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Septic Shock
Objectives
 Introduction & Definition
 Etiology
 Pathophysiology
 Epidemiology
 Diagnosis
 Stages
 Treatment
Introduction & Definition
 Septic Shock: The most common form of vasodilatory shocks that results
from dysfunctional endothelium caused by systemic response to a
microbe
 Vasodilatory shocks include other types:
 Hypoxic lactic acidosis
 CO poisoning
 Decompensated/Irreversible Shocks
Etiology
 Systemic Inflammatory response syndrome “SIRS”, to:
 Severe local infection
 Invasive infection (Bacteremia)
Pathophysiology
 Inflammatory mediators released due to host response to infection
causes damage to endothelium resulting in dysfunctional epithelium
 Endothelium produces large amount of NO by increasing the iNOS which
leads to relaxation of the vascular smooth muscles and therefore
vasodilation
 Vasodilation leads to hypotension and maldistribution of the blood flow
causing hypoperfusion to target tissues and the blood vessels themselves
Pathophysiology
 Large amounts of NO causes the vasodilation to be resistant to vasopressors
 The cycle continues perpetuating the damage to the endothelium
Pathophysiology
Epidemiology
 750,000 case yearly in the US
 High mortality rate of 30%-50%
 Causes 9.3% of deaths
 Mortality rate haven’t changed much even with the advancement in the treatment
Diagnosis
 Diagnosis criteria: manifestations + identification of organism or source of
infection
 High level of suspicion is the first step to diagnose sepsis
 Labs: CBC, Blood and source C&S, Serum lactate, ABGs, CRP, ESR, PTT, PT, INR
Diagnosis
 Clinical Features of sepsis:
 Leukocytosis
 Hyper- or Hypodynamic States (Starts hyper then hypo)
 Hyper: Tachycardia with reduced peripheral resistance (Warm)
 Hypo: Bradycardia with increase peripheral resistance (Cold)
 Hyperglycemia
 End-Organ failure
 Oliguria, Anuria
 CNS: reduced level of consciousness
 GI pain and bleeding
Stages
 SIRS: Inflammatory response without evidence of an infection
 Sepsis: Manifestations + evidence of an infection
 Severe Sepsis: Sepsis + Signs of end-organ damage, SBP<90 mm Hg, Lactate>4mmol
 Septic Shock: persistent severe sepsis
Treatment
 ABC:
 Airway: intubation
 If the patient is severely obtunded and patients whose work of breathing is excessive
 Breathing: ventilation
 Circulation: fluid at least 30ml/Kg within 4-6 hrs.
 Starch-based colloids cause delirium
Treatment
 Antibiotics:
 Empirical ATB depending on the most likely organism and the infection
history of the patient
 Specific ATB depending on microbiologic studies
 To prevent resistance, opportunistic fungus infections, colitis
 Source of infections must be controlled:
 I&D, Debridement, foreign body removal “instrumentation, catheters, …”
Treatment
 Vasopressors:
 1st Line: Norepinephrine
 2nd Line: Epinephrine
 3rd Line: Arginine vasopressin “ADH”
 4th Line: Dobutamine
 In Hypodynamic states (low CO + High SPB or hypoperfusion)
Treatment
 Goal-directed Therapy:
 Continued intervention for maintaining pre- , afterload and contractility
 Reduced CVS collapse from 21.0% to 10.3%
 Reduced 28-day mortality from 49.2 to 33.3%
 Fluid given within first 4-6 hrs. is more but less fluid over 72-hr period
Treatment
 Glucose level control:
 Old way: insulin if >215mg/dl to reach 180-200mg/dl
 New way: maintain within 80-110 mg/dl
 Reduced mortality from 8.0% to 4.6%
 Reduced post-5th day ICU mortality by 42%
 Reduced septicemia episodes by 46%
 Reduced ATB need
 Reduced ventilation time
 Reduced renal replacement therapy
Treatment
 Tidal Volume Control:
 Old way: 12ml/Kg
 New way: 6ml/Kg
 Better outcomes
Treatment
 Steroid Use:
 Controversial
 If SPB<90 mm Hg with vasopressors, try hydrocortisone 50mg 1x4x7 or equivalents IV
infusion
 Fludrocortisone 50ug oral may can also be used
Treatment
 Immune Therapy:
 AB, receptor antagonists, NOS inhibitors
 Not Successful, no improvement

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Septic shock

  • 2. Objectives  Introduction & Definition  Etiology  Pathophysiology  Epidemiology  Diagnosis  Stages  Treatment
  • 3. Introduction & Definition  Septic Shock: The most common form of vasodilatory shocks that results from dysfunctional endothelium caused by systemic response to a microbe  Vasodilatory shocks include other types:  Hypoxic lactic acidosis  CO poisoning  Decompensated/Irreversible Shocks
  • 4. Etiology  Systemic Inflammatory response syndrome “SIRS”, to:  Severe local infection  Invasive infection (Bacteremia)
  • 5. Pathophysiology  Inflammatory mediators released due to host response to infection causes damage to endothelium resulting in dysfunctional epithelium  Endothelium produces large amount of NO by increasing the iNOS which leads to relaxation of the vascular smooth muscles and therefore vasodilation  Vasodilation leads to hypotension and maldistribution of the blood flow causing hypoperfusion to target tissues and the blood vessels themselves
  • 6. Pathophysiology  Large amounts of NO causes the vasodilation to be resistant to vasopressors  The cycle continues perpetuating the damage to the endothelium
  • 8. Epidemiology  750,000 case yearly in the US  High mortality rate of 30%-50%  Causes 9.3% of deaths  Mortality rate haven’t changed much even with the advancement in the treatment
  • 9. Diagnosis  Diagnosis criteria: manifestations + identification of organism or source of infection  High level of suspicion is the first step to diagnose sepsis  Labs: CBC, Blood and source C&S, Serum lactate, ABGs, CRP, ESR, PTT, PT, INR
  • 10. Diagnosis  Clinical Features of sepsis:  Leukocytosis  Hyper- or Hypodynamic States (Starts hyper then hypo)  Hyper: Tachycardia with reduced peripheral resistance (Warm)  Hypo: Bradycardia with increase peripheral resistance (Cold)  Hyperglycemia  End-Organ failure  Oliguria, Anuria  CNS: reduced level of consciousness  GI pain and bleeding
  • 11. Stages  SIRS: Inflammatory response without evidence of an infection  Sepsis: Manifestations + evidence of an infection  Severe Sepsis: Sepsis + Signs of end-organ damage, SBP<90 mm Hg, Lactate>4mmol  Septic Shock: persistent severe sepsis
  • 12. Treatment  ABC:  Airway: intubation  If the patient is severely obtunded and patients whose work of breathing is excessive  Breathing: ventilation  Circulation: fluid at least 30ml/Kg within 4-6 hrs.  Starch-based colloids cause delirium
  • 13. Treatment  Antibiotics:  Empirical ATB depending on the most likely organism and the infection history of the patient  Specific ATB depending on microbiologic studies  To prevent resistance, opportunistic fungus infections, colitis  Source of infections must be controlled:  I&D, Debridement, foreign body removal “instrumentation, catheters, …”
  • 14. Treatment  Vasopressors:  1st Line: Norepinephrine  2nd Line: Epinephrine  3rd Line: Arginine vasopressin “ADH”  4th Line: Dobutamine  In Hypodynamic states (low CO + High SPB or hypoperfusion)
  • 15. Treatment  Goal-directed Therapy:  Continued intervention for maintaining pre- , afterload and contractility  Reduced CVS collapse from 21.0% to 10.3%  Reduced 28-day mortality from 49.2 to 33.3%  Fluid given within first 4-6 hrs. is more but less fluid over 72-hr period
  • 16. Treatment  Glucose level control:  Old way: insulin if >215mg/dl to reach 180-200mg/dl  New way: maintain within 80-110 mg/dl  Reduced mortality from 8.0% to 4.6%  Reduced post-5th day ICU mortality by 42%  Reduced septicemia episodes by 46%  Reduced ATB need  Reduced ventilation time  Reduced renal replacement therapy
  • 17. Treatment  Tidal Volume Control:  Old way: 12ml/Kg  New way: 6ml/Kg  Better outcomes
  • 18. Treatment  Steroid Use:  Controversial  If SPB<90 mm Hg with vasopressors, try hydrocortisone 50mg 1x4x7 or equivalents IV infusion  Fludrocortisone 50ug oral may can also be used
  • 19. Treatment  Immune Therapy:  AB, receptor antagonists, NOS inhibitors  Not Successful, no improvement