Intertrigo (intertriginous dermatitis) is an inflammatory condition of skin folds, induced or aggravated by heat, moisture, maceration, friction, and lack of air circulation.
Intertrigo frequently is worsened by infection, which most commonly is with Candida species. Bacterial, viral, or other fungal infection may also occur.
Intertrigo commonly affects the axilla, perineum, inframammary creases, and abdominal folds. Uncommonly, it can also affect the neck creases and interdigital areas.
Signs and symptoms of intertrigo
Intertrigo usually is chronic with an insidious onset of itching, burning, pain, and stinging in the skin folds.
Intertrigo initially presents as mild erythematous patches on both sides of the skinfold. The erythematous lesions may progress to weeping, erosions, fissures, maceration, or crusting.
Worsening erythema or inflammation could suggest the development of a secondary cutaneous infection.
Etiology of intertrigo
Intertrigo develops from mechanical factors and secondary infection. Heat and maceration are central to the process. Opposing skin surfaces rub against each other, at times causing erosions that become inflamed.
Secondary cutaneous infections can be caused by a variety of gram-positive or gram-negative bacteria or fungi, including various yeasts and dermatophytes.
Diagnosis of intertrigo
Basic microbiologic diagnostic studies can be performed to identify a potential causative agent of intertrigo and guide antimicrobial therapy.
Potassium hydroxide (KOH) test, Gram stain, or culture is useful to exclude primary or secondary infection and to guide intertrigo therapy.
A skin biopsy generally is not required unless the intertrigo is refractory to medical treatment.
Treatment of intertrigo
Simple intertrigo may be treated with drying agents
Infected intertrigo should be treated with a combination of an appropriate antimicrobial agent (antifungal or antibacterial) and low-potency topical steroid.
Prevention of intertrigo
During patient instruction, emphasize topics such as weight loss, glucose control (in patients with diabetes), good hygiene, and the need for daily care and monitoring. Additionally, preventative measures to reduce skin-on-skin friction and moisture can help in the management of current intertrigo and prevent future episodes.
Complications
Since intertrigo frequently is colonized or secondarily infected, secondary cutaneous infections and acute cellulitis can occur.
Intertrigo (intertriginous dermatitis) is an inflammatory condition of skin folds, induced or aggravated by heat, moisture, maceration, friction, and lack of air circulation.[1] Intertrigo frequently is worsened by infection, which most commonly is with Candida. Bacterial, viral or, other fungal infection may also occur. Intertrigo commonly affects the axilla, perineum, inframammary creases, and abdominal folds, and it can also affect the neck creases and interdigital areas.[2, 3] Diaper dermatitis shows significant overlap with intertrigo. Intertrigo is a common complication of obesity and diabetes.[4]
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Intertrigo. Courtesy of DermNet New Zealand (http://www.dermnetnz.org/assets/Uploads/fungal/candida-intertrigo/1308.jpg).
Intertrigo develops from mechanical factors and secondary infection. Heat and maceration are central to the process. Opposing skin surfaces rub against each other, at times causing erosions that become inflamed.[1] Sweat, feces, urine, and vaginal discharge may aggravate intertrigo in both adults and infants.
Initiating factors include skin-on-skin friction, perspiration, maceration, trapping of moisture in deep skin folds, or irritation from stool, urine, drainage, or topical agents.[5] Autoeczematization and infection also may be factors in intertrigo.[1]
Whether infectious agents play a primary role in intertrigo or simply are common secondary agents is controversial.[1]
Intertrigo is common, especially in hot humid environments. Intertrigo is a common complication of diabetes, and it affects many infants as a component of diaper dermatitis.
Race
Intertrigo has no racial predilection.
Sex
Intertrigo has no sex predilection.
Age
Intertrigo affects people who are very old and very young because of reduced immunity, immobilization, and incontinence.
With preventative measures and therapy, the prognosis for each episode of simple intertrigo is excellent; however, recurrence is common. As a complication of more serious disease, intertrigo should be considered a comorbidity. Intertrigo becomes most serious as a source of secondary infection.
During patient instruction, emphasize topics such as weight loss, glucose control (in patients with diabetes), good hygiene, and the need for daily care and monitoring.[6] Additionally, preventative measures to reduce skin-on-skin friction and moisture can help in the management of current intertrigo and prevent future episodes.[1]
Intertrigo usually is chronic with an insidious onset of itching, burning, pain, and stinging in skin folds. When acute discomfort is noted, consider secondary infection.[7]
Intertrigo commonly is seasonal, associated with heat and humidity or strenuous activity in which chafing or skin-on-skin friction occurs.
In addition to obesity and diabetes, hyperhidrosis may be a risk factor for intertrigo. Additional factors that predispose individuals to perineal intertrigo include urinary or fecal incontinence, vaginal discharge, or a draining wound.
The appearance of intertrigo is dependent on the skin area involved and the duration of inflammation. Intertrigo initially presents as mild erythematous patches on both sides of the skinfold. The erythematous lesions may progress to weeping, erosions, fissures, maceration, or crusting. Worsening erythema or inflammation could suggest the development of a secondary cutaneous infection.[1, 7]
Pustules or vesicles may herald infection. In the perineum, depths of the skin folds are involved compared with purely irritant diaper dermatitis in which only convex surfaces are involved. Bluish-green staining of the diaper or underclothing may indicate pseudomonal intertrigo, which can be treated with vinegar soaks.[8, 9] Intertrigo infected by candidal species often presents with satellite lesions.
Any skin fold may be involved with intertrigo. In adults or infants who are obese, skin folds are accentuated, and inflammation may occur under pendulous abdominal folds, in neck creases, or in popliteal or antecubital fossae.
Since intertrigo frequently is colonized or secondarily infected, secondary cutaneous infections and acute cellulitis are threats to occur.[10] These secondary cutaneous infections can be caused by a variety of gram-positive or gram-negative bacteria or fungi, including various yeasts and dermatophytes.[11] An infectious intertrigo may result in serious cellulitis, especially in patients who are diabetic. Additionally, skin fissuring and ulceration can occur, possibly hidden in the deep skin folds of persons who are obese, which can lead to pain, disability, and, potentially, sepsis.
The diagnosis of intertrigo usually is based on history, presentation, and physical examination. The characteristics of the lesions also provide clues to the etiology and severity.
Basic microbiologic diagnostic studies can be performed to identify a potential causative agent of intertrigo and to guide antimicrobial therapy. A skin biopsy generally is not required unless the intertrigo is refractory to medical treatment.
Potassium hydroxide (KOH) test, Gram stain, or culture is useful to exclude primary or secondary infection and to guide intertrigo therapy.
Wood lamp examination can exclude erythrasma or pseudomonal infection.
Perform an appropriate workup if systemic disease is suspected along with the intertrigo (eg, diabetes, acrodermatitis enteropathica, necrolytic migratory erythema secondary to glucagonoma) or if intertrigo responds poorly to treatment.
Consider biopsy if the intertrigo fails to respond to treatment or if severe skin or systemic disorders must be excluded. Skin biopsies are not necessary to diagnose uncomplicated intertrigo. Skin biopsy may help exclude psoriasis vulgaris inversa, Bowen disease, Paget disease, or metastatic carcinoma.
Correcting the causative factors of intertrigo is critical.
Simple intertrigo may be treated with drying agents, while infected intertrigo should be treated with a combination of an appropriate antimicrobial agent and low-potency topical steroid.
Correcting the causative factors of intertrigo is critical.
Take steps to eliminate friction, heat, and maceration by keeping folds cool and dry. These steps can be accomplished by using air conditioning and absorbent powders, wearing moisture-wicking polyester underwear and socks (eg, Orlon) and by exposing skin folds to the air. Compresses with Burow solution 1:40, dilute vinegar, or wet tea bags often are effective, especially if followed by fanning or cool blow-drying. Skin surfaces in deep folds can be kept separated with cotton or linen cloth; however, be sure to avoid tight, occlusive, or chafing clothing or dressings.
Simple intertrigo may be treated with drying agents (eg, talc, cornstarch).
Where appropriate, antimycotic agents (miconazole, clotrimazole) are helpful, especially if used with a mild- to mid-potency (class III-VI) steroid for a short duration. Avoid using stronger topical steroids because the occlusive effect of skin folds can accelerate the development of skin atrophy and striae. Castellani paint (carbol-fuchsin paint) also can be helpful, especially in the toe web spaces.
Formulations combining protective agents, antimicrobials, and topical steroids may be helpful, including the following[17, 18] :
Triple Paste contains petrolatum, zinc oxide paste, and aluminum acetate (Burow) solution applied qs ad (ie, in a sufficient quantity).
Greer goo is composed of nystatin (Mycostatin) powder 4 million U, hydrocortisone powder 1.2 g, and zinc oxide paste 4 oz applied qs ad (ie, in a sufficient quantity).
A thick coat of these protective barrier creams should be applied. Commercially available barrier pastes sold for diaper dermatitis (eg, Desitin) can be helpful, as can absorbent diapers. Tetrix, a prescription dimethicone barrier cream, may be more protective and less greasy than traditional petrolatum-based barrier products such as zinc oxide ointment.
Intertrigo infected by bacteria should be treated with topical (eg, mupirocin) or oral antibiotics (eg, penicillin) along with low-potency topical steroids. Intertrigo infected by yeasts or dermatophytes should be treated with antifungal agents.[19] Intertrigo complicated by erythrasma should be treated with topical or oral erythromycin.[20]
Intertrigo most often involves persons who are helpless or dependent on others (eg, older persons, infants). Since intertrigo in the perineum often is complicated by incontinence, new breakthroughs in absorbent diapers have made diaper dermatitis easier to avoid. However, contact dermatitis in reaction to these diapers, whether irritant or allergic, can occur; therefore, monitor waistlines and leg openings for intertrigo.
Open-toed shoes or sandals may help reduce toe web-space moisture.
Monitor patients closely for the development of striae or a hidden infection if topical steroids are needed to control an inflammatory intertrigo.
Keeping the affected area and additional intertriginous areas dry, free of moisture, and exposed to air is recommended to help prevent recurrences.[4] Additionally, reducing skin-on-skin friction can help prevent intertrigo.[4]
The goals of pharmacotherapy for intertrigo are to clear the intertrigo, reduce morbidity, and prevent complications.
Antifungal agents can be used. Their mechanism of action may involve altering RNA and DNA metabolism or intracellular accumulation of peroxide toxic to fungal cells.[21] Antibacterial agents should be used for bacterially infected intertrigo.
Immunosuppressant agents such as tacrolimus and pimecrolimus are safer than topical steroids for prolonged use or in skin folds.[17, 22]
Clinical Context:
Greer goo consists of nystatin (Mycostatin) powder, 4 million U, hydrocortisone powder, 1.2 g, and zinc oxide paste, 4 oz qs ad (in a sufficient quantity).
Clinical Context:
Carbol-fuchsin is a first aid antiseptic and drying agent. The active ingredient is phenol 1.5%. Inactive ingredients are water, SD alcohol 40B (13%), resorcinol, acetone, and basic fuchsin.
Clinical Context:
Miconazole damages the fungal cell wall membrane by inhibiting biosynthesis of ergosterol. Membrane permeability is increased, causing nutrients to leak out, resulting in fungal cell death. Lotion is preferred in intertriginous areas. If cream is used, apply sparingly to avoid maceration effects.
Clinical Context:
Clotrimazole is a broad-spectrum antifungal agent that inhibits yeast growth by altering cell membrane permeability, causing death of fungal cells.
Antifungal agents exert fungicidal effects by altering the permeability of fungal cell membrane. Their mechanism of action may also involve an alteration of RNA and DNA metabolism or an intracellular accumulation of peroxide toxic to fungal cells.
Clinical Context:
Tacrolimus ointment is a nonsteroidal anti-inflammatory agent. It should not cause steroid-type skin atrophy. Tacrolimus ointment is currently indicated only for atopic dermatitis in nonimmunocompromised patients aged 2 years and older.
Clinical Context:
Pimecrolimus is a nonsteroidal anti-inflammatory agent. It should not cause steroid-type skin atrophy. Pimecrolimus is currently indicated only for atopic dermatitis in nonimmunocompromised patients aged 2 years and older.
These agents exert anti-inflammatory effect by inhibiting T-lymphocyte activation. They are safer than topical steroids for prolonged use or in skin folds.
What is intertrigo?What are the signs and symptoms of intertrigo?What causes intertrigo?Which lab studies are indicated in the workup of intertrigo?How is intertrigo treated?How can intertrigo be prevented?What are the complications of intertrigo?What is intertrigo (intertriginous dermatitis)?What is the pathophysiology of intertrigo?What are the causes of intertrigo?How common is intertrigo?Does intertrigo have a racial predilection?Is intertrigo more common in males or females?Does intertrigo have an age predilection?What is the prognosis of intertrigo?What information should be provided in the patient education on intertrigo?How does intertrigo present?What is the clinical appearance of intertrigo?What complications are associated with intertrigo?What are the differential diagnoses for intertrigo in adults?What are the differential diagnoses for intertrigo by body site?What are the differential diagnoses for Intertrigo?What should be considered in the workup of intertrigo?Which lab studies should be performed to diagnose intertrigo?When should biopsy be performed in the workup of intertrigo?How is intertrigo treated?How are the causes of intertrigo mitigated?How is simple intertrigo treated?How is infected intertrigo treated?How can intertrigo be prevented?What are the complications of intertrigo treatment?How is intertrigo prevented?What are the goals of drug treatment for intertrigo?Which medications in the drug class Corticosteroids, Topical are used in the treatment of Intertrigo?Which medications in the drug class Immunosuppressant agents are used in the treatment of Intertrigo?Which medications in the drug class Antifungal agents are used in the treatment of Intertrigo?Which medications in the drug class Protective agents are used in the treatment of Intertrigo?
Paras Vakharia, PharmD, Medical Student Researcher, Department of Dermatology, Henry Ford Hospital; Medical Student Researcher, Department of Ophthalmology and Department of Radiation Oncology, Oakland University William Beaumont School of Medicine
Disclosure: Nothing to disclose.
Specialty Editors
Richard P Vinson, MD, Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA
Disclosure: Nothing to disclose.
Paul Krusinski, MD, Director of Dermatology, Fletcher Allen Health Care; Professor, Department of Internal Medicine, University of Vermont College of Medicine
Disclosure: Nothing to disclose.
Chief Editor
William D James, MD, Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine
Disclosure: Received income in an amount equal to or greater than $250 from: Elsevier; WebMD.
Additional Contributors
Franklin Flowers, MD, Department of Dermatology, Professor Emeritus Affiliate Associate Professor of Pathology, University of Florida College of Medicine
Disclosure: Nothing to disclose.
Samuel T Selden, MD, Assistant Professor Department of Dermatology Eastern Virginia Medical School; Consulting Staff, Chesapeake General Hospital; Private Practice
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