Current and Upcoming Therapies for Ocular Surface Chemical Injuries

Alireza Baradaran-Rafii, Medi Eslani, Zeeshan Haq, Ebrahim Shirzadeh, Michael J Huvard, Ali R Djalilian, Alireza Baradaran-Rafii, Medi Eslani, Zeeshan Haq, Ebrahim Shirzadeh, Michael J Huvard, Ali R Djalilian

Abstract

Chemical injuries frequently result in vision loss, disfigurement, and challenging ocular surface complications. Acute interventions are directed at decreasing the extent of the injury, suppressing inflammation, and promoting ocular surface re-epithelialization. Chronically, management involves controlling inflammation along with rehabilitation and reconstruction of the ocular surface. Future therapies aimed at inhibiting neovascularization and promoting ocular surface regeneration should provide more effective treatment options for the management of ocular chemical injuries.

Keywords: chemical burn; cornea; limbal stem cell deficiency; ocular chemical burn; ocular surface; stem cell.

Conflict of interest statement

The authors have no commercial or proprietary interest in any concept or product discussed in this article.

Copyright © 2016 Elsevier Inc. All rights reserved.

Figures

Figure 1
Figure 1
Eye after combined chemical and thermal injury to the lids and ocular surface due to an explosion of a pyrotechnic device. There is total corneal epithelial defect and 360°limbal ischemia (Roper-Hall grade IV and Dua’s grade VI).
Figure 2
Figure 2
Algorithm for the management of acute phase after chemical burn.
Figure 3
Figure 3
Severe corneal thinning after severe chemical burn.
Figure 4
Figure 4
Algorithm for the management of chronic phase after chemical burn.
Figure 5
Figure 5
Symblepharon: Severe symblepharon formation.
Figure 6
Figure 6
A: Nasal and temporal pseudopterigia in a case with partial limbal stem cell deficiency due to severe alkaline chemical burn. B: Total LSCD in a case with severe chemical burn.
Figure 6
Figure 6
A: Nasal and temporal pseudopterigia in a case with partial limbal stem cell deficiency due to severe alkaline chemical burn. B: Total LSCD in a case with severe chemical burn.
Figure 7
Figure 7
Upper lid entropion and trichiasis in a case with total LSCD due to severe alkaline chemical burn.
Figure 8
Figure 8
Patient with total LSCD after chemical burn who was successfully treated with CLAU (2 years after surgery).
Figure 9
Figure 9
Keratolimbal allograft surgery in a case with total limbal stem cell deficiency due to acidic chemical burn.
Figure 10
Figure 10
Patient with total LSCD after chemical burn who underwent KLAL and PKP with systemic immunosuppression (18 months after surgery).
Figure 11
Figure 11
Boston Type I keratoprosthesis in a patient with LSCD due to chemical injury (Courtesy of Dr. Maria S. Cortina, University of Illinois at Chicago).

Source: PubMed

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