network. The headache woke him out of sleep, and he experienced sudden vomit­ing at the installation of the complaints. Neurological examination at the emer­gency department showed Glasgow Coma Scale of 12 out of 15. He was restless and anxious, complaining of a throbbing headache. He was not cushingoid, acro­megalic, or eunuchoid and no gynecomastia or galactorrhea was present. Unable to help with the bedside visual acuity test, the patient kept repeating that he could not see well, especially with his left eye. There was a sluggish light reex bilater­ally and a questionable nuchal rigidity. A subarachnoid hemorrhage was the ini­tial diagnostic assumption, as no previous medical history of a sellar lesion existed. A computed tomography (CT) scan (Fig.30.1A–D), however, showed an enlarged sella and an intrasellar lesion that extended to the suprasellar space and protruded towards the cavernous sinuses, particularly on the left. A bright, thin halo on the top of the lesion suggested focal subarachnoid intracranial hemor­rhage. The patient was admitted to the intensive care unit (ICU) with the diagno­sis of apoplectic, previously undiagnosed sellar lesion and routine preoperative exams as well as hormonal serum prole were collected. An endovenous (EV) bolus of hydrocortisone 500mg was administered before surgery, while awaiting the results of the hormonal prole. Five hours after admission he was taken to the operating room (OR) and a microsurgical transsphenoidal surgery with endo­scopic assistance performed. During surgery, the bony sellar oor was found thinned and eroded, with a tense sellar dura prolapsing towards the sphenoidal sinus. Dural opening initially relieved a liquied, reddish bloody content and fur­ther material was collected under the surgical microscope with transsphenoidal microsurgical curettes. The endoscope was introduced to explore the cavity at the end of the procedure and further laterally displaced material removed, except on the right side, where the pituitary gland seemed to have been displaced. The sella oor was closed using a bony fragment reserved from the sphenoidal rostrum dur­ing the approach, supported by Gelfoam cubes. The surgical procedure was undertaken under 150minutes. At the immediate postop period, the patient indi­cated relief both of his headache and visual disturbances. The same-day postop CT scan (Fig.30.1E–H), 17hours after the admission CT, showed adequate sellar decompression. Preop serum prole disclosed only mild elevation of serum pro­lactin, compatible with infundibular compression by a non-secreting pituitary adenoma, later conrmed by histopathology. The postop period was uneventful, during which rst line, EV, analgesic drugs, were administered, when needed, and were enough to control his headache. Oral hydrocortisone was swiftly tapered off while monitoring the urinary density and output. The patient was able to perform a campimetry on the third postop day. He was discharged on the fourth postop day, after repetition of the hormonal prole and having the rst endocrinologic outpatient consultation scheduled within a fortnight. The rst neurosurgical out­patient follow-up, scheduled in four weeks’ time included evaluation of postop magnetic resonance imaging (MRI) and comparative campimetry.