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SHOCK IN CHILDRENSHOCK IN CHILDR...
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DefinitionDefinition
Circulatory...
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Other DefinitionsOther Definitio...
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Oxygen DeliveryOxygen Delivery
•...
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HemodynamicsHemodynamics
Myocard...
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PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Defending the blood pressureDefe...
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• Pre...
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Classification of ShockClassific...
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Other ClassificationsOther Class...
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PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Cardiovascular Changes in ShockC...
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EvaluationEvaluation
• Regardles...
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EvaluationEvaluation
• Early Sig...
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Cardiovascular AssessmentCardiov...
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TreatmentTreatment
Airway manage...
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TreatmentTreatment
CirculationCi...
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PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Vasoactive/Cardiotonic AgentsVas...
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HypovolemicHypovolemic
• # 1 cau...
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Hypovolemic ShockHypovolemic Sho...
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TreatmentTreatment
Solution Na+ ...
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Hemorrhagic ShockHemorrhagic Sho...
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CardiogenicCardiogenic
• Low CO ...
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Cardiogenic ShockCardiogenic Sho...
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Cardiogenic ShockCardiogenic Sho...
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Obstructive ShockObstructive Sho...
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Obstructive ShockObstructive Sho...
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Distributive ShockDistributive S...
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Distributive ShockDistributive S...
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Distributive ShockDistributive S...
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Metabolic IssuesMetabolic Issues...
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Metabolic IssuesMetabolic Issues...
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Metabolic IssuesMetabolic Issues...
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Other StudiesOther Studies
• Loo...
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Other Studies IIOther Studies II...
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ConclusionConclusion
• Goal of t...
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Shock in Children

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Shock in Children

  1. 1. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU SHOCK IN CHILDRENSHOCK IN CHILDREN
  2. 2. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU DefinitionDefinition Circulatory system failure to supplyCirculatory system failure to supply oxygen and nutrients to meet cellularoxygen and nutrients to meet cellular metabolic demandsmetabolic demands
  3. 3. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Other DefinitionsOther Definitions • Blood PressureBlood Pressure BP = CO x SVRBP = CO x SVR • Cardiac OutputCardiac Output CO = SV X HRCO = SV X HR • Vascular Tone (SVR)Vascular Tone (SVR) – Regulated by several mechanismsRegulated by several mechanisms
  4. 4. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Oxygen DeliveryOxygen Delivery • DODO22 = CO x CaO= CO x CaO22 x 10x 10 – Remember: CO depends on HR, preload,Remember: CO depends on HR, preload, afterload, and contractilityafterload, and contractility • CaOCaO22 = Hgb x 1.34 x SaO= Hgb x 1.34 x SaO22 + (PaO+ (PaO22 x 0.003)x 0.003) – Remember: hemoglobin carries more than 99%Remember: hemoglobin carries more than 99% of oxygen in the blood under standardof oxygen in the blood under standard conditionsconditions
  5. 5. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU HemodynamicsHemodynamics Myocardial Contractility Stroke Volume Preload Cardiac Output Afterload Blood Pressure Heart Rate Systemic Vascular Resistance Textbook of Pediatric Advanced Life Support, 1988Textbook of Pediatric Advanced Life Support, 1988
  6. 6. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Defending the blood pressureDefending the blood pressure • Neural SympatheticNeural Sympathetic – BaroreceptorsBaroreceptors • Carotid BodyCarotid Body • Aortic ArchAortic Arch – Volume receptorsVolume receptors • Right AtriumRight Atrium • Pulmonary vascularPulmonary vascular – ChemoreceptorsChemoreceptors • Aortic and carotidAortic and carotid • MedullaryMedullary – Cerebral ischemicCerebral ischemic responseresponse • HumoralHumoral – Adrenal medullaAdrenal medulla • CatecholaminesCatecholamines – HypothalamopituitaryHypothalamopituitary responseresponse • AdrenocorticotropicAdrenocorticotropic hormonehormone • VasopressinVasopressin – Renin-angiotensin-Renin-angiotensin- aldosterone systemaldosterone system
  7. 7. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Cardiovascular functionCardiovascular function • Cardiac OutputCardiac Output  Clinical AssessmentClinical Assessment • peripheral perfusion, temperature, capillaryperipheral perfusion, temperature, capillary refill, urine output, mentation, acid-baserefill, urine output, mentation, acid-base statusstatus  CO = HR x SVCO = HR x SV • HR responds the quickestHR responds the quickest • SV is a function of three variablesSV is a function of three variables – preload, afterload, and myocardialpreload, afterload, and myocardial contractilitycontractility • A noncompliant heart cannot increase SVA noncompliant heart cannot increase SV
  8. 8. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Stroke VolumeStroke Volume • Preload (LVEDV)Preload (LVEDV) – Reflects patient’s volume statusReflects patient’s volume status – CVP or PCWPCVP or PCWP – Starling curveStarling curve • AfterloadAfterload – The resistance to ventricular ejectionThe resistance to ventricular ejection – Two variables:Two variables: • vascular tone and transmural pressurevascular tone and transmural pressure • Myocardial Contractility (“squeeze”)Myocardial Contractility (“squeeze”) – Many factors including coronary perfusion,Many factors including coronary perfusion, baseline myocardial function, use of cardiotonicbaseline myocardial function, use of cardiotonic medicationsmedications
  9. 9. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Classification of ShockClassification of Shock • COMPENSATEDCOMPENSATED – blood flow is normal or increased and may beblood flow is normal or increased and may be maldistributed; vital organ function ismaldistributed; vital organ function is maintainedmaintained • UNCOMPENSATEDUNCOMPENSATED – microvascular perfusion is compromised;microvascular perfusion is compromised; significant reductions in effective circulatingsignificant reductions in effective circulating volumevolume • IRREVERSIBLEIRREVERSIBLE – inadequate perfusion of vital organs; irreparableinadequate perfusion of vital organs; irreparable damage; death cannot be preventeddamage; death cannot be prevented
  10. 10. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Other ClassificationsOther Classifications • Hypovolemic or HemorrhagicHypovolemic or Hemorrhagic • CardiogenicCardiogenic • ObstructiveObstructive • DistributiveDistributive
  11. 11. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Cardiovascular Changes in ShockCardiovascular Changes in Shock TypeType PreloadPreload AfterloadAfterload ContractilityContractility CardiogenicCardiogenic    HypovolemicHypovolemic   No changeNo change DistributiveDistributive    SepticSeptic earlyearly    latelate   
  12. 12. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU EvaluationEvaluation • Regardless of the cause: ABC’sRegardless of the cause: ABC’s – First assess airway patency, ventilation, thenFirst assess airway patency, ventilation, then circulatory systemcirculatory system • Respiratory PerformanceRespiratory Performance – Respiratory rate and pattern, work of breathing,Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertnessoxygenation (color), level of alertness • CirculationCirculation – Heart rate, BP, perfusion, and pulses, liver sizeHeart rate, BP, perfusion, and pulses, liver size – CVP monitoring may be helpfulCVP monitoring may be helpful
  13. 13. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU EvaluationEvaluation • Early Signs of ShockEarly Signs of Shock – sinus tachycardiasinus tachycardia – delayed capillary refilldelayed capillary refill – fussy, irritablefussy, irritable • Late Signs of ShockLate Signs of Shock – bradycardiabradycardia – altered mental status (lethargy, coma)altered mental status (lethargy, coma) – hypotonia, decreased DTR’shypotonia, decreased DTR’s – Cheyne-Stokes breathingCheyne-Stokes breathing – hypotension is a very late signhypotension is a very late sign – Lower limit of SBP = 70 + (2 x age in years)Lower limit of SBP = 70 + (2 x age in years)
  14. 14. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Cardiovascular AssessmentCardiovascular Assessment • Heart RateHeart Rate – Too high: 180 bpm forToo high: 180 bpm for infants, 160 bpm forinfants, 160 bpm for children >1year oldchildren >1year old • Blood PressureBlood Pressure – Lower limit of SBP =Lower limit of SBP = 70 + (2 x age in years)70 + (2 x age in years) • Peripheral PulsesPeripheral Pulses – Present/AbsentPresent/Absent – Strength (diminished,Strength (diminished, normal, bounding)normal, bounding) • Skin PerfusionSkin Perfusion – Capillary refill timeCapillary refill time – TemperatureTemperature – ColorColor – MottlingMottling • CNS PerfusionCNS Perfusion – Recognition ofRecognition of parentsparents – Reaction to painReaction to pain – Muscle toneMuscle tone – Pupil sizePupil size • Renal PerfusionRenal Perfusion – UOP >1cc/kg/hrUOP >1cc/kg/hr
  15. 15. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU TreatmentTreatment Airway managementAirway management – Always provide supplemental oxygenAlways provide supplemental oxygen – Endotracheal intubation and controlledEndotracheal intubation and controlled ventilation is suggested if respiratory failure orventilation is suggested if respiratory failure or airway compromise is likelyairway compromise is likely • elective is safer and less difficultelective is safer and less difficult • decrease negative intrathoracic pressuredecrease negative intrathoracic pressure • improved oxygenation and Oimproved oxygenation and O22 delivery anddelivery and decreased Odecreased O22 consumptionconsumption • can hyperventilate if necessarycan hyperventilate if necessary
  16. 16. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU TreatmentTreatment CirculationCirculation – Based on presumed etiologyBased on presumed etiology – Rapid restoration of intravascular volumeRapid restoration of intravascular volume • PIV-if unstable you have 60-90 secondsPIV-if unstable you have 60-90 seconds • I.O. if less than 4-6 years oldI.O. if less than 4-6 years old • Central venous catheterCentral venous catheter • Use isotonic fluid: NS, LR, or 5% albuminUse isotonic fluid: NS, LR, or 5% albumin • PRBC’s to replace blood loss or if stillPRBC’s to replace blood loss or if still unstable after 60cc/kg of crystalloidunstable after 60cc/kg of crystalloid – anemia is poorly tolerated in the stressed,anemia is poorly tolerated in the stressed, hypoxic, hemodynamically unstable patienthypoxic, hemodynamically unstable patient
  17. 17. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Vasoactive/Cardiotonic AgentsVasoactive/Cardiotonic Agents • DopamineDopamine – 1-5 mcg/kg/min: dopaminergic1-5 mcg/kg/min: dopaminergic – 5-15 mcg/kg/min: more beta-15-15 mcg/kg/min: more beta-1 – 10-20 mcg/kg/min: more alpha-110-20 mcg/kg/min: more alpha-1 – may be useful in distributive shockmay be useful in distributive shock • DobutamineDobutamine – 2.5-15 mcg/kg/min: mostly beta-1, some beta-22.5-15 mcg/kg/min: mostly beta-1, some beta-2 – may be useful in cardiogenic shockmay be useful in cardiogenic shock • EpinephrineEpinephrine – 0.05-0.1 mcg/kg/min: mostly beta-1, some beta-20.05-0.1 mcg/kg/min: mostly beta-1, some beta-2 – > 0.1 to 0.2 mcg/kg/min: alpha-1> 0.1 to 0.2 mcg/kg/min: alpha-1
  18. 18. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Vasoactive/Cardiotonic AgentsVasoactive/Cardiotonic Agents • NorepinephrineNorepinephrine – 0.05-0.2mcg/kg/min: only alpha and beta-10.05-0.2mcg/kg/min: only alpha and beta-1 – Use up to 1mcg/kg/minUse up to 1mcg/kg/min • MilrinoneMilrinone – 50mcg/kg load then 0.375-0.75mcg/kg/min:50mcg/kg load then 0.375-0.75mcg/kg/min: phosphodiesterase inhibitor; results in increasedphosphodiesterase inhibitor; results in increased inotropy and peripheral vasodilation (greater effectinotropy and peripheral vasodilation (greater effect on pulmonary vasculature)on pulmonary vasculature) • PhenylephrinePhenylephrine – 0.1-0.5mcg/kg/min: pure alpha0.1-0.5mcg/kg/min: pure alpha
  19. 19. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU HypovolemicHypovolemic • # 1 cause of death in children worldwide# 1 cause of death in children worldwide • CausesCauses • Water Loss (diarrhea, vomiting with poorWater Loss (diarrhea, vomiting with poor PO intake, diabetes, major burns)PO intake, diabetes, major burns) • Blood Loss (obvious trauma; occult bleedingBlood Loss (obvious trauma; occult bleeding from pelvic fractures, blunt abdominalfrom pelvic fractures, blunt abdominal trauma, “shaken baby”)trauma, “shaken baby”) • Low preload leads to decreased SV andLow preload leads to decreased SV and decreased CO.decreased CO. • Compensation occurs with increased HR andCompensation occurs with increased HR and SVRSVR
  20. 20. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Hypovolemic ShockHypovolemic Shock • Mainstay of therapy isMainstay of therapy is fluidfluid • GoalsGoals – Restore intravascular volumeRestore intravascular volume – Correct metabolic acidosisCorrect metabolic acidosis – Treat the causeTreat the cause • Degree of dehydration often underestimatedDegree of dehydration often underestimated – Reassess perfusion, urine output, vital signs...Reassess perfusion, urine output, vital signs... • Isotonic crystalloid is always a good choiceIsotonic crystalloid is always a good choice – 20 to 50 cc/kg rapidly if cardiac function is20 to 50 cc/kg rapidly if cardiac function is normalnormal – NS can cause a hyperchloremic acidosisNS can cause a hyperchloremic acidosis
  21. 21. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU TreatmentTreatment Solution Na+ Cl- K+ Ca++ Mg++ BufferSolution Na+ Cl- K+ Ca++ Mg++ Buffer NS 154 154 0 0 0 NoneNS 154 154 0 0 0 None LR 130 109 4 3 0 LactateLR 130 109 4 3 0 Lactate Plasmalyte 140 98 5 0 3 AcetatePlasmalyte 140 98 5 0 3 Acetate & Gluconate& Gluconate  Inotropic and vasoactive drugs are not a substitute forInotropic and vasoactive drugs are not a substitute for fluid, however...fluid, however... – Can have various combinations of hypovolemic andCan have various combinations of hypovolemic and septic and cardiogenic shockseptic and cardiogenic shock – May need to treat poor vascular tone and/or poorMay need to treat poor vascular tone and/or poor cardiac functioncardiac function
  22. 22. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Hemorrhagic ShockHemorrhagic Shock • Treatment is PRBCs or whole bloodTreatment is PRBCs or whole blood – Treat the cause if able (stop the bleeding)Treat the cause if able (stop the bleeding) – Transfuse if significant blood loss is known orTransfuse if significant blood loss is known or if patient unstable after 60cc/kg crystalloidif patient unstable after 60cc/kg crystalloid • In an emergency can give group O PRBCsIn an emergency can give group O PRBCs before cross matching is complete or typebefore cross matching is complete or type specific non-cross-matched blood productsspecific non-cross-matched blood products
  23. 23. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU CardiogenicCardiogenic • Low CO and high systemic vascular resistanceLow CO and high systemic vascular resistance • Result of primary cardiac dysfunction:Result of primary cardiac dysfunction:  A compensatory increase in SVR occurs toA compensatory increase in SVR occurs to maintain vital organ functionmaintain vital organ function  Subsequent increase in LV afterload, LVSubsequent increase in LV afterload, LV work, and cardiac oxygen consumptionwork, and cardiac oxygen consumption  CO decreases and ultimately results inCO decreases and ultimately results in volume retention, pulmonary edema, andvolume retention, pulmonary edema, and RV failureRV failure
  24. 24. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Cardiogenic ShockCardiogenic Shock EtiologiesEtiologies • Congenital heartCongenital heart diseasedisease • ArrhythmiasArrhythmias • Ischemic heartIschemic heart diseasedisease • MyocarditisMyocarditis • Myocardial injuryMyocardial injury • Acute and chronicAcute and chronic drug toxicitydrug toxicity • Late septic shockLate septic shock • Infiltrative diseasesInfiltrative diseases – mucopolysaccharidosesmucopolysaccharidoses – glycogen storageglycogen storage diseasesdiseases • ThyrotoxicosisThyrotoxicosis • PheochromocytomaPheochromocytoma
  25. 25. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Cardiogenic ShockCardiogenic Shock • Initial clinical presentation can be identical toInitial clinical presentation can be identical to hypovolemic shockhypovolemic shock • Initial therapy is a fluid challengeInitial therapy is a fluid challenge • If no improvement or if worsens after givingIf no improvement or if worsens after giving volume, suspect cardiogenic shockvolume, suspect cardiogenic shock • Usually need invasive monitoring, furtherUsually need invasive monitoring, further evaluation, pharmacologic therapyevaluation, pharmacologic therapy • Balancing fluid therapy and inotropic support canBalancing fluid therapy and inotropic support can be very difficult.be very difficult. – Call an intensivist and/or a cardiologistCall an intensivist and/or a cardiologist
  26. 26. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Obstructive ShockObstructive Shock • Low CO secondary to a physical obstruction to flowLow CO secondary to a physical obstruction to flow • Compensatory increased SVRCompensatory increased SVR • Causes:Causes: – Pericardial tamponadePericardial tamponade – Tension pneumothoraxTension pneumothorax – Critical coarctation of the aortaCritical coarctation of the aorta – Aortic stenosisAortic stenosis – Hypoplastic left heart syndromeHypoplastic left heart syndrome
  27. 27. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Obstructive ShockObstructive Shock • Initial clinical presentation can be identical toInitial clinical presentation can be identical to hypovolemic shockhypovolemic shock • Initial therapy is a fluid challengeInitial therapy is a fluid challenge • Treat the causeTreat the cause – pericardial drain, chest tube, surgicalpericardial drain, chest tube, surgical interventionintervention – if the patient is a neonate with a ductalif the patient is a neonate with a ductal dependent lesion then give PGEdependent lesion then give PGE • Further evaluation, invasive monitoring,Further evaluation, invasive monitoring, pharmacologic therapy, appropriate consultspharmacologic therapy, appropriate consults
  28. 28. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Distributive ShockDistributive Shock • High CO and low SVR (opposite of hypovolemic,High CO and low SVR (opposite of hypovolemic, cardiogenic, and obstructive)cardiogenic, and obstructive) • Maldistribution of blood flow causingMaldistribution of blood flow causing inadequate tissue perfusioninadequate tissue perfusion • Due to release of endotoxin, vasoactiveDue to release of endotoxin, vasoactive substances, complement cascade activation,substances, complement cascade activation, and microcirculation thrombosisand microcirculation thrombosis • Early septic shock is the most common formEarly septic shock is the most common form
  29. 29. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Distributive ShockDistributive Shock • Goal is to maintain intravascular volume andGoal is to maintain intravascular volume and minimize increases in interstitial fluid (theminimize increases in interstitial fluid (the primary problem is a decrease in SVR)primary problem is a decrease in SVR) – Use crystalloid initiallyUse crystalloid initially – Additional fluid therapy should be based onAdditional fluid therapy should be based on lab studieslab studies – Can give up to 40cc/kg without monitoringCan give up to 40cc/kg without monitoring CVPCVP – Vasoactive/Cardiotonic agents oftenVasoactive/Cardiotonic agents often necessarynecessary – Treat the cause (i.e.. antimicrobial therapy)Treat the cause (i.e.. antimicrobial therapy)
  30. 30. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Distributive ShockDistributive Shock EtiologiesEtiologies • AnaphylaxisAnaphylaxis • Anaphylactoid reactionsAnaphylactoid reactions • Spinal cord injury/spinal shockSpinal cord injury/spinal shock • Head injuryHead injury • Early sepsisEarly sepsis • Drug intoxicationDrug intoxication – Barbiturates, Phenothiazines,Barbiturates, Phenothiazines, AntihypertensivesAntihypertensives
  31. 31. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Metabolic IssuesMetabolic Issues Acid-BaseAcid-Base • Metabolic acidosis develops secondary to tissueMetabolic acidosis develops secondary to tissue hypoperfusionhypoperfusion • Profound acidosis depresses myocardialProfound acidosis depresses myocardial contractility and impairs the effectiveness ofcontractility and impairs the effectiveness of catecholaminescatecholamines • Tx: fluid administration and controlledTx: fluid administration and controlled ventilationventilation • Buffer administrationBuffer administration – Sodium Bicarbonate 1-2meq/kg or can calculate aSodium Bicarbonate 1-2meq/kg or can calculate a 1/2 correction = 0.3 x weight (kg) x base deficit1/2 correction = 0.3 x weight (kg) x base deficit – hyperosmolarity, hypocalcemia, hypernatremia,hyperosmolarity, hypocalcemia, hypernatremia, left-ward shift of the oxyhemoglobin dissociationleft-ward shift of the oxyhemoglobin dissociation curvecurve
  32. 32. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Metabolic IssuesMetabolic Issues ElectrolytesElectrolytes • ElectrolytesElectrolytes – Calcium is important for cardiac function andCalcium is important for cardiac function and for the pressor effect of catecholaminesfor the pressor effect of catecholamines – Hypoglycemia can lead to CNS damage and isHypoglycemia can lead to CNS damage and is needed for proper cardiovascular functionneeded for proper cardiovascular function – Check the BUN and creatinine to evaluate renalCheck the BUN and creatinine to evaluate renal functionfunction – Hyperkalemia can occur from renal dysfunctionHyperkalemia can occur from renal dysfunction and/or acidosisand/or acidosis
  33. 33. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Metabolic IssuesMetabolic Issues Special TopicsSpecial Topics Congenital adrenal hyperplasiaCongenital adrenal hyperplasia • Infant presents in shock, usually in the secondInfant presents in shock, usually in the second week of life, typically a boy, with metabolicweek of life, typically a boy, with metabolic acidosis, hyponatremia, hypoglycemia, andacidosis, hyponatremia, hypoglycemia, and hyperkalemiahyperkalemia HyperammonemiaHyperammonemia • mild elevations are common with shockmild elevations are common with shock • levels > 1000 are consistent with inborn errorslevels > 1000 are consistent with inborn errors of metabolismof metabolism • consider Reye Syndrome, toxins, hepaticconsider Reye Syndrome, toxins, hepatic failurefailure
  34. 34. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Other StudiesOther Studies • Look for etiology of shockLook for etiology of shock • Evaluate hemoglobin, hematocrit, and plateletEvaluate hemoglobin, hematocrit, and platelet countcount – Should be followed as these values may drop afterShould be followed as these values may drop after fluid resuscitationfluid resuscitation • Shock from any etiology can lead to DIC andShock from any etiology can lead to DIC and end organ damageend organ damage – CBC, PT, INR, PTT, Fibrinogen, Factor V, FactorCBC, PT, INR, PTT, Fibrinogen, Factor V, Factor VIII, D-dimer, and/or FDPsVIII, D-dimer, and/or FDPs – Check LFT’s, follow CNS and pulmonary statusCheck LFT’s, follow CNS and pulmonary status
  35. 35. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU Other Studies IIOther Studies II • Think about inborn errors of metabolismThink about inborn errors of metabolism – Lactate and pyruvateLactate and pyruvate – Ammonium, LFTsAmmonium, LFTs – Plasma amino acids, urine organic acidsPlasma amino acids, urine organic acids – Urinalysis with reducing substancesUrinalysis with reducing substances – Urine tox screenUrine tox screen
  36. 36. UTHSCSAUTHSCSA PediatricResidentCurriculumforthePICUPediatricResidentCurriculumforthePICU ConclusionConclusion • Goal of therapy is identification, evaluation, andGoal of therapy is identification, evaluation, and treatment of shock in its earliest stagetreatment of shock in its earliest stage • Initial priorities are for the ABC’sInitial priorities are for the ABC’s • Fluid resuscitation begins with 20cc/kg ofFluid resuscitation begins with 20cc/kg of crystalloid or 10cc/kg of colloidcrystalloid or 10cc/kg of colloid • Subsequent treatment depends on the etiology ofSubsequent treatment depends on the etiology of shock and the patient’s hemodynamic conditionshock and the patient’s hemodynamic condition • Successful resuscitation depends on early andSuccessful resuscitation depends on early and judicious interventionjudicious intervention
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