5 Maggio 2016

Francesco Causin

Neuroradiology

Padua University Hospital

Best treatment of Hemorrhagic StrokeIntracranial Vascular Lesions

AV malformation and fistulas: surgery and embolization

Brain AVMs DAV Fistulas

Heterogeneous group of lesions with

different clinical presentation and most likely

different natural history and outcomes.

Brain AVMs DAV Fistulas

Brain AVMs

• Patients younger than 40 y.o. (peak age 20-40)

• Asymptomatic or different clinical settings

Artero-venous malformations prevalence:

• less than 0.01% in the western world

• the detection rate is about 1 per 100.000 prs/y

Brain AVMs

Estimates for bleeding from unruptured AVMs range from 1.3% to 4% per year with mortality of 10% to 30% from incident

hemorrhage and neurological disability of 20% to 30%.

Clinical presentation could be:

• No clinic, incidental

• Progressive neurological deficit

• Headache (episodic or chronic)

• Seizure (fixed or unstable/focal or gen.)

• Bleeding (intracerebral, ventricular, SAH)

3%

7%

15%

25%

50%

Brain AVMs

Arterio-venous malformations of the brain are a major cause of hemorrhagic stroke in young, healthy individuals.

• Local repression of genes may cause absence of vasoregulatory peptides that modify vasculogenesis and angiogenesis.

• Venous side of primitive capillaries may be involved in structural and cellular abnormalities. This may result from failure of endothelial cells to remodel the primitive embryonic vascular network.

• Many AVMs show upregulated expression of vascular endothelial growth factors (VEGF). This induce increased endothelial cells proliferation and cause inappropriate stimulation of neural and glial cells.

Pawlikowska Stroke 2004

Brain AVMs

• Patients older than 50 y.o. (peak age 40-60)

• More typical progressive symptoms

AV Fistulas

Much less common than AVMs, they exhibit a wide spectrum of clinical signs, that range from relatively benign tinnitus to severe degenerative

symptoms or hemorrhages.

There are few data on incidence and natural hystory

AV Fistulas

While the precise etiology is unknown and controversial, local hypoperfusion in a thromboseddural venous sinus that result in elevated intrasinus

pressure, is the most cited mechanism.

Upregulated angiogenesis within the dural sinus walls occurs after thrombosis.

We are quite sure they are acquired lesions.

AV Fistulas

Artero-venous malformations:

• brain lesions

• probably genetically determined

• errors in the development of the vasculature

• modified by effect of blood flow

• not endovascular first option

Artero-venous fistulas:

• not brain lesions

• mainly acquired lesions

• probably due to thrombophlebitis of dural sinus

• modified by effect of blood flow

• endovascular always first option

Doing something

• Embolizationperi-post procedure (hemorrhagic / ischemic)

• Stereotactic Radiosurgerybleeding after treat./ radio-necrosis

• Microsurgery new neurol. deficit/ death

• Combination of these

per procedure 3%9% new deficit - 13% cured

overall 10%8% new deficit - 38% cured

11%-30%96% cured

?

Brain AVMs

The literature contains a wide range of data on this subject, and by taking

examples from across this spectrum one can easily support any viewpoint.

which is worse, the disease or the cure?

Brain AVMs

The efficacy and risk of treatment vary based on the modality used (surgical, endovascular, or radiosurgical)

and AVM specific location and features.

Patients who present with a hemorrhage from an AVM should be initially stabilized.

The characteristics of a lesion (size & location) and high-risk features will influence risk of rupture, prognosis, as well as help guide management decisions.

Given that rupture is associated with an increased risk of 6% re-rupture in the year following the initial hemorrhage, versus 1 % to 3 % predicted annual risk in non-ruptured lesions, definitive treatment is encouraged after stabilization.

A rest period of 2 to 6 weeks after hemorrhage is recommended before definitive treatment to avoid disrupting friable parenchyma and the hematoma.

Treatment may consist of endovascular embolization, surgical resection, radiosurgery, or a combination of these three interventions based on the lesion.

Although it is usually preferable to defer AVM treatment for a few weeks,acute surgical (open and endovascular) management is essential in specific clinical and radiological settings.

Spighi locatelli

19 aa

23 aa

The annual mortality rate for lesions with cortical venous reflux may be as high as 10.4%, whereas the annual risk for

hemorrhage or nonhemorrhagic neurologic deficits during follow-up is 8.1% and 6.9%, respectively, resulting in an annual

event rate of 15%.

AV Fistulas

Male gender, posterior fossa location, older age at presentation, and focal neurological deficits are associated

with hemorrhagic presentation of DAVFs. Tentorial and anterior fossa DAVFs are reported to have a risk

of hemorrhage as high as 75-95%. Ruptured Borden type II and III carry a high risk of early rebleeding (35% within 2

weeks after the first hemorrhage)

S.V.

G.M.

Different lesions with different clinical

presentation and treatment options and most

likely different natural history and outcomes.

Brain AVMs DAV Fistulas