Pediatric Shock

dr. Lilia Dewiyanti, SpA, MSiMed

 Introduction
 Shock is a syndrome that results from
inadequate oxygen delivery to meet
metabolic demands
 DO2 < VO2

 Untreated this leads to metabolic

acidosis, organ dysfunction and death
 Oxygen Delivery
 Oxygen delivery = Cardiac Output x Arterial
Oxygen Content
(DO2 = CO x CaO2)
 Cardiac Output = Heart Rate x Stroke Volume
(CO = HR x SV)
 SV determined by preload, afterload and
contractility
 Art Oxygen Content = Oxygen content of the
RBC + the oxygen dissolved in plasma
(CaO2 = Hb X SaO2 X 1.34 + (.003 X PaO2)
Figure 1. FACTORS AFFECTING OXYGEN DELIVERY

Hgb

CaO2
A-a gradient
DPG
Acid-Base Balance
Influenced By Blockers
Oxygenation Competitors
Temperature

DO2
Drugs
Influenced By Conduction System
HR

CVP
CO
EDV Venous Volume
Venous Tone
Metabolic Milieu
SV Ventricular Ions
Compliance Acid Base
Temperature
Influenced By
Drugs
ESV Contractility Toxins

Afterload Blockers
Influenced By Temperature Competitors
Drugs Autonomic Tone
 Stages of Shock

 Compensated
– Vital organ function maintained, BP
remains normal.
 Uncompensated
– Microvascular perfusion becomes marginal.
Organ and cellular function deteriorate.
Hypotension develops.
 Irreversible
 Compensatory Mechanisms

 Baroreceptors
– In aortic arch and carotid sinus, stimulated by
high MAP and then excite cardioinhibitory center
leading to vasodilation, decreased BP, HR and CO.
Hyotension will lift the stimulation and result in
vasoconstriction, increased HR, BP and CO.
 Chemoreceptors
– Respond to cellular acidosis and results in
vasoconstriction and respiratory stimulation.
Compensatory Mechanisms
(con’t)
 Renin-angiotensin system
– Decreased perfusion to the kidney leads to renin
secretion. Renin is eventually converted to
Anigiotensin II leading to vasoconstriction and
aldosterone release. Aldosterone leads to sodium
and water reabsorption
 Humoral responses
– catecholamine release leading to increased
contractility and vasoconstriction.
 Autotransfusion
– Reabsorption of interstitial fluid.
 Clinical Presentation
 Early diagnosis requires a
high index of suspicion

 Diagnosis is made through the physical

examination focused on tissue perfusion

 Abject hypotension is a late and

premorbid sign
 Hemodynamic Response to
Hemorrhage
% of Vasc Resistance
Control

100

Blood
Pressure
Cardiac
Output
25% 50%
% Plasma Loss
Initial Evaluation: Physical
Exam

 Neurological: Fluctuating mental

status, sunken fontanel
 Skin and extremities: Cool, pallor,
mottling, cyanosis, poor cap refill,
weak pulses, poor muscle tone.
 Cardio-pulmonary: Hyperpnea,
tachycardia.
 Renal: Scant, concentrated urine
Initial Evaluation: Directed
History
 Past medical history
– heart disease

– surgeries

– steroid use

– medical problems

 Brief history of present illness

– exposures

– onset
Differential Diagnosis of Shock I
 Cardiogenic
– Myocardial
 Hypovolemic – Dysrrhythmia
– Hemorrhage
– CHD-(duct
– Serum/Plasma loss
dependant)
– Drugs
 Obstructive
 Distributive – Pneumo,
– Analphylactic Tamponade,
– Neurogenic Dissection
– Septic  Dissociative
– Heat, CO, Cyanide
Differential Diagnosis of Shock II
 Precise etiologic classification may be
delayed
 Immediate treatment is essential
 Absolute or relative hypovolemia is
usually present
 The size of the cardiac silhouette on
plain film can be used to estimate the
need for volume replacement.
 Neonate in Shock:
Include in differential:
 Congenital adrenal hyperplasia
 Inborn errors of metabolism
 Obstructive left sided cardiac lesions:
– Aortic stenosis
– Hypoplastic left heart syndrome
– Coarctation of the aorta
– Interrupted aortic arch
 Outcome of Pediatric Shock
Chang 1999

2 2 S h o c k K id s

1 1 S e p t ic 7 H y p o v o l e m ic 4 C a r d i o g e n ic

8 2 % D ie d 0 % D ie d 7 5 % D ie d
 Management-General
 Goal: increase oxygen delivery and
decrease oxygen demand:
– Oxygen
– Fluid
– Temperature control
– Antibiotics
– Correct metabolic abnormalities
– Inotropes
 Management-General (con’t)

 Airway
– If not protected or unable to be maintained,
intubate.
 Breathing
– Always give 100% oxygen to start
– Sat monitor
 Circulation
– Establish IV access rapidly
– CR monitor and frequent BP
 Management-General (con’t)
 Laboratory studies:
– ABG
– Blood sugar
– Electrolytes
– CBC
– PT/PTT
– Type and cross
– Cultures
 Management-Volume
Expansion
 Optimize preload
 NS or RL
 Except for myocardial failure use 10-
20cc/kg aliquots q 2-10 minutes
 At 40-60cc/kg reassess and consider:
ongoing losses, adrenal, intestinal
ischemia, obstructive shock. Get CXR.
Consider colloid
 Further fluid therapy guided by response,
labs, possibly CVP, CXR
 Fluid in early septic shock
Carcillo, et al, JAMA, 1991

 Retrospective review of 34 pediatric patients with

culture + septic shock, from 1982-1989.
 Hypovolemia determined by PCWP, u.o and
hypotension.
 Overall, patients received 33 cc/kg at 1 hour and 95
cc/kg at 6 hours.
 Three groups:
– 1: received up to 20 cc/kg in 1st 1 hour
– 2: received 20-40 cc/kg in 1st hour
– 3: received greater than 40 cc/kg in 1st hour
 No difference in ARDS between the 3 groups
 Fluid in early septic shock
Carcillo, et al, JAMA, 1991

Group 1 Group 2 Group 3

(n = 14) (n = 11) (n = 9)
Hypovolemic at 6 6 2 0
hours
-Deaths 6 2 0
Not hypovolemic 8 9 9
at 6 hours
-Deaths 2 5 1
Total deaths 8 7 1
 Management - Cardiotonics I
 Lack of history of fluid losses, history of
heart disease, hepatomegaly, rales,
cardiomegaly and failure to improve
perfusion with adequate oxygenation,
ventilation, heart rate, and volume
expansion suggests a cardiogenic or
distributive component.
 Prior to introduction of cardiotonics, the
goals of therapy and criteria for monitoring
of endpoint should be established
Management - Cardiotonics II

 Dopamine
Epinephrine
– 0.05-1.5 ug/kg/min
– 2-20 ug/kg/min
– increase HR, SVR, contractility
– Lower
– End point:doses,
adequateincreases renal
BP; acceptable and
tachycardia
splanchnic blood flow, & contractility.
 Norepinephrine
– Higher doses increases HR and SVR
0.05-1.0 ug/kg/min
– End
– Point:
Increase SVR Improved perfusion, BP, Urine
– End point: adequate BP
Management - Cardiotonics III
 Dobutamine E-1
Prostaglandin
– 0.05-0.1
1-20 ug/kg/min
ug/kg/min
– maintains
increases contractility,
patency of ductus
may reduce SVR,
PVR
– End Point: Improved perfusion, may
decrease BP
 Hypovolemic Shock

 Most common form of shock world-wide

 Results in decreased circulating blood
volume, decrease in prelaod, decreased
stroke volume and resultant decrease in
C.O.
 Etiology: Hemorrhage, renal and/or GI
fluid losses, capillary leak syndromes
 Hypovolemic Shock
 Clinically, history of vomiting/diarrhea
or trauma/blood loss
 Signs of dehydration: mucous
membranes, tears, skin turgor
 Hypotension, tachycardia without signs
of congestive heart failure
 Hemorrhagic Shock

 Most common cause of shock in the

United States (due to trauma)
 Patients present with an obvious history
(but in child abuse history may be
misleading)
 Site of blood loss obvious or concealed
(liver, spleen,intracranial, GI)
 Hypotension, tachycardia and pallor
 Hypovolemic/Hemorrhagic
Shock: Therapy
 Always begin with ABCs
 Replace circulating blood volume
rapidly: start with crystalloid/colloid
 Blood products as soon as available for
hemorrhagic shock (Type and Cross
with first blood draw)
 Replace ongoing fluid/blood losses &
treat the underlying cause
 Septic Shock
SIRS/Sepsis/Septic shock

Mediator release:
exogenous & endogenous

Maldistribution Cardiac Imbalance of Alterations in

oxygen
of blood flow dysfunction metabolism
supply and
demand

Outcomes of mediator release in systemic inflammatory response

syndrome (SIRS), sepsis, and septic shock
Septic Shock: “Warm Shock”
 Early, compensated, hyperdynamic state
 Clinical signs
– Warm extremities with bounding pulses,
tachycardia, tachypnea, confusion.
 Physiologic parameters
– widened pulse pressure, increased cardiac ouptut
and mixed venous saturation, decreased systemic
vascular resistance.
 Biochemical evidence:
– Hypocarbia, elevated lactate, hyperglycemia
 Septic Shock: “Cold Shock”
 Late, uncompensated stage with drop in
cardiac output.
 Clinical signs
– Cyanosis, cold and clammy skin, rapid, thready
pulses, shallow respirations.
 Physiologic parameters
– Decreased mixed venous sats, cardiac output and
CVP, increased SVR, thrombocytopenia, oliguria,
myocardial dysfunction, capillary leak
 Biochemical abnormalities
– Metabolic acidosis, hypoxia, coagulopathy,
hypoglycemia.
 Septic Shock (con’t)
 Cold Shock rapidly progresses to MOSF or
death, if untreated
 Multi-Organ System Failure: Coma, ARDS,
CHF, Renal Failure, Ileus or GI
hemorrhage, DIC
 More organ systems involved, worse the
prognosis
 Therapy: ABCs, fluid
 Appropriate antibiotics, treatment of
underlying cause
 Cardiogenic Shock
 Etiology:
– Dysrhythmias
– Infection
– Metabolic
– Obstructive
– Drug intoxication
– Congenital heart disease
– Trauma
 Cardiogenic Shock (con’t)
 Differentiation from other types of
shock:
– History
– PE:
 Enlarged liver
 Gallop rhythm
 Murmur
 Rales
– CXR:
 Enlarged heart, pulmonary venous congestion
 Cardiogenic Shock (con’t)
 Management:
– Improve cardiac output::
 Correct dysrhymias
 Optimize preload
 Improve contractility
 Reduce afterload
– Minimize cardiac work:
 Maintain normal temperature
 Sedation
 Intubation and mechanical ventilation
 Correct anemia
 Distributive Shock
 Due to an abnormality in vascular tone
leading to peripheral pooling of blood with a
relative hypovolemia.
 Etiology
– Anaphylaxis
– Drug toxicity
– Neurologic injury
– Early sepsis
 Management
– Fluid
– Treat underlying cause
 Obstructive Shock
 Mechanical obstruction to ventricular
outflow
 Etiology: CHD, massive PE, tension
pneumothorax, cardiac tamponade
 Inadequate C.O. in the face of adequate
preload and contractility
 Tamponade: Narrow pulse pressure and/or
EMD
 Treat underlying cause.
 Dissociative Shock
 Inability of Hemoglobin molecule to give
up the oxygen to tissues
 Etiology: Carbon Monoxide poisoning,
methemoglobinemia,dyshemoglobinemias
 Tissue perfusion is adequate, but oxygen
release to tissue is abnormal
 Early recognition and treatment of the
cause is main therapy
Hemodynamic Variables in
Different Shock States

CO SVR MAP Wedge CVP

Hypovolemic    Or   
Cardiogenic    Or   
Obstructive    Or   
Distributive    Or   Or   Or 
Septic: Early    Or   
Septic: Late      or 
 Final Thoughts
 Recognize compensated shock quickly- have a high
index of suspicion, remember tachycardia is first
sign. Hypotension is late and ominous.
 Gain access quickly- if necessary use an IO line.
 Administer adequate amounts of fluid rapidly.
Remember ongoing losses.
 Correct electrloytes and glucose problems quickly.
 If the patient is not responding the way you think he
should, broaden your differential, think about
different types of shock.