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Patho-Physiology and ICU Management of Septic Shock Dr.T.R.ChandraShekar Director critical care,  K.R.Hospital, Bengaluru
Case Scenario ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Is he in septic shock ? Can we administer anaesthesia right now ?   Do you want to stabilise him before surgery ?
Shock definition  ,[object Object],[object Object]
Sepsis: Defining a Disease Continuum ,[object Object],[object Object],[object Object],[object Object],[object Object],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
Sepsis SIRS Infection/ Trauma Severe Sepsis ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],HYPOTENSION despite adequate fluid resuscitation/Requiring Vasopressors or Inotropes SEPTIC Shock
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
Definitions SIRS Sepsis Severe Sepsis Septic Shock Infection DO WE REQUIRE TO CHANGE THE DEFINITION? MODS
2001 Sepsis Definitions Conference ,[object Object],[object Object],[object Object],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
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
Case Scenario ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Severe SEPSIS
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
Toll receptors
Toll receptors (TLR) ,[object Object],[object Object],[object Object]
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
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
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
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
Role of  Nitric Oxide ,[object Object],[object Object],[object Object],[object Object],Endothelium Neurones Macrophages Smooth muscle Endothelium Vasoplegia-Hypotension
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
CARDIOVASCULAR FAILURE Vasodilatation (nitric oxide release) Hypovolemia Myocardial dysfunction Cell metabolism alteration Decrease vascular resistance  Tachycardia ,  Hypotension, Hypoperfusion
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
Why the microcirculation is important in shock . ,[object Object],[object Object],[object Object],[object Object],Rescue of the  microcirculation =  resuscitation end-point
[object Object],[object Object],[object Object],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
Resuscitation end points ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Micro circulation Macro circulation Tissue hypoperfusion can persist despite normal vital sign.
Normal Lactate and SCVO2 despite MMDS ,[object Object],[object Object],[object Object]
Management of Sepsis the bottom line is ,[object Object],[object Object],[object Object]
DO2 –oxygen delivery  with adequate pressure ,[object Object],[object Object],MV/ oxygen therapy PEEP Blood transfusion Contractility Inotropes Preload Fluids HR Pacing  Isoproterenol  Afterload Vasodialators
Oxygen to mitochondria ,[object Object],[object Object],[object Object],O 2 lactate CO 2 v a Micro-Emboli Maldistribution
MMDS- Prevention ,[object Object],[object Object],[object Object],Microcirculation Monitoring at bedside is difficult Therapeutically Not much can be done at MM level Except early and protocol based treatment
[object Object],[object Object],[object Object],War on Sepsis Society of Critical Care Medicine, European Society of Intensive Care Medicine, International Sepsis Forum + Institute of Healthcare Improvement
Even with the ‘best’ parameters it is not always easy to make the right decision.………
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
Antibiotics  Always look at you  local organisms and resistance patterns Early antibiotic therapy  Right dose
Case Scenario ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],3l of oxygen RBM,   Two BC Inj Meoropenem 500mg tid+ Inj Metrogyl 100 ml tid
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
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Fluid Therapy: Fluid Challenge Grade E Dellinger, et. al.  Crit Care Med 2004, 32: 858-873.
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
Vasopressors ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
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
Case Scenario ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],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.
EGDT
Steroids ,[object Object],[object Object],[object Object]
Supportive care ,[object Object],[object Object],[object Object],[object Object]
Conclusions  ,[object Object],[object Object],[object Object],[object Object]
Thank you

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Patho Physiology And Icu Management Of Septic Shock

  • 1. Patho-Physiology and ICU Management of Septic Shock Dr.T.R.ChandraShekar Director critical care, K.R.Hospital, Bengaluru
  • 2.
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  • 4.
  • 5.
  • 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.
  • 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.
  • 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
  • 13.
  • 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.
  • 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.
  • 23.
  • 24.
  • 25.
  • 26.
  • 27.
  • 28.
  • 29.
  • 30.
  • 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.
  • 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.
  • 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.
  • 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.
  • 41. EGDT
  • 42.
  • 43.
  • 44.