Necrotizing Fasciitis 

Author: Michael Maynor, MD, Clinical Assistant Professor, Department of Hyperbaric/Emergency Medicine, Louisiana State University School of Medicine


For more than a century, many authors have described soft tissue infections. Their occurrence has been on the rise because of an increase in immunocompromised patients with diabetes mellitus, cancer, alcoholism, vascular insufficiencies, organ transplants, HIV, or neutropenia.
Necrotizing fasciitis can occur after trauma or around foreign bodies in surgical wounds, or it can be idiopathic, as in scrotal or penile necrotizing fasciitis. Necrotizing fasciitis also has been referred to as hemolytic streptococcal gangrene, Meleney ulcer, acute dermal gangrene, hospital gangrene, suppurative fascitis, and synergistic necrotizing cellulitis. Fournier gangrene is a form of necrotizing fasciitis that is localized to the scrotum and perineal area.


Necrotizing fasciitis is a progressive, rapidly spreading, inflammatory infection located in the deep fascia, with secondary necrosis of the subcutaneous tissues. Because of the presence of gas-forming organisms, subcutaneous air is classically described in necrotizing fasciitis. This may be seen only on x-ray or not at all. The speed of spread is directly proportional to the thickness of the subcutaneous layer. It moves along the deep fascial plane.


These infections can be difficult to recognize in their early stages, but they rapidly progress. They require aggressive treatment to combat the associated high morbidity and mortality. The causative bacteria may be aerobic, anaerobic, or mixed flora, and the expected clinical course varies from patient to patient.


The majority of necrotizing soft tissue infections have anaerobic bacteria present, usually in combination with aerobic gram-negative organisms. They proliferate in an environment of local tissue hypoxia in those patients with trauma, recent surgery, or medical compromise.
Facultative aerobic organisms grow since polymorphonuclear (PMN) leukocytes exhibit decreased function under hypoxic wound conditions. This growth further lowers the oxidation/reduction potential, enabling more anaerobic proliferation and, thus, accelerating the disease process.


Carbon dioxide and water are the end products of aerobic metabolism. Hydrogen, nitrogen, hydrogen sulfide, and methane are produced from the combination of aerobic and anaerobic bacteria in a soft tissue infection. These gases, except carbon dioxide, accumulate in tissues because of reduced water solubility.


In necrotizing fasciitis, group A hemolytic streptococci and Staphylococcus aureus, alone or in synergism, are frequently the initiating infecting bacteria. However, other aerobic and anaerobic pathogens may be present, including Bacteroides, Clostridium, Peptostreptococcus, Enterobacteriaceae, coliforms, Proteus, Pseudomonas, and Klebsiella. Bacteroides fragilis usually is noted as part of a mixed flora, in combination with Escherichia coli. It does not directly cause these infections, but it does play a part in reducing interferon production and the phagocytic capacity of macrophages and PMNs.


A variant synergistic necrotizing cellulitis is considered to be a form of necrotizing fasciitis, but some authorities feel that it is actually a nonclostridial myonecrosis. It begins in the same manner as necrotizing fasciitis, but it progresses rapidly to involve wide areas of deeper tissue and muscle at an earlier stage than might be expected. Severe systemic toxicity occurs.  Anaerobic streptococci, occasionally seen in drug addicts, cause many forms of nonclostridial myonecrosis. Some cases of necrotizing fasciitis can be caused by Vibrio vulnificus. This organism is seen more often in patients with chronic liver dysfunction, and it often follows the consumption of raw seafood. It may cause subcutaneous bleeding


The overall morbidity and mortality is 70-80%.

  • Fournier gangrene has a reported mortality as high as 75%.

  • The mean age of survivors is 35 years.

  • The mean age of nonsurvivors is 49 years.

History:

  • There often will be a history of trauma or a recent surgery to the involved area. Idiopathic cases are not uncommon.

  • Typically, there is a sudden onset of pain and swelling at the site of trauma or recent surgery. In some cases, the symptoms may begin at a site distant from the initial traumatic insult.

  • Over the next several hours to days, the local pain progresses to anesthesia.

  • Fournier gangrene begins with pain and itching of the scrotal skin.

  • A history of comorbid factors, including diabetes mellitus, should be sought in all cases of suspected necrotizing fasciitis.

Physical:

  • The patient usually appears moderately to severely toxic, but early on, the patient may look deceptively well.

  • Typically, the infection begins with an area of erythema that quickly spreads over a course of hours to days.

  • The redness quickly spreads, and the margins of infection move out into normal skin without being raised or sharply demarcated.

  • As it progresses, the infection gives way to dusky or purplish skin discoloration near the site of insult.

o Multiple identical patches develop to produce a large area of gangrenous skin, as the erythema continues to spread.
o The initial necrosis appears as a massive undermining of the skin and subcutaneous layer.
o If the skin is open, gloved fingers can pass easily between the 2 layers and may reveal yellowish-green necrotic fascia. If the skin is unbroken, a scalpel incision will reveal it.
o The normal skin and subcutaneous tissue are loosened from the rapidly spreading deeper necrotic fascia that is a great distance from the initiating wound.
o Fascial necrosis is typically more advanced than the appearance suggests.

  • Anesthesia in the involved region may be detected, and it usually is caused by thrombosis of the subcutaneous blood vessels, leading to necrosis of nerve fibers.

  • Without treatment, secondary involvement of deeper muscle layers may occur, resulting in myositis or myonecrosis. Normally, however, the muscular layer remains healthy red with normal bleeding muscle under the yellowish-green fascia.

  • Usually, the most important signs are tissue necrosis, putrid discharge, bullae, severe pain, gas production, rapid burrowing through fascial planes, and lack of classical tissue inflammatory signs.

  • There is usually some degree of intravascular volume loss detectable on clinical exam.

  • There may be general signs, such as fever and severe systemic reactions.

  • Fournier gangrene begins with local tenderness, edema, and erythema of the scrotal skin.

o This progresses to necrosis of the scrotal fascia. The scrotum enlarges to several times its normal diameter.
o There can be local crepitation in more than one half of patients.
o If the process continues beyond the penile-scrotal region to the abdomen or the upper legs, the normal picture of necrotizing fasciitis can be seen.
o In males, the scrotal subcutaneous layer is so thin that most of the patients present after the skin is already exhibiting signs of necrosis.
o In 2-7 days, the skin becomes necrotic, and a characteristic black spot can be seen.
o Early on, this infection may resemble acute orchitis, epididymitis, torsion, or even a strangulated hernia.
o In women, Fournier gangrene acts more like necrotizing fasciitis because of the thicker subcutaneous layers involving the labia majora and the perineum

Causes:

  • Surgical procedures may cause local tissue injury and bacterial invasion, resulting in necrotizing fasciitis. These procedures include surgery for intraperitoneal infections and drainage of ischiorectal and perianal abscesses.

  • IM injections and IV infusions may lead to necrotizing fasciitis.

  • Minor insect bites may set the stage for necrotizing infections. Streptococci can be introduced into the wounds, but the bacteriologic pattern changes from hypoxia-induced proliferation of anaerobes.

  • Local ischemia and hypoxia can occur in patients with systemic illnesses (eg, diabetes).

o Host defenses can be compromised by underlying systemic diseases favoring the development of these infections. Illnesses such as diabetes or cancer have been described in over 90% of cases of progressive bacterial gangrene.
o The number of diabetic patients has been reported to be 20-40%. As many as 80% of Fournier gangrene cases occur in diabetics.

  • As many as 35% of patients were alcoholics in some series.

  • Recent studies have shown a possible relationship between the use of nonsteroidal anti-inflammatory agents (NSAIDs), such as ibuprofen, and the development of necrotizing fasciitis during varicella infections. Additional studies are needed to establish whether ibuprofen use has a causal role in the development of necrotizing fasciitis and its complications during varicella infections. This has not previously been described

Lab Studies:

  • CBC with differential

  • Electrolytes, glucose, BUN, and creatinine

  • Blood and tissue cultures

  • Urinalysis

  • Arterial blood gas

Imaging Studies:

  •  Local radiographs can reveal the presence of gas in subcutaneous fascial planes.

o The presence of subcutaneous gas in a radiograph does not necessarily indicate a clostridial infection, as Escherichia coli, Peptostreptococcus species, and Bacteroides species may produce gas under appropriate conditions.
o Misleading subcutaneous gas also can result from the undermining of tissue planes during surgical debridement.
o Perforations of the esophagus, the respiratory tract, and the GI tract related to endoscopy or chest tube insertion can result in the radiographic appearance of gas.

  • CT scanning can pinpoint the anatomic site of involvement by demonstrating necrosis with asymmetric fascial thickening and the presence of gas in the tissues.

  • Magnetic resonance imaging and computerized tomography have been utilized recently in the diagnosis of necrotizing fasciitis. Absence of gadolinium contrast enhancement in T1 images reliably detects fascial necrosis in those requiring operative debridement. Combined with clinical assessment, MRI can determine the presence of necrosis and the need for surgical debridement.

Other Tests:

  • The Gram stain usually shows a polymicrobial flora with aerobic gram-negative rods and positive cocci.

Procedures:

  • Biopsy

o Tissue biopsies are the best method to use when diagnosing necrotizing fasciitis. They can be performed from the spreading periphery of the necrotizing infection or the deeper tissues, reached only in surgical debridement, to obtain proper cultures for microorganisms.
o Avoid doing this procedure from the actual necrosis or granulating center, as many bacteria that neither cause nor add to the infection would be detected.

Emergency Department Care:

  • Aggressively treat the patient with suspected necrotizing fasciitis to reduce morbidity and mortality.

  • Perform endotracheal intubation in patients who are unable to maintain their airway.

  • Provide supplemental oxygen.

  • Obtain IV access. Be careful to not use an infected extremity.

  • Place patient on continuous cardiac monitoring.

  • Begin fluid resuscitation with normal saline or lactated Ringer solution.

  • In patients with suspected hypovolemia, Foley catheterization may be needed to monitor urine output. This procedure probably should be avoided in patients with Fournier gangrene.

  • Begin antibiotics as soon as possible.

Consultations:

  • Obtain early surgical consultation for aggressive debridement.

  • Consider surgical subspecialty consultation for necrotizing fasciitis involving specific anatomic areas, as needed.

  • Obtain urological consultation in cases of Fournier gangrene.

  • Consult with a hyperbaric specialist.

  • Infectious disease consult may be useful to guide initial empiric antibiotic therapy.

     

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