Asteatotic Eczema 

Updated: Aug 07, 2019
Author: Christina K Anderson, MD; Chief Editor: William D James, MD 

Overview

Background

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 the following four 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

Pathophysiology

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. Areas of hypoesthetic skin, such as scar tissue, may be predisposed to developing asteatotic eczema.[2]

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.[3] 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.

Etiology

Overwhelmingly the following are the most frequent contributors to asteatotic eczema:

  • Xerosis and friction
  • Frequent or prolonged bathing in hot water, use of soap on the involved site, and infrequent use of emollients for water retention in the stratum corneum
  • Degreasing agents - Solvents, cleansers
  • Decreased sebaceous and sweat gland activity in elderly persons
  • Low environmental humidity and cold winds that increase the loss of water by convection
  • Atopy
  • Ichthyosis

Multiple more uncommon etiologic factors may coexist to cause asteatotic dermatitis, including the following:

  • Decreased keratin synthesis in elderly persons
  • Radiation
  • Long-term malabsorption of essential fatty acids, including linoleic acid and linolenic acid
  • Nutritional deficiencies - Zinc deficiency [4] ; essential fatty acid deficiency, such as linoleic acid deficiency or linolenic acid deficiency
  • Thyroid disease - Myxedema and other thyroid diseases with diminished sweat and sebaceous gland activity [5]
  • Neurologic disorders - Decreased sweating in denervated areas
  • Drugs - Antiandrogen therapy [6] and diuretic therapy
  • Malignancies - Malignant lymphoma, [7] gastric adenocarcinoma, [8] glucagonoma, angioimmunoblastic lymphadenopathy, [9] breast cancer, large-cell lung carcinoma, and colorectal carcinoma [10]

Epidemiology

Frequency

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.

Sex

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

Age

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

Prognosis

Asteatotic dermatitis responds well to therapy; however, if the causative factors are not eliminated, recurrences are common. Although most cases resolve without ill effects, asteatotic dermatitis can be chronic with relapses frequent during the winter months and during times of low humidity.

Patient Education

For patient education resources, visit the Skin, Hair, and Nails Center. Also, see the patient education article Eczema.

 

Presentation

History

During the winter months, an elderly person classically presents with pruritic and dry skin with dermatitis on the pretibial areas. Sometimes, the dysesthesia may be described as a pinprick or biting sensation.

Asking the patient about pertinent controllable factors, such as the following, is important:

  • Frequency of bathing, showering, and cleansing, and which soaps and cleansers are in contact with the skin

  • Types of skin lubricants used, and method and frequency of application

  • Diet

  • Medications

  • Types of clothing worn (Wool may cause irritation.)

  • The source, the type, and the temperature of heat that may alter the humidity of the environment

If the eruption persists despite therapy, behavioral changes, and treatment compliance, allergic contact dermatitis and irritant contact dermatitis and internal malignancy may require investigation.

Physical Examination

Primary lesions

Slightly scaly, inflamed, curvilinearly cracked and/or fissured skin most commonly involves the pretibial areas, but it may also occur on the thighs, on the hands, and on the trunk (see image below).

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

Secondary lesions

Excoriated, erythematous, edematous patches may result from rubbing or scratching.

Bleeding fissures secondary to the disruption of dermal capillaries have been described in exaggerated eczema craquelé, which begins as superficial cracks in the epidermis.

Generalized lesions

Generalized or extensive asteatotic dermatitis presents with primary lesions and secondary excoriations (see images below).

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

DDx

 

Workup

Laboratory Studies

Appropriate laboratory studies are indicated for identified or suspected associated diseases.

Histologic Findings

Spongiosis and a varying amount of inflammatory dermal infiltrate similar to that of mild, subacute eczema are seen.

 

Treatment

Medical Care

Patients should follow the methods listed below to improve the condition.[11]

Eliminate or reduce the use of soap on the involved areas; use only in the perineum and axillae.

Avoid harsh skin cleansers.

Apply petrolatum-based emollients following bathing, and use moisturizing agents liberally.

Apply topical steroid ointments with or without polyethylene occlusion. Note that steroids can thin the cutaneous barrier and lower the threshold for further insults that lead to dermatitis, especially in elderly patients.

Use humidifiers.

For particularly inflamed or severe disease, soaking and smearing may be instituted for 1-2 weeks to gain control of the condition.[12]

 

Medication

Medication Summary

Topical steroid ointments with 24- to 48-hour occlusion with polyethylene or Unna boots are the treatment of choice for the rapid resolution of asteatotic dermatitis.[13] Unna boots with steroid cream or ointment add to therapeutic efficacy and ease of care, especially in the nursing home population. Boots can be left intact usually for 3-5 days. Many patients heal with mild topical steroids (class III-VI) alone, depending on the severity of the dermatitis, the patient's compliance with treatment, and the reduction in the use of soap and hot water to the involved areas. Several studies have reported on the successful use of pimecrolimus or tacrolimus cream in conditions other than atopic dermatitis, including seborrheic dermatitis and asteatotic eczema, among others. However, more research is needed to clarify the role of topical calcineurin inhibitors in treating these other disorders.[14, 15, 16]

The liberal use of moisturizers, especially petrolatum-based preparations, alone or in combination with topical steroids for mild cases of asteatotic dermatitis is recommended.

The soak-and-smear method of hydrating the skin by bathing or soaking the affected area followed by immediate application of steroid ointment once daily has been shown to clear more that 90% of patients in 4-14 days. This is best performed at night.[12]

Note that steroids can thin the cutaneous barrier and lower the threshold for further insults that lead to dermatitis, especially in elderly patients.

Topical steroids

Class Summary

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body's immune response to diverse stimuli.

Triamcinolone (Aristocort)

Triamcinolone is for inflammatory dermatosis responsive to steroids; it decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability. Triamcinolone is available in ointment (0.1%) and cream (0.025%, 0.1%, 0.5%).

 

Questions & Answers