Phacoantigenic Response to

Ruptured Lens Capsule:

Clinicopathologic Case

Emily Deschler, MD
Charleen Chu, MD, PhD
March 2011
 Brief History and Course

• 58 year-old woman
• Blind left eye since teens – unknown
etiology
• No history of trauma
• Referred to glaucoma service when left
eye became painful
 Initial Physical Exam
• Vision: • Anterior segment
– Right eye: 20/20 – Right eye: Shallow anterior
– Left eye: NLP chamber with patent PI
• IOP: – Left eye: injected
conjunctiva, cornea with
– Right eye: 11 PEE, shallow anterior
– Left eye: 16 chamber with patent PI x2,
• Pupil: iris with florid rubeosis,
posterior synechiae,
– Right eye: 4-3 mature cataract
– Left eye: Irregular • Fundus:
– Right eye: Normal, c/d 0.6
with healthy neuroretinal
rim
– Left eye: no view
 Brief History and Course
• Symptoms initially attributed to ocular
surface disease and treated with artificial
tears, topical steroids

• 1 year later, pain continued and patient

elected to proceed with enucleation
(PHS10-35123)
 Calcific Band Keratopathy
• Gross photo of
the cornea
– entire cornea is
affected
– calcification
spans from
limbus to limbus
 Calcific Band Keratopathy
• Seen clinically as calcific plaques in the
interpalpebral zone
– deposition of calcium in the epithelial basement
membrane, Bowman’s layer, and anterior stroma.
– usually an intervening region of cornea between the
limbus and the calcification that is unaffected
• 6 main causes
– chronic ocular disease (usually inflammatory),
hypercalcemia, hereditary transmission, elevated
serum phosphorus with normal calcium, exposure to
mercury, silicone oil in ahakic eye
• Tx: remove overlying epithelium and then apply
EDTA
 Calcific Band Keratopathy
• H&E
– 1. stippled
basophilia of
Bowman’s layer,
the calcium
deposits merge to
form a linear array
2
along Bowman’s
layer
1
– 2. keratocyte
nuclei
 Neovascularization of the Iris &
Hyphema

1. Neovascularization
of the iris – at this
power cannot see
individual vessels,
but flattened
anterior iris is a clue
2. Hyphema

2
 Disorders Predisposing to
Neovascularization of Iris and Angle
• Systemic vasular disease
– Carotid disease
– Giant cell arteritis
• Ocular vascular disease
– Diabetes
– CRVO
– Coats
– Eales
– ROP
– Persistent fetal vasculature
– Anterior segment ischemia
• Ocular disease
– Cronic uveitis
– Chronic retinal detachment
– Endophthalmitis
– Stickler syndrome
– Retinoschisis
• Intraocular tumors
– Uveal melanoma
– Metastatic disease
– Retinoblastoma
• Ocular therapy
– Radition therapy
 Peripheral Anterior Synechia
• Iris stroma obliterates the
angle recess
• Mechanisms of PAS
formation:
– Contraction of an
inflammatory, hemorrhagic
or vascular membrane, band
or exudate in the angle
– Forward displacement of the
iris-lens diaphragm leading
to a prolonged shallow/flat
anterior chamber
• Extent of PAS may correlate
with visual field damage,
larger vertical cup-to-disc
ratio, and higher untreated
intraocular pressure
• Poor prognosis
• Treat underlying cause
(ischemic retina with PRP)
anti-VEGF, filtering surgery
 1. Chronic Iritis
2. Neovascularization of the Iris
• Lymphocytes
– small cells with
round,
hyperchromatic 1
nuclei and scant
cytoplasm
– found in chronic
inflammatory
process
2
 Chronic Plasmacytic Cycloiritis

• B lymphocytes may
differentiate into
plasma cells and
produce
immunoglobulin
• Eccentric
“cartwheel” or
“clockface” nuclei
Chronic Choroiditis

• Small blue
cells
 Phacoantigenic Response to
Ruptured Lens Capsule

• Granulomatous
reaction
• Macrophages
filled with
degenerated
lens cortical
material
Phacoantigenic Response to
Ruptured Lens Capsule - PAS
 Phacoantigenic vs Phacoanalytic
Glaucoma
Phacoantigenic
– Sensitized to own lens protein
following surgery or
penetrating trauma
– Granulomatous reaction
• Clinically
– Moderate anterior chamber
reaction with KP on
endothelium and lens capsule
– Low grade vitritis
– Synechial formation
– Not commonly associated with
glaucomatous optic
neuropathy
• Treatment
– Corticosteroids, aqueous
suppressants, and if
unsuccessful, remove residual
lens material
Phacolytic
– Leakage of lens proteins
through the capsule of a
mature or hypermature
cataract
– Proteins, phagocytizing,
inflammatory debris obstruct
the uveal meshwork
• Clinically
– Prominent cell and flare with
possible psuedohypopyon in
the anterior chamber
– No KP
– Morgagnian cataract with
wrinkled anterior lens capsule
– Open anterior chamber angle
• Treatment
– IOP lowering medications,
ultimately cataract extraction
 Discussion: Phacoantigenic
response to ruptured lens capsule
• Occurs following surgery or penetrating trauma
causing sensitization to one’s own lens protein
– Granulomatous reaction
– Variable clinical presentation: moderate AC reaction
with KP on corneal endothelium and anterior lens
surface (unlike phacolytic) with moderate AC reaction.
Low grade vitritis, synechial formation, residual lens
material may be in AC
– Not commonly associated with glaucomatous
optic neuropathy.
• Treatment
– Corticosteroids, aqueous suppressants, and if
unsuccessful, remove residual lens material
Discussion: Phacolytic response to
mature cataract
• Proteins, phagocytizing macrophages, and other
inflammatory debris obstruct the trabecular meshwork
• Generally an elderly person with a history of poor vision
presents with sudden onset pain, conjunctival injection,
elevated IOP, corneal edema, prominent cell and flair
without KP and open anterior chamber angle
• Cellular debris may be present in the anterior chamber
presenting as pseudohypopyon. The anterior capsule
may appear wrinkled representing loss of lens material
• Treatment:
– IOP lowering medications, ultimately cataract extraction
• Diagnosis:
– Phacoantigenic immune response to
ruptured lens capsule

• Additional diagnoses:
– Idiopathic chronic panophthalmitis
– Neovascularization of the iris
– Peripheral anterior synechiae
– Calcific band keratopathy
 Sources
• Basic Clinical Science Course Section 10:
Glaucoma. American Academy of
Ophthalmology 2009-2010
• Yanoff, Myron and Fine, Ben. Ocular
Pathology. Mosby. 2002