Sulfur mustard ocular injury

L., Kadar, T. (2002). Topical dexamycin treatment against sulfur mustard ocular injury. US Army Medical Defense Bioscience Review 221. 

The reported proportion of casualties who fully recover from sulfur mustard respiratory injury varies from over 90% (Vedder, 1925) to only 20% (Balali-Mood, 1986). Much of this variation can be explained by differences among patients and by attribution of chronic bronchitic symptoms to previous mustard gas exposure in the presence of ongoing causes such as heavy smoking. Major chronic problems such as bronchiectasis and recurrent pneumonia appear confined to casualties who had severe pulmonary infections complicating the acute injury (Urbanetti, 1988). Ocular and skin injuries generally heal completely but with the need for corneal transplantation or for skin grafting to deal with uncommon complications. 

Bahru, M., Ricketts, K., Gazaway, M., Lee, R., Sweeney, R., Brozetti, J. (2004). A comhination drug treatment against ocular sulfur mustard injury. J. Toxicol. Cutan. Ocul. Toxicol. 23(1) 65-75. 

Bossone, C., Newkirk, K., Schulz, S., Railer, R., Gazaway, M., Shutz, M., Clarkson, E., Estep, S., Subramarian, P., Castro, A. Clinkscales, J., Lukey, B. (2002). Effects of prednisolone acetate on ocular sulfur mustard injury in a rabbit model. Technical report, US Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, MD, 1-22. 

Vidan, A., Luria, S., Eisenkraft, A., Hourvitz, A. (2002). Ocular injuries following sulfur mustard exposure clinical characteristics and treatment. Isr. Med. Assoc. J. 4 511-8. 

In the conjunctiva and cornea, sulfur mustard exposure causes loosening of epithelial cells accompanied by corneal edema and opacification (Warthin Weller, 1919). Even low-dose exposure of sulfur mustard to the eyes can be incapacitating (ocular ICt5o = 50 to 100 mg-min/m3). Only limited studies of sulfur mustard-induced eye injuries in animals are available (Kadar et al., 1996 Maumenee Scholz, 1948 Warthin Weller, 1919). These suggest that the microscopic pathology is similar to most chemical injuries with the exception of acid and alkali bums. 

Schons, M., Shutz, M., Skvorak, K., Sweensy, R. and Brozetti, J. (2002), Corticosteroids offer protection against sulfur mustard induced ocular injury, presented at Bioscience Review 2002, Hunt Valley, Maryland, June 2-7, 2002, U.S. Army Medical Research and Materiel Command, U.S. Army Medical Research Institute of Chemical Defense, p. 272. 

Approximately 90% of soldiers and workers exposed to sulfur mustard in World War I initially presented with symptoms of conjunctivitis, photophobia, and blepharospasm. The subsequent injury progression was observed to follow one of three clinic trajectories (Qasses I-III), which differed based on the nature of the symptoms and the recovery time (Table 38.3) (Hughes, 1945b). Qass I injiuies occurred in 75% of those with ocular presentation, involving mild symptoms without comeal involvement... 

Kadar, T., Dachir, S., Cohen, L., et al., 2009. Ocular injuries following sulfur mustard exposure—pathological mechanism and potential therapy. Toxicology 263 (1), 59-69. 

Ruff, A.L., Jarecke, A.J., Hilber, D.J., et al., 2013. Development of a mouse model for sulfur mustard-induced ocular injury and long-term clinical analysis of injury progression. Cutan. Ocul. Toxicol. 32 (2), 140-149. 

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