keratitis

keratitisBacterial keratitisMost important potential complicationEarly diagnosis and treatment are keyClose follow up , attention toBacterial keratitis remains one of the most important potential complications of contact lens use and refractive corneal surgery. Keeping this in mind, early diagnosis and treatment are key to minimizing any visual-threatening sequelae. In addition, close follow-up, attention to laboratory data, and changing antimicrobials if no clinical improvement is evident are important elements for successful outcome. 2Pathophysiologyalteration in the corneas defense mechanisms that allow bacteria to invade when an epithelial defectThe severity of the disease depends on the strain of the organism, the size of the inoculums, the susceptibility of the host and immune response, the antecedent therapy and the duration of the infectionPathophysiologyInterruption of an intact corneal epithelium and/or abnormal tear film permits entrance of microorganisms into the corneal stroma, where they may proliferate and cause ulceration. Virulence factors may initiate microbial invasion, or secondary effector molecules may assist the infective process. Many bacteria display several adhesins on fimbriated and nonfimbriated structures that may aid in their adherence to host corneal cells. During the initial stages, the epithelium and stroma in the area of injury and infection swell and undergo necrosis. Acute inflammatory cells (mainly neutrophils) surround the beginning ulcer and cause necrosis of the stromal lamellae. Diffusion of inflammatory products (including cytokines) posteriorly elicits an outpouring of inflammatory cells into the anterior chamber and may create a hypopyon. Different bacterial toxins and enzymes (including elastase and alkaline protease) may be produced during corneal infection, contributing to the destruction of corneal substance. The most common groups of bacteria responsible for bacterial keratitis are as follows: Streptococcus, Pseudomonas, Enterobacteriaceae (including Klebsiella, Enterobacter, Serratia, and Proteus), and Staphylococcus species.Up to 20% of cases of fungal keratitis (particularly candidiasis) are complicated by bacterial coinfection.

Corneal infections rarely occur in the normal eye. They are a result of an alteration in the corneas defense mechanisms that allow bacteria to invade when an epithelial defect is present. The orgaknisms may come from the tear film or as a contaminant from foreign bodies, contact lenses or irrigating solutions. The severity of the disease depends on the strain of the organism, the size of the inoculums, the susceptibility of the host and immune response, the antecedent therapy and the duration of the infection. The process of corneal destruction can take place rapidly (within 24hrs with virulent organisms) so that rapid recognition and initiation of treatment is imperative to prevent visual loss. 3 EtiologyKeratitis may develop as a result of:1. Exogenous infection Mostly traumatic, the object causing injury may carry infection to cornea or may come from conjunctival sac (infecting abraded cornea)2. Endogenous Infection (inflammation): this is immunological in nature eg. Phlyctenular keratitis caused by tubercular or staphylococcal hypersensitivity and interstitial keratitis related to measles or syphilis. These conditions are commonly noticed at corneal margin (Marginal Keratitis or Marginal Corneal Ulcer)3. Spread of Infection from neighboring structuresSymptomrapid onset of ocular pain, redness, photophobia, discharge, and decreased visionSymptoms include rapid onset of ocular pain, redness, photophobia, discharge, and decreased vision. The rate of progression of the symptoms is related to the virulence of the infecting organism. 5Physical Ulceration of the epithelium; corneal infiltrate with no significant tissue loss; dense, suppurative stromal inflammation with indistinct edges; stromal tissue loss; and surrounding stromal edema Increased anterior chamber reaction with or without hypopyonFolds in the Descemet membraneUpper eyelid edemaPosterior synechiaeSurrounding corneal inflammation that is either focal or diffuseConjunctival hyperemiaAdherent mucopurulent exudateEndothelial inflammatory plaque

PhysicalExternal and biomicroscopic examination of these patients reveals some or all of the following features:Ulceration of the epithelium; corneal infiltrate with no significant tissue loss; dense, suppurative stromal inflammation with indistinct edges; stromal tissue loss; and surrounding stromal edema Increased anterior chamber reaction with or without hypopyonFolds in the Descemet membraneUpper eyelid edemaPosterior synechiaeSurrounding corneal inflammation that is either focal or diffuseConjunctival hyperemiaAdherent mucopurulent exudateEndothelial inflammatory plaque

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Expanding oval, yellow-white, dense stromal infiltrateStromal suppuration and hypopyon

Central bacterial corneal ulcer with hypopyonMedical theraphyTopical broad spectrum antibiotic therapy should be used until culture results are available. Small non-staining peripheral ulcers may be started on fluoroquinolone drops every 2 to 6 hours. For ulcers with epithelial defects and an anterior chamber reaction, a fluoroquinolone drop every hour around the clock is recommended. Large or vision threatening ulcers (with moderate to severe anterior chamber reaction and/or involving the visual axis) are usually treated with fortified tobramycin or gentamicin (15mg/ml) every hour around the clock alternating with fortified vancomycin (25mg/ml) every hour around the clock. 8Fungal keratitisFungal keratitis is a serious ocular infection with potentially catastrophic visual results. Caused by any of the many species of fungi capable of colonizing human tissue, its occurs worldwide and its incidence is increasing in frequency.

Risk factorTraumaTopical corticosteroid useCorneal surgery such as penetrating keratoplasty, clear cornea (sutureless) cataract surgery, or laser in situ keratomileusis (LASIK) Young malesPrevious history of trauma (vegetable matter)Agricultural occupationsRisk factors include trauma, ocular surface disease, and topical steroid use. Risks and type of fungi also might vary by geographic location and climate1-7. In warmer climates the rule is that the most common organisms are filamentous fungi, like Fusarium spp and Aspergillus spp. with a strong relationship to trauma. Reports from Brazil show the most common isolates in descending order were Fusarium spp in 67%, Aspergillus spp in 10.5%, and Candida spp in 10%. About 40% of the infections were related to trauma.1 In the northern USA, corneal infection by fungus was, until recently, more common in debilitated or immunocompromised patients and the causative organism being a yeast, such as Candida albicans. Filamentous fungi in these latitudes were then rarely reported. A few years ago a breakout of Fusarium keratitis associated to a type of contact lens solution8 displaced yeasts as the most common fungal corneal infection in some areas. This trend persists in the most recent epidemiological reports. Still they are, in most cases, related to contact lens use. It should be noted that the incidence of contact lens-related fungal keratitis was increasing before the Fusarium outbreak. This new distribution means that we no longer can rely on the geographical distribution only to initiate empirical treatment. Broad-spectrum treatment should be administerd once there is a strong probability of a mycotic infection.

10Pathophysiologystarts when the epithelial integrity is broken either due to trauma or ocular surface disease Proteolitic enzymes, fungal antigens and toxins are liberated into the cornea with the resulting necrosis and damage to its architecture thus compromising the eye integrity and function. General Pathology Even thought fungi can be classified as a kingdom due to their complexity and unique characteristics, a simple practical classification for ocular infection is used. Under this method, morphology and type of reproductive method define the type of fungi. They are classified for our purpose as yeast, filamentous septated pigmented and non-pigmented and filamentous without septae. Fungi are present worldwide and can be part of the ocular flora. Are eukaryotic with a defined nucleus surrounded by a membrane. Are either saprophytic, free organisms living out of decaying organic matter or pathologic, those that need a living host for perpetuation. Pathophysiology The infection probably starts when the epithelial integrity is broken either due to trauma or ocular surface disease and the organism gains access into the tissue and proliferates. Proteolitic enzymes, fungal antigens and toxins are liberated into the cornea with the resulting necrosis and damage to its architecture thus compromising the eye integrity and function.

11SymptomSymptoms are similar to any corneal infection including blurred vision, redness, tearing, photophobia, pain, foreign body sensation and secretions.Signs With filamentary fungi the corneal lesion have a white/gray infiltrate with feathery borders. There might be satellite lesions with hypopyon and conjunctival injection as well as purulent secretions. Ulcers caused by yeast are plaque like and slightly more defined, similar to bacterial keratitis. Symptoms Symptoms are similar to any corneal infection including blurred vision, redness, tearing, photophobia, pain, foreign body sensation and secretions. In some cases the lesion are rather indolent which help to delay the diagnosis and hence the treatment. Always be suspicious after trauma with vegetable matter.

12Physicalthe clinical diagnosis of fungal keratitis is based on risk factor analysis and characteristic corneal features. The most common signs on slit lamp examination are nonspecific and include the following: Conjunctival injection

Fungal corneal ulcer, with excessive vascularization. Marginal ulcer, fungus positive.Fungal corneal ulcer, with excessive vascularization. Marginal ulcer, fungus positive. Epithelial defectSuppuration (See images below.)Fungal abscess. Fungal corneal abscess/ulcer. A proven case of fungal infection, 5 days' duration. Intense infiltration around the abscess. Stromal infiltrationAnterior chamber reactionHypopyon13Stromal infiltrationAnterior chamber reactionHypopyonEpithelial defect

Fungal abcess

Pigmented lesionTreatmentNatamycin 5% suspension: frequency will depend on severity of conditionCandida species respond better to Amphotericin B 0.15%Fluconazole 2%Miconazole 1%Scrapping every 24 to 48 hours Treatment is required for 4 6 weeks TreatmentSub-conjunctival injection of Miconazole 5 10 mgm of 10 mgm/ml suspension (indicated in severe form of keratitis, scleritis and endophthalmitis) Systemic: Fluconazole or Ketoconazole is indicated in severe form of keratitis, scleritis and endophthalmitisViral KeratitisHerpetic epithelial keratitis may occur unilaterally or bilaterally (most often in patients with atopic disease) and may be accompanied by a blepharoconjunctivitis, involving lesions of the lid and a follicular response of the conjunctiva. In addition, a palpable preauricular lymph node may be present17Risk factorRisk factors for development of primary HSV involve direct contact with infected lesions, but also may result as exposure to asymptomatic viral shedding. Risk factors for reactivation of disease have been postulated to include sunlight, trauma, heat, menstruation, stress, infectious disease and immunocompromised states. Herpes Simplex KeratitisEpidemiology- 90% of the population are carriers of HSV- corneal infection is always a recurrence

Symtomps: - very painful, photophobia, lacrimation, and swelling of the eyelids-vision may be impaired

19Forms of herpes simplex keratitisDendritic keratitis (epithelial cell)Stromal Keratitis diskiform corneal infiltratesAcute retinal necrosis syndrome Involvement of the posterior eyeball20Treatmentepithelial keratitis : topical antivirals, gentle wiping dbridement Stromal/Endothelial Keratitis : antiviral prophylaxis

Herpes Simplex Keratitis

Herpes Simplex Keratitis

23Herpes Zoster Keratitisendogenous recurrence of chickenpoxaffected the ophthalmic division of the trigeminal nerveSign and symtomps: red eyewith dendritic keratitis, stromal keratitis, and keratouveitis), Hutchinsons sign, Corneal sensitivity is usually decreased or absentTreatment

Acanthamoeba KeratitisAcanthamoeba is a free-living protozoan that thrives in polluted water containing bacteria and organic material.usually associated with soft contact lens wear, including silicone hydrogel lenses, or overnight wear of rigid (gas-permeable) contact lenses to correct refractive errors (orthokeratology)

Acanthamoeba KeratitisAcanthamoeba KeratitisAcanthamoeba is a free-living protozoan that thrives in polluted water containing bacteria and organic material. Corneal infection with acanthamoeba is usually associated with soft contact lens wear, including silicone hydrogel lenses, or overnight wear of rigid (gas-permeable) contact lenses to correct refractive errors (orthokeratology). It may also occur in noncontact lens wearers after exposure to contaminated water or soil.The initial symptoms are pain out of proportion to the clinical findings, redness, and photophobia. The characteristic clinical signs are indolent corneal ulceration, a stromal ring, and perineural infiltrates, but patients often present with changes confined to the corneal epithelium. The diagnosis is established by culturing on specially prepared media (nonnutrient agar with an overlay of E coli). Better specimens are obtained by corneal biopsy than corneal scrape, since histopathologic examination for amebic forms (trophozoites or cysts) can also be undertaken. Impression cytology and confocal microscopy are newer diagnostic techniques. Contact lens cases and solutions should be cultured. Often the amebic forms can be identified in the contact lens case fluid.The differential diagnosis includes herpetic keratitis, with which it is frequently confused, fungal keratitis, mycobacterial keratitis, and nocardia infection of the cornea.In the early stages of the disease, epithelial debridement may be beneficial. Medical treatment is usually started with intensive topical propamidine isethionate (1% solution) and either polyhexamethylene biguanide (0.010.02% solution) or fortified neomycin eyedrops (Tables 61 and 62). Acanthamoeba species may have variable drug sensitivities and may acquire drug resistance. Treatment is also hampered by the organisms' ability to encyst within the corneal stroma, necessitating prolonged treatment. Topical corticosteroids may be required to control the associated inflammatory reaction in the cornea.Keratoplasty may be necessary in advanced disease to arrest progression of the infection or after resolution and scarring to restore vision. Amniotic membrane transplants may be helpful for persistent epithelial defects. If the organism reaches the sclera, medical and surgical treatments are usually fruitless.

26symptomThe initial symptoms: pain out of proportion to the clinical findings, redness, and photophobiaclinical signsindolent corneal ulcerationa stromal ring perineural infiltratesoften present with changes confined to the corneal epithelium

characteristic clinical signs are indolent corneal ulceration, a stromal ring, and perineural infiltrates, but patients often present with changes confined to the corneal epithelium28Epithelial ridges seen in Acanthamoeba keratitis

Perineuritis seen in Acanthamoeba keratitis

Nonspecific infiltration of the corneal stroma caused by Acanthamoeba infection.

differential diagnosisherpetic keratitis, with which it is frequently confusedfungal keratitismycobacterial keratitisnocardia infection of the cornea.The differential diagnosis includes herpetic keratitis, with which it is frequently confused, fungal keratitis, mycobacterial keratitis, and nocardia infection of the cornea.

32treatmentIn the early stagesepithelial debridementMedical treatment topical propamidine isethionate (1% solution) polyhexamethylene biguanide (0.010.02% solution) fortified neomycin eyedrops

PS. may have variable drug sensitivities and may acquire drug resistance, also hampered by the organisms' ability to encyst within the corneal stroma

In the early stages of the disease, epithelial debridement may be beneficial. Medical treatment is usually started with intensive topical propamidine isethionate (1% solution) and either polyhexamethylene biguanide (0.010.02% solution) or fortified neomycin eyedrops (Tables 61 and 62). Acanthamoeba species may have variable drug sensitivities and may acquire drug resistance. Treatment is also hampered by the organisms' ability to encyst within the corneal stroma, necessitating prolonged treatment. Topical corticosteroids may be required to control the associated inflammatory reaction in the cornea.

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