Mustard gas keratopathy

Pleyer, U., Sherif, Z., Baatz, H., Hartmann, C. (1999). Delayed mustard gas keratopathy clinical findings and confocal microscopy. Am. J. Ophthalmol. 128 506-7. 

BlodiFC. Mustard gas keratopathy. Int Ophthalmol Clin. 1971 Fall ll(3) l-13.) ... 

Baradaran-Rafii, A., Javadi, M.A., Rezaei Kanavi, M., et al., 2010. Limbal stem cell deficiency in chronic and delayed-onset mustard gas keratopathy. Ophthalmology 117 (2), 246-252. 

Jafarinasab, M.R., Zarei-Ghanavati, S., Kanavi, M.R., et al., 2010. Confocal microscopy in chronic and delayed mustard gas keratopathy. Cornea 29 (8), 889-894. 

McNuth P., Lyman, M., Swartz, A., et al., 2012b. Architectural and biochemical ejqjressions of mustard gas keratopathy precUnical indicators and pathogenic mechanisms. PLoS One 7 (8), e42837. 

The eyes are the organs most sensitive to SM injury. Acute effects are conjunctivitis, with dry eye, pain and photophobia. More than 60% of eye injuries recover and vision is restored. The remaining patients develop chronic or delayed-onset mustard gas keratopathy (MGK). Khateri et al (2003) reported that 35% of injured veterans had mild ocular injury (dry eye, conjunctival scarring and decreased visual acuity) and 3.6% had moderate injury that included some corneal involvement. Severe symptoms were described in fewer than 1% of patients. MGK is characterized by chronic blepharitis, meibomian gland dysfunction, dry eye, perilimbal conjunctival ischemia. 

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