Skin and Soft tissue infections (SSTIs) encompass a variety of pathological conditions that involve the skin and underlying subcutaneous tissue, fascia, or muscle, ranging from simple superficial infections to severe necrotizing infections that may involve the dermal, subcutaneous, fascia, and muscle layers.
Various systems of classification have been used to describe SSTIs. World Society of Emergency Surgery classifies SSTIs into four principal groups .
Surgical Site infections
Incisional
-Superficial
-Deep
Non-necrotizing SSTIs
Superficial infections (Impetigo, erysipelas, cellulitis)
Simple abscess, boils and carbuncles
Complex abscesses
Infections developing in damaged skin.
Necrotizing SSTIs (NSTIs)
Necrotizing cellulitis
Necrotizing fasciitis
Fournier’s gangrene
Necrotizing myositis
The first group includes the surgical site infections (SSIs). SSIs represent a separate chapter of soft tissue infections. They are post-operative infections and because of their multifaceted aspects should be framed them as a separated group. In many cases they can be prevented. They are classified into 2 groups: incisional and organ and organ/space. The incisional SSIs are further divided into superficial (skin and subcutaneous tissue) and deep (deep soft tissue–muscle and fascia). Organ and organ/space infections are not properly soft tissue infections. The development of an SSI depends on contamination of the wound site at the end of a surgical procedure and specifically relates to the pathogenicity and inoculum of microorganisms present, balanced against the host’s immune response. Numerous patient-related (endogenous) and process/procedures related (exogenous) risk factors for developing an SSI have been described. Some factors, such as age and gender, are obviously not amenable to changes or improvements. However, addressing other potential factors, such as the nutritional status, smoking, proper use of antibiotics and accurate intraoperative technique, can reduce the likelihood of SSI. Prophylactic antibiotic administration is an established approach for reducing the risk of SSIs in various fields of elective surgery
Non-necrotizing soft tissue infections include superficial infections, complex abscesses, and infections developing in damaged skin. Superficial infections encompass either superficial spreading infection and inflammation within the epidermis and dermis that may be treated with antibiotics alone or a well circumscribed abscess that may be treated by drainage alone.
Common sites of origin of complex abscesses may be perineal or perianal infections, perirectal abscesses, diabetic foot or lower-extremity ulcerations, traumatic injuries, chronic cutaneous cysts, intravenous drug injection sites, gastrointestinal pathology with perforation, genitourinary pathology, animal bites, and pressure ulcers. Complicated skin and subcutaneous abscesses are typically well circumscribed and respond to incision and drainage with adjuvant antibiotic therapy. The cornerstone of treatment is early surgical drainage. Antibiotic therapy is required perioperatively if systemic signs of sepsis are present, in immunocompromised patients, if source control is incomplete or for the abscesses with significant cellulitis. The initiating pathogens often differ according to the originating site. Aerobic gram-positive pathogens are isolated in most complicated abscesses. Depending on the origin, anaerobes, Enterobacteriaceae, and Clostridium spp. may also be present
Infections developing in damaged skin is a heterogeneous group that includes soft tissue infections developing in damaged skin such as bite wounds (animal and human bites), burn wounds or in pressure or vascular ulcers. If managed incorrectly, these infections can develop into more complicated soft tissue infections
Necrotizing soft tissue infections (NSTIs) sare life-threatening, invasive, soft tissue infections caused by aggressive, usually gas-forming bacteria. Delay in diagnosing and treating these infections increases the risk of mortality. NSTIs may involve dermal and subcutaneous components (necrotizing cellulitis), fascial component (necrotizing fasciitis), and muscular components (necrotizing myositis) either singularly or in combination. NSTIs may also be classified into three types defined by the bacterial pathogens initiating the infection and their typical clinical characteristics; type 1 – poly-microbial, type 2 – mono-microbial pathogenic β-haemolytic Streptococci or CA-MRSA, type 3 – mono-microbial secondary to a variety of pathogenic bacilli. Initially, distinguishing between cellulitis and a necrotizing soft tissue infection that requires operative intervention may be difficult. Most cases of necrotizing soft tissue infection are originally diagnosed as cellulitis. However, since time to operative debridement is a strong determinant of outcome in NSTIs, timely diagnosis is essential. Patients with necrotizing soft tissue infections usually present with severe pain that is out of proportion to the physical findings. A rapidly progressive soft tissue infection should be initially treated as a necrotizing infection.
In the early phases, necrotizing soft tissue infections, cause localized inflammatory reactions in the involved tissues. Necrosis occurs because of direct cellular injury from bacterial endo/exotoxins, significant inflammatory oedema within a closed tissue compartment, thrombosis of local blood vessels, and tissue ischemia. Circulating toxins may cause systemic illness which can progress to septic shock, multisystem organ dysfunction, and death.
Fournier’s gangrene is a rapidly progressive, variant of necrotizing fasciitis involving the external genitalia and perineum. Due to the complexity of fascial planes, this infection may extend up to the abdominal wall, down into the thigh, into the perirectal and gluteal spaces, and occasionally, into the retroperitoneum. Diagnosis is based on clinical signs and physical examination. Imaging may be needed to confirm clinical suspicions and to help in identifying the extent of the soft tissue involvement, particularly in the peri-rectal and retroperitoneal planes.
Management of patients with soft tissue infections
The treatment of soft tissue infections is based on source control and/or antibiotic therapy. Source control for SSTIs includes drainage of infected fluids, debridement of infected soft tissues, removal of infected devices or foreign bodies. It should also include definite measures to correct any anatomic derangement resulting in ongoing microbial contamination and restoring optimal function.
The most critical factors for reducing mortality from NSTIs are early recognition and urgent operative debridement. Surgical debridement must be aggressive to halt progression of infection. Cultures of infected fluid and tissues should be obtained during the initial surgical debridement and the results used to tailor specific antibiotic management. Radical surgical debridement of the entire affected area should be performed, continuing the debridement into the healthy-looking tissue. Delay in source control for patients with NSTIs has been repeatedly associated with a greater mortality.
Postoperative wound care starts with meticulous haemostasis. Non-adherent compressive dressings should be applied, followed by repeat wound inspection in ≤ 24 hours. Any patient with extensive necrosis or who is considered to have not be adequately debrided at the initial operation should be returned to the operating room in 24–48 hours for a second look. Further debridement should be repeated until the infection is controlled.
In the setting of Fournier’s gangrene, diverting colostomy has been demonstrated to improve the outcome and the need for fecal diversion depends upon severity of the disease. It helps in decreasing sepsis by minimizing bacterial load in the perineal wound thus controlling infection. Diverting colostomy does not eliminate the necessity of multiple debridements, nor reduces the number of these procedures.
Empiric antibiotic therapy should be directed toward the likely pathogens involved. The principal barrier against microbial invasion is the skin. It constantly interacts with the external environment and is colonized with different populations of bacteria. Intact and well vascularized skin is highly resistant to bacterial invasion. The majority of SSTIs involving healthy skin are caused by aerobic Gram-positive cocci, specifically S. aureus and streptococci. Strains of S. aureus and Group A β-haemolytic streptococci (GAS) can produce a variety of toxins that may both potentiate their virulence and affect the soft tissues and allow invasion of the dermis. Polymicrobial infections occur when aerobic Gram negative and anaerobes invade soft tissues.
SSTIs management has recently become more complicated because of the increasing prevalence of multidrug-resistant pathogens.
Methicillin-resistant Staphylococcus aureus (MRSA) is an increasing cause of these infections, particularly in certain countries. Although MRSA has been usually acquired during exposure in hospitals and other healthcare facilities (HA-MRSA), there has been a recent increase in MRSA infections presenting in the community (CA-MRSA). CA-MRSA strains are genetically and phenotypically distinct from HA-MRSA. They may be susceptible to a wider range of anti-staphylococcal antimicrobials (some are resistant only to β-lactams). CA-MRSA infections are becoming increasingly common. They can have a rapid and devastating course and may produce the pathogenic Panton–Valentine leucocidin toxin (PVL), which destroys white blood cells and is an important virulence factor.
For empirical coverage of CA-MRSA in outpatients with SSTI, oral antibiotic options include clindamycin, trimethoprim-sulfamethoxazole (TMP-SMX), a tetracycline (doxycycline or minocycline), and linezolid. If coverage for both β-hemolytic streptococci and CA-MRSA is required, options include clindamycin alone or TMP-SMX or a tetracycline in association with a β-lactam (eg, amoxicillin) or linezolid and tedizolid alone. For hospitalized patients with severe SSTI, in addition to surgical debridement and broad-spectrum antibiotics, empirical therapy for MRSA should be considered, pending culture data. Options include intravenous (IV) vancomycin or teicoplanin, linezolid or tedizolid, daptomycin, clindamycin, tigecycline, ceftaroline, dalbavancin
In the setting of NSTIs appropriate empiric coverage against MRSA should be immediately initiated. Patients whose clinical setting or gram stain suggests rapidly progressive infection potentiated by exotoxins from Gram positive pathogens (S. pyogenes, CA-MRSA, Clostridial species), treatment with antimicrobial agents should be combined with antiribosomal agents (clindamycin or linezolid). Patients who present with rapidly progressive infections with gram stains of tissue demonstrating gram negative pathogens (Aeromonas sp., Eikenella, Vibrio sp) should be treated with antiribosomal agents targeting gram negative pathogens (tetracyclines). Since it is impossible to exclude with certainty a polymicrobial necrotizing infection, an aggressive broad-spectrum empiric antimicrobial therapy should initially be selected to cover gram-positive, gram-negative, and anaerobic organisms until culture-specific results and sensitivities are available. An appropriate de-escalation of antimicrobial therapy is suggested once culture results return.
Early detection of shock and prompt aggressive treatment of the underlying organ dysfunction is an essential component of improving outcome of critical ill patients. Deep soft tissue infections may present with a fulminant course and may be associated with great morbidity and high case-fatality rates, especially when they occur in conjunction with toxic shock syndrome. After initial debridement, and early antimicrobial therapy, patients require early intensive care for haemodynamic and metabolic support. Patients may loss fluids, proteins and electrolytes from a large surgical wound. In addition hypotension is caused by vasodilation induced by the systemic inflammatory response syndrome to infection. Fluid resuscitation and analgesia are the mainstays of support for patients with advanced sepsis usually combined with vasoactive amines associated with mechanic ventilation.
Sartelli M, Malangoni MA, May AK, Viale P, Kao LS, Catena F, et al. World Society of Emergency Surgery (WSES) guidelines for management of skin and soft tissue infections. World J Emerg Surg. 2014 Nov 18;9(1):57.
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