Written em Board Exam

Nailing the Written
Emergency Medicine
Board Examination
Bobby Desai
Brandon R. Allen
Editors
123
Nailing the Written Emergency Medicine
Board Examination
Bobby Desai • Brandon R. Allen
Editors
Nailing the Written

Emergency Medicine
Board Examination
Editors
Bobby Desai, MD, FACEP Brandon R. Allen, MD
Department of Emergency Medicine Department of Emergency Medicine
University of Florida College of Medicine University of Florida College of Medicine
Gainesville, FL Gainesville, FL
USA USA
ISBN 978-3-319-30836-4 ISBN 978-3-319-30838-8 (eBook)

DOI 10.1007/978-3-319-30838-8
Library of Congress Control Number: 2016946055
© Springer International Publishing Switzerland 2016

This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is
concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction
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The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not
imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and
regulations and therefore free for general use.
The publisher, the authors and the editors are safe to assume that the advice and information in this book are
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Printed on acid-free paper
This Springer imprint is published by Springer Nature

The registered company is Springer International Publishing AG Switzerland
For my wife Katie and children Nila and Owen
–Brandon R. Allen
For Alpa, Jayden, Dylan, and Shayan
Your support in this endeavor has been incredible
–Bobby Desai
Contents
Cardiovascular Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
Bobby Desai
Pulmonary Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Michael R. Marchick and Bobby Desai
Gastroenterology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 185
Brandon R. Allen and Bobby Desai
Nephrology and Urology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 261
Bobby Desai
Hematologic and Oncologic Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 309
Bobby Desai
Disorders Affecting the Skin . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349
Bobby Desai
Endocrine/Metabolic/Electrolytes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 389
Bobby Desai
Ears, Nose, and Throat . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 467
Bobby Desai
Environmental Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 517
Neurologic Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 555
Obstetrics and Gynecology. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 617
Bobby Desai and Alpa Desai
Ophthalmology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 637
Bobby Desai
Toxicologic Emergencies. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 675
Matthew Ryan and Bobby Desai
Orthopedic Emergencies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 735
Bobby Desai
Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 813
Henry Young II and Bobby Desai
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 869
vii
Contributors
Brandon R. Allen, MD Department of Emergency Medicine, University of Florida College

of Medicine, Gainesville, FL, USA
Alpa Desai, DO Community Health and Family Medicine, University of Florida College of
Medicine, Gainesville, FL, USA
Bobby Desai, MD, MEd Department of Emergency Medicine, University of Florida,
Gainesville, FL, USA
Michael R. Marchick, MD Department of Emergency Medicine, University of Florida
College of Medicine, Gainesville, FL, USA
Matthew Ryan, MD, PhD Department of Emergency Medicine, University of Florida,
Henry Young II, MD Department of Emergency Medicine, UF Health at the University of
Florida, Gainesville, FL, USA
ix
Cardiovascular Emergencies
Bobby Desai
Contents
Acute Coronary Syndrome 2
Other Causes of Acute Coronary Syndrome 4
Stable and Unstable Angina 6
Acute Myocardial Infarction 7
Arteries and Affected Areas 9
Inferior MI Specifics 13
Right Ventricular Infarction 15
Cardiac Markers 16
Reperfusion in AMI 18
Complications in AMI 22
Congestive Heart Failure 24
Valvular Emergencies 31
Mitral Regurgitation 33
Mitral Valve Prolapse 35
Aortic Stenosis 37
Causes of Aortic Regurgitation 39
Infective Endocarditis 42
Rheumatic Heart Disease 48
Cardiomyopathies (CM) 50
Myocarditis 56
Pericarditis 59
Cardiac Tamponade 62
Abdominal Aortic Aneurysm 64
Aortic Dissection 67
B. Desai, MD, MEd

Department of Emergency Medicine, University of Florida,
e-mail: [email protected]
© Springer International Publishing Switzerland 2016 1
B. Desai, B.R. Allen (eds.), Nailing the Written Emergency Medicine Board Examination,
DOI 10.1007/978-3-319-30838-8_1
2 B. Desai
Hypertension 72
Pulmonary Hypertension 76
Syncope 77
Deep Venous Thrombosis and Pulmonary Embolism 79
Acute Limb Ischemia 87
Pacemakers 89
Left Ventricular Assist Devices (LVAD) 94
EKG Changes Related to Electrolytes and Metabolic Conditions 96
EKG Changes Related to Medications 100
Dysrhythmias 102
Heart Blocks 118
Miscellaneous 127
Acute Coronary Syndrome
Acute Coronary Myocardial

Stable Angina Unstable Angina
Syndrome Infarction
Acute Coronary Number 1 cause of

Syndrome death in the U.S.
Location of Retrosternal left

OR Epigastric region
Angina Pectoris? chest area
Description Radiation
Either
Pressure Crushing Squeezing Diffuse Chest Either Arm Either Hand
Shoulder
May indicate a higher

probability of ACS!
Sharp
Beware of pain May STILL be

described as Stabbing
angina!
Pleuritic
Cardiovascular Emergencies 3
Angina Pectoris
Angina
2–20
Can be minutes
Angina Pectoris Time
variable AMI
Can last
hours
Typically with Associated Classically occurs

exertion symptoms with
B
u
t
N/V Sweats SOB
Can be at rest!
2-fold higher risk

of ischemia Cold Exercise Stress
Plaque Coronary
Rupture Spasm
Classic Cardiac Risk Factors
Prinzmetal’s HTN
Angina Hypercholesterolemia
Diabetes
Poor predictors of ACS!
ACS Physical Exam
Normal
Appearance may vary
Severe distress
Normal
Chronic Hypertension
Blood pressure varies Elevated
Anxiety
Extremes of BP can
be associated with
a worse prognosis Decreased Heart Failure
Decreased preload
RV infarction
Rales
May represent new
Ominous Physical Findings onset
CHF + Cardiogenic shock
S3
4 B. Desai
Pathophysiology
Initial Repeated injury to Atherosclerotic Rupture of the Platelet

Pathophysiology blood vessel walls plaque forms plaque aggregation
Results in vessel Release of

stenosis thrombogenic
substances
After
Vessel occlusion Hypoxia Cell death
aggregation
Time & amount of

hypoxia
determine
Unstable Angina
vs. MI
25–40 % loss
CHF
ventricular function
Affects
Affects pump
Cardiac output
function
>40 % loss Cardiogenic Blood pressure
ventricular function Shock
Effects of myocardial
cell death
Tachydysrhythmias Higher degree blocks

2 o Type II Block
Anterior MI
Dysrhythmias & Type III Block
Extensive MI?
AV Blocks
Type 1 AV Block Ventricular
Inferior MI dysrhythmias
Other Causes of Acute Coronary Syndrome
Vasculitis or other
connective tissue
disease
Lupus
Kawasaki disease
Congenital
Drugs
anomalies
Cocaine
Other Causes of
Thrombotic Acute Coronary
Emboli
processes Syndrome
DIC, TTP + Bacteria
Infectious
diseases
HIV
Cocaine and Chest Pain
Potential coronary
Cocaine effects Vasospasm Due to a–agonism ischemia
May cause premature

Cocaine abuse coronary disease
Only 5–6 % will

Cocaine use Chest pain Acute MI have MI!
MI present with May cause unopposed

cocaine use? Treat the same But… No b–Blockers a–agonist effect
Unopposed a– Worsened Extremely high

agonism vasospasm BP
Treatment Nitroglycerin Benzodiazepines
Atypical Chest Pain
Populations with atypical chest pain
Immune
Women Minorities Elderly Diabetics Lupus
compromised
HIV on HAART
Atypical presentations are typical in

this population
The chest pain may be different
Can occur at Can occur with

rest stress
Associated Sx in Nausea +
Jaw pain Neck pain Back pain
women? Vomiting
Other atypical findings
Pain unrelated Pain relieved Weakness and No chest pain

Palpitations
to exertion with antacids fatigue at all
6 B. Desai
Stable and Unstable Angina
Stable angina Fixed plaque
Pain of stable Crescendo-

Exertional
angina? Decrescendo pattern
Relieved by? Nitroglycerin Rest
Pitfall of stable May progress to

angina? Unstable Angina & Myocardial Infarction
Change in chest Frequency,

Unstable angina Unstable plaque
pain Intensity, Duration
New-onset chest
Unstable angina
pain?
Pain of unstable NOT Palliated by

Exertional OR Rest
angina? nitroglycerin or rest
Greater than 20
Pain duration?
minutes
Pitfall of Have high risk of

unstable angina? Myocardial Infarction & Death
Prinzmetal’s or Variant Angina
Prinzmetal’s Angina
May NOT have

Coronary artery ST-elevation evidence of coronary
Occurs at rest
spasm occurs disease at
catheterization
Similar to STEMI
EKG
EKG
What Factors Predict Prinzmetal’s Angina?
ST elevation
Concave upwards
Convex upwards
May be difficult to
Transient
distinguish with STEMI
Minutes
Prinzmetal’s
Angina
Consider in No reciprocal ST
women depression
More common
No dynamic
changes
Acute Myocardial Infarction
Single best test Should be done within 10 Up to 5 % will be

EKG But…
to perform in ED minutes of arrival to ED NORMAL
EKG’s in AMI
Normal Nonspecific Diagnostic

5–10 % 50–70 % 40–50 %
New ST- ≥ 1 mm elevation in two Positive predictive The elevation typically occurs
elevations anatomically contiguous leads* value for AMI >90 %! over the area of ischemia
Reciprocal ST depression over on ekg areas Predicts increased Predicts potentially larger
changes opposite areas of infarction mortality infarction
New ST-depressions Positive predictive

& T-wave inversions value for AMI only 20 %
ST Segment Transmural Involves full-thickness “Q-wave” “Significant Q wave”= .04 mm

Elevated? infarction of myocardium MI wide & 1/3 the height of R wave
NO ST Segment Subendocardial Does not involve full- “Non Q-wave”

elevated? infarction thickness of myocardium MI
Subendocardial Initially may have lower The long term prognosis

infarction morbidity and mortality is the same or worse ST elevation followed
by T wave inversion
may signify
(*) Except in V2-V3
improvement
Women = 1.5 mm
Men less than 40 = 2.5 mm
Men over 40 = 2 mm
8 B. Desai
How Is the EKG Helpful?
EKG
Identifies
Quickly shows who Conduction
Identifies the STEMI requires emergent Abnormalities Aids in localization
reperfusion of infarction
Dysrhythmias
vs.
May guide
specific
therapy
Non-diagnostic or
Continuous EKG
other “concerning”
monitoring may
findings
show evidence of
reperfusion after e.g., Avoidance
thrombolytic therapy of nitroglycerin
for Inferior MI
The EKG in Acute Myocardial Infarction

Posterior
R>S waves
+ R wave should
ST depression V1 & V2 be >.04 mm
Upright T waves
Right Ventricular
II, III, avF
(Inferior injury) Lateral
+ I, avL, V5, V6
1 mm ST elevation V4R
Anterior
V1–V4
Septal
V1, V2
Inferior
II, III, avF
Causes of ST-Segment Elevation
Acute MI
Bundle branch blocks Prinzmetal’s angina

Vasospasm
Causes of ST
elevation
Ventricular wall
Early repolarization
aneurysm
Usually benign Post-MI
Pericarditis
Global ST elevation
All ST-segment elevation IS

NOT MI!
Arteries and Affected Areas
Posterior Right Coronary
Right Ventricular
Usually accompanies inf MI
4–5 % will be isolated
ALWAYS Right Lateral

Coronary
Inferior Sinus Node Right Coronary (60 %) Septal

Circumflex (40 %)
AV Node Right Coronary (90 %)

Circumflex (10 %)
Anterior MI
Right Coronary (80 %) Left Anterior
Circumflex (20 %) Septal Left Anterior Descending
conduction Descending (100 %)
10 B. Desai
Anterior MI
Center image (Reprinted from Davies A, Scott A. Acute coronary syndromes. In: Davies A, Scott A, editors. Starting to read ECGs (The basics).
New York: Springer Science; 2013. p. 147–59. With permission from Springer Science + Business Media)
Hyperacute T Waves
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
What Factors Predict MI on the EKG?
ST elevation
Horizontal
Convex upwards
Specific for coronary

Q waves
anatomy
After time
Myocardial
Infarction
ST depression
HyperacuteT waves
in reciprocal leads
Occurs early
Dynamic changes
Changes with time
What Factors Predict Early Repolarization?
ST elevation
Concave upwards
Precordial leads
J-point elevation
NOT specific for
No Q waves
coronary anatomy
Early
Repolarization
No reciprocal ST
Men, Young
depression
Muscular
No changes with
time
12 B. Desai
Anterior MI Specifics
Poor prognostic Infarction of

Heart block Due to
sign conduction tissue
Type II 2° Heart Block Potential progression to Consider Transcutaneous

Especially bad Due to
associated with anterior MI? complete heart block or Transvenous Pacing
Sinus Tachycardia
Left ventricular
Pericarditis Anxiety Pain Hypovolemia
failure
Continued sinus tachycardia

carries a poor prognosis
The EKG and Emergent Reperfusion
Emergent Reperfusion
Old Left Bundle Branch

ST Elevation ≥ 1 mm in New Left Bundle Branch
Block with Sgarbossa
2 contiguous leads* Block
criteria
But…new STEMI guidelines from

2013 say this is not a STEMI w/o
ACS symptoms and/or Sgarbossa
Don’t forget about a Posterior criteria
MI!
(will look like ST depression)
Concordant ST ST Depression ≥ 1 mm Discordant ST elevation

Elevation ≥ 1mm in any in V1–V3 ≥ 5 mm
lead
Concordant Same direction as QRS
Discordant Opposite direction as QRS
(*) Except in V2-V3
Women = 1.5 mm
Men less than 40 = 2.5 mm
Men over 40 = 2 mm
Sgarbossa Criteria
Sgarbossa’a Criteria
LBBB/Paced Rhythm V1, V2, V3
≥ 5 mm
Concordant ST Concordant ST
ST elevation > 5 mm in
elevation > 1 mm in depression > 1 mm in
leads with a (–) QRS
leads with a (+) QRS V1–V3
Center image (Reprinted from Allen B, Ganti L, Desai B. Cardiology. In: Allen B, Ganti L, Desai B, editors. Quick hits in emergency medicine.
New York: Springer Science; 2013. p. 71–82. With permission from Springer Science + Business Media)
Inferior MI Specifics
Inferior wall MI
complications
May have
Hypotension Bradycardia conduction
disturbances
Consider Atropine if
Increase preload with required Mobitz I (Wenkebach)
fluids
May need
transcutaneous or
transvenous pacing if
Usually will
refractory to Intermittent
NOT progress
atropine during the first
to higher
3 days
degree blocks
14 B. Desai
Inferior MI
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
Inferior-Posterior MI
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Right Ventricular Infarction
Right ventricular Complicates up to Isolated RV infarction is

infarction 40 % of inferior MI extremely uncommon
Right ventricular Very preload Can develop severe hypotension in response Treated with
infarction sensitive to nitrates or other preload-reducing agents fluids
EKG in RV ST elevation in V1 is the only standard EKG lead that

Infarction? V1 looks directly at the right ventricle
Other EKG ST elevation in Lead III is more “rightward facing” than lead II & more
Tidbits? lead III > lead II sensitive to the injury current produced by the right ventricle
Highly specific EKG If the magnitude of ST elevation in V1 If the ST segment in V1 is isoelectric and the
changes for RV MI? exceeds the magnitude of ST elevation in V2 ST segment in V2 is markedly depressed
Confirmation of Presence of ST elevation in the The most useful Sensitivity of 88 %, specificity of 78 %

RV Infarction? right-sided leads (V3R–V6R) lead is V4R and diagnostic accuracy of 83 %
Right Ventricular Infarction
I aVR V1r V4r
II aVL V2r V5r
III aVF V3r V6r

16 B. Desai
Posterior Infarction
Posterior Accompanies Usually occurring in the context Isolated posterior MI is less

infarction 15–20 % of STEMIs of an inferior or lateral infarction common (3–11 % of infarcts)
Posterior extension of an Implies a much larger area Increased risk of left ventricular
inferior or lateral infarct? of myocardial damage dysfunction and death
Isolated Posterior Indication for emergent Lack of obvious ST elevation in this condition
But…
infarction? coronary reperfusion means that the diagnosis is often missed
EKG in Posterior Horizontal ST Tall, broad R Dominant R wave

Upright T waves
MI (V1–V3) depression waves (>30ms) (R/S ratio > 1) in V2
EKG Leads V7–9 are placed on

Posterior leads
considerations the posterior chest wall
Cardiac Markers
Rise 1–2 hours Tidbits

Earliest detection
Myoglobin
Peak 4–6 hours
Poor specificity
Duration 24 hours (caution in renal failure, trauma)

More specific than CK-MB
CK-MB
Peak 12–24 hours
Marked elevations predict higher
complications and increased
Duration 1–2 days mortality

May have elevation due to
Troponin means other than MI
Peak 12–24 hours
Must compare MB with total CK

Duration 7 days to improve specificity
Other Reasons for Troponin Elevation
Heart block
Tachy or
Stroke or SAH
Bradyarrhythmias
Renal Failure Sepsis
Aortic dissection Hypertrophic Obstructive

Cardiomyopathy
Rhabomyolysis
Cardiac contusion
with cardiac injury
Other Reasons for
Troponin Elevation Coronary
Burns > 25 % BSA
vasospasm
Aortic valve
CHF
disease
Myocarditis Renal Failure
Infiltrative Pulmonary
diseases embolism
Drug toxicity
or toxins
Initial Therapy for ACS
Considering ACS? History + PE + EKG Cardiac monitor Stabilize ABC’s as required
Glycoprotein Iib/IIIa
Oxygen Aspirin Nitrates Morphine Heparins β-Blockers ACE Inhibitors P2Y12inhibitor
Inhibitors
>162–325 mg Sublingual Antiplatelet agent
Non-enteric Topical Consider for
Anti-arrhythmic
Reduce LV
persistent
When added to Indications
(Delays Intravenous ASA -Reduces dysfunction
absorption) pain (+) troponins
risk of AMI and Decreases onset
Anti-ischemic Pts getting PCI
death in of CHF Reduces
Unstable Angina platelet
Contraindicated if
Lowers BP aggregation
Reduces mortality by Phosphodiesterase-5 Use caution for
23 % inhibitors (eg Sildenafil) inferior MI’s! By 56 %! Mechanism Start within
within 24 hours Beware Can give if
24 hours
CHF Blocks binding aspirin
Hypotension of fibrinogen allergic!!
LMWH +ASA = Asthma at receptor
May cause fatal Better with Inferior/RV site that
hypotension! fibrinolysis infarction causes
ASA + Fibrinolytic Bradycardia aggregation In
Therapy reduces USA/NSTEMI
ischemic events Reduces:
Mechanism LWMH = Less Death
thrombocytopen Most AMI
Peripheral + Coronary ia Stroke
Effective
vasodilation Give orally Pts getting
within 24 PCI
LMWH = NOT hours
Decreased Reduces infarct
1st line for PCI
cardiac work size
42 % reduction in
mortality
LMWH = Do not Administer early in
use in renal patients along with
Decreased O2
Improves failure! (Use ASA regardless if
function Heparin) PCI or conservative
demand
management is
planned
Use LMWH in
Decreases
USA
complications
Afterload
reduction
CABG =
withhold for 12–
Decreases 24 hours
mortality by 35 %
Titrate nitroglycerin to Blood

Pressure reduction, not chest pain
resolution
18 B. Desai
Reperfusion in AMI
PCI Thrombolysis Potential benefit

Outcomes better with PCI if provided in a timely manner Cardiogenic shock
≤90 minutes
Constant CP for >6
hours
The longer the symptoms the better the benefit with PCI
Better at Decreases Decreases

Decreases Decreases
establishing death short and intracranial
re-occlusion re-infarction
flow long term hemorrhage
For PCI
Use Glycoprotein IIb/IIIa
inhibitors! (In consultation
with cardiologist
Reduces death
Early PCI in NSTEMI (24–48°) Reduces recurrent ACS
Reduces MI
Use in severely Use for refractory

unstable patients angina
Reperfusion in AMI (2)
EKG findings
Fibrinolytics Indicated for 1 mm ST elevation
Act as Plasminogen activators in 2 or more
STEMI (if PCI contiguous leads
unavailable)
Improves left New LBBB

Improves mortality (controversial)
ventricular function
But… <6–12 hours from

May not fully restore coronary blood flow in 40–50 % of patients! onset (at least >30
min)
After fibrinolytics
Give full-dose anticoagulants for 48 hours
Absolute Contraindications PCI available
Known
Hx intracranial Known cerebral Ischemic stroke Active internal Aortic Dissection
intracranial
hemorrhage AVM in last 3 months bleed or Pericarditis
neoplasm
Relative Contraindications
Hx chronic Other known

Uncontrolled BP Prior ischemic Known bleeding
severe intracranial INR >2–3
(>180/110) stroke >6 months diathesis
hypertension pathology
Noncompressible
Recent trauma Prolonged CPR Major surgery Active Peptic
vascular Pregnancy
(last 2 weeks) (>10 min) (<3 weeks) Ulcer Disease
punctures
Conditions with
Recent internal
potential risk of
bleeding
bleeding
20 B. Desai
Thrombolytic Therapy Complications
Internal Bleeding Intracranial Bleeding Allergic Reactions
2–10 % Approx 1 % Usually minor

Always High mortality
Type and Screen
Beware
Elevated Blood Pressure
Older age >65
Successful Thrombolytic Therapy
Early T-wave
Reperfusion Resolution of ST Resolution of chest inversions may be
Arrhythmias elevation pain highly specific for
reperfusion
Accelerated
idioventricular
rhythm
(highly specific)
Successful Thrombolytic Therapy
Early T-wave
Reperfusion Resolution of ST Resolution of chest inversions may be
Arrhythmias elevation pain highly specific for
reperfusion
Accelerated
idioventricular
rhythm
(highly specific)
Accelerated Idioventricular Rhythm (AIVR)
Return of
Reperfusion phase spontaneous
post-MI circulation following
Most common cause cardiac arrest
Drugs & Medications Heart Disease

Digitalis toxicity Congenital
Sympathomimetics Causes of AIVR Myocarditis
Volatile anesthetics Cardiomyopathy
Metabolic &
Electrolyte
derangements
AIVR: EKG Changes
Rate QRS Complex Rhythm Other
3 or more
50–120 bpm Wide Regular ventricular
complexes
>120 ms Fusion &

Capture beats
present
AIVR Treatment
AIVR
Self-limited Hypotensive? Consider atrial

No treatment pacing
required
22 B. Desai
Complications in AMI
Days after MI Weeks

1 2 3 4 5 6 7 2 >4
Pericarditis
2–7 days post event Ventricular aneurysm
Dressler’s Syndrome
Occurs in 20 % of MI’s formation
NSAID’s May take months to
Fever, friction rub
form
Associated with
Papillary muscle rupture Elevated WBC
chronic ST elevations
3–5 days post event Pericardial & pleural
effusions
Occurs in 1 % of patients
Treatment
Myocardial wall rupture
NSAID’s & steroids
1–5 days post event
Accounts for 10 % of
AMI deaths
Other complications
Recurrent chest Right ventricular Acute mitral Interventricular

CHF Embolism
pain infarction regurgitation septum rupture
Associated with From mural Surgical Anterior or inferior MI
Continued inferior MI thrombus emergency
Cardiogenic shock Results in acute VSD
ischemia vs. RV loses pump
reinfarction function
> 40 % necrosis of LV
Ventricular Significant New holosystolic
Heart becomes Dyspnea
aneurysm pain murmur
preload dependent
Caution with ntg May take months to
High mortality PTCA or CABG develop
& morphine Treatment
Fluids IABP
Liberal use of fluids
Inotropes to augment Afterload Balloon
Surgery
preload reduction pump
What Factors Predict Ventricular Aneurysm on EKG?
ST elevation
Concave upwards or
Convex upwards
Continued ST
elevation
Usually in anterior
leads
NO reciprocal ST
Q waves
Ventricular depression
Usually present Aneurysm
No dynamic changes
No change in old
EKG’s
Rhythm Abnormalities in AMI
May occur in 75–100 %

of patients treated in a CCU
e Ma
aus yc
yc au
Ma se
Related to
Hemodynamic Increases chances for
instability ventricular tachycardia &
Size of ventricular fibrillation
Location
infarction
Anterior MI Worse prognosis Due to Death of conduction tissue

Especially if new BBB
May require early pacing
develops
Sinus Bradycardia May predispose to Hypotension Ventricular dysrhythmias
But
...
May be protective Does NOT increase mortality
Due to decrease in
myocardial O2 demand
PVC’s Don’t treat! Idioventricular Rhythm? Reperfusion!

PVC’s & PAC’s have good prognosis
Sustained ventricular
Early ventricular
tachycardia OR Large infarction ACLS and emergent
> 150 bpm? fibrillation reperfusion
Due to ischemia
Tachycardia in AMI Hemodynamic Abnormal

Hypotension Reperfusion
instability automaticity
Abnormal vagal
New Atrial Fibrillation tone
Atrial infarction Sustained atrial
Electrolyte
± increased atrial fibrillation =
Typically in 1st 24 hours derangements pressures
Usually transient Hypokalemia anticoagulation
Sinus &/or AV nodal
Marker of worse prognosis ischemia
Hypo-Mg Pericarditis 3-fold risk of embolization
Conduction Disturbances in AMI
Good prognosis
Type 1 second
3° AV Block
degree AV block
Wenckebach With INFERIOR MI
ONLY!
Poor prognosis
Type 2 second Persistent

3° AV Block
degree AV block
Sinus Atrial
SVT
Can progress to 3° From ANTERIOR MI tachycardia fibrillation
Increased risk of mortality

New RBBB with Left posterior
New LBBB
hemiblock hemiblock Increased risk of pump failure
Increased mortality Large infarct
Death of
Anterior MI High grade blocks Pacemaker
conduction tissue
24 B. Desai
Congestive Heart Failure
Heart Failure Pathophysiology
Heart Failure
Acute Subacute Chronic
Decompensated
CHF
Acute Acute MI
pulmonary
edema
Cardiogenic shock
The heart is unable to maintain an output

necessary for adequate tissue perfusion
The heart is unable to clear

venous return
Inadequate stroke volume
Depends on
Preload Afterload Contractility

Causes of Heart Failure
Myocardial
Hypertension Dysrhythmias “-itis’es” Aortic Dissection
ischemia
Acute & Chronic Pericarditis
Papillary muscle Myocarditis
rupture Cardiac tamponade Endocarditis
Chordae tendinae (infectious)
Pulmonary
rupture Mitral stenosis embolism
Mitral
Mitral regurgitation
Valvular disorders Aortic stenosis

Aortic
Aortic insufficiency
Prosthetic valve malfunction
Intrinsic myocardial
process Myxedema
Metabolic
Acquired Thyrotoxicosis
cardiomyopathy
Hypertrophic Toxic Cocaine
cardiomyopathy
Restrictive Alcohol
cardiomyopathy
Dilated
cardiomyopathy
High-Output Failure
Paget’s disease of
Anemia Beriberi Thyrotoxicosis A-V Fistula
bone
Systolic Heart Failure (Heart Failure Reduced Ejection Fraction)
Normal ejection
60 %
fraction
Systolic heart Most common

Ejection fraction 40 %
failure Ischemic heart disease
Inability of heart Increased amount of blood Increased intracardiac

to pump blood remaining in heart after systole pressures
Increased intracardiac Inability of heart Pulmonary

Exercise or Stress
pressures to compensate edema
Low cardiac C Renin &

C Afterload
output Angiotensin levels
26 B. Desai
Diastolic Heart Failure (Heart Failure Preserved Ejection Fraction)
Common in elderly women

30–50 % of elderly patients have CHF due to diastolic dysfunction
Diastolic heart Left ventricular hypertrophy
failure
Chronic hypertension
Coronary artery disease
Normal ejection
Contractility Normal
fraction
LV filling is decreased
Ventricular Left ventricle cannot C Atrial pressure
Impaired
relaxation receive blood
Preload dependent
Pulmonary congestion
Too much Preload Due to inadequate

Hypotension
diuresis dependency ventricular filling
Diastolic Systolic
May lead to
dysfunction dysfunction
Left Versus Right Heart Failure
Symptoms & Signs–Isolated Left-sided Failure
Paroxysmal
Dyspnea Orthopnea JVD Cough Weakness
nocturnal dyspnea
Hepatojugular
Fatigue
reflex
Symptoms & Signs – Isolated Left-sided Failure
Peripheral Right upper Hepatojugular

JVD
edema quadrant pain reflex
Due to liver
engorgement
Most common cause

Left heart failure
of right heart failure
Heart Failure Clinical Features and Presentation
Days
1 2 >7
Hypertensive acute CHF Hypotensive acute CHF Normotensive acute CHF

Most common acute presentation Poorest prognosis ~45–50 %
≥50 % ~3–5 %
Tachycardia
Hypotensive acute CHF
Dyspnea
Systolic BP < 90 mm Hg Rales
Altered mental status Symptoms Signs
Narrow pulse pressure
Decreased urine output
Pulmonary edema May have evidence of
end-organ damage Cool extremities
Tachycardia
Normotensive acute CHF
Less dyspnea
Symptoms Normal LV function Signs Rales
(may not be present)
Weight gain May have little edema on
CXR Peripheral edema
Hypertensive acute CHF

Dyspnea Tachycardia
Symptoms Normal LV function Signs
Weight gain Systolic BP > 140 mm Hg Rales
Tachycardia
Severe dyspnea Acute (Flash) Pulmonary
Edema
Symptoms Signs Significant rales & JVD
Usually pts are
Weight gain hypertensive
Cool, diaphoretic skin
28 B. Desai
CHF Diagnosis
Exam
Peripheral
Tachycardia ± Rales S3 JVD Orthopnea Dyspnea
edema
Specificity of Specificity of
99 % 94 % Hepato-jugular
RUQ pain
reflux
If present,
Liver
worse
engorgement
outcomes
Enlarged,
pulsatile liver
CXR Up to 20 % will not have CXR may not show acute

Sensitivity for CHF is low congestion on CXR! abnormalities for up to 6 hours!
Pulmonary Alveolar Prominent Superior

Cardiomegaly Pleural effusion
congestion edema vena cava
Kerley B lines
Upper lung field
hyperemia Labs
Overall increase
in vascular BNP
markings Recommended to aid in
Dx or exclusion of acute Suggests Dx other than
Low
CHF CHF
Obese pts may have But…should not be
Echo/US lower levels used by itself!
Consider lung US for BNP is helpful for

B lines prognosis – elevated
BNP levels are Chronic BNP Increase of 50% from
associated with elevation? baseline is relevant
Confirmatory
increased risk of
death or heart failure
within 6 months
CHF Treatment: General
Supplemental Oxygen
Mild
Pt with CHF Maintain airway
Consider noninvasive Ventilation
exacerbation Moderate control
ventilation
Hemodynamically stable,
Se
ver cooperative pts
e
Endotracheal intubation
Hemodynamically unstable
Preload reduction Afterload reduction Inotropes
IV Nitroglycerin
Nitrates Dobutamine
ACE inhibitors
Diuretics Dopamine
Nitroprusside
Increased mortality
Increased ICU admission rate

Adverse
Morphine
events
Increased need for mechanical ventilation
Use for pain
control only! Prolonged hospitalization
E.g., STEMI
30 B. Desai
CHF Treatment: Specific
Hypotensive Heart Failure

Least common presentation
Always consider ACS as the cause STEMI? Cath Lab
Milrinone
Systolic
Hypotension? Inotropic agent Dobutamine
90–100 mm Hg
± Dopamine
Hypertensive CHF & Acute Pulmonary Edema
Sx improve
Heart is sensitive to Titrate nitroglycerin
Start Nitroglycerin
Afterload rapidly
Until OR
SL first Until BP is
IV if needed BP improves controlled
Increased Worsened renal Use IV diuretics in settings

Diuretics alone Vasodilator
mortality function of volume overload
No improvement Consider May prolong

IV ACE inhibitor?
with IV nitroglycerin? IV nitroprusside survival
Vasodilation Preload
contraindications dependent states
Preload Volume Hypertrophic

RV infarction Aortic stenosis
dependent states depletion cardiomyopathy
Non-cardiogenic Pulmonary Edema
Amniotic fluid
emboli
Strangulation
Toxins
Non-Cardiogenic Salicylates
Pulmonary Phenobarbital
Edema
Carbon monoxide
Fat emboli Opioids
Environmental
High altitude
pulmonary edema
Thermal injury
Drowning
Valvular Emergencies
New Murmur
Anemia Pregnancy
Systolic Murmur Normal Heart Consider High output state
Thyro-
Fever
toxicosis
Diastolic New murmur Urgent Cardiology

OR Echocardiogram
Murmur with Sx at rest referral
Emergent
Echocardiogram Admission
ere Cardiology referral
Sev
Symptoms
No
t se
ver Outpatient
e
Symptoms are most referral
important to
consider, not the
murmur
New Systolic
Syncope Aortic Stenosis
Murmur
Until proven
otherwise New Aortic Surgical
Regurgitation? emergency
Pregnant New Murmur Mitral Stenosis
Until proven
otherwise
32 B. Desai
Mitral Stenosis
Pathophysiology Rheumatic Heart

Tidbits Women > Men
Disease
Prevents Most common

normal diastolic cause
filling
Tricuspid &
d to Pulmonary
May lea valve failure
Decreased
Left Atrial Pulmonary Pulmonary
flow out of the May lead to May lead to
Enlargement Congestion Hypertension May
left atria
lead Right sided
to
Failure
May lead to
May lead to
Ascites
Hepatomegaly
Atrial Pulmonary JVD
Fibrillation Edema Peripheral edema
Symptoms
Exertional Paroxysmal Acute Pulmonary Premature atrial

Hemoptysis Orthopnea
dyspnea Nocturnal Dyspnea Edema contractions
Most May be
common massive
complaint
Systemic Atrial Right sided

emboli Fibrillation failure
20–30 %
Mitral Stenosis Diagnosis
Exam
Diastolic rumble in Opening snap

Loud S1
Mitral area
EKG CXR Echo
Left heart border Loss of pulmonary Left atrial

Biphasic P waves Confirmatory
straightening window enlargement
Right Axis Pulmonary

Deviation congestion
Kerley B lines
Upper lung field
hyperemia
Atrial Fibrillation Overall increase
in vascular
markings
Mitral Stenosis Treatment
Pulmonary
Diuretics
congestion?
Cardioversion
Atrial Other treatment depends
Anticoagulation
Fibrillation? on stability of patient
Medications
High risk of
Anticoagulation
embolism?
Hemoptysis Blood Cardiothoracic

Bronchoscopy
considerations transfusions surgery consultation
Depends on
Disposition
clinical condition
Mitral Regurgitation
MI
MI Blunt Trauma Rheumatic Heart Disease

Papillary muscle Rare
dysfunction Most common cause
Pathophysiology Acute Chordae Rarely
tendinae rupture spontaneous
Chronic Collagen Vascular Disease
Mitral valve
does not close Infective Appetite-suppressant Most patients
endocarditis medications Mitral valve prolapse
adequately
Valve leaflet Phentermine Mitral annulus calcification
perforation Dexfenfluramine
Fenfluramine
Dilated Cardiomyopathy
Retrograde
Left Ventricle Retrograde
blood flow Left Atrium
Blood to
(systole)
Acute retrograde Sudden increase in Sudden increase in Right Early Right sided
flow Left Atrial Pressure Ventricular Pressure Failure
Pulmonary edema
Decrease in stroke Cardiogenic

volume & cardiac output Shock
Chronic Gradual increase in Gradual increase in Right Late Right sided

retrograde flow Left Atrial Pressure Ventricular Pressure Failure
Left atrial enlargement

& compensation
34 B. Desai
Mitral Regurgitation Symptoms
Dyspnea
Cardiogenic
shock
Acute Pulmonary May lead
Acute Symptoms Edema & CHF to
Cardiac Arrest
Right sided failure
Exertional dyspnea
1st symptom
May be
Compensated CHF prompted by
Chronic
Symptoms
± Atrial Fibrillation
Thromboembolism
Mitral Regurgitation Diagnosis

Exam
Holosystolic Palpable heave

Thrill
murmur during systole
EKG CXR Echo
Left atrial
Cardiomegaly Confirmatory
enlargement
Left ventricular Pulmonary

hypertrophy congestion & CHF
Kerley B lines
Upper lung field
hyperemia
Atrial Fibrillation Overall increase
in vascular
markings
Mitral Regurgitation Treatment
Severe acute Afterload ICU Balloon Emergency

MR? reduction admission pump surgery
Depends on
Treat Atrial
Chronic MR? Treat CHF Disposition clinical
Fibrillation
condition
New onset Cardioversion

Other treatment depends
Atrial Anticoagulation
on stability of patient
Fibrillation? Medications
High risk of
Anticoagulation
embolism?
Mitral Valve Prolapse
Mitral Valve The most common valvular Most have no

Women > Men
Prolapse disorder in developed countries issues
Idiopathic myxomatous Displacement of thickened

Pathophysiology
degeneration of mitral valve leaflets leaflets into left atrium
During systole
Higher rate of Mitral

Male > 45
complications? regurgitation
There is a increased There is a possibility of

Pitfalls
incidence of arrhythmias thromboembolic disease
Symptoms
Most are Atypical Chest

Palpitations Dyspnea Weakness Fatigue
asymptomatic Pain
Not
exertional
36 B. Desai
Mitral Valve Prolapse Diagnosis
Exam
Late systolic S2 may be

Mid-systolic click
murmur diminished
Due to
EKG CXR Echo
Non-specific ST-
Usually normal Diagnostic
T waves changes
Ectopy
PSVT
Mitral Valve Prolapse Treatment
β–Blockers may
Chest pain?
be helpful
Embolic disease Anticoagulation
β–Blockers may
Palpitations?
be helpful
β–Blockers may
Anxiety?
be helpful
Mitral Endocarditis
MVP
Regurgitation Prophylaxis
Depends on
Disposition
clinical condition
Aortic Stenosis
Congenital Calcific Rheumatic

biscuspid aortic Heart
valve stenosis Disease
Most common
Most common Second most
cause in
Pathophysiology younger
cause in common
patients adults cause
Maintain diminishing
Prevents
ejection fraction
systolic
ejection of
Women Men
blood
r to
rde
o
In
Decreased Increased
Left Ventricular Diastolic Ischemia on
flow out of the May lead to Leads to myocardial O2 May lead to
Enlargement dysfunction exertion
left ventricle requirements
Over time
As aortic Decreased
outflow Leads to cardiac
diminishes output
Symptoms
May appear late

New murmur
Paroxysmal Sudden Death

Syncope Chest pain Dyspnea Hypotension
Nocturnal Dyspnea from:
Angina 1st symptom Late finding Arrhythmias
Syncope
Acute LV failure
Classic Triad
Bad prognosis Aortic

Pt with AS is
Atrial Fibrillation Aortic Stenosis Stenosis
“SAD” Due to acute
decrease in cardiac Until proven
output otherwise
38 B. Desai
Aortic Stenosis Diagnosis
Exam
Weak carotid pulse Systolic ejection Narrow pulse Paradoxicsplitting Brachioradial

with delayed upstroke murmur pressure of S2, S3, S4 delay
Pulsus parvus et Radiates into neck Difference Any palpable

tardus between delay between
systolic & the brachial
The pulse is small and and radial
diastolic
rises and falls slowly pulses
pressures <25
EKG CXR Echo
LVH with strain Early disease Normal Confirmatory
Left bundle Late disease

branch block
May have Right
bundle branch
block Left atrial Signs of
LVH
enlargement CHF
Aortic Stenosis Treatment
Symptomatic Avoid strenuous Aortic Valve

Admit
Aortic Stenosis? exertion replacement
Cardioversion
New-onset Atrial Anticoagulation Other treatment depends
Fibrillation? on stability of patient
Medications
Pulmonary
Consider Oxygen Diuretics
Edema
Getting a surgical Prophylactic

procedure? antibiotics
Depends on Avoid strenuous

Disposition
clinical condition exertion
Pitfall - Calcium channel

Beta-blockers Nitrates Vasodilators
Meds to Avoid blockers
Causes of Aortic Regurgitation

Infective
endocarditis
Majority of cases
Aortic Dissection Blunt chest

Acute
trauma
At the aortic root
20 % of cases
2nd most common
Congenital
Biscuspid valves
Ankylosing Chronic Rheumatic heart

Spondylitis hypertension Chronic disease
Rheumatoid Symptoms
Arthritis Collagen-Vascular usually late in
disease disease Marfan’s
Reiter’s syndrome
syndrome
Prognosis worse
Conjunctivitis Appetite- once Sx start
Urethritis suppressant Calcific
Arthritis medications degeneration
Phentermine
Dexfenfluramine
Fenfluramine
Syphilitic Aortitis
Aortic Regurgitation
Aortic valve does

not close
adequately
Most have a slow
CHF Aortic blood
course
retrograde to left
Over time, Due to chronic
ventricle
compromises left ventricular
Pathophysiology (diastole)
systolic function remodeling
Pulmonary
edema Increase in Left
Ventricular End-
Diastolic
Pressure
Volume Overload
Left ventricular
dilatation
Until proven
Acute MI AR Aortic Dissection
otherwise
Infective
Complications CHF Arrhythmias
Endocarditis
40 B. Desai
Aortic Regurgitation Symptoms
Typical May have a spectrum

of disease Acute Worsening
Symptoms
May Cardiogenic
Dyspnea Tachycardia Hypotension Cardiac Arrest
lead to shock
Most
common
presenting
Sx
M
lea ay
d to
Acute Pulmonary Edema & CHF
Aortic Regurgitation Diagnosis
Exam
High-Pitched “Water Austin-Flint

blowing diastolic Duroziez sign Quincke’s sign CHF Signs
hammer” pulse murmur
murmur
To-and-fro Pulsatile Diastolic Tachycardia
Lower left Quick rise due femoral blushing of nail rumbling Tachypnea
sternal border to increased murmur beds murmur Rales
stroke volume,
then rapid
collapse due to
fall in diastolic
pressure
EKG in Acute AR EKG in Acute AR EKG in Chronic Echo Contrasted CT

with dissection AR scan
Non-specific Confirmatory May be used to

Ischemic
LVH diagnose aortic
changes
dissection
Most common Will not assess
finding Aortic
valvular
Dissection?
Sinus function
Tachycardia
ST-elevation
Inferior leads Left atrial

enlargement
Transesophageal
Echo
The CXR in Aortic Regurgitation
CXR in Chronic
CXR in Acute AR AR
LVH
Acute Pulmonary Cardiac
enlargement Cardiomegaly
Edema
LAE
Kerley B lines
Upper lung field
hyperemia
Overall increase Aortic Dilatation
in vascular
markings
CHF
CXR Findings with Aortic Dissection
Displacement on
Widened Tracheal Apical pleural Loss of the aortic
Pleural effusion intimal
mediastinum deviation cap knob
calcification
Aortic Regurgitation Treatment
Symptomatic or Acute Immediate surgical

Aortic Regurgitation? Admit Nitroprusside Inotropic agents
intervention
Dobutamine
Augments forward blood Milrinone
Inotropic agents
flow & reduces LVEDP ±Dopamine
Pulmonary
Oxygen Airway control
Edema
Suspected
Antibiotics Surgery
endocarditis?
Afterload Usually started by

Chronic AR? Inotropes
reduction their physicians
ACE Inhibitors Digoxin
Getting a surgical Prophylactic antibiotics In acute AR,

Beta-blockers
procedure? (after replacement) AVOID
Blocks
compensatory
Depends on tachycardia
Disposition
clinical condition
For Acute
Aortic Give Beta-blockers
Dissection
WANT to block
compensatory
tachycardia
42 B. Desai
Infective Endocarditis
Introduction
Infective Endocarditis
Prosthetic valves
HIV infection
M>F Mitral valve prolapse
Prior Hx of
Urban > Rural endocarditis
Pacemakers
IV drug use
Most patients have risk Rheumatic heart

factors or a structural disease
cardiac abnormality
<20 %
Not as common in Poor dental hygiene
children; related to:
Congenital heart
Congenital heart disease disease
Rheumatic heart disease IV drug abuse 15 %
Most have normal Mitral valve prolapse

Nosocomial infections
valves (75 %)
Bicuspid aortic valve
Tricuspid most
>50 % are common (50 %)
>60 years old
S. aureus most
common pathogen
Due to increase in
degenerative valve
disorders and Degenerative heart
replacement disease
S. aureus also
common in Calcific aortic stenosis
prosthetic valve IE (~50 %)
Also due to increase in
invasive procedures
Typically in elderly
Introduction (2)
Valves affected Mitral Aortic Tricuspid Pulmonic
Left side predominates in

native valve IE
Risk factors for Bacterial

mortality in Left Medical therapy
Underlying etiology other
sided native valve CHF without valve
comorbidities than S. aureus
endocarditis surgery
or S. viridans
E.g., DM, HIV, etc.
Pathophysiology
Direct invasion
Valve defects
of endothelium
Pre-existing Intravenous
by virulent
defect drug use
organisms
Congenital
S.aureus
Injury due to
High flow Direct ischemia
Turbulent Endothelium Direct matter present in
strikes
blood flow endocardium damage effect injected material
Talc Cocaine
Deposition Formation Non-bacterial

Transient Colonization
of fibrin and of sterile thrombotic IE
bacteremia of vegetations
platelets vegetations endocarditis
Sterile vegetations
Skin trauma
Mucosa of GI/GU
tracts
Periodontal disease
Acute Versus Subacute Endocarditis
Younger Potential for Higher morbidity

Acute IE patient fulminant course S. aureus
and mortality
50 % will have Organisms may
normal valves be more
virulent
Slower, May be difficult

Subacute IE Older patient Strep.viridans
indolent course to diagnose
Most will have
50–60 %
abnormal valves
44 B. Desai
Left-Sided Versus Right-Sided Endocarditis
Strep. viridans
Left sided S. aureus Emboli CHF
CNS Major
Gram negatives
cause of
Systemic
IV drug users death
Contaminated needles
S. pneumoniae
Pulmonary Less
Right sided S. aureus Emboli Less CHF
infarction mortality
Gram negatives Pulmonary
IV drug users
Indwelling catheters
Organisms
Small # species account

Most common Bacteria
for most cases
Native valves Both Normal valves Abnormal valves

Most common
S. aureus
cause overall
Prosthetic valves
RAPID destruction Myocardial Conduction

S. aureus Pericarditis
of valves abscess abnormalities
Streptococcal Slower disease

endocarditis course
DM
Enterococcal Underlying Underlying risk
endocarditis valvular disease factors
GI/GU procedures
Most common S. aureus

during 1st
Prosthetic valve 2 months S. epidermidis
endocarditis
S. viridans
Late causes Similar to native
Pseudomonas valve endocarditis
Serratia
Organisms (2)
S. aureus Normal valves

Infect
>50 % Tricuspid
IV drug use Contaminated
Skin Flora
endocarditis devices Streptococcal
Abnormal valves
species Infect
Incl. enterococcus Mitral
Aortic
Coagulase (-)
Streptococci
Prosthetic valve Perioperative

endocarditis period S. epidermidis
Candida albicans
Mycotic
Large
prosthetic valve Large emboli
vegetations
endocarditis
Aspergillus
Clinical Findings
Constitutional Cardiac Skin Embolic
Not specific for IE

Emboli to
Early extremities
Murmurs
bacteremia
“Flu-like” Petechiae & Splinter Acute limb ischemia
illness (+) in 85 % hemorrhages
Embolic stroke
Nonspecific Sx N/V
Osler nodes Involving MCA is the
most common CNS Cx
Usually Valve
Malaise Tender nodules
regurgitant incompetence Rupture of
on tips of fingers
& toes mycotic aneurysm
Rupture of
papillary Subarachnoid
Fever
muscle hemorrhage
Janeway
Present in CHF? Rupture of lesions Retinal artery
almost all cases chordae embolism
tendinae Nontender
hemorrhagic plaques Acute monocular
Perforation of on palms & soles blindness
cardiac wall
Elderly? Pericarditis Pulmonary embolic

Roth spots complications
Pulmonary
Immune Retinal infarction
Compromise? hemorrhages with Pneumonia/
central clearing Empyema
May Heart Blocks
NOT Extension of
Antibiotic use? infection into Renal embolic
have
fever the complications
conduction
Renal failure? system Flank pain
Arrhythmias
Hematuria
Severe CHF?
GI embolic
complications
Abdominal pain
Bowel ischemia
46 B. Desai
Diagnosis
Observation High IE
Diagnosis Culture Echo Admission
over time suspicion
There are NO
useful Can evaluate
prediction 3 separate
valvular
rules for IE! sites
abnormalities
Transesophageal
has greater Risk Consider
Fever
sensitivity and Factors IE
There are NO 10 mL for specificity
definitive each bottle
laboratory
tests that can Recommended IV drug
Fever Admission
Dx IE in the for users
ED
Wait 1 hour
between 1st Prosthetic
and last valves Prosthetic
Fever Admission
culture valve
Inadequate
Transthoracic Evidence of
echo New
vasculitis or Admission
No antibiotics murmur
embolization
prior to
cultures High clinical
suspicion of IE
Evaluating
complications
Treatment
Penicillins
Vancomycin
Initial Antibiotic
stabilization therapy May include Surgery
combinations of:
Aminoglycosides
After blood
cultures
Definitive therapy
based on culture Rifampin
results
For prosthetic valve IE
4–6 weeks
Severe valve Relapsing prosthetic

incompetence valve IE
Multiple major Persistent bacteremia

embolic complications despite Abx therapy
Surgical
indications
New conduction defects or

Refractory CHF
arrhythmias 2° infection
Fungal IE Valve ring abscess

Endocarditis Prophylaxis
High risk
conditions for IE
Prosthetic
Unrepaired
Prosthetic History of material used
congenital
valves prior IE for repair of
heart disease
valve
Repaired congenital
Repaired congenital heart disease with Cardiac
heart disease with residual defects at or transplantation with
prosthetic material adjacent to the site cardiac valve disease
or prosthetic device of a prosthetic patch or incompetence
or device
All 30–60 minutes prior to

Gingival manipulation procedure
Dental procedures Periapical dental Oral Amoxicillin 2 g po

Provide
manipulation
prophylaxis for IV Ampicillin 2 g IM/IV
Oral mucosa perforation
Clindamycin 600 mg PO/IV
Oral Dicloxacillin 2 g po
Cephalexin 2 g po
Cephalexin 2 g po PCN allergy
GI/GU Infected skin or Azithromycin 500 mg po
NO prophylaxis musculoskeletal IV Vancomycin 1 g IV
structure Cefazolin/Ceftriaxone 1 g
Clindamycin 600 mg IV/IM IV/IM
Endocarditis Prophylaxis NOT Indicated
Mitral valve
prolapse
Repaired atrial Ventricular septal

septal defects defect
Endocarditis
Physiologic Patent ductus
Prophylaxis
murmurs arteriosus
NOT indicated
Pacemakers Prior CABG
Hypertrophic
cardiomyopathy
48 B. Desai
Rheumatic Heart Disease
Sequelae of Group A Antigen cross-reactivity

Rheumatic Fever
b–Hemolytic Strep with normal tissue
Greatest risk in Latent period

Natural History Pharyngitis Rheumatic Fever
children 4–18 1–5 weeks
Rheumatic Heart Disease: Diagnosis
Jones Criteria
Major Criteria Minor Criteria
“CASES” “4 P’s & an A”
Sydenham’s Previous Hx Prolonged

Carditis PolyArthritis Positive ESR
Chorea of RF PR interval
Pancarditis
Erythema Subcutaneous
Pyrexia Arthralgia
marginatum nodules
Evidence of
Diagnosis 2 major OR 1 major 2 minor preceding
Strep infection
Scarlet Fever
(+) Group A Strep
Rheumatic related valvular disease is the most common throat culture
cause of valvular disease overall Elevated ASO titer
Rheumatic Heart Disease: Treatment
Prevention is key! PEDIATRICS
Streptococcal Appropriate
pharyngitis? antibiotics
Over 2 years of
age
Acute Rheumatic Anti-strep prophylaxis

Penicillin Erythromycin
Fever? for up 5 years
NSAID’s or
Arthritis?
Salicylates
NSAID’s or
Mild carditis?
Salicylates
Moderate to
3° heart block Cardiomegaly CHF Prednisone
severe carditis?
Chorea? Benzodiazepines
50 B. Desai
Cardiomyopathies (CM)
Cardiomyopathy: General
Impairs Electrical
Diseases that Cardiac
Cardiomyopathy myocardial properties of the
directly alter structure
function myocardium
Cardiomyopathy
Primary Secondary
Primary
Hypertrophic Dilated Toxins Amyloid Metabolic
restrictive
Thiamine
EtOH
deficiency
Cocaine Diabetes
Myocarditis Peripartum mellitus
Hypo-&
Hyperthyroidism
Acquired Neuromuscular
disorders
Most common cause of sudden death in athletes

Hypertrophic
2nd most common cause of sudden death in adolescents
Dilated Cardiomyopathy
Most common cause 25 % of all cases 1° reason for cardiac

of Dilated CM? Idiopathic of CHF transplantation in US
Systolic Diastolic LV RV
dysfunction dysfunction contractility contractility
¯ ¯
Low cardiac End End
output systolic pressure diastolic pressure
¯ Ventricular
compliance
Intracavitary
Pressures
Signature LV wall thickness

characteristics? is normal LV dilatation RV dilatation
52 B. Desai
Dilated Cardiomyopathy: Clinical Features
Exam Symptoms & signs of CHF
Peripheral Peripheral
Murmurs Rales PND Orthopnea Dyspnea
edema embolization
Due to poor
closure of CP usually due to lack of vascular reserve
valves, not
necessarily Sudden death is possible
valvular issues
CXR EKG
Pulmonary Poor R wave Rhythm Conduction

congestion Cardiomegaly LVH LAE disturbances
progression defects
CHF Globular heart A. fib
Most common
Kerley B lines Ventricular
findings
ectopy
Upper lung field
hyperemia
Overall increase
in vascular
markings
Echo
Ejection Ventricular Atrial

Systolic volume Diastolic volume
fraction enlargement enlargement
May see a mural thrombus due to

these factors
Dilated Cardiomyopathy: Treatment
Treatment is largely supportive
Chronic therapy Diuretics Digoxin Survival
Survival ACE inhibitors β–blockers
Ventricular
ectopy? Amiodarone AICD
Exacerbation of Treat like CHF Antidysrhythmic

chronic DCM? exacerbation Nitrates Diuretics Anticoagulation agents
See CHF for full
details Mural thrombi Ectopy
Ultimate Cardiac
treatment? transplantation
Depends on
Disposition clinical condition Exacerbation? Admit
Hypertrophic Cardiomyopathy
Hypertrophic Familial, Autosomal Hypertrophy is

LV hypertrophy RV hypertrophy
CM dominant asymmetric
Hypertrophic Primary involves the

CM interventricular septum
¯ LV diastolic LV filling
LV hypertrophy ¯ LV compliance
function pressure
End-systolic End-diastolic
Cardiac output Ejection fraction Normal
volume volume
Clinical ¯ Diastolic ¯ LV filling Dynamic obstruction

Due to
symptoms relaxation of LV outflow
Mitral valve leaflets

block the outflow
tract
54 B. Desai
Hypertrophic Cardiomyopathy: Clinical Features
History & Exam Older? Worse Sx
Family Hx of sudden Dyspnea on Exertional

Murmurs Chest pain Palpitations Sudden death
cardiac death exertion Syncope
Harsh mid- Dysrhythmias? Most frequent
systolic murmur Due to
initial complaint
at LLSB imbalance of Causes LV
O2demand May be Due to exercise diastolic pressure &
and worsened by induced sinus pulmonary venous
availability atherosclerotic tachycardia hypertension
due to LV disease
hypertrophy
May mimic
angina
Murmur Valsalva Standing after

Hypovolemia β–blockers
increased maneuver squatting
¯ Preload
Murmur Volume
Squatting Hand grip α–agonists Trendelenburg
decreased expansion
Afterload
CXR EKG Echo
Normal or SeptalQ Disproportionate septal

LVH LAE
non-specific waves hypertrophy
Hypertrophic Cardiomyopathy: Treatment
Avoid exertion Leads to ↑ Obstruction Arrhythmias
Risk for sudden

Syncope? Admission Echo Holter Due to
cardiac death
Chest pain? β–blockers
Medications to Negative Calcium channel

β–blockers OR
decrease obstruction? inotropes blockers
Surgical Surgical
treatment? myomectomy
Depends on
Disposition Exacerbation? Admit
clinical condition
Restrictive Cardiomyopathy
Sarcoid
Amyloid
Most common cause May be familial Multiple other
Idiopathic
of Restrictive CM? Autosomal dominant causes
Scleroderma
Hemochromatosis
Systolic function Normal or decreased filling of Ventricular wall thickness

Restrictive CM But…
is usually normal one or both ventricles may be normal or increased
Restrictive CM LV end diastolic RV end diastolic Normal LV Early diastolic pressure has a decrease
pressure pressure systolic function followed by a rapid rise & plateau
EF ≥ 50 %
Restrictive Cardiomyopathy: Clinical Features
Exam Symptoms & signs of CHF
Peripheral
JVD Rales PND Orthopnea Dyspnea Right sided CHF
edema
Hepatomegaly
CP uncommon
RUQ pain
Except in amyloidosis
Ascites
CXR EKG
Pulmonary Normal heart Nonspecific ST-T Low voltage may A. Fib may be
congestion size changes be seen seen
CHF
Kerley B lines
Upper lung field
hyperemia
Overall increase
in vascular
markings
Echo
Confirmatory
56 B. Desai
Restrictive Cardiomyopathy: Treatment
Treatment is largely supportive &

depends on type of RCM
Diastolic Calcium channel

OR β–blockers
dysfunction? blockers
Medical
Diuretics ACE inhibitors
management
Less effective
Sarcoid? Steroids
Chelation
Hemochromatosis?
therapy
Depends on
Disposition Exacerbation? Admit
clinical condition
Myocarditis
Introduction
Form of & common cause of

Myocarditis
dilated cardiomyopathy
Causes of Connective
Idiopathic Infectious Chemotherapy
Myocarditis tissue disorders
Inflammation of Systolic function

Myocarditis But…
heart muscle is usually normal
Myocarditis Many episodes Thus many cases Myocarditis may be

tidbits are mild are not diagnosed accompanied by Pericarditis
Natural History Most recover
Complications of Sudden Cardiac Dilated

Myocarditis Death cardiomyopathy
Infectious Causes of Myocarditis
Coxsackie B
Enteroviruses
Parainfluenza Influenza
Viral
Echovirus EBV
Hepatitis B HIV
Lyme Disease
Mycoplasma
Rheumatic fever
pneumoniae
Bacterial
Corynebacterium Neisseria
diphtheriae meningitidis
58 B. Desai
Myocarditis: Clinical Features
History & Exam Symptoms & signs of CHF
Sinus
Flu-like illness Fever Myalgias Headache CHF Dysrhythmias
tachycardia
Severe cases Out of
proportion to
fever
Pericardial
Emboli
friction rub
Chest pain in Retrosternal in May be anginal Usually due to

Common
Myocarditis? location in quality Myopericarditis
CXR EKG
Usually normal or Pulmonary Nonspecific ST-segment QRS

Cardiomegaly AV Blocks
non-diagnostic congestion ST-T changes elevation prolongation
CHF From
Pericarditis
Kerley B lines
Upper lung field
hyperemia Echo
Overall increase
in vascular Myocardial Wall motion Usually
markings depression abnormalities nonspecific
Severe cases
Severe cases
Labs
Elevated cardiac biomarkers
Myocarditis: Treatment
Treatment is largely
supportive
Myocarditis from
Antibiotics
Rheumatic fever?
Myocarditis from
Antibiotics
Diphtheria?
Myocarditis from
Antibiotics
Meningococcus?
Medical
CHF?
management
Depends on CHF
Disposition Admit
clinical condition Exacerbation?
Pericarditis
Causes of Pericarditis
Myxedema Idiopathic
Post-MI Radiation-induced
Dressler’s
syndrome
Malignancy
Drug Induced
Melanoma
Pericarditis
Leukemia
Metastatic lung
cancer
Lymphoma Infectious
Metastatic
breast cancer
Rheumatic
Uremia
diseases
SLE
RA
Polyarteritis nodosa
Dermatomyositis
Scleroderma
Infectious Causes of Pericarditis
Echovirus
HIV Viral Coxsackie
Staph
Streptococcus
pneumoniae
Bacterial Rheumatic fever
Tuberculosis
Histoplasma
Fungal
capsulatum
60 B. Desai
Pericarditis: Clinical Features and Diagnosis
History & Exam
Pericardial Pulsus
CP common Fever Dyspnea Dysphagia Malaise
friction rub paradoxus
Sharp/Stabbing Due to pain on Due to BP lowers on
Sinus
inspiration esophageal inspiration &
Retrosternal or Tachycardia
irritation increases on
Precordial
expiration
Radiates to back, neck, Especially left
L arm or shoulder trapezium ridge
Worse on inspiration or
movement
Worse when supine
Relief on sittingup &
Rub heard better
bending forward
CXR Echo Procedure of choice
Usually normal or Epicardial

Fluid in Separation Separation between
non-diagnostic Fat-Pad sign
pericardial between RV & LV & posterior
On lateral CXR space chest wall pericardium
Only present in
15% of cases
Labs
CT sensitivity? Echo sensitivity
Elevated cardiac biomarkers

Due to associated
myocarditis
Pericarditis: EKG Changes
ST amplitude: T wave
Stage PR Segment ST Segment T wave
amplitude >0.25
Diffuse elevation
Depression,
1 (does not correlate
especially in II, N/A
with coronary
aVF& V4–V6
distribution)
2 Returns to Returns to
baseline baseline N/A
Inversions,
3 N/A Isoelectric especially in I,
V5, V6
4 N/A Isoelectric Normal
Large pericardial effusion Low-voltage QRS complexes Electrical Alternans
Due to attenuation of electrical Due to pendular motion of heart

signals within fluid filled pericardium
Pericarditis: Treatment
Treatment depends on
cause
Viral
NSAID’s Course is benign
pericarditis?
Immune- Hx of oral Large pericardial Onset over Associated

T > 38°C?
compromised? anticoagulant use? effusion? weeks? myocarditis?
Poor prognostic
signs
Depends on Hospitalization Poor prognostic

Disposition But… Admit
clinical condition usually not necessary signs
62 B. Desai
Cardiac Tamponade
Introduction
↑ Fluid in ↑ Pericardial
Pathophysiology
pericardial sac pressure
Continued Pericardial Filling pressure of the Limits Cardiac

collection of fluid? pressure right side of heart ventricular filling Tamponade
Cardiac Depends Pericardial Rate of fluid Intravascular

Tamponade on compliance collection volume
Hypotension
lowers filling
pressures
Causes of Cardiac Tamponade
Myxedema Uremia
Hemorrhage Radiation-induced
Anticoagulant use
Idiopathic
Acute
Drug Induced Chronic
Cardiac
Tamponade Infectious
Tuberculosis
Trauma Bacterial
Rheumatic
Malignancy
diseases
SLE Melanoma
Leukemia
Metastatic lung cancer
Lymphoma
Metastatic breast
cancer
Other metastatic
cancer
Cardiac Tamponade: Clinical Features
History & Exam
Sinus Distant heart Pericardial Distended neck

Dyspnea Dysphagia Low systolic BP
Tachycardia sounds friction rub veins
Both rest & Due to Narrow pulse
Pulsus exertion esophageal pressure
RUQ pain irritation
paradoxus
BP lowers on Hepatic
inspiration & congestion
increases on
expiration
CXR EKG
May or may not + Epicardial ST-segment Electrical

Low voltage PR depression
show enlarged heart Fat-Pad sign elevation alternans
On lateral CXR Epicardial Beat-to-beat
inflammation variation in the
amplitude of
the QRS
Echo Procedure of choice
Right atrial Diastolic collapse of Dilated IVC with no

compression the right ventricle inspiratory collapse
Specific for
tamponade
Cardiac Tamponade: Treatment
Cardiac Volume
Pericardiocentesis Admit
Tamponade? expansion
Definitive treatment
Why Volume ↑ Right Heart ↑ Intravascular

↑ Blood Pressure ↑ Cardiac output
Expansion? Filling volume
64 B. Desai
Abdominal Aortic Aneurysm
Introduction
Dilatation of > 1.5 times Due to Medial Usually

Aneurysms
arterial wall normal diameter degeneration atherosclerotic
All layers of
True Aneurysms
vessel wall
Risk Factors for Connective

Family Hx Atherosclerosis
True Aneurysms tissue disorders
Some layers of Fibrous tissue

Pseudoaneurysm
vessel wall formation
Causes of Fibrous Prior

Prior surgery Trauma Infection
tissue formation catheterization
Mycotic Develops due to Direct extension of Embolization

Due to OR
aneurysm infection in vessel wall neighboring infection from endocarditis
Abdominal Aortic Aneurysm: General
Abdominal Aneurysm >3.0

Aortic Aneurysm cm in diameter
Majority are 18 % of patients with 1st degree relative

AAA Tidbits M>F
infrarenal with AAA have a AAA of their own
Connective
Risk Factors Atherosclerosis Hypertension
tissue diseases
Abdominal Aortic Increased risk of

Consider repair Due to
Aneurysm >5.0 cm? rupture
Symptomatic Abdominal
Emergent repair
Aortic Aneurysm of any size?
Pt with Peripheral Higher risk for

arterial disease? AAA
Aneurysms Higher risk for

elsewhere? AAA
Abdominal Aortic Aneurysm: Symptoms
Most common Abdominal Usually severe 50 % with ripping Constitutional

Back pain
presenting Sx? pain & abrupt or tearing pain Sx
Other Symptoms & Signs
Extremity
GI Bleeding Sudden death Flank pain Shock Tachycardia Tachycardia
ischemia
Aortoenteric Due to Most common
embolization From rupture
fistula misdiagnosis =
from of aneurysm
Renal Colic
aneursymal
thrombus
Severe Until proven

Syncope Severe back pain Ruptured AAA
Abdominal pain otherwise
Occurs in 10 % of From rapid Lack of cerebral

Syncope in AAA? Due to
patients blood loss perfusion
Physical Exam in
Unreliable
AAA? Unusual
Presentations
Abdominal &/or
Classic Triad Pulsatile mass Hypotension
back pain Partial bowel
obstruction
IVC Erosion
AAA Signs
Scrotal or vulvar Inguinal Dissection of May irritate psoas muscle = Psoas sign
hematomas masses retroperitoneal blood May irritate femoral nerve = Femoral neuropathy
Periumbilical
Cullen’s sign
ecchymosis
Flank
Grey-Turner sign
ecchymosis
Presence of
< 50 %!
pulsatile mass?
Abdominal or Decreased
Other signs?
femoral bruits femoral pulses
Massive GI Hx of Aortic Aortoenteric

Bleed Graft Fistula
May have a
“sentinel” bleed
Aortoenteric Most common May cause upper or

Fistula in Duodenum lower GI bleeding
66 B. Desai
Diagnosis
Radiologic Evaluation
Computed
Plain radiography Ultrasound MRI
Tomography
Cannot rule out AAA 90 % sensitive for AAA IV contrast

& can measure
diameter
May show calcified Can assess for free

& bulging aorta Stable patient only Not routinely used
intraperitoneal fluid
65 % with symptomatic
AAA Absence does not rule
out AAA rupture
Can define
Cannott ass
assess for anatomic detail
retroperitoneal
hemorrhage
Lateral AP
Won’t Arch of
Can id
identify
overlie calcification
retroperitoneal
vertebrae to the left
hemorrhage
Pt away
Risk
from ED
Treatment
Suspect Expedited Emergent Vascular Type & Standard resuscitative

ruptured AAA? evaluation Surgery consultation Cross techniques
Bedside U/S Emergent operative 10 units Multiple large bore
repair IV’s, O2, etc.
AAA 3–5 cm Close follow-up
Asymptomatic
Elective repair
AAA >5 cm
Aortic Dissection
Introduction
Acute development of Within tunica

Aortic Dissection
false blood filled lumen media
Aortic Dissection May mimic many other

pitfalls etiologies of chest pain
Aortic Dissection Deadly disease
Mortality without 25 % in 75 % in
treatment 1st 24 hours 1st 2 weeks
Prompt Increases
diagnosis? survival to 90 %
Anatomy
Location of Aortic Majority in

Dissection? Thoracic aorta
Descending Areas distal to left Continues into Ends at the

aorta subclavian artery the diaphragm Celiac artery
Adventitia Outer layer

Composition of
Three layers Media Strongest layer
Aortic wall?
Intima Inner layer
Major structural
Tunica Media
component?
68 B. Desai
Aortic Dissection Risk Factors
Hypertension
Most common
Coarctation of Bicuspid aortic
risk factor
the aorta valve
Parainfluenza Male
Congenital
Acquired
Echovirus Older age

Marfan’s
Syndrome
Most common
Hx of aortic
Drugs cause of AD
aneurysm
<40
Cocaine Annual rate of
Causes cystic
AD increases as
medial
aortic diameter
necrosis
increases
Pregnancy +
Marfans’s =
Greater risk of
AD
Increased Sudden ↑ Aortic shear

Cocaine use? Aortic dissection
catecholamine surge elevation in BP stress
Aortic Dissection Pathophysiology
Between inner &

Tunica media Tear forms in High velocity outer layers of False
degenerates tunica intima blood enters the abnormal Creates
lumen
tunica media
Most common
Sustained
site of tear is
hypertension May
left
worsens obstruct
posterolateral
degeneration the true
portion of aorta
lumen
Above aortic valve
Distal to
subclavian artery
↑ Aortic luminal Propagation of

Anterograde OR Retrograde
pressure dissection
May reenter
through the
intima
Dissect thru the Paths of travel for Dissect thru the

Peritoneal space the dissection Pericardium
Dissect thru the

Pleura
Aortic Dissection Classification
Ascending 60 %
Aortic arch 10 %
10 %
60 %
Descending 30 %
Type I
Anatomy and Classification of Aortic Dissection
False lumen
True lumen
30%
Intimal tears
Type II
DeBakey I II III
A B
Stanford
A = 62 % B = 38 %
Aortic Dissection: Clinical Features
History
CP common Radiation pain to Radiation pain to

Back Pain
neck, jaw, throat abdomen, back, intrascapular region
Abrupt, Sharp/Stabbing Abrupt & Aortic arch Descending
Anterior = Ascending stabbing
All pain may

migrate
Feeling of
Others Diaphoresis Syncope N/V
impending doom
Symptoms & Signs
Neurologic Hyper-or
Myocardial Infarction Stroke Syncope Limb Ischemia
findings hypotension
Aortic Pulse deficit between Mesenteric Asymmetric

Renal infarction Tamponade
regurgitation extremities ischemia pulses
Myocardial 5 % of Type A RCA most Leads to Inferior

Infarction Dissections commonly involved wall MI
70 B. Desai
Aortic Dissection Diagnosis
CXR
Abnormal in Mediastinal Left pleural Obliteration of Loss of

Calcium sign
80–90 % with AD widening effusion aortic knob paratracheal stripe
Most common
12 % with Separation of
finding More common
normal CXR the intimal Depression of left Tracheal
with descending
Seen in 63 % calcification deviation
Findings are aorta mainstem bronchus
with Type A from the outer
often aortic soft
non-specific Seen in 56 % tissue border
with Type B by 10mm
EKG
Ascending AD
31 % are normal involving RCA
Inferior wall MI
Will have same
signs &
symptoms
Almost always
requires further
imaging
Main Findings Other Findings Main Findings

CT Angiography Angiography
Dilation of Pleural effusion
Diagnostic test Site of origin
the aorta The “gold standard”
of choice of the original
Pericardial
Findings Sensitivity varies – dissection
Sensitivity Intimal flap effusion
up to 85 %
95–100 % identification Very specific -
Aortic rupture
Specificity 98 % 98 % Branch artey
Presence of true Branch vessel Logistically involvement
& false lumen Findings
involvement difficult
May have false
negatives due to
Aortic
false lumen
CAN Pericardial Valvular regurgitation
thrombosis
Transthoracic identify effusions abnormalities
Echocardiography Being replaced
(or has been Coronary
Lacks sensitivity replaced by CT)
CANNOT fully Descending artery
77–80 % Aortic arch
visualize aorta involvement
Transesophageal
Echocardiography CAN Pericardial Valvular
Diagnostic test of identify effusions abnormalities
choice in the MRI Labs
unstable patient Limited use in the
Of little value
Sensitivity 98 % ED
Identifies the mobile
Highest Sensitivity
intimal flap that Do not use D-
Specificity 95 % 98 %
separates the true & dimer to exclude
Highest
Can image most false lumen dissection
specificity 98 %
of the thoracic
aorta Type & cross if
going to OR
Aortic Dissection Management
Acute
management
Decrease Minimize
Initial Pain control
the blood the shear
stabilization as needed
pressure pressure
Fentanyl Target
Target heart
preferred with systolic BP is
rate is £ 60
labile blood 100–120 mm
BPM
pressures Hg
1st line b-blocker

Reduce shear pressure Start prior to
medication? by lowering the pulse vasodilators
Esmolol Easily titratable Very short acting
Has both a & b May be used as a single Has a longer Hypotension & bradycardia
Labetalol
properties agent for BP & HR control half-life may be prologed
Selective Metoprolol & Use for COPD or

b-blockers atenolol Asthma
Calcium channel Use Diltiazem

Not Nifedipine
blockers or Verapamil
Additional BP Start after Long term use can potentially

Nitroprusside
control? b-blocker cause cyanide toxicity
Definitive therapy Prompt surgical

for Type A treatment
Definitive therapy Medical Strict blood

for Type B management pressure control
Aortic Dissection Special Circumstance

May use
Cocaine + Benzodiazepines Risk of unopposed
Due to Phentolamine
Dissection? become 1st line therapy alpha hypertension
as well
Fetus Emergent repair

Pregnancy + < 28 weeks? of AD
Dissection?
Same therapy Fetus Emergent repair

C-section
>32 weeks? of AD
b-blockers &
nitroprusside
Between Repair depends on
28–32 weeks? maternal condition
72 B. Desai
Hypertension
Blood Pressure Definitions
Systolic BP Diastolic BP
mm Hg mm Hg
Normal <120 & <80
Prehypertension 120–139 OR 80–89
Stage 1 140–159 OR 90–99
Stage 2 ³160 OR ³100
Hypertensive Severe elevation NO signs or symptoms Initiate Modify

Urgency in BP of end organ damage therapy behavior
Arbitrary BP ³
180/120
Hypertensive Severe elevation Signs or symptoms of Emergent BP

Emergency in BP end organ damage reduction
No specific BP
level!!
End Organs Heart Aorta Brain Eyes Kidney
Hypertensive Emergencies
Hypertensive Malignant Reduce Mean Arterial 30 % in 30

OR
emergency? hypertension? Pressure (MAP) minutes
MAP DBP (SBP-DBP) 3

End Organ and Other Syndromes Related to Hypertension
Heart ACS Aortic dissection CHF
ASA Labetalol Nitro

Nitro or Diuretics
b-Blockers Esmolol+
Nitroprusside
Brain Hemorrhages Stroke Hypertensive

syndromes Encephalopathy
Labetalol
Subarachnoid Labetalol or
or Intracranial or Nitroprusside
Nitroglycerin or
Esmolol or Nicardipine
or Nicardipine or
Labetalol Fenolopam
Hypertension is
or
transient & Papilledema on
Nicardipine
protects the PE
brain
Usually resolves
in hours
Symptoms & Signs –Hypertensive Encephalopathy
Altered mental Headache Vomiting Seizures Visual

status disturbances
Acute Pulmonary Pre-eclampsia&

Lungs Kidneys Renal failure
Edema Eclampsia
Nitroglycerin Labetalol Labetalol

or or or
Nitroprusside Nicardipine Nicardipine
or or or
Enalaprilat Fenolopam Nifedipine
or
Nicardipine Dialysis Hydralazine not
recommended
Seizures? =
Magnesium
Cocaine
± Mental
Drugs Amphetamines Tachycardia Diaphoresis Hypertension
status changes
PCP
Benzodiazepines
Nitroglycerin
Labetalol
Phentolamine
Nicardipine
a+b-blocker is
ideal No b-blocker Unopposed
alone a effect
Labetalol +
Phentolamine
74 B. Desai
Catecholamine
Adrenals Pheochromocytoma
crisis
Labetalol +
Phentolamine
a+b-blocker is
ideal
Alternating periods of
Pheochromocytoma Headache Flushing
hypertension and normal BP
Treat associated
Eyes Exudates Hemorrhages
syndromes
Medication Effects and Side Effects

Medication Effects Side Effects &
Cautions
Arterial, venous, coronary Reflex tachycardia

Nitroglycerin
vasodilator Headache
Onset = immediate
Reflex tachycardia
Arterial & venous Use with b-blocker
Nitroprusside
vasodilator ↑ Increased ICP
Long term use
Onset = 1-2 min Cyanide toxicity
No reflex tachycardia
Labetalol a+b-blocker Do not use in AV blocks, CHF,
or bronchospasm
Onset = 2-5 min
Do not use in bradycardia,

Esmolol β−blocker
CHF, bronchospasm
Onset = immediate
Medication Effects Side Effects &

Cautions
Selective for cerebral &

Nicardipine Do not use in CHF
coronary arteries
Onset = 5–10 min
Cerebrovascular occlusion
Phentolamine a1 & a2 blocker
MI
Onset = 5–10 min
Avoid in pregnancy
Enalaprilat ACE Inhibitor Dizziness
Headache
Onset = 5–10 min
Arteriolar vasodilator
May be used in Reflex tachycardia
Hydralazine Pediatric nephritis Chronic use = “Lupus-like”
Not recommended syndrome
Pregnancy-induced
hypertension
Onset = 10 min
Evaluation of Severe Asymptomatic Hypertension
Completely depends on patient

condition, history, and review of
systems
Commonly ordered investigations
Basic
EKG metabolic CXR Urinalysis
panel
Depends on
Disposition clinical condition
76 B. Desai
Pulmonary Hypertension
Introduction
Pulmonary Dx cannot be
Hypertension made in the ED!
Time between symptom 2 years due to

start and diagnosis lack of specificity
Pulmonary ↑ Pulmonary ↓ Right ventricular

Hypertension Causing
vascular pressure function
Acute Sx in pts Worsening of Complications of Adverse effects Rebound effects due

Dx with PH underlying condition medication administration of drugs to drug stoppage
Symptoms
Sx of underlying Peripheral
Dyspnea Chest pain Fatigue Syncope
disease edema
Most common Poor coronary Poor cardiac
RV failure
Sx blood flow output
On rest or
exertion
Exam may include
Increase in pulmonary Murmur of tricuspid Murmur of Pulmonary Peripheral Hepatic

Ascites
component of 2nd heart sound regurgitation insufficiency edema congestion
Sternal heave JVD

RV Severe cases
hypertrophy
Diagnostic Studies
CXR EKG
Use to show any signs Incomplete RBBB with right
of pulmonary disease RVH
RBBB axis deviation
Confirmatory
Transthoracic Cardiac
PFT’s
echocardiography catheterization
Goal of Treatment
Decrease Improve exercise Consult your pulmonologist

Treatment goals Prolong survival
symptoms tolerance for definitive Rx
Syncope
Introduction
Sudden & brief Inability to maintain Resolves Without medical

Syncope
loss of consciousness postural tone spontaneously intervention
Near or Feeling of syncope

Pre-Syncope without LOC
Syncope Lack of blood flow to Reticular

OR
mechanism? both cerebral cortices activating system
Most common An event that causes a

mechanism? drop in cardiac output
Causes of Syncope
Cardiac Medications
Structural – 4 % 3%
Dysrhythmias –
14 %
Unknown Orthostatic
hypotension
34 % 8%
Syncope
Breath Neurally
holding mediated
Pediatric Vasovagal –18 %

1% Situational –5 %
Carotid sinus
syndrome –1 %
Neurologic Psychiatric
10 % 2%
78 B. Desai
Cardiac Syncope
The most dangerous Have higher risk 6 month Needs timely

etiologies of sudden death mortality >10% evaluation
Structural Heart unable to provide cardiac output to

Cardiac syncope Dysrhythmias
lesions maintain cerebral blood flow & perfusion
Syncope from May be due to

Physical exertion Vasodilation
structural lesions Medications or Heat
Until proven
Elderly? Aortic Stenosis Syncope Angina Dyspnea
otherwise!
Until proven
Young? HOCM
otherwise!
Pulmonary Until proven

Syncope SOB Risk factors
embolism otherwise!
Brady-
Dysrhythmias Tachy-rhythms OR Usually sudden No prodrome
rhythms
Depends on Continued
Disposition Admit
clinical condition syncope?
Vasovagal and Orthostatic Syncope
Vasovagal Inappropriate Slow, progressive onset

Bradycardia
syncope vasodilatation with a prodrome
Both resulting from inappropriate

vagal or sympathetic tone
Negative cardiac Carotid sinus Until proven

Elderly?
evaluation sensitivity otherwise!
Orthostatic Blood shifted to Drop in cardiac May have many

syncope lower body output causes
Evaluation of Syncope
Completely depends on patient

condition, history, and review of
systems
Depends on
Disposition
clinical condition
Deep Venous Thrombosis and Pulmonary Embolism
Introduction
Pulmonary Thrombi Usually form near Portion of venous Lodges in

embolism formation venous valves clot breaks off Pulmonary arteries
Due to slow blood
flow Pre-capillary
Popliteal
Superficial
Pelvic
Femoral
Veins in which
clots can form
Great veins Axillary
Jugular
Pulmonary vessels
PE symptoms
20–30 % occluded
Obstruction of ↑ Ventilation Alveolar dead

pulmonary blood flow ↓ Perfusion space
Hypoxemia in Shunting of
Unpredictable Due to
PE? blood flow
80 B. Desai
Risk Factors for Thromboembolism
Conditions that
allow the Virchow’s Venous Damage Hypercoagulable
formation of Triad stasis of tissue states
clots
Immobilization Trauma Thrombophilic states
Venous
Smoking Cancer
catheters
CHF Post-op Lupus
COPD HIV
Nephrotic Syndrome
Hormonal
Pregnancy
Age Contraceptives
Other risk Obesity

factors
Long-distance
travel
PE: Clinical Features
Patients may have completely

Symptoms
different clinical presentations
CP common Epigastric Altered mental

Dyspnea Syncope Stroke
abdominal pain status
Most common Pleuritic From right Severe cases From cerebral R->L shunt
Sx ventricular hypoxia from patent
2nd most common Sx strain
On rest or foramen ovale
exertion 50 % have no CP
Focal CP can also be
related to pulmonary
infarction
Pain can be anywhere in
the chest or upper
abdomen
Signs
Wheezes or Sinus
Tachycardia Tachypnea Low PO2 ± Fever Dysrhythmias
rales tachycardia
Most have Atrial Out of
Shock DVT’s clear lungs fibrillation proportion to
Pulmonary fever
infarction has
rales over the
affected area
DVT: Clinical Features
Symptoms
Extremity pain Swelling Cramping Erythema ± Fever
Unilateral
Signs
Venous
Erythema U/L swelling ± Fever Homan’s sign
insufficiency
Not sensitive
Hyperpigmentation
or specific
Skin ulcers Calf pain
when
passively
dorsiflexing
the affected
foot
Massive Phlegmasia Cyanotic congested Phlegmasia alba Pale swollen

ileofemoral DVT cerulean dolens extremity dolens extremity
Phlegmasia alba Has associated

Pregnancy
dolens associations arterial spasm
↑ Compartment Possible Requiring Thrombectomy Surgery for

Pitfalls of both
pressure ischemia or Thrombolysis compartment syndrome
Diagnosis
Pitfalls for PE Routine testing usually

Diagnosis shows nonspecific findings
Diagnostic Depends on ↑ Pre-test More aggressive No perfect test

But…
approach? Pre-test probability probability workup exists
Determination of Pre- Clinician’s training

History Physical exam Scoring system
test probability? & experience
Well’s score
Well’s Score
Low < 2
PE Unlikely < 4 Moderate = 2–6
OR
PE Likely > 4 High > 6
PE is leading
Signs and
diagnosis or equally HR > 100 bpm Prior PE or DVT
symptoms of DVT
likely
3 points 3 points 1.5 points 1.5 points
Immobilization
Active malignancy Hemoptysis
within 4 weeks
1.5 points 1 point 1 point

82 B. Desai
Using Pretest Probability in the Diagnosis of PE
D-Dimer normal No further testing

Low or Moderate No
D-dimer PE
Probability
D-dimer elevated Computed tomography
PE
No recent trauma or
Age < 50
surgery
Pulse ox >94 % on room air No hemoptysis

Very low
PERC rule
suspicion for PE
HR < 100 bpm No exogenous estrogen
The overall All 8 must be true
gestalt suggests Rules out PE No prior PE/DVT No clinical signs of DVT
the probability (<2 % chance)
for PE < 15 %
Further testing for other

CT normal
etiology
Computed
High Probability
Tomography
CT abnormal PE
Other Basic Tests
ABG EKG
Most commonly
abnormal Usually abnormal Sinus Incomplete
S1-Q3-T3
but not specific tachycardia RBBB
Nonspecific ST-T
changes
Hypoxemia ↑ A-a gradient
Right axis T-wave inversions
P pulmonale
↑ A-a deviation V1–V4
gradient?
PE more likely
CXR
Usually abnoral Less common

but not specific but more specific
Westermark
Cardiomegaly Atelectasis Hampton hump
sign
Oligemia distal Wedge shaped
Pleural to infarct pulmonary
Infiltrates
effusions infarction
D-Dimer
Qualitative
Break down of Fibrin D-dimer protein Measured by
containing clots into blood Quantitative Qualitative
Quantitative Sensitivity
Usually high for 94–98 %
3 days after (–) D-Dimer + High risk?
NOT sensitive
DVT/PE Imaging
enough
Specificity
50–60 %
NOT specific (+) D-Dimer?
ALL risk factors for
thromboembolism enough Imaging
D-dimer!
Trauma Older age (>70) Pregnancy
Liver disease Active malignancy

False positive
age-adjusted d-dimer
Stroke & MI Infections
Inflammatory
Recent surgery
disease
SLE Within past week
Rheumatoid Also indwelling
arthritis catheters
PE Imaging: CT Angiography
Filling defect in contrasted Exactly like Pulmonary
PE
pulmonary arteries angiography
64 slice > 32 slice Better resolution with Filling defects can be seen in
More detectors
32 slice > 1 slice multi-head scanners Subsegmental pulmonary arteries
Sensitivity 90 %
Specificity 90 %
Not sensitive enough to rule out
PE in high risk patients
Potential alternative Can image the

CT scan benefits
diagnosis legs for DVT
8%
CT scan Anaphylactoid Pulmonary Contrast

Radiation dose
complications response to contrast edema extravasation
Pain
Compartment
syndrome
Thrombophlebitis
84 B. Desai
PE Imaging: Pulmonary Angiography
Angiography Direct treatment Can measure pulmonary Can see filling defects
benefits of PE artery pressures in ³ 3 mm vessels
Lysis of clots
IVC filter
placement
Angiography Not consistently Contrast Cardiac or pulmonary Radiation

Arrhythmias
complications available complications artery perforation exposure
PE Imaging: VQ Scanning
Sensitive enough
Normal V/Q
to rule out PE
Even in high
risk patients!
All other V/Q Nondiagnostic

findings
Venous Ultrasound
Ultrasound ↑ Sensitivity &

Readily available No radiation
benefits Specificity (for DVT)
Sensitivity = 90–95 %
Specificity = 95 %
Need experienced
sonographers
Non-compressible
DVT diagnosis?
veins
Ultrasound Lack of experienced Difficult in obese Prior Hx of DVT + non-

Pain
Pitfalls sonographers patients compressible vein
New vs. old clot
Venography
From CT Filling defect in

Indirect
angiography contrasted veins
Injection of contrast Filling defect in Complication:

Direct
material into foot vein contrasted veins Phlebitis
“Gold standard”
Rarely used
Treatment: Anticoagulation
Venous Systemic Unfractionated Low molecular

OR
thromboembolism? anticoagulation heparin weight heparin
Potential delay May give a dose of LMWH for suspected DVT

High risk Treat!
in diagnosis when imaging is not available for 12–24 hours
Unfractionated
DVT or PE Renal Failure
Heparin
Upper extremity Same Rx as lower

DVT extremity DVT
PE Tidbits
SBP < > 40 % decrease

Massive PE SBP < 90 mm Hg OR OR Sats < 95 %
100 mm Hg in SBP
> 15 min In pt with Hx of
HTN
Ultrasound in
RV hypokinesis RV dilation
massive PE
“Less severe” PE Normal BP Sats> 94 %
Ultrasound in Normal RV
Normal RV size
less severe PE systolic function
Treatment: Fibrinolysis
Hypotension
Respiratory
Right sided strain Criteria for
Failure
Fibrinolysis
On Echo Hypoxia <90 %
Elevated Fibrinolytic Increased work
Troponin agent + Heparin of breathing
or LMWH
Metastatic cancer
Cardiac arrest
Intracranial Fibrinolysis
Uncontrolled HTN
disease Contraindications
Recent major
surgery or trauma
Within 3 weeks
86 B. Desai
Treatment: Embolectomy
Large proximal
Embolectomy Young patient Hypotension
PE
For most severe
cases
Mortality rate =
30 %
Disposition
PE? Admission
DVT No complicating Consider outpatient

features management
Extensive
iliofemoral DVT
Contraindication
Bleeding risks
to LMWH
Complicating
Features
Cardiac disease Concurrent PE
Thrombocytopenia Renal Failure

Acute Limb Ischemia
Introduction
Acute Limb Medical

Ischemia emergency
Acute Limb Smoking & Diabetes are

Men > Women
Ischemia Tidbits most important risk factors
Acute Limb Lack of blood flow to With passage of time have Usually within 6 hours but can occur
Ischemia an affected extremity irreversible cell death sooner due to lack of collateral flow
Typically due to
Thrombosis? Most common Has a slow onset
atherosclerosis
Usually cardiac in
Embolism? Atrial fibrillation Rapid onset
origin
Reperfusion Complete or partial Formation of

injury restoration of blood flow oxygen radicals
Reperfusion Peripheral
Related to time Myoglobinemia Renal Failure
injury muscle infarction
Lab abnormalities in ↑ CK Metabolic

Myoglobinemia ↑ K+
Reperfusion injury acidosis
Clinical Features
Symptoms & Signs
Muscle
Pain Paralysis Pallor Pulselessness Paresthesias Polar
weakness
Severe & With Early Severe cases
Constant continued
Later =
Earliest Sx ischemia
Mottled
Latest =
Necrosis
Symptoms & May not manifest In diseased arteries, collateral

The “6 P’s”
Signs all Sx blood flow may prevent abrupt Sx
Ischemic
Hypoesthesia OR Hyperesthesia
neuropathy
Preservation of Tissue is
light touch? probably viable
Crampypain Relieved with Femoral + Popliteal disease

Claudication
with exertion rest Calf pain
Neurogenic Worsened with Inconsistent response

claudication erect posture to exercise
88 B. Desai
Clinical Diagnosis
History/PE is most useful
Exertional pain Bilateral signs of

Gradual onset Thrombosis
palliated by rest? occlusive disease
Thrombosis Collateral Narrowing of

Diffuse disease
Radiology circulation blood flow
Otherwise normal
Known source Rapid onset Embolism
opposite limb
Embolism NO collateral Abrupt cutoff in

Minimal disease
Radiology circulation blood flow
Ankle-Brachial <1 < 0.25

Index? Chronic disease Severe disease
Diagnosis
Diagnosis EKG Cardiac enzymes Coagulation

panel
Atrial For
Fibrillation anticoagulation
if needed
Myocardial infarction or other cardiac
process
Echo Intracardiac
thrombus
Duplex U/S Can detect flow

obstruction
Arteriography Prior to surgery
Treatment
Acute Limb Dependent

Heparin Aspirin Analgesia
Ischemia? positioning
Optimal therapy for Surgical

acute embolism embolectomy
Catheter directed In consultation with

thrombolysis? a vascular surgeon
Bypass surgery for

Gold standard
atherosclerotic disease
Pacemakers
Emergency Pacing
Types
Transcutaneous Transvenous
AMI Asystole
Symptomatic
AMI bradycardia
Hypotension
Acute MI Indications Bilateral bundle

AMI branch block
New Bifascicular
AMI block
Mobitz type II 2°
AMI
heart block
Asystole within 10 minutes

of arrest
Mobitz type II 2o or 3o heart

block
Hemodynamically unstable
Other Indications Overdrive pacing of a

tachyarrhythmia
Drug-resistant
tachyarrhythmia
Drug overdose
Digoxin, b-blocker, Ca
channel blocker
90 B. Desai
Pacemaker Nomenclature
Response
Chamber Chamber Arrhythmia
to electrical Programming
Paced Sensed control
activity
Programmable rate
A trium Inhibits or output Pacing
Ventricle T riggers Multi-programmable Shock
Dual (A+V) Dual (T+I) Communicating D ual (P+S)
NO ne NOne Rate adaptive NOne

Sensing only
NOne
Unipolar vs Asynchronous
Bipolar vs. Synchronous
Unipolar more Asynchronous are fixed

susceptible to rate only
interference
In newer models,
magnets may not
predictable covert
pacer to asynchronous
mode
Automatic Implantable Cardioverter: Defibrillator Nomenclature
Chamber Anti-tachycardia Tachycardia Anti-bradycardia

Shocked pacing chamber detection pacing chamber
Atrium Electrogram Atrium
Ventricle Hemodynamic Ventricle
Dual (A+V) Dual (A+V)
NOne NOne
Can Tiered Pacing, then

Newer AICD
deliver therapy increasing shocks
All AICD have
Magnets stop
backup VVI
tachyarrhythmia
detection pacing to protect
against post
shock
R-R bradycardia
All AICD Measure
interval
Pacemaker Bipolar
Due to
functions electrodes
92 B. Desai
Specific Pacemaker Malfunctions
Battery or Electromagnetic
Failure to pace Lead problems Oversensing
component failure interference
Pacemaker Dislodgement
does not fire
Wire fracture
when it should
No visible pacing
EKG
spikes
Failure to Low pacing voltage or Battery or

Lead problems Exit block
capture elevated thresholds component failure
Dislodgement Lead displacement
Wire fracture Fibrosis at tip
Metabolic causes
Visible pacer No QRS

EKG
spikes complexes
Low pacing voltage or Battery or

Failure to sense Lead problems Exit block
elevated thresholds component failure
Pacemaker Dislodgement Lead displacement
does not
Wire fracture Fibrosis at tip
detect native
cardiac activity Metabolic causes
Visible pacer None should

EKG
spikes occur
Pacemaker Failure
Signs
Slowing of pacer
Rapid rhythm
rate
Battery depletion Battery depletion
Internal
malfunction
Looks like
Ventricular
tachycardia
CXR EKG
Evaluate lead Rarely, cardiac Assess for sensing Assess QRS

position perforation & capture morphology
Also for lead

fracture
Treatment & Emergent cardiology

Magnet
Disposition evaluation
94 B. Desai
Left Ventricular Assist Devices (LVAD)
Introduction
Bridge to Improves quality of life for

LVAD
transplant those not eligible for transplant
May have no
Stable patients
pulse at baseline!
Aorta
Outflow valve Inflow valve

housing housing
External battery Prosthetic
pack left ventricle
Skin line Vent adapter
and vent filter
System Drive line
controller
LVAD Emergencies
Pt in extremis
LISTEN for humming Check the Use the hand

Check battery Check the lines
sound from machine alarm pump back up
Pt should have Will be 60-90 bpm
travel bag with flashing
extra batteries
LVAD: Patient Assessment
Use manual BP
Check MAP Ideally >65
or Doppler
↓ Preload? Fluids + Blood
↑ Afterload? Nitrates or Anti-hypertensives

Coding with LVAD
May dislodge
MAP present No CPR!
the pump
LVAD Complications
Drive line infection
Look at skin entry site

Cover for hospital
acquired infection
Arrhythmia Gram (-) + MRSA Bleeding
Pts are anticoagulated

Mental status change =
Hemorrhagic stroke
Complications
Pts have acquired Von
Willebrand’s
Pump Thrombosis
LVAD is HOT with high RPM

Bolus Heparin
MI
tPA if decompensating
Pump Failure
Echo Findings
Right heart Give volume +

Big RV Small LV Pulmonary HTN
strain inotropes
Small RV Give volume
Big RV Big LV Pump failure OR Thrombosis
EKG in LVAD
MI Catheterization
But…
No pads over
Arrhythmia Standard ACLS
device!
96 B. Desai
EKG Changes Related to Electrolytes

and Metabolic Conditions
Hypothermia: EKG Changes
PR interval QRS Segment QT Interval 30–32 oC 28–30 oC
Sinus
V. Fib
Bradycardia +
Prolonged Prolonged Prolonged +
Other
Asystole
Arrhythmias
J-waves Other
Slow A. fib
May be present Muscle tremor
artifact
Hypokalemia: EKG Changes
P wave QRS Segment ST Segment T wave U wave
Early
Flat May be
Prominent May widen Depression
Later present
Inversion
Intervals Other
PR
PVC’s
Prolonged
V.Tach
QT
Torsades
Prolonged
Hyperkalemia: EKG Changes
P wave QRS Segment ST Segment T wave
Early
Hyperacute”
“
Flat or May be
Wide Later
Absent elevated
QRS + T = Sine
wave
7.5–8.0 mEq/L 7.5–8.0 mEq/L Early: 6.5–7.5

mEq/L
Intervals Rhythms Blocks
PR
Prolonged Bradycardia
V. Fib AV Blocks
QT Sine Wave
Shortened
6.5–7.5 mEq/L 10–12 mEq/L
Hypocalcemia: EKG Changes
Intervals Rhythms T wave
Ventricular
dysrhythmias
QT
Inversions
Prolonged
Torsades
98 B. Desai
Hypercalcemia: EKG Changes
QRS Segment ST Segment Intervals
PR
May be May be Prolonged
wide depressed QT
Shortened
Hypomagnesemia: EKG Changes
Intervals QRS Segment ST Segment T wave Other
PR PVC’s
Prolonged Flat or V.Tach
Wide Not normal
QT inverted Torsades
Prolonged V. fib
QT
QT prolongation
Hypokalemia
Hypocalcemia
Hypomagnesemia
Hyperphosphatemia
Hypomagnesemia
Usually in association with
hypokalemia + hypocalcemia
Torsades De Pointes
“Twisting of the Polymorphic V. Associated with

Torsades
points” tach prolonged QT
Electrolyte
Causes Medications
abnormalities
TCA’s See prior

Phenothiazines
Procainamide
Quinidine
Overdrive pacing
Cardioversion or
Medications
Defibrillation
NO
Depending on Treatment Lidocaine Amiodarone or
patient condition Isoproterenol Procainamide!
Phenytoin
Magnesium
Shortens QT
Give infusion post
conversion
100 B. Desai
EKG Changes Related to Medications
Digitalis: EKG Changes
Rhythms &
Intervals ST Segment T wave
Blocks
PR Sagging,
Prolonged Concave
Flat or PVC’s (most common)
QT upwards
inverted AV dissociation
Shortened (dig effect and
PAT with blocks
may be normal)
Sinus bradycardia
SA blocks
AV blocks
Bidirectional V.tach
Slow A. Fib
Junctional tachycardia
Sinus Arrest
PAT with block Bidirectional V.

Tach
Pathognomonic Rare but

suggests
Digitalis toxicity
Tricyclic Antidepressants: EKG Changes
Axis QRS Segment QT Interval Rhythms Blocks
Right axis
Sinus
deviation Wide May be
Prolonged tachycardia
>100 ms present
Terminal R wave (most common)
>3mm in aVR
R/S ratio >0.7 in
aVR
Same effect with other Sodium

channel blocking agents
I aVR V1 V4
Quinine
II aVL V2 V5 Propranolol
Antimalarials
(Chloroquine)
Local anesthestics
III aVF V3 V6 (Bupivacaine)
Type 1a antiarrhythmics
(Quinidine, Procainamide)
Type 1c antiarrhythmics
II
(Flecainide, Encainide)
102 B. Desai
Dysrhythmias
Junctional Escape Rhythm (JER)
JER Rate decreases down

Depends on Location
Mechanism the conducting system
Sinus Arrest Sinus Bradycardia
Severe
Blocks
Type II 2oAV Block

3oAV Block
Heart Disease
Sinoatrial block Conditions that
can potentially Acute MI
Drugs & Medications lead to JER CHF
Myocarditis
Digitalis toxicity
β -blocker OD
Ca channel blocker
OD
Metabolic
derangements
Electrolyte
disturbances
Hypo- or
Hyperkalemia
JER: EKG Changes

Rate
P waves PR Interval QRS Complex Rhythm
(Depends on site
of ectopic
pacemaker)
Shortened if P
Absent Usually
wave precedes Regular
May be inverted narrow Atria = <60 bpm
QRS
< 120 ms AV Node =

40–60 bpm
Ventricle =
20–40 bpm
Accelerated
Junctional Rhythm
Retrograde P
waves
Rate =
60–100 bpm
JER Treatment
Hemodynamically Transvenous or
Atropine
Unstable Transcutaneous pacing
JER Treatment
Stable patient
Atropine to speed
Usually none
up rate
Supraventricular Tachycardia (SVT)
SVT
All dysrhythmias arising A. flutter AV nodal re-entry

SVT
above the bindle of His A. fib tachycardia
MAT
Pre-excitation
Hyperthyroidism
syndromes
WPW
Rheumatic Heart
Mitral disease
Disease
Stenosis
Drugs & Medications

Causes of SVT
Caffeine
Tobacco
Alcohol
Acute MI
Digitalis toxicity
Pericarditis
104 B. Desai
SVT: EKG Changes
P waves QRS Complex Rhythm
May be absent
Narrow Regular
May be
retrograde
SVT Treatment
Hemodynamically Synchronized
Unstable cardioversion
Methylxanthines
(Theophylline)=
MORE
Carbamazepine = LESS
Vagal maneuvers Adenosine
Most effective mg
Valsalva 6 12 12
CP, dyspnea, feeling
of doom
SVT Treatment Amiodarone

Procainamide
Preferred for CHF or

Slow in onset
Stable patient low EF
Calcium Channel
b-blockers
Blocker
Diltiazem Esmolol
Verapamil Propranolol
Other Choices for SVT Treatment
SVT 2°
Propranolol
Thyrotoxicosis?
SVT 2° Digoxin Consider Slow correction

Magnesium Lidocaine Phenytoin
Toxicity? Digibind of hypokalemia
Other agents? Procainamide Amiodarone
Depends on
Disposition
clinical condition
Atrial Fibrillation (AF) and Atrial Flutter (AFL)
Most common
AF
supraventricular arrhythmia
Pre-excitation
Thyrotoxicosis
syndromes
WPW
Heart Disease
Acute MI
Pulmonary Embolism
Rheumatic HD ±
Valvular HD
Hypertension
Dilated
Causes of AF/AFl cardiomyopathy
HOCM
Drugs & Medications
Digitalis toxicity
COPD
Sympathomimetics
Metabolic
Pericarditis
derangements
Electrolyte
disturbances
Acid-base
disturbance
106 B. Desai
AF: EKG Changes
P waves QRS Complex Rhythm Other
Usually Irregularly Wandering

Absent baseline
narrow irregular
May have fine

Wide QRS or coarse
Complex fibrillatory
BBB waves
Accessory
pathway
Ashman
Aberrant Phenomenon
conduction
Aberrantly
conducted beats
usually of RBBB
morphology
Due to long
refractory period
of the preceding
RR interval
Atrial Flutter: EKG Changes
Flutter waves QRS Complex Rhythm Other
Regular with Wandering

Usually
Present a fixed AV baseline
narrow
block
II, III,aVF,V1 Variable AV

Wide QRS block =
Irregular
BBB rhythm
Accessory
pathway
Aberrant
conduction Ventricular Rate
Usually
blocked
2:1, 3:1, 4:1

AF/AFL Treatment
Atrial Fib or A. Flutter

Anticoagulate 1st!
> 2 days? AF/AFL >2 days =
Anticoagulate 1st
Diltiazem
Amiodarone AF/AFL b-blockers

Treatment
Stable patient
Digoxin
Slow in onset
Other Tidbits Concerning AF/AFL
All block AV node

Adenosine β-blockers conduction &
increase
AF 2° WPW? Amiodarone OR Procainamide NOT
conduction down
Ca-channel blockers Digoxin the accessory
pathway
AF + ↓ EF Amiodarone OR Diltiazem OR Digoxin
Depends on
Disposition
clinical condition
108 B. Desai
Multifocal Atrial Tachycardia (MAT)
COPD
Most common cause
Theophylline toxicity Causes of MAT CHF
Sepsis
MAT: EKG Changes
P waves QRS Complex Rhythm Intervals
At least 3 different
P wave Usually Irregularly PP, PR, & RR
morphologies narrow irregular intervals vary
Some may not be

conducted; others
may be aberrantly
conducted
Other
Isoelectric baseline
No single dominant
atrial pacemaker
MAT Treatment
Treat the underlying

Primary treatment
condition
Oxygen
MAT
Treatment
Stable patient
Magnesium sulfate Ca-channel blockers
Drug of choice
Premature Ventricular Contractions
Iatrogenic Hyperthyroidism
Digitalis toxicity Acute MI
Sympathomimetics CHF
Alcohol Myocardial
Causes of PVC’s contusion
Caffeine
Cardiomyopathy
Tobacco
Beta agonists
Hypoxia
Metabolic & Electrolyte

Anxiety
derangements
Hypokalemia
Hypomagnesemia
Acid-Base disturbance
110 B. Desai
PVCs: EKG Changes
Compensatory
pause
Absent Wide Varies
Unifocal or
Multifocal
PVC Treatment
Treat the underlying

Primary treatment
condition
Magnesium
Procainamide Considerations for b-blockers

PVC treatment
Stable
DEPENDS ON
CLINICAL
SCENARIO!!
Hemodynamic Cardioversion or
Sustained PVC’s VT > 30 sec
instability Defibrillation
Wolff-Parkinson-White (WPW) Syndrome
Anterograde
Pre-excitation syndrome due to
WPW Pathways Retrograde
abnormal accessory pathway
Bi-directional Majority
Bundle of Kent
Predisposes one to Especially

WPW
tachyarrhythmias Atrial Fibrillation
Orthodromic Antidromic
pathway pathway
SA AV SA AV
RA LA RA LA AV node cannot
slow down
conduction
Rapid ventricular rates

RV LV RV LV can occur
Worse in A. fib, can

degenerate into V. fib!
Normal EKG Wide complex QRS

112 B. Desai
WPW: EKG Changes in Sinus Rhythm
PR interval QRS Complex Delta wave ST segment
ST segment & T
Slurred initial
wave may show
Shortened Wide upstroke of QRS
discordant
may be present
changes
<120 ms > 100 ms May not be seen in

–
tachyarrhythmias
Pseudo-
Infarction
Delta waves are

negatively
deflected in
anterior & inferior
leads
Pseudo Q waves
Prominent R waves
in V1–3
Mimicks posterior
infarction
Atrioventricular Reentry Tachycardias (AVRT): RD
AVRT Type of SVT
Has a reentry circuit

that allows for circus
movement
During
tachyarrhythmias
pre-excitation features
are lost
Direction of reentry
determines shape of
QRS
AVRT with
orthodromic (left) &
antidromic (right)
AV nodal conduction
AVRT: EKG Changes
P waves QRS Complex T waves ST segment Rate
Orthodromic
Buried in Normal May be
QRS or Depression 200–300
inverted
Retrograde
Andromic
Wide
< 120 ms
Orthodromic
Andromic
Atrial Fibrillation/Flutter in WPW: EKG Changes
Rate Rhythm QRS Complex Axis
Irregular
>200 bpm A. Flutter = Wide Stable
Regular
May change in
shape
114 B. Desai
WPW Treatment: Narrow QRS Complex: Stable
Vagal maneuvers Adenosine
Most effective mg Methylxanthines

Valsalva 6 12 12 (Theophylline)=
CP, dyspnea, feeling MORE
of doom
Carbamazepine = LESS
Amiodarone
Procainamide Treatment
Preferred for CHF or
Slow in onset
low EF
Calcium Channel
β-blockers
Blocker
Diltiazem Esmolol
Verapamil Propranolol
WPW Treatment: Unstable: Any Size QRS Complex
WPW Treatment Atrial Fibrillation or Flutter: Stable
WPW + A. Fib Procainamide Slow Onset
WPW Treatment Wide QRS Complex: Stable
WPW + Wide
Procainamide OR Amiodarone
Complex
Preferred for
CHF or low EF
Digitalis
Adenosine
Do NOT Block AV node ↑ Conduction down ↑ Ventricular May lead
USE β-blockers conduction accessory pathway rate to V. Fib
Ca-Channel blockers
Ventricular Tachycardia (VT)
Family Hx of Sudden
Hypoxia
Cardiac Death
Digitalis toxicity Causes of Acute MI

Ventricular
Sympathomimetics Tachycardia CHF
Toxic ingestions Myocardial
contusion
Cardiomyopathy

Age > 35
derangements
Hypokalemia PPV 85%
Hypomagnesemia
Ventricular Tachycardia: EKG Changes
P waves QRS Complex Rhythm Rate
Rate >120
Absent Wide Regular Usually > 150
Unifocal or
Multifocal
Monomorphic
Polymorphic VT
VT
The same QRS

complexes Example:
within each Torsades
lead
116 B. Desai
Other EKG Features of VT
No LBBB or RBBB
QRS > 150 ms
morphology
RSR’ complexes with Extreme Axis

taller left rabbit ear Deviation
Most specific finding (+) QRS in aVR &
of VT Causes of VT (-) in I & aVF
Concordance
AV dissociation
throughout
P’s and QRS
complexes at
different rates
Capture Beats Fusion Beats
SA node “captures” Hybrid beat from

the ventricles simultaneous sinus
producing a normal & ventricular beats
QRS
VT Treatment
Pulse
Hemodynamically
Pulse Defibrillation
Unstable
Amiodarone
Low EF
Lidocaine Procainamide
VT
Stable patient
Magnesium
Torsades
Ventricular Fibrillation (VF)
Hypoxia Pulmonary Embolism
Digitalis toxicity Acute MI

Causes of
Sympathomimetics Ventricular Long QT
Toxic ingestions Fibrillation Cardiomyopathy
R on T
Brugada syndrome
Tamponade
Blunt trauma

Environmental
derangements
Hypo & Hyperkalemia Electrical injuries
Hypothermia Lightning strikes
Hypomagnesemia Drowning
118 B. Desai
Ventricular Fibrillation: EKG Changes
P waves QRS Complex T waves Rhythm Rate
150–500 per
Absent Absent Absent Chaotic
minute
Other
Amplitude
decreases with
duration
Coarse to Fine
Heart Blocks
Left Bundle Branch Block (LBBB)
Ischemic Heart
Aortic stenosis
disease
Drugs & Medications Anterior MI
Digitalis toxicity
Causes of LBBB
Primary cardiac
fibrosis of the
Hypertension
conducting system
Dilated Electrolyte
Cardiomyopathy derangements
Hyperkalemia
Hypermagnesemia
LBBB: EKG Changes
V1 Lateral leads QRS T waves Other
Large R waves Opposite

Dominant S Left axis
(I, aVL, V5, V6) deflection than
wave Wide deviation is
terminal half of
(QS or rS) common
the QRS
No Q Waves
(I, V5,V6) >120 ms
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
Right Bundle Branch Block (RBBB)

Ischemic Heart Right Ventricular
Pulmonary embolism
Disease Hypertrophy
Rheumatic heart
Cor Pulmonale
disease
Causes of RBBB
Primary cardiac
fibrosis of the Congenital heart
conducting system disease
Cardiomyopathy Myocarditis
120 B. Desai
RBBB: EKG Changes
V1 Lateral leads QRS T waves Other
Wide S waves Opposite Axis is variable

Triphasic I, V5, V6 deflection than ST depression &
Wide
QRS (RSR’) terminal half of T wave
Normal septal Q the QRS
waves inversions
I, V6 > 120 ms V1–3
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
II
First-Degree Heart Block (1° HB)
Age-related
Increased vagal tone
degeneration
Heart Disease
Acute Inferior MI
Myocarditis
Drugs & Medications Endocarditis
Mitral valve surgery
Digitalis toxicity
1oHB Congenital
β -blockers Causes of
Ca-channel blockers
Amiodarone
Hypothermia
Electrolyte
Athletic training
derangements
Hypo-or
Hyperkalemia
Hypermagnesemia
1° HB: EKG Changes
P waves PR Interval QRS Complex Rhythm Other
Usually “Marked” 1°HB

Normal Prolonged Regular if PR > 300 ms
narrow
1:1 relationship
> 200 ms of P & QRS
Block at level of
AV node
1° HB Treatment
Transcutaneous
Symptomatic? Atropine
pacing
1oHB Treatment
Stable
Look for underlying

Usually none
cause
122 B. Desai
Second-Degree Type 1 Heart Block (2° Type 1 HB)
Age-related
Increased vagal tone
degeneration
Heart Disease
Acute Inferior MI
Myocarditis
Drugs & Medications Endocarditis
Digitalis toxicity
Causes of 2o Congenital
β -blockers Type 1 HB
Ca-channel blockers
Similar to 1° HB
Amiodarone
Hypothermia
Electrolyte
Athletic training
derangements
Hypo-or
Hyperkalemia
Hypermagnesemia
2° Type 1 HB: EKG Changes
PR & RR
Intervals
PR
Progressively “Marked” 1°HB
Usually
Normal lengthens Regular if PR > 300 ms
narrow
RR 1:1 relationship
Progressively of P & QRS
shortens
Block at level of
Until a beat is AV node
dropped
2° Type 1 HB Treatment
2° Type 1
Treatment
Transcutaneous
Atropine
pacing
Permanent pacing
is rarely required
Second-Degree Type 2 Heart Block

(2° Type 2 HB)
Infiltrative Idiopathic fibrosis of

Myocardial Diseases conducting system
Sarcoid
Amyloidosis
Heart Disease
Hemachromatosis
Acute Anterior MI
Due to infarction of
the bundle branches
Drugs & Medications
Digitalis toxicity Causes of 2° Myocarditis

Type 2 HB
b-blockers
Ca-channel blockers
Autoimmune
Amiodarone disorders
Lupus
Systemic sclerosis
Inflammatory Electrolyte
conditions derangements
Rheumatic Fever Hyperkalemia
Lyme Disease Hypermagnesemia

124 B. Desai
2° Type 2 HB: EKG Changes
P waves PR Intervals QRS Complex Dropped Beats Other
When they occur Block below AV

Normal are of the same Usually wide Present node
duration
Typically with
pre-existing
LBBB or
bifascicular
block
2° Type 2 HB Treatment
2° Type 2
Treatment
Transcutaneous Transvenous +
Bridge to
pacing Permanent pacing
Permanent pacing
may be required
Other Tidbits Concerning 2° Type 2 HB
Severe
Hemodynamic Progression to
2° Type 2 HB 2° Type 1 HB In producing
compromise
symptomatic
3° Heart Block
bradycardia
Risk of Asystole? 30-35% per year
2° Type 2 HB Do not give Accelerates ↓ Ventricular

↓ BP
Pitfall Atropine atrial rate response
Insertion of permanent
Disposition ADMISSION
pacemaker
Third-Degree Heart Block (3° HB)
Infiltrative Idiopathic fibrosis of

Myocardial Diseases conducting system
Sarcoid
Amyloidosis
Heart Disease
Hemochromatosis
Acute MI
Due to infarction of the
bundle branches
Drugs & Medications Both Anterior & Inferior

MI
Digitalis toxicity Myocarditis
Causes of 3° HB
b-blockers
Ca-channel blockers
Essentially the same Autoimmune
Amiodarone as 2° Type 2 HB disorders
Lupus
Systemic sclerosis
Inflammatory Electrolyte
conditions derangements
Rheumatic Fever Hyperkalemia
Lyme Disease Hypermagnesemia

126 B. Desai
3° HB: EKG Changes
P waves PR Intervals QRS Complex Rate Other
Junctional Block at AV
Changes node, bundle of
Normal escape beats Usually severe
randomly His or bundle
Narrow QRS bradycardia branches
with
independent
Ventricular atrial &
ventricular rates No relationship
escape beats between P and
Wide QRS QRS
AV Dissociation (AVD) Similar causes

to 3° HB
3° HB is type of AVD
Rate Other
Atrial rate > Fusion beats are

Ventricular rate common
3° HB Treatment
3° HB Treatment
Narrow Complex Wide Complex
May be transient due

Pacemaker
to vagal tone
Inferior MI
OD’s
R
No Atropine
x
Transcutaneous
Atropine
pacing
Miscellaneous
Brugada Syndrome Introduction
Brugada Structurally Autosomal Common in SE Abnormality in sodium

syndrome normal heart dominant Asia channels of heart
Brugada One of the most common causes

syndrome of death in males <40
Brugada Ventricular
Sudden death Syncope Due to
syndrome fibrillation
Treatment AICD Placement
Fever
Infectious &
Non-infectious
causes
Drugs & Electrolyte
Medications derangements
Cocaine Hypo-&
Hyperkalemia
Alcohol
Brugada Hypercalcemia
a-agonists
Syndrome Hypercalcemia
b-blockers
Factors that may
Nitrates precipitate Vagal maneuvers
dysrhythmias
Na channel blockers
TCA’s Heart Disease
Type 1 antiarrhythmics Ischemia
Hypothermia
128 B. Desai
Brugada Syndrome: EKG Changes
Brugada Sign
ST segments Type 2 Type 3
Type 1
Elevated in
V1 & V2
Coved ST segment
elevation > 2mm ST elevation Morphology of
in V1-3 (only need resembling a Type 1 or 2, but <2
1 lead) followed by saddle > 2mm mm ST elevation
a (-) T wave
“Pseudo RBBB”
Type 1 Type 2 Type 3
V1 V1
V1
V2 V2 V2
V3 V3 V3
Tetralogy of Fallot
PEDIATRICS
Pulmonary stenosis
Tetralogy of Most common cause Consists of RV outflow obstruction Thickened RV wall

Fallot of congenital shunts & Ventricular Septal defect
VSD
Overriding aorta on VSD

Boot shaped Decreased pulmonary
CXR
heart vascular markings
Dyspnea Syncope
Usually precipitated
“Tet Spell” Hemoptysis
by feeding or crying
Hypercyanosis Seizures
Knees to chest or Decreases venous

squatting return & increases
position peripheral resistance
Propranolol Supplemental O2
Potential
treatments for
Tet Spell
Can decrease
Increases systemic
Phenylephrine Morphine sulfate hyperpnea, but can
vascular resistance
decrease BP
Bicarbonate
Decreases acidosis
induced respiratory
drive
Pulmonary Emergencies
Contents
Definitions and Clinical Presentations ............................................................................................................................................................ 132
Pneumothorax ................................................................................................................................................................................................... 135
Asthma ............................................................................................................................................................................................................... 138
Chronic Obstructive Pulmonary Disease ........................................................................................................................................................ 143
Bronchiolitis....................................................................................................................................................................................................... 150
Pertussis ............................................................................................................................................................................................................. 152
Pneumonia ......................................................................................................................................................................................................... 153
Tuberculosis ....................................................................................................................................................................................................... 168
Lung Abscess ..................................................................................................................................................................................................... 172
Acute Respiratory Distress Syndrome ............................................................................................................................................................ 172
Pleural Effusions ............................................................................................................................................................................................... 173
The Airway ........................................................................................................................................................................................................ 179
General Pediatrics ............................................................................................................................................................................................. 181
M.R. Marchick, MD
Department of Emergency Medicine,
University of Florida College of Medicine,
B. Desai, MD, MEd (*)
University of Florida, Gainesville, FL, USA

DOI 10.1007/978-3-319-30838-8_2
132 M.R. Marchick and B. Desai
Definitions and Clinical Presentations
Hypoxemia
Low arterial
Hypoxemia PaO2 < 60 mmHg OR SaO2 < 90 mmHg PaO2 < 60 mmHg
oxygen content
Hypoventilation
Impaired Low ambient O2

diffusion concentration
Emphysema High altitudes
Right->Left
shunting
Does not reverse Causes
with supplemental
O2
Vascular
malformations V/Q mismatch
Cyanotic
congenital PE
heart disease Infection
Atelectasis Asthma
Consolidation COPD
Hypoxia
Insufficient tissue
Hypoxia oxygen delivery
Hypoxemia
#1 cause
Abnormal
hemoglobin Causes Anemia
Methemoglobinemia
Low cardiac
output
Pulmonary Emergencies 133
Hypercapnia
Arterial pCO2 Result of

Hypercapnia
> 45 mmHg hypoventilation
Acute Little renal HCO3 increases 1 mEq/L for

hypercapnia compensation every 10 mmHg increase in pCO2
Chronic HCO3 increases 3.5 mEq/L for

hypercapnia every 10 mmHg increase in pCO2
Arterial-Alveolar Gradient
Arterial-Alveolar
Measured PaO2 Calculated PaO2
Gradient
Quick Normal is 10–15

140 – (PaCO2 + PaO2)
determination (Increases with age)
Decrease in
diffusion
Interstitial disease
V/Q Mismatch
Shunt Causes of Pulmonary
increased A-a embolism
AV Fistula gradient Pneumonia
Atrial septal defect COPD
Cyanosis
Blue discoloration of tongue Abnormal Insufficient lung

Central
and mucous membranes hemoglobin oxygenation
Blue discoloration Abnormal Insufficient lung Peripheral

Peripheral
of extremities hemoglobin oxygenation vasoconstriction
Diminished blood
flow
Obtain formal
Cyanosis present?
ABG
Apparent clinically with

Central cyanosis
> 5 g/dL desaturated Hgb
Overestimates Presence of Presence of

Pulse oximetry? Due to OR
SaO2 Methemoglobin carboxyhemoglobin
Reads as 80–85 % Read as oxygenated
regardless of true SaO2 hemoglobin
Hemoptysis
Hemoptysis Massive Moderate Minor
> 600 mL in 24 20–600 mL in 24 <20 mL in 24

hours hours hours
Bronchitis
#1 cause
Pulmonary
Bronchiectasis
embolism
Common Causes
Lung Abscess Pneumonia
Pulmonary
Malignancy
embolism
Tuberculosis
Bronchiectasis Lung abscess
Causes of Massive Wegener’s

Aspergillosis Hemoptysis granulomatosis
Arterio-bronchial
Angiodysplasia
fistula
Tuberculosis Mitral stenosis

Stabilize airway for Consider ENT or

Initial evaluation
massive hemoptysis GI source!
Massive Attempt to selectively intubate Consider placing patient with

Intubate Failure?
hemoptysis? non-hemorrhaging lung hemorrhaging lung down
After airway Pulmonary Reverse

Bronchoscopy
secure consultation coagulopathy
Coagulation Consider type &

Laboratory CBC
parameters screen
Will miss 20 % of
Imaging CXR
neoplasms
Better sensitivity for

Imaging CT May diagnose PE
carcinomas & bronchiectasis
Pneumothorax
Spontaneous Pneumothorax
No underlying Underlying lung

Primary lung disease Secondary disease
Male
Primary Risk Genetic

Thin build predilection
Factors
Smoking
COPD
#1 cause
Sarcoidosis Asthma
Secondary Risk
Factors
Thoracic P. jiroveci
endometriosis infection
Crack cocaine use Lung abscess

Pneumothorax Diagnosis and Management
Concern for Immediate needle Do not wait for

tension? decompression CXR!!
Needle 16 gauge or larger long 2nd (or 3rd) Midclavicular Subsequent tube
decompression needle / Angiocath intercostal space line thoracostomy
Above rib to avoid

neurovascular
bundle
Look for deep

CXR? 83 % sensitive On supine CXR sulcus sign
Ultrasound Near 100 % sensitive if Absence of Absence of lung

findings experienced operator comet tails sliding
CT? Highly sensitive
Small Consider trial of nitrogen

< 20 %
pneumothorax washout with 100 % oxygen
Moderate Needle Small caliber/ Pigtail 24 Fr chest tube

OR OR
pneumothorax aspiration catheter placement placement
Followed by chest
tube or catheter
Large Chest tube

pneumothorax placement
Iatrogenic PTX
~50 % of cases Thoracentesis Biopsies

Always obtain
Iatrogenic PTX post-procedure
CXR!
~25 % of cases Subclavian CVL
May be difficult to Development Up to 1/3 not idenfied

CXR?
idenfy if supine may be delayed on inial CXR
Similar to
Treatment
spontaneous PTX
Pneumomediastinum
Symptoms & Signs
Pleuritic chest + Hamman’s

pain crunch
Pulmonary
barotrauma
Forceful valsalva
Pulmonary
barotrauma
Endoscopy
Trauma Causes Bronchoscopy
Intubation
Mechanical
ventilation
Esophageal Caustic substance

perforation ingestion
Treat underlying
Treatment cause
Tension
Pneumomediastinum Rare Treatment Pericardiocentesis
Asthma
Introduction
50 % of cases Initial 2:1 predominance
Affects ~ 5 % of Higher in Blacks
Asthma develop among of M:F & equalizes over
US population children < 10 subsequent decades & Puerto-Ricans
Bronchoconstrictor response Airway Reversible airway

Pathology
to a number of triggers inflammation obstruction
Triggering agent
Recruitment of
Air trapping
inflammatory cells
Eosinophils
Neutrophils
Pathophysiology
Mast cells
Lymphocytes
Increased airway Macrophages

Bronchoconstriction
resistance
Mucus
hypersecretion Release of
Airway edema inflammatory
mediators
IgE
Leukotrienes
Recruitment of Cytokines
additional
inflammatory cells
Triggering Agents
Infection Hormonal factors
Viral Pregnancy
Menses
Thyroid disease
Allergens Exercise
Pollutant
Emotional stress
Triggering Agents
Irritants
Food Smoke
preservatives
Dust mites
Dyes Cold Exposure
β-blockers ASA NSAIDs
Clinical Features
Symptoms & Signs
Prolonged
Typical S&S Tachypnea Tachycardia Chest tightness Wheezing Cough
expiratory phase
Severe exacerbations – May indicate Poor Paradoxical Altered mental
No wheezing Hypercapnia
impending respiratory arrest respirations respirations status
Risk Factors for Death

Prior ICU
Prior intubation
admissions
> 3 ED visits in last

Difficulty
year
perceiving severity
of exacerbation
> 2 hospitalizations
in prior year
Prior psychiatric
disease
Risk Factors for
Death Hospitalization or
ED visit for asthma
Prior pulmonary in past month
disease
Use of >2 canisters

Prior of short acting beta
cardiovascular agonist in past
disease month
Current use or
Recreational drug Low socio- recent
use economic status discontinuation of
systemic steroids
Peak Flow
Measure pre and post each Ensure good

Peak Flow
bronchodilator treatment patient effort
Compare to Personal
Peak Flow Age Sex Height
predicted value best
<25 % Concern for impending

predicted respiratory failure
<40 % Poor response to

Measurement
predicted treatment
>70 % Good treatment

Good social
predicted response
support &
follow-up plan
>70 % Good response to treatment,

predicted can likely be discharged
Short-acting
Discharge?
β-agonist
After treatment 40–69 % Individualized decision
<40 %
Generally requires admission Short course of
predicted
systemic
steroids
β-Agonists and Anticholinergics
β-2 adrenergic Primarily dilate small, Short acting agents Long acting agents Not indicated for
agonists peripheral airways have rapid onset have slow onset acute sx
β-2 adrenergic Stimulate adenyl Increase cyclic Decreased Smooth muscle

agonists cyclase AMP intracellular Ca++ relaxation
Rare
Tremor
Side effects Tachycardia HTN Anxiety arrhythmias,
(#1) e.g., MAT
Seen with
theophylline
Systemic No advantage Unless unable to More side

IV infusions
β-agonists over inhaled deliver via inhalation effects
Subcutaneous 0.2–0.5 mL Increased cardiovascular Via β-1

Not β-2 selective
epinephrine 1:1000 solution side effects receptors
Terbutaline 0.25 mg SC β-2 selective
Inhibits parasympathetic Decrease respiratory Primarily affect

Anticholinergics
reflex bronchoconstriction secretions large airways
Poorly absorbed Minimal systemic Slower onset of Less potent action

Ipratropium
from airways side effects action than β-2 agonists
Not appropriate for
monotherapy
Work Commonly given together in

Ipratropium β-blockers
synergistically 3 stacked doses early in ED
Steroids, Methylxanthines, Magnesium, and Leukotriene Modifiers
Reduce recruitment & Reduce release of Increase Onset of action

Corticosteroids activation of pro-inflammatory responsiveness of β-
4-8 hours
inflammatory cells mediators adrenergic receptors
Occasionally used
Bronchodilatory Anti-inflammatory
Methylxanthines Theophylline for chronic
effects effects
management
Narrow Significant Check level on all

Methylxanthines therapeutic arrythmogenic CNS side effects patients taking
window potential theophylline
Modulate
Leukotriene Useful for chronic Not indicated for
inflammatory
modifiers management ED use
response
25–75 mg/kg up
Relaxes bronchial Stabilizes mast cells & Indicated only in
Magnesium severe to 2 g IV over 30
smooth muscle T-lymphocytes exacerbations minutes
Magnesium side Respiratory Muscle

Flushing Nausea Hypotension Reflexes
effects depression weakness
Severe Asthma Management
Induction agent Provides

Ketamine Bronchodilation
to consider sedation
Intubation Continue in-line

After intubation
tidbits nebulizer therapy
Ventilator Increase time for Decrease Decrease Increase inspiratory

management expiration I:E ratio respiratory rate flow rate
Permissive Ensure pulse

Goal?
hypercapnia oximetry > 88 %
Respiratory Disconnect Provide chest Consider bilateral

Provide fluids
arrest? ventilator compressions chest tubes
For putative
pneumothorax
Risk of barotrauma secondary to
Pitfall
with intubation barotrauma
Chronic Obstructive Pulmonary Disease
Introduction
Increasing Only major cause Insidious onset
4th leading cause
COPD prevalence in of death which is typically over
of death in US women increasing decades
FEV 1 FVC
Clinical FEV1/FVC< 70 % FEV1 < 80 %
Forced expiratory Forced vital
definition predicted volume in 1 sec capacity
More severe Further diminishment in

COPD? FEV1 vs. predicted value
Chronic Common overlap

COPD Emphysema Bronchiectasis of these conditions
bronchitis
Chronic bronchitis Productive cough for > 3 months in 2

“blue bloater” Clinical diagnosis
consecutive years without other apparent cause
Emphysema Pathologic
Destruction of small pulmonary airspaces
“pink puffer” diagnosis
Long-term
Cigarette Indoor air Occupational α-1 antitrypsin
Risk factors passive
smoking pollutants dust exposure deficiency
smoking
#1 risk factor Very rare
Cigarette COPD develops in

smoking ~15 % smokers
Interventions which
Smoking Long-term O2 Consider pneumococcal
improve disease
cessation therapy vaccination for all COPD patients
progression
COPD Pathophysiology
Irritants
Arterial
Failed gas constriction Increased
exchange inflammatory
pCO2 cells
T cells
pO2
Polycythemia
Neutrophils
Pathophysiology
Macrophages
Blockage of small
airways
Release of
Tissue destruction inflammatory
mediators
Decreased lung Diminished cross
elasticity sectional area of TNF
vascular bed
Proteases
Leukotriene B4
Mucus secretion
Diminished cross
Arterial Pulmonary Right heart
sectional area of Cor pulmonale
constriction hypertension failure
vascular bed
Acute COPD Exacerbation Causes
Infection
Viral
Bacterial
#1 cause
Idiopathic PE
CHF
Acute COPD
Beta blockers Exacerbation Environmental
Causes changes
Temperature
Humidity
Spontaneous PTX Pollutants
Medication
noncompliance
Must consider potential
comorbid disease: PE, PTX,
PNA, CHF
Diagnostics
Evaluate for
CXR treatable cause of Pneumonia PTX CHF
exacerbation
Chronic CXR Findings
Flat low Narrow cardiac Unless RV hypertrophy/ Ø Lung markings if emphysematous

hemidiaphragm
≠AP diameter silhouette dilation severe
Bullae
changes predominate
Not routinely Consider in patients with Ø mental

ABG necessary status to evaluate for hypercapneic
respiratory failure
Chronic HCO3 ≠ 3.5 mmol/l for Acute HCO3 ≠ 1mmol/l for each
Hypercapnia
each 10 mm Hg ≠ in pCO2 Hypercapnia 10 mm Hg ≠ in pCO2
Less critical than for asthma as

PFT’s bronchospasm generally less prominent
ECG Findings
Right axis Multifocal atrial Atrial Right ventricular S1Q3T3 pattern as result of
Low voltage
deviation tachycardia enlargement hypertrophy right ventricular strain
COPD Exacerbation Management

Positive pressure
O2
ventilation
Administer For respiratory
supplemental to failure
keep SaO2 near Ø Short-term
90 % mortality
Methylxanthines Steroids
Monitor for
Ø Intubation rate
Not indicated for hypercarbia Delayed onset of
ED use Improved action
Check level if symptoms Usually little change
patient uses in ED course
Ø pCO2
these chronically Associated with Ø
relapse
Improved dyspnea
Antibiotics Acute COPD Hyperglycemia
Exacerbation most common
Indicated in patients Management
with evidence of side effect
infection
≠ Sputum
purulence
≠ Dyspnea Bronchodilators
≠ Sputum See asthma
volume section
Respiratory
Organisms S. pneumoniae M. catarrhalis H. influenzae Azithromycin
fluoroquinolones
NIPPV Indications and Contraindications

Moderate to
severe dyspnea
with accessory
muscle use
pH < 7.35 and/or
PaCO2 > 45 mm RR > 25/min
Hg
Indications
Respiratory arrest
Hemodynamic
Craniofacial trauma
instability
Poor mask fit Contraindications Marked obesity
AMS / Aspiration Uncooperative

risk patient
Upper airway Inability to clear

obstruction airway secretions
Indications for Intubation
Respiratory arrest
Contraindication to
¯ Mental status
NIPPV
despite otherwise
maximal treatment
Severe Indications for
hypercapnia Intubation
Severe Failure to improve

acidemia with NIPPV
Severe hypoxia Severe tachypnea
COPD Ventilator Management and Pitfalls
Presence of High risk of PTX due to

blebs? positive pressure ventilation
Obstructed airways
Diminished
subsequent Incomplete
delivered tidal exhalation of
volumes tidal volume
“Air trapping”
Airway effects
Barotrauma
Increased airway
PTX pressures
Avoid
hyperventilation!
↑ Risk of
Dysrhythmias barotrauma Respiratory
alkalosis
Hyperventilation
effects
Seizures
Further metabolic
derangement in
setting of chronic
metabolic alkalosis
Permissive Hypercapnia
Permissive Prolonged Low respiratory Low tidal

Hypercapnia expiratory phase rate volumes
Improved V/Q
matching
Permissive
Less barotrauma Increased cardiac
hypercapnia
from autoPEEP output
benefits
Increased oxygen
unloading
Increased ICP
Permissive
hypercapnia
harms
Decreased
seizure threshold
COPD Exacerbation Disposition
Significantly
worsened
symptoms from
baseline
New oxygen
requirement
Poor social
situation or ADMIT
follow-up
Worsened hypercapnia
Inadequate
Significant
response to ED
comorbidities
treatment
Patient already
taking oral
steroids
³ 5 ED and clinic
HIGH RISK OF
Initial RR > 20 visits for COPD in
RELAPSE
prior year
Acute Bronchitis
Viruses
Most common
cause
Atypical bacteria
Influenza
<10 % cases
Acute Bronchitis
Rhinovirus Close quarter
Inflammation of outbreaks
Most common cause the large airways
of common cold of the lungs Chlamydophila
pneumoniae
Coronavirus Cough ± Mycoplasma
phlegm pneumoniae
Adenovirus
Bordetella
pertussis
RSV
Parainfluenza
virus
Acute Bronchitis Management

Exclude
Symptomatic Rx
pneumonia
Clinically Wheezing?
± CXR Albuterol
Suspect
Sx > 3 weeks?
pertussis?
Consider Azithromycin or
alternative Clarithromycin
diagnoses
Acute Bronchitis Reduces
GERD Management transmission of
B. pertussis
Asthma
Minimal effect on
Chronic symptoms, which
bronchitis often last > 3
weeks
Suspect
influenza?
Oseltamivir
< 48 hours from

onset of
symptoms
Bronchiolitis
Bronchiolitis
PEDIATRICS
Acute
inflammation of
bronchioles
Increased work of Bronchospasm

breathing
Pathophysiology
Edema
Airway resistance
Mucous
production
Atelectasis
Symptoms & Signs
Low grade PE: Wheezing

Typical S&S Rhinorrhea Cough Tachypnea Wheezing
fever & crackles
Severe Accessory
Cyanosis Apnea
exacerbations muscle use
Parainfluenza
Organisms RSV Influenza Adenovirus Rhinovirus
virus
#1 cause
RSV Management
PEDIATRICS
Rapid viral detection

Diagnosis 90 % sensitive Highly specific
of NP secretions
CXR NOT routinely Unless concern Commonly see

Imaging? for alternative Severe illness
indicated diagnosis atelectasis
Mainstay is Humidified Saline nasal Nebulized

Treatment supportive O2 Hydration drops & hypertonic
care suctioning saline
Severe respiratory Refractory Consider mechanical

Severe disease?
distress hypoxemia ventilation
Bronchodilators Should not be Used but no

Limited utility Discontinue
+ steroids? used routinely response?
Ribavirin? Not indicated
Only for coexisting

Antibiotics?
bacterial infection
Bronchiolitis Disposition
PEDIATRICS
Witnessed apnea
Ill appearance Persistent

hypoxemia
Gestational age
Underlying <37 weeks
cardiopulmonary ADMIT
disease
Age < 3 months
Marked
Immunodeficiency
tachypnea
Inability to clear
airway secretions
Bronchopulmonary Dysplasia
PEDIATRICS
Bronchopulmonary Common in premature infants treated Greatly increases risk of

Dysplasia with oxygen ± mechanical ventilation hospitalization in 1st year
Degree of Barotrauma Commonly see

Severity? Steroid use
prematurity from ventilation atelectasis
Airway Airway Obstructive

Pathophysiology ¯Compliance
resistance reactivity physiology
Palivizumab for Routine

Treatment
RSV prophylaxis vaccinations
Pertussis
Introduction
PEDIATRICS
Immunization
Bordetella Gram negative Highly Incubation 1–3
efficacy wanes from
pertussis coccobacillus contagious weeks
late adolescence
Culture on
Diagnosis? NP swab Bordet-Gengou PCR also useful
medium
Paroxysmal Convalescent
Stages of disease Catarrhal Stage
stage stage
Catarrhal Stage Paroxysmal Stage Convalescent Phase
Up to 2 weeks 2–4 weeks 1 week to several months
Sx Sx Sx
Low grade fever & malaise Fever abates Residual cough
Paroxysmal coughing
Congestion
40–50 per day
Conjunctivitis Cough followed by inspiratory

stridor “whoop”
Highest infectivity
Infants may become apneic,
cyanotic, bradycardic
Whoop rare in infants
Pertussis Complications
PEDIATRICS
Pneumonia
#1 complication
Encephalitis Aspiration
Pertussis
Seizures Apnea
Complications
Subconjunctival
Pneumothorax
hemorrhage
Epistaxis Pneumomediastinum
Pertussis Treatment
PEDIATRICS
Rarely shorten course

Treatment Erythromycin OR Azithromycin OR Clarithromycin
or reduce severity
Primary reason Primarily to reduce

for treatment? transmission
Consider
Close contacts?
treatment
Highest
Severe respiratory
Admission Age < 1 year mortality in
distress
those < 1 month
Pneumonia
Pneumonia Classification
New infection ³ 2
Hospitalized ³ 2 Hospital
days after
days in past 90 acquired PNA
admission
days
New infection ³ 2
Ventilator
days after
Patients receiving associated PNA
Long-term care intubation
chronic wound
residents
care
Healthcare- Resistant Lower risk in
associated PNA organisms? CAP patients
(HCAP)
Patients receiving
home IV Hemodialysis
antibiotics patients
Immuno
Patients receiving
compromised
chemotherapy
patients
All others are

Community Acquired
PNA (CAP)
Pneumonia Pathophysiology
Pneumonia Pathogens inhaled or aspirated Overwhelm the lung’s typically

Pathophysiology into respiratory tract robust defense mechanisms
Impaired Chronic
Diminished host Impaired
mucociliary underlying OR Immune disease
defenses cough/gag
transport disease
Impaired
cough/gag AMS Seizure CVA
Impaired
Pre-existing viral
mucociliary Smoking COPD infection
transport
Chronic Cystic Hepatic

Alcoholism AIDS fibrosis failure Cancer ESRD
underlying disease
Hematogenous Otherwise
seeding Pseudomonas S. aureus uncommon
Less intense More indolent

Atypical agents? inflammatory course, mild
response symptoms
Pneumonia Treatment
Patient Type Organisms Treatment
S. pneumoniae
Outpatient Macrolide (preferred)
H. influenza
Previously healthy or
Mycoplasma pneumonia
No Abx within 3 months Doxycycline
Chlamydophila pneumoniae
Comorbidities
Chronic heart, lung, liver, renal Respiratory fluoroquinolone
disease, DM, Alcoholism, Same as above or
Malignancies, Immune disease β-lactam + Macrolide
Same as above + Respiratory fluoroquinolone

Inpatients
Legionella species or
Non-ICU
Aspiration β-lactam + Macrolide
S. pneumoniae β-lactam + either Azithromycin

Staph aureus or Respiratory fluoroquinolone
Inpatients
Legionella species (substitute Aztreonam for the
ICU
Gram (-) bacilli β-lactam if penicillin allergy)
H. influenza
Special Considerations
Pseudomonas a consideration?
Antipneumococcal, Respiratory
antipseudomonal b-lactam fluoroquinolone
OR
Antipneumococcal,
antipseudomonal b-lactam Aminoglycoside Azithromycin
OR
Antipneumococcal, Antipneumococcal
antipseudomonal b-lactam Aminoglycoside fluoroquinolone
Substitute Aztreonam for

penicillin allergy
Very sick (including children) and/or MRSA a

consideration?
Add Vancomycin or Linezolid

Pediatric Pneumonia Tidbits and Treatment
PEDIATRICS
Patient Age Organisms Treatment
Group B Streptococcus Ampicillin + Gentamicin

Birth – 3 weeks E. coli or
Listeria monocytogenese Cefotaxime
S. pneumoniae
Bordetella pertussis Erythromycin
3 weeks – 3 months Chlamydia trachomatis or
H. influenza Cefotaxime
Viral – RSV/Parainfluenza
Viruses
4 months – 4 years S. pneumoniae Same as above
Mycoplasma pneumoniae
Erythromycin
Mycoplasma pneumonia (Doxycyline if >8)
5 years – 15 years
S. pneumoniae or
Cefotaxime
Group B Most common Acquired in Results in a rapid

streptococcus cause utero fulminant disease process
Symptoms & Signs –> 3 weeks – 3 months – Typical bacteria
Decreased Intercostal Severe

feeding Fever Tachypnea Nasal flaring retractions Grunting irritability
Symptoms & Signs –> Chlamydia
Staccato cough Lung

Afebrile Tachypnea Conjunctivitis hyperinflation
Short sudden bursts of cough
Streptococcus pneumoniae
Streptococcus Most commonly

identified Encapsulated
pneumoniae pathogen Gram (+) diplococci
Even in HIV
Symptoms & Signs
Sudden onset May have more

Fever Chest pain Hemoptysis
chills indolent presentation
Parapneumonic
CXR Lobar infiltrate
effusion
Elderly (especially Sickle cell

High risk groups Children <2 HIV
unvaccinated) disease
Potential rapid
Functional or Immunosuppressed
OR development of
surgical asplenia patients
septic shock
Haemophilus influenzae
Type b causes Less common in
Haemophilus Gram negative
majority of children due to
influenzae rod infections immunization
Symptoms & Signs
Pleuritic chest Typical indolent

Fever Dyspnea pain course
Patchy alveolar
CXR Effusion
infiltrates
Poor Sickle cell

High risk groups Alcoholism COPD DM Cancer
nutrition disease
Complication Bacteremia
Similar Highly associated

M. catarrhalis
presentation with COPD
Pseudomonas aeruginosa
Pseudomonas Gram negative Not a common May cause Hematogenous

aeruginosa rod cause of CAP severe illness spread is common
Symptoms & Signs
Severe
Systemic illness Fever Chills Chest pain Vomiting AMS
presentation
Cyanosis
Empyema
Bilateral lower
CXR formation
lobe infiltrates common
Structural lung Patients on

Recent ICU Cystic Immune
High risk groups disease e.g., high-dose
admission Fibrosis bronchiectasis steroids compromised
Consider double
Complication High resistance
coverage
Klebsiella pneumoniae
Klebsiella Gram negative

pneumoniae rod
Symptoms & Signs
Abrupt onset “Currant jelly Necrotizing High incidence of

fever
Rigors Chest pain sputum” infection empyema formation
Abscess
CXR Lobar pattern
formation
History of Pre-existing lung

High risk groups Alcoholics Elderly
aspiration disease
Common producer of
Necrotizing extended spectrum
Antibiotic
Complication Due to
infection β-lactamases resistance
Staphylococcus aureus
Large gram (+) High association
Staphylococcus Uncommon Incidence
cocci in pairs with concomitant
aureus cause of CAP increasing (MRSA)
and clusters influenza infection
Symptoms & Signs
Insidious onset Often

Fever Chills Chest pain
of Sx necrotizing
Patchy, multilobar Pneumatocele Necrotizing

CXR But… Cavitation
infiltrate common formation infection
Nursing home Immuno- Laryngeal CA

High risk groups IVDA Aspiration
residents suppression history
Hematogenous
Complication
spread
Chlamydophila and Mycoplasma pneumoniae

Chlamydophila & Observed in
No organisms on Common causes Children &
Mycoplasma clustered
pneumoniae gram stain of atypical PNA outbreaks young adults
Symptoms & Signs
Non-productive
Gradual onset Sore throat Headache Flu-like Sx Vomiting AMS
cough
Cyanosis
Patchy segmental Interstitial

CXR
infiltrates pattern
Associated with
Mycoplasma
bullous myringitis
Legionella
Observed more Transmitted via inhalation of
Intracellular No person-
Legionella frequently during aqueous aerosols from
organism summer contaminated source to-person
Symptoms & Signs
Watery Relative
Flu-like Sx N/V Classic Hx Transaminitis
diarrhea bradycardia
Altered MS Both later in

Seizures
disease
Patchy infiltrates
Pleural effusion Can progress to
CXR predominantly
lower lobe in up to 1/3 ARDS
Immune
High risk groups Alcoholism Age > 50 Smokers DM COPD
disease
Complications Myocarditis Pyelonephritis Pancreatitis

Zoonotic PNA Etiologies
Direct contact Infected animal Post-tick Onset of high fever,

Tularemia OR cough, adenopathy,
with tissue (Rabbits) bite ulcerated skin lesion
Inhalation of dust contaminated From infected

Q-fever Coxiella burnetti
with tissue or excretions sheep, cattle, goats
Chlamydia Inhalation of droplets/dust

Psittacosis
psittaci from infected birds
Inhalation of Bilateral Respiratory Often fatal

Hantavirus aerosols from pulmonary
rodent feces or urine infiltrates distress No treatment
Most cases in the Cardiac failure
Southwest
Renal failure
Pneumocystis jirovecii (Formerly PCP)
Pneumocystis But does not Predisposed HIV

Fungal etiology But… respond to
jirovecii antifungals! patients Immune compromise
Symptoms & Signs
General Non-productive
Dyspnea Fever Weight loss Night sweats
malaise cough
CXR Appearance Bilateral interstitial Pleural Lobar Hilar

pattern with hilar Risk of PTX
varies! prominence effusion consolidation adenopathy
Most common
Serum lactate Confirm with silver staining or

Diagnosis dehydrogenase immunofluorescence assay of
often elevated sputum or bronchial washings
High dose TMP- Pentamidine can High incidence of

Treatment 21 days if HIV + OR be used if allergic But… severe side
SMX first line to TMP-SMX effects
ABG on room air Alveolar-arterial

Indicated if
Steroids? with PaO2 <70 OR gradient > 35 mm Initiate early!
HIV(+) Hg
mm Hg
Pathogens in HIV
CD4 Community acquired May have atypical

Pitfall
200–500 pathogens appearance on CXR
CD4
CAP TB PCP
<200
Most common
CD4 Mycobacterium
CAP TB PCP CMV Fungi
<50 avium complex
Serum lactate Confirm with silver staining or

Diagnosis dehydrogenase immunofluorescence assay of
often elevated sputum or bronchial washings
Pentamidine can High incidence of

High dose TMP-
Treatment 21 days if HIV + OR be used if allergic But… severe side
SMX first line
to TMP-SMX effects
ABG on room air Alveolar-arterial

Indicated if
Steroids? with PaO2 <70 OR gradient > 35 mm Initiate early!
HIV(+)
mm Hg Hg
Fungal PNA Etiologies
Coccidiodes Desert areas of Acute Typically resolves

uncomplicated without
immitis the Southwest US pneumonia antifungals
Immune Chronic 1st line

OR cardiopulmonary
compromised disease Fluconazole
Treatment
Rapidly 1st line
Life threatening OR May use azoles
progressive Amphotericin B
Histoplasma Blastomyces Ohio and

Mississippi river
capsulatum dermatitides valleys
Hilar
CXR Granulomas
adenopathy
Acute &
No treatment
Asymptomatic
Treatment
Evidence of 1st line
Symptomatic OR
chronic infection Itraconazole
Disposition
Viral pneumonia (esp. Low threshold for Consider IV

HCAP? Admit Varicella) particularly imaging, esp in
smokers acyclovir
severe in pregnancy
Pneumonia Clinical judgment

CAP Decision rules CURB-65 OR must always
severity index supersede
Immune status?
Social situation?
BUN > 19 Respiratory Diastolic BP ≤

CURB-65 factors Confusion rate ≥ 30/min 60 mm Hg Age ≥ 65
mg/dL
2 or more CURB-
Admit
65 factors?
Pneumonia Multiple criteria No high risk

consider pt at Class I Outpatient Rx
Severity Index high risk factors
High risk factors Assign to risk

present? Compute score class
Class II Outpatient Rx
Class III Borderline
Class IV or V Admit
Cultures and Treatment
If indicated, obtain
Cultures
prior to antibiotics
Abscess Pleural Immune

Blood cultures? ICU Pts Alcoholics
formation effusions compromise
Asplenia
Similar indications Limited utility due to Liver Dz

Sputum culture? inability to produce
to blood cultures adequate sample
Urine Legionella Other high risk

ICU patients Alcoholics
antigen? populations
Respiratory Azithromycin/ Least preferred - less

Outpatient CAP? OR OR Doxycycline
fluoroquinolone Clarithromycin S. pneumoniae activity
Respiratory
Inpatient CAP? OR Ceftriaxone Azithromycin
fluoroquinolone
3rd or 4th gen. Respiratory

ICU CAP? cephalosporin, i.e., Vancomycin
fluoroquinolone
ceftriaxone
Antipseudomonal cephalosporin, Respiratory

HCAP? β-lactam, or carbapenem Vancomycin
fluoroquinolone
or Aminoglycoside or Linezolid
Pneumonia in Special Patients

Bacterial pneumonia Viral pneumonia (esp. Low threshold for
Consider IV
Pregnancy similar to that in non- Varicella) particularly imaging, especially
pregnant severe in pregnancy in smokers acyclovir
Transplant Heart, liver, lung

patients at greatest risk
Organisms within
3 months of K. pneumoniae E. coli S. aureus Pseudomonas Legionella Fungi
transplant
Poor prognosis
Organisms within
Especially
6 months of CMV P. jirovecii Fungi
transplant Aspergillus
Organisms > 6
Ordinary CAP
months of Better prognosis
transplant pathogens
Cystic Fibrosis
PEDIATRICS
Most common lethal genetic Autosomal Affects all

Cystic fibrosis
disorder in caucasians recessive exocrine glands
Recurrent respiratory Abnormalities in pancreas Chloride concentration

Cystic fibrosis
infections exocrine function in sweat is high
Other Symptoms & Signs – Present by 1st year
Failure to thrive Recurrent Diabetes Neonatal Hypochloremic

Diarrhea Rectal prolapse
& dehydration pneumonia mellitus jaundice alkalosis
Pulmonary Respiratory
Hemoptysis Pneumothorax Cor pulmonale
emergencies failure
Gastrointestinal Meconium ileus

Early sign Intussusception
emergencies causing obstruction
Fluid & Depletion of

Dehydration Heavy sweating
Electrolytes Na+, K+, Cl-
Pneumonia in
S. aureus Haemophilus
early life
Pneumonia in #1 cause in PNA Burkholderia cepacia also

Pseudomonas
later life in adults common later in life
Mucolytic Chest Empiric

Management
clearance physiotherapy antibiotics
Empiric Anti-pseudomonal Coverage for Tailor based on

penicillin or Aminoglycoside most recent
antibiotics cephalosporin S. aureus culture
Aspiration
Introduction of sterile substance

Inflammatory Aspiration
Aspiration (>20 mL) with pH < 2.5 into lower
respiratory tract response pneumonitis
Development of airspace infection

Aspiration PNA following inhalation of oropharyngeal
contents
Commonly Posterior segments

Aspiration PNA Right lower lobe
affected areas of upper lobes
High gastric
Stroke
pressures
Gastric tube
Seizure
placement
Aspiration Risk Esophageal

GERD
Factors dysmotility
Drug Intoxication Dementia
Emergent
Head Trauma
intubation
Aspiration Management
Aspiration Suction Concern for Decompress

Witnessed? recurrent Intubate pt stomach with
Management airway aspiration? gastric tube
No evidence that
Steroids? corticosteroids
improve outcomes
Wheezing? Bronchodilators
Prophylactic NOT indicated for If sx persist

Treat
antibiotics? pneumonitis >24–48 hours
When to treat Productive New infiltrate on

aspiration for Fever
PNA? cough CXR
Aspiration in Coverage for S. pneumoniae Anaerobic

community? CAP pathogens H. influenzae coverage
Aspiration in health Coverage for Pseudomonas Anaerobic

care setting? HCAP pathogens S. aureus coverage
Admission Nursing home New infiltrate

Chronically ill Hypoxemia Persistent Sx
criteria residents on CXR
Dyspnea
Reliable & Observe x 1 Strict return NO prophylactic Cough
asymptomatic? hour precautions antibiotics
Tachypnea
Dyspnea Wheezing
Cough
Fever
Tuberculosis
TB Tidbits
Responsible for 2nd highest number of

TB
deaths worldwide of any infectious agent
Obligate aerobic Prefers high blood Propensity to affect

TB flow, highly lung apices, kidneys,
rod oxygenated areas bones, brain
Most common Lymphatic

extrapulmonary Lymphadenopathy
site? system
Calcified, necrotic
Ghon focus
granuloma
Associated calcified
Ghon complex Ghon focus
hilar lymph node(s)
Primary Active Occurs in 5–10 % Occurs in up to 20 % of

TB of healthy adults patients with AIDS & children
Most common location

Pott’s Disease Spinal TB
of bone/joint TB
Symptoms & Point tenderness

Fever Back pain Back stiffness
Signs at back
Anterior wedging of vertebral bodies with CT or MRI more

Plain film
destroyed intervertebral disk (late findings) sensitive
TB Pathophysiology
Latent reactivation
Immunocompetent Rapidly
progressive
Primary infection
primary active TB
+/- disseminated
Bacilli inhaled spread
into alveoli
Primarily of
Latent infection lower lobes
PPD becomes Initial infection

positive in 1–2 not contained
months
TB Pathophysiology
Bacilli proliferate
locally
Bacilli Immune
Effective phagocytized problems or
immune small subset of
response
immune
competent pts
May also spread

distally through
lymphatics &
bloodstream to
Immune
areas of high O2
deficiency
content
Reactivation TB
Occurs in up to
5 % within 2 years 5 % subsequent
Reactivation TB 10 % of general
of initial infection lifetime risk
population
AIDS
7–10 % annual risk

Malignancy Immunosuppression
Steroids
Silicosis Increased risk of Transplant

conversion
DM ESRD
Malnutrition Extremes of age

TB Presentation
Primary infection
Asymptomatic
contained?
Primary Active TB
Fever Malaise Weight loss Chest pain ± Cough
Reactivation TB
Fevers Malaise Weight loss Chest pain Hemopytsis Night sweats

Most common
Dyspnea Cough Extrapulmonary Sx
TB Initial Evaluation: PPD and CXR

Place mask on
Suspected active
patient Isolation room
infection? immediately
Read 48–72 hours

PPD after intradermal ≥ 5mm ≥ 10mm ≥ 15mm
injection
High prevalence
HIV groups All others
Immune Patients with
compromise
increased risk of
Close contacts progression
with TB
CXR consistent
Children < 4 years
with TB
Exposure to non-
False positive Prior BCG
tuberculous
PPD vaccination
mycobacteria
Immune
False negative Very recent Improper
compromised
PPD infection administration
patients
CXR Latent Upper lobe & hilar

Infection nodules/fibrosis
Upper lobe or superior

CXR Reactivation
segment lower lobe lesions
TB +/- cavitation
Primary Parenchymal Hilar Unilateral

Infection CXR infiltrate lymphadenopathy pleural effusion
Any lobe Esp. in children

TB Diagnosis
Rapid result, High specificity,

Sputum Stain Ziehl-Neelson OR Fluorochrome
inexpensive 60 % sensitive
Lower if HIV+
Inadequate Gastric aspirate

Pleural fluid OR CSF OR May be used
sputum? (esp. children)
Length of time Slow growing Culture takes 4–8

for culture? bacteria weeks
Tuberculosis Treatments and Side Effects
Isoniazid (INH) Rifampin

Peripheral
Hepatitis
neuropathy
Seizures Thrombocytopenia
Hepatitis Orange / red

discoloration of
Must administer bodily fluids
with pyridoxine to
Pyrazinamide reduce risk of Induces CYP450
neurologic side Decreased Ethambutol
Hepatitis effects levels/efficacy
of: coumadin, Optic neuritis
digitalis, OCPs
Arthralgias
Rash
Hyperuricemia
Tuberculosis
Treatments and
Side Effects
Latent infection? 9 months of INH
Active TB? 4 drug regimen
Concern for
Admit
active infection?
Lung Abscess
Incidence
Lung Abscess declining as PNA
Rx improves
Immuno- Abscess typically result of

Anaerobic bacilli Peptostreptococcus
competent hosts untreated aspiration PNA
Immuno- S. aureus Klebsiella Fungi

More likely to be result
compromised
hosts of hematogenous spread E.coli Pseudomonas TB
Untreated Hematogenous spread

aspiration of bacteria, including
pneumonia septic emboli
#1 cause
Inflammatory
Lung Abscess
disorders, e.g., Malignancy
Causes
Wegener’s,
Sarcoidosis
Pulmonary
Fungal infection
infarction
Diagnosis & Broad spectrum

Blood Cx Admit
Treatment abx
Include anaerobic
coverage!
Acute Respiratory Distress Syndrome

PaO2:FiO2 <300 with Bilateral Not fully explained Onset of sx within
ARDS PEEP or CPAP ≥ 5 pulmonary by volume overload one week of
cm H2O infiltrates or CHF clinical insult
Normal heart size PCWP < 18 mm Hg
Noncardiogenic Leaky alveolar

ARDS Due to
pulmonary edema capillary membranes
MANAGE Mechanical Minimize

Treatment UNDERLYING CAUSE ventilation barotrauma
Maintain O2 sats
> 85 %
Minimize FiO2
Minimize Low tidal Permissive Plateau pressure

High PEEP
barotrauma volume hypercapnia ≤ 30 cm H2O
Minimize airway
pressures
ARDS Causes
Sepsis Air, fat, amniotic

(#1 cause) fluid emboli
Subarachnoid
Pancreatitis
hemorrhage
Toxin/Smoke
Aspiration
inhalation
Drug Overdose ARDS Causes Trauma
ASA, opioids,
TCAs, cocaine High altitude
PE Transfusion
Pleural Effusions
Introduction
150–200 mL needed to be Lateral decubitus view

Pleural Effusions visible on standard more sensitive
PA/lateral CXR (25–50 ml)
Defect in pleural Protein-rich fluid

Exudate accumulation
membrane
Low-protein
↑ Hydrostatic ↓ Oncotic
Transudate OR plasma
pressure pressure
ultrafiltrate
Pleural protein Pleural
Light’s Criteria Pleural LDH>2/3 upper
level/serum OR LDH/serum LDH OR
for Exudates protein >0.5 > 0.6 normal limit serum LDH
One or more of More labs No Light’s

Exudate? Light’s criteria required Transudate? criteria present
present
Labs for
Culture/ AFB
Evaluation of Glucose Cytology pH Amylase
Gram Stain smear
Exudate
<6 = esophageal
rupture
No imminent cardiac or Defer to

Treatment Thoracentesis inpatient setting
respiratory collapse?
Post-expansion
Complications Pneumo/ Lung Transient
Infection pulmonary
Hemothorax laceration hypoxia edema
Due to V/Q Especially
mismatch with >1500 ml
fluid removal
Uncooperative or Coughing, Overlying

Contraindications OR Coagulopathy
moving patient sneezing pt cellulitis
Transudates
CHF
#1 cause in US
SVC obstruction Cirrhosis
Peritoneal Nephrotic
dialysis Transudates syndrome
Constrictive
Hypoalbuminemia
pericarditis
PE Myxedema
Exudates
Infection
Bacterial pneumonia
Tuberculosis
Viral illness
Recent abdominal Lung abscess
Malignancy
surgery
Subphrenic abscess PE
Pulmonary infarction
Exudates
Pancreatitis Malignancy
Esophageal rupture Uremia
Connective tissue
Chylothorax disease ARDS
Empyema
Pus in the
Empyema
pleural space
Symptoms & Signs
Indolent Weight loss Malaise Night sweats
Pleuritic chest
Other Sx Fever Chills Dyspnea
pain
Pleural fluid Gross Glucose LDH Positive gram

findings pH < 7.1
purulence < 40 mg/dL > 1000 iU/L stain
Potential CXR Air-fluid level in Loculated

findings pleural space effusion
Prolonged Drainage via tube Defer to

Treatment
course of IV Abx thoracostomy inpatient setting
Pipercillin- Vancomycin
Antibiotics Cefepime OR
Tazobactam (if MRSA suspected)
Causes of Empyema
Hematogenous or
lymphatic spread
from pneumonia
#1 cause
Other infected Aspiration
fluids pneumonia
Hemothorax
Chylothorax
Hydrothorax Transudates Esophageal rupture
Direct extension of
Mediastinitis
osteomyelitis
Extension from
retropharyngeal Post-procedure
abscess
Thoracotomy
Thoracostomy
Thoracentesis
Mediastinitis
Post cardiac
surgery
#1 cause in US
S. aureus
S. epidermidis
Esophageal
Trauma
perforation
Acute Causes
Local spread from Iatrogenic

perforation of
Osteomyelitis tracheobroncheal
tree
Pneumonia
Deep space
head/neck infection
Surgical
Acute Treatment IV antibiotics consultation
Chronic Rare result of Granulomatous May proceed to

Mediastinitis radiation OR infection cause SVC syndrome
TB
Histoplasmosis
Hiccups
Persistent Consider diaphragm /

Pneumonia
Hiccups phrenic nerve irritation
Chlorpromazine
Treatment 25–50 mg IM
Pneumoconioses
Interstitial lung Inhalation of Typically Very slow to

Pneumoconioses Due to
diseases specific dusts occupational develop
Silicosis Due to Silica dust
Asbestosis Due to Asbestosis Can result in

mesothelioma
Coal Worker’s
Due to Coal dust
Pneumoconioses
Diagnosis CXR
Sarcoid
Not Non-caseating Can affect High prevalence in

Sarcoid
infectious granulomatous disease many systems African-American women
Symptoms & Signs
Fatigue Lack of energy Weight loss Arthralgias Arthritis Dry eyes Blurry vision
Rales on exam Dyspnea Cough Skin lesions
Most commonly Lungs Skin Cardiac involvement

affected organs? #1 #2 varies by race
Lung Interstitial lung Bilateral hilar Infiltrates on

involvement disease adenopathy CXR
Skin Erythema Maculopapular Subcutaneous

Plaques
involvement nodosum eruptions nodules
Eye involvement Uveitis
Symptomatic Rx Complicated cases

Treatment
with NSAIDs need steroids
Superior Vena Cava (SVC) Syndrome
Obstruction of Results in face &

SVC Syndrome
SVC arm edema
Symptoms & Signs
Headache Visual changes Facial plethora Dyspnea Syncope
Radiation +
Treatment May need stenting
chemotherapy
Mediastinal Masses
Most common Bronchogenic
mass in
mediastinum carcinoma
Thyroid
“Terrible”
(Carcinoma) Thymoma
Anterior
mediastinal
masses
Five “T”’s
T cell lymphoma Teratoma

The Airway
Rapid Sequence Intubation
t -10 minutes Preparation
Pre-oxygenation
Pretreatment
Paralysis with
induction
Protection &
Time Zero Positioning
Placement with
Proof
Post-intubation
t + 90 seconds management
Airway Tidbits
3-3-2 Rule
Opening of mouth = 3 fingers
Hyoid-chin distance = 3 fingers
Distance from thyroid cartilage to floor of mouth = 2 fingers
L ook at the anatomy
Class 0 Class I Class II Class III Class IV

E valuate the 3-3-2 rule
M allampati Score
O bstruction
N eck mobility
Tracheostomy and Respiratory Distress
Respiratory Obstruction until Remove inner Suction as best Irrigate with

distress? proven otherwise cannula as possible saline
If no Consider replacing Ensure appropriate May need to do over catheter

improvement entire tracheostomy size is available if any risk of stoma closing
Definitive
ENT evaluation
treatment
(Reprinted from Ramachandran SK, Kheterpal S. The expected diffi- New York: Springer Science; 2013. p. 11–32. With permission from
cult airway. In: Glick DB, Cooper RM, Ovassapian A, editors. The diffi- Springer Science + Business Media)
cult airway: an atlas of tools and techniques for clinical management.
Tracheostomy and Bleeding
Bleeding from Consider tracheo- May occur with new tracheostomies

If new & brisk
site? innominate fistula or those that are poorly fitting
Emergency Hyperinflation of tracheostomy balloon as well

treatment as using the tracheostomy tube as a lever
Intubate from Remove Directly tamponade artery

Unsuccessful? Call ENT!
above tracheostomy with a gloved finger
Definitive Interventional
ENT evaluation
treatment radiology
General Pediatrics
Apparent Life-Threatening Events (ALTE)
PEDIATRICS
Scares the Has a combination of NOT a Usually occurs from

ALTE
parent signs & symptoms diagnosis! 1–3 months of age
Severe Higher risk of sudden Evaluation & Depends on History &

symptoms? infant death syndrome Treatment Physical exam
Symptoms & Signs
Choking or Change in
Color change Apnea gagging muscle tone
Cyanotic Limp
Pale
Occurred during
sleep period
Hx of abuse or Witnessed
other trauma seizure activity
High Risk ALTE
Associated with Lasted > 10

feeding seconds
Hypotonic tone
Selected Causes of ALTE
PEDIATRICS
Idiopathic
Congenital heart
Increased ICP
disease
Intracranial
Arrhythmias
hemorrhage
Airway
Cardiomyopathy
obstruction
Seizures Selected Causes Abuse

of ALTE
Meningitis Munchausen
Gastroesophageal
Hypoglycemia
reflux
Pneumonia Hypocalcemia
Sepsis
Sudden Infant Death Syndrome (SIDS)
PEDIATRICS
Most common cause of death

SIDS
1 month to 1 year of age
High maternal
parity
Substance abuse Low age of

in mother mother
Higher Risk of
SIDS
Higher risk if
Prematurity sibling had SIDS
Higher risk if
infant had ALTE
Infant should sleep Higher risk for prone Upper airway Hypercarbia from
Sleeping position
on back or sides sleeping infants obstruction rebreathing expired air
Lower risk
Gastroenterology
Brandon R. Allen and Bobby Desai
Contents
Pediatric Gastroenterology 186
Constipation 187
Diarrhea 189
Esophageal Emergencies 199
Esophageal Perforation 204
Esophageal Foreign Bodies 207
GERD 210
Peptic Ulcer Disease 212
GI Bleeding 214
Liver and Gallbladder 219
Pancreatitis 229
Ileus 233
Bowel Obstruction 234
Intussusception 236
Volvulus 240
Hernias 242
Bowel Perforation 245
Acute Appendicitis 246
Acute Diverticulitis 248
Mesenteric Ischemia 251
Crohn’s Disease 253
Ulcerative Colitis 256
Irritable Bowel Syndrome 257
Miscellaneous Anorectal Emergencies 257
B.R. Allen, MD (*)

University of Florida College of Medicine, Gainesville, FL, USA
B. Desai, MD, MEd

B. Desai, B.R. Allen (eds.), Nailing the Written Emergency Medicine Board Examination, 185
DOI 10.1007/978-3-319-30838-8_3
186 B.R. Allen and B. Desai
Pediatric Gastroenterology
Pediatric GI Tidbits: Vomiting
PEDIATRICS
Forceful Regurgitation
Vomiting vs spitting up
Infections
Sepsis
Incarcerated
Gastroenteritis Increased ICP
hernia
UTI Shaken baby
syndrome
Inborn errors of
metabolism
Intussusception
Hypoglycemia
Metabolic
Etiologies of Acute acidosis
Constipation
Gut malrotation
Pyloric stenosis Bilious vomiting
Projectile vomiting 50 % Dx in 1st
at end of feeding month of life
Hepatic disease
Necrotizing Enterocolitis
Necrotizing Most common GI Mechanism is Infection? Prematurity is a

Entercolitis emergency in neonates not understood Hypoxia? risk
Symptoms & Signs
Abdominal Shock for

Bloody stools Inability to feed Hematochezia
distention advanced states
Findings on Double density of Intramural Bowel Loss of

Intraportal air
imaging abdominal wall bowel gas dilation haustra
Pneumatosis
Imaging Late finding
intestinalis
Abdominal Fluids
Treatment IV antibiotics
decompression (Pressors if needed)
Gastroenterology 187
Constipation
Introduction
Most common GI
Constipation
complaint in US
Increases with
Constipation
age
Acute Obstruction (until But has multiple

constipation proven otherwise) causes
Symptoms and Signs
Symptoms & Signs
Abdominal Presence of Decreased Potential presence Examine for

pain hernias bowel sounds of masses rectal tone
Rectal Examination
Other masses Fecal impaction Fissures Hemorrhoids Abscesses Stool guaiac
Etiologies of Acute Constipation
GI Causes
Tumors
Volvulus
Neurologic Obstruction Medications
Parkinson’s IBD Narcotics

Paraplegia Anticholinergics
Neuropathy Antipsychotics
Cerebral Palsy Antihistamines
Etiologies of Acute
Electrolyte Constipation
Hypomagnesemia
Hypercalcemia Endocrine
Hypokalemia Hypothyroidism
Common reason Hyperparathyroidism
for ileus mimicking
SBO DM
Rheumatologic Toxic Ingestions
Amyloidosis Iron
Scleroderma Lead
Etiologies of Chronic Constipation
GI Causes
Tumors
Dysmotility
Medications
Narcotics
Anal Pathology
Etiologies of Acute Anticholinergics
Hemorrhoids Constipation
Antipsychotics
Fissures
Antihistamines
Foreign bodies
Other
Lack of exercise
Lack of fiber
Lack of fluid intake
Diagnosis
Labs for
Depends on DDx
Constipation?
No specific labs!
Imaging for Bowel

Plain films Abdominal CT
perforation?
If normal plain
film & high
suspicion
Appearance on Dilated loops of

bowel Air-fluid level
plain film?
Treatment
Depends on Treat underlying

Constipation? Dietary changes Medical adjuncts
etiology cause
Enemas
Cathartics
Diarrhea
Introduction
Increase in normal Increased frequency of A leading cause of

Acute Diarrhea
water content of stool stools of lesser consistency death worldwide
Mechanisms of Decreased intestinal Increased Abnormal Increased

OR OR OR
Diarrhea absorption intestinal secretion motility osmotic load
Infectious Non-infectious
Diarrhea
85 % 15 %
Infectious Viruses
Bacterial Parasitic
diarrhea (Vast majority)
Pediatric GI Tidbits: Diarrhea
PEDIATRICS
Blood in stool of Cow’s milk Swallowed

Anal fissure
infants? intolerance maternal blood
2nd most
Viral causes Rotavirus Most common Adenovirus
common
Most common Viruses more

Bacterial causes
summer cause common in winter
Viral Diarrhea
Increased incidence
Winter & Spring Children Daycare
of viral diarrhea
Specific viruses Rotavirus Adenovirus Calcivirus Enterovirus Norwalk
Most common cause

Rotavirus
of diarrhea in children
Norovirus Leading cause of

(Norwalk-like) gastroenteritis in the US
Viral diarrhea No bloody stools No WBC’s in stool
Bacterial Diarrhea
High likelihood of Potential consumption of Most common cause

Foreign travel
bacterial diarrhea contaminated food & drink of Traveler’s diarrhea
Traveler’s
E. coli C. jejuni Shigella Salmonella
Diarrhea
Consider bacterial
Abdominal pain Fever Bloody stool
diarrhea
Consider bacterial
(+) stool WBC Bleeding
diarrhea
Also (+) stool Depending on
lactoferrin pathogen
Invasive E. coli
Bloody stools Shigella Campylobacter Yersinia
pathogens O157:H7
Non-invasive Enterotoxin Usually food-

pathogens producing organisms borne infections
Diarrhea from Watery, copious

Mild to No Fever Bloody stool WBC’s in stool
toxins diarrhea
Specific Bacterial Pathogens: E. coli
Enterohemorrhagic
E. coli O157:H7 Bloody stool WBC in stools
E. coli
Causes of E. coli Undercooked

Untreated water Raw milk Petting zoos
O157:H7 meat
Complications of Thrombotic Hemolytic-Uremic Antibiotics may

E. coli O157:H7 Thombocytic Purpura Syndrome increase risk of HUS
Adults Children
Traveler’s Enterotoxogenic
Diarrhea E. coli
Traveler’s diarrhea Bismuth Antiperistaltic

Ciprofloxacin OR TMP-SMX
treatment? salicylate agents
Specific Bacterial Pathogens: Shigella
2–6 day incubation

Shigella High infectivity
period
Symptoms of Potential for Bloody diarrhea

Very high fever
Shigella febrile seizures (Dysentery)
Treatment Ciprofloxacin
Specific Bacterial Pathogens: Salmonella
Very common Not as infective

Salmonella pathogen as Shigella
Symptoms of Watery, mucoid

Salmonella stools
Reservoirs of Undercooked
Eggs Chicken Amphibians
Salmonella food
Complications of
Osteomyelitis
Salmonella
Sickle cell disease
Treatment Ciprofloxacin
Specific Bacterial Pathogens: Campylobacter
Most common cause Incubation 2–6

Campylobacter of bacterial diarrhea days
Acquired from contaminated

Campylobacter food or water Fecal-oral spread
Campylobacter
symptoms Fever Bloody diarrhea
Campylobacter
mimics IBD Appendicitis
Campylobacter Acute infection associated with

complication Guillain-Barre syndrome
Treatment Ciprofloxacin Erythromycin
Adults Children
Specific Bacterial Pathogens: Yersinia
Can mimic
Yersinia
appendicitis
Yersinia Colicky (+) Fecal

symptoms Fever abdominal pain leukocytes
May be in the
RLQ quadrant
May persist up
Yersinia
to 2 weeks
Ciprofloxacin or
Treatment OR Supportive
TMP-SMX
Complicated Uncomplicated
Salmonella
Reiter’s Shigella
Arthritis Conjunctivitis Urethritis
syndrome
Yersinia
Campylobacter
Specific Bacterial Pathogens: Vibrio
V.
Raw oysters Clams Shrimp
parahaemolyticus
V. 6–24 hour
parahaemolyticus incubation
V. vulnificus Raw oysters Shellfish
Food or drink contaminated

V. cholera by feces of infected person
Severe fluid & Potentially severe

V. cholera sign Rice water stool electrolyte disturbances & fatal diarrhea
WHO
Treatment Ciprofloxacin rehydration
Or TMP-SMX
Specific Bacterial Pathogens: Staphylococcus
Most common cause Sx within 6

Staph
of food-borne illness hours
Contaminated Meats including

Staph Potato salad Dairy & Eggs
foods poultry
Via pre-formed
toxin
Staph symptoms N/V Watery diarrhea Fever
Treatment No antibiotics!
Specific Bacterial Pathogens: Clostridium perfringens
Sx within 6–24
C. perfringens Large outbreaks hours
Contaminated Meats including

C. perfringens foods Stews
poultry
Spores survive
C. perfringens cooking process Toxins produced
C. perfringens
Watery diarrhea Vomiting Fever
symptoms
C. perfringens
No Fecal WBC’s No RBC’s
stool
Treatment Fluids
Specific Bacterial Pathogens: Bacillus cereus
Anaerobic spore
B. cereus forming organism
Common in Spores germinate when the

B. cereus Vegetables Meats Cereals
fried rice rice is not refrigerated
Severe vomiting 2–3 hours

Vomiting
after ingestion
B. cereus Has 2 forms
Severe diarrhea 6–12 hours
Diarrhea
after ingestion
Supportive due to
Treatment
self-limited nature
Specific Toxins: Scombroid
Scombroid From deep

Mahi-mahi Tuna Mackerel
poisoning ocean fish
Histamine-like 30 minute onset

Scombroid Heat stable toxin
toxin of action
Scombroid Fish has

poisoning “peppery” taste
Scombroid Flushing of Abdominal Chest pain &

Diarrhea Headache
symptoms face pain palpitations
Treatment Antihistamines
Specific Toxins: Ciguatera
Ciguatera Reef Red Fish eat ciguatera toxin

Barracuda Grouper
poisoning fish snapper containing dinoflagellates
Ciguatera Muscle Reversed temperature

Vomiting Diarrhea Paresthesias
symptoms weakness sensation
Perioral
Ciguatera Sx can last for Burning
poisoning years hands &
feet
Worsened with alcohol
Treatment Mannitol Amitriptyline Antihistamines

Specific Protozoan Pathogens: Giardia
Most common cause of “Backpacker’s” Contaminated

Giardia
water-borne diarrhea in US diarrhea rivers & streams
1–4 week
Giardia incubation
Giardia Colicky Audible bowel Frothy foul

symptoms abdominal pain sounds smelling stools
Giardia Send off stool specimens for

diagnosis Ova & Parasites
Treatment Metronidazole
Specific Protozoan Pathogens: Entamoeba histolytica
Fecal-oral
E. histolytica
contact
E. histolytica May have

symptoms bloody diarrhea
Liver abscess Pericarditis

Multiple extra-intestinal
E. histolytica
manifestations
Cerebral amebiasis Pleuropulmonary disease
Treatment Metronidazole
Specific Protozoan Pathogens: Cryptosporidium
Most common cause of From contaminated

Cryptospordium
chronic diarrhea in AIDS water
1 week
Cryptospordium
incubation
Cryptospordium
Abdominal pain Watery diarrhea
symptoms
Cryptospordium Send off stool specimens for

diagnosis Ova & Parasites
Treatment Fluids Nitazoxanide Azithromycin
Antibiotic-Associated Diarrhea
Antibiotic Associated Moderate Abdominal

Fever Fecal leukocytes
Diarrhea diarrhea cramps
Antibiotic Associated C. difficile (until

Diarrhea proven otherwise)
Stop offending
Treatment
antibiotic
Clostridium difficile and Pseudomembranous Enterocolitis
Spore forming Spectrum of

C. difficile Causes Diarrhea Severe colitis
anaerobic bacillus illness
Most common cause of infectious

C. difficile
diarrhea in hospitalized patients
Pseudomembranous Inflammatory Exudative Necrotic intestinal

Covering
enterocolitis bowel process plaques mucosa
Pseudomembranous Antibiotic
Types Neonatal Post-operative
enterocolitis associated
Pseudomembranous Begins 7–10 days

enterocolitis after Abx
Symptoms (May be Profuse Crampy Dehydration &

Fever Leukocytosis
toxic appearing) diarrhea abdominal pain hypovolemia
Colonic
Complications Toxic megacolon
perforation
Diagnosis C. difficile toxin Colonoscopy
Severe disease
Stop offending
Treatment Metronidazole OR Vancomycin
antibiotic
Esophageal Emergencies
Dysphagia
Difficulty Most patients have

Dysphagia an organic etiology
swallowing
Transfer Transport
Dysphagia OR dysphagia
dysphagia
Transfer Early in Difficulty in initiating Neuromuscular

dysphagia swallowing swallowing disorder
Stroke
Transport Later in Sensation of

dysphagia swallowing stuck food
Impaired May be localized

movement of by patient if in
food upper 1/3 of
esophagus
Other Mechanical
Functional dysphagia OR dysphagia
classifications
Progressive
Intermittent
Solids then
liquids
Usually made
Diagnosis outside of ED
Transfer Dysphagia
Transfer Transfer Risk of

Dysphagia Pharynx problems Esophagus Aspiration
Symptoms
Regurgitation Problems initiating

Coughing Gagging
through nose a swallow
Signs
Malnutrition Pneumonia Weight loss

Neuromuscular Causes of Transfer Dysphagia
CNS Processes
CVA
Most common
cause in this Rheumatologic
Toxic & Poison Processes
category
Lead toxicity Parkinson’s Polymyositis 2nd most
common cause
Tetanus Dermatomyositis in this category
Botulism Scleroderma
Neuromuscular
causes of Transfer
Dysphagia
80 %
Liquids > Solids

Myasthenia
Hypothermia Gravis
Endocrine
disorders
Thyroid Disease
Localized Causes of Transfer Dysphagia
Cancer
Tongue
Pharynx
Aphthous ulcers Larynx Abscesses

Progressive
Peritonsillar
dysphagia
Retropharyngeal
Zenker’s
Diverticulum
Localized causes of
Halitosis Transfer Dysphagia
Acquired disease 20 %
Above upper
sphincter
Pts present with Sx Pharyngitis
of neck mass
Candidal
infection Cervical disease
Causes
odynophagia
Immunocompromised
Transport Dysphagia
Transport Transfer ↑ Risk of

Esophagus Stomach
Dysphagia problems Aspiration
Less than transfer
Solids only? Mechanical OR Obstructive
Solids & Liquids? Motility
Symptoms
May have painful

Fullness in chest
swallowing
1st with solids then liquids
Signs
Malnutrition Dehydration Weight loss

Obstructive Causes of Transport Dysphagia
Cancer
Large vessel
Strictures
abnormalities
Occurs from scarring

or inflammation
GERD
Diverticula
Occur in distal
esophagus
Usually with solids

Foreign bodies Obstructive causes
of Transport
Dysphagia
Webs
Schatzki’s Ring 85 %
May occur with
Plummer-Vinson
Most common cause
syndrome
of intermittent
dysphagia with
solids Anterior webs with
iron-deficiency
May occur from anemia + nailbed
GERD spooning
Occur in middle or
Near GE junction
proximal esophagus
“Steakhouse Non-progressive
syndrome” dysphagia
Thyroid
enlargement
Motor Causes of Transport Dysphagia
Nutcracker
esophagus
Common motility
disorder in pts with
noncardiac chest
pain
Achalasia
Esophageal spasm Most common
Motor causes of motility disorder
Sx = chest pain Transport Dysphagia causing dysphagia
May cause chest
pain, regurgitation,
15 % weight loss and
airway Sx
Other inflammatory
Scleroderma
processes
Esophageal Perforation
Partial thickness Most at gastro- Common cause Commonly resolves

Mallory-Weiss
esophageal tear esophageal junction of GI bleeding spontaneously
Mallory-Weiss
Hiatal hernia Alcohol
risk factors
Leakage of Mediastinum Mediastinitis

Esophageal esophageal Can be contained Chemical then
Peritoneum Can Peritonitis
perforation contents within each area infectious
cause
into Pleura Pneumonitis
Full thickness
May ultimately lead
to a shock state
Need early antibiotics!
Severity of Distal Proximal Can be contained locally as Can occur with

perforation? perforation perforation a periesophageal abscess instrumentation
Iatrogenic is most
common cause of
perforation
Spontaneous Left posterolateral wall
perforation of the distal esophagus
Esophageal High mortality Affected Location of Time elapsed for Etiology of

perforation rate by perforation treatment perforation
Causes of Esophageal Perforation
Iatrogenic
Endoscopy
Boerhaave
Infection Risk higher in Syndrome
diseased esophagus
Rare Dilation increases Spontaneous
risk Increase in
Most at pharyngo- intraluminal
esophageal junction pressure
Zollinger-Ellison
Syndrome Gastric Sudden forceful
intubation emesis
Treatment of
varices 10–15 % of
Cancer perforations
Left distal esophagus
Causes of
Esophageal Full thickness tear
Aortic pathology Perforation
Aortic aneurysm
Trauma
Penetrating
Barrett’s 10 % of
Esophagus perforations
Foreign Body Ingestion
Alkaline
Esophageal Perforation Symptoms and Signs
Symptoms
Abdominal
Chest pain Neck pain Back pain Dyspnea Dysphagia Hematemesis
pain
Pain may radiate to

back and shoulders
Vomiting
Mallory-Weiss
Non-toxic patient
Signs
Abdominal Subcutaneous
Cyanosis Hypotension Fever Tachycardia Tachypnea emphysema
rigidity
In cervical
perforations
Swallowing Mediastinal Hamman’s
Pleural effusion
exacerbates pain emphysema crunch
Takes time to Air in In thoracic
develop mediastinum perforations
Absence does moving with the
not rule out heart
perforation
Diagnosis and Treatment
X-ray findings of Left pleural Widened

Pneumothorax Mediastinal air
Esophageal perforation? effusion mediastinum
High amylase in
fluid
Ultimate Dx of Gastrografin
CT scan OR
Esophageal perforation? Upper GI series
Esophageal perforation Resuscitate Broad spectrum Emergent surgical

treatment shock state antibiotics consultation
Esophageal Foreign Bodies
Levels of narrowing in esophagus

Children Adults
Most C6: Cricopharyngeus muscle

80 % T4: Aortic arch
impactions are
Small objects distal T6: Tracheal bifurcation
lodge in T11: Gastroesophageal junction
proximal
esophagus
FB past the Usually continues Sharp or May become lodged

Unless OR Long OR Wide
pylorus? through GI tract irregular distal to the pylorus
> 6 cm > 2.5 Requiring OR vs.

cm endoscopy
FB Esophageal Esophageal Airway

OR OR
Complications perforation strictures obstruction
Esophageal Foreign Body Symptoms and Signs
Center bottom image (Reprinted without modification from James Heilman https://commons.wikimedia.org/wiki/
File:CoinAP.jpg. With permission from the Creative Commons License https://creativecommons.org/licenses/by-sa/3.0/
deed.en)
Symptoms & Signs
Choking or
Chest pain Dysphagia Vomiting Coughing Dysphagia
gagging
Drooling Refusal to eat Neck pain Sore throat Vomiting
Especially in High index of

children suspiciion
Diagnosis and Treatment of Esophageal Foreign Bodies
Suspected FB? Plain film
Esophageal Circular face on May consider Foley

Endoscopy
coin? AP film removal if experienced
Impacted bone Plain films

Consider CT scan Endoscopy
in esophagus? visualize FB <50 %
Object distal to Expectant

pylorus? management
Consider Consider Carbonated Endoscopic

Food impaction? OR OR OR
Glucagon Nitroglycerin beverage retrieval
Most have underlying Monitor for Gaseous
pathology distention to push
hypotension
food into stomach
Button battery lodged Emergent Broad spectrum Burns and perforation Lithium battery =
in esophagus? endoscopy antibiotics in 6 hours worse outcome
Double density
appearance on X-ray
Button battery Expectant

past esophagus? management
Sharp object in Emergent Perforation at

esophagus or stomach? endoscopic removal ileocecal valve
Sharp object distal Asymptomatic Document passage Symptomatic Surgical

to esophagus? patient? with daily plain films patient? consultation
Caustic Ingestions
Esophageal
Oral findings
findings
Caustic
Endoscopy
ingestion?
Caustic Gastric
ingestion? decontamination
Coagulation
Acid ingestion? Less damage
necrosis
Liquefaction
Alkali ingestion? More damage
necrosis
Dilution with
Solid alkali?
water or milk
Hydrofluoric Consider Magnesium Consider IV

acid? neutralization citrate or milk calcium as well
Supportive
Treatment GI consultation
therapy
Early Perforation of
Edema of airway
complications esophagus
Late Esophageal Perforation of

complications stricture esophagus
GERD
Reflux of gastric contents

GERD
into the esophagus
Transient relaxation of
Mechanism
lower esophageal sphincter
Risk factors Pregnancy Alcohol use Tobacco use High fat diet
Other predisposing Impairment of Increased gastric Medications that lower

Hiatal hernia
factors esophageal motility emptying time sphincter pressure
Diabetic
Diabetes mellitus Caffeine
gastroparesis
Achalasia Outlet obstruction Nitrates
Scleroderma Anticholinergics Ca-Channel blockers
Anticholinergics
Estrogens
GERD Inflammatory Barrett’s

Strictures Dysphagia
Complications esophagitis esophagus
Premalignant
condition
Predisposes to
adenocarcinoma
GERD Symptoms and Signs
Symptoms & Signs
Acid taste in Pain with

“Heartburn” Chest pain Odynophagia Hypersalivation Dysphagia
mouth meals
Water brash
Worse recumbent or Relief with

head-down antacids
Better sitting up
Can mimic ischemic cardiac
pain
Less common Symptoms & Signs
Frequent ENT Vocal cord Chronic

Pulmonary Sx Dental erosion Laryngitis Chronic cough
Sx granulomas sinusitis
Asthma Infections
GERD Treatment
Decrease acid Enhance UGI Decrease risk

GERD?
production in stomach tract motility factors
H+ pump inhibitors
Histamine blockers
Ultimate Dx of Gastrografin
CT scan OR
Esophageal perforation? Upper GI series
Esophageal Resuscitate Broad spectrum Emergent surgical

perforation? shock state antibiotics consultation
Esophagitis
Esophagitis
Odynophagia Chest pain
symptoms
Diagnosis Endoscopy Biopsy
Causes of Esophagitis
GERD
Aggressive
treatment with
acid-blocking Immunosuppression
agents
Medications Candida
NSAID’s Most common

Causes of HSV & other herpes
Antibiotics
Esophagitis family
Clindamycin CMV
Doxycycline Other fungi
Mycobacteria
Peptic Ulcer Disease
Introduction
Ulcerations in Ulcerations in
PUD Due to OR
stomach proximal duodenum
Helicobacter
PUD Causes NSAID use
pylori infection
Inflammation of
Gastritis
gastric mucosa
Pathophysiology
Mucosa Mucosa
destructors protectors
Almost all PUD caused
by
Mucosa
HCl acid Pepsin H. Pylori
destructors
NSAID’s
Destroyed by
H. pylori
Mucosa Enhance production Enhance mucosal

Prostaglandins
protectors of mucus & HCO3 blood flow
Inhibited by
NSAID’s
Causes of PUD and Gastritis

Hereditary
factors
Shock states Smoking
Gastritis
Chronic renal
Autoimmune failure
Pernicious
anemia
Renal
Transplantation
Causes of PUD
Medications
H. pylori
NSAID’s
Steroids
Have direct toxic
Cirrhosis
effect in gastritis
Zollinger-Ellison
Emotional stress
syndrome
PUD Symptoms and Signs
Symptoms & Signs
Burning Night-time Abdominal Hematochezia

N/V Back pain Hematemesis
epigastric pain recurrence of pain pain or Melena
May have acute Penetration into
abdomen with the pancreas
perforation Most common
Free air on plain presentation of
films Gastritis
Duodenal = pain
after eating
Gastric = pain
with eating
Worse recumbent or Relief with

head-down antacids
Better sitting up
PUD Diagnosis and Treatment
Suspicion of Endoscopy is
PUD? gold standard
Treatment goals Prevent Prevent

Relieve pain Heal the ulcer
for PUD complications recurrence
NO NSAID’s!
Treatment for Antibiotics vs. Proton pump

Sucralfate Misoprostol
PUD H. pylori inhibitors
Metronidazole Take before Protects ulcer from Prostaglandin

meal acid exposure analog
Amoxicillin For NSAID induced
Allows healing
Clarithromycin PUD
Take after other
meds
Hemorrhage Restore hemodynamic Proton pump Emergent Surgery for

from PUD? stability inhibitors endoscopy refractive cases
Fluids Bolus then

Blood infusion
Perforation from Restore hemodynamic Nasogastric Emergent surgical

PUD? stability suction consultation
Fluids
Blood
Gastric outlet Restore volume Nasogastric Surgical

obstruction from PUD? & electrolytes suction consultation
PUD Complications
PUD most PUD bleeding is most

UGI Bleeding
common cause common in the elderly
Severe epigastric Radiation to the Evidence of

Perforation
pain back pancreatitis
Scarring of gastric outlet

Obstruction
due to chronic PUD
GI Bleeding
Terminology
Bleeding proximal to
UGI Bleed Hematemesis
Ligament of Treitz
Other causes of
black stool
Black coloration Bismuth
Melena UGI Bleed from digestion Beets
Sigmoid
Hematochezia Bright red blood Rectum OR Rapid UGI Bleed
Anus Will be
May be
accompanied hemodynamically
by unstable
hematemesis
Maroon colored
Right colon OR Transverse colon
stool
Introduction: Upper GI Bleeding (UGIB)
Bleeding proximal to
UGI Bleed More common Males Elderly
Ligament of Treitz
Peptic Ulcer Commonest

Disease cause of UGIB
Result from Portal Commonly Alcoholic liver Varices are likely

Variceal Bleeding due to
Hypertension disease to rebleed
Many cirrhotics
do not develop
varices
Erosive Esophagitis NSAID’s &

Due to Alcohol
& Gastritis Salicylates
Mallory-Weiss Mucosal partial thickness Repeated

Due to Hematemesis
Tears tears in the esophagus vomiting
Aortoenteric
Other causes AVM Cancer
Fistula
Preexisting
aortic graft
“Herald” bleed
then massive
bleed
UGIB Symptoms and Signs
Symptoms & Signs Varies depending on severity of bleed
Decreased Cool, clammy Signs of liver Signs of

Tachypnea Tachycardia Hypotension
pulse pressure skin failure coagulopathy
Jaundice Petechiae
Spider angiomata Purpura
Mild Bleed Severe Bleed
Gynaecomastia
Palmar erythema
Ascites
Abdominal Change in
Weight loss Hepatosplenomegaly
pain bowel habits
Malignancy
UGIB Diagnosis and Treatment

CBC
Labs for suspicion Type & Electrolyes + Coagulation
including LFT’s EKG
of UGIB? Crossmatch BUN/Cr studies
platelets
May not Elevated BUN in
UGIB due to Silent
reflect
digestion of ischemia
actual
hemoglobin
blood loss BUN/Cr ≥ 30 =
UGIB
Endoscopy is gold Nasogastric Inspection of NG Gentle gastric

UGIB?
standard intubation aspirate lavage
Assess ongoing bleed

Does not provoke
bleeding with varices
Stabilize Replacement of
Massive Volume Emergent Blood
ABC’s as Medications coagulation
UGIB? Replacement endoscopy indications
needed factors as needed
Protect airway Crystalloids Continued
active bleed
2 large bore IV
Shock states
No change
after several
boluses of
fluid
Proton pump Consider ceftriaxone

Medications Octreotide Vasopressin IV Erythromycin for variceal bleeding
inhibitors
Reduces rebleeding For varices For varices Speeds up gastric

Reduces need for Reduction in emptying
Many
surgery for peptic splanchnic blood complications Consult with GI
ulcers flow Ischemia,
hypertension,
arrhythmias
Delayed Sengstaken- Many adverse st

Variceal Bleeding Blakemore tube Intubate 1 !
endoscopy reactions
Disposition
Image just left of center (Reprinted from Allen B, Ganti L, Desai B. GI bleeding/hemorrhage. In: Allen B, Ganti L, Desai
B, editors. Quick hits in emergency medicine. New York: Springer Science; 2013. p. 83–5. With permission from Springer
Science + Business Media)
Systolic BP (+) Bloody NG Low Hematocrit
Significant UGIB? Hx of liver failure
< 100 mm Hg lavage (<30)
Admit OR (+)
hematemesis
Low risk =
Score of 0
Glasgow-Blatchford
Bleeding Score Any score higher than 0 is "high risk" & may need a medical
intervention of transfusion, endoscopy, or surgery
Introduction: Lower GI Bleed (LGIB)
Bleeding distal to
LGI Bleed
Ligament of Treitz
Most common
UGIB
cause of LGIB
Multiple bouts of
hematochezia
Hemodynamic Low initial

instability hematocrit
High Morbidity in
LGIB
Multiple
Syncope
comorbid factors
Use of
anticoagulants
Some Causes of LGIB
UGI Bleed
Most common
overall
Colitis - Ischemic Diverticular disease

Most common
Usually transient
lower GI cause
Some causes of Painless bleeding

LGIB Erosion into the
penetrating artery
Mesenteric of the diverticulum
ischemia Bleeding distal to
Ligament of Treitz May be massive
May lead to bowel
Some risk factors but 90% resolve
necrosis
Recent MI spontaneously
Causes
Atrial Fibrillation Most located on
- Thrombosis
- Embolism CHF left, but right side
- Venous Postprandial bleed more
thrombosis abdominal pain
- Nonocclusive Weight loss
(low flow state
with
vasoconstriction)
Meckel’s Rule of 2’s
Angiodysplasia Diverticulum -2% of population
Right sided bleed Embryonic tissue - 2 feet from the ileocecal valve
in terminal ileum -2 inches long
Associated with Ectopic gastric -2 types of epithelial tissue
Hypertension tissue
-Presents in the first 2 years
Aortic stenosis Erosion of the
mucosal wall -2:1 Male: Female
Other Causes of LGIB
Cancer
Colitis - Infectious Polyps
Mesenteric Inflammatory
ischemia bowel disease
Other Causes of Anal Fissures

Rectal disease LGIB
Hemorrhoids
Most common Trauma
source of anorectal
bleeding
Ulcers Foreign body
Aortoenteric
Endometriosis
fistula
Inflammatory
Angiodysplasia
bowel disease
LGIB Diagnosis and Treatment
Labs for suspicion Type & CBC Electrolyes + Coagulation

including LFT’s EKG
of UGIB? Crossmatch BUN/Cr studies
platelets
May not Elevated BUN in
UGIB due to Silent
reflect
digestion of ischemia
actual hemoglobin
blood loss BUN/Cr ³30 =
UGIB
Dx of LGIB? Colonoscopy Angiography Scintigraphy CT scanning
Assess site of bleed Sensitive

Allows embolization
Massive Stabilize Replacement of

Volume Emergent Blood
ABC’s as Medications coagulation
LGIB? Replacement colonoscopy indications
needed factors as needed
Protect airway Crystalloids Continued
active bleed
2 large bore IV
Shock states
No change
after several
boluses of
fluid
Failure of Emergency
colonoscopy? surgery
Disposition
Normal vital signs
Good follow-up Negative guaiac
LOW RISK
Normal H&H Negative NG

from baseline lavage
Healthy patient
Liver and Gallbladder
Introduction: Liver
Acute & chronic

Viral infection Alcohol Toxins
hepatitis
Acetaminophen
Primary causes Mushrooms
Injury to Hepatocyte
Hepatitis Leads to Scarring in liver
hepatocytes death
Especially in
chronic disease
Hepatocyte Loss of synthetic and Loss of Vitamin K Loss of Potential for

injury metabolic function clotting factors Protein C & S uncontrolled bleeding
II, III, IX, X
Loss of normal Portal

Liver scarring Leads to Portal shunts
liver structure hypertension
Portal Spontaneous Respiratory

Hypoalbuminemia Ascites Risk of
hypertension bacterial peritonitis issues
Ammonia level alone

Encephalopathy Multiple causes
has poor correlation
Bilirubin Evaluation
Prehepatic
Unconjugated Hepatic causes
causes
Posthepatic
Conjugated causes
Hemolysis
Sepsis Gilbert’s Disease

Hepatocellular
CHF
Unconjugated disease
Viral infection Toxins + Alcohol
Decreased Neonatal Infection Viral hepatitis

conjugation jaundice
Drug-induced
Mass/Tumor Conjugated
hepatitis
Stone Cirrhosis
Obstruction of
Sepsis
biliary ducts
Neonatal Jaundice
PEDIATRICS
Neonatal A common cause

Jaundice of readmission
Physiologic Due to hemolysis Bilirubin rises Peaks at 6 mg/dL during Decreases to

(> 50%) of fetal RBC’s < 5 mg/dL/day the 2nd–4th day of life < 2mg/dL by day 5–7
Jaundice related Higher levels of

to sepsis bilirubin
Breast feeding Bilirubin inhibitors Peaks at 10–27 Cessation of breast feeding causes a
related jaundice
(5–10% of cases) present in breast milk mg/dL by days 10–21 decrease in levels, but not recommended
Unlikely to cause kernicterus
UV light
Treatment
treatment
Otherwise healthy Levels

infants > 1–2 days old ³15 mg/dL
UV light Levels
2–3 days old
treatment ³18 mg/dL
Levels
> 3 days old
³20 mg/dL
Direct
Admission
hyperbilirubinemia?
Hepatitis Symptoms and Signs
Symptoms & Signs Varies depending on chronicity
Abdominal Altered mental Bleeding or Signs of liver Signs of

N/V Fever
pain status easy bruising failure coagulopathy
Epigastric Jaundice Petechiae
RUQ Spider angiomata Purpura
Gynaecomastia
Palmar erythema
Ascites
Hepatosplenomegaly
Tea-colored Dupuytren’s
Pruritis White Stools Presyncope Muscle atrophy
urine contracture
Acholic
Chronic
Laboratory Abnormalities in Hepatitis
Acute Hepatitis
Elevated Elevated indirect Elevated

AST/ALT > 2
AST/ALT bilirubin Urobilinogen
Esp. Alcohol
Chronic Hepatitis & Liver Failure
Elevated Elevated Elevated Elevated direct ± Elevated Elevated

± AST/ALT > 2
AST/ALT PT/INR ammonia bilirubin indirect bilirubin Urobilinogen
Indications for Hospitalization for Any Hepatitis
Encephalopathy
Severe Immunocompromised
electrolyte
abnormalities
Indications for Increased PT/INR

Age > 45 Hospitalization
Concomitant
significant renal
Sepsis
impairment
Bilirubin > 20 Hypoglycemia

Hepatitis A
Fecal-oral route via Most common cause of conjugated No chronic carrier

Hepatitis A
contaminated water or food hyperbilirubinemia in children state
Incubation of
Hepatitis A
15–50 days
Hepatitis A Nausea/Vomiting Jaundice + Light

Dark urine
symptoms & signs & Weakness stools
Hepatitis A
Prophylaxis
vaccine
Immune globulin within

Treatment
2 weeks of exposure
Majority are self-

Prognosis?
limiting
Hepatitis B
Transmission via blood, sexual

Hepatitis B DNA virus
exposure, & parenteral exposure
Hepatitis B Liver 5-10% chronic Hepatitis D co-infection

Cirrhosis
complications cancer carrier state increases risks of complications
Incubation of Pts may be infectious for

Hepatitis B
1–6 months 5–15 weeks after Sx onset
Markers HBsAg HBsAb HBeAg HBcAb
(+) after clearance Marker for high Appears after

(+) early
of HbsAg infectivity HbsAg
Best marker for Risk of Best marker for
immunity contracting HBV prior infection
after exposure
high if source is
HbeAg(+)
Risk of contracting
HB immune Repeat series if HBV after exposure
Treatment Vaccination if not successfully
globulin nonresponder
vaccinated = 6-30%
Unvaccinated 0, 1, 6 months
There are non-

NO TREATMENT HB immune converters to
Treatment If ( -) Vaccination
if HbsAb positive globulin the vaccine
Effective within 1 after
Vaccinated 0, 1, 6 months
week of exposure vaccination!
Hepatitis C
Transmission via Most common cause of

Hepatitis C RNA virus contaminated blood or viral infection with blood
blood products transfusion
Sexual transmission is
rare
Hepatitis C 50% chronic Hepatocellular

disease Cirrhosis carcinoma
complications
Usually
Hepatitis C aymptomatic
acutely
Higher incidence
Hepatitis C in pts with HIV
After exposure No effective post-

Hepatitis C conversion rate is exposure prophylaxis
2%
No vaccine
Hepatitis C available
Hepatitis D
Most commonly
Requires Hepatitis B surface
Hepatitis D from injection drug
antigen for co-infection
use
Hepatitis D Rapidly progressive High short term

complications liver failure mortality
Hepatitis E and G
Fecal-oral Can occur in Higher incidence

Hepatitis E in Russia, Asia &
transmission pregnancy
Africa
Via blood transfusions &

Hepatitis G
sexual exposure
Toxic Hepatitis
Multiple other
Toxic Hepatitis Acetaminophen prescription Mushrooms Alcohol
medications
Most common Amanita
Acetaminophen
N-acetylcysteine
overdose?
INH overdose? Treat with B6
Severe hepatic
Carbon
necrosis with Consider Acetaminophen OR Mushrooms OR
tetrachloride
AST/ALT > 1000?
Hepatic Encephalopathy
Hepatic
Dehydration or Electrolyte
encephalopathy Sedatives Infection GI bleeding
volume loss imbalances
precipitants
Ammonia level Poor correlation
Sleep during
Early sign Sleep inversion day, not night
Other signs Asterixis
“Liver flap”
Pitfall? Hypoglycemia
Treat Decreased
Treatment precipitants Lactulose Neomycin dietary protein
Spontaneous Bacterial Peritonitis
Chronic liver Portal Leakage of

SBP Bowel edema
disease hypertension enteric organisms
Enterococcus
E. coli
Symptoms and Signs
Abdominal Increased
Encephalopathy Fever Hypotension Sepsis
pain ascites
May be shock
May be absent
state
Increased WBC Neutrophils

Diagnosis Paracentesis
(>1000 mm3) > 250 cells/uL
3rd or 4th Levofloxacin or

Treatment generation OR Ciprofloxacin
cephalosporin
Introduction: Gallbladder
Due to gallstone
Biliary colic RUQ pain Vomiting But… No inflammation
obstruction
Most common cause of

Gallbladder Due to
Cholecystitis surgical abdomen in the
inflammation gallstones
elderly
Cholecystitis Obstruction by Distention of Pain & Bacterial

mechanism gallstone GB Vomiting infection Leukocytosis
E. coli
Stones in common Klebsiella
Choledocholithiasis
bile duct
Chronic Repeated episodes of Thickening of GB

Leads to Porcelain GB
cholecystitis gallstone obstruction wall
Calcification
Emphysematous Infection of GB wall by GB gangrene or

cholecystitis perforation High mortality
gas forming organisms
May see pneumobilia
Stone into adjacent Obstruction at

Gallstone ileus GB perforation High mortality
hollow viscus ileocecal valve
Biliary–duodenal fistula
RUQ pain
Ascending
Ascending Bile duct
infection through Charcot’s triad Fever
cholangitis obstruction
biliary tree
Jaundice
Acalculous Cholecystitis
Elderly Major surgery Postpartum

Acalculous Multiple risk
No gallstones Burns TPN Immune disease
cholecystitis factors
Severe illness Diabetes Trauma
Acalculous Pts usually very Higher morbidity

cholecystitis ill and mortality
Acalculous Beware
cholecystitis perforation!
Ascending Cholangitis
RUQ pain
Ascending
Ascending Bile duct
infection through Charcot’s triad Fever
cholangitis obstruction
biliary tree
Jaundice
Reynold’s Altered mental

Charcot’s Triad Shock
pentad status
Pathophysiology
Pure (20%)
Types of Cholesterol stones Pigmented stones
gallstones (70%) (30%)
Mixed (10%)
Radiolucent Radiopaque
Obesity
Risk of GB Large GB Impaired GB

Pregnancy DM
disease volumes contraction
Pts on TPN
Mechanism Infectious Mechanical Chemical
From reflux
of intestinal Inflammatory
contents into mediators
the biliary
tree
Most
commonly
Gram (-)
Can be
mixed
Symptoms and Signs
Symptoms & Signs
Abdominal Belching, bloating, Fatty food

N/V Fever Diaphoresis Dyspepsia
pain flatulence intolerance
RUQ
Epigastric Murphy’s sign
May radiate to
the back, right Cessation of
shoulder, or deep inspiration
scapula when palpating
the GB
High
sensitivity
Pain lasting for

Biliary colic
1–5 hours
Abdominal pain Acute Ascending Acute

Consider OR OR
> 5 hours cholecystitis cholangitis Pancreatitis
Diagnosis
Labs for suspicion Liver function Electrolyes +

of GB disease? CBC tests BUN/Cr
No specific labs!
Elevated ALT, AST

Not specific for Intrinsic hepatic Ascending Common bile
or Alkaline Consider OR OR
Acute cholecystitis disease cholangitis duct stone
Phosphate?
Imaging for Sensitivity = 94%

suspicion of GB RUQ sonography OR HIDA scan OR CT scan
disease? Specificity = 78%
Similar sensitivity & Use when U/S is
Test of choice specificity as U/S equivocal
Increased
Sonographic signs Sonographic Pericholecystic
thickness of GB
of cholecystitis Murphy’s sign fluid
wall
Presence of Most cholecystitis Specific for
tenderness over has wall thickness > cholecystitis
the GB 5 mm
Positive if GB is Obstruction of
Negative U/S? HIDA Scan not seen cystic duct
Identifies biliary
dyskinesia
Stones in bile
ducts? ERCP
Potential for
Gallstone ileus? CT or US
Treatment
Asymptomatic No specific
Refer to surgeon
gallstones treatment
Symptomatic
Biliary colic?
treatment
Acute Symptomatic Surgical

Admission Antibiotics
Cholecystitis? treatment consultation
Surgical or
Ascending Broad spectrum
Admission Endoscopic GB
cholangitis? antibiotics
decompression
Pancreatitis
Introduction and Some Causes of Pancreatitis
Gallstones
Most common
Infection Alcohol
Bacterial Acute
Viral Chronic
Parasites 2nd most common
Drugs and
Autoimmune
Medications
disease
Pancreatitis
Posterior penetrating
Cancer peptic ulcer
Inflammation of
the pancreas Hypertriglyceridemia
Iatrogenic May involve other
surrounding areas
ERCP Hyperparathyroidism
Post-op
Ischemia
Toxins
Organophosphate Trauma
poisoning
Scorpion venom Penetrating
Hypercalcemia
Wide range in Severe pancreatic Multiorgan

Pancreatitis e.g., Mild
disease severity necrosis failure
Complications of Pancreatitis
Pancreatic
necrosis
Cardiovascular
effects Abscess
Hypotension
Pseudocyst
Pericardial effusion
+ Hemorrhage
Pulmonary
effects Ascites
Hypoxemia
Pleural effusion Complications of Bowel infarction

Pancreatitis
ARDS
Hematologic effects
Respiratory failure
DIC
Renal effects Thrombosis
Renal Failure Portal vein

Renal artery or
Splenic vein
vein thrombosis
GI effects Metabolic effects
PUD Hyperglycemia
GI perforation
Hypocalcemia
GI Bleed
Hypertriglyceridemia
Bowel obstruction
Biliary obstruction
Symptoms and Signs
Symptoms & Signs
Abdominal Abdominal Diminished Hypotension +

N/V Fever Tachycardia
pain distention bowel sounds Shock
From associated
RUQ/LUQ
ileus
Epigastric Epigastric Severe disease
May radiate Pulmonary
through to the findings
back
10–20% cases
Worse supine
Relieved sitting
up with knees
flexed
Ecchymosis in
Cullen’s Sign
Umbilical area
Severe necrotizing
Late findings Hemorrhage
pancreatitis
Grey-Turner’s Ecchymosis in
Sign flank area Intraabdominal
Retroperitoneal
Diagnosis
Labs for suspicion
Liver function Electrolyes +
of Pancreatic CBC Lipase
tests BUN/Cr
disease?
3x upper limit
Imaging Pleural or
Sentinel Generalized
considerations for Plain films Identify Free air OR OR OR pericardial
loop ileus
pancreatitis? effusions
Imaging for Look for gallstones

suspicion of Sonography OR CT scan
pancreatic disease? Look for abscess or pseudocysts
Test of choice in
May be limited equivocal cases
Ranson’s Criteria: At Admission and 48 h
Age > 55
LDH > 350 WBC > 16,000

For both admission and 48
Ranson’s Criteria in
hours, 3 positives may predict
the ED
severe disease
(This has poor predictive value)
Used to determine
AST (SGOT) > 250 severity of acute Glucose > 200 mg/dL
pancreatitis
Decrease in
hematocrit > 10%
Base deficit > 4 Increase in BUN > 5

mEq/L mg/dL
Ranson’s Criteria at
48 hours
Rapid fluid
Calcium < 8 mg/dL
sequestration > 6L
PaO2 < 60 mm Hg
Treatment
Monitor
Acute Fluid Correction of Pain & nausea
hemodynamic and
Pancreatitis? resuscitation electrolytes control
volume status
Abscess or
CT guided
potentially infected Antibiotics
drainage
pseudocyst?
Retained common
ERCP
bile duct stone?
Ileus
Cessation of
Ileus NO obstruction
normal peristalsis
Medications
Other stressors Causes of Ileus Infections
Electrolyte
abnormalities
Symptoms & Signs
Continuous Abdominal Hypoactive No passage of flatus or

abdominal pain distention bowel sounds no bowel movements
Plain film for Fluid-filled loops

Ileus? throughout bowel
Usually self-
Treatment? NPO Supportive care
limited
Bowel Obstruction
Introduction and Causes

Inability of bowel
Both require
Obstruction to pass bowel Due to Intrinsic factors OR Extrinsic factors
intervention
contents
Cancer
Adhesions
Most common
Most common
Pseudo-
Ulcerative colitis
Small Bowel Obstruction
Strictures Hernias Large Bowel
Obstruction
Obstruction
Intussusception Fecal impaction
Cancer Intussusception
Lymphoma Diverticulitis Volvulus
Abscess
Incarcerated
inguinal hernia
Gut atresia &

Meconium ileus
stenosis
Early sign of Pediatric Bowel
cystic fibrosis Obstruction Malrotation with
PEDIATRICS
volvulus
1st year causes
Hirshsprung’s
Intussusception
disease
Duplication cyst of
intestine
Bowel Obstruction Pathophysiology
Continued
accumulation of
Development of secretions from Bowel becomes
obstruction stomach, pancreas congested
and liver
Vomiting & Volume depletion +

Potential for shock
Decreased oral electrolyte
and renal failure
intake imbalances
Failure of
absorption of
intestinal contents
Increase in
Bowel becomes
Distention of bowel intraluminal
ischemic
pressure
Exceeds capillary &

lymphatic pressures
Septicemia + Bowel
necrosis
High Mortality
Symptoms and Signs
Symptoms & Signs
Abdominal Abdominal Hyperactive Decreased passing Hypotension +

N/V Mass on exam
pain distention bowel sounds of flatus & stool Shock
Proximal Partial BO may Late finding
obstruction = SBO = Diffuse or
have passage of
Bilious Periumbilical
stool & flatus
Distal
obstruction = LBO =
Feculent Hypogastric
Diagnosis
Center bottom image (Reprinted from Pelaez CA, Agarwal N. The surgical abdomen. In: Pitchumoni CS, Dharmarajan
TS, editors. Geriatric gastroenterology. New York: Springer Science; 2012. 607–13. With permission from Springer Science
+ Business Media)
Labs for suspicion

Electrolyes + Others depending
of Bowel CBC
BUN/Cr on DDx
Obstruction?
No specific labs!
Traverse the
SBO X-ray Step Ladder or Plicae circulares
entire width of the
Appearance? “String of pearls” are seen
bowel
CT is diagnostic
DO NOT traverse
LBO X-ray
Distended colon Haustra are seen the entire width
Appearance?
of the bowel
“Coffee Bean”
Closed loop bowel Competent High risk of
appearance on
obstruction ileocecal valve perforation
plain film?
Diagnostic
method of choice? CT scan
SBO
Treatment
Monitor
Bowel Fluid Correction of Pain & nausea
hemodynamic and
obstruction? resuscitation electrolytes control
volume status
Consider NG
tube placement
Prophylactic
True mechanical
Surgery broad spectrum
obstruction?
antibiotics
Intussusception
(a) Top right image (Reprinted from Yoo S-Y. Non-neonatal gastrointestinal diseases. In: Kim I-O, editor. Radiology
illustrated: pediatric radiology. Heidelberg: Springer Verlag; 2014. p. 629–63. With permission from Springer Verlag).
(b) Bottom right image (Reprinted from Gilger MA, Nazer HM. Gastrointestinal bleeding. In: Elzouki AY, Harfi HA, Nazer
HM, Stapleton FB, Oh W, Whitley RJ, editors. Textbook of clinical pediatrics. Heidelberg: Springer Verlag; 2012. p. 1937–
49. With permission from Springer Verlag)
Most common cause of surgical

Intussusception abdomen & SBO from
3 months to 6 years
Uncommon > 3
Intussusception Rare < 3 months
years
Increased risk with Cystic fibrosis, Henoch-Scholein

Intussusception Purpura, Meckel’s diverticulum & Polyps
Ultrasound
“Sausage shaped” mass Ileocecal valve is
Intussusception
in right side of abdomen most common
Classic plain film Bowel Absent liver

Crescent sign Target sign
findings obstruction edge
Symptoms & Signs
Abdominal
N/V Heme(+)stools
pain
Intermittent Currant jelly

stool is late
Child appears finding
well between
paroxysms of
pain
Coiled Spring sign
Diagnosis
Labs for suspicion Electrolyes + Others depending

CBC
of Intussusception? BUN/Cr on DDx
No specific labs!
Imaging
Plain films Ultrasound Barium Enema
modalities?
Appearance on “Coiled spring”

Barium enema? sign
Treatment
Air contrast Fluid Correction of Pain & nausea

Intussusception?
enema resuscitation electrolytes control
Consider NG
tube placement
No relief with
Surgery
enema?
Pyloric Stenosis
Image just right of center (Reprinted from Yoo S-Y. Non-neonatal gastrointestinal diseases. In: Kim I-O, editors. Radiology
illustrated: pediatric radiology. Heidelberg: Springer Verlag; 2014. p. 629–63 (With permission from Springer Verlag)
PEDIATRICS
3rd week to 3rd month of Most common cause of surgically

Pyloric stenosis
life correctable cause of vomiting in newborns
Increased incidence with High incidence

Pyloric stenosis
1st born males in families
“Olive-shaped” mass in
Pyloric stenosis
right upper quadrant
Symptoms & Signs
Abdominal
N/V Dehydration Heme(+) stools
pain
Non-bilious Intermittent Currant jelly
Classic
stool is late
hypochloremic
Child appears well finding
metabolic
between
alkalosis
paroxysms of pain
Diagnosis

CBC
of Pyloric Stenosis? BUN/Cr on DDx
No specific labs! Will see

hypochloremic
metabolic alkalosis
Imaging for
Ultrasound OR Upper GI Series
Pyloric Stenosis?
“Target sign” (hypertrophied Elongated pylorus Exaggerated peristalsis &

Appearance on “Cervix
hypoechoic muscle surrounding with thickened failure of the pylorus to
ultrasound? sign”
echogenic mucosa) muscle open
Appearance on
“String sign”
Upper GI series?
Treatment
Monitor
Fluid Correction of Pain & nausea
Pyloric stenosis? hemodynamic and
resuscitation electrolytes control
volume status
Pyloric stenosis? Surgery
Hirschsprung’s Disease
PEDIATRICS
Hirshsprung’s Congenital Usually the 1st

Disease megacolon month
Hirschsprung’s Newborn: Failure Children: Chronic

Disease to pass meconium constipation
Hirschsprung’s
Complication Enterocolitis Potentially fatal
Disease
Volvulus
Introduction
Bottom left image (Reprinted from Pelaez CA, Agarwal N. The surgical abdomen. In: Pitchumoni CS, Dharmarajan TS,
editors. Geriatric gastroenterology. New York: Springer Science; 2012. p. 607–13. With permission from Springer Science
+ Business Media)
Bottom right image (Reprinted from Hellinger MD, Steinhagen RM. Colonic volvulus. In: Wolff BG, Fleshman JW, Beck
DE, Pemberton JH, Wexner SD, Church JM, Garcia-Aguilar J, Roberts PL, Saclarides TJ, Stamos MJ, editors. The ASCRS
textbook of colon and rectal surgery. New York: Springer Science; 2007. p. 286–98. With permission from Springer Science
+ Business Media)
Elderly (Old) Young

Most common 20–40
Insidious onset Acute onset
Congenitally freely
mobile cecum
High fiber diet SigmOid Volvulus Debilitated
Cecal Volvulus
Chronic motility
disorders Most common
cause of bowel
obstruction in
Rx pregnancy
Sigmoidoscopy
decompression
Rx
Surgery
Inverted “U” or “Bent Inner Tube”
Loops project to RUQ
Kidney shape loop in LUQ
Loops project to LUQ
Malrotation with Volvulus
PEDIATRICS
Malrotation with Occurs in early Usually the 1st

Volvulus infancy month
Malrotation with Abnormal rotation &

Volvulus fixation of midgut
Malrotation with Early diagnosis is

Prevents Midgut gangrene
Volvulus important
Symptoms & Signs
Abdominal Abdominal Shock

N/V Heme(+) stools
pain distention (potential)
Bilious Rigid
Sudden onset
For ALL types of

volvulus!
Diagnosis

CBC
of Malrotation? BUN/Cr on DDx
No specific labs!
Air-fluid levels in
Appearance on “Double bubble
stomach & in
Imaging? sign”
distended duodenum
Treatment
Monitor
Malrotation with Correction of Pain & nausea
hemodynamic and Fluid resuscitation
Volvulus? electrolytes control
volume status
Consider NG
tube placement
Prophylactic
Malrotation with broad spectrum
Surgery
Volvulus? antibiotics
Prophylactic
Surgical
Other Volvulus? broad spectrum
consultation
antibiotics
Hernias
Introduction
Protrusion of a viscus from

Hernia
its surrounding tissue walls
Hernia is soft & easy to

Reducible hernia replace back through the
defect
Hernia is firm & often painful.

Incarcerated
Unable to be replaced back
hernia
through the defect
Irreducible painful hernia Potential

Strangulated Impairment of Acute surgical
developing as a result of obstruction&
hernia blood flow emergency
incarceration toxicity
May have overlying skin changes Do not reduce!
Inguinal Hernias
Most common
Inguinal Hernia type of hernia for 2/3 are Indirect
males & females
Indirect Inguinal Herniates through Extends into the

Hernia the inguinal canal scrotal sac
Common in boys
Direct Inguinal Herniates through Palpable at the

Hernia the abdominal wall inguinal ligament
Common in older
men
Direct and
Pantaloon
Indirect at the
Hernia
same time
Ventral Hernias
Epigastric
Occur due to Hypogastric

Spontaneous or Named for
Ventral Hernia defect in anterior anatomic location
Acquired
abdominal wall Umbilical
Incisional
Older age
Obesity
Inadequate or Increased tension Wound infection Has a high

Incisional Hernia Due to OR on the abdominal Due to
wound healing recurrence rate
wall Conditions
which cause
increased
abdominal
pressure
Ascites
Adult form is Increased tension Strangulation is
Umbilical Hernia usually acquired Due to on the abdominal Obesity
uncommon
wall
Pregnancy
Congenital Closes by end of

Umbilical Hernia appears in 1st 1st year
month
Other Hernias
Hernia protrudes More likely to have
Mass below the More common in
Femoral Hernia through femoral incarceration &
inguinal ring women
canal strangulation
Increased tension
Lateral ventral Have high rates of
Spigelian Hernia Acquired Due to on the abdominal
hernia incarceration
wall
Abdominal pain with

Difficult to diagnose
Spigelian Hernia an anterior – lateral
Use CT or US
abdominal wall mass
Through the Presents as partial

Obturator Usually in elderly High complication
obturator or complete bowel
Hernia females rate
foramen obstruction
Perforations > 50 %
Pain in medial thigh

Obturator
due to obturator Dx = CT scan
Hernia
nerve compression
Howship – Romberg
sign
Only a portion of bowel wall More often with

May present strangulation due to
Richter Hernia herniates through the
without N/V delay in Dx
abdominal wall
May NOT have obstruction
Diagnosis
Labs for suspicion

No specific labs!
of Hernia?
Imaging for Often not

Plain films
hernias? diagnostic
Operator & body Most useful for

Sonography for
habitus kids & pregnant
hernias?
dependent women
Can identify
“Best” imaging
CT scan uncommon hernia
for hernias?
types
Treatment
Easily reducible Outpatient

hernia? management
Toxicity
Systemic signs Potential for
Tender hernia Obstruction Antibiotics Surgery
or symptoms Strangulation
Peritonitis Do not attempt ED
reduction!
Incarcerated hernia
(NO Attempt reduction
strangulation)? in ED
Bowel Perforation
Introduction
Most common
Cecum
site
Most common
Ulcers cause of
perforation
Inflammation
Appendicitis
Diverticulitis
Colitis
Obstruction Ulceration
Cancer Most common cause

Etiologies of Bowel
Foreign bodies Perforation IBD
Radiation Large bowel > Small Cancer
Bowel PUD
Foreign bodies
Ischemia Trauma
Symptoms & Signs
Abdominal Septic
N/V Fever
pain appearance
Diagnosis
Labs for suspicion

Electrolyes + Others depending
of Bowel CBC
BUN/Cr on DDx
Perforation?
No specific labs!
Plain films may Plain films may

Imaging for Bowel
miss small miss Get upright CXR!
perforation?
amounts of air retroperitoneal air
Diagnostic
CT scan
method of choice?
Treatment
Monitor
Bowel Fluid
hemodynamic and Antibiotics Surgery
perforation? resuscitation
volume status
Prophylactic
True bowel
Surgery broad spectrum
perforation?
antibiotics
Acute Appendicitis
Introduction
Obstruction by fecalith of
Appendicitis
the vermiform appendix
Other causes of
Parasites OR Tumor OR Lymphatic tissue OR Gallstones
Appendicitis
Blockage of Continued Increased Inflammation

Vascular
Appendicitis appendiceal secretion from luminal with potential
insufficiency
lumen luminal mucosa pressure perforation
Visceral pain Parietal pain

Appendicitis
Vague pain Localizes to RLQ
33% have atypical Most common is

Appendicitis But…
presentations still RLQ
Appendicitis Confounders
Pregnancy
Displacement by
gravid uterus
RUQ tenderness
Most common is
still RLQ
Malrotation of Retrocecal
colon appendix
LUQ tenderness Right flank or
Appendicitis
pelvic pain
Confounders
Situs inversus Long Appendix
Suprapubic pain
Testicular pain
Symptoms and Signs
Depends on location of appendix

Symptoms & Signs
and time frame of process
Abdominal Alterations in Pain on

pain Anorexia N/V Fever
bowel function movement
Early Usually follows
Variable
Nonspecific pain
Later
More specific
Flank pain Dysuria Hematuria
May have pain in
other areas
depending on
location Due to proximity
to urinary tract
Sudden
improvement in Consider perforation
pain?
Palpation of LLQ
Rovsing’s sign
worsens RLQ pain
RLQ pain with thigh

Psoas sign extension while patient is
in left lateral decubitus
RLQ pain with internal and

Obturator sign
external rotation of hip
Diagnosis
Labs for suspicion Electrolyes+ U/A

CBC CRP/ESR
of Appendicitis? BUN/Cr (with pregnancy)
No specific labs! May not be helpful
Imaging for
Ultrasound OR CT
Appendicitis?
Appearance on Thickened noncompressible

ultrasound? appendix > 6mm in diameter
CT for Use when Dx is

appendicitis? not clear
Appendicitis Mistaking pyuria

pitfall? for UTI
Treatment
Monitor
Fluid Pain & nausea
Appendicitis? hemodynamic and
resuscitation control
volume status
Prophylactic
Appendicitis? broad spectrum Surgery
antibiotics
Acute Diverticulitis
Introduction: Diverticulitis
Outpouchings through the colonic Increased
Weakening of
Diverticula wall near where vasa recta Due to intraluminal
colonic wall
penetrate bowel wall pressure
Involve only mucosal & submucosal Sigmoid = highest
layers pressures
Erosion of Thickened fecal Inflammation &

Diverticulitis Due to
diverticular wall material microperforation
Free perforation
is rare
In the U.S. Left sided In Asia Right sided

Diverticulitis colonic process Diverticulitis colonic process
Sigmoid
Common Gram (-) rods

Clostridium Peptostreptococci Bacteriodes Fusobacterium
bacterial agents E. coli
Risk Factors for Diverticulitis
Western diet
High fat
Low fiber
High carb
Those who are

Diverticulitis Obesity
sedentary
Potential links
Alcohol
Caffeine
Ingestion of nuts &
seeds
Smoking
Symptoms and Signs
Symptoms & Signs
Abdominal Alterations in
pain Anorexia bowel function N/V Fever Urinary Sx
LLQ in non- Diarrhea or Due to irritation

Asians Constipation of nearby GU
tract
RLQ in Asians
May be
suprapubic
Colicky or
constant
Diagnosis
Labs for suspicion Electrolyes + U/A

CBC CRP/ESR
of Diverticulitis? BUN/Cr (with pregnancy)
No specific labs! May not be helpful
Imaging for CT
OR Ultrasound
Diverticulitis? (Preferred)
Appearance on Inflammatory Colonic Thickened

Phlegmon Abscesses
CT? stranding diverticula bowel wall
Soft tissue Fluid

masses collections
Appearance on Wall Colonic

Inflammation Abscesses
US? thickening diverticula
Fluid
collections
Must refer for colonoscopy after

Diverticulitis
resolution to evaluate for
pitfall?
carcinoma
Treatment
Uncomplicated
Oral antibiotics High fiber diet Discharge
Diverticulitis?
-Non-toxic
-Pain controlled
-Healthy
Complicated Pain and nausea Surgical

IV antibiotics NPO
Diverticulitis? control consultation
Broad spectrum
-Toxic appearing
including
-Vomiting
anaerobic
-Comorbidities
coverage
High mortality Fluid

Perforation IV antibiotics Surgery
rate resuscitation
Mesenteric Ischemia
Introduction
Usually with Hx of Has a high

Mesenteric “Abdominal Usually affects an mortality rate if
cardiovascular
ischemia angina” older population undetected
disease
Mesenteric
Arterial OR Venous OR Nonocclusive
ischemia
From cardiac Severe

Arterial (70%) OR Thrombosis From
embolization atherosclerosis
SMA thrombosis
Hypercoagulable Usually a younger

Venous (10%)
state population
Continued
Nonocclusive
decrease in e.g., Shock states
(20%)
cardiac output
Risk Factors for Mesenteric Ischemia
Hypercoagulable
states
Dysrhythmias
A. fib
Venous
Atherosclerotic Valvular heart

Arterial
disease disease
Hx of prior
thromboembolism
Use of
vasoconstrictors
Most common
Other low flow

Diuretic use
states
Nonocclusive
Prolonged
CHF
hypotension
Shock states
Symptoms and Signs
Symptoms & Signs Depends on time frame
Abdominal
Anorexia Diarrhea N/V Fever Tachycardia
pain
“Out of May be grossly
Food fear
proportion” bloody
Abdominal
Sudden = Peritoneal signs
distention
embolic
Insidious =
thrombotic or
Late findings
nonocclusive
May have pain

“Intestinal
that resolves
ischemia”
following meals
Diagnosis
Labs for suspicion
Electrolytes +
of Mesenteric CBC Lactate ABG
BUN/Cr
ischemia?
Usually elevated May show
Elevated Acidosis
WBC hyperphosphatemia
Mesenteric
Plain films CT
ischemia
Appearance on Paucity of Thickening of

SBO Ileus Bowel wall gas
imaging? bowel gas bowel wall
Pneumatosis
Thumbprinting
intestinalis
Gold standard? Angiography
Mesenteric Not considering

ischemia pitfall? the Dx
Treatment
Monitor
Mesenteric Fluid Prophylactic Early surgical
hemodynamic and
ischemia? resuscitation antibiotics consultation
volume status
Crohn’s Disease
Introduction
Chronic
Involves any part Ileum usually Segmental
Crohn’s Disease granulomatous
of GI tract involved involvement
inflammatory disease
Involves all layers of From mouth to “Skip lesions”
the bowel wall anus
Ulcerations are Fissures

Crohn’s Disease Lead to Fistulas Abscesses
present (not in midline)
Crohn’s Disease
Remission Exacerbation
pattern
Crohn’s Disease 15–40 years old
Symptoms and Signs
Symptoms & Signs Varies from patient to patient
Abdominal May present with Extra-intestinal

Anorexia Diarrhea Weight loss Fever
pain complications manifestations
Chronic cases Bowel obstruction
Present in most Obstipation
patients
Intra-abdominal
abscess
Perianal Toxic
Abscesses Fistulas Rectal prolapse Hematochezia
fissures megacolon
Colonic
involvement
Extraintestinal Manifestations
Arthritic
Sacroiliitis
Renal Ankylosing Eye

spondylitis
Nephrolithiasis Peripheral arthritis Uveitis
Hyperoxaluria Episcleritis
Malnutrition
Hematologic
Extraintestinal
Chronic anemia Manifestations Vascular
Seen in 50 % Vasculitis
Hypercoagulable
state
Skin
DVT
Erythema
Venous
nodosum
thromboembolism
Pyoderma
gangrenosum Arteritis
Hepatobiliary
Cholelithiasis
Hepatitis
Pancreatitis
Cholangiocarcinoma
Pericholangitis
Primary sclerosing
cholangitis
Diagnosis
Pts usually have

Crohn’s Disease?
established diagnosis
Laboratory Electrolytes + U/A LFT’s & Type &

CBC
evaluation? BUN/Cr (add preg test) Lipase Cross
If needed
Imaging for acute

symptoms? CT
Visualization of
Appearance on Mesenteric Thickened bowel
Local abscesses extra-intestinal
CT? edema wall
manifestations
Treatment
Identify & treat

Crohn’s Disease?
complications
Prevention of Nutritional
Crohn’s disease? Symptom relief
complications maintenance
Mild to moderate
Crohn’s disease? Sulfasalazine
Acute
exacerbation of Glucocorticoids
Crohn’s disease?
Antibiotics in Can help induce

Crohn’s disease remission
Ciprofloxacin
Perianal
complications & Metronidazole
Fistulas
Must screen for

Pitfall
malignancy
Ulcerative Colitis
Introduction
Chronic inflammatory Rectum involved Most will have

Ulcerative Colitis Colon only
disease nearly all the time bloody diarrhea
Involves only the Worse from

Major finding
mucosa & submucosa proximal->distal
Mucosal Epithelial
Ulcerative Colitis Lead to Ulcerations Crypt abscesses
inflammation necrosis
Ulcerative Colitis
Remission Exacerbation
pattern
Same extraintestinal
Similar GI Sx as Similar laboratory
Ulcerative Colitis manifestations as
Crohn’s evaluation as Crohn’s
Crohn’s
30 fold increased
Ulcerative Colitis
risk of carcinoma
Toxic Megacolon
Disease process
Ulcerative Colitis Loss of muscular Dilated transverse
Toxic megacolon through all layers
complication of colon tone in colon colon > 6 cm
Continued Distended, painful Systemic toxicity Signs of

Peritonitis
dilation abdomen (F/tachycardia) hypovolemia
Continued Risk of
dilation perforation
Laboratory Electrolyte
Leukocytosis Anemia Hypoalbuminemia
evaluation abnormalities
Imaging Loss of haustra Thumb printing
Toxic Early surgical

megacolon? consultation
Irritable Bowel Syndrome
Irritable bowel Altered gut Altered gut Alterations in

syndrome motility sensation rectal evacuation
Irritable bowel
Abdominal pain Bloating Constipation OR Diarrhea
syndrome
Usually concomitant
Irritable bowel
psychiatric
syndrome
conditions

Abdominal pain for Change in Change in
Improvement
Diagnosis 3 days/month in the frequency of OR appearance of
with defecation
last 3 months bowel movements stools
Treatment Antispasmodics Laxatives OR Antidiarrheals
Depending on
complaints
Miscellaneous Anorectal Emergencies
Hemorrhoids
Engorgement, prolapse,
Hemorrhoids or thrombosis of
hemorrhoidal veins
Internal Proximal to the Not easily Best seen with

Found at 2, 5, & 9 o’clock
hemorrhoids dentate line palpable anoscope
When patient Usually non-
viewed prone tender
Painless, self-
limited bleeding
Tender to
External Distal to the Seen on external
palpation if
hemorrhoids dentate line examination
thrombosed
Warm water Stool Topical

Treatment Analgesia High fiber diet
sitz baths softeners steroids
Thrombosed
Clot excision
hemorrhoid?
Pitfalls of excision Immune Portal

Coagulopathy Pregnancy Children
(Don’t excise) compromised hypertension
Surgical Very large Incarcerated Strangulated Continued

Intractable pain
consultation? hemorrhoid hemorrhoid hemorrhoid bleeding
Risk Factors for Hemorrhoids
Constipation
Straining with
defecation
Older age Pregnancy
Risk factors for

Hemorrhoids
Fibrosis from Portal

radiation therapy hypertension
Ascites Tumors
Anal Fissures
Superficial linear tear Most common
Usually midline
Anal Fissures of the anal canal below cause of painful
& posterior
the dentate line rectal bleeding
Children &
Adults
Non-midline More serious Infectious

fissures pathology
IBD OR etiology
OR Cancer
Until proven
TB
otherwise
Syphilis, GC,
Chlamydia
Sharp, cutting Pain most severe Blood streaked

Anal Fissure Sx
pain with BM during & after BM stools
Pain dissipates
between BM’s
Warm water Stool Topical

Treatment Analgesia High fiber diet
sitz baths softeners steroids
Non-healing Surgical
fissure? consultation
Anorectal Abscesses
Anorectal Begin with blockage of Abscess

Infection Polymicrobial
Abscesses anal crypt & its gland formation
Anorectal abscess Deep postanal

Perianal Intersphincter Ischiorectal Supralevator
locations space
Most
common
Associated with
Can be treated Surgery
Perianal abscess Unless deeper periectal
in ED
abscesses
Abscess Pain before Lessened after Pain worsened by

But… Persists
Symptoms defecation defecation movement & sitting
Deep abscess? IV antibiotics Surgery
Rectal Prolapse
Part or all of rectal In children,

Folds of mucosa
Rectal Prolapse layers protrude intussusception
are circular
through the anal canal more likely
Hemorrhoidal
mucosal folds
radiate out like
wheel spokes
Rectal Prolapse Sensation of

rectal mass
Treatment Reduction
Pitfalls of rectal Edematous Surgical

propalse rectum consultation
Nephrology and Urology
Bobby Desai
Contents
Acute Renal Failure 262
Rhabdomyolysis 274
Chronic Renal Failure 277
Hemodialysis 283
Urinary Tract Infections 288
Hematuria 292
Kidney Stones 293
Renal Transplant 295
Male Genital Emergencies 295
Sexually Transmitted Diseases 301
B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_4
262 B. Desai
Acute Renal Failure
Introduction
Decrease in renal
Acute Renal
function over Due to Prerenal causes OR Renal causes OR Postrenal causes
Failure
hours to days
Decrease in
Prerenal causes perfusion of
normal kidney
Intrinsic renal
Renal causes pathology
Obstruction to
Postrenal causes urinary tract
General Symptoms & Signs Usually no Sx until uremia develops
Sx of underlying
Confusion N/V Fatigue Lethargy Weakness
process
Helps determine Prerenal Renal Postrenal

FENa etiology of renal
failure <1 % >1 % >4 %
Urine Sodium? Prerenal Renal Postrenal

(mmol/L) <20 >40 >40
Loss of End stage

RIFLE criteria Risk Injury Failure
function renal disease
Nephrology and Urology 263
RIFLE Criteria
Risk
1.5 fold increase

in creatinine OR
GFR decrease by
25 % OR
ESRD
Urine output Injury
Complete loss of
<0.5 mL/kg/hr x
kidney function
6 hr 2 fold increase in
for more than 3
creatinine OR
months
GFR decrease by
50 % OR
RIFLE Criteria
Loss
Urine output
<0.5 mL/kg/hr x
Complete loss of 12 hr
kidney function
for more than 4
weeks
Failure
3 fold increase in
creatinine OR
GFR decrease by
75 % OR
Urine output
<0.5 mL/kg/hr x
24 hr OR
Anuria x 12 hr
Common Causes of Acute Renal Failure in Children
PEDIATRICS
Glomerulonephritis
Common Causes of
Postoperative Hemolytic
Acute Renal Failure
complications Uremic Syndrome
in Children
Sepsis
264 B. Desai
Prerenal Failure
Decrease in Renal artery or
Prerenal Acute
perfusion of Due to Hypovolemia OR Cardiogenic shock OR small vessel
Renal Failure
normal kidney disease
Related to
Symptoms
underlying cause
Treat underlying Restore Pressors as

Treatment
cause circulating volume required
Causes of Prerenal Failure
Hypovolemia
GI loss
Skin loss - Burns
Burns, Fever, Sepsis
3rd spacing
Hypoaldosteronism
Medications Hypotension
ACE inhibitors Hemorrhage

Causes of Prerenal Decreased cardiac
NSAIDs Failure output
b-blockers
High output failure
Medications
Renal artery
disease
Electrolyte Embolism from any
cause
Hypercalcemia Thrombosis from
any cause
Dissection
Intrinsic Renal Failure
Vascular disease that

Intrinsic Renal Disease within
OR directly affects renal
Failure kidney
function
Related to
Symptoms
underlying cause
Interstitial
Treat underlying
Treatment disease
cause
Antibiotics
NSAIDs
Antifungals
Small vessel + Other non- Glomerular
disease medication causes disease
HSP
Glomerulonephritis
Tumor lysis
syndrome General Causes of Nephrotic syndrome
Intrinsic Renal
Failure
Hemoglobinuria Myoglobinuria
Tubular disease
ATN
Contrast
Chemotherapy
266 B. Desai
Some Causes of Interstitial Disease
Infiltrative
processes
Lymphoma
Sarcoid
Autoimmune Infection derived

Some Causes of
Interstitial Disease
Lupus Legionella
Acute interstitial
nephritis Urine
Immune mediated Pyuria Treatment
Features Treat underlying
Usually from a drug
Rash process
reaction
Fever WBC Casts
Most commonly
Eosinophilia
NSAIDs & Antibiotics Antibiotics for
(PCN, Sulfa) Eosinophils in infection
May be infectious urine
as well
Some Causes of Glomerular Disease
Malignant
hypertension
Henoch – Schonlein Wegener’s

purpura disease
Diabetic Focal segmental

nephropathy glomerulosclerosis
Membranous Minimal change

glomerulonephritis Some Causes of disease
Glomerular Disease
Goodpasture
Lupus
syndrome
Infection
Poststreptococcal Urine Treatment

glomerulonephritis Features
Hematuria Steroids
Oliguria
Pyuria
Group A β-Hemolytic Edema
RBC Casts
streptococci HTN Immune
Proteinuria suppressants
Immune complexes
in glomeruli
268 B. Desai
Some Causes of Tubular Disease
Acute Tubular Intratubular

Necrosis obstruction
Most common Uric acid

Some Causes of
Tubular Disease
Calcium oxalate
Ischemia due to
Usually oliguric
sepsis & trauma
Amyloid
Usually NOT
Toxin derived
oliguric
Radiocontrast
agents
Aminoglycosides
Rhabdomyolysis
Hemolysis
Multiple myeloma
Ethylene glycol
Risk for Radiocontrast-Induced Nephropathy
Age >70
Concomitant use Hyperuricemia

of diuretics Risk for Radiocontrast
Induced Nephropathy
Risk reduction
Dehydration Avoidance of contrast Existing renal

study disease
Volume expansion
Low osmolar contrast
agents
Multiple Hypo-or
N-acetylcysteine
myeloma Hypertension
Diabetes mellitus Recent contrast

study
Vascular or Related Disease

Thrombosis in
microvasculature
Scleroderma
Vascular or Related
Disease
Malignant Transplant-related
hypertension thrombosis
270 B. Desai
Causes of Microthrombosis
Hemolytic-uremic
syndrome
DIC Causes of Preeclampsia

Microthrombosis
TTP Sickle cell disease Polyarteritis

nodosa
Postrenal Failure
Obstruction of
Postrenal Failure
outflow tract
May have gradual Alternating

Symptoms
onset oliguria & polyuria
Treat underlying
Treatment
cause
General Causes of Postrenal Failure
Urethra & bladder

outlet obstruction
Phimosis
Neurogenic bladder
Meatal stenosis
Urethral calculus
Prostatic
hypertrophy Most common
Anatomic
Retroperitoneal Causes of Postrenal
malformation of
tumor or clot Failure
ureter
Vesicoureteral
reflux
Bilateral ureteral
Papillary necrosis GU Tract trauma
stones
Diabetes mellitus
Sickle cell
Pyelonephritis
272 B. Desai
Some Laboratory Investigations for Renal Failure
Fractional
Prerenal Failure BUN/Cr Urine Na
excretion of Na
<1 % >20 <20 mEq/L
Intrinsic Renal Fractional

BUN/Cr Urine Na
Failure excretion of Na
>1 % <20 >40 mEq/L
Urinalysis Mandatory
Glomerulonephritis (+) RBC Casts Hematuria Proteinuria
Nephrotic Proteinuria
syndrome alone
Probable
WBC Bacteria
infection
Macroscopic Urine
Renal /
Microscopic Nephritic Renal
Gross Hematuria OR Ureteral OR Tumor OR
Hematuria syndrome Trauma
calculus
Microscopic Myoglobinuria OR Hemoglobinuria

Gross Hematuria Hematuria
Microangiopathic
Rhabdomyolysis
hemolytic anemia
TTP, HUS, DIC
Mechanical valve
breakdown of RBC
Urinalysis
Granular casts
Bowman’s
Proximal
capsule
Red cell casts convoluted Tubules
tubule
Glomerulus Acute tubular necrosis
Nephritic syndrome
Descending
White cell casts
Limb of Distal
Loop of convoluted
Interstitium Henle tubule
Collection duct
Acute interstitial nephritis
Ascending
Pyelonephritis Limb of Loop
Loop of Henle of Henle
Eosinophiluria
Interstitium
Acute interstitial
nephritis
Center image (Adapted from Kidney Nephron: https://commons.wikimedia.org/wiki/File:Kidney_Nephron.png. Artwork by Holly Fischer with
permission from Creative Commons License: https://creativecommons.org/licenses/by/3.0/deed.en)
Red cell casts
Glomerulus
Nephritic syndrome
White cell casts Granular casts
Interstitium Tubules
Acute interstitial nephritis Acute tubular necrosis
Pyelonephritis
Eosinophiluria
Interstitium
Acute interstitial
nephritis
274 B. Desai
Rhabdomyolysis
Introduction
Caused by acute Leakage of muscle
Rhabdomyolysis necrosis of skeletal contents into
muscle circulation
Creatine
Muscle contents Myoglobin LDH Potassium
kinase
Pathophysiology Dysfunction of Increased Activation of Production of

of rhabdomyolysis Na-K pump intracellular Ca catabolic enzymes free radicals
Pathophysiology Myoglobin Acute renal In setting of

of renal failure blocks tubules failure hypovolemia
Causes of Rhabdomyolysis
Alcohol
Electrolyte
abnormalities
present in
Neuroleptic alcoholics Prolonged
malignant syndrome contributes to immobility
rhabdomyolysis
Tumor lysis
Intrinsic muscle syndrome
diseases
Causes of Drugs of abuse

Rhabdomyolysis
Seizures Cocaine
Heroin
Amphetamines
LSD
Heat stroke PCP
Infection Trauma Medications
Influenza Crush injury Statins

Legionella Burns SSRI’s
Electrical injury Antipsychotics
TASER AZT
Lithium
Clinical Features of Rhabdomyolysis

Symptoms & Signs
Diffuse Diffuse Dark cola

Acute Myalgias Malaise +Fever
stiffness weakness colored urine
More advanced
N/V Tachycardia Abdominal pain AMS
stage
Diagnosis of Rhabdomyolysis
5 fold or greater Without heart or CK rises 2-12 hours,

Creatine kinase
increase in CK brain injury peaks 24-72 hours
Failure of CK to
Ongoing muscle
decrease over
necrosis
time
Acute rise in
Other marker
creatinine
RBC on
Urine (+) dip for heme
microscopy
Serum
Other labs electrolytes Calcium Phosphorus Uric acid Baseline CBC
with BUN/Cr
Fibrin split Due to potential DIC

Consider PT/PTT Fibrinogen
products as a complication
276 B. Desai
Complications of Rhabdomyolysis
Acute Renal Failure
Oliguric
Most common
Early Metabolic
Complications
Hyperkalemia
Hyperphosphatemia
Hyperuricemia
Hypocalcemia Musculoskeletal
complications
Complications of Compartment
Rhabdomyolysis syndrome
Late Metabolic
Complications Neuropathy
Hypophosphatemia
Hypercalcemia
DIC
Usually
spontaneously
resolves
Treatment of Rhabdomyolysis
Treatment of Treatment of
Urine output
Rhabdomyolysis IV hydration electrolyte
2 cc/kg/hr
derangements
No significant benefit
Mannitol OR Bicarbonate over aggressive
hydration alone
Hypocalcemia? No treatment
Hypercalcemia? Saline diuresis
Oral phosphate
Hyperphosphatemia? binders if >
7 mg/dL
Treat if <1
Hypophosphatemia?
mg/dL
Chronic Renal Failure
Chronic Renal Failure and End-Stage Renal Disease (ESRD)
PEDIATRICS
Build up of toxins
End Stage Renal Irreversible loss of 10 % of normal for
GFR & loss of
Disease (ESRD) renal function age
homeostasis
Accumulation of
Clinical syndrome Fatal without
Uremia Azotemia nitrogen in the
of ESRD therapy
blood
Clinical
syndrome
4 stages of
Chronic Renal Stage 1 Stage 2 Stage 3 Stage 4
Failure
GFR 50–75% of GFR 25–50 % of GFR 10–25 % of GFR <10 % of
normal for age normal for age normal for age normal for age
Elevated urine Chronic renal
failure ESRD
protein
Elevated
Anemia
BUN/Cr
Acidosis
Rickets in
children
Mortality in Cardiovascular Infectious

children (50 %) (20 %)
Most common
Congenital renal Reflux
cause of CRF in Older children Glomerulonephritis
disease nephropathy
younger children
278 B. Desai
Nephrotic Syndrome
PEDIATRICS
Permeability
Nephrotic Chronic disease Loss of protein in
changes in
syndrome in children urine
glomerular wall
Nephrotic
Proteinuria Edema Hypoalbuminemia Hyperlipidemia
syndrome
May be massive Due to salt &

water retention
Especially of face
and periphery
Thromboembolic
Complications Infection
events
DVT/PE High risk for

Streptococcus
pneumoniae
peritonitis
Goals of ED Treat acute

Make the Dx Arrange followup
treatment symptoms
Causes of Nephrotic Syndrome
PEDIATRICS
Minimal change
disease
Membranoproliferative Focal segmental

Nephritis sclerosis
Most common
Primary
Proliferative Membranous
nephritis nephropathy
DM
Systemic infections Drugs (Toxicity)
Gold
HSP
Mercury
Secondary
Sickle cell disease Cancer
HIV Lupus
Syphilis
Renal Tubular Acidosis
PEDIATRICS
Renal Tubular Hyperchloremic Normal GFR

Acidosis (RTA) Wide anion gap
metabolic acidosis
Failure of HCO3 Failure of Inability to acidify the

3 types of RTA reabsorption in excretion of H+ urine in setting of low
proximal tubule ions distally aldosterone
Type 1 Type 2 Type 4
Sequelae of potassium
ED visits Urinary Tract
Failure to thrive derangements (High & Rickets
prompted by Stones
Low)
Depends on
Treatment underlying
condition
280 B. Desai
Polycystic Kidney Disease
Polycystic Autosomal Progressive

Leads to
Kidney Disease dominant process renal failure
Polycystic Associated Cerebral Subarachnoid

Kidney Disease with aneurysms hemorrhages
Symptoms & Signs
Renal failure on
Flank pain Hematuria
lab evaluation
Cardiovascular Complications of Uremia
Mortality due to 10-30 fold higher Preexisting

Due to
CV disease in dialysis patients conditions
Management Other agents may

Present in 80-90%
Hypertension starts with control be considered if
of dialysis patients
of blood volume unsuccessful
Most commonly
Consider uremic AV fistula high
CHF due to Fluid overload
cardiomyopathy output failure
hypertension
Similar treatment
Pulmonary
to non-dialysis Nitrates Diuretics ACE Inhibitors
edema
patients
Pulmonary
vasodilation
Consider when all Dialysis rarely

Uremic
other causes have improves function
cardiomyopathy
been evaluated in these patients
Typical EKG
Usually due to Loud pericardial
Pericarditis changes may be
uremia friction rubs
absent
Beck’s triad is Mental status

Tamponade May have Hypotension Dyspnea
rare changes
Neurologic Complications of Uremia
Stroke causes in Intrinsic Bleeding Anticoagulant Excessive

HTN
dialysis patients disease dyscrasias therapy ultrafiltration
10 times more Bilateral SDH may May only see

Subdural
common in not have focal altered mental
hematomas
dialysis patients deficits status
Uremic Nonspecific Diagnosis of Improve with

encephalopathy neurologic Sx exclusion dialysis
Fails to respond
Dialysis Nonspecific CNS
Progressive with dialysis or Ultimately fatal
dementia Sx
transplant
Frequent Autonomic
Peripheral
manifestation of Lower > Upper dysfunction may
neuropathy
ESRD occur
Symptoms & Signs of Peripheral Neuropathy
Impaired
Paresthesias Decreased DTR Weakness
vibration sense
Symptoms & Signs of Autonomic Neuropathy
Postural Bowel Decreased

Impotence
hypotension dysfunction sweating
Hematologic Complications of Uremia
Anemia caused Dialysis blood Decreased red cell Decreased Usually normocytic,
by loss survival time erythropoietin normochromic
Bleeding CNS & Eye Subcapsular liver

Multifactorial Leads to GI bleeding
diasthesis bleeding hematomas
High morbidity &

Decreased WBC Immunologic
Leads to mortality from
function dysfunction
infectious causes
282 B. Desai
Gastrointestinal Complications of Uremia
Anorexia
Increased Nausea &

incidence of Vomiting
diverticular disease
Gastrointestinal
Complications of
Uremia
Chronic
Gastritis
constipation
Dialysis related
UGI Bleeding
ascites
Idiopathic Higher mortality
Electrolyte Complications of ESRD
Hyperkalemia
Hypermagnesemia Hypokalemia
In dialysed patients
Electrolyte
Complications of
ESRD
Hypomagnesemia Hypocalcemia
Hyperphosphatemia
Hemodialysis
Indications for Emergency Dialysis
Refractive
Hyperkalemia &
Hypercalcemia
Metabolic Refractive
acidosis volume overload
Indications for
Emergency Dialysis
Severe sodium
Imbalance Toxic overdose
Symptomatic
Uremia
Pericarditis
Bleeding
Encephalopathy
Acid-Base Electrolyte Fluid

AEIOU Intoxications Overload Uremic Sx
problems problems
Severe acidosis
Hyperkalemia BUN >100
or alkalosis
284 B. Desai
Complications of Hemodialysis
Infectious
Dialysis site
infection
Bacteremia
High output CHF Thrombosis
Braham sign Most common

cause of
Decrease in inadequate
heart rate after dialysis flow
occlusion of
vascular access May use
Complications of thrombolytics in
Hemodialysis consultation with
vascular surgeon
Hemorrhage
Vascular Vascular
insufficiency aneurysms
“Steal From repeated
syndrome” punctures
Nonhealing. Most are

ulcers asymptomatic
May have
Pain on use of impingement
extremity neuropathy
Cool, pulseless
digits
Infectious Complications of Hemodialysis

May present with
Infections systemic signs of Hypotension Fever
sepsis
Rx with
Gram negative
Organisms Staph aureus Vancomycin ±
organisms
Gentamicin
Complications Epidural abscess Septic arthritis Endocarditis Osteomyelitis

Hemorrhagic Complications of Hemodialysis
Rare but may be

Hemorrhage
life threatening
Control bleeding Observe if

Hemorrhage with direct hemorrhage is
pressure controlled
Other modalities Topical thrombin Protamine DDAVP
Hypotension During Hemodialysis (HD)
Most common
Multiple
Hypotension complication of
differentials
hemodialysis
Rx with
Hypotension Hypovolemia that Gram negative
Vancomycin ±
early in dialysis is preexisting organisms
Gentamicin
Hypotension late Excessive Pericardial

Cardiac disease
in dialysis ultrafiltration disease
Volume depletion
before HD
Pericardial effusion Blood loss during

or tamponade HD
Hemodialyzer loss
Hypotension during
Hemodialysis
Cardiac
dysfunction Medications
Blood loss after

HD
Graft loss
Symptoms & Signs
Nausea &
Tachycardia Dizziness Syncope Anxiety
Vomiting
286 B. Desai
Dialysis Disequilibrium
Dialysis
N/V Hypertension Leads to Seizure Coma Death
Dysequilibrium
Differential Intracranial Hypertensive

Seizures Stroke
diagnosis hemorrhage crisis
Especially SDH
Blood has lower

Clearance of large Fluid shifts into
Natural history osmolality than Cerebral edema
amount solute brain
brain
Treatment Stop HD Mannitol
Increase serum
osmolality
Altered Mental Status in Hemodialysis Patients
Hypotension
Dialysis
Hypoglycemia
dysequilibrium
Altered Mental Status

in Hemodialysis
Patients
Intracranial
Hypercalcemia
hemorrhage
“Psychic moans” SDH
Consider air embolism

CVA Sx, Syncope or
Myocardial ischemia
Peritoneal Dialysis
Most common Abdominal wall PD catheter

Complications Peritonitis
complication hernias infections
Repair ASAP due

to high risk of
incarceration
Peritonitis cell
> 100 WBC/mm3
count
>50% neutrophils
Other Gram Anaerobes &

Organisms S. epidermidis S. aureus
streptococcus negatives Fungi
40 % 15–20 % 15–20 % 10 % 5 % each
Symptoms & Signs
Rebound Cloudy Pain during

Abdominal pain Fever
tenderness peritoneal fluid inflow
Antibiotics in
Treatment
dialysate
288 B. Desai
Urinary Tract Infections
UTI
Kidney
Significant Described by Bladder
UTI Symptoms
bacteriuria location
Urethra
Most risk of
Older men Neonates Girls Young women
infection
Risk of UTI in Age of 1st UTI Maternal Hx of

Sexual activity Diaphragm use
young women <15 UTI
STD
Males <50 With Dysuria OR Frequency (until proven
otherwise) Consider
prostatitis
Males >50 With Dysuria OR Frequency UTI
Urethritis & Lower urinary Usually benign if

tract infections treated
Cystitis appropriately
Flank pain
Upper urinary Usually with Fever
Pyelonephritis tract infection systemic symptoms
N/V
5
Asymptomatic Presence of >10 On 2 successive Treat in Prevents
CFU of single
bacteriuria bacterial species urine cultures pregnancy pyelonephritis
Especially in 3rd
Same organism & Within one trimester
Relapsed UTI
serotype month May cause
miscarriage
Different organism 1-6 months after Multiple Look for

Reinfection
or serotype initial infection reinfections comorbid factors
Complicated Versus Uncomplicated UTI
Uncomplicated No recent GU tract

Young & healthy Nonpregnant No comorbities
UTI instrumentation
Pathogen E. coli Treatment 3 days
More likely to
Abnormal GU Essentially have resistant
Complicated UTI Comorbities everyone else
tract organisms
Pseudomonas
Staphylococcus Proteus
Pathogens
Group D Strep Klebsiella
Enterobacter
Urine culture &

Treatment > 10 days
sensitivities
Perinephric Emphysematous
UTI Complications
abscess pyelonephritis
From contiguous Especially in
spread diabetics
290 B. Desai
Clinical Features of UTI
UTI Diagnosis Bacteriuria Clinical Sx
Symptoms & Signs
Pain in
Dysuria Frequency Hematuria CVA tenderness Hesitancy Fever
suprapubic area
Increase the probability of UTI

Beware of referred
pain!
Urethritis in a Urethral
Dysuria
male discharge
Gonococcal Gram-(-)
intracellular
urethritis diplococci
Sterile pyuria Chlamydia OR TB
Gram stain Chlamydia (until Nonspecific

negative? proven otherwise) urethritis
UTI Diagnosis
U/A Midstream OR Catheterization
Urine >5 WBC/high With appropriate

Abnormal
microscopy powered field symptoms
Centrifuged
>1–2 WBC/high May be significant

In males Bacteria with appropriate
powered field
Sx
Centrifuged
Bacteria in gram
stained specimen of Significant
uncentrifuged urine
Enterococcus
Nitrite >90% specificity Coliform bacteria Nitrite (-) Pseudomonas
Acinetobacter
Leukoctye Supports UTI Does not rule it

(+) test (-) test
esterase diagnosis out (not sensitive)
Urine culture Complicated Relapse or

Pregnancy Adult males Children
required UTI reinfection
Unnecessary in
Imaging
uncomplicated infections
Severely ill Diabetes or

Renal stone Imaging
(Septic) Immune disease
292 B. Desai
Hematuria
Most Common Causes of Hematuria
Infections
Any age
Any location in
GU tract
Glomerulonephritis Nephrolithiasis
<20 years > 20 years
Hematuria
IgA nephropathy Sickle cell anemia
Microscopic
hematuria = >5
Schistosomiasis WBC/HPF Medication
related
Most common >20 years
cause worldwide
Prostatic
hypertrophy Cancer
>60 >40 years
On start of
Urethra OR Bladder
urination
May have clot
formation
End of urination Prostate
Throughout Usually dark

Kidney
urination urine
Kidney Stones
Kidney Stones Diagnosis and Treatment

Paucity of
Supersaturation of
Kidney stones Due to inhibitory Urinary stasis
urine
substances
Calcium oxalate Struvite Uric Acid Cysteine

Types of stones (75 %) (15 %) (10 %) (1 %)
Diseases that
Causes of calcium Inflammatory Small bowel
increase calcium Hyperparathyroidism
oxalate stones Bowel disease resection
excretion
Urea-splitting
Struvite stones Chronic infection organisms Proteus Pseudomonas
Most common Poor antibiotic

Chronic infection,
Struvite stones High urinary pH cause of staghorn penetration into
staghorn Surgical treatment
calculi
25 % of patients
Radiolucent
Uric acid stones with gout will Low urinary pH
stones
develop stones
Inborn error of May form Associated with

Cysteine stones Due to Cysteinuria
metabolism staghorn calculi renal failure
Medications Carbonic
Indinivir Prolonged abuse
predisposing to anhydrase
stone formation (Radiolucent) of laxatives
inhibitors
Ureterovesicular
Common sites of Ureteropelvic
Renal calyx Pelvic brim junction
impaction junction
(most common)
Spontaneous Depends on
Amount of urinary
Size Shape Location
stone passage obstruction
<5 mm = 98 % pass rate
294 B. Desai
High clinical Confirmatory

Kidney stones? U/A
suspicion imaging Renal colic is most
common
Crampy Radiation from misdiagnosis in cases
Clinical suspicion N/V of AAA
intermittent pain flank to groin
Absent in 10-
Hematuria?
20 %
Confirmatory Noncontrast
94–97 % sensitive 96–99 % specific
imaging helical CT
98 % sensitive for
Confirmatory Ultrasound (if CT detecting 64–90 % sensitive 94–100 % specific
imaging contraindicated) hydronephrosis
Except in Opioids as
Treatment Pain control NSAID’s
congenital stones needed
Control of nausea Consider α-

Treatment
& vomiting blockers
Boluses increase Fluids for

Hydration? replacement
pain when vomiting
Urologic
Infected stones? Antibiotics Admission
consultation
Stone Admission Criteria

Concurrent
infection
Ruptured renal Renal insufficiency

capsule or failure
Stone Admission
Criteria
Intractable
vomiting Intractable pain
Solitary kidney
with severe
obstruction
Renal Transplant
Most common
Renal Transplant solid organ Location = pelvis
transplant
Infection Can be subtle
May not have

Rejection Can be subtle Minimal pain
systemic signs
Antirejection
Cyclosporine Is nephrotoxic
meds
Male Genital Emergencies
Scrotal Disorders
Usually from
Antibiotics for
Scrotal abscess infected hair Simple I&D
complicated cases
follicle
Fournier’s Polymicrobial necrotizing

Affects Genital area Perianal area Perineal area
gangrene fasciitis
Starts as simple Microthrombi of

Fournier’s Gangrene of
abscess or Spreads subcutaneous
gangrene vessels overlying skin
cellulitis
immunosuppressed
Risk of
Diabetics Alcohol abusers IV Drug Users
Fournier’s
Symptoms & Signs
Pain at involved Swelling at

Ecchymosis Crepitus Fever
area involved area
Pain out of proportion Pain extending beyond

Foul odor
to findings area of infection
Immunocompromised
Prompt Fluid Polymicrobial Prompt surgical

Treatment
recognition resuscitation antibiotics debridement
Center right image (Reprinted from Wessells H, Sorensen MD. Fournier’s gangrene. In: Wessells H, editor. Urological emergencies: a practical
approach. New York: Humana Press; 2013. p. 141–50. With permission from Springer Science + Business Media)
296 B. Desai
Glans Penis and Foreskin Disorders
Balanoposthitis is
Inflammation of Inflammation of
Balanitis Posthitis inflammation of
glans penis foreskin both
Inadequate Colonization with Recurrent Diabetes until

Usual etiology
hygiene Candida infections proven otherwise
Antifungal creams
Treatment Proper cleansing
or oral
Bacterial Warmth, edema,

Antibiotics
infection swelling
Inability to Urinary
Phimosis Complication Treatment Circumcision
retract foreskin retention
Inability to reduce True emergency– Wrap glans tightly with

Paraphimosis foreskin over the necrosis of glans elastic bandage to Dorsal incision
glans penis (Consult Urology) reduce edema
Can consider methods that
cause osmotic shifts of fluid
Produces Thickened plaque

Peyronie’s Disease progressive penile Painful erections on dorsum of Urologic referral
deformity penis
Traumatic Penis and Foreskin Disorders
PEDIATRICS
Hair-thread Hair wrapped

tourniquet around an Hyperemia Swelling Pain
syndrome appendage
Uncircumcised Hair may be Prompt removal

Around penis Glans swelling
males 3–5 invisible is the cure
Rupture of tunica
Direct trauma to
Penis fracture albuginea of
erect penis
corpus cavernosa
Swollen flaccid Hx of immediate

Physical exam Discoloration
penis detumescence
Retrograde Assess for urethral

Imaging
urethrogram injury
Urological
Treatment
evaluation
Deep dorsal vein

Complications Urethral rupture
injury
Priapism
Glans & Corpus

Pathologic Both cavernosa
Priapism Very painful spongiosum NOT
erection engorged with blood affected
Injection of Agents related to

Medication Hypertension Psychiatric
vasoactive erectile
causes include agents medications
substances dysfunction
Sickle cell
In children
disease
High flow Low flow

Priapism OR
(Nonischemic) (Ischemic)
Traumatic fistula between

Usually Treated with Straddle
High flow cavernosal artery and corpus
painless embolization mechanism
cavernosum
Dx by aspiration of dark SCD

Low flow More common Very painful Spinal cord
intracavernosal blood injuries
Corporal Irrigation with α-

Treatment Analgesia Terbutaline
aspiration agonists
Treatment failure Surgery
Consider
Sickle cell disease? exchange
transfusion
Complications Impotence Urinary retention

298 B. Desai
Testicular Torsion
Testicular Bimodal age Appendix testis Prepubertal

Peak in puberty
Torsion distribution torsion boys
Results from abnormal fixation Bell clapper Free movement Rotation and
Torsion
of testis in tunica vaginalis deformity of testes swinging of testes
Most torsion
Torsion can Periods of Most are aligned
Minor trauma But… occurs without a
occur with testicular growth horizontally
preceding event!
Symptoms & Signs
Severe pain in May have pain in Horizontal lie of Testicle is firm & Absent Absent Prehn’s
N/V
testicle abdominal or inguinal area testes elevated Cremasteric reflex sign
Elevation of the
Blue dot sign for appendix scrotum with
testis torsion improvement of pain
Emergent urologic
Radionuclide Salvage rates
Diagnosis Doppler U/S OR But… consultation if high
scintigraphy decline >6 hours
suspicion
88 % sensitive;
100 % sensitive
90 % specific
Manual detorsion Relief of pain + Still needs Urology

ED Treatment (while waiting for Success
Urology) normal lie & possible OR!
If unsuccessful, try
Bilateral opposite direction
Treatment
orchidopexy “Opening a
book”
Treatment of
appendix testes Pain control
torsion
Epididymitis and Orchitis
Most commonly
Urine reflux Mumps or other
Epididymitis due to bacterial Orchitis
(Inflammation) viral illnesses
infection
Mumps =
Unilateral then
bilateral
involvement
Young boys E. coli Urine reflux
Sexually active
STD’s GC OR Chlamydia
males
Prostatic Urethral
Older males OR E. coli Klebsiella
enlargement stricture
Associated with
Bacterial orchitis
epididymitis
Symptoms & Signs
Gradual onset of pain May have pain in Testicle may be (+) Cremasteric Progression may cause
(+) Prehn’s sign
in scrotum or testicle abdominal or inguinal area firm reflex epididymo-orchitis
May be positive for

Diagnosis U/A WBC, nitrite & U/S Increased flow
bacteria
Cover age Ice packs &

Treatment Antibiotics Analgesics
related causes scrotal support
300 B. Desai
Prostatitis
Same etiologies as Same age related

Prostatitis
epididymitis considerations
Lower urinary
Epididymitis Foley Rectal
Risk factors Phimosis tract
or urethritis catheter intercourse obstruction
E. coli (most
Causative agents Klebsiella Pseudomonas Serratia Staph
common)
Symptoms & Signs
Pain in genital Difficulty in

Pain in perineum Low back pain Frequency Dysuria F/C
area defecating
Enlarged & tender

Urinary retention
prostate – “boggy”
Evaluate for
Diagnosis U/A
GC/Chlamydia
Antibiotics (long
Treatment Analgesics Foley
term = 30 days)
Suprapubic
Severe? IV antibiotics
catheter
Especially for
retention
Urethritis
Purulent urethral
Urethritis
discharge
Whitish Intracellular gram

GC
discharge (-) diplococci
Watery or no Negative gram

Chlamydia
discharge stain
Diagnosis DNA probes U/A
Ceftriaxone Azithromycin
Treatment Treat partners
250 mg IM 1 g po
Urinary Retention
Mechanical causes Prostatic Urethral

Meatal stenosis
of Urinary retention hypertrophy strictures
Neurologic Spinal cord

Diabetes Multiple sclerosis
causes injury
Drugs &
Other causes
medications
Opioids
Sympathomimetics TCA
Cold remedies
Drugs &
medications
Antihypertensives Anticholingerics
D/C with
Treatment Foley catheter
catheter
Cannot pass Urology Suprapubic

catheter consultation catheter
Sexually Transmitted Diseases
Ulcer-Forming Processes
Syphilis
Mite disease Herpes
Lymphogranuloma
Chancroid Ulcer Forming
venerum
Processes
Molluscum
Yeast infections contagiosum
Granuloma
Genital warts inguinale
302 B. Desai
Non-ulcer-Forming Processes
Gonorrhea
Candidal vaginitis Chlamydia
Non-ulcer Forming
Processes
2º & 3º syphilis PID/Cervicitis
Bacterial
vaginosis Trichomonas
Chlamydia
Most frequently Commonly coexists Most are 1–3 week

Chlamydia incubation period
reported STD with gonorrhea asymptomatic
Types of Reiter’s
Urethritis Epididymitis Proctitis
infections in males syndrome
Types of
Sterile pyuria
infections in Cervicitis Urethritis PID
females (Males as well)
Polyarticular Arthritis of the heel

Reiter’s syndrome Conjunctivitis Urethritis
asymmetric arthritis Sausage digits
Symptoms & Signs
Penile (or vaginal) Testicular (or Bleeding

Dysuria Abdominal pain
discharge Pelvic) pain between menses
Complications in Fitz-Hugh-Curtis
PID Ectopic pregnancy Infertility
females syndrome
Diagnosis DNA probe
Azithromycin No intercourse
Doxycycline Refer partner for
Treatment OR until 7 days after
(single dose) (7 days) therapy treatment
Treatment Treat Chlamydia &

considerations Gonorrhea together
Gonorrhea
2nd most Commonly coexists Most are 1–2 week

Gonorrhea frequently
with chlamydia asymptomatic incubation period
reported STD
Types of
Urethritis Epididymitis Prostatitis Proctitis
infections in males
Types of PID
infections in Cervicitis Urethritis (20% of untreated
females females get PID)
Symptoms & Signs
Mucopurulent Testicular (or Bleeding Lower Mucopurulent

Penile discharge Dysuria
anal discharge Pelvic) pain between menses abdominal pain cervicitis
Septic arthritis (most

In males GC conjunctivitis GC Pharyngitis common cause <50 years) In females
Complications in Chronic pelvic

PID Ectopic pregnancy
females pain
Disseminated Petechial rash Fever & Asymmetric

Tenosynovitis Septic arthritis
Gonococcemia on red base Malaise arthralgias
Gram stain of
Diagnosis DNA amplification
urethral swab
IM Doxycycline Azithromycin Treatment of partner & no intercourse

Treatment OR
Ceftriaxone (7 days) 1 g dose until 7 days after treatment
Treatment Evaluation for Evaluation for

IV antibiotics Hospitalization
disseminated GC endocarditis meningitis
Trichomoniasis
High prevalence
Protozoan Infections mostly 3 days to 4 weeks
T.vaginalis of coinfection
infection in women incubation period
with other STD
Symptoms & Signs
Thin, malodorous Lower Inflamed

Vulvar irritation Dysuria Frequency Dyspareunia
watery discharge abdominal pain vaginal mucosa
Punctate cervical May be asymptomatic

in men Urethritis
hemorrhages
Males
Motile organisms
Diagnosis
on microscopy
Refer partner for No intercourse

Treatment Metronidazole until 7 days after
therapy treatment
304 B. Desai
Syphilis
Enters through
Spirochete Consists of three Still sensitive to
Syphilis mucous membranes
disease phases or damaged skin Penicillin
Painless chancre
Incubation Lesions resolve
Primary syphilis with indurated Symptoms
borders period 21 days after 3–6 weeks
3–6 weeks after end of 1º Dull red papular

Secondary Malaise, fever,
stage with spontaneous trunk rash spreads Lymphadenopathy
syphilis to palms & soles headaches
resolution
Secondary Most infectious Lesions contain In moist areas the

Condyloma lata
syphilis stage spirochetes lesions are flat
Involvement of nervous
Seen in 33 % of 3–20 years after
Tertiary syphilis and cardiovascular
patients initial infection systems
Neuropathy
Widespread Thoracic Charcot’s
Tertiary syphilis Meningitis (Tabes Dementia
gummas aneurysm joint
dorsalis)
Dark field FTA-ABS (best Serology is (-) the

Diagnosis RPR sensitivity &
microscopy specificity) first 4–6 weeks
Benzathine Benzathine
Treatment Treatment of Treatment
penicillin IM x 1 penicillin weekly x
1º and 2º dose partners 3º 3 weeks
Fever
Complication of Jarisch-Herxheimer Most frequently In 1st 24 hours of
HA
treatment reaction in early syphilis Myalgias therapy
Due to organism
Jarisch-Herxheimer Lasts a few 50 % Primary Pretreat with
death & release of
reaction hours 90 % Secondary acetaminophen
endotoxins
Herpes Simplex
Exposure of Most genital
Lifelong
HSV infections mucosal surfaces infections caused
infection or nonintact skin by HSV-2
Symptoms & Signs
Painful
Burning Tingling Pain in area Headache Fever Malaise
adenopathy
Prodrome Constitutional
2–24 hours Sx in 75%
Vesicles on red Vesicles erode in Lesions crust and heal

Painful lesions
base hours to days without scarring
Urethral
Shaft of penis Glans of penis Labia Perineum
meatus
Recurrent
Usually milder
outbreak?
Viral culture Tzank smear

Diagnosis Clinical
(Gold standard) (Low sensitivity)
C-section if
Treatment Antivirals
pregnant Neonatal herpes
Acquired at birth
Treatment Antivirals with
recurrent
High mortality
reduced dosages
infections
Aseptic Urinary retention due
meningitis Erythema Transverse
Complications to sacral root ganglia Hepatitis Encephalitis multiforme myelitis
(HSV-2) inflammation
306 B. Desai
Chancroid
H. ducreyi is
Haemophilus If present search
Chancroid Due to cofactor for HIV
ducreyi for other infections
transmission
Painful genital Incubation Painful

Chancroid Lymphadenitis erythematous
ulcers period 4–10 days papule
Painful Lesion is painful &

Lesion erodes & May become
erythematous 1–2 days later 1-2 cm in
papule ulcerates pustular diameter
Tender lymph 1–2 weeks after Spontaneous

Adenopathy Untreated ? Bubo formation
nodes primary infection rupture
Culture medium
Exclude herpes
Diagnosis Clinical grounds Swab for culture not universally
& syphilis available
I&D of
Treatment Ceftriaxone OR Azithromycin OR Ciprofloxacin OR Erythromycin
buboes
Lymphogranuloma Venereum (LGV)
Chlamydia
LGV Due to Serotypes L1,L2, L3
trachomatis
Painless herpes- May not be

Primary lesion Lasts 2-3 days
like ulcer noticed
1-3 weeks after Unilateral inguinal May progress to Spontaneous

OR Firm adenopathy
primary lesion adenopathy suppuration rupture of abscess
Buboes
These are painful
Scarring of Form linear depressions

Groove sign
masses near inguinal ligament
LGV proctitis Rectal bleeding Rectal ulcers Rectal discharge
Symptoms & Signs
Erythema Meningoencephalitis
Fever Chills Arthralgias
nodosum (Rare)
Culture of Complement
Diagnosis Clinical
aspirate fixation titers
Doxycycline for 3
Treatment
weeks
Granuloma Inguinale
Granuloma Calymmatobacterium
Due to Donovaniasis Rare in US
Inguinale granulomatis
Incubation period Subcutaneous Progress to Lesions are

Granuloma
of 2 weeks to 6 nodules on penis painless ulcerative erythematous and
Inguinale months or labia/vulva lesions bleed easily
Granuloma Lesions are

Inguinale mutilating
Granuloma May have

Inguinale adenopathy
Diagnosis Biopsy
Doxycycline for 3
Treatment
weeks
Lesions
Syphilis
Granuloma
inguinale Painless lesions LGV
Chancroid Painful Lesions Herpes

308 B. Desai
Genital Warts
Human Condyloma 15–18 genotypes There is a

Genital Warts Due to
papilloma virus acuminata are oncogenic vaccine available
Flesh colored
1–3 month
Genital warts cauliflower like
incubation period projections
Seen in external
In females Perianal region
genitalia Usually painless
Depending on
Nonhealing Urethral
In males Pruritis location may be
penile ulcers discharge painful
Diagnosis Clinical
Treatment Topical podofilox OR Imiquimod OR Cryotherapy

Hematologic and Oncologic
Emergencies
Bobby Desai
Contents
Anemia 310
Transfusion Therapy 314
Complications of Transfusion Therapy 317
Dyshemoglobinemias 321
Hemostasis Tests 323
Sickle Cell Anemia 325
Hereditary Hemolytic Anemias 329
Specific Labs for Hemolytic Anemia 330
Platelet Disorders 333
Hemophilia 338
Von Willebrand’s Disease 339
Anticoagulants 339
Absolute and Relative Contraindications to Thrombolysis 342
Complications of Malignancy 343
B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_5
310 B. Desai
Anemia
Introduction
Reduced Increased
Decrease in Increase in RBC
Anemia concentration of Due to
production
OR loss
OR destruction of
RBC from baseline RBC
Decrease in
Response to Increase in Stimulation of
Tachycardia systemic vascular
acute anemia cardiac output erythropoietin
resistance
Response to Increase in Stimulation of

chronic anemia plasma volume erythropoietin
Causes of Anemia
Increased
destruction
Sickle cell
Splenic sequestration
Thalessemia
Hemolytic anemia
Hemorrhage May be medication

induced
Impaired
production
Causes of Anemia Iron deficiency

Infectious Folate deficiency
Parvovirus B19 in AIDS Aplastic anemia
Dilutional
Hematologic and Oncologic Emergencies 311
Symptoms and Signs
Symptoms & Rate of Age and condition Extent of

Depend on Comorbidities
Signs development of patient anemia
Most symptoms Hemoglobin of

& signs <7 g/dL
Symptoms & Signs
Dyspnea on Palpitations +
Fatigue Weakness Orthostasis Lethargy
exertion Chest pain
Chronic anemia
Pallor of skin & Wide pulse Systolic ejection
Tachycardia Hepatosplenomegaly Jaundice
mucosal surfaces pressure murmur
Hemolytic
anemia
Resting Palpitations + Altered mental

Acute anemia Hypotension Diaphoresis
dyspnea Chest pain status
Specific Labs for Anemia
Decreased
Anemia Hemoglobin & Decreased RBCs
Hematocrit
Consideration of Look for GI or Reticulocyte Consider sending

CBC
anemia GU bleeding count peripheral smear
Mean corpuscular Red blood cell

MCV
volume size
Red cell Size variability of

RDW
distribution RBC’s
Reticulocyte
RBC production
count
Best indicator for

iron deficiency Serum ferritin
anemia
Direct Coomb’s Demonstrates presence (+) in Hemolytic Transfusion

Test of antibodies on RBC’s anemia reactions
Indirect Coomb’s Demonstrates presence Tested before

Test of antibodies in serum transfusion
312 B. Desai
Classification of Anemia
Classification Based on MCV
Microcytic Macrocytic Normocytic
Low MCV (Microcytic)
Iron deficiency
Low MCV Low ferritin
anemia
Anemia of
Renal failure
chronic disease
Sideroblastic
Low MCV Normal ferritin Hypothyroidism
anemia
Vitamin C
Thalessemia
deficiency
High MCV (Macrocytic)
B12 deficiency Folate deficiency
High MCV Alcohol abuse Liver disease
Aplastic anemia Chemotherapy

Normal MCV (Normocytic)

Anemia of
Renal failure
chronic disease
Normal
Normal MCV Iron deficiency B12 deficiency
reticulocyte count
Folate deficiency
High reticulocyte Positive Coomb’s Autoimmune

Normal MCV
count test related
Hereditary
Sickle cell disease
spherocytosis
High reticulocyte Negative Coomb’s
Normal MCV
count test
Microangiopathic
G6PD deficiency
hemolysis
Treatment
Depends on
Treatment
etiology of anemia
Significant Limited cardiac Evidence of Cardiac Hemodynamic Type & cross-

OR OR OR OR
blood loss reserve hypoxia ischemia instability matched RBC
Iron deficiency
Elemental iron
anemia
B12 or Folate IM
OR PO Folate
deficiency anemia Cyanocobalamin
Sideroblastic Evaluate for

Supportive care
anemia reversible causes
Aplastic anemia Transfusion Supportive care
Anemia of Transfusion as
Supportive care
chronic disease needed
314 B. Desai
Transfusion Therapy
Packed Red Blood Cells (PRBC)

Shock states with
Acute
ED transfusion impaired O2
hemorrhage
delivery
Total blood 5L in 70 kg
volume in adult person
Each unit of Volume of Hematocrit of Increases Hb by Increases Hct by

PRBC 250 cc 55–80 % 1 g/dL 3%
Lasts 42 days Children = 2 g/dL Children = 6 %
May use O Universal

O negative Universal donor Type AB
positive for men recipient
Minimize risk of Prevent sensitization Prevent non-hemolytic

Leukocyte 70–80 % leukocytes
virus transmission for bone marrow febrile reactions due to
reduced PRBC removed
HIV/CMV recipients WBC antibodies
Prevents donor T- Prevents

Use in immune- Transplant
Irradiated RBCs cells from graft vs host Neonates
comprised hosts patients
proliferating process
For plasma
Washed RBCs
hypersensitivity
Higher percentage of RBC’s in a set volume

Decreased infusion of protein antigens in PRBC
Advantages of = decreased autoimmunization
PRBCs compared Less total volume given = less fluid overload
to whole blood Decreased infusion of Potassium in PRBC
Decreased citrate in PRBC = improved
coagulation
Massive Blood Transfusion
Bottom figure image (Reprinted from Allen B, Ganti L, Desai B. Trauma and ATLS. In: Allen B, Ganti L, Desai B, editors. Quick hits in
emergency medicine. New York: Springer; 2013. p. 37–44. With permission from Springer Science + Business Media)
Results in Due to lack of

Class III Class IV Massive Blood
dilutional clotting factors &
hemorrhage hemorrhage Transfusion
coagulopathy platelets
ARDS from
Complications Hypothermia microaggregate Citrate toxicity
debris
TRALI = Transfusion
related acute lung injury
Use blood
Hypothermia
warmer
Normal saline as Calcium in Formation of

Microaggregates Use blood filter
diluent lactated ringers microclots
May cause Increased

Citrate toxicity QT prolongation
hypocalcemia bleeding
316 B. Desai
Platelet Transfusion
Prophylaxis when
ED transfusion Active bleeding
clinically indicated
Each unit of Increases

Platelets from one platelets by up to
unit whole blood 10,000
Give ABO compatible

Platelet pheresis 6 units of Usually from
platelets when
pack platelets single donor
possible
< 10,000
Asymptomatic
<100,000 Indications for <15,000

Platelet
Neurosurgery transfusion Minor bleeding
Coagulation
Cardiac surgery Consider also in disorder
pts with major
bleeding on a
platelet inhibitor
<50,000 <20,000
Invasive procedure Major bleeding
General surgery
Fresh Frozen Plasma

Takes
Frozen within 8
FFP Whole blood RBC & Platelets approximately 30
hours
minutes to thaw
Usually 4 units in
Volume of One unit of each 2 mg of fibrinogen
One unit FFP adults, 15 mL/kg
250 cc coagulation factor per mL
in children
Massive Bleeding
Warfarin
FFP Uses Liver failure transfusion (to DIC from factor TTP
overdose
provide clotting) deficiency
FFP will NOT

Monitoring of lower INR below
PT INR PTT
FFP treatment 1.2 – 1.3!
Isolated factor Use specific

deficiency? factors instead
Cryoprecipitate
Insoluble protein
Cryoprecipitate
fraction of FFP
Volume of 225 mg 80 units Also has

Cryoprecipitate
20–50 cc Fibrinogen Factor VIII & vWF Factor XIII & fibronectin
Cryoprecipitate Replacement of Replacement of

uses fibrinogen vWF
Complications of Transfusion Therapy
Acute Hemolytic Transfusion Reaction

Acute Hemolytic Infusion of
Immediate Antibodies
Transfusion incompatible Usually ABO
reaction destroy RBC’s
Reaction RBC’s
Destruction of Release of
DIC
RBC vasoactive amines
Symptoms & Signs
Pain at
Acute stages Fever Chills Low back pain Dyspnea Tachycardia
transfusion site
More advanced Respiratory Acute tubular

Hypotension Shock Bleeding Hemoglobinuria
stages failure necrosis
Stop May be life

Treatment IV hydration Supportive care
transfusion! threatening!
May require
diuretics or
mannitol
Repeat cross
Evaluation Retype
match
Proportional to
Morbidity amount of blood
given
318 B. Desai
Laboratory Investigation for Acute Hemolytic Transfusion Reaction
CBC
Coagulation
Indirect bilirubin
parameters
Hemoglobinuria Haptoglobin
Laboratory
Investigation for
Haptoglobin Acute Hemolytic Electrolytes
Transfusion Reaction
LDH BUN/Cr
Direct Coomb’s Indirect Coomb’s

test test
Plasma free
hemoglobin
Febrile Nonhemolytic Reaction

Febrile Interaction between Difficult to distinguish
Immediate Most common
Nonhemolytic Due to recipient and donor from early hemolytic
reaction reaction
Reaction non-RBC components reaction
Symptoms & Signs
Fever Chills Rigors Myalgias Headache Tachycardia Dyspnea
Consider
Stop Evaluate for
Treatment Treat fever IV hydration infectious
transfusion! hemolysis
evaluation
May be life-threatening
Natural history Usually mild But… in patients with poor
cardiovascular reserve
Delayed Transfusion Reaction
Delayed
7–10 days after Antigen-antibody
Transfusion Delayed reaction Due to
transfusion reaction
Reaction
Symptoms & Signs
Otherwise
Low grade fever
asymptomatic
Hemolysis
Treatment Stop transfusion!
evaluation
Allergic Transfusion Reaction

Allergic Due to
Immediate Severe
Transfusion Minor To Due to incompatible
reaction anaphylaxis
Reaction plasma proteins
Symptoms & Signs Not dose related
Mild Erythema Urticaria Pruritis
Vasomotor
Severe Bronchospasm Dyspnea Tachycardia Shock
instability
May restart
Treatment for Stop No further
Diphenhydramine transfusion if
mild reaction transfusion! workup
symptoms resolve
Treatment for Stop Treat Hemolysis Don’t restart

severe reaction transfusion! anaphylaxis evaluation transfusion!
May be
indistinguishable
from hemolysis
320 B. Desai
Infectious Complications of Transfusion
For viral, bacterial

Overall risk of
1:500 or parasitic
acquiring infection
infections
Risk of
1:2,000,000
Hepatitis C or HIV
Risk of
1:200,000
Hepatitis B
Risk of
1:10,000
Parvovirus B19
Risk of Most commonly by Grows in

1:500,000
Bacterial sepsis Yersinia enterocolitica refrigerated blood
Other Complications of Transfusion

Transfusion Complication of
related Acute Uncommon FFP or platelet
Lung Injury transfusion
Transfusion Bilateral Syndrome
related Acute pulmonary Within 6 hours clinically similar to
Lung Injury infiltrates ARDS
Usually self
Treatment Supportive But… Can be fatal
resolves
Electrolyte
Uncommon Hypokalemia OR Hyperkalemia OR Hypocalcemia
disturbances
Electrolyte Due to massive Concern in liver or

disturbances transfusions renal failure
Beware in those with Beware in

Due to rapid
Hypervolemia limited cardiopulmonary pediatric pts, esp
volume expansion
reserve infants
Pulmonary Transfuse slowly

Symptoms Dyspnea Hypoxia
edema if possible
2–4 mL/kg/hr
Dyshemoglobinemias
Introduction: Methemoglobin (MHb)

Hemoglobin Prevented from
Dyshemoglobinemia molecule is carrying O2
altered
Iron in normal Ferrous state Oxidizes Ferric state Now Hb incapable

to of carrying O2 Methemoglobin
Deoxyhemoglobin (Fe2+) (Fe3+)
Limited by enzyme
Normal amounts 1–2 % of circulating NADH -> NAD
reduction of ferric to
of methemoglobin hemoglobin reaction
ferrous iron
Produced when enzymatic

Methemoglobinemia reduction hampered by Drugs OR Chemicals OR Congenital
exogenous oxidant stress
> 1.5 g of Hb in Chocolate

Cyanosis
Ferric form brown blood
Often more Due to leftward Reduced release

Reduce O2
Clinical effect symptomatic than shift of O2 of O2 from RBC
content of blood
simple anemia dissociation curve
Blood gas Pulse ox is

Methemoglobinemia PO2 is normal measures dissolved misleading –
O2 80–85 %
Drugs Causing Methemoglobinemia
Antimalarials
Common
Local anesthetics Dapsone
Benzocaine
Most common
Lidocaine
Nitrates/Nitrites
Amyl nitrite
Drugs causing Sodium nitrite

Methemoglobinemia
Both in cyanide
antidote kit
Silver nitrate
Nitroglycerin
Pyridium Rare
Sulfonamides
322 B. Desai
Types of Methemoglobinemia
Acquired Due to Medications
Underdeveloped More suspectible

Well water,
Infants reduction to MHb
spinach
mechanisms accumulation
Enzyme Amino acid

Hereditary OR Hemoglobin M
deficiency substitution in Hb
Clinical Features
No effects until
Healthy patients
MHb >20 %
Symptoms & Signs – MHB 20–30 %
Generalized
Headache Weakness Lightheadedness Tachycardia Tachypnea Cyanosis
weakness
Symptoms & Signs – MHB 50–60 % 70 % = fatal
Myocardial Metabolic
AMS Coma Seizures Arrhythmias
ischemia acidosis
No cyanosis until higher

Sx at lower MHb
Anemic patients percentage of Hb is in
concentrations
ferric form
Treatment
Supportive Supplemental O2 Decontamination

Treatment
measures as appropriate
Clinical
Use in Asymptomatic pts
Antidote Methylene blue improvement in
symptomatic pts with Mhb > 25 %
20 minutes
Pt on Dapsone? Cimetidine
Hemostasis Tests
Bleeding Time
Uremia
Prolonged
Von Willebrand’s
NSAID
disease
Bleeding Time
Prolonged Prolonged
Replaced by platelet
function test
Aspirin
Prolonged
324 B. Desai
Prothrombin Time
Warfarin
Prolonged
Prothrombin Time
(Reported as INR)
DIC Measures extrinsic Liver disease

pathway
Prolonged Prolonged
Tissue Factor
Measures common
pathway
Prothrombin>Thrombin
>Fibrinogen>Fibrin
Deficiency of
Vitamin K
Prolonged
Activated Partial Thromboplastin Time
Heparin
Prolonged
Activated Partial
Von Willebrand’s Thromboplastin Time
Hemophilia
disease
Prolonged Measures intrinsic Prolonged

pathway
Measures common
pathway
Lupus
anticoagulant
Prolonged
Sickle Cell Anemia
Introduction
Under certain
Sickle cell Genetically Due to abnormal
Hemoglobin S conditions causes
disease based Hb molecule
RBC sickling
Cannot pass
Sickled cells through Leads to Ischemia Infarction
microcirculation
Higher rate of
Chronic hereditary
Sickled cells hemolysis than May be icteric
hemolytic anemia
normal RBC
Vaso-occlusive
Usually May Spontaneous
Sickle cell Trait have crisis under
asymptomatic bleeding
extreme conditions
Sickle cell Have a

10–15 %
Anemia reticulocytosis
Higher risk of infection

Sickle cell
with encapsulated Due to Autosplenectomy
Anemia
organisms
Strep pneumoniae
Neisseria
Minimal laboratory Reticulocyte

CBC CXR Urine
investigation count
Sickle Cell Tidbits
PEDIATRICS
Marrow infarction
Early sign of sickle Hand-foot
Dactylitis in bones of hands
cell in children syndrome
& feet
Consider
Hip pain in sickle 30 % of patients
avascular necrosis
cell disease will have this
of femoral head
May consider exchange

30 % of patients
Priapism Same treatment But… transfusion for severe
will have this
cases
May have loud

SCD systolic ejection
murmur
May have chronic poor healing

SCD
leg ulcers around the malleoli
326 B. Desai
Vaso-occlusive Crisis
Vaso-occlusive Obstruction of Sludging of

Due to
Crisis microvasculature sickled cells
Vaso-occlusive Increased
Leads to Ischemia Infarction
Crisis viscosity of blood
Precipitants or Changes in
Infection Dehydration Cold weather
stressors altitude
Manifestations Joint pain Bone pain Muscle pain
Musculoskeletal Most common

Back Arms Legs
pain presentation
2nd most common Cholelithiasis is

Abdominal pain Diffuse Poorly localized
presentation common
Papillary necrosis Microscopic or Treat with Monitoring of

Flank pain
of kidney gross hematuria hydration Hb levels
Treatment Hydration Analgesia Hydroxyurea Folate
Evidence of
Elevated WBC Antibiotics
infection?
Acute Chest Syndrome
Acute Chest New infiltrate on CXR Chest Cough or

involving 1 complete lung Fever Tachypnea
Syndrome segment (usually lower lobes) pain wheeze
Acute Chest Leading cause of 2nd most common Most common in

cause of
Syndrome death hospitalization 2–4 years
Acute Chest Iatrogenic – over hydration

Syndrome Infection Rib infarction Fat emboli leading to pulmonary
Etiologies edema
Infectious Chlamydia Mycoplasma Streptococcus Hemophilus

Staph aureus
organisms pneumoniae pneumoniae pneumoniae influenzae
May be a
Acute Chest May occur during
combination of
Syndrome hospitalization
factors
O2 Pain Broncho- Exchange

Treatment Antibiotics Hydration
control dilators transfusions
Don’t
forget a
macrolide
Aplastic Crisis
PEDIATRICS
RBC production Decrease in More common in

Aplastic Crisis
declines significantly reticulocyte count pediatric patients
Most common
Especially with
cause of Aplastic Infection
Parvovirus B19
Crisis
Bone marrow
Other causes Folate deficiency
infarction
Symptoms & Signs
Generalized
Pallor Fatigue
weakness
Laboratory Low Hb level Low reticulocyte WBC & Platelets

findings from baseline count are normal
Transfusions may be
Self-limiting
Treatment But… required for severe
process
symptoms
Splenic Sequestration
PEDIATRICS
Splenic Sudden enlargement of spleen with acute Most common

Sequestration fall in Hb due to sequestration of RBC in children
Symptoms & Signs
Generalized + LUQ
Pallor Lethargy Hypotension Tachycardia Tachypnea
weakness abdominal pain
Splenic Platelets are Mild

Sequestration also sequestered thrombocytopenia
Fluids may mobilize Exchange Investigation for

Treatment Transfusion OR
some RBC’s transfusion infectious etiology
Splenic Recurrence is
Sequestration common
328 B. Desai
Neurologic Complications of SCD

Ischemic &
Neurologic
Hemorrhagic TIA Seizures Paresthesias
sequelae
stroke
Ischemic in Hemorrhagic in
Strokes adults
children
Cerebral More common

aneurysms in SCD
Exchange
Treatment
transfusion
Neurologic Recurrence is
sequelae common
Infectious Complications of SCD

High risk of infection
Sickle cell Functionally Streptococcus Hemophilus
from encapsulated
disease asplenic organisms pneumoniae influenzae
Chlyamdia Mycoplasma Streptococcus Hemophilus

Pneumonia Staph aureus
pneumoniae pneumoniae pneumoniae influenzae
Osteomyelitis in Salmonella
Staph aureus E. coli
SCD typhimurum
Infectious
Fever OR Early antibiotics
symptoms
Especially
Need
SCD pneumococcal
immunizations vaccine
Hereditary Hemolytic Anemias
G6PD Deficiency
Most common Some may have
X-linked inherited Most patients are
G6PD Deficiency enzyme disease of anemia or chronic
disorder asymptomatic
RBC’s worldwide hemolysis
Likelihood of hemolysis
G6PD Deficiency depends on amount of enzyme
deficiency
G6PD Deficiency Acute hemolytic Neonatal May cause

1st week of life
manifestations anemia in adults jaundice kernicterus
Some Malaria Fava

Aspirin Sulfas Nitrofurantoin Mono
precipitants meds beans
Depends on clinical Treatment of

Treatment
presentation infections
Hereditary Spherocytosis
Unable to pass Increased
Hereditary Autosomal RBCs are
easily through destruction in
Spherocytosis dominant spherical
spleen spleen
Aplastic or Neonatal
Acute hemolytic Cholelithiasis &
Complications megaloblastic hemolysis with
anemia Cholecystitis
crisis jaundice
Depends on clinical Treatment of

Treatment
presentation infections
330 B. Desai
Specific Labs for Hemolytic Anemia
Acquired Hemolytic Anemia
Fragmented Intravascular
Schistocytes
RBCs hemolysis
Peripheral smear
Extravascular
Spherocytes Spheroid RBCs
hemolysis
Potassium Elevated RBC destruction
Lactate
Elevated RBC destruction
dehydrogenase
Intravascular
Haptoglobin Decreased
hemolysis
Free Intravascular
Elevated
Hemoglobin hemolysis
Hemoglobinuria Present
Reticulocyte Production of
Elevated
count RBCs
Total Increased
Bilirubin
Indirect Increased
Urine
Present
Urobilinogen
Microangiopathic Hemolytic Anemia (MAHA)
Thrombotic
Hemolytic uremic
Two syndromes thrombocytopenic purpura
syndrome (HUS)
(TTP)
Neurologic
More common Wider deposition of
TTP symptoms
in adults platelet aggregates
predominate
More common Renal symptoms

HUS
in children predominate
Causes consumptive
TTP
thrombocytopenia
Thrombotic Thrombocytopenic Purpura (TTP)
CNS Renal
TTP Fever MAHA Thrombocytopenia
dysfunction dysfunction
Platelet Schistocytes form when

Endothelial Release of
Pathophysiology aggregation in Due to RBCs shear through
cell damage vWF
microcirculation microcirculation
Microthrombi in CNS Eventual end Renal injury or CVA, TIA,

Tissue ischemia Due to
& Renal capillaries organ damage failure Seizures, Coma
Show evidence Normal Abnormal

TTP Laboratories But… DIC
of hemolysis coagulation coagulation
Etiology Drug induced Pregnancy Infection Idiopathic
Fluoroquinolones May be difficult to HIV

distinguish from
Clopidogrel & HELLP syndrome
Ticlopidine
LFT’s in TTP may
Cyclosporine be normal
Platelet
Treatment Plasmapheresis Steroids Supportive care
transfusion
May acutely start Treat CNS & Worsens condition

FFP, until resources Renal dysfunction due to increased
mobilized consumption
90 % mortality if
May relapse
TTP not treated in 1st
within 2 years
24 hours
332 B. Desai
Hemolytic Uremic Syndrome (HUS)
PEDIATRICS
Most common cause of

Microangiopathic Renal
HUS preventable acute renal Thrombocytopenia
hemolytic anemia dysfunction
failure in childhood
May be bloody
Pathophysiology Infectious
Due to (Hemorrhagic Usually no fever
of HUS diarrhea
colitis)
Shiga-toxin Serotype Other Salmonella, Yersinia, Shigella,

Bacterial agent
producing E. coli O157:H7 pathogens Campylobacter
Ingestion of
2–14 days after
Onset Due to contaminated
diarrhea develops
food or water
Laboratory Evidence of
Hyperglycemia Stool studies Urine studies
investigations hemolytic anemia
Microthrombi Culture for E. coli

affecting pancreas O157:E7
B-cells
Some may
develop DM
Treatment Supportive care
Treat renal
dysfunction
Platelet Disorders
Introduction
More common
Platelet Decreased Decreased Nonpalpable
Petechiae in lower
disorders number function purpura
extremities
Decreased Decreased overall Destruction of Splenic

Platelet loss
number production platelets sequestration
Marrow disorder TTP Sickle cell disease Hemorrhage

Aplastic anemia ITP Liver failure Dialysis
Rubella / HIV HUS
Drugs DIC
Radiation Heparin
B12 / Folate
Some drugs Sulfa
Thiazide
causing Ethanol Aspirin Heparin containing
diuretics
thrombocytopenia antibiotics
Some drugs Some β and Ca

Clopidogrel & Penicillins/
causing platelet NSAIDs Aspirin channel
Ticlopidine Cephalosporin
dysfunction blockers
Symptoms & Signs
Gingival
Epistaxis Hemoptysis Hematochezia Menorrhagia Hematuria
bleeding
Palpable Platelet count

Vasculitis OR Angiopathy
purpura >50,000 – Usually asymptomatic
50–30,000 – bruising with minor trauma
High risk of 30–10,000 – Spontaneous petechiae &
Platelets Especially
spontaneous bruising
<10–20,000 Intracranially
bleeding
334 B. Desai
Idiopathic Thrombocytopenic Purpura (ITP)

Acquired
Petechiae & No other cause
ITP autoimmune Thrombocytopenia
purpura identified
disease
Children Onset of Most cases require no

Infectious
Acute ITP Peak age of 5 petechiae & treatment & resolve in 6
illness
M=F purpura months
Likely to have Only findings are Most cases require

Adults
Chronic ITP underlying petechiae & treatment & last >3
F>M
autoimmune disorder purpura months
Normal except
ITP Laboratories
platelets
Asymptomatic Platelets >

No treatment
patients 50,000
Platelets < Platelets < Treatment

Bleeding OR
50,000 20,000–30,000 required
IV Platelet
Treatment Prednisone Rhogam
Immunoglobulin transfusion
For very low If needed, after 1st
50–75 % remission For Rh+ patients
platelets & dose of steroids or
by 3 wks
bleeding IVIG
Treatment Not always

Splenectomy
failure effective
Etiologies of Disseminated Intravascular Coagulation (DIC)

Activation of Activation of Formation & Depletion of
DIC coagulation fibrinolytic breakdown of coagulation Bleeding
system system clots factors
Bacterial Endotoxin stimulated

Infectious Most common Direct endothelial
Fungal formation of Tissue
etiology cause damage
Viral Factor
Meningococcus is most
extreme
Most common with Blast cells release
Acute Leukemia Promyeloctyic coagulant inducing
leukemia enzymes
Lymphoma Direct endothelial Release of

Adenocarcinoma damage Tissue factor
Extremes of
Trauma Crush injury Brain injury Rhabdomyolysis Fat embolism
temperature
Activation of
Pancreatitis/ Hepatocyte
Liver Pancreatitis coagulation
Liver Failure release of TF
cascade
Direct endothelial Release of

Envenomation
damage Tissue factor
Intrauterine fetal Abruption Amniotic fluid

Pregnancy Septic abortion
demise placentae embolism
Adult respiratory Thrombi in Damage of

distress syndrome pulmonary vessels endothelium
Post incompatible
Bleeding Shock
tranfusion
336 B. Desai
Disseminated Intravascular Coagulation (DIC)
Infectious
Sepsis Bleeding Thrombosis
etiology
Acute Leukemia Bleeding Thrombosis
Adenocarcinoma
Lymphoma
except Prostate Thrombosis Bleeding
Adenocarcinoma
cancer
Trauma Bleeding Thrombosis
Pancreatitis
Bleeding Thrombosis
Liver Failure
Envenomation Bleeding Thrombosis
Pregnancy Bleeding Thrombosis
Adult respiratory
Bleeding Thrombosis
distress syndrome
Post incompatible
Bleeding Thrombosis
tranfusion
Clinical Features of DIC

Depends on Either bleeding or
Clinical features underlying thrombosis
disease predominates
Multiple organ Purpura

Complications Bleeding Thrombosis
failure fulminans
Widespread
Wide range of
Bleeding Petechiae bleeding from
bleeding
multiple sites
Multiple organ Symptoms depend

failure on organs involved
Diffuse arterial &

Purpura
venous Leads to Bacteremia
fulminans
thromboses
Laboratory Findings in DIC
Prothrombin
Time
Prolonged
APTT Platelet count
Prolonged Decreased
Fibrinogen
Schistocytes
Low
May be present
Laboratory Findings in
DIC
Fibrin degradation
D-dimer
products
Elevated Elevated
Factor assays
Depend on factor
Treatment of DIC
Depends on Mostly
Treatment
underlying disease supportive
Multiple organ Purpura Replete

Low fibrinogen Bleeding Leads to
failure fulminans fibrinogen
Platelets Replace
Bleeding
<50,000 platelets
Platelets Replace
<20,000 platelets
DIC associated
FFP Vitamin K Folate
bleeding
DIC associated Consider VERY

thrombosis Heparin controversial
338 B. Desai
Hemophilia
Introduction
Deficiency in Usually appear
Factor VIII & IX is
Hemophilia Bleeding disorder Due to clotting cascade early in life
most common
factor (Males only)
Factor related Bleeding into Deep bruising & Retroperitoneal Intracranial

bleeding joints muscle bleed bleeding bleeding
May cause airway
May cause joint Most common cause
issues; compartment
destruction of hemorrhagic death
syndrome
Inability of platelet derived clot to

Trauma & factor Bleeding may be
Due to be stabilized by fibrin from
deficiency delayed
clotting cascade
Platelet related GI/GU Gingival

Easy bruising Epistaxis Heavy menses
bleeding (GIB/hematuria) bleeding
Most common
Deficiency of Deficiency of
Hemophilia A cause of Hemophilia B
Factor VIII Factor IX
hemophilia in US
Severe Activity levels Severe spontaneous

Hemophilia <1% bleeding
May have
Moderate Activity levels Usually bleed
spontaneous
hemophilia 1–5% with trauma
bleeding
Activity levels May not know Bleeding after

Mild hemophilia
5 – 40 % they have disease severe trauma
PTT may be
Laboratory Unless factor
Abnormal PTT normal in this
abnormalities levels >30–40 %
case
Treatment
Evaluation for
Hemophilia with Factor No major interventions (central lines,
major
bleeding? replacement etc) without factor replacement
complications
Factor Recombinant
replacement factor Plasma derived
Very pure &

May contain other
No risk of
factors increasing
HIV/Hepatitis
risk of DIC
transmission
Mild hemophilia May give Releases vWF

Factor levels >5 % Mild bleeding desmopressin from storage sites
Von Willebrand’s Disease
Introduction: VWD
Most common Deficiency in von Made & stored in
VWD congenital Due to Willebrand factor vascular
bleeding disorder (VWF) endothelial cells
Von Willebrand Cofactor for Carrier protein Leads to platelet activation &
Factor platelet adhesion for factor VIII adhesion to other platelets
GI/GU Gingival
Clinical features Easy bruising Epistaxis Heavy menses
(GIB/hematuria) bleeding
Unless severe
Clinical features NO Hemarthosis
disease
Diagnosis Bleeding time PTT vWF activity
Prolonged
Prolonged Decreased
depending on
severity
Treatment for
Desmopressin
Mild disease
Treatment for Factor VIII

Moderate to Cryoprecipitate OR OR products that
severe disease have vWF
Anticoagulants
Introduction: Warfarin
Disrupts synthesis II, VII, IX, X Extrinsic pathway blocked
Blocks action of
Warfarin of Vitamin K (Has mild thrombotic effect
vitamin K (Also Proteins C&S)
dependent factors through Protein C&S blockade)
Over anti-coagulation will raise PTT as

Therapeutic range
Warfarin dosing Guided by INR But… well due to effect on common final
usually from 2–3
pathway of coagulation
Multiple Change in
Drugs or Albumin
Warfarin interfering hepatic
Medications binding
factors metabolism
NOT in
Warfarin Teratogenic
Pregnancy
Major Warfarin
Bleeding Skin necrosis
complications
340 B. Desai
Bleeding from Warfarin

Amount of
Warfarin Risk increases Greater increase
Bleeding Due to anticoagulant therapy
Complications with INR > 3 with INR > 5
(most important)
Other bleeding GI lesions or Cerebrovascular

Renal disease Hypertension Anemia
risk factors disease disease
Treatment of Identify & Treatment of

Attempt to Hold Monitor
Bleeding & treat cause of Elevated INR with
improve INR Warfarin INR
Elevated INR bleed NO bleed
Elevated INR + Parenteral FFP

Stop Warfarin
Severe bleeding Vitamin K 10–15 mL/kg
Problems with IV may be Problems May

Give slowly May
Parenteral associated with reanticoagulating produce
or give IM overcorrect
Vitamin K anaphylaxis –lasts 2 weeks thrombosis
Prothrombin
Other Concentrates of Works Less volume
complex
considerations II, VII, IX & X immediately than FFP
concentrates
Skin Necrosis from Warfarin
Protein C
Skin necrosis Due to Not exclusively
deficiency
3-8 days after

Thrombosis of
Skin necrosis initiation of Due to
small vessels
warfarin
Use another
Screen for Protein
Treatment Stop Warfarin anticoagulant as Vitamin K
C & S deficiency
needed
Introduction: Heparin
Thrombin & Unfractionated Unfractionated
Binds to
Heparin Factor Xa heparin must be heparin is given in a
Antithrombin
inhibition given parenterally weight based dosing
May be given in Does not cross

Heparin
pregnancy placenta
Therapeutic range =
Unfractionated Requires frequent
Guided by PTT 1.5–2.5 times the
heparin monitoring
normal value
More predictable
Low molecular Allows for b.i.d.
anticoagulant
weight heparin or daily dosing
effect
Use Reduced dose of

Renal failure &
unfractionated OR low molecular
Heparin
heparin weight heparin
Major Heparin Heparin-induced

Bleeding
complications thrombocytopenia
Bleeding from Heparin

May be seen
Bleeding from Unfractionated
without very So… Bleeding Stop Heparin!
Heparin heparin
elevated PTT
1 mg Protamine
50 mg in 10
Other treatment Protamine neutralizes 100 units of Give slowly
minutes
unfractionated heparin
Can have allergic Use only for

Protamine
reactions severe bleeding
Heparin-Induced Thrombocytopenia (HIT)
Platelet count IgG or IgM Tendency for

HIT Due to Thrombocytopenia
may drop antibodies thrombosis
Skin
5-10 days after Arteries
HIT
starting heparin
Veins
Platelets return to
Monitor for
Treatment Stop heparin normal 4 -6 days after
thrombosis
stopping heparin
342 B. Desai
Absolute and Relative Contraindications to Thrombolysis

Hx of hemorrhagic
stroke
Suspected aortic Intracranial surgery

dissection or trauma within 2
months
Absolute
Intraspinal surgery
Contraindications to
or trauma within 2
Thrombolysis
months
Intracranial or
intraspinal tumor,
aneurysm or AV
CVA < 6 months
malformation
Active bleeding
Uncontrolled HTN
from any site
(DBP >120)
Pregnancy or < 10
Hx of GI bleed
days postpartum
Relative
Significant trauma Known active
Contraindications to
< 4 weeks cavitary lung lesion
Thrombolysis
Severe Known severe

thrombocytopenia bleeding disorder
Allergy to agent Prolonged CPR

Complications of Malignancy
Introduction
Due to therapy
N/V
Related
electrolyte
derangements
Metabolic
Hematologic
Hypercalcemia
Complications of Neuropenia &
Hyponatremia Malignancy related
complications
SIADH
Thromboembolism
Adrenal
insufficiency Hyperviscosity
Tumor lysis
syndrome
Local effects
SVC syndrome
Pathologic
fractures
Airway obstruction
Tamponade
Spinal cord
compression
Malignant Airway Obstruction

Result of mass
Malignant Airway Loss of muscle
effect on upper Due to Hemorrhage OR Infection OR
Obstruction tone
or lower airway
Symptoms Dyspnea Stridor Tachypnea
Diagnosis Plain films CT Endoscopy
Symptomatic improvement
Position patient O2
ED Management Heliox of upper airway
for comfort
obstruction due to cancer
Definitive Radiation
management therapy
344 B. Desai
Pathologic Fractures from Bone Metastases
Bony fracture Malignancy

Pathologic Solid Axial Proximal
secondary to disease related Due to
Fractures tumors skeleton limbs
weakening the bone fractures
Benign
Severe localized
Symptoms appearance of
pain
affected limb
Loss of Poorly defined

Diagnosis Plain films
trabeculae margins
Best modality for

Dx of soft tissue MRI
involvement
Radiation
Treatment Pain control Surgery
therapy
Malignant Pericardial Effusion and Tamponade

Malignant Most common is Tamponade severity
Lymphoma
Pericardial lung & breast Melanoma depends on speed of
& leukemia
Effusion cancer development
Other causes of Radiation Infectious

Chemotherapy
pericardial effusion therapy complications
Symptoms & Signs
Narrow pulse Muffled heart Pulses paradoxus Low voltage on Cardiomegaly

JVD Hypotension
pressure tones > 10 mm Hg EKG without CHF
Diagnosis Echocardiogram
Management for Pericardial Radiation Intrapericardial

Pericardiocentesis
severe symptoms window therapy chemotherapy
Malignant Spinal Cord Compression
Malignant Spinal Most Metastatic is

Lung OR Breast OR Prostate
Cord Compression common most common
Renal cell Multiple

Other cancers Lymphoma
carcinoma myeloma
Pathologic Tumor mass

Other etiologies Infection Tumor bleeding
fracture effect
Thoracic Lumbosacral Cervical

Location
60 % 30 % 10 %
No palliating Worse when

Back pain Severe
factors supine
Neurologic Urinary Muscular weakness – common Fecal

Radicular pain
deficits retention in proximal extremities incontinence
MRI of entire
Diagnosis CT Endoscopy
spine
Radiation
ED Management Steroids Surgery
therapy
Superior Vena Cava Syndrome

External
Superior Vena Obstruction of Elevated venous Head, Neck, Face,
Causes Due to compression of SVC
Cava Syndrome SVC blood flow pressure Arms
by malignant mass
Most common Lung Lymphoma

cancers 70 % 20 %
Central Other
Other causes Goiter Radiation TB
lines thrombosis
Symptoms & Signs
Face edema Arm edema Head Neck & upper Face plethora &
Headache Papilledema
(80 %) (50 %) congestion chest congestion telangiectasia
Voice Mediastinal
Dyspnea Cough Sentinel node
hoarseness enlargement on CXR
Diagnosis CT
Emergency Head O2 Radiation Steroids Diuretics

Management elevation
346 B. Desai
Hypercalcemia Due to Malignancy
Hypercalcemia Secretion of PTH- Increasing bone Increased renal

Due to
due to Malignancy like protein resorption of Ca resorption of Ca
Most common
Multiple Squamous cell
associated Breast cancer
myeloma carcinoma of Lung
malignancies
Hypercalcemia Osteolytic Multiple

Due to Lung cancer Breast cancer
due to Malignancy activity myeloma
Symptoms & Signs Severity depends on rate of rise of Ca
Altered mental
Lethargy Dehydration Constipation Weakness Abdominal pain Short QT
status
IV hydration
ED Management Bisphosphonates Calcitonin Steroids Furosemide
2–4 L as tolerated
Not
recommended
for malignancy
related
hypercalcemia
SIADH Due to Malignancy

Most common
SIADH due to Brain Lympho-
with bronchogenic OR OR Pancreas OR Prostate OR
Malignancy cancer sarcoma
carcinoma
Symptoms depend
SIADH due to Ectopic Normovolemic
Due to on rapidity of
Malignancy secretion of ADH hyponatremia
development
Less than
Normovolemic Elevated urinary
Diagnosis Low osmolality maximally dilute
hyponatremia Na excretion
urine
Hypertonic saline for

Find and treat
ED Management Fluid restriction seizures or
cause
arrhythmias
Adrenal Insufficiency Due to Malignancy

Adrenal Adrenal tissue
Adrenocorticoid
Insufficiency due replaced by OR
suppression
to Malignancy metastases
Adrenal
Insufficiency due Due to Dehydration OR Infection OR Surgery OR Trauma
to Malignancy
Consider in
Fever Hypotension Shock Dehydration
cancer patients
Common
Eosinophilia Hypoglycemia Hyponatremia Hyperkalemia
findings
Blood for cortisol

ED Management Steroids
level before Rx
Tumor Lysis Syndrome

Proteins, Potassium, Usually blood
Tumor Lysis Caused by massive 12 hrs to 3 days
Phosphate & Calcium borne
Syndrome lysis of cancer cells after treatment
released malignancies
DNA/RNA Uric acid Acute

Breakdown precipitation nephropathy
Most life-
Potassium
Hyperkalemia threatening Arrhythmias
release
complication
Elevated LDH Extensive lysis
Abrupt
Phosphorus May combine Precipate in Acute
hypocalcemia &
release with calcium renal tubules nephropathy
its complications
Treat electrolyte
Maintain
ED Management abnormalities as
hydration
usual
348 B. Desai
Febrile Neutropenia
Pts may not manifest Most common
Increased risk of Impaired
Neutropenia Due to symptoms due to lack due to bacterial
infection immunity
of neutrophils infection
Absolute Absolute
Severe
Neutropenia neutrophil 1000/mm3 neutropenia
neutrophil 5000/mm3
count count
Neutropenia in
Due to Chemotherapy
cancer patients
Empiric treatment with

ED Management broad spectrum
antibiotics
Hyperviscosity Syndrome Due to Malignancy

Impaired blood flow due
Hyperviscosity Due to increase in Usually immune
to sludging, limited
syndrome serum proteins globulins
perfusion & thromboses
Chronic
Waldenstrom Multiple
Causes OR OR myelocytic OR Polycythemia
macroglobulinemia myeloma
leukemia
Symptoms & Signs
Altered mental
Fatigue Headache Abdominal pain Blurred vision Anorexia Somnolence
status
Retinal Retinal Altered mental

Dyspnea
hemorrhage exudates status
Hyponatremia with
Laboratory Rouleaux
Anemia Hypercalcemia low osmolality &
abnormalities formation
normovolemia
ED Management Hydration Plasmapheresis Phlebotomy

Disorders Affecting the Skin
Bobby Desai
Contents
Generalized Skin Rashes and Disorders 350
Allergic Processes 363
Skin Cancers 365
Infectious Diseases and Associated Skin Lesions 366
Viral Infections 372
Malaria 376
Pediatric Rashes 376
Miscellaneous Skin-Related Disorders 385
B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_6
350 B. Desai
Generalized Skin Rashes and Disorders
Erythema Multiforme
Erythema Has a spectrum of disease defined by EM Stevens-Johnson Toxic Epidermal

Multiforme amount of epidermal detachment Minor syndrome (EM major) Necrolysis
Erythema
Young adults M>F
Multiforme
Epidermal EM Minor SJS TEN

detachment (None) (10–30 %) (> 30 %)
Precipitating causes
(50 % idiopathic) Mycoplasma Herpes Malignancies Antibiotics Anticonvulsants
Hypersensitivity
reaction in all
Symptoms & Signs
Fever Myalgias Malaise Arthralgias Diffuse pruritis
Erythema “Bull’s eye” or Knees &

ON Palms & Soles Elbows
Multiforme “Target” lesions
Symptomatic for More severe cases will need

Treatment admission to ICU/Burn unit
minor cases
Bottom center image (Reprinted from Zaidi Z, Lanigan SW. Vasculitis, common erythemas, and lymphatic disorders. In: Zaidi Z, Lanigan SW,
editors. Dermatology in clinical practice. London: Springer; 2010. p. 253–70. With permission from Springer Verlag)
Disorders Affecting the Skin 351
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN)
Severe bullous Affects 10–30 % of Has mucosal

SJS May be fatal
form of EM body surface area involvement
Affects > 30 % of
TEN
body surface area
Precipitating causes
Mycoplasma Herpes Malignancies Antibiotics Anticonvulsants
(50 % idiopathic)
Hypersensitivity
reaction in all
Common medication Sulfonamides

PCN Thiazides Barbiturates Phenytoin
precipitants Tetracyclines
Symptoms & Signs
Bullous
SJS cutaneous lesions
Stomatitis Conjunctivitis Mucositis Nikolsky’s sign
Very large Severe Skin peels off with
TEN Hypotension Shock Tachycardia light pressure
bullae mucositis
Increased Secondary
Older age Dehydration
mortality infection
Primary causes
Sepsis Pneumonia
of death
Disposition ICU Admission
PEDIATRICS
Right side image (Reprinted from Zaidi Z, Lanigan SW. Exanthems and Hypersensitivity Syndromes. In: Zaidi Z, Lanigan SW, editors. Dermatology
in clinical practice. London: Springer; 2010. p. 271–80. With permission from Springer Verlag)
352 B. Desai
Staphylococcal Scalded Skin Syndrome (SSSS)
PEDIATRICS
Exotoxin related Infants & small Starts as benign Nasopharynx

SSSS disorder children Staph infection Conjunctiva
Mucous membranes
SSSS are spared
Symptoms & Signs
1st – Scarlatiniform Exfoliation of Bullae may + Nikolsky’s

Fever skin appear
rash sign
Electrolyte Vancomycin
Treatment Fluids replacement Antibiotics (Does not alter skin process)
Bottom center image (Reprinted from Zaidi Z, Lanigan SW. Exanthems and hypersensitivity syndromes. In: Zaidi Z, Lanigan SW, editors.
Dermatology in clinical practice. London: Springer; 2010. p. 271–80. With permission from Springer Verlag)
Pemphigus Vulgaris
Pemphigus Generalized bullous rash also Affects patients Poor

Vulgaris affecting mucous membranes Autoimmune 40–60 prognosis
Pemphigus Vesicles or Bullae May appear on 1st affect mucous Bullae break easily,
Vulgaris < 1cm to several cm normal skin membranes, head, trunk leave painful areas
2–3 days Rupture of Painful

Natural History Clear blisters blisters ulcerations
Enlarge
Precipitating Barbiturates ACE inhibitors

causes (Phenobarbital) (Captopril) Penicillamine
Symptoms & Signs
Large flaccid Skin Denuding & Mucous membrane

bullae ulceration exfoliation of skin involvement Nikolsky’s sign
Increased Secondary
mortality Older age Dehydration infection
ICU/Burn Fluid & Electrolyte

Treatment Admission replacement Steroids
Right side image (Reprinted from Zaidi Z, Lanigan SW. Bullous disorders: autoimmune and childhood bullous dermatoses. In: Zaidi Z, Lanigan
SW, editors. Dermatology in clinical practice. London: Springer; 2010. p. 233–52. With permission from Springer Verlag)
354 B. Desai
Bullous Pemphigoid
Bullous Benign chronic Autoimmune

Affects pts > 60 F>M
Pemphigoid bullous rash process (IgE)
Bullous Begins with Formation of Blisters may Leads to

Pemphigoid urticaria tense blisters exceed 10 cm exfoliation
Bullous Minimal involvement of

NO Nikolsky sign
Pemphigoid mucous membranes
Precipitating Medications
Malignancy
causes (Sulfa)
Complications Infection Electrolyte loss
Much more benign course

Treatment Supportive
than pemphigus vulgaris
Right side image (Reprinted from Cashman MW, Doshi D, New York: Springer; 2013. p. 147–73. With permission from Springer
Krishnamurthy K. Vesiculobullous dermatoses. In: Buka B, Uliasz A, Science + Business Media)
Krishnamurthy K, editors. Buka’s emergencies in dermatology.
Exfoliative Dermatitis (Erythroderma)
Exfoliative Skin reaction to exogenous Skin affected with Affects

M>F
Erythroderma agent or to systemic process scaly red dermatitis patients > 40
Exfoliative Onset may be Begins on face Spreads to other areas, Leads to

Erythroderma acute or chronic and trunk eventually most or all of skin exfoliation
Precipitating
Medications Systemic disease Chemicals Malignancy
causes
Symptoms & Signs
Generalized Nikolsky’s sign

Skin warmth NO pain Pruritis NO fever
skin erythema NOT present
Hypothermia due High output CHF due to Electrolyte

Complications Infection
to excess heat loss cutaneous vasodilation loss
Fluid & Electrolyte

Treatment Biopsy Steroids
replacement
356 B. Desai
Drug Rash or Eruption
Drug Rash or Typically soon after Immediate hypersensitivity Delayed

OR
Eruption starting new medication reaction (IgE) hypersensitivity (IgM)
Urticaria Serum sickness
Drug Rash or Usually resolves

Eruption in 1–2 weeks
Drug Rash or Reddish brown papules Erythema multiforme

Urticaria
Eruption Morphology that may coalesce (extreme)
Precipitating
Penicillin Sulfa drugs Cephalosporins
causes
Stevens-Johnson
Complications
syndrome
Discontinue
Treatment Antihistamines Steroids
medication
Erythema Nodosum
Erythema Painful lesions due to Violet in Usually on anterior Noted in

Nodosum localized vasculitis color tibia, arms & trunk females 30–50
Erythema Marker for

Nodosum systemic process
Some selected Inflammatory Leukemia TB or Fungal

causes Sarcoidosis bowel disease Lymphoma infections Drugs
Treat underlying Typical resolution

Treatment cause 3–6 weeks
Bottom center image (Reprinted from Vázquez-Roque MI, De Jesús- New York: Springer; 2012. p. 41–51. With permission from Springer
Monge WE. Cutaneous manifestations of gastrointestinal diseases. In: Science + Business Media)
Sánchez NP, editors. Atlas of dermatology in internal medicine.
358 B. Desai
Eczema
Chronic & itchy
Has association with Allergic rhinitis
Eczema Nasal Polyps (+) Family hx
multiple processes Asthma
Worse in winter
Skin findings Lichenification Crusting Redness Excoriations Pruritis Fissures
Eczema in Face, scalp & Crusting and Resolves by

infants extremities blistering age 2
Antecubital & Dryness and skin

Eczema in adults
Popliteal fossa thickening
Eczema HSV infection with Secondary

Complications
herpeticum underlying eczema infection
Treatment Antipruritics Steroids
Right center image (Reprinted from Silverberg NB. Eczematous dis- New York: Springer; 2012. p. 69–88. With permission from Springer
eases. In: Silverberg NB, editor. Atlas of pediatric cutaneous biodiver- Science + Business Media)
sity: comparative dermatologic atlas of pediatric skin of all colors.
Allergic Contact Dermatitis
Allergic Contact Delayed hypersensitivity 48 hours to days after

Dermatitis reaction allergen contact
Poison Ivy, Oak Nickel in metal

Causes Detergents
or Sumac jewelry
Symptoms & Signs
May be limited to
Erythema Pruritis Vesicles Bullae
area of contact
Treatment Steroids
Psoriasis
Red papules & plaques Chronic Due to overproduction

Psoriasis
with silvery-white scale Starts in 20’s of keratinocytes
May be accompanied by
Psoriasis
psoriatic arthritis
Symptoms & Signs
Removal of scale shows

Auspitz sign Pitting of nails
areas of bleeding
Treatment Steroid creams Tar UV light Methotrexate
Bottom center image (Reprinted from Norman RA, Young, Jr. EM. Psoriasis. In: Norman RA, Young EM Jr, editors. Atlas of geriatric dermatology.
London: Springer; 2014. p. 83–95. With permission from Springer Verlag)
360 B. Desai
Seborrheic Dermatitis
PEDIATRICS
Seborrheic Chronic inflammatory Affects areas of high Scalp, eyebrow,

Dermatitis process sebaceous gland activity axilla, ears, groin
Seborrheic May be associated

Dermatitis with Malassezia furfur
Seborrheic Scales that white or Well Weeping and Cradle cap in

Dermatitis yellow with erythema marginated crusting infants
Ketaconazole Selenium
Treatment
shampoo shampoos
Bottom center image (Reprinted from Silverberg NB. Eczematous dis- New York: Springer; 2012. p. 69–88. With permission from Springer
eases. In: Silverberg NB, editor. Atlas of pediatric cutaneous biodiver- Science + Business Media)
sity: comparative dermatologic atlas of pediatric skin of all colors.
Pityriasis Rosea
PEDIATRICS
Affects F > M Especially in Unknown Not contagious,

Pityriasis Rosea
15–40 spring & fall etiology resolves 1–2 months
Starts with Single salmon colored

PityriasisRosea Seen on trunk 1–5 cm large
“herald patch” lesion with raised border
1–2 weeks Christmas tree

Natural History Herald patch
Pink maculopapular oval patches that follow ribs pattern
Pityriasis Rosea Syphilis

Drug reaction
mimics (no herald patch)
Antihistamines
Treatment Symptomatic
for pruritis
Left side image (Reprinted from Zaidi Z, Lanigan SW. Keratinizing and Right side image (Reprinted from Silverberg NB. Papulosquamous
papulosquamous disorders. In: Zaidi Z, Lanigan SW, editors. disorders. In: Silverberg NB, editor. Atlas of pediatric cutaneous biodi-
Dermatology in clinical practice. London: Springer; 2010. p. 179–209. versity: comparative dermatologic atlas of pediatric skin of all colors.
With permission from Springer Verlag) New York: Springer; 2012. p. 53–60. With permission from Springer
362 B. Desai
Dermatophyte Infections
Scaly patch on
Tinea capitis Affects scalp
head
Large edematous
Kerion DO NOT I&D!
nodule & pustule
On non hairy Annular lesions Spread

Tinea Corporis
parts of body with clear center outwardly
Scrotum is not Affects inner Has sharp demarcation

Tinea Cruris
involved thigh and groin from normal skin
Causes Trichophyton Epidermophyton Microsporum
Treatment Topical or oral

antifungals
Right side image (Reprinted from Zaidi Z, Lanigan SW. Superficial fungal infections. In: Zaidi Z, Lanigan SW, editors. Dermatology in clinical
practice. London: Springer; 2010. p. 73–99. With permission from Springer Verlag)
Tinea Versicolor
PEDIATRICS
Overgrowth of Common in Affects steroid users,

Tinea Versicolor
Malassezia furfur young people oily skin, high humidity
Upper back and chest Hypo-or

Tinea Versicolor Scaly macules
most affected Hyperpigmented lesions
Selenium Ketoconazole
Treatment
shampoo cream or shampoo
Bottom center image (Reprinted from Silverberg NB. Cutaneous New York: Springer; 2012. p. 113–25. With permission from Springer
infections. In: Silverberg NB, editor. Atlas of pediatric cutaneous biodi- Science + Business Media)
versity: comparative dermatologic atlas of pediatric skin of all colors.
Allergic Processes
Urticaria
Affects superficial Allergic

Urticaria Wheals Hives
dermis phenomenon
Usually unknown Usually self

Urticaria IgE mediated
precipitant limited
Mast cell Histamine

Pathophysiology Inciting allergen Release of IgE
activated release
Skin findings Wheals Hives
Epinephrine for
Treatment H1& H2blockers Steroids
severe cases
364 B. Desai
Angioedema
Affects deeper Mediated by Causes increase in Vasodilation of

Angioedema
dermis bradykinin vascular permeability vessels
Decreased metabolism May cause angioedema 66 % in 33 % months to

Ace Inhibitors
of bradykinin at any time hours years after starting
Familial C1 esterase Leads to increased Due to inhibition of Autosomal

angioedema deficiency bradykinin complement cascade dominant
Symptoms & Signs
Edema of face, Edema of Bowel wall

lips and tongue extremities edema
Treatment of Ensure airway is May try standard allergic No standard,

angioedema protected reaction medications effective treatment
Treatment of Familial Responds to fresh C1 esterase inhibitor

angioedema frozen plasma concentrate
Skin Cancers
Malignant Affects ages Affects sun Head, neck, Most common cause of skin
melanoma 30–60 exposed areas truncal areas cancer related deaths
ABCD’s of Asymmetry of Border

Melanoma the lesion irregularity Uneven Color Diameter > 6mm
Congenital or Exposure to UV
Risk factors dysplastic nevi Family Hx Fair skin radiation
Melanoma Metastases are Brain mets may

tidbits common Increasing depth Worse prognosis hemorrhage
Basal cell Most common Does not Affects head & Seen where there
carcinoma skin cancer metastasize neck are hair follicles
Pearl colored rolled border Very slow Very high cure

Basal cell tidbits
with central ulceration growing rate if found early
Squamous cell 2nd most common Metastasizes Affects face, ears,

carcinoma skin cancer early lips, tongue, hands
Exposure to UV
Risk factors Elderly males Fair skin
radiation
Squamous cell Very rapid Raised & indurated

tidbits growth border with central ulcer
366 B. Desai
Infectious Diseases and Associated Skin Lesions
Meningococcemia
PEDIATRICS
Sepsis
Neisseria Encapsulated gram Causes a spectrum
Meningococcemia Meningitis
meningitidis negative diplococcus of diseases
Bacteremia
Petechiae Coalesce to
Rash
1–2 mm purpura
Waterhouse- Adrenal
Shock Petechiae
Friderichsen syndrome infarction
Hypotension Low platelets No

Poor prognosis? Temp > 40ºC Petechiae
or shock state & low WBC meningismus
Symptoms & Signs
Head and neck

Fever Myalgias Rash Sepsis
pain
Rifampin or
Prophylaxis? Close contacts
Ciprofloxacin
Laboratory workup
Diagnosis CSF serology Blood serology
as indicated
Penicillin
Chloramphenicol ICU for shock
Treatment IV antibiotics Isolation
rd states
3 generation
cephalosporin
Right side image (Reprinted from Stamell E, Krishnamurthy New York: Springer; 2013. p. 19–41. With permission from Springer
K. Infectious emergencies in dermatology. In: Buka B, Uliasz A, Science + Business Media)
Krishnamurthy K, editors. Buka’s emergencies in dermatology.
Gonococcemia and GC Arthritis
Gonorrhea
Neiserria Gram negative Also causes
Gonococcemia gonorrheae diplococcus multiple disorders Arthritis
Synovitis
The base is Hemorrhagic Necrotic Usually 1st on

Rash With OR
erythematous vesicles pustules distal extremities
Symptoms & Signs
Vaginal or penile Mono-or Symptoms often begin

Fever discharge Polyarthritis Tenosynovitis Rash during menses
Ankles, knees Wrists, Ankles
Pharyngeal Joint fluid & blood

Diagnosis Genital cultures cultures often negative!
cultures
Cefoxitin with
Treatment Ceftriaxone OR Cefotaxime OR
probenecid
Empirically treat young females with

Pitfall fever & migratory polyarthritis
368 B. Desai
Lyme Disease
Borrelia Transmitted by Reservoirs Tick bites may be

Lyme Disease
burgdoferi bite of Ixode stick Deer, rodents, rabbits asymptomatic
Local Disseminated Chronic/Persistent

Stages of disease
Rash Cardiac & Neuro Arthritis
Erythema Erythematous expanding Spares palms

Rash “Bull’s eye”
chronicum migrans lesion with central clearing and soles
Symptoms & Signs
Localized stage Fever Arthralgias Myalgias Rash-ECM
Neuro manifestations of Peripheral

Meningitis CN VII palsy Encephalitis
Disseminated stage neuropathy
Cardiac manifestations
Pericarditis Myocarditis AV Block
of Disseminated stage
Chronic/Persistent Lyme arthritis Chronic

stage (m.c.= knees) encephalomyelitis
Clinical ELISA Western Blot

Diagnosis If (+)
symptoms (sensitive) (specific)
Probable disease =
treat
Treatment Doxycycline OR Ceftriaxone OR Amoxicillin OR Erythromycin
Right side image (Reprinted from Miró EM, Sánchez NP. Cutaneous manifestations of infectious diseases. In: Sánchez NP, editor. Atlas of derma-
tology in internal medicine. New York: Springer; 2012. p. 77–119. With permission from Springer Science + Business Media)
Leptospirosis
Leptospira Caused by skin contact with Reservoirs Contaminated

Leptospirosis OR
(Spirochete) urine of infected animal Dogs, Rats, Pigs, Cattle water
Mild Asymptomatic Severe

Stages of disease
leptospirosis period leptospirosis
Severe Meningitis / Hepatitis Myocarditis /

Nephritis
leptospirosis Encephalitis Causes coagulopathy Pericarditis
Subconjunctival Renal failure

Weil’s disease Jaundice DIC
hemorrhage (tubular necrosis)
Symptoms & Signs
Mild
Leptospirosis Fever & chills Myalgias Headache
Severe Severe Abdominal

Leptospirosis High fever Rash Vomiting Diarrhea
headache pain
Diagnosis Serology
Treatment Penicillin G OR Doxycycline OR Tetracycline

370 B. Desai
Rocky Mountain Spotted Fever (RMSF)
Rickettsia Caused by bite Common in Endemic in SE US

RMSF
ricketsii from infected tick pts< 15 Most cases April-September
Maculopapular Begins on Spreads to trunk & Eventually

Rash
rash wrists & ankles extremities (face is spared) becomes petechial
Symptoms & Signs
Altered mental
Fever Myalgias Headache Vomiting Rash Encephalitis
status
Relative
Myocarditis Arrhythmias Pneumonitis
bradycardia
Laboratory clues Moderate Usually have

Hyponatremia Mild anemia
to Dx thrombocytopenia normal WBC
Diagnosis Clinical Serology
Treatment Doxycycline OR Chloramphenicol
Gangrene of
Complications CNS issues DIC Renal failure Liver failure
digits
Delirium Azotemia Elevated LFT’s Due to
Seizures vasculitis
Bottom right image (Reprinted from Morgan MB, Smoller BR, Somach clinicopathologic atlas and text. New York: Springer; 2007. p. 125–8.
SC. Rocky mountain spotted fever and the rickettsioses. In: Morgan With permission from Springer Science + Business Media)
MB, Smoller BR, Somach SC, editors. Deadly dermatologic diseases:
Ehrlichiosis
Very similar Caused by bite Two types of Monocytic

Erlichiosis
presentation to RMSF from infected tick disease Granulocytic
Rash Maculopapular
Symptoms & Signs
Sx very similar
Fever Myalgias Headache Rash
to RMSF
Laboratory clues Moderate Mild Elevated

Hyponatremia Leukopenia
to Dx thrombocytopenia anemia LFT’s
Diagnosis Clinical
Treatment Doxycycline OR Tetracycline OR Chloramphenicol
Complications CNS issues DIC Renal failure Liver failure Death
Delirium Azotemia Elevated LFT’s

Seizures
Coma
372 B. Desai
Babesiosis
Babesia Caused by bite Endemic in 2nd most common

Babesiosis
(protozoan parasite) from infected tick NE US blood parasite
Malaria #1
Symptoms & Signs
Signs of Signs of ARDS

Fever Chills Fatigue Malaise Diarrhea (Severe cases)
hemolytic anemia
Hepatomegaly Splenomegaly Jaundice
Blood smear with Protozoa in

Diagnosis Serology “Maltese cross”
intra-RBC parasites blood smear
Treatment Clindamycin Quinine OR Azithromycin Atovaquone
Usually mild Immune

Asplenic Elderly
unless compromised
Viral Infections
TORCHES
PEDIATRICS
TO Toxoplasmosis
R Rubella
C CMV
H Herpes/HIV
E Epstein-Barr Virus
S Syphilis
These organisms are associated

with congenital transmission
Cytomegalovirus (CMV)
PEDIATRICS
Congenital
Most common Member of Herpes 3 disease
CMV Acquired
of the TORCHES virus family processes
Immunocompromised
Liver & spleen

Congenital Chorioretinitis Deafness Rash
enlargement
+ Jaundice
Acquired Usually benign Flu-like illness OR Mono-like illness
CMV effects on
Nephritis Pneumonitis Retinitis Colitis
immunocompromised pts?
Immune
CMV High mortality
compromised
Atypical lymphocytes
Diagnosis ELISA
on peripheral smear
Treatment Ganciclovir Foscarnet
Epstein-Barr Virus (EBV)
PEDIATRICS
Infectious Member of Herpes Common in May be asymptomatic

EBV
mononucleosis virus family adolescents in younger children
Symptoms & Signs
Exudative
Fever Splenomegaly Lymphadenopathy
pharyngitis
Atypical lymphoctyes
Diagnosis Monospot Serology
on peripheral smear
Macular rash if May be

Complications Splenic rupture Thrombocytopenia
given Amoxicillin diagnostic
Instructions for no
Treatment Rest Supportive care
contact sports
374 B. Desai
Herpes Zoster (HZV)
Varicella Member of herpes Located in dorsal root Dermatomal distribution

Herpes Zoster ganglion-Zoster is a
virus virus family of painful vesicles
reactivation process
Disseminated Post-herpetic
Complications Meningitis Pneumonia
VZV neuralgia
Treatment Valacyclovir OR Acyclovir Steroids
Bottom center image (Reprinted from Zaidi Z, Lanigan SW. Viral infections. In: Zaidi Z, Lanigan SW, editors. Dermatology in clinical practice.
London: Springer; 2010. p. 101–23. With permission from Springer Verlag)
Complications of AIDS
Most frequent Hypoxemia with TMP/SMX &

Pulmonary Pneumocystis
infection bilateral infiltrates Steroids
Cryptococcal Most common CNS Dx with CSF

Meningitis Amphotericin B
meningitis fungal infection studies
Most common cause Dx = CT with ring Pyrimethamine

Encephalitis Toxoplasmosis
of encephalitis enhancing lesions & Sulfadiazine
Kaposi’s 2nd most common Seen in No significant

Sarcoma (KS) AIDS manifestation homosexual males morbidity
Painless macular These may Raised strawberry

KS Skin Findings Nonpruritic OR
purple areas coalesce & bleed like plaques
Extracutaneous GI tract, especially Central nervous

Lungs
findings liver & spleen system
Percutaneous Transmission Post exposure prophylaxis

exposure rate 0.3 % recommended for significant exposure
Source with high Contamination due to

Increased Risk Deep injury
viral load hollow bore needle
Post exposure Start meds within 1–2 Multiple drugs Reverse transcriptase Protease
prophylaxis hours, continue for 4 weeks are standard inhibitors inhibitors
Molluscum Contagiosum
PEDIATRICS
Molluscum Viral infection of Usually self HIV–lesions may last

Poxvirus
Contagiosum the skin limited longer & be atypical
Pink or flesh colored 1–5 mm diameter

Rash
dome shaped papules with dimpled center
Face Groin
Autoinoculation Trunk Children Adults
Extremities Genitalia
Close contact with

Transmission Autoinoculation
infected individuals
Bottom center image (Reprinted from Silverberg NB. Cutaneous New York: Springer; 2012. p. 113–25. With permission from Springer
infections. In: Silverberg NB, editor. Atlas of pediatric cutaneous biodi- Science + Business Media)
versity: comparative dermatologic atlas of pediatric skin of all colors.
376 B. Desai
Malaria
Intra-RBC Transmitted via infected Prevalent in Asia, Latin

Malaria
parasite female Anopheles mosquito America & Sub-Saharan Africa
Plasmodium Plasmodium Plasmodium Plasmodium

Organisms
falciparum ovale vivax malariae
Plasmodium Causes more Widespread High likelihood

Most severe Due to
falciparum complications medication resistance of parasitemia
Symptoms & Signs
“ Blackwater
Fever & Chills Splenomegaly Headache Malaise Joint pain N/V
fever”
Cerebral Abnormal Massive
AMS Seizures posturing Opisthotonus hemolysis
malaria
Classic Paroxysm Coldness Shivering Fever
Diagnosis Thick and thin

blood smears
Treatment Depends on organism

and resistance pattern
Pediatric Rashes
Erythema Infectiosum
PEDIATRICS
Erythema
Parvovirus B19 Fifth Disease
Infectiosum
Bright red face & Spares eyelids & “Lace-like” red

Rash Limbs & Trunk
cheeks chin papules
Symptoms & Signs
Rash follows
Fever Headache Myalgias URI/Flu Sx Diarrhea
these Sx
Treatment NSAID’s
Fetal anemia if
Complications Arthritis Aplastic crisis
acquired in pregnancy
Sickle cell
Rubella
PEDIATRICS
Acute viral
Rubella
illness
Spread from
Rash Pink macules
head to feet
Symptoms & Signs
Prominent Posterior auricular,

Fever Headache Sore throat Rash
lymphadenopathy cervical & occipital
Congenital
Complications Arthritis Encephalitis
defects
Immune complex If acquired during
1st trimester
378 B. Desai
Measles (Rubeola)
PEDIATRICS
Acute viral
Measles
illness
Red-brown Spread from

Rash Maculopapular
“morbilliform” head to feet
Appear on buccal Nontender small

Koplik spots “Grains of salt”
mucosa before rash white spots
Symptoms & Signs
Morbilliform
Fever Cough Coryza Conjunctivitis Koplik spots
rash
“The 3 C’s”
Complications Pneumonia Encephalitis Conjunctivitis Otitis

Roseola Infantum
PEDIATRICS
Roseola Exanthem Human herpes Common 6–18

Infantum subitum virus 6 & 7 months
Pink maculopapular Spread from trunk to

Rash Starts on trunk
rash face, neck, & extremities
Symptoms & Signs
Fever Defervescence Rash
Complications Febrile seizures

380 B. Desai
Varicella (Chicken Pox)
PEDIATRICS
Varicella Zoster
Chicken Pox
virus
“Dew drop on a
Rash Macules Papules Vesicles
rose petal”
Symptoms & Signs
Fever Malaise URI Rash
Treatment Acyclovir OR Valacyclovir
Secondary
Complications Pneumonia Encephalitis Otitis media
infection
Immune disease Children &

Prevention Immune globulin Vaccine
Pregnant Adults (non immune)
Avoid salicylates!
May precipitate Reye
syndrome
Hand-Foot-Mouth Disease
PEDIATRICS
Hand-Foot- Caused by Fecal-oral Occurs in

Mouth Disease Coxsackievirus transmission outbreaks
Symptoms & Signs
1–2 mm oral
High fever Sore throat URI Sx Malaise Dysphagia Vomiting
vesicles
Vesicles
Buccal mucosa Tongue Soft palate Gingiva
intraorally
Vesicles also
Hands Feet Soles
present on
Change to gray
Skin lesions Red papules Palms & Soles Buttocks
vesicles
Beware viscous lidocaine

Treatment Analgesia Hydration Seizures
in young children
Aseptic
Complications? Rare Myocarditis Encephalitis
meningitis
382 B. Desai
Henoch-Schonlein Purpura (HSP)
PEDIATRICS
Most common acute Usually resolves

HSP Ages 2–10
vasculitis affecting children spontaneously
Typically from Salmonella Preceding Strep

HSP OR
preceding GI infection Shigella infection
Symptoms & Signs
Palpable
Abdominal pain Hematuria GI Bleeding
purpura
Palpablepurpura Buttocks Legs
No Consider checking
Laboratory
thrombocytopenia renal function
Complications Arthritis Glomerulonephritis Hematuria GI Bleed Intussusception
Right side image (Reprinted from Zaidi Z, Lanigan SW. Vasculitis, common erythemas, and lymphatic disorders. In: Zaidi Z, Lanigan SW, editors.
Dermatology in clinical practice. London: Springer; 2010. p. 253–70. With permission from Springer Verlag
Kawasaki’s Disease
PEDIATRICS
Kawasaki’s Mucocutaneous Typically in males Self-limited

Ages 2–5
Disease lymph node syndrome & of Asian descent vasculitis
Predilection for
coronary arteries
Criteria for Diagnosis Fever >5 days PLUS 4
Eyes Oral Skin Nodes
Bilateral Strawberry Erythematous rash Swelling or Enlarged

conjunctival tongue; Lip starting on palms desquamation of (>15 mm) cervical
injection fissures & cracking & soles fingers & toes lymph nodes
Increased
Laboratory Increased WBC Elevated ESR
platelets
IV
Treatment Aspirin
immunoglobulin
Coronary artery
Complication
aneurysm
384 B. Desai
Scarlet Fever
PEDIATRICS
Caused by toxin from

Scarlet Fever
Group A β−hemolytic Strep
“Sandpaper Starts on neck & Spreads to trunk

Rash
rash” face & extremities
Spares circumoral
area
Red streaks from Axilla, groin, antecubital

PastiaLines
the rash areas & body creases
Symptoms & Signs
Strawberry
Fever Headache Sore throat N/V Lymphadenopathy Rash
tongue
Skin peeling
(palms & soles)
Increasing ASO
Diagnosis Throat swab
titer
Treatment Penicillin
Strep
Complications Otitis media Glomerulonephritis Rheumatic fever
pneumonia
Miscellaneous Skin-Related Disorders
Venous Stasis Ulcers
Venous Stasis Result from chronic Caused by episodes of Poor venous return from LE leading
Ulcers venous insufficiency phlebitis or varicose veins to edema & stasis dermatitis
Prolonged Tall
Risk Factors Older age Female Pregnancy Genetic
standing person
Medial distal legs & pretibial areas Honey crusted Secondary Cellulitis or
Tidbits
most affected for dermatitis lesions or pustules? infection lymphangitis
Ulcers – medial & lateral malleolus
Symptoms & Signs
Dependent Hyperpigmentation Ulceration in

Erythema Pruritis
edema Orange/Brown severe cases
Diagnosis Clinical
Support Anitbiotics for

Treatment Leg elevation
stockings infection
Pilonidal and Sebaceous Cysts and Abscess
Located along These sinuses are lined with Sinuses can get blocked &
Pilonidal Cysts
the gluteal fold squamous epithelium & hair lead to bacterial infection
Organisms Skin flora Staphylococcus spp
Most common
Blockage of sebaceous gland duct

Sebaceous cysts Occur diffusely
may lead to bacterial infection
Symptoms & Signs
Tender, swollen nodule Nodule is May have surrounding

along gluteal fold fluctuant erythema
For pilonidal
Sebaceous may be
located anywhere
Diagnosis Clinical
Incision & Antibiotics generally

Treatment Packing
drainage not needed
Not removing capsule May lead to

Pitfall
of sebaceous cyst recurrence
386 B. Desai
Decubitus Ulcers
Occur when soft tissue is compressed Results in lack of Tissue ischemia

Decubitus Ulcer blood supply
between a bony prominence & a hard surface & death
Areas commonly
Sacrum Posterior scalp Heels
affected
High risk Immobilized Pts with underlying Nursing home Immune-

patients trauma pts neurologic conditions residents compromised
Stages of
Stage 1 Stage 2 Stage 3 Stage 4
decubitus ulcers
Intact skin with Shallow open Full thickness Exposure of
erythema sore, pink base No exposure of muscle, tendon,
muscle, tendon, or bone
or bone
Diagnosis Clinical
Keep affected Decrease pressure

Treatment Pain relief
area moist on the wound
Complications Infection Skin dehiscence
Not rolling at risk patients

Pitfall
to examine their back
Lipoma
Benign tumors Usually small, can Occur on neck,

Lipoma
of fat enlarge to > 6 cm trunk, & extremities
Diagnosis Clinical
Treatment Excision
Hemangiomas
PEDIATRICS
Congenital vascular If palpable, they are soft &

Hemangiomas
malformations mobile with a bluish hue
Infantile Grow rapidly until 90 % spontaneously

hemangiomas 9–10 months of age regress
Head & neck If large may Present as

Biphasic stridor
hemangiomas compromise the airway respiratory distress
Airway lesion? Need endoscopy
Diagnosis CT or MRI
Urgent treatment Compression of

Rapid growth Hemorrhage Infection
needed for nearby structures
388 B. Desai
Lymphangiomas (Cystic Hygroma)
PEDIATRICS
Separation of lymphatic channels that do not Lead to blockage of Slow

Lymphangiomas communicate with the internal jugular system lymphatic channels growing
Can occur anywhere 75 % occur in the Most commonly near the

Lymphangiomas in the body neck jugular chain of lymphatics
Soft, painless, & are

Lymphangiomas Can be very large
compressible
Compression of May cause feeding May compress

Complications surrounding structures problems the airway
Diagnosis Prenatally via US
Treatment Refer for

asymptomatic pts Eventual surgery
(Stable)
Treatment May need tracheostomy for

(Unstable) respiratory distress
Endocrine/Metabolic/Electrolytes
Bobby Desai
Contents
Hypoglycemia 390
Diabetes Mellitus 393
Diabetic Ketoacidosis 395
Alcoholic Ketoacidosis 401
Hyperosmolar Hyperglycemic Nonketotic Syndrome 404
Thyroid Disorders 407
Hypothyroidism and Myxedema Coma 408
Hyperthyroidism and Thyroid Storm 415
Adrenal Insufficiency and Crisis 423
Pheochromocytoma 429
ADH-Related Diseases 430
Electrolytes and Acid-Base 437
The Osmolal Gap 466
B. Desai, MD, MEd


B. Desai, B.R. Allen (eds.), Nailing the Written Emergency Medicine Board Examination, 389
DOI 10.1007/978-3-319-30838-8_7
390 B. Desai
Hypoglycemia
Agents for Glucose Control
Agents causing
hypoglycemia Sulfonylureas
Long duration Chlorpropamide
Stimulate the Chlorpropamine of action Can cause SIADH
pancreas to Glyburide
OD can cause profound
release insulin
Glipizide hypoglycemia
Sulfonylurea Hypoglycemia Admission
α-glucosidase
inhibitors
Agents attenuating Rare to cause lactic

Metformin
hyperglycemia acidosis
Thiazolodenediones
Hypoglycemia
Hepatic disease
Post-Prandial Critical illness
Extrapancreatic
neoplasm
Medications Insulinoma
Insulin
Oral hypoglycemics
Causes of
Hypoglycemia Artifactual
(Laboratory)
Alcohol
Salicylates Leukemia
Barbituates Polycythemia
Hypothermia Infection
Dumping
syndrome AMI
Endocrine
disorders
Hypothyroidism
Adrenal
insufficiency
Pituitary
insufficiency
Endocrine/Metabolic/Electrolytes 391
Hypoglycemia: Clinical Features
Depend on glucose level

and rate of glucose drop
Sympathomimetic Symptoms Can be masked by b-blockers
Tremor Diaphoresis Pallor Nausea Anxiety Palpitations Shivering
Neuroglycopenic Symptoms
Concentration
Confusion Drowsiness Dizziness Tiredness
difficulty
Can have severe
Psychosis obtundation
Coma
Tidbits of Hypoglycemia
Primary energy
Glucose source for brain
Glucagon
Norepinephrine
Role of multiple Cause the
Glucose
counterregulatory Growth Hormone release of liver
control hormones glycogen stores
Epinephrine
Glucocorticoids
Excess exogenous NO measurable C-

insulin peptide level
392 B. Desai
Hypoglycemia Differential Diagnosis

Seizure
Stroke/TIA Precipitant
May have transient
focal deficits
Psychosis Depression
Hypoglycemia
Sympathomimetic Altered mental
Mimics
drug ingestion status
Traumatic brain
injury Multiple sclerosis
Other neurologic
deficits
Treatment of Hypoglycemia
Awake &
Hypoglycemia Oral glucose
alert
15–20 g Disposition
depends on clinical
D 50 Adults condition and
effectiveness of
Standard treatment
treatment D 25 Pediatric use
D 10 Infant use
Confusion or Glucagon not

altered mental Intravenous or effective with
Hypoglycemia Glucagon
status PR glucose depleted glycogen
stores
1 mg IV/IM
Liver disease
Alcoholics
Adrenal Give Thiamine to
Hypoglycemia Insufficiency Hydrocortisone Glucose
these pts
Consider
Magnesium
Sulfonylurea Glucose
Hypoglycemia overdose Octreotide infusion Admit
Inhibits insulin
secretion
Prevents rebound
hypoglycemia
Continued D10
hypoglycemia Infusion
Diabetes Mellitus
Insulin
DM Hyperglycemia Defects in production
Insulin action
Type I Dx
No circulating B-cell
Children
DM 5–10 % insulin dysfunction Teens
Causes ketoacidosis Insulin is required Immune mediated
in untreated cases
90 %
Type II
80–90 % Has circulating Fails to act on Relative insulin Dx
insulin but tissues deficiency Older
Ketoacidosis during
stress Insulin resistance
May lead to HHNS
Tidbits About Hormones
Skeletal muscle
Insulin
Glucose Stimulates Fat tissue
release
Liver
Promote Assists uptake of

Insulin Promote
Acts to glycogen amino acids into
lipogenesis muscle
production
Triglyceride production
from free fatty acids
Prevents triglyceride
breakdown
Breakdown of Increased Catabolic

Inability of cells secretion of
Lack of Insulin protein & fat to counterregulatory (breakdown)
to use glucose provide useful fuel hormones state
Glycogen Gluconeogenesis
Worsens
Primary hormone hyperglycemia
Counterregulatory Glycogenolysis Acetoacetate
hormones Cortisone
Free fatty acid + Convert to
Catecholamines β-hydroxybutyrate
glycerol production ketones
Growth hormone Protein breakdown Acetone
Renin-
Volume Angiotensin- Potassium
Activates
Aldosterone
Exacerbates
depletion
system
loss
394 B. Desai
Types of Insulin
Rapid Short Intermediate Long
Time of Onset 6 – 15 min 15 – 60 min 1– 4 hrs 90 min
Time to Peak 1–2 hrs 2–4 hrs 6–9 hrs No peak
Duration of effect 3–6 hrs 6–8 hrs 6–24 hrs 24 hrs
Insulin Administration
Subcutaneous Most common SC Complication Fibrosis
Preferred method for

Intravenous Rapid onset hyperglycemia
Insulin Pump
Insulin Delivers fixed dose of

pump rapid acting insulin
Usually a basal rate
Priming the pump
Insulin delivery Disconnection

Complications Empty reservoir
Catheter problem
Diabetic Ketoacidosis
Some Causes of Diabetic Ketoacidosis
Noncompliance
with insulin regimen
Pregnancy CVA
Pulmonary
Medications & Embolism
Drugs
Cocaine
Most GI Bleed
Steroids
common
Causes of DKA
Thiazides
Sympathomimetics
Critical Illness
Antipsychotics
Errors in insulin
administration
Infection
Heat stroke
Trauma AMI
Endocrine organ
dysfunction
Pancreatitis
Hyperthyroidism
Insulin Catabolic Despite cellular

Stress Hyperglycemia
deficiency Hormones starvation
May be relative lack
of insulin
Excess production Inability of cell

Hyperglycemia Due to
of glucose to use glucose
Hepatic
gluconeogenesis
396 B. Desai
Effects of Hyperglycemia
Osmotic Leading
Hyperglycemia Causes Dehydration Due to Polydipsia
diuresis to
Osmotic Leading
Causes Polyuria to Hypovolemia Electrolyte Loss
diuresis
Electrolytes Lost
Na+ Cl- K+ Ca2+ Mg+ PO2
Severe
Hypovolemia Leads to Leads to Shock
Dehydration
Systemic &
Intracellular
Worsened by
vomiting that Also ketonuria
accompanies DKA
Systemic Effects of Hyperglycemia
Insulin lack & Protein

Counterregulatory Causes Lipolysis
breakdown
hormones
Muscle breakdown
Nitrogen loss
Production of Leading
Lipolysis Causes to Ketonemia Acidosis
ketoacids
Anion gap
Ketoacidosis Causes Vomiting Ketonuria
metabolic acidosis
Increased
Anion gap ventilation to
Leads to Tachypnea Leads to
metabolic acidosis decrease CO2
Altered mental
Vomiting Leads to Dehydration Leads to Shock
status
Intracellular Potential Leading cause

Acidosis Leads to shift of K+ Leads to arrhythmia of death in DKA
DKA: Clinical Features
Directly related to
Acidosis Volume Depletion Hyperglycemia
Symptoms & Signs
Polyuria Polydipsia AMS Hypotension Dehydration Palpitations Shivering
Fruity breath Tachypnea &

+ Fever odor
Tachycardia
Hyperpnea N/V Abdominal pain
Common in
children
Neuroglycopenic Symptoms
Concentration
Confusion Drowsiness Dizziness Tiredness difficulty
Can have
Psychosis
severe
obtundation
Coma
398 B. Desai
Diagnosis: DKA
Presence of Low HCO3 Moderate

Diagnosis Hyperglycemia pH < 7.3
anion gap ketonemia
May be venous
> 250 mg/dL > 12–15 <15mEq/L pH
Venous pH
is 0.03 lower
CBC +
Basic Labs EKG ABG/VBG Lactate U/A Ketones
‘Lytes
Glucose Look for ± Culture
Calculate hyper-K+
anion gap changes
And K+ may be normal or
Mg + PO4
ischemia elevated
Consider other
studies depending Cardiac LFT’s + Thyroid Head CT
on underlying evaluation Lipase studies + LP
medical conditions Cardiac
enzymes
CXR Looking for DKA
precipitants
DKA Precipitants
ANY acute
Noncompliance
stressor
Psychosis Infection
Precipitants of
Drug or Other
DKA Hyperthyroidism
Ingestion
Myocardial
Traumatic injuries
Infarction
High mortality
Neurologic
Pancreatitis
deficits
DKA Differential Diagnosis
AKA Lactic acidosis
Renal Failure DKA Differentials Starvation
Other alcohol
ingestion Drug Ingestion
Methanol Salicylates
Ethylene glycol
DKA Treatment
Immediate
Suspicion Fluid Bedside Appropriate
Hx DM Glucose of DKA resuscitation glucose
Urine dip +
Labs
EKG
Anion gap?
Correct Treat
Replace
DKA? fluids
metabolic reversible
derangements causes Other electrolytes
Over 24–36
hours Na = Pseudohyponatremia
(correction = 1.6 mEq/L
for every 100 mg/dL
Treatment Replace Correct glucose over 100)
potassium Insulin
order fluids derangements PO4 = Emergent
May need to replacement when level
give K+ even <1 mg/dL (Sx= respiratory
with normal
depression, muscle
levels
weakness, CHF, AMS)
Initial hypokalemia Mg = Replace if Sx or level

May be life
Hypo-K+ threatening!
requires aggressive <2 mg/dL
replacement
Usual deficit Cardiac arrest Before insulin!
is 3-5
mEQ/kg
SQ insulin once
Insulin Continue Anion gap Ketonemia
DKA Normal K+
therapy until closes has resolved
Switch to IV insulin has
stopped
IV drip
400 B. Desai
Bicarbonate in DKA
Rarely
HCO3
indicated!
Impaired
Potential Cerebral Electrolyte Sodium oxygen– Paradoxical
complications edema problems overload hemoglobin CSF acidosis
dissociation
Especially in Curve shifts to Also worsening
Hypo-K+ left intracellular
children acidosis
Hypo-PO4
DKA Complications
Mortality HCO3 Serum Glucose BUN

osmolarity
Precipitating
factors with
highest MI Infection
mortality
Over- Acute
Respiratory
aggressive Distress
fluids? Syndrome
Cerebral New-onset
Young persons
edema DM
High mortality
Cerebral May be Over- Osmotic

edema due to Hypoxemia
hydration changes
Cerebral Edema
Symptoms/Signs
Drowsiness or Pupillary Hypo-or

Bradycardia Headache Incontinence Seizures
Obtundation changes Hyperthermia
Fluid
Treatment Intubation Mannitol
restriction
High mortality
Disposition
Severe DKA Admission
Anion gap Can tolerate Appropriate Potential

Mild DKA
closed po follow-up discharge
Alcoholic Ketoacidosis
Introduction
Abrupt cessation
Alcoholic Wide anion
Due to of alcohol use Causes
ketoacidosis gap acidosis
after chronic use
Can be followed by
vomiting
Nicotinamide Conversion to
Metabolism Alcohol
adenine Alcohol Acetyl
of alcohol dehydrogenase
dinucleotide coenzyme A
NAD
Can be used in the Krebs cycle

Acetyl
Directly metabolized Ketoacids
coenzyme A
Can be used for free fatty acid synthesis
402 B. Desai
Pathophysiology
Decreased Formation Reduction

Alcoholic Depletion Stimulation
aerobic of Ketones of glycogen
ketoacidosis of NAD of lipolysis
metabolism stores
Due to ethanol
metabolism
Growth hormone
Reduction Decreased
Addition of Stimulation
of glycogen insulin Catecholamines
stress of
stores section
Dehydration Glucagon
Illness
Anaerobic metabolism
Further stimulates lipolysis

Lactate
levels are
high
Acetyl Metabolized β-hydroxybutyrate Acetoacetate

coenzyme A to
Ketone
production Predominant in AKA
until NAD returns to Metabolized to acetone
increased
normal
with vomiting May cause an increased
osmolar gap
Alcoholic Ketoacidosis: Clinical Features
Symptoms May be nonspecific
Abdominal
Nausea Vomiting pain
Tremors Hematemesis
Most common
Signs
Abdominal Altered mental

Tachypnea Tachycardia tenderness on exam
Bloody stools status
Hypotension
Usually secondary
to other causes
Most common
May have associated

gastritis or
pancreatitis
Diagnosis
Based on appropriate Laboratory

Diagnosis
scenario findings
Consider CBC ‘Lytes EtOH Lipase LFT’s Ketones
Ca Usually
low or
Mg negative
PO4
Initial ketone Anion gap

level
Required for
calculation
Due to b -HB
Inability of
During recovery
Initial ketone nitroprusside
Low Due to Recovery acetoacetate
level reagent to detect b -
increases
HB
Tests become
positive
Treatment
D5NS MgSO4 Electrolyte

Volume Glucose Thiamine Vitamins
repletion
Stimulates Fluid of Before K+
insulin choice Glucose
production Thiamine Mg++
before
glucose
prevents Controversial
Wernicke
disease
Stops
Insulin
Glucose Stimulates Glucagon
production
production
Endogenous Ketone
Stops Lipolysis
Insulin production
Not
exogenous!
404 B. Desai
Disposition
Resolution Tolerating Potential

AKA
of acidosis po discharge
Other Persistent
AKA Admission
illness acidosis
Hyperosmolar Hyperglycemic Nonketotic Syndrome
Introduction
Hyperosmolar
hyperglycemic Hyperglycemia Hyperosmolarity Usually in Type II Diabetics
state
Often >1000 Often >350 Poor control of

sugars
Elderly or
debilitated
May have decreased
access to water
Hyperosmolar
Higher mortality
hyperglycemic No ketoacidosis Insidious onset
than DKA
state
May have starvation

related ketones
Pathophysiology
Lack of insulin Increased

Osmotic Potential
or resistance to Leading to gluconeogenesis HHNS
diuresis for
insulin & glycogenolysis
Impaired Due to insulin Leads to Often the initial

peripheral use resistance or dehydration presentation of
of glucose deficiency May be profound Type II DM
–8 to 12 liters
Leads to more
hyperglycemia
HHNS: Clinical Features

Comorbid
Symptoms Usually elderly
conditions
Mental status Abnormal vital

Fatigue Weakness Dyspnea Chest pain Anorexia
changes signs
Abdominal Neurologic
pain deficits
Signs
Abnormal vital Signs of other

Dehydration Hypothermia Seizures Lethargy Coma
signs acute illness
Poor skin Poor
Tachycardia Typically focal Typically older Infection
turgor prognostic sign
Typically
Sunken eyes higher glucose MI
Dry mucous Typically more
membranes dehydration CVA
AMS
Precipitating Factors for HHNS
Diabetes
Often the initial
presentation of
Pulmonary NIDDM
GI Bleed
embolism
Medications
β-and Ca channel Uremia
blockers
Lithium
Diuretics Causes of HHS

Infection
Steroids
Phenytoin UTI/Pyelonephritis
Neuroleptics Pneumonia
Cimetidine
Pancreatitis SDH
Renal failure Vascular disease AMI

Common comorbid Common comorbid
condition condition
406 B. Desai
Diagnosis
Severe Elevated serum Negative to mildly Normal pH &

Diagnosis HCO3
hyperglycemia osmolality positive serum ketones
May have
May have moderate
metabolic acidosis
ketonemia–from starvation
–lactic acidosis
Serum
Basic Labs glucose
‘Lytes Osmolality Lactate CBC Ketones
Mg Calculated
&
Calculate Measured
anion gap
Consider other
studies depending Cardiac LFT’s+ Thyroid Head CT
U/A ABG
on underlying evaluation Lipase studies + LP
medical conditions Cardiac + Culture
enzymes
EKG
CXR
Treatment
50 % of fluid
Volume Improves Decreases Remainder over
Fluids deficit over the
depletion perfusion glucose the next 24 hours
first 12 hours
Replace Average
volume before deficit 8-12 L
insulin
Initial 1 L
boluses as
indicated Cerebral edema not as
common as in DKA, but can
occur with rapid fluid
replacement
Respiratory Withhold Insulin Adequate urine

Low K+ Potential for Arrhythmias
arrest until K+ replaced output
Consider
replacement of Mg
HypoK+ = HypoMg+
Disposition
HHS Admission
Thyroid Disorders
Thyroid Hormones
Feedback TRH
inhibition of Hypothalamus
TSH
TSH
Pituitary
Depends on
Thyroid gland
iodine intake
Excess Iodine
blocks hormone
release
T3 Converted to T4
20 % 80 %
4x more
biologically
active than T4
Protein Cell
synthesis metabolism
408 B. Desai
Hypothyroidism and Myxedema Coma
Introduction: Hypothyroidism
Primary
Thyroid
Hypothyroidism hormone Metabolism 2 types
production
Often >1000 Secondary
Females Males
Primary Dysfunction of Most common

Hypothyroidism thyroid gland type
TSH administration
Primary
will not be
Hypothyroidism
effective
Dysfunction of TSH Dysfunction of TRH

Secondary
release from the OR release from the
Hypothyroidism
pituitary hypothalamus
Some Causes of Hypothyroidism
Autoimmune
Hashimoto’s
Thyroiditis
Infection
Medications &
Drugs Surgical ablation
Amiodarone
Lithium In patients with

preexisting Iodine deficiency
Iodine autoimmune Causes of
disease Hypothyroidism
A-interferon
After radiation
Panhypopituitarism
Pituitary adenoma Congenital
Treatment of
Infiltrative disease Idiopathic
Graves’ disease
Lymphoma
Sarcoid
410 B. Desai
Hypothyroidism: Clinical Features
Symptoms
Thinning or loss Weakness & Irregular Cold

Depression Weight gain Constipation
of hair Fatigue menstrual cycles intolerance
Dysfunctional Due to decreased
Muscle and Shortness of uterine bleeding metabolic rate
joint pain breath And…decreased
shivering
Signs
Puffiness Decreased or absent

Pallor Hoarseness Macroglossia Bradycardia Hypoventilation
around orbits bowel sounds
Delay in relaxation Peripheral

Hypothermia Edema Cool dry skin Hypoxemia
of reflexes neuropathy
Severe in Non-pitting “Hung -up” Myxedema coma
Myxedema coma reflexes
Pretibial
myxedema
May also be a
rare sign of
hyperthyroidism
Severe Hypothyroidism: Specific Clinical Features
Cardiopulmonary
Low EKG Distant heart Pericardial &

Angina Bradycardia Cardiomyopathy Hypoventilation
voltage sounds Pleural effusions
Dermatologic
Non-pitting Periorbital
Dry skin Hair loss Macroglossia Facial swelling Ptosis
edema edema
Neuropsychiatric
Delayed DTR’s Dementia Paresthesias Psychosis Depression Confusion Ataxia

Myxedema Coma
Mental
Myxedema Preexisting Some type of
status Hypothermia
Coma hypothyroidism stress
changes
Or coma <35.5oC
Occurs in High Consider in

Myxedema
elderly mortality winter
Coma
females rate months
AMS or
Signs Bradycardia Hypotension Hypoventilation Hypothermia
Coma
Infection may May be in Very

be present
despite these
shock common
signs
Poor prognostic
Persistent
factors for The elderly Bradycardia
hypotension
Myxedema Coma
412 B. Desai
Precipitating Factors of Myxedema Coma

Noncompliance
with medications
Infection MI
Medications &
Drugs
Trauma
Amiodarone
β-blockers
Narcotics Stressors Cold exposure
Phenothiazines
Sedatives
CHF
GI bleed
CVA
Burns
Metabolic
Surgery
conditions
Hyponatremia,
hypoxia,
hypoglycemia,
hypercapnia
Differential Diagnosis of Myxedema Coma
Sepsis
Drug overdose Adrenal crisis
DDx
Infection-
Meningitis
Florid depression
Cold exposure-
CVA Hypothermia
Hypoglycemia CHF
Myxedema Diagnosis
Diagnosis of Laboratory findings

Primarily clinical
Myxedema Coma are secondary
Looking for
Free T4 Free T3 Other laboratories and
Consider TSH precipitating
imaging as needed
factors
Free T4 Free T3 Primary

High TSH
hypothyroidism
Free or Free or Secondary

Low TSH
Total T4 Total T3 hypothyroidism
Other common
May have
laboratory Hyponatremia Anemia
elevated lipids
findings
414 B. Desai
Treatment
Treatment of
Consideration of Thyroid hormone
Supportive care precipitating
Myxedema Coma? replacement
factors
IV T4 IV T3 and large
doses of IV T4 in
Beware of large
the elderly
doses in the elderly
may cause
arrhythmias
Hypotension or Consider Thyroid hormone

Steroids
shock? Vasopressors replacement
Not effective Potential for
without thyroid concurrent adrenal
hormone! insufficiency
More aggressive
measures may be
Passive Warm
Hypothermia Warmed fluids needed for
rewarming Blankets profound
hypothermia
Myxedema Increased Steroids

coma metabolic stress (Hydrocortisone)
Give before 1st

dose of thyroid
hormone
Disposition
Myxedema
Admission
coma
Hyperthyroidism and Thyroid Storm
Introduction: Hyperthyroidism
Circulating Circulating
Hyperthyroidism Thyroid Thyrotoxicosis Thyroid
hormone hormone
From thyroid
From any cause
overproduction
Altered
Life-threatening Adrenergic Presence of
Thyroid Caused peripheral OR
state of hyperactivity With one or more
storm by response to
thyrotoxicosis precipitants
thyroid hormone
Other
Hyperthyroidism
Female > Male autoimmune Family history
risk factors
disease
Excess production
Primary of thyroid
Hyperthyroidism hormone from the
thyroid
Excess production Excess production

Secondary
or TSH from the OR of TRH from the
Hyperthyroidism
pituitary hypothalamus
416 B. Desai
Causes of Primary Hyperthyroidism
Graves disease
Most common
form (85%)
Primary
Hyperthyroidism
Toxic multinodular Toxic nodular

goiter goiter
Second most
common form
Graves’ Disease
Thyrotropin receptor
immunoglobulins stimulate both
Graves disease thyroid hormone synthesis and
secretion
Pre-tibial
myxedema
Rare
Bilateral
Pre-tibial Accumulation of
elevated dermal Waxy skin
myxedema mucopolysaccharides
nodules
Causes of Hyperthyroidism
Thyroiditis
Hashimoto
Drug overdose thyroiditis
Thyroid hormone Initially hyperthyroid
followed by
hypothyroidism
Secondary and
Other Causes of
Drugs & Pituitary
Medications Hyperthyroidism adenoma
Iodine
Amiodarone
Radiation
thyroiditis
Metastatic
Teratoma thyroid cancer
Hyperthyroidism: Clinical Features
Symptoms
Thinning or loss Weakness & Irregular Heat

Pallor Weight loss Diarrhea
of hair Fatigue menstrual cycles intolerance
Dysfunctional
uterine bleeding
Muscle and Shortness of` Chest pain + Confusion + Fullness of

Diplopia
joint pain breath Palpitations Psychosis neck
Not all pts
have a goiter
Signs
Fever+ Thyroid gland

Fine tremor Muscle wasting Exophthalmos Hypertension Sinus tachycardia
Sweating enlargement
Atrial flutter or Hyperactive bowel Pretibial

CHF Hyper-reflexia Anemia
fibrillation sounds myxedema
418 B. Desai
Thyroid Storm: Specific Clinical Features
Cardiopulmonary
Angina Tachycardia Arryhthmias CHF

Atrial flutter or
fibrillation
Constitutional
Fever
May have
hyperthermia
Neuropsychiatric
Seizures Delirium Agitation Psychosis Stupor Confusion Coma
Precipitating Factors of Thyroid Storm
Infection HHNS Trauma
Medications &
DKA
Drugs
Withdrawal of
thyroid meds
Intentional ingestion
of thyroid meds Thyroid storm
MI
precipitants
Iodine
administration
Eclampsia CVA
Idiopathic PE Surgery
Up to 25%
Differential Diagnosis of Thyroid Storm
Infection and
Sepsis
Illicit drug or prescribed Heat stroke /

medication withdrawal Heat exhaustion
DDx
Malignant
Psychosis
hyperthermia
Organophosphate Neuroleptic
poisoning malignant syndrome
Drug ingestion Delirium tremens
Amphetamines
Cocaine
420 B. Desai
Thyroid Storm Diagnosis
Tachycardia out Severe

Diagnosis of Fever > CNS
Primarily clinical of proportion to manifestations of
Thyroid Storm 38oC dysfunction
fever thyrotoxicosis
In those with preexisting
hyperthyroidism
Laboratory findings
are secondary
Free T4 & Serum ‘lytes + EKG +

Consider TSH CBC
Free T3 cortisol LFT’s CXR
Should be
elevated
If considering Thyroid
Graves disease antibody titers
Primary
High TSH
hyperthyroidism
Secondary
Low TSH
hyperthyroidism
Low TSH Free T4 Thyrotoxicosis
Normal T3
Low TSH OR Free T3
Free T4 Thyrotoxicosis
Other common
May have low
laboratory Hypercalcemia Hyperglycemia Elevated LFT’s
cholesterol
findings
Treatment
Consideration Block peripheral Block thyroid Block thyroid Treatment of
Supportive
of Thyroid thyroid hormone hormone precipitating
care
Storm? hormone effects synthesis release factors
Correction of
Supportive care Fluids Steroids electrolyte
imbalances
Decrease
conversion of T4
to T3
Block peripheral
Beware β-blocker
thyroid hormone Propranolol
contraindications!
effects
Also inhibits
peripheral
conversion of T4
toT3
Block thyroid
hormone PTU OR Methimazole
synthesis
Also inhibits
peripheral
conversion of T4
toT3
Block thyroid
Iodine
hormone release
One hour after PTU β-blockers PTU Iodine
Disposition
Thyroid
Admission
storm
422 B. Desai
Apathetic Thyrotoxicosis
Apathetic Usually Presence of Presence of

Rare
Thyrotoxicosis elderly goiter droopy eyelids
Hallmarks of
Slowed Lethargy and Apathy and
Apathetic
mentation weakness depression
Thyrotoxicosis
Signs & Symptoms Atrial fibrillation &

Usually NO Resting
Apathetic CHF resistant to
exophthalmos tachycardia
Thyrotoxicosis treatment
Adrenal Insufficiency and Crisis
Adrenal Hormones
Feedback
inhibition
Gonadcorticoids
Estrogen & Testosterone
Adrenal Adrenal Adrenal Renal Na+ Renal K+

Mineralocorticoids
gland medulla cortex reabsorption excretion
Aldosterone
Inner Outer
layer layer Affects Regulates
Glucocorticoids tissue blood
metabolism glucose
Catecholamines Cortisol
Corticotropin
releasing factor
(Hypothalamus) Renin-
Angiotensin Serum K+
system
Responds to
Hyperkalemia
changes in
increases
volume,
ACTH Diurnal secretion
posture,Na
Pituitary rhythm intake
Higher in am
Lower in pm
Adrenal
Adrenal gland gland
Cortisol Aldosterone
424 B. Desai
Introduction: Adrenal Insufficiency and Crisis
Primary
Adrenal gland
Adrenal
hormone 2 types
Insufficiency
production
Secondary
Worsening of Decreased Increased

Adrenal Crisis adrenal Due to circulating physiologic
insufficiency steroid demand
Primary Cortisol
Dysfunction of
Adrenal Addison disease and
adrenal gland
Insufficiency Aldosterone
Secondary Inadequate ACTH

production due to Cortisol
Adrenal hypothalamic- only
Insufficiency pituitary dysfunction
Some Causes of Primary Adrenal Insufficiency
Adrenal hemorrhage
Idiopathic
or infarction
Meningococcal sepsis
Infiltrative
Infection
Most common diseases
TB infectious cause Amyloid
worldwide
Fungal Sarcoid
Bacterial sepsis Lymphoma
Most common
HIV infectious cause Hemachromatosis
in the US Causes of Metastasis
Primary Adrenal
Insufficiency
Medications
Etomidate
Autoimmune
Surgery Addison disease

70 % of 10
Congenital
Congenital adrenal
hypoplasia
Some Causes of Secondary Adrenal Insufficiency
Sudden cessation of Pituitary necrosis or

chronic steroid therapy bleed
Most common cause Sheehan syndrome
of iatrogenic cause of
acute adrenal crisis
Infection Infiltrative
diseases
TB
Amyloid
Fungal
Sarcoid
Meningitis
Lymphoma
HIV
Hemachromatosis
Causes of Metastasis
Secondary Adrenal
Medications Insufficiency
Most common
Steroids cause overall
Causes adrenal
“Tertiary” atrophy
Surgery Brain tumor
Pituitary Pituitary
Hypothalamic
Trauma to head
426 B. Desai
Adrenal Insufficiency: Clinical Features
Primary
Symptoms & Signs
Mental status Weakness & Increased Nausea &

Weight loss Diarrhea Abdominal pain
changes Fatigue pigmentation vomiting
Cortisol deficiency
Dehydration Hypotension Syncope
May be marked
Aldosterone deficiency
No aldosterone
Secondary
deficiency symptoms
Symptoms & Signs
Cushingoid Other Sx of pituitary

Visual changes Headache Galactorrhea
appearance hormone deficiency
Adrenal Crisis: Clinical Features
Symptoms & Signs
Severe Mental status Profound Nausea &

Lethargy Sepsis Abdominal pain
hypotension changes weakness vomiting
Refractory to Delirium Without fever
pressors
Fever May mimic an
acute abdomen
Laboratory Abnormalities and Testing Considerations
Diagnosis of Adrenal High index of Especially in those with Those with predisposing
Insufficiency suspicion unexplained hypotension features
Primary adrenal
Hyperkalemia Hyponatremia Hypoglycemia
insufficiency
Hyponatremia OR Secondary adrenal

Hypokalemia Hypoglycemia
hypernatremia insufficiency
Other common
Metabolic
laboratory Hypoglycemia Eosinophilia
acidosis
findings
Due to cortisol Due to hypotension Chronic
deficiency & hypovolemia insufficiency
May show Depends on

EKG findings evidence of K+ hyper - or
problems hypokalemia
Looking for
Cortisol ACTH Other laboratories and
Consider precipitating
level stimulation test imaging as needed
factors
Treatment
Consideration of Treatment of
Supportive
Adrenal Steroids precipitating
care
Insufficiency? factors
IVF = D5NS Hydrocortisone Dexamethasone
Corrects Drug of choice Can be given if

hypoglycemia& Provides mineralo - & ACTH simulation
hyponatremia glucocorticoid effects test will be done
Hypotension or Consider
Steroids
shock? Vasopressors
Give 1st Not effective

without steroids!
Due to underlying
High mortality Dysrhythmias Shock
precipitant
Hyperkalemia
428 B. Desai
Disposition
Adrenal
Admission
crisis
Introduction: Hyperadrenalism (Cushing’s Syndrome)
Cushing’s
Cortisol
Syndrome
Prolonged steroid
use
Most common
ACTH secreting Causes of Adrenal

carcinoma Hyperadrenalism neoplasm
Pituitary
adenoma
Hyperadrenalism: Clinical Features
Symptoms & Signs
Hypertension Hirsuitism Truncal obesity Buffalo hump Purple striae Moon facies Edema
On abdomen
Diagnosis of High index of Those with predisposing

Hyperadrenalism suspicion features
Common
laboratory Hypernatremia Hyperglycemia Glucosuria
findings
Due to cortisol Due to hypotension Chronic
deficiency & hypovolemia insufficiency
Treatment
Consideration of Supportive Treatment of

Stop steroids precipitating
Hyperadrenalism? care
factors
Disposition
Depends on
Hyperadrenalism
clinical scenario
Pheochromocytoma
Introduction
Rare cause of Tumor of adrenal Secretes

Pheochromocytoma
hypertension medulla norepinephrine
Usually benign but

Treatable!
can be malignant
Pheochromocytoma: Clinical Features
Symptoms & Signs 5 P’s
Pallor Palpitations Pressure Pain Perspiration
Increased BP Abd pain

Headache
Chest pain
430 B. Desai
Diagnosis
Consideration of
24 hour urine Catecholamines VMA
Pheochromocytoma?
Metabolites
Treatment and Disposition
HTN Phentolamine α-blockade
Depends on
Disposition
clinical condition
ADH-Related Diseases
Antidiuretic Hormone
Feedback
inhibition
Brain
Increased serum osmolality Detected by

Kidneys
& decreased plasma volume receptors
Heart
ADH produced
(Hypothalamus)
Well hydrated?
Pituitary
secretes ADH
Restoration of
plasma volume and
tonicity
Increases renal
water absorption
Introduction: Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)
ADH Urine Fluid Serum

SIADH
secretion production retention sodium
Inappropriately
SIADH concentrated Hyponatremia Normovolemia
urine
Low serum
osmolality
Some Causes of SIADH
CNS disease
Trauma
CVA
Infection
CNS
Pneumonia TB or Fungal
Malignancy
Medications &
Some causes of
Drugs CNS
SIADH
Chlorpropramide Hypothalamic
Diuretics
Vasopressin
Vincristine
Cyclophosphamide
Thioridazine
Cisplatin
Stress
432 B. Desai
SIADH: Clinical Features
Symptoms & Signs Most are asymptomatic
Most S&S are related to

hyponatremia
Mental status Weakness &

Seizures Lethargy Confusion Coma
changes Fatigue
Delirium
Clinical features depend on

rate of decline of Na+
Serum Urine specific Urine Na+ Normal renal, adrenal

SIADH Hyponatremia and thyroid function
osmolarity gravity < 20mEq/L
Urine Serum Other laboratories and

Consider BMP CBC U/A
‘lytes osmolality imaging as needed
Consideration of Treatment of
SIADH? Supportive care precipitating
factors
Mild Slow correction Central pontine

Fluid restriction Prevents
hyponatremia? over 24–48 hours myelinolysis
125 –134 mEq/L Admit
Severe Seizures or 4–6 cc/kg 3 %

Fluid restriction Furosemide
hyponatremia? Coma normal saline
<115 mEq/L Stop when

seizures subside
Goal Na+ > 120 mEq/L

Serum Na+ levels can be
safely raised at a rate of
1–2 mEq/L/hr
High morbidity Serum Na+ < 120
Central Pontine Myelinolysis
Hyponatremia
Central Pontine
corrected too
Myelinolysis
rapidly
Central Pontine Cranial nerve Locked in

Confusion Quadriparesis
Myelinolysis deficits syndrome
Mental status Pseudobulbar

Seizures Dysarthria Dysphagia Coma
changes palsy
Delirium
Other
Other risk factors
Alcoholism electrolyte Malnutrition
for CPM
imbalances
Concomitant use of furosemide can

decrease incidence of CPM
434 B. Desai
Introduction: Diabetes Insipidus
Failure of central
Diabetes Urine
or peripheral ADH
Insipidus response production
Low urine osmolality
Central Failure of ADH secretion
Diabetes
Insipidus
Nephrogenic Kidneys are unresponsive to ADH
Some Causes of Central DI
CNS disease
Neoplasms
Head Trauma
Idiopathic Some causes of Pituitary surgery

Central DI
Granulomas
Some Causes of Nephrogenic DI
Renal disease
Drug Induced Familial

Lithium toxicity
Other nephrotoxic
drugs Some causes of
Nephrogenic DI
Hematologic
Malnutrition
disorders
Electrolyte
Disturbances
Hypercalcemia
Hypokalemia
DI: Clinical Features
Symptoms & Signs Sx can be seen once Na+ >158 mEq/L
Most S&S are related to

hypernatremia
Mental status Increased

Polyuria changes Seizures Coma Polydipsia
muscle tone
Delirium
Can see brain

Clinical features depend
hemorrhages due to
on rate of change of Na+
tearing of blood vessels.
436 B. Desai
Serum Urine specific Urine Na+ 60 -

DI Hyper natremia
osmolarity gravity 100 mEq/L
Urine Serum Other laboratories and

Consider BMP CBC U/A
‘lytes osmolality imaging as needed
Hypocalcemia is frequently
seen in patients with
hypernatremia
Central = concentrates urine

Response to
Diagnosis of DI
Vasopressin
Nephrogenic = no response
Reduce Na+ by Switch to a hypotonic

Diagnosis made Fluids only 10–15 solution once tissue
of DI? mEq/L/day perfusion has improved
Maintain an adequate urine
NS or LR Admit
output
Central DI? Desmopressin
Nephrogenic DI? HCTZ

Electrolytes and Acid-Base
Sodium
Introduction: Hyponatremia
Primarily Concentration
Sodium
extracellular 140 mEq/L
Concentration
Hyponatremia <135 mEq/L
Na+ loss > water

Hyponatremia Due to Water gain
loss
Consequence of <120 mEq/L

Symptoms of more likely to
rate of change
Hyponatremia have Sx
of sodium
Hyponatremia
Symptoms & Signs Most are asymptomatic

Early
N/V Anorexia Muscle cramps Lethargy Confusion
These Sx can be
Late seen with an acute
(<24 h) drop in Na+
Seizures Obtundation Coma

More likely <113
mEq/L
Chronic
Focal weakness Ataxia Hemiparesis

438 B. Desai
Diagnosis + Treatment
Clinically evaluate Calculate plasma Measure plasma

Hyponatremia?
volume Status Osmolality Osmolality
Most
Movement of Intracellular Extracellular common
Osmolality From To
water space space cause is
Hyperglycemia
>295
Normal No treatment
Pseudohyponatremia
Osmolality required
275–295
Replace fluids
Hypovolemic Small boluses
with NS
Assess Volume Correct Water
Osmolality Euvolemic Furosemide
Status underlying cause restriction
If Na <120
<275 Measure urine Salt & Water
Hypervolemic sodium restriction
Causes of Hyponatremia
Hypertonic
hyponatremia
Osm > 295
Hyperglycemia Hyperglycemia
Glycerol therapy For every 100
mg/dL increase in
Mannitol therapy glucose, the Na+
decreases by 1.6–1.8
mEq/L
Some causes of
Hyponatremia
Isotonic
hyponatremia
Osm 275–295
Hyperlipidemia
Hyperproteinemia
Causes of Hypotonic Hyponatremia (Osm < 275)
Hypovolemic
Renal
Diuretics
Nephropathy
Osmotic diuresis
Aldosterone
deficiency
Extra-Renal
GI loss Hypervolemic
3rd spacing
Urine Na+ > 20
Sweating mEq/L
Euvolemic
Renal Failure
SIADH
Urine Na+ < 20
Hypothyroidism mEq/L
Water intoxication Nephrotic syndrome
Medications Cirrhosis
CHF
Introduction: Hypernatremia
Concentration
Hypernatremia >150 mEq/L Increases Thirst
Decrease in Decreased
Increased intake
Hypernatremia Due to total body OR excretion of
of sodium
water sodium
Volume loss a
common etiology
440 B. Desai
Some Causes of Hypernatremia
Inadequate water
intake
Ingestion of large
amount of Na+
Burns
Iatrogenic
Essential
hypernatremia
Mineralocorticoid
Causes of excess
Hypernatremia
Medications &
Drugs Glucocorticoid
excess
Osmotic causes N/V/D
Renal disease
Nephrogenic
Diabetes Insipidus
Central Diabetes
Insipidus
Hypernatremia Symptoms
Symptoms & Signs Sx can be seen once Na+ >158 mEq/L
Mental status Increased

Polyuria Seizures Coma Polydipsia
changes muscle tone
Delirium
Treatment
Reduce Na+ by Switch to a hypotonic

Diagnosis made of
Fluids only 10–15 solution once tissue
Hypernatremia? mEq/L/day perfusion has improved
Maintain an adequate urine
NS or LR Admit output
Usual
replacement
over 48 hours
Too rapid
correction may
lead to cerebral
edema
Potassium
Introduction: Hypokalemia
Concentration Mild hypokalemia

Primarily
Potassium 3.5–5 mEq/L may = severe total
intracellular
(in serum) body deficit
Most located in
Potassium muscle tissue
Serum levels
Concentration
Hypokalemia determine
<3.5 mEq/L
complications
For every 0.1 rise

Maintains
Shifts into in pH, K+ Shifts into
Potassium When pH rises electrical
cells decreases 0.5 cells
mEq/L neutrality
Most common electrolyte

Hypokalemia abnormality in patients
with weakness
Appear sooner <2.5 mEq/L

Symptoms of
with rapid more likely to
Hypokalemia changes have Sx
442 B. Desai
Causes of Hypokalemia
Decreased
dietary intake
Intracellular shifts GI loss
Alkalosis Vomiting
Insulin therapy Diarrhea
β-agonists Malabsorption
NG suctioning
Causes of
Medications &
Drugs Hypokalemia
Renal loss
Lithium
Diuretic therapy
Penicillin
1°& 2°
Aldosteronism
Osmotic diuresis
Hypo-Mg
Renal tubular
acidosis
Heat stroke /
Sweat loss
Hypokalemia Symptoms and Signs
Symptoms & Signs
Worsening of Weakness & Paresthesias &

Hypertension Dysrhythmias EKG changes Reflexes
Digoxin toxicity Fatigue Paralysis
Orthostatic Nephrogenic Glucose

Ileus
hypotension diabetes insipidus intolerance
Replace after Correction of

Correction of
Hypokalemia? urine output antecedent acid -
Hypomagnesemia
confirmed base abnormality
Mg required for
Na-K pump
Intravenous
Hypokalemia? Oral replacement
replacement
Safest No more than

Cardiac
40 mEq /L & no
monitoring is
faster than 40
recommended
mEq /hour
Introduction: Hyperkalemia
Concentration Most common Factitious 2o

Hyperkalemia >5.5 mEq/L phlebotomy
cause
Causes of Hyperkalemia
Pseudohyperkalemia
Hemolysis
Extracellular
shifts Potassium load
Acidosis Supplementation
Lack of Insulin Diet
b-blockers GI bleed
Rhabdomyolysis
Causes of
Medications &
Drugs Hyperkalemia
Digoxin toxicity Renal failure

K+ sparing
diuretics
Thrombocytosis
NSAID’s
Succinylcholine
Leukocytosis
Renal tubular
Lupus
acidosis
Low Aldosterone
444 B. Desai
Hyperkalemia Symptoms and Signs
Symptoms & Signs
Cardiac Ascending Weakness & Paresthesias &

EKG changes N/V/D Areflexia
dysrhythmias paralysis fatigue Paralysis
Stabilize cell Shift K+

Hyperkalemia? Remove excess K+
membrane intracellularly
Continuous
Hyperkalemia? EKG cardiac Recheck sample
monitoring
Assess for If no EKG changes
dysrhythmias and pt is stable
Ca Chloride 3 times as
Cell membrane Calcium gluconate
Beware Digitalis potent as Ca Gluconate
stabilization or chloride
Ca Potentiates
digoxin’s toxic Consider administering Ca
cardiac effects Chloride via central venous
access
Albuterol
Intracellular shift Insulin + Glucose Bicarbonate
(b-agonist)
Sodium
Removal of excess
polystyrene Furosemide Hemodialysis
K+
sulfonate
Calcium
Introduction: Calcium
Most abundant Measured

99 % is bound in
Calcium mineral in the serum level
bone
body 8.5–10.5 mg/dL
Maintained Parathyroid
Calcium Calcitonin Vitamin D
by hormone
Increased Increased
PTH Increased GI
Hypocalcemia? bone resorption
secretion absorption
resorption by kidney
Intravascular 50 % bound to 5 % bound to other

45 % ions
calcium plasma proteins substances
A decrease in protein Physiologically

results in a total active
decrease of Ca
Acidosis
Also affected
Calcium Acid Base status Increases
by
ionized fraction
446 B. Desai
Introduction: Hypocalcemia
Normal ionized
Ionized level
Hypocalcemia level = 2.1–2.6
<2.0 mEq/L
mEq/L
Depends on the
Hypocalcemia < 1.4 –1.6
Start at rapidity of the
Symptoms mEq/L
decrease in Ca
Thyroid or Perioral &

Parathyroid Check for Hyperreflexia fingertip
surgery? paresthesias
Mouth twitch
Chvostek’s sign after tapping
the facial nerve
BP cuff on upper Carpal spasm after

Trosseau’s sign arm inflated to 3 minutes of the
above systolic elevated pressure
More reliable for

hypocalcemia
Causes of Hypocalcemia
Sepsis
Increased Decreased
excretion absorption
Renal failure Vitamin D deficiency
Diuretics
Endocrine
Medications & disorders
Drugs Hypoparathyroidism
Phosphates Causes of Pseudo
Phenytoin & Hypocalcemia hypoparathyroidism
Phenobarbital
Cimetidine
Acute
Heparin Pancreatitis
Glucagon
Norepinephrine
Hypomagnesemia
Glucocorticoids
Sodium
nitroprusside
Magnesium sulfate Rhabdomyolysis
Low Aldosterone
Hypocalcemia Symptoms and Signs
Occur when ionized levels <1.4 –1.6

Symptoms & Signs
mEq/L
Chvostek & Weakness &

Tetany Paresthesias EKG changes reflexes Confusion
Trousseau signs fatigue
Prolonged QT
Rickets Seizures Hallucinations Dry skin CHF Muscle cramps

448 B. Desai
Mild or
Asymptomatic Oral calcium Vitamin D
Hypocalcemia?
IV calcium should
Severe Causes be used with
IV calcium
Hypocalcemia? vasoconstriction caution in patients
taking digitalis
Potentiates
digitalis toxicity
Replace Mg
Hypocalcemia Hypomagnesemia before or with
calcium
Introduction: Hypercalcemia
Total level Ionized level

Hypercalcemia >10.5 mEq/L OR >2.7 mEq/L
Hypercalcemia 90 % due to Malignancy OR Hyperparathyroidism
More common in
ED
Causes of Hypercalcemia
Malignancy
Squamous cell-
Lung
Fungal Infection Endocrine
Breast 1°
Histoplasmosis
Hyperparathyroidism
Kidney
Coccidioidomycosis Pheochromocytoma
Leukemia
Hyperthyroidism
Myeloma
Medications & Causes of

Drugs Hypercalcemia
Thiazides
Lithium
Paget disease of
Sarcoidosis
bone
Tuberculosis
Hypercalcemia Symptoms and Signs
Symptoms & Signs Occur when total levels >12 mEq/L
Weakness &
Polydipsia Stupor & apathy Headache EKG changes Reflexes & tone Confusion
malaise
Shortened QT
Pathologic Rhythm Digitalis

Bone pain Hallucinations Hypertension
fractures disturbances sensitivity
Abdominal
Anorexia N/V Constipation
pain
Peptic ulcer
Pancreatitis Renal failure
disease
Polyuria Kidney stones

450 B. Desai
Correction of Many patients will

Decreased bone have associated
Hypercalcemia? Replace volume underlying
breakdown hypokalemia &
disorder
hypomagnesemia
Hypercalcemia? IV fluids Bisphosphonates Loop diuretics Calcitonin
Works within 2–4 Only after Inhibits bone

2–4 liters
days hydration resorption
Inhibit osteoclast
function
Severe
Dialysis
Hypercalcemia?
Magnesium
Introduction
2nd most Measured

Magnesium abundant serum level
intracellular 1.5 –2.5 mg/dL
cation
Has a role Has a role in Has a role in

ATP Protein
Magnesium in neuromuscular platelet
production synthesis
coagulation activity aggregation
Introduction: Hypomagnesemia
Level <1.5
Hypomagnesemia
mEq/L
Severe
Frequently With With
Hypomagnesemia Alcoholics Malnourished vomiting or
seen in pancreatitis cirrhosis diarrhea
Causes of Hypomagnesemia
Sepsis
Other Hypercalcemic After correction of

states DKA
Potassium
Severe Diarrhea
depletion
Medications &
Drugs Severe burns
Loop diuretics
Causes of
Alcohol Hypomagnesemia Acute
Pancreatitis
Aminoglycosides
Ketoacidosis Alcoholism
1° or 2°
Malnutrition
Aldosteronism
Hyperparathyroidism Malabsorption
Hyperthyroidism
Hypomagnesemia Symptoms and Signs
Symptoms & Signs
Weakness & Altered mental

Tetany Seizures Paresthesias EKG changes reflexes
fatigue status
Ataxia Vertigo Anorexia Nausea Dysphagia CHF
Hypotension Hypokalemia Hypocalcemia Anemia
In presence of normal Calcium EKG changes in Hypomagnesemia

levels may have positive Chvostek or Very similar to hypocalcemia &
Trousseau sign hypokalemia
452 B. Desai
All can present

Hypomagnesemia? Check Potassium Calcium Phosphate with severe
hypomagnesemia
Hypocalcemia does
not develop until
Mg < 1.2 mg/dL
Severe
IV/IM magnesium
Hypomagnesemia?
Introduction: Hypermagnesemia
Seen in perinatal period

Rarely after treatment of
Hypermagnesemia
encountered eclampsia or
preeclampsia
Ingestion of
Most common Magnesium
Hypermagnesemia Renal failure
cause containing
medications
Causes of Hypermagnesemia
Renal Failure
Acute or chronic
Other Hypercalcemic
Untreated DKA
states
Treatment of
preeclampsia or
eclampsia
Medications &
Drugs
Mg - containing Rhabdomyolysis
Causes of
medications
Hypermagnesemia
Lithium ingestion
Adrenal
insufficiency
Hyperparathyroidism Malnutrition
Hypothyroidism
Hypermagnesemia Symptoms and Signs
Symptoms & Signs Rarely produces symptoms
Respiratory
Nausea Drowsiness Hypotension Heart Block reflexes Cardiac arrest
depression
Hypermagnesemia? Check Potassium Calcium
Hyperkalemia Hypercalcemia
Stop Mg Stop Lithium

Hypermagnesemia?
administration (if on)
Hypermagnesemia? Fluids Loop diuretic IV Calcium Dialysis
If no renal failure
Phosphorus
Introduction
Measured serum
Intracellular Hydroxyapatite
Phosphorus level
(15 %) (85 %) 2.5–5.0 mg/dL
Inversely 30 – 40
Phosphorus Calcium Calcium Phosphorus
proportional mg/dL
Proportional
Phosphorus Dietary intake
to
Intravascular 5 % bound to other

Excretion Urine Regulated by PTH
calcium substances
Lowers PO4 by
increasing renal
excretion
454 B. Desai
Introduction: Hypophosphatemia
Normal ionized
Hypophosphatemia Unusual level = 2.1 – 2.6
mEq/L
Specifically 12–
Hypophosphatemia
Start at < 1.0 mEq/L 24 hours after
Symptoms
DKA treatment
Causes of Hypophosphatemia
Decreased oral intake
Redistribution Decreased GI
with glucose absorption
infusion
Alkalosis
Medications & Causes of
Metabolic
Drugs Hypophosphatemia
Respiratory
Antacids
Hyperalimentation
DKA treatment
Increased renal
excretion
Renal tubular
Hyperparathyroidism
defects
Malignancy
associated with
hypercalcemia
Hypophosphatemia Symptoms and Signs
Symptoms & Signs Occur when levels <1.0 mEq/L
Respiratory Impaired myocardial Weakness & Confusion &

Anorexia Paresthesias reflexes
depression function fatigue AMS
Hemolytic Impaired
Tremors Rhabdomyolysis CHF
anemia platelets
Correct underlying Replace

Hypophosphatemia?
disorder Phosphate
Oral
Severe
IV Phosphate
Hypophosphatemia?
Severe Slow rate of

Renal Failure
Hypophosphatemia? replacement
Lower total
Hypercalcemia Hypophosphatemia replacement of
Phosphate
Introduction: Hyperphosphatemia
Usually seen in
Hyperphosphatemia patients with
renal failure
Hyperphosphatemia Concomitant
Due to Hypomagnesemia Hypocalcemia
Symptoms renal failure
Causes of Hyperphosphatemia
Hypoparathyroidism
Renal Failure Renal Failure

Causes of
Hyperphosphatemia
Increased Increased
phosphorus intake Vitamin D
Problems
associated with
hypercalcemia
456 B. Desai
Correct underlying Limit phosphorus

Hyperphosphatemia? disorder intake
Oral
Oral phosphate
Hyperphosphatemia? IV Fluids Acetazolamide binders
Severe
Hyperphosphatemia? Dialysis
Metabolic Derangements
Introduction
pH changes 0.01
Plasma H+ 40 nmol/L pH of 7.4 Thus
of 0.01 nmol /L H+
Decreased buffering capacity
Increased production
Acidosis Increase in H+
H+ addition
Decreased excretion
Alkalosis Decrease in H+
Will have
Acid-Base compensatory
Respiratory OR Metabolic
Disorders mechanisms to limit
pH changes
1° changes in Will NOT return pH
1° changes in PCO2
HCO3 to normal
History and Physical
Medications
Consider events Ingestions

that may cause a
change in acid-
base status Diarrhea
Vomiting
Liver
Evaluate specific
organs involved in
Kidneys
maintaining acid-
base status
Lungs
Laboratory Investigations
Sodium
There is a good
“Chem 7” Arterial
Potassium correlation
or (or venous) blood between pH/CO2
Basic metabolic gases
Specific chemistry Chloride in arterial &
panel
laboratories venous samples
Bicarbonate Except in
Lactate level severe shock
Serum osmolality
Potassium and pH
Low or normal K+
For every 0.1 decrease in
In acidosis Severe intracellular K+
pH, K+ increases by 0.5
depletion
mEq/L
Methanol & Ethylene

Elevated osmolal gaps Seen in
glycol poisoning
458 B. Desai
Metabolic Acidosis
Anion Gap
Relies on principal of
electrical neutrality
Chloride
Charge of Charge of Unmeasured

Must equal
Sodium plasma anions anions
Serum proteins
Principal plasma Bicarbonate Phosphates
cation Sulfates
Organic acids
Chloride
Sodium Anion Gap
Bicarbonate
Lactic
Anion Gap 30 Usually OR DKA
acidosis
For pure wide

anion gap Anion
HCO3-
metabolic Gap
acidosis
Abnormal Anion Gap Without Acid-Base Disturbance
Hypomagnesemia Myeloma
Hypercalcemia Lithium toxicity
High Low
Bromide
Hypermagnesemia
intoxication
Hypokalemia Hypocalcemia
Hypoalbuminemia
Anion Gap Causes
Abrupt cessation of alcohol +

A AKA Ketoacidosis
malnourishment
C Cyanide, Carbon monoxide Toxic Lactic acidosis
A Aspirin Ingestion
T Toluene Toxic
M Methanol Ingestion
U Uremia Renal failure
D DKA Ketoacidosis
P Propylene Glycol, Paraldehyde Ingestion
I Iron, Isoniazid Ingestion Lactic acidosis
L Lactic acidosis Most common cause
E Ethylene Glycol, Ethanol Ingestion
S Salicylates Ingestion
Metabolic Acidosis
Metabolic Wide anion

OR Non-gap
acidosis gap
Exogenous Endogenous
Metabolic
increase in OR increase in OR Loss of HCO3 -
acidosis
acid acid
DKA Vomiting
Loss of HCO3-
Exogenous TPN Endogenous
Enterocutanous Renal tubular
fistulas acidosis
AKA
Decreased Stimulation
Metabolic Increase in
acidosis HCO3- Increased H+ of respiratory
ventilation
centers
Attempt to
lower H+ by
lowering PCO2
Lowest PCO2 in
spontaneous
respiration is 12
mm Hg
460 B. Desai
Lactic Acidosis
Seizures
Antiretrovirals Renal Failure
Liver failure
Toxic alcohols
Sepsis
Hypoxia Causes of Lactic

Acidosis
Lactate produced by Methemoglobin
anaerobic glycolysis
Metformin
Associated with
renal failure Cancer
Myeloma
Hypoperfusion Lymphoma
Leukemia
Ethanol
Usually mild
Non-anion Gap Metabolic Acidosis Causes
H Hypoaldosteronism (Addison disease)

Usually a loss of HCO3-
with loss of Na+
A Acetazolamide
R Renal tubular acidosis
D Diarrhea
Some may have a

U Uterosigmoidostomy tendency to
Hyperkalemia, while
others have a tendency
P Pancreatic fistula
to Hypokalemia
Other causes
Early obstructive Other potassium sparing

Improving DKA Early Uremia uropathy diuretics
Effects of Acidosis
Decreased ventricular Increased energy

Cardiac Decreased contractility
fibrillation threshold requirement for defibrillation
Liver Decreased perfusion
Decreased systemic
Kidney Decreased perfusion
blood pressure
Increased pulmonary
Lungs vascular resistance
Attenuation of Potential for systemic

Adrenals catecholamine effect vascular collapse
General Increased metabolism
Pancreas Insulin resistance

462 B. Desai
Treatment
Restore tissue
Correct underlying
Metabolic Acidosis? perfusion and
disorder
oxygenation
Correct
Poor respiratory
respiratory
compensation?
disorder first
No Bicarbonate
therapy for mild to
moderate acidosis
Metabolic Alkalosis
Introduction
Chloride The major

Metabolic Chloride Chloride
OR & anions
alkalosis sensitive insensitive
HCO3- altered
Metabolic
alkalosis Gain of HCO3- OR Loss of acid
Chloride
Decrease Decrease in Increased Increased Na+ Increased
sensitive reabsorption +
of extracellular aldosterone HCO3-
metabolic
Chloride volume activity K+ & H+
alkalosis generation
secretion
Urine Cl- is
low
Chloride
Hypokalemic,
sensitive Responds to
Hypochloremic
metabolic normal Saline
Alkalosis
alkalosis
Chloride
Normovolemia Increased Urine Cl- is No
insensitive
or aldosterone normal or response
metabolic Hypervolemia activity elevated to NS
alkalosis
Also with
HTN
Causes of Metabolic Alkalosis

Renal artery
Vomiting
stenosis
Renin-secreting
Hyperaldosteronism
tumors
Chloride
Chloride Sensitive
Insensitive
Diarrhea Adrenal
Diuretics Cushing syndrome
hyperplasia
Exogenous
mineralocorticoids
Chloride-wasting
processes Licorice
Enteropathies
Cystic fibrosis
Effects of Alkalosis
Decreased ionized Decreased

Electrolytes calcium
Decreased K+ Decreased Mg
phosphate
Decreased coronary
Cardiac blood flow
Refractory dysrhythmias
Decreased Neuromuscular
Neuro cerebral perfusion Seizures Tetany
instability
May depress respiratory

Lungs drive
Treatment
Correct underlying
Metabolic Alkalosis? Supportive care Acetazolamide
disorder
Respiratory Acidosis
Introduction
Respiratory Alveolar Decreased Increased

Acidosis hypoventilation ventilation PCO2
464 B. Desai
Causes of Respiratory Acidosis
Head trauma
Respiratory
Oversedation Chest trauma
Acidosis
Lung Disease
COPD
May be chronic
Treatment
Respiratory Improve
acidosis? ventilatory status Supportive care
Respiratory Alkalosis
Introduction
Respiratory Alveolar Increased Decreased

Alkalosis hyperventilation ventilation PCO2
Causes of Respiratory Alkalosis
Infections
Sepsis
Iatrogenic CNS tumors
CVA
Respiratory
Anxiety Alkalosis
Hypoxia
Pain Pregnancy
Toxic overdose
Salicylates
Treatment
Respiratory Treat underlying

alkalosis? cause
466 B. Desai
The Osmolal Gap
Introduction
Determined
Osmolal Gap by Sodium Chloride BUN Glucose
Osmolal Gap Measured Calculated 10
Presence of
unmeasured
Osmolal Gap Indicates
low molecular
weight solutes
2 x Na+ + Glucose / 18 + BUN / 2.8 = 280–295
Causes of Elevated Osmolal Gap
Ethanol
Mannitol Ethylene Glycol
Osmolal Gap
precipitants
Glycerol Methanol
Isopropyl alcohol
Ears, Nose, and Throat
Bobby Desai
Contents
Ear 468
Nose 478
Facial Fractures 482
Throat/Neck/Upper Airway Infections 484
Dental Emergencies 490
Neck Masses 494
Edema of Upper Airway 496
Soft Tissue Lesions 497
Intraoral and Tongue Lesions 499
Salivary Gland Disorders 501
Facial Infections 503
Other ENT Emergencies 504
Vertigo 508
B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_8
468 B. Desai
Ear
Introduction: Otalgia
Otalgia Due to Primary causes Referred causes
Primary causes Due to Auricular Periaricular
Cranial nerve innervation Cervical Roots

Referred causes Due to
5, 7, 9, 10 C2, C3
Primary and Referred Causes of Otalgia
Infections
Otitis media
Otitis externa
Mastoiditis
Bullous myringitis
Foreign bodies Trauma
Primary Causes
of Otalgia
Impaction of Around the ear

cerumen Neoplasms
Cellulitis of pinna Cholesteatoma Dental
Dental infections
Sinusitis Dental trauma TMJ disease

Malocclusion
Neck Trigeminal
Some Referred neuralgia
Foreign body Causes of Otalgia
Cervical strain Mouth & Throat

Need good history
& physical Phayngotonsillitis
examination Peritonsillar abscess
Neuralgias Neoplasms
Thyroid disease
Ears, Nose, and Throat 469
Introduction: Tinnitus
Perception of sound No gender Most prevalent

Tinnitus
when none is present predominance between 40–70
Objective Heard by
tinnitus examiner
Subjective More May be due to disease or Side effect of

tinnitus common damage to cochlear hair cells medications
Antibiotics
Aminoglycosides
Aspirin
Refer to
Diagnosis
Otolarynogologist 1st sign of
toxicity
Introduction: Hearing Loss
Sudden hearing Occurs over less No gender Increases with

loss than 3 days predominance age
Hearing loss Vertigo Worse prognosis
Tests for hearing

Rinne test Weber test
loss
Tuning fork next

Rinne test Normal Air conduction Bone conduction
to ear
Conductive
Bone conduction Air conduction
hearing loss
Tuning fork middle Sound is equal in

Weber test Normal
of forehead both ears
Sound greater in Sensorineural defect Conductive defect

OR
one ear on nonlateralizing ear in lateralizing side
470 B. Desai
Causes of Sudden Hearing Loss
Infections
Mumps
Intrinsic ear Herpes Family Rheumatologic
disorders
Syphilis
Otitis media Temporal arteritis
Otitis externa Polyarteritis nodosa
TM rupture Wegener’s
Cerumen impaction
Foreign bodies
Causes of
Sudden Hearing Medications &
Loss Drugs
Meniere’s disease
Acoustic
Hematologic
neuroma
Associated with Sickle cell disease
other CN deficits Leukemia
5, 7
Polycythemia
Neoplasms of ear Metabolic
Hyperlipidemia
DM
Medications and Drugs Causing Sudden Hearing Loss
Alcohols
Ethanol
Propylene glycol
Antibiotics Salicylates
Aminoglycosides Aspirin
Vancomycin
Erythromycin
Medications &
Drugs Causing
Sudden Hearing
Loss
Chemotherapy NSAID’s
Loop diuretics Quinine
Ear Infections
Perichondritis
Perichondritis Inflammation of Layer of connective tissue

perichondrium surrounding cartilage
Perichondritis Post trauma
Symptoms & Signs
Ear pain Fever Ear swelling Redness of ear Warmth
Bacterial agents Staph Proteus Pseudomonas
Treatment? IV antibiotics Admission
Pinna deformation
Complication
if not treated
472 B. Desai
Otitis Externa (OE)

Infection & inflammation
Otitis externa Swimmer’s ear OR Malignant OE
of external auditory canal
Symptoms & Signs
Erythema of Edema of ear Pus from ear Hearing impairment

Ear pain
ear canal canal canal if untreated
Predisposing Elevation of Frequent contact Trauma to external

factors for OE local pH with water auditory canal (EAC)
Bacterial agents Staph Proteus Pseudomonas Enterobacteriaceae
Immune
Fungal agents Humid climates Aspergillus Candida
compromised
Contact
Noninfectious
dermatitis
Topical antibiotics Gentle cleansing Avoidance of

Treatment? Pain control
+ steroids of EAC water in ear
Fluoroquinolones Ear plugs
Center right image (Reprinted from Önerci TM. External ear canal. In: Önerci TM, editors. Diagnosis in otorhinolaryngology: an illustrated
guide. Heidelberg: Springer Verlag; 2010. p. 18–23. With permission from Springer Verlag)
Malignant Otitis Externa (MOE)
Malignant Otitis Life threatening Infection Soft tissue May extend Pseudomonas
Involves
externa of external auditory canal around the pinna into the skull > 90 % of time
Chondritis of Osteomyelitis of
Pathophysiology Simple OE Cellulitis of EAC
outer ear bone
Spread of Mastoid air 7th cranial 9th, 10th, & 11th

Parotid Skull base
infection cells nerve cranial nerves
1st CN to be More severe
affected with disease
cranial
extension of
infection
Predisposing Immune
Diabetics Elderly
factors suppressed
Agents Pseudomonas Staph Strep Fungal
Specifically
Diagnosis? CT of head
Temporal bone
Topical antibiotics Surgical

Treatment? IV antibiotics Pain control
+ steroids debridement
Fluoroquinolones Broad spectrum
to cover
Pseudomonas
Signs and Symptoms of Malignant Otitis Externa
Otalgia
May be severe
Evidence of
Headache
granulation tissue
in the EAC
Erythematous ear
Fever
Signs & Edematous ear

Symptoms of Larger than
Malignant Otitis
unaffected side
Externa
Toxic appearance
Pustular drainage
Pain on
Sigmoid sinus
manipulation of
thrombosis
ear
Parotitis may be
CN deficits
present
7, 9, 10, 11
474 B. Desai
Otitis Media (OM)
PEDIATRICS
Infection & inflammation

Otitis Media
of inner ear
Symptoms & Signs
May have fluid Loss of light

Bulging TM + Fever + Otorrhea Ear pain + Hearing loss
behind TM reflex
Conductive if
Red, yellow or TM perforation
white TM
Most sensitive Decreased movement

sign of TM on insufflation
Streptococcus Hemophilus Moraxella

Bacterial agents Viral
pneumoniae influenza catarrhalis
“Watchful Tympanostomy for

Treatment? Analgesia
waiting” recurrent serous OM
No improvement High dose

Antibiotics
in 48 hours? Amoxicillin
Complications TM Facial nerve Intracranial

Mastoiditis Labyrinthitis
perforation palsy infections
Due to Brain abscess
proximity to Meningitis
middle ear
Bullous Myringitis
Bullous Characterized by bulla Bloody, serous or

Myringitis formation on the TM serosangineous
Symptoms & Signs
Ear pain Middle ear

Bullae + Otorrhea + Hearing loss
effusions
Mycoplasma Chlamydia No clear association

Agents Viral
pneumoniae psittaci with any one agent
Usually the same
agents that cause
OM
Treatment? Analgesia Antibiotic drops Oral antibiotics Admission
For concomitant
OM
Top right image (Reprinted from Önerci TM. Acute otitis media. In: Önerci TM, editors. Diagnosis in otorhinolaryngology: an illustrated guide.
Heidelberg: Springer Verlag; 2010. p. 28–33. With permission from Springer Verlag)
Acute Mastoiditis
Acute Complication of Spread of middle

Mastoid air cells
Mastoiditis Otitis media ear infection
Symptoms & Signs
Erythema Swelling behind Tenderness Downward

Ear pain Fever
behind ear ear behind ear displacement of ear
Specifically
Diagnosis CT scan
Temporal bone
Treatment? IV antibiotics Myringotomy Tympanocentesis Admission
Top right image (Reprinted from Önerci TM. Complications of otitis media. In: Önerci TM, editors. Diagnosis in otorhinolaryngology: an illus-
trated guide. Heidelberg: Springer Verlag; 2010. p. 43–4. With permission from Springer Verlag)
Cholesteatoma
Epidermal collections May be associated with

Cholesteatoma
within the middle ear chronic TM perforation
Symptoms & Signs
Collection of Foul smelling Abnormal inner

Ear pain + Hearing loss
tissue in EAC drainage ear structure
Due to bone
absorbing
substances
Treatment? Surgery
476 B. Desai
Ear Trauma
Auricular Hematoma
Auricular Result from Shearing forces perichondrium Tears blood
Due to Hematoma
Hematomas ear trauma from underlying cartilage vessels
Auricular May accumulate

Hematomas rapidly or over time
Auricular Need complete Aspiration is not Will lead to

Hematomas removal of clot enough deformity
Goals of Remove fluid Maintenance of pressure to

treatment collection prevent fluid reaccumulation
Cauliflower Ear
Formation of new Deforms
Cauliflower ear Asymmetric
cartilage following trauma external ear
Tympanic Membrane Perforation

Blocked eustachian tube Altitude Internal pressure
Tympanic Membrane Result from pressure
Perforation differences on either side of TM Blocked eustachian tube Diving External pressure
Symptoms & Signs
+ Bloody Conductive
Ear pain + Vertigo + Tinnitus
otorrhea hearing loss
Tympanic Membrane Most heal

Perforation spontaneously
Antibiotics not Unless caused by infection

Treatment No water in ear
needed or forceful water entry
Barotrauma
Early Referral Penetrating Posterior
(<24 hours) trauma perforation
Otitis media Blunt trauma
Late Referral
Blunt trauma Noise trauma Causes of Tympanic
(>24 hours)
Membrane
Perforation
Lightning injury Noise trauma
Penetrating
trauma
478 B. Desai
Nose
Epistaxis
Kiesselbach’s plexus Sphenopalatine

Epistaxis Anterior Posterior
(90% of bleeds) artery
Initial Type & Cross for Consider labs as

ABC’s IV access
assessment hemodynamic instability needed
Blood pressure Consider reduction after

& Epistaxis control of hemorrhage
Significant amount of blood Elderly with Bleeding from Uncontrolled bleed

Posterior bleed
in posterior pharynx coagulopathy both nares after packing
Risk factors for Elderly with

Hypertension Atherosclerosis
posterior bleed? coagulopathy
Agents & methods Direct pressure & topical Chemical cautery Thrombogenic
Packing
to control bleeding vasoconstrictors with silver nitrate foams & gels
Controlled
Anterior Bleed Stable Discharge
bleeding
Anterior Bleed Stable Packing Oral Antibiotics ENT referral
Posterior Bleed? Admission

Causes of Epistaxis
Local causes
Deviated septum
Hereditary Digital trauma Rhinosinusitis
hemorrhagic
telangiectasia Inhaled medications
Neoplasia
Chronic renal
failure
Alcoholism
Causes of
Epistaxis
Malignancy Hypertension
Coagulopathy
Warfarin
NSAID use
Hemophilia
Von Willebrand’s
Complications of Posterior Nasal Packing
Toxic shock
Syncope Septal necrosis
Otitis media
Sinusitis
Complications of
Posterior Packing
Airway
Arrhythmias
compromise
Cardiac ischemia
480 B. Desai
Nasal Fractures
Most common Most are Have potential for

Nasal Fractures
facial fractures isolated associated injuries
Initial Look for Septal

Edema Crepitus Epistaxis
assessment deformity hematoma
Clinical exam is
Imaging Insensitive Unnecessary
the best indicator
CSF
Fracture of
CSF rhinorrhea Dx by CT scan
cribiform plate Blood
Dipstick glucose Ring sign on Worse when

CSF Rhinorrhea
> 30 mg/dL coffee filter leaning forward
Septal Appears as a boggy blue Tender to Prevents cartilage destruction

I&D
hematoma swelling to nasal septum palpation & saddle nose deformity
Intranasal
Septal Abscess?
drainage
Septal Requires repair Saddle nose

Untreated?
Perforation by ENT deformity
Untreated infected Contiguous Intracranial Cavernous sinus

Meningitis Osteomyelitis
hematomas spread abscess thrombosis
Allergic Rhinitis
PEDIATRICS
IgE mediated response of Affects 80 % of children with Makes asthma more

Allergic Rhinitis
nasal mucosa to allergen children >2 asthma have this difficult to control
Symptoms & Signs
Clear Conjunctival Purulent nasal

Sneezing Nasal pruritis Eye itching Hyposmia
rhinorrhea hyperemia discharge
Hypertrophy of Clear secretion

nasal turbinates from nares
Avoidance of Nasal saline

Treatment Antihistamines Nasal steroids
precipitating factors sprays
Sinusitis – Introduction
Inflammation of the mucosal Inflammation of the paranasal

Sinusitis Rhinosinusitis
lining of the paranasal sinuses sinuses and nasal cavity
Symptoms & Signs
Purulent nasal
Facial pain + Fever Facial pressure Ear pain Hyposmia
discharge
Blockage and Sinus pain when

Tooth pain
congestion of nose changing head position
Agents of acute Streptococcus Hemophilus Moraxella Viral (most common predisposing

sinusitis pneumoniae influenza catarrhalis factors for bacterial sinusitis)
Agents of Gram-(-) Fungal in immune

Staph aureus Anaerobes
chronic sinusitis bacteria compromised
Imaging not Use CT for potential complications of

Diagnosis Clinical
needed acute disease or for chronic disease
Treatment for Nasal Intranasal

Saline irrigation
Acute Sinusitis? decongestants steroids
Antibiotics for Purulent nasal Severe Sx

Acute sinusitis? secretions > 7 days
Cavernous sinus Skull Intracranial

Complications Orbital cellulitis
thrombosis osteomyelitis infections
Pott’s puffy Brain abscess
tumor Meningitis
Sinusitis
PEDIATRICS
Sinusitis in Commonly involves the

children ethmoid & maxillary sinuses
Form at 3–5 years of

Sphenoid sinus
age
Does not appear until

Frontal sinus
7–8 years of age
Treat for
Chronic sinusitis > 90 days Give for 4 weeks Refer to ENT
anaerobes as well
482 B. Desai
Facial Fractures
Frontal and Zygoma Fractures
Frontal Bone High energy Assess for crepitus to evaluate Dx = CT (As for all
Uncommon
Fractures injury for frontal sinus injury facial fractures)
Frontal Bone Associated with

Fractures intracranial injury
Frontal Bone Frontal sinus

Antibiotics Operative repair
Fracture fracture
Depressed Frontal
IV Antibiotics Admission
Bone Fracture
Zygoma Anterior-lateral
fractures force
Zygomatico- “Tripod” fracture” Zygomatico-frontal Zygomatico- Infraorbital

Injury
maxillary fracture Orbital + Sinus fracture suture temporal junction rim
Symptoms & Signs – Zygoma injury
Flat malar Subconjunctival Infraorbital

Tilted eye Trismus Diplopia Crepitus
eminence hemorrhage anesthesia
Complicated Admission for

Displacement Visual changes IV antibiotics
tripod fractures operative repair
Midface Fractures
Midface LeFort
I, II, III Dx = CT
fractures classification
Symptoms & Signs

3
Bilateral orbital Significant CSF leaks in II &
Hemorrhage
ecchymosis swelling III
Horizontal Hard palate & teeth 2

LeFort I
maxillary fracture move on exam
1
Pyramidal Hard palate & nose are Hardt, N., & Kuttenberger, J.
LeFort II
fracture free floating on exam (2010).Craniofacial trauma: diagnosis
and management. Springer. Fig 3.4, p.
33
Craniofacial Entire face is Globes held in place

LeFort III
malunion mobile by optic nerves
Treatment Admission IV antibiotics
Complications C-spine injury Airway CSF Dental

Bleeding
(> in II & III) or fracture compromise rhinorrhea malocclusion
Retrophayngeal May require
hematoma nasal packing
Consider
awake
intubation
Mandible Fractures
Mandible 2nd most common Look for fracture on Assume open

fractures facial fracture opposite side of ring fracture
Severe Mandible Beware tongue Causes upper

fracture? displacement airway obstruction
Symptoms & Signs
Pain on Jaw deviates to Mandible Anesthesia in inferior alveolar

Malocclusion
movement side of fracture displacement or mental nerve distribution
Tongue Assess in low Bite on tongue blade Blade breaks & Unlikely
Bedside testing
blade test risk patients while MD twists blade patient tolerates? fracture
95%
sensitive
Blood in mouth Open fracture
Risk for facial growth Consider in cases with facial

Children 4–11
disturbances if missed trauma with trismus and TMJ pain
CT
Imaging? Panorex
(complicated injury)
Treatment for Ace wrap over head Outpatient

Analgesia Antibiotics
stable patient? and under mandible followup
Open fracture? Admission Operative repair

484 B. Desai
Throat/Neck/Upper Airway Infections
Pharyngitis and Tonsillitis
Inflammation of posterior Group A β-hemolytic strep is Most pharyngitis is viral –

Pharyngitis
pharyngeal wall most common bacterial organism (GABHS) Rhinovirus most common
Petechial or vesicular pattern

Viral pharyngitis Rhinorrhea Fever
on soft palate & tonsils
No specific Consideration of
Viral pharyngitis Unless
testing infectious mononucleosis
Infectious Posterior cervical Epstein-Barr

Fever Pharyngitis
mononucleosis lymphadenopathy (pathognomic) virus
Rare risk of Spread thru saliva
splenic rupture
with trauma
Symptoms & Signs of GABHS
Erythema of
Sore throat Odynophagia Fever Chills Headache N/V
tonsils & palate
Tonsillar Tender anterior No
exudate cervical nodes Uvular edema No rhinorrhea No cough conjunctivitis
Tonsillar Tender anterior

Centor criteria Fever Cough
exudates cervical nodes
Penicillin is 1st
Treatment Dexamethasone Rheumatic Fever can be prevented
line drug
with Abx treatment
With EBV + To relieve pain
ampicillin, 95% Glomerulonephritis cannot be
will get a rash prevented
Peritonsillar Abscess (PTA)
Peritonsillar Polymicrobial collection of pus beside Most common deep

Rare < 12
Abscess the tonsil in the peritonsillar space space infection in adults
Dental Chronic Prior Hx of

Risk Factors Prior PTA Smoking
disease tonsillitis Abx use
Symptoms & Signs of PTA
Sore throat Odynophagia Fever Malaise Dysphagia Drooling Dehydration
Muffled “hot Displacement of Uvula displacement Tender cervical

Trismus
potato” voice infected tonsil to opposite side adenopathy
Especially for concern of

Diagnosis? CT scan
spread to lateral neck space
Single dose of
Treatment? I&D Antibiotics For pain
high dose steroid
Airway Aspiration of abscess Carotid erosion Spread of

Complications Mediastinitis
obstruction after rupture & hemorrhage infection
Potential location Retropharyngeal Parapharyngeal

for spread? area area
486 B. Desai
Epiglottitis
PEDIATRICS
Inflammation or infection of the May lead to rapid life-

Epiglottitis
epiglottis including the supraglottic area threatening airway obstruction
Most are now seen in 25% caused by

Epiglottitis
adults due to use of vaccine H. influenza b
Symptoms & Signs
Sore throat Odynophagia Dysphagia Drooling Dyspnea Fever Tachycardia
Pain on larynx Inspiratory Cervical Pt usually sitting

palpation stridor adenopathy up, head extended
Diagnosis? Soft tissue X-ray CT scan Laryngoscopy
Prevertebral Disappearance Swelling of Thumb shaped

Soft tissue X-ray
edema of vallecula hypopharynx epiglottis
Immediate ENT Antibiotics Steroids to

Treatment? Humidified O2
(& Anesthesia) consultation (Ceftriaxone) decrease edema
Airway Consider need for early Prepare for Prepare for needle
Complications
obstruction airway intervention cricothyrotomy in adults cricothyrotomy in children
Retropharyngeal Abscess
PEDIATRICS
Retropharyngeal Deep inflammation or infection In children the primary infection

Abscess behind the posterior pharyngeal wall is elsewhere in the head & neck
Retropharyngeal In adults, the infection is due to More likely to extend

Abscess in adults extension from a nearby site into the mediastinum
Symptoms & Signs
Cervical
Sore throat Fever Torticollis Dysphagia Neck pain Neck edema
adenopathy
Muffled or hoarse voice Anterior displacement of

Odynophagia (“Cri du canard” = duck like voice) Stridor posterior pharyngeal wall
CT scan
Diagnosis? Soft tissue X-ray
(Gold standard)
Protrusion of Neck flexion may cause

Soft tissue X-ray
retropharyngeal wall bulge of posterior wall
Immediate ENT Surgical

Treatment? Antibiotics IV hydration
consultation intervention
Airway Extension into

Complications
compromise mediastinum
488 B. Desai
Ludwig’s Angina
Bilateral infection of the submandibular, Involves muscle,

Ludwig’s Angina
sublingual & submental areas connective tissues & fascia
Usually Mixed aerobic In adults, more likely to

Ludwig’s Angina
odontogenic & anaerobic extend into the mediastinum
Symptoms & Signs
Painful swelling of
Fever Dysphagia Odynophagia Poor dentition Dysphonia
submandibular area
Edema of Edema at floor Potential for airway
Voice changes Trismus
upper neck of mouth compromise
Immediate ENT Definitive airway

Treatment? Antibiotics
consultation management
Airway Awake fiberoptic

Complications
compromise intubation
Necrotizing Infections
Necrotizing Patients are

Infections critically ill
Symptoms & Signs
Altered mental + Crepitus on Potential for airway

Fever Tachycardia Hypotension
status exam compromise
Gas in deep Subcutaneous

Diagnosis? CT scan Pus pockets
tissues emphysema
Immediate surgical Definitive airway

Treatment? Antibiotics
consultation management
Extension of
Complications Mediastinum
infection
Mediastinal Great vessel Pleural & Pleural & Retroperitoneal

Risk of
extension erosion pericardial abscess pericardial effusion extension
Croup
PEDIATRICS
Parainfluenza Most common cause Peak at 2

Croup Larygnotracheobronchitis Due to
virus (50 %) of stridor 6 mo–3yr years
Symptoms & Signs
Nasal Low grade

Rhinorrhea Cough Prodrome
congestion fever
Barky cough Hoarseness Stridor Classic croup Sx
Most severe Sx 3–4 days Improvement
Subglottic
Diagnosis Clinical Plain films Steeple sign
narrowing
Nebulized epinephrine
Treatment Oral steroids
(Racemic or L-epi)
After epinephrine must

Disposition
observe for 3–4 hours
Bacterial Tracheitis
PEDIATRICS
Bacterial Can cause life-threatening Often a secondary 5–8 years of Clinically similar
Tracheitis airway obstruction infection after viral URI age to epiglottitis
Symptoms & Signs
Thick purulent Toxic Inspiratory &

Hx of viral URI High fever Stridor Cough sputum appearance expiratory wheeze
Hemophilus
Bacterial agents Staph aureus Strep
influenza
Diagnosis? Bronchoscopy
Plain film Irregular Subglottic narrowing

findings tracheal margins of trachea
Immediate ENT May require

Treatment? Antibiotics Humidified O2
(& Anesthesia) consultation urgent intubation
490 B. Desai
Dental Emergencies
Odontogenic Infections
Odontogenic From infected tooth Following tooth Polymicrobial

Abscess (1-21 days after onset of pain) extraction (aerobes & anaerobes)
Deep neck Most deep neck infections arise from Fascial layers of head & neck have
infection tidbits dental source (esp. mandibular teeth) potential spaces for spread of infection
Localized dental Pulpitis or dental Intermittent pain worse with Rx = root canal
pain caries extremes of temperature or extraction
Inflammation of Inflammation of soft tissues surrounding the Rx = irrigation +

Pericoronitis Due to
gum overlying tooth crown of partially erupted teeth esp. 3rd molars antibiotics
Periapical Most common cause Inflammation & infection Can erode into
abscess of severe dental pain of apical aspect of tooth cortical bone
Periapical abscess draining

Parulis
externally on gums
Infections of May spread to Parapharyngeal

Neck Mediastinum
molar teeth masticator space space
Infections of anterior
Spread to neck
mandibular teeth
Infections of other Spread

mandibular teeth sublingually
Penicillin is 1st
Treatment Clindamycin OR Metronidazole I&D
line drug
Periostitis and Alveolar Osteitis and Post-extraction Bleeding
1-2 days after Trauma of Ice packs & NSAID’s ±

Periosteitis Due to Rx
extraction surgery Head elevation Narcotics
Muscular injury
Complications Trismus Due to TMJ injury Infection
during anesthesia
2-5 days after Dislodgement of Localized

Alveolar osteitis Due to Leads to
extraction clot from socket osteomyelitis
Preexisting pericoronitis Hormone Traumatic

Risk factors Smoking
or other dental process replacement therapy extraction
Local & topical Ribbon gauze pack with

Treatment? Irrigation Antibiotics
anesthesia oil of cloves or eugenol
Referral to dentist
Disposition?
within 24 hours
Post-extraction Displacement of
Bleeding clot
Firm pressure to Topical thrombin/ Cautery with Injection of Lidocaine with epinephrine
Treatment? OR
extraction site Gel foam silver nitrate may tamponade the bleeding
Periodontal Pathology
Gingival Plaque along

Gingivitis Bleeding Due to
inflammation gingiva
Progression of Forms sulci and Bacteriodes

Periodontitis Tooth loss Due to
gingival inflammation periodontal pockets gingivalis
Risk factors for Down’s Diabetes

HIV
severe Periodontitis syndrome mellitus
Most common
Gum disease
cause of tooth loss
Periodontal Entrapment of plaque & other Severe gum Warm saline Antibiotics &
abscess debris in the periodontal pocket pain rinses analgesia
Penicillin is 1st
Treatment Clindamycin OR Metronidazole I&D
line drug
Acute Necrotizing Ulcerative Gingivitis (ANUG)
Trench Caused by: Spirochetes Can be very May spread from gums to
ANUG
mouth & Fusobacteria destructive tissues of face to facial bones
Poor oral Immune Prior necrotizing

Risk factors
hygiene diseases (HIV) gingivitis
Gingival Ulcerated intradental

Diagnosis Severe pain
bleeding papillae
Symptoms & Signs
Red, swollen Ulcerations on Abnormal

Painful gums Foul breath Fever Malaise
gums gums tooth mobility
Pseudomembrane
Lymphadenopathy
formation
Treatment Clindamycin OR Metronidazole

492 B. Desai
Gingival Hyperplasia
Associated with May lead to significant

Gingival Hyperplasia
medications gum bleeding
Phenytoin
Medications
causing Calcium channel
Cyclosporine
gingival blockers
hyperplasia
Dental Trauma: Introduction
Younger patients Pulp of anterior Greater involvement of Older patients have

Leads to
(<12) teeth is large pulp with dental fractures smaller pulp chambers
Dental trauma Length of time Relationship of

outcome prior to treatment fracture to the pulp
Ellis Fractures
Involves enamel No specific Refer to dentist for

Ellis Class I
only treatment cosmetic repair
Ellis Class II Yellowish tinge Increased sensitivity to

Involves dentin
(most common) on white enamel temperature extremes
Early Cover exposed Referral to dentist Delay in treatment increases

Treatment
identification dentin in 24 hours chance for pulpal necrosis
May see blood

Ellis Class III Exposes pulp
from pulp
Early Cover exposed Urgent referral to Delay in treatment increases

Treatment
identification pulp dentist in 24 hours chance for pulpal necrosis
Dental Trauma
Concussion of Trauma to supporting No tooth Tenderness to

Tooth structures of tooth mobility percussion
Treatment Analgesia Soft diet Dental referral
Subluxation of Trauma to supporting Tenderness to

Tooth mobility Mobile tooth
Tooth structures of tooth percussion
Higher incidence
Treatment Analgesia Soft diet Dental referral
of pulpal necrosis
Avulsion of Avulsion of tooth from

Tooth surrounding bone
Quick 1% loss of survival Rinse tooth, do May transport in milk,

Treatment
replantation per minute not scrub saliva or Hank’s solution
Only for May injure No dry storage
permanent periodontal
teeth ligament
After Splint tooth in Urgent dental

Antibiotics
replantation place referral
494 B. Desai
Neck Masses
Neck
PEDIATRICS
Neck Masses Neoplastic Congenital Infectious
75% of lateral neck masses present Most common cause of unilateral neck
In adults > 40
for > 6 weeks are malignant mass is squamous cell carcinoma
Acute retroviral Generalized Risk factors for

syndrome adenopathy HIV
Reactive
Hemangioma lymphadenopathy
Branchial cleft cyst Branchial cleft cyst Thyroglossal duct

Infant Lymphangioma (lateral location) Child
(lateral location) cyst (central location)
Rhabdomyosarcoma
Reactive
Metastatic cancer
lymphadenopathy
Branchialcleft cyst Young Thyroglossal duct Salivary gland

Adult Thyroid disease
(lateral location) adult cyst (central location) disorder
Lymphoma
Mononucleosis Tuberculosis Lymphoma
(Hodgkin’s)
Branchial Cleft Cysts
PEDIATRICS
Branchial Cleft Congenital epithelial cyst on the lateral part of the neck due to
Cysts failure of obliteration of the second branchial cleft
Symptoms & Signs
Painless mass Fluctuant mass Lateral location
Treatment? Surgical excision
May become May enlarge Treat with Excision after

Complications
infected after infection antibiotics treatment
Thyroglossal Duct Cysts
PEDIATRIC
Thyroglossal Fibrous cyst that develops from persistent Usually in

Duct Cysts thyroglossal ducts children
Symptoms & Signs
Usually
asymptomatic mass Soft & mobile Bluish hue
Treatment? Surgical excision
May become May enlarge Treat with Excision after

Complications
infected after infection antibiotics treatment
Larynx Trauma
Compression of larynx on Laryngotracheal Cartilage

Larynx Trauma Mucosal tears
anterior cervical spine separation fractures
Can be due to direct trauma,

Larynx Trauma
hyperflexion/extension, or rotation
Clothesline Motorcycle, ATV, Crushes thyroid May cause immediate Tracheostomy required
injury Football cartilage asphyxiation in these patients
Symptoms & Signs
Anterior neck
Hoarseness Dysphagia Stridor Dyspnea Cough Hemoptysis
pain
Subcutaneous Vascular injury = expanding
Aphonia Apnea hematomas, bruits, pulse deficits
emphysema
Diagnosis? CT scan
Maintenance of Endotracheal Avoid

Treatment OR Tracheostomy
airway intubation cricothyrotomy
496 B. Desai
Edema of Upper Airway
Angioedema
Rapid paroxysmal swelling of dermis, Involves face,

Angioedema
subcutaneous tissue & mucosal tissues extremities & genitalia
Swelling is not NO Pitting &

Angioedema
symmetric Pruritis
Airway All require prompt Protect airway if

Mortality Due to
obstruction airway assessment necessary
Types of Congenital (C1 IgE mediated Reaction to ACE

Idiopathic
angioedema esterase deficiency) reaction inhibitor
C1 esterase Respond poorly Epinephrine may Fresh frozen C1 esterase

deficiency treatment to standard Rx help plasma inhibitor
ACE inhibitor
Epinephrine H1 blocker H2 blocker Steroids
treatment
Uvular Edema
Quincke’s
Uvular Edema
edema
Same factors as Also with Peritonsillar

Uvular Edema Due to Epiglottitis
angioedema infections abscess
Treatment Steroids Antihistamines

Soft Tissue Lesions
Candidiasis
White cottage-cheese like Candida Commonly affects the

Candidiasis Due to
plaques on a erythematous base albicans mouth and throat
HIV
Chemotherapy Antibiotic use
Predisposing
factors for
Dentures Malnourished
Candidal state
infection
Diabetes mellitus Steroids
Extremes of age
Antifungal Topical nystatin

Treatment Fluconazole OR
agents or clotrimazole
HSV infections
Most commonly HSV 2 can also Cannot distinguish

HSV 1 But…
affects oral cavity occur orally between both
Tingling or burning along May occur 3 days

Prodrome Fever Lymphadenopathy
trigeminal distribution before oral lesions
Herpes Vesicular lesions Painful ulcers on oral Decreased fluid

Leads to Leads to
gingivostomatitis appear then rupture mucosa & gingiva intake
Secondary Hard palate &

Lips
infection gingiva
Diagnosis PCR OR Tzanck Smear OR Viral culture
To promote
Treatment Analgesia Acyclovir OR Valacyclovir
hydration
Non-GU Herpetic Group of Non-surgical

Corneal ulcers
pathologies whitlow vesicles on digits treatment
Painful vesicles on
GU pathologies
anus & genitalia
Congenital
Complications Part of TORCHES Encephalitis
transmission
498 B. Desai
Aphthous Stomatitis
Aphthous Red macules

Leads to Painful eschar May be multiple
stomatitis that ulcerate
Aphthous Due to cell mediated immune response to an

stomatitis unidentified triggering agent
Aphthous Usually resolve

stomatitis in 10–14 days
Treatment Topical steroids
Herpangina
PEDIATRIC
Caused by Fecal-oral Spreads to other Usually lasts

Herpangina
Coxsackievirus A transmission children 7–10 days
Symptoms & Signs
1–2 mm oral
High fever Sore throat Headache Malaise Dysphagia Vomiting
vesicles
Oral vesicles Rupture of Painful ulcers

Natural history Constitutional Sx 1–2 days
appear vesicles remain
Vesicle Posterior
Tonsils Soft palate Uvula
appearance pharynx
Vesicles spare Gingiva Tongue Buccal mucosa
Treatment Analgesia Hydration

Distinguished from
Herpes gingivostomatitis
which does affect gingiva
Complications? Rare
Intraoral and Tongue Lesions
Leukoplakia
Whitish plaque on Cannot be Most commonly Most common

Leukoplakia
mucosal surfaces scraped off on buccal mucosa oral precancer
Candidiasis
Alcohol
Tertiary syphilis
Predisposing
factors for
Leukoplakia
Trauma Tobacco
UV radiation HPV
Strawberry Tongue
Strawberry Prominent red spots Erythrogenic toxin producing

Due to
Tongue on white background Streptococcus pyogenes
Antibiotics for
Treatment
Group A Strep
500 B. Desai
Oral Cancer
90 % are Most commonly

Oral Cancer
squamous cell on tongue
Symptoms & Signs
Pain from Most hard lesions Nonhealing Bleeding from

Drooling Hard lesions
ulcerations are painless ulcer ulcers
Fixed lesions to
Lymphadenopathy
surrounding tissue
Candidiasis
HIV Alcohol
Predisposing
factors for Oral
cancer Tobacco
HPV (esp. chewing)
Chronic iron
Excessive sunlight
deficiency
exposure
anemia
Salivary Gland Disorders
Viral Parotitis (Mumps)
PEDIATRIC
Acute infection Uni- or bilateral swelling Caused by Most common

Mumps
of the parotids (usually bilateral) paramyxovirus <15
Symptoms & Signs After 2–3 wk incubation
Salivary gland Parotid is

High fever Myalgias Headache Malaise Arthralgias
swelling painful & tense
No pus from
Mumps
Stensen’s duct
Elevated Leukocytosis with

Diagnosis Clinical Labs
amylase lymphocyte predominance
Orchitis in 20–
Complications Pancreatitis Myocarditis Polyarthritis Meningitis
30 % males
502 B. Desai
Suppurative Parotitis
Suppurative Bacterial infection Impaired Retrograde migration Staph aureus is

Due to
Parotitis of parotid salivary flow of bacteria from mouth most common
Post- Chronic
Risk factors Medications Dehydration Sialolithiasis
operative illness
Symptoms & Signs
Skin over parotid Skin over parotid Pus expressed from

Fever Trismus
is erythematous is tender Stensen’s duct
Normal Leukocytosis with

Diagnosis Clinical Labs
amylase neutrophilic predominance
Imaging U/S OR CT
Optimize salivary Massage & heat

Treatment Hydration Antibiotics
flow (lemon drops) to parotid
Sialolithiasis
Formation of calcium Most common

Sialolithiasis
stone in a salivary duct in men 30–60
80 % occur in Due to ascending course

Sialolithiasis
submandibular gland & viscous secretions
Predisposition to
Diabetes Dehydration
sialolithiasis
Symptoms & Signs
Pain worse Unilateral May palpate

swelling Tenderness Gland is firm
with meals stone in duct
May see on X-ray

Diagnosis Clinical
or CT
May attempt to milk Antibiotics for

Treatment Analgesia Sialogogues
stone from duct concurrent infection
Secondary Staph Recurrent

Complications Strictures
infection obstruction
Facial Infections
Facial Cellulitis
Most commonly caused by Streptococcus Inciting factors

Facial Cellulitis
pyogenes (GABHS) & Staph aureus of piercings
Symptoms & Signs
Erythema Edema Warmth Pain at site
Imaging as needed for

Diagnosis Clinical
suspicion of deep infection
Removal of
Treatment Analgesics Antipyretics Antibiotics
inciting factors
Erysipelas
Cellulitis affecting epidermis, Most commonly Can affect the

Erysipelas
upper dermis & lymphatics affects the LE face
Streptococcus pyogenes
Erysipelas
is most common
Bullous 50 % caused by
More severe form
erysipelas MRSA
Red, raised puffy Sharply defined

Diagnosis
skin appearance border
Treatment Antibiotics
504 B. Desai
Impetigo
Superficial Discrete amber

Impetigo OR Bullae Highly infectious
epidermal infection crusts
Staph aureus Streptococcus

Impetigo OR Staph
alone pyogenes (GABHS)
Nonbullous Start as red, Have surrounding Break down into

impetigo moist vesicles area of redness honey-crusted lesions
Rapidly enlarging Become flaccid bullae Suggests Staph

Bullous impetigo
vesicles with clear yellow fluid infection
Antibiotics to cover Dicloxacillin Mupirocin

Treatment
Staph & Strep Cephaloporins ointment
Not prevented
Complication Glomerulonephritis
by antibiotics
Other ENT Emergencies
Post-tonsillectomy Bleeding
Post-tonsillectomy Most occurs 5–10 Sloughing of clot or Usually see a

Due to
Bleeding days after surgery eschar from tonsil bed gray-white eschar
Initial Emergent ENT

Sit upright NPO IV hydration
stabilization consultation
Coagulation Emergent ENT

Labs CBC Type & Cross
parameters consultation
Direct pressure Packing soaked with

Treatment
to bleeding epinephrine or thrombin
Airway Hemorrhagic
Complications
obstruction shock
Trigeminal Neuralgia
Trigeminal Most common Causes severe

Neuralgia cranial neuralgia facial pain
Trigeminal Maxillary branch of the 5th Most common in

neuralgia cranial nerve is most common females & adults 30–60
Trigeminal Almost always

neuralgia unilateral
Trigeminal Paroxysms of electric- Followed by pain May be triggered by

neuralgia like pain in face free periods stimulation of a trigger point
Trigeminal Has associated contraction of

neuralgia face & masticatory muscles
Referral to
Treatment Carbamazepine
neurologist
Causes of Trismus
Dystonia
Epiglottitis Causes of Trismus Tetany
Hypocalcemia
Tetanus
Abscess
Ludwig’s angina
Peritonsillar
abscess
506 B. Desai
Ramsay Hunt Syndrome
Ramsay Hunt Reactivation of preexisting Herpes Zoster virus

Syndrome in the Geniculate ganglion of the Facial nerve
Geniculate Facial Touch to part of external Taste to anterior

ganglion movement ear and ear canal 2/3 of tongue
Symptoms & Signs
Facial nerve Loss of taste in Erythematous vesicular rash in ear

Ear pain Dry mouth Dry eyes
paralysis anterior tongue canal, tongue &/or hard palate
Hearing loss Tinnitus Vertigo
Treatment Acyclovir OR Valacyclovir Steroids
Cavernous Sinus Thrombosis
Vasculature Veins of face, oral cavity, middle ear &

Tidbit mastoid area drain to cavernous sinus
Cavernous Sinus Blood clot within Complication of a Staph aureus

Thrombosis the cavernous sinus central facial infection most common
Sphenoid or Dental infection Periorbital or

Etiology Nasal furuncle
ethmoid sinus or extraction orbital cellulitis
Symptoms & Signs
Toxic
Chemosis Ptosis Eyelid edema Facial edema Proptosis Fever appearance
Pupillary dysfunction Cranial nerve dysfunction Impaired Retinal

Papilledema
(mydriasis from III dysfunction) (III, IV, V, VI (most common)) corneal reflex hemorrhages
Decreased
visual acuity Headache
Diagnosis CT or MRI
Triad
Head or neck infection +
ophthalmoplegia + venous
Emergent ENT obstruction
consultation
Oculomotor Pituitary
Complications Blindness Hemiparesis
weakness insufficiency
Airway Foreign Body (AFB)
PEDIATRICS
Airway Foreign Most occurs 1–3 Must consider AFB in young Sudden coughing &
Body years of age child with respiratory Sx choking
Symptoms & Signs
May be Decreased
Stridor Hoarseness U/L wheezing
asymptomatic breath sounds
May be normal in May be normal in 75% of AFB in kids

Diagnosis Plain films
50% of tracheal FB 25% of bronchial FB < 3 are radiolucent
Signs of U/L obstructive Ball valve obstruction

Consolidation Atelectasis
radiolucent FB emphysema of affected side
Direct Endotracheal ENT/Anesthesia

Treatment
laryngoscopy intubation consultation
508 B. Desai
Vertigo
Introduction
Perception of movement Peripheral

Vertigo Due to Central causes OR
where none exists causes
Caused by
Central vertigo Cerebellum Brainstem
central disorders
May not necessarily
be distinct
Peripheral Disorders affecting Vestibular
vertigo 8th cranial nerve system
Central Peripheral
Onset Slow Sudden
Severity Less intense Severe spinning
Instances Constant Paroxysmal
Movement aggravated No Yes
Nausea Infrequent Frequent

Horizontal, rotatory-
Nystagmus Vertical vertical
Fatiguability No Yes
Hearing loss No Possible
Tinnitus No Possible
TM No Possible
CNS Symptoms Yes No

Symptoms of Peripheral Vertigo

Intense
symptoms
Tinnitus Nausea/Vomiting
Symptoms of
Peripheral
Vertigo
Hearing loss Diaphoresis
Photophobia
Symptoms of Central Vertigo
Diplopia
Visual Symptoms of
Dysarthria
abnormalities Central Vertigo
More likely to have

neurologic
symptoms & signs
Headache
510 B. Desai
Peripheral Vertigo
Benign Paroxysmal Positional Vertigo (BPPV)

Most common cause of Canalolithiasis – delayed activation of posterior
BPPV Due to
recurrent peripheral vertigo semicircular canal due to impaired endolymph flow
Females > males

BPPV
Mid 50’s
Precipitated by
BPPV
head turning
Position Intensity peaks then diminishes

BPPV 1–5 sec Nystagmus Vertigo
change Duration 5–40 sec
Vertigo & nystagmus fatigue with

BPPV
repeated head movement
Dix-Hallpike
Diagnosis
maneuver
No hearing problems
BPPV
or tinnitus
Particle repositioning
Treatment Medications
maneuvers
Bottom right image (Reprinted from Önerci TM. Vertigo. In: Önerci TM, editors. Diagnosis in otorhinolaryngology: an illustrated guide.
Meniere’s Disease
Meniere’s Increased endolymph Usually unilateral, Females = males

Disease within cochlea may be bilateral 1st attack usually > 65
Meniere’s Sudden onset Roaring Unilateral ear

N/V Hearing loss
Disease vertigo tinnitus fullness
Meniere’s 20 min to 12 Frequency of attacks vary

Disease hours from weekly to monthly
Salt restricted
Treatment Medications
diet
Vestibular Neuronitis
Vestibular Probably viral in

Acute onset URI
Neuronitis etiology
Vestibular
Last several days Does not recur
Neuronitis
Vestibular May lasts for + Unilateral

Intense vertigo Tinnitus
Neuronitis days to weeks hearing loss
Vestibular Worse with Will have positional

Neuronitis change in position nystagmus
Vestibular Patients may have

Neuronitis unsteady gait
512 B. Desai
Perilymph Fistula
Opening in Allows pneumatic changes to be
Perilymph Fistula
round window transmitted to the vestibular system
Causes of round Pressure

Infection Trauma
window pathology changes
Sudden onset of Unilateral

Perilymph Fistula
vertigo hearing loss
Nystagmus with
Diagnosis Hennebert’s sign
pneumatic otoscopy
Treatment Symptomatic Bed rest
Labyrinthitis
Infection of Associated with Bacterial etiology as a
Labyrinthitis Viral in etiolgy
labyrinth measles & mumps sequelae of otitis media
May be caused by
Labyrinthitis
ototoxic medications
Sudden onset of Middle ear

Labyrinthitis Hearing loss
vertigo findings
Complications of
Meningitis
bacterial labyrinthitis
Eighth Cranial Nerve Lesions

Eighth Cranial Produce mild
Nerve Lesions vertigo
Eighth Cranial Acoustic

Meningiomas
Nerve Lesions schwannomas
Eighth Cranial Gradual onset of Hearing loss

Unsteady gait
Nerve Lesions vertigo precedes vertigo
Referral to
Treatment
neurosurgeon
Cerebellopontine Angle Tumors

Cerebellopontine Ipsilateral facial Corneal reflex Cerebellar
Deafness Ataxia
Angle Tumors weakness deficit signs
Cerebellopontine Acoustic
Meningiomas Dermoids
Angle Tumors neuromas
Referral to
Treatment
neurosurgeon
Posttraumatic Vertigo and Post-concussive Syndrome

Post Traumatic Direct injury to Immediate in Associated with
Vertigo labyrinthine membrane onset nauseas & vomiting
Failure to evaluate for

Pitfall
temporal bone fracture
Closed head Exclude intracranial

Vertigo CT/MRI
injury hematoma
Vertigo due to Usually resolves

Labyrinthine trauma in weeks
Post concussive Gait

Dizziness N/V
syndrome unsteadiness
Treatment of
Symptomatic
Post Concussive
514 B. Desai
Central Vertigo
Cerebellar Infarction and Hemorrhage

Cerebellar Infarction Especially in the
Vertigo Not intense Ataxia
& Hemorrhage truncal area
Cerebellar Infarction Not always

Headache N/V
& Hemorrhage present
Cerebellar Infarction (+) Gait Conjugate eye deviation

VI nerve palsy OR
& Hemorrhage Romberg abnormalities away from side of lesion
Neurosurgical
Treatment
evaluation
Wallenberg Syndrome
Wallenberg Lateral medullary Vertigo is part of
Syndrome infarction of the brainstem the syndrome
Wallenberg Syndrome Loss of Facial Horner’s Weakness or paralysis of soft

ipsilateral findings corneal reflex numbness syndrome palate, pharynx & larynx
Dysphagia & dysphonia
Contralateral Loss of pain & temperature

findings in trunk & limbs
Wallenberg May see cranial

6, 7, 8 Leads to Vertigo N/V Nystagmus
Syndrome nerve abnormalities
Emergent neurosurgical
Treatment
consultation
Vertebrobasilar Insufficiency
Vertebrobasilar TIA of the May cause Usually resolve
Insufficiency brainstem vertigo within 24 hours
Bilateral Bilateral long

Other symptoms Diplopia Dysarthria Dysphagia
blindness tract signs
Vertebrobasilar May be provoked Turning head occludes

Insufficiency by position vertebral artery
Neurology
Treatment
consultation
Vertebral Artery Dissection

Vertebral Artery Stroke involving Caused by sudden rotation Trauma, diving
Dissection posterior circulation or extension of neck injury
Unilateral Horner’s
Symptoms Vertigo Headache
syndrome
Diagnosis CT/MRI
Multiple Sclerosis
Multiple Due to May lasts for Does not usually
sclerosis demyelination hours to weeks recur
Multiple Vertigo is not Prominent

sclerosis intense nystagmus
Multiple Ataxia may be Optic neuritis

sclerosis present may be present
Diagnosis MRI
Neurology Consider
Treatment
consultation steroids
516 B. Desai
Migraine-Related Vertigo
Migraine Related May be a symptom Develops over 5–20 min Does not usually
Vertigo of the aura and diminishes in 1 hour recur
Aura has manifestations of

Basilar migraine
vertebrobasilar insufficiency
Decreased Visual
Basilar migraine Vertigo
hearing disturbances
May have
Other symptoms Dysarthria Diplopia
decreased LOC
Treatment NO ergotamine Consult

Basilar migraine or sumatriptan neurology
Environmental Emergencies
Contents
Bites and Envenomations 518
Dysbarism 526
Electrical Injuries 531
High-Altitude Illness 535
Submersion 538
Temperature-Related Illness 540
Radiation 548
Biological Weapons 548
Chemical Weapons 552
Tetanus 554
M.R. Marchick, MD

DOI 10.1007/978-3-319-30838-8_9
Bites and Envenomations
Bees/Wasps
Bee & Wasp Leading cause of fatalities from

stings stings & bites of arthropods
Majority within May occur up to 6 May recur 8–12 hours Most severe
Anaphylaxis? But…
15 minutes hours afterwards after initial reaction reactions occur early
Immediately Infection is
Stinger present? Wash area
remove stinger uncommon
Oral Elevation if
Local reactions NSAIDs Ice
antihistamine significant edema
Systemic 0.3-0.5 mg adults Systemic H1 & Systemic

Epinephrine
reaction 0.01 mg/kg (up to 0.3 mg in kids) H2 antagonists steroids
1:1000
Airway Early airway Inhaled

Bronchospasm?
compromise? protection β-agonist
Continued
IV crystalloids Pressors
hypotension?
Gave epinephrine Minimum 6 hours observation

in ED? for recurrence of Sx
Severe
ICU admission
anaphylaxis?
Systemic Epipen Explicit return

Discharge Allergist referral
reaction prescription instructions
Environmental Emergencies 519
Black Widow Envenomation
Black Widow Throughout Can trigger premature Potentially fatal

Spider continental US labor in pregnancy in children
Symptoms & Signs
Pinprick + Local edema + Local

Initial Sx sensation erythema
15 min –1 hour Can spread to Especially abdomen

Local cramping
later entire body and chest
Severe Sx Hypertension Vertigo Edema Dyspnea N/V Ptosis
Typical Occasionally
resolution 8–12 hours
2–3 days
Tetanus as Local wound

Initial Treatment Ice application needed care
Benzodiazepines For pain and Elevated

ED Treatment Opiates spasm control BP? Antihypertensives
Asymptomatic after 6 Discharge

hours observation?
Severe Latrodectus
Pregnant Children Refractory HTN neurologic sx antivenin
Brown Recluse Envenomation
Primarily south-
Brown Recluse central US
Release of Local tissue Potential severe

Envenomation Vasoconstriction hemolytic enzymes hemolysis in children
necrosis
Symptoms & Signs
Several hours
Local Sx Bull’s eye lesion Local pain after bite
Usually due to
Systemic Sx F/C N/V Malaise Petechiae hypersensitivity reactions
Liver failure
Severe Sx Renal failure (Jaundice) DIC
Tetanus as Local wound Antibiotics if

Treatment Pain control needed care local infection
Consider Prevents local

Medication Dapsone effects
Consider surgical Consider

Severe Sx consultation hyperbaric oxygen
Mammalian Bites
Bites: Introduction
Copious irrigation
Scrub with soap

Evaluate for Initial wound & water if
retained FB or care concern for
teeth rabies
Update tetanus if Debridement if

needed necessary
Avoid primary Immune > 6–12 hours

wound closure compromised after injury
Immune
compromised
Wounds requiring
surgical repair Cat bites
Treat
uninfected
wounds
Hand wounds Human bites
Deep dog bites

Rabies
Raccoons
Most common
reservoir in US
Foxes Rabies reservoirs Bats

Responsible for
most cases
Skunks
Rats
Domesticated Mice
rabbits
Hamsters Squirrels
No prophylaxis
Guinea pigs Chipmunks
Gerbils
Rabies Vaccination
Healthy dog or May observe for Develops signs

Immunize
cat? 10 days or symptoms?
Immunize
Suspect rabies?
immediately
Contact local Consider Immunizing

Unknown?
authorities immediately
Bite from Immunize

OR Exposure to bats
reservoir animal immediately
Rabies Provides a delayed Must be given in Anterolateral Never in gluteal

vaccination antibody response deltoid thigh ok in kids region
Rabies
Days 0, 3, 7, 14
vaccination
Rabies Provides immediate Give as much at Give remainder

immunoglobulin antibody response site as possible distant from vaccine
Rabies
Symptoms Infected saliva
#1 cause
Spreads distally Bite deposits

diffusely into virus in muscle &
Pathophysiology
periphery subcutaneous
tissue
Ascends into CNS Virus enters distal Long

axon incubation
Site of Negri bodies
Deep scratches
Laboratory Other means of Mucous membrane

exposure transmission contact with virus
Negri body Eosinophilic (pink) intracellular
site of viral replication
Pathognomic Organ
transplantation
Rabies Symptoms and Signs

Incubation
period 20–90 days
Symptoms & Signs
Incubation
20–90 days
period
Prodrome
phase 1–7 days Fever Malaise Dyspnea Flu-like Sx
Acute neurologic Onset of signs

phase 7–10 days 80 % “Furious” 20 % “Dumb”
of CNS disease
“Furious” Encephalitic High fever Disorientation Agitation Hallucinations ↑ Salivation
Hydrophobia Aerophobia
“Dumb” Paralytic Fever Paralysis
Untreated? Coma Eventual death

Cat Bites and Scratches

Cats have sharp, Deeper Including bones, High risk of
Cat Bites
narrow teeth inoculation tendon sheaths infection
Primary closure? Avoid
Pasteurella Fairly rapid Amoxicillin-

Organism Treatment
multocida onset of action clavunate 1st line
Cat scratch Bartonella 1–2 week

disease henselae incubation
Cat scratch Region of painful, Flu–like Rare severe multi- Generally self-
disease matted lymph nodes symptoms system involvement limited
Severe case? Azithromycin
Do not I &D May cause

Pitfall
lesions scarring/fistulae
Dog Bites
Most common
Pasteurella Streptococcus Staphylococcus Anaerobes
organisms
Capnocytophaga Encapsulated
canimorsus bacterium
Alcoholics
Immune Sepsis Renal failure
Capnocytophaga Post-splenectomy May lead to
canimorsus compromised pt DIC Death
Immunosuppressant
Capnocytophaga Rarely after cat

canimorsus bites
Risk of infection Immune Give Amoxicillin-

Hand bites
increases compromised prophylactic Abx clavunate 1st line
Not at risk for

Keflex OR TMP-SMX
Capnocytophaga?
Marine Envenomation
Jellyfish Stings
Wash area with Fresh water may cause
Jellyfish Stings Increases pain
sea water discharge of nematocysts
Symptoms & Signs
Erythema Local pain Urticaria
Stinger or tentacles Remove tentacles

identified? with forceps
Wash with Isopropyl Application of hot water Update tetanus

ED treatment OR
vinegar alcohol (45°C) also effective as needed
Indo-Pacific box Often rapidly

jellyfish envenomation fatal
Stingray Stings
Barbed wire Causes Followed by
Stingray stings
apparatus laceration envenomation
Symptoms & Signs
Local injury Local pain Nausea Flushing Sweats Diarrhea Muscle cramps
Deactivates the
ED treatment Hot water
toxin
Snake Bites
Snake Envenomation
Water
Pit Vipers Rattlesnakes Copperheads
moccasins
Spade-shaped Presence of pit between Double row of

Pit Vipers Elliptical eyes
head eye and nostrils caudal plates
Non-venomous Single row of

Rounded head Rounded eyes
Snakes caudal plates
Eastern coral Sonoran Coral Much less dangerous

Elapids
snake (SE US) Snake (AZ, NM) than eastern variety
Red on yellow, Red on black,

Coral Snake King Snake
kill a fellow venom lack
Pit Viper Envenomation

Tissue If no evidence of tissue Up to 25 %
Envenomation Snake bite Dry Bite
Injury injury after ≥ 8 hours of bites
Symptoms & Signs
Worsening
Local Pain Edema Ecchymosis
symptoms
Any Treat with
Systemic AMS Hypotension Tachycardia Paresthesias
Sx antivenom
Coagulopathy Platelets Fibrinogen INR Abnormal?
Immobilize limb in May use Tourniquet use contraindicated,

Initial Treatment
neutral position constriction band as is suction/incision
Serial measurements of limb Mark progression of erythema/ Monitor for

ED Treatment
circumference above & below bite edema every 30 min compartment syndrome
Laboratory Periodic measurement of

investigations Coags, Fibrinogen, CBC
Initial dose 4–6 Give additional if local Additional 2 vials 6,12,18 hours
Antivenom
vials IV control not achieved after local control achieved
Antivenom for Same as adult

children dose
Consider blood products Antivenom most effective

Active bleeding?
in addition to antivenom treatment for coagulopathy
Eastern Coral Snake Envenomation

Eastern Coral Snake Neurotoxic Little tissue Can lead to
Envenomation venom injury respiratory failure
3–5 vials of May be difficult

Definite bite?
antivenom IV to locate
Antivenom Supportive care May need airway

ICU admission
unavailable? protection
Antivenom for Same as adult

children dose
Sonoran Coral Milder Antivenom not

Snake symptoms usually needed
Dysbarism
Introduction
If pressure doubles, Air trapped in body is compressed

Boyle’s Law P1V1 = P2 V2 Thus…
volume must be cut in ½ during descent as pressure increases
Each 33 feet below sea level

corresponds to pressure increase of
1 atm
Barotrauma of Descent: Barotitis Media
Middle ear Most common diving-

Barotitis media
squeeze related complaint
Descent
Can lead to
nystagmus/
vertigo Pressure on TM
from water in ear
Due to caloric canal increases
stimulation
Additional air not

Physiology
forced into middle
ear via auditory
tubes (occlusion)
+ Rupture of TM Using Valsalva

maneuvers
Occlusion
Increased pain
Antibiotics if TM
Treatment No diving Decongestants
rupture
Barotrauma of Descent: Barotitis Interna
Descent
Pressure on TM
Symptoms begin from water in ear
canal increases
Damage to inner Barotitis

Additional air not
ear structures Interna
forced into middle
ear via auditory
Pressure wave tubes (occlusion)
forms if Valsalva Using Valsalva
later performed maneuvers
Occlusion
Pressure gradient
results in
outward
distention of
round window
Symptoms & Signs
Nausea & Severe

Hearing loss Tinnitus Vertigo
Vomiting nystagmus
5–7 days bed rest Avoid Valsalva Urgent ENT referral

Treatment with no diving Decongestants maneuver for hearing loss
Barotrauma of Descent: Barotitis Externa
Descent
Preexisting
Bloody otorrhea blockage of
external auditory
canal
Barotitis Externa (e.g., cerumen)
Increased pain
Air in canal not
replaced by water
Increased
pressure with
descent
Remove any Antibiotics for

Treatment No diving Keep canal dry foreign bodies otitis externa
Sinus Barotrauma
Descent
Symptoms occur Obstructed ostia
Sinus Barotrauma
No air entry to
equalize pressure Due to polyps or
during descent congestion
Symptoms & Signs
Mucosal Infraorbital nerve

Sinus pain Epistaxis
edema paresthesias
Treatment Decongestants Antibiotics
Barotrauma of Ascent
Barotrauma of Trapped air expands

Ascent as pressure decreases
Middle ear
barotrauma of
ascent
Sinus barotrauma
Barodontalgia
of ascent
Related Conditions
Decompression Pulmonary
Sickness (DCS) barotrauma
GI pain
Pneumomediastinum
Arterial gas Pulmonary

Barotrauma Pneumothorax
embolism
Alveolar
hemorrhage
Pulmonary Barotrauma
Pulmonary Rapid uncontrolled Expansion of Must exhale on

“Burst lung”
barotrauma ascent gases ascent
Symptoms & Signs
Potential hemothorax Arterial gas

Pneumothorax Pneumomediastinum Pneumopericardium
from lung injury embolism
Arterial Gas Embolism
Arterial Gas Damage to Air entry into Embolize to Symptoms develop within
Embolism pulmonary vein systemic circulation any site 10 minutes of surfacing
Coronary
Arterial Gas Sudden arteries
Embolism occurrence of Sx Cerebral
arteries
Retinal
arteries
Symptoms & Signs
LOC (the rule) Hemiplegia Confusion Seizures Blindness Deafness Vertigo
Neurologic event most

common presentation
Myocardial
infarction
If embolizedto
coronaries
Neurologic Pulmonary Arterial gas Treat with

symptoms barotrauma embolism recompression
Nitrogen Narcosis
Nitrogen Disorder at From breathing May result in High concentrations of

narcosis depth compressed air drowning nitrogen are neurotoxic
Symptoms & Signs
Decreased Decreased
Euphoria Confusion Disorientation
judgment motor control
Controlled Decrease the amount of

Treatment
ascent dissolved nitrogen in the brain
Decompression Sickness
Decompression Dissolved N2 bubbles Causes obstruction,

Rapid ascent
Sickness re-enter tissues inflammation, & thrombosis
Decompression Symptoms in any part of body

Sickness minutes to hours after ascent
Musculoskeletal Cutaneous
DCS Type 1
symptoms symptoms
Cardiovascular
DCS Type 2 CNS symptoms
symptoms
Symptoms & Signs
Deep pain in muscles,

“The bends” Musculoskeletal
tendons, ligaments or fascia
Mottling Pruritis Cutaneous
“The chokes” Cough Chest pain Dyspnea Pulmonary
Rapid onset ascending Autonomic

Spinal Cord
paralysis dysfunction
CNS
“The staggers”
(Vestibular) Ataxia Vertigo Hearing loss Tinnitus
Barotrauma of Ascent Treatment
Pneumomediastinum Supportive care
Immediate needle
Pneumothorax Thoracostomy
if tension PTX
Arterial gas Rapid recompression

100 % O2 Supine position
embolism with hyperbaric O2
Rapid recompression
DCS 100 % O2
with hyperbaric O2
Nitrogen washout
Recompression Therapy
Recompression Definitive Decompression Arterial gas

For
Therapy treatment sickness embolism
Not having a low Subtle symptoms may develop Minor symptoms

Pitfalls Due to
threshold for treatment after treatment of major symptoms may progress
Time frame for Up to 14 days after

recompression? symptom onset
Electrical Injuries
Introduction
Electrical Injuries High voltage > 1000 Volts Low voltage <1000 Volts
Burns are severe Burns are minor

Significant injury More common
& death
Electrical Arc No passage of current Thermal burn + blast

Burns through tissues injury may still occur
Longer contact Increased Resembles

Higher voltage Worsened injury
time trauma crush injury
Alternating Household electricity, Associated Can produce Worsened effects at a given

Current power lines with V. fib tetany voltage compared with DC
Victim may not
be able to let
go of source
Batteries & Associated with

Direct Current
lightning asystole
Depend on current Increase injury with

Injuries?
& tissue resistance increased resistance
Skin & neurovascular exam may underestimate

Pitfall
injury with deep electrical burns
Electrical Injuries
Cardiac
dysrhythmias
Spinal cord injury Hearing loss
Cognitive deficits Respiratory arrest
Peripheral nerve Electrical

injury Gangrene
Injuries
Cataracts Rhabdomyolysis
GI injury Cutaneous burns
Compartment
syndrome
Can occur with < 1
second exposure
if high-voltage
Mechanisms of Direct tissue damage Trauma from

Injury from electrical current Thermal burn tetanic conduction Blast injury
Burn with damage to Eschar Potential

Oral Electrical Child bites
labial artery Vasospasm separates ~ 5 severe
Cord Burn electrical cord controlled by eschar days later bleeding
Electrical Injury Management
Electrical Injury Careful physical Determine path current Predict tissues at

EKG
Management exam took through body risk
High voltage Continuous cardiac

Abnormal EKG Symptomatic
injury monitoring
Further Compartment Other traumatic

Based on H&P Rhabdomyolysis
evaluation syndrome injuries
< 240 Volts AC Normal EKG Normal exam Discharge
Observe 6 hours
< 600 Volts AC Any symptoms OR EKG abnormality
(or longer)
> 600 Volts AC Admit

Lightning Injury
Lightning often Deep tissue injury Lightning has direct current

Lightning “Flashover”
travels over body less common with high voltage & current
Direct strike Most severe
Nearby object Current travels

Side Flash
struck through air to victim
Object being held

Contact strike
by victim is struck
Current delivered
Ground current Ground is struck
across ground
Heat causes
Thermal burns Sweat OR Clothes burning
sweat to steam
Rapid expansion TM rupture

Blunt trauma Victim thrown
of air due to heat common
Rare extensive Rare renal

Lightning injury Rare deep burns
tissue damage failure
Rapid return of Paralysis of Secondary

Pathophysiology Initial asystole
sinus function respiratory center cardiac arrest
Immediate
Apnea
cause of death?
Possible permanent Cognitive Motor

effects? sequelae dysfunction
Lightning Injuries
Asystole
Most common
cause of death
Neurologic injury Ruptured TM
LOC
Respiratory arrest
Amnesia
Peripheral nerve
damage Cataracts
Immediate or
Keraunoparalysis
delayed
Transient flaccid
paralysis Lightning
Injuries Burns
Linear
Ocular trauma
Punctate
Anisocoria / Contact
Pupillary dilatation
Flash
Due to autonomic
dysfunction, not Lichtenberg
brain injury figures
Fractures
Lichtenberg Disappear in 24 Pathognomonic of

figures Not a true burn hours lightning strike
Lightning Injury Management
Lightning induced Better prognosis relative

cardiac arrest? to other causes of arrest
Cardiac Admit for

Management EKG
monitoring monitoring
Management in
Continue CPR!
the field?
Rare in lightning
Rhabdomyolysis?
injuries
High-Altitude Illness
Introduction
% of oxygen in atmosphere constant With altitude the total atmospheric Decline in partial
Physiology (~21 %) regardless of altitude
But
pressure decreases pressure of O2
Factors affecting development Rate of ascent Sleeping at Hydration

of illness at altitude & final altitude Acclimation altitude status
Prior Hx of Pre-existing Pulmonary

Risk factors cardiopulmonary disease R->L shunts
altitude illness hypertension
Decreased
alveolar O2
Decreased
Renal arterial O2
compensation via
bicarbonate
diuresis Acute
Physiology
With time, will
have increased
Decreased pCO2 Carotid body
RBC production
stimulation
Respiratory
alkalosis
Increased minute
ventilation
Promotes
Treatment Acetalozamide Leads to Acclimatization
bicarbonate diuresis
Acute Mountain Sickness
Acute Mountain Onset within Duration

Sickness hours of ascent 3–4 days
Symptoms & Signs
Frontal
headaches N/V Anorexia Sleeplessness
Worsened by
valsalva
Temporary halting of ascent for Symptomatic

Treatment Acetazolamide Supplemental O 2
12–36 hours treatment of HA
Allows acclimatization NSAIDs
Acetazolamide Metabolic Bicarbonate Increased Increased

effects acidosis diuresis respiratory drive oxygenation
Allows
acclimatization
Acetazolamide Contraindicated May cause Rarely causes

pitfalls in sulfa allergy paresthesias aplasic anemia
Definitive Not necessary unless

Descent severe or refractive Sx
treatment
High-Altitude Cerebral Edema
High Altitude Severe Fatal if untreated or Usually associated

Pulmonary Edema symptoms without descent with HAPE
Symptoms & Signs
Confusion Hallucinations Headaches Ataxia Retinal Visual

hemorrhages Disturbance
Head Use of portable hyperbaric chamber

Treatment Descent Dexamethasone Mannitol with preparation for descent
elevation
High-Altitude Pulmonary Edema
High Altitude Pulmonary Onset 1–4 days Precipitated by

Edema (HAPE) after ascent exertion
Most commonly
on 2nd night at
altitude
Symptoms & Signs
Cough with Noncardiogenic

Dyspnea Rales Cyanosis pink sputum Weakness pulmonary edema
Resting Resting Severe Respiratory Normal sized heart

tachypnea tachycardia hypoxemia alkalosis on CXR
Positive airway Use of portable Consider

Treatment Rest & O2 pressure Descent OR hyperbaric chamber nifedipine
Use of For pulmonary

Nifedipine? hypertension
Definitive
treatment Descent
Prevention Gradual ascent Nifedipine Dexamethasone

Submersion
Drowning
2nd leading cause of 2/3 of overall deaths are

Drowning less than 30 years of age
accidental death in children
Diving reflex Bradycardia & Shunting of Metabolism Children more

after immersion apnea blood to CNS decreases than adults
All submersion Regardless of

Drowning
injuries mortality
Salt vs fresh water

Recovery from
Near drowning No effect on survival
submersion
Secondary
ARDS Delayed death
drowning
Immersion Sudden death in

syndrome cold water
Drowning Freshwater Bathtub drowning

Bathtub Swimming pool
locations by age bodies of water common in elderly
< 1 year old 1–4 years old > 4 years old
Result of Both salt & fresh Interrupt

Wet drowning? 85 % of cases
aspiration water surfactant
Laryngospasm
Dry drowning Hypoxia later 15 % of cases
1st
Electrolyte Require large

OR Hemolysis OR Hemoconcentration Uncommon
abnormalities volume aspiration
Drowning Management
Primary determinant Duration of

of outcome? immersion
Initial Consider C-spine Measure core

ABC’s
management injury temperature
Significant Mechanical Improves

Positive pressure Recruits alveoli
injury? ventilation oxygenation
At risk for Use ventilator strategies

Pitfall
developing ARDS to reduce barotrauma
Hypothermia (low
Poor prognosis? Asystole Need for ED CPR Severe acidosis
core temperature)
But better But some
prognosis if cold survivors of
water
prolonged
Rewarm! submersion
Asymptomatic at Normal Strict return

Normal SaO2 Discharge
6 hours pulmonary exam precautions
Otherwise? Admit
Temperature-Related Illness
Heat Dissipation Versus Generation
Generation of Physical activity

heat Metabolism (Shivering)
Conservation of Peripheral Behavioral

heat vasoconstriction modification
Radiation
Heat dissipation Conduction Convection Evaporation
(1o modality)
Heat loss via Direct contact Circulating air or

electromagnetic liquid
waves
Occurs over 1–2 Decreased set point for

Acclimatization weeks onset of evaporation
Increased Increased Increased

Mechanism aldosterone sodium retention plasma volume
Predisposing Factors for Heat Illness
Vigorous activity
in hot
environment
Obesity Extremes of age
Predisposing
Factors
Cardiovascular
disease Dehydration
Medications
Anticholinergics
Decreased ability
to sweat
Decreased
peripheral blood b -blockers Phenothiazines
flow Central action on
hypothalamus
Medications
Predisposing
to heat illness
Decreased heat Ca-channel
loss Diuretics
blockers
Decreased
plasma volume
Sympathomimetics
Vasoconstriction
Minor/Moderate Heat Illness
Muscular Treat with

Heat Cramps exertion Salt loss electrolyte solutions Oral or IV
Increased aldosterone No treatment

Heat Edema during acclimatization indicated
Heat Rash Plugged sweat Topical

Salicylic acid
(Prickly Heat) pores chlorhexidine
Decreased Peripheral Postural Remove PO/IV

Heat Syncope hypotension from heat hydration
plasma volume vasodilation
Moderate form
Heat Exhaustion
of heat illness
Symptoms & Signs of Heat Exhaustion
Orthostatic Lightheadedness Temperature normal NO CNS

Severe fatigue hypotension N/V Muscle cramps impairment
& Dizziness or slightly elevated
Heat exhaustion
treatment Cooling IV hydration
May progress to heat Even after removal from

Complication
stroke if untreated hot environment!
Heat Stroke
Hyperthermia Neurologic
Heat Stroke > 40o C abnormality
Symptoms & Signs
Ataxia
Seizures Delirium Coma Hemiplegia Posturing Anhidrosis
Early Sx
Cerebellum
sensitive to
hyperthermia
Laboratory Respiratory Metabolic Elevated Variable Na Elevated Mild

(depends on
findings alkalosis acidosis CK volume status) AST/ALT coagulopathy
Immediate Consider immersion Fluid Goal is core

Treatment aggressive cooling (difficult) resuscitation temp of 39o C
Aggressive Removal Complete Tepid Ice packs to

cooling from heat Fan groin & axilla
undressing sprays
Ineffective
cooling? Invasive cooling Bypass Lavage
Will counteract Judicious use of

Complications Shivering
cooling benzodiazepines
No role for antipyretics

Cold Injury Pathophysiology

Maximal
Cooling to 10o C
vasoconstriction
Ice crystal
formation as
blood flow Decreased
further decreases cutaneous blood
and temp flow
decreases
Further cooling
Pathophysiology
Plasma leakage Cycles of cold-
induced
vasodilation
Vessel Cold blood

thrombosis returns to core
Capillary Further decrease

endothelial in blood flow to
damage affected areas
Reperfusion injury can also

occur as rewarming is
initiated
Localized Cold Injuries
Face
Areas most
Feet Ears
affected
Hands Nose
Areas distant from body core

most susceptible, head most
commonly affected overall
Nonfreezing, Prolonged Tissue loss

Trench Foot wet conditions exposure required uncommon Supportive care
Symptoms & Signs
Hyperemic Severe burning

Numbness Paresthesias Early cramps Leads to
phase pain
Nonfreezing, dry Exposure to

Chilblains conditions cold, damp air Supportive care
Symptoms & Signs Grading of severity

difficult visually for
Delayed Erythematous, several weeks post
development of: Paresthesias pruritic lesions injury
Freezing injury Numbness/ Erythema of Edema of

Frostnip affected area
(1st degree) Paresthesias affected area
Freezing injury
Frostbite 2nd degree 3rd degree 4th degree
(More severe)
Blistering Tissue loss Tissue loss

involving entire involving deep
skin thickness structures as
well, poor
prognosis
Management
Prevent Remove Rewarm affected area in Avoid dry heat,

Initial treatment
refreezing clothing circulating 42° C water may cause burns
Further Elevate affected Tetanus as Consider

Apply aloe Ibuprofen
management extremity needed antibiotics
Pain control &
inhibition of
prostaglandin
synthesis
Avoid early surgical

intervention
Hypothermia
Core temperature Standard oral thermometers

Hypothermia o
< 35 C
may not register < 35 o C
Failure to rewarm with Adrenal

standard methods? OR Myxedema state Considerations
insufficiency
Hypoglycemia
Decreased Elderly
metabolic rate
Decreased heat
generation
Predisposing
Sepsis Skin disorders
Factors
Altered Young
sensorium High surface area
Dementia / leads to poor heat
Delirium conservation
Drug & EtOH

abuse
Hypothermia Manifestations
Fall in Cardiac
Cardiac Below 32 o C
output & Pulse
T wave Prolongation of
EKG Changes Osborne J waves
inversions PR, QRS & QT
Dysrhythmias (Risk Sinus Ventricular

Atrial fibrillation Asystole
increases < 30oC) bradycardia fibrillation
Increased blood Increased risk of

viscosity thromboembolism
Respiratory Diminished airway

Respiratory Tachypnea
depression protection reflexes
Decreased Increased toxicity of medications

Liver
hepatic function metabolized by liver
Acute tubular
Kidney
necrosis
CNS Decreased LOC
Hypothermia Treatment
Gently handle Avoid

Treatment patients precipitating V. fib
A: Standard C: Treat only Other rhythms correct

ABC’s B: Warmed O2
intubation indications A. fib & asystole with rewarming
May be persistent with

unpredictable response
to treatment
Cardiovascular status most important

Rewarming determinant of need for rapid rewarming
Life-threatening
Rapid warming? Hypotension arrhythmias
Incidence of Rapid rewarming likely unnecessary

Temp > 30o C? arrhythmias rare if patient otherwise stable
Avoid temperature > 40 °C

Pitfall
in rewarming fluids/O 2
Pronouncement Do not pronounce patient deceased

of death until rewarmed to at least 32 °C
Rewarming Physiology
External
rewarming
Core Peripheral
Temperature vasodilation
Afterdrop
Also caused by
conduction of
heat from core to
colder periphery
External Physiology
rewarming
techniques
often used in Cold blood
conjunction returns to core
with core
rewarming to
minimize this
phenomenon
Preferential Improved
Core rewarming rewarming of heart cardiac function
Rewarming Methods
Passive external
rewarming
Warm blanket
Active core
rewarming
Active external
Warm IV fluids rewarming
40 oC max Methods of Circulating
Gastric lavage
Rewarming warmed air
blanket
Bladder lavage Inhaled warmed
air
Peritoneal lavage
40 o C max
Thoracic lavage
Extracorporeal
methods
Bypass
Multiple methods commonly

used simultaneously
Radiation
Free radical
Radiation effects Ionization DNA damage
formation
a b g
Radiation types
Least penetrating 8 mm penetration (burns) Deep penetration & radiation sickness
Radiation effects LD50 ~450 rad
Earliest symptoms in Hematopoietic system

Radiation cells/tissues with high turnover most sensitive 2nd is GI
Early symptoms? Higher dose Worse prognosis
Massive
GI effects N/V N/V/D fluid/protein loss
125 rads 100–200 rads >500 rads

Acute Radiation Survival unlikely
Syndrome
CNS Least sensitive
May survive
> 1200/uL Good prognosis

Best indicator of Absolute lymphocyte
300–1200/uL Intermediate
prognosis? count after 48 hours
< 300/uL Poor prognosis
Radiation Activated Whole bowel Chelating agents for Potassium iodide

management charcoal irrigation radioactive heavy metals for I-131 ingestion
Biological Weapons
Biological Weapons Tidbits
Biologic Relatively easy Potential for Difficult to

weapons to produce high mortality detect
Stability in
transport
Virulence Infectivity
Characteristics of
ideal biologic
weapons
Toxicity Length of
incubation in host
Ease of
Lethality
transmission
Selected Biological Agents and Toxins
Tularemia
Q fever Bacterial Anthrax
Cholera Plague
Ricin Toxins Botulinum toxin
Hantavirus
Viral hemorrhagic
fevers Viral Smallpox
Venezuelan
equine
encephalitis
Anthrax
Cutaneous
Anthrax 3 forms Gastrointestinal Inhalational
“ Woolsorter’s disease”
Incubation Exposed or infected pts

Anthrax Spore inhalation
1–6 days require no isolation
Symptoms & Signs Inhalational

Profound Productive
Fever & chills N/V Chest pain Sepsis Death
sweats cough
Hemorrhagic Within 24 hours if

mediastinitis untreated
Mediastinal Fullness paratracheally

CXR Infiltrates Pleural effusions
widening & in hilum
Symptoms & Signs Cutaneous

Lesion is No surrounding Pruritic papule turns into a
Chest pain
painless rash vesicle
Resembles a “bug bite”
The vesicle can be
hemorrhagic
Pitfall: Cutaneous Pts may have Including fever & Antibiotics do

Anthrax systemic signs edema not alter course
Vaccine may be Treat for 8 weeks for

Treatment Ciprofloxacin OR Doxycycline
useful confirmed exposure
Plague
Bubonic
Transmitted by flea bite, 3 main
Plague Yersinia pestis Pneumonic
contact or inhalation forms
Septicemic
2–3 day Inhalation of Exposed or infected

Pneumonic
incubation aerosolized bacteria pts require isolation
Symptoms & Signs

Cough productive Liver function
Fever & chills Shock DIC
of bloody sputum abnormalities
Gram stain of
Diagnosis Serology Blood culture
sputum
Extensive lobar Hemorrhagic

CXR
consolidation mediastinitis
Must be given within 24

Treatment Streptomycin OR Chloramphenicol OR Doxycycline
hours to prevent death
Most common Infected fleas bite with Y.pestis No spread from

Bubonic
form entering through a break in the skin person to person
Symptoms & Signs

Swollen & tender
Headache Fever & chills
lymph nodes (buboes)
Complication of
Septicemic
pneumonic plague
Smallpox
Airborne
Smallpox Variola virus transmission Highly infectious Strict quarantine
7–17 day Not contagious One case is a public

Smallpox until rash appears health emergency
incubation
Symptoms & Signs

Muscle aches &
Fever & chills pains Headache Malaise N/V Rash
Diagnosis PCR
Treatment Vaccine
Toxins
Toxin absorbed Toxin binds to preganglionic Inhibits acetylcholine
Botulinum toxin through inhalation membrane of cholinergic synapses release
Symptoms & Signs

Double vision Progresses to Ultimately
(1st) descending paralysis respiratory failure
Pitfall in NO significant
NO miosis
diagnosis respiratory secretions
Inhaled, ingested Inhibits protein

Ricin
or injected synthesis
Diagnosis ELISA
Symptoms & Signs
Hemorrhagic
Airway necrosis Fever & chills Cough Sweats
pulmonary edema
Chemical Weapons
Chemical Weapons
Nerve agents
Cyanide Vesicants
Chemical
weapons
Agents that affect
the lungs Tear gas
Nerve Agents
Sarin,Tabun, All inhibit

Nerve agents Multiple Soman, VX acetylcholinesterase
Most potent? VX Most volatile Sarin
Secondary
Pitfall contamination
Symptoms & Signs – “SLUDGEM” & Killer B’s”

Miosis
Salivation Lacrimation Urination Defecation GI Upset Emesis
(& Muscle spasm)
Bradycardia Bronchorrhea Bronchospasm
Protect self -
Treatment decontaminate Oxygen Atropine 2-PAM
Vesicants
Blister the
Vessicants
dermis
Not a true Skin blanches & has May cause

Phosgene
vessicant wheals without blisters pulmonary edema
Enters via inhalation or Causes necrotic blisters on

Mustard Liquid or gas
through skin – delayed pain mucus membranes and dermis
Causes Increases capillary Shock & end

Lewisite Liquid or gas
immediate pain permeability organ damage
Tetanus
Tetanus
Clostridium Anaerobic Produces Potent

Tetanus tetani gram (+) bacillus tetanus toxin neurotoxin
Crush injury
Devascularized
Burns
tissue
Wounds at
high risk
Wounds > 24
IV drug use
hours old
Postpartum
Soil in wounds
wounds
May occur with May not know of Neonatal 3–10 days after birth
Tetanus
minor wounds injury tetanus Poor prognosis
Symptoms & Signs

Risus
Muscle spasm Rigidity Fever Tachycardia Opisthotonus
sardonicus
Treatment – Tetanus <3 prior immunizations 3 prior Give toxoid only

Simple wounds toxoid or unknown immunizations if last > 10 years
Contaminated wounds, Tetanus Tetanus immune <3 prior immunizations If 3 prior immunizations,
punctures, avulsions, burns toxoid globulin or unknown toxoid if last > 5 years
Neurologic Emergencies
Contents
Dermatomes and Reflexes 556
Altered Mental Status and Coma 556
Cerebrovascular Accidents 557
Seizures 565
CNS Infections 572
Encephalitis 578
Brain Abscess 580
Headache Syndromes 581
Bell’s Palsy 593
Neuromuscular Disorders 594
Movement Disorders 598
Neuropathies 600
Spinal Disorders 600
Miscellaneous Disorders 601
Psychiatric Emergencies 601
Abuse/Neglect/Violence 611
Addictive Behavior and Withdrawal 613
M.R. Marchick, MD
Department of Emergency Medicine, University of Florida College
of Medicine, Gainesville, FL, USA

DOI 10.1007/978-3-319-30838-8_10
Dermatomes and Reflexes
Dermatomes & Reflexes

Dermatome Area
C4 Clavicle
C6 Thumb
C7 Index finger
C8 Ring Finger
T4 Nipple Line
T10 Umbilicus
L1 Inguinal ligament
L2, 3 Medial thigh
L4 Knee
L5 Lateral calf
S1 Lateral foot
S2–4 Perianal
Reflexes Area
C6 Biceps
C7 Triceps
L4 Patellar
S1 Achilles
Altered Mental Status and Coma
Altered Mental Status
Altered Mental Evaluate ABC’s

Status first!
Coma Cocktail Naloxone Glucose Thiamine Oxygen
AEIOU-TIPS
A Alcohol, Acidosis
E Epilepsy, Endocrine, Electrolytes, Encephalopathy
I Insulin
O Opiates, Overdose
U Uremia
T Trauma, Temperature
I Infection
P Poisoning, Psychiatric
S Stroke, Shock
Neurologic Emergencies 557
Coma Testing
Oculovestibular Test in comatose Ensure ear

Cold calorics
reflex patients canals are clear!
Supine patient with head Irrigate canal with

Cold calorics
elevated 30º ice cold water
Intact brainstem Nystagmus with fast component COWS

& cortex? to opposite ear Cold opposite, Warm same
Brainstem Brainstem intact but Eyes deviate

No eye deviation
damaged? cortex damaged? towards cold ear
Oculocephalic Test in comatose Absent in Contraindicated for known

Doll’s eyes
reflex patients awake patients or suspected C-spine injury
Eyes move in opposite Brainstem

Intact brainstem? Eyes are fixed
direction of head movement injured?
Tested in awake Tests CN V and

Corneal reflex
patients VII
Damaged brainstem Decreased direct & consensual

or cortex? blink in response to stimulus
Cerebrovascular Accidents
Stroke Mimics
Hyperosmolar
Hypoglycemia nonketoticstate
Conversion
disorder Hyponatremia
Drug toxicity Bell’s palsy
Hypertensive Complicated
encephalopathy migraine
Risk Factors
Subdural or
epidural bleed Multiple sclerosis
Seizures /
CNS infection
Todd’s paralysis
Brain mass Syncope

Stroke and TIA
Ischemic Anterior circulation: Supplies 80 % of brain

Stroke 80–90 % ischemic
Thrombotic > Embolic Posterior circulation: 20 % of brain
Anterior Anterior Middle cerebral Posterior

circulation cerebral artery artery cerebral artery
Posterior Vertebral Cerebellar type

Basilar artery Lacunar type
circulation arteries stroke
Transient Focal brain, spinal cord, Transient neurologic dysfunction

Ischemic Attack or retinal ischemia without infarction
Transient ~10 % risk of stroke ~5 % risk within Begin antiplatelet therapy

Ischemic Attack within 90 days 48 hours unless contraindicated
Age > 60 BP > 140/90 Clinical Diabetes

ABCD2 score Duration
(+1) (+1) features (+1)
Higher score = Unilateral > 60 minutes
≠2 day stroke weakness (+2)
risk (+/- speech 10-59
impairment) minutes
(+2) (+2)
Speech
impairment
only
(+1)
Anterior Circulation Stroke
Anterior Cerebral Artery
Symptoms & Signs
Contralateral Contralateral Altered mental Impaired Gait

Lower extremities > Arms & Face
weakness numbness status judgment disturbance
Middle Cerebral Artery Most commonly involved artery
Symptoms & Signs
Contralateral Contralateral Dominant Non-dominant

Arms & Face > Lower extremities
hemiparersis sensory loss hemisphere = Aphasia hemisphere = Neglect
Ipsilateral gaze Homonymous

preference hemianopsia
Posterior Cerebral Artery
Symptoms & Signs
Visual field Unilateral Inability to read Light touch

Contralateral homonymous hemianopsia
deficits headache (alexia) deficits
Most common
Visual agnosia Sx Cortical
(Inability to recognize objects) blindness
Tidbit
Contralateral motor & sensory deficits &
contralateral cranial nerve palsies
Vertebrobasilar Infarction
Vertebrobasilar Infarction
Symptoms & Signs
Oculomotor
Vertigo Nystagmus Headache N/V Ataxia
palsies
Ipsilateral cranial Contralateral
Crossed deficits
nerve palsies motor deficits
Locked-in Wallenberg
Quadriplegia Coma Syncope Dysphagia Dysarthria
syndrome syndrome
Locked-in Patient is awake but cannot move or verbally communicate due Diaphragm breathing & vertical
syndrome to complete paralysis of voluntary muscles except for the eyes eye movements spared
Locked-in Basilar artery occlusion Also seen with central pontine

syndrome at level of pons myelinolysis & pontine hemorrhage
Wallenberg Thrombosis of
syndrome vertebral artery
Symptoms & Signs – Wallenberg Syndrome
Oculomotor
Vertigo Nystagmus Ataxia N/V Ataxia
palsies
Decreased pain & Contralateral
Ipsilateral face
temperature sensation body
Ipsilateral Horner’s
Ptosis Miosis Anhidrosis
Syndrome
Lacunar Infarction
Lacunar 15–25 % of Due to disease of smaller Microinfarction Pts usually have

infarction ischemic strokes penetrating arteries of tissue HTN or DM
Lacunar Ataxia- Dysarthria-

Pure sensory Pure motor Mixed
syndromes hemiparesis hemiparesis
Thalamus Pons or Pons or Pons or Weakness
internal internal internal or paralysis
capsule capsule capsule with
ipsilateral
sensory
dysfunction
Prognosis? Usually good
Cerebellar Infarction
Cerebellar Infarction
Symptoms & Signs & Tidbits
Vertigo or N/V Drop attack

Nystagmus Headache Ataxia
dizziness (may be only feature) Sudden inability to walk or stand
≠ Brainstem Potential for Neurosurgical evaluation

Edema
pressure respiratory arrest & close observation
Hydrocephalus
Worse prognosis
Acute Ischemic Stroke Treatment
Determine if potential Determine time of If uncertain, use last

First step
candidate for thrombolysis symptom onset time known normal
Within 4.5 hours Stat Neurology BP control Determine Determine

(Window for IV tPA) noncontrast CT consultation (Goal < 185/110) glucose NIH score
Interventional
Longer window
capability?
Not a tPA Permissive Check Neurology NPO pending

CT or MRI
candidate? hypertension glucose consultation swallowing evaluation
When to give After swallow Intracranial

ASA? evaluation hemorrhage excluded
IV tPA inclusion Ischemic stroke with Symptom onset

Age >18 years
criteria measurable deficit < 4.5 hours ago
Maintain BP < 180/105 mm Hg during No heparin, ASA, warfarin etc.

After tPA
& 24 hours post thrombolytics for 24 hours post thrombolytics
Stroke
Admit
disposition?
Admit, unless these done Head/Neck

TIA disposition Neuro consult Echocardiogram
in ED prior to discharge vascular imaging
IV tPA Exclusions
Significant stroke
or head trauma Prior ICH
within 3 months
Multilobar Intracranial
infarction with neoplasm, AVM,
hypodensity > aneurysm
33% of
hemisphere
Recent
intracranial or
CT head with ICH
spinal surgery
Heparin use
within 48 hours Symptoms of SAH
with ≠ PTT IV tPA Exclusions
Anticoagulant use SBP ≥185,

with PT >15, or DBP ≥ 110
INR >1.7
Glucose
Platelets < 50 mg/dL
< 100,000/mm3
Acute bleeding Active internal
diathesis bleeding
Use of direct
Arterial puncture thrombin
within 7 days - inhibitor or factor
non-compressible Xa inhibitor with
site anticoagulant
effect on labwork
Relative Exclusions for IV tPA

Minor neurologic
deficit
Seizure at onset Rapidly improving

with postictal symptoms
impairment
Relative Exclusions
MI in previous 3
Pregnancy
months
Major
GI or urinary tract
surgery/serious
bleeding within
trauma within 14 Age > 80
21 days
days
Relative Exclusions
Prior ischemic Any oral
for Treatment 3–4.5
stroke + DM anticoagulant use
Hours After Onset
Severe stroke
(NIHSS > 25)
tPA Complications
Symptomatic
~ 5 % incidence
intracranial hemorrhage
D/C
If suspected Stat head CT
thrombolytics
Neurosurgery Consider cryoprecipitate

If diagnosed
consultation + platelets
Oozing from IV, mucosal Can continue

Other bleeding Minor bleeding
bleeding, ecchymoses thrombolytics
Consider discontinuing
Major bleeding
thrombolytics
Typically mild & Contralateral to Typical

Angioedema 1–5 % incidence
transient ischemic hemisphere treatment
Spontaneous Intracranial Hemorrhage
10 % of acute Putamen Thalamus Pons Cerebellum

Spontaneous ICH
CVA’s 45 % 10 –15 % 10 % 10 %
Hypertension
Sympathomimetic
AVM
use - Cocaine
Amyloid
Smoking Risk Factors
angiopathy
Masses Aneurysm
Anticoagulant use
Symptoms & Signs
Marked Neurologic deficit corresponds to Cerebellar hemorrhage

Headache N/V
hypertension affected area, often rapidly progressive Vertigo, Vomiting, Ataxia
Noncontrast Typical initial test of choice Better identification of

Diagnosis MRI structural abnormalities
CT Fast & readily available
Intracranial Hemorrhage Management
Initial Consider airway May have rapidly Anticoagulant Consider seizure

management protection progressive Ø mental status reversal prophylaxis
Blood pressure control CPP = MAP - ICP
Consider aggressive BP reduction

SBP >200mmHg or MAP >150 mmHg
(continuous drip)
Evidence of or Consider ICP Reduce BP (intermittent or continuous

suspected ICP monitoring drip) for goal CPP 61–80 mmHg
NO evidence of or Consider modest BP reduction (target

suspected ICP MAP 110 mmHg or 160/90 mmHg)
Increased ICP Sedation/ Consider invasive

Elevate HOB 30°
management Analgesia monitoring
Large
Indications for Evidence of
GCS < 8 intraventricular Hydrocephalus
invasive monitoring herniation hemorrhage
Other ICP Mannitol Mild hyperventilation (pCO2 30-35 mmHg)

Ventriculostomy
considerations (1 g/kg) Avoid prolonged use
Cerebellar High risk of upward Neurosurgical

hemorrhage? herniation emergency
Seizures
Definitions
Neurologic dysfunction due to inappropriate

Seizure
electrical discharges of brain neurons
Recurrent seizures NOT due

Epilepsy
to secondary, reversible cause
No apparent
Primary seizure
cause identified
Secondary Due to identifiable neurologic

seizure condition (tumor, CVA, trauma)
Occur in otherwise normal individual

Reactive seizure
exposed to insult (e.g., toxin)
Status Seizure activity lasting over 5 minutes or 2

epilepticus consecutive seizures without return to consciousness
Transient focal paralysis

Todd’s paralysis Stroke mimic
following seizure
Psychogenic Voluntary in No loss of

Pseudoseizure No EEG changes
nonepileptic seizures nature consciousness
Seizure Classification: Generalized
Result of simultaneous activity Loss of consciousness

Generalized
involving entire cerebral cortex without aura
Convulsive Positive loss of Rhythmic, bilateral, generally

Muscle rigidity
(Grand mal) consciousness symmetric contractions
Convulsive
Post-ictal state Headache Drowsiness
(Grand mal)
Non-Convulsive Conscious activity Dissociated state Automatisms

(Petit mal) suddenly ceases for several seconds may be present
Non-Convulsive No post-ictal Most common

(Petit mal) confusion in children
Seizure Classification: Focal
Result of localized Consider mass

Focal
electrical discharge lesions
Localized manifestations depending No post-ictal

Simple partial No LOC
on involved area of cortex state
Manifestations
Focal clonic Visual Auditory Gustatory Olfactory Visceral or affective

Paresthesias
movements phenomena phenomena phenomena phenomena symptoms
Has additional May have post - Automatisms Amnesia may be

Complex partial
impairment of cognition ictal state common present
Lip-smacking
These may
Pitfall
generalize
“Jacksonian Focal seizure that may progress

march” to generalized seizure
Causes of Secondary/Reactive Seizures

Intracranial Hypertensive
hemorrhage encephalopathy
Anoxia Infectious
Any meningitis
Encephalitis
Brain abscess
Causes of Secondary/Reactive
Neurocysticercosis
Structural Seizures
Latent syphilis
Neoplasm
HIV
CVA
AVM
Acute
hydrocephalus Trauma
Metabolic Toxic
Hypo/Hyperglycemia Cocaine
Hypo/Hypernatremia Amphetamines
Hypo/Hyperosmolar Lidocaine
states
Isoniazid
Hypo/Hypercalcemia
Bupropion
Thyrotoxicosis
Flumazenil
Uremia
Lithium
TCA’s
Theophylline
Seizure Mimics
Syncope
Most common
mimic
Sandifer
Psychogenic
syndrome nonepilieptic
GERD seizures
Dystonic reaction Hyperventilation

Seizure Mimics
Apparent life
threatening event TIA
Myoclonus /
movement Narcolepsy
disorders
Seizure Versus Syncope
Prodrome of
No aura or nausea,
prodrome lightheadedness,
darkened or
tunnel vision
May not be
present if
Generalized cardiogenic
Seizure
Syncope
Forceful
Post-ictal period tonic-clonic
movements NO post-ictal
May have “twitching”
period
Routine First Seizure Evaluation
Laboratory BMP +
Glucose magnesium Drug screen h CG
studies
Hyponatremia
most common in
afebrile children
<2
Non - contrast Referral for outpatient MRI

Imaging head CT prudent if CT negative
Lumbar CNS infection on

No ICP on CT
puncture? differential
Recurrent Seizure Evaluation
Laboratory Relevant Further testing

Glucose
studies anticonvulsant level determined by H&P
Other Most common cause of seizure Medication

considerations in patient with seizure disorder noncompliance
New seizure
CT scan
pattern
Adult Status Epilepticus Management
ABC’s First! –Treat as required
Specific Benzodiazepines Lorazepam Rapid onset 0.1 mg/kg IV

treatment 1st Line drug of choice Long acting (Also IM)
Other Can be administered

Diazepam Midazolam
benzodiazepines IV, IM, PR, via ETT
Maximum infusion
2nd line Phenytoin 20 mg/kg IV
rate 50 mg/min
Phenytoin Dissolved in May cause hypotension Need cardiac Potential for vascular
pitfalls propylene glycol & bradydysrhythmias monitoring injury & tissue necrosis
20 phenytoin Water soluble Less toxic to tissues

Fosphenytoin
equivalents/kg IV or IM prodrug of phenytoin & may be given IM
Considerations if Induction of Propofol Midazolam

Valproate IV OR
refractory? general anesthesia Pentobarbital Isoflurane
INH Toxicity? Pyridoxine
Emergent
Eclampsia Magnesium
delivery
Need continuous Especially if paralytic used or concern

Pitfall EEG monitoring for non-convulsive status epilepticus
Disposition
Status
Admit
epilepticus?
Return to
baseline mental
status
Reliable social No structural

situation abnormality on
CT
Criteria to Discharge
First Time Seizures
Outpatient
neurology follow-
up
No significant Unremarkable
Otherwise Admit
comorbidities labs
Recurrent Reload anticonvulsant Discharge if back Discuss medication

seizure if subtherapeutic to baseline adjustments with neurologist
Instructions
Do not drive or participate in other potentially
dangerous activities until cleared by a
neurologist
(Driving restrictions vary by jurisdiction)
Febrile Seizures
Most common type

Febrile seizures 2–5 % incidence
of pediatric seizures
Simple febrile 6 months – < 15 minute Only one in

Fever ≥ 38°C
seizure 5 years old duration 24 hours
Complex febrile Seizure associated with fever but not a < 6 m or > 5 yrs > 15 minutes
seizure serious infection and any of the following Focal Multiple
50 % of those < 12 months 30 % of those >12

Recurrence?
have another febrile seizure months have another
Higher risk of Family history of Multiple febrile First seizures at

epilepsy? seizures seizures age < 12 months
Febrile Seizure Evaluation and Management
Well appearing Evaluation focuses

child? on source of fever
Meningeal May not be present Age < 12 months 12–18 months

signs? in young children Strongly consider LP Consider LP
Complex febrile
Consider LP Septic workup
seizure
Prolonged
LP
seizure
Ill-appearing LP
Diazepam per
Treatment
rectum if prolonged
Anticonvulsants
Pitfall
not indicated
Neonatal Seizures (<28 Days)
Neonatal Often not a generalized

seizures tonic-clonic seizure
Intracranial
Apnea/ALTE CNS infection
hemorrhage
Pyridoxine Hypoxic ischemic

Bicycling Eye deviation dependency encephalopathy
Neonatal Seizures Drug withdrawal Congenital brain

Differential
or intoxication malformations
Staring/Rhythmic
Lip smacking Inborn errors of
blinking
metabolism Hypoglycemia
Hypomagnesemia Hypocalcemia
Glucose + Mg + Consider ammonia & lactate Septic

Evaluation Neuroimaging
Na + Ca if inborn error suspected workup
Specific Empirical treatment with

treatment IV antibiotics & acyclovir
Phenobarbital Pyridoxine if
Seizures?
1st Line refractory
Background EEG
Poor prognosis
abnormalities?
CNS Infections
Typical CSF Characteristics
Preterm
Term
Normal Bacterial Viral Fungal TB Abscess Child
Normals
0–25
WBCs <5 > 1000 < 1000 100-500 100-500 10-1000 7.3 ± 13.9
0–7
57
% PMNs 0-15 > 80 < 50 < 50 < 50 < 50 61–84
5
% Lymph > 50 < 50 > 50 > 80 Inc. Mono Varies
65–120
Protein
20-45 > 150 50-100 100-500 100-500 > 50 64.2 ± 24.2
(mg/dL)
5–40
24–63
Glucose
40-65 < 40 40-65 30-45 30-45 45-60 51.2 ± 12.9
(mg/dL)
40–80
Opening 8–11
pressure 6-20 > 25-30 Variable > 20 > 20 Variable < 20
(cm H2O) < 20
Viral profile may be seen with CSF sterilization can occur within 2
Pitfalls
partially treated bacterial meningitis hours of IV antibiotic administration
Meningitis Introduction
Natural history Typically gradual onset of

viral meningitis symptoms over several days
Mechanisms for Entry via upper Contiguous

bacterial meningitis OR
airway spread
Pathophysiology Entry into upper Hematogenous Seeding of

of direct entry airway spread subarachnoid space
Contiguous From multiple Brain abscess, otitis media, sinusitis,

spread? sites mastoiditis, cavernous sinus
Final common Inflammation of Violation of blood

pathway subarachnoid space brain barrier Edema Ischemia
Mechanisms for Hematogenous

fungal meningitis Inhalation spread
Fungal Much more common in Cryptococcus occurs in up Generally CD4

meningitis immunocompromised to 10 % of HIV + patients count < 100
Meningitis
Symptoms & Signs
Altered mental
Fever Headache Photophobia Vomiting Seizures Nuchal rigidity
status
Bulging
Infants Irritability Poor feeding
fontanelle
Exam Findings
Brudzinski’s Jolt accentuation

Skin Rash Kernig’s sign
sign test
Petechiae Passive neck Passive knee Quick
flexion causes extension movement of
N. meningitidis while hips
hip and knee head from side
RMSF flexion flexed causes to side in a
pain horizontal
plane causes
worsening
headache
Common symptoms & exam findings

Pitfall
may not be present in infants & elderly
Causes of Viral Meningitis
Enteroviruses
Vast majority of
cases
Enterovirus
Coxsackievirus
Echovirus
HIV Herpes Simplex
Causes of Viral
Meningitis
Adenovirus Cytomegalovirus
Supportive
Treatment
(except HSV)
Causes of Bacterial Meningitis
Streptococcus
pneumoniae
#1 overall
Highest
> 50 years old morbidity & Neonates
mortality
Streptococcus E. coli
pneumoniae
Group b strep
Listeria
monocytogenes Listeria
monocytogenes
Causes of Bacterial
Meningitis
Children
Streptococcus
pneumoniae
Young adults Neisseria
meningitidis
Streptococcus
pneumoniae Group b Strep
Neisseria Haemophilus
meningitidis influenzae
Consider
Petechial rash?
meningococcus
Risk Factors
Sinusitis Otitis Media
Head trauma /
Endocarditis
CSF leak
S. pneumoniae
Pneumonia Immune
compromise
Risk Factors
Diabetes mellitus Splenectomy
Encapsulated
organisms
Alcoholism
Malignancy
Gram (-) bacilli
L. monocytogenes
Hx of Close living
neurosurgery or conditions
cochlear implant Dorms, barracks
S. aureus N. meningitidis
Meningitis Prophylaxis
Indicated for close contacts of patients

Prophylaxis?
with documented N. meningitidis
Household
contacts
Contact with oral Daycare or school

Prophylaxis
secretions contacts
Intubation
without facemask
or mouth-to-
mouth
resuscitation
Agents? Rifampin OR Ciprofloxacin
Prophylaxis for
Not indicated
S. pneumoniae ?
Evaluation
Suspected bacterial Administer empiric antibiotics

meningitis? prior to LP (and CT if ordered)
Suspected S. pneumoniae Administer dexamethasone prior to or Improved

or H. influenzae? concurrently with initial antibiotic administration neurologic outcome
Other
CBC Blood cultures
considerations
Imaging CT
Altered mental
status
Immune
Papilledema
compromise
Concern for mass Focal neurologic

CT prior to LP
lesion deficit
Malignancy Seizure
Advanced age
Empiric Antibiotic Treatment
Adults, Infants >1 Ceftriaxone Vancomycin Acyclovir Ampicillin

month, Children 2g IV 15–20 mg/kg up to 2 g 10 mg/kg IV 2 g IV
If HSV suspected If L.
monocytogenes
suspected
(> 50 yrs)
Neonatal Ampicillin Cefotaxime OR Gentamicin
Meningitis due Add anaerobic

to sinusitis? coverage
Fungal Meningitis
Cryptococcus
Blastomyces Histoplasma
Causes of Fungal
Meningitis
Coccidiodes Candida
Lumbar CSF cryptococcal antigen India ink 60–80 %

Diagnosis
puncture almost 100 % sensitive sensitive
Specific Often not

Amphotericin OR Flucytosine OR Fluconazole
treatment initiated in ED
Disposition Admit
Encephalitis
Encephalitis: Introduction
Often coexists Presence of a distinct neurologic

Encephalitis
with meningitis deficit is a distinguishing feature
Retrograde spread
Rabies virus Herpes Simplex Herpes Zoster
via axons to CNS
Pathophysiology Hematogenous spread

of others? due to viremia
Symptoms & Signs
Psychiatric Cognitive Movement Meningeal signs Other symptoms of

Seizures
disturbances dysfunction disorders & symptoms respective viral pathogens
Especially
Herpes
Simplex
Encephalitis Causes
Arboviruses
Most common
La Crosse
St. Louis
West Nile
Eastern Equine
Western Equine
Epstein - Barr Rabies
Causes of
Encephalitis
Herpes Zoster Herpes Simplex
Encephalitis Diagnosis and Management
Herpes Simplex
Memory Psychological
HSV Encephalitis
disturbances disturbances
Diagnosis of HSV Neuroimaging is Inferior frontal lobe & medial MRI more
encephalitis helpful temporal lobe hypodense lesions sensitive than CT
Periodic sharp
EEG?
waves
Disposition for all
Admit
CSF? May have RBC’s
Acyclovir
Treatment
10 mg/kg IV every 8 hours
CMV
Ganciclovir
Encephalitis
Herpes Zoster
Acyclovir
Encephalitis
Brain Abscess
Brain Abscess Introduction
Pathogenesis Hematogenous OR Direct extension OR Post-surgical OR Idiopathic
Hematogenous Typically
Polymicrobial
spread multiple
Direct extension Odontogenic OR Sinogenic OR Otogenic
Odontogenic or Anaerobic Gram negative

Otogenic OR Bacteriodes
sinogenic streptococci rods
Gram negative
Post-surgical S. aureus OR rods
Symptoms & Signs Often nonspecific presentation with delayed diagnosis
Focal neurologic Altered mental

Fever Headache Vomiting Nuchal rigidity
deficit status
Most common
symptom
Based on Contrast enhanced CT or Ring enhancing

Diagnosis
imaging MRI (+/- gadolinium) lesion
Management
Suspected brain Emergent neurosurgical Joint decision making on antibiotics

abscess consultation prior to obtaining abscess fluid
Neurosurgical or 4th generation

Vancomycin
trauma history cephalosporin
Oto/sino/
Hematogenous OR Cefotaxime Metronidazole
odontogenic
Disposition Admission
Headache Syndromes
Headache Red Flags: “SNOOP”
Odor Agent
Systemic symptoms Fever, weight loss
Secondary risk factors Cancer, HIV
Neurologic symptoms Altered mental status, focal deficits
Onset Sudden or abrupt onset
Older New onset headache > 50 years old
First headache or change in headache frequency,

Previous history severity or features
Eyes Diplopia, papilledema, red eye, halos around light
Headache Classification
Migraine
Tension Primary Cluster
Masses including Intracranial

metastases hypertension
Acute mountain
CNS infection
sickness
Trigeminal Medication use

neuralgia or withdrawal
Acute angle Secondary Idiopathic

closure glaucoma Headaches intracranial HTN
Central venous
Temporal arteritis
thrombosis
Hypertensive
Cervicogenic
urgency
Post lumbar
Post concussion
puncture
Migraine Introduction
F>M Menses
Migraine
Typical onset in teens to 20’s
Even pregnancy
Nitrite use Physical activity
Potential Triggers
Caffeine use Sleep deprivation
Alcohol use
Symptoms & Signs
Lasts up to 72 Worsened with Phono-or

Gradual onset Unilateral Pulsatile N/V
hours exertion photophobia
Visual
Most common
Scintillating
scotoma
Brainstem Sx Visual field Hemiparesis
Typically < 60 minute duration
deficits
Vertigo, ataxia
Migraine aura Resolves spontaneously
Auras
15 % of overall cases
Aphasia Ophthalmoplegia
Paresthesia
Migraine Treatment
Dopamine
Prochlorperazine OR Metoclopramide OR Droperidol
antagonists
Potential for QTc prolongation with

Pitfall
dystonic reactions high doses of droperidol
Dopamine and
DHE 5HT1B/1D agonist
DHE Patients with Hemiplegic

Pregnancy Basilar migraines
contraindications CAD migraines
High incidence Pretreat with

Pitfalls
of emesis antiemetic
Selective 5HT1D
Triptans Less N/V Prophylactic Treatments
agonists
(Usually not started in ED)
Lifestyle modification
Triptan β–blockers
Patients with HTN Patients with CAD Ca-channel blockers
contraindications
TCA’s
Do not give within Causes increased

Pitfall
24 hours of DHE vasoconstriction
Can be effective for Frequent use may cause

Opioids But…
rescue analgesia rebound/worsened HA
May be effective for

Steroids
status migrainosus
Tension Headache
Symptoms & Signs
Non-pulsatile Lasts minutes No focal NO Phono-or

Bilateral Band-like ±N/V
character to days deficits photophobia
No aggravation
with activity
If severe, consider
Treatment NSAIDs
migraine treatment
Cluster Headache
Cluster More common Unlike other

No prodrome
Headache in men primary syndromes
Symptoms & Signs
Severe unilateral temporal or Duration 15– Ipsilateral Ipsilateral conjunctival Rhinorrhea/

Facial swelling
retro-orbital lancinating pain 180 minutes lacrimation injunction Congestion
Horner’s
Facial flushing
syndrome
Inciting agents Alcohol Nitroglycerin
High flow
Treatment 75 % effective DHE OR Triptans
oxygen
Other treatment Lidocaine 4 %

considerations nasal drops
Steroids with
Prophylaxis Verapamil
taper
Trigeminal Neuralgia
Trigeminal More common in Compression of Consider

Tic douloureux
Neuralgia middle aged women trigeminal nerve multiple sclerosis
Symptoms & Signs
Severe unilateral lancinating Brief episodes Normal

“Electric”
pain in trigeminal distribution (seconds) neurologic exam
Carbamazepine
Treatment
1st line
Surgical
Refractory case?
treatment
Post-lumbar Puncture Headache
Post LP Headache ≠ Needle caliber ≠ Amount of

≠ # attempts
severity increased by (most important) CSF removed
Symptoms & Signs
Worse in upright Pulsatile in

position nature
Consider
Treatment Hydration Analgesia
caffeine
Definitive
Blood patch
treatment
Toxic Metabolic Headache
Toxic Metabolic Usually due vasodilation Fever is most

Headache of pain sensitive arteries common cause
Carbon
Other causes Alcohol Hypoxia
monoxide
Symptoms & Signs
Bilateral Diffuse
Underlying
Treatment
condition
Headache Related to CNS Tumors
Headache most Often worse at

CNS Tumors
common Sx night
Symptoms & Signs
HA may be HA may be new onset or an increase HA worse with HA worse with Sleep Focal neurologic
diffuse or focal in frequency or duration of chronic HA valsalva laying down disturbance deficit
N/V Seizures
Lung
Most common
Colon metastases to
Breast
brain
Genitourinary Melanoma
MRI test of IV contrast

Diagnosis
choice ≠ sensitivity of CT
Treatment of Emergent neurosurgery

Dexamethasone
acute ≠ ICP consultation
Pseudotumor Cerebri (Idiopathic Intracranial Hypertension)
Pseudotumor Young obese Typically with irregular Due to impaired ↑ CSF pressure without
Cerebri females menses & amenorrhea CSF absorption mass or obstruction
Symptoms & Signs
Nausea & Diffuse Papilledema Pain behind Pain with eye

Visual changes Double vision
vomiting headache (90 %) eye movement
NO focal
Tinnitus
deficits
CT shows slit-like or
Imaging No mass effect
normal ventricles
Lumbar puncture shows

Diagnosis
high opening pressure
Shunt if
Treatment Repeated LP’s Acetazolamide
refractory Vision perimetry
testing guides
adequacy of
Other treatment Nerve sheath treatment
Weight loss Steroids
considerations fenestration
Hydrocephalus
PEDIATRICS
Non-
Hydrocephalus Obstructive Communicating Non-obstructive
communicating
Blockage Impaired CSF
Increased CSF
between absorption by
volume with
ventricles & arachnoid
increased CSF
arachnoid granulations
pressure
granulations
Normal pressure
Congenital Acquired hydrocephalus
Arnold-Chiari Masses
malformation Non- Hydrocephalus
Infection Hemorrhage Communicating
Dandy-Walker Communicating ex-vacuo
malformation Hemorrhage
Intrauterine Post-trauma Meningitis
infection
Symptoms & Signs
Altered mental Bulging Increased head

Headache Papilledema N/V Blurred vision
status fontanelle circumference (infants)
Horizontal
Gait instability
diplopia
Diagnosis CT OR MRI
Treatment CSF Shunt

Pediatric Hydrocephalus Tidbits
PEDIATRICS
Arnold-Chiari Malformation of cerebellum with

malformation non-communicating hydrocephalus
Symptoms & Signs Specific to Pediatrics
Increased head 6th nerve

Headache Papilledema N/V Irritability Lethargy
circumference (infants) weakness
Increased lower May have positive “Cracked pot” sign on

Strabismus
extremity tone Babinski sign percussion of skull
Enlarged
Diagnosis
ventricles on CT
Treatment CSF Shunt
Normal Pressure Hydrocephalus
Normal pressure Communicating Uncertain Intermittent intracranial “Wobbly, wacky,

hydrocephalus hydrocephalus etiology hypertension may exist & wet”
Often first Most responsive

“Wobbly” Gait disturbance
finding to treatment
Often misdiagnosed as
“Wacky” Dementia
Alzheimer’s or Parkinson’s
Urinary Typically a late

“Wet”
incontinence finding
Large ventricles out of

Diagnosis CT or MRI
proportion to atrophy
Lumbar Normal opening

puncture pressures
LP with large volume Eventual shunt

Treatment
CSF drainage placement
Ventricular Shunt Headache
Ventricular Evaluate for infection

Shunt Headache or obstruction
Diversion of CSF Can go to a body cavity

VP Shunts
fluid or bloodstream
Mechanism to
VP Shunt valves One way valve
flush CSF
Body cavities
Peritoneal Right atrium Pleura
used for shunts
Incompressible Obstruction until

valve? proven otherwise
Evaluate shunt for Neurosurgery

Treatment
patency consultation
VP Shunt Complications: Malfunction
PEDIATRICS
Shunt Mechanical Slit ventricle CSF Abdominal pseudocyst

Obstruction
malfunction failure syndrome loculation formation
Most
common
CSF protein
Kink of tubing Clot

Causes of
Mechanical Obstruction
Infection
disconnect
Tip migration
Slit ventricle Waxing and Worsened by

syndrome waning symptoms standing or exercise
Overdrainage
Slit ventricle Tissue occlusion

Tissue dislodges
syndrome of proximal shunt
ICP
Symptoms & Signs
Altered mental Bulging Increased head Sundowning–paralysis

Headache Ataxia N/V
status fontanelle circumference (infants) of upward gaze
Resisted compression ICP > 20 cm H2O

of pumping chamber
VP Shunt Complications: Infection
PEDIATRICS
50 % within 2 Up to 10 % > 1
Shunt infection
weeks post-op year post-op
Typical S. epidermidis
S. aureus H. influenzae
pathogens (#1)
Symptoms & Signs
Altered mental Erythema/tenderness

Fever N/V Headache Abdominal pain
status over tubing
Meningismus Sepsis Peritonitis
May have
Pitfall
peritonitis
Diagnosis and Treatment of VP Shunt Complications
Both not 100 % sensitive & if Sx suggestive

Diagnosis CT head Shunt series
Neurosurgery consult mandatory
Suspected
Shunt tap
infection?
Standard LP may
Pitfall
miss shunt infection
Suspected Broad spectrum Neurosurgery

peritonitis? antibiotics consultation
Treatment of Neurosurgery consultation

Elevate head
obstruction for potential shunt revision
Treatment of Vancomycin +
infection Ceftazidime
Cardiopulmonary Sudden worsening Emergent tap of

Coma OR OR
arrest of condition shunt
Venous Sinus Thrombosis
Hypercoagulability
Exogenous Pregnancy &
estrogens post-partum
Risk Factors
Connective tissue Primary CNS
disorders infection
Spread of
infection from
contiguous area
Symptoms & Signs
Neurologic deficit varies

Headache N/V Seizure
with location of thrombus
Diagnosis MRI/MRV OR CT Angiography
Treatment Heparin
Subarachnoid Hemorrhage Introduction
Subarachnoid 75 % due to ruptured Occasionally due 20 % of patients have onset during activities
hemorrhage aneurysm to AVM which ≠ ICP (intercourse, defecation, exercise)
Moyamoya
Hypertension
syndrome
Idiopathic Dissection Family history Smoking
Other Causes Risk Factors
Sympathomimetic Mycotic Polycystic kidney
Heavy EtOH use
drugs aneurysm disease
Tumor Connective tissue
disorders
Marfan’s syndrome
Ehlers-Danlos Type
IV
Symptoms & Signs
Thunderclap Loss of Altered mental Subhyaloid retinal

Nuchal rigidity N/V Seizure
headache consciousness status hemorrhage
Headache
Sentinel bleed
“worst of life”
30–50 % of Sudden focal or generalized May precede aneurysm rupture by

Sentinel bleed
aneurysmal bleeds severe headache hours to months, mean is 2 weeks
SAH Diagnosis
Computed ≠ Time since Near 100 % sensitive Ø Sensitivity

Ø Sensitivity
tomography symptom onset within 6–12 hours after 12 hours
SAH suspected & Lumbar

CT negative? puncture
Lumbar Hemoglobin Yellow discoloration

Bilirubin Xanthochromia
puncture metabolized of CSF
Takes 6–12 hours

Xanthochromia to develop Lasts 3 weeks
RBC count in Does not decrease

collection tubes? from tubes 1 through 4
Positive CT OR Xanthochromia SAH
No
Negative CT < 5 RBC’s No SAH
xanthochromia
SAH Treatment and Tidbits
<24 hours post Highest Maintain patient at baseline BP

SAH hemorrhage rebleeding risk using IV titratable antihypertensive
Avoid
Pitfalls
hypotension
48 hours–3 weeks Nimodipine 60 mg postarted

Vasospasm
post hemorrhage within 96 hours is protective
Seizure Discuss with

Controversial
prophylaxis? neurosurgeon
Disposition? ICU admission

Carotid/Vertebral Artery Dissection
Important cause of stroke in

Dissection
young-middle aged adults
Trauma
Connective tissue Abrupt head

Risk Factors
disorders turning
Chiropractic
manipulation
Symptoms & Signs
Headache / Facial pain Neck pain Horner’s Cranial nerve Neurologic deficits typically
Visual changes
(Typically unilateral) (Typically unilateral) syndrome palsies follow pain by hours to months
MR generally preferred
Diagnosis MRI/MRA OR CT Angiography
for vertebral arteries
Prevent subsequent
Treatment Anticoagulation
embolic stroke
Bell’s Palsy
Lower motor 7th nerve Many cases likely associated

Bell’s Palsy neuron disorder paralysis with herpes virus infection
Symptoms & Signs
Most common Acute onset unilateral upper and

symptoms lower facial muscle paralysis
Less common Posterior Taste Paresthesias/ Poor tear

Hyperacusis Ocular pain
symptoms auricular pain disturbance numbness of cheek/mouth distribution
CVA
Upper face spared CVA affecting CN VI nucleus
Genu VII nerve and CN VII
Bacterial middle,
palsy Patient’s cannot abduct
external ear or
ipsilateral eye
mastoid
infections Differential
Ramsay Hunt Facial nerve most

Trauma
syndrome commonly injured CN
Lyme disease
Treatment Steroids Initiate prednisone if 1 mg/kg (up to 60 mg)

onset within 72 hours X 6 days
Other Consider Acyclovir/Valacyclovir if Modest, if any benefit

Antivirals
considerations high suspicion for viral etiology Concomitant steroids necessary
80–90 % recover Earlier improvement ≠ likelihood of

Prognosis
within 3 months in symptoms full recovery
Neuromuscular Disorders
Multiple Sclerosis
Multiple Inflammation Patchy areas of Episodic neurologic 20’s–30’s peak

sclerosis in CNS demyelination (plaques) dysfunction onset, F>M
Increased
incidence
postpartum
Symptoms & Signs
Cranial nerve Optic neuritis Internuclear ophthalmoplegia Oculomotor Sx

dysfunction 20 % risk of developing MS in next 2 years Eyes cannot look medially (in MS is bilateral) Diplopia & nystagmus
Paresis/ Numbness/ Cerebellar Bowel/bladder Uhthoff’s phenomenon

paraplegia paresthesias dysfunction dysfunction Temporary worsening of symptoms with ≠ body temperature
Mildly ≠ ≠ protein, ~90 % of patients with oligoclonal

CSF Findings
lymphocytes particularly IgG bands of IgG on electrophoresis
Bright white (hyperintense) May be

MRI Often multiple
lesions on T2 images periventricular
Acute exacerbation Most resolve IV methylprednisolone

management without therapy Ø duration of Sx
Other treatment
ACTH Interferon
options
IV steroids Ø rate of
Optic neuritis
development of MS
Guillain-Barre Syndrome
Acute autoimmune demyelination Typically preceded by infection

Guillain-Barre
of peripheral nervous system (rarely following vaccination)
Infectious agents Campylobacter Mycoplasma

CMV EBV
implicated jejuni pneumoniae
Guillain-Barre Pace of Severity of ventilatory

Time to recovery
variables progression compromise
Symptoms & Signs
Progressive, ascending, Variable Signs/symptoms typically Ocular muscles

Loss of DTR’s
symmetrical weakness sensory deficits worse in lower extremities typically spared
Most common
1/2 with autonomic 1/3 require
dysfunction mechanical ventilation
Most common Mildly But may be

≠≠ protein But…
CSF findings ≠ lymphocytes normal
Maintain BP < 180/105 mm Hg during No heparin, ASA, warfarin etc.

After tPA
& 24 hours post thrombolytics for 24 hours post thrombolytics
More likely to need Forced vital capacity Negative inspiratory force (NIF)
mechanical ventilation < 20 mL/kg OR < 30 cm H2O
Plasma
Management Supportive care IVIG OR
exchange
Acute Periodic Paralysis
Acute periodic Progressive extremity weakness in Typically after No pain, sensation

paralysis young males exercise is normal
Thyroid Use of
Associations Hypokalemia Steroids Renal disease
disease alcohol
Hypokalemic Autosomal Variant associated with

periodic paralysis dominant variant thyrotoxicosis
Most common Typically after exercise
Tick Paralysis
Similar to Guillain-
Tick Paralysis Rapidly ascending paralysis Reversible
Barre
Find & remove

Treatment
tick
Myasthenia Gravis
Myasthenia Autoantibodies Destruction Competition with Fatigability + muscle weakness

Gravis to ACh receptors of receptors ACh for binding worsens with repetitive use
Myasthenia Women Men Associated with thymoma

Women > Men
Gravis (20–30) (50–60) (25 % of these pts have it)
Symptoms & Signs
Proximal>distal Respiratory muscle

1st Symptoms Ptosis Diplopia Blurred vision Other symptoms
limb weakness weakness in ~15 %
Edrophonium Increases Ach by inhibiting Increases

Diagnosis
test breakdown of ACh by cholinesterase muscle strength
Consider obtaining a negative

Diagnosis
inspiratory force measurement
Edrophonium may cause Consider

Pitfall
AV block & cardiac arrest atropine first
Not understanding that increased

Pitfall Cholinergic crisis
weakness may be due to over medication
Respiratory Myasthenic crisis Overmedication

arrest causes Exacerbation vs. inadequate treatment Cholinergic crisis
Precipitants of Myasthenic Crisis
Medication
change or missed Infection
dose
Many others Surgery
Metronidazole Aspiration
Macrolides Pregnancy
Risk Factors
Clindamycin Beta-blockers
Calcium channel
Phenytoin
blockers
Neuromuscular
Lidocaine
blockers
Myasthenia Gravis Treatment
Acute myasthenic Airway Plasma

OR IVIG
crisis? protection exchange
Avoid depolarizing & Very sensitive to ≠ Duration of

Pitfall
nondepolarizing paralytic agents effects action
Very unpredictable
Pitfall
response to succinylcholine
Chronic Pyridostigmine
≠ ACh Immunosuppressants Thymectomy
management or neostigmine
Lambert-Eaton Myasthenic Syndrome
Lambert-Eaton Clinically similar to Autoantibodies to Proximal muscle

Ø ACh release
syndrome myasthenia gravis Ca2+ channels weakness
Lambert-Eaton Highly associated with malignancies

syndrome especially small cell lung CA
Repeated
≠ ACh release ≠ Strength
stimulation
Symptoms & Signs
Weakness & fatigue Especially Weakness

of proximal muscles thighs & hips improves with use
Treat underlying
Treatment Plasmapheresis OR IVIG
condition
Syndrome Neuromuscular blockers,

Pitfall worsened by Ca channel blockers, IV contrast
Movement Disorders
Movement Disorders: Dystonic Reaction and Chorea
Dystonic Side effect of Typically seen Many cases likely associated

reaction antipsychotics early in treatment with herpes virus infection
Symptoms & Signs

Spasms/tics of face, neck, & Oculogyric crisis Laryngospasm
back most common Continuous rotatory eye movement rare
Treatment
Diphenhydramine Benztropine Benzodiazepines
options
Abrupt, excessive, dance-like

Chorea
non-rhythmic movements
Huntington’s
disease
Creutzfeldt-Jakob Chronic
disease antipsychotic use
Wilson’s disease Causes Levodopa
Pregnancy Cocaine
Rare
Rheumatic fever
Sydenham’s
chorea
Movement Disorders: Akathisia and Tardive Dyskinesia
Akathisia Subjective and objective Typically seen early in High incidence with
motor restlessness treatment with antipsychotics prochloperazine
Treatment Diphenhydramine Benztropine Propranolol

options (chronic cases)
Tardive Prolonged use of Late onset, chronic, rapid Especially of face, with
dyskinesia anitpsychotics involuntary movements trunk/limb choreoathetosis
Tardive Risk higher with traditional

dyskinesia agents vs atypicals
Treatment Psychiatrist to consider

¯ dose or alternative agent
Often
Pitfall
irreversible
Parkinson’s Disease
Symptoms & Signs
Pill-rolling tremor Cogwheel Posture Bradykinesia/

Dysequilibrium
(decreases with purposeful movement) rigidity changes Akinesia
Parkinson’s
Drug induced Idiopathic
types
Treatment Discontinue e.g., metoclopramide

Drug-induced inciting agent & neuroleptics
Treatment Carbidopa
Benztropine Amantadine
Idiopathic Levodopa
Pitfall of Can cause dysrhythmias, dystonia,

Carbidopa/Levodopa orthostatic hypotension
Avoid haloperidol & Can precipitate

General pitfalls
other neuroleptics tardive dyskinesia
Neuropathies
Peripheral Polyneuropathies
Peripheral Typically bilateral Slowly Lower extremities >

Polyneuropathies stocking-glove distribution progressive Upper extremities
Pain & sensory deficits

Tidbits
precede motor symptoms
Ethanol
Diabetes mellitus Methanol
Heavy metals:
Aminoglycosides Causes
Arsenic, Lead
Phenothiazines HIV
Vitamin
deficiencies
B1 (Beriberi)
Niacin (Pellagra)
Pyridoxine
B12 (Pernicious
anemia)
Gabapentin,
Treatment Glucose control
Pregabalin, or TCAs
Spinal Disorders
Amyotrophic Lateral Sclerosis
Upper & lower motor Unknown

ALS
neuron degeneration etiology
Rapidly progressive muscle atrophy, fasciculations,

ALS
spasticity, hyperreflexia (+ Babinski)
Combination of upper & lower

Diagnosis EEG
motor neuron symptoms
Death due to respiratory

Pitfall
failure & aspiration
Miscellaneous Disorders
Wernicke’s Encephalopathy
Wernicke’s Seen in malnourished Thiamine May result in death

Encephalopathy chronic alcoholics (B1 deficiency) if not treated
Symptoms & Signs
Altered mental status Ophthalmoplegia Short term memory

Nystagmus Ataxia
due to encephalopathy (lateral rectus) impairment
Replete electrolytes Alcohol

Treatment Thiamine Before glucose
especially magnesium abstinence
Glucose oxidation is a May drive the insufficient May precipitate

Treatment pitfall
thiamine intensive process circulating B1 into cells neurologic injury
May lead to Korsakoff’s Recent memory

Disease pitfall Confabulations
psychosis if not treated impairment
Psychiatric Emergencies
Delirium Versus Dementia
Acute/subacute
¯ cognitive Drug
function intoxication/
Consciousness withdrawal
Abnormal VS
impaired
Delirium Hepatic
Infection Common Causes
encephalopathy
Fluctuating Duration
severity Days-weeks
Visual CNS lesions Hypoxia
hallucinations
common
Gradually ¯ Alzheimer’s
cognitive function disease
No acute focal
findings
CT = atrophy
Duration Consciousness
Often permanent Dementia Anoxic brain Parkinson’s
intact Common Causes
injury disease
Can have
superimposed Multi-infarct
dementia
acute worsening
CT = lacunar
of cognition
infarcts
Organic Acute Psychosis Etiologies Medications/Drugs (Including Withdrawal)
EtOH Benzodiazepines
Anticholinergics Cocaine
Digitalis Amphetamines
Medications &
Phenytoin Drugs THC
Tricyclic
antidepressants Opioids
INH PCP
Heavy metals Corticosteroids Antihistamines
Organic Acute Psychosis Etiologies Medical Conditions
Hypoglycemia
Hepatic
Hypercalcemia
encephalopathy
Pellagra (niacin
Hyponatremia
deficiency)
Encephalitis Medical Conditions Hypoxia
Thyroid disease Hypercarbia
Uremia Lupus
Wernicke- Pernicious
Korsakoff anemia (B12
Syndrome deficiency)
Organic Versus Functional Psychosis
Age < 12 & > 40
Recent memory PE/vitals often

impairment abnormal
Hx of substance Pupils abnormal

Organic
abuse ± nystagmus
Emotional lability Sudden onset
Visual & tactile

Disorientation
hallucinations
Age < 40
Remote memory PE/vitals often

impairment normal
Hx of substance Normal physical

Organic
abuse exam
Clear sensorium Gradual onset
Orientation Auditory
hallucinations
Amnesia
Anterograde Retrograde
Amnesia Loss of prior memories
Inability to create new memories
Transient global Inability to form

Lasts < 24 hours Unclear etiology Good prognosis
amnesia new memories
Traumatic After concussive May be anterograde

amnesia event or retrograde
Korsakoff’s Result of thiamine

Amnesia Confabulation
syndrome deficiency
Invented
memories
Major Depression
Major ¯ Interest in usual Typically

Dysphoria OR
Depression activities ≥ 2 weeks episodic
Symptoms & Signs
Sleep Unintentional weight Decreased Decreased Decreased

Guilt Anhedonia
disturbance &/or appetite change concentration activity energy
Psychomotor agitation Thoughts of suicide

or retardation Must screen for this
Underlying
Risk Factors Female Family history
medical condition
Major Often superimposed Other psychiatric

depression with substance abuse conditions
15 % lifetime
Pitfall
suicide risk
Suicide
Frequency of Lethality of
Suicide Women > Men Men > Women
attempts attempts
Advanced age
Pre-existing Non-married,
mental illness especially
widowed
Risk Factors for
Completed Suicide
Comorbid
physical illness Lives alone
Substance abuse Prior attempts
Most common
Drug overdose
attempt method
Most common
Gun shot wound
completed method
Not involuntarily committing patient at

Pitfall
risk to self (or others)
Grief Reaction
Sadness
Somatic Normal Grief Sleep impairment

complaints Reaction
Symptoms
> 2 months
Substance abuse Loss of self-esteem
Abnormal Grief
Reaction
Psychomotor
Guilt
retardation
Thoughts of
death
But, desire to be
with deceased =
normal
Bipolar Disorder
Typical onset
Bipolar Disorder Male = Female
20–30’s
Manic Symptoms
Pressured or Racing
¯ Sleep Activity self esteem Euphoria Risky behavior
rapid speech thoughts
Mania present? Bipolar I
Hypomania only Bipolar II Less severe
Financial, social, &

Sequelae Suicide Substance abuse
employment difficulties
Evaluate for toxic, metabolic,

Evaluation
or CNS disorders
Acute treatment Antipsychotics
Chronic Takes several days for Anticonvulsants

Lithium
treatment therapeutic onset Valproate, Carbamazepine, Lamotrigine
Schizophrenia
Typical onset late

Schizophrenia
adolescence-early adulthood
Symptoms must be 1 – < 6 months < 1 month

Time Frame
present for ≥ 6 months Schizophreniform disorder Brief psychotic disorder
Causes decreased Absence of Not caused by

Schizophrenia
functioning mood disorder substance abuse
Symptoms & Signs
Positive Disorganized Disorganized or

Hallucinations Delusions
symptoms speech catatonic behavior
Negative Emotional
Anhedonia Blunted affect
symptoms withdrawal
Typical antipsychotics More effective against

Treatment
(e.g., haloperidol) positive symptoms
Atypical Aripiprazole, Still risk tardive Less sedation &

But…
antipsychotics? Quetiapine, Risperidone dyskinesia cognitive impairment
Anxiety
Acute coronary
syndrome
Alcohol, Dysrhythmias
benzodiazepine
withdrawal
Mitral valve prolapse

Sympathomimetic
use Organic Conditions
Resulting in Anxiety
Pulmonary embolism
Hypothyroidism
Pheochromocytoma COPD
Hyperthyroidism Asthma
Generalized ≥ 6 months excessive,

Anxiety Disorder persistent anxiety
Anxiety Disorders
Rapid onset of anxiety Autonomic symptoms

Panic Attack
or impending doom Dyspnea, chest tightness, palpitations, tachycardia, diaphoresis
Recurrent panic Fear of future Worry over panic Resulting

Panic disorder OR OR
attacks attacks attack consequences behavior change
Post-traumatic Intrusive memories of Guilt, depression, Substance abuse

stress disorder extremely traumatic event anxiety often results
Irrational fear of
Phobia Avoidance
specific situation
Evaluate for Especially

Evaluation
organic etiology medications & drugs
Obsessive-Compulsive Disorder
Recurrent, intrusive,
Obsessions
unwanted thoughts
Behaviors patient engages in Repetitive hand

Compulsions
to “control” thoughts washing, checking
May occupy significant May cause a significant

Pitfall
amount of time per day lifestyle disruption
Anorexia
Refusal to maintain normal body weight Fear of gaining Distorted body

Anorexia
(>15 % under ideal body weight) weight image
Onset typically
Anorexia Female >> Male
in teens
Symptoms & Signs
Secondary ¯ Cardiac Normochromic

Bradycardia ¯Mg > QTc
amenorrhea contractility anemia
Significant Suicide is a
Pitfall
mortality common cause
Correct electrolyte Admission to inpatient

Treatment
abnormalities treatment center
Bulimia Nervosa
Poor impulse Episodes of Unlike anorexia Onset typically in

Bulimia Nervosa
control binge eating weight often normal teens-early adulthood
Binging typically followed by purging

Bulimia Nervosa OR Excessive exercise OR Fasting
(vomiting, diuretic or laxative abuse)
Symptoms & Signs
Metabolic Mallory-Weiss
Vomiting ¯K ¯ Cl alkalosis tears
Tooth decay
Metabolic
Laxative Abuse ¯ Na ¯K alkalosis
Generally better
Prognosis
than anorexia
Somatoform Disorders
Somatoform Physical No medical Symptoms not

disorders symptoms explanation voluntary
Numerous Multiple organ NO medical

Somatization
symptoms systems affected explanation
Preoccupying fear Persists despite evaluation ≥6 months significant

Hypochondriasis
of serious disease and reassurance distress or impairment
Hypochondriasis No secondary gain
Conversion Single neurological symptom Often triggered Not explained by

disorder (e.g., paralysis, blindness, seizure) by stressor organic disease
Conversion Patient does NOT consciously Symptom onset

disorder produce symptom typically sudden
“La belle Patient with lack of concern

indifference” regarding symptoms, common
Rule out organic

Evaluation Beware MS, SLE
pathology
Malingering, Factitious Disorders, and Munchausen’s Syndrome
Intentionally produced or For secondary May have antisocial

Malingering Motivation
feigned signs & symptoms gain behavior or drug abuser
Secondary gain Disability Drug-seeking

Work avoidance
examples payments behavior
Signs of drug Multiple non- Request specific Multiple visits for

Rapidly dose
seeking behavior narcotic “allergies” medications or dosages same complaint
Disconnect between symptoms & Lack of cooperation

Malingering
physical findings with physician
Factitious Intentionally produced or feigned Assuming the

Motivation
disorder signs & symptoms “sick role”
Example of a
Munchausen's
factitious disorder
Classically dramatic presentations Willing to undergo

Munchausen's Hospitalized desired
with prolonged pattern of behavior painful procedures
Munchausen's Factitious disorder imposed Caretaker produces Typically

by proxy on another symptoms in another person mother -> child
Personality Disorders
Paranoid
Cluster A
Schizoid Schizotypal
“Odd, eccentric”
Antisocial
Cluster B
Narcissistic “Dramatic, Borderline
emotional, erratic”
Histrionic
Avoidant
Cluster C Obsessive-
Dependent compulsive
“Anxious, fearful”
Antisocial, Borderline, Histrionic, and Narcissistic Personality Disorders
Antisocial Responsible for Disrespect for Impulsive Hx of conduct

personality disproportionate # of ED visits law & others behavior disorder as a teen
Behavior
typically
Poor medical
Complications Substance abuse Trauma improves by age
compliance
30
Borderline
Chronically labile Unstable relationships Impulsiveness
personality
Borderline Unstable self- Self mutilation, suicide Difficulty

Splitting
personality image attempts & threats controlling anger
Histrionic Excessively emotional, impulsive, Can lead to

personality attention-seeking behavior suicidal gestures
Narcissistic Inflated sense of self-importance, Leads to impractical

personality abilities, & achievements ambitions
Abuse/Neglect/Violence
Intimate Partner Violence
Intimate Partner Harm (Physical, Psychological,

Victims F >> M
Violence Sexual) by current or former partner
Other risk Low socioeconomic

Young adulthood Pregnancy
factors status
Common Patterns of Injury
Fingernail Injuries in multiple

Broken nails Forearm injuries
scratches healing stages
Pitfall for Victim attempts to

OR When abuse reported
assault risk end relationship
Screen Ensure patient Refer to social services Report to law enforcement

Management
females and child safety & victim advocate as appropriate
Elder Abuse
Neglect or action resulting

Elder Abuse
in harm to elderly
M>F
F>M Typically primary
Substance abuse caregiver
Hx of domestic Cognitive Characteristics of
violence impairment History of Abusers
Risk factors for Mental illness
Elders violence
Lack of social Physical Financial
support dependency
dependence on
elder
Patterns of Injury
Electrolyte Forearm
Decubiti Dehydration Rhabdomyolysis Rape marks
abnormalities injuries
Chronic neurologic conditions and/or

Pitfall
immobility may result in some of these findings
Replete electrolytes Report to Social work to assist with

Management Treat injuries
& fluids authorities placement vs. admission
Sexual Assault
~1/2 assaults have no visible

Sexual assault
genital injury
> 72 hours post Unlikely to find Consider deferring Shared decision making with
assault? evidence forensic exam victim & victim advocate
Must maintain chain of

Pitfall
custody of evidence
Offer pregnancy, STD, HIV

Post evaluation
prophylaxis
ED Staff/Patient Safety
Chemical Typical Atypical Antipsychotic +

Benzodiazepines
restraints antipsychotics antipsychotics benzodiazepine
Droperidol Synergism
Haloperidol Reduced side
effects
Pitfall of physical Failure to reassess physically restrained patients

restraints frequent & document neurovascular status
Neurovascular
Potential injuries Rhabdomyolysis Asphyxia
injury
Violence prevention Screening for Visible and Limited ED

Alarm systems
methods weapons responsive security access
Addictive Behavior and Withdrawal
Substance Abuse/Dependence
Pattern of drug use resulting in

Substance abuse
harm to patient or others
Failure to fulfill
work, school, or
home obligations
Use continues
DSM IV definition Recurrent use in
despite
1 of these in past hazardous
interpersonal
year situations
problems
Use continues
Recurrent legal
problems despite known
physical /
psychological
problem caused
Large amount of by substance Important
time activities given up
obtaining/using/ or reduced
recovering DSM IV definition
Persistent desire
3 of these in past
to ¯ use
year
Withdrawal Tolerance
Substance taken
in larger
amounts/longer
period than
intended
Alcohol Withdrawal
Alcohol Onset 6–48 hours Delirium 48–120 hours

Potentially fatal
Withdrawal after last use Tremens after last use
Symptoms & Signs Withdrawal
Generalized tonic- Tongue

Tremulousness Irritability Tachycardia Hypertension
clonic seizures fasciculations
Must consider trauma or

Pitfall
SDH as etiology of seizure
Symptoms & Signs Delirium Tremens
Visual Elevated
Paranoia Diaphoresis Irritability Tachycardia Hypertension
hallucinations temperature
Uncomplicated Long acting benzodiazepine Lorazepam preferred if hepatic impairment,

withdrawal or seizures? (lorazepam, diazepam or chlordiazepoxide) elderly due to no active metabolites
Phenytoin not useful for

Pitfall
EtOH withdrawal seizures
Delirium High doses of If refractory consider Propofol

tremens? benzodiazepines & airway protection
Chronic IV thiamine, K+, Mg++ often depleted in

alcoholics? glucose, fluids chronic alcoholics
Benzodiazepine Withdrawal
Benzodiazepine Similar symptoms to

But… Rarely fatal
Withdrawal EtOH withdrawal
Withdrawal may Depends on agent Symptoms may not

Pitfall
be delayed half-life develop for 7–10 days
Gradual taper of agent over

Management
up to 10 weeks
Opiate Withdrawal
Symptoms & Signs
Mydriasis Piloerection N/V Diarrhea GI cramping Rhinorrhea Irritability
Body aches
Opiate Not life

Withdrawal threatening
Heroin/oxycodone/other
Onset/Duration Methadone
short acting agents
Onset 36–72 hours after Onset 72–96 hours
last use Duration up to 14
Duration 7–10 days days
Reduces Ineffective for

Treatment Clonidine But…
autonomic sx other symptoms
Buprenorphine Prescribing for addiction limited

& Methadone? to specific facilities/clinicians
Partial opioid
Buprenorphine
agonist & antagonist
Buprenorphine + Heroin Can trigger

use within 24 hours? withdrawal symptoms
Cocaine/Sympathomimetic Withdrawal
Symptoms & Signs
Increased
Fatigue Malaise Depressed mood
appetite
Cocaine/Sympathomimetic
Duration 8–48 hours
Withdrawal
THC Withdrawal
Symptoms & Signs
Decreased
Irritability Mood swings Sleep disturbance
appetite
Relatively
THC Withdrawal
uncommon
Timeline after Onset Duration

quitting 1–2 days 1–3 weeks
Obstetrics and Gynecology
Bobby Desai and Alpa Desai
Contents
Infections 618
Gynecologic Oncology 627
Obstetrics 629

A. Desai, DO
Community Health and Family Medicine,

DOI 10.1007/978-3-319-30838-8_11
618 B. Desai and A. Desai
Infections
Pelvic Inflammatory Disease
Introduction
Infections of the Ascending from Includes a Most common
PID upper the vagina & spectrum of gynecologic cause
reproductive tract cervix diseases of ED visits
Chlamydia Polymicrobial
PID Due to OR Gonorrhea OR
(Most common) (30–40 %)
Including
anaerobes
Prior PID or Multiple sexual IUD in 1st Hx of sexual

Risk factors STD Younger age month abuse
partners
Decreased risk Use of barrier

of PID Pregnancy contraceptives
Most commonly occur early in or at

General Symptoms & Signs the end of menstrual cycle due to
thinning of cervical mucosal barrier
Lower Vaginal Vaginal or postcoital

discharge Dysuria Fever Malaise N/V
abdominal pain bleeding
Cervical motion Uterine Adnexal tenderness Mucopurulent Abdominal guarding Associated

tenderness tenderness (most sensitive finding) cervicitis & rebound peritonitis
Fitz-Hugh-Curtis
RUQ pain Jaundice
syndrome
Laparoscopy Laboratory
Diagnostic tests Ultrasound OR CT OR
(Gold standard) evaluation
Thickened fluid
Ultrasound
filled fallopian Free pelvic fluid Dx of TOA
utility
tubes
Rule out other

CT utility surgical causes
Other diagnostic Mucopurulent Elevated Confirmation of

criteria Temp > 38 cervicitis ESR/CRP GC or Chlamydia
Uterine Adnexal Cervical motion

Empiric therapy For OR
tenderness tenderness tenderness
Cefotetan
Inpatient Ampicillin/
or Doxycycline Clindamycin Gentamicin Doxycycline
treatment Sulbactam
Cefoxitin
Cefotetan
Outpatient Levofloxacin
or Doxycycline Metronidazole OR Metronidazole
treatment or Ofloxacin
Cefoxitin
IUD? Remove IUD

Obstetrics and Gynecology 619
Admission Criteria for PID
Pregnancy
Failed outpatient Other possible

therapy surgical etiology
Admission Criteria
for PID
Tubo-ovarian
abscess Intractable N/V
Compliance
issues
Complications of PID
Ectopic pregnancy
Menstrual
Infertility
irregularities
Complications of Chronic pelvic

Tubo-ovarian PID pain
abscess
Majority resolve
with Abx alone Fitz-Hugh-Curtis
Syndrome
Adhesions Dyspareunia
Fitz-Hugh-Curtis Syndrome
Spillage of purulent
Fitz-Hugh-Curtis Lymphatic
Perihepatitis Due to material from tubes Direct spread OR
Syndrome spread
into abdomen
Referred
Symptoms RUQ pain shoulder pain
Violin string
Laparoscopy adhesions around
liver
Treatment Same as PID

Vulvovaginitis
Introduction
PEDIATRICS
Infections Atrophic vaginitis

Inflammation of Vaginal foreign body
Vulvovaginitis Due to Multiple factors Allergy
vulva &/or vagina
Irritants
Most common Bacterial vaginosis Candidiasis

infectious causes Trichomoniasis
(most common) (2nd most common)
Most common Gyn Less covering of

Exposure to
Vulvovaginitis complaint in Due to introitus by labia Low estrogen irritants
prepuberty majora
Symptoms & Signs
Vaginal + Abdominal
Burning Itching + Pelvic pain
discharge pain
Trichomonas & BV Premature

Low infant birth
complications in rupture of Preterm labor weight
pregnancy membranes
Normal vaginal
pH 4 – 4.5
Sx of vaginitis &
pH 4 – 4.5? Normal OR Candidiasis
Sx of vaginitis &
pH >4.5? BV OR Trichomonas
Bacterial Vaginosis (BV)

Most common Normal lactobacilli vaginal
50 % may be
BV cause of vaginal Due to flora replaced by
asymptomatic
discharge Gardnerella & anaerobes
Intercourse with Vaginal intercourse

Relations with Prior use of
Risk factors uncircumcised following anal
>1 partner antibiotics
partner intercourse
Diagnosis Thin homogenous Clue cells on wet Fishy odor on

prep pH > 4.5 KOH whiff test
(3 of 4 criteria) vaginal discharge
PO or vaginal Treat all pregnant

Treatment OR Clindamycin
Metronidazole patients
Flagellated
Trichomoniasis Due to Common STD
protozoan
Increases risk of
Trichomoniasis HIV/HSV/HPV
Motile
Diagnosis trichomonads on Culture Antigen testing
wet mount
Symptoms & Signs
Vaginal ± Abdominal Strawberry May be

discharge
Irritation Itching ± Pelvic pain pain cervix on exam asymptomatic
Yellow-green Punctate
submucosal
Frothy hemorrhages
Foul smelling
PO
Metronidazole
Trichomoniasis
Flagellated
Trichomoniasis Due to Common STD
protozoan
Increases risk of
Trichomoniasis HIV/HSV/HPV
Motile
Diagnosis trichomonads on Culture Antigen testing
wet mount
Symptoms & Signs
Vaginal ± Abdominal Strawberry May be

discharge
Irritation Itching ± Pelvic pain pain cervix on exam asymptomatic
Yellow-green Punctate
submucosal
Frothy hemorrhages
Foul smelling
PO
Metronidazole
Candida Vaginitis
2nd most common Part of normal

Candida cause of vaginal flora
infections
Oral Diabetes Prior use of

Risk factors Pregnancy
contraceptives mellitus antibiotics
Thick cottage Yeast buds &

Diagnosis cheese vaginal pseudohyphae on pH 4–4.5
discharge wet prep
Symptoms & Signs
Vaginal Vulvar
Leukorrhea Vulvar Itching Dyspareunia Dysuria Vulvar erythema
discharge excoriations
“Cottage cheese” Most common &
most specific Sx Vulvar edema
Topical Topical for

Treatment PO Fluconazole OR imidazoles Pregnancy
More effective
than nystatin
Bartholin Cyst and Abscess
Obstruction on the
Located in labia Provide moisture
Bartholin glands duct may lead to
minora for the vestibule
cyst or abscess
Rare presence of
Abscess Very painful Indurated area Polymicrobial
systemic signs
Infectious agents GC & Chlamydia Bacteriodes E. coli
Treatment I&D of abscess Word catheter

Abdominal and Pelvic Pain in the Nonpregnant

Patient
Ovarian Cysts
Two types of
First 2 weeks of Corpus luteal Last 2 weeks of
functional Ovarian Follicular cyst
menstrual cycle cyst menstrual cycle
cysts
Growths filled
Dermoid cyst with various types
of tissue
Pressure on
Pain from Rupture in
adjacent Torsion
ovarian cysts peritoneum
structures
Sudden onset of
Torsion OR Rupture
unilateral pain
Symptoms & Signs Symptomatic cysts > 3 cm
Lower Vaginal Tender adnexal Cervical motion

abdominal pain Pelvic pain bleeding mass tenderness Malaise N/V
Shock due to
hemorrhage
Transient
Usually
Mittelschmerz (<1 day) mid cycle
unilateral
pain
Imaging test of May see fluid in

choice Pelvic U/S cul-de-sac
Shock or
possible torsion? Laparoscopy
Ovarian or Adnexal Torsion
Ovary twists on Ovarian Surgical Adenexal >

Torsion Due to
oviduct (Adnexa) enlargement emergency Ovarian torsion
Congestion of Ischemia and

Pathophysiology Venous blockage Arterial blockage
ovary potential necrosis
Most associated Dermoid cyst

>50 % on the
Torsion with benign most common
Right
tumors or cysts
Chemical
Pregnancy Large cysts or
Risk factors induction of
(Corpus luteum) tumors
ovulation
Symptoms & Signs
Unilateral constant Vaginal bleeding Tender adnexal Cervical motion

lower abdominal pain N/V is not common mass tenderness
Imaging test of Pelvic U/S with Low flow to

choice Doppler ovary
Treatment Laparoscopy
Endometriosis
Common cause of Endometrial Chronic Mostly in
Endometriosis infertility & pelvic Due to tissue outside of inflammatory
pain uterus reaction reproductive age
Endometrial
Adenomyosis tissue in uterine
wall
Common Ovary Fallopian Abdominal

locations Bladder Lungs
(most common) tubes cavity
May cause
catamenial
pneumothorax
Symptoms & Signs
Chronic lower Pain is cyclical, Dysmenorrhea

Dyspareunia Hypermenorrhea Pelvic pain
abdominal pain associated with menses (most common symptom)
Enlarged Ovarian mass
Infertility
adherent uterus (Chocolate cyst)
Imaging test of
Pelvic U/S
choice
Diagnosis Laparoscopy
Treatment Analgesia Referral

Leiomyomas
Most common
Benign tumors of
Leiomyomas Uterine fibroids pelvic tumor in
uterine muscle African Americans
Pregnancy results
May outgrow May torse if on a
Complications in growth and loss Pain
blood supply pedicle
of blood supply
Symptoms & Signs
Lower Mass on
Pelvic pain Hypermenorrhea
abdominal pain examination
Imaging test of
Pelvic U/S
choice
Treatment Analgesia Referral
Abnormal Vaginal Bleeding
Abnormal Vaginal Bleeding
Vaginal bleeding Premenstrual Midcycle Menstrual Postmenstrual
Bleeding
Heavy Excessive irregular
Menorrhagia Metrorrhagia outside Menometrorrhagia
bleeding normal cycle bleeding
Abnormal vaginal Nonuterine Ovulatory Anovulatory

bleeding in non-
pregnant females bleeding bleeding bleeding
Abnormal Bleeding between

Metrorrhagia
ovulatory bleeding menses
Oral
Treatment NSAIDs
contraceptives
Anovulatory Light & frequent Prolonged amenorrhea

Menometrorrhagia OR OR with intermittent
bleeding bleeding metrorrhagia
Oral
Treatment contraceptives NSAIDs
Consider endometrial cancer in pts > 35!

Ovulatory Bleeding
Tumors
Blood dyscrasias Fibroids
Endometrial
hyperplasia
Ovulatory Bleeding
Polyps Endometriosis
Endometrial Adenomyosis
Malignancy Infections
Cervical cancer Cervicitis
Endometrial cancer PID
Anovulatory Bleeding
Polycystic ovary
Extremes of Endocrine
reproductive age disorders
Anovulatory Oral
Bleeding contraceptives
Eating disorders
Liver diseases
Lower urinary
tract lesions Cirrhosis
Renal diseases
Gynecologic Oncology
Ovarian Cancer
Has highest
2nd most common May be advanced Peak incidence
Ovarian cancer But… mortality rate of
gyn malignancy on diagnosis 55–65
GYN malignancy
Obesity Hx of breast or
Risk factors Infertility Low parity Family history
(high fat diet) colon cancer
Symptoms & Signs
Urinary frequency
Abdominal pain Bloating Weight loss Pleural effusion Ascites Early satiety
or urgency
Unilateral fixed
mass
Rare torsion
Unexplained Gyn neoplasm

until proven
ascites otherwise
Diagnosis Ultrasound OR CT scan
Uterine Cancer
Most common Adenocarcinoma Usually caught Average age

Uterine cancer GYN malignancy 55–58
is most common early
Sarcoma? More aggressive Worse prognosis
Continuous Obesity DM Early menses

Risk factors Nulliparity Late menopause
estrogen (high fat diet) HTN
Symptoms & Signs
Abnormal Uterine
vaginal bleeding Weight loss
enlargement
Endometrial Transvaginal U/S

Diagnosis D&C OR OR
biopsy in postmenopause
Cervical Cancer
Squamous cell is Average age at

Cervical cancer most common Dx is 54
Early coitus &

Prolonged
Risk factors multiple HPV Smoking Hxof STD’s
partners OCP
Symptoms & Signs
Postmenopausal Postcoital Abnormal Vaginal Mass or ulceration

Pelvic pain Leg swelling
bleeding bleeding vaginal bleeding discharge on exam
Cervical cancer AIDS defining

in HIV illness
Diagnosis Cervical biopsy

Obstetrics
Ectopic Pregnancy
Fetus implanted Most commonly in Abdomen

Ectopic
outside of uterine distal fallopian OR Ovary
pregnancy cavity tube Cervix
Prior Tubal Pelvic Infertility

Risk factors PID IUD
ectopic ligation surgery Rx
Symptoms & Signs
Vaginal Adnexal Relative

Abdominal pain Hx amenorrhea Shock Adnexal mass
bleeding tenderness bradycardia
HCG U/S Double gestational sac

Diagnosis (slower than (most IUP FHT
normal rise) sensitive) Yolk sac or fetal pole
U/S & HCG Transvaginal

Transabdominal
(1500–3000 Gestational sac Fetal pole
levels (6000 mIU/mL)
mIU/mL)
No definitive IUP
Consider
IUP on U/S? Ectopic unlikely heterotopic in Indeterminate Close f/u
fertility patients
Serial US & HCG
Embryonic cardiac
High probability Free fluid Adnexal activity outside
NO IUP Diagnostic
U/S in pelvis mass uterus
Laparoscopy if Laparotomy if Continued pain Persistent

Treatment stable &
unruptured unstable after laparoscopy? ectopic
Beware abdominal Ruptured ectopic

Use for tubal No fetal cardiac
Methotrexate pain (most common until proven
mass <4 cm activity side effect) otherwise
Abortions
< 20 weeks Abdominal

Threatened Vaginal bleeding Closed os
gestation cramps or pain
Treatment Vaginal rest
< 20 weeks Abdominal

Inevitable Vaginal bleeding Open os
gestation cramps or pain
Treatment D&C
Tissue noted as Likely to occur at

Incomplete Vaginal bleeding
cervical os 6–14 weeks
Treatment D&C
Passage of all
Complete Vaginal bleeding <20 weeks Closed os
fetal tissue
Fetal death <20 No passage of

Missed D&C
weeks tissue
Infection during
Septic
abortion
Treatment Fluids Antibiotics D&C
RhoGAM
Rhogam Anti-D IgG
0.1 mL of fetal Also can occur

Immunization blood mixing with
mother’s with ectopics
Destruction of Rh+ fetal RBC Antibodies to Rh+ fetal RBC

Pathophysiology Immunization
in maternal circulation which cross placenta
Fetal hemolytic Potential death

Complications Splenomegaly Erythroblastosis
anemia of fetus
Indications in Any type of Placenta Antepartum

Ectopic Trauma
Rh (-) mother abortion abruption hemorrhage
Dose <12 weeks 50 mcg >12 weeks 300 mcg

Gestational Trophoblastic Disease
Gestational
Spectrum of Partial
trophoblastic OR Choriocarcinoma
disease processes hydatidiform mole
Gestational Arises in
trophoblastic trophoblastic cells
disease of the placenta
Hydatidiform Complete is
mole Noninvasive Partial OR Complete
more common
Deformed
Complete No fetus Incomplete nonviable fetus
present
Symptoms & Signs
Vaginal bleeding Passage of “grape-

Hyperemesis Preeclampsia Large uterus
(75–95 %) like” clusters
st
1 Trimester 2nd Trimester
Lucent areas & Elevated HCG

Diagnosis Ultrasound
brighter areas levels
Suction
Treatment
curettage
Amniotic fluid Metastases to

Complications Preeclampsia
embolism lung, liver, brain
Hypertension, Preeclampsia, and Eclampsia
Hypertension in Pregnancy
Chronic Existed prior to Persists > 6 weeks

OR Dx < 20 weeks OR
Hypertension pregnancy after delivery
Complications of Abruptio
Preterm birth Preeclampsia Low birth weight
chronic HTN placentae
Treatment Labetalol OR Methyldopa OB/GYN referral
Resolves within
HTN during Complications to
Transient HTN Proteinuria 2–4 weeks of
pregnancy pregnancy delivery
Preeclampsia
140/90 or SBP >20 After 20

Preeclampsia HTN or DBP >10 over Proteinuria Edema
baseline weeks
Before 20 Consider molar

weeks? pregnancy
Vasospastic disease of Causes end

Pathophysiology
unknown etiology organ damage
Premature Low birth Intrauterine Abruptio

Associations growth
labor weight retardation placenta
DM <20 Multiple Molar

Risk factors Nulliparous HTN Obesity FHx
Renal dis. >40 gestation pregnancy
Symptoms & Signs
Visual
Headache Abdominal pain Edema
symptoms
Treatment Delivery of fetus
Eclampsia
>20 weeks <4 weeks

Eclampsia Preeclampsia Seizures OR
gestational age postpartum
Symptoms & Signs
Headache Visual symptoms Abdominal pain Edema Seizures Hyperreflexia
Treatment of Magnesium
Seizures sulfate
Magnesium Decreased Calcium

Hyporeflexia Treatment
toxicity? respiratory drive gluconate
Treatment of
Hydralazine OR Labetalol
HTN
Liver/spleen Abruptio Intracranial

Complications End organ failure
hemorrhage placenta hemorrhage
HELLP Syndrome
Elevated Liver Clinical variant

HELLP syndrome Hemolysis Low Platelets
enzymes of Preeclampsia
Epigastric RUQ abdominal

HELLP syndrome + HTN OR
abdominal pain pain
HELLP syndrome Multigravid Primigravid
Schistocytes on Platelets Elevated AST Calcium

Diagnosis
peripheral smear <100,000/mcL and ALT gluconate
Same as
Treatment Delivery of fetus Control of BP Magnesium
Preeclampsia
Subcapsular liver Rupture of right

Complications
hematoma lobe of liver
Placental Emergencies
Abruptio Placentae
Separation of 2nd most
Abruptio placenta from Can occur
common cause
Placentae uterine wall spontaneously of fetal death
HTN
(most Advanced Cocaine Hx of abd Prior
Risk factors Trauma Smoking
common) age abuse surgery incidence
Symptoms & Signs
Painful vaginal Uterine

Contractions Abdominal pain Hypotension N/V Back pain
bleeding tenderness
If no bleeding, Tachycardia then Fetal
then concealed Fetal distress
bradycardia decelerations
abruptio
Maternal Hemorrhagic Rupture of Multi-organ

DIC
complications shock uterus failure
Fetal Neurologic Rupture of Multi-organ

Death
complications abnormalities uterus failure
External fetal Indicated for

Not sensitive for
Ultrasound? monitoring more blunt trauma pts
Dx sensitive > 20 weeks
>8 Risk for 3–7 Extend

Fetal monitoring contractions/hr contractions/hr monitoring for
for 4 hours abruption for 4 hours 24 hours
Fluid Blood products Emergent OB

Treatment Fetal monitoring
resuscitation at the ready consultation
> 23 weeks Consideration of

Fetal distress emergent C -
gestation section
Placenta Previa
Placenta near or
Placenta Previa
over the cervical os
Multi- Advanced Cocaine Hx of C-

Risk factors Minorities Smoking
parity age abuse section
Symptoms & Signs
Painless vaginal Uterine

Contractions Abdominal pain Hypotension N/V Back pain
bleeding tenderness
Pelvic Exam Contraindicated
Highly sensitive
Ultrasound?
for Dx
Other Emergencies of Pregnancy, Deliveries, or the Postpartum Period
Tidbits
Asymptomatic Asymptomatic Aggressive

OR
pyuria bacteriuria empirical Rx
Inpatient
Pyelonephritis?
therapy
Complications Preterm labor Sepsis
Most common Higher fetal

Diagnosis may Higher incidence
Appendicitis surgical emergency mortality &
in pregnancy be delayed of rupture maternal morbidity
Diagnosis U/S Surgical consult Consider CT scan
Preterm Birth and Premature Rupture of Membranes (PROM)

Leading cause of
Labor occurring May occur
Preterm birth infant morbidity & OR With PROM
mortality <37 weeks spontaneously
Membrane
PROM rupture <37
weeks gestation
Vaginal Hx of abd Prior

Risk factors Race Hx STD Smoking Infection
bleeding surgery incidence
Limited digital
Examine vaginal Blue is positive =
PROM Diagnosis exams (use sterile Nitrazine test
speculum) fluid pH >6.5
Complications Prolapsed cord Chorioamnionitis

Umbilical Cord Prolapse
Prolapsed
High mortality
umbilical cord
Prolapsed Place mother in

knee to chest
umbilical cord position
Elevate Emergent
Treatment Impede delivery
presenting part C-section
Postpartum Hemorrhage
Most common
Postpartum cause of maternal Primary Secondary
Hemorrhage mortality worldwide In 1st 24 hours >24 hours, < 6 weeks
Primary Retained Lacerations

Uterine Rupture of Inversion Clotting
Postpartum placental of genital
Hemorrhage atony fragments tract uterus of uterus problems
Enlarged uterus Prolonged Multiple

Uterine atony Risk factors Multiparity
(“Doughy”) labor gestations
Treatment IV fluids Fundal massage Oxytocin
Uterine rupture High doses of

Trauma Cocaine Prior C -section
Risks Oxytocin
Symptoms & Copious Absent Tender

Shock Treatment C-section
Signs bleeding FHT uterus
Retained Products Early or delayed

Firm uterus Treatment D&C Oxytocin
of conception painless bleeding
Uterine Excessive traction Non -palpable Obstetric

Mass in vagina
Inversion on umbilical cord uterus Emergency
Tocolytic Do not separate Manual Emergent

Treatment OR
medications placenta reduction laparotomy
Amniotic Fluid Embolism
Occurs when amniotic Immunologic

Amniotic Fluid May simulate
fluid enters the response by High mortality
Embolism maternal circulation anaphylaxis
mother
Abruptio Amnio -
Occurs with C-section Labor Abortion Trauma
placentae centesis
Symptoms & Signs
Acute cardiovascular Seizures

collapse (hypoxic) Shock Dyspnea ARDS DIC Hypoxemia
Immediate
Place in left lateral
Treatment Supportive delivery of the
decubitus position infant
Peripartum Cardiomyopathy
Peripartum Dilated Occurs at any

High mortality
Cardiomyopathy cardiomyopathy stage of gestation
Advanced Multiple Pre-

Risk factors Multiparity HTN EtOH use
age fetuses Eclampsia
Symptoms &
CHF
Signs
Association with
Treatment CHF treatment Heparinization Due to
thrombotic events
Endometritis
Usually
Endometritis
polymicrobial
Symptoms & Signs
Foul-smelling Uterine
Abdominal pain Fever Tachycardia
lochia tenderness
Broad spectrum
Treatment
antibiotics
Pelvic Septic Necrotizing Infected

Complications Peritonitis
abscess thrombophlebitis fasciitis hematomas
Mastitis
Breast ducts
Mastitis Infection Staph
blocked
Symptoms & Signs
Breast pain Erythema Edema Fever
Continue breast
feeding
Ophthalmology
Bobby Desai
Contents
Neuro-ophthalmology 638
Pupil Abnormalities 640
Visual Field Deficits 641
External Eye 642
Conjunctiva 648
Cornea 653
Corneal Abrasion, Laceration, and Ulcers 657
Uveitis and Iritis 660
Vitreous and Intraocular Cavities 661
Retina 663
Optic Nerve 666
Temporal Arteritis 668
Glaucoma 669
Trauma 670
Blow-Out Fractures 673
Retrobulbar Hematoma 673
Chemical Burns 674
Lacerations to Refer 674
B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_12
638 B. Desai
Neuro-ophthalmology Eye Movements: Right Eye
Eye Muscles: Left Eye Superior Inferior

rectus Oblique
SR
O
S
Lateral Medial
rectus rectus
VI
MR LR
Inferior Superior
rectus oblique
IV
IR
LR6(SO4)3
Cranial Nerves
All innervated by Lateral Rectus Superior Oblique

Eye muscles Except
CN 3 6 4
Eyelid opened by
Eyelid closed by 7
Eyelid Control CN 3 &
(hook closing lid) Sympathetic chain
Bell’s palsy affects Horner’s syndrome
eye closure + 3rd nerve palsies
cause ptosis
Pupillary fibers
Compression of Ipsilateral fixed
CN 3 dilated pupil Run on outer part of nerve
Posterior Affected in uncal

communicating herniation
artery aneurysm until
proven otherwise
CN 3
Medial
Diabetic CN 3
Pupil is spared Ptosis Abnormal gaze Upwards
palsy
Downwards
Dysfunction of Can’t look

CN 6 laterally
Dysfunction of Affecting entire Can’t completely Potential for

Bell’s Palsy close eyelids on abrasions &
CN 7 face affected side keratitis
Consider Ramsay
Hunt
Bell’s Palsy Eye lubricant

Antivirals Steroids Protect eye with eye shield
Treatment drops
Ophthalmology 639
Sympathetic Chain and Horner’s Syndrome
Sympathetic chain Travels with the Abnormalities can

internal carotid occur anywhere
Anatomy through the neck along this path
Sympathetic Chain Smooth muscle Facial sweat

to elevate eyelid Pupil dilation
Innervation glands
Mueller muscle “Fight or Flight”

response
Elevates upper
eyelid by 2 mm
Loss of Horner’s
Ptosis Miosis Anhidrosis
Sympathetic chain Syndrome
Evaluation of CT angiogram of
Horner’s CT of brain and
CXR head & neck
syndrome cervical spine vessels
Carotid or vertebral
Pancoast tumor
dissection
CVA Aneuryrsm
Neuroblastoma Tumors
(esp. at lung apex)
Children Causes of Horner’s
Syndrome
Lymphoma Trauma
Carotid Artery
Herpes Zoster
Dissection
640 B. Desai
Pupil Abnormalities
Introduction
Surgery
Inspect pupil Teardrop shaped Acute Trauma
Irregular pupil
shape pupil with iris rupture
Remote trauma
Normal pupillary Tests cranial Direct & consensual

light reflex nerves II & III response to light
Parasympathetic Runs with Causes pupillary

Pupillary control
chain cranial nerve III constriction
Sympathetic “Fight or Flight”

Pupillary control Dilates the pupil
chain response
Intrinsic optic nerve

Afferent pupillary Optic nerve Disorders preventing pathology
light from reaching Retinal pathology
defect (APD) disorder optic nerve Vitreous pathology
Marcus-Gunn pupil
Swinging Pupils will be equal Affected pupil will

APD Diagnosis? due to consensual have no response to
flashlight test response light directed at it
Conditions that Multiple Vitreous

Optic neuritis Tumors Glaucoma
cause APD? sclerosis hemorrhage
Argyll Robertson Small irregular Accommodation preserved No reaction to light

with bilateral pupillary
pupil pupil constriction in affected eye
Ophthalmology 641
Visual Field Deficits
Visual Field Deficits
Monocular vision loss
Globe
Retina
Optic nerve
Temporal arteritis
Visual Fields Retina

Bitemporal
hemianopsia
R Optic nerve
Optic chiasm L
Pituitary tumor 1
1 Optic chiasma
Aneurysm
2
3 Optic tract
2
Lateral geniculate
body
3
Homonymous Optic radiation

hemianopsia 4
Optic tract 4
CVA
Most common field
deficit in CVA 5
Occipital cortex
Bottom right image (Reprinted from Galloway NR, Amoaku WMK, diseases and their management. London: Springer Verlag; 2006.
Galloway PH, Browning AC. Neuro-ophthalmology. In: Galloway NR, p. 179–88. With permission from Springer Verlag)
Amoaku WMK, Galloway PH, Browning AC, editors. Common eye
642 B. Desai
External Eye
Lids
Hordeolum (External and Internal)
Infection of eyelash
External Pustule at eyelid
follicle & sebaceous or Usually bacterial
hordeolum (Stye) sweat gland margin
At lid margin Staph
Internal Infection of Pustule is on

surface of tarsal
hordeolum meibomian glands plate
Symptoms & Signs
Pain Redness Eyelid swelling
Topical ointment
Warm
Hordeolum Rx to prevent
compresses infection
Erythromycin
Refer to
Need I&D?
ophthalmology
Center right image (Reprinted from Khairallah M, Kahloun R. Infections of the eyelids. In: Tabbara KF, Abu El-Asrar AM, Khairallah M, editors.
Ocular infections. Heidelberg: Springer Verlag; 2014. p. 51–61. With permission from Springer Verlag)
Chalazion
Chronic inflammation of eyelid Mid portion of upper

Chalazion due to blockage of Meibomian Usually painless
glands in the tarsal pate lid away from margin
Lid may have mild
erythema
Difficult to distinguish from

Chalazion Same treatment
internal hordeolum
Associated with
Chalazion squamous cell
carcinoma
Warm Topical ointment Ophthalmology

Chalazion Rx to prevent
compresses infection referral
Erythromycin
Center right image (Reprinted from Khairallah M, Kahloun R. Infections of the eyelids. In: Tabbara KF, Abu El-Asrar AM, Khairallah M, editors.
Ophthalmology 643
Blepharitis
Inflammation of Chronic Staph

Blepharitis
eyelid epidermidis infection
Symptoms & Signs
Conjunctival Crusting Eyelid redness +

+ Eye pain Pruritis + Ulceration
injection around lids swelling
Blepharitis Seborrheic Atopic Staph aureus

Lice infestation
Associations dermatitis dermatitis infection
Daily cleansing Topical

Treatment with baby
shampoo antibiotics
Bottom right image (Reprinted from Khairallah M, Kahloun R. Infections of the eyelids. In: Tabbara KF, Abu El-Asrar AM, Khairallah M, editors.
644 B. Desai
Dacryocystitis
Infection of Strep
Dacryocystitis Usually Staph OR
lacrimal sac pneumoniae
Red, tender Below the inner

Dacryocystitis Inferior-medial
swelling canthus
Symptoms & Signs
Pressure over lacrimal sac Eyelid redness +

Low grade fever Excess tearing Crusting
= pus through punctum swelling
Lower eyelid
Dacryocystitis Associated with

Corneal ulceration
complication Strep pneumoniae
Warm Relief of duct

Treatment Oral antibiotics Decongestants
compresses obstruction
Ophthalmology
consult
Top right image (Reprinted from Khairallah M, Attia S. Infections of the orbit. In: Tabbara KF, Abu El-Asrar AM, Khairallah M, editors. Ocular
infections. Heidelberg: Springer Verlag; 2014. p. 37–43. With permission from Springer Verlag)
Dacryoadenitis
Inflammation of
Dacryoadenitis Bacterial or Viral
lacrimal gland
Red, tender Outer portion of

Dacryoadenitis
swelling upper lid
Acute causes? Mumps EBV Staph Gonococcus
Chronic causes? Sarcoid Neoplasm Sjogren’s
Symptoms & Signs
Eyelid redness + Preauricular

Tenderness swelling Excess tearing
lymph nodes
Upper eyelid
Warm Incision &

Treatment Oral antibiotics
compresses Drainage
Ophthalmology
consult
Ophthalmology 645
Periorbital and Orbital Cellulitis
Introduction: Orbital Infections
Preseptal Postseptal
Subperiosteal Orbital Cavernous sinus
Orbital infections cellulitis cellulitis
(Periorbital) (Orbital) abscess abscess thrombosis
Least severe Most severe
Preseptal Infection of eyelids

Anterior to orbital Treated as
(Periorbital) and tissues around Usually benign
Cellulitis septum outpatient
the eye
Postseptal Infection of orbital Posterior to orbital Treated as

Vision threatening
(Orbital) Cellulitis soft tissues septum inpatient
Closed space IV antibiotics

Outward
appearance of May be similar + Surgery
both?
Mechanism of Hematogenous
Local infection Skin disruption
spread? spread
Common < 2 y.o.
Staphylococcus Streptococcus Streptococcus

Organisms (aureus & H. influenza
epidermidis) species pneumoniae
Less common
Specific
None
laboratories?
Definitive
CT scan
diagnosis?
646 B. Desai
Preseptal Cellulitis
PEDIATRICS
Hordeolum
Preseptal Associated with Especially
upper respiratory Eyelid problems Chalazion
cellulitis infections sinusitis
Insect bites or other
skin trauma
Preseptal Childhood
<10 years old
cellulitis disease
Symptoms & Signs
Low grade Eyelid redness +

URI Sx Excess tearing
fever swelling
Preseptal No eye Painless ROM Normal visual Normal pupillary

cellulitis involvement of eye acuity reactivity
Amoxicillin/Clavulanate
Mild Preseptal 24 hour
cellulitis Outpatient Rx Hot packs
1st generation follow-up
cephalosporin
Moderate – Vancomycin
Ophthalmology
Severe Preseptal Inpatient Rx Admission
cellulitis consult
Ceftriaxone
Preseptal
< 5 years Septic workup
cellulitis
Ophthalmology 647
Postseptal Cellulitis
Intraocular FB
Postseptal Associated with Especially ethmoid
Hematogenous
sinus & denta l sinusitis Other factors spread
cellulitis infections (most common cause)
Insect bites or other
skin trauma
Postseptal Usually
Staph aureus S. pneumoniae Anaerobes
cellulitis polymicrobial
Symptoms & Signs
Often high Eyelid is dark red Pain on eye

URI Sx Facial pressure Chemosis Proptosis
fever + swelling movement
Abnormal
Postseptal Painful ROM of + Decreased
Eye is involved pupillary
cellulitis eye visual acuity reactivity
Elevated IOP
Diagnosis CT
Amoxicillin/Sulbactam
Postseptal Ophthalmology
Inpatient Rx Metronidazole
cellulitis 3rd generation consult
cephalosporin
Debridement
Orbital Cellulitis Complications
Meningitis
Most common
Subperiosteal
abscess Septicemia
Brain abscess
Orbital Cellulitis
Vision loss Complications
Due to increased Usually seen on CT

IOP decreasing Orbital abscess
retinal blood flow
Subdural empyema Epidural abscess
Cavernous sinus Frontal bone

thrombosis osteomyelitis
Involvement of Pott’s puffy
CN 3, 4, or 6 tumor
648 B. Desai
Conjunctiva
Conjunctivitis
Introduction
Inflammatory
Common cause
Conjunctivitis condition of the
conjunctiva of the red eye
Viral (m.c.) Fungal

Usually benign &
Conjunctivitis Multiple causes Bacterial Allergic
self-limited
Parasitic Chemical
Symptoms & Signs
Red eye Chemosis Excess tearing
Normal visual Normal pupillary

Conjunctivitis
acuity reactivity
Blepharoconjunctivitis Blepharitis Conjunctivitis
Corneal Punctate ulcerations

Keratoconjunctivitis Conjunctivitis
inflammation in cornea
Conjunctivitis Failure to stain Herpetic

Miss Corneal abrasion OR Corneal ulcer OR
pitfall cornea dendrite
Ophthalmology 649
Bacterial Conjunctivitis
Symptoms & Signs
Injected Uni - or Bilateral

No eye pain Clear cornea Excess tearing Chemosis
conjunctiva mucopurulent discharge
Unless keratitis
present
Preauricular Consider
adenopathy Gonococcus
Typical Streptococcus
Staphylococcus
pathogens species
Gonococcus &
Other pathogens Pseudomonas
Chlamydia
Ophthalmia Contact lens
neonatorum wearers
Gonococcal Can invade Can be self - Parenteral + Emergent

ophthalmology
conjunctivitis intact cornea inoculated Topical Abx consult
Topical Warm
Treatment Severe = Culture Patching
antibiotics compresses
Can relieve pain…but

Fluoroquinolone
not for use in contact
for Pseudomonas lens wearers
650 B. Desai
Ophthalmia Neonatorum
PEDIATRICS
Chemical Other bacterial

Ophthalmia Conjunctivitis in
Chlamydial
neonatorum the 1st 28 days
Gonococcal Viral
1st 2 days Resolves within Negative gram

Chemical
postpartum 48 hours stain
Bilateral Copious (+) Gram

Gonococcal 2–7 days of life conjunctival Chemosis purulent
stain
injection discharge
Evaluation for
GC Treatment disseminated IV Abx
disease
GC Corneal Corneal
Complications ulceration perforation
Most common Bilateral Bilateral

Chlamydial conjunctivitis conjunctival purulent
(5–14 days of life) injection discharge
Chlamydia
PO Erythromycin
Treatment
Chlamydia Associated with Trachoma = most

chlamydial Staccato cough Otitis media common cause of
Complications pneumonia blindness worldwide
Keratitis Hx of
Bilateral lid Conjunctival
Viral (Herpes) 6–14 days of life (Corneal maternal
edema injection dendrites) herpes
Herpes Evaluation for IV & topical

disseminated
Treatment disease Acyclovir
Center right image (Reprinted from Galloway NR, Amoaku WMK, editors. Common eye diseases and their management. London:
Galloway PH, Browning AC. Common diseases of the conjunctiva and Springer Verlag; 2006. p. 45–60. With permission from Springer
cornea. In: Galloway NR, Amoaku WMK, Galloway PH, Browning AC, Verlag)
Ophthalmology 651
Viral Conjunctivitis
Symptoms & Signs
Injected Uni - or Bilateral Preauricular

No eye pain watery discharge Clear cornea Excess tearing Chemosis adenopathy
conjunctiva
Unless keratitis One eye followed Unless keratitis
present present Common
by the other
Esp. with
Adenovirus
Viral Usually resolves Typically Highly

conjunctivitis spontaneously preceded by URI contagious
Typical Epidemic
Adenovirus
pathogens keratoconjunctivitis
Frequent hand
Treatment Warm compresses Patching
washing
Epidemic Keratoconjunctivitis (EKC)
Virulent strain of Tends to occur in Extremely

EKC
Adenovirus epidemics contagious
Muscle
EKC Preceded by Cough Fevers Malaise N/V
aches
Symptoms & Signs
Very injected Swelling & Preauricular

Eye pain Chemosis Excess tearing FB sensation
conjunctiva redness of eyelid adenopathy
Ipsilateral
Papillae of inferior Subconjunctival Corneal stippling on
conjunctiva hemorrhages slit lamp exam
Sx may persist for

EKC
2–3 weeks
Cycloplegic Ophthalmology
EKC Treatment Artificial tears Cool compresses
agents consult
Severe
photophobia
652 B. Desai
Allergic Conjunctivitis (AC)
Symptoms & Signs
Papilla on inferior Injected Red swollen Watery

Pruritis Excess tearing Chemosis
conjunctiva conjunctiva eyelids discharge
Allergic No eye pain or

conjunctivitis visual issues
Mild-Moderate Topical
Artificial tears
AC Treatment antihistamines
Severe AC Consider topical

Treatment steroids
In conjunction
with
ophthalmology!
Subconjunctival Hemorrhage
Subconjunctival Rupture of fragile conjunctival Usually resolves

Hemorrhage vessels within 2 weeks
Increased pressure
Causes Trauma OR OR Hypertension OR Spontaneous
from Valsalva
Exam Otherwise normal
Recurrent Evaluate for coagulation

hemorrhage? abnormalities
Cavernous sinus
Trauma thrombosis
Subconjunctival Mistaken for Raised circular
Due to
Hemorrhage Pitfall bloody chemosis lesions Perforation of sclera Coagulopathy
Ophthalmology 653
Cornea
Keratitis
Introduction
Viral Drugs
Inflammation of
Keratitis Multiple causes Bacterial Exposure
the cornea
Fungal Sjorgren’s
Redness
Keratitis “Perilimbic flush” circumferential of
sclera at corneal edge
Can disrupt Make the cornea

Keratitis corneal epithelial susceptible to
layers infection
Usually due to Immunocompromised

Fungal Keratitis
organic FB patients
654 B. Desai
Bacterial Keratitis
Due to Staph Strep

Bacterial inflammation or
Severe keratitis
Keratitis injury to cornea
Pseudomonas Gonococcus
Contact lenses
Symptoms & Signs
Decreased White spots on

Red eye + IOP Eye pain Hypopyon
vision cornea
Pus in anterior Bacterial until
chamber proven otherwise
Bacterial
May cause iritis
Keratitis
Dx of Bacterial May not be clear

Gram Stain Culture
Keratitis cut
Bacterial Keratitis Topical Ophthalmology

IV Antibiotics
Treatment antibiotics consult
Complication Corneal scarring
Center right image (Reprinted from Mete G, Turgut Y, Osman A, Gülşen Ü, Hakan A. Anterior segment intraocular metallic foreign body
causing chronic hypopyon uveitis. J Ophthalmic Inflamm Infect. 2011;1(2):85–7. With permission from Springer Verlag)
Ophthalmology 655
HSV Keratitis
Can affect eyelids,

Herpes Simplex conjunctivitis & Hx of cold sores OR Genital herpes
cornea
Symptoms & Signs
Decreased + Skin Decreased

Red eye + IOP Eye pain Photophobia
vision involvement corneal sensation
Typical vesicular
eruptions
Dx of HSV Fluorescein Herpetic Linear branching

OR Geographic ulcer
Keratitis staining dendrites pattern
“Amoeba -like”
Dx of HSV May not be clear May not see the

Keratitis cut dendrites
HSV Affecting
Oral Acyclovir
Lids?
HSV Affecting Topical

Conjunctiva? Trifluridine
HSV Keratitis Topical Erythromycin Ophthalmology

Cycloplegics
Treatment Trifluridine ointment consult
To prevent 2º
bacterial infection
HSV Keratitis
Corneal scarring
Complication
Center right image (Reprinted from Sundmacher R. Herpes simplex guide to clinical management. Heidelberg: Springer Verlag; 2008.
virus (HSV) diseases of the anterior segment and the adnexa. In: p. 5–112. With permission from Springer Verlag)
Sundmacher R, editor. Color atlas of herpetic eye disease: a practical
656 B. Desai
Herpes Zoster Ophthalmicus
Herpes Zoster Shingles in 1st Has ocular Involves upper Does not cross
Ophthalmicus division of CN V involvement eyelid the midline
Rare V2/V3
Symptoms & Signs
Facial Pain Paresthesias Fever Headache Malaise Red eye Blurred vision
+ Cranial nerve
+ Optic neuritis Photophobia Eye pain + IOP
palsies
Hutchinson’s Cutaneous lesion Involvement of High likelihood of Sight

nasociliary ocular
sign on tip of nose dermatome involvement threatening!
Herpes Zoster Non-staining mucous plaque HSV has erosion

Pseudodendrites
Ophthalmicus with no epithelial erosion and staining
Herpes Zoster
Ophthalmicus Eye Retinitis Choroiditis Uveitis Keratitis Iritis
involvement
HZV Affecting
Oral antivirals
Skin?
Ophthalmology
HZV Iritis?
consultation
Herpes Zoster Erythromycin Ophthalmology

Ophthalmicus IV acyclovir Admission
ointment consult
Treatment
To prevent 2º
bacterial infection
Center image (Reprinted from Sundmacher R. Varicella zoster virus guide to clinical management. Heidelberg: Springer Verlag; 2008.
(VZV) diseases of the anterior segment and the adnexes. In: p. 113–57. With permission from Springer Verlag)
Sundmacher R, editor. Color atlas of herpetic eye disease: a practical
Ophthalmology 657
Ultraviolet Keratitis
Ultraviolet UV light causes

Welder’s keratitis Snow Blindness death of corneal
Keratitis epithelial cells
Symptoms & Signs
No visual Conjunctival
FB sensation Eye pain Tearing Photophobia changes injection Corneal edema
On slit lamp
Blepharospasm
Ultraviolet Usually a delay of

Keratitis 6–12 hours
Ultraviolet Diffuse, bilateral

punctate lesions on
Keratitis cornea
Ultraviolet Keratitis Patch for

Cycloplegics Analgesia
Treatment comfort
Corneal Abrasion, Laceration, and Ulcers
Corneal Abrasion
Contact lenses Fingernails

Corneal abrasion Corneal scratch Due to
Dust Other FB
Symptoms & Signs
No visual Mild corneal + Subconjunctival

FB sensation Eye pain Tearing + Photophobia
changes injection hemorrhage
Unless full
thickness corneal
Blepharospasm Lid swelling laceration
Relief of pain with

Corneal abrasion
topical anesthesia
Appears green after

Dx of Corneal Irregular corneal
fluorescein staining
abrasion defect under cobalt blue light
Corneal abrasion Topical Patch for

Cycloplegics Topical NSAIDs
Treatment antibiotics comfort
Decreases pain Does not impair healing
Patching eye
Corneal abrasion Metal FB causing Not examining Dispensing topical
abrasions due to
pitfalls abrasion under the lids anesthestics organic matter
Consider Retained FB Retards healing Increases
intraocular FB infection risk
“Ice rink sign”
658 B. Desai
Corneal Lacerations
Full thickness Small lacerations

Anterior chamber
Corneal can close
Laceration perforation spontaneously
Symptoms & Signs
Teardrop Change in Shallow anterior Iris pigment may be

Misshapen iris Hyphema
shaped pupil visual acuity chamber seen at wound edge
Dx of Corneal Fluorescein on eye is

Seidel Test washed away by leaking
Laceration aqueous humor
Corneal Emergent
Avoidance of
Laceration Ophthalmology Eye Shield
Treatment consult eye movements
Extrusion of
vitreous with eye
muscle contraction
Corneal laceration Failure to consider Performing

pitfalls globe perforation Tonometry
Need CT scan if
Contraindicated
globe injury is
considered
Corneal Traumatic
Laceration Endophthalmitis Vision loss
Complications Cataracts
Ophthalmology 659
Corneal Ulcers
Infection of Trauma Dry eyes

Breaks in
Corneal Ulcer multiple layers of Due to
epithelial layer
the cornea Infection Contact lens
Pseudomonas
Symptoms & Signs
+ Subconjunctival Mild corneal No visual

FB sensation Eye pain Tearing + Photophobia
hemorrhage injection changes
Unless full thickness
Mucopurulent corneal laceration
Blepharospasm Lid swelling Associated iritis
discharge Or ulcer at visual
axis
Miotic pupil
Slit Lamp May Show

Dx of Corneal Round or Whitish on
Cells & Flare = Iritis Culture
Ulcer irregular defect appearance + Hypopyon
Corneal Ulcer Topical Ophthalmology

Cycloplegics
Treatment antibiotics consult
Decrease pain
Corneal abrasion Not referring to

Patching eyes
pitfalls Ophthalmology
Worsen
Pseudomonas
infection
Corneal Ulcer Corneal Corneal

Synechiae Glaucoma Cataracts
Complications perforation scarring
Bottom right image (Reprinted from Heiligenhaus A, Heinz C, Schmitz Reinhard T, Larkin F, editors. Cornea and external eye disease.
K, Tappeiner C, Bauer D, Meller D. Amniotic membrane transplanta- Heidelberg: Springer Verlag; 2008. p. 15–36. With permission from
tion for the treatment of corneal ulceration in infectious keratitis. In: Springer Verlag)
Corneal Foreign Bodies
Corneal Foreign Usually

Bodies superficial
Symptoms & Signs
No visual
FB sensation Blurred vision Tearing Edema of lids Chemosis Photophobia
changes
If present for Metal will diffuse

Metallic FB prolonged period Rust ring
into cornea
of time
Corneal Foreign Removal in ED or Topical

Cycloplegics
Body Treatment by Ophthalmology antibiotics
Failure to assess Failure to refer to

Corneal Foreign Failure to evert
for globe ophthalmology when
Body Pitfalls penetration lid metallic FB removed
Will see Rust may
“Ice rink” sign
hyphema reaccumulate
660 B. Desai
Uveitis and Iritis
Introduction
Inflammation in Iris
Multiple
Iritis anterior segment Choroid
of uveal tract etiologies
Ciliary body
Symptoms & Signs
Conjunctival Decreased
Eye Pain Photophobia Perilimbal flush Cells & Flare + Systemic Sx
injection vision
U/L, but may be B/L Red eye Ciliary spasm Injection is On slit lamp Arthritis
in systemic irritates trigeminal greatest around
processes nerve the limbus Urethritis
May be consensual Poorly reactive
miotic pupil
Ophthalmology Dilation &

Iritis Treatment Cycloplegics
consult Steroids
Decrease pain
Differential Diagnosis of Iritis
Malignancies
Leukemia
Viral Lymphoma
Trauma
Zoster Melanoma
Corneal foreign body
Adenovirus
UV Keratitis
HSV
Bacterial
Lyme disease Differential

Diagnosis of Iritis Systemic
TB
Sarcoidosis
Syphilis
Reiter’s syndrome
Ulcerative colitis
Parasitic Ankylosing spondylitis
Toxoplasmosis Behcet’s syndrome
Ophthalmology 661
Vitreous and Intraocular Cavities
Endophthalmitis
Penetrating globe
Inflammation of Postsurgical injuries
Endophthalmitis aqueous or Leads to Loss of vision Due to
vitreous humor Most common Hematogenous
spread
Usually infectious
Rare
Septic emboli
Right eye 2x more
affected due to
blood supply
Symptoms & Signs
Headache Eye pain Eye discharge Photophobia Visual loss Lid swelling Lid erythema
Conjunctival Associated Cotton wool

Chemosis Hypopyon
injection uveitis spots
Dependent on Gram positive

Infectious causes
source most common
Endophthalmitis 3 rd generation
Vancomycin Gentamicin OR Amphotericin B
treatment cephalosporin
If fungal etiology
suspected
Endophthalmitis Not consulting

pitfall Ophthalmology
662 B. Desai
Vitreous Hemorrhage
Firmly adherent Trauma to these areas

Vitreous Vitreous is
to specific cause hemorrhage
Hemorrhage avascular structures behind the vitreous
Vitreous
Diabetic Vitreous
Hemorrhage Ocular trauma
causes retinopathy detachment
Shaken baby Elderly
syndrome
Symptoms & Signs
Sudden painless Appearance of Unilateral hazy

visual loss black spots in vision vision
Consider Vitreous Sickle cell

Diabetics
Hemorrhage disease
Vitreous
Failure to check Not referring to
Hemorrhage
INR Ophthalmology
pitfalls
In those patients
on Warfarin
Ophthalmology 663
Retina
Central Retinal Artery Occlusion (CRAO)
Central Retinal Sudden painless May be preceded

Due to Embolism True emergency
Artery Occlusion visual loss by Amaurosis fugax
Symptoms & Signs
Monocular Afferent Fixed dilated Cherry red spot “Box car” appearance
Pale retina
blindness pupillary defect pupil in macula to retinal artery
Due to decreased
flow
CRAO Goals of Allows emboli to

Lower IOP
Treatment move peripherally
Within 90
minutes
Anterior
Gentle globe Increase Topical
CRAO Treatment Acetazolamide chamber
massage PCO2 β-blocker paracentesis
Dislodge Dilates Decrease
By ophtho
emboli retinal aqueous
artery humor
Breathe production
into paper
bag
Center right image (Reprinted from Galloway NR, Amoaku WMK, Common eye diseases and their management. London: Springer
Galloway PH, Browning AC. Systemic disease and the eye. In: Verlag; 2006. p. 165–78. With permission from Springer Verlag)
Galloway NR, Amoaku WMK, Galloway PH, Browning AC, editors.
664 B. Desai
Etiologies of Central Retinal Artery Syndrome
Emboli
Carotid
Sickle cell disease Cardiac Thrombosis
Vasospasm
Trauma
Migraine
Elevated IOP Etiologies of Acute Vasculitis

Central Retinal
Glaucoma SLE
Artery Syndrome
Polyarteritis nodosa
Hypercoagulable
Temporal arteritis
states
Low retinal blood

flow
Hypertension
Carotid disease
Lack of fluid intake
Ophthalmology 665
Central Retinal Vein Occlusion (CRVO)
Central Retinal Thrombosis of Retinal

Varying severity Causes Hemorrhage
Vein Occlusion CRV edema
DM Hypertension
Cerebrovascular Cardiovascular
disease disease
CRVO Risk Factors
Orbital tumors Dyslipidemia
Glaucoma Vasculitis
Symptoms & Signs
Variable loss of Optic disk Diffuse retinal Cotton wool

vision edema hemorrhages spots
“Blood &
Thunder”
appearance
No specific Refer to
CRVO Treatment
treatment Ophthalmology
Center right image (Reprinted from Galloway NR, Amoaku WMK, Common eye diseases and their management. London: Springer
Galloway PH, Browning AC. Systemic disease and the eye. In: Verlag; 2006. p. 165–78. With permission from Springer Verlag)
Galloway NR, Amoaku WMK, Galloway PH, Browning AC, editors.
666 B. Desai
Retinal Detachment
Separation of the
Retinal Ophthalmologic
retina from its
Detachment supporting layers emergency
Symptoms & Signs
“Curtain” over Decreased Decreased Vitreous Grey retina

Flashes of light Floaters peripheral vision
field of vision central vision hemorrhage with folds
DM Sickle cell disease
Retinal Detachment
Trauma Retinopathy
Risk Factors
Prior Hx of
detachment
Retinal Emergent Inferior Superior

Detachment ophthalmology
consult detachment detachment
Treatment
Elevate head Lay flat
Optic Nerve
Optic Neuritis
Multiple sclerosis
Inflammation of Causing acute Over hours to
Optic Neuritis until proven
optic nerve reduction in vision days otherwise
Symptoms & Signs
Afferent Optic disc Loss of color + Visual field Change in

Eye pain
pupillary defect swelling vision deficits visual acuity
Usually U/L, Mild to
but can be B/L Papillitis Primarily red profound
Especially with
movement
Optic Neuritis Ophthalmology Neurology

Treatment IV steroids consult consult
Ophthalmology 667
Papilledema and Pseudotumor Cerebri
Increased
Bilateral optic disc
Papilledema Due to intracranial
swelling pressure
Malignant
Hypertension
Pseudotumor
Causes of cerebri
CNS Tumors
Papilledema Idiopathic intracranial
hypertension
Hydrocephalus
Pseudotumor
Papilledema Increased ICP Normal CT/MRI Normal CSF
cerebri
Can occur at any But…elevated
age opening pressure
Symptoms & Signs
Nausea & Vision is Blurred disc

Headache Diplopia + CN 6 palsy
Vomiting preserved margins
Horizontal
diplopia
Pseudotumor
Papilledema
cerebri
Papilledema Pseudotumor Neurosurgery

Depends on cause Acetazolamide
Treatment cerebri consult
Top right image (Reprinted from Galloway NR, Amoaku WMK, Galloway their management. London: Springer Verlag; 2006. p. 179–88. With
PH, Browning AC. Neuro-ophthalmology. In: Galloway NR, Amoaku permission from Springer Verlag)
WMK, Galloway PH, Browning AC, editors. Common eye diseases and
668 B. Desai
Temporal Arteritis
Involves medium
Temporal Systemic Painless ischemic Can progress
sized arteries in the
Arteritis vasculitis optic neuropathy bilaterally
carotid circulation
Bilateral blindness
in 50 % of
untreated patients
Temporal Decreased
Temporal Arteritis New onset
Age > 50 artery pulsations in ESR > 50
Dx headache artery
tenderness
3 of 5
Symptoms & Signs
Jaw Temporal artery

Headache Myalgias Fatigue Fever Impaired vision
claudication abnormalities
Polymyalgia
Near temple rheumatica + Afferent Tenderness
Pale optic disc
Worse at night pupillary defect Warmth
Worsens over
time Pulselessness
Worse at night
Vision impairment Loss of vision in one eye

Posterior ciliary May present as 2nd eye affected 2-
in Temporal due to a lack of blood
artery amaurosis fugax 3 weeks after 1st
Arteritis flow to the retina
Sign of impending stroke
Temporal Arteritis Followed by oral Ophthalmology &

Initial IV steroids
Treatment steroids Neurology consult
Discuss with Ophthalmology & Neurology!

Ophthalmology 669
Glaucoma
Acute Angle-Closure Glaucoma

Disorder of Impairment of
Acute Angle
increased Due to aqueous humor Causes Optic neuropathy Vision loss
Closure Glaucoma
intraocular pressure outflow
Ocular emergency
Acute Angle Corneal edema

Preceded by Pupillary dilation Causes Increased IOP Causes
Closure Glaucoma & haziness
Farsighted people Dim light
Parasympatholytic
Inhaled β-agonists
agents
Topical
Systemic
Familial
Some risk factors
DM
for Acute Angle
Anything else Closure Glaucoma
Sympathomimetic
causing pupillary agents
dilation
Topical
Systemic
HTN Cocaine
Acute Angle-Closure Glaucoma

Symptoms and Signs
Eye Symptoms & Signs
“Steamy” or Non-reactive
Abrupt in onset Red eye Eye pain pupil Blurred vision
hazy cornea
Mid-fixed & Conjunctival

Hard globe injection Elevated IOP
dilated pupil
Perilimbic
flush 60–80 mm Hg
Normal is
10–20 mm Hg
Systemic Symptoms & Signs
Abdominal
Headache pain N/V
Rare
670 B. Desai
Acute Angle-Closure Glaucoma Treatment
Emergent
Glaucoma Decrease aqueous Increase drainage Reduce volume of
Ophthalmology
Treatment humor production of aqueous humor aqueous humor consult
Lower IOP
Decrease aqueous Topical

Topical β-blockers α -adrenergic IV Acetazolamide
humor production agonists
Beware in sickle
Timolol Apraclonidine cell disease
Note usual
contraindications
Increase drainage Topical miotic Use after IOP is

Use in both eyes
of aqueous humor agents decreased
Pilocarpine Due to increased

IOP-induced
ischemic paralysis
of iris
Reduce volume of
Mannitol
aqueous humor
Osmotic
decompression of
eye
Trauma
Blunt Eye Trauma
Initial Anterior
Visual acuity Globe integrity
Assessment Chamber
Projectiles to Penetration of
globe until proven
eye otherwise
Penetration of
Eyelid Lacerations near
OR globe until proven
lacerations the orbit otherwise
Hammering or Penetration of
globe until proven
grinding metal otherwise
Flat anterior Emergent

Ruptured globe Ophthalmology Eye shield
chamber consult
Decreased sensation
Injury to inferior
below the eye or
orbital nerve
ipsilateral nose?
The apex of the pupil will

Pupillary
point to the site of “Tear drop” pupil
irregularity?
penetration or rupture
Prying the eyes Using contact

Pitfalls
open tonometry
May worsen
May raise IOP
condition
IV Update
Ophthalmology
Treatment Tetanus if Analgesia CT/MRI
Antibiotics needed consult
No MRI for
metal FB
Ophthalmology 671
Signs and Symptoms of Blunt Ocular Trauma and Globe Rupture
Flat Anterior
Chamber
Due to lowered
IOP
Hyphema Eye pain
Most globe
ruptures will have
this Pupillary
irregularity
Tear drop pupil

Lens dislocation
Subconjunctival
Signs & Symptoms hemorrhage
Traumatic Iritis
of Blunt Ocular
Trauma & Globe Large
Cells & flare on slit
lamp Rupture
Lid laceration
Restricted gaze
Up
Afferent pupillary
Lateral defect
Periorbital
Uveal prolapse (+) Seidel Test + Decreased IOP
ecchymosis
Involvement of
CN 3, 4, or 6
672 B. Desai
Hyphema
Microhyphema
Circulating red blood cells
Grade I
< 1/3 anterior chamber vol.
Blood or clots in
Hyphema Traumatic OR Spontaneous
anterior chamber
Grade II
1/3 - 1/2 anterior chamber vol.
Traumatic Bleeding from iris

Hyphema vessel Grade III
> 1/2 anterior chamber vol.
Spontaneous Bleeding from Sickle cell

OR Grade IV
Hyphema anticoagulants disease Total anterior chamber vol.
“eight ball hyphema”
Hyphema Topical or oral

Elevate head Dilate pupil Control IOP
Treatment steroids
Settles RBC’s Consult with Consult with
Same as glaucoma
inferiorly ophtho! ophtho!
No acetazolamide
for SC patients
Promotes sickling
due to decreased
pH
Hyphema Increased risk Corneal Impaired

Rebleed Adhesions
complications of glaucoma staining vision
Most common
May be worse
than original
bleed
Ophthalmology 673
Blow-Out Fractures
Sites for blow Inferior wall into Medial wall into Most common Caused by direct
out fractures the maxillary sinus the ethmoid sinus orbital wall fx trauma to orbit
Subcutaneous Orbital rupture

Medial wall fx
emphysema into sinus or nose
Contents of orbits Restriction of

Inferior wall fx through orbital Diplopia
floor upward gaze
Decreased sensation Injury to inferior

below the eye or
ipsilateral nose? orbital nerve
Blowout fx until
Epistaxis Eye Trauma Nasal trauma
proven otherwise
Dx of Blowout CT Water’s view Opacity in Blood or tissue

OR X-ray
fracture (Better) maxillary sinus in sinus
Isolated Blow Referral for repair

Entrapment
Out in 3-10 days
Update
PO Ophthalmology &
Treatment Tetanus if Analgesia CT
Antibiotics Face consult
needed
Not referring to Using contact

Pitfalls ophthalmology & Not giving Abx
Face tonometry
May worsen
All will need
condition
dilated exam
Retrobulbar Hematoma
Retrobulbar Bleeding behind Traumatic

Hematoma orbit exophthalmos
Decreased blood
Large hematoma Increase in IOP Acute glaucoma flow to optic nerve Retinal ischemia
& retina
Symptoms & Signs
Decreased Afferent
Eye pain Proptosis
vision pupillary defect
Penetration of
Increased IOP Lateral Medications to
globe NOT Measure IOP
suspected (>40) canthotomy reduce IOP
Blood in Tenon’s
Diagnosis CT
capsule
674 B. Desai
Chemical Burns
Chemical Burns True emergency
Immediate 1–2 L
Chemical Burns irrigation before
examination
Household Liquefaction Continues to burn

Alkali burns cleaners Worse than acids
Ammonia, Lye necrosis until treated
Damaged area
Coagulation Usually no deep
Acid burns Chlorine, Sulfur coagulates and
necrosis penetration prevents deeper burns
Continuous Emergent
Topical
Treatment irrigation until pH Ophthalmology
anesthetic is normal consult
7.4
Loss of eye from Permanent loss

Complications corneal Corneal scarring
perforation of vision
Super glue to Topical Refer to

erythromycin to Remove clumps
eye? eye ophthalmology
Lacerations to Refer
Lid Margin
Any significant Within 6-8 mm of

tissue loss medial canthus
Lacerations to Refer
Wounds involving
Require specialist Involving lacrimal
orbital septum
repair for proper lid duct or sac
function & lacrimal
system function
Any wounds
Inner surface of
causing ptosis eyelid
Tarsal plate
Toxicologic Emergencies
Matthew Ryan and Bobby Desai
Contents
General Approach to the Poisoned Patient 676
Data Interpretation 685
Toxidromes 687
Specific Toxins and Poisons 692
M. Ryan, MD, PhD • B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_13
676 M. Ryan and B. Desai
General Approach to the Poisoned Patient
Primary Survey
Very similar to trauma Should be performed

Primary Survey primary survey on all patients
Rapid
Survey algorithm Primary
resuscitation
“ABCDE” Airway Breathing Circulation Disability Exposure
What, when,
route, dose,
co-ingestions,
why
Consider Pill Bottles

modified-release
medications
Toxicology
History
Consider body
packing or Review medical
stuffing record
Have family, EMS
or police search
the patient’s
house
Toxicologic Emergencies 677
Airway Assessment
Airway Evaluate for FB & Obstruction to

Assess patency Assess gag reflex
assessment pooling of secretions airway
E.g., facial fractures
Tongue most
common cause of
obstruction
Breathing Assessment
Signs of Manage as
Assess breathing Respiratory rate Retractions
aspiration needed
Airway protection
& intubation
Circulation Assessment
Circulation Heart rate & Volume Peripheral

Pallor Diaphoresis
assessment Blood pressure status pulses
Disability Assessment
Disability
Assess GCS Pupils
assessment
Exposure
Complete
Skin/soft tissue
exposure of Wounds Track marks Pressure ulcers
infections
patient
Other Decontaminate
considerations as needed
Not searching
Pitfall
patient
Primary Survey Adjuncts
Coma Cocktail Dextrose Supplemental O2 Naloxone Thiamine
Flumanzenil? Use caution!! May precipitate

seizures
Known Antidote if available

intoxicant? & indicated
Adults Pediatrics Neonates

Dextrose 1 g/kg
D50W D25W D10W
Can be given
Naloxone 2 mg bolus No effect? 10 mg repeat
IV/IM/SL/SC/ETT
0.01 mg/kg 0.1 mg/kg

Pediatrics?
bolus repeat
Thiamine 100 mg IV/IM Before glucose
Other Call poison

considerations control
Laboratory Studies
Laboratory Serum BMP + CK ASA

CBC EtOH ECG
studies osmolarity + Glucose APAP
Important
Renal function Potassium Bicarbonate
aspects of BMP?
Assess for
CK?
rhabdomyolysis
Consideration of Prothrombin Assess for

Liver enzymes
APAP toxicity? time hepatotoxicity
Other Blood gas for Serum drug

Urine toxicology
considerations A-a gradient levels
Ischemic Assess for prolonged Conduction

EKG Arrhythmias
changes QT Intervals defects
Head & C-spine Others as clinically

Imaging tidbits CXR KUB
CT indicated
Assess for Assess for
As indicated for
aspiration radio-dense
possible
foreign bodies
trauma, CHI
or pills
Toxicology Screens
Urine toxicology Not always Most drugs are Initial screen Positive findings
tidbits indicated not screened may be negative may be unrelated
Rarely impacts Many drugs
management not have half lives:
Cocaine, Benzos
Initial screen Too soon to Delayed gastric Extended release

Bezoars
negative? ingestion emptying medications
Urine is better Can detect metabolites 2–3 days Check blood levels on all drugs in
Urine vs Blood
than serum after ingestion or injection which levels can guide therapy
Relying on screens to rule May have false positives

Pitfall
in or rule out exposure or false negatives
Amphetamines
Pseudoephedrine
Tricyclic
PCP
antidepressants
Ketamine False positive Cyclobenaprine
drug screens
Dextromethorphan Phenothiazines
Diphenhydramine
May not present

False negative Methadone
on opioid screen
Urinalysis Tidbits
Ketones in
Dehydration OR Ketosis OR Toxic alcohols Ethanol
urine?
Metabolic
pH
acidosis
Assess for
Blood Hyperthermia OR Cocaine
rhabdomyolysis
Consider
Crystals
Ethylene glycol
Urine drug
As needed
screen?
Secondary Survey and Adjuncts
Secondary Head to toe Specific antidotes for

Survey examination of patient known ingestions
Physical exam Track Pressure Skin/Soft tissue Skin Check groin &
features marks ulcers infections popping axilla for sweat
“Toxicology
handshake”
Other Other Dx that mimic a

Trauma? Toxidromes?
considerations? toxic ingestion
No clinical trials to date Best performed within

Gastric lavage
have shown efficacy 1–2 hours of ingestion
Environmental Shower or Cutaneous

Pesticides
exposure? irrigation exposure
Modified release
Whole bowel
medication or
irrigation
ingestion?
Activated Within 1 hour of Must be awake Risk of

charcoal ingestion & cooperative aspiration
Elimination Forced saline

Alkalinization Dialysis
strategies diuresis
TCA & ASA
Charcoal Tidbits
Activated 1st line for GI Administer within 1 Massive overdose may

1 g/kg
charcoal decontamination hour of ingestions require extra doses
Activated Decreases enterohepatic Prevents

charcoal recirculation re-absorption of agent
Lithium Bases
Not effective for ionic or
Pitfall
charged substances
Acids Heavy Metals
Sustained release
Lithium
drugs
Alkali Iron Salicylates Theophylline
Medications that Multidose

bind poorly Charcoal
Acids Cyanide Carbamazepine Phenobarbital
Alcohols Hydrocarbons
Altered mental
Contraindications Caustics Ileus OR Obstruction
status
Using multidose Cause electrolyte

Pitfall
cathartics problems & dehydration
Other Methods of Drug Elimination
Charcoal Drug must be

Carbamazepine Theophylline Phenobarbital
Hemoperfusion protein bound
Whole Bowel Iron, Lithium, Sustained release Drug packers

Metals
Irrigation (WBI) Lead medications Cocaine
Pitfalls to WBI Ileus OR Obstruction
Urine
INH Phenobarbital Salicylates Urine pH 7–8
alkalinization
Pitfalls to urine Need for

alkalinization replacement of K+
Dialysis Tidbits
Must have toxic

level of dialyzable
substance
Must be water Must have small

soluble volume of
distribution
Ideal agents for
Dialysis
Must have slow Must have poor

renal clearance plasma binding
Must have low

molecular weight
Lithium
Some antibiotics Aspirin
Some dialyzable
medications
Anticonvulsants Alcohols
Phenobarbital Ethanol
Toxins That Alter Thermoregulation or Cause Temperature Changes
Anticholinergics
Throxine Sympathomimetics
Hyperthermia
Methylxanthines Serotoninergics
Salicylates
Opiates
Insulin & long

Sedatives &
Hypothermia acting oral
Hypnotics
hypoglycemics
Phenothiazines Alcohols
Toxins That Cause Hypoglycemia
Salicylates
Oral
Hypoglycemia Acetaminophen
hypoglycemics
Alcohol Insulin
Select Antidotes
Agent/ Drug Antidote
Acetaminophen N-Acetylcysteine
Anticholinesterase Atropine/Pralidoxime
Anticholinergics Physostigmine
Benzodiazepines Flumanezil
b-blockers Glucagon
Calcium-channel blockers Glucagon
Coumadin Phytonadione
Cyanide Amyl nitrate, Sodium nitrite, Sodium

thiosulfate or Hydroxocobalamin
Digoxin Digibind
Extrapyramidal symptoms Diphenhydramine
Ethylene glycol Fomepizole
Heparin Protamine sulfate
Insulin reaction Glucose
Iron Deferoxamine
Lead Dimercapol, EDTA
Narcotics Naloxone
TCA’s Sodium bicarbonate
Overdose Odor Pearls
Odor Agent
Burnt Almonds Cyanide
Carrots Water Hemlock
Fruity breath Ethanol, Acetone, Isopropanol, Hydrocarbons
Garlic Arsenic, arsenates
Glue Toluene, Benzene, Polyaromatic hydrocarbons

& other solvents
Pears Chloral hydrate, Paraldehyde
Rotten eggs Hydrogen Disulfide
Wintergreen Topical Salicylate, e.g., Methyl Salicylate

Data Interpretation
Arterial-Alveolar Gradient
Arterial-alveolar Difference between arterial

Gradient versus alveoli oxygenation
Ambient gas minus what displaces it

Alveolar gas
from the internal environment
PAO2 Inspired O2 CO2 0.8
A-a gradient PAO2 PaO2
Normal A-a
(Age/4) + 4
gradient?
Anion Gap
Measured Measured
Anion gap
cations anions
Sodium Chloride Bicarbonate

Anion gap
(Na+) (Cl–) (HCO3–)
Normal anion
10–15
gap?
Largely due to
Anion gap
albumin
Hypo-
Lower anion gap Malnourished Chronically ill
albuminemic pts
Anion gap CAT MUDPILES

Toxins Associated with Anion Gap
Toxins Tidbits
CO/CN Inhibits oxidative phosphorylation
Ethanol (Alcohol) Acidosis, Respiratory depression, Dehydration
Toluene
Methanol Formic acid
Uremia
Paraldehyde Acetic and Chloracetic acid
Isoniazid Lactic acidosis
Iron Inhibits oxidative phosphorylation
Lactic acidosis Sepsis
Ethylene glycol Oxalic acid
Salicylates Acidosis & Inhibits oxidative phosphorylation
Osmolar Gap
Measured Calculated
Osmolar Gap
osmolality osmolality
Normal osmolar –15 up to +10

Usually < 10
gap? (mean +2)
Normal gap due

Calcium Lipids Proteins
to ?
Differential
Increased
diagnosis of OR Alcohols OR Hyperglycemia OR Ketosis OR Acidosis
protein
osmolar gap
Presence of Consider toxic

OR AKA OR DKA OR Mannitol
osmolar gap? alcohols
Most common
Ethanol
cause of gap?
Toxidromes
Anticholinergic Toxidrome
Hot as a hare, red as a beet, dry as a bone, blind as a bat, mad as

hatter
Symptoms & Signs
Cutaneous Dry mucous Urinary Decreased Altered mental

Hyperthermia Mydriasis
flushing membranes & skin retention bowel motility status
Similar to sympathomimetic Check axilla or

Tidbit Will be dry
crisis except NO diaphoresis groin for sweat
Anticholinergic Causes
Antihistamines
Botanicals
Jimson weed Tricyclic

Anticholinergic
antidepressants
Causes
Belladonna
Mandrake
Other agents
Scopolamine
Anti-diarrheals
Atropine
Ipatropium
Bladder spasm
medications
Anticholinergic Treatment Tidbits
Agitation or
OR Seizures Benzodiazepines
Delirium
Giving Giving Will worsen

Pitfall OR
Phenothiazines Haloperidol condition
Wide complex Sodium

tachycardia? bicarbonate
Dysrhythmias? Lidocaine Amiodarone Cardioversion
Torsades? Magnesium Overdrive pacing Cardioversion
Medication Will worsen

Phenytoin Procainamide
Pitfalls condition
Physostigmine Refractory Ventricular Malignant Severe

Hyperthermia
indications? seizures dysrhythmias hypertension hypotension
Physostigmine Tricyclic
Heart block
contraindications? overdose
Cholinergic Toxidrome
“SLUDGEM” + “KILLER B’s”

“DUMBELS”
(Muscarinic Effects)
Symptoms & Signs – “SLUDGEM” & Killer B’s”
Miosis
Salivation Lacrimation Urination Defecation GI Upset Emesis
(& Muscle spasm)
Bradycardia Bronchorrhea Bronchospasm
Symptoms & Signs – Nicotinic Effects
Muscle Respiratory
Fasciculations
weakness failure
Respiratory
Pitfalls Seizures Coma
failure
Cholinergic Causes
Organophosphates
Muscarinic
Cholinergic Carbamates
agents
Causes
Physiostigmine &
Some nerve gases
Pyridostigmine
Opioid Toxidrome
Symptoms & Signs
Respiratory
Obtundation Miosis Coma Hypotension
depression
Not always
seen!
Consider acetaminophen ARDS as a severe

Pitfalls
co-ingestion sequelae of overdose
Clonidine overdose can

Tidbit
mimic opioid overdose
Common Opioids
Morphine
Propoxyphene Oxycodone
Common Hydrocodone
Hydromorphone
Opioids
Codeine Methadone
Meperidine Fentanyl
Sedative Toxidrome
Symptoms & Signs
Respiratory Decreased level of

Hypotension
depression consciousness
Considerations for Sedative Toxidrome
Ethanol
Gamma
Benzodiazepines
hydroxybutyrate
K12 & Synthetic Common Toxic alcohols

cathinones Sedatives
Spice Barbituates
Sepsis Trauma
Sympathomimetic Toxidrome
Symptoms & Signs
Tachycardia Hypertension Tachypnea Myridiasis Diaphoresis
May resemble Due to CNS

Pitfalls Due to
acute psychosis stimulation
Skin findings Diaphoresis
Sympathomimetic Agents
Amphetamines
Common
Sympathomimecs
Cocaine Smulants
Withdrawal Symptoms
Withdrawal Can mimic

Symptoms toxidromes
Symptoms & Signs – Depends on Syndrome
Tachycardia Hypertension Tachypnea Mydriasis Diaphoresis Diarrhea Muscle cramps
Insomnia Agitation Piloerection
Opioid Mimics
Usually not fatal
withdrawal cholinergic crisis
Benzodiazepine Withdrawal from

withdrawal extended use may be fatal
Alcohol Mimics
Can be fatal
withdrawal sympathomimetic crisis
Mimics
Hypoglycemia
sympathomimetic crisis
Specific Toxins and Poisons
Alcohols: Introduction
Overdoses cause anion

Methanol Ethanol Ethylene glycol Osmolar gap
gap metabolic acidosis
Isopropyl Metabolized to Does NOT cause Causes osmolar

But…
alcohol? acetone anion gap acidosis gap
Metabolism of By alcohol
alcohols? dehydrogenase
Methanol Formic Acid
Ethanol Acetaldehyde Acetic acid
Ethylene glycol Glycoaldehyde Glycolic acid Oxalic acid
Positive birefringent calcium

Oxalic acid
oxalate crystals excreted in urine
Isopropyl alcohol Acetone

Alcohols: Methanol
Paint thinner Anion & Osmolar

Methanol Solvent found in Windshield wiper fluid
Gasoline additives gap in OD
Methanol Can cause anion From formic acid

overdose gap acidosis production
Formic acid Snowstorm Eventual May see disc

Toxic to retina
effects vision blindness hyperemia
Symptoms & Signs May be delayed 12–18 hours
Respiratory
N/V Seizures Pancreatitis Blindness
failure
Repletion of Repletion of
Initial Treatment ABC’s IV Fluids
Thiamine electrolytes & glucose
Agitation &/or
Benzodiazepines
seizures?
Specific Inhibits conversion of Allows methanol to be directly

Fomepizole
antidote? methanol to formic acid excreted unchanged by the kidneys
Alcohol dehydrogenase preferentially

Other Treatment Ethanol
metabolizes it over methanol & ethylene glycol
Indications for Serum methanol Altered mental Metabolic No response to

hemodialysis > 25 mg/dL status acidosis standard therapy
Alcohols: Ethanol
Causes euphoria In small to moderate Anion & Osmolar

Ethanol
& disinhibition amounts gap in OD
CNS Toxic Effects
Decreased Altered mental

Slurred speech Obtundation Coma Death
reflexes status
Alcohol toxicity
Respiratory Alcoholic
Hypothermia Hypotension Hypoglycemia
depression ketoacidosis
Agitation &/or
Benzodiazepines
seizures?
Indications for Depressed vital Significant

Coma
hemodialysis signs overdose
Ethanol Most require a period of observation and

intoxication can be discharged when clinically sober
Ethanol Tidbits
Withdrawal Withdrawal Delirium

The shakes
syndromes seizures tremens
6–8 hours after May have visual

The Shakes
last drink hallucinations
Withdrawal 6–48 hours after Treat with

seizures last drink benzodiazepines
Delirium Confusion & Patients are

Fever Tachycardia
tremens Agitation extremely ill
Thiamine Multivitamins
Treatment Fluids Magnesium Benzodiazepines
(Vitamin B1) & Folate
Wernicke’s Oculomotor
Confusion Ataxia Nystagmus CN VI Palsy
encephalopathy crisis
Korsakoff’s Retrograde
Confabulation
Psychosis amnesia
Disulfiram
Alcohol Metronidazole
reaction
Disulfiram
Flushing Diaphoresis N/V Headache
reaction
Severe Disulfiram
Arrhythmias Seizures Hypotension
reaction
Alcohols: Ethylene Glycol
Anion & Osmolar

Ethylene Glycol Solvent found in Antifreeze
gap in OD
Early stages similar to Later stages of toxicity CNS

Ethylene Glycol Progressive toxin
ethanol intoxication leads to renal failure deficits
Due to complex Oxalic aciduria
metabolite profile
Ethylene Glycol Broken down by alcohol

Oxalic acid Glycolic acid
Metabolism dehydrogenase
Other laboratory Renal failure

Hypocalcemia Hematuria
abnormalities (elevated BUN/Cr)
Glycolic acid Causes acidosis
Precipitates with calcium to

Oxalic acid
form calcium oxalate crystals
Agitation &/or
Benzodiazepines
seizures?
Specific Inhibits conversion of

Fomepizole
antidote? ethylene glycol to oxalic acid
Treatment Requires supplemental Both are consumed in the

tidbits Pyridoxine & Thiamine metabolism of ethylene glycol
Indications for High ethylene Altered mental Metabolic No response to

hemodialysis glycol level status acidosis standard therapy
Alcohols: Isopropyl Alcohol
Overdose causes
Isopropyl alcohol Solvent found in Rubbing alcohol
osmolar gap
½ metabolized Rest excreted by

Metabolism
to acetone lungs & kidney
Presents similar to But…NO anion Ketosis is

Isopropyl alcohol
ethanol toxicity gap acidosis present
Isopropyl alcohol toxicity
Hemorrhagic Hypotension Pulmonary

CNS depression Hypoglycemia
gastritis (may be severe) edema
Indications for Serum level Altered mental

Hypotension
hemodialysis > 400 mg/dL status
Amphetamine Examples
Ephedrine
Methamphetamine Amphetamine Pseudoephedrine

Examples
MDMA ADHD
medications
“Ecstacy” Lisdexamfetamine
“Molly” Methylphenidate
Dextroamphetamine
Amphetamines
Prescription Sympathomimetic
Amphetamines Drugs of abuse
medication syndrome
Signs & Symptoms
Hypertension Tachycardia Hyperthermia Restlessness Agitation Psychosis Seizures
Cooling measures Cardiac

Initial Treatment IV fluids
as needed monitoring
Agitation &/or
Benzodiazepines
seizures?
Acidification of urine is
Pitfall
NOT recommended
Medications to Causes unopposed

b–blockers
avoid a stimulation
Unopposed a Diffuse
Ischemia Hypertension
stimulation vasoconstriction
Analgesics: Acetaminophen
Most commonly used over-the- Also found in

Acetaminophen
counter pain medication in the US combination agents
First pass These are saturable processes

Metabolism Sulfation Glucuronidation
kinetics especially in overdose
Major
pathways
Other metabolic Oxidation by cytochrome P-450 Greater oxidation Hepatotoxic metabolite

pathway system after saturation of above occurs in overdose NAPQI produced
> 4 g/day
Symptoms & Signs Progression of poisoning in stages
May be
Early stage N/V asymptomatic
Mid Stage N/V RUQ pain
Fulminant Coagulation Alerted mental

Late stage hepatic failure Jaundice Lactic acidosis disorders status
Acetaminophen Rare Due to different

OD in kids? hepatotoxicity metabolic pathways
Rumack-Matthew Nomogram
Based on Rumack -
Antidose dosing
Matthew Nomogram
5000 5000
Acetaminophen plasma concentration (µmol/L)

2000 2000
1000 1000
500 500
Po
ss Probable hepatic toxicity
ibl
eh
200 ep 200
ati
ct
No hepatic toxicity ox
100 ici
ty 100
50 50
25%
20 20
10 10
4 8 12 16 20 24
Hours after ingestion
Rumack matthew nomogram
A level of > 150 mg/dL at the four Treat multiple ingestions as a single
Tidbits
level requires treatment with NAC ingestion initiated at the first ingestion
Nomogram Less useful for delayed presentations > 24

pitfall hours or for modified-release formulations
Acetaminophen Overdose Treatment
Specific May be of value Do not delay

NAC But…
antidote? > 24 hours treatment with NAC!
Prevents NAPQI May also reduce NAPQI

NAC actions
from binding to liver back to acetaminophen
Provides cofactors to allow production Lack of NAC results with the liver’s
NAC importance
of inert metabolites of acetaminophen production of toxic metabolites
Load Followed by
NAC Dosing
140mg/kg po 70 mg/kg every 4 hours for 17 doses
Consult poison control +

IV NAC?
board certified toxicologist
Safe in May use charcoal with oral NAC

NAC tidbits
pregnancy without a decrease in effectiveness
Ingestions not May be discharged Consider repeating acetaminophen level

requiring NAC? if no other issues prior to discharge to ensure it is not present
Other indications
Co-ingestions Acute psychosis Suicidal intent
for admission
Co-ingestions with May delay absorption &

Pitfall
anticholinergic agent cause a false negative level
Salicylate Examples
Aspirin
Topical pain relief Salicylate Oil of

medications Examples Wintergreen
Some migraine Bismuth

preparations subsalicylate
Analgesics: Salicylates
Salicylate Uncouples oxidative Leads to metabolic

overdose phosphorylation and lactic acidosis
Anion gap Respiratory Due to increased

Classic finding alkalosis respiratory rate
metabolic acidosis
Salicylate overdose alters Neutral salicylates can

Other Tidbits glucose metabolism cross blood -brain barrier
Symptoms & Signs Presentation is dose dependent
Sweating
< 150 mg/kg N/V GI upset
(esp. in kids)
Tachypnea
150–300 mg/kg N/V AMS Tinnitus
(esp. in kids)
>300 mg/kg Altered mental Unstable vital

ARDS Seizures Dysrhythmias
(Severe) status signs
Chronic More CNS & Less Level may not correlate

poisoning GI symptoms with symptoms
Salicylate Overdose Treatment
Initial Treatment ABC’s IV Fluids O2 Cardiac monitor
Laboratory Salicylate BMP + LFT Others as

CBC ABG ECG
studies level + Glucose needed
Anion gap Respiratory

Classic finding
metabolic acidosis alkalosis
Other findings Hypoglycemia T3/T4 levels
Overdose within Consider

1 hour? charcoal
Definitive Urinary 150 mEq NaHCO3 Maintain urine output

Urine pH 7.5–8
treatment alkalinization in 1 L of D5W of 1–2 cc/kg/hr
Alkalinization will Replete electrolytes

Pitfall
worsen hypokalemia as needed
Indications for Refractory or Worsening acid- Unstable vital

hemodialysis worsening symptoms base derangements signs
Medication Oil of wintergreen has

Very toxic
pitfall high salicylate level
Nonsteroidal Anti-Inflammatory Agents
Celecoxib
Combination
Diclofenac
formulations
Naproxen Etodolac
Nonsteroidal Anti-
Nabumetone Inflammatory Ibuprofen
Agents
Meoxicam Indomethicin
Ketorolac Ketoprofen
Analgesics: NSAIDs
Inhibit COX Decrease prostaglandin

NSAID overdose
enzymes synthesis
Most common Renal Both more common in

GI bleeding
problems insufficiency casual use than in overdose
Overdose within Consider

1 hour? charcoal
Other Intentional
Co-ingestions Suicidal intent
considerations overdose
Anticonvulsants: Valproate
Valproate Supportive
overdose treatment
Signs & Symptoms
Severe Altered mental

Dysrhythmias Hypotension Coma Hepatic failure
overdose status
Rare, but fatal
complication
Initial Valproate Coagulation Phosphorus

Electrolytes Liver function
Laboratories level studies level
Initial Treatment Supportive
Altered mental Unstable vital

Hemodialysis
status signs
Anticonvulsants: Carbamazepine
Carbamazepine Supportive
overdose treatment
Symptoms & Signs
Classic triad Nystagmus Ataxia Dizziness
Other
Slurred speech Sleepiness
neurologic Sx
Severe
Seizures Coma Arrhythmias
symptoms
Other
GI upset
symptoms
Initial Carbamazepine Coagulation

Electrolytes Liver function
Laboratories level studies
Other treatment Charcoal Multidose Sodium bicarbonate

considerations hemoperfusion charcoal if QRS > 100 ms
Anticonvulsants: Phenytoin and Fosphenytoin
Phenytoin Blocks sodium CNS & cardiac Fosphenytoin is a pro-drug

mechanism channels activity with a safer side effect profile
Acute vs Chronic
Considerations Oral vs IV
ingestion
IV is more IV Phenytoin is diluted in propylene glycol which

IV Phenytoin
cardiovascular toxic itself can cause hypotension & bradycardia
Symptoms & Signs
Vertical, horizontal
Common Sx Nystagmus Ataxia Dysarthria Hyporeflexia Hypotonia
or both
Respiratory
Severe AMS Seizures Coma
failure
Conduction
Cardiovascular Hypotension Bradycardia AV Blocks Tachydysrhythmias
delays
Initial Others as
Phenytoin level Electrolytes ECG
Laboratories needed
ABC’s, O2, Activated Decreases absorption & Dialysis NOT

Initial Treatment
Cardiac monitor charcoal enhances elimination useful
Seizures? Benzodiazepines
Bradycardia? Pacing OR Atropine
Antihistamines
Antihistamine Central &

Diphenhydramine Doxylamine
examples peripheral action
Antihistamine Anticholinergic Sodium channel

QT prolongation
overdose effects blockade
Definitive
Supportive
Treatment
Agitation or Avoid
Benzodiazepines
psychosis? phenothiazines
Severe Consider
symptoms? physostigmine
Antimicrobials
Antimicrobial Most Sx are self- Hypersensitivity

GI symptoms
overdose limiting reactions
Aminoglycoside Hydrate to prevent

Nephrotoxic Ototoxic
overdose and abate symptoms
CNS Sx including Depend on renal

b-lactams Hydration status
seizures function
Isoniazid
Isoniazid Decreases vitamin This is necessary for May lead to

overdose B6 GABA production intractable seizures
Neurotoxic & Even at

Isoniazid
hepatotoxic therapeutic doses
Depletes Decreases GABA Decreases seizure

Isoniazid
Pyridoxine stores stores threshold
Toxicity
Peripheral Altered mental Metabolic

Coma N/V Seizures Elevated CK
neuropathy status acidosis
Replete 1 g Pyrixodine for

Initial Treatment
Pyridoxine each gram isoniazid
Consider in intractable Unintentional

Pitfall
pediatric seizures overdose
Cardiac Medications: β-Blockers
Binds to β1 receptors Blocks production

β-blockers
of the myocardium of cAMP
Negative iotrope and Causes

β-blocker effects Vasoconstrictor Hypoglycemia
chronotrope effects on heart bronchospasm
Toxicity
Conduction
Hypotension Bradycardia Dysrhythmias AV Block Hypoglycemia
delays
Specific Glucagon 0.1 mg/kg bolus up to 10 mg/hr High dose insulin up to 2 mg/kg/hr
Treatment thereafter as a continuous infusion OR OR & dextrose
Refractory Epinephrine
hypotension? infusion
High grade
Pacemaker
blocks?
Topical medications can

Pitfall
cause systemic toxicity
Cardiac Medications: Calcium Channel Blockers
Calcium Channel Block the effects of Ca on Most Nifedipine/

Diltiazem Verapamil
Blockers smooth & cardiac muscle common Nicardipine
Calcium Channel Most common causes of death

Blockers from cardiovascular drugs
Long acting formulations require at least

Pitfall
24 hours of continuous cardiac monitoring
Toxicity
Conduction
Hypotension Bradycardia Dysrhythmias
delays
Specific Calcium Glucagon 0.1 mg/kg bolus up to 10 mg/hr High dose insulin up to 2 mg/kg/hr
OR
Treatment gluconate thereafter as a continuous infusion & dextrose
Refractory Epinephrine
hypotension? infusion
Bradycardia? Atropine
Cardiac Medications: Clonidine
Centrally acting a2- Has some peripheral

Clonidine
agonist effects as well
Can cause opioid- Respiratory

Clonidine effects Coma Seizures Miosis
like symptoms depression
Symptoms & Signs
Central effects Hypotension Bradycardia
Peripheral Hypertension followed

effects by hypotension
CNS effects Lethargy Apnea Miosis Hyporeflexia
Cardiac effects AV blocks
Specific Naloxone may be Greatest effect is on

Treatment of some benefit reversal of CNS depression
Refractory
Pressors
hypotension?
Bradycardia? Atropine
Clonidine
Hypertension Anxiety Tachycardia Sweating
withdrawal
Cardiac Medications: Digitalis
A cardiac glycoside that inhibits

Digitalis
the Na-K-ATPase pump
Increases Increases Ca2+ in the K+ leaks Increased cardiac

Digitalis
intracellular Na+ sarcoplasm reticulum extracellularly contractility
Children or Accidental or
Acute toxicity
young adults intentional overdoses
Due to decreased
Chronic toxicity Older patients
renal excretion
Symptoms & Signs
Altered mental
Acute toxicity Dysrhythmias N/V Visual changes Hyperkalemia
status
Ventricular PVC’s
Dysrhythmias SVT AV Block Bradycardia Tachycardia
tachycardia (most common)
PAT with block

(Pathognomonic)
Decreased Generalized Altered mental

Chronic toxicity N/V Dysrhythmias
excretion weakness status
Digitalis Management and Treatment
Laboratory Electrolytes Others as

EKG Digitalis level
investigations (May see elevated K+) needed
Specific
Digibind Hyperkalemia
Treatment
Unstable vital
Renal Failure
Start with 5–10 Discuss with signs
Amount?
vials initially poison control
Digibind indications
Avoid repleting Potassium,

Pitfall
Calcium and Magnesium
Altered mental Ventricular
status dysrhythmias
Replace May cause cardiac arrest Digitalis level

Calcium? in face of Dig Toxicity > 10 mg/mL
Treat hyperkalemia with all other modalities

Hyperkalemia?
(Fluids, glucose/insulin, sodium bicarbonate and enhanced GI elimination)
Ventricular dysrhythmia Use least amount Myocardial May lead to

Due to
requiring cardioversion? of joules possible irritability V. Fib
Carbon Monoxide (CO) Poisoning
Leading cause of CO binds to hemoglobin, Carboxyhemoglobin has an affinity for

CO Poisoning
toxic death myoglobin & cytochrome A3 O2 that is 250 times > Hemoglobin
Shifts oxyhemoglobin Inhibits O2 release

Pathophysiology
dissociation curve to the left from hemoglobin
Symptoms & Signs
Headache Nausea Confusion Seizures NO cyanosis
Carboxyhemoglobin Pulse ox not

Diagnosis
level reliable
Initial Treatment ABC’s 100 % O2 Cardiac monitor Hyperbaric O2
Room Air 100 % O2 Hyperbaric O2

Half-life of CO
320 minutes 90 minutes 20 minutes
Neurologic Hyperbaric
sequelae? chamber
CO crosses the Fetal hemoglobin Not considering cyanide toxicity

Pitfall
placenta has high CO affinity with smoke inhalation & acidosis
Caustic Agents: Acids
Coagulation Eschar formation stops

Acids Stomach Esophagus
necrosis further progression
Depends on type Concentration of Volume of

Severity? pH
of acid substance ingestion
Symptoms & Signs
Burning in Burning in Burning in

mouth stomach chest
Laboratory
Chemistries CBC ABG
investigations
Assess for
Imaging CXR
perforation
For large Symptomatic

Endoscopy? OR
ingestions patient
Diluting the acid except

Pitfall Giving charcoal Giving cathartics
for hydrofluoric acid
Hydrofluoric acid Dilute with milk or

ingestion? magnesium citrate
Specific Acid: Hydrogen Fluoride
Hydrogen Acts like an Can cause deep Systemic

Weak acid
Fluoride alkali cutaneous injury hypocalcemia
Symptoms & Signs
Severe burning
pain at site
Calcium Multiple Gel, infiltration,

Treatment
gluconate modalities intra-arterial
Calcium binds
Pathophysiology Pain improves
with fluoride
Stopping treatment without

Pitfall
complete resolution of pain
Caustic Agents: Alkali
Liquefactive Worse than acids due to continued tissue More common

Alkali
necrosis of tissue damage causing a full thickness burn than acid injury
Depends Solid vs Time Concentration of Volume of

Severity? pH
on agent liquid presenting substance ingestion
IV Fluids
Initial Treatment ABC’s O2 Cardiac monitor
(prevent shock)
May dilute solid agent with milk Dilution is contraindicated in May lead to
Dilution?
or water if able to tolerate po any other caustic ingestion vomiting
Laboratory
Chemistries CBC ABG
investigations
Assess for
Imaging CXR
perforation
Esophageal Assess for

Pitfall
perforation perforation
Severe burns Stridor

Concern for Symptomatic Ingestion of
Endoscopy? OR OR
perforation patient button battery
Vomiting Rigid abdomen
Lodged in the
Diluting liquid esophagus
Pitfall Giving charcoal Giving cathartics alkali
Chlorine
Has a very Affects moist

Chlorine Gaseous
pungent odor membranes
Symptoms & Signs
Irritation of Irritation of
Eye irritation Dermal injury
throat upper airway
Severe Pulmonary ARDS in severe

Rare
exposure? edema exposure
Treatment Supportive care Humidified O2
Sodium Household Typically causes mild stomach Other Sx similar

hypochlorite bleach irritation if swallowed to chlorine

Cocaine
CNS and cardiac

Cocaine
stimulant
Cocaine & Chest Abnormal EKG May be early But if ST Requires

pain may be seen repolarization elevation? cardiology consult
Normal cardiac markers

Disposition No EKG changes May discharge
after 6–12 hours
Symptoms & Signs
Agitation Tachycardia Hypertension
Initial
ABC’s O2 Cardiac monitor
Management
Nitroglycerin Avoid
Treatment Benzodiazepines
(for chest pain) Haloperidol
Evaporative
Hyperthermia? Cooling blankets
cooling
Medications to May increase

β–blockers Labetalol
avoid cardiac ischemia
Medications to May increase

Lidocaine
avoid seizure activity
Cocaine Tidbits
Whole bowel irrigation May have positive plain

Body packers Transporters
until all packets pass film
Ingestors attempting Observe until

Body stuffers
to avoid detection asymptomatic
Symptoms in Admit if symptomatic for continued

any? medical & potential surgical management
Cyanide and Nitriles
Fires
Synthetic rubber
Burning plastic
Fumigation Metal processing
Jewelers
Common
Apricot pits sources
Nitroprusside Direct exposure
Wood treatment
Cyanide
Binds more avidly Disrupts the mitochondrial

Cyanide
to Fe3+ than O2 electron transport chain
Block electron ↓ ATP ↓ H+ ↑ metabolic/

Mechanism
transport production metabolism lactic acidosis
Symptoms & Signs
Decreased mental Decreased Labile heart rate Metabolic Bitter almond Cherry red color
status + coma respiratory rate & blood pressure acidosis odor especially of blood
Secondary to ↓ O2
Normal PaO2 &
metabolism No cyanosis Abdominal pain No cyanosis Acidosis
O2 saturation
Initial IV Fluids
ABC’s O2 Cardiac monitor
Management (prevent shock)
Other initial Decontaminate Poison control

management skin & clothing assistance
Laboratory Shows anion gap

Chemistries CBC ABG acidosis
investigations
Lactic acidosis
from anaerobic
metabolism
Cyanide Treatment
Induce controlled methemoglobinemia Use of Nitrites to

Treatment goal
to compete for cyanide create methemoglobin
Sodium Nitrite Sodium Thiosulfate

Treatment Amyl nitrite
3 % IV infusion 25 % IV 50 mL bolus
Pearls are
crushed &
inhaled
Sodium
Cyanide Thiocyanate Renal excretion
thiosulfate
Fire victim? Thiosulfate only
Combines with Forms

Hydroxocobalamin B12 precursor Renally excreted
CN Cyanocobalamin
May occur in ICU patients on

Pitfall
prolonged nitroprusside
Hallucinogens
LSD
Anticholinergics Amphetamines
Jimson weed
Common
sources
Mushrooms
Cannabinoids
Amanita causes
most deaths
Mescaline PCP
Hallucinogens
Serotonin
Pathophysiology
antagonism
Symptoms & Signs
Myridiasis ↑HR and BP Agitation Labile behavior Psychosis Hyperthermia
Initial
ABC’s IV Fluids O2 Cardiac monitor
Management
Agitation? Benzodiazepines Haloperidol
Hyperthermia? Cooling
IV fluids to maintain
Rhabdomyolysis?
adequate urinary output
Phencyclidine (PCP)
Symptoms & Signs
Rotatory
↑HR and BP Agitation Seizures Psychosis Hyperthermia
nystagmus
Initial
Management
Agitation? Benzodiazepines Haloperidol
Hyperthermia? Cooling
IV fluids to maintain
Rhabdomyolysis?
adequate urinary output
Pitfall Acidifying urine

Metals and Metalloids
Arsenic
Metal Fume Metals and

Iron
Fever Metalloids
Mercury Lead
Arsenic
GI symptoms are common May have unstable

Arsenic Gastroenteritis
presenting features vital signs
Symptoms & Signs
Acute Secondary Altered mental Pulmonary In addition to GI Sx of

Renal failure Rhabdomyolysis
Symptoms status edema N/V & Abdominal pain
Chronic Peripheral Cognitive

Skin rashes Nail changes Mees’ Lines Metallic taste
exposure neuropathy dysfunction
Initial
Management
Diagnosis 24 hour urine
Acute Whole bowel

intoxication? irrigation
BAL Succimer
Antidote? OR
3–5 mg/kg IM every 4 hours For patients able to tolerate PO
Iron
Essential nutrient found in multivitamins Absorbed by upper Bound to transferrin

Iron
& iron-specific supplements small bowel in plasma
Toxicity Stages
Up to 6 hours
Stage 1 N/V Diarrhea Hematemesis Hematochezia
after ingestion
Up to 12 hours Gi symptoms Pt is still ill due to mounting

Stage 2
after ingestion improve metabolic acidosis
Metabolic
Stage 3 > 12 hours Shock Coma Coagulopathy
acidosis
Coagulopathy
Stage 4 12–48 hours Liver failure
worsens
Small bowel Continued Continual GI

Stage 5 2–6 weeks GI scarring
obstruction abdominal pain upset
Iron Treatment and Management
Need to quantify amount of Number of Pills?

History
elemental iron ingested Concentration?
Imaging Assess for radio-

KUB
consideration opaque tablets
Initial O2
ABC’s IV Fluids Cardiac monitor
Management
Whole bowel
Large ingestion?
irrigation
Laboratory 4 hour serum BMP, LFT

PT, PTT ABG
investigations iron level CBC
Deferoxamine
Antidote?
15mg/kg/hr continuous IV infusion
Fe level Unstable vital Altered mental status

Indications Seizures
> 350 µg/dL signs including coma
Lead
Most poisoning is chronic due to Disrupts neural tissue both Due to interference with
Lead
exposure of lead laden paints centrally and peripherally enzyme activity
Symptoms & Signs
Altered mental Memory and

CNS Symptoms Coma Seizures Ataxia
status Cognitive deficits
Peripheral Wrist drop is
PNS Symptoms
neuropathy classic
Children Headache Encephalopathy Anorexia Abdominal pain
Imaging May show lead KUB may show

Long bones
consideration lines lead paint chips
Basophilic stippling > 10 µg/dL are toxic

Diagnosis Serum lead level
of RBCs noted > 50 µg/dL are severe
Initial O2
Management
Lead pain chips Whole bowel

on KUB? irrigation
Antidote? BAL or Dimercaptol or EDTA
Lead level
Indications Symptomatic
> 70 µg/dL
Mercury
Toxicity depends on amount, Metallic mercury has no effects if ingested,

Mercury
type, & route of exposure but severe effects if injected or inhaled
Symptoms & Signs
Altered mental
CNS Symptoms Depression Memory loss Ataxia
status
GI Symptoms Abdominal pain N/V
Renal Acute tubular

symptoms necrosis
24 hour urine
Diagnosis
collection
BAL Succimer
Antidote? OR
3–5 mg/kg IM every 4 hours 10 mg/kg PO every 8 hours
Child swallowed
This mercury is Not absorbed
thermometer
inert by GI tract
mercury?
Metal Fume Fever
Metal Fume Cause from breathing in fumes Can result from the preparation of coinage
Fever secondary to welding metals: copper, silver and gold
Symptoms & Signs
Flu-like
URI symptoms F/C Nausea Malaise Myalgias Headaches
Symptoms
Hydrocarbons
Gasoline & Fuels
Solvents and
Oils
refrigerants
Hydrocarbons
Benzene and
Paint thinners
Toluene
Kerosene & Lamp

oils
Hydrocarbons: Introduction
Hydrocarbon Depends on viscosity High volatility worse Low viscosity worse

toxicity and volatility than low volatility than high viscosity
Consider Petroleum jelly (high viscosity/low volatility)

Example
versus Benzene (low viscosity/high volatility)
Other toxicity Route of exposure

Amount of agent Type of agent
dependents (inhaled, ingested, skin)
Halogenated
Liver toxic
agents
High risk of Highly-volatile low-

aspiration? viscosity agents
Direct effects of Secondary to

CNS effects?
agents on CNS hypoxia
Peripheral
Due to
nervous system
demyelination
effects?
Due to catecholamine Sensitization of myocardium from sniffing

Cardiac effects?
response to hypoxia or huffing which may cause dysrhythmias
Pulmonary Due to pneumonitis from

toxicity? aspiration of low viscosity agents
Hydrocarbon: Treatment and Management
Mostly Decontaminate
Treatment
supportive as required
Initial O2
Management
Charcoal and cathartics CXR may have delayed findings

Pitfall
are of no benefit 4–6 hours after exposure
General rule for Aspiration Unless the hydrocarbon has an inherent systemic
“CHAMP”
lavage outweighs benefits toxicity or has additives that cause systemic toxicity
Gastric lavage Halogenated

Camphor Aromatics Metals Pesticides
indications hydrocarbons
Carbon Toluene Leaded gas
tetrachloride
Benzene
PVC
Symptomatic
Admission
patient?
Asymptomatic If normal CXR may be discharged if

patient? medically cleared
Hypoglycemic Agents
Hypoglycemic Concern when Patient is

OR
Agents Glucose < 60 mg/dL symptomatic
Short acting Replete glucose with Give a meal (e.g., turkey and cheese sandwich D/C if asymptomatic
agent? IV & oral modalities which contains protein, carbohydrates and fat after observation
Long acting May cause serious Requires

Sulfonylureas
agents symptoms admission
Risk factors for

Liver or kidney Use of β-
sulfonylurea Old or young Alcohol use Poor nutrition
insufficiency blockers
toxicity
Sulfonylurea Toxicity
Altered mental Unstable vital Continuous hypoglycemia

status signs despite treatment
Initial O2
Management
Initial treatment IV bolus of D50
No effect or Every 1–2 hour 2 mg/kg D25 for children

IV infusion D5NS
continued Sx? blood glucose 2 mg/kg D10 for neonates
Gastric
May consider Glucagon D10 drip
decontamination
Non- No May cause lactic

Metformin?
sulfonylureas? hypoglycemia acidosis
Lithium
Used to treat Small therapeutic Most pts under long term therapy
Lithium
manic depression window will develop toxicity at some time
Excreted by Hypovolemia or hyponatremia

Lithium tidbits
kidneys will increase toxicity
Symptoms & Signs
Early CNS
Fatigue Confusion Tremor
Symptoms
CNS Symptom Altered mental

Ataxia
progression status
Late CNS
Clonus Rigidity Seizures Coma
Symptoms
Renal Diabetes Decreased ability to

Polyuria
Symptoms insipidus concentrate urine
GI Symptoms N/V Diarrhea Anorexia
Cardiac QT
Arrhythmias
Symptoms Prolongation
Maculopapular
Skin Symptoms
rash
Lithium Toxicity Treatment
Initial O2
Management
Clinical status Levels may be normal even when

Lithium level? Not helpful
more important toxicity is present in acute ingestions
Aggressive hydration
IV fluids?
with normal saline
Replete electrolytes and Li is largely

Other treatment
rehydrate patient excreted in urine
Other Sodium polystyrene

GI elimination
considerations sulfonate
Severely toxic
Hemodialysis
patient?
Rising levels of Worsening Renal Severe toxicity with Li level

Indications
lithium mental status failure > 4 mg/dL after fluid challenge
Lithium toxicity Phenytoin decreases

Pitfall
induces seizures excretion of lithium
Use
Seizures? OR Phenobarbital
benzodiazepines
Monoamine Oxidase Inhibitor (MAOI) Overdose
Used in
MAOI’s Parkinson’s
depression
Block degradation Serotonin, norepinephrine

Physiology
of catecholamines & epinephrine
Symptoms & Signs May be delayed 6–12 hours after taking
HTN
Headache Tachycardia Hyperthermia Seizures
(May be severe)
Hypertensive Red wine

Fava beans Cheese Amphetamines
crisis causes (Tyramines)
IV Fluids O2
Treatment ABC’s Cardiac monitor
(may have severe dehydration)
No role for dialysis or

Pitfall
multidose charcoal
Severe Treatment usually If used, no Use nitroprusside,

But…
hypertension? not necessary β-blockers nitroglycerine or phentolamine
Hyperthermia? Cooling methods
Mushrooms: Amanita
3–12 hours post

Amatoxin GI upset N/V Abdominal pain
ingestion
Hepatorenal 3–7 days

Final outcome Coma Death
failure thereafter
Symptoms
Benign course
within 2 hours?
Symptoms
Higher chance of
delayed > 6 Toxic ingestion
liver & kidney failure
hours?
GI
Treatment IV fluids
decontamination
Amanita Toxin is GABA

NO liver toxicity
muscaria agonist
Symptoms Delirium Seizures Hallucinations

Mushrooms: Others
Hydrazine used as a
Gyromitrins
fuel & propellant
Hepatorenal 6–12 hours post

Gyromitrins N/V Seizures
failure ingestion
GI Benzodiazepines &
decontamination Pyridoxine for seizures
Muscarinic
Muscarines DUMBELS Psychoactive
effects
GI Supportive Atropine for Bradycardia, Bronchorrhea,

Treatment
decontamination care “Killer B’s” Bronchospasm
Cutaneous Due to increased

Corpines N/V Tachycardia
flushing acetaldehyde production
Narcotics
Toxidromes Overdose Withdrawal
Symptoms & Signs
Respiratory
Overdose Obtundation Miosis
depression
Respiratory Respiratory Decreased Aspiration Pulmonary
Septic emboli
complications depression cough reflex pneumonia edema
Similar to
Withdrawal Yawning Piloerection
cholingeric crisis
2 mg initial dose and up Continuous infusion = ½ the dose given

Antidote? Naloxone
to 10 mg if no response to elicit response given each hour
Half lives of Methadone, Modified-release morphine & Oxycodone have long half-lives
Pitfall
narcotics is variable and may require repeated dosing of Naloxone and continuous infusion
Higher doses of Propoxyphene, Methadone,

naloxone Fentanyl, Codeine
Bacterial Skin & Soft

Complications Rhabdomyolysis
endocarditis tissue infections
IVDA Bacterial Right sided Left sided S. aureus most

endocarditis Staph aureus Pseudomonas common overall
Skin & Soft Look for sites of injection, track Abscess at injection site
tissue infections marks & retained foreign bodies or distal to site (CNS)
Organophosphates (OP) and Carbamates
OP & Structurally distinct Both inhibit Builds up In both neuronal &

Carbamates compounds acetylcholinesterase acetylcholine motor synapses
Symptoms & Signs
Respiratory
CNS effects Coma
depression
Muscarinic see Cholinergic
“SLUDGEM” “Killer B’s”
effects toxidrome
Nicotinic Muscle Respiratory
Cramps Weakness
effects fasiculations failure
Presentation of If presence of
“DUMBELS” Intubation!
patient? “Killer B’s”
Other Patient may smell of insecticide

presentation? or have a chemical smell
Treatment and Management
Initial
Decontamination!!
Management
Other Intubation as O2
ABC’s Cardiac monitor
Management required
Atropine 1–2 mg IV every 10 For muscarinic

Initial treatment
minutes until secretions dry up effects
Definitive Pralidoxime Can reverse acetylcholinesterase inhibition if For nicotinic

treatment (2-PAM) patient presents within 24–36 hours of exposure effects
Not indicated for

Pitfall of 2-PAM
carbamate poisoning
Phenothiazines
Compazine
Phenergan Prochlorperazine
Phenothiazines
Chlorpromazine Promethazine
Fluphenazine Mesoridazine
Lipophilic, membrane- Have long half- Unpredictable

Phenothiazines
bound agents lives absorption
Symptoms & Signs
Torticollis Tremor Rigidity Dysphagia

Extrapyramidal Dystonic
symptoms reactions Facial Oculogyric Prolonged involuntary upward
grimacing crisis deviation of the eyes
Other neurologic Inability to sit Tardive Involuntary lip &

Akathesia
symptoms still dyskinesia tongue movements
Quinidine-like Anticholinergic Peripheral

Prolonged QT Arrhythmias
effects symptoms α-blockade
Other Excessive Urinary

Hypotension Acute psychosis Seizures Heat stroke
Symptoms sedation retention
Overdose may cause neuroleptic

Pitfall
malignant syndrome
Treatment and Management
Initial O2
Management
Extrapyramidal
Diphenhydramine OR Benztropine
symptoms?
Sodium
Dysrhythmias? Lidocaine
bicarbonate
Other Consider GI
considerations decontamination
Neuroleptic Malignant Syndrome (NMS)
Not related to doses of May occur due to dopamine antagonism

NMS Rare syndrome
medications ingested or lack of dopamine agonists
Symptoms & Signs
Altered mental
CNS effects Rigidity Opisthotonus Opisthotonus
status
Constitutional Severe
symptoms hyperthermia
Cardiovascular
Tachycardia Hypertension
effects
Laboratory ↑CK, ↑WBC, ↑BUN/Cr,

abnormalities ↑LFTs, metabolic acidosis
Consider Consider
Treatment Control fever Benzodiazepines
Dantrolene Bromocriptine
Cooling blankets
Cool IV fluids
Medications
may not be
effective
Need to Use nondepolarizing

intubate? agent
Serotonin
Serotonin syndrome occurs Rigidity is Except in lower extremities where
syndrome
soon after starting medications greater in NMS in serotonin syndrome it is greater
comparison
Serotonin Syndrome
Serotonin Combination of 2 or more drugs Commonly after ↑ dosage of an Antidepressants

syndrome increases total serotonin levels agent, adding another agent most common
Symptoms & Signs
Altered mental Hypertonicity/

CNS effects Coma Seizures Hallucinations Ocular clonus
status Clonus
Constitutional Severe
symptoms hyperthermia
Cardiovascular Hypo-or
Tachycardia
effects Hypertension
Diagnosis Hunter criteria
Consider cyproheptadine Antiserotonergic

Treatment Control fever Benzodiazepines
or chlorpromazine agents
Cooling blankets Cyproheptadine: Only
Cool IV fluids available PO, or per
NG/OG
Medications
may not be
effective
Hunter Criteria for Serotonin Syndrome

Spontaneous
clonus
Hypertonicity
and Hunter Criteria Inducible Clonus
Fever (>38 °C)
with Agitation or
and Ocular
Diagnosis can be Diaphoresis
Clonus or
made if 1 criteria
Inducible Clonus
is present
Ocular Clonus
Tremor and
with Agitation or
Hyperreflexia
Diaphoresis
No serotonin
None of these?
syndrome
Agents Causing Serotonin Syndrome
Meperidine Dextromethorphan
LSD Fentanyl
Agents Causing
Cocaine & Serotonin Levodopa
Amphetamines Syndrome
Tramadol Linezolid
Triptans Lithium
Sedative-Hypnotics: Barbiturates
Wide volume of Except for modified release

Barbituates Lipophilic agents
distribution agents which are ionized
Short-acting Metabolized by
Pentobarbital
Barbituates liver
Long-acting Excreted by Dialyzable in

Phenobarbital
Barbituates kidneys overdose
Pupillary Persists even

response? when obtunded
Symptoms & Signs
Respiratory Cutaneous
Coma Shock Hypothermia Hypotension Bad prognosis
depression bullae
Initial ABC’s O2
IV Fluids Cardiac monitor
Management (Especially “A”)
Definitive Urinary
treatment alkalinization
Long acting
Hemodialysis
agent?
Sedative-Hypnotics: Benzodiazepines
Long & short Variable active

Benzodiazepines Variable potency
acting agents metabolites
Symptoms & Signs
Altered mental Depressed level Respiratory

Coma Seizures Ataxia Hypotension
status of consciousness depression
Initial ABC’s O2
Use of May cause

Pitfall
Flumazenil intractable seizures
Risk factors for

Hx of seizure Other Hx of increased
intractable Chronic users
disorders co-ingestants intracranial pressure
seizures
Definitive
Supportive
treatment
Sedative-Hypnotics: Gamma-Hydroxybutyrate (GHB)
Used as “rave” NOT detected on

GHB Analog of GABA
drug or “date rape” routine drug screens
Symptoms & Signs
Sudden Agitation followed Decreased level Respiratory

Sleepiness Coma
agitation by euphoria of consciousness depression
Initial ABC’s O2
Concomitant use Will need to

Pitfall
of alcohol observe longer
Similar to alcohol & other

Withdrawal
sedative-hyponotic withdrawal
Definitive May self extubate

Supportive
treatment & leave ED
Strychnine Toxicity
Blocks inhibition of spinal cord motor End result is

Strychnine Toxic alkaloid
neurons & some brainstem receptors hyperstimulation of CNS
Symptoms & Signs
Facial Severe muscle Pt remains

Muscle spasms Opisthotonus
grimacing twitches conscious
Initial ABC’s Consider

Benzodiazepines
Management (Especially “A”) paralytics
Paralysis of medulla
Pitfall
with death
Tricyclic Antidepressants (TCA)
Amitriptyline
Trimipramine Amoxapine
Protriptyline Tricyclic Desipramine

Antidepressants
Nortriptyline Doxepin
Imipramine
Tricyclic Antidepressants (TCA)
Broad effects due to engagement Has anticholinergic, Na+ channel

TCA
of multiple receptors blocker, and α-blockade effects
Symptoms & Signs Usually occur within 6 hours of ingestion

Anticholinergic
“DUMBELS”
effects
Bundle branch Wide QRS
Cardiovascular AV Block Tachycardia Hypotension S in I, R in aVR
block complex
CNS effects Confusion Seizures Coma Delirium Ataxua
Initial O2
Management
Treatment of Multidose Sodium Maintain Especially for hypotension

ingestions charcoal bicarbonate serum pH ~7.5 or Wide QRS > 100 ms
Agitation or
OR Seizures Benzodiazepines
Delirium
Overdrive pacing
Dysrhythmias? Lidocaine Magnesium Cardioversion
for Torsades
Medication Will worsen

Phenytoin Procainamide
Pitfalls condition
Xanthines
Inhibit breakdown Cause excess Theophylline

Xanthines
of cAMP adrenergic output Caffeine
Symptoms & Signs
Multifocal atrial
Cardiovascular Tachycardia
tachycardia
Other effects Vomiting Seizures
Theophylline In acute overdose, levels In chronic overdose, may have

Diagnosis
levels correlate with toxicity high toxicity with low levels
Other laboratory Metabolic

Hypokalemia Hypomagnesemia Hypophosphatemia
findings acidosis
Initial O2
Management
Treatment of Multidose Charcoal

Dialysis
overdose charcoal hemoperfusion
Seizures? Phenobarbital
Malignant Hyperthermia
Malignant Hypermetabolism Triggered by inhalation

Inherited disorder
Hyperthermia involving skeletal muscle anesthetics & succinylcholine
Calcium released from sarcoplasmic reticulum of skeletal muscle and

Pathophysiology
causes a hypermetabolicstate after exposure to triggering agents
Symptoms & Signs
Muscle Hyperthemia
Muscle rigidity Tachypnea Tachycardia Rhabdomyolysis Mottled skin
stiffness (> 40.5 °C)
Some laboratory
Acidosis Hyperkalemia Myoglobinuria
findings
Initial O2
Management
Further Discontinue Cooling of

Dantrolene
Management affecting agent patient
Interferes with Lowers

Dantrolene
muscle contraction temperature
Complications DIC Cardiac failure Renal failure

Orthopedic Emergencies
Bobby Desai
Contents
Tidbits 736
The Hand 738
Fractures and Dislocations of the Wrist 750
The Forearm 756
The Elbow 760
The Humerus and Shoulder 766
Nontraumatic Hip Disorders 777
The Femur 781
The Knee 782
The Leg 791
The Ankle 795
The Foot 797
Osteomyelitis 800
Thoracic and Lumbar Pain 801
Rheumatologic Emergencies 808
B. Desai, MD, MEd


DOI 10.1007/978-3-319-30838-8_14
736 B. Desai
Tidbits
Growing Bone Anatomy
Epiphysis
Physis (growth plate)
Metaphysis
Diaphysis
Center image (Reprinted from Abdelgawad A, Naga O. Introduction

to orthopedic nomenclature. In: Abdelgawad A, Naga O, editors.
Pediatric orthopedics: a handbook for primary care physicians.
New York: Springer; 2014. p. 1–14. With permission from Springer
Orthopedic Emergencies 737
Salter-Harris Fractures
PEDIATRICS
Most common in males
10–16
Metaphysis Infants &

Diaphysis S toddlers
(Shaft) S Slip through the growth plate
Growth plate 6%
Epiphysis
A Above the growth plate
Complete
Growth issues
physeal fx
related to: L Lower than the growth plate
Amount of
fragmentation
T Through the growth plate
A L
Size of fracture
75 % 10 % fragment
R Ram the growth plate
Extent of
epiphyseal
Most Chip fx of Physeal fx extends Fractures due to epiphyseal growth
injury
common metaphysis thru epiphysis plate being weaker than supporting
Worst ligaments
prognosis
Crush or May result in growth
compression complications
with severe
T R abduction or
10 % <1 % adduction
Knee/Ankle
Most common Physeal fx+ most
epiphyseal fx+ Increase in complications from I–V
in distal common
humerus metaphyseal fx Compression fx IV & V – future growth impairment
of growth plate
Blood supply to growth plate
Long bones in children I&V comes from epiphysis
All involve growth plate or X-ray may be negative Greater the injury to epiphysis, higher
surface of joint likelihood of growth disturbances
738 B. Desai
The Hand
Nerves of the Hand
Sensory Motor
Radial Radial
Dorsal web space

Finger/Wrist
between index finger
extension
& thumb R
R
U
U M
M
Median Median
M M
M
Flexion of index &

Thumb, index, long
middle fingers +
and ½ of ring finger
Thumb opposition
Ulnar Ulnar
Finger adduction &

½ of little & ring
abduction + flexion
fingers
of ring & little fingers
DrCuMa
Drop Hand = Radial

Recurrent Median Nerve Dorsal branch of Radial
Pure motor nerve to Claw Hand = Ulnar Nerve
thenar muscles Finger Apposition = Median Pure sensory
Amputation of the Digit (Look in Trauma)
Place digit in Do NOT place Clean & sharp

Initial plastic bag in But… digit directly on wounds have best
management water ice! prognosis
Multiple digits
Consider any part

Thumb
for reimplantation
in a child Better prognosis
proximal to IP joint
Indications for
Reimplantation
Single digit
Wrist or Forearm between PIP & DIP
Metacarpal (Palm)
area
Hand Infections
Most hand Most frequent

Pathophysiology Due to Staph OR Strep
infections colonizers of skin
Some hand Due to Anaerobes Polymicrobial Both common Neisseria

infections with mouth flora
IV drug users Abscesses Due to Staph aureus Gram negatives
Eikenella Amoxicillin-
Human bites Fusobacterium Staph
corredens Clavulate for these
Atypical
DM + HIV Mycobacterium Candida albicans
organisms
Cellulitis that May form Same antibiotics

Cat/Dog Bites Pasteurella
rapidly spreads abscess as human bite
Drain obvious Provide broad

General Rx for Immobilize Elevate
superficial spectrum
hand infections abscesses
extremity extremity antibiotics
Position of
function
Position of IP joints MCP joints Wrist

function 5–15o flexion 50–90o flexion 15–30o flexion
740 B. Desai
Felon
Pulp space
Felon Due to Staph aureus
infection
Occurs in distal
Felon fingertip
Incision & Antibiotics vs

Treatment
drainage Staph
Volar
longitudinal
incision
Starts 3 to
5 mm from
the distal
interphalangeal
joint
a b
d e
Top right image (Reprinted from Dailana ZH, Rigopoulos N. Infections of the hand. In: Bentley G, editor. European surgical orthopaedics and
traumatology. Heidelberg: Springer Verlag; 2014. p. 2009–31. With permission from Springer Verlag)
Paronychia
Acute nailbed
Paronychia Due to Staph aureus
infection
Chronic Candida or other

Paronychia Due to
infection fungi
Incision & Antibiotics NOT

Treatment Soaks
drainage indicated
Osteomyelitis
Complication
(if not improving)
I&D herpetic May result in

Pitfall
whitlow herpetic myositis
Eponychium
Pus beneath Germinal
eponychial fold matrix
Nail
Hyponychium
Sterile matrix
Top right image (Reprinted from Dailana ZH, Rigopoulos N. Infections of the hand. In: Bentley G, editor. European surgical orthopaedics and
traumatology. Heidelberg: Springer Verlag; 2014. 2009–31. With permission from Springer Verlag)
742 B. Desai
Collar Button Abscess
Collar Button Infection of Between Erupts Palmar aponeurosis

Spreads
Abscess hand metacarpals dorsally presents volar extension
Collar Button Dorsal & volar abscess

Due to Foreign body OR Splinter
Abscess connected by a tract
Incision & Urgent orthopedic

drainage consultation
Flexor Tenosynovitis
Flexor Surgical Failure to Dx will result in loss Penetrating Staph most

Due to
Tenosynovitis emergency of both digit & hand function trauma common
May have
anaerobes
Diagnosis Kanavel’s signs
Tenderness over
Symmetric Pain with passive Flexed posture
Kanavel’s signs flexor tendon
finger swelling extension of digit
sheath
Tenderness along
tendon sheath
Finger held
in flexion
Fusiform
swelling
Pain with passive

extension
Treatment IV antibiotics Surgical I&D
Bottom right image (Reprinted from Dailana ZH, Rigopoulos N. Infections of the hand. In: Bentley G, editor. European surgical orthopaedics
and traumatology. Heidelberg: Springer Verlag; 2014. p. 2009–31. With permission from Springer Verlag)
Sporotrichosis
Fungal infection Sporothrix Occurs in Rose

Sporotrichosis Due to
with skip lesions schenckii gardeners
Supersaturated
Treatment Itraconazole OR
potassium iodide
Boutonniere Deformity
Central slip extensor
Boutonneire Forced flexion at
hood disruption near Due to
Deformity PIP joint
PIP joint
Boutonneire Lateral bands of extensor hood

Deformity split to become PIP flexors
Boutonneire deformity
Boutonneire May have concomitant Flexed PIP
Deformity avulsion fracture
Extended DIP
PIP flexion
+
Splint PIP in
Treatment DIP extension
extension
744 B. Desai
Mallet Finger
Extensor tension Forced flexion at

Mallet Finger Due to
disruption of the DIP DIP joint
Swan neck deformity
Something hitting a
fully extended digit
Avulsion fx of dorsal
Mallet Finger
base of distal phalanx
Splint DIP in
Treatment
extension
X-ray
Bottom left image (Reprinted from Almusa E, Peterson II WM, Bianchi S, Jacob D, Hoffman D. Radiological investigations. In: Chick G, editor.
Acute and chronic finger injuries in ball sports. Paris: Springer Verlag; 2013. p. 89–124. With permission from Springer Verlag)
Gamekeeper’s (Skier’s) Thumb
Gamekeeper’s Injury to ulnar collateral Forced radial abduction

Due to
Thumb ligament of thumb MCP of MCP joint
Ulnar collateral Important for grasp &

pincher function of Skier’s thumb
ligament thumb
Gamekeeper’s May have concomitant

Thumb avulsion fracture Ulnar collateral
ligament of the
thumb
X-ray
Thumb spica
Treatment Partial tear Complete tear Surgery
splint
Chronic instability
Pitfall
of thumb
Bull rider’s Thumb
>40o radial angulation Surgical RCL injury
Complication
indicates complete rupture consultation
Center left image (Reprinted from Almusa E, Peterson II WM, Bianchi S, Jacob D, Hoffman D. Radiological investigations. In: Chick G, editor.
Acute and chronic finger injuries in ball sports. Paris: Springer Verlag; 2013. p. 89–124. With permission from Springer Verlag)
Herpetic Whitlow
Herpetic Viral infection of Contact with oral

Due to Herpes simplex Due to
Whitlow distal finger herpetic infection
Associated with
Adults HSV 2 Children gingivostomatitis
HSV-1
Symptoms & Signs
Red, tender Potential

Burning Pruritis Vesicular bullae
lesion induration of finger
Mistaken for
Pitfall DO NOT I&D!
felon
Usually self Consider

Treatment
limited antiviral agents
746 B. Desai
De Quervain’s Tenosynovitis
De Quervain’s Excessive use of Tenosynovitis of extensor pollicis

Due to
Tenosynovitis thumb or wrist brevis & abductor pollicislongus
Radial aspect of wrist

Pain
radiating to thumb or wrist
Painful ROM of Pain over distal Positive

Diagnosis
thumb radial styloid Finkelstein’s test
Abductor pollicis Extensor pollicis

longus brevis
Immobilize thumb Anti-inflammatory
Treatment
& wrist with splint medications
Carpal Tunnel Syndrome

Entrapment of
Carpal Tunnel
Polyneuropathy Due to median nerve in Causing Sx
Syndrome the carpal tunnel
Radial aspect of Palmar aspect of

Paresthesias Long finger Index finger
ring finger thumb
Radiation of pain Waking up at Numbness with

Other Sx to forearm & night with burning Tingling in hand prolonged flexed
shoulder pain hand
Overuse CHF Hypothyroidism

Etiology
Pregnancy Renal disease Rheumatoid arthritis
Tapping over the Flexing wrist for

Diagnosis Tinel’s sign Phalen’s sign
median nerve 1 min
More sensitive &
specific
Referral to hand
Treatment Volar splint NSAIDs
surgeon
Fractures of the Hand: Phalanx
Crush or Tuft fx can be associated Fx at the base may be associated with

Distal phalanx Due to
shearing forces with nail bed lacerations flexor or extensor tendon involvement
Treatment Splinting
Middle & Most fx are stable May be Rx with

proximal phalanx & nondisplaced buddy taping
Splint from
Unstable Fx? Hand follow-up
elbow to DIP
Spiral or intra-
Internal fixation
articular fx?
Fractures of the Hand: Metacarpals

Displacement
Metacarpal Caused by direct May result in Consider human bite
causes poor
Head fx blow or crush intraarticular fx if laceration present
outcome
Metacarpal neck Metacarpal neck is Boxer’s Fracture of the neck All will have
fx most common hand fx Fracture` of the 5th metacarpal volar angulation
Direct impaction force Unstable
Acceptable Ring (4th)

5th
angulation of < 35 degrees
<45 degrees
metacarpal neck?
Ulnar gutter Radial gutter

Treatment 5th & Ring Index & Middle
splint splint
Any rotation
PItfall requires urgent
hand followup
Metacarpal Shaft Usually with rotational Caused by axial

fx deformity & shortening force or direct blow
Index & middle

Angulation of Index Long
Not acceptable tolerate less
metacarpal shaft? 10 degrees 20 degrees
angulation
Rotational Corrected with

deformity operative fixation
Ulnar gutter splints do

Pitfall not provide any
correction of rotation
Metacarpal Base Associated with Caused by axial Base of 4th & 5th may result in paralysis
fx carpal bone fractures force or direct blow or motor branch of ulnar nerve
748 B. Desai
Special Fractures of the Metacarpals

Caused by axial
Bennett’s Intraarticular fracture with dislocation At ulnar aspect of base of
load with a closed
Fracture hand
or subluxation at metacarpal joint thumb at metacarpal joint
Thumb spica
Treatment Will require ORIF
splint
Comminuted fracture Fx is
Rolando Fracture Worse prognosis
at base of metacarpal intraarticular
Hand
Treatment Thumb spica
consultation
Finger Dislocation
Distal
Have firm
interphalangeal Uncommon attachments
joint
Proximal
Axial load &
interphalangeal Common hyperextension
joint
Dorsal Rupture of the Causes ulnar Rupture radial

Very common Due to Due to
dislocation volar plate deviation collateral ligament
Digital Distraction & Splint at 30o

Treatment Reduction block hyperextension Reposition
flexion
Unable to Volar plate Operative

Pitfall reduce entrapment fixation
Metacarpophalangeal Less common Caused by Ruptures volar Dorsal

joint than PIP hyperextension plate dislocation
Treatment Reduction Splint in flexion
If present may Caused by

Thumb IP Joint Rare be open hyperextension
Hyperextension
Thumb MCP mechanism
High-Pressure Injection Injury
High Pressure Caused by injection of substances with

2000–10,000 PSI
Injection Injury high pressure in soft tissues of hand
Ischemia of Chemical
Mechanism Tissue edema Due to
tissues inflammation
Initial benign
Pitfall
appearance
Symptoms & Signs
Severe tenderness Signs of compartment

Edema Pallor
to palpation syndrome
Plain film may show Subcutaneous

Diagnosis
radiopaque substance emphysema
Immobilize & Surgical Broad spectrum

Treatment Debridement
elevate decompression antibiotics
Amputation rate
Complication
30 %
750 B. Desai
Fractures and Dislocations of the Wrist
Colles’ Fracture
Most common fx Fall on

Colles’ Fracture Due to
in adults > 50 outstretched hand
Distal radial Dorsal “Dinner fork May have fx of

Colles’ Fracture
metaphysis fx angulation deformity” ulnar styloid
Lateral view has best

Diagnosis Plain film
view of angulation
X-ray
Treatment Closed reduction Sugar tong splint
> 20o of Involvement of Significant > 1 cm of

Unstable fx?
angulation joint comminution shortening
Median nerve
Complications Malunion Joint instability Arthritis
injury
Center right image (Reprinted from Raby N. Imaging of wrist trauma. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand and
wrist. Heidelberg: Springer Verlag; 2013. p. 141–69. With permission from Springer Verlag)
Smith’s Fracture
“Reverse Fall or direct blow

Smith’s Fracture Due to
Colles’” on dorsum of hand
Distal radial “Garden spade

Smith’s Fracture Volar angulation
metaphysis fx deformity”
Lateral view has best

view of angulation
X-ray
Treatment Closed reduction Sugar tong splint
Median nerve Flexor tendon

Associations
injury injury
Complications Same as Colles’
Center image (Reprinted from Raby N. Imaging of wrist trauma. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand and wrist.
752 B. Desai
Scaphoid Fracture
Scaphoid Most common Fall on dorsiflexed

Due to
Fracture carpal fracture hand or axial load
Pain along radial Pain in anatomic

Symptoms
aspect of wrist snuffbox
Initial x-rays may

be negative
X-ray
Thumb spica Orthopedic

Treatment
splint referral
Not splinted Not repeating Bone scan in 3 CT or MRI as

Pitfalls films in several
suspected fx days days alternative
If continued pain
Avascular
Complications
necrosis
Center image (Reprinted from Raby N. Imaging of wrist trauma. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand and wrist.
Triquetral Fracture
Triquetrum 2nd most common May be an

Fracture carpal fracture avulsion fx
Pain along dorsum of

Symptoms wrist distal to ulnar styloid Pain to flexion
X-ray
Orthopedic
Treatment Splint referral
Center bottom image (Reprinted from Raby N. Imaging of wrist trauma. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand and
Other Hand Fracture Tidbits
Occurs with other Fall on

Lunate Fracture Due to
carpal injuries outstretched hand
Risk of avascular
Pitfall
necrosis
May be difficult to isolate

lunate from other carpals
Orthopedic
Treatment Splint
referral
Avascular Kienbock Lunate Decreased

Osteoarthritis Chronic pain
necrosis disease collapse grip
754 B. Desai
Scapholunate Dissociation
Scapholunate Scapholunate ligament is most

Dissociation commonly injured ligament of the wrist
Scapholunate Pain & swelling at

Dissociation Sx radial side of wrist
Widening of scapholunate
joint space > 3mm
X-ray
Treatment Radial gutter Orthopedic

splint referral
Arthritis if
Complications
untreated
Center image (Reprinted from Raby N. Imaging of wrist trauma davies. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand and
Perilunate and Lunate Dislocations
Perilunate
Perilunate& Lunate aligned but capitate
Forced Fall on displaced
Lunate Due to
hyperextension outstretched hand
Dislocations Lunate
Capitate aligned but lunate
displaced
Lateral view has
best view
a b a b
X-ray
Lunate Perilunate
“Piece of pie”
Treatment Closed reduction Long arm splint
Avascular
Median nerve
Complications necrosis if Scaphoid fx Arthritis Malunion
injury
lunate fx
Center left image (Reprinted from Raby N. Imaging of wrist trauma davies. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand
and wrist. Heidelberg: Springer Verlag; 2013. p. 141–69. With permission from Springer Verlag)
Center right image (Reprinted from Raby N. Imaging of wrist trauma davies. In: Davies AM, Grainger AJ, James SJ, editors. Imaging of the hand
and wrist. Heidelberg: Springer Verlag; 2013. p. 141–69. With permission from Springer Verlag)
756 B. Desai
The Forearm
Ulnar Nightstick Fracture
Ulnar Nightstick Nondisplaced ulnar Direct blow to

Due to Defense injury
Fracture shaft fracture forearm
X-ray
Immobilized in Orthopedic
Nondisplaced fx
splint referral
Displaced fx ORIF
Unstable fx? > 10oof > 50 % Proximal 1/3 of

angulation displacement ulna
Missed Radiohumeral Radial nerve

Complications Nonuniuon
Monteggia fx dislocation injury
Center right image (Reprinted from De Boeck H, Haentjens P, Handelberg F, Casteleyn PP, Opdecam P. Treatment of isolated distal ulnar shaft
fractures with below-elbow plaster cast. Arch Orthop Trauma Surg. 1996;115(6):316–20. With permission from Springer Verlag)
Galeazzi Fracture
Fx of distal 1/3 Dislocation of distal Fall on

Galeazzi Fracture Due to OR Direct blow
of radial shaft radioulnar joint outstretched hand
Usually
Galeazzi Fracture
displaced
Local tenderness & swelling

Symptoms
over distal radius & wrist
MUGR X-ray
Monteggia – Ulna
Galeazzi - Radius
Treatment ORIF Sugar tong splint
Ulnar nerve
Complications Malunion injury
Lower right image (Reprinted from Haugstvedt JR. Galeazzi’s fracture and Essex-Lopresti injuries: dislocation fractures of the forearm. In: Hove LM, Lindau
T, Hølmer P, editors. Distal radius fractures: current concepts. Heidelberg: Springer Verlag; 2014. p. 391–401. With permission from Springer Verlag)
758 B. Desai
Monteggia Fracture
Monteggia Fx of proximal Dislocation of

Fracture 1/3 of ulna radial head
Monteggia May miss the radial

Fracture head dislocation

Symptoms
over the elbow
X-ray
Treatment ORIF
Radial nerve Radial head

Complications Malunion
injury fracture
Bottom center image (Reprinted from Casado-Sanz E, Barco R, of the limbs. Zug: Springer International Publishing; 2014. p. 1–8.
Antuña SA. Complex fractures of the proximal humerus. In: With permission from Springer International Publishing)
Rodríguez-Merchán EC, Rubio-Suárez JC, editors. Complex fractures
Both Ulna and Radius Fractures
Both Ulna & Requires Are usually MVC

Due to
Radius Fractures significant force displaced Fall from height

Symptoms
over the forearm
X-ray
Adults Greenstick Other fx in kids

Treatment Children
ORIF Immobilization ORIF
Inability to
Neurovascular Compartment Non-or
Complications supinate & Osteomyelitis
injury syndrome malunion
pronate
Volkmann’s Ischemic Contracture

Volkmann’s Decreased
Typically from unrecognized or delayed Caused by
Ischemic Due to circulation to the
Contracture forearm
treatment of compartment syndrome compressive states
Volkmann’s
Pronation of Flexion of wrist Paralysis of
Ischemic
Contracture
forearm & digits intrinsic muscles
Symptoms & Signs
Swelling &
Pain Paresthesias
edema of digits
Forearm Inappropriately
Causes Elbow fracture
fractures tight casts
Damage is irreversible Need for prompt

Pitfall
in 6 hours recognition & treatment
Cast Pain Numbness Removal of cast

760 B. Desai
The Elbow
Soft Tissue Injuries
Most are Involve Repetitive trauma Sudden or prolonged

Biceps Rupture Due to
proximal long head & overuse contraction against resistance
Symptoms & Signs
Pain
Snapinoranterior
pop is Pain in anterior Swelling, tenderness, & Flexion of elbow causes pain
heard
shoulder
& felt shoulder crepitus over bicipial groove and produces avmidarm “ball”
Sling, ice, Referral to

Treatment
analgesics orthopedic surgeon
Distal Fall on outstretched Direct blow to

Triceps Rupture Due to OR OR Spontaneous
injury hand olecranon
Hyperparathyroidism
Symptoms & Signs
Pain in posterior Complete ruptures cause Partial tears may have some Swelling & tenderness posteriorly
elbow inability to extend the elbow function proximal to olecranon
Sling, ice, Referral to

Treatment
analgesics orthopedic surgeon
Bursitis
Acute or chronic Olecranon Prepatellar Repetitive

Bursitis Due to
inflammation of bursa in elbow in knee trauma
Not recognizing
Pitfall
septic bursitis
Abrupt onset of swollen,

Septic bursitis
hot, red & tender area
Aspiration of Both diagnostic Some may need

Diagnosis
fluid & therapeutic open debridement
Organisms MRSA Strep
Treatment
RICE NSAID’s
non-septic
PO vs IV Depends on
Treatment septic
antibiotics clinical condition
Epicondylitis
Lateral Overuse of
“Tennis elbow” Due to
Epicondylitis forearm extensors
Symptoms & Signs
Tenderness of Pain on forced extension & supination

lateral epicondyle of forearm against resistance
Anti-
Treatment RICE Immobilization
inflammatories
Medial Overuse of
“Golfer’s elbow” Due to
Epicondylitis forearm flexors
Symptoms & Signs
Tenderness of Pain on forced flexion & pronation of

medial epicondyle forearm, wrist & digits against resistance
Sling, ice, Anti-

Treatment Immobilization
analgesics inflammatories
Ulnar
Complication
neuropathy
762 B. Desai
Nursemaid’s Elbow
PEDIATRICS
Nursemaid’s Subluxation of the radial head Arm being May have tear of Typically ages
Due to
Elbow beneath the anular ligament pulled anular ligament 1–4
Symptoms & Signs
Child reluctant Forearm flexed

to move arm and pronated
X-rays
Diagnosis Clinical Hx
unnecessary!
Reduction by supination Hyperpronation/

Treatment OR
forearm & flexing elbow forced pronation
Flexion
Supination
Supination-flexion Hyperpronation
Elbow Dislocation
Elbow Vast majority Fall on

Due to
dislocation (90%) are posterior outstretched hand
Ulnar nerve
Most common nerve
Elbow Pt presents with Must assess Brachial injury
dislocation elbow in 45o flexion neurovascular status artery
Radial nerve
Most common
arterial injury Median nerve
Consider Arterial
No radial pulse Open dislocation Arteriogram
injury?
Children may have

Coronoid
X-ray associated medial Unstable
process fx?
epicondyle fx
Longitudinal traction Long arm Orthopedic

Treatment Closed reduction
of wrist & forearm posterior splint consultation
Causes bleeding
Pitfalls Hyperextension
from arterial injury
Median nerve
Complications Malunion Joint instability Arthritis
injury
Left center image (Reprinted from Spina V, Baldini L. Imaging of the elbow. In: Celli A, Celli L, Morrey BF, editors. Treatment of elbow lesions:
new aspects in diagnosis & surgical techniques. Milan: Springer Verlag; 2008. p. 21–38. With permission from Springer Verlag)
764 B. Desai
Elbow Fracture Tidbits
Elbow Fractures Radial head Proximal ulna Distal humerus
A small one may Large one is

Radiologic signs Anterior fat pad “Sail sign”
be seen normally abnormal
Radiologic signs Posterior fat pad Never normal
Intraarticular Intracapsular Occult radial Gout, synovitis or

Posterior fat pad OR OR OR
hemorrhage hemorrhage head fx other infections
Anterior Picks up occult In normal imaging, the anterior aspect of the humerus
humeral line test supracondylar fx bisects middle 1/3 of capitellumon the lateral view
Radial Head Fracture
Radial Head Most common Fall on Radial head is driven May have
Due to
Fracture fx of the elbow outstretched hand into the capitellum additional injury
Most common Capitellum fx
occult fx in adults
Coronoid fx
Symptoms & Signs Olecranon fx
Elbow dislocation
Lateral elbow Lateral elbow Tenderness of Pain with passive MCL injury
pain swelling radial head rotation of forearm
Avulsion fx of
medial
epicondyle
Diagnosis Plain film Look for fat pads
X-ray
Treatment
Immobilization RICE
Non-displaced
Displaced Fx OR Decreased ROM Surgical repair
Restricted elbow
Complications Chronic pain
ROM
Right center image (Reprinted from Daneshvar P, Pollock JW, Athwal Right image (Reprinted from Daneshvar P, Pollock JW, Athwal
GS. Fractures and dislocations of the proximal ulna and radial head. GS. Fractures and dislocations of the proximal ulna and radial head.
In: Antuña S, Barco R, editors. Essentials in elbow surgery. London: In: Antuña S, Barco R, editors. Essentials in elbow surgery. London:
Springer Verlag; 2014. p. 61–89. With permission from Springer Springer Verlag; 2014. p. 61–89. With permission from Springer
Verlag) Verlag)
Supracondylar Fracture
Supracondylar Most common fx of Extension type Flexion type

Fracture OR
the elbow in children (>95 %) (<5 %)
Posterior displacement Anterior displacement
Fall on Direct force anteriorly

Extension type Flexion type
outstretched hand to a flexed elbow
Symptoms & Signs
Edema around Tenderness of Prominent Depression + medial or lateral

elbow elbow olecranon proximal to elbow displacement
X-ray
Treatment Emergent orthopedic

Reduction
Displaced fx consultation
Brachial artery Compartment Eventual

Complications Nerve injury Volkmann’s
injury syndrome contracture
Vascular Median
compromise Radial
Left center image (Reprinted from Abdelgawad A, Enes Kanlic. Orthopedic trauma. In: Abdelgawad A, Naga O, editors. Pediatric orthopedics:
a handbook for primary care physicians. New York: Springer; 2014. p. 409–83. With permission from Springer Science + Business Media)
766 B. Desai
The Humerus and Shoulder
Proximal Humerus Fracture
Proximal Humerus Occur in elderly Fall on outstretched hand

Due to
Fracture osteoporotics with elbow extended
Symptoms & Signs
Shoulder Crepitus near Arm held near

Shoulder pain Ecchymosis
swelling shoulder chest wall
Diagnosis Classified into Displacement of fracture There can be

Plain film
fractures of “parts” fragment is a “part” up to 4 parts
One part No displacement Displacement Angulation

OR OR
fracture at all < 1 cm < 45º
X-ray
Treatment Immobilization Orthopedic

with sling & RICE Analgesics
One-Part Fx swathe referral
Treatment of Ortho More

Due to
multi-part fx consultation complications
Brachial plexus Axillary nerve Axillary artery

Complications
injury injury injury
Most common nerve Most common artery
injury injury
Deltoid muscle
Right center image (Reprinted from Erhardt JB, Roderer G, Grob K, Forster TN, Stoffel K, Kuster MS. Early results in the treatment of proximal
humeral fractures with a polyaxial locking plate. Arch Orthop Trauma Surg. 2009;129(10):1367–74. With permission from Springer Science +
Business Media)
Humerus Shaft Fracture

Occur in elderly
Humerus Shaft Fall on Direct Transverse
osteoporotics & Due to Spiral fx
Fracture young men outstretched hand blow fx
Most commonly in
middle 1/3 of humerus
Symptoms & Signs
Localized Abnormal Crepitus on May have shortening

Arm swelling Arm pain
tenderness mobility palpation with displaced fx
Displacement of fx Actions of
Diagnosis Plain film Due to
fragments is common various muscles
a b
X-ray
Immobilization Orthopedic
Treatment with sling & RICE Analgesics
swathe referral
Radial is most Wrist drop & decreased

Brachial artery Radial, median or
Complications common nerve sensation at dorsal thumb-
or vein injury ulnar nerve injury injury index web space
Left center image (Reprinted from Ristevski B, Hall J. Humeral shaft fractures. In: Sethi MK, editor. Orthopedic traumatology: an evidence-
based approach. New York: Springer Science. 2014. p. 129–40. With permission from Springer Science + Business Media)
Nontraumatic Shoulder Pain
Nontraumatic
Intrinsic causes Extrinsic causes
Shoulder Pain
Heart Gallbladder Spleen

Extrinsic causes Referred pain
Lungs Liver Neck
Rotator cuff Impingement Adhesive

Intrinsic causes
tendinitis syndrome capsulitis
Rotator cuff Secondary to Active ROM Passive ROM is Impingement

repetitive over syndrome can
tendinitis head use of arm painful & limited full & impeded occur
Rotator cuff Supraspinatus Infraspinatus Teres minor Subscapularis
Rotator cuff
Immobilization strengthening
Treatment RICE Analgesics
for comfort exercises
Adhesive After long period Painful & limited Both active &
capsulitis of immobilization ROM passive
768 B. Desai
Sternoclavicular Injuries
Sternoclavicular Sudden forcing of Pain & swelling RICE, sling,

Due to the shoulder Treatment
Sprain forward to the joint analgesics
Sternoclavicular Sports Posterior Shoulder forward + direct blow

Due to MVC OR
dislocation injury Anterior (m.c.) Shoulder backwards + direct blow
Symptoms & Signs
Shoulder Pain worsened with Shoulder Shoulder rolled Anterior have prominent Posterior may impinge on contents
pain arm movement shortened forward clavicle anterior to sternum of superior mediastinum
Contrast for suspected Evaluate for

Diagnosis CT
posterior dislocation thoracic injury
Emergent
Treatment Orthopedic
If uncomplicated reduction not Sling Analgesia
Anterior necessary referral
Complications Associated with life Injury to Injury to Injury to

PTX
Posterior threatening injury great vessels esophagus trachea

Posterior in OR
Acromioclavicular (AC) Injuries
Acromioclavicular Direct trauma to Fall with arm

Due to
Sprain AC joint adducted
Diagnosis Clinical
Symptoms & Signs
Shoulder Painful to move arm across

Tender at AC joint
pain body
Type Injury Imaging
Type 1 Sprain of AC ligament Normal
Type 2 AC rupture, coracoclavicular (CC) ligament sprain Clavicle 25–50 % above acromion
Type 3 AC rupture, CC rupture AC joint dislocated 100 %, CC interspace widened up to 100 %
Type 4 All supporting structures ruptured Appear similar to 2 & 3
Types 5 & 6 have AC dislocation, gross deformity and have potential for multiple associated injuries
Immobilization
Treatment Types Orthopedic
1&2 swathe referral
Treatment Types Orthopedic

Severe injury Surgical repair
3–6 evaluation
Clavicle Fracture
770
~80 % in middle ~5 % in medial ~20 % in distal

Clavicle Fracture Due to Direct blow
1/3 1/3 1/3
Most common in
children
Symptoms & Signs
Deformity Arm inward & down, needing

Swelling over clavicle Tender clavicle Ecchymosis
around clavicle support from other arm
May miss fx at the

Diagnosis Plain film CT may be needed
end of the clavicle
Imaging b c
Emergent ortho Open fx or skin Neurovascular Severe fx Significant

OR OR OR
consultation? tenting injury communition displacement

RICE Analgesics
uncomplicated fx with sling & swathe referral
Rupture of Medial
Distal Needs Intrathoracic
Complications coracoclavicular clavicle
clavicle surgery injury
ligament injury
Has significant Subclavian
medial elevation artery & vein
Left center image (Reprinted from Geddes CR, McKee MD. Clavicle fractures. In: Sethi MK, editor. Orthopedic traumatology: an evidence-based approach. New York: Springer Science. 2014.
B. Desai
p. 87–102. With permission from Springer Science + Business Media)

Scapula Fracture
Fall on Most common

Scapula Fracture Due to OR Direct blow
outstretched hand Fx of body & glenoid neck
Symptoms & Signs
Ipsilateral arm Movement

Localized pain
in adduction worsens pain
High association Ribs

Pitfall Lung Shoulder
of other injury (most common)
Diagnosis Plain film OR CT scan
a b
X-ray
Immobilization
Treatment Orthopedic
uncomplicated swathe referral
Bottom center image (Reprinted from Cole PA, Hill BW. Scapula fractures. In: Sethi MK, editor. Orthopedic traumatology: an evidence-based approach. New York: Springer Science. 2014.
771
772 B. Desai
Shoulder Dislocations: Anterior
Shoulder Anterior Posterior

Inferior Luxatio erecta
dislocations 99 % <1 %
Anterior Shoulder Subcoracoid

Subglenoid Subclavicular Intrathoracic
dislocations (most common)
Anterior to Inferior & Between the
Medial to
glenoid &
anterior to coracoid below ribs & thoracic
inferior to
glenoid the clavicle cavity
coracoid
Indirect blow to Arm is abducted, extended

Mechanism
arm & externally rotated
Shoulder dislocation Humerus Clavicle
Glenoid
Scapula
Inferior dislocation
Normal Anterior Posterior
anatomy dislocation dislocation
Anterior d/l with

Hill-Sach’s Symptoms & Signs
deformity (bottom)
Arm in abduction & Resists abduction & Potential axillary

external rotation internal rotation nerve injury
Bottom left image (Reprinted from Missiroli C, Singh A. Emergencies of the biliary tract. In: Singh A, editor. Emergency radiology: Imaging of
acute pathologies. New York: Springer Science; 2013. p. 11–25. With permission from Springer Science + Business Media)
Diagnosis and Treatment: Anterior
Diagnosis Plain film AP Scapular Y views
Distinguishes b/w
Y view?
anterior & posterior
Associated bony Fx of anterior Bankart’s Compression fx Hill-sach’s

injuries? glenoid lip fracture of humeral head deformity
Predisposes to
recurrent
dislocations
Recurrent Vascular
Complications Bony injury Nerve injury Other
dislocation injury
Most common Rare Bankart lesion Axillary nerve Rotator cuff tear
Adhesive
Axillary artery Hill-Sach’slesion capsulitis
Avascular necrosis Greater
tuberosity fx
Continued pain
Pitfall Rotator cuff tear 2–4 weeks after Needs MRI
injury
774 B. Desai
Shoulder Dislocations: Posterior
Posterior shoulder Force that produces internal Fall/direct Electric

Due to OR Seizure OR
dislocations rotation & adduction blow shock
Commonly
Pitfall
missed
Symptoms & Signs
Prominent Inability to externally rotate

posterior shoulder Anterior flattening
or abduct the affected arm
Diagnosis Plain film AP Scapular Y views
Treatment
Closed reduction
uncomplicated
Neurovascular injuries are less

Complications Fractures
common than in anterior dislocations
Shoulder Dislocations: Inferior
Inferior shoulder Hyperabduction Tearing inferior Pushing humeral

Luxatio erecta Due to
dislocation force capsule head inferiorly
Symptoms & Signs
Humerus is Arm raised with Arm held near

Elbow is flexed Ecchymosis
fully abducted hand above head chest wall
Orthopedic
Treatment Closed reduction RICE Analgesics
referral
Proximal Rotator cuff Severe soft Inability to

Complications
humerus fx injuries tissue injury reduce
All patients will
Will need surgery
have this
Rotator Cuff Injuries
Rotator Cuff Typically 40–50 Tear of SITS Partial tear is

Due to
Injuries years of age muscles more common
SITS Muscles Supraspinatus Infraspinatus Teres Minor Subscapularis
Symptoms & Signs
Muscle Decreased Decreased Arm held near

Atrophy
weakness abduction external rotation chest wall
Muscles of Rotator Cuff

MRI may be Subscapularis Supraspinatus Infraspinatus
Diagnosis Clinical
needed
Most common
Supraspinatus
muscle injury?
Front view Back view

Teres minor
776 B. Desai
Thoracic Outlet Syndrome (TOS)
Brachial plexus
Thoracic Outlet Compression As they pass through Associated with
Due to Subclavian artery
Syndrome of: the thoracic outlet a cervical rib
Subclavian vein
Symptoms & Signs
Pain in upper
Weakness Numbness Paresthesias Neck pain Cool extremity
extremity
Most common? Neurologic
Most serious? Arterial Least common
Elevated arm Hands above Open & close hands

Diagnosis
stress test head for 3 minutes
Paresthesias & Pt unable to

Positive test
Claudication complete test
Test for arterial Palpate both radial pulses while

Adson’s test
TOS head turned to each side
Loss of pulse? Positive test

Nontraumatic Hip Disorders
Legg-Calve-Perthes Disease
PEDIATRICS
Legg-Calve- Occur in boys Idiopathic avascular necrosis May be Typically

Due to
Perthes Disease aged 4–8 of the femoral head bilateral self-limited
Symptoms & Signs
Pain may Pain worsened by Decreased

Hip pain Limp
radiate to groin internal hip rotation ROM of hip
MRI may be Bone scan is Labs may be

needed diagnostic normal
Imaging
Orthopedic
Treatment Pain control
referral
Left center image (Reprinted from Abdelgawad A, Naga O. The hip. In: Abdelgawad A, Naga O, editors. Pediatric orthopedics: a handbook for
primary care physicians. New York: Springer; 2014. p. 85–116. With permission from Springer Science + Business Media)
778 B. Desai
Slipped Capital Femoral Epiphysis
PEDIATRICS
Slipped Capital Occur in obese May be Typically self-

Unknown cause
Femoral Epiphysis boys aged 10–16 bilateral limited
Slipped Capital Most common cause of hip

Femoral Epiphysis disability in adolescents
Symptoms & Signs
Pain may Pain worsened by Decreased

Hip pain Limp
radiate to groin internal hip rotation ROM of hip
“Melting ice
Diagnosis Plain film Frog leg view
cream cone”
Mild Moderate Severe

0–1/3 1/3–2/3 2/3–complete
Change in apposition, AP projection
Imaging
Mild Moderate Severe

0–30° 30°–60° 60°–90°
Slip angle, true lateral projection
No weight
Treatment ORIF
bearing
Right center image (Reprinted from Abdelgawad A, Naga O. The hip. In: Abdelgawad A, Naga O, editors. Pediatric orthopedics: a handbook
for primary care physicians. New York: Springer; 2014. p. 85–116. With permission from Springer Science + Business Media)
Septic Arthritis
PEDIATRICS
Most common Usually from

Occur in all age cause of painful
Hip & knee most
Septic arthritis hematogenous
ranges hip in infants common spread
H. N. Gram
Organisms Salmonella S. aureus Strep spp
influenza gonorrhoeae negatives
Most
Sickle cell common
Adolescents
Symptoms & Signs May be subtle!
Refusal to Decreased
Pseudoparalysis Fever Localizing signs Erythema Hip tenderness
ambulate ROM of hip
Infants Older children
Frequently May see widening Fat lines may be

Plain films
nondiagnostic early of joint spaces displaced
May see joint

Ultrasound
effusion
May see elevated

Diagnosis Arthrocentesis Labs
WBC & CRP
Joint drainage by
orthopedics
Septic Arthritis Tidbits
Septic arthritis Hematogenous

Direct extension
mechanisms spread
Staphylococcus Group B
Newborn causes Neisseria Enterobacter
aureus Streptococcus
Staphylococcus Streptococcus Streptococcus Hemophilus Other Gram

Children
aureus pyogenes pneumoniae influenzae (-) bacilli
Young sexually Staphylococcus

Streptococcus Neisseria
active adults aureus
Staphylococcus aureus
Direct extension
most common
Sickle cell
Salmonella
disease
Early Late
Joint prosthesis
Staphylococcus Gram (-)’s
Involves axial
IV Drug Users Pseudomonas
skeleton
780 B. Desai
Toxic Synovitis
PEDIATRICS
Most common cause of Fever may be

Toxic Synovitis Cause unknown
painful hip in children < 10 present
Toxic Synovitis
Post trauma Viral illness Allergic reaction
Associations
Symptoms & Signs
Inability to bear Decreased

Limp Hip pain Hip tenderness
weight ROM of hip
Frequently
Plain films
nondiagnostic
Exclude septic May see elevated

Diagnosis Arthrocentesis
arthritis ESR on lab work
Treatment NSAIDs Supportive care

The Femur
Femoral Shaft Fracture
Femoral Shaft Occur in High energy

Due to MVC Falls
Fracture younger patients trauma
Fx types due to Transverse Oblique or spiral

OR OR Comminuted
direct trauma (most common) oblique fx
Primary bone Osteogenic Breast, lung,

Pathologic fx Due to OR Metastases
tumors sarcoma prostate
Symptoms & Signs
Shortening of Inability to bear

Leg deformity Leg swelling Severe pain
leg weight
Fracture types
Imaging
Oblique Comminuted Spiral Compound
Traction splint & Not for open fracture Potential for These need
Treatment But… OR
Ortho consult with contaminated ends sciatic injury ORIF!
Neurovascular Post traumatic

Complications Fat emboli Hemorrhage
injury arthritis
782 B. Desai
The Knee
The Knee Tidbits
Tests for ACL More sensitive

tears Lachman test OR Pivot Shift test OR Anterior Drawer
for ACL tears
Positive > 5 mm displacement

Lachman? compared to opposite knee
Hemarthrosis of Most likely an “Pop” with swelling

knee? within hours? ACL injury
ACL tear
Posterior Typically do not Posterior drawer

cruciate injury? occur alone! test
Imaging for
Typically show MRI may be
ligamentous OR Will be normal
injury? joint effusion needed
Avulsion fracture
at lateral tibial ACL rupture
condyle?
Tests for Apley

meninscal injuries McMurray test
compression test
Treatment for Knee Early ROM &

ligamental & RICE NSAIDs
meninscal injury immobilizers ambulation
Medial collateral Medial Significant

Terrible triad ACL tear Due to
ligament tear meninscus injury lateral force
Ottawa Knee Rules
Age > 55
Tenderness at
head of fibula
Ottawa Knee
Inability to Rules
transfer weight
Radiograph if 1
for 4 steps criterion is met
immediately after
Rules are valid in
injury & in the ED Isolated
children as well
tenderness of
patella
Inability to flex
knee to 90º
Patellar Fractures
Patellar Typically a Transverse fx More likely to Associated with extensor

Due to
Fractures direct blow most common be displaced mechanism disruption
Symptoms & Signs
Local patella
Knee swelling Knee effusion Ecchymosis
tenderness
X-ray
Treatment Knee Orthopedic

RICE Analgesics
non-displaced Immobilizer referral
Surgical Displacement Severe Rupture of extensor

OR Open fracture OR OR
treatment? > 3mm comminution mechanism
Left center image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute
pathologies. New York: Springer Science; 2013. p. 277–98. With permission from Springer Science + Business Media)
Center image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute pathol-
ogies. New York: Springer Science; 2013. p. 277–98. With permission from Springer Science + Business Media)
784 B. Desai
Patellar Dislocation
Patella More common Twisting injury to Displaced May tear medial

Due to
dislocation in women an extended knee laterally joint capsule
May recur
Symptoms & Signs
Laterally
Knee pain
displaced patella
Confirm with
Diagnosis Clinical
imaging
Hyperextension Sliding patella in

Treatment Reduction Hip flexion
of knee place
Knee Partial weight Progress to full Isometric quadriceps

Post-reduction
immobilizer bearing weight bearing exercises
Tibial Plateau Fractures
Tibial plateau Axial load with rotational e.g., MVC In older Lateral is more
Due to force driving femoral
fractures condyle into tibia Fall from height population common
Lateral plateau ACL & MCL Medial plateau PCL & LCL
Associations
fx injuries fx injuries
Symptoms & Signs
Knee pain Knee swelling Knee effusion Limited ROM
CT may be
needed
X-ray
Treatment ORIF
Neurovascular Deep peroneal

Complications nerve injury DVT Arthritis
injury
Popliteal artery Occurs with

lateral fractures
Test 1st dorsal
web space!
786 B. Desai
Knee Dislocation
Often Will be unstable in

Severe ligamental Anterior is most
Knee Dislocation spontaneously multiple
disruption common
reduce directions
Symptoms & Signs
Loss of distal
Knee pain Unstable knee Knee deformity Late
pulses
Popliteal artery Peroneal nerve Ligamental

Complications Meninscal injury
injury injury injury
Arteriogram Evaluate for popliteal

Diagnosis Clinical Plain films
(or CT Angio) artery injury
X-ray
Immediate
Treatment
reduction
No pulse after Emergent vascular Return of pulse Emergent ankle- Vascular surgery
reduction? surgery consultation after reduction? brachial index consult
Delay of reduction High rate of

Pitfall
6-8 hours amputation
Tendon Rupture: Quadriceps and Patella
Forceful contraction Fall onto flexed

Tendon Rupture Due to OR
of quadriceps knee
Past Hx steroid Quadriceps

Patella rupture < 40 OR ORinjections > 40
tendinitis tendon rupture
Symptoms & Signs
Inability to extend a flexed

Pain Diffuse swelling
knee against resistance
Diagnosis Patella High riding

tendon rupture Plain film
patella
Surgical repair of
Treatment
involved tendon
788
Osteochondritis Dissecans
Osteochrondritis Unknown Subchondral Found in Typically unilateral &

Dissecans etiology fracture adolescents affects medial condyle
Symptoms & Signs
Knee pain Knee swelling
Diagnosis Plain film May be negative
a b
X-ray
Treatment Activity
Analgesics
Open Epiphysis modification & PT
Treatment Detached
Arthroscopy
Closed Epiphysis fragments
Locked joint due

Complications
to loose bodies
Left center image (Reprinted from Abdelgawad A, Naga O. The knee/leg. In: Abdelgawad A, Naga O, editors. Pediatric orthopedics: a handbook for primary care physicians. New York:
Springer; 2014. p. 117–56. With permission from Springer Science + Business Media)
B. Desai
Osgood-Schlatter Disease
Osgood- Patella tendon Males Repeated normal Microavulsions
Schlatter Disease apophysitis 10–15 Due to stress or overuse of ossification centers
May be bilateral
Symptoms & Signs
Chronic anterior knee Swelling over the Tender patellar Activity aggravates Erythema over
pain, intermittent tibial tubercle tendon the pain site
Soft tissue Prominence of

Diagnosis Plain film swelling tibial tuberosity But… May be normal
X-ray
Avoidance of
Treatment Self limited NSAIDs Rest knee extension
Left center image (Reprinted from Abdelgawad A, Naga O. The knee/leg. In: Abdelgawad A, Naga O, editors. Pediatric orthopedics: a handbook for primary care physicians. New York:
Springer; 2014. p. 117–56. With permission from Springer Science + Business Media)
789
790 B. Desai
Baker’s Cyst
Inflammation of May mimic

Baker’s Cyst
gastrocnemius bursa thrombophlebitis
Symptoms & Signs
Tender at
Painful knee Painful calf Swollen knee Swollen calf
popliteal fossa
Diagnosis Ultrasound
Baker’s
cyst
Back view of leg muscles

Imaging
Normal knee
joint fluid
Baker’s
cyst
Side view of knee joint
Treatment RICE Analgesics

The Leg
Tibial Shaft Fractures
Tibial Shaft Tibia is most commonly Often result in Due to Minimal

Fractures fractured long bone open fx subcutaneous tissue
Fracture type Transverse Direct blow Spiral Rotational force
Symptoms & Signs
Painful leg Swollen leg Bone

protrusion
Diagnosis Plain films Imaging
Treatment Analgesics Splinting Orthopedic

Closed consultation
Treatment Analgesics IV antibiotics ORIF

Open
Complication Compartment
syndrome
Toddler’s Twisting of foot Dx via imaging Splint entire leg NOT child abuse
Fracture with a planted leg
Left center image (Reprinted from Lichte P, Pape H-C. Tibial shaft fractures. In: Oestern HJ, Trentz O, Uranues S, editors. Bone and joint injuries: trauma surgery III. Heidelberg: Springer Verlag;
2014. p. 341–46. With permission from Springer Verlag)
791
792 B. Desai
Compartment Syndrome
Compartment Increased pressure within a space compromises

syndrome the circulation & overall function within the space
Symptoms & Signs
Pain Pulselessness
Pallor Paresthesias Poikilothermia Paralysis
earliest Sx (Late)
Compartment Normal Compartment

Diagnosis Clinical !
pressures (adjunct) < 10 mm Hg syndrome > 30 mm Hg
Compartment pressures
Surgery?
40–50 mm Hg
Irreversible damage
Pitfall
in 4–6 hours!
Remove Place limb at the

dressings or cast level of the heart
No success? Fasciotomy
Causes of Compartment Syndrome
Fractures
Distal radius
Tibial shaft
Most common
Bleeding
Crush injury
disorders
Causes of
Compartment
Syndrome
Prolonged
compression
Bleeding -
hematoma Tight casts
High pressure
Infection
injection injury
Pilon (Tibial Plafond) Fracture
Crushing of High or low energy High Low

Pilon fx Due to
distal tibia mechanism MVC Sporting injury
Significant soft Extensive

High energy
tissue damage comminution of bone
Minimal soft Less comminution of

Low energy
tissue damage bone
Diagnosis Plain film CT
Compartment Vertebral body

Associations Especially L1
syndrome fractures
X-ray
Surgical
Treatment
treatment
Bottom center image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute pathologies. New York: Springer Science; 2013.
793

794 B. Desai
Fibula Fracture
External rotation Medial malleolus or Interosseous Proximal

Maisonneuve fx Due to
of the foot deltoid ligament injury membrane tear fibula fx
Any medial ankle swelling Maisonneuve fx until

& pain after trauma proven otherwise!
Treatment Eventual Surgery Treatment
May be missed
Pitfall
on plain film
Midshaft fibula Associated with Isolated injury

fx tibia fx can occur
Knee Elastic bandage

Intact tibia? OR
immobilizer for distal fx
Right center image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute
Achilles Tendon Rupture
Largest & strongest Typical pt is a Sudden eccentric force

Achilles Tendon
tendon in the body middle aged man applied to a dorsiflexed foot
Risk factors Prior Quinolone

Older age Prior steroid use
use
Symptoms & Signs
Feel/hear a Inability to Noticeable defect 2–6 cm Unable to

Sudden pain Calf swelling
“pop” palpate tendon proximal to calcaneus stand on toes
Failure of foot to plantar

Radiographs Consider MRI or
Diagnosis Thompson test flex when calf if
unnecessary US
squeezed
US is operator
dependent
Foot slightly Orthopedic
Treatment Short leg cast
plantar flexed referral
Gastrocnemius Rupture
Gastrocnemius Same Medial head is most

Rupture “Push off”
mechanism commonly injured
Thompson test Foot does plantar flex

Diagnosis Achilles is intact Consider MRI
is negative when calf if squeezed
Foot slightly Orthopedic

Treatment Short leg cast
plantar flexed referral
The Ankle
Ankle Sprains
Most common Inversion injury with

Ankle Sprains Due to
to lateral ankle ankle plantar flexed
Evaluate for
Isolated Associated Tear of
Medial Injury? Eversion OR Maissoneuve
injury is rare with fibular fx syndesmosis
fx!
Anterior Posterior
Ankle ligaments Calcaneofibular
talofibular Talofibular
Symptoms & Signs
Inability to
Ankle pain Ankle swelling Painful ROM Ecchymosis
ambulate
Ottawa ankle
Diagnosis Clinical
rules for imaging
Depends on
Treatment Stable RICE Analgesics
stability of ankle
Orthopedic
Unstable Splint
referral
Ottawa Ankle Rules
Point tenderness
over the navicular
bone
Tenderness along
Inability to bear Ottawa Ankle posterior edge of
weight Rules the distal 6 cm of
immediately after Radiograph if 1 either the lateral
injury & in the ED criterion is met or medial
malleolus
Point tenderness
over the proximal
base of the 5th
metatarsal
796
Ankle Dislocations
Anterior Lateral
Ankle Can occur in
May be open!
dislocations 4 planes
Posterior (m.c.) Upwards
Posterior Rupture of Lateral malleolus

OR
associated with talofibular ligaments fx
Symptoms & Signs
May have signs of

Deformity Severe pain Ecchymosis
vascular compromise
Unless vascular Emergent reduction is

Diagnosis Plain film 1st
compromise present indicated
X-ray
Orthopedic IV antibiotics
Treatment Reduction Immobilization Analgesics
consult if open
Neurovascular Avascular Conversion from

Complications
compromise necrosis closed to open
Left center image (Reprinted from Ríos-Luna A, Villanueva-Martínez, M, Fahandezh-Saddi H, Pereiro J, Martín-García A. Isolated dislocation of the ankle: two cases and review of the literature.
Eur J Orthop Surg Traumatol. 2007;17(4):403–7. With permission from Springer Verlag)
B. Desai
The Foot
Calcaneal Fractures
Calcaneus Require a large Associated injuries

Due to Fall from height
Fractures compressive force are common
Associated Injury to other Injury to other GU & renal

Lumbosacral fx
injuries extremities calcaneus injuries
Symptoms & Signs
Tender
Foot pain Foot swelling Ecchymosis Low back pain
hindfoot
Plain film Bohler’s angle may be Normal 20-40 CT may be

Diagnosis
lateral view reduced with fx degrees needed
Imaging &
Boehler’s angle
20˚-40˚
Bohler’s angle
Orthopedic
Treatment Immobilization Posterior splint Analgesics
referral
Right center image (Reprinted from García-Rey E. Complex fractures of the calcaneus. In: Rodríguez-Merchán EC, Rubio-Suarez JC, editors.
Complex fractures of the limbs. Zug: Springer International Publishing; 2014. p. 95–9. With permission from Springer International Publishing)
798
Lisfranc Injuries
2nd metatarsal
Occurs at the tarsal- Range from sprains to MVC
Lisfranc Injuries needed for
metatarsal joint fracture-dislocations Football injury
midfoot stability
Common
mechanisms
Symptoms & Signs
Pain on passive Inability to

Foot pain flexion of foot walk
Plain film 1 mm displacement b/w the Unstable CT is study of

Diagnosis ( ± Stress views) bases of the 1st & 2nd metatarsal injury! choice
X-ray

Non-displaced with splint RICE Analgesics referral
Treatment of
Displaced fx Unstable fx ORIF
Compartment
Complications syndrome
Left center image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute pathologies. New York: Springer Science; 2013.
B. Desai
Metatarsal Fractures
5th Metatarsal Styloid fx proximal Diaphyseal

3 forms Jones Fracture
Fracture to the joint stress fractures
Has high
Transverse fx at Common in athletes Treatment is
Jones Fracture incidence of
proximal diaphysis that run & jump ORIF
nonunion
Dancer’s Avulsion fx of 5th Near attachment Treatment is

Inversion injury
Fracture metatarsal base of peroneus brevis cast shoe
Jones fracture
Imaging Pseudo-jones/
tennis fracture
Stress fracture
Jones fracture
Avulsion fracture
Other metatarsal Displacement > 10 degree

OR ORIF
fx tidbits 3–4 mm angulation
Stress fx of 2nd Repeated

March fracture
metatarsal pushing off
Tarsal Tunnel Syndrome
Tarsal Tunnel Entrapment Posterior tibial Motor to foot Sensory to

Syndrome neuropathy nerve muscles bottom of foot
Nighttime foot Has a Tinel’s sign as

Associations
pain well for aid in diagnosis
Treatment Analgesia Walking boot
Complication Claw toe

800 B. Desai
Osteomyelitis
Fungus Results in bone Direct spread – 80 %

Osteomyelitis Bone infection Due to change &
Bacteria destruction Hematogenous – 20 %
Long bones most

Hematogenous More common Hematogenous Spine most
commonly
spread in children affected spread in adults commonly
Most common
Staph aureus
agent?
Symptoms & Signs
Pain at the site Warmth Erythema Swelling
Plain film is Later shows bone Periosteal

Imaging Late lytic lesions
normal early demineralization elevation
Preferred
imaging? MRI
Laboratory ESR Often elevated Blood cultures
Treatment
IV Abx Admission
Acutely ill
Bottom right image (Reprinted from Abdelgawad A, Naga O. Musculoskeletal infections. In: Abdelgawad A, Naga O, editors. Pediatric
orthopedics: a handbook for primary care physicians. New York: Springer; 2014. p. 561–84. With permission from Springer Science + Business
Media)
Risk Factors and Likely Agents for Osteomyelitis
Neonates Children
Grp B Strep Staph + MRSA
Staph + MRSA
Postoperative Elderly
Staph aureus Staph + MRSA
Coagulase (-) Gram (-)’s
staph
Risk Factors &
Likely Agents for Human bite
Osteomyelitis
Sickle cell disease Staph is most Streptococci
Salmonella has a common overall Anaerobes
higher incidence Eikenella
Foot puncture
Animal bite
wound
Pasteurella Pseudomonas
Diabetes + vascular
IV Drug user
insufficiency
Staph + MRSA Staph aureus
Pseudomonas Strep agalactiae
Strep pyogenes
Anaerobes
Thoracic and Lumbar Pain
Back Pain Tidbits

A common problem 2nd only to URI’s Common cause of Most common
Back pain which typically resolves cause of disability
for MD visits work disability
spontaneously < 50
Fractures &
Considerations Tumor or Consider Consider Congenital & other
other
< 18 & > 50 infection > 50 < 18 bony abnormalities
processes
History & Search for red

Back pain thorough exam flags
is paramount
Major risk factor Major risk factor

Trauma? for fx IV drug use for infection
Fevers, chills,
Constitutional Rheumatologic
sweats, weight Infection OR Malignancy OR
complaints? process
loss
Achy pain that worsens with Radicular back pain in the distribution
Benign back pain movement & is palliated by rest Sciatica of a lumbar or sacral nerve root
Pain worsened by Bilateral sciatic pain Relived with rest

Disk herniation? cough, valsalva or Spinal stenosis worsened with walking & forward flexion
prolonged sitting & extension
Hx of urinary Check post void Concern for

incontinence? residual > 100 mL cauda equina
Straight leg raise 70–80 % sensitive for Crossed straight Radicular pain down Specific for
test L4-L5 or L5-S1 leg raise test affected leg when other herniated disk
herniated disk leg raised
802 B. Desai
Red Flags
HIV positive
Chronic infections IV Drug Abuse
Hx of cancer “Red Flags” Unexplained

weight loss
Pain unrelieved with
Cancer
rest
Other immune
Fever
disorders
Prolonged
Night time pain
duration of pain
Back Pain Workup
Back pain Failure to improve Elderly with

Red flags OR Trauma OR OR
imaging? after 4–6 weeks back pain
Definitive Best for tumors Fractures, vertebral

MRI CT
modality & infections bodies, facets
Unnecessary
Laboratories
unless red flags
Lumbar Strain/Nonspecific Back pain
Mild-moderate Aggravated by Mechanism may

Lumbar Strain Palliated by rest
pain movement be lifting or turning
Diagnosis Clinical
Treatment Analgesia Early movement
Disk Herniation
No diagnostic No diagnostic
Diagnosis Clinical
tests required tests required
Treatment for no Conservative

Follow up
red flags? treatment
Spinal Stenosis
More common Narrowing of May have facet Ligamentum

Spinal Stenosis Due to
in elderly lumbar canal hypertrophy flavum thickening
May have Other physical findings

Spinal Stenosis
associated sciatica may be absent
Symptoms & Signs
Low back pain worsened with Pain relieved with rest Low back & lower extremity
standing & extension of spine & forward flexion pain with walking
Neurogenic
claudication
Diagnosis CT OR MRI
Analgesia,
Treatment Leg exercises Physical therapy Epidural steroids
NSAIDs
Ankylosing Spondylitis
Ankylosing Autoimmune Affects spine & Associated with May be Trauma

Spondylitis arthritis pelvis HLA-B27 & infection
Ankylosing
Spondylitis Pts < 40 Males 3:1
Symptoms & Signs
Waking with low back pain &

stiffness that improves with activity Malaise Fatigue
Diagnosis Thorough Hx Imaging Sacroilitis “Bamboo spine”
Referral to
Treatment NSAIDs rheumatology
804 B. Desai
Cauda Equina Syndrome
Cauda Equina Surgical Difficult to

Syndrome emergency diagnose early
Symptoms & Signs
Perianal ± Urinary Overflow Fecal Sciatica in one

Back pain Leg weakness
anesthesia retention incontinence incontinence or both legs
Most common
finding
Probable cauda Urinary retention Fecal

Bilateral sciatica
equina > 500 mL incontinence
Diagnosis MRI
Treatment Dexamethasone
consultation
For tumor
Causes of Cauda Equina
Spinal canal
hemorrhage
Massive midline Spinal epidural

disk herniation abscess
Causes of cauda
equina
Tumors of the Other spinal

epidural space canal infections
Tumors of the
spine
Transverse Myelitis
Transverse Inflammatory Involves complete transverse Causes T>L>C

Myelitis disorder section of the cord demyelination Spine
Viral infection MS Spinal infarction

Schistosomiasis Lyme Disease
Triggers Differential
MS & Lupus Post vaccination
Cord
Cancer Malignancy
compression
Symptoms & Signs
Neck or back Bilateral motor, sensory & Urinary & fecal Urinary & Fecal Sciatica in one
Leg weakness Fever
pain autonomic dysfunction retention incontinence or both legs
Neurologic Depends on level Rapidly progressive

deficit of involvement over hours to days
Elevated protein & Normal in

Diagnosis MRI
lymphocytes in CSF 40 %
Steroids Plasma
Treatment
(Unclear benefit) exchange
From complete Improvement maximal

Prognosis varies
recovery to death at 3–6 months
Spinal Infections
Vertebral Disk space Irregular vertebral Bony

Imaging
osteomyelitis narrowing end plates destruction
Diagnosis Imaging Elevated ESR
90 % with severe Wakens them at No change with

Diskitis
back pain night rest
May have 90 % have

Diskitis Fever in 70 %
neurologic deficits elevated ESR
Epidural abscess Neurologic

Severe back pain Fever All 3 in < 15 %
triad deficits
Imaging may be
Diagnosis Elevated ESR
normal
Treat for Neurosurgical

Staph aureus evaluation
806 B. Desai
Diskitis
L-spine most Acute onset more common

Diskitis Often insidious onset
common in children
Immune
Risk Factors Spinal surgery OR OR IV drug use
compromise
S. aureus
Most common
Fungal Pseudomonas
Pathogens
TB Klebsiella
Proteus
Symptoms & Signs
± Radicular
Fever Localized pain
symptoms
Imaging Elevated ESR & Blood cultures

Diagnosis
MRI best CRP may be (+)
Broad spectrum antibiotics Neurosurgery

Treatment
including Vancomycin consultation
Spinal Epidural Abscess
Spinal epidural Typically a result of Often involves multiple

T/L >> C spine
abscess hematogenous spread adjacent vertebral segments
S. aureus
Most common
Fungal Pseudomonas
Pathogens
Streptococcus
TB
spp
E. coli
Symptoms & Signs
Fever common - Radicular symptoms

Back pain
not always present late finding
Imaging Elevated ESR & Blood cultures

Diagnosis
MRI best CRP may be (+)
Surgical CT guided Broad spectrum antibiotics

Treatment OR
decompression drainage including Vancomycin
808 B. Desai
Risk Factors for Epidural Abscess
IV drug use
Chronic renal
Cancer
failure
Indwelling
catheter or Risk Factors for
device Diabetes mellitus
Epidural Abscess
Pacemaker
Immune Recent spinal

compromise surgery
Recent spine fx Alcohol abuse
Rheumatologic Emergencies
Joint Fluid Analysis
Non-
Normal Inflammatory Septic
Inflammatory
Translucent to
Clarity Transparent Transparent Opaque
opaque
Yellow to
Color Clear Yellow tinged Yellow tinged
green
WBC
< 200 200–2000 2,000–50,000 >50,000
(per mm3)
PMN’s (%) < 25 < 25 ≥ 50 ≥ 75
Culture Negative Negative Negative Often positive
None or
Crystals None None None
multiple
Gout, pseudogout,
Conditions Osteoarthritis Staph, GC
Lupus
Joint Fluid Tidbits
Testing includes Cell count Gram stain Culture Crystals
Most important Distinguishes between inflammatory,

Cell count
test non-inflammatory & septic conditions
Other Glucose may be low in Septic

Protein Glucose
considerations arthritis & Rheumatoid arthritis
Gout and Pseudogout
Precipitation of Overproduction of uric acid Decreased renal

Gout Due to OR
uric acid crystals due to multiple causes excretion
Precipitation of calcium Associated with

Pseudogout May be idiopathic OR
pyrophosphate crystals hypercalcemia
Needle shaped
Gout Non-specific imaging
crystals
Rhomboid
Pseudogout Chondrocalcinosis
shaped crystals
Radiographic densities in cartilage due to

Chondrocalcinosis
deposition of calcium pyrophosphate crystals
Steroids for
Treatment NSAID’s
severe cases
Rheumatoid Arthritis
Rheumatoid Increased Labs show elevated

Joint edema
arthritis flare arthralgias CRP & ESR
Treatment NSAID’s Steroids
Rheumatoid Have cervical Especially at Beware even minor trauma

arthritis pitfalls instability C1–C2 in this group of patients
Treatment with
Predispose to serious
disease modifying
bacterial infections
agents
Rheumatoid
Tidbit Felty syndrome Neutropenia Enlarged spleen
arthritis
810 B. Desai
Antiphospholipid Syndrome
Antiphospholipid Autoimmune Not Primary process is arterial

Syndrome syndrome inflammatory! & venous thrombosis
Cerebral infarction
Severe = multi Myocardial infarction

organ failure
Ischemia of
placenta with Selected syndromes
Retinal ischemia
fetal loss
due to thrombosis
Multiple
miscarriages
Pulmonary
Low platelets embolism
Life long
Treatment
anticoagulation
Systemic Lupus Erythematosus (SLE) Tidbits
Affects females Many are African- Waxing-waning

SLE 16–55 years old American pattern is typical
Typical
symptoms Fever Rash Joint pain
Symptoms & Signs May have multiple Sx at the same time
Rheumatologic Arthralgias Myalgias Tenosynovitis
Constitutional Fatigue Fever Anorexia Malaise
Persistent Possible
Renal Lupus nephritis chronic failure
proteinuria
Classic butterfly Scaly red plaques on

Skin Discoid lupus
facial rash face, head, & neck
Pleural Pulmonary
Pulmonary Pneumonitis Pleurisy effusions infarcts PE
Most common Pericardial

Cardiac Pericarditis MI ACS risk factor Myocarditis effusions
cardiac presentation
Intestinal
GI Ulcerations vasculitis
Chronic
Neurologic Stroke Seizures Neuropathy
migraines
Hematologic Low platelets Anemia Thrombosis Due to antiphospholipid

syndrome
Treatment Steroids
Trauma
Henry Young II and Bobby Desai
Contents
Introduction 814
Spinal Injuries 826
Spinal Cord Injuries 830
Penetrating Neck Injury 835
Chest Trauma 838
Abdominal Trauma 847
Pelvis and Hip Trauma 852
Extremity Injuries 856
Trauma in Special Populations 858
H. Young II, MD
Department of Emergency Medicine, UF Health at the University
of Florida, Gainesville, FL, USA

B. Desai, B.R. Allen (eds.), Nailing the Written Emergency Medicine Board Examination ,
DOI 10.1007/978-3-319-30838-8_15
814 H. Young II and B. Desai
Introduction
Most common Systemic approach Provide
Establishment of
Trauma cause of death created to decrease multidisciplinary
morbidity & mortality trauma centers care
<45
Vary state to Trauma center

Trauma systems
state designations fall to states
24/7 availability of surgical Injury prevention

Level 1 trauma Trauma research 24/7
subspecialists, including & education
center? Neurosurgery presence programs Hemodialysis
Basis of trauma Anatomy &

Mechanism
triage? Physiology
Not at trauma Expeditious Transfer to trauma

center? evaluation center after stabilization
Primary Survey
Quickly identify and treat Should be performed

Primary Survey
life threatening injuries on all trauma patients
Rapid Diagnostic Ultimate

Survey algorithm Primary Secondary
resuscitation testing triage
“ABCDE” Airway Breathing Circulation Disability Exposure
Airway
obstruction
Cardiac Massive
tamponade hemorrhage
Life threatening
injuries
Open
Flail chest pneumothorax
Tension
pneumothorax
Trauma 815
Airway Assessment
Airway Evaluate for FB & Obstruction to

Assess patency pooling of Assess gag reflex
assessment secretions airway
Ex: facial fractures
Tongue most
common cause of
obstruction
C-spine Concomitant with Always assume

stabilization? airway control! C-spine injury!
Consider Consider
Airway NOT Remove Perform jaw Suction
placement of endotracheal
patent? obstruction thrust airway
OPA intubation
Avoid head tilt- Avoid NPA in
disrupts C-spine setting of facial OPA
stabilization! trauma Oropharyngeal airway
Avoid NPA for NPA
concern of basilar Nasopharyngeal airway
skull fracture
Protect Optimize Condition with high likelihood GCS < 8 or

Severe
Intubation? airway oxygenation of progression that could severe
patency or ventilation compromise airway agitation hypotension
Burns/CNS injury See pg. 10
Intubation Rapid sequence intubation

technique with C-spine stabilization
Unable to
Surgical airway
intubate?
Contraindications
Basilar skull Maxillofacial
to nasotracheal Apnea
intubations fracture trauma
Breathing Assessment
Assess for Sucking chest Paradoxical chest Assess Intubation

Inspection
deviated trachea wound wall motion success
Tension Place occlusive Reposition ETT if
Flail chest
pneumothorax dressing needed
Needle thoracostomy
then chest tube
Palpate Crepitus Pneumothorax Treat!
Pneumothorax Inappropriate
Symmetrical If decreased
Auscultate ETT placement
breath sounds? consider
Hemothorax Displacement
Obstruction
Pneumothorax
Tube in Esophagus
O2 via Needle thoracostomy Presence of

Treatment
nonrebreather for all then chest tube Hemopneumothorax?
Tension If > 1500 mL initially =
pneumothorax thoracotomy
If > 200 mL/hr x 4 hrs=
Pneumothorax thoracotomy
Circulation Assessment
Circulation Level of Peripheral Blood Assessment

Skin color
assessment consciousness pulses pressure of Shock
Carotid pulse = BP>60 mm Hg Femur = 1000 mL

Normal blood 5 L or 7 % of body Significant blood
Femoral pulse = BP>70 mm Hg
volume? weight loss from fx Pelvic = 1000–2000 mL
Radial pulse = BP > 80 mm Hg
Blood loss Pulse pressure Decreased Blood loss

Decreased BP
> 15 %? narrows capillary refill > 30 %?
Infusion of warm External

Initial treatment 2 large bore IV Direct pressure
crystalloid bleeding?
Unable to obtain Intraosseous vs

IV? central access
Hypotensive 3 mL fluid = O negative Later = type

Consider blood Blood?
after 2L fluid? 1 mL blood initially specific
O positive
Typically PRBC but in males
Blood
whole blood can
replacement
be used
Transfusing large quantities of PRBC in the absence

Massive Give PRBC, Platelets,
>10 units of other blood components may create a dilutional
transfusion & FFP in 1:1:1 ratio coagulopathy and hypovolemia
1 blood volume
Muffled heart tones
Consideration of Significant
Pericardial Beck’s triad Hypotension Pericardiocentesis hemorrhage may
tamponade? not be noted in
JVD
young healthy
Hypotension adults!
FAST exam
without a source?
Trauma 817
Classification of Hemorrhage
Blood loss Cardiovascular Neurologic Skin Renal
HR normal or
Warm, pink,
< 15 % slightly Normal or
Class I normal Normal output
< 750 ml increased; BP slightly anxious
capillary refill
normal
irritable, Cool, mottling, Oliguria,

15–30 % Tachycardia,
Class II confused, delayed increased spec.
750-1500ml BP normal
combative capillary refill gravity
Significant
tachycardia, Cool, mottling,
Lethargic,
30–40 % thready pulse, pallor, Oliguria,
Class III diminished
1500-2000ml hypotension, prolonged elevated BUN
metabolic pain response
capillary refill
acidosis
Severe
tachycardia & Cold
>40 % Lethargic,
Class IV hypotension, extremities, Anuria
>2000ml coma
thready central pallor, cyanosis
pulse
Disability Assessment
Disability Pupil size & Movement & strength Check of blood

Mental status
assessment reactivity of extremities glucose
GCS
AVPU (see below)
Low GCS Increased morbidity Consider airway

(< 8) & mortality protection
Alert - Patient is Verbal - Patient responds Pain - Patient responds Unresponsive or

AVPU
awake and alert to verbal stimuli only to painful stimuli only Unarousable
Intoxicated Not a cause of AMS until

patient? head injury evaluated!
Patient with Consider early Identifies those who could benefit

altered mental
status? Head CT from early neurosurgical intervention
GCS
Eye opening Best verbal Best motor

4-Spontaneous 5-Oriented/converses 6-Obeys
3-Verbal command 4-Disoriented/converses 5-Localizes pain
2-Pain 3-Inappropriate words 4-Withdraw to stim
1-No response 2-Incomprehensible 3-Abn ext/decert
1-No response 2-Abn ext/decer
1-No response
Center bottom image (Reprinted from Allen B, Ganti L, Desai B. Trauma and ATLS. In: Allen B, Ganti L, Desai B, editors. Quick hits in emergency
medicine. New York: Springer Science; 2013. p. 37–45. With permission from Springer Science + Business Media)
Exposure
Maintenance
Complete Midline back Prevent
Exposure Log roll of spinal
exposure of pt precautions palpation hypothermia!
For step offs Warm blankets
Other areas to Back for lesions,

Perineum Gluteal cleft
examine? wounds, etc
Trauma 819
Secondary Survey
Head to toe Identify as
Secondary Consultations
examination of many injuries AMPLE Hx FAST exam
Survey patient as possible as needed
Allergies PMH
AMPLE Hx Events of injury
Medications Time of Last meal
AMPLE Mechanism Blood loss at Damage at Tetanus

Pregnancy?
considerations of injury scene scene status
Secondary BMP + Glucose Type & Urine drug

EtOH Pregnancy
Survey Labs + CBC screen screen
Secondary Extremities as
CXR Pelvis
Survey Imaging needed
Multi-system Consider CT’s of chest,

trauma? abdomen/pelvis
Traumatic Arrest and ED Thoracotomy
Absolute Penetrating Cardiac activity

Signs of life
indication chest trauma in ED
Pre-hospital or
ED
Palpable pulse
Pupil Organized Purposeful Respiratory
Signs of life or blood OR OR OR OR
pressure reactivity cardiac rhythm movement effort
Liberal Abdominal Cardiac Requiring cross clamping Blunt chest trauma with
OR
indications trauma activity of aorta to get to OR loss of vital signs in ED
Return of
spontaneous Operating room
circulation?
Must open Avoids phrenic Inadvertent cross

Pitfalls?
pericardium vertically nerve clamping of esophagus
Head Trauma Introduction
Head trauma Cranium is enclosed Intracranial pressure Brain Blood

CSF
tidbits & has a fixed volume determined by parenchyma flow
Normal = 10–15 mm Hg
Monroe-Kellie Expansion of one Reduction in Baseline ICP will

OR
doctrine compartment volume of another increase
Late &
Sudden Respiratory
Cushing Reflex Due to Hypotension Bradycardia unreliable sign
increase in ICP irregularity of increased ICP
Head trauma Accounts for 50 % Higher risk of Males MVA/MCC Elderly falls
tidbits of trauma deaths head injury Ages 15–30 Assaults Alcoholics
Sudden acceleration
Mechanisms Direct trauma OR Indirectly
or deceleration
Cerebral blood flow changes

Auto-regulation of Affected by Cerebral perfusion Pressure gradient needed
& adapts to the needs of the
cerebral perfusion pH, PO2, pCO2 pressure to perfuse cerebral tissue
tissue
Often damaged in Alkalosis &
hypocarbia cause CPP = MAP - ICP
traumatic brain injury vasoconstriction MAP = Mean arterial pressure
Increased morbidity
ICP > 20 mm Hg?
& mortality
Headache Nausea
Scalp laceration May bleed enough to
in children? cause shock state! Hypertension Vomiting
Signs of increased
ICP
Serious head Evaluate for cervical
Bradycardia Seizure
injury? spine fracture!
Agonal
respirations Lethargy
Trauma 821
Brain Herniation
Due to increased
Brain herniation
ICP
Brain herniation Uncal Central Upward

Cerebellotonsilar
syndromes transtentorial transtentorial Posterior Fossa
Most common
Uncus of the temporal lobe Occasionally opposite

Fixed & dilated Contralateral
Uncal herniation herniates inferiorly through corticospinal tract is
pupil motor paralysis compressed
the tentorium
Due to mass effect from Compression of Compression of
edema or hemorrhage parasympathetic Ipsilateral hemiplegia
cerebral peduncle
fibers of 3rd Compression of
cranial nerve
ipsilateral
Brainstem
Coma corticospinal tract
compression?
Bilateral pinpoint Bilateral Conjugate

Pinpoint pupils Pinpoint pupils Flaccid paralysis
pupils Babinski’s sign downward gaze
Cerebellotonsillar
Central
transtenorial Upward herniation
herniation transtentorial Cerebellar tonsils
herniation herniate thru the
Earliest sign is
CN 6 palsy foramen magnum
Increased muscle Absence of vertical

Sudden death Respiratory arrest
tone eye movements
Treatment of Elevated ICP
Elevate head of Increase CSF outflow

Elevated ICP?
bed to 30º from skull base
Maintain PCO2 O2 saturation Mechanically Maintenance of

Elevated ICP?
at 35–40 mm Hg > 95 % ventilated? appropriate sedation
Agitation increases
ICP
Avoid Decreases
Elevated ICP?
hypotension cerebral perfusion
Prevention of Beware in
Other treatment Mannitol
seizures hypotension!
Seizures Osmotic agent

increase ICP than can lower ICP
30 min. onset,
lasts 6 hours
1 g/kg
Recommended for brief periods in

Hyperventilation?
the event of impending herniation
Consider invasive
GCS < 8 Intubation
monitoring
Traumatic Seizures
Immediate &
Seizure? Non focal exam No treatment
brief?
High risk of Depressed skull Penetrating injury Focal

GCS< 10
seizures? fracture to cranium examination
Treatment Phenytoin OR Levetiracetam
Can occur within Increased with bleeds

Delayed seizures
the 1st year & skull fractures
Mild Traumatic Brain Injury (TBI)

Impairment in brain Based on clinical assessment of
Traumatic Brain Temporary or Uses GCS
function as a result of patients level of consciousness not
Injury permanent system
mechanical force the actual underlying injury to brain
80 % of head 15 % of pts with GCS 15 will < 1 % will need

Mild TBI GCS 14–15
injuries have lesion on Head CT neurosurgical intervention
Symptoms & Signs
Asymptomatic Headache Confusion Amnesia Brief LOC Nausea Vomiting
Large subgaleal Focal neurological

swelling deficit
Drug/alcohol Focal neurologic

Higher risk of findings Coagulopathy Vomiting
intoxication significant injury
with mild TBI Non contrast head
Skull fracture Coagulopathy CT in patients with
GCS < 15 Severe headache
mild TBI and no LOC
Age > 60 Signs of basilar Age > 65

skull fx
Dangerous
mechanism
Ejection after MVC
Pedestrian struck
Positive CT scan? by motor vehicle
consultation
Fall from height >3
feet or 5 stairs
Moderate and Severe TBI

Accounts for 10 % 40 % have 8 % of these require May
GCS
Moderate TBI of patients with abnormal CT neurosurgical deteriorate
9–13
head trauma scan intervention to severe TBI
Accounts for 10 %
GCS 4 % of severe TBI
Severe TBI of patients with Mortality = 40 %
<9 have cervical injury
head trauma
Trauma 823
Cerebral Contusions
Most common Associated with

Cerebral Contre-coup Contusions opposite
Frontal, Temporal, Subarachnoid
Contusions Occipital lobes hemorrhages injury to site of trauma
Intracerebral Can occur days after Patient on Increased risk of Admission for
hemorrhage in at sites of resolving
contusions? contusions anticoagulants? delayed bleeding monitoring
Concussion
Transient alteration in mental Lack of focal No sports until

Concussion LOC?
status after head injury neurologic findings re-evaluated
Second Impact Syndrome
Second Impact Irreversible brain injury after 2nd Speculated to be due to

Syndrome head injury after a concussion disordered autoregulation
Postconcussive Syndrome
Post concussive Physical, emotional & Can persist 1 month-

After TBI
syndrome cognitive symptoms > 1 year after injury
Post concussive Physical exam & HA common in Prognosis is

headache imaging are normal - children excellent
Symptoms & Signs
Decreased Memory Sleep

Headache Dizziness Irritability Depression
concentration problems disturbances
Visual Judgment
Anxiety Vertigo
disturbances problems
Basilar Skull Fracture
Basilar Skull Most commonly occur within

Fracture petrous portion of temporal bone
Symptoms & Signs
Facial Loss of smell or

CSF leak Hemotympanum Raccoon eyes Battle sign Diplopia
weakness hearing
CSF otorrhea Periorbital Retoauricular
ecchymosis ecchymosis
CSF rhinorrhea
Takes hours to
May develop develop & may
meningitis not be present
Consider upon initial
evaluation
prophylactic Abx
Basilar Skull CT is often

Fracture negative
Air-fluid levels in Air in posterior

CT findings
sphenoid sinus fossa
Ring of clear fluid beyond

Other test Ring test for CSF
blood tinged fluid
CSF is glucose
positive
Skull Fracture
CT scan to Skull X-rays

Skull Fracture?
characterize limited value
Depressed Skull If greater than full Due to increased likelihood

Surgical repair
Fracture? thickness of skull of direct brain compression
Open Skull Antibiotics

Fracture? indicated
Trauma 825
Intracranial Hemorrhage
Subarachnoid Due to disruption of parenchyma Most common CT abnormality

hemorrhage & subarachnoid vessels with moderate-severe TBI
Symptoms & Signs
Meningeal
Headache Photophobia
signs
Blood within Due to Disruption of Arterial bleed

Epidural Emergent
space b/w temporal skull middle meningeal causes rapid
hematoma fracture artery expansion surgery
dura & skull
Biconcave bleed
CT scan
(lens shaped)
Symptoms & Signs
Dilated
Immediate LOC Lucid interval Skull fracture
ipsilateral pupil
Due to rapid Increased risk Due to cerebral

Subdural Disruption of
acceleration & Alcoholics atrophy & greater
hematoma bridging veins deceleration Elderly shear forces
Symptoms & Signs
Meningeal Decreased May have lucid

OR LOC
signs mental status interval
CT scan Crescent shaped
Acute Sub-Acute Chronic

Subdural
< 24 hours 1 day-2 weeks >2 weeks
hematoma Isodense on CT Dark on CT
White on CT
Pediatric Head Trauma
PEDIATRICS
Differences in
More waxing & More non-surgical
pediatric head Weaker skull
trauma waning of GCS lesions
Non-surgical Concussion Diffuse cerebral Diffuse axonal

Brain contusions
lesions syndrome edema shear
Diffuse cerebral
hyperemia
Increased risk for Fractures much Especially in

Children < 2 Due to Thinner skull
serious head injuries easier parietal area
Scalp Possible fracture 90 % of fractures Especially in parietal

hematoma? present have hematomas & temporal areas
Spinal Injuries
Spinal Injury Introduction

Cervical spine is 90 % of spinal cord 10 % C-spine fractures
C5/6 most
Spinal Injury most commonly injuries related to associated with
injured common in adults another spinal fracture
MVC
Region in C-spine most commonly C5/6 most common

Spinal Injury
associated with fx is C5 subluxation in adults
Denis 3 column Spine divided Used to assess stability

principle into 3 columns of spine following injury
Anterior wall of Anterior longitudinal

Anterior column Anterior annulus
vertebral body ligament
Posterior wall of Posterior

Middle column
vertebral body annulus fibrosis
Bony complex of the Posterior

Posterior column
posterior vertebral arch ligamentous complex
Ligamentous injury can cause unstable

Unstable spinal Spinal injury within thorax or lumbar Can use MRI or flexion
injuries that are not always associated
injury region disrupting 2 or more columns with fractures extension films for Dx
Unstable
> 25 % of 3rd to 7th > 50 % in T or L
compression
injuries cervical vertebrae vertebrae (acute)
Trauma 827
Cervical Spine Clearance
Imaging for Not always Clinical criteria Canadian C-

NEXUS
Cervical clearance needed that can be used spine rule
Apply to those that are To those pts who

Canadian C-
Better sensitivity Better specificity unlikely to have significant are awake and
spine rule cervical injury alert
No posterior
midline tenderness
No focal neurologic
No intoxication
deficits NEXUS criteria 99 % sensitive
Failure to meet any
Normal level of 1 = need for No distracting
consciousness imaging injury
Low risk by Thorough Full exam of C- Active ROM of

either criteria? neurologic exam spine C-spine
Altered mental
Distracting injury OR Intoxication OR NO clearance!
status
Cervical Spine Evaluation
PEDIATRICS
Anatomy Anterior Posterior

Spinolaminar Spinous process
(4 lines) longitudinal longitudinal
Important Peds < 5 mm Prevertebral 6 mm at C2

measurements on Predental space
plain films Adults < 3 mm space 22 mm at C6
AP, Lateral, & Must see ALL 7

Imaging tidbits X-rays = 3 views Top of T1
Odontoid vertebrae on film
20 % C-spine
injuries occur at
Plain films miss Negative plain films
Imaging tidbits C7
15 % of injuries do not rule out injury!
Plain film
CT
inadequate?
CT instead of High risk Those receiving Suspected head

Age > 65
plain film? mechanism CT of other areas trauma or AMS
Pseudosubluxation
Common below Typically occurs 2–3 mm anterior

Pseudosubluxation Pediatric C-spine
8 years of age C2 on C3 misalignment
Normal alignment of
Pseudosubluxation
the spinolaminar line
Stable Cervical Fractures
Type of Fracture Mechanism Tidbits
May be unstable if loss of

Wedge Fracture Flexion
>50 % of vertebral height
Flexion against contracted Most common at C7

Clay Shoveler’s Fracture
posterior muscles Can occur at C6 & T1
Transverse Process Fracture Flexion
Disruption of posterior ligament

complex
Unilateral Facet Flexion & Rotation “Bow-Tie” deformity on lateral X-Ray
Is potentially unstable
Becomes unstable if fracture

Burst Fracture Vertical compression fragments enter spinal canal
Isolated fractures of articular

Vertical compression
pillar & vertebral body
Stable when isolated

Posterior Neural Arch of C1 Hyperextension
Arch may be congenitally absent
Unstable Cervical Fractures
Jefferson Bit Off A Hangman’s Thumb
C1 Burst Fracture Axial load with vertical Lateral masses of C1 are

(Jefferson Fracture) compression (Diving injury) displaced outward
High incidence of spinal cord

Bilateral facet dislocation Flexion injuries
May see > 5mm subluxation
Odontoid Type II or III Flexion or Extension See next page
Atlantoaxial
Atlantoaxial or Atlanto-occipital Atlantoaxial or Atlanto-occipital C1/2 disruption
(or Any Fx/dislocation) = Flexion or extension Rheumatoid arthritis or ankylosing
spondylitis
Bilateral Fx of pedicles of C2 with

Hangman’s Fracture Extension forward movement of C2 on C3
Flexion? = extreme flexion with complete

ligamentous disruption
Extension? = Hyperextension; Associated
Teardrop fractures Flexion or Extension with central cord syndrome; anterior
longitudinal ligament avulses inferior part
of vertebral body
Trauma 829
Odontoid Fractures
Atlanto-dens interval
Odontoid Increase in Most common cervical
3 types 5 mm in pediatrics
Fractures prevertebral space fracture in children 3 mm in adults
Avulsion at tip of
Type 1 Stable
dens
At the junction of
Type 2 Most common Unstable
odontoid & body of C2
Fracture at base
Type 3 Unstable
of dens
Thoracolumbar Fractures
Not injured as
Increased Higher incidence Narrower spinal
Thoracic spine frequently as C Due to But… Due to
or L spine rigidity of cord injury canal
Part of vertebra located between

Minor Transverse Spinous process Pars the inferior & superior articular
thoracolumbar fx process fx fx Interarticularis processes of the facet joint
Wedge Compression
Fracture Flexion
Flexion with compression of

anterior elements and
Flexion-distraction Fracture
distraction of posterior
elements
Translational Fracture Shear
Horizontal fracture & is UNSTABLE due

Flexion around an anterior to disruption of posterior ligament
Chance Fracture Usually at L1 or L2
axis associated with lap belt Beware Bowel, Spleen & Liver injury!!
Ileus may occur
L1> L2> T12

Disruption of anterior & middle
Burst Fracture Vertical compression columns = Unstable fracture
Unstable if > 50 % loss of height
Consider calcitonin spray for Rx
Spinal Cord Injuries
Spinal Cord Syndromes
Incomplete lesions of the spinal cord
Central cord syndrome

Posterior
Anterior
Anterior cord syndrome

Posterior
Anterior
Brown-sequard syndrome
Posterior
Corticospinal
tract
Spinothalamic
tract Anterior
Trauma 831
Incomplete Spinal Cord Injury

Central cord
syndrome
Anterior Cord
SCIWORA syndrome
Incomplete Spinal
Cord Injury
Posterior cord Brown-Sequard

syndrome syndrome
Transverse cord
syndrome
Central Cord Syndrome
Central cord Hyperextension Buckling of the Compression of May occur in older

syndrome injury ligamentous flavum the central cord patients with DJD
Central cord Most common incomplete

syndrome spinal cord injury
Symptoms & Signs
May have loss of May have decreased

Weakness Sacral sparing
bladder control sensation
Arms > Legs Distal pain & Rectal tone is
Temperature present
Good
prognostic
sign
Anterior Cord Syndrome
Anterior cord Flexion or Vascular injury of the Injury due to retropulsion Disc herniation is
OR
syndrome extension anterior spinal artery of bony fragments common
Symptoms & Signs
Ipsilateral Loss of vibration & Contralateral loss of pain &

motor paralysis proprioception temperature sensation
Needs surgical
Treatment
intervention
Brown-Sequard Syndrome
Brown-Sequard Penetrating Hemisection of Classic crossed

Syndrome injury spinal cord findings
Stab wound to
the spine
Symptoms & Signs
Complete Preservation of vibration & Loss of pain &

motor paralysis proprioception temperature sensation
Below injury Below injury
Transverse Cord Syndrome
Transverse Cord Transverse

Rule of T’s OR Tumors OR Trauma
Syndrome myelitis
Symptoms & Signs
Complete loss of ALL

No sacral sparing
motor & sensation
Below injury
Trauma 833
Posterior Cord Syndrome
Posterior Cord Extension from

B12 deficiency OR OR Tertiary syphilis
Syndrome trauma
Symptoms & Signs
Loss of position &

vibration
Below injury
SCIWORA
PEDIATRICS
More flexible Injury can cause 2/3 spinal cord injury is

Pediatric spine
than adults SCIWORA SCIWORA in this population
Consider Pt with neurologic Absence of

SCIWORA symptoms radiographic evidence
Spinal Cord Injury Without Involves Most common Can be seen in

SCIWORA But…
Radiographic Abnormalities cervical cord in children any age group
Normal
Diagnosis Complete exam MRI
radiographs
Surgery may be Especially for

Treatment
beneficial for some disc herniation
Spinal Shock
Partial or complete Transient reflex depression of all Reflex function below the level of the
Spinal shock Causes
injury of spinal cord cord function below the injury injury spontaneously returns in 1–2 days
Symptoms & Signs
Flaccid Loss of bladder

Priapism
paralysis & bowel control
First reflex to Bulbocavernous Reflexive contraction of anal sphincter when

return? reflex glans penis is squeezed or foleyis pulled
Early return of Associated with

this reflex? better outcomes
Typical clinical Initial return of Hyperreflexia Hyperreflexia

course reflexes alone with spasticity
1–3 days 1 week – 1 month 1 month – 1 year
Loss of neurological function can cause an incomplete Not able to determine true
Pitfalls
spinal cord injury to mimic a complete one effect until resolution
Neurogenic Shock
Neurogenic Loss of sympathetic Unopposed Usually affects Evaluate for

Causes
Shock outflow parasympathetic effects T1 and above other causes
Unlikely below For Sx below
T4 this level
Symptoms & Signs
Flaccid Loss of Peripheral

Loss of reflexes Hypotension Bradycardia
paralysis autonomic tone vasodilation
Below lesion Skin is warm,
flushed & dry
Maintain a MAP Provides adequate perfusion to

Treatment IV crystalloids
of 85–90 mm Hg prevent secondary cold injury
BP not improving Positive inotropes Norepinephrine

with fluids? may be needed is preferred agent
Trauma 835
Penetrating Neck Injury
Penetrating Neck Injury Introduction
Houses major vessels, spinal Any of these can

Neck anatomy
cord, esophagus & airway be injured
Symptoms Associated with Neck Trauma
Subcutaneous
Stridor Dysphonia Hemoptysis Hematemesis Dyspnea
emphysema
Hard Signs Associated with Neck Trauma Associated with Significant injury
Active arterial Diminished Expanding Lateralizing Hemothorax>

Hypotension Thrill or bruit
bleed carotid pulse hematoma signs 1000mL
Air bubbling
Hemoptysis Hematemesis
from wound
Death from
Airway Extreme
penetrating neck Due to Intubate early CNS injury
injury compromise bleeding
Apply pressure to
active bleeds
Respiratory
distress
Expanding neck Airway
hematoma obstruction
Indications for Do tracheostomy
Pitfall Fractured larynx
intubation Massive instead
Altered mental subcutaneous May result in
status emphysema complete
transection or
Tracheal shift creation of false
lumen
Zones of the Neck
Zone 1 Clavicles Cricoid
Zone 1
Vertebral & Proximal Major thoracic Superior Lungs &

Thoracic duct Spinal cord Esophagus
carotid artery vessels mediastinum Trachea
Angiography/
Thoracic surgical
Treatment Stable? Esophagram or endoscopy/ Unstable?
Bronchoscopy approach
Angle of
Zone 2 Cricoid
mandible
Zone 2
Vertebral & carotid

Jugular veins Trachea Larynx Spinal cord Esophagus
artery
Angiograghy/ Unstable or Hard Surgical

Treatment Stable? Esophagram or endoscopy/
Bronchoscopy signs? exploration
Surgery also an option
Angle of
Zone 3 Base of skull
mandible
Zone 3
Vertebral & Distal

Pharynx Spinal cord
carotid artery
May require disarticulation

Treatment Stable? Angiograghy Unstable?
of mandible
Center image (Reprinted from Ustin J. Access to the neck in penetrat-

ing trauma. In: Velmahos GC, Degiannis E, Doll D, editors. Penetrating
trauma. Heidelberg: Springer Verlag; 2012. p. 37–45. With permission
from Springer Verlag)
Trauma 837
General Treatment of Penetrating Neck Trauma
Violation of the Emergent surgical Do not explore Any vascular injuries need NO blind
But…
platysma? consultation at bedside! proximal & distal control clamping!
Apply direct No blind

Active bleeding?
pressure clamping!
NO violation of Minor neck No signs of structural damage Careful D/C after 4-6 hours
the platysma? trauma to nerves or major vessels closure in ED of observation
CT scan of neck Plain radiographs

Diagnostic tools
+ chest of chest & C-spine
Pitfall? Air embolism May be fatal
Airway Classic machinery

Embolism murmur
Left lateral Prevents migration

Treatment Trendelenburg
decubitus position of air bubble
Pharynx Trauma
Larynx trauma
see ENT
Blunt or Same with

Pharynx Trauma
penetrating trauma esophageal trauma
Symptoms & Signs
Pneumomediastinal Retropharyngeal
Hematemesis Odynophagia SQ emphysema
air air
Cervical soft Consider Consider

Diagnosis esophageal
tissue plain films endoscopy imaging
If stable to leave
ED
Broad spectrum
Treatment NPO
antibiotics
Blunt Neck Trauma
Blunt neck trauma Car dashboard

Direct trauma Shear forces Seat belt
mechanisms Steering wheel
Injuries may be
Pitfall? Require imaging!
subtle
Carotid or
Dissection Pseudoaneurysm
vertebral injury
Hyperextension
Intraoral trauma Mechanisms of Hyperflexion

Pseudoaneurysm
formation
Basilar skull fx Direct trauma
CT scan of neck
Diagnostic tools
with contrast
CT angiogram
Chest Trauma
Chest Trauma Tidbits
25 % of trauma
Chest trauma
deaths
Hypotension due Pelvic fracture Abdominal Thoracic Consider other reasons other
to blunt trauma #1 reason injury injury than thoracic structures
Hypotension due
Lung
to penetrating Heart Great vessels
trauma
#1 reason
Trauma 839
Pneumomediastinum (PM)
Air within the Injury to air containing

PM No trauma? Ruptured alveoli
mediastinum structures in thoracic cavity
Air containing Major

Pharynx Larynx Trachea Esophagus
structures bronchi
Restraints with Mechanical Ruptured

Spontaneous? Valsalva Sneezing
combative pts ventilation bleb
Subcutaneous Crunching sound over

Signs Hamman’s sign
emphysema heart during systole
Contrast For evaluation of

Diagnosis CT scan OR Endoscopy
esophagram esophageal injury
Pneumothorax (PTX)
Accumulation of air
Pneumothorax
within pleural space
Symptoms & Signs
Ipsilateral decreased or Hyperresonance Subcutaneous

Chest pain Dyspnea
absent breath sounds to percussion emphysema
Subcutaneous PTX until proven Findings can be Repeat CXR if Sx

No PTX on CXR delayed by 4–6 hrs!
emphysema otherwise! persist
Diagnosis CXR Ultrasound CT
Expiratory
Ipsilateral low
Ipsilateral decreased Subcutaneous Decubitus CXR has higher
CXR findings lateral diaphragm
lung markings emphysema (Deep sulcus) sensitivity than upright CXR
As accurate as Supine US has higher negative

Ultrasound
CT predictive value than CXR
Pneumothorax Treatment
< 1 cm from Upper 1/3 of

Small PTX
chest wall chest
100 % O2 Accelerates rate of Decreases alveolar Repeat CXR in

Treatment
pleural air absorption pressure of nitrogen 4–6 hours
Consider needle decompression or chest Intubation & positive pressure can

All other
Chest tube tube placement prior to intubation if convert a simple PTX into a tension
traumatic PTX
needed PTX
Needle 2nd intercostal space

thoracostomy at midclavicular line
Failure of lung May be a large tear

2nd chest tube OR Bronchial injury
expansion? in lung parenchyma
No improvement
Surgical
with 2nd chest
tube? intervention
Air moves in and 3-sided Eventual chest

Open PTX Treatment
out of wound petrolatum gauze tube
Place at
different site
Dressing can create Remove dressing
Pitfall open PTX than wound on
a tension PTX! for increased SOB!
ipsilateral chest
Tension Pneumothorax
Accumulation of air within pleural Clinical

Tension PTX
space that is under pressure diagnosis!!
Symptoms & Signs
Ipsilateral decreased or Hyperresonance Contralateral Distended neck

Hypotension Dyspnea
absent breath sounds to percussion tracheal deviation veins
Decreased venous
Hypoxemia Cardiac arrest
return
Immediate needle Leave catheter Follow with a

Treatment
decompression in place chest tube
Waiting for a
Pitfall? May be fatal
CXR
Trauma 841
Hemothorax
25 % are
Accumulation of blood A hemthorax can hold 40% Intercostal
Hemothorax associated
within pleural space of circulating blood volume with PTX artery injury
Symptoms & Signs
Ipsilateral decreased or Dullness to

absent breath sounds percussion
Blunting of Greater than

Diagnosis Upright CXR
costophrenic angle 250 cc blood
Haziness may be seen Layers out on Large volumes

Supine CXR? But… Up to 1 L!
with > 100 cc blood supine film may be missed
Large bore chest Consider

Treatment 36–40 french
tube autotransfusion
> 1000 mL 150–200 mL blood

OR Thoracotomy
immediately per hour for 4 hours
Other
Persistent air
thoracotomy Unstable patient
indications leak
Rib Fractures
Most common chest Assume fx with localized 50 % are not

Rib fractures
injury in adults pain & pain on inspiration seen on CXR
Rib fracture Pulmonary

Vascular injuries PTX
associations contusion
High risk Underlying Multiple rib Consider

Elderly Smokers
patients lung disease fractures admission
Multiple rib
Increased risk Liver, kidney, spleen Higher incidence Aspiration
fracture
considerations for other injuries potential injury of fat emboli pneumonitis
Lower ribs
Pain control & Allow pt to maintain Prevents atelectasis Consider intercostal

Treatment lung volumes
incentive spirometry & pneumonia nerve blocks
1st & 2nd Rib Have increased incidence Greater

Due to Greater force
fractures of occult injury mortality
1st & 2nd Rib Myocardial Consider

fracture Bronchial tears Vascular injuries
contusion angiogram
associations
Flail Chest
Free floating segment of ribs not connected to thorax Sx more severe as pulmonary
Flail chest
with fx of 3 or more adjacent ribs in 2 or more places compliance worsens
Symptoms & Signs
Ipsilateral decreased Decreased Decreased venous

breath sounds ventilation return
Paradoxical chest wall

Diagnosis CXR CT scan of chest
motion on physical exam
Pain Chest Prevent fluid Intubation &

Treatment O2
control physiotherapy overload mechanical ventilation
Leads to
pulmonary
High risk for edema
Hypoxemia Due to Contused lung
ARDS
3 or more Severe head

associated injuries trauma
Negative inspiratory AMS

force < 25
Indications for
intubation Comorbid
RR > 30/min pulmonary disease
Fx of 8 or more
Age > 65
ribs
Sternal Fracture
Associated with
Sternal Fx
head on MVC
Sternal fx Blunt myocardial

Aortic injury
associations injury
Symptoms & Signs
Anterior point tenderness

Palpable deformity
over sternum
Diagnosis Lateral CXR
Adequate
Treatment
analgesia
Normal EKG at Normal EKG at 6

Disposition Normal VS Discharge
presentation hours
Otherwise admit
Trauma 843
Pulmonary Contusion
Pulmonary Direct damage Associated with

Leads to Hemorrhage Edema
contusion to lung flail chest
Fluid administration Development of edema in unaffected

Pitfall Secondary insult Due to
during resuscitation lung due to reflex shunting of blood
Beware aggressive
fluid resuscitation
Pulmonary Most common significant Elasticity of

Due to
contusion chest injury in children chest wall
Symptoms & Signs
Decreased compliance of Hemoptysis

Hypoxemia
lung (common)
CT is more
Diagnosis CXR OR CT
accurate
Opaque patches Patchy alveolar May be delayed

CXR findings OR
of lung infiltrates up to 6 hours
Respiratory Consider PEEP &

Treatment Analgesia Pulmonary toilet
support permissive hypercapnia
Consider If > 28 % of lung 1 lobe = 18 % total

intubation affected lung volume
Severe Decubitus Uninjured lung Enhances ventilation

contusion? position down & perfusion
Tracheobronchial Injuries
Tracheobronchial Associated with Typically occurs within High mortality

Due to Deceleration
Injuries shear forces 2cm of the carina with rupture
Continuous
Bronchopleural
bubbling in
chest tube? fistula
Symptoms & Signs
Hamman’s Subcutaneous
Chest pain Dyspnea Hypoxemia Hemoptysis
crunch emphysema
CT is more
Diagnosis CXR CT
accurate
CXR findings PTX OR Pneumomediastinum Rib fractures
Treatment Oxygenation Ventilation Chest tube

Cardiac Trauma
Most commonly due Right ventricle greatest risk of

Cardiac trauma
to penetrating trauma injury due to anterior location
Location between nipples, Penetrating trauma here causes

Cardiac box
sternal notch & xiphoid potential cardiac damage
Cardiac Tamponade
Cardiac Most commonly due Fluid within pericardial cavity resulting in elevation of intra-
Tamponade to penetrating trauma pericardial pressure that decreases ventricular filling pressures
As little as 65 ml can increase intra-pericardial pressures
Muffled heart All 3 rarely

Beck’s Triad JVD Hypotension
sounds present
Symptoms & Signs
Sinus Narrow pulse Elevated central Pulsus Low voltage Electrical Enlarged cardiac
tachycardia pressure venous pressure paradoxus QRS alternans silhouette
Lower systolic
Alternating
pressure with
inspiration QRS direction
Diagnosis Echocardiogram
Removal of 5–10 mL fluid may

Treatment Pericardiocentesis Thoracotomy
increase stroke volume by 50 %
Trauma 845
Cardiac Contusion
Cardiac Blunt myocardial 20 % MVC deaths

contusion injury due to this
Direct precordial Deceleration or Causes tear in heart

Mechanisms Blast injury
impact torsion at point of fixation
Right atrium
Symptoms & Signs
Vena cava
Chest pain Tachycardia Arrhythmia
Wall rupture Valve injuries Contusion Septal rupture

Injuries
90 % die at scene Aortic most common RV most common
Coronary artery thrombosis Coronary artery laceration Pericardial injury
No definitive Troponin 4–6 Consider

Diagnosis EKG Monitoring
screening tests hrs post injury echocardiogram
Wall motion
O2 to maintain IVF & pressors defects
Treatment PaO2 >80 (Hypotensive pts)
Post-trauma Ventricular
Complications VSD Valve defects Tamponade
pericarditis aneurysm
2nd most common Sudden death due Caused by impact to chest wall 10-30
Commotio cordis cause of death in to blunt trauma to milliseconds before T wave that induces
young athletes chest ventricular fibrillation
Associated with baseball, Football – Direct

Commotio cordis blow to sternum
hockey, & lacrosse
Traumatic Aortic Injury (TAI)
Deceleration
Traumatic Aortic 90 % with blunt trauma 50 % of the rest die High speed side
Mechanism impact
Injury (TAI) & TAI die at scene within 24 hours
Penetrating trauma
Most common Proximal Survivors who Have tear at

region injured descending aorta reach ED ligamentum arteriosum
Symptoms & Signs
Unequal BP in Intrascapular bruits Retrosternal Pulse difference

Dysphagia Dyspnea Stridor
extremities or murmurs chest pain b/w UE & LE
Elevated BP in Harsh systolic
UE, Decreased in murmur
LE
Transesophageal
Diagnosis CXR CT – angio scan
echo
Maintain systolic Heart rate of 60

Treatment Avoid Valsalva Surgery
BP < 120 mm Hg bpm
CXR Findings Suggestive of Aortic Injury

Esophageal
deviation
Widened Loss of distinct

mediastinum aortic knob
Width > 8 cm on
supine AP film
Sensitivity =
50–92 %
Specificity = CXR Findings Widening of right
10 % Suggestive of paratracheal stripe
Aortic Injury
Displacement of
left mainstem
bronchus 40º Loss of paraspinal
below horizontal stripe
Loss of pleural
apical cap
10 % of initial CXR’s are

normal!
Diaphragmatic Injury
Diaphragmatic Usually penetrating Chest or upper Usually left Right side is missed
Injury trauma abdomen posterolateral more often due to liver
Difficult to Leads to delay in Small injuries will

Pitfall
diagnose diagnosis continue to enlarge
Symptoms & Signs
Appearance of Bowel sounds in

Dyspnea Orthopnea Chest pain
scaphoid abdomen thorax
Diagnosis CXR CT MRI
Abdominal viscera
CXR findings Hemothorax
within thorax
Treatment Surgery
Trauma 847
Abdominal Trauma
Abdominal Trauma Introduction

Serial exams are
Abdominal 15–20 % of all Approximately 2/3 Single PE is not
critical in awake, alert
Trauma trauma deaths blunt & 1/3 penetrating sensitive for Dx pts
In penetrating trauma, external

Bruising & “Seat belt Increased likelihood
Inspection exam may underestimate
distention sign” of abdominal injuries
internal damage
Mesenteric Tears of hollow Diaphragm

Seat belt injuries Chance fracture
laceration viscus rupture
Distention may not be apparent until

Palpation
loss of 50–60 % of blood volume
>35 % of blunt trauma pts with Pts with solid organ injury Especially in younger pts &
Pitfalls initial benign exam are later found may present with minimal Sx those with head injury or
to have a significant injury & nonspecific findings distracting injuries
Deceleration May produce duodenal Causes

Duodenum Retroperitoneal
injury hematoma or duodenal rupture obstruction
Retroperitoneal May have delayed FAST & DPL cannot

Difficult to Dx
injuries presentation of Sx adequately assess
Penetrating Lower chest, flank, Abdominal injury until

trauma pelvis wounds proven otherwise
CT & plain films for

Gun shot Direct trauma & Transabdominal Surgical
evaluation of trajectory &
wounds Blast effect injuries GSW? intervention
Penetrating Abdominal Trauma
May not penetrate No positive Conservative

Stab wounds
the peritoneum findings? management
Indications for Evisceration Gross blood via Unstable +

GSW Impalement
laparatomy of organs OG or rectal positive FAST
Abdominal Signs
Kehr’s
Left shoulder
referred pain
Due to splenic
injury or
diaphragmatic
irritation
Grey -Turner’s Cullen’s

Flank Periumbilical
discoloration ecchymosis
Retroperitoneal Ectopic
hematoma Abdominal Signs pregnancy
May be seen in
hemorrhagic Hemorrhagic
pancreatitis pancreatitis
Rovsing’s
RLQ pain due to
LLQ palpation
Appendicitis
Abdominal Trauma Imaging
Routine plain films

Imaging
not indicated
Solid organs Pancreas

CT Sensitive Retroperitoneum Insensitive Hollow organ
Bony structures Diaphragm
Intra-peritoneal May be done during

FAST Evaluation Hemothorax Hemopericardium
fluid primary survey
Positive PPV > 90 % for significant Negative Cannot rule 1/3 of pts with blunt trauma
FAST intra-abdominal injury FAST out injury & (–) FAST require laparatomy
Consider
Blunt trauma Positive FAST Hypotension
laparatomy
Cannot assess Cannot assess Difficult in obese Cannot tell blood

FAST Pitfalls
hollow viscus retroperitoneum patients from other fluids
CT indications High concern for

Stable patient Positive FAST OR Negative FAST
after FAST injury
Diagnostic Open or closed Pelvic fracture & Open technique

peritoneal lavage technique doing a DPL? above umbilicus
Diagnostic Positive 10 mL of frank blood > 100,000 RBC/mL Bile, feces or

OR OR
peritoneal lavage test on initial draw in lavage fluid urine obtained
10,000 RBC/mL
Diagnostic Replaced by FAST penetrating trauma
NOT 1st line
peritoneal lavage & CT scanning
Trauma 849
Spleen and Liver Trauma
Solid organ injury Spleen most Also consider with Solid organ injury Liver most
with blunt trauma commonly injured left lower rib injuries penetrating trauma common
Symptoms & Signs
LUQ pain Kehr’s sign R shoulder pain RUQ pain Shock

Spleen Spleen Liver Liver For both
Diagnosis CT
Depending on extent of injury may

Treatment
consider non-operative management
After Appropriate Risk of encapsulated Neisseria

Due to S.pneumoniae
splenectomy vaccinations organism sepsis meningitidis
Pancreas/Stomach/Duodenum/Intestine Trauma
Commonly injured Deceleration Steering wheel Bicycle

Pancreas
in blunt trauma injury injury handlebar
Also duodenum
Retroperitoneal
Pain May be delayed Due to
location
Diagnosis CT
Depends on
Treatment
extent of injury
Stomach & Commonly injured in Duodenal injury

Duodenum penetrating trauma associated with liver injury
Commonly injured in May have multiple Sx may be Associated with

Small intestine
penetrating trauma locations of injury delayed lumbar spine injuries
Typically transverse
Large intestine Due to Location
colon injured
Diagnosis of
hollow viscus May be difficult
injuries
Penetrating Flank and Buttock Injuries
Penetrating Flank Consider rectal Look for gross Bowel injury until
Blood on exam?
& Buttock Injuries exam blood & rectal tone proven otherwise
GSW to flank
entering Laparatomy
peritoneum?
Hemodynamically Triage based on

Wound to flank
stable? CT results
Surgical Antibiotics for anaerobic

Unstable pt?
consultation & Gram (–) coverage
No CT evidence Observation for

Stable pt
of injury 6 hours
Diagnosis CT U/A CBC Type & screen
Possible bowel CT with oral &

injury? rectal contrast
Kidney Injuries
Flank bruising
Present in 10 % of pts
Kidney injuries Higher risk with Lower rib fx
with abdominal trauma
Hematuria
Penetrating
Mechanism Compression Deceleration
trauma
Gross Renal injury until

hematuria? proven otherwise!
Absence of ANY Does NOT exclude

hematuria? renal injury!
Pt with renal 80 % will have

Skeletal OR Visceral
injury? other injuries
Gross Suspicion for Deceleration Multiple Imaging

Blunt trauma
hematuria renal trauma injuries trauma (CT)
Penetrating Imaging Suspicion of renal

trauma to flank or Hematuria Angiogram
abdomen (CT) vascular injury?
Contrast Early Ongoing

Type of CT?
enhanced CT extravasation hemorrhage
Delayed CT CT done 10 minutes Extravasation from Genitourinary

scan? after contrast kidney, ureter or bladder injury
Renal vascular Associated with May not have Must revascularize

Pitfall
injury multiple trauma hematuria within 12 hours
Trauma 851
Genitourinary Injuries: Bladder and Ureter Injury
Direct blow to Penetrating Associated with

Bladder injury OR
distended bladder trauma pelvic fx
Symptoms & Signs
Lower Scrotal Inability to

Gross hematuria
abdominal pain ecchymosis urinate
Retrograde
Diagnosis
cystogram
Contrast into Intraperitoneal Contrast into Extraperitoneal

Surgery Foley
peritoneum bladder rupture retroperitoneum bladder rupture
Extraperitoneal
Most common?
bladder rupture
Penetrating
Ureteral injury Due to
trauma
Diagnosis Contrasted CT
Genitourinary Injuries: Urethral Injury
Perineum Look for gross Vaginal

Inspection Genitals Speculum exam
Gluteal folds blood bleeding?
Abnormal
Consider position of
Boggy Blood at Perineal Scrotal
Urethral trauma prostate prostate meatus ecchymosis hematoma
Anterior urethral Iatrogenic

Due to Fracture of penis Straddle injuries
injury (foreign body) Dysuria
Hematuria
Posterior Deceleration
Due to Pelvic fracture MVC
urethral injury (Fall from height)
Retrograde No Foley until

Diagnosis
urethrogram this is done!
May need
Treatment Primary repair
suprapubic catheter
Complications
Fistula Strictures CBC
Anterior Injury
Complications
Incontinence Impotence
Posterior injury
Genitourinary Injuries: Testicular Injury
Most common in blunt

Testicular injury
or straddle injury
Symptoms & Signs
Scrotal
Hematuria Scrotal pain Scrotal edema
ecchymosis
Diagnosis Ultrasound Nuclear scan
Complications Infertility Abscess Hydrocele
Pelvis and Hip Trauma
Introduction
Requires Associated with Mortality of all

Pelvis Trauma 5%
significant force multiple trauma pelvic fx
Pedestrian vs
Mechanisms MVC Fall from height
MVC
Iliac vessels
Pelvic fx Significant Neurologic Close proximity to
Due to Lumbar plexus
associations hemorrhage injury major vessels & nerves
Sacral plexus
Diagnosis Radiographs CT scan
Young-Burgees
Classification
Based on Can predict likelihood
System mechanism of severe hemorrhage
Avulsion &
Three Types Major ring fx Acetabular fx
Single bone fx
Symptoms & Signs
Tenderness to Pelvis instability with lateral Pelvis instability with posterior

Destot’s sign Earle’s sign
palpation of pelvis compression of iliac crests compression at pubic symphysis
Hematomas Ability to
Perineal over scrotum palpate pelvic
lacerations or inguinal fracture line
ligament on rectal exam
Open fx
Trauma 853
Major Ring Fractures
Major Ring Lateral Anterior-Posterior Vertical shear

Fractures compression compression force
Lateral
Due to Horizontal force T-bone MVC OR Pedestrian vs car
compression fx
Lateral Transverse fracture Ipsilateral or contralateral Most common

Mortality = 13 %
compression fx of pubic rami to posterior injury major ring fx
Anterior-Posterior Symphyseal Longitudinal Associated with

Vertical fx
compression Fx diastasis rami fx Head on MVC
Vertical shear Symphyseal Vertical Associated with Associated with

OR
force fx diastasis displacement fall from height severe hemorrhage
Up to 75 %
May have combination of

Fractures!
Center bottom image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute
Acetabular and Avulsion/Single Bone Fx
Associated with knee Associated with

Acetabular Fx Displaced fx? Surgery
striking dashboard sciatic nerve injury
Avulsion/Single Associated with Forceful muscle Conservative

OR
Bone Fx falls contraction treatment
Center image (Reprinted from Zamora-Carrera E, Rubio-Suarez Springer International Publishing; 2014. p. 51–60. With permission
JC. Complex fractures of the acetabulum. In: Rodríguez-Merchán EC, from Springer International Publishing)
Rubio-Suarez JC, editors. Complex fractures of the limbs. Zug:
Pelvic Radiograph Tidbits
If one fx is Look for another Disruption of pubic SI joint

Pelvis is a ring OR OR
located fx! symphysis anteriorly posteriorly
Pelvic Oblique hemi

AP view Inlet view Outlet view
radiographs pelvis view
Most useful Will show the

AP view
view most pelvic fx
Oblique hemi Assesses

pelvis view acetabular fx
Assesses antero-
Inlet view
posterior displacement
Assesses superior-
Outlet view
inferior displacement
Extent of fx is underestimated
Pitfall
with plain films
Posterior arch
Superior to plain
CT of pelvis Assesses Hemorrhage
films
Acetabulum
Treatment of Pelvic Fractures
Minimize Surgical
Unstable pelvis? Displaced fx?
manipulation! evaluation
Open book Pubic symphysis Decreases pelvic Tamponades

OR Pelvic binder
pelvis fx widening volume bleeding vessels
Emergent
Unstable patient Positive FAST
laparatomy
Pt with significant Evaluate for

Angiography
bleeding? embolization
Transfusion of 4U
of PRBC in 24 hrs
Large pelvic Persistent

hematoma on CT hypovolemia
After treatment
Indications for
of other
Embolization?
bleeding sources
Transfusion of 6U Persistent
of PRBC in 48 hrs hypotension
Trauma 855
Complications of Pelvic Fractures
Retrograde Prior to Foley

Urethral injury Clinical suspicion
urethrogram catheter
Vaginal Associated with Bimanual exam for

Blood on exam? Speculum exam
laceration anterior pelvic fx females with pelvic fx
Other Nerve root

Rectal injuries May be delayed
complications injuries
Hip Dislocation Introduction
Hip Dislocations 3 types Anterior Central Posterior
Anterior hip
Anterior force Medial force Abducted leg
dislocation
Central hip Direct trauma

dislocation through acetabulum
Posterior hip Force directed posteriorly Most common Associated with

dislocation through a flexed knee hip dislocation acetabular fractures
Posterior hip Flexed knee strikes

Due to Head on MVC
dislocation dashboard
Patient’s Internally
Shortened ADducted
extremity? rotated
Plain
Diagnosis CT
radiographs
Adequate
analgesia
Complications
Avascular necrosis From prolonged
Posterior hip
dislocation of femoral head dislocation
Bottom right image (Reprinted from Kaewlai R, Singh A. Lower extremity trauma. In: Singh A, editor. Emergency radiology: imaging of acute
Extremity Injuries
Introduction
Assess for
Pulse presence Color of
neurovascular Warmth Capillary refill Sensation
injury & strength extremity
Hard signs of arterial injury Emergency surgical consult
Absent or Obvious arterial Expanding Pulsatile

Audible bruit Palpable thrill
diminished pulse bleeding hematoma hematoma
Coolness
Distal ischemia Pain Pallor Paresthesias
poikilothermia
Soft signs of arterial injury
Small stable Injury to anatomically Unexplained Hx of Proximity of injury to Complex

hematoma related nerve hypotension hemorrhage major vascular structures wound
Soft arterial Associated with true vascular Most do not require

injury signs injury only 35 % of the time surgical intervention
Ankle brachial May be normal in

Diagnosis Pseudoaneurysm OR Intimal flaps
index non-occlusive injuries
Can use to compare BP’s on

Assess presence of Injured SBP/Uninjured
Dopplers injured extremity proximal Arteriogram
nonpalpable pulses to injury to uninjured side SBP <0.9?
Direct No blind clamping Repair within Major venous

Treatment Repair!
pressure or tourniquets 6 hours injury?
Small arterial No active

Observe
injury bleeding
Trauma 857
Amputations
Amputated body Cleaned with Wrapped in saline Placed in closed Placed on ice which
parts sterile saline soaked gauze plastic bag extends viability
Amputated Re-implant
penis? within 6 hours
Amputated great Not

Reimplant Other toes?
toe? re-implanted
Fingertip
4 categories Zone 1 Zone 2 Zone 3 Zone 4
amputations
Distal Exposed
Amputation Amputation
amputation bone of
of entire near DIP
distal
Nail bed & nail bed joint
phalanx
bone intact
Local wound
Require reimplantation
care
by hand surgeon
Never leave Rongeur bone for

Pitfalls
bone exposed soft tissue coverage
Every effort should be made to re-

Pediatric pitfalls
attach thumb, index finger & digits
Trauma in Special Populations
Pediatric Trauma
Pediatric Trauma Tidbits
PEDIATRICS
Leading cause of Severely injured children should

Most morbidity Traumatic
Pediatric trauma death & disability be stabilized & transferred to
& mortality brain injury nearest trauma center
> 1 year
2nd most common cause Beware

Burns
of death < 5 years old inhalation injury!
Most sensitive &

Hypotension is a
earliest sign of Tachycardia late finding
volume loss?
Fluid 20 mL/kg isotonic No response Warm all fluids

10 mL/kg PRBC
resuscitation? crystalloid after 2 boluses? to 40 oC
C1–C4 most Cord injuries more

Pediatric C-spine Fx rare Due to Flexion injury
common < 8 common than fx
SCIWORA
Pediatric spleen Injury managed non-operatively

Thicker capsule more often than adults
& liver
Pediatric Acute pancreatitis most often Most common Handlebar Symptoms may be
pancreas caused by abdominal trauma mechanism? injury mild or delayed
Chest wall in More pliable Less likely to More likely to have pulmonary
Pediatrics than adults have rib fx & cardiac contusion!
Rib fx in Great force Consider child

Rare
Pediatrics applied abuse
GU trauma in Higher incidence Less peri- Relatively

Due to
pediatrics than adults adipose tissue enlarged kidneys
Trauma 859
Pediatric Trauma Airway and Breathing
PEDIATRICS
Pediatric airway & Pre-oxygenation Small cricothyroid

Enlarged occiput
breathing pitfalls is more difficult membrane
Difficulty in pre- Children have higher Smaller lung Smaller functional

Due to
oxygenation metabolic rates volumes residual capacity
Enlarged occiput Causes flexion of Padding may be needed under shoulders

pitfall? head when laid flat to maintain in-line stabilization
Cricothyroid Cricothyrotomy not Surgical airway Needle

membrane pitfall recommended < 10 years old of choice cricothyrotomy
Facial trauma & Infants < 6 Obligate nose Facial trauma + Potential
airway pitfall? months breathers nasopharynx bleeding respiratory distress
Upper airway Large Large Significant Upper airway Difficult to see

pitfall? tongues epiglottis redundant tissue obstruction vocal cords
Larynx & vocal Airway more Use Miller Better Displaces large
Lifts tongue
cord pitfall? anterior blade visualization tongue easier
Endotracheal Diameter of ETT Uncuffed Narrowest part of Over-inflation of cuff may

Due to
tube > 1 = (16+age)/4 < 8 years airway is cricoid lead to laryngeal injury
Depth of
insertion of ETT 3 x tube size
Unable to Transtracheal jet Temporizing Allows

But… Poor ventilation
intubate? ventilation measure oxygenation
Indications for Transfer to Pediatric Trauma Center
PEDIATRICS
Ejection from
vehicle
Fall from height

MVC with death
Mechanism of
of another injury
vehicle occupant Prolonged
extrication
Multiple severe
trauma
Severe head
> 3 long bone fractures
trauma
Penetrating head,
Severe facial
Anatomic injury chest, or
trauma
abdominal trauma
Amputations Spinal cord injury
Spinal fractures
Nonaccidental Trauma
PEDIATRICS
Mechanism of
injury not
consistent with
sustained injuries
Pattern injuries
Skeletal fx in
different stages Non-Accidental
of healing Trauma Retinal
hemorrhage
Poor prognosis
Unexplained
bruising
Trauma 861
Child Abuse
PEDIATRICS
Typically a delay Inconsistent Certain patterns Undiagnosed child abuse

Child abuse
in diagnosis history of injury has high 2 year mortality
Child abuse Diffuse cerebral

Shaken baby
syndromes injury with edema
Cigarette burns Low back
Immersion into Contact with hot Genitalia

Burns Neck
hot bath object
May be in a stocking-
glove distribution
Contusions
Face Buttocks
Metaphyseal
Bilateral fx Long bone Cerebral

hemorrhage
Suspicious Fractures
Sternum for Abuse Spine
Head injury
patterns
Any < 1 year of
Skull age SAH SDH
Posterior ribs
Geriatric Trauma
Geriatric Trauma Introduction

Increased morbidity & mortality Falls are most common MVC are most common
Geriatric trauma
compared to younger persons cause of injury > 65 cause of death
Elderly more susceptible to injury Less able to Increased incidence

Geriatric trauma
from low energy mechanisms compensate of complications
Multiple Physiologic Consider thesepts as both

Pitfalls Polypharmacy
comorbidities changes medical & surgical pts!
Medication Potential masking Sensitivity to

pitfalls of vital signs narcotics
Comorbidity Decreased cardiac Aggressive fluids may

pitfall function lead to pulmonary edema
Radiograph May be difficult to Low threshold

pitfall see fx on plain film for CT
Age is independent risk factor

Head trauma Due to Brain atrophy
for morbidity & mortality
Subdural Increased stress on More susceptible

Due to
hematoma bridging veins in brain to tearing
For each rib fx in Pneumonia risk Mortality

Chest trauma
the geriatric pt increases 27 % increases 19 %
Trauma 863
Trauma in Pregnancy
Introduction
Most common blunt trauma = MVC
Leading cause of non-obstetric
Trauma
morbidity & mortality in pregnancy Most common penetrating trauma = GSW
Physiologic Difficult to
Pitfall
changes interpret VS
Heart rate increase Blood pressure

Vital signs
10–20 blm decreases 10–15 mm Hg
Physiologic Blood volume RBC mass increases Pt may lose 35 % of blood volume
Pitfall
anemia increases to a lesser degree before manifesting signs of shock
Supine
When a pregnant Compresses Decrease in Tilt pt to left 30
hypotension
female is supine inferior vena cava venous return degrees
syndrome
Bladder ascends to Increases risk Most common cause of

Anatomic pitfalls Splenic injury
abdomen in 3rd trimester of injury abdominal hemorrhage
Fetal mortality Late 2nd–3rd

Uterine rupture? Not common
of 100 % trimester
Risk factors for

Prior C-section VBAC
rupture?
Symptoms & Signs of uterine rupture
Loss of uterine Able to palpate

Shock Abdominal pain Fetal demise
contour fetal parts
Complications of Abruptio
Preterm labor See OB/GYN
trauma placenta
Maternal-Fetal Well-Being
Depends on maternal
Fetal well being
stability & survival
Emergent C- 75 % fetal Presence of fetal Procedure done at 1st

At > 26 weeks
section? survival rate heart tones sign of fetal distress
CPR & emergent Continue CPR As well as for a short time

C-section? during procedure after the procedure
Perimortem Only after optimal Done within 5 minutes

> 23 weeks
C-section? resuscitation of maternal death
Burns
Burn Classification
1st degree
Epidermis only
No blisters
Painful
Ex: Sunburn
4th degree Burn 2nd degree burn

Entire Classification Dermis involved
epidermis,
(+) blisters
dermis, bone,
fat, and muscle Painful
3rd degree
Full thickness
Charred, pale, &
leathery
Eschar formed
NO PAIN
Burn Tidbits
The pts palm
Rule of palms
= 1 % BSA
Adults Pediatrics
Burn estimation
Rule of 9’s Lund-Browder
4 mL x kg weight x %BSA ½ of volume over the 1st 8

Parkland formula
per day of lactated ringers hours, the rest over 16 hours
More fluid required for Follow urine Consider foley

Pitfall > 1 mL/kg/hr
pulmonary or electrical burns output placement
Potential for
Early intubation
airway burn?
Other
Update tetanus
considerations
Inhalational Seared nasal History of being in

Soot in mouth
injury? hairs an enclosed space
Trauma 865
Burn Estimation
Head = 9 %
(front and back)
Back =
18 %
Chest = 18%
Right arm = Left arm =

9% 9%
Head = 18 %
(front and
back)
Back =
18 %
Chest =
Perineum = 18%
1% Right arm = Left arm =
9% 9%
Perineum =
1%
Right leg =
Left leg =
18 %
18 %
Right leg = Left leg =

13.5 % 13.5 %
Adult Child
Parkland formula = LR 4ml/kg/% burn TBSA in
first 24 hrs + maintain fluids w/half in first 8 hrs + second half in last 16 hrs.
Center image (Reprinted from Allen B, Ganti L, Desai B. Trauma and ATLS. In: Allen B, Ganti L, Desai B, editors. Quick hits in emergency medi-
cine. New York: Springer Science; 2013. p. 37–45. With permission from Springer Science + Business Media)
Indications for Transfer to Burn Center
2nd degree burns

involving > 25 %
BSA: Ages 10–50
Burns
2nd degree burns
complicated by fx
involving > 20 %
or other trauma
BSA: Ages < 10 or
> 50
Electrical &
chemical burns
Indications for
3rd degree burns
transfer to burn
> 10 % BSA in any
All inhalational center
age
injuries
Circumferential Burns involving

burns of an hands, feet, face,
extremity feet, perineum
Burns in high risk Burns crossing

Children < 1 year
patients major joints
Burn Complications
From shock Direct pulmonary

ARDS
states injury
Other gram
Infection Pseudomonas
negatives
DIC from tissue

Hematologic
injury
Carbon
Toxins Cyanide
monoxide
Barotrauma
Blast injury
from explosions
Long term Stress ulcers GI bleeding

Trauma 867
Escharotomy
Escharotomy Full thickness Full thickness

indications chest wall burns circumferential limb burns
Limb burn Vascular Poor pulses &

indications? insufficiency capillary refill
Chest wall Inadequate

indications? chest rise
Cut along sides Avoid

Technique
on the long axis vasculature!
Chest technique Chest wall box
Will have a “popping” sensation Will have minimal

Tidbits
as the tissues expand after cutting bleeding
Center right image (Reprinted from Sjöberg F. Pre-hospital, fluid and volume 1. Vienna: Springer-Verlag/Wien; 2012. p. 105–16. With
early management, burn wound evaluation. In: Jeschke MG, Kamolz permission from Springer-Verlag/Wien)
L-P, Sjöberg F, Wolf SE, editors. Handbook of burns: acute burn care
Blast Injuries
Blast Injury Classification
Barotrauma
Type I Pulse pressure
effects
Penetrating
Type II Flying debris
trauma
Person is thrown Deceleration

Type III
from pulse wave impact
Type IV Toxic gas Radiation Burns
Air emboli from

CNS Symptoms LOC Concussion
ruptured arteries
Ear injuries TM rupture Ossicle injury
Rupture of
GI injury
hollow viscus
Pulmonary injury Pneumothorax

Index
A diagnosis, 248
AAA. See Abdominal aortic aneurysm (AAA) symptoms and signs, 247
Abdominal and pelvic pain, nonpregnant patient treatment, 248
endometriosis, 624 Acute bronchitis, 149
leiomyomas, 625 Acute chest syndrome, 326
ovarian/adnexal torsion, 624 Acute constipation, etiologies of, 187
ovarian cysts, 623 Acute COPD exacerbation causes, 145
Abdominal aortic aneurysm (AAA) Acute coronary syndrome (ACS)
description, 64 angina pectoris, 3
diagnosis, 66 atypical chest pain, 5
general, 64 causes, 4
signs, 65 cocaine and chest pain, 5
symptoms, 65 description, 2
treatment, 66 initial therapy, 17
Abdominal trauma pathophysiology, 4
abdominal signs, 848 physical exam, 3
bladder and ureter injury, 851 Prinzmetal’s/variant angina, 6, 7
imaging, 848 stable and unstable angina, 6
kidney injuries, 850 Acute diverticulitis. See Diverticulitis
pancreas/stomach/duodenum/intestine trauma, 849 Acute hemolytic transfusion reaction
penetrating, 847 description, 317
penetrating flank and buttock injuries, 850 laboratory investigations, 318
spleen and liver trauma, 849 Acute ischemic stroke treatment, 561
testicular injury, 852 Acute limb ischemia
urethral injury, 851 clinical diagnosis, 88
Abnormal vaginal bleeding, 625 clinical features, 87
Abortions, 630 description, 87
Abruptio placentae, 633 diagnosis, 88
Abuse/neglect/violence treatment, 88
ED staff/patient safety, 612 Acute mastoiditis, 475
elder abuse, 611 Acute mountain sickness, 536
intimate partner violence, 611 Acute myocardial infarction (AMI)
sexual assault, 612 complications, 22
AC. See Allergic conjunctivitis (AC) conduction disturbances, 23
Acalculous cholecystitis, 227 description, 7
Accelerated idioventricular rhythm (AIVR) EKG, 8
description, 21 reperfusion, 18, 19
EKG changes, 21 rhythm abnormalities, 23
treatment, 21 Acute necrotizing ulcerative gingivitis (ANUG), 491
Acetaminophen, 697 Acute periodic paralysis, 595
overdose treatment, 699 Acute renal failure
Rumack-Matthew nomogram, 698 in children, 263
Achilles tendon rupture, 794 description, 262
Acquired hemolytic anemia, 330 glomerular disease causes, 267
ACS. See Acute coronary syndrome (ACS) interstitial disease causes, 266
Acute angle-closure glaucoma intrinsic renal failure, 265
symptoms and signs, 669 laboratory investigations, 272
treatment, 670 macroscopic urine, 272
Acute appendicitis microthrombosis, 270
appendicitis confounders, 247 postrenal failure, 270–271
description, 246 prerenal failure, 264

DOI 10.1007/978-3-319-30838-8
870 Index
Acute renal failure (cont.) Anemia

radiocontrast-induced nephropathy, 269 causes, 310
RIFLE criteria, 263 classification, 312
tubular disease causes, 268 description, 310
urinalysis, 273 high MCV (macrocytic), 312
vascular/related disease, 269 low MCV (microcytic), 312
Acute respiratory distress syndrome (ARDS) normal MCV (normocytic), 313
causes, 173 specific labs, 311
description, 172 symptoms and signs, 311
Addictive behavior and withdrawal treatment, 313
alcohol withdrawal, 614 Angina pectoris, 3
benzodiazepine withdrawal, 614 Angioedema, 364, 496
cocaine/sympathomimetic withdrawal, 616 Anion gap, 685
opiate withdrawal, 615 Ankle
substance abuse/dependence, 613 dislocations, 796
THC withdrawal, 616 Ottawa rules, 795
ADH-related diseases sprains, 795
diabetes insipidus, 434–436 Ankylosing spondylitis, 803
SIADH, 431–433 Anorectal abscess, 259
Adrenal insufficiency and crisis Anorectal emergencies
adrenal hormones, 423 anal fissures, 258
causes of primary, 424 anorectal abscess, 259
causes of secondary, 425 hemorrhoids, 257–258
clinical features, 426 rectal prolapse, 259
disposition, 428 Anorexia, 607
laboratory abnormalities and testing considerations, 427 Anovulatory bleeding, 626
treatment, 427 Anterior circulation stroke, 559
Adult status epilepticus management, 569 Anterior cord syndrome, 832
AF. See Atrial fibrillation (AF) Anterior MI, 10
AFL. See Atrial flutter (AFL) specifics, 12
Airway Anthrax, 550
rapid sequence intubation, 179 Antibiotic-associated diarrhea, 197
tracheostomy and bleeding, 181 Anticholinergics, 141
tracheostomy and respiratory distress, 180 Anticholinergic toxidromes
Airway foreign body (AFB), 507 causes, 687
AIVR. See Accelerated idioventricular rhythm (AIVR) treatment, 688
Akathisia, 599 Anticoagulants
Alcoholic ketoacidosis heparin, 341
clinical features, 402 warfarin, 339–340
description, 401 Anticonvulsants
diagnosis, 403 carbamazepine, 702
disposition, 404 phenytoin and fosphenytoin, 703
pathophysiology, 402 valproate, 702
treatment, 403 Antidotes, 684
Alcohols Antihistamines, 703
description, 692 Antimicrobials, 704
ethanol, 693–694 Antiphospholipid syndrome, 810
ethylene glycol, 695 Antisocial personality disorders, 610
isopropyl alcohol, 695 Anxiety
methanol, 693 description, 606
Alcohol withdrawal, 614 disorders, 607
Allergic conjunctivitis (AC), 652 Aortic dissection
Allergic rhinitis, 480 anatomy, 67
Allergic transfusion reaction, 319 classification, 69
ALTE. See Apparent life-threatening events (ALTE) clinical features, 69
Altered mental status description, 67
description, 556 diagnosis, 70
in hemodialysis, 286 management, 71
AMI. See Acute myocardial infarction (AMI) pathophysiology, 68
Amnesia, 603 risk factors, 68
Amniotic fluid embolism, 635 special circumstance, 71
Amphetamine, 696 Aortic regurgitation
Amyotrophic lateral sclerosis, 600 causes, 39
Anal fissures, 258 CXR, 41
Analgesics description, 39
acetaminophen, 697–699 diagnosis, 40
NSAIDs, 701 symptoms, 40
salicylate, 699–700 treatment, 41
Index 871
Aortic stenosis Bacterial vaginosis (BV), 621

description, 37 β-agonists, 141
diagnosis, 38 Baker’s cyst, 790
treatment, 38 Barbituates, 729
Apathetic thyrotoxicosis, 422 Barotitis externa, 527
Aphthous stomatitis, 498 Barotitis interna, 527
Aplastic crisis, sickle cell anemia, 327 Barotitis media, 526
Apparent life-threatening events (ALTE) Barotrauma of ascent, 528
causes, 182 Barotrauma of ascent treatment, 530
description, 181 Bartholin cyst and abscess, 622
Appendicitis confounders, 247 Basilar skull fracture, 824
ARDS. See Acute respiratory distress syndrome (ARDS) β-blockers, 705
Arsenic, 715 Bees/wasps, 518
Arterial-alveolar gradient, 133, 685 Bell’s palsy, 593
Arterial gas embolism, 529 Benign paroxysmal positional vertigo (BPPV), 510
Arteries and affected areas, 9 Benzodiazepines, 730
Ascending cholangitis, 227 Benzodiazepine withdrawal, 614
Aspiration Bilirubin evaluation, 220
description, 166 Biological agents and toxins, 549
management, 167 Biological weapons, 548
Asthma anthrax, 550
anticholinergics, 141 plague, 551
β-agonists, 141 selected biological agents and toxins, 549
clinical features, 139 smallpox, 551
description, 138 toxins, 552
leukotriene modifiers, 141 Bipolar disorder, 605
magnesium, 141 Bites
methylxanthines, 141 bees/wasps, 518
peak flow, 140 black widow envenomation, 519
risk factors for death, 140 brown recluse envenomation, 519
severe asthma management, 142 mammalian bites, 520–523
steroids, 141 Black widow envenomation, 519
triggering agents, 139 Bladder and ureter injury, 851
Atrial fibrillation (AF) Blast injuries, 867
description, 105 Bleeding
EKG changes, 106 from heparin, 341
treatment, 107 and tracheostomy, 181
WPW syndrome, 112–113 from warfarin, 340
Atrial flutter (AFL) Blepharitis, 643
EKG changes, 106 Blood pressure definitions, 72
treatment, 107 Blow out fractures, 673
WPW syndrome, 112–113 Blunt eye trauma, 670
Atypical chest pain, 5 Blunt neck trauma, 838
Auricular hematoma, 476 Blunt ocular trauma and globe rupture, 671
Automatic implantable cardioverter, 91 Bone anatomy, 736
Borderline personality disorders, 610
Boutonniere deformity, 743
B Bowel obstruction
Babesiosis, 372 causes, 234
Bacillus cereus, 194 description, 234
Back pain, 801 diagnosis, 235–236
Back pain workup, 802 pathophysiology, 235
Bacterial conjunctivitis, 649 symptoms and signs, 235
Bacterial diarrhea treatment, 236
description, 190 Bowel perforation
pathogens description, 245
B. cereus, 194 diagnosis, 246
Campylobacter, 192 treatment, 246
C. perfringens, 194 BPPV. See Benign paroxysmal positional vertigo (BPPV)
E. coli, 191 Brain abscess, 580
Salmonella, 191 Brain herniation, 821
Shigella, 191 Branchial cleft cysts, 494
Staphylococcus, 193 Bronchiolitis
Vibrio, 193 bronchopulmonary dysplasia, 151
Yersinia, 192 description, 150
Bacterial keratitis, 654 disposition, 151
Bacterial meningitis, 575 RSV management, 150
Bacterial tracheitis, 489 Bronchopulmonary dysplasia, 151
872 Index
Brown recluse envenomation, 519 Cerebral contusions, 823

Brown-Sequard syndrome, 832 Cerebral edema, 400
Brugada syndrome, 127–128 Cerebrovascular accidents
Bulimia nervosa, 608 acute ischemic stroke treatment, 561
Bullous myringitis, 474 anterior circulation stroke, 559
Bullous pemphigoid, 354 cerebellar infarction, 561
Burns intracranial hemorrhage management, 564
classification, 864 IV tPA exclusions, 562
complications, 866 lacunar infarction, 560
escharotomy, 867 relative exclusions for IV tPA, 562
estimation, 865 spontaneous intracranial hemorrhage, 563
indications, 866 stroke and TIA, 558
stroke mimics, 557
tPA complications, 563
C vertebrobasilar infarction, 560
Calcaneal fractures, 797 Cervical cancer, 628
Calcium, 445 Cervical spine clearance, 827
hypercalcemia, 448–450 Cervical spine evaluation, 827
hypocalcemia, 446–448 Chalazion, 642
Calcium channel blockers, 705 Chancroid, 306
Campylobacter, 192 Chemical burns, 674
Candida vaginitis, 622 Chemical weapons, 552
Candidiasis, 497 nerve agents, 553
Carbamazepine, 702 vesicants, 553
Carbon monoxide (CO) poisoning, 707 Chest pain
Cardiac contusion, 845 atypical, 5
Cardiac markers, 16 and cocaine, 5
Cardiac medications Chest trauma, 838
β-blockers, 705 cardiac contusion, 845
calcium channel blockers, 705 cardiac tamponade, 844
clonidine, 706 cardiac trauma, 844
digitalis, 706–707 CXR findings of aortic injury, 846
Cardiac syncope, 78 diaphragmatic injury, 846
Cardiac tamponade, 844 flail chest, 842
causes, 62 hemothorax, 841
clinical features, 63 pneumomediastinum, 839
description, 62 pneumothorax, 839–840
treatment, 63 pulmonary contusion, 843
Cardiac trauma, 844 rib fractures, 841
Cardiomyopathy (CM) sternal fracture, 842
dilated, 51–53 tracheobronchial injuries, 843
general/description, 50 traumatic aortic injury, 845
hypertrophic, 53–54 Children, acute renal failure in, 263. See also Pediatrics
restrictive, 55–56 Chlamydia, 302
Carotid/vertebral artery dissection, 593 Chlamydophila pneumoniae, 160
Carpal tunnel syndrome, 746 Chlorine, 710
Cat bites and scratches, 523 Cholesteatoma, 475
Cauda equina syndrome, 804 Cholinergic toxidromes, 688–689
Cauliflower ear, 476 Chronic constipation, etiologies of, 188
Caustic agents Chronic obstructive pulmonary disease (COPD)
acids, 708 acute bronchitis, 149
alkali, 709 acute COPD exacerbation causes, 145
Cavernous sinus thrombosis, 506 description, 143
Central cord syndrome, 831 diagnostics, 145
Central pontine myelinolysis, 433 exacerbation disposition, 148
Central retinal artery occlusion (CRAO), 663 exacerbation management, 146
Central retinal vein occlusion (CRVO), 665 intubation, indications, 147
Central vertigo NIPPV indications and contraindications, 146
cerebellar infarction and hemorrhage, 514 pathophysiology, 144
migraine-related vertigo, 516 permissive hypercapnia, 148
multiple sclerosis, 515 ventilator management and pitfalls, 147
symptoms, 509 Chronic renal failure
vertebral artery dissection, 515 and end-stage renal disease, 277
vertebrobasilar insufficiency, 515 nephrotic syndrome, 278–279
Wallenberg syndrome, 514 polycystic kidney disease, 280
Cerebellar infarction, 514, 561 renal tubular acidosis, 279
Cerebellopontine angle tumors, 513 uremia, 280–282
Index 873
Ciguatera, 195 Decubitus ulcers, 386

Clonidine, 706 Deep venous thrombosis (DVT)
Clostridium difficile, 198 clinical features, 81
Clostridium perfringens, 194 diagnosis, 81
Cluster headache, 584 disposition, 86
CM. See Cardiomyopathy (CM) Defibrillator nomenclature, 91
CNS infections Delayed transfusion reaction, 319
meningitis, 573–578 Delirium vs. dementia, 601
typical CSF characteristics, 572 Dental emergencies
Cocaine ANUG, 491
and chest pain, 5 dental trauma, 493
description, 711 ellis fractures, 492
sympathomimetic withdrawal, 616 gingival hyperplasia, 492
Cold injury pathophysiology, 543 odontogenic infections, 490
Collar button abscess, 742 periodontal pathology, 491
Colles’ fracture, 750 periostitis and alveolar osteitis and post-extraction
Coma testing, 557 bleeding, 490
Compartment syndrome, 792 Dental trauma, 493
Complicated vs. uncomplicated UTI, 289 De Quervain’s tenosynovitis, 746
Concussion, 823 Dermatophyte infections, 362
Congestive heart failure Diabetes insipidus (DI)
causes of, 25 causes of central DI, 434
diagnosis, 28 causes of nephrogenic DI, 435
diastolic heart failure, 26 clinical features, 435
pathophysiology, 24 laboratory abnormalities and testing considerations, 436
systolic heart failure, 25 treatment and disposition, 436
treatment, 29, 30 Diabetes mellitus (DM)
Conjunctivitis, 648 about hormones, 393
allergic, 652 insulin pump, 394
bacterial, 649 types of insulin, 394
EKC, 651 Diabetic ketoacidosis (DKA)
ophthalmia neonatorum, 650 bicarbonate, 400
subconjunctival hemorrhage, 652 causes of, 395
viral, 651 cerebral edema, 400
Constipation clinical features, 397
description, 187 complications, 400
diagnosis, 188 diagnosis, 398
etiologies, 187–188 differential diagnosis, 399
symptoms and signs, 187 disposition, 401
treatment, 189 precipitants, 398
COPD. See Chronic obstructive pulmonary disease (COPD) treatment, 399
Cornea, 653–657 Dialysis disequilibrium, 286
Corneal abrasion, 657 Diaphragmatic injury, 846
Corneal foreign bodies, 659 Diarrhea
Corneal lacerations, 658 antibiotic-associated, 197
Corneal ulcers, 659 bacterial, 190
Cranial nerves, 638 C. difficile, 198
Crohn’s disease description, 189
description, 253 pseudomembranous enterocolitis, 198
diagnosis, 254 viral, 190
extraintestinal manifestations, 254 Diastolic heart failure, 26
symptoms and signs, 253 DIC. See Disseminated intravascular coagulation (DIC)
treatment, 255 Digitalis
Croup, 489 description, 706–707
Cryoprecipitate, 317 EKG changes, 100
Cryptosporidium, 197 Dilated cardiomyopathy
Cushing’s Syndrome. See Hyperadrenalism clinical features, 52
Cyanide and nitriles, 712–713 description, 51
Cyanosis, 134 treatment, 53
Cytomegalovirus, 373 Disk herniation, 802
Diskitis, 806
Disseminated intravascular coagulation (DIC)
D clinical features, 336
Dacryoadenitis, 644 description, 336
Dacryocystitis, 644 etiologies, 335
D-Dimer, 83 laboratory findings, 337
Decompression sickness, 530 treatment, 337
874 Index
Diverticulitis Eighth cranial nerve lesions, 513

description, 248 EKG
diagnosis, 250 in AMI, 8
risk factors, 249 changes related to
symptoms and signs, 249 electrolytes and metabolic conditions, 96–99
treatment, 250 medications, 100–101
Dog bites, 523 and emergent reperfusion, 12
Drowning, 538–539 MI predicting factors, 11
Drug rash/eruption, 356 ventricular aneurysm predicting factors, 22
Dysbarism Elbow
arterial gas embolism, 529 bursitis, 761
barotitis externa, 527 dislocation, 763
barotitis interna, 527 epicondylitis, 761
barotitis media, 526 fracture, 764
barotrauma of ascent, 528 nursemaid’s elbow, 762
barotrauma of ascent treatment, 530 radial head fracture, 764
decompression sickness, 530 soft tissue injuries, 760
nitrogen narcosis, 529 supracondylar fracture, 765
pulmonary barotrauma, 529 Elder abuse, 611
recompression therapy, 531 Electrical injuries
sinus barotrauma, 528 description, 531
Dyshemoglobinemias lightning injury, 533–534
clinical features, 322 management, 532
methemoglobin, 321 Electrolyte complications, of ESRD, 282
methemoglobinemia Electrolytes and acid-base
drugs causing, 321 calcium, 445–450
types, 322 magnesium, 450–453
treatment, 322 metabolic acidosis, 458–462
Dysphagia, 199 metabolic alkalosis, 462–463
Dysrhythmias metabolic derangements, 456–457
atrial fibrillation and atrial flutter, 105–107 phosphorus, 453–456
junctional escape rhythm, 102–103 potassium, 441–444
multifocal atrial tachycardia, 108–109 respiratory acidosis, 463–464
premature ventricular contractions, 109–110 respiratory alkalosis, 464–465
supraventricular tachycardia, 103–105 sodium, 437–440
ventricular fibrillation, 117–118 Ellis fractures, 492
ventricular tachycardia, 115–117 Emergency dialysis, indications for, 283
Wolff-Parkinson-White syndrome, 111–114 Emergency pacing, 89
Dystonic reaction and chorea, 598 Emergent reperfusion and EKG, 12
Empyema, 175
Encephalitis
E causes, 579
Ear description, 578
acute mastoiditis, 475 diagnosis and management, 579
auricular hematoma, 476 Endometriosis, 624
bullous myringitis, 474 Endometritis, 636
cauliflower ear, 476 Endophthalmitis, 661
cholesteatoma, 475 End organ and other syndromes, 73–74
hearing loss, 469–471 End-stage renal disease (ESRD), 277
malignant otitis externa, 472–473 Entamoeba histolytica, 196
otalgia, 468 ENT emergencies
otitis externa, 472 airway foreign body, 507
otitis media, 474 causes of trismus, 505
perichondritis, 471 cavernous sinus thrombosis, 506
tinnitus, 469 post-tonsillectomy bleeding, 504
tympanic membrane perforation, 477 Ramsay Hunt syndrome, 506
Early repolarization, predicting factors, 11 trigeminal neuralgia, 505
Eastern coral snake envenomation, 525 Epidemic keratoconjunctivitis (EKC), 651
Eclampsia, 632 Epididymitis, 299
E. coli, 191 Epiglottitis, 486
Ectopic pregnancy, 629 Epistaxis, 478–479
Eczema, 358 Erysipelas, 503
Edema of upper airway Erythema multiforme, 350
angioedema, 496 Erythema nodosum, 357
uvular edema, 496 Escharotomy, 867
ED staff/patient safety, 612 Esophageal emergencies
Ehrlichiosis, 371 dysphagia, 199
Index 875
transfer dysphagia, 199–201 traumatic penis and, 296

transport dysphagia, 202–204 Fractures, 747
Esophageal foreign bodies Fresh frozen plasma (FFP), 316
caustic ingestions, 209 Frontal and zygoma fractures, 482
description, 207 Fungal meningitis, 578
diagnosis and treatment, 208
symptoms and signs, 207
Esophageal perforation G
causes, 205 Gallbladder
description, 204 acalculous cholecystitis, 227
diagnosis and treatment, 206 ascending cholangitis, 227
symptoms and signs, 206 description, 226
Esophagitis, 211 diagnosis, 228
Ethanol, 693–694 pathophysiology, 227
Ethylene glycol, 695 symptoms and signs, 228
Exacerbation disposition, asthma, 148 treatment, 229
Exacerbation management, asthma, 146 Gamekeeper’s thumb, 745
Exfoliative dermatitis, 355 Gamma-hydroxybutyrate, 730
External eye Gastrocnemius rupture, 794
lids, 642–644 Generalized skin rashes and disorders
periorbital and orbital cellulitis, 645–647 angioedema, 364
Extremity injuries bullous pemphigoid, 354
amputations, 857 dermatophyte infections, 362
description, 856 drug rash/eruption, 356
Exudates, 174 eczema, 358
Eye movements, 638 erythema multiforme, 350
Eye muscles, 638 erythema nodosum, 357
exfoliative dermatitis, 355
pemphigus vulgaris, 353
F pityriasis rosea, 361
Facial cellulitis, 503 psoriasis, 359
Facial fractures seborrheic dermatitis, 360
frontal and zygoma fractures, 482 SJS and TEN, 351
mandible fractures, 483 skin cancers, 365
midface fractures, 483 SSSS, 352
Facial infections tinea versicolor, 363
erysipelas, 503 Genital warts, 308
facial cellulitis, 503 GERD
impetigo, 504 description, 210
Factitious disorders, 609 symptoms and signs, 210
Febrile nonhemolytic reaction, 318 treatment, 211
Febrile seizures, 570–571 Geriatric trauma, 862
Felon, 740 Gestational trophoblastic disease, 631
Femoral shaft fracture, 781 Giardia, 196
FFP. See Fresh frozen plasma (FFP) GI bleeding
Fibula fracture, 794 LGIB (see Lower GI bleeding (LGIB))
Finger dislocation, 748 terminology, 214
First-degree heart block (1° HB) UGIB (see Upper GI bleeding (UGIB))
description, 120 Gingival hyperplasia, 492
EKG changes, 121 Glans penis and foreskin disorders, 296
treatment, 121 Glaucoma, 669–670
Fitz-Hugh-Curtis syndrome, 619 Glomerular disease, causes, 267
Flail chest, 842 Gonorrhea, 303
Flexor tenosynovitis, 742 G6PD deficiency, 329
Foot Granuloma inguinale, 307
calcaneal fractures, 797 Graves disease, 416
lisfranc injuries, 798 Grief reaction, 605
metatarsal fractures, 799 Guillain-Barre syndrome, 595
tarsal tunnel syndrome, 799 Gynecologic oncology
Forearm cervical cancer, 628
Galeazzi fracture, 757 ovarian cancer, 627
Monteggia fracture, 758 uterine cancer, 627
ulna and radius fractures, 759
ulnar nightstick fracture, 756
Volkmann’s ischemic contracture, 759 H
Foreskin disorders Haemophilus influenzae, 158
glans penis and, 296 Hallucinogens, 713–714
876 Index
Hand hemolytic uremic syndrome, 332

Boutonniere deformity, 743 hereditary
carpal tunnel syndrome, 746 G6PD deficiency, 329
collar button abscess, 742 hereditary spherocytosis, 329
De Quervain’s tenosynovitis, 746 microangiopathic hemolytic anemia, 331
felon, 740 thrombotic thrombocytopenic purpura, 331
finger dislocation, 748 Hemolytic uremic syndrome (HUS), 332
flexor tenosynovitis, 742 Hemophilia
Gamekeeper’s thumb, 745 description, 338
herpetic whitlow, 745 treatment, 338
high-pressure injection injury, 749 Hemoptysis, 134–135
infections, 739 Hemorrhage, 514
Mallet finger, 744 Hemorrhoids
nerves, 738 description, 257
paronychia, 741 risk factors, 258
sporotrichosis, 742 Hemostasis tests
Hand-foot-mouth disease, 381 activated partial thromboplastin time, 324
Headache syndromes bleeding time, 323
carotid/vertebral artery dissection, 593 prothrombin time, 324
classification, 581 Hemothorax, 841
cluster headache, 584 Henoch-Schonlein Purpura, 382
CNS tumors, 586 Heparin
headache red flags, 581 bleeding from, 341
hydrocephalus, 587–588 description, 341
migraine, 582–583 Heparin-induced thrombocytopenia (HIT), 341
post-lumbar puncture headache, 585 Hepatic encephalopathy, 225
pseudotumor cerebri, 586 Hepatitis
subarachnoid hemorrhage, 591–592 hepatic encephalopathy, 225
tension headache, 583 hepatitis A, 223
toxic metabolic headache, 585 hepatitis B, 223
trigeminal neuralgia, 584 hepatitis C, 224
venous sinus thrombosis, 591 hepatitis D, 224
ventricular shunt headache, 589 hepatitis E and G, 224
VP shunt complications, 589–590 indications for hospitalization, 222
Head trauma, 820 laboratory abnormalities, 222
Hearing loss, 469 symptoms and signs, 221
causes of, 470 toxic, 225
medications and drugs, 471 Hepatitis A, 223
Heart blocks Hepatitis B, 223
first-degree heart block, 120–121 Hepatitis C, 224
left bundle branch block, 118–119 Hepatitis D, 224
right bundle branch block, 119–120 Hepatitis E and G, 224
second-degree type 1 heart block, 122–123 Hereditary spherocytosis, 329
second-degree type 2 heart block, 123–125 Hernias
third-degree heart block, 125–126 description, 242
Heart failure diagnosis, 244
clinical features and presentation, 27 inguinal, 242
congestive (see Congestive heart failure) treatment, 244
left vs. right, 26 ventral, 243
Heart failure preserved ejection fraction. See Diastolic heart failure Herpangina, 498
Heart failure reduced ejection fraction. See Systolic heart failure Herpes Simplex, 305
Heat dissipation vs. generation, 540 Herpes Zoster, 374
Heat stroke, 542 Herpes Zoster ophthalmicus, 656
HELLP syndrome, 633 Herpetic whitlow, 745
Hemangiomas, 387 Hiccups, 176
Hematuria, causes, 292 High-altitude cerebral edema, 536
Hemodialysis (HD) High-altitude illness, 535
altered mental status, 286 acute mountain sickness, 536
complications, 284 high-altitude cerebral edema, 536
dialysis disequilibrium, 286 high-altitude pulmonary edema, 537
emergency dialysis, indications for, 283 High-altitude pulmonary edema, 537
hemorrhagic complications, 285 High MCV (macrocytic), 312
hypotension during, 285 High-pressure injection injury, 749
infectious complications, 284 Hip dislocation, 855
peritoneal dialysis, 287 Hirschsprung’s disease, 239
Hemolytic anemias Histrionic personality disorders, 610
acquired hemolytic anemia, 330 HIT. See Heparin-induced thrombocytopenia (HIT)
Index 877
Hordeolum, 642 diagnosis, 456

HSV infections, 497 treatment, 456
HSV keratitis, 655 Hypertension
Humerus and shoulder blood pressure definitions, 72
acromioclavicular injuries, 769 description, 631
anterior dislocations, 772 end organ and other syndromes, 73–74
clavicle fracture, 770 hypertensive emergencies, 72
diagnosis and treatment, 773 medication effects, 74–75
inferior dislocations, 775 pulmonary, 76
nontraumatic pain, 767 severe asymptomatic hypertension, 75
posterior dislocations, 774 side effects, 74–75
proximal fracture, 766 Hypertensive emergencies, 72
rotator cuff injuries, 775 Hyperthyroidism
scapula fracture, 771 causes of, 416, 417
shaft fracture, 767 clinical features, 417
sternoclavicular injuries, 768 description, 415
thoracic outlet syndrome, 776 Graves disease, 416
HUS. See Hemolytic uremic syndrome (HUS) Hypertrophic cardiomyopathy
Hydrocarbons clinical features, 54
description, 719 description, 53
treatment and management, 720 treatment, 54
Hydrocephalus Hyphema, 672
description, 587 Hypocalcemia
normal pressure, 588 causes of, 447
pediatric, 588 description, 446
Hyperacute T waves, 10 diagnosis, 448
Hyperadrenalism EKG changes, 97
clinical features, 428 symptoms and signs, 447
disposition, 429 treatment, 448
laboratory abnormalities and testing considerations, 429 Hypoglycemia
treatment, 429 agents for glucose control, 390
Hypercalcemia clinical features, 391
causes of, 449 description, 683
description, 448 differential diagnosis, 392
diagnosis, 450 treatment, 392
EKG changes, 98 Hypoglycemic agents, 721
symptoms and signs, 449 Hypokalemia
treatment, 450 causes of, 442
Hypercapnia, 133 description, 441
Hyperglycemia diagnosis, 443
effects of, 396 EKG changes, 96
systemic effects of, 397 symptoms and signs, 442
Hyperkalemia treatment, 443
causes of, 443 Hypomagnesemia
diagnosis, 444 causes of, 451
EKG changes, 97 description, 450
symptoms and signs, 444 diagnosis, 452
treatment, 444 EKG changes, 98
Hypermagnesemia symptoms and signs, 451
causes of, 452 treatment, 452
diagnosis, 453 Hyponatremia
symptoms and signs, 453 causes of, 438
treatment, 453 causes of hypotonic hyponatremia, 439
Hypernatremia description, 437
causes of, 440 diagnosis, 438
description, 439 treatment, 438
symptoms, 440 Hypophosphatemia
treatment, 440 causes of, 454
Hyperosmolar hyperglycemic nonketotic syndrome (HHNS) diagnosis, 455
clinical features, 405 symptoms and signs, 454
diagnosis, 406 treatment, 455
disposition, 406 Hypotension, during hemodialysis, 285
pathophysiology, 404 Hypothermia
precipitating factors, 405 description, 545
treatment, 406 EKG changes, 96
Hyperphosphatemia manifestations, 546
878 Index
Hypothyroidism ITP. See Idiopathic thrombocytopenic purpura (ITP)

causes of, 409 IV tPA exclusions, 562
clinical features, 410
specific clinical features, 410
Hypoxemia, 132 J
Hypoxia, 132 Jellyfish stings, 524
Junctional escape rhythm (JER)
description, 102
I EKG changes, 102
Iatrogenic pneumothorax, 136 treatment, 103
Idiopathic intracranial hypertension. See Pseudotumor cerebri
Idiopathic thrombocytopenic purpura (ITP), 334
Ileus, 233 K
Impetigo, 504 Kawasaki’s disease, 383
Incomplete spinal cord injury, 831 Keratitis, 653
Infectious diseases and associated skin lesions bacterial, 654
babesiosis, 372 Herpes Zoster ophthalmicus, 656
cytomegalovirus, 373 HSV, 655
ehrlichiosis, 371 ultraviolet, 657
hand-foot-mouth disease, 381 Kidney injuries, 850
Henoch-Schonlein purpura, 382 Kidney stones
Herpes Zoster, 374 diagnosis and treatment, 293–294
Kawasaki’s disease, 383 stone admission criteria, 294
leptospirosis, 369 Klebsiella pneumoniae, 159
lyme disease, 368 Knee
malaria, 376 Baker’s cyst, 790
measles, 378 dislocation, 786
meningococcemia, 367 Osgood-Schlatter disease, 789
Molluscum contagiosum, 375 osteochondritis dissecans, 788
rocky mountain spotted fever, 370 Ottawa rules, 782
roseola infantum, 379 patellar dislocation, 784
rubella, 377 patellar fractures, 783
scarlet fever, 384 tendon rupture, 787
varicella, 380 tibial plateau fractures, 785
Infective endocarditis
acute vs. subacute, 43
clinical findings, 45 L
description, 42 Labyrinthitis, 512
diagnosis, 46 Lacerations, 674
left-sided vs. right-sided endocarditis, 44 Lactic acidosis, 460
organisms, 44–45 Lacunar infarction, 560
pathophysiology, 43 Lambert-Eaton myasthenic syndrome, 597
prophylaxis, 47 Larynx trauma, 495
treatment, 46 Lead, 717
Inferior MI, 14 Left bundle branch block (LBBB)
Inferior MI specifics, 13 description, 118
Inferior-posterior MI, 14 EKG changes, 119
Inguinal hernias, 242 Left-sided vs. right-sided endocarditis, 44
Interstitial disease, causes, 266 Left ventricular assist devices (LVAD)
Intimate partner violence, 611 coding, 95
Intracranial hemorrhage, 564, 825 complications, 95
Intraoral and tongue lesions description, 94
leukoplakia, 499 echo findings, 95
oral cancer, 500 EKG, 95
strawberry tongue, 499 emergencies, 94
Intrinsic renal failure, 265 patient assessment, 94
Intubation Left vs. right heart failure, 26
indications, 147 Leg
rapid sequence intubation, 179 Achilles tendon rupture, 794
Intussusception compartment syndrome, 792
description, 236–237 fibula fracture, 794
diagnosis, 237 gastrocnemius rupture, 794
treatment, 238 pilon fracture, 793
Iron, 716 tibial shaft fractures, 791
Irritable bowel syndrome, 257 Legg-Calve-Perthes disease, 777
Isoniazid, 704 Leiomyomas, 625
Isopropyl alcohol, 695 Leptospirosis, 369
Index 879
Lesions, 307 tumor lysis syndrome, 347

Leukoplakia, 499 Malignant hyperthermia, 733
Leukotriene modifiers, 141 Malignant otitis externa (MOE), 472–473
LGV. See Lymphogranuloma venereum (LGV) Malingering, 609
Lids Mallet finger, 744
blepharitis, 643 Mammalian bites
chalazion, 642 cat bites and scratches, 523
dacryoadenitis, 644 description, 520
dacryocystitis, 644 dog bites, 523
hordeolum, 642 rabies, 521–522
Lightning injury, 533–534 Mandible fractures, 483
Lisfranc injuries, 798 Marine envenomation
Lithium, 721–722 eastern coral snake envenomation, 525
Liver jellyfish stings, 524
bilirubin evaluation, 220 pit viper envenomation, 525
description, 219 snake bites, 524
hepatitis (see Hepatitis) stingray stings, 524
neonatal jaundice, 221 Massive blood transfusion, 315
spontaneous bacterial peritonitis, 226 Mastitis, 636
Localized cold injuries, 543–544 MAT. See Multifocal atrial tachycardia (MAT)
Lower GI bleeding (LGIB) Measles, 378
causes, 217, 218 Mediastinal masses, 178
description, 217 Mediastinitis, 176
diagnosis and treatment, 218 Meniere’s disease, 511
disposition, 219 Meningitis
Low MCV (microcytic), 312 bacterial, 575
Ludwig’s angina, 488 description, 573
Lumbar strain, 802 empiric antibiotic treatment, 577
Lung abscess, 17, 172 evaluation, 577
LVAD. See Left ventricular assist devices (LVAD) fungal, 578
Lyme disease, 368 prophylaxis, 576
Lymphangiomas, 388 risk factors, 576
Lymphogranuloma venereum (LGV), 306 viral, 574
Meningococcemia, 367
Mercury, 718
M Mesenteric ischemia
Macroscopic urine, 272 description, 251
Magnesium diagnosis, 252
description, 141 risk factors, 251
hypermagnesemia, 452–453 symptoms and signs, 252
hypomagnesemia, 450–452 treatment, 252
MAHA. See Microangiopathic hemolytic anemia (MAHA) Metabolic acidosis
Major depression, 604 abnormal anion gap without acid-base disturbance, 458
Major ring fractures, 853 anion gap, 458
Malaria, 376 causes of anion gap, 459
Male genital emergencies effects, 461
epididymitis and orchitis, 299 lactic acidosis, 460
foreskin disorders non-anion gap causes, 461
glans penis and, 296 treatment, 462
traumatic penis and, 296 Metabolic alkalosis
priapism, 297 causes of, 463
prostatitis, 300 description, 462
scrotal disorders, 295 effects, 463
testicular torsion, 298 treatment, 463
urethritis, 300 Metabolic derangements
urinary retention, 301 description, 456
Malignancy, complications of history and physical, 457
adrenal insufficiency, 347 laboratory investigations, 457
airway obstruction, 343 Metal fume fever, 718
febrile neutropenia, 348 Metatarsal fractures, 799
hypercalcemia, 346 Methanol, 693
hyperviscosity syndrome, 348 Methemoglobin (MHb), 321
pathologic fractures from bone metastases, 344 Methemoglobinemia
pericardial effusion and tamponade, 344 drugs causing, 321
SIADH, 346 types, 322
spinal cord compression, 345 Methylxanthines, 141
superior vena cava syndrome, 345 Microangiopathic hemolytic anemia (MAHA), 331
880 Index
Microthrombosis, causes, 270 thyroglossal duct cysts, 495

Midface fractures, 483 Necrotizing enterocolitis, 186
Migraine Necrotizing infections, 488
description, 582 Neonatal jaundice, 221
treatment, 583 Neonatal seizures, 571
Migraine-related vertigo, 516 Nephrotic syndrome
Mild traumatic brain injury (TBI), 822 causes, 279
Minor/moderate heat illness, 541 description, 278
Miscellaneous skin-related disorders Nerve agents, 553
decubitus ulcers, 386 Neurogenic shock, 834
hemangiomas, 387 Neuroleptic malignant syndrome (NMS), 727
lymphangiomas, 388 Neuromuscular disorders
venous stasis ulcers, 385 acute periodic paralysis, 595
Mitral regurgitation Guillain-Barre syndrome, 595
description, 33 multiple sclerosis, 594
diagnosis, 34 myasthenia gravis, 596–597
symptoms, 34 tick paralysis, 595
treatment, 35 Neuro-ophthalmology
Mitral stenosis cranial nerves, 638
description, 32 eye movements, 638
diagnosis, 32 eye muscles, 638
treatment, 33 sympathetic chain and Horner’s syndrome, 639
Mitral valve prolapse Neuropathies, 600
description, 35 NIPPV indications and contraindications, 146
diagnosis, 36 Nitrogen narcosis, 529
treatment, 36 Nonaccidental trauma, 860
Moderate and severe TBI, 822 Non-cardiogenic pulmonary edema, 30
Molluscum contagiosum, 375 Nonsteroidal anti-inflammatory agents (NSAIDs), 701
Monoamine oxidase inhibitor (MAOI) overdose, 723 Nontraumatic hip disorders
Movement disorders Legg-Calve-Perthes disease, 777
akathisia, 599 septic arthritis, 779
dystonic reaction and chorea, 598 slipped capital femoral epiphysis, 778
Parkinson’s disease, 599 toxic synovitis, 780
tardive dyskinesia, 599 Non-ulcer-forming processes, 302
Multifocal atrial tachycardia (MAT) Normal MCV (normocytic), 313
description, 108 Normal pressure hydrocephalus, 588
EKG changes, 108 Nose
treatment, 109 allergic rhinitis, 480
Multiple sclerosis, 515, 594 epistaxis, 478–479
Munchausen’s syndrome, 609 nasal fractures, 480
Mushrooms, 723–724 sinusitis, 481
Myasthenia gravis
Lambert-Eaton myasthenic syndrome, 597
precipitants, 596 O
treatment, 597 Obsessive-compulsive disorder, 607
Mycoplasma pneumoniae, 160 Obstetrics
Myocarditis abortions, 630
clinical features, 58 abruptio placentae, 633
description, 56 amniotic fluid embolism, 635
infectious causes, 57 eclampsia, 632
treatment, 58 ectopic pregnancy, 629
Myxedema coma endometritis, 636
description, 411 gestational trophoblastic disease, 631
differential diagnosis, 413 HELLP syndrome, 633
disposition, 414 hypertension, 631
precipitating factors, 412 mastitis, 636
treatment, 414 peripartum cardiomyopathy, 636
placenta previa, 634
postpartum hemorrhage, 635
N preeclampsia, 632
Narcissistic personality disorders, 610 preterm birth and premature rupture of membranes, 634
Narcotics, 724 RhoGAM, 630
Nasal fractures, 480 umbilical cord prolapse, 635
Neck, 494 Odontogenic infections, 490
Neck masses Odontoid fractures, 829
branchial cleft cysts, 494 Ophthalmia neonatorum, 650
larynx trauma, 495 Opiate withdrawal, 615
neck, 494 Opioid toxidromes, 689–690
Index 881
Optic nerve treatment, 854

optic neuritis, 666 Pemphigus vulgaris, 353
papilledema and pseudotumor cerebri, 667 Penetrating abdominal trauma, 847
Optic neuritis, 666 Penetrating flank and buttock injuries, 850
Oral cancer, 500 Penetrating neck injury, 835
Orchitis, 299 blunt neck trauma, 838
Organic acute psychosis etiologies medical conditions, 602 general treatment, 837
Organic acute psychosis etiologies medications/drugs, 602 pharynx trauma, 837
Organic vs. functional psychosis, 603 zones of neck, 836
Organophosphates (OP) and carbamates, 725 Peptic ulcer disease (PUD)
Orthostatic syncope, 78 causes, 212
Osgood-Schlatter disease, 789 complications, 214
Osmolal gap, causes, 466 description, 212
Osmolar gap, 686 diagnosis and treatment, 213
Osteomyelitis, 800, 801 gastritis, 212
Otalgia, 468 pathophysiology, 212
Otitis externa (OE), 472 symptoms and signs, 213
Otitis media (OM), 474 Pericarditis
Ottawa rules causes, 59
ankle, 795 clinical features and diagnosis, 60
knee, 782 EKG changes, 61
Ovarian/adnexal torsion, 624 infectious causes, 59
Ovarian cancer, 627 treatment, 61
Ovarian cysts, 623 Perichondritis, 471
Overdose odor pearls, 684 Perilymph fistula, 512
Ovulatory bleeding, 626 Periodontal pathology, 491
Periorbital and orbital cellulitis
complications, 647
P description, 645
Pacemakers postseptal cellulitis, 647
automatic implantable cardioverter, 91 preseptal cellulitis, 646
emergency pacing, 89 Periostitis and alveolar osteitis and post-extraction bleeding, 490
failure, 93 Peripartum cardiomyopathy, 636
malfunctions, 92 Peripheral polyneuropathies, 600
nomenclature, 90 Peripheral vertigo
Packed red blood cells (PRBC), 314 BPPV, 510
Pancreas/stomach/duodenum/intestine trauma, 849 cerebellopontine angle tumors, 513
Pancreatitis eighth cranial nerve lesions, 513
causes, 229 labyrinthitis, 512
complications, 230 Meniere’s disease, 511
diagnosis, 231 perilymph fistula, 512
Ranson’s criteria, 232 posttraumatic vertigo and post-concussive syndrome, 513
symptoms and signs, 231 symptoms, 509
treatment, 232 vestibular neuronitis, 511
Papilledema and pseudotumor cerebri, 667 Peritoneal dialysis, 287
Parkinson’s disease, 599 Peritonsillar abscess (PTA), 485
Paronychia, 741 Permissive hypercapnia, 148
Pediatric gastroenterology, 186 Personality disorders, 610
Pediatrics Pertussis
apparent life-threatening events, 181–182 complications, 152
head trauma, 825 description, 152
hydrocephalus, 588 treatment, 153
sudden infant death syndrome, 183 Pharyngitis and tonsillitis, 484
Pediatric trauma, 858 Pharynx trauma, 837
airway and breathing, 859 Phencyclidine (PCP), 714
child abuse, 861 Phenothiazines, 726–727
indications, 860 Phenytoin and fosphenytoin, 703
nonaccidental trauma, 860 Pheochromocytoma
Pelvic inflammatory disease (PID) clinical features, 429
admission criteria, 619 diagnosis, 430
complications, 619 treatment and disposition, 430
diagnosis and treatment, 618 Phosphorus
Pelvis and hip trauma, 852 description, 453
acetabular and avulsion/single bone Fx, 853 hyperphosphatemia, 455–456
complications, 855 hypophosphatemia, 454–455
hip dislocation, 855 PID. See Pelvic inflammatory disease (PID)
major ring fractures, 853 Pilon fracture, 793
pelvic radiograph, 854 Pit viper envenomation, 525
882 Index
Pityriasis rosea, 361 toxins, 683

Placenta previa, 634 urinalysis, 680
Plague, 551 Polycystic kidney disease, 280
Platelet disorders Postconcussive syndrome, 823
description, 333 Posterior cord syndrome, 833
disseminated intravascular coagulation, 335–337 Posterior infarction, 16
idiopathic thrombocytopenic purpura, 334 Post-lumbar puncture headache, 585
Platelet transfusion, 316 Postpartum hemorrhage, 635
Pleural effusions Postrenal failure
description, 173 causes, 271
empyema, 175 description, 270
exudates, 174 Postseptal cellulitis, 647
hiccups, 176 Post-tonsillectomy bleeding, 504
mediastinal masses, 178 Posttraumatic vertigo and post-concussive syndrome, 513
mediastinitis, 176 Potassium
pneumoconioses, 177 hyperkalemia, 443–444
sarcoid, 177 hypokalemia, 441–443
superior vena cava syndrome, 178 PRBC. See Packed red blood cells (PRBC)
transudates, 174 Preeclampsia, 632
Pneumoconioses, 177 Premature ventricular contractions (PVCs)
Pneumocystis jirovecii, 161 description, 109
Pneumomediastinum, 137, 839 EKG changes, 110
Pneumonia treatment, 110
aspiration, 166, 167 Prerenal failure
classification, 153 causes, 264
C. pneumoniae, 160 description, 264
cultures and treatment, 164 Preseptal cellulitis, 646
cystic fibrosis, 165 Preterm birth and premature rupture of membranes (PROM), 634
disposition, 163 Priapism, 297
fungal PNA etiologies, 162 Prinzmetal’s angina
H. influenzae, 158 description, 6
K. pneumoniae, 159 predicting factors, 7
Legionella, 160 Prostatitis, 300
M. pneumoniae, 160 Protozoan pathogens
P. aeruginosa, 158 Cryptosporidium, 197
pathogens in HIV, 162 E. histolytica, 196
pathophysiology, 154 Giardia, 196
pediatric pneumonia, 156 Pseudomembranous enterocolitis, 198
P. jirovecii, 161 Pseudomonas aeruginosa, 158
S. aureus, 159 Pseudosubluxation, 828
special considerations, 155 Pseudotumor cerebri, 586
in special patients, 164 Psoriasis, 359
S. pneumoniae, 157 Psychiatric emergencies
treatment, 154 amnesia, 603
zoonotic PNA etiologies, 161 anorexia, 607
Pneumothorax anxiety, 606–607
description, 839–840 bipolar disorder, 605
diagnosis and management, 136 bulimia nervosa, 608
iatrogenic, 136 delirium vs. dementia, 601
pneumomediastinum, 137 factitious disorders, 609
spontaneous, 135 grief reaction, 605
Poisoned patient major depression, 604
airway assessment, 677 malingering, 609
antidotes selection, 684 Munchausen’s syndrome, 609
breathing assessment, 677 obsessive-compulsive disorder, 607
charcoal, 681 organic acute psychosis etiologies medical conditions, 602
circulation assessment, 677 organic acute psychosis etiologies medications/drugs, 602
dialysis, 682 organic vs. functional psychosis, 603
disability assessment, 677 personality disorders, 610
exposure, 678 schizophrenia, 606
laboratory studies, 679 somatoform disorders, 608
methods of drug elimination, 682 suicide, 604
overdose odor pearls, 684 PUD. See Peptic ulcer disease (PUD)
primary survey, 676 Pulmonary barotrauma, 529
primary survey adjuncts, 678 Pulmonary contusion, 843
secondary survey and adjuncts, 681 Pulmonary embolism (PE)
toxicology screens, 680 anticoagulation treatment, 85
Index 883
basic tests, 82 description, 48

clinical features, 80 diagnosis, 48
CT angiography, 83 treatment, 49
description, 79 Rheumatologic emergencies
disposition, 86 antiphospholipid syndrome, 810
embolectomy, 86 gout and pseudogout, 809
fibrinolysis, 85 joint fluid, 809
massive and less severe, 85 joint fluid analysis, 808
pretest probability, 82 rheumatoid arthritis, 809
pulmonary angiography, 84 systemic lupus erythematosus, 811
venography, 84 RhoGAM, 630
venous ultrasound, 84 Rib fractures, 841
VQ scanning, 84 RIFLE criteria, 263
Pulmonary hypertension, 76 Right bundle branch block (RBBB)
Pupil abnormalities, 640 description, 119
PVCs. See Premature ventricular contractions (PVCs) EKG changes, 120
Pyloric stenosis Right ventricular infarction, 15
description, 238 Rocky mountain spotted fever, 370
diagnosis, 239 Roseola infantum, 379
treatment, 239 Rubella, 377
R S
Rabies, 521–522 Salicylate, 699–700
Radiation, 548 Salivary gland disorders
Radiocontrast-induced nephropathy, 269 sialolithiasis, 502
Ramsay Hunt syndrome, 506 suppurative parotitis, 502
Ranson’s criteria, 232 viral parotitis, 501
Rapid sequence intubation, 179 Salmonella, 191
RBBB. See Right bundle branch block (RBBB) Salter-Harris fractures, 737
Reactivation tuberculosis, 169 Sarcoid, 177
Recompression therapy, 531 SBP. See Spontaneous bacterial peritonitis (SBP)
Rectal prolapse, 259 Scarlet Fever, 384
Red flags, 802 Schizophrenia, 606
Renal transplant, 295 SCIWORA, 833
Renal tubular acidosis, 279 Scombroid, 195
Respiratory acidosis Scrotal disorders, 295
causes of, 464 Seborrheic dermatitis, 360
description, 463 Second-degree type 1 Heart Block (2° type 1 HB)
treatment, 464 description, 122
Respiratory alkalosis EKG changes, 122
description, 464 Second-degree type 2 Heart Block (2° type 2 HB), 125
Respiratory distress and tracheostomy, 180 EKG changes, 124
Restrictive cardiomyopathy treatment, 124
clinical features, 55 Second impact syndrome, 824
description, 55 Sedative-hypnotics
treatment, 56 barbituates, 729
Retina benzodiazepines, 730
central retinal artery occlusion, 663 gamma-hydroxybutyrate, 730
central retinal vein occlusion, 665 Seizures
etiologies of central retinal artery syndrome, 664 adult status epilepticus management, 569
retinal detachment, 666 causes of, 566
Retinal detachment, 666 definitions, 565
Retrobulbar hematoma, 673 disposition, 570
Retropharyngeal abscess, 487 febrile, 570–571
Rewarming methods, 547 focal classification, 566
Rewarming physiology, 547 generalized classification, 565
Rhabdomyolysis mimics, 567
causes, 274 neonatal, 571
clinical features, 275 recurrent seizure evaluation, 568
complications, 276 routine first seizure evaluation, 568
description, 274 vs. syncope, 567
diagnosis, 275 Serotonin syndrome
treatment, 276 agents, 729
Rheumatic heart disease Hunter criteria, 728
884 Index
Severe asthma management, 142 lithium, 721–722

Severe asymptomatic hypertension, 75 malignant hyperthermia, 733
Sexual assault, 612 mercury, 718
Sexually transmitted diseases metal fume fever, 718
chancroid, 306 monoamine oxidase inhibitor overdose, 723
chlamydia, 302 mushrooms, 723–724
genital warts, 308 narcotics, 724
gonorrhea, 303 neuroleptic malignant syndrome, 727
granuloma inguinale, 307 organophosphates and carbamates, 725
Herpes Simplex, 305 phencyclidine, 714
lesions, 307 phenothiazines, 726–727
lymphogranuloma venereum, 306 sedative-hypnotics, 729–730
non-ulcer-forming processes, 302 serotonin syndrome, 728–729
syphilis, 304 strychnine, 731
Trichomoniasis, 303 tricyclic antidepressants, 731–732
ulcer-forming processes, 301 xanthines, 732
Sgarbossa Criteria, 13 Spinal cord injuries
Shigella, 191 anterior cord syndrome, 832
SIADH. See Syndrome of inappropriate antidiuretic hormone Brown-Sequard syndrome, 832
secretion (SIADH) central cord syndrome, 831
Sialolithiasis, 502 incomplete spinal cord injury, 831
Sickle cell anemia, 325 neurogenic shock, 834
acute chest syndrome, 326 posterior cord syndrome, 833
aplastic crisis, 327 SCIWORA, 833
description, 325 spinal cord syndromes, 830
infectious complications, 328 spinal shock, 834
neurologic complications, 328 transverse cord syndrome, 832
splenic sequestration, 327 Spinal cord syndromes, 830
vaso-occlusive crisis, 326 Spinal disorders, 600
SIDS. See Sudden infant death syndrome (SIDS) Spinal epidural abscess, 807, 808
Sinus barotrauma, 528 Spinal infections, 805
Sinusitis, 481 Spinal injuries, 826
SJS and TEN, 351 cervical spine clearance, 827
Skin cancers, 365 cervical spine evaluation, 827
Skull fracture, 824 odontoid fractures, 829
Smallpox, 551 pseudosubluxation, 828
Smith’s fracture, 751 stable cervical fractures, 828
Snake bites, 524 thoracolumbar fractures, 829
Sodium unstable cervical fractures, 828
hypernatremia, 439–440 Spinal shock, 834
hyponatremia, 437–439 Spinal stenosis, 803
Soft tissue lesions Spleen and liver trauma, 849
aphthous stomatitis, 498 Splenic sequestration, 327
candidiasis, 497 Spontaneous bacterial peritonitis (SBP), 226
herpangina, 498 Spontaneous intracranial hemorrhage, 563
HSV infections, 497 Spontaneous pneumothorax, 135
Somatoform disorders, 608 Sporotrichosis, 742
Specific toxins and poisons SSSS. See Staphylococcal scalded skin syndrome (SSSS)
alcohols, 692–695 Stable angina, 6
amphetamine, 696 Stable cervical fractures, 828
analgesics, 697–701 Staphylococcal scalded skin syndrome (SSSS), 352
anticonvulsants, 702–703 Staphylococcus, 193
antihistamines, 703 Staphylococcus aureus, 159
antimicrobials, 704 Sternal fracture, 842
arsenic, 715 Steroids, 141
cardiac medications, 705–707 Stingray stings, 524
caustic agents, 708, 709 Strawberry tongue, 499
chlorine, 710 Streptococcus pneumoniae, 157
cocaine, 711 Stroke and TIA, 558
cyanide and nitriles, 712–713 Stroke mimics, 557
hallucinogens, 713–714 Strychnine, 731
hydrocarbons, 719–720 ST-segment elevation, causes of, 9
hydrogen fluoride, 708 Subarachnoid hemorrhage (SAH)
hypoglycemic agents, 721 description, 591
iron, 716 diagnosis, 592
isoniazid, 704 treatment, 592
lead, 717 Subconjunctival hemorrhage, 652
Index 885
Submersion, 538–539 Thoracolumbar fractures, 829

Substance abuse/dependence, 613 Throat/neck/upper airway infections
Sudden infant death syndrome (SIDS), 183 bacterial tracheitis, 489
Suicide, 604 croup, 489
Superior vena cava (SVC) syndrome, 178 epiglottitis, 486
Suppurative parotitis, 502 Ludwig’s angina, 488
Supraventricular tachycardia (SVT) necrotizing infections, 488
description, 103 peritonsillar abscess, 485
EKG changes, 104 pharyngitis and tonsillitis, 484
treatment, 104, 105 retropharyngeal abscess, 487
Sympathetic chain and Horner’s syndrome, 639 Thromboembolism, risk factors, 80
Sympathomimetic toxidromes, 691 Thrombolysis, absolute and relative contraindications, 342
Syncope Thrombolytic therapy
cardiac, 78 complications, 20
causes, 77 successful, 20
description, 77 Thrombotic thrombocytopenic purpura (TTP), 331
evaluation, 79 Thyroglossal duct cysts, 495
vasovagal and orthostatic syncope, 78 Thyroid disorders, 407
Syndrome of inappropriate antidiuretic hormone secretion (SIADH) Thyroid hormones, 407
causes of, 431 Thyroid storm
central pontine myelinolysis, 433 diagnosis, 420
clinical features, 432 differential diagnosis, 419
laboratory abnormalities and testing considerations, 432 disposition, 421
treatment and disposition, 433 precipitating factors, 418
Syphilis, 304 specific clinical features, 418
Systolic heart failure, 25 treatment, 421
Tibial shaft fractures, 791
Tick paralysis, 595
T Tinea versicolor, 363
Tardive dyskinesia, 599 Tinnitus, 469
Tarsal tunnel syndrome, 799 Torsades De Pointes, 99
TB. See Tuberculosis (TB) Toxic hepatitis, 225
Temperature-related illness Toxic megacolon, 256
cold injury pathophysiology, 543 Toxic metabolic headache, 585
heat dissipation vs. generation, 540 Toxidromes
heat stroke, 542 anticholinergic, 687–688
hypothermia, 545–546 cholinergic, 688–689
localized cold injuries, 543–544 opioid, 689–690
minor/moderate heat illness, 541 sedative, 690
predisposing factors, 540 sympathomimetic, 691
radiation, 548 withdrawal symptoms, 692
rewarming methods, 547 Toxins, 552
rewarming physiology, 547 associated with anion gap, 686
Temporal arteritis, 668 ciguatera, 195
Tension headache, 583 hypoglycemia, 683
Testicular injury, 852 scombroid, 195
Testicular torsion, 298 that alter thermoregulation/cause temperature changes, 683
Tetanus, 554 tPA complications, 563
Tetralogy of Fallot, 129 Tracheobronchial injuries, 843
THC withdrawal, 616 Tracheostomy
Third-degree heart block (3° HB) and bleeding, 181
description, 125 and respiratory distress, 180
EKG changes, 126 Transfer dysphagia
Thoracic and lumbar pain localized causes, 201
ankylosing spondylitis, 803 neuromuscular causes, 200
back pain, 801 Transfusion therapy
back pain workup, 802 complications
cauda equina syndrome, 804 acute hemolytic transfusion reaction, 317–318
disk herniation, 802 allergic transfusion reaction, 319
diskitis, 806 delayed transfusion reaction, 319
lumbar strain, 802 febrile nonhemolytic reaction, 318
red flags, 802 infectious complications, 320
spinal epidural abscess, 807, 808 cryoprecipitate, 317
spinal infections, 805 fresh frozen plasma, 316
spinal stenosis, 803 massive blood transfusion, 315
transverse myelitis, 805 packed red blood cells, 314
Thoracic outlet syndrome (TOS), 776 platelet transfusion, 316
886 Index
Transport dysphagia U
description, 202 Ulcerative colitis
motor causes, 204 description, 256
obstructive causes, 203 diagnosis, 257
Transudates, 174 irritable bowel syndrome, 257
Transverse cord syndrome, 832 toxic megacolon, 256
Transverse myelitis, 805 treatment, 257
Trauma Ulcer-forming processes, 301
abdominal, 847–852 Ultraviolet keratitis, 657
airway assessment, 815 Umbilical cord prolapse, 635
basilar skull fracture, 824 Unstable angina, 6
blast injuries, 867 Unstable cervical fractures, 828
blunt eye, 670 Upper GI bleeding (UGIB)
blunt ocular trauma and globe rupture, 671 description, 215
brain herniation, 821 diagnosis and treatment, 216
breathing assessment, 815 disposition, 216
burns, 864–867 symptoms and signs, 215
cerebral contusions, 823 Uremia
chest (see Chest trauma) cardiovascular complications of, 280
circulation assessment, 816 gastrointestinal complications of, 282
classification of hemorrhage, 817 hematologic complications of, 281
concussion, 823 neurologic complications of, 281
disability assessment, 818 Urethral injury, 851
elevated ICP, 821 Urethritis, 300
exposure, 818 Urinalysis, 273
extremity injuries, 856–857 Urinary retention, 301
geriatric, 862 Urinary tract infections (UTI)
head trauma, 820 clinical features, 290
hyphema, 672 complicated vs. uncomplicated, 289
intracranial hemorrhage, 825 description, 288
mild TBI, 822 diagnosis, 291
moderate and severe TBI, 822 Uterine cancer, 627
pediatric, 858–861 UTI. See Urinary tract infections (UTI)
pediatric head trauma, 825 Uveitis and iritis, 660
pelvis and hip, 852–855 Uvular edema, 496
penetrating neck injury, 835–838
postconcussive syndrome, 823
pregnancy, 863 V
primary survey, 814 Valproate, 702
secondary survey, 819 Valvular emergencies
second impact syndrome, 824 aortic regurgitation, 39–41
skull fracture, 824 aortic stenosis, 37–38
spinal cord injuries, 830–834 mitral regurgitation, 33–35
spinal injuries, 826–829 mitral stenosis, 32–33
traumatic arrest and ED thoracotomy, 819 mitral valve prolapse, 35–36
traumatic seizures, 822 new murmur, 31
Traumatic aortic injury, 845 Variant angina. See Prinzmetal’s angina
Traumatic penis and foreskin disorders, 296 Varicella, 380
Traumatic seizures, 822 Vascular/related disease, 269
Trichomoniasis, 303, 621 Vaso-occlusive crisis, sickle cell anemia, 326
Tricyclic antidepressants (TCA), 731–732 Vasovagal syncope, 78
EKG changes, 101 Venous sinus thrombosis, 591
Trigeminal neuralgia, 505, 584 Venous stasis ulcers, 385
Triggering agents, 139 Ventilator management and risks, 147
Trismus, 505 Ventral hernias, 243
Troponin elevation, reasons for, 17 Ventricular aneurysm, predicting factors on EKG, 22
TTP. See Thrombotic thrombocytopenic purpura (TTP) Ventricular fibrillation (VF)
Tuberculosis (TB), 168 description, 117
diagnosis, 171 EKG changes, 118
initial evaluation, 170 Ventricular shunt headache, 589
pathophysiology, 169 Ventricular tachycardia (VT)
PPD and CXR, 170 description, 115
presentation, 170 EKG changes, 115
reactivation, 169 EKG features, 116
treatments and side effects, 171 treatment, 117
Tubular disease, causes, 268 Vertebral artery dissection, 515
Tympanic membrane perforation, 477 Vertebrobasilar infarction, 560
Index 887
Vertebrobasilar insufficiency, 515 candida vaginitis, 622

Vertigo description, 620
central (see Central vertigo) trichomoniasis, 621
description, 508
peripheral (see Peripheral vertigo) W
Vesicants, 553 Wallenberg Syndrome, 514
Vestibular neuronitis, 511 Warfarin
VF. See Ventricular fibrillation (VF) bleeding from, 340
Vibrio, 193 description, 339
Viral conjunctivitis, 651 skin necrosis from, 340
Viral diarrhea, 190 Wernicke’s encephalopathy, 601
Viral meningitis, 574 Wolff-Parkinson-White (WPW) syndrome
Viral parotitis (Mumps), 501 atrial fibrillation/flutter, 112–113
Visual field deficits, 641 atrioventricular reentry tachycardias, 112–113
Vitreous and intraocular cavities description, 111
endophthalmitis, 661 EKG changes in sinus rhythm, 112
vitreous hemorrhage, 662 treatment, 114
Vitreous hemorrhage, 662 Wrist
Volkmann’s ischemic contracture, 759 Colles’ fracture, 750
Volvulus perilunate and lunate dislocations, 755
description, 240 scaphoid fracture, 752
diagnosis, 241 scapholunate dissociation, 754
malrotation with, 241 Smith’s fracture, 751
treatment, 242 triquetral fracture, 753
Vomiting, 186
Von Willebrand’s disease (VWD), 339 X
VP shunt complications, 589–590 Xanthines, 732
VT. See Ventricular tachycardia (VT)
Vulvovaginitis
bacterial vaginosis, 621 Y
bartholin cyst and abscess, 622 Yersinia, 192

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What are the main topics covered in the book?

What are the main topics covered in the book?

What are some of the major medical conditions discussed?

What are some of the major medical conditions discussed?

Nailing the Written

Nailing the Written

ISBN 978-3-319-30836-4 ISBN 978-3-319-30838-8 (eBook)

Library of Congress Control Number: 2016946055

© Springer International Publishing Switzerland 2016

Printed on acid-free paper

This Springer imprint is published by Springer Nature

Brandon R. Allen, MD Department of Emergency Medicine, University of Florida College

B. Desai, MD, MEd

Acute Coronary Syndrome

Acute Coronary Myocardial

Acute Coronary Number 1 cause of

Location of Retrosternal left

May indicate a higher

Beware of pain May STILL be

Typically with Associated Classically occurs

2-fold higher risk

Poor predictors of ACS!

ACS Physical Exam

Initial Repeated injury to Atherosclerotic Rupture of the Platelet

Results in vessel Release of

Time & amount of

Tachydysrhythmias Higher degree blocks

Other Causes of Acute Coronary Syndrome

Cocaine and Chest Pain

May cause premature

Only 5–6 % will

MI present with May cause unopposed

Unopposed a– Worsened Extremely high

Treatment Nitroglycerin Benzodiazepines

Atypical Chest Pain

Populations with atypical chest pain

Atypical presentations are typical in

The chest pain may be different

Can occur at Can occur with

Other atypical findings

Pain unrelated Pain relieved Weakness and No chest pain

Stable and Unstable Angina

Stable angina Fixed plaque

Pain of stable Crescendo-

Relieved by? Nitroglycerin Rest

Pitfall of stable May progress to

Change in chest Frequency,

Pain of unstable NOT Palliated by

Pitfall of Have high risk of

Prinzmetal’s or Variant Angina

May NOT have

What Factors Predict Prinzmetal’s Angina?

Acute Myocardial Infarction

Single best test Should be done within 10 Up to 5 % will be

Normal Nonspecific Diagnostic

New ST-depressions Positive predictive

ST Segment Transmural Involves full-thickness “Q-wave” “Significant Q wave”= .04 mm

NO ST Segment Subendocardial Does not involve full- “Non Q-wave”

Subendocardial Initially may have lower The long term prognosis