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AVM ruptured

In fact, as was shown by Hillman (2001), the rupture of an AVM is as devastating as that of an aneurysm. While aneurysm rupture is more lethal than AVM rupture (21% vs 9%), a good outcome is obtained less frequently in AVM than in aneurysm ruptures (49% vs 56%), due to the high incidence of parenchymal hematoma. [Pg.61]

In cases where the hemorrhage is clearly due to AVM rupture the treatment is aimed primarily at the AVM. The first embolization procedure maybe performed after the acute phase, as for ruptured brain AVM not associated with aneurysms. [Pg.91]

In case the subarachnoid hemorrhage or parenchymal hematoma cannot be obviously ascribed to FAA or AVM rupture, the aneurysm should be treated in emergency (Pucheu). The treatment should indeed focus on the lesion presenting the more important risk of rebleeding and likely more severe clinical consequences. [Pg.91]

In the series of Cunha e Sa et al. (1992) the site of rupture was the aneurysm in 46% of cases, the AVM in 33% of cases, and undetermined in 21% of cases. In other series (Batjer et al. 1986 Piotin et al. 2001), the source of hemorrhage in patients harboring brain AVMs and associated aneurysms was identified as an aneurysm in approximately 80% of cases. [Pg.58]

In a relatively small series of patients, Spetzler et al. (1992) evaluated the perfusion pressure of AVM arterial feeders. The difference between mean arterial blood pressure and the feeding artery pressure was higher in ruptured than in non-ruptured AVMs. Moreover, smaller AVMs had significantly higher feeding artery pressure than larger AVMs and were associated with larger hematomas. These results were partially confirmed by Kader et al. (1994), who... [Pg.59]

On the basis of retrospective analysis, the rupture of brain AVMs is estimated to be less severe than that of intracranial aneurysms, with mortality between 10% and 15% and an overall morbidity of less than 50% (The Arteriovenous Malformation Study Group 1999). Hemorrhages of brain AVMs are subarachnoidal (30%), parenchymal (23%), intraventricular (16%), and in combined locations in 31% of cases (Hartmann et al. 1998). Parenchymal hemorrhages were most likely to result in a neurological deficit (52%). Overall, in the series of Hartmann et al. (1998), 47% of patients... [Pg.61]

Patients presenting with ruptured AVMs are usually examined in the acute phase by a CT scan. MRl is currently used in case of unruptured AVM or to find the underlying lesion in case of lobar hematoma, generally days or weeks after the bleeding. [Pg.66]

As shown in Section 3.3.2.1, many anatomic factors have to be analyzed to evaluate the risk of rupture of an AVM and to decide which treatment is appropriate. Despite recent developments, CTA and MRA are currently not sufficient to obtain a precise description of the AVM from an anatomic and hemodynamic point of view. Selective angiography is still always necessary to make a decision regarding the treatment. In summary the diagnosis of an AVM nowadays is usually based on CT or MR the exact and therapeutically relevant anatomic and functional information still has to be obtained by catheter angiography. [Pg.72]

Imaging strategy is closely related to the clinical presentation (rupture of the AVM or not) and the clinical status of the patient. [Pg.73]

In case of unruptured AVM associated with INA or ruptured AVM with INA not responsible for the bleeding, there is no need to perform the treatment in the acute phase. The first embolization procedure should be performed several weeks after bleeding and must be targeted at the compartment of the AVM harboring the INA. [Pg.92]

Fig. 3.13a-i. A 23-year-old man presenting with sudden headaches and vomiting but no neurologic deficit or consciousness disturbance. CT scan shows right cerebellar hematoma with intraventricular rupture and moderate ventricular dilatation (a). Left vertebral artery injection in AP (b) and lateral (c) views show an AVM of the right cerebellar... [Pg.94]

While it is difficult to obliterate multiple arteriovenous connections via the feeding arteries, this can be easily achieved by packing the lumen of the single venous channel of the lesion. Although this might induce transient pressure elevation inside the nidus, rupture and bleeding does not occur, as the nidus is located within the dura and is surrounded by thick walls, reinforced by connective tissue proliferation (Houdart et al. 1993). In contrast to brain AVMs, venous occlusion is feasible... [Pg.153]

Fig. S.12a,b. A 9-year-old boy with acute headache and initially misdiagnosed as meningitis. Lumbar puncture revealed SAH due to a ruptured cervical AVM... Fig. S.12a,b. A 9-year-old boy with acute headache and initially misdiagnosed as meningitis. Lumbar puncture revealed SAH due to a ruptured cervical AVM...
Although these formations are often asymptomatic, they may cause central nervous symptoms such as seizures and ischemia, among other conditions. Locahzed effects such as hearing and vision loss have also occurred (Lasjaunias et al., 1986). Treatment for comphcations associated with AVMs is focused on treating the symptoms of the morbidity. Embolization and resection are used in cases where the physical presence of the AVM poses a concern, such as the structure contacting nerves or, in the presence of endothelium weakening or calcification, a potential for rupture. Treatment typically... [Pg.574]


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See also in sourсe #XX -- [ Pg.72 ]




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