Soft Tissue Infection
David Morris
Babak Sarani
I. Introduction
Soft tissue infections are common, with most responding to antibiotic therapy. Some infections cause systemic symptoms and require inpatient treatment or surgical debridement. This chapter describes the basic anatomic structure of the soft tissue, common etiologies of soft tissue infections, and principles of treatment. Special attention will be paid to necrotizing soft tissue infections (NSTIs), as these infections are increasing in incidence, difficult to diagnose, treat, and require urgent surgical exploration and debridement.
II. Anatomy
Each of the anatomical layers of the body wall can be infected from the superficial epidermis to the deep muscle and can behave in a very distinct fashion. In some cases, multiple layers are infected; the more layers and when deeper layer are involved generally denotes more serious illness with systemic manifestations. Although these infections are generally referred to as “soft tissue infections,” a patient may have an infection of the skin (erysipelas, cellulitis), subcutaneous tissue (necrotizing cellulitis or adipositis), fascia (necrotizing fasciitis), or the muscle (necrotizing myositis) or multiple layers. The skin is made up of the epidermis and dermis; beneath are other tissues that are not skin but part of the soft tissue.
Epidermis. The epidermis is the most superficial skin layer of stratified squamous epithelium cells arising from the deeper basal lamina. The cells are gradually filled with keratin as they are pushed upward. The keratinized cell layer performs a barrier function, limiting water loss, preventing entry of microbes, and regulating temperature.
Dermis. The dermis is located deep to the epidermis and is attached to it via hemidesmosomes. The dermis houses blood vessels, which nourish the epidermis via the basal cell layer. It also contains the sensory nerves and skin appendages: Sweat glands and hair follicles. In addition, the dermis provides tensile strength to the skin with type I collagen comprising the major structural protein responsible for tensile strength.
Subcutaneous tissue. Deep to the dermis is the subcutaneous tissue. This tissue varies in thickness and cellular composition in different areas of the body and generally consists of adipocytes, fibroblasts, macrophages, blood and lymph vessels, fibrous anchoring bands, nerves, and occasional skeletal muscle (e.g., platysma), glandular tissue (salivary glands, breast tissue), and bursae. The subcutaneous tissue provides cushioning for the deeper tissues and acts as insulation to help regulate internal body temperature.
Investing fascia. Deep to the subcutaneous tissue is a layer of investing fascia that covers the skeletal muscle. This fibrous layer surrounds muscles, nerves, and vascular structures. It consists of collagen fibers that provide tensile strength.
Muscle. The skeletal muscle is invested by the fascia and is connected to the bony skeleton. It is generally well vascularized and is largely resistant to infection, except in circumstances described below.
Table 54-1 Organisms Isolated in Type I (Polymicrobial) Necrotizing Soft Tissue Infections
Organism
Percent of isolates n = (162) (Anaya and Dellinger, 2007)
Percent of isolates n = (272) (Anaya et al., 2005)
Streptococcus
19
17
S. aureus
16
22
Klebsiella
10
E. coli
7
Gram Negatives
18
Anaerobes
7
18
Clostridia sp.
Rare
Rare
III. Risk Factors
Any patient may develop a soft tissue infection, with or without skin disruption. Cellulitis is a frequent complication of even minor wounds encountered. Patients at risk for NSTI generally are immunocompromised from a variety of causes that include diabetes mellitus, malignancy, HIV, and use of immunosuppressive
medications such as corticosteroids, infliximab, antitumor chemotherapy, or anti-rejection drugs. Patients with chronic skin conditions such as psoriasis may also be predisposed to these infections due to the breakdown of the barrier function of the epidermis. In addition, other factors that contribute to local tissue ischemia, such as peripheral vascular disease and cigarette smoking, may increase the risk of NSTI. Recent reports describe otherwise healthy young patients with none of the above risk factors developing an aggressive NSTI, often caused by methicillin-resistant Staphylococcus aureus (MRSA). The microbiologic factors contributing to these infections will be discussed.
medications such as corticosteroids, infliximab, antitumor chemotherapy, or anti-rejection drugs. Patients with chronic skin conditions such as psoriasis may also be predisposed to these infections due to the breakdown of the barrier function of the epidermis. In addition, other factors that contribute to local tissue ischemia, such as peripheral vascular disease and cigarette smoking, may increase the risk of NSTI. Recent reports describe otherwise healthy young patients with none of the above risk factors developing an aggressive NSTI, often caused by methicillin-resistant Staphylococcus aureus (MRSA). The microbiologic factors contributing to these infections will be discussed.
IV. Necrotizing Soft Tissue Infections (NSTI)
NSTIs are known by many names, including necrotizing fasciitis, gas gangrene, Fournier’s gangrene, Meleney’s ulcer, and in the popular media as “flesh-eating bacterial infections.” They are rapidly progressing and may result in significant tissue loss or death, if not treated aggressively.
Types. Several different classification systems have been developed in an attempt to uniformly describe NSTIs consistently from. One widely used schema is based on the microbiology of the infection.
Type I infections are the most common, comprising 55% to 75% of all NSTIs, and are polymicrobial in nature. Tissue isolates demonstrate an average of four organisms in most wounds. The most commonly isolated bacteria are gram-positive cocci, gram-negative rods, and anaerobes (Table 54-1). These infections tend to occur in immunocompromised (including diabetic) and obese patients.
Type II infections are monomicrobial in nature. Classically, the causative organism was group A Streptococcus (GAS) but MRSA is becoming more prevalent. These infections tend to occur in relatively young and healthy patients, although they can also cluster in intravenous drug users.
Pathophysiology. Microbial invasion of the subcutaneous tissues from an external source most often occurs after trauma; the most common internal source is direct spread from a perforated colon, rectum, anus, or urogenital organ. One less common route of entry is in-dwelling vascular or enteral catheters. The inciting event may be unknown in as many as 50% of cases.
The bacteria then proliferate in the subcutaneous tissues, producing endo- and exotoxins that cause tissue ischemia and liquefactive necrosis. As the innate immune cascade develops, systemic illness can occur. The infection may spread rapidly – as fast as 1 in./h with little overlying skin change.
The seriousness of a given infectious process depends heavily on the presence or absence of endo- and exotoxins elaborated by the microbes involved. Clostridia species produce α-toxin, which leads to extensive tissue necrosis locally and hypotension and shock systemically. S. aureus and Streptococci produce a wide variety of virulence factors including the surface proteins M-1 and M-3, exotoxins A, B, C, streptolysin O, and superantigen. M-1 and M-3 allow the microbe to escape phagocytosis. Exotoxins A and B cause a loss of endothelial integrity with tissue
edema and increased oxygen diffusion distance. CD4 cells and macrophages are stimulated by these toxins to produce tumor necrosis factor-α, interleukin-1, and interleukin-6, which may lead to systemic inflammatory response syndrome (SIRS), sepsis, septic shock, multiorgan system dysfunction, or death. S. aureus strains can produce Panton–Valentine leukocidin (PVL) which is a pore-forming exotoxin that results in destruction of leukocytes. PVL has been identified in the majority of community-acquired methicillin-resistant strains of S. aureus and leads to necrotizing skin infections. The various bacteria also produce superantigens which lead to complement activation and stimulation of the bradykinin–kallikrein system and coagulation cascade. The end result is local tissue ischemia, which creates a favorable environment for further bacterial proliferation and spread. The lack of perfusion therefore prevents effective delivery of antibiotics, making surgical debridement absolutely necessary to eradicate the infection.Related posts:
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