Thyroid Disorders

William E. Clutter

HYPERTHYROIDISM

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 media^a)
Painless thyroiditis
Subacute thyroiditis
Factitious hyperthyroidism (ingestion of thyroid hormone)

^aIodine 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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