The role of thyroid dysfunction in the critically ill: a review of the literature.

During critical illness, patients with no known history of thyroid disorders may experience multiple alterations in their serum thyroid hormone levels. Such alterations have been termed sick euthyroid syndrome or, more recently, non-thyroidal illness syndrome (NTIS). The laboratory parameters of NTIS usually include low serum levels of triiodothyronine (T3), normal or low serum levels of thyroxine (T4) and normal or low serum levels of thyroid-stimulating hormone (TSH). The magnitude of the alteration in thyroid function correlates with the severity of the illness and its outcomes in critically ill patients with NTIS. The pathogenetic mechanisms involved in NTIS include a decreased conversion of T4 to T3 in extrathyroidal tissues and alterations in thyroid hormones' binding to serum proteins. In cases of protracted critical illness, a decrease in the pulsatile frequency of TSH secretion, resulting from reduced thyrotropin-re leasing hormone (TRH) release by the hypothalamus, may also occur. Several medications or clinical conditions that are commonly present in critically ill patients may be responsible for lowering serum concentrations of thyroid hormone. Among those who study the condition, the question of whether NTIS is a protective adaptation of the organism to illness or a maladaptive response to a stressful insult remains unanswered. In either case, thyroid hormone abnormalities are likely to play a role in the critically ill patient.However, there is currently no convincing evidence to suggest that restoring physiological thyroid hormone concentrations in unselected patients with NTIS would be beneficial.