🎓 DNB Anaesthesiology — December 2025, Paper III (Solved)

Opioid-Free Anaesthesia (OFA) — Definition

OFA is a multimodal anaesthetic technique in which NO intra-operative systemic opioid (IV, IM, neuraxial, intracavitary or intra-articular) is administered; analgesia and suppression of the sympathetic/nociceptive response are achieved instead by a combination of non-opioid analgesics, sympatholytics and regional/local anaesthesia. It is the logical extension of Opioid-Sparing Anaesthesia (where opioids are minimised but not eliminated), and is a core element of Enhanced Recovery After Surgery (ERAS).

Rationale

• Nociception (not "pain", which needs consciousness) can be blunted without μ-opioid agonism by targeting other pathways — α2, NMDA, sodium channel, cyclo-oxygenase, dexamethasone, magnesium.
• Avoids the well-recognised opioid-related adverse events and the phenomenon of opioid-induced hyperalgesia (OIH) and acute tolerance.

Advantages

• Eliminates opioid-related adverse effects: postoperative nausea & vomiting (PONV), respiratory depression, sedation, ileus/constipation, urinary retention, pruritus.
• Reduces opioid-induced hyperalgesia and acute tolerance, and lowers postoperative opioid requirement — relevant to the opioid epidemic and to chronic-pain/opioid-dependent patients.
• Faster recovery of bowel function and earlier mobilisation → shorter length of stay (fits ERAS pathways).
• Particularly valuable in the morbidly obese and OSA patient (avoids depression of respiratory drive), in day-case surgery, and in patients with a history of substance-use disorder.
• Attenuation of the surgical stress response and possible (unproven) benefit on cancer-recurrence/immune function.
• Better preservation of hypoxic and hypercapnic ventilatory drive.

Disadvantages / Limitations

• The individual agents carry their own adverse effects: dexmedetomidine/clonidine → bradycardia, hypotension, delayed sedation; ketamine → dysphoria, hallucinations, hypertension, salivation; lignocaine → LA systemic toxicity; magnesium → potentiation of neuromuscular block, hypotension; NSAIDs → renal, GI and platelet effects.
• More complex to conduct — needs multiple infusions, precise titration and more vigilance; risk of drug errors.
• Intra-operative haemodynamic control may be less predictable; awareness is a theoretical concern if depth is not adequately monitored.
• Not suitable for all surgeries — poor evidence/insufficient for some major procedures; regional block may be contraindicated (coagulopathy, sepsis, refusal).
• Residual effects of long-acting adjuvants (e.g. dexmedetomidine) may delay discharge.
• Robust evidence of superiority over modern opioid-sparing techniques for hard outcomes is still limited (e.g. POFA trial showed more adverse events with a dexmedetomidine-based OFA protocol).

Patient (pre-operative) factors

• Pre-existing liver disease: cirrhosis, chronic hepatitis, NAFLD/NASH, alcoholic liver disease — high Child-Pugh class and high MELD score are the strongest predictors.
• Acute hepatitis (viral, alcoholic, drug-induced) — elective surgery is contraindicated until resolved.
• Obstructive jaundice / biliary obstruction (endotoxaemia, coagulopathy, hepatorenal risk).
• Portal hypertension, hypoalbuminaemia, coagulopathy (raised INR), ascites, encephalopathy.
• Age, malnutrition, sepsis, diabetes, obesity, right heart failure/congestive hepatopathy.

Surgical & anaesthetic factors

• Site & magnitude of surgery: hepatobiliary, cardiac (CPB) and upper-abdominal surgery carry the highest risk (proximity + reduced hepatic blood flow).
• Emergency surgery, prolonged surgery, large blood loss and massive transfusion.
• Intra-operative hypotension, hypoxaemia and low cardiac output → hepatic ischaemia (the liver's O₂ supply is uniquely dependent on hepatic-arterial buffer response).
• Raised intra-abdominal pressure (laparoscopy/pneumoperitoneum) reducing portal flow.
• Hepatotoxic/older volatile agents (historically halothane), and hypercarbia/PEEP reducing hepatic venous drainage.
• Sepsis, drugs (antibiotics, paracetamol, TPN) and transfusion-related injury.

1. Prehepatic — bilirubin overload / haemolysis (unconjugated)

• Resorption of a large haematoma or bruising.
• Haemolysis: transfusion of stored/old blood, transfusion reactions, mechanical (prosthetic valve, CPB), G6PD deficiency, sickle cell.
• Gilbert's syndrome unmasked by fasting/stress.

2. Intrahepatic — hepatocellular dysfunction (mixed)

• Ischaemic/hypoxic hepatitis ('shock liver') from intra-operative hypotension, hypoxia, low cardiac output, sepsis.
• Drug-induced (halothane hepatitis, paracetamol, antibiotics, TPN-associated cholestasis).
• Benign postoperative intrahepatic cholestasis (multifactorial — bilirubin load + reduced hepatic function).
• Decompensation of pre-existing liver disease; sepsis-associated cholestasis.

3. Posthepatic — obstructive (conjugated)

• Iatrogenic bile-duct injury or ligation (cholecystectomy).
• Retained common-bile-duct stone, biliary stricture.
• Ascending cholangitis, pancreatitis, or external compression.

Systemic effects relevant to anaesthesia

• CVS: bradycardia, ↓ contractility & cardiac output, pericardial effusion, ↑ diastolic BP, blunted baroreceptor reflex → prone to hypotension.
• Respiratory: ↓ hypoxic & hypercapnic ventilatory drive, hypoventilation, risk of CO₂ narcosis and sensitivity to sedatives/opioids; possible pleural effusion, macroglossia/OSA.
• CNS/metabolic: slow mentation, ↓ BMR, hypothermia, hypoglycaemia, hyponatraemia (impaired free-water clearance).
• GI/other: delayed gastric emptying (aspiration risk), constipation/ileus, anaemia, coagulopathy (acquired vWF deficiency), adrenal insufficiency association.
• Airway: goitre may cause airway compromise / difficult intubation; myxoedematous tissue infiltration.

Anaesthetic management

• Preop: optimise to euthyroid; continue thyroxine on the day (long half-life ~7 days). Assess airway/goitre, cardiac status, electrolytes, glucose. Consider stress-dose steroid if adrenal insufficiency suspected.
• Intra-op: cautious, reduced doses of induction agents, opioids and sedatives (exquisite sensitivity); anticipate hypotension (have vasopressors); use invasive monitoring in severe disease. Prevent hypothermia (warming, warm fluids); monitor glucose and Na.
• Ventilation: titrate carefully — impaired CO₂ response; delayed awakening/extubation is common.
• Regional anaesthesia is often preferable where feasible (avoids airway & respiratory-depressant issues).
• Postop: risk of delayed recovery, hypoventilation, ileus and, in severe cases, myxoedema coma — monitor accordingly.

Uses in anaesthesia

• PONV prophylaxis: 4–8 mg IV at induction — a first-line antiemetic (works best given at induction, not emergence).
• Analgesic adjunct: reduces postoperative pain and opioid requirement (part of multimodal/OFA analgesia); prolongs peripheral nerve-block duration (as IV or perineural adjuvant).
• Airway oedema: reduces post-extubation stridor / airway swelling and in croup; used before extubation of the difficult/oedematous airway.
• Reduction of raised ICP due to vasogenic oedema around tumours (peri-tumoural oedema) — NOT for traumatic/ischaemic oedema.
• Adrenal replacement / stress cover and treatment of adrenal crisis; component of the WHO surgical/anaesthesia armamentarium.
• Antiemetic & anti-inflammatory in chemotherapy, and dexamethasone-suppression testing; adjunct in bacterial meningitis and in COVID-19.

Cautions / adverse effects

• Transient hyperglycaemia — monitor in diabetics (does not contraindicate a single dose).
• Perineal burning/itching on rapid IV bolus in the awake patient — give slowly/diluted.
• Theoretical immunosuppression / impaired wound healing and infection risk with repeated dosing; caution in active systemic infection.
• A single perioperative dose is generally safe; avoid unnecessary repeated dosing.

Cardiovascular

• Low cardiac output syndrome (LCOS) — myocardial stunning, inadequate myocardial protection, incomplete revascularisation.
• Arrhythmias (AF, heart block, VF), and vasoplegia (low SVR, distributive shock from SIRS).
• Hypovolaemia/bleeding vs. fluid overload; tamponade; residual/new valvular or surgical lesion; myocardial ischaemia (graft problem, air/embolism to coronaries).

Haematological & coagulation

• Coagulopathy: heparin effect / heparin rebound, protamine reactions, platelet dysfunction & thrombocytopenia, fibrinolysis, dilution, hypothermia-induced coagulopathy → bleeding.
• Haemolysis and transfusion requirements.

Respiratory

• Atelectasis, pulmonary oedema, 'post-pump lung' (SIRS/ARDS), pleural effusion, phrenic nerve injury (cold cardioplegia).

Metabolic, renal, neurological & thermal

• Electrolyte/acid-base derangement: hyperkalaemia (cardioplegia) or hypokalaemia, hypocalcaemia, hypomagnesaemia, metabolic acidosis, hyperglycaemia.
• Acute kidney injury (hypoperfusion, haemolysis, non-pulsatile flow).
• Neurological: stroke, delirium, cognitive dysfunction (micro-emboli, hypoperfusion).
• Hypothermia and rewarming shivering (↑ O₂ demand); systemic inflammatory response / capillary leak.

Causes (a diagnostic framework of preload / contractility / afterload / rate-rhythm / mechanical)

• Preload: hypovolaemia, bleeding, vasodilation, tamponade, RV dysfunction.
• Contractility: myocardial stunning, inadequate protection, ischaemia/infarction, pre-existing poor LV.
• Afterload: high SVR (poor LV) or vasoplegia (low SVR).
• Rate/rhythm: bradycardia, AF, heart block.
• Mechanical/surgical: residual valve lesion, graft failure, coronary air embolism, tamponade.

Treatment (systematic, cause-directed)

• Confirm diagnosis: TOE, cardiac output monitoring (PAC/pulse-contour), SvO₂, lactate; exclude/treat tamponade & surgical bleeding.
• Optimise preload: guided fluid boluses to an optimal filling pressure; correct bleeding/coagulopathy.
• Optimise rate & rhythm: pace to ~80–90/min (AV sequential), cardiovert/treat arrhythmias, correct K⁺/Mg²⁺/Ca²⁺.
• Optimise contractility (inotropes): adrenaline, dobutamine, milrinone (inodilator, also lowers PVR — good for RV failure), levosimendan; calcium for acute support.
• Optimise afterload: vasodilators (GTN/nitroprusside/milrinone) if SVR high; vasopressors (noradrenaline, vasopressin) for vasoplegia.
• Ensure adequate oxygenation, normocarbia, normothermia, and correct acidosis/electrolytes.
• Mechanical support if refractory: Intra-Aortic Balloon Pump (IABP), then ECMO/VAD; consider return to CPB and surgical revision (graft/valve).
• Treat RV failure specifically: reduce PVR (iNO, milrinone, avoid hypoxia/hypercarbia/acidosis), inotropic RV support, optimise preload without overload.

Mechanisms of benefit

• Hyperoxygenation — greatly increased dissolved O₂ delivers oxygen even without functioning haemoglobin (e.g. CO poisoning, severe anaemia).
• Reduction of bubble volume (Boyle's law) — treats gas emboli and decompression sickness.
• Vasoconstriction (reduces oedema), enhanced leucocyte killing, angiogenesis/neovascularisation, fibroblast proliferation and antibacterial effects.

Accepted indications (UHMS-approved)

• Carbon monoxide poisoning (especially with LOC, neurological signs, cardiac involvement, pregnancy).
• Decompression sickness ('the bends') and air/gas embolism.
• Gas gangrene (clostridial myonecrosis) and necrotising soft-tissue infections.
• Crush injury, compartment syndrome and other acute traumatic ischaemias.
• Enhancement of healing in selected problem wounds (e.g. diabetic foot ulcers, Wagner grade ≥3).
• Compromised skin grafts and flaps.
• Delayed radiation injury (osteoradionecrosis, soft-tissue radionecrosis, radiation cystitis/proctitis).
• Refractory osteomyelitis; severe anaemia (when transfusion not possible); intracranial abscess; thermal burns; sudden sensorineural hearing loss / central retinal artery occlusion (selected).

1. Barotrauma (pressure-related)

• Middle-ear barotrauma — the commonest complication (ear pain, TM rupture).
• Sinus and dental ('aerodontalgia') barotrauma.
• Pulmonary barotrauma → pneumothorax (risk of tension pneumothorax on decompression), air embolism.
• Inner-ear barotrauma (vertigo, hearing loss).

2. Oxygen toxicity

• CNS (Paul Bert effect): grand-mal seizures — the most feared acute toxicity (more likely >2.8–3 ATA); premonitory VSCELL features (visual, tinnitus, nausea, twitching, irritability).
• Pulmonary (Lorrain Smith effect): tracheobronchitis, retrosternal pain, reduced vital capacity, pulmonary oedema with prolonged exposure.
• Ocular: reversible myopia, and cataract acceleration / worsening with repeated long courses; retinopathy of prematurity risk in neonates.

3. Other effects

• Claustrophobia/anxiety in the chamber.
• Fire hazard (100% O₂ environment).
• Hypoglycaemia in diabetics; reversible worsening of congestive cardiac failure (afterload/oxidative effects).
• Decompression sickness in attendants; difficulty accessing/monitoring a critically ill patient in the chamber.

Key components

• Permissive (hypotensive) resuscitation — accept a lower target BP (e.g. SBP ~80–90 mmHg or a palpable radial pulse / mentation) until bleeding is controlled, to avoid 'popping the clot' and dilution — EXCEPT in traumatic brain injury, where normotension is maintained.
• Haemostatic resuscitation — early, balanced transfusion of blood products in ~1:1:1 ratio of packed red cells : plasma (FFP) : platelets; minimise crystalloid.
• Rapid haemorrhage control — direct pressure, tourniquets, pelvic binder, and early damage-control surgery / interventional radiology.
• Tranexamic acid — give early (within 3 h; CRASH-2), 1 g over 10 min then 1 g over 8 h.
• Correction and prevention of the lethal triad — aggressive rewarming, correct acidosis (perfusion, not just bicarbonate), replace calcium, and use point-of-care coagulation testing (ROTEM/TEG) to guide products.
• Massive transfusion protocol activation and use of a validated trigger/score (e.g. ABC score).

The three (four) stages

• Stage 0 — recognition & DCR: identify the patient who needs DCS (hypothermia <35 °C, acidosis pH <7.2/base deficit, coagulopathy, high transfusion requirement) and begin damage control resuscitation.
• Stage 1 — abbreviated surgery: rapid control of bleeding (packing, ligation, temporary vascular shunts) and of contamination (staple/close bowel, no anastomosis); temporary abdominal closure ('open abdomen', e.g. Bogota bag / negative-pressure dressing).
• Stage 2 — ICU physiological restoration: rewarming, correction of acidosis and coagulopathy, ongoing resuscitation and organ support over 24–48 h.
• Stage 3 — definitive surgery: return to theatre once physiology is restored for definitive repair, anastomosis, reconstruction and abdominal closure (may need repeated 're-look' laparotomies).

Key anaesthetic concerns

• Positioning: often sitting/park-bench/prone — risk of VAE (surgical site above the heart), postural hypotension, pressure injuries, quadriplegia from neck flexion (allow ≥2 finger-breadths chin–chest), macroglossia, peripheral nerve injury, and pneumocephalus.
• Venous air embolism & paradoxical air embolism (right-to-left shunt / PFO — screen with pre-op echo).
• Brainstem manipulation → sudden bradycardia/asystole, hypertension, arrhythmias (surgeon must be warned to pause); cardiovascular instability.
• Cranial-nerve involvement → loss of airway-protective reflexes and risk of postoperative bulbar dysfunction, apnoea and aspiration → delayed/cautious extubation.
• Need for a smooth, immobile field and rapid emergence for neuro assessment; brain relaxation (avoid ↑ICP/coughing).
• Haemodynamic monitoring: invasive arterial line (transducer at the level of the external auditory meatus/circle of Willis to reflect cerebral perfusion in the sitting position), central line (right atrial catheter for air aspiration), precordial Doppler/capnography.

Anaesthetic management points

• Preop: assess for PFO (contrast echo), cardiorespiratory reserve, and raised ICP; plan monitoring.
• Induction/maintenance: smooth induction, secure reinforced (armoured) ETT well fixed, TIVA or balanced technique preserving CO₂ reactivity and cerebral autoregulation, avoid N₂O once VAE risk begins (it enlarges bubbles).
• Careful positioning with graded head-up, MAP maintained for cerebral perfusion, and vigilance for VAE throughout.
• Emergence: assess airway reflexes and consciousness; be prepared for delayed extubation and postoperative ventilation.

Methods of detection (most → least sensitive)

• Transoesophageal echocardiography (TOE) — most sensitive; detects tiny air and paradoxical embolism, but invasive/needs expertise.
• Precordial Doppler ultrasound — very sensitive, non-invasive; classic 'mill-wheel'/roaring change in sound (placed over the right heart, 3rd–6th right parasternal space).
• End-tidal CO₂ — a sudden fall in EtCO₂ (increased alveolar dead space) is the most practical, continuous monitor.
• End-tidal nitrogen (EtN₂) — rises with air entrainment (early, but less available).
• Pulmonary artery pressure — rises; and fall in SpO₂/PaO₂.
• Clinical/haemodynamic: hypotension, arrhythmias, 'mill-wheel' murmur on auscultation (late), and cardiovascular collapse.
• A right-atrial catheter also allows aspiration of entrained air (both a monitor and a treatment).

Treatment of VAE

• Alert the surgeon — flood the field with saline and pack/wax bone edges to stop further air entry; lower the head (below heart level) if possible.
• Stop N₂O immediately and give 100% oxygen.
• Aspirate air from the right-atrial (central) catheter.
• Apply jugular venous compression (raises venous pressure at the surgical site to identify and stop the entry point).
• Position: left lateral decubitus (Durant's manoeuvre) ± head-down to trap air in the RV apex, away from the outflow tract.
• Cardiovascular support: fluids, vasopressors/inotropes; CPR if arrest; treat arrhythmias.
• Refractory/paradoxical cases: consider hyperbaric oxygen (for cerebral/coronary air embolism) and supportive intensive care.

Severe pre-eclampsia — definition & implications

Pre-eclampsia is new-onset hypertension (≥140/90 mmHg) after 20 weeks with proteinuria and/or maternal organ dysfunction. It is 'severe' when BP ≥160/110 mmHg, or there is thrombocytopenia, renal/hepatic involvement, pulmonary oedema, or cerebral/visual symptoms. It is a multisystem endothelial disorder — the anaesthetic implications flow from every affected system.

Anaesthetic implications (multisystem)

• CVS: severe hypertension with exaggerated pressor response to laryngoscopy (risk of cerebral haemorrhage, LV failure); intravascular volume depletion despite oedema.
• CNS: risk of eclamptic seizures, cerebral oedema/haemorrhage; headache, hyperreflexia, visual disturbance are warning signs.
• Respiratory: laryngeal/airway oedema → difficult intubation and higher failed-intubation rate; pulmonary oedema.
• Haematological: thrombocytopenia and coagulopathy (may contraindicate neuraxial block); HELLP syndrome.
• Hepatic: HELLP (Haemolysis, Elevated Liver enzymes, Low Platelets), subcapsular haematoma / hepatic rupture, epigastric pain.
• Renal: proteinuria, oliguria, AKI.
• Uteroplacental: reduced placental perfusion, IUGR, fetal compromise; risk of abruption.
• Drug interactions: magnesium potentiates neuromuscular block and causes hypotension.

Preoperative optimisation

• Control BP: keep <160/110 mmHg — labetalol, hydralazine or nifedipine (avoid precipitous falls that harm placental perfusion).
• Seizure prophylaxis/treatment: magnesium sulphate (loading 4 g IV then infusion) — monitor for toxicity (loss of reflexes, respiratory depression); antidote is calcium gluconate.
• Assess platelets/coagulation (usually need platelets >70–80 ×10⁹/L and normal coagulation for neuraxial block), airway, and fluid status; secure large-bore IV access, group & save.
• Judicious fluids (risk of pulmonary oedema) — avoid aggressive preloading.

Regional anaesthesia (preferred technique)

• Neuraxial (spinal, epidural, or combined spinal-epidural) is the technique of choice if platelets/coagulation are adequate and no other contraindication — it avoids airway instrumentation and the hypertensive response, and improves uteroplacental flow.
• Modern evidence shows spinal is acceptable in severe pre-eclampsia — hypotension is often LESS severe than in healthy parturients; treat hypotension with phenylephrine and cautious fluids.
• Epidural gives a slower, controllable block and good postoperative analgesia.

General anaesthesia (when regional contraindicated)

• Indications: thrombocytopenia/coagulopathy, maternal refusal, eclampsia with reduced consciousness, fetal distress needing immediate delivery, or pulmonary oedema.
• Anticipate a DIFFICULT AIRWAY (oedema) — smaller ETT, difficult-airway equipment ready, experienced assistance.
• Obtund the pressor response to laryngoscopy: e.g. IV labetalol, esmolol, fentanyl/alfentanil, magnesium, or lignocaine — a critical step to prevent cerebral haemorrhage.
• Rapid-sequence induction with cricoid; remember magnesium prolongs neuromuscular blockade — titrate relaxants with a nerve stimulator.
• Maintain BP control at extubation (another pressor surge) and continue magnesium and monitoring postoperatively.

Causes / contributing factors

• Shunt through the collapsed non-dependent lung (main cause).
• Impaired hypoxic pulmonary vasoconstriction (HPV) — inhibited by volatile agents (dose-dependent), vasodilators (GTN, nitroprusside, dobutamine), hypocapnia, very high/low PA pressures.
• Malposition of the double-lumen tube (DLT) or bronchial blocker — the commonest correctable cause; verify with fibreoptic bronchoscopy.
• V/Q mismatch and reduced FRC/atelectasis in the dependent lung (lateral position, weight of mediastinum, absorption atelectasis with high FiO₂).
• Pre-existing lung disease, low cardiac output (low mixed-venous O₂), and secretions/blood obstructing the airway.

Management of hypoxaemia during OLV (stepwise)

• Increase FiO₂ to 1.0.
• Check DLT/blocker position with fibreoptic bronchoscopy and confirm both lungs; suction secretions/blood.
• Ensure adequate cardiac output and Hb; confirm no equipment/circuit problem.
• Apply CPAP (5–10 cmH₂O with O₂) to the non-dependent (operative) lung — after a recruitment breath (most effective specific measure).
• Apply PEEP (5 cmH₂O) to the dependent, ventilated lung (helps if atelectatic; may worsen shunt if it over-distends and diverts flow).
• Intermittent re-inflation / two-lung ventilation if severe or persistent.
• Surgical clamping of the pulmonary artery to the operative lung (during pneumonectomy) abolishes the shunt.
• Optimise ventilation: lung-protective settings, avoid factors inhibiting HPV.

1. Preoperative

• Detect and treat anaemia early — iron (oral/IV), B12/folate, and erythropoietin where indicated.
• Stop/optimise antiplatelet and anticoagulant drugs where safe; treat coagulopathy.
• Autologous predonation in selected elective cases; restrictive transfusion thresholds (Hb 7–8 g/dL).
• Plan surgery/technique to minimise loss.

2. Intraoperative

• Meticulous surgical haemostasis; minimally invasive/laparoscopic approaches; tourniquets where appropriate.
• Controlled (deliberate) hypotension where safe.
• Acute Normovolaemic Haemodilution (ANH) — remove blood at induction, replace volume, re-infuse later.
• Intraoperative Cell Salvage (autotransfusion) — collect, wash and re-infuse the patient's own shed blood (avoid in malignancy/infection unless leucodepletion filter used).
• Antifibrinolytics — tranexamic acid (strong evidence), aminocaproic acid.
• Positioning to reduce venous congestion; maintain normothermia, normal pH and calcium (all improve haemostasis); point-of-care ROTEM/TEG-guided, targeted product use.
• Topical haemostatic agents (fibrin sealants, etc.).

3. Postoperative

• Postoperative cell salvage from drains; restrictive transfusion triggers.
• Minimise iatrogenic (phlebotomy) blood loss; continue iron/erythropoietic support.
• Prompt management of surgical bleeding and coagulopathy.

Patient (predisposing) factors

• Advanced age — the single strongest risk factor.
• Pre-existing cognitive impairment / low cognitive reserve, low educational level.
• Cerebrovascular disease, prior stroke/TIA, and vascular risk factors (hypertension, diabetes, atherosclerosis).
• Depression, alcohol misuse, frailty and poor functional status; genetic factors (e.g. ApoE4 — evidence mixed).
• History of previous POCD or postoperative delirium.

Surgical & perioperative (precipitating) factors

• Major/prolonged and emergency surgery; the systemic inflammatory (neuro-inflammatory) response to surgery.
• Intra-operative and postoperative complications: hypotension/hypoperfusion, hypoxaemia, hypo-/hyperglycaemia, embolic events.
• Postoperative pain, sleep disturbance and postoperative delirium (a strong predictor of subsequent POCD).
• Deep anaesthesia / possible burst suppression, and polypharmacy (long-acting sedatives, anticholinergics, benzodiazepines).
• Postoperative infection/sepsis, second surgery, and prolonged ICU stay/hospitalisation.
• (The independent role of anaesthetic type — general vs regional — remains unproven.)

Prevention (reduce the triad)

• Minimise oxidiser: use the lowest FiO₂ that maintains safe SpO₂; avoid nitrous oxide; allow time for O₂ to dissipate before using cautery.
• Use laser-resistant (laser-safe) tracheal tubes for laser airway surgery; fill the cuff with saline (± dye) to detect/quench rupture.
• Control ignition: surgeon warns before activating laser/cautery; keep power low; allow prep solutions to dry fully.
• Team briefing and a fire risk assessment before high-risk cases; wet swabs/gauze around the field; saline immediately available.

Immediate management of an airway fire (drill)

• STOP and simultaneously: STOP the flow of all airway gases (disconnect the circuit) and REMOVE the tracheal tube.
• Pour saline/water into the airway to extinguish and cool.
• Remove any other flammable/burning material from the airway and field.
• Then: re-establish ventilation by mask (avoiding supplemental O₂/N₂O until sure the fire is out); re-intubate — ideally examine the airway with rigid/flexible bronchoscopy to assess thermal injury.
• Assess airway damage (bronchoscopy), consider steroids/humidified oxygen, and plan ICU care; keep the patient intubated/ventilated if significant injury.
• Save the involved materials and report the incident.