Physical principle: whole blood (~0.36mL) in a cylindrical cup; a pin on a torsion wire oscillates 4°45' every 10s (4–5Hz); clot formation transmits torque from cup to pin, plotted as the TEG waveform.

Systems: TEG (Haemonetics, oscillating cup) vs ROTEM (rotating pin, stationary cup) — not interchangeable.

Activators: kaolin (intrinsic/trauma); tissue factor (rapid TEG); heparinase (neutralises heparin, cardiac surgery); functional fibrinogen (isolates fibrinogen).

Structure: multivesicular liposomes (15–30μm) with dozens–hundreds of aqueous chambers containing bupivacaine, walls of natural phospholipids.

Release: macrophage/fibroblast uptake, lipid walls degrade over 72–96h; Cmax at 24–48h (vs 15–30 min for plain bupivacaine).

Key value: 72h analgesia without catheter infrastructure → true ambulatory surgery, opioid-sparing, faster discharge.

Cost ~$300–350/vial vs <$5 plain bupivacaine — cost-effective mainly when it avoids admission/catheter costs.

Structure: modified gamma-cyclodextrin — 8 glucose units in a torus with hydrophobic interior and 8 negatively-charged side chains.

Mechanism: steroidal nucleus of rocuronium docks into the hydrophobic cavity → 1:1 inclusion complex (essentially irreversible) → encapsulated rocuronium inaccessible to NMJ → plasma level falls → rocuronium dissociates from receptors → block reversed.

Specificity: works on aminosteroid NMBs only (rocuronium>vecuronium>pancuronium); CANNOT reverse benzylisoquinoliniums (atracurium, cisatracurium).

DAS 2015: sugammadex 16mg/kg given SIMULTANEOUSLY with FONA preparation, not as an alternative to it.

VACTERL: ~50% have associated anomalies — Vertebral, Anal atresia, Cardiac (~35%, most important), TE fistula, Renal, Limb.

Echocardiogram (mandatory, determines side of thoracotomy); CXR; renal USS; spinal X-ray; blood glucose monitoring.

Optimisation: head-up 30°; continuous Replogle tube suction of upper pouch; IV access; delay surgery if severe RDS/prematurity.

Induction: avoid bag-mask ventilation; inhalational induction maintaining spontaneous ventilation; intubate WITHOUT NMB; advance ETT into right main bronchus then withdraw until bilateral breath sounds heard (tip just above carina, distal to fistula), or use fibreoptic bronchoscope directly.

Ventilation: lowest peak pressure maintaining SpO₂/ETCO₂; permissive hypercapnia (PaCO₂ 50–60); if gastric distension → emergency gastrostomy.

Postop: elective ventilation 24–72h; neck flexed 7–10 days; parenteral nutrition; monitor for anastomotic leak and tracheomalacia.

VOO/DOO = asynchronous (fixed rate) modes used under magnet; VVIR = VVI with rate-adaptive function.

Preop: identify device type; determine pacemaker-dependency; contact device clinic for reprogramming to asynchronous mode if monopolar diathermy planned; deactivate ICD anti-tachycardia therapy before surgery.

Intraoperative: use bipolar diathermy where possible; short bursts <5s, minimum power, return pad away from device; external pacing/defibrillation immediately available; continuous ECG + SpO₂.

Postop: device interrogated and reprogrammed to original settings; document management in anaesthetic record.

Aspirin: continue throughout — incremental bleeding risk modest vs high thrombosis risk if stopped.

Clopidogrel: if surgery can wait — defer to ≥6 months, then stop 5 days before surgery. If cannot defer — cardiologist involvement; bridging with IV GPIIb/IIIa inhibitors is observational-evidence only and largely not recommended by current ACC/AHA guidance; if continued through surgery — accept higher bleeding risk, use cell salvage, avoid neuraxial.

Standard cemented THR BCIS protocol: FiO₂ 1.0 pre-cementation, fluid preload, ephedrine ready, canal lavage, venting.

VTE prophylaxis: mechanical from induction; LMWH from 12h postop, coordinated with haematology if clopidogrel continued.

Neurological: document level/completeness of paraplegia; autonomic dysreflexia risk if lesion above T6.

Obstetric: gestational age; fetal wellbeing; obstetric team involvement; emergency CS plan.

TB status: which ATT drugs (HRZE); liver function (rifampicin hepatotoxicity); sputum status.

Drug interactions: rifampicin is a potent CYP450 inducer → reduces duration of opioids, NMBs (vecuronium); minimal effect on volatiles.

Pregnancy: oedematous airway, reduced FRC, rapid desaturation, aspiration risk → RSI protocol mandatory.

Positioning: lateral decubitus for anterolateral decompression — maintain left lateral tilt even in lateral position to avoid aortocaval compression.

GA with RSI: antacid prophylaxis; rocuronium 1.2mg/kg (avoid succinylcholine if paraplegia >6 months — hyperkalaemia risk).

Maintenance: sevoflurane <1MAC; avoid N₂O; maternal MAP ≥65mmHg for uteroplacental perfusion.

Continuous CTG intraoperatively if >24 weeks gestation; emergency CS trolley/neonatology on standby.

NMB dosing: rifampicin shortens vecuronium/rocuronium duration — monitor with quantitative TOF; reverse with sugammadex.

Analgesia: IV morphine PCA; avoid NSAIDs >32 weeks (ductus arteriosus closure).

TB precautions: respiratory isolation, staff PPE, resume ATT within 24–48h.

Continuous CTG 24h postop; VTE prophylaxis (paraplegia + pregnancy = very high risk).

RCOG Category 1: immediate threat to mother/fetus; decision-to-delivery target <30 min. If functioning epidural → top-up (fastest); if not, single-shot spinal (5–10 min available) or GA with RSI (immediately life-threatening).

Pre-eclampsia worsens the airway: facial/laryngeal oedema, higher Mallampati class; video laryngoscope first-line.

Modified RSI: attenuate hypertensive response to laryngoscopy with alfentanil 10–20mcg/kg or remifentanil 1mcg/kg or labetalol 10–20mg, plus thiopentone 4–5mg/kg and rocuronium 1.2mg/kg.

Standard block: heavy bupivacaine 0.5% 2–2.5mL + fentanyl 15–25mcg + morphine 100mcg, T4–T6 level; co-load 500mL with spinal (not pre-load) to avoid pulmonary oedema.

Target: systolic <160mmHg, diastolic <110mmHg; avoid acute MAP reduction >20–25% (uteroplacental perfusion is pressure-dependent).

IV labetalol 20mg boluses (max 300mg, avoid in asthma); IV hydralazine 5–10mg; oral nifedipine 10mg if no IV access.

Left DLT preferred (right DLT risks RUL orifice occlusion), even for right-sided VATS; size 39/41 Fr for male patient; confirm with fibrescope.

Bronchial blocker (Arndt/EZ-Blocker) if DLT placement anticipated difficult.

Dependent lung ventilation: TV 4–6mL/kg IBW, PEEP 5cmH₂O, plateau ≤25cmH₂O, FiO₂ 1.0 initially.

If hypoxia (<90%): FiO₂ 1.0 → PEEP dependent lung → recruitment → CPAP to operative lung → switch to TIVA → consider brief two-lung ventilation.

Thoracic epidural (T4–T6) is gold standard for open thoracotomy; for VATS, paravertebral block (equivalent analgesia, fewer side effects) increasingly preferred.

Serratus anterior plane block (emerging); multimodal with paracetamol/NSAIDs/low-dose opioids.

Withheld traditionally due to lactic acidosis risk if renal function deteriorates (metformin accumulates, inhibits Complex I). For minor procedures under topical anaesthesia (no fasting, no contrast) metformin can generally be CONTINUED per updated SIGN/NHS guidance.

Long-term steroids suppress the HPA axis — relative adrenal insufficiency under stress. Cataract under topical = MINOR stress (~5–10mg hydrocortisone equivalent) — does NOT require additional cover beyond usual morning dose. If GA used → hydrocortisone 25mg IV at induction (moderate stress).

Target 6–10 mmol/L perioperatively; usual oral agents continued for this topical anaesthesia case; steroids cause hyperglycaemia — vigilance for postop rise.

Trigeminovagal reflex: traction on extraocular muscles/globe pressure → V1 afferent → brainstem → vagal efferent → bradycardia/asystole. Management: surgeon releases traction immediately; atropine 0.3–0.6mg IV if persistent; prophylactic atropine not routinely recommended.

Definition: TOFR <0.9 at extubation/recovery, measured by quantitative monitoring (acceleromyography/EMG) at adductor pollicis.

Incidence: 20–40% with clinical criteria alone; ~40% with neostigmine reversal; >98% achieve TOFR≥0.9 within 3 min with sugammadex 2mg/kg.

• Upper airway obstruction — genioglossus/pharyngeal dilators more sensitive than adductor pollicis; impaired at TOFR 0.7–0.8
• Impaired swallowing/aspiration — cricoarytenoid sensitivity
• Blunted hypoxic ventilatory response (~50% of normal at TOFR<0.9)
• Hypoventilation and CO₂ retention
• Grosse-Sundrup (Lancet 2012): sugammadex vs neostigmine reduced pneumonia, reintubation, unplanned ICU admission

Hydrotherapy, TENS, massage/acupuncture/hypnobirthing — modest analgesic effect, no maternal/fetal side effects.

Entonox (50% N₂O/O₂): onset 30–45s, inhaled before contraction peak; ~50–60% find helpful but most progress to epidural; nausea/dizziness common; occupational exposure risk to staff.

Uniquely suited to labour PCA (onset 30–90s, context-sensitive half-time 3 min) — timed to contraction cycle.

Protocol: 40mcg bolus, 2-min lockout, no background infusion. Superior to pethidine, inferior to epidural.

Achieves complete/near-complete pain relief in >95%; Cochrane review confirms superiority over all other methods; NICE recommends offering to all who request it.

Technique: L2–L3/L3–L4; test dose 3mL 2% lidocaine + adrenaline 1:200,000; loading 10–15mL 0.1% bupivacaine + fentanyl.

'Walking epidural': 0.0625–0.1% bupivacaine + fentanyl — preserves motor function.

Complications: PDPH (1–2%), inadequate analgesia (5–15%), hypotension, motor block, urinary retention; rare: epidural haematoma/abscess, total spinal.

CSE: intrathecal bupivacaine 2.5mg + fentanyl 25mcg gives immediate dense analgesia within 5 min; catheter for maintenance — faster onset than epidural alone.

Pudendal block: perineal analgesia for delivery/instrumental delivery only, no uterine pain relief. Paracervical block: largely abandoned (fetal bradycardia risk).

TV 6–7mL/kg IBW; RR ↑15–25% for CO₂ absorption; PEEP 6–10cmH₂O; I:E 1:2 (extend to 1:2.5 if pressures high); permissive hypercapnia (PaCO₂ 50–55) if plateau >30cmH₂O; continuous capnography, ABG every 60–90min.

After prolonged Trendelenburg (3–5h): facial/conjunctival/laryngeal oedema. Perform cuff leak test before extubation; IV dexamethasone 8mg; head elevated 30–60 min pre-extubation; have Airway Exchange Catheter ready.

CO₂ absorbs infrared light at 4.26μm (mid-IR). Absorbance = ε × C × L — absorbed light directly proportional to CO₂ concentration.

Sidestream: gas aspirated at 150mL/min, slight delay (1–3s), suitable for non-intubated patients. Mainstream: sensor at airway, no delay, requires ETT.

RSI: persistent consistent waveform over ≥6 breaths confirms tracheal placement; flat line/2 waves then zero suggests oesophageal intubation.

Cardiac arrest: ETCO₂<10mmHg = poor CPR quality/poor prognosis; sudden rise to ≥35–40mmHg = ROSC indicator, precedes palpable pulse.

Located in each non-O₂ gas line; held open only when O₂ supply pressure ≥30psi is present; if O₂ pressure falls → all other gases shut off.

Mechanically (Ohmeda Link-25) or pneumatically (Dräger ORC) links O₂/N₂O flow control to ensure FiO₂ ≥25%. Limitation: ensures the FLOWMETER RATIO is correct, but cannot detect pipeline crossing.

Intrinsic response of pulmonary arteriolar smooth muscle to regional alveolar hypoxia (PAO₂<70mmHg) — can reduce blood flow to a collapsed segment by ~50%.

Phase 1 (seconds–minutes): ↓PAO₂ → altered mitochondrial ROS signalling → inhibits voltage-gated K⁺ channels (Kv1.5/Kv2.1) → depolarisation → L-type Ca²⁺ channel activation → Ca²⁺ influx → MLCK activation → smooth muscle contraction. Simultaneously ↓NO/prostacyclin removes tonic vasodilation.

Phase 2 (hours–days): Prolonged hypoxia → HIF-1α stabilisation → ↑endothelin-1, ↑VEGF, ↓eNOS — sustained structural component underlying pulmonary hypertension of chronic hypoxaemia.

During OLV, maximal HPV stimulus in the collapsed lung reduces its flow by ~50%, but ~35–50% shunt persists. TIVA preserves HPV → 15–25mmHg higher PaO₂ vs equiMAC volatile.

Stepwise hypoxia management: FiO₂ 1.0 → PEEP to ventilated lung → recruitment → CPAP to operative lung → brief two-lung ventilation as last resort.

Low λ → poor blood sink → rapid rise in alveolar concentration → fast induction/emergence. Metabolism: CYP2E1 → hexafluoroisopropanol (non-toxic, glucuronidated) + inorganic fluoride (peaks 15–30μmol/L, below the 50μmol/L nephrotoxic threshold; no demonstrated clinical nephrotoxicity).

Non-pungent — ONLY volatile suitable for inhalational induction in adults/children. Bronchodilator; useful in asthma.

vs desflurane: GWP 130 vs 2540 (19× lower); atmospheric lifetime 1.1yr vs 14yr; no sympathetic activation tachycardia; standard room-temperature vaporiser vs heated pressurised TEC-6.

MAC = alveolar concentration at 1 atm preventing purposeful movement to skin incision in 50% of unpremedicated subjects at steady state (age 40, reference standard).

Why alveolar? At steady state alveolar partial pressure = brain partial pressure (Henry's law); alveolar concentration is measurable via ETCO₂-like monitoring.

MAC measures spinal cord-mediated immobility, NOT unconsciousness (which occurs at ~0.3–0.4 MAC = MAC-awake). At 1MAC, 50% move; 1.3MAC≈ED95.

Not significantly affected: sex, height, duration of anaesthesia, PaCO₂ (20–90mmHg), PaO₂>40mmHg, mild acid-base changes.

Two ACh molecules joined via acetyl groups (bisquaternary ammonium).

Phase I block: binds and ACTIVATES nicotinic AChR (fasciculations) → NOT hydrolysed by AChE (requires plasma pseudocholinesterase) → sustained depolarisation → Na⁺ channel inactivation → flaccid paralysis. NO fade on TOF; augmented (not antagonised) by anticholinesterases.

Hydrolysis by plasma pseudocholinesterase → succinylmonocholine → choline+succinic acid; duration 10–15 min; onset 60–90s at 1–1.5mg/kg.

With repeated/prolonged dosing (>3–5mg/kg), block develops non-depolarising characteristics: FADE on TOF, post-tetanic potentiation, PARTIALLY reversible by neostigmine — from receptor desensitisation.

• RSI — fastest onset of all NMBs with short duration; rocuronium+sugammadex now an equivalent alternative
• Laryngospasm treatment: 0.5–1mg/kg IV (or 3–4mg/kg IM)
• Brief procedures (ECT) where rapid offset is advantageous

Unionised LA crosses axonal membrane, re-ionises intracellularly, and binds the Na⁺ channel from the cytoplasmic face (domain IV-S6) → blocks Na⁺ influx → conduction fails.

Use-dependent block: the receptor site is accessible only when channels are OPEN/INACTIVATED. High-frequency-firing C fibres (pain) accumulate more block at a given concentration — the basis of differential block.

Order of block: autonomic B fibres → C fibres (pain/temp) → A-delta → A-beta (touch) → A-alpha (motor). C fibres block first (small, high-frequency firing); motor blocked only at higher concentrations.

Walking epidural application: 0.0625–0.1% bupivacaine gives sensory block while preserving motor function.

Layers penetrated: skin → subcutaneous fat → supraspinous ligament → interspinous ligament → ligamentum flavum (LOR) → epidural space → dura mater → arachnoid mater (true puncture) → subarachnoid space (CSF).

Safe insertion: L3–L4 or L4–L5 (conus ends at L1 in adults, L3 in neonates). CSF volume ~35–60mL, lower in elderly/obese/pregnant → wider spread per dose.

Position: sitting or lateral decubitus, full lumbar flexion. Needle: 25–26G pencil-point (Whitacre/Sprotte) — lower PDPH (1–2%) vs cutting bevel (10–15%).

Identification: free-flowing clear CSF confirms subarachnoid position; rotate 90° if no CSF; withdraw if blood-stained or paraesthesia.

Baricity is most important: hyperbaric sinks to dependent areas; isobaric is position-independent. Position during/after injection determines settling in hyperbaric solutions. Dose/volume matters most for isobaric; age/height affect spread per dose.

Contents: epidural fat (LA depot), Batson's venous plexus (engorged in pregnancy → reduced volume), spinal nerve roots. LF thickest at L3–L4 (5–6mm).

Loss of Resistance (LOR): 16–18G Tuohy needle through supraspinous→interspinous→ligamentum flavum with continuous pressure on saline-filled syringe; sudden easy injection confirms entry.

Catheter threaded 3–5cm into space. Test dose: 3mL 2% lidocaine + 1:200,000 adrenaline — IV catheter → tachycardia ≥20bpm within 60s; intrathecal catheter → dense bilateral motor block within 3–5min.

Accidental dural puncture (1–2%): re-site adjacent level, or thread intrathecal catheter for continuous spinal, or blood patch. Epidural haematoma (<1:150,000): urgent MRI, decompression within 8h. Epidural abscess: MRI, IV antibiotics ± drainage. High/total epidural: manage as total spinal.

Autosomal dominant; RYR1 mutations (~70%), CACNA1S (~1%). Normal contraction: T-tubule depolarisation → DHPR conformational change → RyR1 opens → controlled SR Ca²⁺ release → contraction → SERCA reuptake.

MH event: mutant RyR1 is abnormally sensitive/slow to close; trigger contact → massive uncontrolled Ca²⁺ release → sustained contraction (rigidity) → ATP consumed at enormous rate → anaerobic glycolysis → lactic acidosis → heat → hyperthermia → rhabdomyolysis → AKI, hyperkalaemia, arrhythmia.

Cooling: ice packs axillae/groin/neck, cold IV saline 4°C 15mL/kg, target <38.5°C. Hyperkalaemia: calcium gluconate, insulin+dextrose, bicarbonate. Rhabdomyolysis: fluids, urine alkalinisation to prevent AKI. Arrhythmia: procainamide/lidocaine, avoid CCBs.

General incidence: Sandin (Lancet 2000) 0.18%; NAP5 UK (2014) 1 in 19,600 (0.005%) with potential harm.

• Obstetric emergency CS under GA — highest risk, 1 in 250 (0.4%)
• Cardiac surgery — 1 in 500 (opioid-based technique, bypass dilutes volatile)
• Trauma RSI — 1 in 500 (haemodynamic instability limits depth)
• Difficult airway/failed intubation, chronic alcohol/opioid use, equipment failure (vaporizer/pump/disconnection)

Maintain volatile ≥0.7 MAC-equivalent (above MAC-awake 0.3–0.4); benzodiazepine premedication in high-risk groups; TIVA requires reliable propofol delivery with anti-free-flow pumps and pressure-monitoring lines.

If detected intraoperatively: immediately deepen anaesthesia, reassure verbally, give midazolam 2mg IV for amnesia.

Postop: structured interview (Modified Brice Interview) in all high-risk/reporting patients. Transparent disclosure is ethically mandatory. PTSD develops in ~30% of those with awareness — early psychological referral (CBT/EMDR) can prevent full PTSD. Document, report via incident system/national database, investigate the anaesthetic record for the likely cause.

The vomiting centre (medullary reticular formation) receives afferent input from four sources, each with specific neurotransmitters — the targets of antiemetic drugs.

• TIVA with propofol instead of volatile (reduces PONV 25–30%)
• Minimise opioids via multimodal analgesia
• Adequate IV hydration
• Avoid N₂O and neostigmine where possible (use sugammadex)
• Adequate preoperative anxiolysis

Apfel 0–1: minimal/no prophylaxis. Apfel 2: two antiemetics, different classes. Apfel 3: three antiemetics + consider TIVA. Apfel 4: maximum multimodal (TIVA + 3–4 antiemetic classes + scopolamine patch). Treatment of established PONV: use a DIFFERENT class from any prophylaxis already given; do not repeat the same agent within 6 hours.

Autoimmune mechanism: MG results from autoantibody-mediated destruction and functional impairment of the postsynaptic nicotinic acetylcholine receptor (nAChR) at the neuromuscular junction; Anti-AChR antibodies are present in 85% of patients (complement-activating IgG1 and IgG3); Anti-MuSK (musclespecific kinase) antibodies in 10%; seronegative MG (~5%) — antibodies against LRP4 or other targets Thymic abnormality in ~80%: thymoma in 10–15% (often aggressive, paraneoplastic); thymic hyperplasia in 60–70%; the thymus drives autoreactive T-cell sensitization against AChR — thymectomy produces remission in 30–40%, improvement in 70–80%

NMJ consequence: Anti-AChR Ab → complement activation → receptor degradation, cross-linking and endocytosis → fewer functional AChRs → smaller end-plate potential for each ACh quantum released → more quanta needed to reach action potential threshold → with repetitive stimulation, the ACh store depletes faster than it is replenished → progressive failure of neuromuscular transmission = FATIGABLE WEAKNESS — the hallmark of MG

Osserman Classification Features Anaesthetic Risk

Class I — Ocular Ptosis and diplopia only; no bulbar or limb weakness Lowest risk; rarely requires post-op ventilation

Class IIa — Mild generalised Generalised weakness, predominantly limb; mild bulbar Moderate risk; monitor closely post-op

Class IIb — Moderate generalised Moderate generalised weakness with significant bulbar involvement High risk; plan for post-op ventilatory support

Class III — Acute severe Rapid onset of severe generalised weakness; respiratory muscles ± Very high risk; plan ICU post-op

Class IV — Late severe Severe generalised from Class I/II after ≥2 years Very high risk

Class V — Intubated Requiring intubation for respiratory failure (myasthenic crisis) In crisis; stabilise before any elective surgery

Spirometry: FVC and FEV1 — FVC <2.9 L = high post-operative ventilation risk; FVC <40 mL/kg = very high risk

NIF (Negative Inspiratory Force): worse than −25 cmH₂O = likely ventilator-dependent post-operatively

ABG: CO₂ retention (elevated PaCO₂) indicates severe disease with impaired ventilatory reserve

CT chest: thymoma size, tracheal deviation, substernal extension, mediastinal involvement

Drug Perioperative Management Rationale Pyridostigmine (neostigmine, Continue on morning of surgery with sip of water; do NOT Abrupt withdrawal → myasthenic crisis; helps maintain NMJ function mestinon) abruptly withdraw through induction Steroids (prednisolone) Continue; give stress dose hydrocortisone 100 mg IV at Adrenal suppression from long-term steroids; surgical stress dose induction required Azathioprine, mycophenolate Continue; note immunosuppression increases infection risk Abrupt cessation can worsen disease Plasmapheresis (3–5 sessions) If poorly controlled — start 2–4 weeks before elective Removes circulating anti-AChR antibodies; temporary improvement Plasmapheresis (3–5 sessions) If poorly controlled — start 2–4 weeks before elective Removes circulating anti-AChR antibodies; temporary improvement thymectomy (4–8 weeks) IVIG 2 g/kg over 5 days Alternative to plasmapheresis for preoperative optimisation Modulates immune response; effect lasts 4–8 weeks

Standard IV induction: propofol or thiopentone; ketamine relatively contraindicated (increases sympathetic tone and may worsen laryngospasm in bulbar MG)

Airway: careful assessment for bulbar weakness and aspiration risk; rapid sequence induction if bulbar MG present (aspiration risk from impaired swallowing) Topical airway anaesthesia for awake fiberoptic intubation if severely compromised

Continuous quantitative NMJ monitoring (acceleromyography/TOF-Watch) at the ulnar nerve throughout — mandatory; set a TOF ratio threshold of ≥0.9 for extubation, same as in non-MG patients but even more critically enforced

Standard monitoring: SpO₂, ETCO₂, invasive arterial BP (for blood gas assessment and beat-to-beat BP during sternotomy/VATS approach), CVP if mediastinal surgery

Temperature monitoring — hypothermia worsens NMJ transmission impairment in MG BIS or entropy monitoring for depth of anaesthesia — important if volatile agents are used as the primary "muscle relaxant" at high doses

TIVA preferred by many centres: propofol + remifentanil infusion; remifentanil provides excellent intraoperative analgesia with very brief post-infusion effects; propofol does not significantly affect NMJ function; no volatile agent effects on respiratory function at emergence

If volatile used: sevoflurane preferred (less airway irritation, suitable for potential bronchoscopy); desflurane is acceptable; halothane AVOIDED (exacerbates NMJ block)

Parameter Detail Extubation TOF ratio ≥0.9 (quantitative monitoring); FVC ≥15 mL/kg (ideally ≥20 mL/kg); NIF better than −25 cmH₂O; alert, following commands; adequate criteria (MG) swallow/gag reflex; normothermia; pain controlled; no ongoing residual NMB Post-op Plan for ICU admission; ventilate overnight; gradually wean using pressure support; daily extubation readiness assessment; restart pyridostigmine via ventilation (if NGT when bowel sounds return Leventhal ≥3) Myasthenic Acute respiratory failure from worsening MG — triggers: inadequate immunosuppression, infection, stress, drugs, surgery itself; treatment: intubate crisis and ventilate, plasmapheresis (most rapid effect), IVIG, increase steroids, eliminate trigger; withhold anticholinesterases if excessive secretions (cholinergic crisis possible)

Cholinergic Both cause weakness — differentiate by edrophonium (Tensilon) test: 2 mg IV → if myasthenic crisis → temporary improvement; if cholinergic crisis crisis vs → worsens (excessive ACh); or by clinical signs: cholinergic = SLUDGE (salivation, lacrimation, urination, defecation, GI cramps, emesis) + myasthenic bradycardia + miosis crisis Analgesic Thoracic epidural or paravertebral block (VATS/sternotomy); minimise systemic opioids (respiratory depression particularly hazardous); NSAIDs + strategy paracetamol as baseline multimodal; avoid morphine PCA without close monitoring

Beach chair / sitting position (45–90° trunk elevation): posterior fossa neurosurgery (Fowler's position — head in Mayfield pins, trunk upright), shoulder arthroscopy, ENT procedures; creates the risks described below

Key anatomical problem: the brain is above the level of the heart → cerebral venous pressure is subatmospheric (negative) → open dural sinuses and bone marrow sinuses act as open tubes at negative pressure → air can be entrained with each inspiration or surgical manipulation

Hypotension — The Most Common Complication Venous pooling in the lower limbs from gravity → ↓ venous return → ↓ cardiac output → ↓ MAP; compounded by general anaesthesia (vasodilation, reduced cardiac reserve)

Critical CPP calculation for sitting position: MAP is measured at arm/heart level, but the brain is above this reference point; for every centimetre of head elevation above the right atrium, subtract 0.77 mmHg from the measured MAP to obtain actual cerebral perfusion pressure at the level of the Circle of Willis: CPP = MAP(measured at heart) − (height of brain above heart in cm × 0.77) − ICP

Target: maintain CPP ≥70 mmHg at brain level; this may require MAP at arm level of 80–100 mmHg if the head is 30–40 cm above the heart (30 cm × 0.77 = 23 mmHg correction)

Management: adequate IV fluid loading before positioning; graduated compression stockings + abdominal binders to reduce venous pooling; vasopressors titrated to maintain corrected CPP ≥70 mmHg; arterial line at the level of the external auditory meatus (EAM) for accurate "brain-level" blood pressure measurement in some centres

Open venous structures in the surgical field (dural sinuses, diploic veins of skull, epidural veins) + subatmospheric venous pressure (brain above the heart) → pressure gradient drives room air into the venous system with each surgeon's cut, dissection, or drill → air enters right atrium and right ventricle → large air bolus can obstruct the right ventricular outflow → pulmonary arterial air lock → acute right heart failure, sudden loss of cardiac output → death. Small boluses: air distributes to the pulmonary vasculature → microvascular obstruction → ventilation-perfusion mismatch → pulmonary hypertension → increased dead space → ETCO₂ falls.

Incidence: 25–40% by precordial Doppler in posterior fossa surgery in the sitting position; clinically significant in 10–15%

Paradoxical Air Embolism (PAE): if a patent foramen ovale (PFO) is present (~25–30% of the general population), air in the right atrium can cross to the left atrium via the PFO → arterial circulation → coronary air embolism (MI), cerebral air embolism (stroke); PAE makes VAE potentially lethal even with small volumes of air

Minimum Volume Rank Monitor What It Detects Detectable 1 (Most Precordial Doppler frequency shift from air bubbles in the right heart — characteristic "mill wheel" murmur (loud, As little as 0.05 mL/kg of air sensitive) Doppler churning, machinery-like sound); probe placed over the right cardiac border (4th intercostal space, right sternal edge) 2 Transoesophageal Direct visualisation of air bubbles in right atrium and right ventricle; also detects PFO (bubble test — ~0.05 mL/kg; same echocardiography injection of saline agitated with air through a peripheral vein; bubbles seen crossing from right to left sensitivity as Doppler but (TOE/TEE) atrium = PFO); most specific monitor and can guide aspiration via CVP catheter more specific 3 ETCO₂ Sudden fall in ETCO₂: air emboli create pulmonary dead space (capillaries obstructed → no gas Clinically significant VAE (capnography) exchange → CO₂ not eliminated → ETCO₂ falls despite unchanged ventilation) (~0.5 mL/kg); less sensitive than Doppler for small emboli 4 ETCO₂ − PaCO₂ Pulmonary dead space increase → PaCO₂ rises (CO₂ not eliminated) while ETCO₂ falls or plateaus Significant VAE gradient widens → the arterial-to-end-tidal CO₂ gradient increases (normal <5 mmHg); requires arterial line for simultaneous ABG 5 Expired N₂ monitor Air (78% N₂) entering the pulmonary circulation → N₂ detected in expired gas; requires specialised Small to moderate VAE gas analyser; not routine 6 (Least CVP rise, BP fall, Late signs of haemodynamically significant VAE; CVP rises from right heart outflow obstruction; Large, haemodynamically sensitive) arrhythmia, SpO₂ hypotension from reduced cardiac output; dysrhythmia from right heart distension significant VAE; already a fall crisis

Complication Mechanism Prevention Cerebral Reduced CPP from MAP fall + gravity reduction at brain level; posterior circulation Maintain corrected CPP ≥70 mmHg; arterial line for ischaemia (vertebrobasilar) particularly vulnerable in the sitting position (long route from heart to brain continuous beat-to-beat monitoring; vasopressors; from with gravity against it) avoid excessive head flexion (reduces vertebral artery hypotension blood flow) Quadriplegia Excessive neck flexion → cervical cord ischaemia or direct compression; particularly Lateral skull pins for head fixation; neutral neck position; (catastrophic) dangerous if there is pre-existing cervical stenosis; the "two-finger rule" — maintain at least pre-operative MRI of cervical spine in elderly or patients two finger-breadths between chin and sternum to prevent excessive neck flexion and with known spondylosis; monitor SSEP and MEP vertebral artery compression intraoperatively Paradoxical Air crossing PFO to systemic circulation → cerebral embolism Pre-operative bubble echocardiogram to exclude PFO; air embolism if large PFO present, reconsider sitting position; → stroke intraoperative TOE for detection Peripheral Stretch to brachial plexus from arm position; pressure on ulnar nerve; sciatic nerve stretch Careful arm positioning (neutral, supported, no nerve injuries from extreme hip flexion in beach chair abduction >90°); padding at all bony prominences; avoid extreme hip flexion

Mechanism Pathophysiology Threshold Distinguishing Feature 1. Direct pressure on a nerve against an underlying bony As little as 30 mmHg external Produces maximum injury at the compression Compression prominence → compression of vasa nervorum (the small blood pressure sustained for 2 hours point; endoneurial oedema proximal and distal vessels supplying the nerve fascicles) → ischaemia of nerve → can produce significant to the injury; most common in thin, Wallerian degeneration of axons; also direct mechanical ischaemic nerve injury; lower malnourished patients with reduced protective deformation of nerve fibres at the compression site pressures for longer durations = subcutaneous fat padding equivalent injury 2. Stretch Excessive elongation of a nerve beyond its elastic limit → <15% stretch = tolerable Injury distributed along the stretched segment intraneural fibrosis → disruption of blood supply along the (reversible); >15% sustained (not localised to one point); particularly stretched segment; a nerve tolerates <15% elongation from stretch = ischaemia and axonal common with brachial plexus (arm abduction resting length before ischaemia begins; beyond this threshold, injury; >20% = fascicle rupture >90°), ulnar nerve (extreme elbow flexion), progressive axonal injury occurs and sciatic nerve (extreme hip flexion + knee extension) 3. Ischaemia Hypotension, excessive tourniquet time, arterial occlusion from Vulnerable in: hypotensive Systemic factors (hypotension, anaemia, (vasa positioning (axillary artery compression in lateral position), or patients, those with peripheral vasopressor use) combine with positional nervorum vascular disease reduces oxygen delivery to the nerve fascicles vascular disease, diabetes (pre- factors; explain why the same position that is compromise) below the critical threshold for aerobic metabolism → nerve existing reduced vasa nervorum safe in a healthy patient causes injury in a ischaemia → injury; compounds the effects of compression and blood flow), prolonged cases diabetic or hypotensive one stretch with low MAP

Position at Nerve Mechanism Clinical Deficit Prevention Risk Ulnar Supine, lateral, Compression at medial epicondyle (cubital Clawing of ring and little fingers Supinate or neutral forearm position on arm nerve prone tunnel); especially if forearm is pronated (intrinsic paralysis); weak flexion of ring boards; foam padding at the medial epicondyle; (most (moves the nerve medially, directly over and little fingers; sensory loss over avoid elbow flexion >90°; check arm boards are common the epicondyle) and the elbow is resting on medial 1.5 fingers and medial hand; at same level as body overall — a hard surface without padding; body reduced grip strength; wasting of first ~28% of habitus: males > females (different dorsal interosseous all PNI) anatomy at cubital tunnel)

Brachial Supine, lateral, Stretch: arm abduction >90° from body → Upper plexus (Erb's — C5-C6): weak Never abduct arm >90°; shoulder brace lateral plexus Trendelenburg, excessive tension on upper trunk (C5-C6); shoulder abduction (deltoid), elbow (not medial); axillary roll in lateral position (second prone shoulder brace positioned too medially in flexion (biceps), forearm supination; (placed in axilla, NOT in axilla — the roll should most Trendelenburg → compresses plexus wrist drop (C7 if involved); Lower be placed distal to the axilla at the thoracic wall common) against clavicle and 1st rib; lateral position plexus (Klumpke's — C8-T1): intrinsic to lift the thorax off the dependent shoulder, without axillary roll → compression of lower hand muscle paralysis; claw hand; NOT compress the axilla); check arm position plexus by weight of thorax sensory loss medial forearm and hand every 30 minutes in long cases Radial Lateral, prone, Compression in the spiral groove of the Wrist drop (extensor carpi Ensure arm boards are wide enough; check nerve supine (if arm humerus (where the nerve winds around radialis/ulnaris paralysis); inability to arm position after any repositioning; pad the allowed to fall the mid-humerus) against a hard surface; extend fingers at MCP joints; loss of mid-humerus over the spiral groove; arm should off the arm arm allowed to hang off the side of the arm thumb abduction; sensory loss dorsum never be allowed to hang unsupported board) board in a dependent position of hand (especially 1st web space) and radial aspect of forearm Common Lithotomy, Compression at the fibular head (lateral Foot drop (paralysis of ankle Well-padded stirrups (Lloyd-Davies preferred peroneal lateral knee) — the nerve winds around the fibular dorsiflexion and eversion); inability to over candy-cane for nerve protection); ensure (fibular) decubitus neck immediately subcutaneous; candy- walk on heels; high-stepping gait; no lateral pressure on fibular head; check knee nerve cane stirrups apply direct lateral pressure; sensory loss dorsum of foot and lateral position after every adjustment; limit lithotomy (most lateral decubitus position with weight on lower leg; complete loss of eversion time common the lateral knee (distinguish from L4-L5 disc prolapse leg which affects only dorsiflexion) injury) Femoral Lithotomy, Compression by inguinal ligament from Weak hip flexion; weak knee extension Avoid excessive hip flexion/abduction/external nerve prone extreme hip flexion + external rotation + (quadriceps); absent/reduced knee rotation combination; limit retractor pressure abduction → ligament compressed against reflex; sensory loss anteromedial thigh duration; 2-hour maximum in extreme positions iliopsoas; retractor pressure during pelvic and medial leg (via saphenous surgery branch); difficulty climbing stairs Sciatic Lithotomy, Stretch from hip flexion combined with Mixed deficit depending on division Avoid combined hip flexion >90° + knee nerve prone knee extension (particularly in the modified affected: tibial division — weak extension; adequate padding in prone position; lithotomy position); piriformis muscle plantarflexion, foot inversion, loss of limit total lithotomy time to <4 hours; check compression in prone position; may be Achilles reflex, sensory loss plantar nerve function every hour in prolonged cases compressed by leg holders in lithotomy if foot; peroneal division — foot drop poorly padded Obturator Lithotomy Compression by thigh support against Weak hip adduction; sensory loss Avoid extreme external rotation in lithotomy; nerve obturator canal with extreme hip flexion medial thigh; patient cannot cross legs padded leg holders and external rotation

Padding at all bony prominences: foam, gel pads, or specialised pressure-relieving materials at every point where a nerve is superficial — medial epicondyle (ulnar), fibular head (common peroneal), spiral groove (radial), lateral malleolus (sural), olecranon Arm boards at 90° maximum abduction — NEVER allow arm to abduct more than 90°; check with a protractor or a simple visual reference for long cases

The axillary roll in lateral position: placed under the chest DISTAL to the axilla (at the 4th–5th rib level), NOT in the axilla itself; functions by lifting the thorax off the underlying arm and shoulder, reducing compression of the brachial plexus and axillary vessels by the weight of the body

Time limits: extreme positions (lithotomy, Trendelenburg) should be limited; many recommendations suggest repositioning or reverting every 2–4 hours; at minimum, check and document limb position every 30–60 minutes

Maintain adequate MAP: hypotension compounds positional nerve injury through ischaemia; a MAP ≥65 mmHg is generally recommended intraoperatively; diabetic or vascular disease patients may need higher MAPs

Documentation: document the exact position, padding used, time of positioning, and any position changes in the anaesthetic record — essential for medicolegal defence if PNI occurs; "If it isn't written, it didn't happen"

Pre-existing neuropathy: diabetic patients, those with pre-existing compression neuropathy or cervical/lumbar radiculopathy are at significantly higher risk — identify pre-operatively, document baseline deficit, use extra padding and more conservative positions

Medicolegal Perspective — The "Double Crush" Syndrome Many perioperative nerve injuries may not be caused by a single intraoperative insult but by "double crush" — a nerve that is already partially compromised by pre-existing entrapment or neuropathy (subclinical carpal tunnel syndrome, diabetic neuropathy) becomes symptomatic from an additional minor intraoperative insult that alone would be insufficient to cause injury. This explains why some patients develop PNI despite apparently good positioning — and why pre-operative documentation of neurological baseline status is crucial for both clinical management and medicolegal defence.

The Mapleson classification (1954) categorises non-rebreathing circuits by the relative position of three key components: the fresh gas flow (FGF) inlet, the reservoir bag/APL valve, and the patient connector Bain circuit = Mapleson D (coaxial modification): the FGF enters near the patient end (the machine-end inner tube delivers FGF to the patient connector); the reservoir bag and APL valve are at the MACHINE END — both features defining Mapleson D; the Bain circuit is simply a coaxial version of the Mapleson D, with the inner tube carrying fresh gas and the outer corrugated tube carrying expired gas Mapleson Classification FGF Location Bag/APL Location Rebreathing Efficiency A (Magill's) Near bag (machine end) Near patient (patient end) Most efficient for spontaneous breathing (FGF ≈ MV); least efficient for IPPV B Near patient Near patient Moderate efficiency C (Waters to-and-fro) Near patient Near patient Moderate efficiency D (Bain) Near patient (via inner tube) Machine end Most efficient for IPPV; needs higher FGF for SB than Mapleson A E (Ayre's T-piece) Near patient Open end (no bag) For paediatric use; low resistance F (Jackson-Rees) Near patient Open-ended bag Paediatric standard; allows manual IPPV

The Bain circuit consists of a narrow inner tube (typically 7 mm diameter) running centrally within a wider corrugated outer tube (22 mm diameter). Fresh gas flows: from the FGF inlet at the MACHINE END → along the inner tube → to the PATIENT END (patient connector) — delivering fresh anaesthetic gas close to the patient's airway. Expired gas flows: from the patient → into the outer corrugated tube (surrounding the inner tube) → back toward the MACHINE END where the reservoir bag and APL valve are located.

Thermal exchange advantage: the warm expired gas flowing backward through the outer tube warms the incoming fresh gas in the central inner tube — a counter-current heat exchange effect that helps warm and humidify the fresh gas before it reaches the patient; reduces respiratory heat and moisture loss compared to standard Mapleson D

Length: standard adult Bain circuit is 1.8 metres (some circuits 1.5 m); this length provides adequate reservoir of expired gas in the outer tube while maintaining low resistance

Introduced by: Bain and Spoerel in 1972 in Anaesthesia — hence the eponym

In the Bain/Mapleson D during spontaneous breathing, FGF must be high enough to prevent rebreathing of expired CO₂ from the outer tube

During expiration: expired gas enters the outer tube and fills the corrugated reservoir; during inspiration, if FGF is insufficient, the patient may inhale expired gas from the near end of the outer tube — rebreathing occurs Minimum FGF for spontaneous breathing = 2–3 times the minute volume (MV); for an adult with MV = 5 L/min: FGF = 10–15 L/min; this is higher than Mapleson A (which only needs FGF ≈ MV) — making Bain less efficient than Mapleson A for spontaneous breathing

Mode Required FGF Rationale Spontaneous 2–3× MV = 10–15 L/min Must flush expired CO₂ from the outer tube reservoir before the next inspiration; high FGF requirement breathing (adult) Controlled 70–100 mL/kg/min — During IPPV, gas is actively delivered by the ventilator/hand ventilation, and the pattern of gas flow is more ventilation (IPPV) approximately 5–7 L/min for predictable; partial rebreathing is acceptable and controlled; this lower FGF makes Bain more economical — normocapnia average adult than for spontaneous breathing Paediatric (per 1000 mL/min for infants + 100 Paediatric circuits use Mapleson E/F (Ayre's T-piece, Jackson-Rees) rather than Bain for most children <25– weight) mL/min/kg (simplified Mapleson 30 kg E/F paediatric rule)

Lightweight and portable — no heavy CO₂ absorber or unidirectional valves

Suitable for head and neck surgery — the long circuit keeps the machine away from the surgical field Inspired gas warming by counter-current heat exchange (reduces respiratory heat and moisture loss)

Easy to clean and sterilise — no valves or complex components

Low resistance — suitable for spontaneous breathing (no unidirectional valves to open)

Scavenging easy — single exhaust port at the APL valve

Feature Gastroschisis Omphalocele (Exomphalos) Location of Para-umbilical — ALWAYS to the RIGHT of the umbilicus (very rarely THROUGH the umbilicus — the umbilical ring fails to close; umbilical cord defect left); the umbilical cord is intact and normally inserted inserts at the apex of the sac Sac/covering NO SAC — bowel is completely bare, directly exposed to amniotic fluid; SAC PRESENT — peritoneal sac covered by a membrane; sac may rupture bowel appears thickened, matted, and covered with an inflammatory but initially contains bowel and possibly liver fibrinous "peel"

Associated Rare — isolated bowel malrotation; NO chromosomal associations; 50% associated with chromosomal anomalies (Trisomy 18, 13, 21); cardiac anomalies 15% intestinal atresia (from intrauterine vascular accident) defects in 30%; Beckwith-Wiedemann syndrome (organomegaly, hypoglycaemia, macroglossia)

Surgical EMERGENCY — bare bowel exposed → progressive ischaemia, Semi-elective — sac provides protection; allows 24–48 hours for urgency inflammation, bacterial contamination; surgery within hours cardiac/chromosomal evaluation if stable; ruptured sac = emergency

Liver Liver rarely herniates — too large to exit small paraumbilical defect Liver herniates in ~50% of large defects — makes primary closure much more herniation difficult Bowel Foreshortened, inflamed, matted, no normal peristalsis; prolonged ileus If sac intact: bowel usually normal appearance and function; if sac ruptured: condition at expected post-operatively (weeks); TPN required similar to gastroschisis surgery

Wrap eviscerated bowel immediately in warm, saline-moistened gauze swabs; then cover with transparent cling film (occlusive dressing) — reduces evaporative loss of heat and fluid; maintains bowel warmth; allows visual inspection of bowel colour and perfusion without repeated dressing changes

Positioning: right lateral decubitus — the weight of the bowel falls to the right, preventing kinking of the mesenteric vessels at the bowel-abdominal wall junction; reduces vascular compromise of the herniated gut Never squeeze, compress, or attempt to reduce the bowel manually at the bedside — forced reduction without anaesthesia dramatically raises intraabdominal pressure → inferior vena cava compression → cardiac arrest

Evaporative losses from the exposed bowel in a 2 kg neonate are 3–5× normal insensible losses; neonates have a very small total blood volume (~80–90 mL/kg = 160–180 mL for this 2 kg baby) and limited cardiovascular reserve

IV access: umbilical venous catheter (UVC) — fastest and most reliable access in the neonate; the umbilical vein is large, catheterisation is quick; position tip at the inferior vena cava/right atrial junction (confirmed by X-ray or ETCO₂ monitoring); peripheral IV as backup

Initial fluid bolus: 10–20 mL/kg of normal saline or Ringer's lactate over 10–15 minutes; reassess perfusion; repeat as needed; target urine output >1 mL/kg/hr, improving capillary refill (<3 seconds), improving HR toward 120–160 bpm, restoring MAP ≥40 mmHg in a neonate

Maintenance: 5–10% dextrose in 0.45% NaCl at 4–6 mL/kg/hr; glucose infusion rate 4–6 mg/kg/min to prevent hypoglycaemia (neonatal glycogen stores limited, especially in a stressed, unwell gastroschisis neonate); monitor glucose 1-hourly

NGT decompression: decompress the stomach and bowel via NGT on free drainage — reduces bowel distension, decreases the volume that must be reduced at surgery

Thermal management: overhead radiant warmer; warming mattress; all IV fluids warmed; the neonate's large surface area:body mass ratio makes hypothermia extremely rapid without active warming

Antibiotics: broad-spectrum IV antibiotics immediately (ampicillin + gentamicin ± metronidazole) — the exposed bowel is an open portal for bacterial contamination AVOID mask ventilation/CPAP/bag-mask ventilation before intubation — gas insufflation would distend the bowel, making reduction at surgery even more difficult

Full stomach/aspiration risk from GI obstruction and NGT (stomach not empty) → modified RSI Atropine 20 mcg/kg IV (minimum 100 mcg) before induction — neonates are highly vagotonic; laryngoscopy without prior atropine can cause severe reflex bradycardia and cardiac arrest

Induction: propofol 2–3 mg/kg IV or thiopentone 4–5 mg/kg IV; ketamine 1–2 mg/kg is an alternative (maintains cardiovascular stability in haemodynamically compromised neonate)

Muscle relaxant: suxamethonium 2 mg/kg IV for RSI (neonates require relatively higher doses than adults for equivalent block); alternatively rocuronium 1.2 mg/kg IV with sugammadex 16 mg/kg available

Intubation: use uncuffed ETT (neonatal airway is funnel-shaped — the narrowest point is the subglottis where the cricoid ring constricts the airway; a correctlysized uncuffed tube provides an airtight fit at this level); size: weight/10 + 3.5 = (2/10) + 3.5 = 3.7 → use 3.5 mm ID ETT; depth: weight + 6 = 8 cm at lip

Sevoflurane or isoflurane in O₂/air (avoid N₂O — distends bowel); TIVA with propofol/remifentanil is alternative

Fluid management: maintenance + replacement of surgical losses; gastroschisis surgery involves significant "third-space" losses into the peritoneum as the bowel is handled; typical additional intraoperative losses 10–20 mL/kg/hour; use crystalloid (Ringer's lactate) and colloid (albumin 4.5% if significant haemodynamic instability) Warm all gases and fluids; maintain temperature ≥36.5°C; operating theatre temperature 28°C (neonate) AVOID 100% O₂ — use minimum FiO₂ to maintain SpO₂ 94–98% in preterm; hyperoxia causes retinopathy of prematurity

Post-operative ventilation: almost all gastroschisis neonates require mechanical ventilation post-operatively; primary closure raises IAP → diaphragmatic splinting → impaired spontaneous ventilation; plan ICU admission and continued ventilation for 24–72 hours minimum

Prolonged ileus: the inflamed, peel-covered bowel of gastroschisis recovers function slowly — bowel sounds and function may not return for 2–6 weeks; parenteral nutrition (TPN) via a central line is essential until bowel function is confirmed (absence of bile in NGT, passage of stool, tolerance of enteral feeds)

Analgesia: morphine infusion (10–20 mcg/kg/hr) — provides analgesia and reduces respiratory effort against the ventilator; regional analgesia (caudal or spinal) is rarely feasible in the immediate post-operative period given the abdominal pathology

NEC surveillance: increased risk of necrotising enterocolitis post-gastroschisis (bowel ischaemia from vascular compromise, bacterial colonisation of inflamed bowel, immature gut immunity); monitor for abdominal distension, bloody stools, rising inflammatory markers

Parameter Value Total CSF volume (adult) ~140–150 mL; neonates: 10–60 mL Production rate 500 mL/day (0.35 mL/min); produced continuously by choroid plexus (70%) + ependymal cells (30%) Normal ICP (lateral recumbent) 10–15 mmHg (7–10 mmHg in neonates with open fontanelle) Lateral ventricles (choroid plexus production) → Foramen of Monro (interventricular foramina) → Third ventricle → Aqueduct of Sylvius (most common site of obstruction → non-communicating hydrocephalus) → Fourth ventricle → Foramina of Magendie (median) + Luschka (lateral ×2) → Subarachnoid space (basal cisterns → cerebral convexities) → Arachnoid granulations (Pacchionian bodies) → Superior sagittal sinus (venous absorption)

Drug effects on CSF production: ↑ production: vasodilators, volatile anaesthetics (halothane most, sevoflurane/desflurane least), N₂O; ↓ production: acetazolamide (carbonic anhydrase inhibitor), furosemide, steroids; ↑ absorption: mannitol (raises osmotic gradient), furosemide

Monroe-Kellie doctrine: total intracranial volume = brain + blood + CSF = constant (skull is a rigid box); ↑ in any one component must be compensated by ↓ in another; compensation buffers ICP initially (CSF displaced to spinal subarachnoid space, venous blood expelled); once compensatory mechanisms exhausted → exponential ICP rise

Type Mechanism CSF Pressure Common Causes Obstructive Block WITHIN the ventricular system — CSF cannot flow from High Aqueduct stenosis (most common), tectal glioma, Chiari (non- ventricles to subarachnoid space; all ventricles proximal to the malformation, colloid cyst of 3rd ventricle, posterior fossa communicating) block are dilated tumours Communicating Block OUTSIDE the ventricular system — CSF flows from High (usually) Post-meningitic fibrosis of arachnoid granulations, postventricles to subarachnoid space but absorption at arachnoid SAH blood products blocking granulations, carcinomatous granulations is impaired; all four ventricles dilated meningitis Normal Communicating hydrocephalus with normal or intermittently normal Normal (10–15 Hakim's triad: Wet (urinary incontinence) + Wacky Pressure ICP; pathogenesis incompletely understood; classic triad: Hakim's mmHg) but (dementia) + Wobbly (gait apraxia/ataxia); idiopathic in Hydrocephalus triad intermittent elderly; responds to VP shunt (NPH) spikes Hydrocephalus Apparent ventricular enlargement from brain tissue loss (atrophy); Normal Alzheimer's disease, chronic ischaemia, post-traumatic; ex vacuo ICP is NORMAL; not true hydrocephalus distinguished from true hydrocephalus by normal ICP and lack of periventricular oedema on MRI

Preoperative Assessment

Clinical ICP assessment: Cushing's triad (hypertension + bradycardia + abnormal respirations) indicates severely elevated ICP with brainstem compression — anaesthetic induction in this state requires extreme care (avoid further ICP elevation from laryngoscopy, coughing, straining) GCS, pupillary reflexes, CT scan (ventricle size, midline shift, evidence of herniation) Full stomach? — urgent VP shunt for acute hydrocephalus → aspiration precautions mandatory

Induction — The Most Critical Phase in Raised ICP

Tier Intervention Mechanism 1 Head position: 15–30° head-up; neutral neck Improves jugular venous drainage → reduces cerebral venous blood volume → lowers ICP 2 Normocapnia (PaCO₂ 35–40 mmHg); normoxia (SpO₂ >95%); Hypercapnia → cerebral vasodilation → ↑CBV → ↑ICP; hypoxia → cerebral oedema; fever normothermia → ↑CMRO₂ → ↑CBF → ↑ICP 3 Osmotherapy: mannitol 0.5–1 g/kg IV or 3% hypertonic saline Osmotic gradient draws interstitial water out of brain → reduces cerebral volume → 3–5 mL/kg reduces ICP; effect within 15–20 minutes; lasts 3–4 hours 4 Controlled hyperventilation (PaCO₂ 30–35 mmHg) — Hypocapnia → cerebral vasoconstriction → ↓CBV → ↓ICP; effect immediate but tolerance TEMPORARY ONLY develops within 4–6 hours; brain ischaemia risk if prolonged; used ONLY as bridge to definitive treatment 5 Barbiturate coma (thiopentone 3–5 mg/kg boluses, infusion 1– Maximum CMRO₂ reduction (burst-suppression EEG = 50% CMRO₂ reduction); reserves (salvage) 5 mg/kg/hr) targeting burst-suppression EEG; decompressive for refractory ICP not controlled by tiers 1–4 craniectomy

Device Key Feature Sizes Specific Advantage Arndt Wire- Contains a wire loop at the tip that couples to the fiberoptic bronchoscope (FOB) — the FOB 5, 7, 9 Fr Most widely used; the wire-loop coupling Guided is threaded through the loop, then advanced under direct vision into the target bronchus; the makes bronchoscope-guided positioning Blocker blocker follows the bronchoscope and wire; once positioned, the wire is removed leaving the very reliable; 9 Fr has a large central channel lumen allowing CPAP to the operative lung Cohen Tip- A wheel mechanism at the proximal end deflects the blocker tip up to 90° in any direction — 9 Fr More directional control; useful when the Deflecting allows steering into the target bronchus under FOB vision; no need for wire coupling Arndt wire cannot reach the target bronchus; Blocker large central lumen for CPAP Fuji Pre-shaped curved tip; positioned under FOB guidance; no wire; simple design; the curve 5, 9 Fr Simplest design; can be used with any Uniblocker directs the blocker toward the target bronchus when rotated single-lumen ETT ≥7.5 mm ID; lower cost (Coopdech) EZ-Blocker A Y-shaped device with two cuffs — one for each main bronchus; inserted through the ETT Universal Can switch operative side quickly; positioned (Y-shaped) and positioned at the carina; one cuff is inflated to block the operative bronchus; allows at carina (very stable — rarely displaced); switching to block either side without FOB repositioning the Y-shape means it straddles the carina Torque Designed for paediatric use; smaller profile; positioned under FOB guidance Paediatric Provides OLV option in children where DLTs Control sizes are not available (<8 years, <30 kg) Blocker (Vitaid)

ETT size requirement: a standard single-lumen ETT of at least 7.5–8.0 mm ID is needed to accommodate both the bronchial blocker and the fiberoptic bronchoscope simultaneously (the FOB occupies ~4 mm; the blocker ~5–9 Fr); some centres use a dedicated multiport airway adapter that allows simultaneous passage of the blocker, bronchoscope, and ventilation circuit without circuit disconnection Step-by-step (Arndt wire-guided example): 1. Intubate with a ≥7.5 mm ETT; connect multiport adapter to ETT hub 2. Insert the Arndt blocker through the blocker port of the multiport adapter (blocker wire loop at the tip) 3. Insert the FOB through the bronchoscope port of the adapter; thread the FOB through the wire loop of the Arndt blocker 4. Advance the FOB under direct vision into the TARGET bronchus (left for left-sided surgery; right for right-sided surgery in most cases); once the FOB is in the correct bronchus, the blocker wire loop guides the blocker to follow the FOB into the same bronchus 5. Remove the FOB; inflate the blocker cuff with 5–8 mL air under direct FOB vision (re-insert FOB to confirm blocker position) — cuff inflated in the bronchus creates the seal for OLV 6. Remove the wire; ventilate the contralateral lung through the ETT lumen; the blocker allows the operative lung to collapse through passive resorption of gas through the inflated cuff

Feature Bronchial Blocker (via SLT) Double-Lumen Tube (DLT)

Ease of Easier overall — DLT requires specific technique; BB allows use of familiar SLT; FOB More complex; requires correctly-sized DLT (left DLT most insertion guidance ensures accuracy common — avoids right upper lobe orifice occlusion); DLT malposition is common Lung Adequate; but lung collapse takes LONGER (10–15 min via passive gas resorption vs 3– Faster lung collapse — the bronchial lumen can be actively isolation 5 min with DLT active venting) suctioned and the lung deflated; better surgical exposure quality more rapidly

Ability to Limited — the central lumen of the blocker is narrow (allows CPAP delivery but not Full suctioning capability through the bronchial lumen; can suction effective suctioning); cannot clear secretions from operative lung clear blood, secretions from operative lung operative lung

CPAP to Possible through the central lumen of larger blockers (9 Fr): apply 5 cmH₂O CPAP to the Possible through the bronchial lumen; same CPAP strategy operative partially collapsed operative lung to improve oxygenation available lung

Risk of HIGHER — the blocker can migrate proximally during surgical manipulation; Lower displacement risk once correctly secured; DLT is displacement displacement mid-surgery restores two-lung ventilation suddenly; displacement distally more rigid and secured at the ETT hub level can cause complete contralateral bronchial occlusion Preferred Difficult airway (use existing SLT); already intubated with SLT; children (no appropriate Elective thoracic surgery; rapid lung collapse needed; need clinical DLT size); tracheostomy; right upper lobe surgery (right-sided DLT risks RUL occlusion) for frequent intraoperative suctioning; most thoracic cases scenarios in adults Post-op Deflate cuff; remove blocker; leave SLT for post-op ventilation; can extubate from the SLT Must exchange DLT for SLT post-operatively if mechanical management directly ventilation needed (DLT is uncomfortable and highresistance for prolonged ventilation)

Risk Factor Higher Risk Lower Risk Device type Hollow-bore needle (higher volume blood inoculation — syringes, IV Solid needle (suture needle, lancet — less blood volume transferred) cannulae, blood gas needles) Depth of injury Deep puncture wound (needle passed completely through tissue) Superficial scratch

Visible blood on YES — visible blood increases viral inoculation volume No visible blood device Source patient High viral load (AIDS, untreated HIV, AIDS-defining illness, CD4 <200) Undetectable viral load on effective ART (extremely low risk — but viral load PEP still recommended) Exposure route Parenteral (needle/sharp); mucous membrane to high-titre blood Intact skin contact (essentially no risk) Bloodborne Transmission Risk (hollow-bore needle) Risk Modifiers Virus HIV ~0.3% (1 in 333) Deep injury + visible blood + high viral load → up to 0.9%; undetectable viral load → much lower but not zero HBV 6–30% depending on HBeAg status (HBeAg positive source = up to Highest risk of all three BBVs; vaccination provides near-complete protection 30%; HBeAg negative = 1–6%) HCV ~1.8% (1 in 55) No effective PEP or vaccine; higher risk if HCV RNA positive source

HBV Exposure HCW Vaccination Status Anti-HBs Titre Action Vaccinated and responder Anti-HBs ≥10 No action needed — fully protected; document and reassure mIU/mL Vaccinated but non-responder or <10 mIU/mL or Check anti-HBs titre immediately; if <10: HBIG 0.06 mL/kg IM + HBV booster dose simultaneously (in different unknown titre unknown sites); retest anti-HBs at 1–2 months Unvaccinated N/A HBIG 0.06 mL/kg IM within 24 hours of exposure (most effective within 12 hours) + initiate full HBV vaccination series (0, 1, 6 months) simultaneously HCV Exposure There is NO effective PEP for HCV and NO vaccine available

Management: baseline HCV antibody (anti-HCV) and HCV RNA at time of exposure; repeat HCV RNA at 4–6 weeks (HCV RNA becomes detectable 1–2 weeks after infection — earlier than antibody); repeat anti-HCV and ALT at 3 and 6 months

If HCV infection is confirmed (HCV RNA positive): refer to hepatologist; modern direct-acting antivirals (DAAs — sofosbuvir-based regimens) can achieve >95% SVR (sustained virological response = cure) when treatment is started in the acute phase (within weeks of infection); early treatment during acute HCV is the current management strategy

Follow-up Protocol (All BBVs)

HIV: HIV Ag/Ab (4th generation test) at baseline, 6 weeks, 3 months, 6 months post-exposure; if all negative at 6 months — exposure did not result in HIV infection

HBV: LFTs at baseline and 3 months; if HBV infection occurs — refer to hepatologist

HCV: as above; LFTs at baseline, 6 weeks, 3 months, 6 months

Counsel on risk reduction during the window period: use condoms, avoid blood donation, avoid breastfeeding, avoid sharing needles; advise on the meaning of the window period (infection may be present before tests become positive)

GOLD Stage FEV1 (% predicted) Anaesthetic Risk

I — Mild ≥80% Low; managed as routine

II — Moderate 50–79% Moderate; respiratory physiotherapy, bronchodilators, plan for regional if possible

III — Severe 30–49% High; aggressive preoperative optimisation, plan for postoperative HDU/ICU

IV — Very severe <30% Very high; multidisciplinary decision; consider alternatives to general anaesthesia; ICU post-op

Intervention Specific Action & Evidence Smoking Immediate cessation reduces carboxyhaemoglobin within 12 hours and improves mucociliary clearance within 2–4 weeks; maximum respiratory cessation benefit at 8 weeks (secretion production normalises); warn against "cutting back" — partial smoking cessation does not reduce PPC risk as much as complete cessation

Bronchodilators Optimise inhaler therapy: SABA (salbutamol MDI 100–200 mcg QID) + LABA (salmeterol 50 mcg BD) + LAMA (tiotropium 18 mcg OD); bronchodilators should be continued until morning of surgery with a sip of water; IV aminophylline if severe bronchoconstriction not responding to inhalers (monitor levels — narrow therapeutic index) Treat infection Course of oral or IV antibiotics if purulent sputum/fever — guided by sputum culture where possible; standard: amoxicillin-clavulanate or cotrimoxazole for community-acquired exacerbation Steroids Short course oral prednisolone 30–40 mg for 5 days for COPD exacerbation (GOLD Guidelines); then continue inhaled corticosteroids (budesonide/formoterol); stress dose steroids perioperatively (hydrocortisone 100 mg IV at induction) for patients on systemic steroids >2 weeks Chest Breathing exercises, incentive spirometry, postural drainage; reduces secretion retention and improves baseline lung function pre-operatively physiotherapy Pulmonary FEV1, FVC, FEV1/FVC ratio; if FEV1 <0.8 L → very high risk of post-op ventilatory failure; 6-minute walk test for functional capacity; ABG for CO₂ function tests retention (PaCO₂ >50 mmHg at rest = severe disease and high risk of post-op hypercapnic respiratory failure) Nutritional COPD + malnutrition = very high PPC risk; optimise nutrition if BMI <18 with supplemental enteral feeding pre-operatively status

Anaesthetic Technique Choice Regional anaesthesia preferred where feasible — epidural or spinal anaesthesia for abdominal surgery avoids airway manipulation, maintains spontaneous ventilation, provides excellent post-operative analgesia (reducing opioid need and splinting), and is associated with lower PPC rates than general anaesthesia

Laparoscopic radical cholecystectomy: requires GA (pneumoperitoneum + Trendelenburg not compatible with spontaneous ventilation); combine with epidural for analgesia

Open cholecystectomy: thoracic epidural (T6–T8) provides surgical anaesthesia ± sedation as an alternative to GA in selected cases; more commonly combined with GA for better intraoperative control Intraoperative Ventilator Settings for COPD

Intervention Evidence Epidural / regional analgesia Epidural analgesia reduces splinting → allows deep breathing and coughing → reduces atelectasis and pneumonia; continues for 48– post-operatively 72 hours post-op in major abdominal surgery Early mobilisation Sitting out of bed day 1 post-op → improves FRC and reduces atelectasis; nurse physiotherapist-supervised ambulation Incentive spirometry Pre- and post-operative deep breathing exercises reduce atelectasis rate by 30–50% NIV/CPAP readiness In GOLD III–IV patients: plan for NIV (BiPAP) prophylactically post-extubation; CPAP 5–8 cmH₂O + IPAP 12–16 cmH₂O in pressure support mode; reduces need for reintubation Minimise opioids Opioid-induced respiratory depression + cough suppression directly causes PPC; use multimodal analgesia (paracetamol + NSAIDs + epidural + regional) to minimise systemic opioid requirement ARISCAT risk stratification Use ARISCAT score preoperatively to predict PPC risk: includes age, SpO₂, anaemia, incision site, surgery duration, emergency status, respiratory infection

Known cause: irreversible structural brain injury (TBI, massive stroke, anoxic brain injury, hypoxic-ischaemic encephalopathy) — must be established; no unknown or reversible causes

Exclude reversible causes of coma: hypothermia (core temp must be ≥36°C); metabolic derangement (Na, glucose, ammonia within normal limits); drug intoxication (sedatives, neuromuscular blockers, barbiturates, alcohol — must have cleared; if uncertain, drug levels should be measured and/or a minimum of 4–5 half-lives must have elapsed)

Haemodynamic stability: MAP ≥60 mmHg; patient must not be in cardiovascular shock

Duration: in India, observation period of at least 6 hours from the onset of coma before first testing is recommended

Test Method Brain Dead Response GCS Standard assessment GCS = 3 (E1V1M1) — no eye opening, no verbal, no motor response to any stimulus Pupillary light Bright light in each eye Pupils fixed and dilated (4–9 mm); NO constriction to reflex light; tests CN II (afferent) and CN III (efferent — parasympathetic to iris sphincter) Corneal reflex Touch cornea gently with sterile cotton wisp No blink; tests CN V (afferent trigeminal) and CN VII (efferent facial nerve to orbicularis oculi) Oculocephalic Rapidly rotate head side-to-side (ONLY after cervical spine cleared); contraindicated if C- In brain death: eyes remain fixed and do NOT move — reflex (Doll's spine injury they move WITH the head (absent reflex); normally eyes eye) lag behind head movement (brisk reflex = intact brainstem) Oculovestibular Irrigate 50 mL ice cold water into each external auditory meatus (with head 30° elevated); Brain dead: no eye movement; normally produces tonic reflex (Cold observe for 1 minute deviation of eyes toward the irrigated side (brainstem caloric) intact); most sensitive brainstem test Gag reflex Stimulate posterior pharynx with suction catheter No gag; tests CN IX (afferent glossopharyngeal) and CN X (efferent vagus) Cough reflex Pass suction catheter to carina via ETT No cough — complete absence of cough response to tracheal suctioning Pain response Apply painful stimulus (supraorbital pressure, nail bed pressure) No motor response; spinal reflexes (limb withdrawal) may be present — these are spinal cord reflexes, NOT brainmediated, and do NOT exclude brain death Apnoea test Pre-oxygenate with 100% O₂ for 10 minutes; confirm PaCO₂ 35–45 mmHg; disconnect No respiratory effort at PaCO₂ ≥60 mmHg = confirms (most ventilator; deliver passive O₂ via catheter in trachea at 6 L/min; observe for respiratory absent respiratory drive = confirms brainstem death; important movements for 10 minutes; check ABG at end — PCO₂ must rise to ≥60 mmHg (or 20 abort test if SpO₂ <85%, haemodynamic instability, or single test) mmHg above baseline) cardiac arrhythmia

Brain Death Certification Committee (India) Under THO Act, brain death must be certified by a panel of four doctors: 1. Medical Administrator/Registered Medical Practitioner nominated by the hospital 2. Neurologist or Neurosurgeon 3. The treating doctor/intensivist 4. An independent doctor (not from the treating team)

Two sets of tests must be performed — first set, then a second set after an observation interval (minimum 6 hours from first set for adults; 24 hours for neonates/children). Both sets must confirm brain death. The time of death is certified at the time the second set of tests confirms brain death. The death certificate is then issued, and organ donation can proceed with family consent.

Investigation Finding in Brain Death When Used

EEG Electrocerebral silence — isoelectric (flat) EEG at maximum sensitivity When apnoea test cannot be performed (severe pulmonary (Electroencephalogram) for ≥30 minutes disease); drug intoxication suspected; medico-legal requirement CT/MRI Angiography Absence of intracranial blood flow — no filling of cerebral vessels Most specific — absence of cerebral circulation is definitive; above the skull base preferred confirmatory test in many guidelines Transcranial Doppler Reverberating flow or absent flow in the major intracranial arteries Bedside, non-invasive; widely available; reverberating flow = net (TCD) (MCA, ACA, PCA) — systolic spikes only, no forward diastolic flow zero flow = no cerebral circulation Radionuclide brain "Hollow skull sign" — isotope does not cross the blood-brain barrier into Highly specific; demonstrates absent cerebral blood flow and scan (99mTc HMPAO) brain parenchyma; only scalp uptake cellular metabolic activity SSEP (Somatosensory Bilateral absence of N20 cortical response (the cortical component is Useful when EEG unreliable; tests cortical function Evoked Potentials) absent bilaterally)

Fixed position: once the robot is docked, the patient cannot be quickly repositioned; access to the airway is severely restricted (the robot arms are above the chest); any airway emergency requires complete undocking of the robot — a 3–5 minute process during which the airway cannot be managed Pneumoperitoneum + steep Trendelenburg: the combination produces multiplicative physiological effects on the respiratory and cardiovascular systems far worse than either alone

Duration: 2–4 hours in position — prolonged physiological insult accumulates (CO₂ absorption, ICP elevation, facial/conjunctival oedema, positional nerve injuries)

Patient population: elderly males with prostate cancer frequently have concurrent cardiovascular disease, hypertension, and reduced cardiac reserve — making the cardiovascular stress of the combined insult potentially poorly tolerated

System Effect Mechanism Management

Respiratory — FRC falls 30–50% from baseline; Abdominal contents pushed cranially by gravity Lung-protective ventilation: TV 6–7 mL/kg IBW; FRC reduction peak airway pressures rise 40– (Trendelenburg) + pneumoperitoneum compression of PEEP 6–10 cmH₂O; RR adjusted for 50%; compliance falls diaphragm from below; combined displacement severely normocapnia; accept permissive hypercapnia restricts diaphragmatic movement; FRC may fall below (CO₂ absorption from pneumoperitoneum → closing capacity → widespread atelectasis + shunt PaCO₂ rises 10–15 mmHg → increase MV by 15–25%); recruitment manoeuvres at position change CO₂ ETCO₂ progressively rises 10–20 CO₂ insufflation gas absorbed across peritoneal surface Increase RR by 15–25% after insufflation; absorption mmHg above pre-insufflation into mesenteric blood; the rate depends on peritoneal monitor ETCO₂ continuously; perform ABG every baseline surface area, absorption rate, and insufflation pressure; 60–90 minutes to confirm ETCO₂–PaCO₂ must increase minute ventilation to compensate gradient is stable (the gradient may widen with prolonged pneumoperitoneum from ↑dead space)

Cardiovascular Initial: ↑CO (Trendelenburg IAP 12–15 mmHg compresses IVC → reduces venous Maintain adequate preload before insufflation; increases venous return); return → ↓preload → ↓CO after 15–30 min; CO₂ absorption vasopressors (phenylephrine/noradrenaline) for sustained: ↓CO from ↑IAP; ↑SVR → sympathetic activation → ↑catecholamines → ↑HR and hypotension; arterial line for continuous BP (from CO₂ absorption → SVR; in patients with impaired cardiac reserve, the ↓CO monitoring; avoid high PEEP (further reduces sympathetic activation); ↑MAP from IVC compression is not compensated venous return) initially then risk of hypotension from venous compression Intracranial ICP rises significantly (by 5–15 Steep head-down → venous blood pools in cerebral In patients with pre-existing intracranial pressure mmHg) during RARP position vasculature (impaired jugular venous drainage from gravity) pathology (previous stroke, tumour, → cerebral venous hypertension → rises ICP; hydrocephalus) RARP position is potentially pneumoperitoneum worsens this by raising CVP and IVC dangerous; maintain normocapnia (do NOT pressure, transmitting to the jugular system; ETCO₂ rises → permit hypercapnia in neuro-compromised PaCO₂ rises → cerebral vasodilation → further ICP rise patients); keep head as flat as possible; avoid excessive PEEP Ocular Raised intraocular pressure (IOP); Venous congestion in ophthalmic circulation from raised Avoid excessive fluid administration (worsens risk of ischaemic optic neuropathy ICP and CVP; mean IOP may double (from ~15 mmHg to venous congestion and IOP); position the head (ION) in prolonged cases 30+ mmHg) during RARP position; prolonged elevated IOP to minimise venous obstruction; case duration → retinal artery pressure may approach IOP → potential should be minimised; report any visual retinal ischaemia symptoms post-operatively immediately

Preoxygenation: thorough 3–5 minutes; consider CPAP 10 cmH₂O during preoxygenation — extends safe apnoea time and buffers against the FRC reduction after induction

Airway: cuffed ETT with pilot balloon accessible (the cuff must be positioned for easy deflation/re-inflation — airway access is restricted once robot is docked); some centres use armoured ETT (flexible — less kinking in extreme position)

IV access and monitoring: large-bore IV access; arterial line (right radial — patient's right arm accessible despite robot docking); urinary catheter; temperature probe; compression stockings and pneumatic compression devices (DVT risk from immobility and venous stasis) Secure ETT and IV lines VERY carefully before docking — any disconnection after docking requires full robot undocking (3–5 min) to manage; use ETCO₂ waveform continuously to confirm ETT position; check ETT depth after each position change

NGT decompression: decompress the stomach before Trendelenburg positioning to reduce the volume of abdominal contents pressing on the diaphragm

Maintenance: TIVA preferred (propofol + remifentanil) — TIVA does not alter HPV, provides smoother depth control with precise recovery; alternatively volatile agent with careful monitoring

Facial/airway oedema: prolonged steep Trendelenburg causes significant venous engorgement in the head and neck — facial oedema, conjunctival chemosis, and potentially airway oedema (glottic and supraglottic); assess airway before extubation; if significant airway oedema suspected, consider cuff-leak test; have a plan for difficult extubation/re-intubation

Hypothermia: prolonged surgery with large body surface area exposed + CO₂ insufflation heat loss; active warming essential throughout

Shoulder pain: referred pain from diaphragmatic irritation by CO₂ (phrenic nerve, C3–C5 → referred to shoulder tip); NSAID + paracetamol; most resolves within 24–48 hours as CO₂ is absorbed

PONV: high risk (laparoscopy + opioids + position); aggressive PONV prophylaxis (ondansetron + dexamethasone + scopolamine patch)

Difficult airway: the clinical situation in which a conventionally trained anaesthesiologist experiences difficulty with: (1) face mask ventilation; (2) direct laryngoscopy/intubation; or (3) supraglottic airway placement; or (4) surgical airway (cricothyrotomy)

Difficult mask ventilation (DMV): inability to maintain SpO₂ >90% or to prevent/reverse signs of inadequate ventilation during mask ventilation using 100% O₂ and positive pressure

Difficult laryngoscopy: inability to visualise any portion of the vocal cords with conventional laryngoscopy (Cormack-Lehane Grade III–IV)

Failed intubation: proper insertion of the ETT in the trachea cannot be achieved after multiple attempts

Test What It Assesses High-Risk Finding Sensitivity/Specificity Mallampati Pharyngeal space (size of tongue relative to pharyngeal opening); patient Class III (only soft palate visible) or IV Sensitivity ~50%, Specificity score opens mouth and protrudes tongue — no phonation (soft palate not visible): predicts difficult ~85%; poor alone but laryngoscopy valuable in combination Thyromental Distance from thyroid notch to chin in full neck extension; measures space <6.5 cm → difficult laryngoscopy; <6 cm Sensitivity ~50%, Specificity distance available for tongue displacement during laryngoscopy → strongly predictive ~80% (TMD) Sternomental Distance from sternum to chin in full extension; overall neck mobility <12.5 cm → reduced neck extension → Low sensitivity; useful in distance assessment difficult laryngoscopy combination Interincisor Distance between upper and lower incisors in maximum mouth opening <3 cm (two finger breadths) → restricted Specific but insensitive; gap (mouth mouth opening; limits laryngoscope important combined with opening) blade insertion other factors

ULBT (Upper Patient bites their upper lip with lower incisors: Class I = bite above Class III → likely difficult laryngoscopy; Sensitivity ~50%, Specificity Lip Bite Test) vermilion border, Class II = below, Class III = cannot bite at all — assesses better predictor than Mallampati in some ~85% mandibular prognathism and tongue space studies Neck Active flexion/extension range; atlanto-occipital extension; presence of Extension <80° of normal; cervical Important contextual movement collar/fusion/arthritis collar; rheumatoid C-spine instability assessment; cannot be (atlanto-axial subluxation risk) quantified easily LEMON L=Look externally; E=Evaluate 3-3-2 rule; M=Mallampati; O=Obstruction; Any LEMON component positive → Validated in ED setting; easy score N=Neck mobility anticipate difficulty; used in emergency to apply rapidly airway assessment The 3-3-2 Rule (LEMON "E") 3 fingers = interincisor gap (mouth opening); 3 fingers = hyoid-chin distance (mandibular space for tongue); 2 fingers = thyroid-floor of mouth distance (laryngeal height); any measurement less than the finger widths suggests a potentially difficult airway.

Plan Action Maximum Attempts Proceed If Plan A Direct laryngoscopy (DL) / Video laryngoscopy — optimise: HELP/BURP, 3 attempts maximum (including 1 SpO₂ maintained; can still ventilate bougie, different blade; videolaryngoscope if available; give 100% O₂; with an experienced colleague); after 3 by mask call for help after first failed attempt failed attempts → declare failed intubation → move to Plan B

Plan B Supraglottic airway device (SAD): 2nd generation SAD (i-gel or Proseal 2 SAD insertion attempts; if SAD fails Oxygenation maintained with SAD

LMA — better seal for positive pressure ventilation); use as conduit for → Plan C → use as conduit for FOI; if not → intubation via fibrescope Plan C

Plan C Face mask ventilation — 2-person technique (two-hand grip, jaw thrust, Maximum mask ventilation effort; if can Can maintain SpO₂ ≥90% → wake

Plan C Face mask ventilation — 2-person technique (two-hand grip, jaw thrust, Maximum mask ventilation effort; if can Can maintain SpO₂ ≥90% → wake +oral/nasal airway); attempt to maintain oxygenation while waking the maintain SpO₂ → wake up patient; if up patient; then consider options patient up (if not already paralysed or relaxant has worn off) CANNOT ventilate → CICO → Plan D (awake FOI, tracheostomy, LA technique, abort surgery)

Plan D — Front-of-Neck Access (FONA): scalpel-bougie-tube cricothyrotomy IMMEDIATELY — do NOT delay; this Always — CICO is immediately lifeCICO (DAS recommended technique); simultaneously give sugammadex 16 is a life-or-death emergency threatening; FONA must not be Emergency mg/kg IV if rocuronium was used; 4 mm Melker emergency delayed cricothyrotomy kit (scalpel or needle technique)

Indication: anticipated difficult airway (Mallampati IV, TMD <6 cm, cervical spine instability, obesity with obstructive airway, known previous difficult airway, upper airway mass or tumour); the patient who might lose their airway under GA must be intubated AWAKE Sedation protocol (cooperative sedation, not general anaesthesia): Glycopyrrolate 200 mcg IM 30 minutes before (dries secretions — improves visualisation; secretions coat the lens) Dexmedetomidine 1 mcg/kg over 10 minutes then 0.5–0.7 mcg/kg/hr infusion — produces cooperative sedation without respiratory depression; patient remains rousable and able to follow commands; maintains airway tone and reflexes Midazolam 1–2 mg IV (anxiolysis) ± fentanyl 1 mcg/kg IV (analgesia) — small doses only; avoid over-sedation which abolishes protective reflexes Topical anaesthesia of the airway (most important step):

Oropharynx: lidocaine spray 4% + gargle

Nasopharynx (nasal route): lidocaine gel 2% + vasoconstrictor (xylometazoline) in each nostril; co-phenylcaine spray

Supraglottic: transtracheal injection or spray-as-you-go (SAYGO) — lidocaine 4% 2–3 mL injected through the cricothyroid membrane or through the working channel of the bronchoscope as it advances Total lidocaine dose <9 mg/kg (using 4% — 1 mL = 40 mg; total <400 mg for 70 kg patient)

Technique: pass lubricated FOB through ETT (size 7.0 loaded on the scope); advance the FOB through the nasal or oral route under direct vision; identify the epiglottis, arytenoids, vocal cords; pass the FOB through the cords under direct vision; confirm tracheal rings and carina; railroad the ETT over the FOB into the trachea; remove FOB; confirm placement with ETCO₂ waveform; induce GA (propofol) only after ETT confirmed in trachea

Colour / Container Waste Category Treatment/Disposal Anaesthesia Examples YELLOW bag Human anatomical waste (tissues, organs); animal Incineration (temperature ≥1200°C) Bloody gauze swabs; blood-contaminated waste; microbiology waste; soiled waste (cotton, at CBWTF (Common Biomedical drapes; expired IV drugs; placenta (obstetric); gauze, bandages, gowns contaminated with Waste Treatment Facility); or deep surgical tissue specimens sent intraoperatively blood/body fluids); expired medicine burial in specific cases

RED bag Non-chlorinated plastic waste: IV tubing, IV bags, Chemical treatment + shredding + IV administration sets; Bain circuit; breathing catheters, single-use gloves (non-contaminated), urine recycling at authorised recycler; circuit components; LMA (single-use); face bags, oxygen masks, nasogastric tubes; any non- autoclave NOT used (risk of dioxin masks; suction catheters; ETT (after use); sharp plastic recyclable from patient care release from chlorinated plastics) syringe bodies (without needles)

WHITE/PUNCTURE- Sharps: needles, syringes with needles, lancets, Autoclave + shredding at CBWTF; or ALL needles (drawing up needles, IV cannula PROOF container blades, broken glass, glass ampoules encapsulation in cement; or needle needles, spinal needles, epidural Tuohy (Sharps bin) destruction in needle cutters needles, nerve block needles); scalpel blades; glass ampoules; broken glass vials BLUE bag/box Glassware (non-sharp), metallic implants Autoclave/microwave then disposal Empty glass drug vials (intact); glass syringes at municipal solid waste site or (if applicable) recycling

BLACK bag General municipal solid waste (non-biomedical): food Municipal solid waste disposal; no Uncontaminated outer drug packaging; waste, packaging materials NOT contaminated with special treatment needed newspaper; administrative paper waste; nonbody fluids, paper, office waste contaminated cardboard drug cartons

KEY RULE — Sharps NEVER in plastic bags; always in puncture-proof container The most common BMW violation in anaesthesia is discarding needles into soft plastic bags or bins — creating a needlestick injury risk for housekeeping staff. All sharps go ONLY into the labelled white puncture-proof sharps container. Fill to 75% capacity only; do not force needles in; never recap with two hands (one-handed scoop technique only).

Waste Type Container Special Consideration Expired anaesthetic drugs Yellow bag (expired Controlled substances (opioids) require specific documentation and destruction procedures under (propofol, fentanyl, muscle medicine) NDPS Act — witnessed destruction by two staff, signed register; cannot simply discard in yellow bag relaxants) without documentation Residual drug in Yellow bag for liquid, Red for Separate the needle from the syringe body before disposal; needle in white sharps bin; body in red bag syringes/vials plastic syringe body, White for needle

Used breathing circuits, Red bag Single-use circuits: red bag; reusable equipment (laryngoscope blades, handles, fiberscopes) require LMAs, ETTs proper sterilisation before reuse — contaminated items not BMW waste but infection control waste (decontamination) CO₂ absorbent (spent soda Yellow or black bag Soda lime directly in the breathing circuit — contaminated with exhaled patient air and humidity; treat lime) depending on patient contact as patient contact waste; yellow bag preferred level Vaporizer filling devices and Hazardous chemical waste — Spilled or expired volatile agents are hazardous chemical waste (flammable, environmental pollutant); halogenated liquid agent NOT BMW require specific chemical waste handling; NOT to be poured down drain

Term Definition Example in Anaesthesia Artificial The broad field of computer science dedicated to creating systems that perform Computer programs that interpret ECG rhythms, diagnose airway Intelligence tasks that would normally require human intelligence — reasoning, problem- images, or generate anaesthetic plans (AI) solving, learning, perception Machine A subset of AI where algorithms learn patterns from data without being explicitly An algorithm trained on thousands of hypotensive episodes learns Learning (ML) programmed with rules; the algorithm improves its performance with more data to predict the hemodynamic pattern before the event occurs and experience Deep A subset of ML using artificial neural networks with many layers (deep networks) Image recognition of airway anatomy on video laryngoscopy; Learning (DL) — most powerful for image recognition, speech, and complex pattern recognition recognition of EEG burst suppression patterns for depth of tasks anaesthesia monitoring Natural AI subset enabling machines to understand and process human language (text or Automated extraction of preoperative comorbidities from Language speech) unstructured clinical notes to populate risk scores; voice-activated Processing anaesthetic documentation (NLP)

Application System/Tool Evidence/Validation Hypotension Hypotension Prediction Index (HPI — Edwards Lifesciences): an ML algorithm that Multiple RCTs (HYPE trial) show HPI-guided Prediction analyses the arterial waveform in real-time and outputs a probability (0–100) of vasopressor use reduces duration and severity of intraoperative hypotension in the next 15 minutes; uses machine learning on >20 arterial intraoperative hypotension by 50–70%; now cleared by waveform features FDA and CE mark; available in Acumen IQ sensor Closed-loop SEDASYS (now withdrawn from market but concept continues); closed-loop propofol Multiple RCTs show closed-loop TIVA achieves better anaesthesia drug TIVA using BIS feedback — the algorithm automatically adjusts propofol infusion rate to BIS time-in-target than manual titration; closed-loop delivery maintain target BIS 40–60 without manual titration; closed-loop vasopressor systems vasopressor reduces hypotension time in trials (CLMA — phenylephrine titrated by ML algorithm to MAP target) Difficult airway ML algorithms trained on preoperative airway assessment data (Mallampati, TMD, BMI, Proof-of-concept; not yet clinical standard; accuracy prediction etc.) to predict difficult intubation probability; some systems use facial image analysis via superior to single clinical variables but not yet smartphone cameras validated at population level Preoperative risk ML-enhanced versions of ASA, ACS-NSQIP, and APACHE scoring — algorithms trained Multiple validation studies show ML risk scores scoring on large perioperative databases predict individualised mortality, ICU admission, and outperform traditional scoring on discrimination metrics complication probability more accurately than point-score calculators (AUC 0.85–0.92 vs 0.75–0.80 for conventional scores) Depth of Machine learning-based EEG analysis for depth of anaesthesia (Sedline, Masimo); AI AI-enhanced EEG depth monitoring commercially anaesthesia/brain interpretation of processed EEG spectrograms; burst-suppression detection algorithms; available; research phase for real-time awareness monitoring automated alerting for accidental awareness risk detection Postoperative ML algorithms predict PONV, delirium, readmission, and unplanned ICU admission in Several hospital-deployed systems; validation ongoing; outcome real-time during the intraoperative period using intraoperative vital sign patterns; NLP not yet standard practice prediction algorithms extract risk factors from preoperative notes

Black box problem: deep learning algorithms are not interpretable — they produce outputs without explaining their reasoning; clinicians cannot understand why the algorithm recommended a specific action; this reduces trust and makes error analysis difficult

Training data bias: algorithms trained on data from specific populations (predominantly Western, specific hospital systems) may perform poorly in different patient populations (Indian patients, paediatric, rare diseases); biased training data → biased (and potentially harmful) outputs

Regulatory approval: most AI/ML devices in anaesthesia are approved only as decision-support tools, not autonomous treatment systems; the clinician retains legal responsibility for all patient care decisions regardless of AI recommendation

Data privacy: AI systems require large datasets of patient information for training; ethical data governance, consent, and privacy regulations (DPDP Act India 2023; GDPR in Europe) must be complied with

Alert fatigue: AI systems that generate too many false-positive alerts (like all monitoring systems) can lead to alarm fatigue — the very real danger that clinicians learn to ignore AI warnings, including true positives

Fully autonomous closed-loop anaesthesia machines (induction + maintenance + emergence, all algorithm-controlled); currently regulatory frameworks prohibit fully autonomous administration without human oversight in most jurisdictions Preoperative AI-generated anaesthetic plans tailored to individual patient genomics, comorbidities, and predicted drug metabolism Real-time voice-activated anaesthetic documentation — NLP extracts and records events from the spoken intraoperative narrative without manual charting AI-assisted surgical team communication and cognitive load management — real-time situational awareness tools that alert the team to developing physiological trends

GWP (100Agent Atmospheric Lifetime Clinical Equivalent year, CO₂ = 1) Nitrous 265 114 years Also depletes stratospheric ozone; longest-persisting anaesthetic greenhouse gas — 1 L of N₂O delivered = Oxide (N₂O) 265 L CO₂ equivalent; used in huge volumes globally Isoflurane 510 3.2 years Medium impact; 1 L liquid isoflurane at 1 L/min FGF releases ~510 kg CO₂ eq over its lifetime Sevoflurane 130 1.1 years Lowest GWP of halogenated agents; preferred environmentally; short atmospheric lifetime Desflurane 2540 14 years Most potent greenhouse anaesthetic gas; 1 hour at 1 MAC, 2 L/min = driving 235 km; UK NHS banned desflurane from formulary in 2021; Australia, Canada, and several EU nations phasing out Propofol ~3.5 Metabolised — not The environmentally superior anaesthetic choice per MAC-hour; 97% less carbon footprint than desflurane (TIVA) (manufacturing exhaled into for equivalent anaesthesia time + disposal) atmosphere

Other contributors: single-use equipment manufacturing and disposal (anaesthesia circuits, LMAs, ETTs, gloves, syringes — lifecycle analysis shows a reusable LMA has 1/10th the carbon footprint of single-use equivalents over 40 uses); operating theatre energy consumption (3–6× normal hospital areas per m²); patient transport and building heating

N₂O infrastructure leakage: pipeline N₂O systems routinely leak 10–30% of delivered N₂O into the building atmosphere; reducing N₂O infrastructure use reduces both intentional and leak emissions

Strategy Impact & Evidence 1. Eliminate Single highest-impact action: switching from desflurane to sevoflurane for 1 hour at 2 L/min reduces CO₂ equivalent emissions by ~95%; UK NHS desflurane removed desflurane from national formulary 2021 citing lack of meaningful clinical advantage over sevoflurane combined with catastrophic environmental cost; at the individual clinical level — desflurane provides only marginally faster early emergence (5–10 min) vs sevoflurane, with no difference in actual PACU discharge time or patient outcomes 2. Low-flow / Fresh gas flow (FGF) directly determines volatile agent consumption and atmospheric release; reducing FGF from 4–6 L/min (high-flow) to 0.5–1 L/min minimal-flow (low-flow) in the circle system reduces volatile agent consumption by 70–80%; at metabolic flow (0.35 mL/min), only the patient's metabolic uptake is anaesthesia replaced; requires circle system with CO₂ absorber (not Bain circuit); simultaneously saves cost and reduces operating room pollution 3. TIVA (Total Propofol-based TIVA produces zero volatile greenhouse gas emissions; propofol is metabolised and excreted — not exhaled into atmosphere; the IV environmental cost is propofol manufacturing and packaging, substantially less per MAC-hour than volatile agents; TIVA is the "greenest" general Anaesthesia) anaesthetic option; growing advocacy for TIVA adoption on environmental grounds in addition to its established clinical benefits (reduced PONV, no MH triggering, no HPV inhibition) 4. Eliminate N₂O (GWP 265, atmospheric lifetime 114 years) also depletes stratospheric ozone; clinical alternatives exist for every indication (opioids provide or minimise analgesia; volatile agents provide hypnosis; ketamine provides dissociative anaesthesia); N₂O elimination from routine anaesthesia removes the longestN₂O lasting anaesthetic greenhouse gas; multiple centres have eliminated N₂O from their formulary without impact on patient outcomes 5. Regional Every regional technique (peripheral nerve block, neuraxial) that successfully avoids GA eliminates 100% of volatile agent emissions for that case; the anaesthesia "Regional First" philosophy aligns environmental sustainability with established clinical benefits (reduced opioid consumption, faster PACU discharge, preference lower PONV, superior analgesia); expanding regional anaesthesia is one of the most effective department-level environmental strategies ("Regional First") 6. Volatile Systems (SageTech MARU — Medical Agent Recovery Unit) that capture exhaled volatile agent from scavenging systems and reconstitute it into liquid agent capture form for reuse; pilot programmes in UK and Scandinavia demonstrating both environmental and economic benefit; requires regulatory framework for and recycling recycled agent use (quality assurance); prevents atmospheric release from scavenging exhaust 7. Reduce Where infection risk allows: use reusable LMAs (sterilised between cases — lifecycle analysis shows 90% reduction in carbon footprint vs single-use); single-use metal laryngoscope blades (sterilised) vs single-use plastic; reusable temperature probes; audit single-use vs reusable decisions against infection risk equipment evidence rather than defaulting to single-use for convenience

NHS Net Zero commitment (UK 2020): first national health system to commit to net-zero carbon by 2040; explicit desflurane ban (2021); anaesthesia sustainability targets in NHS contracts; green theatre champions programme

ESA Sustainability Task Force: green anaesthesia guidelines (2021); mandatory sustainability education in anaesthesia training programmes

India: desflurane is already rare in most Indian centres (cost-driven); sevoflurane predominates; formalising low-flow protocols and eliminating routine N₂O would meaningfully reduce Indian anaesthesia's carbon footprint without additional cost; TIVA availability expanding with propofol generic manufacturing

Individual anaesthesiologist: each anaesthesiologist makes hundreds of agent selection, FGF, and equipment choices annually — collectively determining a department's carbon footprint; professional responsibility now explicitly includes environmental stewardship in modern anaesthesia training frameworks

Infection: pathological process caused by microbial invasion of normally sterile tissue

Sepsis: life-threatening organ dysfunction caused by a dysregulated host response to infection; defined clinically as: suspected or confirmed infection + acute increase in SOFA score ≥2 points (indicating acute organ dysfunction); a SOFA score ≥2 is associated with >10% in-hospital mortality in the general ICU population

Septic shock: a subset of sepsis with circulatory, cellular, and metabolic dysfunction that is profound enough to substantially increase mortality; defined as: sepsis PLUS vasopressor requirement to maintain MAP ≥65 mmHg AND serum lactate >2 mmol/L despite adequate fluid resuscitation; hospital mortality for septic shock exceeds 40%

Quick SOFA (qSOFA): a bedside screening tool (not a diagnostic criterion) to identify patients outside the ICU at risk of sepsis: ≥2 of the following: altered mentation (GCS <15), RR ≥22/min, systolic BP ≤100 mmHg; qSOFA ≥2 → high risk of poor outcome → initiate full SOFA assessment and sepsis workup SOFA Parameter Score 0→4 Component Respiratory PaO₂/FiO₂ ratio ≥400 → 0; 300–399 → 1; 200–299 → 2; 100–199 + MV → 3; <100 + MV → 4 Coagulation Platelet count (×10³/ ≥150 → 0; 100–149 → 1; 50–99 → 2; 20–49 → 3; <20 → 4 μL) Hepatic Bilirubin (mg/dL) <1.2 → 0; 1.2–1.9 → 1; 2.0–5.9 → 2; 6.0–11.9 → 3; >12 → 4 Cardiovascular MAP/vasopressors MAP ≥70 → 0; MAP <70 → 1; Dopamine ≤5 or dobutamine → 2; Dopamine 5–15 or NE ≤0.1 → 3; Dopamine >15 or NE >0.1 → 4 CNS GCS 15 → 0; 13–14 → 1; 10–12 → 2; 6–9 → 3; <6 → 4 Renal Creatinine (mg/dL) / <1.2 → 0; 1.2–1.9 → 1; 2.0–3.4 → 2; 3.5–4.9 or UO<500 → 3; >5 or UO<200 → 4 UO

Pathogen (bacteria/virus/fungi) + host susceptibility → Pattern Recognition Receptors (PRRs: TLR-4 for LPS; NOD-like receptors) on innate immune cells → activation of NF-κB transcription factor → massive cytokine release (TNF-α, IL-1β, IL-6, IL-8 — the "cytokine storm") → systemic endothelial activation and injury → four simultaneous cascades producing multi-organ dysfunction: Cascade Mechanism Clinical Consequence Vascular NO overproduction (iNOS) → pathological vasodilation + increased vascular permeability; loss of Distributive shock: low MAP, high CO, low SVR; dysfunction vascular autoregulation; catecholamine resistance from downregulated adrenergic receptors warm extremities; relative hypotension despite high output Coagulation Endothelial injury + TF expression → thrombin generation → microthrombi in capillary beds → Microvascular occlusion → end-organ activation simultaneous consumption of clotting factors → fibrinolysis activation → DIC ischaemia despite normal/high CO; bleeding from factor depletion Mitochondrial Cytokines (TNF-α) + NO → inhibition of mitochondrial electron transport chain (Complex I and Rising lactate in the presence of normal or high dysfunction Complex IV) → cells cannot use oxygen even when delivered → aerobic glycolysis → lactate cardiac output; explains why improving cardiac (cytopathic production → Type B lactic acidosis in well-perfused tissue output does not always resolve lactate in hypoxia) advanced sepsis Immunoparalysis Initial hyperinflammation (cytokine storm) is followed by profound immunosuppression: Patients die of secondary nosocomial infections (late sepsis) lymphocyte apoptosis (programmed cell death), monocyte deactivation, T-cell exhaustion, HLA- (Candida, Aspergillus, reactivated CMV, MDR DR downregulation on monocytes → impaired pathogen clearance → secondary infections bacteria) rather than the original pathogen dominate late clinical course

The costoclavicular space (CCS): the anatomical compartment bounded superiorly by the clavicle, inferiorly by the first rib, anteriorly by the subclavius muscle, and posteriorly by the serratus anterior muscle; this space is traversed by the subclavian/axillary vessels and the three cords of the brachial plexus as they pass from the neck to the axilla

Plexus level: the CCS approach targets the brachial plexus at the level of the CORDS (divisions have just formed the cords at or just proximal to this level) — one anatomical level below the supraclavicular approach (which targets trunks/divisions) and one level above the conventional coracoid infraclavicular approach (which also targets cords but deeper and more lateral)

Cord arrangement at the CCS: the three cords are clustered in a compact triangular arrangement immediately lateral to the axillary artery at this level — the lateral cord is supero-lateral to the artery, the medial cord is infero-medial, and the posterior cord is posterior; this compact arrangement (compared to the more dispersed arrangement deeper in the axilla) makes the CCS an excellent target for a single-injection block

Key relationships: the cephalic vein runs in the deltopectoral groove nearby; the axillary artery is the primary vascular landmark; the pleura is relatively distant from the injection site (greater safety margin from pneumothorax compared to supraclavicular approach); pectoralis major muscle is the superficial landmark for needle entry

Structure Ultrasound Appearance Position Axillary Round, pulsatile, anechoic; does not compress with probe pressure; Central landmark — the anchor for cord identification artery confirmed with colour Doppler Lateral cord Hyperechoic (bright) nodular oval structure Supero-lateral to axillary artery (at approximately 10–12 o'clock position relative to artery) Medial cord Hyperechoic nodular oval Infero-medial to axillary artery (approximately 5–6 o'clock position) Posterior Hyperechoic nodular oval Posterior to axillary artery (approximately 6–9 o'clock position, behind the cord artery) Subclavius Hypoechoic muscle belly with linear fibres Between the clavicle (hyperechoic bony shadow above) and the muscle plexus/vessels Pectoralis Hypoechoic layered muscle Most superficial layer; the probe is placed below the clavicle in the major deltopectoral groove region

First rib / First rib: hyperechoic line deep to vessels; pleura: bright sliding line below Deep to the plexus — the posterior limit of the CCS; deeper than in the pleura first rib supraclavicular approach

Patient Positioning and Probe Placement Patient supine; head turned 30–45° away from the side to be blocked; ipsilateral arm adducted at the side (neutral — no abduction required; this is an advantage over the coracoid infraclavicular approach which benefits from arm adduction but can be done in any position) High-frequency linear probe (10–15 MHz) placed just below the medial clavicle in the deltopectoral groove, oriented in a para-sagittal plane (probe indicator pointing cephalad); the probe is tilted to optimise cord visualisation in the CCS

Needle Approach

In-plane from lateral to medial (lateral approach): the needle enters the skin lateral to the probe and advances medially in the plane of the ultrasound beam — the entire needle shaft and tip are visible throughout the approach; this is the preferred approach for the CCS block

Target: the needle tip is directed to the space posterior to the axillary artery — between the artery and the posterior cord — which is the centre of the compact cord triangle; a single injection here achieves circumferential spread around all three cords

Injection: aspirate before each injection; inject 2–3 mL and observe spread; the local anaesthetic should spread to surround all three cords in a "donut" pattern around the artery; total volume: 20–25 mL of 0.5% ropivacaine or 0.375% bupivacaine; hydrodissection (small saline boluses) used to develop the plane and confirm needle position before LA injection

Key safety check: confirm no intravascular injection (negative aspiration, low injection pressure, no patient report of peri-oral tingling); confirm LA is spreading around the cords (not sub-pectoral, not into the axillary sheath only)

Feature Costoclavicular Approach Conventional Coracoid Infraclavicular Depth of More superficial (2–3 cm) — cords are at the level of the CCS, closer to the Deeper (3–5 cm) — plexus is deeper beneath the pectoralis muscles plexus skin at the coracoid level

Needle Better — shorter needle path, more superficial target, in-plane approach; entire Can be challenging — deep target; steep needle angle required; visualisation needle visible long needle path Cord Cords are most compact at the CCS — single injection more reliably blocks all Cords begin to separate as they approach the axilla — may require compactness three cords multiple injections

Arm position Neutral arm position — no abduction needed; suitable for patients with painful Arm abduction 90° improves cord separation and visualisation; not required shoulders, fractures, limited ROM possible in shoulder pathology

Onset time Faster — more compact target, better spread with single injection; studies Moderate onset; similar total success rates with experienced show 5–10 min advantage operators

Complication Incidence (USG-guided) Prevention Vascular puncture (axillary <1% with USG guidance Direct visualisation of artery; stay posterior to artery; aspiration artery/vein) before injection Pneumothorax <0.1% — lower than supraclavicular (first rib and pleura are deeper Identify first rib and pleura before needle insertion; do not advance and more distant in CCS) beyond the posterior cord LAST Rare with incremental injection and aspiration Test dose; incremental injection; have LAST rescue plan (intralipid available)

Cephalic vein puncture Small risk — cephalic vein runs nearby in deltopectoral groove Identify cephalic vein on ultrasound before needle insertion; avoid it during approach Phrenic nerve palsy Very low (<5%) — distant from phrenic nerve at this level No specific precautions needed; far from phrenic nerve path

TIVA: induction AND maintenance of general anaesthesia using only intravenous drugs, without any inhalational anaesthetic agent; requires at least three pharmacological components:

Hypnotic agent (produces unconsciousness): propofol (almost universally); alternatives: thiopentone, ketamine, dexmedetomidine as adjuncts

Analgesic agent (blunts surgical pain response): remifentanil (preferred — ultra-short context-sensitive half-time, titrable); alternatives: fentanyl, alfentanil, ketamine Neuromuscular blocking agent (facilitates intubation and surgical relaxation, if required): rocuronium, vecuronium, cisatracurium

Component Target Concentration Effect Rationale

Propofol Induction: 4–6 mcg/mL Ce Unconsciousness, amnesia; Dose-dependent reduction of CMRO₂ and CBF (neuroprotective); lowest PONV (Schnider); Maintenance: 3–4 mild muscle relaxation at incidence of all agents; no HPV inhibition; environmentally clean; predictable recovery mcg/mL Ce (surgery); higher concentrations; with TCI

Sedation: 1–1.5 mcg/mL Ce antiemetic at subanaesthetic concentrations

Remifentanil Blunt intubation response: 4– Analgesia; suppression of Unique organ-independent ester hydrolysis metabolism → context-sensitive half-time = 8 ng/mL; Maintenance: 2–5 haemodynamic response to 3 min regardless of infusion duration; no drug accumulation; predictable emergence ng/mL (depending on surgical stimulation; reduces even after 12-hour infusion; CRITICAL: provide post-op analgesia (morphine/NSAIDs) stimulation); Emergence: propofol requirement by 30– before stopping remifentanil as its analgesic effect disappears within 5–10 min of reduce to 1–2 ng/mL 40% stopping

Unlike volatile anaesthesia (where ETCO₂ confirms drug delivery and MAC multiples correlate with depth), TIVA has no exhaled gas indicator of delivery or depth — processed EEG monitoring is essential

BIS (Bispectral Index): 0–100 scale; target 40–60 for surgical anaesthesia; values <40 suggest excessive depth (burst suppression); >60 → inadequate depth and awareness risk; specifically validated for propofol and volatile agents

Entropy (Spectral Entropy): State Entropy (SE) and Response Entropy (RE); similar utility to BIS; uses different mathematical processing of the EEG spectrum pEEG (Patient-State Index, Narcotrend): alternative processed EEG monitors; similar principle to BIS

Important limitation: all processed EEG monitors fail to reliably predict awareness in the concentration range where awareness most commonly occurs (0.2– 0.4 MAC equivalent of propofol); they provide a trend indicator, not an absolute guarantee of unconsciousness

Advantage Clinical Basis Lowest PONV incidence Propofol has intrinsic antiemetic properties (5-HT3 antagonism at sub-anaesthetic concentrations); absence of volatile agents (which are emetogenic); absence of N₂O; TIVA reduces PONV by ~25–30% vs inhalational techniques No HPV inhibition Propofol does not inhibit hypoxic pulmonary vasoconstriction (unlike volatile agents) → superior oxygenation during one-lung ventilation; preferred for thoracic anaesthesia No MH triggering Propofol and opioids are safe in MH-susceptible patients; TIVA is mandatory when volatile agents are contraindicated (MH, suspected MH susceptibility) No operating room No volatile agent exhaled into the OR environment; protects OR staff from chronic low-level anaesthetic exposure pollution Environmental No halogenated greenhouse gas emissions; environmentally superior to all volatile agent techniques sustainability Predictable recovery with Remifentanil's flat CSHT (3 min) means recovery time is independent of infusion duration; propofol's moderate CSHT rises slowly — propofol-remifentanil suitable for even very long cases (8+ hours) with predictable emergence Suitable for remote TIVA requires only a syringe pump and IV access — no anaesthetic machine, vaporizer, or gas supplies needed; ideal for MRI (no locations ferromagnetic components), remote sites, transport anaesthesia

Definition: BCIS is defined as hypoxia (SpO₂ fall >10% from baseline), hypotension (systolic BP fall >20% from baseline), or both, occurring at the time of cementation, prosthesis insertion, reduction of the joint, or deflation of a tourniquet during orthopaedic surgery using PMMA bone cement Grade Clinical Features Incidence Mortality Grade 1 Moderate hypoxia (SpO₂ fall >10%) OR moderate hypotension (systolic BP Common — up to 30% Near-zero direct mortality (Mild) fall >20%) — not both; brief, self-limiting of cemented THRs Grade 2 Severe hypoxia (SpO₂ <94%) AND/OR severe hypotension (systolic BP fall ~5–10% Low but non-trivial; associated with increased (Moderate) >40%) AND/OR unexpected loss of consciousness postoperative complications Grade 3 Cardiovascular collapse requiring cardiopulmonary resuscitation — cardiac ~0.5–1% of cemented Very high — approaching 100% in full cardiac (Severe) arrest THRs arrest without immediate CPR

Risk Factor Specific Risk Factors Category Patient Advanced age (>70 years — greater intramedullary fat content, more fragile vasculature); male sex (larger intramedullary cavities); pre-existing factors cardiorespiratory disease (impaired ability to compensate for acute pulmonary embolism); PFO (paradoxical embolism risk); hypovolaemia at time of cementation; pathological bone (osteoporosis, Paget's, metastatic disease — more intramedullary blood and fat, more friable); pulmonary hypertension (reduced reserve for additional right ventricular afterload) Surgical Cemented implant (vs cementless — cementless arthroplasty does not cause BCIS); revision surgery (larger canals, more debris); long-stem prostheses factors (greater medullary surface area → more material driven into veins); inadequate canal cleaning before cementation (more marrow content → more embolic material); cement pressurisation technique; cement mixing (higher monomer content with improper mixing) Anaesthetic Hypovolaemia at time of cementation (reduced cardiac reserve for haemodynamic response); inadequate preloading; general anaesthesia reduces factors cardiovascular reserve vs regional; the haemodynamic challenge of BCIS may be tolerated better under spinal/epidural anaesthesia (better maintained cardiovascular reserve in spinal vs GA)

Preventive Measures

Communication: surgeon must verbally announce BEFORE cementation — "I am about to cement" — this is a mandatory communication point; the anaesthesiologist must be at full vigilance at the critical moment

Pre-cementation fluid loading: ensure the patient is euvolaemic or mildly hypervolaemic before cement is introduced; a small preloading fluid bolus (250–500 mL crystalloid) 5–10 minutes before cementation ensures adequate intravascular volume to buffer the haemodynamic response

FiO₂ to 1.0: increase to 100% O₂ immediately before cementation is announced; this maximises the oxygen reservoir in the FRC to buffer any hypoxic episode

ETCO₂ monitoring: a sudden fall in ETCO₂ is an early sign of massive embolism (reduced pulmonary blood flow → reduced CO₂ delivery to alveoli → ETCO₂ falls); warns the anaesthesiologist before SpO₂ falls

Surgical technique: thorough canal lavage (irrigation before cementation removes loose marrow and blood); use of cement restrictors (reduces the intramedullary volume receiving cement pressure); retrograde cementing technique (fills the canal from distal to proximal — minimises air entrapment); venting holes drilled by surgeon (releases intramedullary pressure) Management of Cardiovascular Collapse (Grade 3 BCIS)

Principle Application to End-of-Life Care Autonomy The patient's right to refuse or accept treatment, including life-sustaining measures; expressed through informed consent, advance directives (living will, healthcare proxy), and verbal refusal; must be respected even when the clinician disagrees with the patient's decision; a competent adult's refusal of CPR or ventilation is legally and ethically binding Beneficence Act in the patient's best interest; in end-of-life care, this requires understanding what constitutes "best interest" beyond mere prolongation of biological function — quality of life, freedom from suffering, dignity, and the patient's own values determine best interest Non- "First, do no harm" — in end-of-life care, this principle supports withholding treatments that produce suffering without meaningful benefit; continuing maleficence painful, invasive treatments in a terminally ill patient who cannot benefit is a form of harm; overly aggressive treatment at the end of life violates nonmaleficence Justice Fair allocation of resources; when ICU resources are limited, justice requires that they be directed toward patients who can benefit; withdrawing futile ICU care also has a justice dimension — freeing resources for patients who can meaningfully benefit Doctrine of An action that is intended for a good purpose (relieving pain/suffering) but has a known adverse side effect (possibly hastening death from respiratory

Double depression) is ethically permissible if: the action itself is not inherently wrong; the bad effect is foreseen but not intended; the good effect outweighs the Effect bad; this principle underpins the use of opioids and sedation for palliative purposes even when there is a theoretical risk of respiratory depression

Definition: a DNR/DNAR order is a specific medical order instructing healthcare providers not to perform CPR (cardiopulmonary resuscitation) in the event of cardiac or respiratory arrest; it does NOT mean withdrawal of all treatment — it only refers to CPR attempts

Indications for DNR discussion: terminal malignancy with no curative treatment; advanced end-organ failure (GOLD IV COPD, NYHA IV heart failure, ESRD); severe neurological injury (persistent vegetative state, brainstem death); patient's own expressed wish to avoid CPR; clinical judgment that CPR would be futile or cause more harm than benefit

Perioperative DNR — the anaesthesiologist's challenge: a patient with a pre-existing DNR order who requires surgery for quality-of-life purposes (pain relief, obstruction relief) presents a specific ethical dilemma; the anaesthesiologist does not automatically suspend the DNR during surgery; the standard approach is: Pre-operatively discuss the DNR order with the patient/family and surgeons

The patient has three options: (1) suspend the DNR during the perioperative period (the resuscitation risks of anaesthesia and surgery justify temporary DNR suspension); (2) require procedure-directed DNR (only resuscitate for anaesthesia-caused arrests, not disease-related arrests); (3) retain DNR in full (no resuscitation for any cause) Document the agreed modification clearly in the notes before proceeding

Legal status in India: there is no specific statute governing DNR orders in India; the Supreme Court of India judgment (Common Cause vs Union of India, 2018) affirmed the right to die with dignity and the validity of advance medical directives (living wills); hospitals are expected to develop policies aligned with this ruling; end-of-life orders should be documented clearly, reviewed with families, and counter-signed by senior medical staff

Ethical basis: withholding and withdrawing futile treatment are ethically equivalent; prolonging life with no prospect of meaningful recovery is not a benefit to the patient; WLST is not "killing" the patient — it is removing an impediment to natural death; the patient dies of their underlying disease, not from the withdrawal Decision process (ICU):

Senior clinician assessment: confirm that treatment is futile (no prospect of recovery to a quality of life the patient would value, based on clinical evidence and the patient's expressed values)

Family meeting: structured, compassionate communication with the family/surrogate decision-maker; explain the clinical situation honestly; establish what the patient would have wanted; allow time for family to process; avoid false hope without being brutal

Multidisciplinary agreement: consensus from the treating intensivist, nursing team, relevant specialists, and chaplaincy/social work if appropriate; document the decision clearly in the notes

Ethical committee consultation: for difficult cases or family disagreement; not required for straightforward clinical decisions where family and clinical team agree

Process of withdrawal: ensure comfort medications are in place BEFORE withdrawal (morphine infusion, midazolam infusion — titrate to comfort, not to hasten death); then remove ventilator support gradually or extubate; family may be present; provide dignified, peaceful environment; post-withdrawal monitoring for comfort (pain, dyspnoea, agitation) and adjustment of medications; notify death and complete documentation; provide family support

Concept Definition Ethical Status Palliative The use of sedative drugs to reduce consciousness in patients with terminal illness and refractory Ethically permissible under the doctrine of sedation suffering — symptoms that cannot be adequately controlled by any other means (pain, dyspnoea, double effect; legally supported in India and agitation, existential distress); the goal is relief of suffering, not hastening of death; depth of sedation most jurisdictions; distinct from euthanasia ranges from mild (rousable) to deep (unconscious) (where the intent is to end life) Euthanasia Deliberate administration of a lethal drug specifically intended to end the patient's life; NOT the same as Illegal in India; ethical debate ongoing globally; palliative sedation; NOT legal in India or most countries NOT part of anaesthesia/ICU practice in India Physician- Physician prescribes a lethal drug that the patient self-administers; NOT legal in India Illegal in India; legal in Netherlands, Belgium, Assisted Canada, Oregon (USA) Suicide (PAS)

Drugs for palliative sedation: midazolam (most common — 1–10 mg/hr SC or IV infusion); morphine (for pain and dyspnoea — primary analgesic with titration; not intended as the sedating agent); phenobarbitone (for seizures or refractory agitation in terminal patients); propofol (for deeply distressing cases requiring rapid sedation in inpatient palliative/ICU settings); combination midazolam + morphine most commonly used Anaesthesiologist's specific role: expertise in drug titration and pharmacology; experienced in airway management (relevant if sedation produces airway compromise); able to manage the physiological consequences of advanced disease; liaison between the palliative team and ICU; providing terminal sedation when palliative care team requests specialist support for difficult symptom control

Feature Acute Pain Chronic Pain Duration <3 months; recent onset; expected to resolve as tissue heals Persists >3 months; beyond expected healing time; often persists after original injury has healed

Biological Adaptive — warns of tissue damage; promotes protective Maladaptive — no longer serves a protective purpose; becomes a disease in its own purpose behaviour (rest, seeking care); essential for survival right ("chronic pain syndrome") Neurobiology Nociceptive signals from tissue damage → ascending pain Central sensitisation; neuroplastic changes in the dorsal horn and brain; descending pathways → cortical pain perception; proportional to damage inhibitory pathway failure; pain independent of (or out of proportion to) peripheral stimulus Treatment Treat underlying cause; multimodal analgesia; short-term Biopsychosocial model; multidisciplinary team; minimise opioid exposure; focus on approach opioids acceptable function not pain elimination

Type Mechanism Characteristics Examples Treatment Nociceptive Activation of A-delta (sharp, fast pain) and C Well-localised; proportional to stimulus; Bone pain, muscle pain, NSAIDs; — Somatic fibres (slow, burning pain) in somatic tissues improves with rest and analgesics; described incisional pain, trauma paracetamol; by noxious stimuli (mechanical, thermal, as sharp, aching, throbbing; responds to opioids; regional chemical) — signalling to the dorsal horn → NSAIDs and opioids blocks thalamus → somatosensory cortex Nociceptive Activation of visceral afferents by distension, Poorly localised; colicky or pressure-like; Bowel obstruction, biliary Opioids; N-butyl — Visceral ischaemia, or inflammation of hollow organs; associated with autonomic responses (nausea, colic, ureteric colic, scopolamine travels via sympathetic nerves; referred pain sweating, pallor); referred to somatic areas cardiac ischaemia (antispasmodic); via shared dermatomes with somatic fibres (e.g., MI → left arm pain; appendicitis → treat underlying periumbilical then RIF) cause Neuropathic Initiated or caused by a primary lesion or Burning, shooting, electric shock-like, tingling Diabetic peripheral Gabapentinoids disease in the somatosensory nervous system (dysaesthesia); allodynia (pain from normally neuropathy, post-herpetic (pregabalin, (peripheral or central); pathological changes in non-painful stimulus — light touch causes neuralgia, phantom limb, gabapentin); TCAs neural signalling — ectopic discharge from severe pain); hyperalgesia (exaggerated pain complex regional pain (amitriptyline); injured axons, central sensitisation, loss of response to painful stimulus); often associated syndrome (CRPS), SNRIs (duloxetine); descending inhibitory control, glial activation with sensory deficit in the painful area; often chemotherapy-induced, topical poorly responsive to NSAIDs/opioids post-surgical (chronic lidocaine/capsaicin; post-surgical pain) nerve blocks; spinal cord stimulation Nociplastic Altered nociception from changed functioning Widespread, diffuse pain; poor correlation with Fibromyalgia; irritable Exercise; cognitive (Central of the somatosensory nervous system without tissue findings; associated with fibromyalgia, bowel syndrome; tension- behavioural therapy Sensitisation) clear evidence of actual tissue damage or irritable bowel, tension headache; fatigue; type headache; (CBT); SNRIs nerve damage; the pain is real but arises from sleep disturbance; often has psychological widespread (duloxetine); TCAs; a sensitised central nervous system (changes comorbidities musculoskeletal pain low-dose naltrexone in dorsal horn transmission, supraspinal (experimental); processing, descending modulation) multidisciplinary rehabilitation

The Biopsychosocial Model — Framework for All Interventions The biopsychosocial model (Engel, 1977) recognises that chronic pain is determined by three interacting dimensions: biological (tissue pathology, neural sensitisation, genetics, pharmacology), psychological (depression, anxiety, catastrophising, fear-avoidance behaviour, sleep disturbance), and social (employment, social support, compensation claims, cultural attitudes to pain); effective chronic pain management must address all three dimensions simultaneously Component Interventions Evidence Level 1. Step 1 (mild pain): paracetamol 500–1000 mg QID; NSAIDs (ibuprofen, naproxen, celecoxib) — WHO analgesic ladder (adapted for chronic Pharmacological most evidence for acute/inflammatory pain; limit <10 days; GI/renal/cardiovascular risk monitoring pain); NICE guidelines (NG173); NNT for

Step 2 (moderate pain): weak opioids (codeine, tramadol) + step 1; tramadol (SNRI + opioid) neuropathic agents: duloxetine NNT 6.5; particularly useful for neuropathic pain; gabapentinoids (pregabalin 75–300 mg BD; gabapentin 300– pregabalin NNT 7.7; amitriptyline NNT 6.4 1200 mg TID) for neuropathic

Step 3 (severe/neuropathic): strong opioids (morphine, oxycodone, fentanyl patch) — ONLY for chronic pain with demonstrated benefit and documented risk-benefit discussion; buprenorphine patches (7-day) — less euphoric, ceiling effect, suitable for chronic pain; duloxetine 60–120 mg OD (SNRI with level 1 evidence for diabetic neuropathy, fibromyalgia, MSK pain); amitriptyline 10–75 mg nocte (low-dose TCA — analgesic, sleep aid, also antidepressant) 2. Interventional Nerve blocks: diagnostic and therapeutic; e.g., coeliac plexus block (pancreatic cancer pain), NICE (NG59) — SCS for FBSS and CRPS; / Procedural stellate ganglion block, sympathetic blocks level 1 evidence for SCS in selected

Epidural steroid injection: lumbar radiculopathy, cervical radiculopathy — reduces nerve root populations; RFA supported by multiple inflammation; short-to-medium term benefit RCTs for facet pain

Radiofrequency ablation (RFA): thermal or pulsed RFA of facet joint medial branches for chronic facet pain; cryoablation of sensory nerves

Spinal Cord Stimulation (SCS): implanted lead in the dorsal epidural space; dorsal column electrical stimulation produces paresthesia overlying the painful area; excellent evidence for CRPS, failed back surgery syndrome (FBSS), refractory angina; NNT ~2.4 for CRPS

Intrathecal drug delivery (ITDD) systems: implanted pump delivering opioids/baclofen/ziconotide directly into the CSF; for cancer pain or spasticity; reduces systemic opioid requirements

TENS (Transcutaneous Electrical Nerve Stimulation): surface electrodes; modulates pain via gate control theory (large-fibre stimulation closes the gate to C-fibre transmission); simple, noninvasive; evidence moderate but patient-driven 3. Psychological Cognitive Behavioural Therapy (CBT): the most evidence-based psychological treatment for Cochrane reviews: CBT reduces pain chronic pain; addresses catastrophising, fear-avoidance, maladaptive pain behaviours; teaches intensity (SMD −0.4) and disability (SMD coping strategies, activity pacing, relaxation; delivered individually or in group settings; best evidence −0.3) in chronic low back pain; psychological for fibromyalgia, CLBP, headache; NNT ~3–5 for significant improvement in disability interventions are NICE-recommended as

Acceptance and Commitment Therapy (ACT): focuses on accepting pain rather than eliminating it; core components of chronic pain increasing psychological flexibility; newer evidence base but growing; particularly useful in patients management where pain cannot be eliminated

Mindfulness-Based Stress Reduction (MBSR): 8-week structured programme; meditation, body scan, yoga; reduces pain catastrophising and improves quality of life; level 2 evidence for chronic pain

Pain neuroscience education (PNE): teaching patients the neuroscience of pain processing reduces catastrophising and improves outcomes; shifts the patient's conceptual model from "pain = damage" to "pain = overactive alarm system" 4. Physical / Exercise therapy: the single most evidence-based physical intervention for chronic pain; aerobic Cochrane reviews: exercise vs no treatment Rehabilitative exercise, resistance training, and specific exercise programmes (e.g., McKenzie for CLBP, graded for CLBP — moderate quality evidence for activity); mechanisms include endorphin release, central sensitisation reversal, anti-inflammatory improved pain and function; exercise is NICE effects; supervised exercise superior to home exercise first-line recommendation for CLBP

Physiotherapy: manual therapy (mobilisation, manipulation) for musculoskeletal pain; specific exercise prescription; postural correction

Hydrotherapy: warm water exercises reduce joint loading while allowing mobility; excellent for fibromyalgia, OA, rheumatoid arthritis

Occupational therapy: activity grading, adaptive devices, return-to-work planning; particularly for patients with chronic pain and disability

Cardiac Output (CO): the volume of blood ejected by the left ventricle per minute; CO = Stroke Volume (SV) × Heart Rate (HR); normal = 4–8 L/min; Cardiac Index (CI) = CO/BSA; normal CI = 2.5–4.0 L/min/m²

Stroke Volume (SV): the volume ejected per beat (normal 60–100 mL); determined by preload, afterload, and contractility; SV variation (SVV) and pulse pressure variation (PPV) are dynamic indices of preload responsiveness in mechanically-ventilated patients — if SVV >13% or PPV >13%, the patient is likely preload-responsive (will increase SV with fluid challenge) Most non-invasive monitors estimate CO or SV indirectly through physical principles (thermodilution, Fick, bioreactance, Doppler) — each with its own assumptions, limitations, and sources of error

Accuracy vs Method / Device Principle Invasiveness Key Advantages Key Limitations PAC Oesophageal A flexible probe (6 mm) placed in the Minimally Good Real-time continuous; the Requires intubation and Doppler Monitor oesophagus at the level of the invasive — concordance most validated non-PAC CO sedation; operator skill for (ODM) — CardioQ descending thoracic aorta; emits requires with PAC (bias monitor; FTc provides probe positioning; not continuous Doppler ultrasound at 4 MHz; intubated/sedated within ±20%); unique stroke volume index reliable in AF (irregular measures red blood cell velocity in the patient; placed validated in and preload assessment; stroke volumes); descending aorta → waveform analysis like NGT; not multiple large OPTIMISE trial showed overestimates CO if probe provides stroke volume, corrected flow possible in awake trials ODM-GDT reduces not correctly aligned with time (FTc), and cardiac output estimate; patients or with complications in major aortic blood flow; only assumes a fixed proportion of CO passes oesophageal surgery; NICE-approved measures CO indirectly through the descending aorta (roughly pathology (MTG3) for use in major (assumes fixed descending 70%) surgery aorta fraction) Pulse Contour Analyses the arterial pressure waveform Minimally Moderate Continuous real-time CO; Accuracy degrades

Analysis — to calculate stroke volume from the area invasive — concordance also provides SVV and PPV significantly with arterial PiCCO, LiDCO, under the systolic portion of the pressure requires arterial with PAC; (fluid responsiveness waveform distortion FloTrac/Vigileo wave; requires an arterial line (radial or line (standard accuracy indices); PiCCO additionally (vasopressors, arrhythmia, femoral); some systems require anaesthetic decreases in: provides extravascular lung vasoconstriction); intermittent external calibration (PiCCO monitoring); no high-dose water and intrathoracic calibrated systems need uses transpulmonary thermodilution; additional central vasopressors, blood volume; suitable for periodic recalibration LiDCO uses lithium dilution); venous access irregular rhythms major surgery and ICU; (position change, FloTrac/Vigileo uses a proprietary needed for (AF), severe FloTrac requires only a haemodynamic instability); algorithm based on patient demographics FloTrac; PiCCO peripheral standard arterial line FloTrac less accurate than without external calibration and LiDCO vasoconstriction, calibrated systems in require calibration cardiac haemodynamically bolus arrhythmias, unstable patients aortic regurgitation Thoracic Alternating electrical current is passed Non-invasive — Moderate Completely non-invasive — Lower accuracy than ODM Electrical through the thorax via surface electrodes surface concordance no needles; suitable for or calibrated pulse contour Bioimpedance / on the neck and chest; changes in electrodes; no with PAC in non-intubated patients; can in high acuity; affected by Bioreactance transthoracic impedance (related to the arterial line stable patients; monitor awake patients in patient movement (NICOM, Cheetah) aortic blood volume change with each required; fully poor accuracy in: ICU or stepdown; useful for (artefact); unreliable in heartbeat) are used to calculate SV; non-invasive obesity, trend monitoring pulmonary oedema, severe bioreactance (NICOM) measures the cardiac pulmonary obesity, thoracic surgery phase shift of the AC signal rather than monitoring oedema (fluid patients amplitude — more specific to aortic flow, alters less affected by pleural fluid or body impedance), composition arrhythmias, after cardiac surgery (altered thoracic anatomy and fluid) Transoesophageal A phased-array ultrasound transducer on Minimally Excellent Provides qualitative AND Requires intubated patient; Echocardiography an oesophageal probe; provides direct invasive — accuracy when quantitative data; directly needs formal training (TOE/TEE) imaging of cardiac chambers, valves, and requires performed by a visualises the cause of (BSE/EACVI TOE great vessels; SV calculated from the intubation and competent haemodynamic instability accreditation); not portable velocity-time integral (VTI) of the LVOT sedation; operator; (tamponade, LV/RV or continuously available in Doppler multiplied by the LVOT cross- operator considered a dysfunction, hypovolaemia, all settings; time-intensive sectional area (2D echo measurement); expertise reference PE, valve per measurement; relative provides the gold standard for direct required; requires standard for regurgitation/stenosis); contraindications visualisation of cardiac function, wall formal TOE perioperative cannot be replicated by any (oesophageal disease, motion, pericardial effusion, and competency haemodynamics; other non-invasive monitor; variceal bleeding risk) haemodynamic instability training limited not by provides wall motion (EACVI/ASE accuracy but by assessment for ischaemia accreditation) operator skill and detection access Non-Invasive Continuous non-invasive blood pressure Non-invasive — Moderate Completely non-invasive; Accuracy reduced by Haemodynamic measurement from a finger cuff using the finger cuff; accuracy for suitable for monitoring in peripheral vasoconstriction; Monitor (CNAP — volume clamp method (Finapres suitable for trending; may awake patients, procedural requires regular calibration continuous non- technology); uses the continuous BP awake patients underestimate in sedation, obstetrics (non- cycles; less accurate than invasive arterial waveform to compute CO via pulse peripheral invasive BP + CO), arterial line-based systems pressure + Nexfin) contour analysis; completely non-invasive vasoconstriction monitored care settings in haemodynamically — finger cuff only and overestimate unstable patients in warm vasodilated patients

Concept: GDT uses real-time CO/SV monitoring to guide fluid and vasopressor therapy toward specific haemodynamic targets — aiming to optimise oxygen delivery (DO₂) to tissues rather than simply normalising conventional vital signs (MAP, HR, urine output); key targets: CO/CI, SV, SVV/PPV (fluid responsiveness), and derived DO₂ OPTIMISE Trial (Pearse et al., BMJ 2014; n=734): high-risk major gastrointestinal surgery patients randomised to ODM-guided GDT vs standard care; GDT group received targeted colloid boluses to maximise SV and maintain FTc 35–40 ms; GDT significantly reduced postoperative complications (44.3% vs 51.0% — adjusted risk ratio 0.84) — the largest pragmatic RCT of CO-guided therapy in major surgery

Fluid responsiveness assessment: SVV >13% (mechanically-ventilated patients in sinus rhythm) or a passive leg raise (PLR) test predicts fluid responsiveness; if fluid responsive → 250 mL crystalloid/colloid bolus → reassess SV; if SV increases >10% → repeat; if SV increase <10% → patient is on the flat part of the Frank-Starling curve → additional fluid will not increase SV → use vasopressors instead

During third stage of labour, the placenta separates and the uterus must contract rapidly to compress the spiral arteries of the placental bed — these arteries supply the placenta at a rate of approximately 500 mL/min at term; without uterine contraction, these open vessel sinuses bleed at this rate, producing potentially fatal haemorrhage within minutes Normal uterine contraction is mediated by oxytocin (from the posterior pituitary) acting on uterine myocyte oxytocin receptors → intracellular Ca²⁺ → myosin light chain kinase activation → smooth muscle contraction; prostaglandins (PGE₂, PGF₂α) and ergometrine (α-adrenergic stimulation + 5-HT-mediated) independently support uterine tone

Atony occurs when: oxytocin receptor downregulation (from prolonged IV oxytocin during labour); myometrial fatigue (prolonged labour, grand multiparity); mechanical failure to contract (fibroids, distension from polyhydramnios, multiple gestation, macrosomia); retained placental tissue preventing uniform contraction; drug-induced uterine relaxation (volatile anaesthetic agents, magnesium sulphate, tocolytics, nifedipine)

T Category Specific Risk Factors

T1 — Uterine atony Grand multiparity (≥5 deliveries — exhausted myometrium); overdistended uterus (multiple pregnancy, polyhydramnios, macrosomia —

TONE — failure of LGA baby >4 kg); prolonged labour (myometrial fatigue); precipitate labour; induction/augmentation with oxytocin (receptor uterine downregulation); uterine fibroids (prevent uniform contraction); general anaesthesia with volatile agents (dose-dependent uterine muscle to relaxation); magnesium sulphate infusion (tocolytic); chorioamnionitis contract

T2 — Retained Retained placenta or placental fragments (prevents normal uterine retraction and contraction); succenturiate lobe (accessory lobe — TISSUE products of frequently retained); placenta accreta spectrum (accreta/increta/percreta — placenta abnormally adherent, cannot separate normally; conception major risk for catastrophic PPH); placenta praevia (abnormally located, prevents normal third stage)

T3 — Genital tract Cervical tears (especially after rapid delivery); vaginal lacerations; perineal tears (1st–4th degree); uterine rupture (rare but catastrophic); TRAUMA lacerations uterine inversion (fundus turns inside out — rare; causes profound haemorrhage and shock); episiotomy; forceps/ventouse delivery; and injuries caesarean incision extension

T4 — Coagulopathy Pre-existing coagulopathy (ITP, vWD, haemophilia carrier); obstetric causes of coagulopathy: abruptio placentae (DIC from thromboplastin THROMBIN release), amniotic fluid embolism (DIC), HELLP syndrome, pre-eclampsia; dilutional coagulopathy from massive transfusion; anticoagulant therapy (LMWH, warfarin)

OP compound (lipid-soluble; absorbed via skin, inhalation, ingestion, conjunctiva) → covalently phosphorylates the serine hydroxyl group at the active site of acetylcholinesterase (AChE) → AChE is IRREVERSIBLY INHIBITED → cannot hydrolyse acetylcholine (ACh) at cholinergic synapses → ACh accumulates at: (1) all parasympathetic postganglionic nerve-effector junctions (muscarinic receptors); (2) nicotinic receptors at the NMJ (skeletal muscle); (3) autonomic ganglia — sympathetic and parasympathetic (nicotinic ganglionic receptors); (4) CNS synapses (muscarinic and nicotinic receptors in brain and spinal cord) → prolonged, excessive stimulation of ALL cholinergic receptors simultaneously → the CHOLINERGIC CRISIS.

SLUDGE (Muscarinic) = Salivation, Lacrimation, Urination, Defecation, GI cramps/Emesis DUMBELS = Defecation/Diarrhoea, Urination, Miosis, Bradycardia/Bronchospasm/Bronchorrhoea, Emesis, Lacrimation, Salivation System Receptor Features Mnemonic Aid MUSCARINIC M1, M2, Salivation (excessive drooling), Lacrimation (tearing), Urination (incontinence), Defecation (diarrhoea), GI SLUDGE + DUMBELS; (parasympathetic M3 cramps, Emesis; ADDITIONALLY: MIOSIS (pinpoint pupils — pathognomonic), bradycardia, "wet and small" — nerve-effector receptors bronchospasm, BRONCHORRHOEA (copious secretions in airways — the most life-threatening feature), excessive secretions + junctions) hypotension, diaphoresis, urinary incontinence miosis NICOTINIC (NMJ N1 NMJ stimulation → initial FASCICULATIONS (visible muscle twitching — brief initial stimulation phase) → "Paralysis follows + autonomic (ganglionic) progressing to PARALYSIS (continuous receptor depolarisation → end-plate depolarisation block → fasciculations" — never ganglia) and N2 flaccid paralysis); diaphragm paralysis → respiratory failure (the primary cause of death); GANGLIONIC use succinylcholine (NMJ) stimulation → tachycardia (may coexist with or override bradycardia), hypertension (early), pallor, (pseudocholinesterase receptors mydriasis (may counteract or compete with muscarinic miosis) inhibited → prolonged paralysis) CNS Central Anxiety, restlessness, delirium, seizures (classically intractable — resistant to standard anticonvulsants "Seizures + coma" — muscarinic alone; require benzodiazepines + atropine for adequate control); coma; central respiratory depression CNS cholinergic storm and (compounding NMJ paralysis); in severe poisoning, all three mechanisms combine to produce apnoea nicotinic receptors

Grade Clinical Features Management Mild Alert; salivation, lacrimation, miosis, diarrhoea; RR normal; no Observation; atropine titration; supportive respiratory compromise Moderate Confusion; significant bronchorrhea, bronchospasm; mild respiratory ICU admission; IV atropine; pralidoxime; monitor RR closely — may deteriorate distress; RR increased; fasciculations prominent rapidly Severe Coma; seizures; severe bronchorrhoea and bronchospasm; respiratory Immediate intubation + mechanical ventilation; IV atropine titration; pralidoxime; failure (apnoea); bradycardia + hypotension; paralysis benzodiazepines for seizures; ICU; prolonged ventilatory support

PERSONAL PROTECTION FIRST: OP compounds are highly lipid-soluble and absorbed through skin; all healthcare staff must wear gloves, gown, and eye protection before approaching the patient; remove and bag the patient's contaminated clothing before they enter the department

Decontamination: thorough washing of all exposed skin surfaces with soap and water (for 10–15 minutes) if dermal exposure; flush eyes with saline for conjunctival exposure; in ingestion cases: gastric lavage via NGT (within 1 hour of ingestion) + activated charcoal 50 g via NGT (if airway protected); emesis is CONTRAINDICATED (risk of aspiration, and rapid loss of consciousness)

Mechanism: pralidoxime (PAM; 2-PAM chloride) is an oxime compound that attacks the OP-AChE bond BEFORE ageing occurs → reactivates AChE by removing the OP group from the serine active site → restored AChE can resume hydrolysing ACh; this specifically reverses the NMJ (nicotinic) effects of OP poisoning (reverses fasciculations and paralysis) in addition to reducing the ACh burden at muscarinic synapses

Critical timing: pralidoxime MUST be given BEFORE AGEING; ageing rate depends on the specific OP compound — for most pesticide OPs, ageing occurs over hours; give pralidoxime as soon as diagnosis is made (ideally within 6–12 hours for most pesticides)

Dose: 1–2 g IV over 15–30 minutes; then 200–500 mg/hr infusion for 24–48 hours; continue until patient is asymptomatic and off atropine

Controversy: a large RCT from Sri Lanka (Eddleston et al., Lancet 2009) showed no mortality benefit of pralidoxime in agricultural OP poisoning — ongoing debate about its clinical utility in pesticide poisoning; still recommended in WHO and Indian guidelines; most useful early, before ageing

Seizures: benzodiazepines (diazepam 10 mg IV or midazolam 5–10 mg IV) — first-line; phenytoin is relatively ineffective for OP seizures (which are cholinergic in origin); continue until seizures stop

Monitor: ECG (QT prolongation from OP toxicity + atropine; AF, VT); blood glucose (OP poisoning causes hyperglycaemia from glycogen mobilisation); RBC cholinesterase activity (reflects AChE inhibition — correlates with severity); plasma cholinesterase (pseudocholinesterase — also inhibited but recovers faster)

Physical principle: a small sample of whole blood (~0.36 mL) is placed in a cylindrical cup; a pin suspended by a torsion wire is lowered into the blood; the cup oscillates through an arc of 4°45' at a rate of 1 oscillation every 10 seconds (4–5 Hz); as the blood clots, the fibrin strands form between the cup wall and the pin, and the rotational movement of the cup is transmitted to the pin through the clot — the more rigid the clot, the greater the angular displacement transmitted to the pin; this mechanical coupling is measured electronically and plotted as the TEG waveform (torque vs time)

Modern systems: original TEG (Haemonetics) uses the oscillating cup described above; ROTEM (Tem Innovations — rotational thromboelastometry) uses a rotating pin in a stationary cup — same principle, different geometry; the two systems are not directly interchangeable (different parameter names and reference ranges)

Activators used in different TEG channels: kaolin (activates the intrinsic/contact pathway — most common for trauma and general coagulopathy assessment); tissue factor/TF (extrinsic pathway — rapid TEG); heparinase cup (same as kaolin but heparinase added to neutralise heparin — used intraoperatively in cardiac surgery to measure true coagulation status excluding heparin effect); functional fibrinogen (platelet inhibitor GPIIb/IIIa added — measures fibrinogen contribution only, excluding platelet contribution to clot strength)

Normal Parameter What It Measures Abnormal → Interpretation → Action Range R Time from placement of blood in the cup to first detectable fibrin formation 5–10 ↑R (prolonged): factor deficiency; anticoagulant effect (Reaction (when the waveform amplitude first reaches 2 mm); represents the time for minutes (heparin, warfarin, NOACs); haemophilia; → give FFP time) sufficient thrombin to be generated to initiate fibrin polymerisation; reflects the (kaolin- (replaces factors II, V, VII, IX, X, XI, fibrinogen); if CLOTTING FACTORS (both intrinsic and extrinsic pathways) activated) heparin-related → protamine ↓R (shortened): hypercoagulable state; thrombophilia K Time from R (first fibrin formation) to when the clot amplitude reaches 20 mm; 1–3 ↑K: low fibrinogen; thrombocytopenia; anticoagulants → (Kinetics represents the speed of clot formation — mainly reflects FIBRINOGEN function minutes give cryoprecipitate (fibrinogen concentrate); platelets if time) and platelet contribution to clot development thrombocytopenic ↓K: hypercoagulable Alpha The angle of the tangent to the TEG curve at 2 mm amplitude; represents the 53–72 ↓Alpha angle (flat curve): low fibrinogen; low platelets; angle (α) rate of fibrin build-up and cross-linking — more steeply rising curve = faster degrees → cryoprecipitate + platelets fibrin polymerisation; reflects FIBRINOGEN concentration and platelet-fibrin ↑Alpha angle: hypercoagulable; pregnancy (high interaction fibrinogen physiologically) MA The maximum width of the TEG waveform — the peak clot strength; reflects the 55–73 mm ↓MA: thrombocytopenia; platelet dysfunction (aspirin, (Maximum total clot strength from the interaction of fibrin and PLATELETS (primarily — clopidogrel, uraemia, liver disease); low fibrinogen → Amplitude) approximately 80% of MA is platelet-dependent; 20% is fibrinogen-dependent); give platelets (if platelet count low or function impaired); MA is the most clinically important parameter for platelet function assessment consider desmopressin (if platelet dysfunction from aspirin/vWD) ↑MA: hypercoagulable; post-trauma hypercoagulability; may predict thrombosis LY30 The percentage decrease in clot amplitude at 30 minutes after MA is reached; <8% lysis ↑LY30 (>8%): hyperfibrinolysis — the clot is dissolving (Lysis at represents FIBRINOLYSIS — how much of the clot has been dissolved by 30 at 30 too rapidly (e.g., after trauma, liver failure, amniotic fluid 30 minutes after maximal clot formation minutes embolism, cancer surgery); → give TRANEXAMIC ACID minutes) (normal (antifibrinolytic); this is the specific TEG indication for fibrinolytic TXA activity) ↓LY30 (near 0%): fibrinolytic shutdown (common in trauma after initial hyperfibrinolysis) — do NOT give TXA (may worsen hypercoagulability) CL60 (Clot As LY30 but at 60 minutes; used in ROTEM as LI60 or CLT60 <15% Same interpretation as LY30 but with more time elapsed; lysis at 60 useful for monitoring TXA efficacy minutes)

Pattern Appearance Interpretation Treatment Normal Classic "footprint" shape — narrow at base (R), All coagulation parameters normal None required widening through K and Alpha, maximum width at MA, mild narrowing after Factor deficiency Elongated R time; normal or slightly reduced MA Slow initial clot formation from factor FFP (or specific factor concentrate if identified) and Alpha angle deficiency; clot strength may be adequate once formed Fibrinogen Normal R; prolonged K; reduced Alpha angle; Initial factor activation normal; fibrin Cryoprecipitate 10 units or fibrinogen concentrate deficiency reduced MA formation slow and weak; clot is thin 2–4 g and fragile Platelet Normal R; normal K and Alpha; markedly reduced Coagulation cascade and fibrinogen Platelet transfusion; desmopressin if dysfunction dysfunction / MA normal; poor platelet contribution to thrombocytopenia clot strength Hyperfibrinolysis Normal R/K/Alpha/MA initially; then dramatic Clot forms normally but is rapidly Tranexamic acid 1 g IV immediately progressive narrowing of the waveform after MA — lysed by fibrinolysis (↑LY30 >8%) the "onion peel" or "glass vase" appearance Global Prolonged R; reduced K; reduced Alpha; very low All components of coagulation are Massive transfusion protocol: FFP + coagulopathy MA; often increased LY30 depleted; typical of late trauma DIC, cryoprecipitate + platelets + TXA in targeted (DIC) obstetric DIC, sepsis-induced DIC fashion based on which parameters are most abnormal

Standard Tests (PT, APTT, Fibrinogen, Platelet Feature TEG / ROTEM Count) Sample Whole blood (includes platelets, RBCs, WBCs — holistic) Plasma (platelets removed by centrifugation — platelet function NOT assessed by PT/APTT) Result time 10–30 minutes for actionable results (MA visible at ~20–30 min) 45–90 minutes (laboratory processing time)

Fibrinolysis YES — directly measured as LY30/LY60 NO — PT/APTT cannot detect fibrinolysis; D-dimer detection is indirect

Platelet function YES — MA reflects platelet-fibrin interaction; specific platelet mapping TEG channels NO — platelet count does not assess function; available specific tests (PFA-100, aggregometry) needed Point-of-care YES — bedside in theatre or ICU; results during active haemorrhage NO — requires central laboratory; results after clinical decision must be made Evidence for Multiple RCTs show TEG/ROTEM-guided transfusion reduces blood product use 30–40% Used for baseline assessment and monitoring; less guiding and improves outcomes in cardiac surgery, trauma, and liver transplantation suitable for real-time resuscitation guidance transfusion

DepoFoam particle structure: liposomal bupivacaine consists of multivesicular liposomes (MVLs) — each particle (15–30 μm diameter) contains dozens to hundreds of aqueous chambers (vesicles) separated by lipid membranes; each aqueous chamber contains dissolved bupivacaine base; the particles are suspended in normal saline for injection; the particle walls are composed of natural phospholipids (same composition as cell membranes — biodegradable and biocompatible)

Release mechanism: after injection into tissue, the liposomal particles are taken up by tissue macrophages and fibroblasts, and the lipid walls are slowly degraded by tissue lipases and phospholipases over 72–96 hours; as each membrane breaks down, bupivacaine is released into the local tissue environment in a controlled, sustained fashion; the release is not immediate but follows an extended profile — Cmax (peak plasma concentration) occurs at approximately 24–48 hours after injection (much later than plain bupivacaine which peaks at 15–30 minutes), and plasma levels remain above the analgesic threshold for 72– 96 hours

Comparison with standard bupivacaine: plain bupivacaine (0.5%) injected as a nerve block or wound infiltration produces high initial plasma concentrations (Cmax within 15–30 minutes), providing 6–8 hours of analgesia before plasma levels fall below the effective threshold; liposomal bupivacaine provides a much lower Cmax (reduced LAST risk from the rate-controlled release), sustained analgesic levels for 72 hours, and a pharmacokinetic profile that is independent of the vascularity of the injection site (because drug is released from the particles, not simply absorbed) Parameter Plain Bupivacaine 0.5% Liposomal Bupivacaine (Exparel) Tmax (time to peak plasma 15–30 minutes 24–48 hours level) Cmax (peak plasma Higher (higher peak with equivalent dose) Lower (slower release rate → reduced peak) concentration) Duration of analgesia 6–8 hours (nerve block) to 2–4 hours (wound Up to 72 hours infiltration) LAST risk profile Higher initial Cmax → higher early LAST risk Lower Cmax → theoretically lower peak LAST risk, but cumulative exposure prolonged Maximum recommended dose 2–2.5 mg/kg (plain) 266 mg (single dose in adults; do not exceed)

Application Technique Evidence Wound Single-shot injection into surgical wound layers at wound RCT (Haas, Anesth Analg 2012): haemorrhoidectomy — liposomal bupivacaine infiltration closure; diluted with NS to increase volume for wide-area wound infiltration significantly reduced pain scores and opioid use for 72 hours vs (surgical site infiltration; FDA-approved for bursectomy, haemorrhoidectomy placebo; one of the strongest FDA approval trials infiltration) TAP block Ultrasound-guided bilateral TAP block with 266 mg liposomal Golf et al. RCT (2011): single-injection liposomal bupivacaine TAP block reduced (Transversus bupivacaine diluted to 60 mL; provides prolonged abdominal pain scores and opioid consumption for 72 hours after colectomy; FDA-approved Abdominis wall analgesia for laparotomy, colectomy, hysterectomy, C- indication for TAP block; growing use in ERAS (Enhanced Recovery After Surgery) Plane block) section pathways Interscalene 266 mg ultrasound-guided interscalene block; provides 72- Multiple RCTs comparing liposomal bupivacaine ISB vs catheter-based continuous nerve block hour analgesia for total shoulder arthroplasty and rotator cuff interscalene block; liposomal bupivacaine provides non-inferior analgesia in some (shoulder repair — avoiding the need for a catheter; suitable for but not all trials; enables truly ambulatory shoulder arthroplasty (no catheter pump surgery) ambulatory shoulder surgery to manage at home) Local Surgeon intraoperatively infiltrates the periarticular tissues Bramlett RCT (Reg Anesth Pain Med 2012): liposomal bupivacaine LIA in TKA infiltration (posterior capsule, fat pad, periosteum) with liposomal reduced opioid consumption 30% over 48 hours vs placebo; results vs spinal with analgesia (LIA) bupivacaine during joint replacement; reduces post-TKA pain intrathecal morphine are more mixed — some studies show equivalence, others — knee/hip for 72 hours show spinal superiority arthroplasty Mastectomy / Pectoralis plane block or wound infiltration with liposomal Growing evidence; widely used in breast surgery ERAS programmes; reduces breast surgery bupivacaine provides prolonged analgesia avoiding thoracic length of stay epidural; enables ambulatory mastectomy

ERAS integration: the key value proposition of liposomal bupivacaine in ERAS is providing 72 hours of analgesia from a single injection without catheter infrastructure (no pump, no home nursing, no catheter dislodgement risk, no risk of perineural infection) — this enables true ambulatory surgery for procedures previously requiring admission for catheter analgesia management; it reduces opioid consumption (opioid-sparing) → less PONV, earlier mobilisation, faster discharge

Cost-effectiveness debate: at approximately $300–350 USD per vial (vs <$5 for plain bupivacaine), liposomal bupivacaine is significantly more expensive; cost-effectiveness is demonstrated only when the extended duration reduces hospital length of stay or avoids the cost of catheter infrastructure (pump, tubing, nursing management, hospital admission); for inpatient surgery where any nerve block catheter would be placed, the cost advantage over a well-functioning catheter may not be demonstrated; for ambulatory surgery enabling same-day discharge for procedures previously requiring admission — the costeffectiveness argument is much stronger

Local anaesthetic systemic toxicity (LAST): the extended-release pharmacokinetics mean that LAST risk is not eliminated — it is temporally shifted; the peak LAST risk occurs at 24–48 hours rather than immediately post-injection; patients must be monitored for delayed LAST presentations in the ambulatory setting (patient education about LAST symptoms is important for home discharge)

Structure: sugammadex is a modified gamma-cyclodextrin — a cyclic oligosaccharide of 8 glucose units arranged in a toroidal (doughnut) shape; the interior of the torus is hydrophobic; 8 negatively-charged carboxymethyl thioether side chains extend from the exterior of the ring, conferring aqueous solubility and electrostatic attraction to the guest molecule

Host-guest inclusion complex: the steroidal nucleus of rocuronium (or vecuronium) "docks" into the hydrophobic central cavity of the sugammadex torus — shape complementarity + hydrophobic interactions + electrostatic interactions between the carboxymethyl chains and the quaternary N⁺ of rocuronium form a 1:1 inclusion complex with extremely high binding affinity (Kd ~10⁻²⁵ mol/L — essentially irreversible under physiological conditions)

Pharmacodynamic consequence: encapsulated rocuronium within the sugammadex cage is COMPLETELY INACCESSIBLE to the neuromuscular junction nicotinic receptor; free plasma rocuronium concentration falls sharply as it is sequestered into the complex → rocuronium dissociates from the NMJ receptors along the new plasma concentration gradient → NMJ function restored → neuromuscular block reversed

Specificity: the cyclodextrin cavity accommodates the steroidal skeleton of aminosteroid NMBs (rocuronium > vecuronium > pancuronium); it has essentially no affinity for benzylisoquinolinium NMBs (atracurium, cisatracurium, mivacurium) — their non-steroidal structures do not fit the cavity; therefore sugammadex

CANNOT reverse atracurium or cisatracurium

No receptor activity: sugammadex has no activity at any receptor — no cholinergic, anticholinergic, or cardiovascular effects from the mechanism itself; it is a purely pharmacokinetic intervention (drug sequestration, not pharmacodynamic antagonism)

Clinical Scenario NMJ Monitor Status Sugammadex Dose Expected Recovery to TOFR ≥0.9 Routine reversal at end of case TOF count ≥2 (T2 present — at least 2 visible 2 mg/kg IV (based on actual ~3 minutes (moderate block) responses to TOF stimulation) body weight) Deep block reversal PTC 1–2 (TOF count = 0, but 1–2 post-tetanic 4 mg/kg IV (actual body ~3–4 minutes twitches present) weight)

CICO emergency reversal — Profound block: within 3 minutes of rocuronium 1.2 16 mg/kg IV (actual body ~2–3 minutes to restoration of adequate immediate mg/kg (PTC = 0, TOF = 0) weight) — push dose spontaneous ventilation

Consideration Detail Renal failure Sugammadex-rocuronium complex is excreted renally unchanged; in severe renal impairment (eGFR <30 mL/min), both drug and complex are retained; the complex may dissociate at very low concentrations, potentially releasing rocuronium → re-paralysis hours later; avoid sugammadex in severe renal failure or use with extreme caution (extended monitoring for at least 24 hours post-administration); dialysis can remove the complex

Re-paralysis After a full 16 mg/kg CICO dose: residual sugammadex will bind any subsequently administered rocuronium unpredictably; do NOT administer — when to rocuronium for at least 24 hours after a 16 mg/kg dose; if re-paralysis is needed within 24 hours → use a benzylisoquinolinium NMB (cisatracurium, reintroduce atracurium) which is NOT encapsulated by sugammadex and has predictable pharmacokinetics; after routine 2 mg/kg reversal: wait at least 5 minutes NMBs before rocuronium if repeat block needed (sugammadex still present); for elective re-paralysis: use cisatracurium Hormonal Progesterone (and related hormones in combined oral contraceptive pills and progesterone-only pills) may bind to the sugammadex cyclodextrin cavity contraception — reducing the effective plasma progesterone concentration; this is equivalent pharmacokinetically to missing one dose of the combined OCP; advise the patient to use additional contraception for 7 days after sugammadex administration (as stated in the prescribing information) Toremifene Toremifene has high affinity for the sugammadex cyclodextrin and competes with rocuronium for encapsulation → may significantly delay or reduce (oestrogen reversal efficacy; avoid sugammadex in patients receiving toremifene; use neostigmine-based reversal if rocuronium was used, or use a different NMB antagonist for breast cancer)

Sugammadex Neostigmine (acetylcholinesterase inhibitor): only works when TOF count ≥2 (significant block remaining cannot be reversed); requires co-administration vs of anticholinergic (glycopyrrolate/atropine) to prevent bradycardia and excess secretions; cannot fully reverse block to TOFR ≥0.9 reliably — residual Neostigmine block persists in a significant proportion; maximum dose 0.07 mg/kg. Sugammadex: works at ANY depth of block (2/4/16 mg/kg); no anticholinergic required; reliably achieves TOFR ≥0.9; much faster onset; preferred for all routine and emergency reversal where available; much more expensive

Type Description Incidence

Type A Oesophageal atresia ALONE — no fistula; blind upper pouch, normal lower oesophagus with no connection to trachea; "pure oesophageal 7% atresia" Type B Oesophageal atresia with proximal TEF — the upper pouch connects to the trachea; rare 1% Type C Oesophageal atresia with DISTAL TEF — the upper oesophagus ends in a blind pouch; the lower oesophagus (from the stomach) connects to 87% (Most the TRACHEA via a fistula; this is the type with the greatest risk of positive-pressure ventilation inflating the stomach (gas goes via trachea → common) fistula → lower oesophagus → stomach); incidence ~87% of all TEF cases Type D Oesophageal atresia with BOTH proximal and distal TEF; rare 1% Type E TEF WITHOUT oesophageal atresia — an isolated fistula connecting the trachea and oesophagus; the oesophagus is intact and the neonate 4% (H-type) can swallow; diagnosis may be delayed (recurrent aspiration pneumonia, choking with feeds, abdominal distension); classically in the shape of an "H" on contrast oesophagram; most difficult type to diagnose

VACTERL association: approximately 50% of TEF infants have associated anomalies — Vertebral (sacral agenesis, hemivertebrae), Anal atresia (imperforate anus), Cardiac (VSD, ASD, TOF — most important; cardiac anomaly present in ~35%), Tracheo-Esophageal fistula, Renal (horseshoe kidney, absent kidney), Limb (radial aplasia, polydactyly)

Preoperative assessment: echocardiogram (mandatory — identify cardiac anomaly and right or left aortic arch — determines surgical approach; right arch → left thoracotomy; left arch → right thoracotomy); chest X-ray (coiled NGT in the upper pouch = Type C; gasless abdomen = Type A no distal fistula); renal ultrasound; spinal X-ray; blood group and crossmatch; blood glucose monitoring (neonatal hypoglycaemia risk)

Preoperative optimisation: head-up positioning (30°) to reduce gastric acid aspiration into lungs via fistula; continuous upper pouch suction via Replogle tube (prevents saliva accumulation and aspiration from the blind upper pouch); IV access for fluids and glucose; antibiotics if aspiration pneumonia suspected; temperature maintenance; delay surgery if severe pneumonia or prematurity with RDS requiring high ventilatory pressures — HFOV may be needed first

Induction — The Core Dilemma

IV — Rate

Position I — Chamber Paced II — Chamber Sensed III — Response to Sensing Modulation Letters O=None; A=Atrium; V=Ventricle; O=None; A=Atrium; V=Ventricle; O=None; I=Inhibited; T=Triggered; D=Dual (I+T) O=None; R=Rate-

D=Dual (A+V) D=Dual (A+V) modulated

Example: V=Ventricle paced V=Ventricle sensed I=Inhibited (pacemaker output inhibited when native (no rate modulation)

VVI ventricular beat is sensed)

Example: D=Both chambers paced D=Both chambers sensed D=Inhibited by native beat + Triggered by P wave (no rate modulation

DDD shown)

Common VVI — standard single-chamber pacemaker; DDD — physiological dual-chamber pacemaker; VOO/DOO — asynchronous (fixed rate, no sensing) modes modes used under magnet; VVIR — VVI with rate-adaptive function (accelerometer responds to patient activity)

EMI Source Effect on Pacemaker Effect on ICD Monopolar The EMI from the monopolar diathermy current path (from active electrode to return pad) can be ICD interprets diathermy signal as VF → delivers surgical sensed by the pacemaker as native cardiac electrical activity → pacemaker is INHIBITED (it inappropriate HIGH-ENERGY SHOCK (20–40 J) diathermy "thinks" the patient is generating their own beats) → paced output is suppressed → asystole in to the fully conscious or anaesthetised patient → (most common pacemaker-dependent patients; also: rapid diathermy can trigger pacemaker reversion to backup pain, burns, possibility of inducing true VF or and dangerous) rate (fixed rate mode) atrial fibrillation

Bipolar surgical Minimal risk — current flows only between the two tips of bipolar forceps; extremely localised EMI; Minimal risk; preferred diathermy does not affect implanted devices in most circumstances; preferred diathermy technique in patients with pacemakers/ICDs

MRI (strong Older devices: reed switch activation → asynchronous pacing; rapid pacing from strong RF field; Inappropriate shock delivery; lead heating; reed magnetic field) device damage; heating of leads (myocardial burns); reed switch function may not reliably revert switch; generally contraindicated unless MRIto sensing mode. MRI-conditional devices: specifically tested for use at 1.5T (some 3T) under conditional ICD defined conditions; conditional devices can safely undergo MRI with appropriate programming Radiofrequency Similar to monopolar diathermy; device reprogramming may be required; avoid ablation catheters Similar to diathermy — inappropriate shock; ICD ablation near the device leads must be reprogrammed to no-therapy mode before ablation Peripheral Low risk; use the stimulator on the opposite side from the pacemaker generator and leads Minimal risk nerve stimulator (neuromuscular monitor)

Preoperative Identify the device type, manufacturer, model, and implant date (from patient's device card or cardiologist records); determine if the patient is PACEMAKERDEPENDENT (no underlying rhythm — asystole if pacing inhibited) vs non-dependent Assess underlying rhythm via 12-lead ECG; determine current programming mode

Contact the device clinic/cardiologist: if surgery is >6 inches (15 cm) from the device AND monopolar diathermy use is expected → reprogramming to asynchronous mode (VOO/DOO) is strongly recommended; OR prepare a magnet for intraoperative use

For ICDs: ICD anti-tachycardia therapy (shock delivery) must be DEACTIVATED (suspended) before surgery if monopolar diathermy is to be used — inappropriate ICD shock during surgery is dangerous and can induce true VF; suspend ICD by reprogramming (preferred) or by magnet application

Magnet Application — Mechanism and Use

Minimum Safe Interval Before Elective Stent Type Rationale Surgery Bare Metal Stent (BMS) 4–6 weeks minimum (preferably 3 months) Endothelialisation of BMS is complete by 4 weeks; after 4 weeks, aspirin alone is sufficient and surgery is feasible Drug-Eluting Stent (DES) — 1st 12 months minimum DES polymer coating inhibits endothelialisation; incomplete endothelialisation gen (sirolimus/paclitaxel) persists for up to 12 months; stent thrombosis risk remains very high if DAPT is stopped before this

DES — 2nd gen 6 months minimum; many guidelines now Faster endothelialisation with newer DES; 2022 ESC guidelines suggest 3 (everolimus/zotarolimus — thin accept 3 months for newer-generation DES in months is acceptable for newer-generation DES if surgery cannot be deferred strut, biocompatible polymer) high-risk surgery

Continue aspirin throughout perioperative period: aspirin should not be stopped for THR even in the presence of orthopaedic surgery unless the surgeon has a specific reason (unusual bleeding site); the incremental bleeding risk of aspirin for THR is modest (slightly increased wound ooze); the thrombosis risk of stopping aspirin in a DES patient is much higher; aspirin 75–100 mg should be continued up to and including the morning of surgery and restarted as soon as haemostasis is confirmed postoperatively Clopidogrel management (the difficult decision):

If surgery can wait: DEFER until ≥6 months post-DES and complete the full DAPT course; then stop clopidogrel 5 days before surgery; continue aspirin

If surgery cannot be deferred: cardiologist must be involved in the decision; options include "bridging" with IV eptifibatide or tirofiban (IV GP IIb/IIIa inhibitors with short half-lives — stopped 4 hours before surgery, provide platelet inhibition until the moment of surgery with rapid offset); however bridging is only supported by observational data, not RCTs, and has fallen out of favour in some guidelines; most recent ACC/AHA guidelines do not recommend bridging DAPT If proceeding with surgery with clopidogrel continued (surgeon and cardiologist agree): accept higher intraoperative and postoperative bleeding risk; use cell salvage; avoid spinal/epidural (LCRP/anticoagulation contraindication)

Pre-operative optimisation: coronary function assessment (stress test or functional status evaluation); echocardiogram (LV function, wall motion); anaesthesia preassessment for cardiac risk (RCRI or ACS-NSQIP cardiac risk calculator)

Neuraxial vs General Anaesthesia Technique Advantages for THR Specific Considerations with DAPT Spinal Reduces blood loss (~30% reduction vs GA); lower DVT/PE If clopidogrel has been stopped ≥5 days: spinal is safe; ACCP and ESRA guidelines anaesthesia incidence; reduces PONV; better postoperative analgesia; avoids allow spinal/epidural if clopidogrel stopped ≥5 days; if clopidogrel is continued: (preferred general anaesthesia risks; reduces cognitive dysfunction in elderly spinal contraindicated (epidural haematoma risk with dual antiplatelet therapy) for THR) General Allows surgery regardless of antiplatelet status; no risk of epidural Higher blood loss than spinal; more PONV; suitable if neuraxial is contraindicated anaesthesia haematoma (DAPT continued, patient refusal, anatomical difficulty) (GA) Combined Spinal for surgery + epidural for post-op analgesia Same antiplatelet restrictions as neuraxial above; epidural catheter removal must Combined Spinal for surgery + epidural for post-op analgesia Same antiplatelet restrictions as neuraxial above; epidural catheter removal must spinal- also be timed carefully relative to antiplatelet therapy epidural (CSE)

BCIS prevention: pre-cementation FiO₂ 1.0; fluid preload; ephedrine drawn; surgeon announcement before cementing; thorough canal lavage; venting holes — standard protocol for all cemented THR (see Q20); this patient's cardiac disease makes BCIS particularly dangerous

VTE prophylaxis: mechanical (pneumatic compression) from induction; LMWH starting 12 hours post-operatively; if clopidogrel was continued through surgery, coordinate with haematology for postoperative LMWH timing (risk of additive bleeding); resume aspirin + clopidogrel as early as safely possible postoperatively (within 24 hours if haemostasis adequate)

Neurological: document exact level and completeness of paraplegia (sensory and motor); autonomic dysfunction assessment — patients with high thoracic/cervical cord lesions can develop autonomic dysreflexia during surgery; baseline bladder and bowel function; pressure sores from immobility

Obstetric: gestational age; fetal wellbeing (biophysical profile, CTG); placental position; planned fetal monitoring during surgery; obstetric team involvement; plan for emergency CS if fetal compromise during surgery

TB disease status: duration of ATT; which drugs (HRZE — Isoniazid, Rifampicin, Pyrazinamide, Ethambutol); current liver function (rifampicin hepatotoxicity); sputum status (open vs closed TB); isolation precautions; airway TB involvement (laryngeal TB)

Drug interactions from ATT: rifampicin is a potent inducer of CYP450 enzymes (CYP3A4, CYP2C19) → increases metabolism of many anaesthetic drugs including: opioids (morphine, fentanyl — reduced duration); neuromuscular blocking agents (vecuronium — shorter duration, may need higher doses); propofol (modest effect); volatile agents (minimal clinically significant effect); benzodiazepines (faster metabolism); anticonvulsants; warfarin

Airway

Pregnancy-related airway changes: oedematous mucosa (Mallampati class may have risen), reduced FRC, rapid desaturation during apnoea, increased aspiration risk (reduced gastroesophageal sphincter tone + raised intra-abdominal pressure) — RSI protocol required Check for laryngeal TB (unusual but possible in miliary TB) — hoarseness, stridor; consider awake fiberoptic intubation if laryngeal involvement suspected

Neuraxial anaesthesia: NOT suitable as primary anaesthetic — spinal TB at the surgical level makes spinal/epidural technically impossible at that level and contraindicated due to direct needle insertion through infected tissue; consider neuraxial at a remote unaffected level for postoperative analgesia only after consulting with the neurosurgeon and confirming the anatomy is uninvolved

Positioning

Anterolateral decompression: typically lateral decubitus position; pregnancy complicates this — ensure aortocaval decompression is maintained (left lateral tilt) even in the lateral position to prevent supine hypotension syndrome; the gravid uterus requires a supporting roll/padding Autonomic dysreflexia precautions if thoracic cord lesion is above T6 — sudden hypertension, bradycardia, sweating from surgical stimulation below the cord injury level; treated with vasodilators (hydralazine, GTN); deepening anaesthesia

General anaesthesia with RSI: antacid prophylaxis (sodium citrate + H₂ blocker); rocuronium 1.2 mg/kg for RSI (succinylcholine acceptable if no contraindications from paraplegia — avoid succinylcholine if paraplegia >6 months as denervation upregulates extrajunctional AChRs → life-threatening hyperkalaemia from succinylcholine)

Maintenance: volatile agent (sevoflurane — minimal uterine relaxant effect at <1 MAC; maintain adequate fetal uteroplacental perfusion by maintaining maternal MAP ≥65 mmHg); avoid N₂O (potential teratogenicity in first trimester; bowel distension)

Fetal monitoring: continuous CTG intraoperatively in viable gestations (>24 weeks); dedicated obstetrician monitoring and interpreting the CTG; plan for emergency CS — caesarean trolley in theatre; neonatology team on standby

NMB dosing: vecuronium/rocuronium may have shorter duration due to rifampicin CYP induction; monitor with quantitative TOF and redose as needed; reverse with sugammadex at end of case

Analgesia: IV morphine PCA (paracetamol + NSAIDs if obstetric team agrees; NSAIDs avoided in >32 weeks gestation — premature closure of ductus arteriosus); neuraxial analgesia at an unaffected spinal level if technically feasible and neurosurgeon approves

TB precautions: respiratory isolation in recovery room and ward; staff PPE; continue ATT postoperatively (most can be resumed orally within 24–48 hours)

Fetal monitoring: continuous CTG for 24 hours postoperatively; obstetric review daily; plan for preterm labour monitoring

VTE prophylaxis: paraplegia + pregnancy = very high VTE risk; pneumatic compression stockings intraoperatively; LMWH from 6–12 hours post-op (obstetric team timing guidance)

Category 1 CS (RCOG classification): immediate threat to life of mother or fetus; decision-to-delivery interval target <30 minutes

Anaesthetic choice dilemma: if the patient has a functioning epidural (labour epidural in situ) → top-up with 20 mL 2% lidocaine + 1:200,000 adrenaline (fastest route to surgical anaesthesia via existing catheter — achieves T4 block in 5–10 minutes); if no epidural in situ → decision between rapid-sequence spinal vs general anaesthesia depends on urgency: if delivery urgency allows 5–10 minutes → single-shot spinal (faster than GA in skilled hands, avoids difficult obstetric airway, avoids neonatal drug exposure); if delivery truly immediately life-threatening (catastrophic fetal heart rate, cord prolapse, abruption) → GA with RSI (fastest to surgical conditions, avoids setup time of spinal)

Pre-eclampsia specifically worsens the obstetric airway: facial and laryngeal oedema (from hypertensive systemic oedema and low albumin) → Mallampati class higher than non-pre-eclamptic patient; laryngeal oedema causes stridor in severe cases; the "obstetric difficult airway" incidence is higher in preeclampsia than in non-hypertensive parturients

Pre-GA airway assessment: Mallampati class, thyromental distance, mouth opening, neck extension; if possible, briefly assess even for emergency GA; have video laryngoscope as first-line for pre-eclamptic patients

Modified RSI for pre-eclampsia: the hypertensive response to laryngoscopy in a pre-eclamptic patient is dramatically amplified (catecholamine surge → acute severe hypertension → risk of intracranial haemorrhage); attenuate this response with: alfentanil 10–20 mcg/kg IV just before laryngoscopy (rapid-onset opioid — reduces catecholamine response); OR remifentanil 1 mcg/kg IV; OR lignocaine 1.5 mg/kg IV; OR labetalol 10–20 mg IV (alpha and beta blockade); co-administer with thiopentone 4–5 mg/kg (preferred over propofol in emergency CS for faster loss of consciousness and proven fetal safety) or propofol 2 mg/kg; rocuronium 1.2 mg/kg for rapid intubation (preferred over succinylcholine if MgSO₄ infusion — see D below)

Spinal anaesthesia is SAFE in severe pre-eclampsia — the historical concern that pre-eclamptic patients would develop catastrophic hypotension from spinalinduced vasodilation has been disproven; pre-eclamptic patients actually have LESS hypotension after spinal than healthy parturients (their high SVR provides a partial buffer)

Standard single-shot spinal: heavy bupivacaine 0.5% 2–2.5 mL + fentanyl 15–25 mcg + morphine 100 mcg; T4–T6 level for CS

Fluid management with spinal: co-load (simultaneous with spinal — 500 mL colloid or crystalloid) rather than pre-load (pre-eclamptic patients have low colloid osmotic pressure from hypoalbuminaemia + impaired sodium excretion → excessive fluid administration risks pulmonary oedema); phenylephrine or noradrenaline infusion to treat spinal-induced hypotension

Interaction Mechanism & Clinical Consequence Management Non-depolarising Mg²⁺ inhibits ACh release from the presynaptic terminal (competes with Ca²⁺ at the presynaptic Reduce NDMR dose by 30–50%; use NMBs (rocuronium, Ca²⁺ channels required for ACh vesicle fusion) AND reduces motor end-plate sensitivity to ACh; quantitative TOF monitoring throughout; vecuronium, both mechanisms potentiate NDMR block; clinical effect: standard doses of NDMR produce sugammadex for reversal (not neostigmine atracurium) deeper and more prolonged block than normal; TOFR may not recover within expected time — hypermagnesaemia impairs neostigmine efficacy) Succinylcholine Mg²⁺ inhibits ACh release → reduces initial stimulation of the NMJ → reduces the intensity of Succinylcholine still effective but may show succinylcholine-induced fasciculations; prolongs succinylcholine's Phase I block duration; at high altered onset; prefer rocuronium with Mg²⁺ levels (>4 mmol/L), onset of succinylcholine paralysis may be delayed sugammadex availability in MgSO₄-infused patients Volatile anaesthetic MgSO₄ + volatile agents: additive CNS and cardiovascular depression; reduces MAC requirement; Reduce volatile agent concentration; agents monitor for excessive cardiovascular depression monitor BIS; maintain MAP with vasopressors Calcium channel MgSO₄ + nifedipine → additive vasodilation + negative inotropy → profound hypotension; MgSO₄ Monitor BP closely; be ready to treat blockers (nifedipine itself is a Ca²⁺ channel blocker (competes with Ca²⁺); nifedipine amplifies this effect hypotension aggressively; prefer IV — used for labetalol or IV hydralazine over oral antihypertensive in nifedipine in the emergency perioperative pre-eclampsia) setting

Target: systolic BP <160 mmHg (above this → maternal ICH risk); diastolic BP <110 mmHg; do NOT reduce MAP by >20–25% acutely (uteroplacental perfusion is pressure-dependent and not autoregulated; acute hypotension → fetal distress) IV labetalol 20 mg IV bolus (alpha + beta blockade); repeat 40 mg, 80 mg if needed; maximum 300 mg total; contraindicated in asthma IV hydralazine 5–10 mg over 2 minutes; repeat every 15–20 minutes; slower onset than labetalol; may cause reflex tachycardia Oral nifedipine 10 mg (if IV access not yet established); onset 10–15 minutes

Investigation Findings & Significance Spirometry (FEV1, FVC, FEV1 78% predicted → mild obstructive-borderline; FEV1/FVC determines obstruction; optimise preoperatively with bronchodilators and FEV1/FVC) smoking cessation DLCO (Diffusing capacity The single best predictor of postoperative respiratory complications and mortality; reduced DLCO indicates parenchymal gas exchange for CO) impairment; if DLCO <40% predicted → very high risk regardless of FEV1 ABG (Arterial blood gas) PaO₂ <60 mmHg or PaCO₂ >45 mmHg at rest → very high operative risk (chronic respiratory failure) CT chest/PET-CT Tumour size, location, hilar/mediastinal nodes, pleural involvement; determines resectability and surgical approach

CPET (Cardiopulmonary VO₂max (maximal oxygen consumption): VO₂max >20 mL/kg/min → low risk; 10–20 → moderate risk; <10 → very high risk and likely Exercise Test) inoperable; the functional gold standard for operative risk in lung resection Predicted Postoperative Function (ppoFEV1)

For VATS lobectomy in this patient: Left double-lumen tube (DLT) — preferred; right DLT avoided as a general rule (risk of RUL orifice occlusion); left DLT placed for right-sided VATS (the right lung = operative lung; left lung = ventilated lung)

Size selection: male patient, likely tall → 39 or 41 Fr DLT; confirm position with fibrescope after placement and after lateral positioning

Alternative: bronchial blocker (Arndt, EZ-Blocker) if DLT placement anticipated difficult (previous neck surgery, difficult airway history, tracheostomy)

Lung-protective ventilation of the dependent (left) lung: TV 4–6 mL/kg IBW; PEEP 5 cmH₂O; RR adjusted to maintain PaCO₂ 40–50 mmHg; FiO₂ 1.0 initially; plateau pressure ≤25 cmH₂O

HPV optimisation: TIVA (propofol-remifentanil) preferred over volatile anaesthesia — volatile agents inhibit HPV in the non-ventilated (operative) right lung, worsening shunt; TIVA preserves HPV and improves oxygenation during OLV (supported by multiple RCTs) If hypoxia develops (SpO₂ <90%) during OLV: FiO₂ 1.0 → PEEP 5 cmH₂O dependent lung → recruitment manoeuvre → CPAP 5 cmH₂O to operative lung → switch to TIVA if on volatile → consider surgeon return to two-lung ventilation briefly

Ventilator-induced lung injury (VILI) prevention: low tidal volume is most important; avoid high plateau pressures in the remaining single lung (already under greater than normal workload); this single lung must not be injured perioperatively as it will be the patient's primary respiratory organ post-resection

Thoracic epidural analgesia (TEA): gold standard for open thoracotomy; for VATS (minimally invasive), effectiveness vs other approaches is debated; TEA at T4–T6 provides excellent analgesia enabling deep breathing and coughing; inserted preoperatively or postoperatively

Paravertebral block (PVB): single injection or continuous catheter paravertebral block at the surgical level; equivalent analgesia to thoracic epidural for unilateral thoracic surgery with fewer side effects (no bilateral sympathectomy, no hypotension, suitable in patients who cannot receive epidural); increasingly preferred for VATS over TEA

SERRATUS anterior plane block: newer US-guided block for VATS; blocks lateral cutaneous branches of the thoracic intercostal nerves; simpler to perform; emerging evidence base

Multimodal analgesia: all regional techniques should be combined with paracetamol, NSAIDs (if renal function normal), and low-dose opioids; minimise opioids (impair respiratory effort and cough); gabapentin for neuropathic component of post-thoracotomy pain

Technique Method Advantages Indications for GA Topical anaesthesia Oxybuprocaine 0.4% or proxymetacaine eye drops; Safest — no injection-related complications; Failure of topical; uncooperative (preferred for supplemented by intracameral lignocaine 1% injection; fastest; suitable for day-case; no orbicularis patient; conversion to open phacoemulsification) NO injection, NO needle; patient must be able to block (patient can close eye if needed); surgery needed; complex cooperate (fixate, keep still, no sudden movement) preserves visual acuity during surgery surgery (vitreoretinal) Peribulbar block Injection of LA outside the muscle cone (peribulbar Complete akinesia (patient cannot move the Prolonged surgery; patient who space); needle passed inferior or superior to the globe; eye); suitable for longer or more complex cannot cooperate for topical; 6–8 mL LA mixture (2% lidocaine + 0.5% bupivacaine + procedures; no risk of retrobulbar haemorrhage surgeon preference hyaluronidase) or globe penetration if correctly performed General anaesthesia Standard GA with supraglottic airway device (LMA — Complete control; suitable for children and non- Children; intellectual disability; laryngoscopy not required; reduces IOP spike) cooperating adults extreme anxiety; failed regional; bilateral simultaneous; claustrophobia in operating microscope

Why withhold metformin? Metformin increases the risk of lactic acidosis if renal function deteriorates perioperatively (contrast nephropathy, reduced perfusion from anaesthesia, NSAIDs) — metformin is exclusively renally excreted and accumulates in renal impairment → inhibits Complex I of the mitochondrial ETC → lactic acidosis

Standard guidance: omit metformin on the day of surgery if the patient is fasting; for minor procedures (cataract surgery under topical anaesthesia — no fasting required, no IV contrast, minimal physiological disruption) → metformin can usually be continued; NHS and SIGN guidelines now recommend metformin can be continued for procedures where renal function is unlikely to be compromised

For this patient: cataract surgery under topical anaesthesia requires no general anaesthetic, no IV contrast, minimal physiological stress → metformin is generally safe to continue; if GA is used (LMA) with general perioperative fasting: omit metformin on the morning of surgery and resume when the patient is eating and drinking normally and renal function confirmed stable (same day for short procedures)

HPA axis suppression: long-term systemic steroids (prednisolone >10 mg/day for >3 weeks) suppress the hypothalamic-pituitary-adrenal (HPA) axis; the adrenal glands atrophy and cannot produce the normal surge of cortisol in response to surgical stress → relative adrenal insufficiency → hypotension, circulatory collapse in the perioperative period

Surgical stress classification: Cataract surgery under topical/local anaesthesia = MINOR surgery — stress equivalent to approximately 5–10 mg hydrocortisone release; does NOT require additional steroid cover beyond the patient's usual morning oral steroid dose; the stress of topical cataract surgery is less than the normal daily fluctuation in endogenous cortisol

If GA is used for cataract surgery: GA represents moderate surgical stress → give hydrocortisone 25 mg IV at induction; patient resumes usual oral steroid postoperatively Continue patient's usual morning steroid dose on the day of surgery with a sip of water regardless of the fasting period

Target blood glucose perioperatively: 6–10 mmol/L (108–180 mg/dL) — avoids hypoglycaemia (which is acutely dangerous and impairs wound healing, immune function, and cognitive function) while avoiding significant hyperglycaemia (worsens infection risk, impairs healing, causes osmotic diuresis)

For this topical anaesthesia case (no fasting, no general anaesthetic): usual T2DM medications can be continued including oral agents; if patient normally skips breakfast, adjust accordingly; check blood glucose 1 hour before and immediately after procedure Steroids cause hyperglycaemia (increase hepatic gluconeogenesis and reduce insulin sensitivity) — particular vigilance for post-operative hyperglycaemia in this patient; may require insulin sliding scale if glucose >14 mmol/L persistently

Mechanism: the oculocardiac reflex is a trigeminovagal reflex — traction on the extraocular muscles or direct pressure on the globe activates the short and long ciliary branches of the ophthalmic division (V1) of the trigeminal nerve → brainstem → dorsal motor nucleus of the vagus → increased vagal tone → sinus bradycardia, junctional rhythm, VT, asystole; most common trigger: medial rectus traction; classically occurs in children undergoing strabismus surgery under GA, but can occur during phacoemulsification or under any type of anaesthesia including topical

Management: surgeons must release traction immediately when the OCR occurs; most OCR episodes resolve spontaneously when traction ceases; if persistent bradycardia: IV atropine 0.3–0.6 mg (NEVER rely on Atropine-only prophylaxis — prophylactic atropine is not recommended as first-line OCR prevention); deepening anaesthesia (light anaesthesia augments OCR); retrobulbar block or peribulbar block (local anaesthetic interrupts the afferent trigeminal arc) provides OCR prophylaxis; anticholinergic (atropine 20 mcg/kg IM) as premedication in children undergoing strabismus surgery

Definition: TOF ratio (TOFR) <0.9 at the time of tracheal extubation or in the recovery room, measured by quantitative neuromuscular monitoring (acceleromyography or electromyography) at the adductor pollicis

Incidence with quantitative monitoring: approximately 20–40% of patients have TOFR <0.9 in the PACU when clinical reversal criteria were met (head lift, grip strength, sustained tetanus — all insensitive at TOFR 0.4–0.9) With neostigmine reversal + clinical assessment alone: TOFR <0.9 in approximately 40% of patients; neostigmine does not reliably achieve TOFR ≥0.9 With sugammadex 2 mg/kg (TOF ≥2): TOFR ≥0.9 in >98% of patients within 3 minutes — dramatically lower PRNB incidence

Upper airway obstruction: the genioglossus and other pharyngeal dilator muscles are more sensitive to NDMR block than the adductor pollicis (the monitoring site); at TOFR 0.7–0.8, pharyngeal muscle function is impaired → upper airway collapses on inspiration → obstructive apnoea episodes → hypoxia; clinically the patient may appear conscious (cortex is unaffected by NMBs) but unable to maintain airway patency

Impaired swallowing and aspiration: the cricoarytenoid muscles that protect the airway from aspiration are sensitive to residual block; at TOFR <0.9 → disordered swallowing coordination → aspiration risk during the immediate post-extubation period when the patient is in a vulnerable state

Impaired hypoxic ventilatory response: residual NMB blunts the ventilatory response to hypoxaemia (the normal reflex increase in respiratory rate and effort triggered by falling SpO₂) — at TOFR <0.9, the hypoxic ventilatory response is approximately 50% of normal; patients do not increase their respiratory effort when SpO₂ falls, making hypoxia self-perpetuating

Hypoventilation and CO₂ retention: residual respiratory muscle weakness → reduced tidal volume → hypercapnia → worsening respiratory acidosis

Outcome data: Grosse-Sundrup et al. (Lancet 2012): sugammadex reversal (vs neostigmine) reduced postoperative complications including pneumonia, reintubation, and unplanned ICU admission — directly linking reversal quality to patient outcomes

Risk Factor Mechanism / Evidence Long-acting NMBs Pancuronium has the longest duration and highest incidence of PRNB; largely replaced by intermediate-acting agents (pancuronium) Inadequate reversal agent or Neostigmine at incorrect dose, administered at wrong TOF count, or in the presence of deep block → incomplete reversal dose Absence of quantitative NMJ Without TOF ratio measurement, PRNB cannot be detected — clinical signs are insensitive until TOFR <0.4 monitoring Hypothermia Cold slows NMB metabolism and prolongs duration; potentiates NDMR block; reduces neostigmine efficacy Metabolic alkalosis Alkalosis potentiates NDMR block (reduced ionised calcium and altered neuromuscular excitability) Renal or hepatic failure Impaired elimination of NMBs (vecuronium, rocuronium dependent on hepatic/renal clearance); use atracurium/cisatracurium (Hofmann elimination) in organ failure Drug interactions Aminoglycosides, magnesium, calcium channel blockers — all potentiate NDMR block; volatile agents; lithium

Strategy Evidence-Based Recommendation Quantitative NMJ Acceleromyography (TOF-Watch) or electromyography at adductor pollicis; confirm TOFR ≥0.9 BEFORE extubation; this is the only reliable monitoring method to exclude PRNB; endorsed by AHA, ESAIC, and ASA as the standard of care (mandatory)

Sugammadex for For rocuronium or vecuronium: sugammadex 2 mg/kg (TOF ≥2) achieves TOFR ≥0.9 in >98% of cases within 3 minutes; dramatically aminosteroid NMBs outperforms neostigmine; Grosse-Sundrup Lancet 2012 showed sugammadex reduced serious pulmonary complications vs neostigmine Neostigmine (if 0.04–0.07 mg/kg IV; administer only when TOF count ≥2 (deeper block → neostigmine ineffective); co-administer glycopyrrolate 0.2 mg per 1 mg sugammadex neostigmine (prevents bradycardia, excess secretions); confirm TOFR ≥0.9 with quantitative monitor before extubation even after neostigmine unavailable) Use intermediate- Rocuronium (1.2 mg/kg RSI; 0.6 mg/kg intubating; 0.15 mg/kg maintenance) and cisatracurium instead of longer-acting pancuronium; predictable acting NMBs duration with appropriate dosing preferentially Avoid unnecessary Titrate NMB dose to surgical requirements using TOF monitoring; avoid top-up doses when TOF count ≥3 (unnecessary deepening of block) deep block

Hydrotherapy (warm water immersion in a birthing pool): evidence supports reduction in analgesic requirement; reduces maternal perception of pain intensity; no fetal harm at temperatures <37.5°C; not suitable after membrane rupture in some centres

TENS (Transcutaneous electrical nerve stimulation): modest analgesic effect; most effective in early labour; gate control theory (large fibre A-beta stimulation inhibits C-fibre pain transmission); patient-controlled; no maternal or fetal side effects; endorphin release

Massage, acupuncture, hypnobirthing, breathing techniques: psychological/CNS modulation; individual variability in effectiveness; no pharmacological side effects

Mechanism: inhalation provides analgesic (NMDA antagonism + endogenous opioid release) and anxiolytic effects; onset in 30–45 seconds; rapid offset when removed; self-administered via demand valve (the patient controls their own dosing)

Use: inhale Entonox 30 seconds before the expected peak of a contraction (to coincide the peak analgesic effect with the contraction peak); 4–5 deep breaths at contraction onset

Limitations: modest analgesic efficacy — approximately 50–60% of women find it helpful but most progress to epidural; nausea, dizziness, light-headedness (common); occupational exposure risk to midwives in poorly-ventilated delivery rooms; cannot be used in first trimester (teratogenic concern); not suitable with B12 deficiency (N₂O irreversibly oxidises vitamin B12 → methionine synthase inhibition)

Remifentanil PCA: the major advance in non-epidural labour analgesia of the last decade; remifentanil is uniquely suitable for labour PCA because of its very rapid onset (30–90 seconds) and ultra-short context-sensitive half-time (3 minutes) — it can be timed to the contraction cycle without excessive intercontraction sedation

Protocol: remifentanil 40 mcg IV bolus, lockout 2 minutes, no background infusion; patient presses the button at the START of the contraction (peak effect 60– 90 seconds later coincides with contraction peak); this contraction-synchronised self-dosing makes it far more effective than fixed-rate IV opioid infusions

Efficacy: superior to pethidine (meperidine) IV for labour analgesia; inferior to epidural for pain scores but significantly better maternal satisfaction than pethidine; approximately 40–50% of women achieve adequate analgesia with remifentanil PCA alone

Safety: maternal respiratory depression (SpO₂ <94% in approximately 10–15% of patients) — requires CONTINUOUS maternal SpO₂ monitoring and 1:1 midwife nursing throughout remifentanil PCA use; supplemental O₂ available at the bedside; rapid response protocol if SpO₂ <90%; fetal: crosses the placenta rapidly (similar to other opioids) but is metabolised by fetal esterases — neonatal respiratory depression usually transient; APGAR scores not significantly different from epidural in most studies

Efficacy: the most effective method of labour analgesia; achieves complete or near-complete pain relief in >95% of patients; Cochrane review (Anim-Somuah 2018, 40 trials, 11,000 women): epidural provides superior pain relief compared to all other methods; NICE recommends epidural analgesia should be offered to all labouring women who request it

Technique: epidural catheter placed at L2–L3 or L3–L4 interspace; test dose 3 mL 2% lidocaine + adrenaline 1:200,000 (tachycardia if intravascular; motor block if intrathecal); loading dose 10–15 mL 0.1% bupivacaine + fentanyl 2 mcg/mL; maintenance via PCEA (patient-controlled epidural analgesia) with background infusion + patient-controlled boluses Low-dose "walking epidural": 0.0625–0.1% bupivacaine + fentanyl 2 mcg/mL (or sufentanil) — preserves motor function and proprioception while providing excellent analgesia; allows ambulation ("mobile epidural"); preferred over higher concentrations in modern practice

Complications of epidural: dural puncture with the Tuohy needle → PDPH (1–2% incidence with experienced operators); inadequate analgesia (5–15%); hypotension (treat with IV fluid + vasopressor); motor block preventing ambulation at higher concentrations; urinary retention (Foley catheter often inserted); very rarely: epidural haematoma (<1:150,000), epidural abscess (<1:50,000), total spinal (if catheter migrates intrathecally); does NOT increase C-section rate (proven by Cochrane and multiple RCTs — the historical association was from confounding); slightly prolongs second stage (30–60 minutes)

Intrathecal injection of bupivacaine 2.5 mg + fentanyl 25 mcg (or sufentanil 10 mcg) provides immediate, dense analgesia within 5 minutes; the epidural catheter is then placed for maintenance

Advantage over epidural alone: faster onset of analgesia (particularly useful in rapid labourers, advanced cervical dilation, or when rapid relief is essential); the intrathecal opioid component provides excellent visceral analgesia with minimal motor block → "walking spinal"

Disadvantage: slightly higher rate of fetal heart rate changes (from rapid uterine relaxation after sudden pain relief causing uterine tachysystole); higher rate of pruritus (from intrathecal opioid)

Pudendal nerve block: blocks the pudendal nerve (S2–S4) — provides perineal analgesia for delivery, episiotomy repair, and instrumental deliveries; transvaginal injection of 10 mL lidocaine 1% at the ischial spine bilaterally; no systemic effect; limited to perineal region — does not relieve uterine contraction pain; used primarily at second stage

Paracervical block: injection of LA at the lateral fornix of the cervix (where the uterine nerve bundles pass) — provides good first-stage uterine analgesia; significant risk of fetal bradycardia (from vasospasm of the uterine artery by LA or direct fetal absorption) — largely abandoned in modern obstetric anaesthesia practice

System Effect of Combined Position + Pneumoperitoneum Magnitude Respiratory FRC ↓ 30–50% (Trendelenburg elevates diaphragm; CO₂ compresses from below); peak airway pressures ↑ Major — most immediately life40–50% for same TV; significant atelectasis in dependent lung regions; CO₂ absorption raises PaCO₂ 10–20 threatening mmHg above baseline requiring ↑ MV by 15–25% Cardiovascular Initial ↑ CO from Trendelenburg-increased venous return; then ↓ CO as IAP ≥15 mmHg compresses IVC; ↑ Major; vasopressors often required MAP (initially); ↑ SVR (CO₂ absorption → sympathetic activation); ultimately ↓ CO in prolonged cases Intracranial Trendelenburg → impaired cerebral venous drainage → ↑ CVP → ↑ ICP; CO₂ absorption → hypercapnia → ICP may rise 8–15 mmHg above pressure cerebral vasodilation → further ↑ ICP; PEEP further reduces cerebral venous drainage baseline; significant in patients with pre-existing ICP pathology Intraocular Venous congestion of ophthalmic circulation → ↑ IOP; mean IOP may double (15 → 30+ mmHg); prolonged Important for case duration decisions pressure elevated IOP → retinal artery pressure may approach IOP → retinal ischaemia; ischaemic optic neuropathy (ION) is a rare but devastating complication Renal ↑ IAP → renal vein compression → ↓ renal blood flow → reduced urine output; transient oliguria expected Expected; monitor UO and document intraoperatively; resolves after desufflation Hepatic / ↑ IAP → portal vein compression → ↓ hepatic blood flow; combined with Trendelenburg displacement of Moderate; relevant for hepaticallysplanchnic hepatic venous return; drug clearance may be reduced for prolonged cases metabolised drug dosing in very long cases

TV: 6–7 mL/kg IBW (lung-protective; prevents over-distension of dependent atelectatic lung)

RR: increase 15–25% above pre-pneumoperitoneum baseline to compensate for CO₂ absorption

PEEP: 6–10 cmH₂O (prevents atelectasis formation; improves compliance; may reduce post-operative pulmonary complications) I:E ratio: 1:2 standard; if airway pressures very high, extend to 1:2.5

Permissive hypercapnia: accept PaCO₂ 50–55 mmHg if maintaining normocapnia requires pressures >30 cmH₂O plateau

Monitoring: continuous capnography; ABG every 60–90 minutes; plateau pressure monitoring

After prolonged steep Trendelenburg (3–5 hours): significant facial, conjunctival (chemosis), and pharyngeal/laryngeal oedema from dependent venous engorgement; the glottic structures may be significantly oedematous

Pre-extubation assessment: perform cuff leak test before extubation (deflate ETT cuff and listen for air leak around the cuff at end-inspiration with IPPV — no air leak = significant laryngeal oedema); if no cuff leak → consider delayed extubation; apply IV dexamethasone 8 mg (may reduce glottic oedema); keep the head elevated 30° for 30–60 minutes before attempting extubation Have an Airway Exchange Catheter (AEC) ready before extubation — if the patient cannot be re-intubated after extubation due to laryngeal oedema, the AEC provides a guide for re-intubation while maintaining some oxygenation

Post-extubation monitoring: stridor suggests laryngeal oedema → nebulised adrenaline (1 mL 1:1000 + 4 mL saline via nebuliser); heliox if available; reintubation if oedema progresses

CO₂ (a polyatomic molecule with asymmetric bonds) absorbs infrared light at specific characteristic wavelengths — the peak IR absorption wavelength for CO₂ is 4.26 μm (mid-infrared range)

Beer-Lambert Law: Absorbance = ε × C × L; where ε = molar absorption coefficient (specific to CO₂ at 4.26 μm), C = concentration of CO₂ in the sample gas, L = path length through which the IR beam passes; the amount of 4.26 μm IR light absorbed by the gas sample is directly proportional to the CO₂ concentration

Sidestream capnography: gas is continuously aspirated from the breathing circuit at 150 mL/min through a thin sampling tube to a remote analyser where the IR measurement occurs; slight delay (1–3 seconds transport time); suitable for non-intubated patients with sampling adapters

Mainstream capnography: IR sensor cuvette placed directly at the patient airway (between ETT and breathing circuit); no transport delay; heavier but faster response; requires ETT

CO₂ Phase Gas Sampled Clinical Meaning if Abnormal

Concentration

Phase I — Baseline Anatomical dead space gas (trachea, main bronchi) ≈ 0 mmHg ↑ Baseline above 0 → rebreathing CO₂; exhausted soda lime; (start of expiration) — has NOT participated in gas exchange; CO₂ near incompetent expiratory valve; inadequate FGF in Mapleson zero circuits

Phase II — Ascending Transitional mix: dead space gas washing out, Rapidly rising Prolonged/sloped ascending limb → obstructive disease (COPD, limb progressively replaced by alveolar gas; CO₂ rises from 0 to near- asthma — uneven alveolar emptying); ETT cuff leak steeply plateau

Phase III — Alveolar Pure alveolar gas; the ETCO₂ maximum at the end of 35–45 mmHg Upward-sloping plateau ("shark fin") → bronchospasm/COPD; plateau (expiratory expiration = the monitored ETCO₂ value (normal) flat plateau = normal uniform emptying; the peak of Phase III = plateau) ETCO₂

Phase 0 — Inspiratory Fresh gas from circuit (CO₂ ≈ 0) rapidly replaces Rapidly falls to Slow or incomplete return to zero → rebreathing; inadequate FGF downstroke expired CO₂ at the start of inspiration zero in non-rebreathing circuits

Pattern Appearance Diagnosis & Action ETCO₂ → 0 Waveform disappears completely Oesophageal intubation (most critical); ETT disconnection; complete airway obstruction; ventilator failure → (flat line) immediate ETT position check Sudden ↓ Waveform present but ETCO₂ Massive pulmonary embolism (↓ pulmonary blood flow → ↓ CO₂ delivery to alveoli); cardiac arrest; massive ETCO₂ drops acutely from 35 to <15 mmHg haemorrhage; severe hypoventilation → immediate assessment of haemodynamics (abrupt fall) Progressive ↑ Gradual baseline rise over minutes Hypoventilation (↓ RR or TV); ↑ CO₂ production: malignant hyperthermia (FIRST SIGN — dramatic rapid rise), ETCO₂ fever, laparoscopic CO₂ absorption → increase MV; if MH suspected → activate MH protocol immediately "Shark fin" — No distinct plateau; Phase II and III Obstructive airway disease (COPD, asthma — heterogeneous alveolar emptying; slow-emptying high-CO₂ sloped Phase merge into prolonged upward slope alveoli continue to contribute late in expiration) → treat bronchospasm III ↑ Baseline Waveform never returns to zero CO₂ rebreathing: exhausted soda lime; faulty unidirectional valve; inadequate FGF → check and replace CO₂ (Phase I > 0) absorbent; check valves Cardiogenic Small rhythmic oscillations in Phase Cardiac contractions transmit pressure changes to adjacent lung → CO₂ concentration oscillations; benign oscillations III synchronous with heart rate variant; common during apnoea or in thin patients; no intervention required

RSI ETT confirmation: ETCO₂ is the mandatory confirmation of tracheal intubation after RSI; a persistent, consistent capnograph waveform over ≥6 breaths confirms tracheal placement; a flat line or 2 brief waves then zero strongly suggests oesophageal intubation (initial CO₂ from gastric CO₂ pool is exhaled then disappears); ETCO₂ confirmation is mandated by all intubation guidelines including DAS and AHA ETCO₂ during CPR: ETCO₂ reflects cardiac output generated by chest compressions (CO₂ delivery to lungs depends on pulmonary blood flow) ETCO₂ <10 mmHg despite confirmed intubation and adequate compressions → poor CPR quality OR very poor prognosis Sudden rise in ETCO₂ to ≥35–40 mmHg during CPR = ROSC indicator — spontaneous cardiac output suddenly delivers a large CO₂ load to the lungs; this ETCO₂ spike often precedes the palpable pulse by 30–60 seconds; stop compressions and check for pulse when this pattern is seen

AHA 2020 ACLS: ETCO₂ persistently <10 mmHg after 20 minutes of high-quality ACLS is one factor supporting consideration of resuscitation termination (not a sole criterion)

Location: in the gas supply line of EACH non-oxygen gas (N₂O, air, CO₂, helium) — between the pipeline/cylinder supply and the flowmeter needle valve

Mechanism: a pressure-sensitive valve held OPEN only when adequate oxygen supply pressure is present (≥30 psi); if oxygen supply pressure falls → spring closes the valve → all non-oxygen gas flows are shut off → the patient receives NOTHING rather than pure N₂O

Specific limitation: responds to OXYGEN SUPPLY PRESSURE — not to oxygen flow or oxygen concentration; if the oxygen pipeline has been incorrectly connected to an N₂O supply (pipeline crossing), the N₂O in the "oxygen" pipeline maintains full supply pressure → the fail-safe valve STAYS OPEN → N₂O flows freely into the system mislabelled as oxygen → patient receives N₂O without any alarm

Ohmeda Link-25: mechanically links the O₂ and N₂O flow control needle valves via a chain-and-sprocket mechanism (14-tooth sprocket on O₂ valve; 29-tooth sprocket on N₂O valve); the gear ratio ensures N₂O cannot be increased beyond a ratio that would reduce FiO₂ below 25% Dräger ORC (Oxygen Ratio Monitor Controller): pneumatic system — uses O₂ supply pressure to regulate N₂O supply pressure proportionally; achieves the same ≥25% minimum FiO₂ in the total gas flow

Specific limitation: ensures the FLOWMETER RATIO of O₂:N₂O produces ≥25% FiO₂ — but cannot detect pipeline crossing; if the gas in the "oxygen" pipeline is actually N₂O, the proportioning system faithfully delivers 25% "O₂" (which is actually 25% N₂O + 75% N₂O = 100% N₂O to the patient)

System Application Mechanism Limitation PISS (Pin Medical gas Each gas cylinder valve has a specific pin pattern: O₂ = pins at Only protects against single-cylinder misconnection; can fail with Index CYLINDERS positions 2,5; N₂O = pins 3,5; CO₂ = pins 1,6; the cylinder yoke on worn pins; does NOT apply to pipeline connections Safety only the anaesthesia machine has corresponding holes for only one gas System) type → wrong cylinder physically cannot connect to the wrong yoke DISS PIPELINE Each gas pipeline probe (Schrader valve probe) has a gas-specific Protects against single-hose misconnection at the machine end; (Diameter connections diameter and thread pitch: O₂ probe cannot physically connect to the does NOT protect against the WALL SOCKET end being plumbed Index at the N₂O Schrader socket and vice versa; gas-specific connectors at the incorrectly during hospital construction — if O₂ and N₂O wall Safety machine machine end sockets are installed in wrong positions, DISS cannot detect this System)

The inspired oxygen analyser (paramagnetic or galvanic fuel cell) continuously measures FiO₂ in the INSPIRED gas at the patient airway; alarms if FiO₂ falls below the set threshold (typically 19–21%) This is the ONLY safety feature that actually tests what gas the patient is breathing — all other safety systems (fail-safe, proportioning system, PISS, DISS) test gas pressure, flow ratios, or connector geometry; only the inspired O₂ analyser detects a genuinely wrong gas mixture Must be calibrated before each use (21% in room air; 100% in pure O₂); alarm thresholds correctly set; probe correctly positioned on the inspiratory limb of the breathing circuit

Pipeline gas verification: before every case in every theatre (especially new or recently serviced), connect the pipeline and test the gas from the wall socket directly with the O₂ analyser probe to confirm it is actually delivering oxygen before connecting to the machine and patient circuit

Alarm Trigger Immediate Response High peak airway Peak pressure exceeds set limit (typically 40 cmH₂O) Check for kinking, secretions, ETT obstruction, bronchospasm, pneumothorax, patient pressure biting ETT Low minute Exhaled MV falls below set threshold; or no breath Circuit disconnection; ETT displacement; patient has resumed spontaneous ventilation (if volume / apnoea detected for >apnoea time excessively light); check circuit integrity O₂ supply failure O₂ supply pressure below threshold; O₂ cylinder Switch to backup O₂ cylinder; reduce FGF; call for maintenance approaching empty FiO₂ alarm (low) Inspired O₂ concentration falls below set minimum MOST CRITICAL — check pipeline gas identity; O₂ analyser calibration; blender malfunction; pipeline failure

Definition: HPV is an intrinsic response of pulmonary arteriolar smooth muscle (predominantly precapillary arterioles of 30–300 μm diameter) to regional alveolar hypoxia (PAO₂ <70 mmHg), resulting in vasoconstriction of the supplying arteriole and diversion of blood flow to better-ventilated lung units The pulmonary arterioles CONSTRICT in hypoxia — the OPPOSITE of systemic vasculature; this unique response is intrinsic to the pulmonary vascular smooth muscle cell (PVSMC) and does not require neural input or systemic hormones, though both can modulate it HPV can reduce blood flow to a collapsed lung segment by approximately 50% — significantly limiting the intrapulmonary shunt fraction from that segment during OLV

Phase 1 — Rapid (Seconds to Minutes): Mitochondrial O₂ Sensing ↓ PAO₂ (alveolar O₂ falls) → pulmonary vascular smooth muscle cells sense O₂ through their mitochondria (the inner mitochondrial membrane contains an NADH oxidase complex that generates reactive oxygen species [ROS] in proportion to O₂ tension) → in hypoxia, mitochondrial ROS generation is ALTERED (recent evidence — hypoxia changes ROS flux from Complex III) → this altered ROS signal inhibits voltage-gated K⁺ channels (Kv channels — specifically Kv1.5 and Kv2.1) on the PVSMC plasma membrane → K⁺ cannot flow out → cell DEPOLARISES → activates voltage-gated L-type Ca²⁺ channels (VDCC — voltage-dependent Ca²⁺ channels) → Ca²⁺ influx into the cytoplasm → calmodulin-myosin light chain kinase (MLCK) activation → smooth muscle CONTRACTION → arteriolar vasoconstriction.

Simultaneously: hypoxia reduces endothelial production of NO (nitric oxide) and prostacyclin (PGI₂) — both potent pulmonary vasodilators → their reduction removes a tonic vasodilatory influence → unopposed vasoconstriction TRPV4 channels (transient receptor potential vanilloid 4) may also contribute — mechanosensitive channels activated by cell volume changes during hypoxic vascular stress

Phase 2 — Sustained (Hours to Days): HIF-1α Transcriptional Response Prolonged hypoxia → HIF-1α (Hypoxia-Inducible Factor-1α) stabilisation and nuclear translocation → transcriptional upregulation of vasoconstrictor gene expression: endothelin-1 (ET-1) production ↑; VEGF ↑; downregulation of eNOS (endothelial NO synthase) expression ET-1 (endothelin-1) is one of the most potent pulmonary vasoconstrictors known — directly activates ETA receptors on PVSMC → additional sustained Ca²⁺mediated contraction; explains the longer-lasting, more structural component of HPV in chronic hypoxaemia (pulmonary hypertension of high altitude, COPD, sleep apnoea) The Phase 2 response underlies the development of sustained pulmonary hypertension in chronic hypoxaemic states

Effect on Factor Mechanism Clinical Significance HPV Volatile anaesthetic INHIBIT HPV Volatile agents activate K⁺ channels (reversing the Kv channel inhibition During OLV: volatile agents allow blood to agents (dose- — the most that drives HPV) AND enhance NO/PGI₂ production from the pulmonary continue flowing through the collapsed (nondependent) clinically endothelium → both actions promote PVSMC relaxation, opposing the ventilated, hypoxic) operative lung → high shunt important hypoxic vasoconstriction; dose-dependent: halothane > isoflurane ≈ fraction → arterial hypoxaemia; TIVA with anaesthetic sevoflurane ≈ desflurane at equiMAC concentrations; clinically significant propofol does NOT inhibit HPV → superior factor above 0.5 MAC oxygenation during OLV Propofol (TIVA) Does NOT Propofol does not activate pulmonary K⁺ channels or enhance pulmonary TIVA is preferred for thoracic surgery and OLV; inhibit HPV NO/PGI₂ synthesis at clinical concentrations; HPV operates normally multiple RCTs demonstrate higher PaO₂ during — no during propofol anaesthesia OLV with TIVA vs volatile significant effect on PVSMC tone at clinical doses Vasodilators INHIBIT HPV Non-selective pulmonary vasodilation — reduce HPV-mediated Any intraoperative vasodilator may worsen V/Q (nitroprusside, GTN, constriction alongside systemic vasodilation; the degree of HPV inhibition mismatch during OLV; use with caution; calcium channel varies by agent phenylephrine (alpha-1 agonist — no blockers, hydralazine) pulmonary vasodilator effect) is preferred over vasodilators for treating intraoperative hypotension during OLV Pulmonary arterial Reduces When baseline PAP is already high (pulmonary hypertension), the Pre-existing pulmonary hypertension blunts pressure ↑ HPV vascular bed has limited capacity for additional HPV-mediated HPV response to atelectasis effectiveness vasoconstriction Hypocapnia (↓ PaCO₂) INHIBITS Hypocapnia causes pulmonary vasodilation (CO₂ has vasoconstrictor Avoid hyperventilation during OLV — maintain HPV effects on pulmonary vasculature); hyperventilation removes CO₂ → normocapnia (PaCO₂ 40 mmHg) to preserve pulmonary vasodilation → opposes HPV HPV Acidosis AUGMENTS Acidosis (↓ pH) potentiates HPV by further reducing K⁺ channel activity in Permissive hypercapnia (mild acidosis) during HPV PVSMCs and directly activating Ca²⁺ entry pathways OLV may augment HPV and improve oxygenation — one reason some OLV protocols allow PaCO₂ to rise slightly Infection/inflammation INHIBITS Cytokines (TNF-α, IL-1β), prostaglandins, and NO overproduction from Clinical paradox: the most diseased, most in the hypoxic lung HPV locally activated macrophages/endothelium in pneumonia or ARDS override HPV hypoxic lung regions have the least HPV — specifically in the most inflamed regions; explains why pneumonia causes maximising shunt from precisely the areas that disproportionate shunt — the most hypoxic regions lose HPV protection most need redirection of blood flow

During OLV: operative (non-dependent, non-ventilated) lung collapses → PAO₂ in that lung = 0 → maximal HPV stimulus → HPV constricts the operative lung arterioles → blood flow from the collapsed lung reduced by ~50%; despite maximal HPV, ~35–50% of the shunt persists (HPV cannot eliminate flow completely) → PaO₂ typically 80–120 mmHg on FiO₂ 1.0 during OLV

TIVA vs volatile for OLV: propofol-remifentanil TIVA preserves HPV → maximises diversion of operative lung blood flow to the ventilated lung → higher PaO₂ during OLV; multiple RCTs confirm 15–25 mmHg higher PaO₂ with TIVA vs equiMAC volatile during OLV; TIVA is the preferred anaesthetic technique for thoracic surgery and OLV in most current guidelines

When hypoxia occurs despite TIVA during OLV: stepwise management — FiO₂ 1.0 → PEEP 5 cmH₂O to ventilated lung → recruitment manoeuvre → CPAP 5 cmH₂O to operative lung → request surgeon to allow brief re-inflation → resume two-lung ventilation as last resort

Property Sevoflurane Value Comparison Chemical name Fluoromethyl-2,2,2-trifluoro-1- Fully halogenated (fluorine only — no chlorine); not flammable at any clinical concentration in O₂ or N₂O (trifluoromethyl)ethyl ether Molecular weight 200 g/mol Heavier than desflurane (168) but lighter than isoflurane (184) Boiling point 58.5°C Higher than desflurane (23.5°C — requires heated pressurised vaporiser); sevoflurane uses a standard Tec-7 vaporiser at room temperature SVP at 20°C 157 mmHg (21.3 kPa) Allows standard draw-over vaporiser delivery (unlike desflurane) Blood-gas partition 0.65 Low — 2nd lowest after desflurane (0.42); lower than isoflurane (1.4); rapid equilibration between blood coefficient (λ) and alveolar gas → fast induction and emergence MAC (in O₂, 40-year- 2.0% MAC 1.8–2.0%; with N₂O 65%: MAC ≈ 0.66%; elderly (>65 years): MAC reduced ~6% per decade above old adult) 40; reduced by hypothermia, opioids, alpha-2 agonists Oil-gas partition 47–54 Lower than isoflurane (91) — less lipid-soluble; contributes to faster context-sensitive offset from fat coefficient compartments

Uptake and distribution: low blood-gas λ (0.65) means blood is a poor sink for sevoflurane; minimal first-pass uptake by blood → rapid rise in alveolar concentration (FA/FI ratio) → rapid equilibration with brain → fast induction; at equilibrium, 65% of administered sevoflurane is eliminated by the lungs; approximately 2–3% undergoes hepatic metabolism

Metabolism: CYP2E1 metabolises sevoflurane → hexafluoroisopropanol (HFIP) + inorganic fluoride (F⁻) ions; HFIP is rapidly glucuronidated and excreted in urine (non-toxic); inorganic fluoride peak levels reach 15–30 μmol/L after 1 MAC-hour — BELOW the traditionally cited nephrotoxic threshold of 50 μmol/L associated with methoxyflurane; sevoflurane nephrotoxicity from fluoride is not clinically demonstrated in humans at clinical doses

Emergence: rapid — FA/FI falls rapidly after stopping vaporiser due to low λ; context-sensitive emergence is predictable and fast for sevoflurane even after prolonged infusions; emergence faster than isoflurane but slightly slower than desflurane at equivalent durations

Formation mechanism: in the presence of the strong alkali catalysts (NaOH, KOH) in soda lime — particularly at high temperature (desiccated soda lime) — sevoflurane undergoes base-catalysed beta-elimination → Compound A (fluoromethyl-2,2-difluoro-1-[trifluoromethyl]vinyl ether); Compound A concentration is higher with: low fresh gas flow (less dilution), higher temperature soda lime, high sevoflurane concentrations, desiccated absorbent

Toxicity: Compound A is nephrotoxic in rats at concentrations of 150–200 ppm; rat renal tubules have high beta-lyase enzyme activity that activates Compound A into its toxic form; human renal beta-lyase activity is 10–30 times LOWER than rat → human kidneys are substantially resistant to Compound A; multiple prospective RCTs in humans (including patients with pre-existing renal impairment) have demonstrated NO clinically significant renal injury from Compound A at clinical concentrations achieved during low-flow sevoflurane anaesthesia

FDA recommendation: minimum FGF of 1 L/min with sevoflurane (US regulatory requirement to reduce Compound A concentration by dilution); many European and Asian anaesthesia societies consider this unnecessarily conservative given clinical evidence — low-flow sevoflurane (<1 L/min) with Amsorb Plus (no NaOH/KOH — minimal Compound A generation) is widely accepted

Parameter Effect at 1 MAC Sevoflurane Comparison Myocardial Dose-dependent depression (↓ ~20% at 1 MAC); well-tolerated in most patients Less depressant than halothane; similar to contractility isoflurane at equiMAC Heart rate Minimal change (slight ↑ or no change) — unlike desflurane (marked tachycardia from Cardiovascular stability is sevoflurane's key sympathetic activation during abrupt increases) and halothane (bradycardia) advantage over halothane and desflurane Blood pressure Dose-dependent ↓ MAP (~15–20% at 1 MAC) from peripheral vasodilation Less hypotension than desflurane (which causes Blood pressure Dose-dependent ↓ MAP (~15–20% at 1 MAC) from peripheral vasodilation Less hypotension than desflurane (which causes sympathetic tachycardia) at abrupt concentration changes

Coronary Coronary vasodilator — potential for coronary steal in patients with severe coronary artery Similar to isoflurane; clinically relevant coronary vasodilation disease (theoretical, clinically debated) steal is not consistently demonstrated in RCTs

Cardiac Minimal — unlike halothane (which markedly sensitises the myocardium to arrhythmias from Safe with adrenaline infiltration (ENT, plastic sensitisation to adrenaline) surgery); adrenaline up to 10 mcg/kg is safe with catecholamines sevoflurane Ischaemic Sevoflurane produces anaesthetic preconditioning — protective against myocardial Clinically meaningful benefit in cardiac surgery; preconditioning ischaemia-reperfusion injury; mediated through KATP channel activation and protein kinase C evidence supports sevoflurane-based activation; may reduce perioperative myocardial infarction in high-risk cardiac patients maintenance in CABG over TIVA for myocardial protection

Respiratory effects: dose-dependent ↓ tidal volume; ↑ RR (partially compensatory); net ↓ minute ventilation → mild CO₂ retention; dose-dependent ↓ hypoxic and hypercapnic ventilatory responses; bronchodilation (useful in asthma); NO airway irritation at clinical concentrations (unlike desflurane and isoflurane which are pungent)

Inhalational induction: sevoflurane is the ONLY volatile agent suitable for inhalational induction in adults and children — its lack of airway irritation (nonpungent, pleasant odour) allows smooth induction without breath-holding, coughing, laryngospasm; 6–8% sevoflurane in O₂ achieves loss of consciousness in 30–60 seconds; desflurane and isoflurane are too pungent for inhalational induction Advantages over desflurane:

GWP 130 vs desflurane 2540 — 19× lower environmental impact Atmospheric lifetime 1.1 years vs 14 years for desflurane Suitable for inhalational induction (desflurane is not) No sympathetic activation tachycardia on rapid concentration increases (desflurane causes marked sympathetic activation when concentration is rapidly ↑) Standard vaporiser (room temperature) vs desflurane's heated pressurised TEC-6 vaporiser (expensive, complex, requires electrical power) Lower cost per MAC-hour at equivalent flow rates

Definition (Merkel and Eger, 1963): MAC is the minimum alveolar concentration of an inhaled anaesthetic at 1 atmosphere of pressure (101.3 kPa) that prevents purposeful movement (not reflex withdrawal) in response to a standard surgical stimulus (skin incision) in 50% of unpremedicated subjects at steadystate equilibrium between the alveolar and brain concentrations; defined at age 40 in adults, at sea level, in a 40-year-old patient (the reference standard) Why ALVEOLAR concentration? at steady state, alveolar partial pressure equals brain partial pressure (Henry's law — dissolved concentration is proportional to partial pressure); the alveolus is accessible for measurement (via ETCO₂-like monitoring); brain concentration cannot be directly measured; alveolar = brain at equilibrium is the fundamental assumption of MAC

What MAC measures: the spinal cord (not the brain) is the primary mediator of the motor response to painful stimulation; MAC measures the concentration that prevents spinal cord-mediated reflex movement — it reflects IMMOBILITY, not unconsciousness; amnesia and loss of consciousness occur at LOWER concentrations than MAC (MAC-awake ≈ 0.3–0.4 MAC)

Population-level statistic: MAC is the ED50 for immobility — at 1 MAC, 50% of patients move to incision; at 1.3 MAC ≈ ED95; dose-response relationship for volatile agents is steep, so 1.2–1.3 MAC provides adequate anaesthesia in ~95% of patients

Agent MAC in O₂ (40-year adult) MAC with 65% N₂O (MAC-N₂O) Halothane 0.75% 0.29% Isoflurane 1.15% 0.50% Sevoflurane 2.0% 0.66% Desflurane 6.0% 2.8% Nitrous oxide 105% (hyperbaric required for sole agent) N/A Xenon 63–71% N/A

Factor Direction Mechanism / Magnitude Age ↓ with increasing age MAC reduces by ~6% per decade above 40 years; elderly have reduced CNS neurotransmitter activity, reduced synaptic density; a 70-year-old requires only ~65% of the MAC needed in a 40-year-old for the same agent Hypothermia ↓ MAC (significant) Each 1°C reduction in core temperature reduces MAC by ~5%; hypothermia reduces CMRO₂ and CNS synaptic activity; at 25°C, MAC is approximately 50% of normothermic value Nitrous oxide ↓ MAC of volatile N₂O has its own MAC (105%); N₂O concentrations used clinically (65–70%) reduce the volatile agent MAC by ~50% agents (additive) (65% N₂O contribution = 0.62 MAC-N₂O equivalents subtracted from volatile agent requirement) Opioids (pre- ↓ MAC Opioids synergistically reduce MAC by reducing CNS pain processing; fentanyl, morphine, remifentanil all reduce MAC medication, co- dose-dependently; remifentanil 4 ng/mL reduces sevoflurane MAC by ~50% administration) Alpha-2 agonists ↓ MAC Central noradrenergic inhibition reduces general CNS arousal; dexmedetomidine reduces sevoflurane MAC by 35–50% (dexmedetomidine, at typical infusion rates clonidine) Benzodiazepines, ↓ MAC GABAergic CNS depression reduces the volatile agent requirement; midazolam premedication reduces MAC by ~15– barbiturates, 25% propofol Pregnancy ↓ MAC (~25–40%) Progesterone (which enhances GABA activity and reduces sympathetic tone) reduces MAC from early pregnancy; at term: MAC is approximately 25–40% lower than non-pregnant; also relevant for neonatal MAC (neonatal MAC is higher than adults — not lower) Hyperthyroidism / ↑ MAC Increased CNS metabolic activity and synaptic transmission increases anaesthetic requirement; fever raises MAC ~5% fever per degree Celsius Chronic alcohol ↑ MAC Cross-tolerance between alcohol and volatile anaesthetics through shared CNS mechanisms (GABA, NMDA); chronic use (tolerance) alcoholics require higher volatile agent concentrations for equivalent anaesthesia Hypernatraemia ↑ MAC Hypernatraemia increases CNS neuronal excitability Altitude (reduced ↓ MAC expressed as At altitude, a lower % concentration delivers the same partial pressure; MAC as partial pressure remains constant; e.g., atmospheric % (but not as partial at 2000m: barometric pressure 596 mmHg → sevoflurane MAC = 2.0% × (760/596) = 2.55% by concentration, but still pressure) pressure) 11.4 mmHg partial pressure Factors That Do NOT Significantly Affect MAC Sex, height, duration of anaesthesia, PaCO₂ (in the physiological range 20–90 mmHg), PaO₂ (above 40 mmHg), anaemia (haematocrit >10%), metabolic acidosis or alkalosis (mild-moderate)

Value Variant Definition Clinical Use (sevoflurane) MAC- The alveolar concentration at which 50% of patients will open ~0.3–0.4 Sets the LOWER limit for safe anaesthesia — FET (functional endawake their eyes on command and respond to verbal stimulation — MAC = ~0.6– tidal) concentration must be maintained above MAC-awake at all defines the transition between conscious and unconscious 0.8% times; the BIS 60 target corresponds approximately to MAC-awake; states; below MAC-awake → risk of awareness; above MAC- sevoflurane relevant to setting minimum volatile agent concentration before adding awake → patient is unconscious and amnestic neuromuscular block MAC- The alveolar concentration required to prevent 50% of patients ~1.3 MAC = Explains why induction of anaesthesia alone is insufficient for intubation from showing laryngeal or respiratory reflex responses to ~2.6% intubation without NMB or opioids; laryngoscopy requires deeper laryngoscopy and tracheal intubation (a much more intense sevoflurane anaesthesia than skin incision; used in historical studies of volatilestimulus than skin incision) only induction-intubation without NMB (rare in modern practice) MAC-BAR The alveolar concentration required to block the autonomic ~1.4–1.7 The concentration required for haemodynamic stability during high(Block (adrenergic) cardiovascular response (tachycardia, MAC = ~2.8– stimulation surgery without opioid supplementation; explains why Adrenergic hypertension) to surgical incision in 50% of patients; reflects 3.4% volatile agents alone at standard MAC produce haemodynamic Response) blunting of the sympathetic stress response, not just motor sevoflurane responses to surgical stimuli — supplemental opioids are needed to immobility reduce MAC-BAR and provide haemodynamic stability at lower volatile concentrations

Structure: succinylcholine is two acetylcholine molecules joined through their acetyl groups → a bisquaternary ammonium compound (a "double ACh" molecule); chemical name: diacetylcholine or bis-trimethylammonioethyl succinate

Mechanism — Phase I (Depolarising) Block: 1. Succinylcholine binds to the postsynaptic nicotinic AChR and ACTIVATES it (like ACh) → end-plate depolarisation → action potential in the muscle → FASCICULATIONS (visible all-over muscle twitching — the brief initial stimulation phase before block) 2. Unlike ACh (hydrolysed in <1 ms by AChE), succinylcholine is NOT hydrolysed by AChE (requires pseudocholinesterase which is not at the NMJ) → succinylcholine remains at the receptor for minutes → sustained end-plate depolarisation → sodium channels INACTIVATE (cannot reopen during sustained depolarisation) → the muscle cannot repolarise and respond to the next nerve impulse → FLACCID PARALYSIS despite the membrane still being "on" 3. Phase I block characteristics: NO FADE on TOF stimulation (the presynaptic mobilisation mechanism works normally since succinylcholine does not block presynaptic nicotinic autoreceptors); all TOF twitches uniformly reduced; augmented (not antagonised) by anticholinesterases (neostigmine increases ACh at synapse, compounding depolarisation)

Hydrolysis and duration: succinylcholine is hydrolysed by PLASMA PSEUDOCHOLINESTERASE (butyrylcholinesterase) → succinylmonocholine (weak block) → choline + succinic acid (inactive); normal duration 10–15 minutes; onset 60–90 seconds after 1–1.5 mg/kg IV

With repeated doses or prolonged infusion of succinylcholine: the character of the block changes from Phase I (depolarising) to Phase II (also called "desensitisation block" or "dual block") — the neuromuscular junction develops characteristics of a non-depolarising block

Phase II characteristics: FADE appears on TOF stimulation (unlike Phase I); post-tetanic potentiation present; the block can be partially reversed by neostigmine (unlike Phase I where neostigmine deepens the block)

Mechanism not completely understood: receptor desensitisation (the receptor becomes unresponsive even to ACh despite continued presence of succinylcholine) is the leading hypothesis; channel enters an "open channel block" configuration; more common with large total doses (>3–5 mg/kg) or in patients with atypical pseudocholinesterase

RSI (Rapid Sequence Induction and Intubation): the primary indication — fastest onset of all NMBs (60–90 seconds to ideal intubating conditions) with short duration (10–15 minutes); provides rapid onset for emergency airway management AND relatively rapid offset if intubation fails; rocuronium 1.2 mg/kg with sugammadex 16 mg/kg available is now an equivalent alternative that avoids succinylcholine's contraindications

Laryngospasm treatment: 0.5–1 mg/kg IV (or 3–4 mg/kg IM in emergencies without IV access) → rapidly abolishes laryngospasm by relaxing the adducted vocal cords; rapid offset means ventilation can be resumed quickly Brief intubation for electroconvulsive therapy (ECT), endoscopy, other short procedures where rapid offset is advantageous

Complication / Mechanism Specific Context Contraindication HYPERKALAEMIA → Depolarisation of the muscle membrane → K⁺ efflux from cells; in Absolute contraindication in: denervation injury

Cardiac arrest (most NORMAL patients: K⁺ rises ~0.5 mEq/L (benign); in patients with (paraplegia/quadriplegia >48 hours); severe burns (>10% BSA, from important absolute UPREGULATED EXTRAJUNCTIONAL AChRs (denervation injury, 48 hours to 2 years post-burn); prolonged immobility (>1 week); contraindication) burns >10% BSA, immobilisation, disuse atrophy, critical illness crush injury/rhabdomyolysis; severe sepsis with muscle myopathy, severe infection): K⁺ can rise 5–10 mEq/L → fatal cardiac involvement; myopathies (Duchenne, Becker — progressive arrest extrajunctional receptor upregulation); closed head injury with prolonged ICU stay Malignant Succinylcholine is a POTENT MH TRIGGER — combination of Absolute contraindication in known or suspected MH susceptibility; Hyperthermia (MH) succinylcholine + any volatile agent produces the most rapid and family history of MH or unexplained perioperative death; history of triggering severe MH reactions; mechanism involves abnormal RyR1 receptor- MH on previous anaesthesia; masseter muscle rigidity after mediated Ca²⁺ release from the sarcoplasmic reticulum in susceptible succinylcholine is an early warning sign of possible MH — if individuals masseter spasm occurs after succinylcholine, cancel surgery and investigate for MH susceptibility Pseudocholinesterase Succinylcholine is hydrolysed by plasma pseudocholinesterase; if Congenital atypical PChE (autosomal recessive, 1:2500 deficiency (PChE PChE is absent or functionally impaired → succinylcholine is not homozygous); acquired: liver disease (reduced synthesis), deficiency) hydrolysed → prolonged paralysis (hours to days) requiring prolonged pregnancy (reduced levels), organophosphate poisoning, ventilation; dibucaine number (DN) quantifies PChE quality: normal DN plasmapheresis; ALSO: OP pesticide exposure inhibits PChE 80; heterozygous atypical DN 60; homozygous atypical DN 20 → paralysis for 1–4 hours Masseter muscle Jaw stiffness after succinylcholine (inability to open mouth fully, or If MMR occurs: cancel surgery; monitor closely for signs of MH rigidity (MMR) complete jaw lock) — can be an early sign of MH but can also occur as (rising temperature, rising ETCO₂, rigidity, metabolic acidosis, an isolated exaggerated succinylcholine response without MH; difficult rhabdomyolysis); if signs of MH develop: activate MH protocol; to distinguish at the time of occurrence investigate with CHCT/IVCT or genetic testing post-event Increased IOP Succinylcholine-induced fasciculations contract the extraocular muscles Relative contraindication in penetrating open globe injury; if RSI is (Intraocular Pressure) → raise IOP by 6–12 mmHg for 2–6 minutes; risk of vitreous expulsion required for open globe: use rocuronium 1.2 mg/kg with prefrom an open globe injury if IOP is raised treatment to prevent succinylcholine-induced IOP rise; the IOP rise from succinylcholine is TRANSIENT but potentially catastrophic in the open globe Raised ICP Fasciculations raise intracranial pressure transiently (mechanism: Relative contraindication in head-injured patients with raised ICP; fasciculation-induced arterial CO₂ change + direct muscle contraction the transient ICP rise from succinylcholine is clinically debated — → raised venous return to brain → raised ICP); the ICP rise is transient most evidence suggests it is not clinically significant in the RSI (~1–2 minutes) and modest (~5 mmHg) context where the intubation itself is critical to manage the airway and ICP; rocuronium is preferred where possible

Myotonia In patients with myotonic dystrophy or myotonia congenita: Absolute contraindication in all myotonic conditions (myotonic succinylcholine depolarisation → prolonged sustained muscle dystrophy types 1 and 2, myotonia congenita, Schwartz-Jampel contraction (RIGIDITY, not relaxation) — the myotonic muscle cannot syndrome) relax because the voltage-gated Na⁺ channels cannot be inactivated; these patients may become impossible to intubate due to jaw clenching and may have respiratory compromise from chest wall rigidity Bradycardia and Succinylcholine stimulates muscarinic receptors (M2) on the sinoatrial Paediatric RSI: always co-administer atropine 20 mcg/kg IV before asystole node → bradycardia; particularly in children, repeated doses, and in succinylcholine; adults: atropine usually not routinely required for parasympathetic-dominant individuals; atropine pre-treatment (20 single-dose RSI but should be available mcg/kg IV or IM) prevents this in paediatric RSI

Class Linkage Metabolism Allergy Examples Esters –COO– Plasma pseudocholinesterase; PABA metabolite → true IgE allergy possible; more Cocaine, tetracaine (amethocaine), benzocaine, t½ minutes; no liver required common than amide allergy chloroprocaine, procaine Amides –NH– Hepatic CYP450; t½ 1–3 hours; True allergy extremely rare (usually preservative Lidocaine, bupivacaine, ropivacaine,

CO– requires liver methylparaben — PABA-like structure); safe in ester allergy levobupivacaine, mepivacaine, prilocaine, articaine

Unionized (lipid-soluble) LA crosses the axonal membrane → inside the cell, re-equilibrates to ionized (charged) form → the ionized form enters the Na⁺ channel pore from the CYTOPLASMIC face and binds to the LA receptor site on the domain IV-S6 α-subunit transmembrane segment → physically occludes the channel → prevents Na⁺ influx → action potential blocked → conduction fails

State-dependent (use-dependent) binding: the LA receptor site is accessible only when the Na⁺ channel is OPEN or INACTIVATED (not in the RESTING/CLOSED state); during high-frequency stimulation, channels cycle rapidly through open and inactivated states → more LA binds with each cycle → progressively deeper block at the same LA concentration; C fibres (pain) have higher firing frequency → more use-dependent block at lower LA concentrations → differential sensory block

Property Effect Clinical Correlate pKa (determines Lower pKa → more unionized at physiological pH → faster Lidocaine (pKa 7.9): 25% unionized → moderate onset; Bupivacaine (pKa 8.1): unionized membrane penetration → faster onset; pKa 7.6 (mepivacaine) → 15% unionized → slower onset; Why LAs fail in infected tissue: acidic pH → fraction at pH fast; pKa 8.1 (bupivacaine) → slower onset more ionized → cannot cross membrane 7.4) Protein binding Higher protein binding → longer duration of action (drug remains Bupivacaine 95% bound → 6–8 hours; lidocaine 65% bound → 1–2 hours; bound to channel protein longer; slower dissociation from neural procaine 6% bound → 30–60 minutes tissue) Lipid solubility Higher lipid solubility → greater potency (more drug crosses Bupivacaine more lipid-soluble than lidocaine → approximately 4× more membrane for a given concentration) → lower dose needed for potent; same applies to toxicity → lower absolute dose produces toxicity equivalent block

Autonomic B fibres (preganglionic) → C fibres (pain, temperature) → A-delta (sharp pain) → A-beta (touch, pressure) → A-alpha (motor)

C fibres (pain) are blocked before A-alpha (motor): small unmyelinated → shorter nodal length requiring block → also high frequency firing → use-dependent block predominates; A-alpha (motor) are large myelinated → require longer axon length to be blocked → blocked only at higher concentrations

Clinical application — walking epidural: 0.0625–0.1% bupivacaine provides C fibre sensory block for labour analgesia while preserving A-alpha motor function (the patient can walk and push)

Agent Max dose (plain) Max dose (+ adrenaline) Lidocaine 3–4 mg/kg 7 mg/kg Bupivacaine 2–2.5 mg/kg 3 mg/kg Ropivacaine 3 mg/kg — Prilocaine 5–6 mg/kg 8 mg/kg

Layers penetrated by the spinal needle from outside to inside: skin → subcutaneous fat → supraspinous ligament (connects spinous process tips) → interspinous ligament (between adjacent spinous processes) → ligamentum flavum (tough yellow elastic ligament — LOR to saline/air) → epidural space → dura mater (tough outer meningeal layer) → arachnoid mater (the barrier layer — the actual meningeal puncture) → subarachnoid space (CSF here — free flow of clear CSF through needle confirms subarachnoid position) → conus medullaris (L1 in adults, L3 in neonates)

Safe insertion level: L3–L4 or L4–L5 interspace in adults (the conus ends at L1 — below L1, the cauda equina floats freely in CSF and the needle pushes nerve roots aside rather than penetrating the cord); Tuffier's line (line connecting iliac crests) crosses at L4 in most adults

CSF volume in lumbar subarachnoid space: approximately 35–60 mL; lower in elderly, obese, pregnant patients → same dose spreads more widely

Position: sitting (best for obese, CSF identification easier) or lateral decubitus (better tolerated by ill/anxious patients); full lumbar flexion to open interspinous space ("shrimp" position)

Needle: 25G or 26G pencil-point (Whitacre/Sprotte) — separates rather than cuts dural fibres → lower PDPH rate (1–2%) vs Quincke cutting bevel (10–15% at 25G); orient the bevel of Quincke parallel to dural fibres (longitudinal axis) to reduce the dural defect size

Identification of subarachnoid space: clear, free-flowing CSF through the needle hub (no need to aspirate with 25–26G needles — capillary action brings CSF); if no CSF: rotate needle 90°; if blood-stained: withdraw and re-attempt; if paraesthesia into a leg: withdraw slightly before injecting

Drug Concentration/Baricity Dose Range Block Duration Heavy Hyperbaric (glucose 8%) — denser than CSF 2–4 mL (10–20 2–4 hours motor; 3–5 hours sensory (hyperbaric) → sinks with gravity to dependent areas; most mg) for most bupivacaine predictable spread; GOLD STANDARD for procedures; 1.5– 0.5% spinal 2 mL for CS

Isobaric Isobaric — same density as CSF → position- 2–3 mL for lower Similar to hyperbaric bupivacaine independent spread; more variable but limb/pelvic 0.5% unaffected by position changes surgery Fentanyl 10–25 mcg added to bupivacaine 10–25 mcg Enhances quality of block; reduces dose of LA needed; no significant post-op (intrathecal respiratory depression at these doses adjuvant) Morphine 100–300 mcg (preservative-free morphine 100–200 mcg for 12–24 hours postoperative analgesia from intrathecal morphine — valuable for (intrathecal) only) CS; 100–300 major surgery and CS; delayed respiratory depression risk 6–24 hours postmcg for major injection → patient must be monitored; NEVER use preserved morphine surgery intrathecally Clonidine 15–45 mcg added to bupivacaine 15–45 mcg Prolongs sensory and motor block; provides some postoperative analgesia; (intrathecal) causes hypotension and sedation at higher doses

Baricity (most important): hyperbaric → sinks to dependent areas; isobaric → position-independent; hypobaric → floats to non-dependent areas

Patient position during and after injection: with hyperbaric solution, position determines where the block settles; supine → spread cephalad from lumbar lordosis to thoracic kyphosis (T4 for CS); lateral → block denser on dependent side; head-down Trendelenburg → rapid cephalad spread of hyperbaric solution

Dose and volume: higher dose and larger volume → more extensive spread; most important for isobaric solutions; less critical for hyperbaric

Speed of injection: faster injection → more turbulent mixing → slightly wider spread (modest effect)

Age and height: elderly have reduced CSF volume → wider spread per dose; shorter patients → higher block per mL (less CSF volume to dilute)

Complication Mechanism Management Hypotension Sympathetic block → vasodilation (↓ SVR) + relative bradycardia; worse in Prophylactic fluid co-loading; vasopressors: phenylephrine (first-line in (most hypovolaemia and with high blocks (T1–T4 blocks sympathetic cardiac obstetrics — does not cause tachycardia; maintains uteroplacental blood common — accelerators) flow); ephedrine (mixed alpha/beta — preferred if bradycardic); atropine up to 30%) for bradycardia; elevate legs; reduce block height if possible High/total Block ascends to C3–C5 (phrenic nerve — diaphragm paralysis) → 100% O₂ immediately; secure airway (RSI if unconscious); vasopressors spinal respiratory failure; and to cervical sympathetic → severe hypotension and (ephedrine + adrenaline if cardiovascular collapse); CPR if arrest; bradycardia; cardiovascular collapse; causes: excessive dose, head-down patient is awake and terrified if cervical block — reassure and sedate position, accidental intrathecal epidural top-up (10× concentration difference) PDPH CSF leak through dural puncture → low CSF pressure → traction on pain- See Q16 detailed management; epidural blood patch 15–20 mL if sensitive structures (see Q16) conservative measures fail after 24 hours Transient Bilateral buttock and leg pain 6–24 hours post-spinal; no motor deficit; NSAIDs + reassurance; avoid hyperbaric 5% lidocaine; use bupivacaine Neurological complete resolution in 5 days; associated with hyperbaric lidocaine 5% instead Symptoms (TNS) Urinary Sacral parasympathetic block prevents detrusor contraction; most common Urinary catheterisation until block resolves; monitor urine output retention with long-acting agents (bupivacaine) and intrathecal morphine

Boundary Structure Superior (cranial) Fusion of periosteal and spinal dura at the foramen magnum — epidural space ends here Inferior (caudal) Sacrococcygeal membrane at the sacral hiatus — accessed percutaneously for caudal epidural Anterior (ventral) Posterior longitudinal ligament covering vertebral bodies and discs Posterior (dorsal) Ligamentum flavum — the primary posterior boundary; characteristic "loss of resistance" as needle exits the LF into the epidural space Lateral Pedicles of vertebral arches and intervertebral foramina through which spinal nerve roots exit

Contents: epidural fat (primary content — acts as lipid depot for LA); Batson's venous plexus (valveless epidural veins — engorged in pregnancy, reducing epidural volume); spinal nerve roots in dural sleeves (primary site of LA uptake); radicular arteries

Ligamentum flavum thickness: thickest at L3–L4 (5–6 mm); thinner at thoracic (2–4 mm); identified by characteristic "gritty" resistance as needle advances, followed by sudden loss of resistance as it exits into the epidural space

Loss of Resistance (LOR) technique: advance the 16–18G Tuohy needle through the supraspinous → interspinous → ligamentum flavum layers (increasing resistance) with continuous pressure on a 10 mL syringe filled with saline (or air, though saline preferred — air can cause patchy block and pneumocephalus); at the moment of LOR (sudden easy injection of saline → the epidural space has been entered)

Catheter placement: thread the epidural catheter 3–5 cm into the epidural space; fixate securely; catheter tip should be at the level of intended surgery (lumbar for abdominal; thoracic for thoracic/upper abdominal) Test dose (3 mL 2% lidocaine + 1:200,000 adrenaline):

Intravascular catheter: IV adrenaline → tachycardia ≥20 bpm within 60 seconds → positive test dose → resite

Intrathecal catheter: 3 mL 2% lidocaine intrathecally → dense bilateral motor block within 3–5 minutes → positive → resite

Negative test dose: no tachycardia, no spinal block → proceed with full dose incrementally

Factor Effect Mechanism

Volume of injectate Most important — ↑ volume → ↑ spread Rule of thumb: 1–1.5 mL per spinal segment; 15–20 mL for T4–S5 block in an adult Concentration Determines intensity (motor vs sensory); NOT spread 0.1% bupivacaine → sensory only; 0.5% → motor + sensory

Age Elderly: greater spread per volume (~2×) Less epidural fat; calcified foramina (less lateral leakage); reduced epidural volume Pregnancy Greater spread → reduce dose 25–30% Engorged Batson's plexus from IVC compression → reduced epidural volume Site of injection Closer to target → smaller volume needed Thoracic epidural for thoracotomy: 8–10 mL; lumbar for lower limb: 15–20 mL

Clinical Goal Drug Choice Dose/Concentration Labour analgesia (walking epidural) Bupivacaine 0.0625–0.1% + fentanyl 2 mcg/mL 10–15 mL loading; 5–10 mL/hr PCEA maintenance Postoperative analgesia (major Bupivacaine 0.125% or ropivacaine 0.2% + fentanyl 2–4 6–12 mL/hr background + 5 mL PCEA boluses abdominal) mcg/mL Surgical anaesthesia (caesarean 2% lidocaine + 1:200,000 adrenaline ± fentanyl 50 mcg; OR 15–20 mL in 5 mL incremental doses with T4 level section top-up) 0.5% bupivacaine confirmation Thoracic epidural (post-thoracotomy) Ropivacaine 0.2% + fentanyl 2 mcg/mL or sufentanil 0.5 Inserted T4–T8; 5–8 mL/hr; reduces opioid requirement, Thoracic epidural (post-thoracotomy) Ropivacaine 0.2% + fentanyl 2 mcg/mL or sufentanil 0.5 Inserted T4–T8; 5–8 mL/hr; reduces opioid requirement, mcg/mL facilitates extubation

Accidental dural puncture (ADP): 1–2% incidence with 16G Tuohy needle; CSF freely flowing through needle confirms; PDPH in 70–80% without treatment; options: re-site epidural at adjacent level (leaving original needle in place as guide); OR thread intrathecal catheter for continuous spinal anaesthesia; OR prophylactic epidural blood patch; formal EBP if PDPH occurs >24 hours later

Hypotension: from sympathetic block — fluid preload, vasopressors (phenylephrine or ephedrine)

Epidural haematoma: <1:150,000 — risk increased with coagulopathy, anticoagulants; presents as back pain + motor deficit post-block; MRI urgently; emergency surgical decompression within 8 hours of symptom onset (return of neurological function depends on speed of decompression)

Epidural abscess: <1:50,000; risk with immunocompromised patients, prolonged catheters; fever + back pain + progressive neurological deficit; MRI; IV antibiotics ± surgical drainage; remove epidural catheter

High or total epidural: excessive spread of epidural LA to cervical level; respiratory failure, cardiovascular collapse; manage as per total spinal above

Failed or patchy block: asymmetric block (plica mediana dorsalis); catheter migration out of epidural space; inadequate volume; re-dose and reposition; may need resiting

Boundary Structure Superior (cranial) Fusion of periosteal and spinal dura at the foramen magnum — epidural space ends here Inferior (caudal) Sacrococcygeal membrane at the sacral hiatus — accessed percutaneously for caudal epidural Anterior (ventral) Posterior longitudinal ligament covering vertebral bodies and discs Posterior (dorsal) Ligamentum flavum — the primary posterior boundary; characteristic "loss of resistance" as needle exits the LF into the epidural space Lateral Pedicles of vertebral arches and intervertebral foramina through which spinal nerve roots exit

Contents: epidural fat (primary content — acts as lipid depot for LA); Batson's venous plexus (valveless epidural veins — engorged in pregnancy, reducing epidural volume); spinal nerve roots in dural sleeves (primary site of LA uptake); radicular arteries

Ligamentum flavum thickness: thickest at L3–L4 (5–6 mm); thinner at thoracic (2–4 mm); identified by characteristic "gritty" resistance as needle advances, followed by sudden loss of resistance as it exits into the epidural space

Loss of Resistance (LOR) technique: advance the 16–18G Tuohy needle through the supraspinous → interspinous → ligamentum flavum layers (increasing resistance) with continuous pressure on a 10 mL syringe filled with saline (or air, though saline preferred — air can cause patchy block and pneumocephalus); at the moment of LOR (sudden easy injection of saline → the epidural space has been entered)

Catheter placement: thread the epidural catheter 3–5 cm into the epidural space; fixate securely; catheter tip should be at the level of intended surgery (lumbar for abdominal; thoracic for thoracic/upper abdominal) Test dose (3 mL 2% lidocaine + 1:200,000 adrenaline):

Intravascular catheter: IV adrenaline → tachycardia ≥20 bpm within 60 seconds → positive test dose → resite

Intrathecal catheter: 3 mL 2% lidocaine intrathecally → dense bilateral motor block within 3–5 minutes → positive → resite

Negative test dose: no tachycardia, no spinal block → proceed with full dose incrementally

Factor Effect Mechanism

Volume of injectate Most important — ↑ volume → ↑ spread Rule of thumb: 1–1.5 mL per spinal segment; 15–20 mL for T4–S5 block in an adult Concentration Determines intensity (motor vs sensory); NOT spread 0.1% bupivacaine → sensory only; 0.5% → motor + sensory

Age Elderly: greater spread per volume (~2×) Less epidural fat; calcified foramina (less lateral leakage); reduced epidural volume Pregnancy Greater spread → reduce dose 25–30% Engorged Batson's plexus from IVC compression → reduced epidural volume Site of injection Closer to target → smaller volume needed Thoracic epidural for thoracotomy: 8–10 mL; lumbar for lower limb: 15–20 mL

Clinical Goal Drug Choice Dose/Concentration Labour analgesia (walking epidural) Bupivacaine 0.0625–0.1% + fentanyl 2 mcg/mL 10–15 mL loading; 5–10 mL/hr PCEA maintenance Postoperative analgesia (major Bupivacaine 0.125% or ropivacaine 0.2% + fentanyl 2–4 6–12 mL/hr background + 5 mL PCEA boluses abdominal) mcg/mL Surgical anaesthesia (caesarean 2% lidocaine + 1:200,000 adrenaline ± fentanyl 50 mcg; OR 15–20 mL in 5 mL incremental doses with T4 level section top-up) 0.5% bupivacaine confirmation Thoracic epidural (post-thoracotomy) Ropivacaine 0.2% + fentanyl 2 mcg/mL or sufentanil 0.5 Inserted T4–T8; 5–8 mL/hr; reduces opioid requirement, Thoracic epidural (post-thoracotomy) Ropivacaine 0.2% + fentanyl 2 mcg/mL or sufentanil 0.5 Inserted T4–T8; 5–8 mL/hr; reduces opioid requirement, mcg/mL facilitates extubation

Accidental dural puncture (ADP): 1–2% incidence with 16G Tuohy needle; CSF freely flowing through needle confirms; PDPH in 70–80% without treatment; options: re-site epidural at adjacent level (leaving original needle in place as guide); OR thread intrathecal catheter for continuous spinal anaesthesia; OR prophylactic epidural blood patch; formal EBP if PDPH occurs >24 hours later

Hypotension: from sympathetic block — fluid preload, vasopressors (phenylephrine or ephedrine)

Epidural haematoma: <1:150,000 — risk increased with coagulopathy, anticoagulants; presents as back pain + motor deficit post-block; MRI urgently; emergency surgical decompression within 8 hours of symptom onset (return of neurological function depends on speed of decompression)

Epidural abscess: <1:50,000; risk with immunocompromised patients, prolonged catheters; fever + back pain + progressive neurological deficit; MRI; IV antibiotics ± surgical drainage; remove epidural catheter

High or total epidural: excessive spread of epidural LA to cervical level; respiratory failure, cardiovascular collapse; manage as per total spinal above

Failed or patchy block: asymmetric block (plica mediana dorsalis); catheter migration out of epidural space; inadequate volume; re-dose and reposition; may need resiting

Genetic basis: autosomal dominant inheritance; mutations in the RYR1 gene (ryanodine receptor type 1 — the SR calcium release channel in skeletal muscle) account for approximately 70% of MH susceptibility; mutations in the CACNA1S gene (dihydropyridine receptor — the T-tubule voltage sensor that triggers RyR1) account for approximately 1%; over 100 different RYR1 mutations have been identified; variable penetrance — not all RYR1 mutation carriers develop MH on every triggering exposure

Normal skeletal muscle calcium regulation: during normal muscle contraction — action potential in the T-tubule → DHPR (voltage sensor) conformational change → mechanical coupling to RyR1 on the SR membrane → controlled Ca²⁺ release from the sarcoplasmic reticulum (SR) into the myoplasm → Ca²⁺ binds troponin C → actin-myosin cross-bridge cycling → contraction; after contraction — Ca²⁺ is pumped BACK into the SR by SERCA (SR Ca²⁺-ATPase); energy (ATP) is consumed in both contraction and Ca²⁺ reuptake

MH molecular event: in MH-susceptible individuals, the mutant RyR1 channel is functionally abnormal — it is abnormally sensitive to activation and abnormally slow to close; when a triggering agent (volatile anaesthetic or succinylcholine) comes into contact with the mutant RyR1 → massive, uncontrolled, sustained Ca²⁺ release from the SR into the myoplasm → myoplasmic Ca²⁺ concentrations rise to extremely high levels → sustained muscle contraction (RIGIDITY — the hallmark sign) → ATP is consumed at an enormous rate to power the contractile machinery AND the SERCA pumps working frantically to restore Ca²⁺ to the SR → oxidative metabolism is overwhelmed → anaerobic glycolysis → lactic acidosis → heat production → hyperthermia → if untreated → cell membrane disruption → rhabdomyolysis → myoglobinuria → AKI; K⁺ released from ruptured muscle cells → hyperkalaemia → cardiac arrhythmia

Sign Details MH Specificity Unexplained Rapid, dramatic, unexplained rise in ETCO₂ despite adequate ventilation; first detectable Most sensitive early warning; any unexplained ETCO₂ ETCO₂ rise sign because CO₂ production increases from hypermetabolism before temperature rises rise should prompt MH consideration (EARLIEST sign) significantly; ETCO₂ may double within 10–20 minutes of MH onset Masseter Jaw stiffness after succinylcholine — inability to open the mouth (may be just stiffness or Pathognomonic concern for MH; cancel elective surgery; muscle rigidity complete lock-jaw); occurs 30–60 seconds after succinylcholine; may precede monitor for full MH development; all cases should be (MMR) generalised rigidity; MMR is a specific early warning in the succinylcholine-triggered reported and investigated context Tachycardia Unexplained sinus tachycardia disproportionate to the clinical context; HR may exceed Non-specific but common; in combination with other 140–180 bpm signs → activate MH protocol Hyperthermia Rapid rise in core temperature; may exceed 40°C and rise at 1°C every 3–5 minutes; If temperature >38.8°C during GA with triggering agents (not the first fever is NOT the first sign (metabolic derangement precedes temperature rise); late → MH until proven otherwise sign) presentation of temperature indicates delay in diagnosis Muscle rigidity Generalised skeletal muscle rigidity; the patient becomes difficult to ventilate (chest wall Highly specific for MH when occurring under volatile rigidity); "stiff as a board" anaesthesia; distinguish from neuromuscular cause (no NMB given) — MH rigidity is not reversed by additional NMB Metabolic Mixed metabolic and respiratory acidosis (CO₂ ↑ + lactate ↑); pH may fall precipitously; ABG demonstrating metabolic acidosis + raised ETCO₂ acidosis base excess markedly negative (−10 to −20); lactate >10 mmol/L in severe cases = strong combined indicator Rhabdomyolysis Serum CK rising (often delayed — peak at 12–24 hours post-event); myoglobinuria (dark Confirms the diagnosis retrospectively; severity brown or cola-coloured urine); in late or untreated MH: CK >20,000 IU/L; electrolyte correlates with extent of muscle damage abnormalities from rhabdomyolysis: hyperkalaemia, hypocalcaemia

After an MH event or suspected event: refer to a specialist MH investigation centre; Caffeine-Halothane Contracture Test (CHCT — North American standard) / In Vitro Contracture Test (IVCT — European standard) — fresh muscle biopsy from the vastus lateralis is exposed in vitro to caffeine and halothane; susceptible muscle contracts at lower doses than non-susceptible; definitive diagnostic standard; positive → lifelong advice to avoid all MH triggers; provide MH alert bracelet and medic-alert documentation

Type Definition Incidence Harm Potential Explicit The patient is CONSCIOUS during surgery AND can RECALL specific events after ~0.1–0.2% of GAs Psychological trauma; PTSD awareness with recovery — the classic "awareness" scenario; they remember sounds, voices, (1–2 per 1000); in approximately 30% of recall (conscious sensations, or pain; the recalled content may be distressing or non-distressing higher in specific those with awareness; major awareness) high-risk populations medicolegal implications Explicit The patient shows signs of consciousness intraoperatively (responds to commands, More common than Less psychological harm (no awareness moves) but has NO recall of events postoperatively; detected by intraoperative awareness with recall) but potential without recall observation but not volunteered by the patient; may include sedated but responsive recall; specific undetected distress if pain patients during MAC procedures incidence difficult to was experienced determine Implicit Intraoperative processing of sensory information that influences post-operative Poorly defined; Largely unknown; generally awareness behaviour and emotional responses WITHOUT conscious recall — the patient cannot suggested by considered less harmful than (subcortical report awareness but may display evidence of implicit memory (e.g., therapeutic experimental data but explicit awareness processing suggestions made intraoperatively influence recovery) controversial clinically without conscious recall) Dreaming during Hypnagogic or hypnopompic dreams during light anaesthesia or emergence — NOT Common (~20% of Usually benign; patients anaesthesia true awareness; patient is unconscious during the dream; recalled as a "dream" rather patients) should be informed this is than as real events normal

General incidence: Sandin et al. (Lancet 2000, n=11,785): 0.18% awareness with recall; Sebel et al. (Anesth Analg 2004, n=19,575): 0.13%; NAP5 (UK National Audit Project 5, 2014, n=2.8 million GAs): 1 in 19,600 (0.005%) of awareness with potential harm — this lower figure reflects the rarity of truly distressing awareness with pain High-risk patient populations:

Obstetric (emergency CS under GA): highest risk — 1 in 250 (0.4%); deliberate use of light anaesthesia (to minimise fetal drug exposure) + challenging intubation conditions + modified RSI

Cardiac surgery: 1 in 500 — deliberate use of opioid-based high-dose techniques with reduced volatile agent to maintain haemodynamics; cardiopulmonary bypass dilutes volatile agent

Trauma RSI: 1 in 500 — haemodynamic instability requires reduced anaesthetic depth; delayed awareness assessment

Difficult airway (DAS failed intubation): periods of paralysis without adequate anaesthesia depth Chronic alcohol/benzodiazepine/opioid use → increased anaesthetic requirement; standard doses produce lighter-than-expected anaesthesia Accidental vaporizer malfunction, circuit disconnection, syringe pump failure (TIVA)

Maintain adequate volatile agent concentration ≥0.7 MAC equivalent (MAC-awake ≈ 0.3–0.4 MAC; maintaining ≥0.7–1.0 MAC provides a substantial safety margin above MAC-awake); do NOT reduce volatile below 0.5 MAC without supplementary agents

Pre-medication: benzodiazepines (midazolam 1–2 mg IV) reduce awareness risk through amnesia and reduced anaesthetic requirement; particularly important in high-risk groups

TIVA with propofol: low incidence of awareness with TIVA if correctly delivered; propofol produces reliable amnesia at plasma concentrations achieved with correct TCI targeting; however, pump malfunction or line disconnection in TIVA can cause immediate awareness without the capnograph or vaporizer warning that volatile agent delivery has failed

Neuromuscular blockade awareness: when NMB is used, the patient cannot move or signal intraoperative consciousness → monitoring is CRITICAL; paralysed patients who are aware but cannot move are the most traumatised group

BIS (Bispectral Index): targets 40–60 for surgical anaesthesia; BIS >60 suggests inadequate depth and possible consciousness; BIS <40 → excessive depth

Evidence — conflicting:

B-Aware trial (Myles et al., Lancet 2004): BIS-guided anaesthesia reduced awareness rate from 0.91% to 0.17% in high-risk patients — suggested BIS monitoring reduced awareness B-Unaware trial (Avidan et al., NEJM 2008, n=2000 high-risk patients): BIS-guided vs ETAC (end-tidal anaesthetic concentration) ≥0.7 MAC — NO significant difference in awareness rates between groups; ETAC-guided anaesthesia was equivalent to BIS in preventing awareness

BAG-RECALL trial (Avidan, Lancet 2011): same result — end-tidal concentration monitoring ≥0.7 MAC-equivalent was non-inferior to BIS for awareness prevention

Conclusion: BIS is a useful adjunct but ETAC monitoring ≥0.7 MAC is at least as effective for awareness prevention in volatile-based anaesthesia; for TIVA (no ETAC available): BIS is particularly important and should be used routinely; for volatile anaesthesia: ETAC is the primary monitor with BIS as supplementary

Pre-use machine check: confirm vaporizer loaded and functional; O₂ analyser calibrated; circuit intact

TIVA safety: use dedicated syringe pumps with anti-free-flow mechanisms; use pressure-monitoring integrated IV lines (detect disconnection); IV line check before and after position changes; TIVA is particularly vulnerable to awareness from syringe pump failure or line disconnection (no ETAC warning)

Minimum alveolar concentration monitoring: use ETAC (end-tidal anaesthetic concentration) monitoring with alert if ETAC <0.7 MAC-equivalent; many modern anaesthetic machines display MAC-age equivalents directly

Immediate Intraoperative Response If awareness is DETECTED intraoperatively (patient moves, signals, or verbally communicates): immediately deepen anaesthesia (propofol bolus, increase volatile, add opioid); reassure the patient verbally ("You are safe, you are in the operating theatre, we are taking care of you — I am giving you more medication right now and you will not feel anything"); administer midazolam 2 mg IV (provides immediate amnesia for any recall from the awareness period) + additional analgesic if pain was involved Postoperative Disclosure and Support ALL patients at high risk of awareness AND any patient reporting post-operative recall should be interviewed using a structured awareness questionnaire (Modified Brice Interview: routine questions about what was the last thing remembered before sleep; first thing recalled on waking; any dreams or unusual experiences between these two points; any pain or distress during the operation)

Transparent disclosure: if awareness is confirmed — the patient must be told honestly and clearly, with empathy; they must understand what happened, why it happened, that it is being taken seriously, and what follow-up support is available; denial or minimisation is ethically indefensible and legally dangerous

Psychological support: PTSD develops in approximately 30% of patients with awareness — early psychological intervention (trauma-focused cognitive behavioural therapy, EMDR — Eye Movement Desensitisation and Reprocessing) can prevent the development of full PTSD if offered promptly; provide referral to a clinical psychologist or psychiatrist; give contact information for specialist awareness counselling services

Anaesthetic documentation and incident reporting: document the awareness event fully in the anaesthetic record; file an adverse incident report through the hospital governance system; report to national databases (NAP5 equivalent) for quality improvement; future anaesthetic alert for this patient (document triggers, pharmacology, monitoring used, and what was found during the investigation)

Investigation: review the anaesthetic record for periods of light anaesthesia; check for equipment malfunction (vaporizer output, pump function, line disconnection); calculate MAC equivalents throughout the case; identify the most likely period of awareness and the probable cause

The Vomiting Centre and Its Afferent Inputs The vomiting centre (VC — also called the emetic centre) is located in the medullary reticular formation (nucleus tractus solitarius and nearby dorsal vagal complex) — it coordinates the complex motor act of vomiting (diaphragm contraction, retroperistalsis, glottis closure, respiratory muscle coordination) The VC receives afferent input from FOUR principal sources, each mediated by specific neurotransmitters and receptors that are the targets of antiemetic drugs: Afferent Source Neurotransmitters Triggers Antiemetic Target Chemoreceptor Trigger Zone (CTZ) — Dopamine (D2 Opioids; chemotherapy; morphine and D2 antagonists (haloperidol, droperidol, area postrema, floor of 4th ventricle; receptors); Serotonin (5- other opioids; uraemia; ketamine; metoclopramide); 5-HT3 antagonists (ondansetron); OUTSIDE the blood-brain barrier → HT3 receptors); digitalis; high CO₂; motion sickness NK1 antagonists (aprepitant); steroids (mechanism directly samples blood and CSF for Substance P (NK1 through vestibular input uncertain but potent antiemetic) emetic stimuli receptors); opioid receptors Vestibular system (labyrinthine Histamine (H1); Motion; opioids (sensitise vestibular H1 antagonists (cyclizine, promethazine); apparatus, CN VIII) Acetylcholine (M1 system); position changes anticholinergics (scopolamine/hyoscine patch) muscarinic) Gastrointestinal tract afferents (vagal Serotonin (5-HT3 from Gastric distension; chemotherapy 5-HT3 antagonists (ondansetron, granisetron); and splanchnic afferents from the gut) enterochromaffin cells); mucosal damage (serotonin released metoclopramide (prokinetic + D2 antagonist in the substance P (NK1) from EC cells); opioid-induced gut); NK1 antagonists gastroparesis; abdominal surgery; peritoneal irritation

Cerebral cortex Multiple — cortical Anxiety, unpleasant odours, pain, Anxiolytics (benzodiazepines); adequate processing of olfactory, psychological triggers; higher cortical preoperative preparation and anxiolysis; TIVA visual, emotional inputs inputs integrate with the VC (propofol has direct antiemetic properties at subanaesthetic concentrations — central 5-HT3 and D2 receptor modulation)

Reduce volatile anaesthetic exposure: TIVA with propofol instead of volatile agents — propofol has intrinsic antiemetic properties (reduces PONV by 25–30% vs volatile maintenance); eliminates volatile-induced emetogenesis

Minimise opioid use: multimodal analgesia (NSAIDs, paracetamol, regional techniques) reduces postoperative opioid requirements → reduces PONV; use opioid-sparing analgesic techniques

Adequate hydration: IV fluid replacement reduces PONV by approximately 30% vs dehydrated patients Avoid N₂O (emetogenic — increases PONV risk particularly for prolonged procedures) Avoid neostigmine (muscarinic stimulation → nausea/vomiting) — if possible use sugammadex instead Adequate preoperative anxiolysis (anxiety increases PONV)

Drug Class / Prophylaxis Dose & Mechanism Treatment Dose Specific Side Effects Agent Timing 5-HT3 Block 5-HT3 (serotonin) receptors in the CTZ and Ondansetron 4 mg IV at end Ondansetron 4 mg IV Headache; constipation; QTc antagonists vagal afferents from the GI tract; most effective of surgery (just before for established PONV prolongation (check ECG in (Ondansetron — against opioid-induced and postoperative nausea; emergence); granisetron 1 — if not used for patients on other QTc-prolonging first-line) no sedation mg IV; palonosetron 0.075 prophylaxis drugs); serotonin syndrome risk mg IV (longer acting, with serotonergic drugs superior for delayed PONV) Corticosteroids Mechanism not fully elucidated — likely reduces Dexamethasone 4–8 mg IV Second dose at 6 Transient hyperglycaemia (monitor (Dexamethasone) prostaglandin synthesis centrally and inhibits at INDUCTION of hours post-op if in diabetics); perineal burning on serotonin release from the enterochromaffin cells; anaesthesia (slow onset PONV persists; note: rapid IV injection; theoretical wound also reduces post-operative pain (anti- means it's ineffective if given single dose healing concern with multiple doses inflammatory) contributing to opioid sparing; onset at end of surgery); dexamethasone does (single dose is safe); avoid in is slow (30–60 min to peak effect — give at betamethasone 4 mg IV not cause adrenal uncontrolled diabetes or INDUCTION not at end) alternative suppression or impair immunocompromised (relative) wound healing D2 antagonists Block dopamine D2 receptors in the CTZ; Droperidol 0.625–1.25 mg IV Same doses as Droperidol: QTc prolongation (Droperidol, droperidol (butyrophenone) was widely used but at end of surgery; prophylaxis doses for (dose-related); extrapyramidal Haloperidol, withdrawn in many countries due to FDA black haloperidol 0.5–1 mg IV at rescue reactions (akathisia, acute dystonia Metoclopramide) box warning for QTc prolongation and arrhythmia induction; metoclopramide — more with metoclopramide); at higher doses; low-dose droperidol (0.625–1.25 10 mg IV at end (less haloperidol similar mg) is safe and effective effective for PONV than other agents — primarily a prokinetic) NK1 antagonists Block substance P at NK1 (neurokinin-1) Aprepitant 40–80 mg oral 1– IV fosaprepitant for Headache; hiccups; fatigue; (Aprepitant, receptors in the CTZ, vestibular nucleus, and 2 hours before surgery; or rescue (high cost; CYP3A4 inhibition → drug Rolapitant, NTS; the most effective single agent for PONV IV fosaprepitant 115 mg (but mainly used for interactions (warfarin, oral Fosaprepitant) prevention particularly for chemotherapy-induced high cost); most effective in prevention) contraceptives); relatively nausea (CINV) and for delayed PONV (>24 combination with other expensive hours); substance P is a key emetic antiemetics for high-risk neurotransmitter that other classes do not target patients Antihistamines / H1 and/or M1 (muscarinic) receptor blockade in Cyclizine 50 mg IV/IM at end Cyclizine 50 mg IV for Sedation; dry mouth; urinary Anticholinergics the vestibular nucleus and NTS; particularly of surgery; promethazine rescue; promethazine retention; blurred vision; (Cyclizine, effective for motion sickness-related PONV and 12.5–25 mg IV; scopolamine 12.5 mg IV anticholinergic delirium in elderly Promethazine, vestibular-mediated nausea (e.g., ear surgery, transdermal patch applied (avoid promethazine in elderly); Scopolamine opioid-induced vestibular sensitisation) the night before surgery scopolamine: amnesia, confusion in patch) (onset 4 hours; peak 12 elderly hours; worn behind ear) Propofol Sub-anaesthetic propofol concentrations modulate Propofol TIVA as primary Propofol 20 mg IV in Transient burning on injection; (antiemetic via central 5-HT3 and D2 receptor activity → inherent anaesthetic technique; recovery for respiratory depression at higher TIVA) antiemetic effect; TIVA with propofol reduces "propofol rescue" 20 mg IV established PONV doses PONV by 25–30% vs volatile anaesthesia by both: bolus for established PONV (brief antiemetic (1) eliminating volatile-induced emetogenesis and in PACU (provides transient effect; 30–60 min (2) propofol's own antiemetic properties antiemetic effect) duration)

Apfel 0–1: no prophylaxis or single antiemetic only; prioritise baseline risk reduction

Apfel 2: two antiemetics from different classes at surgery (e.g., ondansetron 4 mg + dexamethasone 8 mg at induction)

Apfel 3: three antiemetics (ondansetron + dexamethasone + droperidol 0.625 mg); consider TIVA; scopolamine patch the night before

Apfel 4: maximum multimodal prophylaxis: TIVA + ondansetron + dexamethasone + droperidol/haloperidol + scopolamine patch ± aprepitant; minimise opioids; total intravenous fluid replacement

Treatment of established PONV: if prophylaxis was given, do NOT repeat the same agent within 6 hours; give an antiemetic from a DIFFERENT class; if no prophylaxis given, ondansetron 4 mg IV is first-line rescue

Parameter Definition Clinical Meaning Volume of The apparent volume into which a drug distributes to produce the observed Large Vd → drug distributes extensively into peripheral tissues →

Distribution plasma concentration: Vd = Dose / Cp; expressed in L or L/kg smaller plasma concentration for a given dose → longer elimination half(Vd) life; e.g., propofol Vd ~200–500 L (large — distributes into fat widely) Clearance Volume of plasma cleared of drug per unit time (mL/min or L/hr); CL = Dose / High clearance → drug eliminated rapidly from plasma → short duration; (CL) AUC; depends on hepatic blood flow (for flow-limited drugs like propofol, propofol CL ~1.5–2 L/min (very high — entire hepatic blood flow) fentanyl) or hepatic enzyme capacity (capacity-limited) Half-life t½ = 0.693 × Vd / CL; the time for plasma concentration to halve; for drugs Terminal t½ is often misleading for clinical practice — a drug with large (t½) with large Vd or low CL → long t½ Vd has long t½ even with high CL because drug continues to return from peripheral compartments; CSHT is more clinically relevant Context- The time for plasma concentration to fall 50% after stopping an infusion of a The most clinically relevant parameter for infusions: remifentanil CSHT = Sensitive specific duration ("context" = infusion duration); accounts for redistribution from 3 min (flat — no accumulation, organ-independent ester hydrolysis); Half-Time peripheral compartments back into plasma after stopping; CSHT INCREASES propofol CSHT rises slowly (short cases ~5 min; 8 hr case ~40 min — (CSHT) with longer infusion duration as peripheral compartments become still manageable); thiopentone CSHT rises steeply (very long — not progressively saturated suitable for infusion)

Drug Vd CL t½β CSHT Protein Binding Key Clinical Feature

Propofol Large: 200– Very high: Biphasic: α- Short and 98% protein Rapid induction AND relatively predictable recovery from 500 L (3- 1.5–2 L/min phase 2–4 only bound (albumin); infusions; suitable for TIVA; cardiorespiratory depression compartment) (exceeds min moderately reduced in dose-dependent; pain on injection (use large vein, lidocaine hepatic blood (redistribution, increasing: 5 hypoalbuminaemia pre-treatment) flow — responsible min after 1- → enhanced extrahepatic for clinical hr infusion; effect metabolism: recovery); β- ~40 min lung, kidney) phase 1–3 after 8-hr hours infusion

Thiopentone Large: ~400 Low: 0.15– Very long: 8– Rises very 80% protein Rapid induction from redistribution; single induction dose = L 0.25 L/min 12 hours (but steeply — bound brief action because drug redistributes to fat/muscle; repeat clinical offset becomes doses = accumulation in peripheral compartments → is from clinical prolonged recovery; still used for RSI and ICP reduction redistribution hangover (burst-suppression) not with elimination) repeated doses or infusion; NOT suitable for maintenance

Ketamine Large: 3 L/kg Moderate: 1 2–3 hours Moderate — 27% protein Dissociative anaesthesia; NMDA antagonist; preserves (highly lipid L/min suitable for bound airway reflexes and spontaneous ventilation; soluble) (hepatic N- bolus or sympathomimetic (raises BP/HR — useful in demethylation short haemodynamically compromised patients); bronchodilator; to infusion; increases ICP and IOP (controversial — may be used with norketamine norketamine sedation in ventilated patients); emergence delirium — active (active (benzodiazepine premedication reduces incidence) metabolite) metabolite) prolongs clinical effects

Etomidate Moderate: 4 High: 1 L/min 2–5 hours Moderate — 77% protein Most cardiovascularly stable induction agent — minimal L/kg (hepatic ester suitable for bound effect on MAP, HR, cardiac output; drug of choice for hydrolysis to induction; haemodynamically compromised patients (septic shock, inactive acid) not used for cardiogenic shock, cardiac tamponade) and for cardiac maintenance surgery induction; adrenal suppression (inhibits 11βhydroxylase → reduces cortisol and aldosterone synthesis for up to 12 hours after single dose — controversial, avoid in septic shock where adrenal function already stressed); myoclonus and pain on injection; increases seizure threshold (used in ECT)

Central compartment (V1 — blood + highly perfused organs) ↔ Peripheral compartment 1 (V2 — muscle — rapid equilibration) ↔ Peripheral compartment 2 (V3 — fat — slow equilibration)

After IV induction: drug rapidly enters the brain (part of V1 — high blood flow) → onset of effect; drug simultaneously redistributes to V2 (muscle) → plasma concentration falls → drug leaves the brain along the new gradient → patient wakes up; this redistribution-mediated recovery is why even thiopentone (long t½) produces short induction duration from a single bolus

With prolonged infusion: V2 and V3 progressively fill with drug; when the infusion stops, drug continues to return from V2 and V3 back to plasma → slows the fall in plasma concentration → CSHT rises with infusion duration; the extent of this depends on the lipid solubility and Vd of V3 (fat compartment) — drugs with very high fat solubility (thiopentone) have steeply rising CSHT; drugs with moderate fat solubility (propofol) have slowly rising CSHT

Nerve stimulation: a peripheral nerve (ulnar nerve at the wrist — most common; facial, posterior tibial as alternatives) is stimulated with surface or needle electrodes delivering supramaximal current pulses (20–60 mA for 0.1–0.2 ms; calibrated to exceed the maximum that produces maximum twitch — ensures all motor units are activated)

Response measurement: the mechanical or electrical response of the innervated muscle is measured; at the adductor pollicis (ulnar nerve → thumb adduction); quantitative devices measure the force or acceleration of thumb movement with each stimulus

Principle: residual NMB reduces the amplitude or number of twitches in proportion to the degree of receptor occupancy; the specific pattern of response varies by stimulation pattern and type of block (depolarising vs non-depolarising)

Pattern Description What It Detects Clinical Application Single Single supramaximal stimulus at 0.1 Hz (every 10 sec); Overall degree of block vs baseline; T1 = 0% Basic monitoring; requires a baseline preTwitch compares height to baseline (pre-NMB) twitch height; T1 = complete block; T1 = 25% → adequate NMB measurement; less used than TOF in expressed as % of baseline intubating conditions with most NMBs practice Train-of- Four supramaximal stimuli at 2 Hz (0.5 sec intervals) TOF count: 0 = profound block; 1 = deep The primary monitoring tool; no baseline Four (TOF) every 10–15 seconds; counts responses (TOF count = 0, block; 2–3 = moderate block; 4 = recovering; needed (counts 0–4 twitches); TOFR is the 1, 2, 3, or 4); measures ratio T4/T1 = TOFR TOFR: ratio of 4th to 1st twitch; TOFR <0.9 = criterion for safe extubation; fade pattern clinically significant residual block; TOFR (T4<T1) is pathognomonic for NON≥0.9 = adequate recovery depolarising block; no fade in depolarising (Phase I) block Double Two short bursts of 3 stimuli each at 50 Hz, separated by Detects residual block at TOFR 0.6–0.9 Useful for tactile/visual assessment when Burst 750 ms; easier to detect fade visually than TOF because better than TOF tactile assessment; fade in quantitative monitors unavailable; better Stimulation two larger responses are compared rather than four DBS (second response weaker than first) sensitivity than TOF for detecting residual (DBS) smaller ones indicates residual block block near extubation Tetanic Sustained high-frequency stimulation (usually 50 Hz for 5 Fade to tetanus indicates non-depolarising Confirms non-depolarising block character; Stimulation seconds); produces sustained muscle contraction block; sustained tetanus indicates either no used before PTC assessment (tetanus (50 or 100 (tetanus); in the presence of NON-depolarising block: block or Phase I depolarising block; NOT mobilises ACh stores for post-tetanic Hz) tetanic stimulation is not sustained → FADE of the tetanic routinely used (painful in awake patients); potentiation) contraction; in DEPOLARISING block (Phase I): no fade used in research Post- A 50 Hz tetanic stimulus for 5 seconds → 3-second Used when TOF count = 0 (no response to Guides decision between routine reversal Tetanic pause → single twitches at 1 Hz counted; the tetanic TOF); PTC 1–2 = deep block (→ (TOF≥2 → sugammadex 2 mg/kg) and deep Count stimulation temporarily mobilises ACh → post-tetanic sugammadex 4 mg/kg for reversal; reversal (PTC 1–2 → sugammadex 4 (PTC) potentiation → some twitches visible that were not neostigmine inadequate); PTC 0 = profound mg/kg) present before tetany; count the number of single block; PTC >10 = recovery imminent (TOF twitches detectable count about to reappear)

Feature Qualitative (Tactile/Visual) Quantitative (Acceleromyography — TOF-Watch) Method Anaesthesiologist feels or sees the response to TOF stimulation; Accelerometer attached to the thumb; piezoelectric transducer measures estimates fade by comparing T4 to T1 feel acceleration of thumb adduction; outputs TOFR as a number (0–1.0) TOFR threshold Fade detected only when TOFR <0.4 (60% of receptor occupancy); Provides exact TOFR; can detect TOFR 0.7, 0.8, 0.9 — the clinically for detection at TOFR 0.4–0.9 — "feels normal" to the clinician despite clinically dangerous range that qualitative monitoring misses completely dangerous residual block Clinical Patients extubated with TOFR 0.4–0.9 → postoperative residual Confirms TOFR ≥0.9 before extubation → eliminates PORC; Grosseconsequence of curarisation (PORC) → impaired airway protection, aspiration, Sundrup Lancet 2012: sugammadex + quantitative monitoring → significantly limitation hypoventilation, PTSD reduced pulmonary complications Evidence-based Insufficient for routine practice ASRA/AHA consensus 2018: quantitative monitoring should be the standard recommendation of care whenever NMBs are used; endorsed by major anaesthesia societies globally

Temperature effect: cool fingers → reduced acceleromyography signal → falsely low apparent block may be underestimated; ensure hand and monitoring site are warm; consider TOF at the corrugator supercilii (facial nerve) — less temperature-sensitive and more relevant for the diaphragm/airway muscles than adductor pollicis (which is more resistant to NMB than facial muscles)

Neuromuscular junction variability: different muscles have different sensitivities; adductor pollicis is MORE RESISTANT to NMB than the diaphragm and genioglossus; paradox: if TOF is measured at the thumb and TOFR = 0.7, the critical airway muscles (genioglossus, pharynx) may have TOFR = 0.4–0.5 → inadequate for safe extubation; this is why the TOFR threshold for extubation must be ≥0.9 at the adductor pollicis to ensure airway muscles are adequately recovered

8 glucose units in a ring (gamma-cyclodextrin); hydrophobic core encapsulates the steroidal nucleus of rocuronium or vecuronium → 1:1 high-affinity inclusion complex (Kd ~10⁻²⁵ mol/L); free plasma rocuronium concentration falls → rocuronium dissociates from NMJ receptors → NMJ function restored; no receptor activity — purely pharmacokinetic mechanism; inactive complex excreted renally

Clinical Situation NMJ Monitor Dose Expected Recovery Routine reversal (moderate block) TOF count ≥2 2 mg/kg actual body weight TOFR ≥0.9 within ~3 min Deep block reversal PTC 1–2 (TOF count = 0) 4 mg/kg actual body weight TOFR ≥0.9 within ~3 min

CICO emergency — immediate Within 3 min of rocuronium 1.2 mg/kg RSI 16 mg/kg actual body weight (push Spontaneous ventilation restored in ~2– reversal dose dose) 3 min

Issue Management Renal failure (eGFR <30) Complex excreted renally; accumulation with renal failure may cause delayed re-paralysis; use with caution; extended monitoring ≥24 hours; dialysis removes complex Oral contraceptives Progesterone may bind cyclodextrin cavity → reduced contraceptive efficacy equivalent to missing one OCP dose; advise additional barrier (OCP) contraception for 7 days post-administration Toremifene (breast High cyclodextrin affinity → displaces rocuronium → delayed/incomplete reversal; avoid sugammadex; use neostigmine or alternative NMB cancer treatment) Re-paralysis after 16 Sugammadex still present for hours; subsequent rocuronium/vecuronium doses will be unpredictably bound; if NMB needed within 24 hours mg/kg dose → use cisatracurium (not encapsulated by sugammadex)

Step 1: Is the surgery urgent/emergent? If emergency surgery → proceed with optimal medical management; no time for cardiac investigations; alert surgical team to cardiac risk; prepare haemodynamic monitoring plan

Elective laparoscopic colectomy → proceed with structured assessment

Step 2: Active Cardiac Conditions (ACS, decompensated HF, severe valvular disease, symptomatic arrhythmia) If present → postpone elective surgery, treat cardiac condition first; stabilise for at least 6–8 weeks after ACS before elective surgery This patient (stable IHD, NYHA II) → no active conditions → proceed to Step 3 Revised Cardiac Risk Index (RCRI / Lee's Index) RCRI Factor Present? Score High-risk surgery (suprainguinal vascular, intrathoracic, intraperitoneal) YES — laparoscopic colectomy is intraperitoneal 1 History of ischaemic heart disease YES — previous NSTEMI + stent 1 History of congestive heart failure If NYHA II = mild, evaluate carefully; if compensated → 0 0 History of cerebrovascular disease Not stated → 0 0 Diabetes on insulin Not stated → 0 0 Preoperative creatinine >2 mg/dL Not stated → 0 0 RCRI = 2 → predicted 30-day MACE rate ~7%; RCRI ≥3 → >11% MACE risk; this patient = intermediate-high risk Use ESC/ESA 2022 ACS-NSQIP or RCRI ≥3 → consider functional capacity assessment and/or further cardiac testing before proceeding

Functional Capacity — METs Assessment ≥4 METs (can climb 2 flights of stairs, brisk walk) → adequate functional reserve → proceed without further cardiac testing; perioperative MACE risk is low despite cardiac history <4 METs or unable to assess → consider non-invasive cardiac testing (stress echocardiography, MPS) to identify significant stress-inducible ischaemia

CPET (cardiopulmonary exercise test): anaerobic threshold ≥11 mL/kg/min → low perioperative risk; <11 → higher risk

Assessment Action ECG (12-lead) Baseline; compare with previous if available; identify LVH, bundle branch block, ischaemic changes, arrhythmia Echocardiogram Assess LV function (EF); wall motion abnormalities (prior MI territory); diastolic dysfunction; valvular disease; if EF <35% → high-risk patient requires detailed discussion and ICU plan Troponin Elevated pre-operative troponin predicts perioperative MACE; guides risk stratification; if elevated: cardiology review before surgery Beta-blockers If already on beta-blocker → CONTINUE; never stop perioperatively (rebound ischaemia); if not on beta-blocker → do NOT start de novo for noncardiac surgery within 24 hours (POISE trial: acute beta-blocker initiation increased mortality despite reducing MACE) Statins CONTINUE perioperatively; pleiotropic effects (endothelial stabilisation, anti-inflammatory) independently reduce perioperative cardiac risk; do not stop Aspirin If on aspirin alone → CONTINUE for most non-cardiac surgery (modest bleeding increase vs high cardiac benefit); discuss with surgeon for highbleeding procedures (neurosurgery, posterior eye surgery) DAPT (if DES <6 Do NOT stop clopidogrel within 6 months of DES — stent thrombosis risk 45% mortality; see Q31 management months)

Element Strategy & Rationale Monitoring Standard + 5-lead ECG (leads II and V5 simultaneously — II for inferior ischaemia/arrhythmia; V5 for anterolateral ischaemia — the most sensitive lead for LV ischaemia); arterial line for continuous BP; ST-segment trend analysis; consider TOE for direct wall motion assessment in high-risk/EF<40% patients Avoid Tachycardia (HR >100) dramatically increases myocardial O₂ demand and reduces coronary filling time (coronary blood flow occurs during diastole — tachycardia shorter diastole with tachycardia → ischaemia in compromised coronary territories); target HR 60–80 bpm intraoperatively; short-acting beta-blocker (esmolol infusion) to manage intraoperative tachycardia Avoid MAP <65 mmHg → subendocardial ischaemia (particularly in hypertrophied LV); MAP target ≥65–70 mmHg; vasopressors (phenylephrine, noradrenaline) hypotension for vasodilatory hypotension (regional techniques, volatile agents); inotropes (dobutamine) for cardiogenic hypotension with low EF Anaesthetic Sevoflurane preferred over desflurane for cardiac patients — anaesthetic preconditioning (mitoKATP protection); avoids the rapid sympathetic tachycardia technique and hypertension on concentration increase that desflurane causes; TIVA (propofol) is the alternative — no ischaemic preconditioning but excellent haemodynamic stability with careful titration; combined GA + epidural for laparotomy provides superior analgesia and reduces sympathetic stress response Prevent Hypothermia → shivering → ↑ O₂ demand → ischaemia; active warming throughout; temperature ≥36.5°C hypothermia Blood Anaemia → ↓O₂ delivery → myocardial ischaemia; maintain Hb ≥80 g/L (transfuse if Hb <70 g/L in most settings, ≥80 g/L in IHD with high ischaemia risk); conservation cell salvage for anticipated major blood loss

POMI (Perioperative Myocardial Injury): troponin should be measured at 24 and 48 hours post-operatively in high-risk patients (RCRI ≥3, known IHD) — the VISION trial showed 18% of high-risk non-cardiac surgery patients had troponin rise without symptoms (perioperative myocardial injury) associated with 30-day mortality of 15%; most POMI is not a Type 1 STEMI but Type 2 MI (demand ischaemia from haemodynamic stress) Any symptomatic chest pain, new ECG changes, or haemodynamic instability post-operatively → urgent ECG + troponin; if STEMI → emergency cath lab activation; if NSTEMI → medical management + early cardiology review Resume all cardiac medications as soon as possible post-operatively (same day for most oral medications)

Enhanced recovery: early mobilisation, VTE prophylaxis, adequate analgesia to reduce sympathetic stress

GOLD Stage FEV1 Anaesthetic Risk Post-op Recommendation I (Mild) ≥80% Low — near-normal reserve Standard care; consider incentive spirometry II (Moderate) 50–79% Moderate — significant symptom burden Bronchodilators optimised; NIV plan post-op III (Severe) 30–49% High — this patient (42%); PPCs >30% Aggressive preoperative optimisation; HDU/ICU post-op; TEA analgesia IV (Very severe) <30% Very high; consider surgery alternatives MDT decision; ICU post-op; may need post-op ventilation

ARISCAT risk score: incorporates age, SpO₂ (<96% = highest risk — this patient 90%!), anaemia, upper abdominal/intrathoracic incision, duration >2 hours, emergency surgery, respiratory infection; this patient scores very high on SpO₂ alone (90% at rest) PaCO₂ >45 mmHg at rest → severe disease with CO₂ retention → very high post-op ventilatory failure risk; check ABG preoperatively

Intervention Specific Action Smoking Absolute cessation ≥8 weeks before surgery; immediate cessation improves carboxyhaemoglobin within 12 hours and mucociliary function within 2–4 cessation weeks Bronchodilators Optimise existing LABA/LAMA/ICS regimen; add SABA (salbutamol MDI) PRN pre-operatively; continue all inhalers on morning of surgery with sip of water; spirometry re-check 4 weeks post-optimisation Physiotherapy Pre-operative breathing exercises, incentive spirometry (IS), and chest physiotherapy for secretion clearance; IS 10 repetitions hourly pre- and postoperatively reduces atelectasis rate by 30% Treat acute If purulent sputum/fever → antibiotics for ≥4–6 weeks before surgery; elective surgery during active exacerbation is contraindicated (triples PPC risk) exacerbation Pulmonary 4–8 week supervised exercise programme if FEV1 <50% and surgery is semi-elective; improves functional capacity and reduces PPCs rehabilitation

Regional Anaesthesia Preference Thoracic epidural (TEA) T6–T8: provides surgical anaesthesia ± sedation for laparotomy in selected patients; avoids GA and its airway/ventilatory consequences; reduces PPCs by 30% compared with GA; insert epidural preoperatively; combined epidural+GA preferred (epidural → superior post-op analgesia → better respiratory function post-op)

If GA Required (Laparoscopic Colorectal)

Bronchodilator pre-treatment: nebulised salbutamol 2.5 mg before induction via nebuliser

Induction: avoid histamine-releasing drugs (atracurium, morphine, thiopentone — all can cause bronchospasm); propofol (bronchodilator) preferred for induction; rocuronium for intubation

Airway: ETT preferred over LMA (secure airway needed for abdominal surgery + risk of bronchospasm); however LMA can be used for selected procedures if leak pressure >25 cmH₂O Ventilatory Settings for COPD Parameter Setting Rationale Tidal Volume 6–8 mL/kg IBW Lung-protective; avoid overdistension of already hyperinflated lung Respiratory Rate 8–12 breaths/min Lengthens expiratory time → complete exhalation → prevents gas trapping and auto-PEEP build-up (LOW) I:E ratio 1:3 or 1:4 (prolonged Standard 1:2 inadequate for obstructive physiology; prolonged expiratory time allows complete emptying through expiration) narrowed airways PEEP Minimal (3–5 cmH₂O) or Auto-PEEP already present; extrinsic PEEP >auto-PEEP level adds to air trapping; measure auto-PEEP by expiratory zero hold Permissive Accept PaCO₂ 50–60 Avoid normalising PaCO₂ at cost of excessive airway pressures; this patient may normally retain CO₂ (chronic hypercapnia mmHg hypercapnia — check preop ABG baseline) Volatile agent Sevoflurane preferred Bronchodilator properties; avoid desflurane (airway irritant, may trigger bronchospasm)

Epidural analgesia: continue thoracic epidural for 48–72 hours post-op → allows deep breathing and productive coughing → reduces splinting → reduces atelectasis and pneumonia; superior to IV morphine for COPD patients

NIV/CPAP: plan for immediate BiPAP support post-extubation in GOLD III/IV patients; BiPAP settings: EPAP 5 cmH₂O + IPAP 12–16 cmH₂O; reduces reintubation rate; may be used prophylactically for first 24 hours

Early mobilisation: sitting out of bed day 1 post-op; physiotherapy-supervised ambulation; improves FRC and reduces atelectasis

Minimise opioids: opioid-sparing multimodal analgesia (TEA + paracetamol + NSAIDs); opioid-induced respiratory depression is catastrophic in this patient

HDU/ICU: book ICU/HDU bed preoperatively; plan for extended monitoring; daily spontaneous breathing trials if intubated post-op

Parameter Change by Term Mechanism Anaesthetic Implication Blood ↑ 40–50% (plasma ↑45%, RBC Progesterone → aldosterone activation → Na⁺/water Physiological anaemia of pregnancy (Hb <100 = Volume ↑20%) — dilutional anaemia (Hb retention; oestrogen → renin-angiotensin; plasma pathological); increased blood volume provides falls to 105–110 g/L at term) expansion exceeds RBC production haemorrhage buffer but masks volume depletion Cardiac ↑ 40–50% by 28–32 weeks; CO ↑ Blood volume, ↓ SVR (progesterone → High CO masks underlying cardiac pathology; cardiac Output = HR × SV; HR ↑15–25 bpm; SV vasodilation), ↑ metabolic demand of the feto- disease patients may decompensate in late pregnancy; CO ↑25–30%; further ↑ 15% during placental unit peaks 32–36 weeks not at term labour contractions SVR ↓ 20% (vasodilation from Progesterone → smooth muscle relaxation; Low SVR → relative hypotension; regional anaesthesia → progesterone + prostacyclin) prostacyclin production ↑; results in low-resistance further ↓ SVR → risk of severe hypotension particularly in hyperdynamic circulation pre-existing vasoconstricted states Aortocaval Supine hypotension syndrome in Gravid uterus compresses IVC (right side) and aorta ALWAYS left lateral tilt (15°) for supine procedures after 20 Compression 10–15% at term; IVC (left lateral reduces this) when supine; collateral weeks; for cardiac arrest in pregnancy: manual uterine compression → ↓ venous return circulation (paravertebral, azygous veins) displacement + left lateral tilt during CPR; perimortem CS → ↓ CO → hypotension compensates partially in most patients within 5 minutes if no ROSC

Parameter Change Anaesthetic Implication FRC ↓ 20% (400 mL) — most important respiratory ↓ Oxygen reservoir → rapid desaturation during apnoea; SpO₂ falls faster than in non-pregnant; change; diaphragm is pushed up 4 cm by gravid preoxygenation mandatory and may be less effective; closing capacity may exceed FRC in the uterus supine position → airway closure → shunt → worse oxygenation O₂ ↑ 20–30% at term (metabolic demands of fetus Rapid O₂ consumption + ↓ FRC → very short safe apnoea time; preoxygenate with 100% O₂ for 3–5 Consumption + uterus) minutes ALWAYS before obstetric RSI Tidal Volume TV ↑ 40%; RR ↑ 15%; MV ↑ 50%; driven by Hyperventilation of pregnancy: PaCO₂ falls to 30–32 mmHg (normal for pregnancy); "normal" PaCO₂ + MV progesterone stimulating the respiratory centre 40 mmHg indicates CO₂ retention in a pregnant patient; pH maintained by renal bicarbonate excretion (HCO₃⁻ falls to 18–21 mEq/L) Airway Oedema + hyperaemia of upper airway Smaller ETT (6.5–7.0 mm vs 7.5–8.0 mm standard); use nasal airways with extreme caution mucosa (oestrogen effect); capillary engorgement → (epistaxis); video laryngoscopy first-line for all obstetric intubations; Mallampati class increases as increased bleeding with instrumentation pregnancy progresses

Gastric emptying: progesterone relaxes lower oesophageal sphincter (LOS) → ↓ LOS tone → regurgitation risk; mechanical displacement of stomach by uterus changes gastric axis; opioids during labour dramatically slow gastric emptying → a labouring woman who received opioids should be treated as having a full stomach regardless of fasting time

Gastric acid: ↑ gastric acid production (gastrin from placenta); the combination of ↓ LOS tone + ↑ gastric acid = "at risk for aspiration" from 16–20 weeks gestation

Aspiration prophylaxis: ranitidine 150 mg oral or 50 mg IV (↓ gastric acid pH); sodium citrate 30 mL oral (non-particulate antacid — immediate neutralisation of gastric acid); metoclopramide 10 mg IV (↑ gastric emptying, ↑ LOS tone); RSI protocol for any general anaesthesia after 16–20 weeks; clear liquid fasting 2 hours, light meal 6 hours (but treat as full stomach if in active labour with opioids)

Physiological anaemia: dilutional (plasma ↑45%, RBC ↑20%); Hb 105–115 g/L normal at term; true anaemia in pregnancy = Hb <100 g/L

Hypercoagulability: Virchow's triad complete in pregnancy — hypercoagulability (↑ clotting factors I, VII, VIII, X, XII; ↓ protein S; acquired resistance to protein C), venous stasis (↑ venous pressure in legs; ↓ venous tone from progesterone), and endothelial injury (from placental trauma, delivery); DVT risk ↑5× vs nonpregnant; PE is leading cause of maternal mortality in the UK

VTE prophylaxis: LMWH for high-risk pregnancies (immobility, thrombophilia, previous DVT); graduated compression stockings; early ambulation; timing of neuraxial anaesthesia relative to last LMWH dose (unfractionated 4 hours; LMWH 12 hours prophylactic or 24 hours therapeutic dose)

Platelet count: mild thrombocytopenia of pregnancy (gestational thrombocytopenia — Plt 70–150 × 10⁹/L at term) — benign; does NOT contraindicate epidural; contraindication threshold for neuraxial anaesthesia: Plt <70–80 × 10⁹/L (institution-specific) with normal platelet function

Parameter Change Drug Effect Plasma Albumin ↓ 20–30% → less drug protein-bound → more free (active) Propofol, thiopentone, local anaesthetics: increased free fraction → greater protein drug effect per dose; reduce doses accordingly binding Renal GFR ↑50% → creatinine falls to 0.5–0.6 mg/dL (normal pregnant); Renally-cleared drugs (aminoglycosides, digoxin) have shorter t½ → may need clearance renal tubular secretion ↑ higher/more frequent doses MAC MAC ↓ 25–40% from early pregnancy (high progesterone → Standard MAC concentrations produce deeper anaesthesia in pregnant (volatile GABAergic CNS depression) patients; doses should be reduced; risk of cardiovascular depression agents) Epidural LA Epidural veins engorged (↓ epidural space volume) → same LA volume Reduce epidural and spinal doses by 25–30%; a "standard" dose produces a dose spreads further → blocks are 25–30% more extensive higher block than expected in pregnancy

Category Examples Full stomach / known Emergency surgery (<6 hours from last solid meal); trauma (pain + opioids delay gastric emptying); inadequate fasting (non-compliant aspiration risk patient, unknown time of last meal); post-pyloric obstruction (ileus, bowel obstruction); hiatus hernia + severe GORD with symptoms at rest Physiological/anatomical Pregnancy (>16–20 weeks); opioid administration within 4 hours; diabetic gastroparesis (particularly insulin-dependent); renal failure; acute delay in gastric abdominal emergency (pain reflex slows gastric emptying) emptying Raised intra-abdominal Morbid obesity; ascites; peritoneal dialysis; bowel obstruction pressure

1. Preoxygenation: 3–5 minutes 100% O₂ via tight-fitting face mask (SpO₂ ≥99%); 4 vital capacity breaths as alternative if time critical; head-up 20° position increases FRC and tolerance of apnoea 2. Pre-oxygenation assessment: confirm difficult airway assessment completed; DAS algorithm available; team briefed; sugammadex 16 mg/kg drawn and ready if rocuronium used 3. Induction agent (rapid IV): thiopentone 4–5 mg/kg IV (classic choice — extremely rapid and reliable LOC in <30 sec; reduces ICP; propofol 2–2.5 mg/kg is the modern alternative — more cardiovascular depression but associated with less PONV and lower aspiration risk from earlier return of reflexes) 4. Cricoid pressure (Sellick's manoeuvre): applied simultaneously with induction drug injection by a trained assistant; 10 N (cricoid just visibly displaces) during awake phase → 30 N after LOC; maintained until ETT position confirmed; specific technique: steady downward pressure on the cricoid cartilage (not thyroid) compresses the cricoid ring against the vertebral body → occludes the upper oesophagus → prevents passive regurgitation of gastric contents into the pharynx 5. Succinylcholine 1.5 mg/kg IV: the classic RSI NMB; fastest onset (60 seconds) of any NMB; OR rocuronium 1.2 mg/kg (equivalent intubating conditions at 60 sec; sugammadex 16 mg/kg available for reversal if CICO) 6. No bag-mask ventilation between induction and intubation in classic RSI (avoids gastric insufflation); if SpO₂ falls <93% during apnoea → gentle bag-mask ventilation acceptable (modern modification) with cricoid pressure maintained 7. Intubation at 60 seconds: laryngoscopy + intubation at the time of peak NMB effect; no waiting for response to painful stimuli; direct or video laryngoscopy based on anticipated airway 8. Confirm ETT position: ETCO₂ waveform (sustained over 6 breaths) + bilateral breath sounds + SpO₂ maintenance; inflate cuff; release cricoid pressure once position confirmed; secure ETT

Sellick's Manoeuvre — What the Evidence Shows

Arguments FOR: Reduces regurgitation in cadaveric studies; still recommended by RCOA, DAS 2018, and most obstetric guidelines as standard of care

Arguments AGAINST: Reduces LOS competence at 30 N (paradoxically may allow regurgitation); impairs laryngoscopic view in up to 20% of cases; incomplete protection (only works against passive regurgitation, not active vomiting); no randomised controlled trial demonstrating reduced aspiration morbidity; may cause oesophageal rupture if the patient vomits against closed cricoid

DAS 2018 guidance: Cricoid pressure should be applied but must be released immediately if it impairs laryngoscopic view or interferes with intubation attempt; the airway takes priority over aspiration prevention

Rocuronium 1.2 mg/kg provides equivalent intubating conditions to succinylcholine 1.5 mg/kg at 60 seconds; sugammadex 16 mg/kg immediately available for reversal if CICO

Advantages over succinylcholine: no contraindications in burns, denervation, MH susceptibility, pseudocholinesterase deficiency, hyperkalaemia risk; longer clinical duration (30–45 min vs 10 min) which can be an advantage (no recurarisation) or disadvantage (if airway fails and spontaneous recovery is needed)

CICO scenario: rocuronium RSI + CICO → sugammadex 16 mg/kg → spontaneous ventilation returns in 2–3 min → "wake and manage awake" strategy; this converts a catastrophic situation into a recoverable one

Where succinylcholine still preferred: where briefest possible duration is specifically needed (very brief intubation, hyperkalemia acceptable, no CICO concern with established airway plan)

STOP-BANG for OSA: Snoring (loud enough to be heard through closed door?), Tired (tired/fatigued during daytime?), Observed apnoeas (by partner?), blood Pressure (hypertension?), BMI >35, Age >50, Neck circumference >40 cm, Gender male; ≥5 positive = high risk for severe OSA; this patient with BMI 52 + hypertension + female = at minimum moderate risk

Airway assessment: Mallampati class (higher in obese); neck circumference >40–45 cm is the strongest predictor of difficult intubation in obese patients (independently of Mallampati); limited neck extension; LEMON score; plan for video laryngoscopy as first-line tool

Investigations: ECG (RVH, LVH from chronic hypoxaemia/hypertension); echocardiogram (pulmonary hypertension, RV function); spirometry (restrictive pattern — ↓ FVC, ↓ FRC, ↓ ERV, normal FEV1/FVC; severe OSA with pulmonary hypertension = very high risk); ABG if suspected daytime CO₂ retention (obesity hypoventilation syndrome)

CPAP pre-admission: if OSA diagnosed — patient should be on home CPAP; bring CPAP machine to hospital; use throughout recovery and post-op

Ramped position (HELP position — Head Elevated Laryngoscopy Position): pillows/foam wedge under head and shoulders to align the external auditory meatus with the sternal notch; this optimises the laryngoscopic view (brings glottis into line of sight) in obese patients and simultaneously maximises the FRC benefit of head-up positioning; the HELP position reduces failed first-attempt intubation rates in obese patients by ~50%

Preoxygenation: 3–5 minutes 100% O₂; consider non-invasive ventilation (BiPAP/CPAP 5–10 cmH₂O) during preoxygenation — applies positive pressure to stent open collapsed small airways in obese patients, increasing FRC and O₂ reserve; high-flow nasal O₂ (HFNO) 60 L/min through apnoeic period extends safe apnoea time; target ETO₂ >90% at end of preoxygenation to confirm denitrogenation Safe apnoea time is markedly reduced in morbid obesity — SpO₂ may fall to critical levels within 90 seconds of apnoea vs 8+ minutes in a normal-weight patient; this is the most important practical implication of FRC reduction in obesity

Drug Dosing in Obesity Drug Dose Basis Rationale Propofol Lean Body Weight (LBW) for induction dose; LBW for induction — obese patients have proportionally less increase in central compartment (induction) Total Body Weight (TBW) for maintenance volume vs LBW; TBW for maintenance — larger volume of distribution for fat-soluble propofol infusion Succinylcholine Total Body Weight (TBW) NMBs distribute into extracellular fluid which increases in proportion to TBW in obesity / Rocuronium Sugammadex Actual Body Weight (ABW/TBW) Must encapsulate total circulating rocuronium based on TBW dosing; underdosing causes incomplete reversal Fentanyl / Lean Body Weight (LBW) Opioids should be dosed conservatively in obese patients — increased sensitivity to respiratory Morphine depression; avoid boluses; prefer remifentanil infusion for precise titration Local Ideal Body Weight (IBW) LA does not distribute into fat; TBW dosing would cause LAST; reduce dose as epidural space anaesthetics smaller (fatty infiltration) (regional)

Ventilation Strategy (Laparoscopic — Trendelenburg + Pneumoperitoneum)

Lung-protective ventilation: TV 6–8 mL/kg IBW (NOT TBW — obese lungs are not proportionally larger); using TBW for TV in obesity = massive overventilation = VILI PEEP 10–12 cmH₂O: morbidly obese patients develop rapid atelectasis; higher PEEP than standard needed to prevent alveolar collapse in dependent lung regions; Trendelenburg + pneumoperitoneum → severe FRC reduction → PEEP 10–12 required

Recruitment manoeuvre: 30 cmH₂O sustained inflation for 30 seconds at position change and after pneumoperitoneum then maintain PEEP 10–12; reduces atelectasis significantly

FiO₂: avoid 100% O₂ unnecessarily — absorption atelectasis; target SpO₂ ≥95% with minimum necessary FiO₂

Complication Risk in Obese Prevention Hypoxaemia / Very high; OSA + opioids + supine positioning + upper Semi-recumbent position (30–45° head-up) in recovery; CPAP immediately postObstructive abdominal incision extubation; supplemental O₂; nurse 1:1 in recovery; SpO₂ monitoring ≥12 hours apnoea post-op; avoid opioids DVT/PE ↑ VTE risk 2–3× vs normal weight (venous stasis + LMWH (dose based on TBW for adequate anti-Xa levels — standard prophylactic hypercoagulability + immobility) dose often insufficient); pneumatic compression stockings; early mobilisation; consider extended LMWH prophylaxis for 28 days post-bariatric surgery Wound Impaired wound healing (poor oxygenation of subcutaneous Laparoscopic preferred to open (fewer SSIs); adequate subcutaneous closure; complications fat); SSI 2–3× higher antimicrobial sutures; glycaemic control (<10 mmol/L) Rhabdomyolysis Specific to morbidly obese patients positioned on standard Adequate padding under all pressure points; limit case duration; CK monitoring operating tables; pressure necrosis of dependent muscle post-operatively for cases >3 hours; IV fluids to maintain UO ≥1 mL/kg/hr groups (particularly buttocks in lithotomy, back in supine)

Feature Infant/Child Adult Clinical Consequence Laryngeal C3–C4 in neonates (high and anterior) C4–C5 More difficult to align larynx with the line of sight during laryngoscopy; straight position Miller blade preferred in neonates (lifts the epiglottis directly) Epiglottis Long, stiff, omega-shaped (Ω); floppy Short, flat; flexible Miller blade (straight) more effective for direct lift of epiglottis; Macintosh blade (curved, fits vallecular) less reliable in infants Narrowest Subglottis (cricoid ring) — funnel-shaped airway; Glottis (true vocal ETT that passes through the cords may still be too tight at the subglottis; too point the cricoid ring is the non-distensible narrowest cords) large a tube → subglottic oedema → post-extubation stridor; a small air leak at point 15–20 cmH₂O is the correct fit indicator for uncuffed tubes Head and Large occiput → passive neck flexion in supine Smaller occiput; In neonates: a small shoulder roll under the shoulders (not the head) brings the occiput position → relative anterior laryngeal position neck extension larynx into the line of sight; neutral "sniffing" position or slight extension; NO needed for pillow under the head intubation Tongue Relatively large tongue for the oral cavity size → Proportionally Higher aspiration and obstruction risk; jaw thrust more important; LMA insertion more easily obstructs airway; more likely to fall smaller may be more challenging back in unconscious child Rib cage Horizontal ribs → FRC-dependent breathing; Downward- Neonates desaturate extremely rapidly (≤60 seconds in a neonate vs 8+ higher closing capacity relative to FRC → small sloping ribs allow minutes in healthy adults); keep preoxygenation time adequate; work fast during airway closure at FRC → rapid desaturation active increase in apnoea FRC

Parameter Formula Example (5-year-old) Uncuffed ETT internal diameter (Age/4) + 4 = ID in mm (5/4) + 4 = 5.25 → use 5.0 mm uncuffed Cuffed ETT internal diameter (Age/4) + 3.5 = ID in mm (5/4) + 3.5 = 4.75 → use 4.5 mm cuffed ETT length at lips (oral) (Age/2) + 12 cm (5/2) + 12 = 14.5 cm at lip ETT length at nostril (nasal) (Age/2) + 15 cm (5/2) + 15 = 17.5 cm at nostril LMA size <5 kg = size 1; 5–10 kg = 1.5; 10–20 kg = 2; 20–30 kg = 2.5; 30–50 kg = 3; >50 kg = 4 20 kg child = LMA size 2.5

Anticipated difficult airway: plan in advance; assemble the paediatric difficult airway trolley (range of LMAs, paediatric video laryngoscope [Karl Storz DCI or CMAC paediatric blade], paediatric fiberoptic bronchoscope [2.8 mm minimum for ETT loading], paediatric cricothyrotomy kit); experienced paediatric anaesthesiologist; ENT surgeon on standby for possible surgical airway

Inhalational induction (spontaneous breathing maintained): the safest technique for anticipated difficult airway in children — induction with sevoflurane in 100% O₂, maintaining spontaneous ventilation throughout; once adequately anaesthetised, direct laryngoscopy ± video laryngoscopy attempted; if fails → LMA; if LMA → use as conduit for FOI; if all fails → wake up (spontaneous breathing maintained throughout → safe to allow the child to recover)

Video laryngoscopy in paediatrics: paediatric-sized blades (C-MAC size 0, 1, 2; Karl Storz DCI Miller size 0, 1); improving first-attempt intubation success vs direct laryngoscopy; increasingly recommended as first-line for anticipated difficult airway in children

Fibreoptic intubation (awake FOI in paediatrics): rarely practical in young children (unlike adults); infants do not cooperate for topical airway anaesthesia; preferred approach: sedated (dexmedetomidine infusion) or lightly anaesthetised FOI with spontaneous ventilation; technique: 2.8 mm or 3.5 mm paediatric fibrescope through a face mask or LMA while child breathes spontaneously; ETT railroaded over the scope once in trachea

Front-of-Neck Access (FONA) in children: true cricothyrotomy is technically challenging in infants (small cricothyroid membrane); needle cricothyrotomy (14G IV cannula) with jet ventilation is the primary emergency technique in children <8 years; surgical cricothyrotomy and tracheostomy for older children/adolescents

Higher O₂ consumption per kg (6–8 mL/kg/min vs 3 mL/kg/min adults); very small functional residual capacity → rapid desaturation; safe apnoea time in a neonate ≈ 60–90 seconds Higher heart rate (normal neonatal HR 120–160 bpm; infants 100–120 bpm); cardiac output is rate-dependent in neonates (cannot increase SV significantly — immature Frank-Starling mechanism) → bradycardia = fall in cardiac output; ALWAYS give atropine 20 mcg/kg before laryngoscopy in neonates/young infants

Temperature regulation: high surface area:body mass ratio → rapid heat loss; all fluids warmed; warming blanket; theatre temperature 28°C for neonates; temperature monitoring mandatory

Effect Mechanism Intraoperative Management ↑ SVR (early IAP compression → mesenteric vasoconstriction; CO₂ absorption MAP rises initially; may require vasodilators in hypertensive patients; volatile and → sympathetic activation → ↑ catecholamines → vasoconstriction; agents and deeper anaesthesia help manage hypertension from CO₂ absorption sustained) IAP 12–15 mmHg → SVR ↑30–50% ↓ Venous IAP >12 mmHg → IVC compression → ↓ preload; initial ↑ CO from Adequate preloading before insufflation (250–500 mL crystalloid); vasopressors Return → ↓ leg-emptying into central circulation then falls as IVC compression for sustained hypotension; Trendelenburg position modifies venous return (↑ in CO predominates head-down; ↓ further in head-up laparoscopy) (intermediate) ↑ HR Sympathetic activation from CO₂ absorption and surgical stress; Adequate depth of anaesthesia; beta-blocker if needed for rate control (moderate) partially offset by vagal tone from peritoneal stretching Cardiac Hypercapnia (CO₂ absorption) → ↑ catecholamines → arrhythmia; Atropine available; adequate hyperventilation to prevent hypercapnia; if arrhythmia also vagal reflex from peritoneal stretching at insufflation onset → arrhythmia → check ETCO₂ and ABG; consider desufflation bradycardia → asystole (rare)

↓ FRC and lung compliance: diaphragm displaced cranially by pneumoperitoneum → FRC reduced 10–20% beyond position-related reduction; peak airway pressures rise 40–50% for same TV; atelectasis in dependent lung regions

CO₂ absorption: CO₂ gas diffuses from the peritoneal cavity into systemic blood → ETCO₂ rises 10–20 mmHg above pre-insufflation baseline within 10–20 minutes; must increase MV by 15–25% to maintain normocapnia; in patients with severe COPD or very limited reserve, maintaining normocapnia may not be possible without dangerous airway pressures → accept permissive hypercapnia

Gas embolism risk: direct IV insufflation of CO₂ (rare but catastrophic) → sudden fall in ETCO₂ + cardiovascular collapse; CO₂ is more water-soluble than air → reabsorbed faster from the blood; management: stop insufflation; left lateral Durant's position; aspiration via CVP catheter; CPR

Renal: IAP >15 mmHg → renal vein compression → ↓ renal blood flow → oliguria (transient — resolves on desufflation); not associated with post-op AKI in healthy patients; ensure adequate hydration; monitor urine output; avoid NSAIDs peri-operatively if oliguric intraoperatively

ICP rise: CO₂ absorption → hypercapnia → cerebral vasodilation → ↑ CBF → ↑ ICP; compounded by ↑ CVP from IAP raising venous pressure; head-down Trendelenburg further raises ICP; relevant in patients with pre-existing raised ICP or ventriculoperitoneal shunts

Subcutaneous emphysema: CO₂ tracks along fascial planes from the peritoneal cavity into subcutaneous tissue; presents as crepitus on palpation; may cause extensive tracking to the mediastinum and neck; results in massive CO₂ absorption → very high ETCO₂ → increase MV further; does not require specific treatment unless compromising airway or mediastinal structures

Airway: ETT mandatory (positive pressure needed; aspiration risk from raised IAP; patient may need Trendelenburg); LMA is used for brief, non-obese patients in selected units with second-generation supraglottic devices (higher seal pressure)

Ventilation settings: TV 6–8 mL/kg IBW; PEEP 5–8 cmH₂O; RR adjusted to maintain normocapnia (increase by 15–25% from baseline after CO₂ insufflation); monitor ETCO₂ continuously; check ABG at 30–60 minutes if significant patient complexity; accept permissive hypercapnia in COPD patients rather than use excessive driving pressures

PONV: laparoscopy is one of the highest PONV risk procedures; full multimodal PONV prophylaxis based on Apfel score; TIVA with propofol reduces PONV incidence by 25–30% vs volatile; ondansetron + dexamethasone minimum for all laparoscopic procedures

Analgesia: port-site local anaesthetic infiltration (bupivacaine 0.5% at each port before closure); IV paracetamol + NSAIDs; opioid-sparing; TAP block for larger ports/incisions; intraperitoneal local anaesthetic instillation (bupivacaine) reduces post-operative visceral pain after laparoscopy

Desufflation awareness: sudden desufflation may cause vasovagal reaction (brief hypotension + bradycardia); anaesthesiologist should be informed before desufflation; have atropine ready

Normal MVA = 4–6 cm²; symptoms begin at MVA <2.5 cm²; MVA 1.0–1.5 = severe; MVA <1.0 = very severe

Mechanism: stenotic mitral valve → ↑ LA pressure → pulmonary venous hypertension → pulmonary oedema; chronic LA pressure ↑ → pulmonary arterial hypertension → RV hypertrophy and failure; fixed outflow from LA → any ↑ HR shortens diastolic filling time → less time for blood to cross the stenotic valve → sudden ↑ LA pressure → acute pulmonary oedema (the key clinical insight) AF is almost universal in significant MS (atrial dilation drives AF); loss of atrial systole ("atrial kick") removes 20–30% of ventricular filling → additional haemodynamic compromise

Regional Anaesthesia (Preferred)

Spinal anaesthesia: technically simple but produces sudden sympathectomy → acute hypotension → reflex tachycardia → catastrophic in MS; spinal is RELATIVELY CONTRAINDICATED for major surgery in MS because the sympathectomy is abrupt and may cause severe tachycardia from reflex sympathetic activation; if used → titrated slowly (combined spinal-epidural with very small initial intrathecal dose + epidural top-up) or avoided

Epidural anaesthesia: preferred for regional technique — allows gradual titration of sympathectomy level; maintains more haemodynamic control than spinal; place thoracic epidural for laparoscopic hysterectomy; slow top-up in 5 mL increments; use vasopressor (phenylephrine) to maintain SVR; monitor closely for tachycardia

General Anaesthesia (for Laparoscopic Case)

Induction: etomidate (most cardiovascularly stable) or carefully titrated propofol; AVOID ketamine (↑ HR → ↑ LA pressure → pulmonary oedema); fentanyl 1–2 mcg/kg with induction to blunt laryngoscopy response

Maintenance: sevoflurane preferred (moderate rate reduction; preconditioning); avoid desflurane (sympathetic activation → tachycardia)

Intraoperative tachycardia management: esmolol 0.5–1 mg/kg IV bolus; or digoxin if not already digitalised; metoprolol 1–2 mg IV bolus

Fluid management: conservative; avoid large volume crystalloid boluses; pulmonary artery catheter or TOE for haemodynamic monitoring in MVA <1.0 cm²

CO₂ pneumoperitoneum in MS: ↑ IAP → ↑ SVR (helps maintain MAP) and initial ↑ CO₂ absorption → sympathetic activation → tachycardia (harmful); maintain ETCO₂ strictly in normal range (increase MV to manage absorbed CO₂)

Trendelenburg position: increases venous return to an already volume-loaded right heart → may precipitate acute pulmonary oedema; head-down tilt must be gradual; monitor closely

Post-desufflation: sudden ↓ IAP → venous pooling → ↓ preload → ↓ CO; prepare vasopressor

HDU/ICU level monitoring for 24 hours post-op; cardiac monitoring (continuous ECG); resume rate-control medications immediately post-op; watch for AF with rapid ventricular rate; fluid balance (restrict fluids post-op; furosemide if signs of pulmonary congestion); anticoagulation for AF (warfarin or DOAC — check thromboembolism vs bleeding balance post-surgery); resume warfarin/DOAC within 24 hours if haemostasis adequate

Item Fasting Period Rationale Clear liquids (water, black 2 hours before Clear fluids empty from the stomach within 30–60 minutes; gastric pH improves with fluid consumption (dilutes coffee, clear fruit juice without induction acid); preoperative carbohydrate drink (200–400 mL of 12.5% carbohydrate solution 2 hours before surgery) pulp, sports drinks, carbonated reduces insulin resistance and anxiety, improves postoperative outcomes — integral to ERAS protocols drinks) Breast milk (infants) 4 hours Breast milk empties from the stomach faster than formula or cow's milk due to its whey-dominant protein composition and lower fat content Infant formula / non-human milk 6 hours Higher fat and protein content → slower gastric emptying Light meal (toast, crackers, 6 hours Light meals typically empty within 4–5 hours; 6-hour fasting ensures adequate buffer simple carbohydrate meal — low fat, low protein) Full/fatty/fried meal (heavy meal 8 hours High-fat meals significantly slow gastric emptying; fat delays gastric acid secretion reduction; high-protein meals — high fat, meat, fried food) minimum are digested slowly; in practice: a large evening meal → fast from midnight (8+ hours) is appropriate (some guidelines: overnight fast)

Patient Modification Rationale Group Pregnancy Treat as full stomach regardless of fasting time (in active labour + opioids); RSI mandatory; Progesterone reduces LOS tone; opioids (>16–20 sodium citrate 30 mL oral + H₂ blocker before all GA dramatically slow gastric emptying; risk persists weeks) through full postoperative period Morbid Apply standard fasting times; however, gastric emptying may be delayed; some centres treat Obesity associated with raised intra-abdominal obesity morbidly obese patients with raised aspiration risk as "full stomach" for GA pressure and higher gastric residual volumes; GORD common Diabetes Establish surgery as first on the list (shortest fasting); monitor blood glucose hourly; variable rate Diabetic gastroparesis delays gastric emptying; mellitus insulin infusion (VRIII) if glucose >14 mmol/L; resume oral agents when eating and drinking; omit prolonged fasting → hypoglycaemia; insulin on the metformin if GA with fasting (standard glucose-containing fluids in prolonged fasting) morning of surgery without food → severe hypoglycaemia Emergency Treat as full stomach regardless; RSI if GA; aspiration prophylaxis; check last oral intake as part Emergency surgery cannot wait for fasting to surgery of pre-operative history complete; RSI is the mechanism for managing fullstomach risk when anaesthesia must proceed Gastro- Continue proton pump inhibitor (PPI) preoperatively (omeprazole 20 mg oral OD); consider PRN GORD with severe symptoms/hiatus hernia → oesophageal antacid pre-operatively; apply RSI if severe symptoms/hiatus hernia with regurgitation at rest elevated aspiration risk even with adequate fasting reflux disease (GORD)

200–400 mL of a specialised clear carbohydrate drink (12.5% maltodextrin — e.g., PreOp, Nutricia) given 2–3 hours before induction as part of the ERAS protocol

Evidence: reduces insulin resistance by 50%; reduces preoperative thirst, hunger, anxiety; reduces length of hospital stay by 0.5–1 days in colorectal ERAS programmes

Safe: gastric emptying is complete within 90 minutes for this formulation; not associated with increased aspiration risk vs water; contraindicated in: diabetics with gastroparesis; morbid obesity with delayed gastric emptying; immediate emergency surgery

Property Desflurane Sevoflurane Blood-gas partition 0.42 (lowest of all volatile agents) 0.65 coefficient (λ) MAC (O₂, 40-year adult) 6.0% 2.0% Boiling point 23.5°C (near room temp → requires heated pressurised TEC-6 vaporiser with 58.5°C (standard draw-over TEC-7 vaporiser; no electrical power) heating required) Global Warming Potential 2540 (most potent greenhouse gas anaesthetic); atmospheric lifetime 14 years 130; atmospheric lifetime 1.1 years (GWP 100-year)

Inhalational induction NOT suitable — pungent; causes coughing, laryngospasm, breath-holding; cannot Suitable — non-pungent, pleasant odour; gold suitability be used for gas induction standard for paediatric gas induction; smooth and rapid

Cardiovascular effects — Causes marked sympathetic activation (tachycardia + hypertension) when Minimal sympathetic activation with concentration abrupt concentration concentration rapidly increased → dangerous in ischaemic heart disease; requires changes; smoother cardiovascular profile increase gradual titration Metabolism Minimal (<0.02%) — essentially no hepatic metabolism; no nephrotoxic metabolites 2–3% hepatic metabolism → inorganic fluoride + HFIP; Compound A from soda lime degradation Recovery speed Fastest of all volatile agents; significant time advantage in long cases (>6–8 hours); Rapid — marginally slower than desflurane; in (emergence) clinically meaningful in very long procedures procedures <6 hours: discharge time equivalent to desflurane Vaporiser Expensive TEC-6 heated and pressurised vaporiser required; electrically powered; Standard TEC-7 vaporiser; no power required; not portable portable; cheaper Anaesthetic Less data than sevoflurane; some evidence of preconditioning Well-documented ischaemic preconditioning effect preconditioning (mitoKATP channels); benefit in cardiac surgery

When desflurane might be preferred: cases expected >8 hours (morbid obesity, hepatobiliary surgery) where the faster emergence from desflurane provides meaningful time advantage; patients with high risk of prolonged emergence where rapid assessment is clinically important; very long neurosurgical cases requiring rapid wake-up testing

When sevoflurane is clearly preferred: paediatric anaesthesia (gas induction); cardiac surgery (preconditioning benefit); all routine cases (<6 hours, which is the vast majority) where recovery times are equivalent; all environmentally-conscious practice; any patient with ischaemic heart disease (desflurane sympathetic activation on concentration changes is contraindicated)

Environmental decision: UK NHS has banned desflurane from formulary (2021); ESA recommends desflurane should be reserved for exceptional clinical indications only; for the same MAC-hour, desflurane produces 19× more CO₂ equivalent emissions than sevoflurane; switching a department from desflurane to sevoflurane is among the highest-impact individual actions an anaesthesiologist can take for environmental sustainability

Mechanism: NMDA receptor antagonism (the primary mechanism for analgesia and sedation); inhibits nicotinic ACh receptors; modulates opioid receptors (μreceptor agonist — contributes to analgesia and some physical dependence); activates TREK-1 two-pore potassium channels (contributes to sedation)

Properties: colourless gas; sweet smell; no hepatic metabolism; excreted unchanged by the lungs; blood-gas partition coefficient = 0.47 (low — rapid onset and offset); MAC = 105% (requires hyperbaric conditions for surgical anaesthesia as sole agent; clinically used at 50–65% to provide MAC-equivalent of approximately 0.6 MAC)

Analgesia: significant analgesic effect at 30–50% concentrations — equivalent to moderate-dose opioids for procedural pain; the mechanism: endogenous opioid release + NMDA antagonism; Entonox (50% N₂O/50% O₂) provides effective labour analgesia, dental analgesia, and procedure analgesia

Cardiovascular: mild myocardial depression (direct) but sympathomimetic (↑ catecholamines) → net: relatively stable BP and HR; less vasodilatory than volatile agents; suitable for cardiac surgery supplementation

Controversy Mechanism Clinical Evidence Expansion of N₂O is 34× more blood-soluble than N₂; diffuses into gas-filled spaces faster than Strong evidence; absolute contraindication in known gas-filled N₂ leaves → expanding gas volumes (pneumothorax, bowel obstruction, middle pneumothorax, bowel obstruction, middle ear surgery (Jobsonspaces ear, pneumocephalus, intraocular gas bubbles post-vitreoretinal surgery) Horne tympanoplasty), intraocular gas (>3 months after vitreoretinal surgery with gas tamponade), pneumocephalus, and air embolism; N₂O triples/quadruples trapped gas volume PONV N₂O activates opioid receptors in the gut → ↑ PONV; also activates vomiting ENIGMA trial (Myles PS, Lancet 2007; n=2050): N₂O-free increase centre directly; meta-analyses confirm N₂O increases PONV incidence by anaesthesia significantly reduced severe PONV; eliminating N₂O approximately 20–30% relative to N₂O-free anaesthesia from routine practice is one of the most effective PONV prevention strategies Vitamin B12 / N₂O irreversibly oxidises cobalt (Co²⁺→Co³⁺) in the active site of vitamin B12 Clinically relevant in: prolonged exposures (>6 hours); patients Methionine (cobalamin) → inactivation of methionine synthase → impaired methionine with pre-existing B12 deficiency (vegans, elderly, pernicious synthase synthesis → impaired DNA synthesis (folate-methyl trap); single anaesthetic anaemia, malabsorption); ICU patients on prolonged N₂O; patients inhibition exposure → 50% reduction in methionine synthase activity within 2–6 hours; bone on antifolate drugs (methotrexate); subacute combined marrow depression with megaloblastic changes within 24 hours after prolonged degeneration of the cord reported in N₂O abuse and chronic exposure occupational exposure Environmental GWP = 265; atmospheric lifetime 114 years; also depletes stratospheric ozone Multiple hospitals have eliminated N₂O from routine use without impact (similar mechanism to CFCs); N₂O pipeline systems leak 10–30% of delivered patient outcome impact; the ENIGMA trial in fact showed improved gas into building; healthcare N₂O accounts for approximately 5% of all healthcare outcomes in the N₂O-free arm; environmental + PONV evidence greenhouse gas emissions globally together strongly support N₂O elimination from routine anaesthesia

Primary: non-competitive antagonist of the NMDA (N-methyl-D-aspartate) glutamate receptor — binds within the ion channel pore (open channel block) → prevents Ca²⁺ influx → inhibits glutamate-mediated excitatory neurotransmission; NMDA receptors mediate pain transmission in the dorsal horn, memory formation in the hippocampus, and consciousness in the thalamo-cortical circuits

Secondary: sigma receptor agonist (contributes to dissociative hallucinations); mu-opioid receptor agonist (weak analgesic contribution); muscarinic receptor antagonist (bronchodilation, tachycardia); voltage-gated sodium channel blockade (local anaesthetic-like effect at high concentrations)

Dissociation: ketamine produces EEG dissociation between the thalamus and limbic system — the thalamus (which normally relays sensory information to the cortex) is blocked while the limbic system (emotion and memory) continues activity; this produces the unique "dissociative" state: the patient appears conscious (open eyes, preserved nystagmus, intact airway reflexes) but is profoundly analgesic and amnestic and does not respond purposefully to stimuli

Highly lipid-soluble → rapid CNS penetration (peak brain concentration within 1 minute of IV administration); Vd = 3 L/kg (large — widely distributed); protein binding = 27% (low)

Hepatic metabolism: CYP3A4 → norketamine (an active metabolite — 20–30% of parent potency; contributes to prolonged clinical effect); norketamine → hydroxynorketamine metabolites (water-soluble, renally excreted) t½ = 2–3 hours; clinical duration of single bolus induction dose: 10–15 minutes (recovery from redistribution, not elimination); sub-anaesthetic infusion duration variable

Routes: IV (1–2 mg/kg induction; 0.5–1 mg/kg for procedural sedation); IM (4–6 mg/kg — useful when IV access unavailable; onset 5–15 minutes); oral, nasal, rectal (subanesthetic analgesic doses in paediatrics and chronic pain)

System Effect Mechanism Clinical Application Cardiovascular ↑ MAP, ↑ HR, ↑ CO Inhibition of noradrenaline reuptake → ↑ circulating Ideal induction agent for haemodynamically (sympathomimetic); catecholamines + direct sympathetic stimulation → ↑ SVR + ↑ compromised patients (trauma, cardiac tamponade, myocardial depression HR + ↑ CO; in catecholamine-depleted states (severe tension pneumothorax, septic shock when directly (but masked by haemorrhagic shock), the direct myocardial depressant effect catecholamine stores are intact); provides sympathomimetic effect in may be unmasked → hypotension paradoxically anaesthesia while maintaining or improving most patients) haemodynamics Respiratory Minimal respiratory Bronchial smooth muscle relaxation from muscarinic Bronchodilator of choice for severe depression at analgesic antagonism and catecholamine release → useful in status bronchospasm/status asthmaticus; useful for doses; preserves airway asthmaticus; airway reflexes are preserved relative to other IV sedation in spontaneously breathing patients; avoids reflexes (relatively); agents but NOT completely — aspiration can still occur; do not apnoea seen with propofol/benzodiazepines bronchodilator rely on preserved reflexes for full stomach patients

Haemodynamically unstable RSI: induction dose 1–2 mg/kg IV; maintains cardiovascular stability when other agents would cause hypotension

Procedural sedation: 0.5–1 mg/kg IV or 4 mg/kg IM; ideal for brief, painful procedures (fracture reduction, joint manipulation, wound debridement) — maintains spontaneous ventilation and airway reflexes; use with midazolam 0.05 mg/kg to reduce emergence hallucinations

Subanesthetic analgesia: 0.1–0.5 mg/kg/hr infusion; reduces opioid consumption by 30–40% in acute pain; prevents opioid-induced hyperalgesia (NMDA antagonism blocks the central sensitisation that increases pain perception with opioid use); useful in complex regional pain syndrome, burn wound care, and multimodal analgesia

Status asthmaticus: 1–2 mg/kg IV or 0.5 mg/kg/hr infusion; bronchodilation helps while providing sedation for intubated patients with severe bronchospasm

Acute depression (S-ketamine/Esketamine): intranasal esketamine (Spravato) — FDA-approved for treatment-resistant depression; administered in clinic under observation; rapid antidepressant effect within hours (unlike conventional antidepressants — weeks); mechanism via NMDA antagonism and AMPA receptor potentiation in prefrontal cortex

Emergence delirium/hallucinations: unpleasant vivid dreams, hallucinations, and psychedelic experiences during recovery; more common in adults than children (>15%); can be profoundly distressing; prevented by: benzodiazepine premedication (midazolam 0.05 mg/kg IV) markedly reduces incidence; quiet, calm environment during recovery; avoid unnecessary stimulation during emergence; propofol sub-anesthetic infusion co-administered

Contraindications: severe hypertension/pre-eclampsia (raises BP further → hypertensive crisis); raised ICP/IOP (raises both — traditionally contraindicated in head injury; however, in adequately ventilated/sedated ICU patients this is disputed — recent evidence suggests ketamine does not raise ICP when used with other drugs in the context of mechanical ventilation); history of schizophrenia or acute psychosis (NMDA antagonism can exacerbate psychotic symptoms); thyrotoxicosis (catecholamine surges dangerous)

α₂ Receptor Location Effect of Agonism Clinical Consequence Locus coeruleus (brainstem ↓ noradrenaline release → ↓ activity in the ascending arousal system → sedation The unique "co-operative sedation" — patients noradrenergic nucleus — the and hypnosis; crucially, this sedation resembles natural sleep (NREM stage 2 — can be woken easily by verbal stimulation but primary site for delta waves) rather than anaesthetic unconsciousness; the brainstem arousal return to calm sedation when stimulation stops dexmedetomidine's sedative circuits are inhibited, not the cortex directly → rousable sedation and hypnotic effects) Dorsal horn (spinal cord α₂ ↓ substance P and glutamate release from C fibre terminals → ↓ pain signal Significant analgesic effect (not as potent as receptors on presynaptic transmission → analgesia; also post-synaptically modulates dorsal horn neuron opioids but clinically meaningful); opioid-sparing nociceptive terminals) excitability (reduces morphine requirements 30–40%); reduces opioid-induced hyperalgesia Peripheral vasculature (α₂ Vasoconstriction at high doses → initially ↑ BP; at lower plasma concentrations, Bradycardia and hypotension (the most receptors on vascular smooth the presynaptic α₂ receptors on sympathetic nerve terminals are activated → ↓ common and important side effects); typically: ↑ muscle) noradrenaline release → sympatholysis → ↓ HR + ↓ BP (the predominant effect BP during loading dose followed by bradycardia at clinical infusion rates) + hypotension; atropine for severe bradycardia

Protein binding: 94%; Vd: 118 L (extensive distribution); t½: 2 hours; hepatic glucuronidation + CYP2A6 metabolism to inactive metabolites (renally excreted)

Dose: loading infusion 1 mcg/kg over 10–20 minutes (AVOID rapid loading — causes hypertension from peripheral vasoconstriction; many protocols omit loading and start at maintenance rate directly for ICU use); maintenance 0.2–1.4 mcg/kg/hr

Application Dose Advantage Over Alternatives ICU sedation 0.2–1.0 mcg/kg/hr infusion; no SEDCOM trial (Riker RR, JAMA 2009): dexmedetomidine vs midazolam ICU sedation — dexmedetomidine reduced (non-intubated loading dose recommended in delirium duration by 22% and time on ventilator; less respiratory depression → earlier extubation; PADIS 2018 and intubated ICU; titrate to RASS target 0 guidelines: dexmedetomidine preferred over benzodiazepines for ICU sedation patients) to −2 Awake 1 mcg/kg loading over 10 The ideal sedation for awake procedures — patient is cooperative on verbal command (can perform motor tasks for craniotomy / minutes then 0.5–0.7 awake cortical mapping; can follow commands for awake intubation), analgesic (reduces topical LA requirement), awake mcg/kg/hr maintenance and anti-anxiety; no respiratory depression (unlike benzodiazepines/propofol); dissipates rapidly when infusion fiberoptic stopped intubation (AFOI) MAC (Monitored 0.5–1 mcg/kg loading then Suitable for procedures under regional anaesthesia (prevents patient movement while maintaining cooperation when Anaesthesia 0.2–0.7 mcg/kg/hr needed); reduces supplement GA required for regional block procedure anxiety Care) sedation Attenuation of Added to propofol-remifentanil Reduces haemodynamic response to laryngoscopy, intubation, and extubation; reduces emergence agitation in sympathetic TIVA or as premedication paediatrics (reduces tachycardia and hypertension on emergence) responses Paediatric 0.5–1 mcg/kg loading over 10 Children sedated with dexmedetomidine are arousable → able to follow instructions for MRI positioning; minimal sedation min + infusion for MRI respiratory depression → safer than propofol in children without an anaesthesiologist for non-procedural imaging sedation

PRIS: a syndrome of new-onset metabolic acidosis (lactate acidosis — unexplained metabolic acidosis in an ICU patient on propofol infusion), rhabdomyolysis, renal failure, and cardiac failure (specifically brady-arrhythmia progressing to right bundle branch block → complete heart block → cardiovascular collapse) occurring in patients receiving high-dose propofol infusions

Incidence: approximately 1.1% of ICU patients on propofol infusions; mortality: 33–85% once the full syndrome is established; more common than recognised because early features are attributed to other causes

Propofol (particularly at high doses and prolonged infusions) → inhibition of mitochondrial Complex I (NADH-ubiquinone oxidoreductase) AND Complex II (succinateubiquinone oxidoreductase) of the electron transport chain → impaired oxidative phosphorylation → cells cannot use oxygen for ATP synthesis despite adequate O₂ delivery → cells switch to anaerobic metabolism → lactic acidosis. Simultaneously: propofol phenol ring → impairs mitochondrial β-oxidation of free fatty acids (the primary fuel source for cardiac muscle and skeletal muscle in critically ill patients who are frequently on carbohydrate-restricted or lipid-heavy nutrition) → free fatty acids and their acylcarnitine intermediates accumulate → directly toxic to the mitochondrial and cell membranes → rhabdomyolysis of cardiac and skeletal muscle → acute cardiac failure + skeletal myolysis → myoglobinaemia → AKI Risk Factors Risk Factor Mechanism Dose >4–5 mg/kg/hr for >48 hours Exceeds the mitochondrial capacity to process propofol metabolites; accumulation of toxic phenol metabolites High catecholamine state (severe illness, Catecholamines switch cellular metabolism toward fat oxidation → cells become MORE dependent on β-oxidation catecholamine infusions) pathways that propofol specifically impairs High-fat/low-carbohydrate intake Further increases reliance on fat oxidation; propofol vehicle (Intralipid — 1.1 kcal/mL) itself adds significant lipid load Mitochondrial disease Pre-existing mitochondrial impairment → much lower propofol dose required to tip into PRIS Paediatric patients Originally described in children; PRIS was first recognised as a distinct entity in paediatric critical care after reports of unexplained cardiac arrest in children on propofol sedation Concomitant steroids + catecholamines Steroids impair mitochondrial function; catecholamines increase fat metabolism; combination with propofol = perfect storm

Feature Clinical/Laboratory Finding Metabolic lactic Unexplained metabolic acidosis (↑ lactate >4 mmol/L, ↓ pH); FIRST and most consistent early feature; check lactate every 4–6 hours in patients on acidosis propofol >4 mg/kg/hr Rhabdomyolysis Rising CK (often dramatic >10,000 IU/L); myoglobinuria (dark brown urine); muscle tenderness Cardiac New right bundle branch block (RBBB) → progressing to complete heart block → cardiovascular collapse; new-onset bradycardia refractory to dysfunction atropine; cardiomegaly on CXR; LV failure on echo Lipaemia Hyperlipidaemia (lipid load from Intralipid vehicle); visible lipaemia in plasma samples AKI Rising creatinine from rhabdomyolysis-induced renal tubular necrosis; myoglobin casts in tubules

Phaeochromocytomas arise from chromaffin cells of the adrenal medulla (90%) or extra-adrenal sympathetic ganglia (10% — paragangliomas); secrete catecholamines (adrenaline, noradrenaline, dopamine) constitutively or in paroxysms Noradrenaline-secreting tumours → predominantly hypertension from α₁ vasoconstriction; adrenaline-secreting → mixed hypertension and tachycardia + β₂ vasodilation (can cause paradoxical hypotension); dopamine-secreting → hypertension from indirect catecholamine release

Rule of 10: 10% bilateral; 10% extra-adrenal; 10% malignant; 10% familial (MEN2A, MEN2B, VHL, SDH mutations); 10% in children; 10% discovered incidentally Chronic catecholamine excess → hypertrophied cardiovascular system with REDUCED intravascular volume (chronic vasoconstriction → pressure natriuresis + relative hypovolaemia); catecholamine cardiomyopathy (catecholamine-induced cardiac toxicity); increased sensitivity to vasodilators after tumour removal

Monitoring (all before induction) Arterial line (radial artery — beat-to-beat BP monitoring throughout); large-bore IV access (2× 14G); central venous catheter (CVP monitoring, vasopressor access); TOE or PA catheter for high-risk patients (EF <40%, bilateral tumour); temperature monitoring

Induction

Avoid laryngoscopy-induced catecholamine surge: lidocaine 1.5 mg/kg IV + fentanyl 2–3 mcg/kg + esmolol 0.5 mg/kg immediately before laryngoscopy; or high-dose opioid induction (remifentanil 2–3 mcg/kg)

Avoid: histamine-releasing drugs (morphine, atracurium — can trigger catecholamine release from the tumour or direct histamine release); succinylcholineinduced fasciculations raise intra-abdominal pressure potentially triggering tumour catecholamine release; droperidol (triggers catecholamine release from phaeochromocytoma in rare cases) Hypertensive Crisis During Tumour Manipulation Drug Dose Mechanism Phentolamine (non- 2–5 mg IV bolus; repeat Competitive α₁ + α₂ blockade → acute vasodilation; rapid onset (2 min); duration 10–15 min; drug of choice for selective reversible every 2–3 minutes until BP intraoperative hypertensive crisis management α-blocker) controlled Sodium nitroprusside 0.5–8 mcg/kg/min infusion Nitric oxide → direct arterial + venous vasodilation; immediate onset; very titratable; risk of cyanide toxicity at high (SNP) doses or prolonged use; most powerful vasodilator available; useful as infusion for sustained hypertension during tumour handling Nicardipine (IV 5–15 mg/hr infusion Dihydropyridine CCB → arterial vasodilation; does not cause reflex tachycardia to the same degree as SNP; calcium channel increasingly used as an alternative first-line infusion blocker) Magnesium sulphate 2 g IV bolus Inhibits catecholamine release from the tumour; inhibits catecholamine receptor sensitivity; useful adjunct

Assessment of Hyperthyroidism

Symptoms and clinical assessment: weight loss, heat intolerance, tremor, palpitations, anxiety, exophthalmos (Graves' disease), goitre size; assess for signs of heart failure (AF in 10–15%); thyroid bruit

Investigations: TFTs (TSH, free T4, free T3); ECG (AF, sinus tachycardia, LVH); CXR/CT neck (tracheal deviation, retrosternal extension, compression of trachea or oesophagus); flow-volume loop if significant tracheal compression; calcium and parathyroid function (risk of hypoparathyroidism post-thyroidectomy)

Airway assessment: palpate the goitre; assess tracheal position; review CT for tracheal diameter at narrowest point; if tracheal compression >50% → awake fiberoptic intubation; tracheal softening (tracheomalacia) may occur with long-standing retrosternal goitre → risk of tracheal collapse after ETT removal Achieving Euthyroid State Drug Mechanism Duration to Euthyroid Carbimazole or Inhibit thyroid peroxidase → ↓ T3 and T4 synthesis; PTU also inhibits peripheral 4–6 weeks for biochemical euthyroid state; continue up to Propylthiouracil conversion of T4→T3 day of surgery (PTU) Lugol's iodine Wolff-Chaikoff effect: excess iodide transiently inhibits thyroid hormone synthesis and Used for 10–14 days pre-operatively after anti-thyroid (KI 65%) release; also reduces vascularity of the thyroid gland (reduces intraoperative bleeding) drugs started; reduces vascularity and bleeding — an additional surgical benefit intraoperatively Beta-blockers Blocks peripheral sympathetic effects of excess T3/T4 (HR, tremor, anxiety); propranolol Immediate symptom control; continue until surgery; must (propranolol) also inhibits peripheral T4→T3 conversion (PTU-like effect) be used alongside anti-thyroid drugs (treats symptoms, not the thyroid excess)

Tracheal deviation and compression: large goitres may displace or compress the trachea; CT neck identifies the minimum tracheal diameter; if compressed <50% diameter → standard intubation with smaller ETT (6.0–6.5 mm); if >50% → consider awake fiberoptic intubation (maintains airway tone and spontaneous ventilation throughout — safest approach)

Reinforced (armoured) ETT: used for thyroid surgery to prevent ETT kinking in the extended neck position; allows surgeon access to the anterior neck without ETT obstruction

Recurrent Laryngeal Nerve (RLN) monitoring: the RLN runs in the tracheo-oesophageal groove adjacent to the thyroid; inadvertent RLN injury → immediate hoarseness or voice change (unilateral) → bilateral injury → aphonia + stridor + airway emergency; intraoperative neuromonitoring (IONM) uses a specialised ETT (NIM-EMG tube — electromyography electrodes embedded on the ETT surface monitor the RLN via laryngeal muscle EMG); if RLN is stimulated, the EMG records a response; loss of signal = nerve impaired; requires specific endotracheal tube and specific drug considerations

RLN monitoring — NIM ETT implications: NMBs MUST be allowed to wear off completely before placing the NIM tube (EMG response requires muscle activity — NMB prevents it); use the shortest-acting NMB (rocuronium 0.3–0.6 mg/kg initial dose + TOF monitoring); confirm T4 (all four twitches) on TOF before baseline NIM signal is obtained

Tracheomalacia: rare complication of long-standing retrosternal goitre; cartilaginous rings soften and lose support when external tumour pressure is suddenly removed → trachea collapses inward on extubation → immediate post-extubation stridor → may require re-intubation or even tracheostomy; anticipate by performing "cuff leak test" before extubation in long-standing large goitre

GCS and focal neurological deficit documentation (baseline for post-operative comparison); pupil assessment (unequal pupils → herniation → emergency);

NIHSS if focal deficits present

CT/MRI: tumour location and size; degree of midline shift; presence of hydrocephalus; oedema extent (vasogenic vs cytotoxic); vascular supply (hypervascularity → blood loss risk)

Medication review: dexamethasone (started by neurology — reduces vasogenic oedema; must continue perioperatively; stress dose not routinely needed for steroids already prescribed); anti-epileptic drugs (continue perioperatively); anticoagulation history Clinical Cushing's triad: hypertension + bradycardia + abnormal breathing = impending herniation → urgent CT + possible emergency ventricular drainage before anaesthesia

Goal Target How Achieved Maintain CPP CPP = MAP − ICP ≥ 60 mmHg Arterial line for continuous BP; vasopressors (phenylephrine) for MAP; ICP reduction strategies Reduce ICP / brain ICP <20 mmHg; slack brain at craniotomy Mannitol; moderate hyperventilation; head-up 15–30°; TIVA; steroids pre-operatively; relaxation CSF drainage Control CMRO₂ Reduce metabolic demand; prevent secondary injury Adequate depth; normothermia; normoglycaemia (6–10 mmol/L); normocapnia Rapid, smooth Awake, oriented, able to follow commands within 15– TIVA with propofol + remifentanil; short-acting agents; no residual NMB emergence 20 min of surgery end (sugammadex); avoid hypothermia (delays emergence) Avoid secondary PaO₂ >80 mmHg; PaCO₂ 35–40 mmHg; MAP ≥65 Mandatory monitoring; active warming; arterial blood gas monitoring every 60 min injury factors mmHg; Temperature 36–37°C

Agent Choice

TIVA preferred for craniotomy: propofol reduces CMRO₂ and ICP, maintains cerebral autoregulation; remifentanil provides precise analgesic control and allows rapid emergence (context-sensitive half-time 3 min); no effect on ETCO₂ monitoring interpretation

Volatile agents: acceptable at ≤0.5 MAC (low doses preserve cerebral autoregulation); above 0.5 MAC → cerebral vasodilation → ↑ CBV → ↑ ICP; desflurane causes cerebral vasodilation and sympathetic activation → avoid; sevoflurane preferred if volatile is used

N₂O: avoid in craniotomy — increases CMRO₂ and CBF; expands any pneumocephalus; may worsen PONV Avoid ketamine (↑ CMRO₂ and ICP; cerebral vasodilation) Brain Relaxation ("Slack Brain") Strategies Strategy Drug/Intervention Mechanism Osmotherapy Mannitol 0.5–1 g/kg IV over 15–20 min; 7.5% hypertonic Osmotic gradient draws water from brain interstitium into plasma → reduces cerebral water saline 3–5 mL/kg IV alternatively → reduces ICP; effect begins at 15 min, peaks at 30–60 min, lasts 3–4 hours; monitor serum osmolality (<320 mOsm/L); avoid repeat doses if hypernatraemic Head 15–30° head-up; neutral neck Improves jugular venous drainage → reduces cerebral venous volume → reduces ICP position Controlled Normocapnia (PaCO₂ 35–40 mmHg) for routine Hypocapnia → cerebral vasoconstriction → ↓ CBV → ↓ ICP; effect immediate but tolerance ventilation maintenance; moderate hyperventilation (PaCO₂ 30–35 develops within 4–6 hours; ischaemia risk with prolonged hyperventilation; use ONLY as mmHg) if brain tight at opening — TEMPORARY only bridge to surgical decompression Position at Local anaesthetic at pin sites + remifentanil bolus before Pin insertion through the scalp into the outer table of the skull is extremely painful; Mayfield pins pin insertion inadequate analgesia → massive sympathetic surge → hypertension + ↑ ICP (skull clamp) Surgical CSF Surgeon opens cisterna magna or places intraventricular CSF removal directly reduces ICP and brain volume → provides surgical access without drainage drain excessive brain retraction

Smooth emergence critical: coughing, straining, bucking on ETT during emergence → ↑ ICP → brain herniation through the craniotomy defect → catastrophic; ensure adequate analgesic level before emergence; use remifentanil to bridge until patient can follow commands without response to ETT; lidocaine 1.5 mg/kg IV 3–5 minutes before extubation reduces cough response to ETT

Immediate neurological assessment: is there a new deficit? Is the patient at the same GCS as pre-operatively? Can they squeeze both hands, follow commands bilaterally, speak? Any new deficits → urgent CT to exclude haematoma/oedema/ischaemia; haematoma within hours of craniotomy → reexploration

When NOT to extubate: prolonged surgery (>8 hours); significant brain swelling requiring dural closure under tension; haemodynamic instability; GCS baseline was low pre-operatively; posterior fossa surgery (risk of respiratory centre compression); brainstem surgery; plan for ICU intubated

PONV prevention mandatory: even mild vomiting → ↑ ICP → dangerous; full multimodal PONV prophylaxis (ondansetron + dexamethasone + droperidol); TIVA reduces PONV substantially vs volatile

Parameter Neonate/Infant Adult Clinical Implication Heart rate CO = HR × SV; SV is FIXED in neonates (immature Can increase SV Bradycardia = cardiac arrest in neonates; ALWAYS give atropine 20 mcg/kg dependency Frank-Starling mechanism — stiff, non-compliant substantially (min 100 mcg) before laryngoscopy; normal neonatal HR 120–160 bpm; HR myocardium cannot increase SV significantly); CO (preload reserve, <100 = emergency is entirely rate-dependent Starling mechanism) Transitional Foetal shunts (PDA, foramen ovale) may reopen in No foetal shunts Maintain SpO₂ ≥94–98%; avoid hypoxia, acidosis, hypothermia — all trigger circulation hypoxia, acidosis, hypothermia, or surgical stress (all closed) ductal reopening; give O₂ carefully in prematurity (retinopathy risk with high → right-to-left shunting → cyanosis; particularly in SpO₂) first weeks of life Circulating 80–90 mL/kg (neonates); 70–80 mL/kg (infants); 65–70 mL/kg Meticulous blood loss monitoring (weigh swabs in grams — 1 g = 1 mL); blood even 5 mL blood loss can = 5–10% of total blood transfusion triggers lower (Hb <80 g/L in most neonates, <70 g/L in older volume volume in a 1 kg premature neonate children); use small (10 mL) syringes for fluid management; calculate maximum allowable blood loss preoperatively Glycogen Limited glycogen reserves → rapid hypoglycaemia Adequate hepatic Dextrose-containing maintenance IV fluids mandatory during nil-by-mouth stores with fasting; premature neonates particularly glycogen for periods in neonates and infants ≤6 months; blood glucose hourly monitoring vulnerable; high glucose consumption rate (6 moderate fasting intraoperatively; target 4–8 mmol/L mg/kg/min)

Parameter Neonate/Infant Clinical Implication O₂ 6–8 mL/kg/min (vs 3 mL/kg/min in adults) — very high Rapid desaturation during apnoea (SpO₂ falls to critical in 60–90 seconds in neonates); consumption metabolic rate preoxygenate adequately; work fast during airway management FRC relative FRC only 3× TV (vs 7× TV in adults); closing capacity may Rapid onset of hypoxia; needs higher FiO₂ baseline; PEEP 3–5 cmH₂O even during routine to TV exceed FRC → small airway closure at FRC in infants → spontaneous ventilation under anaesthesia shunting even during spontaneous ventilation Chest wall Highly compliant; ribcage collapses inward during During respiratory distress: see "see-saw" breathing (chest wall sinks in, abdomen compliance respiratory distress rather than stabilising to generate protrudes) — an emergency sign requiring immediate intervention negative pressure (paradoxical breathing) Apnoea risk Post-conceptional age <60 weeks → immature respiratory All ex-premature infants under 60 weeks PCA must have apnoea monitoring for minimum in ex- centre → risk of postoperative apnoea for up to 12–24 12 hours post-GA; regional anaesthesia preferred to GA where possible in this group; premature hours after GA caffeine 10 mg/kg IV preoperatively reduces post-op apnoea incidence infants

Neonates and infants have: very large body surface area:mass ratio (4–5× adult); thin skin with minimal subcutaneous fat; no shivering mechanism in neonates (brown adipose tissue thermogenesis — "non-shivering thermogenesis" — instead, which consumes large amounts of O₂ and generates heat from BAT oxidation); immature hypothalamic thermoregulation

Under GA: all anaesthetic agents abolish behavioural thermoregulation and impair the autonomic thermoregulatory vasoconstriction threshold → body temperature falls rapidly to ambient; at 20°C theatre temperature, a neonate can become hypothermic in minutes

Prevention mandatory: theatre temperature 26–28°C for neonates (adults find this uncomfortably hot); warm all IV fluids and blood; forced-air warming blankets; warming mattress; warm cotton blankets; humidified gases; minimise exposed skin area; temperature probe mandatory throughout

Consequences of hypothermia: impaired drug metabolism → prolonged anaesthesia; coagulopathy; cardiac arrhythmia; impaired immune function → infection; hypoglycaemia (thermogenesis depletes glucose); prolonged post-op recovery

Parameter Neonate/Infant vs Adult Clinical Implication Volume of ↑ Total body water (neonates 80% body weight vs 60% adults); drugs distributing to TBW Higher weight-based dose of NMBs, antibiotics; neonates distribution have larger Vd → need higher mg/kg doses for equivalent plasma concentration; e.g., need larger mg/kg loading doses of many drugs water-soluble drugs (NMBs, aminoglycosides) Hepatic CYP450 enzyme systems immature at birth; CYP2C9, CYP2D6, CYP3A4 all below adult Prolonged half-lives of hepatically metabolised drugs metabolism activity levels; reached adult activity at 6 months–3 years depending on the isoenzyme (morphine, propofol, midazolam) in neonates; start low and titrate carefully; risk of accumulation Renal GFR 25–30% of adult value at birth; reaches adult GFR per body surface area by 18–24 Renally cleared drugs (vancomycin, aminoglycosides, excretion months; tubular secretion also immature NMBs) have prolonged half-lives; reduce dose frequency or extend intervals; monitor drug levels Protein Lower albumin and α₁-acid glycoprotein in neonates → more free (active) drug for given Enhanced effects of protein-bound drugs (local anaesthetics binding total plasma concentration — higher LAST risk; propofol; thiopentone); reduce doses accordingly MAC MAC is highest in neonates (1–6 months), falls with increasing age; term neonates: Neonates require HIGHER volatile concentrations for (volatile sevoflurane MAC ~3.3% (vs 2.0% in adults); falls to adult value by age 10–12 years equivalent depth of anaesthesia than children or adults — agents) counter-intuitive but well-established

Glucose: neonates have limited glycogen stores and high glucose utilisation; hypoglycaemia (blood glucose <2.6 mmol/L) causes seizures and brain injury; maintain dextrose infusion throughout GA; check glucose hourly; prolonged preoperative fasting without IV dextrose is contraindicated

Calcium: neonates (especially premature) have immature calcium regulation; hypocalcaemia (ionised Ca²⁺ <1.1 mmol/L) causes cardiac depression, apnoea, and seizures; check ionised calcium before major neonatal surgery; give calcium gluconate 10% 0.5 mL/kg IV for hypocalcaemia

Acid-base: neonatal kidneys have limited bicarbonate reabsorption capacity → any acid load causes metabolic acidosis more readily than adults; standard base excess target slightly more negative acceptable in neonates (−4 to +2 mEq/L)

Drug toxicity — succinylcholine and atropine: succinylcholine causes more pronounced bradycardia in children (high vagal tone); ALWAYS give atropine 20 mcg/kg before succinylcholine in children; succinylcholine-induced hyperkalaemia and cardiac arrest from undiagnosed muscular dystrophy (Duchenne muscular dystrophy — DMD) in boys → succinylcholine increasingly avoided in paediatric elective cases

Category Definition DDI Target Anaesthetic Priority 1 — Immediate threat to life of mother or fetus; examples: severe fetal <30 minutes Fastest available safe technique; epidural top-up Immediate bradycardia, cord prolapse, placental abruption with acute fetal compromise, (ideally <15 if in situ; rapid-sequence spinal if no epidural; threat to life uterine rupture, maternal haemodynamic collapse minutes for cord RSI-GA if spinal not feasible prolapse) 2 — Not immediately life-threatening but requires urgent delivery; examples: non- <75 minutes Regional anaesthesia preferred; time allows Maternal or reassuring CTG, failure to progress with maternal compromise careful spinal or epidural top-up fetal compromise 3 — No Early delivery needed but no current compromise; examples: failed induction, Within a scheduled Standard elective spinal or epidural anaesthesia; compromise prolonged latent phase time frame no time pressure 4 — Elective Elective CS at a time convenient to patient and team Elective scheduled Full preoperative assessment; standard spinal anaesthesia

Fastest Route to Surgical Anaesthesia from a Functioning Labour Epidural Check epidural function first (10–15 seconds): ask patient if she can still feel the block; test cold/warm sensation; if dense bilateral block present → proceed to top-up; if patchy or one-sided → may need rapid-sequence spinal instead

Top-up drug: 2% lidocaine with adrenaline 1:200,000 + optional fentanyl 50–100 mcg — fastest-onset epidural solution for surgical anaesthesia; inject 15– 20 mL in 5 mL increments (2–3 mL test dose first to re-confirm not intravascular); onset of T4 sensory block in 5–10 minutes (faster than 0.5% bupivacaine which takes 15–20 minutes)

Alternative: 0.5% levobupivacaine 15–20 mL (slower onset than 2% lidocaine; onset 12–15 min) or 3% chloroprocaine (if available — fastest epidural agent, onset 3–5 minutes; suitable for true Category 1)

Simultaneous actions while topping up: left lateral tilt; IV fluid co-load 500 mL crystalloid; phenylephrine infusion running (prevent spinal hypotension); supplemental O₂ by face mask; fetal monitoring (CTG off for delivery); surgical team ready; neonatologist present

Assess level: confirm T4 level by cold/pinprick test before incision; if inadequate despite full top-up dose → proceed to RSI-GA (do not delay surgery waiting for inadequate epidural)

When appropriate: no epidural in situ; patient haemodynamically stable; no significant coagulopathy; uncomplicated expected airway; DDI is <30 minutes (achievable with spinal)

Drug choice: hyperbaric bupivacaine 0.5% 2 mL + fentanyl 15–25 mcg + morphine 100–150 mcg (intrathecal morphine provides 12–24 hours post-op analgesia — significant advantage over GA for post-CS pain); onset of surgical T4 level within 5–8 minutes

Simultaneous preparation: position patient in lateral decubitus or sitting; one hand on the patient, one drawing up drugs — no time for separate preparation; assistant preparing vasopressor; left lateral tilt immediately after injection; do not wait for full block to assess — check block level at 3 minutes (usually adequate T4 by then)

Failed spinal: if block is inadequate after 5 minutes → RSI-GA; do NOT give a second spinal (risk of total spinal from accumulated doses)

Indications for RSI-GA over Regional Patient refusal of regional; coagulopathy (HELLP, DIC, thrombocytopenia); severe haemodynamic instability (cannot tolerate sympathectomy of spinal); local anaesthetic allergy (rare); severe urgency where time for spinal is unavailable; failed spinal or epidural top-up; major placenta praevia with active major haemorrhage Modified RSI Protocol for Obstetrics Step Detail Obstetric-Specific Modification Aspiration Sodium citrate 30 mL oral + ranitidine 50 mg IV + Mandatory pre-GA in pregnancy >16 weeks; reduce gastric acid pH and volume prophylaxis metoclopramide 10 mg IV Preoxygenation 100% O₂ × 3–5 minutes (head-up 20°); ETO₂ >90% Reduced safe apnoea time in pregnancy (↓FRC + ↑O₂ consumption); mandatory full preoxygenation; HFNO 60 L/min during apnoea Induction agent Thiopentone 4–5 mg/kg IV (classic; proven fetal safety) Reduce dose 20% in pre-eclampsia (enhanced CNS sensitivity); MAC reduced 25–40% in OR propofol 2–2.5 mg/kg pregnancy NMB Succinylcholine 1.5 mg/kg IV (classic RSI); OR Both acceptable; succinylcholine provides shortest duration (10 min) if airway fails; rocuronium 1.2 mg/kg + sugammadex 16 mg/kg rocuronium provides CICO rescue option available Cricoid Applied at induction; release if impairs laryngoscopy Higher risk of regurgitation in pregnancy; cricoid pressure standard; video laryngoscope pressure (DAS 2018) first-line Intubation Confirm with ETCO₂ × 6 breaths; 6.5–7.0 mm ETT Higher failed intubation rate in obstetrics (1:224 vs 1:1800 general surgical); video (oedematous obstetric airway → smaller tube) laryngoscope as first-line for all obstetric GA; have DAS failed intubation plan ready Maintenance Volatile agent (sevoflurane 1.0–1.5 MAC) + opioid after Awareness risk until delivery (deliberately reduced anaesthetic to minimise fetal exposure); delivery; N₂O 50% optional give fentanyl after cord clamped; must increase anaesthetic depth after delivery

Condition Definition Hypertension SBP ≥140 mmHg OR DBP ≥90 mmHg on at least two occasions ≥4 hours apart after 20 weeks gestation in pregnancy

Pre- New hypertension after 20 weeks PLUS one or more of: proteinuria (≥300 mg/24h or spot PCR ≥30 mg/mmol); thrombocytopenia (<150,000/μL); renal eclampsia insufficiency (creatinine >88 μmol/L); impaired liver function (↑ LFTs); pulmonary oedema; new-onset headache unresponsive to medication; visual disturbances Severe pre- Pre-eclampsia with severe hypertension (SBP ≥160 mmHg or DBP ≥110 mmHg on two occasions) OR end-organ dysfunction (neurological symptoms, eclampsia HELLP syndrome, pulmonary oedema, severe renal impairment) Eclampsia New-onset grand-mal seizures in a patient with pre-eclampsia (or other hypertensive disorder of pregnancy); seizures in the context of hypertension and proteinuria HELLP Haemolysis (LDH >600 IU/L, abnormal blood film) + Elevated Liver enzymes (AST/ALT ≥2× ULN) + Low Platelets (<100,000/μL) — a severe variant of syndrome pre-eclampsia

Abnormal placentation (failure of trophoblast invasion of spiral arteries) → inadequate placental blood flow → placental ischaemia → release of anti-angiogenic factors (sFlt-1 — soluble FMS-like tyrosine kinase 1 — antagonises VEGF and PlGF) → systemic maternal endothelial dysfunction → widespread vasospasm (hypertension) + endothelial permeability ↑ (oedema, proteinuria) + platelet activation (thrombocytopenia, DIC) + organ ischaemia (renal, hepatic, cerebral)

Haemodynamics: paradox — pre-eclamptic patients have HIGH BP (vasospasm) but LOW intravascular volume (protein leaks out of vessels into interstitial space; venous tone ↑); vasodilators reduce BP but may worsen the already-contracted intravascular volume; fluid management is a delicate balance

Cerebral: vasospasm → headache, scotomata, altered consciousness; loss of cerebral autoregulation at high BP → breakthrough cerebral oedema → eclamptic seizures → cerebral haemorrhage (leading cause of maternal death in pre-eclampsia)

Indication: severe pre-eclampsia → MgSO₄ for seizure prophylaxis (MAGPIE trial: MgSO₄ reduced eclampsia rate by 58% vs placebo in severe preeclampsia; NNT = 63); ACTIVE eclampsia → MgSO₄ is first-line treatment (superior to diazepam or phenytoin for controlling eclamptic seizures —

Collaborative Eclampsia Trial)

Dosing: loading dose 4 g IV over 5–15 minutes; maintenance 1–2 g/hr IV infusion; continue for 24 hours after delivery (or 24 hours after last fit)

Toxicity monitoring — the clinical signs of hypermagnesaemia:

Therapeutic range: 2–3.5 mmol/L (serum Mg)

Loss of patellar reflexes: first sign of toxicity — Mg 3.5–5 mmol/L; CHECK PATELLAR REFLEXES HOURLY on MgSO₄ infusion

Respiratory depression: Mg 5–6.5 mmol/L; monitor RR ≥12 breaths/min

Cardiac arrest: Mg >7.5 mmol/L

Also maintain: UO ≥25 mL/hr (Mg is renally cleared; renal failure → rapid Mg accumulation) Antidote for MgSO₄ toxicity: calcium gluconate 10% 10 mL IV over 10 minutes (competes with Mg at the receptor; reverses respiratory and cardiac effects); have at bedside of every patient on MgSO₄ infusion

Regional preferred: spinal anaesthesia is SAFE in severe pre-eclampsia (the historical concern about catastrophic hypotension is not supported by evidence — Dyer RA et al.: pre-eclamptic patients have LESS hypotension after spinal than healthy parturients, because their high baseline SVR provides a buffer against the sympathectomy-induced fall in SVR); epidural also safe and allows gradual titration

Platelet threshold: neuraxial anaesthesia safe if platelets ≥70,000/μL (most institutional guidelines 70–80,000); review trend (rapidly falling counts are more concerning than a stable 80,000); check recent result (<6 hours in rapidly deteriorating HELLP)

If GA required: oedematous obstetric airway — use 6.5 mm ETT; video laryngoscope first-line; attenuate laryngoscopy response (alfentanil 10 mcg/kg or remifentanil 1 mcg/kg or labetalol 10 mg IV 1 minute before laryngoscopy — pre-eclamptic patients have exaggerated hypertensive response to laryngoscopy → stroke risk); esmolol NOT preferred in CS (crosses placenta → neonatal bradycardia)

Postoperative: HDU monitoring minimum 24 hours; continue MgSO₄ 24 hours post-delivery; continued antihypertensive therapy; watch for late eclampsia (can occur up to 48 hours post-delivery — the most dangerous time is actually the first 24 hours postpartum)

Traditional care pathways allowed or amplified the surgical stress response: prolonged fasting → catabolism, insulin resistance; hypothermia → impaired coagulation and immune function; large-volume IV fluids → bowel oedema and anastomotic leak; opioid analgesia → ileus, nausea, sedation, respiratory depression; immobility → DVT, deconditioning, pneumonia

ERAS systematically addresses each factor: carbohydrate loading reduces pre-operative insulin resistance by 50%; targeted fluid therapy prevents both hypovolaemia and fluid overload; regional analgesia eliminates systemic opioids; early feeding and mobilisation restore gut motility and physical function; the combined effect reduces the magnitude of the catabolic stress response from major surgery, allowing early functional recovery Kehlet's original concept (1997): Henrik Kehlet (Lancet 1997) demonstrated that major colonic surgery could be performed with a 2-day hospital stay using multimodal opioid-sparing analgesia, early oral nutrition, and early mobilisation — the founding evidence for ERAS

Phase ERAS Component Evidence/Mechanism Pre- Patient education and counselling Patients who understand the ERAS plan and their role in recovery comply better with early feeding and mobilisation; operative anxiety reduction → lower analgesic requirements Preoperative carbohydrate loading Reduces insulin resistance by 50%; reduces preoperative thirst/hunger/anxiety; improves postoperative muscle (200–400 mL 12.5% carbohydrate function; supported by Cochrane review — reduces hospital stay by 0.5–1 day drink, 2–3 hours before surgery) Clear fluid fasting up to 2 hours Evidence-based replacement for "NPO from midnight"; no increased aspiration risk; reduces preoperative (solid food up to 6 hours) discomfort; reduces catabolism from prolonged fasting Bowel preparation (OMIT for most Traditional mechanical bowel prep dehydrates patients and worsens electrolyte imbalance without reducing colorectal surgery) anastomotic leak rates (Cochrane 2011) — omitted in most ERAS colorectal protocols Anaemia assessment and Preoperative anaemia is a major risk factor for transfusion and complications; correcting Hb ≥100 g/L reduces treatment (if Hb <100 g/L → iron transfusion requirement and length of stay supplementation or erythropoietin if time allows) Intra- TIVA or volatile anaesthesia with PONV causes delayed oral intake and prolonged bed rest — specifically addressed in ERAS; TIVA reduces PONV operative multimodal PONV prophylaxis (min. 2 25–30%; dexamethasone also reduces fatigue and pain agents: ondansetron + dexamethasone) Avoidance of long-acting opioids; Intraoperative opioids contribute to postoperative ileus; remifentanil provides precise intraoperative analgesia with remifentanil intraoperative immediate offset; no contribution to postoperative ileus when stopped at end of surgery; regular NSAIDs and paracetamol for post-op baseline analgesia

Goal-directed fluid therapy (GDT) OPTIMISE trial: ODM-GDT reduced postoperative complications by 20%; avoids both hypovolaemia (anastomotic — ODM or FloTrac guided ischaemia) and hypervolaemia (bowel oedema, anastomotic leak, cardiorespiratory complications); targeted fluid to optimise SV; vasopressors for vasodilatory hypotension rather than volume Temperature maintenance Hypothermia increases wound infection, coagulopathy, cardiac events; active warming — forced-air blanket, warm (normothermia ≥36.5°C) fluids, warm gases, theatre temperature 21–22°C; NICE recommends core temp >36°C throughout surgery

Minimally invasive surgery Laparoscopic colorectal surgery: reduced pain, faster bowel recovery, shorter hospital stay vs open; smaller (laparoscopic vs open) incisions → less incisional pain → less splinting → better respiratory function; does not eliminate the need for ERAS (laparoscopic + ERAS = best outcomes) Thoracic epidural or paravertebral Thoracic epidural analgesia for open colorectal: reduces opioid requirements, allows early mobilisation, reduces block for open surgery; TAP block ileus, reduces PPCs; for laparoscopic: bilateral TAP blocks + NSAIDs + paracetamol replaces epidural for laparoscopic Post- Early oral nutrition (day 0 — same Traditionally, patients were "nil by mouth until bowel sounds return" — no evidence base for this; early oral nutrition operative day as surgery) maintains gut mucosal integrity, reduces infection risk, reduces ileus by stimulating gut motility via the gastrocolic reflex; NGT removal before end of surgery; clear fluids within 2–4 hours of operation; diet as tolerated from day 1 Early mobilisation (out of bed day Immobility → DVT, deconditioning, pneumonia, prolonged ileus; early ambulation reverses these; supervised 1, with target of 2 hours out of bed physiotherapy from day 1; functional milestones set daily increasing daily) Opioid-sparing analgesia — Opioids → ileus + respiratory depression + PONV; multimodal opioid-sparing analgesia maintains adequate pain NSAIDs + paracetamol + regional ± control while dramatically reducing opioid-related complications low-dose oral opioid PRN Urinary catheter removal day 1 (if Urinary catheter delays mobilisation and increases UTI risk; removed as soon as epidural is stopped or day 1 if no no epidural) epidural IV fluid discontinuation / removal IV fluids → sedentary behaviour + fluid overload; oral fluids maintain hydration without restricting mobilisation of IV cannula by day 1–2

Varadhan KK et al. (BJA 2010, meta-analysis): ERAS for colorectal surgery reduces LOS by 2.5 days (from 7.5 to 5.0 days average) and reduces complication rate by 30% vs traditional care; no increase in readmission rates — demonstrating that early discharge is safe

Gustafsson UO et al. (Arch Surg 2011): higher compliance with individual ERAS elements correlates directly with better outcomes — the benefit is additive; implementing only some elements produces partial benefit; full protocol compliance produces maximal benefit

Cost savings: reduced LOS → significant cost savings per patient; ERAS implementation has positive return on investment even accounting for the cost of multidisciplinary programme establishment

ERAS Society: publishes specialty-specific guidelines for colorectal, gynaecological, liver, bariatric, thoracic, and urological surgery; all follow the same core principles adapted for specific surgical and physiological contexts

The nociceptive cascade has multiple targets: pain from surgical tissue injury involves: peripheral sensitisation (PGs, bradykinin, substance P at the wound — target: NSAIDs, local anaesthetics); ascending spinal transmission (dorsal horn — target: opioids, α₂ agonists, ketamine); central processing (thalamocortical — target: paracetamol, opioids, gabapentinoids); descending modulation (from brainstem — target: SNRIs, α₂ agonists); no single drug blocks ALL of these simultaneously

Synergy: paracetamol + NSAID produces significantly better analgesia than either alone at the same individual doses; opioid + NSAID shows opioid-sparing effect of 30–40% (less opioid needed for equivalent analgesia); combination allows adequate pain control with individually lower (and safer) doses of each drug

Opioid-sparing: reducing systemic opioid consumption reduces: PONV, sedation, respiratory depression, ileus, urinary retention, cognitive impairment, and opioid-induced hyperalgesia — all of which are major barriers to early recovery in ERAS

Level Drug / Technique Mechanism Dose/Route Key Evidence Foundation Paracetamol Inhibits prostaglandin synthesis centrally 1 g IV/oral every 6 hours; Reduces opioid consumption 20% vs placebo; (all (acetaminophen) (COX-3 in CNS); also modulates descending reduce dose in liver well tolerated; no platelet, renal, or GI effects; patients) serotonergic inhibitory pathways; DOES NOT disease and <50 kg body should be prescribed regularly for ALL inhibit peripheral COX (no anti-inflammatory weight postoperative patients unless contraindicated effect in tissues) Foundation NSAIDs (ibuprofen, COX-1 and COX-2 inhibition → ↓ Ibuprofen 400–600 mg Opioid-sparing 25–35% vs placebo; celecoxib (all diclofenac, ketorolac, prostaglandin synthesis BOTH peripherally TID oral; ketorolac 15–30 equivalent to non-selective NSAIDs for pain; patients) celecoxib) (reduces sensitisation of nociceptors at mg IV every 6 hours avoid in renal impairment (↓GFR from PG wound) AND centrally (reduces PG-mediated (max 5 days); celecoxib inhibition in kidney); avoid in active peptic ulcer; central sensitisation in dorsal horn) 200–400 mg oral avoid in coagulopathy; avoid in cardiovascular (selective COX-2 — high-risk patients (long-term COX-2 selective) better GI safety) Second Gabapentinoids Bind α₂δ subunit of voltage-gated Ca²⁺ Gabapentin 300–600 mg Reduces acute postoperative pain scores by 20– level (gabapentin, channels on presynaptic terminals in dorsal oral preoperatively + 300 30%; reduces opioid consumption 30–40%; pregabalin) horn → ↓ Ca²⁺ influx → ↓ release of mg TID for 2–3 days prevents chronic post-surgical pain development glutamate, substance P, and CGRP → post-op; pregabalin 75– (prevention of central sensitisation); sedation reduces central sensitisation and neuropathic 150 mg oral BD and dizziness at higher doses — dose reduction pain component; also supraspinal anxiolytic needed in elderly and renal impairment effects Second Ketamine (sub- NMDA antagonist → blocks central 0.1–0.5 mg/kg IV loading Cochrane meta-analysis: intraoperative ketamine level anaesthetic) sensitisation ("wind-up") at the spinal cord then 0.1–0.2 mg/kg/hr reduces 24-hour morphine consumption by level; specific efficacy against opioid- infusion for 48 hours; or approximately 8 mg (30%) and reduces resistant and neuropathic pain components; 0.5 mg/kg IV at wound postoperative pain scores at rest and on ALSO reduces opioid tolerance development closure movement; particularly beneficial for major (prevents opioid-induced hyperalgesia) surgery (thoracotomy, major orthopedic) Third level Opioids (morphine, Mu-opioid receptor agonism in brain and Morphine: 0.1 mg/kg IV; Should NOT be used as the sole agent; ERAS (for oxycodone, tramadol, spinal cord; reduces pain perception; PCA 1 mg bolus with 5- philosophy: regular paracetamol + NSAID ± moderate- codeine) sedation; respiratory depression; min lockout; oxycodone gabapentinoid as baseline; opioids as PRN severe constipation and ileus (GI opioid receptors); 5–10 mg oral 4–6 hourly; rescue for breakthrough pain only, not as the pain) tolerance with prolonged use; physical and tramadol 50–100 mg TID primary analgesic psychological dependence risk (weak opioid + SNRI effect) Regional Epidural, nerve blocks Local anaesthetic blockade of afferent nerve Site-specific techniques; Thoracic epidural analgesia = gold standard for techniques (TAP, paravertebral, conduction → complete interruption of standard blocks major abdominal surgery; reduces systemic (opioid- femoral, popliteal, etc.), nociceptive transmission from the surgical described in separate opioid requirement to near-zero; best PPCs free wound infiltration with site; the most powerful analgesic intervention questions reduction; PROSPECT guidelines provide analgesia) bupivacaine/ropivacaine available procedure-specific recommendation for which block is evidence-based for each operation

Principle and Programming

Concept: patient activates a syringe pump (by pressing a button) to self-administer a pre-set bolus dose of IV opioid; the system prevents overdose through lockout intervals; the patient "titrates" to their own analgesic requirement, accounting for interindividual pharmacokinetic variability that makes fixed-dose nurseadministered regimens suboptimal Standard Adult Parameter Setting Rationale (Morphine) Bolus dose 1–2 mg morphine Sufficient for analgesic effect in most adults; enough to "feel" the bolus working Lockout 5 minutes Allows peak effect of each bolus before next dose can be activated; prevents double-stacking; morphine Tmax ~5–10 min after IV interval dose Background NOT routinely Background infusion removes the self-limiting safety feature — if a patient falls asleep (indicating sufficient analgesia/sedation), infusion recommended for they stop pressing the button; background infusion continues regardless → respiratory depression while sedated; ONLY use opioid-naive adults background infusion in opioid-tolerant patients with careful monitoring 4-hour limit 20–30 mg/4 hours Prevents very high total opioid consumption; triggers review if frequently hit

Safety Features

Lockout interval (primary safety): prevents re-dosing within the lockout period even if button pressed repeatedly 4-hour limit: nurse reviews if maximum 4-hour dose is reached; may indicate inadequate analgesia requiring reassessment of the regimen

Anti-siphon valve: prevents gravity-assisted free-flow of opioid from the syringe if the pump is placed below patient level

Tamper-evident syringe: prevents drug diversion

One-way valve on the dedicated IV line: prevents bolus of opioid being pushed backward into a concurrent running IV line (avoiding inadvertent bolusing) Monitoring Requirements for PCA Continuous SpO₂ monitoring throughout PCA use (standard of care — most guidelines); hourly sedation score; hourly RR; 4-hourly pain score; only the patient must press the PCA button — family or staff pressing the button on behalf of the patient ("PCA by proxy") bypasses the self-limiting safety feature and causes respiratory arrest

Anatomy: the lateral abdominal wall has three muscle layers: external oblique (most superficial), internal oblique (middle), and transversus abdominis (deepest, just above the peritoneum); the intercostal nerves T10–L1 (supplying the anterior abdominal wall from the umbilicus to the groin) travel within the fascial plane between the internal oblique and transversus abdominis — the TAP (Transversus Abdominis Plane); injection of LA into this plane bathes the nerve trunks as they fan out across the abdominal wall Approaches:

Lateral TAP (midaxillary approach): probe in the mid-axillary line between the iliac crest and costal margin; image the three muscle layers; inject 20 mL 0.25% bupivacaine (or 0.2% ropivacaine) into the TAP layer (between IO and TA); covers T10–L1 (lower abdomen and groin); best for lower abdominal surgery (appendicectomy, hernia repair, Pfannenstiel incision)

Subcostal TAP: probe obliquely from the xiphoid toward the ASIS; targets T6–T9 nerves in the TAP layer below the costal margin; covers upper abdomen; for laparoscopic port sites below the costal margin

Bilateral TAP: bilateral injection for midline laparotomies or bilateral laparoscopic port sites; 20 mL each side = 40 mL total (stay within LA maximum dose)

Sonoanatomy: high-frequency (12–15 MHz) linear probe; identify three muscle layers (EO = thin superficial layer; IO = middle, usually thickest; TA = deepest, most echogenic with deep fascia); the TAP lies between IO and TA; visualise the fascial plane as a bright line; inject LA to see hypoechoic spread in the plane (if "dome" appears in TA → too deep, peritoneum injected; if injection raises IO → too superficial)

QL Type Needle Target Coverage Indication QL1 (anterior) Anterior to the QL muscle, T10–L1 (lateral cutaneous branches); similar to lateral TAP Lower abdominal surgery, hip lateral to the transversalis surgery fascia QL2 Posterior to the QL muscle, T7–L1; better posterior cutaneous coverage than QL1; may provide Laparotomy, colectomy, renal (lateral/posterior) in the thoracolumbar fascia some visceral analgesia via epidural-like spread in the thoracolumbar surgery fascia QL3 Between the QL and psoas T5–L1; most extensive coverage; may reach the paravertebral space; Major abdominal surgery, (transmuscular) major muscles (anterior QL) provides both somatic and visceral analgesia components hysterectomy, colectomy as epidural alternative Intramuscular Within the belly of the QL Variable; less commonly used Selected cases QL muscle QL technique (lateral decubitus approach — most common): patient lateral decubitus; low-frequency curved array probe (3–5 MHz) placed on the posterior flank, lateral to the spine; identify the "shamrock sign" — the three muscles (psoas major, QL, erector spinae) meeting at the L4 transverse process like a three-leaf shamrock; place the needle tip at the correct fascial plane relative to the QL (depending on QL1, QL2, or QL3 target); inject 20–30 mL 0.375% ropivacaine or 0.25% bupivacaine; bilateral for midline surgery

Feature TAP Block QL Block Coverage T10–L1 (lateral TAP); T6–T9 (subcostal); cannot reliably T5–L1 (QL3); broader coverage including posterior abdominal wall and potentially level cover upper abdomen from a single approach visceral component via thoracolumbar fascia spread

Visceral None — purely somatic abdominal wall Some visceral analgesia from QL2/QL3 (thoracolumbar fascia spread toward analgesia paravertebral space)

Ultrasound Easier — superficial, familiar anatomy; suitable for trainees More difficult — requires identification of the shamrock sign; deeper target; more difficulty variable anatomy Duration 8–12 hours (plain bupivacaine); 24–36 hours with continuous Similar; some studies show longer duration with QL (15–16 hours) due to the fascial catheter or liposomal bupivacaine depot providing slower diffusion

Evidence Moderate — effective for port-site analgesia in laparoscopic Growing — QL3 provides superior analgesia to TAP for open colectomy in multiple for surgery; less effective than epidural for open laparotomy RCTs; increasingly used as epidural alternative when epidural is contraindicated laparotomy

PROSPECT recommendation 2022: bilateral TAP blocks (subcostal + lateral) recommended for laparoscopic colectomy (Grade A evidence); QL2 or QL3 block for open colectomy as alternative to epidural; single-shot TAP for Pfannenstiel CS incision analgesia (combined with intrathecal morphine)

Liposomal bupivacaine TAP: 266 mg liposomal bupivacaine (Exparel) diluted to 60 mL for bilateral TAP → provides 72-hour analgesia from a single injection; FDA-approved indication for TAP block; allows ambulatory colectomy/hysterectomy without epidural catheter management

Maximum LA dose: bilateral blocks consume twice the dose; for bilateral TAP or bilateral QL: use 0.2–0.25% ropivacaine (lower concentration × larger volume) to maintain total dose <3 mg/kg; avoid bilateral blocks with high-concentration solutions in obese patients where the total dose may approach toxic levels

Criterion Specification Timing Within 1 week of a known clinical insult OR new/worsening respiratory symptoms Chest imaging Bilateral opacities on CXR or CT — not fully explained by effusions, lobar/lung collapse, or nodules Origin of oedema Not fully explained by cardiac failure or fluid overload; echocardiography if no risk factor for ARDS Oxygenation (on PEEP ≥5 cmH₂O) Mild: PaO₂/FiO₂ 200–300 mmHg; Moderate: PaO₂/FiO₂ 100–200 mmHg; Severe: PaO₂/FiO₂ <100 mmHg

Global Definition 2023 (Matthay et al.): expands Berlin to include patients on high-flow nasal O₂ ≥30 L/min with SpO₂/FiO₂ ≤315 (mild), and patients in resource-limited settings without PEEP-capable ventilators; acknowledges ARDS can be diagnosed without intubation

Trigger (direct: pneumonia, aspiration, COVID-19; indirect: sepsis, trauma, pancreatitis, transfusion) → inflammatory cascade (neutrophil activation, macrophage cytokine storm: IL-1β, IL-6, IL-8, TNF-α) → alveolar-capillary membrane disruption → protein-rich fluid floods alveoli → hyaline membrane formation → Type II pneumocyte damage → impaired surfactant production → alveolar collapse → severe V/Q mismatch → refractory hypoxaemia. Simultaneously: fibroblast activation → fibrin deposition → fibrosing alveolitis in survivors (fibrotic phase after 5–7 days)

Phase Timing Pathology Clinical

Exudative Days 1– DAD, hyaline membranes, neutrophil infiltration, oedema, Refractory hypoxaemia, bilateral infiltrates, poor compliance (acute) 7 protein exudate

Proliferative Days 7– Type II pneumocyte proliferation, early fibroblast activation, Some improvement in oxygenation; risk of ventilator-induced lung injury 14 beginning repair Fibrotic >2 Collagen deposition, lung fibrosis, emphysema-like bullae Prolonged ventilator dependence; barotrauma risk; survivors: long-term weeks reduced DLCO

Therapy Evidence When to Use

Neuromuscular ACURASYS trial (2010): early NMBA improved 90-day mortality by 9% vs placebo in moderate-severe ARDS; Severe ARDS (P/F <150) + failure blockade ROSE trial (2019): NMBA not superior to light sedation target (contradictory); current: NMBA for severe of sedation alone to prevent (cisatracurium dyssynchrony, refractory hypoxaemia, or prone positioning dyssynchrony; facilitate prone 48h) Recruitment Sustained inflation (40 cmH₂O × 40 sec) or PEEP incremental staircase; improves oxygenation acutely; ART After ETT suctioning, accidental manoeuvres trial showed no mortality benefit and possible harm in moderate ARDS; not routinely recommended; use disconnection, or circuit change selectively in severe ARDS after derecruitment events Inhaled nitric Selective pulmonary vasodilator → improves V/Q matching → ↑PaO₂; does not improve mortality; use as Refractory hypoxaemia as bridge oxide (iNO) bridge to lung transplant or ECMO decision therapy

ECMO (VV- EOLIA trial (Combes A, NEJM 2018): VV-ECMO for severe ARDS (P/F <50–80 despite optimal ventilation); Severe ARDS (P/F <80) at ECMOECMO) significant reduction in 60-day mortality (35% vs 46%); rescue therapy when conventional management fails capable centre; bridge to recovery or transplant

Conservative FACTT trial: conservative fluid management (target CVP <4 cmH₂O vs liberal CVP <10) reduced ventilator- Haemodynamically stable ARDS — fluid strategy free days and ICU days without worsening renal outcomes; reduce fluid once haemodynamically stable switch from resuscitative to conservative fluid balance

Domain Criteria for Readiness Cause of The primary reason for ventilatory support is improved or resolved (pneumonia improved, pulmonary oedema resolved, post-operative recovery respiratory adequate) failure Oxygenation PaO₂/FiO₂ ≥150–200 mmHg on FiO₂ ≤0.4–0.5 with PEEP ≤5–8 cmH₂O; SpO₂ ≥90% on these settings Ventilation Stable spontaneous respiratory effort; pH ≥7.25; PaCO₂ at or near baseline; RR ≤35 breaths/min spontaneously

Haemodynamics Stable — MAP ≥65 mmHg without escalating vasopressor requirements; no active ischaemia; HR ≤120 bpm Neurological Patient awake and following commands (GCS ≥8 if no sedation); capable of protecting the airway (cough and gag reflex present); secretion management — can clear secretions (not requiring suctioning more than every 2 hours) Sedation SAT (Spontaneous Awakening Trial) has been performed — sedation stopped or weaned to allow patient to demonstrate neurological readiness; Ely

EW (NEJM 2008): SAT + SBT combined strategy reduces ventilator days by 3 days and 1-year mortality by 14% vs SBT alone

Mode: T-piece (patient breathes entirely spontaneously through the ETT circuit with no ventilator support) OR low-level pressure support (PS 5 cmH₂O +

PEEP 5 cmH₂O — overcomes ETT resistance while minimising support); duration: 30–120 minutes

Success criteria (pass SBT): all of the following maintained throughout: SpO₂ ≥90% (or PaO₂ ≥60 mmHg on ≤40% O₂) RR ≤35 breaths/min No accessory muscle use or paradoxical breathing HR 50–140 bpm; MAP ≥65 mmHg; no new arrhythmia

No agitation, diaphoresis, or distress

Failure criteria (abort SBT): any of the above reversed — reinstate full ventilatory support; do NOT retry SBT for at least 24 hours (patient needs rest); identify and treat the cause of SBT failure

After passing SBT: assess for extubation readiness (additional criteria beyond ventilation ability)

RSBI = f/VT where f = respiratory rate (breaths/min) and VT = tidal volume (litres) measured during 1 minute of spontaneous breathing (T-piece or minimal PS)

Normal: RSBI <105 breaths/min/L (the original Yang & Tobin 1991 threshold); values below this predict successful extubation with sensitivity 97%, specificity 64%

Practical interpretation: patient breathing at 25 breaths/min with TV 0.35 L → RSBI = 25/0.35 = 71 → favourable for extubation; patient breathing at 35/min with TV 0.20 L → RSBI = 175 → very high risk of extubation failure

Limitations: alone insufficient — high sensitivity but lower specificity; must be combined with clinical assessment; not validated in chronically ventilated patients or COPD; some guidelines now use RSBI <80 as a stricter threshold for high-confidence extubation

Additional extubation criteria beyond passing SBT: adequate cough force (peak cough flow >60 L/min); secretion burden manageable (<2-hourly suctioning); upper airway intact — cuff leak test positive (if failed cuff leak → laryngeal oedema → consider IV dexamethasone 8 mg, delay extubation 24 hours, consider airway exchange catheter before extubation); no recent high aspiration risk episode

High-risk extubation: patients with >2 risk factors for re-intubation (age >65, underlying cardiac/respiratory disease, ≥2 comorbidities, BMI >30, weak cough, excessive secretions, prolonged ventilation >7 days) should receive preventive NIV (BiPAP) immediately post-extubation for at least 24 hours — reduces reintubation rate by 20–30%

High-flow nasal O₂ (HFNO) post-extubation: alternative to NIV; delivers heated-humidified O₂ at 30–60 L/min; reduces work of breathing from washout of dead space; evidence (FLORALI trial): HFNO equivalent to NIV for post-extubation respiratory failure in non-hypercapnic patients; now widely used as default post-extubation support

Reintubation: 15–20% of extubated patients require reintubation within 48–72 hours; associated with significantly higher mortality; early reintubation (within 6 hours of extubation failure signs) is associated with better outcomes than delayed reintubation after prolonged failed rescue NIV

Domain SSC 2021 2024 Updates/Evolving Evidence Fluid type Balanced crystalloids preferred PLUS trial (NEJM 2022; n=5037): Plasmalyte-148 vs 0.9% NaCl in ICU — NO significant difference in 90-day over 0.9% NaCl (SMART trial — mortality or AKI; raises questions about the magnitude of benefit of balanced vs saline; current consensus: balanced ↓ AKI); weak balanced crystalloids remain preferred but the benefit is modest recommendation Fluid volume 30 mL/kg crystalloid bolus in CLASSIC trial (NEJM 2022; n=1554): restrictive vs standard fluid in septic shock — restrictive (boluses only if Hour-1 for hypotension/lactate severe hypoperfusion; target CVP ≤5) vs standard: NO significant difference in 90-day mortality; confirms that the ≥4; reassess after each 500 mL traditional 30 mL/kg "mandate" is not evidence-based beyond the initial resuscitation; current emphasis: titrate fluid to dynamic fluid responsiveness markers (SVV, PLR), not a fixed volume Vasopressor Noradrenaline first-line (strong); VANCS trial: vasopressin vs noradrenaline in septic shock — vasopressin first-line non-inferior, fewer arrhythmias; choice vasopressin second (weak); ongoing debate; noradrenaline remains standard first-line; vasopressin as second agent to reduce noradrenaline consider terlipressin dose (catecholamine-sparing) Corticosteroids IV hydrocortisone 200 mg/day if CAPE-COVID, APROCCHSS trials: hydrocortisone + fludrocortisone in septic shock → significant 90-day mortality noradrenaline ≥0.25 mcg/kg/min reduction; growing evidence that corticosteroids benefit a broader population than previously defined; threshold for for ≥4 hours (weak initiation may be lower than noradrenaline 0.25 mcg/kg/min recommendation; ADRENAL trial basis) Lactate-guided Measure lactate; if >2 mmol/L → LACTATES trial: lactate-guided vs usual care in septic shock — lactate-guided resuscitation did not improve resuscitation reassess every 2 hours; lactate outcomes; questions whether lactate normalisation is the appropriate endpoint; tissue oxygenation markers and clearance ≥10% per 2 hours is a organ function (creatinine, bilirubin, mental status) may be equally or more relevant endpoints target

The SSC 2021 Hour-1 bundle (measure lactate, blood cultures before antibiotics, broad-spectrum antibiotics within 1 hour, 30 mL/kg crystalloid if hypotensive, vasopressor if MAP <65) has been validated in multiple observational studies showing that compliance with all 5 elements is associated with reduced mortality

Controversy: the 1-hour antibiotic target for all sepsis (not just septic shock) — some evidence that for less severe sepsis without shock, the 1-hour target may lead to unnecessary broad-spectrum antibiotic use and antibiotic resistance, without clearly improving outcomes; the 2024 updates may refine the antibiotic timing based on clinical severity

Antibiotic de-escalation: increasingly emphasised in 2024 updates — broad-spectrum antibiotics started in Hour-1 must be de-escalated as soon as culture results and clinical response allow (typically at 48–72 hours); de-escalation reduces resistance, side effects (C. difficile, nephrotoxicity), and costs

Agent Role in 2024 Guidelines Specific Advantage

Noradrenaline FIRST LINE — strong recommendation; start early Best evidence base; predictable dose-response; less tachyarrhythmia than dopamine (De (norepinephrine) (before completing 30 mL/kg if MAP <65) Backer trial)

Vasopressin SECOND LINE — add when noradrenaline dose V1 receptor vasoconstriction — no catecholamine effects; may preserve renal blood flow; ≥0.25 mcg/kg/min; reduces noradrenaline reduces relative vasopressin deficiency of septic shock requirement Hydrocortisone Add when noradrenaline ≥0.25 mcg/kg/min (2021 Not a vasopressor per se but restores catecholamine receptor sensitivity (corticosteroidthreshold; 2024 may lower this) deficient state → reduced receptor responsiveness to noradrenaline; hydrocortisone restores this) Dopamine NOT recommended as first-line; alternative only if De Backer NEJM 2010: dopamine → more arrhythmias + higher mortality in cardiogenic shock noradrenaline unavailable subgroup vs noradrenaline Angiotensin II Rescue therapy for refractory shock on high-dose AT1 receptor agonist → vasoconstriction independent of catecholamine pathway; ATHOS-3 (Giapreza) noradrenaline + vasopressin trial: improved MAP in refractory vasodilatory shock; expensive, limited availability

Haemorrhage → hypothermia (heat loss from haemorrhage, exposure, resuscitation with cold fluids) + acidosis (tissue hypoperfusion → lactic acidosis) + coagulopathy (dilution by crystalloids + consumption of clotting factors + direct hypothermia/acidosis impairment of coagulation enzyme activity) → these three form a positive feedback loop: hypothermia impairs coagulation enzymes → worse coagulopathy → more bleeding → more acidosis → more cooling → death Component Mechanism Consequence Hypothermia Blood and tissue heat loss; cold IV fluids; OR exposure; factor activity falls 10% for Progressive coagulopathy despite "normal" laboratory (<35°C) every 1°C below 37°C; platelet function impaired at <33°C; fibrinogen activity coagulation tests (which are performed at 37°C — not impaired at <30°C reflecting the patient's actual temperature) Acidosis (pH Tissue hypoperfusion → lactate accumulation → metabolic acidosis; pH <7.2 reduces Even normal factor levels fail to generate adequate thrombin at <7.2) coagulation enzyme activity by 50%; inhibits thrombin generation low pH — coagulopathy despite normal PT/APTT Coagulopathy Factor dilution by crystalloids; factor consumption; hyperfibrinolysis (plasmin Fibrinogen is consumed first (critical threshold <1.5 g/L in activation); hypothermia/acidosis-induced enzyme failure; early trauma-induced trauma); then factor V, VIII, XI; then platelet dysfunction coagulopathy (TIC — before any resuscitation)

TEG/ROTEM: whole blood point-of-care coagulation tests; provide results within 10–20 minutes vs 60+ minutes for standard laboratory coagulation tests; guide targeted blood product replacement: TEG R time prolonged → FFP; MA reduced → platelets; LY30 elevated → tranexamic acid; fibrinogen reduced (Alpha angle low) → cryoprecipitate/fibrinogen concentrate

Standard lab tests during MTP: FBC (Hb, Plt), PT/APTT/fibrinogen, ABG (pH, lactate, calcium, glucose, temperature), TEG if available — all repeated every 30–60 minutes during active haemorrhage

Rotational thromboelastometry (ROTEM): equivalent to TEG but uses different parameter names (CT = R time; MCF = MA; LI30 = LY30); EXTEM/FIBTEM/INTEM/APTEM channels provide comprehensive haemostatic profile in <30 minutes

MTP termination criteria: haemorrhage surgically or radiologically controlled; haemodynamic stability with reducing vasopressor requirements; normal coagulation parameters (TEG normalised; pH >7.25; temperature >35°C)

Post-haemostasis care: switch from DCR (permissive hypotension, haemostatic resuscitation) to damage control surgery phase: repair injuries in planned stages; prevent abdominal compartment syndrome; reverse hypothermia aggressively; correct remaining acidosis; ICU monitoring for multi-organ failure in the subsequent days

Thromboprophylaxis after MTP: VTE risk is extremely high post-trauma; start LMWH as soon as haemostasis is secure and surgical team agrees (usually 12–24 hours after haemostasis); mechanical compression devices from admission

Definition (World Allergy Organisation 2011): anaphylaxis is a severe, life-threatening, generalised hypersensitivity reaction; clinical diagnosis: "highly likely when ONE of the following 3 criteria is fulfilled": Acute onset with skin/mucosal involvement + either respiratory compromise OR reduced BP/end-organ dysfunction

Two or more of: skin/mucosal involvement, respiratory compromise, reduced BP, GI symptoms — occurring after EXPOSURE to a LIKELY ALLERGEN Reduced BP after exposure to a KNOWN allergen Immunological (IgE-mediated — Type I hypersensitivity): previous sensitisation → IgE antibodies bound to mast cells and basophils; re-exposure → allergen cross-links IgE → mast cell degranulation → histamine, tryptase, leukotrienes, prostaglandins, PAF → vasodilation + vascular permeability ↑ + bronchospasm + GI effects Non-immunological (anaphylactoid — no prior sensitisation needed): direct mast cell degranulation without IgE; drugs that cause this: opioids (morphine, codeine — direct mast cell degranulation; NOT IgE-mediated), hyperosmolar solutions, contrast media, aspirin (via COX pathway → ↑ leukotrienes), dextrans, protamine (complement activation)

Key mediators: histamine (H1 → bronchospasm, vasodilation; H2 → ↑ gastric acid); tryptase (the most specific mast cell marker — peaks at 60–90 min postanaphylaxis; used for diagnostic confirmation); leukotrienes C4 and D4 (potent bronchoconstrictors); prostaglandins; platelet activating factor (PAF)

Finding Detail Most common NMBAs 50% (suxamethonium 26%, rocuronium 14%); antibiotics 15% (teicoplanin, co-amoxiclav, cefuroxime); chlorhexidine 9%; patent blue dye 6%; triggers latex 2%; all others 18% Incidence 1 in 10,000 general anaesthetics (estimated); true incidence uncertain due to under-reporting; approximately 266 cases identified in a 12-month period across UK Mortality 9 deaths in the audit period; estimated UK mortality from perioperative anaphylaxis: 3–9 per million GAs

Cardiovascular In perioperative anaphylaxis: cardiovascular collapse is the predominant feature (73%) in contrast to community anaphylaxis where skin and predominance respiratory symptoms predominate; skin features may be absent due to vasoconstriction/surgical drapes masking urticaria Under- Only 60% of confirmed cases were referred for formal allergy investigation; many patients discharged without follow-up testing — leaving them at risk investigation of recurrence without knowing their triggers Key practice Initial adrenaline dosing often inadequate or delayed; 25% received adrenaline >10 minutes after first symptoms; some received non-adrenaline concerns vasopressors first (noradrenaline — inadequate in anaphylaxis which requires both alpha + beta effects)

ACUTE TRYPTASE SAMPLES — MANDATORY after every suspected anaphylaxis:

Sample 1: as soon as possible after reaction (within 30 minutes of onset)

Sample 2: 1–2 hours after reaction (peak tryptase — typically 60–90 minutes)

Sample 3: 24 hours (baseline tryptase — to exclude mastocytosis as an underlying cause) Serum tryptase >20 mcg/L (or >2× baseline + 2) confirms mast cell degranulation → supports anaphylaxis diagnosis Refer to allergy clinic at 4–6 weeks: this is the mandatory post-event investigation window; earlier testing is unreliable (residual drug/antibodies may interfere) Skin testing (SPT — skin prick test + ID — intradermal): gold standard for identifying the causative agent; each drug used during the anaesthetic is tested individually at non-irritating concentrations; a positive SPT (wheal ≥3 mm) confirms IgE sensitisation to that drug; helps identify the trigger and guide future safe anaesthesia

RAST/ImmunoCAP (specific IgE ELISA): blood test for specific IgE antibodies against drugs/allergens; less sensitive than skin testing for NMBAs but useful for penicillin allergy, latex, and chlorhexidine; complements skin testing

Future anaesthesia document: after full investigation, a written report must be provided to the patient specifying the identified trigger, safe alternative agents, and a detailed future anaesthesia plan; this document should be worn as a medical alert bracelet or kept with the patient's records

Grade Features Management Mild Wheeze on auscultation; ↑ peak airway pressure 20–30%; SpO₂ maintained; ETCO₂ Deepen anaesthesia; salbutamol MDI via ETT adapter; upsloping plateau; patient comfortable under adequate anaesthesia continue monitoring Moderate Audible wheeze; peak airway pressure ↑30–50%; SpO₂ 90–94%; clear shark-fin ETCO₂; Salbutamol 5 mg nebulised via circuit; increase volatile agent increased work of breathing if spontaneously ventilating concentration; IV magnesium 2 g; reduce RR to lengthen expiratory time Severe Severe wheeze or silent chest (no air entry — life-threatening); peak airway pressure Emergency protocol (see below); IV adrenaline; ketamine; IV ↑>50% or cannot ventilate; SpO₂ <90%; potential auto-PEEP development and aminophylline; consider whether this is anaphylaxis cardiovascular compromise

Common triggers: intubation/laryngoscopy in light anaesthesia; aspiration of gastric contents or secretions; airway irritation (ETT irritation, suctioning); histamine-releasing drugs (atracurium, morphine, thiopentone at high doses); anaphylaxis; irritant volatile agents (desflurane — most pungent; isoflurane); cold dry gas; GORD; active smoking; uncontrolled asthma

Cause Distinguishing Features Action ETT obstruction Unilateral or no breath sounds; passes suction catheter easily (if secretion plug) or does not pass (if Suction ETT; reposition; replace ETT if (kink, secretion, kinked); pass suction catheter immediately — rules out/confirms most ETT obstruction causes kinked bite) Endobronchial Unilateral breath sounds only; ↑ airway pressure; hypoxia; SpO₂ falls; confirm with fibreoptic or pull Withdraw ETT 1–2 cm; confirm bilateral intubation back ETT slowly until bilateral sounds return breath sounds Pneumothorax Absent unilateral breath sounds; hypotension; tracheal deviation; JVP raised; cardiovascular collapse if Emergency needle decompression 2nd (tension) tension; immediate clinical diagnosis; confirm with CXR or POCUS ICS MCL if tension; formal chest drain True BILATERAL wheeze; shark-fin ETCO₂; bilateral reduced air entry; responsive to bronchodilators; no Bronchodilators; deepen anaesthesia; bronchospasm sudden cardiovascular collapse (unless anaphylaxis) ventilation adjustment Anaphylaxis Bronchospasm + cardiovascular collapse + urticaria/flush (may be masked by drapes); tryptase Adrenaline IM/IV; IV fluids; full elevated; multiple drug exposures anaphylaxis protocol

1. FiO₂ 1.0 immediately — maximum oxygenation while managing airway 2. Deepen anaesthesia: increase volatile agent to 1.5–2 MAC (sevoflurane/isoflurane — inherent bronchodilators); propofol bolus 1–2 mg/kg IV (bronchodilator properties); avoid desflurane (airway irritant) 3. Salbutamol (albuterol): 5–10 puffs MDI via ETT adapter (actuate MDI into the circuit during inspiration); or 5 mg nebulised via the inspiratory limb; the fastest and most effective initial bronchodilator; mechanism: β₂ agonist → airway smooth muscle relaxation → bronchodilation + mast cell stabilisation 4. Ventilation adjustments: reduce RR to 8–10 breaths/min (extend expiratory time → reduce auto-PEEP); I:E ratio 1:4; reduce TV if necessary (accept permissive hypercapnia rather than high airway pressures); if patient fighting ventilator → NMBA (rocuronium 0.6 mg/kg) to eliminate respiratory dyssynchrony 5. IV Magnesium sulphate: 2 g IV over 10–20 minutes — inhibits Ca²⁺-mediated smooth muscle contraction; modest bronchodilator; well tolerated; safe to give empirically 6. IV Ketamine: 0.5–1 mg/kg IV — bronchodilator via catecholamine release and direct smooth muscle relaxation; also provides additional depth of anaesthesia; particularly useful if patient is light under anaesthesia 7. IV Aminophylline: 5 mg/kg loading over 20 minutes (reduce to 3 mg/kg if on theophylline); phosphodiesterase inhibitor → ↑ cAMP → bronchodilation; narrow therapeutic index — requires ECG monitoring (tachyarrhythmia risk) 8. IV Adrenaline: if severe, life-threatening, or anaphylaxis suspected — 50–100 mcg IV boluses; activates β₂ receptors → most powerful bronchodilator; also reverses any anaphylaxis component 9. IV Hydrocortisone: 200 mg IV — anti-inflammatory; effect delayed 4–6 hours but appropriate for medium-term management; reduces airway inflammation perpetuating bronchospasm

Preoperative optimisation: ensure asthma is well-controlled (PEFR ≥80% predicted); continue all inhalers on morning of surgery; consider salbutamol nebulisation 20–30 minutes before induction; avoid elective surgery during active exacerbation

Induction: topicalise the airway (lignocaine spray) before intubation; ensure adequate depth (sevoflurane >1 MAC or propofol 2.5 mg/kg) before laryngoscopy; LMA preferred over ETT in reactive airway disease if surgically feasible (avoids subglottic stimulation); avoid histamine-releasing NMBs (atracurium → use rocuronium or cisatracurium); avoid thiopentone in high-dose (histamine release); propofol preferred induction agent

4 Hs Perioperative Context 4 Ts Perioperative Context Hypoxia ETT displacement, oesophageal intubation, airway Tension Central line insertion, barotrauma, laparoscopy CO₂ tracking, obstruction, failed oxygenation; FIRST thing to exclude Pneumothorax ARDS over-ventilation; absent breath sounds + sudden — check bilateral breath sounds, SpO₂, ETCO₂ cardiovascular collapse; immediate needle decompression Hypovolaemia Surgical haemorrhage, aortocaval compression Tamponade Cardiac surgery complication, central line perforation, chest (pregnancy), fluid deficit; PEA in context of surgery and (cardiac) trauma; PEA after cardiac surgery is tamponade until proven haemorrhage; transfuse blood products immediately otherwise; pericardiocentesis or surgical drainage Hypo/Hyperkalaemia Succinylcholine in denervated patients, renal failure, Thrombosis PE during surgery (DVT, air embolism, fat embolism, amniotic fluid transfusion; ECG changes; calcium gluconate for (pulmonary) embolism); sudden hypoxia + hypotension + reduced ETCO₂; hyperkalaemia; calcium for hypocalcaemia thrombolyse if PE confirmed in arrest Hypothermia Prolonged surgery + inadequate warming; VF refractory Toxins Drug overdose (opioids, local anaesthetics), volatile agent to defibrillation below 28°C; warm the patient before overdose, anaphylaxis, medication errors; specific antidotes: lipid declaring death; "not dead until warm and dead" emulsion (LAST), naloxone (opioids), sugammadex (CICO), adrenaline (anaphylaxis)

Airway already managed: ETT usually in situ → confirm bilateral breath sounds and ETCO₂ waveform first (excludes oesophageal intubation as arrest cause); ensure 100% O₂; ventilate manually at 10 breaths/min (not continuous ventilation — pauses for CPR compression are acceptable if ETCO₂ waveform visible)

IV access established: use existing IV/central access; if fluids are running → check for medication errors or anaphylaxis-triggering drug

Abandon the surgical field: inform the surgeon immediately; control haemorrhage if possible; non-critical surgery → close and focus on resuscitation

Team roles: anaesthesiologist leads CPR and drug management; surgeon manages surgical cause if relevant; ODP/nurse circulates drugs; second anaesthesiologist for airway relief; immediate defibrillator application

Immediate defibrillation for VF/pVT: 200J biphasic immediately; do not delay defibrillation for any other intervention in shockable rhythms

Higher quality CPR target in operating theatre: sternal compression 5–6 cm depth at 100–120/min; full chest recoil; minimal interruptions; CPR feedback device if available

Mechanism: bupivacaine "fast in, slow out" cardiac Na⁺ channel block → VF/VT refractory to standard ACLS

Management: standard CPR; 20% lipid emulsion 1.5 mL/kg IV bolus immediately; then 0.25 mL/kg/min infusion; may repeat bolus once after 5 minutes; max 12 mL/kg total; AVOID propofol as the lipid source (not adequate lipid content for LAST at clinical doses); avoid vasopressin in LAST; adrenaline doses ≤1 mcg/kg (higher doses may worsen outcomes in LAST); consider ECMO early if LAST arrests persist despite lipid emulsion

Mechanism: massive vasodilation + myocardial depression + bronchospasm → PEA or VF

Management: FULL DOSE adrenaline 1 mg IV every 3–5 minutes (standard ACLS dose — do NOT use reduced dose in anaphylaxis arrest); IV fluids 1–2 L crystalloid rapidly; lie flat, legs up; stop causative drug; chlorphenamine and hydrocortisone are secondary — do not delay CPR for these; once ROSC: vasopressor infusion (noradrenaline); tryptase samples; allergy follow-up

Mechanism: air in the pleural space under pressure → compresses the lung, mediastinum, and great veins → reduced venous return → obstructive shock →

PEA arrest

Recognition during anaesthesia: sudden ↑ airway pressure + sudden ↓ ETCO₂ + sudden ↓ BP → absent breath sounds unilaterally

Management: immediate needle decompression 2nd intercostal space, mid-clavicular line (anterior approach — 14G IV cannula; confirm by hiss of air under pressure and haemodynamic improvement); formal chest drain after needle decompression; do NOT delay for CXR in arrest; if bilateral pneumothorax suspected (both sides absent breath sounds, bilateral raised airway pressures in ARDS) → bilateral needle decompression simultaneously

Immediate check: is the correct drug drawn up? Syringe labelling error? Dose calculation correct? Weight entered correctly into TCI?

Opioid-induced arrest: naloxone 400 mcg IV; propofol overdose: supportive CPR + lipid emulsion if unresponsive

Potassium bolus error (concentrated KCl given as IV push): hyperkalaemia → VF → calcium gluconate 1 g IV immediately; sodium bicarbonate 50 mEq IV; insulin-dextrose; defibrillate for VF; dialysis

Targeted Temperature Management (TTM): cool to 32–36°C for 24 hours in comatose post-cardiac arrest patients (TTM2 trial 2021: 33°C vs 37.5°C — no mortality difference; maintain normothermia at minimum; avoid hyperthermia >37.5°C); continuous EEG monitoring for seizures (post-anoxic seizures are common)

Haemodynamic optimisation: MAP ≥65–70 mmHg; avoid hypotension post-ROSC; vasopressor infusion; coronary angiography if STEMI suspected as cause

Neuroprognostication: defer formal neurological assessment until 72 hours post-arrest (and 24 hours after stopping TTM); use multimodal approach: EEG, SSEP, CT brain, MRI brain, biomarkers (NSE, S100β)

Hypothalamic thermostat: the preoptic nucleus of the anterior hypothalamus integrates thermal signals from the skin (peripheral warm/cold receptors) and the blood temperature (central core sensing); it maintains core temperature within a narrow range (36.5–37.5°C) by triggering heat gain or loss responses

Heat production mechanisms: shivering (skeletal muscle tremor — increases metabolic heat production 2–5×); non-shivering thermogenesis (brown adipose tissue in neonates and some adults — uncoupled oxidative phosphorylation); piloerection (traps insulating air — minimal in humans)

Heat loss mechanisms: vasodilation (increases skin blood flow → radiation and convection); sweating (evaporative cooling — most powerful heat loss mechanism at high ambient temperatures); radiation (60% of normal heat loss), convection (15%), evaporation (22%), conduction (3%)

Interthreshold range: the range of core temperatures at which no thermoregulatory response is triggered (approximately 0.2°C wide in awake humans); anaesthesia widens this range dramatically (2–4°C under GA and neuraxial anaesthesia) → the body tolerates a much wider temperature fluctuation without triggering a corrective response

Redistribution hypothermia (Phase 1 — first hour): the most important mechanism; GA abolishes the vasoconstrictor response that normally maintains a temperature gradient between the warm core (vital organs) and the cooler periphery (arms, legs, skin); vasodilation from anaesthetic agents → peripheral blood vessels dilate → warm core blood redistributes to the cool periphery → core temperature falls rapidly (1–1.5°C in first 30 minutes despite no net heat loss from the body — the heat has moved from core to periphery); this cannot be prevented by any warming measure alone Heat loss to the environment (Phase 2 — hours 1–3): the patient loses heat to the cool operating theatre environment (typically 18–20°C ambient) through radiation from exposed skin, convection from unwarmed gas flows, and conduction from cold fluid infusions and preparation solutions; the rate of heat loss exceeds metabolic heat production under anaesthesia New equilibrium (Phase 3 — after 3 hours): core temperature stabilises at a new (lower) equilibrium when heat loss and production balance

Contributing factors: cold operating theatre (18–20°C vs optimal 21–22°C); unwarmed IV fluids and blood products (stored at 4°C); unwarmed irrigation solutions; large exposed body cavities (abdominal, thoracic); prolonged surgery; regional anaesthesia (vasodilates below the block level); neonates and extremes of age; thin patients with low body fat

Consequence Mechanism Evidence Surgical Site Hypothermia → vasoconstriction of skin/subcutaneous tissue → ↓ O₂ delivery to the Kurz A (NEJM 1996): maintaining normothermia (36.6°C vs Infection wound → ↓ oxidative bacterial killing by neutrophils → ↑ SSI rate; also impairs 34.7°C) reduced SSI rate from 18% to 6% in colorectal (SSI) collagen deposition surgery — a 3× reduction; this landmark trial established warming as a patient safety standard Coagulopathy Each 1°C below 37°C → 10% reduction in coagulation enzyme activity; platelet Frank SM (Anesthesiology 1997): hypothermic patients (34°C) function impaired; fibrinolysis altered; coagulopathy occurs at "normal" PT/APTT required 20% more blood transfusion than normothermic (tested at 37°C in the lab, not at the patient's actual temperature) patients in hip arthroplasty Cardiac Vasoconstriction → ↑ SVR → ↑ cardiac workload; shivering → ↑ O₂ consumption; Frank SM (JAMA 1997): hypothermic patients had significantly events tachycardia → ↑ myocardial O₂ demand; hypothermia → arrhythmias (AF below 35°C, more morbid cardiac events (MI, unstable angina) in the 24 VF below 28°C) hours after major non-cardiac surgery Prolonged Hypothermia reduces hepatic and renal blood flow → ↓ drug metabolism; ↓ plasma NMB duration prolonged by 30–60% at core temperature drug action pseudocholinesterase activity → prolonged succinylcholine; ↓ cytochrome P450 34°C; extends post-operative recovery room time activity; volatile agents: MAC falls ~5% per °C below 37°C → deeper anaesthesia at lower vaporiser settings than expected Patient Post-anaesthetic shivering occurs in 20–60% of patients; increases O₂ consumption Shivering: treat with pethidine 25 mg IV (most effective) or discomfort 400–500%; increases CO₂ production → impairs wound oxygenation; profoundly ondansetron; prevent with active warming and shivering uncomfortable — frequently rated by patients as the worst part of their surgical experience (worse than pain)

Seal Pressure Generation Features Examples (OLP) First Inflatable cuff; no gastric drainage channel; suitable for spontaneous breathing only or Classic LMA (Brain's original); Portex 15–20 cmH₂O (low generation very low-pressure IPPV; cuff repositions with each inflation; requires inflating balloon to Soft Seal; LMA Unique (single-use) — limits positive (classic) achieve seal pressure ventilation use) Second Higher seal pressures (25–30 cmH₂O); integrated gastric drainage channel (allows NGT i-gel (non-inflatable cuff); LMA 25–35 cmH₂O generation passage and decompresses stomach, reducing aspiration risk); drainage port separates ProSeal (inflatable cuff + gastric (allows positive (advanced) the respiratory and GI tracts; some have bite block and alignment features; suitable for drain); LMA Supreme (single-use + pressure ventilation positive pressure ventilation during surgery gastric drain); LMA Protector; Air-Q for most surgical procedures)

Cuff material: non-inflatable thermoplastic elastomer (TPE) gel — formulated to match the soft consistency of perilaryngeal tissues; the gel cuff moulds to the individual anatomy of the patient's hypopharynx, laryngeal inlet, and perilaryngeal anatomy at body temperature without requiring inflation; eliminates the complications of cuff inflation (cuff over-inflation, cuff herniation, cuff leak)

Structure: a short, curved airway tube connecting to a widened cuff that sits in the hypopharynx sealing around the laryngeal inlet; an integrated gastric drainage channel runs parallel to the main airway lumen, terminating at the oesophageal inlet (allows NGT insertion for gastric decompression); a bite block at the proximal end prevents jaw closure from occluding the airway

Sizes: 1 (neonates); 1.5 (infants 5–12 kg); 2 (children 10–25 kg); 2.5 (25–35 kg); 3 (small adult 30–60 kg); 4 (adult 50–90 kg); 5 (large adult >90 kg); selected by patient weight

Advantages: rapid insertion (no cuff inflation step); higher OLP (oropharyngeal leak pressure — 24–30 cmH₂O) than first-generation LMAs; integrated gastric drain (drainage of regurgitated gastric contents via the second channel reduces (but does NOT eliminate) aspiration risk); single-use (infection control); suitable for fibreoptic intubation conduit; suitable as second line (Plan B) in DAS failed intubation algorithm

Indications Contraindications Elective surgery under GA where ETT is not mandatory (most ENT, orthopaedic, Full stomach / aspiration risk (RSI with ETT preferred); predicted difficult SAD superficial surgery, gynaecological laparoscopy in non-obese); IPPV during placement (limited mouth opening <2.5 cm; fixed neck with pharyngeal surgery (2nd generation SADs can withstand 25–30 cmH₂O to allow controlled pathology; severe pharyngeal/laryngeal pathology); morbid obesity for ventilation); ambulatory anaesthesia (faster emergence, less PONV than ETT); prolonged procedures; high airway resistance/low pulmonary compliance rescue airway in failed intubation (DAS Plan B); cardiac arrest — all ILCOR requiring peak pressures >30 cmH₂O; surgery requiring full neuromuscular guidelines accept SADs as alternative to ETT in cardiac arrest (AHA 2020); bridge blockade with high airway pressures (thoracic, steep Trendelenburg in obese to fibreoptic intubation (Aintree Intubation Catheter through i-gel) patients); head-and-neck surgery where access to the SAD is lost during the case

The i-gel, once placed and ventilation confirmed, can be used as a conduit for fibreoptic-guided intubation (DAS Plan B — after failed intubation, maintain oxygenation with SAD then attempt intubation through it): pass a lubricated fibrescope through the i-gel airway tube → visualise the vocal cords through the SAD aperture → advance a tracheal tube over the fibrescope → confirm intubation with ETCO₂; then remove the i-gel over the ETT

Aintree Intubating Catheter (AIC) technique: a 56 cm catheter (4.7 mm OD) is passed through the fibrescope into the trachea; fibrescope is removed; then a 7.0–8.0 mm ETT is railroaded over the AIC through the i-gel into the trachea; the AIC is then removed; this technique allows intubation through an i-gel with a standard-sized adult ETT

Success rate: approximately 96% intubation success through second-generation SADs in multiple studies; specific i-gel success rate 93–97% for intubation via FOI conduit

Cardiac arrest: ILCOR 2020 and AHA 2020: "SADs are an acceptable alternative to tracheal intubation for airway management during cardiac arrest"; a SAD by a practitioner with limited ETT skill provides equivalent outcomes to ETT in multiple randomised trials; i-gel specifically: AIRWAYS-2 trial (Benger JR, JAMA 2018; n=9,296 out-of-hospital cardiac arrest patients): i-gel vs ETT for cardiac arrest airway management — no difference in neurologically intact survival (primary outcome); i-gel had faster insertion and fewer complications

Select size by weight; lubricate cuff with water-based lubricant (NOT silicone — degrades TPE gel); head in neutral or slightly extended position; open mouth; grasp i-gel with thumb on the bite block; introduce into the mouth aiming the cuff toward the hard palate; rotate and guide the device posteriorly along the hard palate then downward into the pharynx in a single smooth movement until resistance is felt (cuff seated against laryngeal inlet); confirm ventilation (ETCO₂ waveform, bilateral chest movement, absence of epigastric sounds); if poor seal → reinsert or change size

FGF Bag/APL Min FGF Min FGF System Efficiency Explanation Position Position (SB) (IPPV) A (Magill) Near the Near the MV 2–3× MV During SB: expired gas pushes to the patient-end APL → alveolar gas (CO₂-rich) vents first; bag patient (alveolar (10–15 fresh gas fills the space; VERY EFFICIENT for SB (least FGF). For IPPV: PPV pushes (machine (patient ventilation) L/min) mixed gas toward the bag → CO₂-rich gas is not selectively vented; fresh gas wasted — end) end APL) ≈ 4–5 INEFFICIENT for IPPV L/min B Near Near 2–2.5× MV 2–2.5× MV Intermediate efficiency; FGF near patient means fresh gas is available at each inspiration patient patient but expired gas accumulates in the same reservoir C (Waters to- Near Near 2× MV 2× MV Similar to B; CO₂ absorber canister between bag and patient; dead space includes the and-fro) patient patient absorber; largely obsolete in modern practice D (Bain — Near Machine 2–3× MV 70–100 During SB: expired gas may be inhaled from the outer tube before FGF flushes it away — coaxial) patient end (bag) (10–15 mL/kg/min INEFFICIENT for SB (high FGF needed). For IPPV: controlled pattern allows efficient (via inner L/min) (5–7 L/min) flushing of expired gas during expiration → EFFICIENT for IPPV (low FGF sufficient) coaxial tube) E (Ayre's T- Near Open- 2.5–3× MV N/A (no bag No valve or bag; all expired gas vents freely through the expiratory limb; high FGF needed piece) patient ended for IPPV) to prevent rebreathing (must flush entire expiratory limb before next inspiration); simple, (lateral expiratory low-resistance; standard for neonates/infants spontaneously breathing limb) limb (no bag/APL) F (Jackson- Near Open- 2.5–3× MV Available Modification of E with open-ended bag allowing visual monitoring of breathing, manual Rees patient ended bag (manually IPPV, and CPAP; standard paediatric anaesthesia circuit; allows TPEF (total positive modification) on compress the expiratory flow) monitoring expiratory open-ended limb bag)

Key question: at the end of expiration, just before the next inspiration, which gas is positioned nearest to the patient — fresh gas or CO₂-rich expired alveolar gas?

Mapleson A during SB: FGF enters at the bag end (far from patient); during expiration, the patient exhales → dead space gas first (CO₂-free) → then alveolar gas (CO₂-rich); the alveolar gas pushes toward the patient-end APL valve, which vents it out; the fresh gas from the machine end fills the remaining space; at end-expiration, fresh gas + dead space gas are nearest the patient — essentially no CO₂ near the patient; next breath = minimal rebreathing; only needs FGF ≈ alveolar ventilation (3–5 L/min) to maintain this; MOST EFFICIENT for SB

Mapleson D (Bain) during SB: FGF enters at the patient end (via inner tube); expired gas fills the outer tube moving toward the bag; the FGF must flush the entire outer tube of expired gas during expiration before the next breath; if FGF is insufficient, the patient inhales expired gas from the nearest part of the outer tube — rebreathing; needs 2–3× MV to reliably flush; LEAST EFFICIENT for SB

Mapleson D (Bain) during IPPV: controlled pattern of expiration → predictable FGF flushing of the outer tube; lower FGF can maintain normocapnia; 70–100 mL/kg/min sufficient; EFFICIENT for IPPV

Coaxial design: inner tube carries FGF from machine end to patient end; outer corrugated tube carries expired gas from patient toward the machine-end bag/APL; counter-current heat exchange between inspired FGF (cooler) and expired gas (warmer) warms and humidifies inspired gas — an advantage over standard Mapleson D Pethick's test: mandatory pre-use safety check for inner tube integrity; occlude patient end → turn on FGF → reservoir bag should inflate (FGF is being delivered to the patient end, blocked, and fills the circuit); then release → bag should deflate (Venturi effect from FGF venturi draws the bag down); if bag does NOT inflate when occluded → inner tube disconnected (FGF not reaching patient end) → circuit unsafe → DO NOT USE

Applications: head and neck surgery (machine remote from the airway); long cases where inspiratory gas warming is beneficial; controlled ventilation where efficiency is highest; NOT ideal for spontaneous breathing cases (high FGF required)

Mapleson E (T-piece) for neonates and infants <10–15 kg under spontaneous breathing (low resistance, simple, lightweight) Mapleson F (Jackson-Rees) for manual IPPV and continuous monitoring of breathing in children; the open-ended bag provides visual confirmation of tidal volume and allows CPAP/PEEP application Adult circle system at >25–30 kg (when resistance of circle valves is proportionally less important and CO₂ absorption economics justify the setup)

Standard soda lime composition: Ca(OH)₂ (calcium hydroxide) ~80%; NaOH (sodium hydroxide) ~4%; KOH (potassium hydroxide) ~1%; SiO₂ (silica — hardening agent to reduce dust); water 14–19% (critical — desiccated absorbent is more reactive with volatile agents) Chemical reaction (two-step):

Step 1: CO₂ + H₂O → H₂CO₃ (carbonic acid forms in the water film on granules)

Step 2: H₂CO₃ + 2NaOH → Na₂CO₃ + 2H₂O; and H₂CO₃ + Ca(OH)₂ → CaCO₃ + 2H₂O

Net: CO₂ is neutralised; water and heat are produced (the canister becomes warm — indicates active absorption); Na₂CO₃ and CaCO₃ are the end products (the "spent" absorbent)

Capacity: 1 kg of soda lime absorbs approximately 100–120 L of CO₂ before exhaustion; each breath generates approximately 200 mL of CO₂ → a 1 kg canister lasts approximately 8–10 hours of normal use in a circle system

Conditions Favoring Byproduct Agent Mechanism Clinical Significance Formation Compound A Sevoflurane High temperature soda Sevoflurane + NaOH/KOH → Nephrotoxic in rats at 150+ ppm (high renal beta-lyase ONLY lime; DESSICATED base-catalysed beta-elimination activity); NOT clinically demonstrated in humans (10– absorbent; high sevoflurane → Compound A (fluoromethyl- 30× lower renal beta-lyase activity); FDA requires concentrations; low FGF 2,2-difluoro-1-[trifluoromethyl]vinyl minimum FGF 1 L/min with sevoflurane in US; Amsorb (less dilution) ether) Plus contains no NaOH/KOH → minimal Compound A generation Carbon Monoxide (CO) Desflurane DESSICATED soda lime Volatile agent haloalkyl groups + Clinically significant CO poisoning reported in patients; >> (critical — water content dessicated NaOH/KOH → CO COHb can reach 30–35% in severe cases; diagnosis Enflurane <5%); highest temperature production via free radical difficult — SpO₂ reads normally (not affected by >> Monday morning case mechanism; desflurane produces COHb); measured with co-oximetry on ABG Isoflurane (absorbent left with dry gas most CO (difluoromethyl ether (NOT flowing all weekend) group most reactive) sevoflurane, NOT halothane) Formaldehyde/Methanol Desflurane Severe dessication Further degradation products Theoretical toxicity; not prominently reported clinically + from desflurane dessicated absorbent

Feature Soda Lime Amsorb Plus Composition Ca(OH)₂ + NaOH/KOH + water Ca(OH)₂ + Ca(OH)₂ (no NaOH or KOH — no strong alkali); CaCl₂ + Ca(SO₄) hardening agents; water

Compound A Yes — NaOH/KOH catalyses Compound A Essentially ZERO — no strong alkali to catalyse beta-elimination; no FDA FGF minimum production from sevoflurane restriction needed with Amsorb Plus

CO production from Yes — dessicated NaOH/KOH reacts with Essentially ZERO — no strong alkali dessication desflurane/isoflurane → CO CO₂ absorption Slightly higher (NaOH/KOH contribute to Slightly lower CO₂ absorption capacity (pure calcium hydroxide less efficient); larger canister capacity absorption capacity) needed for equivalent capacity Cost Lower Higher; but the improved safety profile and elimination of toxic byproducts justifies the premium, particularly for sevoflurane and desflurane

Indicator dyes: ethyl violet (most common) — turns from colourless to VIOLET/PURPLE when the absorbent is exhausted (the rising CO₂ in the spent granules lowers local pH → activates the indicator); alternative: ethyl violet turns purple in acid → spent granules; some formulations use atropine red (red when fresh, colourless when spent)

Important limitation — colour regeneration: ethyl violet can regenerate (return to near-colourless) when the gas flow stops (resting in the dark); a canister that appears fresh may actually be exhausted — colour change cannot be relied upon as the SOLE indicator of absorbent exhaustion; use TIME-based replacement (replace after approximately 8–10 hours of clinical use, or based on ETCO₂ rise as the definitive functional indicator) Canister management: Never allow the absorbent to dessicate (do not leave high-flow dry gas flowing through the circuit when not in use — this is the "Monday morning phenomenon" that produces CO from desflurane)

Replace when: ≥50% of indicator has changed colour; ETCO₂ rises unexpectedly in the circle system; more than 8–10 hours of use Never pack the granules too tightly (prevents channelling of gas flow through the absorbent) Record date of installation; use the oldest canister first from storage

The CO₂ absorbent allows the circle system to operate at FGF as low as 0.35 L/min (metabolic flow) — essentially replacing only the O₂ consumed and the agent absorbed by the patient; at metabolic flow, volatile agent consumption falls by 80–90% compared to high-flow techniques; this dramatically reduces both cost (1 mL liquid sevoflurane = approximately £1.00; saving 30 mL per hour = £30/hour) and environmental volatile agent release

Volume/Capacity Definition Normal Value Measured By Tidal Volume (TV) Volume of one normal breath at rest 500 mL (7 Spirometry mL/kg) Inspiratory Reserve Volume Maximum additional volume inhaled after normal ~3000 mL Spirometry (IRV) inspiration Expiratory Reserve Volume Maximum volume exhaled after normal expiration ~1000 mL Spirometry (ERV) Residual Volume (RV) Volume remaining after maximum forced ~1200 mL NOT by spirometry — requires helium dilution, nitrogen expiration — CANNOT be exhaled washout, or body plethysmography Functional Residual Capacity Volume in the lungs at end of normal expiration — ~2200 mL Body plethysmography or gas dilution (NOT spirometry) (FRC = ERV + RV) the "resting lung volume" Total Lung Capacity (TLC = VC Maximum volume in the lungs after maximum ~6000 mL Plethysmography or gas dilution + RV) inspiration Vital Capacity (VC = IRV + TV + Maximum volume exhaled from maximum ~4500 mL Spirometry ERV) inspiration (~70 mL/kg) FEV1 Volume exhaled in the first second of a forced >80% Spirometry (forced) expiration from TLC predicted FEV1/FVC ratio The proportion of VC exhaled in the first second ≥0.70 (70%) Spirometry; FEV1/FVC <0.70 = OBSTRUCTION by ATS/ERS definition

Normal flow-volume loop: inspiration (bottom of loop) is effort-dependent and effort-independent portions; expiration (top of loop) shows a sharp early peak (maximum flow = PEF) followed by a linear decline down to RV; the loop shape depends on lung mechanics Pattern Flow-Volume Loop Appearance Spirometry Clinical Examples Obstructive Scooped/concave expiratory curve (reduced flow at low lung FEV1/FVC <0.70; FEV1 reduced more COPD; asthma (reversibility: ≥12% + 200 mL volumes); expiratory peak flow reduced; loop is wider (↑ RV) than FVC; RV ↑ (air trapping); TLC may FEV1 increase post-bronchodilator); and shorter (↓ VC); the characteristic "shark fin" appearance be ↑ (emphysema) or normal; FVC may emphysema; bronchiectasis with concave expiratory limb be ↓ in severe COPD Restrictive Smaller loop (all volumes reduced proportionally); normal FVC ↓; FEV1 ↓ proportionally; Pulmonary fibrosis; obesity (FRC falls below shape (expiratory limb straight, not scooped); peak flow may FEV1/FVC NORMAL or ↑ (preserved closing capacity); neuromuscular disease be normal relative to lung size; loop is narrower and shorter ratio); TLC <80% predicted (definitive (diaphragm weakness); chest wall deformity but proportionally similar shape to normal criterion for restriction); RV normal or ↓ (kyphoscoliosis); pleural disease Fixed upper Both inspiratory AND expiratory flow plateaus are truncated FEV1/FVC may be normal or mildly Fixed tracheal stenosis; foreign body; airway (flattened) — a "box shape" loop; the fixed obstruction limits abnormal; the specific flattened loop subglottic stenosis; bilateral vocal cord palsy obstruction both inspiratory and expiratory flow equally shape is diagnostic Variable Expiratory flow plateau only (during expiration, positive Characteristic asymmetric flattening of Tracheomalacia; intrathoracic tracheal intrathoracic pleural pressure collapses the obstruction further → worsens expiratory limb tumour obstruction flow limitation); normal inspiratory limb Variable Inspiratory flow plateau only (during inspiration, negative Characteristic asymmetric flattening of Vocal cord dysfunction; large goitre; extrathoracic pleural pressure draws the extrathoracic obstruction inward inspiratory limb extrathoracic tracheal tumour; unilateral obstruction → worsens flow limitation); normal expiratory limb vocal cord palsy

Definition: DLCO (Diffusing capacity for carbon monoxide) measures the ability of the alveolar-capillary membrane to transfer gas from the alveolus to the blood; measured by having the patient inhale a small amount of CO (non-toxic test concentration) and measuring how much is absorbed into the blood over a period; CO is used because it binds haemoglobin with very high affinity (200× O₂) → its uptake is entirely membrane and Hb-limited, not flow-limited

Normal: 25–30 mL/min/mmHg; expressed as % predicted (normal ≥75% predicted) Clinical significance:

Reduced DLCO: emphysema (loss of alveolar-capillary surface area); pulmonary fibrosis (↑ membrane thickness); pulmonary hypertension (↓ blood volume in capillaries); pulmonary haemorrhage (competing CO binding)

Elevated DLCO: polycythaemia (more Hb available for CO binding); pulmonary haemorrhage (blood in alveoli binds CO); left-to-right cardiac shunt (increased pulmonary blood flow) DLCO is the single best preoperative predictor of postoperative pulmonary complications and mortality after lung resection — superior to FEV1 alone; ppoDLCO <40% = very high risk regardless of FEV1

Predicted postoperative values (ppo): both ppoFEV1 and ppoDLCO must be calculated and must both exceed 40% predicted for resection to proceed safely

Formula: ppoFEV1% = preop FEV1% × [1 − (segments resected / total segments)]; total segments = 19 (right lung 10, left lung 9); e.g., right lower lobectomy = 5 segments: ppoFEV1 = FEV1% × (14/19) = FEV1% × 0.74

CPET (Cardiopulmonary Exercise Test): if ppoFEV1 or ppoDLCO <30–40% → CPET for further risk stratification; VO₂max >20 mL/kg/min → low risk; 10–20 → moderate risk; <10 → very high risk (likely inoperable) 6-minute walk test: surrogate for CPET if unavailable; <400 m → high risk; predicts post-resection outcomes

Direction Boundary Structure Clinical Notes Superior Fusion of periosteal dura and spinal dura at the foramen Epidural drugs cannot spread intracranially under normal conditions; high blocks can impair (cranial) magnum; the epidural space is a closed cavity cranially cranial nerve function if drug reaches cervical cord (but not intracranial) Inferior Sacrococcygeal membrane (sacral hiatus) — the natural Caudal block: sacral hiatus between sacral cornua; typically 5 mL LA for perineal surgery; 20 (caudal) termination of the spinal canal; accessed for caudal mL for lumbar anaesthesia in adults; 1 mL/kg in children epidural blocks Anterior Posterior longitudinal ligament covering the vertebral The anterior epidural space is narrow at the midline (epidural veins concentrate (ventral) bodies and intervertebral discs anterolaterally); catheter tip may impinge on the posterior longitudinal ligament anteriorly Posterior Ligamentum flavum (flavum = yellow; elastic, dense Loss of resistance technique targets the moment the needle tip exits the ligamentum flavum (dorsal) collagenous ligament connecting adjacent laminae); and into the epidural space; LF is thickest at L3–L4 (5–6 mm) and thinnest at C1 (1–1.5 mm) the posterior surface of the vertebral arch/laminae Lateral Pedicles of the vertebral arches and the intervertebral The lateral spread through intervertebral foramina is partially limited by the dural sleeve (bilateral) foramina; drug spreads laterally through the foramina to around each nerve root; elderly patients have calcified foramina reducing lateral leakage → surround exiting nerve roots more drug confined to the epidural space → wider spread per volume

Epidural fat: the primary content; distributed in lobules throughout the space; acts as a pharmacological depot — lipophilic drugs (opioids, particularly fentanyl and sufentanil) are taken up into epidural fat; acts as a physical spacer determining available volume for drug spread; reduced in elderly (less fat → more drug spreads per unit volume) Batson's venous plexus (epidural veins): an extensive valveless venous network of large, thin-walled veins lying predominantly anterolaterally within the epidural space; drain the spinal cord and vertebral column into the azygous, hemiazygous, and vertebral veins; valveless → blood flows in any direction depending on pressure gradients; during the Valsalva manoeuvre or in pregnancy (IVC compression → elevated epidural venous pressure → engorged veins → reduced epidural space volume → wider spread of same drug volume); veins are a source of significant risk during epidural catheter placement (catheter in vein → intravascular injection of LA → LAST)

Spinal nerve roots and dural sleeves: nerve roots pass laterally from the dural sac to the intervertebral foramina surrounded by dural sleeves (extensions of the dura); these are the primary site of LA uptake and block in epidural anaesthesia; the sleeves provide a surface for drug uptake and spread along the nerve

Radicular arteries: branches of the lumbar and intercostal arteries pass through the intervertebral foramina to supply the spinal cord; vascular injection of LA → immediate LAST; adrenaline in epidural solutions causes vasoconstriction of these vessels (decreasing LA systemic absorption and increasing block duration)

Plica mediana dorsalis: an inconstant fibrous median fold at the back of the epidural space that may divide it partially into two lateral compartments; can cause asymmetric or "one-sided" epidural blocks when a catheter tip is directed into one lateral compartment

The epidural space is a POTENTIAL space (the dura is normally pressed against the ligamentum flavum by the higher pressure in the subarachnoid space); it contains a small volume of fluid between the dural surface and the surrounding structures

Negative pressure: in most adults (particularly in the thoracic region), the epidural pressure is slightly negative relative to atmospheric pressure; mechanism: the dura is normally apposed to the surrounding structure by cerebrospinal fluid pressure + small negative epidural pressure; the negative pressure was the basis for the historical "hanging drop" technique (a drop of saline in the needle hub would be aspirated into the epidural space when the needle exits the LF) — less reliable than loss of resistance but still used by some clinicians

Pressure variation: epidural pressure rises with Valsalva, coughing, straining, and in pregnancy (engorged veins transmit pressure); abdominal compression during thoracic epidural catheter placement → veins engorge → increased risk of intravascular placement at that moment

Factor Effect on Spread Magnitude Volume of ↑ Volume → ↑ spread; THE MOST IMPORTANT FACTOR; rule of thumb: 1–1.5 mL per dermatome (segment) for adults Major — predominant injectate determinant Concentration Determines motor vs sensory block intensity but NOT spread; 0.1% bupivacaine → sensory only; 0.5% → motor + Minimal effect on spread Concentration Determines motor vs sensory block intensity but NOT spread; 0.1% bupivacaine → sensory only; 0.5% → motor + Minimal effect on spread sensory Age ↑ Age → ↑ spread per volume; elderly have reduced epidural fat, calcified foramina (less lateral leakage), and reduced Major — reduce dose 30– compliance of the space; same volume spreads ~2× further in a 70-year-old vs a 20-year-old 50% in elderly Pregnancy Engorged epidural veins (from IVC compression) → reduced epidural space volume → same volume spreads further; Major — well established reduce dose 25–30% in pregnant patients clinically Height Taller patients have larger epidural space → slightly less spread per volume; clinical effect modest Minor Weight/Obesity ↑ Intra-abdominal pressure → engorged epidural veins → reduced volume → wider spread; similar to pregnancy effect Moderate Site of Thoracic epidural spreads more cephalad than caudad from the injection point; lumbar epidural spreads more bilaterally Moderate — influences injection choice of insertion level Speed of Faster injection → slightly more turbulence → slightly wider spread; effect modest in clinical practice Minor injection Position of Gravity has modest effects on epidural drug spread (less than in spinal); lateral position → slightly more dependent side Minor for epidural (vs patient block; sitting position → sacral block more reliable major for spinal)

Dural puncture → CSF leak through the dural defect into the epidural space (at approximately 0.1–0.2 mL/min) → CSF volume in the subarachnoid space decreases → CSF pressure falls → the buoyant support of the brain in CSF is reduced → the brain descends slightly with gravity when upright → traction on pain-sensitive structures (the meningeal blood vessels, cranial nerves — particularly the trigeminal nerve = frontal/temporal headache, and the vagus and glossopharyngeal nerves = nausea and vomiting) → postural headache

The two mechanisms: (1) direct traction on pain-sensitive structures from CSF hypotension; (2) reflex cerebral vasodilation (adenosine-mediated) compensatory to the CSF loss — additional vascular headache component; the cerebral vasodilation component explains why caffeine (vasoconstrictor) provides partial temporary relief

IIH (intracranial pressure reduction): CSF pressure may fall from normal 10–15 cmH₂O to <5 cmH₂O; measured as "low opening pressure" on lumbar puncture

Risk Factor Effect Needle gauge Smaller gauge → smaller dural defect → less CSF leak → lower PDPH risk; 25G Whitacre: 1–2% PDPH; 22G Quincke: 25–30% PDPH; 16G

Tuohy (accidental ADP): 70–80% PDPH Needle type/design Pencil-point (Whitacre/Sprotte — separates rather than cuts dural fibres): much lower PDPH rate than cutting (Quincke); for equivalent gauge, pencil-point has 5× lower PDPH rate

Quincke bevel Bevel parallel to dural longitudinal fibres: lower PDPH rate (smaller functional defect); perpendicular: higher rate orientation

Age Young patients (especially obstetric population): high PDPH risk; elderly: lower risk (reduced CSF pressure and flow; more compliant meninges)

Gender Female: higher risk than male (hormonal differences and obstetric population); pregnancy further increases risk Previous PDPH Strong risk factor for recurrence — may reflect individual susceptibility in dural compliance Diagnostic criteria (IHS — International Headache Society): headache that develops within 5 days of dural puncture; worsens within 15 minutes of sitting/standing and resolves (or improves significantly) within 15 minutes of lying flat; accompanied by at least one of: neck stiffness, tinnitus, hypacusis, photophobia, nausea

Severity grades: mild (tolerated; no limitation of daily activities); moderate (limits daily activities; patient confined to bed part of the time); severe (complete bed rest; unable to ambulate); very severe (cranial nerve palsies — 6th nerve palsy from traction most common → diplopia)

Bed rest: lying flat relieves the headache by reversing the gravitational traction; but strict bed rest does NOT reduce the rate of EBP requirement or speed recovery — provide for comfort only

Analgesics: paracetamol 1 g QID; NSAIDs (ibuprofen 400 mg TID); simple analgesics for symptomatic relief while awaiting natural dural sealing

IV/oral hydration: adequate hydration supports CSF production; no evidence that supernormal hydration accelerates recovery

Caffeine: caffeine sodium benzoate 500 mg oral or IV; causes cerebral vasoconstriction (adenosine antagonist) → reduces the vascular component of PDPH → temporary partial relief (12–24 hours); does NOT seal the dural hole; approximately 70% of patients report temporary improvement; reassess at 24 hours — if still symptomatic, EBP should be discussed

ACTH/Cosyntropin: ACTH 1.5 IU/kg IV once → stimulates adrenal cortisol production → increases CSF production (aldosterone effect on choroid plexus); some trials showing modest benefit; not widely used

Sumatriptan: some evidence in case reports; not standard treatment

Reassurance: PDPH naturally resolves in most patients within 7–14 days as the dural hole heals; 85% of patients improve without EBP if managed conservatively for 14 days

Site of action: mu-opioid receptors (MOR) in the substantia gelatinosa (laminae I and II) of the dorsal horn; PRESYNAPTIC: opioid binds MOR on C/Aδ fibre terminals → ↓ Ca²⁺ influx → ↓ release of substance P, glutamate, CGRP → reduced nociceptive transmission; POSTSYNAPTIC: ↑ K⁺ conductance → hyperpolarisation → reduced responsiveness to nociceptive input The dual mechanism provides potent, segmental analgesia without affecting motor, sympathetic, or non-pain sensory modalities — the key clinical advantage over LA agents

Property Fentanyl (lipophilic, log P 4.05) Morphine (hydrophilic, log P 0.9) Onset 5–15 minutes (rapidly absorbed into spinal cord 30–60 minutes (slow diffusion through aqueous CSF) lipid) Duration 2–4 hours (rapid redistribution out of cord) 12–24 hours (persists in CSF; slow clearance)

CSF spread Minimal — absorbed before spreading rostrally Extensive — remains in CSF → bulk flow cephalad to brainstem

Delayed respiratory Minimal — early (0–4h) from systemic absorption HIGH RISK at 6–24 hours — morphine accumulates near respiratory centre in depression only medulla

Systemic vascular uptake High — much of epidural fentanyl is systemic, not Low — primarily spinal mechanism spinal IT dose (adult) 20–25 mcg added to spinal LA 100–300 mcg (100–150 mcg for CS; up to 300 mcg for major surgery) Epidural dose 50–100 mcg bolus; 2–4 mcg/mL infusion 2–4 mg epidural; 0.05–0.1 mg/mL infusion

Scenario Recommended Drug Dose Benefit Caesarean section Morphine 100–150 mcg + Fentanyl Added to hyperbaric bupivacaine 2 mL Morphine: 12–24h post-CS analgesia; Fentanyl: augments — IT 20–25 mcg intraoperative block quality Major orthopaedic Morphine 200–300 mcg Added to spinal LA 18–24h postoperative analgesia; reduces opioid surgery — IT requirements

Labour analgesia — Fentanyl 2 mcg/mL in dilute LA Bupivacaine 0.0625–0.1% + fentanyl 2 Walking epidural; dense block without motor impairment epidural mcg/mL at 5–10 mL/hr Post-thoracotomy — Fentanyl or sufentanil 0.5 mcg/mL in 5–8 mL/hr thoracic epidural infusion Facilitates extubation; reduces PPCs epidural ropivacaine 0.2%

Mechanism: morphine slowly migrates cephalad in CSF via bulk flow over 6–12 hours → reaches the fourth ventricle near the pre-Bötzinger complex (respiratory rhythm generator) → mu-receptor activation → ↓ respiratory drive → progressive hypoventilation → hypoxia

Risk factors: IT morphine >300 mcg; co-administered systemic opioids/sedatives; elderly; obesity/OSA; poor respiratory reserve

Mandatory monitoring: hourly RR and sedation score for 24 hours; SpO₂ monitoring; supplemental O₂ available; naloxone at bedside; monitored ward (HDU level)

Treatment: RR <8 or SpO₂ <90%: naloxone 0.04–0.4 mg IV titrated (start 0.04 mg increments to preserve analgesia); then naloxone infusion 2–5 mcg/kg/hr (morphine duration exceeds naloxone t½ of 45–90 min → re-narcotisation without infusion)

Pruritus: 50–100% incidence with IT morphine; direct MOR activation in trigeminal nucleus → facial and truncal itch; treat: ondansetron 4 mg IV (5-HT3 antagonism), nalbuphine 5–10 mg IV, or low-dose naloxone 0.04 mg IV

PONV: 20–40%; multimodal prophylaxis; ondansetron at emergence

Urinary retention: sacral MOR activation → detrusor relaxation; catheterise if symptomatic

At the supraclavicular level, the brachial plexus roots C5–T1 have formed into three TRUNKS: superior (C5–C6), middle (C7), inferior (C8–T1); they lie compactly as a cluster posterolateral to the subclavian artery, above the first rib, deep to the clavicle

Sonoanatomy: high-frequency linear probe (10–15 MHz) in the supraclavicular fossa, coronal oblique plane; the subclavian artery appears as a large pulsatile anechoic circle; the brachial plexus trunks appear as a "bunch of grapes" — hypoechoic cluster — posterolateral to the artery; the first rib is a bright hyperechoic line with acoustic shadow deep to the plexus; pleura visible just deep to the first rib The "corner pocket": the zone at the corner between the lateral border of the subclavian artery and the superior surface of the first rib; the inferior trunk (C8– T1 → ulnar nerve) sits specifically here; targeted injection in this corner ensures complete block of all three trunks including the ulnar nerve territory — the most commonly missed nerve with supraclavicular techniques

1. Patient supine, head turned 45° away; high-frequency probe in supraclavicular fossa; coronal oblique plane 2. In-plane needle approach lateral to medial; 22G 50 mm needle; advance toward the corner pocket first (lateral subclavian artery border + first rib superior surface) 3. Hydrolocation: 1–2 mL saline to confirm tip position (fluid surrounds inferior trunk in the corner; if fluid goes deep to first rib → withdraw — pleural puncture risk) 4. Inject 5–10 mL LA into the corner pocket (inferior trunk coverage); then reposition needle superiorly and inject 15–20 mL more to cover superior and middle trunks; total 20–30 mL 0.375% ropivacaine or 0.25% bupivacaine

Complication Incidence Mechanism Management Pneumothorax 4% landmark; <0.5% Pleura is immediately deep to the first rib — the deep margin of Small (<15%) — O₂ + observation; Large (>15%) or ultrasound-guided the injection target; needle past first rib → pleural puncture → symptomatic → chest drain; CXR if any respiratory delayed pneumothorax (may present 1–6 hours post-block) symptoms develop post-block Phrenic nerve 40–60% standard Phrenic nerve lies on the anterior scalene adjacent to the Clinically inconsequential with normal contralateral palsy volumes; 20–30% brachial plexus; LA spreads medially → baths the phrenic function; CONTRAINDICATED if: contralateral phrenic with reduced volumes nerve → ipsilateral hemidiaphragm paralysis → ↓ FVC 25% palsy, contralateral pneumonectomy, severe COPD (FEV1 (5–10 mL) <50%) Horner's 1–4% Stellate ganglion (T1 sympathetic) adjacent to plexus; LA Benign and self-limiting; reassure patient (warn them Syndrome spreads medially → sympathetic chain block → ipsilateral preoperatively) ptosis, miosis, anhidrosis LAST <1% with US Large LA volume adjacent to subclavian artery; intravascular Incremental injection with aspiration every 5 mL; LAST guidance injection protocol

Best for: surgery from the elbow to the hand; forearm fractures; wrist/hand surgery; more reliable than axillary block for elbow procedures (musculocutaneous nerve reliably blocked at this level); more reliable ulnar coverage than interscalene (with corner pocket technique)

Compared to interscalene: supraclavicular has less phrenic nerve palsy risk (though still 20–30%); better ulnar nerve coverage; less good for true shoulder surgery (interscalene preferred) Intercostobrachial nerve NOT covered (medial upper arm skin from T2); supplement with subcutaneous ring injection if medial arm tourniquet is planned

The interscalene groove lies between the anterior scalene muscle (anteriorly) and the middle scalene muscle (posteriorly); the brachial plexus roots C5, C6, and C7 exit the intervertebral foramina and enter this groove at approximately the C6 level (cricoid cartilage level)

Sonoanatomy — "traffic light sign": high-frequency linear probe transversely at C6 level; the three roots C5, C6, C7 appear as three hypoechoic oval structures stacked between the anterior and middle scalene muscles — resembling traffic lights; the vertebral artery is deep (anteromedial) and must be identified and avoided; the internal jugular vein and carotid artery are medial

Critical relation: the phrenic nerve (C3–C4–C5) lies directly on the ANTERIOR SURFACE of the anterior scalene at this level; any injection sufficient to block C5–C6 roots simultaneously bathes the adjacent phrenic nerve

The phrenic nerve forms from C3–C4–C5 roots and descends on the anterior surface of the anterior scalene muscle; at the C5–C6 interscalene level, the phrenic nerve is anatomically inseparable from the brachial plexus injection target — it lies on the muscle surface directly adjacent to the C5–C6 roots Any volume of LA sufficient to block C5–C6 (the primary targets) inevitably spreads anteriorly to the phrenic nerve; Urmey (Anesth Analg 1991) demonstrated by hemidiaphragm ultrasound that 100% of patients have ipsilateral hemidiaphragm paralysis after interscalene block regardless of technique or volume

Clinical consequence: ipsilateral hemidiaphragm paralysis → ↓ FVC ~25%; well tolerated in patients with normal contralateral function; catastrophic if contralateral reserve is limited

Contralateral phrenic nerve palsy (bilateral phrenic palsy → complete diaphragm paralysis → respiratory failure) Contralateral pneumonectomy (single functioning lung → loss of ipsilateral hemidiaphragm → severe compromise) Severe COPD (FEV1 <50% predicted) where 25% FVC reduction would cause respiratory failure Contralateral vocal cord paralysis (combined impairment) Local infection; coagulopathy; patient refusal

Procedure Block Role Total shoulder arthroplasty (TSA), Gold standard; complete shoulder anaesthesia; continuous catheter for 48–72h dramatically reduces opioid use and reverse TSA improves rehabilitation Shoulder arthroscopy (rotator cuff, Single-shot + GA or sedation; 6–12h post-op analgesia; beach chair positioning requires careful MAP management labrum) Clavicle fracture fixation May need supplemental superficial cervical plexus block (C3–C4) for medial clavicle skin not covered by brachial plexus Proximal humerus fractures Excellent coverage; continuous catheter; reduces pain and aids physiotherapy

Complication Mechanism / Management Horner's syndrome (1– Stellate ganglion (T1 sympathetic) adjacent → LA spread → ipsilateral ptosis, miosis, anhidrosis; benign, self-limiting; warn patient 4%) preoperatively Recurrent laryngeal Hoarseness and voice change; avoid bilateral interscalene in singers/voice professionals; self-limiting nerve palsy

Vertebral artery Catastrophic — even 1 mL IV → cerebral circulation → immediate seizure; deep anteromedial vessel; identify on ultrasound before needle injection insertion; always aspirate before injecting Spinal / epidural Needle through intervertebral foramen → intrathecal space → high or total spinal at cervical level → immediate respiratory arrest; use US injection guidance and advance cautiously; always aspirate

Boundaries: superior (inguinal ligament), lateral (sartorius), medial (adductor longus); floor: iliopsoas laterally + pectineus medially

Contents lateral to medial — NAVY: Nerve (femoral nerve), Artery (femoral artery), Vein (femoral vein), Y-fronts (lymphatics/lymph nodes) Femoral nerve (L2–L4) lies just lateral and slightly deep to the femoral artery; divides immediately below the inguinal ligament into anterior division (purely sensory — medial and intermediate cutaneous nerves of the thigh) and posterior division (saphenous nerve + motor branches to all four quadriceps heads)

A fascial tunnel in the middle third of the thigh; boundaries: roof = sartorius; lateral wall = vastus medialis; posteromedial wall = adductor longus then adductor magnus

Contents: saphenous nerve (PURELY SENSORY at this level — all motor branches to quadriceps have already branched off proximal to the canal); femoral artery; femoral vein; descending genicular artery

Key concept: the motor branches to the quadriceps (rectus femoris, vastus lateralis, vastus intermedius, vastus medialis) ALL originate within the femoral triangle or proximal thigh — ABOVE the adductor canal; the saphenous nerve within the canal is exclusively sensory

Feature Femoral Nerve Block (FNB) Adductor Canal Block (ACB) Target Entire femoral nerve in femoral triangle (motor + sensory Saphenous nerve within the adductor canal (sensory only at this level) branches)

Quadriceps motor COMPLETE — all four quadriceps heads paralysed; patient PRESERVED — motor branches all originate proximal to the canal; block cannot extend knee → cannot weight-bear safely completely unaffected Analgesia quality Excellent anterior knee; partial posterior knee Equivalent anterior and medial knee (same saphenous nerve territory); with for TKR IPACK for posterior → comprehensive coverage

Falls risk High — quadriceps weakness → falls documented in multiple Very low — normal quadriceps strength maintained studies Rehabilitation Delayed until block resolves (12–18h); physiotherapy postponed Day 1 physiotherapy achievable; reduces hospital LOS by ~1 day PROSPECT 2022 NOT recommended (motor weakness/falls) RECOMMENDED as primary block for TKR + IPACK for posterior knee recommendation

ACB technique: supine with thigh externally rotated; high-frequency probe at mid-thigh level; identify sartorius (superficial, triangular shape), femoral artery; saphenous nerve appears as a small hyperechoic oval adjacent to the artery within the fascial compartment; inject 15–20 mL 0.25–0.375% ropivacaine or 0.25% bupivacaine; visualise spread within the canal on ultrasound IPACK block (Infiltration between Popliteal Artery and Capsule of the Knee): complements ACB by covering the posterior knee capsule — popliteal branches of the sciatic, obturator, and genicular nerves; 15–20 mL LA injected posterior to the knee between the capsule and popliteal artery; performed at end of surgery under ultrasound or arthroscopically

Fascia Iliaca Block: large volume (40 mL) deep to fascia iliaca → spreads to femoral nerve, LFCN, sometimes obturator; landmark technique; used for hip fracture analgesia in ED by non-anaesthesiologists; less reliable for surgical anaesthesia

When the femoral nerve enters the femoral triangle below the inguinal ligament, its posterior division immediately starts giving off motor branches to the quadriceps: nerve to rectus femoris, nerve to vastus lateralis, nerve to vastus intermedius, and nerve to vastus medialis — ALL of these motor branches originate within the femoral triangle (above or at the level of the inguinal ligament); by the time the saphenous nerve (the sensory continuation of the posterior femoral nerve division) reaches the adductor canal, it has already lost ALL its motor branches and is purely sensory; therefore, an ACB at mid-thigh level blocks ONLY sensory afferents without any motor component

System ESRD Effect Clinical Action Cardiovascular Hypertension (80%); LVH; accelerated atherosclerosis; Pre-op echo (LV function); ECG; arterial line; careful fluid management; avoid rapid uraemic cardiomyopathy; pericardial effusion; arrhythmias boluses in diastolic dysfunction (hyperkalaemia, hypomagnesaemia) Haematological Normochromic normocytic anaemia (↓EPO); uraemic Pre-op: EPO + iron; target Hb ≥80–90 g/L; DDAVP 0.3 mcg/kg IV pre-op (releases vWF platelet dysfunction; thrombocytopenia (hypersplenism) → improves platelet adhesion); AVOID NSAIDs (worsen platelet dysfunction) Electrolytes Hyperkalaemia (K⁺ 5.5–7.5 mEq/L common); metabolic Check K⁺ DAY OF SURGERY; K⁺ >6.0 → postpone → emergency dialysis; AVOID acidosis; hypocalcaemia; hyperphosphataemia Hartmann's/Ringer's Lactate (contains K⁺ 4 mEq/L — FATAL in hyperkalaemic ESRD); use 0.9% NaCl ONLY; ECG monitoring throughout Fluid/Volume Fluid overloaded or depleted depending on dialysis; most Compare with dry weight; cautious fluid administration; echo for volume assessment patients should be dialysed 12–24h before elective surgery

Drug Problem in ESRD Recommendation Morphine Morphine-6-glucuronide (M6G — active, renally cleared) accumulates → prolonged sedation AVOID morphine in ESRD; use fentanyl (hepatic and respiratory depression → inactive metabolites; safe) Fentanyl Hepatic metabolism to inactive norfentanyl; no renally-cleared active metabolites Safe — preferred opioid in ESRD; dose as normal with careful monitoring Succinylcholine K⁺ release 0.5–1.0 mEq/L → cardiac arrest if baseline K⁺ ≥5.5 mEq/L; also reduced AVOID if K⁺ >5.5 mEq/L; use rocuronium 1.2 pseudocholinesterase in severe uraemia mg/kg + sugammadex 16 mg/kg for CICO Atracurium / Organ-independent Hofmann elimination (pH/temperature-dependent chemical degradation) + PREFERRED NMBs in ESRD; cisatracurium

Cisatracurium ester hydrolysis — NOT renally cleared; predictable duration regardless of renal function preferred (3× more potent; less laudanosine production) Vecuronium 3-desacetyl-vecuronium (active metabolite) renally cleared → accumulates → prolonged block Avoid; if used, reduce doses and monitor TOF carefully Rocuronium Primarily hepatic elimination; some renal excretion; t½ modestly prolonged Generally safe with TOF monitoring; sugammadex reversal preferred for reliability NSAIDs COX inhibition → ↓ renal prostaglandins → ↓ GFR further; worsens uraemic platelet ABSOLUTELY AVOID ALL NSAIDs in ESRD; use dysfunction; risk of AKI paracetamol for baseline analgesia Midazolam 1-hydroxymidazolam glucuronide (active, renally cleared) accumulates → prolonged sedation Use cautiously; reduce dose; prefer shorter-acting alternatives for ICU sedation

Laudanosine is a byproduct of atracurium Hofmann elimination; a tertiary amine that crosses the BBB; CNS stimulant/potentially epileptogenic at high concentrations in animals; in humans, clinical doses of atracurium/cisatracurium produce laudanosine concentrations well below toxic thresholds; cisatracurium produces ~3× less laudanosine than atracurium per equivalent NMB dose (because it is more potent and lower doses are used) Clinically safe at recommended doses even in ESRD; prefer cisatracurium for prolonged ICU infusions in ESRD

AV Fistula — absolute rules: NO BP cuff on fistula arm; NO IV cannula in fistula arm; NO arterial line in fistula arm; clearly label the fistula arm; pad to avoid positional compression; check for bruit/thrill pre- and post-operatively

Dialysis timing: perform dialysis 12–24 hours before elective surgery to normalise K⁺ (<5.5 mEq/L), optimise volume status (reach dry weight), and correct metabolic acidosis; avoid dialysis immediately before surgery (post-dialysis hypotension from volume depletion; heparin effect — withhold 4–6 hours)

Regional anaesthesia advantage: avoids systemic drugs with renally-altered kinetics; superior analgesia without NSAIDs; neuraxial is safe if platelet count and coagulation acceptable; check platelet count and recent coag profile in uraemic patients before neuraxial

Parameter 1 Point 2 Points 3 Points Encephalopathy None Grade 1–2 Grade 3–4 Ascites Absent Mild Moderate-severe Bilirubin (μmol/L) <34 34–51 >51 Albumin (g/L) >35 28–35 <28 Prothrombin time (sec prolonged) <4 4–6 >6 Child-Pugh A (5–6 pts): 30-day surgical mortality ~10%; Child-Pugh B (7–9 pts): ~30%; Child-Pugh C (10–15 pts): ~76–82% — elective surgery generally contraindicated

MELD score: = 3.78 × ln(bilirubin mg/dL) + 11.2 × ln(INR) + 9.57 × ln(creatinine mg/dL) + 6.43; MELD <10 low risk; >15 high risk; >20 very high; >25 ≈50% mortality for major surgery; superior to Child-Pugh for predicting 90-day surgical mortality

Derangement Mechanism Clinical Implication

Coagulopathy — ↓ synthesis of procoagulant factors (II, V, VII, IX, X) INR is unreliable for predicting bleeding risk in liver disease (rebalanced "rebalanced AND anticoagulant factors (Protein C, S, antithrombin); haemostasis — some patients with high INR bleed little; some with "normal" INR bleed haemostasis" thrombocytopenia (hypersplenism); primary fibrinolysis; massively from portal hypertension); use TEG/ROTEM (measures the full clot formation the INR ONLY measures procoagulant factor and fibrinolysis process in whole blood at physiological conditions); TEG-guided blood deficiency — misses the simultaneous anticoagulant product administration uses significantly less product than INR-guided with equivalent factor reduction haemostasis Hepatic Ammonia + gut-derived neuroactive substances + AVOID benzodiazepines (exquisite sensitivity; precipitates or worsens encephalopathy); encephalopathy astrocyte failure; GABA receptor dysfunction; cerebral avoid opioids where possible; lactulose pre-operatively; maintain haemodynamic stability oedema in acute liver failure (encephalopathy worsens with hypotension) Hyperdynamic Portal hypertension → ↑ NO/prostacyclin → splanchnic AVOID NSAIDs absolutely; maintain MAP ≥65 mmHg (vasopressors not fluids in fluidcirculation + vasodilation → low SVR, high CO; reduced effective overloaded cirrhosis); careful fluid balance; avoid hepatotoxic drugs and contrast without hepatorenal risk circulating volume despite high CO; renal adequate prehydration; HRS type 1 (acute renal failure) → terlipressin + albumin vasoconstriction → HRS risk from: NSAIDs, nephrotoxins, hypotension, paracentesis without albumin Hepatopulmonary Intrapulmonary vascular dilatation → arteriovenous Pre-op SpO₂ and ABG; supplemental O₂; echo to exclude portopulmonary hypertension syndrome shunting → hypoxaemia worsening on standing (PAP >35 mmHg) (orthodeoxia)

Drug Effect Recommendation Benzodiazepines Hepatic metabolism to active metabolites; prolonged t½; enhanced CNS AVOID in liver disease; can precipitate or worsen hepatic sensitivity in encephalopathy encephalopathy

Opioids Morphine: hepatic glucuronidation (relatively preserved) but M6G clearance Titrate carefully; prefer remifentanil (ester hydrolysis — organreduced; fentanyl: prolonged t½ with reduced clearance and protein binding independent, safe in liver failure); avoid high doses Atracurium / Hofmann elimination — organ-independent; safe in liver failure; duration First-choice NMBs in liver disease Cisatracurium NOT prolonged Rocuronium, Hepatic elimination → prolonged duration in severe liver disease (Vd Use cautiously; reduce repeat doses; TOF monitoring; sugammadex Vecuronium increases with ascites) for reversal Volatile agents Halothane → immune-mediated hepatic necrosis (20% subclinical hepatitis; AVOID halothane; sevoflurane preferred — least hepatotoxic volatile; — halothane rare fulminant failure) maintain hepatic blood flow (avoid hypotension and deep anaesthesia) Propofol Hepatic + extrahepatic metabolism; moderately reduced clearance; ↑ free Safe but reduce induction dose; titrate carefully; BIS monitoring during fraction (↓ albumin) TIVA

Child-Pugh A → acceptable risk for most elective surgery; Child-Pugh B → 30% mortality; careful MDT review, optimise first; Child-Pugh C → generally contraindicated for elective surgery; only life-saving surgery; consider liver transplantation evaluation Sugammadex preferred over neostigmine for NMB reversal in liver disease (neostigmine metabolised hepatically; unpredictable in severe disease; sugammadex reversal organ-independent)

Surgical stress → ↑ cortisol, catecholamines, glucagon, growth hormone → all counter-regulatory (hyperglycaemic) → ↑ hepatic glucose production + ↑ insulin resistance; in T1DM the compensatory pancreatic response is absent → uncontrolled hyperglycaemia

Consequences of perioperative hyperglycaemia: SSI rate ↑ 2–3× for each 1 mmol/L above 10 mmol/L; ↓ neutrophil function; ↓ wound collagen synthesis; osmotic diuresis above 15–20 mmol/L; risk of HHS or DKA

Assessment Action HbA1c HbA1c ≥69 mmol/mol (8.5%) → POSTPONE elective surgery; refer diabetes team for optimisation; HbA1c 53–69 → proceed with caution + enhanced monitoring; HbA1c <53 (<7%) → well-controlled, proceed as planned Diabetic Autonomic neuropathy (↓ cardiovascular reflexes → orthostatic hypotension, silent MI, impaired tachycardia response to hypovolaemia); renal function complications (eGFR affects drug dosing); peripheral neuropathy (pre-existing deficit — document before regional anaesthesia)

Drug Morning of Surgery Rationale Metformin OMIT day of surgery Metformin + perioperative hypoperfusion → lactic acidosis; resume when eating and renal function confirmed (and 48h before contrast/major surgery) SGLT2 inhibitors OMIT ≥24–72 hours SGLT2i → euglycaemic DKA risk: blocks glucose reabsorption → glucosuria → shifts metabolism to fat → (empagliflozin, before surgery ketogenesis ↑; fasting + surgical stress + SGLT2i = DKA despite NORMAL blood glucose; check betadapagliflozin, hydroxybutyrate (ketones) if SGLT2i taken within 72h + acidosis present canagliflozin) Sulphonylureas OMIT morning dose Risk of hypoglycaemia; long half-life; check glucose hourly throughout day (gliclazide, glibenclamide) Long-acting insulin Give 80% of normal Do NOT omit completely in T1DM — always needs basal insulin to prevent ketogenesis; 80% reduces (glargine, detemir) dose the night before hyperglycaemia without hypoglycaemia risk Short/rapid-acting OMIT morning dose Only give prandial insulin when eating; if VRIII started → short-acting not separately required insulin

Hypoglycaemia (<4 mmol/L): STOP VRIII; 150–200 mL 10% dextrose IV over 15 min; recheck at 15 min; once >6 mmol/L → restart VRIII at lower rate; do NOT stop basal insulin in T1DM (stops it → risks DKA)

DKA recognition: glucose >11 mmol/L (OR normal glucose if on SGLT2i = euglycaemic DKA) + ketones >3 mmol/L + pH <7.3, HCO₃⁻ <18 → start DKA protocol: fixed rate insulin 0.1 units/kg/hr + IV fluids + K⁺ replacement + hourly monitoring + endocrinology/diabetes team

Criterion Eligible Requires Overnight Admission ASA ASA I, II; selected well-optimised ASA III ASA IV; unstable ASA III; recent decompensation BMI BMI up to 35–40; BADS 2019: BMI alone should NOT exclude patients; assess BMI >40 with severe OSA + major surgery; obesity individually hypoventilation syndrome OSA Mild-moderate OSA on CPAP + minor surgery; brings own CPAP device Severe OSA (AHI >30) with opioid requirement post-op Social Responsible adult to drive home and stay 24h; within 60–90 min of hospital; telephone Lives alone; remote from medical care; unable to understand access; able to follow instructions discharge instructions Procedure Expected duration <3 hours; pain controllable with oral analgesia; manageable blood loss Major surgery; significant expected blood loss; complex wound management

Element Day-Surgery Recommendation Rationale Induction Propofol 2–2.5 mg/kg IV — preferred Antiemetic properties; pleasant emergence; faster return to street fitness vs thiopentone Maintenance Propofol TIVA (propofol + remifentanil TCI) OR sevoflurane; TIVA TIVA: lower PONV (propofol antiemetic); no volatile emissions; sevoflurane preferred for Apfel ≥3 suitable for shorter cases; desflurane: fastest recovery for long cases but environmental concerns NMB Short-acting NMBs; sugammadex reversal (faster and more reliable than Residual NMB delays discharge; neostigmine → nausea adds to PONV neostigmine); ideally avoid NMB (LMA + spontaneous breathing for burden suitable cases) Analgesia Regional where possible; paracetamol 1 g IV at induction + ketorolac 15 Opioids → PONV + sedation at home → most common cause of failed day mg IV; wound infiltration bupivacaine 0.25%; prescribe 3–5 days surgery; adequate multimodal analgesia enables discharge paracetamol + NSAID for home PONV Minimum 2 antiemetics for Apfel ≥2: ondansetron 4 mg at end + PONV is #1 cause of unplanned admission; every Apfel point = +20% risk; prophylaxis dexamethasone 4–8 mg at induction; consider TIVA for Apfel ≥3; maximum prevention is cost-effective prescribe rescue antiemetics for home Airway LMA preferred over ETT where safe — reduces sore throat, coughing, Smooth emergence without coughing prevents PONV and cardiovascular laryngospasm; i-gel or ProSeal for controlled ventilation stress; less stimulating extubation with LMA

Parameter Score 2 Score 1 Score 0 Vital signs ≤20% change from pre-op baseline 20–40% change >40% change Ambulation Steady gait; no dizziness Requires assistance Unable to ambulate Nausea/Vomiting Minimal; oral treatment sufficient Moderate; parenteral medication needed Severe; continues despite treatment Pain Minimal; controlled with oral analgesics; acceptable to patient Moderate; requires parenteral analgesia Severe; not controlled Surgical bleeding Minimal; no dressing change Moderate; 1–2 dressing changes Severe; >2 dressing changes

Discharge criterion: PADSS ≥9 out of 10 required; developed and validated by Chung et al. (J Clin Anesth 1995) specifically for ambulatory surgery

PONV (35–40% of failures): most common; prevent with Apfel-stratified multimodal prophylaxis; prescribe rescue antiemetics for home; discharge only when PONV PADSS score ≥1 Inadequate pain control (25–30%): pain too severe for home management; multimodal analgesia pre-discharge; VAS ≤3/10 at discharge; written pain management plan; adequate take-home analgesia

Surgical complications: haemorrhage requiring return to theatre; urinary retention (particularly after spinal with opioids — ensure void before discharge); wound concerns

Residual anaesthetic effects: prolonged sedation, dizziness, residual NMB; avoid long-acting benzodiazepines; quantitative NMB monitoring

Stage When Leader Key Items Sign Before anaesthesia induction Anaesthesiologist 1. Patient identity confirmed verbally (name + DOB against wristband + In notes) 2. Procedure and site confirmed (including marking) 3. Consent signed and present 4. Pulse oximeter functioning and applied 5. Known allergy? → state allergen 6. Difficult airway/aspiration risk? → equipment ready 7. Blood loss risk ≥500 mL? → IV access, cross-match, blood products ordered Time Before surgical incision (patient draped, all Surgeon or team leader; any 1. All team members introduce themselves and roles Out team assembled) member may initiate 2. Surgeon + anaesthesiologist + nurse verbally confirm: patient name, procedure, site 3. Surgeon: anticipated critical steps, expected duration and blood loss 4. Anaesthesiologist: patient-specific concerns (allergy, airway, cardiac risk) 5. Nursing team: equipment sterility confirmed, essential equipment available 6. Antibiotic prophylaxis given within 60 min of incision if required 7. Imaging confirmed displayed and correct patient Sign Before patient leaves the operating room Nursing team (scrub/circulating) 1. Procedure recorded by name Out 2. Instrument, sponge, and needle count completed and documented 3. Specimen labelling confirmed (patient name, DOB, procedure, surgeon on label) 4. Equipment problems to address 5. Key concerns for recovery: surgeon and anaesthesiologist verbally handover to recovery team

Haynes AB et al. (NEJM 2009): 8 hospitals, 8 countries, n=7,688 surgical patients; WHO SSC reduced: overall complications 11.0% → 7.0% (36% relative reduction); in-hospital mortality 1.5% → 0.8% (47% reduction); SSI 6.2% → 3.4% (45% reduction); benefit was significant in all income settings de Vries EN et al. (Lancet 2010): SURPASS trial, Netherlands; 11-step checklist across multiple perioperative time points; complications 15.4% → 10.6%; mortality 1.5% → 0.8% — independently confirmed Haynes findings

Implementation challenges: despite strong evidence, compliance <50% in many audits; primary barriers: tick-box exercise without engagement; time pressure (OR schedule); hierarchical culture (junior reluctant to pause senior surgeon); checklist fatigue

Aviation research and human factors science (Reason — Swiss cheese model, 1990): most high-consequence errors occur from team communication breakdowns, not individual failures; the SSC embeds structured communication into the surgical routine

TeamSTEPPS core strategies: SBAR (Situation-Background-Assessment-Recommendation) for structured handover; closed-loop communication (receiver explicitly confirms the message); call-out and check-back; the Time Out team introduction step specifically breaks down hierarchical barriers and creates a culture where any team member can halt the procedure

Challenging authority: the SSC gives every team member — including the most junior nurse — specific authorisation to raise a safety concern; the ABCDE framework for challenging decisions: Assert concern clearly; call Supervisor; call Expert help; Explain to the team; Document concerns

Leads the Sign In — the most complex section, requiring knowledge of both the patient's medical history and the anaesthetic plan; confirms all anaestheticspecific safety items (allergy, airway, aspiration, blood loss risk) Contributes specific expertise at all three pause points; at Time Out: states patient-specific anaesthetic concerns: "this patient is allergic to penicillin — please ensure a non-penicillin antibiotic is used"; "this patient has known difficult airway — video laryngoscope is in the room"; "this patient is on anticoagulation — the surgeon should anticipate increased bleeding" Has a duty to halt the procedure if the checklist reveals an unresolved safety concern — patient identity discrepancy, unsigned consent, absent blood crossmatch in a high-blood-loss case, unavailable specialised equipment; escalate through the chain of command if the initial concern is dismissed

Air enters a venous sinus or vessel held open by surrounding anatomy (bone, surgical retractors, tethered dura) where the venous pressure is below atmospheric → negative pressure gradient drives air into the venous system → right atrium → right ventricle → pulmonary vasculature

Air-lock mechanism: large amounts (2–5 mL/kg at rapid rate) → air accumulates in the right ventricle → impedes RV ejection → acute cor pulmonale → ↓ CO → cardiovascular collapse; simultaneously pulmonary arteriolar obstruction → ↑ dead space → rising then falling ETCO₂ as cardiac output falls

Paradoxical air embolism (PAE): patent foramen ovale (PFO — present in 25–30% of population) → right atrial pressure elevated by VAE → reverses atrial pressure gradient → air crosses PFO from right to left atrium → systemic arterial circulation → coronary artery (MI) or cerebral (stroke, seizures) air embolism; PAE can occur even with relatively small VAE amounts

Monitor Sensitivity Details

Transoesophageal Most sensitive: Visualises air bubbles directly in right atrium and ventricle; detects paradoxical embolism across PFO; impractical for echo (TOE) detects 0.01–0.02 routine use — requires expertise, limits positioning mL/kg

Precordial Very sensitive: Placed over the right precordium (right sternal border, 2nd–4th ICS); characteristic churning "mill-wheel" quality change in Doppler detects 0.05–0.1 Doppler signal; STANDARD MONITOR for sitting-position neurosurgery; non-invasive; cannot quantify volume mL/kg

ETCO₂ Moderate: detects Initially ↑ CO₂ then ↓ as CO falls; non-specific; part of routine monitoring; the first bedside indicator in most cases (capnography) >0.5 mL/kg

Pulmonary artery Sensitive: detects 0.25 Direct PA pressure rise; allows air aspiration via PA catheter; invasive — not routine catheter mL/kg CVP / CVC Moderate CVP rises with right heart obstruction; allows air aspiration via right atrial catheter

Oesophageal Least sensitive — Mill-wheel murmur only with massive embolism; delayed detection; backup only stethoscope detects only very large VAE

Setting VAE Incidence Mechanism Sitting position Up to 45% by Doppler; 1–2% Surgical site far above heart → cranial venous sinuses at sub-atmospheric pressure → nonneurosurgery clinically significant collapsible (held open by bone) → air entrainment Posterior fossa surgery 15–25% by Doppler Same mechanism; dural venous sinuses (prone/sitting) Total hip arthroplasty Varies; BCIS related Intramedullary pressurisation during cementing → fat + air embolism (Bone Cement Implantation

Syndrome)

Laparoscopic surgery Rare CO₂ embolism if trocar in CO₂ embolism: 25× more soluble than air → less severe; sudden ETCO₂ fall + CVS collapse vein

CVC insertion/removal Air embolism during Prevent: Trendelenburg + Valsalva during removal; immediately occlude on removal disconnection Caesarean section 30–50% by TOE but almost all Open uterine veins during closure; vast majority are clinically irrelevant small amounts subclinical

FES is a clinical syndrome caused by embolisation of fat globules from the bone marrow into the systemic circulation following long bone or pelvic fractures (or other triggers: liposuction, total hip arthroplasty, sickle cell crisis, pancreatitis); incidence after closed femoral shaft fracture: 0.5–2% clinical FES; incidence of fat emboli in the bloodstream (without syndrome): nearly 100%; the syndrome requires an inflammatory amplification beyond simple fat embolisation

Mechanism Details Mechanical Disruption of bone marrow fat cells → fat droplets enter disrupted marrow sinusoids → enter the venous system → travel to the pulmonary vasculature (embolic) → mechanical obstruction of pulmonary arterioles → impaired gas exchange; fat droplets large enough to traverse the pulmonary capillaries or cross theory through a PFO → systemic embolisation to brain, skin, retina, kidneys Biochemical Fat droplets in the bloodstream undergo hydrolysis by lipases (plasma and tissue lipases) → release of FREE FATTY ACIDS (FFAs); FFAs are directly (inflammatory) toxic to: pulmonary endothelium (causing capillary leak → non-cardiogenic pulmonary oedema → ARDS); cerebral vasculature (cerebral oedema); theory — the platelet membranes (platelet aggregation → thrombocytopenia, DIC); the systemic inflammatory response amplifies this injury through cytokine release; primary this biochemical theory explains why ARDS onset is delayed (12–72 hours — time for lipases to generate sufficient FFAs) rather than immediate as mechanism would be expected from mechanical obstruction alone for FES

Timing: characteristically presents 24–72 hours after injury; the lucid interval — the patient may initially be alert and oriented after the fracture, then gradually deteriorates with increasing confusion, agitation, and dyspnoea over the subsequent 24–48 hours

The classic triad: respiratory failure (most constant — present in 75–90% of FES; ARDS pattern; bilateral infiltrates; hypoxaemia refractory to supplemental O₂); neurological dysfunction (confusion, agitation, headache, seizures, coma — in 86%); petechial rash (in 50–60% — pathognomonic)

Other features: acute anaemia (haemolysis and marrow fat release); thrombocytopenia; fever; retinal fat emboli (Purtscher's retinopathy — white retinal patches visible on fundoscopy)

Investigations: ABG (hypoxaemia, ↓ PaO₂/FiO₂); CXR (bilateral infiltrates — "snowstorm" appearance); CT thorax (bilateral ground-glass opacities); MRI brain (DWI — "starfield" pattern of multiple small white matter diffusion restriction lesions — pathognomonic for cerebral fat embolism); FBC (thrombocytopenia, anaemia); serum lipase and urinary fat globules; urinalysis (lipiduria)

No specific antidote — treatment is primarily SUPPORTIVE; the syndrome is self-limiting if the patient survives the acute phase

Respiratory support: supplemental O₂; early CPAP/NIV for mild-moderate hypoxaemia; mechanical ventilation with lung-protective settings (6 mL/kg IBW, PEEP 8–12 cmH₂O, plateau ≤30 cmH₂O) for ARDS; prone positioning for severe ARDS (PaO₂/FiO₂ <150)

Haemodynamic support: IV fluids cautiously (avoiding fluid overload which worsens pulmonary oedema); vasopressors for hypotension; albumin may help bind and transport FFAs reducing free toxicity (theoretical)

Neurological: seizure control (benzodiazepines); maintain cerebral perfusion pressure; avoid hypoxia and hypotension (worsen cerebral injury); EEG monitoring for subclinical seizures

Early fracture fixation: definitive surgical fixation of the fracture reduces ongoing fat embolisation from the fracture site; early IMN (intramedullary nailing) is associated with lower rates of pulmonary complications than traction alone; however, reaming the intramedullary canal during nailing transiently increases fat embolisation — use of unreamed or solid nails, or reaming with suction, reduces this risk

Corticosteroids: prophylactic methylprednisolone (1.5 mg/kg every 8 hours for 3 doses) has been shown in some trials to reduce FES incidence in high-risk patients (multiple long bone fractures); not universally adopted; no evidence for therapeutic role once FES is established

System Effect During Inflation Mechanism Cardiovascular ↑ Circulating blood volume (+10–15% central volume); ↑ MAP; Exsanguination of the limb by Esmarch bandage before inflation + tourniquet inflation ↑ CVP; ↑ CO initially; ↑ HR → up to 1 L of blood redistributed from the limb to the central circulation → autotransfusion effect; raises preload, afterload, and myocardial work; may precipitate pulmonary oedema in patients with limited cardiac reserve

Metabolic — Complete ischaemia of the limb distal to the tourniquet → No arterial inflow; ischaemic reprogramming of cellular metabolism within 1–2 hours; limb anaerobic metabolism → lactic acid accumulation; K⁺ leaks safe limit is approximately 90–120 minutes before irreversible ischaemic damage from ischaemic cells; endothelial activation; neutrophil begins sequestration in capillaries; progressive tissue hypoxia Neurological Nerve injury from direct mechanical compression (at the Compression neuropraxia; ischaemic axonal damage; high cuff pressures + tourniquet edge) occurs at the periphery; ischaemia within the prolonged time → risk of permanent nerve injury; preserve by minimising pressure compressed zone; most nerve damage occurs at the (see below) tourniquet EDGE not the ischaemic limb distally

Parameter Safe Limit Rationale Inflation Systolic BP + 50–75 mmHg (or LOP × 1.2–1.4 where LOP = limb occlusion Lowest effective pressure reduces nerve injury and tissue damage; pressure — pressure); minimum pressure to occlude arterial flow only avoid arbitrary fixed pressures (e.g., 300 mmHg) which may be upper limb excessive Inflation Systolic BP + 75–100 mmHg; or LOP × 1.2–1.4; typically 250–300 mmHg for the Larger muscles and higher venous pressures in the lower limb pressure — thigh require higher tourniquet pressures for complete arterial occlusion lower limb Maximum 90–120 minutes maximum single inflation; if longer surgery anticipated: Beyond 90–120 minutes: progressive ischaemic myopathy, inflation time deflate for 10–15 minutes (reperfusion interval) then re-inflate for up to a further endothelial injury, nerve damage, and skin injury become 90 minutes irreversible Cuff width Widest cuff that fits the limb segment without wrapping beyond the surgical site Pressure per unit area is inversely proportional to cuff width; wider — wider cuffs achieve occlusion at lower pressures cuff = lower pressure needed = less nerve injury

Tourniquet released → sudden re-perfusion of the ischaemic limb → massive washout of accumulated metabolites into the systemic circulation: lactic acid → metabolic acidosis (pH falls 0.1–0.2 units within minutes); K⁺ (2–4 mEq/L rise — risk of hyperkalaemic arrhythmia particularly in patients with pre-existing ↑ K⁺); CO₂ → ETCO₂ rises sharply (10–15 mmHg) within 2–3 minutes; hypotension (vasoactive metabolites + reactive hyperaemia in the reperfused limb acts as a "third space" drawing blood volume away from the central circulation)

Ischaemia-reperfusion injury mechanism: on re-oxygenation, xanthine oxidase in ischaemic endothelium generates reactive oxygen species (ROS) → oxidative damage to cell membranes → increased capillary permeability → oedema; neutrophils, sequestered in the ischaemic capillaries during tourniquet inflation, are activated by reperfusion mediators → massive ROS and protease release → amplification of local tissue injury; this explains why post-tourniquet limb swelling and pain can be disproportionate to the surgical injury alone

Anaesthetic management at tourniquet release: warn the surgeon to deflate gradually (slow release); increase minute ventilation to manage ETCO₂ rise; vasopressors for hypotension; monitor K⁺ if prolonged tourniquet time or pre-existing hyperkalaemia; monitor ECG for hyperkalaemia changes (peaked T waves, wide QRS)

Tourniquet pain (tourniquet tolerance) — pain or discomfort under a pneumatic tourniquet despite an apparently adequate regional anaesthetic block — develops in 30–60 minutes of inflation and becomes progressively more severe; affects 55–70% of patients with a functioning peripheral nerve block

Mechanism: the tourniquet compresses the skin and subcutaneous tissue at the cuff level; the pain fibres in this zone (C fibres) may escape block because: the cuff is often at the level of the sensory block margin (the most poorly blocked zone); C fibres are notoriously difficult to block reliably for prolonged periods; the slow onset of tourniquet pain suggests involvement of deep pain pathways (possibly spinal sensitisation) that are different from surgical pain pathways Management:

Supplement the regional block with IV analgesics: opioids (fentanyl 25–50 mcg IV), ketamine (0.25–0.5 mg/kg IV), or NSAIDs before tourniquet pain becomes established Sedation (midazolam, propofol sub-anaesthetic) can reduce the cortical processing of tourniquet pain TIVA with propofol-remifentanil can be added to maintain patient comfort while the regional block provides post-operative analgesia

If pain is intolerable: convert to GA

Double-cuff tourniquet: inflate the distal cuff first (over anaesthetised skin from the block); then inflate the proximal cuff (less discomfort as this is on the analgesia-free side); deflate the distal cuff; this technique delays but does not prevent tourniquet pain

Severe peripheral vascular disease (ischaemic limb — tourniquet-induced ischaemia in already-compromised tissue → limb-threatening ischaemia) Sickle cell disease (sickling may be precipitated in the ischaemic limb → vaso-occlusive crisis; if tourniquet essential → hydroxyurea pre-operatively, optimal oxygenation, avoid hypothermia) History of compartment syndrome of the relevant limb Severe crush injury of the limb (tourniquet on already-injured tissue) DVT in the limb (exsanguination before inflation → systemic embolisation of clot)

Perfusion (Q): gravity causes blood to preferentially perfuse the dependent (lower) lung; pulmonary arterial pressure in the dependent lung is higher (hydrostatic gradient adds to zone 2 and zone 3 conditions → active blood flow); the dependent lung receives approximately 60% of total pulmonary blood flow

Ventilation (V): in the awake spontaneously breathing patient in the lateral position, the dependent hemidiaphragm is better positioned for contraction — it is higher (pushed up by mediastinal weight and abdominal pressure) and in a more efficient mechanical position (like a well-stretched muscle starting on the steep part of the length-tension curve); the dependent diaphragm moves more with each breath → dependent lung receives more ventilation (approximately 55–60% of tidal ventilation to the dependent lung)

Result (awake): V/Q matching is approximately preserved — the lung that gets more blood (dependent) also gets more ventilation → good oxygenation; this is the optimal physiological state

Effect on ventilation: paralysis eliminates the active diaphragm advantage of the dependent side; the non-dependent (upper) lung has BETTER compliance under anaesthesia — it is less compressed, higher FRC, less atelectasis-prone; controlled ventilation distributes gas preferentially to the most compliant lung → the non-dependent lung receives more ventilation (the opposite of the awake state)

Effect on perfusion: gravity still preferentially perfuses the dependent (lower) lung → this does NOT change with anaesthesia; the dependent lung continues to receive ~60% of pulmonary blood flow

The critical mismatch: under anaesthesia, the non-dependent lung is WELL VENTILATED (high V) but receives less blood flow (low Q) → high V/Q ratio → dead space effect; the dependent lung is WELL PERFUSED (high Q) but receives less ventilation (low V due to compression, atelectasis, and splinting by mediastinal weight) → low V/Q ratio → shunt effect → hypoxaemia

Magnitude: FRC of the dependent lung decreases significantly (compression from mediastinal structures + abdominal pressure against the dependent diaphragm); closing capacity may exceed FRC in the dependent lung → small airway closure → atelectasis → intrapulmonary shunt

PEEP strategy for lateral decubitus: PEEP applied to the dependent lung helps recruit collapsed airways and restore dependent lung ventilation (reapproaches the awake V/Q relationship); PEEP titration to the dependent lung is the key ventilatory strategy during lateral decubitus under GA

Venous return: the lateral position with a kidney bridge or flexed table can compress the IVC (depending on the flexion position) → ↓ venous return → ↓ CO; conversely, the Trendelenburg component (head-down) increases venous return; careful positioning with padding avoids abdominal compression

Dependent arm complications: the dependent arm may have impaired venous drainage, particularly with arm boards or in prolonged procedures — monitor the arm position carefully; avoid direct compression of the axillary vessels

Mediastinal shift: in open thorax (thoracotomy), the mediastinum may shift toward the operative (non-dependent) side during spontaneous breathing → paradoxical mediastinal movement → further impairs gas exchange

Nerve/Structure Mechanism Prevention

Brachial plexus Stretching of the brachial plexus from: dependent arm excessively abducted + Axillary roll placed BELOW the axilla (at the thoracic cage level, (dependent head turned away; axillary roll too high (pushing into the axilla rather than below not in the axilla itself); limit abduction to <90°; neutral head arm) it) → compresses the neurovascular bundle in the axillary region; dependent arm position; pad under the dependent shoulder; pillow between weight pulling on the shoulder knees; check arm position every 30 min Common Compression of the CPN as it winds around the head of the fibula; the lateral Generous padding (gel pad or foam) under the dependent knee; peroneal nerve aspect of the dependent knee presses against the table without adequate pillow between knees prevents the upper knee from compressing (dependent leg) padding the lower CPN; confirm the fibular head is well-padded before draping Lateral femoral Compression of the LFCN at the anterior superior iliac spine region when the Pad the dependent iliac crest; avoid kidney bridge position that cutaneous iliac crest is pressed against the table; particularly with kidney bridge positioning directly compresses the ASIS region nerve (LFCN) Eye (dependent Direct pressure on the dependent eye from inadequate head support → central Confirm eye position is NOT under pressure (headrest positioned eye) retinal artery occlusion (rare but devastating) → permanent blindness; also from behind the ear, not over the orbit); check eyes by lifting the head oedema from Trendelenburg component slightly immediately after positioning; document in anaesthetic chart

Indications: anticipated haemodynamic instability (major vascular surgery, cardiac surgery, severe haemorrhage risk); need for frequent ABG sampling; patients requiring vasopressor/inotrope titration; severe hypertension; difficult-to-measure NIBP (obesity, arrhythmias); phaeochromocytoma; deliberate hypotension

Technique — radial artery (most common): Allen's test (optional — confirm dual circulation); 20G cannula; Seldinger or direct technique; sterile preparation; connect to non-compliant pressure tubing + transducer (compliant tubing distorts the waveform — "damping"); transducer levelled at the phlebostatic axis (4th

ICS, mid-axillary line) and zeroed to atmospheric pressure

Waveform components: upstroke = systole (rate reflects LV contractility); peak = systolic BP; dicrotic notch = aortic valve closure (separates systole from diastole); downslope = diastolic runoff; trough = diastolic BP; area under the curve = MAP; pulse pressure variation during IPPV indicates fluid responsiveness

Complications: haematoma; arterial occlusion (more likely with smaller arteries, prolonged cannulation, haematoma); distal ischaemia; infection; accidental intra-arterial drug injection (catastrophic — label all arterial lines prominently)

CVP measures right atrial pressure (normally 0–8 mmHg); the waveform contains: a wave (atrial contraction); c wave (tricuspid valve closure); x descent (atrial relaxation); v wave (venous filling with closed tricuspid valve); y descent (tricuspid valve opens → passive ventricular filling)

Limitations as a fluid responsiveness marker: CVP does NOT reliably predict fluid responsiveness in clinical practice; Marik (Chest 2008; systematic review of 24 studies): CVP was not correlated with blood volume and could not predict haemodynamic response to a fluid challenge; patients with low CVP may or may not respond to fluid; patients with high CVP may respond; CVP is influenced by venous tone, intrathoracic pressure, RV compliance, and many other factors independent of volume status

Current role: CVP provides information about right heart function and filling; useful for comparison over time; useful for CVP waveform analysis (cannon a waves in complete heart block, blunt y descent in tamponade); still useful to guide vasopressor vs fluid therapy in certain scenarios; SHOULD NOT be the sole guide for fluid resuscitation

Parameter Normal Value Clinical Interpretation PAWP (pulmonary artery 6–12 mmHg Left atrial filling pressure; PAWP >18 mmHg → cardiogenic pulmonary oedema; PAWP <8 with hypotension → wedge pressure) hypovolaemia or vasodilatory shock Cardiac Output 4–8 L/min Low CO → cardiogenic or obstructive shock; high CO + low SVR → septic, anaphylactic, hepatic failure (thermodilution) SVR (systemic vascular 800–1200 Low SVR = vasodilatory shock (sepsis); high SVR = cardiogenic shock (reflexive vasoconstriction) resistance) dynes·sec/cm⁵ Mixed venous O₂ sat (SvO₂) 65–75% Low SvO₂ (<65%) → inadequate O₂ delivery or ↑ O₂ extraction (anaemia, high output demand); high SvO₂ (>80%) → distributive shock (O₂ not extracted — shunting) The PAC's clinical utility has been questioned by multiple randomised trials (PACMAN, ESCAPE) showing no mortality benefit and possible harm from its complications; it retains specific roles in: complex cardiac surgery (post-cardiopulmonary bypass haemodynamic management), severe pulmonary hypertension assessment, refractory shock characterisation when less invasive measures are insufficient

Oesophageal Doppler Monitor (ODM): a small Doppler probe placed in the oesophagus (at 35–40 cm from the incisors) and positioned adjacent to the descending aorta; measures aortic blood flow velocity using a 4 MHz Doppler signal; allows continuous, real-time assessment of: stroke volume (SV), cardiac output (CO), corrected flow time (FTc — a surrogate for preload), and peak velocity (a surrogate for LV contractility); non-invasive and minimally invasive alternative to PAC for CO measurement

Goal-Directed Therapy (GDT) using ODM: algorithm-based fluid and vasopressor management targeting specific physiological endpoints: fluid challenges of 200–250 mL crystalloid/colloid → assess if SV increases >10% (fluid responsive → give more fluid) or <10% (non-responsive → stop fluid, consider vasopressor or inotrope); targets: FTc 0.35–0.40 seconds; SV index >35 mL/m²; CO optimisation OPTIMISE trial (Pearse RM, BMJ 2014; n=734 high-risk major GI surgery patients): ODM-guided GDT (stroke volume optimisation using colloid challenges) vs standard care; result: ODM-GDT significantly reduced the rate of postoperative complications (36.6% vs 43.4%) without increasing hospital mortality; meta-analysis including OPTIMISE confirms GDT reduces postoperative complications and hospital length of stay in high-risk surgical patients

Dynamic fluid responsiveness markers: SVV (stroke volume variation during IPPV >13% = fluid responsive); PPV (pulse pressure variation >13% = fluid responsive); PLR test (raise legs → ↑ CO ≥10% = fluid responsive) — these are superior to CVP/PAWP for predicting fluid responsiveness

PiCCO (Pulse Index Continuous Cardiac Output) uses transpulmonary thermodilution (cold saline injected via CVC; measured via a thermistor in the femoral artery) for intermittent CO measurement calibrating a continuous pulse contour analysis algorithm; provides: CO (continuous); GEDVI (global end-diastolic volume index — a volumetric preload marker superior to CVP); EVLWI (extravascular lung water index — measures pulmonary oedema quantitatively; EVLWI >10 mL/kg = pulmonary oedema; >14 mL/kg = severe oedema); SVV (continuous fluid responsiveness marker) Particularly useful in ARDS management (EVLWI allows quantification and monitoring of pulmonary oedema), post-cardiac surgery, and complex septic shock where distinguishing between fluid overload and under-resuscitation is difficult

Receptor Location Effect When Stimulated α₁ adrenergic Peripheral vascular smooth muscle; skin, splanchnic, Vasoconstriction → ↑ SVR → ↑ MAP; pupil dilation; urethral sphincter contraction renal vessels α₂ adrenergic Presynaptic nerve terminals (central + peripheral); Central: sedation, analgesia, ↓ sympathetic outflow; peripheral: vasoconstriction (lower vascular smooth muscle potency than α₁) β₁ adrenergic Cardiac sinoatrial node, AV node, myocardium ↑ Heart rate (chronotropy), ↑ contractility (inotropy), ↑ AV conduction, ↑ myocardial O₂ demand β₂ adrenergic Vascular smooth muscle; bronchial smooth muscle; Vasodilation → ↓ SVR; bronchodilation; uterine relaxation; mast cell stabilisation; ↑ insulin uterus; mast cells release DA₁ Renal and splanchnic vasculature Vasodilation → ↑ renal/splanchnic blood flow; historically thought to provide "renal (dopamine) protection" — now disproven V₁ Vascular smooth muscle Vasoconstriction independent of catecholamine pathway; particularly useful in (vasopressin) catecholamine-resistant vasodilatory shock

Drug Receptor Profile Haemodynamic Effect Primary Indication Key Safety Point Noradrenaline α₁ >> β₁; minimal β₂ ↑ SVR (↑ MAP); modest ↑ HR; no FIRST LINE for septic shock (SSC 2021); Peripheral ischaemia with (norepinephrine) significant vasodilation; maintains first line for most vasodilatory shock; extravasation (use central line); CO via afterload-mediated LV maintains MAP ≥65 mmHg; preferred over reflex bradycardia at high doses; optimization dopamine (De Backer NEJM 2010) splanchnic vasoconstriction at very high doses Adrenaline β₁ + β₂ at low doses; Low dose: ↑ CO, ↑ HR, ↓ SVR (β₂ Cardiac arrest (1 mg IV every 3–5 min); Tachyarrhythmias (high dose); (epinephrine) α₁ added at high dominant); High dose: ↑↑ SVR, anaphylaxis (0.5 mg IM or 50–100 mcg IV); metabolic acidosis (lactic acid from doses ↑↑ HR, ↑↑ MAP; universal potent severe refractory shock; low cardiac output β₂ glycogenolysis and impaired effect with hypotension tissue perfusion at high doses); myocardial ischaemia; hyperglycaemia Vasopressin V₁ receptor: vascular Vasoconstriction via V₁ Vasodilatory shock refractory to Coronary and mesenteric (ADH) smooth muscle (independent of adrenergic noradrenaline alone (adds V₁ vasoconstriction at high doses — vasoconstriction; V₂ receptors); ↑ SVR; ↑ MAP; no vasoconstriction via a different receptor ischaemia risk; hyponatraemia (V₂ receptor: renal water direct chronotropy or inotropy; pathway); vasodilatory shock post-CPB effect — SIADH-like); skin necrosis reabsorption reduces noradrenaline (vasopressin deficiency after bypass); with high doses and extravasation; requirements (catecholamine- relative vasopressin deficiency of septic typical ICU dose: 0.03–0.04 sparing) shock (vasopressin levels paradoxically low units/min (do not increase above in septic shock) this) Phenylephrine Pure α₁ agonist; no β ↑ SVR; ↑ MAP; reflex bradycardia Perioperative hypotension from vasodilation Reflex bradycardia; if used in activity (baroreceptor response to ↑ BP); (regional anaesthesia, volatile agents) — cardiogenic shock → worsens NO increase in HR or contractility first-line vasopressor for this; obstetric spinal cardiac output (↑ afterload on failing hypotension (preferred — no tachycardia, heart without ↑ inotropy); avoid in maintains uteroplacental blood flow); heart failure or low CO states preserves HR (useful if baseline tachycardia) Dopamine DA₁ (low dose <5 Low dose: ↑ renal/splanchnic Not recommended as first-line vasopressor Significantly more arrhythmias than mcg/kg/min); β₁ blood flow (historically "renal (De Backer NEJM 2010: dopamine → more noradrenaline; "low-dose dopamine" (medium dose 5–10); protection" — NOT proven); arrhythmias than noradrenaline + more for renal protection is NOT evidenceα₁ (high dose >10 Medium: ↑ CO; High: deaths in cardiogenic shock subgroup); only based and should be abandoned mcg/kg/min) vasoconstriction alternative if noradrenaline unavailable Dobutamine β₁ >> β₂; minimal α ↑ Contractility (↑ CO, ↑ SV); ↑ Cardiogenic shock (↑ CO in failing heart); Tachycardia and arrhythmias; Dobutamine β₁ >> β₂; minimal α ↑ Contractility (↑ CO, ↑ SV); ↑ Cardiogenic shock (↑ CO in failing heart); Tachycardia and arrhythmias; HR; ↓ SVR (β₂ vasodilation); net: acute decompensated heart failure (reduced worsens myocardial ischaemia (↑ O₂ ↑ CO, may ↓ BP if SVR falls more EF <35% + hypoperfusion); post-cardiac demand); tachyphylaxis with than CO rises surgery low output syndrome; often prolonged use; NOT for vasodilatory combined with noradrenaline (dobutamine ↑ shock (will ↓ SVR further) CO, noradrenaline maintains SVR) Milrinone PDE-III inhibitor ↑ Contractility + ↓ SVR + ↓ PVR; Acute decompensated heart failure Hypotension (significant vasodilation (phosphodiesterase the "inodilator" — lowers both (particularly in patients with β-blocker- — often requires concomitant type 3 inhibition → ↑ SVR and PVR while increasing induced receptor downregulation where vasopressor support); arrhythmias; cAMP in cardiac CO; does NOT act via adrenergic dobutamine is less effective); post-cardiac long t½ (2–3 hours) makes titration muscle → inotropy; ↑ receptors → useful when surgery LCOS (low cardiac output slow; renal excretion → accumulates cAMP in vascular downregulation of β-receptors syndrome); pulmonary hypertension (↓ PVR); in renal failure smooth muscle → has occurred (chronic HF) right heart failure vasodilation)

Type of Shock Primary Agent Second Agent Septic/Distributive shock (↑ CO, Noradrenaline 0.1–1 mcg/kg/min Vasopressin 0.03 units/min if noradrenaline >0.25 mcg/kg/min; ↓ SVR) hydrocortisone 200 mg/day if vasopressor-refractory Cardiogenic shock (↓ CO, ↑ SVR) Dobutamine (↑ CO, ↓ SVR) + Noradrenaline if hypotensive Milrinone if β-receptor downregulated; levosimendan (Ca²⁺ (↑ SVR to counteract dobutamine vasodilation) sensitiser — Europe) for acute-on-chronic decompensation Anaphylactic shock (↓ CO, ↓ Adrenaline (α₁ for vasoconstriction + β₂ for bronchodilation + Vasopressin for refractory anaphylaxis (V₁ vasoconstriction SVR, bronchospasm) β₁ for ↑ CO) — the ONLY appropriate first-line agent independent of epinephrine); noradrenaline if adrenaline inadequate Perioperative vasodilatory Phenylephrine (pure α₁ — restores SVR without Noradrenaline infusion for sustained hypotension hypotension (regional/volatile tachycardia) for hypotension alone; ephedrine if bradycardic agent) Right heart failure + pulmonary Milrinone (↓ PVR + ↑ RV contractility) + Vasopressin Inhaled NO (selective pulmonary vasodilation); prostacyclin hypertension (maintains systemic BP without worsening PVR) analogues

Step Assessment Action

C — Catastrophic External haemorrhage from limb or junctional wound Tourniquet (limb haemorrhage); wound packing with haemostatic gauze haemorrhage visible BEFORE airway assessment (junctional/non-compressible); direct pressure; pelvic binder for pelvic fracture

A — Airway with C- Is airway patent? Can patient speak? Assess for Manual in-line stabilisation (MILS) of the C-spine during all airway manoeuvres; jaw spine control obstruction (blood, vomit, teeth, foreign body, soft thrust (not head tilt/chin lift); suction; nasopharyngeal airway (NPA) or OPA; RSItissue oedema, facial/laryngeal fracture) intubation if unable to maintain airway; surgical airway if CICO

B — Breathing and RR; oxygen saturation; bilateral breath sounds; High-flow O₂ via non-rebreather mask 15 L/min; needle decompression + chest drain ventilation tracheal deviation; subcutaneous emphysema for tension pneumothorax; chest drain for haemothorax; seal open chest wound with 3sided dressing

C — Circulation and HR, BP, CRT, skin colour, consciousness (surrogate Large-bore IV access (2× 14G or intraosseous); activate MTP; permissive hypotension haemorrhage control for cerebral perfusion); identify source of (SBP 80–90 mmHg until surgical haemostasis); blood products in 1:1:1 ratio; TXA haemorrhage (external/internal) within 3 hours of injury

D — Disability GCS (Eyes 4/Motor 6/Verbal 5); pupil size and Maintain CPP ≥70 mmHg in TBI (MAP ≥90 + ICP monitoring if GCS ≤8); C-spine (Neurological) reactivity; limb movements; AVPU immobilisation; anticonvulsants for TBI seizures; neurosurgical consultation for (Alert/Voice/Pain/Unresponsive) deteriorating GCS

E — Complete undressing (log-roll with spinal Active warming: warm blankets, warm IV fluids, warm theatre; prevent heat loss (wet Exposure/Environment precautions); assess posterior injuries; temperature clothing removed); temperature monitoring

Permissive hypotension: accept SBP 80–90 mmHg (MAP 50–65 mmHg) until surgical or radiological haemostasis achieved; rationale: high BP displaces blood clots from injured vessels, worsening haemorrhage; permissive hypotension maintains marginal tissue perfusion while allowing clot formation;

EXCEPTION: TBI — maintain MAP ≥80 mmHg (brain needs adequate CPP); severe thoracic aorta injury (risk of complete rupture) Haemostatic resuscitation (1:1:1): packed RBC : fresh frozen plasma : platelets in 1:1:1 ratio — PROPPR trial (JAMA 2015): 1:1:1 vs 1:1:2 → significantly better 24h and 30d survival with 1:1:1; provides volume replacement AND replaces all clotting factors AND replaces platelets simultaneously — treats the coagulopathy rather than just the volume deficit

Tranexamic acid (TXA): CRASH-2 (Lancet 2010; n=20,211): 1 g IV within 3 hours of injury → 15% relative mortality reduction; second dose 1 g IV over 8 hours if bleeding continues; TXA >3 hours after injury: NO benefit and possible harm (procoagulant effect may worsen thromboembolic complications once fibrinolysis has already resolved); give EARLY — the most time-sensitive intervention in trauma

Minimise crystalloids: large-volume crystalloids dilute clotting factors, worsen acidosis, cause hypothermia, and worsen outcomes; limit to <1.5 L during active haemorrhage resuscitation; blood products are the primary volume expanders in DCR

Calcium replacement: citrate in FFP and blood products chelates ionised calcium → hypocalcaemia impairs clotting and cardiac function; 10 mL 10% calcium gluconate IV per 4 units transfused rapidly; check ionised Ca²⁺ every 30 minutes

Challenge Management Full stomach RSI mandatory for all trauma patients regardless of fasting status; rapid loss of consciousness and NMB with immediate intubation; no mask ventilation (aspiration unless hypoxia threatened (SpO₂ <93%) risk) Potential MILS (Manual In-line Stabilisation) by assistant throughout laryngoscopy; do NOT remove cervical collar during intubation until cleared by imaging; cervical spine video laryngoscope (C-MAC, McGrath) as first-line — achieves intubation without neck extension; difficult intubation plan (bougie, fibreoptic) prepared injury in advance

Haemodynamic Induction agents: ketamine 1–2 mg/kg IV (sympathomimetic — maintains BP; bronchodilator — useful if aspiration suspected); if critically shocked (BP compromise <70 systolic): etomidate 0.2 mg/kg IV (most cardiovascularly stable) or ketamine at reduced dose (0.5–1 mg/kg); AVOID propofol in haemorrhagic shock (vasodilatory → cardiac arrest) NMB choice Succinylcholine 1.5 mg/kg IV (fastest intubating conditions; 60 seconds) — check for contraindications (burns >48h → hyperkalaemia; crush injuries with denervation); OR rocuronium 1.2 mg/kg (60-second equivalent intubating conditions; sugammadex 16 mg/kg available)

TBI Avoid: hypotension (↓ CPP → secondary brain injury); hypoxia (SpO₂ <90% even briefly); hypercapnia (↑ CBF → ↑ ICP); maintain: MAP ≥80 mmHg; management EtCO₂ 35–40 mmHg (normocapnia); consider lidocaine 1.5 mg/kg IV before laryngoscopy to blunt ICP response (evidence weak but commonly used) during RSI

The "damage control" concept — do MINIMAL surgery now to control haemorrhage and contamination; leave definitive repair for later when the patient is physiologically resuscitated from the lethal triad: abbreviated laparotomy (suture major vessels; pack the abdomen; leave the bowel stapled but not anastomosed); temporary abdominal closure (TAC — negative pressure wound dressing); transfer to ICU for resuscitation; return to theatre 24–48 hours later for definitive repair

Intraoperative considerations during damage control: permissive hypothermia acceptance (warming is a secondary concern to surgical haemostasis); goal is to terminate the surgical bleeding source as fast as possible; ICU bed should be booked before entering theatre

Burn wound: Zone of coagulation (central — irreversible cell death); Zone of stasis (middle — potentially salvageable with optimal resuscitation — inadequate fluid → extends the irreversible injury); Zone of hyperaemia (peripheral — minimal injury, will recover)

Systemic inflammatory response: massive cytokine release → capillary leak → interstitial oedema (not just locally at the burn wound — generalised); distributive shock from vasodilation; bacterial translocation from gut (mucosal barrier disruption from shock); hypermetabolism persists for months (catecholamines, glucagon → ↑ resting metabolic rate 150–200% of predicted — the most severe hypermetabolic state of any disease)

Cardiovascular phases: Early (0–24h): ↓ CO, ↑ SVR (shock), myocardial depression (from burn toxins and inflammatory mediators); Late (24–72h onward): hyperdynamic — ↑ CO, ↓ SVR, ↑ HR (from hypermetabolism and sepsis)

Type Mechanism Clinical Features Management Carbon CO binds Hb with 200× affinity of O₂ → COHb → left- Headache, confusion, seizures, coma; 100% O₂ (reduces CO t½ from 5 hours to 60 min); Monoxide shifted O₂ dissociation curve → impaired O₂ delivery cherry-red colour (unreliable); SpO₂ hyperbaric O₂ (35–90 min at 2.5 atm → t½ 20–30 min) (CO) despite normal PaO₂; inhibits mitochondrial FALSELY NORMAL (co-oximetry on for: COHb >25%; neurological symptoms; cardiac poisoning cytochrome oxidase ABG required); carboxyHb >20% → compromise; pregnancy neurological damage; >60% → fatal Upper Direct heat injury to supraglottic structures (larynx, Singed nasal hairs, facial burns, eyebrow EARLY intubation is critical — delay allows airway pharynx); steam and hot gases cause oedema which burns, hoarseness, stridor; initial airway progressive oedema to make intubation impossible; thermal can completely obstruct the upper airway within hours may appear adequate but oedema is once hoarse or stridorous → intubate IMMEDIATELY injury progressive with the largest possible ETT; awake FOI if cooperative; surgical airway if intubation fails Lower Products of combustion (aldehydes, acids, HCN, CO) Productive cough, wheezing, Humidified O₂; nebulised N-acetylcysteine (mucolytic); airway damage the tracheobronchial mucosa and alveoli → bronchospasm; late: bronchopneumonia, bronchoscopy and lavage for cast removal; ventilator chemical mucosal necrosis, cast formation, bronchospasm, ARDS; bronchoalveolar lavage showing support with lung-protective settings; prophylactic injury impaired mucociliary clearance → pneumonia; true carbonaceous particles confirms lower antibiotics controversial (selective digestive acid burns to the lower airway airway injury decontamination evidence weak)

Change Early Phase (0–48h) Late/Hypermetabolic Phase Succinylcholine SAFE in the first 24–48 hours post-burn CONTRAINDICATED after 48 hours until 2 years post-burn: upregulated extrajunctional AChRs from denervation of burned skin → K⁺ efflux 5–10 mEq/L → cardiac arrest; use rocuronium instead Non- Reduced protein binding (↓ albumin) → RESISTANCE to NDMR develops (upregulated AChRs bind more drug without equivalent effect); need depolarising enhanced effect; reduced Vd in early 2–3× higher doses; use TOF monitoring to titrate NMBs shock Opioids Normal initially; reduced binding with ↓ ↑ Clearance from hypermetabolism + ↑ Vd (oedema); patients may need very high doses for adequate protein analgesia Propofol Normal ↑ Volume of distribution; ↑ clearance; increased dose requirements; AVOID prolonged high-dose propofol (PRIS risk, especially in paediatric burns)

Temperature regulation: burns patients are profoundly hypothermic-prone (loss of skin barrier → massive heat and water evaporation); theatre temperature must be raised to 28–30°C; all fluids warmed to 40°C; forced-air warming; minimise exposed body surface area; temperature monitoring mandatory

Blood loss: burns excision and grafting can cause massive haemorrhage (1 mL/cm² burn area excised); blood products must be available; large-bore IV access; cell salvage; topical thrombin or adrenaline-soaked dressings (reduce surgical blood loss); tourniquets for limb excisions

IV access difficulty: extensive burns may make peripheral IV access impossible; central venous access through burned skin (sterility maintained) or through non-burned areas

Repeated anaesthetics: burns patients often require 10–20 or more anaesthetics over months; opioid tolerance and opioid-induced hyperalgesia develop rapidly; multimodal analgesia (ketamine, gabapentinoids, regional techniques) essential; ketamine specifically useful in burns — procedural sedation and analgesia during dressing changes (0.5–1 mg/kg IV or 2–4 mg/kg IM in paediatric burns)