RESUMO
Blister aneurysms are rare cerebrovascular lesions for which the treatment methods are reviewed here, with a focus on endovascular options. The reported pathogenesis of blister aneurysms varies, and hemodynamic stress, arterial dissection, and arteriosclerotic ulceration have all been described. There is consensus on the excessive fragility of blister aneurysms and their parent vessels, which makes clipping technically difficult. Open surgical treatment is associated with high rates of complications, morbidity, and mortality; endovascular treatment is a promising alternative. Among endovascular treatment options, deconstructive treatment has been associated with higher morbidity compared with reconstructive methods such as direct embolization, stent- or balloon-assisted direct embolization, stent monotherapy, and flow diversion. Flow diversion has been associated with higher technical success rates and similar clinical outcomes compared with non-flow diverting treatment methods. However, delayed aneurysm occlusion and the need for antiplatelet therapy are potential drawbacks to flow diversion that must be considered when choosing among treatment methods for blister aneurysms.
Assuntos
Vesícula/cirurgia , Procedimentos Endovasculares/métodos , Aneurisma Intracraniano/cirurgia , Stents , Angiografia Digital , Vesícula/complicações , Vesícula/diagnóstico por imagem , Procedimentos Endovasculares/instrumentação , Humanos , Aneurisma Intracraniano/complicações , Aneurisma Intracraniano/diagnóstico por imagem , Resultado do TratamentoRESUMO
STUDY DESIGN: Retrospective cohort study. OBJECTIVE: The purpose of this study was to see whether upgrades in newer generation robots improve safety and clinical outcomes following spine surgery. METHODS: All patients undergoing robotic-assisted spine surgery with the Mazor X Stealth EditionTM (Medtronic, Minneapolis, MN) from 2019 to 2022 at a combined orthopedic and neurosurgical spine service were retrospectively reviewed. Robot related complications were recorded. RESULTS: 264 consecutive patients (54.1% female; age at time of surgery 63.5 ± 15.3 years) operated on by 14 surgeons were analyzed. The average number of instrumented levels with robotics was 4.2 ± 2.7, while the average number of instrumented screws with robotics was 8.3 ± 5.3. There was a nearly 50/50 split between an open and minimally invasive approach. Six patients (2.2%) had robot related complications. Three patients had temporary nerve root injuries from misplaced screws that required reoperation, one patient had a permanent motor deficit from the tap damaging the L1 and L2 nerve roots, one patient had a durotomy from a misplaced screw that required laminectomy and intra-operative repair, and one patient had a temporary sensory L5 nerve root injury from a drill. Half of these complications (3/6) were due to a reference frame error. In total, four patients (1.5%) required reoperation to fix 10 misplaced screws. CONCLUSION: Despite newer generation robots, robot related complications are not decreasing. As half the robot related complications result from reference frame errors, this is an opportunity for improvement.
RESUMO
OBJECTIVES: Neuroprotective benefits of ethanol (EtOH) and normobaric oxygenation (NBO) were previously demonstrated in transient and permanent ischemic stroke. Here we sought to identify whether the enhanced lactic acidosis and increased expression of monocarboxylate transporters (MCTs) observed after stroke might be attenuated by single and/or combined EtOH and NBO therapies. METHODS: Sprague-Dawley rats (n=96) were subjected to right middle cerebral artery occlusion (MCAO) for 2 or 4h (transient ischemia), or 28 h (permanent ischemia) followed by 3, 24h, or no reperfusion. Rats received: (1) either an intraperitoneal injection of saline (sham treatment), one dose of EtOH (1.5 g/kg), two doses of EtOH (1.5 g/kg at 2h of MCAO, followed by 1.0 g/kg 2h after 1st dose), or (2) EtOH+95% NBO (at 2h of MCAO for 6h in permanent ischemia). Lactate levels were detected at 3 and 24h of reperfusion. Gene and protein expressions of MCT-1, -2, -4 were assessed by real-time PCR and western blotting. RESULTS: A dose-dependent EtOH neuroprotection was found in transient ischemia. Following transient ischemia, a single dose of EtOH (in 2h-MCAO) or a double dose (in 4h-MCAO), significantly attenuated lactate levels, as well as the mRNAs and protein expressions of MCT-1, MCT-2, and MCT-4. However, while two doses of EtOH alone was ineffective in permanent stroke, the combined therapy (EtOH+95% NBO) resulted in a more significant attenuation in all the above levels and expressions. CONCLUSIONS: Our study demonstrates that acute EtOH administration attenuated lactic acidosis in transient or permanent ischemic stroke. This EtOH-induced beneficial effect was potentiated by NBO therapy in permanent ischemia. Because both EtOH and NBO are readily available, inexpensive and easy to administer, their combination could be implemented in the clinics shortly after stroke.