Medical Aspects of Chemical Warfare (2008) - The Black Vault

VesicantsabcdFig. 8-6. Transient hyperpigmentation of the injured skin is frequently observed following mustard exposure. It is causedby the collection of melanin from dead melanocytes at the base of the soon-to-desquamate epidermis and resolves whenthe involved skin desquamates. Hyperpigmentation is not dependent on the formation of bullae. (a) An Iranian casualty isshown 5 days following exposure to mustard. Note the extensive desquamation of hyperpigmented skin on his back andthe normal appearance of the underlying skin. This patient developed a profound leukopenia (400 cells per µL) and a bronchopneumoniaof 10 days’ duration. Resolution of these problems required a 5-week hospitalization. (b) A different Iraniancasualty, seen 12 days after exposure to mustard, has darkening of the skin, desquamation, pink areas showing regenerationof the epidermis, and yellow-white areas of deeper necrosis. (c) Another casualty’s blackening of the skin and beginningdesquamation of the superficial layer of the epidermis is shown 15 days after mustard exposure. Note the prominence ofthese changes in the skin of the axilla. (d) The appearance on light microscopy of a hyperpigmented area. Note the melaninin the necrotic epidermal layer, under which is a layer of regenerating epidermis.Reproduced with permission from: Willems JL. Clinical management of mustard gas casualties. Ann Med Milit Belg. 1989;3S:13,18, 29, 30.hypopigmentation can be extremely distressing topatients, because similar appearing skin changes areoften associated with diseases such as leprosy andsyphilis. Punctate repigmentation can be seen startingat and around hair follicles where the melanocyteswere not destroyed (Figure 8-7).Cytopathology. The major change at the dermalepidermaljunction, visualized by light microscopy,is liquefaction necrosis of epidermal basal cell keratinocytes(Figure 8-8). Nuclear swelling within basalcells starts as early as 3 to 6 hours after exposure, andprogresses to pyknosis of nuclei and disintegrationof cytoplasm. 31,67 The pathological process can be describedas follows (Figure 8-9 further illustrates thisprocess).By a coalescence of neighboring cells undergoingthe process of swelling, vacuolar degeneration, orhydropic degeneration (“liquefaction necrosis”) andrupture, spaces of progressively increasing size areformed. This usually involves dissolution of cells of thebasal layer, resulting in defects in the basal portion ofthe epidermis and separation of the upper layers of theepidermis from the corium. At first there are multiplefocal areas of such microvesicle formation, with septaof as yet uninvolved epidermal cells. 68,69 Progressivedissolution of the cells of such septa follows, and althoughintact or partially degenerated basal cells mayinitially remain in the floor of the microvesicles, these269