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Emergency lectures - Septic shock
 

Emergency lectures - Septic shock

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    Emergency lectures - Septic shock Emergency lectures - Septic shock Presentation Transcript

    • Septic ShockDr Alastair D McR MeyerBSc(Hons) BMedSci MBBS FACEM FCEM(UK) FRCP(Edin)Emergency PhysicianCasey Hospital, Melbourne, Australia.Hue, Vietnam, March 2012.
    • Melbourne from 1000m
    • Shock• Shock is a clinical syndrome where tissue perfusion, and hence oxygenation, is inadequate to maintain normal metabolic function.• Insufficient ATP is generated within the cell, leading to dysfunction of the cell, a switch to anaerobic metabolism, resulting in oxygen debt & tissue acidosis & death
    • • Three broad categories of shock – Hypovolaemic (trauma) • Nothing to pump/leaking pipes – Cardiogenic (cardiac arrest) • Broken pump – Septic • Pump and pipe failure
    • Septic shock• Sepsis – Evidence of infection and two or more of • tachypnoea (> 20/min or pCO2 <32 or ventilated min vol >10l/min) • tachycardia (>90 bpm) • hyper- or hypo- thermia (<360C, >380C) • elevated or reduced WCC (<4, >12cells/ul)• Septic Shock – Sepsis + hypotension (<90/<40) or > 40 below base line, despite adequate fluid resuscitation
    • Pathophysiology• Infection of bacterial, viral or fungal origin• Nidus of infection through multiplication of infective organism, releasing various mediators which consist of structural components of the organism and/or exotoxins and endotoxins (from the dead invading organism)• Over 100 mediators have been identified (include: tissue necrosis factors, interleukins)• Circulatory & cardiac ‘toxic’
    • • Circulatory changes: – Nitric oxide overproduction in response to these mediators results in peripheral vasodilatation, decreased systemic vascular resistance, fluid leak from capillaries – Capillary blood flow is reduced• Cardiac Dysfunction – Ventricular dilatation with decreased ejection fraction, decreased stroke volume – Leads to increased heart rate (&O2 demand)
    • • Mortality – 28-50% – High risk groups • Age (>55), burns & sepsis, alcohol dependence, diabetes, immunosuppression, chronic cardio-respiratory disease, malnutrition, multi-trauma (&septic)
    • • Clinical signs – Early: tachycardia, tachypnoea, temperature instability, oliguria, altered mental state, peripheral vasodilatation • Be wary at age extremes – Later: reduced capillary refill, hypotension, poor urine output, myocardial dysfunction, metabolic acidosis – Evidence of septic source (often not obvious)
    • • Investigations – FBE, UEC, coagulation profile, LFT, pregnancy test, ABG (or VBG), blood cultures – Urine cultures – CXR & ECG – Directed investigations towards presumed site of sepsis (eg sputum, wound swab….)
    • Clinical Management• Early recognition and early definitive therapy is the key• Much research has concluded that the most important steps are: – Fluid • Normal saline 20-40ml/kg initial bolus – Antibiotics (early use, big dose, broad spectrum, narrow as results become available, knowledge of possible organisms) – Inotropic support – Monitor interventions
    • Septic Shock:A Brief Case Study, Mr TP• 33 yo man (builder), Mr TP, presents to the Emergency Department• ’flu-like illness for 3-4days, now severe pleuritic chest pain, productive cough, myalgia, arthralgia, feels terrible, looks very unwell• Lightheaded, dizzy, GCS 15• Febrile: 40.5 deg, tachycardic (140), hypotensive (90/50)• Clinically dehydrated
    • …Mr TP (continued)• Past: – Heavy alcohol use – Smokes tobacco, heroin, crack cocaine (on occasion) – No previous illnesses – No other medications
    • Obs chart: presentation T=40.5Sat 99% P=140bpm BP=90/55mmHgRR =30
    • Initial management• Team approach• Resuscitate and investigate simultaneously• IV access (peripheral x 2 & draw bloods)• Commence IV fluid (lots and fast) • Much debate over which fluid and why, the essential point is just do it! Do it now!• IV antibiotics (early!): as soon as IV goes in– Evidence that this takes > 1 hr!• Begin investigations: CXR, Bloods, cultures• Central monitor/lines• Arrange disposition/destination bed (ICU)
    • Team ApproachResuscitated and Investigated simultaneously
    • …Mr TP• IV x 2• Blood drawn• Broad spectrum antibiotics- azithromycin and ceftriaxone (presumed source-chest infection)• IV fluid x 3 litres
    • Mr TP Investigations: CXR
    • Early monitor• Standard BP, pulse, pulse oximetery• CV line-essential – CVP, CV O2 sat• Urinary catheter
    • Response: Obs chart: + 3 litresfluid T=40.5 After fluid challenge, initial improvement with pulse. P= 85, BP 90/55 (still hypotensive), CVP 5mmHg P=140 BP=90/55
    • Early inotropic support• Much debate – Dobutamine, dopamine, adrenaline or noradrenaline – Learn one, learn it well• Noradrenaline (= norepinepherine) – alpha-1 & beta-1 adrenergic receptor activity – Potent peripheral vasoconstrictor – Less myocardial O2 demand (compared to adrenaline) – First line inotrope for sepsis
    • …Mr TP• Noradrenaline infusion commenced• Titrated to MAP >65mmHg• BP rose, urine flowed• Patient improved
    • Therapy goals• Begin therapy immediately• CVP 8-12mmHg• MAP >65mmHg• Urine > 0.5ml/kg/hr• CV O2 sat >70% (or mixed venous > 65%) – If not achieved consider further fluid – Pack cells if Hct <30%
    • Obs chart: + inotropic agents T=40.5 After fluid challenge, initial improvement with pulse. P= 85, BP 90/55 P=140 (+noradren) P=80-90 BP 130/80 BP=90/55
    • Outcome, Mr TP• Transferred to ICU• Fluid balance• Inotropes 24 hrs• Discharged to ward• Home 3 days later• Vows to stop drinking EtOH & to stop smoking heroin & crack cocaine
    • This case illustrates:• Early recognition of the shock syndrome• Early vigorous fluid challenge/resuscitation• Early broad spectrum antibiotics• Early vigorous monitoring• Early judicious use of inotropic support
    • References• Cameron et al. 2004 “Textbook of Adult Emergency Medicine” 2nd Edition. Churchill Livingston, Sydney• Gooneratne et al. “Use of vasopressors and inotropes” www.uptoddate.com• Kumar et al. “Early combination antibiotic therapy yields improved survival compared with monotherapy in septic shock; a propensity-matched analysis.” Critical Care Medicine. 2010 38(9):1773-1785• Levinson et al. “Reducing Mortality in Severe Sepsis and Septic Shock” Seminars in respiratory and critical care medicine 2011 32(2):195-205• Levy et al. “The surviving sepsis campaign”. Critical Care Medicine. 2010 38(2):368.• Rivers et al. “Fluid therapy in septic shock” Current opinion in critical care. 2010 16:297-308• Scmidt et al. “Management of severe sepsis and septic shock in adult” www.uptodate.com• Surviving Sepsis Campaign www.survivingsepsis.org
    • Dr Alastair D McR Meyer BSc(Hons)(Melb) BMedSci MBBS(Tas) FACEM FCEM(Lond) FRCP(Edin) Emergency Physicianalastair.meyer22@hotmail.com