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DNB Final Anesthesiology — December 2025 Paper 1

Comprehensive Model Answers (10 Marks Each)

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QUESTION 1: THRIVE [10 Marks]

THRIVE — Transnasal Humidified Rapid-Insufflation Ventilatory Exchange

Definition

Mechanism of Action

Key Physiology

• During apnea, O₂ consumption (250 mL/min) exceeds CO₂ production (200 mL/min) — net negative pressure draws O₂ into alveoli
• CO₂ rises at ~3 mmHg/min (slower than with standard apneic oxygenation) due to the flushing effect
• Normal apnea tolerance extends from ~8 min (standard) to >15–20 min with THRIVE

Device

• Optiflow™ (Fisher & Paykel) or AirVO™ system
• Flow rates: Adults 30–70 L/min; Children 2 L/kg/min (max 50 L/min)
• Temperature: 37°C; Humidity: 44 mg H₂O/L

Clinical Applications

1. Preoxygenation — THRIVE at 60 L/min for 3 minutes is as effective as tidal volume preoxygenation by facemask (Miller's Anesthesia 10e)
2. Difficult airway management — Awake fiberoptic intubation (AFOI); provides safety margin during laryngoscopy
3. "Cannot intubate, cannot oxygenate" (CICO) scenarios — Bridge while preparing for surgical airway
4. ENT/airway surgeries — Shared airway procedures (rigid bronchoscopy, laryngoscopy, microlaryngoscopy)
5. Bariatric patients — Head-up position combined with THRIVE significantly extends apnea time
6. Pediatric patients — RCTs confirm safety in children (Br J Anaesth, 2017)
7. ICU — Prevention of desaturation during intubation

Advantages

• Non-invasive; well-tolerated by awake patients
• Maintains verbal communication during AFOI
• Reduces need for bag-mask ventilation (BVM)
• No risk of gastric insufflation

Limitations

• Does NOT provide ventilation — PaCO₂ still rises (acidosis risk with prolonged use)
• Contraindicated with nasal obstruction, base of skull fractures
• High flows may cause discomfort; oral breathing reduces efficacy
• Not a substitute for definitive airway

Comparison: Standard vs. THRIVE Preoxygenation

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QUESTION 2: CDH — Management and Concerns [10 Marks]

Congenital Diaphragmatic Hernia (CDH) — Anesthesia Management and Concerns

Definition

Pathophysiology

Diaphragmatic defect → Visceral herniation → Pulmonary compression
           ↓
Pulmonary hypoplasia (bilateral, ipsilateral > contralateral)
           ↓
Reduced pulmonary vascular bed + Vascular remodeling
           ↓
Pulmonary Hypertension (PH)
           ↓
R→L shunting (PFO/PDA) → Profound hypoxemia

Preoperative Assessment and Concerns

• Liver herniation into chest
• Lung-to-head ratio (LHR) < 1.0
• Total fetal lung volume < 25% predicted
• Right-sided CDH
• Associated cardiac anomalies (VSD, ASD — present in 25%)

• Immediate gastric decompression (NG tube) — prevents gaseous bowel distension
• Avoid bag-mask ventilation — air enters gut, worsening compression
• Immediate intubation (awake or rapid sequence)
• Gentle ventilation: PIP < 25 cmH₂O; permissive hypercapnia (PaCO₂ 45–60 mmHg)
• Pre-ductal SpO₂ target: >85%; post-ductal > 70%
• ECMO if refractory: available as rescue

Anesthetic Concerns and Management

• Avoid triggers: hypoxia, hypercarbia, acidosis, hypothermia, pain, agitation
• iNO (inhaled nitric oxide): 20–40 ppm
• Sildenafil, prostacyclins as adjuncts
• Avoid high-dose vasodilators that cause systemic hypotension

• High-frequency oscillatory ventilation (HFOV) if conventional fails
• Low tidal volumes (4–6 mL/kg), high rate
• PEEP 3–5 cmH₂O (avoid overdistension of contralateral lung)
• Pre-ductal monitoring (right hand SpO₂, right radial arterial line)

• Awake intubation preferred in severely compromised neonates
• Avoid N₂O (causes bowel distension, worsens herniation)
• Isoflurane/sevoflurane in low concentrations (caution — vasodilation may worsen PH)
• TIVA (fentanyl + midazolam + vecuronium) preferred

• Dopamine 5–10 mcg/kg/min for systemic hypotension
• Avoid excessive fluid overload (pulmonary edema risk)
• Maintain ductal patency initially if PH is severe (keep R→L shunt as "pop-off")

• Pre- and post-ductal SpO₂ simultaneously
• Invasive arterial (right radial preferred — pre-ductal)
• Central venous pressure
• Temperature monitoring (neonates prone to hypothermia)
• Capnography (ETCO₂ underestimates PaCO₂ — rely on arterial blood gas)

• Abdominal approach (laparoscopic or open)
• Lung expansion after repair is AVOIDED — forceful inflation of hypoplastic lung → pneumothorax
• Contralateral pneumothorax is a catastrophic complication

• ICU — continue mechanical ventilation
• Watch for pulmonary hypertensive crisis (treat with iNO, sedation, paralysis)
• Chest drain on ipsilateral side only if tension pneumothorax
• ECMO bridging if required

ECMO Criteria in CDH

• Oxygenation Index (OI) > 40 for 4 hours
• PaO₂ < 40 for >2 hours
• Inability to maintain pre-ductal SpO₂ > 85%

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QUESTION 3: BARIATRIC SURGERY ANESTHESIA MANAGEMENT [10 Marks]

Definition

Physiological Concerns of Morbid Obesity

• Reduced FRC (functional residual capacity) — worse supine, critical in Trendelenburg
• OSA (obstructive sleep apnea) in 70–80%
• OHS (obesity hypoventilation syndrome)
• Increased O₂ consumption, increased CO₂ production
• Rapid desaturation on induction (reduced O₂ reserve relative to demand)

• Biventricular hypertrophy, diastolic dysfunction
• Increased cardiac output, blood volume
• Pulmonary hypertension
• Higher incidence of coronary artery disease, hypertension

• High gastric volume, low pH — aspiration risk
• Hiatus hernia common
• Fatty liver (NASH)

• Increased volume of distribution (lipophilic drugs)
• Altered protein binding
• Use Ideal Body Weight (IBW) for most drugs; Total Body Weight (TBW) for succinylcholine and some volatile agents

Preoperative Assessment

• Airway assessment (Mallampati, neck circumference >40 cm = difficult airway)
• Sleep study (CPAP titration)
• Echocardiogram if significant cardiopulmonary disease
• ABG if OHS suspected
• Optimize comorbidities: diabetes (HbA1c < 8%), hypertension, GERD
• Preoperative CPAP use

Premedication

• Continue CPAP, antihypertensives, statins
• Aspiration prophylaxis: ranitidine/omeprazole + metoclopramide
• Avoid benzodiazepine premedication (respiratory depression risk in OSA)
• DVT prophylaxis: LMWH (increased dose), TED stockings, pneumatic compression

Intraoperative Management

• Ramped position (head-elevated laryngoscopy position, HELP) — ear-to-sternal notch alignment
• Improves laryngoscopy view and preoxygenation
• Reverse Trendelenburg during emergence

• 25° head-up position + THRIVE (60 L/min) for 3 min
• Target EtO₂ > 90% or SpO₂ 100%

• RSI with cricoid pressure
• Video laryngoscope as primary choice
• Have surgical airway backup
• Double-lumen tube if thoracic component
• Succinylcholine: 1.5 mg/kg TBW; Rocuronium: 1.2 mg/kg IBW

• Propofol: 1–2 mg/kg IBW (reduced dose)
• Ketamine/etomidate if hemodynamically compromised
• LMA not recommended (aspiration risk)

• Desflurane preferred (faster emergence, low solubility)
• Avoid N₂O (bowel distension, pneumoperitoneum issues)
• TIVA with propofol/remifentanil — good option
• Multimodal analgesia (reduce opioid requirement)

• Tidal volume: 6–8 mL/kg IBW
• PEEP 10–12 cmH₂O (prevent atelectasis)
• Recruitment maneuvers during pneumoperitoneum
• Monitor plateau pressure < 30 cmH₂O
• Pneumoperitoneum (15 mmHg) further reduces FRC

• Restrictive strategy (no bowel prep, short fasting)
• Goal-directed fluid therapy

• Arterial line if BMI >55, OHS, or severe cardiac disease
• BIS or entropy monitoring
• Temperature monitoring
• Neuromuscular monitoring essential — sugammadex preferred

• TAP block / wound infiltration
• Paracetamol + NSAIDs (if no contraindication)
• Opioid-sparing: ketamine, dexmedetomidine, lidocaine infusion
• Epidural for open procedures

Emergence and Extubation

• Full reversal of NMB (TOF ratio > 0.9 — use sugammadex)
• Extubate awake, sitting up (45°)
• Continue CPAP immediately post-extubation
• Avoid excessive opioids in PACU

Postoperative Care

• Enhanced Recovery After Surgery (ERAS) for bariatrics
• CPAP, respiratory physiotherapy
• Early ambulation (DVT prevention)
• VTE prophylaxis continued for 4 weeks post-discharge (major risk)

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QUESTION 4: BRONCHIAL BLOCKERS + DIASTOLIC DYSFUNCTION [10 Marks]

PART A: BRONCHIAL BLOCKERS

Definition

Types of Bronchial Blockers

Indications for Bronchial Blockers (When DLT Not Feasible)

1. Difficult airway — tracheostomy, small trachea, airway distortion
2. Pediatric patients (< 8 years) — no DLT available for small airways
3. Need to remain intubated postoperatively — avoid tube exchange
4. Selective lobar blockade — isolate single lobe (lobe resection)
5. Thoracoscopic procedures via standard ETT
6. Cervical spine instability — avoid excessive neck manipulation for DLT

Placement Technique

• Standard ETT (≥7.5 mm ID for adults) placed first
• Fiberoptic bronchoscope used to guide and confirm placement
• Cuff inflated (5–8 mL air or saline) in target bronchus
• Suction port allows lung deflation (slower than DLT)

Advantages Over DLT

• No need for tube exchange at end of surgery
• Useful when DLT contraindicated/impossible
• Selective lobar blockade possible
• Less airway trauma

Disadvantages

• Slower lung collapse (no communication valve)
• More susceptible to displacement
• Limited suction capability
• Difficult CPAP application to operative lung
• Higher malposition rate

Complications

• Endobronchial migration → complete atelectasis
• Proximal displacement → bilateral blockade
• Cuff herniation → airway obstruction
• Bronchial rupture (rare but reported — Miller's Anesthesia 10e)

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PART B: DIASTOLIC DYSFUNCTION AND ANESTHETIC IMPLICATIONS

Definition

Grading (ASE/EACVI Classification)

Causes

• Hypertension (most common), elderly, obesity, diabetes, CAD, aortic stenosis, hypertrophic cardiomyopathy

Pathophysiology

↓ LV relaxation + ↑ LV stiffness
        ↓
High filling pressures needed to maintain CO
        ↓
Dependent on preload, heart rate, sinus rhythm, and afterload

Anesthetic Implications

1. Maintain sinus rhythm — atrial contraction contributes 40% of CO (vs. 20% in normal hearts)
2. Control heart rate — tachycardia reduces diastolic filling time → acute decompensation
   • Target HR: 60–80 bpm
3. Maintain preload — these patients are preload-dependent; hypovolemia → ↓ CO
4. Avoid acute increases in afterload — SVR increases → further impaired emptying
5. Avoid aggressive fluid loading — stiff LV → rapid rise in LVEDP → pulmonary edema

• Atrial fibrillation → sudden hemodynamic collapse
• Pulmonary edema from fluid overload or tachycardia
• Hypotension from vasodilating anesthetics
• Worsening with high PEEP (reduces preload)

• Invasive arterial monitoring
• TEE intraoperatively — assess filling, grade of DD, presence of diastolic failure
• PA catheter (PCWP often elevated but CO may be preserved)
• BIS — prevents light anesthesia/tachycardia

• Beta-blockers maintained perioperatively (heart rate control)
• Phenylephrine for hypotension (preserves SVR without tachycardia)
• Avoid ketamine (tachycardia, ↑ SVR)
• Careful fluid management — goal-directed using TEE
• Amiodarone for AF treatment
• Diuresis if pulmonary edema develops

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QUESTION 5: SPINAL ADDITIVES + NEUROLOGICAL COMPLICATIONS OF SPINAL + FACTORS AFFECTING PDPH [10 Marks]

PART A: SPINAL ADDITIVES (Intrathecal Adjuvants)

Purpose: Enhance quality, duration, and analgesic profile of spinal anesthesia

Opioids

α₂ Agonists

• Clonidine: 15–75 mcg — prolongs motor and sensory block, provides analgesia; ↓ BP, bradycardia, sedation
• Dexmedetomidine: 5–10 mcg — superior to clonidine; shorter duration of hypotension

Vasoconstrictors

• Epinephrine: 0.1–0.2 mg — prolongs block by 50%, reduces systemic absorption of LA, provides alpha-2 mediated analgesia
• Phenylephrine: 2–5 mg — prolongs sensory block

Ketamine

• 0.1–0.5 mg/kg intrathecal — NMDA antagonism provides prolonged analgesia; concern for neurotoxicity (preservative-free only)

Neostigmine

• 25–75 mcg — anticholinesterase; visceral analgesia; significant N&V limits routine use

Magnesium

• 50–100 mg — NMDA blockade; prolongs block, reduces opioid requirement; safe profile

Adenosine

• 1000 mcg — analgesic; reduces allodynia; not used routinely

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PART B: NEUROLOGICAL COMPLICATIONS OF SPINAL ANESTHESIA

1. Transient Neurological Symptoms (TNS)

• Bilateral buttock/lower extremity aching after spinal, resolving within 72 hours
• Most common with lidocaine (especially hyperbaric 5%)
• Management: NSAIDs, reassurance

2. Cauda Equina Syndrome

• Permanent loss of bowel/bladder function + lower extremity sensorimotor deficits
• Caused by: concentrated lidocaine (microcatheters), neurotoxic preservatives (chlorhexidine contamination)
• Mechanism: pooling of local anesthetic around sacral nerve roots

3. Arachnoiditis

• Inflammatory fibrosis of arachnoid mater
• Caused by: contamination with antiseptics (chlorhexidine), blood, foreign material
• Presents: chronic pain, progressive neurological deficit

4. Epidural Hematoma

• Most common with: anticoagulant use, coagulopathy
• Presents: severe back pain → paraplegia
• Emergency MRI + surgical decompression within 6–8 hours

5. Spinal Cord Ischemia

• Anterior spinal artery syndrome: paraplegia with preserved posterior column function
• Causes: hypotension, adrenaline in LA, vasoconstrictors in high concentrations

6. Anterior Spinal Artery Syndrome

• Rare; caused by profound hypotension or direct injection

7. Meningitis

• Bacterial (break in sterile technique) or aseptic (chemical irritants)

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PART C: FACTORS AFFECTING POST-DURAL PUNCTURE HEADACHE (PDPH)

Patient Factors (Increasing Risk)

Needle Factors (Most Modifiable)

Technique Factors

• Accidental dural puncture (ADP) during epidural: 70% PDPH risk with 16–18G Tuohy
• Multiple attempts: increased risk
• Paramedian approach: slightly lower risk

Treatment

1. Conservative: Bed rest, oral hydration, caffeine (500 mg orally or IV)
2. Epidural Blood Patch (EBP): Gold standard — 15–20 mL autologous blood; 90% efficacy
3. Sumatriptan, ACTH, cosyntropin — second-line
4. Prophylactic intrathecal morphine after ADP reduces PDPH

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QUESTION 6: NEUROTOXICITY IN CHILDREN + AUTONOMIC CHANGES IN SPINAL CORD TRANSECTION [10 Marks]

PART A: NEUROTOXICITY OF ANESTHESIA IN CHILDREN

Background

Agents Implicated

• NMDA antagonists: Ketamine, N₂O, xenon
• GABA-A agonists: Volatile agents (isoflurane, sevoflurane, desflurane), propofol, benzodiazepines, barbiturates

• NMDA antagonism → ↓ glutamate-mediated survival signals → apoptosis
• GABA-A activation in immature neurons (depolarizing in early life) → excitotoxicity
• Mitochondrial dysfunction, dendritic pruning, synaptic remodeling

Critical Period

• Most vulnerable: synaptogenesis (perinatal through ~3 years in humans; equivalent to postnatal days 7–10 in rodents)
• Effect is dose-dependent and duration-dependent

Human Evidence

• FDA Warning (2016): Repeated or lengthy (>3 hours) use of anesthetics in children <3 years old may affect brain development
• GAS trial (NEJM, 2016): Sevoflurane 1 hour for inguinal hernia repair — no difference in neurodevelopmental outcome at 5 years vs. regional anesthesia
• PANDA study: Single, short anesthetic < 3 years — no difference in sibling controls
• MASK study (Mayo Clinic): Multiple exposures — subtle processing speed deficits, but no IQ difference
• Conclusion: Single short exposure appears safe; multiple prolonged exposures in young infants remain concerning

Risk Factors

• Age < 3 years (especially < 1 year)
• Prolonged exposure (> 3 hours)
• Multiple exposures
• Pre-existing neurological conditions
• Systemic illness (hypoxia, hypoglycemia compound toxicity)

Clinical Recommendations (Barash 9e)

1. Defer elective surgery in children <3 years when possible
2. Regional anesthesia preferred as primary or adjunct
3. Dexmedetomidine — relatively sparing of NMDA/GABA, potential neuroprotective
4. Use lowest effective concentrations and minimize duration
5. Preoperative discussion with parents (informed consent regarding this risk)

Protective Strategies

• Melatonin, lithium, hypothermia (animal studies)
• Neurosteroids (allopregnanolone) — early research
• Xenon (neuroprotective — NMDA antagonism with anti-apoptotic properties)

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PART B: AUTONOMIC CHANGES IN SPINAL CORD TRANSECTION

Acute Phase (Spinal Shock — 0 to 3 weeks)

• Flaccid paralysis and areflexia below level of lesion
• Cardiovascular: Profound bradycardia and hypotension
  • Loss of sympathetic tone below lesion
  • Unopposed vagal tone → bradycardia (especially cervical lesions)
  • Loss of vasomotor tone → massive venous pooling → ↓ SVR
• Neurogenic shock: bradycardia + hypotension (distinguished from hemorrhagic by bradycardia)
• Treatment: Atropine, dopamine, phenylephrine; aggressive volume resuscitation

Chronic Phase (Hyperreflexia — after 3–6 weeks)

• Most critical autonomic complication — life-threatening
• Occurs with lesions at or above T6 (above splanchnic outflow)
• Triggered by any noxious stimulus below the lesion (bladder distension most common, bowel, skin pressure, surgical stimulation)

Noxious stimulus below T6
        ↓
Massive sympathetic discharge below lesion
        ↓
Severe hypertension (SBP >200 mmHg)
        ↓
Baroreceptors detect → vagal reflex bradycardia
        ↓
Reflex above lesion: flushing, sweating, headache above level
Below lesion: pallor, piloerection (unable to reflexly vasodilate)

• Severe pounding headache
• Flushing and sweating above lesion
• Pallor below lesion
• Bradycardia
• Hypertensive crisis → intracerebral hemorrhage, seizures, death

1. Prevention: Adequate regional anesthesia/analgesia
2. Identify and remove trigger: Catheterize bladder, empty bowel
3. Acute treatment:
   • Sit patient up (reduces BP)
   • Nifedipine (bite and swallow, 10 mg)
   • GTN (glyceryl trinitrate) sublingual/IV
   • Hydralazine, labetalol IV
   • Phentolamine (alpha blocker) — best for refractory
4. Spinal anesthesia for procedures: blocks sympathetic efferents below lesion — preferred for surgeries (TURP, obstetric)

Other Chronic Autonomic Changes

• Temperature dysregulation: Poikilothermia (cannot sweat or vasoconstrict below lesion)
• Respiratory: Cervical lesions → phrenic nerve paralysis (C3–C5), require ventilatory support
• Cardiovascular: Orthostatic hypotension, loss of cardiac acceleration reflex
• Succinylcholine: CONTRAINDICATED after 72 hours (until ~1 year) — massive K+ release from denervation hypersensitivity → cardiac arrest
• DVT: High risk from stasis

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QUESTION 7: HEMORRHAGIC SHOCK + HYPERVOLEMIA IN RESUSCITATION + REGIONAL ANESTHESIA FOR TRAUMA [10 Marks]

PART A: HEMORRHAGIC SHOCK

Classification (ATLS 4-Class System)

Pathophysiology

• Decreased O₂ delivery → anaerobic metabolism → lactic acidosis
• Lethal triad: Hypothermia + Acidosis + Coagulopathy
• Trauma-induced coagulopathy (TIC): consumption + dilution + dysfunction + fibrinolysis

Modern Resuscitation — Damage Control Resuscitation (DCR)

1. Permissive hypotension (hypotensive resuscitation):
   • Target SBP 80–90 mmHg until surgical hemorrhage control
   • Exception: head injury (maintain CPP) and elderly
2. Hemostatic resuscitation:
   • Blood products early: 1:1:1 ratio (PRBC: FFP: Platelets)
   • Minimize crystalloid
   • Cryoprecipitate early (fibrinogen < 1.5 g/L)
   • Tranexamic acid: 1g IV within 3 hours of injury (CRASH-2 trial)
3. Damage control surgery: Rapid hemorrhage control, pack and close, ICU resuscitation, definitive repair later

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PART B: ISSUES WITH HYPERVOLEMIA IN RESUSCITATION

The Problem with Liberal Fluid Resuscitation

Key Principle: "Stop the Bleed, Not Dilute It"

• Each liter of crystalloid reduces hematocrit by ~3%
• 3L crystalloid for Class III shock → dilutes clotting factors by 50%
• Glycocalyx disruption from isotonic saline worsens edema formation

Balanced Approach

• Limited crystalloid (< 1L before definitive hemostasis)
• Early blood products
• Vasopressors (noradrenaline) to maintain BP while limiting fluid volume
• Goal-directed therapy guided by thromboelastography (TEG/ROTEM)

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PART C: ADVANTAGES OF REGIONAL ANESTHESIA FOR TRAUMA

Physiological Advantages

1. Avoidance of airway manipulation — critical in suspected C-spine injury, facial trauma, burns
2. Reduced opioid requirement — avoid respiratory depression, improved chest wall movement (rib fractures)
3. Preservation of consciousness — ongoing neurological assessment
4. Reduced sympathoadrenal stress response — beneficial in cardiovascular compromise
5. Improved pulmonary function — thoracic epidural or intercostal blocks for rib fractures → better respiratory mechanics, prevents pneumonia

Specific Benefits by Region

• Thoracic epidural/paravertebral: Multiple rib fractures — superior pain control to IV opioids; reduces ICU stay, pneumonia, mortality
• Femoral/fascia iliaca/adductor canal blocks: Femur fractures — reduces pain, reduces blood loss, avoids GA risks
• Brachial plexus block: Upper limb trauma/surgery
• Spinal anesthesia: Lower limb trauma — avoids GA in hemodynamically compromised (lower dose, titrated)
• PECS/serratus blocks: Thoracic trauma without epidural

Considerations/Cautions

• Coagulopathy — contraindication to neuraxial and deep blocks (TEG to guide)
• Compartment syndrome — regional anesthesia may mask symptoms (controversial; most surgeons accept if appropriate monitoring)
• Infection — local infection at block site contraindicated
• Patient cooperation — required for awake blocks
• Systemic toxicity (LAST) — high vascularity of trauma patients; use ultrasound guidance

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QUESTION 8: MALIGNANT HYPERTHERMIA — TRIGGERING AGENTS, TREATMENT, ASSOCIATED SYNDROMES [10 Marks]

Definition

Genetics

• Autosomal dominant, variable penetrance
• RYR1 gene (chromosome 19q12–13.2) — ryanodine receptor type 1 mutation (70%)
• CACNA1S gene — dihydropyridine receptor (DHP) α-1 subunit (1%)

• 300 known mutations; severity varies

Pathophysiology

Triggering agent → Opens RyR1 receptor → Massive Ca²⁺ release from SR
        ↓
Sustained muscle contraction (rigidity)
        ↓
↑↑ ATP consumption → Glycolysis + oxidative phosphorylation overdrive
        ↓
Heat generation (hyperthermia: 1–2°C/5 min)
CO₂ production ↑↑ (EtCO₂ rises first!)
O₂ consumption ↑↑
Lactic acidosis
Rhabdomyolysis → CK, myoglobinuria, renal failure
K+ release → Hyperkalemia → arrhythmias

TRIGGERING AGENTS

• Propofol, barbiturates, etomidate, ketamine
• Benzodiazepines, opioids
• N₂O (safe)
• Non-depolarizing NMBAs (vecuronium, rocuronium, atracurium, cisatracurium)
• Local anesthetics (amide and ester)
• Neostigmine, atropine

Clinical Presentation (MHAUS Criteria)

1. ↑ EtCO₂ (earliest and most sensitive sign)
2. Masseter spasm (jaw rigidity after succinylcholine)
3. Tachycardia
4. Metabolic/respiratory acidosis
5. Generalized muscle rigidity
6. Hyperthermia (late sign — if temperature rising, crisis is established)
7. Rhabdomyolysis: CK > 20,000 U/L, myoglobinuria, dark urine

TREATMENT

• Discontinue all volatile agents immediately
• Stop succinylcholine
• Call for help, activate MH protocol

• Dose: 2.5 mg/kg IV bolus (repeat every 5 min up to 10 mg/kg total)
• Maintenance: 1 mg/kg every 6 hours for 24–48 hours (prevent recurrence)
• Mechanism: Blocks RyR1 receptor → reduces Ca²⁺ release
• Preparation: Each vial = 20 mg; reconstitute in 60 mL sterile water → 36 vials for 70 kg patient (stock minimum)
• Must be readily available in all anesthetizing locations (MHAUS guideline)

• 100% O₂ at 10L/min, increase fresh gas flow to maximum
• Flush breathing circuit (do NOT delay surgery to change machine)
• Target: Normalization of EtCO₂

• Arterial line: ABG, electrolytes, CK, coagulation every 30 min
• Foley catheter: urine color and output
• Temperature: continuous monitoring

• ICU admission for 24–48 hours
• Dantrolene for 24–48 hours
• Patient and family counseling
• Refer for caffeine-halothane contracture test (CHCT) / RyR1 genetic testing
• Medic alert bracelet

SYNDROMES ASSOCIATED WITH MALIGNANT HYPERTHERMIA

• Neuroleptic Malignant Syndrome (NMS): Dopamine blockade (antipsychotics); treated with dantrolene + bromocriptine; not triggered by volatile agents
• Serotonin Syndrome: 5-HT excess; does NOT respond to dantrolene
• Thyroid storm, pheochromocytoma: Differential diagnoses — elevated catecholamines cause hyperthermia

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QUESTION 9: SUPINE CAVAL SYNDROME + HEMATOLOGICAL CHANGES IN PREGNANCY [10 Marks]

PART A: SUPINE CAVAL SYNDROME (Aortocaval Compression)

Definition

Anatomy of Compression

• IVC compression: Enlarged uterus compresses IVC against vertebral column → ↓ venous return → ↓ cardiac output (up to 25–30% fall)
• Aortic compression (Poseiro effect): Partial obstruction of distal aorta → ↓ uteroplacental blood flow
• IVC is more susceptible than aorta (lower pressure vessel)

Incidence

• Subclinical IVC compression in nearly ALL term pregnancies in supine position
• Frank supine hypotensive syndrome in 8–10% of pregnancies at term (Morgan & Mikhail 7e)

Symptoms in the Mother

• Sudden hypotension (10–20 mmHg drop in SBP)
• Dizziness, nausea, pallor
• Bradycardia (vasovagal reflex)
• Syncope in severe cases
• Anxiety, restlessness

Compensatory Mechanisms

1. Increased sympathetic tone
2. Venous collateral flow via azygos system (maintains partial venous return)
3. Epidural venous plexus engorgement (Batson's plexus)
4. Tachycardia

Fetal Consequences

• Reduced uteroplacental blood flow → fetal hypoxia
• Fetal bradycardia, late decelerations
• Emergency C-section risk

Anesthetic Implications

1. Left uterine displacement (LUD) from 20 weeks: 15° left lateral tilt (wedge under right hip) — mandatory for all obstetric procedures
2. Under spinal anesthesia, sympathetic block exacerbates hypotension — prophylactic phenylephrine infusion (vasopressor of choice in obstetrics — maintains uteroplacental blood flow)
3. Obstetric epidural: slow titration prevents sudden sympathectomy
4. Maternal hypotension → fetal distress: phenylephrine or ephedrine to treat; phenylephrine preferred (maintains fetal pH)
5. Prevention: preloading with colloid; co-loading with crystalloid during spinal
6. Manual LUD if wedge not available during CPR

CPR in Pregnancy

• Left lateral tilt or manual uterine displacement
• Perimortem C-section within 4–5 minutes if CPR unsuccessful (restores aortocaval decompression → improves maternal CPR success)

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PART B: HEMATOLOGICAL CHANGES AND IMPLICATIONS IN PREGNANCY

Blood Volume

• Plasma volume increases 40–50% by term
• Red cell mass increases 20–30%
• Net result: Physiological dilutional anemia of pregnancy
  • Hb: 11–12 g/dL (normal for pregnancy)
  • Hematocrit: 32–35%
  • MCV and MCHC: relatively normal

Red Blood Cells

White Blood Cells

• Leukocytosis: WBC increases to 12,000–15,000/μL (up to 20,000 in labor)
• Primarily neutrophilia; lymphocytes slightly decreased
• Monocytes unchanged; eosinophils decreased
• Implication: WBC not reliable for diagnosing infection during pregnancy

Platelets

• Gestational thrombocytopenia: mild ↓ (normal >100,000; consider > 80,000 for neuraxial)
• Platelet count: 150,000–300,000 → ~200,000 at term
• Platelet function may be mildly impaired
• HELLP syndrome: Microangiopathic hemolytic anemia + elevated liver enzymes + low platelets

Coagulation — Hypercoagulable State of Pregnancy

Anesthetic Implications of Hematological Changes

1. Neuraxial anesthesia threshold:
   • Platelets >80,000 generally safe for spinal; >100,000 for epidural
   • Gestational thrombocytopenia must be distinguished from ITP, TTP, HELLP
2. Coagulopathy in obstetric emergencies:
   • Abruptio placentae: DIC (fibrinogen consumption)
   • AFE (amniotic fluid embolism): catastrophic DIC
   • Pre-eclampsia/HELLP: thrombocytopenia + hemolysis
3. Transfusion: Tolerate lower Hb (11 g/dL) given expanded volume, but target > 8 g/dL in labor
4. Thromboembolism: Major risk — DVT/PE is leading cause of maternal mortality
   • LMWH prophylaxis; stockings; early ambulation
5. Iron deficiency: Most common cause of anemia in pregnancy; ferrous sulfate supplementation
6. Iron infusion preferred for severe anemia (<8 g/dL or intolerance) in third trimester

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QUESTION 10: NEUROPHYSIOLOGICAL MONITORING IN SCOLIOSIS [10 Marks]

Background

Goals of IONM in Scoliosis

1. Early detection of iatrogenic spinal cord injury (before irreversible damage)
2. Alert surgeon to correct/remove offending instrumentation
3. Guide surgical and anesthetic decisions intraoperatively
4. Reduce false negatives (missed injuries) and false positives (unnecessary alarms)

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MODALITIES USED

A. Somatosensory Evoked Potentials (SSEPs)

• >50% decrease in amplitude OR
• >10% increase in latency → Alert surgeon immediately

• Well-established, robust technique
• Continuous monitoring

• Monitors posterior cord only — does NOT monitor motor tracts
• 50–75% sensitivity for paralysis; 25% of motor injuries missed (anterior cord)
• Affected by temperature, anemia, volatile agents

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B. Motor Evoked Potentials (MEPs)

• >50% decrease in amplitude (more commonly used)
• Complete loss of response (most concerning)
• Significant change in threshold

• Monitors anterior cord (motor tracts) — detects motor injury SSEPs miss
• SSEPs + MEPs together have >95% sensitivity for spinal cord injury

• Requires total intravenous anesthesia (TIVA) — volatile agents suppress MEPs at concentrations > 0.5 MAC
• Contraindicated: pacemaker, cortical implants, skull defects
• Tongue biting risk (bite block mandatory)
• Jaw and limb movements during stimulation

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C. Electromyography (EMG)

Spontaneous EMG (Free-run EMG)

• Continuous recording from myotomes innervated by nerve roots at surgical level
• Spontaneous bursts indicate nerve root irritation/traction
• Continuous "neurotonic discharge" = nerve root at risk

Triggered EMG (Pedicle Screw Stimulation)

• Electrical stimulation through pedicle screws
• Tests pedicle wall integrity
• Threshold > 8–10 mA = intact pedicle wall (no medial cortex breach)
• Threshold < 6 mA = possible medial wall breach → nerve root at risk

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D. Wake-Up Test (Stagnara)

• Historically the gold standard
• Patient awakened mid-surgery and asked to move feet/hands
• Detects motor function only at one time point
• Now replaced by MEP monitoring
• Still used: when IONM signals are equivocal, or as confirmation before closure

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ANESTHETIC CONSIDERATIONS FOR IONM

Recommended Anesthetic Protocol for Scoliosis with MEP Monitoring:

• Propofol infusion (75–100 mcg/kg/min) — least effect on MEPs
• Remifentanil infusion — opioid-sparing; no significant SSEP/MEP effect
• Dexmedetomidine — adjunct; reduces anesthetic requirements; minimal IONM interference
• Ketamine low-dose — may enhance SSEPs; antihyperalgesic
• Avoid: Volatile agents > 0.5 MAC; N₂O; neuromuscular blockers (except for intubation — reversed before monitoring begins)

Confounders of IONM Signals

1. Hypotension (MAP < 65 mmHg) → reduced spinal cord perfusion → signal loss
2. Hypothermia → increases latency
3. Anemia (Hb < 8 g/dL) → decreased O₂ delivery → signal loss
4. Hypoxia, hypercapnia
5. Electrical interference
6. Position changes

Response to IONM Alert

1. Anesthesia — ensure no recent change (bolus, volatile dose change)
2. Blood pressure — raise MAP ≥ 80 mmHg
3. Check temperature — rewarm if hypothermic
4. Distraction/correction — inform surgeon to reverse instrumentation
5. Evaluate — repeat signals; consider wake-up test

Spinal Cord Perfusion Pressure (SCPP)

• SCPP = MAP − Intrathecal pressure
• During correction of scoliosis: SCPP may fall due to ↑ cord tension
• Target MAP ≥ 80 mmHg (some centers ≥ 90 mmHg during correction)
• Consider intrathecal papaverine or cerebrospinal fluid drainage in high-risk cases

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Summary Table: Key References

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