DIAGNOSIS AND DISCUSSION:
Massive adenohypophysial necrosis (few weeks old) corresponding to "respirator pituitary".
Pituitary necrosis in patients kept alive on mechanical respirator was first described by McCormick and Halmi in 1970 (7). Subsequently several authors reported an increased incidence of pituitary necrosis in artificially ventilated patients (2,10). The incidence of pituitary necrosis which can be called respirator pituitary in patients maintained on respirators is 18-30% compared with 1-5% found in unselected autopsy material (2,6). The lesion is characterized by areas of necrosis of variable extent and can be regarded morphologically as ischemic infarct. It involves the central portion of the adenohypophysis leaving a rim of surviving parenchyma at the periphery underneath the fibrous capsule (2). The extent of necrosis varies from focal detachment of cells from the basement membrane to small or large infarcts involving up to 90 % of the adenohypophysis (2,7). Depending on the duration of artificial ventilation, the lesion may represent acute coagulating necrosis or a more chronic lesion such as capillary rich, loose connective tissue or a scar. Necrosis of the neurohypophysis may also occur in 3-40% of the cases (2,7). In many cases brain injury such as softening, swelling, infarcts of various sizes can also be demonstrated. For the cerebral lesion the term respirator brain was applied (7). However, no close correlation exists in the incidence and extent of cerebral and pituitary lesions (6,7).
The pathogenesis of pituitary infarction in patients on a mechanical respirator is not clear. Based on the morphologic findings it is evident that the lesion in the adenohypophysis is due to ischemia (3,6). Histologically identical infarcts have been found in several other conditions, such as obstetric shock, epidemic hemorrhagic fever, diabetes mellitus and section of the pituitary stalk (3,4,5,8,11). The arrest of blood flow to the adenohypophysis may be caused by vasospasm (2) or thrombosis (10) of the vessels supplying the adenohypophysis with blood. Increased intracranial pressure, severe hypotension may interfere with adenohypophysial blood flow and lead to ischemic infarction (7). The artificial ventilation per se cannot be implicated in the pathogenesis. The role of artificial ventilation is that this intervention prolongs the life of the patient and permits the progression of the lesion to histologically recognizable infarction (6). The question arises whether massive destruction of adenohypophysial cells leads to life threatening hypopituitarism. The pituitary has a remarkable reserve capacity. Previous studies showed that at least 80-90% of the pituitary parenchyma has to be removed or destroyed before symptoms of hypopituitarism may develop (3). Since adenohypophysial cells are not capable of adequate regeneration and the proliferation rate of adenohypophysial cells are very low, in patients with massive loss of hormone producing cells, normal endocrine function cannot be restored. Barber evaluated adenohypophysial function in 50 patients on mechanical respirators and found 7 cases (14%) who developed hypopituitarism (1). In his cases, hypopituitarism was transient and did not appear to affect survival. Sugimoto et al found decreased blood levels of ACTH, GH, PRL, TSH, LH and vasopressin in ventilated patients with necrosis of the hypothalamus and pituitary (9). Patients with postpartum pituitary necrosis may develop permanent hypopituitarism which, if not treated, may cause severe endocrine abnormalities and demise of the patients (8). In our case endocrinologic investigation was not performed, but it is known that patients kept alive on mechanical respirators may develop hypopituitarism (1). In these patients investigation of pituitary function should be carried out and if needed substitution therapy should be introduced.
Contributed by Mubarak Al-Gahtany, Kalman Kovacs and Juan M. Bilbao