Approach to paediatric shock dr jason

approach

1. Approach to Paediatric Shock Presented by: Dr Jason Dsouza Moderator : Dr Sowmya S G Friday, February 19, 2021

2. Shock: Definition A physiologic state characterized by inadequate tissue perfusion to meet metabolic demand and tissue oxygenation .

3. Epidemiology 2% of all hospitalized infants and children

4. Few terminologies: Blood Pressure BP = CO x SVR Cardiac Output CO = SV X HR Stroke Volume: • Preload (LVEDV): Volume of blood present in ventricle before contraction – Reflects patient’s volume status • Afterload: The resistance to ventricular ejection Two variables: Vascular tone and transmural pressure • Myocardial Contractility: Many factors including coronary perfusion,baseline myocardial function, use of cardiotonic medications

5. Few terms(cont.) Oxygen Delivery to tissues DO2 = CO x CaO2 x 10 – Remember: CO depends on HR, preload, afterload, and contractility CaO2 = Hgb x 1.34 x SaO2 + (PaO2 x 0.003) -- Remember: Hemoglobin carries more than 99% of oxygen in the blood under standard conditions

6. Hypotension formula: 5 th centile PALS : 1-10 year – ( age in years x 2 )+ 70 , >10 year – 90 mm Hg Do you remember how to quickly estimate blood pressure by pulse? 60 80 70 90 If you palpate a pulse, you know SBP is at least this number

7. Stages of Shock Compensated Vital organ function maintained, BP remains normal. Hypotensive (Uncompensated) Microvascular perfusion becomes compromised. Organ and cellular function deteriorate. Hypotension develops. Irreversible - Inadequate perfusion of vital organs; irreparable damage; death cannot be prevented

8. Pathophysiology Types of shock (pathogenesis) Hypovolemic Cardiogenic Distributive: Septic, Neurogenic,Anaphylactic Obstructive

9. 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: Blood loss:Hemorrhage , Plasma loss: Burns,Nephrotic syndrome Water/Electrolyte loss: Vomiting,diarrhoea

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

11. Hemorrhagic Shock Most common cause of shock due to trauma Site of blood loss obvious or concealed (liver, spleen, intracranial, GI, long bone fracture) Hypotension, tachycardia and pallor

12. 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

13. Hypovolemic shock – How the body reacts >30%-45% Volume loss Mild/compensated vs severe/moderate hypotensive shock correlates with an acute blood loss of 30%

14. <20 -30% volume loss Sympathetic vasoconstriction maintains BP – Increase in diastolic BP Tachycardia Fall in urine output Prolonged CFT MAP SVR CO Blood volume lost 10% 30% 40%

15. Decrease in blood volume > 30% Hypotensive shock Decrease in systolic BP Decrease in CO(Despite rise in SVR) Weak central pulses Cardiac arrest is imminent MAP SVR CO Blood volume lost 10% 30% 40%

16. 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

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

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

19. 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.

20. 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 Septic Shock

21. Cardiogenic Shock Myocardial contractility is affected leading to systolic or diastolic dysfunction Etiology: Arrhythmias Congenital heart disease Cardiomyopathies : Infective,dilated or restrictive Metabolic,Ischemia Drug intoxication, Trauma

22. Cardiogenic Shock Tachypnoea, cool extremities, poor capillary filling time, poor central and peripheral pulses, declining mental status and urine output Exam: Enlarged liver Gallop rhythm Murmur Rales CXR: Enlarged heart, pulmonary venous congestion

23. 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

24. Obstructive Shock Mechanical obstruction to ventricular outflow Etiology: Congenital heart disease, massive pulmonary embolism, tension pneumothorax , cardiac tamponade Inadequate Cardiac Output inspite of adequate preload and contractility Treat underlying cause.

25. 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

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

27. Types of shock – Based on specific mechanism and treatment Causes that require primarily volume infusion – Hypovolemic - GI , 3 rd spacing Hemorrhagic - Traumatic Require an improvement of pump function Cardiogenic Late septic shock Require volume support and vasopressor support Septic shock Anaphylactic shock

28. Types of shock – Further classification Require immediate relief from obstruction to cardiac output Pneumothorax Cardiac tamponade Cellular poisons require specific antidote Methemoglobinemia Cyanide

29. Clinical features : Shock Early signs (compensated) Increased heart rate Poor systemic perfusion Late signs (decompensated / hypotensive ) Weak central pulses Altered mental status ( may not be present till late ) Hypotension

30. Septic shock is unique Hypotension (may be early) and poor end-organ perfusion may be present despite “good” skin perfusion. Hypotension is still a sign of decompensation.

31. Common signs / symptoms Altered Consciousness Confusion Tachypnea Pulses Skin perfusion BP

32. CFT – Capillary Filling Time COLD SHOCK (Prolonged CFT >3 sec) FLASH /BRISK

33. BP interpretation Systolic BP used for diagnosis Systolic BP – Lowest acceptable PALS – 1-10 year - age in years x 2 + 70 , >10 year – 90 mm Hg Mean BP – better indicator of tissue perfusion Not affected by cuff size, artery chosen

34. Mean BP Mean arterial pressure (MAP) = Diastolic + 1/3 rd of pulse pressure For adequate tissue perfusion, maintain MAP 1month to 3 years > 50 mm Hg > 3 years > 60 mmHg

35. Diastolic BP Required for coronary perfusion Minimum diastolic tolerated >25% of Systolic BP

36. Clinical - Capillary refill time/ BP Normalization of systolic blood pressure for age and CFT <=3seconds – reduced mortality (5.06% vs 16.37%)

37. Type of shock - Pulse pressure Narrow pulse pressure - (< 25% of systolic ) , prolonged CFT – hypovolemic shock , cardiogenic shock (Cold shock) Wide pulse pressure - (>50% of systolic ) Brisk CFT – high cardiac output with vasodilatation (Warm shock - Early sepsis )

38. Can we differentiate clinically ? Hypovolemic Shock – Narrow pulse pressure - apparent loss of fluid externally (or 3 rd spacing ) with usually normal consciousness unless severe . Distributive shock – Wide pulse pressure (bounding pulses ) Disproportionate tachypnea, tachycardia Cardiogenic – Narrow pulse pressure , no apparent volume loss with severe tachycardia , rales in chest with grunting

39. 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

40. 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

41. 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

42. Management-General A irway If not protected or unable to be maintained, intubate. B reathing Always give 100% oxygen to start Sat monitor C irculation Establish IV access rapidly CR monitor and frequent BP

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

44. What are the targets of management ? Pulse rate (Normal for age) Mean BP – Lowest normal (5 th centile ) CFT - 2 sec Diff between skin temp and core (rectal) temperature < 3C Urine output > 1ml/kg/hour (If > 2.5 ml /kg/hour decrease intake ) Improved mental status Lactate: normal value within 6 hours Central venous O 2 saturation > 70%

45. Management-Volume Expansion Optimize preload Normal saline (NS) or lactated ringer’s (RL) Except for myocardial failure use 5-10ml/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. Approxmimately 3ml of crystalloid is required to replace 1 ml of blood lost

46. Antibiotics and source control : within 1 hour of sepsis identification Corticosteroids in fluid refractory, cathecholamine resistant shock: High dose therapy for 23 hours Must be started within 8 hours Mechanical ventilation Blood and plasma products Glycemic control(<180mg/dl)

47. 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. Persistent hypotension: If no response even after 40-60ml/kg of crystalloid, start a vasopressor (norepinephrine, dopamine, etc ) and titrate to effect Goal: MAP > 60 Consider adrenal insufficiency: hydrocortisone 100 mg IV

48. Final Thoughts Shock is a state of oxygen deficiency; it can be classified as hypovolemic, cardiogenic, obstructive and distributive Clinically it can be recognized by HR & RR, abnormal CFT and pulses, hypotension and altered mental status Diastolic BP and mean BP are important to manage shock and pulse pressure is important in classification 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 intraosseous 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.

49. References and Recommended Reading Uptodate : Initial Management of Shock in Pediatric patients Nelson’s Textbook of Pediatrics American Heart Association PALS guidelines