Example Of Necrotizing Fasciitis Research Paper

Necrotizing Fasciitis

Necrotizing fasciitis is a deep seated infection of subcutaneous tissue that results in progressive destruction fascia and fat but may spare the skin itself. Approximately there is an estimate of 500-1500 cases of necrotizing fasciitis per year in the United States. Over the past decade, necrotizing fasciitis due to invasive group A streptococcus have been observed with increasing frequency . Typically, necrotizing fasciitis affects elderly patients or individuals with diabetes, alcohol abuse, chronic cardiac disease or peripheral vascular disease. However, group A streptococcal necrotizing fasciitis often occurs in young, previously healthy patients. Mortality rates range from 20 to 40 percent. Higher mortality rates are visible in people with diabetes, malnutrition, obesity, arteriosclerosis, and advancing age .
Necrotizing fasciitis is a rare but often fatal infection involving the superficial fascial layers of the neck, extremities, abdomen, and perineum. Hippocrates first described the disease in the fifth century. The disease also has other names, such as streptococcal, hospital or galloping gangrene. The original designation for this illness was hospital gangrene. Fournier, a respected French dermatologist was the man who discovered the disease in a group of men in the form of cellulitis in the groin in the year 1883 . Hence, the disease also has another name, Fournier’s gangrene. In 1924, Meleny recognized that this condition rapidly became a fatal systemic disease. Most recently, the lay press has labeled it the ‘flesh-eating disease’. Wilson coined the term necrotizing fasciitis in the year 1952.
There exist two clinical types of necrotizing fasciitis. Type 1 necrotizing fasciitis is a mixed infection caused by aerobic and anaerobic bacteria and occurs most commonly after surgical procedures, in diabetic patients, or in those with peripheral vascular disease . Nonclostridial anaerobic cellulitis and synergistic necrotizing cellulitis are both variants of the same syndrome. In addition to its spontaneous occurrence in diabetic patients, type 1 necrotizing fasciitis may also develop as a result of breach of the integrity of mucous membranes from surgery or instrumentation. Group A streptococcus bacteria are responsible for type II necrotizing fasciitis, also previously called as streptococcus gangrene . In contrast to patients with type I necrotizing fasciitis, patients with type II are usually younger with no complicated medical illnesses, and have a history of blunt trauma or penetrating injury.
In most cases of necrotizing fasciitis caused by group A streptococcus, infection occurs deep in tissues at a site of minor trauma such as a bruise, muscle strain and many others. Within 24 hours, breakage in the skin is apparent. Symptoms such as malaise, myagias and anorexia may be present in the patients . In some cases, mild overlying erythema is also visible. In other cases, excruciating pain in the absence of any cutaneuos findings is the only clue of infection. Within 24 to 48 hours, erythema may darken to a reddish-purple color, with overlying blisters and bullae. Conversely, erythema may be absent and the characteristics bullae develop in normal appearing skin.
Early diagnosis is crucial in optimizing the outcome of the disease. The diagnosis is predominantly clinical, but both ultrasonography and magnetic resonance imaging (MRI) scans are useful in supporting such a diagnosis. These tests as well as plain x-ray sometimes show gas in the soft tissues. Differentiating early necrotizing fasciitis from the more common cellulitis is difficult in the diagnosis process. One clue is severe pain that often accompanies necrotizing fasciitis. Laboratory risk indicator for necrotizing fasciitis (LRINEC) helps to determine and assist in the diagnosis of necrotizing fasciitis. It uses a panel of hematological and biochemical test results, such as C –creative protein, serum creatinine, total white blood cell count, hemoglobin, blood glucose, and serum sodium in order to provide a scoring system for the risk of having necrotizing fasciitis .
Extensive surgical debridement or fasciotomy is the mainstay of effective treatment of necrotizing fasciitis. Occasionally, amputuation is necessary. Antimicrobial therapy directs towards the results of initial gram stain. Initial therapy with a β-lactam/β-lactamase inhibitor with broad-spectrum coverage against Gram-negative bacilli, staphylococci, streptococci, and anaerobes, such as piperacillin or tazobactam are effective treatment procedures . In septic patients, ciprofloxacin is an additive medication. In patients with serious penicillin allergy, empiric therapy with ciprofloxacin plus metronidazole is administrable. Other effective antibiotics are Benzyl penicillin with a combination of nafcillin, metronidazole, quinolone, clindamycin and quinolone, carbapenem, meropenem with fluconazole, and piperacillin with tazobactam . In severe cases, medications to raise blood pressure, blood transfusions, intravenous immunoglobin are also effective treatments.
According to the Centers for Disease Control, 2000 to 3000 people die each year due to necrotizing fasciitis . There are over 10000 to 15000 known cases of necrotizing fasciitis. Preventive measures of necrotizing fasciitis should focus on adhering to aseptic and sterile techniques and standard precautions with all patients. Control of endogenous infection with prompt cleansing and debridement of traumatic wounds helps to halt the spread of bacteria . Frequent handwashing, sterile technique for dressing changes and appropriate use of prophylactic antibiotics are also effective preventive measures. A great recommendation is to reduce exogenous or environmental sources of contamination, including airborne microorganisms. In the case of serious sequelae, it is advisable to allow the wound to heal naturally and prevent necrotizing fasciitis.

References

Acton, Q. A. (2012). Necrotizing Fasciitis: New Insights for the Healthcare Professional. Atlanta, GA: Scholarly Editions.
Bolognia, J. L., Rapini, R. P., & Jorizzo, J. L. (2008). Dermatology. Gulf Professional Publishing.
Schlossberg, D. (2008). Clinical Infectious Disease. Cambridge University Press.