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Pediatric Shock Critical Concepts Course Recognition, Classification and Initial Management.

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Presentation on theme: "Pediatric Shock Critical Concepts Course Recognition, Classification and Initial Management."— Presentation transcript:

1 Pediatric Shock Critical Concepts Course Recognition, Classification and Initial Management

2 Introduction  Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands  Oxygen delivery (DO 2 ) is less than Oxygen Consumption (< VO 2 )  Untreated this leads to metabolic acidosis, organ dysfunction and death

3 Oxygen Delivery  Oxygen delivery = Cardiac Output x Arterial Oxygen Content (DO 2 = CO x CaO 2 )  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 (CaO 2 = Hb X SaO 2 X 1.34 + (.003 X PaO 2 )


5 Stages of Shock n Compensated – Vital organ function maintained, BP remains normal. n Uncompensated – Microvascular perfusion becomes marginal. Organ and cellular function deteriorate. Hypotension develops. n Irreversible

6 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

7 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

8 Initial Evaluation: Directed History Past medical history – heart disease – surgeries – steroid use – medical problems Brief history of present illness – exposures – onset

9 Differential Diagnosis of Shock  Hypovolemic Hemorrhage Fluid loss Drugs  Distributive Analphylactic Neurogenic Septic  Cardiogenic Myocardial dysfunction Dysrrhythmia Congenital heart disease  Obstructive Pneumothorax, CardiacTamponade, Aortic Dissection  Dissociative Heat, Carbon monoxide, Cyanide Endocrine

10 Differential Diagnosis of Shock  Precise etiologic classification may be delayed  Immediate treatment is essential  Absolute or relative hypovolemia is usually present

11 Neonate in Shock: Include in differential: nCongenital adrenal hyperplasia nInborn errors of metabolism nObstructive left sided cardiac lesions: –Aortic stenosis –Hypoplastic left heart syndrome –Coarctation of the aorta –Interrupted aortic arch

12 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

13 Management-General  Airway If not protected or unable to be maintained, intubate.  Breathing Always give 100% oxygen to start Sat monitor  Circulation Establish IV access rapidly CR monitor and frequent BP

14 Management-General nLaboratory studies: –ABG –Blood sugar –Electrolytes –CBC –PT/PTT –Type and cross –Cultures

15 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.

16 Fluid in early septic shock Carcillo, et al, JAMA, 1991 nRetrospective review of 34 pediatric patients with culture + septic shock, from 1982-1989. nHypovolemia determined by PCWP, u.o and hypotension. nOverall, patients received 33 cc/kg at 1 hour and 95 cc/kg at 6 hours. nThree groups: –1: received up to 20 cc/kg in 1 st 1 hour –2: received 20-40 cc/kg in 1 st hour –3: received greater than 40 cc/kg in 1 st hour nNo difference in ARDS between the 3 groups

17 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 -Deaths -Deaths662200 Not hypovolemic at 6 hours -Deaths -Deaths829591 Total deaths 871

18 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.

19 Hypovolemic Shock n Most common form of shock world-wide n Results in decreased circulating blood volume, decrease in preload, decreased stroke volume and resultant decrease in cardiac output. n Etiology: Hemorrhage, renal and/or GI fluid losses, capillary leak syndromes

20 Hypovolemic Shock n Clinically, history of vomiting/diarrhea or trauma/blood loss n Signs of dehydration: dry mucous membranes, absent tears, decreased skin turgor n Hypotension, tachycardia without signs of congestive heart failure

21 Hemorrhagic Shock n Most common cause of shock in the United States (due to trauma) n Patients present with an obvious history (but in child abuse history may be misleading) n Site of blood loss obvious or concealed (liver, spleen, intracranial, GI, long bone fracture) n Hypotension, tachycardia and pallor

22 Hypovolemic/Hemorrhagic Shock: Therapy n Always begin with ABCs n Replace circulating blood volume rapidly: start with crystalloid n Blood products as soon as available for hemorrhagic shock (Type and Cross with first blood draw) n Replace ongoing fluid/blood losses & treat the underlying cause

23 SIRS/Sepsis/Septic shock Mediator release: exogenous & endogenous Maldistribution of blood flow Cardiacdysfunction Imbalance of oxygen supply and demand Alterations in metabolism Septic Shock

24 Septic Shock: “Warm Shock”  Early, compensated, hyperdynamic state  Clinical signs Warm extremities with bounding pulses, tachycardia, tachypnea, confusion.  Physiologic parameters widened pulse pressure, increased cardiac ouptut and mixed venous saturation, decreased systemic vascular resistance.  Biochemical evidence: Hypocarbia, elevated lactate, hyperglycemia

25 Septic Shock: “Cold Shock”  Late, uncompensated stage with drop in cardiac output.  Clinical signs Cyanosis, 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 abnormalities Metabolic acidosis, hypoxia, coagulopathy, hypoglycemia.

26 n Cold Shock rapidly progresses to mutiorgan system failure or death if untreated n Multi-Organ System Failure: Coma, ARDS, CHF, Renal Failure, Ileus or GI hemorrhage, DIC n More organ systems involved, worse the prognosis n Therapy: ABCs, fluid n Appropriate antibiotics, treatment of underlying cause Septic Shock

27 Cardiogenic Shock nEtiology: –Dysrhythmias –Infection (myocarditis) –Metabolic –Obstructive –Drug intoxication –Congenital heart disease –Trauma

28 Cardiogenic Shock nDifferentiation from other types of shock: –History –Exam: nEnlarged liver nGallop rhythm nMurmur nRales –CXR: nEnlarged heart, pulmonary venous congestion

29 Cardiogenic Shock nManagement: –Improve cardiac output:: nCorrect dysrhthymias nOptimize preload nImprove contractility nReduce afterload –Minimize cardiac work: nMaintain normal temperature nSedation nIntubation and mechanical ventilation nCorrect anemia

30 Distributive Shock nDue to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia. nEtiology –Anaphylaxis –Drug toxicity –Neurologic injury –Early sepsis n Management – Fluid – Treat underlying cause

31 Obstructive Shock n Mechanical obstruction to ventricular outflow n Etiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax, cardiac tamponade n Inadequate C.O. in the face of adequate preload and contractility n Treat underlying cause.

32 Dissociative Shock n Inability of Hemoglobin molecule to give up the oxygen to tissues n Etiology: Carbon Monoxide poisoning, methemoglobinemia, dyshemoglobinemias n Tissue perfusion is adequate, but oxygen release to tissue is abnormal n Early recognition and treatment of the cause is main therapy

33 Hemodynamic Variables in Different Shock States  or   Septic: Late   Or   Septic: Early  Or  Distributive  Obstructive  Cardiogenic  HypovolemicCVPWedgeMAPSVRCO

34 Recognition and Classification

35 Initial Management of Shock

36 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.

37 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

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