RISK OF INTRACRANIAL ARTERIOVENOUS MALFORMATION RUPTURE DUE TO VENOUSDRAINAGE IMPAIRMENT - A THEORETICAL-ANALYSIS

Background and Purpose Increased resistance in the venous drainage of intracranial arteriovenous malformations (AVMs) may contribute to thei r increased risk of hemorrhage. Venous drainage impairment may result from naturally occurring stenoses/occlusions, or if draining veins (DV s) undergo occlusion before feeding arteries during surgical removal, or after surgery in the presence of ''occlusive hyperemia.'' We employ ed a detailed biomathematical AVM model using electrical network analy sis to investigate theoretically the hemodynamic consequences and the risk of AVM rupture due to venous drainage impairment. Methods The AVM model consisted of a noncompartmentalized nidus with 28 vessels (24 p lexiform components and 4 fistulous components), 4 arterial feeders, a nd 2 DVs. An expression for the risk of AVM nidus rupture was derived on the basis of functional distribution of the critical radii of compo nent vessels. Risk was calculated from biomathematical simulations of volumetric how rate with both DVs patent and for four stages of venous drainage obstruction: (1) 25%, (2) 50%, (3) 75%, and (4) 100%. Each s tage of occlusion was applied to each DV while the other DV was patent and then to the patent DV while the other DV was totally occluded. Re sults For flow through the AVM when both DVs were unobstructed, the ba seline risk of AVM nidus rupture ranged from 4.4% to 91.2%. Theoretica l rupture occurred in nidus components proximal to the DVs when the ri sk exceeded 100%, as was observed with the obstruction of DV1 and a pa tent DV2. The ranges for risk of rupture across the nidus for the four stages were (1) 4.7% to 90.5%, (2) 5.9% to 86.9%, (3) 0% to 98.4%, an d (4) 0% to 106.3%, respectively. Rupture was observed for an 86% occl usion of DV1 (ie, the DV fed by the intranidal fistula) and DV2 patent , primarily because of the dramatic shift in the hemodynamic burden to ward the weaker plexiform nidus vessels. Conclusions On theoretical gr ounds, venous drainage impairment was predictive of AVM nidus rupture and was strongly dependent on AVM morphology (presence of intranidal f istulas and their spatial relation to DVs) and hemodynamics. Specifica lly, stenosis/occlusion of a high-flow DV induces a rapid redistributi on of blood into the weak plexiform vessels of the opposing region of the nidus, causing a hemodynamic overload and an increased risk of rup ture. These findings should be carefully considered among all factors affecting the natural history of intracranial AVMs and the mechanisms implicated in their spontaneous rupture. They may also provide a theor etical rationale for some of the hemorrhagic complications that occur during and after surgical treatment.