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DNB Final Anesthesia — Dec 2025, Paper 1

Model Answers (20 Marks Each)

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Q1. THRIVE | CDH Management and Concerns

Part A: THRIVE (Transnasal Humidified Rapid-Insufflation Ventilatory Exchange)

Mechanism

• Apnoeic oxygenation: Alveolar O₂ uptake exceeds CO₂ elimination (O₂ absorbed at ~250 mL/min vs CO₂ diffusion limited by gradient); bulk flow of O₂ from upper airway maintains oxygenation even during apnoea.
• CO₂ clearance: High-flow gas generates a degree of nasopharyngeal CPAP (2–7 cmH₂O at flows >30 L/min), maintaining upper airway patency and slowing CO₂ rise (~rate of rise CO₂ 0.15 kPa/min with THRIVE vs 0.3–0.5 kPa/min without).
• Washout effect: Flushes nasopharyngeal dead space, optimizing FiO₂ delivered.

Equipment

• Optiflow/Fisher & Paykel AIRVO 2 system
• Heated humidifier (37°C, 100% RH)
• Flow rates: 15–70 L/min (typically 70 L/min for adults)

Clinical Applications

Evidence (Barash ClinicalAnesthesia, 9e)

• Patel & Nouraei 2015: Extended safe apnoea time up to 65 minutes in elective patients.
• Flow ≥30 L/min needed for appreciable CPAP effect.
• CO₂ rises slowly; however, duration still limited in patients with pre-existing pulmonary disease.

Limitations

• Does not prevent aspiration
• High flows cause noise, patient discomfort
• CO₂ accumulates over time → respiratory acidosis if prolonged
• Not a substitute for definitive airway

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Part B: CDH (Congenital Diaphragmatic Hernia) — Anaesthetic Management and Concerns

Pathophysiology

• Herniation of abdominal viscera (left > right, 85:15) through Bochdalek defect → ipsilateral and contralateral pulmonary hypoplasia
• Pulmonary hypertension (PHT) due to abnormal vascular remodelling — the primary determinant of outcome
• Associated anomalies: cardiac (VSD, ASD), chromosomal (Trisomy 18, 21), CNS

Preoperative Stabilisation (Delayed Surgery Concept)

• Allow spontaneous transition of pulmonary circulation
• Target: SpO₂ > 85–95% (pre-ductal), PaO₂ > 50 mmHg, pH 7.35–7.45
• Avoid bag-mask ventilation (gastric distension worsens lung compression)
• Intubate immediately after birth if respiratory distress
• Place orogastric tube to decompress bowel
• Echocardiography: assess PHT severity, direction of ductal shunt

Anaesthetic Concerns (Miller's 10e)

Intraoperative Anaesthesia

• Induction: IV (ketamine 1–2 mg/kg or fentanyl based) — avoid N₂O (bowel distension)
• Maintenance: Low-dose volatile (not >1 MAC due to PHT vasodilatory concerns) + opioid infusion
• Ventilation strategy: Low tidal volume (4–6 mL/kg), high RR, permissive hypercapnia, PEEP 3–5 cmH₂O
• Monitoring: Pre-ductal (right hand) and post-ductal SpO₂, arterial line, CVP
• Surgical approach: Open vs VATS/laparoscopic (laparoscopic increases intraabdominal pressure — may worsen PHT)

Postoperative

• ICU ventilation, weaning guided by echocardiography
• Avoid unnecessary stimulation (triggers PHT crises)
• Adequate analgesia (caudal/epidural reduces opioid requirement)

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Q2. Bariatric Surgery — Anaesthetic Management

Preoperative Assessment

• BMI cutoff: ≥35 with comorbidities, or ≥40 without
• Comorbidities: OSA, T2DM, HTN, CAD, NAFLD, GERD, DVT/PE risk, OHS
• Airway assessment: Mallampati, neck circumference (>43 cm in men → difficult intubation), thyromental distance. 3-3-2 rule.
• Cardiopulmonary: ECG, Echo if suspected cardiomyopathy, PFTs in OHS
• OSA: STOP-BANG ≥3 → sleep study; pre-op CPAP if moderate-severe OSA for at least 2 weeks
• Labs: ABG (hypercapnia in OHS), HbA1c, LFTs
• Premedication: Avoid BZD; ranitidine/PPI + prokinetic for aspiration prophylaxis

Positioning

• Ramped position (ear-to-sternal notch horizontal) — improves laryngoscopic view and FRC
• Head-up tilt 20–30° — improves FRC, reduces regurgitation risk
• Reverse Trendelenburg during induction for preoxygenation

Preoxygenation

• 3–5 min 100% O₂; THRIVE if available
• NIV/CPAP during pre-oxygenation significantly prolongs safe apnoea time (FRC is reduced in obesity)

Induction

• RSI mandatory (GERD, high aspiration risk)
• Succinylcholine (ideal body weight + 20% for RSI) or rocuronium 1.2 mg/kg IBW + sugammadex availability
• Video laryngoscopy preferred

Drug Dosing (Miller's 10e)

Maintenance

• TIVA (propofol + remifentanil) preferred: reduced PONV, faster recovery
• Volatile agents: desflurane (fastest emergence) — but concerns re global warming and higher cost
• Nitrous oxide avoided (bowel distension, PONV)
• Lung-protective ventilation: Tidal volume 6–8 mL/kg IBW, PEEP 8–10 cmH₂O, FiO₂ titrated to SpO₂ 94–98%, recruitment manoeuvres

Multimodal Analgesia (ERAS for Bariatric)

• Paracetamol + NSAIDs (if no renal/GI contraindication)
• Dexamethasone 8 mg (antiemetic + anti-inflammatory)
• Ketamine 0.25–0.5 mg/kg (opioid-sparing)
• TAP block / wound infiltration
• Avoid excess opioids (respiratory depression in OSA)

Airway Management

• Video laryngoscopy preferred (GlideScope, C-MAC)
• Awake FOI if predicted very difficult airway
• LMA as rescue only; do not use as primary in bariatric

Extubation

• Fully awake, reversed neuromuscular block (TOF ratio >0.9 with sugammadex)
• 30–45° head-up position
• Have CPAP ready immediately post-extubation
• Delay extubation if desaturation <94% on 100% O₂

Postoperative

• HDU/ICU if OHS or complex comorbidities
• CPAP for OSA patients from night 1
• VTE prophylaxis (LMWH dose adjustment + compression stockings)
• Thromboprophylaxis: higher doses of enoxaparin (0.5 mg/kg BD) often needed

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Q3. Bronchial Blockers | Diastolic Dysfunction and Anaesthetic Implications

Part A: Bronchial Blockers

Definition

Indications (Morgan & Mikhail, 7e; Miller 10e)

• Difficult airway where DLT placement not feasible
• Pre-existing tracheostomy
• Paediatric patients (<8 years) — DLT too large
• Need for selective lobar collapse
• ICU patients requiring OLV while remaining intubated
• Haemorrhage from one bronchus (tamponade)

Types of Bronchial Blockers

Placement Technique

1. Single-lumen ETT placed first
2. Fibreoptic bronchoscope used to guide blocker into target bronchus
3. Balloon inflated to seal bronchus
4. Lung deflation occurs over 10–20 min (slower than DLT)
5. Check position with bronchoscopy after positioning patient

Advantages over DLT

• Applicable in difficult airway
• No need to change tube for postoperative ventilation
• Selective lobar isolation possible
• Less trauma to larynx/trachea (smaller outer diameter)

Disadvantages

• Slower deflation of operative lung
• Risk of displacement with patient movement
• No ability to suction/CPAP isolated lung (except Arndt with open channel)
• Inadequate seal if anatomy is abnormal

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Part B: Diastolic Dysfunction — Pathophysiology and Anaesthetic Implications

Definition

Grades (ASE/EACVI 2016)

Anaesthetic Implications

• Acute pulmonary oedema risk with any rapid fluid bolus or systemic HTN
• AF/arrhythmia → loss of atrial kick → acute LV failure
• Tachycardia is poorly tolerated (shortened diastole)
• Hypotension must be treated carefully: vasopressors (phenylephrine, vasopressin) preferred over excessive fluid
• Neuraxial anaesthesia: sympathectomy → preload reduction → catastrophic fall in CO; slow titration mandatory

• Intraoperative TOE recommended for major surgery
• PA catheter or PICCO if severely impaired
• Watch for diastolic filling pattern changes on echo

• Avoid tachycardia (beta-blockade, adequate anaesthesia depth)
• Judicious fluid therapy guided by SVV/PPV or TOE
• Maintain sinus rhythm; have DC cardioversion ready
• Vasopressors early for hypotension (avoid fluid overload)
• Regional anaesthesia with caution and slow titration

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Q4. Spinal Additives | Neurological Complications of Spinal Anaesthesia + Factors Affecting PDPH

Part A: Spinal Additives (Intrathecal Adjuvants)

Opioids

Alpha-2 Agonists

• Clonidine 15–75 µg: prolongs both sensory and motor block, reduces shivering, provides analgesia without respiratory depression. Caution: hypotension, sedation.
• Dexmedetomidine 3–5 µg: newer; superior to clonidine in extending block duration without significant haemodynamic effects.

Neostigmine

• 25–50 µg intrathecally
• Mechanism: inhibits breakdown of acetylcholine at spinal cord dorsal horn
• Provides visceral analgesia
• Significant side effects: severe nausea, bradycardia — limits routine use

Ketamine

• 50–100 mg (preservative-free): NMDA antagonism at dorsal horn
• Caution: neurotoxicity concerns with preservative-containing formulations
• Not routinely recommended

Magnesium

• 50–100 mg intrathecally
• NMDA antagonism; prolongs sensory and motor block
• Caution: neurotoxicity risk at higher doses

Vasoconstrictors (historically used)

• Adrenaline 100–200 µg: prolongs block, reduces systemic absorption
• Reduced use due to concerns about spinal ischaemia

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Part B: Neurological Complications of Spinal Anaesthesia

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Part C: Factors Affecting Post-Dural Puncture Headache (PDPH)

Patient Factors

• Age: Young patients (20–40 years) — highest risk; elderly less affected (reduced CSF pressure, fibrotic dura)
• Gender: Female > male (especially obstetric population)
• BMI: Obese → higher intraabdominal/intrathecal pressure → reduced leak
• Pregnancy: High risk (obstetric population)
• Previous PDPH: Increased risk of recurrence
• Chronic headache history: Possible association

Needle Factors

Technique Factors

• Midline vs paramedian: No significant difference
• Direction of dural fibres: Parallel insertion reduces leak
• Experience of operator: Fewer accidental dural taps with experienced anaesthetist

Physiological Factors

• CSF pressure: Higher pressure forces more CSF through dural defect
• Dehydration: May worsen headache
• Coughing/straining: Increases CSF leak

Management of PDPH

1. Conservative: Supine rest, adequate hydration (not prolonged bed rest), paracetamol, caffeine (300–500 mg oral/IV)
2. Pharmacological: Caffeine IV, sumatriptan, theophylline, ACTH, neostigmine
3. Definitive: Epidural Blood Patch (EBP) — 15–20 mL autologous blood; success rate 70–98%; repeat if needed; timing: >24h after dural puncture optimal

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Q5. Neurotoxicity in Children | Autonomic Changes in Spinal Cord Transection

Part A: Anaesthetic Neurotoxicity in Children

Background

Agents Implicated

Critical Period (Animal Data)

• Maximal brain vulnerability = period of rapid synaptogenesis
• Rodents: 7–10 days postnatal
• Primates: 3rd trimester to 2 years postnatal
• Humans: estimated 3rd trimester to age 3 years (most vulnerable <6 months)

Human Evidence

• GAS Trial (McCann 2019, Lancet): Sevoflurane ≤1h single exposure in infants <60 weeks PMA → no significant difference in neurodevelopmental outcomes at 5 years (Bayley-III cognitive score)
• PANDA Study: Siblings discordant for early single anaesthesia exposure → no difference in IQ or neuropsychological outcomes
• MASK Study (Warner 2018): Single exposure — no difference; multiple exposures → modest association with learning disability and ADHD-like symptoms
• SPS3/FDA Warning (2016): FDA labelled general anaesthetic agents for repeated/prolonged use in children <3 years and pregnant women (3rd trimester)

Risk Factors for Harm (if any)

• Age <3 years (especially <6 months)
• Duration >3 hours
• Multiple anaesthetic exposures
• Pre-existing neurological vulnerabilities

Current Clinical Guidance (ASA/AAP 2017; UK SNAP 2018)

1. Avoid unnecessary delay of essential surgery in young children — untreated surgical conditions are also harmful
2. For elective surgery: Consider delaying to ≥3 years if clinically safe to do so
3. For necessary surgery, use shortest effective duration of anaesthesia
4. Inform parents appropriately (shared decision making)
5. Consider regional techniques where feasible to reduce GA duration
6. Dexmedetomidine as an adjunct may be neuroprotective

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Part B: Autonomic Changes in Spinal Cord Transection

Acute Phase — Spinal Shock (1–6 weeks)

• Loss of all autonomic reflexes below lesion
• Flaccid paralysis, areflexia, loss of sympathetic outflow below injury
• Neurogenic shock: Hypotension (loss of sympathetic tone) + bradycardia (vagal predominance if cervical/high thoracic)
• Cardiovascular: HR ≤60, BP ≤90/60 in cervical lesions
• Temperature regulation lost: Poikilothermia
• Urinary retention, ileus

Chronic Phase — Return of Reflex Activity

• Reflex arc returns below lesion (spinal cord neurons reorganise)
• Autonomic Dysreflexia (AD) — major anaesthetic concern

Autonomic Dysreflexia (AD)

• Occurs in injuries at or above T6 (loss of supraspinal inhibition over splanchnic sympathetics)
• Triggered by stimuli below the level of lesion: Bladder distension (most common), bowel distension, pressure sores, surgical stimulation, UTI, ingrown toenail

Noxious stimulus below T6
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Afferent signals → spinal cord → massive sympathetic discharge below lesion
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Vasoconstriction → severe HTN (BP can reach 300/200 mmHg)
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Baroreceptors detect HTN → vagal response above lesion
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Bradycardia, flushing, sweating, headache ABOVE lesion
(no compensatory vasodilation below lesion — sympathetics still active there)

• Pounding headache, blurred vision
• Flushing and sweating above lesion
• Pallor, piloerection below lesion
• Severe hypertension (may cause stroke, MI, retinal haemorrhage)
• Bradycardia/reflex tachycardia

• Prevention: Ensure no triggers (empty bladder before procedure, adequate regional block)
• Regional anaesthesia preferred (spinal > epidural) — blocks afferent trigger arc
• General anaesthesia: Volatile agents effective but less reliable
• Acute AD during surgery: Remove trigger; sit patient up; immediate antihypertensives
  • Nifedipine 10 mg sublingual (first line in emergency)
  • GTN patch/spray
  • Hydralazine, labetalol, phentolamine
• Continuous arterial line monitoring for major procedures

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Q6. Haemorrhagic Shock | Issues with Hypervolaemia in Resuscitation | Advantages of Regional Anaesthesia for Trauma

Part A: Haemorrhagic Shock — Classification and Management

ATLS Classification

Damage Control Resuscitation (DCR)

1. Permissive hypotension — target SBP 80–90 mmHg (MAP 50–65) until surgical haemostasis; avoid aggressive fluid until bleeding controlled (prevents clot disruption, dilution coagulopathy)
   • Exception: TBI — maintain MAP ≥80 mmHg (avoid cerebral ischaemia)
2. Haemostatic resuscitation (1:1:1) — RBCs:FFP:Platelets in equal ratios (PROPPR Trial 2015: 1:1:1 ratio improved 24h survival vs 1:1:2)
   • Rationale: replaces blood with blood (not crystalloid); delivers coagulation factors early
   • Tranexamic acid 1g IV within 3 hours of injury (CRASH-2 Trial) — reduces mortality; dose repeated at 8h
3. Damage control surgery — abbreviated initial surgery, temporary measures, ICU resuscitation, then definitive surgery

Resuscitation Endpoints

• Lactate <2 mmol/L
• Base deficit correction
• Normalisation of pH (>7.35)
• Temperature >35°C
• INR <1.5, fibrinogen >2 g/L
• Urine output >0.5 mL/kg/hr

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Part B: Issues with Hypervolaemia in Resuscitation

• Crystalloids (0.9% saline, Hartmann's): Expand interstitial space more than intravascular; ratio 3:1 to replace blood
• Colloids (albumin, Gelofusine, Haemaccel): Better volume expansion but cost, anaphylaxis risk; no survival advantage
• Blood products preferred in haemorrhagic shock

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Part C: Advantages of Regional Anaesthesia for Trauma

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Q7. Malignant Hyperthermia — Triggering Agents, Treatment, Syndromes

Part A: Triggering Agents

Definite Triggers

• All volatile halogenated anaesthetic agents: Halothane, isoflurane, sevoflurane, desflurane, enflurane
• Succinylcholine (suxamethonium)

Mechanism of Triggering

Safe (Non-triggering) Agents

• All intravenous agents: Propofol, ketamine, etomidate, thiopentone, opioids, benzodiazepines
• Non-depolarising NMBDs: Rocuronium, vecuronium, atracurium, cisatracurium
• Local anaesthetics (amide and ester)
• Nitrous oxide
• Dexmedetomidine
• Neostigmine/Sugammadex

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Part B: Clinical Features and Treatment of MH

Clinical Features (MHAUS Grading/Clinical Signs)

• Masseter spasm after succinylcholine (may be early warning)
• Unexplained tachycardia, tachypnoea
• Increasing end-tidal CO₂ (earliest reliable sign)

• Hyperthermia (temperature rises >2°C/h; can reach >42°C)
• Hyperkalaemia
• Metabolic + respiratory acidosis
• Myoglobinuria (cola-coloured urine) → AKI
• DIC
• Muscle rigidity (generalised)
• Rhabdomyolysis: CK >20,000 IU/L

Treatment Protocol (MHAUS 2020 Guidelines)

1. Discontinue all triggering agents immediately
2. Call for help, activate MH protocol
3. Switch to TIVA (propofol-based) if continuing surgery
4. Hyperventilate with 100% O₂ at 10 L/min (flush volatile from circuit); change to clean machine if possible or use activated charcoal filters
5. Dantrolene sodium 2.5 mg/kg IV bolus (initial dose) — repeat 1 mg/kg every 5 min until signs resolve; maximum 10 mg/kg (occasionally higher)
   • Mechanism: Blocks Ca²⁺ release from SR by inhibiting RYR1
   • Mix in sterile water (not saline — precipitates)
   • Stock minimum 36 vials (each 20 mg) in any institution giving GA

• Cool patient: Ice packs groin/axilla/neck, cold IV fluids, cold nasogastric lavage; target <38.5°C
• Bicarbonate for metabolic acidosis (2–4 mEq/kg)
• Insulin + dextrose for hyperkalaemia (Ca gluconate for cardiac protection)
• Maintain urine output >1 mL/kg/hr (hydration ± mannitol) — prevent myoglobinuric AKI
• Treat arrhythmias: Amiodarone (avoid calcium channel blockers — interact with dantrolene)
• Monitor: Continuous core temp, serial ABGs, electrolytes, CK, coagulation, urinalysis
• ICU admission: Continue dantrolene 1 mg/kg IV q6h for 24–48h (rebound MH possible)

• Genetic counselling; test first-degree relatives (IVCT — In Vitro Contracture Test or next-gen sequencing)
• Medical alert bracelet
• Register with MHAUS

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Part C: Syndromes Associated with MH

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Q8. Supine Caval Syndrome | Haematological Changes in Pregnancy

Part A: Supine Caval (Aortocaval Compression) Syndrome

Anatomy

Pathophysiology

• IVC compression → ↓ venous return → ↓ preload → ↓ cardiac output (CO falls 10–30%)
• Aortic compression → reduced uterine artery flow → uteroplacental insufficiency
• Collateral circulation (paravertebral, azygous veins) partially compensates
• 5–10% women develop symptomatic syndrome (supine hypotension syndrome)
• ALL parturients have some degree of compression

Clinical Features

Anaesthetic Relevance

• Mandatory left lateral tilt (15°) with wedge under right hip for all parturients >20 weeks
  • Displaces uterus left, relieves IVC compression
  • 15° tilt may still allow some compression — manual uterine displacement (MUD) may be needed
• Spinal/epidural anaesthesia removes sympathetic compensatory vasoconstriction → more severe hypotension → aggressive management needed
• Spinal anaesthesia for LSCS: Hypotension occurs in >80% → vasopressor infusion (phenylephrine preferred over ephedrine per recent meta-analyses — better FHR outcomes)
• Prevention: pre-load with 500–1000 mL crystalloid, lateral tilt, phenylephrine infusion

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Part B: Haematological Changes in Pregnancy and Anaesthetic Implications

Blood Volume

• Total blood volume increases 40–50% by 34 weeks (plasma +50%, RBC mass +25%)
• Net result: Physiological anaemia — Hb 10.5–11.0 g/dL (dilutional)
• Protects against blood loss at delivery (average 500 mL SNVD, 1000 mL LSCS)

Red Blood Cells

• Hb falls due to disproportionate plasma expansion
• MCV unchanged or slightly increased (folate demand)
• Iron requirements: 1000 mg total; supplement from 12–16 weeks
• Iron deficiency anaemia most common — target Hb >10 g/dL before term

White Blood Cells

• WBC increases to 9,000–16,000/µL (mainly neutrophilia)
• Further ↑ in labour (up to 25,000) — physiological, do not attribute to infection alone
• NK cell activity reduced (maternal immune tolerance)
• Susceptibility to viral infections increased (influenza, COVID)

Platelets

• Slight decrease (125,000–150,000/µL) — "gestational thrombocytopaenia"
• Increased consumption at uteroplacental interface
• Below 80,000: Risk of bleeding; reconsider regional anaesthesia
• Below 50,000: Regional anaesthesia contraindicated
• Causes of severe thrombocytopaenia: ITP, HELLP, TTP, DIC

Coagulation — Hypercoagulable State

• LMWH thromboprophylaxis for high-risk patients
• Compression stockings

Anaesthetic Implications of Haematological Changes

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Q9. Neurophysiological Monitoring in Scoliosis

Rationale

Modalities Used

1. Somatosensory Evoked Potentials (SSEPs)

• Pathway: Peripheral nerve stimulation (median/ulnar/posterior tibial nerve) → dorsal column → thalamus → cortex
• Monitors: Posterior cord (sensory) function
• Interpretation:
  • Warning criteria: Amplitude ↓ >50% AND/OR latency ↑ >10%
  • Sensitive to ischaemia, cord compression
• Limitations: Does NOT monitor motor tract; can miss isolated motor injury

2. Motor Evoked Potentials (MEPs)

• Pathway: Transcranial electrical stimulation → corticospinal tract → peripheral muscle response
• Monitors: Anterior cord (motor) function
• Interpretation:
  • Warning criteria: Amplitude ↓ >50–80% or loss of response
  • More sensitive for motor injury
• Advantages: Detects anterior spinal artery injury that SSEPs may miss
• Requirements: No muscle relaxant (or minimal — Train-of-4 1/4); patient must be immobile
• Contraindications: Metal in skull, seizure disorder, cardiac pacemaker

3. Combined SSEP + MEP (Gold Standard)

• Bimodal monitoring recommended for all major scoliosis corrections
• High sensitivity (93%) and specificity (98%) for cord injury when combined

4. Electromyography (EMG)

• Free-running (spontaneous) EMG: Monitors nerve root irritation — bursts of activity = nerve root at risk
• Triggered EMG: Tests pedicle screw placement accuracy (current threshold >10 mA = screw in bone; <5 mA = possible medial breach)
• Essential for screw-based instrumentation

5. Wake-up Test (Stagnara)

• Historically used, now supplementary
• Patient awakened intraoperatively, asked to move lower limbs
• Limitations: One-time assessment, requires light anaesthesia, risk of air embolism/ETT displacement
• Confirmed by MEPs — no longer routine

Anaesthetic Requirements for Monitoring

Factors that Affect Monitoring Quality

• Temperature: Hypothermia ↓ amplitude ↑ latency
• Blood pressure: MAP <60 mmHg → ischaemia → signal loss
• Anaemia: Hb <7 g/dL → cord ischaemia
• Positioning: Stretch on brachial plexus/peripheral nerves → false positives
• Electrode impedance: Poor contact → noise

Response to Warning Signals

1. Alert surgeon immediately
2. Reverse last surgical manoeuvre (loosen distraction)
3. Raise MAP to ≥80 mmHg (vasopressors)
4. Optimise Hb (transfuse if <9 g/dL)
5. Correct hypothermia, acid-base
6. Reduce anaesthetic depth (↓ volatile, ↑ O₂)
7. If signals do not recover → wake-up test
8. Consider removing implants
9. Post-op neurological assessment mandatory

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Summary Table — Mark Allocation (Approximate)

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• Miller's Anesthesia, 10th Edition (Gropper et al.)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9th Edition
• Morgan & Mikhail's Clinical Anesthesiology, 7th Edition
• MHAUS Malignant Hyperthermia Guidelines 2020
• CRASH-2 Trial (Lancet 2010) — Tranexamic acid
• PROPPR Trial (JAMA 2015) — 1:1:1 resuscitation
• GAS Trial (Lancet 2019) — Paediatric neurotoxicity
• FDA Drug Safety Communication 2016 — Anaesthetic neurotoxicity
• ASE/EACVI 2016 Guidelines — Diastolic dysfunction grading
• ATLS 10th Edition — Haemorrhagic shock classificationAll 10 questions answered comprehensively. Here is a quick orientation guide to using these answers:

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How to Use These Answers in Exam

• Definitions to anchor the answer
• Tables for rapid readability (examiners appreciate structured answers)
• Mechanisms and pathophysiology for depth
• Clinical management protocols with specific doses/targets
• Recent guidelines cited (MHAUS 2020, PROPPR Trial, GAS Trial, FDA 2016, CRASH-2)

Key High-Yield Points Per Question