The Stress Response of Critical Illness: Metabolic and Hormonal Aspects by Jean-Charles Preiser

Author:Jean-Charles Preiser
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

11.2 Alterations in the Thyroid Axis in Acute and Prolonged Critical Illness

Patients suffering from a variety of critical illnesses present with uniform alterations within the thyroid axis (Fig. 11.2). During acute and severe physical stress, caused by illness, surgery, or trauma, T3 plasma concentrations decline rapidly, whereas circulating rT3 concentrations increase. The concentration of T4 is only shortly elevated and subsequently returns to the normal physiological range, although in more severely ill patients, T4 concentration can also decrease [12]. In contrast with primary hypothyroidism, low plasma T3 concentration perseveres in the presence of normal TSH. This constellation, with low plasma T3 but normal TSH in the context of illness, has been described as “euthyroid sick syndrome,” “low T3 syndrome,” or “nonthyroidal illness (NTI).” The reduction in circulating T3 during the first hours after ICU admission reflects the severity of illness and correlates with outcome [13, 14].

Fig. 11.2Changes in the thyroid axis during acute and chronic critical illness. The upper panel displays reduced TRH gene expression in the hypothalamus of prolonged critically ill rabbits (Adapted from [28]). The middle panel illustrates schematically the observed adaptations in circulating TSH and TH of acute and prolonged critically ill patients. The bottom panel summarizes the findings in deiodinase tissue activity of acute and prolonged critically ill patients

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