Case #1
A 55-year-old woman complained of a five-day-old leg rash. She also had non-insulin-dependent diabetes, hyperlipidemia, and hypertension, which she managed with insulin, atorvastatin, and labetalol and nifedipine, respectively. A unilateral ill-defined erythematous plaque with a surface texture like orange peel occupied most of her left shin. Dystrophic left toenails and scaly plaques on the dorsal left foot were diagnosed by KOH preparation as onychomycosis and tinea pedis, respectively. The leg was tender to palpation. Doppler studies demonstrated normal vascular flow. The patient's temperature was 38.2°C, and her WBC count was 16,500/µL with 77% neutrophils. Blood cultures were taken.
Case #2
The patient, a 65-year-old white woman with a history of coronary artery disease, hypertension, hypercholesterolemia, and type 2 diabetes, presented with an existing leg eruption that had been worsening for two weeks. Current medications included aspirin, atorvastatin (Lipitor), ezetimibe (Zetia), glyburide, and hydrochlorothiazide. Scaly erythematous plaques that began on the lower leg and extended to the knees were topped by yellow-brown crusts. The eruption was pruritic but did not burn or hurt. Arterial pulses were palpable. Examination revealed tinea pedis. The patient was afebrile. Her past medical history was significant for recurrent leg cellulitis. OTC hydrocortisone 1% cream had not been beneficial.
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CASE #1: Cellulitis
Cellulitis is an infection of the subcutaneous fat that is so closely related to erysipelas, an infection of the dermis, that some authorities use the terms interchangeably. Unlike erysipelas, the borders of cellulitis are not raised or sharply demarcated. Cellulitis is marked by warmth, erythema, edema, and tenderness. Erythematous streaks may radiate from the affected tissue. The skin may be smooth or have the texture of orange peel. Occasionally ulcers or bullae are seen.
Most cellulitis is caused by Streptococcus pyogenes or Staphylococcus aureus. Other bacteria, such as non-group A streptococci (i.e., groups B, C, and G) and the gram-negative microorganisms Escherichia coli, Pseudomonas, Proteus, Serratia, Enterobacter, Citrobacter, and marine Vibrios, can also cause cellulitis. IV drug abusers who “skin pop” (inject liquid drugs into the fat rather than blood vessels) have been reported to suffer from cellulitis due to Enterococcus faecalis and Enterobacteriaceae organisms that otherwise only very rarely cause cellulitis, as well as Bacteroides and Clostridium species. Rare causes of cellulitis include atypical mycobacteria and deep fungal pathogens, the most common being cryptococci.
The estimated incidence of cellulitis is two to three cases per 100 people per year (24.6/1,000 person-years). Cellulitis affects men and women equally in most studies, although a higher incidence among males has recently been reported. Most cases involve the leg. Facial cellulitis and perianal cellulitis are most common in children. Breast cellulitis is most often caused by streptococcus and occurs primarily in women with breast cancer or in those who have undergone lumpectomy with lymph node dissection for stage 1 or 2 breast cancer.
No test is particularly sensitive or specific for cellulitis. A WBC count >10,000/µL with fever is present in up to 42% of patients. Needle aspiration of the advancing edge of cellulitis may be subjected to Gram's stain and cultured. Culture is diagnostic in approximately 30% of patients. Blood cultures have a higher positive yield in facial and periorbital cellulitis. Ultrasonography can diagnose an underlying abscess and help guide needle aspiration. CT or MRI may rule out underlying fasciitis or osteomyelitis. Radiographs reveal gas in the tissues, helping to establish diagnoses of fasciitis or gangrene, which require immediate surgical intervention.
The differential diagnoses for leg cellulitis include stasis dermatitis, allergic contact dermatitis, necrobiosis lipoidica diabeticorum, necrotizing fasciitis, toxic epidermal necrolysis, and gas gangrene, all of which are similarly painful. Facial cellulitis must be distinguished from Stevens-Johnson syndrome, angioedema, rosacea, allergic contact dermatitis, and lupus. Perianal cellulitis can be confused with diaper dermatitis but will not respond to topical antifungal agents or barrier creams. Both facial and perianal cellulitis tend to be unilateral. Impetigo results in alteration of the epidermis but not the dermis or fat and is not typically painful.
With the increasing prevalence of methicillin-resistant S. aureus (MRSA), choosing the correct antibiotic for empiric treatment is more important than ever. In healthy patients, mild cellulitis may be treated on an outpatient basis with oral antibiotics. I use trimethoprim-sulfamethoxazole 160/800 mg (Bactrim DS, Septra DS) b.i.d., which does not cover streptococcus but does cover many cases of community-acquired MRSA, with cefdinir (Omnicef) 300 mg b.i.d. (to cover streptococcus). Avoid using quinolones, as rapidly emerging resistance can extend to other classes of antibiotics.
IV antibiotics should be given for more extensive cellulitis; cellulitis involving burns or ulcers, fever, and elevated WBCs; and cellulitis in the context of immunosuppression (e.g., diabetes). At the very least, patients should receive amoxicillin-clavulanic acid (Augmentin) or piperacillin-tazobactam (Zosyn). Whether the IV antibiotic should always be vancomycin is arguable; a first-generation cephalosporin (e.g., cefazolin [Kefzol, Ancef]) administered with vancomycin can increase the potency of the regimen. Empiric vancomycin is necessary when the patient has impaired circulation or immune dysfunction (e.g., secondary to diabetes).
Gram-negative coverage is not generally needed but can be added if testing finds a gram-negative pathogen or if the patient fails to improve. Abscesses must be drained for antibiotic treatment to be effective. Underlying osteomyelitis requires an extended treatment regimen that can last six weeks.
Our patient's fever and WBC count normalized within four days of starting empiric vancomycin and cefepime. After one week of trimethoprim-sulfamethoxazole 160/800 mg b.i.d. with cefdinir 300 mg b.i.d., the cellulitis had abated altogether. The causative pathogen was not identified.
CASE # 2: Stasis dermatitis
A type of spongiotic dermatitis that almost always occurs on the leg, stasis dermatitis (SD) is thought to be related to chronic venous insufficiency with venous hypertension. An age-related decrease in valve competency is usually to blame.
SD plaques are often scaly, rough, dry, red, or pruritic; some are moist, oozing crusts and erosions. Usually an isolated condition, SD can be associated with lymphedema, cellulitis, venous leg ulceration, atrophie blanche, and lipodermatosclerosis. Besides venous insufficiency, underlying conditions include diabetes, hypertension, peripheral vascular disease, high lipid levels, morbid obesity, and cardiac failure.
In the United States, SD occurs in 6%-7% of persons aged 50 years and older. After age 70, the prevalence may be >20%. Women are slightly more likely to be affected, perhaps due to the effect of pregnancy on the venous system of the leg. Deep venous thrombosis (DVT), vein stripping, saphenous-vein harvesting, or traumatic injury can severely impair the function of the lower-extremity venous system, leading to SD. In persons younger than 50, SD is more often related to surgery, trauma, a history of DVT, or repeated cellulitis.
The first symptom is pruritus, followed by scaly pink, red, erythematous, and/or brown plaques, which can be associated with edema. Rarely, SD can manifest with red friable and purple nodules termed pseudo-Kaposi sarcoma or acroangiodermatitis. SD often manifests first on the medial ankle, the foot, or the calf and extends to the knee. The id reaction is a papular eruption distant from the SD itself.
Differential diagnoses include asteatotic eczema, cellulitis, allergic contact dermatitis, necrobiosis lipoidica, nummular dermatitis, benign pigmented purpura, and pretibial myxedema. Staphylococcal superinfected SD with its telltale yellow crusts must be distinguished from cellulitis. A classic inverted champagne-bottle appearance identifies lipodermatosclerosis, which, like cellulitis, involves the dermis and fat.
One proposed etiology of SD involves pericapillary fibrin cuffs, which may act as a barrier to the diffusion of oxygen and nutrients, resulting in tissue anoxia, intracellular spongiosis, cell death, and sometimes ulceration. Whether pericapillary fibrin cuffs are barriers or markers for endothelial cell damage or part of an overall mechanism of macromolecular leakage and trapping is uncertain. Leg ulcers resulting from causes other than venous hypertension do not possess fibrin cuffs. Other hypotheses include the trapping of growth factors by macromolecules that have leaked from the vasculature and damage to epithelial cells in the microcirculation due to adherence of WBCs. Secondary or acute-onset SD may result from impaired deep venous circulation, a hypercoagulable state, DVT, or severe valve damage due to past thrombosis.
Treatment of SD depends on its stage, duration, and underlying conditions. Elastic support hose worn to at least knee height at 30 mm of pressure can help reduce edema and improve venous return. Raising the lower extremities above the level of the heart when sitting and minimizing standing reduces fluid buildup. If erythema is a prominent manifestation, low- and medium-potency topical corticosteroids can help reduce inflammation. I often start the patient on triamcinolone 0.1% cream (Kenalog), then taper to hydrocortisone valerate cream 0.2%. Dry-skin care using only mild soaps or cleansers and bland emollients (such as petrolatum) after showering or bathing is sometimes helpful. Complex moisturizers and topical antibiotics can induce allergic contact dermatitis.
SD is usually a progressive and chronic condition that re-quires lifelong care. If superinfection and cellulitis are present, they must be treated to avoid exacerbation of the SD.
This patient's erythema abated with two weeks of triamcinolone 0.1% cream, but the underlying brawny dyspigmentation and lichenification remained.
Dr. Scheinfeld is assistant clinical professor of dermatology at Columbia University in New York City, where he has a private practice.