Septic ShockSeptic ShockDr Alastair D McR MeyerBSc(Hons) BMedSci MBBS FACEM FCEM(UK) FRCP(Edin)Emergency PhysicianCasey Hospital, Melbourne, Australia.

Hue, Vietnam, March 2012.

Dr Alastair D McR MeyerBSc(Hons) BMedSci MBBS FACEM FCEM(UK) FRCP(Edin)Emergency PhysicianCasey Hospital, Melbourne, Australia.

Hue, Vietnam, March 2012.

Melbourne from 1000mMelbourne from 1000m

ShockShock

• 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 shockSeptic 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

PathophysiologyPathophysiology

• 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 ManagementClinical 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 TPSeptic 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)…Mr TP (continued)

• Past: – Heavy alcohol use– Smokes tobacco, heroin, crack cocaine (on

occasion)– No previous illnesses– No other medications

Obs chart: presentationObs chart: presentation

T=40.5T=40.5

P=140bpmP=140bpm

BP=90/55mmHgBP=90/55mmHg

Sat 99%Sat 99%

RR =30RR =30

Initial managementInitial 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 simultaneouslyTeam ApproachResuscitated and Investigated simultaneously

…Mr TP…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: CXRMr TP Investigations: CXR

Early monitorEarly monitor

• Standard BP, pulse, pulse oximetery• CV line-essential

– CVP, CV O2 sat

• Urinary catheter

Response: Obs chart: + 3 litres fluidResponse: Obs chart: + 3 litres fluid

T=40.5T=40.5

P=140P=140

BP=90/55BP=90/55

After fluid challenge, initial improvement with pulse. P= 85, BP 90/55 (still hypotensive), CVP 5mmHg

After fluid challenge, initial improvement with pulse. P= 85, BP 90/55 (still hypotensive), CVP 5mmHg

Early inotropic supportEarly 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…Mr TP

• Noradrenaline infusion commenced• Titrated to MAP >65mmHg

• BP rose, urine flowed• Patient improved

Therapy goalsTherapy 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 agentsObs chart: + inotropic agents

T=40.5T=40.5

P=140P=140

BP=90/55BP=90/55

After fluid challenge, initial improvement with pulse. P= 85, BP 90/55

After fluid challenge, initial improvement with pulse. P= 85, BP 90/55

(+noradren)P=80-90BP 130/80

(+noradren)P=80-90BP 130/80

Outcome, Mr TPOutcome, 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: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

ReferencesReferences

• 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 MeyerBSc(Hons)(Melb) BMedSci MBBS(Tas)

FACEM FCEM(Lond) FRCP(Edin)

Emergency Physicianalastair.meyer22@hotmail.com