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
Test yourself…
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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