Hand, foot, and mouth disease (HFMD) is a common childhood viral illness characterized by vesicles in the mouth, hands, feet, and sometimes the buttocks. HFMD has a predilection for the summer and autumn seasons, and historically has been treated with supportive care. Coxsackievirus A16 and enterovirus 71 are the most commonly reported viruses responsible for HFMD. Coxsackievirus A6 (CVA6), however, has been associated with more widespread skin lesions and profound tissue destruction. Recently, the term eczema coxsackium (EC) was coined to describe patients with underlying atopic dermatitis who present with an eczema herpeticum-like eruption caused by CVA6 with vesicles and erosions in pre-existing areas of eczema. Enteroviral infections, particularly CVA6, should be on the clinicians’ differential diagnosis of children who present with extensive erosions and vesicles, and with a history of eczema. We present the first case, to our knowledge, that documents wet wrap therapy (WWT) as a viable treatment option for CVA6 EC, a condition that previously has only been treated with supportive measures. Our patients were 8-month-old former 36-week fraternal twin boys with medical histories significant for eczema. A few days before their January admission, the eczema of both patients were noted to be worsening and not responding to step-up therapy. The primary care physician had escalated therapy from daily moisturizing, as needed over-the-counter class VII topical corticosteroids (TCS), and twice a week diluted bleach baths, to a class V TCS, Hydrocortisone Valerate 0.2% cream (Perrigo Pharmaceuticals, Bronx, New York, New York). The patients were presented to the emergency department with rapid progression of a vesiculobullous rash that involved the face, particularly the perioral area, upper and lower extremities, and trunk. Of note, twin B was diagnosed with otitis media on the day before presentation to the hospital, for which his pediatrician started him on cefdinir. The infants were referred for admission because of worsening skin lesions, fussiness, and dehydration. Laboratory evaluation included a complete blood cell count with differential, comprehensive metabolic panel, and blood cultures. Vesicular fluid was aspirated and sent for herpes PCR, enterovirus PCR, and viral cultures. Intravenous acyclovir and ceftriaxone were started for empiric treatment of herpes and possible bacterial superinfection. Differential diagnosis included eczema herpeticum, varicella, EC from HFMD, and a severe eczema flare with secondary bacterial infection. Complete blood cell count and comprehensive metabolic panel results were within normal limits. Results of herpes PCR, viral cultures, and blood cultures were negative. The enteroviral PCR results were positive. Further testing by the Centers for Disease Control and Prevention confirmed CVA6. Ceftriaxone and acyclovir were stopped when blood cultures and erpes simplex virus PCR results were negative, and WWT and low-potency Class VI TCS (desonide 0.05% ointment, Taro Pharmaceuticals Inc., Brampton, Ontario, Canada) were started. Although it is well known that WWT, in conjunction with TCS, is an effective and safe treatment for severe flares of atopic dermatitis refractory to increased TCS strength, to our knowledge there is no literature that mentions the use of WWT for treatment of EC. The benefits of WWT include an occlusive barrier that prevents scratch-induced skin trauma, increased skin hydration, decreased pruritus and inflammation by cooling of the skin, and increased penetration of the TCS. Complications, such as maceration of the skin or secondary skin infections, are possible but have been shown to be uncommon with proper application of WWT. Because standard skin therapy was unsuccessful for these patients before admission and because results of enteroviral PCR were positive, which raised our suspicion that this was a possible EC case, we considered the risks and benefits of increasing the potency of the TCS further, commensurate with the severity of the flare, versus implementing WWT with a low-potency TCS. Although there have been no reported complications with patients with CVA6 EC, there are no studies that evaluated whether the use of TCS, or occlusion from WWT, increases the risk of complication. Furthermore, there are no studies that evaluated whether the use of TCS, or occlusion from WWT, increases the risk of worsening the cutaneous findings of EC by immunosuppression and leads to more disseminated viral growth. When considering the large body surface area involved, and balancing the uncertainty of the theoretical risks of higher-potency corticosteroids inCVA6ECwith the knownbenefits ofWWTand TCS, we chose to continue treatment with a low-potency TCS with the addition of WWT. Systemic adverse effects from WWT with corticosteroid use were considered; however, prolonged suppression of the hypothalamic-pituitary-adrenal axis has not been reported after short-term treatment with WWT and TCS. Therefore, we pursued only short-term use of combined WWT and low-dose TCS for 3 days. Wet wraps were applied 3 times a day, with the morning and evening wraps to include Aquafor (Beiersdorf, Hamburg, Germany) to unaffected areas and desonide 0.05% ointment to the affected areas, and the mid day wrap included Aquafor head to toe. The morning and mid day wraps wereworn for an hour, and the eveningwrapswereworn overnight. Within 24 hours, the patients demonstrated significant clinical improvement, and were discharged after extensive family education to continue the same WWT regimen at home. Twin B also was discharged on cefdinir for the previously diagnosed otitis media. By day 3 after discharge, the patients had improved dramatically, and WWT was discontinued. The twins were seen for follow-up 5 days after discharge and were noted to have had an