Skin Disorders Guide

Diagnostic Hallmarks

1. Distribution: areas of solvent exposure or maceration (weak irritant), areas conforming to patient history of specific contact (strong irritant)
2. Discontinuation of exposure leads to improvement

Presentation

The relatively common problem of irritant contact dermatitis occurs because of environmental damage to the outer layers of the epidermis. Two types of irritant contact dermatitis are recognized that resulting from strong irritants and that resulting from weak irritants.

Strong-irritant contact dermatitis occurs after a single exposure and a short latent period. Because of the direct connection between the exposure and the reaction, patients can usually identify the cause with little difficulty. Examples of strong irritants include chemicals that markedly change pH (acid and alkali “burns”) or temperature (thermal burns and frostbite). Sunburn can also be conceptualized as a strong-irritant contact dermatitis, The reactions caused by strong irritants are characterized by inflammation, pain, and epithelial disruption. The latter often occurs in the form of skin necrosis. The relative lack of pruritus and scale formation often results in an appearance that meets the morphologic requirements of the eczematous group only because of fissuring and other erosion formation.

Weak-irritant contact dermatitis requires multiple exposures and, consequently, is associated with a long latent period. Because of this latency, the connection between the exposures and the reaction is often not apparent to the patient.

Fortunately, only one environmental modification (that of a change in moisture content of the skin) accounts for the majority of problems. This change in moisture content results in skin that is too dry (xerosis) or too wet (maceration). Thus, on the one hand, solvents (of which detergents and hot water exposure are the most common) dry the skin by removing the lipid layer on the outer surface of the epidermis. Without a normal lipid layer the superficial epidermal cells lose moisture because of evaporative loss, and the cells then shrink in size. This shrinkage leads to cell separation with resultant cracking and fissuring. When the fissures are very shallow and are noninflammatory, the process is known as chapping or xerosis. When the fissures are deeper and are accompanied by inflammation, the process is appropriately called irritant contact dermatitis or xerotic eczema.

Weak-irritant contact dermatitis is associated with dusky redness and mild to moderate scale formation. The skin looks taut and shiny; it feels dry and rough on palpation. Weeping, crusting, and excoriation are usually not prominent.

Irritant contact dermatitis from solvent exposure occurs mostly on the hands. A history of excess solvent exposure can usually be elicited. Alternatively, in the process known as maceration, the constant entrapment of too much fluid (water, sweat, urine, etc.) against the skin results in over hydration, swelling, and eventually epidermal cell death.

Irritant contact dermatitis from maceration is suggested by localization of the eczematous process to the feet or to intertriginous areas. When maceration is mild and is unaccompanied by evidence of epithelial disruption, the process is known as intertrigo. When the inflammation of intertrigo is acompanied by epithelial disruption (weeping or yellow scale) the term “irritant contact dermatitis” can be used. When maceration occurs intermittently rather than constantly, the picture becomes more like that seen with excess solvent exposure. The shiny, dry, cracked appearance of the toes in tennis shoe foot” and the fingers in patients with hyperhidrosis represents good examples of this phenomenon.

The diagnosis of either type of irritant contact dermatitis is made clinically; proof of the correct diagnosis requires resolution of the disease following removal of the irritant or modification of the suspected environmental factors.

Course and Prognosis

Removal of the offending environmental irritant is usually all that is needed to end the episode of dermatitis. In most cases this is easy to do, but in other instances (notably hand eczema resulting from solvent exposure and diaper dermatitis resulting from urine retention) it may be quite difficult. In such situations the addition of topically applied steroids will also be necessary. Finally, in some cases the itch-scratch cycle will become superimposed on the irritant contact dermatitis. Failure to end the scratching results in continuation of eczematous disease, even though the environmental factors are suitably modified.

Pathophysiology

In most cases of strong-irritant contact dermatitis, damage is caused because of a direct destructive effect on the exposed epithelial cells. In weak-irritant contact dermatitis the damageis done more indirectly. Epithelial cells, like cells elsewhere in the body, require a certain moisture content for health and function. Loss of moisture (solvent action) or the presence of excess moisture (maceration) eventually results in cell death. In all instances of irritant contact dermatitis, epithelial cell death leads to exposure of cutaneous nerve endings and the conveyance of burning, tingling, or itching to the central nervous system. If the itching sensation is translated into scratching (such as often happens in atopic individuals), prolongation and worsening of the epithelial damage can be expected.

Weak-irritant contact dermatitis, is most often caused from excess exposure to the solvent action of soap and water. Our hands will generally tolerate about 5 soap and water exposures! day. Five to ten exposures will result in mild chapping that can be controlled by lubrication. More than 10 exposures!day (a level frequently reached by housewives and mothers) will result in more severe damage, with superimposition of inflammatory changes against a background of cracking and fissuring. The skin over the rest of our body is not as resistant. Bathing twice a day leads to mild xerosis; more frequent bathing frequently results in the development of inflammatory changes also.

The deleterious effect of maceration is harder to quantitate. Skin of the groin and feet tolerates entrapment of moisture for several hours quite well, but exposures longer than this (as with chronically wet diapers or chronic hyperhidrosis of the feet) result in the appearance of eczematous disease.

Less often, weak-irritant contact dermatitis develops as a result of direct, repetitive mild trauma. Thus, constant handling of rough materials, such as stone or brick, or repeated wiping of the hands because of wet work will eventually cause the hands to become eczematized. This trauma causes direct damage to epithelial cells, but it also causes removal of the protective lipid layer, as occurs in solvent exposure.

Therapy

The first step in the treatment of contact dermatitis is the removal of the offending contactant. Of course to do this, the correct contactant must be identified. In instances of irritant contact dermatitis this is generally not too difficult, since a reasonably accurate history regarding solvent exposure, moisture entrapment, and mechanical trauma can usually be obtained. In an industrial setting this may be somewhat more difficult, but even here the number of possible solvents can usually be narrowed down to a few prime suspects.

In all instances the use of soap and detergents should be minimized. Bath oils or Cetaphil can be used instead of soap and washing, and the skin can be patted, rather than rubbed, dry. The temperature of wash water can be decreased. In situations of maceration, wet clothing (stockings, diapers, etc.) can be changed frequently and nonporous items of clothing made of nylon, plastic, or rubber can be avoided.

Once the environment has been modified, the second step is to restore a protective lipid layer. This is carried out through the application of lubricants as these emollients need to be applied frequently (4 to 6 times/ day), but some care should be taken in treating intertriginous areas such that excess sweat is not trapped.

Topically applied steroids may or may not be necessary. Generally, if itching is present or if more than a minimal degree of inflammation is present, their use is desirable.