 
                                 OUTFLOW

                                   VII

                         The Aqueous Circulation

            The aqueous humor is thought to be secreted by the
       epithelium of the ciliary body.  That this may not be the
       only structure from which aqueous originates was suggested
       to me some years ago when I took care of a patient who had
       sustained blunt trauma to the globe of his right eye.  When
       one looked at the eye with the slit lamp, one saw what
       appeared to be lens and iris lying under the nasal
       conjunctiva.  The anterior chamber was deep and clear.  The
       iris and lens were absent.  The vitreous face was intact.
       On indirect ophthalmoscopy with scleral indentation one
       could see a temporal retinal detachment.  Anterior to the
       ora serrata, no ciliary body structures could be identified.
       I inferred, therefore, that the ciliary body had been
       avulsed together with the lens and the iris.  Initially the
       intraocular pressure was normal, but over a period of months
       the tension rose to the high thirties and proved, as a
       matter of fact, rather intractable to treatment.  I
       concluded that in this patient, at least, the retina must
       have contributed significantly to the production of aqueous.

            Whatever its origin, the phenomenon of pupillary block
       leaves no question that the aqueous flows from the posterior
       into the anterior chamber.  On occasion when one makes a
       laser iridotomy, one sees a jet of aqueous come forward
       carrying its particles of pigment.  Particles of pigment or
       cells, whenever they can be identified in the anterior
       chamber aqueous, are seen to rise in the posterior part of
       the chamber and descend near its corneal boundary,
       indicating that the fluid in the chamber is in continuing
       motion.  rising by convection as it is warmed by the iris,
       and similarly falling as it is cooled by the cornea.

            That the aqueous leaves the eye through structures in
       the anterior chamber angle may be inferred from the
       circumstance that in the great majority of eyes where
       gonioscopy shows the anterior angle to be closed, glaucoma
       supervenes, and the pressure rises.  Gonioscopy also
       suggests that a substantial proportion of the outflow occurs
       in an area of the angle just posterior to Schwalbe's line.
       One may infer as much from the observation that angle
       closure does not provoke glaucoma until the anterior half of
       the ring that extends from the scleral spur to Schwalbes
       line is occluded, so that, if one can see scleral spur one
       may say with confidence that the filtering portion of the
       angle is not occluded.  Occasionally when the intraocular
       pressure is low, one sees just anterior to the scleral spur
       a thin reddish band.  This is thought to be blood in
       Schlemm's canal and quickly disappears if one increases the
       intraocular pressure as, for example, by pressing against
       the sclera with ones finger.  On the surface of the globe
       one may on occasion be able to identify the aqueous veins
       that collect the aqueous once it has traversed the sclera in
       the collector channels.  The pressure in the episcleral
       veins is approximately 9 mm Hg which corresponds to the
       pressure at the distal end of the capillary as it is cited
       in standard physiology texts.  Thus the pressure gradient
       across the outflow channels of the eye ranges from two or
       three to perhaps 12 mm Hg, is 6mm, plus or minus 5 mm Hg.
       That is as much as one can observe through the slit lamp and
       with the ophthalmoscope.

            The simple operative maneuvre of paracentesis, where a
       narrow, oblique incision is made through the cornea into the
       anterior chamber with a thin, needle-like knife, serves to
       demonstrate, in the absence of pupillary block, that the
       anterior chamber is under the same pressure as the posterior
       chamber, and serve to demonstrate in the presence of
       pupillary block that the direction of flow is from the
       posterior chamber anterior through the pupil.  Where
       resistance to flow is defined as that characteristic of a
       conduit which limits the flow that may be produced by any
       given pressure.  Algebraically, one stipulates that
       resistance shall equal the pressure divided by the flow.  In
       this equation, then, when pressure is treated as the
       independent variable, an increase in pressure is
       attributable either to an increase in resistance or to an
       increase in flow.  Surely this is the case where the angle
       is grossly occluded as in angle closure and synechial
       glaucoma.  The evidence that open angle glaucoma is also
       attributable to an increase in outflow resistance is almost
       as great.  Hypersecretion glaucoma, if it occurs at all,
       must be very rare.

            What is in this context of greater importance is the
       interpretations of fluctuations in intraocular pressure,
       given the existence of glaucoma.  The traditional
       explanation is that such fluctuations reflect not variations
       in the severity of the glaucoma, i.e., one assumes that the
       resistance to outflow remains constant, but that they
       reflect changes in the amount of aqueous produced.  The
       evidence for this assumption is slight, for one cannot, in
       general, reproduce such pressure fluctuations by giving a
       patient a water load by mouth, concerning which one might
       infer wth some certainty that it enhances the production of
       aqueous.

            The salient issue here is whether or not, or to what
       extent, glaucoma represents a fixed anatomic deformation of
       the outflow channels and to what extent, if any it
       represents an impairment of a control mechanism that
       maintains the resistance to outflow at physiologic levels.
       Before addressing this question, we must take another look
       at the anatomy of thr outflow system, necessarily, through
       the microscope.  The measurement of outflow resistance both
       in the laboratory by perfusion techniques and in the clinic
       by tonography leaves little room for doubt that the cause
       of increased pressure in the vast majority of glaucomas
       results from an increased resistance.


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Copyright 2006, Ernst Jochen Meyer
