Classical pituitary apoplexy: clinical features, management and outcome

OBJECTIVE The term classical pituitary apoplexy describes a clinical syndrome characterized by sudden headache, vomiting, visual impairment and meningismus caused by the rapid enlargement of a pituitary adenoma usually due to haemorrhagic infarction of the tumour. Most published reports looking at the clinical features and management of pituitary apoplexy have not differentiated between patients with clinical and subclinical apoplexy, the latter diagnosed at surgery. Furthermore, little is reported on the clinical outcome, in particular visual and endocrinological, and the role of radiotherapy. The purpose of this study was to observe not only the clinical presentation but also the possible predisposing events, investigations, management, clinical outcome as well as the role of radiotherapy in patients presenting with classical pituitary apoplexy. PATIENTS AND DESIGN In a retrospective analysis 1985–96, the medical records of 21 male and 14 female patients (mean age 49.8 years, range 30–74) with classical pituitary apoplexy were reviewed. This represents all patients seen with this condition over the stated period. MEASUREMENTS In all patients, pre‐ and post‐ operative measurements were made of FT4, FT3, TSH, PRL, LH, FSH, cortisol (0900 h), GH, oestradiol (females) and testosterone (males). Pituitary imaging was by computerized tomography (CT) scan, magnetic resonance imaging (MRI) or both. RESULTS Patients were followed for up to 11 years (mean 6.3 years: range 0.5–11). Headache (97%) was the commonest presenting symptom, followed by nausea (80%) and a reduction of visual fields (71%). Hypertension, defined as a systolic > 160 mmHg and/or a diastolic > 90 mmHg, was seen in 26% of patients. MRI correctly identified pituitary haemorrhage in 88% (n = 7), but CT scanning identified haemorrhage in only 21% (n = 6). By immunostaining criteria, null‐cell adenomas were the most common tumour type (61%). Transsphenoidal surgery resulted in improvement in visual acuity in 86%. Complete restoration of visual acuity occurred in all patients operated on within 8 days but only in 46% of patients operated on after this time (9–34 days). Long‐term steroid or thyroid hormone replacement was necessary in 58% and 45% of patients, respectively. Of the male patients, 43% required testosterone replacement, and long‐term desmopressin therapy was required in 6%. Only two patients (6%) with tumour recurrence after transsphenoidal surgery for the initial apoplectic event, subsequ