Abstract

Abnormal thyroid markers are a frequent occurrence in emergency and intensive care medicine. Correct interpretation of their clinical relevance and distinction from a primary thyroid disease, particularly prior to potential administration of iodine-containing antiarrhythmic drugs such as amiodaron or radiocontrast agents, are both essential and challenging. This article aims to present the pathophysiology of abnormal thyroid markers in acute or protracted critical disease. Their relevance for administration of amiodaron or iodine-containing radiocontrast agents is discussed, and concrete practical recommendations are presented. The current work comprises a discussion of expert recommendations, guidelines, and basic research. Approximately one third of intensive care patients develop non-thyroidal illness syndrome (NTIS) during the course of their critical disease. NTIS is characterized by a reduction in the serum concentration of fT3 and, during the course, also in those of thyroid-stimulating hormone (TSH) and fT4, despite an organically intact thyroid gland. A greater extent of the deviations correlates with a worse overall prognosis. The mechanisms involved are manifold and influence different levels of hormonal signaling axes. They are mediated by interaction with acute stress signals such as inflammatory factors and elevated cortisol levels and are influenced by medication. The components vary depending on disease severity and the protracted course. NTIS does not require any specific treatment; the focus is on treating the underlying disease. Latent hyperthyroidism in particular must be distinguished from NTIS. In unclear situations and high-risk constellations, perchlorate is indicated before (and after) iodine exposure.

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