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Abstract
Necrotizing fasciitis is a rapidly progressive soft-tissue infection characterized by widespread necrosis of subcutaneous tissue and fascia, with secondary necrosis of the overlying skin. Muscle is usually spared and the disease is usually accompanied by systemic toxicity.
It was first described by Confederate surgeon, during the Civil war as ”hospital gangrene ”. A variety of terms have been used to describe this condition, including necrotizing erysipelas, progressive bacterial synergistic gangrene, Meleney ulcer and hemolytic streptococcal gangrene. The term necrotizing fasciitis, first introduced by Wilson in 1952, is perhaps the most accurate for describing the key features of this infectious process.
The initiating factors may be unknown; but surgery and trauma (including burns and lacerations) are the commonest. It has been also reported after intravenous drug abuse, dental extraction and varicella.
Reported risk factors for necrotizing fasciitis include age greater than 50 years, peripheral vascular disease, diabetes mellitus, malnutrition, atherosclerosis, obesity, hypoalbuminemia, and chronic alcoholism.
Necrotizing fasciitis has been divided into 2 types on the basis of microbiological cultures. Type 1 necrotizing fasciitis is caused by a polymicrobial infection consisting of both aerobic and anaerobic bacteria . Type 2 necrotzing fasciitis is identified by the existence of Streptococcus pyogenes alone or with staphylococci.
The underlying pathogenesis of type- I necrotizing fasciitis is poorly understood. It is suggested that diverse bacterial species work together to enhance the spread of infection, and the growth of invading microbes is synergistic. The virulence factors of group A streptococcus, the cause of type II necrotizing fasciitis, include factors that mediate attachment to host cells, such as protein F, lipotechoic acid and M protein ,extracellular exotoxins such as streptokinase, streptolysin O and S, hyaluronidase, and deoxyribonucleases.
Once bacteria invade the subcutaneous space, local tissue destruction is thought to occur as a result of bacterial production of exotoxins and proteinases. Poorly perfused or necrotic tissue allowing for bacterial proliferation, continuing toxin production and further tissue destruction. Initially, tissue destruction spreads horizontally within the subcutaneous tissues and superficial fascia. As the disease progresses, however, the overlying skin and underlying muscle may develop ischemic necrosis secondary to toxin-induced vasoconstriction or thrombosis of the nourishing vessels.
There has been a five-fold increase in the incidence of necrotizing fasciitis over the last decade. It is found mainly in elderly male patients, it can affect any area of the body, but it most commonly involve the abdomen, perineum, and lower extremities. The condition present as an extremely tender, erythematous, hot and swollen area of extensive cellulitis which does not respond to the usual antibiotics. Lymphadenitis and lymphangitis are rare. As the infection progresses, the skin becomes increasingly tense and erythematous with indistinct margins. It may change colour sequentially from a red-purple to a dusky blue before progressing to necrosis and formation of bullae and eventually becoming haemorrhagic. Crepitus of the affected area may be palpated. Pain is gradually replaced by anesthesia due to cutaneous nerve destruction. The condition is accompanied by sever systemic manifestation. Several clinical subtypes of necrotizing fasciitis have been described with hyperacute and subacute variants.
Early diagnosis of necrotzing fasciitis is critical and may be life saving, as early diagnosis leads to early treatment. The clinician should have a high index of suspicion and begin therapy immediately based on the clinical findings, Tissue biopsies are the best method to use when diagnosing necrotizing fasciitis.
Histopathological findings include coagulation necrosis of the fascia and subcutaneous fat, neutrophilic infiltration of the dermis and fascia, and thrombosis of the adjacent vessels. Gram stain of the tissue reveals the presence of microorganisms in the dermis and destroyed fascia. The underlying muscle is not involved.
Laboratory and radiologic testing should be ordered to confirm the diagnosis. Laboratory investigations include; complete blood count, serum calcium levels, PH of the blood, erythrocyte sedimentation rate, C- reactive protein, liver and renal functions. Culture of the exudate or blood are important to identify the causative organisms. Radiologic testing may detect air within the tissue, highly suggestive of necrotizing fasciitis. Plain x-rays and ultrasound can be used; however, computed tomographic scans and magnetic resonance imaging produce better quality images. Several diagnostic adjuncts have been developed recently to help in early recognition of necrotizing fasciitis. These include a Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) and transcutaneous soft issue oximetry. A positive ”finger” test is pathognomonic for necrotizing fasciitis.
Cellulitis, progressive postoperative bacterial synergistic gangrene, clostridial gas gangrene, clostridial cellulitis, synergistic necrotizing cellulitis and pyoderma gangrenosum should all be considered in the differential diagnosis of necrotizing fasciitis.
Mortality rate from this condition varies from 25% to 60%. Death is usually due to sepsis, respiratory failure, renal failure, or multiple organ system failure. The prognosis of necrotizing fasciitis depends on age, site of infection, comorbidities and severity of the septic syndrome .The most important factor affecting survival is early diagnosis and immediate surgical debridement.
The management of this life threatening condition depends mainly on early and complete surgical debridement of the necrotic tissue, often requiring multiple surgical procedures. Hemodynamic support, appropriate antibiotics, wound care, nutritional support, and analgesia are other essential components of therapy. Hyperbaric oxygen and intravenous immunoglobulins has been used as an adjunct in the treatment of necrotizing fasciitis.
Fournier’s gangrene is an infectious necrotizing fasciitis of the perineum and genital region. It is synergistic infection caused by a mixture of aerobic and anaerobic organisms. Anorectal, genitourinary infections, and cutaneous injuries are the most frequent sources of infection. The diagnosis of Fournier’s gangrene is mainly on clinical grounds and there should be a high index of suspicion. The development and progression of the gangrene is often fulminating and can rapidly cause multiple organ failure and death. Prompt surgical excision of necrotic tissue, along with broad-spectrum antibiotics and aggressive supportive care, is paramount to improved survival.
So, it can be concluded that necrotizing fasciitis is not a new disease entity but it has been known for about one century. However, it is now noticed in increased incidence. In addition, more and more is being understood about its exact pathogenesis and its causative organisms. With a high index of suspicion, early diagnosis and an aggressive approach to its management, the mortality and morbidity associated with serious condition can be reduced.