This document discusses various types of peripheral non-infectious keratitis, including Mooren ulcer, Terrien marginal degeneration, dellen, furrow degeneration, neurotrophic keratitis, and exposure keratitis. It provides details on the pathogenesis, signs and symptoms, clinical presentation, diagnostic considerations, and management approaches for each condition. The conditions are characterized by thinning and/or ulceration preferentially affecting the peripheral rather than the central cornea. Management involves identifying and treating underlying causes, using lubricants, bandage contact lenses, amniotic membrane grafts, tarsorrhaphy, and in some cases immunosuppression or surgery.
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2. Peripheral corneal thinning
Thinning and/or ulceration preferentially affecting the
peripheral rather than the central cornea, and spreading
around the margin.
It should be noted that any cause of corneal ulceration can
affect the periphery
3. Types
Mooren ulcer.
Terrien marginal degeneration.
Dellen.*
Associated with systemic autoimmune disease.
Others; Ocular rosacea, furrow degeneration* (mild
peripheral thinning in the elderly, usually benign), pellucid
marginal degeneration
4. Dellen
Localized corneal disturbance associated with drying of a focal
area
Usually associated with an adjacent elevated lesion as
pinguecula or large subconjunctival haemorrhage that impairs
physiological lubrication.
Generally mild though can occasionally be severe.
8. Rare autoimmue disease
Characterized by:
progressive,
peripheral,
circumferential,
stromal corneal ulceration
slightly central to the corneoscleral limbus
with later central spread
11. Signs
Peripheral ulceration*
involving the superficial one-third of the stroma,
variable epithelial loss,
Several distinct foci may be present and subsequently coalesce
Undermined and infiltrated leading edge is characteristic**
Progressive circumferential and central stromal thinning**
Vascularization involving the bed of the ulcer up to its leading edge but
not beyond.
The healing stage* is characterized by thinning, vascularization and
scarring
20. Complications
Severe astigmatism due to extensive vascularization & fibrosis
Perforation following minor trauma (spontaneous perforation is
unlikely)
Secondary bacterial infection
Cataract
Glaucoma
23. Management
Topical :
Steroids (Q1hr combined with A.B)
Cyclosporin (weeks to show signiificant effect)
Artificial tears
Collagenase inhibitors (acetylcystine)
bandage contact lenses may reduce discomfort and promote
epithelial healing.
24. Conjunctival resection
may be combined with excision of necrotic tissue
performed if there is no response to topical steroids.
The excised area should extend 4 mm back from the limbus
and 2 mm beyond the circumferential margins.
Keratoepithelioplasty (suturing of a donor corneal lenticule
onto the scleral bed) may be combined to produce a physical
barrier against conjunctival regrowth and further melting.
Steroids are continued postoperatively
25. Systemic
Immunosuppression should be instituted earlier for
bilateral disease
advanced involvement at presentation
Systemic collagenase inhibitors such as doxycycline may be
beneficial.
Lamellar keratectomy involving dissection of the residual
central island in advanced disease may remove the stimulus
for further inflammation.
27. Prognosis
Most patients who have unilateral disease respond fairly well
to topical corticosteroids and conjunctival resection.
For more severe bilateral cases, the prognosis is poor, and
the primary goal is to reduce the likelihood of perforation
and preserve the structure of the eye.
29. Peripheral ulcerative keratitis
Destructive inflammation of the peripheral cornea associated
with corneal epithelial sloughing and keratolysis.
Severe peripheral corneal infiltration, ulceration or thinning
unexplained by evident ocular disease should prompt
investigation for a (potentially life-threatening) systemic
collagen vascular disorder.
The mechanism includes immune complex deposition in
peripheral cornea, episcleral and conjunctival capillary
occlusion with secondary cytokine release and inflammatory
cell recruitment, the upregulation of collagenases and
reduced activity of their inhibitors.
30. Systemic associations
Rheumatoid arthritis (most common).
PUK is bilateral in 30% and tends to occur in advanced RA.
Wegener granulomatosis (2nd
most common)
In contrast to RA ocular complications are the initial presentation in
50%.
Other conditions include polyarteritis nodosa, relapsing
polychondritis and SLE.
32. Signs
Crescentic ulceration*
with an epithelial defect, thinning and stromal infiltration at the limbus
Spread is circumferential and occasionally central
in contrast to Mooren ulcer, extension into the sclera may occur.
Limbitis, episcleritis or scleritis are usually present; as with a Mooren
ulcer, there is no separation between the ulcerative process and the
limbus.
Contact lens cornea*
Perforation.
Rheumatoid paracentral ulcerative keratitis (PCUK)*
thought to be a distinct entity
punched-out more centrally located lesion with little infiltrate in a quiet eye.
Perforation can occur rapidly
usually a good response to topical ciclosporin, with bandage contact lens and
tissue glue application if necessary, rather than systemic treatment.
39. Management
Principally with systemic immunosuppression in collaboration
with a rheumatologist.
Topical
Artificial tears (preservative-free).
Antibiotics as prophylaxis if an epithelial defect is present.
Steroids may worsen thinning so are generally avoided
Systemic
Steroids (via pulsed IV administration) are used to control acute
disease, with immunosuppressive therapy and biological blockers for
longer-term management.
Tetracycline for its anticollagenase effect.
Surgical management is generally as for Mooren ulcer, including
conjunctival excision if medical treatment is ineffective.
43. Idiopathic thinning of the peripheral cornea
Young adult to elderly patients
Uncommon
75% males
Usually bilateral
Although usually categorized as a degeneration, some cases
are associated with episodic episcleritis or scleritis.
45. Signs
Fine yellow–white refractile stromal opacities*, frequently
associated with mild superficial vascularization,
usually start superiorly,
spread circumferentially
separated from the limbus by a clear zone.
no epithelial defect, and on cursory examination the condition may
resemble arcus senilis.
Slowly progressive circumferential thinning*
results in a peripheral gutter, the outer slope of which shelves
gradually, while the central part rises sharply. A band of lipid is
commonly present at the central edge
Perforation is rare but may be spontaneous or follow blunt
trauma.
Pseudopterygia* sometimes develop
49. Pseudopterygium vs Pterygium
Results from corneal burns, perforation or longstanding
corneal ulcer.
Differentiated by:
Hx of prior inflammation
Unilateral
Location
Configuration other than the wing shape
Nonprogressive
Inability to pass a probe under the neck
50. Management
Safety spectacles if thinning is significant.
Contact lenses for astigmatism. Scleral or soft lenses with
rigid gas permeable ‘piggybacking’.
Surgery – crescentic or annular excision of the gutter with
lamellar or full-thickness transplantation.
52. Pathophysiology
Loss of trigeminal innervation to the cornea resulting in
partial or complete anaesthesia.
Also it leads to intracellular oedema, exfoliation, loss of
goblet cells and epithelial breakdown with persistent
ulceration.
The trophic ulceration results from abnormal repair of
corneal epithelium secondary to abnormal epithelial cell
turnover and reduced reflex tearing
53. Normally, a bidirectional interaction occurs between epithelial
cells and nerve endings.
Adrenergic stimulation leads to increased cAMP, which
inhibits mitosis.
Cholinergic stimulation leads to increased cGMP, which
increases cell turnover
Substance P may play a role in normal and abnormal epithelial
cell turnover
Disruption of the sensory and sympathetic pathways is thought to
lead to decreased cell division.[
Cells therefore fail to resist the effects of trauma (microtrauma)
and desiccation, which normally lead to reflex tearing
54. Causes
Trigeminal ganglion surgical ablation for neuralgia,
stroke,
tumour,
peripheral neuropathy due to DM,
ocular disease such as herpes simplex and herpes zoster keratitis
(the most common causes).
55. Causes
Toxicity of certain topical medications :
Anasthetics
NSAID
B blockers
Carbonic anhydarse inhibitors
56. Ocular manifestation
three stages of neurotrophic keratitis.
Stage 1*: interpalpebral epithelial irregularity and staining,
with mild opacification, oedema and tiny focal defects (SPKs)
Stage 2*: is characterized by a frank epithelial defect,
which typically is associated with mild anterior stromal
inflammation. Folds in Descemet’s membrane often develop.
The epithelium at the edges of the defect tends to be
characteristically “heaped up” with grayish, swollen
epithelium.
Stage 3*: involves stromal melting and occasionally
perforation
67. Management
Discontinuation, if possible, of potentially toxic medications.
Topical lubricants (non-preserved) for associated dry eye or
corneal exposure.
Anticollagenase agents: topical (e.g. acetylcysteine,
tetracycline ointment) or systemic (e.g. tetracyclines).
Protection of the ocular surface:
Simple taping of the lids, particularly at night, may provide modest
protection.
Botulinum toxin-induced ptosis.
Tarsorrhaphy.
Therapeutic silicone contact lenses may be fitted, provided the eye is
carefully monitored for infection.
Amniotic membrane patching with temporary central tarsorrhaphy.
68. Prognosis
Patients with superficial punctate staining should be
maintained on regular lubrication .
Persistent defects respond best to tarsorrhaphy.
Signs of infection must be followed closely. Patients should
be advised that neurotrophic ulcers tend to recur and
are difficult to heal. More severe, progressive, sterile or
infectious ulcers may progress to descemetocele or
perforation
70. Pathogensis
Results from incomplete lid closure (lagophthalmos), with
drying of the cornea despite normal tear production.
Mild exposure is normal in some individuals but may become
symptomatic if poor bell`s phenomenon.
76. Signs
Mild punctate epithelial changes involving the inferior third
of the cornea, particularly with nocturnal lagophthalmos.
Epithelial breakdown*
Stromal melting*, occasionally leading to perforation.
Inferior fibrovascular change with Salzmann degeneration
may develop over time.
Secondary infection*
82. Reversible exposure
Artificial tears (unpreserved) during the day and ointment at
night.
Taping the lid closed at night may be an alternative to
ointment.
Bandage silicone hydrogel or scleral contact lenses.
Management of proptosis by orbital decompression if
necessary.
Temporary tarsorrhaphy.
83. Permanent exposure
Permanent tarsorrhaphy.
Gold weight upper lid insertion for facial nerve palsy.
Permanent central tarsorrhaphy, amniotic membrane
grafting or conjunctival flap when vision is poor.