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Microsoft PowerPoint - Sepsis SMI [Compatibility Mode]

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    Microsoft PowerPoint - Sepsis SMI [Compatibility Mode] Microsoft PowerPoint - Sepsis SMI [Compatibility Mode] Presentation Transcript

    • Septic Shock
    • Maternal Mortality - Safe Motherhood Initiative - In 2002 the “Safe Motherhood Initiative” was launched as a joint venture between NYS Dept of Health and ACOG District II. The goals of the program : 1. - Overall decrease in maternal mortality: 2. - Eliminates the disparity between white and black women
    • Maternal Mortality - Safe Motherhood Initiative - Reporting Maternal Deaths through the S.M.I. was on a voluntary basis from 8/03 through 6/05 there were 37 Maternal Deaths reported to ACOG District II through the S.M.I.
    • Maternal Mortality - Safe Motherhood Initiative - Most common causes of M.M. Embolism 24% PIH 24% Hemorrhage 15% Infectious 15% Cardiac 6%
    • Maternal Mortality - Safe Motherhood Initiative - 1.- Hemorrhage Protocol 2.- Preconceptional counselling 3.- Management of Sepsis and septic shock 4.- Obesity 5.- Critical Care in Obstetrics
    • Septic Shock - Case presentation - Mrs X , 36y old P2 at 34wks C/O - Fever, nausea, vomiting 2-3d - Other fam members same symptoms V.S. -Temp 104, BP 97/57, Pulse 150, R.R. 22 P.E. - Non-focal: Lungs clear, Abd non-tender Labs - WBC 8,000 Hct 33%, Hb 11g Fever etiology ?? - Hydration, Temp, EFM - Sepsis workup
    • Septic Shock - Case presentation - Hospital Course Initial FHR: - Bseline 200bpm, variability, no decels 2hrs after Adm: - Temp 102, BP 94/45, Pulse 150, R.R. 18, O Sat 95% 4 hrs after Adm: - FHR Decelerations 430 hrs after Adm: - Decision for C/S
    • Septic Shock - Case presentation - Adhesion molecules
    • Septic Shock -Case presentation –
    • Septic Shock - Case presentation - Delivery 401 A.M. (EBL=800cc) To R.R. 430 A.M. 4:45A.M. Temp 98.9o F 5:00A.M. BP 80/40 Ephedrine BP 100/55 6:45A.M. O2 Sat 85%, -75% O2 Rpt Sat 95% 7:00A.M. pH=7.27 pO2=47 pCO2=41 HCO3=18 7:30A.M. Temp 99.5o F, CxR Bil pleural effusion
    • Septic Shock - Case presentation - Delivery 401 A.M. (EBL=800cc) To R.R. 430 A.M. Urinary Output 5A.M. 50cc 6A.M. 50cc 7A.M. 45cc 8A.M. 25cc 9A.M. 25cc 10A.M. 20cc 11A.M. 10cc Fluids 12P.M. 30cc 1P.M. 60cc
    • Septic Shock - Case presentation - Pregnancy Post surgery R/O Pulmonary Embolus Ac resp distress - 8A.M. Heparin theray started - CT of chest requested Temp 99-101o F, O2 Sat 95-97%, UO > 30cc/h - 2P.M. CT - No evidence of Emboli - Infiltrates sugg of pulm. edema
    • Septic Shock - Case presentation - CT Bil Infiltrates Rpt WBC 15,000 Fever 1010 F Pneumonia – Sepsis -ARDS O2 desaturation Low BP’s - 5P.M. Antibiotic Rx ICU -10P.M. Respiratory Distress Intubated Vent (PEEP=15cm H2 O) Rpt CxR ARDS
    • Septic Shock - Case presentation - Day 1-7 No improvement Pulmonary Status Levophed Maintain BP’s Blood Culture Strep Pneumonia Rx Imipenem, Gentamycin Xigris (APC) started Day 8-9 WBC’s 18-33,000 Temp 102-103 F 2nd Septic Source ?
    • Septic Shock - Case presentation - 2nd Septic Source CxR No empyema No other studies done (Pat unstable) #9 Explor laparotomy TAH* in ICU Temp’s 98-100 F Pulmonary – No Change WBC’s 17,000 Pressor agents – No Change #14 Cardiac Arrest Death * Endomyometritis with abcess formation
    • Septic Shock - Case presentation - Mrs X , 36y old P2 at 34wks 2A.M. -Delay in Dg -Delay in initiation of antibiotic therapy -Delay in initiation of hemodynamic monitoring - Delay in initiation of aggressive fluid management ICU Admission in Septic Shock 5 P.M. Maternal Mortality 2wks later
    • Septic Shock Consensus conference of American College of Chest Physicians and Society of Critical Care Medicine on Sepsis and related disorders – 1992 - Systemic inflamatory response syndrome - Sepsis - Severe Sepsis - Septic Shock - Multiple Organ Dysfunction Syndrome
    • Systemic Inflamatory Response Syndrome
    • Septic Shock SIRS* Definition The organisms response to any insult - Infectious, Trauma, Toxic Diagnosis >2 of the following : -Temperature >380C or <360C - Heart Rate > 90 bpm - Respiratory Rate >20/min - WBC >12,000 or <4,000 - Organ dysfunction (Neuro, Renal, Clotting, Acidosis, etc) *Systemic Inflamatory Response Syndrome
    • Septic Shock Presence of bacteria Bacteremia in the blood Systemic Inflamatory SIRS Response Syndrome Documented infection + Sepsis Evidence of SIRS Sepsis associated with Severe sepsis organ dysfunction (MODS) Sepsis induced hypotension Septic Shock despite adequate hydration
    • Septic Shock Increasingly severe 1.- Individual entities ? responses to same insult 2.- Do they develop Progression after sequentially ? hospitalization ? 3.- Risk of specific ARDS, DIC, ARF end-organ failure ? 4.- Mortality Rates ?
    • Septic Shock A large study of 2,527 patients that met at least 2 criteria for SIRS and were followed for 28d in the hospital or until discharge/death. Rangel-Fausto et al JAMA-1995
    • Septic Shock Final Diagnosis SIRS 1301 (52%) Sepsis 649 (26%) Severe Sepsis 467 (18%) Septic Shock 110 (4%) Rangel-Fausto et al JAMA-1995
    • Septic Shock Final Dg Present on Progressed in Admission Hospital Sepsis 56% 44% Severe Sepsis 42% 58% Septic Shock 29% 71% Rangel-Fausto et al JAMA-1995
    • Septic Shock SIRS Advance to Advance to higher level Septic Shock 2 criteria 32% 11% 3 criteria 36% 21% 4 criteria 45% 27% Rangel-Fausto et al JAMA-1995
    • Septic Shock ⊕ Blood Cultures Sepsis 16% Severe Sepsis 25% Septic Shock 69% Rangel-Fausto et al JAMA-1995
    • Septic Shock Dg ARDS DIC ARF SIRS-2 2% 8% 9% SIRS-3 3% 15% 13% SIRS-4 6% 19% 19% Sepsis 6% 16% 19% Severe Sepsis 8% 18% 23% Septic Shock 18% 38% 31% Rangel-Fausto et al JAMA-1995
    • Septic Shock
    • Septic Shock Conclusions SIRS and related conditions represent a hierarchical continuum of increased inflammatory response to infection End organ failure rates blood culture rates and mortality rates are all increased with each subsequent stage of systemic inflamatory response. Rangel-Fausto et al JAMA-1995
    • Septic Shock Diagnosis - Clinical presentation - Lab workup Pathophysiology Treatment
    • Septic Shock - Pathophysiology - Infection Bacteremia Release of toxins Complex inflammatory response Multiple Organ Dysfunction Death
    • Septic Shock - Pathophysiology - Bacteremia Coagulation system Endothelium Bacterial toxins Cell metabolism Lungs Inflamatory Kidney Response Cardio-vascular
    • Septic Shock -Coagulation – Procoagulants Anticoagulants - Coagulation cascade - TF Inhibitor - Platelet Activation Factor - AT Complex - Vasoconstriction - Prot C Complex - Fibrinolysis
    • Septic Shock - Coagulation - Activated Protein C - Inhibits Factor VIII-a, V-a Anticoagulant - TF expression - Inhibits PAI – 1 Fibrinolysis - Leukocytes adhesion Anti-Inflamatory - TNF levels Septic Shock Low Prot C and APC Mortality Rates
    • Septic Shock - Coagulation - Bacterial Toxins Bacterial Toxins Anticoagulants Procoagulants - Expression of TF - levelTF Inhibitor - Edothelial damage - level ofAT - Platelet agregation - level of Prot C - Prot C to APC - Fibrinolysis Microvascular thrombosis
    • Septic Shock - Cellular metabolism - Sepsis -Hypoxemia - Hypotension -Microvascular abn Microvascular thrombosis Shunting Tissue hypoxia Mitochondrial dysfunction Anaerobic metabolism ATP Lactic ac
    • Septic Shock - Cellular metabolism - Acidosis ( pH < 7.35 ) Respiratory Metabolic pCO2 > 45mmHg HCO3 < 22mEq/L HCO3 22-26 mEq/L ⊕Anion Gap ∅ Anion Gap -Lactic ac -Renal ac -Ketoacidosis -Intoxication Anion Gap = (Na + K ) – (Cl + HCO3 ) ⊕ Anion Gap >14mEq/L
    • Septic Shock - Endothelial Cell - Endothelial cell - Prevent coagulation TM,, APC receptors TF - Prevent migration of cells Adhesion molecules - Regulate vasopermeability Leukocyte activation - Regulate microcirculation Vasoactive substances
    • Septic Shock - Endothelial Cell - Sepsis Endothelial cells Adhesion molecules Permeability Complement activation Coagulation TF, PAF Leakage Edema Microvascular thrombosis Cell death
    • Septic Shock - ARDS - Endothelial Capillary permeability cell injury Alveolar flooding Lung compliance Shunting Hypoxemia Recovery Pulmonary fibrosis Death Pulmonary HTN
    • Septic Shock - ARDS - Onset Acute Hypoxemia PaO2 / FiO2 < 200mmHg Chest X-ray Bilateral alveolar or interstitial infiltrates PCWP < 18mmHg
    • Septic Shock - Cardio-vascular - Sepsis Myocardial Depression Refractory Vasodilation Capillary permeability Hypotension Loss of intravascular Tissue perfusion volume Cell Death
    • Septic Shock - Diagnosis - Coagulation -D.I.C. Pulmonary - Hypoxemia - Thrombosis - CxR changes Tissue - Metabolic ac. Renal -Ac renal failure metabolism (Anion gap) - Lactic acid Liver -Hepatic failure Cardio -Decreased E.F. C.N.S. -Alteration of vascular -Hypotension mental status
    • Septic Shock - Diagnosis - Fever - Common symptom Pulse - Anxiety - Viral syndrome - Pain - Non infectious BP -Regional anesthesia WBC’s - Pregnancy -Supine hypotension - Steroids (FLM) - Labor Output - NPO - Nausea/Vomiting
    • Septic Shock - Diagnosis - Coagulation -Fibrinogen, FSP, PT, PTT, INR, Plts Tissue metabolism - pH, HCO3 BD, Anion gap, Lactate Cardio-vascular -Low BP (Refractory), PCWP, EF Pulmonary - O2 Sat, CxR Renal - Urinary Output, BUN, CR, Lytes Liver - Liver function tests C.N.S. - Physical exam
    • Septic Shock - Diagnosis - Acidosis Fever Oliguria Abn WBC’s BP, Hypotension Pulse Hypoxemia R.R. Coagulopathy Abn mental status Prompt Dg and Management
    • Septic Shock - Management - Patients seen in the E.R. with the Dg of septic shock were randomly allocated to 1.- Standard therapy (n=133) 2.- Early goal-directed therapy (n=130) Rivers et al NEJM 2001
    • Septic Shock - Management - “Early goal directed therapy” is a complex approach to septic shock involving manipulation of cardiac preload afterload and contractility to achieve a balance between O2 delivery and O2 demand. End points used to confirm that balance - Mixed venous O2 Sat - Lactate level - Base Deficit - pH Rivers et al NEJM 2001
    • Septic Shock - Management - Controls A-lines, CVP placed Management of fluids, drugs up to MD’s Study A-line, CVP placed Fluids 500cc q 30min CVP = 8-12mmHg If MAP < 65mmHg Vasopressors If CV O2 Sat < 70% Blood Hct > 30% If CV O2 Sat still < 70% Dobutamine During the 1st 6hrs Rivers et al NEJM 2001
    • Septic Shock - Management - Therapy 0-6hrs 0-72hrs Fluids-Control 3,499ml 13,300ml Fluids-Study 4,981ml* 13,400mlns Blood-Control 18% 44% Blood-Study 64%* 68%* Dobutamine-Control 1% 9% Dobutamine-Study 14%* 15%ns *p< 0.01 Rivers et al NEJM 2001
    • Septic Shock - Management - End-Point Baseline 0-6hrs 7-72hrs CVP-C 6.1 11.8 11.6 CVP-S 5.3ns 13.8* 11.9ns MAP-C 76 81 80 MAP-S 74ns 95* 87* Lactate-C 6.9 4.9 3.9 Lactate-S 7.7ns 4.3* 3.0* Base Deficit-C 8.9 8.0 5.1 Base deficit-S 8.9ns 4.7* 2.0* C Control, S Study *p< 0.01 Rivers et al NEJM 2001
    • Septic Shock - Management - End-Point Baseline 0-6hrs 7-72hrs PT-C 16.5 17.5 17.3 PT-S 15.8ns 16.0* 15.4ns PTT-C 32.9 37.6 37.0 PTT-S 33.3ns 32.6* 34.6* FSP-C 39 54.9 62.0 FSP-S 44ns 45.8ns 39.2* MODS-C 7.3 6.8 6.4 MODS-S 7.6ns 5.9* 5.1* C Control, S Study *p< 0.01 Rivers et al NEJM 2001
    • Septic Shock - Management - Mortality Controls Study (n=133) (n=130) All inpatients 59(46%) 38(30%)* 28 day 61(49%) 40(33%)* 60 Day 70(57%) 50(44%)* *p< 0.01 Rivers et al NEJM 2001
    • Septic Shock - Management - Objective To determine the impact of delays in initiating adequate antibiotic therapy on mortality rates of patients in septic shock Kumar et al Crit Care Med, 2006
    • Septic Shock - Management - Methods A retrospective cohort study including 14 ICU’s in the USA and Canada. A total of 2,731 adult patients with documented septic shock were included. Kumar et al Crit Care Med, 2006
    • Septic Shock - Management - Methods A. The primary outcome variable was survival to hospital discharge. B. The primary independent variable was the time to initiation of effective antimicrobial therapy relative to the first occurrence of shock (persistent hypotension) Kumar et al Crit Care Med, 2006
    • Septic Shock - Management - Outcome A. Mortality for the entire population 56% B. Survival was similar: - Infection documented or suspecetd - A plausible pathogen identified or not - Bacteremia present or absent Kumar et al Crit Care Med, 2006
    • Septic Shock - Management - Antibiotics Rx Mortality Rates (from onset of shock) < 1hr 82% At 6hrs 42% Kumar et al Crit Care Med, 2006
    • Septic Shock - Management - Antibiotics Rx Mortality Rates (from onset of shock) < 1hr 82% Each hour of delay was associated with a in survival of 7.6% At 6hrs 42% Kumar et al Crit Care Med, 2006
    • Septic Shock - Management - Antibiotic Rx and Intensive therapy (goal directed therapy ) started at the earliest stages of severe sepsis/septic shock Lower mortality rates