22.Holland EJ, Schwartz GS (1999) Herpes simplex virus keratitis classiÞcation and treatment. Clinical Signs Ophthalmol 14:1Ð19

23.Goldblum D, Bachmann C, Tappeiner C et al (2008) Comparison of oral antiviral therapy with valacyclovir or acyclovir after penetrating keratoplasty for herpetic keratitis. Br J Ophthalmol 92:1201Ð1205

24.Holland EJ (2003) In post-keratoplasty patients: a safer alternative to prednisolone? Data on Þle, Bausch & Lomb pharmaceuticals

4.2Descemet’s Stripping Endothelial Keratoplasty

4.2.1 Introduction

Endothelial cornea dysfunction has previously been treated with full thickness cornea transplantation. Fuchs endothelial dystrophy, pseudophakic bullous and aphakic bullous keratopathy are conditions that are the results of endothelial dysfunction.

Pseudophakic bullous keratopathy remains the leading indication for keratoplasty [1, 2]. Fuchs endothelial dystrophy is a very common indication for cornea transplant as well, with an incidence falling just behind regraft and keratoconus [1]. Fuchs endothelial dystrophy demonstrates clinical signs that range from asymptomatic cornea guttata to a decompensated cornea with stromal edema, subepithelial Þbrosis, and epithelial bullae. Onset of the condition is typically after the age of 50 and there is a female preponderance. Some cases may be sporadic but others demonstrate autosomal dominant transmission [3].

Histopathological analysis of excised corneal buttons of patients with clinically diagnosed Fuchs dystrophy demonstrates thickening of DescemetÕs membrane, multiple guttata of varying size and shape, and attenuation of the corneal endothelium [4]. Guttata are focal excrescences of altered basement membrane material synthesized by abnormal endothelial cells [5]. The histopathological changes are noted in the central cornea and underlay areas of clinical edema. The peripheral cornea is usually clear clinically and shows little histologic change [4].

Clinically, Fuchs dystrophy progresses slowly over a period of 20 or more years with the patient Þrst developing asymptomatic cornea guttata and later developing corneal edema with decreased vision and pain [6]. Symptoms usually do not appear until middle age but some pathologic studies have suggested abnormalities in endothelial function occurring early in life [6].

Traditionally, PK was the only surgical procedure available for the correction of endothelial dysfunction. Full-thickness keratoplasty for endothelial dysfunction is complicated by the same issues that complicate PK. High astigmatism, suture-related problems, and ineffective wound healing are some of these [7]. When only the posterior layers of the cornea are diseased, it