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Holzheimer RG, Mannick JA, editors. Surgical Treatment: Evidence-Based and Problem-Oriented. Munich: Zuckschwerdt; 2001.

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Surgical Treatment: Evidence-Based and Problem-Oriented.

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Soft tissue infections

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Introduction

Soft tissue infections are classified by anatomic extent and pathophysiologic process. Thus, they may be focal or diffuse; the most severe have associated tissue necrosis; and when this is combined with systemic toxic effects the results are devastating. But most cases are easily diagnosed and treated. Awareness of the harbingers of necrotizing infection and knowledge of the complicating factors in toxic infections are essential to avoid loss of limb and life. Although most treatment has been empirical, strategies for diagnosis and treatment are emerging, that yield improved results (fig. 1).

Figure 1. Schema of approach to soft tissue infection.

Figure 1

Schema of approach to soft tissue infection.

Presentation and pathogenesis

Simple focal infections

These infections arise in the skin or in the adenexal skin structures, particularly the follicles. The commonest examples are impetigo contagiosa and folliculitis. Impetigo contagiosa is an infection of minor skin abrasions on the face or limbs of children caused by S. aureus or Strep. pyogenes. In folliculitis staphylococcal pyodermas of the hair follicles may extend to form furuncles or coalesce to form carbuncles.

Necrotizing focal infections

Focal necrotizing infections occur far less commonly. The best examples are Meleney's Progressive bacterial Synergistic Gangrene and Fournier's Idiopathic Scrotal Gangrene. Progressive synergistic gangrene (1) is characterized by three concentric zones of erythema, cyanosis, and necrosis at sites of synergistic infection of operative wounds or pressure sores by a microaerophilic nonhemolytic streptococcus and a hemolytic S. aureus or gram-negative bacillus. Idiopathic scrotal gangrene as described by Fournier (2) is caused by anaerobic streptococci and differs from the perineal form of Gram-negative bacterial synergistic gangrene commonly given this name today. The onset is dramatic and progression to gangrene of the scrotum occurs within 24 hours.

Toxic non-necrotizing focal infections

These infections occur still less often and include the Staphylococcal scalded skin syndrome (SSSS) and toxic shock syndrome (TSS). SSSS occurs most frequently in young children and sometimes in neonates (pemphigus neonatorum). It presents as a diffuse rash that follows a staphylococcal infection, and progresses to generalized bullae that break and slough. An exfoliative toxin has been identified that splits the epidermis so that the bullae develop. In TSS fever and a generalized macular rash develops in a patient with vaginitis associated with menstruation and the use of superabsorbent tampons. Enterotoxin F produced by group I phage strains of S. aureus is responsible for this constellation of symptoms and for the multiple organ failure that commonly ensues.

Diffuse non-necrotizing infection: cellulitis

Cellulitis is a diffuse infection of the skin and subcutaneous tissues characterized by local spreading erythema, warmth, tenderness and swelling. Most infections are mild and are caused by S. aureus or group A streptococci (3). Systemic signs such as fever, chills, and leucocytosis indicate severe cellulitis that usually requires intravenous antibiotic therapy. Patients should be investigated for underlying diseases including diabetes mellitus and peripheral arterial occlusive disease that worsen the prognosis.

Infections at some sites are regarded as high risk cellulitis because they are prone to serious complications. These include facial and orbital cellulitis (4), post adenectomy and postvenectomy cellulitis of the extremities, and infected animal and human bites of the hands. Facial cellulitis that originates in the teeth or gums is odontogenic. It occurs typically in the lower face of older children. Most facial cellulitis is non-odontogenic and occurs in the upper face of infants and younger children. Typical examples are erysipelas and Haemophilus influenzae type B (HIB) cellulitis. The peau d'orange cellulitis of erysipelas follows streptococcal upper respiratory infection that invades the dermis and lymphatics of the cheek. Similar infection by Haemophilus influenzae type B results in the characteristic “bruised cheek” appearance of HIB cellulitis now uncommon with the use of H. influenzee vaccine (5).

Postadenectomy and postvenectomy cellulitis are caused by lymphedema that is secondarily infected by non-group A streptococci. High risk hand infections include erysipeloid and infected human and animal bites. Erysipeloid is diagnosed when a spreading violaceous wound appears at the site of a minor wound on the hand of a worker handling fish, meat, or poultry. The infection is caused by the gram positive bacillus Erysipelothrix rhusiopathae. Animal and human bites are dangerous when secondary infection occurs and tenosynovitis develops in deep tendons. Pasteurella multocida in cat bites, and Eikenella corrodens in human bites are common pathogens. Delay in seeking treatment and anaerobic conditions in deep hand infections favor tissue necrosis and rapid progression (6).

The spread of infection in cellulitis is associated with toxins and enzymes produced by the offending organisms. Further, a disparity has been noted between the low frequency of positive culture of deep aspirates of these wounds and the marked inflammation observed. This has recently been attributed to cytokines such as interleukin-1 and tumor necrosis factor produced by specific dendritic cells of Langerhans in the stratum spinosum of the skin when they are exposed to bacterial components. The inflammatory response may therefore persist even when the bacteria have been killed by antibiotics.

Diffuse necrotizing cellulitis

These conditions are described fully in the chapter that follows. In general, they include necrotizing infections in which inflammatory cells are absent or sparse on biopsy, particularly clostridial myonecrosis, and those conditions in which inflammatory cells are abundant on histologic examination or Gram's stain of deep aspirates. Meleney's streptococcal gangrene, clostridial cellulitis, necrotizing fasciitis as described by Wilson and gram-negative bacterial synergistic necrotizing cellulitis are all encompassed by the latter group. A high index of suspicion is essential for early recognition and treatment of diffuse necrotizing cellulitis. Key markers of the disease include subcutaneous edema out of proportion to erythema progressing to skin vesicles and later skin anesthesia, discoloration, and patchy necrosis, and gas in the subcutaneous tissues identified on plain radiographs or as clinical crepitus. Necrotizing soft tissue infections owe their rapid progression to impaired host resistance, anaerobic conditions and bacterial synergy in the wound, and to lytic enzymes and toxins produced by the organisms involved. In the recently described variant, streptococcal necrotizing fasciitis with toxic shock syndrome (STSS), the explosive nature of the “flesh-eating disease” is related to pyrogenic exotoxins produced by group A streptococci that stimulate mononuclear cells and lymphocytes to produce cytokines that cause fever, shock and tissue injury. They also act as superantigens that interact with T-lymphocytes by methods that are more rapid and universal than those employed by conventional antigens, so that massive activation occurs and the damaging cytokines are poured out in abundance to exert their dramatic effect.

Diagnosis

A systematic approach to diagnosis that includes, needle aspiration, blood sampling for risk assessment, aerobic and anaerobic culture and diagnostic imaging is employed except in the simplest and most obvious cases.

Needle aspiration

Needle aspiration for sampling of tissue fluid or collections is preferable to superficial culture (7). It supplies the best information for improving on empirical therapy with semisynthetic penicillins.

Blood sampling

Blood sampling aids in assessment of the risk of the infection to the patient, and is an important reminder of the importance on outcome of conditions affecting the immune state of the patient . Diabetes, severe malnutrition and organ failure are all important.

Culture

Culture of the tissue aspirate is positive for organisms in only 20 to 30% of patients, but allows revision of antibiotic therapy in difficult cases. Blood culture was formerly done routinely, but is seldom positive, and should only be obtained by specific indication (8).

Diagnostic imaging

Plain roentgenographs of the affected site should be obtained except in mild disease. They may provide the only evidence of gas in the tissues, complicating deep infection such as osteomyelitis, or of a retained foreign body. Isotope imaging performed with technetium (99mTc) pyrophosphate detects areas of increased blood flow or newbone formation. Gallium citrate and indium chloride indicate sequestered polymorphonuclears cells and macrophages in areas of inflammation. By combining the two or using phased 99mTc pyrophosphate scans one may distinguish between soft tissue and bome inflammation. But the best method of identifying osteomyelitis complicating soft tissue infection of the extremities is by use of magnetic resonance imaging (MRI) with gadolinium contrast (9). MRI with also differentiates necrotizing from non-necrotizing soft tissue infection by failure of the necrotic fascia to enhance with gadolinium.

Treatment

Strategies for optimal treatment follow naturally from the schema suggested in figure 1. Simple focal lesions are readily treated with oral or topical antibiotics, such as mupirocin 2% ointment applied three times per day, and cloxacillin 250 or 500 mg every 6 hours for 7 days, local cleansing of the wounds, and attention to hygiene. On the other hand, focal necrotizing disease and focal lesions with toxic symptoms require intravenous fluid resuscitation and combined antibiotics such as amoxycillin 1 to 2 g every six hours and gentamicin 1.5 mg/kg every 8 hours or monotherapy such as ticarcillin disodium/clavulanate potassium 3 × 1 g every six hours. In TSS the culprit vaginal tampon must be removed, and wide debridement is best in progressive synergistic gangrene and idiopathic scrotal gangrene. Among the diffuse infections, mild cellulitis responds well to oral antibiotics and local care; but severe and high risk cellulitis require intravenous antibiotics. Current strategies using long acting intravenous antibiotics such as ceftriaxone and antibiotics e.g. quinolones that are equally effective by oral or intravenous route allow rapid conversion to out-patient intravenous or oral antibiotics (10, 11). Certain types of high risk cellulitis require specific antibiotics - cefuroxime for HIB cellulitis, cloxacillin (not erythromycin) for human bites, and amoxicillin-clavulanic acid for dog and cat bites. The diffuse necrotizing infections also demand aggressive surgical debridement. The antibiotics and need for further debridement should both be reviewed after 36 to 48 hours. In STSS intravenous clindamycin has also been recommended to slow the M protein synthesis essential for exotoxin production; and human immunoglobulin 2 g with or without subsequent booster doses is given to neutralize existing exotoxin.

References

1.
Meleney F L. Bacterial synergism in disease processses with confirmation of the synergistic bacterial etiology of a certain type of progressive gangrene of the abdominal wall. Ann Surg. (1931);94:961–981. [PMC free article: PMC1391509] [PubMed: 17866704]
2.
Fournier J A. : Etude clinique de la gangréne foudroyante de la verge. Sem Médicale. (1884);4:69–70.
3.
Hook E W, Hooton T M, Horton C A, Coyle M B, Ramsey P G, Turck M. Microbiologic evaluation of cutaneous cellulitis in adults. Arch Intern Med. (1986);146:295–297. [PubMed: 3947189]
4.
Uzcz∨tegui N, Warman R, Smith A, Howard CW (1998) Clinical Practice Guidelines for the management of Orbital Cellulitis J Pediatr Opthalmol Strabismus 35: 73–79 . [PubMed: 9559505]
5.
Unkel J H, McKibben D H, Fenton S J, Nazif M M, Moursi A, Schuit K. Comparison of odontogenic and nonodontogenic facial cellulitis in a pediatric hospital population. Pediatric Dentistry. (1997);19:476–479. [PubMed: 9442541]
6.
Bunzli W F, Wright D H, Dahms R D, Hass W F, Rotschafer J C. Current management of human bites. Pharmacotherapy. (1998);18:227–234. [PubMed: 9545141]
7.
Lebre C, Girard-Pipau F, Roujeau J C, Revuz J, Saiag P, Chosidow O. Value of fine-needle aspiration in infectious cellulitis. Arch Dermatol. (1996);132:842–843. [PubMed: 8678588]
8.
Sadow K B, Chamberlain J M. ]: Blood cultures in the evaluation of children with cellulitis. Pediatrics. 1998;101:E4. [PubMed: 9481023]
9.
Croll S D, Nicholas G G, Osborne M A, Wasser T E, Jones S. : Role of magnetic resonance imaging in the diagnosis of osteomyelitis in diabetic foot infections. J Vasc Surg. (1996);24:266–270. [PubMed: 8752038]
10.
Tice A D, Poretz D, Cook F, Zinner D, Strauss M J. : Medicare coverage of outpatient ambulatory: a program that pays for itself. Clin Infect Dis. (1998);27:1415–1421. [PubMed: 9868653]
11.
Lipsky B A, Baker P D, Landon G C. Antibiotic therapy for diabetic foot infections: Comparison of two parenteral-to-oral regimens. Clin Infect Dis. (1997);24:643–648. [PubMed: 9145738]
Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6971

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