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Myasthenia Gravis (MG): Anaesthetic Management for Thymectomy & Myasthenic Crisis

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What is Myasthenic Crisis?

• Occurs in 15–20% of MG patients, usually within the first 2 years of disease onset
• A progression in severity of the underlying disease, often amplified by a trigger

• Cardiovascular: beta-blockers, calcium channel blockers, quinidine, procainamide, lidocaine
• Antibiotics: aminoglycosides, tetracyclines, clindamycin, fluoroquinolones, polymyxin B
• Others: neuromuscular blockers, corticosteroids (paradoxical worsening), phenytoin, thyroid replacement

1. Secure airway — respiratory failure arises from muscle weakness, not hypoxia; supplemental O₂ alone is inadequate
2. Plasma exchange — first-line for severe crisis; effective in up to 95% of cases; multiple exchanges over 1–2 weeks
3. IVIG — 2 g/kg in divided doses over several days; equivalent efficacy, easier to administer
4. Both are combined with high-dose oral prednisolone (60 mg/day) — but steroids can transiently worsen weakness, so always give alongside PE or IVIG
5. Reinstate or adjust pyridostigmine (60–120 mg orally q4–6h) if crisis was precipitated by dose reduction

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Anaesthetic Management for Thymectomy

Preoperative Assessment

• Document disease class (MGFA Classification I–V) — class, affected muscle groups, bulbar/respiratory involvement
• Identify predictors of postoperative ventilation requirement:
  • Disease duration > 6 years
  • Vital capacity < 4 mL/kg (or < 2–2.9 L)
  • Peak inspiratory pressure < –25 cmH₂O
  • Pyridostigmine dose > 750 mg/day
  • Coexisting pulmonary disease
• Optimise before surgery: patients with respiratory or oropharyngeal weakness should receive preoperative IVIG or plasmapheresis; if strength normalises, postoperative complication risk approaches that of a non-myasthenic patient
• Screen for coexisting autoimmune disorders (hypothyroidism, rheumatoid arthritis, SLE)
• Review all drugs for potential MG exacerbation

Premedication

• Avoid or use with great caution: opioids and benzodiazepines — MG patients are hypersensitive to respiratory depressant effects
• Consider H₂-blocker or proton pump inhibitor (aspiration risk with bulbar involvement)
• Continue anticholinesterase medications up to the morning of surgery in most patients; discuss with the surgical/neurological team

Induction & Airway

• Standard induction agents can be used, but even moderate doses of propofol or opioids may cause marked respiratory depression
• Volatile agent-based anaesthesia is preferred — deep inhalational anaesthesia alone (sevoflurane/desflurane) frequently provides sufficient relaxation for intubation and surgery without any NMB

Neuromuscular Blocking Agents (NMBs)

• Neuromuscular monitoring is mandatory — train-of-four throughout; confirm full recovery before extubation
• Sugammadex is the preferred reversal agent if rocuronium is used (avoids anticholinesterase accumulation)
• Neostigmine reversal may be used cautiously; remember it also inhibits plasma cholinesterase, theoretically prolonging succinylcholine and ester local anaesthetic action

Maintenance

• Volatile agents (sevoflurane/isoflurane) provide dose-dependent relaxation and are the backbone of MG anaesthesia
• Supplement with short-acting opioids titrated carefully
• Target multimodal analgesia to minimise opioid requirement (NSAIDs, paracetamol, regional techniques where feasible)
• Thoracic epidural analgesia is an excellent option for open transsternal thymectomy — reduces opioid requirement and facilitates early extubation

Surgical Note

• Preserve phrenic nerves — critical; inadvertent phrenic nerve injury is catastrophic in an already weak patient
• Complete resection of all mediastinal fatty areolar tissue is required to remove ectopic thymic tissue

Extubation & Postoperative Care

• Extubate only after confirming adequate neuromuscular recovery (TOF ratio > 0.9) and ventilatory function
• Predictors of need for postoperative mechanical ventilation (see preoperative assessment above) must guide planning
• Have ICU/HDU bed available for all MG thymectomy patients
• Restart anticholinesterase agents as soon as oral intake resumes postoperatively; if oral route unavailable, give parenterally at 1/30th the oral dose
• Intensive pulmonary physiotherapy, early mobilisation, avoid respiratory depressants
• Watch for postoperative myasthenic crisis — infection, residual NMB, pain-limited respiration, and medication delays are all triggers

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• Morgan and Mikhail's Clinical Anesthesiology, 7e — Anaesthetic Considerations, Myasthenia Gravis
• ROSEN's Emergency Medicine — Myasthenic Crisis Management
• Sabiston Textbook of Surgery — Perioperative Management for Thymectomy
• Miller's Anesthesia, 10e — Postoperative Myasthenic Crisis Predictors

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Anaesthetic Management: 90-Year-Old Female for Total Hip Replacement (THA)

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Preoperative Assessment

Age-Related Physiological Changes to Consider

Specific Preoperative Workup

• Full history and examination: document functional status, exercise tolerance, comorbidities (HTN, IHD, DM, COPD, CVA), current medications (anticoagulants, antiplatelet agents, steroids, antihypertensives)
• Investigations: ECG, CXR, FBC (haemoglobin — correct anaemia preoperatively), RFT/electrolytes, coagulation profile, blood group and save/crossmatch
• Cardiac evaluation: consider echocardiography if signs of heart failure or severe valvular disease; aortic stenosis is common in elderly women and is high risk
• Respiratory: PFTs if significant COPD; optimise if active infection or bronchospasm
• Airway assessment: assess for cervical spine disease, limited neck movement (common in elderly), temporomandibular stiffness
• Cognitive baseline: Mini-Mental State Examination or Mini-Cog as baseline
• Frailty assessment: frailty significantly predicts perioperative morbidity — assess with validated tool
• Antithrombotic medications: VTE prophylaxis planning; if on warfarin/DOAC, plan appropriate bridging

Preoperative Optimisation

• Correct anaemia: IV iron infusion, or if elective with sufficient time, recombinant erythropoietin + iron/B12/folate supplementation; maintain Hb >10 g/dL before surgery
• Correct electrolyte disturbances and dehydration
• Optimise cardiac failure, COPD, glycaemic control
• Continue antihypertensives (except ACE inhibitors/ARBs on the day of surgery)
• Tranexamic acid: clinical practice guidelines recommend routine administration prior to incision to reduce blood loss (both IV and topical routes supported)
• Inform patient and family of high perioperative risk; shared decision-making

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Choice of Anaesthesia

• Decreased mortality
• Reduced incidence of deep vein thrombosis and pulmonary embolism
• Reduced postoperative delirium
• Decreased all-cause infections
• Reduced acute kidney injury
• Better postoperative analgesia
• Reduced blood loss (sympathectomy reduces venous pooling in lower limbs; also reduces platelet reactivity and attenuates postoperative changes in factor VIII, von Willebrand factor, and antithrombin III)

Spinal Anaesthesia — Practical Points

• Agent: Hyperbaric or isobaric bupivacaine (0.5%) — isobaric preferred if patient positioned laterally
• Level: T10 provides adequate coverage for THA
• Dose reduction: Elderly patients require smaller doses (reduced CSF volume, decreased spinal cord blood flow, reduced protein binding); typically 1.5–2 mL of 0.5% isobaric bupivacaine
• Adjuvants: Intrathecal opioids (morphine 100–150 mcg or fentanyl 10–25 mcg) extend postoperative analgesia — but morphine requires close monitoring for delayed respiratory depression (up to 18–24 h)
• Hypotension: Very common in the elderly due to sympathectomy on a background of reduced cardiac reserve and pre-existing hypertension. Treat promptly with:
  • Vasopressors: phenylephrine (pure alpha) preferred if tachycardic; ephedrine if bradycardic
  • Judicious IV fluids — avoid overload in diastolic dysfunction
  • Pre-loading or co-loading with crystalloid

Combined Spinal-Epidural (CSE)

• Allows lower spinal dose (reduces hypotension) with epidural catheter for top-up and postoperative analgesia
• Particularly useful if prolonged surgery anticipated

General Anaesthesia (if neuraxial contraindicated or fails)

• Contraindications to neuraxial: patient refusal, therapeutic anticoagulation, coagulopathy, local infection, severe spinal deformity
• Use total intravenous anaesthesia (TIVA) with propofol + remifentanil (dose-reduced) or volatile agent (MAC reduced by ~6% per decade after 40 years)
• Airway: anticipate difficult airway — reduced neck mobility, poor dentition, possible cervical spondylosis
• Avoid: prolonged use of anticholinergics and benzodiazepines (increase delirium risk); meperidine (normeperidine metabolite causes neurotoxicity); ketamine has analgesic/opioid-sparing role but evidence for delirium prevention is mixed

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Intraoperative Management

Positioning

• Lateral decubitus (most common for posterior approach) — pad all pressure points carefully; bony prominences especially vulnerable in elderly with thin skin
• Axillary roll to protect the brachial plexus
• Ensure eyes are protected and head is neutral

Monitoring

• Standard ASA monitoring: SpO₂, ETCO₂, ECG, NIBP, temperature
• Invasive arterial line (radial): strongly recommended in a 90-year-old for continuous BP monitoring (frequent hypotension episodes, beat-to-beat response to cementing) and blood gas sampling
• Consider central venous access if poor peripheral access or significant cardiac disease
• Temperature monitoring and active warming — elderly lose heat rapidly; hypothermia increases blood loss and infection risk

Bone Cement Implantation Syndrome (BCIS) — Critical Risk

• Hypoxia (increased pulmonary shunt)
• Hypotension / cardiovascular collapse
• Arrhythmias — heart block, sinus arrest
• Pulmonary hypertension and decreased cardiac output

• Increase FiO₂ to 1.0 before cementing
• Ensure euvolemia and maintain adequate MAP
• Have vasopressors drawn up and ready
• Surgical measures: vent hole in distal femur, high-pressure lavage of femoral shaft
• If severe collapse: CPR, vasopressors, treat as massive embolism

Blood Loss Management

• THA involves significant blood loss (average 500–1000 mL; more in revision)
• Tranexamic acid IV (15 mg/kg) prior to incision — single dose reduces transfusion requirement
• Cell salvage (intraoperative) — consider for major blood loss risk
• Transfusion threshold: Hb < 8 g/dL (or < 10 g/dL if symptomatic or cardiac disease)
• Large-bore IV access; fluid warmer

DVT/VTE Prophylaxis

• Mechanical: graduated compression stockings + intermittent pneumatic compression devices
• Pharmacological: LMWH (e.g., enoxaparin) starting 12 h postoperatively (or 12 h pre-op), or direct oral anticoagulants (rivaroxaban/apixaban) postoperatively
• Neuraxial timing around anticoagulant dosing must strictly follow ASRA guidelines:
  • Prophylactic LMWH: wait ≥12 h after last dose before neuraxial; catheter removal ≥12 h after last dose; next dose ≥4 h after removal

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Postoperative Management

• HDU/ICU bed: all 90-year-old THA patients need enhanced postoperative monitoring
• Analgesia (multimodal — minimise opioids):
  • Intrathecal morphine (extended coverage up to 18–24 h; monitor for respiratory depression)
  • Fascia iliaca compartment block / lumbar plexus block for opioid-sparing analgesia
  • Regular paracetamol ± NSAIDs (use NSAIDs cautiously — renal function, GI bleeding risk in elderly)
  • Avoid morphine/opioids as first-line — use minimum effective dose; naloxone available
• Delirium prevention: early mobilisation; avoid delirium-precipitating drugs; restore glasses/hearing aids; maintain orientation; adequate hydration; treat pain adequately
• Early mobilisation: key to preventing DVT, chest complications, pressure ulcers, functional decline
• Temperature: maintain normothermia (forced-air warming)
• Physiotherapy: begin day 1 postoperatively
• Monitor for: BCIS complications, fat embolism syndrome (petechiae, hypoxia, neurological signs 1–3 days post-op), surgical site infection, urinary retention, pressure injuries

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Summary of Key Priorities in This Patient

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Inhalational Anaesthetic Agents

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Classification

• Halogenated ethers: Isoflurane, Sevoflurane, Desflurane, Enflurane
• Halogenated alkane: Halothane (largely withdrawn)

• Nitrous oxide (N₂O)
• Xenon (Xe) — experimental/specialised use

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Key Pharmacological Concepts

Minimum Alveolar Concentration (MAC)

• Higher MAC = less potent agent
• MAC-awake = concentration at which consciousness/recall is lost (~0.4–0.5 MAC)
• MAC in 60–70% N₂O is significantly reduced (N₂O has an additive/synergistic effect)

Blood:Gas Partition Coefficient (Ostwald Coefficient)

• Measures solubility of the agent in blood relative to alveolar gas
• Lower blood:gas coefficient → less uptake by blood → faster equilibration → more rapid induction and emergence
• Order (fastest to slowest emergence): Desflurane (0.42) > N₂O (0.46) > Sevoflurane (0.65) > Isoflurane (1.46) > Enflurane (1.9) > Halothane (2.5)

Oil:Gas Partition Coefficient

• Correlates with potency (Meyer-Overton theory of lipid solubility)
• Higher oil:gas coefficient = more potent (lower MAC)

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Physicochemical Properties (Comparative Table)

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Individual Agents

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1. Isoflurane

• Most potent of the modern volatile agents (MAC 1.17%)
• Isomer of enflurane
• Pungent odour — not suitable for inhalational induction (causes airway irritation, laryngospasm, coughing)
• Used for maintenance after IV induction

• 99% excreted unchanged by lungs; only 0.2% metabolised

• Dose-dependent ↓ BP primarily via ↓ SVR (vasodilation)
• Cardiac output well-maintained (unlike halothane which depresses contractility)
• May cause reflex tachycardia
• Potent coronary vasodilator — theoretical coronary steal syndrome but large clinical trials show no increase in myocardial infarction
• Anaesthetic preconditioning — protects myocardium from ischaemia-reperfusion injury

• Concentration-dependent ↓ tidal volume; ↑ respiratory rate
• Potent bronchodilator
• Irritating to airway — not for mask induction
• ↓ ventilatory response to CO₂ and hypoxia

• ↓ CMRO₂ in dose-dependent manner; can produce isoelectric EEG at high doses
• ↑ CBF at doses >0.5 MAC; may raise ICP — use with caution in raised ICP
• Hypocapnia blunts cerebrovascular dilation

• Potentiates non-depolarising NMBs (reduces dose by 30–40%)
• Relaxes skeletal and uterine muscle
• Trigger for malignant hyperthermia (MH)

• Minimal hepatotoxicity; no cases of halothane-like hepatitis
• Reduces renal blood flow and GFR at higher doses

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2. Sevoflurane

• Most widely used volatile agent for both induction and maintenance
• Pleasant, sweet smell — preferred for inhalational (mask) induction in children and adults
• Low blood:gas coefficient (0.65) → rapid induction and emergence
• 2–5% metabolised by hepatic CYP2E1 → inorganic fluoride + hexafluoroisopropanol

• Induction: 2–4% in O₂ ± N₂O
• Maintenance: 1–2.5%
• Ideal for paediatric anaesthesia and day case surgery

• Dose-dependent ↓ BP (vasodilation) and ↓ cardiac output
• Does not cause tachycardia (unlike desflurane/isoflurane) — preferred in ischaemic heart disease
• QTc prolongation may occur at high doses
• Anaesthetic preconditioning against myocardial ischaemia

• ↓ tidal volume, ↑ respiratory rate → net ↑ PaCO₂
• Least irritating to airways of all volatile agents — potent bronchodilator
• Best bronchodilator for use in asthmatic patients

• Similar to isoflurane: ↓ CMRO₂, ↑ CBF at >1 MAC
• Emergence delirium in children — short-lived, no long-term sequelae

• Reacts with soda lime CO₂ absorbent to form Compound A (pentafluoroisopropenyl fluoromethyl ether) — nephrotoxic in rat models
• Large clinical studies show no increase in creatinine, BUN, or urinary enzymes in humans
• Minimum fresh gas flow of 2 L/min recommended when used with circle system

• Exothermic reaction with desiccated CO₂ absorbent → airway burns, spontaneous ignition, CO production

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3. Desflurane

• Least soluble in blood (blood:gas 0.42) → fastest onset and recovery of all volatile agents
• Least potent (MAC 6.6%)
• Boiling point 24°C — requires a heated, pressurised vaporiser (Tec 6 type)
• <0.02% metabolised → negligible hepatic and renal toxicity

• Not suitable for inhalational induction — highly pungent, causes severe airway irritation, bronchospasm, laryngospasm, coughing, excessive secretions
• Used for maintenance in adult patients
• Ideal for long cases where rapid wake-up is desired (bariatric surgery, obese patients, elderly)

• Dose-dependent ↓ BP via ↓ SVR
• Rapid increases in concentration cause sympathetic stimulation → tachycardia, hypertension (due to airway irritation and sympathetic surge) — avoid rapid increments

• Highly irritating to airways — can trigger bronchospasm
• Potentiates NMBs similarly to other volatile agents

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4. Halothane

• Most potent of the common agents (MAC 0.75%)
• High blood:gas coefficient (2.5) → slow induction and emergence
• Was preferred for paediatric inhalational induction; largely replaced by sevoflurane
• 15–20% metabolised by CYP2E1 — highest metabolism of any modern agent

• ↓ BP by direct myocardial depression (negative inotropy) + ↓ SVR
• Cardiac output ↓ significantly
• Sensitises myocardium to catecholamines → arrhythmias (VT/VF) — adrenaline doses must be restricted during halothane

• Type 1 (mild, reversible): 20–30% of patients; subclinical enzyme elevation
• Type 2 (fulminant hepatic necrosis): 1 in 10,000–35,000 exposures; immune-mediated, via trifluoroacetyl chloride hapten formed during metabolism; high mortality; contraindication to re-exposure

• Contains thymol preservative
• Not stable in moist CO₂ absorber
• Trigger for MH

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5. Enflurane

• Isomer of isoflurane; largely obsolete
• MAC 1.63%; blood:gas 1.9 → slower induction
• 2–8% metabolised → fluoride ions; risk of nephrotoxicity at prolonged high concentrations
• Lowers seizure threshold → epileptiform EEG activity; contraindicated in epilepsy
• Decreases BP by myocardial depression + ↓ SVR
• Not in widespread use in modern anaesthesia

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6. Nitrous Oxide (N₂O)

• Colourless, odourless, sweet-tasting gas; not flammable but supports combustion
• MAC 104% — cannot produce surgical anaesthesia alone at atmospheric pressure
• Low blood:gas coefficient (0.46) → rapid equilibration
• Negligible metabolism (0.004%) — 99.9% excreted unchanged by lungs

• Used as an adjunct (up to 70% with 30% O₂) to reduce requirements for volatile agents (~0.5 MAC sparing effect)
• Analgesia at sub-anaesthetic concentrations (Entonox = 50% N₂O / 50% O₂ for labour, procedures)

• Rapid uptake of N₂O from alveoli concentrates co-administered volatile agents, speeding induction

• On discontinuation, N₂O rapidly diffuses from blood → alveoli, diluting O₂ and CO₂
• Administer 100% O₂ for 5–10 min at end of anaesthesia to prevent hypoxia

• Mild myocardial depressant in isolation
• But stimulates sympathetic nervous system → in practice, BP and HR maintained or slightly elevated
• Increases pulmonary vascular resistance — avoid in pulmonary hypertension

• N₂O is 34× more soluble than nitrogen; diffuses into air-filled spaces faster than N₂ leaves
• Contraindicated in: pneumothorax, bowel obstruction (may double/triple size), middle ear surgery, pneumocephalus, intraocular gas bubbles (retinal detachment surgery), air embolism
• Can expand a pneumothorax to 2–3× its size within 10–30 minutes

• Oxidises vitamin B₁₂ (methionine synthase inhibition) — megaloblastic anaemia and subacute combined degeneration of spinal cord with prolonged exposure
• Environmental impact: potent greenhouse gas; ozone-depleting
• Contraindicated in patients with MTHFR deficiency or recent methotrexate use

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System-by-System Effects Summary

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Special Concerns

• All volatile agents (including halothane) are potent triggers
• Presents as: rapidly rising temperature, masseter spasm, ↑ ETCO₂, metabolic acidosis, rhabdomyolysis, tachycardia
• N₂O is not a trigger
• Treatment: dantrolene 2.5 mg/kg IV, discontinue trigger agent, supportive care

• Desiccated CO₂ absorbent (water content <5%) degrades desflurane, isoflurane, and sevoflurane to carbon monoxide (toxic)
• Sevoflurane also generates Compound A in wet soda lime

• All volatile agents are potent greenhouse gases with global warming potential (GWP) far exceeding CO₂
• GWP order: Desflurane >> Isoflurane > Sevoflurane >> N₂O
• Low fresh gas flows reduce atmospheric release; xenon is environmentally neutral

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Anaesthetic Management: 69-Year-Old for Emergency Laparotomy — Intestinal Perforation

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Preoperative Assessment & Resuscitation

Rapid Clinical Assessment

• History: nature and duration of symptoms, last oral intake, comorbidities (IHD, HTN, DM, COPD, CKD, anticoagulants), functional status
• Physical examination: haemodynamic status (HR, BP, capillary refill), level of consciousness, abdominal findings, airway assessment
• Sepsis scoring: SOFA score, qSOFA — identify septic shock early

Investigations (point-of-care + urgent labs)

Resuscitation Priorities (Sepsis Bundle — within 1 hour)

• IV access: two large-bore peripheral cannulae; consider central venous access (CVC) if shocked or poor peripheral access
• Fluid resuscitation: 20–30 mL/kg crystalloid bolus; target MAP >65 mmHg, UO >0.5 mL/kg/h, lactate clearance
• Vasopressors: if fluid-refractory hypotension — norepinephrine (noradrenaline) via CVC or, temporarily, peripherally
• Blood cultures then broad-spectrum IV antibiotics (e.g., piperacillin-tazobactam + metronidazole, or meropenem in severely unwell patients) — do not delay surgery for antibiotic administration if patient is deteriorating
• Urinary catheter: monitor hourly urine output
• Nasogastric tube: to decompress stomach — reduces aspiration risk and facilitates surgery; aspirate before induction
• Correct coagulopathy: FFP if INR >1.5; vitamin K if on warfarin; consider 4-factor PCC for urgent reversal
• Treat hyperkalaemia, severe acidosis if present
• Blood transfusion: if Hb <8 g/dL or symptomatic anaemia

Key principle: The surgery IS the resuscitation — source control (closing the perforation, peritoneal lavage) is the definitive treatment. Do not delay surgery indefinitely for optimisation. Accept that the patient will be brought to theatre in a suboptimal state.

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Premedication & Aspiration Prophylaxis

• Sodium citrate (30 mL orally, 0.3 mol/L) — immediate-acting non-particulate antacid; neutralises gastric acid
• Ranitidine 50 mg IV or omeprazole 40 mg IV — reduces gastric acid secretion (slower onset; administer early)
• Metoclopramide 10 mg IV — promotes gastric emptying, raises lower oesophageal sphincter tone; has limited effect in ileus
• Avoid oral sedative premedication — increases aspiration risk and can cause cardiovascular depression in a septic patient
• Anxiolysis if necessary: small IV midazolam 1–2 mg with caution, only after haemodynamics are secured

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Anaesthetic Technique

• Coagulopathy (common in sepsis/DIC)
• Haemodynamic instability
• Active sepsis/bacteraemia (risk of epidural abscess/meningitis)
• Duration and extent of procedure unpredictable

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Induction — Rapid Sequence Induction (RSI)

Pre-oxygenation

• 100% O₂ for 3–5 minutes (tidal breathing) or 8 deep breaths in 60 seconds if time critical
• Target EtO₂ > 90%; target SpO₂ 100%
• In elderly patients, functional residual capacity is reduced — denitrogenation is critically important; apnoeic time before desaturation is shorter than in younger patients
• Position: head-up (reverse Trendelenburg, 20–30°) or ramped position — improves FRC, reduces aspiration risk

Airway Preparation

• Full difficult airway trolley immediately available
• Video laryngoscope as first choice in elderly (reduced neck mobility, poor dentition, potential cervical spondylosis)
• Bougie immediately to hand
• Suction (Yankauer) powered and immediately available
• Pre-drawn vasopressors (phenylephrine/ephedrine/norepinephrine)

RSI Drugs

In a 69-year-old with septic peritonitis: ketamine (1–2 mg/kg) or etomidate (0.3 mg/kg) are preferred. If haemodynamically stable, low-dose propofol is acceptable. All doses must be significantly reduced in the elderly (reduced cardiac output, reduced protein binding, reduced redistribution).

• Fentanyl 1–2 mcg/kg IV (50–100 mcg) — attenuates pressor response to laryngoscopy; reduces induction agent dose requirements
• Caution in hypotension — may worsen haemodynamics

• Apply 10 N (awake) increasing to 30 N at loss of consciousness
• Maintained until endotracheal tube cuff inflated and position confirmed
• Controversial — effectiveness questioned; release if it impedes intubation or view

Intubation

• Rapid direct laryngoscopy or video laryngoscopy
• Cuffed endotracheal tube (7.0–7.5 mm for female) — confirm with capnography (gold standard) + bilateral breath sounds
• Inflate cuff before commencing ventilation

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Maintenance of Anaesthesia

• Volatile agent (sevoflurane 1–2%) or TIVA (propofol + remifentanil infusion) — both acceptable; TIVA may offer more haemodynamic control in septic patients
• Supplement with IV opioids (fentanyl boluses or morphine; remifentanil infusion in TIVA)
• Nitrous oxide — avoid: risk of bowel distension (N₂O diffuses into gas-filled spaces), worsening an already compromised gut; also an immunosuppressant
• Neuromuscular blockade: maintain with rocuronium (0.3–0.6 mg/kg boluses) or atracurium (useful in renal/hepatic impairment — Hofmann elimination); monitor with TOF
• Volatile agent dose reduction: MAC decreases 6% per decade after age 40 — in a 69-year-old, roughly a 20% MAC reduction is expected; titrate carefully to avoid overdose

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Monitoring

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Intraoperative Management

Haemodynamic Goals

• MAP ≥65 mmHg (or higher if pre-existing hypertension — target 20% below baseline)
• Vasopressors: norepinephrine (noradrenaline) infusion is first-line vasopressor in septic shock
• Vasopressin 0.03–0.04 units/min can be added as a second agent to spare norepinephrine dose
• If myocardial depression evident (poor cardiac output despite adequate filling): dobutamine or adrenaline

Fluid Management

• Goal-directed fluid therapy: use dynamic parameters (pulse pressure variation, stroke volume variation) if in sinus rhythm
• Balanced crystalloids (Hartmann's/Ringer's lactate) preferred over normal saline (0.9% saline → hyperchloraemic metabolic acidosis; worsens existing acidosis)
• Avoid excessive fluid — risks bowel oedema, abdominal compartment syndrome, ARDS, coagulopathy
• Blood products: transfuse RBCs if Hb <7–8 g/dL (or <10 if cardiovascular disease); FFP for coagulopathy; platelets if <50 × 10⁹/L; cryoprecipitate if fibrinogen <1.5 g/L
• Tranexamic acid 1 g IV over 10 minutes if significant haemorrhage expected or occurring

Temperature

• Active warming throughout: forced-air warming blanket, warmed IV fluids, warming mattress
• Hypothermia (core temp <36°C) worsens coagulopathy, increases infection risk, prolongs drug metabolism
• Target normothermia (36–37°C)

Antibiotics

• Ensure broad-spectrum antibiotics are running intraoperatively
• Repeat dose for prolonged surgery (>3–4 hours) or major blood loss

Positioning

• Supine for laparotomy
• Protect pressure areas in elderly (thin skin, reduced subcutaneous tissue)

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Emergence and Extubation

Extubate in Theatre If:

• Haemodynamically stable and vasopressor dose low/weaning
• Core temperature ≥36°C
• Coagulopathy corrected
• Alert, following commands, adequate respiratory effort (TOF ratio >0.9)
• No respiratory failure (SpO₂ >95% on FiO₂ ≤0.4, good tidal volumes)
• Minimal aspiration risk on emergence

Keep Intubated & Transfer to ICU If:

• Ongoing haemodynamic instability or high vasopressor requirements
• Hypothermia
• Significant metabolic acidosis (pH <7.2) or high lactate
• Respiratory compromise (ARDS pattern, poor oxygenation)
• Massive fluid resuscitation (bowel oedema, abdominal compartment syndrome risk)
• Altered consciousness or high-grade sepsis

In most 69-year-old patients with faecal peritonitis and septic shock, planned ICU admission with continued intubation is the appropriate disposition.

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Postoperative Care

• ICU/HDU admission — all emergency laparotomies in septic elderly patients
• Ventilation strategy: lung-protective ventilation (tidal volume 6 mL/kg IBW, PEEP 5–8 cmH₂O, plateau pressure <30 cmH₂O)
• Vasopressors: wean as haemodynamics permit, guided by lactate clearance
• Analgesia (multimodal — opioid-sparing):
  • Paracetamol IV (1g q6h)
  • NSAIDs: caution in elderly — renal toxicity, GI bleeding, platelet dysfunction
  • Low-dose ketamine infusion (0.1–0.2 mg/kg/h) — opioid-sparing, anti-hyperalgesic
  • IV morphine/fentanyl PCA or nurse-controlled (dose-reduced in elderly)
  • Epidural analgesia (if coagulopathy resolves) — excellent for abdominal surgery but inserted postoperatively once contraindications cleared
• Sepsis management: follow surviving sepsis guidelines; continue antibiotics; repeat cultures; reassess source control
• DVT prophylaxis: LMWH once surgical haemostasis secure + compression stockings
• Nutrition: early enteral feeding (within 24–48 h if bowel function permits) — reduces catabolism, maintains gut barrier, improves outcomes
• Glycaemic control: insulin infusion targeting 6–10 mmol/L
• Delirium prevention: early mobilisation, sensory orientation, adequate analgesia, minimise sedation, restore sleep-wake cycle
• Renal monitoring: AKI is common — monitor creatinine, urine output; avoid nephrotoxins (aminoglycosides, high-dose NSAIDs, contrast)

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Summary of Key Priorities

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Postoperative Vision Loss (POVL) Following Spine Surgery

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Overview & Incidence

• POVL is defined as permanent or sustained visual impairment (ranging from partial field loss to complete blindness) occurring before discharge from an acute care facility
• Analysis of the ASA POVL Registry: 83 of 93 initial cases were due to ischaemic optic neuropathy (ION)
• In 94% of ION cases in the registry, anaesthetic duration exceeded 6 hours
• POVL can range from monocular partial field loss to complete bilateral blindness

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Causes / Aetiology of POVL

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1. Ischaemic Optic Neuropathy (ION) — The Dominant Cause

Anterior ION (AION)

• Ischaemia of the anterior portion of the optic nerve via short posterior ciliary artery compromise
• Features: painless visual loss, afferent pupillary defect (APD), disc oedema or pallor, altitudinal visual field defects
• Presentation may be delayed until the first postoperative day
• More strongly linked to cardiovascular comorbidities and cardiac surgery
• Note: NOT typically caused by emboli (which preferentially lodge in the central retinal artery)

Posterior ION (PION) — Predominant in Spine Surgery

• Ischaemia of the retrolaminar optic nerve (pial vessel compression, compromised collateral flow)
• Features: APD or non-reactive pupil; no disc oedema (unlike AION); bilateral blindness more common
• Delayed symptom onset possible (symptom-free period before vision loss)
• CT in early postoperative period may show optic nerve enlargement; optic atrophy on later MRI
• Only ~11% of PION cases associated with cardiac surgery; majority are spinal/neck surgery

Prone positioning
  ↓ venous drainage from head/orbit
  ↑ orbital venous pressure
  ↑ intraocular pressure (IOP)
  ↓ ocular perfusion pressure (OPP = MAP − IOP)

Combined with:
  Deliberate hypotension → ↓ MAP
  Massive blood loss → anaemia → ↓ O₂ carrying capacity
  Large crystalloid administration → periorbital oedema → ↑ orbital venous pressure → ↑ IOP
  Prolonged duration → sustained ischaemia of watershed optic nerve zones

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2. Central Retinal Artery Occlusion (CRAO)

• Ocular equivalent of a cerebral stroke
• Presentation: sudden, profound, painless monocular vision loss

• 90% non-arteritic in origin; ipsilateral carotid atherosclerosis is common

• Other causes: cardiogenic embolism, hypercoagulable states, vasospasm, retrograde embolism from injections around neck/sinus
• Fundoscopy: pale oedematous retina with cherry-red spot at the fovea; platelet-fibrin or cholesterol emboli in retinal arterioles
• External pressure on the globe in prone position can directly raise IOP → CRAO
• Management: urgent ophthalmology review; treat as vascular emergency (similar to stroke protocol)

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3. Cortical Blindness

• Damage to the visual cortex (parietooccipital region) or optic radiation
• Causes: profound hypoperfusion, thromboembolic events, hypoxaemia, posterior cerebral artery occlusion, watershed infarction
• Features: bilateral vision loss; normal optic disc; normal pupillary reflexes; loss of optokinetic nystagmus; normal eye motility
• CT/MRI: occipital infarcts; posterior cerebral artery thrombosis
• Prognosis best of all POVL causes — recovery more likely in previously healthy patients
• Prevention: maintain adequate systemic perfusion; minimise air/particulate embolism in cardiac surgery

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Risk Factors for POVL in Spine Surgery

Patient-Specific (Pre-existing)

Surgery & Anaesthesia Factors

The landmark 2012 multicenter study (first with detailed perioperative data) identified as independent risk factors: male sex, obesity, Wilson frame use, prolonged anaesthesia, greater blood loss, and lower-percent colloid administration. Pre-existing comorbidities (hypertension, diabetes, atherosclerosis) were not statistically significant independent factors — suggesting intraoperative management may dominate.

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ASA Practice Advisory — Intraoperative Preventive Strategies

Blood Pressure Management

• In high-risk patients, maintain MAP within 24% of estimated baseline MAP
• Minimum average systolic BP of 84 mmHg recommended
• If deliberate hypotension is used: apply only in patients without uncontrolled hypertension; case-by-case basis in high-risk patients
• Continuous BP monitoring; invasive arterial line recommended for high-risk patients
• Consider CVP monitoring in high-risk patients

Fluid Management

• Avoid excessive crystalloid-only resuscitation — large crystalloid volumes raise IOP via orbital venous pressure
• Use balanced colloid and crystalloid administration to maintain intravascular volume
• Excessive crystalloid → periorbital oedema → ↑ orbital venous pressure → ↓ optic nerve perfusion pressure

Anaemia Management

• Monitor haemoglobin periodically in high-risk patients with substantial blood loss
• There is no established transfusion threshold proven to prevent POVL, but permissive anaemia should be avoided in high-risk patients
• Transfuse severely anaemic patients at risk of ION

Positioning

• Head level with or higher than the heart whenever possible
• Avoid Trendelenburg or excessive head-down positions in high-risk patients
• Head in neutral forward position — avoid neck flexion, extension, lateral flexion, and rotation
• Use padded foam headrest (Mayfield/Wilson type) — ensure no direct pressure on the globe
• Check eyes frequently throughout the procedure (every 30–60 minutes in prone patients)
• Confirm eyes are in the opening of the headrest, not compressed

Staging of Surgery

• For procedures anticipated to last >6.5 hours with blood loss >44.7% estimated blood volume: consider staged procedures
• Dividing a lengthy spinal fusion into two separate anaesthetics reduces cumulative physiological insult

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Diagnosis and Postoperative Recognition

Clinical Presentation

• PION: Bilateral visual loss; may be delayed hours to days; no disc oedema; afferent pupillary defect
• AION: Unilateral or bilateral; disc oedema/pallor; altitudinal field defect; APD
• CRAO: Sudden profound unilateral loss on waking; cherry-red spot; afferent pupil defect
• Cortical blindness: Bilateral; normal fundoscopy; normal pupils; ocular motility preserved

Assessment

• Assess vision as soon as the patient is alert enough (not while still sedated from anaesthesia)
• Urgent ophthalmology consultation — within hours of discovery
• MRI brain and orbits: identify intracranial causes, optic nerve signal changes; detect cortical infarcts
• CT brain: detects posterior cerebral artery occlusion, basilar artery lesions
• Fundoscopy: disc oedema, pallor, cherry-red spot, cotton-wool spots
• Echocardiogram, carotid Doppler: if embolic source suspected

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Treatment

There is no proven effective treatment for perioperative ION once it occurs — prevention is paramount.

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Summary: Key Teaching Points

1. ION (predominantly posterior) is the most common cause of POVL after spine surgery
2. Most cases occur in prolonged (>6 hours) prone spinal fusion with significant blood loss (>1 litre)
3. The triad of prone position + significant haemorrhage + low colloid-to-crystalloid ratio dramatically raises risk
4. Deliberate hypotension in high-risk patients carries particular risk; keep MAP within 24% of baseline
5. Wilson frame use and obesity are independent risk factors via abdominal compression raising venous pressure
6. Eyes must be checked regularly during prone procedures; external orbital compression must be zero-tolerated
7. Consider staged surgery for predicted lengthy high-blood-loss procedures
8. Vision assessment on emergence is critical — diagnose before the patient is discharged from recovery
9. There is no proven treatment — all management is preventive; once ION occurs, prognosis is generally poor
10. Surgical team communication is essential — if high-risk features accumulate intraoperatively, consider interrupting and staging

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Supine Hypotension Syndrome (Aortocaval Compression Syndrome)

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Definition

A decrease in mean arterial pressure of >15 mmHg with a rise in heart rate of >20 beats/min, occurring when the gravid uterus compresses the inferior vena cava (IVC) and abdominal aorta in the supine position.

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Anatomy & Pathophysiology

IVC Compression (Dominant Mechanism)

• The IVC runs on the right side of the spine and is the most vulnerable vessel
• At term, the IVC is nearly completely occluded in the supine position in almost all parturients
• Compression ↓ venous return from the lower body → ↓ right heart preload → ↓ stroke volume → ↓ cardiac output (10–20% compared to lateral position)
• Collateral venous return develops via epidural, azygos, and vertebral veins → these become engorged, explaining the increased risk of accidental intravascular injection during epidural placement in pregnancy

Aortoiliac Compression (Secondary)

• Significant aortic compression occurs in 15–20% of patients
• Direct ↓ in blood flow to the lower extremities and uteroplacental circulation
• Uterine contractions → reduce IVC compression but worsen aortic compression
• Fetal umbilical artery Doppler shows reduced diastolic flow during aortic compression

Why Only 8–10% are Symptomatic?

1. Reflexive increase in sympathetic activity → ↑ SVR → maintains MAP despite ↓ CO
2. Collateral venous return via paravertebral veins
3. Failure of compensation (symptomatic syndrome) appears linked to inadequacy of paravertebral collateral blood supply, not a failure of baroreceptor response

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Timeline and Onset

• IVC compression begins around week 20 of gestation as the uterus rises out of the pelvis
• Cardiac output decreases from supine→lateral position from approximately 20 weeks onwards
• Full symptomatic syndrome typically requires >20–30 minutes in the supine position
• At term, turning from left-lateral recumbent to supine can reduce cardiac output by 25–30%

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Clinical Features

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Effects on the Fetus and Neonate

• Fetal hypoxaemia → late decelerations on CTG (bradycardia pattern)
• Fetal acidosis and acidaemia
• Reduced fetal movement
• In severe or prolonged cases: fetal asphyxia, neurological damage, fetal demise

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Anaesthetic Implications

• Spinal anaesthesia for caesarean section: most common clinical scenario; sudden profound sympathectomy + aortocaval compression = severe maternal hypotension
• Labour epidural: slower onset, but hypotension still occurs in ~20% without preventive measures
• General anaesthesia: similarly impairs compensation; also associated with decreased uteroplacental perfusion during induction

• Accidental intravascular catheter placement during epidural insertion
• Intravascular injection of local anaesthetic → systemic toxicity

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Prevention

1. Left Uterine Displacement (LUD) — Cornerstone of Prevention

• Placing the patient in the full left lateral position (most effective)
• Left lateral tilt of the operating table (15–30°)
• Wedge/roll under the right hip (elevating right hip 10–15 cm; Cardiff wedge = 27° tilt)
• Foam or hard wedges maintain tilt more effectively than pillows

Current evidence (MRI study): The IVC volume does not significantly differ between supine and 15° left tilt, but 30° left tilt does increase IVC volume. This has challenged the traditional recommendation of 15° tilt. Despite this, LUD remains standard of care — the appropriate degree should be determined on a case-by-case basis, with at least 15–30° tilt during neuraxial anaesthesia induction and during maternal hypotension or fetal compromise.

2. IV Fluid Preloading / Co-loading

• Crystalloid co-loading (1000 mL Hartmann's or Ringer's lactate) administered simultaneously with spinal block — reduces but does not eliminate hypotension
• Colloid preloading is more effective than crystalloid preloading at preventing hypotension

3. Vasopressors

• Phenylephrine (pure α₁ agonist): currently preferred first-line vasopressor for neuraxial hypotension in obstetrics — human clinical trials show less fetal acidosis and better umbilical artery pH than ephedrine
• Phenylephrine infusion (25–50 mcg/min, titrated) rather than boluses, for prophylaxis at spinal anaesthesia for elective caesarean section
• Ephedrine (α + β agonist): previously considered first-line; remains useful for hypotension with bradycardia; associated with more neonatal acidaemia (crosses placenta and stimulates fetal metabolism)
• Norepinephrine: emerging evidence supports its use

4. Avoid Femoral/Saphenous IV Access

• During resuscitation of a pregnant woman at >20 weeks gestation, avoid IV access below the diaphragm — aortocaval compression can impede delivery of IV drugs to the central circulation

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Treatment of Established Syndrome

1. Immediate left lateral positioning — usually corrects haemodynamics promptly
2. IV fluid bolus — 500–1000 mL crystalloid rapidly
3. Supplemental oxygen — 100% O₂ via face mask for maternal and fetal benefit
4. Vasopressors — IV phenylephrine or ephedrine for persistent hypotension
5. Fetal monitoring — continuous CTG; watch for late decelerations or bradycardia
6. If fetal distress persists despite all measures → expedite delivery

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Chronic Effects of Partial Aortocaval Compression in Third Trimester

• Venous stasis in lower extremities → ankle oedema, varicose veins
• Increased DVT risk (lower limb deep vein thrombosis)
• Engorgement of paravertebral venous plexus including epidural veins
• Backflow of blood via azygos system → transient ↑ in venous return when contractions relieve compression

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Postpartum Considerations

• Sudden autotransfusion from the contracting uterus further increases cardiac output
• Patients with underlying cardiac disease (fixed valvular lesions, cardiomyopathy) may not tolerate this acute rise in preload → pulmonary oedema, cardiac decompensation

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Summary

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Mendelson Syndrome (Aspiration Pneumonitis)

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Historical Background

• Aspiration in 66 patients (1 in 667)
• Most recovered within 24–36 hours
• Only 2 deaths (1 in 22,008)

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Definition

Mendelson syndrome (aspiration pneumonitis) is an acute chemical inflammatory injury of the lung parenchyma resulting from the aspiration of regurgitated sterile acidic gastric contents, occurring in patients with impaired consciousness and loss of protective airway reflexes.

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Pathophysiology

Two-Phase Injury Model

• Direct caustic effect of acid on pulmonary epithelium
• Airspace oedema, alveolar haemorrhage, atelectasis
• Immediate bronchospasm from acid contact with airway mucosa
• Destruction of surfactant-producing type II pneumocytes

• Neutrophil recruitment to the lung
• Neutrophil-mediated injury via:
  • Reactive oxygen species (ROS) — NADPH oxidase generates superoxide anion; xanthine oxidase is also a source
  • Proteases released by activated neutrophils
  • NF-κB activation → transcription of pro-inflammatory cytokines (TNF-α, IL-8)
  • NETosis (neutrophil extracellular traps)
• This results in diffuse alveolar damage → pattern indistinguishable from ARDS

Pathological Changes

• Airspace oedema and haemorrhage
• Hyaline membrane formation
• Bronchospasm (from acid irritation of bronchial smooth muscle via vagal reflex)
• Loss of surfactant → alveolar collapse
• Increased capillary permeability → non-cardiogenic pulmonary oedema
• Intrapulmonary shunting → profound hypoxaemia

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Risk Factors / Predisposing Conditions

Conditions Associated with Full Stomach / Increased Gastric Volume

Conditions Impairing Airway Protection

GLP-1 receptor agonists (semaglutide/ozempic, liraglutide) — now of special concern: the ASA advises holding daily preparations 1 day and weekly preparations 1 week before surgery. If not held, treat as full-stomach precautions.

• Reduced lower oesophageal sphincter (LOS) tone (progesterone effect — from early pregnancy)
• Delayed gastric emptying in labour (pain, opioids, fear)
• Increased intra-abdominal pressure from gravid uterus
• Aspiration incidence in obstetric general anaesthesia: 1 in 430–1547 — 2–3× higher than general surgery

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Clinical Presentation

• 64% (42 patients) were completely asymptomatic
• 13 required mechanical ventilation for >6 hours
• 4 died

• Tachycardia, tachypnoea
• Bronchospasm (wheezing, rhonchi)
• Rales/crepitations bilaterally
• Fever
• Diminished breath sounds
• Frothy or bloody sputum (severe cases)
• Hypotension (massive aspiration)

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Diagnosis

• Clinical: History of aspiration (witnessed or strongly suspected) in a patient with depressed consciousness + respiratory symptoms
• Arterial blood gas: Hypoxaemia (↓ PaO₂, ↓ SpO₂); respiratory alkalosis early, then acidosis in severe disease
• Chest X-ray: Bilateral airspace infiltrates, typically dependent segments (posterior segments of upper and lower lobes, superior segment of lower lobe in supine patients); may initially be normal
• CT chest: More sensitive; diffuse bilateral ground-glass opacities; consolidation in dependent regions
• Bronchoscopy: Airway erythema, oedema, gastric contents visible; useful to confirm diagnosis and rule out other causes
• No pathognomonic laboratory test: Procalcitonin cannot reliably distinguish aspiration pneumonitis from aspiration pneumonia

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Aspiration Pneumonitis vs Aspiration Pneumonia

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Management

Immediate Actions (on recognition or suspicion of aspiration)

1. Head-down position (Trendelenburg) + lateral decubitus — allow gastric contents to drain out of the pharynx rather than down into the trachea
2. Suction the upper airway thoroughly (Yankauer suction)
3. Secure the airway — endotracheal intubation if patient cannot protect airway
4. Tracheal suctioning — clear as much aspirate as possible
5. FiO₂ 1.0 (100% oxygen) immediately
6. Bronchoscopy — if particulate aspiration suspected; remove solid material; diagnostic

Respiratory Support

• Non-invasive ventilation (NIV/BiPAP): for mild-moderate hypoxaemia in alert, cooperative patients
• Mechanical ventilation with lung-protective strategy if severe:
  • Tidal volume: 6 mL/kg ideal body weight
  • PEEP: 5–10 cmH₂O (titrate to oxygenation)
  • Plateau pressure: < 30 cmH₂O
  • FiO₂: titrate to maintain SpO₂ 92–96%
• Prone positioning: consider for severe ARDS (PaO₂/FiO₂ < 150)
• ECMO: in refractory severe ARDS unresponsive to conventional ventilation

Bronchodilators

• Inhaled salbutamol (β₂-agonist) for bronchospasm
• Ipratropium bromide (anticholinergic)
• IV lignocaine/lidocaine or propofol for bronchospasm under anaesthesia

Fluids and Haemodynamic Support

• Maintain adequate hydration
• Avoid excessive fluid (exacerbates non-cardiogenic pulmonary oedema)
• Vasopressors if haemodynamic instability (norepinephrine preferred)

Antibiotics

• Prophylactic antibiotics are NOT recommended for uncomplicated chemical aspiration pneumonitis — overuse selects resistant organisms
• Delay antibiotic initiation if symptoms (fever, leukocytosis, infiltrates) develop within 48 hours — these may reflect chemical pneumonitis, not bacterial infection
• Antibiotic therapy is appropriate when:
  • Aspiration occurs in context of small bowel obstruction (colonised gastric contents)
  • Patients on acid-suppressive therapy or tube feeds (gastric contents colonised)
  • Pneumonitis fails to resolve within 48 hours (suggests bacterial superinfection)
  • Empiric broad-spectrum agents; anaerobic cover not routinely required in hospital-acquired aspiration
  • Organisms: E. coli, Klebsiella, Staphylococcus, Pseudomonas, Bacteroides

Corticosteroids

• Role is controversial and not established
• Glucocorticoids used since 1955; limited efficacy as monotherapy (limited effect on neutrophil-mediated ROS injury)
• Not routinely recommended — may increase risk of superinfection
• May be considered in severe refractory cases

Emerging Therapies

• HAT therapy (Hydrocortisone + Ascorbic acid + Thiamine): case reports show dramatic responses in aspiration-induced ARDS; Vitamin C inhibits NADPH oxidase and NETosis; randomised trials underway — not yet standard of care

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Prevention (The Focus in Anaesthesia)

1. Preoperative Fasting (ASA 2017 Guidelines)

2. Aspiration Prophylaxis Drugs

Note: No drug reliably prevents aspiration. Their goal is to reduce the volume and acidity of gastric contents — not eliminate risk. Routine use in low-risk patients is not recommended by ASA guidelines.

3. Rapid Sequence Induction (RSI)

• Standard technique for all patients at risk of aspiration
• See emergency anaesthesia management (discussed separately)
• Sellick manoeuvre (cricoid pressure): compresses cervical oesophagus → prevents passive regurgitation; effectiveness controversial but remains standard of care

4. Airway Protection During Recovery

• Keep patient intubated until fully awake with return of laryngeal reflexes
• Extubate in left lateral head-down position for high-risk patients
• Ensure TOF ratio >0.9 before extubation (reversal of NMB)

5. Nasogastric Tube

• Consider preoperative NGT to decompress the stomach in obstruction, ileus, delayed gastric emptying
• In full-stomach patients: place NGT before induction if possible and aspirate contents; however, NGT does not eliminate risk (doesn't prevent regurgitation from incompetent LOS)

6. Avoid LMA in High-Risk Patients

• LMA does not reliably protect lungs from regurgitated gastric contents
• Avoid in patients with: obesity, GERD, hiatal hernia, emergency surgery, GI pathology, full stomach

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Prognosis

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Summary — Key Points

1. Definition: Chemical pneumonitis from aspiration of acidic gastric contents — requires pH < 2.5 and volume > 20–25 mL for significant injury
2. Two-phase injury: Immediate caustic injury → delayed neutrophil/ROS-mediated ARDS-like injury
3. Most common cause in anaesthesia practice: altered consciousness + lost protective airway reflexes
4. Highest risk groups: Pregnant women, obese patients, emergency surgery, full stomach, GLP-1 agonist users, diabetics
5. Earliest sign: Hypoxia
6. Treatment: Supportive — airway suction, oxygenation, lung-protective ventilation; antibiotics only if bacterial infection confirmed or suspected
7. Prevention: NPO guidelines, aspiration prophylaxis drugs in high-risk patients, RSI with cricoid pressure, secure endotracheal intubation
8. Corticosteroids and prophylactic antibiotics: not routinely recommended
9. Modern obstetric anaesthesia (neuraxial preferred over GA, sodium citrate routine, RSI for GA): has dramatically reduced mortality compared to Mendelson's original era

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HELLP Syndrome

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Nomenclature and Definition

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Epidemiology

• Occurs in 0.1–0.9% of all pregnancies
• Occurs in 10–20% of women with severe preeclampsia
• Mortality rate: 7.4–34% (varies with severity and access to care)
• 70% of cases develop antepartum (usually in the third trimester after week 27)
• 20% of cases occur before week 28 of gestation
• 30% of cases occur postpartum (within 48–72 hours of delivery) — may occur despite no obvious preeclampsia at delivery
• More common in multigravid women (unlike preeclampsia, which is more common in primigravidae)

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Pathogenesis

1. Defective spiral artery remodelling → placental ischaemia → excess sFlt-1 and endoglin release
2. Systemic endothelial cell activation and injury → increased vascular permeability
3. Platelet activation and consumption at sites of endothelial damage → thrombocytopenia
4. Microangiopathic haemolytic anaemia (MAHA) — RBCs forced through fibrin-occluded microvasculature → schistocytes (fragmented RBCs)
5. Hepatic ischaemia — fibrin deposition in hepatic sinusoids, periportal haemorrhage, hepatocellular necrosis → elevated transaminases
6. Elevated inflammatory markers (CRP, IL-1Ra, IL-6) and complement activation (30–40% have complement gene mutations)
7. Elevated soluble HLA-DR compared to preeclampsia alone

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Diagnostic Criteria

ACOG Task Force on Hypertension in Pregnancy Criteria

• Schistocytes and burr cells on peripheral blood smear
• Serum bilirubin ≥1.2 mg/dL
• Low serum haptoglobin
• Severe anaemia unrelated to blood loss

• AST or ALT ≥ twice the upper limit of normal
• LDH ≥ twice the upper limit of normal

• Platelet count < 100,000/mm³

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Classification Systems

Tennessee Classification (Sibai)

1. Microangiopathic haemolytic anaemia + abnormal blood smear + low haptoglobin + elevated LDH
2. Serum LDH > 600 IU/L (or 2× ULN) AND serum AST > 70 IU/L (or 2× ULN) OR serum bilirubin > 1.2 mg/dL
3. Platelet count < 100,000/μL

Mississippi Triple-Class Classification (Martin)

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Clinical Features

Symptoms (% affected)

Key clinical trap: Hypertension may be absent or mild initially — the predominant complaints of epigastric pain, nausea, and vomiting make HELLP easy to misdiagnose as gastroenteritis, cholecystitis, hepatitis, pancreatitis, or pyelonephritis. Any woman >20 weeks gestation presenting with abdominal pain or up to 7 days postpartum should be evaluated for HELLP.

Laboratory Findings (median values from Sibai series)

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Investigations

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Maternal Complications

Hepatic Complications — The Defining Organ

• Hepatic histology: periportal haemorrhage, sinusoidal fibrin deposition, hepatocellular necrosis
• Subcapsular haematoma: right lobe > left; presents with severe RUQ pain; may be contained
• Hepatic rupture: catastrophic; haemoperitoneum → hypovolaemic shock; surgical emergency
  • Presents with severe RUQ pain, shoulder pain (diaphragmatic irritation), sudden hypotension
  • Diagnosis: USS → hemoperitoneum; CT/MRI → subcapsular haematoma
  • Management: hepatic artery embolisation → if inadequate → liver repair by experienced surgeon; rarely, liver transplantation

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Differential Diagnosis

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Comparison: HELLP vs HUS/TTP vs AFLP

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Anaesthetic Implications

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Management

Immediate Stabilisation (in all cases)

1. Hospital admission — ICU/HDU setting
2. Maternal monitoring: BP, SpO₂, urine output, clinical assessment
3. IV magnesium sulphate — seizure prophylaxis (load 4–6 g IV over 15–20 min; maintenance 1–2 g/h); prevent and treat eclampsia; monitor for toxicity (loss of deep tendon reflexes is first sign; antidote: calcium gluconate 10 mL of 10% IV)
4. Antihypertensive therapy if BP ≥150/100 mmHg:

1. Correct coagulopathy: Fresh frozen plasma (FFP) for INR/APTT correction; cryoprecipitate if fibrinogen < 1.5 g/L
2. Platelet transfusion: if platelets < 20,000/mm³ (spontaneous bleeding risk) or < 50,000/mm³ pre-caesarean section, or < 70–80,000/mm³ if neuraxial anaesthesia planned

Delivery — Timing

• Mode of delivery: Vaginal delivery preferred if cervix favourable and fetal condition reassuring; caesarean section if obstetric indications
• No difference in outcomes between induced labour and caesarean in retrospective studies

Corticosteroids (Antenatal + Adjunct)

• Betamethasone or dexamethasone (antenatal course): for fetal lung maturity if <34 weeks — standard of care
• High-dose dexamethasone as adjunct HELLP management: a randomised controlled trial showed no benefit on overall outcomes; post-hoc analysis suggests possible benefit in platelet recovery in Class I (platelet <50,000) — further studies needed; not standard of care

Plasmapheresis

• Used based on pathophysiological similarities to TTP
• No clear antepartum benefit — limited case series with mixed results; risks include fetal compromise from reduced placental blood flow
• May be indicated postpartum if TTP has not been excluded (plasma exchange is curative in TTP)

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Fetal Complications

• Prematurity (iatrogenic — from early delivery to preserve maternal health)
• IUGR — from impaired uteroplacental blood flow
• Placental abruption
• Fetal distress/asphyxia
• Perinatal and neonatal mortality: ~10% worldwide; higher with earlier gestational age

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Postpartum Course

• Laboratory abnormalities typically worsen before improving, then normalise within 3–5 days after delivery
• 20% of cases develop in the postpartum period — monitor all preeclamptic women after delivery
• Eclampsia can occur postpartum; magnesium should be continued 24–48 hours postpartum
• Long-term: increased risk of hypertension, cardiovascular disease, and recurrence in future pregnancies

Recurrence

• HELLP recurs in future pregnancies but usually does not recur in the same form
• Risk of preeclampsia in subsequent pregnancies is increased
• Low-dose aspirin (75–150 mg daily from 12 weeks) reduces recurrence risk

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Key Points Summary

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Anaesthesia for Retained Placenta

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Definition and Background

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Why Anaesthesia is Needed

1. Adequate analgesia/anaesthesia — the procedure is painful and requires uterine access
2. Uterine relaxation — a contracted/spastic uterus (cervical spasm) prevents the operator's hand from entering the uterine cavity
3. Haemodynamic management — significant blood loss may have already occurred or may occur during the procedure

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Pre-procedure Assessment

• FBC (haemoglobin, platelets)
• Coagulation profile (INR, APTT, fibrinogen)
• Group and crossmatch (2–4 units pRBC)
• Urea/electrolytes/creatinine

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Anaesthetic Options

Option 1: Extend a Pre-existing Epidural (Preferred if Available and Haemodynamically Stable)

• This is the safest and most practical option
• Top-up with a concentrated local anaesthetic solution:
  • Lignocaine (lidocaine) 2% (alkalized or plain) — rapid onset
  • Chloroprocaine 3% — fastest-onset epidural agent
  • Bupivacaine 0.5% — if more prolonged cover needed
• Target sensory level: T10 — provides anaesthesia for uterine and perineal procedures
• Advantage: avoids risks of spinal (sudden hypotension in potentially hypovolaemic patient) and risks of general anaesthesia (failed airway, aspiration)

Option 2: Spinal Anaesthesia (if no epidural; patient haemodynamically stable)

• Appropriate if no pre-existing epidural, no coagulopathy, and patient is haemodynamically compensated
• Spinal is the standard neuraxial technique for operative obstetrics
• Drug: Hyperbaric bupivacaine 0.5% (1–1.5 mL = 5–7.5 mg) ± intrathecal fentanyl 10–25 mcg for analgesia
• Target level: T10
• Key concern: Sudden sympathectomy in a woman who is already volume-depleted from haemorrhage → precipitous hypotension → worse PPH → fetal/maternal compromise
• Pre-load/co-load with crystalloid; phenylephrine infusion prophylactically

Contraindications to neuraxial (spinal/epidural): active haemorrhage with haemodynamic instability, coagulopathy (platelets <70–80 × 10⁹/L, INR >1.5), patient refusal, local infection

Option 3: General Anaesthesia (mandatory in certain situations)

• Haemodynamic instability / active haemorrhage → neuraxial contraindicated (sympathectomy would worsen hypotension; coagulopathy risk)
• Coagulopathy (DIC, thrombocytopenia) → neuraxial contraindicated
• Neuraxial technique failed or contraindicated
• Urgency — no time for regional technique
• Need for profound uterine relaxation (when tocolysis alone is insufficient)
• Suspected placenta accreta spectrum requiring laparotomy/hysterectomy

1. Pre-oxygenation — 100% O₂ for 3–5 minutes; parturients desaturate rapidly (↓ FRC, ↑ O₂ consumption)
2. Aspiration prophylaxis: sodium citrate 30 mL + ranitidine 50 mg IV / omeprazole 40 mg IV; metoclopramide 10 mg IV
3. Rapid Sequence Induction (RSI) — mandatory:
   • Induction agent:
     • Propofol 1–2 mg/kg (reduce dose if haemodynamically compromised)
     • Ketamine 1–2 mg/kg — preferred if haemodynamically compromised (sympathomimetic; maintains BP; uterotonic at high doses but bronchodilator)
     • Etomidate 0.3 mg/kg — cardiovascularly neutral (note: adrenal suppression)
   • NMB: Succinylcholine 1.5 mg/kg IV or rocuronium 1.2 mg/kg IV (with sugammadex available)
4. Cricoid pressure until ETT cuff inflated and position confirmed
5. Airway: use smaller ETT (6.0–6.5 mm) — airway oedema in parturients; video laryngoscope as first-line or immediately available
6. Maintenance:
   • Volatile anaesthetic agent (sevoflurane/desflurane/isoflurane) — provides uterine relaxation in a dose-dependent manner
   • At 1.5–2 MAC → profound uterine relaxation — advantageous for retained placenta MROP
   • Note: volatile agents inhibit myometrial contractions induced by oxytocin in a dose-dependent fashion; therefore, after placenta is removed, reduce volatile to ≤0.5 MAC and use N₂O/opioids to maintain anaesthesia, allowing uterotonic drugs to work effectively

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Uterine Relaxation — The Key Technical Requirement

Pharmacological Uterine Relaxation

Key principle: IV nitroglycerin 50–150 μg administered while the patient has adequate IV analgesia (fentanyl/ketamine) or existing neuraxial block is the current preferred approach — it provides brief, controllable uterine relaxation without requiring general anaesthesia, thus avoiding airway risks in a postpartum patient.

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Anaesthesia Decision Algorithm for Retained Placenta

Retained Placenta (>30 min post-delivery)
            ↓
Assess haemodynamic status + existing analgesia
            ↓
  ┌─────────────────────────────────────────────────────┐
  │                                                     │
  ↓                                                     ↓
Haemodynamically STABLE                    Haemodynamically UNSTABLE
No coagulopathy                            Active haemorrhage / DIC
            ↓                                             ↓
  ┌─────────────────────────┐                    GENERAL ANAESTHESIA
  │                         │                    + RSI (ketamine preferred)
  ↓                         ↓                    + volatile agent ≥1.5 MAC
Functioning              No epidural              + uterotonic after delivery
Epidural                      ↓
  ↓                   GTN 50–150 μg IV +
Top-up with            IV fentanyl/ketamine
concentrated               (if neuraxial                     
local anaesthetic      not possible/safe)
(lignocaine 2%         OR Spinal if stable
or bupivacaine 0.5%)
            ↓
    Manual Removal Under Neuraxial Block

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Intraoperative Management

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Uterotonics After Successful Manual Removal

• B-Lynch uterine compression sutures
• Internal iliac artery ligation
• Uterine artery embolisation (interventional radiology)
• Peripartum hysterectomy — definitive; last resort

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Special Situation: Placenta Accreta Spectrum (PAS)

• Placenta accreta: villi attach to myometrium (no decidua basalis)
• Placenta increta: villi invade myometrium
• Placenta percreta: villi penetrate through myometrium (may involve bladder, bowel)

• Average blood loss 3–5 litres (ranges to 20+ litres)
• Planned caesarean hysterectomy at 34–36 weeks under controlled conditions
• Multidisciplinary team planning: anaesthesiology, MFM, urology, vascular surgery, interventional radiology, haematology, blood bank
• Invasive monitoring: arterial line mandatory; consider central venous access
• Massive transfusion protocol activated from the outset
• Anaesthetic choice: CSE (combined spinal-epidural) preferred for planned PAS — allows awake delivery, then convert to GA for hysterectomy if massive haemorrhage; neuraxial associated with less blood loss than GA alone
• Even if neuraxial planned, patient must be counselled about conversion to GA
• Cell salvage: intraoperative blood salvage recommended
• Vascular occlusion balloons (internal iliac/aorta): used in some centres but ACOG does not currently recommend

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Postoperative Care

• All women who required MROP under general anaesthesia → recovery room monitoring with full monitoring
• Delay extubation until: alert, following commands, TOF ratio >0.9, adequate respiratory effort, SpO₂ ≥96% on FiO₂ ≤0.4
• Continue uterotonic infusion postoperatively
• Monitor for continued PPH, coagulopathy (DIC), fluid overload
• Analgesia postoperatively:
  • If epidural in situ: epidural infusion/PCA
  • If GA: paracetamol + NSAIDs (with caution) + PRN opioids
• Arrange ICU/HDU if significant haemorrhage, coagulopathy, or haemodynamic instability occurred intraoperatively

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Summary

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Textbook References

1. Morgan GE, Mikhail MS, Murray MJ. Morgan and Mikhail's Clinical Anesthesiology. 7th ed. New York: McGraw-Hill; 2022.
   • Chapter 41: Obstetric Anesthesia — Postpartum Hemorrhage; General Anesthesia for Vaginal Delivery; Indications Table 41-3
2. Barash PG, Cullen BF, Stoelting RK, et al. Barash, Cullen, and Stoelting's Clinical Anesthesia. 9th ed. Philadelphia: Wolters Kluwer; 2022.
   • Chapter 41: Obstetric Anesthesia — Inhalation Analgesia and General Anesthesia; Postpartum Hemorrhage; Placenta Accreta Spectrum; Uterotonic Therapy (Table 41-5)
3. Creasy RK, Resnik R, Iams JD, et al. Creasy & Resnik's Maternal-Fetal Medicine: Principles and Practice. 9th ed. Philadelphia: Elsevier; 2023.
   • Chapter: Retained Placenta (pp. 3250–3256)
   • Chapter 70: Hemorrhage in the Peripartum Period — Placenta Accreta Spectrum; Anaesthetic Management (pp. 6248–6258)
   • Chapter 58: Postpartum Hemorrhage
4. Miller RD, Cohen NH, Eriksson LI, et al. Miller's Anesthesia. 10th ed. Philadelphia: Elsevier; 2023.
   • Chapter 58: Obstetric Anesthesia — Aortocaval Compression; Uterine Blood Flow; Other Obstetric Emergencies
5. Katzung BG, Vanderah TW. Katzung's Basic and Clinical Pharmacology. 16th ed. New York: McGraw-Hill; 2021.
   • Chapter: Effects of Volatile Anesthetics on Uterine Smooth Muscle

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Key Journal References (Cited in Textbooks)

1. Magpie Trial Collaborative Group. Do women with pre-eclampsia, and their babies, benefit from magnesium sulphate? The Magpie Trial: a randomised placebo-controlled trial. Lancet. 2002;359(9321):1877–1890.
2. WOMAN Trial Collaborators. Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet. 2017;389(10084):2105–2116. (Key evidence for tranexamic acid in PPH)
3. Combs CA, Murphy EL, Laros RK Jr. Factors associated with postpartum hemorrhage with vaginal birth. Obstet Gynecol. 1991;77(1):69–76.
4. Weeks AD. The retained placenta. Best Pract Res Clin Obstet Gynaecol. 2008;22(6):1103–1117.
5. Dyer RA, Reed AR, van Dyk D, et al. Hemodynamic changes associated with spinal anesthesia for cesarean delivery in severe preeclampsia. Anesthesiology. 2008;108(5):802–811.

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Clinical Guideline References

1. American College of Obstetricians and Gynecologists (ACOG). Practice Bulletin No. 183: Postpartum Hemorrhage. Obstet Gynecol. 2017;130(4):e168–e186.
2. Royal College of Obstetricians and Gynaecologists (RCOG). Green-top Guideline No. 52: Prevention and Management of Postpartum Haemorrhage. London: RCOG; 2016.
3. Obstetric Anaesthetists' Association (OAA) / Difficult Airway Society (DAS). Guidelines for the management of difficult and failed intubation in obstetrics. Anaesthesia. 2015;70(11):1286–1306.
4. American Society of Anesthesiologists Task Force on Obstetric Anesthesia. Practice guidelines for obstetric anesthesia. Anesthesiology. 2016;124(2):270–300.

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Anaesthetic Management of Emergency Lower Segment Caesarean Section (LSCS)

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Classification of Urgency (Lucas Categories)

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Common Indications for Emergency LSCS

• Fetal distress / non-reassuring CTG / fetal bradycardia
• Cord prolapse
• Placental abruption with fetal distress
• Uterine rupture
• Antepartum haemorrhage (placenta praevia with bleeding)
• Failure to progress / dystocia with fetal compromise
• Eclampsia / severe preeclampsia unresponsive to treatment
• Malpresentation with imminent delivery
• Maternal cardiac arrest — perimortem caesarean

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Pre-anaesthetic Assessment

• FBC (Hb, platelets)
• Coagulation profile
• Group and crossmatch / blood bank activation
• Blood glucose

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Aspiration Prophylaxis (Mandatory in ALL Emergency LSCS)

Sodium citrate is the most time-critical agent — give immediately before induction. H₂-blockers/PPIs take 1–2 hours to work; give earlier if time permits.

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Choice of Anaesthetic Technique

Emergency LSCS
     ↓
Assess urgency, existing epidural, haemodynamic status
     ↓
┌─────────────────────────────────────────┬──────────────────────────────────────┐
│ Functioning epidural in situ            │ No epidural / epidural failed        │
│ (from labour analgesia)                 │                                      │
│               ↓                         │       ↓                              │
│ EPIDURAL TOP-UP                         │  Haemodynamically stable?            │
│ (fastest safe option)                   │       ↓              ↓               │
│                                         │      YES              NO / coag fail  │
│                                         │       ↓               ↓              │
│                                         │   SPINAL          GENERAL            │
│                                         │ ANAESTHESIA       ANAESTHESIA        │
└─────────────────────────────────────────┴──────────────────────────────────────┘

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Option 1: Epidural Top-Up (Fastest and Safest When Epidural in Situ)

• Target level: T4 (level of the nipple line) — to anaesthetise the peritoneum and viscera
• Always administer as incremental fractionated doses with a test dose (3 mL lignocaine 2% + adrenaline 1:200,000) first to exclude intravascular or intrathecal placement
• If existing block is partial, add fentanyl 50–100 μg epidurally to improve quality

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Option 2: Spinal Anaesthesia (Technique of Choice When No Epidural)

• Rapid, reliable, dense block within 5 minutes
• Avoids GA risks (aspiration, failed intubation)
• Less fetal drug exposure
• Mother awake at birth
• Better postoperative analgesia with intrathecal opioids

• Haemodynamic instability/active haemorrhage (sympathectomy worsens hypotension)
• Coagulopathy (platelets <70–80 × 10⁹/L; INR >1.5)
• Local infection at insertion site
• Patient refusal
• Raised ICP

1. Position: Lateral decubitus or sitting — sitting may be faster in obese patients
2. Needle: 25-gauge pencil-point (Whitacre/Sprotte) — reduces PDPH risk
3. Level: L3–4 or L4–5 interspace
4. Drug:

1. After injection: Immediately position supine with left uterine displacement (right hip wedge/table tilt 15–30°)
2. Sensory level testing: Cold sensation or sharp/blunt; target T4 bilaterally (level of nipple)
3. Blood pressure: Monitor every 1–2 minutes; have phenylephrine drawn up

• Phenylephrine is now first-line vasopressor — less fetal acidosis than ephedrine; give as prophylactic infusion (25–50 mcg/min titrated) or bolus 50–100 mcg IV
• Ephedrine 5–10 mg IV — use if bradycardic or if phenylephrine causes bradycardia
• IV fluid co-loading — crystalloid 500–1000 mL at time of spinal injection (co-loading more effective than preloading)
• Left uterine displacement maintained throughout

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Option 3: General Anaesthesia (When Neuraxial Contraindicated or Extreme Urgency)

• Fetal bradycardia/collapse requiring immediate delivery (<10 min)
• Cord prolapse with severe fetal compromise
• Major haemorrhage with haemodynamic collapse
• Coagulopathy/DIC (neuraxial contraindicated)
• Failed/refused neuraxial block
• Uterine rupture
• Maternal cardiac arrest (perimortem CS)
• Severe pre-eclampsia with airway oedema or obtunded consciousness

• Risk of failed intubation (8× more common in obstetrics than general surgery — 1 in 224–390 obstetric GAs vs 1 in 1000–2000 general population)
• Aspiration risk
• Neonatal depression from anaesthetic agents (especially with prolonged induction-to-delivery interval)
• Awareness risk higher (1 in 256 for LSCS vs 1 in 19,000 general)
• Greater haemodynamic instability

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General Anaesthesia Technique for Emergency LSCS

Step 1: Preparation (Simultaneous with Surgical Prep)

• Aspiration prophylaxis as above (sodium citrate 30 mL orally immediately)
• Patient positioned supine with 15–30° left lateral tilt (wedge under right hip)
• Pre-oxygenation: 100% O₂ via tight-fitting face mask for 3–5 minutes (FiO₂ >90% endtidal); or 4 maximal deep breaths in 30 seconds if time critical
• Nasal cannula O₂ during laryngoscopy to extend safe apnoea time (apnoeic oxygenation)
• Standard monitoring: SpO₂, ECG, NIBP, ETCO₂, temperature
• Large-bore IV access confirmed and patent
• Draw up vasopressors (phenylephrine, ephedrine); emergency drugs ready
• Video laryngoscope available (recommended as first-line or immediately available for all obstetric GAs per OAA/DAS guidelines)
• Obstetric team scrubbed and ready to incise immediately after intubation confirmed
• Neonatal resuscitation team present

Step 2: Rapid Sequence Induction (RSI) — Mandatory

Step 3: Maintenance of Anaesthesia

• Volatile agent (sevoflurane preferred) in oxygen + nitrous oxide (50:50) or oxygen alone
• Historical practice: 0.5 MAC volatile to limit fetal exposure → unacceptably high awareness rate (BIS >60 in many patients on this regimen)
• Current recommendation: 0.75–1.0 MAC volatile (sevoflurane ~1.5–2%) from induction — reduces awareness without clinically significant neonatal depression when delivery occurs within 10 minutes
• After delivery: increase opioids (fentanyl 1–2 mcg/kg IV); maintain adequate volatile concentration
• Add N₂O 50% (if no concern for bowel distension or neonatal exposure)
• Avoid awareness: use BIS monitoring if available; target BIS 40–60
• Keep surgeons informed of anaesthetic depth

• When delivery occurs within 10 minutes of induction — neonatal depression from anaesthetic agents is minimal
• Beyond 10 minutes → neonatal Apgar scores and pH decline
• Neonates delivered >3 minutes after uterine incision have lower Apgar scores regardless of technique

Step 4: Post-Delivery

1. Give oxytocin — 0.3–1 IU slow IV bolus over 1 minute, then infusion 5–10 IU/h (avoid rapid bolus → profound hypotension)
2. Increase anaesthetic depth (no longer restricted to protect fetus)
3. Add opioid analgesia (fentanyl, morphine)
4. Transition to multimodal analgesia

Step 5: Emergence and Extubation

• Extubate only when patient is fully awake, obeying commands, with intact laryngeal reflexes
• TOF ratio >0.9 confirmed before extubation
• Extubate in slightly head-up / left lateral position — reduces aspiration risk on emergence
• Have suction ready
• Do NOT extubate in deep plane (high aspiration risk)

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Failed Intubation in Emergency LSCS

1. First attempt fails → optimise position (ramped/head-elevated), use video laryngoscope, bougie
2. Second attempt (maximum 2 attempts at direct + 1 at video laryngoscopy) → if fails:
   • Declare failed intubation — do not persist
   • Call for help
3. Maintain oxygenation: bag-mask ventilation with cricoid pressure; OR insert supraglottic airway device (LMA) — ProLMA/LMA Supreme
4. Decision: Can surgery continue with LMA + cricoid pressure?
   • Yes: if fetal distress persists — proceed under LMA (LMA does NOT protect against aspiration)
   • No: If maternal condition allows → wake patient up → reassess → consider awake fibreoptic intubation or regional

• Front-of-neck access (emergency surgical airway): scalpel-bougie-tube cricothyroidotomy
• This is a true emergency — have scalpel kit immediately available in all obstetric theatres

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Pre-eclampsia with Emergency LSCS — Special Considerations

• Airway: grossly oedematous larynx/pharynx — use smaller ETT (6.0 mm); video laryngoscopy first-line
• Induction: Avoid ketamine (raises BP); use propofol + labetalol 20 mg IV or esmolol 0.5–1.5 mg/kg or remifentanil 1 mcg/kg to attenuate hypertensive response to laryngoscopy
• Magnesium sulphate: if receiving MgSO₄ — potentiates NMBs (reduce dose of rocuronium); reduces MAC; monitor clinically
• Spinal: generally safe; phenylephrine infusion for hypotension; avoid excessive volume preload (pulmonary oedema risk)

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Neonatal Considerations

• Neonatal resuscitation team must attend all emergency LSCS under GA (lower 1-minute Apgar scores with GA vs neuraxial)
• Short induction-to-delivery interval minimises neonatal drug exposure
• Apgar score at 1 and 5 minutes
• Umbilical artery blood gas — pH and base excess assess fetal condition

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Postoperative Analgesia

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Summary Table

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Uteroplacental Circulation and Anaesthetic Effects

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1. Anatomy of Uteroplacental Circulation

Maternal Side

• Uterine blood flow is supplied by the uterine arteries (branches of the internal iliac arteries) and, to a lesser extent, the ovarian arteries
• At term, uterine blood flow increases from approximately 100 mL/min (nonpregnant state) to 700–900 mL/min (~10% of maternal cardiac output)
• Uterine arteries branch into arcuate arteries → radial arteries → spiral arteries, which open into the intervillous space of the placenta
• Maternal blood bathes the chorionic villi in the intervillous space and drains via uterine veins

Fetal Side

• Fetal blood flows to the placenta via two umbilical arteries (carrying deoxygenated blood from the fetus)
• Oxygenated blood returns via a single umbilical vein
• Fetal capillaries within the chorionic villi are separated from maternal blood in the intervillous space by the placental membrane (syncytiotrophoblast + cytotrophoblast + fetal endothelium) — functional exchange surface ≈1.8 m²

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2. Determinants of Uterine Blood Flow

Uterine Blood Flow = Uterine Perfusion Pressure / Uterine Vascular Resistance

Uterine Perfusion Pressure = Uterine Arterial Pressure − Uterine Venous Pressure

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3. Factors That Reduce Uterine Blood Flow

A. Decreased Uterine Arterial Pressure (Hypotension)

B. Increased Uterine Vascular Resistance (Vasoconstriction)

C. Increased Uterine Venous Pressure

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4. Placental Exchange

Mechanisms of Transfer

Oxygen Transfer

• Fetal O₂ consumption at term: ~7 mL/min/kg
• Fetal PaO₂ normally only 30–35 mmHg — fetus tolerates this because:
  • Fetal Hb has higher O₂ affinity (OHbDC shifted left; P50 = 18 mmHg vs maternal 27 mmHg)
  • Fetal Hb concentration: 15 g/dL (vs ~12 g/dL maternal)
  • Double Bohr effect — maternal CO₂ release from placenta → maternal Hb shifts right (↓ affinity) → fetal Hb shifts left (↑ affinity) → O₂ transfer enhanced
  • Maximum fetal PaO₂ never exceeds 60 mmHg even if mother breathes 100% O₂
• Fetal O₂ consumption can be maintained despite ↓ O₂ delivery until maternal O₂ delivery falls to ~50% of normal

Carbon Dioxide Transfer

• CO₂ diffuses readily across placenta
• Transfer is blood flow-limited, not diffusion-limited
• Maternal hyperventilation (↓ PaCO₂) increases gradient for CO₂ transfer from fetus
• Severe maternal hypocapnia (PaCO₂ < 20 mmHg) from excessive hyperventilation → reduces uterine blood flow AND causes left shift of maternal Hb curve (↑ O₂ affinity) → impairs O₂ offloading to fetus

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5. Factors Governing Placental Drug Transfer

Ion Trapping

• Weakly basic drugs (local anaesthetics, opioids) cross as unionised molecules
• In the more acidic fetal circulation → become ionised → cannot diffuse back → accumulate in fetal blood
• During fetal acidaemia (fetal distress) → even greater ion trapping → higher fetal drug concentrations

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6. Anaesthetic Effects on Uteroplacental Blood Flow

A. Intravenous Induction Agents

B. Volatile Inhalational Agents

Clinical guidance: use 0.5–0.75 MAC volatile for LSCS maintenance (before delivery) to balance awareness prevention with minimal uterotonic inhibition. Reduce to 0.5 MAC after delivery to allow oxytocin to work.

• Nitrous oxide: minimal to no effect on UBF when combined with volatile agents; in animal studies, N₂O alone can cause uterine arterial vasoconstriction — not a significant clinical concern at standard concentrations

C. Opioids

D. Local Anaesthetics

E. Neuraxial Anaesthesia (Regional)

F. Vasopressors — The Ephedrine vs Phenylephrine Debate

Key principle: Small doses of phenylephrine (40 mcg bolus) may actually increase UBF in normal parturients by restoring arterial pressure. Large doses of all α-agents can produce tetanic uterine contractions by α₁-receptor stimulation on uterine muscle.

G. Oxytocin and Uterotonic Drugs

H. Benzodiazepines

• Readily cross placenta
• Diazepam accumulates in fetal tissues (long t½ of active metabolite)
• Midazolam crosses rapidly but shorter-acting
• Neonatal effects: hypotonia, respiratory depression — avoid if possible

I. Neuromuscular Blocking Agents

• Non-depolarising NMBs (rocuronium, vecuronium, atracurium): ionised, high MW, poor lipid solubility → minimal placental transfer → fetus is not paralysed
• Succinylcholine: low MW but highly ionised → does not cross placenta at clinical doses

J. Glycopyrrolate vs Atropine

• Glycopyrrolate: highly ionised, large MW → minimal placental transfer → preferred over atropine for maternal bradycardia (does not cause fetal tachycardia)
• Atropine: crosses placenta → causes fetal tachycardia; still used when rapid effect needed

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7. Fetal First-Pass Effect and Protective Mechanisms

1. ~75% of umbilical venous blood passes through the fetal liver first → hepatic drug metabolism before reaching brain/heart
2. Drugs entering via ductus venosus are diluted by drug-free blood from the fetal lower body
3. Fetal liver enzyme activity is lower than adults but still provides some drug metabolism

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8. Summary: Clinical Principles

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Uteroplacental Circulation

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Definition

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Anatomy

Maternal Vascular Supply

• Uterine arteries (primary supply) — branches of the internal iliac (hypogastric) arteries
• Ovarian arteries — anastomose with uterine arteries

Aorta → Common iliac → Internal iliac → Uterine artery
  → Arcuate arteries (in myometrium)
    → Radial arteries
      → Spiral arteries (in endometrium/decidua)
        → Intervillous space (bathes chorionic villi)
          → Uterine veins → Internal iliac vein → IVC

Fetal Vascular Supply

Fetal heart → Descending aorta → Two umbilical arteries (deoxygenated)
  → Placental capillaries within chorionic villi
    → Single umbilical vein (oxygenated) → umbilical cord → fetus

• Two umbilical arteries: carry deoxygenated, nutrient-depleted blood from fetus to placenta
• One umbilical vein: carries oxygenated, nutrient-rich blood back to fetus
• Fetal capillaries within villi are separated from maternal blood by the placental membrane

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Quantitative Changes in Pregnancy

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Spiral Artery Remodelling — Key to Normal Uteroplacental Circulation

1. Interstitial invasion — into the decidua
2. Endovascular invasion — replacing the endothelial and muscular layers of spiral arteries up to the myometrial segments

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Physiology of Uterine Blood Flow

Governing Equation

• Uterine vasculature is maximally vasodilated at term — no autoregulation
• Therefore UBF is entirely dependent on perfusion pressure and vascular resistance
• Has α-adrenergic receptors (vasoconstriction) and β-adrenergic receptors (vasodilation) — not under significant neural control

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Factors Reducing Uterine Blood Flow

1. Decreased Uterine Arterial Pressure (Hypotension)

2. Increased Uterine Vascular Resistance

3. Increased Uterine Venous Pressure

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Placental Structure and Exchange

Anatomical Organisation

MATERNAL SIDE:
Spiral artery → Intervillous space (maternal blood)
                      ↕ Exchange occurs across placental membrane
FETAL SIDE:
Umbilical arteries → Chorionic villi capillaries

• Cotyledons: functional units of the placenta (15–30 at term), each supplied by one spiral artery
• Placental membrane: syncytiotrophoblast + cytotrophoblast + fetal vascular endothelium

Mechanisms of Placental Exchange

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Oxygen and Carbon Dioxide Transfer

Oxygen Transfer

• Fetal PaO₂ in umbilical vein: 30–35 mmHg (never exceeds 60 mmHg even with 100% maternal O₂)
• Fetal O₂ consumption: ~7 mL/min/kg
• Fetal SaO₂: ~80% (umbilical vein)

• Redistribution of blood flow to brain, heart, placenta, adrenal glands (diving reflex)
• ↓ O₂ consumption
• Anaerobic glycolysis — metabolic acidosis

Carbon Dioxide Transfer

• CO₂ diffuses very readily — transfer is blood flow-limited, not diffusion-limited
• Maternal hyperventilation (↓ maternal PaCO₂) → steepens CO₂ gradient → promotes fetal CO₂ excretion
• Fetal Haldane effect: as O₂ loads on fetal Hb in placenta → fetal Hb releases CO₂ more readily → facilitates CO₂ transfer to mother

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Fetal Circulation — Key Features for Anaesthesia

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Drug Transfer Across the Placenta

Pharmacokinetic Determinants

Drugs with Minimal Placental Transfer

Drugs that Cross Readily

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Uterine Contractions and Blood Flow

• Each uterine contraction transiently reduces UBF:
  • Intrauterine pressure rises → compresses intramyometrial arteries
  • Uterine venous pressure ↑ → reduces perfusion gradient
  • Blood flow nearly ceases at peak of contraction (intrauterine pressure 50–80 mmHg)
• The fetus normally tolerates this because it has adequate O₂ reserve between contractions
• Hypertonic contractions (oxytocin excess, abruptio) → prolonged ↓ UBF → fetal distress

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Summary Diagram

                    UTEROPLACENTAL CIRCULATION
                    
    MATERNAL                                    FETAL
    
  Aorta                                     Fetal heart
    ↓                                           ↓
  Uterine artery                         2 Umbilical arteries
    ↓ (700-900 mL/min at term)               (deoxygenated)
  Arcuate → Radial                              ↓
    ↓                                    Placental capillaries
  Spiral arteries                         within chorionic villi
    ↓                                              ↕
  INTERVILLOUS SPACE ←————— EXCHANGE ————→ Fetal villi
    ↑                      (O₂, CO₂,
  Drains into               nutrients,
  Uterine veins             drugs)
    ↓                                              ↓
  IVC                                      Umbilical vein
                                           (oxygenated)
                                               ↓
                                         Ductus venosus + liver
                                               ↓
                                         Fetal heart/brain

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Clinical Implications

1. Prevent maternal hypotension — the single most important anaesthetic intervention to protect UBF
2. Left uterine displacement — mandatory from 20 weeks to prevent aortocaval compression
3. Adequate pain relief — epidural analgesia reduces catecholamine-mediated uterine vasoconstriction
4. Avoid hyperventilation — target maternal PaCO₂ 28–32 mmHg in pregnancy
5. Treat uterine hyperstimulation promptly — terbutaline/GTN to relax uterus
6. Monitor fetal wellbeing — CTG, fetal pH/lactate sampling — detect ↓ UBF effects on fetus early
7. Drug dosing — timing relative to delivery, minimum effective dose, awareness of ion trapping in fetal acidosis

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