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Homonymous hemianopia due to cerebral air embolism from central venous catheters.

cedure was done, however, the small amount of pituitary tissue in the otherwise empty sella had basophilic hyperplasia and no adenoma. In addition, partial pituitary hypofunction is suggested by plasma gonadotropin levels that were inappropriately low for her postmenopausal state. Thyroid function was normal. Several management issues arose during the course of this patient's illness that deserve comment. Selective venous catheterization would have been helpful in establishing the pituitary as the source of inappropriate ACTH production. In a case of pituitary-dependent Cushing's and an empty sella, it is probably still warranted to surgically explore the pituitary fossa for a possible adenoma. Bilateral adrenalectomy remains, however, a reasonable treatment alternative. The question of whether this patient had Cushing's disease or Cushing's syndrome on another basis cannot ultimately be settled without a postmortem examination. The weight of the evidence suggests a pituitary basis. The factors supporting a primary pituitary aberration are the inappropriate rise in the ACTH level (though still within the normal range) in the presence of extreme hypercortisolism and its partial suppressibility. Other possible causes for Cushing's syndrome appear to be reasonably excluded. Documentation by CT scan of enlargement of both adrenal glands rules out a unilateral adrenocortical adenoma as the source of this patient's hypercortisolism. An ectopic source for ACTH is also unlikely for several reasons. The patient's long clinical course (six years), negative findings on a chest x-ray film, normal 24-hour urinary excretion of 5-hydroxyindoleacetic acid and partially suppressible hypercortisolism are inconsistent with an ectopic source for ACTH. Furthermore, the ACTH level in this paraneoplastic syndrome tends to be much higher than occurred in this patient. The failure of high-dose dexamethasone to suppress urinary 17-hydroxycorticosteroid excretion by at least 50% may argue against pituitary-dependent Cushing's disease, but 15% to 30% of these patients fail to suppress to this degree.14 This case also has potentially interesting implications concerning the natural history of Cushing's disease. If this patient's primary defect was at the level of the hypothalamus resulting in inappropriate stimulation of the pituitary, this would have caused development of a pituitary adenoma, ACTH hypersecretion and cushingcid features. Infarction of the adenoma may have then occurred, resulting in an empty sella. Of other possible causes of an empty sella, a developmentally incomplete sellar diaphragm cannot be completely excluded, whereas involution of a previously hypertrophied and overstimulated pituitary due to end-organ failure appears highly unlikely.