Initially, excess water loss from the epidermis results in dehydration of the stratum corneum with upward curling of corneocytes. A significant decrease in free fatty acids in the stratum corneum is present in people with asteatotic dermatitis. Stratum corneum lipids act as water modulators and cutaneous loss of these lipids can increase transepidermal water loss to 75 times that of normal skin. When the stratum corneum loses water, the cells shrink and a significantly decreased cellular volume can stress the skin's elasticity, creating fissures. Edema in the dermis leads to additional stretch on the overlying epidermis.
Fissures rupture dermal capillaries, causing clinical bleeding.
The disruption of cutaneous integrity can result in inflammation with risk of infection. Transepidermal absorption of allergens and irritants is increased as the epidermis is damaged, thus increasing susceptibility to allergic and irritant contact dermatitis. Allergic and irritant contact dermatitis may be a cause for a persistent and possibly more extensive dermatitis despite therapy. Furthermore, low environmental humidity contributes to xerosis, creating an asteatotic dermatitis picture in some dermatologic conditions such as atopic dermatitis. The frequency of asteatotic dermatitis is increased in the northern United States, particularly during the winter season.