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Emergency And Acute Medicine: Hyperthyroidism
Basics
Description Hyperthyroidism is caused by excessive thyroid hormone production, producing a continuum of disease due to direct metabolic effects of thyroid hormones and increased sensitivity to catecholamines. Clinical states range from subclinical or mild hyperthyroidism to thyrotoxicosis and, in 1–2% of cases, life-threatening thyroid storm. Thyroid regulation occurs through hypothalamic TRH stimulating pituitary TSH release, which increases thyroidal secretion of T4 and T3. Most circulating hormone is T4, which is peripherally converted to the more biologically active T3. Genetic predisposition plays a role, particularly in Graves disease, which is associated with HLA-B8 and HLA-DR3, and in some familial cases of nontoxic goiter with autosomal dominant inheritance.
Etiology Primary hyperthyroidism includes Graves disease, toxic multinodular or uninodular goiter, iodine-induced hyperthyroidism, and thyroiditis (postpartum, radiation, subacute de Quervain, and chronic lymphocytic). Other causes include metastatic thyroid cancer, ectopic thyroid tissue such as struma ovarii, pituitary adenoma, drug-induced hyperthyroidism (amiodarone, lithium, interferon, interleukin-2, iodinated contrast), factitious thyrotoxicosis from excess hormone ingestion, and aspirin overdose.
Diagnosis
Alert Thyroid storm is a medical emergency and may be precipitated by infection, trauma, surgery, diabetic ketoacidosis, myocardial infarction, stroke, chemotherapy, organophosphate intoxication, or abrupt withdrawal of antithyroid medications.
Signs and symptoms Findings reflect heightened end-organ responsiveness to thyroid hormone. Common signs include fever, tachycardia with widened pulse pressure, diaphoresis, tremor, hyperreflexia, goiter, thyromegaly, thyroid bruit, exophthalmos, lid lag, pretibial myxedema, congestive heart failure, shock, and psychosis. Symptoms include weight loss despite increased appetite, palpitations, chest pain, heat intolerance, diarrhea, vomiting, weakness, anxiety, insomnia, menstrual irregularities, and fatigue. Thyroid storm presents with exaggerated manifestations including extreme tachyarrhythmias, heart failure, shock, delirium, coma, seizures, and thromboembolic events.
Geriatric considerations Apathetic hyperthyroidism often presents with subtle findings such as refractory atrial fibrillation, heart failure, weight loss, depression, tremor, and emotional lability rather than classic hyperadrenergic features.
History Typically reveals gradual onset of symptoms.
Physical exam May show fever, tachycardia, systolic hypertension with widened pulse pressure, tachypnea, alopecia, fine diaphoretic skin, irregularly irregular rhythm, lung rales, RUQ tenderness, jaundice, proximal muscle weakness, tremor, and altered mental status.
Essential workup Identify underlying cause and precipitating factors. Plasma TSH is the preferred initial test; a normal TSH generally excludes hyperthyroidism. Low TSH with normal T4 requires T3 measurement to rule out T3 thyrotoxicosis. If laboratory testing is delayed or unavailable, strong clinical suspicion should prompt treatment.
Diagnosis tests and interpretation
Laboratory TSH is typically suppressed, with elevated free T4. Approximately 5% of patients have isolated T3 thyrotoxicosis. Additional testing may include CBC, chemistry panel, liver enzymes, ABG, glucose, and cardiac markers to evaluate complications or precipitants.
Imaging Chest radiograph is useful in heart failure or infection.
Diagnostic procedures ECG commonly shows sinus tachycardia or new-onset atrial fibrillation and helps identify ischemia as a precipitating factor.
Differential diagnosis Pheochromocytoma, sepsis, sympathomimetic intoxication, psychosis, heat stroke, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, hypothalamic stroke, hypothyroidism with apathetic presentation, and factitious thyrotoxicosis.
Treatment
Prehospital Supportive care and stabilization.
Initial stabilization/therapy Manage airway, breathing, and circulation. Initiate cardiac monitoring, provide oxygen and IV fluids, and begin cooling measures. Use acetaminophen for fever and avoid aspirin, which increases free thyroid hormone levels.
Emergency department management Identify and treat precipitating causes. In suspected thyroid storm, initiate treatment based on clinical suspicion without delay. Inhibit hormone synthesis with thioamides, preferably propylthiouracil, which also reduces peripheral T4-to-T3 conversion; methimazole is an alternative. Block hormone release with iodine preparations only after thioamide administration and at least one hour later. Block peripheral effects using beta-blockers, with propranolol preferred due to inhibition of T4-to-T3 conversion; esmolol may be used when beta-1 selectivity is needed. Reduce peripheral conversion with corticosteroids. Adjunctive therapies include cholestyramine to reduce enterohepatic circulation of thyroid hormone and lithium if iodine is contraindicated. Manage heart failure, dehydration, hyperthermia, and associated conditions concurrently.
Medication Propylthiouracil, propranolol, iodine solutions (Lugol), methimazole, esmolol, hydrocortisone or dexamethasone, cholestyramine, lithium, guanethidine, and reserpine as indicated based on clinical context.
Pregnancy considerations Physiologic changes may mimic hyperthyroidism. Poorly controlled disease increases risks of hyperemesis gravidarum, preeclampsia, preterm labor, low birth weight, miscarriage, and stillbirth. PTU is preferred at the lowest effective dose; propranolol may be used cautiously. Radioactive iodine is contraindicated. Thyroidectomy is an option when medications are not tolerated. Postpartum thyroiditis occurs in up to 10% of patients and often resolves within one year.
Follow-up and disposition
Admission criteria Thyroid storm, need for IV rate control, or significant instability.
Discharge criteria Mild symptoms responsive to oral therapy with reliable follow-up.
Follow-up recommendations Arrange timely primary care or endocrinology follow-up.
Key points Thyroid storm is highly lethal without prompt treatment and often requires empiric therapy. Never administer iodine before blocking hormone synthesis with a thioamide. Radioactive iodine is contraindicated in pregnancy.
Basics
Description Hyperthyroidism is caused by excessive thyroid hormone production, producing a continuum of disease due to direct metabolic effects of thyroid hormones and increased sensitivity to catecholamines. Clinical states range from subclinical or mild hyperthyroidism to thyrotoxicosis and, in 1–2% of cases, life-threatening thyroid storm. Thyroid regulation occurs through hypothalamic TRH stimulating pituitary TSH release, which increases thyroidal secretion of T4 and T3. Most circulating hormone is T4, which is peripherally converted to the more biologically active T3. Genetic predisposition plays a role, particularly in Graves disease, which is associated with HLA-B8 and HLA-DR3, and in some familial cases of nontoxic goiter with autosomal dominant inheritance.
Etiology Primary hyperthyroidism includes Graves disease, toxic multinodular or uninodular goiter, iodine-induced hyperthyroidism, and thyroiditis (postpartum, radiation, subacute de Quervain, and chronic lymphocytic). Other causes include metastatic thyroid cancer, ectopic thyroid tissue such as struma ovarii, pituitary adenoma, drug-induced hyperthyroidism (amiodarone, lithium, interferon, interleukin-2, iodinated contrast), factitious thyrotoxicosis from excess hormone ingestion, and aspirin overdose.
Diagnosis
Alert Thyroid storm is a medical emergency and may be precipitated by infection, trauma, surgery, diabetic ketoacidosis, myocardial infarction, stroke, chemotherapy, organophosphate intoxication, or abrupt withdrawal of antithyroid medications.
Signs and symptoms Findings reflect heightened end-organ responsiveness to thyroid hormone. Common signs include fever, tachycardia with widened pulse pressure, diaphoresis, tremor, hyperreflexia, goiter, thyromegaly, thyroid bruit, exophthalmos, lid lag, pretibial myxedema, congestive heart failure, shock, and psychosis. Symptoms include weight loss despite increased appetite, palpitations, chest pain, heat intolerance, diarrhea, vomiting, weakness, anxiety, insomnia, menstrual irregularities, and fatigue. Thyroid storm presents with exaggerated manifestations including extreme tachyarrhythmias, heart failure, shock, delirium, coma, seizures, and thromboembolic events.
Geriatric considerations Apathetic hyperthyroidism often presents with subtle findings such as refractory atrial fibrillation, heart failure, weight loss, depression, tremor, and emotional lability rather than classic hyperadrenergic features.
History Typically reveals gradual onset of symptoms.
Physical exam May show fever, tachycardia, systolic hypertension with widened pulse pressure, tachypnea, alopecia, fine diaphoretic skin, irregularly irregular rhythm, lung rales, RUQ tenderness, jaundice, proximal muscle weakness, tremor, and altered mental status.
Essential workup Identify underlying cause and precipitating factors. Plasma TSH is the preferred initial test; a normal TSH generally excludes hyperthyroidism. Low TSH with normal T4 requires T3 measurement to rule out T3 thyrotoxicosis. If laboratory testing is delayed or unavailable, strong clinical suspicion should prompt treatment.
Diagnosis tests and interpretation
Laboratory TSH is typically suppressed, with elevated free T4. Approximately 5% of patients have isolated T3 thyrotoxicosis. Additional testing may include CBC, chemistry panel, liver enzymes, ABG, glucose, and cardiac markers to evaluate complications or precipitants.
Imaging Chest radiograph is useful in heart failure or infection.
Diagnostic procedures ECG commonly shows sinus tachycardia or new-onset atrial fibrillation and helps identify ischemia as a precipitating factor.
Differential diagnosis Pheochromocytoma, sepsis, sympathomimetic intoxication, psychosis, heat stroke, delirium tremens, malignant hyperthermia, neuroleptic malignant syndrome, serotonin syndrome, hypothalamic stroke, hypothyroidism with apathetic presentation, and factitious thyrotoxicosis.
Treatment
Prehospital Supportive care and stabilization.
Initial stabilization/therapy Manage airway, breathing, and circulation. Initiate cardiac monitoring, provide oxygen and IV fluids, and begin cooling measures. Use acetaminophen for fever and avoid aspirin, which increases free thyroid hormone levels.
Emergency department management Identify and treat precipitating causes. In suspected thyroid storm, initiate treatment based on clinical suspicion without delay. Inhibit hormone synthesis with thioamides, preferably propylthiouracil, which also reduces peripheral T4-to-T3 conversion; methimazole is an alternative. Block hormone release with iodine preparations only after thioamide administration and at least one hour later. Block peripheral effects using beta-blockers, with propranolol preferred due to inhibition of T4-to-T3 conversion; esmolol may be used when beta-1 selectivity is needed. Reduce peripheral conversion with corticosteroids. Adjunctive therapies include cholestyramine to reduce enterohepatic circulation of thyroid hormone and lithium if iodine is contraindicated. Manage heart failure, dehydration, hyperthermia, and associated conditions concurrently.
Medication Propylthiouracil, propranolol, iodine solutions (Lugol), methimazole, esmolol, hydrocortisone or dexamethasone, cholestyramine, lithium, guanethidine, and reserpine as indicated based on clinical context.
Pregnancy considerations Physiologic changes may mimic hyperthyroidism. Poorly controlled disease increases risks of hyperemesis gravidarum, preeclampsia, preterm labor, low birth weight, miscarriage, and stillbirth. PTU is preferred at the lowest effective dose; propranolol may be used cautiously. Radioactive iodine is contraindicated. Thyroidectomy is an option when medications are not tolerated. Postpartum thyroiditis occurs in up to 10% of patients and often resolves within one year.
Follow-up and disposition
Admission criteria Thyroid storm, need for IV rate control, or significant instability.
Discharge criteria Mild symptoms responsive to oral therapy with reliable follow-up.
Follow-up recommendations Arrange timely primary care or endocrinology follow-up.
Key points Thyroid storm is highly lethal without prompt treatment and often requires empiric therapy. Never administer iodine before blocking hormone synthesis with a thioamide. Radioactive iodine is contraindicated in pregnancy.
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