Position-dependent pressure pneumocephalus after transsphenoidal surgery: illustrative case.

BACKGROUND: Intracranial air may become trapped inside the cranial vault after cranial surgery, causing tension pneumocephalus with a variety of possible neurological symptoms. The authors reported a unique case in which position-dependent tension pneumocephalus developed after standard pituitary adenoma resection, causing severe intermittent visual symptoms. OBSERVATIONS: A tiny hole in the sellar floor after transsphenoidal surgery created a valve mechanism, allowing pressurized air accumulation inside the tumor capsule that periodically compressed the optic chiasm. This caused acute visual field defects only when the patient was in an upright position. Symptoms resolved when the patient lay down because pressurized air was allowed to escape from the cranial vault and compression of the optic chiasm was relieved. This phenomenon was verified with consecutive magnetic resonance imaging sequences demonstrating the relaxation of suprasellar space, after the intracranial air had escaped in a horizontal imaging position. LESSONS: Imperfect sealing of the sellar floor after transsphenoidal surgery is not uncommon. Even a tiny defect may in rare cases work in a valve-like manner, leading to intermittent air accumulation in the suprasellar space and causing corresponding visual symptoms. Pressure pneumocephalus inside an empty tumor capsule should be kept in mind as a possible rare complication after transsphenoidal surgery.

Early ischemic lesion on computed tomography: predictor of poor outcome among survivors of aneurysmal subarachnoid hemorrhage.

OBJECT: Identifying ischemic lesions after subarachnoid hemorrhage (SAH) is important because the appearance of these lesions on follow-up imaging correlates with a poor outcome. The effect of ischemic lesions seen on computed tomography (CT) scans during the first days of treatment remains unknown, however. METHODS: In 156 patients with SAH, clinical course and outcome, as well as the appearance of ischemic lesions on serial CT scans, were prospectively monitored for 3 months. At 3 months after SAH, magnetic resonance imaging was performed to detect permanent lesions that had not been visible on CT. RESULTS: Of the 53 patients with no lesions on any of the follow-up CT scans, four (8%) had a poor outcome. Of the 52 patients with a new hypodense lesion on the first postoperative day CT, 23 (44%) had a poor outcome. Among the remaining 51 patients with a lesion appearing later than the first postoperative morning, 10 (20%) had a poor outcome (p < 0.001). After adjusting for patient age; clinical condition on admission; amounts of subarachnoid, intracerebral, and intraventricular blood; and plasma glucose and D-dimer levels, a hypodense lesion on CT on the first postoperative morning was an independent predictor of poor outcome after SAH (odds ratio 7.27, 95% confidence interval 1.54-34.37, p < 0.05). CONCLUSIONS: A new hypodense lesion on early postoperative CT seems to be an independent risk factor for poor outcome after SAH, and this early lesion development may be more detrimental to clinical outcome than a later lesion occurrence.

Risk factors for ischemic lesions following aneurysmal subarachnoid hemorrhage.

OBJECT: The aim of this study was to test whether enoxaparin treatment (40 mg subcutaneously once daily) reduces the risk of cerebral infarction after subarachnoid hemorrhage (SAH) and to investigate predictive risk factors for permanent ischemic lesions visible on follow-up computerized tomography (CT) scans obtained 3 months after SAH. METHODS: After undergoing surgery for a ruptured aneurysm, 170 patients were randomized in a prospective, double-blind, placebo-controlled trial to test the effect of enoxaparin on the occurrence of ischemic lesions, which were demonstrated on follow-up CT scans available for 156 patients. The presence of lesions correlated highly with an impaired outcome, as assessed using both the Glasgow Outcome and modified Rankin Scales (p < 0.01). Lesions occurred in 101 (65%) of the 156 patients. In half of the patients (51 patients) no lesion was visible on the CT scan obtained on the 1st postoperative day in 51 patients. On univariate analysis, the presence of lesions at 3 months post-SAH was not associated with enoxaparin treatment but did correlate with several clinical, radiological, and prehemorrhage variables. Significant independent risk factors for lesions consisted of an impaired initial clinical condition (odds ratio [OR] 2.63, 95% confidence interval [CI] 1.03-6.73), amount of subarachnoid blood (OR 6.51, 95% CI 2.27-18.65), nocturnal occurrence of SAH (that is, between 12:01 a.m. and 8:00 a.m.; OR 4.32, 95% CI 1.28-14.52), fixed symptoms of delayed ischemia (OR 5.21, 95% CI 1.02-26.49), duration of temporary artery occlusion during surgery (OR 1.66 per minute, 95% CI 1.20-2.31), and body mass index (OR 1.13/kg/m2, 95% CI 1.01-1.28). CONCLUSIONS: The presence of ischemic lesions can be predicted by the severity of bleeding, delayed cerebral ischemia, excess weight, duration of temporary artery occlusion, and occurrence of nocturnal aneurysm rupture.

No effect of enoxaparin on outcome of aneurysmal subarachnoid hemorrhage: a randomized, double-blind, placebo-controlled clinical trial.

OBJECT: From the moment an intracranial aneurysm ruptures, cerebral blood flow is impaired, and this impairment mainly determines the outcome in patients who survive after the initial bleeding. The exact mechanism of impairment is unknown, but activation of coagulation and fibrinolysis correlate with clinical condition and outcome after aneurysmal subarachnoid hemorrhage (SAH). The purpose of this study was to determine whether enoxaparin, a low-molecular-weight heparin, which is a well-known anticoagulating agent, has any effect on the outcome of aneurysmal SAH postoperatively. METHODS: In this randomized, double-blind, single-center clinical trial, 170 patients (85 per group) with aneurysmal SAH were randomly assigned to receive either enoxaparin (40 mg subcutaneously once daily) or a placebo, starting within 24 hours after occlusion of the aneurysm and continuing for 10 days. Analysis was done on an intention-to-treat basis. Outcome was assessed at 3 months on both the Glasgow Outcome and modified Rankin Scales. Patients were eligible for the study if surgery was performed within 48 hours post-SAH, and no intracerebral hemorrhage was larger than 20 mm in diameter on the first postoperative computerized tomography scan. At 3 months, there were no significant differences in outcome by treatment group. Of the 170 patients, 11 (6%) died, and only 95 (56%) had a good outcome. Principal causes of unfavorable outcome were poor initial condition, delayed cerebral ischemia, and surgical complications. There were four patients with additional intracranial bleeding in the group receiving enoxaparin. The bleeding was not necessarily associated with the treatment itself, nor did it require treatment, and there were no such patients in the placebo group. CONCLUSIONS: Enoxaparin seemed to have no effect on the outcome of aneurysmal SAH in patients who had already received routine nimodipine and who had received triple-H therapy when needed. Routine use of low-molecular-weight heparin should be avoided during the early postoperative period in patients with SAH, because this agent seems to increase intracranial bleeding complications slightly, with no beneficial effect on neurological outcome.

Relationship of local infarctions to cognitive and psychosocial impairments after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Previous studies suggest that cognitive and psychosocial impairments after subarachnoid hemorrhage (SAH) result from diffuse brain damage caused by the initial bleeding rather than from focal lesions. We describe the relationship of local infarctions to these impairments and explore how well test and questionnaire results explain psychosocial outcome. METHODS: A total of 170 patients, selected from a consecutive series of patients with aneurysmal SAH, underwent neurological and neuroradiological examinations, and 138 of them were assessed with neuropsychological tests and questionnaires 1 year after SAH. RESULTS: Patients with left and bilateral infarctions performed worse on verbal memory tests than the other patients, and patients with left infarctions had more impaired working capacity than those with no infarction. The indices of the severity of SAH were related to reductions in both working capacity and social activity but less clearly to poor test performances. Whereas the modified Rankin scale was the most important correlate of working capacity, performance on cognitive tests was associated with return to work, and questionnaire ratings of mental impairments correlated with reduced working capacity and decreased social activity. CONCLUSION: Left-hemisphere infarctions cause deficits in verbal memory and working capacity. The severity of SAH is associated with impairments in working capacity and social activity rather than with specific cognitive deficits. Patients' and partners' opinions on patients' mental impairments could provide complementary information to clinical grades and cognitive tests in the evaluation of outcome after SAH.