6 Soft Tissue Infections and Antibiotics in Plastic Surgery Abstract Skin and soft tissue infections (SSTIs) include infections of skin, subcutaneous tissue, fascia, and muscle. Clinical presentation is variable, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis. It is imperative to distinguish necrotizing from nonnecrotizing infections in order to avoid unnecessary delays of lifeand limb-saving treatments. Eron’s classification of SSTIs is based on the severity of local and systemic signs and provides information regarding the therapeutic approach for each category. Surgical site infections (SSIs) are the most common health care–associated infections, representing a considerable burden in terms of postoperative morbidity and mortality, delays in discharge, and hospital costs. Clinical management of SSIs is based on a combination of surgical, supportive, and antimicrobial therapies. On the other hand, infection is a leading cause of morbidity complicating breast implant surgery and is reported in 2–2.5% of interventions. Treatment goals are to eradicate infection and rescue the implant if possible. Several studies have revealed the presence of bacteria on the surface of breast implants and suggested an association between these findings and capsular contracture. The mechanisms of action, spectrum of activity, clinical uses, route of excretion, and toxic effects of the antimicrobial agents most commonly used in SSTIs are reviewed in this chapter. Keywords: alloplastics infections, breast implant biofilm, broad-spectrum antimicrobials, capsular contracture, necrotizing fasciitis, skin and soft tissue infections, surgical site infections In this chapter skin and soft tissue infections (SSTIs) are addressed, with particular emphasis in general clinical and surgical management. In this sense, distinguishing severe from nonnecrotizing infections and knowing the main microorganisms involved, as well as the most commonly used antimicrobials, are crucial in the implementation of a prompt and effective therapy. In addition, the management of breast implant–associated infections is described, along with the role of biofilm and its relationship with capsular contracture. SSTIs include infections of skin, subcutaneous tissue, fascia, and muscle. Clinical presentation is variable, ranging from simple cellulitis to rapidly progressive necrotizing fasciitis. There are several factors that may predispose a patient to developing SSTIs, such as a breach in the epidermis, immunosuppression (malnutrition, hypoproteinemia, burns, diabetes mellitus, HIV infection), chronic venous or lymphatic insufficiency, and chronic neuropathy. On initial assessment it is imperative to distinguish necrotizing from nonnecrotizing infections to avoid delaying a treatment that may otherwise save a life or a limb. Note Infection, which is different from colonization, develops when microbial pathogenicity overcomes the host’s immunological defenses. SSTIs may be classified according to the layer of infection ( Table 6.1 Type of infection according to the layer of skin/soft tissue affected
6.1 Introduction
6.2 Skin and Soft Tissue Infections
6.2.1 Classification
Table 6.1), severity of infection, and microbiological etiology. According to severity, the practice guidelines of the Infectious Diseases Society of America (IDSA) classifies SSTIs into five categories: superficial uncomplicated infections (e.g., impetigo, erysipelas, and cellulitis), necrotizing infections, infections associated with bites and animal contact, surgical site infections (SSIs), and infections in the immunocompromised host. Of note, Eron’s classification, also based on the severity of local and systemic signs, incorporates information on management besides the clinical features of each group (
Table 6.2).
Anatomical structure | Infection | Microbiological etiology |
Epithelium | Varicella Measles | Varicella virus Measles virus |
Keratin layer | Ringworm | Dermatophyte fungi |
Epidermis | Impetigo | Streptococcus pyogenes Staphylococcus aureus |
Dermis | Erysipelas | Streptococcus pyogenes |
Hair follicles | Folliculitis, boils, carbuncles | Staphylococcus aureus |
Sebum glands | Acne | Propionibacterium acnes |
Subcutaneous fat | Cellulitis | β-Hemolytic streptococci |
Fascia | Necrotizing fasciitis | Streptococcus pyogenes Mixed anaerobic infection |
Muscle | Myositis Gangrene | Toxic strains of Staphylococcus aureus Clostridium perfringens |
Table 6.2 Eron’s classification of skin and soft tissue infections
Category | Clinical features | Management |
Class 1 | SSTI but no signs or symptoms of systemic toxicity or comorbidities | Drainage (if required) and oral antibiotics as outpatient |
Class 2 | Either systemically unwell or systemically well but with comorbidity that may complicate or delay resolution | Oral or outpatient intravenous antibiotic therapy; may require short period of observation in hospital |
Class 3 | Toxic and unwell (fever, tachycardia, tachypnea and/or hypotension) | Likely to require inpatient treatment with parenteral antibiotics |
Class 4 | Sepsis syndrome and life-threatening infection | Likely to require admission to intensive care unit, urgent surgical assessment, and treatment with parenteral antibiotics |
6.2.2 General Management
The general management of SSTIs includes proper assessment of the indications for conservative or surgical treatment, the collection of samples for culture, and the instauration of an empirical or antibiogram-oriented therapy when needed. Uncomplicated SSTIs pose little risk to life and generally respond well to either source control (e.g., drainage or debridement) or a simple course of antibiotics, whereas complicated SSTIs, such as complicated abscesses, infected burn wounds, infected ulcers, infections in diabetics, and deep space wound infections, are often limbor life-threatening conditions requiring surgical intervention.
Note
The timing of treatment initiation in skin and soft tissue infections is important for patient outcomes; failure to give antibiotics within 8 hours of presentation is associated with prolonged patient hospitalization.
Role of Swabs, Cultures, and Biopsies
Tissue biopsy or aspiration sampling of infected tissue is the gold standard for culture of SSTI and is especially important in cases of severe infection, systemic toxicity, or failure of initial therapy. A bacterial count of 105 organisms per gram of tissue has been regarded as the threshold for clinical infection. Swab cultures are probably the most commonly used method to determine the resistance pattern of skin pathogens in nursing home residents and are widely used in a number of other settings as well; however, they are controversial, especially when obtained from chronic wounds. If material superficial to the infected tissue is sampled, colonizers may be isolated. Furthermore, swab cultures should not be used to determine if a wound is acutely infected, but rather to identify potential pathogens when deep tissue biopsy is not elected.
Empirical Antibiotic Treatment
The microbiological diagnosis of any infection is ideally based on data from bacterial or fungal culture or serologic testing; however, it usually takes 24 to 72 hours for these results to become available, which is sometimes a prohibitively long period to wait without intervention. On the other hand, the most likely pathogens can usually be inferred from the clinical presentation. Thus, once pus samples are sent for culture and antimicrobial sensitivity testing, empirical oral or intravenous (IV) antimicrobial therapy should be started based on the severity of infection. A common approach is to use broad-spectrum antimicrobial agents as initial empirical therapy (sometimes involving a combination of antibiotics) so as to cover multiple possible pathogens commonly associated with the specific clinical entity.
Indications for IV antibiotics include a limbor life-threatening severe soft tissue infection, signs and symptoms of systemic illness, immunosuppression, and elderly patients. The timing of initial therapy should be guided by the urgency of the situation. In critically ill patients, such as those in septic shock and febrile neutropenic patients, empirical therapy should be initiated immediately after or concurrently with collection of diagnostic specimens. In more stable clinical circumstances, antimicrobial therapy should be deliberately withheld until appropriate specimens have been collected and submitted to the microbiology laboratory. Premature initiation of antimicrobial therapy in these circumstances may suppress bacterial growth and preclude the opportunity of establishing an accurate microbiological diagnosis, which is critical in the management of these patients, who usually require several weeks to months of directed antimicrobial therapy.
Note
Microbiological diagnosis and susceptibility testing are of increasing importance in the current era of multidrug-resistant bacteria and have a major role in promoting appropriate prescription of antibiotics.
General Laboratory Workup
Patients with uncomplicated SSTIs do not usually require any investigations or hospital admission. However, patients with symptoms and signs of systemic compromise, including hemodynamic changes (e.g., tachycardia and hypotension) should undergo the following tests: blood culture and drug susceptibility, complete blood count with differential and creatinine, bicarbonate, creatine phosphokinase, and C-reactive protein levels. Additional investigations may be indicated depending on the severity of systemic illness. Once a pathogenic microorganism is identified in culture, most microbiology laboratories then run an antimicrobial susceptibility testing (AST), which measures the ability of a specific organism to grow in the presence of a particular drug in vitro and is performed using guidelines established by the Clinical and Laboratory Standards Institute. The goal of AST is to predict the clinical success or failure of the antibiotic being tested against a particular organism. Data are reported in the form of minimum inhibitory concentration, which is the lowest concentration of an antibiotic that inhibits visible growth of a microorganism, and interpreted by the laboratory as susceptible, resistant, or intermediate, according to Clinical and Laboratory Standards Institute criteria. A report of susceptible indicates that the isolated pathogen is likely to be inhibited by the usually achievable concentration of a particular antimicrobial agent when the recommended dosage for the particular site of infection is used.
Note
Patients showing symptoms and signs of systemic compromise, such as tachycardia and hypotension, should undergo blood culture and drug susceptibility together with complete blood count with differential and creatinine, bicarbonate, creatine phosphokinase, and C-reactive protein levels.
Antibiogram-oriented Therapy
Once microbiological or antimicrobial susceptibility data are available, every attempt should be made to narrow the antibiotic spectrum. This is a critically important component of antibiotic therapy because it can reduce costs and toxicity and prevent the development of antimicrobial resistance in the community.
Bactericidal versus Bacteriostatic Therapy
A commonly used distinction among antibacterial agents is whether they are bactericidal or bacteriostatic. On the one hand, bactericidals, which cause death and disruption of the bacterial cell, include drugs that act primarily on the cell wall (e.g., β-lactams), cell membrane (e.g., daptomycin), or bacterial DNA (e.g., fluoroquinolones). Bacteriostatic agents, on the other hand, inhibit bacterial replication without killing the microorganism. Most bacteriostatic drugs, including sulfonamides, tetracyclines, and macrolides, act by inhibiting protein synthesis. The distinction is not absolute, and some agents that are bactericidal against certain organisms may be bacteriostatic against others and vice versa. Although in most cases this distinction is not significant in vivo, bactericidal agents are preferred in cases of serious infections, such as necrotizing fasciitis.
Use of Antimicrobial Combinations
Although single-agent antimicrobial therapy is generally preferred, a combination of two or more agents is sometimes recommended, such as to: (1) treat infections that are frequently caused by bacteria resistant to multiple antibiotics; (2) treat infections that are thought to be caused by more than one microorganism; and (3) prevent the development of resistant mutants in a bacterial population, which is generally the result of selective pressure from antimicrobial therapy.
Surgical Treatment
Some SSTIs require operative drainage or debridement, especially in cases where the bioburden is very high or in the presence of purulent collections (e.g., abscess), for which the penetration and activity of antimicrobial agents are often inadequate. Thus any abscess, regardless of size, must be drained for complete resolution. The drainage incision should be made parallel to a natural skin crease, at the most prominent part and going all the way into the abscess cavity. Care should be taken when incising abscesses near major vessels and nerves, where it is more prudent to access the cavity by blunt dissection. Any necrosed or unhealthy skin on the roof of the abscess should be excised completely. Necrotizing fasciitis is a surgical emergency, and early surgical treatment has been shown to optimize outcomes in these patients. Staged debridements until dermal bleeding is seen on the edges of the skin should be done in order to minimize damage to healthy tissue. Finally, there are no absolute contraindications for incision, drainage, and/or debridement of SSTIs. Patients whose physical condition is compromised should be stabilized and rendered fit for anesthesia before surgery.
6.2.3 Surgical Site Infections
SSIs are the most common health care–associated infection, representing a considerable burden in terms of postoperative morbidity and mortality, delays in discharge, and hospital costs (
Table 6.3). Since plastic surgery interventions have increased in number, frequency, and complexity, postoperative complications, particularly SSIs, have also increased. Data regarding incidence and risk factors for SSIs in plastic surgery are limited and sometimes refer to specific interventions. Moreover, according to current literature, SSI rates in plastic surgery interventions in relation to a specific preoperative contamination class are widely variable, ranging from 2 to nearly 20% in clean elective operations (e.g., excisional surgery and breast augmentation or reduction) and from 23 to 37% in clean-contaminated interventions (e.g., skin grafting of lower extremity vascular ulcers and burn wounds).
Table 6.3 Definition criteria for surgical site infection
Superficial incisional SSI | Occurs within 30 days postoperatively and involves skin or subcutaneous tissue of the incision and at least one of the following: 1. Purulent drainage from the superficial incision. 2. Organisms isolated from an aseptically obtained culture of fluid or tissue from the superficial incision. 3. At least one of the following signs or symptoms of infection: pain or tenderness, localized swelling, redness, or heat, and superficial incision is deliberately opened by surgeon and is culture positive or not cultured (a culture-negative finding does not meet this criterion). 4. Diagnosis of superficial incisional SSI by the surgeon or attending physician. |
Deep incisional SSI | Occurs within 30 days after the operative procedure if no implant is left in place or within 1 year if implant is in place and the infection appears to be related to the operative procedure, involves deep soft tissues (e.g., fascial and muscle layers) of the incision, and the patient has at least one of the following: 1. Purulent drainage from the deep incision but not from the organ/space component of the surgical site. 2. A deep incision spontaneously dehisces or is deliberately opened by a surgeon and is culture positive or not cultured, and the patient has at least one of the following signs or symptoms: fever (> 38°C) or localized pain or tenderness (a culture-negative finding does not meet this criterion). 3. An abscess or other evidence of infection involving the deep incision is found on direct examination, during reoperation, or by histopathological or radiologic examination. 4. Diagnosis of a deep incisional SSI by a surgeon or attending physician. |
Organ/space SSI | Involves any part of the body, excluding the skin incision, fascia, or muscle layers, that is opened or manipulated during the operative procedure. Specific sites are assigned to organ/space SSI to further identify the location of the infection (e.g., endocarditis, endometritis, mediastinitis, vaginal cuff, and osteomyelitis). Organ/space SSI must meet the following criteria: 1. Infection occurs within 30 days after the operative procedure if no implant is in place or within 1 year if implant is in place and the infection appears to be related to the operative procedure. 2. Infection involves any part of the body, excluding the skin incision, fascia, or muscle layers, that is opened or manipulated during the operative procedure. 3. The patient has at least one of the following: (a) purulent drainage from a drain that is placed through a stab wound into the organ/space, (b) organisms isolated from an aseptically obtained culture of fluid or tissue in the organ/space, (c) an abscess or other evidence of infection involving the organ/space that is found on direct examination, during reoperation, or by histopathologic or radiologic examination, and (d) diagnosis of an organ/space SSI by a surgeon or attending physician. |
Source: Reproduced with permission from Stevens DL, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections (Infectious Diseases Society of America Guideline). Clinical Infectious Diseases 2005;41:1371–1406. | |
Etiology
The normal skin flora comprises numerous species of microorganisms residing in the epidermis, which in the unwounded skin of a healthy individual are usually nonpathogenic. However, when skin is breached these microorganisms have the potential to penetrate into the dermis and subcutaneous tissue and cause infection. Infection, which is distinct from colonization, develops when microbial pathogenicity overcomes the host’s immunological defenses. The majority of SSIs are monomicrobial and caused mainly by gram-positive or gram-negative bacteria, most often Staphylococcus aureus. The presence of methicillin-resistant S. aureus (MRSA) represents an important risk factor in the development of complications. SSIs can also be polymicrobial, in which case a synergistic effect may develop, increasing pathogenicity and complicating therapy.
Clinical Presentation
The severity of SSIs depends on a series of factors, and the clinical spectrum ranges from mild to life-threatening variants. SSIs are considered complicated SSTIs with potentially devastating consequences and therefore require early recognition and prompt management. Moreover, SSIs caused by highly pathogenic strains of common organisms (e.g., S. aureus expressing Panton–Valentine’s leukocidin, or toxigenic strains of Streptococcus pyogenes) may present with systemic toxicity in immunocompetent individuals. These infections tend to spread rapidly and are considered medical emergencies necessitating urgent surgical debridement and high doses of antibiotics.
Diagnosis
Swabs of pus or tissue samples from open wounds usually provide the best diagnostic value. Samples from deeper tissues or exudate are the most appropriate for microbiological diagnosis and should be obtained after debridement and cleansing of superficial debris. Imaging techniques can provide structural information about deep tissue infections and differentiate necrotizing from nonnecrotizing infections by detecting the presence of edema along the fascial plane in the former. Radiography and computed tomography can be used to detect gas in tissues, which is indicative of necrotizing infection, whereas ultrasonography is useful for diagnosing and draining collections under direct vision. Magnetic resonance imaging has a particularly high sensitivity for the diagnosis of infections involving soft tissue and bone and can be used to determine the extent of deep tissue involvement.
Treatment
Management of SSIs involves a combination of supportive, antimicrobial, and surgical therapies (
Fig. 6.1).
In general, small abscesses are treated primarily by incision and drainage, with antibiotics indicated for patients who do not respond to these measures and those with either large collections or located in an area that is difficult to drain. Rapid progression of infection, signs of systemic illness, comorbidities, and immunosuppression are also indications for systemic antibiotic therapy. Negative pressure dressings, especially with silver-coated foams, can be used for infections with excessive exudate or for large wounds, always maintaining close vigilance on the wound and patient’s evolution. Once infection is resolved, reconstructive procedures, including revascularization of critically perfused limbs, skin grafting, and flap closure may be needed. Regarding antibiotics, the timing of (effective) treatment initiation is critical—failure to give antibiotics within 8 hours of presentation is associated with prolonged patient hospitalization. Furthermore, the treating surgeon needs to be aware of microbial and patient factors that may render an empirical treatment inappropriate and guide therapeutic decisions accordingly. Inappropriate treatment, defined as the administration of an antimicrobial that has no activity against the isolated pathogen(s), is more likely in patients with a device-associated infection or an infection due to MRSA.
Fig. 6.2 A 27-year-old man came to the outpatient clinic with a 3-week history of a red, tender, pusfilled facial bump. Furuncles often rupture and drain spontaneously or following treatment with moist heat.
6.2.4 Nonnecrotizing Infections
Folliculitis, Furuncles, and Carbuncles
Furuncles are infections of the hair follicle, usually caused by S. aureus, in which suppuration extends through the dermis and into the subcutaneous tissue, leading to the formation of a small abscess (
Fig. 6.2). Folliculitis is characterized by a more superficial inflammation, with pus limited to the epidermis. Clinically, furuncles are inflammatory nodules with overlying pustules through which hair emerges. They often rupture and drain spontaneously or following treatment with moist heat. Infection involving several adjacent furuncles produces a carbuncle, which is seen as a coalescent inflammatory mass with pus draining from multiple follicular orifices. Carbuncles are typically larger and deeper than furuncles and develop most commonly on the back of the neck, particularly in diabetics. Most large furuncles and all carbuncles should be treated with incision and drainage. Systemic antimicrobials are usually unnecessary, unless fever or other evidence of systemic toxicity is observed.
Erysipela
Erysipela is an infection of the upper dermis that extends into the superficial lymphatics. Clinically, it presents as an erythematous indurated plaque with sharply demarcated borders. It is almost always caused by group A and B streptococci and less commonly by group G or C. In rare cases, other microorganisms, including S. aureus, Streptococcus pneumoniae, enterococci, and a variety of aerobic gram-negative bacilli, have been recovered from patients with erysipelas.
Cellulitis
Cellulitis is an acute, spreading, pyogenic inflammation of the dermis and subcutaneous tissue that lacks sharp demarcation from uninvolved skin. Prior to the introduction of Haemophilus influenzae type b conjugated vaccine in the immunization schedule, buccal cellulitis due to H. influenzae was responsible for up to 25% of cases of facial cellulitis in children between 3 and 24 months; today such disease is rare. Cellulitis is most commonly caused by β-hemolytic streptococci, especially groups A and B, and less often by groups C and G, as well as S. aureus. Importantly, the incidence of community-acquired SSTIs due to MRSA is currently increasing.
Identifying the source of cellulitis (cutaneous, subjacent, or bacteremic) can provide clues as to the causative microorganism. Animal or human bites can cause cellulitis due to skin flora of the recipient or oral flora from the biter (e.g., Pasteurella multocida, Erysipelothrix rhusiopathiae). Specific pathogens should be suspected when infection follows exposure to seawater (Vibrio vulnificus), freshwater (Aeromonas hydrophila), aquacultured fish (Streptococcus iniae), or fish aquaria (Mycobacterium marinum). Subcutaneous injection of drugs (i.e., skin popping) can result in cellulitis due to unusual microorganisms, such as Clostridium tetani, Clostridium botulinum, Clostridium sordellii, Clostridium novyi, or Bacillus cereus. Cellulitis is not uncommon in lymphedematous arms following radical mastectomy and radiotherapy and in legs of patients who have had vein grafts harvested. Crepitant cellulitis is produced by either clostridia or non-spore-forming anaerobes (e.g., Bacteroides species, Peptostreptococcus species) either alone or mixed with facultative pathogens, particularly Escherichia coli, Klebsiella species, or Aeromonas species. Crepitant cellulitis of the left thigh may be associated with a colonic diverticular abscess. Though not frequently, cellulitis can occur secondary to bacteremia. Pneumococcal cellulitis of the face or limbs may occur in patients with diabetes mellitus, alcoholism, systemic lupus erythematosus, nephrotic syndrome, or hematological malignancy. Meningococcal cellulitis is rare and usually presents as periorbital cellulitis in children, whereas in adults it typically affects the extremities. Bacteremic cellulitis due to Vibrio vulnificus with prominent hemorrhagic bullae may follow the ingestion of raw oysters in patients with cirrhosis, hemochromatosis, or thalassemia. Bacteremia caused by gram-negative bacteria (e.g., E. coli, Enterobacter species, Proteus species) occasionally causes soft tissue infections, including cellulitis. Pseudomonas aeruginosa cellulitis may follow bacteremia in neutropenic patients, whereas less common opportunistic pathogens (e.g., Helicobacter cinaedi) may affect HIV patients.
Skin Abscesses
Cutaneous abscesses are collections of pus within the dermis and deeper layers. They usually present as tender, fluctuant, red nodules, often surmounted by a pustule and encircled by a rim of erythematous swelling. S. aureus is the sole pathogen in most cases, with a substantial number caused by MRSA strains. Skin abscesses can be polymicrobial, containing regional skin flora or organisms from adjacent mucous membranes. Incision and drainage of pus and debris, and probing of the cavity to break up loculations, provides effective treatment of these lesions.
Hidradenitis Suppurativa
Hidradenitis suppurativa (HS) is a chronic inflammatory, recurrent follicular disease affecting apocrine gland–bearing regions. It usually occurs in healthy adolescents and adults and is characterized by comedo-like follicular occlusion, mucopurulent discharge, and progressive scarring. Predisposing risk factors include genetic susceptibility, smoking, obesity, immunosuppression, hormonal changes (puberty, menstruation, menopause), and emotional and social stress. It has been suggested that HS is primarily a disease of the follicular epithelium that becomes secondarily infected, most commonly with S. epidermidis and S. aureus. Arthropathy is usually associated with HS. HS is classified in three stages, depending on the presence and extent of sinus tracts and scarring (Table 6.4). Diagnosis of HS is mainly clinical and is based on three main pillars: the presence of typical lesions, their characteristic distribution, and recurrence. Typical (primary) lesions include painful erythematous papules, nodules, or abscesses; draining sinuses; dermal contractures; or double-ended comedones. Regarding distribution, as already mentioned, HS affects areas containing apocrine glands, which include the axillae and groin, and perineal, perianal, and interand inframammary areas (
Fig. 6.3).
Note
Diagnosis of hidradenitis suppurativa is based on the presence of typical lesions, characteristic distribution, and recurrence.
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