ISNVD Abstract Book

PRINCIPLE CONSIDERATIONS ON
VENOUS STASIS AND VENOUS
REFLUX
COMPARTMENTALIZATION IN VENOUS
STASIS
In a vascular compartment affected by
venous obstruction, pressure rises to that
level at which (also adaptive enhancement
in local) arterial inflow is balanced out by
compensatory rises in collateral venous
outflow.
Any rise in pressure in an obstructed venous
drainage domain depends on limitations
to collateral venous drainage from the
affected vascular domain. Owing to the
rigid channeling of cerebral venous passages
by dura mater and cranial bones, it is in
the cranial cavity that critical degrees of
compartmentalization of venous excess
pressures to particular cerebral venous
territories preferably occur.
COMPARTMENTALIZATION OF VENOUS
REFLUX
Tending to arise during even short-lived
vein compression, reflux works through
intermittent, at times turbulent, back and
forth flow. It washes out its passages, strains
corpuscular vein content and - dependent on
channeling, speed and massivity - eventually
affects the venous periphery.
Peripheral impacts will be harder and tighter,
the more the veins involved in venous reflux
are engorged. Crucial importance is thereby
attained not by the duration or even the
volume, but by the peak value in the speed of
venous reflux.
A vascular compartment affected by venous
reflux accordingly has its source domain,
connecting domain and target domain, each
marked by different venous flow behaviors.
Apart from transcranial doppler observations
of exspiratory venous reflux, the findings
of CCSVI tell little about flow behavior in
a cerebral or spinal venous reflux‘ source,
connecting domain or target domain. Eventual
damaging of cerebral or spinal venous
structures can be identified either at post
mortem or, in vivo, on MRI.
Cerebral angiography, 3D CCT and MRV
present development potential for mapping out
pathways of venous reflux. The structure of, and
short-term flow behavior in, a venous reflux’
source and connecting domain can be traced
in some detail by IVUS, MR flow mapping and
conventional phlebography.
SOURCE DOMAIN: THE WAYS IN WHICH
VENOUS REFLUX EMERGES
Without at least some transient block in
normal flow direction, abrupt vein compression
displaces blood chiefly towards the heart.
Peripheral vein pressure is hardly ever
substantially raised. The more pronounced
a venous stenosis, the more it is apt to boost
peripheral reflux.
Any segment of a main venous pathway
related to brain and spinal canal, by its
being obstructed heartwards and then
compressed headwards, may become a
source of venous reflux. With incompetent
IJV valves, intracranial reflux may start in a
brachiocephalic and superior cava vein, right
atrium, in an incompetent tricuspid valve in the
heart, or else as far down as the inferior cava
vein.
Higher up, any kind of IJV or deep cervical vein
obstruction is liable to turn such a vein into a
source of brainwards directed reflux.
Reflux into the spinal canal tends to emerge,
especially in the abdomen, during compression
of engorged prevertebral collecting veins.
For such a reflux to gain critical momentum,