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Asteatotic Eczema

  • Author: Christina K Anderson, MD; Chief Editor: William D James, MD  more...
Updated: Sep 01, 2015


First described by Brocq in 1907, using the term eczema craquelé, asteatotic dermatitis is characterized by pruritic, dry, cracked, and polygonally fissured skin with irregular scaling. It most commonly occurs on the shins of elderly patients, but it may occur on the hands and the trunk.

In 1971, Domonkos described the appearance of this dermatitis as cracked porcelain. The pattern of cracking has been likened to a crazy pavement pattern. In 1999, Fitzpatrick likened asteatotic eczema to a dried-up riverbed. According to Caplan, superficial bleeding and fissures can occur as the epidermis loses water, as it splits, and as it cracks deeply enough to disrupt papillary dermal capillaries. The inflammation can be associated with asymmetric leg edema. Eczema with increased lichenification occasionally supervenes as patients rub and scratch the pruritic areas.

The eruption can be generalized or localized. Generalized asteatosis is a distinct entity and should provoke a search for possible associated diseases. Guillet divides the localized forms into 4 types:

  • Asteatotic eczema of the lower extremities in elderly persons secondary to aging, dehydrated skin, and malnutrition
  • Cracked erythema secondary to irritant contact dermatitis from soaps or detergents
  • Eczema craquelé in areas in which corticosteroid therapy was discontinued
  • Asteatotic eczema in neurologic disorders


Initially, excess water loss from the epidermis results in dehydration of the stratum corneum with upward curling of corneocytes. The outer keratin layers require 10-20% water concentration to maintain their integrity. 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 healthy skin.[1] Elderly persons with decreased sebaceous and sweat gland activity, patients on antiandrogen therapy, people using degreasing agents, and people bathing without replacing natural skin emollients lost to bath water are at risk for asteatotic eczema.

When the stratum corneum loses water, the cells shrink. 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, increasing susceptibility to allergic contact dermatitis and irritant contact dermatitis.[2] Allergic contact dermatitis and irritant contact dermatitis may cause a persistent and possibly more extensive dermatitis despite therapy. Furthermore, low environmental humidity contributes to xerosis, creating a clinical picture of asteatotic dermatitis in some dermatologic conditions, such as atopic dermatitis.




Seasonality is prominent, and most patients present in the winter months, especially in areas where indoor humidity is decreased by heating. The frequency of asteatotic dermatitis is increased in the northern United States, particularly during the winter season.


Men older than 60 years develop asteatotic dermatitis more commonly than women.


The median patient age at presentation is 69 years. Asteatosis can also occur in young people.

Contributor Information and Disclosures

Christina K Anderson, MD Consulting Staff, Department of Dermatology, CentraCare Clinic

Christina K Anderson, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.


Susan Cooper, MB, ChB, MD, FRCP MRCGP, FRCP, Consultant Dermatologist and Honorary Senior Clinical Lecturer, Department of Dermatology, Churchill Hospital, UK

Susan Cooper, MB, ChB, MD, FRCP is a member of the following medical societies: Royal College of Physicians

Disclosure: Nothing to disclose.

O Fred Miller, III, MD Emeritus Director, Department of Dermatology, Geisinger Medical Center

O Fred Miller, III, MD is a member of the following medical societies: American Academy of Dermatology, Pennsylvania Medical Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Christen M Mowad, MD Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, Noah Worcester Dermatological Society, Pennsylvania Academy of Dermatology, American Academy of Dermatology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Abby S Van Voorhees, MD Assistant Professor, Director of Psoriasis Services and Phototherapy Units, Department of Dermatology, University of Pennsylvania School of Medicine, Hospital of the University of Pennsylvania

Abby S Van Voorhees, MD is a member of the following medical societies: American Academy of Dermatology, Women's Dermatologic Society, National Psoriasis Foundation, American Medical Association, Phi Beta Kappa, Sigma Xi

Disclosure: Received honoraria from Amgen for consulting; Received honoraria from Abbott for consulting; Partner received salary from Merck for management position; Received honoraria from Abbott for speaking and teaching; Received honoraria from Amgen for review panel membership; Received honoraria from Centocor for consulting; Received honoraria from Leo for consulting; Received none from Merck for other.

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Asteatotic dermatitis on the lower extremity.
Asteatotic dermatitis on the lower extremity.
Asteatotic dermatitis on the lower extremity.
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