LENS-INDUCED (PHACOGENIC) GLAUCOMAS

In this group IOP is raised secondary to some disorder
of the crystalline lens. It includes following subtypes:
1. Phacomorphic glaucoma
Causes. Phacomorphric glaucoma is an acute
secondary angle-closure glaucoma caused by :
Intumescent lens i.e., swollen cataractous lens
due to rapid maturation of cataract or sometimes
following traumatic rupture of capsule is the main
cause of phacomorphic glaucoma.
Anterior subluxation or dislocation of the lens
and spherophakia (congenital small spherical
lens) are other causes of phacomorphic glaucoma.
Pathogenesis. The swollen lens pushes the iris
forward and oblitrates the angle resulting in
secondary acute angle closure-glaucoma. Further,
the increased iridocorneal contact also causes
potential pupillary block and iris bombe formation.
Clinical presentation. Phacomorphic glaucoma
presents as acute congestive glaucoma with features
almost similar to acute primary angle-closure
glaucoma (see page 229) except that the lens in always
cataractous and swollen (Fig. 9.20).
Treatment should be immediate and consists of :
Medical treatment to control IOP by i.v. mannitol,
systemic acetazolamide and topical betablockers.
Cataract extraction with implantation of PCIOL
(which is the main treatment of phacomorphic
glaucoma) should be performed once the eye
becomes quite,
2. Phacolytic glaucoma (Lens protein glaucoma)
Pathogensis. It is a type of secondary open angle
glaucoma, in which trabecular meshwork is clogged
by the lens proteins and macrophages which have
phagocytosed the lens proteins. Leakage of the lens
proteins occurs through an intact capsule in the
hypermature (Morgagnian) cataractous lens.
Clinical features. The condition is characterised by:
Features of congestive glaucoma due to an acute
rise of IOP in an eye having hypermature cataract.
Anterior chamber may become deep and aqueous
may contain fine white protein particles.
Management. It consists of medical therapy to lower
the IOP followed by extraction of the hypermature
cataractous lens with PCIOL implantation.3. Lens particle glaucoma
Pathogenesis. It is a type of secondary open angle
glaucoma, in which trabecular meshwork is blocked
by the lens particles floating in the aqueous humour.
It may occur due to lens particles left after accidental
or planned extracapsular cataract extraction or
following traumatic rupture of the lens.
Clinical features. Raised IOP associated with lens
particles in the anterior chamber.
Management includes medical therapy to lower IOP
and irrigation-aspiration of the lens particles from the
anterior chamber.
4. Glaucoma associated with phacogenic uveitis
Pathogenesis. In this condition IOP is raised due to
inflammatory reaction of the uveal tissue excited by
the lens matter. Basically, it is also a type of secondary
open angle glaucoma where trabecular meshwork is
clogged by both inflammatory cells and the lens
particles.
Management consists of medical therapy to lower
IOP, treatment of iridocyclitis with steroids and
cycloplegics. Irrigation-aspiration of the lens matter
from anterior chamber (if required) should always be
done after proper control of inflammation.
5. Glaucoma associated with phacoanaphylaxis
In this condition, there occurs fulminating acute
inflammatory reaction due to antigen (lens protein) –
antibody reaction. The mechanism of rise in IOP and
its management is similar to that of phacogenic
uveitis.
GLAUCOMAS DUE TO UVEITIS
The IOP can be raised by varied mechanisms in
inflammations of the uveal tissue (iridocyclitis). Even
in other ocular inflammations such as keratitis and
scleritis, the rise in IOP is usually due to secondary
involvement of the anterior uveal tract.
Types. Glaucomas associated with uveitis can be
divided into two main groups:
1. Hypertensive uveitis.
2. Post-inflammatory glaucoma.
1. Hypertensive uveitis
Hypertensive uveitis refers to acute inflammation of
the anterior uvea associated with raised IOP.It includes:
i. Non-specific hypertensive uveitis, and
ii. Specific hypertensive uveitis syndromes
i. Non-specific hypertensive uveitis. It includes all
cases of acute inflammation of the anterior uveal tract
associated with raised IOP, other than the specific
hypertensive uveitis syndromes, but inclusive of
postoperative inflammation.
Mechanisms of rise in IOP. A secondary open-angle
glaucoma occurs due to trabecular clogging (by
inflammatory cells, exudates and turbid aqueous
humour), trabecular oedema (due to associated
trabeculitis), and prostaglandin–induced rise in IOP.
Management. It includes treatment of iridocyclitis and
medical therapy to lower IOP by use of hyperosmotic
agents, acetazolamide and beta- blocker eyedrops
(timolol or betaxolol).
ii. Specific hypertensive uveitis syndromes. These
include:
Fuchs’ uveitis syndrome (see page 160) and
Glaucomatocyclitic crisis (see page 160).
2. Post-inflammatory glaucoma
In it IOP is raised due to after-effects of the
iridocyclitis.
Mechanisms of rise in IOP. include :
Pupillary block due to annular synechiae or
occlusio pupillae,
Secondary angle-closure with pupil block
following iris bombe formation,
Secondary angle-closure without pupil block
due to organisation of the inflammatory debris in
the angle.
Secondary open-angle glaucoma due to
trabecular scarring and obstruction of the
meshwork.
Management. It includes prophylaxis and curative
treatment.
1. Prophylaxis. Acute iridocylitis should be treated
energetically with local steroids and atropine to
prevent formation of synechiae.
2. Curative treatment. It consists of medical therapy
to lower IOP (miotics are contraindicated). Surgical
or laser iridotomy may be useful in pupil block
without angle closure. Filtration surgery may be
performed (with guarded results) in the presence
of angle closure.