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![Global tissue hypoxia
SIRS
Endothelial activation
Disruption of:
Coagulation
Vascular permeability
Vascular tone
Microcirculatory failure
Precipitated by:
Cytokines
[Over]production
of nitric
oxide
Results in:
Loss of vasomotor
control
Under‐perfusion of
tissues
Hypotension
Ait‐Oufella H, et al. Intensive Care Med 2010;26:1286‐1298.
Rivers E, et al. NEJM 2001;345:1368‐1377.
Organ dysfunction
Heart
Lungs
Brain
Kidneys
Liver](https://image.slidesharecdn.com/approachtohypovolemicandsepticshock-140911101035-phpapp01/75/Approach-to-hypovolemic-and-septic-shock-21-2048.jpg)
Uploaded byAhmed Bahamid
Approach to hypovolemic and septic shock
This document discusses approaches to hypovolemic and septic shock in children. It defines shock and describes the pathophysiology, stages, and management. Shock results from inadequate oxygen delivery to tissues. Initially, compensatory mechanisms attempt to maintain blood pressure, but the condition can progress to decompensated then irreversible shock without treatment. Sepsis causes an inflammatory response that can lead to organ dysfunction if uncontrolled. Early intervention is important to improve outcomes from shock.
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Approach to hypovolemic and septic shock
- 1. 11 September 2014 APPROACH TO HYPOVOLEMIC AND SEPTIC SHOCK Prepared by: Dr. Ahmed M. Bahamid pediatric resident at Alsabeen hospital
- 2. OBJECTIVES Definitionof shock Pathophysiology, common types and etiologies of shock Clinical manifestations and diagnosis Management of child with septic and Hypovolemic shock
- 3. DEFINITION Shockis 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 Shockoccurs 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 inseptic 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 Aninitial 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 thesecompensatory 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 Triggersshock Decreased perfusion Compensatory mechanisms Compensated shock Decompensated shock Tissue damage Multisystem organ failure Death
- 11. In adequate O2at tissue level Anaerobic metabolism with resultant progressive LACTIC ACIDOSIS Inadequa te 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 itimportant 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
- 18. In septicshock 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 tissuehypoxia with lactic acidosis ↓ ATP, ↑ H+, ↑ lactate In vascular smooth muscle ↑nitric oxide synthase ↑ vasopressin secretion ↓ vasopressin stores ↓ plasma vasopressin Open K ATP Vasodilatation ↑nitric oxide Open K Ca ↓ cytoplasmic Ca 2+ ↑ cGMP ↓ phosphorylated myosin
- 20. SYSTEMIC INFLAMMATORY RESPONSESYNDROME 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. Global tissue hypoxia SIRS Endothelial activation Disruption of: Coagulation Vascular permeability Vascular tone Microcirculatory failure Precipitated by: Cytokines [Over]production of nitric oxide Results in: Loss of vasomotor control Under‐perfusion of tissues Hypotension Ait‐Oufella H, et al. Intensive Care Med 2010;26:1286‐1298. Rivers E, et al. NEJM 2001;345:1368‐1377. 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 oxidereleased 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 inflammatorycascade 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 mayinitially 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 ofthe 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 DECREASEDPERFUSION 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 BP, only
- 31. CRITERIA FOR ORGANDYSFUNCTION Organ system Criteria for dysfunction Cardiovascul ar Despite administration of isotonic IV fluid bolus ≥ 60 mL/kg in 1 hour: decrease in BP (hypotension) < 5th 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 ORGANDYSFUNCTION Organ system Criteria for dysfunction Respirator y 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 Neurologi c GCS score ≤ 11 OR Acute change in mental status with a decrease in GCS score ≥ 3 points from abnormal baseline
- 33. CRITERIA FOR ORGANDYSFUNCTION Organ system Criteria for dysfunction Hematologi c 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 Hypovole mic Cardiogen ic Distributiv e Obstructi ve Septic
- 35. WHY IS ITIMPORTANT 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 Becauseof 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 ofetiology, 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 clinicalfindings 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.
- 50. Sepsis isdefined 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 OFSEPSIS SIRS From infection Sepsis Severe sepsis Death MODS Septic shock 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 INDIFFERENT SHOCK STATES Type of shock CO SVR MAP CWP CVP HYPOVOLEM IC ↓ ↑ ↔ OR ↓ ↓↓↓ ↓↓↓ CARDIOGENI C: SYSTOLIC ↓↓ ↑↑↑ ↔ OR ↓ ↑↑ ↑↑ DIASTOLIC ↔ ↑↑ ↔ ↑↑ ↑ OBSTRUCTIV E ↓ ↑ ↔ OR ↓ ↑↑ Ω ↑↑ Ω DISTRIBUTIV E ↑↑ ↓↓↓ ↔ OR ↓ ↔ OR ↓ ↔ OR ↓ SEPTIC: EARLY ↑↑↑ ↓↓↓ ↔ OR ↓ ‡ ↓ ↓ LATE ↓↓ ↓↓ ↓↓ ↑ ↑ or ↔
- 55. DIAGNOSIS Shockis diagnosed clinically on the basis of a thorough history and physical exam.
- 56. DIFFERENTIAL DIAGNOSIS OFTHE 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.
- 58. TESTING SKIN PINCHFOR 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.
- 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 Airwaymanagement 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 O2 delivery and decreased O2 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
- 75. CARDIOVASCULAR DRUG TREATMENTOF SHOCK Drug Effects 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 Norepinephri ne Potent vasoconstriction 0.05-1.5 micro/kg/min ↑ BP 2ndry to ↑ SVR No significant effect on cardiac contractility ↑ left ventricular afterload
- 76. VASODILATORS/AFTERLOAD REDUCERS DrugEffects Dosing range comments Nitroprossid e Vasodilator (mainly arterial) 0.5-4 mic/kg/min Rapid effect Risk of cyanide toxicity with use >96hr Nitroglyceri ne Vasodilator (mainly venous) 1-20 mic/kg/min Rapid effect Risk of ↑ ICP Prostagland in 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
- 77. GOAL-DIRECTED THERAPY OFORGAN 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
- 78. GOAL-DIRECTED THERAPY OFORGAN DYSFUNCTION IN SHOCK Syste m 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
- 79. GOAL-DIRECTED THERAPY OFORGAN DYSFUNCTION IN SHOCK System Disorder Goal Therapies Hematologi c Coagulopathy (DIC) Prevent/treat; bleeding Vitamin K Fresh frozen plasma Platelets Thrombosis Prevent/treat; abnormal clotting Heparinization Activated protein C
- 80. GOAL-DIRECTED THERAPY OFORGAN DYSFUNCTION IN SHOCK Syste m 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
- 81. GOAL-DIRECTED THERAPY OFORGAN DYSFUNCTION IN SHOCK System Disorder Goal Therapies Endocrin e 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.
- 82. 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.
- 83. SEPTIC SHOCK Ininfants and children Community acquired N. meningitides can be treated with 3rd 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
- 84. 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.
- 85. SEPTIC SHOCK Nosocomial sepsis should generally be treated at least 3rd or 4th 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.
- 86. 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
- 87. 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
- 88. Regardless ofthe 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.
- 89. STEROIDS Hydrocortisonereplacement 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.
- 90. STEROIDS Steroidsmay also be considered in patients with shock that is unresponsive to fluid resuscitation and catecholamines.
- 91.
Editor's Notes
- #6 Shock Often masked in pediatrics because the inherent reserve in a child allows for the maintenance of vital organs in the normal range, even in the presence of severe hemodynamic instability (pediatric secrets, 5th edition)
- #11 Compensatory mechanisms attempts to maintain BP by: Increase CO increase SVR increase O2 extraction - Redistributing blood flow to the brain, kidneys, and heart (at expense of
- #14 Because shock is a progressive process. As will be reviewed, data show that intervention in early stages leads to better outcomes. Management often differs based on stage of shock.
- #26 Hypothetical pathophysiology of the septic process
- #42 1- abnormalities of vasomotor tone due to loss of venous and arterial capacitance 2- causes: Anaphylaxis Neurologic; loss of sympathetic vascular tone secondary to spinal cord or brainstem injury Drugs
- #49 Hypovolemic: third spacing of fluids into the extracellular, interstitial space Distributive: early shock with decreased afterload Cardiogenic :depression of myocardial function by endotoxins
- #55 Ω = wedge pressure, CVP, & pulmonary artery diastolic pressure are equal ‡ = wide pulse pressure CO = CARDIAC OUTPUT SVR= SYSTEMIC VASCULAR RESISTANCE MAP= MEAN ARTERIAL PRESSURE CWP= CAPILLARY WEDGE PRESSURE CVP= CENTRAL VENOUS PRESSURE
- #78 PEEP= positive end-expiratory pressure ECMO= extracorporeal membrane oxygenation