الفهرس 
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Abstract
The concept of adrenal insufficiency during critical illness remains a highly debated disease. There is no consensus about the diagnostic criteria of this context. Also, there exists considerable conflict about what cortisol level is ”normal” or ” adequate ” in critical illness, what constitutes an adequate response to ACTH, and what dose of synthetic ACTH should be used for stimulation testing.
The overall prevalence of adrenal insufficiency in critically ill medical patients about 10–20%, with a rate as high as 60% in patients with septic shock. Absolute adrenal insufficiency is rare with incidence of 3%, relative adrenal insufficiency not uncommon in critical illness with variable incidence (0-70%) depending on the population of patients studied and the diagnostic criteria. However, the use of terms absolute or relative adrenal insufficiency are best avoided in the context of critical illness, as the differentiation of absolute and relative adrenal insufficiency remains controversial.
Several studies have addressed how to diagnose or treat this condition but have often controversial. The main reason for the controversy is the fact that the pathophysiology is not completely understood. It is caused by adrenal insufficiency together with tissue corticosteroid resistance and is characterized by an exaggerated and prolonged proinflammatory response; recently, new insights in the pathophysiology of the hypothalamic–pituitary–adrenal axis response to critical illness were generated. It was revealed that high circulating levels of cortisol during critical illness are explained more by reduced cortisol breakdown than by elevated cortisol production. Which in turn reduce plasma ACTH concentrations via feedback inhibition, which with time may lead to an under stimulation and hereby a dysfunction of the adrenal cortex. This could explain the high incidence of adrenal insufficiency in the prolonged phase of critical illness.
Assessing adrenal insufficiency or relative adrenal insufficiency in critically ill patients is difficult. Laboratory assays of plasma cortisol concentration and response to adrenocorticotropic hormone (ACTH) stimulation are likely unreliable in critically ill patients. The initial diagnosis of suspected RAI starts with the clinical presentation. Hypotension refractory to fluid resuscitation and vasopressors may be signs of CIRCI, even when other symptoms of adrenal failure are absent. Suggested diagnostic criteria for CIRCI have been based on one landmark study that identified a plasma cortisol incremental response < 9 mcg/dl after the injection of 250 mcg ACTH in the face of a high baseline plasma cortisol concentration (> 34 mcg/dl) as most indicative for an increased risk of death. However, these findings have not been repeated by other investigators, which explain why there is currently no consensus on the diagnostic criteria for CIRCI.