Labour Analgesia — 30-Mark Model Answer (Anaesthesia MD Examination)

Introduction

1. Physiology and Pathways of Labour Pain (5 marks)

First Stage of Labour

• Pain is visceral in origin - from uterine contractions, cervical dilation, and lower uterine segment distension.
• Afferent impulses travel via the uterine and cervical plexuses through sympathetic nerves, entering the spinal cord at T10-L1.
• Character: crampy, poorly localised, referred to the umbilicus, lower abdomen, and lumbar region.

Second Stage of Labour

• Pain becomes somatic as the presenting part descends and distends the vagina, perineum, and pelvic floor.
• Afferent impulses travel via the pudendal nerve (S2-S4) and posterior cutaneous nerve of the thigh.
• Sensory block must extend from T10 to S4 to cover both stages.

Physiological Consequences of Untreated Labour Pain

2. Non-Pharmacological Methods (3 marks)

• Breathing techniques - Lamaze, Bradley method, LeBoyer technique
• Continuous labour support - doula or partner presence; Cochrane review of 26 trials (n=15,858) showed shorter labour, more spontaneous vaginal deliveries, less pharmacological analgesia
• Hydrotherapy (water immersion / warm bath)
• TENS (Transcutaneous Electrical Nerve Stimulation) - stimulates Aβ fibres, activates gate control mechanism
• Acupuncture/acupressure - Cochrane review of 28 RCTs (n=3,960): acupuncture minimally reduces labour pain and increases maternal satisfaction; acupressure showed no clear benefit over sham
• Massage - Cochrane review of 10 RCTs: reduces pain in first stage; increases sense of control
• Hypnosis - Cochrane review of 9 trials (n=2,954): reduced systemic analgesia use; no clear difference in neuraxial use
• Intradermal sterile water injections, aromatherapy, biofeedback

3. Pharmacological Methods

3a. Systemic Analgesics (4 marks)

Opioids

Non-opioid Systemic Agents

• Nitrous oxide (Entonox - 50% N2O + 50% O2) - self-administered via facemask at onset of contraction; rapid onset/offset; minimal uterine effects; provides mild-moderate analgesia; safe for fetus; widely used in the UK
• Low-dose ketamine (10–15 mg IV) - excellent analgesia in 2–5 min without loss of consciousness; most useful just prior to delivery or as adjuvant to regional; doses >1 mg/kg cause hypertonic uterine contractions
• Midazolam (≤2 mg IV) - anxiolytic adjunct to neuraxial blockade; chronic diazepam use associated with fetal depression
• NSAIDs - avoid in labour (premature closure of ductus arteriosus)

3b. Regional (Neuraxial) Techniques (12 marks)

"Using a local anaesthetic-opioid mixture for lumbar epidural analgesia during labor significantly reduces drug requirements when compared with using either agent alone." - Morgan & Mikhail, 7e

I. Epidural Analgesia

1. Patient positioned sitting or left lateral; sterile technique
2. Identify L3-L4 or L2-L3 interspace; loss of resistance technique (saline or air) for epidural space identification
3. Test dose - 3 mL of 1.5% lidocaine + epinephrine 1:200,000; wait 5 minutes
   • Tachycardia (+20-30 bpm) = intravascular placement
   • Rapid dense motor/sensory block = intrathecal placement
4. If test dose negative: administer 10-15 mL of LA-opioid mixture in 5 mL increments
5. Place supine with left uterine displacement; monitor BP every 1-2 min for 15 min

• Bupivacaine 0.0625–0.1% + fentanyl 2 mcg/mL
• Ropivacaine 0.1% + fentanyl 2 mcg/mL (less motor block, safer cardiac profile than bupivacaine)
• Bupivacaine 0.125% + sufentanil 0.5–1 mcg/mL

• First stage: T10–L1
• Second stage: T10–S4

II. Combined Spinal-Epidural (CSE) Analgesia

1. Epidural needle placed in epidural space as standard
2. Spinal needle (25G Whitacre or Sprotte pencil-point) passed through epidural needle until dural puncture confirmed by CSF
3. Intrathecal injection of opioid ± low-dose LA
4. Spinal needle withdrawn; epidural catheter threaded and secured

• Fentanyl 15–25 mcg (opioid alone - no motor block; "walking epidural")
• Sufentanil 5–7.5 mcg
• Bupivacaine 2.5 mg + fentanyl 15 mcg (excellent initial analgesia)

• Faster onset (2–5 minutes vs 20 min for epidural)
• Dense analgesia; particularly useful for advanced labour
• Low-dose intrathecal component preserves ambulation ("walking epidural")
• Epidural catheter allows top-up for prolonged labour or operative delivery

III. Spinal (Intrathecal) Analgesia

• Single-shot intrathecal opioid ± LA
• Provides rapid but time-limited analgesia (1.5–3 hours)
• "Saddle block" - hyperbaric tetracaine 3–4 mg or bupivacaine 2.5–5 mg + fentanyl 12.5–25 mcg for second stage/operative vaginal delivery
• Continuous spinal analgesia via intrathecal catheter: used after accidental dural puncture; provides excellent analgesia and utilises the wet tap

IV. Other Regional Techniques

• Blocks S2-S4 (pudendal nerve), covering perineum/vaginal outlet
• Technique: transvaginal injection beneath ischial spine through sacrospinous ligament, using Koback needle/Iowa trumpet guide; 10 mL of 1% lidocaine or 2% chloroprocaine per side
• Useful for second stage and perineal repair
• Complications: intravascular injection, retroperitoneal haematoma, retropsoas/subgluteal abscess

• Injections at 4 o'clock and 10 o'clock lateral to cervix
• Controls first-stage pain only
• No longer used for viable fetuses - high rate of transient fetal bradycardia (uterine artery proximity, direct fetal drug absorption); risk of injecting into fetal head
• Still used for intrauterine fetal demise, D&C, D&E procedures

4. Complications of Neuraxial Analgesia (4 marks)

5. Effect on Labour and the Neonate (2 marks)

• Labour progress: Dilute LA-opioid combinations do NOT prolong labour or increase operative (caesarean or instrumental) delivery rates - this is a Class A evidence finding (Morgan & Mikhail, 7e)
• Fetus/Neonate: Neuraxial analgesia is vastly superior to systemic opioids for fetal safety; systemic opioids (especially meperidine/morphine) cross placenta and cause neonatal respiratory depression, lower Apgar scores, and neurobehavioural depression; neuraxial drugs - being highly dilute - have minimal neonatal effects
• Maternal catecholamines: Effective analgesia reduces catecholamines, improving uteroplacental perfusion

6. Contraindications to Neuraxial Analgesia

Summary Table

Conclusion

• Miller's Anesthesia, 2-Volume Set, 10th Edition (Elsevier, 2023)
• Morgan & Mikhail's Clinical Anesthesiology, 7th Edition (McGraw Hill, 2022)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9th Edition

Anaesthesia for Awake Craniotomy — Comprehensive MD Exam Answer

1. Introduction and Rationale

2. Indications

3. Presurgical Evaluation

Preoperative Neurological Workup

• Wada test (intracarotid sodium amobarbital test) - selective hemisphere anaesthesia to lateralise speech dominance and test bilateral memory representation
• Video-telemetry with EEG electrode placement - for epilepsy surgery, to record and localise ictal events
• Functional MRI (fMRI) / PET scan - non-invasive cortical mapping
• Neuropsychological baseline assessment - establishes cognitive/language function for intraoperative comparison

Patient Selection Criteria

• Motivated, cooperative, psychologically prepared patient
• Able to follow commands and communicate during testing
• No severe anxiety, claustrophobia, or panic disorder
• No obstructive sleep apnoea (high sedation risk with prone/lateral positions)
• No significant language barrier
• No uncontrolled cough, nausea, or movement disorders

• Severe anxiety or inability to cooperate (relative)
• Morbid obesity (airway management challenges with inaccessible airway)
• Obstructive sleep apnoea
• Uncontrolled cough or movement disorder
• Severe nausea or GERD
• Raised intracranial pressure with risk of herniation
• Children (generally not suitable; poor cooperation)
• Patients unable to understand the procedure

• Detailed explanation of all phases (most important - reduces anxiety and intraoperative failure)
• Psychological rehearsal ("walk-through") of the awake testing phase
• Consider anxiolytic premedication carefully - avoid benzodiazepines if ECoG-based seizure focus localisation is planned (anticonvulsant effect masks EEG activity)
• Anti-emetics (ondansetron, dexamethasone) - routine, especially if opioids are planned
• Anticonvulsants: continue or reduce by half depending on whether intraoperative EEG activation is needed
• NPO as per standard guidelines; IV access, arterial line

4. Anaesthetic Techniques

Technique 1: Monitored Anaesthesia Care (MAC) / Sedation Throughout ("Awake-Awake-Awake")

• Patient is sedated at a light-to-moderate level throughout
• Spontaneous ventilation maintained with unprotected airway
• Titrated sedation reduced during mapping phase
• Best for cooperative patients with good tolerance

Technique 2: Asleep-Awake-Asleep (AAA) with Supraglottic Airway (LMA)

• Most widely practiced technique
• Three distinct phases:

• During the awake phase, the patient communicates with the neuropsychologist/surgeon
• LMA is preferred over ETT for easier removal and less stimulation

Technique 3: Asleep-Awake-Asleep with Endotracheal Tube (ETT)

• Customised ETTs with local anaesthetic installation in glottis/trachea allow awake extubation without cough
• Used when airway concerns preclude LMA
• More stimulating; technically demanding
• Reported but less commonly used than LMA technique

5. Scalp Nerve Block - The Cornerstone

• Unilateral (ipsilateral to craniotomy) or bilateral depending on incision
• Local anaesthetic: ropivacaine 0.5-0.75% or bupivacaine 0.25-0.5% with or without adrenaline
• Maximum dose calculations mandatory - volumes can be substantial when combined with surgeon's pin-site infiltration and dural infiltration
• Surgeon supplements with local infiltration of pin sites, skin incision, and dura (especially subtemporal dura - most painful area)
• The anesthesiologist must track cumulative LA dose to prevent toxicity

6. Sedation and Drug Regimens

1. Minimise patient discomfort during painful phases (positioning, pinning, craniotomy)
2. Ensure patient responsiveness and cooperation during mapping
3. Minimal respiratory depression - airway inaccessible in pin fixation
4. Minimal suppression of EEG activity (if ECoG planned)
5. Rapid offset to allow prompt awakening for testing

Drug Options

A. Propofol-Based Regimens

• Propofol infusion (50-150 mcg/kg/min) - most widely used; rapid offset; excellent titrability
• Often combined with remifentanil (0.02-0.05 mcg/kg/min) for analgesia during painful phases
• Or combined with dexmedetomidine (0.2 mcg/kg/h)
• Critical limitation: Propofol must be discontinued at least 15 minutes before EEG/ECoG recording - it leaves a residual high-frequency, high-amplitude beta activity footprint that can obscure seizure activity
• Propofol + remifentanil: synergistic respiratory depression - great caution in pin-fixed patient

B. Dexmedetomidine-Based Regimens

• Dexmedetomidine (α2-adrenergic agonist): loading dose 0.5-1 mcg/kg over 10-20 min, then infusion 0.2-0.7 mcg/kg/h
• Key advantages:
  • Sedation AND analgesia with minimal respiratory depression - safest agent for spontaneous ventilation
  • Cooperative, arousable sedation - patients respond to verbal commands
  • Does not suppress EEG - can be maintained during ECoG recording (0.1-0.5 mcg/kg/h during testing)
  • Anxiolytic without full amnesia - patients remain cooperative
• Disadvantage: Bradycardia, hypotension; slower onset; occasional delays in arousal; less analgesic than opioid combinations
• Comparative study (Barash, 9e): propofol-remifentanil vs dexmedetomidine - similar sedation and mapping efficacy but lower rates of respiratory depression with dexmedetomidine
• Functional testing has been successfully performed with dexmedetomidine 0.1-0.2 mcg/kg/h during neurocognitive testing

C. Remifentanil Alone or Combinations

• Remifentanil infusion: excellent analgesia with rapid offset (context-sensitive half-life ~3 min); risk of respiratory depression and chest wall rigidity; requires vigilant monitoring
• Combination options:
  • Propofol + remifentanil (most commonly used for MAC)
  • Dexmedetomidine + remifentanil (excellent; minimal respiratory depression)
  • Propofol + fentanyl + dexmedetomidine

D. Drugs to Avoid

7. Monitoring

8. Intraoperative Phases and Management

Phase 1: Positioning and Pin Fixation

• Most painful phase (pericranium)
• Adequate scalp block before pin application
• Bolus sedation/analgesia at time of pinning
• Patient positioning critical: maximise neck extension and atlanto-occipital positioning before final head holder lockdown - this widens the airway and allows more latitude for sedation
• Visual access to patient's face must be maintained throughout - for speech testing (naming objects) and detecting motor responses during mapping
• Temperature management, pressure-area padding

Phase 2: Skin Incision and Craniotomy

• Moderately to deeply sedated
• Scalp block analgesia covering the incision
• Surgeon infiltrates incision line additionally
• Monitoring SpO2 and ETCO2 continuously

Phase 3: Dural Opening

• Subtemporal dura traction is particularly painful - ensure adequate dural infiltration with LA
• Commence reducing sedation in preparation for awake phase
• If LMA-based AAA: commence waking patient; remove LMA when responsive

Phase 4: Awake Cortical Mapping (Critical Phase)

• Patient fully awake and cooperative
• Electrocorticography (ECoG): cortical surface EEG to localise seizure foci
  • If no spontaneous activity: provocative agents used
  • Methohexital 0.3 mg/kg - safe, effective seizure activation agent
  • Etomidate 0.05-0.1 mg/kg - alternative
  • Alfentanil bolus 30-50 mcg/kg; Remifentanil 2.5 mcg/kg - under GA
  • Hyperventilation - helps activate foci
• Direct cortical stimulation mapping: bipolar stimulator applied to brain surface
  • Motor mapping: observe for movement in contralateral limbs/face
  • Speech mapping: naming task (patient asked to name images) - speech arrest or errors indicate language cortex
  • Sensory mapping: patient reports tingling/paraesthesia
• Dexmedetomidine can be maintained at low rates (0.1-0.2 mcg/kg/h) during mapping without interfering with testing

Phase 5: Tumour Resection and Closure

• Sedation resumed; LMA reinserted if AAA technique
• Anaesthesia for closure

9. Complications and Management

10. Postoperative Management

• PACU or ICU observation (neurological observations every 15-30 min initially)
• Multimodal analgesia: paracetamol, NSAIDs (cautiously), scalp infiltration of long-acting LA
• Nausea prophylaxis continued
• Anticonvulsant medication maintained/resumed
• Monitoring for: delayed seizures, neurological deterioration, haematoma (headache, reduced GCS), raised ICP, pneumocephalus
• Steroids (dexamethasone) to reduce cerebral oedema
• VTE prophylaxis when appropriate

11. Summary Comparison - Anaesthetic Approaches

Key Examination Points

1. The essential element is the scalp nerve block - sedation cannot compensate for inadequate local anaesthesia
2. Six nerves of the scalp must be blocked: supratrochlear, supraorbital, zygomaticotemporal, auriculotemporal, lesser occipital, greater occipital
3. Propofol must be stopped ≥15 min before ECoG - residual beta activity obscures seizure focus
4. Dexmedetomidine advantage: sedation + analgesia with minimal respiratory depression; can be maintained during mapping at 0.1-0.2 mcg/kg/h
5. Capnography is essential - airway is all but inaccessible with head in pin fixation
6. Avoid benzodiazepines as premedication if ECoG is planned
7. Seizures during mapping - cold saline first; then propofol 0.5-1 mg/kg; wait before giving propofol in case self-limiting
8. Conversion to GA is pre-planned - video laryngoscope must be immediately available

• Miller's Anesthesia, 2-Volume Set, 10th Edition (Chapter 53: Awake Craniotomy and Seizure Surgery)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9th Edition (Chapter: Awake Craniotomy)
• Morgan & Mikhail's Clinical Anesthesiology, 7th Edition

Brain Death and Organ Harvesting — 30-Mark Model Answer (Anaesthesia MD Examination)

1. Definition and Historical Context

• First codified by the Harvard Ad Hoc Committee in 1968, following the world's first cardiac transplant by Dr Christiaan Barnard in 1967
• Incorporated into the Uniform Determination of Death Act (USA) and legally recognised in most countries
• The legal time of death is the moment the apnoea test confirms PaCO2 criteria are met in the absence of any respiratory effort
• Equivalent terms: death by neurological criteria (DNC), brain stem death (BSD - UK terminology)

2. Causes of Brain Death

3. Prerequisites Before Brain Death Testing (5 marks)

A. Establish Irreversible Cause of Coma

• Known, structural, irreversible catastrophic neurological injury
• Neuroimaging (CT/MRI) explains the coma
• Patient has received aggressive treatment (osmotherapy, ICP management, surgery) and further treatment is futile

B. Exclude Confounding Conditions

C. Qualified Examiners

• Two independent doctors (in most countries) - neither involved in transplant team
• Senior physicians (consultant/attending) qualified in neurology, neurosurgery, or intensive care
• Two separate examinations, separated by an appropriate observation period (institution-dependent)

4. Clinical Examination for Brain Death (8 marks)

A. Level of Consciousness

• Unresponsive to all stimuli
• No purposeful motor response to painful stimulation (deep pressure on condyles of TMJ, supraorbital notch, nail beds, sternal rub)
• Motor responses from spinally-mediated reflexes (Lazarus sign - arms rising and meeting midline) may still occur and are not incompatible with brain death, but require explanation
• Decerebrate or decorticate posturing IS incompatible with brain death

B. Brainstem Reflexes - All Must Be Absent Bilaterally

• Nystagmus or spontaneous eye movements
• Conjugate eye deviation
• Pinpoint pupils (suggests opioid effect)
• Decerebrate/decorticate posturing
• Grimacing to pain

C. Apnoea Test

• Systolic BP ≥100 mmHg (vasopressors if needed)
• PaO2 ≥200 mmHg (pre-oxygenate with 100% O2 for 10 minutes)
• Normalise PaCO2 to baseline (35-45 mmHg) by adjusting ventilator

1. Obtain baseline ABG confirming normocapnia and adequate oxygenation
2. Disconnect from ventilator
3. Deliver 100% O2 via catheter at carina level (6 L/min) - apnoeic oxygenation maintains SpO2
4. Observe for any respiratory effort (chest/abdominal excursion, gasping) for 8-10 minutes
5. Obtain ABG at end of observation period

• No respiratory effort is observed AND
• PaCO2 ≥60 mmHg OR a rise of ≥20 mmHg from a normal baseline PaCO2

• SpO2 falls below 85-90% (despite apnoeic oxygenation)
• Severe haemodynamic instability (hypotension, severe arrhythmia)
• In these cases, proceed to ancillary/confirmatory tests

5. Ancillary (Confirmatory) Tests

• Clinical exam cannot be completed (e.g., severe facial trauma, severe lung disease preventing apnoea test)
• Confounders cannot be fully excluded
• Legal or institutional requirements
• Religious/cultural objections to clinical criteria alone

6. Communication with Family

• Family should not be surprised by brain death - they should have been counselled about the prognosis from the time of severe brain injury
• Announcement: "Your loved one has died but is being supported by machines"
• Organ donation discussion occurs separately from the brain death declaration - by organ procurement organisation (OPO) personnel, not the treating team
• In the USA: federal law requires physician to contact the OPO
• Cultural/religious sensitivity mandatory - some faiths (Orthodox Jewish, Japanese tradition) may not accept brain death criteria
• Family refusal remains a major cause of lost donor potential

7. Types of Organ Donation

A. Donation After Brain Death (DBD)

• Heart-beating donor
• Optimal organ quality (warm ischaemia avoided)
• Allows time for full evaluation and multiple organ procurement
• Accounts for ~70% of deceased donors (USA)

B. Donation After Circulatory (Cardiac) Death (DCD)

• Non-heart-beating donor
• Maastricht Classification:

• Controlled DCD (Cat III) most common: life support withdrawn in OT; organ procurement begins after 5-minute "no-touch" period of confirmed cardiac arrest
• Warm ischaemia time is longer in uncontrolled DCD - reduces organ quality
• DCD accounted for 30.2% of deceased donors in USA in 2021 (Miller's Anesthesia, 10e)

8. Pathophysiology Following Brain Death - "The Catecholamine Storm" (4 marks)

Phase 1: Autonomic Storm (Cushing Response/Catecholamine Surge)

• As intracranial pressure rises and herniation occurs, brainstem ischaemia triggers an intense sympathetic discharge
• Plasma catecholamines rise 10-100x above baseline
• Cardiovascular effects: severe hypertension, tachycardia, arrhythmias, myocardial ischaemia, reversible left ventricular dysfunction (catecholamine cardiomyopathy)

Phase 2: Post-Herniation Cardiovascular Collapse

• Loss of sympathetic tone → systemic vasodilation, increased venous capacitance, relative hypovolaemia
• Exacerbated by prior osmotherapy (mannitol), diuresis, and inadequate fluid resuscitation
• Progressive hypotension requiring vasopressors

Phase 3: Hypothalamic-Pituitary Axis Disruption

Phase 4: Systemic Consequences

• Hypothermia - loss of hypothalamic temperature regulation
• Coagulopathy - DIC from thromboplastin release from injured brain
• Pulmonary oedema - neurogenic (sympathetic storm) + aspiration risk
• Anaemia - from haemorrhage, haemodilution
• Infection - ICU-acquired, aspiration pneumonia

9. ICU Management of the Brain-Dead Organ Donor (5 marks)

The "Rule of 100s" (Trauma Surgery guideline)

• Systolic BP >100 mmHg
• Urine output >100 mL/h
• PaO2 >100 mmHg

A. Haemodynamic Goals

• Vasopressors: Noradrenaline (norepinephrine) first choice; vasopressin has dual benefit (vasopressor + treats DI); avoid high-dose dopamine
• Fluid resuscitation: balanced crystalloids; albumin; avoid synthetic starches
• Inotropes (dopamine, dobutamine) if cardiogenic dysfunction

B. Respiratory Goals (Critical for Lung Donation)

• Frequent suctioning; HOB 30-45°; avoid ventilator-associated pneumonia
• Lung-protective ventilation critical for lung procurement

C. T4 Hormonal Resuscitation Protocol

D. Specific Organ Targets

E. Diabetes Insipidus Management

• Urine output >3-4 mL/kg/h + rising serum Na+ + low urine osmolality (hypotonic)
• Vasopressin (desmopressin DDAVP 0.5-2 mcg IV q6h, or vasopressin infusion)
• Replace fluid losses with 0.45% NaCl or 5% dextrose
• Target sodium: 130-155 mmol/L

10. Anaesthesia for Organ Procurement (Harvesting) in the Operating Theatre (6 marks)

Role of the Anaesthesiologist

1. Verify the brain death certificates
2. Confirm family consent is in order
3. Confirm no absolute contraindications to donation (e.g., active HIV, active malignancy)
4. Continue ICU-level haemodynamic support
5. Manage spinal reflexes and haemodynamic responses to surgical stimulation

Why Anaesthesia is Required Despite Brain Death?

• Spinal cord reflexes remain intact and may cause gross movements (Lazarus reflex, limb movements) during surgical stimulation, which is distressing to the surgical team
• Haemodynamic reflexes - surgical stimulation can cause spinal-sympathetic reflex responses: hypertension and tachycardia (without pain perception), which can worsen catecholamine-mediated organ injury
• Volatile agents may provide ischaemic preconditioning - theoretical benefit for organ protection
• Muscle relaxants provide optimal surgical conditions

"Neuromuscular blockade required to inhibit spinal motor reflexes... volatile anaesthetics due to theoretical advantage of ischaemic preconditioning... brain death may cause haemodynamic response to noxious stimuli; hypertension should be avoided." (BC Transplant Anaesthesia Guidelines, 2024)

Monitoring in OT

Anaesthetic Technique

• Neuromuscular blockade (NMB): suxamethonium/rocuronium; maintain throughout
• Volatile anaesthetic (isoflurane/sevoflurane): 0.5-1 MAC - suppresses spinal motor reflexes; ischaemic preconditioning
• Opioids (fentanyl): to attenuate haemodynamic responses to incision - not for analgesia (brain dead) but to reduce reflex hypertension
• Continue vasopressors and inotropes as per ICU management
• Ventilation: lung-protective strategy as per ICU

• Continue vasopressin infusion for DI
• Insulin to maintain glucose 6-10 mmol/L
• Methylprednisolone if not already given
• NAC (N-acetylcysteine) 30 mg/kg 1 hour before procurement; 300 mg via portal vein before cross-clamp - shown to improve graft survival
• Prophylactic broad-spectrum antibiotics (cephalosporin)
• Heparin IV bolus (300-400 units/kg) before aortic cross-clamping - to prevent vascular thrombosis during cold flush

Surgical Sequence (Multi-organ Procurement)

1. Midline incision - suprasternal notch to pubis
2. Thoracic dissection - heart, lungs mobilised
3. Abdominal dissection - liver, pancreas, kidneys, bowel
4. Heparin given before cross-clamping
5. Aortic cross-clamp (supradiaphragmatic) + cold perfusion with preservation solution begins
   • At cross-clamp: all vasopressors ceased; ventilator stopped
   • Cardioplegia for heart
6. Sequential organ removal in order of ischaemia tolerance:
   • Heart (most sensitive - 4h cold ischaemia)
   • Lungs (6h cold ischaemia)
   • Liver (12-24h)
   • Pancreas (12-24h)
   • Kidneys (24-36h)
   • Intestines (8-12h)
7. Corneas, skin, bones - post-cardiac death

11. Donation After Circulatory Death (DCD) - Anaesthetic Implications

• Life support withdrawn in OT (Maastricht III) - comfort care drugs (morphine, midazolam) given to relieve any distress
• No-touch period of 2-5 minutes after cardiac arrest (permanent cardiac arrest confirmed)
• Rapid organ retrieval begins immediately after no-touch period
• Warm ischaemia time is the critical variable - shorter warm ischaemia = better organ outcomes
• Ex-vivo machine perfusion (normothermic or hypothermic) increasingly used to recondition DCD organs

12. Ethical and Legal Considerations

13. Summary - Key Examination Points

1. Harvard criteria 1968 - first formalised brain death; 25 assessments required
2. Three absolute requirements for brain death: deep coma (known irreversible cause) + all brainstem reflexes absent + apnoea test positive (PaCO2 ≥60 mmHg or rise ≥20 mmHg, no respiratory effort)
3. Five confounders to exclude before testing: hypothermia, drugs, NMB, metabolic, hypotension
4. Ancillary tests (EEG, CTA, SPECT, TCD) - not routinely required; used when clinical exam incomplete
5. Catecholamine storm → haemodynamic collapse → hypothalamic-pituitary failure → DI, hypothyroidism, adrenal failure
6. T4 protocol: methylprednisolone + T3/T4 + vasopressin + insulin
7. Anaesthesia in OT: NMB + volatile agent + opioids = suppress spinal reflexes + haemodynamic responses; NOT for consciousness (brain dead)
8. CVP strategy: low (4-8) during heart/lung harvesting; raise (10-12) for kidney procurement
9. Dead donor rule and separation of teams are non-negotiable ethical principles
10. DCD donors now account for 30% of deceased donors in the USA; Maastricht classification

• Miller's Anesthesia, 2-Volume Set, 10th Edition
• Bradley & Daroff's Neurology in Clinical Practice, 8th Edition
• Plum & Posner's Diagnosis and Treatment of Stupor and Coma, 5th Edition
• Mulholland & Greenfield's Surgery: Scientific Principles and Practice, 7th Edition
• BC Transplant - Anesthesia for Donors following Death by Neurological Criteria (2024)
• NOTTO (National Organ & Tissue Transplant Organisation) India - OT Guidelines