Asteatotic eczema
Salient features
·
Dry, rough, scaly and inflamed skin with superficial cracking
that resembles a “dried riverbed”
·
Sites of predilection are the shins, arms and hands but
also the trunk
·
Associated with aging, xerosis, low relative humidity, and
frequent bathing
Introduction
Asteatotic eczema is a common pruritic
dermatitis that occurs especially in older persons during winter living in
rooms with a high environmental temperature and low relative humidity.
Asteatotic eczema can occur in anyone
with very dry skin.
Dry skin
(xerosis, asteatosis) may result from both exogenous and endogenous causes: a
dry climate or low indoor humidity; excessive exposure to water, soaps and
surfactants; marasmus and malnutrition; renal insufficiency and hemodialysis;
and heritable conditions such as ichthyosis vulgaris and atopic dermatitis. The
most common cause of xerosis is aging. Rarely, but especially when widespread
and refractory to therapy, asteatotic eczema may be related to an underlying
systemic lymphoma.
Epidemiology
Age
Elderly
people over the age of 60 years are predominantly affected and prevalence
increases with increasing age.
Pathogenesis
Xerosis
of aging skin is not caused by deficient sebum production, but by a complex
dysfunction of the stratum corneum. The condition is thought to be due to a
decrease in skin surface lipid. There is a decrease
of intercellular lipids with a deficiency of all key stratum corneum
lipids and an altered ratio of fatty acids esterified to ceramide 1; this,
plus a persistence of corneodesmosomes and premature expression of
involucrin and formation of the cornified envelope, results in corneocyte
retention and marked impairment of barrier recovery. The water-binding capacity
of the stratum corneum layer is reduced owing to decreased synthesis of
“natural moisturizing factor” (NMF), which contains urea and degradation
products of filaggrin. Consequently, the stratum corneum desiccates, loses its
pliability and forms small cracks, which render the skin surface dull, rough
and scaly.
Mild xerosis is asymptomatic, but
if more pronounced, the skin conveys unpleasant sensations such as itching and
stinging. Inflammation is enhanced by the release of proinflammatory cytokines
secondary to barrier perturbation, mechanical factors (scratching, rubbing),
and the application of irritating or sensitizing substances in topical
preparations and skin care products.
Occasionally, eczema craquelé can appear in the setting of acute
edema, e.g. from congestive heart failure or the re-feeding of patients with
anorexia nervosa. One theory is that this is related to the rate of distention
of the skin.
Clinical Features
Itching in this form of eczema is often intense, and worse
with changes of temperature, particularly on undressing at night. Asteatotic
eczema usually affects the legs, arms and hands but also the trunk of elderly people in the context of dry skin. Xerosis first
arises on the shins. Xerotic skin is dry, dull, with fine bran-like scales
which may be released as powdery clouds when patients take off their stockings and show accentuation
of the skin lines. Excessive drying on the
lower legs may eventually become so severe that red plaques with long, horizontal superficial fissures of the horny layer appear. The fissures
eventually develop a cracked porcelain or “crazy paving” pattern when short
vertical fissures connect with the horizontal fissures. The term eczema craquelé“or dried riverbed” is
appropriately used to describe this pattern. The skin
becomes rough, and it may develop an appearance similar to ichthyosis vulgaris
(“pseudo-ichthyosis”). In some
patients the fissures may become hemorrhagic. In more advanced stages of
asteatotic eczema, these horizontal
fissures become deep and wide and acute eczematous
lesion finally develops with oozing, crusting and abundant
excoriations.
The surface of the backs of the
hands is marked in a criss‐cross
fashion. The finger pulps are dry and cracked, producing distorted prints and
retaining a prolonged depression after pressure (‘parchment pulps’).
Complications and co‐morbidities
As
with all forms of eczema, secondary infection may occur due to a reduction in
skin barrier function. Like other forms of eczema on
the lower
leg,
it can eventually result in widespread secondary disseminated eczema
(autosensitisation).
Disease
course and prognosis
Without treatment, the condition is usually chronic,
relapsing each winter and clearing in the summer, but eventually becoming
permanent. Scratching, rubbing or contact irritants and sensitizers cause
further eczematous changes or spread.
Treatment
Avoid
over bathing with soap, especially tub baths and use tepid water baths
containing bath oils for hydration, followed by immediate liberal application
of emollient ointments, such as hydrated petrolatum. The patient's immediate environment may need
to be adjusted. Central heating should be humidified where possible by
increasing the ambient humidity to > 50%, by using room humidifiers and
abrupt temperature changes should be avoided. Wool is usually poorly tolerated
and possibly damaging due to irritation. Soap substitutes should also be prescribed to
reduce irritation from soap.
Asteatotic eczema usually clears
within a few days of the application of topical corticosteroid ointment. Weak
topical corticosteroids are often prescribed, and those contained in a urea
base are very appropriate in this situation as urea encourages hydration.
Proper attention must be given to the care of xerosis in
order to avoid relapses: regular use of emollients, including petrolatum-,
urea-, ceramide- or lactic acid-containing preparations and the elimination of
factors that aggravate dry skin. Topical calcineurin inhibitors have also been
used.
Treatment ladder
First line
·
Humidify environment and avoid
sudden temperature changes
Second line
·
Emollients, with or without urea,
and soap substitute
Third line
·
Mild topical corticosteroids; pimecrolimus 1% cream to be effective after 4
weeks of treatment
