Section 8. Allergic, Eczematous, Irritant, and Light-Related Dermatoses

This condition is the most common of all pediatric dermatoses. For the majority of patients, the onset occurs during infancy. The classic clinical appearance in this age group is illustrated in Figs. 8-1, 8-2, 8-3. There are symmetrical patches of erythema, exudation, and scale involving the cheeks and chin. It is not unusual also to see widespread involvement of the trunk and extensor extremities during infancy; the diaper area is most often spared.

Figure 8-4 shows similar distribution in an older child. In this case, impetiginization may be contributing to the crusted appearance of the lesions. Pruritus is a cardinal feature of atopic dermatitis and may be evidenced in the infant by irritability, scratching, and rubbing against nearby objects. Atopic dermatitis is an inherited disorder. Children with the disease most often have a family history of the atopic diathesis (atopic dermatitis, asthma, or allergic rhinitis) and may themselves manifest asthma or allergic respiratory disease.

When the diagnosis of atopic dermatitis is in doubt, the search for associated clinical findings is often helpful. Two such near-pathognomonic cutaneous signs of atopic dermatitis are pictured here. The Dennie-Morgan line (Fig. 8-5) is a double fold under the eye, which is seen in many children with atopic dermatitis. Figure 8-6 shows another telltale sign: a fissure at the junction of the pinna of the ear and the face. Other associated findings related to atopic dermatitis include pityriasis alba (Figs. 8-16 and 8-17), keratosis pilaris (Figs. 8-46 and 8-47), lichen spinulosus (Figs. 9-56 and 9-57), and ichthyosis vulgaris (Figs. 12-1, 12-2, 12-3). Children with atopic dermatitis are also frequently noted to have hyperlinear palms and soles. Keratoconjunctivitis and cataracts may occur in the child with atopic dermatitis.

During childhood, the most common locations of atopic dermatitis are the antecubital and popliteal fossae and the posterior neck. Pictured here are children in whom the involvement is more widespread. The lesions show the characteristic erythema, oozing, and crusting of acute atopic dermatitis. This appearance correlates with the histopathology. Spongiosis and intracellular edema are cardinal features of acute lesions; chronic plaques show acanthosis and hyperkeratosis. The pathogenesis of atopic dermatitis remains a mystery. Patients with the disease seem to have altered autonomic function and increased plasma histamine levels. Many have elevated levels of IgE, but some are completely normal in this respect. Finally, there is evidence of diminished cell-mediated immunity in atopics. However, none of these observations has yet provided a basis for understanding the chronic and recurrent skin lesions of atopic dermatitis.

These are illustrations of atopic dermatitis on the elbow (Fig. 8-9) and in a popliteal space (Fig. 8-10) in a 5-year-old child. As mentioned above, the latter is a very common site for involvement in this age group. The majority of children with atopic dermatitis experience resolution of their disease and have normal skin as adults. However, the severe pruritus and the unpleasant appearance of the skin that accompany the exacerbations of this condition can be extremely troubling to the parent and child alike. The role of diet in the treatment of atopic dermatitis remains controversial. Despite evidence that some children with atopic dermatitis display a significant histamine response to some foods, it is fair to say that the majority of children with the disease do not respond to modifications of their diet. However, any foods that cause an obvious worsening of the condition should be avoided. Occasionally, food allergy in the atopic child may even be manifested by the rapid evolution of contact urticaria on the face and hands.

Figure 8-11 illustrates an area that is scaly and lichenified. Figure 8-12 shows atopic dermatitis involving one toe. The treatment of atopic dermatitis should include the establishment of a routine of skin care that maintains adequate hydration of the skin. Parents should be encouraged to apply a lubricating ointment to the child's skin several times a day. Topical corticosteroid ointments are currently the mainstay of medical management. Many children do well with proper use of the milder, nonfluorinated ointments, but some require stronger preparations for brief periods of time. The dangers of local atrophy and stria formation and of systemic absorption must be considered carefully with the use of the stronger formulations. Important adjuncts to therapy include topical calcineurin inhibitors, oral antihistamines and, occasionally, a brief course of oral antibiotics to reduce skin colonization with streptococcus and staphylococcus.

These figures show erythema and fissuring on the weight-bearing surface of the foot. This disorder, which tends to be worse in the winter months, is called juvenile plantar dermatitis. It is much more common in children with atopic dermatitis. Juvenile plantar dermatitis, which has also been called wet-dry foot syndrome, is caused by excessive sweating of the feet in occlusive footwear and rapid drying in a low-humidity environment. The use of emollient ointments is extremely helpful.

Illustrated here are fine, erythematous, and flesh-colored papules on the elbows. This pruritic eruption, also termed as summer prurigo or summertime pityriasis, occurs most commonly but not exclusively in children with the atopic diathesis. The rash is seen most frequently between the ages of 4 and 10 years and tends to recur seasonally in the late spring or early summer. Some children also have lesions on the knees and dorsa of the hands.

This is a condition that is characterized by blotchy areas of hypopigmentation with or without scale. The lesions are usually asymptomatic. In older children, the cheeks are a favored location, but in infants, the process may be more generalized. Both figures illustrate how the borders of the lesions tend to fade into the surrounding normal skin. This contrasts with vitiligo (Figs. 24-12, 12-13, 12-14, 24-15), another common cause of pigment loss. In vitiligo, the areas of involvement tend to be a whiter white and are more sharply demarcated. Pityriasis alba is more common among children with atopic dermatitis and may represent a form of postinflammatory hypopigmentation. There may or may not be a preceding inflammatory dermatosis in the same area. It is important to reassure the parent and child that the loss of pigment is temporary and that complete restoration of normal skin color will occur. The use of a mild topical steroid may speed the process.

This is a chronic, recurrent eruption of the hands and feet that is often accompanied by severe pruritus. It is considerably more common among individuals with an atopic history or with a family history of atopic disease. These photographs show a number of deep-seated vesicles and pustules on the palm and sole. Small, firm vesicles along the sides of the fingers are a particularly common clinical sign. At times, bullae may occur. Patients who develop pompholyx often tend to have hyperhidrosis of the hands and feet. Some observers note that episodes of the disease are brought on by stress. Management of this condition is best achieved by the use of drying agents and topical corticosteroid creams or ointments with or without tar.

This is a common and benign self-limited childhood dermatosis that is easily diagnosed from its classic appearance. Onset is usually between the ages of 3 and 10 years, and it is rare in young infants, adolescents, and adults. The lesions consist of pink, flesh-colored, or slightly hypopigmented flat-topped papules that evolve in a linear array following lines of Blaschko. As pictured in Figs. 8-20 and 8-21, the linear course of the papules may eventually traverse the major part of an extremity. The area of involvement is often noted to become wider as it advances and may even include the nails.

These figures demonstrate lichen striatus following Blaschko's lines on the trunk (Fig. 8-22) and face (Fig. 8-23). The lesions of lichen striatus are usually asymptomatic but may last from months to years. Postinflammatory hypopigmentation occurs following the initial inflammatory process. The etiology of the condition is unknown. Treatment is not strictly necessary, but mild topical steroids tend to speed the process of resolution.

This condition is a T cell-mediated delayed hypersensitivity response to a variety of different antigens. Acute lesions are characterized by erythema, vesiculation, and oozing, whereas chronic areas of involvement may be dry and lichenified. The diagnosis of allergic contact dermatitis is a simple one when there is a clear history of exposure to an allergen or when the distribution of the lesions provides a strong clue. At other times, the identification of the causative agent can be very difficult. A number of different plants are capable of causing contact dermatitis. By far, the most common are members of the genus Toxicodendron: poison ivy, oak, and sumac. These are illustrations of contact dermatitis from poison ivy, the most common single cause of contact dermatitis in childhood. The linear array of vesicles and bullae in Fig. 8-24 reflects the pattern in which the resin was transferred from leaf to skin. Figure 8-25 shows a more diffuse reaction. Children who experience recurrent episodes of this phytodermatitis should be encouraged to learn to recognize the causative plants.

These photographs illustrate two other common causes of allergic contact dermatitis. The young girl in Fig. 8-26 has developed an area of vesiculation and crusting because she is allergic to the nickel in her earrings. The same rash may develop under the metal buttons on blue jeans or beneath a wristwatch. Coating the surface of these metallic objects with clear nail polish will sometimes protect the skin from the allergen. In Fig. 8-27, a band of erythema and vesiculation has appeared on a thigh of a girl who has become sensitive to some component of rubber in an undergarment. Synthetic rubber contains many potential allergens, but the most common offenders are antioxidants and rubber accelerators. The treatment of allergic contact dermatitis is based on the successful identification and avoidance of the skin allergen. When the cause is not obvious, the use of a standard patch test kit may be of enormous benefit. The resolution of acute episodes of contact dermatitis is hastened by the application of topical corticosteroids; a brief course of oral prednisone is sometimes indicated in widespread disease.

The allergic contact dermatitis in this figure was caused by a sandal. Note how the eruption conforms, like a patch test, to the design of the thongs. Shoe dermatitis should be considered in any eczematous eruption on the dorsum of the foot in a child. The agent responsible for the rash in this photograph was a tanning agent or dye. The other common causes of shoe dermatitis are rubber and rubber accelerators, adhesives, and leather. If the allergen is correctly identified by patch testing, it is possible to select the footwear that is tolerable.

This picture demonstrates the use of patch testing done for determining the cause of an allergic contact dermatitis and illustrates a positive reaction in the form of vesiculation at 48 hours in a person who has been sensitized to the offending agent.

Figure 8-30 illustrates the result of sensitization to an ingredient in lipstick. Lipstick cheilitis may be caused by indelible dyes, perfumes, or lanolin derivatives. The child in Fig. 8-31 has an allergic contact dermatitis resulting from the repeated application of a preparation containing neomycin. The development or worsening of an eczematous eruption after the use of a topical medication, either prescribed or over-the-counter, should alert the physician to the possibility of a contact dermatitis (dermatitis medicamentosa). In addition to neomycin, common offenders are the stabilizer ethylenediamine and the paraben preservatives.

The development of an itchy eczematous eruption near the umbilicus is virtually pathognomonic for contact dermatitis to nickel. The source is the small metal snap in the blue jeans or the metal belt buckle. The simultaneous occurrence of an id reaction, sometimes with small lichenoid papules on the elbows and knees, is very common. Lesions can be treated effectively with topical corticosteroids, but the only cure results from strict avoidance of nickel. This is easier said than done. Parents must buy jeans without snaps or sew in a small piece of fabric to protect the underlying skin. Families should be reminded that wearing jeans with a metal snap for just several hours out of the month would reactivate the entire process. Children with contact dermatitis to nickel should also avoid metal jewelry and should be advised against ear piercing.

Allergy to nickel is one of the most common causes of contact dermatitis in children. Infants may present with skin lesions corresponding to the location of snaps on their pajamas or other garments. Older children may show reactions to watches, chains, belt buckles, or earrings.

Contact allergy to temporary tattoos has become an increasingly common phenomenon. In most cases, the tattoo material does not contain pure henna, but is a mixture of brown henna with paraphenylenediamine (PPD) called black henna. The patient is allergic to PPD in the tatto. In fact, the concentration of PPD in black henna is higher than that seen in commercial hair dyes. After resolution of the eczematous skin eruption, postinflammatory hyperpigmentation may persist for a considerable period of time.

Irritant contact dermatitis is an eczematous eruption that results from the application of an irritating substance to the skin. Examples would include strong acids or alkalis, harsh soaps, and bleaches. In these cases, Tcell–mediated allergy is not involved. The irritant in Fig. 8-37 is saliva. The child pictured here has developed a habit of licking his lips. Some children do this as compulsively as others suck their thumbs or bite their nails. Notice how the design of the inflammatory lesions conforms to the extent to which the lips can be drawn into the mouth or licked by the tongue. In Fig. 8-38, postinflammatory hyperpigmentation is shown in a child who has recovered from inflammation induced by chewing and blowing bubble gum.

Where skin is in natural apposition (for example, in the axillae, intergluteal folds, and neck folds) or where the skin is occluded, it is susceptible to the effects of wetness, higher temperature, friction, and accumulated debris. An area of slight erythema in the neck fold is illustrated here. The skin is superficially inflamed from excessive maceration of the stratum corneum, caused by retention of wetness from washing and insufficient drying or from retained sweat. Group A B-hemolytic strep and Candida albicans infections need to be considered.

The most common form of diaper dermatitis is related to the combination of moisture and friction. The result is illustrated in Fig. 8-40. Note that the areas of involvement are folds of skin that are in direct apposition to the diaper itself; the skin creases tend to be spared. The bright erythema and shiny appearance of the involved skin are typical. Rashes of this type must be differentiated from candidiasis, seborrheic dermatitis, and psoriasis.

Inflammation that results from the precipitating factors of wetness, heat, friction, and debris in intertriginous places varies directly with the intensity and duration of those precipitating factors. The inflammation may be merely a slight erythema, a tumid, beefy redness with serous exudation, or an area of ulceration. The punched-out ulcers illustrated here is typical of the erosive diaper dermatitis of Jacquet. This severe irritant dermatitis responds to the use of barrier creams, mild topical steroids, and frequent diaper changes. Evaluation for candidiasis or bacterial infection should be considered in those who do not respond to treatment.

This term refers to a granulomatous eruption of infancy that is usually confined to the diaper area but may also involve other intertriginous parts. The lesions are typically large nodules with a red or purplish hue; their alarming appearance may falsely suggest the presence of a neoplasm. The cause of this dermatosis seems to be a combination of local inflammation and, sometimes, cutaneous candidiasis. It may be aggravated by the use of fluorinated topical steroids. These lesions may persist for months. Good diaper care is essential for resolution of this condition.

This unique diaper dermatitis was originally described in the skin surrounding urostomies, but can occur as a result of chronic diarrhea (sometimes from Hirschsprung's disease), encopresis, or urinary incontinence. The flat topped or round lesions are shiny, erythematous, and moist. They resolve completely when the problem causing chronic irritation in the diaper area has been corrected.

This is an asymptomatic condition that is often familial and is sometimes associated with atopic dermatitis or ichthyosis vulgaris. Pictured here are typical lesions in the two most common areas of involvement: the lateral aspect of the upper arms and the anterior thighs. The lesions are fine keratotic papules; each represents a plug in the upper part of a hair follicle. The appearance of the involved areas is often likened to chicken skin or gooseflesh; the sensation on palpation is a grater-like roughness. Keratosis pilaris tends to worsen during the winter months and abates somewhat after puberty. Keratolytics and emollients are somewhat helpful.

Children with keratosis pilaris sometimes develop the condition's typical follicular papules on the cheeks. When this occurs, there may also be erythema associated with the roughness. This condition is sometimes termed keratosis pilaris rubra faciei. Again, mild keratolytics are sometimes helpful.

This eruption is sometimes confused with infantile acne, in which comedones are found along with papules, pustules, and sometimes cysts. The prognosis of facial keratosis pilaris is good, although this condition may persist on the extremities.

The accentuation of skin markings and fine scale illustrated here are typical of xerosis. The tendency toward dry skin tends to be inherited and is more common in families with a history of atopy. Low humidity, usually related to dry heat during the winter months, is an aggravating factor. Treatment of xerosis is aimed at rehydrating the stratum corneum. Emollients containing urea or alpha-hydroxy acids are particularly effective. Excessive bathing and the use of alkaline soaps must be avoided.

Patients being treated with naproxen may experience an eruption characterized by the development of erythema, vesicles, and shallow atrophic scars after sun exposure. In many patients, frank vesicles are not appreciated. The acute eruption may persist for a few weeks after the medication has been stopped.

Patients with this condition develop papules, papulovesicles, or erythematous plaques in response to sun exposure. The lesions erupt a few hours to several days after the subject has been exposed to sunlight. Lesions are most often located on the face, upper chest, and exposed parts of the extremities. Ocular inflammation and cheilitis may also occur. Among North American and Latin American Indians, polymorphous light eruption tends to be a familial disease with childhood onset. Figure 8-52 shows an area of erythema and edema. The butterfly rash illustrated in Fig. 8-53 gives a sense that polymorphous light eruption can sometimes be difficult to differentiate from the cutaneous findings in systemic lupus erythematosus. Both immunofluorescence and serology are useful techniques in differentiating the two diseases. Sunscreens, antimalarial medications, topical corticosteroids, and psoralens with ultraviolet light (PUVA) are among the treatments used for polymorphous light eruption.

In addition to sunburn and polymorphous light eruption, there are several other abnormal cutaneous reactions in which sunlight is a part of the causative mechanism. Among these are photoallergic (Fig. 8-54) and phototoxic (Fig. 8-55) dermatitides. In the former, sensitization and subsequent clinical reactions develop to a topically applied or internally administered substance that has been activated to allergenicity by sunlight. The topical halogenated salicylanilides are among the most common causative agents in photoallergy. In phototoxic reactivity, no immunologic mechanism is involved, and the patient reacts as anyone would to a primary irritant. Phototoxic drugs and chemicals include some dyes, coal tar derivatives, and psoralens. Drugs that may cause a phototoxic reaction include the sulfonamides, tetracyclines, and thiazides.

This condition is a special kind of photoreaction in which the skin becomes slightly inflamed and quickly develops hyperpigmentation. The cutaneous changes are the result of contact with a photosensitizing chemical, followed immediately by sunlight. The most common causative agents are furocoumarins (psoralens). These figures illustrate the form of this condition that results from the application of a psoralen-containing perfume, such as oil of bergamot. Note that the hyperpigmentation follows the exact distribution in which the perfume was applied. In addition to perfumes, a number of plants, grasses, fruits, and vegetables contain psoralen as a photosensitizer.

In addition to perfumes, a number of plants, grasses, fruits, and vegetables contain psoralen as a photosensitizer. The child who helps mother or father slice limes before a trip to the park may develop an identical eruption on the hands. Celery and parsley may present similar problems. It is important to recognize this entity since some affected infants and children have been mistakenly thought to have bruising from child abuse.

This is a rare blistering and scarring eruption of sun exposed skin. It most often occurs during childhood and resolves spontaneously over time. The itching and burning papules develop within hours after sun exposure and rapidly progress to vesicles or blisters. The eyes may also be involved with a mild keratoconjunctivitis. Sun avoidance, the proper applications of high sun protection factor (SPF) sunscreens, and sun protective clothing are strongly advised. Other light induced disorders, which may occur in childhood, such as erythropoietic protoporphyria, must be ruled out. A hydroa vacciniforme-like lymphoma may clinically resemble this entity.

This term refers to a disease with its onset in early childhood. Patients develop an intensely pruritic eruption in response to sunlight. The papules, vesicles, and crusted plaques tend to favor areas of exposed skin but may become generalized. The disease process is most severe during the late spring and summer. Illustrated in both figures is the inflammatory pruritic dermatitis on a common location, the pinnae of the ears. The relationship between the disease called actinic prurigo (or Hutchinson's summer prurigo) and polymorphous light eruption (Figs. 8-52 and 8-53) has been an area of controversy. Some observers believe that the diseases are identical, but others feel that actinic prurigo is a distinct entity. Treatment for children with this clinical syndrome consists of maximal protection from sunlight. Topical steroids are of some benefit during exacerbations.