PATRICK DUFF, M.D. SEPTIC SHOCK

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PATRICK DUFF, M.D. SEPTIC SHOCK

  1. 1. PATRICK DUFF, M.D.
  2. 2. SEPTIC SHOCK OVERVIEW Etiology Microbiology Pathophysiolog y Diagnosis Management
  3. 3. SEPTIC SHOCK IMPACT Results in approximately 215,000 deaths annually in the U.S. Similar in frequency to MI as a cause of death
  4. 4. SEPTIC SHOCK PREDISPOSING FACTORS Extended hospitalization Advanced age Debilitating illness Immunodeficiency disorder Ventilator > 48 h
  5. 5. SEPTIC SHOCK PREDISPOSING FACTORS Disseminated malignancy Hyperalimentation Biliary tract surgery Genital tract surgery
  6. 6. SEPTIC SHOCK MORTALITY Underlying IllnessUnderlying Illness Mortality %Mortality % Rapidly fatalRapidly fatal 8080 Ultimately fatalUltimately fatal 4040 Non-fatalNon-fatal <10<10
  7. 7. SEPTIC SHOCK MICROBIOLOGY
  8. 8. The Perfect Storm
  9. 9. SEPTIC SHOCK PATHOPHYSIOLOGY Endotoxinstimulation of humoral and cellular immune systemsactivation of complement sequence and coagulation cascade
  10. 10. SEPTIC SHOCK PATHOPHYSIOLOGY Activation of coagulation cascade activation of fibrinolytic system DIC
  11. 11. SEPTIC SHOCK PATHOPHYSIOLOGY Complement activationchemotaxis of PMNs, degranulation of mast cells, and release of histamine and inflammatory mediatorsincreased capillary permeability
  12. 12. SEPTIC SHOCK PATHOPHYSIOLOGY INFLAMMATION release of catecholamines and prostaglandins generalized vasoconstriction
  13. 13. SEPTIC SHOCK PATHOPHYSIOLOGY VASOCONSTRICTION decreased perfusion of vital organs tissue hypoxia metabolic acidosis
  14. 14. SEPTIC SHOCK PATHOPHYSIOLOGY METABOLIC ACIDOSIS capillary pooling decreased circulating blood volume decreased venous return decreased cardiac output
  15. 15. SEPTIC SHOCK PATHOPHYSIOLOGY DECREASED CARDIAC OUTPUT decreased coronary and cerebral blood flow intractable hypotension, coma, multiorgan failure DEATH
  16. 16. SEPTIC SHOCK CLINICAL MANIFESTATIONS Altered mental status Thermal instability Cardiac dysfunction Respiratory compromise
  17. 17. SEPTIC SHOCK CLINICAL MANIFESTATIONS Bleeding Jaundice Ileus Skin changes
  18. 18. SEPTIC SHOCK DIFFERENTIAL DIAGNOSIS Cardiogenic shock Hypovolemic shock Venous or AF embolism Cardiac tamponade
  19. 19. SEPTIC SHOCK DIFFERENTIAL DIAGNOSIS Hemorrhagic pancreatitis Diabetic ketoacidosis Aortic dissection
  20. 20. SEPTIC SHOCK DIAGNOSTIC TESTS Laboratory TestLaboratory Test ResultResult WBCWBC Decreased, then increasedDecreased, then increased HCTHCT VariableVariable PLTPLT Decreased with DICDecreased with DIC FibrinogenFibrinogen Decreased with DICDecreased with DIC
  21. 21. SEPTIC SHOCK DIAGNOSTIC TESTS Laboratory TestLaboratory Test ResultResult Fibrin degradation productsFibrin degradation products Increased with DICIncreased with DIC PT, PTT, TTPT, PTT, TT Prolonged with DICProlonged with DIC pHpH DecreasedDecreased Lactic acidLactic acid Increased (poor prognosticIncreased (poor prognostic factor)factor)
  22. 22. SEPTIC SHOCK DIAGNOSTIC TESTS Laboratory TestLaboratory Test ResultResult pO2pO2 DecreasedDecreased pCO2pCO2 IncreasedIncreased HCO3HCO3 DecreasedDecreased K+K+ IncreasedIncreased
  23. 23. SEPTIC SHOCK MICROBIOLOGY STUDIES Urine culture Blood culture Culture of peritoneal fluid Culture of abscess Sputum culture
  24. 24. SEPTIC SHOCK IMAGING STUDIES Chest x-ray Abdominal films IVP CT MRI Ultrasound
  25. 25. SEPTIC SHOCK OTHER DIAGNOSTIC STUDIES ECG Right heart catheterization
  26. 26. SEPTIC SHOCK MANAGEMENT Monitoring CO PCWP BP ABGs Urine output
  27. 27. SEPTIC SHOCK MANAGEMENT Restore circulating blood volume Packed red blood cells Maintain hemoglobin of 7 to 9 g/l Crystalloid Ringer’s lactate Normal saline
  28. 28. SEPTIC SHOCK MANAGEMENT “7 – 3 rule” for fluid replacement Infuse 150-200 ml/10 minutes If PCWP increases > 7mm Hg, discontinue infusion temporarily If PCWP increases < 3 mm Hg, infuse a second increment
  29. 29. SEPTIC SHOCK GOALS OF FLUID RESUSCITATION Central venous pressure of 8 to 12 mm Hg Mean arterial pressure > 65 mm Hg Urine output > 0.5 ml/kg/h Central venous or mixed venous oxygen saturation > 70%
  30. 30. SEPTIC SHOCK VASOPRESSORS Dopamine Starting dose 1-3 mcg/kg/min Norepinephrine 5 to 15 mcg/min Vasopressin 0.01 to 0.03 U/min
  31. 31. SEPTIC SHOCK VASOPRESSORS In patients with septic shock, there is no difference in mortality in patients treated with dopamine vs norepinephrine vs vasopressin Dopamine is associated with more arrhythmic events than norepinephrine Events serious enough to require discontinuation of medication
  32. 32. SEPTIC SHOCK INOTROPIC THERAPY Dobutamine - first choice inotrope for patients with low CO in the presence of adequate LV filling pressure Dose 0.5 to 1 mcg/kg/min Maximum – 40 mcg/kg/min
  33. 33. SEPTIC SHOCK MANAGEMENT Corticosteroids
  34. 34. SEPTIC SHOCK TREATMENT WITH HYDROCORTISONE Dose – 200-300 mg/day for 7 days in 3 or 4 divided doses or by continuous infusion Reverses shock more rapidly Variable effect on mortality Increases frequency of superinfection
  35. 35. SEPTIC SHOCK SURGICAL INTERVENTION Drainage of abscess Debridement of infected wound Removal of infected organ
  36. 36. SEPTIC SHOCK ANTIBIOTIC THERAPY Antibiotics should be started within one hour of diagnosis of sepsis/hypotension improved survival Initial empiric regimen should target most likely pathogens, e Reassess regimen after 48-72 hours Total duration of treatment- 7 to 10 days
  37. 37. SEPTIC SHOCK SPECIALIZED ANTIBIOTICS Anti- staphylococcal agents Linezolid Quinupristin plus dalfopristin Vancomycin Anti-fungal agents
  38. 38. SEPTIC SHOCK POSSIBLE MODIFICATIONS IN ANTIBIOTIC ADMINISTRATION Prolong the intravenous infusion to 3 to 4 hours For ventilator-related infections, administer nebulized antibiotics
  39. 39. SEPTIC SHOCK MINIMIZING INFLAMMATION Recombinant human activated protein C (rhAPC) Inflammatory response is integrally linked to procoagulant activity and endothelial activation rhAPC is an endogenous anticoagulant with anti-inflammatory properties
  40. 40. SEPTIC SHOCK MINIMIZING INFLAMMATION Recombinant human activated protein C Inhibits thrombin Inhibits neutrophil recruitment Inhibits apoptosis Improves survival in patients with multi-organ dysfunction Dose - 24 micrograms/kg/min x 96 hours
  41. 41. SEPTIC SHOCK RESPIRATORY SUPPORT Administer oxygen Monitor ABGs Initiate mechanical ventilation early Avoid barotrauma Use PEEP as indicated
  42. 42. EFFECT OF ARDS ON MORTALITY IN SEPTIC SHOCK ConditionCondition Mortality %Mortality % Septic shock withoutSeptic shock without ARDSARDS 5050 Septic shock withSeptic shock with ARDSARDS 9090
  43. 43. MANAGEMENT OF SEPTIC SHOCK OTHER SUPPORTIVE MEASURES Maintain normal temperature Correct coagulation abnormalities Maintain glucose < 150 mg/dl Administer WBC transfusion DVT prophylaxis
  44. 44. SEPTIC SHOCK PREVENTIVE MEASURES Stabilize pre-existing illnesses prior to surgery Avoid unnecessary preoperative hospitalization
  45. 45. SEPTIC SHOCK PREVENTIVE MEASURES Diagnose and treat operative site infections immediately Be ever vigilant
  46. 46. SEPTIC SHOCK CONCLUSIONS Predisposing factors Microbiology Fluid resuscitation Surgical intervention Antibiotic therapy Importance of early intervention
  47. 47. REFERENCES Dellinger RP, et al. Surviving sepsis campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004; 32: 858-73. Russell JA. Management of sepsis. N Engl J Med 2007: 355:1699-713. Sprung CL, et al. Hydrocortisone therapy for patients with septic shock. N Engl J Med 2008; 358:111-24.
  48. 48. REFERENCES Parrillo JE. Septic shock – vasopressin, norepinephrine, and urgency. N Engl J Med 2008; 358: 954-55 DeBacker D, et al. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010; 362:779-89. Peleg AY, Hooper DC. Hospital-acquired infections due to gram-negative bacteria. N Engl J Med 2010; 362:1804- 13.

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