Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

Chapter 152: Soft Tissue Infections

Elizabeth W. Kelly; David Magilner

INTRODUCTION

This chapter discusses soft tissue infections in adults; impetigo and other soft tissue infections in children are discussed in chapter 141, "Rashes in Infants and Children."

The skin consists of the superficial epidermis, dermis, and deeper subcutaneous tissues including fat (Figure 152-1). The lymphatics run parallel with the blood vessels (not shown in the figure). Cellulitis is an infection of the dermis and subcutaneous tissues of the skin. Cellulitis is divided clinically as purulent or nonpurulent, and management of the two types is different.^1,2 Purulent cellulitis is cellulitis with an abscess, or cellulitis with drainage or exudate in the absence of a drainable abscess. Nonpurulent cellulitis has no purulent drainage or exudate and no associated abscess.^1,2 Erysipelas traditionally has been defined as a more superficial skin infection involving the upper dermis with clear demarcation between involved and uninvolved skin with prominent lymphatic involvement. However, in many countries, the term erysipelas is considered synonymous with cellulitis.² Folliculitis is an infection of the hair follicle, often purulent, but is superficial without involvement of the deeper tissues. Skin abscesses are collections of pus within the dermis and deeper skin tissues, potentially involving the subcutaneous tissues. Abscesses should be differentiated from simple cellulitis, because abscesses should be treated with incision and drainage.¹ Furuncles (or boils) are single, deep nodules involving the hair follicle that are often suppurative.² Carbuncles are formed by multiple interconnecting furuncles that drain through several openings in the skin.² Necrotizing soft tissue infections are necrotizing infections involving any of the soft tissue layers including the dermis, subcutaneous tissues, fascia, and muscle.³

FIGURE 152-1.

Schematic diagram of the architecture of the skin. This diagram shows the anatomy of the skin, including the epidermis, dermis, and deeper subcutaneous tissues. Also shown are the blood vessels and a hair follicle. [Reproduced with permission from Wolff et al: Fitzpatrick's Dermatology in General Medicine, 7th ed. © 2008, McGraw-Hill, Inc., New York.]

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CELLULITIS AND ERYSIPELAS

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EPIDEMIOLOGY

Cellulitis accounts for approximately 1.3% of all ED visits. General risk factors for cellulitis are listed in Table 152-1.^4,5 Risk factors for specific organisms causing cellulitis are listed in Table 152-2.^{1,4,6,7,8,9,10,11} Cellulitis is observed more frequently among middle-aged and elderly patients, whereas erysipelas is more common among children and elderly patients.¹² Patient characteristics demonstrate a male predominance (61%) and a mean age of 46 years, and the vast majority of infections involve either the lower or upper extremities (48% and 41%, respectively). Approximately 10% of patients diagnosed with cellulitis are hospitalized, the majority of these patients are over age 64 years.

TABLE 152-1General Risk Factors for Cellulitis and Erysipelas

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TABLE 152-1 General Risk Factors for Cellulitis and Erysipelas

Risk Factors

Lymphedema

Skin breakdown/site of entry

Venous insufficiency

Leg edema

Obesity

Neutropenia

Immunocompromise

Hypogammaglobulinemia

Chronic renal disease

Cirrhosis

TABLE 152-2Risk Factors for Specific Organisms Causing Cellulitis

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TABLE 152-2 Risk Factors for Specific Organisms Causing Cellulitis

Organism(s)

Risk Factors

Methicillin-resistant Staphylococcus aureus (MRSA)

Purulent soft tissue infections

Antibiotic use in past month

Previous MRSA infection or colonization

Patient report of suspected spider bite

Previous history of hospitalization or surgery within the past year

Residence in a long-term care facility within the past year

Hemodialysis

Crowded living environments including daycare or homeless shelters, soldiers, prisons

Contact sports

IV drug users

Men who have sex with men

Household contacts with MRSA infection

Children

β-Hemolytic streptococci

Nonpurulent cellulitis that is culture negative by needle aspiration

Gram-negative bacteria

Elderly patients, cirrhosis, diabetic foot infections, fish bone injury

Aeromonas hydrophila

Fresh water lacerations, contact with wet soil

Vibrio vulnificus, Vibrio parahaemolyticus

Salt water lacerations, fish fin or bone injuries, cirrhosis

Pseudomonas aeruginosa

Neutropenia, IV drug use, hot tub exposure

Anaerobic bacteria including clostridia

Bite wounds,^* diabetes mellitus, necrotizing infections, gas in tissues

Polymicrobial

Diabetic foot injections, bite wounds^*

Pasteurella species

Dog and cat bites^*

Capnocytophaga canimorsus

Dog and cat bites^*

Mycobacterium marinum

Fish tank exposure

Streptococcus pneumoniae and Haemophilus influenzae

Nonimmunized children and adults

^*See chapters 46 and 211-213, "Puncture Wounds and Bites," "Bites and Stings," "Reptile Bites," and "Marine Trauma and Envenomation."

MICROBIOLOGY

Approximately 80% of cellulitis cases are caused by gram-positive bacteria. Community-acquired Methicillin-resistant Staphylococcus aureus (MRSA) is now the most common cause of skin and soft tissue infections presenting to the ED,^6,13 regardless of patient risk factors. The Infectious Diseases Society of America recommends differentiation of purulent from nonpurulent cellulitis (see detailed definitions above) for treatment decisions.¹ MRSA is likely to be the causative agent in purulent cellulitis. For nonpurulent cellulitis, the role of MRSA is unknown, and empirical therapy for β-hemolytic streptococcal infection with β-lactams is recommended.^1,14,15

Gram-negative aerobic bacilli are the third most common etiology. Other less common pathogens causing cellulitis are listed in Table 152-2 with associated risk factors.

Erysipelas is usually caused by β-hemolytic streptococci.¹² Bullous erysipelas is a more severe form, and can represent synergy with beta-hemolytic streptococci and methicillin-resistant staphylococcal aureus.¹⁶

PATHOPHYSIOLOGY

Most symptoms of cellulitis are secondary to a complex set of immune and inflammatory reactions triggered by cells within the skin itself. Although bacterial invasion is what triggers the inflammation, the organisms are largely cleared from the site within the first 12 hours, and the infiltration of cells, such as Langerhans cells and keratinocytes, releases the cytokines interleukin-1 and tumor necrosis factor that enhance skin infiltration by lymphocytes and macrophages. The net effect is a rapid clearing of bacteria but with significant inflammatory response.

CLINICAL FEATURES

Cellulitis

In cellulitis, the affected skin is tender, warm, erythematous, and swollen, and typically does not exhibit a sharp demarcation from uninvolved skin. Edema can occur around hair follicles that leads to dimpling of the skin, creating an orange peel appearance referred to as "peau d'orange" (Figure 152-2). Symptoms develop gradually over a few days. Lymphangitis and lymphadenopathy are seen occasionally in previously healthy patients, but purely local inflammation is much more common. In cases of purulent cellulitis, exudate drains from the wound¹; an abscess may or may not subsequently form. Systemic signs of fever, leukocytosis, and bacteremia are more typical in the immunosuppressed. Recurrent episodes of cellulitis can lead to impairment of lymphatic drainage, permanent swelling, dermal fibrosis, and epidermal thickening. These chronic changes are known as elephantiasis nostra and predispose patients to further attacks of cellulitis.

FIGURE 152-2.

Cellulitis of the right leg characterized by erythema and mild swelling. [Photo contributed by Lawrence B. Stack, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.]

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Erysipelas

In erysipelas, the onset of symptoms is usually abrupt, with fever, chills, malaise, and nausea representing the prodromal phase. Over the next 1 to 2 days, a small area of erythema with a burning sensation develops. As infection progresses, the affected skin becomes indurated with a raised border that is distinctly demarcated from the surrounding normal skin. The "peau d'orange" appearance is also common in erysipelas. A classic description is a "butterfly" pattern over the face (Figure 152-3). Complete involvement of the ear is the "Milian ear sign" and is a distinguishing feature of erysipelas because the ear does not contain deeper dermis tissue typically involved in cellulitis. Lymphatic inflammatory changes, known as toxic striations, and local lymphadenopathy are common. Purpura, bullae, and small areas of necrosis warrant a search for possible necrotizing soft tissue infection. On resolution of the infection, desquamation of the site often occurs.

FIGURE 152-3.

Butterfly rash of erysipelas. The sharp demarcation between the salmon-red erythema and the normal surrounding skin is evident. [Reproduced with permission from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006, McGraw-Hill, New York.]

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DIAGNOSIS

The diagnosis of cellulitis and erysipelas is clinical. Management should be guided by the clinical differentiation between purulent and nonpurulent soft tissue infections.^1,2 Presence of an abscess defines the soft tissue infection as purulent; purulent cellulitis is defined as cellulitis with drainage or exudate in the absence of a drainable abscess.

Mild disease, for both purulent and nonpurulent forms of cellulitis, is distinguished by the absence of systemic symptoms. In cases of mild infection, blood cultures, needle aspiration, punch biopsy, leukocyte count, or other lab data are of little benefit and are not recommended.² Needle aspiration of the leading edge of an area of cellulitis produces organisms in 15.7% of cultures (range, 0% to 40%), and punch biopsy reveals an organism only 18% to 26% of the time.¹⁴ Areas with abscess formation have significantly higher yields; wound culture is recommend when the decision has been made to place the patient on antibiotics for purulent cellulitis.² Blood cultures are positive in only 5% of cases. For both purulent and nonpurulent cellulitis, in patients with systemic toxicity, extensive skin involvement, underlying comorbidities, immunodeficiency, immersion injuries, failed initial therapy, or recurrent episodes, or in circumstances such as animal bites, cultures of pus, bullae, or blood are recommended.^2,17,18, Routine radiographic evaluation is unnecessary but should be considered if osteomyelitis (see chapter 281, "Hip and Knee Pain") or necrotizing soft tissue infections are suspected (see section below). Table 152-3 lists differential diagnoses and characteristics that help distinguish cellulitis from the listed disorder.

TABLE 152-3Differential Diagnosis of Cellulitis and Erysipelas

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TABLE 152-3 Differential Diagnosis of Cellulitis and Erysipelas

Diagnosis

Distinguishing Clinical Characteristics

Bursitis

Characteristic locations such as suprapatellar or olecranon, may have palpable fluid collection

Contact dermatitis

Pruritus instead of pain, absence of fever, may have bulla, but patient is nontoxic in appearance.

Cutaneous abscess

Abscess may appear similar to cellulitis initially; eventual fluctuance and purulent drainage

Deep vein thrombosis

Typically not associated with skin redness or fever

Drug reactions

Temporal relation to new drug exposure, pruritus instead of pain, absence of fever

Gouty arthritis

Pronounced pain with involved joint movement

Herpes zoster

Characteristic vesicles, dermatomal pattern

Insect stings

Pronounced pain most at onset

Necrotizing soft tissue infection

Rapid progression; triad of severe pain, swelling, and fever; pain out of proportion to exam; severe toxicity; hemorrhagic or bluish bullae; gas or crepitus; skin necrosis or extensive ecchymosis

Osteomyelitis

Deeper involvement, prolonged course, comorbidities

Superficial thrombophlebitis

Typically not associated with fever, limited to venous path

Toxic shock syndrome

Hypotension, multiorgan involvement, severe toxicity

Bedside US is useful to exclude occult abscess.¹⁹ Doppler studies may be indicated to distinguish lower extremity deep venous thrombosis from cellulitis. The most important diagnosis to exclude is necrotizing soft tissue infection (see section below).

TREATMENT

General Treatment

Treatment is elevation of the affected area, incision and drainage of any abscess found (see section below), antibiotics for cellulitis, and treatment of underlying conditions. Elevation helps drainage of edema. Treat skin dryness with topical agents because skin dryness and cracking further exacerbate symptoms. Treat predisposing conditions such as tinea pedis (see chapter 253, "Skin Disorders: Extremities") and refer to primary care for treatment of lymphedema and chronic venous insufficiency.

Treatment for Purulent Cellulitis or Suspected Methicillin-Resistant Staphylococcus aureus

See Table 152-4 for empiric antibiotic recommendations for purulent cellulitis or when MRSA is suspected.² Identify and thoroughly drain an abscess. Bedside US will aid this procedure. Provide empiric therapy for MRSA for patients who have failed initial non-MRSA therapy, those with a previous history of or risks for MRSA, or those who live in an area with a high prevalence of community-associated MRSA infections.²⁰ For patients with severe infection or systemic toxicity, consider necrotizing fasciitis (see later section on necrotizing fasciitis). It may be difficult to clinically distinguish MRSA cellulitis from methicillin-susceptible S. aureus cellulitis. Treatment failure rates are similar for both β-lactam antibiotics and MRSA-specific antibiotics such as trimethoprim-sulfamethoxazole.^21,22

TABLE 152-4Empiric Antibiotic Treatment of Purulent Cellulitis* and/or Soft Tissue Abscess

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TABLE 152-4 Empiric Antibiotic Treatment of Purulent Cellulitis* and/or Soft Tissue Abscess

Guide by Severity of Illness

Antibiotics

Comments

No antibiotics for mild disease:

Drainable abscess found with no signs of systemic infection

None required for immunocompetent patients where abscess drainage is complete after procedure

Presence of an abscess should be carefully investigated clinically and drained; consider use of US.

Oral antibiotics for moderate disease:

Purulent cellulitis* without signs of systemic infection

Or drainable abscess in the presence of mild to moderate signs of systemic infection

If immunocompromised, see below.

Trimethoprim-sulfamethoxazole double-strength 1–2 tablets twice per day PO for 7–10 d^†

Or doxycycline 100 milligrams PO twice per day for 7–10 d^†

Or clindamycin, 300–450 milligrams PO four times daily for 7–10 d^†‡

Wound culture is recommended in cases where antibiotics are given.
Patients who have failed to improve on outpatient antibiotics or are unable to tolerate oral antibiotics should be admitted to the hospital and receive IV antibiotics; see below.

IV antibiotics for severe disease:

Purulent cellulitis* with signs of systemic infection

Or drainable abscess in the presence of moderate to severe signs of systemic infection^# or sepsis^ƒ

Or an immunocompromised patient

For MRSA coverage:

Vancomycin 15 milligrams/kg IV every 12 h

Or linezolid 600 milligrams IV every 12 h^†

Or daptomycin 4 milligrams/kg IV every 24 h^†

Or telavancin 10 milligrams/kg IV every 24 h^†

Or clindamycin 600 milligrams IV every 8 h^†‡

Admit to the hospital.
Additional antibiotic coverage is listed below.
Consider admission to intensive care unit for patients who meet criteria for sepsis (see also chapter 151, Sepsis).

5. For all patients with severe disease, see later section on necrotizing fasciitis.

Additional coverage for patients with sepsis or for patients with selected indications (see last column to the right)

For patients with sepsis, or for unclear etiology, add:

Piperacillin-tazobactam, 4.5 grams IV every 6 h^†

Or meropenem, 500–1000 milligrams IV every 8 h^†

Or imipenem-cilastatin, 500 milligrams IV every 6 h^†

For fresh water exposure (Aeromonas species) or for salt water exposure (Vibrio species) consider adding Doxycycline 100 milligrams IV every 12 hours,^† plus ceftriaxone 1 gram IV every 24 hours^†

Abbreviation: MRSA = methicillin-resistant Staphylococcus aureus.

^*Purulent cellulitis is defined as cellulitis with drainage or exudate in the absence of a drainable abscess. In all cases of purulent cellulitis, the presence of an abscess should be carefully investigated clinically and drained. Bedside US can help diagnose occult abscess formation and verify complete drainage after procedure.

^†Optimal treatment duration has not been established. For mild to moderate disease, 5-day oral treatment regimens have been successful but are recommended only in settings where follow-up at 5 days is feasible.

^‡Not recommended if local resistance is greater than 10%.

^#Physicians should use their clinical judgement; there are no validated criteria to differentiate moderate from severe signs for systemic infection.

^ƒCriteria for sepsis in the presence of an infection are two or more of the following: temperature >38°C, tachycardia (>90 beats/min), tachypnea (respiratory rate >24 breaths/min), WBC count <400 cells/μL or >12,000 cells/μL), or immunocompromised patients (see chapter 151, Sepsis). Hypotensive patients should be admitted to the ICU.

Treatment of Nonpurulent Cellulitis/Erysipelas

Guidelines no longer differentiate the treatment of nonpurulent cellulitis from erysipelas.² Oral antibiotics are sufficient for simple cellulitis or erysipelas in otherwise healthy adult patients. See Table 152-5 for guideline-recommended antibiotic options.² Consider surgical consultation in patients with bullae, crepitus, pain out of proportion to examination, or rapidly progressive erythema with signs of systemic toxicity, because these signs and symptoms suggest necrotizing infection (see later section on necrotizing fasciitis).

TABLE 152-5Empiric Treatment of Nonpurulent Cellulitis*/Erysipelas

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TABLE 152-5 Empiric Treatment of Nonpurulent Cellulitis*/Erysipelas

Guide by Severity of Illness

Antibiotics

Comments

Oral antibiotics for mild disease:

Typical cellulitis/erysipelas with no focus of purulence, and no signs of systemic infection

Cephalexin, 500 milligrams PO every 6 h^†

Or dicloxacillin, 500 milligrams PO every 6 h^†

Or clindamycin, 150–450 milligrams PO every 6 h^†

Cultures are not recommended because of poor yields.

Monotherapy IV antibiotics for moderate disease:

Typical cellulitis/erysipelas with mild to moderate systemic signs of infection‡

Ifimmunocompromised, see below

Ceftriaxone 1 gram IV every 24 h^†

Or cefazolin 1 gram every 8 h^†

Or clindamycin 600 milligrams IV every 8 h^†

Patients who have failed to improve on outpatient antibiotics or are unable to tolerate oral antibiotics should be admitted to the hospital and receive IV antibiotics, with coverage dependant on severity of illness.

Broad-spectrum antibiotics for severe disease (including necrotizing fasciitis):

Those with sepsis# or those with clinical signs of deeper infection such as bullae, skin sloughing, hypotension, or evidence of organ dysfunction

Or an immunocompromised patient

Vancomycin 15 milligrams/kg IV every 12 h^†

Plus piperacillin-tazobactam, 4.5 grams IV every 6 h^†

Or meropenem, 500–1000 milligrams IV every 8 h^†

Or imipenem-cilastatin, 500 milligrams IV every 6 h^†

1. Consider immediate consultation with surgery for possible debridement (see later section on necrotizing fasciitis for further recommendations).

2. Blood cultures recommended in this treatment group.

Different/additional coverage for patients with selected indications

Fresh water exposure (suspected Aeromonas species):

Doxycycline 100 milligrams IV every 12 h^†

Plus ciprofloxacin 500 milligrams IV every 12 h^†

Salt water exposure (suspected Vibrio species):

Doxycycline 100 milligrams IV every 12 h^†

Plus ceftriaxone 1 gram every 24 h^†

Suspected Clostridium species:

Clindamycin 600–900 milligrams IV every 8 h^†

Plus penicillin 2–4 million units IV every 4 h^†

1. Consider immediate consultation with surgery for possible debridement (see later section on necrotizing fasciitis below for further recommendations).

2. Blood cultures recommended in this treatment group.

^*If exudate or abscess is found on exam, the patient should be treated for purulent cellulitis, see Table 152-4 for treatment recommendations

^†Optimal treatment duration has not been established. For mild to moderate disease, 5-day treatment regimens have been successful but are recommended only in settings where follow-up at 5 days is feasible.

^‡Physicians should use their clinical judgment; there are no validated criteria to differentiate moderate from severe signs of systemic infection.

^#Criteria for sepsis in the presence of an infection are two or more of the following: temperature >38°C, tachycardia (>90 beats/min), tachypnea (respiratory rate >24 breaths/min), WBC count <400 or >12,000 cells/mm³, or immunocompromised state (see chapter 151 "Sepsis"). Hypotensive patients should be admitted to the intensive care unit.

DISPOSITION AND FOLLOW-UP

Admit patients with cellulitis or erysipelas and evidence of systemic toxicity and those with underlying comorbidities such as diabetes mellitus, alcoholism, or immunosuppression (see later section on necrotizing fasciitis). Healthy patients without systemic toxicity can be discharged to home with follow-up and a list of warning signs to prompt return. Follow-up intervals depend on initial presentation, but generally 2 or 3 days are sufficient to evaluate the success of treatment. Mark the patient's skin with an indelible marker along the perimeter of infection so healing can be determined at follow-up; marks also aid the patient in evaluating worsening infection. Reported risk factors for failure of empiric antibiotic therapy include fever, lymphedema or chronic edema, chronic leg ulcers, prior cellulitis in the same area, and cellulitis at a wound site.²³

CUTANEOUS ABSCESSES, FURUNCLES, AND CARBUNCLES

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Furuncles and carbuncles involve the epidermis, and abscesses involve the deeper soft tissue.² Skin abscesses, furuncles, and carbuncles can develop in otherwise healthy patients with no risk factors other than skin or nasal carriage of S. aureus. Persons in close contact with those who have an active infection with a skin abscess are at increased risk.

PATHOPHYSIOLOGY

Skin abscesses typically begin as a local superficial cellulitis. Many organisms that colonize normal skin can cause necrosis and liquefaction with subsequent accumulation of leukocytes and cellular debris; however, MRSA causes the majority of skin abscesses presenting to the ED in the United States.^6,13 Loculation and subsequent walling off of these products of infection lead to abscess formation. As the infection progresses and the area of liquefaction increases, the abscess wall thins and ruptures spontaneously, draining either cutaneously or into an adjoining tissue compartment.

Infection can be caused by one or multiple pathogens that typically include skin flora or organisms from adjacent mucous membranes. Pathogens implicated in folliculitis are those that can cause furuncles and carbuncles, namely Pseudomonas, Candida, and others.

Any process causing a breach in the skin barrier heightens the risk for a skin abscess. Examples include trauma, such as abrasions or shaving; skin foreign bodies; insect bites; and IV drug abuse involving needle injection. Other risk factors for abscess development include diabetes mellitus and immunologic abnormalities. Patients with oral, rectal, or vulvovaginal abscesses are more likely to be infected with multiple organisms, including gram-negative and anaerobic organisms.

CLINICAL FEATURES

Skin abscesses are fluctuant, tender, erythematous nodules, often with surrounding erythema (Figure 152-4). Spontaneous drainage of purulent material may occur, and local lymphadenopathy may be present. Signs of systemic toxicity, fever, or chills are rare in the case of simple abscesses. In uncommon cases, skin abscesses may be the result or cause of bacteremia.

FIGURE 152-4.

Subcutaneous abscess is noted in the axilla. [Reproduced with permission from Slaven EM, Stone SC, Lopez FA: Infectious Diseases: Emergency Department Diagnosis & Management, © 2006, McGraw-Hill, New York.]

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Furuncles are clinically very similar to abscesses, and systemic toxicity is rare. Carbuncles are larger infections commonly associated with fever and malaise. Carbuncles are most common on the upper back, chest, buttocks, hips, and axilla but can occur in any hair-bearing region of the body.

DIAGNOSIS

The diagnosis of skin abscesses, furuncles, and carbuncles is clinical; however, physical exam is unreliable for nonsuperficial abscesses.²⁴ Bedside US is an invaluable tool for distinguishing deep abscess from cellulitis, identifying a foreign body within an abscess, and determining the adequacy of drainage^19,25,26 (Figure 152-5).

FIGURE 152-5.

Long-axis sonogram of a deep midline buttock abscess in the region of the gluteal fold. The skin and immediate subcutaneous tissue exhibit relatively normal echogenicity. The deeper tissues surrounding the rounded abscess cavity appear more hyperechoic and edematous. Note that the superior edge of this large abscess cavity is 3.5 cm from the skin surface (arrow). Knowledge of the depth of this abscess cavity was crucial to the individual performing the drainage procedure. [Reproduced with permission from Ma OJ, Mateer JR, Reardon RF, Joing SA: Ma & Mateer's Emergency Ultrasound, 3rd ed. 2014, McGraw-Hill Inc., New York. From Chapter 18: Musculoskeletal, Soft Tissue, and Miscellaneous Applications, Figure 18-105, p. 561.]

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Radiography is not needed routinely, unless a radiopaque foreign body or underlying osteomyelitis is suspected. Disorders that can mimic abscesses include folliculitis, hidradenitis suppurativa, sporotrichosis, leishmaniasis, tularemia, and blastomycosis, as well as conditions in immunocompromised persons such as Nocardia and Cryptococcus. Wound cultures are not recommended for simple abscess drainage; however, guidelines recommend cultures when antibiotics are given.²

TREATMENT

It is best to drain extremely large abscesses or those in deep areas in the operating room. Abscesses of the palms, soles, or nasolabial folds can be associated with complications and usually require a specialist.²⁷ Input from an appropriate specialist is also recommended in areas of the body with cosmetic concerns due to the expected scar formation.²⁷

In the case of small furuncles (boils), warm compresses can be used to promote drainage, and no other treatment is needed. Sitz baths are helpful for furuncles in the buttock or perineal regions. Repeat evaluation in 2 to 3 days is best to determine whether suppuration has occurred and surgical drainage is required.

Large furuncles, carbuncles, and skin abscesses require incision and drainage.²⁸ Simple needle aspiration of abscesses is inadequate to treat abscesses caused by MRSA.²⁹ Prior recommendations for endocarditis prophylaxis in patients undergoing incision and drainage have changed (see chapter 155, "Endocarditis"). If indicated by the severity of valvular heart disease, the most common regimen is either clindamycin 600 milligrams IV or vancomycin 1 gram IV, 30 to 60 minutes before the procedure.

Incision and Drainage Procedure

Before the incision and drainage procedure, obtain consent and explain complications. Use universal precautions, including a face shield with eye protection, because many abscesses are under pressure. There are few complications with superficial abscesses, but these include residual local numbness, the risk of injury to deeper nerves and blood vessels, and poor or delayed wound healing, especially in those with diabetes or peripheral vascular disease. Plan the incision along tension lines to minimize scaring if possible, especially in areas of cosmetic significance.

Position the patient for good access to the abscess. Prepare the area with povidone-iodine solution and drape in a sterile fashion. To provide local anesthesia, approach the abscess from the side and slowly infiltrate the skin over the abscess. Then infiltrate deeper until resistance of the wall of the abscess cavity is overcome. Distend the abscess with several milliliters of lidocaine, taking care to shield the patient and operator from any material forced from the wound due to pressure. The inflamed abscess wall absorbs the lidocaine and lessens pain associated with the procedure.

After appropriate anesthesia, using a No. 11 or 15 scalpel blade, incise the abscess over the area of greatest fluctuance, using the results of preparatory US evaluation to guide the length of the incision. Incisions that are too small or superficial are not likely to provide effective drainage. Express as much pus as possible by gentle compression. Insert a hemostat into the abscess cavity, opening and closing the jaws to break up loculations.

Irrigation of the cavity with saline followed by packing with gauze ribbon to promote drainage is commonly done, but the benefit is uncertain.^30,31 Less painful alternatives to packing include placing a catheter,³² or tying in a rubber drain after placing two small stab incisions, using a small forceps to reach into one incision, coming out the other, and pulling the drain back through the track before making a knot.³³ Primary closure after abscess drainage shortens healing time for patients treated in the operating room³⁴ and has been studied in a small randomized controlled trial in the ED;³⁵ however, recommendations for its use await larger trials.

If placed, maintain packing, catheter, or drain long enough for the cavity to heal from the inside out and to prevent recollection of pus. Patients should apply warm compresses or soaks three times a day. Schedule a follow-up visit in 2 to 3 days for recheck. Maintain catheter or replace packing if the cavity is still draining at the follow-up visit.

Adjuvant Antibiotics

Antibiotics are generally unnecessary after incision and drainage of uncomplicated abscesses without significant surrounding cellulitis in healthy patients.^6,36,37 Guidelines recommend antibiotics for patients with multiple lesions, extensive surrounding cellulitis, immunosuppression, or signs of systemic infection; see Table 152-4 for indications and specific antibiotics recommended.²

DISPOSITION AND FOLLOW-UP

Most patients with skin abscess, furuncles, and carbuncles are treated as outpatients. Those with systemic toxicity or severe infection may require parenteral treatment and hospital admission. For those discharged to home, remind patients to keep the wound covered and practice frequent hand washing to prevent spread of the infection to household contacts.²⁸ Patients with open wounds should not participate in activities involving skin-to-skin contacts, such as wrestling or football, until wounds are fully healed. Individuals should not share items such as towels, clothing, soap, razors, or other items that come in contact with a contaminated wound.

NECROTIZING SOFT TISSUE INFECTIONS

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Necrotizing soft tissue infections are a spectrum of illnesses characterized by fulminant, extensive soft tissue necrosis, systemic toxicity, and high mortality. Early in their course, these infections can appear deceptively benign.^3,38 Terms used to describe necrotizing soft tissue infections are Fournier's gangrene (see chapter 93, "Male Genital Problems"), necrotizing fasciitis, necrotizing soft tissue infection, or gas gangrene. Risk factors for necrotizing soft tissue infections are advanced age, diabetes mellitus, alcoholism, peripheral vascular disease, heart disease, renal failure, human immunodeficiency virus, cancer, nonsteroidal anti-inflammatory drug use, decubitus ulcers, chronic skin infections, IV drug abuse, and immune system impairment.^39,40 However, infections also occur in young and healthy individuals. The incidence is increasing, but mortality has decreased in the United States from 25% to 10% over the last 20 years.⁴¹ Bacteremia is reported in 25% to 30% of cases and is a strong predictor of mortality. Other patient factors that increase mortality are age <1 year old or >60 years old; IV drug use; comorbid conditions, especially cancer, chronic renal disease, and congestive heart failure; and certain characteristics of the clinical course such as positive blood culture, trunk or perineal involvement, infection related to peripheral vascular disease, and delayed time to diagnosis or treatment.

MICROBIOLOGY

Type I (polymicrobial) infections include 55% to 75% of all necrotizing soft tissue infections, and the causative microbes are a combination of gram-positive cocci, gram-negative rods, and anaerobes. Clostridial infections are now uncommon causes due to improvements in hygiene and sanitation.³⁸ Type II (monomicrobial) infections are most commonly caused by group A Streptococcus. Type II infection is less common (20% to 30%) than type I infection and tends to occur on an extremity in an otherwise healthy host who often has a history of trauma or has had a recent operative procedure at the site of the infection. Community-acquired MRSA is a cause of type II (monomicrobial) infection, particularly in IV drug abusers, athletes, and institutionalized patients.^42,43 Necrotizing infection caused by Vibrio vulnificus is classified as a type III infection. This infection is more common in Asia and may occur in patients who have an apparently insignificant break in their skin in a seawater environment. Type IV is associated with fungal infections, primarily in immunocompromised patients.⁴⁴

PATHOPHYSIOLOGY

The rapid necrotizing process typically begins with direct invasion of subcutaneous tissue from external trauma (IV injection, surgical incision, abscess, insect bite, or ulcer) or direct spread from a perforated viscus (usually colon, rectum, or anus). Although spontaneous development is rare, it does occur, and risk factors include diabetes and underlying malignancy. Bacteria proliferate, invade subcutaneous tissue and deep fascia, and release exotoxins that lead to tissue ischemia, liquefaction necrosis, and systemic toxicity.³⁹

Skin involvement is secondary to vasculitis and thrombosis of perforating blood vessels. The ischemic tissue environment promotes bacterial growth, propagating the process and resulting in rapid spread of the infection. Infection can spread as fast as 1 inch/h. Because thrombosis of large numbers of capillary beds must occur before skin findings develop, early infection has little overlying skin change to indicate the extent of infection.³⁸ As the disease progresses, widespread gangrene of the skin, subcutaneous fat, fascia, and even skeletal muscle occurs.³⁹

In polymicrobial infections, a symbiotic relationship between the different kinds of bacteria seems to promote the necrotizing soft tissue infection. Facultative gram-negative organisms lower the oxygen reduction potential of the tissue and facilitate anaerobic organism growth. Anaerobic organisms impede phagocyte function, favoring aerobic bacterial growth. The alpha-toxin produced by the Clostridium species causes tissue necrosis and cardiovascular collapse. S. aureus and streptococci produce exotoxins and cause the release of tumor necrosis factor and cytokines that can produce the systemic inflammatory response syndrome and lead to septic shock, organ failure, and death.

The tissue ischemia produced in all such infections impedes immune system destruction of bacteria and prevents adequate delivery of antibiotics.³⁹ Thus, antibiotics alone are rarely effective, and immediate surgical intervention remains the cornerstone of successful management.

CLINICAL FEATURES

Classic symptoms of necrotizing soft tissue infections are severe pain, anxiety, and diaphoresis.³⁸ Pain is often out of proportion to physical examination findings with tenderness beyond the area of erythema and thus is perhaps the single most important feature to make the diagnosis early. However, some patients may have little pain, and as the condition progresses, the affected areas may become insensate. About 10% to 40% of the time, patients report trauma or a break in the skin roughly 48 hours before onset of symptoms.

On examination, the painful area may demonstrate a brawny edema, and crepitus caused by bacterial gas production may be present. The lack of crepitus does not rule out the diagnosis. Two different studies reported that the only signs present in >50% of patients were erythema, tenderness, or marked edema beyond the area of redness; crepitus was present in only 13% to 31% of patients. Late in the course of the infection, the skin can develop a bronze or brownish discoloration with a malodorous serosanguineous discharge, and bullae may be present (Figure 152-6).

FIGURE 152-6.

Necrotizing soft tissue infection. Large cutaneous bullae are seen on the leg of this patient with necrotizing fasciitis. Note the dark purple fluid in the bullae. [Photo contributed by Lawrence B. Stack, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.]

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Systemic manifestations include a low-grade fever with tachycardia out of proportion to the fever. In fulminant necrotizing infections, particularly from V. vulnificus, patients may have cardiovascular collapse due to release of bacterial toxins and release of cytokines, and they may be confused, irritable, or have a rapid deterioration of mental status.

DIAGNOSIS

The diagnosis is based on clinical assessment in combination with laboratory tests and imaging when the clinical picture is unclear. One or more "hard" signs of necrotizing fasciitis—crepitus, skin necrosis, bullae, hypotension, or gas on x-ray—are present in less than half of patients.⁴⁵ Many laboratory abnormalities have been investigated to aid in the diagnosis,^{46,47,48,49,50,51,52} including the laboratory risk indicator for necrotizing fasciitis.^46,47 Since its derivation, the laboratory risk indicator for necrotizing fasciitis has proven to miss many cases of necrotizing fasciitis,⁵¹ especially those cause by Vibrio species,⁴⁸ and neck infections.⁵² Table 152-6 lists laboratory factors and imaging findings associated with necrotizing fasciitis to help clinicians with medical decision making.^45-55 Clinicians are encouraged to consult surgery for possible debridement early when the diagnosis of necrotizing fasciitis is being considered rather than waiting for confirmatory studies that may yield equivocal results. There is no single test or sign that can reliably confirm the diagnosis of necrotizing fasciitis early in the course of this disease process. The finger test has been advocated, which involves making a 2-cm incision over involved tissue down to the fascia after local anesthesia, observing for normal blood flow, and inserting a gloved finger to test for normal tissue firmness.⁴⁶ A positive test is lack of normal bleeding, or friable tissue to minimal finger pressure. However, its use has never been studied formally.

TABLE 152-6Laboratory and Imaging Results Associated with Necrotizing Fasciitis

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TABLE 152-6 Laboratory and Imaging Results Associated with Necrotizing Fasciitis

Laboratory Factors Associated with Necrotizing Fasciitis

Laboratory Test

Threshold

Comments

C-reactive protein

>150 milligrams/L

Positive result adds 4 in LRINEC score

WBC count

>15,000 cells/mm³

Positive result adds 1 in LRINEC score, level >25,000 cells/mm³ adds 2

Hemoglobin

<13.5 grams/dL

Positive result adds 1 in LRINEC score,^* level <11 grams/dL adds 2 in LRINEC score^*

Sodium

<135 mmol/L

Positive result adds 2 in LRINEC score^*

Creatinine

>1.6 milligrams/dL

Positive result adds 2 in LRINEC score^*

Glucose

>180 milligrams/dL

Positive result adds 1 in LRINEC score^*

Potassium

>5.0 mEq/L

Associated with extremity infections

Band count

>7%

Associated with Vibrio species

Serum albumin

≤2.0 grams/dL

Associated with Vibrio species

Platelets

≤80,000

Associated with Vibrio species

Imaging Findings Associated with Necrotizing Fasciitis

Imaging Test

Finding

Comments

MRI with contrast

Extensive thickening of the intermuscular fasciae with an appearance suggesting incomplete vascularization

1. Presence of gas is highly specific for necrotizing infection (but not common).

2. Absence of MRI abnormalities of the intermuscular fasciae virtually rules out necrotizing fasciitis.

CT with contrast

1. Fascial thickening of deep facial planes

2. Nonenhancing deep fascia on contrast imaging suggesting necrosis

1. Presence of gas is highly specific, but found in one third of cases or less.

2. Accurate diagnosis requires contrast; acute kidney injury is common in patients with necrotizing fasciitis and may contraindicate IV contrast.

Ultrasonography

1. Fluid collections along the fascial plane

2. Fascia irregularity

3. Subcutaneous air

Radiologists warn that abnormal superficial hyperechogenicity absorbs US and may block diagnostic deeper findings and give false reassurance.

Plain radiographs

Gas in soft tissues

Poor sensitivity

Abbreviation: LRINEC = laboratory risk indicator of necrotizing fasciitis.

^*LRINEC score of ≥6 is associated with increased risk of necrotizing fasciitis but misses many cases and therefore should not be used in isolation for the diagnosis and management.

Plain x-rays may reveal subcutaneous gas in a minority of patients but may miss deep fascial gas and is therefore a poor screening tool. CT with contrast is more sensitive (80% to 97%) but has a false-positive rate of 19%. The most reliable sign of necrosis on CT is nonenhancing deep tissues, which requires contrast, or gas, seen in only ≤36% of patients.⁵⁴ IV contrast is a significant risk in this group of patients who frequently sustain acute renal failure due to sepsis. MRI has better sensitivity (90% to 100%), but false-positive rates are as high as 39%.⁵⁵ Finally, MRI imposes significant delays to treatment. Bedside US has been advocated,⁵³ but radiologists caution against excluding necrotizing fasciitis based its findings.

TREATMENT

Begin aggressive fluid resuscitation immediately. Transfusion of packed red blood cells may be needed to correct anemia from hemolysis. Avoid vasoconstrictors, if at all possible, because vasoconstrictors will decrease perfusion to already ischemic tissue.

Early surgical consultation is indicated for all suspected cases of necrotizing fasciitis. Surgery is the gold standard for diagnosis and treatment. Surgical intervention may include fasciotomy, debridement, and/or amputation. Mortality skyrockets if debridement is delayed >24 hours. See Table 152-5, "Empiric Treatment of Nonpurulent Cellulitis/Erysipelas," the row titled "Broad-spectrum antibiotics for severe disease," for patients with selected indications. Provide tetanus prophylaxis as indicated. Controversial therapies that are typically the decision of the surgical consultant include IV immunoglobulin therapy and hyperbaric oxygen therapy.

OTHER SOFT TISSUE INFECTIONS

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FOLLICULITIS

Folliculitis is an inflammation of hair follicles related to infection, chemical irritation, or physical injury to the skin. It typically involves a superficial bacterial infection of the hair follicles with purulent material in the epidermis.

Epidemiology/Microbiology

Folliculitis is usually caused by S. aureus, and nasal carriage of this organism is a risk factor for folliculitis. "Hot tub folliculitis" or "whirlpool-associated folliculitis" is often attributed to Pseudomonas species and occurs in inadequately chlorinated hot tubs, whirlpools, and swimming pools. Symptoms of uncomplicated folliculitis and whirlpool-associated Pseudomonas folliculitis are often mild and self-limited, and patients do not seek medical attention.

Individuals exposed to whirlpool footbaths at nail salons are at risk for mycobacterial furunculosis. Candida species are implicated in patients receiving broad-spectrum antibiotics or glucocorticoids or who are otherwise immunocompromised.²

Clinical Features

The most common sites of involvement for folliculitis are the apocrine areas of the upper back, chest, buttocks, hips, and axilla, but folliculitis can develop in any hair-bearing region of the body, especially in areas of repeated shaving. Folliculitis presents with clusters of pruritic, erythematous lesions that are usually <5 mm in diameter, with pustules sometimes present at the centers.² Pseudomonal folliculitis can develop over areas exposed to contaminated water, and lesions are often larger (up to 3 cm in diameter).

Pseudofolliculitis is a related noninfectious condition more commonly seen in blacks secondary to shaving. It occurs when the hair follicle becomes trapped and, instead of exiting the follicle, curls and grows into the follicular wall. Such findings in the beard region are called "sycosis barbae" or "folliculitis barbae" and can progress to deep infections that can cause facial scarring (see chapter 250, "Skin Disorders: Face and Scalp").

Diagnosis

Folliculitis is diagnosed clinically. It should be differentiated from other disorders, such as acne vulgaris, impetigo, fungal infections, contact dermatitis, scabies, insect bites, and viral disorders such as herpes.

Treatment/Disposition and Follow-Up

For simple cases of uncomplicated folliculitis or hot tub folliculitis, stopping exposure or removing the offending agent and twice-daily cleansing with mild hand soap often suffices. Lesions usually resolve spontaneously, but if desired, warm compresses may be applied several times daily, and a topical antibiotic such as bacitracin or polymyxin B can also be used. Shaving should be avoided in the involved areas. Pseudofolliculitis is managed by allowing the hairs to grow 2 to 3 mm above the surface and afterward using commercially available razors designed for this condition. For painful or more extensive cases, oral antibiotics with activity against Streptococcus and Staphylococcus, such as cephalexin, dicloxacillin, or azithromycin, are recommended.

HIDRADENITIS SUPPURATIVA

Hidradenitis suppurativa is a recurrent, suppurative, and scarring disease of the apocrine glands, most commonly found in the axillae and pubic regions of women and people of African descent. The disorder is neither contagious nor due to poor hygiene. Diagnosis is clinical. Identification and treatment are discussed in chapter 252, "Skin Disorders: Groin and Skinfolds."

PILONIDAL ABSCESS

Pilonidal abscesses are located along the superior gluteal fold. Some think that a pilonidal sinus forms along the gluteal fold possibly at the time of embryogenesis, although others believe it to be an acquired condition secondary to local soft tissue trauma. The sinuses are lined with squamous epithelium and hair, and blockage of the sinus tract with hair and other keratinous material leads to bacterial invasion and infection. The causative organisms typically are normal skin flora, with Staphylococcus species being the most common. Contamination with peritoneal and fecal organisms is also possible.

Clinical Features

Patients tend to develop symptoms in their late teens and early twenties, and without definitive surgical treatment, they tend to suffer recurrent infections, sometimes developing a chronic draining fistulous tract. Pilonidal abscess is a tender, swollen, and fluctuant nodule located along the superior gluteal fold (Figure 152-7).

FIGURE 152-7.

Pilonidal abscess. Redness, fluctuance, and tenderness in the gluteal cleft are seen with a pilonidal abscess. [Photo contributed by Louis La Vopa, MD. Reproduced with permission from Knoop K, Stack L, Storrow A, Thurman RJ: Atlas of Emergency Medicine, 3rd ed. © 2010, McGraw-Hill, New York.]

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Treatment

ED treatment is incision and drainage, with care taken to remove excess hair and debris from the abscess cavity. See "Incision and Drainage Procedure" given earlier for further recommendations. Antibiotics generally are not needed. Outpatient surgical referral should be recommended for definitive treatment. This typically consists of wide surgical excision and healing by secondary intention. Surgical treatment, although often successful, may involve difficult wounds and a long healing time. There is a debate in the surgical literature over primary closure versus open healing for pilonidal abscesses. When surgical treatment involves primary closure, wounds heal more quickly but are associated with an increased risk of recurrence.⁵⁶ Performing less extensive procedures whenever possible is often in the patient's best interest.

INFECTED EPIDERMOID AND PILAR CYSTS

Epidermoid cysts originate from the epidermis, and pilar cysts originate from hair follicles; both contain a thick, cheesy collection of keratin, not sebum. True sebaceous cysts, as these cysts have erroneously been called in the past, are rare. Sebaceous glands occur diffusely throughout the body. Blockage of the duct of a sebaceous gland may lead to development of a glandular cyst that can exist for a long period without becoming infected. Once bacterial invasion occurs, abscess formation is common. An infected epidermoid or pilar cyst is an erythematous, tender, fluctuant cutaneous nodule. Simple incision and drainage is the appropriate ED treatment. The cyst always contains a capsule that must be removed to prevent further infection. Capsule excision is typically done at follow-up when the initial inflammation has improved or resolved. Occasionally, the wall of the sac can be grasped with a forceps and removed at the time of drainage.

BARTHOLIN GLAND ABSCESS

Bartholin gland abscesses are common in women of reproductive age. An abscess in a perimenopausal woman requires gynecologic follow-up to exclude carcinoma. The Bartholin glands are a pair of pea-sized glands located in the labia minora in the 4 and 8 o'clock positions. They are not palpable if in a noninfected state. Infections are polymicrobial, including vaginal flora, anaerobes, and, in an important minority, Neisseria gonorrhoeae and Chlamydia trachomatis. Examination of the labia typically reveals a fluctuant 2- to 4-cm mass.

Definitive treatment is marsupialization of the abscess to prevent recurrence. The technique is detailed in Figure 152-8. See chapter 102, "Vulvovaginitis" for further discussion.

FIGURE 152-8.

Incision and insertion of the Word catheter. A. Make a 0.5-cm-long stab incision on the mucosal surface of the labia minora. B. The cavity has been evacuated and the Word catheter inserted. C. The balloon is inflated with saline. [Reproduced with permission from Reichman EF, Simon RR: Emergency Medicine Procedures, © 2004, Eric F. Reichman, PhD, MD, and Robert R. Simon, MD.]

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PARONYCHIA AND FELONS

Paronychia and felons are discussed in chapter 283, "Nontraumatic Disorders of the Hand."

PERIRECTAL ABSCESSES

Perirectal abscesses are discussed in chapter 85, "Anorectal Disorders."

SPOROTRICHOSIS

Sporotrichosis is a mycotic infection caused by the fungus Sporothrix schenckii.

Epidemiology

Sporotrichosis occurs worldwide but is most common in tropical and subtropical zones. It is endemic in Central and South America and in Africa. The organism is found most commonly in soil, sphagnum moss, and decaying vegetable matter. It is a common disease among florists, gardeners, and agricultural workers. Inoculation into the host most often occurs when a spine or barb on a plant punctures the skin during handling. Approximately 10% to 62% of patients relate infection to penetrating trauma from plant thorns, wood splinters, or contaminated organic material. The largest outbreak of sporotrichosis in the United States occurred in 1988 and involved 15 states and 84 persons, all of whom handled conifer seedlings shipped in sphagnum moss contaminated with S. schenckii.

Transmission from infected animals, especially cats, has been documented. Veterinary workers, animal handlers, and cat owners are therefore at increased risk. The typical patient is a healthy young adult, but the infection can also occur in immunocompromised individuals such as those with alcoholism, diabetes mellitus, hematologic malignancy, organ transplantation, or human immunodeficiency virus infection.

Pathophysiology

S. schenckii is a thermally dimorphic fungus that changes from its mycelial form to its yeast form on entering a body temperature environment. Disease is usually limited to local cutaneous or lymphocutaneous areas. Osteoarticular involvement, including osteomyelitis, septic arthritis, bursitis, and tenosynovitis, occurs and may extend from a local cutaneous infection or may be secondary to hematogenous spread. Although less common, transmission may occur through inhalation of the fungus through the upper respiratory tract, and subsequent hematogenic dissemination can occur. When inhaled, granulomatous pneumonitis with cavitation may arise.

Clinical Features

The incubation period averages 3 weeks following initial inoculation, but varies from a few days to several weeks. After the fungus enters the body through a break in the skin, three types of localized infections may occur. The fixed cutaneous type is characterized by lesions restricted to the site of inoculation and may appear as a crusted ulcer or verrucous plaque (Figure 152-9). Local cutaneous type infections also remain local but present as a subcutaneous nodule or pustule. The surrounding skin becomes erythematous and may ulcerate, resulting in a chancre. Local lymphadenitis is common. The lymphocutaneous type is the third and most common type. It is characterized by an initial painless nodule or papule at the site of inoculation that later develops subcutaneous nodules with clear skip areas along local lymphatic channels (Figure 152-10). The local reactions in all three types of infections tend to be relatively painless but show no signs of improvement without treatment.

FIGURE 152-9.

Fixed sporotrichosis. The ulcer and surrounding erythema of fixed cutaneous sporotrichosis could be confused with a brown recluse spider bite. [Reproduced with permission from Knoop K, Stack L, Storrow A: Atlas of Emergency Medicine, 2nd ed. © 2002, McGraw-Hill, New York.]

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FIGURE 152-10.

Sporotrichosis. Chronic lymphocutaneous type—an erythematous papule at the site of inoculation on the index finger with a linear arrangement of erythematous dermal and subcutaneous nodules extending proximally in lymphatic vessels of the dorsum of the hand and arm. [Reproduced with permission from Wolff K, Johnson RA: Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 6th ed. © 2009, McGraw-Hill, New York.]

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Patients occasionally develop extracutaneous illness from what is most probably hematogenous spread. Most cases of extracutaneous sporotrichosis involve the skeletal system. An indolent form of monoarticular arthritis is the most common symptom. Osteomyelitis, tenosynovitis, and carpal tunnel syndrome are occasionally seen as well. Multiarticular arthritis is usually only seen in patients with immunocompromise. Pulmonary involvement is rare, typically occurring in elderly alcoholic males and clinically resembling tuberculosis. Chronic lymphocytic meningitis can be a delayed complication of sporotrichosis infection and should be considered in patients with chronic meningeal symptoms.

Diagnosis

History and physical findings are the keys to diagnosis. Fungal cultures are the best way to isolate the fungus, and tissue biopsy cultures often are diagnostic. Pus, synovial fluid, sputum, blood, or tissue fragment is suitable for culture.

Routine laboratory tests are nonspecific, but an increased WBC count, eosinophil count, and erythrocyte sedimentation rate may occur. The differential diagnosis includes tuberculosis, subcutaneous abscesses of tularemia, cat-scratch disease, leishmaniasis, staphylococcal lymphangitis, paracoccidioidomycosis, chromoblastomycosis, blastomycosis, bacterial pyoderma, primary syphilis, and infections caused by atypical mycobacteria such as Mycobacterium marinum.

Treatment

Itraconazole (100 to 200 milligrams daily for 3 to 6 months) is the treatment of choice for localized and systemic infections. Fluconazole is less effective than itraconazole and should be reserved for those few patients not tolerating itraconazole. Ketoconazole has shown even poorer results than fluconazole. IV amphotericin B is effective, but adverse reactions limit its use to disseminated forms of the disease. In endemic regions or in epidemic outbreaks, a saturated solution of potassium iodide is an effective low-cost alternative.

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FIGURE 152-1.

EPIDEMIOLOGY

MICROBIOLOGY

PATHOPHYSIOLOGY

CLINICAL FEATURES

Cellulitis

FIGURE 152-2.

Erysipelas

FIGURE 152-3.

DIAGNOSIS

TREATMENT

General Treatment

Treatment for Purulent Cellulitis or Suspected Methicillin-Resistant Staphylococcus aureus

Treatment of Nonpurulent Cellulitis/Erysipelas

DISPOSITION AND FOLLOW-UP

PATHOPHYSIOLOGY

CLINICAL FEATURES

FIGURE 152-4.

DIAGNOSIS

FIGURE 152-5.

TREATMENT

Incision and Drainage Procedure

Adjuvant Antibiotics

DISPOSITION AND FOLLOW-UP

MICROBIOLOGY

PATHOPHYSIOLOGY

CLINICAL FEATURES

FIGURE 152-6.

DIAGNOSIS

TREATMENT

FOLLICULITIS

Epidemiology/Microbiology

Clinical Features

Diagnosis

Treatment/Disposition and Follow-Up

HIDRADENITIS SUPPURATIVA

PILONIDAL ABSCESS

Clinical Features

FIGURE 152-7.

Treatment

INFECTED EPIDERMOID AND PILAR CYSTS

BARTHOLIN GLAND ABSCESS

FIGURE 152-8.

PARONYCHIA AND FELONS

PERIRECTAL ABSCESSES

SPOROTRICHOSIS

Epidemiology

Pathophysiology

Clinical Features

FIGURE 152-9.

FIGURE 152-10.

Diagnosis

Treatment

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