An Atypical Case of Allergic Contact Dermatitis in a Pediatric Patient

AUTHORS:

Claire Overholt, BS1; Bliss Colao, BS1; Michele Lossius, MD, FAAP2; Kendall Steadmon, MD2
1University of Florida College of Medicine, Gainesville, Florida
2Department of Pediatrics, University of Florida, Gainesville, Florida

CASE REPORT | PUBLISHED SPRING 2025 | Volume 45, Issue 2

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Abstract

Allergic contact dermatitis is a common rash caused by an immune reaction to an allergen that touches the skin. Allergic contact dermatitis is a type IV hypersensitivity reaction, and it presents clinically as a well-demarcated, pruritic rash that typically exhibits bright erythema and edema. It can also have vesicles, oozing, and blistering. There are many triggers of allergic contact dermatitis, including metals, cosmetics, topical medications, and various plants. We present an atypical case of allergic contact dermatitis on the plantar foot in a 7-year-old male who was initially diagnosed with cellulitis. His physical exam was significant for a large bulla on his plantar foot. The presumed trigger for our patient was a Toxicodendron plant, as he had a history of swimming and walking barefoot outside. Toxicodendron plants (poison ivy, poison oak, and poison sumac) contain urushiol, which can trigger allergic contact dermatitis. Treatment for allergic contact dermatitis is typically topical steroids, with systemic steroids recommended in more severe cases, such as our patient’s case. Definitive treatment is the removal of the triggering allergen. A high index of suspicion is needed in cases of allergic contact dermatitis, particularly in cases of atypical presentation.

Introduction

Allergic contact dermatitis (ACD) is a common rash caused by an immune reaction to an allergen that touches the skin.1 Common allergens include metals (e.g., nickel), personal care products, cosmetics, topical medications, plastics, glues, rubber materials, and various plants.1 ACD is considered a type IV delayed-response hypersensitivity reaction and presents clinically as a well-demarcated, pruritic rash that usually has bright erythema and edema.2 Vesicles, oozing, and blistering can be associated with the rash, making it difficult to distinguish from infections (i.e., cellulitis) or irritant contact dermatitis.2 We present an atypical ACD on the plantar foot in a 7-year-old male diagnosed initially with cellulitis.

Primary Objective

Be able to identify an atypical presentation of ACD, understand the pathology of ACD, and accurately treat cases of ACD.

Case Presentation

A 7-year-old male presented to our emergency department (ED) with a chief concern of redness, swelling, and blisters on the right plantar foot for four days. His past medical history was significant for seasonal allergies, and he was not taking any medications at the time. Five days before the presentation, he reported boating and swimming in a river. The patient was barefoot but did not recall stepping on any rocks or sustaining injuries to his right foot. Over the next 48 hours, his right foot became pruritic, and blisters appeared. The blistering worsened and was associated with significant pain that prevented the patient from ambulating. He denied pain unless pressure was placed on his right foot. He had no other symptoms, such as fever, chills, or joint pain. Due to worsening symptoms, his mother took him to an outside hospital two days after the itching started, where he was diagnosed with cellulitis. He was prescribed topical mupirocin ointment and a course of oral cephalexin.

The blister increased in size over the next two days, and his foot pain persisted. Thus, he returned to the ED. At the outside ED, the patient received one gram of ceftriaxone intramuscularly (IM) and one intravenous (IV) saline bolus. His labs at presentation were significant for a white blood cell count of 10.5 × 103/µL, with 47.6% neutrophils and 18.4% eosinophils and lactic acid of 1.5 mmol/L. An X-ray of the right foot displayed soft tissue abnormality on the plantar aspect, with no acute osseous abnormality or radiopaque foreign body.

The patient was then transferred to our ED, where a physical exam showed erythema, swelling, and multiple large bullae on the plantar aspect of his right foot (Figure 1). The patient was afebrile and hemodynamically stable. The erythema was marked with a pen, and the patient was started on IV clindamycin due to concern for cellulitis (Figure 2). One dose of cefepime was given to address the fears of Pseudomonas aeruginosa infection, and pediatric surgery was consulted.

Figure 1: Clinical presentation in our emergency department showing multiple large bullae on the plantar aspect of the patient’s right foot.

Figure 2: Clinical presentation showing bullae on patient’s right plantar foot, with surrounding edema and erythema.

Pediatric surgery recommended consulting orthopedic surgery to evaluate the right foot for potential bone or tendon involvement. Orthopedic surgery conducted a bedside deroofing procedure that removed the circumferential epidermis from all affected areas. Afterwards, the wound was cleaned and bandaged. The patient received an IM injection of ketorolac for pain control and had acetaminophen as needed for pain. His antibiotics were changed from IV clindamycin to oral cephalexin. Dermatology was consulted and noted pink desquamated plaques with peripheral residual detached skin of bullae on the right plantar foot status post debridement (Figure 3) and non-erythematous vesicles versus small bullae on the left lateral foot and third toe web space. They determined this was likely ACD due to Toxicodendron species, without concern for cellulitis or other infectious etiology.

Figure 3: Clinical presentation showing desquamated plaques with peripheral residual detached skin of bullae on right plantar foot status post debridement.

Physical therapy was consulted to assist with ambulation, and wound care was involved. The patient was afebrile, hemodynamically stable, and had adequate intake and output upon discharge. The patient was discharged on a course of oral prednisolone (2mg/kg/day for 5 days) and was to follow up with his primary care physician and orthopedic surgery after discharge. At the orthopedic follow-up one week after discharge, the patient’s foot was healing well.

Discussion

This presentation demonstrates the difficulty that can be encountered in diagnosing ACD and determining the underlying cause. This is not an uncommon issue, with some studies estimating the prevalence of ACD as high as 20% in the general population with a wide range of allergens that can serve as triggers.3,4 Additionally, due to the delayed onset of presentation, identifying the causative agent can be complicated. Groups with a higher risk of developing ACD are those with a personal or family history of atopy (as with our patient), those who have increased environmental exposures to allergens, and female sex.4 The rates of ACD in children are reported to be similar to those of adults; however, many childhood cases are likely underdiagnosed.5 ACD can occur at any age, with some reports of ACD in infancy, although prevalence increases with age.5

The proposed pathophysiology of ACD includes a sensitization phase and an elicitation phase. Sensitization occurs when exposed to a low-molecular-weight allergen or hapten, which is taken up by a dermal dendritic cell and presented to a T-cell in a draining lymph node.2,6 The elicitation phase occurs upon re-exposure to the allergen, which causes the dermatitis, with a peak inflammatory process occurring 72 hours after re-exposure.2,6 This type IV delayed-response hypersensitivity reaction is primarily mediated by Th1 cells and Th2, Th17, and Th22 cells.2

There are many triggers for ACD, with the most common being nickel.7 Other common allergens are methylisothiazolinone, formaldehyde, and methylchloroisothiazolinone, which are preservatives in everyday products, and fragrance mixes.2,7 Topical medications, such as antibiotics and corticosteroids, are also commonly implicated in ACD.2,7 The plants most likely to cause ACD are poison ivy, oak, and sumac, which fall under the Toxicodendron genus.1,8 Toxicodendron plants contain urushiol, which can trigger ACD.8 A thorough history to determine the trigger for the rash is central to making the diagnosis. It is essential to elucidate the location of the lesions, when they developed, how they have evolved, exposures, and previous treatment.4 For our patient, who had a history of swimming and walking barefoot outside, his dermatitis was likely secondary to a plant in the Toxicodendron genus, which is widespread throughout North America.8

ACD commonly presents on the hands or face, or as a scattered or generalized distribution.7 The dermatitis distribution patterns can be helpful in diagnosis because they reflect the area of contact with the allergen.3,4 In our case, the plantar foot was an unusual location for ACD, which could have contributed to the initial misdiagnosis of cellulitis.4

The first-line treatment for ACD involves short-term mid- to high-potency topical corticosteroids, such as triamcinolone 0.1% or clobetasol 0.05%.9,10 Systemic corticosteroids can also be used and are specifically helpful in quickly calming the inflammatory response associated with ACD secondary to Toxicodendron plants, as in the case of our patient.4 A two to three-week taper of oral corticosteroids is typically recommended in cases of ACD to Toxicodendron plants due to the risk of rebound dermatitis.8,10 Surgical intervention, as seen in our patient, is not a routine treatment for ACD.10 However, surgery can be employed in cases of cellulitis to drain abscesses.10 This further emphasizes the need for timely and accurate diagnosis of ACD to ensure proper treatment.

Definitive treatment is the identification and removal of the causative agent to prevent recurrent or chronic dermatitis.9 As mentioned, identifying the causative agent can be challenging. Patch testing can be used when the etiology is unknown or if the patient’s dermatitis is worsening or unresponsive to treatment.10,11 Patch testing uses various allergens suspended in a vehicle (commonly white petroleum) exposed to the skin to recreate an allergic reaction.5,10 Patch testing can also be used for patients at high risk for ACD, such as healthcare workers, cosmetologists, and construction workers.4,11

Pediatricians need to be familiar with diagnosing and treating cases of ACD, as many pediatric patients will present initially to their pediatrician. This case highlights the importance of clinical history in diagnosing allergic contact dermatitis. A high index of suspicion is needed in cases of ACD, particularly in cases of atypical presentation.

References

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