10.4

Flow Velocity and Pressure Measurements in Brain AVMs and DAVFs

These studies were conducted by the author between 1993 and 1997 at Charité, Berlin (Benndorf et al. 1994 a,b, 1995, 1997). A total of 24 patients with intracranial AVMs and DAVFs were included, undergoing 42 measurements during endovascular treatment. The FloWire was usually advanced via a 5-F or 6-F coaxial catheter system into the dural sinuses of interest, such as the superior sagittal sinus, transverse sinus or straight sinus.

In this series, maximum flow velocities up to 166 cm/s were measured in arterialized sinuses (directly draining the arteriovenous shunt), indicating disturbed or even turbulent flow (Hassler 1986), while a maximum of 57 cm/s was found in non-ar- terialized sinuses. The pulsatility index was found to be similar in arterialized and non-arterialized sinuses with a trend to somewhat lower values in the latter (Fig. 10.2)

In DAVFs, increased pulsatility was found not only in the region of the fistula itself (transverse sinus PI = 3.5), but also upstream in the parietal superior sagittal sinus (PI = 1.86). Disturbed flow was found in AV shunt draining sinuses only when the Doppler probe was positioned close to the nidus, or where the main draining vein entered a larger sinus. In four patients without AV shunt a clear pulsatile flow pattern was recorded as well. Pressure measurements revealed values between 6–16 mm Hg in non-arterial- ized versus 19–41 mmHg in arterialized sinuses.

Major changes in flow pattern were found in DAVFs. In one patient, who suffered from a distressing bruit, the DSA showed a partial retrograde opacification of the transverse sinus in the early arterial phase, which caused a contrast “wash out” of the normal anterograde flow in this sinus during the venous phase of the angiogram. This sinus segment remained non-opacified during the late venous phase, mimicking possible thrombosis or even occlusion. Retrograde catheterization, however, demonstrated a patent sinus that exhibited extremely disturbed flow (Fig. 10.3). This flow turbulence was apparently caused by two opposing flow components: the normal antegrade flow from the SSS and the AV shunting retrograde flow. It can be considered a point of “reversal”, which position depends on the degree of AV shunting and may shift upor downstream by either the natural course of the fistula or by inter-

vening endovascular treatment. In the case shown here, TAE of ECA feeders diminished the retrograde component and established normal antegrade flow in this sinus as was documented by continuous recording during the injection of glue. The patient’s associated symptoms subsided.

10.5

Hemodynamics and Pathophysiology in CSFs

The ophthalmic artery mainly supplies the retinal and choroidal circulation. The retinal arteries supply the inner retinal layers and the choroidal arteries, which contain the main blood volume and supply the high metabolic demand of the outer retinal layers (Sanders and Hoyt 1969). Because both the retinal and choroidal vessels are subjected to the intraocular pressure, this circulatory system requires an intraluminal pressure that exceeds the intraocular pressure (normal between 10 and 20 mm Hg). The entire blood circulation of the eye depends on the arteriovenous pressure gradient that, if reduced, will impede the eye blood circulation. The pressure gradient may be lowered by either decreased arterial pressure (hypotension, arteriovenous shunt) or by increased venous pressure (glaucoma, arteriovenous shunt). Whenever this pressure gradient is reduced, the orbital circulation will adjust, mostly by lowering the peripheral resistance through the opening of precapillary shunts and dilatation of small venules (Sanders and Hoyt 1969). These compensatory mechanisms may be exhausted and the blood circulation will be insufficient to meet metabolic demands of the retina that then becomes hypoxic causing loss of visual acuity. If such a condition persists, intraretinal hemorrhages may follow.

An arteriovenous shunt at the CS will, especially when draining anteriorly, cause a significant elevation in the venous ophthalmic pressure that will retard normal antegrade flow in afferent tributaries or even cause flow reversal. It will increase flow in other efferent veins such as the IPS or the PP and may cause “steal effects” in small dural arteries supplying cranial nerves.

Most important for the clinical symptomatology of CSFs are the effects on the orbital venous circulation. Here the AV shunt may cause a drastic reduction in the normal arteriovenous

pressure gradient required to allow normal blood supply to the retina and other intraorbital tissues. As elaborated by Sanders and Hoyt (1969), the elevated venous pressure generates reduced perfusion pressure, which may be further raised by increased intraocular pressure. The eye will attempt to adapt to these changes by lowering the peripheral resistance through microcirculatory changes consisting of capillary shunting, dilatation and venous dilatation. These compensations of the ocular circulation become visible in conjunctival changes with tortuousities, dilatation and thickening of arterialized veins. Fluorescein angiography may show the development of microaneurysms and perivenous leakage.

It is assumed that the orbital circulation, especially the flow in the SOV and IOV, is less affected and has more mechanisms for compensation:

Arterial collateral circulation from external carotid arteries to increase the arterial pressure (Sanders and Hoyt 1969).

The SOV is widely connected through to the facial vein, through the CS with the IPS and multiple other efferent and afferent veins.

Dilatation of some of these major veins will lower the overall venous pressure which is indirectly beneficial for small orbital veins including the central retinal vein.

These compensatory mechanisms explain why in some patients with moderate or high flow in the CS/ SOV, the IOP is only moderately elevated and the vision may be normal.

The situation becomes entirely different when venous outflow restriction develops due to thrombosis, which is often associated with dural arteriovenous shunts of the CS. Therefore, in many DCSFs with “low-flow shunts”, the venous pressure, and subsequently the IOP, may be significantly elevated, particularly if thrombosis of the SOV occurs. If this thrombosis results in an acute SOV occlusion, the venous system of the orbit may not be able to adapt fast enough and the IOP may rise to extreme levels as seen in one of our patients (76 mmHg, see Case Report VI). In such a fistula, the AV shunting volume plays a minor role in the pathophysiology, as it is the elevated venous pressure that causes the reduction in the normal arteriovenous gradient in the ocular circulation leading to reduced retinal perfusion.

10.6

Flow Velocity and

Pressure Measurements in DCSFs

Venous flow velocity and pressure were assessed before, during and after TVO of the CS in three patients (Table 10.1).

Case #1: A Type D fistula with dominant posterior drainage into the SPS and leptomeningeal veins (Fig. 10.4). The opacification of the AV shunt on DSA images was relatively slow. The direct intrasinus measurements revealed 5–14 cm/s in the left CS that showed minimal drainage into a presumably thrombosed IPS; values are considered low for an AV shunting lesion.

With up to 30 cm/s the flow velocity was more increased in the right CS, where posterior drainage into the SPS and leptomeningeal veins was present.

Interestingly, these pressure values were inversed with lower values on the right (39 mm Hg) and higher values on the left side (28 mm Hg).

Case #2: A Type D fistula with venous outflow restriction due to thrombosis of both SOVs. The flow velocity reached maximal 18 cm/s, while the intrasinus pressure was measured at 30 mm Hg. During the coil packing the mean intrasinus pressures reached 60 mm Hg, then fluctuated and decreased again towards the end of the procedure, but remained above levels of adjacent sinuses (IPS).

Case #3: A Type D fistula, the flow was angiographically very low or stagnant due to thrombosis of the SOV and the CS itself (see also Case report III). The Doppler probe did not detect any measurable flow, while the PressureWire documented significantly elevated intrasinus pressure with 40 mmHg (Figs. 10.5).

Table 10.1. Measurement of venous flow velocity and pressure in three DCSFs

a

c

P = 39 mm Hg

V= 5–14 cm/s

e

b

**

d

P = 28 mm Hg

V= 30 cm/s

Fig. 10.4 a–d. Intracavernous measurements of pressure and flow (Case #1): a, b Type D fistula at the posterior right CS (black asterisk), no anterior drainage, but leptomeningeal venous drainage via the right SPS (arrow). Note the minimal drainage on the left side, indicating outflow restriction. c,d Road mapping of transvenous catheterization from right to left with assessment of intracavernous pressure and flow using sensor-tipped guidewires. The flow velocity in the left CS was 5–14 cm/s, the venous pressure reached 39 mm Hg. In the right CS, the velocity increased with 30 cm/s, while the pressure was lower with 28 mm Hg. This difference may be explained by the less restricted outflow in the right CS, where the AV shunt utilized the SPS and leptomeningeal veins for drainage. Note that there is no visible anterior drainage, corresponding with the patients minor dilataion of cunjunctival veins (e). Towards the end of the coil occlusion, pressure values slightly increased, likely due to the tight packing causing additional mechanical pressure. Following TVO, the patient fully recovered without cranial nerve dysfunction. (Benndorf et al. 2001)