Infection and sepsis

11 min read Last updated April 8, 2026

Surgical approach (source control — what the surgeon typically does)

  • Principle: treat sepsis with early source control + antibiotics + resuscitation
    • Drain pus/collections (percutaneous radiological drainage vs open surgical drainage)
    • Debride necrotic/infected tissue (e.g. necrotising soft tissue infection)
    • Remove infected foreign material (lines, prostheses where feasible)
    • Resect perforated/ischaemic bowel; lavage; stoma formation if required
  • Common emergency operations for septic source control
    • Laparotomy/laparoscopy for perforation, peritonitis, ischaemic bowel, anastomotic leak
    • Incision & drainage (abscess), washout (septic arthritis), debridement (nec fasc)
    • Urological decompression (obstructed infected kidney: stent/nephrostomy)
    • ENT drainage (deep neck space infection), thoracic drainage (empyema)
  • Timing: aim for source control as soon as feasible once resuscitation started; do not delay for complete physiological normalisation

Anaesthetic management (sepsis / septic shock for source control surgery)

  • Type of anaesthesia
    • GA usually required (often emergency laparotomy/debridement/drainage)
    • Regional/neuraxial: may be inappropriate in shock, coagulopathy, thrombocytopenia, anticoagulation, or severe sepsis with instability; consider peripheral blocks for analgesia if coagulation acceptable
  • Airway device
    • ETT preferred (full stomach, aspiration risk, need for controlled ventilation, high FiO2/PEEP, potential postoperative ventilation)
    • SGA generally unsuitable in unstable septic patients / intra-abdominal sepsis
  • Duration
    • Variable: I&D 0.5–1 h; debridement 1–3 h; laparotomy 2–4+ h; anticipate return to theatre for re-look
  • Pain
    • Often moderate–severe (laparotomy, extensive debridement); multimodal analgesia; consider epidural only if stable and coagulation normal; consider TAP/rectus sheath/QL blocks
  • Pre-op priorities (parallel processing)
    • A–E, treat immediately; call for senior help/ICU early
    • Give antibiotics within 1 hour of recognising sepsis (after cultures if this does not delay)
    • Blood cultures, lactate, FBC, U&E, LFT, coagulation, ABG/VBG; group & save/crossmatch
    • Fluid resuscitation with balanced crystalloid; start vasopressor early if hypotension persists
  • Monitoring & access
    • Arterial line early; large-bore IV access; consider central line for vasopressors; urinary catheter (hourly output)
    • Temperature monitoring and active warming (but fever may be present)
  • Induction and maintenance (key risks: vasodilation + myocardial depression)
    • Pre-induction optimisation: vasopressor ready (noradrenaline), fluid bolus if responsive, correct severe acidosis/hyperkalaemia where possible
    • Induction: haemodynamically stable technique (e.g. ketamine or etomidate where appropriate; cautious propofol); RSI if aspiration risk
    • Ventilation: lung-protective strategy; consider higher PEEP if ARDS; avoid excessive hyperventilation; target normocapnia unless specific indication
    • Vasopressors/inotropes: noradrenaline first-line; add vasopressin if refractory; consider dobutamine if low cardiac output with adequate MAP
  • Transfusion/coagulation
    • Check for DIC; treat bleeding with blood products guided by labs/viscoelastic testing where available
    • Restrictive RBC transfusion strategy (often Hb threshold ~70 g/L) unless ongoing bleeding/ischaemia
  • Post-op disposition
    • High likelihood of ICU/HDU; many require postoperative ventilation, ongoing vasopressors, renal support
    • Continue sepsis bundle: antibiotics, lactate clearance, source control reassessment, glucose control, VTE prophylaxis, stress ulcer prophylaxis where indicated

Definitions and clinical criteria

  • Infection: invasion of normally sterile tissue by organisms with host response
  • Bacteraemia: bacteria in blood (may be transient); not synonymous with sepsis
  • Sepsis (Sepsis-3): life-threatening organ dysfunction caused by a dysregulated host response to infection
    • Operationalised as suspected infection + acute increase in SOFA ≥ 2
  • Septic shock: sepsis with profound circulatory/metabolic abnormalities
    • Despite adequate fluids: need vasopressors to maintain MAP ≥ 65 mmHg AND lactate > 2 mmol/L
  • Screening tools
    • qSOFA (screen): RR ≥ 22, altered mentation, SBP ≤ 100 (not a definition; limited sensitivity)
    • NEWS2 used widely in UK to trigger escalation; think sepsis if infection + physiological derangement

Pathophysiology (what drives organ failure)

  • Host response: PAMPs/DAMPs → innate immune activation → cytokines (TNF-α, IL-1, IL-6), complement, coagulation activation
  • Circulation: vasodilation (NO-mediated), capillary leak, relative hypovolaemia, maldistribution of flow (microcirculatory dysfunction)
  • Myocardial depression: reduced contractility; may have high CO early then low CO; catecholamine resistance can occur
  • Cellular/metabolic: mitochondrial dysfunction, impaired oxygen utilisation, stress hyperglycaemia, lactic acidosis (often from impaired clearance + adrenergic drive, not purely hypoxia)
  • Coagulation: endothelial injury → tissue factor activation → microthrombosis; consumption coagulopathy → DIC
  • Organ dysfunction patterns
    • CNS: delirium/encephalopathy
    • Respiratory: ARDS, V/Q mismatch, increased dead space
    • Renal: AKI (pre-renal + intrinsic + microcirculatory)
    • Hepatic: cholestasis, impaired drug metabolism

Microbiology and common sources

  • Common sources: lungs, urinary tract, abdomen, skin/soft tissue, intravascular devices
  • Typical organisms (context-dependent)
    • Community: Streptococcus pneumoniae, Staph aureus, E. coli and other Enterobacterales
    • Healthcare-associated: MRSA, Pseudomonas, Enterococcus, ESBL producers; consider Candida in high-risk
    • Necrotising soft tissue infection: Group A Strep, mixed anaerobes/Gram negatives; consider toxin-mediated disease
  • Cultures and sampling
    • Blood cultures (2 sets), urine, sputum, wound/abscess; consider CSF if meningitis; take samples before antibiotics if no delay

Recognition and initial management (UK sepsis approach)

  • Immediate priorities: oxygen, IV access, bloods (including lactate), cultures, antibiotics, fluids, monitor urine output
  • Antibiotics
    • Give early; choose empiric regimen based on source, local policy, allergy, renal/hepatic function; de-escalate when cultures return
    • Consider toxin suppression (e.g. add clindamycin for suspected GAS nec fasc) per local guidance
  • Fluids
    • Balanced crystalloid boluses with frequent reassessment (dynamic measures of responsiveness preferred)
    • Avoid fluid overload; capillary leak common; consider early vasopressors if hypotension persists
  • Vasopressors/inotropes
    • Noradrenaline first-line to target MAP ≥ 65 (individualise: chronic hypertension, cerebral perfusion)
    • Add vasopressin if escalating noradrenaline; adrenaline as alternative; dobutamine if myocardial dysfunction with low CO
  • Oxygenation/ventilation
    • Treat hypoxaemia; consider early intubation if work of breathing high, altered consciousness, refractory shock, or need for urgent surgery
  • Lactate and perfusion targets
    • Use lactate as a marker of severity and response; aim for improving lactate/clinical perfusion rather than a single number

Anaesthetic implications (pharmacology and physiology)

  • Cardiovascular
    • Profound vasodilation → induction hypotension; reduced SVR; possible relative adrenal insufficiency
    • Septic cardiomyopathy: reduced EF, impaired response to fluids/vasopressors; consider echo
  • Respiratory
    • Increased dead space; ARDS risk; higher oxygen requirements; lung-protective ventilation (6 ml/kg PBW, plateau pressure control)
  • Renal/hepatic
    • Altered drug handling: reduced clearance, increased Vd (capillary leak) → unpredictable effect-site concentrations
  • Coagulation
    • Thrombocytopenia/DIC common → neuraxial often contraindicated; check platelets/INR/fibrinogen
  • Neuromuscular blockers
    • Prolonged blockade possible (organ failure, acidosis, hypothermia); monitor with nerve stimulator; consider cisatracurium in organ failure
  • Steroids
    • In septic shock requiring ongoing vasopressors, ICU may use hydrocortisone (e.g. 200 mg/day) per local protocol; intra-op consider if refractory shock and not yet given

Investigations and scoring

  • Key labs: lactate, ABG (acid-base), FBC, U&E, LFT, coagulation, CRP/procalcitonin (trend), glucose, calcium/magnesium/phosphate
  • Imaging: CXR, CT abdomen/pelvis, ultrasound (biliary/urinary), echo if shock unclear
  • SOFA components: PaO2/FiO2, platelets, bilirubin, MAP/vasopressors, GCS, creatinine/urine output

Special situations relevant to anaesthetists

  • Sepsis in pregnancy
    • Physiology may mask severity; early senior involvement; fetal considerations; avoid aortocaval compression; early antibiotics/source control
  • Neutropenic sepsis
    • Medical emergency; broad-spectrum antibiotics immediately; strict asepsis; consider fungal infection if persistent fever
  • Meningococcal sepsis / toxic shock
    • Rapid progression; early antibiotics; aggressive haemodynamic support; DIC common; anticipate difficult vascular access
  • Necrotising soft tissue infection
    • Time-critical debridement; severe pain out of proportion; systemic toxicity; consider clindamycin + broad spectrum; expect major physiological derangement

Perioperative antibiotic prophylaxis vs treatment (common FRCA confusion)

  • Prophylaxis: given to prevent infection in clean/clean-contaminated surgery; narrow spectrum; timed within 60 min of incision (agent-dependent)
  • Treatment: suspected/confirmed infection; broad empiric initially; do not delay for theatre; continue post-op and tailor to cultures
Define sepsis and septic shock (current definitions). How do they differ from SIRS?

Examiners want modern Sepsis-3 definitions and awareness that SIRS is not the definition of sepsis.

  • Sepsis: life-threatening organ dysfunction caused by dysregulated host response to infection; operationally suspected infection + SOFA rise ≥ 2
  • Septic shock: sepsis with need for vasopressors to maintain MAP ≥ 65 and lactate > 2 mmol/L despite adequate fluids
  • SIRS: physiological criteria (temp, HR, RR/PaCO2, WCC); can occur without infection and may miss sepsis; no longer defines sepsis
You are called to ED for a hypotensive febrile patient with suspected abdominal sepsis. Talk through your first 10 minutes.

Structure as A–E with parallel tasks and early escalation.

  • A/B: high-flow oxygen if hypoxaemic; assess work of breathing; prepare for early intubation if deteriorating
  • C: 2 large-bore IVs; take bloods incl lactate, cultures; start balanced crystalloid boluses with reassessment; start noradrenaline early if persistent hypotension
  • D: assess GCS, glucose; treat hypoglycaemia; consider encephalopathy
  • E: temperature, examine for source; urine output catheter; start active warming if hypothermic
  • Give broad-spectrum antibiotics within 1 hour (after cultures if no delay)
  • Escalate: ICU/anaesthetic senior review; plan imaging and source control; consider theatre
Explain why septic patients become hypotensive. Include macro- and microcirculatory factors.

Aim: vasodilation + leak + myocardial depression + microcirculatory dysfunction.

  • Reduced SVR: inflammatory mediators (NO) → vasodilation and vasoplegia
  • Relative/absolute hypovolaemia: capillary leak, venodilation, third spacing, poor intake
  • Myocardial depression: septic cardiomyopathy, reduced contractility, arrhythmias
  • Microcirculatory shunting and endothelial dysfunction → maldistributed flow; impaired oxygen extraction/utilisation
Discuss lactate in sepsis: causes, interpretation, and how you use it perioperatively.

Examiners like: not purely hypoxia; use trends; correlate clinically.

  • Raised lactate may reflect hypoperfusion, impaired hepatic clearance, adrenergic stimulation (β2), mitochondrial dysfunction
  • High lactate indicates severity and worse prognosis; use serial measurements for response (lactate clearance) alongside perfusion markers (cap refill, urine output, mental state)
  • Perioperative: rising lactate may indicate ongoing source, inadequate resuscitation, excessive vasoconstriction, hypoxia/anaemia, seizures, or drug effects
How does sepsis alter anaesthetic drug pharmacology and your choice of induction agent?

Key: reduced SVR, altered Vd/clearance, increased sensitivity/unpredictability.

  • Increased Vd (capillary leak) and reduced protein binding can change free drug levels; organ dysfunction reduces clearance → prolonged effects
  • Induction: avoid large propofol doses (vasodilation, myocardial depression); consider ketamine or etomidate; titrate to effect; vasopressor ready
  • Volatile agents can worsen hypotension; use balanced technique; consider opioid-sparing where haemodynamics permit
Outline your intraoperative haemodynamic strategy for septic shock during emergency laparotomy.

Examiners want: monitoring, fluids, vasopressors, echo, perfusion endpoints.

  • Monitoring: arterial line, frequent ABGs/lactate, temperature; consider cardiac output monitoring and bedside echo
  • Fluids: balanced crystalloid boluses guided by dynamic responsiveness; avoid overload; consider albumin only per local policy/ICU practice
  • Vasopressors: noradrenaline first-line to MAP target; add vasopressin if refractory; adrenaline alternative
  • Inotrope: dobutamine if low cardiac output with adequate filling and MAP support
  • Endpoints: MAP (individualised), urine output, lactate trend, capillary refill, mental state (post-op), ScvO2 if used
What is DIC? How might it present in sepsis and what are the anaesthetic implications?

Definition + labs + practical consequences (bleeding, thrombosis, neuraxial contraindication).

  • DIC: systemic activation of coagulation → microthrombi + consumption of platelets/clotting factors → bleeding
  • Labs: thrombocytopenia, prolonged PT/APTT, low fibrinogen, raised D-dimer; clinical bleeding/oozing, purpura, organ dysfunction
  • Implications: avoid neuraxial; secure blood products; use point-of-care coagulation if available; treat underlying cause (source control) and replace components if bleeding/procedures
Discuss antibiotics in sepsis: timing, cultures, and perioperative considerations.

Timing is critical; avoid delays; consider renal dosing and allergy.

  • Give IV antibiotics as early as possible (often within 1 hour of recognition) after cultures if this does not delay
  • Choose empiric therapy based on likely source, severity, local resistance; add MRSA/Pseudomonas/anaerobic cover when indicated
  • Adjust dose for renal/hepatic dysfunction; consider extended/continuous infusions for time-dependent antibiotics per ICU policy
  • De-escalate when cultures/sensitivities return; document indication and review date
A patient with suspected necrotising fasciitis needs emergency debridement. What features suggest the diagnosis and what is your anaesthetic plan?

Time-critical; severe systemic toxicity; anticipate difficult physiology and repeat debridements.

  • Suggestive features: pain out of proportion, rapidly progressive swelling/erythema, skin discolouration/bullae, crepitus (may be absent), systemic toxicity, lactate rise
  • Plan: GA with ETT; arterial line; large-bore access; early noradrenaline; broad-spectrum antibiotics + toxin suppression per policy; aggressive resuscitation; prepare for ICU postop
  • Analgesia: multimodal; consider peripheral blocks if coagulation acceptable; avoid neuraxial if unstable/coagulopathic
When would you consider hydrocortisone in septic shock, and what is the rationale?

They want: refractory shock on vasopressors; relative adrenal insufficiency/vasopressor responsiveness.

  • Consider in septic shock with ongoing vasopressor requirement despite adequate fluids and vasopressor therapy (per ICU/local protocols)
  • Rationale: improves vasopressor responsiveness; may shorten shock duration; monitor for hyperglycaemia, infection risk, neuromuscular weakness
Explain 'source control'. Give examples and discuss timing relative to resuscitation.

Core sepsis concept: remove/drain the source; do not delay excessively.

  • Source control: physical measures to eliminate infection focus and stop ongoing contamination/toxin production
  • Examples: drain abscess/empyema, debride necrotic tissue, remove infected line, resect perforated bowel, relieve obstruction (e.g. obstructed pyelonephritis)
  • Timing: start resuscitation immediately but aim for early source control once feasible; prolonged delay worsens outcome
How do you decide whether a septic patient should go to theatre now or to ICU first?

Balance immediate source control vs need for stabilisation; aim for parallel resuscitation.

  • Assess: likely surgical source, time-critical pathology (perforation, nec fasc), response to initial resuscitation, airway/ventilation needs, availability of ICU/theatre
  • If clear surgical source requiring urgent control, proceed with ongoing resuscitation (vasopressors, invasive monitoring) and plan ICU postop
  • If diagnosis uncertain or patient requires immediate organ support (e.g. severe hypoxaemia needing stabilisation), consider ICU for optimisation and imaging while maintaining urgency
Write short notes on: (a) Sepsis definitions and scoring systems (b) Initial management bundle (c) Septic shock vasopressor choice.

Common written-paper format: structured headings + key numbers.

  • Definitions: Sepsis-3; septic shock criteria; SOFA and qSOFA; NEWS2 as UK trigger
  • Bundle: oxygen, IV access, lactate, cultures, antibiotics early, fluids, urine output, escalation and source control
  • Vasopressors: noradrenaline first-line; MAP target 65; add vasopressin; consider inotrope if low CO
Discuss the pathophysiology of sepsis and relate it to anaesthetic management for emergency surgery.

Link mechanisms to practical consequences.

  • Vasodilation/capillary leak → induction hypotension; need invasive monitoring, vasopressors, careful fluids
  • Myocardial depression → consider echo, inotropes, cautious fluid loading
  • ARDS risk → lung-protective ventilation, avoid fluid overload, plan ICU
  • Coagulopathy/DIC → blood products, avoid neuraxial, anticipate bleeding
Outline the causes of raised lactate in the perioperative period and how you would investigate a rising lactate postoperatively.

Often examined as a differential + approach question.

  • Causes: sepsis/shock, hypovolaemia/bleeding, hypoxaemia, anaemia, seizures, β-agonists/adrenaline, liver failure, mesenteric ischaemia, mitochondrial dysfunction
  • Approach: A–E, review haemodynamics, Hb/ABG, infection markers/cultures, imaging for source/ischaemia, assess perfusion and urine output, review drugs/infusions

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