• We studied the hormonal milieu and possibility of altered thyroid function in 25 patients in a surgical intensive care unit (ICU) who had severe life-threatening illnesses. Sixteen patients had septic complications and nine patients had multiple-system injuries. On admission to the ICU, serial measurements were begun of thyroxine (T4), triiodothyronine (T3), T4-binding globulin, thyrotropin (thyroid-stimulating hormone [TSH]), corticotropin (adrenocorticotropic hormone [ACTH]), cortisol, prolactin, human growth hormone, catecholamine, insulin and glucose, lactate, retinol-binding protein, prealbumin, and transferrin levels. All patients initially had low normal levels of T4 (4.5 ± 2 μg/dL) and T3 (55 ± 26 ng/dL), with normal TSH levels (2.3±2.3 μU/mL) (the "low T3 syndrome"). The 11 surviving patients had their levels increase to normal before leaving the ICU (T4, 7.0 ±2.1 μg/dL; T3, 110±48ng/dL; and TSH, no change). The 14 patients who died showed further decreases before death (T4, 2.6±2.1 μg/dL; T3, 30.6 ± 23.5 ng/dL; and TSH, 0.9 ± 0.7 μU/mL). The corticotropin, cortisol, prolactin, and growth hormone levels were normal throughout the study. Catecholamine levels were high initially and decreased in surviving patients. Epinephrine levels increased greatly in nonsurvivors before death, and the norepinephrine-epinephrine ratio decreased from 5.7:1 to 2:1. After protirelin (thyroid-releasing hormone [TRH]) stimulation, the TSH level increased either minimally or not at all in six patients who eventually died. This indicates hypothalamicpituitary dysregulation or suppression, and altered release and/or peripheral metabolism of T4. Whether this represents a deficiency of thyroid hormone for cell and organ function remains to be established.
(Arch Surg 1984;119:1125-1132)