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Distinguishing cellulitis from its mimics

Cleveland Clinic Journal of Medicine. 2012 August;79(8):547-552 | 10.3949/ccjm.79a.11121
August 1, 2012|Cleveland Clinic Journal of Medicine
Emily C. Keller, MD;Kenneth J. Tomecki, MD;M. Chadi Alraies, MD, FACP
Author and Disclosure Information

Emily C. Keller, MD
Department of Dermatology, Cleveland Clinic

Kenneth J. Tomecki, MD
Vice Chairman, Department of Dermatology, Cleveland Clinic

M. Chadi Alraies, MD, FACP
Clinical Assistant Professor of Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, and Department of Hospital Medicine, Cleveland Clinic

Address: M. Chadi Alraies, MD, FACP, Department of Hospital Medicine, A13, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH 44195; e-mail alraiec@ccf.org

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.

KEY POINTS

  • 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.

LYMPHEDEMA

Figure 5. In a woman who underwent lumpectomy of the left breast, lymphedema of the dependent portion of the breast presented as a new-onset erythematous, orange-colored indurate plaque without epidermal or nipple changes.

Lymphedema is characterized by localized edema of an affected extremity, with induration, erythema, and secondary cutaneous changes such as hyperkeratosis, dyspigmentation, and wart-like architecture (Figure 5).

Primary lymphedema appears in the setting of congenital abnormalities, whereas secondary lymphedema results from an interruption of a previously functioning lymphatic system (eg, after radical mastectomy).

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Patients often present with unilateral nonpitting edema and erythema in the absence of systemic symptoms.12 Many patients presenting with lower-extremity lymphedema are overweight or obese, as the weight they carry causes obstruction of the inguinal lymphatics.6

The pathophysiology is not clearly delineated but is thought to be a consequence of decreased oxygenation of tissue secondary to extravasated lymph. As the oxygen is compromised, macrophages and fibroblasts are recruited, resulting in fibrosis.6

Patients with lymphedema are more susceptible to superficial and deep skin infections, as the natural defense system in the epidermis and papillary dermis is compromised by impaired lymphatic drainage.15

Figure 6. Diffuse, warm, and indurated erythema with superficial desquamation affecting both lower extremities in an overweight patient with long-standing lymphedema. This patient had a systemic reaction to a medication, which caused an exfoliative dermatitis superimposed on the existing lymphedema.

To differentiate uncomplicated lymphedema from a secondary cutaneous infection, the clinician should take into account the presence or absence of warmth, pain, increased erythema, and systemic symptoms (Figure 6).

Tip: Primary lymphedema will most likely present in childhood with no inciting factors and will require a full workup. Obtaining a history should make secondary lymphedema a relatively straightforward diagnosis: Has the patient undergone lymph node dissection? Has the patient had an injury in the affected leg? Lymphedema is overwhelmingly unilateral and nonpitting, and is often seen in overweight people (if no precipitating factor is present).

EOSINOPHILIC CELLULITIS

Figure 7. Eosinophilic cellulitis, also called Wells syndrome, on the right volar forearm in this patient presented as an acute-onset,  pruritic, erythematous plaque without warmth or pain. The patient had no systemic symptoms and had noted similar episodes in the past.

Eosinophilic cellulitis, or Wells syndrome, was first described in 1971 as a granulomatous dermatitis.16 It is a recurrent hypersensitivity reaction to a drug, to a vaccine, or to an insect bite, or to a viral or fungal infection that presents on the extremities as localized erythema, edema, and induration with sharp borders and a green or gray hue (Figure 7).17–19 The lesions commonly progress to firm, indurated plaques that resemble morphea. The plaques may take weeks or years to resolve, but they do so without scarring.12,17,20,21

As patients tend to have recurrent bouts of eosinophilic cellulitis, they may have lesions in different stages of healing. Patients tend to report itching and burning that precedes the onset of plaques.22 The complete blood count typically shows a transient hypereosinophilia.12,16,17,23–25

Tip: This diagnosis often requires biopsy for confirmation, but helpful clues are a history of recurrent episodes, the color of the lesions, and peripheral eosinophilia.

PAPULAR URTICARIA

Papular urticaria is a dermal hypersensitivity reaction to an insect bite, most commonly from a flea or mosquito.26 Patients are often children, as their immune system may be hypersensitive. But children often develop tolerance before puberty.27

Figure 8. Papular urticaria on the medial left knee and lower leg showed proximal urticarial papules with pinpoint erythematous papules coalescing to form the well-demarcated, distal plaque. The plaque was intensely pruritic, was nontender, and lacked warmth.

The presentation may vary, from numerous urticarial papules near the site of a bite, to generalized, large, indurated, erythematous plaques reminiscent of cellulitis (Figure 8).5,26 The lesions usually develop within hours of a bite and persist for an average of 1 to 2 weeks.28 The areas typically affected are the head and neck or the upper or lower extremities; the palms, soles, and trunk are usually spared.27

Patients most often complain of intense itching.12 The pathogenesis is proposed to be mediated by the immune complex, and tissue biopsy study shows increased eosinophils. The eosinophils stimulate mast cells, causing release of histamine, leading to increased vascular permeability, edema, and erythema.28,29

Tip: Biopsy may be necessary to confirm the diagnosis, though often the history may be sufficient. The patient may or may not recall a bite, so probe into recent activities such as outdoor sports or contact with a new pet. The papules and plaques are generally very pruritic but not painful.

DERMATOLOGY CONSULT

If the clinical presentation and history do not correlate, or if the skin condition has been treated with antibiotics yet has failed to respond, the possibility of other cutaneous dermatoses should be entertained. A dermatology consult can help determine the diagnosis, the need for further evaluation, and the best treatment course.

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