Winter 2019 Issue
Volume 11 | Number 1
Christopher Larrimore, M.Sc
Rogerio Faillace, M.D.
Nova Southeastern University
Fort Lauderdale, FL
Dyshidrotic eczema is a type of dermatitis of unknown etiology that is characterized by pruritic vesicular eruptions of both the hands and feet. While the exact cause is unknown, it is often associated with hyperhidrosis and atopy. Diagnosing dyshidrotic eczema can be challenging as clinical presentation can mimic Tinea pedis or cellulitis from bacterial infections. For this reason, if the differential diagnosis is limited to fungal or bacterial etiologies, prolonged and reoccurring episodes will result. In this clinic case report we describe a case of an eight-year-old boy from South Florida with chronic interdigital pruritic erythematous lesions located on both hands and feet. Following several unsuccessful fungal and bacterial treatments, infection was ruled out and dyshidrotic eczema was added to the differential diagnosis. Once treatment was modified to target dyshidrotic eczema, the patient’s condition greatly improved. This case report emphasizes the importance of eliciting a thorough history from patients presenting with recurring skin infections. The inclusion of hyperhidrosis in the patient history was principal in expanding the differential diagnosis, which ultimately lead to an improvement in patient treatment
Dyshidrotic eczema is a type of dermatitis of unknown etiology that is characterized by intensely pruritic, vesicular eruptions of both the hands and feet. It is a relatively rare type of dermatitis with an unknown prevalence, but is estimated to account for five to twenty0 percent of all cases of hand dermatitis.1,2 Episodes often start with pruritus, followed by symmetrical vesicular eruptions on the fingers, toes, palms and soles. Vesicles are typically deep-seated and multilocular, but may later merge into larger bullae. While feet can be an area of involvement, between 70 to 80 percent of patients will only present with eczema on the hand.3 This is typically preceded by a history of excessive perspiration in the areas of involvement.
The frequency of episodes can vary, ranging between self-limiting to chronic, with the possibility of secondary skin infections. Typically, vesicles and bullae will persist for weeks before resolving. However, if untreated, secondary infections can develop.1,3 The most common secondary infections include Staphylococcus aureus and Tinea pedis.4 Increased frequency of episodes can result in lichenified, red scaling patches with fissures. This is more common in warm climates or in patients with emotional or physical stress.4
While the etiology is unknown, it is likely multifactorial. Some of the most common associated factors include hyperhidrosis, a history of atopy, exposure to contact allergens or irritants and emotional stress.4,6-8 Interestingly, while hyperhidrosis is a predominant associated finding in 40 percent of those affected, a 2009 case report provided histopathologic evidence that sweat glands are not involved.5 Regardless of pathogenesis, clinical diagnosis is relatively achievable as it is based upon clinical findings, symptoms and history.
Diagnosis does not require biopsy. Instead, clinicians should look for deep-seated vesicles localized on the hands, feet or lateral surfaces of the fingers. In addition, a history of intense pruritis with recurrent episodes that is preceded by rapid onset is required. Hyperhidrosis may or may not be reported, but should be considered. A differential diagnosis should include atopic dermatitis, contact dermatitis, bullous tinea, herpetic infection, cellulitis and Tinea pedis.
The management of dyshidrotic eczema first requires the identification of severity. Avoidance of causative factors should be achieved, if possible. Patients should keep affected areas clean and dry, lotions can be applied to prevent excessive dryness which may be an aggravating factor. Secondary infections should be treated accordingly (antibiotic or antifungal). Topical corticosteroids should be applied for patients with moderate severity, systemic corticosteroids can be used for more severe cases.4
An eight-year-old boy presented to the pediatric clinic with a one-year history of recurring skin infections. During the first office visit, the child’s parents described a pruritic erythematous lesion located between the first and second toe of the right foot. During the two-months prior to this visit, the parent’s applied over-the-counter anti-fungal creams but reported no improvement. Tinea pedis was diagnosed and 1% topical terbinafine was prescribed. The child was instructed to keep his feet clean and dry and to apply the topical medication daily. Seven months later, the child returned to the clinic for a well visit. During examination, the mother reported a recurring pruritic interdigital rash located on the right hand. She stated that the rash typically self-resolved within three weeks. The rash was described as “red, bumpy and itchy.” At this time, the child was diagnosed with atopy.
|Figure 1: Pruritic vesicular eruptions of the left foot, both feet were equally affected.|
|Figure 2: Left foot one month after topical steroid was applied, vesicular eruptions are noted to have improved.|
Within one month, the child developed bilateral pruritic erythematous vesicular eruptions located between his toes. The parents attempted various treatments which included over-the-counter antifungal creams, soaking the child’s feet in hydrogen peroxide and applying Listerine to the affected areas of the skin. After two months with no improvement, the boy returned to the clinic. Physical examination revealed bilateral pruritic vesicular eruptions between the toes and on the forefoot (figure 1). Tinea pedis was diagnosed and oral terbinafine (250 mg Q.D.) was prescribed. Two weeks later, the patient returned with no improvement. During examination no pus or discharge was noted, however, small papules located on both hands were present with a small lesion located on the left hand. Additionally, his hands felt cold and sweaty to touch. Laboratory testing was ordered and revealed negative results. Testing included skin culture, complete blood count (CBC) and antistreptolysin (ASO). Further discussion with the parents revealed a history of hyperhidrosis on both the hands and feet of the child. Additionally, the mother reported having increased sweat production of her hands, similar to her child’s. Dyshidrotic eczema was diagnosed.
The child was prescribed a topical corticosteroid (fluocinonide 0.1%, q12hr) and instructed to apply to the surrounding areas that did not have ruptured lesions. Additionally, he was also prescribed a topical antibiotic (Bactroban 2%, q12hr) and instructed to apply this to the areas of ruptured lesions. He was asked to keep the affected areas clean and dry. During a follow-up appointment one month later, the lesions (figure 2) appeared improved.
Indicators that this patient presented with dyshidrotic eczema include a history of hyperhidrosis, recurring pruritic-erythematous lesions of the hands and feet, interdigital vesicles, and poor response to anti-fungal therapies. Further supporting this diagnosis, was the mother’s reporting of similar patterns of hyperhidrosis. Because this disorder can be inherited, the mother’s excessive sweating located in her hands and feet, suggest a pattern of inheritance between mother and child.
The differential diagnosis for this case included atopy, Tinea pedis and S. aureus infection, which were all later ruled out. Failure to respond to anti-fungal medications ruled out Tinea pedis. Negative skin cultures and ASO titers ruled out bacterial infection. Improvement in symptoms following medical therapy that was in align with dyshidrotic eczema, ultimately confirmed the diagnosis.
Because dyshidrotic eczema can vary in severity, altering the therapeutic approaches may be required. Here the patient had increased frequency of episodes and slow response to standard treatment. This suggest a more severe form of dyhidrotic eczema which will require more aggressive therapies in the future. Standard care for less severe cases would be topical corticosteroid and maintaining a clean and dry surface. However, for more severe cases, systemic corticosteroids or biologics should be considered.
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