Compressive hematoma and deep arteriovenous malformation: Emergency endovascular occlusion via a venous approach with surgical evacuation of the hematoma

Abstract

Compressive hematoma associated with deep arterio-venous malformation is a difficult surgery. Arterial presurgical embolization is often indicated but rarely effective. Endovascular occlusion via a venous approach is a technique that has recently been undertaken successfully to treat certain types of sub-pial vascular malformation.

The venous endovascular approach has succeeded in a 20-year-old man of who presented with a compressive hematoma due to rupture of a deep arteriovenous malformation. By fully endovascular occlusion, the surgery consisted of surgical removal of the hematoma, with reduced cortical damage.

Background

Emergency surgery on a ruptured deep arteriovenous malformation (AVM) is challenging, especially when it is associated with an exclusively deep cerebral hematoma. Presurgical arterial embolization of the vascular malformation is one of the therapeutic options that is often considered although this endovascular treatment is often incomplete and also difficult because of tiny, twisted arterial pedicles. Endovascular occlusion via a venous approach is a technique that has recently been undertaken successfully to treat certain types of sub-pial vascular malformation. Here we report a case of emergency treatment of an arteriovenous malformation associated with a deep cerebral hematoma, by endovascular repair of the vascular malformation via a venous approach followed by surgical evacuation of the hematoma with stereotactic guidance.

Case presentation

The patient was a 20-year-old man, right-handed, without any particular history. In April 2014, he experienced malaise followed by tonic-clonic movements and impaired consciousness. On admission, his Glasgow score was 4 and he showed bilateral myosis. A computed tomography (CT) scan revealed a deep intraparenchymatous hematoma in the left hemisphere, measuring 65 mm along its longest axis (Figure 1). An intracranial pressure monitor installed in Intensive Care showed high intracranial pressure (40 mm H₂O). Arteriography showed a deep arteriovenous malformation (AVM) supplied by a lenticulostriate artery and draining into a left lateral ventricular vein (Figure 2). It was decided to evacuate the hematoma but, given the depth of the malformative nidus, it seemed wiser to perform endovascular occlusion of the AVM before the craniectomy.

Figure 1.

Left deep haematoma on the initial computed tomography.

Figure 2.

Cerebral angiography with selective injection in a lenticulostriate artery. Lateral view: nidus supplied by lenticulo-striate network (black arrow). Single venous drainage of the arterio-venous malformation in a left lateral ventricular vein (white arrow).

Treatment

The origin of the lenticulostriate artery supplying the malformation was catheterized but, given the artery’s tortuosity and small size, the end of the catheter could not be installed distally. Given the small size of the nidus and the fact that the malformation was only draining into a vein, it was decided to make a venous approach. The right jugular vein was punctured and a French 6 introducer was inserted. Then a 4F catheter (4F BER tempo4 Cordis Corporation, USA) was mounted in the right lateral sinus then the right sinus with its distal end ultimately installed in the great cerebral vein. A microcatheter (UltraFlow eV3, CA, USA) was mounted coaxially in the 4F catheter and its distal end was placed in the deep vein as close as possible to the nidus of the malformation. Careful injection into microcatheter showed that it was in the right position by shadowing a pseudoaneurysm next to the nidus where the arteriovenous malformation ruptured. Diluted glue (Histoacryl Braun and Lipiodol) was injected to rupture the pseudoaneurysm and occlude it as well as the malformed vessels and the vein draining the malformation (Figure 3). Follow-up arteriography after embolization showed disappearance of the malformation and its draining vein as well as intact lenticulostriate arteries (Figure 4). At the end of the procedure, hemodynamics were stable and the patient’s pupils were contracted. Before evacuation of the hematoma, neuronavigation with CT guidance was undertaken. With the patient lying on his back, a broad flap was cut out after crossbow temporo-parieto-frontal skin incision. After opening of the dura mater, a transfrontal path (F3) was created with a Cushing trochar and then this was dilated with a balloon. The hematoma was aspirated without visible bleeding. At the end of the intervention, because of the intracranial hypertension, the dura mater was not closed and the flap was not put back in place.

Figure 3.

Injection of glue through the microcatheter placed in the drainage vein of the arteriovenous malformation, showing a false-aneurysm (black arrows). The microcatheter was mounted coaxially through a 4F catheter placed in the Galien vein (white arrow).

Figure 4.

Post-embolization angiogram: Complete occlusion of the arteriovenous shunt.

After withdrawal of the sedation, the patient was conscious and cooperative, with spontaneous movement of the left body but aphasia and hemiplegia on the right. Rehabilitation was started and the bone flap was replaced after three months.

Outcome and follow-up

The patient was seen again after six months with magnetic resonance imaging (MRI) and cerebral arteriography. Although the aphasia had improved, certain words still failed him. He could walk but his right arm function was still impaired. Arteriography showed occlusion of the AVM and MRI showed a reduced cortical stigma from the surgery and a cavity in the deep brain (Figure 5).

Figure 5.

Six-month follow-up magnetic resonance imaging: post-hematoma deep cavity with reduced cortical stigma from the surgery (white arrows).

Discussion

How to manage deep AVMs when they rupture is particularly challenging for two reasons: First, there is a high risk of re-bleeding, and the annual risk of rupture has been estimated at 10%–34% with a mortality rate of more than 60%;^1,2 second, neurosurgery on such deep malformations is riskier than with cortical malformations. A very experienced team³ recently reported on a highly selected series of deep AVMs with complete resection in 71% of cases and complications in 29%. The risk of treatment is also greater for other treatment modalities: Arterial embolization is very rarely curative and has a rate of permanent morbidity of between 10% and 60%;² the delayed effects of radiosurgery represent a major disadvantage of this technique, which often leads to complications in deep AVMs as well as being less effective.⁴

In this case, the strategy was to combine complete endovascular repair of the malformation via a venous approach with stereotactic evacuation of the hematoma in order to minimize cortical damage in the left hemisphere. Because of the high intracranial pressure, surgical evacuation of the hematoma was considered as an emergency, and the combined treatment was carried out immediately. Embolization via a venous approach has been shown to be effective in the treatment of dural fistulae, aneurysms of the great cerebral vein and peripheral AVMs. However, many endovascular surgeons are reticent about this technique for the treatment of sub-pial malformations because accidental occlusion of draining veins during embolization can raise pressure inside the malformation and cause vessel rupture, usually with catastrophic consequences.

Some 30 cases of AVM embolization via a venous approach have been reported in the literature with complete occlusion of the nidus and few complications.^5–8 Unlike our case, reported venous embolizations were not carried out as a matter of emergency before the surgery of a compressive hematoma. In these cases, the venous approach was attempted when no other technique—surgery, radiotherapy, arterial embolization—was possible, when the AVM was small and when drainage was into a single vein. In addition, the venous approach: precludes the need for risky attempts to catheterize the lenticulostriate arteries, which are very small and tortuous; avoids possible ischemic complications of arterial embolization in the lenticulostriate territory; provides easier access by virtue of dilation of the vein draining the malformation, thereby cutting down operating time; and finally and most important, may succeed in completing occlusion of the AVM. On the last point, positioning the end of the embolization microcatheter at the venous point of convergence of the malformed capillary shunts would seem to allow centrifugal filling of the malformation during embolization that would be better than that afforded by an arterial approach,⁵ and would account for the improvement in occlusion rate. Despite the success of this procedure, prudence is indicated vis-à-vis a venous approach because of the fragility of the vessels’ walls and especially the risk of high pressure inside the vascular malformation following occlusion of the draining vein. In our case, this risk was illustrated during the injection of glue by the rupture of an aneurysm in the nidus—luckily with no repercussions. While awaiting bigger studies and according to Consoli et al.,⁵ the indication for endovascular treatment of an AVM via a venous approach should be conditioned by: a risk of re-bleeding from the malformation; other therapeutic options being impossible or difficult; a very small malformative nidus; a single draining vein; and endovascular navigation being possible. Accordingly, indications for a transvenous approach are not dependent or limited by age and sex of patients, but rather the angioarchitectural aspect of the malformation, and the difficulties of conventional treatments.^5–8

No consensus exists on the surgical evacuation of the intracerebral hematomas. Most of the published data from randomized trials, such as the recent second Surgical Trial in Lobar Intracerebral Hemorrhage (STICH II) Study,⁹ concerned surgery for spontaneous lobar brain hematomas and showed no improvement in outcome after surgical evacuation. In a meta-analysis,¹⁰ there was a suggestion that surgery might be beneficial in certain, selected patients: Selection criteria seem to be: less than 69 years of age, superficial hematoma, Glasgow score of over 8, and finally the absence of concomitant intraventricular bleeding. The justification for evacuation of the hematoma was debatable in this situation: deep insular hematoma (≥1.5 cm), initial Glasgow score of 4, and ventricular effraction. In our case, the intracranial hypertension and, most of all, the patient’s age, were crucial factors in our decision to perform surgery.

Funding

This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.

Conflicting interest

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.