ANZCA Final
Critical Care
Emergency Surgery
High Evidence

Anaesthesia for the Septic Patient

Sepsis is life-threatening organ dysfunction caused by dysregulated host response to infection, with septic shock defined as sepsis with persistent hypotension requiring vasopressors despite adequate fluid...

Updated 2 Feb 2026
2 min read
Citations
88 cited sources
Quality score
54 (gold)

Clinical board

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Urgent signals

Safety-critical features pulled from the topic metadata.

  • Septic shock with refractory hypotension
  • Multi-organ dysfunction syndrome (MODS)
  • Adrenal insufficiency in sepsis
  • Lactic acidosis >4 mmol/L

Exam focus

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  • ANZCA Final Written
  • ANZCA Final Clinical Viva

Editorial and exam context

ANZCA Final Written
ANZCA Final Clinical Viva
Clinical reference article

Quick Answer

Sepsis is life-threatening organ dysfunction caused by dysregulated host response to infection, with septic shock defined as sepsis with persistent hypotension requiring vasopressors despite adequate fluid resuscitation and lactate >2 mmol/L. Definitions (Sepsis-3): qSOFA (quick SOFA) ≥2 points (RR ≥22, altered mentation, SBP ≤100) identifies high-risk patients; SOFA score ≥2 indicates organ dysfunction. Pathophysiology: Inflammatory cascade (cytokine storm), endothelial dysfunction (capillary leak, tissue oedema), vasodilation (nitric oxide, prostacyclin), myocardial depression (TNF-α, IL-1β), microvascular thrombosis, mitochondrial dysfunction (cytopathic hypoxia). Anaesthetic considerations: Emergency source control surgery (drainage of abscess, debridement of necrotizing fasciitis, cholecystectomy, bowel resection); high-risk anaesthesia due to hemodynamic instability, coagulopathy, multi-organ failure. Preoperative optimisation: 30 mL/kg crystalloid resuscitation (goal MAP ≥65 mmHg), antibiotics within 1 hour, source control as soon as possible (within 6-12 hours), noradrenaline first-line vasopressor (0.01-3 μg/kg/min), vasopressin (0.03 units/min) if refractory, corticosteroids (hydrocortisone 50 mg IV q6h if refractory shock). Induction: Ketamine 1-2 mg/kg preferred (maintains sympathetic tone, less cardiovascular depression than propofol/thiopental), etomidate 0.2-0.3 mg/kg if severe cardiovascular collapse (adrenal suppression risk), cautious fluid loading (risk of fluid overload, ARDS), anticipate difficult intubation (capillary leak, airway oedema), RSI with ketamine or etomidate, suxamethonium or rocuronium (sugammadex ready). Maintenance: TIVA with ketamine/propofol and remifentanil; low-dose vasopressor support; lung-protective ventilation (6 mL/kg IBW, PEEP 5-15 cm H₂O, FiO₂ minimum to maintain SpO₂ 88-95%); permissive hypercapnia if needed (avoid high airway pressures). Monitoring: Arterial line, central access, cardiac output monitoring (PiCCO, FloTrac), urine output (≥0.5 mL/kg/hour), lactate clearance (target >10% in 2 hours), dynamic fluid responsiveness (SVV, PPV, passive leg raise). Postoperative: ICU admission, continued sepsis management (antibiotics, source control, organ support), consider drotrecogin alfa (activated protein C) no longer recommended, thromboprophylaxis, glycaemic control (6-10 mmol/L), renal replacement therapy if AKI. Indigenous patients: Higher sepsis rates due to higher rates of diabetes, renal disease, and late presentation for infection; aggressive early management essential. [1-10]