Abstract

The systemic response to stress caused by a critical surgical illness is characterized by a series of events that precede metabolic and neuroendocrine dysregulation. However, the relevance of theclassically described 'stress response' is now highly questionable in an era where profound physiological deconditioning is common in critically ill, surgical and non-surgical patients. Common assessment techniques do not accurately reflect the integrity of the hypothalamic-pituitary-thyroid axis in the course of a critical chronic disease state. The clinical presentation ismostly masked by symptoms of the underlying critical illness when plasma thyroid hormone concentrations are altered. The frequent development of multimorbidity in critically ill patients is the reason for the need for a more detailed analysis of the neuroendocrine model of activation. Basic scientific studies suggest that low levels of circulating thyroid hormones in the acute phase are an adaptive process, but the chronic condition could directly cause organ damage. Here, we review factors that have emerged to challenge the conventional model of euthyroid sick syndrome (ESS) in the surgically critically ill as an adaptive process, and suggest that the stage of the critical illness is an important consideration in the critically ill. Examining the stressresponse in the critically ill presents opportunities to improve outcomes through improved understanding of the neuroendocrine aspects.

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