Approach to hypovolemic and septic shock

Approach to hypovolemic and septic shock.
reference: Nelson text book of pediatrics, 19th edition

1. Approach to Hypovolemic and septic shock Prepared by: Dr. Ahmed M. Bahamid pediatric resident at Alsabeen hospital 28 August 2014

2. objectives Definition of shock Pathophysiology, common types and etiologies of shock Clinical manifestations and diagnosis Management of child with septic and Hypovolemic shock

3. definition Shock is an acute syndrome characterized by the body’s inability to deliver adequate oxygen to meet the metabolic demands of vital organs and tissues.

4. epidemiology Shock occurs in 2% of all hospitalized patients in USA. Death usually occur due to complications rather than during hypotensive phase The presence of MODS in patients with shock substantially increases the probability of death

5. Mortality in septic shock as low as 3% in previously healthy children & 6-9% in children with chronic illness Early effects of O2 deprivation on the cell are REVERSIBLE Early intervention reduces mortality Often masked in pediatrics . Why?

6. Pathophysiology An initial insult triggers shock, leading to inadequate O2 delivery to organs and tissues Compensatory mechanisms attempts to maintain BP

7. Compensatory mechanisms Increase HR, stroke volume, & vascular smooth muscle tone. Regulated through sympathetic NS & neurohormonal responses. Increased RR with greater CO2 elimination is a compensatory response to the metabolic acidosis & increased CO2 production from poor tissue perfusion

8. Compensatory mechanisms Renal excretion of H ions & retention of bicarbonate also increase in an effort to maintain normal body pH. Maintenance of intravascular volume is facilitated via sodium regulation through the renin-angiotensin- aldosterone & atrial natriuretic factor axes, cortisol & catecholamine synthesis & release, and ADH secretion.

9. Despite these compensatory mechanisms, the underlying shock and host response lead to vascular endothelial cell injury and significant leakage of intravascular fluids into interstitial extracellular space.

10. Initial insult Triggers shock Decreased perfusion Compensatory mechanisms Compensated shock Decompensated shock Tissue damage Multisystem organ failure Death

11. In adequate O2 at tissue level Anaerobic metabolism with resultant progressive LACTIC ACIDOSIS Inadequate perfusion persist Adverse VASCULAR, INFLAMMATORY, METABOLIC, CELLULAR, ENDOCRINE, AND SYSTEMIC responses Physiological instability

12. Stages of shock Pathophysiology of shock passes into 3 progressive stages; ( INTERVENE EARLY ) 1)- compensated shock 2)- decompensated shock 3)- irreversible sock

13. Why is it important to identify the stage of shock?

14. Compensated shock Compensatory mechanisms attempts to maintain BP NORMAL BLOOD PRESSURE Unexplained tachycardia Mild tachypnea Delayed capillary refill Orthostatic changes in pressure or pulse irritability

15. Decompensated shock It is a state of inadequate end-organ perfusion Compensatory mechanisms fails and HYPOTENSION occurs. Increased tachycardia, increased tachypnea Altered mental state, low urine output, Poor peripheral pulses. Capillary refill markedly delayed Cool extremities

16. Irreversible shock It occurs as a consequence of decompensated shock not managed properly and at right time. Permanent cellular damage & MODS. Recovery does not occur even with adequate restoration of circulatory volume Death occurs due to refractory acidosis, myocardial and brain ischemia.

17. Pathophysiology of shock Extracorporeal fluid loss Hypovolemic shock may be due to direct blood loss through hemorrhage or abnormal loss of body fluids ( diarrhea, vomiting, burns, diabetes mellitus or insipidus, nephrosis ) Lowering plasma oncotic pressure Hypovolemic shock may also result from hypoproteinemia ( liver injury, or as a progressive complication of increased capillary permeability) Abnormal vasodilation Distributive shock ( neurogenic, anaphylaxis, or septic shock ) occur when there is loss of vascular tone- venous, arterial or both ( sympathetic blockade, local substance affecting permeability, acidosis, drug effects, spinal cord transection ) Increased vascular permeability Sepsis may change vascular permeability in the absence of any change in capillary hydrostatic pressure ( endotoxins from sepsis, and excess histamine release in anaphylaxis) Cardiac dysfunction Peripheral hypoprfusion may result from any condition that affects the heart’s ability to pump blood efficiently ( ischemia, acidosis, drugs, constrictive pericarditis, sepsis )

18. In septic shock it is important to distinguish between the inciting infection and the host inflammatory response. Normally host immunity prevents the development of sepsis via activation of the reticular endothelial systems. This host immune response produces an inflammatory cascade of toxic mediators, including hormones, cytokines, and enzymes If this inflammatory cascade is uncontrolled, derangement of the microcirculatory system leads to subsequent organ and cellular dysfunction

19. Sepsis or tissue hypoxia with lactic acidosis ↓ ATP, ↑ H+, ↑ lactate In vascular smooth muscle ↑nitric oxide synthase ↑ vasopressin secretion ↓ vasopressin stores ↓ plasma vasopressin Vasodilatation Open K ATP ↑nitric oxide Open K Ca ↓ cytoplasmic Ca 2+ ↑ cGMP ↓ phosphorylated myosin

20. Systemic inflammatory response syndrome SIRS is an inflammatory cascade that is initiated by the host response to an infectious or noninfectious trigger. This inflammatory cascade is triggered when the host defense system does not adequately recognize and/or clear the triggering event The inflammatory cascade initiated by shock can lead to hypovolemia, cardiac & vascular failure, ARDS, insulin resistance, decreased CYP450 activity, coagulopathy,..etc

21. Ait‐ Oufella H, et al. Intensive Care Med 2010;26:1286‐1298. Rivers E, et al. NEJM 2001;345:1368‐1377 . SIRS Endothelial activation Disruption of: Coagulation Vascular permeability Vascular tone Global tissue hypoxia Microcirculatory failure Precipitated by: Cytokines [Over]production of nitric oxide Results in: Loss of vasomotor control Under‐perfusion of tissues Hypotension Organ dysfunction Heart Lungs Brain Kidneys Liver

22. TNF & other mediators increase vascular permeability , causing diffuse capillary leak , decreased vascular tone , and an imbalance between perfusion and metabolic demands of tissues TNF & IL-1 stimulates the release of pro-inflammatory and anti-inflammatory mediators causing fever and vasodilation Arachidonic acid metabolites lead to the development of fever, tachypnea, ventilation-perfusion abnormalities, and lactic acidosis.

23. Nitric oxide released from the endothelium or inflammatory cells, is a major contributor to hypotension. Myocardial depression is caused by myocardium-depressant factors, TNF, and some interleukins through direct myocardial injury, depleted catecholamines, increased -endorphin, and production of myocardial nitric oxide

24. The inflammatory cascade is initiated by toxins or superantigens via macrophage binding or lymphocyte activation. The vascular endothelium is both a target of tissue injury and a source of mediators that may cause further injury. The balance between these mediator groups for an individual patient contributes to the progression of disease and affects the chance for survival.

25. Focus of infection Superantigens or toxins Activated inflammatory cells Activation of host defense Activ . Of complement system Activ . Of coagulation system Endogenous mediator release Pro-inflammatory cytokines Anti-inflammatory cytokines Platelet activating factor Arachidonic acid metabolites Myocardial depressant substance Endogenous opiates Activated endothelium increased expression endothelial derived adhesion molecules Decreased thrombomodulin Increased plasminogen activator inhibitor Thrombosis & antifibrinolysis Hypovolemia, cardiac & vascular failure, capillary leak/endothelial damage, ARDS, DIC, decreased steroid synthesis Shock MODS Death

26. Inflammatory mediators Pro-inflammatory mediators Anti-inflammatory mediators Tumor necrosis factor (TNF) Interleukin-1 Interleukin-6 Interleukin-8 Interleukin-gamma HMGB-1 (high mobility group box chromosomal protein 1) Interleukin-4 Interleukin-10 Soluble receptor and receptor antagonists

27. Clinical manifestations Categorization is important, but there may be significant overlap among these groups, especially in septic shock. The clinical presentation of shock depends in part on the underlying etiology. If unrecognized and untreated all forms of shock progresses ultimately to irreversible shock and death.

28. Shock may initially manifest as only tachycardia or tachypnea. Progression leads to ; Decreased urine output Poor peripheral perfusion Respiratory distress or failure Alteration of mental status Low blood pressure

29. Because of the compensatory mechanisms hypotension is often a late finding and is not a criterion for the diagnosis of shock Tachycardia with or without tachypnea , may be the first or only sign of early compensated shock Hypotension reflects an advanced state of decompensated shock and is associated with increased mortality.

30. Signs of decreased perfusion Organ dysfunction ↓ Perfusion ↓↓ Perfusion ↓↓↓ Perfusion CNS __ Restless, apathetic, anxious Agitated/confused, coma Respiration __ ↑ Ventilation ↑↑ Ventilation Metabolism __ Compensated metabolic acidemia Uncompensated metabolic acidemia Gut __ ↑ Motility Ileus Kidney Decreased urine volume Oliguria < 0.5 mL/kg/hr Oliguria/ anuria Increased specific gravity Skin Delayed capillary refill Cold extremities Mottled, cyanotic, cold extremities CVS Increase heart rate 2* increase HR 2* increase HR Decreased P. pulses Decreased BP, only central pulses

31. Criteria for organ dysfunction Organ system Criteria for dysfunction Cardiovascular Despite administration of isotonic IV fluid bolus ≥ 60 mL/kg in 1 hour: decrease in BP (hypotension) < 5 th percentile for age or systolic BP < 2 SD below normal for age OR Need for vasoactive drug to maintain BP in normal range (dopamine> 5 micro/kg/min or dobutamine, epinephrine, or norepinephrine at any dose) OR Tow of the following : Unexplained metabolic acidosis: base deficit > 5 mEq/L Increased arterial lactate: > 2x upper limit of normal Oliguria: urine output < 0.5 mL/kg/hr Prolonged capillary refill: > 5 seconds Core to peripheral temperature gap > 3◦C

32. Criteria for organ dysfunction Organ system Criteria for dysfunction Respiratory PaO2/Fio2 ratio < 300 in the absence of cyanotic heart disease or pre-existing lung disease OR PaCO2 > 65 torr or 20 mm Hg over baseline PaCO2 OR Proven need for >50% FiO2 to maintain saturation ≥ 92% OR Need for non-elective invasive or non-invasive mechanical ventilation Neurologic GCS score ≤ 11 OR Acute change in mental status with a decrease in GCS score ≥ 3 points from abnormal baseline

33. Criteria for organ dysfunction Organ system Criteria for dysfunction Hematologic Platelet count < 80,000/mm³ or a decline of 50% in the platelet count from the highest value recorded over the last 3 days (for the patient with chronic hematologic or oncologic disorders) OR INR > 2 Renal Serum creatinine ≥ 2x upper limit of normal for age or 2-fold increase in baseline creatinine value Hepatic Total bilirubin ≥ 4mg/dL (not applicable for newborn) Alanine transaminase level 2x upper limit of normal for age

34. Types of shock SHOCK Hypovolemic Cardiogenic D istributive O bstructive S eptic

35. Why is it important to identify the type of shock? Because successful management often depends on correct interpretation of the classification of shock, and often, its specific etiology. For example, the interventions for obstructive or Cardiogenic shock will be different from the interventions for distributive shock (which will also change depending on whether the etiology is anaphylaxis or sepsis).

36. Hypovolemic shock Most common cause of shock in children worldwide Decreased preload due to internal or external losses Water /electrolyte loss (diarrhea & vomiting) Blood loss (hemorrhage) Plasma loss (burns & nephrotic syndrome)

37. Hypovolemic shock Tachycardia and an increase in systemic vascular resistance are the initial compensatory response to maintain cardiac output and blood pressure Manifests initially as orthostatic hypotension Associated with dry mucous membranes, dry axillae, poor skin turgor, and decreased urine output.

38. Hypovolemic shock Depending on the degree of the dehydration, the patient with hypovolemic shock may present with either normal or slightly cool distal extremities, and peripheral or central (femoral) pulses may be normal, decreased, or absent.

39. Cardiogenic shock Cardiac pump failure 2ndry to poor myocardial function CHD Cardiomyopathies ( infectious or acquired, dilated or restrictive) Ischemia or arrhythmias Myocardial contractility affected leading to systolic and/or diastolic dysfunction

40. Cardiogenic shock Because of decreased CO and compensatory peripheral vasoconstriction, the presenting signs of cardiogenic shock are: Tachypnea Cool extremities Delayed capillary refill Poor peripheral and/or central pulses Declining mental status Decreased urine output

41. Distributive shock Inadequate vasomotor tone, which leads to capillary leak and maldistribution of fluid into the interstitium Sepsis, hypoxia, poisonings, anaphylaxis, spinal cord injury, or mitochondrial dysfunction. ↓ in SVR accompanied with maldistribution of blood flow from vital organs and a compensatory increase in CO This process leads to decrease in preload and afterload

42. Distributive shock Distributive shock manifests early as peripheral vasodilation and increased but inadequate cardiac output

43. Obstructive shock Caused by a lesions that creates a mechanical barrier that impedes adequate CO Decreased CO secondary to direct impediment to right or left heart outflow or restriction of all cardiac chambers.

44. Obstructive shock Pericardial tamponade, tension pneumothorax, pulmonary embolism, ductus-dependant CHD Anterior Mediastinal masses. Critical coarctation of the aorta

45. Obstructive shock Obstructive shock often manifests as inadequate cardiac output due to a physical restriction of forward blood flow; the acute presentation may quickly progress to cardiac arrest

46. Regardless of etiology, uncompensated shock, with hypotension, high vascular resistance, decreased cardiac output, respiratory failure, obtundation, and oliguria, occurs late in the progression of the disease.

47. Additional clinical findings in shock include cutaneous lesions such as petechiae, diffuse erythema, ecchymoses, erythema gangrenosum, and peripheral gangrene. jaundice can be present either as a sign of infection or as a result of MODS.

48. Septic shock Usually involves a more complex interaction of distributive, Hypovolemic, and Cardiogenic shock Bacterial Viral Fungal (immunocompromised patients are at increased risk)

49. Septic shock

50. Sepsis is defined as SIRS resulting from a suspected or proven infectious etiology. Severe sepsis (the presence of sepsis combined with organ dysfunction. Septic shock (severe sepsis plus the persistence of hypoperfusion or hypotension despite adequate fluid resuscitation or a requirement for vasoactive agents), MODS, and possibly death.

51. The progression of sepsis Outcomes improve with early recognition and treatment

52. Septic shock The initial sign and symptoms are; Alteration in temperature regulation (hypo or hyperthermia) Tachycardia and tachypnea In early stages (hyperdynamic phase or warm shock) the cardiac output increases in an attempt to maintain adequate O2 delivery and meet the metabolic demands

53. Septic shock As septic shock progresses, cardiac output falls in response to the effects of numerous inflammatory mediators, leading to a compensatory elevation in SVR and the development of cold shock

54. Hemodynamic variables in different shock states Type of shock CO SVR MAP CWP CVP HYPOVOLEMIC ↓ ↑ ↔ OR ↓ ↓↓↓ ↓↓↓ CARDIOGENIC: SYSTOLIC ↓↓ ↑↑↑ ↔ OR ↓ ↑↑ ↑↑ DIASTOLIC ↔ ↑↑ ↔ ↑↑ ↑ OBSTRUCTIVE ↓ ↑ ↔ OR ↓ ↑↑ Ω ↑↑ Ω DISTRIBUTIVE ↑↑ ↓↓↓ ↔ OR ↓ ↔ OR ↓ ↔ OR ↓ SEPTIC: EARLY ↑↑↑ ↓↓↓ ↔ OR ↓ ‡ ↓ ↓ LATE ↓↓ ↓↓ ↓↓ ↑ ↑ or ↔

55. diagnosis Shock is diagnosed clinically on the basis of a thorough history and physical exam.

56. Differential diagnosis of the child presenting with shock Bleeding shock — History of trauma ,Bleeding site Dengue shock syndrome — Known dengue outbreak or season, History of high fever ,Purpura Cardiac shock — History of heart disease , congested neck veins and liver Septic shock — History of febrile illness ,Very ill child Known outbreak of meningococcal infection Shock associated with severe dehydration — History of profuse diarrhea ,Known cholera outbreak

57. Child with shock

58. Testing Skin pinch for assessing dehydration

59. Laboratory findings Thrombocytopenia & anemia Prolonged PT & PTT Reduced fibrinogen level Elevation of fibrin split products Elevated neutrophil count and immature forms, vacuolation of neutrophils, toxic granulations, and Döhle bodies can be seen with infection Neutropenia & leukopenia are ominous sign of overwhelming sepsis.

60. Laboratory findings Glucose dysregulation (hyper or hypoglycemia) is a common stress response Electrolyte abnormalities are hypocalcemia, hypoalbuminemia, and metabolic acidosis. Renal and/or hepatic function may be abnormal Patients with ARDS or pneumonia have impairment of oxygenation (decreased PaO2) as well as ventilation (increased PaCO2) in the later stage of lung injury.

61. Laboratory findings The hallmark of uncompensated shock is an imbalance between O2 delivery and O2 consumption. This state manifests clinically by increased lactic acid production (high anion gap, metabolic acidosis) due to anaerobic metabolism and a low mixed venous oxygen saturation

62. Laboratory findings Serum lactate measurement along with mixed venous oxygen saturation may be used as a marker for the adequacy of oxygen delivery and the effectiveness of therapeutic interventions.

63. treatment

64. Initial management Early recognition and prompt intervention are extremely important in the management of all forms of shock.

65. Initial management Regardless of the cause: ABC’s First assess airway patency, ventilation, then circulatory system Respiratory Performance Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertness Circulation Heart rate, BP, perfusion, and pulses, liver size CVP monitoring may be helpful

66. Initial management Airway management Always provide supplemental oxygen Endotracheal intubation and controlled ventilation is suggested if respiratory failure or airway compromise is likely elective is safer and less difficult decrease negative intrathoracic pressure improved oxygenation and O 2 delivery and decreased O 2 consumption

67. Initial management Neonates and infants in particular may have profound glucose dysregulation in association with shock Glucose levels should be checked routinely and treated appropriately, especially early in the course of the illness.

68. Initial management Given the predominance of sepsis and hypovolemia as the most common causes of shock in the pediatric population, most therapeutic regimens are based on guidelines established in these settings.

69. Initial management Immediately after establishment of IV or IO access, aggressive, early goal-directed therapy (EGDT) should be initiated unless there significant concerns for cardiogenic shock as an underlying pathophysiology.

70. Initial management Rapid IV administration of 20 mL/kg isotonic saline or, less often colloid should be initiated in an attempt to reverse the shock state Bolus should be repeated quickly up to 60-80 mL/kg. Rapid fluid resuscitation using 60-80 mL/kg or more is associated with improved survival without an increased incidence of pulmonary edema.

71. Initial management Fluid resuscitation in increments of 20 mL/kg should be titrated to normalize HR, urine output (to 1 mL/kg/hr), capillary refill time(<2 seconds), and mental status. Normalization of BP alone is not a reliable endpoint for assessing the effectiveness of resuscitation.

72. Initial management Although the type of fluid (crystalloid vs colloid) is an are of debate, fluid resuscitation in the first hour is unquestionably essential to survival in septic shock, regardless of the fluid type administered. If shock remains refractory following 60-80 mL/kg resuscitation, inotrope therapy should be instituted while additional fluid are administred

73. Initial management Inotropic and vasoactive drugs are not a substitute for fluid, however... Can have various combinations of hypovolemic and septic and cardiogenic shock May need to treat poor vascular tone and/or poor cardiac function

74. Cardiovascular drug treatment of shock Drug Effect s Dosing range comments Dopamine ↑ cardiac contractility 3-20 microg /kg/min ↑ risk of arrhythmias with high doses Significant peripheral vasoconstriction at > 10 micro/kg/min Epinephrine ↑ HR, ↑ cardiac contractility 0.05-3 mic /kg/min May ↓ renal perfusion at high doses Potent vasoconstrictor ↑ myocardial O2 consumption Risk of arrhythmias at high doses Dobutamine ↑ cardiac contractility 1-10 micro/kg/min ___ Peripheral vasodilator Norepinephrine Potent vasoconstriction 0.05-1.5 micro/kg/min ↑ BP 2ndry to ↑ SVR No significant effect on cardiac contractility ↑ left ventricular afterload Phenylephrine Potent vasoconstriction 0.5-2 micro/kg/min Cause sudden hypertension ↑ O2 consumption

75. Vasodilators/afterload reducers Drug Effects Dosing range comments Nitroprosside Vasodilator (mainly arterial) 0.5-4 mic /kg/min Rapid effect Risk of cyanide toxicity with use >96hr Nitroglycerine Vasodilator (mainly venous) 1-20 mic /kg/min Rapid effect Risk of ↑ ICP Prostaglandin E1 vasodilator 0.01-0.2 mic /kg/min Can lead to hypotension Risk of apnea Maintain an open ductus arteriosus Milrinone Increased cardiac contractility Load 50 mic /kg over 15 min Phosphodiestrase inhibitor – slow cyclic adenosine monophosphate breakdown Improves cardiac diastolic function 0.5-1 mic /kg/min Peripheral vasodilation

76. Goal-directed therapy of organ dysfunction in shock System Disorder Goals therapies Respiratory ARDS Prevent/treat; hypoxia & respiratory acidosis Oxygen Respiratory muscle fatigue Prevent barotrauma Early endotracheal intubation & mechanical ventilation Central apnea Decrease work of breathing PEEP Permissive hypercapnia High-frequency ventilation ECMO

77. Goal-directed therapy of organ dysfunction in shock System Disorder Goal Therapies Renal Prerenal failure Renal failure Prevent/treat; hypovolemia, hypervolemia, hyperkalemia, metabolic acidosis, hypernatremia/hyponatremia, & hypertension. Monitor serum electrolytes Judicious fluid resuscitation Low-dose dopamine Establishment of normal urine output & BP for age Furosemide (Lasix) Dialysis, ultrfiltration, hemofiltration

78. Goal-directed therapy of organ dysfunction in shock System Disorder Goal Therapies Hematologic Coagulopathy (DIC) Prevent/treat; bleeding Vitamin K Fresh frozen plasma Platelets Thrombosis Prevent/treat; abnormal clotting Heparinization Activated protein C

79. Goal-directed therapy of organ dysfunction in shock System Disorder Goal Therapies GIT Stress ulcer Prevent/treat; gastric bleeding Avoid aspiration, abdominal distension Histamine H2 receptor-blocking agents or proton pump inhibitors Nasogastric tube Ileus Bacterial translocation Avoid mucosal atrophy Early enteral feedings

80. Goal-directed therapy of organ dysfunction in shock System Disorder Goal Therapies Endocrine Adrenal insufficiency, primary or secondary to chronic steroid therapy Prevent/treat; adrenal crisis Stress-dose steroid in patients previously given steroids Physiologic dose for presumed primary insufficiency in sepsis Metabolic Metabolic acidosis Correct etiology Normalize pH Treatment of hypovolemia (fluids) & poor cardiac function (fluids, inotropic agents) Improvement of renal acid excretion Low-dose (0.5-2 mEq/kg) sodium bicarbonate if the patient is not showing response, pH < 7.1, and ventilation (CO2 elimination) is adequate.

81. Septic shock Early administration of broad spectrum antimicrobial agents is associated with a reduction in mortality. Neonates should be treated with ampicillin plus cefotaxime and/or gentamicin. Acyclovir should be added if herpes simplex virus is suspected clinically.

82. Septic shock In infants and children Community acquired N. meningitides can be treated with 3 rd generation cephalosporin (Ceftriaxone or cefotaxime) or high dose penicillin. H. influenzae can be treated with ceftrixone or cefotaxime The presence of resistant S. pneumoniae often requires the addition of vancomycin

83. Septic shock Suspicious of community or hospital acquired MRSA infection warrants the coverage with vancomycin. If intra-abdominal process is suspected, anaerobic coverage should be included with an agents such as Metronidazole, Clindamycin, or piperacillin-tazobactam.

84. Septic shock Nosocomial sepsis should generally be treated at least 3 rd or 4 th generation cephalosporin or piperacillin-tazobactam. An aminoglycoside should be added as the clinical situation warrants. Vancomycin should be added to the regimen if the patient has an indwelling medical device, gram positive cocci are isolated from the blood, or MRSA is suspected or as empiric coverage for S. pneumoniae.

85. Septic shock Empirical coverage for fungal infections should be considered for selected immunocompromised patients. These broad, generalized recommendations must be tailored to the individual clinical scenario and to the local resistance pattern of the community and/or hospital

86. Hypovolemic shock Mainstay of therapy is fluid Goals Restore intravascular volume Correct metabolic acidosis Treat the cause Degree of dehydration often underestimated Reassess perfusion, urine output, vital signs... Isotonic crystalloid is always a good choice

87. Regardless of the etiology of shock, metabolic status should be meticulously maintained. Electrolytes should be monitored closely and corrected as needed. Hypoglycemia is common and should be promptly treated. Hypocalcemia which may contribute to myocardial dysfunction, should be treated.

88. Steroids Hydrocortisone replacement may be beneficial in pediatric shock. Up t0 50% of critically ill patient may have absolute or relative adrenal insufficiency. Patients at increased risk for adrenal insufficiency include those with congenital adrenal hyperplasia, abnormalities of hypothalamic-pituitary axes, recent therapy with corticosteroids, and should receive stress doses of hydrocortisone.

89. Steroids Steroids may also be considered in patients with shock that is unresponsive to fluid resuscitation and catecholamines.

90. Thank you