Purpose. To study changes in astigmatism throughout a 20-year period using keratometry and refraction in patients who underwent penetrating keratoplasty (PKP) for keratoconus.
Methods. We reviewed the charts of patients who underwent PKP for keratoconus from 1975 to 1979 and recorded preoperative refraction, stage of keratoconus, laterality of surgery, graft size, suture technique, time of suture removal, keratometry, subjective refraction at 1, 3, 5, 7, 10, 15, 20, and 25 years after suture removal, and slit-lamp findings.
Results. Eighty eyes with a mean follow-up of 20 years (range, 15–25) were included in the study. Graft size, suture technique, and time of suture removal had no significant influence on the astigmatism at the last examination. We observed a stabilization of keratometric astigmatism in the first 7 years (4.05 ± 2.29 D 1 year after suture removal, 3.90 ± 2.28 D at year 3, 4.03 ± 2.49 D at year 5, 4.39 ± 2.48 D at year 7) followed by a progressive increase from 10 years after suture removal until the last follow-up visit (5.48 ± 3.11 D at year 10, 6.43 ± 4.11 D at year 15; 7.28 ± 4.21 D at year 20, and 7.25 ± 4.27 D at year 25). The mean absolute value of the difference vector (DV) calculated by vector analysis was 7.17 ± 4.35 D (0–18.33). In 70% of cases, progression of the astigmatism was evident with mean absolute DV of 9.10 ± 3.65 D. There was a significant correlation between the preoperative and final axis of astigmatism (Pearson r = 0.39, p = 0.0008). There was also a slight positive correlation coefficient between the DV of the eyes in bilateral cases, but it was not significant (Spearman's r = 0.2226, p = 0.34). The major late slit-lamp finding was a peripheral crescent-shaped thinning at the graft-host junction with absence of Bowman's layer on histopathology.
Conclusion. In spite of refractive stability obtained during the first years after PKP for keratoconus, increasing astigmatism thereafter suggests that there is a progression of the disease in the host cornea.
Keratoconus is a noninflammatory ectatic corneal disorder characterized by localized conical protrusion and thinning of the corneal stroma. Its diagnosis is based on progressive myopic astigmatism identified by refraction, keratometry, or corneal topographic analysis. The prevalence of keratoconus has been estimated in various studies to be as high as 2.2 per 1,000 1 to as low as 4 per 100,000. 2 Several investigators have studied the association of keratoconus with disease entities such as atopy, vernal conjunctivitis, asthma, Down syndrome, and other systemic collagen diseases. 2–4 While the role of heredity has been well recognized, the mode of inheritance is yet to be established. 2,3
The earliest histopathologic change in keratoconus is the presence of fibrillations, irregularities, and interruptions in Bowman's layer. Activated stromal keratocytes and corneal epithelial cells may project into the interruptions of Bowman's layer. 2,5–8 The corneal epithelium may show loss of normal architecture, thinning, and weakened interlamellar adhesions, leading to focal stromal thinning. The proposed biochemical mechanism that brings about this ectasia is an increase in the degradative protein enzymes such as lysosomal acid phosphatase, acid esterase, acid lipase, and cathepsin B. Conversely, the inhibitors α1 proteinase inhibitor (α1 PI) and α2-macroglobulin are reduced in the basal layer of the corneal epithelium. 2,9,10
Keratoconus typically progresses during the second and third decades of life. 2,4 Initial management of keratoconus includes meticulous contact lens fitting once spectacle correction becomes inadequate for good visual acuity. Surgical alternatives such as orthokeratology, epikeratophakia, deep lamellar keratoplasty, intrastromal segments, PRK, and LASIK have been considered. 2 However, penetrating keratoplasty (PKP) remains the most accepted surgical procedure for its correction, with a 5-year graft survival ranging from 90% to 100% and graft rejection episodes occurring in about 20% to 30%. 2,11–14
It has generally been accepted that corneal ectasia in keratoconus is confined to the central cornea and that by performing PKP, the diseased tissue is excised. However, keeping in mind the latest histopathologic and biochemical findings, we tend to question why it starts in the center and whether it actually affects the entire cornea.
Cases of recurrent keratoconus after PKP have been reported over the past two decades, 4–8,15,16 but the etiology of this recurrence remains uncertain. We performed a retrospective study of keratoconus patients who underwent PKP at our institution with a minimum follow-up of 15 years to analyze the postoperative astigmatic change and its possible causes.
From Centro de Oftalmología, Barcelona, Spain.
Submitted November 13, 2002.
Revision received February 24, 2003.
Accepted March 5, 2003.
Address correspondence and reprint requests to Juan Alvarez de Toledo, M.D., Barraquer Centro de Oftalmología, Muntaner 314, 08021 Barcelona, Spain. E-mail: firstname.lastname@example.org