Necrotizing fasciitis overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Necrotizing fasciitis or fasciitis necroticans, commonly known as “flesh-eating bacteria,” is a rare infection of the deeper layers of skin and subcutaneous tissues, easily spreading across the fascial plane within the subcutaneous tissue. Many types of bacteria can cause necrotizing fasciitis (eg. Group A streptococcus, Vibrio vulnificus, Clostridium perfringens, Bacteroides fragilis), of which Group A streptococcus (also known as Streptococcus pyogenes) is the most common cause. It is severe inflammation of the muscle sheath that leads to necrosis of subcutaneous tissue and adjacent fascia.[1][2]
Historical Perspective
Necrotizing fasciitis was first described by Hippocrates in the fifth century B.C. as the complication of erysipelas.[3][4]It was described as "hospital gangrene" by confederate army surgeon Joseph jones.[5][6]Meleney reported a series of 20 patients in 1924 as having hemolytic streptococcal gangrene, later called Meleney's gangrene.[7]Necrotizing fasciitis of perineum was described in 1883 by the French physician, Jean Alfred Fournier.[8]
Classification
Necrotizing fasciitis may be classified according to international classification of diseases-10 (ICD-10) into M72.6 Necrotizing fasciitis.[9]Based on microbiological findings, necrotizing fasciitis may be classified into four types (type I, type II, type III, type IV). Necrotizing fasciitis is further classified based on anatomic location and severity of symptoms.[10]
Pathophysiology
The pathophysiology of necrotizing fasciitis is common to all types but the speed of development and associated clinical features differs depending on the causative organisms. Following transmission, the bacteria uses the entry site to invade the fascial planes which causes the wide spread necrosis of superficial fascia, deep fascia, subcutaneous fat, nerves, arteries, and veins. Necrotizing fasciitis can be a serious complication of omphalitis in the neonate.The pathogenesis of necrotizing fasciitis is the result of bacterial and host factors. The exact pathogenesis of type 1 necrotizing fasciitis is not fully understood but polymicrobial species work together to enhance the spread of infection (Synergistic). Group A streptococcus is the most common causative agent of type 2 NF. Bacterial virulence factors, exotoxins, superantigens and host immune system plays a major role in the pathogenesis of type II NF. Recurrent NF is caused by MRSA. On gross pathology, the characteristic findings of NF include subcutaneous emphysema, skin sloughing, bulae and necrosis. Inflammatory changes are seen on microscopic histopathology.[1]
Causes
The causative organisms vary depending on the type of necrotizing fasciitis. Type I (polymicrobial), Type II (monomicrobial), Type III (gram negative monomicrobial including marine related organisms) and Type IV (fungal).[1]
Differentiating Necrotizing fasciitis overview from Other Diseases
Necrotizing fasciitis must be differentiated from other diseases that cause erythema, pain, edema and necrosis of soft tissues such as sun burn, cellulitis, erysipelas, diabetic myonecrosis and vasculitis.[11]
Epidemiology and Demographics
The incidence of necrotizing fasciitis in adults is 0.40 cases per 100,000 people/year and the incidence in children is higher at 0.08 cases per 100,000 people/year.The overall mortality rate in the United states from 2003- 2013 was 4.8/1,000,000 per year. Patients from all age groups can develop necrotizing fasciitis but slightly more common among >50 years age and effects men and women equally.The incidence rate of necrotizing fasciitis is high in black, Hispanic, and American Indian individuals compared to Whites and low in Asian individuals.
Risk Factors
Common risk factors in the development of necrotizing fasciitis include trauma, alcoholism, diabetes, intravenous drug abuse, immunosupression and burns.[1]
Screening
According to the U.S. Preventive Service Task Force (USPSTF), there is insufficient evidence to recommend routine screening for necrotizing fasciitis.
Natural History, Complications, and Prognosis
If left untreated, the acute inflammatory changes spread quickly, accompanied by high fever and extreme weakness leading to necrosis of soft tissue. Common complications of necrotizing fasciitis include limb loss, sepsis, toxic shock syndrome, disseminated intravascular coagulation(DIC). Depending on the extent of the necrotizing fasciitis at the time of diagnosis, the prognosis may vary. The prognostic factors associated with necrotizing fasciitis include diabetes mellitus, acute renal failure, admission serum creatinine >2mg/dl and admission white blood cells >30,000 cells/mm3.
Diagnosis
History and Symptom
During early stages, the symptoms of necrotizing fasciitis are non specific and the diagnosis requires high degree of suspicion. The disease is often indistinguishable from cellulitis or abscess early in its evolution.
Physical Examination
Physical examination of patients with necrotizing fasciitis is usually remarkable for local soft tissue signs such as warmth, tenderness beyond margins of erythema, swelling , erythema with ill defined margins, Blistering/bullae, skin discoloration, foul discharge (greyish or brown discharge), fluctuance, crepitus, skin sloughing or necrosis, absence of lymphangitis or lymphadenopathy (lymphangitis is rarely seen in necrotizing fasciitis), sensory and motor deficits (e.g. localized anesthesia).
Diagnostic Criteria
LRINEC is a diagnostic scoring system used to distinguish necrotizing fasciitis from other soft tissue infections.
Laboratory Findings
Laboratory findings consistent with the diagnosis of necrotizing fasciitis include positive blood and tissue culture, elevated inflammatory markers, leucocytosis and elevated serum creatinine. LRINEC is a diagnostic scoring system used to distinguish necrotizing fasciitis from other soft tissue infections.
Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Prevention
References
- ↑ 1.0 1.1 1.2 1.3 Misiakos EP, Bagias G, Patapis P, Sotiropoulos D, Kanavidis P, Machairas A (2014). "Current concepts in the management of necrotizing fasciitis". Front Surg. 1: 36. doi:10.3389/fsurg.2014.00036. PMC 4286984. PMID 25593960.
- ↑ Hakkarainen TW, Kopari NM, Pham TN, Evans HL (2014). "Necrotizing soft tissue infections: review and current concepts in treatment, systems of care, and outcomes". Curr Probl Surg. 51 (8): 344–62. doi:10.1067/j.cpsurg.2014.06.001. PMC 4199388. PMID 25069713.
- ↑ Descamps V, Aitken J, Lee MG (1994). "Hippocrates on necrotising fasciitis". Lancet. 344 (8921): 556. PMID 7914656.
- ↑ Hasham S, Matteucci P, Stanley PR, Hart NB (2005). "Necrotising fasciitis". BMJ. 330 (7495): 830–3. doi:10.1136/bmj.330.7495.830. PMC 556077. PMID 15817551.
- ↑ WILSON B (1952). "Necrotizing fasciitis". Am Surg. 18 (4): 416–31. PMID 14915014.
- ↑ Janevicius RV, Hann SE, Batt MD (1982). "Necrotizing fasciitis". Surg Gynecol Obstet. 154 (1): 97–102. PMID 7031943.
- ↑ Sadasivan J, Maroju NK, Balasubramaniam A (2013). "Necrotizing fasciitis". Indian J Plast Surg. 46 (3): 472–8. doi:10.4103/0970-0358.121978. PMC 3897089. PMID 24459334.
- ↑ Chennamsetty A, Khourdaji I, Burks F, Killinger KA (2015). "Corary diagnosis and management of Fournier's gangrene". Ther Adv Urol. 7 (4): 203–15. doi:10.1177/1756287215584740. PMC 4580094. PMID 26445600.
- ↑ ICD-10 version:2016. http://apps.who.int/classifications/icd10/browse/2016/en#/M72.6 2016 Accessed on August 25,2016
- ↑ Lancerotto L, Tocco I, Salmaso R, Vindigni V, Bassetto F (2012). "Necrotizing fasciitis: classification, diagnosis, and management". J Trauma Acute Care Surg. 72 (3): 560–6. doi:10.1097/TA.0b013e318232a6b3. PMID 22491537.
- ↑ Wong CH, Wang YS (2005). "The diagnosis of necrotizing fasciitis". Curr Opin Infect Dis. 18 (2): 101–6. PMID 15735411.