A 57-year-old man with a history of diabetes mellitus and hypertension presents to the emergency department (ED) with a 2-week history of vesiculobullous lesions on his feet and hands. The lesions first appeared on both of his feet and have been increasing in size and number; over the last several days, they have begun to develop on both of his palms and on the sides of the fingers. The patient was seen at a different clinic approximately 1 week ago and was given an ointment to treat the lesions; this has not resulted in any improvement. The lesions are extremely pruritic. The patient has not had any recent travel history, and he lives alone, without any pets, in a regularly cleaned apartment. He has had no discernible new exposures and has not experienced any fevers or constitutional symptoms. The patient is on insulin, labetalol, and a combination pill of lisinopril/hydrochlorothiazide plus omeprazole; he has been on these medications for a long time and has had no prior complications. The patient has no known allergies.
On physical examination, the patient is well-appearing at rest, without any signs of undue anxiety or discomfort. His vital signs show a temperature of 98.7ºF (37.1ºC), blood pressure of 130/85 mm Hg, heart rate of 70 bpm, respiratory rate of 18 breaths/min, and oxygen saturation of 98% while breathing room air. Fluid-filled vesicles ranging in size from 1 mm to 3 cm are present on the instep and plantar aspects of his feet (see Figures 1 & 2). The vesicles are present on the palms of his hands and the sides of the fingers as well. The lesions are all skin-colored, without any surrounding erythema. No other lesions are found anywhere else on the patient’s body. The lesions are nontender to palpation; additionally, his legs exhibit nonpitting edema up to the knees and reduced sensation to light touch, both long-standing conditions. The oropharynx is clear of any lesions, and the rest of the physical examination is unremarkable.
| What is the skin condition being described?Hint: Pay particular attention to the anatomic clustering of the lesions. | |||
| Allergic contact dermatitis | |||
| Herpes simplex | |||
| Impetigo | |||
| Dyshidrotic eczema | |||
stepowl said,
March 20, 2008 @ 5:07 am
The diagnosis of dyshidrotic eczema, also known as pompholyx (Greek for “bubble”), was made on the basis of the patient’s history and the results of the physical examination. Additional testing (described below) ruled out any alternative diagnoses. The pruritic lesions were progressive in number and size, but they were restricted to the hands and feet. The blisters were classically vesiculobullous in nature, without any surrounding erythema. Lesions in multiple stages of development, from emerging vesicles to ruptured bullae, were concurrently present. The history did not reveal any etiologic factors, such as recent exposures to allergens, new medications, or animal-borne vectors. The patient did not have any systemic symptoms and was afebrile. No evidence of concurrent cellulitis or lymphangitis was apparent.
Dyshidrotic eczema is estimated to be present in 0.5-1% of the population, with an equal distribution between men and women. The majority of cases present before the patients reach 40 years of age, and there is no racial predominance. It is more commonly found in warmer, more humid climates, especially during the spring and summer. Recurrences may occur throughout a patient’s lifetime, with or without treatment. The pathophysiology of dyshidrotic eczema has not been definitively established,[5] but several hypotheses have been proposed. The term “dyshidrosis” is a misnomer that refers to the original hypothesis of sweat gland dysfunction, which has fallen out of favor. In addition, patients are not typically noted to experience hyperhidrosis. There is interest in the association of the condition with atopy,[4] as approximately 20% of patients experience concomitant hand eczema and approximately 50% of patients have a general disposition to an atopic diathesis (eg, asthma, hay fever, and sinusitis).[2] Other exogenous factors that have been implicated and may trigger episodes include contact dermatitis to heavy metals (such as with exposure to costume jewelry, nickel,[2,5] cobalt,[5] or chromates); sensitivity to ingested metals[5]; exposure to other contact allergens such as balsam,[5] paraphenylenediamine, and sesquiterpene lactones; and infection by dermatophytes or bacteria. Emotional stress (many patients report recurrences during stressful periods of their life) and environmental factors (eg, seasonal changes, hot or cold temperatures, and humidity) are also reported to exacerbate dyshidrosis.[2,5] There have also been case reports of dyshidrotic eczema occurring in patients recently treated with intravenous immunoglobulin therapy; in HIV-positive patients with an immune reconstitution inflammatory syndrome shortly after starting active antiretroviral therapy[5]; with the use of aspirin or oral contraceptives; and with cigarette smoking. In most cases, the condition remains idiopathic.
Dyshidrotic eczema is a recurrent or chronic, relapsing form of vesicular dermatitis. The classic presentation is of crops of vesicles or bullae that erupt bilaterally on the palms and the lateral aspects of the fingers. The vesicles may coalesce over time to form multiloculated bullae. The majority of cases involve the hands alone (cheiropompholyx), but roughly 10% of patients have lesions on both the hands and feet, and another 10% have lesions on just the feet (podopompholyx). The lesions may be intensely pruritic, leading to secondary desquamation and erosions and ulcerations from scratching. Dyshidrotic eczema developing near the tips of the fingers or toes may lead to dystrophic changes of the nails. Cellulitis, lymphangitis, or infection of the lesions themselves may all develop with the long-standing presence of lesions and/or poor hygiene. The vesicular crops usually resolve spontaneously after 3-4 weeks, leaving behind collarettes of scale. Although self-limited, outbreaks will frequently alternate with disease-free intervals of weeks to months and, if severe, may be extremely disabling.[5]
The differential diagnosis includes immunobullous disorders, such as bullous pemphigoid and pemphigus vulgaris, or other dermatoses, such as contact dermatitis, herpes simplex virus infection, bullous tinea pedis, and pustular psoriasis. The diagnosis is usually made on the basis of the clinical history, the physical examination, and the exclusion of alternative diagnoses. Bacterial culture and sensitivities may be evaluated for secondary infections. Additionally, potassium hydroxide wet mount preparations may be useful for excluding dermatophyte infections. A skin biopsy may also be useful for confirming the clinical impression in unresponsive cases and for excluding alternative diagnoses. It can be difficult to differentiate dyshidrotic eczema from an id reaction (autoeczematization), which is a cutaneous eruption that develops in response to a variety of infectious and inflammatory stimuli at a distant site from the primary dermatosis.[5]
Treatment for dyshidrotic eczema begins with topical corticosteroid therapy; topical class I steroids are the first-line treatment regimen, with oral steroids reserved for more severe cases. Large lesions should be drained, but not unroofed, in order to prevent rupture and subsequent infection. Wet compresses will help shrink bullae, and the physician could consider a course of oral antibiotics if infection is suspected. In many patients, antihistamines or other antipruritic agents may be extremely helpful for symptomatic relief. The patient should make appropriate modifications to daily activities and should avoid scratching in order to limit unwarranted skin irritation, exacerbation, and subsequent infection. In addition, there are a number of other adjuvant therapies, such as ultraviolet light, botulinum toxin, irradiation, occlusive dressings, and immunosuppressive agents, which may be helpful on a case-by-base basis for refractory patients. Unfortunately, there is no established preventive therapy except for avoidance in patients with well-established triggers. Untreated dyshidrotic eczema can lead to concomitant infections; therefore, prompt detection and treatment is essential.
One of the bullae, measuring approximately 3 cm by 1.5 cm, was percutaneously drained with a 10 cc syringe. Approximately 3 mL of a yellow, cloudy fluid was aspirated. The roof of the vesicle was left intact. In order to confirm the diagnosis and exclude alternative diagnoses, a punch biopsy of the skin was performed from the foot (see Figures 1-3). Histologically, spongiotic dermatitis and an intraepidermal vesicle were present, which were consistent with the diagnosis of dyshidrotic eczema. A periodic acid-Schiff (PAS) stain performed on this specimen did not reveal any fungal elements; scrapings of skin from the feet were negative for fungal infection as well. The patient was instructed to begin a regimen of topical steroids and moisturizing emollient, as well as wet compresses. An over-the-counter moisturizer was recommended, and prescriptions for Burrow’s solution (10% aluminum acetate) and clobetasol propionate were written. Additionally, prophylactic antibiotics were prescribed to prevent superinfection by typical organisms. The patient was instructed to limit his ambulation to avoid further blister rupturing. At a follow-up visit, the patient underwent patch testing, but a causative contact allergen was not identified.
Although dyshidrotic eczema is frequently idiopathic, which one of the following has not been described as being associated with an outbreak of dyshidrotic eczema?
Answer: Person-to-person contact
The exact etiology of dyshidrotic eczema is not completely understood; however, studies have elucidated associations with contact allergens (notably nickel), IVIg therapy, emotional stress, and concomitant tinea pedis infection. Unfortunately, in many cases, the causative agent is not discovered. There is no evidence to support person-to-person transmission.
What is the most common anatomic location for the presentation of dyshidrotic eczema?
Answer: Hands
Approximately 80% of cases of dyshidrotic eczema are localized to the hands only; 10% of cases are limited to the feet only; and 10% include both the hands and the feet, as in the patient in this case. Vesicles are rarely found elsewhere on the body.
dermlive said,
April 25, 2008 @ 10:59 pm
yup i agree, i recently had a case with both palmsand soles involved. biopsy wasnt supportive(psoriasiform dermatitis) they have improved with potent topical steroids but they always relapse. trating herproved 2 b a challange. the strange thing about this case is thie asssocoation with keratoderma but since she s old it may be present well before the onset of bulla.
the best clearance she had wad when she wasadmitted in our hospital wheere she enjoyed almost free disease period(2moths) after dicharge without treatment