Sepsis and septic shock

11 min read Last updated April 8, 2026

Surgical approach (source control)

  • Principle: identify and control the source early (often within 6–12 h if feasible; immediately if life-threatening)
    • Drain pus/collections: percutaneous drainage (IR) vs open surgical drainage
    • Remove infected devices: central lines, urinary catheters, prostheses if implicated
    • Debridement: necrotising soft tissue infection (NSTI) requires urgent wide debridement; repeat “re-look” operations common
    • Resection/repair: perforated viscus, ischaemic bowel, anastomotic leak; consider stoma formation
    • Biliary sepsis: ERCP for cholangitis; cholecystostomy/cholecystectomy depending on physiology
  • Intra-op priorities: minimise delay to theatre, obtain cultures (blood + source), haemostasis, avoid hypothermia, plan for ICU post-op

Anaesthetic management (typical for septic source control surgery)

  • Type of anaesthesia: usually GA (often rapid sequence induction). Regional/neuraxial generally avoided in unstable septic shock; consider peripheral blocks as adjunct if coagulation allows
    • Neuraxial concerns: hypotension from sympathectomy; thrombocytopenia/coagulopathy; bacteraemia (relative contraindication)
  • Airway: ETT preferred (high aspiration risk, need for controlled ventilation, high FiO2/PEEP, prolonged case). SGA rarely appropriate
  • Duration: variable (30 min drainage to 3–6 h laparotomy/debridement); anticipate re-look surgery
  • Pain: moderate–severe depending on procedure; multimodal analgesia with opioid titration, ketamine, paracetamol; NSAIDs often avoided in AKI/shock; consider regional (TAP/fascial plane) if safe
  • Monitoring/lines: A-line early; large-bore IV access; CVC for vasopressors; consider cardiac output monitoring/echo; urinary catheter; temperature
  • Induction/maintenance: haemodynamically stable induction (ketamine/etomidate commonly used; cautious propofol). Early vasopressor support (noradrenaline) and gentle ventilation strategy
    • Expect vasoplegia: induction can precipitate cardiovascular collapse—start vasopressor before/at induction if shocked
  • Fluids/blood: balanced crystalloids first-line; avoid fluid overload; early blood products if haemorrhage/DIC; aim Hb appropriate to context (often transfuse if Hb <70 g/L unless ongoing ischaemia/bleeding)
  • Post-op: most require ICU/HDU; ongoing vasopressors, ventilation, renal support, lactate clearance monitoring

Definitions and diagnostic criteria

  • Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection
    • Operationalised as acute increase in SOFA score ≥2 from baseline in a patient with suspected/confirmed infection
  • Septic shock: subset of sepsis with profound circulatory/metabolic abnormalities
    • Clinical criteria: despite adequate fluid resuscitation, requires vasopressors to maintain MAP ≥65 mmHg AND lactate >2 mmol/L
  • qSOFA (screening outside ICU): RR ≥22, altered mentation, SBP ≤100 (≥2 suggests high risk). Not a diagnostic tool; do not delay treatment
  • Sepsis-3 emphasises organ dysfunction; older SIRS criteria are less specific but may still be encountered in exams
    • SIRS: ≥2 of T >38 or <36, HR >90, RR >20/PaCO2 <4.3 kPa, WCC >12 or <4 or >10% bands

Epidemiology and common sources

  • Common sources: pneumonia, intra-abdominal sepsis (perforation, anastomotic leak), urinary tract, skin/soft tissue (cellulitis/NSTI), line-related infection
  • Common organisms: Gram-negative (e.g., E. coli), Gram-positive (e.g., Staph aureus), anaerobes (abdominal), fungi (immunosuppressed/TPN/long ICU stay)
  • Risk factors: extremes of age, immunosuppression, diabetes, CKD, malignancy, indwelling devices, recent surgery, burns/trauma

Pathophysiology (what drives shock and organ failure)

  • Dysregulated inflammation: PAMPs/DAMPs → cytokines (TNF-α, IL-1, IL-6), complement, leukocyte activation
  • Vasoplegia: NO-mediated vasodilation + relative vasopressin deficiency → low SVR, maldistributed flow
  • Capillary leak and endothelial dysfunction: third spacing, oedema, reduced effective circulating volume; glycocalyx injury
  • Myocardial depression: sepsis-induced cardiomyopathy (often reversible) → reduced EF, impaired diastolic function; may coexist with high CO state
  • Microcirculatory dysfunction: shunting, impaired oxygen extraction; lactate may reflect stress/adrenergic drive as well as hypoperfusion
  • Coagulation derangement: tissue factor activation, consumption, impaired anticoagulant pathways → DIC risk; thrombocytopenia common
  • Mitochondrial dysfunction/cytopathic hypoxia: impaired cellular oxygen utilisation contributes to organ dysfunction

Clinical features and organ dysfunction

  • General: fever or hypothermia, tachycardia, tachypnoea, altered mental state, mottling, oliguria, ileus
  • Respiratory: hypoxaemia, ARDS (bilateral opacities, non-cardiogenic), increased work of breathing
  • Cardiovascular: hypotension, wide pulse pressure early, cool peripheries late; arrhythmias (AF), myocardial ischaemia
  • Renal: AKI, rising creatinine/urea, oliguria; consider obstruction and nephrotoxins
  • CNS: delirium/encephalopathy; reduced GCS
  • Haematology: thrombocytopenia, coagulopathy, DIC; anaemia
  • Metabolic: hyperglycaemia, lactic acidosis; hypocalcaemia; adrenal insufficiency (relative)

Investigations (initial and ongoing)

  • Bedside: ABG/VBG (lactate, acid-base), glucose, ECG, CXR/POCUS, urine output, temperature
  • Bloods: FBC, U&E/creatinine, LFTs, CRP/procalcitonin (trend), coagulation, fibrinogen, group & save/crossmatch
  • Microbiology: blood cultures (2 sets) before antibiotics if no delay; culture suspected source (sputum, urine, wound, line tips)
  • Imaging: CT abdomen/pelvis for source; ultrasound for biliary/renal; echocardiography to assess volume status and myocardial function
  • Monitoring response: lactate clearance, capillary refill time, ScvO2/SvO2 (selected), dynamic fluid responsiveness tests
    • Dynamic tests: passive leg raise with stroke volume change; pulse pressure variation (limitations with arrhythmia/low VT)

Immediate management (time-critical bundle)

  • A–E approach; call for senior help early; treat hypoxia and hypotension immediately
  • Oxygen/ventilation: titrate to target saturations; early intubation if airway compromise, severe work of breathing, refractory hypoxaemia, or to facilitate source control
  • Cultures then antibiotics: give IV broad-spectrum antibiotics within 1 hour of recognition of sepsis/septic shock (do not delay for cultures if difficult)
    • Choose based on likely source, local guidelines, resistance risk; add MRSA/anaerobic/fungal cover when indicated; de-escalate with results
  • Fluids: initial bolus commonly 30 mL/kg crystalloid in septic shock, but individualise; reassess frequently to avoid overload
    • Preferred: balanced crystalloids; avoid starches; albumin may be considered when large volumes required (unit-dependent practice)
  • Vasopressors: noradrenaline first-line to target MAP ≥65 mmHg; start early (even peripherally via a large-bore cannula while securing CVC, with close monitoring)
    • Add vasopressin (fixed dose) if escalating noradrenaline; adrenaline as alternative/add-on; consider angiotensin II where available
    • Inotrope: dobutamine if myocardial dysfunction with persistent hypoperfusion despite adequate MAP/volume
  • Source control: urgent surgical/IR intervention when indicated; remove infected lines; drain collections
  • Steroids: consider hydrocortisone 200 mg/day (e.g., 50 mg QDS or infusion) if shock remains refractory to fluids + vasopressors
  • Glycaemic control: avoid severe hyperglycaemia; typical target 6–10 mmol/L (avoid hypoglycaemia)
  • VTE prophylaxis and stress ulcer prophylaxis: assess bleeding risk; LMWH + mechanical prophylaxis; PPI/H2 blocker if risk factors

Anaesthetic considerations in septic shock (FRCA focus)

  • Pre-op optimisation: resuscitate in ED/ICU if possible but do not delay urgent source control; ensure antibiotics given; correct hypoglycaemia, severe hyperkalaemia, and treat arrhythmias
  • Induction strategy: high risk of peri-induction collapse due to vasodilation + relative hypovolaemia + myocardial depression
    • Consider: ketamine or etomidate; reduce induction dose; opioid sparing initially; have vasopressor boluses ready (metaraminol/phenylephrine/adrenaline as appropriate)
    • RSI: aspiration risk (ileus, reduced GCS); use rocuronium; consider sugammadex availability; cricoid pressure per local practice
  • Ventilation: lung-protective strategy if ARDS risk (VT ~6 mL/kg PBW, plateau pressure <30 cmH2O), appropriate PEEP; permissive hypercapnia if tolerated
  • Haemodynamics: aim MAP ≥65 (higher if chronic HTN/cerebrovascular disease); use echo to guide fluids/inotropes; avoid chasing CVP alone
  • Renal protection: avoid nephrotoxins; maintain perfusion; adjust drug doses; consider early RRT in refractory acidosis/hyperkalaemia/fluid overload/uraemia
  • Coagulation: check platelets/INR/fibrinogen; anticipate DIC; use blood products guided by labs/TEG/ROTEM where available
  • Temperature: active warming; hypothermia worsens coagulopathy and outcomes
  • Analgesia/sedation: opioid sensitivity may be altered; consider ketamine infusion; avoid excessive benzodiazepines; daily sedation breaks in ICU where appropriate

ICU management overview

  • Ongoing resuscitation: repeated assessment of perfusion (mental state, urine output, lactate trend, capillary refill) and fluid responsiveness
  • Vasopressor strategy: noradrenaline first-line; add vasopressin; consider adrenaline; consider inotrope if low cardiac output
  • Ventilation: ARDSnet principles; prone positioning if severe ARDS; conservative fluid strategy once shock resolved
  • Renal: CRRT commonly used in unstable patients; manage fluid balance and electrolytes
  • Antibiotic stewardship: daily review, de-escalation, stop if infection excluded; therapeutic drug monitoring (e.g., vancomycin/aminoglycosides)
  • Nutrition: early enteral feeding if feasible; avoid overfeeding; consider refeeding risk

Special situations

  • Neutropenic sepsis: medical emergency—broad-spectrum antibiotics immediately (per local policy), consider antifungal if persistent fever; isolate and involve haematology
  • Pregnancy: maintain uteroplacental perfusion; left lateral tilt; early senior obstetric/ICU involvement; antibiotics safe in pregnancy per guidance
  • Paediatrics: different physiology and thresholds; use paediatric sepsis guidance; early senior help
  • Perioperative sepsis: consider anastomotic leak, intra-abdominal collection, line infection; early CT and source control
Define sepsis and septic shock (Sepsis-3).

Be precise and include the operational criteria.

  • Sepsis: life-threatening organ dysfunction due to dysregulated host response to infection
  • Organ dysfunction: acute increase in SOFA score ≥2 from baseline
  • Septic shock: sepsis with need for vasopressors to maintain MAP ≥65 mmHg AND lactate >2 mmol/L despite adequate fluids
How would you recognise sepsis quickly on the ward? What is qSOFA and what are its limitations?

Examiners often want: rapid bedside recognition + escalation + not over-relying on scores.

  • Look for infection + organ dysfunction: new confusion, oliguria, hypotension, tachypnoea/hypoxia, mottling, rising lactate
  • qSOFA: RR ≥22, altered mentation, SBP ≤100; ≥2 suggests high risk of poor outcome
  • Limitations: not diagnostic; insensitive early; should not delay antibiotics/resuscitation; better as a prompt to escalate
Outline your immediate management of septic shock in the first hour.

Structure as A–E and time-critical actions.

  • A–E, senior help, high-flow oxygen, monitor (ECG, SpO2, NIBP), gain IV access, measure lactate
  • Blood cultures (2 sets) and relevant samples; then IV broad-spectrum antibiotics within 1 hour
  • Fluid resuscitation with balanced crystalloids; reassess response and fluid responsiveness
  • Start noradrenaline early to target MAP ≥65; insert arterial line and CVC as soon as practical
  • Arrange urgent source control (surgery/IR), remove infected lines, escalate to ICU
Discuss fluid therapy in septic shock: what fluid, how much, and how do you decide when to stop?

Aim: adequate perfusion without overload; demonstrate dynamic assessment.

  • Initial resuscitation often 30 mL/kg crystalloid in shock, but individualise (elderly, heart failure, ARDS risk)
  • Use balanced crystalloids; avoid hydroxyethyl starch; consider albumin if large volumes required (unit policy dependent)
  • Assess response: MAP, urine output, mental state, lactate trend, capillary refill; use dynamic tests (PLR with SV change, echo)
  • Stop/slow fluids when not fluid responsive or signs of overload (rising CVP with no SV gain, pulmonary oedema, worsening oxygenation)
Which vasopressors/inotropes are used in septic shock and why?

Link drug choice to vasoplegia and myocardial depression.

  • Noradrenaline first-line: α1 vasoconstriction increases SVR; some β1 support
  • Vasopressin: add-on in refractory vasoplegia; catecholamine-sparing (fixed low dose commonly used)
  • Adrenaline: alternative/add-on (α and β); may increase lactate and tachyarrhythmias
  • Dobutamine: inotrope for low cardiac output/sepsis-induced cardiomyopathy with ongoing hypoperfusion despite adequate MAP
A septic patient needs emergency laparotomy. How will you induce anaesthesia safely?

Examiners want anticipation of collapse, preparation, and a controlled RSI plan.

  • Resuscitate while preparing: antibiotics given, ongoing fluids, start noradrenaline early; arterial line if time; two large-bore IVs
  • Pre-oxygenate; plan RSI due to aspiration risk; have vasopressor boluses drawn up; consider push-dose adrenaline if profoundly unstable
  • Induction agent: reduced-dose ketamine or etomidate; cautious opioid; avoid full-dose propofol in shock
  • Post-intubation: lung-protective ventilation; maintain MAP ≥65; temperature control; early ICU handover
Explain why lactate is elevated in sepsis and how you use lactate clinically.

Avoid stating lactate always equals hypoxia; show nuance.

  • Mechanisms: tissue hypoperfusion/anaerobic metabolism; impaired clearance (hepatic dysfunction); adrenergic-driven glycolysis; mitochondrial dysfunction
  • Use: risk stratification, monitoring response to resuscitation (trend/lactate clearance), prompt search for ongoing hypoperfusion/source
  • Pitfall: normal lactate does not exclude sepsis; high lactate can persist despite adequate macro-haemodynamics
What is sepsis-induced cardiomyopathy and how does it change management?

Often appears in FRCA vivas as ‘why is the echo showing low EF in sepsis?’

  • Reversible myocardial depression (systolic ± diastolic) occurring in sepsis; can coexist with vasoplegia
  • Diagnosis: echocardiography (LV/RV function), haemodynamic profile, response to fluids/vasopressors
  • Management: maintain perfusion pressure with noradrenaline; add inotrope (dobutamine) if low output with hypoperfusion; avoid fluid overload
Discuss the role of steroids in septic shock.

Keep it pragmatic and guideline-consistent.

  • Indication: refractory septic shock (ongoing vasopressor requirement despite adequate fluids and vasopressors)
  • Regimen: hydrocortisone total 200 mg/day (e.g., 50 mg QDS or infusion); taper/stop when vasopressors no longer required (local practice varies)
  • Rationale: treat relative adrenal insufficiency; may shorten shock duration; monitor hyperglycaemia, neuromuscular weakness, infection risk
How do you decide on targets: MAP, urine output, Hb, and oxygenation in septic shock?

Targets are common exam territory; show individualisation.

  • MAP: aim ≥65 mmHg; consider higher target (e.g., 75–85) in chronic hypertension or cerebrovascular disease if perfusion concerns
  • Urine output: typically ≥0.5 mL/kg/h as a perfusion marker (interpret with CKD/obstruction/diuretics)
  • Hb: restrictive transfusion threshold ~70 g/L in stable ICU patients; higher if active bleeding, myocardial ischaemia, severe hypoxaemia (individualise)
  • Oxygenation: treat hypoxaemia; if ARDS use lung-protective ventilation and accept lower PaO2/SpO2 targets per ARDS strategy while avoiding harm
A patient has suspected necrotising fasciitis with septic shock. What are your priorities?

This is a classic FRCA scenario: ‘time-critical surgery + profound physiology’.

  • Immediate broad-spectrum antibiotics including toxin suppression (e.g., add clindamycin for streptococcal toxin inhibition per local policy) and urgent surgical debridement
  • Aggressive resuscitation: early noradrenaline, balanced fluids guided by responsiveness, correct coagulopathy, active warming
  • GA with RSI; invasive monitoring; anticipate major vasopressor requirement and repeated operations; ICU post-op
What are the key differences between septic shock and anaphylactic shock (perioperative differential)?

Often asked when hypotension occurs after induction/antibiotics.

  • Both can cause vasodilation and hypotension; anaphylaxis often has bronchospasm, urticaria/angioedema, rapid onset after exposure (but skin signs may be absent under drapes)
  • Sepsis: usually infectious prodrome, fever/hypothermia, raised inflammatory markers, lactate; may have warm peripheries early
  • Management overlap: ABC, fluids, vasopressors; anaphylaxis requires IM/IV adrenaline early and tryptase sampling; sepsis requires antibiotics and source control

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