Common Dermatologic Presentations in Emergency Medicine

Authors: Gregory A. Jeppesen, DO, St. Vincent Mercy Medical Center, Toledo, OH; and Catherine A. Marco, MD, FACEP, Clinical Professor, Department of Surgery, Medical College of Ohio; Attending Physician, St. Vincent Mercy Medical Center, Toledo, OH.

Peer Reviewers: Sandra M. Schneider, MD, FACEP, Professor and Chair, Department of Emergency Medicine, University of Rochester, NY; and Steven M. Winograd, MD, FACEP, Attending Physician, Emergency Department, Adena Regional Medical Center, Chillicothe, OH.

Dermatologic complaints commonly are seen in emergency medicine and may pose a diagnostic dilemma for the clinician. Although a detailed understanding of all dermatologic conditions is beyond the scope of practice of emergency physicians, recognition of categories of disease, particularly emergent conditions, is essential. Knowledge of basic disease lesions, patterns, diagnostic tests, and emergent management is crucial to the appropriate treatment of patients with cutaneous disease. This article presents an organized approach to the diagnosis and management of cutaneous conditions, including brief discussions of selected dermatologic complaints. The Editor

Introduction

Dermatologic complaints in emergency medicine are common, both as the chief complaint or as discovered while performing the history and physical examination. The skin is the largest organ system and, likewise, the number of diseases potentially affecting the integument also is large. Some dermatologic disorders are straightforward, but often it is difficult to sort out the etiology and management of a particular dermatologic complaint. Many dermatologic conditions initially are misdiagnosed.1 A wide spectrum of dermatologic disorders, from the benign to life-threatening skin disorders, may be encountered. This article is intended to provide a structured approach to common dermatologic presentations in the emergency department. The authors present a unique question-based approach to dermatologic complaints. (See Table 1.)

Table 1.
Eleven Questions to Lead Physicians
to the Diagnosis and Management

Dermatologic findings are particularly common among pediatric emergency patients. More than 50 infectious agents have been identified that may cause exanthems in the pediatric population.2 One study demonstrated that 72% of cases of fever and rash in the pediatric population were caused by viruses, and 20% by bacteria.3 Many exanthems have specific patterns of lesions, distributions, and clinical history, and some of the more common exanthems are detailed in this article. However, many viral exanthems are nonspecific, and establishing a definitive etiology may not be feasible.

A sound understanding of the basic anatomy and physiology of the skin can be helpful when evaluating a dermatologic problem. The skin is comprised of three layers: the epidermis, dermis, and subcutaneous layer. (See Figure 1.)

Figure 1.
Three Layers of Normal Skin, Including
Epidermis, Dermis, and Subcutaneous Layers

The epidermis is a thin layer of stratified squamous epithelium mainly consisting of keratinocytes which progress through stages of differentiation as they move from the basal to the superficial layer. These layers are respectively named: stratum germinativum, stratum spinosum, stratum granulosum, and stratum corneum. These layers act as a barrier from the environment. The epidermis also includes melanocytes and Langerhans cells. Melanocytes produce the pigment melanin, which functions to absorb harmful ultraviolet radiation. Langerhans cells are a component of the immune system and, as part of their function, these cells ingest and process foreign antigens.

The epidermis is devoid of blood vessels and depends upon the dermis for nutrients and waste disposal by diffusion through the dermal-epidermal junction. This junction consists of two layers, the lamina lucida and the lamina densa. The interface is irregular, with many finger-like projections from both the epidermis and dermis that greatly increase surface area for diffusion. This junction also is the site of immunologic injury resulting in the bulla in bullous pemphigoid and epidermolysis bullosa.

The dermis is a thicker layer consisting of connective tissue, blood vessels, lymphatic vessels, nerve endings, immune cells, and epidermal appendages, all of which are surrounded by mucopolysaccharides. The epidermal appendages are epithelial lined structures with the ability to differentiate and form hair follicles, sweat glands, sebaceous glands, and apocrine glands. The main function of the dermis is to sustain the epidermis and contribute to the protective functions of the skin. Fibroblasts are the primary cell type in the dermis and are responsible for producing procollagen and elastic fibers used to form the connective tissues that give support and elasticity to the skin. Sweat glands and the vast network of blood vessels provide a thermoregulatory function.

The subcutaneous layer is composed of loose connective tissue and adipose tissue and functions to cushion the overlying skin and contains lymph and neurovascular structures.

History and Physical Examination

As with all emergency department cases, emergency stabilization is the first priority. Airway, breathing, and circulation must be evaluated and addressed immediately. For example, a toxic, lethargic, or confused patient with a rash requires immediate action. For more routine dermatologic complaints, historical information can be valuable, and should include details including time of onset, duration of symptoms, and relation to any new potential allergens, such as foods, medications, soaps, pets, jewelry, etc. Information about evolution of the rash over time should be sought, including whether the rash has progressed, improved, or waxed and waned. Other historical features such as associated pain, pruritus, fever, sexual history, occupation, or hobbies may be relevant. Past medical history should be obtained, including such conditions as general medical conditions, previously diagnosed skin conditions, medications, illicit drug use, allergies, recent travel, sunlight exposure, and family history.

A detailed physical examination is essential. The physical examination of the skin should be performed in a private area with adequate lighting, and a systemic and thorough visual exam from the head to the soles of the feet should be performed, including skin, mucosa, and genitalia. Lesions may be palpated (wearing gloves) to determine texture, blanching, or sloughing characteristics. A test for Nikolsky’s sign may be performed in which gentle rubbing of the skin results in sloughing of the epidermis. Primary and secondary lesions, characteristics, and patterns should be identified.

The identification and description of lesions is essential to making the correct diagnosis and determining the appropriate management. Lesions may be categorized as primary or secondary. Primary lesions are those that arise as a result of the disease process and have not been altered. Secondary lesions result from additional forces such as scratching, treatment, healing, or complicating infections. (See Figure 2.)

Figure 2.
Extensive Excoriations Secondary to
Toxicodendron Exposure (Poison Ivy)

Appropriate terminology allows one to accurately describe cutaneous findings, form a differential diagnosis, and communicate with colleagues or consultants. Primary and secondary lesions are listed with descriptions in Tables 2 and 3.

Table 2. Primary Lesions

 
Table 3. Secondary Lesions

Following the thorough physical examination, diagnostic tests should be considered. For the nontoxic patient, laboratory tests often are unnecessary. Blood tests for secondary syphilis or heterophile antibodies (mono-spot) and throat swabs for rapid testing and culture of Group A streptococcus may be indicated. For the toxic or unstable patient, complete blood count (CBC), blood cultures, lumbar puncture studies, electrolytes, blood urea nitrogen (BUN), creatinine, glucose, and liver function tests should be considered.

Categories of Cutaneous Conditions

When formulating a differential diagnosis it is useful to place the disorder into a general category. Dermatologic conditions may be categorized by lesion, distribution, or etiology. For purposes of organization, the authors choose to organize dermatologic conditions by distribution. Table 4 demonstrates this organizational scheme.

Selected Dermatologic Presentations

As not all dermatologic presentations can be discussed in a single article, several important cutaneous diseases have been selected for review in this article.

Erythema multiforme (EM) is an acute inflammatory disease that is a spectrum of disease and can be further divided into EM minor and major. EM minor manifests as erythematous macular or papular eruptions generally located on the extensor surfaces, palms, soles, and face and affects no more than one mucosal surface. The classically described lesion is an erythematous macule that over 1-2 days develops central clearing and forms what resembles a target. Mucosal involvement may include vesicles and bullae. The lesions may be painful or pruritic. Also, as the name implies, this disease usually is minor and resolves in 2-4 weeks with little if any sequelae. Etiologies of EM minor include bacterial or viral infections, various drugs, and malignancies. Herpes simplex virus often is implicated and frequently is the cause in recurrent EM minor. The cause is undetermined as often as 50% of time. EM major (Stevens-Johnson syndrome) is a systemic disease with greater skin involvement, two or more mucosal surfaces, and often affects internal organs. It typically is preceded by diffuse malaise, myalgias, and fever. Morbidity is much worse, and mortality reaches 5-15%. Treatment depends on the severity of disease and may include treatment of the underlying disease, steroids, skin care, hydration, and, in severe cases, intensive care unit (ICU) or burn unit admission for supportive care.4,5

Secondary syphilis is a dermatologic condition that mimics many other common rashes and often is misdiagnosed. Syphilis is caused by the spirochete Treponema pallidum that penetrates mucous membranes or breaks in the skin. Reported syphilis rates have fallen drastically since reports began in 1941; however, there was a slight increase in the rates in 2001 and 2002 in the South and select urban areas in the specific population of men who have sex with men.6 Untreated syphilis should be considered as a diagnostic possibility, particularly in an era in which many sexually transmitted diseases (STDs) are treated with oral agents not providing adequate treatment for incubating syphilis. The first symptom is a painless genital chancre that appears approximately four weeks after inoculation and then remains for 3-6 weeks before resolution. If untreated, in another 3-6 weeks the patient develops generalized malaise, fatigue, fever, lymphadenopathy, and a maculopapular or pustular erythematous rash that usually begins on the trunk and extends peripherally and may include the soles and palms. (See Figure 4.) Lesions of primary and secondary syphilis are contagious and should be examined with gloved hands. Treponema pallidum remains sensitive to penicillin in most areas of the United States, and primary syphilis easily is treated with a single dose of benzathine penicillin G(Bicillin-LA) 2.4 million units intramuscularly. For those allergic to penicillin, tetracycline or doxycycline may be used. Secondary syphilis should be treated with three weekly doses of benzathine penicillin G.7

Figure 4.
Maculopapular Lesions Resulting
from Secondary Syphilis

Toxic epidermal necrolysis (TEN) is a generalized exfoliative skin disease with significant morbidity and mortality. The pathophysiology is thought to be immune-complex mediated and results in a confluent morbiliform rash that may progress to large bullae formation caused by disruption at the dermal-epidermal junction. Although TEN often is idiopathic, there are many potential identifiable causes, with drug reactions being the most common. Sulfonamides, penicillins, cephalosporins, nonsteroidal anti-inflammatory drugs, anticonvulsants, and antituberculosis medications are among those found to have caused TEN. Malignancy, radiation therapy, and viral infections are other identified causes. Symptoms typically begin as vague generalized malaise, fatigue, fever, and upper respiratory infection symptoms, and the generalized rash follows. The rash is tender, erythematous, hot, and develops into large bullae that slough easily with shearing pressure (Nikolsky sign). Mucous membranes commonly are affected. Complications may include electrolyte disturbances, secondary infections, dehydration, pneumonia with respiratory failure, and gastrointestinal hemorrhage. Mortality rates are 15-40%, with geriatric patients having the worst overall prognosis. Treatment mainly is supportive and includes aggressive fluid management, wound care, and treatment of subsequent complications, all of which may be accomplished effectively in a burn unit or ICU.3,8

Drug reactions commonly are seen in the emergency department and may present a diagnostic dilemma. (See Figures 5 and 6.)

Figure 5.
Vasculitis, Which May Occur as a Drug Reaction

Figure 6.
Vasculitis Resulting from Sulfonamide Medication

Drug eruptions can present as nearly any form of rash and, therefore, medication history is vital in evaluating all patients with dermatologic complaints. All medications started within the last two months should be identified. Routes of medication administration are important as topical and intramuscular routes have higher rates of cutaneous reactions. Cutaneous drug reactions may occur sporadically after multiple uses of the same drug, and may occur immediately or delayed following administration of the drug. Reactions may be classified into allergic and nonallergic. The allergic reactions further may be described using the Gell-Coombs classification in which there are four types of allergic reactions: type I is immediate hypersensitivity reaction (i.e., anaphylaxis, urticaria, angioedema, etc.); type II is a cytotoxic antibody reaction (i.e., purpura, hemolysis, etc.); type III is immune complex reaction (i.e., vasculitis, angioedema, serum sickness, etc.); type IV is delayed-type hypersensitivity reaction (i.e., contact dermatitis, photoallergic reactions, etc.). Nonallergic reactions are more common and may be the result of drug-drug interactions, toxicity, disruption of normal flora, exacerbation of pre-existing skin conditions, triggering of mast cell activation through nonimmunologic pathways, or systemic effects of bacterial endotoxins released by antibiotic mediated cell destruction. Immunocompromised patients (including those with HIV infection, malignancy, etc.) have a 10-fold greater risk of developing drug eruptions, and women have a 35% higher incidence than men. These reactions may be mild and short-lived or may be extensive and life-threatening. Severe reactions include but are not limited to toxic epidermal necrolysis, erythema multiforme, Stevens-Johnson syndrome, vasculitis, hypersensitivity syndrome, and anticoagulant skin necrosis erythroderma. Diagnostic tests rarely are useful, although a complete blood count and skin biopsy may be indicated. Treatment includes identification and removal of the offending agent and symptomatic and supportive treatment as indicated by the severity of the condition.9

Meningococcemia is a serious and potentially life-threatening bacterial infection caused by the encapsulated organism Neisseria meningitides. Infection is preceded by colonization of the mucus membranes in the nasopharynx with subsequent invasion into the blood stream. Some of the population (2-10%) are asymptomatic carriers. The organism resists phagocytosis by virtue of a polysaccharide capsule, is able to shed large amounts of endotoxin, and has an immunoglobulin A1 protease that increases intracellular survival. Transmission occurs via upper respiratory secretions, which include airborne droplets. This infection may be manifested by meningitis alone or meningococcemia with or without meningitis. Symptoms begin as a vague viral syndrome with sore throat, headache, and cough and rapidly progress to include high sudden fever, severe headache, meningeal signs, altered mental status, and rash. The rash classically is described as petechial or purpuric, typically first appears on the trunk, and may progress to extremities including the palms and soles. These lesions may evolve rapidly into confluent palpable papules. Patients typically appear toxic and may have unstable vital signs at presentation. Because most commercially available vaccines do not provide adequate protection against serogroup B, meningococcemia should be considered in the appropriate clinical context, even among immunized individuals. Indicated laboratory studies include: complete blood count, blood cultures, and analysis and culture of cerebral spinal fluid. Prompt treatment is absolutely vital and should not be delayed to obtain the cerebral spinal fluid or other diagnostic tests. Cephalosporins, especially ceftriaxone (Rocephin), penicillin G, and vancomycin (Vancocin), are appropriate antibiotics. Aggressive supportive care and ICU admission are indicated for patients with unstable vital signs. Mortality is high (5-28%) even with optimal treatment. Persons with four hours of close contact or intimate exposure to upper respiratory secretions (including emergency department personnel) should receive antibiotic prophylaxis.3,10

Erythema nodosum is a nodular disease caused by inflammation of the subcutaneous adipose tissue. Lesions generally are located on the anterior lower extremities but can be found on the upper extremities or trunk. The lesions are warm, tender, erythematous nodules. Possible etiologies include bacterial, viral, fungal, and parasitic infections; pharmacologic agents; sarcoidosis; leukemia; lymphoma; inflammatory bowel disease; and idiopathic cases. Treatment is focused on management of the underlying cause and systemic nonsteroidal anti-inflammatory agents.11

Necrotizing fasciitis is a life-threatening infection of the soft tissues that does not penetrate the fascial layer deep to the subcutaneous fat. Most cases are polymicrobial, including microbes such as Streptococcus, Peptostreptococcus, Staphylococcus aureus, Pseudomonas, Escherichia coli, and Klebsiella. Often the infection results from local trauma, insect bites, or recent surgical procedures, although comorbid conditions such as diabetes may have a contributory role. The infection typically begins locally and progresses rapidly, with severe pain, discharge, subcutaneous gas formation, bullae, and tissue necrosis. Mortality may be as high as 70-80%. Treatment should be instituted with fluid and/or blood resuscitation as clinically indicated, broad spectrum antibiotics, early surgical debridement, and hyperbaric oxygen therapy.12,13

Insect bites and stings are encountered often in the emergency department. Most are not serious, causing a local histamine reaction of urticaria or inflammation. (See Figures 3 and 7.)

Figure 3.
Hemorrhagic Reaction to Insect Bites

Figure 7.
Vesicular and Papular Lesions
Secondary to Insect Bites

However, more serious complications such as cellulitis, local tissue necrosis, transmission of a disease, or anaphylaxis can result. Insects of the order of Hymenoptera (which includes wasps, ants, and bees) are responsible for sting injuries and most insect-related anaphylaxis. Brown recluse spider bites may cause local tissue necrosis. These bites often have central clearing at the bite site that looks like a small target and also result in neurological or autonomic system dysfunction. Mosquitoes and ticks of various types may transmit disease through the bite. Lyme disease transmitted by the bite of the Ixodes tick and caused by the spirochete Borrelia burgdorferi results in the pathognomonic skin lesion erythema migrans. (See Figure 8.) Treatment of insect bites is dependent on the specific etiology and spectrum of symptomatology. Antihistamines may be sufficient to treat local reactions; antibiotics are indicated for Lyme disease or other transmitted diseases; aggressive wound care may be indicated for necrotic lesions; and epinephrine with antihistamines as well as aggressive supportive care are indicated to treat anaphylaxis.14-17

Figure 8.
Erythema Migrans Associated with Lyme Disease

Tinea infections are fungal skin conditions that are named and treated according to the area of the body affected. Tinea capitis refers to the scalp and is characterized by scaly, pruritic patches that may result in alopecia. Treatment requires systemic antifungal therapy for 4-6 weeks. Tinea corporis involves the trunk, arms, and legs and is widely inappropriately known as "ringworm" because it is characterized by a pruritic, scaly, raised, sharply demarcated annular lesion that clears centrally. Tinea cruris, which is similar in appearance, involves the groin. Tinea versicolor typically involves the upper trunk and limbs and is manifested as superficial scaly lesions that vary in color and may be tan, pink, or white. These lesions may be pruritic and do not tan with sun exposure. Tinea corporis, cruris, and versicolor all are treated with topical antifungal agents. Tinea versicolor should be treated with topical selenium sulfide solution. Tinea unguium refers to the nails and results in thickened, opaque, cracked, or crumbled appearance. The great toe most commonly is affected. Treatment with prolonged systemic antifungal therapy may be necessary.18

Herpes zoster is caused by the reactivation of a previously acquired varicella zoster infection that has been dormant in the dorsal root ganglia. Reactivation usually is caused by a decrease in cellular immunity, and the virus travels along the ganglion’s dermatomal distribution to the surface. Symptoms usually begin with pain or paresthesias along the involved dermatome for 2-3 days, followed by eruption of the classic vesicular lesions on an erythematous base that progress to pustules and crusts before resolving. (See Figure 9.)

Figure 9. Herpes Zoster

Involvement of the second branch of the trigeminal nerve may implicate ocular disease that may result in blindness if untreated. It is important to perform a slit lamp exam with fluorescein dye to look for dendritic corneal lesions in such cases. Even if ocular involvement is not identified, if the infection involves the face, especially the tip of the nose, urgent ophthalmological consultation is warranted. Ramsay Hunt syndrome is involvement of the geniculate ganglion and is characterized by temporary unilateral facial paralysis and lesions on the external ear or tympanic membrane. Herpes zoster is considered disseminated if the rash is found on more than two dermatomes, and also may have visceral involvement. Disseminated zoster may be found in immunocompromised individuals and can be fatal. Pain that persists after resolution of the rash, postherpetic neuralgia, can be quite bothersome and may persist for up to a year. Treatment for herpes zoster should be instituted with oral antiviral medication (such as acyclovir [Avirax, Zovirax], famciclovir [Famvir], or valacyclovir [Valtrex]), analgesics including nonsteroidal anti-inflammatory drugs or narcotics, and appropriate referrals as warranted.19 Topical capsaicin has demonstrated efficacy for pain relief in some patients. Systemic steroids should be administered for patients within the first 48 hours of symptoms to reduce the incidence of postherpetic neuralgia.

Lice infestation is caused by one of three types of ectoparasites. Pediculus humanus capitis, Pediculus humanus corporis, and Pthirus pubis are, respectively, head, body, and pubic lice. Head lice primarily infest the scalp with predilection to the occipital and postauricular areas. The eggs of head lice are called nits and are attached to the base of the hair shaft 3-4 mm from the scalp. Body lice, as named, primarily infest the body but can include the scalp margins. Nits from the body louse may be attached to the patient’s clothing. Pubic lice primarily infest the pubic and anogenital regions. Pediculosis typically is acquired from close contact with an infested person or sharing of items such as hair brushes, clothing, and headgear. All age groups and races are affected, with a slightly higher prevalence in females. Hair length and hygiene do not affect infestation rates. Symptoms include pruritis, which leads to excoriation and potentially secondary skin infections with regional lymphadenopathy. The treatment of choice is topical permethrin.20 There are a number of topical treatments arranged in kits that can be purchased over-the-counter or by prescription. Most treatments should be repeated in 7-10 days to kill recently hatched nits. Treatment also should include washing clothing and linens in water greater than 55° C for 5 minutes or longer. Unwashable small items such as stuffed animals may be sealed in a plastic bag for 12-14 days.21

Conclusions

Dermatologic presentations are common in emergency medicine. An understanding of common dermatologic definitions and a systematic approach to the diagnosis and therapy can be useful in the appropriate management of dermatologic complaints.

References

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