Increased Intracranial Pressure

and other Neurological Trauma

Intervention on 1st only if

significant

UNIT 2, CHAPTER 6

NEUROLOGIC AFFECTATION caused

by:

INTRACRANIAL PRESSURE

ICP is the pressure exerted in

the cranium by its contents: the
brain, blood, and CSF.

ICP is measured with a monitor

in the ventricle, brain
parenchyma, or the subarchnoid
space. Recognition of increased
ICP is one of the most important
assessments made by the nurse
for neurologic disorders.

Influenced by adburpt changes

on intrathoracic pressures such
as COUGHING, VALSALVA
(Queckenstedt's Maneuver),
communication with the
VASCULATURE (venous and
arterial system).

Brain volume

Blood

CSF in dura mater

The brain and the cranium

Munro Kellie hypotesis:

Cranium cannot expand when

any of its components expand

Skull's components are

incomprehensible

Volume inside the cranium is

fixed

Notes:
7-15 mmgh: normal ICP
>20 mmhg: needs intervention

Cerebral Perfusion Pressure:

Mgt:

- Is the amount of blood from the

systemic circulation required to
provide adequate oxygen and glucose
for brain metabolism.

Check for neurologic changes

Assessment
Intervention on 2nd, 3rd, 4th
assessment only

Formula:
CPP = MAP ICP

Where: MAP = SP + (DP x 2) / 3

An obstruction to the outflow of

CSF (cerebral infarct)

Presence of abscess secondary

to brain injury

Ingestion or accumulation of
toxin that impairs blood flow to
and / or from the brain.

Systemic hypertension

Vasodilation from increases CO2

(PaO2)

Increased Intrathoracic Pressure

Increase venous pressure

Note:
MAP- mean arterial pressure
Normal CPP- 72 mmhg
Pedia CPP- 60 mmgh
At rest: intrapulmonary 760
mmHg, intrapleural 756 mmgh
Inspiration: intrapulmonary 757
mmgh, intrapleural 754 mmgh
Expiration: intrapulmonary 763
mmgh, intrapleural 754 mmgh

ICP MEASUREMENT

INTRAVENTRICULAR
CATHETER- attached thru ct
scan, a hole in the skull is made

Subdural screw (aka bolt)boring of the skull. Placed in

between brain and spinal cord.
Used during emergency
situations (lasts for several days
to weeks.

Epidural sensor- plaCP

ETIOLOGY OF INCREASED ICP

Increased ICP is most often

associated with space
occupying lesions such as
tumor, edema, or bleeding.

Note: Increase venous pressured/t venous sinus thrombosis,

heart failure, obstructiono of
superior mediastinal or jugular
vein

RISK FACTORS FOR INCREASED

ICP

Head Injury

Brain Tumors

Cerebral Bleeding

Hydrocephalus

Edema from Surgery or Trauma

CAUSATIVE FACTORS &

MANIFESTATIONS
PRECIPITATING FACTOR:

1. Cerebral Edema & Brain

Swelling

1B. BRAIN SWELLING:

-

2. Herniation Syndrome
3. Cerebral Perfusion

Increase in the brain bulk

caused by an increase in
cerebral blood volume from
dilated cerebral blood vessels.

Note: Cerebral edema and brain

swelling are not the same

CAUSATIVE FACTORS &

MANIFESTATIONS
1A. CEREBRAL EDEMA:
-

Increase in the brain bulk

caused by an increase in the
fluid surrounding the tissue of
the brain, such as in the
extracellular spaces or the
white matter, or within the cells
themselves.

Note: Happens when there is

disruption in blood brain barrier

Manifestations of Cerebral Edema:

-

No single set of clinical

manifestations occur in all
patients.

Clinical manifestations are

subtle.

Common clinical manifestations

includes:
1. Alteration in Level of
Consciousness and Decrease in
GCS.

Fluids: electrolytes, protein, blood

2. Aphaxia (partial or complete)
Post surgery- cerebral edema is
expected but does not last for
long (2-3days only)
Mannitol (osmotic diuretic) and
steroids are prescribed post
surgery
Mannitol- check for hypotension
(IV bolus so it will not retain in
CSF)

3. Pupillary Reactivity, Blurring,

Double Vision
4. Motor and Sensory Disability
5. Changes in Cardiac Rate and
Rhythm
6. Headache and Vomiting
(projectile)
7. Cushings Triad

8. Hyperthermia

d. Cingulate Herniation

Note: Sublte- not obvious

2.

Infratentorial (Tonsillar)

HS
RIC- greatest manifestation;
restlessness, irritability, and
confusion
Cushing's triad- increase in
systolic pressure, wide pulse
pressure (N=30-40 mmgh) , and
bradycardia (seen on severe head
trauma)
Hyperthermia- affectation on
hypothalamus

DIAGNOSING Cerebral Edema:

1. Skull Radiography (X- ray)
2. CT Scan
3. MRI

Note: Herniation- last resort

before displacement happens. All
berniation are considered
EMERGENCY

SUPRATENTORIAL HS:
A. Transcalvarial Herniation
-

It occurs with open head injury

when brain tissues are
extruded through an unstable
skull force.

Note: Brain is forced.

Manifestation varies to which part
of the brain is affected
Medications- given to control
swelling

Note: Skull xray- lesser accuracy

Lumbar function- not considered
because of cerebral herniation on
spinal cord
2. HERNIATION SYNDROME:
Five Types of H.S:
1. Supratentorial Herniation
a. Transcalvarial H.
b. Central Transtentorial H.
c. Lateral Transtentorial H.

B. CENTRAL TRANSTERORIAL
HERNIATION
-

Is the downward displacement

of the diencephalon through
the tentorial notch.

Note: (+) rapid change in LOC

As ICP increase, chyne stokes
respiration (slow shallow
respiration >> rapid deep
respiration >> slow shallower
respiration >> apnea for 10-20
seconds)

D. CINGULATE HERNIATION
C. LATERAL TRANSTEntorial
HERNIATION

AKA Uncal Herniation

Uncal Herniation: because as

the temporal lobe is
compressed, the UNCUS (the
anteromedial portion of the
hippocampus) of the
hippocampal gyrus shifts FROM
THE MIDDLE FOSSA through
the tentorial notch into the
POSTERIOR FOSSA.

Occurs from displacement from

by masses in or along temporal
lobe.

It occurs when the frontal lobes of the

cerebrum are compressed, resulting in
compression of the cingulate
gyrus (an arch shaped convolution
situated just above the corpus
collosum) under the Falx cerebri.
Note: Reslust of edema, increased
ICP
Manifestations similar with lateral

2. INFRATENTORIAL (TONSILLAR)
HERNIATION SYNDROME

Occurs when the cerebral tonsil

shifts through the foramen
magnum, compressing the
medulla and upper potion of the
spinal cord.

Increasing pressure in the

posterior fossa, often secondary
to cerebellar bleeding, is the
usual underlying problem.

Note: Ipsilateral- Side of the pupil

affectedside of the brain
affected
Decreased level of consiousness
Manifestations- Stupor,
unconsious, coma followed by
chyne stokes
Central Neurogenic
hyperventilation- CNH is
characterized by deep and rapid
respirations (not less than 25
breathes per minute) a
compensatory to acquire oxygen
(involuntary; increased metabolic
rate causing COMA)
Extremities will decorticate or
deceribrate (COMA)

Note: Aka cerebellar tonsilar

herniation
Erratice changes in bp, pr, hr, and
rr
Decrease LOC
Tonsillar herbiation- manifestation
include stiff neck
Quadriparesis- most prominent
sign

which bruises and lacerate brain

tissues.
Traumatic Brain Injury

Is an insult to the brain that is

capable of producing physical,
intellectual, emotional, social,
and vocational changes.
People who encounters this type
of injury can either result to:

a. Short or Long term

Hospitalization
b. Chronic Disability
c. Persistent Vegetative State
(PVS)
d. Death

Motor vehicle accidents are

the leading cause of head
injuries. Other causes include
assaults, falls, and sportsrelated injuries.

Mechanism of Traumatic Brain

Injury
Pathophysiologic Principles:
1. The brain is unable to move
inside the skull, movement of
the brain can result in injuries in
different locations.
2. Primary injuries result in direct
impact that causes the brain to
move and scrapes the skulls
irregular inner prominences,

3. Disruption of the brains small

surface blood vessels may
occur.
Note: Small bleeding- causes
neurological dysfunction
Types of Traumatic Head Injuries
1. Coup Contrecoup Injuries
Coup injury occurs under the site of
impact with an object.
Contrecoup injury occurs on the side
opposite the area that was impacted.
2.

Penetrating Trauma
Are forms of primary injury
caused by a head wound made
by a foreign object (e.g. knives
or bullets) or those made by
bone fragments from a skull
fracture.

3. Skull Fractures

Are cause by force sufficient to

fracture the skull and cause
brain injury.

Three (3) Types of Skull Fracture:

a. Linear Skull Fracture
b. Depressed Skull

Fracture

c. Basilar Skull Fracture

d. Compound fracture

e. Diastatic skull fracture

Note: Compound- hole +
irregularities
Depression- (-) fragments, high
risk of creating hemorrhage (brain
might also by affected)

Is one of the most common and

devastating types of traumatic
brain injury;

Damage occurs over a more

widespread area than in focal brain
injury.
Classified as:

Basilar- base of the skull (racoon's

eye, battle's sign, halo sign)

a. Mild

Linear- line

b. Moderate

Diastatic- fracture is located

where sutures are placed
(lambdoidal suture MC)

c. Severe
Note: May lead to permanent
vegetative state

Cold compress for 24 hours

4. Concussion and
Contusion

Classification- determined by the

extent of unconsiousness

6-24 hours MILD,

associated with short
term disability

>24 hours with

incomplete recovery
upon awakening
MODERATE

Prolonged formT,
abnormal
extension/flexion of
the extremities with
hypertension, fever
and iicp

Concussion: a head trauma that may

result to loss of consciousness for 5
minutes
Contusion: With extensive damage
than the previous resulting to bruised
brain
Note: Latin concuture: to shake
violently
Concussion: May cause temporary
disorientation, temporary memory
loss, unconsiousness
Contusion: may cause permanent
damage
5. Diffuse Axonal Injury
(DAI)

May lead to multiple sclerosis

(myelin sheath)

Focal Injuries
1. Epidural Hematoma

Manifestations:
1. Unconsciousness or transient
LOC

2. Subdural Hematoma
a. Acute

2. A conscious client usually have

severe headache

b. Chronic

3. Irritability

3. Intracerebral Hematoma
1. Epidural Hematoma
Buildup of blood occurs between the
dura mater and the skull.
Manifestations:

4. Lapses of coma state

Subdural Hematoma
B. Chronic Subdural
Hematoma

a. Unconsciousness immediately
after the head trauma
b. The client awakens but is quite
lucid
c. Pupil dilation occurs rapidly on
the same side of the hematoma
d. The client may have periodic
coma state
2. Subdural Hematoma

Is the collection of blood in the

subdural space.

Tearing of the bridging veins over the

brain causes the bleeding.
A. Acute Subdural Hematoma

Results from brain or blood

vessel laceration

Results from stretching of the

bridging veins. These veins
becomes rigid and easily
ruptures.

Manifestations:
1. Drowsiness, inattentiveness
2. Incoherence
3. Personality change
4. Hemiparesis
5. Transient LOC
Note: May be related with
hypertension.
Managed surgically (crainiotomy)
3. Intracerebral Hematoma

Results from bleeding directly

from the brain tissue and may
occur at the area of injury.

Manifestations are the same

with epidural or subdural
hematoma

Note: Non traumatic may become

intracerebral hematoma
Types of brain hematoma:
summary

Abnormal Changes Resulting from

Altered Perfusion: Affecting the
Cerebral Cortex
1. Altered level of consciousness
2. Altered perception of time, then
place, lastly person
3. Motor deficits

Epidural: between skull and dura

mater
Subdural: between dura mater and
brain
Intracranial hemorrhage: reached
the brain tissue
SIGNIFICANT CONSIDERATIONS IN
PATIENT ASSESSMENT (WITH IICP)
1. CHANGE is the key word.
2. After performing therapeutic
interventions such as suctioning
and changing in position, the
patient may exhibit changes.

4. Speech deficits
5. Memory deficits
6. Hyperreflexia
7. Babinskis Sign
8.

Seizures

9.

Decorticate rigidity

10.Emotional ability
11. Altered sensory perception
12.Cheyne Stokes Respiration
13.. Headache
14.Nausea and Vomiting
15.Papilledema

3. Observe for short and transient

changes or deterioration
Normal Neurologic Response
1. Alert, oriented to person, place
and time.
2. Responds appropriately to
verbal commands.
3. Eyes open spontaneously with
any stimulus, unless in a deep
sleep.

Abnormal Changes Resulting from

Altered Perfusion: Affecting the
INFERIOR PART of the Cerebral
Cortex
1. Papillary changes
2. Loss of reaction to direct light
3. Visual Field Loss
Abnormal Changes Resulting from
Altered Perfusion: Affecting the
DIENCEPHALON

1. Altered Temperature
2. Cheyne Stokes Respiration
Abnormal Changes Resulting from
Altered Perfusion: Affecting the
POSTERIOR PITUITARY GLAND
1. Diabetes Insipidus

2. Flaccidity
Abnormal Changes Resulting from
Altered Perfusion: Affecting the
MEDULLA
1. Dysfunction of CN VIII
2. Dysfunction of CN IX
3. Dysfunction of CN X

Abnormal Changes Resulting from

Altered Perfusion: Affecting the
MIDBRAIN
1. Dysfunction of CN III
2. Dysfunction of CN IV
3. Central Neurogenic
Hyperventilation
Abnormal Changes Resulting from
Altered Perfusion: Affecting the
UPPER PONS
1. Dysfunction of CN V
2. Dysfunction of CN VI
3. Dysfunction of CN VII
4. Central Neurogenic
Hyperventilation
5. Abnormal extension posture
6. Pinpoint pupils
Abnormal Changes Resulting from
Altered Perfusion: Affecting the
LOWER PONS
1. Apneustic breathing

4. Dysfunction of CN XI
5. Dysfunction of CN XII
6. Projectile vomiting
7. Cushings Triad
8. Ataxic
MANAGING IICP:
1. To maintain cerebral
oxygenation
1. The swollen or bruised brain has
an increased need for oxygen
and glucose. Keep PaO2 must
be kept between 90 100
mmHg.
2. Routine prophylactic
hyperventilation (with the use
of mechanical ventilator) must
be avoided unless the client
shows evidence of cerebral
herniation.
3. Steroid may be prescribed by
the physician.
2. To decrease IICP
1. Maintain proper ABCs

2. Hypoxemia and Hypotension

should be expected in head
injuries.
3. Administration of osmotic
diuresis
4. Monitor renal function and blood
pressure.

1. A score of 8 or less indicates

coma;
2. The following criteria may
indicate invalid GCS, but other
observable cues will be
documented and used :

5. Elevate the head.

a. The client is intubated and

cannot speak

6. Hypertonic Saline Solutions per

IV

b. Eyes are swollen closed

7. Prevent complications
8. Closely monitor the glucose
level
9.

Monitor Intracranial pressure

and GCS.

10.Prevent Intracranial
Hypertension
Note:
2. Any vascular problems initiate
ventilation
3. problem: mannitol- has the
tendency to retain on the brain of
the pt. and may lead to
continuously decreasing fluid
which is also not good. Deliver
mannitol bodies the faster it gets
in the body the faster it get
excreted.

3. To maintain optimal neurologic

function
Closely monitor the GCS of the
patient. Consider the ff:

c. The client has commnication

(language) barrier
d. The client has hearing loss
e. The client is blind
f.

The client has aphasia

g. The client is paralyzed or

hemiplegic
3. The first GCS score recorded
will be the baseline score.
4. Subsequent scores are used to
monitor development or deterioration
5. A single measurement or score
is not used to predict the outcome of
the condition.
6. The first change in patients
with altered cerebral tissue perfusion
is deterioration on the level of
consciousness.
4. To prepare for rehabilitation
1. This event can only be assumed
after medical and surgical
clearances.

2. Assess readiness of the patient

and the family.
3. Take time in assisting the
patient. Do not rush the
rehabilitative procedures,
outcomes, and expectations.
NURSING CARE
Nsg. Dx: Airway Clearance

2. Monitor neurologic examination

as per unit standard.
3. Maintain ICP < 20 mmHg. Treat
ICP > 25 mmHg with diuresis,
SCF drainage, mild
hyperventilation.
Note: CSF changes not only
should be monitored but to know
specifically the cause

Goal: Patient will be free from

respiratory distress
Intervention:
1. Maintain patent airway using
suctioning or coughing

Nsg. Dx: Intracranial Adaptive

Capacity
Goal: The client will be free from
seizure and have a functional
neurologic status.

2. Elevate head to 30 degrees

3. Assess client ability to maintain
own airway
4. Assess patency of artificial
airway
5. Monitor oxygenation using pulse
oximetry
6. Provide oxygen support
Nsg. Dx: Tissue Perfusion
Goal: Patient will maintain cerebral
perfusion
Intervention:
1. Maintain blood pressure within
ordered range. Assess
hemodynamic (blood
movement) to ensure
appropriate cardiac output.

Interventions:
1. Assess neurologic status as per
unit standard. Include mental
status, motor, sensory, and the
cranial nerves.
2. Monitor ICP to ensure oxygen
and nutrients are delivered to
the brain.
3. Monitor for seizures. Administer
antiseizure medications as
ordered.
Nsg. Dx: Fluid Volume: Deficit or
Excess
Goal: Client will maintain fluid and
electrolytes within normal limits and
will maintain a regular diet.
Interventions:

1. Monitor acid base balance,

fluid intake and output, and
electrolyte results.

3.

Assess the clients level of pain

and if the client s not able to
verbally express pain, use other
pain assessment tools.

4.

Educate the client about

analgesics and appropriate
management of pain using
various types of analgesia.

2. Assess fluid volume status.

3. Provide fluid and electrolytes
via IV access until patient can
able to take oral fluids.
Nsg. Dx: Hyperthermia
Goal: The client will be maintained
without fever
Interventions:
1. Monitor temperature per unit
standard.
2. Initiate treatment of fever once
temperature is >38.5 c

5. Provide information about the

sedative effects of certain
analgesics.
Note: To prevent drug
dependency, when the right time
to tolerate pain and when to use
medication.
Nsg. Dx: Nutrition Imbalance
Goal: The client will maintain a
normal weight and will consume a
balanced diet.
Interventions:

Nsg. Dx: Acute or Chronic Pain

1. Assess caloric consumption

Goal: The client will have pain control

and will not become depressed as a
result of pain.

2. Provide information about

appropriate dietary intake

Interventions:

3. Educate regarding weight loss

or weight gain as appropriate.

1. Educate the client regarding

medications, dosage, and side
effects.
2. Provide information about
appropriate pain management
and weaning from pain
medication.

Nsg. Dx: Urinary Retention

Goal: The client will be continent and
without bladder distention
Interventions:

1. Assess for bladder distention,

particularly after urinary
catheter is removed.
2. Insert urinary catheter if unable
to void, has history of urinary
retention, or prostatic
hypertrophy or had urine output
of less than 250 ml / day.
3. Assess for volume, color, odor
of urine; frequency of urination,

difficulty with urination , or over

urination.