Necrotizing Fasciitis (NF): Causes and Treatment

Necrotizing Fasciitis (NF): Causes and Treatment Abstract Necrotizing Fasciitis (NF) is a rare but severe type of bacterial infection that affects the soft tissue and fascia. Because of how rapidly the infection spreads it has a high mortality rate and the key to a successful recovery is early diagnosis and treatment. Since the discovery of this disease, little progress has been made to decrease the mortality rate, further emphasizing the importance of healthcare providers ability to detect and treat the infection early so that the patient will have a fighting chance. This article will discuss the history, pathophisiology, clinical manifestations, diagnostics and treatments, and interventions as it relates to the Nurse practitioners role in caring for a patient with NF. History and Background Necrotizing Fasciitis (NF) is a rare but rapidly progressing inflammatory infection that results in the extensive destruction of soft tissue and fascia. In the earlier stages of the infection muscle and skin are not affected (Ruth-Sahd Gonzalez, 2006). NF involves the superficial fascia, subcutaneous fat (which has nerves and vascular structures) and deep fascia (Green, Dafoe, Raffin, 1996). Thrombosis of the microvasculature occurs but there is an absence of myonecrosis (Giuliano, Lewis, Hadsley, Blaisdel, 1977). NF was first described as a complication of erysipelas by Hippocrates in the 5th century B.C. (Descamps, Aithen, Lee, 1994). During the civil war confederate army surgeon Joseph Jones described it as hospital gangrene in which 46% of the 2,642 soldiers who were infected died from NF complications. The cause of the disease was identified as a bacterial infection in 1915. It wasnt until 1952 that the soft tissue infection was named necrotic Fasciitis by Wilson (Wilson, 19 52). Cases of NF were sporadically occurring throughout the 19th and 20th century but remained restricted to military hospitals during the war with a few outbreaks occurring in civilian populations. Epidemiology The centers for Disease control and Prevention (CDC) reported that rates of NF increased worldwide from the mid 1980s to early 1990s. According to the CDC the increases in the rate and severity of NF are correlated with increase in the prevalence of toxin producing strains of S. Pyogenes (M-1 and M-3 serotypes). The CDC reported approximately 600 cases of NF in the U.S. in 1999 (Hu, 2002). Disease progression NF develops when bacteria enters the body usually through a minor trauma for example a laceration, bruise, or bug bite. Some cases occur after surgeries for example abdominal surgeries; the bacterium enters the surgical incision. The bacteria attacks the soft subcutaneous tissue releasing toxins that kill the tissue and affect blood flow to the infected area causing it to become gangrenous. If left untreated the skin, fat, muscle sheath, and later the muscle become involved. The infection spreads unseen moving up the affected body part at a rate of 3 centimeters per hour up to 1 inch of tissue per hour (Ruth-Sahd and Gonzales, 2006). Once necrosis of the tissue occurs that area has to be surgically removed. The bacteria can also cause the patient to go into systemic shock, which can lead to hypotension, respiratory failure, renal failure, and heart failure. If the infection is severe death can occur within 18 hours (Astorino, Genrich, MacGregor, Victor, Eckhouse, Barbour Barbour, 20 09) Pathophysiology Tissue destruction is possible once the bacterium has been introduced under the skin via a cut or penetrable wound. The pathogens begin to rapidly multiply spreading from the subcutaneous tissue along fascial planes, and then invading the blood vessels and lymphatic system. The bacteria release toxins that decrease the protective tissue factors in order to inhibit the immune systems ability to combat the bacteria. In the bodies attempt to combat the bacteria at the tissue level. The blood vessels in the area begin to leak due to the effects of the bacteria in the tissue, the immune response becomes hyperactive, which results in blood vessel dilation in order to facilitate the immune response to the area affected. Unfortunately the cells in the tissue begin to die as the blood vessels leak and decrease the oxygen supply to the cells due to the increase in permeability. Since there is a decrease in blood flow and oxygen supply to the tissue from the infection, tissue necrosis and ische mia occur. As tissue necrosis worsens, nerve damage takes place, which can be seen, as the patient will report the decrease or absence of pain at the area affected. As the infection progresses septicemia will also develop (Astorino, et al. 2009). Causative factors NF is caused by a bacterium named Streptococcus pyogenes or Group A streptococcus (GAS). GAS can be found in peoples throats or on their skin and they will be asymptomatic. S. pogenes is a cause for non-invasive GAS diseases for example rheumatic fever, strep throat, and skin infections like impetigo. When GAS travels to areas of the body where bacteria isnt found it is called invasive GAS disease example would be blood or lungs. More than 10 million non-invasive GAS cases occur annually. A rare but most severe case of invasive GAS is NF. These bacterium evolve quickly and scientist believe that GAS makes proteins that cause the immune system to attack the tissue directly thus the body destroys itself (Hu, 2002). NF has been classified into two types based upon the bacterium identified upon culture. Type 1 in a polymicroial infection including both gram-positive and gram- negative bacteria that can be anaerobic or aerobic. Type 1 is the most common, making up 90% of all the cases, st riking abdominal or peritoneal tissue. Underlying risk factors include postoperative, advanced age, or diabetes (McGee, 2005). Type 2 also known as the Flesh eating Bacteria is the rarest out of the two making up about 10% of the cases. It is the most dangerous of the infections usually affecting the arms or legs and involves the Group A (beta)- hemolytic streptococcus with or without staphylococcus aureus. Type 2 does not discriminate on age, race, or sex (Astorino, et al. 2009). Signs and Symptoms Early detection of NF is crucial it can be the difference between life and death. Health care providers need to be knowledgeable about the signs and symptoms of NF so that treatment can be started right away. Initial signs may be vague and are often confused with cellulitis, signs include pain, edema, erythema, and fever. A definitive diagnosis can be made by visualization and dissection of the necrotic fascia. A key factor of NF is pain, which is disproportionate to the amount of redness. If suspected cellulitis fails to respond to antibiotics within 24-48 hours NF should be considered (Varma and Stashower, 2006). Early symptoms including pain, malaise, fever, and thirst occur within the first 24 hours of invasion of bacteria. This is the time NF is usually misdiagnosed because progression of the disease is not visible until tissue destruction has already stated (McGee, 2005). Walter (2004) states that the hallmark of NF is erythema that spreads quickly with a margin of redness that extends to normal skin and is not raised. Advance symptoms occur 48-72 hours later and are characterized by significant pain at the wound site, increasing erythema, edema, and warmth. The skin tissue then becomes discolored and deteriorates further. The redness turns to dusky or blue and bullae (vesicles) appear. These bullae enlarge and then rupture leaking out dishwater pus a foul smelling, thin dirty gray liquid (Kessenich, 2004); (Ruth-Sahd and Gonzales, 2008). 4-5 days after appearance of the first symptoms patients can begin to demonstrate critical symptoms ranging from numbness and hypotension to toxic shock and unconsciousness. From there the patient can develop gangrene, sepsis, and then death may occur (McGee, 2005). When the initial symptoms are found it can be difficult to differentiate between NF and celluitis thus it is important to remember the hallmark of NF. After 3-5 days of onset when there is skin breakdown, bullae, and cutaneous gangrene present which are defin itive signs of NF and the involved area is usually not painful due to the are becoming anesthetic secondary to thrombosis of small vessels and nerve destruction located in the necrotic subcutaneous tissue Mandell, Bennett, and Dolin, 2005). Laboratory and Imaging Studies Common laboratory studies used in diagnosing NF include complete blood cell count with differential (CBC), Electrolytes, Blood urea nitrogen (BUN), Creatinine phoshokinase (CPK), rapid streptococcus test, and a culture and sensitivity. CBC may show an increase in WBC greater than 14,000/ul and the electrolytes may show a sodium level less than 135 mmol/L, which are both indicative of NF (Schwartz, 2006). The BUN may also be elevated to 15 mg/ml and the CPK may be elevated, indicating the presence of tissue breakdown. A C S with a Gram stain can determine whether the infection is Type 1 or Type 2, which will help to determine what antibiotics to prescribe. Computed tomography (CT) scan and magnetic resonance imaging (MRI) can be used to help diagnose NF. Ct scans can visualize the subcutaneous air and find the anatomic site of involvement by detecting necrosis with asymmetric fascial thickening (Maynor, 2006). MRI is helpful with guided rapid debridement of the wounds. Treatment In order to prevent significant disfigurement and/or death in the patient with NF is a quick diagnosis and very aggressive treatment is needed from the start. Broad spectrum antibiotics that treat gram-positive and negative aerobes and anaerobes are prescribed around the clock until the specific strain of the bacteria can be identified and treated appropriately. Due to the amount of antibiotics being administered and possible toxicity involved, Kidney and Liver function should be monitored during therapy. The patient will also need intravenous fluids, pain management, and possibly TPN. All necrotic tissue on the patient needs to be debrided with diligence in removing fascia, skin and subcutaneous tissue involved as early as possible, which may need to be performed multiple times to effectively remove all necrotic tissue. Hyperbaric therapy may be prescribed as an additional therapy. Role of the NP The NP needs to be able to recognize the early symptoms of NF so that he or she will be able to begin treatment quickly. A collaborative multidisciplinary care approach needs to be used for the care of this type of patient. The care team will need to include Critical/Acute care, Dietitian, Physical therapy, and Wound care Nurse. The patient will need a lot of education and psychological support as well. Conclusion Necrotizing Fasciitis is a very aggressive and debilitating disease that has a very rapid progression. Since the disease is very easily transmitted into the body with the potential of detection not until later stages due to the similarities to cellulitis. Rapid diagnosis and treatment is essential to prevent severe dismemberment and or death. So this makes the Nurse Practitioner working in ambulatory care the first line of defense against this rapidly debilitating disease.