Presentation on theme: "Pediatric Shock Recognition, Classification and Initial Management"— Presentation transcript:
1Pediatric Shock Recognition, Classification and Initial Management Critical Concepts Course
2IntroductionShock 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
3Oxygen 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 contractilityArt Oxygen Content = Oxygen content of the RBC + the oxygen dissolved in plasma(CaO2 = Hb X SaO2 X (.003 X PaO2)
5Stages of Shock Compensated Vital organ function maintained, BP remains normal.UncompensatedMicrovascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops.Irreversible
6Clinical Presentation Early diagnosis requires a high index of suspicionDiagnosis is made through the physical examination focused on tissue perfusionAbject hypotension is a late and premorbid sign
10Differential Diagnosis of Shock Precise etiologic classification may be delayedImmediate treatment is essentialAbsolute or relative hypovolemia is usually present
11Include in differential: 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
12Management-GeneralGoal: increase oxygen delivery and decrease oxygen demand:For all children:OxygenFluidTemperature controlCorrect metabolic abnormalitiesDepending on suspected cause:AntibioticsInotropesMechanical Ventilation
13Management-General Airway Breathing Circulation If not protected or unable to be maintained, intubate.BreathingAlways give 100% oxygen to startSat monitorCirculationEstablish IV access rapidlyCR monitor and frequent BP
14Management-General Laboratory studies: ABG Blood sugar Electrolytes CBCPT/PTTType and crossCultures
15Management-Volume Expansion Optimize preloadNormal 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.
16Fluid in early septic shock Carcillo, et al, JAMA, 1991 Retrospective review of 34 pediatric patients with culture + septic shock, fromHypovolemia 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 cc/kg in 1st hour3: received greater than 40 cc/kg in 1st hourNo difference in ARDS between the 3 groups
17Fluid 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-Deaths62Not hypovolemic at 6 hours8951Total deaths7
18Inotropes 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.
19Hypovolemic 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
20Hypovolemic 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
21Hemorrhagic 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
22Hypovolemic/Hemorrhagic Shock: Therapy Always 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
23Septic Shock SIRS/Sepsis/Septic shock Mediator release: exogenous & endogenousMaldistributionof blood flowCardiacdysfunctionImbalance of oxygensupply and demandAlterations inmetabolism
25Septic Shock: “Cold Shock” Late, 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.
26Septic ShockCold 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 cause
28Cardiogenic Shock Differentiation from other types of shock: History Exam:Enlarged liverGallop rhythmMurmurRalesCXR:Enlarged heart, pulmonary venous congestion
29Cardiogenic Shock Management: Improve cardiac output:: Correct dysrhthymiasOptimize preloadImprove contractilityReduce afterloadMinimize cardiac work:Maintain normal temperatureSedationIntubation and mechanical ventilationCorrect anemia
30Distributive ShockDue to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia.EtiologyAnaphylaxisDrug toxicityNeurologic injuryEarly sepsisManagementFluidTreat underlying cause
31Obstructive Shock Mechanical obstruction to ventricular outflow Etiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax, cardiac tamponadeInadequate C.O. in the face of adequate preload and contractilityTreat underlying cause.
32Dissociative 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
33Hemodynamic Variables in Different Shock States or Septic: Late Or Septic: EarlyDistributiveObstructiveCardiogenicHypovolemicCVPWedgeMAPSVRCO
36Final 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.
37References, Recommended Reading, and Acknowledgments Uptodate: Initial Management of Shock in Pediatric patientsNelson’s Textbook of PediatricsSome slides based on works by Dr. Lou DeNicola and Dr. Linda Siegel for PedsCCMAmerican Heart Association PALS guidelines