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Necrotizing fasciitis

Necrotizing fasciitis is a serious but rare infection of the deeper layers of skin and subcutaneous tissues (fascia). Many types of bacteria can cause necrotizing fasciitis (eg. Group A streptococcus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis), of which Group A streptococcus is the most common cause. more...

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Necrotizing fasciitis: a diagnostic challenge
From American Family Physician, 7/1/97 by Daniel L. Meltzer

Necrotizing fasciitis is a deep infection of the subcutaneous tissues that results in progressive destruction of fat and fascia.[1] While group A streptococci are the most common causative organisms, many other bacteria can give rise to necrotizing fasciitis. Predominant aerobes include Staphylococcus aureus and Escherichia coli. Predominant anaerobes include Bacteroides fragilis, and Peptostreptococcus and Clostridium species.[2]

Invasion by group A streptococci causes the host to release cytokines, including interleukin-2, tumor necrosis factor and gamma-interferon.[3,4] These substances, in combination with the bacterial toxin, can cause vascular thrombosis and ischemic gangrene of the overlying skin.[5] The infection can advance rapidly, producing a highly lethal situation.

Illustrative Case

A 59-year-old woman was admitted to the hospital with a five-day history of swelling and redness in the right leg, accompanied by fever and chills. Before this leg problem developed, the patient had been in good health. She reported no history of trauma or injury to the leg. Her medical history was significant for a seizure disorder, which was well controlled with phenytoin and phenobarbital. She had no history of diabetes mellitus.

The physical examination revealed an obese woman in no acute distress. Her temperature was 37.9 [degrees] C (100.3 [degrees] F), her pulse rate was 95 per minute, and her respiratory rate was 18 per minute. The patient's blood pressure was 102/58 mm Hg.

Examination of the right lower leg revealed an edematous, erythematous area below the knee, extending over the anterior tibia and the medial malleolus. The affected area was approximately 10 cm x 9 cm in size. Violaceous bullae were noted over the medial malleolus and medial calf. Each bulla measured approximately 3 cm x 3 cm (Figure 1).


The patient's leg showed no evidence of trauma or abrasions, but she was noted to have tinea pedis. The leg was warm and exquisitely tender to palpation, with pitting edema. Dorsalis pedis and posterior tibial pulses were normal. No sensory deficits were detected, and the patient had full range of motion in the affected leg. The remainder of the physical examination was within normal limits.

The patient's white blood cell count was 19,500 per [mm.sup.3] (19.5 [10.sup.9] per L), with 91 percent (0.91) neutrophils and 8 percent (0.08) lymphocytes. The hemoglobin mass concentration was 12.6 g per dL (126 g per L), the hematocrit was 37.3 percent (0.37), and the platelet count was 160,000 per [mm.sup.3] (160 [10.sup.9] per L). Other laboratory values were as follows: sodium, 131 mEq per L (131 mmol per L); potassium, 3.6 mEq per L (3.6 mmol per L); chloride, 97 mEq per L (97 mmol per L); bicarbonate, 23 mEq per L (23 mmol per L); blood urea nitrogen, 23 mg per dL (8.0 mmol per L); creatinine, 1.1 mg per dL (100 [micro]mol per L); glucose, 120 mg per dL (6.7 mmol per L); calcium, 7.8 mg per dL (1.94 mmol per L); phosphorus, 1.9 mg per dL (0.60 mmol per L); albumin, 2.1 g per dL (21 g per L), and creatine kinase, 2,449 U per L.

A presumptive diagnosis of cellulitis was made. A surgeon was consulted, and the patient was started on intravenously administered cefazolin.

The next day, an infectious disease specialist was consulted because the patient was having more severe pain, the redness in her leg was spreading and more bullae were developing. The diagnosis of necrotizing fasciitis was made, and clindamycin was added to the patient's medications.

Debridement confined to the distal calf and the anterior foot was performed by a plastic surgeon. This procedure revealed generalized necrotic tissue with many layers of thrombosed blood vessels but no gross purulence (Figure 2). Gram staining revealed cocci in pairs, consistent with group A streptococci. The presence of group A streptococci was later verified by culture. Hyperbaric oxygen therapy was instituted, and the patient continued to receive intravenously administered cefazolin and clindamycin.


Over the next two days, the patient's temperature rose to 38.3 [degrees] C (101.0 [degrees] F), and her white blood cell count increased to 24,000 per [mm.sup.3] (24.0 x [10.sup.9] per L). In addition, increased induration and erythema were noted in the popliteal region of the affected leg.

On the fourth hospital day, the patient was taken back to the operating room for wider debridement of necrotic tissue over the ankle and foot. On debridement, deep necrotic tissue was observed along the fascial plane of the leg (Figure 3). Antibiotics and hyperbaric oxygen therapy were continued.


On the fifth hospital day, the patient's temperature was still 38.3 [degrees] C (101.0 [degrees] F), and her white blood cell count was 20,400 per [mm.sup.3] (20.4 x [10.sup.9] per L). Further migration of erythema and induration in the lateral calf up to the popliteal area was noted. The infectious process was thought to be progressing proximally, with increased erythema and blistering at the knee. Consequently, debridement at the fascial plane of almost all areas of proximally extending erythema was performed (Figure 4).


On the day following the third debridement, the patient's temperature was 37.7 [degrees] C (100 [degrees] F), and the white blood cell count was 17,500 per [mm.sup.3] (17.5 x [10.sup.9] per L). There was no further evidence of an ascending process or new blistering. The foot was still viable and was thought to be improving. Whirlpool treatments were begun to assist in cleansing the wound. Hyperbaric oxygen treatments and intravenous antibiotic therapy were continued.

Over the next week, the patient became afebrile, and her white blood cell count decreased to 8,900 per [mm.sup.3] (8.9 x [10.sup.9] per L). Hyperbaric oxygen therapy was continued, and zinc and vitamin C supplements were added to aid wound healing.

On hospital day 15, the patient underwent split-thickness skin grafting (Figure 5). A large amount of skin was taken from the right and left thigh and was grafted to cover the wound. After a five-day course of physical therapy, the patient was discharged.


Predisposing Factors

Predisposing factors for necrotizing fasciitis caused by infection with group A streptococci include any inciting injury that disrupts the integrity of the skin, including minor cuts, burns, injection-drug use, surgical procedures, insect bites and varicella infection. Noninvasive injuries such as blunt trauma may also be predisposing factors for the development of this infection.[6] Persons with diabetes and arterial insufficiency may be at increased risk for necrotizing fasciitis. Occasionally, as in the illustrative case, a specific inciting event may not be identified.

Clinical Manifestations

Distinguishing between cellulitis and necrotizing fasciitis can be difficult on the basis of the clinical findings alone. Evaluation by a multidisciplinary team that includes the primary care physician and various subspecialists is generally necessary.

The distinction between cellulitis and necrotizing fasciitis is crucial, since the treatment approach and prognosis for these conditions are dramatically different. Cellulitis is characterized by a red, hot, tender area of skin. The first clinical clue to streptococcal necrotizing fasciitis is diffuse swelling of an extremity, followed by the appearance of bullous lesions filled with a fluid that is initially clear but rapidly becomes violaceous.[6]

While bullae formation is significant when present, it is absent in up to 70 percent of necrotizing skin infections.[7] Patients with streptococcal necrotizing fasciitis may present with severe systemic toxicity and pain out of proportion to the degree of observed skin involvement. While the majority of infections affect the extremities, they may also occur in other parts of the body, such as the perirectal area.

Leakage into the perineal area results in a syndrome called Fournier's gangrene, a form of necrotizing fasciitis that affects the male genitals. This infection is characterized by edema of the scrotum and penis, with extension into the perineum, the abdominal wall and the legs. Fournier's gangrene is an example of so-called type I necrotizing fasciitis. An infection of this type is polymicrobic, with anaerobes most often predominant.


Various strategies have been used to make a definitive diagnosis of necrotizing fasciitis. Gram staining and blood culture are inexpensive initial methods that may suggest the diagnosis. Elevated serum creatine kinase levels indicate involvement of underlying muscle. Radiographs, although not particularly sensitive, may reveal gas in the soft tissues.

Computed tomography and magnetic resonance imaging (MRI) may be very useful in diagnosing necrotizing fasciitis. Scans obtained with either of these techniques show involvement of the fascia in advance of obvious symptoms or signs. Of the two techniques, MRI is more sensitive and does not require the administration of intravenous contrast agents.[7]

The most accurate diagnostic test for necrotizing fasciitis is surgical biopsy of the involved area. When the clinical picture is consistent with necrotizing fasciitis or the diagnosis is in doubt despite serious constitutional manifestations, surgical exploration is indicated. Surgery can establish a definitive diagnosis by providing specimens for gram staining, culture and histopathologic examination. Furthermore, direct observation of the nature and extent of the underlying process can help guide treatment.[1]

The mortality rate has been lower and fewer overall operations have been necessary in patients with suspected necrotizing soft tissue infections who underwent definitive surgical therapy within 24 hours of admission, compared with patients in whom surgery was delayed more than 24 hours.[7]


Depending on the situation, necrotizing fasciitis may be treated with simple drainage, surgical debridement or, in extreme cases, amputation.

Although not a substitute for surgery, antibiotics are an integral part of the treatment of necrotizing fasciitis. Penicillin, while traditionally extremely effective against group A streptococcal infections, may have reduced efficacy in necrotizing fasciitis.[8] Clindamycin (Cleocin), which has been proposed as the antibiotic of choice for this infection, may have increased efficacy[8] by inhibiting exotoxin production[9] and M-protein synthesis.[10] Some experts recommend combining high-dose penicillin with clindamycin.[11] Until culture results are available, broad-spectrum coverage might include a penicillin, an aminoglycoside or a third-generation cephalosporin, and either clindamycin or metronidazole (Flagyl).[5,12]

The beneficial effects of hyperbaric oxygen therapy in necrotizing fasciitis have been advocated by the Undersea and Hyperbaric Medical Society.[13] This therapy helps to reestablish a normal or elevated partial oxygen pressure, which may provide protection against infection, ischemia and a reduction in host defenses. Furthermore, hyperbaric oxygen therapy enhances the action of antibiotics by facilitating their transport across cell walls, and it also induces fibroblast proliferation, collagen synthesis and angiogenesis.

In one study,[14] the mortality rate was lower and fewer debridements were necessary in some patients with necrotizing fasciitis who received hyperbaric oxygen therapy in addition to surgical and antibiotic treatment, compared with patients who were treated with just surgery and antibiotics. However, a well-matched retrospective study[12] found that adjunctive hyperbaric oxygen did not significantly decrease mortality or morbidity rates in patients with necrotizing fasciitis. Thus, doubt exists concerning the overall usefulness of hyperbaric oxygen therapy in the management of necrotizing fasciitis.[12]

Final Comment

Despite the attention tie lay press has given to "flesh-eating bacteria," necrotizing fasciitis remains a relatively uncommon disease. Nonetheless, primary care physicians, who are often the first to encounter this problem, must be able to recognize the condition and involve appropriate specialists early. Doing so can mean the difference between life and death.

The authors thank Robert Pollack, M.D., for assisting in the surgical management of the patient presented in the illustrative case. The authors also thank Joseph Scherger, M.D., M.P.H., for his review of the manuscript.


[1.] Bisno AL, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med 1996;334:240-5.

[2.] Brook I, Frazier EH. Clinical and microbiological features of necrotizing fasciitis. J Clin Microbiol 1995;33:2382-7.

[3.] Hackett SP, Stevens DL. Streptococcal toxic shock syndrome: synthesis of tumor necrosis factor and interleukin-1 by monocytes stimulated with pyrogenic exotoxin A and streptolysin O. J Infect Dis 1992;165:879-85.

[4.] Hackett SP, Stevens DL. Superantigens associated with staphylococccal and streptococcal toxic shock syndrome are potent inducers of tumor necrosis factor-beta synthesis. J Infect Dis 1993;168:232-5.

[5.] Schwartz SN, Roman DL, Grosserode MH, Rowland MD. Streptococcal necrotizing fasciitis ("flesh-eating strep infection"). J Okla State Med Assoc 1995;88:472-4.

[6.] Stevens DL. Invasive group A streptococcus infections. Clin Infect Dis 1992;14:2-11.

[7.] Lille ST, Sato TT, Engrav LH, Foy H, Jurkovich GJ. Necrotizing soft tissue infections: obstacles in diagnosis. J Am Coll Surg 1996;182:7-11.

[8.] Stevens DL, Yan S, Bryant AK. Penicillin-binding protein expression at different growth stages determines penicillin efficacy in vitro and in vivo; an explanation for the inoculum effect. J Infect Dis 1993;167:1401-5.

[9]. Stevens DL, Maier KA, Mitten JE. Effect of antibiotics on toxin production and viability of Clostridium perfringens. Antimicrob Agents Chemother 1987;31:213-8.

[10.] Gemmell CG, Peterson PK, Schmeling D, Kim Y, Mathews J, Wannamaker L, et al. Potentiation of opsonization and phagocytosis of Streptococcus pyogenes following growth in the presence of clindamycin. J Clin Invest 1981;67:1249-56.

[11.] Sanford JP, Gilbert DN, Sande MA. Guide to antimicrobial therapy. 26th ed. Dallas: Antimicrobial Therapy, Inc., 1996.

[12.] Feingold DS, Weinberg AN. Group A streptococcal infections. An old adversary reemerging with new tricks? [Editorial] Arch Dermatol 1996;132:67-70.

[13.] Shupak A, Shoshani O, Goldenberg I, Barzilai A, Moskuna R, Bursztein S. Necrotizing fasciitis: an indication for hyperbaric oxygenation therapy? Surgery 1995;118:873-8

[14.] Riseman JA, Zamboni WA, Curtis A, Graham DR, Konrad HR, Ross DS. Hyperbaric oxygen therapy for necrotizing fasciitis reduces mortality and the need for debridements. Surgery 1990;108:847-50.

DANIEL L. MELTZER, M.D., M.P.H. currently is a resident in family practice at the University of California, San Diego, School of Medicine. Dr. Meltzer received his medical degree from Boston University Medical School. Previously he earned a master's degree in public health from San Diego State University.

MARTIN KABONGO, M.D., PH.D. is a faculty member in the Sharp Family Practice Residency Program in San Diego. Dr. Kabongo graduated from the Universidad Autonoma in Juarez, Chihuahua, Mexico, and completed a family practice residency at Bon Secours Hospital, Grosse Pointe, Mich. He also earned a doctoral degree in microbiology and dermatopathology at the University of Cincinnati/St. Thomas Institute.

Address correspondence to Martin Kabongo, M.D., Ph.D., Sharp Family Practice Residency Program, 5525 Grossmont Center Dr., Suite 200, La Mesa, CA 91942.

COPYRIGHT 1997 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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