Hemodynamic Changes Caused by the Occlusion of Dural Arteriovenous Fistula

Hemodynamic Changes Caused by the Occlusion of Dural Arteriovenous Fistula

Perspectives Commentary on: Rapid and Progressive Venous Thrombosis After Occlusion of High-Flow Arteriovenous Fistula by Gonzalez et al. pp. E359-E36...

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Perspectives Commentary on: Rapid and Progressive Venous Thrombosis After Occlusion of High-Flow Arteriovenous Fistula by Gonzalez et al. pp. E359-E365.

Mika Niemela¨, M.D., Ph.D. Associate Professor, Department Neurosurgery Head of Section, Helsinki University Central Hospital

Hemodynamic Changes Caused by the Occlusion of Dural Arteriovenous Fistula Anna Piippo and Mika Niemela¨

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ural arteriovenous fistulas may cause tinnitus, sometimes headache, neurologic deficits, or hemorrhage. The clinical presentation is determined by the pattern of venous drainage (1, 2, 7). Retrograde flow into the venous sinuses without cortical venous drainage (CVD) in Borden type I fistulas can result in increased intracranial pressure (3, 4). CVD predicts an aggressive clinical course. Dural arteriovenous fistulas with CVD may manifest with hemorrhage and neurologic deficits secondary to local venous congestion, brain edema, or ischemia (3, 5, 7, 11). The symptoms may be reversible after treatment (5).

Management of these lesions requires careful planning. Despite developments in both endovascular and microsurgical techniques, treatment still carries significant risks that should be weighed against the achievable benefits. The risks related to interfering with the pathologic venous drainage have been recognized, and the treatment strategy has changed over the decades. Benign Borden type I fistulas are treated conservatively aiming at palliative symptom relief. In Borden type II and type III fistulas, a simple procedure disconnecting the CVD is preferred. However, certain complex fistulas with several draining veins simply cannot be managed by simple CVD disconnection and require total obliteration of the fistula to prevent an aggressive course. In our series of 261 dural arteriovenous fistulas, we observed complications in 18% of the procedures, of which 8.4% were severe (large infarction, intracerebral hemorrhage, epidural hematoma, brain swelling) (9). Severe bleeding occurred in 14% of the craniotomies performed. There were 5 procedure-related deaths, 3 after embolization and 2 after microsurgical occlusion of the fistula.

Key words Arteriovenous - Dural - Fistulas - Onyx - Pial - Sinus thrombosis - Surgical clipping -

Abbreviations and Acronyms CVD: Cortical venous drainage

WORLD NEUROSURGERY 80 [6]: e211-e212, DECEMBER 2013

Two of the patients developed progressive sinus thrombosis after glue embolization, and in one of them glue was seen in the sigmoid sinus at autopsy. Both patients treated with microsurgery had sudden severe brain edema during surgery. All of the fistulas were Borden type I and were treated with the goal of complete occlusion, which was the treatment strategy at that time. Occluding the venous outflow, particularly a major venous sinus or a large draining vein, may be hazardous and cause infarction or hemorrhage if it drains the normal brain. In our 2 surgical cases, this kind of hemodynamic change in venous outflow resulted in severe uncontrollable brain swelling and bleeding in one of the endovascular cases. Similar complications have been reported in the literature (6, 8, 10). Gonzalez et al. described in their case report another problem caused by a major change in hemodynamics after treatment. Two patients with pial and dural arteriovenous fistulas and large venous pouches developed progressive massive sinus thrombosis after treatment. In the first case, the sluggish venous blood flow was observed already during the endovascular procedure. The thrombosis progressed despite placing the patient on heparin drip. The authors assumed that the thrombosis developed because of decreased flow from the feeding arteries after endovascular and surgical occlusion. In our 2 patients with massive sinus thrombosis observed after treatment, the angiogram showed normal venous flow. However, migration of the glue into the venous system initiating the coagulation cascade was seen in 1 patient, in contrast to the case of Gonzalez et al. The other patient developed sinus thrombosis without any

Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland To whom correspondence should be addressed: Mika Niemelä, M.D., Ph.D. [E-mail: [email protected]] Citation: World Neurosurg. (2013) 80, 6:e211-e212. http://dx.doi.org/10.1016/j.wneu.2013.01.068

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obvious predisposing factors. In this case, the change in venous flow may have been the activating factor of the coagulation cascade. The authors demonstrated that if a significant venous stasis is observed after closure of a large venous pouch, strict therapeutic anticoagulation may be necessary to prevent venous thrombosis. It may be problematic after surgery as well as after

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embolization if the patient develops hemorrhage secondary to impaired venous outflow. Venous thrombosis carries high morbidity and mortality rates, as the cases of this report and our study showed, and anticoagulation therapy is justified. As the authors pointed out, neurosurgeons should be aware of this devastating complication.

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Citation: World Neurosurg. (2013) 80, 6:e211-e212. http://dx.doi.org/10.1016/j.wneu.2013.01.068 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com

9. Piippo A, Niemela M, van Popta J, Kangasniemi M, Rinne J, Jaaskelainen J, Hernesniemi J: Characteristics and long-term outcome of 251 patients with

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