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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:
– Right eye: 20/20
– Left eye: NLP
• IOP:
– Right eye: 11
– Left eye: 16
• Pupil:
– Right eye: 4-3
– Left eye: Irregular
• Anterior segment
– Right eye: Shallow anterior
chamber with patent PI
– Left eye: injected
conjunctiva, cornea with
PEE, shallow anterior
chamber with patent PI x2,
iris with florid rubeosis,
posterior synechiae,
mature cataract
• 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
along Bowman’s
layer
– 2. keratocyte
nuclei
2
1
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
1
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
nuclei and scant
cytoplasm
– found in chronic
inflammatory
process
1
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