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Pediatric Shock

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

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Pediatric Shock

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  1. PediatricShock Recognition, Classification and Initial Management Critical Concepts Course

  2. Introduction • Shock is a syndrome that results from inadequate oxygen delivery to meet metabolic demands • Oxygen delivery (DO2 ) is less than Oxygen Consumption (< VO2) • Untreated this leads to metabolic acidosis, organ dysfunction and death

  3. Oxygen Delivery • Oxygen 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)

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

  5. 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

  6. Initial Evaluation: Physical Exam Findings of Shock Neurological: Fluctuatingmental 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

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

  8. 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

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

  10. Neonate in Shock: Include in differential: • Congenital adrenal hyperplasia • Inborn errors of metabolism • Obstructive left sided cardiac lesions: • Aortic stenosis • Hypoplastic left heart syndrome • Coarctation of the aorta • Interrupted aortic arch

  11. 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

  12. 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

  13. Management-General • Laboratory studies: • ABG • Blood sugar • Electrolytes • CBC • PT/PTT • Type and cross • Cultures

  14. 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.

  15. Fluid in early septic shockCarcillo, 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 hour • 2: received 20-40 cc/kg in 1st hour • 3: received greater than 40 cc/kg in 1st hour • No difference in ARDS between the 3 groups

  16. Fluid in early septic shockCarcillo, et al, JAMA, 1991

  17. 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.

  18. Hypovolemic 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

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

  20. Hemorrhagic Shock • Most 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

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

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

  23. 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

  24. Septic Shock: “Cold Shock” • Late, uncompensated stage with drop in cardiac output. • Clinical signs • Cyanosis, cold and clammy skin, rapid threadypulses, 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.

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

  26. Cardiogenic Shock • Etiology: • Dysrhythmias • Infection (myocarditis) • Metabolic • Obstructive • Drug intoxication • Congenital heart disease • Trauma

  27. Cardiogenic Shock • Differentiation from other types of shock: • History • Exam: • Enlarged liver • Gallop rhythm • Murmur • Rales • CXR: • Enlarged heart, pulmonary venous congestion

  28. Cardiogenic Shock • Management: • Improve cardiac output:: • Correct dysrhthymias • Optimize preload • Improve contractility • Reduce afterload • Minimize cardiac work: • Maintain normal temperature • Sedation • Intubation and mechanical ventilation • Correct anemia

  29. Distributive Shock • Due to an abnormality in vascular tone leading to peripheral pooling of blood with a relative hypovolemia. • Etiology • Anaphylaxis • Drug toxicity • Neurologic injury • Early sepsis • Management • Fluid • Treat underlying cause

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

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

  32. CO SVR MAP Wedge CVP Hypovolemic    Or    Cardiogenic    Or    Obstructive    Or    Distributive    Or   Or   Or  Septic: Early    Or    Septic: Late      or  Hemodynamic Variables in Different Shock States

  33. Recognition and Classification

  34. Initial Management of Shock

  35. 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.

  36. 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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