OUTFLOW
IV
The Optic Disc
The blood circulates through the eye in flaccid vessels
as through a pressurized sphere. Where the intravascular
pressure is less than the intraocular pressure, the blood
vessels are collapsed. Where the intravascular pressure is
greater than the intraocular pressure, the blood vessels are
distended. Stresses within the vessel walls are
proportionate to the difference between the extravascular
and intravascular pressures. These stresses, depending on
their direction, may collapse a vessel or dilate it. They
may also, less obviously, lengthen the vessel and under some
circumstances bring about its concomitant constriction.
One often observes an increase in the ratio of the
width of the retinal veins to that of the arteries. Such
apparent widening of the veins may be a consequence of
engorgement and distention, as when outflow is obstructed by
venous thrombosis. Apparent widening of the veins may,
however, also result from arterial insufficiency, when
inadequate filling of the veins results in their partial
collapse. The recognition that with impairment of the
circulation the veins in the retina may collapse also
provides an explanation for arteriovenous nicking. At the
a-v crossing, the rigidity of the overlying artery prevents
tangentially oriented collapse of the vein. Instead there
may be radially oriented collapse as the vein passes under
the artery, presenting the profile of the lesser diameter of
the elliptical cross section of the vein to the observer and
giving the appearance of a localized constriction.
The walls of the retinal vessels, be they arteries,
capillaries, or veins, are subjected to stresses
proportional to the difference between the intravascular and
intraocular pressures. Intuitively it is immediately
apparent that if the intravascular pressure is greater than
the extravascular pressure, the diameter of the vessel will
tend to expand. What is not so readily apparent is that
increased intravascular pressure may bring about not only
dilation but also elongation of the vessel, which, if its
ends are tethered, will become tortuous. Furthermore, if
the elastic modulus, i.e. the resistance to circumferential
expansion is disproportionately high, then the stretching of
the vessel may actually produce circumferential contraction
of its walls and narrowing of its lumen.
We distinguish deformations that are promptly
reversible upon removal of the inducing stress from
deformations that persist long after the stress has been
removed. For example, when digital pressure on the globe
causes the collapse of a segment of vein on the optic disc,
the deformation is reversible, because as soon as the finger
is removed, the intraocular pressure falls to its prior
value; the collapsed vein again fills with blood and
recovers its prior shape. Here we need only look to the
balance of forces exerted by the intravascular and
extravascular pressures for an explanation of the phenomenon
that we see. On the other hand, the tortuosity of an artery
or vein that has been subjected to increased intraluminal
pressure is reversed very slowly if at all when the
intravascular pressure is reduced or the extravascular
pressure increased. In this instance we may not attribute
the morphologic changes that we see solely to the elastic
characteristics of the tissue. Nonetheless it is axiomatic
that the pressure induced stress does produce some
deformation, however small, and we may ask whether such
small deformation, if it persists day after day and week
after week, might not suffice to determine a pattern of
tissue growth that ultimately produces the observed
configuration. We do not know what effects protracted
mechanical stress will have on the structural development of
tissue. For the time being, we note the similarity between
the deformation expected if the tissue were elastic, and the
observed non-elastic change, whatever its nature may be.
FIGURE 1 - Schematic representation of retinal vein leaving
the eye at the optic disc. At point 1U and 1L, the vein is
distended because intravenous pressure exceeds intraocular
pressure. The external (intraocular) pressure does not
express the contents of the vein at these points because of
the downstream resistance at points 2U and 2L. The
intraocular pressure does express the contents of the vein
at point 2U and 2L, because the pressure within the optic
nerve (point 3) is very low. As the intraocular pressure
expresses the contents of the vein, its cross-section
becomes smaller and the resistance to flow becomes greater.
From the circumstance that the length of segment 2U is
greater than 2L, one infers that either the flow through 2U
is less or that it is less tightly compressed than 2L,
giving it a lower resistance per unit length, since the
pressure gradient across 2U must be the same as the pressure
gradient across 2L. If intraocular pressure increases,
resistance to flow increases because the vein becomes more
tightly compressed or because the collapsed segment becomes
longer, or both. If intraocular pressure decreases, the
converse is the case. Thus the collapse of the vein creates
in effect a self-adjusting pressure reducing valve.
On the surface of the disc we observe the dynamics of
venous outflow from the retina. We cannot, to be sure,
measure the intravenous pressure directly, but we are in a
position to make reliable inferences about it. In the first
place, we know that since the venous wall is flaccid, the
intravenous pressure of the distended vein within the globe
must be no less than the intraocular pressure of which we
can make reliable measurements. In the second place, we
know that in the cavernous sinus at the base of the brain
the venous pressure is negligible, and may, when the patient
is upright, even be negative. The venous pressure in the
optic nerve immediately posterior to the lamina cribrosa is
likely to be almost as low. On the optic disc, therefore,
there is within a fraction of a millimeter a precipitous
drop in pressure, from the 12 or 15 or 20 or 25 mm. Hg. or
whatever the intraocular pressure happens to be, to a very
low value, perhaps five or three mm Hg. The drop in
pressure is associated with correspondingly large resistance
to flow. Resistance is defined as the quotient of pressure
difference divided by flow. Given a constant volume of flow
per unit time, the large pressure difference indicates a
proportionately large resistance.
The mechanism by which flow resistance on the disc is
increased can be readily seen. With the ophthalmoscope, one
can observe that on the optic disc the increase in
resistance to flow is brought about by the pressure induced
collapse of the retinal veins. The vein collapses, of
course, from a disparity between intravascular and
extravascular, i.e. intraocular pressures. The
intravascular pressure is low because of a lack of down-
stream resistance. There is literally nothing, no
resistance, no friction, no back pressure, to prevent the
blood in the retinal vein from draining freely into the
veins behind the globe. That is why on the disc there
collapses a segment of vein sufficient in length to
establish a channel of high resistance to flow which will in
effect maintain the intravascular pressures within the eye
at above intraocular pressure. It is this resistance which
holds back, as it were, the contents of the venous bed in
the retina, and prevents its being expressed by the
intraocular pressure. Since the volume flow per unit time
remains the same, the velocity of flow will increase as the
cross section of the vein becomes smaller.
It is instructive now to observe, how this collapsed
segment of vein which serves as a reducing valve, responds
to changes in the various forces to which it is subject. By
lightly placing a finger over the lateral rectus muscle and
making pressure on the sclera, one may increase the
intraocular pressure, and simultaneously looking through the
ophthalmoscope one notes that the segment of collapsed vein
becomes longer, up to a point, beyond which additional
pressure will cause no further extension of the collapse of
the vessel. In other eyes even the initial increase of
intraocular pressure brings about no change in the length of
the compressed vein. In all eyes, as intraocular pressure
increases, so does the resistance to venous drainage. This
increase in venous outflow resistance comes about by two
mechanisms which act independently or in combination: 1. As
the flattened vein is yet further compressed, its cross-
section may become even smaller. 2. Segments of hitherto
distended vein may collapse, thereby increasing the overall
extent of flattened vein.
An analogous phenomenon may be observed in those eyes
which have spontaneous pulsation of veins on the disc.
There the fluctuation in the length of the collapsed segment
is caused by pulsations in the intraocular pressure. It is
the arterial pulse of the choroid which propagates through
the aqueous and vitreous, contained within the relatively
inelastic sclera, inducing small periodic fluctuation of
intraocular pressure. This in turn changes venous dynamics
in just the manner we have described and produces
spontaneous pulsation of the retinal veins.
FIGURE 2 - Venous drainage on the glaucomatous optic disc.
The upper and lower poles of the disc drain into more peripheral
segments of retinal vein at 1U and 1L. These peripheral segments
are distended with blood whose pressure is at or above the
intraocular pressure. As the intraocular pressure rises, so
does the pressure at 1U and 1L. On the other hand, venous
drainage of the temporal and nasal poles, 1T and 1N, is into
segments of retinal vein (2U and 2L), which are already
collapsed by intraocular pressure. The venous pressure at
2U and 2L is substantially lower than intraocular pressure.
Perhaps even more important, the venous collapse at 2U and
2L insulates this segment of vein and its tributaries from
increases in intraocular pressure. The estimates of venous
pressure assume an intraocular tension of 30 mm Hg. The
highest venous pressures are expected in those areas of the
disc that are must susceptible to glaucomatous damage. In
the areas most resistant to glaucomatous damage, venous
pressure remains low inspite of elevation of intraocular
tension. Consider also the effects on the length of
collapsed vein of variations of retinal arterial flow. When
flow through the vein increases, there is some small
diminution in the length of the collapsed vein at its distal
end. Conversely, as is often the case, when, as from
arteriosclerotic obstruction of the feeding vessels, there
is a diminution of flow, the length of collapsed vein
increased. This relationship becomes obvious from purely
algebraic considerations, inasmuch as the pressure gradient
is the product of flow times resistance. If the pressure
gradient is to remain the same, then when the flow per
minute decreases, the resistance must increase. The
resistance will increase either as a result of more complete
or of more extensive collapse. Whether the change in
resistance comes about as the result of more complete or
more extensive collapse will be a function of the elastic
properties of the vein. The less pliable, the more
sclerotic the vein, the longer will be the segment required
to bring about the requisite pressure gradient for any given
amount of flow. Similarly, the lower the minute volume of
flow, the longer will be the segment required to account for
any given pressure gradient. We observe that when the flow
diminishes beyond a point that is critical for any given
value of wall stiffness, the reduction in pressure will no
longer remain localized. The pressure will then be reduced
in the entire venous tree. All the large veins of the
fundus will then flatten, and their visible profiles will
broaden as described in the preceding issue of the Glaucoma
Letter.
These observations in physiology, in addition to their
explanatory value for a-v nicking and the increased v/a
ratio commonly seen in obstructive retinal vascular disease
of all kinds, will also shed some light on the possible
etiology of glaucomatous disc damage. Observation with the
ophthalmoscope, readily confirmed with fluorescein
angiography, reveals that the temporal and nasal poles of
the disc, those areas in other words subserving the macula
and the temporal field which are most resistant to
glaucomatous damage, have a venous drainage through small
horizontally coursing veins which enter the central retinal
vein near the center of the disc in the proximity of the
lamina cribrosa. The central vein in this area is almost
always collapsed and the pressure within it is substantially
lower than the intraocular pressure. Equally important is
the circumstance that when the intraocular pressure rises,
the venous pressure in this central segment of vein is
unaffected. It is different with the venous drainage from
the upper and lower poles of the optic disc. There drainage
feeds into the superior and inferior retinal veins at or
near the disc margin, where the retinal veins are distended
with blood at or above the intraocular pressure. Therefore
venous drainage from the upper and lower poles of the disc
which show the greatest sensitivity to glaucomatous damage,
occurs into a segment of vein at or slightly above the
intraocular pressure. Occasionally, when intraocular
pressure rises, the distended segment of vein into which
drainage takes place collapses with a resulting fall in
intravenous pressure. More commonly such collapse does not
occur, and the venous pressure against which the upper and
lower poles must drain, at minimum equals the intraocular
tension. At least as important, when the intraocular
pressure rises, unless, as is usually not the case, the area
of collapse extends to this region, the pressure against
which the capillary drainage from the upper and lower poles
of the disc must contend, increases with the intraocular
pressure.
Consider then what might happen to the venous
circulation on the disc as the intraocular pressure is
increased. The venous drainage from the temporal and nasal
portions of the disc remains unaffected, inasmuch as it
flows into a segment of retinal vein which is collapsed, and
therefore under lower pressure, and insulated from any
increase in intraocular tension. The venous drainage, on
the other hand, from the upper and lower poles of the disc
flows into branches of the retinal vein which are not
usually collapsed either at normal or at elevated
intraocular pressures. This fact means that the venous
pressure in these segments is equal to or slightly higher
than the prevailing intraocular pressure and, more
importantly, that as intraocular pressure rises, the
pressure in this segment of vein rises with it. At the
upper and lower poles of the disc, as distinct from the
temporal and nasal poles, the veins act like funnels which
serve to conduct increases of intraocular pressure into the
disc substance. It may not be coincidence that those areas
of the disc most susceptible to atrophy and excavation from
elevated intraocular pressure are the same areas in which
elevated intraocular pressure induces increased venous
pressure. It may also not be coincidence that the small
splinter hemorrhages which are sometimes seen on the disc
margin in open angle glaucoma are not unlike hemorrhages
seen with venous obstruction elsewhere in the fundus.
One may make these observations without presuming to
have discovered the "cause" of glaucomatous disc damage.
The term "cause" is ambiguous, a trap which it is better to
avoid. It is likely that several factors contribute to the
glaucomatous destruction of the optic disc, and impairment
of venous drainage may be one of them.
* * * * *
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Copyright 2006, Ernst Jochen Meyer