Curative embolization of arteriovenous malformations.

07:00 EST 5th February 2019 | BioPortfolio

Summary of "Curative embolization of arteriovenous malformations."

Arteriovenous malformations have a significant cumulative risk for hemorrhage. Treatment options include observation, microsurgical resection, stereotactic radiosurgery, embolization, and multimodal treatment. Treatment selection and timing are based upon AVM features including size, location in eloquent versus non-eloquent parenchyma, pattern of venous drainage, surgical access, rupture status, and prior treatments. Spetzler-Martin grading is the most commonly used classification system used to select treatment, with grades I and II lesions amenable to surgical resection alone, grade III lesions typically treated via a multimodal approach entailing pre-operative embolization followed by microsurgical resection, and grades IV and V lesions generally observed unless ruptured. Embolization in the treatment of AVMs is thus most commonly used as a pre-operative or, occasionally, pre-radiosurgical adjunct. The concept of curative AVM embolization is an attractive one which has emerged within the past few decades, with increasing clinical evidence for its safety and efficacy in recent years. Obliteration rates for curative AVM embolization will be improved by innovation in endovascular techniques and technologies.


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Name: World neurosurgery
ISSN: 1878-8769


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Medical and Biotech [MESH] Definitions

A method of hemostasis utilizing various agents such as Gelfoam, silastic, metal, glass, or plastic pellets, autologous clot, fat, and muscle as emboli. It has been used in the treatment of spinal cord and INTRACRANIAL ARTERIOVENOUS MALFORMATIONS, renal arteriovenous fistulas, gastrointestinal bleeding, epistaxis, hypersplenism, certain highly vascular tumors, traumatic rupture of blood vessels, and control of operative hemorrhage.

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A congenital disorder that is characterized by a triad of capillary malformations (HEMANGIOMA), venous malformations (ARTERIOVENOUS FISTULA), and soft tissue or bony hypertrophy of the limb. This syndrome is caused by mutations in the VG5Q gene which encodes a strong angiogenesis stimulator.

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