SINCE Brougham et al6 in 1950 reviewedthe literature and reported five new cases of pituitary apoplexy, there has been an increasing interest in the subject. Subsequent physicians 22,26,45 reporting their clinical experiences have cited other recorded cases so that the total number now stands at or near 85. 2-11,13-15,17-26, 30-33,35-49 We have recently treated two additional patients with spontaneous hemorrhage into pituitary adenomata. The details of these are reported here.Clinical Summaries Case 1.\p=m-\A 63-year-old bricklayer was transferred from another hospital on April 29, 1960, for evaluation of headache, diplopia, drowsiness, nausea, and vomiting of five days duration. In 1954 a routine chest x-ray had shown multiple pulmonary densities which were thought to represent silicosis. However, metastatic tumor was considered, and a lateral skull film taken as part of a routine metastatic bone series showed an enlarged sella turcica. Endocrine studies showed normal 17-ketosteroid and 17-hydroxysteroid excretion values, but protein bound iodine was 1.5/¿g%. A tenta¬ tive diagnosis of chromophobe adenoma was made. In 1956 the sella had increased in size. Cortisone (12.5 mg) and thyroid extract, (60 mg) were begun daily and testosterone propionate 25 mg twice weekly.On April 24, 1960, the patient suddenly developed intense frontal headache, nausea, vomiting, and leth¬ argy. Blood pressure on admission to another hospital was 230/120. Within a few hours he developed left ophthalmoplegia and two days later, right ophthalmo-plegia. Visual acuity decreased but by confrontation testing fields were full.On transfer five days later he was still drowsy. Temperature was 102.6 F (39.44 C). Total left ophthalmoplegia was present, but the right VI cranial nerve was thought to be functioning. He could scarcely read 5 mm letters with the left eye and could read only 10 mm letters with the right one. There was mild weakness of the left side of the face and left upper extremity. Neurological examination was other¬ wise physiologic.Laboratory data: Hb 13.5 gm%. Hct 40%. WBC 7,700 cu mm with 62% neutrophils, 33% lymphocytes, and 5% band forms. Eosinophil count was 125 cu mm. Urinalysis showed specific gravity 1.019; there was a trace of albumin but no sugar, acetone, or cells. Fast¬ ing blood sugar 136 mg%. BUN 24 mg%. Cholesterol 189 mg%. Sodium 138 mEq/liter. Potassium 4.0 mEq/liter. Chloride 104 mEq/liter. Carbon dioxide 30.1 mEq/liter. Phosphorus 3.2 mg%. Alkaline phosphatase 3.0 units. Twenty-four hour 17-ketosteroid excretion 0.0; corticoid 8.9, 8.3 mg. Urinary corticoid response to corticotropin was delayed for 24 hours and was submaximal (ie, 17.4, 18.6 mg). Free plasma 17-OHCS response to corticotropin was markedly re¬ duced.
