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Anginal Chest Pain and Cardiac Failure in Hyperthyroidism

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Underlying Haemodynamic Changes

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1. Cause of Anginal Chest Pain

A. In Patients with Pre-existing CAD (Type 2 MI / Demand Ischemia)

• Tachycardia shortens diastolic filling time, further reducing coronary perfusion
• The increased cardiac work (rate x pressure product) escalates oxygen consumption
• In older hyperthyroid patients with known or suspected CAD, this increased cardiac workload reliably triggers anginal episodes

B. In Patients with Normal Coronary Arteries (Coronary Vasospasm)

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2. Cause of Cardiac Failure

A. High-Output Failure (Predominantly Right Heart)

1. Pulmonary hypertension develops - Systemic vascular resistance falls in hyperthyroidism but pulmonary vascular resistance does not. Because of the greatly increased output delivered to the pulmonary circulation, pulmonary arterial pressure rises.
2. This leads to elevated mean venous pressure, hepatic congestion, and peripheral edema - the picture of right-sided heart failure.
3. The kidneys respond to the high-output state by increasing sodium reabsorption (via renin and aldosterone stimulation), further expanding plasma volume and worsening congestion.

Note: The exercise intolerance seen in many hyperthyroid patients is not purely cardiac - it also results from skeletal and respiratory muscle weakness, and the reduced cardiac reserve (cardiac output cannot rise further during exercise because it is already near maximum at rest).

B. Tachycardia-Mediated (Low-Output) Cardiomyopathy

1. The persistently elevated heart rate creates a tachycardia-mediated cardiomyopathy - a well-recognized cause of dilated cardiomyopathy
2. The left ventricle dilates and ejection fraction falls
3. As the LV dilates, mitral regurgitation may develop, further reducing forward output
4. Pulmonary congestion develops - producing dyspnea, orthopnea, and paroxysmal nocturnal dyspnea
5. The clinical picture becomes indistinguishable from conventional heart failure with reduced ejection fraction

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Atrial Fibrillation as an Amplifying Factor

• Increases ventricular rate irregularly, worsening tachycardia-mediated injury
• Reduces effective cardiac output (loss of atrial kick)
• Creates risk of systemic embolism and stroke
• May be the first presenting symptom of hyperthyroidism in older adults, in whom the classic sympathomimetic features (anxiety, tremor) are less prominent

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Summary Table

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• Braunwald's Heart Disease, Chapter 96 (Heart Failure in Overt and Subclinical Hyperthyroidism; CHD in Hyperthyroidism)
• Tietz Textbook of Laboratory Medicine, 7th Ed. (Signs and Symptoms of Thyrotoxicosis - Cardiovascular System)
• Fuster and Hurst's The Heart, 15th Ed. (Thyroid Cardiomyopathy)
• Harrison's Principles of Internal Medicine, 22nd Ed. (High-Output States)
• Katzung's Basic and Clinical Pharmacology, 16th Ed. (Pathophysiology of Heart Failure)

Angina & Cardiac Failure in Hyperthyroidism

MD Exam Summary

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Core Mechanism (Learn This First)

• ↑ Heart rate + ↑ contractility + ↑ stroke volume → ↑ Cardiac output (2-3x normal)
• ↓ Systemic vascular resistance (peripheral vasodilation)
• ↑ Blood volume (T3 stimulates renin-aldosterone → Na+ and water retention)
• Net effect: High-output state with massively increased myocardial oxygen demand

T3 targets: β-adrenergic receptors, contractile apparatus, Na+/K+-ATPase, sarcoplasmic reticulum Catecholamines are actually normal - but β-blockers still work by blunting T3's adrenergic-mimicking effects

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I. Anginal Chest Pain - Two Mechanisms

Type 1 - Demand Ischemia (Pre-existing CAD)

• Most common mechanism
• ↑ Heart rate + ↑ contractility → ↑ myocardial O2 demand
• Tachycardia shortens diastolic filling time → ↓ coronary perfusion
• Fixed coronary stenosis cannot meet the demand → ischemia
• Seen in: older patients with known/suspected CAD
• Rx: Beta-blockers (symptomatic relief) + restoration of euthyroidism (definitive)

Type 2 - Coronary Vasospasm (Normal Coronaries)

• Seen in: younger women, chest pain at rest, ischemic ECG changes
• Angiography shows normal coronary arteries but vasospasm (like Prinzmetal's angina)
• MI is rare
• Rx: Calcium channel blockers / nitroglycerin

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II. Cardiac Failure - Two Mechanisms

Mechanism A - High-Output Right Heart Failure

Key exam point: SVR ↓ but PVR unchanged - this asymmetry explains pulmonary hypertension and right heart failure

Mechanism B - Tachycardia-Mediated Cardiomyopathy (Low-Output Failure)

1. Sustained tachycardia or AF → tachycardia-mediated cardiomyopathy
2. LV dilates → EF falls → low cardiac output
3. LV dilation causes functional mitral regurgitation → further ↓ forward output
4. Pulmonary congestion → dyspnea, orthopnea, PND
5. Picture of dilated cardiomyopathy / HFrEF

Key exam point: This is reversible - rate control alone (beta-blocker) can improve LV function even before antithyroid therapy

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III. Role of Atrial Fibrillation

• T3 shortens action potential duration + refractory period of atrial myocardium → substrate for AF
• AF may be the first presentation in elderly (classic sympathomimetic features absent in old age)
• AF amplifies failure: irregular rate, loss of atrial kick, risk of embolism/stroke

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One-Line Mechanisms for MCQs

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High-Yield Exam Points

1. Cardiovascular complications = highest morbidity/mortality in hyperthyroidism
2. Catecholamines are normal - symptoms are T3-mediated, not catecholamine excess
3. High-output failure = NOT the same as typical HF - CO is elevated, SVR is low
4. Tachycardia-mediated cardiomyopathy is the mechanism for true LV failure
5. Rate control precedes antithyroid therapy in managing LV failure
6. Thyroid cardiomyopathy is potentially reversible with treatment
7. Elderly patients present with apathetic hyperthyroidism - AF and cardiac failure without classic features

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Metabolic Changes in Thyrotoxicosis

MD Exam Summary

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Core Principle

↑ Basal metabolic rate (BMR) by 30-60% in severe thyrotoxicosis

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Molecular Basis of Increased BMR

1. Na+/K+-ATPase upregulation - T3 transcriptionally induces both α and β subunits of the Na/K pump in muscle, liver, and kidney. Increased pump activity consumes more ATP → ↑ O2 consumption and heat generation. A compensatory Na+/K+ leak creates a futile cycle (energy consumed, no useful work done).
2. Mitochondrial uncoupling - T3 upregulates uncoupling proteins (thermogenin/UCP) in brown adipose tissue. Mitochondria consume O2 and produce heat without generating ATP.
3. ↑ β-adrenergic receptor expression - Catecholamine levels are normal, but T3 increases tissue sensitivity by upregulating β-receptors in heart, skeletal muscle, and adipose tissue → amplified adrenergic thermogenesis.

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1. Carbohydrate Metabolism

Exam point: Despite driving gluconeogenesis AND glycogenolysis, plasma glucose is usually normal because insulin rises in parallel. However, thyrotoxicosis can unmask/worsen diabetes mellitus.

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2. Protein Metabolism

Exam point: Proteolysis > synthesis → net catabolism → negative nitrogen balance. This is why thyrotoxic patients have proximal muscle weakness.

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3. Lipid Metabolism

Exam point: Thyrotoxicosis → ↓ cholesterol (opposite of hypothyroidism). Cholesterol rises when patient becomes hypothyroid after treatment.

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4. Energy Metabolism / Thermogenesis

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5. Bone / Calcium Metabolism

Exam point: Thyrotoxicosis is a recognised secondary cause of osteoporosis (important in post-menopausal women on T4 replacement).

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6. Vitamin and Drug Metabolism

High-yield exam point: Thyrotoxicosis potentiates warfarin - dose reduction needed. Mechanism: increased catabolism of vitamin K-dependent clotting factors.

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Summary Table for Revision

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High-Yield MCQ Points

1. BMR rises 30-60% in severe thyrotoxicosis
2. Catecholamines are normal - but β-receptor expression is upregulated
3. Blood glucose is usually normal despite ↑ gluconeogenesis (pancreas compensates)
4. Negative nitrogen balance due to net protein catabolism
5. Cholesterol is low (not high) - hypothyroidism causes hypercholesterolaemia
6. Osteoporosis occurs from direct osteoclast stimulation by T3
7. Warfarin dose must be reduced in thyrotoxicosis (increased clotting factor catabolism)
8. Weight loss occurs despite increased appetite (polyphagia) - net energy expenditure exceeds intake
9. Futile cycles (simultaneous synthesis + degradation) are the core molecular mechanism for ↑ O2 consumption

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Thyrotoxicosis in Relation to Anaesthesia

MD Exam Summary

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Why This Matters Perioperatively

• Haemodynamic instability under anaesthesia
• Thyroid storm precipitated by surgery/stress
• Airway difficulty from goitre
• Drug interactions (altered drug clearance, catecholamine sensitivity)
• Postoperative complications (RLN injury, hypocalcaemia after thyroidectomy)

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I. Preoperative Assessment and Preparation

Goals

1. Achieve euthyroid state before elective surgery - essential to minimise risk
2. Assess and control end-organ effects (arrhythmias, heart failure)
3. Evaluate airway - degree of tracheal compression/deviation (CT/MRI)

Preoperative Drug Regimen

Key exam point: Iodide must never be given before antithyroid drugs - it can initially worsen thyrotoxicosis before the Wolff-Chaikoff effect kicks in.

Key exam point: Propranolol is the beta-blocker of choice - it is the only one that also blocks T4→T3 peripheral conversion.

Fitness for Surgery

• Marker of adequate control: normalised free T4 + absence of overt symptoms (TSH lags and may not normalise for weeks)
• All antithyroid medications are continued on the morning of surgery
• Emergency surgery in uncontrolled thyrotoxicosis: achieve heart rate <90 bpm with beta-blockers; add dexamethasone + SSKI

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II. Airway Considerations

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III. Intraoperative Anaesthetic Management

Choice of Agents

Key Intraoperative Principles

1. Induction may be slower than in euthyroid patients and may require higher volatile agent concentrations - because of the elevated cardiac output (increased drug distribution and clearance)
2. Maintain adequate anaesthetic depth to blunt sympathetic responses to surgical stimulation
3. Vasopressors: use direct-acting (phenylephrine) rather than indirect-acting (ephedrine) - avoids catecholamine release in a catecholamine-sensitised patient
4. Muscle relaxants: the incidence of myasthenia gravis is increased in hyperthyroidism → reduce initial NMB dose; use a nerve stimulator (twitch monitor) to guide dosing
5. NIM tube for RLN monitoring: avoid muscle relaxants and topical laryngeal anaesthesia if using NIM endotracheal tube

Haemodynamic Profile to Anticipate

• Systolic hypertension + widened pulse pressure
• ↓ Systemic vascular resistance
• Sinus tachycardia / AF / high-output heart failure
• Increased sensitivity to catecholamines (upregulated β-receptors)

Beta-Blockers Intraoperatively (Mainstay)

• Control tachycardia, arrhythmias
• Esmolol infusion (50-350 mcg/kg/h, titrated) for acute rate control
• Test dose: 0.1-0.2 mg/kg esmolol; if heart rate slows without worsening heart failure - continue infusion
• Remember: beta-blockers do NOT prevent thyroid storm

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IV. Thyroid Storm - The Critical Emergency

What Triggers It

Clinical Features

Thyroid Storm vs. Malignant Hyperthermia (Critical Exam Distinction)

Management of Thyroid Storm

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V. Postoperative Complications (After Thyroidectomy)

Exam point: Laryngospasm after thyroidectomy should make you think hypocalcaemia first.

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VI. Special Situations

Emergency Surgery in Uncontrolled Hyperthyroidism

• Optimise with antithyroid drugs + SSKI + propranolol (oral) pre-induction
• Target HR <90 bpm
• Use direct-acting vasopressors only
• Avoid ketamine, ephedrine, anticholinergics
• Have esmolol infusion ready
• Glucocorticoids (dexamethasone) for severe disease

Subclinical Hyperthyroidism

• Still carries increased risk of AF and MACE perioperatively
• Monitor and control heart rate

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High-Yield Exam Points

1. Achieve euthyroidism before elective surgery - free T4 is the operative marker, not TSH
2. MAC is unchanged in hyperthyroidism; induction may be slower (high cardiac output)
3. Propofol infusion rate must be increased (increased clearance and Vd)
4. Avoid ketamine, pancuronium, anticholinergics, ephedrine, adrenaline-containing LAs
5. Use phenylephrine (direct-acting) for hypotension
6. Reduce NMB dose - association with myasthenia gravis
7. Propranolol = beta-blocker of choice (also blocks T4→T3 conversion)
8. Beta-blockers do NOT prevent thyroid storm
9. Thyroid storm = postoperative, hypokalemia, no ↑ ETCO2 → distinguishes from MH
10. After thyroidectomy: laryngospasm = hypocalcaemia until proven otherwise

Complete Anaesthetic Management of Hyperthyroidism

From Miller's Anesthesia (10e) & Barash/Stoelting's Clinical Anesthesia (9e)

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PREOPERATIVE MANAGEMENT

1. Primary Goal

"The most important goal in managing the hyperthyroid patient is to make the patient euthyroid before surgery, if possible." — Stoelting's (Barash), Ch. 47

2. Preoperative Assessment

• Cardiovascular: arrhythmias (especially AF), heart failure, systolic hypertension, widened pulse pressure
• Airway: degree of tracheal compression/deviation from goitre; review CT or MRI
• End-organ effects: muscle weakness (myopathy), bone loss, electrolytes
• Subclinical hyperthyroidism: even with normal T3/T4 and low TSH (<0.5 mU/L) - still increased risk of AF, MACE, heart failure
• Operative fitness criterion: normalisation of free T4 + absence of overt symptoms (TSH lags - do not wait for TSH normalisation)

3. Drug Therapy - Preoperative Preparation

Antithyroid Drugs (6-8 weeks required)

• Both are thiourea derivatives
• Normal glands store enough hormone to maintain euthyroidism for months even after synthesis is abolished - hence 6-8 weeks needed
• Toxic reactions (uncommon): skin rash, nausea, fever, agranulocytosis, hepatitis, arthralgias
• Continue all antithyroid medications on the morning of surgery

Beta-Blockers

• Dose: Propranolol titrated to effect + potassium iodide (2-5 drops every 8 hours)
• Preparation time: 7-14 days
• Beta-blockers do NOT inhibit hormone synthesis and do NOT prevent thyroid storm
• In heart failure: use with caution; small test dose of esmolol (0.1-0.2 mg/kg) - if HR slows without worsening failure, continue infusion at 50-350 mcg/kg/h

Potassium Iodide (SSKI) - Wolff-Chaikoff Effect

• Mechanism: inhibits iodide organification AND reduces synthesis and release of thyroid hormones; also reduces size and vascularity of the hyperplastic gland
• Onset: faster symptom control (7-10 days) vs. 2-6 weeks with antithyroid drugs alone
• Use: added when rapid preparation needed (e.g. before urgent thyroidectomy)
• CRITICAL: Antithyroid drugs must be started before iodide - iodide alone may initially worsen thyrotoxicosis
• Iopanoic acid (iodide-based contrast agent) has similar effects

Glucocorticoids

• Dexamethasone 8-12 mg/day (or hydrocortisone 50-100 mg IV every 6h)
• Indications: severe thyrotoxicosis; emergency surgery in uncontrolled hyperthyroid patient
• Mechanism: reduces thyroid hormone secretion + inhibits peripheral T4→T3 conversion

Emergency Surgery Protocol (Uncontrolled Hyperthyroid)

1. Antithyroid drug (PTU/methimazole)
2. SSKI after antithyroid drug
3. Beta-blocker to HR <90 bpm
4. Dexamethasone
5. Target: free T4 normalised + symptomatic control

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INTRAOPERATIVE MANAGEMENT

4. Airway

5. Drug Selection - What to Use and Avoid

AVOID

SAFE / PREFERRED

6. Key Intraoperative Principles (Miller's)

1. Slower induction: elevated cardiac output increases drug distribution and clearance - higher concentrations of volatile agents or higher propofol infusion rates may be needed
2. Adequate depth: maintain depth sufficient to prevent exaggerated sympathetic response to surgical stimulation
3. MAC unchanged: do not adjust inhalational agent MAC targets
4. Muscle relaxants - reduce initial dose: hyperthyroidism is associated with increased incidence of myasthenia gravis → use twitch monitor (nerve stimulator) for all subsequent NMB dosing
5. NIM tube for RLN monitoring: if using Nerve Integrity Monitor (NIM) endotracheal tube - avoid muscle relaxants and topical laryngeal anaesthesia (interfere with EMG signal)
6. Vasopressors: use direct-acting only (phenylephrine) - not indirect agents (ephedrine)
7. Invasive monitoring: individualised based on haemodynamic stability and procedure; especially useful in patients with significant LV dysfunction

7. Haemodynamic Profile Intraoperatively

• Systolic hypertension + widened pulse pressure
• ↓ Systemic vascular resistance
• Sinus tachycardia / AF / high-output heart failure
• Increased sensitivity to catecholamines (upregulated β-adrenergic receptors)

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THYROID STORM - INTRAOPERATIVE EMERGENCY

Recognition

Differential Diagnosis (Critical - from Stoelting's & Morgan Mikhail)

No laboratory test is diagnostic for thyroid storm. Free T4 often markedly elevated but diagnosis is clinical.

Management of Thyroid Storm (Stoelting's Table 47-3)

Invasive haemodynamic monitoring is especially useful in guiding treatment of patients with significant LV dysfunction.

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POSTOPERATIVE MANAGEMENT

After Thyroidectomy - Complications to Monitor

After Non-Thyroid Surgery in Hyperthyroid Patient

• Monitor for signs of thyroid storm (first 18 hours)
• Resume all antithyroid medications immediately
• Adequate analgesia (pain is a trigger for storm)

RLN Monitoring Protocol (Barash)

• Evaluate vocal cord function before AND after surgery (laryngoscopy or ask patient to phonate "E")
• If using NIM tube: muscles relaxants and topical laryngeal LA must be avoided
• Succinylcholine or small dose rocuronium acceptable for intubation only

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SUMMARY - High-Yield Points for MD Exam

From Miller's Anesthesia (10e)

1. Euthyroidism before surgery = normalised free T4, not TSH (TSH lags)
2. MAC is unchanged by hyperthyroidism
3. Induction may be slower (↑ cardiac output → ↑ drug distribution)
4. Propofol clearance and Vd increased → increase infusion rates for TIVA
5. Avoid ketamine, anticholinergics, pancuronium, ephedrine
6. Phenylephrine for hypotension (direct-acting)
7. Reduce NMB dose + use twitch monitor (myasthenia gravis association)
8. Subclinical hyperthyroidism still increases perioperative MACE and AF risk
9. Thyroid storm can occur up to 18 hours postoperatively

From Stoelting's/Barash Clinical Anesthesia (9e)

1. Propranolol = beta-blocker of choice (also blocks T4→T3 conversion)
2. Iodide AFTER antithyroid drugs - never before (can worsen thyrotoxicosis initially)
3. Combination: propranolol + SSKI (2-5 drops q8h) = standard pre-op preparation; takes 7-14 days
4. Dexamethasone (8-12 mg/day) for severe disease or emergency surgery
5. Beta-blockers do not prevent thyroid storm
6. HR <90 bpm = target for emergency surgery
7. Thyroid storm: hypokalemia distinguishes it from MH (which causes hyperkalemia)
8. In thyroid storm: aspirin is contraindicated as antipyretic
9. Difficult intubation 5-8% in goitre surgery; cancer (not goitre size) is the predictor
10. Laryngospasm post-thyroidectomy = hypocalcaemia until proven otherwise

• Phase 1 (Weeks 0-8): Antithyroid drugs (PTU/Methimazole) - the backbone of preparation
• Phase 2 (ongoing): Propranolol - for heart rate and symptom control, with the bonus of T4→T3 blockade
• Phase 3 (Day -7 to -10): SSKI added for rapid gland preparation before surgery
• Phase 4 (emergency only): Dexamethasone for severe or urgent cases
• Day of Surgery: Continue all drugs; fitness criterion is free T4 normalised + HR <90

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Anaesthesia in Hyperthyroidism

MD Theory Exam & Viva Answer

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THEORY ANSWER FORMAT (Long Essay / Short Note)

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Introduction

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A. PREOPERATIVE MANAGEMENT

1. Assessment

• Cardiovascular: palpitations, AF, heart failure, systolic hypertension, widened pulse pressure
• Airway: stridor, dyspnoea, dysphagia (tracheal/oesophageal compression from goitre)
• Neuromuscular: proximal muscle weakness, tremor
• Metabolic: weight loss, heat intolerance, diarrhoea

• Free T4, T3, TSH (free T4 is the operative fitness criterion - TSH lags)
• ECG (AF, sinus tachycardia, LVH)
• Echocardiography if heart failure suspected
• CT/MRI neck and chest - mandatory for large goitres to assess tracheal deviation, substernal extension
• Indirect laryngoscopy (baseline vocal cord function)
• U&E (hypokalaemia, hypercalcaemia)
• Blood glucose (risk of unmasking DM)

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2. Preoperative Preparation - The Timeline

Primary goal: Achieve euthyroidism before elective surgery (Miller's, Stoelting's)

Step 1 - Antithyroid Drugs (weeks 0 to 6-8)

• Takes 6-8 weeks to achieve euthyroidism
• Toxic effects: rash, agranulocytosis, hepatitis, arthralgias
• Continue on morning of surgery

Step 2 - Beta-Blockers (start early; can be added at any stage)

• Controls: tachycardia, tremor, anxiety, heat intolerance
• Any beta-blocker acceptable; long-acting agents more convenient
• Combination: propranolol + SSKI standard pre-op regimen (7-14 days)
• Does NOT prevent thyroid storm
• Does NOT inhibit hormone synthesis

Step 3 - Potassium Iodide/SSKI (day -7 to -10 before surgery)

• Wolff-Chaikoff effect: blocks iodide organification → inhibits synthesis AND release
• Also reduces gland size and vascularity (important for thyroidectomy)
• Faster control: 7-10 days vs 6-8 weeks with antithyroid drugs alone
• Dose: 2-5 drops every 8 hours (or sodium iodide 250 mg q6h)
• ⚠️ MUST start antithyroid drugs first - iodide alone can worsen thyrotoxicosis

Step 4 - Glucocorticoids (severe disease / emergency surgery)

• Dexamethasone 8-12 mg/day or hydrocortisone 50-100 mg q6h
• Reduces thyroid hormone secretion + blocks T4→T3 conversion
• Reserved for: severe thyrotoxicosis, emergency surgery, thyroid storm

Emergency Surgery Protocol

1. PTU/methimazole immediately
2. SSKI after antithyroid drug
3. Propranolol → HR < 90 bpm
4. Dexamethasone
5. Proceed when haemodynamically stable

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B. AIRWAY MANAGEMENT

• General endotracheal anaesthesia (standard)
• LMA - allows real-time vocal cord visualisation with spontaneous breathing (Stoelting's)
• Bilateral superficial cervical plexus block - for limited thyroidectomy

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C. INTRAOPERATIVE MANAGEMENT

1. What to AVOID

2. Safe / Preferred Drugs

3. Key Intraoperative Principles

1. Induction may be slower - elevated cardiac output increases drug distribution; higher agent concentrations required
2. MAC unchanged - do not alter volatile agent targets
3. Maintain adequate depth - prevent exaggerated sympathetic response to surgical stimulation
4. Muscle relaxants - reduce initial dose - increased incidence of myasthenia gravis in hyperthyroidism
5. Use nerve stimulator (twitch monitor) for all subsequent NMB dosing (Stoelting's)
6. Direct vasopressors only for hypotension (phenylephrine)
7. Invasive monitoring individualised - especially if significant LV dysfunction
8. NIM tube for RLN monitoring: avoid NMB and topical LA if used

4. Expected Haemodynamic Profile

• Systolic hypertension + widened pulse pressure
• ↓ SVR with ↑ cardiac output
• Sinus tachycardia / AF
• Increased catecholamine sensitivity (↑ β-receptor density)

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D. THYROID STORM

Triggers

Clinical Features

Thyroid Storm vs MH - The Critical Distinction

Management of Thyroid Storm (Stoelting's Table 47-3)

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E. POSTOPERATIVE COMPLICATIONS (after Thyroidectomy)

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VIVA QUESTIONS & MODEL ANSWERS

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To achieve euthyroidism before elective surgery. The operative fitness criterion is normalisation of free T4 with absence of overt symptoms - not TSH, which lags weeks behind clinical response.

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Propranolol is unique among beta-blockers because it not only controls hyperadrenergic symptoms (tachycardia, tremor, anxiety, heat intolerance) but also inhibits the peripheral conversion of T4 to the more active T3 - an effect seen over 1-2 weeks. Other beta-blockers lack this additional antithyroid mechanism.

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Iodide (SSKI) works via the Wolff-Chaikoff effect to block hormone synthesis and release. However, if given alone initially, it can paradoxically worsen thyrotoxicosis (by transiently increasing hormone availability or through Jod-Basedow effect). Starting antithyroid drugs first ensures that any hormone released by iodide cannot contribute to toxicity.

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No. MAC is not altered by hyperthyroidism (Miller's, Stoelting's). However, induction may be slower because the elevated cardiac output increases drug distribution volume and clearance, requiring higher concentrations. Propofol TIVA infusion rates must be increased for the same reason.

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Hyperthyroidism is associated with an increased incidence of myasthenia gravis (an autoimmune overlap). Myasthenic patients are highly sensitive to non-depolarising NMBs. The initial dose should be reduced and a nerve stimulator (twitch monitor) used to guide all subsequent dosing.

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The key distinguishing features are: thyroid storm typically presents postoperatively, with hypokalemia, no rise in ETCO2, no muscle rigidity, and no elevation of CK. MH presents intraoperatively during volatile/succinylcholine exposure with early rise in ETCO2, hyperkalemia, rigidity, massively elevated CK, and severe metabolic acidosis. MH responds to dantrolene; thyroid storm does not.

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Aspirin displaces T4 from thyroid-binding globulin, increasing the concentration of free (active) T4 in circulation - this worsens the thyrotoxic state. Paracetamol (acetaminophen) is the safe antipyretic of choice.

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A substernal goitre behaves like an anterior mediastinal mass and can cause intrathoracic airway obstruction after induction of general anaesthesia due to loss of negative intrathoracic pressure and muscle tone supporting the airway. CT/MRI must be reviewed preoperatively. An awake fibreoptic approach should be considered.

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Hypocalcaemia due to inadvertent parathyroid removal (hypoparathyroidism). Symptoms develop 24-96 hours after total thyroidectomy. Laryngeal stridor progressing to laryngospasm is one of the first signs of hypocalcaemic tetany. Treatment: IV calcium chloride or calcium gluconate; also check and correct magnesium.

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Hyperthyroidism upregulates β-adrenergic receptor density in the heart, skeletal muscle, and adipose tissue, making the patient highly sensitive to catecholamines. Indirect vasopressors (ephedrine) work by releasing endogenous catecholamines, which in this sensitised state can precipitate severe hypertension, tachyarrhythmias, and myocardial ischaemia. Direct-acting vasopressors (phenylephrine) bypass this mechanism and are safe.

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No. Beta-blockers only provide symptomatic control by blunting the hyperadrenergic manifestations. They do not inhibit thyroid hormone synthesis or secretion and cannot prevent thyroid storm. Only achieving euthyroidism (via antithyroid drugs) reduces that risk.

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Apathetic hyperthyroidism occurs in elderly patients who present with depression, withdrawal, and cardiac features (AF, heart failure) without the classic sympathomimetic features (anxiety, tremor, weight loss). It is relevant because the diagnosis may be missed preoperatively, and these patients are at high risk of haemodynamic instability and thyroid storm under anaesthesia without appropriate preparation.

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One-Line Revision Points

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Extubation Strategy After Thyroid Surgery

From Miller's Anesthesia (10e) & Barash/Stoelting's Clinical Anesthesia (9e)

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Why Extubation is High-Risk After Thyroid Surgery

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The Core Principle

"Gentle emergence from anaesthesia is necessary to avoid coughing on the ETT and the possibility of haematoma formation from venous engorgement." — Miller's Anesthesia 10e

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Step-by-Step Extubation Strategy

Step 1 - Pre-extubation Checklist (Before Any Attempt)

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Step 2 - Smooth Emergence (Prevent Coughing)

Key point from Miller's: Deep extubation is NOT recommended after thyroid surgery despite reducing coughing - the risk of airway obstruction outweighs the benefit.

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Step 3 - Assess for Tracheomalacia Before Extubation

1. Do not extubate in the operating theatre - transfer to ICU with ETT in situ
2. Consider planned tracheostomy intraoperatively (discuss with surgeon)
3. If extubation attempted - use Airway Exchange Catheter (AEC) strategy (see Step 5)

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Step 4 - RLN Assessment at Extubation

• Ask patient to phonate: say the sound "E" (Stoelting's)
• Normal phonation = bilateral cord function likely intact
• Hoarse/weak voice = suspect unilateral injury (usually tolerated; observe)
• No voice / aphonia + stridor = suspect bilateral injury → do NOT extubate; reintubate or proceed to tracheostomy

• Intraoperative EMG monitoring provides real-time RLN data
• Surgeon should communicate nerve integrity status before extubation

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Step 5 - The "Staged / Bailey Manoeuvre" Extubation

• Long-standing/substernal goitre (tracheomalacia risk)
• Difficult original intubation
• Significant intraoperative airway oedema
• Bilateral RLN at risk (e.g. completion thyroidectomy, central neck dissection)
• Any doubt about post-extubation airway safety

1. Preoxygenate fully (FiO2 1.0) before extubation
2. Lubricate AEC; select AEC with external diameter closest to internal diameter of the reintubation ETT
3. Insert AEC to depth of ETT bevel (match depth markings on AEC with markings on ETT)
4. Aim for mid-tracheal positioning of AEC tip to avoid endobronchial placement
5. Remove ETT carefully while holding AEC position
6. Leave AEC in situ as a guide rail for reintubation if needed
7. AEC has a central lumen - can provide supplemental O2 (jet ventilation in emergency)
8. Keep AEC in place for 30-60 minutes post-extubation while monitoring in theatre or recovery
9. If reintubation required: advance ETT over AEC; if hang-up at glottis - lift tongue with laryngoscope + rotate ETT 90° anticlockwise

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Step 6 - Post-Extubation Position and Monitoring

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Post-Extubation Emergencies - Recognition and Response

1. Haematoma (Most Time-Critical)

2. Bilateral RLN Palsy

3. Tracheomalacia

4. Hypocalcaemia / Laryngospasm

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Summary - Extubation Decision Framework

Before extubation:
    ├─ Long-standing goitre? → Test for tracheomalacia (cuff test / bronchoscopy)
    ├─ Difficult original intubation? → Use AEC strategy
    ├─ RLN at high risk? → Phonate "E" + laryngoscopy before extubation
    └─ All clear?
           ↓
    Smooth emergence:
    → Remifentanil infusion 0.01-0.05 mcg/kg/min
    → Avoid deep extubation
    → Fully awake, cooperative, NMB reversed
           ↓
    Extubate in 30-45° head-up position
           ↓
    AEC left in situ if ANY doubt (staged extubation)
           ↓
    Recovery: SpO2 monitoring + wound checks q15 min
           ↓
    Voice check before discharge from recovery

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Viva Points on Extubation

Although deep extubation prevents coughing and reduces haematoma risk, it is avoided because there is a significant risk of airway obstruction - both from cord oedema/palsy and tracheomalacia. Recovery of airway reflexes is needed to protect against obstruction. (Barash/Stoelting)

A low-dose remifentanil infusion (0.01-0.05 mcg/kg/min) is a popular technique to allow smooth, awake extubation without coughing - preserving airway reflexes while blunting the cough reflex. This prevents venous engorgement and haematoma formation. (Miller's)

With the ETT still in situ, the cuff is deflated. If the patient can breathe around the ETT, there is adequate tracheal lumen and tracheomalacia/oedema is less likely to cause obstruction after extubation. Failure suggests critical narrowing.

Haematoma typically presents within the first few hours with visible neck swelling and progressive stridor - relieved partially by wound opening. Tracheomalacia presents immediately on extubation as sudden airway collapse without external swelling; requires reintubation and tracheostomy.

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The Bailey Manoeuvre

From Miller's Anesthesia (10e) & Barash/Stoelting's Clinical Anesthesia (9e)

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Definition

"An alternative extubation technique, known as the Bailey maneuver, involves exchanging an ETT for an SGA while the patient is under deep anaesthesia." — Miller's Anesthesia, 10e

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The Problem It Solves

• Smooth like deep extubation (no coughing on ETT)
• Protected like awake (SGA maintains airway until patient wakes fully)

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Indications

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How It Is Performed - Step by Step

Prerequisites Before Starting

• Patient is deeply anaesthetised (surgical stage III)
• Neuromuscular blockade fully reversed
• Oropharynx suctioned under deep anaesthesia
• Bite block placed (rolled gauze between molars - not OPA, which can cause dental damage) (Miller's)
• Patient preoxygenated (FiO2 1.0)
• Size-appropriate LMA selected and checked

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The Technique (Barash/Stoelting, Ch. 28)

Step 1:
Patient deeply anaesthetised; ETT still in situ
              ↓
Step 2:
Deflate LMA cuff completely
              ↓
Step 3:
Insert the deflated LMA into the oropharynx
BEHIND the in-situ ETT
(slide LMA posteriorly into hypopharynx around the ETT)
              ↓
Step 4:
Confirm LMA tip seated in hypopharynx
              ↓
Step 5:
Remove the ETT (withdraw over the LMA)
              ↓
Step 6:
Inflate the LMA cuff
              ↓
Step 7:
Confirm airway patency via capnography / chest rise / SpO2
              ↓
Step 8:
Allow patient to emerge via LMA
(smooth, no laryngeal stimulation, no coughing)
              ↓
Step 9:
Remove LMA when fully awake - either:
  (a) Deeply anaesthetised, OR
  (b) After full return of protective reflexes + patient opens mouth on command

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Variant - When SGA Was Used as Intubation Conduit

• At end of surgery, deflate the SGA cuff and leave device in situ
• Remove the ETT, leaving the SGA as the primary airway
• Conduct emergence via SGA

"This technique can be of great benefit in cases in which an ETT is needed intraoperatively but coughing or hypertension during emergence would be deleterious." (Barash/Stoelting)

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Advantages of the Bailey Manoeuvre

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Disadvantages / Limitations

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Bailey Manoeuvre vs. AEC vs. Deep Extubation

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LMA Removal During/After Bailey Manoeuvre

1. While deeply anaesthetised - smooth, no stimulation
2. After protective reflexes fully returned - patient can open mouth on command

Avoid removal during stage II excitation - associated with coughing and laryngospasm.

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Relevance to Thyroid Surgery Specifically

• Need for ETT intraoperatively: surgical access, RLN monitoring (NIM tube), airway protection
• Need to avoid coughing at extubation: prevents venous engorgement and haematoma

• Full intraoperative ETT + NIM monitoring
• Smooth exchange to LMA under deep anaesthesia at end of surgery
• Patient waking on LMA without ever coughing on the tracheal tube

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Viva Questions

Exchanging an endotracheal tube for a supraglottic airway device (typically LMA) while the patient is under deep anaesthesia, allowing smooth cough-free emergence while maintaining airway control.

The LMA cuff is deflated and the LMA is inserted into the oropharynx behind the in-situ ETT. The ETT is then withdrawn, the LMA cuff is inflated, and the patient emerges through the LMA.

Patients at high risk of bronchospasm in whom tracheal intubation was required for surgery - the LMA causes far less bronchospasm than an ETT on emergence.

The AEC is recommended by the ASA as first-line for difficult airway extubation because it provides a direct guide rail for immediate reintubation if the airway is lost after extubation. The Bailey manoeuvre does not provide this safety feature - if the LMA fails, standard laryngoscopy is required with no pre-positioned guide. (Miller's)

Full stomach / aspiration risk - the LMA does not protect against regurgitation. Also avoid with very limited mouth opening.

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Is the Preoperative Preparation According to Latest Guidelines?

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Side-by-Side Comparison

1. Antithyroid Drugs - UPDATED GUIDANCE

Key update: Methimazole is the first-line drug. PTU is second-line due to hepatotoxicity risk. For the MD exam, always state methimazole as preferred and know the dose-titration scheme.

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2. Beta-Blockers - CONSISTENT WITH UPDATES

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3. Potassium Iodide / Lugol's Solution - UPDATED GUIDANCE

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4. Glucocorticoids - CONSISTENT

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5. Rapid Preparation Regimen - NEW IN GUIDELINES (Not in Textbooks)

Option A - Iodide-based rapid preparation (ATA / current reviews)

Option B - Iodinated contrast agent (iopanoic acid / iodide)

These rapid protocols are increasingly used in real clinical practice but are not in Miller's or Stoelting's - important for viva.

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6. Cholestyramine - MENTIONED IN TEXTBOOKS, CONFIRMED IN GUIDELINES

• 4g q6h used as adjunct (bile acid sequestrant)
• Interrupts enterohepatic recirculation of thyroid hormones
• Confirmed as useful adjunct in rapid preparation regimens
• ✅ Consistent between textbooks and guidelines

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7. Fitness Criterion for Surgery - UPDATED

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What the Textbooks Get Right

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What the Textbooks Miss or Understate

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For Your MD Exam and Viva - What to Say

"The preoperative preparation taught in Miller's and Stoelting's is broadly consistent with ATA 2016 guidelines. However, current guidelines clarify that methimazole is the preferred first-line antithyroid drug over PTU due to PTU's hepatotoxicity risk. PTU is now reserved for first-trimester pregnancy, thyroid storm, and methimazole intolerance. The methimazole dose should be titrated to the degree of fT4 elevation. Iodide should not be continued beyond 10 days due to the risk of Wolff-Chaikoff escape. In patients intolerant of thionamides, a rapid preparation regimen using Lugol's solution, dexamethasone, and beta-blockers can achieve clinical euthyroidism within 7-10 days. T3 levels should be monitored separately from fT4 as the criterion for euthyroidism, as T3 may remain elevated despite fT4 normalisation."

Preoperative Preparation for Hyperthyroidism Before Surgery

Exam Answer (ATA 2016 + AAES 2020 + Current Evidence)

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Introduction

1. Achieve euthyroidism before elective surgery
2. Minimise risk of thyroid storm perioperatively
3. Reduce intraoperative blood loss (for thyroidectomy)
4. Control cardiovascular manifestations

Fitness criterion: Normalisation of free T4 AND T3 + absence of overt symptoms + HR <80 bpm (Do NOT wait for TSH - it lags weeks behind clinical response)

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STEP 1 - Antithyroid Drugs (Weeks 0 to 6-8)

Drug of Choice: Methimazole (ATA 2016 - First Line)

• Monitor TFTs every 4-8 weeks
• Monitor T3 separately - may remain elevated even when fT4 normalises
• Reduce to maintenance (5-10 mg/day) as thyroid function improves
• Continue on the morning of surgery

When to Use PTU Instead (ATA 2016 - Second Line Only)

1. First trimester of pregnancy
2. Thyroid storm
3. Methimazole intolerance or side effects

⚠️ PTU is NOT first-line due to risk of hepatotoxicity (hepatic failure, agranulocytosis). ETA 2022 states it "should not be used" routinely.

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STEP 2 - Beta-Blockers (Start Early; Can Add at Any Stage)

Drug of Choice: Propranolol

• Controls hyperadrenergic symptoms within 12-24 hours
• Uniquely also inhibits peripheral T4→T3 conversion (over 1-2 weeks)
• No other beta-blocker has this additional antithyroid effect

• Does NOT inhibit hormone synthesis
• Does NOT prevent thyroid storm
• Use cautiously in heart failure - test with small dose of esmolol (0.1-0.2 mg/kg) first

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STEP 3 - Potassium Iodide / Lugol's Solution (Day -10 to Day -1 Before Surgery)

Mechanism - Wolff-Chaikoff Effect

Preparation

Key Rules (ATA 2016)

1. ALWAYS start antithyroid drug BEFORE iodide
   • Iodide given alone can initially worsen thyrotoxicosis
   • Optimal: give iodide 1 hour after thionamide dose
   • Exception: In patients intolerant of thionamides, iodide + beta-blocker alone may still be used
2. Do NOT continue iodide beyond 10 days
   • Risk of Wolff-Chaikoff escape after 10 days: gland adapts, resumes hormone synthesis
   • Textbooks do not mention this - important exam point
3. Benefits for thyroid surgery specifically:
   • Reduces thyroid blood flow and vascularity
   • Reduces intraoperative blood loss
   • Some guidelines recommend iodide in all Graves' thyroidectomy patients (even if euthyroid) for this haemostatic benefit

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STEP 4 - Glucocorticoids (Severe Disease / Emergency Surgery)

Indications

• Severe thyrotoxicosis
• Emergency surgery in uncontrolled hyperthyroid patient
• Thyroid storm

Regimen

Glucocorticoids block T4→T3 conversion - the same mechanism as propranolol and PTU. Triple blockade of T4→T3 conversion (propranolol + PTU + dexamethasone) is used in thyroid storm.

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STEP 5 - Cholestyramine (Adjunct)

• Dose: 4 g every 6 hours
• Mechanism: Bile acid sequestrant - interrupts enterohepatic recirculation of thyroid hormones
• Reduces circulating T4/T3 load faster
• Used as adjunct in rapid preparation and thyroid storm

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Standard Preoperative Timeline

WEEKS 0-6                WEEK 6-8               DAY -10 to -1         DAY OF SURGERY
─────────────────────────────────────────────────────────────────────────►
│ Methimazole           │ Confirm euthyroid    │ Add SSKI/Lugol's    │ Continue ALL drugs
│ (dose per fT4)        │ Free T4 + T3 normal  │ 2-5 drops q8h       │ in morning
│                       │                      │ Max 10 days only     │
│ Propranolol           │ HR <80 bpm           │                     │ Check HR, fT4
│ (titrate to HR)       │                      │                     │
└───────────────────────┴──────────────────────┴─────────────────────┴──────────────────

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Emergency / Rapid Preparation (When Surgery Cannot Wait)

For patients who can take thionamides:

1. Methimazole (high dose) or PTU
2. SSKI / Lugol's (1 hour after thionamide)
3. Propranolol (HR <80 bpm)
4. Dexamethasone
5. Cholestyramine (adjunct) → Target: 7-10 days to clinical euthyroidism

For patients intolerant of thionamides (ATA 2016 exception):

Iopanoic acid (iodinated contrast) based regimen:

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Fitness for Surgery - Checklist

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Summary - Key Exam Points

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Intraoperative Management of Hyperthyroidism

MD Exam Answer (Miller's 10e + Stoelting's/Barash 9e)

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Introduction

"To achieve a depth of anaesthesia that prevents an exaggerated sympathetic response to surgical stimulation, while avoiding drugs that stimulate the sympathetic nervous system." — Stoelting's (Barash), Ch. 47

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A. MONITORING

Standard Monitoring (All Cases)

• ECG (continuous - detect AF, tachyarrhythmias)
• SpO2
• ETCO2 (capnography - also helps distinguish thyroid storm from MH)
• Temperature (continuous - detect early hyperthermia)
• Non-invasive blood pressure

Enhanced / Invasive Monitoring (Individualised)

• Haemodynamic instability preoperatively
• Significant LV dysfunction / heart failure
• Uncontrolled AF or high-output failure

"Invasive haemodynamic monitoring is especially useful in guiding treatment of patients with significant left ventricular dysfunction." - Stoelting's

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B. AIRWAY MANAGEMENT

Preoperative Airway Assessment (Review Before Induction)

• Review CT/MRI for tracheal deviation, substernal extension, airway narrowing
• Indirect laryngoscopy - document baseline vocal cord function
• Assess mouth opening, neck extension, Mallampati

Expected Difficulties

Airway Plan

Tube Size and Position

• Standard ETT unless nasal intubation needed (transoral thyroidectomy)
• NIM (Nerve Integrity Monitor) ETT if surgeon requires RLN monitoring intraoperatively
• Confirm tube position after head and neck repositioning for surgical exposure

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C. INDUCTION

Agent of Choice: Propofol

Avoid at Induction

Induction Speed

• Induction may be slower than expected - elevated CO distributes drug rapidly
• Higher inhalational concentrations or higher propofol doses may be required

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D. MAINTENANCE OF ANAESTHESIA

Inhalational Agents

TIVA (Total Intravenous Anaesthesia)

Depth of Anaesthesia - Critical Principle

• Maintain adequate anaesthetic depth throughout surgery
• Inadequate depth → sympathetic surge → tachycardia, hypertension, risk of storm
• Use BIS/entropy monitoring if available to guide depth
• Deepen anaesthesia before skin incision and during stimulating surgical steps

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E. DRUGS TO AVOID - COMPLETE LIST

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F. SAFE / PREFERRED DRUG CHOICES

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G. MUSCLE RELAXANTS - SPECIAL CONSIDERATION

"The incidence of myasthenia gravis is increased in hyperthyroid patients; thus, the initial dose of muscle relaxant should be reduced, and a twitch monitor should be used to titrate subsequent doses." — Stoelting's (Barash)

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H. CARDIOVASCULAR MANAGEMENT

Expected Haemodynamic Profile

Intraoperative Haemodynamic Targets

Rate Control Intraoperatively

• Test dose: 0.1-0.2 mg/kg IV bolus
• If HR slows without worsening heart failure → start infusion
• Infusion: 50-350 mcg/kg/h, titrate to HR

• Beta-blockers used cautiously
• Controlled HR improves diastolic filling and cardiac function
• Short-acting esmolol titrated by clinical response

Vasopressors

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I. FLUID MANAGEMENT

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J. TEMPERATURE MANAGEMENT

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K. THYROID STORM - INTRAOPERATIVE RECOGNITION AND RESPONSE

Intraoperative Signs (occur during or within 18 hours post-op)

Immediate Management of Thyroid Storm (Stoelting's Table 47-3)

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L. POSITIONING

• Neck extension for thyroid surgery - can cause haemodynamic changes and stress on cervical vessels
• Ensure adequate padding under neck/shoulders
• Recheck ETT/NIM tube position after final positioning
• Head-up tilt (15-20°) reduces venous engorgement and surgical bleeding

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M. RLN MONITORING (When NIM Tube Used)

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Summary Table for Exam

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Anaesthetic Management in Hypothyroidism

MD Exam Answer — Miller's 10e + Barash/Stoelting 9e

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Introduction

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Causes

• Autoimmune: Hashimoto thyroiditis (most common worldwide)
• Previous radioiodine (131I) therapy
• Surgical removal of thyroid
• Drugs: PTU, methimazole, amiodarone, lithium
• Severe iodine depletion
• Infiltrative disease (amyloidosis, sarcoidosis)

Distinguish from Euthyroid Sick Syndrome (critical illness): low T3/T4 with near-normal TSH; no treatment required - resolves with underlying illness (Miller's)

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Pathophysiology - Multi-system Effects

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A. PREOPERATIVE MANAGEMENT

1. Assessment

• Duration and severity of hypothyroidism
• Current thyroid replacement therapy and compliance
• Symptoms: fatigue, cold intolerance, constipation, cognitive slowing, voice change, OSA symptoms
• Cardiovascular symptoms: chest pain, dyspnoea, ankle swelling

• Macroglossia, goitre, periorbital oedema, hoarse voice
• Bradycardia, BP (narrow pulse pressure)
• Signs of pericardial effusion (muffled heart sounds, raised JVP)
• Signs of heart failure

• TSH, free T4, T3
• ECG: bradycardia, low voltage, prolonged QTc, flat/inverted T waves
• Echocardiography: pericardial effusion, LV dysfunction
• Haemoglobin (anaemia common)
• Electrolytes: hyponatraemia, hypoglycaemia
• Coagulation screen (von Willebrand factor deficiency)
• Cholesterol (often elevated)
• Cortisol (if adrenal insufficiency suspected)

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2. When to Operate - Severity Guide (Miller's + Stoelting's)

"Anesthesia management has few implications in patients with mild to moderate hypothyroidism." - Miller's

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3. Preoperative Thyroid Replacement

Special rule for CAD patients: Thyroid replacement can unmask or worsen angina - initiate at low dose and titrate slowly. In symptomatic/unstable CAD: delay thyroid replacement until after coronary revascularisation (Stoelting's)

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4. Adrenal Insufficiency Consideration

• Longstanding or severe hypothyroidism → blunted stress response → risk of adrenal insufficiency
• Give stress-dose hydrocortisone perioperatively if suspected
• Hydrocortisone 100 mg IV at induction; continue 25 mg q6h for 24 hours

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B. AIRWAY MANAGEMENT

Airway Strategy

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C. INDUCTION

Preferred Agent: Ketamine (Stoelting's - unique to hypothyroidism)

"Ketamine has been proposed as the ideal induction agent because it stimulates the sympathetic nervous system." - Stoelting's

• Counteracts the bradycardia, ↓ CO, and ↓ SVR of hypothyroidism
• Maintains heart rate and blood pressure
• Contrast with hyperthyroidism (where ketamine is absolutely contraindicated)

Propofol / Other Agents

• Can be used, but:
  • Vasodilatory and cardiodepressant effects exaggerated in hypothyroidism
  • Use reduced doses - severe disease has ↓ cardiac output, ↓ drug clearance, ↑ sensitivity
  • Profound hypotension can result from standard doses

Key Principle

• All induction agents have exaggerated haemodynamic effects in severe hypothyroidism due to:
  • Already reduced cardiac output
  • Fixed bradycardia
  • Decreased intravascular volume (narrow pulse pressure)

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D. MAINTENANCE

Inhalational Agents

• All acceptable
• MAC: little if any decrease in hypothyroidism (Stoelting's)
• However, vasodilatory + cardiodepressant effects can exaggerate hypotension - use lower concentrations in severe disease

TIVA

• Propofol safe at reduced doses
• Drug clearance decreased (↓ hepatic blood flow, ↓ cardiac output) → drugs last longer
• Avoid high infusion rates; titrate carefully

Regional Anaesthesia

• Excellent choice in hypothyroid patients (Stoelting's)
• Avoids respiratory depression, prolonged sedation
• Caveat: maintain intravascular volume - sympathetic blockade from neuraxial anaesthesia + already reduced SVR → profound hypotension

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E. DRUGS TO USE CAREFULLY OR AVOID

Safe/Preferred

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F. CARDIOVASCULAR MANAGEMENT

Expected Intraoperative Haemodynamic Profile

Key Considerations

1. Monitor for hypotension - cardinal intraoperative risk; direct monitoring (arterial line) in severe cases
2. Bradycardia - treat with atropine or glycopyrrolate; chronotropic agents may be needed
3. Pericardial effusion - tamponade risk; echocardiography preoperatively if suspected
4. Prolonged QTc - risk of ventricular arrhythmias; avoid QT-prolonging drugs
5. Congestive heart failure - rarely occurs without coexisting heart disease; but monitor for it

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G. RESPIRATORY MANAGEMENT

Implications

• Consider controlled ventilation intraoperatively (do not rely on spontaneous breathing in severe cases)
• Postoperative: high risk for respiratory depression and prolonged ventilation
• Extubate only when fully awake, with good tidal volumes and reversal confirmed
• Monitor closely for OSA in recovery

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H. TEMPERATURE MANAGEMENT

• Hypothyroid patients are already hypothermic (reduced basal metabolic rate)
• Active warming mandatory: forced-air warming blanket, warm IV fluids, warm theatre
• However, Stoelting's states: "Cover to conserve body heat; no warming blankets" in myxedema coma (risk of vasodilation causing cardiovascular collapse)
• Monitor temperature continuously

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I. METABOLIC AND ELECTROLYTE MANAGEMENT

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J. POSTOPERATIVE MANAGEMENT

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K. MYXEDEMA COMA - THE EMERGENCY

Definition

Precipitants

Features

Anaesthetic Rule

"Only lifesaving surgery should proceed in the face of myxedema coma." - Stoelting's

Management (Stoelting's Table 47-5)

Expected response: improvements in HR, BP, and temperature within 24 hours of thyroid replacement

⚠️ Thyroid replacement can precipitate myocardial ischaemia - especially in patients with CAD

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Summary Tables for Exam

Hypothyroidism vs Hyperthyroidism - Anaesthetic Contrast

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High-Yield Exam Points

1. Mild/moderate hypothyroidism: no compelling reason to postpone surgery (Stoelting's)
2. Severe hypothyroidism: postpone elective surgery until partially treated
3. Ketamine is the preferred induction agent (sympathomimetic) - contrast with hyperthyroidism
4. MAC is not significantly reduced (Stoelting's)
5. Drug clearance is decreased - all drugs last longer; use reduced doses
6. Opioids and sedatives exaggerate already-impaired ventilatory responses - use judiciously
7. Regional anaesthesia is excellent - but maintain volume (hypotension risk)
8. Coagulopathy from acquired vWS - check coagulation; DDAVP available
9. T4 replacement can cause angina in CAD patients - titrate slowly
10. In CAD: delay T4 replacement until after coronary revascularisation (Stoelting's)
11. Myxedema coma: only lifesaving surgery; IV T4 200-300 mcg loading; IV hydrocortisone; NO active warming
12. Myxedema mortality: 25-50%
13. Euthyroid sick syndrome: do not treat - resolves with underlying illness

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Eye Signs in Graves' Ophthalmopathy

MD Exam Answer

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Introduction

Key distinction: Lid retraction and lid lag from sympathetic overactivity occur in ALL causes of thyrotoxicosis. True Graves' ophthalmopathy (proptosis, ophthalmoplegia, chemosis) is unique to Graves' disease and is autoimmune in origin - it can occur even without hyperthyroidism (10% of cases).

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Pathophysiology

• TSH receptor antibodies cross-react with antigens on orbital fibroblasts and extraocular muscle cells
• This triggers lymphocytic infiltration and deposition of glycosaminoglycans in retro-orbital and orbital tissues
• Results in: swelling of extraocular muscles + proliferation of orbital fat → increased orbital pressure → proptosis
• Late stage: fibrosis → muscle tethering → restrictive ophthalmoplegia

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Classification of Eye Signs

Group A - Non-specific (Sympathomimetic - Any Thyrotoxicosis)

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Group B - Specific to Graves' Ophthalmopathy (Infiltrative/Autoimmune)

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Clinical Images (Kanski's Clinical Ophthalmology, 10th Ed.)

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NO SPECS Classification (Harrison's 22e)

⚠️ Patients do not necessarily progress sequentially through classes - class 6 (optic neuropathy) can occur without severe proptosis. EUGOGO (European Group on Graves' Orbitopathy) scoring is now preferred in clinical practice as it assesses disease activity separately from severity.

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Summary Table - All Named Eye Signs

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Clinical Course (Harrison's 22e)

• Typically worsens over 3-6 months, then plateaus 12-18 months, then partial improvement
• Thyroid dysfunction can worsen eye signs; but ophthalmopathy follows its own independent course from thyroid disease
• Can precede or follow thyrotoxicosis by years
• Radioiodine therapy (especially in smokers) can worsen ophthalmopathy - use steroids cover if radioiodine given in active disease
• Smoking is the single most important modifiable risk factor

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Urgent Referral Criteria (Scott-Brown's)

• Visual acuity deteriorating
• Colour vision affected
• Corneal exposure / ulceration
• Papilloedema
• Severe periorbital oedema with inability to close eye

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High-Yield Exam Points

1. Graves' ophthalmopathy occurs in ~1/3 clinically; most have subclinical orbital changes on imaging
2. 10% have ophthalmopathy without hyperthyroidism (euthyroid ophthalmopathy)
3. Von Graefe, Dalrymple, Stellwag, Kocher = sympathomimetic (non-specific)
4. Proptosis, chemosis, ophthalmoplegia = infiltrative (Graves' specific)
5. Most serious complication = compressive optic neuropathy (→ permanent blindness)
6. Most common motility deficit = inferior rectus fibrosis → defect in elevation (mimics SR palsy)
7. NO SPECS: 0-1 (lid signs) → 2 (soft tissue) → 3 (proptosis) → 4 (EOM) → 5 (cornea) → 6 (sight)
8. Smoking = biggest modifiable risk; radioiodine can worsen active disease
9. Course of ophthalmopathy is independent of thyroid disease
10. Thyroid dermopathy (pretibial myxoedema) almost always accompanies moderate-severe ophthalmopathy