Migratory Serpiginous Corneal Epitheliopathy
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Disease Entity
Migratory serpiginous corneal epitheliopathy (MSCE)
Disease
Migratory serpiginous corneal epitheliopathy (MSCE) was first characterized by Mohanty et al. in a case series of four patients.[1] It is characterized by typically unilateral, well-demarcated, elevated, epithelial lesions that take on serpiginous or amoeboid patterns within the interpalpebral area. Recurrence after debridement was reported, and new lesions emerged at different interpalpebral sites, prompting the term migratory.[1] Pathological samples from debrided epithelium in MSCE cases reveal no cellular atypia or dysplasia, and the conjunctiva is spared.
Etiology
Currently, the cause of MSCE is not well understood. Mohanty et al. propose that it is caused by exaggerated tissue response to trivial trauma, creating an abnormal reparative process. The serpiginous, amoeboid appearance of the lesion often raise suspicion for bacterial or viral serpiginous keratitis or ulceration; however, the original case series found no evidence of infectious organisms.[1] More recently, a case report describing a clinically similar presentation identified HSV-1 in corneal epithelial scrapings, suggesting a possible viral association in some cases.[2]
Risk Factors
Risk factors include younger age and possibly low-impact trauma to the eye. No predisposing genetic or immunological factors have been identified thus far, including no nutritional deficiencies, ocular surgery, foreign body, contact lens wear, exposure to toxic substances, diabetes, ocular cicatricial pemphigoid, or allergic disorders.[1]
General Pathology
Histopathology of tissue obtained from debridement or corneal scrapings showed folded epithelial strips with full-thickness keratinizing squamous metaplasia with parakeratosis. Further findings include intraepithelial edema with cytoplasmic ballooning and degenerative changes.[1] In the case report that identified HSV-1, histopathology showed perinuclear haloes in some epithelial cells, suggestive of viral cytopathic effects.[2] (For histopathology photos, see Reference 1, Mohanty)
Pathophysiology
The epithelial defects seen in MSCE shown on histopathology demonstrated loose epithelial cell adherence and discontinuity between the epithelial basement membrane and Bowman membrane. This finding is likely due to dysfunction in cell to cell and cell to matrix adhesion. Additionally, the delayed healing and recurrent lesions signify that, in MSCE, there is likely a defect in epithelial cell migration and proliferation.[1][3]
Diagnosis
MSCE is diagnosed clinically using a slit-lamp examination. Furthermore, MSCE is often considered a diagnosis of exclusion and requires the following information to complete the diagnosis:
History
This disease presents unilaterally in young patients 14 to 31 years of age. These patients typically experience a gradual decrease in visual acuity over four to ten weeks. Sometimes patients have been treated with antiviral medications without any symptomatic or clinical improvement. In all reported cases, patients denied any environmental exposure and any restrictions or changes in diet. Additionally, the patient may have had trivial, untreated trauma to the eye.[1]
Physical Examination
In all reported patients, a slit-lamp examination revealed a unilateral corneal lesion with greyish-white raised epithelium and a well-demarcated border in an amoeboid pattern. Minimal subepithelial haze was noted within the border of each amoeboid pattern. Moderate conjunctival congestion and serous discharge was reported. Punctate fluorescein staining was noted in a serpiginous pattern in each case. No corneal edema, infiltrates, opacities or neovascularization was observed in the area surrounding the lesion.[1] (For clinical photos, see Reference 1, Mohanty)
Symptoms
Patients present with progressive blurry vision for four to ten weeks prior to presentation. Reported symptoms include ocular irritation, redness, photophobia, foreign body sensation, and tearing. These symptoms dissipate one to eight weeks after treatment with debridement followed by a bandage contact lens for two weeks, topical lubricants and antibiotics. [1]
Clinical Diagnosis
The diagnosis of MSCE is guided by signs, symptoms, and diagnostic procedures, including slit-lamp examination, anterior segment ocular coherence tomography, and histopathological samples obtained from debridement. As this is often a diagnosis of exclusion, corneal scrapings can be used for gram stain and cultures to rule out an infectious source.
Diagnostic Procedures
Corneal scrapings can be used for gram stain and cultures. Imaging is not essential for the diagnosis, but anterior segment optical coherence tomography of affected corneas has revealed elevated hyperreflective epithelial surface lesions and no stromal involvement.[1]
Laboratory test
Gram stain and culture/sensitivity are recommended to rule out infectious etiologies.[1]
Differential diagnosis
Common corneal pathologies that could appear similar to MSCE include bacterial or viral serpiginous keratitis/ulcer, advanced wavelike epitheliopathy (AWE), corneal dysplasia, carcinoma in situ, squamous cell carcinoma, hereditary benign intraepithelial dyskeratosis, corneal pannus, corneal epithelial keratinization, contact lens-induced keratopathy, superior limbic keratoconjunctivitis, or prominent epithelial basement membrane dystrophy.[4][5][6][7][8][9][10][11][12][13][14][15]
Management
Management consists initially of a medical regimen of lubricants and antibiotics. Corneal debridement of the lesion removes the excess tissue and allows for microbiologic and histopathologic investigations. The cornea must be monitored frequently and assessed whether additional corneal debridement is necessary.[1]
Medical therapy
Reported cases of MSCE have been treated with topical lubricants and antibiotics combined with corneal debridement and bandage contact lens (BCL) placement. Mohanty et al. initially treated patients in the case series with gatifloxacin 0.5% and carboxymethylcellulose 0.5% for two weeks, and if no improvement, proceeded with corneal debridement followed by BCL placement, topical antibiotics and lubricants.[1] Time to improvement ranged from one to eight weeks. Recurrence of lesions was reported, but ultimately resolved with repeated scraping and continued topical antibiotics and lubricants. The authors also described using loteprednol etabonate 0.3% for the first 15 days of treatment to decrease ocular surface inflammation.[1] Further studies are needed to prove these effective empirical treatments. Consistent follow up during medical management is recommended, particularly to identify and treat recurrences.
Surgery
Corneal debridement may be indicated in patients with MSCE. Epithelial debridement promotes appropriate healing of the corneal epithelium with minimal scarring. Epithelial debridement is essential when lesions occur in the visual axis. A bandage contact lens should be placed after epithelial debridement to protect the healing epithelium from the microtrauma and friction resulting from blinking.[1][16][17]
Surgical follow up
After corneal debridement and bandage contact lens placement, the bandage contact lens should remain in place for two to three weeks. After this time period, bandage contact lens should be removed and the healing process observed.[1][16][17]
Complications
The known complications include corneal scarring and recurrent lesions despite aggressive treatment with corneal debridement, bandage contact lens placement, lubricant, and antibiotic eye drops.[1]
Prognosis
With treatment, the ameboid-shaped lesions commonly resolve within one month, with vision returning to baseline or near baseline.[1]
References
- ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 Mohanty A, Mittal R, Khurana A, Chanda S, Priyadarshini S, Sahu SK. Migratory serpiginous corneal epitheliopathy (MSCE)- details of 4 cases. The Ocular Surface. 2020;18(4):742-747. doi:10.1016/J.JTOS.2020.08.002
- ↑ 2.0 2.1 Shields C, Buggareddigari S, Jakati S, Basu S, Donthineni PR. Atypical Migratory Serpiginous Corneal Epitheliopathy: Unmasking Herpes Simplex Virus Association. Cornea. 2025 Aug 18. doi: 10.1097/ICO.0000000000003966. Epub ahead of print. PMID: 40823852.
- ↑ Vaidyanathan U, Hopping GC, Liu HY, et al. Persistent Corneal Epithelial Defects: A Review Article. Med Hypothesis Discov Innov Ophthalmol. 2019;8(3):163-176.
- ↑ D’Aversa G, Luchs JL, Fox MJ, Rosenbaum PS, Udell IJ. Advancing Wavelike Epitheliopathy. Ophthalmology. 2020;104(6):962-969. doi:10.1016/s0161-6420(97)30199-7
- ↑ Waring GO, Rodrigues MM, Laibson PR. Corneal dystrophies. I. Dystrophies of the epithelium, Bowman’s layer and stroma. Survey of Ophthalmology. 1978;23(2):71-122. doi:10.1016/0039-6257(78)90090-5
- ↑ Babu K, Narasimha Murthy KY, Ramachandra Murthy K. Wavelike epitheliopathy after phacoemulsification: Role of in vivo confocal microscopy. Cornea. 2007;26(6):747-748. doi:10.1097/ICO.0B013E31804F59F3
- ↑ Erdem U, Hurmeric V, Muftuoglu O, Kerimoglu H. Linear Corneal Epithelial Keratitis with a Horseshoe Pattern. http://dx.doi.org/101080/09273940701244210. 2009;15(2):131-134. doi:10.1080/09273940701244210
- ↑ Miller DD, Hasan SA, Simmons NL, Stewart MW. Recurrent corneal erosion: a comprehensive review. Clinical Ophthalmology (Auckland, NZ). 2019;13:325. doi:10.2147/OPTH.S157430
- ↑ Waring GO, Roth AM, Ekins MB. Clinical and Pathologic Description of 17 Cases of Corneal Intraepithelial Neoplasia. American Journal of Ophthalmology. 1984;97(5):547-559. doi:10.1016/0002-9394(84)90371-4
- ↑ Mas Tur V, AlMaazmi A, AlSaadi A, et al. Columnar keratopathy: An early manifestation of limbal stem cell deficiency. Journal of EuCornea. 2019;3(3-5):1-4. doi:10.1016/J.XJEC.2019.10.001
- ↑ Campbell RJ, Bourne WM. Unilateral Central Corneal Epithelial Dysplasia. Ophthalmology. 1981;88(12):1231-1238. doi:10.1016/S0161-6420(81)34867-2
- ↑ Reed JW, Cashwell LF, Klintworth GK. Corneal Manifestations of Hereditary Benign Intraepithelial Dyskeratosis. Archives of Ophthalmology. 1979;97(2):297-300. doi:10.1001/ARCHOPHT.1979.01020010149011
- ↑ Von Sallmann L, Paton D. Hereditary Benign Intraepithelial Dyskeratosis: I. Ocular Manifestations. AMA Archives of Ophthalmology. 1960;63(3):421-429. doi:10.1001/ARCHOPHT.1960.00950020423004
- ↑ Bloomfield SE, Jakobiec FA, Theodore FH. Contact Lens Induced Keratopathy: A Severe Complication Extending the Spectrum of Keratoconjunctivitis in Contact Lens Wearers. Ophthalmology. 1984;91(3):290-294. doi:10.1016/S0161-6420(84)34308-1
- ↑ Sendele DD, Kenyon KR, Mobilia EF, Rosenthal P, Steinert R, Hanninen LA. Superior Limbic Keratoconjunctivitis in Contact Lens Wearers. Ophthalmology. 1983;90(6):616-622. doi:10.1016/S0161-6420(83)34507-3
- ↑ 16.0 16.1 McGrath LA, Lee GA. Corneal epithelial debridement for diagnosis and therapy of ocular surface disease. Clin Exp Optom. 2015 Mar;98(2):155-9. doi: 10.1111/cxo.12213. Epub 2014 Oct 20. PMID: 25331183.
- ↑ 17.0 17.1 Vaidyanathan U, Hopping GC, Liu HY, et al. Persistent Corneal Epithelial Defects: A Review Article. Med Hypothesis Discov Innov Ophthalmol. 2019;8(3):163-176.
