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PATRICK DUFF, M.D. SEPTIC SHOCK

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PATRICK DUFF, M.D. SEPTIC SHOCK PATRICK DUFF, M.D. SEPTIC SHOCK Presentation Transcript

  • PATRICK DUFF, M.D.
  • SEPTIC SHOCK OVERVIEW
    • Etiology
    • Microbiology
    • Pathophysiology
    • Diagnosis
    • Management
  • SEPTIC SHOCK IMPACT
    • Results in approximately 215,000 deaths annually in the U.S.
    • Similar in frequency to MI as a cause of death
  • SEPTIC SHOCK PREDISPOSING FACTORS
    • Extended hospitalization
    • Advanced age
    • Debilitating illness
    • Immunodeficiency disorder
    • Ventilator > 48 h
  • SEPTIC SHOCK PREDISPOSING FACTORS
    • Disseminated malignancy
    • Hyperalimentation
    • Biliary tract surgery
    • Genital tract surgery
  • SEPTIC SHOCK MORTALITY Underlying Illness Mortality % Rapidly fatal 80 Ultimately fatal 40 Non-fatal <10
  • SEPTIC SHOCK MICROBIOLOGY
  • The Perfect Storm
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • Endotoxin  stimulation of humoral and cellular immune systems  activation of complement sequence and coagulation cascade
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • Activation of coagulation cascade  activation of fibrinolytic system  DIC
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • Complement activation  chemotaxis of PMNs, degranulation of mast cells, and release of histamine and inflammatory mediators  increased capillary permeability
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • INFLAMMATION  release of catecholamines and prostaglandins  generalized vasoconstriction
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • VASOCONSTRICTION  decreased perfusion of vital organs  tissue hypoxia  metabolic acidosis
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • METABOLIC ACIDOSIS  capillary pooling  decreased circulating blood volume  decreased venous return  decreased cardiac output
  • SEPTIC SHOCK PATHOPHYSIOLOGY
    • DECREASED CARDIAC OUTPUT  decreased coronary and cerebral blood flow  intractable hypotension, coma, multiorgan failure  DEATH
  • SEPTIC SHOCK CLINICAL MANIFESTATIONS
    • Altered mental status
    • Thermal instability
    • Cardiac dysfunction
    • Respiratory compromise
  • SEPTIC SHOCK CLINICAL MANIFESTATIONS
    • Bleeding
    • Jaundice
    • Ileus
    • Skin changes
  • SEPTIC SHOCK DIFFERENTIAL DIAGNOSIS
    • Cardiogenic shock
    • Hypovolemic shock
    • Venous or AF embolism
    • Cardiac tamponade
  • SEPTIC SHOCK DIFFERENTIAL DIAGNOSIS
    • Hemorrhagic pancreatitis
    • Diabetic ketoacidosis
    • Aortic dissection
  • SEPTIC SHOCK DIAGNOSTIC TESTS Laboratory Test Result WBC Decreased, then increased HCT Variable PLT Decreased with DIC Fibrinogen Decreased with DIC
  • SEPTIC SHOCK DIAGNOSTIC TESTS Laboratory Test Result Fibrin degradation products Increased with DIC PT, PTT, TT Prolonged with DIC pH Decreased Lactic acid Increased (poor prognostic factor)
  • SEPTIC SHOCK DIAGNOSTIC TESTS Laboratory Test Result pO2 Decreased pCO2 Increased HCO3 Decreased K+ Increased
  • SEPTIC SHOCK MICROBIOLOGY STUDIES
    • Urine culture
    • Blood culture
    • Culture of peritoneal fluid
    • Culture of abscess
    • Sputum culture
  • SEPTIC SHOCK IMAGING STUDIES
    • Chest x-ray
    • Abdominal films
    • IVP
    • CT
    • MRI
    • Ultrasound
  • SEPTIC SHOCK OTHER DIAGNOSTIC STUDIES
    • ECG
    • Right heart catheterization
  • SEPTIC SHOCK MANAGEMENT
    • Monitoring
      • CO
      • PCWP
      • BP
      • ABGs
      • Urine output
  • 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
  • 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
  • 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%
  • 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
  • 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
  • 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
  • SEPTIC SHOCK MANAGEMENT
    • Corticosteroids
  • 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
  • SEPTIC SHOCK SURGICAL INTERVENTION
    • Drainage of abscess
    • Debridement of infected wound
    • Removal of infected organ
  • 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
  • SEPTIC SHOCK SPECIALIZED ANTIBIOTICS
    • Anti-staphylococcal agents
      • Linezolid
      • Quinupristin plus dalfopristin
      • Vancomycin
    • Anti-fungal agents
  • SEPTIC SHOCK POSSIBLE MODIFICATIONS IN ANTIBIOTIC ADMINISTRATION
    • Prolong the intravenous infusion to 3 to 4 hours
    • For ventilator-related infections, administer nebulized antibiotics
  • 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
  • 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
  • SEPTIC SHOCK RESPIRATORY SUPPORT
    • Administer oxygen
    • Monitor ABGs
    • Initiate mechanical ventilation early
      • Avoid barotrauma
      • Use PEEP as indicated
  • EFFECT OF ARDS ON MORTALITY IN SEPTIC SHOCK Condition Mortality % Septic shock without ARDS 50 Septic shock with ARDS 90
  • MANAGEMENT OF SEPTIC SHOCK OTHER SUPPORTIVE MEASURES
    • Maintain normal temperature
    • Correct coagulation abnormalities
    • Maintain glucose < 150 mg/dl
    • Administer WBC transfusion
    • DVT prophylaxis
  • SEPTIC SHOCK PREVENTIVE MEASURES
    • Stabilize pre-existing illnesses prior to surgery
    • Avoid unnecessary preoperative hospitalization
  • SEPTIC SHOCK PREVENTIVE MEASURES
    • Diagnose and treat operative site infections immediately
    • Be ever vigilant
  • SEPTIC SHOCK CONCLUSIONS
    • Predisposing factors
    • Microbiology
    • Fluid resuscitation
    • Surgical intervention
    • Antibiotic therapy
    • Importance of early intervention
  • 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.
  • 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.