Pediatric Shock

Recognition, Classification and

Initial Management

Critical Concepts Course

Introduction
 Shock is a syndrome that results from
inadequate oxygen delivery to meet
metabolic demands
 Oxygen delivery (DO2 ) is less than
Oxygen Consumption (< 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
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
 Initial Evaluation: Physical
Exam Findings of Shock

 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
 Cardiogenic
 Hypovolemic  Myocardial dysfunction
 Hemorrhage  Dysrrhythmia
 Fluid loss  Congenital heart
 Drugs disease
 Distributive  Obstructive
 Analphylactic  Pneumothorax,
 Neurogenic CardiacTamponade,
Aortic Dissection
 Septic
 Dissociative
 Heat, Carbon
monoxide, Cyanide
 Endocrine
Differential Diagnosis of Shock
 Precise etiologic classification may be
delayed
 Immediate treatment is essential
 Absolute or relative hypovolemia is
usually present
 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
Management-General
 Goal: increase oxygen delivery and
decrease oxygen demand:
For all children:
○ Oxygen
○ Fluid
○ Temperature control
○ Correct metabolic abnormalities
Depending on suspected cause:
○ Antibiotics
○ Inotropes
○ Mechanical Ventilation
Management-General

 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

 Laboratory studies:
– ABG
– Blood sugar
– Electrolytes
– CBC
– PT/PTT
– Type and cross
– Cultures
Management-Volume Expansion
 Optimize preload
 Normal saline (NS) or lactated ringer’s
(RL)
 Except for myocardial failure use 10-
20ml/kg every 2-10 minutes. Reasses
after every bolus.
 At 60ml/kg consider: ongoing losses,
adrenal insufficiency, intestinal
ischemia, obstructive shock. Get CXR.
May need inotropes.
 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
 Inotropes and Vasopressors
 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.
 Consider Appropriate inotropic or
vasopressor support.
 Hypovolemic Shock

 Most common form of shock world-wide

 Results in decreased circulating blood
volume, decrease in preload, decreased
stroke volume and resultant decrease in
cardiac output.
 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: dry mucous
membranes, absent tears, decreased
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, long bone
fracture)
 Hypotension, tachycardia and pallor
Hypovolemic/Hemorrhagic
Shock: Therapy
 Always begin with ABCs
 Replace circulating blood volume
rapidly: start with crystalloid
 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
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
 Cold Shock rapidly progresses to mutiorgan
system failure 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 (myocarditis)
– Metabolic
– Obstructive
– Drug intoxication
– Congenital heart disease
– Trauma
 Cardiogenic Shock
 Differentiation from other types of
shock:
– History
– Exam:
 Enlarged liver
 Gallop rhythm
 Murmur
 Rales
– CXR:
 Enlarged heart, pulmonary venous congestion
Cardiogenic Shock
 Management:
– Improve cardiac output::
 Correct dysrhthymias
 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: Congenital heart disease,
massive pulmonary embolism, tension
pneumothorax, cardiac tamponade
 Inadequate C.O. in the face of adequate
preload and contractility
 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 
Recognition and Classification
Initial Management of Shock
Final Thoughts
 Recognize compensated shock quickly- have a
high index of suspicion, remember tachycardia is
an early sign. Hypotension is late and ominous.
 Gain access quickly- if necessary use an
intraoseous line.
 Fluid, fluid, fluid - Administer adequate amounts of
fluid rapidly. Remember ongoing losses.
 Correct electrolytes 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.
References, Recommended
Reading, and Acknowledgments
 Uptodate: Initial Management of
Shock in Pediatric patients
 Nelson’s Textbook of Pediatrics
 Some slides based on works by Dr.
Lou DeNicola and Dr. Linda Siegel for
PedsCCM
 American Heart Association PALS
guidelines