PEMICU 2

BLOK KEGAWATDARURATAN
MEDIK
KELOMPOK 22

Kelompok 22
Tutor: dr Samuel
Anggota:

Definition
A physiological state that results in
inadequate organ perfusion and tissue
oxygenation
Downward spiral of impaired perfusion
leading to impaired function
Results in multiple organ failure and death

Ghana Emergency Medicine

Collaborative

Basic Physiology
Oxygen Delivery = CO x arterial content of O2
Cardiac Output = HR x Stroke Volume
Stroke Volume is a function
Preload
Afterload
Myocardial Contractility

Ghana Emergency Medicine

Collaborative

Pathophysiology
Blood loss
Release of endogenous catecholamines
Increase cardiac output
Increase heart rate
Vasoconstriction of less vital organs
skin, muscle
Results in higher diastolic BP (narrow PP)

Continue to perfuse vital organs as long as

possible (brain, heart, kidney)
Ghana Emergency Medicine
Collaborative

Initial Patient Assessment

Recognition of Shock
Clinical signs and symptoms depends
on the severity of the shock
Early manifestations include tachycardia
and cutaneous vasoconstriction

Ghana Emergency Medicine

Collaborative

Clinical Pathophysiology of
Shock

General / Vital signs

Cardiovascular- tachycardia
Skin- vasoconstriction vs. vasodilation
Respiratory- increased RR
Urinary- decrease urine output
Neurologic- confusion, agitation
Extremities- cold vs. warm
Ghana Emergency Medicine
Collaborative

Clinical Endpoints of Shock

DECREASED BLOOD FLOW TO BRAIN AND HEART
Restless, agitated, confused, lethargy
Hypotension
Tachycardia
Tachypnea

END-STAGE SHOCK
Bradycardia
Arrythmias
Death
Ghana Emergency Medicine
Collaborative

Classifying Shock
Hypovolemic
Hemorrhagic

Distributive /Vasogenic
Sepsis, Anaphylactic

Cardiogenic
Neurogenic
Spinal cord injury

Ghana Emergency Medicine

Collaborative

Shock Types & Physiology

Shock

CVP/PCWP

CO

SVRI

either

Cardiogenic

Neurogenic

Hypoadrenal

either

Anaphylactic

Hemorrhagic
Septic

Severity of Shock
Compensated shock: patient is developing
shock but body still able to maintain perfusion.
Decompensated shock: patient developed shock
but body no longer can compensate.
Irreversible shock: patient developed shock but
body is unable to maintain perfusion to organs.

Jenis syok

Mekanisme

Etiologi

Hipovolemik

Pengurangan volume
darah yang
disebabkan oleh
kehilangan darah,
plasma, atau cairan
tubuh yang
akut/banyak sekali :
1.Perdarahan
2.Dehidrasi :
GIT
Penguapan

1. Perdarahan
ekternal/internal
2. Muntah, diare
3. Luka bakar
4. Pankreatitis , luka
bakar

Kardiogenik

Kegagalan pompa
jantung akibat
penurunan
kontraktilitas jantung

1. Infark miokard
2. Payah jantung

Hilangnya tonus
1. Sepsis
pembuluh darah yang 2. Anafilaktif
normal sehingga
3. Neurogenik

Derajat Syok
Syok Ringan
Penurunan perfusi hanya pada jaringan dan organ
non vital seperti kulit, lemak, otot rangka, dan
tulang.
Jaringan ini relatif dapat hidup lebih lama dengan
perfusi rendah, tanpa adanya perubahan jaringan
yang menetap (irreversible).
Kesadaran tidak terganggu, produksi urin normal atau
hanya sedikit menurun, asidosis metabolik tidak ada
atau ringan.

 Syok Sedang
Perfusi ke organ vital selain jantung dan otak
menurun (hati, usus, ginjal).
Organ-organ ini tidak dapat mentoleransi hipoperfusi
lebih lama seperti pada lemak, kulit dan otot.
Pada keadaan ini terdapat oliguri (urin kurang dari 0,5
mg/kg/jam) dan asidosis metabolik. Akan tetapi
kesadaran relatif masih baik.

 Syok Berat
Perfusi ke jantung dan otak tidak adekuat.
Mekanisme kompensasi syok beraksi untuk
menyediakan aliran darah ke dua organ vital.
Pada syok lanjut terjadi vasokontriksi di semua
pembuluh darah lain.
Terjadi oliguri dan asidosis berat, gangguan
kesadaran dan tanda-tanda hipoksia jantung (EKG
abnormal, curah jantung menurun).

Syok Hipovolemik
Definisi :
terganggunya sistem sirkulasi akibat dari
volume darah dlm pembuluh darah yg ber
(-)

Etiologi
Syok hipovolemik
Perdarahan

Hematom subkapsular hepar

Aneurisma aorta pecah
Perdarahan GIT
Perlukaan berganda

Kehilangan plasma

Luak bakar luas

Pankreatitis
Deskuamasi kulit
Sindrom Dumping

Kehilangan cairan
ekstraseluler

Muntah
Dehidrasi
Diare
Terapi diuretik yang sangat
agresif
Diabetes insipidus
Inssufiensi adrenal

Patofisiologi
Mikrosirkulasi : MAP < 60mmHg fs organ terganggu
Neuroendokrin : baroreseptor & kemoreseptor
KV : pengisian ventrikel volume sekuncup
(kompensasi : frekuensi jantung)
GI : absorpsi endotoksin o/ bakt gram yg mati dlm
usus vasodilatasi, metabolisme, depesi jantung
Ginjal :
Menahan garam + air
Tahanan arteriol aferen u/ me (-) LFG
Aldosteron & vasopresin : produksi urin

Gejala Klinis

kerja simpatis
Hiperventilasi
Pembuluh vena kolaps
Pelepasan hormon stres
Ekspansi besar untuk pengisian volume
PD dgn cairan intersisial, intraselular
produksi urin

Gejala Klinis
Ringan
(<20% vol darah)

Sedang
(20-40% vol darah)

Berat
(>40% vol darah)

Ekstremitas dingin

Sama, ditambah:

Sama, ditambah:

Waktu pengisian
kapiler meningkat

Takikardia

Hemodinamik tak
stabil

Diaporesis

Takipnea

Takikardia bergejala

Vena kolaps

Oligouria

Hipotensi

Cemas

Hipotensi ortostatik

Perubahan
kesadaran

Klasifikasi

http://www.studyblue.com/notes/note/n/su1-05-shock/deck/3390917

Syok hipovolemik karena dehidrasi

(muntah, diare)
Klasifikasi

Penemuan klinis

Pengelolaan

Dehidrasi ringan :
Kehilangan cairan tubuh
sekitar 5%

Selaput lendir kering,

nadi
normal atau sedikit
meningkat

Penggantian volume
dengan cairan
kristaloid (NaCl 0,9%
atau RL)

Dehidrasi sedang :
Kehilangan cairan
tubuh sekitar 10%

Selaput lendir sangat

kering
Status mental tampak
lesu.
Nadi cepat.
Tekanan darah mulai
menurun.
Oliguria.

Dehidrasi berat :
Kehilangan cairan
tubuh >15%

Selaput lendir pecahpecah.

Pasien mungkin tidak
sadar.
Tekanan darah turun.
Anuria.

Diagnosis
Ketidakstabilan hemodinamik / adanya
sumber perdarahan
Ht di awal bukan pegangan
Hilangnya plasma, tanda :
hemokonsentrasi
Hilangnya cairan bebas , tanda :
hipernatremia

Pemeriksaan Penunjang Syok

Hipovolemik
Analisa gas darah arteri/ panel
Penurunan defisit basa
Peningkatan nilai laktat
Merefleksikan asidosis laktat akibat hipoperfusi

Pemeriksaan laboratorium
Sonografi abdominal terfokus untuk trauma (FAST,
Focused Abdominal Sonography for Trauma)
Lavase peritoneal diagnostik
CT scan
Foto polos

Variabel yang Dimonitor pada Syok

Hipovolemik
PENGUKURAN

NILAI NORMAL

NILAI KHAS pada SYOK

Tekanan darah pada pembuluh

nadi
Denyut nadi
Tekanan vena sentral
Hematokrit

120/80
80/menit
4-8cm saline
35-45%

<90 mmHg sistolik

>100/menit
<3cm
<35 %

7,4
95 mmHg
40 mmHg
23-25 mEq/liter
12 mg/liter

7,3
85 mmHg
<30 mmHg
<23 mEq/liter
>20 mg/100ml

50 ml/jam
1,015-1,025
300-400 m Osm/kg air

<20 ml/jam
>1,025
>700 m Osm/kg air

Darah arteri
pH
pCO2
HCO3
Asam laktat
Air kemih
Volume
Berat molekul
Osmolalitas

Tanda Perbaikan Kondisi Syok

Peningkatan tekanan darah

Meningkatkan tingkat kesadaran
Meningkatkan perfusi perifer
Penurunan tachycardia
Penurunan laktat
pH asam/basa normal

DD
Syok kardiogenik
Sama2 : CO & kompensasi simpatis
Beda : distensi v.jugularis, ronki & gallop
S3

Tatalaksana
Menempatkan pasien dgn posisi kaki lebih tinggi
Menjaga jalur pernapasan
Berikan resusitasi cairan intra vena/ CVP/
intrarterial
Cairan : 2-4 L dlm 20-30 mnt
garam isotonus yg ditetes cepat (hati2 pd
asidosis hiperkloremia) atau dgn RL
menggunakan jarum infus yg terbesar (koloid
blm terbukti)

 Kateter Swan-Ganz
Pemeriksaan baji paru
Tujuan : mengetahui apakah cairan sudah
cukup memenuhi kebutuhan untuk
meningkatkan tekanan pengisian ventrikel

 Transfusi darah
Hemodinamik belum stabil setelah pemberian
cairan
Kadar Hb <10 g/dl
Lakukan cross-match sebelum digunakan
Sangat darurat : PRC tipe darah yg sesuai /
Onegatif

 Hipovolemia berat & berkepanjangan :

Dopamin /
Untuk kekuatan ventrikel
Vasopressin /
Kebutuhan vol.darah dicukupi
dahulu
Dobutamin.
NE infus tdk bermanfaat
MAP : Nalokson bolus 30mcg/kh 3-5mnt
60mcg/kg 1jam dalam dekstros 5%

 Menjaga saluran pernapasan

Kebutuhan O2 terpenuhi
Bila diperlukan lakukan intubasi

Figure 57-20 Femoral vein (A) anatomy and (B)

cannulation technique. (From American Heart
Association: Textbook of Pediatric Advanced Life
Support. Dallas, American Heart Association, 1994,
with permission. 1994, American Heart
Association.)

Early Goal Directed Treatment

Terapi Hipovolemik pd Anak

Fluid bolus of 20 mL/kg of normal saline or lactated Ringer solution
should be given rapidly.
If it is not possible to insert an intravenous catheter into a peripheral
vein within 90 sec or within three attempts intraosseous needle
Children in severe hypovolemic boluses totaling 60-80 mL/kg within
the first 1-2 hr of presentation.
Fresh frozen plasma, albumin, whole blood, or packed red blood
cells
The use of dextrans (hydroxyethyl starch) or gelatins may be
indicated if there is a need to increase plasma oncotic pressure but
blood component therapy cannot be administered or is ineffective
(-) : osmotic renal injury and predisposes the patient to acute renal
failure

 Still poor perfusion and shock vasoactive agents

Oxygen delivery need not exceed (supranormal) normal
expectations ("supply-dependency)
GOAL : restore oxygen delivery to vital tissues.
Improving oxygen-carrying capacity (maintain normal
hematocrit at 35-40%)
Improving oxygen saturation (95-99%) and Pao 2 (if
severely anemic)
Enhancing a depressed cardiac output. with direct
therapy (anticonvulsants, antipyretic agents)

Komplikasi
Kerusakan organ akhir jarang terjadi
dibandingkan syok septik / traumatik
Bisa terjadi kerusakan organ di
SSP
Hati
Ginjal :
Nekrosis tubular akut (interaksi antar syok, sepsis, obt
nefrotoksik : aminoglikosida & media kontras angiografi)
GGA : sgt jarang krn cepatnya pemberian cairan
pengganti

Prognosis
Hasil tergantung pada etiologi dan pemulihan yang cepat
dengan perfusi yang memadai.
Dilakukan monitor yang terus-menerus terhadap
kecukupan resusitasi (misalnya stabilisasi TD, perbaikan
takikardi, perfusi yang baik pada saat pemeriksaan,
resolusi asidosis, produksi urine yang memadai)

Syok Septik

Definisi

Keadaan di mana terjadi penurunan tekanan darah

<SBP <90mmHg atau penurunan SBP lebih dari
40mmHg) disertai tanda kegagalan sirkulasi, meskipun
memerlukan vasopresor untuk mempertahankan
tekanan darah dan perfusi organ

Definition

septic shock is a decrease in peripheral vascular

resistance that occurs despite increased levels of
vasopressor catecholamines

Etiology

Epidemiology

>200.000 death in US/year

Sepsis-related incidence and mortality rates increase
with age and preexisting comorbidity

Syok dan Mekanisme Hemodinamik

Syok gangguan hemodinamik perfusi jaringan

tidak adekuat dan mengganggu metabolisme sel &
jaringan
8 faktor hemodinamik yang berperan dalam
terjadinya syok

Volume intravaskular
Jantung
Resistensi vaskular
Mikrosirkulasi & kapiler
Resistensi venula
Hubungan arteri vena tanpa memalui kapiler
Volume sirkulasi sistemik
Pembuluh darah

Faktor hemodinamik yg berperan dalam terjadinya syok

1.Volume intravaskular

-Mempertahankan tekanan & aliran balik vena ke jantung

2.Jantung
-Mempengaruhi sirkulasi hemodinamik (curah jantung,
frekuensi, irama, kontraktilitas, keseimbangan preload, afterload)
3.Resistensi vaskular (Perbedaan tonus arteriol pada organ
maldistribusi volume darah ketidakseimbangan suplai &
oksigen)
4.Mikrosirkulasi & kapiler (transportasi cairan dan nutrisi)
-Gangguan sirkulasi mikrovaskular gangguan
metabolisme sel
-Peningkatan permeabilitas kapiler edema interstisial

5.Resistensi Venula
- Peningkatan resistensi venula & tekanan hidrostatik
keluarnya cairan intravaskular ke interstisial
6.Hubungan arteri vena tanpa kapiler hipoksia & gangguan
transport nutrisi
7.Penurunan tonus vena & peningkatan kapasitas vena
mempengaruhi volume sirkulasi sistemik
8.Patensi pembuluh darah
-Obstruksi pembuluh darah penurunan aliran balik vena

http://www.nejm.org/doi/full/10.1056/NEJMra1208623

Neurogenic Shock
Terjadi akibat gangguan pada jaras simpatis
desenden di servikal atau torakal atas hilangnya
tonus vasomotor dan inevarsi simpatis ke jantung.

Neurogenic Shock
Causes:
1.Spinal cord injury
2.Regional anesthesia
3.Drugs
4.Neurological disorders

Syok
Neurogenik

Manifestasi Klinis
Hampir sama dengan syok pada umumnya tetapi
pada syok neurogenik terdapat tanda TD turun, HR
tidak bertambah cepat, bahkan dapat lebih lambat
(bradikardi) kadang disertai dengan adanya defisit
neurologis berupa quadriplegia atau paraplegia.
Pada keadaan lanjut, sesudah pasien menjadi
tidak sadar nadi bertambah cepat
Pengumpulan darah di dalam arteriol, kapiler dan
vena kulit terasa agak hangat dan cepat
berwarna kemerahan.

Diagnosis Banding
sinkop vasovagal
Keduanya sama-sama menyebabkan hipotensi
karena kegagalan pusat pengaturan vasomotor
tetapi pada sinkop vasovagal hal ini tidak
sampai menyebabkan iskemia jaringan
menyeluruh dan menimbulkan gejala syok.

syok septik
syok anafilaksis

Penatalaksanaan
Baringkan pasien dengan posisi kepala
lebih
rendah
dari
kaki
(posisi
Trendelenburg).
Pertahankan
jalan
nafas
dengan
memberikan oksigen, sebaiknya dengan
menggunakan masker.
Pada pasien dengan distress respirasi dan
hipotensi yang berat, endotracheal tube
dan ventilator mekanik

Resusitasi cairan
Cairan kristaloid seperti NaCl 0,9% atau
Ringer Laktat diberikan per infus secara
cepat
250-500
cc
bolus
dengan
pengawasan yang cermat terhadap
tekanan darah, akral, turgor kulit, dan urin
output untuk menilai respon terhadap
terapi.

Bila tekanan darah dan perfusi perifer tidak segera pulih,

berikan obat-obat vasoaktif
Dopamin
Merupakan obat pilihan pertama. Pada dosis > 10
mcg/kg/menit, berefek serupa dengan norepinefrin. Jarang
terjadi takikardi.
Norepinefrin
Efektif jika dopamin tidak adekuat dalam menaikkan
tekanan darah.
Monitor terjadinya hipovolemi atau cardiac output yang
rendah jika norepinefrin gagal dalam menaikkan tekanan
darah secara adekuat.

 Diberikan per infus.

Awasi pemberian obat ini pada wanita hamil,
karena dapat menimbulkan kontraksi otot-otot
uterus.
Epinefrin
Dobutamin
Berguna jika tekanan darah rendah yang
diakibatkan oleh menurunnya cardiac output.
Dobutamin dapat menurunkan tekanan darah
melalui vasodilatasi perifer

Komplikasi
ARDS
Ginjal : oligouria, azotemia, proteinuria,
Gangguan koagulasi : trombositopenia,,
kerusakan
endotel,
mikrovaskular
trombosis
Kelemahan motorik bagian distal

 Bentuk dari syok kardiogenik yang terjadi

akibat kesukaran mekanik pd sirkulasi, yg
menyebabkan menurunnya CO, bukan
kegagalan jantung primer

Tension Pneumothorax
reduced filling of the right side of the heart
from either increased intrapleural pressure
secondary to air accumulation

Manifestations

respiratory distress (in an awake patient),

hypotension
decreasd breath sounds
hypertympany to percussion
jugular venous distention
shift of mediastinal structures to the
unaffected side with tracheal deviation

Treatment
Pleural decompression
Chest tube

Cardiac Tamponade
increased intrapericardial pressure
precluding atrial filling secondary to blood
accumulation
accumulation of blood within the
pericardial sac (~2000mL)
usually from penetrating trauma or chronic
medical conditions (heart failure or
uremia)

Manifestation

Dyspnea
Orthopnea
Peripheral edema
Chest pain
Tachycardia
Elevated central venous pressure
Hypotension, muffled heart tones, jugular
venous distention (becks triad)

Treatment
Dx : Echocardiography detecting
pericardial fluid
Pericardiocentesis under ultrasound

Cardiogenic Shock
Cardiogenic shock results from low cardiac
output due to myocardial pump failure
due to intrinsic myocardial damage
(infarction),
ventricular
arrhythmias,
extrinsic
compression
(cardiac
tamponade), or outflow obstruction (e.g.,
pulmonary embolism).

Cardiogenic Shock
Cardiogenic shock is characterized by
systemic hypoperfusion due to :
Severe depression of the cardiac index
[<2.2 (L/min)/m2] and sustained systolic
arterial hypotension (<90 mmHg)
despite filling pressure [pulmonary
capillary wedge pressure (PCWP) > 18
mmHg]

Cardiogenic Shock
Circulatory failure cardiac dysfunc.
primary myocardial failure most
common : secondary to AMI less
frequent : cardiomyopathy or myocarditis
or cardiac tamponade.
Shock is typically associated with ST
elevation MI (STEMI) and is less common
with non-ST elevation MI.

Cardiogenic Shock
LV failure accounts for ~80% of the
cases of CS complicating acute MI.
Remainder : Acute severe mitral
regurgitation,
ventricular
septal
rupture,
predominant
right
ventricular failure, and free wall
rupture or tamponade.

*Release
of
inflammatory cytokines
after
myocardial
infarction may lead to
inducible nitrous oxide
expression, excess NO,
and
inappropriate
vasodilation.
A vicious
progressive
dysfunction
ultimately
death if
interrupted.

spiral of
myocardial
occurs that
results in
it is not

Cardiogenic Shock
A
systemic
inflammatory
response
syndrome
may
accompany
large
infarctions and shock inflammatory
cytokines, inducible nitric oxide synthase,
and excess nitric oxide and peroxynitrite
may contribute to the genesis of CS as
they do to other forms of shock.

Cardiogenic Shock
Severe acidosis (pH < 7.25) reduces
the efficacy of endogenous and
exogenously
administered
catecholamines.
Refractory sustained ventricular or
atrial tachyarrhythmias can cause or
exacerbate cardiogenic shock.

Cardiogenic Shock
2/3 patients with CS have flowlimiting stenoses in 3 major
coronary arteries, & 20% : left main
coronary artery stenosis.

Cardiogenic Shock
Shock is present on admission in only 1/4
patients who develop CS complicating MI;
1/ develop it rapidly thereafter, within 6 h
4
of MI onset.
Another quarter develop shock later on the
first day. Subsequent onset of CS may be
due to reinfarction, marked infarct
expansion, or a mechanical complication.

Clinical Findings
Most : continuing chest pain and dyspnea,
appear
pale,
apprehensive,
and
diaphoretic.
Mentation
may
be
altered,
with
somnolence, confusion, and agitation.
The pulse is typically weak and rapid, often
in the range of 90110 beats/min, or
severe bradycardia due to high-grade
heart block may be present.

Clinical Findings
Systolic blood pressure is reduced (<90
mmHg) with a narrow pulse pressure (<30
mmHg).
Tachypnea, Cheyne-Stokes respirations,
and jugular venous distention may be
present.
S1 is usually soft, S3 gallop may be
audible.

Laboratory Findings
Prior to support with supplemental O2,
arterial blood gases : hypoxemia and
metabolic
acidosis,
compensated
by
respiratory alkalosis.
Cardiac markers, creatine phosphokinase
and its MB fraction, are markedly elevated,
as are troponins I and T.

Imaging Findings
Chest Roentgenogram :
CXR : pulmonary vascular congestion
and often pulmonary edema, may be
absent in up to a third of patients.
The heart size is usually normal when CS
results from a first MI but is enlarged
when it occurs in a patient with a
previous MI.

Imaging Findings
Echocardiogram :
Doppler : a left-to-right shunt in
patients with VSR and the severity
of MR when the latter is present.

Cardiogenic Shock
Differential Diagnoses :
Shock Secondary to RV Infarction
Mitral Regurgitation
Ventricular Septal Rupture
Free Wall Rupture
Acute Fulminant Myocarditis

Vasopressors
Norepinephrine
first line is a potent vasoconstrictor and inotropic
stimulant that is useful for patients with CS
Fewer adverse events, including arrhythmias,
compared to a dopamine randomized trial of patients
Started at a dose of 2 to 4 g/min and titrated upward
as necessary.
If systemic perfusion or systolic pressure cannot be
maintained at >90 mmHg with a dose of 15 g/min

Dopamine : infusion rate of 25 g/kg per min,

and the dose is increased every 25 min to
a maximum of 2050 g/kg per min
low doses ( 2 g/kg per min):dilates the renal
vascular bed, not been demonstrated
conclusively
moderate doses (210 g/kg per min) :
positive chronotropic and inotropic effects
as a consequence of -adrenergic receptor
stimulation.
higher doses: vasoconstrictor

 Dobutamine is a synthetic
sympathomimetic amine
low doses (2.5 g/kg per min) :positive
inotropic action and minimal positive
chronotropic activity
higher doses: moderate chronotropic activity
> 10 g/kg per min : vasodilating activity
precludes its use when a vasoconstrictor
effect is required

ANAPHYLACTIC SHOCK

Syok Anafilaksis
Anafilaksis suatu sindrom klinik yang terjadi akibat reaksi
alergik (reaksi imunologis) bersifat sistemik yang cepat
mengenai beberapa organ, meliputi :
Respirasi
Sirkulasi
Perncernaan
Kulit, dll
Sindrom tersebut menyebabkan syok syok anafilaksis
ditangani dengan cepat dan tepat KEMATIAN
Syok anafilaksis adalah gangguan perfusi jaringan akibat
adanya reaksi antigen antibodi yang mengeluarkan histamine
dengan akibat peningkatan permeabilitas membran kapiler dan
terjadi dilatasi arteriola sehingga venous return menurun

Reaksi Anafilaktoid NonImunologik

Reaksi anafilaksis reaksi imunologik
Mekanisme belum jelas
Gejala = reaksi imunologis tetapi lebih
ringan
Lebih banyak ditemukan dibanding dengan
reaksi imunologis

Insidens Syok Anafilaksis

Sangat jarang
Di Amerika :
40 60 % gigitan serangga
20 40 % kontras radiografi
10 20 % penisilin 9% fatal

Etiologi Syok Anafilaksis

Gigitan
serangga,
latex, makanan, dll
Antibiotik : penisilin
dan sefalosporin
Kontras radiografi
Anestetik lokal
NSAID

Opiate
Aspirin
Tubocurarin
Mannitol
Dextran

Manifestasi Klinis Syok

Anafilaksis

Reaksi Lokal : Biasanya hanya urtikaria dan edema

setempat , tidak fatal
Reaksi sistemik : Biasanya mengenai saluran napas
bag atas , sistem kardiovaskular, GIT, dan kulit,
reaksi tersebut timbul segera atau 30 menit setelah
terpapar antigen
a.Ringan : mata bengkak , hidung tersumbat , gatalgatal , bersin, timbul 2 jam setelah terpapar
b.Sedang : Bronkospasme, edema laring , mual ,
muntah
c.Berat : Bronkospasme, edema laring , stridor , sesak
napas ,muntah2 , sianosis , henti jantung , disfagia ,
nyeri perut , kejang , hipotensi , aritmia jantung ,
koma

Anaphylactic shock
Anaphylactic A life threatening syndrome (IgE
mediated) characterized by multiorgan
involvement and rapid onset
Anaphylactoid reaction A syndrome clinically
similar to anaphylaxis that is not mediated by
IgE

Etiologi

Risk Factors
Economic status in people of higher
economic status
Age &sex women > 30 years
Season Summer & early fall

Pathophysiology

Clinical manifestations
One cardinal feature of an anaphylactic reaction rapid
onset
5-30 minutes after parenteral exposure
2 hours after ingestion
Symptoms can resolve & recur hours later biphasic
anaphylaxis

First clinical manifestation pruritus, urticaria,

angioedema, flushing
Followed by mild to severe respiratory distress
cough chest tightness, dyspnea, wheeze (bronchospasm)
Hoarseness, Throat tightness, odynophagia (laryngeal
edema/oropharyngeal angioedema)

Fatal cardiovascular collapse or respiratory failure

Clinical manifestations

Diagnosis
Anaphylaxis is high likely when any one of the
following three criteria fulfilled :
1. Acute onset of an illness (minutes to several
hours) with involvement of the skin, mucosal
tissue, or both (pruritus, flushing, swollen lipstongue-uvula, generalized hives)
AND AT LEAST ONE OF THE FOLLOWING :
a) Respiratory compromise (dyspnea, brochospasm,
stridor, reduced PEF, Hypoxemia)
b) Reduced BP or associated symptoms of endorgan dysfunction (collapse, syncope, incontinence)

2. Two or more of the following occuring rapidly

(minutes to several hours) after exposure to a
likely allergen for that patient:
a) Involvement of the skin-mucosal tissue (itch-flush,
swollen lips-tongue-uvula, generalized hives)
b) Respiratory compromise
c) Reduced BP or associated symptoms
d) Persistent GI symptoms (crampy abdominal pain,
vomiting)

3. Reduced BP after exposure to known allergen for

that patient (minutes to several hours):
a) Infants & children : low systolic BP (age specific) or
in systolic BP> 30%
b) Adults : systolic BP < 90 mmHg or > 30% from that
persons baseline

DD

Carcinoid syndrome
Vasovagal reaction
Epiglotitis
Supraglotitis
Shock (cardiogenic, hemorrhagic/hypovolemic,
septic, obstruction)

Prevention
1.
2.
3.
4.

Get thorough drug allergy and atopic history

Check all drugs for proper labelling
Give drug orally rather than parenterally when possible
Give drug in distal extremity if possible when parenteral route
necessary
5. Always have resuscitation equipment available when
administering antigenic compounds
6. Ensure that patients wait in ED 30 minutes after drug
administration
7. Use unrelated drugs when feasible in susceptible population
8. Predisposed patients should carry warning identification
9. Predisposed patients are taught self-injection of epinephrine, and
patients are instructed to carry treatment kit at all times
10. Patients should avoid known antigens