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SHOCK

SHOCK. September 6, 2005 Andrew Filiatraut. In General. Shock Clinical syndrome defined as hypoperfusion Hypotension and Cellular Hypoxia Elevated lactate Oliguria Hepatic/GI dysfunction Mental status changes . In General. Four Classifications Hypovolemic Cardiogenic Obstructive

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SHOCK

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  1. SHOCK September 6, 2005 Andrew Filiatraut

  2. In General • Shock • Clinical syndrome defined as hypoperfusion • Hypotension and Cellular Hypoxia • Elevated lactate • Oliguria • Hepatic/GI dysfunction • Mental status changes

  3. In General • Four Classifications • Hypovolemic • Cardiogenic • Obstructive • Distributive • Septic, Addison’s, Anaphylactic, Neurogenic, Thyrotoxicosis, Beriberi, Paget’s, Cirrhosis, Chroinc Anemia, Osler-Weber-Rendu

  4. Hemodynamic Profiles

  5. Septic Shock

  6. Epidemiology • 751,000 cases of severe sepsis /year • Up to half develop shock • Overall mortality rate of 45% • Cause • Gram+ 35-40% • Gram- 55-60% • Slightly higher incidence in men, older adults (55-60 yrs)

  7. Definitions • Infection • Inflammation against microorganism • Bacteremia • Viable bacteria in blood

  8. Definitions • SIRS • Evidence of inflammation NOT necessarily infection • 2 or more of the following • Temp>38 or <36 • HR >90bpm • RR >20 or PaCo2 <32 • WBC’s >12,000 or <4000 or >10% bandemia

  9. Definitions • Sepsis • systemic inflammatory response as a result of infection • Severe Sepsis • sepsis associated with organ dysfunction • Lactic acidosis, oliguria, mental status change • Septic shock • sepsis-induced hypotension with presence of perfusion abnormalities

  10. Definitions • Sepsis-induced hypotension • SBP<90 or reduction of 40mm Hg from baseline without other cause • Multiple Organ Dysfunction Syndrome • Altered organ dysfunction in acutely ill patient requiring intervention to maintain homeostasis

  11. Pathophysiology

  12. Pathophysiology • Focus of infection • Pneumonia, UTI, cellulitits, abscess, indwelling device • ICU: catheters, sinusitis, acalculus cholecystitis, C. diff, resistant organism, fungal infection • Blood stream invasion or proliferation of organism at site • Exogenous toxin release • Activation of endogenous mediators

  13. Molecular Mediators in Pathophysiology • Three phases • Induction • Cytokine synthesis & secretion • Cascade

  14. Molecular Mediators in Pathophysiology • Induction • Interaction of microbial molecules with host • Mediators activated that amplify & transmit the microbial signal to other cells • Ex LPS binds to LPS binding protein which is detected by CD14 releasing TNF-alpha • Peptidoglycan & lipoteichoic acid of gram (+) induce similarly

  15. Molecular Mediators in Pathophys • Cytokine cascade • Activation & release of central mediators • TNF-alpha and IL-1 • Release of secondary mediators • IL-6, IL-8, PAF, PG’s, leukotrienes • Activation of neutrophils, complement system, vascular endothelial cells • Synthesis of acute phase reactants

  16. Molecular Mediators in Pathophys • Parallel to SIRS is CARS • Compensatory Anti-inflammatory Response System • Attempts to down regulate the SIRS response • IL-4, IL-10, transforming growth factor beta, CSF, soluble receptors to TNF, antagonists to TNF-alpha and IL-1 • If CARS reaction is severe it will manifest as anergy and infection susceptibility

  17. Vasoactive Mediators in Pathophys • Nitric Oxide • Produced by endothelium • Increased levels during shock • Actions at high levels • Mediator of vasodilation & hypotension • Direct cellular toxicity • Myocardial depression • Increased permeability

  18. Clinical Features

  19. Clinical Features • Constitutional • Hyper/hypothermia • Tachycardia • Tachypnea • Wide pulse pressure • Mental status change • Most likely obtunded

  20. Clinical Features • Cadiovascular • Early, vasodilators predominate • Cardiac output is increased with tachycardia • CO=SV x HR • i.e. Initially patients will have warm extremities • If not treated aggressively decompensation ensues • Typically hypotension is not reversible with fluids alone

  21. Clinical Features • Pulmonary • Sepsis is most common condition associated with ARDS • Lung edema from increased permeability • Alveolar edema dyspnea, hypoxemia, opacities on CXR • B/L infiltrates, wedge pressure <18 • Endotoxin, TNF-alpha, IL-1, IL-6, IL-8, bactericidal/permeability-increasing (BPI) protein

  22. Clinical Features • Pulmonary • ARDS • B/L pulmonary infiltrates • PCWP <18 (non-cardiogenic pulm edema) • PaO2/FiO2 <200 • If PaO2/FiO2 >200, but <300 then ALI

  23. Clinical Features • Renal • Acute renal failure w/ azotemia, oliguria, active urinary sediment • Hypotension/Dehydration, aminoglycosides, pigmenturia (e.g. myoglobinuria) • Immune complex deposition • IgG, IgM,C3, bacterial antigens & antibodies • Tubulointersitial disease • S. pneumoniae, S. pyogenes, Legionella, salmonellosis, brucellosis, diptheria

  24. Clinical Features • Gastrointestinal • Accelerated apoptosis of GI epithelial cells • Can lead to blood loss anemia • Cholestatic jaundice (most frequent abnormality) • Transaminase/Alkaline phosphatase 1-3x normal • Bilirubin concentrations, usually not >10mg/dL • Hemolysis of RBC’s, hepatocellular dysfunction due to endotoxin

  25. Clinical Features • Hematologic • Minor blood loss secondary to erosions in mucosal layer of stomach/duodenum • Accelerated apoptosis of lymphocytes • Possibly due to elevated glucocorticoids • Most frequent changes are neutrophilia or neutropenia, thrombocytopenia, DIC

  26. Clinical Features • Hematologic • Neutrophilia • Most common • Left shift • Demargination & release of less mature granulocytes from BM • C3a causes release of neutrophil releasing substance • Sustained neutrophilia is secondary to CSFs

  27. Hematologic continued Neutropenia Increases mortality Increased peripheral use of cells, damage to cells by bacterial byproducts, depression of marrow by inflammatory mediators Morphological changes of WBC’s in sepsis Toxic granulations, Dohle bodies, vacuolization Functional changes of WBC’s Increased phagocytic/cytotoxic activities Clinical Features

  28. Clinical Features • Hematologic continued • RBC production & survival are decreased • Usually does not cause anemia unless infection is prolonged • Low serum Fe concentrations • Decrease by 50% • Influx into liver & other reticuloendothelial cells

  29. Clinical Features • Hematologic continued • Thrombocytopenia • Usual a consequence of DIC • May be early sign of bacteremia • Inhibition of thrombopoiesis, increased platelet turnover, increased endothelial adherence, increased destruction

  30. Clinical Features • DIC • Clotting & fibrinolytic systems activated • Consumption of coagulation factors & platelets • Clotting system activated through the extrinisic clotting system by bacteria, viruses, fungi, endo/exotoxins • Gram(-) precipitate DIC more readily than gram (+) • Fibrinolytic system is activated by tissue type plasminogen activator • As sepsis progresses, increase release of plasminogen activator inhibitor type 1

  31. Clinical Features • DIC continued • Two forms • Compensated • “slower” generalized activation • Bleeding prevented by increasing coagulation factor production in liver, release of platelets from reserve, synthesis of inhibitors at accelerated rate • Decompensated • Clinical bleeding and/or thrombosis • Thrombocytopenia, prolonged PT/PTT, decreased fibrinogen & antithrombin III, increased fibrin monomer/fibrin split products/D-dimer

  32. Clinical Features • Endocrine • Hyperglycemia • Increased catecholamines, cortisol, glucagon, peripheral insulin resistance, impaired glucose use, decreased insulin secretion • Significant risk for adverse outcome • Must maintain tight control w/insulin infusion to keep b/w 80-100 mg/dl (NEJM Nov 8, 2001; vol 345, #19) • Hypoglycemia • Assoc. w/S. pneumoniae, S. aureus, S. pyogenes, Listeria, Neisseria meningitidis, H. flu, Enterobacteriaceae

  33. Clinical Features • Acid/Base • Early in sepsis  resp alkalosis • Metabolic acidosis suggests inadequate perfusion, impaired hepatic clearance of lactate/pyruvate, increased glycolysis • Hypoxemia often present due to vent/perfusion mismatch

  34. Clinical Features • Cutaneous • Direct bacterial involvement • Cellulitis, erysipelas, fasciitis • Lesions as a consequence of sepsis/hypotension/DIC • Acrocyanosis & necrosis of peripheral tissue • Lesions secondary to intravascular infection • Microemboli &/or immune complex vasculitis

  35. Diagnosis

  36. Diagnosis • Pt presents with • Hypotension not responsive to fluid bolus • Inadequate perfusion • Complaints attributable to a serious infection • Hot flushed skin • Mental obtundation or agitation • Widened pulse pressure • Hyperventilation • Dysthermia • **beware of the old, young, immunocompromised

  37. Diagnosis • Differential Diagnosis • Other causes of shock • Cardiogenic • Neurogenic • Hypovolemic • Anaphylactic • Obstructive (PE, tamponade) • Endocrine (adrenal insufficiency, thyroid storm)

  38. Diagnosis • H & P • Basic lab and x-rays are usually successful in identification of source • CNS • Meningitis (nuchal rigidity, MS change, petechiae) • Brain abscess, sub/epi dural empyemas • Viral CNS infections

  39. Diagnosis • Pulmonary • Acute bacterial pneumonia • Intra-abdominal processes • Most common source of infection leading to sepsis • Acute pancreatits • Cholangitis • Septic abortion/endometritis/myometritis • Pyelonephritis • Occult Abscess • Skin • Cellulitis (S.aureus, S.pyogenes) • Decubitus ulcer(s)

  40. Diagnosis • No obvious source • Endocarditis • Primary bacteremia • S.aureus, S.pneumoniae, N.meningitidis • Asplenia • Salmonella, H flu, S pneumo, N. meningitidis • IVD users, Pseudomonas & gram(-) bacteria • Skin abscess from “popping”

  41. Diagnosis • Ancillary Studies • CBC • DIC panel (PT,PTT,fibrinogen,D-dimer, ATIII) • CMP (include Mag, Ca, Phosphate) • Lactate level • ABG • UA • CXR • Cultures (blood, urine) • If H&P suggest • LP, CT (abd . . .) • Consider • CRP, pro-calcitonin, IL-6 level

  42. Standard Treatment

  43. Standard Treatment • ABC’s! • Maintain O2 sat’s above 90% • Hemodynamic Stabilization • Rapid fluid administration • Rate of 0.5L of NS every 5-10min • May require 2-6L in initial stabilization phase • Be careful with heart failure patients • Monitor response with BP, HR, RR, mental status, urine output (1cc/kg/hr), CVP, skin perfusion

  44. Standard Treatment ▪ Inotropic support • If no response to fluids or signs of fluid overload present • Goal is to keep MAP above 65 mm Hg • Dopamine 5-20 micrograms/kg/min • Beta-1, dopaminergic and alpha adrenergic activity • Norepinephrine • Beta-1 and alpha adrenergic stimulation • Short term vasopressin infusion (0.04 units/min for 4-16h) • Vasodilatory septic shock

  45. Standard Treatment • End points • Early goal directed therapy provides significant benefit & improves outcome • Rivers et al. NEJM vol. 345:1368, 2001 • Maintain CVP b/w 8-12 • Hct 30% • SVO2 >70% • Reduction in mortality from 44% in control group to 29% in intervention group

  46. Standard Treatment • Empiric Antimicrobial Therapy • Start ASAP • Try to get culture samples before • Select based on adequate coverage of potential pathogens • Should cover gram +/- • Give maximum dose allowed • Give IV

  47. Empiric Antibiotics in Sepsis • Table 32-3

  48. Standard Treatment • Removal of Source of Infection • Indwelling catheters  send tip for culture • Replace Foley catheters • Intra-abdominal or soft tissue sites of pus require urgent drainage

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