From the Department of Ophthalmology, Queen Alexandra Hospital, Portsmouth, United Kingdom.
The authors have no financial or proprietary interest in the materials presented herein.
Address correspondence to Sameer Trikha, MRCOphth, Department of Ophthalmology, Queen Alexandra Hospital, Portsmouth PO6 3LY, United Kingdom.
Primary pterygia, particularly in children, remain a poorly understood phenomenon and surgical management in cases of considerable symptomatology pose regular, and often considerable, challenges. Usually located nasally on the bulbar conjunctiva, the precise etiology of pterygia are uncertain, although ultraviolet light exposure, genetic predisposition, human papilloma virus, and chemical pollutants have been implicated as causative factors.1,2
Histologically, pterygia represent a degeneration of the conjunctival stroma with replacement by thickened, tortuous elastotic fibers.3 Activated fibro-blasts in the leading edge of these lesions invade and fragment Bowman’s layer and a variable amount of the superficial corneal stroma.3
Pterygia in children are unusual and, to our knowledge, only five cases have previously been reported.4 No specific treatment guidelines for childhood pterygia currently exist, although excision with adjunctive conjunctival autograft, shown to be effective in adults,5 would be a logical choice of treatment because histopathologically they are identical in both age groups. We describe the management of a case of childhood pterygium and discuss the possible etiology because adult predisposing factors are uncommonly encountered in this age group.
A 9-year-old boy was referred with a medial bulbar conjunctival lesion encroaching on the nasal limbus and clear cornea but not involving the visual axis (Fig. 1). His uncorrected Snellen visual acuity was 6/4 in both eyes with no astigmatic refractive error. His only symptom was progressive grittiness despite the regular use of topical lubricants. In addition, he was becoming increasingly upset at having to explain the nature of his lesion at school.
Figure 1. Nasal Pterygium Encroaching on the Cornea in the Right Eye. The Patient Complained of Significant Ocular Discomfort.
In view of his significant symptomatology, he underwent uncomplicated excision of the conjunctival lesion under general anesthetic with conjunctival autograft and was discharged with topical steroids and antibiotics in addition to his lubricants for 1 month. Review at this time showed a moderately injected intact graft with polyglactin 910 (Vicryl; Ethicon, Somerville, NJ) sutures that resolved with an additional month of topical steroid treatment (Fig. 2). Histopathologic analysis, illustrating elastotic degeneration within the subepithelial fibrous tissue from the specimen, concurred with the clinical diagnosis of pterygium (Figs. 3 and 4).
Figure 2. Inflammation of the Autograft with No Evidence of Recurrence.
Figure 3. Degeneration of Conjunctival Stroma with Thickening of Elastotic Fibers Consistent with Pterygium (Hematoxylin–Eosin, Original Magnification ×100).
Figure 4. Elastotic Degeneration Illustrated Using the Van Giesen Staining Technique, a Method to Differentiate Staining of Collagen (pink) and Other Connective Tissue (original Magnification ×100).
Six months postoperatively, the eye was white with excellent cosmesis and no evidence of recurrence (Fig. 5). He had no residual dry eye symptoms consistent with a stable tear film and no corneal stain. His vision remained intact and repeat refraction revealed no astigmatism attributable to his surgery. He was delighted to stop all lubricants.
Figure 5. The Patient Reported Significant Improvement in Symptoms. On Examination, No Signs of Recurrence Were Detected.
Pterygia are a disease of unknown origin. Childhood pterygia are rare and their presence in 12-year-old twins implies a genetic or developmental predisposition.4 The children were born at 31 weeks’ gestation, with a dichorionic, diamniotic placenta implying dizygosity. Furthermore, both twins were left eye dominant and the pterygia occurred in one twin’s right eye and the other’s left eye, with the fellow eye free of any lesions. Jensen described patients closing their nondominant eye in conditions of bright sunlight.6 By inference, ultraviolet light exposure may not be the most important causative factor because then both twins’ left eyes would have been affected.4
Similarly, early onset of pterygia has been described in children 6 and 4 years old in a Saudi Arabian family.7 Multiple attempts at surgical removal with the use of both the topical antimetabolite mitomycin C and conjunctival autograft failed to prevent recurrence. Family pedigrees of pterygia have also been reported in three generations.8 These cases question the original theory of etiology being principally degenerative.
Although there was no family history of pterygia in the current case, the possibility of an underlying genetic cause cannot be refuted. The role of herpes simplex and human papilloma virus has been questioned in pterygia formation.9 Piras et al. reported 54% of all pterygium biopsies contained human papilloma virus,2 but this was not detected in our sample using cellular localization through microscopy. However, specific polymerase chain reaction for Herpesviridae was not conducted. The patients’ family denied any previous exposure to either virus or to herbicides or pesticides, which have also been implicated in pterygia formation.2 Childhood pterygia may potentially result from a viral or environmental “trigger” involving a multi-stage process. An underlying genetic predisposition may precede this in certain cases.
The superior bulbar conjunctiva, protected from ultraviolet light exposure by the upper eyelid, remains the traditional site of harvest for conjunctival autograft. This case has demonstrated that pterygia in children appear histologically identical to their adult counterparts. Excision with conjunctival autograft of childhood pterygia, indicated in cases of significant symptomatology, visual compromise, and unacceptable cosmesis, may be a safe and effective treatment in certain patients.
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- Reid TW, Dushku N. Does human papillomavirus cause pterygium?Br J Ophthalmol. 2003;87:806–808. doi:10.1136/bjo.87.7.806 [CrossRef]
- Cameron ME. Histology of pterygium: an electron microscopic study. Br J Ophthalmol. 1983;67:604–608. doi:10.1136/bjo.67.9.604 [CrossRef]
- Bloom AH, Perry HD, Donnenfeld ED, Pinchoff BS, Solomon R. Childhood onset of pterygia in twins. Eye Contact Lens. 2005;31:279–280. doi:10.1097/01.ICL.0000165281.48056.15 [CrossRef]
- Fernandes M, Sangwan VS, Bansal AK, et al. Outcome of pterygium surgery: analysis over 14 years. Eye. 2005;11:1182–1189. doi:10.1038/sj.eye.6701728 [CrossRef]
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- Islam SI, Wagoner MD. Pterygium in young members of one family. Cornea. 2001;20:708–710. doi:10.1097/00003226-200110000-00007 [CrossRef]
- Zhang JD. An investigation of aetiology and heredity of pterygium: report of 11 cases in a family. Acta Ophthalmologica (Copenhagen). 1987;65:413–416. doi:10.1111/j.1755-3768.1987.tb07016.x [CrossRef]
- Detorakis ET, Sourvinos G, Spandidos DA. Detection of herpes simplex virus and human papilloma virus in ophthalmic pterygium. Cornea. 2001;20:164–167. doi:10.1097/00003226-200103000-00010 [CrossRef]