Erysipelas and cellulitis are now considered as variants of the same bacterial disease.

17 Erysipelas/Cellulitis

INTRODUCTION

Erysipelas and cellulitis are now considered as variants of the same bacterial disease.

Erysipelas is a more superficial and more acute infection of the upper subcutaneous tissue and dermis. Cellulitis affects the deeper loose subcutaneous tissue. As in any continuum of disease, some overlap can occur. Despite their common etiology, significant differences in presentation, signs, and clinical course are noted.

CLINICAL APPLICATION QUESTIONS

A 27-year-old park ranger presents at your office with a spreading erythema of the right volar forearm. He complains that the area has been sensitive to touch since he scratched the forearm while clearing brush at a campsite 3 days before.

1. What disorders should you consider in this patient?

2. What additional history should you attempt to obtain from this patient?

3. To establish a diagnosis of cellulitis, what physical findings may be present?

4. What treatment is appropriate for this patient?

APPLICATION GUIDELINES Specific History

Onset

Erysipelas starts abruptly and can spread with impressive rapidity, often in a matter of hours. Systemic symptoms of fever, chills, and general feeling of malaise often occur, and constitutional symptoms may be quite severe. The most common site is the lower limb, where a distal portal-of-entry wound is often evident in the form of an abrasion, ulcer, interdigital fissure, or paronychia. The face is the second most frequent area to be affected.

Cellulitis evolves more slowly. Usually patients indicate that symptoms developed gradu- ally over a period of days or even a few weeks, and systemic symptoms usually occur only with longstanding disease. Cellulitis is also seen most frequently on the lower limb and face; however, involvement of skin over the perineum or abdominal wall is not uncommon.

Evolution of Disease Process

Untreated or ineffectively treated erysipelas/cellulitis will progressively spread, resulting in an ascending lymphyangiitis and sometimes septicemia. Deep extension can result in dermal necrosis, subcutaneous abscess formation, fasciitis, gangrene, and even muscle destruction. Facial involvement with erysipelas and periorbital or orbital cellulitis

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From: Current Clinical Practice: Dermatology Skills for Primary Care: An Illustrated Guide D.J. Trozak, D.J. Tennenhouse, and J.J. Russell © Humana Press, Totowa, NJ

can, on rare occasions, result in dread complications such as cavernous sinus thrombosis, brain abscess, meningitis, or periorbital abscess formation.

Evolution of Skin Lesions

Erysipelas begins with the classic signs of infection. Areas of bright red erythema (rubor) develop in the form of sharply demarcated palpable plaques. If the margin edge is inked, spread beyond the markings is noted within a matter of hours. The area is palpably warmer (calor) than the adjacent skin and the involved area is either tender to palpation (dolor) or at the very least is hypersensitive to touch. Sometimes skin sensitivity is the ear- liest sign. Superficial vesicles or bullae are common. Hemorrhage into the blisters may occur, and in older patients hemorrhage into the intact skin is not unusual. Cellulitis also shows the classic signs of infection but there are subtle differences. The erythema is more of a pink rather than a bright red color, and the affected part has a feel of deeper doughy swelling. The margin of color change is indistinct and there is no clearly defined plaque. The afflicted area is palpably warmer than adjacent skin and the area is painful to palpation; how- ever, it is a deep discomfort and not the hyperalgesia noted in early erysipelas. Hypoalgesia or anesthesia with either of these conditions is an ominous sign signaling fascial or deeper compartment involvement. Very rare complications include chronic lymphedema of the affected skin, glomerulonephritis, or cardiovascular complications of septicemia.

Provoking Factors

A simple scratch or nick can trigger an episode. On the face and head, infection may be secondary to fissuring of chronic eczema or may complicate trauma to the auditory meatus as patients manipulate the canal while relieving the itch of a chronic dermatitis. In children, periorbital cellulitis has been associated with middle-ear infections, and orbital cellulitis has been associated with chronic sinusitis in older children and in adults. On the lower extremities, fissuring from dermatophytosis or chronic stasis ulceration is a predis- posing factor. These conditions often act in concert with long-standing lymphatic injury from old trauma or chronic phlebitis. A recently defined syndrome of recurrent cellulitis of the lower extremities has been reported in cardiac bypass patients where vessel har- vesting in the lower extremities has disrupted the normal venous and lymphatic return.

Diabetes mellitus, neutropenia, IV drug abuse, and immunosuppression predispose patients to the more severe forms of cellulitis and a wider array of organisms.

Self-Medication

Self-treatment is not a problem in erysipelas/cellulitis.

Supplemental Review From General History

When the cause such as a local trauma is obvious, extensive review is not essential.

When there is no obvious cause, then a history for possible predisposing factors should be sought. This is especially important in cases of recurrent infection.

2. Dermatologic Physical Exam Primary Lesions

1. Sharply defined, bright red, sensitive plaques that are warmer than the adjacent or

contralateral skin (erysipelas: see Photo 27).

2. Indistinct macular areas of pink erythema that are tender to deep palpation. They are warm, and the affected part may be visibly or palpably edematous (cellulitis:

see Photo 28).

3. Vesicles and bullae (see Photo 29).

Secondary Lesions

1. Purpura secondary to dermal hemorrhage.

2. Erosions.

3. Ulceration.

4. Gangrene.

Distribution

Microdistribution: None.

Macrodistribution: The lower extremity is the most common site for both forms of infection. The next most common is the facial skin. Cellulitis is common in periorbital locations and is also fairly common on the perineal and lower abdominal skin (see Fig. 3).

Configuration None

Indicated Supporting Diagnostic Data

In most cases, the diagnosis is clear and supporting laboratory data are not indicated.

When there is a question regarding the diagnosis, or special circumstances prevail, the fol- lowing laboratory testing may be indicated.

1. CBC: Elevated white count with leukocytosis.

2. Sedimentation rate: Elevated.

3. Culture: Culture may be taken if the diagnosis is in question, when there is lack of response to standard therapy, or where circumstances suggest the possibility of an unusual organism. Culture of the nasopharynx may be helpful with facial involvement, and culture of intact vesicles or bullae will sometimes reveal the offending bacteria. Cultures of entry wounds are often misleading and help only if they correlate with other cultures. If the victim is septic, blood cultures are an excellent source. In a desperate situation, aspiration of involved skin after saline infiltration or culture of minced tissue from a carefully obtained punch biopsy may identify an organism, but the yield is low.

Therapy

Group A streptococci remain the overwhelming cause of erysipelas and cellulitis. On rare occasions, Group C or G strep may be responsible, and in neonates group B strains have been reported. Occasionally, Staphylococcus aureus has been implicated in celluli- tis. Childhood facial and periorbital cellulitis is commonly caused by H. influenzae type b.

With the introduction of effective vaccines against Hemophilus bacteria in the last decade,

an immunization history is critical. Facial or periorbital cellulitis in an immunized child is

now likely to be some other organism. Rare causes of an erysipelas/cellulitis-like picture

include Aeromonas hydrophilia (fresh water or soil wound contamination), Pasturella

multocida (animal bites), or Vibrio species (salt or brackish water exposure or contact with raw seafood). Immunocompromised patients may be infected by a number of unusual organisms and vigorous attempts at culture are indicated.

Antimicrobial Therapy

Early or mild episodes of erysipelas can be treated with 250 to 500 mg oral penicillin V (phenoxoymethyl penicillin) QID. In penicillin-sensitive patients, 250 to 500 mg eryth- romycin orally QID is a reasonable alternative. Severe or advanced cases should be hos- pitalized and treated with 600,000 to 2 million units IV aqueous penicillin every 6 hours.

Early cellulitis of suspect streptococcal origin can be treated in a similar fashion but usu- ally requires maximal dosing and more often demands hospitalization. Rest, elevation, and immobilization of the affected part are an important part of therapy for cellulitis.

When response to therapy is slow or when staphylococcal organisms are suspected, treatment should consist of 500 to 1000 mg oral oxacillin QID, or in the case of more severe

Figure 3: Macrodistribution of erysipelas cellulitis.

infections, 1.0 to 1.5 g iv nafcillin every 4 hours. In penicillin-sensitive patients with severe cellulitis, or cases in which the patient is neutropenic or otherwise immunologically com- promised, consultation with an infectious disease specialist is recommended. Periorbital dis- ease, especially when associated with developing proptosis, pain, loss of extraocular motion, change in pupil reaction, or visual acuity, should prompt appropriate scans and an ophthal- mologic or combined ENT consult. Periocular cellulitis in children was classically due to H. influenzae prior to the advent of the HIB vaccine. Initial therapy now recommended for this condition is IV cefotaxime or ceftriaxone until culture and sensitivity results are avail- able. The patient’s vaccine history should also be reviewed. If the response to therapy is not prompt, a subperiosteal or orbital abscess should be suspected.

Topical Therapy

Topical medications are indicated when surface changes occur that breach the integrity of the overlying epidermis. This fragile tissue should be elevated to reduce edema and pro- mote the delivery of the systemic antimicrobials. A foot cradle prevents additional trauma, and if the surface is moist or exudative, evaporative soaks of 0.25% acetic acid solution cleanse, dry, and inhibit secondary infection. Once the exudative phase is past, applications of an ointment containing polymyxin B sulfate and bacitracin is recommended.

Prevention

Treatment of any local skin condition that is near the site of acute infection is essen- tial. This is particularly important with interdigital tinea and intertrigo in diabetics, or with patients who have chronic lymphatic damage to the lower extremities from trauma, phlebitis, or surgery. If recurrent erysipelas/cellulitis occurs despite these measures, pro- phylaxis with chronic low-dose 250 mg erythromycin BID or 250 mg cephalexin BID is usually effective and can be justified on the basis of both overall cost and prevention of progressive lymphatic destruction.

Conditions That May Simulate Erysipelas/Cellulitis Allergic Contact Dermatitis

This may at first seem strange; however, early erysipelas and an acute contact reac- tion show similar degrees of erythema and induration, and both have a sharp margin with small vesicles. Contact dermatitis lacks the warmth seen in erysipelas. Although both may itch, the pruritus of erysipelas rapidly gives way to tenderness or frank pain while the itch of a contact reaction intensifies. Contact dermatitis does not have the constitutional symp- toms that often accompany erysipelas.

Erysipeloid

This is an infection caused by a Gram-positive facultative anaerobic rod named

Erysipelothrix insidiosa (former name: rhusiopathiae). It is usually acquired by occupa-

tional exposure, and is common among veterinarians, butchers, poultry handlers, and

seafood handlers. The infection occurs 1 to 4 days after exposure through a minor skin

breach or scratch. The dorsal fingers, hand, wrist, and distal forearm are the most common

sites. A slow-moving area of dusky violaceous erythema develops, often around an obvi-

ous injury site. Central clearing with peripheral extension may occur. Throbbing and burn-

ing are prominent; however, there is no pitting edema and no increasing pain with

palpation. Although erysipeloid can resolve spontaneously, symptoms may persist for a year or more and demand therapy. In addition, diffuse and septicemic forms occur as potentially fatal complications.

Angioneurotic Edema

The edema can simulate an erysipelas; however, the warmth, redness, and tenderness of an infectious process are all absent.

Other More Virulent Soft-Tissue Infections

Early stages of gangrenous and gas-forming types of cellulitis may fall into the dif- ferential diagnosisof erysipelas/cellulitis. These infections can advance with extraordinary rapidity and produce profound systemic toxicity. They usually require intensive general care and antimicrobial therapy, and almost always need surgical intervention. These dis- orders must always be kept in mind when treating common soft-tissue infections, and should be thought of especially when infection arises in the context of trauma, surgery, burns, malignancy, diabetes, advanced age, general debilitation, or when a foreign body is present. These infections represent clinical entities caused in some instances by a single organism, while others are caused by multiple organisms acting synergistically. This chap- ter will not deal with them in depth, and will only address the major clinical clues point- ing to their presence. Prompt action and combined multidisciplinary care are essential because of the high morbidity and mortality rates.

Clostridial and nonclostridial crepitant cellulitis: Crepitant cellulitis is more likely to follow local trauma or surgery where wounds are contaminated by bowel flora.

Extensive subcutaneous gas accumulation develops with minimal signs of cellulitis and minimal pain. Infection can progress rapidly. A nonclostridial form is common in diabet- ics and is often associated with a putrid odor.

Necrotizing fasciitis: This is a necrotizing process that develops at the level of the superficial fascia and subcutis. It is always more extensive than it appears clinically.

Originally called hemolytic streptococcal gangrene, it is caused by several organisms. It follows minor trauma or surgery, and presents with prominent systemic toxicity. In the early stages, skin signs may be minimal. The usual picture is that of an acutely ill patient with a cellulitis that is progressing despite antimicrobial treatment. Erythema and edema are variable and may be minimal. The presence of blistering, cyanosis, and especially anesthesia point to this diagnosis. Pain is present, progression is rapid, and gas and putrid odor may occur with the mixed infection type.

Progressive bacterial synergistic gangrene: Also known as Meleney’s ulcer, this gangrenous process usually occurs at an abdominal or thoracic operative site that contains wire-retention sutures. Ulceration and gangrene develop at the wound site, where a gan- grenous ulcer with a border of purple cellulitis is seen. Mixed organisms are present.

Despite pain and enormous tissue damage, there is little systemic toxicity.

Clostridial myonecrosis: Clostridial myonecrosis develops after penetrating trauma,

bowel surgery, bowel infarction, or perforation. It progresses rapidly with localized pain

and marked systemic toxicity. Crepitus may or may not be clinically evident. Skin over

the site is initially blanched and tense. Later, bronze discoloration develops, followed by

bullae and necrosis. True gas gangrene has a sweet or “mousy” odor.

Nonclostridial myositis: Nonclostridial myositis also follows local trauma. It is caused by various organisms, most often anaerobic strep. Onset is gradual over several days. Minimal pain and systemic signs appear early, but may become severe in late stages.

Gas formation is rare and sparse when present. Skin findings consist of erythema. Odor may be foul.

Synergistic necrotizing cellulitis: Typically seen in diabetics, necrotizing cellulitis presents as an acute infection with marked systemic toxicity. It usually involves the per- ineum, causing patchy skin necrosis with small ulcers discharging foul “dishwater” pus.

Crepitus may be present. Biopsy shows muscle necrosis without vascular occlusion. This is a mixed synergistic process with very high mortality.

ANSWERS TO CLINICAL APPLICATION QUESTIONS History Review

A 27-year-old park ranger presents at your office with a spreading erythema of the right volar forearm. He complains that the area has been sensitive to touch since he scratched the forearm while clearing brush at a campsite 3 days before.

1. What disorders should you consider in this patient?

Answer:

a. Cellulitis.

b. Toxicodendron dermatitis (rhus dermatitis).

2. What additional history should you attempt to obtain from this patient?

Answer:

a. Prior history of toxicodendron dermatitis.

b. Exposure to suspicious plant materials.

3. To establish a diagnosis of cellulitis, what physical findings may be present?

Answer:

a. Sharply defined bright-red warm sensitive plaques.

b. Discrete vesicles and bullae (as distinguished from the confluent vesicles and bullae of toxicodendron dermatitis).

c. Lymphangitic streaking.

d. Regional adenopathy.

4. What treatment is appropriate for this patient?

Answer:

a. Systemic antimicrobial therapy is needed if there is any possibility of an acute cellulitis.

b. Rest and elevation of the affected part.

c. Follow-up at 5 to 7 days, but immediate telephone call to your office if

there is progression of lesions or systemic symptoms develop.