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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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Necrotizing soft-tissue infections

, M.D., , M.D, and , M.D.

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Necrotizing soft-tissue infections (NSTI) encompass a diverse disease process characterized by extensive, rapidly progressive soft tissue inflammation and necrosis. NSTIs are increasingly more common, and continue to be associated with a fulminant course and high mortality rates. These infections comprise a spectrum of diseases ranging from necrosis of the skin to life-threatening infections involving the fascia and muscle with systemic toxicity. They vary in predisposing and causative factors, anatomic location, offending bacteria, and tissue level of involvement.

The nomenclature of NSTI can be confusing with many terms used to describe the variable presentations. The original description of “hospital gangrene” was made by Joseph Jones in 1871 (1) following his experience during the U.S. Civil War. Additional terms used in the past included Fournier gangrene (2), acute hemolytic streptococcus gangrene (3), and gas gangrene (clostridial myonecrosis). The term “necrotizing fasciitis” was popularized by Wilson (4) in 1952, and remains in use today.

The terminology of NSTI is of secondary concern when surgeons are challenged by a patient with this aggressive illness. Primary emphasis must be focused on rapid recognition and appropriate aggressive treatment. A high index of suspicion leading to early diagnosis, aggressive surgical intervention and appropriate antimicrobial therapy is essential to reducing the mortality of NSTIs.

Presentation and diagnosis

The presentation of NSTI is highly variable and can range from early sepsis with obvious skin involvement to minimal cutaneous manifestations with a disproportionate (even alarming) underlying necrotizing fasciitis. The usual clinical presentation begins with localized pain and a deceptively benign appearance. Clinical “clues” which may assist in establishing an early diagnosis are: edema beyond the area of erythema, small skin vesicles, crepitus and the absence of lymphangitis (5). Additional local signs suggesting deep infection may include cyanosis or bronzing of the skin, induration, dermal thrombosis, epidermolysis or dermal gangrene. Classic signs of fever, diffuse crepitus, and shock are late signs. Once large blisters and gangrene develop, the infectious process is already at an advanced stage.

Early recognition is the sine qua non for the assessment of risk factors. Multiple risk factors increase the probability of a life-threatening infection. These co-morbid conditions include diabetes mellitus, peripheral vascular disease, malnutrition, malignancy, immunocompromised states (AIDS, steroid therapy), obesity, chronic alcohol or intravenous drug abuse (610). In the urban setting, intravenous and subcutaneous injection of illicit substances has become a more prevalent risk factor and should raise one's suspicion (8, 11). Our recent experience with NSTIs (1990–1995) revealed that 67% of patients were actively practicing parental drug use (8).

The etiologies for NSTI are not always obvious, and often the initiating event is surprisingly minor. The most common etiologies include postoperative wound complications, penetrating and blunt trauma, cutaneous infections, intravenous or subcutaneous illicit substance injection, peri-rectal abscesses, strangulated hernias, and idiopathic causes (7, 8, 10).

Establishing an early diagnosis depends on a high index of suspicion and a willingness to proceed with appropriate treatment. Plain x-rays may demonstrate subcutaneous air or a foreign body but are usually not necessary. Interest in the use of MRI scanning (12) and frozen section biopsy (13, 14) to aid in diagnosis has been reported. Early and aggressive surgical intervention should not be delayed by these ancillary studies. At exploration, the diagnosis can be confirmed by the presence of necrotic fascia, the absence of gross pus and easy finger dissection along the fascial planes.

Bacteriology

The bacteriology of NSTI is well recognized, and the infectious process is independent of specific bacteria (8, 11, 1517). Most NSTI are polymicrobial, involving organisms behaving synergistically. In our series of patients treated 78% of cases were polymicrobial, and 2.8 organisms were recovered per patient (8). Anaerobes, skin flora, and gram negative rods are commonly encountered (table I).

Table I. Bacteriologic findings in patients with necrotizing soft-tissue infections (from Bosshardt TL, Henderson VJ, Organ CH Jr (1996) Necrotizing soft-tissue infections. Arch Surg 131: 846–854).

Table I

Bacteriologic findings in patients with necrotizing soft-tissue infections (from Bosshardt TL, Henderson VJ, Organ CH Jr (1996) Necrotizing soft-tissue infections. Arch Surg 131: 846–854).

Monomicrobial infections are usually caused by hemolytic group A streptococcus, Staphylococcus aureus, or clostridial species. Group A streptococcal NSTI not uncommonly involve younger patients, the extremities, and are associated with a streptococcal toxic shock-like syndrome (18, 19). There has been a recent rise in cases of necrotizing fasciitis caused by group B streptococcus (20). Marine vibrio species have also been associated with NSTI (16).

The sharp increase in NSTI caused by parental drug abuse is at least in part attributable to Black Tar Heroin (8). This substance is manufactured in Mexico using crude processing methods, which result in low purity and a high water content. This may support bacterial growth and explain the high incidence of necrotizing fasciitis with subcutaneous black tar heroin use.

Treatment

The treatment of NSTI must be aggressive and rapid. All infections should be treated as potentially life-threatening emergencies. Previous studies (11, 21, 22) have documented the efficacy of a unified approach to successful treatment. The essential elements of treatment are resuscitation, antimicrobial therapy, surgical debridement, and supportive care. Aggressive resuscitative measures are required early with invasive monitoring to achieve fluid, electrolyte, and hemodynamic stability. Massive volumes of fluid are often required secondary to third spacing and sepsis.

Antimicrobial therapy consists of broad-spectrum antibiotics. Empiric coverage with high dose penicillin G, an aminoglycoside, and clindamycin or metronidazole is recommended (7, 8, 10). Single agent coverage with imipenem-cilastin is an alternative choice (14). Antibiotics can be adjusted once cultures are reported. The tetanus status of the patient must be addressed.

Surgical debridement is paramount, and must be performed early and aggressively. It should not be delayed if the patient is in septic shock. Debridement is best performed under general anesthesia and all necrotic tissue must be excised. Debridement is considered adequate when finger dissection no longer easily separates the subcutaneous tissue from the fascia. The deep muscle should be inspected. Parallel counter incisions may be made if indicated to exclude additional spread of infection (17). Amputation may be necessary for massive involvement of an extremity. The wound is packed open and kept moist with saline or 0.25% Dakin's solution. Patients should undergo re-exploration and debridement every 24 hours (or earlier if indicated) until progression of the necrosis has been halted.

Post-operatively, patients are monitored in the intensive care unit until deemed stable. Early nutritional support is initiated, and physical therapy can be started once sepsis has resolved. Coverage of the wound should be delayed until the infection has clinically resolved and healthy granulation tissue is present. Split-thickness skin grafts usually provide coverage, although more extensive wounds may require a flap procedure.

Controversy surrounds the routine use of hyperbaric oxygen (HBO) in treating NSTI (23). Supporters claim a decrease in mortality when infections involve anaerobic bacteria, specifically the clostridial species (10, 24, 25). However, no survival benefit has been demonstrated by a prospective, randomized trial for HBO in treating nonclostridial NSTI. Its use should not delay appropriate and adequate surgical debridement. For these reasons, HBO should be considered as an adjunctive therapy and in no way should diminish the importance of proper surgical management.

Mortality

Despite advances in intensive medical care, mortality rates for NSTI remain substantial (table II). Recent large series continue to demonstrate rates in excess of 20% (7, 8, 10). The number of risk factors present, extent of infection, delay in first debridement, and degree of organ system dysfunction at admission have been shown to be predictors of outcome (610, 21). Retrospective reviews (21, 22, 26) have clearly demonstrated that a delay in presentation, debridement, or both contribute to the high mortality rates. Time is a critical element in successful management of NSTI, and delays must be avoided.

Table II. Mortality rates of necrotizing soft-tissue infections.

Table II

Mortality rates of necrotizing soft-tissue infections.

Summary

Necrotizing soft-tissue infections have been recognized for many years and appear to be increasing as evidenced by recent published reports. NSTI continues to be associated with significant morbidity and mortality. Early recognition with prompt aggressive surgical therapy is essential for a successful outcome.

References

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Copyright © 2001, W. Zuckschwerdt Verlag GmbH.
Bookshelf ID: NBK6876

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