Hemodynamic disturbances associated with endovascular embolization.
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Publications and source records attributed to K Terbrugge.
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BACKGROUND AND PURPOSE: Inadvertent foreign body embolization is a rarely diagnosed and neglected complication of cerebral angiography that has not been studied systematically. METHODS: We undertook a comprehensive 5-year retrospective study of all available postmortem cases of postangiographic neurologic complications, as well as a comprehensive histologic examination of all surgically resected central nervous system arteriovenous malformations, at our institution. RESULTS: Among the autopsy series, we found 3 patients for whom cerebral infarction, sometimes catastrophic, is attributable to inadvertent cotton fiber, Gelfoam, or polyvinyl alcohol particulate emboli during cerebral angiography. All cases described had concurrent atherosclerotic vascular disease. Particulate embolization, which is usually cotton fiber, is present in as many as 25% of resected arteriovenous malformations: the risk of finding such emboli is in part dependent on a history of prior interventional (as opposed to diagnostic) angiographic procedures. It is not surprising that the amount of tissue examined also increases the risk of finding such emboli. CONCLUSIONS: Unintentional foreign body emboli remain common in modern angiographic practice and are probably underappreciated clinically. Although such emboli are usually asymptomatic, they can be clinically devastating, and a high index of suspicion is required for diagnosis. Foreign body emboli should be included in the differential diagnosis of postangiographic ischemia or infarction.
The association between the formation of intracranial aneurysms and situations of increased blood flow in certain areas of the brain is well accepted today. It has been seen in association with arteriovenous malformations of the brain, carotid occlusion, and Moyamoya disease. The occurrence of aneurysms in small arteries of the skull base, with the exception of the intracavernous carotid artery, however, is rare. We report a case of a 55-year-old woman who presented with an intracerebral hemorrhage caused by a ruptured anterior ethmoidal artery aneurysm. To the best of our knowledge, this is only the second case of documented intracranial bleeding from such a lesion.
The management of Brain Arteriovenous Malformations continues to be challenged by a lack of understanding and control of pathophysiological processes implied in the clinical symptoms. New data from functional MRI with diffusion-weighted, perfusion-weighted and neuronal activation highlight abnormal brain areas near or remote to the AVM nidus. Moreover, these techniques are able to show hemodynamic and neuronal adaptative phenomena involved in brain plasticity. They reflect the instantaneous hemodynamic brain conditions that may help to correlate the clinical symptoms with the anatomical and functional substratum and to influence any invasive therapy.
Intracranial pial and dural arteriovenous shunts may exist at different sites in the same patient. The etiology, natural history and treatment of these associated conditions have not been completely determined. We reviewed the records of 765 cases of pial arteriovenous malformation and 137 dural arteriovenous fistulae and malformations. We selected eight patients with both pial and dural arteriovenous shunts, separate anatomically, with distinct feeding arteries and draining veins, representing 1% of pial and 17% of dural shunts. Presentation was related to the dural lesion in 5 cases (62.5 %) and to the pial malformation in three (37.5%). Treatment of these lesions should be considered separately based on their angio-architecture and natural history.
BACKGROUND: Problems of clinical management of neurovascular diseases are very complex. This is caused by the chronic character of the diseases, a long history of symptoms and diverse treatments. If patients are to benefit from treatment, then treatment decisions have to rely on reliable and accurate knowledge of the natural history of the disease and the various treatments. METHODS: Recent developments in statistical methodology and experience from electronic patient records are used to establish an information infrastructure based on a centralized register. RESULTS: A protocol to collect data on neurovascular diseases with technical as well as logistical aspects of implementing a database for neurovascular diseases are described. The database is designed as a co-operative tool of audit and research available to co-operating centres. CONCLUSION: When a database is linked to a systematic patient follow-up, it can be used to study prognosis. Careful analysis of patient outcome is valuable for decision-making.
The purpose of this report is to determine the role of various imaging modalities, and the outcome of early intervention in neonates with high flow pial arteriovenous malformations (AVM). This report describes 4 neonates with pial AVM associated with congestive cardiac failure, and reviews previous reports. Among the 4 infants in our series, 3 underwent early surgical resection of the AVM, complete in 2 and partial in 1. One infant suffered hemorrhagic infarction postoperatively and has a mild deficit on clinical follow-up; the other 2 patients had no worsening of mild neurologic deficits after surgery, and subsequent development has been normal. The fourth infant had absent deep venous drainage and died from intracranial hemorrhage following transvenous embolization. A single vessel arteriogram in 1 infant led to underestimation of the lesion and unexpected findings at surgery. Complete angiographic study is important in planning treatment, as the vascular anatomy of the lesions may be complex. Cranial ultrasound is useful in early diagnosis, but may miss the superficial lesions. Untreated infants with pial AVM have a poor prognosis due to cardiac failure or progressive cerebral ischemia and neurologic regression. This series illustrates the benefits of complete angiographic investigation and early treatment.
Ninety-seven patients were referred to the Toronto Hospital (Western Division) between January 1984 and January 1992 for selective angiographic embolization (108 embolizations, including repeat procedures) to control intractable or recurrent severe epistaxis. Eighty-one patients (comprising 94 embolizations) were referred on an emergent basis because of failure of conventional conservative therapy, consisting of anterior and posterior packing. The remaining 16 patients (14 embolizations) were referred electively for recurrent epistaxis. A retrospective review of these cases was performed, with long-term telephone follow-up achieved in over 95% of cases. Embolization safely controlled active hemorrhage in 88% of the emergent cases. The success rate increased to 90% when two cases in which the source of epistaxis was found to be from the internal carotid artery were excluded (because these vessels could not be safely embolized). Of the patients whose epistaxis was initially controlled by embolization, 82% had no further nosebleeds (follow-up time ranged from 2 to 82 months; average, 26.8 months). More than half of the long-term failures were seen in patients with Osler-Weber-Rendu disease. Overall, the mortality rate was 0% and the long-term morbidity rate was 2% (one cerebral vascular accident and one case of skin slough in the territory of the superficial temporal artery.
PURPOSE: To present the MR findings of intracranial dural arteriovenous malformations with cortical venous drainage, emphasizing the parenchymal changes. METHODS: Conventional MR and x-ray angiograms in 13 patients with dural arteriovenous malformations and cortical venous reflux were reviewed. The site of the shunt, location of the venous reflux, and presence of venous stenosis were assessed on the angiograms. Parenchymal changes, dilated vessels, and venous occlusive disease were assessed on MR. RESULTS: On MR, 10 of the 13 patients (77%) had dilated pial vessels. Two patients had hydrocephalus. Two patients presented with parenchymal bleeds, one with a subdural component, both remote from the nidus. Two patients presented with subarachnoid hemorrhage. One patient had a parenchymal bleed 9 months after presentation. Venous occlusion was evident on MR in 2 patients. Diffuse white matter edema in the cerebellar or cerebral hemispheres was present on MR in 4 patients and correlated with neurologic deficits. In 2 of these 4 patients, gadolinium enhancement was seen in the periphery of the involved hemisphere. CONCLUSIONS: On MR a surplus of pial vessels suggests a dural arteriovenous malformation with cortical venous drainage. The MR finding of white matter edema deep in the cerebral or cerebellar hemispheres is direct evidence of a venous congestion.
Forty-three patients with vein of Galen aneurysmal malformations (VGAM) referred to us for endovascular treatment between 1985 and 1990 and 335 additional cases published in the literature were reviewed with particular attention to the presence of ventricular enlargement and outcome after shunting. Hydrocephalus was the second most frequent symptom (46.8%); it is more frequent in infants (73%) than in children, adults (30%) or neonates (15%). Of the patients reported in the literature, 17.9% had undergone shunting. Within the shunted population there was an overall morbidity of 41% and a mortality of 10% (especially in the infant group). In our series 17 patients (39.5%) were shunted and a significant difference in the clinical outcome was noted between the shunted and the nonshunted group. Of the nonshunted patients, 66.6% were free of any neurological deficit or mental retardation and fewer than 5% presented with significant mental retardation. On the other hand, only 33.3% of the shunted patients had a favorable outcome and more than 15% developed significant mental retardation. Among the various causes of hydrocephalus in patients with VGAMs, such as obstruction of the aqueduct, subarachnoid hemorrhage, or ex vacuo hydrocephalus, high venous pressure may be of particular importance. In this article a physiopathological interpretation of the hydrodynamics in VGAMs is developed and a speculative explanation for CSF disorders related to ventricular shunting proposed. Treatment of hydrocephalus in VGAMs can be achieved through obliteration of the malformation or at least diminishing the venous pressure; surgical ventricular shunting does not have to be the first treatment of hydrodynamic disorders associated with VGAMs, especially in infants.
The artery of Adamkiewicz infrequently originates from the same radicular vessel that also supplies a dural arteriovenous fistula. This variant is not adequately emphasized in the neuroradiological literature. Awareness of this entity is essential to prevent catastrophic complications during embolization. We report such a case, and our experience with attempted embolization. We are unaware of any previously reported instance of such an attempt being made.
Embolization of cerebral arterio-venous malformations (A.V.M.s) is nowadays recognized as belonging to the therapeutic panel applied to these lesions. After an hemorrhagic accident, embolization is most often performed several weeks later. We report three cases of intracerebral hematoma due to A.V.M. rupture (cortico-ventricular rolandic, lateral ventricle subependymal, cortical anterior temporal A.V.M.s). These were treated by endovascular methods, using fluid material (N.B.C.A.), in emergency or semi emergency (hours, days). This had been done for direct preoperative purposes or medical reasons (heparinization in thrombophlebitis). If, at Bicêtre, the treatment of A.V.M.s by embolization is daily performed, this type of emergent treatment is rare (3 cases on the 350 patients treated till now). No complication was reported for these three patients. The efficiency of such an "emergent procedure" is unknown and cannot be compared to similar experiences. The empiric data we obtained make us think that embolization, necessarily done without heparin, is possible and may constitute an important help to surgery without delaying it. It reduces the risk of rebleeding by targetting the treatment on angio-architectural weakness points (false aneurysms). It redistributes the arterial blood, lowers the venous hyper-pressure, improves the locoregional perfusion and finally leads to a better final neurological status.
The authors present four consecutive cases of multiple dural arteriovenous (AV) shunts in children. This entity represents a rare but severe clinical situation. The etiology of the shunts is not known. There is clinical and radiological evidence that they are evolutionary lesions. The clinical presentation in this series was usually by cardiac manifestations (one case), cerebrospinal fluid disorders (two cases), neurological symptoms (three cases), including intracranial hemorrhage (two cases), and cranial bruits (four cases). No radical treatment leading to anatomical cure of all dural AV shunts was thought to be possible using current methods, including modern endovascular and surgical techniques, in any of the four cases. Therefore, treatment was only symptomatic and directed at some of the AV shunts. Targeted arterial embolization with permanent embolic agents represents the most rational technique for symptomatic relief in these patients. However, clinical recurrence often happens without evidence of recanalization. Secondary multifocal pial AV shunts opening into the abnormal sinus occurred in two of the cases; they may have been induced by venous sump from the sinus draining the dural AV shunts. Mechanical occlusion (or excision) in multiple dural AV shunts in children does not represent a satisfactory goal, as the shunts can be the expression of a more complex and yet unknown disease.
Since 1984 we have been involved in the management of 30 children who had cardiac manifestations secondary to cerebrocranial arteriovenous shunts. Aneurysm malformation of the vein of Galen was the most common vascular lesion observed (73% of cases). In 77% of the patients the cardiac symptoms were the main presenting complaint. Medical treatment and/or endovascular therapy were indicated, depending on the age of the patients and the severity of the cardiac manifestations. Following embolization, the cardiac symptoms resolved (73%) or improved (18%) in 1 or 2 sessions. Mortality in the embolized group was 9%, and transient nonneurologic morbidity occurred in one case. Overall mortality, including four patients rejected for embolization, was 20%. These results compare favorably with medical and/or surgical management, alone or combined. The technique, challenges, indications and contraindications of endovascular therapy are discussed. Embolization represents an effective adjunct treatment to control, improve or cure the congestive cardiac manifestations caused by cerebrocranial arteriovenous shunts.
We report two types of venous patterns associated with great cerebral vein (vein of Galen) absence or unavailability. Developmental venous anomalies or vein of Galen arteriovenous malformations (VGAM) serve as an illustrative material. A diencephalic pattern that collects the thalamo-striate veins into the tentorial sinus is recognized in most VGAM. A telencephalic arrangement connecting the striate veins with the rostral afferents to the basal vein is less frequent. Both patterns reproduce embryonic stages preceding the development of the great cerebral vein, thus confirming Raybaud's hypothesis that in VGAM the pouch is not the vein of Galen but the medial vein of the prosencephalon. The prognostic value of each pattern can then be appreciated and the therapeutic strategies rationalized; some unexplained complications of the venous approach for non selected VGAM can thus be avoided.
4 patients with acquired arteriovenous shunts located in the wall of an ectatic vein of Galen (VG) are reported. They represent so-called VG dural arterio-venous malformations (DAVM). These shunts involve the vasa vasorum normally present in the VG wall. Physiopathology, clinical signs and age groups are usually the same as those encountered in other DAVMs; conversely they are totally different from the other mural shunts of the VG, detected in the pediatric population (true VG arteriovenous malformations), and leading to different clinical symptoms. Venous approach in these VG DAVMs is almost always contraindicated unless secondary occlusion of VG afferent has spontaneously excluded the pouch from the cerebral venous circulation.
The authors present their protocol for spinal angiography in their investigation of dural arteriovenous fistula (DAVF). The protocol has been used in approximately 120 patients from 1983 to the present at Bicetre Hospital. The approach is based on the fact that venous congestion is responsible for the myelopathy of DAVF. If the venous phase of the spinal circulation is normal, this alone rules out DAVF as the cause of the patient's symptoms. If there is stasis in the spinal circulation, this is consistent with DAVF, and thus complete spinal angiography is necessary. Complete angiography includes the selective intercostal arteries, including the lateral sacrals, as well as the supply to the cervical cord and posterior fossa.
From our series of 203 patients with cerebral vascular lesions, 18 (9%) could be included in the multiple arteriovenous malformation category. There were five patients with Rendu-Osler-Weber, one with Wyburn-Mason syndromes and two with concurrent arteriovenous malformations. The remaining ten patients (4%) had multiple brain arteriovenous malformations. Careful angiography with magnification is necessary to try to diagnose multiple brain AVMs, since these sometimes become apparent only after embolization of a larger dominant AVM. The incidence of multiple brain arteriovenous malformations is likely to have been underestimated due to the failure to recognize micro-arteriovenous malformations associated with larger arteriovenous malformations.