Emergency Internal Medicine

Rizal Hafiz
 Kegawatan Penyakit Dalam
1. Nefro : CKD, ggg. Cairan & elektrolit, asam basa
2. Cardio : SKA, aritmia, syok cardio, oedem pulmo akut
3. Gastro : PSCBA, encephalopati hepar, pankreatitis akut
4. Endokrin : hipoglikemia, KAD, HONK, krisis tiroid
5. Pulmo : asma akut, hemoptoe, gagal nafas
6. Hema : febrile neutropeni, sindr lisis tumor, sindr
paraneoplasia
7. Rheuma : SLE
8. Tropik : DHF, sepsis
9. Geriatri : konfusio akut, hipertermi, stroke
 Nefrology
Kegawatan Uremi
(Tx utama = dyalisis)
1. Asidosis metabolik :
koreksi bicnat bila pH<7 atau HCO3<12meq
0,5x0,3xBExBB (dalam 150cc D5% habis 4 jam)1 flash
bicnat 25meq
2. Hiperkalemi
 ringan-sedang (5,5-7,5) Ca polystirene 4x15gr
 Berat (>7,5) Ca Glukonas 0,5mg/KgBB + bicnat 45-90meq +
10-20 U insulin reguler dlm 25-50gr D40% habis 4 jam
 Nefro..
3. Overhidrasi :
 O2 masker
 Furosemid 40-80mg s/d 250mg
 Morfin 2,5mg
4. Hipertensi
 Emergency : diturunkan sesuai target dlm 1 jamNikardipin 5mg/jam
dinaikkan 2,5mg/5menit max 30mg/jam, target 10-15% MABP atau
diastolik 110
 Urgency : dgn antihipertensi oral, diturunkan dlm 24jam
5. Kejang uremik : diazepam 5-10mg iv pelan
6. Perdarahan : dialisis
7. Infeksi : antibiotik
 Hipertensi emergency
• Hipertensi emergensi : meningkatnya tekanan
darah secara akut dan cepat yang menyebabkan
kerusakan organ target. Umumnya tekanan
diastolik > 120 mmHg. Pengendalian tekanan
darah diharapkan dalam 1 jam
• Hipertensi urgensi : tekanan diastolik > 120
mmHg tanpa disertai kerusakan organ.
Pengendalian tekanan darah diharapkan dalam
24 – 48 jam.
• Hipertensi berat : sistolik > 180 mmHg dan
diastolik > 110 mmHg.
End-Organ Damage Associated Hypertensive Emergencies

End-Organ Damage Type No of Cases (%)

Cerebral Infarction 26 (24.5)
Intracerebral or sub-arachnoid
5 (4.5)
hemorrhage
Hypertensive encephalopathy 18 (16.3)
Acute pulmonary edema 24 (22.5)
Acute congestive heart failure 15 (14.3)
Acute myocardial infarction or unstable
13 (12.0)
angina pectoris
Eclampsia 5 (4.5)
Aortic dissection 2 (2.0)

Zampaglione, et al. AHA ; 27 (1) : 144

 SIMPLE APPROACH TO HYPERTENSIVE CRISIS

BP > 220/120 mmHg

Neurological sign Headache

(encephalopathy or stroke) No neurological signs
Retinopathy grade 3-4 No target organ damage
Severe chest pain
(Ischemia or dissecting
URGENCY
aneurism)
Pulmonary edema
Eclampsia Identify the cause
Cathecolamine excess In panic attacks or anxiety use
Acute renal failure analgesic, anxiolytics
Otherwise use oral antihypertensive
agents
EMERGENCY recheck in 6-24 hours

Captopril, clonidine, labetalol

Intravenous therapy
 JNC 7 Recommendation for
Hypertensive Emergency
Drugs Dosage Onset Duration
Sodium 0.25-10 ugr/kg/min Immediate 1-2 minutes
nitroprusside after infusion
stopped
Nitroglycerin 5-500 ug/min 1-3 minutes 5-10 minutes
Labetolol HCl 20-80 mg every 10-15 min or 5-10 minutes 3-6 minutes
0.5-2 mg/min
Fenoldopan 0.1-0.3 ug/kg/min <5 minutes 30=60 minutes
HCl
Nicardipine 5-15 mg/h 5-10 minutes 15-90 minutes
HCl
Esmolol HCl 250-500 ug/kg/min IV bolus, 1-2 minutes 10-30 minutes
then 50-100 ug/kg/min by
infusion; may repeat bolus
after 5 minutes or increase
infusion to 300 ug/min

JNC 7, 2003
 AHA 2007 Recommendation for
Hypertensive Emergency

Drug I.V. Bolus Dose Continous Infus Rate

Labetalol 5 – 20 mg every 15’ 2 mg/min (max 300mg/d)

Nicardipine NA 5-15 mg/h
Esmolol 250 ug/kg IVP loading dose 25-300 ug/kg/m
Enalapril 1,25-5 mg IVP every 6 h NA
Hydralazine 5 – 20 mg IVP every 30’ 1,5-5 ug/kg/m
Nipride NA 0,1-10 ug/kg/m
NTG NA 20-400 ug/m

AHA/ASA Guideline, 2007 update. Stroke. 2007;38: 2001-2023.)

 CHEST 2007 Recommendation for
Hypertensive Emergency
Acute Pulmonary edema / Nicardipine, fenoldopam, or nitropruside combined with
Systolic dysfunction nitrogliceryn and loop diuretic
Acute Pulmonary edema/ Esmolol, metoprolol, labetalol, verapamil, combined with
Diastolic dysfunction low dose of nitrogliceryn and loop diuretics
Acute Ischemia Coroner Labetalol or esmolol combined with diuretics
Hypertensive encephalopaty Nicardipine, labetalol, fenoldopam
Acute Aorta Dissection Labetalol or combined Nicardipine and esmolol or combine
nitropruside with esmolol or IV metoprolol
Preeclampsia, eclampsia Labetalol or nicardipine
Acute Renal failure / Nicardipine or fenoldopam
microangiopathic anemia
Sympathetic crises/ cocaine Verapamil, diltiazem, or nicardipine combined with
oveerdose benzodiazepin
Acute postoperative Esmolol, Nicardipine, Labetalol
hypertension
Acute ischemic stroke/ Nicardipine, labetalol, fenoldopam
intracerebral bleeding
CHEST, 2007
 INASH 2008 Recommendation for
Hypertensive Emergency
Drugs Preparations Caution
Clonidine 150 mcg/ampoule Rebound effects

Diltiazem 10 mg dan 50 mg/amp Use carefully in patients

with heart conduction
insufficiency and heart
failure
Nicardipine 2 mg dan 10 mg/ -
amp
Labetalol NA in Indonesia -

Nitroprusside NA in Indonesia -

INASH, 2008
 Commonly used drug in
Hypertensive emergency

CLONIDINE
• Reduce peripheral sympathetic tone by central
stimulation of 2- receptor.

• Unpredictable onset of action.

• Adverse effect : sedation, dry mouth, constipation

and a tendency to a overshoot or
rebound hypertension on withdrawn.
W.H. Frishman, et al., Cardiovascular Pharmacotherapy, 1996
 Commonly used drug in
Hypertensive Emergency

NITROGLISERIN

• Strong vasodilator (arterial- and veno-dilator).

• Direct interacting with nitrate receptors on vascular smooth
muscle.
• A rapid onset and duration of action.
• Adverse effect : headache, tachycardia, nausea, vomiting.
 Commonly used drug in
Hypertensive Emergency

DILTIAZEM.
Þ Useful for hypertensive emergency and urgency.
Þ Acts as calcium slow-channel blockers.
Þ Dose-dependent :
• Predictable onset of action
• Rapidly reduced BP.
• No rebound on withdrawn
Þ Adverse effect : bradycardia, hypotension, headache, flushing.
Þ Has antiischemic and antiarrhythmic effect (class-IV)
 Commonly used drug in
Hypertensive Emergency

NICARDIPINE

is a second generation dihydropyridine derivative

Calcium Channel Blocker with high vascular
selectivity and strong cerebral and coronary
vasodilatory activity
Onset of actions : 1 to 5 min,
Duration of actions of 4 to 6 h
IV Nicardipine has been shown to reduce both
cardiac and cerebral ischemia
CHEST, 2007
 NICARDIPINE

 The Only Calcium Antagonist Recommended by

JNC 7 ,AHA 2007, and CHEST 2007
 Rapid and stable antihypertensive effect
 Increased blood flow in major organs
 No risk of blood pressure rebound after discontinuation
 Nicardipine has favorable renal effect by increase GFR ,
Renal Blood Flow and reduce
Total Renal Vascular Resistance
 Obat yang tidak direkomendasikan
untuk hipertensi krisis

• Nifedipine : penurunan tekanan darah yang

cepat, sulit dikendalikan, menyebabkan iskhemia
organ target
• Nitroglycerine : venodilator kuat, ‘preload’ dan
‘cardiac output’ turun, iskhemik organ target
• Hydralazine ; vasodilator kuat, sulit diprediksi,
efek lama
• Diuretika : kecuali pada keadaan ‘volume
overload’

Varon J and Marik PE. Critical Care 2003

Intravenous Drugs
for Hypertensive Emergency

DRUGS DOSAGE ONSET of ACTION

Nitropruside 0.25 – 10 g/kg/min as IV Infusion Instantaneous
Nitroglycerin 5 – 100 g/min as IV Infusion 2 – 5 min
Nicardipine 5 – 15 mg/hours IV 5 – 10 min
Hydralazine 10 – 20 mg IV 10 – 20 min
10 – 50 mg IM 20 – 30 min
Enalapril 1.25 – 5 mg q 6 hours 15 min
Fenoldopam 0.1 – 0.3 g/kg/min < 5 min
Phentolamine 5 – 15 mg IV 1 – 2 min
500 g/kg/min for 4 min, then 150 –
Esmolol 1 – 2 min
300 g/kg/min IV
20 – 80 mg IV bolus every 10 min
Labetolol 5 – 10 min
2 mg/min IV Infusion

Braunwald , 2001
Commonly Used Parenteral Antihypertensive Drugs

Lancet 2000; 356: 411–17

 DILTIAZEM-Injection
Dosage and Administration
Each
Eachampoule
ampouleof
ofDILTIAZEM-Injection
DILTIAZEM-Injectionshould
shouldbe
bedissolve
dissolvein
in
at
atleast
least55mL
mLaquadest
aquadestor
orNaCl
NaClor
orglucose
glucosesolution
solutionbefore
beforeuse.
use.

BOLUS I.V. INJECTION

0.20 – 0.35 mg/kg BW

Adult (50kg) : 1 Ampoule (1 – 3 minutes)

DRIP I.V. INFUSION (Flat)

5 – 15 mcg/kg BW/min
Adult (50kg) : 15mg/hour – 45 mg/hour

DRIP I.V. INFUSION (maintenance)

1 – 5 mcg/kg BW/min
Adult (50kg) : 5mg/hour – 15 mg/hour
Bolus I.v.
0.2 mg/kg
10% MBP reduction
10’ From Baseline
Drip infusion
50 mg/hour
20% MBP reduction
20’ From Baseline
Drip infusion
30 mg/hour
Target MBP
30’ Level
Drip infusion
5-10 mg/hour

Every 30-60 minutes observation

Switch to Oral
DILTIAZEM 180SR
 Nefro…
Gangguan keseimbangan cairan
1. Hipovolemik
“air dan Na keluar dlm jumlah yg sama”
koreksi dgn RL/NaCl isotonik, jumlah dan
kecepatan disesuaikan dg klinis kehilangan cairan :
ringan (<20%)
sedang (20-40%) x6%xBB
berat (>40%)
 Nefro….
2. Dehidrasi
“kehilangan air>Na”  hipernatremi
koreksi dg D5% sesuai kebutuhan :
FD : 0,4xBBx((Na Plasma/140)-1)
kecepatan koreksi tdk >0,5meq/jam
Ex : pria 60kg, dehidrasi dg Na160meq, IWL 40cc/jam, UO 1,5L/24jam
Answ : delta Na : 20kec.koreksi 20/0,5 = 40 jam
FD : 0,4x60x((160/140)-1) = 3,42L
IWL : 24X40cc = 0,96L
UO : = 1,5L
5,89L dlm 40 jam = 0,15L/jam
 Nefro…
 Ggg keseimbangan elektrolit
1. Natrium
 hipoNa :
 Na>125 : NaCl 3x500mg po
 Na<125 : (135-X)x0,6xBBNaCl 3%
 akut<48jam : 5meq dlm 1 jam I, selanjutnya
1meq/jam s/d Na 130meq
 Kronik>48jam : perlahan 0,5meq/jam
 Nefro…
hiperNa
koreksi dg D5% sesuai kebutuhan :
FD : 0,4xBBx((Na Plasma/140)-1)
kecepatan koreksi tdk >0,5meq/jam
Ex : pria 60kg, dehidrasi dg Na160meq, IWL 40cc/jam, UO
1,5L/24jam
Answ : delta Na : 20kec.koreksi 20/0,5 = 40 jam
FD : 0,4x60x((160/140)-1) = 3,42L
IWL : 24X40cc = 0,96L
UO : = 1,5L
5,89L dlm 40 jam = 0,15L/jam
 Nefro…
2. Kalium
hipoK
 K>3,5 : KCl 3x1tab
 K<3,5 : (4,5-X)x0,4xBB = Ymeq inj KCl 7,46%
25meq/25cc, kecepatan 2meq/jam (SP Y/2=Z)Ymeq
habis dlm Z jam
hiperK
 ringan-sedang (5,5-7,5) Ca polystirene 4x15gr
 Berat (>7,5) Ca Glukonas 0,5mg/KgBB + bicnat 45-
90meq + 10-20 U insulin reguler dlm 25-50gr D40% habis
4 jam
 Nefro..
3. Magnesium
HipoMg Ringan : renapar/aspar 3x1tab
hipoMg berat : inj MgSO4 20%/40% 25cc
3gr dlm D5% habis 3jam, dilanjut 6gr dlm 21jam (3-3-6-1)
4. Calcium
HipoCa ringan : CaCO3 3x500mg
hipoCa berat : Ca glukonas iv bolus 10-30cc dlm D5%
150cc selama 10menit
hiperCa : hidrocortison 200-300mg iv, furosemid, atasi
volume defisit
 Nefro..
 Ggg. Keseimbangan Asam-basa
1. Konfirm BGA :
24(pCO2/HCO3) tdk lebih dr 10% pH x fc
koreksi (setiap kenaikan 0,1 pH dikali 0,8 dan
setiap turun 0,1 dikali 1,25)
2. Tentukan ggg asam-basa dgn melihat pH,
pCO2 dan HCO3
 Nefro..
3. Tentukan kompensasi :
Asidosis met : pCO2 : (1,5xHCO3)+8
Asid resp : akut  HCO3 1meq setiap pCO2 10
kronik HCO3 3,5meq setiap pCO2 10
Alk met : pCO2 : 40+0,6(delta HCO3)
Alk resp : HCO3 2meq setiap pCO2 10 (akut)
: HCO3 5-7meq setiap pCO2 10 (kronik)
 Nefro..
4. Jika asid met hitung anion gap
AG : Na-(HCO3+Cl)-12 (N + 2)
AG : KAD, intox metanol/salisilat
AG : 2,5meq setiap alb 1gr/dl
AG (N) hitung AG urin (Na+K)-Cl dlm urin
jika (+), maka asid met dari Renal (RTA)
jika (-), maka asid met dari TGI (diare)
5. Koreksi :
asid met : 0,5x0,3xBExBBbicnat
alk met: 0,3xBBx(HCO3-24)HCl/asetazolamid
 Cardiology
Sindrom koroner akut
UAP & NSTEMI Tx=STEMI kecuali reperfusi
STEMI
- oksigen, infus, monitor
- nitrat  ISDN : 2,5-10mg s.l bila nyeri
cedocard : 1-5mg/jam
nitrogliserin 10-20mcg/min
- morfin : 2,5-5mg iv bolus
- aspirin  loading 160mg dilanjutkan 1x80mg
- clopidogrel loading 300mg dilanjut 1x75mg
- heparin UFH : 60 IU/KgBB lanjut 12 IU/KgBB (target PTTK 1,5-2,5)
LMWH : 1mg/KgBB s.c 2xsehari
-B blocker, statin
 Cardio…
- reperfusi :
 Fibrinolitik : streptokinase 1,5 juta IU dlm D5% 100cc
habis dlm 1 jam
 Door to needle<30min
 Cath lab tdk ada/door to ballon>90min
 Akses vaskuler sulit
 Onset<3jam
 PCI :
 Door to ballon <90min
 Killip 3-4
 KI thd fibrinolitik
 Onset>3jam
 Infark vent. Kanan
• Pertahankan pre load
• Ivfd NaCl 1-2L (jam I)200cc/jam (target CVP>10mmHg)
• Hindari nitrat dan furosemid
• Atasi AV block & bradikardi
• Beri inotropik jika dgn cairan cardiac output tdk meningkat
• Turunkan afterload (vasodilator)
• Reperfusi
• Lain2 sama
 Cardio..
Edema paru akut
- O2 8-10lpm masker rebreath
- intubasi bila diperlukan
- morfin 2-4mg iv bolus pelan
- inj furosemid 0,5-1mg/KgBB
- nitrogliserin 10-20mcg/min TDS>90
- nitropusside 0,5-5mcg/KgBB/min
 Cardio..
 SYOK
- Volume  perbaiki defisit cairan, vassopress
- Irama  atasi aritmia
- Pompa  inotropik
TDS 70-100 syok (-) : Dobutamin 2-20mcg/KgBB/min
syok (+) : dopamin
TDS <70  Norepinefrin 0,5-30mcg/min
 Cardio..
Aritmia
Takiaritmia
- O,I,M
- stabil? (hipotensi? Kesadaran? Tanda syok? Nyeri dada? GJ akut?)
- stabil (-) sync cardiversion (AF 120-200J, SVT 50J, VT 100J)
- stabil (+) QRS lebar : amiodarone, adenosin
QRS sempit : vagal manuver, adenosin
*) adeosin hanya diberikan pd QRS teratur, reguler, monomorfik
dosis : 6mg-12mg-12mg bolus cepat diflush
*) amiodarone : 150mg dlm 100cc NaCl selama 10menit dilanjut
1mg/min dlm 6 jam0,5mg/min dlm 18jam
 Cardio..
Bradiaritmia
- O,I,M
- stabil observasi
- tdk stabil 
a) TPM (AV blok derajat 2 tipe 2, TAVB)
b) SA 0,5mg diulang tiap 5 min s/d max 3mg
respon (-)
dopamin 2-10mcg/KgBB/min
respon (-)
epinefrin 2-10mcg/KgBB/min
 Gastro
PSCBA
• Etilogi tersering di INA : hipertensi portal, gastrtitis erosiv,
ulkus peptikum
Pengelolaan dasar
- Ass cepat status kegawatan (KU,GCS,TV, UO,syok?)
- Px Lab (DR, gol darah, cross match, studi koagulasi)
- Resusitasi
 Hemodinamik : kristaloid?Koloid?Tranfusi PRC?WB? Trombo? FFP?
 Respirasi : jalan nafas? O2? Intubasi? NGT?
 Monitoring ketat
-Pemeriksaan data dasar lengkap (Ax+PF+lab)
- obat anti sekresi asam, sitoproteksi
 Gastro..
Pengelolaan intensif/kontrol perdarahan
- Medikamentosa :
1. vasopressin : 0,5 U/min selama 20-60min
2. somatostatin : 250mcg bolus250mcg/jam
3. octreotid : 100mcg bolus25-50mcg/jam
- Tampon mekanik  SB-tube
- Endoskopi cito  STE/LVE
- Bedah cito TIPS
Pengelolaan definitifcari causa
 Gastro..
 Encephalopati hepar
Pencetus : GI bleeding, elektrolit, metabolik, infeksi,
konstipasi, azotemi, drug (sedatif), diet tinggi prot
Patfis :
- Peningkatan permeabilitas sawar darah otak
- Adanya substansi neurotoksin
- Ggg. Fx neurotransmiter
- Ggg. Suplai energi otak
 Gastro..
Klinis :
- derajat I : perubahan pola tidur
II : apatis/somnolen
III : sopor
IV : koma
- flapping tremor
- foetor hepatikum
 Lab : studi koagulasi, DR, GDS, elektrolit, Ur, Cr, amoniak
 Gastro..
Management:
- Supportif : cairan, elektrolit, AB
- Spesifik
• Menurunkan prod amoniak :
– Diet : prot 0,7gr/KgBB/hari, 45kal/BB/hari
– Infus AARC
– Sterilisasi usus : laktulosa, neomisin
• Terapi ggg transport as.amino : levodopa, bromokriptin
 Gastro..
 Pankreatitis akut
Etiologi
- struktural ( batu empedu, spasm singter oddi)
- toxin (alkohol, azatriopin, furosemid)
- infeksi
- metabolik (hiperTG, hiperCa)
- vaskuler (atherosklerosis)
- kongenital, idiopatik
 gastro..
Patfis :
- fase inflamasi : fc pencetusaktivasi dini
zimogen autodigesti pankreas
- fase SIRSsepsis
- fase MODS
Berdasar PA :
1. pankreatitis akut intertitial
2. pankreatitis akut nekrotik hemoragik
 Gastro..
Klinis : nyeri perut hebat mendadak, tdk berkurang
dg analgetik biasa, mual, muntah, obstipasi,
demam
Lab : amilase darah & urn, lipase serum, CRP, DR,
albumin, LDH, elektrolit, BGA
Imaging : USG abd, CT scan abd, ERCP
 Gastro..
Management :
1. Supportif
- Resusitasi cairan, nutrisi, elektrolit
- Analgetik kuat : pethidin, KI : morfin (spasm sfi.oddi)
- AB (quinolon, imipenem)
- Bantuan respirasi
- Monitoring
2. Menekan prod. Enz. Pankreas
- NGT : dekompresi, menurunkan gastrin
- Menurunkan as lambung
- Glukagon , kalsitonin, approtinin : menurunkan enz pankreas
- Somatostatin: octrotid 3x0,5mg s.c
- Memutus rantai SIRS
 Gastro..
Causatif :
- ERCP
- sfingterektomi
- stop alkohol
indikasi bedah :
1. perburukan dlm 72 jam tx intensif
2. sepsis
3. peritonitis
4. obst. sal,. Empedu
5. perdarahan intestinal >500cc/24jam
 Endokrin
 KAD & HONK
 Kontraktilitas miokard 
 Cardiac output 
 Tensi 
 Perfusi ke organ2  KAD
 Respon vaskular thd katekolamin 
 Syok hipovolemi
 Syok hipovolemi HONK
 Trombo-emboli
 Data Laboratorium klinik
LABORATORIUM KAD HONK
Glukosa plasma (mg/dl) > 250 > 600
pH < 7.3 > 7.3
HCO3 serum (mEq/L) < 15 > 20
Keton urine  3+  1+
Keton serum (+) pengenceran 1:2 (-) pada pengenceran 1:2
Osmolalitas serum (mOsm/Kg) Bervariasi  330
Natrium serum (mEq/L) 130 – 140 145 – 155
Kalium serum (mEq/L) 5–6 4–5
BUN (mg/dl) 18 - 25 20 - 40

Panduan klinik praktis untuk membedakan KAD & HONK

Dengan pengertian sekitar 30% penderita KAD dapat
Tampil dalam kondisi HONK
 Endo..
 Tujuan terapi :
- menurunkan glukosa darah
- koreksi cairan dan elektrolit
- menghilangkan fc pencetus
• Infeksi
• Penghentian insulin
• New onset DM
- menghilangkan keton dari darah KAD
 Endo..
 Rehidrasi
NaCl1 jam I : 2L
1 jam II : 1L
 Insulin (short/rapid acting)
- Cepat menurunkan glukosa
- Tdk menyebabkan hipoglikemi
Sp insulin 0,1U/BB/jam,
Bila GDS tdk turun 50-100mg/dldosis naik 2x s/d 100U/jam
bila GDS turun<250, dosis turun ½, infus ganti D5%
(mencegah hipoglikemi + menghilangkan ketonemia)
 Endo..
sliding scale :
GDS INSULIN
<150 -
150-200 5
201-250 10
251-300 15
>300 20
 Antibiotik
 Supportif : elektrolit, asam basa, nutrisi
 Endo..
mengapa HONK berbeda dgn KAD?
 Insulin  (tdk adekwat mengatasi hiperglikemi)
 Counter regulatory hormones  (tdk setinggi
pada ketoasidosis)
 Osmolalitas   menekan lipolisis (sumber
elemen keton bodies)
 Endo..
 Krisis tiroid
Trias klinis :
1. menghebatnya tanda hipertiroid
2. penurunan kesadaran
3. hiperpireksia
 Kriteria diagnostik untuk Krisis Tiroid
Disfungsi pengaturan panas Disfungsi kardiovaskuler
Suhu 99- 99.0 5 Takikardi 99-109 5
100-100.9 10 110-119 10
101-101.9 15 120-129 15
102-102.9 20 130-139 20
103-103.9 25 >140 25
>104.0 30 Gagal jantung
Efek pada susunan saraf pusat Tidak ada 0
Tidak ada 0 Ringan (udem kaki) 5
Ringan (agitasi) 10 Sedang ( rhonchi basal) 10
Sedang (delirium,psikosis,letargi berat) 20 Berat (udem paru) 15
Berat (koma,kejang) 30
Disfungsi gastrointestinal-hepar Fibrilasi atrium
Tidak ada 0 Tidak ada 0
Ringan (diare, nausea/muntah/nyeri perut) 10 Ada 10
Berat (ikterus tanpa sebab yang jelas) 20 Riwayat pencetus
Negatif 0
Positif 10
Pada kasus toksikosis pilih angka tertinggi, >45 highly suggestive, 25-44 suggestive of impending storm, di
bawah 25 kemungkinan kecil.
 Endo..
Supportif : cairan, elektrolit, nutrisi, oksigenasi
Koreksi hipertiroid
- blok sintesisPTU 600-1000mg, dilanjut 200mg/4jam,
max 1000-1500mg
- mencegah sekresi tiroidlugol 10tetes/6jam
- hambat konversi T4-T3propranolol 20-40mg/6jam
Insuf adrenal relatifhidrokortison 100mg/8jam
Antipiretikacetaminophen, KI : aspirin, kompetitif tiroksi
thd prot binding
Digoxinbila AF
Atasi pencetus
 Endo..
 Koma miksedem
Klinis : riwayat hipotiroid ditambah :
-penurunan kesadaran
- hipoventilasi
- hipotermi
- bradikardi
- hipoglikemi
- hiponatremi
Pencetus : infeksi, post OP, obat narkotik/hipnotik
 Endo..
 Management :
-Supportif
- Tiroksin (T4) 300-500mcg bolus iv50mcg/hari atau
T3 25mcg/8jam12,5mcg/8jam
- Hidrokortison 100mg/8jam
- atasi fc pencetus
 Pulmonology
Hemoptisis
Ekspektorasi dahak yg mengandung bercak darah dan berasal dari sal.nafas bag
bawah
Hemptisis masif :
- batuk darah >600cc/24jam
- <600cc/24jam tp Hb<10gr%
- >250cc/24jam, Hb>10gr tp tdk berhenti dlm obs selama 48 jam
Etiologi : 95% berasal dari a. bronkialis
-TB paru
- aspergilosis
- bronkhiektase
- abses paru
- pneumonia
-Ca paru
 Pulmo..
 Asma Bronkhial
O2 max 8lpm
Inhalasi B2 agonis dosis tinggi
- salbutamol 5mg
-terbutalin 10mg
Steroid iv dosis tinggi
- prednison 60mg/hidrokortison 200mg
- maintanance : hidro 200mg/6jam
Bronkhodilator
- aminofilin 250mg dlm 30 menit
- salbutamol 200mcg/terbutalin 250mcg
 Pulmo..
Dampingi pasien sampai ada respon
Bila respon baik nebulasi/6jam
Bila respon buruk ulangi nebulasi+ipaproprium bromid 0,5mg
Bila msh belum respon jg pertimbangkan :
-aminofilin 0,5-0,9mg/BB/jam
-salbu/terbutalin 2-30mcg/min
Evaluasi
- APE dipanttau 4x/hari sampai kondisi stabil
-BGA/6jam
-kadar aminofilin serum, kalium, GDS
Kontraindikasi : SEDATIF!!
 Pulmo..
 Indikasi ICU :
 PO2<60mmHg dg O2 60%
PCO2>50mmHg menetap dlm 6 jam
Tanda kelelahan
Penurunan kesadaran
Henti nafas
 Indikasi pulang :
APE>75% prediksi
Variasi diurnal <25%
Sesak malam hari (-)
 Klasifikasi beratnya asma eksaserbasi
Tanda / Gejala Ringan Sedang Berat AncamanGagal Nafas

Sesak nafas Berjalan Berbicara Istirahat

Dapat terlentang Lebih suka duduk Membungkuk

Berbicara Membuat kalimat Membuat frase Membuat kata

Kesadaran Mungkin gelisah Selalu gelisah Selalu gelisah Mengantuk atau
bingung

Laju pernafasan Meningkat Meningkat > 30/menit

Otot tambahan retraksi Tidak Biasa ada Biasa ada Pergerakan poradok
suprasternal torako abdominal

Wheezing Sedang sering pada keras Sangat keras Tidak ada wheezing.
saat ekspirasi

Nadi/menit < 100 100 - 120 > 120 Bradikardi

Pulsus paradoksus < 10 mmHg 10 – 25 mmHg > 25 mmHg Tidak ada
Dicurigai adanya kelelahan
otot nafas.

APE > 80% 60 – 80 % < 60 %

PaO2 Normal > 60 mmHg < 60 mmHg
PaCO2 < 45 mmHg < 45 mmHg > 45 mmHg
SaO2% > 95 % 91 – 95 % <90 %
Algoritme managemen eksaserbasi asma
Penilaian awal (anamnesis dst)
Terapi awal

Dinilai setelah 1 jam

Kriteria : Episode sedang Kriteria : Episode Berat

Dinilai setelah 1-2 jam

Respon baik dlm 1-2 jam Respon sebagian dlm 1-2 jam Respon buruk dlm 1-2 jam
Masuk ke perawatan akut Masuk ICU

Penilaian berkala
Respon buruk  lihat atas
ICU
Perbaikan: kriteria pulang Respon sebagian
 ICU jika tidak membaik 6-12
jam

Perbaikan
Penilaian awal :
anamnesis, pemeriksaan fisik, pem penunjang:
saturasi oksigen, FEV1 dan PEF

Terapi awal:
1. Oksigen hingga saturasi mencapai 95%
2. Β2 agonist rapid acting inhalasi terus menerus hingga 1 jam
3. Glukokortiokosteroid sistemik jika tdk ada respon segera/jika pasien
sebelumnya mendapat glukokortikosteroid oral
4. Sedasi merupakan KI

Reassess: pem fisik, PEF, sat O2, dan tes lain yang diperlukan
Kriteria : Episode sedang:
1. PEF 60-80% nilai prediksi
2. pem fisik: gejala moderate, pemakaian otot bantu napas
Terapi :
Oksigen
Β2 agonist inhalasi dan antikolinergik inhalasi setiap 60 menit
Glukokortikosteroid oral
Lanj terapi hingga 1 – 3 jam, hingga tercapai perbaikan

Kriteria : Episode Berat:

1. PEF < 60 % nilai prediksi
2. pem fisik: gejala berat, retraksi dinding dada
3. Tidak ada perbaikan setelah terapi awal

Terapi :
Oksigen
Β2 agonist inhalasi dan antikolinergik inhalasi
Glukokortikosteroid sistemik
Mg intravena
Good Respon/ respon baik:
1. Respon bertahan minimal 60 menit setelah terapi terakhir
2. Pem fisik: normal, tidak ada distress
3. PEF > 70%
4. Saturasi O2 > 90%

Incomplete Respon/ sebagian: Terapi:

1. Faktor risiko Oksigen
2. Pem fisik: tanda ringan - sedang Β2 agonist inhalasi dan antikolinergik inhalasi
3. PEF > 60%
4. Saturasi O2 tidak membaik Glukokortikosteroid sistemik (iv)
MG iv
Monitor PEF, sat O2, pulse

Terapi:
Incomplete Respon/ buruk: 1. Oksigen
1. Faktor risiko 2. Β2 agonist inhalasi dan antikolinergik inhalasi
2. Pem fisik: tanda berat,
konfusio, drowsiness 3. Glukokortikosteroid sistemik
• PEF < 30% 4. Pertimbangkan: Β2 agonist iv
• PCO2 > 45% 5. Pertimbangkan: teofiline iv
• PO2 < 60% 6. Intubasi/ pemasangan ET, ventilator mekanik.
 Kriteria dipulangkan:
- PEF > 60% prediks
- Terapi obat secara oral dan
inhalasi diteruskan

Terapi di rumah:
1.Teruskan Β2 agonist inhalasi
2.Pertimbangkan: glukokortikosteroid oral
3.Edukasi pasien:
- pakai obat secara benar
- review action plan
 BERDASAR GAMBARAN KLINIS

Intermiten Persisten Persisten Persisten

Ringan Sedang Berat
Gejala < 1x/ minggu > 1x seminggu, Setiap hari Setiap hari
< 1x sehari
Eksaserbasi singkat Mempengaruhi Mempengaruhi sering
aktivitas dan aktivitas dan
tidur tidur
Gejala malam Tidak > 2 x dlm > 2x dalam 1 > 1 x dalam Sering,
hari 1 bulan bulan seminggu pembatasan
aktivitas
FEV1/PEF ≥ 80% prediksi ≥ 80% prediksi 60-80% 60-80%
prediksi prediksi
Variasi PEF/ < 20% < 20 – 30% > 30% > 30%
VEF1

Tidak lagi direkomendasikan sebagai dasar untuk membuat keputusan pengobatan

yang sedang berlangsung
 BERDASAR TINGKAT PENGENDALIAN ASMA

TERKENDALI TIDAK
Karakteristik TERKENDALI
SEBAGIAN TERKENDALI

Gejala siang hari Tidak ada (2x / > 2 x perminggu Tiga atau lebih
< per minggu) gambaran dari asma
Pembatasan aktivitas Tidak ada Ada terkendali/terkontrol
sebagian muncul
Gejala malam hari Tidak ada Ada beberapa minggu
/terbangun
Perlu reliever Tidak ada (2x / > 2 x perminggu
< per minggu)
Fungsi paru PEF/ VEF1 normal < 80% prediksi

Eksaserbasi Tidak ada Satu / > per tahun Beberapa kali dalam
beberapa minggu

Istilah terkendali  mengindikasikan pencegahan bahkan pengobatan

TUJUAN Mencapai dan mempertahankan kontrol klinis

OBAT-OBATAN
GOAL RELIEVERS GOAL CONTROLLERS

rapid acting β2 agonist Glukokortikosteroid inhalasi

inhalasi dan sistemik
Antikolinergik inhalasi Leukotriene modifiers

Teophiline short acting Long acting β2 agonist +

glukokortikosteroid inhalasi
rapid acting β2 agonist oral Teophiline SR

Steroid sparing sistemik

 GLUKOKORTIKOSTEROID INHALASI

Dosis harian Dosis harian sedang Dosis harian tinggi

OBAT
rendah (μg) (μg) (μg)

Beclomethasone 200 – 500 > 500 – 1000 > 1000 – 2000

dipropionat
Budeso 200 – 400 > 400 – 800 > 800 -1600
nide
Ciclesonide 80 – 160 > 160 – 320 > 320 – 1280

Flunisolide 500 – 1000 > 1000 – 2000 > 2000

Fluticasone 100 – 250 > 250 – 500 > 500 - 1000

Mometasone furoate 100 – 250 > 400 – 800 > 800 - 1200

Triamcinolone acetonide 200 - 400 > 1000 – 2000 > 2000

 Pulmo..
 Gagal Nafas
Etiologi :
- hipoventilasi
- ventilasi/perfusi missmatch
- shunt
- konbinasi 1-3
GN tipe I (hipoksemi)
- paru gagal memenuhi kebutuhan O2, eliminasi CO2 msh
normal
- etiologi : kelainan intrapulmoner (V/Q missmatch, shunting, ggg
difusi/alveolar block)
- PaO2 <50 ; PCO2 normal/turun
 Pulmo..
GN tipe II
- etiologi : kelainan extraparu (hipoventilasi), V/Q
missmatch, kombinasi
- PaO2 turun; PCO2>50
ARDS (acute Respiratory distress syndrome)
sindrom yg ditandai peningkatan permeabilitas
membran alveo-kapiler disertai kerusakan difus
dan akumulasi cairan yg mengandung protein dlm
parenkim paru
 Pulmo..
Fase eksudatif : edema intertitial & alveolar,
nekrosis pneumosit tipe I
Fase proliferatif : proliferasi pneumosit tipe II
Fase fibrosis : pembentukan kolagen, fibrotisasi
parenkim paru
Dx :
1. BGAPO2/FiO2<200
2. Foto thorax infiltrat difus bilateral
3. PCWP< 18mmHg (bukan edema kardiogenik)
 PATOGENESIS
• Pada keadaan normal terdapat keseimbangan
antara tekanan onkotik dan hidrostatik antara
kapiler paru dan alveolar.

• Teraktivasinya kaskade inflamasi yang berasal

dari suatu fokus kerusakan jaringan tubuh.
Neutrofil yang teraktivasi akan melepaskan
toksin / sitokin.Sebagai hasilnya: kerusakan
endotel → Peningkatan permeabilitas kapiler
alveoli.
• Alveoli penuh eksudat kaya protein, banyak neutrofil
dan sel inflamasi → membran hialin
• Pada tahap awal terjadi peningkatan kandungan
cairan jaringan interstisial antara kapiler dan alveoli
Kriteria Diagnosis:
1.Riwayat pencetus.
2.Hipoksemia refrakter dengan terapi oksigen
PaO2/FiO2 <200 .
3.X Foto thorak : infiltrat bilateral difus.
4.Tidak ada gejala edema paru kardiogenik dan
tekanan baji ≤ 18 mmHg.
Pada ARDS nilai AaDO2 >300.
 Penatalaksanaan

1.Mengobati penyakit dasarnya

2.Penatalaksanaan suportif
A.Continuous positive airways pressure (CPAP).
Tidak boleh terlalu tinggi→ trauma. Diberikan
dengan tidal volume 8-9ml/kgbb.
B.Management cairan dan hemodinamik
Restriksi cairan: ↓ edema pulmo.
Keseimbangan antara tata laksana ARDS dan
volume intravaskuler.
C. Terapi surfaktan
D. Vasodilator pulmonal : NO inhalasi
E. Glukokortikoidfase akut.
Belum dilakukan secara rutin/jangka lama:
karena peningkatan resiko infeksi.
 Hematology
 Trombosis

Trombofilia atau Hiperkoagulabilitas adalah merupakan

suatu kondisi dimana terdapat peningkatan risiko untuk
terjadinya trombosis.

 Diturunkan
 Didapat
 PLATELET

COAGULATION FIBRINOLYSIS

INHIBITOR INHIBITOR
VESSELS

THROMBOSIS BLEEDING
 THROMBI
ARTERIAL VENOUS
Abnormalities of blood vessels Abnormalities of blood flow
(atherosclerosis) Hypercoagulability

Risk factors: Hypertension, Risk factors: immobility,

Diabetes, Hyperlipidemia surgery, age, cancer, etc.
 PATHOGENESIS
Virchow’s Triad (1856)

 Venous stasis
 Vascular injury
 Hypercoagulability

 Acquired
 Inherited
 RISK FACTORS AND CONDITIONS PREDISPOSING TO (VTE)

PATIENT FACTORS:
Previous VTE

Age over 40 Years

Pregnancy, Puerperium

Obesity

Inherited Hypercoagulable: Def PC, PS, AT

Hyperhomocysteinaemia (hereditary + acquired)

 UNDERLYING CONDITION AND ACQUIRED
FACTORS
Malignancy: adeno Ca + (surgery – CT)

Estrogen use: OC, HRT

Prolonged immobility, paralysis

Surgery: orthopaedic, pelvic, abdominal

 Acquired hypercoagulable: APS, SLE, MPD

Medical illness: CHF, AMI, Acute resp. failure

 Clinical Features of Acute DVT

 Calf pain
 Swelling with pitting edema
 Swelling below knee (distal DVT), up to groin
(proximal DVT)
 Increased skin temperature
 Cyanosis (severe obstruction)
 Superficial venous dilatation
 DIAGNOSIS OF DEEP VEIN THROMBOSIS

Physical findings alone suggest DVT: unreliable

Confirmation of a suspected DVT requires one
or more investigations: compression USG, D-
dimer, venography
The confirmation rate rises with the number
of risk factors
CLINICAL FEATURES CLINICAL FEATURES
+ +
RISK FACTORS ALTERNATIVE
DIAGNOSIS

DVT MORE LIKELY DVT LESS LIKELY

 MODIFIED PRETEST PROBABILITY FOR DVT

• Tenderness along entire deep vein 1.0

• Swelling of the entire leg 1.0
• >3cm difference in calf circumference 1.0
• Pitting edema 1.0
• Collateral superficial veins 1.0
• Active cancer 1.0
• Prolonged immobility or paralysis 1.0
• Recent surgery or major medical illness 1.0
• Alternative diagnosis -2.0
Score>2: high, 1-2: moderate, <1: low probability
 Pulmonary Embolism

 Dyspnoea, chest pain PE

 Syncope
 Hemoptysis
 RR >20/m, tachycardia
 Wheezing
 Pulmonary hypertension DVT

 Right heart failure

 Signs of DVT
 DIAGNOSIS OF PULMONARY EMBOLISM

Pulmonary angiography
Helical CT
Ventilation-perfusion scan
Diagnostic test positive for DVT
 CLINICAL PROBABILITY FOR PE
DVT suspected
 Clinical features of DVT 3
 Recent prolonged immobility or surgery 1.5
 Active Cancer 1
 History for DVT or PE 1.5
Hemoptysis 1
Resting heart rate > 100 beat/min 1.5
No alternative explanation for acute 3
breathlessness or pleuritic chest pain

>6 high (60%); 2-6 moderate (20%); <1.5 low (3-4%) Turpie AGG, 2002
 Hema..
 DIC
• DIC is an acquired syndrome, characterized by
intravascular activation of coagulation and
deposition of fibrin within the micovasculature
• DIC leads to organ ischaemia and infarction

The consumption of clotting factors and platelets

in the diffusely distributed thrombi may lead to a
hemorrhagic diathesis and clinical bleeding.
 CAUSES DIC
INFECTIONS:
• Gram-negative or Gram-positive septicemia (endotoxin)
• Viruses(e.g. Epstein-Barr virus, cytomegalovirus, human
immunodeficiency virus)
• Miliary tuberculosis
• Fungi
• Parasites (malaria, Toxoplasma spp.)
 CAUSES DIC:
RELEASE OF TISSUE FACTOR
• Malignancy, especially if disseminated
• Obstetric complications:
 abruptio placentae
 amniotic fluid embolism
 eclampsia and pre-eclampsia
 retained dead fetus
 CAUSES DIC:
RELEASE OF TISSUE FACTOR
• Extensive trauma, burn, surgery
• Large aortic aneurysm
• Snake, spider venoms
• Acute hemolytic transfusion reactions
 CLINICAL PRESENTATION: ACUTE DIC

• Acute DIC occurs with endotoxemia, extensive

tissue trauma, preeclampsia, placental
abruption or amniotic fluid embolism.
• Also in patients experiencing hypotension or
shock for any reason: difficult surgical
procedure, massive stroke, heart attack
 CLINICAL PRESENTATION: CHRONIC DIC

• Chronic DIC is associated with malignancies,

aortic aneurysms and large hemangiomas,
retained dead fetus
• Malignancies:
 Risk factors: older age, male, advanced cancer and necrosis in
the tumor
 Most type of cancers: adenocarcinoma of the lung, breast,
prostate or colorectum
 The survival is worse than that of cancer patients without DIC
 PATHOGENESIS OF DIC
Involves simultaneous dysregulation of
several homeostatic mechanisms:
A. Excessive activation of coagulation
B. Down-regulation of physiologic
anticoagulation pathways
C. Inhibitition of fibrinolysis
 SCORE GLOBAL COAGULATION TEST RESULTS:
Platelet count
>100.000=0, <100.000=1, <50.000=2
D-Dimer
no increase (<500)=0, moderate (500-1000)=2, strong (>1000)=3
Prolonged prothrombin time (PT)
<3sec.=0, 4-6sec.=1, >6sec=2
Fibrinogen level
<100mg/dl=1, >100mg/dl=0
Calculate score
If ≥5: overt DIC; If <5: suggestive for non-overt DIC:
repeat next 1-2 days
 MANAGEMENT OF DIC

• Treatment of underlying disease (sepsis)

• Blood component (cryoprecipitate and
platelet) substitution therapy
• Anticoagulants (chronic DIC)
• Restoration of anticoagulant pathways:
ATIII, PCa