How Would You Diagnose This Man’s Erythematous Plaques?

A 44-year-old otherwise healthy man presented with pruritic linear erythematous plaques on his left wrist. Two weeks prior, the patient had been doing some garden work in his backyard while wearing shorts and a T-shirt. By the following morning, he developed a pruritic vesiculobullous erythematous eruption on the left wrist in streak-like arrangements. 

The patient applied an over-the-counter 1% hydrocortisone cream and polysporin ointment several times a day on the affected area but without much improvement of the rash or pruritus. There was no history of insect bites or contact with animals. The patient suspected that the eruption was related to a plant that he accidentally cut in the backyard. The plant had 3 leaflets per stem. 

Physical examination revealed well-demarcated erythematous-brown linear streaks on the left wrist. The rest of the physical examination was normal. 

What's Your Diagnosis?

A. Phytophotodermatitis
B. Chemical irritant dermatitis
C. Poison ivy dermatitis
D. Steven-Johnson syndrome
E. Arthropod bites

(Answer and discussion on next page)

Answer: Poison Ivy Dermatitis

Poison ivy dermatitis is the most common allergic contact dermatitis in the United States.¹ The condition was first described by Nicholson in 1899 who reported a young woman with contact dermatitis after pruning a creeper.² Her father ordered a servant to cut the plant down and the servant developed a widespread allergic contact dermatitis. The plant was subsequently identified to be poison ivy.

Poison ivy belongs to the genus Toxicodendron (previously classified as in the genus Rhus) and the family Anacardiaceae.² Eastern poison ivy (T radicans) is a small shrub or climbing vine that grows mainly east of the Rocky Mountains.³ Western poison ivy (T rydbergii) is a nonclimbing shrub that grows mainly in the northern United States and in Southern Canada.³ The leaves of poison ivy are usually notched and in groups of 3. The flowering branches arise from axillary positions on a single stem.⁴

Epidemiology 

Approximately 50% to 75% of the adult population in the United States is clinically sensitive to poison ivy.⁵ The peak frequency of sensitization occurs between 8 and 14 years of age.⁵ In the eastern states, poison ivy dermatitis usually occurs in the spring and summer whereas in southwestern states, poison ivy dermatitis occurs the whole year round.⁶ Poison ivy dermatitis is a hazard for people who work outdoors or engage in outdoor activities, such as hiking and camping. Farmers, forestry workers, and firefighters are at risk. The condition is slightly more common in males. 

Etiopathogenesis

Poison ivy dermatitis is caused by a type IV, T-cell mediated, delayed hypersensitivity reaction to urushiol, which is found in the sap from damaged leaves or plants of Eastern poison ivy (T radicans) or Western poison ivy (T rydbergii). The dermatitis primarily results from direct contact with the urushiol or indirect contact via contaminated clothing or even smoke from burning poison ivy. Urushiol is stable in high temperature and can be carried in the air by smoke particles when the plants are burned. Damage to the plant is required for poison ivy to release the chemical. Therefore, slight contact with the intact poison ivy plant is usually innocuous and does not cause dermatitis.⁶

Urushiol is composed of a mixture of 3-n-pentadecylcatechols, which are potent allergens. After initial contact, 3-n-pentadecylcatechols penetrate the outer layer of the skin within minutes and become activated to quinone intermediates, which can then bind to antigen-presenting cells.⁶ The antigen-presenting cells present the processed antigen to CD4 T-helper lymphocytes with resultant formation of a clone of urushiol-specific T-effector and T-memory lymphocytes.⁶ With re-exposure to urushiol, these clonal lymphocytes elicit a cell-mediated cytotoxic immune response.⁶

Urushiol is colorless or amber color in the natural state. Due to the enzyme laccase found in the oleoresin, urushiol may oxidize, polymerize, and turn black when exposed to air in a warm, humid environment.⁶

Clinical Manifestations 

Following contact with the sap of poison ivy, a sensitized person typically develops an intensely pruritic eruption within 48 hours of exposure.⁶ The eruption may appear as early as 5 hours or as late as 14 days after exposure.⁴ Intense pruritus is the most common presenting symptom and often precedes the appearance of the eruption. Streaks of erythema and papules in linear arrangements confined to the area that has come in contact with the offending plant agent soon follow. Vesicles may develop hours later and may enlarge into bullae. Mild cases often lack vesicles whereas the more severe ones may present with confluent bullae and edema. The fluid content of vesicles and bullae does not contain urushiol and will not spread the eruption.^5,6 The severity of the dermatitis depends on the level of sensitization, individual susceptibility, the skin thickness at the site of contact, degree of exposure, and the amount of urushiol that binds with the skin.^3,6 The arms, legs, and, the face in children, are sites of predilection.³ At times, the genitalia may become involved from contact with urushiol-contaminated hands.³

Black spot poison ivy dermatitis is a rare clinical variant.⁷ The condition occurs when sufficient concentration of urushiol is left on the skin and oxidized via a dopa oxidase-mediated oxidation process in the presence of oxygen and moisture and turns black.⁷ Typically, black spot poison ivy dermatitis presents with asymptomatic shiny black spots with surrounding erythema on the skin that cannot be washed off.⁴ This is followed by the typical skin eruption of poison ivy dermatitis.⁵

Diagnosis 

The diagnosis is a clinical one. Key elements are taking a history of exposure to a plant with 3 leaflets and familiarity in recognizing the clinical appearance of the lesion (typically linear). 

Differential Diagnosis

Poison ivy dermatitis should be differentiated from phytophotodermatitis. Phytophotodermatitis results from the interaction of solar radiation and photosensitizing compounds (furocoumarins) in various plants. The most common plant families high in furocoumarin content and capable of provoking phototoxic reactions are Rutaceae (eg, limes, lemons, oranges, tangerines).⁸ Phytophotodermatitis is characterized by bizarre configurations of erythema with a sharply demarcated border confined to the area that has come in contact with the offending plant agent and consequent sun exposure.⁸ Vesicles and bullae may develop after 24 hours and peak at 72 hours, and often accompanied by subsequent desquamation and denudation. Pruritus does not seem to be common.⁸ In contrast, poison ivy dermatitis occurs on both covered and uncovered parts of the body and do not require sunlight for its development. Intense pruritus is a characteristic feature of poison ivy dermatitis. Other differential diagnosis include other sources of allergic contact dermatitis, chemical irritant dermatitis, arthropod bites, dyshidrotic eczema, toxic epidermal necrolysis, bullous pemphigoid, bullous tinea, bullous impetigo, Steven-Johnson syndrome, neurotic excoriations, and nummular eczema. Black spot poison ivy dermatitis should be differentiated from a melanoma.

Complications

Secondary bacterial infections with Staphylococcus aureus and group A ß-hemolytic streptococcus are the most common complication.⁴ Another common complication is transient post-inflammatory hyperpigmentation, which is more pronounced in dark-skinned individuals.⁶ The hyperpigmentation usually resolves within months without treatment. Rare complications include urticaria, erythema multiforme, urinary retention due to penile edema, and nephropathy due to immune complex deposition in the kidney.^4-6

Prognosis

The condition is usually self-limiting, lasting approximately 3 weeks.⁵ 

Prevention

The best preventive measure is avoiding contact with poison ivy. The aphorism “leaves of 3, leave them be” refers to the characteristic leaflets per stem of poison ivy and aptly applies to remind people to stay away from the plant. Wearing long-sleeve clothing while gardening or in the woods can be helpful. If contact with poison ivy is suspected, the exposed skin should be gently washed with water and a mild soap. Overly enthusiastic scrubbing should be avoided.⁵ Contaminated clothing should be removed as soon as possible.

Management 

In the majority of cases, ultrapotent topical corticosteroids used early in the course of the dermatitis are the cornerstone of therapy. On the other hand, a mid-potency topical corticosteroid should be considered when the dermatitis involves the face, genitalia, or intertriginous areas. In patients with refractory or severe and widespread dermatitis, particularly involving the face, genitalia, or intertriginous areas, a short course of oral corticosteroids or cyclosporine is indicated.⁴ 

Symptomatic treatment includes alleviating itching by the use of a topical antipruritic agent (eg, methanol/pramoxine hydrochloride) and/or a systemic antihistamine (eg, hydroxyzine hydrochloride). The latter is often prescribed for its antipruritic and sedative effect. Consider swab for culture and sensitivity if there are features of infection, and appropriate systemic antibiotic should be prescribed if there is suspected secondary bacterial infection. A skin biopsy or referral to a dermatologist should also be considered if there is any diagnostic doubt.

Outcome of the Case

The patient was treated with ultrapotent topical steroids twice a day for 10 days and the rash and itch promptly resolved.

Alexander K.C. Leung, MD, is a clinical professor of pediatrics at the University of Calgary and a pediatric consultant at the Alberta Children’s Hospital in Calgary, Alberta, Canada.

Benjamin Barankin, MD, is a dermatologist and the medical director and founder of the Toronto Dermatology Centre in Toronto, Ontario, Canada. 

References:

1. Stibich AS, Yagan M, Sharma V, et al. Cost-effective post-exposure prevention of poison ivy. Int J Dermatol. 2000;39(7):
2. 515-518.
3. Nicholson F. A case of acute dermatitis caused by handling Rhus Toxicodendron. Br Med J. 1899;1(1992):530.
4. Boelman DJ. Emergency: treating poison ivy, oak, and sumac. Am J Nurs. 2010;110(6):49-52. 
5. Prok L, McGovern T. Poison ivy (Toxicodendron) dermatitis. UpToDate. www.uptodate.com/contents/poison-ivy-toxicodendron-dermatitis. Accessed August 11, 2015.
6. Gladman AC. Toxicodendron dermatitis: poison ivy, oak, and sumac. Wildernes Environ Med. 2006;17(2):120-128.
7. Fisher AA. Poison ivy/oak/sumac. Part II. Specific features. Cutis. 1996;58(1):22-24.
8. McClanahan C, Asarch A, Swick BL. Black spot poison ivy. Int J Dermatol. 2014;53(6):752-753.
9. Leung AK, Barankin B. A hyperpigmented right forearm. Consultant. 2014;54(7):629-630.