Necrotizing fasciitis is a severe soft tissue infection that is largely uncommon but when it occurs, it is an aggressive source of mortality and morbidity. In the 5th century B. C Hippocrates recorded one of the first known descriptions of these severe soft tissue infections. Hippocrates noted that in the event of a trivial occurrence such as a skin injury, the affected developed erysipelas throughout their bodies and the disease progressed to a point where sinews, flesh and bones fell apart.
He noted that the disease caused many deaths. However, the modern description of necrotizing fasciilitis as hospital gangrene is drawn from the 1971 descriptions of the disease by Confederate Army Surgeon; Joseph Jones. He referred to the disease as hospital gangrene even though the term necrotizing fasciliitis had been in medical literature since 1952. as such it is prudent to note that there exist a number of terminologies that has been employed over time in reference to the disease.
For instance necrotizing erysipelas, necrotizing cellulitis, haemolytic streptococcal gangrene, bacterial synergistic gangrene, nonclostridal gas gangrene,, nonclostridal crepitant cellulitis and gangrenous erypiselas (Irwin & Ripe 2007). CDC estimates that 10,000-15,000 infections with invasive group A streptococcus occur in the United States every year. Out of this number, 5%-10% are necrotizing fasciilitis and the prevalence has been on an increase since the 1990s.
Necrotizing fasciilitis can be described as a disease process whose entry into the target tissues occurs when the skin barrier is compromised. As the disease progresses it rapidly spreads into surrounding soft tissues hence thrombosis of venous, arterial and lymphatic vessels as well as the necrosis of underlying tissue networks. When a histological examination is done, superficial fascia necrosis, suppuration and thrombosis of veins that traverse the fascia is revealed. As the infection systemically spreads it causes serious toxic shock syndrome or sepsis.
These effects are directly associated to the release of streptococcal exotoxin. These exotoxins are produced bacterial structural genes that are chromosomally encoded. These genes are the streptococcal pyogenic exotoxin A and B genes. Since these genes are responsible for the secretion of the exotoxin, they are thus determinative of the virulence and the pathogenicity of the infecting organism(Irwin & Ripe 2007). Due to the effects of the disease on the affected tissue, the disease is sometimes said to be caused by a “flesh eating bacteria”.
Although the term is a misnomer in the sense that the pathogenic bacterial species do not in any way eat the tissue, it is descriptive of the effects of the toxins on muscle, skin and other underlying tissues. The exotoxins are the virulence factors. The most studied exotoxins are the streptococcal pyogenic exotoxins and the S. pyogenes exotoxins(usually known as the superantigen). The latter has the ability of non specific activation of T-cells resulting in the overproduction of cytokines.
In a nutshell, necrotizing fasciilitis is descriptive of the infectious process that leads to the progressive destruction of the subcutaneous fascia and fat but with relative sparing of the muscular tissues. Although there are cases where the disease has been found to extend even to the perineum and the abdominal wall, it commonly affects the extremities(Wilson et al 2001). Causative Agent of the Disease The term necrotizing fasciilitis is used to specifically refer to a disease caused by the haemolytic group A streptococcal infection.
This specificity in the bacterial aetiology was reached after it was demonstrated that these are the most common isolates from infected tissues. However, when the disease is critically analyzed, it has been shown that the bacterial aetiology of the disease is often nonstreptococcal and polymicrobial in origin in some cases. The organisms that are most often isolated from the wounds include streptococci, enterococci, Escherichia coli, staphylococci, Klebsiella, Proteus, Pseudomonas, Citrobacter, Bacteriodes, peptostreptococci, Clostridia and other fungal species(Irwin & Ripe 2007).
In Type I necrotizing infection which is descriptive of a polymicrobial infection, all the bacterial causative agents are incriminated. Type I infections are caused by Streptococcus pyogenes, Vibrio vulnificus, Staphylococcus aureas, Bacteroides fragilis and Clostridium perfringens. It has also has been conclusively determined that most of the Type II necrotizing fasciilitis infections are caused by group A streptococcus. Owing to the significant increase in the prevalence of necrotizing infections, methicillin resistant Staphylococcus aureas has been responsible for a large proportion of the cases(Lee et al 2007).
For the bacteria to gain entrance into the target tissue there are a host of other causative events that must accompany the infection. Foot ulcers, surgical wounds, abscesses, intravenous drug use, perforated viscus, decubitus ulcers, traumatic wounds and strangulated hernia are some of the predisposing causative events of necrotizing fasciilitis. Some researchers have also documented liposuction, invasive rectal cancer, enterocutenous fistula, infected arteriovenous graft and a percutenous gastronomy tube site as other possible causative events.
Signs and Symptoms During the initial stages of the disease there is considerable semblance to cellulitis but as it progresses, severe pain and significant indications of systemic toxicity become prevalent. In most cases, edema extends beyond the location of cutaneous inflammation. The infection rapidly spreads along fascial planes and subsequently through venous and lymphatic channels. If the bacteria is in deep tissues, the infection may be non apparent on the skin but as the disease progresses, the infected tissue becomes swollen.
If the infection is close to the surface of the skin, signs of an inflammation like swelling, redness and heat are observed and felt. The colour of the skin changes to violet as blisters form. Evidence of cutaneous necrosis may be observed. This is followed by patchy cutaneous anaesthesia and the development of gangrene which extensively undermines the subcutaneous tissue such as the nerves and the vascular structures. During this stage of disease development patients will appear toxic followed by hypotension and the subsequently the onset of organ failure (Wilson et al 2001).
Patients with the disease also vomit and diarrhoea accompanied with severe fever. Diagnosis and Treatment of Necrotizing Fasciilitis The surgical confirmation of the presence of grey necrotic fascia in the absence of frank pus indicates a necrotizing fasciilitis infection. Other histopathologic findings are fascial necrosis, confirmation of the presence of pathologic micro organisms through Gram staining techniques and the thrombosis of small arteries and veins. Based on the bacterial aetiology the disease syndromes are classified as Type 1 necrotizing fasciilitis which is basically a polymicrobial process of infection.
This classification is reached at when the isolation and characterization of the infecting pathogens yields at least a single anaerobic bacterial species (in most cases Peptostreptococcus or Bacteroides or both) occurs with other facultative species like gram negative bacilli(streptococci(not GAS) or the Enterobacteriaceae family). Type 2 necrotizing fasciilitis is specifically caused by invasive GAS in combination with another bacterial species like S. aureas. In some cases, aspiration cultures taken from the edge of the wound or from punch biopsy’s may also are used as confirmatory diagnosis.
Due to the fact that almost 80% of diagnosis is often false diagnostic results, aspiration is deemed to be superior to either aspiration or injection using normal saline. Deep biopsy is also used as a confirmatory diagnosis. Frozen histopathological sections are used in differentiating necrotizing fasciilitis from other integumentary infections like toxic epidermal necrolysis (Baranoski & Ayello 2003). Differential diagnosis of necrotizing fasciilitis includes clostridial myonecrosis, cellulitis, myositis as well as other necrotizing representations of cellulitis.
In all instances where necrotizing fasciilitis is present, both aerobic and anaerobic cultures and subsequent Gram staining should be done to specifically determine the species of microorganisms present in the infected tissue. The initial therapy is thus driven by the results of the isolation and characterization results of bacterial analysis. Based on the morphology of the bacterial species present, only effective antimicrobials are administered. In cases where only the streptococci are observed after Gram stain, a high dose of penicillin G is effective against the infection.
When S. pyogenes is the most prevalent species, a combination of penicillin and clindamycin is advised. Clindamycin interferes with the streptococcal production of the necrotizing toxin. However, given the fact that necrotizing fasciilitis infections are not often monomicrobial, the presence of several bacterial morphologies calls for a broad spectrum antibacterial therapy that is directed at both the gram negative and gram positive anaerobic, aerobic or facultative organisms.
Polymicrobial Gram stain results indicate the presence of Type 1 necrotizing fasciilitis, nonclostridal anerobic cellulitis and progressive synergistic gangrene. The treatment regimen includes the administration of a third generation cephalosporin combined with clindamycin or metronidazole or a combination of gentamicin or penicillin combined with clindamycin or metronidazole. A third option would be to administer tazobactam/peracillin monotherapy. The disease can also be treated with imipenem monotherapy. Thus, in most cases antibacterial treatment is presumptive.
Apart from antibacterial therapies, patients who are highly suspected to be infected are often taken for surgical treatment. Aggressive surgical debridement aids in keeping necrotizing fasciilitis from spreading to adjacent tissues. A visual examination of the affected tissue is enough to yield a conclusive diagnosis even before samples are taken for microscopic analysis. With the development of massive wounds and destruction of tissues, hyperbaric oxygen treatment is resorted to as an adjunctive therapy but it is not largely recommended.
In severe destruction of the extremities, amputation may become the only reliable treatment mode followed by more explorations intended to remove necrotic tissues. The end result is a large wound that cannot heal in the absence of skin grafting. The profound nature of the systemic inflammatory response implies that intense monitoring of the patient in the intensive care unit is compulsory(Escobar et al 2005). Currently, researchers are studying the efficiency of topical negative pressure in the treatment of necrotizing fasciilitis (Martin et al 2008).
Prognosis and Long term effects of the Disease All in all, the prognosis of the disease is highly dependent on early recognition of necrotizing fasciilitis followed by the institution of antimicrobial therapy coupled to an early debridement of devitalized tissue. It is always important to diagnose the disease while still in its early stages so as to decrease the mortality and morbidity rates. As the treatment regimen continues be it antimicrobial therapy before or following surgical treatment, the patient should be provided with adequate nutritional supplements to aid in tissue recovery.
In intensive care, hemodynamic support and wound are critical for quick patient recovery. Additionally, even though surgical incision and debridement remains the only effective form of treatment, concomitant antibiotic therapy should not be forgotten. The patient should be closely monitored to prevent re-infection from remaining necrotic tissues. It is not until surgical debridement removes all these tissues that a patient may be allowed to continue with the treatment in a home environment under the periodic monitoring of the physician.
Apart of using surgery as a treatment intervention, surgery also helps in the reconstruction of anatomical defects and in the restoration of defective functions. Necrotizing fasciitis can cause long term disease specific morbidity of the patient as well as the long term psychological impairment of the patient. For this reason surgery coupled with dressings has been used to avoid these long term effects by stimulating spontaneous healing. Active reconstruction is necessary to heal the huge scars that the massive wounds leave on the patient.
If spontaneous healing is allowed top take place without the help of surgical reconstruction, these extended wounds will shrink leading to the impairment of not only the functional component of the affected tissues but also the aesthetic result. The extent of reconstructive surgery is therefore dependent on the severity of the infection and the extension of the wound. Morbidity and other associated complications of the disease are highly variable. Inflammation considerably affects adjacent healthy organs and in some cases may lead to the organ failure.
Other complications that should be dealt with include squamous cell carcinoma in the scarred tissue, fatal tetanus or the occurrence of the disease. Interventions intended to prevent the severity of any long term effects should therefore take into account these associated complications. References Bananoski, S & Ayello, E. A. (2003. Wound care essentials: practice principles. Lippincott Williams & Wilkins, 2003; 375 Escobar, S. J. , Slade, J. B. , Hunt, T. K. , Cianci, P (2005). Adjuvant hyperbaric oxygen therapy (HBO2) for treatment of necrotizing fasciitis reduces mortality and amputation rate.
Undersea Hyperb Med 32 (6): 437–43 Irvin, R. S. , & Rippe, J. M. (2007). Irwin and Rippe’s intensive care medicine. Lippincott Williams & Wilkins; 1804-1808 Lee, T. C. , Carrick, M. M. , Scott, B. G. (2007). Incidence and clinical characteristics of methicillin-resistant fasciitis in a large urban hospital. Am J Surg 194: 809–813 Martin, D. A. , Nanci, G. N. , Marlowe, S. I. , Larsen, A. N. (2008). Necrotizing fasciitis with no mortality or limb loss. American Surgeon 74 (9): 809–812. Wilson, W. R. , Sande, M. A. , Drew, W. L. (2001). Current diagnosis & treatment in infectious diseases. McGraw-Hill Professional; 186-190Sample Essay of Custom-Writing