Cardiac surgery using cardiopulmonary bypass produces a generalized systemic inflammatory response, resulting in increased postoperative morbidity and mortality. Under these circumstances, a typical pattern of thyroid abnormalities is seen in the absence of primary disease, defined as sick euthyroid syndrome (SES). The presence of postoperative SES mainly in small children and neonates exposed to long bypass times and the pharmacological profile of thyroid hormones and their effects on the cardiovascular physiology make supplementation therapy an attractive treatment option to improve postoperative morbidity and mortality. Many studies have been performed with conflicting results. In this article, we review the important literature on the development of SES in paediatric postoperative cardiac patients, analyse the existing information on thyroid hormone replacement therapy in this patient group and try to summarize the findings for a recommendation.
IntroductionDuring systemic illness, especially after cardiac surgery using cardiopulmonary bypass (CBP), abnormalities in the circulating thyroid hormone levels are found in the absence of primary thyroid disease; this is collectively called the sick euthyroid syndrome (SES). Some argue that it is unclear if the clinical picture of SES is an adaptive process, a marker of the severity of illness or even if treatment is warranted in these patients.The many effects of thyroid hormones on the cardiovascular system have been described in detail elsewhere [1][2][3]. The biological actions of thyroid hormones on the cardiovascular system make these hormones attractive as a potential treatment option in the management of patients after cardiac surgery.We review the actual literature on the development of SES in children after cardiac surgery and discuss the relevant literature on hormone replacement. Finally, a critical appraisal of the potential effects of hormone replacement and the studies performed is sought.
Sick euthyroid syndromeIt is well known that several severe diseases can cause abnormalities in the circulating thyroid hormone levels in the absence of primary thyroid disease (i.e., non-thyroidal illness or SES) [4].The most common pattern is a decrease in total and unbound triiodothyronin (T3) with normal levels of thyroid stimulating hormone (TSH) and thyroxin (T4). This is classified as SES type 1 (SES-1) or low-T3 syndrome. The de-ionidation from T4 to T3 via peripheral (hepatic) enzymes (inhibition of 5′-deionidase, a selenoenzyme [5,6]) is impaired, leading to a decrease of T3 and an increase in reverse T3 that is biologically inactive [7]. Inflammatory cytokines have been linked to the development of SES [8] and the levels of cytokines seem to influence the severity of SES [9,10]. Elevated serum levels of steroids as part of a stress response may influence the de-ionidase activity and TSH and T3 response in SES [8,[11][12][13]. Additionally, tissue-specific thyroid hormone bioactivity is reduced during cellular hypoxia and contributes to the low T(...