Abstract

Objective:To analyze alterations in thyroid function and the correlation between results of thyroid function test and mortality in medical and surgical intensive care unit (ICU) patients. It also aimed to evaluate the effect of thyroid dysfunction in ICU patients and their need for mechanical ventilation (MV).Methods:A single-center, prospective, observational study was conducted on patients admitted to medical and surgical ICU between 2013-2014.. Clinical and paraclinical findings (free triiodothyronine, free thyroxine and thyroid stimulating hormone) were documented for all patients. Regression analysis and chi-square were used for death and MV outcome variables.Results:We included 502 patients. Of these, 340 (67.7%) were admitted to the medical ICU. Results of thyroid function tests were normal in 320 (64%) and 162 (32.3%) medical and surgical ICU patients, respectively. Euthyroid sick syndrome (ESS) was documented in 86 patients (17%). Mortality was twice higher among surgical ICU patients with ESS compared to those with normal thyroid function (p=0.085), which is not statistically significant. Based on thyroid function status, no differences in the risk to be mechanically ventilated was found between medical or surgical ICU patients.Conclusion:There is a significant association between ESS and mortality in ICU patients. Future studies should determine whether abnormal thyroid function increases the risk for MV in ICU patients.

Highlights

  • Thyroid hormones play an essential part in human metabolism.[1]

  • Table-I: Baseline characteristics of the patients stratified by thyroid function status[1]

  • No difference in mortality was found between medical and surgical intensive care unit (ICU) patients based on thyroid function status with p value of 0.75 and 0.082 consecutively

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Summary

Introduction

Thyroid hormones play an essential part in human metabolism.[1]. Thyroid hormones support anabolism, intricate in cardiovascular system function (increase heart contractility and cardiac output), and reduce triiodothyronine/reverse1. Deiodination from T4 to T3 through marginal (hepatic) enzymes (inhibition of 5′- deionidase) leads to a reduction of T3 and proliferation in rT3 that is biologically inactive.[5]

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