The adrenal glands are of intrinsic importance in the physiological response to stress, responsible for maintenance of blood pressure and electrolyte homeostasis . In critically ill patients, unrecognised and untreated adrenal insufficiency is usually fatal  and as the presentation of acute adrenal insufficiency is variable and non-specific, a high degree of clinical suspicion is required.
Clinical features associated with adrenal insufficiency caused by adrenal haemorrhage include pain, fever, nausea, vomiting, fatigue, weakness, obtundation, anorexia, and hypotension. Laboratory features include hyponatraemia, hyperkalaemia, uraemia, hypoglycaemia, eosinophilia and anaemia. The clinical and laboratory features may or may not all be present, and thus it is extremely important to remain alert to the possibility of this diagnosis in patients at risk for developing adrenal haemorrhage [3, 4].
Bilateral adrenal haemorrhage is a rare cause of acute adrenal failure, generally occurring in hospitalised patients who are septic, coagulopathic or who have thromboembolic disorders. The post-operative or post-myocardial infarction states are risk factors. Adrenal haemorrhage secondary to sepsis most typically occurs in the presence of meningococcaemia and is referred to as Waterhouse-Friederichsen Syndrome. There is increasing evidence of hypothalamic-pituitary-adrenal insufficiency in critically ill septic patients which appears to result from circulating suppressive factors released during systemic inflammation. This is associated with both primary and secondary adrenal insufficiency . The prevalence of adrenal insufficiency in septic shock varies but is estimated to occur in approximately half of all septic shock cases [4, 5].
The pathogenesis of adrenal haemorrhage is typically multifactorial. The adrenal gland receives a rich blood supply from the aorta and the inferior phrenic and adrenal arteries, which form a subcapsular plexus. Necrosis and haemorrhage may occur during hypotension and stress as a result of ischemia or during adrenal stimulation from vascular engorgement and stasis -. Ligation of the right adrenal vein during orthotopic liver transplantation is a recognised cause of adrenal infarction leading to haemorrhage .
Platelet aggregation followed by venous thrombosis, vasoconstriction, disruption of the vascular endothelium and regional hypotension are major contributors to the pathogenesis of adrenal haemorrhage, all of which lead to intramedullary ischaemia. Bleeding ensues with reperfusion of these damaged vessels .
The diagnosis of adrenal insufficiency resulting from adrenal haemorrhage is often overlooked because of the nonspecific nature of the clinical presentation. Until recently, most diagnoses of adrenal haemorrhage were made at postmortem examination. The reported incidence of adrenal haemorrhage in general hospital autopsy studies is 0.14% to 1.8% .
Adrenal insufficiency may be established in patients with a random serum cortisol level . This condition can be excluded if the serum cortisol is >34 μg/dL. Conversely, the diagnosis is likely if the serum cortisol is <15 μg/dL. After intravenous administration of 250 μg of cosyntropin, a serum cortisol value at 30 or 60 minutes later of <14.9 μg/dL also points towards adrenal insufficiency . Before testing, dexamethasone can be used as corticosteroid replacement because it is not measured by the cortisol assay.
The criteria for biochemical diagnosis of adrenal insufficiency in the critically ill patient remain unclear and are controversial. Some critically ill patients produce inappropriately low amounts of cortisol in relation to their needs because of the severity of their disease, even with apparently normal basal serum cortisol levels, so called relative adrenal insufficiency . In these patients, a simultaneous measurement of serum cortisol and corticotrophin level is useful. The serum cortisol level will be inappropriately low in relation to the serum corticotrophin level. Of course, while corticotrophin stimulation is helpful in the diagnosis, it is not practical in patients with impending or established shock. In practice, a decrease in inotropic requirement and clinical improvement following administration of corticosteroids suggests adrenal insufficiency.
Ultrasound, CT, and magnetic resonance imaging (MRI) can all be used to suggest and/or confirm the diagnosis of adrenal haemorrhage, but CT is probably most useful and easily performed in critically ill patients. A hyperdense mass seen on non-intravenous contrast-enhanced CT scanning with no enhancement after intravenous contrast or enhancement only in a pattern of a thin peripheral rim can be valuable in discriminating a haematoma from adrenal tumours .
The treatment of adrenal insufficiency consists of prompt administration of parenteral hydrocortisone, tapered to maintenance oral hydrocortisone once the acute illness resolves . In primary adrenal insufficiency, mineralocorticoids can be added once the dose of hydrocortisone is <50 mg daily, however in a published case series, prolonged mineralocorticoid replacement was usually not required in patients with adrenal insufficiency due to bilateral adrenal haemorrhage .