Hypothyroidism is a clinical syndrome caused by insufficient thyroid hormone production, which slows cell metabolism. Hypothyroidism is common in areas where iodine deficiency is common, particularly inland areas where there is no access to marine foods. In iodine-sufficient areas, chronic autoimmune destruction of thyroid gland (e.g., Hashimoto’s thyroiditis) and iatrogenic causes from treatment of Graves’ disease are the leading causes of hypothyroidism (after thyroidectomy or radioactive iodine ablation). The prevalence of hypothyroidism increases with age, and the disorder is nearly 10 times more common in females than in males.¹ Subclinical hypothyroidism is more prevalent than overt hypothyroidism in all age groups and can be seen in 4% to 15% of women, especially the elderly.^2,3

Hypothyroidism occurs in 1% to 32% of patients taking amiodarone.¹

Primary hypothyroidism is caused by the intrinsic dysfunction of the thyroid gland, and this is the most common type. Secondary hypothyroidism is caused by a deficiency of thyroid-stimulating hormone from the pituitary gland or deficiency of thyrotropin-releasing hormone from the hypothalamus. Table 228-1 lists common causes of hypothyroidism. Euthyroid sick syndrome or low thyroxine syndrome, also called nonthyroidal illness, is the term used for patients with low triiodothyronine and thyroxine levels and a normal or low thyroid-stimulating hormone level, but who are clinically euthyroid. This condition is found in critically ill patients or those with severe systemic illness.

Triiodothyronine is the major form of thyroid hormone. The ratio of triiodothyronine to thyroxine released in the blood is about 10:1. Peripherally, triiodothyronine is converted to the active thyroxine, which is three to four times more potent than triiodothyronine. The half-life of triiodothyronine is 7 days, and the half-life of thyroxine is about 1 day.

Symptoms can manifest in all organ systems and range in severity based on the degree of hormone deficiency (Table 228-2).

The common clinical features of hypothyroidism are listed in Table 228-2. Additional cardiopulmonary findings include angina, bradycardia, distant heart sounds from pericardial effusion, low voltage on the electrocardiogram, pleural effusions, cardiomyopathy, or hypoventilation.

Figure 228-1 and 228-2 show some characteristic findings of myxedema.

Table 228-3 describes the differences between primary and secondary hypothyroidism.

Myxedema crisis is a state of metabolic and multiorgan decompensation characterized by uncorrected hypothyroidism, mental status changes or coma, and hypothermia (usually <35.5°C [95.9°F]).¹ In hypothyroid patients, myxedema coma can be precipitated by a number of conditions, including infection, anesthetic agents, cold exposure, trauma, myocardial infarction or congestive heart failure, cerebrovascular accident, GI hemorrhage, metabolic conditions, hypoxia, hypercapnia, hyponatremia, hypoglycemia, surgery, burns, medications (e.g., β-blockers, sedatives, narcotics, phenothiazine, amiodarone), or thyroid medication noncompliance.