Lens-induced glaucoma in the elderly
Clinical Interventions in Aging
Lens-induced glaucoma in the elderly
0 Department of Ophthalmology, University of Athens , Athens , Greece
Lens-induced glaucoma comprises a number of different glaucomatous processes occurring in the elderly that share in common the role of the crystalline lens in the mechanism of increase in intraocular pressure. We will review the anatomic predisposing factors, their physiology, signs and symptoms, and therapeutic approach. We will consider two studies and discuss the visual results and risk factors associated with these pathologic conditions.
with the trabecular meshwork and lead to angle-closure
glaucoma. This mechanism is facilitated by the anatomic
predisposing factors that were mentioned previously.
A senile cataractous lens that has progressed enough to
become intumescent, has an increased anteroposterior length,
which could lead to pupillary block. This type of glaucoma
is named phacomorphic (Figure 1).
18 Phacomorphic glaucoma often occurs from a mature
l-u20 cataract, but may also occur from spherophakia in
-J2 Weill–Marchesani syndrome. Phacomorphic glaucoma
1no could present asymptomatically as chronic angle-closure
.121 glaucoma, however it more often presents as acute
angle.59 closure glaucoma. Acute angle-closure glaucoma will cause a
.323 significant increase in IOP, which is characterized by ocular
y12 pain, headache, blurred vision, perception of halos around
/bm lights (due to the corneal edema), and also nausea, vomiting,
.cso bradycardia, and diaphoresis due to the vasovagal response.
se Symptoms usually occur at night because mid-dilation
.rvdoepww ll.syeuon predisposes relative pupillary block.
The clinical examination reveals reduced visual
/w an acuity secondary to corneal edema, conjuctival injection,
ttph rspe a mid-dilated pupil, and, in the case of phacomorphic
from roF glaucoma, an intumescent cataractous lens which pushes the
de iris forward and reduces the depth of the anterior chamber
loda peripherally. The latter also shows cells and flare. The
now fellow eye shows the same anatomic predisposing factors
ndg and probably a cataract (phacomorphic).10
igA Treatment focuses on two objectives: lower the IOP as
isn soon as possible and prevent the diseased and fellow eye
itnno from another episode.11
agents (mannitol IV) are the mainstay of medical treatment.
Parasympathomimetic agents (pilocarpine 1% or 2%) tend
to increase pupillary block, so they should be used with
caution.12 When this approach fails to lower IOP, then
some other methods can be recruited: corneal depression
with a Zeiss 4-mirror lens, iridectomy with the Nd:YAG
laser, gonioplasty with an argon laser, coreoplasty with
an argon laser, and application of digital massage.11,13,14
If the fellow eye is also anatomically predisposed to
angleclosure glaucoma, prophylactic laser iridotomy should be
In the case of phacomorphic glaucoma, after IOP control
and establishing intraocular inflammation, we proceed to
cataract extraction, which erases the major causative factor
of angle-closure glaucoma.
This clinical entity may present as an isolated inherited form
such as ectopia lentis and ectopia lentis et pupillae. Ectopia
lentis may also be associated with systemic disorders such
as Marfan’s syndrome, homocystinuria, Weill–Marchesani
syndrome, hyperlysinemia, and sulfite oxidase deficiency.
The biochemical defects in these conditions result in
defective zonular apparatus and subluxation/dislocation of
the lens often occurs (Figures 2, 3).
Dislocation of the crystalline lens may be secondary to
Symptoms vary according to the individual state of the
lens. Minimal subluxation may be asymptomatic. Progressive
disruption of the zonules allows the lens to assume a more
spherical shape, which results in increasing degrees of
myopia. If the lens is shifted within the pupillary axis, then
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monocular diplopia may ensue. The loss of zonular support
results in difficulties with accommodation and near vision.
Complete dislocation from the pupillary axis renders the
patient hyperopic because of an aphakic optical condition.
When dislocation results in pupillary block and angle-closure
glaucoma is present, the patient experiences a red and painful
eye, decreased visual acuity, and sometimes headache,
nausea, and vomiting.
Signs include phacodonesis, iridodonesis, shallowing of
the anterior chamber either symmetrically or asymmetrically,
and a difference in the depth of the anterior chamber between
the two eyes. Gonioscopically, the iris may be seen to assume
the shape of a volcano with the pupil forming the central
crater. This is the result of the anterior movement of the lens
and increased contact with the middle third of the iris.
The therapeutic approach depends on the degree
of dislocation and the symptoms. In cases of partial
subluxation within the pupillary space that does not
cause significant visual impairment or pupillary block
glaucoma, a conservative nonintervention strategy could
be followed. When the previous condition is accompanied
by pupillary block, then a laser peripheral iridectomy
is the appropriate solution. Total anterior dislocation
requires removal of the lens. Dislocation in the vitreous
cavity may be followed carefully as long as the cataract
is not hypermature and no inflammation or glaucoma is
noticed. If any of these factors are present, removal of
the lens is indicated.
Ciliary block (malignant) glaucoma sometimes may
be confused with phacomorphic glaucoma in cases where
the anterior chamber is too shallow. However, malignant
glaucoma in its classic form occurs after surgery for
glaucoma and is characterized by the misdirection of aqueous
fluid into the vitreous cavity.16–31
This acute open-angle glaucoma is the result of the leakage
of lenticular material from senile hypermature or Morgagnian
cataract through an intact lens capsule (Figure 4). The
presentation is a red and painful eye, history of gradual decline
of visual acuity reflecting the slow maturation of the cataract,
corneal edema, high IOP, an open–angle in gonioscopy,
a heavy flare, and aqueous cells larger than the lymphocytes
seen in uveitis. These cells are thought to be macrophages
swollen with eosinophilic lenticular material which they
have engulfed.32 Soft white patches on the lens capsule can
be observed, which are aggregates of macrophages trying to
seal the site of leakage.33 The fellow eye usually has a mature
cataract and a deep anterior chamber.
The original theory about the pathogenesis of this
condition was that the macrophages were the major culprit
of increase in IOP by blocking the trabecular meshwork.33,34
Later research by Epstein and colleagues,35 Yanoff and
Scheie,32 and Dueker36 emphasized the role of heavy
molecular proteins (HMW) leaking from the lens in the
obstruction of the aqueous outflow and de-emphasized the
role of the macrophages. As a consequence, the examination
of the anterior chamber fluid for the presence of HMW
protein has become an important diagnostic aid in suspected
and atypical cases of phacolytic glaucoma, but is not yet
The majority of patients with phacolytic glaucoma can be
managed through topical cycloplegia, topical steroids, and
aqueous suppressants. If despite intensive antiglaucomatous
therapy, IOP continues to increase, emergency admission
may be advocated, and in rare instances urgent cataract or
vitreoretinal surgery may be required.37–41
In contrast to phacolytic glaucoma, this form of lens-induced
glaucoma is associated with a grossly disrupted capsule and
the presence of obvious fragments of lens material in the
anterior chamber. It may occur after cataract surgery, trauma
to the lens, or Nd:YAG posterior capsulotomy. The IOP
increase is due to the obstruction of the aqueous outflow by
the lens particles.32 Despite the presence of macrophages as
scavengers of the lens material, their role in the pathogenesis
of the glaucoma is not significant.
Initially, a trial of medical antiglaucomatous therapy
may be attempted, but miotics should be avoided. Mild to
moderate steroid therapy can help to prevent synechiae,
.rvdoepww ll.syeuon pgluapuiclloamrya misesmebvrearneeasn,dc/yosrt othideremiascualalarrgedeeammao, uenttc.oIfflethnes
/:/sw noa material in the anterior chamber, its surgical removal should
h pe be undertaken.
Phacoanaphylactic glaucoma is an inflammatory reaction
directed against lenticular antigens with elevation of the
IOP due to involvement of the trabecular meshwork by the
inflammation or by obstruction from inflammatory cells.
A less usual mechanism is the formation of synechiae
resulting in pupillary block.
The series of events leading to the IOP rise is as follows:
the patient is sensitized to his own lens antigens and these
proteins are kept in an immunologically privileged site
within the lens capsule. After an eye surgery or other trauma
to the lens capsule, these lens antigens are exposed to the
circulation, they may be recognized as ‘foreign’ by the
individual’s immune system and they incite an inflammatory
response. A matter not completely elucidated is why some
patients develop this reaction and others do not.
The time interval between the trauma and the onset
of inflammation is 24 hours to 14 days. The clinical signs
include lid edema, chemosis, conjuctival injection, corneal
edema, heavy anterior chamber reaction, posterior synechiae,
and mutton fat keratic precipitates.
Pathologically, a granulomatous reaction is noted with
polymorphonuclear, epithelioid, and giant cells surrounding
lenticular material. Phacoanaphylaxis is not the correct name of
this condition since it is not an allergy. Eosinophils may be found
but not immunoglobulin E (IgE). The mechanism causing the
reaction seems to be an Arthus-type immune complex reaction
mediated by IgG and the complement system.42,43 In the past,
the differentiation between phacoanaphylaxis and sympathetic
ophthalmia was confusing, but once it is understood that the
former involves only the anterior segment of the eye, the
diagnosis is easy.44,45
The first step in therapy is the effort to control the IOP
and inflammation medically. If this proves unsuccessful
then the next phase is surgical removal of the remaining
Epidemiology: prognostic factors
There are two studies from the Indian Journal of
Ophthalmology that investigate lens-induced glaucomas, more
specifically phacomorphic and phacolytic glaucomas.
The first study47 deals with the clinical modes of
presentation, the postoperative visual results, and the risk
factors that relate to the visual outcome of such cases. The
percentage of phacomorphic glaucomas (52.7%) is slightly
higher than phacolytic (47.3%) and the latter is more common
with increasing age probably due to aggregation of high
molecular weight proteins in the crystalline lens over time.
After surgical management with extracapsular cataract
extraction, 57% of phacomorphic and 61% of phacolytic
cases had good visual acuity (6/12 or better) and 10.2% of
phacomorphic and 13.6% of phacolytic cases had poor visual
recovery (6/60 or less). The conclusion in this study was that
there was no statistically significant difference between the
two groups on the final postoperative visual recovery. When
they investigated the risk factors they found a statistically
marginally significant increased risk (p = 0.05) of females
having these glaucomas. Also, males had a slightly higher
risk of obtaining poor postoperative visual acuity (odds
ratio [OR] = 2.2; 95% confidence interval [CI]: 0.88–5.66),
but this statement has to be analyzed with caution, because
the mean age of males was higher than the females and age
may be a confounding factor. A significant risk of poor
visual acuity was found when the duration between the onset
of pain and surgery exceeded five days (OR = 3.1; 95%
CI: 1.21–8.13). Marginally significant risk of poor visual
outcome was observed in cases of age higher than 60 years
when compared with younger patients. Finally, between
the level of preoperative IOP and final visual acuity, no
significant association was found (p = 0.07).
The second study48 dealt with the frequency and types
of lens-induced glaucoma, the reasons for late presentation,
and the outcome of current management. The percentage of
phacomorphic glaucomas was higher in this study (72%) than
the phacolytic (28%). A similar result occurred in relation
to gender since the ratio of females:males was 1.7:1. The
comparison between the two studies is difficult when we
look at the visual results because the groups are different.
In the latter study, 38.6% achieved a visual acuity of 6/60 or
better, 31.2% less than 6/60, and 30.2% less than 3/60. In the
phacolytic group, 65.9% had a poor outcome compared with
59.8% of the phacomorphic group. This poor outcome was
associated in the latter group with a longer distance from the
hospital, longer duration of pain, and higher IOP at
presentation. In the phacolytic group, only the distance was found to
influence negatively the visual outcome. In this series, the
final visual outcome is worse than in other studies, probably
because the majority of the patients reported later than ten
days after the onset of pain.
In conclusion, lens-induced glaucoma comprises a
number of different glaucomatous processes occurring in
the elderly that share in common the role of the crystalline
lens in the mechanism of increase in IOP. Early diagnosis
and treatment of mature cataract is very important since
delayed treatment of lens-induced glaucoma may result in
poor visual outcome.
The authors report no conflicts of interest in this work.
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Clinical Interventions in Aging is an international, peer-reviewed
journal focusing on evidence-based reports on the value or lack thereof
of treatments intended to prevent or delay the onset of maladaptive
correlates of aging in human beings. This journal is indexed on PubMed
Central, MedLine, the American Chemical Society’s ‘Chemical
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