Non-Infectious keratitis

Mooren ulcerPeripheral ulcerative keratitis

Neurotrophic keratitisExposure keratitis

Non infectious keratitis

Peripheral corneal thinningThinning 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

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

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.

Dellen

Furrow degeneration

Mooren ulcer

Rare autoimmue disease

Characterized by: progressive, peripheral, circumferential, stromal corneal ulceration slightly central to the corneoscleral

limbus with later central spread

Forms

Symptoms Severe pain

Photophobia

Blurring of vision

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

Local peripheral ulceration

Local peripheral ulceration & Undermining

Undermining

Circumferential

Circumferential

Healing

ComplicationsSevere astigmatism due to extensive

vascularization & fibrosis

Perforation following minor trauma (spontaneous perforation is unlikely)

Secondary bacterial infection

Cataract

Glaucoma

DDx

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.

Conjunctival resectionmay be combined with excision of necrotic tissueperformed 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

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.

Surgery

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.

Peripheral ulcerative karatitis

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.

Systemic associationsRheumatoid 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.

Symptoms Foreign body sensation

Pain,

Photophobia

Blurred Vision

SignsCrescentic ulceration*

with an epithelial defect, thinning and stromal infiltration at the limbus

Spread is circumferential and occasionally centralin 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 entitypunched-out more centrally located lesion with little infiltrate in

a quiet eye. Perforation can occur rapidlyusually a good response to topical ciclosporin, with bandage

contact lens and tissue glue application if necessary, rather than systemic treatment.

Crescentic ulceration

Crescent shaped ulceration and stromal infiltration at the limbus

Contact lens cornea

Contact lens cornea

PCUK

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

SystemicSteroids (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.

Terrien marginal degeneration

Idiopathic thinning of the peripheral corneaYoung adult to elderly patientsUncommon75% malesUsually bilateral

Although usually categorized as a degeneration, some cases are associated with episodic episcleritis or scleritis.

Symptoms Asymptomatic, but gradual visual deterioration can occur

due to astigmatism. A few patients experience episodic pain

and inflammation

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

Pseudopterigium

Pseudopterygium vs PterygiumResults from corneal burns, perforation or

longstanding corneal ulcer.Differentiated by:

Hx of prior inflammationUnilateralLocationConfiguration other than the wing shapeNonprogressiveInability to pass a probe under the neck

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.

Neurotrophic keratitis

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

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

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).

Causes Toxicity of certain topical

medications :Anasthetics NSAIDB blockers Carbonic anhydarse inhibitors

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

Stage 1

Stage 1

Stage 2

Stage 2

Stage 2

Stage 3 with infection

Large epithelial defect and stromal infiltratrion

Stromal melting

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.

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

Exposure keratopathy

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.

Facial palsy

Eyelid scaring

Severe proptosis

Symptoms

Foreign body sensation

Tearing

Photophopia

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*

Inferior epithelial changes

Epithelial defect

Stromal melting

Secondary infection

Management

Treatment depends on the severity of exposure and whether recovery is anticipated.

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.

Permanent exposurePermanent tarsorrhaphy.

Gold weight upper lid insertion for facial nerve palsy.

Permanent central tarsorrhaphy, amniotic membrane grafting or conjunctival flap when vision is poor.

Thank you