CORNEAL ULCERSCorneal ulcer, , is an inflammatory or more seriously, infective condition of thecorneainvolving disruption of its epitheliallayer with involvement of the cornealstroma. It is a common condition in humans particularly in the tropics and the agrarian societies. In developing countries, children afflicted by Vitamin A deficiency are at high risk for corneal ulcer and may become blind in both eyes, which may persist lifelong. In ophthalmology, a corneal ulcer usually refers to having an infectious etiology while the term corneal abrasion refers more to physical abrasions.

Corneal ulcer

CAUSESINFECTIOUS Bacterial Fungal Viral Protozoal Chlamydia trachomatis

NON INFECTIOUS

trauma chemical injury contact lenses abrassions post surgical exposure keratopathy neurotropic ulcers nutritional keratitis nearby(contagious )ocular surface inflamation

BACTERIAL ULCERS

Bacterial keratitis is caused byStaphylococcus aureus,Streptococcus viridans,Escherichia coli,Enterococci,Pseudomonas,Nocardiaand many other bacteria.

BACTERIAL ULCERS

Presentation is with pain, photophobia, blurred vision and mucopurulent or purulent discharge. Signs in chronological order: An epithelial defect associated with a larger infiltrate Stromal oedema, folds in Descemet membrane and anterior uveitis. Chemosis and eyelid swelling in severe cases. Rapid progression of infiltration with an enlarging hypopyon Severe ulceration may lead to descemetocele formation and perforation, particularly in Pseudomonas infection Endophthalmitis is rare in the absence of perforation. Scarring, vascularization and opacification.

uveitis

FUNGAL ULCERS

Fungal keratitis causes deep and severe corneal ulcer. It is caused byAspergillussp.,Fusariumsp.,Candidasp., as alsoRhizopus,Mucor, and other fungi. The typical feature of fungal keratitis is slow onset and gradual progression, where signs are much more than the symptoms. Small satellite lesions around the ulcer are a common feature of fungal keratitis andhypopyonis usually seen.

Fungal corneal ulcer, with excessive vascularizationMarginal ulcer, fungus positive.

Candida and filamentous keratitis Clinical features The diagnosis is often delayed unless there is a high index of suspicion, and often infection will initially have been presumed to be bacterial. 1 Presentation is with a gradual onset of pain, grittiness, photophobia, blurred vision and watery or mucopurulent discharge. 2 Signs a Candida keratitis Yellow-white densely suppurative infiltrate A collar-stud morphology may be seen. b Filamentous keratitis A grey or yellow-white stromal infiltrate with indistinct fluffy margins. Progressive infiltration, often with satellite lesions Feathery branch-like extensions or a ring-shaped infiltrate may develop. Rapid progression with necrosis and thinning can occur. Penetration of an intact Descemet membrane may occur and lead to endophthalmitis without evident perforation. c An epithelial defect is not invariable and is sometimes small when present. d Other features include anterior uveitis, hypopyon, endothelial plaque, raised IOP, scleritis and sterile or infective endophthalmitis.

Viral keratitis causes corneal ulceration. It is caused most commonly byHerpes simplex,Herpes ZosterandAdenoviruses. Also it can be caused bycoronaviruses& many other viruses. Herpes virus cause adendritic ulcer, which can recur and relapse over the lifetime of an individual.

dendritic ulcer Images

HERPES SIMPLEXEPITHELIAL KERATITIS

Epithelial (dendritic or geographic) keratitis is associated with active virus replication. 1 Presentation may be at any age with mild discomfort, redness, photophobia, watering and blurred vision. 2 Signs in chronological order: Swollen opaque epithelial cells arranged in a coarse punctate or stellate pattern Central desquamation results in a linear-branching (dendritic) ulcer, most frequent located centrally. The ends of the ulcer have characteristic terminal buds and the bed of the ulcer stains well with fluorescein The virus-laden cells at the margin of the ulcer stain with rose bengal Corneal sensation is reduced. Inadvertent topical steroid treatment may promote progressive enlargement of the ulcer to a geographical or amoeboid configuration . Mild associated subepithelial haze is typical. Elevated IOP may occur. Following healing, there may be persistent punctate epithelial erosions and irregular epithelium which settle spontaneously . Mild subepithelial scarring may develop after healing

Herpes simplex virus dendritic ulcer stained with rose bengal.

HERPES ZOSTERPathogenesis

The varicella-zoster virus (VZV) causes both chickenpox (varicella) and shingles (herpes zoster). VZV belongs to the same subfamily of the herpes virus group as the HSV and the two viruses are morphologically identical but antigenically distinct. Herpes zoster ophthalmicus (HZO) describes shingles involving the dermatome supplied by the ophthalmic division of the 5th cranial (trigeminal) nerve. Mild ocular involvement can also occasionally occur when the disease affects the maxillary division alone.

Mechanisms of ocular involvement

1 Direct viral invasion may lead to conjunctivitis and epithelial keratitis. 2 Secondary inflammation and occlusive vasculitis may cause episcleritis, scleritis, keratitis, uveitis, optic neuritis and cranial nerve palsies. Inflammation and destruction of the peripheral nerves or central ganglia, or altered signal processing in the CNS may be responsible for postherpetic neuralgia. Cicatrizing complications may arise following severe eyelid, periocular skin and conjunctival involvement. 3 Reactivation causes necrosis and inflammation in the affected sensory ganglia, causing corneal anaesthesia that may result in neurotrophic keratitis.

Risk of ocular involvement

1 Hutchinson sign describes involvement of the skin supplied by the external nasal nerve, a branch of the nasociliary nerve supplying the tip, side and root of the nose.. 2 Age. HZO occurs most frequently in the 6th and 7th decades. In the elderly, signs and symptoms tend to be more severe and to be of longer duration. 3 AIDS patients tend to have more severe disease, and shingles can be an early indicator of HIV infection. The development of shingles in children or young adults should also prompt a search for immunodeficiency or malignancy, though this will be found in only a minority

PROTOZOAN KERATITISACANTHAMEOBAPathogenesis Acanthamoeba spp. Are free-living protozoa commonly found in soil, fresh or brackish water and the upper respiratory tract. The cystic form is highly resilient. Under appropriate environmental conditions, the cysts turn into trophozoites, which produce a variety of enzymes, leading to tissue penetration and destruction. In developed countries keratitis is most frequently associated with contact lens wear, especially if tap water is used for rinsing.

Early misdiagnosis as herpes simplex keratitis is relatively common. In advanced disease the possibility of fungal keratitis should be remembered. 1 Presentation is with blurred vision and pain, which may be severe and disproportionate to the clinical signs. 2 Signs In early disease the epithelial surface is irregular and greyish. Epithelial pseudodendrites that may be mistaken for herpes simplex keratitis. Limbitis with diffuse or focal anterior stromal infiltrates Perineural infiltrates are seen during the first 14 weeks and are pathognomonic. Gradual enlargement and coalescence of the infiltrates to form a ring abscess Scleritis may develop and is generally reactive rather than extension of infection. Slowly progressive stromal opacification and vascularization. Corneal melting may occur at any stage when there is stromal disease. The melt often develops at the periphery of the area of infiltrate.

MELTING ULCERSMelting ulcers are a type of corneal ulcer involving progressive loss of stroma in a dissolving fashion. This is most commonly seen inPseudomonasinfection, but it can be caused by other types ofbacteriaorfungi. These infectious agents produceproteasesandcollagenaseswhich break down the corneal stroma. Complete loss of the stroma can occur within 24 hours. Treatment includes antibiotics and collagenase inhibitors such as (penetrating acetylcysteine. Surgery in the form of corneal transplantation keratoplasty) is usually necessary to save the eye.

MELTING ULCERS

RECURRENT CORNEAL ABRASIONSETIOLOGYThey can be caused by damage to corneal epithelium or epithelial basement memberane from one of the followingAnt. corneal dystrophy reis buckler meesmann Previous traumatic corneal abrasionsStromal corneal dystrophyKeratorefractive ,corneal trasplant or catract surgery

RECURRENT CORNEAL ABRASIONS IMAGE

SYMPTOMS recurrent attacks of acute acular pain photophobia fb sensation tearingSIGNS localized roughening of corneal epi corneal abrasion epi dots or small cysts fingerprint pattern or map like lines

CHEMICAL INJURIESChemical injuries range in severity from the trivial to the potentially blinding.

The majority are accidental, and a few due to assault. Two-thirds of accidental burns occur at work and the remainder at home.

Alkali burns are twice as common as acid burns since alkalis are more widely used both at home and in industry.

Alkalis tend to penetrate more deeply than acids, as the latter coagulate surface proteins, forming a protective barrier. The most common involved alkalis are ammonia, sodium hydroxide and lime.

The commonest acids implicated are sulphuric, sulphurous, hydrofluoric, acetic, chromic and hydrochloric.

Pathophysiology

1 Damage by severe chemical injuries occurs in the following order: Necrosis of the conjunctival and corneal epithelium with disruption and occlusion of the limbal vasculature. Loss of limbal stem cells may result in conjunctivalization and vascularization of the corneal surface, or persistent corneal epithelial defects with sterile corneal ulceration and perforation. Other long-term effects include ocular surface wetting disorders, symblepharon formation and cicatricial entropion. Deeper penetration causes the breakdown and precipitation of glycosaminoglycans and stromal corneal opacification. Anterior chamber penetration results in iris and lens damage. Ciliary epithelial damage impairs secretion of ascorbate which is required for collagen production and corneal repair. Hypotony and phthisis bulbi may ensue in severe cases. 2 Healing of the corneal epithelium and stroma takes place as follows: The epithelium heals by migration of epithelial cells which originate from limbal stem cells. Damaged stromal collagen is phagocytosed by keratocytes and new collagen is synthesized.

CONTACT LENS RELATED ULCERSYMPTOMS pain photophobia fb sensation dec vision red eye itching discharge burning contact lens intoleranceETIOLOGY infectious corneal infiltrate(bacterial/acanthameoba) white corneal lesion which stains with fluorescein giant papillary conjunctivitis contact lens deposits tight lens syndrome displaced contact lens

EXPOSURE KERATOPATHYPathogenesis Exposure keratopathy is the result of incomplete lid closure (lagophthalmos). Lagophthalmos may only be present on blinking or gentle lid closure, but absent on forced lid closure. The result is drying of the cornea despite normal tear productionCAUSES 1 Neuroparalytic, 2 Reduced muscle tone 3 Mechanical 4 Abnormality of globe position

EXPOSURE KERATOPATHY IMAGES

Neurotrophic ulcerationNeurotrophic ulceration is caused by failure of re-epithelialization resulting from corneal anaesthesia, often exacerbated by other factors such as drug toxicity. 1 Signs A non-healing epithelial defect, sometimes after prolonged topical treatment The stroma beneath the defect is grey and opaque and may become thin. Secondary bacterial or fungal infection may occur.

OCULAR SURFACE INFLAMATION Lids n lashes(ectropion,entropion,trichiasis, lid defects ETIOLOGY involutional.aging cicatrical.conjuntival scarring spastic..surgical trauma occular irritaion blepherospasm

Skin..SJ syndrome, ocular rosacea,ocular pemphigoid Lacrimal gland..KCS NUTRITIONAL KERATITIS.due to vit A deficiency

EVALUATIONSLIT LAMP BIOMICROSCOPY

Epithelial defects detected which take up flourocein stain

SLIT LAMP BIOMICROSCOPY

LABORATORY STUDIES

Corneal scraping

They may not be required for a small infiltrate, particularly without an epithelial defect and away from the visual axis. Scraping may be delayed off treatment for 12 hours if antibiotics have previously been commenced. A non-preserved topical anaesthetic is instilled Scrapings are taken either with a disposable scalpel blade, the bent tip of a larger diameter hypodermic needle, or a sterile spatula (e.g. Kimura). The easiest way to plate scrapings without breaking the gel surface is with a spatula. If a fresh spatula is not available for each sample a single instrument should be flame-sterilized between scrapes (heat for 5 seconds, cool for 2030 seconds). Alternatively, a fresh scalpel blade or needle can be used for each pass. In scraping it is necessary to first carefully remove loose mucus and necrotic tissue from the surface of the ulcer. The margins and base (except if very thin) of the lesion are scraped

CULTURE MEDIA FOR SCRAPING

MediumSpecificityBlood agar Most bacteria and fungi except Neisseria, Haemophilus and MoraxellaChocolate agar Fastidious bacteria, particularly H. Influenzae, Neisseria and MoraxellaSabouraud dextrose agarFungiNon-nutrient agar seeded with E. coliAcanthamoebaBrain heart infusionDifficult-to-culture organisms; particularly suitable for streptococci and meningococci. Supports yeast and fungal growthCooked meat brothAnaerobic (e.g. Propionibacterium acnes) as well as fastidious bacteria Lwenstein-JensenMycobacteria, Nocardia

2 Conjunctival swabs may be worthwhile in addition to corneal scraping, particularly in severe cases, as occasionally an organism may be cultured when a corneal scrape is negative. 3 Contact lens cases, as well as bottles of solution and lenses themselves should be obtained when possible and sent to the laboratory for culture. 4 Gram staining Differentiates bacterial species into Gram-positive and Gram-negative based on the ability of the dye (crystal violet) to penetrate the cell wall. Bacteria that take up crystal violet are Gram-positive and those that allow the dye to wash off are Gram-negative Other stains, generally not requested at initial investigation, are given in Refrigerated media should be gently warmed to room temperature prior to sample application.

Stains for corneal and conjunctival scrapes

StainOrganismGramBacteria, fungi, MicrosporidiaGiemsaBacteria, fungi, Acanthamoeba, MicrosporidiaCalcofluor white (fluorescent microscope)Acanthamoeba, fungi, MicrosporidiaAcid-fast stain (AFB) e.g. ZiehlNeelsen, Auramine O (fluorescent) Mycobacterium, Nocardia spp. Grocott-Gmri methenamine-silverFungi, Acanthamoeba, MicrosporidiaPeriodic acid-Schiff (PAS)Fungi, Acanthamoeba

5 Sensitivity reports are sent out at 1 or 2 days, 7 days and 2 weeks. When determining drug sensitivity for an isolated organism, the results are reported as follows: a Susceptible indicating that the organism is sensitive to a normal dose of the antimicrobial agent. b Intermediate indicating that the organism is likely to be sensitive to a high dose of the antimicrobial agent. c Resistant means that the organism is not sensitive to the antimicrobial agent at the tested dose.

6 Corneal biopsy is indicated in the absence of clinical improvement after 34 days and if no growth develops from scrapings after a week. A 23mm block should be taken, using a technique similar to the scleral block excision during trabeculectomy. The excised block is sent for culture and histopathological analysis.7 Confocal microscopy is rarely available, but may permit identification of organisms in vivo.

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