Improvement of chronic corneal opacity in ocular surface disease with prosthetic replacement of the ocular surface ecosystem (PROSE) treatment

Abstract

Purpose: To demonstrate clearing of chronic corneal opacities and improvement of visual acuity with the use of BostonSight prosthetic replacement of the ocular surface ecosystem (PROSE) treatment in ocular surface disease.

Observations: We undertook retrospective analysis of the medical records of a series of patients who underwent PROSE treatment from August 2006 to December 2014. Patients were referred for ocular surface disease of various etiologies. Primary inclusion criterion was corneal opacity that improved with PROSE treatment. Patients were excluded if topical steroids or adjuvant therapy used once PROSE treatment was initiated. Underlying disease, prior treatment, clinical presentation, and clinical course were extracted from the medical record. Four patients are included in this series. There were three females and one male; median age at time of treatment initiation was 30 years (range = 0.5-58 years). Median duration of PROSE treatment at time of retrospective analysis was 3.5 years (range = 1-8 years). Two cases had corneal opacification in the context of neurotrophic keratopathy: a unilateral case due to presumed herpes simplex keratitis and a bilateral case due to congenital corneal anesthesia associated with familial dysautonomia. One case had corneal opacity from exposure related to seventh nerve palsy, and one had corneal opacification associated with recurrent surface breakdown, neurotrophic keratopathy, and limbal stem deficiency of uncertain etiology. After consistent wear of prosthetic devices used in PROSE treatment for support of the ocular surface, visual acuity improved and clearing of the opacities was observed, without use of topical steroids or adjuvant therapy.

Conclusions and importance: These cases demonstrate clearing of chronic corneal opacity with PROSE treatment for ocular surface disease. This clearing can occur with no adjuvant therapy, suggesting that restoration of ocular surface function and integrity allows for corneal remodeling.

Keywords: Corneal scar; Dry eye syndrome; Ocular surface disease; Opacity; PROSE treatment; Scleral lenses; Scleral prosthetic devices.

Fig. 1

Acute persistent epithelial defect (PED) and stromal thinning as observed in patient described in case report #1. A) PED with B) 20–30% stromal thinning in the left eye in 2006.

Fig. 2

Corneal opacity regression in a case of presumed Herpes Simplex Virus Type 1 (HSV1). A) Dense corneal opacity after persistent epithelial defect in 2007 with best corrected visual acuity (BCVA) 20/200 at baseline, and after prosthetic replacement of the ocular surface ecosystem (PROSE) treatment B) in 2010 with BCVA 20/70, C) in 2012 and, D) 2013 with BCVA 20/50 as observed in patient described in case report #1.

Fig. 3

Corneal opacity regression in a case of Familial Dysautonomia. A) Dense corneal opacity after persistent epithelial defect in 2008 at baseline, B) after 3 months of prosthetic replacement of the ocular surface ecosystem (PROSE) treatment, C) in 2010, D) in 2011 and, E) 2014 as observed in patient described in case report #2.

Fig. 4

Corneal opacity regression in a case of chronic exposure. A) Opacification and neovascularization as a result of chronic exposure in at baseline, and B) January 2014, after prosthetic replacement of the ocular surface ecosystem (PROSE) treatment, as observed in patient described in case report #3.

Fig. 5

Corneal opacity regression in a case of neurotrophic keratopathy and limbal stem cell deficiency of unknown etiology. A) Opacification and neovascularization in the left eye, at baseline November 2013, and B) January 2014, and C) May 2014 after prosthetic replacement of the ocular surface ecosystem (PROSE) treatment as observed in patient described in case report #4.