-BACKGROUND: Neurocritical management of aneu-rysmal subarachnoid hemorrhage focuses on delayed ce-rebral ischemia (DCI) after aneurysm repair.-METHODS: This study conceptualizes the pathophysiology of cerebral ischemia and its management using a brain oxy-gen -directed protocol (intracranial pressure [ICP] control, eubaric hyperoxia, hemodynamic therapy, arterial vasodila-tion, and neuroprotection) in patients with subarachnoid hemorrhage, undergoing aneurysm clipping (n = 40).-RESULTS: The brain oxygen -directed protocol reduced LbO2 (PbtO2 [partial pressure of brain tissue oxygen] <20 mm Hg) from 67% to 15% during acute brain attack (<24 hours of ictus), by increasing PbtO2 from 11.31 +/- 9.34 to 27.85 +/- 6.76 (P< 0.0001) and then to 29.09 +/- 17.88 within 72 hours. Day-after-bleed, FiO2 change, ICP, hemoglobin, and oxygen saturation were pre-dictors for PbtO2 during early brain injury. Transcranial Doppler -ltrasonography velocities (>20 cm/second) increased at day 2. During DCI caused by territorial sonographic vasospasm (TSV), middle cerebral artery mean velocity (Vm) increased from 45.00 +/- 15.12 to 80.37 +/- 38.33/second by day 4 with concomitant PbtO2 reduction from 29.09 +/- 17.88 to 22.66 +/- 8.19.Peak TSV (days 7-12) coincided with decline in PbtO2. Nicardipine mitigated LbO2 during peak TSV, in contrast to n imodipine, with survival benefit (P < 0.01). Intravenous and cisternal nicardipine combination had survival benefit (Cramer F = 0.43 and 0.327; G2 = 28.32; P< 0.001). This study identifies 4 zones of LbO2 during survival benefit (Cramer F = 0.43 and 0.3) TSV, uncompensated; global cerebral ischemia, compen-sated, and normal PbtO2. Admission Glasgow Coma Scale score (not increased ICP) was predictive of low PbtO2 (b= 0.812, R2 = 0.661, F1,30 = 58.41; P< 0.0001) during early brain injury. Coma was the only credible predictor for mortality (odds ratio, 7.33/>4.8*; c2 = 7.556; confidence interval, 1.70-31.54; P < 0.01) followed by basilar aneurysm, poor grade, high ICP and LbO2 during TSV. Global cerebral ischemia occurs immediately after the ictus, persisting in 30% of patients despite the high therapeutic intensity level, superimposed by DCI during TSV. -CONCLUSIONS: We propose implications for clinical practice and patient management to minimize cerebral ischemia.

The objective of this study was to examine the clinical determinants of incidence and prognosis of arrhythmias in the setting of acute brain injury. Acute brain injury is known to cause electrocardiographic abnormalities and cardiac arrhythmias. The relation between partial brain tissue oxygen (PBTO) and intracranial pressure (ICP) with arrhythmia incidence and prognosis remains unknown. Consecutive patients with acute brain injury and intracranial bleed admitted to the neurosurgical intensive care unit were enrolled in the study. Baseline characteristics [demographics, medical history, etiology of brain injury, Glasgow Coma Scale (GCS) score, blood pressure, and respiratory rate] were documented. Patient's telemetry recordings were reviewed for daily mean heart rates and arrhythmias. If arrhythmia was noted, PBTO levels at the beginning of arrhythmia, ICP, brain tissue temperature, and outcomes were recorded. A total of 106 subjects (53% men, age 39 ± 18 years, 65 traumatic and 41 nontraumatic brain injuries) were studied. Overall, 62% of subjects developed a total of 241 arrhythmia episodes. Ventricular arrhythmias were associated with significantly higher daily mean heart rates, low PBTO levels, and low GCS scores, whereas atrial arrhythmias were associated with lower daily mean heart rates, normal PBTO levels, and higher GCS and ICP. Three or more episodes of arrhythmia predicted worse outcomes, including mortality ( P = 0.001). In patients with acute brain injury, poor PBTO levels are associated with higher incidence of ventricular tachyarrhythmias. In contrast, atrial tachyarrhythmias occur in patients with normal PBTO levels and higher ICP. Incidence of ventricular arrhythmia in those with poor PBTO is associated with increased mortality.

Pseudotumor cerebri is characterized by headaches, visual field changes, papilledema and an elevated cerebrospinal fluid opening pressure without evidence of an intracranial mass. In the setting of failed medical therapy, surgical options such as ventriculoperitoneal shunts and optic nerve sheath fenestrations are considered. Recently, venous sinus stenting has emerged as a new treatment option for patients with pseudotumor cerebri. We review the role of cerebral venous sinus stenting in the management of patients with medically refractory pseudotumor cerebri. Although long- term studies are needed in this field, the current reports indicate a favorable outcome for preventing vision loss and symptom control.

Predictive modeling of emergent behavior, inherent to complex physiological systems, requires the analysis of large complex clinical data streams currently being generated in the intensive care unit. Brain tissue oxygen protocols have yielded outcome benefits in traumatic brain injury (TBI), but the critical physiological thresholds for low brain oxygen have not been established for a dynamical patho-physiological system. High frequency, multi-modal clinical data sets from 29 patients with severe TBI who underwent multi-modality neuro-clinical care monitoring and treatment with a brain oxygen protocol were analyzed. The inter-relationship between acute physiological parameters was determined using symbolic regression (SR) as the computational framework. The mean patient age was 44.4±15 with a mean admission GCS of 6.6±3.9. Sixty-three percent sustained motor vehicle accidents and the most common pathology was intra-cerebral hemorrhage (50%). Hospital discharge mortality was 21%, poor outcome occurred in 24% of patients, and good outcome occurred in 56% of patients. Criticality for low brain oxygen was intracranial pressure (ICP) ≥22.8 mm Hg, for mortality at ICP≥37.1 mm Hg. The upper therapeutic threshold for cerebral perfusion pressure (CPP) was 75 mm Hg. Eubaric hyperoxia significantly impacted partial pressure of oxygen in brain tissue (PbtO2) at all ICP levels. Optimal brain temperature (Tbr) was 34-35°C, with an adverse effect when Tbr≥38°C. Survivors clustered at [Formula: see text] Hg vs. non-survivors [Formula: see text] 18 mm Hg. There were two mortality clusters for ICP: High ICP/low PbtO2 and low ICP/low PbtO2. Survivors maintained PbtO2 at all ranges of mean arterial pressure in contrast to non-survivors. The final SR equation for cerebral oxygenation is: [Formula: see text]. The SR-model of acute TBI advances new physiological thresholds or boundary conditions for acute TBI management: PbtO2≥25 mmHg; ICP≤22 mmHg; CPP≈60-75 mmHg; and Tbr≈34-37°C. SR is congruous with the emerging field of complexity science in the modeling of dynamical physiological systems, especially during pathophysiological states. The SR model of TBI is generalizable to known physical laws. This increase in entropy reduces uncertainty and improves predictive capacity. SR is an appropriate computational framework to enable future smart monitoring devices.

Controversy exists on the role of hyperoxia in major trauma with brain injury. Hyperoxia on arterial blood gas has been associated with acute lung injury and pulmonary complications, impacting clinical outcome. The hyperoxia could be reflective of the physiological interventions following major systemic trauma. Despite the standard resuscitation of patients with acute traumatic brain injury, up to 60% demonstrate low brain oxygen upon admission to the ICU. While eubaric hyperoxia has been beneficial in experimental studies, clinical brain oxygen protocols incorporating intracranial pressure control, maintenance of cerebral perfusion pressure, and the effective use of fraction of inspired oxygen adjustments to maintain cerebral oxygenation levels >20 to 25 mmHg have demonstrated mortality reductions and improved clinical outcomes. The risk of low brain oxygen is most acute in the first 24 to 48 hours after injury. The administration of a high fraction of inspired oxygen (0.6 to 1.0) in the emergency room may be justifiable until ICU admission for the placement of invasive neurocritical care monitoring systems. Thereafter, fraction of inspired oxygen levels need to be careful titrated to prevent low brain oxygen levels.

Intracranial suppurative disorders (ICSDs; brain abscess, empyema, and purulent ventriculitis), have been a scourge through the ages and attempts at curative surgery, as for cranial trauma, are considered to be one of the first true neurosurgical interventions performed. ICSDs, seen initially as a consequence of poor socioeconomic conditions and neglected otorhinogenic infections, predominantly manifest today as postsurgical complications, and/or in immunocompromised patients where they continue to result in significant neurologic morbidity and death. The reduction in the incidence of "old world" classic ICSDs can be attributed to the modernization of society, driven inter alia by a shift from an agricultural to an industrial economic society. It can also be coupled with pivotal achievements in public health and the dramatic developments in medicine in the 20th century. This trend was first noted in developed countries but now, with improved socioeconomic circumstances and globalization of medical technology, it is occurring in the developing regions of the world as well. Although ICSDs have undergone a metamorphosis in their clinical profile and despite their rarity in contemporary "developed world" neurosurgical practice, they still have undoubted potential for fatal consequences and continue to pose a significant challenge to the 21st-century neurosurgeon.

OBJECTIVE: Brain abscess (BA) is a neurosurgical emergency and despite significant medical advances, it remains a surgical challenge. A single institution's two decade computed tomography era management experience with BA is reported.METHODS: A retrospective analysis of patients with BA, admitted to the Department of Neurosurgery, Wentworth Hospital, Durban, KwaZulu-Natal, South Africa, was performed. The medical records were analyzed for demographic, clinical, neuroimaging, neurosurgical and otolaryngology management, microbiological characteristics, and their relationship to outcome.RESULTS: During a 20-year period (1983-2002), 973 patients were treated. The mean age was 24.36 +/- 15.1 years (range: 0.17-72 years) and 74.2% (n = 722) were men. The mean admission Glasgow Coma Score was 12.5 +/- 2.83. The majority of BAs were supratentorial (n = 872, 89.6%). The causes were otorhinogenic (38.6%), traumatic (32.8%), pulmonary (7%), cryptogenic (4.6%), postsurgical (3.2%), meningitis (2.8%), cardiac (2.7%), and "other" (8.6%). Surgical drainage was performed in 97.1%, whereas 19 patients had nonoperative management. The incidence of BA decreased during the study period. Patient outcomes were good in 81.3% (n = 791), poor in 5.3% (n = 52), and death (13.4%, n = 130) at discharge. The management morbidity, which included postoperative seizures, was 24.9%. Predictors of mortality were cerebral infarction (odds ratio [OR] 31.1), ventriculitis (OR 12.9), coma (OR 6.8), hydrocephalus (OR 5.1), dilated pupils (OR 4.8), bilateral abscesses (OR 3.8), multiple abscesses (OR 3.4), HIV co-infection (OR 3.2), papilledema (OR 2.6), neurological deterioration (OR 2.4), and fever (OR 1.7).CONCLUSIONS: Optimal management of BA involves surgical drainage for medium-to-large abscesses (>= 2.5 cm) with simultaneous eradication of the primary source, treatment of associated hydrocephalus, and administration of high doses of intravenous antibiotics. The incidence of BA is directly related to poor socioeconomic conditions and therefore, still poses a public health challenge in developing countries.

To the Editor: We read with great interest the recent article by Moskowitz et al.1 The authors describe their experience with posterior fossa duraplasty in different pathology using various materials to achieve closure and raises significant issues with the use of collagen matrix. Although the method and type of duraplasty, the role of multilayer closure and method of exposure of posterior fossa contents (craniectomy vs craniotomy; midline vs lateral approach) have been implicated in complications following posterior fossa surgery, the principal factor responsible for hydrodynamic complications is associated hydrocephalus, which may be unrecognized prior to surgery or underappreciated in the postoperative period. The role of hydrocephalus as a major contributor to failure of cerebrospinal fluid (CSF) containment (pseudomeningocele, CSF leak) has been shown to be independent of the methods of duraplasty. We,2–4 as well as others,5,6 have reported that water-tight dural closure in posterior fossa surgery is not mandatory. Table 1 documents all previous reports of the clinical use of bovine collagen duraplasty (DuraGen®) (supratentorial and posterior fossa) in various conditions, inclusive of Chiari malformations.5 Analysis of these studies revealed the rate of CSF leakage ranges from 0% to 4.5%, the formation of pseudomeningoceles ranges between 3.8% to 15.4% and the development of wound infections ranges from 1.9% to 6.1%. Hydrodynamic complications following cranial surgery reported by studies using subfascial drains2–4 vs those with no drains5,6 were: CSF leakage 4.5% vs 1.8%; and pseudomeningocele formation 6.5% vs 15.4%. Aseptic meningitis using bovine collagen duraplasty was reported at 0% for all studies. Furthermore, even in spinal surgery where the risk of CSF leak may be higher due to the hydrostatic pressure when standing, the reported risk of hydrodynamic complications with7 and without6 drains is significantly lower than that reported by the authors for posterior fossa surgery. However, the largest study published to date on posterior fossa duraplasty (n=454) using various materials,8 reported a useful metric: pseudomeningocele rate of 12.3% and CSF leak rate of 4.6%. In our experiences with on lay DuraGen® (sponge and matrix), we have reported on comparable posterior fossa CSF leak rates of consistently below 5%.2–4 In our most recent experience with posterior fossa collagen matrix duraplasty, we reported that early and timeous use of CSF diversion with ventriculostomy drainage during the primary surgery (31% of patients), multi-layered wound closure, and closed suction wound drainage to obliterate the dead space protected the suture line resulting in no CSF leaks.4TABLE 1: Incidence of complications following posterior fossa duraplasty using bovine collagen (Duragen®) based grafts.aMoskowitz et al1 report significantly higher “failure of CSF containment” or hydrodynamic complications in all groups using the bovine collagen with the highest being in the suturable type collagen (25%). Even the 22 patients who had primary closure of the dura had a higher than normal complication rate (18.2%) with 2 patients (9.1%) having a CSF leak despite no reported hydrocephalus in this group. The authors mention that 18 patients had CSF diversion during the perioperative period, (17 ventriculostomies for hydrocephalus and 1 prophylactic lumbar subarachnoid drain), however in Table 2 of the original manuscript, 14 patients and 9 patients in the results section are reported to have hydrocephalus. The authors do not document the presence of hydrocephalus prior to surgery and whether CSF diversion was practiced a priori in these patients. Furthermore, how many patients with pre-operative hydrocephalus who did not have temporary or permanent CSF diversionary procedures went on to have hydrodynamic complications? What is the author's definition of delayed hydrocephalus and how many patients developed this complication? The use of craniotomy vs craniectomy to access the posterior fossa contents may also influence the rate of hydrodynamic complications. Midline craniectomy is associated with an increased incidence of post-operative CSF leak, pseudomeningocele, and wound reclosures. CSF leaks are in turn associated with CSF and wound infections. The authors report an unusually high incidence of aseptic meningitis with nearly two-thirds of patients (12 of 19 patients in Table 2) in the bovine collagen group, reporting a higher than normal 12% rate of aseptic meningitis per procedure. How was the diagnosis made, as no details are provided? Surprisingly, given their high hydrodynamic complication rate, the authors do not report on patients that may have had bacterial meningitis, ventriculitis, wound infections or other forms of intracranial suppuration. Similarly, in Table 2, 19 CSF leaks (12%) were reported for all procedures. Given that the authors report total CSF leaks in 15 patients and aseptic meningitis in 13 patients, it implies that even following revision repair, temporary and or permanent CSF diversion, some of their patients continued to have hydrodynamic complications either after repeat surgery and or in a delayed fashion. This may represent on-going under-recognized hydrocephalus. The authors should clarify this further. Stendel et al6 recently reported that the multiple fixation of collagen matrix resulted in a higher rate of infections and CSF leaks. No information is provided by the authors as to their method of fixation (on-lay, single, multiple or continuous suture) for the suturable collagen. Majority of the patients had a neoplastic etiology, did the authors look at steroid use as a possible relationship to their complication rate. Did the authors analyze hydrodynamic complications per age as the series includes a pediatric population? Until the report of Moskowitz et al1 complications associated with posterior fossa bovine collagen duraplasty had only been reported as an on lay graft technique using collagen sponge (original formulation; Duragen®)2 and collagen matrix (newer formulation; Duragen Plus™).4–6,8 Over a 3-year period, the author's (N.N.) personal experience with suturable Duragen (water-tight closure; no drains) in combination with a sealant (Duraseal; Confluent Surgical, Waltham, MA) during 27 posterior fossa craniectomies for resection of tumors resulted in hydrodynamic complications (CSF leak) in a single patient (3.7%). This patient required temporary CSF drainage to control for temporary hydrocephalus and revision surgery. No wound infections or aseptic meningitis were recorded. The recognition and management of hydrocephalus remains a major priority in preventing hydrodynamic complications associated with posterior fossa surgery. We therefore agree with the comments of J.D. Day that the recognition of hydrocephalus is of prime importance, which makes the choice of graft material or closure method irrelevant, with regards the development of hydrodynamic complications. Narendra Nathoo Council Bluffs, Iowa Pradeep K Narotam Terre Haute, Indiana

OBJECT:Cerebral ischemia is the leading cause of preventable death in cases of major trauma with severe traumatic brain injury (TBI). Intracranial pressure (ICP) control and cerebral perfusion pressure (CPP) manipulation have significantly reduced the mortality but not the morbidity rate in these patients. In this study, the authors describe their 5-year experience with brain tissue oxygen (PbtO(2)) monitoring, and the effect of a brain tissue oxygen-directed critical care guide (PbtO(2)-CCG) on the 6-month clinical outcome (based on the 6-month Glasgow Outcome Scale score) in patients with TBIs.METHODS:One hundred thirty-nine patients admitted to Creighton University Medical Center with major traumatic injuries (Injury Severity Scale [ISS] scores >or= 16) and TBI underwent prospective evaluation. All patients were treated with a PbtO(2)-CCG to maintain a brain oxygen level > 20 mm Hg, and control ICP < 20 mm Hg. The role of demographic, clinical, and imaging parameters in the identification of patients at risk for cerebral hypooxygenation and the influence of hypooxygenation on clinical outcome were recorded. Outcomes were compared with those in a historical ICP/CPP patient cohort. Subgroup analysis of severe TBI was performed and compared to data reported in the Traumatic Coma Data Bank.RESULTS:The majority of injuries were sustained in motor vehicle crashes (63%), and diffuse brain injury was the most common abnormality (58%). Mechanism of injury, severity of TBI, pathological entity, neuroimaging results, and trauma indices were not predictive of ischemia. Factors affecting death included gunshot injury, poor trauma indices, subarachnoid hemorrhage, and coma. After standard resuscitation, 65% of patients had an initially low PbtO(2). Data are presented as means +/- SDs. Treatment with the PbtO(2)-CCG resulted in a 44% improvement in mean PbtO(2) (16.21 +/- 12.30 vs 23.65 +/- 14.40 mm Hg; p < 0.001), control of ICP (mean 12.76 +/- 6.42 mm Hg), and the maintenance of CPP (mean 76.13 +/- 15.37 mm Hg). Persistently low cerebral oxygenation was seen in 37% of patients at 2 hours, 31% at 24 hours, and 18% at 48 hours of treatment. Thus elevated ICP and a persistent low PbtO(2) after 2 hours represented increasing odds of death (OR 14.3 at 48 hours). Survivors and patients with good outcomes generally had significantly higher mean daily PbtO(2) and CPP values compared to nonsurvivors. Polytrauma, associated with higher ISS scores, presented an increased risk of vegetative outcome (OR 9.0). Compared to the ICP/CPP cohort, the mean Glasgow Outcome Scale score at 6 months in patients treated with PbtO(2)-CCG was higher (3.55 +/- 1.75 vs 2.71 +/- 1.65, p < 0.01; OR for good outcome 2.09, 95% CI 1.031-4.24) as was the reduction in mortality rate (25.9 vs 41.50%; relative risk reduction 37%), despite higher ISS scores in the PbtO(2) group (31.6 +/- 13.4 vs 27.1 +/- 8.9; p < 0.05). Subgroup analysis of severe closed TBI revealed a significant relative risk reduction in mortality rate of 37-51% compared with the Traumatic Coma Data Bank data, and an increased OR for good outcome especially in patients with diffuse brain injury without mass lesions (OR 4.9, 95% CI 2.9-8.4).CONCLUSIONS:The prevention and aggressive treatment of cerebral hypooxygenation and control of ICP with a PbtO(2)-directed protocol reduced the mortality rate after TBI in major trauma, but more importantly, resulted in improved 6-month clinical outcomes over the standard ICP/CPP-directed therapy at the authors' institution.

OBJECT:Complete dural closure is not always possible following posterior fossa surgery, often requiring a graft to secure complete closure. The authors report their experience of using a collagen matrix as an onlay dural graft for repair of a posterior fossa dural defect.METHODS:A retrospective analysis was performed in 52 adult patients who had undergone collagen matrix duraplasty for the posterior fossa. Complications directly related to the dural graft, the presence or absence of hydrocephalus, and the role of closed suction wound drainage in relation to postsurgical pseudomeningoceles were analyzed.RESULTS:The indication for posterior fossa surgery was tumors in 32 patients, vascular abnormalities in 9 patients, and spontaneous cerebellar hemorrhage in 11 patients. Closed suction wound drainage was used in 23 patients (44.2%). Forty-eight (92.3%) of 52 patients had a dural defect > 2 cm. Nine (81.8%) of 11 patients with hydrocephalus required ventriculoperitoneal shunts. Complications of the surgery included pseudomeningoceles in 2 patients (3.8%; no closed suction wound drainage); superficial wound infections in 1 patient (1.9%; with closed suction wound drainage); and unexplained eosinophilia in 1 patient.CONCLUSIONS:Duraplasty using a collagen matrix is safe and effective in the posterior fossa, and is easy to use and time efficient. Meticulous layered wound closure, the detection and effective control of hydrocephalus, and the use of closed suction wound drainage reduces complications related to collagen matrix duraplasty for the posterior fossa.

OBJECT:Inappropriate sudden blood pressure (BP) reductions may adversely affect cerebral perfusion. This study explores the effect of nicardipine on regional brain tissue O(2) (PbtO(2)) during treatment of acute hypertensive emergencies. METHODS:A prospective case-control study was performed in 30 patients with neurological conditions and clinically elevated BP. All patients had a parenchymal PbtO(2) and intracranial pressure bolt inserted following resuscitation. Using a critical care guide, PbtO(2) was optimized. Intravenous nicardipine (5-15 mg/hour) was titrated to systolic BP < 160 mm Hg, diastolic BP < 90 mm Hg, mean arterial BP (MABP) 90-110 mm Hg, and PbtO(2) > 20 mm Hg. Physiological parameters-intracranial pressure, PbtO(2), central venous pressure, systolic BP, diastolic BP, MABP, fraction of inspired O(2), and cerebral perfusion pressure (CPP)-were compared before infusion, at 4 hours, and at 8 hours using a t-test. RESULTS:Sixty episodes of hypertension were reported in 30 patients (traumatic brain injury in 13 patients; aneurysmal subarachnoid hemorrhage in 11; intracerebral and intraventricular hemorrhage in 3 and 1, respectively; arteriovenous malformation in 1; and hypoxic brain injury in 1). Nicardipine was effective in 87% of the patients (with intravenous beta blockers in 4 patients), with a 19.7% reduction in mean 4-hour MABP (115.3 +/- 13.1 mm Hg preinfusion vs 92.9 +/- 11.40 mm Hg after 4 hours of therapy, p < 0.001). No deleterious effect on mean PbtO(2) was recorded (26.74 +/- 15.42 mm Hg preinfusion vs 27.68 +/- 12.51 mm Hg after 4 hours of therapy, p = 0.883) despite significant reduction in CPP. Less dependence on normobaric hyperoxia was achieved at 8 hours (0.72 +/- 0.289 mm Hg preinfusion vs 0.626 +/- 0.286 mm Hg after 8 hours of therapy, p < 0.01). Subgroup analysis revealed that 12 patients had low pretreatment PbtO(2) (10.30 +/- 6.49 mm Hg), with higher CPP (p < 0.001) requiring hyperoxia (p = 0.02). In this group, intravenous nicardipine resulted in an 83% improvement in 4- and 8-hour PbtO(2) levels (18.1 +/- 11.33 and 19.59 +/- 23.68 mm Hg, respectively; p < 0.01) despite significant reductions in both mean MABP (120.6 +/- 16.65 vs 95.8 +/- 8.3 mm Hg, p < 0.001) and CPP (105.00 +/- 20.7 vs 81.2 +/- 15.4 mm Hg, p < 0.001). CONCLUSIONS:Intravenous nicardipine is effective for the treatment of hypertensive neurological emergencies and has no adverse effect on PbtO(2).

OBJECT:The repair of dural defects is controversial in contemporary neurosurgery. To date, collagen-based products remain a continued area of interest in the development of dural grafts. The authors conducted a prospective case-control study in which they evaluated collagen matrix in the repair of dural defects following cranial and spinal surgery by using specific clinical and magnetic resonance (MR) imaging outcome measures. METHODS:Enrolled in the study were 79 patients, 36 male (45.6%) and 43 female (54.4%), with a mean age of 53 +/- 15.8 years. The pathological diagnosis was brain tumor in 49 cases (62%), vascular conditions in 16 (20.2%), degenerative spine in 10 (12.7%), trauma in two (2.5%), and other in two (2.5%). Most of the patients underwent supratentorial craniotomy (57; 72.2%), whereas 11 patients (13.9%) each underwent posterior fossa and spinal surgery. Sixty-three patients (79.7%) completed the study, which included clinical and MR imaging evaluations at 3 months postsurgery. There were no cerebrospinal fluid (CSF) leaks or delayed hemorrhages. The neurosurgical wound infection rate was 3.8%: superficial wound infection in two cases and deep infection and brain abscess in one case (recurrent brain tumor following radiation therapy). Among the 63 patients in whom 3-month postsurgery imaging data were available, asymptomatic small pseudomeningoceles were detected on MR imaging in two (3.2%); a minor subgaleal fluid collection, which resolved spontaneously, was apparent in another patient (1.6%). Nonspecific dural enhancement was demonstrated on images obtained in seven patients (11.1%), and asymptomatic spinal epidural enhancement was observed on images obtained in two of three patients who had undergone lumbar laminectomy for spinal stenosis. CONCLUSIONS:When used as a dural onlay graft, collagen matrix had a 100% CSF containment rate but might be associated with occult radiological abnormalities.

Introduction: Trauma is the commonest cause of death in the pediatric population, which is prone to diffuse primary brain injury aggravated by secondary insults (eg, hypoxia, hypotension). Standard monitoring involves intracranial pressure (ICP) and cerebral perfusion pressure, which do not reflect true cerebral oxygenation (oxygen delivery [Do,]). We explore the merits of a brain tissue oxygen-directed critical care guide.Methods: Sixteen patients with major trauma (Injury Severity Score, > 16/Pediatric Trauma Score [PTS], < 7) had partial pressure of brain tissue oxygen (PbtO(2)) monitor (Licox; Integra Neurosciences, Plainsboro, NJ) placed under local anesthesia using twist-drill craniostomy and definitive management of associated injuries. PbtO(2) levels directed therapy intensity level (ventilator management, inotrops, blood transfusion, and others). Patient demographics, short-term physiological parameters, PbtO(2), ICP, Glasgow Coma Score, trauma scores, and outcomes were analyzed to identify the patients at risk for low DO2.Results: There were 10 males and 6 females (mean age, 14 years) sustaining motor vehicle accident (14), falls (1), and assault (1), with a mean Injury Severity Score of 36 (16-59); PTS, 3 (0-7); and Revised Trauma Score, 5.5 (4-11). Eleven patients (70%) had low DO2 (PbtO(2), < 20 mm Hg) on admission despite undergoing standard resuscitation affected by fraction of inspired oxygen, PaO2, and cerebral perfusion pressure (P=.001). Eubaric hyperoxia improved cerebral oxygenation in the low-DO2 group (P=.044). The Revised Trauma Score (r = 0.65) showed moderate correlation with PbtO(2) and was a significant predictor for low DO2 (P=-001) In patients with PbtO(2) of less than 20 mm Hg, PTS correlated with cerebral oxygenation (r = 0.671, P =.033). The mean 2-hour PbtO(2) and the final PbtO(2) in survivors were significantly higher than deaths (21.6 vs 7.2 mm Hg [P =.009] and 25 vs 11 mm Hg [P =.01]). Although 4 of 6 deaths were from uncontrolled high ICP, PTS and 2-hour low DO2 were significant for roots for mortality.Conclusions: PbtO(2) monitoring allows for early recognition of low-Do, situations, enabling appropriate therapeutic intervention. (c) 2006 Elsevier Inc. All rights reserved.