الفهرس يوجد فقط 14 صفحة متاحة للعرض العام
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المستخلص
The definition of what constitutes a ’normal’ adrenal response to critical illness is unclear. Consequently, published studies have used a variety of biochemical criteria to define ’Adrenal Insufficiency’.
These criteria have been based on the baseline cortisol level or the increment in cortisol following corticotropin administration. However, in critically ill patients there are a number of confounding factors that make interpretation of these tests difficult. Furthermore, in those patients who are most likely to benefit from treatment with low-dose glucocorticoids, there is no evidence that treatment should be based on adrenal function testing. In those patients in whom the diagnosis of Adrenal Insufficiency may be important, this diagnosis may best be made based on the free cortisol level or the total cortisol level stratified by serum albumin.
Cortisol is the predominant corticosteroid secreted from the adrenal cortex in humans. In a healthy, unstressed person, cortisol is secreted according to a diurnal pattern under the influence of corticotropin released from the pituitary gland. Corticotropin secretion, in turn, is under the influence of hypothalamic corticotropin-releasing hormone and both hormones are subject to negative feedback control by cortisol itself. Circulating cortisol is bound to corticosteroid-binding globulin, with less than 10 percent in the free, bioavailable form. With severe infection, trauma, burns, illness, or surgery, there is an increase in cortisol production by as much as a factor of six that is roughly proportional to the severity of the illness Diurnal variation in cortisol secretion is also lost. These effects are due to increased production of corticotropin-releasing hormone and corticotropin and a reduction in negative feedback from cortisol Stimulation of the hypothalamic–pituitary–adrenal axis in this context is caused by elevated levels of circulating cytokines, among other factors.
Severe illness and stress activate the hypothalamic-pituitary-adrenal (HPA) axis and stimulate the release of corticotropin (also known as adrenal corticotropic hormone [ACTH]) from the pituitary, which in turn increases the release of cortisol from the adrenal cortex. This activation is an essential component of the general adaptation to illness and stress, and contributes to the maintenance of cellular and organ homeostasis. Animals that have had adrenalectomies succumb rapidly to hemorrhagic and septic shock, and steroid replacement is protective against these challenges. Even minor degrees of Adrenal Insufficiency increase the mortality of critically ill or injured patients. Chronic primary Adrenal Insufficiency, as first described by Addison in the mid-1800s, is a rare disease. However, acute Adrenal Insufficiency is a common and largely unrecognized disorder in critically ill patients. We review basic actions of glucocorticoids, etiologies for Adrenal Insufficiency in critically ill patients, factors affecting the release and action of cortisol, new criteria for evaluation of adrenal function during critical illness, and the treatment of Adrenal Insufficiency.