Adrenal insufficiency is a relatively rare but potentially lethal disease if missed during acute settings [1, 2]. Symptoms, signs and biological markers associated with adrenal failure are well known by clinicians [3, 4]. However the relative importance of these symptoms, signs and markers has not been fully studied in patients admitted in acute medical wards. Adrenal insufficiency is defined as primary or secondary. Autoimmune and tuberculous adrenalitis are the principal etiologies for primary adrenal failure, which is characterized by low cortisol levels and elevated plasma concentrations of ACTH. Impairment of the hypothalamic-pituitary corticotropic axis is responsible for secondary causes of adrenal insufficiency. These situations are characterized by low circulating levels of cortisol and ACTH. The most frequent cause of secondary adrenal insufficiency is a tumour of the hypothalamic-pituitary region but administration of supraphysiologic doses of glucocorticoids may alter a normal hypothalamic response with secondary adrenal failure once individuals are weaned from the glucocorticoid treatment. Bilateral adrenalectomy or drug-induced adrenal insufficiency may be considered as iatrogenic etiologies for adrenal failure.
Symptoms commonly associated with adrenal insufficiency are “fatigue” (lack of energy or stamina), abdominal pain, nausea, and dizziness (hypotension symptoms). The patient history may include a key element related to previous glucocorticoid treatment, thus increasing the risk of secondary adrenal failure related to glucocorticoid withdrawal. Signs associated with adrenal insufficiency are low blood pressure, vitiligo and/or skin changes. Biological markers of the disease include hyperkalemia, hyponatremia, acidosis, hypercalcaemia and eosinophilia. Nevertheless, the proportion of individuals with one or more symptoms or signs associated with adrenal insufficiency is not clearly described in the literature.
Evaluating adrenal function is a difficult task in clinical practice . Cortisol response to ACTH administration may depend upon the biological stress of the patients (intensive care versus stable conditions), the cut-off values for cortisol levels and the use of low (1 μg) versus high (250 μg) dose ACTH-stimulation test [6–9]. Basal cortisol levels inaccurately assess adrenal function . Conversely, the high dose ACTH-stimulation test (“Synacthen® test”, cosyntropin stimulation test or tetracosactide test) is generally accepted as reliable to evaluate adrenal function in everyday practice, and considered as the easiest to perform [11–13]. If this test is recognized as gold standard in various clinical situations, it may be more difficult to define cut-off values for cortisol levels in intensive care. Patel and co-authors described expected values of basal serum cortisol (> 250 nmol/l) and peak cortisol (> 600 nmol/l) after 250 μg intramuscular tetracosactrin in acute hospital admissions . However, the optimal cut-off for peak cortisol levels avec ACTH challenge has been questioned by several authors and current recommendations seem to include a minimum of > 18-20 μg/dl (> 500–550 nmol/l) to consider the ACTH response as adequate. These normal values vary dependent on laboratory and assay. In our department, the 550 nmol/l cut-off is considered as a normal response to the ACTH challenge. The minimum increment in serum cortisol is considered by Patel  and others as invalid to diagnose adrenal failure, because individuals who have a high basal concentration, due to normal circadian rhytmicity or acute stress, may be unable to increase further cortisol secretion.
The aim of this study was to identify the clinical and biological determinants associated with adrenal insufficiency in patients admitted to an acute medical ward.