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Object: An intracranial pressure (ICP) monitor, from which cerebral perfusion pressure (CPP) is estimated, is recommended in the care of severe traumatic brain injury (TBI). Nevertheless, optimal ICP and CPP management may not always prevent cerebral ischemia, which adversely influences patient outcome. The authors therefore determined whether the addition of a brain tissue oxygen tension (PO2) monitor in the treatment of TBI was associated with an improved patient outcome., Methods: Patients with severe TBI (Glasgow Coma Scale [GCS] score < 8) who had been admitted to a Level I trauma center were evaluated as part of a prospective observational database. Patients treated with ICP and brain tissue PO2 monitoring were compared with historical controls matched for age, pathological features, admission GCS score, and Injury Severity Score who had undergone ICP monitoring alone. Therapy in both patient groups was aimed at maintaining an ICP less than 20 mm Hg and a CPP greater than 60 mm Hg. Among patients whose brain tissue PO2 was monitored, oxygenation was maintained at levels greater than 25 mm Hg. Twenty-five patients with a mean age of 44 +/- 14 years were treated using an ICP monitor alone. Twenty-eight patients with a mean age of 38 +/- 18 years underwent brain tissue PO2-directed care. The mean daily ICP and CPP levels were similar in each group. The mortality rate in patients treated using conventional ICP and CPP management was 44%. Patients who also underwent brain tissue PO2 monitoring had a significantly reduced mortality rate of 25% (p < 0.05)., Conclusions: The use of both ICP and brain tissue PO2 monitors and therapy directed at brain tissue PO2 is associated with reduced patient death following severe TBI.

Object: Nimodipine has been shown to improve neurological outcome after subarachnoid hemorrhage (SAH); the mechanism of this improvement, however, is uncertain. In addition, adverse systemic effects such as hypotension have been described. The authors investigated the effect of nimodipine on brain tissue PO2., Methods: Patients in whom Hunt and Hess Grade IV or V SAH had occurred who underwent aneurysm occlusion and had stable blood pressure were prospectively evaluated using continuous brain tissue PO2 monitoring. Nimodipine (60 mg) was delivered through a nasogastric or Dobhoff tube every 4 hours. Data were obtained from 11 patients and measurements of brain tissue PO2, intracranial pressure (ICP), mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were recorded every 15 minutes. Nimodipine resulted in a significant reduction in brain tissue PO2 in seven (64%) of 11 patients. The baseline PO2 before nimodipine administration was 38.4+/-10.9 mm Hg. The baseline MABP and CPP were 90+/-20 and 84+/-19 mm Hg, respectively. The greatest reduction in brain tissue PO2 occurred 15 minutes after administration, when the mean pressure was 26.9+/-7.7 mm Hg (p < 0.05). The PO2 remained suppressed at 30 minutes (27.5+/-7.7 mm Hg [p < 0.05]) and at 60 minutes (29.7+/-11.1 mm Hg [p < 0.05]) after nimodipine administration but returned to baseline levels 2 hours later. In the seven patients in whom brain tissue PO2 decreased, other physiological variables such as arterial saturation, end-tidal CO2, heart rate, MABP, ICP, and CPP did not demonstrate any association with the nimodipine-induced reduction in PO2. In four patients PO2 remained stable and none of these patients had a significant increase in brain tissue PO2., Conclusions: Although nimodipine use is associated with improved outcome following SAH, in some patients it can temporarily reduce brain tissue PO2.

Object: Increased intracranial pressure (ICP) is well known to affect adversely patients with head injury. In contrast, the variables associated with ICP following aneurysmal subarachnoid hemorrhage (SAH) and their impact on outcome have been less intensely studied., Methods: In this retrospective study the authors reviewed a prospective observational database cataloging the treatment details in 433 patients with SAH who had undergone surgical occlusion of an aneurysm as well as ICP monitoring. All 433 patients underwent postoperative ICP monitoring, whereas only 146 (33.7%) underwent both pre- and postoperative ICP monitoring. The mean maximal ICP was 24.9 +/- 17.3 mm Hg (mean +/- standard deviation). During their hospital stay, 234 patients (54%) had elevated ICP (> 20 mm Hg), including 136 of those (48.7%) with a good clinical grade (Hunt and Hess Grades I-III) and 98 (63.6%) of the 154 patients with a poor grade (Hunt and Hess Grades IV and V) on admission. An increased mean maximal ICP was associated with several admission variables: worse Hunt and Hess clinical grade (p < 0.0001), a lower Glasgow Coma Scale (GSC) motor score (p < 0.0001); worse SAH grade based on results of computerized tomography studies (p < 0.0001); intracerebral hemorrhage (p = 0.024); severity of intraventricular hemorrhage (p < 0.0001); and rebleeding (p = 0.0048). Both intraoperative cerebral swelling (p = 0.0017) and postoperative GCS score (p < 0.0001) were significantly associated with a raised ICP. Variables such as patient age, aneurysm size, symptomatic vasospasm, intraoperative aneurysm rupture, and secondary cerebral insults such as hypoxia were not associated with raised ICP. Increased ICP adversely affected outcome: 71.9% of patients with normal ICP demonstrated favorable 6-month outcomes postoperatively, whereas 63.5% of patients with ICP between 20 and 50 mm Hg and 33.3% with ICP greater than 50 mm Hg demonstrated favorable outcomes. Among 21 patients whose raised ICP did not respond to mannitol therapy, all experienced a poor outcome and 95.2% died. Among 145 patients whose elevated ICP responded to mannitol, 66.9% had a favorable outcome and only 20.7% were dead 6 months after surgery (p < 0.0001). According to results of multivariate analysis, however, ICP was not an independent outcome predictor (odds ratio 1.26, 95% confidence interval 0.28-5.68)., Conclusions: Increased ICP is common after SAH, even in patients with a good clinical grade. Elevated ICP post-SAH is associated with a worse patient outcome, particularly if ICP does not respond to treatment. This association, however, may depend more on the overall severity of the SAH than on ICP alone.

Object: Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease., Methods: The study focused on seven patients (mean age 30.6 +/- 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management., Conclusions: All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 +/- 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 +/- 11 mm Hg) and an increase in CPP (81 +/- 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 +/- 13.8 mm Hg to 45.5 +/- 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.

The authors reviewed the hospital charts of 415 pediatric patients treated for benign or malignant primary brain tumors over the past 20 years at the Children's Hospital Medical Center, Seattle. Patients' ages ranged from the neonatal period to 18 years. A shunt was placed in 152 patients (37%), 45 before and 94 after surgery. Confirmation of extraneural metastases was based on clinical and diagnostic examination. Factors analyzed as possibly influencing the occurrence of extraneural metastases were: 1) the shunt: type, valve, location, filter, and revisions; 2) extent of resection; 3) pathology; and 4) treatment regimen. Eight of the 415 patients developed extraneural metastases during life. All eight patients had a medulloblastoma (cerebellar primitive neuroectodermal tumor). These eight patients were separated into Group A (without a shunt) and Group B (with a shunt). In Group A (five patients), the mean interval from primary diagnosis to metastasis was 15 months. Two children had gross total resection of the tumor. The predominant location of metastases in Group A was: bone (two cases); cervical lymph nodes (one); lung/bone (one); and retroperitoneal pelvic mass (one). Three Group A patients had a simultaneous central nervous system (CNS) recurrence. Of the three Group B patients, two had a ventriculoperitoneal (VP) shunt and one a ventriculoatrial (VA) shunt; all were placed postoperatively. One Group B patient had a simultaneous CNS recurrence. No shunt revisions were performed in these three patients. The mean time from primary diagnosis to metastasis was 25 months. One patient had a total tumor resection. The predominant location of metastases was bone (one case), retroperitoneal pelvic mass (one), and abdominal cavity with ascites (one case). Only one patient in the entire series had a filter placed; this resulted in shunt obstruction and was removed 1 month following placement. It is concluded that cerebrospinal fluid shunts, regardless of type, location, revision rate, or filter insertion, do not predispose pediatric patients with brain tumors to develop extraneural metastases. A diagnosis of shunt-related metastases should be based on the development of intra-abdominal (VP shunt) or pulmonary (VA shunt) dissemination primarily with or without additional sites. The diagnosis of medulloblastoma is an important factor related to metastasis occurrence while the extent of resection and postoperative therapy are not influential.

Twenty-two patients with primary or metastatic brain tumors were evaluated with computerized tomography (CT) and intraoperative ultrasound. Tumor volume was estimated using a geometric formula based on CT and intraoperative ultrasound measurements. In most cases, tumor margins were marked with indigo carmine injected by ventricular cannula or with Silastic ventricular catheters placed under ultrasonographic control. Nine tumors had previously been operated on and irradiated (Group A). In this group, intraoperative ultrasound tended to overestimate the tumor volume compared to CT (intraoperative ultrasound findings 141.39% +/- 37.73% of CT findings (mean +/- standard deviation]. Sixteen patients were operated on for the first time (Group B), and in this group the volume estimates were comparable (intraoperative ultrasound findings 101.69% +/- 24.65% of CT findings). The difference between the means was statistically significant (p less than 0.01). Ultrasonography improved intraoperative delineation of tumor margins, as depicted by CT, thus maximizing the extent of resection; however, with recurrent tumors, intraoperative ultrasound tended to overestimate the tumor volume. Gliosis may account for this difference.

Computerized tomography (CT) infusion scanning can confirm the presence or absence of an aneurysm as a cause of spontaneous intracerebral hemorrhage. Eight patients who presented with spontaneous hemorrhage were examined using this technique. In five patients the CT scan showed an aneurysm which was later confirmed by angiography or surgery; angiography confirmed the absence of an aneurysm in the remaining three patients. This method is an easy effective way to detect whether an aneurysm is the cause of spontaneous intracerebral hemorrhage.