Distinguishing cellulitis from its mimics

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ABSTRACTDistinguishing true cellulitis from its many imitators is challenging but critical if we are to avoid unnecessary use of antibiotics and delays in treatment. Common imitators of cellulitis are stasis dermatitis, lipodermatosclerosis, contact dermatitis, lymphedema, eosinophilic cellulitis, and papular urticaria. Specific criteria do not exist for the diagnosis of cellulitis, but the alert physician can find clues in the history and physical examination that point toward cellulitis.


  • Cellulitis is rarely bilateral.
  • Patients with cellulitis often have systemic symptoms, such as fever and leukocytosis.
  • A chronic course points to a diagnosis other than cellulitis.
  • Plaques with a “bound-down” appearance or dark pigmentation point to a chronic disease rather than cellulitis.
  • Stasis dermatitis is the most common mimic of cellulitis.



More than 10% of patients labeled as having cellulitis do not have cellulitis.1 This is unfortunate, as it leads to excessive and incorrect use of antibiotics and to delays in appropriate therapy.2 However, it is not surprising, given the number of conditions that bear a striking similarity to cellulitis. A familiarity with the features of true cellulitis and with the handful of conditions that can bear a striking similarity to it is the way out of this potential diagnostic quagmire.


The key characteristics of cellulitis are redness, warmth, tenderness, and swelling of the skin. A history of trauma and pain in the affected area and evidence of leukocytosis3 suggest cellulitis. A symmetric or diffusely scattered pattern indicates a condition other than cellulitis, which is overwhelmingly unilateral, with smooth, indistinct borders4,5 Other factors pointing to cellulitis are underlying immunosuppression, a more rapid progression, previous episodes, systemic symptoms (eg, fever, leukocytosis), new medications, new travel or outdoor exposure, and comorbidities such as diabetes and peripheral vascular disease. A long-standing, slowly progressive course and a history of unsuccessful treatment with antibiotics are strong indicators of a condition other than cellulitis.

Consultation with a dermatologist is recommended to narrow the differential diagnosis. The dermatologist can determine if biopsy is necessary, as many dermatoses that mimic cellulitis can be diagnosed by visual recognition alone.


Figure 1. The right lower extremity in a morbidly obese patient with stasis dermatitis has an ill-defined erythematous plaque with overlying pigment changes and superficial desquamation, as well as nonpitting edema. Stasis dermatitis typically affects both lower extremities.

The most common mimic of cellulitis is stasis dermatitis (Figure 1).2 Patients can present with ill-defined, bilateral, pitting edema of the lower extremities, typically with erythema, hyperpigmentation, serous drainage, and superficial desquamation.3,6,7

The inciting factor is chronic venous insufficiency, leading to interstitial edema, extravasation of red blood cells, and decreased tissue oxygenation. This process causes micro-vascular changes and microthrombi that up-regulate transforming growth factor beta and fibroblastic growth factor.7 If the process is allowed to continue, stasis dermatitis may progress to lipodermatosclerosis.

Tip: Stasis dermatitis is generally bilateral, the process will have been ongoing for years, there is often pitting edema, and the legs should be nontender.


Figure 2. Lipodermatosclerosis typically affects the lower third of both lower extremities. This obese patient presented with a well-demarcated, woody, erythematous induration with light brown pigmentary changes and small white scarred plaques. The lower legs have the characteristic “inverted champagne bottle” shape.

Lipodermatosclerosis is a sclerosing panniculitis classically described as an “inverted champagne bottle” or “inverted bowling pin” appearance of the leg, ie, the diameter of the leg is sharply narrowed directly below the calf (Figure 2).

There is an acute and a chronic phase. The acute phase is characterized by inflammation and erythema, and the chronic phase is characterized by fibrosis.8 The acute phase presents with severe lower-extremity pain above the medial malleolus, erythema, edema, and warmth; there is no sharp demarcation between affected and unaffected skin.9,10 This phase can be difficult to distinguish from cellulitis, so the history plays a key role. Known venous insufficiency, cutaneous changes of stasis dermatitis, and the absence of systemic symptoms all point to lipodermatosclerosis.

The chronic phase is characterized by unilateral or bilateral, indurated, sclerotic plaques with a “bound-down” appearance (ie, they appear as if tethered—or bound—to the subcutaneous tissue) affecting the skin from below the knee to the ankle; there is a sharp demarcation between affected and unaffected skin.9–11 The skin is often bronze or brown secondary to hemosiderin deposits. There can be prominent varicosities and scattered ulcerations depending on the course of the disease.

This condition is thought to be the result of long-standing chronic venous insufficiency.7,8,9,11 It is proposed that venous incompetence leads to extravasation of interstitial fluid and red blood cells, decreased diffusion of oxygen to the tissues, and eventual tissue and endothelial damage. As the endothelium is damaged, microthrombi formation and infarction ensue, stimulating fibroblasts to form granulation tissue.

Tip: The history helps to distinguish acute lipodermatosclerosis from cellulitis. Chroniclipodermatoslcerosis will have been ongoing for years, the legs should be nontender, the skin will be bound-down, and the diameter of the leg will sharply decrease from knee to ankle.


Figure 3. In this patient, irritant contact dermatitis affected the left dorsal foot where the skin was in contact with the shoe, which had been cleaned with bleach. The lesion is a painful, nonpruritic, well-demarcated, erythematous, weeping plaque with scattered vesicles at the periphery, as well as superficial desquamation and scaling.

Allergic and irritant forms of contact dermatitis are often mistaken for cellulitis. Irritant contact dermatitis (Figure 3) presents with erythematous patches and plaques with well-defined borders, often in a geometric distribution where the skin was exposed to an irritant.12 Allergic contact dermatitis is a delayed hypersensitivity dermatitis that can be secondary to something ingested, applied to the skin, or airborne (Figure 4). It presents as erythematous macules, papules, and plaques that may have serous drainage or vesiculation. Lesions of allergic contact dermatitis are usually confined to the site of contact with the allergen, but they can infrequently be found at distant sites, in which case it is considered systemic contact dermatitis.3,5 Depending on the severity of the allergy, patients may complain of intense pain and pruritus.3

Figure 4. Allergic contact dermatitis of the right lower extremity in a patient who recently underwent knee replacement presented as a warm, erythematous plaque confined to the regions of the leg brace. In addition, groups of vesicles and bullae flank the incision at sites of adhesive bandages. This represents an allergy to the rubber or rubber accelerator of the brace.

Additionally, chronic, nonhealing leg ulcers may have a confounding allergic contact dermatitis.7 Although patients may believe they are helping the ulcer heal by applying topical antibiotics or other lubricants, they may in fact be impeding the healing process. Always inquire as to what the patient is applying if he or she has leg ulceration with surrounding edema and erythema that has not resolved with conventional treatments.13,14

Tip: The key to distinguishing contact dermatitis from cellulitis is the history. For example, ask about recent changes in medications, soaps, and laundry detergents, new hobbies, or recent surgeries. The involved site is often confined to the area where the allergen contacted the skin, except in cases of exposure to an airborne allergen.

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