Acute Dermatologic Complaints

Herschel R. Lessin MD, FAAP

Pradeep Sharma MD

Urticaria and Angioedema

INTRODUCTION

Urticaria, commonly known as hives, consists of episodic pruritis with swelling of the skin as a result of histamine release from mast cells in the epidermis. In angioedema, the mast cells involved lie in the dermis. In this instance, histamine release leads to a more localized swelling, which is not itchy or only mildly itchy.

PATHOPHYSIOLOGY

The pathology of urticaria and angioedema varies with etiology. Urticaria is an acute vasodilatory response to an insult. The characteristic wheal arises from the increased vascular permeability of this vasodilatory event. When swelling is more diffuse, widespread, and accompanied by deeper tissue involvement, the process is described as angioedema. Histamine release from mast cells underlies the swelling.

In allergic urticaria, histamine (and, to some extent, bradykinin) is activated by an IgE-mediated degranulation of mast cells. This degranulation is an allergic response to an antigen to which the child has been previously sensitized (Friedmann, 1999).

Urticaria can also occur without antigenic stimulation. In these cases, mast cells will release histamine spontaneously (twitchy mast cell syndrome), as seen in patients with physical urticaria. Inflammatory cells, including eosinophils, monocytes, and neutrophils, are not prominent in acute urticaria. These cells can be seen in patients with chronic urticaria who may also exhibit signs of vasculitis.

Immunogenic Urticaria

Hives caused by immunologic reactions can be further classified using the traditional Bell and Combs method for classification of allergic reactions.

Type 1 hypersensitivity reaction. This involves the IgE antibody. When exposed to antigens to which they were previously sensitized, allergic individuals may develop urticaria of varying intensity. Type 1 reaction is often associated with other signs of an acute allergic reaction, including wheezing, sneezing, and acute anaphylaxis. The most common etiology in pediatrics is an allergic reaction to hymenoptera, foods, drugs, or exposure to animal dander or saliva. See Chapter 48, Environmental Hazards, for further discussion on the diagnosis and management of anaphylaxis.
Type II hypersensitivity reaction. Rarely seen in children, type II reactions occur as urticaria resulting from blood transfusion reactions involving IgG and IgM cytotoxic antibodies.
Type III hypersensitivity reaction. In this condition, antigen-antibody complexes trigger a serum-sickness type of reaction which may include urticaria, arthralgia, and fever.
Hereditary angioedema. This is a very rare but potentially life-threatening condition that presents as acute angioedema of the upper airway, face, and the gastrointestinal tract. This condition is caused by either an absent or dysfunctional C1 esterase inhibitor. This leads to a cascade of the complement system as a result of trauma, infection, or stress.
Aspirin and nonsteroidal anti-inflammatory drug (NSAID) use. Unlike most drug allergies, aspirin sensitivity does not involve IgE antibody but, rather, the prostaglandin pathway. This trigger to urticaria and angioedema is seen mostly in adults who have chronic urticaria.

Nonimmunogenic Urticaria

Causes not mediated by the immune system include the following:

Direct histamine releasing agents. Certain drugs (such as codeine and morphine), foods, and radiocontrast materials may cause direct release of histamine from mast cells, with consequent and prompt development of pruritus and urticaria.
Physical response. This is a major cause of urticaria and may be a result of twitchy mast cell syndrome (where mast cells release contents with minimal provocation).
Cold urticaria. Exposure to cold is the trigger. Children and young adults will present with urticaria after swimming in cold water, or with outdoor winter activities. Cold exposure can lead to massive release of histamine in these individuals, resulting in urticaria. Although rare, shock, and drowning (for swimmers), can occur.

The most common form of cold urticaria is the acquired idiopathic type. Diagnosis can be established by placing an ice cube on the forearm, which will lead to development of localized urticaria with itching. The familial variety is very rare and transmitted as an autosomal dominant trait. These individuals develop urticaria after prolonged exposure to cold. Fever, arthralgia, and headaches may accompany.
Cholinergic urticaria. Exposure to a hot environment or heat as a result of physical activity can cause cholinergic urticaria in affected individuals. This is a fairly common form of urticaria. The lesions tend to be wheals, which are 2 to 3 mm in diameter and extremely pruritic. This condition is occasionally associated with
exercise-induced anaphylaxis, wherein intense exercise can lead to pruritus, cholinergic urticaria, and anaphylaxis.
Dermatographia. One of the leading causes of physical urticaria, dermatographia is seen in 20% of in-patients with chronic urticaria (Tharpe, 1996). Urticarial lesions are seen over friction- and trauma-prone areas of the body, such as the waist. Simply stroking the skin with pressure can provoke hives.
Solar. This variant occurs because of histamine release from mast cells due to sunlight. The lesions develop over exposed skin upon exposure to sunlight.
Papular urticaria. Children who have been bitten by mosquitoes, black flies, fleas, or other biting insects may present with papular urticaria. The lesions, seen mostly over the lower limbs, consist of pruritic wheals. The reaction may involve IgE antibody to the saliva of the biting insect. Occasionally, a delayed type 4 component may also be present.
Bacterial and viral infections. One of the leading causes of acute urticaria may be bacterial and viral infections. It may also be seen with infectious mononucleosis.

Vasculitis. Urticaria associated with vasculitis is seen in a small number of patients with chronic urticaria. The urticarial lesions here tend to persist for 1 to 2 days and may be associated with signs of autoimmune diseases such as arthralgia and arthritis.
Urticaria pigmentosa. When local mast cells infiltrate the dermis, small, hyperpigmented lesions develop which may urticate upon stroking (Darrier’s sign). Urticaria pigmentosa is a rarer and milder condition in children than in adults.
Psychogenic urticaria. This can be a chronic form. Stress is a cause, but more so in adults than in children.

EPIDEMIOLOGY

Urticaria and angioedema affect approximately 10% of the population. Often seen in children, it is usually a transient acute phenomenon. Chronic urticaria, which is a vexing problem in adults, fortunately is only rarely seen in children (Tharpe, 1996).

HISTORY, PHYSICAL EXAM, AND DIAGNOSTIC CRITERIA

A history of lesions establishes the diagnosis of urticaria. However, parents bring their children to the provider wanting to know what precisely is causing these hives. This question can rarely be answered. A detailed history may help to establish an etiology, especially using the classification as outlined.

Physical urticaria can be confirmed by history. Dermatographia can be established by stroking the skin. Cold urticaria can be proven by the ice cube test. Cholinergic urticaria can be diagnosed by a good history. Exercising a patient on a treadmill is not necessary.

DIAGNOSTIC STUDIES

Because urticaria is usually an acute, transient problem, a laboratory or allergy work-up is not generally necessary.

Acute urticaria due to type I reaction (acute allergic/anaphylaxis) can be diagnosed by history. Hives may be associated with signs of anaphylaxis. There will often be history of antigen exposure (usually an ingestant such as medication, drugs, or food) or by injection via hymenoptera sting. In this situation, an allergy work-up or laboratory work-up may be necessary immediately, not because of urticaria but because of the anaphylaxis which may be associated with it.

Chronic urticaria is occasionally associated with an autoimmune phenomenon. Hence, an erythrocyte sedimentation rate (ESR), antinuclear antibody (ANA), and rheumatoid factors should be obtained. In suspected hereditary angioedema, C2, C4, and C1 esterase inhibitor levels should be obtained. These will be low in patients with active disease.

MANAGEMENT

Treatment is based on etiology. In cases of urticaria due to type I reactions, avoidance of the allergen, when known, is most important. Allergen-specific immunotherapy may be necessary in type I urticaria associated with life-threatening anaphylaxis, if appropriate antigens are available. These include hymenoptera venoms.

PHARMACOTHERAPY

In patients with active lesions, antihistamines (H₁-blockers) are the mainstay of treatment. Nonsedating antihistamines should be used, especially in school-aged or older children. Ceterizine (Zyrtec) and loratadine (Claritin) are available in a syrup form. Syrup formulation is a big advantage for children unable to swallow pills or capsules. A dosage of 5 to 10 mg once daily may be sufficient. Diphenhydramine may be added as a rescue medication at a dose of 25 to 50 mg, and repeated every 4 to 6 hours if necessary.

In urticaria not responding to H₁-blockers, the addition of H₂-blockers such as ranitidine can be helpful. Tricyclic antidepressants such as doxepin are reported to be about 80 times more potent than diphenhydramine and, hence, may be used in children with urticaria not responding to H₁– and H₂-blockers. However, sedation can be a problem with doxepin.

Corticosteroids may be necessary in acute urticaria, especially for angioedema that does not respond to H₁– and H₂-blockers.
Sympathomimetics such as epinephrine are useful in the emergency treatment of acute, severe urticaria, or associated angioedema or anaphylaxis.

Cromolyn sodium can help the itching of mastocytosis, but its effect on urticaria appears to be minimal.

Because urticaria can sometimes be unresponsive to the aforementioned medications, newer drugs are being looked into. These include the LTD4 receptor antagonists Singulair and Accolate. These plus the calcium channel blocker nifedipine have shown promise when used in conjunction with H₁-blockers (Tharpe, 1996).

Referral Point

The majority of patients with urticaria respond to H₁ receptor antagonists promptly and require no work-up or referral. The provider should consider referral if the urticaria occurs as part of an acute anaphylactic event. The clinician should also refer the child to a pediatric allergist if the urticaria is a chronic problem (lasting more than 4–6 weeks), if it does not respond to H₁– and/or H₂-blockers, if it is associated with systemic disease, or if the diagnosis of urticaria is in doubt.

Bacterial Infections

INTRODUCTION

Although the skin has many built-in defenses, bacterial skin infections are quite common in children. Children are prone to breaks in the mechanical barriers of the skin, and their often notorious lack of concern for hygiene predisposes to invasion by the countless numbers of organisms to which they are exposed on a daily basis.

Although bacterial skin infections can be caused by a broad array of pathogens, the most common causative organisms are group A β-hemolytic streptococci (GABHS) and Staphylococcus aureus. The different clinical presentations depend on the depth of the infection and its location on the body. Impetigo, ecthema, folliculitis, furuncles, carbuncles, and cellulitis are the clinical manifestations of bacterial infections progressing from the most superficial to the deeper layers of the skin.

PATHOPHYSIOLOGY AND PHYSICAL EXAM

Impetigo

Impetigo is a superficial, highly contagious skin infection. It occurs in all ages, but most frequently in younger children. Lesions can involve any skin surface but are most common on exposed areas. The causal organisms are streptococci and S. aureus. In the past, a distinction was made between impetigo with a bullous presentation and other forms, because it was felt that staphylococcus was the etiologic agent in bullous lesions, as opposed to the classic variety in which streptococci predominated. Today the term bullous impetigo is purely descriptive, because in reality, staphylococci are the most common cause in all lesions of impetigo.

Impetigo usually begins with a small break in the skin, which soon becomes infected. The lesions start with small erythematous macules or bullae surrounded by a thin erythematous ring. The lesions go on to enlarge and often develop the classic golden yellow crusts but can also have a smooth, red, “weepy” appearance or appear simply as enlarging bullae. The weepy exudate from the lesions or from broken bullae can be spread by contact to the patient or to others, creating the spread of new lesions.

Ecthyma

Ecthyma typically begins similarly to impetigo and has the same etiology. Bacterial penetration, however, goes deeper through the epidermis, resulting in a punched-out, ulcerative-appearing lesion. The initial lesion can start as a bulla, which eventually produces a thick crust. When this crust is removed, the shallow ulcer remains. Ecthymal lesions are most common on the lower extremities and often occur at the site of insect bites. They tend to have a more chronic course than the lesions of impetigo and can be quite painful.

Folliculitis

Folliculitis is a superficial infection of the hair follicle, usually caused by S. aureus. The lesions appear as small papules or pustules that are associated with hair follicles. They often occur in crops and are usually painless. In increasingly common subset is the so-called hot tub folliculitis, which is noted after bathing in an infected hot tub. The follicular lesions will often be more prominent in areas covered by bathing suits and are nodular or pustular. The causative organism is not staph, but pseudomonas.

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