Cellulitis, Necrotizing Fasciitis, Subcutaneous Tissue Infections
Are you sure of the type of soft tissue infection you are dealing with? What should you expect to find?
Infections of the skin and soft tissues range from mild superficial processes that can be managed in outpatients to life-threatening infections requiring hospitalization, intensive care, and combined surgical and medical support.
Important considerations include:
History and epidemiologic factors (exposures to specific pathogens, mechanisms of injury)
Microbiologic factors (virulence and drug susceptibility of invasive pathogens)
Host factors (underlying immunosuppression, immunodeficiency, trauma, metabolic disorders, etc.)
The major syndromes of skin and soft tissue infection are generally approached from superficial to deep processes
Infections of the superficial dermis
Impetigo is a superficial skin infection that often begins as a vesicular process which evolves to form crusted and intermittently weeping lesions. Small vesicles typically develop on exposed areas, sometimes associated with a narrow halo of surrounding erythema. The vesicles become pustular in appearance, and readily drain seropurulent material which has a classic golden appearance. The involved areas may be pruritic, and scratching can exacerbate the process with spread to uninvolved areas. Fever and systemic symptoms are uncommon, although regional lymphadenopathy may be present.
Antibiotic therapy (by organism) for the treatment of invasive soft tissue infection
Bullous impetigo and staphylococcal scalded skin syndrome
Bullous impetigo occurs primarily in infants and children and is caused by S. aureus strains carrying bacteriophages which express exfoliative toxins. The toxins weaken the adherence of epithelial cells, leading to the formation of vesicles. The vesicles enlarge to form large flaccid bullae containing clear yellow fluid which contain staphylococci on Gram stain and culture. The surrounding skin typically lacks a significant inflammatory halo. Methicillin-sensitive strains of S. aureus respond to the conventional anti-staphylococcal agents noted above. MRSA infections generally respond to oral co-trimoxazole. Widespread disease may be treated with oral linezolid or parenteral vancomycin or linezolid (see below).
Staphylococcal scalded skin syndrome (SSSS) is a more generalized form of bullous impetigo, with widespread Bulla formation and subsequent exfoliation. As with bullous impetigo, this is usually seen in young children. Fever and generalized scarlatina form rash are early signs which progress to the formation of large flaccid bullae. These bullae readily open with minimal friction (Nikolsky sign), and lead to widespread denudation with erythematous, weeping dermis requiring management as a severe second degree burn injury. Unlike limited bullous impetigo, S. aureus is often not recovered from the widely denuded areas, but may be found at the site of an initial soft tissue injury. The major differential diagnostic consideration is toxic epidermal necrolysis, which is an often generalized skin injury process associated with a variety of triggers including drug reactions and rarely systemic infections such as Mycoplasma pneumoniae infection. Skin biopsy or recovery of sloughed bullae ("jelly roll preparation") distinguish between the intraepidermal cleavage seen with SSSS from the sub-epidermal separation seen with toxic epidermal necrolysis. Parenteral therapy is recommended for SSSS; initial vancomycin therapy to cover possible MRSA is appropriate for this severe illness, with transition to an antistaphylococcal penicillin or cephalosporin if MSSA is isolated.
Folliculitis is caused by bacterial or fungal infection within hair follicles and apocrine glands.
Deeper Dermal Infections
A furuncle or boil is a deeper localized inflammatory process that arises from a folliculitis lesion and extends into the adjoining subcutaneous tissue. Multiple furuncles may coalesce in the subcutaneous fat, creating multiple draining abscesses that are separated in part by bands of connective tissue. These deep, draining, intercommunicating lesions are recognized as carbuncles and are associated with S. aureus infection.
When patients develop recurrent furunculosis, efforts to reduce skin trauma and staphylococcal carriage and improve overall hygiene are appropriate. Daily chlorhexidine scrubs followed by a gradually reduced frequency and avoidance of autoinoculation through patient manipulation of lesions are important measures; assessment of staphylococcal nasal carriage and consideration of nasal mupirocin administration (twice daily for 5 days using mupirocin nasal ointment) for nasal carriers is appropriate. Combined topical and systemic antibiotic therapy using rifampin and doxycycline may be considered in occasional patients with ongoing recurrent disease.
Ecthyma is a localized ulcerating dermal infection that is generally associated with group A streptococcal infection.
Erysipelas is a distinctive rapidly spreading infection of the dermis (cellulitis) caused almost always associated with Group A streptococcal infection.
Infections primarily involving subcutaneous tissue
Cellulitis reflects deeper cutaneous infection than that seen with erysipelas, with involvement of the dermis as well as the deeper subcutaneous structures. As a result, the dermal erythema and edema may be less well-demarcated.
Additional risk factors for the development of cellulitis are similar to those leading to erysipelas. Lymphatic stasis due to primary lymphedema, congenital anomalies of the lower extremity, or surgery involving the lymphatics may increase the risk of cellulitis. A variety of surgical procedures have been particularly associated with cellulitis, including saphenous vein harvesting for coronary artery bypass grafting, mastectomy or lumpectomy and axillary dissection, pelvic procedures including radical pelvic surgery with pelvic and/or inguinal node dissection, pelvic irradiation, etc. Less invasive procedures such as liposuction, body piercing, and injection drug use may also increase the risk of post-procedure cellulitis.
Cellulitis syndromes with particular anatomic foci in normal hosts
Cellulitis syndromes associated with particular environmental exposures
There are several cellulitis syndromes associated with specific pathogens and/or body sites: (
Cellulitis syndromes in immunocompromised hosts
Gangrenous (necrotizing) cellulitis
Gangrenous cellulitis is a severe and rapidly progressive infection of the skin and subcutaneous soft tissue that results in necrosis of the overlying skin and subcutaneous tissues. Several processes, each with distinctive clinical features and microbiologic findings, may cause gangrenous cellulits: (
Gangrenous (necrotizing) cellulitis
Empiric antibiotic recommendations are listed below. High dose intravenous antibiotic regimens are utilized to cover streptococci (both hemolytic and microaerophilic/anerobic species), gram negative bacilli (particularly Enterobacteriaceae), and anerobic species including Clostridia and Bacteroides. In immunocompromised hosts, empiric coverage of Pseudomonas should be included as well. Use of vancomycin for possible staphylococcal infection and a beta lactam/beta lactmase inhibitor combination such as piperacillin/tazobactam or a penem agent such as imipenem or meropenem are appropriate initial therapies prior to Gram stain assessment. In the presence of hypotension and possible toxic shock, intravenous clindamycin should be added to suppress possible toxin production, and administration of high dose IVIG to bind circulating toxin may be considered. Reexploration at 24-48 hours for possible additional debridement of any residual necrotic tissue is important.
Necrotizing fasciitis, like gangrenous (necrotizing) cellulitis, is uncommon. It is characterized by infection extending to the superficial (and often to the deep) fascial layers, with a rapid and progressive course, marked toxicity, and the absolute need for surgical exploration as part of comprehensive management.
The infection progresses over the course of one or a few days, despite antibiotic therapy, with gradual skin discoloration from initial erythema to areas of frank necrosis. Bullae containing hemorrhagic fluid develop at the affected areas. In contrast to other deep infections, sensation in the involved areas is often lost due to local microvascular and nerve injury. The soft tissue edema may be quite dramatic, and when involving the extremities raises concern for a possible compartment syndrome with risk of secondary myonecrosis. Gas formation is often present in the presence of mixed infection containing anerobic or microaerophilic species, especially in diabetic patients. High fever and clinical toxicity are common.
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