Contact dermatitis occurs when a material or chemical contacts skin and results in signs or symptoms that are typically inflammatory. There are two main forms of contact dermatitis, irritant and allergic. ICD is a nonimmunologically mediated process that occurs when a physical agent is applied long enough or in a high enough concentration to damage cells and disrupt skin integrity and function. ICD is the most common type of contact dermatitis and results from exposure that could cause a reaction in all human skin equally, for example, a strong acid.

A key feature of ICD is that the inflammatory response is limited to the contact site, which often itches or burns, depending on the nature of the contactant. The most common etiologies for ICD include excessive chronic washing with soap and water which can dry and irritate the skin. Chronic excoriation and rubbing further exacerbate the problem. Other predisposing factors include age (worse in the very young and very old), occlusion, and mechanical irritation. Management primarily includes avoiding contact with the offending agent. Other therapeutic modalities include using a physical barrier (ie, Liner-Liner prosthetic sock, Knit-Rite, Inc.) and topical barrier (eg, Desitin paste, Johnson & Johnson Consumer Co, Inc. and A&D ointment, Merck & Co., Inc.), emollients (ie, Aquaphor, Beiersdorf AG), and possibly corticosteroids (eg, hydrocortisone). Frictional ICD (Figure 2) is a distinct subtype that results from recurrent low-grade friction and results in hyperkeratosis and lichenification.¹⁴ However, most friction-related dermatoses are classified later in this chapter; they are typically of higher grade and more directly explain the underlying etiology.

In contrast to ICD, agents triggering an allergic response set off an immunologic hypersensitivity cascade in select persons, generally following repeated allergen exposure. This is referred to as allergic contact dermatitis (ACD) (Figure 3). More specifically, ACD is a delayed hypersensitivity reaction to an allergen developing upon reexposure. Lesions from ACD are acutely well-defined involving erythema, edema, and occasionally, vesicles or exudate. Key distinguishing features of ACD include visible reaction upon second but not first exposure. Further, not all persons will react to the offending agent of an ACD, in contrast to irritants that trigger ICD in anyone. Chemicals and materials used in prosthetic fabrication, maintenance, and repair are commonly suspect in contact dermatitis reactions.¹⁷ Varnishes, lacquers, plastics, epoxies, resins, cements, leathers, and others are suspect. Patients with ACD are more likely to have an atopic background (ie, family history of atopic dermatitis, asthma, allergic rhinitis, etc.) in addition to the predisposing factors previously listed for ICD.

Conducting a careful and thorough history is extremely important and necessary to determine if a new exposure outside of the prosthesis (eg, a skin care product) is the offending agent as opposed to a prosthetic component. It may not be possible to differentiate ACD and ICD, especially in the chronic phase, as the signs and symptoms begin to overlap. Patch testing is the benchmark for determining or excluding an immunologic allergen^8,14 (Figure 4). One complication with patch testing before completing a thorough history could be that, following the test, the patient’s immune system initiates a new response to a material that was historically used without problem in the patient’s prosthesis. This would introduce a new problem and could represent a new allergic reaction unrelated to the patient’s rash, thus creating a false-positive reaction. In addition, patch testing is not perfect and could fail to detect a true allergy, referred to as a false-negative reaction. False-negative reactions have been estimated to occur in as many as 30% of patients tested.¹⁸ However, if done correctly, discordant reactions are typically observed in less than 5% of tested cases.^19,20 If history and patch testing are successful, removal of the inciting antigen is routinely curative for the dermatitis. If not, then symptom relief becomes the primary goal, at least temporarily. Conservative topical treatment options for symptomatic relief beyond avoidance include antipruritics (eg, Sarna Lotion, Stiefel Co., Research Triangle Park), topical corticosteroids (eg, hydrocortisone), and cool compresses.^10,21,22 In more aggressive cases or if symptoms are refractory to topical therapy, systemic corticosteroid administration may be necessary but should be used with caution.

Although the dermatitis discussed thus far results in inflammation locally at the contact site, there is a possibility of inflammation at a distant site far from the source. A classic example occurs with a dermatophyte fungal infection on a distal extremity that then results in an eczematous patch on the trunk. This has been termed a “dermatophytid,” or more simply, an “id” reaction. Other terms such as autoeczematization, autosensitization, angry skin syndrome, and disseminated eczema have all been used to describe this poorly understood process that does not have to be related to an infection. Although unclear, systemic dissemination of an irritant, allergen, or immune cells (ie, activated memory T lymphocytes) likely plays a key role in inflammation at a site distant from the primary inflammatory source and has been speculated to be one source of false-positive reactions in patch testing. Management of id reactions is centered on recognizing and providing treatment at the primary source. Emollients and corticosteroids often are the most beneficial in treatment of just the distant eczematous patch(es).

Psoriasis is a common, chronic immune-mediated systemic inflammatory condition that is characterized by a well-demarcated erythematous patch or plaque with white-colored to silver-colored scales (Figure 5). Many patients are genetically predisposed, and an external trigger is possible (eg, infection, hypocalcemia, or medications such as beta blockers). Lesions classically occur on extensor surfaces and are known to occur in areas of friction. In fact, injury may lead to a plaque of psoriasis directly in the traumatized skin that is often linear, as in a scraped knee, known as the Koebner phenomenon (Figure 6). For this reason, it is quite possible for psoriasis of the residual limb to develop in an amputee, and it would be beneficial to check the elbows, knees, groin, digits, and scalp as well. It is of great service to the patient if the prosthetist can recognize this condition and refer them to their primary care physician or dermatologist. In addition to the skin involvement, approximately one-third of patients have an associated psoriatic arthritis as well as an increased risk of diabetes and cardiovascular complications. Most patients are treated with prescription medications. Topical therapeutic options include corticosteroids, vitamin D creams, retinoids, tar, salicylic acid, and calcineurin inhibitors (eg, tacrolimus).²³ The application of topical therapies is most beneficial if applied when the prosthesis is not on the body, such as during sleeping hours. Collaboration between the prosthetist and dermatologist will ensure prosthetic use is not undermining dermatologic treatment and vice versa in conditions such as psoriasis. Extensive skin involvement, severe symptoms, or arthritis should be managed with systemic therapies such as ultraviolet phototherapy, biologic agents, chemotherapeutic agents, or systemic retinoids.²⁴

Intertrigo is a dermal inflammatory response caused by friction between two skin surfaces that are in constant opposition with each other (Figure 7). Areas commonly involved in the nonamputee include the axilla, the submammary areas, and intergluteal cleft. In persons with obesity, intertrigo can develop between tissue folds of the abdomen or thigh and is common on the residual limbs in amputees, particularly where scars are involved. Here, two skin surfaces on either side of an invaginated scar are in constant direct contact while squeezed together inside an artificial interface, often a gel liner.²⁵ Heat, perspiration, and maceration are present in the semiocclusive environment on the residual limb, coupled with elevated mechanical forces associated with movement that begin breaking down protective keratin and result in inflammation. The compromised tissue is subject to further mechanical irritation and secondary infection. Fissures, eczema, pigment alteration, ulceration, or lichenification can result in chronic cases. Intertrigo is the nonspecific label given to dermatitis in contacting surfaces when no other pathology is present. However, steps should be taken to identify an active comorbid infection or specific underlying pathology. For example, inverse psoriasis may affect just the skin folds as an unusual manifestation of psoriasis and be misdiagnosed as intertrigo. Similarly, many cutaneous infections mimic intertrigo as well, such as erythrasma or fungi. A skin biopsy or microbial culture may be necessary to correctly diagnose underlying pathology in a persistent intertriginous lesion. It is therefore prudent to refer the patient with intertrigo who is unresponsive to conservative treatment beyond a 2-week time period.

General management recommendations include good hygiene practices as previously mentioned, which can be modified as needed along with the application of a topical barrier, emollient, corticosteroid, or some combination thereof, depending on the clinical presentation. Furthermore, appropriately selected, fitted, and aligned prosthetic componentry are vital in minimizing undue stress in the invaginated region. It could be that components are worn beyond their service life, ill-fitting/malfunctioning, or that they are contaminated. Once prosthetic components are functioning optimally, care, maintenance, and cleaning are reviewed with the patient to ensure maximal residual limb protection. Finally, if an underlying cause or secondary infection is isolated, it should be treated as indicated.

Obstruction of eccrine sweat ducts or malfunction of their integrity is known as miliaria, or more commonly, heat rash (Figure 8). Miliaria has been categorized by the depth of pathology and ranges from superficial to deep. Miliaria crystallina is characterized by small subcorneal epidermal clear vesicles that are easily ruptured. Miliaria rubra, or prickly heat, is characterized by occluded sweat that leaks into the lower epidermis or superficial dermis and elicits an inflammatory response with erythematous macules, patches, and papules. These first two types are often described in infants who have been swaddled snugly, creating an excessively warm environment. Miliaria pustulosa may be at the same level as rubra and often occurs after a bout of prickly heat rash. The third type, miliaria profunda, results from sweat leaking into the deeper dermis. Among patients with an amputation, prickly heat rash is likely the subtype that will be seen under the prosthetic device because of the artificial interface with sustained exposure to friction and elevated temperatures. Typically, resolution will occur rapidly if the device is not worn for a day or two, usually requiring no further treatment. However, it should be noted that anhidrosis, or a lack of sweating, commonly follows a true heat rash for almost 2 weeks as the ducts need time to repair and restore physiologic function. Because eccrine sweat glands discharge their contents directly onto the skin surface, they are independent of the hair follicle, unlike apocrine and sebaceous glands. Therefore, they are unrelated to epidermal inclusion cyst formation, which is discussed later.

Urticaria is a type of dermatitis commonly referred to as hives (Figure 9). Urticaria is characterized by transient pruritic raised wheals formed from central pale dermal edema and surrounded by erythema that blanches with pressure. Individual wheals can resolve as rapidly as within an hour, or persist for an entire day. Wheals that stay in the same location longer than 1 day should be biopsied to rule out an underlying process, such as urticarial vasculitis or systemic lupus erythematosus. However, acute urticaria is defined as lesions that continue to come and go within a 6-week period and chronic urticaria occurs beyond 6 weeks. Physical urticarias are caused by a direct physical agent such as water (aquagenic), brisk stroking of the skin (dermatographism), sweat (cholinergic), cold, heat, solar, pressure, or vibration. Physical urticaria is recognized as a distinct subtype of urticaria but since most cases persist longer than 6 weeks it is generally a chronic urticaria.²⁶ Although not commonly documented in the prosthetic literature, it is possible to see many of the physical urticarias because of the pressure, heat, and perspiration present in the artificial interface and they should be considered in the differential diagnosis. A careful history should help elucidate if the patient indeed has hives or physical urticaria. Testing physical urticarias should not be done unless the practitioner is trained and equipped to provide treatment for a possible anaphylactic reaction. Treatment of physical urticarias often includes oral antihistamines but topical corticosteroids provide some benefit.²⁶

Folliculitis is defined as hair follicle inflammation (Figure 10). It is a common problem related to microbial infection in patients with an amputation. Lesions are characterized by a small pustule centered about a hair follicle. It is more prevalent in individuals with hyperhidrosis, increased hair, or oily skin. Other predisposing factors include obesity, shaving, and friction as seen under a prosthetic device or with tight clothing. Mechanical stress escalates symptoms, particularly in summer months, with higher ambient temperatures, increased perspiration, and exacerbated by the lack of evaporative cooling under the prosthesis.^12,27 These infections are typically caused by the bacteria Staphylococcus aureus but other bacteria and even fungi, such as Malassezia are also common. It is paramount to recommend against shaving and to emphasize keeping the area cool and as friction-free as possible. Other therapies generally include over-thecounter (OTC) topical antimicrobials (eg, benzoyl peroxide 2% to 5%), prescription topical antimicrobial agents (eg, clindamycin solution, ketoconazole shampoo), and even systemic antibiotics (eg, doxycycline) depending on the severity and microbes involved. For recurrent lesions, permanent laser epilation can also be considered.

A dermal infection deeper than folliculitis is termed a furuncle, or more commonly, a boil.^28,29 A pustule is not visualized in these lesions. Instead, furuncles present as an indurated erythematous nodule, often with tenderness or irritation. Furuncles are generally found on areas of mechanical friction and increased sweating.^10,29 Commonly affected areas include the neck, axilla, and groin, so it is not surprising to see them on the residual limb of a patient with an amputation. Associated systemic disorders include diabetes, immunosuppression, alcoholism, and malnutrition. If more than one follicle is involved the lesion is termed a carbuncle.

Boils are typically caused by S aureus and may spontaneously resolve. Furuncles are often managed in a manner similar to that of folliculitis. Recurrent folliculitis or furunculosis may also require antimicrobial soaps or cleansers (eg, chlorhexidine) several times per week, and can be purchased OTC without a prescription, though a discussion with a dermatologist is advisable depending on the previous rate of skin problems and hygiene regimen success among other factors. If the infection involves more surrounding and deeper tissues, it may result in a fluctuant and very painful abscess. An abscess could result in systemic symptoms and a wound culture should be obtained to determine the microbial etiology and susceptibility to antibiotics. Treatment must include incision and drainage of these purulent lesions. Although systemic antibiotics are commonly used, they are generally not necessary as long as the lesion is drained appropriately.