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Sepsis nuts&bolts

May 31, 2015




Cons. general surgery

  • 1. Dr.shenawiCons. general surgeryM.g.hMBBCh,MsC,MrCs(irelanD)

2. I,m not an intensivist &apologize for deficiency itmight encountered on the mini lecture. Thanks& greeting to all my colleagues& staff inMGH,for their sympathy and support given to meduring my assignment in hajj duty. Accept my appology for any missbehave mighthappen from me during my duty.Dr.abdulfattah alshenawi 3. Its common and increasing in frequency as thepopulation ages Its associated with high risk of death and longlength of stayWe could make a Its expensivedifference AND. The good new is: There are interventions proven to reducemortality & cost. However implementation of these interventionsare not routinely done in all hospitals!! 4. 35% diagnosed in hospital wards. 52% diagnosed in ED. 13 % diagnosed in ICU. Hospitalization for sepsis & sepsis relatedillness has doubled in the states from year2000 -2008. 5. Sever sepsis & septic shock is the leadingcause of death in the non coronary carewith mortality rate of 20 -50%.Ischemic stroke 1-2%STEMI 3-5% 6. Cost 14-18 billion USD /y.Cost 18.000 USD/case. 7. Inflammation is a war! Non specific localized tissue response to injury. Purpose: Destroy Dilute Dam-off result is healing Regeneration (hyperplasia) Fibrosis (scarring) Collateral damage may occur(SIRS) 8. 1. Stimulus: Initiators of inflammation 2. Local dilation of capillaries: increased bloodflow 3. Microvascular structural changes: escape of plasma proteins from bloodstream 4. Leukocyte transmigration throughendothelium and accumulation at injury site 5. Phagocytosis / Oxygen burst: Cellular injury 9. Leucocytic response.(organism specific) Margination&migration of neutrophils(90min) Phagocytosis .(physiologic debridment) Monocyte migration(24hrs)-macrophage. Release of cytokines. 10. Definition: Any messenger that acts on blood vessels,inflammatory cells, or other cells to contribute to aninflammatory response. (Pretty much anything...) 11. Plasma proteins such as complement andantibodies. Other proteins such as sPLA2 and acute phasereactants. Cytokines and chemokines. Lipids such as prostaglandins and PAF. Amines such as histamine. Gasses such as NO and O2-. Kinins such as bradykinin. Neuropeptides such as substance P. 12. Systemic absorption of locally generatedinflamatory mediators. Non specific response!!! May be due to infectious or non infectious causes. 13. Fever>100 pulse.>100 SBP20May be caused by infections(sepsis) Altered mental status Hyperglycemia or noninfections(burn,trauma,pancreatitis,ischemia,reperfusion,chemical) 14. SIRSSEPSISSEVER SEPSISSEPTIC SHOCK 15. SIRS+INFECTION(known or suspected)Infection may bebacterial,viral ,fungal etc. 16. TRAUMABURNSINFECTION SSEEPPSSIISS SIRSPANCREAITISBACTEREMIA 17. SSEEPPSSIISS++22OORRGGAANNddyyssffuunnccttiioonn 18. SEVER SEPSIS+ REFRACTORYHYPOTENSION 19. Normal response to infection.Recognition of foreign antigen.Immune system release inflammatorymediators(PG,TNF,cytokines,interleuk)Platlet activating factors.Promote recovery of the affectedtissues. 20. Uncontrolled response toinfection(sepsis syn) Flood of inflammatory mediatorsCapillary leak. Activation of clotting cascade. Tissue hypoxia & hypoperfusion. Septic shock.Microcirculatory failure is the key!!! 21. Figure B, page 948, reproduced with permission from Dellinger RP. Cardiovascularmanagement of septic shock. Crit Care Med 2003;31:946-955. 22. Site of oxygen exchange.Central role of the immune system.During septic shock,it the first to go & lateto recover.Rescue microcirculation is theresuscitation end point. 23. InfectionInflammatoryMediatorsEndothelialVasodilation DysfunctionHypotension Microvascular PluggingVasoconstriction EdemaMaldistribution of Microvascular Blood FlowIschemiaCell DeathOrgan Dysfunction 24. Oxygen won,t go whereblood don,t flow.Early goal directedtherapy(EGDT) IS to restoremicrocirculation beforemitochondia is permenantlydamaged. 25. Acute organ dysfunction isthe marker of sever sepsis.One organ damage lead to20% increase mortality&double thereafter. 26. A clinician, armed with the sepsis bundles,attacks the three heads of severe sepsis:hypotension, hypoperfusion and organdysfunction. 27. Recognition& screening for sepsis. ivf Early antibiotics. Transfer trigger tool. Emergency dept. initiation of 6hs bundle. 28. Non specific symptoms in elderly pt. Fever may be absent.13% in pt>65y& 4% inpt100 F Pulse>100/min SBP20/min Spo2 10% every hour. Normalisation within 6 hs.Associated with reduced mortality. Half life of lactate is 20 min. 36. 20 -30 ml /kg initial fluidbolus.Minimum 1 L bolus.Minimum of 30ml/kg in the first3hrs. 37. Each 1 h delay in effective antibiotics isassociated with decrease in survival by7.6%. Triage time to appropriateantibiotics4mmol/lPERSISTENT HYPOTENSION DESPITEFLUID CHALLENGEMORE THAN TWO ORGANDYSFUNCTION 41. To be completed within 3 hs!!Measure lactate.Bl. Culture prior to antibiotics.Antibiotics. Infusion of 30ml/kg crystalloids inhypotension or lactate >4mmol/l 42. Apply vasopressors for those notresponding to fluid challenge to maintainMAP>65 mmhg. Persistent hypotension despit fluids,measureCVPScvO2 Re measure lactate if initially elevated. 43. 1. CVP of 10mmhg forunventilated &12-15 mmhg forthe ventilated2. MAP >65mmhg3. Hemoglobin > 9 gm/dL4. ScvO2 > 70%5. UOP>0.5ml/h 44. 3 hs bundle (culture, crystalloid, lactate,&antibiotic.)6 hs bundleContinue resuscitationCvp,monitor,follow lactate.Consider inotropes 45. Screen pt . For sepsis. In ED&wards. Evaluate all pt. with sepsis fororgan dysfunction to identify seversepsis. Implement sepsis bundles for allpts with sever sepsis & septicshock. 46. Obtain lactate when 2 SIRS or suspectedinfection. Begin 3hrs bundle when screen is +ve. For ED pt. u have 3 hrs from arrival todetermine pt has an infection, find thelikely source,& begin the appropriatetherapy. Clock is not your friend!

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