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Patho Physiology And Icu Management Of Septic Shock

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  • 1. Patho-Physiology and ICU Management of Septic Shock Dr.T.R.ChandraShekar Director critical care, K.R.Hospital, Bengaluru
  • 2. Case Scenario
    • 35 year old male patient brought to ICU with 3 day old perforation, Posted for emergency Lapratomy
    • Has chills with fever
    • Tachypneic- RR 40/mt, has respiratory distress,
    • Tense abdomen, bilateral crepts,
    • Spo2 on 89% on room air.
    • Pulse 130/mt well felt, BP 80/60 mm Hg, Restless,
    • Investigations
    • WBC – 19,000 T.B 3.5, Enzymes Normal
    • SC-2.0 INR 2.0, Platelets 1.2 lac
    • Lactate 5.0 SCVO2 60%,
    Is he in septic shock ? Can we administer anaesthesia right now ? Do you want to stabilise him before surgery ?
  • 3. Shock definition
    • Shock is defined as a life-threatening, generalized maldistribution of blood flow resulting in failure to deliver and/or utilize adequate amounts of oxygen, leading to tissue dysoxia.
    • Hypotension [SBP < 90 mmHg, SBP decrease of 40 mmHg from baseline, or mean arterial pressure (MAP) < 65 mmHg], while commonly present, should not be required to define shock . Shock requires evidence of inadequate tissue perfusion on physical examination .
  • 4. Sepsis: Defining a Disease Continuum
    • A clinical response arising from a nonspecific insult, including  2 of the following:
      • Temperature  38 o C or  36 o C
      • HR  90 beats/min
      • Respirations  20/min
      • WBC count  12,000/mm 3 or  4,000/mm 3 or >10% immature neutrophils
    SIRS Systemic Inflammatory Response Syndrome SIRS with a presumed or confirmed infectious process Sepsis SIRS Infection Severe Sepsis SEPTIC SHOCK Inflammatory response to microorganisms or invasion of normally sterile tissues
  • 5. Sepsis SIRS Infection/ Trauma Severe Sepsis
    • Sepsis with  1 sign of organ failure
      • Cardiovascular ( hypotension)
      • Lungs: (ARDS):
      • Kidneys
      • Liver
      • Digestive
      • Brain - confusion
    HYPOTENSION despite adequate fluid resuscitation/Requiring Vasopressors or Inotropes SEPTIC Shock
  • 6. Relationship Of Infection, SIRS, Sepsis Severe Sepsis and Septic Shock Bacteria Fungus Parasites Virus SIRS INFECTION PANCREATITIS BURNS TRAUMA OTHER SEPSIS SEVERE SEPSIS SEPTIC SHOCK
  • 7. Definitions SIRS Sepsis Severe Sepsis Septic Shock Infection DO WE REQUIRE TO CHANGE THE DEFINITION? MODS
  • 8. 2001 Sepsis Definitions Conference
    • Current definitions will remain unchanged
    • However, will accept the uncertainty of definitions
    • SIRS expanded to signs and symptoms
    Although none of these is specific of sepsis, the unexplained presence of several in combination should raise suspicion of sepsis Expanded list of SIRS signs and symptoms
  • 9. Arterial hypotension Tachycardia Altered skin perfusion Decreased U.O Hyperlactatemia – Altered WBC count Increased CRP, PCT concentrations Rigor– fever Tachypnea Positive fluid balance – edema General signs & symptoms General inflammatory reaction Hemodynamic alterations Signs of organ dysfunction Hypoxemia Coagulation abnormalities Altered mental status Expanded signs of SIRS
  • 10. Case Scenario
    • 35 year old male patient brought to ICU with 3 day old perforation, Posted for emergency Lapratomy
    • Has chills with fever
    • Tachypneic- RR 40/mt, has respiratory distress,
    • Tense abdomen, bilateral crepts,
    • Spo2 on 89% on room air.
    • Pulse 130/mt well felt, BP 80/60 mm Hg, Restless,
    • Investigations
    • WBC – 19,000 T.B 3.5, Enzymes Normal
    • SC-2.0 INR 2.0, Platelets 1.2 lac
    • Lactate 5.0 SCVO2 60%,
    Severe SEPSIS
  • 11. Pathogenesis of shock Microcirculatory Mitochondrial dysfunction Cardiac dysfunction, Microemboli, Microvasular injury, increased Nitric oxide- Vasoplegia Cytokines & inflammatory mediator cascade Interaction with human cells- macrophages Monocytes, Neutrophils, Endothelial cells Infectious trigger
  • 12. Toll receptors
  • 13. Toll receptors (TLR)
    • Key mediators of the innate immune system
    • Expressed on macrophage, dendritic cells, neutrophils, endothelial cells and mucosal epithelial cells
    • TLR are transmembrane proteins with the ability to promote signaling pathways downstream, triggering cytokine release and neutrophil activation and stimulating endothelial cells
  • 14. Toll receptors Pathogen-associated molecular patterns (PAMPs) Host factors Immunosuppressed Extremes of age Malnutrition Alcohol, Drug Abuse Malignancy HIV/AIDS Chronic Health Issues – Diabetes, Liver Failure, Heart Disease, Corticosteroids, Chemotherapy Multiple invasive procedures or invasive lines
  • 15. PRO INFLAMMATORY Promotes-Inflammation Coagulation Inhibits-Anti-coagulants, Fibrinilysis. IL-1; TNF IL-6; IL-8 ANTI-INFLAMATORY Inhibits- Inflammation Coagulation Immunosupression Anti-Inflammatories: IL-1ra; IL-4; IL-10 S MONOCYTE DERIVED CYTOKINES INFECTION/MICROBIAL TRIGGER SIRS CARS Systemic Inflammatory Response Syndrome Compensatory Anti- Inflammatory Response Syndrome
  • 16. Crit Care Med 2000, 28(4):N105-N113 with modification Infection Immune Response Sepsis Uncontrolled Pro-inflammatory Mechanisms Dysregulated anti-inflammatory Mechanisms SIRS MODS/MOF
  • 17. Why some patients do well others die ? Death Infection Toxins Host defenses Overwhelming infection Death Sepsis Excessive Survival MODS Adequate Coordinated Infection control Survival Why? Why? Unregulated Host factors Delayed therapy Genetic predisposition HLA class III genes TNF a gene promoter Inadequate
  • 18. Role of Nitric Oxide
    • L – arginine
    • eNOS iNOS
    • nNOS
    • NO
    Endothelium Neurones Macrophages Smooth muscle Endothelium Vasoplegia-Hypotension
  • 19. Coagulation in Sepsis Bernard GR, et al. New Engl J Med, 2001;344:699-709. Coagulation Inflammation Fibrinolysis Micro-emboli Inflammatory Response Inflammatory Response to Infection Thrombotic Response to Infection Fibrinolytic Response to Infection Endothelium TAFI PAI-1 Suppressed fibrinolysis Neutrophil Monocyte IL-6 IL-1 TNF  Bacterial, viral, fungal or parasitic infection/endotoxin Bacterial, viral, fungal or parasitic infection/endotoxin IL-6 Tissue Factor Tissue Factor COAGULATION CASCADE Factor Va Factor VIIIa THROMBIN Fibrin Fibrin clot
  • 20. CARDIOVASCULAR FAILURE Vasodilatation (nitric oxide release) Hypovolemia Myocardial dysfunction Cell metabolism alteration Decrease vascular resistance Tachycardia , Hypotension, Hypoperfusion
  • 21. Final pathway in sepsis Sepsis is a disease of the microcirculation Vasoplegia , Cardiac dysfunction, Capillary leak Hypovolemia,Maldistribution Microemboli Microcirculatory Mitochondrial Dysfunction syndrome (MMDS) Cell death-Organ injury –MODS- Death
  • 22. Why the microcirculation is important in shock .
      • It is where oxygen exchange takes place.
      • It plays a central role in the
      • immune system.
      • During sepsis and shock it the first to go and last to recover.
    Rescue of the microcirculation = resuscitation end-point
  • 23.
    • TIME
    • is
    • TISSUE
    Oxygen Don’t Go Where the Blood Won’t Flow! From these two statements three things are obvious Early therapy before mitochondria gets damaged. Macro circulation should be optimised first. Micro circulation optimisation to prevent Mitochondrial injury is the target
  • 24. Resuscitation end points
    • CVP 8–12 mm Hg
    • (MAP) >=65 mm Hg
    • Urine output >=to 0.5 mL/kg/hr
    • SCVO2(superior vena cava) >=70% or SVO2 >= 65%,
    • Lactate < 2 mmol/L
    • SCVO2 > 70%
    Micro circulation Macro circulation Tissue hypoperfusion can persist despite normal vital sign.
  • 25. Normal Lactate and SCVO2 despite MMDS
    • No extraction of oxygen-mitochondrial damage
    • Shunting of blood away from microcirculation
    • Although ScvO 2 tracked SvO 2 , it is tended to 7 ± 4 % higher
  • 26. Management of Sepsis the bottom line is
    • Blood to be oxygenated
    • Have Adequate pressure
    • Deliver this blood into microcirculation early before Mitochondria are damaged
  • 27. DO2 –oxygen delivery with adequate pressure
    • Arterial oxygen content X Cardiac out put
    • SaO2/Pao2 x Hb%
    MV/ oxygen therapy PEEP Blood transfusion Contractility Inotropes Preload Fluids HR Pacing Isoproterenol Afterload Vasodialators
  • 28. Oxygen to mitochondria
    • Patient may have defective oxygen extraction or oxygen may not reach the cells due to micro emboli or shunting of blood.
    • Defective extraction may be due to Mitochondrial injury.
    • Shunting of blood
    O 2 lactate CO 2 v a Micro-Emboli Maldistribution
  • 29. MMDS- Prevention
    • Optimize Macro-circulation.
    • rhAPC- Prevents coagulation enhances fibrinolysis.
    • Vasodilators
    Microcirculation Monitoring at bedside is difficult Therapeutically Not much can be done at MM level Except early and protocol based treatment
  • 30.
    • Surviving Sepsis Campaign- Phase II
    • 25% reduction in sepsis mortality within 5 years
    • - by 2009
    War on Sepsis Society of Critical Care Medicine, European Society of Intensive Care Medicine, International Sepsis Forum + Institute of Healthcare Improvement
  • 31. Even with the ‘best’ parameters it is not always easy to make the right decision.………
  • 32. EGDT Suspected infection Blood cultures Obtain two or more BCs One or more BCs should be percutaneous One BC from each vascular access device in place more than equal to 48 hrs Culture other sites as clinically indicated. Other diagnostic/imaging as indicated Appropriate Empirical Antibiotics with in 1 hr/ source control Host factors/ local antibiogram/ suspected site Combination antibiotics/ right dose SBP< 90 even after 20-30ml/kg fluid or Lactate > 4mmol/l
  • 33. Antibiotics Always look at you local organisms and resistance patterns Early antibiotic therapy Right dose
  • 34. Case Scenario
    • 35 year old male patient brought to ICU with 3 day old perforation, Posted for emergency Lapratomy
    • Has chills with fever
    • Tachypneic- RR 40/mt, has respiratory distress,
    • Tense abdomen, bilateral crepts,
    • Spo2 on 89% on room air.
    • Pulse 130/mt well felt, BP 80/60 mm Hg, Restless,
    • Investigations
    • WBC – 19,000 T.B 3.5, Enzymes Normal
    • SC-2.0 INR 2.0, Platelets 1.2 lac
    • Lactate 5.0 SCVO2 60%, K+4.5
    3l of oxygen RBM, Two BC Inj Meoropenem 500mg tid+ Inj Metrogyl 100 ml tid
  • 35. Suspected infection Blood cultures SBP< 90 even after 20-30ml/kg fluid or Lactate > 4mmol/l Appropriate Empirical Antibiotics with in 1 hr/ source control CVP MAP Goal achieved SCVO2 < 8 Fluids NS, RL/ Colloid 8-12 >60-90mmHg < 60-90 Vasopressors Noradrenaline/dopamine <70% < 30 HCt-Packed cells SCVO2< 70% Inotrope Dobutamine SCVO2 >70% Decrease Oxygen consumption
  • 36.
    • Fluid challenge in patients with suspected hypovolemia may be given
        • 500 - 1000 mL of crystalloids over 30 mins
        • 300 - 500 mL of colloids over 30 mins
        • Repeat based on response and tolerance
        • Input is typically greater than output due to venodilation and capillary leak
        • Most patients require continuing aggressive fluid resuscitation during the first 24 hours of management
    Fluid Therapy: Fluid Challenge Grade E Dellinger, et. al. Crit Care Med 2004, 32: 858-873.
  • 37. Suspected infection Blood cultures SBP< 90 even after 20-30ml/kg fluid or Lactate > 4mmol/l Appropriate Empirical Antibiotics with in 1 hr/ source control CVP MAP Goal achieved SCVO2 < 8 Fluids NS, RL/ Colloid 8-12 >60-90mmHg < 60-90 Vasopressors Noradrenaline/dopamine <70% < 30 HCt-Packed cells SCVO2< 70% Inotrope Dobutamine SCVO2 >70% Decrease Oxygen consumption
  • 38. Vasopressors
    • MAP >=65 mm Hg.
    • Noradrenaline or dopamine as the first choice
    • Adrenaline/ Vasopressin be the first chosen alternative agent in septic shock that is poorly responsive to norepinephrine or dopamine.
    • Low-dose dopamine not be used for renal protection.
    • Arterial catheter placed
    • Inotropic Therapy
    • Dobutamine -myocardial dysfunction
    • Do not use a strategy to increase cardiac index to predetermined supranormal levels
  • 39. Suspected infection Blood cultures SBP< 90 even after 20-30ml/kg fluid or Lactate > 4mmol/l Appropriate Empirical Antibiotics with in 1 hr/ source control CVP MAP Goal achieved SCVO2 < 8 Fluids NS, RL/ Colloid 8-12 >60-90mmHg < 60-90 Vasopressors Noradrenaline/dopamine <70% < 30 HCt-Packed cells SCVO2< 70% Inotrope Dobutamine SCVO2 >70% Decrease Oxygen consumption
  • 40. Case Scenario
    • 35 year old male patient brought to ICU with 3 day old perforation, Posted for emergency Lapratomy
    • Has chills with fever
    • Tachypneic- RR 40/mt, has respiratory distress,
    • Tense abdomen, bilateral crepts,
    • Spo2 on 89% on room air.
    • Pulse 130/mt well felt, BP 80/60 mm Hg, Restless,
    • Investigations
    • WBC – 19,000 T.B 3.5, Enzymes Normal
    • SC-2.0 INR 2.0, Platelets 1.2 lac
    • Lactate 5.0 SCVO2 60%, K+4.5
    1-2 litrs NS/ RL still hypotensive Add noradrenaline and adrenaline BP 130/70 mmHg, lactate 3 mmol/l, SCVO2 68% CVP 8 cms H20/ UO 1ml/kg/mt If he continues to improve for first 6 hrs I may plan to administer anesthesia for his surgery.
  • 41. EGDT
  • 42. Steroids
    • Treat patients who still require vasopressors despite fluid replacement with hydrocortisone 200-300 mg/day, for 7 days in three or four divided doses or by continuous infusion.
    • ACTH stimulation test is not recommended.
    • Steroid therapy may be weaned once vasopressors are no longer required.
  • 43. Supportive care
    • Deep vein thrombosis prophylaxis.
    • Stress ulcer prophylaxis.
    • Glucose control.
    • Maintain a Plateau pressure of less than equal to 30 cmH2O and low tidal volume 4-6 ml/kg of Predicted body weight for mechanically ventilated patients .
  • 44. Conclusions
    • Sepsis is a disease of microcirculation.
    • Oxygen Don’t Go Where the Blood Won’t Flow- Optimise the Macrocirculation first.
    • Monitoring microcirculation at bedside is difficult- Lactate/ SCVO2 are most important parameters to be monitored, validated by studies.
    • Treatment –SS guidelines
  • 45. Thank you