World neurosurgery · 2025
Cerebral Air Embolism After Percutaneous Kyphoplasty: A Case Report and Systematic Review of Mechanisms and Management.
СтатьяСистематический обзорКлинический случайПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Fang Tianci, Xue Zhifang, Yang Lianda, He Zhaohui, Yang Huilin, Liu Hao, Zhang Junxin, Zhou Feng
Аннотация
OBJECTIVE: Cerebral air embolism (CAE) is a rare but catastrophic complication of percutaneous kyphoplasty (PKP), with only 6 documented cases in spinal surgery literature. This study presents a novel case of CAE following PKP, resulting in a vegetative state despite hyperbaric oxygen therapy (HBOT), and synthesizes existing evidence to elucidate pathogenesis and propose prevention protocols.
METHODS: A systematic literature review (PubMed/Embase, 2000-2023) identified all reported CAE cases after spinal surgery. We integrated a new case of PKP-induced CAE in an 84-year-old male with an L4 compression fracture. Data were analyzed to define mechanisms (anatomic pathways, procedural factors), diagnostic patterns, and management outcomes.
RESULTS: Among the 7 total cases (including ours), CAE manifested as acute neurological decline (coma, Babinski sign) within minutes postoperatively. Anatomical vulnerabilities (intravertebral vacuum clefts, posterior wall defects) and trocar-related air ingress were key pathogenic factors. All 3 patients receiving HBOT survived, but our case progressed to a vegetative state. Prevention strategies include preoperative computed tomography/magnetic resonance imaging screening for vertebral defects and cardiopulmonary shunts; intraoperative technical refinements (airtight trocar placement, temperature-modulated cement delivery); and postoperative vital/neurological monitoring.
CONCLUSIONS: CAE demands protocol-driven vigilance in PKP and analogous spinal procedures. Preoperative risk stratification, standardized intraoperative safeguards, and immediate HBOT initiation are critical to mitigate this complication. Our proposed multiphase protocol provides actionable guidelines for prevention and acute management.
METHODS: A systematic literature review (PubMed/Embase, 2000-2023) identified all reported CAE cases after spinal surgery. We integrated a new case of PKP-induced CAE in an 84-year-old male with an L4 compression fracture. Data were analyzed to define mechanisms (anatomic pathways, procedural factors), diagnostic patterns, and management outcomes.
RESULTS: Among the 7 total cases (including ours), CAE manifested as acute neurological decline (coma, Babinski sign) within minutes postoperatively. Anatomical vulnerabilities (intravertebral vacuum clefts, posterior wall defects) and trocar-related air ingress were key pathogenic factors. All 3 patients receiving HBOT survived, but our case progressed to a vegetative state. Prevention strategies include preoperative computed tomography/magnetic resonance imaging screening for vertebral defects and cardiopulmonary shunts; intraoperative technical refinements (airtight trocar placement, temperature-modulated cement delivery); and postoperative vital/neurological monitoring.
CONCLUSIONS: CAE demands protocol-driven vigilance in PKP and analogous spinal procedures. Preoperative risk stratification, standardized intraoperative safeguards, and immediate HBOT initiation are critical to mitigate this complication. Our proposed multiphase protocol provides actionable guidelines for prevention and acute management.