Physiology
In acute states of severe stress, cortisol secretion by the adrenal gland increases up to sixfold, parallel to the severity of the condition. This is partly due to an increased secretion of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH). Several cytokines have been also shown to interfere with the HPA axis at multiple levels. There is also an increase in the number and affinity of glucocorticoid receptors. Levels of corticosteroid-binding globulin (CBG) and albumin, which normally bind cortisol, are decreased, resulting in increased levels of free cortisol. Furthermore, anaesthesia drugs like etomidate could interfere with the HPA axis. The secretion also loses its normal diurnal pattern of morning peak levels and evening and night time troughs. Nevertheless, secretion remains pulsatile and there is a marked variation in blood samples from the same individual.
High blood levels of cortisol during critical illness could theoretically be protective because of several reasons. They modulate metabolism (for example, by inducing high blood sugar levels, thereby providing energy to the body). They also suppress excessive immune system activation and exert supporting effects on the circulatory system. Increased susceptibility to infections, hyperglycemia (in patients already prone to stress hyperglycemia), gastrointestinal bleeding, electrolyte disturbances and steroid-induced myopathy (in patients already prone to critical illness polyneuropathy) are possible harmful effects.
Blood levels of dehydroepiandrosterone increase, and levels of dehydroepiandrosterone sulfate decrease in response to critical illness.
In the chronic phase of severe illness, cortisol levels decrease slowly and return to normal when the patient recovers. ACTH levels are however low, and CBG levels increase.
Read more about this topic: Critical Illness-related Corticosteroid Insufficiency
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