Acute Acquired Adrenoprivic Hypocorticalism

Abstract

The commonest cause of acute acquired adrenocortical insufficiency of primary adrenal origin was formerly regarded as bilateral adrenal haemorrhage (so-called adrenal apoplexy), such as occurs in the Waterhouse-Friderichsen syndrome (p. 277) with meningococcal septicaemia. Further studies, however, have quite clearly demonstrated that bilateral adrenal haemorrhage is rarely associated with overt biochemical evidence of acute adrenal insufficiency. It is worth noting, for example, that surgical extirpation of both adrenal glands and without substitution therapy is not followed by the overt manifestation of adrenocortical insufficiency within a period of 24–48 h, such as is said to occur following adrenal haemorrhage in fulminating septicaemia. Furthermore, plasma Cortisol levels have been measured in the Waterhouse-Friderichsen syndrome and found to be elevated (Migeon et al. 1967) as one would anticipate of the adrenal in response to stress. In addition, most cases of neonatal adrenal haemorrhage (p. 277), even when the haemorrhage is bilateral and massive, are still capable of a spontaneous and full recovery without the need for steroid replacement therapy (Black and Williams 1973). Hence, most cases of adrenocortical haemorrhage and necrosis can no longer be regarded as a primary cause of life-threatening adrenal insufficiency. Rather, in adults and children, it would appear to be relegated to a possible contributory factor to the demise of the patient but not a primary cause due to acute adrenocortical steroid insufficiency.