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Virtually all patients admitted to an ICU have low levels of serum triiodothyronine (T3), and 30% to 50% have low levels of thyroxine (T4) with normal or low levels of serum thyrotropin (TSH).
Patients who have a T4 level of less than 3.0µg/dL despite normal levels of T4-binding proteins have a 68% to 84% mortality rate.
T3 is the logical choice for critically ill patients requiring thyroid hormone replacement.
Early intubation and mechanical ventilation are crucial for successful treatment of myxedema coma.
Management of myxedema coma should include administration of glucocorticoids while the adrenal status is being assessed.
Alterations in thyroid function change the metabolism of almost all drugs, and the doses need careful adjustment to prevent drug toxicity or decreased efficacy.
Autonomous hypersecretion and exogenous overdose of thyroid hormone are the most common causes of severe thyrotoxicosis.
Hyperpyrexia and altered mental status are the hallmarks of thyroid storm.
Medical treatment of severe hyperthyroidism usually normalizes circulating thyroid hormone levels in 2 to 3 weeks, except under circumstances of iodine overload, in which case hyperthyroxinemia may persist for months.
Blockade of hormonal secretion is best accomplished by the addition of stable iodine to an antithyroid drug regimen.
In severe thyrotoxicosis, treatment with iopanoic acid can be lifesaving.
β-Blockers prevent thyroid storm in the thyrotoxic patient undergoing surgery, and they may ameliorate cardiovascular dysfunction in thyroid storm, but their side effects often interfere with therapy in the elderly, in patients with asthma, and in patients with cardiomyopathy.
Amiodarone-induced thyrotoxicosis in a critically ill patient should be managed with methimazole (30-50 mg/d), potassium perchlorate (500 mg twice a day), and prednisone (30-40 mg/d).
After gastric aspiration and lavage, only symptomatic and supportive treatment is needed in cases of levothyroxine overdose.
Neonatal thyrotoxicosis can be life threatening; it is usually caused by transplacental transfer of thyroid-stimulating antibodies. It is transient and requires only short-term treatment.
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HYPOTHYROIDISM, NONTHYROIDAL ILLNESS, AND MYXEDEMA COMA
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Hypothyroidism is a state of tissue deprivation of thyroid hormone. It is manifested by general reduction of the metabolic rate accompanied by specific symptoms and signs. Usually, hypothyroidism is caused by a decreased supply of thyroid hormone due to one of the following: (1) failure of the gland to synthesize and secrete thyroid hormone, (2) failure of the pituitary to secrete thyrotropin (thyroid-stimulating hormone [TSH]), or (3) hypothalamic disease resulting in a deficiency of thyrotropin-releasing hormone (TRH).
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Perhaps the most controversial, if not the most challenging, aspects of thyroidology for the intensivist are how to interpret thyroid function tests in critically ill patients and what to do when the test results are abnormal. Clinically important hypothyroidism in its most severe form usually is seen in patients with primary hypothyroidism who then develop some intercurrent illness; it develops over several weeks and culminates in myxedema coma. Equally challenging are the thyroid function abnormalities seen ...