Septic shock is a life-threatening condition that occurs when a person's blood pressure drops dramatically low due to their body's overwhelming and dysfunctional response to an infection. It results in severely low blood pressure and abnormalities in microcirculation that can lead to organ damage and failure. Diagnosis involves identifying signs of infection along with low blood pressure and lactate levels. Treatment focuses on identifying and treating the infection with antibiotics, supporting vital organ functions, and administering vasopressors to increase blood pressure such as norepinephrine. Even with advanced treatments, septic shock continues to have a high mortality rate of 30-50%.

1. 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

7. Pathophysiology

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