Level 2 of 6Must-remember

Thyroid emergencies: thyroid storm and myxoedema crisis

Assess, manage and stay safe — enough on its own

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The card — assess, manage, caution

Assessment— look, ask, measure

Two opposite emergencies, both diagnosed clinically: thyrotoxic crisis (thyroid storm), whose mortality is 8–25%, and myxoedema crisis, whose classical mortality is about 50% — in both, the biochemistry is confirmatory rather than diagnostic and treatment is started on suspicion.
Recognise storm by the combination: fever often high and out of proportion to any infection, central nervous system disturbance progressing from agitation through delirium to stupor, seizure and coma, marked tachycardia often above 140/min or rapid atrial fibrillation, cardiac failure, and gastrointestinal–hepatic dysfunction with nausea, vomiting, profuse diarrhoea, abdominal pain and unexplained jaundice.
Look for the background thyrotoxicosis: weight loss despite a normal or increased appetite (about 5% gain weight), heat intolerance and sweating, warm moist skin, palmar erythema, palpitations, dyspnoea, angina, systolic hypertension with a wide pulse pressure, tremor, irritability, emotional lability, psychosis, hyper-reflexia with ill-sustained clonus, proximal myopathy, diarrhoea, vomiting, lid retraction and lid lag.
Spend thirty seconds on the neck and the eyes: a diffuse soft goitre with a bruit is Graves disease, an irregular knobbly gland a multinodular goitre, and a fresh scar changes the entire differential; exophthalmos, periorbital oedema, diplopia, pretibial myxoedema and acropachy are specific to Graves, whereas lid lag and lid retraction occur with every cause.
Recognise myxoedema crisis by the classical patient: an older woman, cold, slow, swollen and not fully rousable, whose temperature has not been properly measured — with hypothermia that may reach 25°C, absent shivering and absent fever despite sepsis.
Take a rectal temperature with a low-reading thermometer in any drowsy, cold or elderly patient: an ordinary thermometer that will not read below 35°C simply reports "35" and conceals the diagnosis.
The rest of the myxoedema picture: somnolence, obtundation, stupor or coma, seizures in a substantial minority, cerebellar ataxia, psychosis ("myxoedema madness"), and delayed relaxation of the tendon reflexes — sought at the ankle, watching the return rather than the kick.
Face, airway and chest in myxoedema: periorbital puffiness, purplish lips, malar flush, pallor or a lemon-yellow carotenaemic tint, loss of the lateral eyebrows, dry coarse skin and hair, non-pitting oedema of hands, feet and eyelids, a hoarse low-pitched voice, a large tongue, deafness, hypoventilation, type 2 respiratory failure and pleural effusion.
Circulation and gut in myxoedema: bradycardia, hypertension early and hypotension late, pericardial effusion, constipation and ileus — and hypotension characteristically refractory to vasopressors until thyroid hormone is replaced.
Danger signs in thyrotoxicosis: core temperature ≥ 38.5°C without infective explanation; altered consciousness; heart rate ≥ 140/min; new or worsening pulmonary oedema; new atrial fibrillation with compromise; hypotension; jaundice.
Danger signs in hypothyroidism: core temperature < 35°C measured rectally with a low-reading thermometer; any depression of consciousness; hypercapnia; bradycardia < 50/min; hypotension; seizure; hyponatraemia; hypoglycaemia.Not available at your setup — Serum electrolytes.
Hunt the precipitant in every case — it is what kills the patient. For storm: infection (much the commonest), thyroidectomy in a patient not rendered euthyroid, radio-iodine therapy, abrupt withdrawal of antithyroid drugs, trauma, surgery, anaesthesia, parturition, an iodine load from amiodarone or contrast, myocardial infarction, pulmonary embolism or ketoacidosis. For myxoedema: cold exposure, sedatives, antipsychotics, anaesthetics and above all opioids, infection often without fever, cessation of levothyroxine, hyponatraemia, cardiac failure, gastrointestinal haemorrhage, stroke and myocardial infarction.
Score the storm but do not be governed by it: on the Burch–Wartofsky Point Scale a score ≥ 45 is highly suggestive of thyroid storm, 25–44 indicates impending storm and should be treated as such, and < 25 makes storm unlikely — but a lower score with a goitre, a precipitant and organ decompensation still warrants treatment.
Bedside tests in both syndromes: capillary glucose immediately, blood gas with lactate (a rising PaCO₂ with a falling pH decides ventilatory support), 12-lead ECG, full blood count with differential, cultures before antibiotics, β-hCG in every woman of childbearing potential, and serum cortisol before the first hydrocortisone if that costs no time.Not available at your setup — Arterial blood gas, Blood culture.
The numbers do not grade the storm: free T4 and T3 in crisis are no higher than in far milder thyrotoxicosis, so a modestly raised FT4 never excludes storm; and T3 toxicosis accounts for about 5% of thyrotoxic presentations, so a normal FT4 with an undetectable TSH does not exclude thyrotoxicosis — request FT3.
Consider the mimics: sepsis, heat stroke, neuroleptic malignant and serotonin syndromes, toxidromes and sedative withdrawal, phaeochromocytoma crisis and primary tachyarrhythmia for storm; exposure or septic hypothermia, hypercapnic COPD, sedative or opioid overdose and adrenal crisis for myxoedema — remembering that sepsis and sedatives are also the leading precipitants, so both may be present at once.

Management— do this, in order

Treat before you confirm: draw the samples, then treat — waiting for a TSH result in myxoedema crisis costs hours the patient does not have, and in storm there is no threshold hormone concentration to wait for.
Storm — resuscitate and cool: oxygen, continuous cardiac monitoring and an early twelve-lead ECG; rehydrate with 0.9% sodium chloride in measured aliquots of 250–500 mL, reassessing after each, with much greater caution where there is cardiac failure.
Storm — antipyresis: tepid sponging and fanning plus paracetamol 1 g orally, by nasogastric tube or per rectum every 6 hours (maximum 4 g daily), or in children 15 mg/kg per dose 4–6 hourly, maximum 60 mg/kg daily. Salicylates must not be used.
Storm — the order of drugs is β-blocker, then thionamide, then wait one hour, then iodine, then glucocorticoid.
1. β-blockade, first because it works within minutes: propranolol 40–80 mg orally or by nasogastric tube four times daily, or 0.5–2 mg by slow intravenous bolus repeated as required with continuous ECG monitoring; esmolol 250–500 micrograms/kg intravenously then 50–100 micrograms/kg/min where titratability matters; verapamil is the alternative in asthma.Doctor / Nurse
β-blockade in children: propranolol 0.5–2 mg/kg/day orally in divided doses 6–8 hourly; intravenously 0.01–0.1 mg/kg over at least 10 minutes, maximum 1 mg in infants and 3 mg in older children.Doctor / Nurse
2. Thionamide, to stop new hormone synthesis and always before iodine: propylthiouracil 200–250 mg every 4 hours orally or by nasogastric tube (many authorities load with 500–1000 mg), or carbimazole 20 mg every 6 hours — treatment is never delayed to obtain propylthiouracil. Children: propylthiouracil 5–10 mg/kg/day divided 4–6 hourly, carbimazole or methimazole 0.5–1 mg/kg/day in divided doses.Doctor / Nurse
3. Iodine, not less than one hour after the thionamide: saturated potassium iodide or Lugol's solution 0.25 mL every 6 hours orally or by nasogastric tube, or sodium ipodate 500 mg daily orally; either should restore serum T3 to normal within 48–72 hours. Where iodine is contraindicated use lithium carbonate 300 mg every 6–8 hours, titrated to a serum level of 0.6–1.0 mmol/L.Doctor / NurseNot available at your setup — Serum electrolytes.
4. Glucocorticoid, given early: hydrocortisone 100 mg intravenously every 8 hours (an initial 300 mg load is often used), or dexamethasone 2 mg intravenously every 6 hours; children hydrocortisone 1–2 mg/kg intravenously every 6 hours.Doctor / Nurse
5. Treat the precipitant: take cultures and give broad-spectrum antibiotics where infection is suspected — and it usually is — searching chest, urine, abdomen, skin, any surgical wound and the neck itself, and manage myocardial infarction, pulmonary embolism and obstetric emergencies in parallel.Doctor / NurseNot available at your setup — Blood culture.
Thyrotoxic atrial fibrillation: it is characteristically little influenced by digoxin but responds to the addition of a β-blocker, and anticoagulation is required unless contraindicated because thromboembolic complications are particularly common.Doctor / Nurse
Myxoedema — airway and ventilation first, because this is where these patients die: high-flow oxygen and a blood gas; a rising PaCO₂ with a falling pH in an obtunded hypothermic patient mandates ventilatory support, and obtundation, bulbar weakness and macroglossia often force intubation — anticipate a difficult airway.Doctor / NurseNot available at your setup — Arterial blood gas, Endotracheal intubation kit, Mechanical ventilator.
Myxoedema — glucocorticoid before or with the thyroid hormone, never after: hydrocortisone 100 mg as an intravenous bolus, then 200 mg per day as a continuous infusion or 50 mg intravenously every 6 hours; children 1–2 mg/kg intravenously every 6 hours.Doctor / Nurse
Myxoedema — thyroid hormone, begun before biochemical confirmation: levothyroxine loading dose 200–400 micrograms, then 1.6 micrograms/kg/day, with the dose reduced by 25% if the intravenous route is used; use the lower end (200 micrograms) in the small, frail or elderly patient and in anyone with known or suspected ischaemic heart disease, with cardiac monitoring whenever a loading dose is given.Doctor / Nurse
Liothyronine may be added: 2.5–10 micrograms every 8 hours alongside levothyroxine; where intravenous levothyroxine is unavailable, liothyronine 20 micrograms every 8 hours as sole agent, or an intravenous bolus of 10–20 micrograms followed by 10 micrograms every 8–12 hours for 48 hours; where no parenteral preparation exists, levothyroxine tablets may be crushed down a nasogastric tube accepting unreliable absorption.Doctor / Nurse
Myxoedema — supportive measures given simultaneously: rewarm slowly and passively with blankets, a warm room, warmed fluids and warmed humidified oxygen; give cautious intravenous fluids in small measured volumes; correct hyponatraemia slowly, no more than 8–10 mmol/L in 24 hours; correct hypoglycaemia; and give broad-spectrum antibiotics after cultures.Doctor / NurseNot available at your setup — Serum electrolytes, Blood culture.
Judge the myxoedema response clinically: in survivors body temperature rises within 24 hours, and after 48–72 hours it is usually possible to convert to oral levothyroxine 1.6 micrograms/kg daily; conscious level typically lags the biochemistry by days.Doctor / Nurse
When storm does not respond within 24–48 hours, or thionamides are contraindicated by agranulocytosis or severe hepatotoxicity: colestyramine 4 g orally four times daily to interrupt enterohepatic recirculation, therapeutic plasma exchange as a bridge, emergency thyroidectomy after stabilisation, and mechanical circulatory support in thyrotoxic cardiogenic shock.Doctor / NurseNot available at your setup — Liver function tests, ICU / HDU bed.

Caution— what harms

Never give salicylates in thyrotoxicosis: aspirin displaces thyroid hormone from binding proteins and raises the free concentration, precisely the opposite of the therapeutic aim — paracetamol is the antipyretic of choice.
Never give iodine before a thionamide: iodine given to an unblocked gland is substrate, the Wolff–Chaikoff effect is unreliable in an autonomous or antibody-stimulated gland, and administration one hour after the thionamide limits the risk of stimulating hormone release.
Iodine is contraindicated in amiodarone-induced thyrotoxicosis, where iodine excess is the problem, and in true allergy — use lithium carbonate 300 mg every 6–8 hours instead.Not available at your setup — Serum electrolytes.
Never give levothyroxine before glucocorticoid in suspected myxoedema crisis: thyroid hormone given to a cortisol-deficient patient raises metabolic demand and cortisol clearance and can precipitate adrenal crisis.
Never accept an ordinary thermometer in a cold patient — it will not read below 35°C, reports "35" and conceals a core temperature that may be 25°C.
Avoid sedation and opioids in myxoedema crisis wherever possible: they are among the commonest precipitants, drug handling is grossly impaired and a conventional dose behaves as an overdose.
Avoid aggressive active external rewarming: warming the skin vasodilates a patient with a fixed low cardiac output and causes hypotension — rewarm slowly and passively.
Correct hyponatraemia by no more than 8–10 mmol/L in 24 hours; faster correction causes osmotic demyelination, and mild dilutional hyponatraemia usually improves with fluid restriction and thyroid hormone alone.Not available at your setup — Serum electrolytes.
β-blockade in thyrotoxic cardiac failure is contested territory: the thyrotoxic heart in failure may be rate-dependent and β-blockade can precipitate collapse — titrate in small increments with a short-acting agent and never bolus; verapamil is negatively inotropic and effective only against the tachycardia.
Do not rely on digoxin for thyrotoxic atrial fibrillation — it is characteristically little influenced, probably because of increased digoxin clearance.
Never start a thionamide on a blood test alone: non-thyroidal illness ("sick euthyroidism") typically shows a low TSH with a raised T4 and a normal or low T3 in a systemically ill patient with no clinical evidence of thyroid disease — do not even request thyroid function in that setting.
A normal or modestly raised FT4 never excludes storm, and serum T3 is unhelpful in suspected hypothyroidism and should not be requested.
A febrile patient on carbimazole or propylthiouracil has agranulocytosis until an urgent differential white cell count says otherwise — it affects 1–2 per 1000, is unpredictable, and is reversible on stopping the drug; propylthiouracil also carries a small but real risk of hepatotoxicity that has caused liver failure and death.Not available at your setup — Liver function tests.
Do not be reassured by a normal temperature in myxoedema — the patient cannot mount a fever, so a normal temperature excludes nothing in a person whose baseline is 30°C; and do not be reassured by the absence of hyperkinetic features in an older patient, because apathetic thyrotoxicosis storms just as readily.
Do not escalate the levothyroxine dose blindly when myxoedema fails to improve: ask instead whether there is an untreated precipitant, whether the hormone is being absorbed at all, and whether there is unrecognised adrenal insufficiency, hypoglycaemia, hypercapnia or a drug still on board.
Stridor after thyroid surgery is an airway emergency — an expanding neck haematoma — and thyroidectomy also causes transient hypocalcaemia in about 10%, permanent hypoparathyroidism in about 1% and recurrent laryngeal nerve palsy in about 1%.

Refer / escalate

Escalate or transfer urgently for any suspected thyroid storm (Burch–Wartofsky ≥ 45, or 25–44 with organ decompensation) or myxoedema crisis, and immediately for a rising PaCO₂ with a falling pH, coma or seizure, hypotension refractory to fluid, cardiac failure or arrhythmia, or failure to respond within 24–48 hours of first-line treatment.

The card — assess, manage, caution

Thyroid emergencies: thyroid storm and myxoedema crisis — Level 1: CorePrevious Thyroid emergencies: thyroid storm and myxoedema crisis — Level 3: Core practiceNext

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