pediatric shockll

8/8/2019 Pediatric ShockLL

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PediatricPediatric ShockShock

dr. Liliadr. Lilia DewiyantiDewiyanti,, SpASpA,, MSiMedMSiMed


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IntroductionIntroduction Shock is a syndrome that results fromShock is a syndrome that results from

inadequate oxygen delivery to meetinadequate oxygen delivery to meetmetabolic demandsmetabolic demands

DODO22 < VO< VO22

Untreated this leads to metabolicUntreated this leads to metabolicacidosis, organ dysfunction and deathacidosis, organ dysfunction and death


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Oxygen DeliveryOxygen Delivery

Oxygen delivery = Cardiac Output x ArterialOxygen delivery = Cardiac Output x ArterialOxygen ContentOxygen Content

(DO(DO22 = CO x CaO= CO x CaO22))

Cardiac Output = Heart Rate x Stroke VolumeCardiac Output = Heart Rate x Stroke Volume((CO = HR x SV)CO = HR x SV)

SV determined by preload, afterload andSV determined by preload, afterload andcontractilitycontractility

Art Oxygen Content = Oxygen content of theArt Oxygen Content = Oxygen content of theRBC + the oxygen dissolved in plasmaRBC + the oxygen dissolved in plasma

(CaO(CaO22 = Hb X SaO= Hb X SaO22 X 1.34 + (.003 X PaOX 1.34 + (.003 X PaO22))


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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 CompetitorsDrugs Autonomic Tone

Metabolic MilieuIons

Acid Base

Temperature

Drugs

Toxins

Influenced By

Influenced By

Influenced By

Influenced By


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Stages of ShockStages of Shock

CompensatedCompensated

Vital organ function maintained, BPVital organ function maintained, BPremains normal.remains normal.

UncompensatedUncompensated

Microvascular perfusion becomes marginal.Microvascular perfusion becomes marginal.Organ and cellular function deteriorate.Organ and cellular function deteriorate.Hypotension develops.Hypotension develops.

IrreversibleIrreversible


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Compensatory MechanismsCompensatory Mechanisms

BaroreceptorsBaroreceptors

In aortic arch and carotid sinus, stimulated byIn aortic arch and carotid sinus, stimulated by

high MAP and then excite cardioinhibitory centerhigh MAP and then excite cardioinhibitory centerleading to vasodilation, decreased BP, HR and CO.leading to vasodilation, decreased BP, HR and CO.Hyotension will lift the stimulation and result inHyotension will lift the stimulation and result invasoconstriction, increased HR, BP and CO.vasoconstriction, increased HR, BP and CO.

ChemoreceptorsChemoreceptors Respond to cellular acidosis and results inRespond to cellular acidosis and results in

vasoconstriction and respiratory stimulation.vasoconstriction and respiratory stimulation.


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Compensatory MechanismsCompensatory Mechanisms

(cont)(cont)ReninRenin--angiotensin systemangiotensin system

Decreased perfusion to the kidney leads to reninDecreased perfusion to the kidney leads to renin

secretion. Renin is eventually converted tosecretion. Renin is eventually converted toAnigiotensin II leading to vasoconstriction andAnigiotensin II leading to vasoconstriction andaldosterone release. Aldosterone leads to sodiumaldosterone release. Aldosterone leads to sodiumand water reabsorptionand water reabsorption

Humoral responsesHumoral responses

catecholamine release leading to increasedcatecholamine release leading to increasedcontractility and vasoconstrictioncontractility and vasoconstriction..

AutotransfusionAutotransfusion Reabsorption of interstitial fluid.Reabsorption of interstitial fluid.


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Clinical PresentationClinical Presentation Early diagnosis requires aEarly diagnosis requires a

high index of suspicionhigh index of suspicion

Diagnosis is made through the physicalDiagnosis is made through the physicalexamination focused on tissue perfusionexamination focused on tissue perfusion

Abject hypotension is a late andAbject hypotension is a late andpremorbid signpremorbid sign


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Hemodynamic Response toHemodynamic Response to

HemorrhageHemorrhage

25% 50%

% Plasma Loss

% of

Control

100

Vasc Resistance

Cardiac

Output

BloodPressure


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Initial Evaluation: PhysicalInitial Evaluation: Physical

ExamExam

Neurological:Neurological: FluctuatingFluctuating mentalmental

status, sunken fontanelstatus, sunken fontanel Skin and extremities:Skin and extremities: Cool, pallor,Cool, pallor,

mottling, cyanosis, poor cap refill,mottling, cyanosis, poor cap refill,

weak pulses, poor muscle tone.weak pulses, poor muscle tone. CardioCardio--pulmonary:pulmonary: Hyperpnea,Hyperpnea,

tachycardia.tachycardia.

Renal

Renal:: Scant, concentrated urineScant, concentrated urine


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Initial Evaluation: DirectedInitial Evaluation: Directed

HistoryHistoryPast medical historyPast medical history

heart diseaseheart disease

surgeriessurgeries

steroid usesteroid use

medical problemsmedical problemsBrief history of present illnessBrief history of present illness

exposuresexposures

onsetonset


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Differential Diagnosis of ShockDifferential Diagnosis of Shock II

HypovolemicHypovolemic

HemorrhageHemorrhage

Serum/Plasma lossSerum/Plasma loss DrugsDrugs

DistributiveDistributive

AnalphylacticAnalphylactic

NeurogenicNeurogenic

SepticSeptic

CardiogenicCardiogenic MyocardialMyocardial

DysrrhythmiaDysrrhythmia

CHDCHD--(duct(duct

dependant)dependant)

ObstructiveObstructive

Pneumo,Pneumo,Tamponade,Tamponade,

DissectionDissection

DissociativeDissociative

Heat, CO, CyanideHeat, CO, Cyanide

EndocrineEndocrine


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Differential Diagnosis of Shock IIDifferential Diagnosis of Shock II Precise etiologic classification may bePrecise etiologic classification may be

delayeddelayed

Immediate treatment is essentialImmediate treatment is essentialAbsolute or relative hypovolemia isAbsolute or relative hypovolemia is

usually presentusually present

The size of the cardiac silhouette onThe size of the cardiac silhouette onplain film can be used to estimate theplain film can be used to estimate theneed for volume replacement.need for volume replacement.


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Neonate in Shock:Neonate in Shock:

Include in differential:Include in differential:Congenital adrenal hyperplasiaCongenital adrenal hyperplasia

Inborn errors of metabolismInborn errors of metabolism

Obstructive left sided cardiac lesions:Obstructive left sided cardiac lesions:

Aortic stenosisAortic stenosis

Hypoplastic left heart syndromeHypoplastic left heart syndrome

Coarctation of the aortaCoarctation of the aorta

Interrupted aortic archInterrupted aortic arch


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Outcome of Pediatric ShockOutcome of Pediatric Shock

Chang 1999Chang 1999

82% Died

11 Septic

0% Died

7 Hypovolemic

75% Died

4 Cardiogenic

22 Shock Kids


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ManagementManagement--GeneralGeneralGoal: increase oxygen delivery andGoal: increase oxygen delivery and

decrease oxygen demand:decrease oxygen demand:

OxygenOxygen FluidFluid

Temperature controlTemperature control

AntibioticsAntibiotics

Correct metabolic abnormalitiesCorrect metabolic abnormalities

InotropesInotropes


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ManagementManagement--General (cont)General (cont)

AAirwayirway

If not protected or unable to be maintained,If not protected or unable to be maintained,intubate.intubate.

BBreathingreathing

Always give 100% oxygen to startAlways give 100% oxygen to start

Sat monitorSat monitor

CCirculationirculation Establish IV access rapidlyEstablish IV access rapidly

CR monitor and frequent BPCR monitor and frequent BP


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ManagementManagement--General (cont)General (cont)Laboratory studies:Laboratory studies:

ABGABG

Blood sugarBlood sugar

ElectrolytesElectrolytes

CBCCBC

PT/PTTPT/PTT Type and crossType and cross

CulturesCultures


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ManagementManagement--VolumeVolume

ExpansionExpansion Optimize preloadOptimize preload

NS or RLNS or RL

Except for myocardial failure use 10Except for myocardial failure use 10--20cc/kg aliquots q 220cc/kg aliquots q 2--10 minutes10 minutes

At 40At 40--60cc/kg reassess and consider:60cc/kg reassess and consider:ongoing losses, adrenal, intestinalongoing losses, adrenal, intestinalischemia, obstructive shock. Get CXR.ischemia, obstructive shock. Get CXR.Consider colloidConsider colloid

Further fluid therapy guided by response,Further fluid therapy guided by response,

labs, possibly CVP, CXRlabs, possibly CVP, CXR


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Fluid in early septic shockFluid in early septic shock

Carcillo, et al, JAMA, 1991Carcillo, et al, JAMA, 1991

RetrospectiveRetrospective review of 34 pediatric patients withreview of 34 pediatric patients withculture + septic shock, from 1982culture + septic shock, from 1982--1989.1989.

Hypovolemia determined by PCWP, u.o andHypovolemia determined by PCWP, u.o andhypotension.hypotension.

Overall, patients received 33 cc/kg at 1 hour and 95Overall, patients received 33 cc/kg at 1 hour and 95cc/kg at 6 hours.cc/kg at 6 hours.

Three groups:Three groups:

1: received up to 20 cc/kg in 11: received up to 20 cc/kg in 1stst

1 hour1 hour 2: received 202: received 20--40 cc/kg in 140 cc/kg in 1ststhourhour

3: received greater than 40 cc/kg in 13: received greater than 40 cc/kg in 1ststhourhour

No difference in ARDS between the 3 groupsNo difference in ARDS between the 3 groups


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Fluid in early septic shockFluid in early septic shockCarcillo, et al, JAMA, 1991Carcillo, et al, JAMA, 1991

Group 1Group 1

(n = 14)(n = 14)

Group 2Group 2

(n = 11)(n = 11)

Group 3Group 3

(n = 9)(n = 9)

Hypovolemic at 6Hypovolemic at 6hourshours

--DeathsDeaths

66

66

22

22

00

00

Not hypovolemicNot hypovolemic

at 6 hoursat 6 hours

--DeathsDeaths

88

22

99

55

99

11

Total deathsTotal deaths 88 77 11


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ManagementManagement -- CardiotonicsI

CardiotonicsI

Lack of history of fluid losses, history ofLack of history of fluid losses, history ofheart disease, hepatomegaly, rales,heart disease, hepatomegaly, rales,cardiomegaly and failure to improvecardiomegaly and failure to improveperfusion with adequate oxygenation,perfusion with adequate oxygenation,ventilation, heart rate, and volumeventilation, heart rate, and volumeexpansion suggests a cardiogenic orexpansion suggests a cardiogenic ordistributive component.distributive component.

Prior to introduction of cardiotonics, thePrior to introduction of cardiotonics, thegoals of therapy and criteria for monitoringgoals of therapy and criteria for monitoringof endpoint should be establishedof endpoint should be established


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ManagementManagement -- CardiotonicsII

CardiotonicsII

EpinephrineEpinephrine

0.050.05--1.5 ug/kg/min1.5 ug/kg/min

increase HR, SVR,increase HR, SVR,contractilitycontractility

End point: adequate BP;End point: adequate BP;acceptable tachycardiaacceptable tachycardia

NorepinephrineNorepinephrine

0.050.05--1.0 ug/kg/min1.0 ug/kg/min Increase SVRIncrease SVR

End point: adequate BPEnd point: adequate BP

DopamineDopamine 22--20 ug/kg/min20 ug/kg/min

Lower doses,Lower doses,increases renal andincreases renal andsplanchnic bloodsplanchnic bloodflow, & contractility.flow, & contractility.Higher dosesHigher doses

increases HR andincreases HR andSVRSVR

End Point: ImprovedEnd Point: Improvedperfusion, BP, Urineperfusion, BP, Urine


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ManagementManagement -- CardiotonicsIII

CardiotonicsIII

DobutamineDobutamine

11--20 ug/kg/min20 ug/kg/min

increasesincreasescontractility, maycontractility, mayreduce SVR, PVRreduce SVR, PVR

End Point: ImprovedEnd Point: Improved

perfusion, mayperfusion, maydecrease BPdecrease BP

Prostaglandin EProstaglandin E--11

0.050.05--0.1 ug/kg/min0.1 ug/kg/min

maintains patency ofmaintains patency ofductusductus


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Hypovolemic ShockHypovolemic Shock

Most common form of shock worldMost common form of shock world--widewide

Results in decreased circulating bloodResults in decreased circulating bloodvolume, decrease in prelaod, decreasedvolume, decrease in prelaod, decreasedstroke volume and resultant decrease instroke volume and resultant decrease inC.O.C.O.

Etiology: Hemorrhage, renal and/or GIEtiology: Hemorrhage, renal and/or GIfluid losses, capillary leak syndromesfluid losses, capillary leak syndromes


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Hypovolemic ShockHypovolemic Shock

Clinically, history of vomiting/diarrheaClinically, history of vomiting/diarrheaor trauma/blood lossor trauma/blood loss

Signs of dehydration: mucousSigns of dehydration: mucousmembranes, tears, skin turgormembranes, tears, skin turgor

Hypotension, tachycardia without signsHypotension, tachycardia without signs

of congestive heart failureof congestive heart failure


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Hemorrhagic ShockHemorrhagic Shock

Most common cause of shock in theMost common cause of shock in theUnited States (due to trauma)United States (due to trauma)

Patients present with an obvious historyPatients present with an obvious history(but in child abuse history may be(but in child abuse history may bemisleading)misleading)

Site of blood loss obvious or concealedSite of blood loss obvious or concealed(liver, spleen,intracranial, GI)(liver, spleen,intracranial, GI)

Hypotension, tachycardia and pallorHypotension, tachycardia and pallor


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Hypovolemic/HemorrhagicHypovolemic/Hemorrhagic

Shock: TherapyShock: TherapyAlways begin with ABCsAlways begin with ABCs

Replace circulating blood volumeReplace circulating blood volumerapidly: start with crystalloid/colloidrapidly: start with crystalloid/colloid

Blood products as soon as available forBlood products as soon as available forhemorrhagic shock (Type and Crosshemorrhagic shock (Type and Cross

with first blood draw)with first blood draw)

Replace ongoing fluid/blood losses &Replace ongoing fluid/blood losses &treat the underlying causetreat the underlying cause


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SIRS/Sepsis/Septic shockSIRS/Sepsis/Septic shock

Mediator release:Mediator release:

exogenous & endogenousexogenous & endogenous

MaldistributionMaldistribution

of blood flowof blood flow

CardiacCardiac

dysfunctiondysfunction

Imbalance ofImbalance ofoxygenoxygen

supply andsupply anddemanddemand

Alterations inAlterations in

metabolismmetabolism

Outcomes of mediator release in systemic inflammatory responseOutcomes of mediator release in systemic inflammatory response

syndrome (SIRS), sepsis, and septic shocksyndrome (SIRS), sepsis, and septic shock

Septic ShockSeptic Shock


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Septic Shock: Warm ShockSeptic Shock: Warm Shock

Early, compensated, hyperdynamic stateEarly, compensated, hyperdynamic state

Clinical signsClinical signs

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

Physiologic parametersPhysiologic parameters widened pulse pressure, increased cardiac ouptutwidened pulse pressure, increased cardiac ouptut

and mixed venous saturation, decreased systemicand mixed venous saturation, decreased systemicvascular resistance.vascular resistance.

Biochemical evidence:Biochemical evidence: Hypocarbia, elevated lactate, hyperglycemiaHypocarbia, elevated lactate, hyperglycemia


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Septic Shock: Cold ShockSeptic Shock: Cold Shock Late, uncompensated stage with drop inLate, uncompensated stage with drop in

cardiac output.cardiac output.

Clinical signsClinical signs Cyanosis, cold and clammy skin, rapid, threadyCyanosis, cold and clammy skin, rapid, thready

pulses, shallow respirations.pulses, shallow respirations.

Physiologic parametersPhysiologic parameters

Decreased mixed venous sats, cardiac output andDecreased mixed venous sats, cardiac output andCVP, increased SVR, thrombocytopenia, oliguria,CVP, increased SVR, thrombocytopenia, oliguria,myocardial dysfunction, capillary leakmyocardial dysfunction, capillary leak

Biochemical abnormalitiesBiochemical abnormalities Metabolic acidosis, hypoxia, coagulopathy,Metabolic acidosis, hypoxia, coagulopathy,

hypoglycemia.hypoglycemia.


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Cold Shock rapidly progresses to MOSF orCold Shock rapidly progresses to MOSF ordeath, if untreateddeath, if untreated

MultiMulti--Organ System Failure: Coma, ARDS,Organ System Failure: Coma, ARDS,CHF, Renal Failure, Ileus or GICHF, Renal Failure, Ileus or GIhemorrhage, DIChemorrhage, DIC

More organ systems involved, worse theMore organ systems involved, worse the

prognosisprognosis

Therapy: ABCs, fluidTherapy: ABCs, fluid

Appropriate antibiotics, treatment ofAppropriate antibiotics, treatment of

underlying causeunderlying cause

Septic Shock (cont)Septic Shock (cont)


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Cardiogenic ShockCardiogenic ShockEtiology:Etiology:

DysrhythmiasDysrhythmias

InfectionInfection

MetabolicMetabolic

ObstructiveObstructive

Drug intoxicationDrug intoxication Congenital heart diseaseCongenital heart disease

TraumaTrauma


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Cardiogenic Shock (cont)Cardiogenic Shock (cont)Differentiation from other types ofDifferentiation from other types of

shock:shock:

HistoryHistory PE:PE:

Enlarged liverEnlarged liver

Gallop rhythmGallop rhythm

MurmurMurmur

RalesRales

CXR:CXR:

Enlarged heart, pulmonary venous congestionEnlarged heart, pulmonary venous congestion


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Cardiogenic Shock (cont)Cardiogenic Shock (cont)Management:Management:

Improve cardiac output::Improve cardiac output::

Correct dysrhymiasCorrect dysrhymiasOptimize preloadOptimize preload

Improve contractilityImprove contractility

Reduce afterloadReduce afterload

Minimize cardiac work:Minimize cardiac work:Maintain normal temperatureMaintain normal temperature

SedationSedation

Intubation and mechanical ventilationIntubation and mechanical ventilation

Correct anemiaCorrect anemia


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Distributive ShockDistributive Shock Due to an abnormality in vascular toneDue to an abnormality in vascular tone

leading to peripheral pooling of blood with aleading to peripheral pooling of blood with arelative hypovolemia.relative hypovolemia.

EtiologyEtiology

AnaphylaxisAnaphylaxis

Drug toxicityDrug toxicity

Neurologic injuryNeurologic injury

Early sepsisEarly sepsis

ManagementManagement

FluidFluid

Treat underlying causeTreat underlying cause


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Obstructive ShockObstructive Shock Mechanical obstruction to ventricularMechanical obstruction to ventricular

outflowoutflow

Etiology: CHD, massive PE, tensionEtiology: CHD, massive PE, tensionpneumothorax, cardiac tamponadepneumothorax, cardiac tamponade

Inadequate C.O. in the face of adequateInadequate C.O. in the face of adequate

preload and contractilitypreload and contractility Tamponade: Narrow pulse pressure and/orTamponade: Narrow pulse pressure and/or

EMDEMD

Treat underlying cause.Treat underlying cause.


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Dissociative ShockDissociative Shock Inability of Hemoglobin molecule to giveInability of Hemoglobin molecule to give

up the oxygen to tissuesup the oxygen to tissues

Etiology: Carbon Monoxide poisoning,Etiology: Carbon Monoxide poisoning,methemoglobinemia,dyshemoglobinemiasmethemoglobinemia,dyshemoglobinemias

Tissue perfusion is adequate, but oxygenTissue perfusion is adequate, but oxygen

release to tissue is abnormalrelease to tissue is abnormal Early recognition and treatment of theEarly recognition and treatment of the

cause is main therapycause is main therapy


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Hemodynamic Variables inHemodynamic Variables inDifferent ShockStatesDifferent ShockStates

oo orormmooqqqqooooqqqqSeptic: LateSeptic: Lateqqqqmm OrOrqqqqqqqqooooooSeptic: EarlySeptic: Early

mm OrOrqqmm OrOrqqmm OrOrqqqqqqqqooooDistributiveDistributive

oooooooomm OrOrqqooqqObstructiveObstructive

oooooooomm OrOrqqooooooqqqqCardiogenicCardiogenic

qqqqqqqqqqqqmm OrOrqqooooHypovolemicHypovolemic

CVPCVPWedgeWedgeMAPMAPSVRSVRCOCO


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Final Thoughts

Final Thoughts

Recognize compensated shock quicklyRecognize compensated shock quickly-- have a highhave a highindex of suspicion, remember tachycardia is first sign.index of suspicion, remember tachycardia is first sign.Hypotension is late and ominous.Hypotension is late and ominous.

Gain access quicklyGain access quickly-- if necessary use an IO line.if necessary use an IO line.

Administer adequate amounts of fluid rapidly.Administer adequate amounts of fluid rapidly.Remember ongoing losses.Remember ongoing losses.

Correct electrloytes and glucose problems quickly.Correct electrloytes and glucose problems quickly.

If the patient is not responding the way you think heIf the patient is not responding the way you think heshould, broaden your differential, think aboutshould, broaden your differential, think aboutdifferent types of shock.different types of shock.

pediatric shockll

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