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      Drugs & Diseases > Plastic Surgery

      Necrotizing Fasciitis Clinical Presentation

      Updated: Oct 12, 2022
      • Author: Steven A Schulz, MD; Chief Editor: Michael Stuart Bronze, MD  more...
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      Presentation

      History

      Diagnosis of necrotizing fasciitis can be difficult and requires a high degree of suspicion. In many cases of necrotizing fasciitis, antecedent trauma or surgery can be identified. Surprisingly, the initial lesion is often trivial, such as an insect bite, minor abrasion, boil, or injection site. Idiopathic cases are not uncommon, however.

      Olafsson et al indicate that the hallmark symptom of necrotizing fasciitis is intense pain and tenderness over the involved skin and underlying muscle. [59] The intensity of the pain often causes suspicion of a torn or ruptured muscle. This severe pain is frequently present before the patient develops fever, malaise, and myalgias.

      In some cases, the symptoms may begin at a site distant from the initial traumatic insult. Pain may be out of proportion to physical findings. Over the next several hours to days, the local pain progresses to anesthesia.

      Other indicative findings include edema extending beyond the area of erythema, skin vesicles, and crepitus. McHenry et al and others have noted that the subcutaneous tissue demonstrates a wooden, hardened feel in cases of necrotizing fasciitis. [38] The fascial planes and muscle groups cannot be detected by palpation.

      A history of comorbid factors, including diabetes mellitus, should be sought in all cases of suspected necrotizing fasciitis. A retrospective, multicenter study by van Stigt et al of 58 patients with necrotizing fasciitis found cardiovascular disease to be the most common comorbidity (39.7% of patients). [49]

      Next:

      Physical Examination

      Physical findings may not be commensurate with the degree of patient discomfort. Early in the disease course, the patient may look deceptively well; unfortunately, this may interfere with early detection, which is key to a favorable outcome. Soon, however, the patient will usually begin to appear moderately to severely toxic.

      Typically, the infection begins with an area of erythema that quickly spreads over a course of hours to days. The redness quickly spreads, and its margins move out into normal skin without being raised or sharply demarcated. As the infection progresses, the skin near the site of insult develops a dusky or purplish discoloration. Multiple identical patches expand to produce a large area of gangrenous skin, as the erythema continues to spread.

      Iwata et al reported that 2 of 3 patients who lacked inflammatory signs such as redness and heat experienced fulminant progression of necrotizing fasciitis and death. [60]

      The initial necrosis appears as a massive undermining of the skin and subcutaneous layer. 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.

      The normal skin and subcutaneous tissue become loosened from the rapidly spreading deeper necrotic fascia that is a great distance from the initiating wound. 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 classic tissue inflammatory signs.

      Usually, some degree of intravascular volume loss is detectable on clinical examination. Other general signs, such as fever and severe systemic reactions, may be present.

      Local crepitation can occur in more than one half of patients. This is an infrequent finding, specific but not sensitive, particularly in cases of nonclostridial necrotizing fasciitis.

      Fournier gangrene in males begins with local tenderness, itching, edema, and erythema of the scrotal skin. This progresses to necrosis of the scrotal fascia. The scrotum enlarges to several times its normal diameter. 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.

      In males, the scrotal subcutaneous layer is so thin that most patients present after the skin is already exhibiting signs of necrosis. In 2-7 days, the skin becomes necrotic, and a characteristic black spot can be seen. Early on, this infection may resemble acute orchitis, epididymitis, torsion, or even a strangulated hernia.

      In women, Fournier gangrene acts more like necrotizing fasciitis because of the thicker subcutaneous layers involving the labia majora and the perineum.

      Complications

      Complications may include the following:

      Metastatic cutaneous plaques may occur in necrotizing fasciitis. Septicemia is typical and leads to severe systemic toxicity and rapid death unless appropriately treated.

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