Pediatric Shock

Critical Concepts Course

Recognition, Classification and Initial Management

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

DO2

CaO2

CO

SV

HR

Oxygenation

Hgb

A-a gradient DPG

Acid-Base Balance Blockers

Competitors Temperature

Drugs Conduction System

Ventricular Compliance

EDV

ESV Contractility

CVP Venous Volume

Venous Tone

Afterload Blockers Temperature Competitors Drugs Autonomic Tone

Metabolic Milieu Ions

Acid Base Temperature

Drugs Toxins

Influenced By

Influenced By

Influenced By

Influenced By

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

HypovolemicHemorrhageFluid lossDrugs

DistributiveAnalphylacticNeurogenicSeptic

CardiogenicMyocardial dysfunctionDysrrhythmiaCongenital heart

disease Obstructive

Pneumothorax, CardiacTamponade, Aortic Dissection

DissociativeHeat, Carbon

monoxide, CyanideEndocrine

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

AirwayIf not protected or unable to be maintained,

intubate.

BreathingAlways give 100% oxygen to startSat monitor

CirculationEstablish IV access rapidlyCR 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 shockCarcillo, 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 shockCarcillo, et al, JAMA, 1991

Group Group 11(n = 14)(n = 14)

Group Group 22(n = 11)(n = 11)

Group Group 33(n = 9)(n = 9)

Hypovolemic Hypovolemic at 6 hours at 6 hours

-Deaths-Deaths

66

66

22

22

0 0

00

Not Not hypovolemic hypovolemic at 6 hours at 6 hours

-Deaths-Deaths

88

22

99

55

9 9

11

Total deathsTotal deaths 88 77 11

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

SIRS/Sepsis/Septic shockSIRS/Sepsis/Septic shock

Mediator release:Mediator release:

exogenous & endogenousexogenous & endogenous

MaldistributionMaldistribution

of blood flowof blood flow

CardiacCardiac

dysfunctiondysfunction

Imbalance of Imbalance of oxygenoxygen

supply and supply and demanddemand

Alterations inAlterations in

metabolismmetabolism

Septic Shock

Septic Shock: “Warm Shock” Early, compensated, hyperdynamic state Clinical signs

Warm extremities with bounding pulses, tachycardia, tachypnea, confusion.

Physiologic parameterswidened 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 signsCyanosis, 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 abnormalitiesMetabolic acidosis, hypoxia, coagulopathy,

hypoglycemia.

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

Septic Shock

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 liverGallop rhythmMurmurRales

– 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

or or Septic: Septic: LateLate

Or Or Septic: Septic: EarlyEarly

Or Or Or Or Or Or DistributivDistributivee

Or Or ObstructiveObstructive Or Or CardiogeniCardiogeni

cc

Or Or HypovolemiHypovolemicc

CVPCVPWedgWedgee

MAPMAPSVRSVRCOCO

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