SHOCK

Akbar Sepadan / Andhika Pangestu /

Andhiny Rezkia Enhas / Annisa Zakiroh
 Epidemiology
• Shock occurs in approximately 2% of all hospitalized
infants, children, and adults in developed countries,
and the mortality rate varies substantially
• Depending on the etiology and clinical
circumstances. Most patients who do not survive,
do not die in the acute hypotensive phase of shock,
but rather as a result of associated complications
and multiple organ dysfunction syndrome (MODS).
Types of Shock
 Pathophysiology

Hypotension

Blood pressure is maintained

Hypovolemic Shock
 Hypovolemic Shock
• Most common shock in pediatric, etiology:
– Vomitting,
– Diarrhea,
– Plasma leakage (e.c. DHF),
– Sepsis,
– Trauma,
– Burn wound,
– Gastrointestinal bleeding,
– Intracranial bleeding.
 Hypovolemic Shock
• Loss of fluid  ↓ preload  ↓ cardiac output
 ↓ stroke volume  Baroreseptor  ↑
heart rate and vasoconstriction to maintain
stroke volume and blood pressure.
• Long hypovolemic shock  multiorgan
disfunction.
– Renal,
– Heart,
– Hepar
 Therapy
• Crystaloid 10-20 ml/kg in 10-30 minutes, while
assessing respond of the body.
• ↑ intracellular volume  ↑ cardiac output
and ↓ heart rate.
• In severe cases, add more crystaloid 10 ml/kg
while assessing patients’ respond.
• Give the fluid until it comes to normovolemic,
you can also use koloid.
Septic Shock
 Septic Shock
• Septic shock is often a unique combination of
distributive, hypovolemic, and cardiogenic shock.
• Hypovolemia from intravascular fluid losses
occurs through capillary leak.
• Cardiogenic shock results from the myocardial-
depressant effects of sepsis
• Distributive shock is the result of decreased SVR.
preload, afterload, and myocardial contractility.
Pathophysiology
of septic shock
Management of Septic Shock
 Initial Resuscitation
• Respiratory distress and hypoxemia  face
mask oxygen, high flow nasal cannula oxygen,
nasopharyngeal CPAP (NP CPAP)
• Circulation  peripheral intravenous access or
intraosseous access can be used for fluid
resuscitation and inotrope infusion when a
central line is not available
• Initial therapeutic end points of resuscitation of septic shock:
- capillary refill of ≤2 sec,
- normal blood pressure for age
- normal pulses with no differential between peripheral
and central pulses
- warm extremities
- urine output >1 mL kg−1 hr−1
- normal mental status
- ScvO2 saturation ≥70%
- cardiac index between 3.3 and 6.0 L/min/m2
 Antibiotics and Source control
• Empiric antibiotics should be administered within 1 hour of
the identification of severe sepsis.
*Blood cultures should be obtained before administering antibiotics when possible but this
should not delay administration of antibiotics.

• Clindamycin and antitoxin therapies for toxic shock

syndromes with refractory hypotension.
• Early onset neonatal sepsis  broad-spectrum antibiotics:
ampicillin and gentamicin or amikacin.
• Late onset neonatal sepsis  broad-spectrum antibiotics, if
meningitis suspected  cefotaxime, suspected central line
sepsis  Vancomycin.
Fluid Resuscitation Inotropes/Vasopressors/Vasodilators
• initial resuscitation of • Begin peripheral inotropic
hypovolemic shock begins support until central venous
with infusion of isotonic access can be attained in
children who are not responsive
crystalloids or albumin with to fluid resuscitation.
boluses of up to 20 mL/kg • Patients with low cardiac output
crystalloids (or albumin and elevated systemic vascular
equivalent) over 5-10 resistance states with normal
minutes. blood pressure should be given
vasodilator therapies in addition
to inotropes.
Extracorporeal Membrane Oxygenation
(Ecmo) CORTICOSTEROIDS
• Consider ECMO for • Hydrocortisone therapy is
refractory pediatric septic reserved in children with
shock and respiratory catecholamine resistant
failure. shock and suspected or
proven absolute (classic)
adrenal insufficiency.
Protein C And Activated Protein
Concentrate Blood Products And Plasma Therapies
• Use of APC is not • Consider targeting
recommended due to a lack transfusion to a Hb goal of
of evidence of benefit and greater than 10 g/dl to
an increase in bleeding achive an ScvO2 > 70%, so
complications. enhancing oxygen delivery.
Mechanical Ventilation SEDATION/ANALGESIA/DRUG TOXICITIES
• Lung-protective strategies • We recommend use of
during mechanical sedation with a sedation goal
ventilation. in critically ill mechanically
ventilated patients with
sepsis.
• Monitor drug toxicity labs
because drug metabolism is
reduced during severe sepsis,
putting children at greater risk
of adverse drugrelated
events.
 Diuretics And Renal Replacement
Glycemic Control Therapy
• Control hyperglycemia using • Use diuretics to reverse
a similar target as in adults fluid overload when shock
(≤180 mg/dL). Glucose has resolved, and if
infusion should accompany unsuccessful then
insulin therapy in newborns continuous venovenous
and children because some hemofiltration (CVVH) or
hyperglycemic children intermittent dialysis to
make no insulin whereas prevent >10% total body
others are insulin resistant. weight fluid overload.
Deep Vein Thrombosis (DVT) Prophylaxis Stress Ulcer (SU) Prophylaxis
• No recommendation on the • Early enteral feeding is not
use of DVT prophylaxis in possible  H2 bolckers or
prepubertal children with PPI should be used in
severe sepsis. patients with severe sepsis.
NUTRITION
• Enteral nutrition given to
children who can be fed
enterally, and parenteral
feeding in those who
cannot.
Anaphylaxis Shock
 Anaphylaxis shock
• Anaphylaxis is defined as a serious allergic reaction
that is rapid onset and may cause death.
• Anaphylaxis occurs when there is a sudden release of
potent biologically active mediators from mast cells
and basophils, leading to cutaneous (urticaria,
angioedema, flushing), respiratory (bronchospasm,
laryngeal edema), cardivascular (hypotension,
dysarhytmias, myocardial ischemia), and
gastrointestinal (nausea, colickly abdominal pain,
vomiting, diarrhea) symptoms.
 Patohysiology
• Mediator inflammatory has been released
from mast cell and basofil after patient has
been exposed allergen that has been
sensitized.
Manifestasi klinis
Treatment
Cardiogenic Shock
 Shock Cardiogenic
• The clinical definition of cardiogenic shock is
decreased cardiac output and evidence of
tissue hypocia in the presence of adequate
intravascular volume
• The sign and symptoms of cardiogenic shock is
– Hypotension
- Absence hypovolemia
- Clinical sign of poor tissue perfusion ex:
oliguria, cyanosis, cool extremities, altered
mentation
• Physical examination in cardiogenic shock
- Skin is cyanotic and cool
- Peripheral pulses are rapid and faint
- Jugular venous distention and crackles in the lung
- Patient show sign of hypoperfusion, such as
altered mental status and decreased urine output
- Systemic hypotension
Treatment
 References
• Kliegman MD, Robert M. 2016. Nelson
Textbook of Pediatrics, Twentieth Edition.
Canada: Elsevier.
• Ikatan Dokter Anak Indonesia. 2011. Buku Ajar
Pediatri Gawat Darurat. Jakarta: Badan
Penerbit Ikatan Dokter Anak Indonesia.