DAVF

Definition

A disease of the vein/sinus where AV shunt is contained within leaflets of dura mater

Exclusively supplied by branches of

Carotid arteries or
Vertebral arteries

Aetiology

Acquired

venous thrombosis

In patients with acquired or genetically determined prothrombotic disorders
prothrombotic states constitute no more than 30% of cases of DAVF

Congenital (e.g. some types of vein of Galen aneurysms

Location usually adjacent to dural venous sinuses

Transverse (lateral) Sinus

Most common
Slight left side predominance (65%)
With the epicentre almost always at junction of transverse and sigmoid sinus
Supplied by the post. Meningeal branch of the vertebral artery

Tentorium

Posterior cavernous sinus

Supplied by the meningohypohyseal trunk
Draining into transverse and sigmoid sinus
Within 1 cm of the junction

Numbers:

10-15% of all intracranial AVM

DAVF 1/3 rate of AVM

Present between 40-50 yrs

60% female

Rare in children but if forms will be bilateral

Annual haemorrhage rate for Borden 2 and 3

20%
Mortality 3%

Pathophysiology

one or more fistulae centred either

Fistula on the bridging vein (bridging between the leptomeningeal veins and dural venous sinus)

fistulae within the wall of veins contained within dura (including dural venous sinuses).

No cortical venous HTN: low bleeding risk

Cortical venous hypertension/drainage: will have high bleeding risk

Zipfel 2009

haemorrhage risk

Symptomatic (cortical venous HTN present) 7.4-7.6%
Asymptomatic (cortical venous HTN absent) 1.4-1.5%

Haemorrhage

Re-haemorrhage rate: 35% within the first 2 weeks of hospitalization
See Cognard and Borden classification

Complication

Venous aneurysm
Arterial aneurysm

Clinical findings

Sign/symptom	No. (%)
pulsatile tinnitus	25 (92%)
occipital bruit	24 (89%)
headache	11 (41%)
visual impairment	9 (33%)
papilledema	7 (26%)

Symptoms can change and need re-evaluation

Classification

Cognard Classification

Type	Description	Notes	Annual risk of haemorrhage
1	Direct to sinus • Antegrade flow in sinus Anterograde drainage into the main sinus F/u for asymptomatic lesions: annual Doppler studies	Does not drain into cortical veins hence does not affect cerebral profusion —> MORE BENIGN Despite good prognosis 2% will progress —> require f/u studies	0%
2a	Direct to sinus • Retrograde flow in sinus --> sinus can be non-functional but if other veins can help doing the drainage Blood is flowing in the wall of the venous sinus and not within the venous sinus Drainage into main sinus with reflux into another sinus F/u for asymptomatic lesions: annual Doppler studies Can cause raised ICP	As above —> MORE BENIGN	10
2b	Direct to sinus • Retrograde flow into cortical veins	When cortical veins affected it can cause reduce drainage from normal cerebrum causing venous ischaemia in that region—> high risk of bleeding and intracranial hypertension
2a+b	Direct to sinus • Retrograde flow into sinus • Retrograde flow into cortical veins	As above
3	Direct to cortical venous drainage • without venous ectasia Partial occlusion		40
4	Direct to cortical venous drainage • With venous ectasia ◦ dilatation of veins (>5mm and 3x larger than the diameter of the draining cortical vein)		65
5	Drainage into spinal perimedullary (a spinal) vein More likely to present with ischaemic than haemorrhagic Di Chiro Type 1 Barrow Intradural dorsal spinal AVF	Description: spinal venous drainage in addition to all of the above Course: progressive myelopathy in 50%

Borden classification

Borden type	Features	Annual Risk of haemorrhage
Type I:	Via meningeal artery → drains anterograde to the venous sinus	0%
Type II:	Via meningeal artery → drains anterograde to venous sinus and sinus drains retrograde to subarachnoid (cortical) veins	6%
Type III	Via meningeal artery → drains retrograde direct to subarachnoid (cortical) veins	10% without venous ectasia 21% with venous ectasia

Radiology

Non-contrast CT

Can see complications of high-grade fistulas,

Haemorrhage
White matter oedema from venous hypertension.

MRI

Usually normal

oedema

suggesting back flow

Engorgement of pial veins

DSA

test of choice

Lateral angiogram of a Borden type III Right transverse sinus that was thrombosed distally. The catheter is situated in the proximal left transverse sinus, which has multifocal severe stenosis that functionally isolate the arterialized right transverse sinus pouch and force venous drainage retrograde. Contrast material refluxes into the superior sagittal sinus and supratentorial veins, as well as into the galenic system, occipital sinuses, and cerebellar veins

CTA

Look for vessels penetrating the skull from the extracranial circulation that then feeds into the fistula at the dura venous sinuses.

Differential diagnosis

Features	AVM	DAVF
Artery	Pial artery	Dural/meningeal artery
Fistula	Parenchymal nidus Fistula located proximal to Bridging veins	Always at the dura Fistula located distal to Bridging veins
Vein	Pial vein that eventually drains into a venous sinus	Always a venous sinus (There can be retrograde flow into the cortical veins)

Management

Complete obliterate fistula (by closing the drainage)

IF NOT ABLE TO

At least downgrade it to reduce short term haemorrhage rates

Strategy

Identify and close the venous collector
Functional channels in walls of sinus -superselective catheterization and balloon protection
Non-functional sinus sacrifice

Indicated for type 2B and below if

Neurological dysfunction
Haemorrhage
Refractory symptoms

Conservative

Indication

Lesions with a benign venous drainage pattern (Borden I or Cognard I/IIa)

Due to low risk of haemorrhage or neurological deficit.

Options

Spontaneous regression of low-grade DAVFs, especially in fistulas involving the cavernous sinus.
Manual carotid self-compression

Rt hand Compress left carotid (so that if ischaemic the hand will drop off) —> reduce blood flow to the left side causes thrombosis of AVF
Thrombosis rate 22%
Clinical improvement rate 33%

F/u clinically and radiographically, tof-MRA

1% to 3% chance of conversion from a benign to an aggressive drainage pattern.

If symptoms change look for if there is an upgrade in grade

Intervention

Indication

Borden 2 and Cognard 2b and above
Controversial

(Borden I or Cognard I/IIa) incapacitating bruit, ocular symptoms, or headache, but this is quite controversial

Complication

Catheter entrapment
Cranial nerve damage
DMSO toxicity
Radiation injury caused by prolonged fluoroscopic time.

Endovascular embolization

1st line

Indication

Sinus and/or cortical vein fistulation

Onyx

Properties

Ethylene vinyl alcohol copolymer dissolved in dimethyl sulfoxide (DMSO)
Onyx contains micronized tantalum powder

After injection into the bloodstream, the DMSO leaves the mixture, causing the Onyx to precipitate without adhesion to the arterial lumen.

Onyx solidifies within the vessel from outside to inside over several minutes, which allows it to be further pushed through the artery.
Nonadhesive property that makes Onyx advantageous

Decreases the risk of gluing in the catheter
Allows the operator to more aggressively penetrate the fistula nidus.

Can have reflux of onyx and can block an artery

Especially true with skull base DAVF and facial nerve palsy
Can see

Artery into vein injection.

Most AVF best tx endovascularly

Options

Transarterial embolization

Most frequently used route
microcatheter should be advanced to the distal arterial feeder, and the embolic material should be injected into both the fistula pouch and the proximal draining vein
Outcome

Rate of cure of 59% to 80% for malignant DAVF
Complication

permanent neurological: 0% to 3%.

Transvenous embolization

Before the widespread use of Onyx, transvenous embolization was considered the first-line endovascular treatment for DAVFs
Technique

Retrograde catheterization of the draining sinus or cortical vein AND
Occlusion of the recipient venous pouch with coils, glue, or a combination of both

involved sinus is often defunctionalized, which reduces the risk of concomitant venous infarction
If the sinus still has some component of normal drainage, then embolization of the sinus should be avoided because it can lead to venous stroke and hemorrhage.

Complication

Vessel perforation
Intracranial haemorrhage
Venous infarction

combined approaches

Microsurgery

Indication

Failed endovascular tx

Esp: SSS and anterior fossa

owing to the long distance that a microcatheter is required to travel to treat these lesions endovascularly

Isolated cortical venous drainage not involving sinus
Unfavourable physiological anastomoses

Goal

Disconnect the vein from the fistula point, which leads to a cure of the lesion

Surgical options:

Point-disconnection of cortical drainage

Exposing the fistula with coagulation of direct arterial feeders as necessary

Then the arterialized veins of the fistula are coagulated, clipped, or ligated in a location that is as close to the fistula point as possible, taking care to spare nonarterialized veins

indocyanine green angiography and intraoperative digital subtraction angiography, when available, to confirm the obliteration of the fistula

Isolation of sinus
Packing of sinus channels

Complication

Heavy blood loss

High blood flow into sinus —> inc. risk of bleeding if sinus is cut (8 units in 4 mins)

Do not use craniotome
Use a lot of dural tack up sutures

From scalp, bone, dura, or fistula vessels themselves.
Pre-op embolization can help reduce bleeding

SRS

Used with or without embo

Indication

Reserved for benign DAVF that have failed other tx
Salvage therapy for higher risk lesions that are felt to be too dangerous to approach endovascularly or surgically.

Dose

20 Gy

Cons

Latency for which haemorrhage may occur

4 yrs delay before occlusion

Complications

Headache
Nausea
Delayed cyst formation.

Outcome

Cure rates ranging from 50% to 93%
Higher cure rate in

cavernous sinus DAVF
SRS + Embolization

Outcome

Low grades (Cognac 1 or 2A) --> High grades

0.8-2%/yrs

Tx DAVF

0.8-2%/yrs