Thyroid storm

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Thyroid storm occurs when the physiological effects of hormone excess overwhelm organ reserve, often after a second insult. Hyperthermia, catecholamine sensitivity and high metabolic demand produce tachyarrhythmia and cardiac dysfunction; the central nervous system becomes agitated, delirious or obtunded; and vomiting, diarrhoea, abdominal pain or jaundice signal visceral involvement. Older patients may have less dramatic agitation but severe cardiac failure.

Diagnosis is clinical. Scoring systems such as Burch-Wartofsky can structure observations and support communication, but fever or tachycardia from sepsis can inflate a score and a subthreshold score cannot overrule compelling decompensation. Treat the competing diagnosis as well: sepsis and storm frequently coexist, and delaying antimicrobials while debating attribution is dangerous.

Therapy attacks several points at once: control adrenergic effects, stop new hormone synthesis, block subsequent hormone release, reduce peripheral conversion, support adrenal reserve, clear circulating hormone when indicated and treat the trigger. Exact formulations and high-intensity regimens are safety-critical and can change; use the current BNF, Society for Endocrinology or locally ratified emergency policy at the bedside with endocrine-pharmacy support.

Key points

Storm is thyrotoxicosis with acute multisystem decompensation, commonly fever, severe tachycardia or atrial fibrillation, heart failure, agitation or delirium, and gastrointestinal or hepatic dysfunction.
Free T4 and free T3 concentrations overlap with uncomplicated hyperthyroidism, so no biochemical cutoff can confirm or exclude the diagnosis.
Infection, abrupt antithyroid withdrawal, surgery, childbirth, iodine load, diabetic ketoacidosis, myocardial infarction and stroke are recognised precipitants.
Resuscitate first: oxygenation and ventilation, monitoring, cautious circulation support, active external cooling and treatment of immediately reversible rhythm or metabolic threats.
Use paracetamol and physical cooling for pyrexia; avoid aspirin because salicylates can increase free thyroid hormone and add bleeding or metabolic risk.
For adult thyrotoxic crisis, the propylthiouracil SmPC gives 200 mg orally every 4–6 hours for the first 24 hours, then dose reduction as the crisis subsides; give a pharmacy-verified iodine regimen only after thionamide, ordinarily at least 1 hour later.
Glucocorticoid provides adrenal support and reduces peripheral conversion, while the trigger needs simultaneous antibiotics, source control or cardiovascular, neurological or metabolic treatment.
Beta blockade can rapidly reduce adrenergic load but may precipitate collapse in low-output heart failure; agent and titration belong with senior critical-care assessment.
Propylthiouracil also reduces T4-to-T3 conversion but carries serious hepatic risk; if carbimazole is selected instead, use the exact live BNF or approved local storm regimen because the agents are not dose-equivalent.
Clinical improvement is judged by organ function, temperature, rhythm, perfusion and cognition, not by forcing TSH to recover during the first hours.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Uncontrolled thyrotoxicosis

Graves disease, toxic nodular disease or another synthesis-driven cause provides the underlying high thyroid-hormone state in susceptible patients.

Acute physiological trigger

Infection, surgery, trauma, childbirth, infarction or abrupt treatment disruption can overwhelm organ reserve and precipitate decompensation.

Iodine or medicine-related worsening

Iodine exposure and selected medicine changes can intensify hormone production or action in a susceptible thyrotoxic patient.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Thyroid-hormone effects intensify
Excess hormone increases metabolic demand, thermogenesis and tissue sensitivity to catecholamines across cardiovascular and neurological systems.
2
A trigger overwhelms organ reserve
Sepsis or another acute stress adds inflammatory, haemodynamic and metabolic demand that compensated thyrotoxicosis can no longer meet.
3
Cardiovascular failure develops
Tachyarrhythmia, high-output stress and sometimes cardiomyopathy progress to pulmonary oedema, hypotension or circulatory collapse while the condition remains active.
4
Central and visceral dysfunction follows
Hyperthermia, agitation, delirium, vomiting, diarrhoea and jaundice signal multisystem decompensation rather than uncomplicated biochemical hyperthyroidism as the process continues.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Thermoregulatory failureRed flag

High fever, profuse sweating, dehydration and marked weakness in a thyrotoxic patient indicate excessive metabolic drive; hypothermia can occur very late in circulatory collapse.

Central nervous system involvementRed flag

Severe anxiety, agitation, delirium, psychosis, seizure, stupor or coma differentiates organ decompensation from ordinary tremor and requires airway, glucose and neurological assessment.

Cardiovascular collapseRed flag

Marked sinus tachycardia, rapid atrial fibrillation, pulmonary oedema, cardiogenic shock, chest pain or a new murmur indicates threatened circulation; high-output physiology can evolve into low-output failure.

Gastrointestinal or hepatic involvementRed flag

Persistent vomiting, diarrhoea, abdominal pain, ileus, jaundice or coagulopathy supports storm and changes medicine route, fluid, hepatic-risk and critical-care decisions.

Precipitating infectionRed flag

Cough, urinary symptoms, focal pain, device infection or recent procedure may coexist, but absence of a clear focus does not rule out sepsis; culture and treat according to probability.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Continuous ABCDE observations and core temperatureFirst step
Why
Define organ failure and immediate response to resuscitation.
Interpretation and limitations
Trend mental state, temperature, rhythm, blood pressure, oxygenation, capillary refill and urine output; worsening physiology outweighs a borderline diagnostic score.
02
TSH, free T4 and free T3
Why
Confirm underlying thyrotoxicosis and provide a biochemical baseline.
Interpretation and limitations
TSH is usually suppressed and peripheral hormones raised, but levels do not distinguish storm; severe illness may lower T3 and must not create false reassurance.
03
ECG, troponin and echocardiography
Why
Characterise tachyarrhythmia, myocardial injury and high- versus low-output failure.
Interpretation and limitations
Atrial fibrillation is common, while ventricular dysfunction or ischaemia changes beta-blocker safety, fluid strategy and the need for mechanical or vasoactive support.
04
Blood gas, lactate, glucose and ketones
Why
Detect respiratory failure, shock, hypoglycaemia or diabetic ketoacidosis as a trigger.
Interpretation and limitations
Rising lactate or acidosis indicates inadequate perfusion or a second metabolic emergency; DKA must be managed through its validated pathway alongside thyroid treatment.
05
Full blood count, renal, liver and coagulation profile
Why
Assess infection, organ injury and the safety of antithyroid choices.
Interpretation and limitations
Neutropenia can reflect prior thionamide toxicity; hepatic injury may be part of storm or medicine-related and requires senior selection between carbimazole, PTU and alternatives.
06
Cultures and source-directed imaging
Why
Find infection that may have precipitated decompensation.
Interpretation and limitations
Obtain cultures before antibiotics when this creates no delay, but begin local severe-infection therapy promptly; interpret fever as potentially dual-cause.
07
Pregnancy assessment when relevant
Why
Alter medicine choice, imaging and obstetric monitoring immediately.
Interpretation and limitations
A positive result requires concurrent maternal medicine and endocrine care; use specialist-selected thionamide strategy and avoid radioiodine.
08
Toxicology and precipitant tests
Why
Identify medicines, iodine, stimulant use or another endocrine mimic.
Interpretation and limitations
Review prescriptions, adherence, recent contrast and recreational exposure; targeted tests should not delay the core storm bundle when clinical probability is high.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Sepsis

Fever, tachycardia, hypotension and delirium overlap and infection often precipitates storm, so both diagnoses may require simultaneous treatment.

Malignant hyperthermia

Peri-anaesthetic hyperthermia, rigidity and rapid carbon-dioxide rise suggest an anaesthetic-triggered syndrome rather than primary thyrotoxic decompensation.

Serotonin syndrome

Serotonergic exposure, clonus and hyperreflexia favour serotonin toxicity, while thyroid history, goitre and hormone results support storm.

Phaeochromocytoma crisis

Paroxysmal hypertension, catecholamine history and metanephrine evidence suggest chromaffin tumour physiology, although both conditions cause adrenergic collapse.

Additional chapter-specific clues

Alternative decompensation

Sepsis without storm, serotonin syndrome, neuroleptic malignant syndrome, stimulant toxicity, malignant hyperthermia, pheochromocytoma crisis and severe alcohol withdrawal can resemble the syndrome and may demand parallel treatment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First minutesResuscitate decompensated thyrotoxicosisFirst stepThyrotoxicosis accompanies fever and acute organ dysfunction.

1Call critical care, endocrinology and pharmacy; perform ABCDE, attach continuous ECG and invasive monitoring when required, and obtain wide-bore access.
2Support airway and ventilation, give cautious fluids guided by cardiac status, correct glucose and electrolytes, and use external cooling plus paracetamol rather than aspirin.
3Take thyroid, liver, haematology, cardiac, culture and pregnancy samples rapidly while starting treatment for storm and its likely precipitant in parallel.

02Hormone blockadeSequence synthesis before releaseSenior review agrees that storm treatment should proceed.

1If propylthiouracil is selected for adult crisis, give 200 mg orally every 4–6 hours for the first 24 hours under the current SmPC, then reduce as the crisis subsides; if carbimazole is selected, use the live BNF or approved local regimen and account for pregnancy, liver injury and previous adverse reactions.
2Give inorganic iodine only after thionamide has inhibited organification, ordinarily waiting at least 1 hour. Pharmacy must verify the stocked preparation, concentration and prescribed elemental iodine dose because aqueous iodine and potassium iodide products and drop sizes are not interchangeable.
3Give stress-dose hydrocortisone and consider specialist adjuncts such as cholestyramine when severe disease or slow response justifies additional hormone clearance.

03Cardiac controlReduce adrenergic load without crashing outputSevere tachycardia or atrial fibrillation contributes to instability.

1Use bedside echocardiography and perfusion assessment to identify low-output failure before administering a long-acting or high-dose beta blocker.
2AlternativeWhen beta blockade is appropriate, use a short-acting titratable strategy or carefully dosed alternative under critical-care supervision with immediate haemodynamic observation.
3Treat pulmonary oedema, ischaemia and atrial-fibrillation stroke risk through their own urgent pathways while hormone control reduces the ongoing trigger.

04Trigger controlReverse the precipitating insultInfection, drug withdrawal, iodine, vascular or metabolic stress is possible.

1Start local broad-spectrum antimicrobial therapy and source control when sepsis is plausible, then refine treatment using cultures, imaging and organ function.
2Manage DKA, myocardial infarction, stroke, trauma or obstetric complications simultaneously with the relevant specialist team and validated emergency pathway.
3DefinitiveOnce stabilised, confirm Graves, autonomy, thyroiditis or exogenous cause and create a definitive prevention plan before discharge from specialist care.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

Stops new thyroid hormone synthesis as the first pharmacological block in the sequence.

Carbimazole or propylthiouracil synthesis blockade

For adult thyrotoxic crisis, give propylthiouracil 200 mg orally every 4–6 hours for the first 24 hours, then reduce as the crisis subsides. If carbimazole is chosen instead, use the exact current BNF or approved local storm regimen; do not infer dose equivalence.

Check prior reactions, neutrophils, liver injury and pregnancy. PTU adds peripheral-conversion inhibition but serious hepatic toxicity; carbimazole carries agranulocytosis, pancreatitis and reproductive warnings.

Acutely inhibits release of newly available thyroid hormone after synthesis blockade is established.

Inorganic iodine after thionamide

After the first thionamide dose, wait at least 1 hour, then give the pharmacy-verified local aqueous iodine or potassium iodide regimen. Record product, concentration and elemental iodine dose; never copy a volume or drop count between preparations.

Giving iodine first can supply substrate for further synthesis. Verify formulation carefully, review allergy history and recent iodine exposure, and involve pharmacy because products and concentrations differ.

Supports adrenal reserve and reduces peripheral conversion of T4 to active T3.

Hydrocortisone in thyroid storm

The BNF adult regimen is 100 mg intravenously every six hours during acute treatment, reviewed frequently by critical care and endocrinology as haemodynamics and diagnosis evolve.

Monitor glucose, sodium, potassium, fluid balance, infection and gastrointestinal risk. Do not let cortisol sampling delay treatment, and plan taper or cessation with specialist advice.

Reduces dangerous catecholamine-mediated rate, tremor and myocardial oxygen demand.

Short-acting beta blockade when haemodynamically suitable

Use critical-care titration from the current protocol, favouring an immediately adjustable intravenous strategy when ventricular function or output is uncertain rather than an inflexible ward dose.

Can precipitate cardiovascular collapse in severe low-output failure; assess ventricular function and perfusion first. Also consider asthma, conduction disease, pregnancy and concurrent rate-control medicines.

Reduces fever burden while definitive hormone and precipitant treatments take effect.

Paracetamol with physical cooling

Use the current BNF adult paracetamol regimen with weight, liver function and total daily exposure checked, alongside cooling blankets, ice packs and environmental measures.

Avoid overdose from combination products and reduce or avoid according to hepatic risk. Do not use aspirin for storm pyrexia because salicylates can increase free hormone.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Arrhythmia and heart failure

Extreme adrenergic and metabolic stress causes atrial fibrillation, ventricular rhythm disturbance, pulmonary oedema and cardiogenic shock.

Neurological failure

Agitation and delirium can progress to seizure, coma and secondary injury through hyperthermia and poor perfusion.

Liver and gastrointestinal injury

Vomiting, diarrhoea, abdominal pain and jaundice cause dehydration and may signal hepatic dysfunction within multisystem failure.

Thromboembolism

Atrial fibrillation, dehydration, immobility and critical illness increase embolic stroke and venous thromboembolism risk during thyroid storm.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Use continuous ECG and close blood-pressure monitoring, escalating to invasive haemodynamics when shock, vasoactive support or titratable beta blockade makes it necessary.
Record core temperature, neurological state, respiratory support, capillary refill and urine output frequently to judge whole-organ response rather than biochemical response alone.
Repeat glucose, electrolytes, renal, liver and coagulation tests according to instability, replacing potassium, magnesium or phosphate through critical-care protocols.
Follow free T4 and free T3 at endocrine-selected intervals; TSH remains suppressed and should not be used as the early recovery target.
Review thionamide route and absorption after vomiting or ileus, and monitor urgently for new neutropenia, hepatic deterioration or pancreatitis symptoms.
Reassess cultures, source control and imaging every day, narrowing antimicrobials when evidence allows and treating unresolved precipitant disease aggressively.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Numbers do not define storm

A patient with modest free-hormone elevation can decompensate after infection, while another with higher concentrations remains stable; organ dysfunction creates the diagnosis.

Scores support, not command

A scoring system can standardise observations and prompt treatment, but overlapping sepsis features and population limitations demand senior clinical judgement.

Sequence prevents iodine fuel

Thionamide must inhibit organification before iodine is introduced; otherwise substrate can be delivered to a gland still capable of synthesising hormone.

Fast rate may hide poor output

Not every thyrotoxic heart is high-output. Cardiomyopathy and shock make indiscriminate beta blockade dangerous, so bedside haemodynamic assessment matters.

Two diagnoses can coexist

Pneumonia may precipitate storm and explain fever, but neither diagnosis excludes the other; both treatment bundles should proceed while evidence develops.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for an extreme free T4 value before treating convincing organ decompensation.
02
Using a diagnostic score as a substitute for bedside judgement and specialist escalation.
03
Giving iodine before a thionamide has blocked new synthesis.
04
Administering aggressive long-acting beta blockade without assessing low-output failure.
05
Using aspirin routinely for fever in thyrotoxicosis.
06
Forgetting that severe vomiting or ileus makes oral absorption unreliable.
07
Treating thyroid hormone while under-investigating sepsis, infarction, DKA or another precipitant.
08
Copying a historical high-dose regimen without checking current BNF, local formulation and pregnancy or hepatic constraints.