P. Kestelyn

Delay in diagnosis and outcome of Acanthamoeba keratitis

PurposeTo evaluate the outcome of Acanthamoeba keratitis with respect to the delay in diagnosis.MethodsA retrospective review of the records of 14 patients treated for Acanthamoeba keratitis was carried out. Delay in diagnosis was correlated with risk factors, clinical presentation, method of diagnosis, final visual acuity and need for penetrating keratoplasty.ResultsBased on the time interval between the first symptoms and the diagnosis of Acanthamoeba keratitis, it appeared that patients could be divided into two groups: an early treatment group (group I), consisting of six patients treated within 18 days of onset of symptoms, and a late treatment group (group II), composed of eight patients treated beyond that time. There were no statistically significant differences between the two groups as far as risk factors, clinical presentation, accuracy of diagnosis and method of diagnosis were concerned, although more extensive and deeper corneal involvement was noted in group II. Improvement in visual acuity following medical therapy was seen in all six patients in the early group and in three (37%) of the eight patients in the late group. One patient in group I needed urgent penetrating keratoplasty for corneal necrosis. In group II, two patients underwent penetrating keratoplasty à chaud to prevent corneal perforation and three patients needed penetrating keratoplasty to restore functional visual acuity.ConclusionA diagnostic delay of less than 18 days between onset of symptoms and start of anti-amoebic treatment results in a better final VA after medical treatment and obviates the need for urgent and elective penetrating keratoplasty.

Clinical and electrophysiological findings in autosomal dominant vitreoretinochoroidopathy : report of a new pedigree

Abstract.Purpose: To report the clinical and electrophysiological findings in a three-generation pedigree with autosomal dominant vitreoretinochoroidopathy. Methods: Sixteen members of a three-generation pedigree with autosomal dominant vitreoretinochoroidopathy were examined clinically, including measurement of the corneal diameter. In 14 persons, Goldmann perimetry, axial length determination and electro-oculography were carried out. Electroretinography, according to ISCEV standards, was performed in 11 of 12 affected persons. Results: Characteristic annular peripheral pigmentary changes were present in all affected members, as well as chorioretinal atrophy varying from a tigroid aspect to marked atrophy. Four patients presented a microcornea and shallow anterior chamber without microphthalmia. The visual fields appeared to narrow with ageing. The electro-oculography was pathological in the affected patients and normal in the unaffected. The electroretinographic amplitude responses tended to worsen with age, with maintenance of near normal latencies. Conclusion: The clinical presentation of autosomal dominant vitreoretinopathy is variable. Electro-oculography seems to be a discriminative test. The condition may be associated with anterior segment abnormalities other than presenile cataract, such as microcornea, shallow anterior chamber and angle closure glaucoma.

Let this be lattice? Dendritiform erosion in lattice dystrophy type I, a source of confusion

Lattice dystrophy type I is an autosomal dominant corneal dystrophy, which appears in the first decade of life [1, 2, 4]. Corneal involvement in lattice dystrophy type I is usually bilateral and symmetric. In the early stages, the lesions can appear as irregular, thin branching refractile lines and/or whitish, ovoid dots in the anterior axial stroma with clear intervening stroma. The lines start centrally and increase in size and number with time. They extend to the periphery and involve both the deeper and the superficial stromal tissue. The typical lattice filaments are radially oriented and branch dichotomously near their central terminations. As they overlap one another at various stromal levels, they create the typical lattice pattern. Indirect or retroillumination shows the lattice lines as refractile filaments with a double contour and a clear core. Refractile, glassy, homogeneous, discrete dots or more irregular opacities are seen with the filaments. With time, the opacities coalesce, and a diffuse groundglass haze may develop in the anterior and mid-stroma [1, 2, 4]. The predominant anterior involvement of this dystrophy commonly leads to recurrent erosions and irregularity of the epithelial surface, with accompanying visual disturbances [1, 2, 4]. Lattice dystrophy type I is a primary, localized corneal amyloidosis. Histologically, the epithelium is of variable thickness, with degeneration of the basal epithelium. The basement membrane is thickened and continuous but without normal hemidesmosomes. A variably thick, eosinophilic layer separating the epithelial basement membrane from Bowman’s layer is present and is composed of amyloid and collagen. Bowman’s membrane may be thicker or thinner than normal and is frequently fragmented in its periphery. The stroma contains large irregular deposits that distort the normal configuration of the corneal lamellae. There is a decrease in the number of keratocytes. Descement’s membrane and the endothelium are usually normal [1, 2, 4]. V. Vanlerberghe (&) S. De Craene Ph. Kestelyn Ghent University Hospital, Ghent, Belgium e-mail: vanlerbergheveerle@gmail.com