 
                     Angle Closure Glaucoma

                               III

                            Treatment

     Unlike our aim in treating open angle glaucoma, which is
solely to achieve permanent control of intraocular pressure at
such levels as will prevent destruction of nerve fibers at the
optic disc, our concerns in the treatment of angle closure are
more complex.  Not only do we seek to protect the integrity of
the optic nerve, but we wish also to prevent the meshwork and the
angle from being damaged by chronic closure, which if allowed to
persist, may cause permanent structural damage with consequent
intractable tension elevation.  Perhaps most important, we wish
to protect these and all other intraocular structures from the
ravages of an acute attack, which can severely damage not only
the meshwork and the angle, but the cornea, the lens, the iris,
the macula, and the optic nerve as well.  It is seldom possible
to predict with certainty what permanent effects angle closure
will have on the integrity of the angle and of the meshwork.
Other factors being equal, the higher the pressure, the greater
the inflammation, and the longer the duration of closure, the
more likely that the angle will be permanently damaged.  Thus,
even when the tension poses no immediate risk to the disc, angle
closure glaucoma requires treatment because of the likelihood
that without early therapy, irreversible damage to the angle will
supervene.  In later stages of the disease, when everything pos-
sible has been done to open the angle, treatment is reoriented
toward preserving the disc and the visual field and then becomes
very similar to the treatment for open angle glaucoma.

     The threshold question with regard to therapy of angle clo-
sure glaucoma is whether, at any given time, treatment should be
begun.  This issue must be construed broadly enough to include
the possibility that therapy should be postponed, in some in-
stances indefinitely, which amounts to saying that in some in-
stances there should be no treatment at all.  It is erroneous to
assume that every disease should be treated as soon as it is dis-
covered.  Sometimes the best treatment is to wait and to do noth-
ing.  The patient may not understand.  "Do I have glaucoma or
don't I?" he asks, thereby implicitly translating the unpre-
dictable issue of pathophysiology into a question of nomencla-
ture.  If I have glaucoma, he reasons, it should be treated, and
if what I have doesn't need treatment, it can't be as serious as
glaucoma.  In response to this argument, the ophthalmologist is
tempted to coin a new term to designate the disease before it re-
quires treatment and to use a different name for the later stage
when it does.  Such conceptual manipulation may satisfy the pa-
tient's desire for certainty, but it adds nothing to the physi-
cian's understanding of the disease.  Indeed, the postulate that
there are two distinct diseases is misleading when one cannot
identify them in practice.  The determination whether the patient
has "only" narrow angles or whether he has actual angle closure
glaucoma, is identical with the decision whether or not the angle
closure glaucoma, construed more broadly, now requires treatment.
What is important to understand is that angle closure glaucoma,
like many another disease, passes imperceptibly from a stage in
which treatment would be premature to a stage where treatment is
imperative.  There are many threatening situations where the best
move is to do nothing.  In those circumstances, the physician's
duty is to stand by, to observe, himself to accept the uncertain-
ty and to make it acceptable to the patient.  Because of the the
progression of the disease is unpredictable, the physician will,
in retrospect, sometimes be blamed for having initiated treatment
either too early or too late.

     In the case of chronic angle closure glaucoma, there is a
period of time during which the disease is developing, and the
uncertainty whether it will ever cause the patient any problem is
so great that the diseconomies of treatment clearly outweigh its
potential benefits.  There is a second stage during which the ev-
idence is equivocal and the decision to treat or not to treat is
discretionary with the physician.  In a third stage where angle
closure is the obvious cause of increased intraocular pressure,
prompt treatment is imperative and delay would threaten sight it-
self.  It is true that with diligence the uncertainty of when to
begin treatment of early chronic angle closure glaucoma can be
reduced, but it can surely not be eliminated entirely.  The need
to do something about *acute* angle closure glaucoma, on the oth-
er hand, is never in doubt, provided the eye retains the capacity
for useful vision.  Once a protracted period of time from the on-
set of the attack has elapsed, one has much reason to fear that
treatment will be too late.

     The first task in the treatment of angle closure glaucoma is
to try to reopen those portions of angle that have been closed
and to forestall closure of any additional sectors.  The most ob-
vious means of achieving this goal is suggested by the circum-
stance that dilation of the pupil may in susceptible eyes precip-
itate a disease otherwise indistinguishable from angle closure
glaucoma.  Therefore miotics are sometimes employed to counteract
the effects of mydriatic and cycloplegic drops.  Pilocarpine is
used to constrict the pupil and to try to draw the iris away from
the angle.  For years this was the favored treatment for angle
closure glaucoma and it is on occasion remarkably effective in-
deed.  However, especially in higher concentrations, miotics also
tend to make the anterior chamber more shallow and cause the an-
gle to close.  Three mechanisms that explain this effect immedi-
ately come to mind.  In the first place, stimulation of the cil-
iary muscle tends to displace the lens-iris diaphragm forward.
Secondly miosis tends to enlarge the area of iris lens apposition
and thereby increase the resistance to flow through the pupil.
Such an enhancement of relative pupillary block will push the
iris anterior, shallow the chamber and narrow the angle.  Final-
ly, any reduction in intraocular pressure will, if all other fac-
tors remain equal, in itself cause the lens-iris diaphragm to
move forward.

     The hydrodynamic link between intraocular pressure and ante-
rior chamber depth has been generally overlooked, probably be-
cause it is often masked by other determinants.  Intuitive repre-
sentation of the forces affecting the position of the retina and
choroid tends to ignore the circumstance that the intraocular
pressure is exerted not only radially but also tangentially to
these tissues.  The retina and choroid are tethered to the sclera
at the optic disc; the choroid is bound to sclera by the vortex
veins.  When the intravascular pressures within either retina or
choroid increase, these tissues expand and creep forward.  Con-
versely, since neither retina nor choroid are tethered rigidly to
the anterior sclera, the intraocular pressure, when it rises,
tends to push them backwards.  It follows that if intravascular
pressures remain constant, the lens-iris diaphragm tends to move
forward when intraocular pressure falls, and tends to move back-
ward when intraocular pressure rises.  This hydrodynamic model is
strikingly corroborated when, on occasion, central retinal vein
occlusion causes unilateral angle closure.  Then, when venous
outflow is blocked, capillary and venous pressures rise to the
arteriolar level and the expanding vascular bed pushes the cil-
iary body forward.  Corroboration from a different perspective
must be inferred from observation of the eye at death.  Then, al-
though its pressure vanishes, the anterior chamber nonetheless
remains formed, because the pressures in the choroidal and reti-
nal circulations also drop to zero.

     The effect of miotics on angle closure glaucoma is unpre-
dictable.  The two opposing influences, the widening of the angle
from sphincter contraction and its narrowing from the other ef-
fects of miotics, make their appearance at variable intervals, so
that the same pilocarpine concentration which initially widens
the angle may in the course of time cause it to close.  It be-
hooves one therefore, if one undertakes to treat angle closure
with miotics, to gonioscope the eye before and just after initi-
ating treatment, and to repeat gonioscopy at sufficiently fre-
quent intervals to make certain that the medication does not make
the glaucoma worse.  The foregoing considerations apply also to
the use of miotics to prevent the development of angle closure in
an anatomically narrow angle.  It is certainly the case that many
such angles are dramatically widened by use of pilocarpine, but
it is also true that other angles, which, in the absence of medi-
cation might not have closed at all, are precipitated into clo-
sure by instillation of miotics.

     The width of the angle is also affected by carbonic anhy-
drase inhibitors, presumably because these medications decrease
aqueous secretion.  Administration of such drugs might be expect-
ed to tend to relieve or prevent angle closure, inasmuch as any
decrease in aqueous flow would tend to decrease the partial
pupillary block that pushes the iris forward into the trabecular
meshwork.  Thus oral administration of carbonic anhydrase in-
hibitors by itself is likely to make a significant difference in
the width of the angle.  Carbonic anhydrase inhibitors also deep-
en the anterior chamber in the presence of a patent iridectomy,
but the mechanism of this effect is not apparent.  Their occa-
sionally dramatic effect in relieving angle closure should not
lead one to rely on them for permanent control.  Many patients
become intolerant to these drugs, and even if the medications can
be continued, they occasionally lose their effectiveness.  When
angle closure recurs under such circumstances, one of the most
valuable of temporary therapies has been exhausted.

     The beta adrenergic blocking agent timolol has a role in the
treatment of angle closure glaucoma similar to that of carbonic
anhydrase inhibitors.  Timolol resembles them in that it also
tends to widen the angle, presumably by inhibiting aqueous secre-
tion.  Topical epinephrine, on the other hand, which is thought
to lower intraocular pressure by a similar mechanism, is consid-
ered inadvisable in the treatment of angle closure glaucoma be-
cause the risk of the mydriasis which it causes is assumed to
outweigh any benefits of aqueous suppression that it might bring
about.  The circumstance that both of these drugs very likely af-
fect the tonus and therefore the pressure within the choroidal
vascular beds is usually overlooked.  Atropine and atropine-like
agents, as is well-known, dilate the pupil, push the iris against
the meshwork, and often precipitate angle closure.  However,
these drugs also retract the lens-iris diaphragm.  They tend to
deepen the anterior chamber, and sometimes, paradoxically, in
eyes with malignant glaucoma, they are the only pharmacological
tools at the physician's disposal for opening the angle.

     Three drugs which transiently increase the osmolarity of the
blood, mannitol intravenously, glycerol and sorbitol by mouth,
have limited but very specific value in the treatment of angle
closure glaucoma.  For an hour or two after they are adminis-
tered, they lower the intraocular pressure by creating an osmotic
gradient between the intraocular and the intravascular fluids,
transfering water from the former into the latter compartments.
The transient lowering of intraocular pressure, by reestablishing
the sensitivity of the iris sphincter to parasympathomimetic
stimuli or perhaps by other as yet unrecognized mechanisms, some-
times breaks the cycle of positive feedback that has precipitated
an attack of glaucoma.  The administration of osmotic agents may
be repeated, but many patients tolerate them poorly, and there is
some danger in patients with cardiac disease, of producing acute
heart failure, and in patients with impaired renal function, se-
vere electrolyte imbalance.  Osmotic agents at best are temporary
expedients in helping to abort an attack of angle closure glauco-
ma; the patient should be in the operating room before their ef-
fect has worn off.

     Notwithstanding the availability of medication that may open
the angle and reduce the tension in angle closure, the basic
treatment of this disease is surgical, the mechanical establish-
ment of a pupillary bypass.  This is the case because relative
pupillary block is usually the decisive factor in precipitating
angle closure, and pupillary block can be relieved definitively
only by making a passage peripheral to the pupil through which
aqueous may flow into the anterior chamber.  Under these circum-
stances it appears unwise to accept the uncertainties of pharma-
cological treatment.

     When the mechanism of pupillary block was first discovered,
the pupillary bypass operation was commonly attempted by punctur-
ing the iris with a needle-knife introduced into the anterior
chamber.  Because of the proximity of the iris to the anterior
lens capsule, lens injury was a not infrequent complication.  It
was also observed that the pin-point opening made with the nee-
dle-knife often closed, and that pupillary block then recurred.
For these reasons, iridotomy was abandoned in favor peripheral
iridectomy, and for some decades this remained the standard
treatment for angle closure glaucoma.  The clear disadvantage of
peripheral iridectomy is that it is an intraocular operation
which requires opening of the anterior chamber, thus entailing
the unavoidable risks of infection, hemorrhage, and wound leak-
age.  The argon laser became available to a generation of oph-
thalmologists who had no experience with iridotomy and were unim-
pressed by the limitations of this procedure.  It is not surpris-
ing, therefore, that to their minds the value of being able to
perforate the iris without opening the eye far outweighs the dis-
advantages of a pinpoint iris lesion which not infrequently clos-
es.

     Thus surgical peripheralridectomy has largely been replaced,
at least for the time being, by laser iridotomy.  The uncritical
enthusiasm with which the argon laser "operation" was accepted by
the ophthalmologist is a reflection largely of his frustration
and anxiety with the established intra-ocular procedure.  The
laser, this miracle weapon for inner and outer space, lavishly
promoted by its manufacturer, attractively styled to enhance the
decor of the physician's office, promises to circumvent the dif-
ficulties posed by conventional diagnosis and treatment.  The
purported ease and safety of its use seem to decrease the re-
quirements of conclusive diagnosis.  Where it appears so simple
to burn a pinpoint perforation through the iris, one is inclined,
I think unwisely, to dispense with the darkroom test and proceed
with the laser surgery.

     The eagerness with which laser iridotomy has been accepted
becomes plausible when one reconstructs the perplexity that con-
fronted the ophthalmologist who was required to intervene with
surgery for an asymptomatic disease which manifested itself only
with an occasional fleeting elevation of tension, and to do so by
means of an operation, iridectomy, which, no matter how meticu-
lously performed, entailed the risk, albeit small, of complica-
tions that could lead to loss of the eye.  It is true that as the
experience of the profession with peripheral iridectomy in-
creased, its complications became less frequent and less devas-
tating, but it remained nonetheless a formidable task for an oph-
thalmolgist to advise a patient who had had no symptoms, whose
vision was 2020, and whose only evidence of glaucoa was a tran-
sient tension elevatio, that the risk of intraocular surgey to
both eyes was less that the risk of medical treatment or of no
tatment at all.

     The cost-benefit tio of peripheral iridectomy was a fnction
at one and the same time of the accuracy of diagnosis and of the
complication rate of surgery.  If oneeserved peripheral iridecto-
myfor those patients who had unequivocally positive darkroom
tests or tension elevation in the presence of unmistakable angle
closure, and if one then performed the operation without intro-
ducing instruments into the anterior chamber and without losing a
sufficient amount of aqueous to require its reformation, then the
cost benefit ratio was favorable indeed and a large proportion of
patients subjected to it were literally cured of their glaucoma.

     The risks of iridectomy is least in the patient who has a
reactive pupil and whose glaucoma is incipient  or  has  been
temporarily relieved with medication.  It is useful to premedi-
cate the eye to be operated on with one drop of pilocarpine 2%
about one hour prior to surgery, then under retrobulbar anesthe-
sia, to make a 5 mm peritomy at the limbus.  One opens the ante-
rior chamber with an ab externo incision near the limbus, just
anterior to the projected root of the iris.  Before one enters
the anterior chamber, a single suture of 8-0 vicryl is preplaced.
The incision, necessarily somewhat longer on the scleral surface,
has the shape of a triangle whose apex is at Descemets membrane.
As soon as iris, or a drop of aqueous appears in the wound, the
incision is complete.  Gentle indentation of the posterior lip of
the wound will now cause the iris to prolapse sufficiently that
it may be grasped with .12 mm toothed forceps.  A small segment
of tissue is excised.  Since pupillary block has now been re-
lieved, further stroking of the edges of the wound will tend to
free the iris, and the miotic pupil will pull it into the anteri-
or chamber.  In many instances the amount of aqueous lost is so
small that no shallowing of the chamber is apparent.  The ends of
the preplaced suture are threaded through the conjunctiva before
the knot is laid down.  Two days later the visual acuity will
usually have returned to its pre-operative value.



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Copyright 2006, Ernst Jochen Meyer
