Surgical approach
- Aim: control contamination, treat source, washout, restore GI continuity (or divert), and drain
- Typical operations (depend on site/cause)
- Perforated peptic ulcer: laparoscopic/open exploration → omental (Graham) patch ± biopsy; peritoneal lavage; drains selectively
- Small bowel perforation (e.g. ischaemia, typhoid, trauma): resection of non-viable bowel ± primary anastomosis vs stoma; washout
- Appendiceal perforation: appendicectomy ± washout; consider drainage if abscess
- Diverticular perforation: Hartmann’s procedure vs resection + primary anastomosis ± defunctioning ileostomy; laparoscopic lavage in selected cases
- Colonic malignancy perforation: oncological resection often with stoma; damage control if unstable
- Approach: laparoscopy if stable/early disease; open laparotomy common in diffuse peritonitis, haemodynamic instability, gross contamination, or uncertain diagnosis
- Damage control surgery (DCS) in profound shock: abbreviated laparotomy, rapid source control, temporary abdominal closure, ICU resuscitation, planned re-look
Anaesthetic management (overview)
- Type of anaesthesia: General anaesthesia with endotracheal intubation
- RSI usually indicated (full stomach, ileus, opioids, sepsis-related gastroparesis)
- Avoid SGA (aspiration risk, need for controlled ventilation, pneumoperitoneum/Trendelenburg, potential for prolonged surgery)
- Duration: typically 1–4+ hours (longer if laparotomy, extensive contamination, resection/stoma, DCS/re-look)
- How painful: moderate–severe (laparotomy > laparoscopy); high opioid requirement unless multimodal/neuraxial used
- Key physiological problems: hypovolaemia (third spacing), sepsis/vasodilation, metabolic acidosis, AKI risk, aspiration risk, coagulopathy, hypothermia
- Monitoring/lines: consider arterial line early; 2 large-bore IVs; central access if vasoactive infusions/poor access; urinary catheter; temperature monitoring
- Post-op destination: HDU/ICU common (sepsis, vasopressors, ventilation, lactate/acidosis, frailty/comorbidity, major laparotomy)
Definition and causes
- Perforated viscus = full-thickness breach of GI tract (or biliary) with leakage of gas/contents → peritonitis ± sepsis
- Common causes
- Upper GI: perforated peptic ulcer (H. pylori, NSAIDs, steroids), iatrogenic (endoscopy)
- Small bowel: obstruction/closed loop, ischaemia, inflammatory bowel disease, infection, trauma
- Lower GI: diverticulitis, malignancy, stercoral perforation, IBD, iatrogenic (colonoscopy), anastomotic leak
- Physiology: contamination → inflammatory cascade → capillary leak/third spacing → hypovolaemia; bacterial translocation/endotoxin → vasodilation, myocardial depression, distributive shock; ileus → aspiration risk
Presentation and diagnosis (anaesthetic relevance)
- Symptoms/signs: sudden severe abdominal pain, guarding/rigidity, peritonism, fever, tachycardia, hypotension, confusion; may be subtle in elderly/immunosuppressed
- Investigations
- Bloods: FBC, U&E/creatinine, LFT, CRP, coagulation, venous/arterial gas (lactate, base deficit), group & save/crossmatch
- Imaging: CT abdomen/pelvis with contrast often diagnostic; erect CXR may show free air (not always)
- Risk stratification: sepsis screening; consider P-POSSUM/NELA context for laparotomy; frailty and physiological reserve matter
Pre-operative priorities (time-critical)
- Resuscitate in parallel with surgical decision-making (do not delay source control in deteriorating patient)
- Sepsis management (Sepsis Six principles adapted to theatre pathway)
- Oxygen as needed; target SpO2 appropriate to patient (avoid hyperoxia in some COPD but prioritise perfusion/oxygen delivery)
- Blood cultures and lactate; repeat lactate for response
- IV broad-spectrum antibiotics within 1 hour of recognition (follow local policy; include anaerobic cover; consider antifungal if high risk/ICU guidance)
- IV fluids: balanced crystalloid boluses guided by response; early vasopressors if fluid-refractory hypotension
- Monitor urine output (catheter); target ≥0.5 mL/kg/h (contextual)
- Aspiration risk reduction
- NG tube for decompression if vomiting/obstruction/ileus (does not eliminate aspiration risk)
- Consider non-particulate antacid ± H2 blocker/PPI per local practice (do not delay theatre)
- Optimise physiology: correct severe electrolyte derangements (K+, Ca2+), treat hypoglycaemia, start warming, consider stress-dose steroids if chronic steroids/adrenal insufficiency
- Consent/communication: high-risk emergency laparotomy discussion; blood products availability; ceilings of care and ICU plan
Anaesthetic technique (details)
- Induction: haemodynamically cautious RSI
- Pre-induction: resuscitate, A-line if time/feasible, vasopressor ready (metaraminol/phenylephrine boluses; noradrenaline infusion early if septic shock)
- Induction agents: ketamine or etomidate often suitable in shock; titrated propofol if stable; consider opioid-sparing if hypotensive
- Paralysis: rocuronium (with sugammadex available) or suxamethonium; consider hyperkalaemia/neuromuscular disease contraindications
- Cricoid pressure: apply if trained assistant; release if impedes ventilation/intubation; prioritise oxygenation and first-pass success
- Maintenance: volatile or TIVA; controlled ventilation; avoid excessive PEEP if hypotensive; lung-protective ventilation (6–8 mL/kg IBW) especially in sepsis
- Monitoring: standard + invasive BP; consider cardiac output monitoring in high-risk laparotomy; frequent blood gases (lactate, Hb, electrolytes)
- Fluids and haemodynamics
- Balanced crystalloid for initial resuscitation; avoid chloride load where possible; reassess after each bolus (stroke volume response, BP, cap refill, lactate trend, urine output)
- Early vasopressors for distributive shock; target MAP ~65 mmHg (individualise: chronic HTN, cerebral perfusion)
- Blood: crossmatch if major laparotomy/anaemia/bleeding risk; transfuse guided by Hb, physiology, ongoing losses; consider cell salvage if contamination policy allows (often avoided in gross faecal contamination)
- Analgesia (multimodal)
- Opioids: titrate carefully in shock; consider fentanyl/alfentanil boluses; morphine cautiously if hypotensive/renal impairment
- Paracetamol IV if not contraindicated; NSAIDs often avoided (AKI risk, sepsis, hypovolaemia, perforated ulcer context)
- Regional: epidural may be excellent for open laparotomy but often limited by sepsis, coagulopathy, urgency, anticoagulation, haemodynamic instability; consider alternative (TAP blocks, rectus sheath, wound catheters)
- Ketamine infusion (analgesic dose) can reduce opioid and support haemodynamics; lidocaine infusion sometimes used (local policy, contraindications)
- Antibiotics: ensure given pre-incision; re-dose intra-op if prolonged/major blood loss as per guidelines
- Temperature and glucose: active warming (forced air, warmed fluids); avoid hypothermia-related coagulopathy; maintain reasonable glycaemic control
Post-operative care
- Extubation vs ICU ventilation: consider ongoing shock/vasopressors, acidosis, hypothermia, high lactate, poor respiratory mechanics, aspiration, frailty
- Critical care priorities: source control achieved? continue sepsis bundle, vasopressors, fluid balance, renal support if needed, early nutrition plan, DVT prophylaxis when safe
- Analgesia: continue multimodal; epidural if in situ with close haemodynamic monitoring; consider PCA if extubated and stable
- Complications to anticipate: intra-abdominal sepsis/collections, anastomotic leak, ileus, AKI, ARDS, wound complications, delirium
Key differentials and special situations
- Differentials for acute abdomen/free air: perforated ulcer, perforated diverticulitis, ischaemic bowel, pancreatitis (no free air usually), ruptured AAA (mimic), mesenteric ischaemia
- Steroids/immunosuppression: blunted signs; higher infection risk; consider peri-op steroid replacement
- Anticoagulation/coagulopathy: impacts neuraxial options and bleeding risk; correct coagulopathy if possible (vit K, PCC/FFP, platelets) guided by urgency and labs/TEG
- Pregnancy: aspiration risk, aortocaval compression, fetal considerations; left uterine displacement; early obstetric input
You are called to anaesthetise a 70-year-old with a suspected perforated viscus for emergency laparotomy. Talk through your pre-operative assessment and immediate priorities.
Structure: assess severity (sepsis/shock), resuscitate, reduce aspiration risk, prepare for high-risk induction and post-op critical care.
- Rapid ABC assessment: airway risk (vomiting/ileus), breathing (SpO2, RR), circulation (BP, HR, perfusion), disability (confusion), exposure (peritonism, temp)
- Identify and treat sepsis/shock: lactate, base deficit; repeat after resuscitation; start broad-spectrum antibiotics urgently
- IV access: 2 wide-bore cannulae; send bloods incl. FBC/U&E/coagulation, group & save/crossmatch; consider arterial line pre-induction if unstable
- Fluid resuscitation with balanced crystalloid boluses; assess response; early vasopressors if hypotension persists
- Aspiration precautions: NG decompression if appropriate; plan RSI; antacid per local policy without delaying theatre
- Analgesia and antiemetics; avoid NSAIDs if hypovolaemic/septic/AKI risk
- Plan post-op destination (ICU/HDU) and discuss ceilings of care; ensure blood availability and warming strategy
How would you induce anaesthesia in a septic, hypotensive patient with peritonitis and a full stomach?
Goal: secure airway rapidly while avoiding cardiovascular collapse; treat distributive + hypovolaemic components.
- Preparation: pre-oxygenate; suction ready; head-up if tolerated; vasopressor drawn up; consider A-line before induction if feasible
- Resuscitate to a reasonable starting point (fluid bolus, start noradrenaline early if needed) but do not delay source control in extremis
- RSI with haemodynamically stable agent: ketamine (1–2 mg/kg titrated) or etomidate (0.2–0.3 mg/kg); cautious opioid dosing
- Neuromuscular blocker: rocuronium (1.0–1.2 mg/kg) with sugammadex available, or suxamethonium if appropriate
- Manage post-induction hypotension proactively: vasopressor boluses and infusion; treat reversible causes (hypovolaemia, acidosis, hypoxia)
- Ventilation: lung-protective strategy; avoid excessive PEEP if preload-dependent
What monitoring and vascular access would you choose for emergency laparotomy for perforation, and why?
- Standard monitoring + temperature + neuromuscular monitoring
- Arterial line early for beat-to-beat BP, frequent gases (lactate, Hb, electrolytes) and vasopressor titration
- Two large-bore peripheral IV cannulae; consider rapid infuser if major contamination/bleeding risk
- Central venous access if poor peripheral access, need for noradrenaline/vasopressin, or anticipated prolonged vasoactive support (not mandatory if reliable peripheral vasopressor pathway exists)
- Urinary catheter for hourly output; consider CVP only if specific question (limited utility as volume marker)
- Consider advanced haemodynamic monitoring in high-risk laparotomy (e.g. oesophageal Doppler/pulse contour) to guide fluids/vasopressors
Discuss fluid therapy in perforated viscus with sepsis. What endpoints would you use?
- Pathophysiology: third spacing + vasodilation → relative and absolute hypovolaemia; aim to restore perfusion while avoiding overload
- Use balanced crystalloids for boluses; reassess frequently; avoid large unstructured volumes
- Endpoints: MAP (often ≥65 mmHg), improving capillary refill/skin perfusion, decreasing lactate/base deficit, urine output trend, stroke volume response if monitored, mental state
- If fluid non-responsive: start/uptitrate vasopressors (noradrenaline first-line); consider inotrope if myocardial depression suspected
- Blood products guided by Hb, physiology and losses; correct coagulopathy if bleeding/major surgery (TEG/ROTEM if available)
How would you provide analgesia for an emergency laparotomy for perforation? Discuss epidural pros/cons.
- Multimodal: paracetamol + opioids titrated; consider ketamine infusion; regional blocks (TAP/rectus sheath) or wound catheters
- Epidural benefits: superior dynamic analgesia, improved respiratory function, reduced systemic opioid requirements, may facilitate early mobilisation
- Epidural risks/limitations in this setting: time-critical case; sepsis-related hypotension; potential coagulopathy/anticoagulants; technical difficulty; risk of epidural abscess (rare) and masking evolving abdominal pathology
- Pragmatic approach: if stable, not coagulopathic, and expertise available, consider epidural; otherwise use blocks + PCA and escalate in ICU if needed
What are the key intra-operative complications you anticipate and how would you manage them?
- Hypotension at induction/after source control: treat with vasopressors, fluids if responsive, correct acidosis/hypoxia; consider myocardial depression
- Aspiration: head-down suction, secure airway, bronchial toilet, increase FiO2/PEEP as needed; consider bronchoscopy; post-op ICU if significant
- Bleeding: activate major haemorrhage protocol if needed; balanced transfusion; calcium replacement; warming; TXA if indicated
- Hypothermia: forced-air warming, warmed fluids, minimise exposure; monitor core temperature
- Worsening acidosis/hyperkalaemia/AKI: frequent gases; adjust ventilation; treat K+; avoid nephrotoxins; optimise perfusion
When would you plan post-operative ICU admission and/or continued ventilation?
- Ongoing vasopressor requirement or persistent shock; high lactate/metabolic acidosis; significant hypothermia; major blood loss; severe comorbidity/frailty
- Respiratory concerns: aspiration, poor gas exchange, high ventilatory requirements, reduced consciousness, high opioid requirement, abdominal compartment concerns
- Surgical factors: damage control laparotomy, open abdomen/temporary closure, planned re-look, extensive contamination
A previous FRCA-style theme: ‘Discuss the anaesthetic implications of sepsis for emergency abdominal surgery.’ Apply it to perforated viscus.
- Cardiovascular: vasodilation + capillary leak + myocardial depression → hypotension; need early vasopressors; cautious induction; invasive monitoring
- Respiratory: increased O2 demand, risk of ARDS; lung-protective ventilation; careful fluid balance
- Renal: AKI risk; avoid nephrotoxins; maintain perfusion; monitor urine output; dose-adjust drugs
- Coagulation: sepsis-associated coagulopathy; check coagulation/platelets; impacts neuraxial and bleeding risk
- Pharmacology: altered Vd/protein binding; increased sensitivity to induction agents in shock; consider reduced doses and titration
- Metabolic: acidosis, hyperglycaemia, electrolyte derangements; frequent gases; temperature control
A previous FRCA-style theme: ‘Outline your approach to rapid sequence induction and discuss cricoid pressure.’ How does perforated viscus influence your answer?
- Perforated viscus commonly implies ileus/obstruction, opioids, pain, sepsis → high aspiration risk → RSI with ETT is standard
- Cricoid pressure: intended to reduce passive regurgitation; must be applied correctly; may worsen laryngoscopy/ventilation—release if it impedes airway management
- First-pass success: experienced intubator, videolaryngoscope availability, bougie, suction, clear plan for failed intubation in full-stomach patient
- Haemodynamic strategy: vasopressor prepared, titrated induction, early noradrenaline in septic shock
How would your management differ for laparoscopic vs open surgery for suspected perforated peptic ulcer?
- Laparoscopy: pneumoperitoneum can reduce venous return and increase SVR; may worsen hypotension in sepsis—ensure adequate resuscitation and vasopressors; adjust ventilation for CO2 absorption
- Positioning: Trendelenburg/reverse Trendelenburg affects haemodynamics and airway pressures; secure ETT well
- Open: often more painful and fluid shifts may be greater; consider epidural/blocks; higher risk of hypothermia—aggressive warming
- Conversion readiness: plan for longer duration and increased losses; ensure blood availability and robust access
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