Thyroid Hormone in the Pediatric Intensive Care Unit.

Abstract

Thyroid hormones are key factors necessary for normal growth and development in children. They have tight control of metabolic rate and, as a result, frequently become altered in their synthesis and/or release during times of stress or critical illness. Disturbances in thyroid hormone homeostasis have been well described in several pathologic states, including sepsis/septic shock, renal failure, trauma, severe malnutrition, and following cardiopulmonary bypass. Specifically, a decrease in serum triiodothyronine (T3) and a concomitant increase in reverse triiodothyronine (rT3) levels are the most common changes observed. It is further noteworthy that serum thyroxine (T4), rT3, and T3 levels change in relation to severity of nonthyroidal illness. Many past investigators have speculated that these alterations are a teleological adaptation to severe illness and the increased metabolic demands that critical illness bears. However, this paradigm has been challenged through multiple avenues and has lost support over the past few years. Instead the "inflammatory hypothesis" has emerged implicating a cytokine surge as the mediator of thyroid hormone disruption. Overall, the demonstrated association between low thyroid hormone levels and poor clinical outcomes, the beneficial effects of thyroid hormone supplementation in multiple critically ill subpopulations, and the well-established safety profile of T3 therapy make thyroid hormone supplementation in the pediatric ICU worth consideration.