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Al-Rodhan, Nayef R. F.; Sundt, Thoralf M.; Piepgras, David G.; Nichols, Douglas A.; Rßfenacht, Daniel; Stevens, Lorna N.

Occlusive hyperemia: a theory for the hemodynamic complications following resection of intracerebral arteriovenous malformations

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  • Medientyp: E-Artikel
  • Titel: Occlusive hyperemia: a theory for the hemodynamic complications following resection of intracerebral arteriovenous malformations
  • Beteiligte: Al-Rodhan, Nayef R. F.; Sundt, Thoralf M.; Piepgras, David G.; Nichols, Douglas A.; Rßfenacht, Daniel; Stevens, Lorna N.
  • Erschienen: Journal of Neurosurgery Publishing Group (JNSPG), 1993
  • Erschienen in: Journal of Neurosurgery
  • Sprache: Nicht zu entscheiden
  • DOI: 10.3171/jns.1993.78.2.0167
  • ISSN: 0022-3085
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:p content-type="fine-print">✓ An alternative theory is proposed to explain the brain edema and hemorrhage that may occur after resection of high-flow intracerebral arteriovenous malformations (AVM's). This theory, termed “occlusive hyperemia,” is based on a retrospective analysis of operative dictations along with postoperative imaging studies (191 angiograms and 273 computerized tomography scans) in 295 cases of intracerebral AVM's operated on at the Mayo Clinic between 1970 and 1990. In this series, 34 cases (12%) of postoperative deterioration were documented, of which 15 were due to incomplete resection of the AVM. Of the remaining 19 cases, six had brain edema alone and 13 had hemorrhage with edema, despite complete excision of the AVM. In these 19 cases, the AVM's were greater than 6 cm in diameter in 10 patients, between 3 and 6 cm in six, and less than 3 cm in three. Obstruction of the venous drainage system was observed in 14 (74%) of the 19 cases. Ten of these 14 were due to obstruction of the primary venous drainage of the brain parenchyma immediately surrounding the lesions, while four were due to obstruction of other venous structures. In no case was a rapid circulation identified on postoperative angiograms. The flow pattern was slow or stagnant in former AVM feeders and their parenchymal branches. It is proposed that postoperative intracranial hemorrhage and/or brain edema in AVM patients may be due to: 1) obstruction of the venous outflow system of brain adjacent to the AVM, with subsequent passive hyperemia and engorgement; and 2) stagnant arterial flow in former AVM feeders and their parenchymal branches, with subsequent worsening of the existing hypoperfusion, ischemia, and hemorrhage or edema into these areas. Supportive hemodynamic evidence for this theory was derived from the literature.</jats:p>