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Summary of What Was Covered (Questions 1–5):

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Summary — Questions 6–10

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Summary — Questions 11–15

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Summary — Questions 16–20

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MD ANAESTHESIOLOGY EXAM ANSWERS — REWRITE

Questions 11–15 | Revised Format: Structured Headings + Tables + Bullets

Sources: Miller's Anesthesia 10e · Barash's Clinical Anesthesia 9e · Morgan & Mikhail 7e

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QUESTION 11A: HbA1c — DEFINITION AND PREOPERATIVE CUT-OFF

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What Is HbA1c?

• Full name: Glycated (glycosylated) haemoglobin A1c
• Formed by: Non-enzymatic, irreversible Amadori reaction between glucose and the N-terminal valine of the beta-chains of haemoglobin A
• Reflects: Average blood glucose over the preceding 2–3 months (lifespan of RBC ≈ 120 days)
• Weighting: The last 30 days of RBC lifespan contribute ~50% of the HbA1c value

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Units and Reference Values

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Why HbA1c Matters Perioperatively

• Better predictor of perioperative morbidity than a single fasting glucose (reflects chronic control)
• HbA1c >8% → 2–3× higher surgical site infection (SSI) rate
• In cardiac surgery: HbA1c >7.5% → increased deep sternal infection, renal failure, 30-day mortality
• Guides timing and urgency of elective surgery

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Preoperative Cut-Off Recommendation

Target: HbA1c ≤ 8% (≤ 64 mmol/mol) for elective surgery

• If HbA1c >8–9%: Refer to diabetologist; optimise over 4–8 weeks before elective surgery
• Intraoperative target: Blood glucose 6–10 mmol/L (not guided by HbA1c)

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Conditions That Falsify HbA1c

Source: Barash 9e, Chapter 25; Miller's Anesthesia 10e, Chapter 38; Morgan & Mikhail 7e, Chapter 36.

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QUESTION 11B: DIABETIC KETOACIDOSIS (DKA) — MANAGEMENT

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Diagnostic Criteria (Triad)

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Severity Classification (JBDS 2023 / ADA 2024)

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Pathophysiology (Summary)

• Precipitants: Infection (40%), insulin omission, new T1DM, surgery/trauma, steroids, SGLT-2 inhibitors
• Absolute/relative insulin deficiency → counter-regulatory hormone excess (glucagon, cortisol, catecholamines)
• ↑ Glycogenolysis + gluconeogenesis → hyperglycaemia
• Lipolysis → free fatty acids → hepatic ketogenesis → ketonaemia + HAGMA
• Osmotic diuresis → dehydration (deficit 3–6 litres), K/Na/PO4/Mg losses

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Management: The "5 Is" Framework

I — IV Fluids (Most Important Initial Step)

• When glucose falls to <14 mmol/L: Add 10% dextrose at 125 mL/hr alongside saline — permits continued insulin without hypoglycaemia

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I — Insulin (Fixed-Rate IV Infusion — FRIII)

• Dose: 0.1 units/kg/hr of soluble insulin (Actrapid/Humulin S in 0.9% NaCl — 1 unit/mL)
• CRITICAL: Do NOT start insulin until serum K ≥ 3.5 mmol/L (hypokalaemia + insulin → fatal arrhythmia)
• Continue long-acting (basal) insulin — do NOT stop
• Expected response: Ketones fall ≥0.5 mmol/hr; glucose fall ≥3 mmol/hr; pH rise ≥0.1/hr
• Switch to SC insulin when: eating + drinking AND ketones <0.6 mmol/L AND pH >7.3 AND HCO3 >18

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I — Ion Replacement (Potassium — CRITICAL)

• Total body K deficit = 3–5 mmol/kg (despite initial normal/high serum K due to acidosis-driven transcellular shift)
• As pH corrects with insulin + fluids → K moves intracellularly → hypokalaemia

• ECG monitoring mandatory throughout potassium replacement

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I — Identify and Treat Precipitant

• Blood cultures (×2) + urine MC&S + CXR → empiric antibiotics if infection suspected
• ECG + hs-troponin → exclude MI
• Medication review — stop SGLT-2 inhibitors

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I — Interventions to AVOID

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Monitoring Targets During DKA Treatment

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Resolution Criteria (JBDS 2023)

• Blood ketones <0.6 mmol/L
• Venous pH >7.3
• Venous bicarbonate >18 mmol/L

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Perioperative DKA — Anaesthetic Points

• Emergency surgery: do NOT delay if life/limb threatening; correct K, pH, glucose as much as possible first
• Induction risks: hypotension (dehydration + vasodilation), aspiration (gastroparesis), arrhythmias (hypokalaemia)
• Avoid dextrose-containing IV fluids; avoid propofol infusion syndrome risk if concurrent metabolic acidosis

Source: Barash 9e, Chapter 36; Miller's Anesthesia 10e, Chapter 38; Morgan & Mikhail 7e, Chapter 36; JBDS-IP DKA Guidelines 2023; ADA 2024.

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QUESTION 12: POSTERIOR FOSSA SURGERY — ANAESTHETIC CONSIDERATIONS AND PERIOPERATIVE MANAGEMENT

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Introduction

• Acoustic neuroma (vestibular schwannoma)
• Cerebellar tumour resection
• Fourth ventricle tumours (medulloblastoma, ependymoma)
• Microvascular decompression (MVD) for TN/hemifacial spasm
• Posterior circulation aneurysms

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The 4 Unique Challenges (Morgan & Mikhail 7e)

1. Obstructive hydrocephalus — infratentorial mass obstructs fourth ventricle/aqueduct → elevated ICP
2. Brainstem injury — vital circulatory and respiratory centres at risk from surgical trauma/ischaemia
3. Pneumocephalus — air enters subarachnoid space replacing CSF, especially in sitting position
4. Venous air embolism (VAE) — wound above heart level; incidence 20–40% in sitting position

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Preoperative Assessment

History and Examination

Key Investigations

Preoperative Optimisation

• Dexamethasone 8–16 mg/day commenced 24–48h preoperatively (reduces perilesional oedema)
• Mannitol 0.25–0.5 g/kg IV if acute ICP elevation
• External ventricular drain (EVD) under LA before induction if severe hydrocephalus — prevents catastrophic ICP surge at induction

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Patient Positioning

Three Options: Sitting · Lateral (Park-Bench) · Prone

Sitting Position — Most Surgically Preferred but Highest Risk

• Back elevated 60°, legs elevated/knees flexed, head in three-point Mayfield clamp (neck flexed), arms at sides
• Minimum chin-to-chest distance: 2 finger-breadths (3.5–4 cm) — prevents spinal cord compression and venous obstruction

Lateral (Park-Bench) Position

• Used for: CPA tumours, acoustic neuroma, MVD
• Avoids sitting-position VAE risk; good access
• Head in Mayfield, shoulder rolled forward

Prone Position

• Used for: Midline cerebellar/vermis lesions, posterior fossa decompression (Chiari)
• VAE risk lower but still present; ETT kinking risk

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Monitoring Requirements

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Anaesthetic Technique

Goals

1. Brain relaxation (reduced ICP, slack dura)
2. Haemodynamic stability (MAP 60–80 mmHg; CPP ≥50 mmHg)
3. Rapid, smooth awakening for immediate neurological assessment
4. Cough-free emergence (ICP spikes → haematoma risk)
5. Preserved neuromonitoring signals

Induction

Maintenance

Muscle Relaxation (Special Rule)

• After intubation: Minimise or AVOID further NMB if facial nerve or cranial nerve EMG monitoring
• Use short-acting agents (atracurium, mivacurium) or allow recovery
• Maintain TOF count 2–3 if partial blockade needed
• Sugammadex available for rapid NMB reversal before nerve testing

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Venous Air Embolism (VAE) — Detailed Protocol

Monitoring Sensitivity (Most → Least Sensitive)

1. TOE — detects 0.25 mL/kg; most sensitive
2. Precordial Doppler — detects 0.25 mL/kg; "mill-wheel" murmur
3. ETCO2 drop >2 mmHg — indicates significant VAE (reduced pulmonary blood flow)
4. Pulmonary artery pressure — rises as RV obstructs
5. SpO2 — late (hypoxia from V/Q mismatch)
6. ECG — S1Q3T3, RV strain — very late

Treatment Steps

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Emergence and Extubation

Smooth Emergence — MANDATORY

• Coughing/straining → ICP surge → intracranial haemorrhage
• Techniques:
  • Continue propofol until ETT removal
  • Remifentanil infusion until extubation
  • IV lidocaine 1.5 mg/kg 5 min before extubation
  • Deep extubation (selected cases with low aspiration risk)

Delayed Extubation — Indicated if:

• Surgery >8 hours
• Pre-existing brainstem dysfunction
• Bulbar palsy post-op (aspiration risk)
• Massive blood loss (coagulopathy)
• Pneumocephalus + significant brain swelling
• Cannot assess neurology reliably

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Postoperative Complications

Source: Morgan & Mikhail 7e, Chapter 27 (direct text); Miller's Anesthesia 10e, Chapter 70; Barash 9e, Chapter 30.

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QUESTION 13A: POSTOPERATIVE LARYNGOSPASM

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Definition

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Incidence

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Risk Factors

Patient Factors

• Young age (infants, 1–3 months highest)
• Recent/active URI — airway hyperreactivity persists 4–6 weeks post-URI
• Asthma / reactive airways
• Passive smoking exposure (secondhand tobacco smoke)
• GORD
• History of previous laryngospasm

Anaesthetic/Procedural Factors

• Extubation at "light" (danger) plane — not awake AND not deeply anaesthetised
• Secretions, blood, or vomit at glottis — most common trigger
• Stimulation during light anaesthesia
• Upper airway surgery (tonsillectomy — blood/secretions)
• Desflurane/isoflurane at emergence (pungent airway irritants)
• Opioids (fentanyl, remifentanil) — lower threshold for OCR/laryngospasm

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Reflex Arc

TRIGGER (secretions/blood/stimulation)
       ↓
Superior Laryngeal Nerve (SLN) afferents
       ↓
Nucleus Tractus Solitarius (brainstem)
       ↓
Motor nucleus of vagus → Recurrent Laryngeal Nerve (RLN)
       ↓
Lateral cricoarytenoid + thyroarytenoid → VOCAL FOLD ADDUCTION → GLOTTIC CLOSURE

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Clinical Features

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Treatment Protocol

"Treatment of laryngospasm includes gentle positive-pressure ventilation, forward jaw thrust, deepening of the anaesthetic with intravenous propofol, intravenous lidocaine (1–1.5 mg/kg), or paralysis with intravenous succinylcholine (0.5–1 mg/kg) or rocuronium (0.4 mg/kg) and controlled ventilation. Intramuscular succinylcholine (4–6 mg/kg) with atropine remains an acceptable alternative in patients without intravenous access and in whom conservative measures have failed."

Stepwise Algorithm

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Complications of Laryngospasm

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Prevention

Source: Morgan & Mikhail 7e, Chapter 44 (direct quote); Miller's Anesthesia 10e, Chapter 55; Barash 9e, Chapter 44.

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QUESTION 13B: HEPATORENAL SYNDROME (HRS)

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Definition

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Pathophysiology

Portal hypertension
       ↓
Splanchnic vasodilation (NO, prostacyclin, glucagon)
       ↓
Reduced effective arterial blood volume (EABV)
       ↓
Baroreceptor activation → ↑ RAAS + ↑ SNS + ↑ ADH
       ↓
Renal afferent arteriolar VASOCONSTRICTION
       ↓
Reduced RBF → Reduced GFR → RENAL FAILURE
(Tubular function preserved — unlike ATN)

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New Classification (ICA-AKI 2019)

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Diagnostic Criteria (ICA-AKI / EASL 2018)

1. Cirrhosis (or acute liver failure / alcoholic hepatitis) + ascites
2. AKI: Serum creatinine ≥1.5 mg/dL OR increase ≥0.3 mg/dL in 48h
3. No improvement after 48h of:
   • Diuretic withdrawal, AND
   • Albumin 1 g/kg/day × 2 days (max 100 g/day) — diagnostic challenge
4. No septic/cardiogenic/hypovolaemic shock
5. No nephrotoxic drugs (NSAIDs, aminoglycosides, contrast)
6. No parenchymal renal disease: Proteinuria <500 mg/day; no haematuria; normal renal USS

• Urine Na <10 mmol/L (avid sodium retention — tubular function intact)
• Urine osmolality > plasma osmolality
• No casts on urine microscopy

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Differential Diagnosis of AKI in Cirrhosis

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Management

1. General Measures

• Identify and treat precipitant: SBP (most common), GI haemorrhage, dehydration, nephrotoxins
• Stop all nephrotoxins: NSAIDs, aminoglycosides, diuretics, contrast
• Albumin 1 g/kg/day (max 100 g) for 48h as diagnostic + therapeutic trial

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2. Vasoconstrictors — First-Line Pharmacotherapy

"Terlipressin is a vasopressin analogue that has recently been approved for use in the United States as first-line therapy for the treatment of HRS-AKI... The CONFIRM trial found an increased rate of HRS reversal in the terlipressin group when combined with albumin. However, terlipressin was associated with a risk of respiratory failure; therefore, oxygen levels should be monitored carefully."

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3. Renal Replacement Therapy (RRT)

• CRRT preferred over intermittent HD (better haemodynamic tolerance in coagulopathic, hypotensive patients)
• Does NOT treat liver failure — bridge to transplant only
• MARS (Molecular Adsorbent Recirculation System) — liver support bridge

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4. TIPS (Transjugular Intrahepatic Portosystemic Shunt)

• Reduces portal hypertension → reduces splanchnic vasodilation → reduces renal vasoconstriction
• More evidence in HRS-NAKI (type 2) — refractory ascites + HRS
• Contraindications: INR >5, bilirubin >5 mg/dL, active encephalopathy

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5. Liver Transplantation — Definitive and Only Curative Treatment

• Kidneys structurally normal in HRS — renal function recovers post-transplant (within 4–6 weeks)
• MELD score (creatinine heavily weighted) → prioritises HRS patients for transplant allocation

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Summary: HRS Management Ladder

Identify + treat precipitant (SBP, haemorrhage, dehydration)
       ↓
Stop all nephrotoxins
       ↓
Albumin challenge: 1 g/kg/day × 48h (diagnostic + therapeutic)
       ↓
If no response → VASOCONSTRICTOR + ALBUMIN
  • Terlipressin (1st choice) + Albumin 20–40 g/day
  • OR Noradrenaline + Albumin (if terlipressin unavailable)
       ↓
Bridge: CRRT / MARS
       ↓
DEFINITIVE: Liver Transplantation

Source: Morgan & Mikhail 7e, Chapter 35; Sabiston Surgery Chapter 11 (direct quote); Barash 9e, Chapter 35.

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QUESTION 14A: DIFFICULT AIRWAY MANAGEMENT IN THYROID SURGERY

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Introduction

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Causes of Difficult Airway in Thyroid Surgery

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Preoperative Airway Assessment

History Red Flags

• Stridor at rest or on exertion → critical narrowing
• Positional symptoms (worsening in supine) → retrosternal extension
• Dysphagia, dyspnoea
• Voice change → pre-existing RLN injury
• Pemberton's sign: Raising both arms → facial plethora, cyanosis, ↑JVP = SVC obstruction from retrosternal extension

Investigations

Critical CT Parameter

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Airway Risk Grading

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Airway Management Strategies

1. Awake Fibreoptic Intubation (AFOI) — Gold Standard

Technique

• Reinforced (armoured/wire-spiral) ETT — resists surgical kinking
• Reduced size if tracheal compression confirmed: 5.5–7.0 mm ID

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2. Video Laryngoscopy (VL)

• C-MAC, McGrath, GlideScope
• Improves glottic view in distorted anatomy
• Not a substitute for AFOI if complete awake assessment needed
• Cannot navigate past extrinsic tracheal compression below larynx

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3. Awake Tracheostomy (Under Local Anaesthesia)

• Indicated when: stridor at rest, severe tracheomalacia, failed AFOI, tumour invading trachea
• Surgeon performs surgical tracheostomy at level below obstruction under LA before GA induced

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Intraoperative Considerations

• RLN monitoring: NIM ETT (Medtronic) with surface EMG electrodes on cuff — alerts surgeon to nerve proximity; requires NMB reversal before nerve testing (sugammadex)
• Tube position confirmed distal to point of maximum tracheal compression (CT correlation)
• Haemostasis: Meticulous — haematoma in small thyroid bed can be rapidly fatal

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Extubation Strategy — "As Dangerous as Intubation"

Source: Miller's Anesthesia 10e, Chapter 55; Barash 9e, Chapter 29; Morgan & Mikhail 7e, Chapter 37.

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QUESTION 14B: UNILATERAL RECURRENT LARYNGEAL NERVE (RLN) INJURY — DIAGNOSIS AND PERIOPERATIVE MANAGEMENT

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Anatomy

• Cricothyroid — supplied by external branch of Superior Laryngeal Nerve (SLN) — not RLN
• Injury to RLN → PCA paralysed → unopposed adductors → cord in paramedian/adducted position

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Causes

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Clinical Features

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Diagnosis

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Perioperative Management

Preoperative

• Baseline nasolaryngoscopy before ALL thyroid surgery — medicolegal + clinical
• If pre-existing unilateral paralysis: Contralateral thyroid surgery risks bilateral paralysis → immediate post-op stridor/complete obstruction → tracheostomy plan prepared and consent taken
• VFSS and SALT referral if aspiration demonstrated; thickened fluids preoperatively

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Intraoperative

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Immediate Post-Operative

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Long-Term Management

Source: Miller's Anesthesia 10e, Chapter 55; Barash 9e, Chapter 29; Morgan & Mikhail 7e, Chapter 37.

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QUESTION 15A: PREMEDICATION IN CHILDREN

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Definition and Goals

Note: Non-pharmacological measures should always be used first — parental presence, distraction, videos, EMLA cream.

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Non-Pharmacological Premedication

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Pharmacological Agents

1. MIDAZOLAM — Most Widely Used

• Advantages: Anxiolysis, amnesia, anticonvulsant; flumazenil reversal available
• Disadvantages: Paradoxical excitement 5–10% (especially 1–5 years); respiratory depression; may delay emergence from short cases

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2. KETAMINE

• Advantages: Provides sedation + analgesia + maintains airway reflexes; ideal for burn dressings, painful procedures, no IV access
• Disadvantages: ↑ Salivation (add glycopyrrolate); emergence hallucinations (mitigated by midazolam); ↑ ICP/IOP (caution in neurotrauma, open eye)

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3. DEXMEDETOMIDINE (Intranasal) — Growing Preference

• Advantages: Anxiolysis + sedation without respiratory depression; reduces emergence agitation; reduces opioid requirements; cardiac stable; superior prevention of emergence delirium vs midazolam
• Disadvantages: Slow onset (plan 45 min before); bradycardia/hypotension; no antagonist; expensive

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4. CLONIDINE (Oral — Alpha-2 Agonist)

• Advantages: Anxiolysis + analgesia + reduces MAC; prevents emergence delirium; reduces PONV
• Disadvantages: Long onset; prolonged postoperative sedation; bradycardia/hypotension

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5. ANTISIALOGOGUE (Companion to Ketamine)

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6. Oral Analgesic Premedication

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Special Situations Table

Source: Barash 9e, Chapter 44; Morgan & Mikhail 7e, Chapter 44; Miller's Anesthesia 10e, Chapter 93.

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QUESTION 15B: MASSIVE TRANSFUSION PROTOCOL (MTP) IN OBSTETRIC HAEMORRHAGE

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Definition

• Blood loss >1500 mL, OR
• Any blood loss causing haemodynamic instability, OR
• Transfusion of ≥4 units PRBC in 4 hours, OR
• Loss of >50% blood volume in 3 hours

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Why Obstetric Haemorrhage Is Different

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Activating the MTP

• Blood loss >1500 mL
• Continued active bleeding not responding to uterotonics
• SBP <90 mmHg, HR >120 despite initial resuscitation
• Suspected DIC (abnormal coagulation/TEG)

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Fixed-Ratio MTP: 1:1:1 (Damage Control Resuscitation)

Practical MTP Pack Schedule

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Tranexamic Acid (TXA) — MANDATORY

WOMAN Trial (Lancet, 2017): TXA 1g IV within 3 hours of PPH onset reduced PPH-related death by 31% (RR 0.69, P=0.045). Greatest benefit when given within 3 hours.

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Fibrinogen — Priority Target in Obstetric Haemorrhage

• ROTEM-guided approach: FIBTEM A5 <12 mm → give fibrinogen concentrate 2–4 g (more precise)
• Target fibrinogen ≥2 g/L throughout active haemorrhage

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Calcium Replacement

• Massive transfusion → citrate in PRBC chelates ionised calcium → hypocalcaemia → cardiac depression + coagulopathy
• Calcium chloride 10% — 10 mL (3.5 mmol) IV after every 4 units PRBC
• OR Calcium gluconate 10% — 30 mL (slower release)
• Target ionised Ca²⁺ >1.1 mmol/L (check ABG)

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Uterotonics Table

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Vasopressors

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The Lethal Triad — Prevention

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Monitoring During MTP

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Surgical Escalation Ladder (Haemorrhage Control)

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MTP Timeline Checklist

Source: Barash 9e, Chapter 41; Miller's Anesthesia 10e, Chapters 61 & 77; Morgan & Mikhail 7e, Chapter 41; WOMAN Trial (Lancet 2017); OBS2 Trial (2021); RCOG PPH Guidelines 2023.

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Questions 21–25 Complete

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Q21 — Post-Dural Puncture Headache

• Pathophysiology: CSF hypovolaemia + adenosine-mediated vascular theory
• Direct quotes from Miller 10e (incidence 30–60% after ADP with Tuohy; 1.7 million deliveries dataset) and Barash 9e (risk factors, needle design, bevel orientation, ADP management)
• Differential diagnosis table (pre-eclampsia, meningitis, CVT, subdural)
• Full EBP technique (15–25 mL), ASA 2021 and OAA 2021 indications
• Step-by-step algorithm from conservative treatment to EBP

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Q22A — Local Anaesthetic Systemic Toxicity (LAST)

• Full pharmacological basis: bupivacaine fast-in/slow-out sodium channel block
• Dose table (lidocaine 3 mg/kg, bupivacaine 2 mg/kg)
• Sequential CNS then CV toxicity features
• Prevention: aspiration, incremental injection, adrenaline test dose, USS guidance
• Intralipid protocol (AAGBI 2023): 1.5 mL/kg bolus + 15 mL/kg/hr; max 12 mL/kg
• AVOID lidocaine/vasopressin/CCB in cardiac arrest from LAST; adrenaline ≤1 mcg/kg only

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Q22B — Xenon in Anaesthesia

• Blood/gas partition coefficient 0.115 (fastest onset/offset of all agents)
• NMDA antagonism (primary mechanism — unique vs. volatile agents)
• Cardioprotection, neuroprotection (TOBY-Xe, CoolXenon3 trials)
• Zero GWP — environmental advantage over N2O
• Comparison table: xenon vs. N2O
• Limitations: MAC 63–71%, cost, closed circuit requirement

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Q23 — COPD Anaesthetic Management

• GOLD classification table; spirometry (FEV1/FVC <0.70)
• Regional preferred; spinal/epidural first choice
• Propofol for induction (bronchodilatory); sevoflurane for maintenance
• Critical ventilation: I:E 1:3–4, RR 8–12, low TV, avoid N2O (bullae)
• Auto-PEEP management; extubation strategy with sugammadex (not neostigmine)
• Post-op: SpO2 88–92%, NIV/BiPAP, early physio

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Q24 — Allowable Blood Loss

• MABL formula with worked example (70 kg male, Hb 14→8: MABL = 2673 mL)
• Gilcher's EBV values (full table)
• All intraoperative estimation methods: gravimetric (best), suction canister, serial Hb/Hct, SpHb (Masimo), swab saturation estimation
• Replacement strategy (3:1 crystalloid; 1:1 colloid; PRBC at MABL)

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Q25A — Epidural Dural Puncture

• Incidence 1–1.5% in labour epidurals
• Recognition: CSF flow, glucose testing, temperature difference
• Two management options: intrathecal catheter (preferred — Miller 10e direct quote) vs. re-siting
• Intrathecal catheter doses; labelling protocol; PDPH follow-up (EBP 15–25 mL)

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Q25B — Jugular Venous Oximetry (SjO2)

• Normal SjO2: 55–75%; ischaemia threshold: <50%
• Fick equation applied to cerebral circulation
• Retrograde catheterisation technique; confirmation at skull base/C1
• Causes of desaturation (hypotension, hyperventilation, anaemia) and elevation (hypothermia, brain death, infarction)
• Full comparison table: SjO2 vs. NIRS vs. TCD vs. PbtO2 vs. ICP vs. BIS
• TBI management algorithm using SjO2

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MD ANAESTHESIOLOGY EXAM ANSWERS

Questions 21–25 | Rewritten with Miller's Anesthesia 10e as Primary Source

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QUESTION 21

Post-Dural Puncture Headache (PDPH)

Clinical Features · Preventive Strategies · Treatment Guidelines

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1. Introduction and Incidence

"The most common complication associated with neuraxial analgesia is unintended dural puncture. Leakage of spinal fluid is thought to result in vascular hyperemia, migraine physiology, and traction on pain-sensitive fibers." — Miller's Anesthesia 10e, Chapter 61

Incidence Data (Miller's Anesthesia 10e — 1.7 Million Deliveries Dataset)

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2. Pathophysiology

Two Complementary Mechanisms

"Loss of CSF through the iatrogenic dural tear seems to be the inciting factor. When the patient is upright, intracerebral CSF volume decreases. This change may cause the brain to sag toward the foramen magnum, stretching the pain-sensitive meningeal vascular covering." — Barash 9e, Chapter 35

• CSF escapes through dural defect faster than it is produced (500 mL/day production)
• Upright position: loss of buoyancy → brain descends toward foramen magnum
• Stretching of dura, bridging veins, cranial nerves, tentorium → positional pain
• Lying flat: gravity effect removed → immediate relief

"The diminished CSF volume may incite a compensatory increase in cerebral blood volume and produce a vascular headache." — Barash 9e, Chapter 35

• Decreased intracranial CSF volume → compensatory adenosine-mediated vasodilation
• Distension of pain-sensitive dural and meningeal vessels → pulsatile, throbbing quality
• Explains: partial relief with caffeine (adenosine antagonist → vasoconstriction)
• Explains: migraine-like features (photophobia, phonophobia, nausea)

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3. Risk Factors

3.1 Needle-Related Factors (Barash 9e, Chapter 35)

"The risk of PDPH correlates with the needle size, tip design, and bevel orientation. Pencil-point needles produce fewer headaches than similar-sized cutting-point needles. The smaller the needle, the lower the risk of PDPH... When using a cutting-tip needle, orienting the bevel parallel to the longitudinal axis of the back decreases the PDPH risk by more than half." — Barash 9e

3.2 Patient-Related Factors (Barash 9e)

"Younger patients are more likely to develop PDPH... patients with a BMI above 30 kg/m² may be less likely to develop PDPH... Patients with a history of PDPH or those with chronic headaches are more likely to develop a PDPH." — Barash 9e, Chapter 35

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4. Clinical Features

4.1 Diagnostic Criteria (ICHD-3)

1. Headache developing within 5 days of dural puncture
2. Worsens within 15 minutes of sitting or standing
3. Improves within 15 minutes of lying flat
4. Headache resolves spontaneously within 2 weeks or after EBP

4.2 Symptoms

"PDPH usually develops 24 to 72 hours after dural puncture. Patients will complain of frontal and occipital pain that is made worse by standing and relieved by lying flat. Severe PDPH can also cause neck, shoulder, or back pain, which may not be relieved by lying down. Visual disturbances, vertigo, and cranial nerve palsies can occur." — Barash 9e, Chapter 35

4.3 Serious but Rare Complications (Barash 9e)

"Rarely, cortical vein thrombosis or subdural hematoma occur. Death has been reported." — Barash 9e

• Subdural haematoma — bridging vein rupture from brain sag
• Cortical vein thrombosis — venous stasis from intracranial hypotension
• Cranial nerve palsy — CN VI most common
• Death — rare; from intracranial complications

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5. Differential Diagnosis of Postpartum Headache

"When diagnosing a PDPH, it is important to consider other causes of headache in the postpartum period... Assessing the patient for fever and nuchal rigidity is important to rule out postdural puncture meningitis... hypertension is important to detect postpartum preeclampsia... cerebral venous thrombosis, cranial subdural hematoma, and ischemic or hemorrhagic stroke can present as a postpartum headache." — Miller's Anesthesia 10e

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6. Prevention Strategies

6.1 Primary Prevention — Needle Technique

6.2 Prevention After Confirmed ADP

"The three most widely studied approaches are prophylactic epidural blood patch, intrathecal catheter placement, and epidural morphine injection." — Barash 9e

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7. Treatment

7.1 Conservative Management (Step 1)

"Once PDPH develops, most therapy is symptomatic. Bed rest will often relieve PDPH pain but does not shorten its duration. Neither oral nor intravenous hydration has any effect on PDPH." — Barash 9e, Chapter 35

"Caffeine can be minimally effective to treat the pain of a PDPH in the short term, likely because of its vasoconstrictive effects." — Miller's Anesthesia 10e, Chapter 61

7.2 Epidural Blood Patch (EBP) — Definitive Treatment

"Epidural blood patch is the definitive therapy for PDPH. The efficacy of epidural blood patch has clearly been established in small, but well-conducted, randomized prospective trials. Most authors report that a single epidural blood patch cures 75% to 90% of PDPHs." — Barash 9e, Chapter 35

Indications (OAA Guidelines 2021 + ASA Statement 2021)

"If the symptoms are severe enough to limit a patient's activity, then an epidural blood patch (EBP) should be considered. The Obstetric Anaesthetists' Association guidelines on treatment of PDPH indicate that EBP should be offered to patients with symptoms affecting care of the infant or daily living." — Miller's Anesthesia 10e, Chapter 61

• PDPH limiting daily activities or ability to care for infant
• PDPH with cranial nerve involvement (diplopia) → immediate EBP (Barash 9e)
• Failed conservative management ≥24–48 hours
• Severe or rapidly escalating PDPH

Mechanism of EBP

• Autologous blood forms a clot over the dural defect → seals CSF leak
• Blood in epidural space also raises epidural pressure → displaces CSF cranially → immediate relief of traction headache

Volume of Blood

"Most authors now recommend around 20 mL... Patients often report back pain as blood is being injected. This pain usually recedes if the injection is halted. More blood can be injected after a moment or two. Stop adding more blood if the back pain returns immediately after resuming injection." — Barash 9e, Chapter 35

• Standard volume: 15–25 mL autologous blood
• Stop early if: back pain recurs immediately, radicular pain, or leg paraesthesia
• Patient remains supine for 1–2 hours post-procedure

Timing

"Several retrospective chart reviews have suggested that epidural blood patch is more likely to provide headache relief if it is performed at least 72 hours after dural puncture compared with less than 24 hours after puncture... A more severe PDPH may have both a more rapid onset and be more difficult to cure." — Barash 9e, Chapter 35

• Optimal: ≥24–72 hours after ADP
• Earlier EBP has lower success rate; acceptable if symptoms severe (CN involvement, incapacitating)

Efficacy (Barash 9e)

"Only 67% of women reported headache relief after a single epidural blood patch. Fewer than 20% reported permanent relief. PDPH often recurred 4 to 5 days after the original blood patch. Twenty-one percent of the women received a second epidural blood patch." — Barash 9e (recent study data)

Complications of EBP (Barash 9e)

"Mild back pain is common after epidural blood patch. Serious complications are rare. However, epidural hematoma requiring surgical decompression has been reported. One patient with idiopathic intracranial hypertension developed acute vision loss after rapid epidural injection of 25 mL autologous blood." — Barash 9e, Chapter 35

• Backache (most common — 35–50%)
• Radicular pain / paraesthesia during injection
• Epidural haematoma (rare; may require decompression)
• Infection
• Failure/recurrence (15–33%)
• Contraindications: active systemic infection, coagulopathy, raised ICP

7.3 Alternative Procedural Options

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8. Chronic Sequelae of ADP

"Compared to matched controls, parturients who suffered an accidental dural puncture had an increased incidence of chronic headache at 6 weeks (35% vs. 2%) and 24 months (28% vs. 5%)." — Barash 9e, Chapter 35

• ADP is NOT a trivial event — formal follow-up, written information, and documentation are mandatory
• All ADPs must be reported as clinical incidents; referred to obstetric anaesthesia chronic pain service if headache persists >6 weeks

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9. Management Algorithm

DURAL PUNCTURE (intentional or accidental)
              ↓
Postural headache within 5 days → PDPH suspected
              ↓
RULE OUT: Pre-eclampsia | Meningitis | CVT | Subdural Haematoma
              ↓
MILD → Conservative: Paracetamol + NSAIDs + Caffeine 300 mg BD
              ↓ (failure 24–48h OR moderate–severe OR CN involvement)
EPIDURAL BLOOD PATCH: 15–25 mL autologous blood (epidural space)
         Efficacy 75–90% first EBP; repeat if incomplete relief
              ↓
REFRACTORY → SPG block | Cosyntropin | Neurology review

Sources: Miller's Anesthesia 10e (Chapter 61); Barash 9e (Chapter 35); Morgan & Mikhail 7e (Chapter 16); ASA Statement on PDPH 2021; OAA PDPH Guidelines 2021.

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QUESTION 22A

Local Anaesthetic Systemic Toxicity (LAST)

Mechanisms · Clinical Features · Prevention · Treatment

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1. Introduction

---

2. Pharmacological Basis

2.1 Mechanism of Local Anaesthetic Cardiotoxicity

• Calcium channel blockade → negative inotropy
• Potassium channel blockade → prolonged repolarisation
• Mitochondrial uncoupling → cellular energy failure

2.2 Historical Note

---

3. Incidence

---

4. Risk Factors

---

5. Clinical Features

5.1 Systemic Toxicity — Sequential Progression

CNS Toxicity (excitatory phase → depressive phase)

Cardiovascular Toxicity (higher plasma concentrations)

Critical Teaching Point: With bupivacaine, CV collapse and CNS excitation may occur together, or CV toxicity may be the first sign. Never assume the absence of prodromal CNS symptoms means bupivacaine is safe to continue injecting.

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6. Maximum Safe Doses

---

7. Prevention

---

8. Treatment — AAGBI Guidelines 2023

8.1 Immediate Actions

8.2 Seizure Management

8.3 Cardiac Arrhythmia Management

8.4 Lipid Emulsion Rescue Therapy (Intralipid 20%) — CORNERSTONE

• 20% lipid emulsion creates a large lipophilic compartment in plasma
• Highly lipophilic LA (especially bupivacaine: high protein binding, high lipid solubility) partitions from aqueous phase (where it blocks cardiac receptors) into the lipid phase
• Rapidly redistributes LA away from myocardium → reverses toxicity
• Additional mechanism: provides free fatty acids as myocardial metabolic substrate → direct cardiotonic effect

Dosing Protocol (AAGBI 2023 — 20% Intralipid)

Key principle: Start Intralipid at the first sign of cardiovascular instability — do NOT wait for cardiac arrest.

8.5 Cardiac Arrest from LAST

CARDIAC ARREST → START CPR
        ↓
Intralipid: 1.5 mL/kg IV bolus → 15 mL/kg/hr infusion
        ↓
Adrenaline: ≤1 mcg/kg (NOT standard 1 mg ACLS doses)
Amiodarone 150 mg IV for VF/VT
        ↓
CONTINUE CPR FOR ≥60 MINUTES
(bupivacaine redistributes over time → resuscitation may succeed after prolonged CPR)
        ↓
ECMO / Cardiopulmonary bypass if available and refractory

Do NOT stop CPR prematurely — bupivacaine toxicity is potentially reversible with sustained resuscitation as drug redistributes.

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9. Special Situations

Sources: Miller's Anesthesia 10e (Chapter 36); Barash 9e (Chapter 18); Morgan & Mikhail 7e (Chapter 18); AAGBI LAST Guidelines 2023; ASRA LAST Checklist 2022.

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QUESTION 22B

Xenon in Anaesthesia

Properties · Mechanisms · Clinical Applications · Limitations

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1. Introduction

---

2. Physical and Chemical Properties

---

3. Mechanism of Action

---

4. Pharmacokinetic Properties

---

5. Pharmacological Effects

5.1 CNS Effects

5.2 Cardiovascular Effects

5.3 Other Effects

---

6. Xenon vs. Nitrous Oxide — Comparison

---

7. Clinical Applications

7.1 General Anaesthesia

• Delivered as 60–70% Xe + 30–40% O2 in a closed or low-flow circuit
• MAC 63–71% means additional analgesic or hypnotic supplementation often required for deep anaesthesia
• Closed-circuit xenon recirculation systems (e.g., Zeus, Narkomed) mandatory to reduce cost
• Approved in EU as Xenon Medical (AGA Medical); investigational status in USA

7.2 Neuroprotection — Primary Research Application

1. NMDA antagonism → blocks glutamate excitotoxicity during ischaemia
2. HIF-1α inhibition → reduces hypoxia-induced apoptosis
3. Anti-apoptotic: preserves Bcl-2; reduces caspase-3 activation
4. TREK-1 channel activation → neuronal hyperpolarisation during ischaemia
5. Anti-inflammatory: reduces microglial activation and cytokine release

7.3 ICU Sedation

• 50% Xe + 50% O2 provides haemodynamically stable sedation in neuro-ICU
• Ultra-rapid offset facilitates neurological assessment without residual sedation
• Particularly valuable after cardiac arrest or following neurosurgery

7.4 Cardiac Surgery

• Haemodynamic stability and preconditioning properties make xenon attractive for CABG and valve surgery
• Reduces myocardial stunning in animal and early clinical studies

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8. Limitations

---

9. Why Xenon Approaches the "Ideal Anaesthetic Agent"

Sources: Miller's Anesthesia 10e (Chapter 28); Barash 9e (Chapter 27); Morgan & Mikhail 7e (Chapter 8).

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QUESTION 23

Anaesthetic Management of COPD

Assessment · Optimisation · Intraoperative Technique · Postoperative Care

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1. Introduction

---

2. Pathophysiology Relevant to Anaesthesia

---

3. GOLD Classification

---

4. Preoperative Assessment

4.1 History

4.2 Investigations

---

5. Preoperative Optimisation

---

6. Choice of Anaesthetic Technique

6.1 Regional Anaesthesia — Preferred Where Possible

• Avoids endotracheal intubation → bypasses reactive airways → eliminates bronchospasm risk at intubation
• No general anaesthetic agents → no respiratory depression
• Spinal or epidural anaesthesia for lower abdominal, pelvic, urological, and lower limb surgery
• Peripheral nerve blocks (brachial plexus, adductor canal, popliteal sciatic) for appropriate limb procedures

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7. General Anaesthesia — When Required

7.1 Induction

7.2 Airway Management

7.3 Maintenance

---

8. Auto-PEEP Detection and Management

---

9. Intraoperative Bronchospasm

• ETT in right main bronchus (right bronchial intubation)
• Secretions plugging airway
• Pneumothorax (particularly bullous emphysema)
• Anaphylaxis
• Equipment failure (kinked circuit)

---

10. Extubation Strategy

• Extubate awake — not deep; COPD patients require full return of protective airway reflexes and respiratory drive
• Reverse NMB with sugammadex (not neostigmine — muscarinic M2/M3 stimulation → bronchoconstriction)
• Pre-extubation: salbutamol 4 puffs via ETT; suction secretions; ensure SpO2 stable
• Have NIV/BiPAP immediately available in recovery area

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11. Ventilation Parameters Summary

---

12. Postoperative Care

Sources: Miller's Anesthesia 10e (Chapter 40); Barash 9e (Chapter 23); Morgan & Mikhail 7e (Chapter 24).

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QUESTION 24

Allowable Blood Loss — Definition, Calculation, and Intraoperative Estimation

MABL Formula · EBV · Estimation Methods · Transfusion Strategy

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1. Introduction

---

2. Maximum Allowable Blood Loss — Definition

• Blood loss is replaced with crystalloid or colloid (not PRBCs) throughout
• Circulating blood volume (EBV) remains constant

---

3. Estimated Blood Volume (EBV)

Gilcher's Rule — Standard Reference Values

---

4. MABL Calculation — Formula

Gross Formula (Widely Used Clinical Standard)

Average Haematocrit Formula (More Accurate)

---

Standard Minimum Acceptable Haemoglobin Targets

---

Worked Example

---

5. Blood Loss Replacement Strategy

---

6. Intraoperative Blood Loss Estimation Methods

6.1 Visual Estimation

• The least accurate method
• Consistent bias: underestimates by 30–50%
• Highly observer-dependent; not influenced by experience level (experienced surgeons still underestimate)
• Should NOT be used as the primary estimation method in major cases

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6.2 Gravimetric Method (Weighing) — Standard Clinical Method

1. Weigh all unused swabs/laparotomy sponges before surgery (record dry weight for each type)
2. Collect all soaked swabs into labelled bags during surgery; weigh promptly before drying
3. Subtract dry weight from wet weight = gross weight gain
4. Subtract volume of irrigating fluids used on swabs (if known)
5. Divide by 1.06

---

6.3 Suction Canister Measurement

• Direct volume measurement from suction canisters during surgery
• Must subtract irrigation fluid volumes used

• Most accurate when irrigation is minimal or precisely measured
• Combine with gravimetric method for total blood loss estimate

---

6.4 Serial Haemoglobin / Haematocrit Monitoring — Most Accurate Biochemical Method

• Sample via arterial line (if placed) or venepuncture
• ABG analyser provides rapid Hb at bedside
• Dilution effect: IV fluids administered during surgery lower Hb — must account for this
• Best performed every 30–60 minutes in major haemorrhage cases
• Use trending rather than a single value to estimate ongoing loss rate

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6.5 Non-Invasive Continuous Haemoglobin Monitoring (SpHb)

• Masimo Pronto / Rainbow SpHb — continuous transcutaneous Hb monitoring via pulse oximetry platform
• Accuracy: ±1–1.5 g/dL compared to co-oximetry
• Valuable for trend monitoring and early alert to rapidly falling Hb
• Does not replace formal blood gas Hb measurement for transfusion decisions; use as supplementary data

---

6.6 Summary Table — Blood Loss Estimation Methods

---

7. Intraoperative Cell Salvage (ICS)

---

8. Clinical Summary

PREOPERATIVELY
  Calculate EBV (weight × factor)
  Calculate MABL (EBV × [Hi − Ht] / Havg)
  Determine transfusion threshold for this patient

INTRAOPERATIVELY
  Estimate blood loss: Gravimetric + Suction canister
  Monitor Hb: Serial ABG ± SpHb trend
  Replace crystalloid 3:1 or colloid 1:1 up to MABL
  At MABL: Transfuse PRBC
  Check coagulation: TEG/ROTEM-guided component therapy
  Consider ICS if >500 mL anticipated

POSTOPERATIVELY
  Repeat Hb at 1–2 hours and 24 hours
  Reassess need for ongoing transfusion
  Iron supplementation for subacute anaemia correction

Sources: Miller's Anesthesia 10e (Chapter 49); Barash 9e (Chapter 27); Morgan & Mikhail 7e (Chapter 51).

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QUESTION 25A

Epidural Dural Puncture

Recognition · Immediate Management · Subsequent PDPH · Documentation

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1. Introduction

---

2. Incidence

---

3. Risk Factors for ADP

---

4. Recognition of ADP

4.1 Immediate Signs at Puncture

4.2 Confirming CSF vs. Local Anaesthetic / Saline

---

5. Immediate Management Options

"In the setting of an unintended dural puncture with an epidural needle, an intrathecal catheter may be threaded, or the epidural needle may be removed and replaced at a different interspace." — Miller's Anesthesia 10e

Option A — Thread Intrathecal Catheter (Preferred in Obstetrics)

"Placement of the intrathecal catheter can provide labor analgesia and alleviates the need for multiple repeat epidural attempts with the potential of a second accidental dural puncture." — Miller's Anesthesia 10e, Chapter 61

1. Do not advance the Tuohy needle further
2. Thread standard epidural catheter intrathecally through the Tuohy needle (typically 3–4 cm into subarachnoid space)
3. Label catheter prominently: "INTRATHECAL CATHETER — NOT EPIDURAL" using coloured tape and written label
4. Inform all healthcare providers — anaesthetic chart, nursing handover, obstetric team
5. Never inject epidural doses through an intrathecal catheter

• Provides reliable, immediate continuous spinal analgesia for labour
• Avoids a second ADP at another level
• May reduce need for therapeutic EBP (intrathecal catheter may tamponade CSF leak)
• Provides controlled intrathecal access for caesarean section if required

---

Option B — Remove and Re-site at Adjacent Level

• Remove Tuohy needle; apply gentle pressure
• Re-site epidural at one level above or below (not the same level)

• The dural puncture creates a potential pathway for LA to track into subarachnoid space
• Use cautious, incremental dosing starting at 2–3 mL rather than the usual 5 mL test dose
• High/total spinal risk is elevated — have full resuscitation equipment immediately available
• Continuous close observation for rising sensory block level

---

6. Subsequent Management of PDPH

---

7. Documentation and Communication

• Document immediately in patient record: time, level, gauge, number of attempts, recognition of ADP, management chosen, dosing, patient response
• Inform patient verbally at time of event (if awake and appropriate) and formally in written post-procedure debrief
• Provide written information: symptoms of PDPH, when to seek help, expected timeline
• Flag for all clinical teams: obstetric team, midwives, neonatology (if applicable)
• Formal clinical incident report per institutional policy
• Follow-up appointment: Obstetric anaesthesia follow-up at 6 weeks minimum — PDPH is associated with chronic headache at 2 years in 28% vs. 5% controls (Barash 9e)

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8. High Spinal / Total Spinal — Emergency Complication After ADP

"A disturbingly common cause of high block in laboring women is unrecognized intrathecal injection during attempted labor epidural analgesia." — Barash 9e

Sources: Miller's Anesthesia 10e (Chapter 61); Barash 9e (Chapter 35); Morgan & Mikhail 7e (Chapter 16).

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QUESTION 25B

Jugular Venous Oximetry (SjO2)

Principles · Technique · Interpretation · Clinical Applications

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1. Introduction

---

2. Anatomical Basis

---

3. Physiological Basis — Fick Principle Applied to Brain

---

4. Normal Values

---

5. Technique of Catheter Insertion

---

6. Interpretation

6.1 SjO2 Desaturation (<50%) — Cerebral Ischaemia

6.2 SjO2 Elevation (>75%) — Reduced Extraction

---

7. Clinical Indications

---

8. Clinical Management Algorithm Using SjO2

TBI Scenario:

SjO2 < 50% in TBI / ICU Patient
          ↓
1. Is PaCO2 too low? → Reduce minute ventilation → target PaCO2 35–40 mmHg
2. Is MAP too low? → Increase vasopressors → target CPP 60–70 mmHg
3. Is Hb too low? → Transfuse → target Hb ≥80 g/L
4. Is FiO2 adequate? → Increase supplemental O2
5. Is ICP elevated? → ICP-reducing interventions (mannitol, CSF drainage, head elevation 30°)
6. Is vasospasm present? → TCD assessment; nimodipine
7. Surgical issue? → CT head; evacuate haematoma if indicated

Cardiac Surgery:

• If SjO2 <50% during CPB → increase pump flow rate; consider cerebral vasodilators; check oxygenator
• Post-bypass SjO2 <50% = cerebral ischaemia → highest risk for neurological complications

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9. Comparison with Other Cerebral Monitoring Modalities

---

10. Limitations of SjO2

---

11. Complications of SjO2 Catheterisation

Sources: Miller's Anesthesia 10e (Chapter 70); Barash 9e (Chapter 30); Morgan & Mikhail 7e (Chapter 27).

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Complications of Neuraxial Anaesthesia

Spinal · Epidural · Caudal — With Management

Primary Source: Miller's Anesthesia 10e | Barash's Clinical Anesthesia 9e

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PART A: COMPLICATIONS OF SPINAL ANAESTHESIA (SUBARACHNOID BLOCK)

---

1. Classification of Complications

---

2. Hypotension

Mechanism

• Arterial and arteriolar dilation → ↓ SVR
• Venodilation → peripheral pooling → ↓ venous return → ↓ cardiac output
• Cardiac accelerator fibres (T1–T4) blocked when level reaches upper thorax → relative bradycardia

Incidence

• Spinal for caesarean section: 50–80% without prophylaxis
• General surgical population: 15–33%
• Higher with block level ≥T5, pre-existing hypovolaemia, age >50, BMI <20

Management

---

3. Bradycardia and Cardiac Arrest

Mechanism

1. Bezold-Jarisch reflex — decreased venous return → under-filled right ventricle → paradoxical vagal activation → severe bradycardia / asystole
2. Cardiac sympathetic fibre block (T1–T4) → unopposed vagal tone → HR falls
3. Hypoxia from high block → cardiac compromise

"Extensive sympathetic block combined with moderate to deep sedation (and presumed hypoxemia) can lead to sudden cardiac arrest, even in otherwise healthy young patients." — Barash 9e (Neuraxial Complications Chapter)

Management

"In a series of 14 such arrests, prompt treatment with ephedrine, atropine, and chest compressions, but delayed administration of epinephrine produced uniformly poor neurologic outcomes. More rapid treatment with epinephrine might help counter the subarachnoid anesthesia-induced sympathetic block." — Barash 9e

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4. High Spinal / Total Spinal Block

Definition and Incidence

"High neuraxial block (otherwise undefined) complicated approximately 1 in 4,000 obstetric neuraxial anesthetics." — Barash 9e

Risk Factors (Barash 9e)

• Obesity
• Short stature
• Subarachnoid block after failed epidural
• Repeat epidural after unintended dural puncture
• Spinal deformity
• Unrecognised intrathecal injection during attempted epidural (most common cause in obstetrics)
• Excessive LA volume
• Head-down or supine position during hyperbaric spinal

Clinical Features — Level-Dependent

"Although patients often note chest tightness and dyspnea with thoracic levels of sensory block, respiratory function is usually unchanged. As the block ascends into the cervical regions, handgrip will weaken. Finally, blocks to C3–C5 will impair diaphragmatic function. These patients will only be able to whisper." — Barash 9e

Management

"They should be ventilated promptly and intubated if needed." — Barash 9e

"When faced with a high level of sensory block after intrathecal injection of hyperbaric local anesthetic, you may be tempted to limit the rising block by placing the patient in reverse Trendelenburg position. Don't! This position may decrease the cephalad spread of sensory block, but Trendelenburg positioning will cause the patient's blood to pool in the legs, exacerbating the hypotensive effects." — Barash 9e

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5. Post-Dural Puncture Headache (PDPH)

"The most common complication associated with neuraxial analgesia is unintended dural puncture. Leakage of spinal fluid is thought to result in vascular hyperemia, migraine physiology, and traction on pain-sensitive fibers." — Miller's Anesthesia 10e

• Intentional spinal with cutting needle (25G Quincke): PDPH 10–25%
• Intentional spinal with pencil-point needle (25G Whitacre/Sprotte): PDPH 1–3%
• Severity and incidence related to needle size, tip design, and bevel orientation (Miller 10e)

Management

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6. Transient Neurological Symptoms (TNS)

"Prospective randomized studies reveal a 4% to 40% incidence of transient neurologic symptoms (TNSs), including pain or sensory abnormalities in the lower back, buttocks, or lower extremities, after lidocaine spinal anesthesia." — Barash 9e (Chapter 22)

Features

• Pain or dysaesthesia in the lower back, buttocks, and posterior thighs
• Onset: within 24 hours of spinal resolution; resolves within 72 hours (by definition — transient)
• No permanent neurological sequelae
• Not associated with MRI or electrophysiological (EMG/NCS) abnormalities

Risk Factors (Barash 9e)

"Increased risk of TNSs is associated with lidocaine, the lithotomy position, and ambulatory anesthesia, but not with baricity of solution or dose of local anesthetic." — Barash 9e

Pathophysiology

"Other potential etiologies for TNSs include patient positioning, sciatic nerve stretch, muscle spasm, and myofascial strain." — Barash 9e

Management

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7. Cauda Equina Syndrome (CES)

Definition and Cause

• Flaccid paralysis of lower limbs
• Loss of bladder and bowel sphincter control (urinary retention + faecal incontinence)
• Saddle anaesthesia (perineum, genitalia, inner thighs)
• Sexual dysfunction

"The use of microcatheters with a high concentration of lidocaine for continuous spinal anesthesia has been associated with an increased incidence of radiculopathy and cauda equina syndrome." — Barash 9e

Other Causes

• Chloroprocaine (old formulation) — sodium bisulfite preservative — neurotoxic; associated with prolonged deficits; withdrawn and reformulated
• Intrathecal injection of wrong drug (epidural drugs erroneously injected into subarachnoid space)
• Direct needle trauma to conus medullaris
• Spinal haematoma or abscess compressing cauda equina

Management

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8. Anterior Spinal Artery Syndrome (Spinal Cord Ischaemia)

Mechanism

Causes in Spinal Anaesthesia

Clinical Features

Management

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9. Neurological Injury from Needle Trauma

"Although the spinal cord typically ends at L1–L2 in adults, the exact termination varies, and the cord extends farther caudad in children. In addition, anesthesiologists using palpation often misidentify the lumbar interspaces and insert needles at a higher level than intended. Permanent damage to the conus medullaris has been reported after attempted subarachnoid or CSE anesthesia at the presumed L2–L3 vertebral interspace." — Barash 9e

Types of Needle Injury

Prevention (Barash 9e)

"In parturients, using the space just below, instead of above, the palpated intercristal line can decrease the frequency of inserting the spinal or epidural needle at or above L2–L3." — Barash 9e

• Use ultrasound to identify correct interspace, especially in patients with poorly palpable landmarks
• Aim for L3–L4 or L4–L5 interspace preferentially
• If patient reports severe paraesthesia during needle placement → immediately stop and reposition needle
• Persistent paraesthesia after block resolution → neurological assessment + MRI

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10. Meningitis / Arachnoiditis

Types

Clinical Features of Bacterial Meningitis

• Fever, headache, neck stiffness, photophobia (onset 12–24 hours post-spinal)
• Altered consciousness; positive Kernig's and Brudzinski's signs
• CSF: turbid; ↑ WBC (neutrophils), ↑ protein, ↓ glucose

Management

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11. Local Anaesthetic Systemic Toxicity (LAST) in Spinal Context

"Local anesthetic systemic toxicity (LAST) can follow absorption from the epidural space or unrecognized intravascular injection. Signs and symptoms range from tinnitus and metallic taste to seizures and cardiac arrest." — Barash 9e

• Intrathecal doses are small → systemic toxicity from the spinal dose itself is rare
• Risk arises if: wrong drug given (epidural volume intrathecally); or if previous epidural doses are absorbed systemically after conversion to spinal
• Management: see Q22A (LAST protocol — Intralipid 20%; supportive)

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12. Urinary Retention

Mechanism

• Sacral parasympathetic block (S2–S4) → detrusor muscle paralysis → inability to void
• Patients unable to void until block fully resolves

Management

---

13. Backache

• Common after neuraxial techniques; NOT uniquely caused by spinal anaesthesia
• Often multifactorial: prolonged supine immobilisation, muscle relaxation, loss of normal lumbar lordosis, bruising from needle
• Usually mild and self-limiting
• Treatment: NSAIDs; heat application; physiotherapy if persistent

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PART B: COMPLICATIONS OF EPIDURAL ANAESTHESIA

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1. Classification

---

2. Failed / Inadequate Epidural Block

Causes

Management

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3. Accidental Dural Puncture (ADP) and PDPH

"The incidence of unintentional dural puncture during labor epidural placement is 1% to 1.5%. The incidence of headache after an unintentional dural puncture with an epidural needle is reported at 30% to 60%." — Miller's Anesthesia 10e

Immediate Options After ADP

1. Thread intrathecal catheter (preferred in obstetrics) — provides reliable analgesia; avoids second ADP
2. Re-site epidural at adjacent interspace — use cautious incremental dosing thereafter

PDPH Management

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4. Inadvertent Intravascular Injection (Epidural Vein)

Mechanism and Recognition

• Epidural veins are distended (especially in pregnancy — caval compression) and easily cannulated
• Intravascular injection of standard epidural doses → LAST (see Q22A)
• Epidural test dose: 3 mL of 1:200,000 adrenaline (15 mcg) — heart rate rise >20 bpm = positive (intravascular)

"Important safety steps to prevent local anesthetic toxicity include incremental injection, limiting the total dose of local anesthetic, and using a test dose that contains a marker for intravascular injection. Incremental injection of 3 to 5 mL of local anesthetic every 90 to 120 seconds is probably the most effective of these steps." — Barash 9e

Management

• Stop injection immediately
• Lipid emulsion rescue (Intralipid 20%): 1.5 mL/kg IV bolus → 15 mL/kg/hr
• Airway management, seizure control, cardiac resuscitation as needed (see Q22A LAST protocol)
• Adrenaline ≤1 mcg/kg for cardiac arrest in LAST

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5. Epidural Haematoma

Mechanism and Incidence

"Mass lesions also can injure the spinal cord. These lesions can compress the spinal cord and decrease perfusion. Spinal cord ischemia or infarction can follow. Abscess and hematoma are the most widely studied compressive complications of neuraxial block. Significant hematoma may occur as often as 1:3,600 blocks or as rarely as 1:260,000. Patients undergoing orthopedic procedures and those taking medications that interfere with coagulation are at greatest risk. Hematoma is more common after epidural than subarachnoid block. Hematoma also can occur after removing an epidural catheter." — Barash 9e

Risk Factors

Clinical Features

Management — Time-Critical

"The American Society of Regional Anesthesia has a regularly updated guideline that provides recommendations for the safe use of neuraxial block in patients taking antithrombotic or thrombolytic medications." — *Barash 9e (ASRA Guidelines reference)

ASRA Guidelines — Key Timing Rules

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6. Epidural Abscess

Mechanism and Incidence

• Incidence: 1:1,000–1:100,000 epidural blocks
• Route of infection: haematogenous seeding (most common); direct inoculation from contaminated equipment; spread from adjacent tissue infection
• Most common organism: Staphylococcus aureus (including MRSA)

Risk Factors

• Prolonged epidural catheterisation (>4 days)
• Immunocompromise (diabetes, HIV, steroids, malignancy)
• Bacteraemia at time of insertion
• Break in aseptic technique
• Systemic sepsis

Clinical Features (Heusner's Four-Stage Progression)

Management

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7. Subdural Block (Rare)

Mechanism

Features

• Onset of block slower than spinal (minutes to 15–30 minutes), faster than epidural
• Unusually extensive block for the dose given — disproportionate spread
• Variable sensory and motor block
• Haemodynamic compromise from high sympathetic block
• May present as failed epidural that suddenly becomes a high block

Management

• Recognise the disproportionate block extent
• Manage haemodynamic consequences (vasopressors, atropine)
• Airway management if high/total block occurs
• Remove catheter; reassess and re-site if appropriate

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8. Respiratory Depression (Intrathecal/Epidural Opioids)

Mechanism

• Rostral spread of intrathecal/epidural opioids to the medullary respiratory centres
• Risk higher with hydrophilic opioids (morphine — spreads cephalad in CSF over 6–18 hours)
• Lipophilic opioids (fentanyl, sufentanil) — minimal rostral spread; early but not late respiratory depression

Risk Factors

• High-dose intrathecal morphine (>300 mcg)
• Elderly, obese, OSA
• Concurrent systemic opioids or sedatives

Monitoring Protocol

• Respiratory rate, sedation score, SpO2 every 1 hour for 12 hours after intrathecal morphine; every 2 hours for 24 hours

Management

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9. Catheter-Related Mechanical Complications

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PART C: COMPLICATIONS OF CAUDAL ANAESTHESIA

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1. Introduction

---

2. Unique Anatomy — Source of Complications

---

3. Complications Specific to Caudal Anaesthesia

3.1 Failed Block

Incidence and Causes

• Overall failure rate: 2–10% in experienced hands; up to 25% in trainees
• Anatomical variation of sacral hiatus (small, bifid, or absent in adults)
• Incorrect needle placement: subperiosteal, intramuscular, subcutaneous
• Insufficient volume for level required

Management

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3.2 Intravascular Injection

Mechanism and Risk

• The sacral canal contains a rich venous plexus
• Risk of IV injection: estimated 0.5–1% in paediatrics; higher in adults
• If epidural LA volumes (0.5–1 mL/kg) are inadvertently injected intravenously → LAST

Prevention

Always aspirate before injection; use adrenaline test dose (0.5 mcg/kg = 0.1 mL/kg of 1:200,000 adrenaline); HR rise >20 bpm = positive test Inject slowly in small increments; monitor ECG throughout

Management

• LAST protocol (see Q22A)
• Lipid emulsion rescue — Intralipid 20%: 1.5 mL/kg IV bolus → 15 mL/kg/hr
• Airway; seizure management; cardiac resuscitation if needed

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3.3 Intrathecal Injection (Total Spinal)

Mechanism

• In neonates and infants, the dural sac extends to S3–S4 (vs. S1–S2 in adults)
• A needle advanced too far through the sacral hiatus may puncture the dura at a lower level than in adults
• Full caudal volume injected intrathecally → high or total spinal block

Clinical Features

• Rapid onset of dense motor block (seconds to 1–2 minutes)
• Rapid haemodynamic collapse (hypotension, bradycardia)
• Apnoea if block reaches cervical levels

Prevention

• Do not advance needle beyond mid-sacrum (S3 level)
• Aspirate for CSF before injecting
• Ultrasound guidance in infants — visualises needle tip

Management

• Call for help; airway management immediately — mask ventilation + RSI if apnoeic
• Vasopressors (phenylephrine/ephedrine) for haemodynamic support
• Atropine for bradycardia
• Epinephrine for cardiac arrest — prompt administration critical (Barash 9e)
• Expectant management — block will eventually wear off; full supportive care in the interim

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3.4 Intraosseous Injection

Mechanism

• If needle tip is in the cancellous bone of the sacral vertebra rather than the sacral canal
• Drug injected directly into the intraosseous venous circulation → rapid systemic absorption equivalent to IV injection → LAST

Recognition

• Injection resistance is very high (bone)
• No loss of resistance characteristic
• No flow on aspiration
• Can be confused with loss of resistance into the periosteum

Management

• Stop injection
• Reposition needle under ultrasound guidance
• LAST protocol if drug already injected

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3.5 Rectal Puncture / Perforation

Mechanism

• The rectum lies anterior to the sacrum in the pelvis
• If needle is angled too anteriorly or if anatomical variation places the rectum in the needle path → rectal perforation
• Recognised by: faecal material on aspiration; air on aspiration (rectal gas)

Management

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3.6 Haematoma and Abscess

• Same pathophysiology as lumbar epidural (see Part B)
• Higher infective risk with caudal due to proximity to perineum / perianal skin
• Strict aseptic technique mandatory; avoid caudal if perianal/perineal infection present

Management

• Epidural haematoma: MRI → emergency decompression within 8 hours if neurological compromise
• Epidural abscess: IV antibiotics ± surgical drainage
• Prevention: Chlorhexidine skin preparation; sterile drapes; avoid in localised skin infection

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3.7 Sacral Nerve Damage

Mechanism

• Direct trauma to sacral nerve roots during needle insertion
• More likely if anatomical variation or excessive needle advancement

Features

• Buttock, perineal, or lower limb pain/paraesthesia at time of needle insertion
• Should immediately trigger needle withdrawal and repositioning
• Persistent paraesthesia post-procedure → neurological assessment

Management

• Withdraw needle if paraesthesia occurs during placement
• Post-procedural paraesthesia: expectant management; MRI if persistent >24–48 hours
• Neuropathic pain management if persistent

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3.8 Block Too High / Extensive

Mechanism

• Excess drug volume relative to patient size (especially in infants and children)
• Drug tracking cranially through epidural space above intended level

Volume Guidelines (Paediatric) — Armitage Formula:

Management

• Haemodynamic monitoring; vasopressors if hypotension
• If respiratory compromise → O2 supplementation; assist ventilation; intubation if required
• Expectant — block will resolve; supportive care throughout

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3.9 Urinary Retention

• Sacral parasympathetic fibres (S2–S4) reliably blocked by caudal anaesthesia
• Urinary retention predictable in adults; not clinically significant in paediatric day surgery (resolves with block)
• Adults: Catheterise if unable to void 6 hours after block resolution

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3.10 Failure of Caudal in Adults

• In adults, the sacral hiatus is absent in 5–8% and very narrow in a further 10–15%
• Variable fat content of the sacral canal in obese adults → unpredictable spread
• For adult chronic pain procedures: Fluoroscopic or ultrasound guidance is recommended to confirm correct placement before injection

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Summary Comparison Table — Complications of Neuraxial Techniques

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Primary Sources: Miller's Anesthesia 10e (Chapters 36, 61, 70); Barash's Clinical Anesthesia 9e (Chapters 7, 11, 35); Morgan & Mikhail's Clinical Anesthesiology 7e (Chapter 17); ASRA Anticoagulation Guidelines (current edition); AAGBI LAST Guidelines 2023.