Synopsis
Recognise clinical thyrotoxic decompensation, initiate coordinated critical-care treatment in the correct pharmacological sequence, and reverse the precipitating illness without delay.
- 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.
Key red flags
High fever, profuse sweating, dehydration and marked weakness in a thyrotoxic patient indicate excessive metabolic drive; hypothermia can occur very late in circulatory collapse.
Severe anxiety, agitation, delirium, psychosis, seizure, stupor or coma differentiates organ decompensation from ordinary tremor and requires airway, glucose and neurological assessment.
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.
Persistent vomiting, diarrhoea, abdominal pain, ileus, jaundice or coagulopathy supports storm and changes medicine route, fluid, hepatic-risk and critical-care decisions.
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.
Investigation priorities
Define organ failure and immediate response to resuscitation.
Management branches
Thyrotoxicosis accompanies fever and acute organ dysfunction.
- Call critical care, endocrinology and pharmacy; perform ABCDE, attach continuous ECG and invasive monitoring when required, and obtain wide-bore access.
- Support airway and ventilation, give cautious fluids guided by cardiac status, correct glucose and electrolytes, and use external cooling plus paracetamol rather than aspirin.
- Take thyroid, liver, haematology, cardiac, culture and pregnancy samples rapidly while starting treatment for storm and its likely precipitant in parallel.