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KEGAWATDARURATAN DI
BIDANG ILMU PENYAKIT DALAM
Pendahuluan
Pendekatan gawat darurat berdasarkan tanda
dan gejala
Basic Life Support
43 topik kajian dalam modul IMELS, tema
disajikan berdasarkan kekerapan ditemui dalam
keseharian pasien2 penyakit dalam
Menjaga serta meningkatkan kompetensi dokter
SpPD
Mampu memberikan pelayanan kegawatdarutan
yg optimal demi peningkatan pelayanan bagi
masyarakat.
Kegawatdaruratan Di Bidang
Ilmu Penyakit Dalam
Syok hipovolemik
Syok anafilaktik
Henti jantung
Intoksikasi dengan ancaman hidup
Sindrom distres pernafasan akut
Pneumonia berat
Pneumotoraks
Efusi pleura masif
Jejas paru karena suhu (trauma inhalasi)
Emboli paru
Gagal hati akut
Kegawatdaruratan Di Bidang
Ilmu Penyakit Dalam
Ensefalopati hepatikum
Kolangitis akut
Pankreatitis
Kolesistitis akut
Hematemesis melena
Hematoskezia
Ileus paralitik
Krisis hipertensi
Hipokalemia
Hiperkalemia
Hiponatremia
Kegawatdaruratan Di Bidang
Ilmu Penyakit Dalam
Hematuria masif
Gangguan ginjal akut
Bradikardia simtomatik
Takikardia dengan pulse
Sindroma koroner akut
Edema paru akut kardiogenik
Sindrom delirium akut
Koagulasi intravaskular diseminata
Sindrom vena kava superior
Sindrom lisis tumor
Ketoasidosis diabetikum
Kegawatdaruratan Di Bidang
Ilmu Penyakit Dalam
Hipoglikemia
Krisis tiroid
Sepsis
Leptospirosis (sindrom Weil)
Malaria berat
Tifoid toksik
Keracunan makanan
Tertelan zat korosif
Gigitan binatang berbisa
Sengatan panas
Shock
Definition
Epidemiology
Physiology and Pathophysiology
Classes of Shock
Clinical Presentation
Management
Controversies
Definition
A physiologic state characterized
by
Inadequate tissue perfusion
Clinically manifested by
Hemodynamic disturbances
Organ dysfunction
Epidemiology
Mortality
Septic shock 35-40% (1 month
mortality)
Cardiogenic shock 60-90%
Hypovolemic shock
variable/mechanism
Physiology
Basic unit of life = cell
Cells get energy needed to stay alive
by reacting oxygen with fuel (usually
glucose)
No oxygen, no energy
No energy, no life
Physiology
Cardiovascular System
Transports oxygen, fuel to cells
Removes carbon dioxide, waste products
for elimination from body
Cardiovascular system must
be able to maintain sufficient
flow through capillary beds to
meet cells oxygen and fuel
needs
Flow =
Perfusion
Adequate Flow
= Adequate
Perfusion
Inadequate Flow
= Indequate
Perfusion
(Hypoperfusion)
Hypoperfusio
n = Shock
Physiology
What is needed to maintain
perfusion?
Pump
Pipes
Fluid
: Heart
: Blood vessels
: Blood
Pathophysiology
Imbalance in oxygen supply and demand
Conversion from aerobic to anaerobic
metabolism
Appropriate and inappropriate metabolic
and physiologic responses
Characterized by three stages
Preshock (warm shock, compensated shock)
Shock
End organ dysfunction
Pathophysiology
Compensated shock
Low preload shock tachycardia, vasoconstriction,
mildly decreased BP
Low afterload (distributive) shock peripheral
vasodilation, hyperdynamic state
Shock
Initial signs of end organ dysfunction
Tachycardia
Tachypnea
Metabolic acidosis
Oliguria
Cool and clammy skin
Pathophysiology
End Organ Dysfunction
Progressive irreversible dysfunction
Oliguria or anuria
Progressive acidosis and decreased CO
Agitation, obtundation, and coma
Patient death
Classification
Schemes are designed to simplify
complex physiology
Major classes of shock
Hypovolemic
Cardiogenic
Distributive
Hypovolemic Shock
Results from decreased preload
Etiologic classes
Hemorrhage - e.g. trauma, GI bleed,
ruptured aneurysm
Fluid loss - e.g. diarrhea, vomiting,
burns, third spacing, iatrogenic
Hypovolemic Shock
Hemorrhagic
Shock
Parameter
I
II
III
IV
<750
7501500
15002000
>2000
<15%
1530%
3040%
>40%
Pulse rate
(beats/min)
<100
>100
>120
>140
Blood pressure
Normal
Decreased
Decreased
Decreased
Respiratory rate
(bpm)
1420
2030
3040
>35
>30
2030
515
Negligible
Normal
Anxious
Confused
Lethargic
Urine output
(ml/hour)
CNS symptoms
Crit Care. 2004; 8(5): 373
381.
Cardiogenic Shock
Results from pump failure
Decreased systolic function
Resultant decreased cardiac output
Etiologic categories
Myopathic
Arrhythmic
Mechanical
Extracardiac (obstructive)
Distributive Shock
Results from a severe decrease in
SVR
Vasodilation reduces afterload
May be associated with increased CO
Etiologic categories
Sepsis
Neurogenic / spinal
Other (next page)
Distributive Shock
Other causes
Systemic inflammation pancreatitis,
burns
Toxic shock syndrome
Anaphylaxis and anaphylactoid
reactions
Toxin reactions drugs, transfusions
Addisonian crisis
Myxedema coma
Distributive Shock
Septic Shock
Clinical Presentation
Clinical presentation varies with type
and cause, but there are features in
common
Hypotension (SBP<90 or Delta>40)
Cool, clammy skin (exceptions early
distributive, terminal shock)
Oliguria
Change in mental status
Metabolic acidosis
Evaluation
Done in parallel with treatment!
H&P helpful to distinguish type of shock
Full laboratory evaluation (including H&H,
cardiac enzymes, ABG)
Basic studies CxR, EKG, UA
Basic monitoring VS, UOP, CVP, A-line
Imaging if appropriate FAST, CT
Echo vs. PA catheterization
CO, PAS/PAD/PAW, SVR, SvO2
Treatment
Manage the emergency
Determine the underlying cause
Definitive management or support
Case
85 y/o M 4 hours postop S/P sigmoid
resection for perforated diverticulitis
is hypotensive on a monitored bed at
70/40
Best actions for the first 5 minutes?
Definitive Management
Hypovolemic Fluid resuscitate (blood
or crystalloid) and control ongoing loss
Cardiogenic - Restore blood pressure
(chemical and mechanical) and prevent
ongoing cardiac death
Distributive Fluid resuscitate,
pressors for maintenance, immediate
abx/surgical control for infection,
steroids for adrenocortical insufficiency
Controversies
IVF Resuscitation
Limited resuscitation in penetrating trauma
Use of hypertonic saline resuscitation in
trauma
Endpoints for prolonged resuscitation
Pressors
Best pressors for distributive shock
Monitoring
Most appropriate timing and use for PA
catheterization or intermittent echocardiogram