Anesthesia

Domain Key Recommendation Assessment Tool

P — Pain Assess pain routinely; use analgesia-first approach (treat pain before sedation); non-opioid NRS (Numeric Rating Scale 0–10) for analgesics first (paracetamol, NSAIDs if appropriate, regional techniques); opioids titrated to communicative; BPS (Behavioural Pain Scale) or VAS/NRS ≤3/10 CPOT (Critical-Care Pain Observation Tool) for non-communicative

A — Agitation Light sedation target (RASS 0 to −2) preferred over deep sedation (RASS −3 to −5); reduces RASS (Richmond Agitation-Sedation Scale −5 to (Sedation) ventilator days, ICU stay, delirium; dexmedetomidine preferred over benzodiazepines for non- +4) deeply sedated patients

D — Delirium Routine delirium screening; multicomponent non-pharmacological bundle (reorientation, sleep CAM-ICU (Confusion Assessment Method for hygiene, early mobilisation, family involvement, natural lighting); avoid benzodiazepines (delirium ICU) — validated for intubated patients; takes <2 risk); antipsychotics (haloperidol) do not reliably prevent delirium but may treat hyperactive minutes delirium symptoms

I — Immobility Early mobilisation within 24–48 hours of ICU admission where safe; reduces ICU-acquired ABCDEF bundle: Awaken + Breathe + (Rehabilitation) weakness, delirium, and ventilator days; structured progressive rehabilitation (passive ROM → Coordinate + Delirium + Early mobility + Family active assisted → active → sitting → standing → walking)

S — Sleep Promote sleep-wake cycling; minimise nighttime interruptions; reduce light and noise; avoid Richards-Campbell Sleep Questionnaire (RCSQ) benzodiazepines and propofol for sleep (both suppress N3 and REM sleep); melatonin or for patient self-report dexmedetomidine may promote more physiological sleep architecture

Score Level Description +4 Combative Overtly combative, violent, immediate danger to staff +3 Very agitated Pulls or removes tubes/catheters; aggressive +2 Agitated Frequent non-purposeful movement, fights ventilator +1 Restless Anxious but movements not aggressive or vigorous 0 Alert and calm Spontaneously alert and calm — TARGET for most ICU patients −1 Drowsy Not fully alert; sustained awakening (eye opening >10 seconds to voice) −2 Light sedation Brief awakening to voice (eye opening <10 seconds); acceptable light sedation target −3 Moderate sedation Movement or eye opening to voice; no eye contact −4 Deep sedation No response to voice; movement or eye opening to physical stimulation −5 Unarousable No response to voice or physical stimulation

Daily SAT (Kress JB — NEJM 2000; Ely EW NEJM 2008): all sedation stopped (or significantly reduced) every morning for up to 4 hours to assess the patient's neurological status and wakefulness; if the patient demonstrates adequate spontaneous breathing, awakens appropriately, and does not require immediate re-sedation for agitation/self-extubation → proceed to SBT; Ely NEJM 2008 (SAT + SBT): combining daily SAT with daily SBT reduced 1-year mortality by 14% and reduced ventilator days by 3 days vs SBT alone

SAT safety screen: active seizures; active alcohol withdrawal; open abdomen; FiO₂ >0.5 or PEEP >8 (too sick for SAT); actively receiving therapeutic neuromuscular blockade; resting agitation before SAT (cannot safely stop sedation in already-agitated patient)

Failed SAT: agitation, anxiety, pain, RR >35, SpO₂ <88%, new arrhythmia or haemodynamic instability during the SAT → restart sedation at half the previous dose

Four CAM-ICU features (ALL four must be assessed):

Feature 1: ACUTE ONSET OR FLUCTUATING COURSE — new change or fluctuation in RASS score or GCS within the last 24 hours? (Yes → proceed)

Feature 2: INATTENTION — "Squeeze my hand every time you hear the letter A" test (reading a series of letters including multiple As); errors in squeezing on non-A letters or not squeezing on A letters = positive; OR picture recognition test in non-English speakers

Feature 3: ALTERED LEVEL OF CONSCIOUSNESS — current RASS other than 0; if yes → CAM-ICU positive (delirium without needing Feature 4)

Feature 4: DISORGANISED THINKING — can patient answer 4 simple yes/no questions correctly? Can patient follow 2 commands? CAM-ICU positive = delirium if Features 1 + 2 present AND either Feature 3 OR Feature 4 is positive

Types of delirium: hyperactive (agitated, pulling lines, fighting ventilator — obvious); hypoactive (quiet, withdrawn, blunted — frequently missed; worse prognosis than hyperactive); mixed (fluctuating between both)

Management: non-pharmacological first (reorientation, early mobilisation, sleep hygiene, family presence, remove unnecessary lines and catheters); pharmacological: haloperidol 0.5–2 mg IV BD (most widely used; evidence weak for prevention but useful for symptom management of hyperactive delirium); dexmedetomidine (MENDS trial — less delirium than midazolam; SEDCOM — less delirium than midazolam)

Multiple RCTs (Kress NEJM 2000, Girard NEJM 2008, Strøm BJA 2010) consistently demonstrate: light sedation (RASS 0 to −2) vs deep sedation (RASS −3 to −5) produces: shorter mechanical ventilation duration (2–3 days fewer); shorter ICU stay; fewer delirium days; LOWER 1-year mortality in some analyses; no increase in patient recall of unpleasant experiences (patients sedated to RASS −2 do not remember being ventilated in the vast majority of cases) Analgesia-first approach (Strøm BJA 2010): protocol of morphine boluses for pain + paracetamol + no background sedation → significantly less sedation exposure, shorter MV time, and no increase in patient distress or self-extubation vs standard propofol-based sedation; analgesia-first is now endorsed by PADIS 2018 as the foundation of ICU pain and sedation management

Finding Ultrasound Sign Interpretation Normal lung Lung sliding (shimmering movement of pleural line with each breath Normal aerated lung; lung sliding confirms visceral pleura is moving → no — the visceral and parietal pleura moving against each other); A- pneumothorax at this site lines (horizontal reverberation artefacts from the pleural line — equidistant, repeating) Pneumothorax ABSENT lung sliding (the pleural line is static — visceral pleura is Absent lung sliding + absent B-lines + barcode sign on M-mode = separated from the parietal pleura by air); B-lines are absent; on M- pneumothorax; more sensitive than CXR for detecting pneumothorax; the mode: "Barcode sign" (static horizontal lines instead of the normal lung point (the anatomical border where the pneumothorax ends — sliding "seashore sign" in a healthy lung) reappears) confirms and localises the pneumothorax Pleural Anechoic (dark) fluid above the diaphragm in the dependent pleural Volume of effusion can be estimated by POCUS; guides thoracocentesis effusion space; the "curtain sign" — lung collapses away from the dependent needle placement under real-time visualisation pleural space; can be guided real-time drainage Pulmonary B-lines (formerly "lung rockets"): vertical, hyperechoic, laser-like Diffuse bilateral B-lines = cardiogenic pulmonary oedema OR ARDS; focal oedema (B- artefacts arising from the pleural line, extending to the far field, unilateral B-lines = pneumonia or contusion; the pattern (bilateral vs focal) and lines) moving with lung sliding, erasing A-lines; 3 or more B-lines in one clinical context distinguish cardiogenic from non-cardiogenic view = interstitial syndrome Consolidation Hypoechoic tissue-like appearance replacing the normal air-filled Pneumonia; pulmonary contusion; lobar collapse; the presence of dynamic air pattern; hepatisation of the lung; air bronchograms (hyperechoic bronchograms (moving with breathing) suggests patent bronchi and potentially spots moving with respiration within the consolidation) reversible atelectasis

Question Finding Clinical Decision

Is there Pericardial effusion: anechoic fluid surrounding the heart; cardiac Effusion with RV diastolic collapse → tamponade → emergency Effusion? tamponade: diastolic collapse of the right ventricle and right atrium (the pericardiocentesis or pericardial window; PEA in the context of pericardial first sign of haemodynamically significant tamponade) effusion → tamponade until proven otherwise

Is cardiac LV function: visual estimation of LV ejection fraction (EF); hyperdynamic Severely reduced LV function in shock → cardiogenic shock → inotropes Ejection (EF >70%: walls touch in systole), normal (40–70%), or reduced (EF (dobutamine, milrinone); NOT give more fluid; hyperdynamic LV in adequate? <40%: poor wall motion) hypotensive patient → distributive shock → vasopressors Are the RV:LV size ratio; normally RV is smaller; RV dilation (RV:LV >0.6 in any Massive PE; acute cor pulmonale; RV MI; D-sign in a shocked hypoxic Equalities of view) + D-sign (interventricular septal flattening — septal bowing into patient → consider pulmonary embolism → consider thrombolysis RV and LV LV) suggests massive PE or RV failure appropriate? Are the Exits Aortic and pulmonary valve assessment; IVC size and collapsibility (a IVC <2 cm collapsing with inspiration → low CVP → likely hypovolaemia patent? surrogate for CVP and volume status) (volume responsive); IVC >2.5 cm non-collapsing → raised CVP → cardiogenic or obstructive cause of shock Is the motion Regional wall motion abnormalities (RWMA) — segments of the LV wall New RWMA in a patient with chest pain + ECG changes → STEMI → Expected? that are hypokinetic or akinetic = myocardial ischaemia or previous MI activate cath lab; RWMA in post-cardiac surgery patient → graft failure

ETT confirmation: probe placed transversely on the anterior neck at the level of the trachea; normal: trachea shows a single hyperechoic curve with posterior acoustic shadowing (air column in the trachea); ETT in trachea: the ETT appears as two hyperechoic curves (the anterior and posterior walls of the ETT) within the trachea — the "double lumen" sign; oesophageal intubation: the oesophagus (soft tissue structure posterior to the trachea) shows a "snowstorm" pattern with air entering it; real-time confirmation: as the ETT cuff is inflated, the hyperechoic cuff appears in the trachea; this is an immediate, real-time confirmation of correct ETT placement

Subglottic anatomy for cricothyrotomy: probe placed longitudinally on the anterior midline neck; identify: thyroid cartilage (superior hyperechoic curved structure); cricothyroid membrane (CTM — the relatively flat area between the thyroid and cricoid cartilages); cricoid cartilage (inferior hyperechoic curved structure); the CTM is identified as the hypoechoic (soft tissue) region between the two cartilage landmarks; ultrasound-guided identification of the CTM before difficult airway cases reduces the risk of misidentification (particularly in obese patients where the CTM is difficult to identify by external palpation)

Central venous access: real-time ultrasound guidance for internal jugular (IJV) or subclavian vein cannulation; reduces: first-attempt failure (by 57%), arterial puncture (by 78%), haematoma, pneumothorax (for subclavian); the vein (anechoic, compressible, distends with Valsalva) is distinguished from the artery (pulsatile, non-compressible, round, thick-walled); the IJV typically lies anterolateral to the common carotid artery

Peripheral IV access: ultrasound-guided peripheral IV in patients with difficult access (obesity, prior IV drug use, multiple previous venepunctures); allows cannulation of deep veins (basilic, brachial) that are not visible or palpable

Arterial line: real-time ultrasound guidance for radial, femoral, or brachial artery cannulation; reduces first-attempt failure and haematoma; the artery is identified as a pulsatile, round, non-compressible structure

DVT diagnosis: compressibility test of the femoral and popliteal veins; normal vein compresses completely with probe pressure; DVT: vein fails to compress (blood clot within the lumen prevents collapse); quick bedside assessment for high-risk ICU/trauma patients

Plan Goal Technique Maximum Attempts

Plan A — Safe tracheal Position optimised (ramped, HELP, head-up); direct laryngoscopy OR video laryngoscopy as first Maximum 3 intubation Primary intubation on line (DAS 2015 does not mandate video laryngoscopy for all but recommends considering it from the attempts; if all 3 fail → Intubation the first attempt start in any anticipated difficulty); bougie as standard adjuvant (not as a rescue — should be the first- DECLARE FAILED choice adjuvant with any suboptimal view); maximum 3 attempts at intubation in Plan A, each with INTUBATION and move to optimisation (position, blade, assistant pressure) Plan B

Plan B — Maintain INSERT a supraglottic airway device (SAD — i-gel or LMA ProSeal as second-generation devices Maximum 2 SAD insertion Oxygenation oxygenation preferred); if SAD achieves adequate ventilation → continue surgery if immediately life-saving; if attempts; if both fail → move via SAD after failed elective → WAKE THE PATIENT UP (allow full recovery, plan definitive airway management before to Plan D (CICO) tracheal rescheduling); if SAD fails to ventilate → CICO → Plan D intubation; buy time

Plan C — Attempt face- Resume face-mask ventilation (two-person, two-handed technique); CALL FOR HELP (senior As many attempts as needed Final mask ventilation anaesthesiologist, ENT surgeon, ODP, nursing support); if face-mask ventilation maintains SpO₂ to buy time; the goal is to call Attempt at while preparing >90% → time to prepare for Plan D or wake the patient up; if SpO₂ still falling → CICO emergency for help and prepare for Oxygenation for CICO if SAD CICO also fails; ensure the team is assembled

Plan D — Emergency Scalpel cricothyrotomy: palpate the cricothyroid membrane (CTM); single horizontal stab incision No limit — do it as fast as CICO oxygenation via with a No.10 scalpel through the CTM; rotate the blade 90° (to widen the incision); insert a bougie possible; every second of Emergency a surgical (caudally into the trachea); railroad a size 6.0 cuffed ETT or specific cricothyrotomy tube over the CICO = hypoxic brain injury; — Front of airway when bougie; confirm ETCO₂ waveform; inflate cuff; ventilate; this is the DAS recommended technique — scalpel-bougie Neck ALL other the "scalpel-bougie" method (has replaced needle cricothyrotomy as the preferred CICO technique cricothyrotomy can be Access methods have for adults in UK practice based on superior reliability) completed in 30–60 seconds (FONA) failed by a trained practitioner

CICO is defined as: failure to intubate the trachea despite optimal positioning and multiple attempts (Plans A and B have failed) AND failure to maintain adequate oxygenation by face mask or SAD; SpO₂ is falling despite all efforts; this is an IMMEDIATE LIFE-THREATENING emergency

The DAS 2015 CICO declaration: any patient in whom SpO₂ cannot be maintained >90% using ALL available non-surgical airway means is in CICO; the 90% threshold is chosen because brain injury risk becomes significant and quickly progressive below this level; do NOT delay FONA waiting for absolute zero — act at 90% and falling The ONLY correct response to true CICO is immediate FRONT OF NECK ACCESS (FONA) using the scalpel-bougie technique; no other intervention is appropriate once CICO is confirmed

The difficult airway does not end at intubation — extubation of a patient who was difficult to intubate carries SIGNIFICANT RISK (loss of the established airway in a patient who may be more difficult to re-intubate after surgical trauma, oedema, bleeding)

DAS Extubation Guidelines (2012): every patient who was difficult to intubate should have an explicit extubation plan that includes: can the patient be safely re-intubated if needed post-extubation? (assess risk); what is the procedure for safe extubation? Extubation technique for at-risk airway:

Awake extubation: patient is fully awake, following commands, with intact reflexes, confirmed T4 on TOF, and normothermia BEFORE the ETT is removed; this is the safest option for the at-risk airway

Airway exchange catheter (AEC): a long hollow catheter (e.g., Cook AEC) is inserted through the ETT into the trachea before the ETT is removed; the ETT is removed over the AEC; the AEC remains in the trachea as a guide for immediate re-intubation if needed; can be used for jet ventilation as a bridge if reintubation is necessary; the AEC should remain in place for 30–60 minutes until the patient is confirmed stable and airway oedema risk has passed

Cuff leak test before extubation: deflate the ETT cuff and check if the patient can breathe around it (leak should be audible); no leak suggests airway oedema → consider IV dexamethasone 8 mg → delay extubation 24 hours → repeat cuff leak test before extubating

Indications: predicted difficult airway by assessment (Mallampati IV, limited mouth opening, limited neck extension, significant facial/cervical pathology); fixed anatomical obstruction; unstable cervical spine; patient preference after discussion Technique:

Sedation: dexmedetomidine (ideal — cooperative, rousable, no respiratory depression) OR midazolam + low-dose remifentanil TCI (careful — respiratory depression risk)

Topical airway anaesthesia: nebulised lidocaine 4% (4 mL × 4 min before procedure) + transtracheal injection of lidocaine 4% 2 mL through CTM (cough response then suppresses tracheal reflexes) + spray-as-you-go technique (lidocaine 2% sprayed via the working channel of the fibrescope as you advance)

Approach: nasal (better tolerated, steadier platform, passes naturally behind the soft palate → vocal cords) or oral (with Berman or Ovassapian airway guide)

Confirm ETT placement: ETCO₂ waveform; visualise carina through the fibrescope before removing it to confirm tracheal (not oesophageal) position

Principle: a peripheral nerve (median nerve at wrist for upper limb; posterior tibial nerve at ankle for lower limb) is stimulated with small electrical pulses; the signal travels via the dorsal column (posterior spinal cord) → brainstem → thalamus → somatosensory cortex; scalp electrodes record the cortical response; the response is averaged over hundreds of stimuli to extract from background EEG noise

What it monitors: the integrity of the POSTERIOR spinal cord (dorsal column — the sensory pathway); does NOT monitor the ANTERIOR spinal cord (corticospinal tracts — the motor pathway); therefore a pure anterior cord injury (from anterior spinal artery occlusion) may be missed by SSEP alone but detected by MEP

Signal parameters: latency (time from stimulus to cortical response; normally 15–25 ms for upper limb SSEP); amplitude (height of the waveform peak); alert criteria: ≥50% amplitude reduction OR ≥10% latency increase from baseline = significant change requiring surgical intervention

Surgical applications: scoliosis surgery (most common — monitoring for distraction-related cord injury); aortic surgery (monitoring during aortic cross-clamp); posterior fossa surgery; carotid endarterectomy (cerebral perfusion monitoring)

Principle: transcranial electrical stimulation (TES) or magnetic stimulation (TMS) is applied to the motor cortex (electrodes placed on the scalp at C3/C4 positions); the electrical impulse travels via the corticospinal tract (ANTERIOR spinal cord) → anterior horn cells → peripheral motor nerve → muscle; the response is recorded as a compound muscle action potential (CMAP) from muscles (tibialis anterior, abductor hallucis for lower limbs; thenar muscles for upper limbs)

What it monitors: the integrity of the ANTERIOR spinal cord (corticospinal tract — the motor pathway); complementary to SSEP — monitors the pathway that SSEP misses; together SSEP + MEP provide comprehensive spinal cord monitoring covering both sensory and motor pathways

Alert criteria: ≥80% CMAP amplitude reduction from baseline; loss of all MEP signals; new asymmetry between left and right limb responses = significant alert requiring surgical pause and intervention

Critical anaesthetic consideration: MEPs are ABOLISHED by neuromuscular blocking agents (NMBs); the CMAP is recorded from muscles and requires intact neuromuscular junction; even partial NMB (TOF ratio 0.5) significantly suppresses MEP amplitude; during MEP monitoring: do NOT use NDMR boluses; if NMB is essential for intubation, use a short-acting agent and allow complete recovery before MEP baseline is established; NMB infusions are completely incompatible with MEP monitoring

Safety consideration: TES can cause patient movement at the time of stimulation (the transcranial stimulus causes brief generalised muscle contraction); the surgeon must be warned before each stimulus train; particularly important during procedures near the spinal cord (sudden movement during posterior instrumentation could cause injury) — TES is temporarily paused during the most critical surgical steps

Processed EEG (BIS, Entropy, SEDLine): the raw EEG is processed by mathematical algorithms (bispectral analysis, spectral entropy) to produce a dimensionless number (BIS 0–100; 40–60 = appropriate depth for GA; >60 = at risk of awareness; <40 = overly deep); BIS monitoring is the standard processed EEG tool for TIVA awareness prevention

Raw EEG for cerebral ischaemia: during carotid endarterectomy (CEA), 8-lead or 16-lead raw EEG is recorded continuously; the EEG changes predictably with ischaemia: first, high-frequency activity decreases; then delta waves emerge; then progressive slowing; then burst suppression; finally, isoelectric EEG; these changes occur within 1–3 minutes of ischaemia onset and precede irreversible injury → if detected, the surgeon can immediately insert a carotid shunt to restore perfusion; EEG sensitivity for detecting significant CEA-related ischaemia: approximately 90%

Agent Effect on SSEP/MEP/EEG IONM Compatibility Volatile agents Dose-dependent suppression of SSEP amplitude (20–50% at 1 MAC); MEP Can be used at low doses (<0.5 MAC) alongside TIVA; above (sevoflurane, amplitude suppressed 50–80% at 1 MAC; high-frequency EEG suppressed 0.5 MAC → signals may become uninterpretable; AVOID for isoflurane, MEP-intensive monitoring desflurane) Nitrous oxide Significant MEP amplitude suppression (additional 50% reduction when added to AVOID in IONM cases; use air-O₂ mixture instead (N₂O) propofol); SSEP amplitude also reduced Propofol (IV Dose-dependent EEG suppression (dose-dependent BIS reduction); SSEP Well tolerated for IONM; TIVA with propofol is the preferred infusion) amplitude modestly reduced but maintained at clinical doses; MEP amplitude technique reduced but maintained at doses used for maintenance TIVA Remifentanil (IV Minimal direct effect on SSEP or MEP at clinical doses; provides analgesia Excellent — ideal TIVA combination: propofol 2–4 mcg/mL + infusion) without significant IONM signal interference remifentanil 2–6 ng/mL Ce provides adequate anaesthesia with minimal IONM signal suppression NMBs (non- ABOLISH MEP (muscle-recorded CMAPs cannot be generated through a CONTRAINDICATED during MEP monitoring; only acceptable depolarising) blocked NMJ); no effect on SSEP (recorded from scalp, not from muscles) for SSEP-only monitoring Ketamine INCREASES cortical excitability → ENHANCES SSEP and MEP amplitude; Beneficial adjuvant for IONM; sub-anaesthetic ketamine (0.5 antagonises the amplitude-suppressing effects of other agents mg/kg bolus + 0.25 mg/kg/hr infusion) as part of a balanced TIVA technique improves IONM signal quality

Phaeochromocytoma secretes adrenaline and/or noradrenaline (and dopamine in some extra-adrenal tumours) — episodically or continuously; during tumour manipulation at surgery, massive catecholamine surges produce: extreme hypertension (SBP up to 300+ mmHg); tachycardia and arrhythmias; diaphoresis; headache; pallor; hyperglycaemia; after tumour vein ligation: sudden catecholamine withdrawal → profound vasodilation → hypotension

Alpha-blockade MUST precede beta-blockade: if beta-blockers are given before alpha-blockers → the vasodilatory β₂ effects are blocked leaving only α₁ vasoconstriction unopposed → PARADOXICAL SEVERE HYPERTENSION; alpha-blockers first allow β₂-mediated vasodilation to counterbalance the α₁ vasoconstriction of the catecholamines, making blood pressure more manageable before beta-blockade is added Phenoxybenzamine (irreversible non-selective α-blocker): historically the gold standard; oral 10–20 mg BD, titrated up over 1–3 weeks; produces noncompetitive (irreversible) alpha-blockade — unresponsive to high catecholamine surges during surgery (the block persists regardless of catecholamine level); well-established safety record; side effects: orthostatic hypotension, nasal stuffiness (nasal α₁ vasoconstriction blocked), reflex tachycardia (α-blockade → vasodilation → reflex HR increase → this is why beta-blocker is then added); disadvantage: long duration of action causes prolonged hypotension postoperatively Doxazosin (selective α₁-blocker; competitive): increasingly preferred in many centres; shorter half-life → post-operative hypotension less prolonged; oral titration starting at 2 mg OD; competitive blockade — may be overcome by very high catecholamine surges (but manageable intraoperatively with vasoactive drugs)

Beta-blockade: added after adequate alpha-blockade (at least 1–2 weeks) ONLY if reflex tachycardia or arrhythmias develop; propranolol or atenolol; DO

NOT start beta-blockade until alpha-blockade is established

Adequacy of pre-operative blockade criteria: BP controlled <130/80 for 24 hours; orthostatic hypotension (confirms adequate vasodilation from alphablockade); nasal congestion; no ECG changes of ischaemia; HR 60–80 bpm (if on beta-blocker) High-salt diet + IV fluid loading: pre-operatively; chronic catecholamine excess causes contracted plasma volume; normalising volume with high-Na diet and adequate hydration reduces the magnitude of post-tumour-ligation hypotension

Surgical Haemodynamic Response Management Phase Induction Hypertensive surge from laryngoscopic stimulus + Fentanyl 3–5 mcg/kg before laryngoscopy; lignocaine 1.5 mg/kg IV 90 sec before; avoid and surgical stress succinylcholine if possible (may stimulate catecholamine release via ganglionic stimulation); laryngoscopy ketamine AVOIDED (stimulates catecholamine release); propofol induction (least haemodynamically stimulating) Tumour MASSIVE catecholamine surge → SBP may reach Pre-prepared syringes: phentolamine (non-selective α-blocker) 1–5 mg IV bolus for acute manipulation 250–300 mmHg; tachycardia; arrhythmias hypertension; sodium nitroprusside (SNP) 0.25–8 mcg/kg/min infusion for rapid BP titration; labetalol for combined α/β effect; nicardipine 1–10 mg/hr; magnesium sulphate 2–4 g IV (inhibits catecholamine release from adrenal medulla — may reduce surges) Tumour vein SUDDEN catecholamine withdrawal → profound Alert surgeon 2–3 minutes before ligation; pre-load with IV crystalloid 500 mL; immediately ligation and vasodilation → precipitous hypotension (SBP may fall to start noradrenaline infusion (0.1–1.0 mcg/kg/min) — typically required for 12–24 hours postremoval 50 mmHg in seconds); this is the most dangerous operatively; dopamine or vasopressin as adjuncts; discontinue ALL antihypertensive infusions haemodynamic event the moment the tumour vein is ligated Post- Continued vasodilatory hypotension from ICU monitoring 24–48 hours; vasopressor infusion as required; blood glucose monitoring (risk operative catecholamine withdrawal; hypoglycaemia (insulin of hypoglycaemia post-resection); hydrocortisone 50 mg QDS if bilateral adrenalectomy period secretion resumes when catecholamine stimulation of performed (adrenal insufficiency) α₂ islet cell receptors is removed); continued alphablocker effect

Monitoring: arterial line (mandatory — beat-to-beat BP); central venous catheter (vasoactive drug delivery + CVP monitoring); TOE (where available — useful for assessing LV function and preload in real-time); temperature monitoring

AVOID in anaesthesia for phaeochromocytoma: succinylcholine (ganglionic stimulation may trigger catecholamine release); ketamine (direct catecholaminereleasing effect); morphine (histamine release may destabilise BP); atracurium high doses (histamine release); metoclopramide (BLOCKS central dopamine receptors → may worsen BP in dopamine-secreting tumours); halothane (sensitises myocardium to catecholamine-induced arrhythmias); pancuronium (catecholamine-releasing sympathomimetic properties)

PREFERRED agents: propofol (induction + maintenance or TIVA); fentanyl/remifentanil (opioid component); isoflurane or sevoflurane at low MAC if volatile desired; rocuronium (NMB without histamine release or catecholamine stimulation); vecuronium (similarly safe)

Monro-Kellie doctrine: the skull is a rigid, non-expandable box containing three components: brain parenchyma (~80% of volume); CSF (~10%); cerebral blood volume (CBV, ~10%); the total volume within the skull is constant; an increase in any one component must be accompanied by a compensatory decrease in another — otherwise ICP rises; normal ICP = 5–15 mmHg ICP determinants:

Cerebral blood volume (CBV): most rapidly modifiable component; PaCO₂ is the most potent regulator (see below); volatile agents increase CBV by causing cerebral vasodilation

CSF: produced by choroid plexus at 0.35 mL/min (450–500 mL/day); reabsorbed at the arachnoid granulations; drainage via EVD (external ventricular drain) is the most effective means of rapidly reducing ICP in acute raised ICP

Brain tissue: cerebral oedema (vasogenic — blood-brain barrier disruption; cytotoxic — cellular swelling from ischaemia); mass lesions (tumour, haematoma, abscess)

Intracranial compliance: the relationship between volume and pressure is exponential — initially, small volume additions are compensated without ICP rise (the compensated phase: CSF is displaced into the spinal subarachnoid space; veins compress); eventually the compensatory reserve is exhausted — any further increase in volume causes a steep, rapid ICP rise (the decompensated phase — a surgical sponge or a cough can now fatally raise the ICP)

Cerebral autoregulation: the capacity of cerebral arterioles to maintain constant cerebral blood flow (CBF ≈ 50 mL/100g/min) over a wide range of MAP (approximately 60–150 mmHg) by intrinsic myogenic and metabolic vasoconstriction/dilation; below MAP 60 mmHg → autoregulation fails → CBF falls proportionally (ischaemia); above MAP 150 mmHg → autoregulation overwhelmed → CBF rises → cerebral hyperaemia → vasogenic oedema; volatile anaesthetic agents impair autoregulation dose-dependently at >0.5 MAC

CO₂ reactivity: the most powerful modulator of CBF in the physiological range; a rise in PaCO₂ of 1 mmHg → approximately 4% increase in CBF (cerebral vasodilation from CO₂-mediated perivascular acidosis → smooth muscle relaxation); a fall in PaCO₂ of 1 mmHg → approximately 3% decrease in CBF (cerebral vasoconstriction); PaCO₂ of 35–40 mmHg = optimal for most neuroanaesthesia (normocapnia); hyperventilation to PaCO₂ 30–35 mmHg → reduces CBF → reduces CBV → reduces ICP (useful for acute ICP crisis but not sustained — effect wanes after 4–6 hours as CSF bicarbonate equilibrates) CPP = MAP − ICP; target CPP ≥60–70 mmHg in TBI (Brain Trauma Foundation Guidelines); if MAP maintained but ICP rises, CPP falls → ischaemia; both MAP maintenance and ICP reduction are required simultaneously

Intervention Mechanism Target Head Head-up 30° → ↓ venous pooling in cerebral veins → ↑ cerebral venous drainage → ↓ CBV → ↓ ICP; head 30° head-up; neutral neck position; positioning must be in neutral position (neck rotation → compresses IJV → ↑ cerebral venous pressure) avoid venous compression from tight cervical collars or ETT tape Mannitol 20% mannitol 0.25–1 g/kg IV over 15–20 min; osmotic gradient draws water from brain parenchyma into the Acute ICP crisis (herniation); bridge to (osmotherapy) vasculature → ↓ brain water content → ↓ ICP; onset: 15–30 min; duration: 4–6 hours; monitor serum definitive treatment; use as a bolus, not osmolality (maintain <320 mOsm/kg; above this → risk of renal tubular damage) infusion Hypertonic Osmotic mechanism (similar to mannitol); additionally raises serum Na → ↑ osmolality → ↓ brain water; does 3% NaCl: 150–200 mL IV over 20 min; saline (3%, NOT cause osmotic diuresis (unlike mannitol — which can cause hypovolaemia with repeated doses); target serum Na 145–155 mEq/L; 7.5%, 23.4%) growing evidence that hypertonic saline is as effective or superior to mannitol for ICP reduction 23.4% NaCl: 30 mL IV for acute herniation Controlled PaCO₂ 35–40 mmHg for routine neuroanaesthesia (normocapnia); PaCO₂ 30–35 mmHg for acute ICP crisis Routine: 35–40 mmHg; acute ICP ventilation — (deliberate hyperventilation — reduces CBF/CBV/ICP temporarily); avoid PaCO₂ <30 mmHg (profound crisis: 30–35 mmHg (temporary bridge CO₂ target vasoconstriction → ischaemia) only) CSF drainage External ventricular drain placed in the lateral ventricle → direct CSF removal → immediate ICP reduction; Drain set at 10–15 cmH₂O above the (EVD) most effective intervention for acute hydrocephalus-related ICP rise foramen of Monro; allows controlled CSF removal Steroids Dexamethasone 8–16 mg loading → 4 mg QDS; reduces vasogenic oedema around brain tumours Brain tumours with vasogenic oedema; (disrupted BBB); NOT effective for cytotoxic oedema (TBI, ischaemia) does NOT improve outcome in TBI (CRASH trial)

Temperature management: every 1°C fall in temperature → 6–7% reduction in cerebral metabolic rate for O₂ (CMRO₂); mild hypothermia (33–35°C) was studied for brain protection — but the landmark IHAST trial (Todd MM — NEJM 2005; n=1000 aneurysm surgery patients) found that intraoperative mild hypothermia did NOT improve neurological outcome vs normothermia in good-grade subarachnoid haemorrhage surgery; current recommendation: strict normothermia; prevent hyperthermia (every 1°C above normal → 6–7% increase in CMRO₂ → increased vulnerability to ischaemia)

Glucose management: hyperglycaemia worsens neurological outcomes after cerebral ischaemia (lactate accumulation in anaerobic metabolism; increased infarct volume); NICE-SUGAR trial confirmed tight glucose control (<6 mmol/L) increases mortality; current recommendation for neurological patients: maintain glucose 6–10 mmol/L (avoids both hyperglycaemia and hypoglycaemia — both are harmful)

Volatile anaesthetics vs TIVA: volatile agents (particularly isoflurane) provide PRECONDITIONING and POSTCONDITIONING of the brain against ischaemia (volatile-induced ischaemic tolerance — via mitochondrial K+ATP channel activation and other mechanisms); BUT volatile agents also cause cerebral vasodilation → ↑ CBV → ↑ ICP; TIVA (propofol) reduces CMRO₂ and ICP without the vasodilation effect; choice depends on the specific neurosurgical context: raised ICP → TIVA preferred; operations where cerebral ischaemia risk is high (aneurysm clipping, carotid surgery) → volatile preconditioning may be beneficial

Burst suppression: propofol or thiopentone infusion titrated to burst suppression on EEG (complete electrical silence interrupted by brief bursts of activity) represents maximal CMRO₂ reduction — used during temporary aneurysm clipping (to maximally reduce metabolic demand during the period of reduced blood flow); thiopentone 3–5 mg/kg bolus → infusion to achieve burst suppression; propofol 100–200 mcg/kg/min similarly

Stimulus Pattern What it Detects Clinical Use Mode TOF (Train- 4 supramaximal 0.2 TOF count (T1–T4 present or absent) during profound/moderate Standard monitoring throughout anaesthesia; TOF count of-Four) ms pulses at 2 Hz block; TOF ratio (T4/T1 amplitude) during recovery guides dosing; TOF ratio guides extubation decision (2 per second), delivered every 12– 15 seconds

PTC (Post- 50 Hz tetanic Post-tetanic potentiation: the tetanic stimulus increases ACh Monitoring PROFOUND block when TOF count = 0; PTC 1–2 Tetanic stimulus for 5 mobilisation at the nerve terminal → more ACh available → = very deep block; PTC 10–15 = moderately deep; as PTC Count) seconds → pause 3 subsequent stimuli produce detectable responses even when increases → TOF count will soon reappear seconds → then TOF count = 0; PTC counts (1–15) the number of post-tetanic TOF twitches DBS 2 short bursts of 50 Fade between the 2 responses is more easily detectable by Allows detection of moderate residual block (TOF ratio 0.6– (Double- Hz tetanic tactile assessment than TOF fade; DBS₃,₃ is the standard; DBS 0.9) that is MISSED by visual/tactile TOF assessment; useful Burst stimulation (3 ratio ≈ TOF ratio at the end of anaesthesia when qualitative assessment of fade Stimulation) pulses per burst), is needed but quantitative acceleromyography is not available separated by 750 ms Tetanic 50 or 100 Hz Fade during tetanic stimulation indicates residual non- Sensitive indicator of residual block; painful in the awake stimulation continuous depolarising block (normal: sustained contraction; residual patient → only for use under deep anaesthesia or general stimulation for 5 block: fading contraction during tetanus) anaesthesia seconds Single Single 0.2 ms T1 height as % of baseline; T1 suppression during block Calibrating baseline before NMB; monitoring during very deep twitch supramaximal pulse relaxant block when all 4 TOF twitches are absent at 0.1–1 Hz

Level of Block TOF Count PTC Clinical Intense/Ultra- 0/4 (no twitches) PTC = 0 Maximum surgical relaxation (intubating conditions, rigid abdomen); used for specific procedures deep block (retroperitoneal surgery, ophthalmic surgery) Profound block 0/4 PTC 1–5 Good surgical relaxation; recovery will occur within 10–30 min depending on drug and dose Deep block 0–1/4 PTC >10 Acceptable for most abdominal surgery; spontaneous recovery approaching Moderate block 1–3/4 N/A (TOF count Inadequate for adequate closure of abdomen; reversal with neostigmine may be attempted but not at TOF present) 1/4 Shallow block 4/4 with fade N/A Patient can breathe but may have residual dysfunction; TOF ratio 0.4–0.9 = clinical RNMB; requires reversal Adequate 4/4 with TOF N/A Safe for extubation; pharyngeal and airway reflexes are clinically intact at TOF ratio ≥0.9 recovery ratio ≥0.9

Sustained head lift for 5 seconds: requires TOF ratio ≥0.6 only — INSENSITIVE; a patient failing the head lift test has very significant RNMB, but a patient who can lift their head for 5 seconds may still have TOF ratio as low as 0.6 → still unsafe to extubate Hand grip strength, ability to open eyes, tongue depressor test — all insensitive; do not reliably detect TOF ratio 0.6–0.9 (the clinically dangerous range of

RNMB)

Tactile and visual TOF fade assessment: cannot reliably detect fade when TOF ratio >0.4; the eye and finger cannot detect fade at TOF ratio 0.4–0.9 → qualitative monitoring misses the most dangerous range of residual block

Conclusion: quantitative TOF monitoring (acceleromyography — Mechanosensor®, TOFscan®, TetraGraph®) is the only reliable method to confirm TOF ratio ≥0.9; this is now the standard of care recommendation (PORC prevention guidelines; 2020 European recommendations)

Phase Description Physiological Basis Phase I Flat baseline at CO₂ = 0 Dead space gas from the airways and breathing circuit; no CO₂ if circuit is functioning correctly; elevated baseline = (Inspiratory mmHg REBREATHING (inadequate CO₂ absorber, incompetent expiratory valve, insufficient fresh gas flow in Mapleson system) baseline) Phase II Rapid rise in CO₂ as Mixing of dead space and alveolar gas; slope of Phase II reflects the homogeneity of alveolar emptying; steeper = more (Expiratory exhaled gas transitions uniform; prolonged gradual slope = V/Q inhomogeneity (COPD, bronchospasm) upstroke) from dead space to alveolar gas Phase III Relatively flat plateau at Predominantly alveolar gas exhaled; the slope of the plateau is slightly upward in normal lungs; steep upward slope (shark fin (Alveolar or near ETCO₂ value pattern) = BRONCHOSPASM (inhomogeneous alveolar emptying — obstructed alveoli empty slowly and their higher CO₂ plateau) concentration is reached later in exhalation); in normal lungs: plateau slope ≤2 mmHg; in COPD/asthma: >5 mmHg Phase 0 Rapid fall in CO₂ as Inspiratory fresh gas washout of CO₂; abrupt fall; the point of maximum CO₂ before this fall = ETCO₂ value (Phase IV fresh gas is inspired — Inspiration)

Waveform Appearance Diagnosis Pattern Oesophageal ETCO₂ absent or rapidly falling to zero (a few Immediate diagnosis of oesophageal intubation; this is the most important airway safety application intubation small waves diminishing over 5 breaths then of capnography; if no sustained ETCO₂ waveform → ETT is NOT in the trachea until proven nothing — CO₂ in the stomach from mask otherwise ventilation exhausted) Bronchospasm Phase II prolonged (gradual rise); Phase III Bronchospasm (or severe COPD exacerbation); inhomogeneous airway resistance → alveoli with — "Shark Fin" steep upward slope; sharp peak replacing the high resistance empty slowly → CO₂ concentration continues to rise throughout expiration → steep or "Reverse normal flat plateau; the overall waveform Phase III slope Shark" resembles a shark's dorsal fin Rebreathing Phase I baseline elevated above zero (ETCO₂ Inspired CO₂; causes: exhausted soda lime; incompetent expiratory valve; insufficient FGF in baseline >0 mmHg) Mapleson system; rebreathing increases ETCO₂ and PaCO₂ → respiratory acidosis Cardiac arrest Sudden sharp fall in ETCO₂ to near-zero ETCO₂ is a surrogate for cardiac output (CO₂ delivery to the lungs requires pulmonary blood flow); or severe ↓ CO (despite continued ventilation); the CO₂ sudden fall in ETCO₂ during surgery = cardiac arrest, massive PE, severe haemorrhage; during reaching the alveoli falls dramatically when CO CPR: ETCO₂ >10 mmHg correlates with adequate chest compression quality; ETCO₂ rise to >35 is absent mmHg during CPR = early sign of ROSC Curare notch Notch or dip within Phase III (the plateau) Insufficient neuromuscular blockade — the patient is making respiratory efforts during the Phase III (cleft in plateau; each effort draws fresh gas briefly, producing a dip in CO₂; a sign of inadequate relaxation plateau) or recovering block — assess TOF count

Limitation Mechanism Clinical Implication Carbon monoxide Standard 2-wavelength pulse oximeter cannot distinguish COHb from Require co-oximetry ABG to measure COHb directly; SpO₂ is poisoning (COHb) OxyHb (both absorb identically at 660 nm); SpO₂ reads FALSELY HIGH USELESS for diagnosis of CO poisoning; clinical suspicion even when functional O₂ saturation is critically low; patient appears well- must guide diagnosis in fires and closed-space exposure oxygenated while CO is occupying 40–60% of haemoglobin Methaemoglobinaemia MetHb absorbs at both 660 nm and 940 nm equally (absorption ratio Suspect if SpO₂ plateau at 85% despite increasing FiO₂; (MetHb) approaches 1.0); the pulse oximeter reads SpO₂ as approximately 85% causes: dapsone, prilocaine (>600 mg → EMLA cream large regardless of the actual MetHb level; MetHb >20% → SpO₂ stuck at ~85% area), nitrites, benzocaine, rasburicase; treat with methylene (does not accurately reflect the true severity) blue 1–2 mg/kg IV (reduces MetHb to functional Hb) Low-perfusion states Peripheral vasoconstriction (hypothermia, shock, vasopressors) reduces Unreliable in hypothermia or shock; move probe to a betterperipheral pulsatile flow → the SpO₂ signal becomes weak, inaccurate, or perfused site (ear, forehead reflectance probe) or use coabsent; the probe may read the venous plethysmographic wave rather than oximetry ABG as the gold standard the arterial signal if pulsatile flow is very low Nail polish and Dark nail polish absorbs at the measurement wavelengths → falsely low Ask about nail polish pre-operatively; remove or use alternative artificial nails SpO₂; remove or use side-of-finger placement to avoid the nail probe placement

P-V loops plot airway pressure (x-axis) against tidal volume (y-axis) during a single breath; modern ventilators display these in real-time; a normal P-V loop is roughly elliptical: the inspiratory limb shows increasing volume with increasing pressure; the expiratory limb shows passive deflation; hysteresis (the loop area) represents the energy consumed in overcoming airway resistance and lung viscoelasticity Clinical applications:

Upper inflection point (UIP): kink in the inspiratory limb at high pressures where compliance suddenly decreases (lung overdistension) → if tidal volume exceeds this point, barotrauma and volutrauma risk; PEEP should be set BELOW the UIP

Lower inflection point (LIP): kink at low pressures where compliance improves suddenly (alveolar recruitment) → PEEP should be set ABOVE the LIP to maintain open alveoli and prevent atelectrauma; the "open lung" strategy: PEEP between LIP and UIP Increased area of the loop (wider loop) = increased resistance (bronchospasm) — the pressure required to move the tidal volume is disproportionately high, creating a characteristic "peanut-shaped" loop in severe bronchospasm Birds-beak appearance at the beginning of inspiration = patient-triggered breath with flow limitation (auto-PEEP/gas trapping) — the loop does not start at zero pressure but at a positive pressure baseline

System Change Clinical Relevance Respiratory ↓ FRC (supine position → abdominal fat compresses diaphragm → FRC may fall below closing Rapid desaturation during apnoea (lowest FRC capacity → atelectasis); ↑ O₂ consumption; ↑ CO₂ production; restrictive pattern (↓ TLC, ↓ FVC); + highest O₂ demand); difficult preoxygenation; obstructive sleep apnoea in 70–80% of morbidly obese challenging ventilation; atelectasis-prone under GA Cardiovascular ↑ Blood volume (↑ CO, ↑ stroke volume); LVH (pressure and volume overload); ↑ HR; systemic and Cardiac assessment essential; diastolic failure pulmonary hypertension; diastolic dysfunction; obesity cardiomyopathy; ↑ atherosclerosis risk → sensitive to fluid overload; higher perioperative cardiac risk Airway Difficult mask ventilation (Mallampati IV, large tongue, retrognathia, short thick neck, excess Anticipated difficult airway; RSI or awake FOI; pharyngeal tissue); difficult laryngoscopy (reduced cervical flexion, excessive chest fat limiting video laryngoscopy as first-line laryngoscope handle movement); high risk of aspiration (↑ gastric volume, ↑ intragastric pressure, ↑ GERD) Gastric ↑ Gastric volume; ↑ intragastric pressure from abdominal fat; ↑ GERD; ↑ aspiration risk RSI for GA induction; anti-aspiration precautions; ranitidine or PPI pre-operatively

OSA screening: STOP-BANG questionnaire (Snoring, Tired, Observed apnoea, Pressure, BMI >35, Age >50, Neck ≥40 cm, Male Gender); score ≥3 = high risk of OSA; ≥5 = high risk of severe OSA; all morbidly obese patients should be considered for pre-operative sleep study (polysomnography or home sleep test) and CPAP therapy optimisation before elective bariatric surgery

Respiratory: spirometry (to identify coexisting COPD or severe restriction); ABG (if suspect O₂ desaturation or CO₂ retention — obesity hypoventilation syndrome); CXR or CT chest for preoperative planning; resting SpO₂ on air (if <95% → investigate for OHS)

Cardiovascular: ECG; echocardiography if clinical suggestion of cardiomyopathy, pulmonary hypertension, or significant dyspnoea; establish exercise tolerance (METS)

Medications: CPAP therapy — patient should bring their CPAP machine to hospital for immediate post-operative use; ensure CPAP settings documented

HELP (Head-Elevated Laryngoscopy Position): 25–30° reverse Trendelenburg (head-up tilt of the whole table) + careful ramping of the upper body with a purpose-built ramp or folded blankets (the external auditory meatus should be at the same horizontal level as the sternal notch); this position: extends the intubation duration by reducing mediastinal and abdominal fat compression on the diaphragm → extends the safe apnoea time; improves laryngoscopic view by aligning the oral-pharyngeal-laryngeal axes more effectively; reduces FRC decrease during the apnoeic intubation phase

Pre-oxygenation: 100% O₂ for minimum 5 minutes in HELP position before induction; use 25° head-up for pre-oxygenation (even before ramping for intubation) — head-up position during pre-oxygenation significantly extends safe apnoea time in obese patients (Boyce JR ANESTH 2003); HFNO (high-flow nasal O₂ 60–70 L/min during apnoea — transnasal humidified rapid insufflation ventilatory exchange — THRIVE) extends safe apnoea time further

Airway strategy: video laryngoscopy as first-line intubation tool (DAS recommendation for obese patients — greater Cormack-Lehane grade I-II rate vs direct laryngoscopy); RSI for all obese patients due to aspiration risk; difficult airway trolley at the bedside; backup plan (SAD, AFOI) documented in pre-op assessment

Use Drug Use TBW Use AdjBW IBW Succinylcholine No TBW (plasma pseudocholinesterase activity correlates with — TBW; underdosing on IBW → inadequate intubating conditions) Rocuronium No IBW (avoid overdose and prolonged block; the NMJ drug — (intubating binding is related to lean body mass not fat) dose) Propofol No No Lean Body Weight (LBW) or IBW for induction dose; TBW overestimates and induction causes overdose; IBW may underdose large individuals; LBW or dose-titrate to effect Propofol No No LBW with Schnider model (Schnider automatically calculates LBW from maintenance height/weight/age/gender) (TCI) Remifentanil No No IBW (or LBW) for remifentanil TCI — using TBW significantly overdoses Fentanyl No No LBW or dose cautiously — accumulates in fat; titrate to effect Morphine IBW No — Gentamicin / No No AdjBW = IBW + 0.4 × (TBW − IBW) antibiotics

LPV in obesity: tidal volume 6–8 mL/kg IBW (NOT TBW — using TBW produces dangerously high tidal volumes in obese patients); PEEP 8–12 cmH₂O (higher PEEP needed to prevent atelectasis in obese patients — the increased abdominal pressure elevates closing volume); FiO₂ 0.5 during surgery (highest FiO₂ worsens atelectasis via absorption atelectasis); intraoperative recruitment manoeuvres (sustained inflation 40 cmH₂O for 40 seconds) improves oxygenation and prevents atelectasis

Post-operative: CPAP immediately post-extubation for known OSA (patient's home CPAP settings); nursing in head-up or lateral position (not supine) in recovery; supplemental O₂; careful opioid avoidance (opioids worsen OSA — multimodal analgesia with TAP block, IV paracetamol, NSAIDs, dexamethasone 8 mg); TIVA with propofol preferred (lower PONV than volatile agents; earlier return to CPAP use)

Immunological: AHTR (ABO incompatibility); FNHTR (antibodies to white cell antigens); allergic/anaphylactic (IgE-mediated to plasma proteins); TRALI (antibody-mediated lung injury); platelet refractoriness

Non-immunological: TACO (circulatory overload); septic transfusion reaction (bacterial contamination — most common from platelet concentrates); air embolism; hypothermia; hyperkalaemia; hypocalcaemia (citrate toxicity)

Pathophysiology: ABO-incompatible blood (e.g., type A blood given to a type O patient) → pre-formed IgM antibodies in the recipient (anti-A, anti-B) bind donor RBCs → complement activation → intravascular haemolysis → massive haemoglobin release → renal tubular haemoglobin precipitation → acute tubular necrosis → acute kidney injury; simultaneous: DIC (from tissue factor release from haemolysed RBCs + complement activation); systemic inflammatory cytokine storm; hypotension; shock

Clinical features: in the awake patient: burning pain at the IV site; lumbar/flank pain (renal haemoglobin deposition); fever and rigors; hypotension; haemoglobinuria (dark/red urine); in the ANAESTHETISED patient (most dangerous — all symptoms masked): unexplained hypotension; unexplained haemoglobinuria (dark urine in the catheter); oozing from surgical wounds (DIC); haemoglobin in the urine Management: STOP the transfusion immediately; send the blood bag and fresh patient blood sample to the transfusion laboratory (with the transfusion number documented to identify the specific unit) IV fluid resuscitation (maintain urine output ≥1 mL/kg/hr to prevent renal tubular precipitation of haemoglobin); monitor urine colour

Treat DIC: FFP, cryoprecipitate, platelets as guided by TEG/ROTEM; transfuse with compatible blood only Vasopressors for hypotension; monitor for AKI (creatinine, urine output, K⁺); renal replacement therapy if established AKI Notify blood bank, transfusion physician, and haematology; SHOT (Serious Hazards of Transfusion) reporting

Feature TRALI (Transfusion-Related Acute Lung Injury) TACO (Transfusion-Associated Circulatory Overload) Mechanism Non-cardiogenic pulmonary oedema; donor antibodies (anti-HLA or anti-neutrophil) in Cardiogenic pulmonary oedema; volume overload from the transfused blood activate recipient neutrophils → neutrophil sequestration in transfusion in a patient with limited cardiac reserve → ↑ pulmonary capillaries → neutrophil degranulation → capillary leak → interstitial and hydrostatic pressure in pulmonary capillaries → fluid alveolar oedema transudation into alveoli Risk factors Multiparous female donors (higher anti-HLA antibody prevalence); male donors Pre-existing heart failure (EF <40%); elderly; renal failure; increasingly used for plasma/FFP to reduce TRALI risk; surgery, mechanical rapid large-volume transfusion; anaemia (lower threshold for ventilation, active infection (priming the neutrophil "second hit") transfusion, larger volume gap) Clinical onset During or within 6 hours of transfusion; often within 1–2 hours During or within 6 hours of transfusion; often during the transfusion itself Respiratory Acute hypoxaemia (PaO₂/FiO₂ <300 mmHg); bilateral pulmonary infiltrates on CXR Acute hypoxaemia; bilateral pulmonary infiltrates; frothy pink features (non-cardiogenic pattern); frothy white sputum if severe sputum Haemodynamic Normal or LOW blood pressure (inflammatory vasodilation); JVP normal or low; NO ↑ Blood pressure (hypertension); ↑ JVP; ↑ CVP; evidence of evidence of cardiac overload; no response to diuretics (not cardiogenic) cardiac overload; responds to diuretics BNP/NT- Normal or mildly elevated Markedly elevated (BNP >250 pg/mL; NT-proBNP >1500 proBNP pg/mL) ECHO/TOE Normal or hyperdynamic LV; no pericardial effusion Reduced EF; dilated LV; ↑ LVEDP; pericardial effusion (if chronic HF) Management STOP transfusion; supportive: O₂ → NIV → IPPV with ARDS-protective ventilation if STOP or slow transfusion; furosemide 40–80 mg IV; O₂ → needed; NO diuretics (not fluid overload); NO steroids (no proven benefit); notify blood NIV; treat underlying cardiac failure; vasodilators if bank; save blood bag for donor antibody testing hypertensive Mortality 5–10%; leading cause of transfusion-related death (SHOT data); severe TRALI has 5%; lower than TRALI with appropriate management; higher 25–40% mortality with ARDS in severe cardiac failure 25–40% mortality with ARDS in severe cardiac failure

Febrile non-haemolytic transfusion reaction: temperature rise ≥1°C during or within 4 hours of transfusion; caused by cytokines in stored blood products (IL-6, IL-8, TNF — accumulate during storage) OR recipient antibodies reacting against donor HLA antigens on white cells; now less common since universal leucodepletion (removal of WBCs from blood products) in the UK

Management: STOP the transfusion; assess the patient (rule out AHTR — haemolysis; rule out septic reaction); if fever is mild and isolated (no haemoglobinuria, no haemodynamic compromise, no rigors): can cautiously restart at a slower rate after paracetamol 1 g oral/IV and 15–30 minutes observation; if fever >2°C, rigors, or any other concerning features → do NOT restart; full AHTR workup (DAT, blood cultures, transfusion laboratory)