Major clinical findings in hyperthyroidism are listed in Table 27.1. Cardiac findings may be prominent including tachycardia, atrial fibrillation, heart failure, and exacerbation of coronary artery disease. Rarely, severe hyperthyroidism may be associated with fever and delirium, sometimes called “thyroid storm.”
Major causes of hyperthyroidism are listed in Table 27.2. Graves’ disease (which may also cause proptosis) is the most common.
When hyperthyroidism is diagnosed in a critically ill patient, plasma thyroid stimulating hormone (TSH) and free thyroxine (T4) should be measured. Clinical hyperthyroidism suppresses TSH to <0.1 µU/mL, so a nonsuppressed plasma TSH excludes the diagnosis of hyperthyroidism. Plasma TSH may also be suppressed by severe nonthyroidal illness (about 10% of patients in intensive care units have plasma TSH <0.1 µU/mL) and by therapy with dopamine or high dose glucocorticoids. Thus, a suppressed plasma TSH alone does not establish the diagnosis.
If plasma TSH is suppressed and plasma free T4 is elevated, the diagnosis of hyperthyroidism is established. If plasma free T4 is not elevated, one of the other causes of suppressed plasma TSH listed earlier is more likely. Heparin therapy may artifactually increase plasma free T4, so in heparin-treated patients, plasma total T4 should be measured instead.
TABLE 27.1 Major Clinical Findings in Hyperthyroidism
Common
Seen primarily in severe hyperthyroidism
Heat intolerance
Weight loss
Palpitations
Sinus tachycardia
Atrial fibrillation
Brisk tendon reflexes
Fine tremor
Lid lag
Proximal muscle weakness
Heart failure
Exacerbation of coronary artery disease
Fever and delirium (“thyroid storm”)
TABLE 27.2 Major Causes of Hyperthyroidism
Associated with increased radioactive iodine uptake
Graves’ disease
Toxic multinodular goiter
Thyroid adenoma
Associated with decreased radioactive iodine uptake
Iodine-induced hyperthyroidism (due to amiodarone or iodine-containing contrast mediaa)
Painless thyroiditis
Subacute thyroiditis
Factitious hyperthyroidism (ingestion of thyroid hormone)
a Iodine excess can cause both hyper- and hypo-thyroidism depending on the patients’ underlying thyroid function and basal iodine consumption.
Treatment
The etiology of hyperthyroidism determines the best long-term therapy, but differential diagnosis can be deferred in the critically ill patient. Emergency therapy (Table 27.3) is indicated when hyperthyroidism exacerbates heart failure or an acute coronary syndrome, or when thyroid storm is present. It includes rapid inhibition of thyroid hormone synthesis (and conversion of T4 to tri-iodothyronine [T3]) by the thionamide propylthiouracil (PTU), inhibition of thyroid hormone secretion by iodine, and inhibition of the cardiovascular effects of hyperthyroidism by beta-adrenergic antagonists. Hydrocortisone is usually recommended because it also inhibits T4 conversion to T3.
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