Anesthesia

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