A 2-year-old African American girl was brought to the pediatric emergency department by her parents with a chief complaint of buttocks lesions. The parents stated that their daughter had been taken to the day care center that morning in her usual state of good health. They had dressed her that morning and denied seeing any lesions whatsoever on her buttocks. The child spent several uneventful hours at the day care center with no reported incidence of injury or illness. They picked her up as usual and took her home. Her lesions were discovered when they changed her clothes that evening. The parents reportedly called the day care center immediately, but could not reach anyone.
The child's medical history was unremarkable. She was not taking any medications and had no known allergies. Her immunizations were current. She lived at home with her parents and was "toilet trained." A review of systems yielded normal results.
The physical examination demonstrated a well-nourished, normally developed, playful little girl who appeared to be cared for well. The results of the physical examination were normal except for her buttocks. She had multiple, erythematous, linear and curvilinear lesions (Figure), some of which appeared to "frame" the buttocks circumferentially. Some of these "welts" had a "train-track" look. Additionally, there were a few scattered papules and plaques. Whereas most of the lesions were deep red, some had a purplish appearance. They were nontender, mildly pruritic, and slightly indurated.
The relationship between the patient and her parents seemed normal and loving. Although the parents displayed a great deal of anxiety over their child's lesions, their interaction with the emergency department staff was respectful and appropriate. No laboratory studies or radiographs were ordered.
The initial impression of the medical team was that the child had suffered nonaccidental physical abuse. Buttocks bruises (and immersion burns) are commonly seen in children who are "punished" for toÜet-training accidents. The color of the lesions suggested that they had occurred within the past few days. However, it is important to recognize that the practice of "dating" injuries by the progression of color changes is imprecise.1 Although the history implicated the day care center, the parents also had to be considered as potential perpetrators. Attempts by the emergency department staff to contact an administrator or staff member from the day care center were unsuccessful. Child Protective Services was consulted.
Accidental trauma is the most common explanation for most childhood injuries. Bruises (contusions) make up most of these "minor'' injuries. On the other hand, cutaneous manifestations (especially bruises) are also the most common findings in cases of physical abuse. The table lists some features of bruising that should prompt suspicion for physical abuse. In our case, both the distribution and the morphology of the lesions argued against accidental trauma. Buttocks bruises are extremely rare in nonabused infants and toddlers.2 Furthermore, the linearity of this child's lesions could not be explained by an accidental fall or other trauma.
Figure. Buttocks lesions at presentation. Note the multiple linear and curvilinear lesions.
Bruise Characteristics Suggesting Abuse
"Coining" or "cao gio" ("scratch the wind") is a common Vietnamese and Cambodian folk medicine remedy for various illnesses. The afflicted region of the body is usually oiled and then rubbed with the edge of a coin with intent to rid the body of "bad winds." This process usually produces sharp borders of petechiae and purpura that are often bilaterally symmetric.3 The erythematous linearity of the lesions on our patient would not likely be explained by coining. Additionally, the chest and back are the commonly "coined" body regions. Furthermore, this family was not of southeast Asian descent.
Henoch-Schönlein purpura is frequently associated with buttocks lesions. These purpura are often red to purple and may be palpable or nonpalpable. However, Henoch-Schönlein purpura would be unlikely to involve the buttocks and spare the lower extremities completely. Furthermore, the lack of other organ system involvement (eg, gastrointestinal tract, joints, or kidneys) would also argue against HenochSchönlein purpura. Purpura fulminans could present initially with localized bruises or purpura, but not in a playful and well child. Mongolian spots, although a common "cause" of apparent buttocks "bruising," present as flat patches of bluish discoloration, not as erythematous welts.
Coagulation disorders such as hemophilia or von Willebrand disease may present with an easy ability to bruise, but this diagnosis is unlikely without any previous history and with bruises located only on the buttocks region. Ehlers-Danlos syndrome is also associated with an easy ability to bruise, but was not likely in this situation. Besides the "focality" ruling against it, this inherited syndrome is associated with joint hypermobility and skin hyperelasticity, neither of which were present in our patient.
Erythema multiforme may present with erythematous macules and patches that may progress to areas of apparent ecchymoses. Usually, however, mere is a history of recent or intercurrent infection or medication use. Furthermore, this eruption is usually more generalized and characterized by "target" lesions. Phytophotodermatitis, a phototoxic skin response to the "psoralens" of plants, may resemble localized bruises. There are several reports of "hand" or "loop" marks on the skin of children touched by adults who had handled the juices of lemons and limes.4'5 Our patient, however, had no history of psoralen contact or exposure of the buttocks to sunlight.
An investigation by Child Protective Services could not substantiate an allegation of abuse by either the child's parents or the day care personnel. Instead, an interesting coincidence was detected at the day care center - other children had recently had similar complaints of buttocks irritation. An investigation discovered that the day care center had changed bathroom cleansers a few weeks prior to our patienf s presentation. The toilet seat cleanser contained a "new and improved" disinfectant chemical. When the child's buttocks marks were carefully mapped and measured, it became clear that the curvilinear lesions that appeared to frame the buttocks matched perfectly with the dimensions of the toilet seat. Our initial working diagnosis of child abuse now appeared to be a case of contact dermatitis.
There are two major types of contact dermatitis: allergic and irritant. Allergic contact dermatitis is a type IV (cell-mediated) immunologic reaction to a specific antigen to which an individual has been previously sensitized. Irritant contact dermatitis is a nonimmunologic reaction in which a substance, without previous sensitization, causes direct damage to the skin.6 Distinguishing between the two is often clinically difficult. It may even be possible for a single exposure to induce both sensitization and subsequent allergic contact dermatitis.7
The pathogenesis of allergic contact dermatitis is divided into a sensitization phase and an elicitation phase. Sensitization occurs when antigens on the skin penetrate the epidermis to combine with antigen-presenting cells (epidermal Langerhans' cells). This complex is transported via the lymphatics to regional lymph nodes. These antigens are then processed and presented to T lymphocytes. Proliferation of effector T lymphocytes specifically programmed to recognize these antigens then occurs. These lymphocytes travel back to the skin via the bloodstream and await immunologic "activation." This phase commonly takes 5 to 7 days in the case of strong allergens, but it may take weeks to months with weaker allergens.8
The elicitation phase of allergic contact dermatitis begins when the antigen comes into contact with the skin again. The antigen-bearing Langerhans' cells interact with antigen-specific T lymphocytes. Cytokine-induced activation, Tlymphocyte proliferation, and inflammatory mediator release occur, all of which initiate and perpetuate the clinical manifestations of the allergic response. This phase usually occurs within 12 to 24 hours of reexposure to the antigen.9
Irritant contact dermatitis occurs when strong chemicals penetrate an intact epidermis or weaker chemicals penetrate a breached epidermal barrier.8 This reaction commonly is seen with only a single contact and usually occurs more quickly than an allergic contact dermatitis response. As previously stated, however, it is still often difficult to distinguish irritant contact dermatitis from true "allergic" contact dermatitis.
Some think that without "patch testing," it is impossible to distinguish allergic contact dermatitis from irritant contact dermatitis.10 The patch test involves placing known substances in "standard" concentrations on a patient's skin (beneath a patch) and looking for an allergic skin reaction during the next several days. Patch test reactions, properly interpreted, are accepted medicolegally as "scientific proof of the cause of a dermatitis.11
Unfortunately, even patch testing does not always reliably distinguish between allergic contact dermatitis and irritant contact dermatitis. A positive response may simply be due to an irritating concentration of a potent chemical.11 Furthermore, many patients have clinical reactions that are combinations of both irritant and allergic contact dermatitis. Because our patient did not undergo patch testing, it was not possible to distinguish between allergic contact dermatitis and irritant contact dermatitis.
Although it is difficult to ascertain the true prevalence of allergic contact dermatitis, the literature suggests that at least 20% of children are at risk.912 Actually, allergic contact dermatitis can be induced in virtually all normal children, but most do not have this reaction under natural conditions. Most experts agree that genetic predisposition plays an important role. Additionally, the circumstances of the exposure are of obvious importance. The body site, the integrity of the integument, and the duration and frequency of the exposure are all important variables in the sensitization process. Finally, both the concentration of the substance and its intrinsic allergenic potential are also crucial.11 The most common allergens responsible for allergic contact dermatitis (in order) are uroshiol (poison ivy, oak, or sumac), nickel (a metal), neomycin (a topical antibiotic), potassium dichromate (a tanning agent), and thimerosal (a preservative).13
Contact dermatitis (irritant or allergic) usually begins as an eczematous process characterized by pruritis, erythema, and edema. Vesicle formation, oozing, and crusting often follow. Occasionally, however, the reaction may be noneczematous with papular, plaque, purpuric, or "erythema multiforme-like" eruptions.11'1415 This somewhat atypical presentation of contact dermatitis seems to best describe our case. Our patient had papules and plaques, and deep red to purplish lesions that resembled purpura.
The treatment of allergic contact dermatitis is glucocorticoids. Topical therapy is sufficient when the dermatitis involves less than 10% of the skin surface. A steroid ointment of moderate potency, applied twice daily for 2 to 3 weeks, is an effective regimen. When more than 10% of the skin surface is involved, oral therapy is indicated. Facial lesions may also require such systemic therapy. Prednisone, given once daily at 1 to 2 mg/kg/d for 7 to 10 days, is the usual initial regimen. A taper during the next 2 to 3 weeks is then recommended to prevent a "rebound" exacerbation of the dermatitis.9,13 Obviously, the offending allergen should be identified and avoided.
The literature is replete with unusual cases of dermatitis involving the ano-genital region. Our patient's presentation fit perfectly the previously described "toilet seat dermatitis."11 This dermatitis is produced by strong detergents used to cleanse the seat (as in our case) or the lacquer or paint on the seat itself. Another example is "toilet paper dermatitis," from the use of moistened, perfumed, or colored toilet paper.1116 Other reports implicate the clothing of infants and children as the sensitizing agent. One example of a true "diaper dermatitis" is a buttocks rash secondary to the rubber chemicals used in certain brands of diapers.17 "Bikini bottom" dermatitis, a type of occlusive folliculitis, occurs in children who wear a damp swimsuit all day.11
Finally, similar to our own case, there are many reported presentations of buttocks lesions that initially were believed to be child abuse, but turned out to be contact dermatitis. In one such case, a child initially suspected to have herpes genitalis was ultimately diagnosed as having allergic contact dermatitis secondary to nickel in the child's bed-wetting alarm.18 Additionally, a laxative-induced dermatitis of the buttocks was incorrectly suspected to be abusive burns in a case series of four. Each of these children had an irritant contact dermatitis after ingesting a laxative that contained the active ingrethent "senna."19
Clearly, contact dermatitis (allergic or irritant) can rnimic a myriad of diagnoses. In this instance, as with most cases of contact dermatitis, it was the distribution of the lesions that ultimately "clinched" the diagnosis. Even more important, however, was the examination of the child's home and day care environments by Child Protective Services. This investigation uncovered the important "clues" that allowed a medical explanation to become possible.
Some health care practitioners may cite cases such as this one as a prime example of their "reluctance to report" presentations of suspected abuse that are equivocal. Certainly, we must all be cognizant of the legal and emotional ramifications of reports that are later not substantiated (due to lack of evidence or due to alternative explanations). On the other hand, we cannot lose sight of the fact that child abuse remains a major threat to the health and safety of children.
All members of the health care team must maintain a high degree of vigilance toward the possibility of child abuse. An organized approach entails taking the history, performing a physical examination, and sometimes ordering laboratory or radiologic tests. These are then combined with the observed interactions between the caregivers and the child. If this "building block" approach yields a high enough degree of suspicion, a "reporting threshold" should be reached.20 It is at this point that a report should be filed and the investigation initiated.
What must be remembered is that filing a report is not analogous with an accusation of abuse. Rather, it is the mechanism by which we as health care professionals call a "consult" with Child Protective Services to investigate a suspicious or puzzling case that could involve the safety and well-being of a child. Although the prospect of these "false positives" is unsettling, the fear of missing a "true positive" is more haunting.
1. Giardino AP, Christian CW, Giardino ER. Skin: bruises and burns. In: Giardino AP, Christian CW, Giardino ER. A Practical Guide to the Evaluation of Child Physical Abuse and Neglect. Thousand Oaks, CA: Sage Publications; 1997:61-95.
2. Sugar NF, Taylor JA, Feldman KW. Bruises in infants and toddlers. Arch Pediatr Adolesc Med. 1999;153:399-403.
3. Romberg AE. Skin and soft tissue injuries. In: Ludwig S, Kornberg AE, eds. Child Abuse: A Medical Reference, 2nd ed. New York: Churchill Livingstone; 1992:91-104.
4. Bays J. Conditions mistaken for child abuse. In: Reece RM, ed. Child Abuse: Medical Diagnosis and Management. Philadelphia: Lea & Febiger; 1994:358-385.
5. Barradell R, Addo A, McDonagh AJ, Cork MJ, Wales JK. Phytophotodennatitis mimicking child abuse. Eur J Pediatr. 1993,152291-292.
6. del Savio B, Sherertz EF. Is allergic contact dermatitis being overlooked? Arch Pam Med. 1994;3:537-543.
7. Kanerva L, Tarvainen K, Pinola A, et al. A single accidental exposure may result in a chemical bum, primary sensitization and allergic contact dermatitis. Contact Dermatitis. 1994;31:229-235.
8. Weston WL, Lane AT, Morelli JG. Dermatitis. In: Weston WL, Lane AT, Morelli JG. Color Textbook of Pediatric Dermatology. St. Louis: Mosby; 1996:30-49.
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10. Belsito DV. The diagnostic evaluation, treatment, and prevention of allergic contact dermatitis in the new millennium. J Allergy Clin Immunol. 2000;105:409-420.
11. Rietschel RL, Fowler JF, eds. Fisher's Contact Dermatitis, 4th ed. Baltimore: Williams and Wilkins; 1995:1-8, 11-20, 33-36, 41-43, 81-82, 92.
12. Mortz CG, Anderson KE. Allergic contact dermatitis in children and adolescents. Contact Dermatitis. 1999;41:121-130.
13. Weston WL, Bruckner A. Allergic contact dermatitis. Pediatr Clin North Am. 2000;47:897-907.
14. Torinuki W. Generalized eryfhema-multiforme-like eruption following allergic contact dermatitis. Contact Dermatitis. 1990;23:202-203.
15. Goh CL. Urticarial papular and plaque eruptions: a noneczematous manifestation of allergic contact dermatitis. Int J Dermatol. 1989;28:172-176.
16. Minet A, Eggers S, Willocx D, Bourlond A, Lachapelle JM. Allergic contact dermatitis from Kathon CG in moist toilet paper. Contact Dermatitis. 1989;21:107-108.
17. Belhadjali H, Giordano-Labadie F, Ranee F, Bazex J. "Lucky Luke" contact dermatitis from diapers: a new allergen? Contact Dermatitis. 2001;44:248.
18. Hanks JW, Venters WJ. Nickel allergy from a bed-wetting alarm confused with herpes genitalis and child abuse. Pediatrics. 1992,-90:458-460.
19. Leventhal JM, Griffin D, Duncan KO, Starling S, Christian CW, Kutz T. Laxative-induced dermatitis of the buttocks incorrectly suspected to be abusive burns. Pediatrics. 2001;107:178-179.
20. Ludwig S. Child abuse. In: Fleisher GR Ludwig S, eds. Textbook of Pediatric Emergency Medicine, 4th ed. Philadelphia: Lippincott Williams & Wilkins; 2000:1669-1704.
Bruise Characteristics Suggesting Abuse