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The author acknowledges the use of substantial material from this chapter in the previous edition.
Infection of soft tissues can involve the skin, subcutaneous tissues, fascia, and skeletal muscle or a combination of these structures. The subcutaneous compartment is continuous over the entire body and consists of fat and loose connective tissue containing blood and lymphatic vessels underlying the dermis. The fascia is subdivided into superficial and deep components. The superficial fascia, between the dermis and the deep fascia, is further subdivided into two layers. The outer layer, which is closest to the dermis, has various thicknesses and contains loose collagenous tissue and fat. The inner layer of the superficial fascia is a thin membrane that has relatively little fat but is rich in elastic tissue. Superficial arteries, veins, nerves, and lymphatics lie within the superficial fascia. The deep fascia is a membranous sheet surrounding muscles and separating them into functioning units, and it forms the deepest boundary of the subcutaneous tissue compartment.
Infections of the skin and subcutaneous tissues can be classified by the depth of involvement, whether there is necrosis ( Box 73.1 ) and as primary, secondary, or tertiary, depending on the mechanism of infection. Primary infections originate directly in skin that grossly appears to be clinically normal, although minor breaks in the integrity of the barrier function may be required (see Chapter 68 ). Some infections, such as cellulitis, folliculitis, furunculosis, carbunculosis, and paronychia, evolve into abscesses and occasionally extend from the epidermis or dermis to involve deeper subcutaneous tissues.
Breast abscess
Carbuncle (see Chapter 68 )
Furuncle (see Chapter 68 )
Paronychia (see Chapter 68 )
Periporitis (i.e., sweat gland abscess)
Perirectal abscess
Cellulitis
Erysipelas
Secondarily infected ulcers: decubitus, diabetic
Folliculitis
Majocchi granuloma (variant of tinea corporis)
Anaerobic cellulitis
Clostridial
Nonclostridial
Bacterial synergistic gangrene
Meleney (post-surgical) ulcer
Gangrenous cellulitis
Necrotizing fasciitis
Type I: mixed flora (85% polymicrobial)
Type II: Streptococcus pyogenes and/or Staphylococcus aureus
Other monomicrobial infections
Fournier (perineal or external genital) gangrene
Noma (orofacial gangrene)
Tropical ulcer
Synergistic necrotizing cellulitis
Myositis (see Chapter 74 )
Pyomyositis (see Chapter 74 )
Secondary infections , which occur in previously diseased or wounded skin, include infection of cysts (e.g., epidermal inclusion, pilar cyst), ulcers (e.g., decubitus ulcer), wounds (e.g., surgical or traumatic wound; burns; scalp electrode sites; arthropod, animal, or human bites; burrows due to scabies, flies, or fleas), and those occurring in areas of dermatitis (e.g., atopic dermatitis, psoriasis). These infections also can spread contiguously to deeper subcutaneous tissue.
Tertiary infections develop when pathogens are spread hematogenously or through lymphatics to soft tissues from a distant focus (e.g., Clostridium septicum necrotizing fasciitis or myonecrosis, Staphylococcus aureus metastatic abscess). These infections can involve any of the deeper soft tissues, but they usually spare direct involvement of the epidermis. Compromise of blood flow within nutrient vessels or extension of an infectious and inflammatory nidus to the epidermis and dermis can result in cutaneous disease.
Many conditions predispose patients to subcutaneous tissue infections and abscesses ( Box 73.2 ). The infections also can be classified as nonpurulent (i.e., erysipelas, cellulitis, and necrotizing fasciitis) or purulent (i.e., furuncles, carbuncles, and abscesses).
Alteration of normal skin flora
Burn wound
Chronic dermatoses
Corticosteroid therapy
Foreign body
Immunodeficiency diseases
Chédiak-Higashi syndrome a
a Associated with abscess formation.
Chronic granulomatous disease a
Congenital neutropenia a
Cyclic neutropenia a
Griscelli syndrome
Hyperimmunoglobulin E and immunodeficiency syndrome a
Leukocyte adhesion deficiency a
Leukocyte alkaline phosphatase deficiency a
Neutrophil-specific granule deficiency a
Transient hypogammaglobulinemia of infancy a
Wiskott-Aldrich syndrome a
X-linked hypogammaglobulinemia a
Multiple innate immune defects
Intravenous drug abuse
Malnutrition
Peripheral vascular disease
Obstruction of drainage
Ischemia
Skin trauma
Surgical wound
Circumcision
Umbilical cord stump
Systemic disease
Cachexia
Cirrhosis
Diabetes mellitus
Neoplasia
Leukemia, lymphoma
Solid tumor
Organ transplantation
Renal tubular acidosis
Renal failure
This chapter describes infections that lead to abscess formation and tissue necrosis involving subcutaneous tissues as deep as the inner layer of the superficial fascia. Infections that commonly extend into the deep fascia and muscle are discussed elsewhere (see Chapter 74 ).
The cause of abscesses and subcutaneous infections in children is not always clear. Microbial etiology can vary both by predisposing host factors (e.g., primary or secondary immunodeficiency, various genetic conditions) and route of infection (e.g., hematogenous, superficial trauma allowing infection from skin flora, penetrating trauma inoculating environmental microbes). S. aureus, including both methicillin-susceptible and -resistant strains (MSSA and MRSA), is the most commonly isolated pathogen overall. Infection can be due to a single pathogen or polymicrobial.
Identification of the pathogens causing a particular subcutaneous soft tissue infection or, in some cases, exclusion of a variety of noninfectious conditions in the differential diagnosis of subcutaneous tissue infections ( Box 73.3 ), requires proper use of diagnostic tests and interpretation of results. If the surface of a wound or site of infection is sampled with a swab, several organisms can be isolated that are colonizing the area but may not be contributing to the disease process. If an organism is suggested by Gram stain (or special stains in the case of fungi) and identified by culture, the likelihood of its pathogenicity is increased. Chances of identifying the true pathogen are improved further if culture specimens are obtained by decontaminating the skin and performing an incision to express material or fine-needle aspiration, by swabbing the exudate from a site of suppuration, or by performing a punch or excisional biopsy.
Acne conglobata
Acne fulminans
Hidradenitis suppurativa
Jellyfish, scorpion, snake, and spider (e.g., brown recluse) bites
Factitial disease
Panniculitis
Polyarteritis nodosa
Purpura fulminans
Pyoderma gangrenosum
Sweet syndrome (i.e., acute febrile neutrophilic dermatosis)
Cultures should be obtained for routine and fastidious, aerobic and anaerobic organisms when appropriate. Sampling to identify fungi and viruses, including herpes simplex virus (HSV) and cytomegalovirus (CMV), particularly in immunocompromised patients, usually is appropriate. Susceptibility testing should be performed on isolated pathogens to guide antibiotic selection.
This chapter describes infections that lead to abscess formation and tissue necrosis involving subcutaneous tissues as deep as the inner layer of the superficial fascia. Infections that commonly extend into the deep fascia and muscle are discussed elsewhere (see Chapter 75 ).
An abscess is a localized, usually inflamed, walled-off collection of purulent exudate formed by a collection of white blood cells (WBCs), bacteria, and disintegration or necrosis of tissue. An abscess is recognized clinically as a firm, tender, erythematous nodule that is fluctuant. The initial skin lesion commonly can be mistaken for a spider bite.
A subcutaneous abscess most commonly evolves by local extension of a primary infectious process from the epidermis or dermis, such as a cutaneous abscess originating from a skin appendage such as a pilosebaceous unit (e.g., furuncle, carbuncle, infundibular cyst, periporitis ) or secondarily from a site of skin disease or injury. A subcutaneous abscess also can arise by direct traumatic implantation or invasion of pathogens into subcutaneous tissue or occasionally by hematogenous spread.
In the patient with an abscess, constitutional symptoms usually are absent initially, unless the process has extended into deeper tissues or the bloodstream or has originated from the bloodstream. Often, no predisposing factor can be identified, although several processes that disrupt the integrity of the barrier function of the skin or the integrity of local immunologic processes, particularly neutrophil function, are associated with abscess formation. Patients with hyperimmunoglobulin E syndrome and chronic granulomatous disease are prone to abscesses. Despite the extensive list of immunodeficiency diseases associated with abscess formation, most people with recurrent abscesses lack evidence of immunodeficiency.
The principal pathogens of subcutaneous abscesses in children are shown in Box 73.4 and vary by body site. The single most common pathogen is S. aureus . CA-MRSA strains, especially the USA 300 clone, became dominant worldwide in the early 2000s. In the later 2010s, MSSA isolates, including USA 300 strains without methicillin resistance, exceeded MRSA isolates among children with invasive S. aureus infections in the US. , Strain diversity appears to be rising with evidence of the declining prevalence of USA 300 (see also Chapter 115 , S. aureus ).
Staphylococcus aureus (i.e., CA-MRSA and CA-MSSA)
Streptococcus pyogenes, streptococci (e.g., α-hemolytic, nonhemolytic), group B Streptococcus
Aeromonas hydrophilia
Actinomyces
Bacteroides fragilis
Brucella
Clostridium
Eikenella corrodens
Enterococcus
Fusobacterium
Haemophilus parainfluenzae
Mycobacterium
Neisseria gonorrhoeae
Nocardia
Peptococcus
Peptostreptococcus
Porphyromonas
Prevotella
Propionibacterium acnes
Pseudomonas aeruginosa
P. mallei
P. pseudomallei
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