A 5-year-old male child is admitted post valvular surgery to cardiac ICU. A consultation is sent saying that there is a suspicion of secondary hypo-thyroidism. The results are as below • T3–80 ng/dL (94–269 ng/dL) • T4–3 μg/dL (7–15 μg/dL) • TSH–0.02 μ IU/mL (0.5–5.0 μ IU/L) What is the clinical diagnosis in this case? What is the next step in evaluation of this patient? What other parameters can help in the diagnosis? The child was evaluated for other evidences of hypopituitarism as below The child is in the 5th centile which is expected as the child had untreated cyanotic congenital heart disease because of which the growth is stunted so probably growth hormone deficiency does not exist. The child has no evidence of micropenis so hypopituitarism was less of a possibility as it can be a marker of hypopituitarism. The child is maintaining blood pressure and is not requiring any ionotropic support which is an indirect evidence of normal cortisol levels. Thus, the clinical diagnosis in this child is kept as sick euthyroid syndrome as the other pituitary hormones are normal and there is no clinical evidence of hypopituitarism in this child. The levels of FT4 and FT3 are also done and FT4 is found to be in the normal range for age while FT3 is low. The other anterior pituitary hormones including random serum cortisol, FSH, LH and prolactin are measured in this child and the levels are found to be normal as per the clinical state of the patient. An IGF-1 level is done to screen for growth hormone deficiency and it is found to be in the normal range for age and sex matched controls. Different critical illness states leading to NTIS • Sepsis and trauma • Starvation • Cardiac dysfunction • Renal disease • Hepatic disease • Nonseptic shock • Burns • Respiratory failure • Other disease states like systemic sclerosis
Do these patients benefit from hormone supplementation?
Medicine
Treatment with thyroid hormone is controversial. The studies done so far have not conclusive benefit with levothyroxine replacement therapy in patients with sick euthyroid syndrome. Intravenous T3 administration is preferred as the peripheral conversion of T4 to T3 is decreased due to the reduced activity of 5’deiodinase enzyme.
Moreover, the use of thyroxine in patients with sick euthyroid syndrome may induce subclinical hyperthyroidism and T3 administration may exert negative effect on protein and fat metabolism and causes a rise in catechola-mine levels.
Thus the use of T3 in patients with NTIS and cardiac disease remains controversial. In some studies intravenous infusion of T3 has not shown any mortality benefit while in few it has been shown that after elective coronary artery bypass grafting the need of ionotropic support, incidence of postoperative myocardial ischemia and need of mechanical ventilation was reduced in patients who were given triiodothyronine. In acute renal failure and burn patients, thyroid hormone supplementation has not been shown to provide any mortality benefits. Thyrotropin releasing hormone (TRH) has been tried and has been shown to normalize the thyroid hormone values in a single day in critically ill patients and could be a safer alternative to thyroid hormone supplementation in such patients.
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