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Severe Sepsis Bridging the gap between Clinician & the Microbiologist

Severe Sepsis Bridging the gap between Clinician & the Microbiologist. Dr. Pratibha Dileep M.D. Consultant Critical Care & Hospital Infection control, Director, Critical Care, Sterling Hospital, Ahmedabad. History. Derived from Greek word SEPO- meaning “I Rot” in eight century B.C.

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Severe Sepsis Bridging the gap between Clinician & the Microbiologist

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  1. Severe SepsisBridging the gap between Clinician & the Microbiologist Dr. Pratibha Dileep M.D. Consultant Critical Care & Hospital Infection control, Director, Critical Care, Sterling Hospital, Ahmedabad

  2. History • Derived from Greek word SEPO- meaning “I Rot” in eight century B.C. • 1914 sepsis leading to bacteremia was termed as Septicemia • The major advance in the therapy of severe sepsis was introduction of ABX 65 years ago • Incidence is rising world over by 8.7%/yr. with an adjusted rate of increase around 300% since 1979

  3. Rising incidence of Sepsis • Aging population >65yrs are >13 times more prone to sepsis • Chronic diseases leading to organ failure • Immunocompromised state, • Invasive diagnostic & therapeutic procedures, • Cytotoxic drugs, • Auto immunity, • Stress, substance abuse • ABX resistance

  4. Sepsis • Most common cause of death in ICU • 800,000 cases/yr: Incidence increasing • Mortality is 10% to 90%. Average 40% • Average Hospital stay = 19 days • Cost = Rs 25,000-30K / day • <50% have a positive blood culture • 50% need ICU, 17% need ventilator

  5. SIRS – MODS • Term coined in 1992 • Is a result of various clinical insults leading to tissue injury manifesting as two or more of the followings • Temp> 38⁰C or <36⁰C • HR >90 beats/min • RR >20 bpm, PaCO2 <32mm Hg • WBC >12K/mcl or <4k/mcl or 10% band cells

  6. Severe Sepsis • Sepsis with organ hypoperfusion: one of the following: • Hypotension <90mm systolic • Acute mental status change • Pa02 <60mm on room air (pO2/FiO2 <250) • Increased lactic acid /acidosis • Oliguria (urine output <0.5ml/kg) • D.I.C /Thrombocytopenia <80 K

  7. See discussion on next slide Figure B, page 948, reproduced with permission from Dellinger RP. Cardiovascular management of septic shock. Crit Care Med. 2003;31:946-955.

  8. The physiological changes occurring in patients with severe sepsis and septic shock are myriad and include changes that are clearly detrimental such as decreased contractility of the left and right ventricle, increased venous capacitance, increased pulmonary vascular resistance, and capillary leak. Increased ventricular compliance and sinus tachycardia are likely adaptive responses allowing the ventricle to maintain, and even manifest increased cardiac input, following volume resuscitation in despite decreased contractility. The decreased arteriolar resistance may also be adaptive, although when profound, produces detrimental and potentially lethal hypotension.

  9. Metabolic Abnormalities • Mitochondrial dysfunction occurs due to sepsis • Even if the blood flow is normal, O2extraction is impaired • Sepsis induces a hyper metabolic state •  Protein & Fat catabolism • Negative nitrogen balance • Hyperglycemia &  Gluconeogenesis •  resting O2 consumption

  10. Hemostatic abnormalities • Endothelial dysfunction • Microvascular thrombosis • Impaired Fibrinolysis • Excessive intravascular activation of coagulant factors • Direct stimulation of coagulation cascade by cytokines • Release of endogenous anticoagulants • Cellular injury

  11. Evolution of organisms causing sepsis • 1950s GPC MSSA • 1960s & 1970s GNBs predominated • 1980s & 1990s resistant GPC (MRSA, penicillin resistant Streptococci, Enterococci) • Late 90s ESBL producer GNBs • 2000 onwards MRSA from community, MDR GNBs, VRE & Fungal Sepsis • NOW- ADR GNB, MRSA, VRSA & Fluconazole resistant fungal infection

  12. Septic Shock • Systolic BP <90mm Hg or MAP <60 mm • Drop in MAP >40 mm Hg in HPN • Organ hypoperfusion: signs? • Unresponsive to IV fluids • Dependent on pressors: Dopamine/ NE

  13. Identifying Acute Organ Dysfunction as a Marker of Severe Sepsis Tachycardia Hypotension Altered CVP Altered PAOP Altered Consciousness Confusion Psychosis Tachypnea PaO2 <70 mm Hg SaO2 <90% PaO2/FiO2300 Oliguria Anuria  Creatinine Jaundice  Enzymes  Albumin PT  Platelets  PT/APTT  Protein C  D-dimer Balk RA. Crit Care Clin 2000;16:337-52.

  14. What does a clinician expect from a microbiologist while treating a severe Sepsis patient?

  15. Need for urgency • Quality assurance • Answerability • Communication • Skills • Conviction

  16. Sampling • The most crucial link between the Clinician & the Microbiologist • Proper collection, site preparation • Transport, transport medium • Processing & preserving in the ward while waiting for the sample to be collected

  17. Common specimen of interest • Sputum- expectorated mucus & not saliva • Sinuses- secretions, washes, curettage & Bx material during endoscopy NOT nasal swab • Urine– midstream clean catch, straight catheterization, suprapubic aspiration or cystoscopic urine & NOT sample from catheter or Bag • Wound – aspiration of pus, normal saline wash & NOT wound swabs, if a swab is needed then from beneath the dermis

  18. Diarrhea- freshly passed stool, endoscopically collected sample & Not rectal swab • Blood– 2-3 samples from separate venipuncture ~each 20ml & NOT clotted blood or less than 10ml

  19. Handling the specimen • Sterile container • Swabs must be kept moist using holding medium • Use anaerobic transport if anaerobic growth is expected • Transport time should be as low as possible, if delay is anticipated then proper handling medium must be used • Blood C&S must be inoculated directly & NOT in the syringe or Clotted blood • Serology – serum must be separated within 4 hrs

  20. Ideal specimen • Sputum- < 25 SEC/10x field • ET-- <25 SEC/10x field and bacteria in at least one out of 20 fields • BAL-- < 1% cells are SEC • Urine--<3+ SEC • Superficial wound- gram stain, <2+SEC • Stool- presence of pus cells in an Outpatient or in an Inpatient admitted for less than 72 hours

  21. Non culture techniques

  22. Gram stain- the forgotten art • Simple, quick & reliable technique • Dominant organism is likely to be a pathogen • Presence of ABX may inhibit the growth of organism • Can even show dead organisms • Is the quickest non-culture technique • Can determine empiric choice of ABX

  23. Others • KOH • ZN stain • Fluorescent staining

  24. Molecular tests • PCR- MRSA - MTB -HCV -HIV -HPV -Parvo virus

  25. Serological tests • Collect serum in sterile test tube without anticoagulants • Specimen should be stored in ice or refrigerated until clots are removed • Clots should be removed as early as possible within hours • Can be stored for few days at 4ο C for few days -Up to 1 month -12ο C ->1month -70ο C • Avoid repeated freezing & thawing

  26. MIC & Break point • Are two different levels • MIC is the lowest level of the drug to inhibit the growth of the organism in vitro • While break point is the level achieved in the particular tissue, which differentiates the susceptible from resistant organism • Hence selection of an ABX based on the MIC value alone can be totally erroneous.“

  27. Synergy test • Particularly helpful in MDR organism particularly in Enterococcal infection, Pseudomonas, Enterobacter • Not very easy to perform in vitro

  28. Management of Sepsis EGDT • Stabilize: fluids, oxygen • Empiric Antibiotics-EARLY! Hold BP medications Keep NBM • Determine source of sepsis- cultures, LFTs, amylase, gram stain

  29. Fluid Resuscitation • If evidence of organ hypoperfusion • rapidinitiation of ISOTONIC crystalloids (Lactated Ringers or normal saline only) • Only 250cc remains intravascularly after 1L of IV fluid given • Initial bolus is 20ml/Kg isotonic fluids or corresponding Colloids • 4-6 L may be required in first 6 hours • Monitor goals of fluid therapy frequently

  30. Fluids - Crystalloids vs. Colloids • Crystalloids - ALWAYS USE FIRST! • Colloids: • FFP if coagulopathy • PCV if HCT <30, especially if risk of CAD • Starch (Penta or Heta) 500cc if BP still low (CCM 2002:300) • Avoid Albumin ( increase ECF, cost,) • No difference in mortality as long as resuscitation goals are met (Metanalysis CHOI:CCM:1999:200-210)

  31. Vasopressors • Persistent hypotension after correcting hypovolemia is treated with vasopressors • NE & Dopamine is the choice of vasopressor in septic shock • Dobutamine is the the cxhoice of vasopressor if SCVO2 is <70mm • Vasopressin can restore vascular tone and BP

  32. Selection of ABX • Presumed site of infection • Gram stain results • Suspected or known organism (includes risk for fungal infection) • Resistance patterns of the hospital • empirical

  33. Antibiotic Therapy • Reassess antimicrobial regimen at 48 - 72 hours • Microbiologic and clinical data • Narrow-spectrum antibiotics • Noninfectious cause identified • Prevent resistance, reduce toxicity, reduce costs

  34. Therapy induced Dysfunction • High tidal volumes required for ventilation (>10 ml/kg) • Excess blood products • Nephrotoxic agents • Invasive devices • Hyperglycemia

  35. Antibiotics / Sugar control • Early antibiotic administration reduces mortality • Adequate coverage: mortality 28% vs. 62% if empiric coverage poor. Usually Candida or staph. (Ebrahim :Chest 2000:118:146) • Intensive Insulin therapy : control sugar <110 reduces mortality in CV surgery ICU (NEJM:2001:Nov 8 )

  36. Strict glycemic control < 110 mg/dl Reduces ICU and hospital mortality of surgical ICU patients • Prevented complications : • Severe infections and inflammation • Acute renal failure and need for dialysis • Prolonged ventilator dependency • Need for transfusions • Prolonged ICU stay

  37. Sepsis Survivors…Multimodality • Recognize early • Remember essentials • Fluids • Antibiotics • Ventilate • Assess: severity of sepsis • Consider Steroids (Low dose Please!!)

  38. Mortality • Varies from 5% to 90% depending on stage SIRS - 10%; Shock / organ dysfunction 30-60%; • 28 day mortality in shock – 40% Poor predictors: MOD >2 systems Lactate > 2.8mm/L Cortisol response APACHE >25

  39. Severe Sepsis Therapy: Conventional Care • Source control • Antibiotics • Hemodynamic support • Mechanical ventilation • Renal replacement therapy • Sedation/analgesia • Adequate nutrition • Hematological support • Other supportive measures Wheeler AP, Bernard GR. N Engl J Med 1999;340:207-14.

  40. Sepsis • Do patients with sepsis have a failure of their immune systems? • Anergy is a state of unresponsiveness to antigen • Autopsies indicate that patients with sepsis have a profound loss of • B cells • CD4+ and CD8+ T cells • Follicular dendritic cells and NK cells

  41. What’s new but so far useless in sepsis!! • Human monoclonal Ab • E5 murine monoclonal Ab • LPS receptor antagonists • Nitric Oxide • High dose Steroids • TNF antagonists • Bactericidal or Permeability increasing protein (BPI) • Immunoglobulins • Drotecogin Alpha

  42. Lets us aggressively fight the war against sepsis!!! Thank You

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