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AJNR - American Journal of Neuroradiology

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American Journal of Neuroradiology 21:1255-1267 (7 2000)
© 2000 American Society of Neuroradiology

ARTICLE

Can Induction of Systemic Hypotension Help Prevent Nidus Rupture Complicating Arteriovenous Malformation Embolization?: Analysis of Underlying Mechanisms Achieved Using a Theoretical Model

Tarik F. Massoud^,a, George J. Hademenos^a, William L. Young^a, Erzhen Gao^a and John Pile-Spellman^a

^a From the Division of Interventional Neuroradiology and Department of Radiological Sciences (T.F.M., G.J.H.), University of California at Los Angeles School of Medicine, Los Angeles; Departments of Radiology (T.F.M., W.L.Y., J.P.-S.), Anesthesiology (W.L.Y.), and Neurological Surgery (W.L.Y., J.P.-S.), College of Physicians and Surgeons, and the Department of Electrical Engineering (E.G.), Columbia University, New York, New York.

BACKGROUND AND PURPOSE: Nidus rupture is a serious complication of intracranial arteriovenous malformation (AVM) embolotherapy, but its pathogenetic mechanisms are not well described. An AVM model based on electrical network analysis was used to investigate theoretically the potential role of hemodynamic perturbations for elevating the risk of nidus vessel rupture (R_rupt) after simulated AVM embolotherapy, and to assess the potential benefit of systemic hypotension for preventing rupture.

METHODS: Five separate hypothetical mechanisms for nidus hemorrhage were studied: 1) intranidal rerouting of blood pressure; 2) extranidal rerouting of blood pressure; 3) occlusion of draining veins with glue; 4) delayed thrombosis of draining veins; and 5) excessively high injection pressures proximal to the nidus. Simulated occlusion of vessels or elevated injection pressures were implemented into the AVM model, and electrical circuit analysis revealed the consequent changes in intranidal flow, pressure, and R_rupt for the nidus vessels. An expression for R_rupt was derived based on the functional distribution of the critical radii of component vessels. If AVM rupture was observed (R_rupt 100%) at systemic normotension (mean pressure [P] = 74 mm Hg), the theoretical embolization was repeated under systemic hypotension (minor P = 70 mm Hg, moderate P = 50 mm Hg, or profound P = 25 mm Hg) to assess the potential benefit of this maneuver in reducing hemorrhage rates.

RESULTS: All five pathogenetic mechanisms under investigation were able to produce rupture of AVMs during or after embolotherapy. These different mechanisms had in common the capability of generating surges in intranidal hemodynamic parameters resulting in nidus vessel rupture. The theoretical induction of systemic hypotension during and after treatment was shown to be of significant benefit in attenuating these surges and reducing R_rupt to safer levels below 100%.

CONCLUSION: The induction of systemic hypotension during and after AVM embolization would appear theoretically to be of potential use in preventing iatrogenic nidus hemorrhage. The described AVM model should serve as a useful research tool for further theoretical investigations of AVM embolotherapy and its hemodynamic sequelae.

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