Pediatric Shock

Critical Concepts CourseRecognition, Classification and Initial Management

IntroductionShock is a syndrome that results from inadequate oxygen delivery to meet metabolic demandsOxygen delivery (DO2 ) is less than Oxygen Consumption (< VO2)

Untreated this leads to metabolic acidosis, organ dysfunction and death

Oxygen DeliveryOxygen 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

A-a gradient

DPG

Acid-Base Balance

Blockers

Competitors

Temperature

CaO2

Influenced By

Oxygenation

DO2

Drugs

Conduction System

Influenced By

HR

CVP

Venous Volume

Venous Tone

EDV

CO

Metabolic Milieu

Ions

Acid Base

Temperature

Drugs

Toxins

Ventricular Compliance

SV

Influenced By

Contractility

Afterload Blockers

TemperatureCompetitors

Drugs Autonomic Tone

ESV

Influenced By

Stages of ShockCompensatedVital organ function maintained, BP remains normal.Uncompensated Microvascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops.Irreversible

Clinical PresentationEarly 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 ShockNeurological: Fluctuating mental status, sunken fontanelSkin 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 HistoryPast medical historyheart diseasesurgeriessteroid usemedical problemsBrief history of present illnessexposuresonset

Differential Diagnosis of ShockHypovolemicHemorrhageFluid lossDrugsDistributiveAnalphylacticNeurogenicSeptic

CardiogenicMyocardial dysfunctionDysrrhythmiaCongenital heart diseaseObstructivePneumothorax, CardiacTamponade, Aortic DissectionDissociativeHeat, Carbon monoxide, CyanideEndocrine

Differential Diagnosis of ShockPrecise etiologic classification may be delayedImmediate treatment is essentialAbsolute or relative hypovolemia is usually present

Neonate in Shock:Include in differential:Congenital adrenal hyperplasiaInborn errors of metabolismObstructive left sided cardiac lesions:Aortic stenosisHypoplastic left heart syndromeCoarctation of the aortaInterrupted aortic arch

Management-GeneralGoal: increase oxygen delivery and decrease oxygen demand:For all children:Oxygen Fluid Temperature controlCorrect metabolic abnormalitiesDepending on suspected cause:AntibioticsInotropesMechanical Ventilation

Management-GeneralAirwayIf not protected or unable to be maintained, intubate.BreathingAlways give 100% oxygen to startSat monitorCirculationEstablish IV access rapidlyCR monitor and frequent BP

Management-GeneralLaboratory studies:ABGBlood sugarElectrolytesCBCPT/PTTType and crossCultures

Management-Volume ExpansionOptimize preload Normal saline (NS) or lactated ringers (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 hour2: received 20-40 cc/kg in 1st hour3: received greater than 40 cc/kg in 1st hourNo difference in ARDS between the 3 groups

Fluid in early septic shock Carcillo, et al, JAMA, 1991

Group 1(n = 14)Group 2(n = 11)Group 3(n = 9)Hypovolemic at 6 hours -Deaths6

62

20

0Not hypovolemic at 6 hours -Deaths8

29

59

1Total deaths871

Inotropes and VasopressorsLack 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 ShockMost common form of shock world-wideResults 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 ShockClinically, history of vomiting/diarrhea or trauma/blood lossSigns of dehydration: dry mucous membranes, absent tears, decreased skin turgorHypotension, tachycardia without signs of congestive heart failure

Hemorrhagic ShockMost 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: TherapyAlways begin with ABCsReplace circulating blood volume rapidly: start with crystalloidBlood 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 shockMediator release:exogenous & endogenousMaldistributionof blood flowCardiacdysfunctionImbalance of oxygensupply and demandAlterations inmetabolismSeptic Shock

Septic Shock: Warm ShockEarly, compensated, hyperdynamic stateClinical signsWarm 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 ShockLate, uncompensated stage with drop in cardiac output.Clinical signsCyanosis, cold and clammy skin, rapid thready pulses, shallow respirations.Physiologic parametersDecreased mixed venous sats, cardiac output and CVP, increased SVR, thrombocytopenia, oliguria, myocardial dysfunction, capillary leakBiochemical abnormalitiesMetabolic acidosis, hypoxia, coagulopathy, hypoglycemia.

Cold Shock rapidly progresses to mutiorgan system failure or death if untreatedMulti-Organ System Failure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DICMore organ systems involved, worse the prognosisTherapy: ABCs, fluidAppropriate antibiotics, treatment of underlying causeSeptic Shock

Cardiogenic ShockEtiology:DysrhythmiasInfection (myocarditis)MetabolicObstructiveDrug intoxicationCongenital heart diseaseTrauma

Cardiogenic ShockDifferentiation from other types of shock:HistoryExam:Enlarged liverGallop rhythmMurmurRalesCXR: Enlarged heart, pulmonary venous congestion

Cardiogenic ShockManagement:Improve cardiac output::Correct dysrhthymiasOptimize preloadImprove contractilityReduce afterloadMinimize cardiac work:Maintain normal temperatureSedationIntubation and mechanical ventilationCorrect anemia

Distributive ShockDue to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia.EtiologyAnaphylaxisDrug toxicityNeurologic injuryEarly sepsisManagementFluidTreat underlying cause

Obstructive ShockMechanical obstruction to ventricular outflowEtiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax, cardiac tamponadeInadequate C.O. in the face of adequate preload and contractilityTreat underlying cause.

Dissociative ShockInability of Hemoglobin molecule to give up the oxygen to tissuesEtiology: Carbon Monoxide poisoning, methemoglobinemia, dyshemoglobinemiasTissue perfusion is adequate, but oxygen release to tissue is abnormalEarly recognition and treatment of the cause is main therapy

Hemodynamic Variables in Different Shock States

Recognition and Classification

Initial Management of Shock

Final ThoughtsRecognize 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 AcknowledgmentsUptodate: Initial Management of Shock in Pediatric patientsNelsons Textbook of PediatricsSome slides based on works by Dr. Lou DeNicola and Dr. Linda Siegel for PedsCCMAmerican Heart Association PALS guidelines

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