Atopic Dermatitis and Contact Dermatitis in the Emergency Department
Peck Y. Ong, MD,*y Mark Boguniewicz, MDz
Atopic dermatitis and contact dermatitis are common dermatologic conditions that may be encountered in the emergency department (ED). Atopic dermatitis is a chronic inflammatory skin disease with an undulating course characterized by remissions and exacerbations. Patients may present to the ED because of chronic disease or acute flares that fail to respond to routine treatments or because of secondary infections. The article reviews the ED management of exacerbations of atopic dermatitis as well as various common skin infections associated with this disorder, including specifically Staphylococcus aureus and eczema herpeticum. Although contact dermatitis can be chronic, patients usually present with acute symptoms. The article discusses the diagnosis and ED management of common types of contact dermatitis, including allergic and irritant chronic dermatitis, photodermatitis, and contact urticaria. Clin Ped Emerg Med 8:81-86 2007 Published by Elsevier Inc. KEYWORDS atopic dermatitis, contact dermatitis, staphylococcus aureus, eczema herpeticum, emergency department, topical corticosteroid
topic dermatitis (AD) and contact dermatitis (CD) are fairly common dermatologic conditions that will be encountered in caring for children in the emergency department (ED). This article reviews the pathophysiology, clinical presentation, and ED management of exacerbations of AD, as well as various common skin infections associated with this disorder. The article discusses the diagnosis and ED management of acute presentations of the common types of CD, including allergic and irritant CD, photodermatitis, and contact urticaria.
Atopic Dermatitis
AD is a common chronic inflammatory skin disease of childhood, affecting about 15% of children in United States [1]. It is characterized by a relapsing course and severe pruritus. Affected children often experience sleep loss, school absences, and psychosocial disturbances. In addition, the disease is frequently complicated by secondary skin infections. Atopic dermatitis accounts for up to 4% of all ED visits [2].
Pathophysiology
*Division of Clinical Immunology/Allergy, Childrens Hospital Los Angeles, Los Angeles, CA. yDepartment of Pediatrics, University of Southern California Keck School of Medicine, Los Angeles, CA. zDivision of Pediatric Allergy-Immunology, National Jewish Medical and Research Center, Denver, CO. Department of Pediatrics, University of Colorado School of Medicine, Denver, CO. Reprint requests and correspondence: Peck Y. Ong, MD, Childrens Hospital Los Angeles, 4650, Sunset Blvd, MS# 75, Los Angeles, CA 90027. (E-mail: pyong@chla.usc.edu) 1522-8401/$ - see front matter 2007 Published by Elsevier Inc. doi:10.1016/j.cpem.2007.04.002
The skin barrier (stratum corneum) functions of AD patients are defective [3]. As a result, this disease is characterized by dryness and hypersensitivity to environmental triggers. Acutely, patients with AD present with erythematous lesions and acute pruritus. Acute lesions are characterized by T-helper type 2mediated inflammation, which is associated with an increased production of interleukins 4 and 13 [3]. Chronic AD lesions are characterized by lichenification, which is a result of thickened, hyperpigmented epidermis. Chronic lesions 81
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Table 1 Diagnostic criteria for atopic dermatitis.
P.Y. Ong, M. Boguniewicz
For patients who would be discharged from the ED, daily skin care should be reviewed. General recommendations for all patients include avoidance of nonspecific skin irritants such as synthetic fabrics (use cotton clothing as much as possible), wool, nonessential toiletries such as bubble baths or perfumes, and highly fragranced or artificially colored soaps and detergents. Patients with AD should take daily warm baths or showers for approximately 10 minutes to hydrate the skin. Baths should be followed by gentle pat drying and immediate application of a topical anti-inflammatory medication (a topical corticosteroid or a topical calcineurin inhibitor) on the affected areas and a moisturizer on the asymptomatic areas. The choices of topical corticosteroids are listed in Table 3 according to their potency. Medium-potency topical corticosteroids (classes III-IV) may be sufficient to treat moderate flares. In general, ointment-based medications may be tolerated better by most patients during an acute flare. Topical calcineurin inhibitors, including tacrolimus ointment 0.03% and pimecrolimus cream 1%, are nonsteroidal topical immunosuppressants that are approved in the United States for children 2 years and older. Tacrolimus ointment 0.1% is also available for adults. These medications are particularly useful for treatment of AD lesions on the thinner skin areas (face, groin, axillae)
Table 2 Differential diagnosis for atopic dermatitis.
The presence of itchy skin plus 3 or more of the following: 1. History of dermatitis involving flexural areas (elbows, behind the knees, fronts of ankles, or around the neck (or on the cheeks for patients b10 y) 2. A personal history of asthma or allergic rhinitis (or family history of atopic disease in a first-degree relative for patients b4 y) 3. A history of generalized dry skin in the past year 4. Visible dermatitis involving flexural areas (or dermatitis on the cheeks/forehead and outer aspects of the limbs for patients b4 y) 5. Onset of the skin condition b2 y (this criterion only applies to patients z4 y) Modified from Williams et al [7].
are characterized by T-helper type 1mediated inflammation, which is associated with an increased production of the cytokine interferon-c . This defective skin barrier also renders the skin of these patients susceptible to a wide range of microbial pathogens. Almost all acute AD lesions are colonized by Staphylococcus aureus . A defect of cutaneous innate immunity further increases the risk for bacterial and viral skin infections [4,5].
Diagnosis
The diagnosis of AD is based on a constellation of clinical signs and symptoms. The most frequently used criteria in clinical studies are those proposed by Hanifin and Rajka [6]. These criteria have been refined and simplified by the United Kingdom Working Party (Table 1) [7]. More than 90% of patients have the onset of AD before 5 years of age. Therefore, new-onset AD in older children or adults should raise suspicion for other diagnoses. Table 2 shows the differential diagnosis of AD. Although most patients with AD (70%-80%) have elevated total serum immunoglobulin (Ig) E levels, up to 30% will have a normal total serum IgE. Therefore, a normal total serum IgE does not preclude the diagnosis of AD.
AD in the ED
AD Flare and Erythroderma
The clinical course of AD is characterized by relapsing episodes of symptom flares. During these episodes, patients may present to the ED with complaints of intense itching and failure of routine treatments such as topical corticosteroids. There are several situations in which admission to the hospital should be considered: 1. Patients with generalized erythema and exfoliation (erythroderma). 2. Patients with severe, generalized itching who have failed outpatient topical treatments [8]. 3. Patients with severe skin infections (discussed in the next sections).
Dermatologic diseases Seborrheic dermatitis Irritant or allergic contact dermatitis Psoriasis Nummular pilaris Keratosis pilaris Lichen simplex chronicus Pityriasis rosea Nonbullous congenital ichthyosiform erythroderma Neoplastic diseases Cutaneous T-cell lymphoma (mycosis fungoides, Sezary syndrome) Letterer-Siwe disease (Langerhans cell histiocytosis) Necrolytic migratory erythema associated with pancreatic tumor Immunodeficiencies Hyper-IgE syndrome Wiskott-Aldrich syndrome Severe combined immunodeficiency syndrome Infectious diseases Human immunodeficiency virusassociated eczema, scabies, candidiasis, tinea versicolor Congenital and metabolic disorders Netherton syndrome Phenylketonuria Zinc deficiency Essential fatty acid deficiency Histidine deficiency Infantile-onset multiple carboxylase deficiency
Atopic dermatitis and contact dermatitis in the emergency department
Table 3 Topical corticosteroid potency ranking.
83 sensation at the site of application. This is typically a transient phenomenon. Patients with more severe flares of AD may require a short course of an oral corticosteroid. The corticosteroid dose should be tapered over 1 week to decrease the chance of a rebound effect when coming off systemic corticosteroids [10]. Caution should be used in prescribing oral corticosteroids in cases where superinfection with herpes simplex virus (HSV) cannot be ruled out. Wet dressing treatments applied over topical corticosteroids have also been shown to be effective during AD flares [11]. However, this procedure should be recommended only by physicians familiar with this therapy because of potential complications [12]. There is no convincing evidence that H1 antihistamines decrease itching in AD [13], although the sedative effects of antihistamines such as diphenhydramine, hydroxyzine, or doxepin may be useful in preventing scratching and help patients with secondary sleep disturbance. Therefore, these medications are best used at bedtime. Up to 30% to 40% of children with moderate to severe AD have food allergies [14]. These patients may present to the ED with acute food allergic reactions. Patients with a systemic food allergic reaction (eg, choking or trouble breathing) should be prescribed and instructed on the use of self-administered epinephrine: Epipen Jr or Twinject 0.15 mg for patients weighing up to 30 kg, or Epipen or Twinject 0.3 mg for patients weighing 30 kg or more. For patients with severe AD or for those having repeated visits to the ED, a referral (either by the ED or the primary physician) to a specialist may be necessary.
Group I (most potent) Betamethasone dipropionate (Diprolene) 0.05% cream, ointment Clobetasol propionate (Temovate) 0.05% cream, ointment Diflorasone diacetate (Psorcon) 0.05% ointment Halobetasol dipropionate (Ultravate) 0.05% cream, ointment Group II Amcinonide (Cyclocort) 0.1% ointment Betamethasone dipropionate (Diprosone) 0.05% cream, ointment Desoximetasone (Topicort) 0.05% gel; 0.25% cream, ointment Fluocinonide (Lidex) 0.05% solution, gel, cream, ointment Halcinonide (Halog) 0.1% solution, cream, ointment Mometasone furoate (Elocon) 0.1% ointment Group III Amcinonide (Cyclocort) 0.1% lotion, cream Betamethasone valerate (Valisone) 0.1% ointment Diflorasone diacetate (Florone) 0.05% cream Fluticasone propionate (Cutivate) 0.005% ointment Group IV Triamcinolone acetonide (Kenalog) 0.1% cream, ointment Fluocinolone acetonide (Synalar) 0.025% ointment Mometasone furoate (Elocon) 0.1% lotion, cream Group V Hydrocortisone valerate (Westcort) 0.2% cream, ointment Betamethasone valerate (Valisone) 0.1% lotion, cream Fluticasone propionate (Cutivate) 0.05% cream Fluocinolone acetonide (Synalar) 0.025% cream Desonide (Tridesilon) 0.05% ointment Group VI Alclometasone dipropionate (Aclovate) 0.05% cream, ointment Fluocinolone acetonide (Synalar) 0.01% solution, cream Desonide (Tridesilon) 0.05% cream Group VII (least potent) Hydrocortisone (Hytone) 1%/2.5% lotion, cream, ointment
Bacterial Infections
Staphylococcus aureus is the most common cause of bacterial infections in children with AD. The severity of infections ranges from minor local skin infections to serious invasive infections including cellulitis, abscesses, bacteremia, sepsis, osteomyelitis, or endocarditis [15]. Secondary skin infections may present as erythema with oozing or honey-colored crusts. Topical mupirocin can be considered for isolated infected lesions. For generalized skin infections, systemic antibiotics should be used.
Table 4 Common oral antibiotics for treatment of skin infections in children. Cephalosporins Cephalexin 25-50 mg/kg/d divided every 6-8 h Cefadroxil 30 mg/kg/d divided every 12 h Cefprozil 20 mg/kg every 24 h b -Lactamase inhibitor Amoxicillin/Clavulanate 25-45 mg (amoxicillin component) divided every 12 h Macrolides Erythromycin 30-50 mg/kg/d divided every 6-8 h Clarithromycin 15 mg/kg/d divided every 12 h
where repeated applications of topical corticosteroids may result in skin atrophy or striae. Although the US Food and Drug Administration has issued a bblack boxQ warning because of concerns that long-term continuous treatment with topical calcineurin inhibitors may lead to cancer, to date, there has been no evidence for a causal link to cancer and the use of these medications. The Topical Calcineurin Inhibitor Task Force of the American College of Allergy, Asthma, and Immunology and the American Academy of Allergy, Asthma, and Immunology reviewed all available data and concluded that the risk/ benefit ratio of topical pimecrolimus and tacrolimus is similar to those of most conventional therapies for the treatment of chronic relapsing eczema [9]. Therefore, patients who may benefit from these medications should be encouraged to discuss this treatment option further with their treating physician. A common known adverse effect of topical calcineurin inhibitors is a burning
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Table 5 Differential diagnosis of contact dermatitis.
P.Y. Ong, M. Boguniewicz
involvement with meningitis, and encephalitis [5]. The mortality of EH was as high as 75% before the introduction of acyclovir. The diagnosis can be supported by a Tzanck smear and confirmed by HSV culture or DNA polymerase chain reaction from the blister fluid [5]. However, these tests may be falsely negative if the samples are inadequate. Ideally, the sample fluid should be obtained by unroofing one or more fresh intact vesicles. The mainstay of treatment for EH is intravenous acyclovir. The usual dose of intravenous acyclovir is 30 mg/kg/d divided every 8 hours (for patients less than a year old) or 1500 mg/m2/d divided every 8 hours (for patients 1 year or older) for 7 to 21 days, depending on the clinical course. Lumbar puncture should be considered if meningitis is suspected, but the presence of infected lesions over the lumbar area should preclude this procedure. Ophthalmology consultation should be obtained for patients with periocular or suspected eye involvement.
Inflammatory disorders Atopic dermatitis Dyshidrotic eczema, psoriasis Lichen simplex dermatitis Seborrheic dermatitis Lichen planus Drug eruptions Rosacea dermatitis Infectious disorders Shingles Insect bites Scabies Erysipelas Cellulitis Impetigo Vascular disorders Thrombosis Compartmental syndromes
Table 4 lists some of the common oral antibiotics that can be used for uncomplicated bacterial skin infections in AD. In patients with fever and signs of systemic infection, intravenous antibiotics should be considered. Blood and skin lesion cultures should be obtained to assess antibiotic sensitivity. Cefazolin may be used as an initial empirical antibiotic against gram-positive bacteria. Of note, community-acquired methicillin-resistant S aureus is becoming more prevalent. If methicillin-resistant S aureus is suspected, clindamycin or trimethoprimsulfamethoxazole should be considered as alternatives to cefazolin. If the patient appears septic, then intravenous vancomycin would be recommended. In patients with persistent fevers or localized pain, a workup for invasive S aureus infections (endocarditis, arthritis, osteomyelitis, bursitis, fasciitis) should be pursued [15]. In addition to S aureus , streptococcal species are also a significant and growing cause of skin infections and serious invasive complications in patients with AD [16].
Eczema Vaccinatum
Since the eradication of smallpox, routine vaccination for smallpox was discontinued in the United States in the early 1970s. However, because of the potential threats of bioterrorism in recent years, there has been a resurgence of need to provide smallpox vaccination [17,18]. Smallpox vaccine (vaccinia virus) is contraindicated in patients with AD because of the risk of developing eczema vaccinatum (EV) [19]. This contraindication also includes patients with a history of AD who currently may not have any active AD lesions [20]. There is also a risk of patients with AD contracting EV by contact with persons who have been vaccinated with vaccinia virus. The clinical symptoms of EV include fever and large disseminated blisters and pustules [5]. Because most physicians have not seen EV, the Centers for Disease Control and Prevention provides some useful pictures of EV on their Web site [21,22]. The treatment for EV is the administration of vaccinia immune globulin, which is available through the Centers for Disease Control and Prevention.
Eczema Herpeticum
Because of their defective skin barrier functions and local skin immunodeficiency, AD patients are also susceptible to viral skin infections. This topic has recently been reviewed [5]. Eczema herpeticum (EH) is an infection caused by HSV. AD patients with EH can present as a medical emergency. Clinically, patients may present with fever, malaise, and disseminated eruptions of dome-shaped vesicles that may or may not be superimposed on areas of eczematous rashes. The head, neck, and trunk are commonly affected. Blistering lesions may crust over and may be mistaken for impetiginized lesions. Alternatively, HSV-infected lesions can become secondarily infected with resulting local or systemic manifestations. Complications of EH include keratoconjunctivitis, viremia, multiorgan
Table 6
Other common causes of allergic contact dermatitis.
Facial or eyelid dermatitis Cosmetics, fragrances, hair sprays, or shampoos Scalp dermatitis Hair dye that contains paraphenylenediamine Axillary dermatitis Deodorants Stasis dermatitis Topical medications, moisturizers, shaving cream, stocking materials Genital dermatitis Douches, spermicides, latex condoms, lubricants, toilet papers, or bubble bath
Atopic dermatitis and contact dermatitis in the emergency department
85
Contact Dermatitis
The common types of CD encountered in the ED include allergic contact dermatitis (ACD), irritant contact dermatitis (ICD), photodermatitis, and contact urticaria. Acute CD may present with erythematous papules, vesicles, or even bullae [23]. ACD may be differentiated from ICD in that itching is the predominant symptom in the former, whereas pain and burning are the chief complaints of the latter [24,25]. Photodermatitis may have a similar appearance to first-degree burns, with patients complaining of a burning sensation as opposed to itching [24]. Urticaria is a less common presentation of CD, which can sometimes be overlooked [23]. The differential diagnosis of CD is shown in Table 5.
Irritant Contact Dermatitis
ICD is caused by a direct epidermal cytotoxic effect of the irritants [24]. Common offending agents include water, soaps/detergents, and juices of food products [23]. Most of the chemicals in industry are irritants, rather than allergens. Occupational-related CD is obviously rare in children. Patients with an impaired skin barrier such as AD are especially susceptible to ICD.
Photodermatitis
Phytophotodermatitis is a phototoxic reaction in skin exposed to sunlight after the skin has been in contact with plants containing furocoumarins (psoralens). The rash is similar in appearance to sunburn; and symptoms include pain, vesiculation, erythema, and edema. Plants that contain furocoumarins include limes, lemons, celery, parsley, parsnips, and wild carrots. A careful medical history will often reveal prolonged contact with lime or lemon juice [31,32]. In addition, children may present with this reaction more frequently during the summer when furocoumarins are most abundant in gardens where children play [23]. Sunscreens, as a group, are the most common cause of photoallergic CD [23]. Because sunscreens are often present in cosmetics, moisturizers, lip preparations, foundations, etc, a detailed history of the patients topical medications may narrow down potential offending agents.
Allergic Contact Dermatitis
The symptoms of ACD appear 24 to 48 hours after contact with the offending agent. It is a type IV cellmediated hypersensitivity reaction. Unfortunately, other than a few obvious offending agents such as nickel or plant-associated ACD, history alone can usually identify the sensitizing agent in only 10% to 20% of the cases [23]. The criterion standard test for the diagnosis of ACD remains patch testing. Plants of the Rhus (Toxicodendron ) group such as poison ivy, poison oak, and poison sumac are the most common causes of plant-associated ACD in children in United States [23]. The offending antigen is known as urushiol. The clinical reaction typically results in vesicles and bullae with a characteristic linear pattern. Some of the reactions may also result in soft tissue swelling. Of note, the fluid content of vesicles is not antigenic; but the urushiol can be transferred by handling exposed animals, clothing, sports equipment, etc. [23]. Urushiol is also found in cashew nut trees, Japanese lacquer, Ginkgo biloba , and mango skin. Ingestion of cashews or contact with mango skin can cause a similar rash [26]. Rhus patch testing is not recommended because of its significant sensitizing capacity. Other common causes of ACD are listed in Table 6. Systemic ACD is a generalized rash that is caused by systemic administration of a drug, chemical, or food to which the patient has previously been sensitized through topical exposure [27]. Patients with sensitivity to ethylenediamine may react systemically to systemic administration of aminophylline or antihistamines that contain piperazine or ethanolamine groups [23]. Patients who have been sensitized to topical diphenhydramine or neomycin can also develop systemic ACD from systemic administration of these drugs [23]. Reactions have also been noted in patients who have been sensitized to topical corticosteroids with the administration of systemic corticosteroids [28-30]. Nickel-sensitized patients may develop systemic reactions from ingestion of nickel in tap water, from foods cooked in nickel utensils, and from eating canned foods [23].
Contact Urticaria
Contact urticaria may be associated with concomitant systemic symptoms such as itchy eyes, sneezing, wheezing, or even anaphylactic shock [23]. Patients with atopy are at a higher risk for developing allergic contact urticaria (type I IgE-mediated reactions) [24]. Allergic contact urticaria may occur as an occupational hazard in food handlers. Contact with latex gloves is a wellrecognized cause of allergic contact urticaria or CD [24,33]. In contrast to allergic contact urticaria, non immunological-mediated contact urticaria may be caused by benzoic acid, sorbic acid, cinnamic acid, or nicotinic acid esters, which are found in ice cream, soft drinks, chewing gum, shampoos, perfumes, mouthwashes, or topical creams [24]. Patients may present with erythema and burning without pruritus. Other organ systems are usually uninvolved [24].
Acute Management of CD
For isolated lesions, topical corticosteroids are the firstline medications (Table 3). Patients with sensitivity to preservatives may use preservative-free corticosteroids such as Synalar ointment or Disprosone ointment [23]. Wet and cold compress with or without Burrow solution (aluminum acetate) several times a day may provide patients with additional comfort [24,27]. For patients with more than 20% to 30% body involvement, severe
86 plant-associated ACD, or systemic ACD, systemic corticosteroids are often required. The recommended dose is 0.5 to 1 mg/kg prednisone-equivalent daily for 5 to 7 days [27]. However, the course of ACD, even after removal of the offending agent, may vary and can persist from 14 to 28 days. Therefore, there may be a need to prolong systemic corticosteroid treatment and taper the dose over an extended period. Topical or systemic antibiotics are occasionally indicated for secondary skin infections. Antihistamines such as diphenhydramine or hydroxyzine may offer some benefit by reducing itching in contact urticaria. However, these medications are contraindicated in patients with contact sensitivity due to topical diphenhydramine or ethylenediamine, respectively [27]. Patients with anaphylaxis should be treated accordingly with epinephrine and bronchodilators. Most importantly, avoidance of the offending agent (if identified) is the key management strategy in CD.
P.Y. Ong, M. Boguniewicz
14. Sampson HA, Scanlon SM. Natural history of food hypersensitivity in children with atopic dermatitis. J Pediatr 1989;115:2327. 15. Benenson S, Zimhony O, Dahan D, et al. Atopic dermatitisa risk factor for invasive Staphylococcus aureus infections: two cases and review. Am J Med 2005;118:1048251. 16. Brook I, Frazier EH, Yeager JK. Microbiology of infected atopic dermatitis. Int J Dermatol 1996;35:79123. 17. Engler RJ, Kenner J, Leung DYM. Smallpox vaccination: risk considerations for patients with atopic dermatitis. J Allergy Clin Immunol 2002;110:357265. 18. Chan YF, Agag RL, Kalira D, et al. Rule out smallpox in the ED: an interesting case of streptococcus pyoderma. Am J Emerg Med 2006;24:24324. 19. Moses AE, Cohen-Poradosu R. Eczema vaccinatuma timely reminder. N Engl J Med 2002;346:1287. 20. Wharton M, Strikas RA, Harpaz R, et al. Recommendations for using smallpox vaccine in a pre-event vaccination program. Supplemental recommendations of the Advisory Committee on Immunization Practices (ACIP) and the Healthcare Infection Control Practices Advisory Committee (HICPAC). MMWR Recomm Rep 2003;52(RR7):1216. 21. Centers for Disease Control and Prevention. Smallpox vaccination and adverse events. Department of Health and Human Services. Available at: http://www.bt.cdc.gov/training/smallpoxvaccine/reactions/ec_vac.html.Accessed 4/14/07. 22. Centers for Disease Control and Prevention. Vaccine reaction images. Department of Health and Human Services. Available at: http://www.bt.cdc.gov/agent/smallpox/vaccineimages.asp. Accessed 4/14/07. 23. Boguniewicz M, Beltrani VS. Contact dermatitis In: Leung DYM, Sampson HA, Geha RS, Szefler SJ, editors. Pediatric allergy: principles and practice. Philadelphia, PA: Mosby; 2003. p. 584-94. 24. Ferrera PC, Dupree ML, Verdile VP. Dermatologic problems encountered in the emergency department. Am J Emerg Med 1996;14:5882601. 25. Krasteva M. Contact dermatitis. Int J Dermatol 1993;32:547260. 26. Weinstein S, Bassiri-Tehrani S, Cohen DE. Allergic contact dermatitis to mango flesh. Int J Dermatol 2004;43:19526. 27. Beltrani VS, Bernstein IL, Cohen DE, et al. Contact dermatitis: a practice parameter. Ann Allergy Asthma Immunol 2006;97: S12S38. 28. Bircher AJ, Levy F, Langauer S, et al. Contact allergy to topical corticosteroids and systemic contact dermatitis from prednisolone with tolerance of triamcinolone. Acta Derm Venereol 1995;75: 49023. 29. Chew AL, Maibach HI. Multiple corticosteroid orally elicited allergic contact dermatitis in a patient with multiple topical corticosteroid allergic contact dermatitis. Cutis 2000;65:307211. 30. Bircher AJ, Bigliardi P, Zaugg T, et al. Delayed generalized allergic reactions to corticosteroids. Dermatology 2000;200:349251. 31. Weber IC, Davis CP, Greeson DM. Phytophotodermatitis: the other blimeQ disease. J Emerg Med 1999;17:23527. 32. Wagner AM, Wu JJ, Hansen RC, et al. Bullous phytophotodermatitis associated with high natural concentrations of furanocoumarins in limes. Am J Contact Dermat 2002;13:1024. 33. Woods JA, Lambert S, Platts-Mills TA, et al. Natural rubber latex allergy: spectrum, diagnostic approach, and therapy. J Emerg Med 1997;15:71-85.
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