✓ Two cases of metastatic glioma with hypercalcemia are presented. Elevated serum calcium secondary to metastatic central nervous system tumors may be more common than is generally supposed, and the symptoms of hypercalcemia may be mistaken for those of increased intracranial pressure.
Report of two cases
Paul R. Cooper, Gleb N. Budzilovich, Peter H. Berczeller, Abraham Lieberman, and Arthur Battista
Michael G. Brandel, Robert C. Rennert, Arvin R. Wali, David R. Santiago-Dieppa, Jeffrey A. Steinberg, Christian Lopez Ramos, Peter Abraham, J. Scott Pannell, and Alexander A. Khalessi
Preoperative embolization of meningiomas can facilitate their resection when they are difficult to remove. The optimal use and timing of such a procedure remains controversial given the risk of embolization-linked morbidity in select clinical settings. In this work, the authors used a large national database to study the impact of immediate preoperative embolization on the immediate outcomes of meningioma resection.
Meningioma patients who had undergone elective resection were identified in the National (Nationwide) Inpatient Sample (NIS) for the period 2002–2014. Patients who had undergone preoperative embolization were propensity score matched to those who had not, adjusting for patient and hospital characteristics. Associations between preoperative embolization and morbidity, mortality, and nonroutine discharge were investigated.
Overall, 27,008 admissions met the inclusion criteria, and 633 patients (2.34%) had undergone preoperative embolization and 26,375 (97.66%) had not. The embolization group was younger (55.17 vs 57.69 years, p < 0.001) with a lower proportion of females (63.5% vs 69.1%, p = 0.003), higher Charlson Comorbidity Index (p = 0.002), and higher disease severity (p < 0.001). Propensity score matching retained 413 embolization and 413 nonembolization patients. In the matched cohort, preoperative embolization was associated with increased rates of cerebral edema (25.2% vs 17.7%, p = 0.009), posthemorrhagic anemia or transfusion (21.8% vs 13.8%, p = 0.003), and nonroutine discharge (42.8% vs 35.7%, p = 0.039). There was no difference in mortality (≤ 2.4% vs ≤ 2.4%, p = 0.82). Among the embolization patients, the mean interval from embolization to resection was 1.49 days. On multivariate analysis, a longer interval was significantly associated with nonroutine discharge (OR 1.33, p = 0.004) but not with complications or mortality.
Relative to meningioma patients who do not undergo preoperative embolization in the same admission, those who do have higher rates of cerebral edema and nonroutine discharge but not higher rates of stroke or death. Thus, meningiomas requiring preoperative embolization represent a distinct clinical entity that requires prolonged, more complex care. Further, among embolization patients, the timing of resection did not affect the risk of in-hospital complications, suggesting that the timing of surgery can be determined according to surgeon discretion.
Peter Abraham, J. Scott Pannell, David R. Santiago-Dieppa, Vincent Cheung, Jeffrey Steinberg, Arvin Wali, Mihir Gupta, Robert C. Rennert, Roland R. Lee, and Alexander A. Khalessi
In vivo and in vitro studies have demonstrated histological evidence of iatrogenic endothelial injury after stent retriever thrombectomy. However, noncontrast vessel wall (VW)–MRI is insufficient to demonstrate vessel injury. Authors of this study prospectively evaluated iatrogenic endothelial damage after stent retriever thrombectomy in humans by utilizing high-resolution contrast-enhanced VW-MRI. Characterization of VW-MRI changes in vessels subject to mechanical injury from thrombectomy may allow better understanding of the biological effects of this intervention.
The authors prospectively recruited 11 patients for this study. The treatment group included 6 postthrombectomy patients and the control group included 5 subjects undergoing MRI for nonvascular indications. All subjects were evaluated on a Signa HD× 3.0-T MRI scanner with an 8-channel head coil. Both pre- and postcontrast T1-weighted Cube VW images as well as MR angiograms were acquired. Sequences obtained for evaluation of the brain parenchyma included diffusion-weighted, gradient echo, and T2-FLAIR imaging. Two independent neuroradiologists, who were blinded to the treatment status of each patient, determined the presence of VW enhancement. Patient age, National Institutes of Health Stroke Scale score on presentation, location of occlusion, stroke etiology, type of device used, number of device deployments, Thrombolysis in Cerebral Infarction (TICI) reperfusion score, stroke volume, and 90-day modified Rankin Scale score were also noted.
Postcontrast T1-weighted VW enhancement was detected in the M2 segment in 100% of the thrombectomy patients, in the M1 segment in 83%, and in the internal carotid artery in 50%. One patient also demonstrated A1 segment enhancement, which was attributable to thrombectomy treatment of that vessel segment during the same procedure. None of the control patients demonstrated VW enhancement of their intracranial vasculature on T1-weighted images.
The study findings suggest that VW injury incurred during stent retriever thrombectomy can be reliably detected utilizing contrast-enhanced 3-T VW-MRI. The results further demonstrate that endothelial injury is associated with oversizing of stent retrievers relative to the treated vessel. Further studies are needed to evaluate the clinical significance of endothelial injury and to characterize the differential effects of various devices.
Abraham Kader, James T. Goodrich, William J. Sonstein, Bennett M. Stein, Peter W. Carmel, and W. Jost Michelsen
✓ Angiography has been considered to be the gold standard to judge the success of treatment for cerebral arteriovenous malformations (AVMs). Patients without residual nidus or early draining veins on postoperative angiograms are considered cured, with the risk of hemorrhage eliminated. A series of five patients with recurrent AVMs after negative postoperative angiography is described. All patients had hemispheric AVMs, presented initially with hemorrhage, and were between 5 and 13 years of age. Recurrence was noted 1 to 9 years later (at 12–16 years of age); after a hemorrhage in three patients, seizures in one, and on follow-up magnetic resonance imaging in one. Four patients underwent angiography that showed recurrence of the AVM at or adjacent to the original site. Three years postsurgery, the fifth patient died from a large intracerebral and intraventricular hemorrhage originating in the previous location of the AVM; however, the patient did not undergo angiography at the time of recurrence. The initial negative angiograms obtained postoperatively in these patients may be explained by postoperative spasm or thrombosis of a small residual malformation. However, in the authors' cumulative experience with 808 patients who have undergone complete surgical removal of AVMs (of whom 667 were older than 18 years of age), no case of recurrent AVM has been observed in an adult. Therefore, actual regrowth of an AVM may occur in children and could be a consequence of their relatively immature cerebral vasculature and may involve active angiogenesis mediated by humoral factors. The present findings argue against the assumption that AVMs are strictly congenital lesions resulting from failure of capillary formation during early embryogenesis. It is concluded that delayed imaging studies should be considered in children at least 1 year after their initial negative postoperative arteriogram to exclude a recurrent AVM.
Michael F. Stiefel, Gregory G. Heuer, John M. Abrahams, Stephanie Bloom, Michelle J. Smith, Eileen Maloney-Wilensky, M. Sean Grady, and Peter D. Leroux
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.
Christian Lopez Ramos, Robert C. Rennert, Michael G. Brandel, Peter Abraham, Brian R. Hirshman, Jeffrey A. Steinberg, David R. Santiago-Dieppa, Arvin R. Wali, Kevin Porras, Yazeed Almosa, Jeffrey S. Pannell, and Alexander A. Khalessi
Safety-net hospitals deliver care to a substantial share of vulnerable patient populations and are disproportionately impacted by hospital payment reform policies. Complex elective procedures performed at safety-net facilities are associated with worse outcomes and higher costs. The effects of hospital safety-net burden on highly specialized, emergent, and resource-intensive conditions are poorly understood. The authors examined the effects of hospital safety-net burden on outcomes and costs after emergent neurosurgical intervention for ruptured cerebral aneurysms.
The authors conducted a retrospective analysis of the Nationwide Inpatient Sample (NIS) from 2002 to 2011. Patients ≥ 18 years old who underwent emergent surgical clipping and endovascular coiling for aneurysmal subarachnoid hemorrhage (SAH) were included. Safety-net burden was defined as the proportion of Medicaid and uninsured patients treated at each hospital included in the NIS database. Hospitals that performed clipping and coiling were stratified as low-burden (LBH), medium-burden (MBH), and high-burden (HBH) hospitals.
A total of 34,647 patients with ruptured cerebral aneurysms underwent clipping and 23,687 underwent coiling. Compared to LBHs, HBHs were more likely to treat black, Hispanic, Medicaid, and uninsured patients (p < 0.001). HBHs were also more likely to be associated with teaching hospitals (p < 0.001). No significant differences were observed among the burden groups in the severity of subarachnoid hemorrhage. After adjusting for patient demographics and hospital characteristics, treatment at an HBH did not predict in-hospital mortality, poor outcome, length of stay, costs, or likelihood of a hospital-acquired condition.
Despite their financial burden, safety-net hospitals provide equitable care after surgical clipping and endovascular coiling for ruptured cerebral aneurysms and do not incur higher hospital costs. Safety-net hospitals may have the capacity to provide equitable surgical care for highly specialized emergent neurosurgical conditions.
Arnaud J. P. E. Vincent, Maria del C. Esandi, Gerry van Someren, Juus L. Noteboom, Cees J. J. Avezaat, Charles Vecht, Peter A. E. Sillevis Smitt, Dirk W. van Bekkum, Dinko Valerio, Peter M. Hoogerbrugge, and Abraham Bout
✓ The authors constructed recombinant adenoviral vectors to investigate their potential for gene therapy treatment of leptomeningeal metastases. Several human cell lines that were derived from tumors occurring as leptomeningeal metastases and that were infected in vitro with major late promoter recombinant adenovirus containing the luciferase (luc) gene (IG.Ad.MLP.luc.) showed high levels of expression. When these human tumor cell lines were infected in vitro with recombinant adenovirus harboring the herpes simplex virus—thymidine kinase (HSV-tk) gene (IG.Ad.MLP.TK), they were highly sensitive to the killing effects of ganciclovir (GCV). Transduction efficiency of leptomeningeal tumor cells in vivo was assessed by injecting 9-L rat brain tumor cells into the cerebrospinal fluid of Fischer rats via the cisterna magna. After 3 days, recombinant adenovirus containing the lacZ reporter gene (IG.Ad.MLP.lacZ) was injected via the same route. Six days after tumor cell injection, expression of the reporter gene was observed in tumor cells along the total neural axis. Subsequently, rats with leptomeningeal metastases were treated 3 days after tumor cell injection with HSV-tk. Beginning on the next day, GCV was injected intraperitoneally for 10 days. The rats that developed neurological symptoms were killed immediately. The symptom-free latency of every rat was determined. The rats treated with HSV-tk and subsequent GCV had significantly longer (p < 0.01) symptom-free latency than all control groups. This study demonstrates the feasibility and efficacy of this therapeutic approach in a rat model. Clinically, it should be used in the palliative treatment of patients with leptomeningeal metastases.
Oliver G. S. Ayling, Raphaele Charest-Morin, Matthew E. Eagles, Tamir Ailon, John T. Street, Nicolas Dea, Greg McIntosh, Sean D. Christie, Edward Abraham, W. Bradley Jacobs, Christopher S. Bailey, Michael G. Johnson, Najmedden Attabib, Peter Jarzem, Michael Weber, Jerome Paquet, Joel Finkelstein, Alexandra Stratton, Hamilton Hall, Neil Manson, Y. Raja Rampersaud, Kenneth Thomas, and Charles G. Fisher
Previous works investigating rates of adverse events (AEs) in spine surgery have been retrospective, with data collection from administrative databases, and often from single centers. To date, there have been no prospective reports capturing AEs in spine surgery on a national level, with comparison among centers.
The Spine Adverse Events Severity system was used to define the incidence and severity of AEs after spine surgery by using data from the Canadian Spine Outcomes and Research Network (CSORN) prospective registry. Patient data were collected prospectively and during hospital admission for those undergoing elective spine surgery for degenerative conditions. The Spine Adverse Events Severity system defined minor and major AEs as grades 1–2 and 3–6, respectively.
There were 3533 patients enrolled in this cohort. There were 85 (2.4%) individual patients with at least one major AE and 680 (19.2%) individual patients with at least one minor AE. There were 25 individual patients with 28 major intraoperative AEs and 260 patients with 275 minor intraoperative AEs. Postoperatively there were 61 patients with a total of 80 major AEs. Of the 487 patients with minor AEs postoperatively there were 698 total AEs. The average enrollment was 321 patients (range 47–1237 patients) per site. The rate of major AEs was consistent among sites (mean 2.9% ± 2.4%, range 0%–9.1%). However, the rate of minor AEs varied widely among sites—from 7.9% to 42.5%, with a mean of 18.8% ± 9.7%. The rate of minor AEs varied depending on how they were reported, with surgeon reporting associated with the lowest rates (p < 0.01).
The rate of major AEs after lumbar spine surgery is consistent among different sites but the rate of minor AEs appears to vary substantially. The method by which AEs are reported impacts the rate of minor AEs. These data have implications for the detection and reporting of AEs and the design of strategies aimed at mitigating complications.