Occlusion of the pig superior sagittal sinus, bridging and cortical veins: multistep evolution of sinus-vein thrombosis

Abstract

Cerebral sinus-vein thrombosis may lead to severe hemodynamic changes, elevated intracranial pressure (ICP), and brain edema. It is supposed that progression of the thrombus from the sinus into bridging and cortical veins plays a key role in the development of these pathophysiological changes, but this hypothesis lacks experimental proof. The aim of this study, using a novel animal model of sinus-vein thrombosis, was to evaluate the effects of a standardized occlusion of the superior sagittal sinus and its bridging and cortical veins on hemodynamic alterations, on brain water content, and on ICP in domestic pigs. In 10 animals, the middle third of the superior sagittal sinus was occluded with a catheter-guided balloon. Five of these pigs received an additional injection of 1 ml fibrin glue into the superior sagittal sinus anterior to the inflated balloon, leading to an obstruction of bridging and cortical veins. In five control animals the balloon was inserted but not inflated. Five pigs underwent cerebral angiography. Four hours after occlusion, the brains were frozen in liquid nitrogen, and coronal slices were examined for Evans blue dye extravasation, regional water content, and histological changes. Occlusion of the superior sagittal sinus alone did not affect ICP or cerebral perfusion pressure (CPP). The additional injection of fibrin glue caused an obstruction of cortical and bridging veins as well as severe increases in mean (+/- standard deviation) ICP to 49.4 +/- 14.3 mm Hg, compared with 8.3 +/- 4.5 mm Hg in sham-treated controls and 7.1 +/- 3.9 mm Hg in animals with occlusion of the superior sagittal sinus alone. There was also a steep fall in the mean CPP to 34.2 +/- 19.6 mm Hg compared with 96.4 +/- 13.8 mm Hg in the control group. White-matter water content anterior to the occlusion site was elevated to 81.9 +/- 3.7 gm/100 gm frozen weight in the fibrin group as compared to 70.7 +/- 2.2 gm/100 gm in controls. Posterior to the occlusion site, water content did not differ among the three groups. Angiography demonstrated collateral flow via cortical and bridging veins in animals with occlusion of the superior sagittal sinus alone. Additional fibrin glue obstructed these collateral vessels. The data suggest a multistep process of pathophysiological alterations in patients with sinus-vein thrombosis and may explain why these patients present with a wide variety of symptoms: minor neurological deficits or headache might indicate thrombosis of the superior sagittal sinus and/or its bridging veins.(ABSTRACT TRUNCATED AT 400 WORDS)

Experimental Cerebral Venous Thrombosis: Evaluation Using Magnetic Resonance Imaging

“…Experimental data suggest that severe increases of rcp occur in response to thrombosis of cortical bridging veins (Fries et al, 1992;Frerichs et al, 1994). The con tribution of increased ICP to the reduction of CBF, how ever, is still controversial, and the elevation of the ve nous pressure and the decreased cerebral perfusion pres sure have been proposed as more important factors (Wagner and Traystman, 1983;Gotoh et al, 1993).…”

Frequency and Topographic Distribution of Brain Lesions in Pediatric Cerebral Venous Thrombosis

“…The severity of parenchymal injuries in experimental CSVT models has been considered proportional to the degree of venous occlusion. 5 The lack of correlation between the extent and site of thrombosis in the dural sinuses and location of brain lesions has been suggested in adults. 6 In this study, our aims were to evaluate the frequency and topographic distribution of brain lesions associated with CSVT in children and to try and compare the topographic distribution of brain lesions with known normal venous drainage and anatomy.…”

From presentation to follow-up: diagnosis and treatment of cerebral venous thrombosis

“…4,40 Infarctions occur in ~ 50% of cases. 24 It is in these patients in whom more immediate and aggressive treatment is indicated.…”

“…Clinicians must watch postoperatively for a decrease in the hematocrit level and clinical signs of hypovolemia, and they must transfuse as needed. 24 Additionally, Curtin, et al 15 demonstrated the usefulness of a combination of approaches in treating CVT. Balloon angioplasty, direct rtPA, and Angiojet thrombectomy were used due to lack of clinical improvement after 1 modality.…”

“…One major advantage of this therapy is the immediate angiographic restoration of flow. 28 The AngioJet system is associated with some complications, including intravascular hemolysis, 19 dilutional anemia 24 resulting from excess infusion of saline, and aspiration anemia due to suctioning of blood into the system. Clinicians must watch postoperatively for a decrease in the hematocrit level and clinical signs of hypovolemia, and they must transfuse as needed.…”