Browse the corpus

CHAPTER 152: Soft Tissue Infections 1005 Soft Tissue Infections Elizabeth W. Kelly INTRODUCTION More than 4 in 100 people seek treatment for skin and soft tissue infec tions each year in the United States, and these infections are about 20 times more likely to be ambulatory treated than inpatient treated. 1 Abscess or cellulitis are the most common of these infections, with the majority of patients treated in the outpatient setting. 1 This chapter discusses skin and soft tissue infections in adults; impetigo and other soft tissue infections in children are discussed in Chapter 142, “Rashes in Infants and Children. ” Perirectal abscess and pilonidal abscess are discussed in Chapter 85, “ Anorectal Disorders. ” Bartholin gland abscess is discussed in Chapter 102, “Vulvovaginitis. ” Hidradenitis suppurativa is discussed in Chapter 252, “Skin Disorders: Groin and Skinfolds. ” Paronychia and felons are discussed in Chapter 283, “Nontraumatic Disor ders of the Hand. ” ANATOMY AND DEFINITIONS 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. Cellulitis is an infection of the dermis and subcutaneous tissue and is divided clinically as purulent or nonpurulent. Management of the two types is different. 2,3 Purulent cellulitis is a skin or soft tissue infection with purulent drainage or an underlying abscess. Nonpurulent cellulitis has no purulent drainage or exudate and no associated abscess. 2,3 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. Folliculitis is an infection of the hair follicle, often purulent, but is superficial without involvement of the deeper tis sues. Skin abscesses are collections of pus within the dermis and deeper skin tissues, potentially involving the subcutaneous tissues. Furuncles (or boils) are single, deep nodules involving the hair follicle that are often suppurative. 3 Carbuncles are formed by multiple interconnecting furuncles that drain through several openings in the skin. 3 Necrotizing soft tissue infections are characterized by microbial triggered necrosis involving any of the soft tissue layers including the dermis, subcutane ous tissues, fascia, and muscle.4 CELLULITIS AND ERYSIPELAS  EPIDEMIOLOGY Cellulitis accounts for approximately 1.3% of all ED visits. General risk factors for cellulitis are listed in Table 152-1. 5,6 Risk factors for specific organisms causing cellulitis are listed in Table 152-2. 2,5,7-12 Cellulitis is observed more frequently among middle-aged and elderly patients, whereas erysipelas is more common among children and elderly patients. 13 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%, respec tively). Approximately 10% of patients diagnosed with cellulitis are hospitalized, and the majority of these patients are over age 64 years. CHAPTER Papillary dermis Reticular dermis Subcutis Superficial vascular plexus Deep vascular plexus capillaries around hairs and glands Subcutaneous vascular plexus Papillary loops Arteries and veins Vascular segments: Epidermis FIGURE 152-1. Schematic diagram of the architecture of the skin.

nts are over age 64 years. CHAPTER Papillary dermis Reticular dermis Subcutis Superficial vascular plexus Deep vascular plexus capillaries around hairs and glands Subcutaneous vascular plexus Papillary loops Arteries and veins Vascular segments: Epidermis 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 K, et al: Fitzpatrick’s Dermatology in General Medicine, 7th ed. © 2008, McGraw-Hill, Inc., New York.] Tintinalli_Sec13_p0997-1100.indd 1005 8/2/19 8:11 PM

skin, including the epidermis, dermis, and deeper subcutaneous tissues. Also shown are the blood vessels and a hair follicle. [Reproduced with permission from Wolff K, et al: Fitzpatrick’s Dermatology in General Medicine, 7th ed. © 2008, McGraw-Hill, Inc., New York.] Tintinalli_Sec13_p0997-1100.indd 1005 8/2/19 8:11 PM 1006 SECTION 13: Infectious Diseases  MICROBIOLOGY Approximately 80% of cellulitis cases are caused by gram-positive bac teria. Community-acquired methicillin-resistant Staphylococcus aureus (MRSA) is now the most common cause of skin and soft tissue infec tions presenting to the ED, 7,14 regardless of patient risk factors. The Infectious Diseases Society of America recommends differentiation of purulent from nonpurulent cellulitis (see detailed definitions earlier) for treatment decisions. 2 MRSA is likely to be the causative agent in puru lent cellulitis. For nonpurulent cellulitis, the role of MRSA is unknown, and empirical therapy for β-hemolytic streptococcal infection with β-lactams is recommended. 2,15-18 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. 13 Bullous erysipelas is a more severe form and can represent synergy with β-hemolytic streptococci and MRSA.  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. The subsequent inflammatory response is caused by the infiltration of cells, such as Langerhans cells and keratinocytes, which release the cytokines interleukin-1 and tumor necrosis factor that enhance skin infiltration by lymphocytes and macrophages.  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 wound 2; an abscess may or may not subsequently form. Systemic signs of fever, leukocytosis, and bacteremia are more typical in the immuno suppressed. 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. 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 erysip elas 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.

over the face ( Figure 152-3). Complete involvement of the ear is the “Milian ear sign” and is a distinguishing feature of erysip elas 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 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 152-2 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 hospitalization or surgery within the past year Residence in a long-term care facility within the past year Hemodialysis Crowded living environments including day care or homeless shelters, soldiers, prisons Contact sports Injection 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, injection 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 to 213, “Puncture Wounds and Bites,” “Bites and Stings,” “Snake Bites,” and “Marine Trauma and Envenomation,” respectively. 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, Inc., New York.] Tintinalli_Sec13_p0997-1100.indd 1006 8/2/19 8:11 PM

. 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, Inc., New York.] Tintinalli_Sec13_p0997-1100.indd 1006 8/2/19 8:11 PM CHAPTER 152: Soft Tissue Infections 1007 necrotizing soft tissue infection. On resolution of the infection, des quamation of the site often occurs.  DIAGNOSIS The diagnosis of cellulitis and erysipelas is clinical. Management should be guided by the clinical differentiation between purulent and nonpurulent soft tissue infections.2,3 Presence of an abscess or purulent drainage from the area of cellulitis defines the soft tissue infection as purulent. 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. 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. 15 Areas with abscess formation have significantly higher yields; wound culture is recom mend when the decision has been made to place the patient on antibiotics for purulent cellulitis. 3 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, immu nodeficiency, immersion injuries, failed initial therapy, or recurrent episodes, or in circumstances such as animal bites, cultures of pus, bullae, or blood are recommended. 3,20,21 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 later section). Table 152-3 lists differential diagnoses and characteristics that help distinguish cellulitis from the listed disorder. POCUS is useful to exclude occult abscess. 22 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 later section).  TREATMENT General Treatment Treatment is elevation of the affected area, inci sion and drainage of any abscess found (see later section), 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 predispos ing 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 MRSA Etiology See Table 152-4 for empiric antibiotic recommendations for purulent cellulitis or when MRSA is suspected. 3,23 Identify and thoroughly drain an abscess. POCUS 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. For patients with severe infection or systemic toxicity, consider nec rotizing fasciitis (see later section on necrotizing fasciitis). It may be difficult to clinically distinguish MRSA cellulitis from methicillinsusceptible S. aureus cellulitis. Treatment failure rates are similar for both β-lactam antibiotics and MRSA-specific antibiotics such as trimethoprim-sulfamethoxazole.

ider nec rotizing fasciitis (see later section on necrotizing fasciitis). It may be difficult to clinically distinguish MRSA cellulitis from methicillinsusceptible S. aureus cellulitis. Treatment failure rates are similar for both β-lactam antibiotics and MRSA-specific antibiotics such as trimethoprim-sulfamethoxazole. 25,26 Treatment of Nonpurulent Cellulitis/Erysipelas Guidelines no longer differentiate the treatment of nonpurulent cellulitis from erysipelas. 3,23 Oral antibiotics are sufficient for simple cellulitis or erysipelas in otherwise healthy adult patients. In cases where there is no evidence of drainage or identifiable abscess, empiric MRSA coverage is not necessary. 17,18,27 POCUS to confirm lack of an abscess is highly recommended. MRSA coverage should be considered in patients who are diabetic, immunosuppressed, have peripheral vascular disease, have a history of IV drug abuse, or require hospitalization. 17,18 See Table 152-5 for guideline-recommended antibiotic options.3,23 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).  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 close follow-up in 2 to 3 days. 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 FIGURE 152-3. Butterfly rash of erysipelas. The sharp demarcation between the salmon-red erythema and the normal surrounding skin is evident. [Reproduced with permis sion from Shah BR, Lucchesi M: Atlas of Pediatric Emergency Medicine, © 2006, McGraw-Hill, Inc., New York.] 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 Stasis dermatitis Bilateral, long-standing, pitting edema, mild tenderness only 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 Tintinalli_Sec13_p0997-1100.indd 1007 8/2/19 8:11 PM

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 Tintinalli_Sec13_p0997-1100.indd 1007 8/2/19 8:11 PM 1008 SECTION 13: Infectious Diseases 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. CUTANEOUS ABSCESSES, FURUNCLES, AND CARBUNCLES Furuncles and carbuncles involve the epidermis, and abscesses involve the deeper soft tissue. 3 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; how ever, MRSA causes the majority of skin abscesses presenting to the ED in the United States. 7,14 Loculation and subsequent walling off of these products of infection lead to abscess formation. As the infection pro gresses 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. Other risk factors 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 puru lent 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. 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. 29 POCUS is an invaluable tool for distinguishing deep abscess from cel lulitis, identifying a foreign body within an abscess, and determining the adequacy of drainage 22,30,31 (Figure 152-5). 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.

e 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. 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 healthy immunocompetent patients where abscess drainage is complete after procedure 1. 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 †‡ 1. Wound culture is recommended in cases where anti biotics are given. 2. 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 sepsisf 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 † 1. Admit to the hospital. 2. Additional antibiotic coverage is listed below. 3. Consider admission to intensive care unit for patients who meet criteria for sepsis (see also Chapter 151, “Sepsis”). 4. 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 >10%. #Physicians should use their clinical judgment; there are no validated criteria to differentiate moderate from severe signs for systemic infection. fCriteria 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/mm 3 or >12,000 cells/mm3, or immunocompromised patients (see Chapter 151, “Sepsis”).

re signs for systemic infection. fCriteria 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/mm 3 or >12,000 cells/mm3, or immunocompromised patients (see Chapter 151, “Sepsis”). Hypotensive patients should be admitted to the intensive care unit. Tintinalli_Sec13_p0997-1100.indd 1008 8/2/19 8:11 PM

re signs for systemic infection. fCriteria 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/mm 3 or >12,000 cells/mm3, or immunocompromised patients (see Chapter 151, “Sepsis”). Hypotensive patients should be admitted to the intensive care unit. Tintinalli_Sec13_p0997-1100.indd 1008 8/2/19 8:11 PM CHAPTER 152: Soft Tissue Infections 1009  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. 32 Input from an appropriate specialist is also recommended in areas of the body with cosmetic concerns. 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. 33 Simple needle aspiration of abscesses is inadequate to treat abscesses caused by MRSA. 34 Prior recommendations for endocarditis prophylaxis in patients undergoing incision and drainage have changed (see Chapter 156, “Endocarditis”). If indicated by the severity of val vular 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 super ficial 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 scarring if possible, especially in areas of cosmetic significance. Position the patient for good access, prepare the area with povidoneiodine solution, and drape in a sterile fashion. To provide local anes thesia, 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 mil liliters 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. 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. Consider MRSA coverage in patients who are diabetic or immunosuppressed, have peripheral vascular disease or history of IV drug abuse, or require hospitalization. Monotherapy IV antibiotics for moderate disease: Typical cellulitis/erysipelas with mild to moderate systemic signs of infection ‡ If immunocompromised, 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 dependent on severity of illness.

xone 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 dependent on severity of illness. Broad-spectrum antibiotics for severe disease (includ ing 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 for further recommendations). 2. Blood cultures recommended in this treatment group. Abbreviation: MRSA = methicillin-resistant Staphylococcus aureus. *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. FIGURE 152-4. Subcutaneous abscess is noted in the axilla. [Reproduced with permis sion from Slaven EM, Stone SC, Lopez FA: Infectious Diseases: Emergency Department Diagnosis & Management, © 2006, McGraw-Hill, Inc., New York.] Tintinalli_Sec13_p0997-1100.indd 1009 8/2/19 8:11 PM

be admitted to the intensive care unit. FIGURE 152-4. Subcutaneous abscess is noted in the axilla. [Reproduced with permis sion from Slaven EM, Stone SC, Lopez FA: Infectious Diseases: Emergency Department Diagnosis & Management, © 2006, McGraw-Hill, Inc., New York.] Tintinalli_Sec13_p0997-1100.indd 1009 8/2/19 8:11 PM 1010 SECTION 13: Infectious Diseases  DISPOSITION AND FOLLOW-UP Most patients with skin abscess, furuncles, and carbuncles are treated as outpatients. Those with systemic toxicity or severe infection typically require parenteral treatment and hospital admission. Age, failed oral antibiotics, and injection drug use impact admission decisions. 46 For those discharged to home, remind patients to keep the wound covered and practice frequent hand washing to prevent spread of the infection. 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 Necrotizing soft tissue infections are a spectrum of illnesses character ized by fulminant, extensive soft tissue necrosis, systemic toxicity, and high mortality. Early in their course, these infections can appear decep tively benign. 4,47 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, NSAID use, decubitus ulcers, chronic skin infections, IV drug abuse, and immune system impairment. 48,49 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 past 20 years. 50 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 cultures, trunk or peri neal 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 necrotiz ing soft tissue infections, and the causative microbes are a combination of gram-positive cocci, gram-negative rods, and anaerobes. Clos tridial infections are now uncommon causes due to improvements in hygiene and sanitation. 47 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 infec tion. Community-acquired MRSA is a cause of type II (monomicrobial) infection, particularly in IV drug abusers, athletes, and institutionalized patients. 51,52 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.

rotizing 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.  PATHOPHYSIOLOGY The rapid necrotizing process typically begins with direct invasion of subcutaneous tissue from external trauma (IV injection, surgical inci sion, 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 under lying malignancy. Bacteria proliferate, invade subcutaneous tissue and deep fascia, and release exotoxins that lead to tissue ischemia, liquefac tion necrosis, and systemic toxicity. Skin involvement is secondary to vasculitis and thrombosis of perfo rating blood vessels. The ischemic tissue environment promotes bacte rial growth, propagating the process and resulting in rapid spread of the 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 drain age. 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. 35,36 Less painful alternatives to packing include placing a catheter,37 or tying in a rubber drain after placing two small stab inci sions, 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. 38 Primary closure after abscess drainage shortens healing time for patients treated in the operating room39 and has been studied in a small randomized controlled trial in the ED40; 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 re-collection 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 followup visit. Adjuvant Antibiotics Recent studies suggest that in patients with a simple abscess, MRSA antibiotic coverage in conjunction with incision and drainage improves short-term outcome. 41-43 However, the benefit of antibiotics as an adjunct to sufficient abscess drainage must be weighed against the known side effect profile, especially in healthy patients without significant surrounding cellulitis. 44,45 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. 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 hyper echoic and edematous. Note that the superior edge of this large abscess cavity is 3.5 cm from the skin surface ( arrow). [Reproduced with permission from Ma OJ, Mateer JR, Reardon RF, Joing SA: Ma & Mateer’s Emergency Ultrasound , 3rd ed. New York, NY: McGraw-Hill, Inc.; 2014. From Chapter 18: Musculoskeletal, Soft Tissue, and Miscellaneous Applications, Figure 18-105, p.

his large abscess cavity is 3.5 cm from the skin surface ( arrow). [Reproduced with permission from Ma OJ, Mateer JR, Reardon RF, Joing SA: Ma & Mateer’s Emergency Ultrasound , 3rd ed. New York, NY: McGraw-Hill, Inc.; 2014. From Chapter 18: Musculoskeletal, Soft Tissue, and Miscellaneous Applications, Figure 18-105, p. 561.] Tintinalli_Sec13_p0997-1100.indd 1010 8/2/19 8:11 PM

his large abscess cavity is 3.5 cm from the skin surface ( arrow). [Reproduced with permission from Ma OJ, Mateer JR, Reardon RF, Joing SA: Ma & Mateer’s Emergency Ultrasound , 3rd ed. New York, NY: McGraw-Hill, Inc.; 2014. From Chapter 18: Musculoskeletal, Soft Tissue, and Miscellaneous Applications, Figure 18-105, p. 561.] Tintinalli_Sec13_p0997-1100.indd 1010 8/2/19 8:11 PM CHAPTER 152: Soft Tissue Infections 1011 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, Inc., New York.] 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/mm 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. infection, which 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. 47 As the disease progresses, widespread gangrene of the skin, subcutaneous fat, fascia, and even skeletal muscle occurs.48 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.

n. 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.  CLINICAL FEATURES Classic symptoms of necrotizing soft tissue infections are severe pain, anxiety, and diaphoresis. 47,48 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. 48 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 infec tion, the skin can develop a bronze or brownish discoloration with a malodorous serosanguineous discharge, and bullae may be present (Figure 152-6). Systemic manifestations include a low-grade fever with tachycardia out of proportion to the fever. In fulminant necrotizing infections, par ticularly 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, bul lae, hypotension, or gas on radiograph—are present in less than half of patients. 54 Many laboratory abnormalities have been investigated to aid in the diagnosis,55-61 including the laboratory risk indicator for necrotizing fasciitis (LRINEC score).55,56 Since its derivation, the LRINEC score ≥ 6 has been proven to miss many cases of necrotizing fasciitis, 60 especially those caused by Vibrio species,57 and neck infections.61 Table 152-6 lists laboratory factors and imaging findings associated with necrotizing Tintinalli_Sec13_p0997-1100.indd 1011 8/2/19 8:11 PM

.55,56 Since its derivation, the LRINEC score ≥ 6 has been proven to miss many cases of necrotizing fasciitis, 60 especially those caused by Vibrio species,57 and neck infections.61 Table 152-6 lists laboratory factors and imaging findings associated with necrotizing Tintinalli_Sec13_p0997-1100.indd 1011 8/2/19 8:11 PM 1012 SECTION 13: Infectious Diseases fasciitis to help clinicians with medical decision making.55-64 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 early diagnosis of necrotizing fasciitis. 48,49 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. 55 A positive test is lack of normal bleeding, or friable tissue to minimal finger pressure. However, its use has never been studied formally. Plain radiographs may reveal subcutaneous gas in a minority of patients, but may miss deep fascial gas and are therefore a poor screening tool. CT with contrast is more sensitive (80% to 97%) but has a falsepositive rate of 19%. The most reliable sign of necrosis on CT is non enhancing deep tissues, which requires contrast, or gas, seen in ≤36% of patients. 63 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%. Finally, MRI imposes significant delays to treatment. Bedside US has been advocated, 62 but radiologists caution against excluding necrotizing fasciitis based on its findings.  TREATMENT The tissue ischemia produced in necrotizing skin infections impedes immune system destruction of bacteria and prevents adequate delivery of antibiotics. 48 Thus, antibiotics alone are rarely effective, and immediate surgical consultation and intervention remain the cornerstone of successful management. 49 Begin aggressive fluid resuscitation immediately as well as transfusion of packed red blood cells as needed. Avoid vasoconstrictors, if at all possible, because vasoconstrictors will decrease perfusion to already ischemic tissue. Surgery is the gold standard for diagnosis and treatment; however, treatment standards are primarily expert consensus based, rather than evidenced based. 49 Surgical intervention may include fasciotomy, debridement, and/or amputation. Mortality skyrockets if debridement is delayed >24 hours. 48 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  FOLLICULITIS Folliculitis is an inflammation of hair follicles related to infection, chemical irritation, or injury. 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.

ology/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. Clinical Features The most common sites of involvement for follicu litis 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. 3 Pseudomonas 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 com monly seen in persons of African descent secondary to shaving. It occurs when the hair follicle becomes trapped and, instead of exiting the fol licle, 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 uncom plicated folliculitis or hot-tub folliculitis, stopping exposure or remov ing the offending agent and twice-daily cleansing with mild hand soap often suffice. 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 allow ing 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.  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 through out 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 procedure 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 forceps and removed at the time of drainage.

s 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 forceps and removed at the time of drainage.  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. 65 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. 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 bodytemperature environment. Disease is usually limited to local cutane ous 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. Tintinalli_Sec13_p0997-1100.indd 1012 8/2/19 8:11 PM