Journal: Anaesthesia 63(9):1001-1005, 2008. 23 References
Reprint: United Lincolnshire Hospitals, NHS Trust, Lincoln County Hospital, Greetwell Road, Lincolnshire LN2 5QY, UK (JN Wilkinson, FRCA)
Faculty Disclosure: Abstracted by S. Ouellette, who has nothing to disclose.
Thyroid storm is a potentially life-threatening endocrinologic emergency and is due to exacerbation of a hyperthyroid state. Trauma as the inciting factor is rare. This case report describes a 38-year-old woman who presented initially as the driver in a road traffic accident, with a Glasgow Coma Score of 14, agitated, tachypneic and hypertensive. The combination of an abnormal CT scan and clinical findings led to the decision to perform an emergency laparotomy. Persistent tachycardia of 160 beats/min, hypertension of around 200/110 mmHg and a core temperature of 39ºC were noted throughout the procedure with no apparent trigger factors despite adequate anesthesia and analgesia.
Persistent symptoms and laboratory results revealed acute thyroid storm: TSH of <0.10 IU/L, free T4 of 59.8 pmol/L and free T3 of 20.20 pmol/L. On discussion with the patient's partner it was discovered that the patient had been diagnosed with an over-active thyroid gland 3 months previously. She had been suffering from moderate unintentional weight loss, palpitations, diarrhea and mood changes. She was treated for thyroid storm and made an uneventful recovery following treatment for bronchopneumonia.
Thyroid storm is a clinical syndrome marked by exaggerated manifestations of thyrotoxicosis. It represents the most serious complication of hyperthyroidism and carries a high mortality even with treatment. Serum thyroid hormones are always elevated .Reported mortality rate ranges from 10% to 75% in hospitalized patients. Due to the high mortality of the condition, it is vital to initiate treatment as soon as the diagnosis is strongly suspected.
Management involves general supportive measures as well as four main specific measures: inhibition of hormone production and release; counteraction of ongoing effects of thyroid hormone in the periphery; therapy against systemic decompensation; and management of the precipitating illness. Thyroid storm should always be managed in the ICU. Invasive hemodynamic monitoring is required due to cardiac arrhythmias, congestive heart failure and large fluid shifts that occur as part of the syndrome. Temperature reduction decreases the metabolic demands and the percentage of free T4. Paracetamol rather than salicylates should be used for temperature reduction since salicylates inhibit thyroid hormone binding and could increase free hormone. Glucose and vitamins are also important since metabolic demands are increased several-fold.
Propylthiouracil reduces new hormone production and peripheral de-iodination of T4 to T3. Potassium iodide or Lugol's iodine solution inhibits acute hormone release from the gland. It is essential to administer iodine 1 hour after the antithyroid drug to allow the latter to prevent the excess iodine from being incorporated into new hormone. The plasma half life of thyroxine is 6-8 days. Five to seven days of therapy should be adequate. Peritoneal dialysis and plasmapheresis deplete the large vascular pool of thyroxine and can result in rapid reduction of symptoms. Reduction of the hyperadrenergic state using propranolol is helpful. Esmolol is also useful as it offers a more cardioselective treatment and its effects wear off rapidly. Aggressive fluid management is necessary as large losses occur due to sweating, diarrhea and vomiting. Glucocorticoids or dexamethasone have been given on the belief that adrenal insufficiency may be present and they block conversion of T4 to T3. The precipitating illness must be addressed. |
