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Transcript of Sepsis - FOMA District 2 · PDF fileSepsis/SIRS Severe Sepsis Septic Shock MODS ... Systemic...

  • Sepsis

    Purvin Shah, DO, MS, FCCP, MBA 5/15/2014

    15th Annual CV & Medicine Symposium

  • Outline

    1. Introduction 2. Definitions 3. Epidemiology 4. Pathophysiology 5. Evaluation & Management 6. Prognosis 7. Conclusion

  • Introduction Why do we care so much about sepsis?

    Sepsis and its advanced forms (severe sepsis and septic shock): Are major healthcare problems Affect millions of people around the world each year Kill 1 in 4 patients (and often more) Are increasing in incidence

    Just like MI and Stroke, the outcome of patients with sepsis is highly dependent on the speed and appropriateness of therapy in the initial hours after sepsis develops.

  • Introduction

    As a non-ICU physician, how do YOU play a role in caring for patients with sepsis?

    Surviving Sepsis Campaign (SSC) Guidelines:

    the committee believes that the greatest outcome improvement can be made through education and process change for those caring for severe sepsis patients in the non-ICU setting and across the spectrum of acute care.

    Critical Care Medicine, Feb. 2013, Vol. 41, No. 2, pp 577-637

  • Surviving Sepsis Campaign (SSC) Guidelines 2004 Initial SSC guidelines were published in 2004 and incorporated

    evidence available through the end of 2003

    2008 Updated SSC guidelines in 2008 based on evidence available through the end of 2007

    2012 Revised SSC guidelines based on literature through Fall 2012

    Quality of evidence = high (A) to very low (D) Strength of recommendations = strong (1) or weak (2)

  • Definitions

    Spectrum of severity of illness:

    Sepsis/SIRS Severe Sepsis Septic ShockMODS

    1991 initially defined by ACCP and SCCM

    2001 reconsidered by ACCP, SCCM, ATS, ESICM, SIS (Surg. Inf. Soc.)

    2012 SCCM and ESICM (European Society of Inten. Care Medicine)

  • Definitions

    Infection presence of bacteria in a normally sterile tissue Bacteremia presence of bacteria in blood Sepsis complicates severe infection SIRS complicates a non-infectious insult Severe Sepsis hypoperfusion or organ dysfunction Septic Shock sepsis-induced hypotension despite fluids MODS Multiple Organ Dysfunction Syndrome

  • Definitions Sepsis

    Problem with regulating the bodys inflammatory response to an infection Characterized by the cardinal signs of inflammation in tissues remote from the infection:

    Vasodilation Leukocyte accumulation Increased microvascular permeability

    SIRS Systemic Inflammatory Response Syndrome Identical to Sepsis BUT complicates a non-infectious insult:

    Pancreatitis, Surgery, Burns, Autoimmune D/O, Trauma, Thromboembolism, etc.

    Massive and uncontrolled release of pro-inflammatory mediators leads to widespread tissue injury and possibly MODS (high mortality)

  • Definitions

    Diagnostic Criteria for Sepsis = probable or documented infection PLUS some systemic manifestations of infection:

    General: Temp. >38.3 C or 90/min. or >2 std. dev. above normal value for age Resp. Rate > 20/min. Altered mental status

    Inflammatory variables: WBC > 20K or < 4K Normal WBC with >10% immature forms (e.g. Bands) Plasma Procalcitonin more than 2 std. dev. above normal value

  • Definitions

    Diagnostic Criteria for Sepsis (continued): Hemodynamic variables:

    SBP < 90 mmHg MAP < 70 mmHg SBP decrease > 40 mmHg, or SBP < 2 std. dev. Below normal for age

    Organ Dysfunction variables: Hypoxemia (PaO2 / FiO2 < 300) Oliguria (urine output < 0.5 mL/kg/hr for >2 hrs. despite fluids) Platelets < 100K Plasma total bilirubin > 4 mg/dL

  • Definitions

    Diagnostic Criteria for Severe Sepsis = sepsis-induced tissue hypoperfusion (low BP, high lactate or oliguria) or organ dysfunction (any of the following thought to be due to the infection):

    Sepsis-induced hypotension Lactate > ULN (upper limits of normal) U.O. < 0.5 mL/kg/hr. for >2 hrs. despite adequate fluid resuscitation Acute lung injury (PaO2/FiO2 1.5

  • Definitions

    Septic Shock: sepsis-induced hypotension that persists despite adequate fluid resuscitation (30 mL/kg of crystalloids some of this may be albumin)

    MODS: progressive organ dysfunction The severe end of the illness spectrum Primary MODS organ dysfunction occurs early and directly from the insult

    (e.g. renal failure due to rhabdomyolysis) Secondary MODS organ failure is NOT due to the insult itself but rather is a

    consequence of host response (e.g. ARDS in patients with pancreatitis) Includes: PaO2/FiO2 ratio, Platelet count, Bilirubin, Creatinine, Low BP, GCS

  • Epidemiology

    Incidence: More than 1,665,000 cases diagnosed in the U.S. annually.

    An analysis reported increased rates from 13 to 78 cases per 100,000 between 1998 and 2009.

    Greatest in African-American males, during winter and patients > 65 yrs of age.

  • Epidemiology

    Pathogens: Gram-positive bacteria more than Gram-negative. Also, fungal sepsis has increased over the past decade. Disease Severity: Increase in disease severity is noted e.g., severe

    sepsis increased from 26% to 44% over a 10-year period. Most common organ dysfunctions: ARDS, AKI, DIC. Mortality: High mortality rate (12 to 50%). Increases stepwise: SIRS = 7%, Sepsis = 16%, Severe Sepsis = 20%, Septic Shock = 46% Mortality remains elevated at one-year among survivors of sepsis.

  • Risk Factors for Sepsis

    Bacteremia (study of 270 blood cultures: 95% of positive blood cultures were associated with sepsis, severe sepsis, or septic shock)

    Advanced age (>65 yrs) age is an independent predictor of mortality Immunosuppression neoplasm, renal failure, hepatic failure, AIDS,

    asplenism or immunosuppressant medications Diabetes Community-acquired pneumonia (CAP): severe sepsis develops in

    48% of patients with CAP

  • Pathophysiology

    Normal Response to Infection: - Host immune cells (esp. macrophages)

    recognize and bind to microbial components

    - Activates an inflammatory response (release of proinflammatory cytokines TNF / IL-1, chemokines, NO, etc.)

    - Polymorphonuclear leukocytes (PMN) become activated, migrate to injury site, release mediators causing inflammation (edema, erythema, warmth) and tissue repair & healing.

  • Pathophysiology

    Transition to Sepsis: - the normal inflammatory response

    becomes uncontrolled and generalized because a large quantity of proinflammatory cytokines are released

    - Complement cascade gets activated - Bacterial cell wall components and

    bacterial products may enhance progression to sepsis

  • Pathophysiology

    Systemic effects:

    - widespread cellular injury - derangements in metabolic auto-regulation - imbalances in coagulation and fibrinolytic systems - mitochondrial dysfunction - delayed apoptosis of activated macrophages and neutrophils

  • Pathophysiology

    Organ-specific effects:

    - Hypotension (from diffuse vasodilation), myocardial depression - Pulmonary edema, V/Q mismatch, hypoxemia - Translocation of bacteria and endotoxin in the GI tract - Liver dysfunction - Acute renal failure - Encephalopathy

  • Evaluation & Management

    Early Management: First, stabilize airway & breathing supplemental O2, monitor pulse ox, may need to intubate and place on mechanical ventilation. Check PCXR and ABG. Then, assess & restore perfusion if low BP, then insert A-line catheter for accurate BP. EXAM: HR>90/min, obtundation / restless, oliguria / anuria, cool vasoconstricted skin. LABS: lactate > 4mmol/L Insert central venous catheter for infusion of meds & fluids / blood draws / measuring CVP and central venous O2 sat. (ScvO2).

  • Evaluation & Management

    Goals of initial resuscitation: (SSC Guidelines) within 1st 6 hours based on an EGDT trial of 263 patients (and a meta-analysis) with targeting of specific goals resulted in lower mortality (31% vs. 47%):

    - ScvO2 > 70% - CVP = 8-12 mmHg - MAP > 65 mmHg - U.O. > 0.5 mL/kg/hour

    Rivers E et al. Early Goal-Directed Therapy in the treatment of severe sepsis and septic shock; NEJM 2001; 345: 1368-1377

  • Evaluation & Management

    Lactate clearance targeting a lactate clearance of >10% (versus targeting ScvO2 > 70%) gives same mortality benefit, hospital LOS, ventilator-free days, or incidence of multi-organ failure.

    Recommend targeting normalization of lactate level if initially elevated.

    Other targets (besides ScvO2, CVP, MAP, U.O.) radial pulse pressure, aortic blood flow peak velocity, brachial artery blood flow velocity, passive leg raising, etc. can be used to guide fluid resuscitation.

  • Evaluation & Management

    Screening recommend routine screening for Sepsis in potentially infected seriously ill patients (so treatment can be started early)

    Diagnosis 2 sets of blood cultures BEFORE Abx Tx is started (as long as there is no significant delay >45 min. in starting Abx).

    - blood cultures (peripheral and through each vascular access device) - sputum cultures - urine cultures - wound cultures - rapid influenza antigen testing (during the flu season) - appropriate imaging studies (to identify abscess for I&D, etc.)

  • Evaluation & Manag