Peripheral Keratitis Research Articles

Bilateral Peripheral Infiltrative Keratitis After LASIK

PurposeTo present a case of peripheral infiltrative keratitis mimicking infectious keratitis on the flap margin and limbus, which appeared on the first postoperative day after the laser in situ keratomileusis (LASIK).MethodsA 36-year-old woman who underwent uneventful bilateral simultaneous LASIK developed multiple round infiltrate along the flap margin reaching to limbus from the 11 o'clock to 6 o'clock area in both eyes.ResultsThe flap was lifted and irrigation was performed with antibiotics. but infiltration seemed to appear again. The infiltrate was more concentrated at the periphery and was extended to the limbus. Direct smear and culture for bacteria and fungus were negative. Topical prednisolone acetate 1% eye drops was added, infiltrative condition was resolved.ConclusionsLASIK induced peripheral infiltrative keratitis, in which infectious origin was ruled out, is reported

Oculocutaneous tyrosinaemia or tyrosinaemia type 2: a case report

Oculo-cutaneous tyrosinaemia type II is an autosomal recessive disease due to an abnormality of tyrosine metabolism, probably because of a deficiency of cytoplasmic tyrosine aminotransferase. It presents as a varying association of focal palmoplantar keratosis, bilateral keratitis and mental retardation. Herein, we report an 8-year-old boy with palmoplantar hyperkeratosis with peripheral oozing and dendritic keratitis appearing after the skin lesions. There was no mental deterioration despite the long delay in diagnosis of the disorder. The diagnosis was confirmed by the presence of hypertyrosinaemia and the absence of hepatorenal lesion. The child exhibited a remarkable degree of improvement in the hyperkeratotic lesions and keratitis after the dietary modifications were instituted. In conclusion, chronic focal bullous palmoplantar hyperkeratosis along with keratitis should alert the clinician to screen for abnormal serum and/or urine tyrosine level. Awareness of the presenting signs and symptoms may speed up the diagnosis and initiation of a tyrosine and phenylalanine-restricted diet that is most efficient in improving the symptoms and preventing visual and cognitive impairment.

Peripheral Interstitial Keratitis

To report a case of peripheral interstitial keratitis in a patient with mastocytosis. Clinical case description and immunohistologic examination of biopsied ocular tissue. A 22-year-old woman with biopsy-proven urticaria pigmentosa, a subset of mastocytosis, presented with an active peripheral interstitial keratitis with vascularization associated with foreign body sensation and itching. Biomicroscopy of the cornea showed deep corneal inflammatory infiltrates and midstromal vascularization adjacent to a region of superior bulbar conjunctiva, which was mildly chemotic and inflamed. Topical mast cell stabilizers and a short course of topical steroids produced dramatic resolution of the lesion. Biopsy of the erythematous conjunctiva adjacent to the area of corneal inflammation showed the presence of mast cells. This is the first case of corneal inflammatory infiltration in a patient with mastocytosis. Therapy for this condition consists of a combination of topical mast cell stabilizers, topical steroids, and systemic antihistaminic therapy.

Bilateral Peripheral Infiltrative Keratitis After LASIK

To report a case of peripheral infiltrate between the flap edge and limbus, which appeared on the first postoperative day after laser in situ keratomileusis (LASIK). A 22-year-old man underwent uneventful bilateral simultaneous LASIK but developed a thick band of infiltrate between the flap margin and limbus extending from 2 o'clock to 9 o'clock in both eyes. The flap edge was not involved. The infiltrate was more concentrated at the periphery and faded centrally and progressed diffusely into the interface leading to typical diffuse lamellar keratitis. The infiltrate responded to topical prednisolone acetate 1% eye drops. This entity was referred to as LASIK-induced bilateral peripheral infiltrative keratitis with a probable immune-mediated etiology.

Nodular scleritis and panuveitis with erythema elevatum diutinum

PurposeTo report a case of nodular scleritis and panuveitis associated with erythema elevatum diutinum, a rare immunocomplex-mediated skin disease. DesignObservational case report. MethodsA 22-year-old woman who was diagnosed with erythema elevatum diutinum developed nodular scleritis and panuveitis of the right eye. She had experienced peripheral ulcerative keratitis with corneal perforation. ResultsAll other known causes of nodular scleritis and panuveitis were investigated and ruled out. ConclusionsErythema elevatum diutinum should be considered as an underlying systemic disease associated with nodular scleritis and panuveitis as well as peripheral keratitis.

Peripheral keratitis associated with erythema elevatum diutinum

PurposeTo describe a case of peripheral keratitis associated with erythema elevatum diutinum (EED), an unusual immune-complex-mediated cutaneous vasculitis. DesignObservational case report. MethodsA 25-year-old man who was diagnosed 15 months previously with erythema elevatum diutinum presented with an inflammatory peripheral keratitis of the left eye. ResultsSerologic investigations for systemic disorders associated with vasculitic peripheral ulcerative keratitis were unremarkable. As the sclerokeratitis was thought to represent an ocular extension of the patient’s cutaneous vasculitis, dapsone therapy was initiated and resulted in a rapid response of both the cutaneous and the ocular inflammation. ConclusionsErythema elevatum diutinum should be included in the differential diagnosis of vasculitic peripheral keratitis.

Rhinosporidiosis and Peripheral Keratitis

Report of a case of peripheral keratitis caused by Rhinosporidium seeberi. The patient was seen in a referral practice. Corneal scraping was performed on a middle-aged female patient presenting with peripheral keratitis and progressive nasal obstruction that revealed spores suggestive of rhinosporidiosis. The patient was started on topical amphotericin B 0.15% eye drops. Ear, nose, and throat (ENT) examination showed presence of a polypoid lesion in the left nostril for which a polypectomy was performed. Histopathological examination confirmed rhinosporidiosis. Complete resolution of the keratitis was observed. Topical amphotericin B is an effective drug in the management of this condition. Keratitis secondary to rhinosporidial infection has not been described although occasional patients with limbal and scleral involvement have been reported. Corneal scraping was effective in helping us make a tentative diagnosis.

Detection of staphylococcal superantigens from contact-lens-induced inflammatory diseases.

We investigated the correlation between the production of superantigens in Staphylococcus-aureus-induced ulcer and contact-lens-induced peripheral ulcer (CLPU) and infiltrative keratitis (IK). Twenty-five S. aureus strains used in the study were isolated either from CLPU cases (six), or IK events (13) or asymptomatic eyes (six). A polymerase chain reaction (PCR) was employed to detect genes for superantigenic staphylococcal enterotoxins A-D, toxic shock syndrome toxin-1 and exfoliative toxins A and B. Reversed passive latex aggregation, enzyme-linked immunosorbent assay (ELISA) and immunoblot were used to examine the production of staphylococcal enterotoxins A-D and toxic shock syndrome toxin-1. The frequency of the superantigenic genes was not significantly different among the clinical isolates when asymptomatic isolates were compared with the strains isolated from CLPU and IK events. ELISA and immunoblot showed non-specific protein cross-reactions. The results suggest that detection of superantigenic toxin genes in ocular strains of S. aureus by PCR is a specific, sensitive, rapid and inexpensive alternative to traditional immunological assays. The role, if any, of the S. aureus superantigens in the production of CLPU/IK remains uncertain.

Suppurative keratitis caused by Streptococcus pneumoniae after cataract surgery.

Six elderly patients are described (age range 76-86 years) in whom a characteristic peripheral suppurative keratitis developed 1-36 months after uncomplicated cataract surgery. A corneal section had been used in all patients and four or five interrupted nylon sutures were present at the time of onset. Streptococcus pneumoniae was cultured from a corneal scrape in all cases. Treatment with appropriate antibiotics resulted in slow resolution though supplementary topical steroids were necessary in five of the six patients, and corneal opacification persists in all cases.

Early Corneal Findings in Cogan's Syndrome

We evaluated the ocular manifestations of Cogan's syndrome in 13 consecutive patients. The most frequent and earliest ocular finding was bilateral peripheral subepithelial keratitis consisting of faint, nummular lesions. The subepithelial keratitis was responsive to topical administration of corticosteroids. Peripheral subepithelial keratitis was seen in four patients and strongly suspected on review of history in three additional patients. Deep stromal keratitis was seen in two patients, while only one patient developed classic findings of Cogan's syndrome, ie. interstitial keratitis with vascularization. Additionally, five patients presented with noncomeal ocular inflammatory disease and deafness (atypical Cogan's syndrome). Early subepithelial keratitis in Cogan's syndrome may be mistakenly diagnosed as trival ocular inflammatory disease, and suppressed by topical corticosteroids, resulting in delayed diagnosis of Cogan's syndrome in the absence of classic corneal findings. Early diagnosis of Cogan's syndrome is important inasmuch as prompt treatment of cochlear symptoms with systemic corticosteroids may prevent or ameliorate deafness.

Ocular Chlamydial Infections

To the Editor.— The excellent article by King K. Holmes, MD, PhD, "TheChlamydiaEpidemic" (1981;245:1718), corroborates what I have long suspected. As an ophthalmologist, I find adult inclusion conjunctivitis is not at all rare if one's suspicion is high. While in training at a county hospital I saw it often and continue to see it even in private practice. Clinical features are a follicular conjunctival reaction with mucoid discharge, and sometimes peripheral corneal vascularization or keratitis (corneal erosions). The diagnosis can be confirmed by a Giemsa stain of a conjunctival scraping; in adults the inclusions typically are not seen in epithelial cells, but the distinctive presence of polymorphonuclear cells and particularly plasma cells (in the presence of the clinical follicular reaction) substantiates the diagnosis. A standard adult treatment is 500 mg of tetracycline, three times a day for three weeks. My main problem has been explaining the transmission of

MARGINAL DEGENERATION OF THE CORNEA WITH PERFORATION.

Introduction Marginal degeneration of the cornea, also identified as peripheral furrow keratitis by Gifford, 1 senile marginal atrophy by Fuchs, 2 and ectatic corneal dystrophy by Terrien, 3 is infrequently encountered in practice. Its exact incidence is difficult to ascertain as there are many clinical variants, and some of the milder cases may be easily overlooked. One unusual complication of this relatively benign disease is spontaneous perforation of the cornea. Francois 4 found this to be present in 15% of the 130 cases with this diagnosis reported in the literature prior to 1936. Recently six patients were observed in varying stages of marginal degeneration. Surprisingly, in four of these patients there was a corneal perforation evidenced either by iris incarceration in the wound and resultant pupillary distortion, or prolapse of a nubbin of iris through the perforation. Report of Cases 1. Marginal Degeneration. —Early stage, 1; age 72; white male.

MARGINAL DEGENERATION OF CORNEA

As marginal degeneration of the cornea is not rare but is being overlooked because of its mildness, it seems timely to report a case. First described by Trümpy¹in 1881 as a peculiar deformity of the cornea, it has been given a variety of names, such as peripheral furrow keratitis, by Schmidt-Rimpler,²in 1889 ; ectatic marginal dystrophy, in 1900; peripheral sclerosis and atrophy, by Fuchs,³in 1901; peripheral corneal ectasis, by Lauber,⁴in 1905, and senile marginal atrophy, by Fuchs, in 1915.^4a <h3>REPORT OF A CASE</h3> A white man aged 21 presented himself at the Research and Educational Hospitals, University of Illinois, complaining of recurring attacks of irritation and slight photophobia of the right eye for the past year and similar attacks in the left eye during the previous month. Each attack lasted a few days. <h3>History.</h3> —The history did not reveal anything relevant. The