No abstract

Recent radiological studies have shown that arteriovenous malformations with impaired venous drainage may be susceptible to hemorrhage. To evaluate this hypothesis using a hemodynamic approach, we measured intravascular pressure during surgery in three patients with arteriovenous malformation. In three patients we measured intravascular pressures in the draining venous system and the feeding arteries simultaneously before removal of arteriovenous malformations with marked segmental stenotic or occlusive draining veins and evidence of hemorrhage. The draining vein pressures at prestenotic (or preocclusive) sites in the three patients were 38, 25, and 40 mm Hg, respectively, all significantly above the normal cortical venous pressure, whereas pressure measurements in poststenotic sites and the sagittal sinus pressure in the venous drainage system approached normal values. The feeding artery pressures in the patients were lower than normal cortical artery pressure because of the arteriovenous shunt. Intraoperative vascular pressure measurements support the hypothesis that arteriovenous malformations with impaired venous drainage may be associated with a local increase in venous pressure and thus may be susceptible to hemorrhage.

During a five-year period, 18 patients with cystic hygroma were treated as follows: 8 patients were treated surgically, 3 patients were treated by sclerosing therapy with Bleomycin (BLM) and 9 patients including 2 secondary to incomplete surgical therapy were treated by sclerosing therapy with OK-432 (Picibanil; Chugai Pharmaceutical Co. Ltd., Tokyo). OK-432 therapy for cystic hygroma showed excellent results; cure was noted in 8 patients, and marked regression with the expectation of subsequent cure was noted in the other patient. Complete excision of the cystic hygromas was possible in 4 patients and resulted in cure; but only partial excisions could be performed in the other 4 patients because of the surrounding tissue and the results were unfavorable. BLM therapy gave insufficient results and was not considered a favorable treatment.

It was demonstrated that (1) chronic hypoperfusion induced impairment of the upper limit of autoregulation and (2) sudden fistula closure under hypertensive conditions caused vasodilation of the arterioles. These findings suggest that rapid restoration of perfusion pressure is possibly followed by a pressure breakthrough phenomenon in a chronically hypoperfused cerebrovasculature.

A case of arteriovenous malformation (AVM) in which postoperative hemorrhagic infarction developed, probably because of occlusion of the former draining veins, is reported. The hemorrhage developed in the temporal lobe 3 days after the initial operation and was located in the immediate vicinity of the site of the AVM. The following findings suggest that the postsurgical hemorrhage probably resulted from a venous thrombosis: 1) no evidence of residual AVM; 2) delayed onset of the hemorrhage, inconsistent with the time course of a hemorrhage developing according to the breakthrough theory or with insufficient hemostasis with a high-pressure afterload; 3) good correlation between the location of the hemorrhage and the occlusion of the draining veins; and 4) multifocal hemorrhage affecting both the gray matter and the subcortical white matter. Postoperative hemorrhagic infarction caused by thrombosis in the draining veins is rare, but it should be considered as a distinct postoperative complication after removal of an AVM.