Necrotizing fasciitis pathophysiology

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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

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 synergistically to enhance the spread of infection. Group A streptococcus is the most common causative agent of type 2 necrotizing fasciitis. Bacterial virulence factors, exotoxins, superantigens and host immune system plays a major role in the pathogenesis of type II necrotizing fasciitis. Recurrent necrotizing fasciitis is caused by MRSA. On gross pathology, the characteristic findings of necrotizing fasciitis include subcutaneous emphysema, skin sloughing, bulae and necrosis. Inflammatory changes are seen on microscopic histopathology.[1]

Pathophysiology

The pathophysiology of necrotizing fasciitis is common to all types of necrotizing fasciitis, but the speed of development and associated clinical features differs depending on the causative organisms.[1]

  • The transmission of pathogens occurs through the following routes:[2][3]

Necrotizing fasciitis in neonate

  • Necrotizing fasciitis can be a serious complication of omphalitis in the neonate.
  • The omphalitis may progress resulting in purplish discoloration and periumbilical necrosis.
  • The necrosis may extend to the flanks and even onto the chest wall.

Pathogenesis

The pathogenesis of necrotizing fasciitis is the result of bacterial and host factors.[4][5]

Type 1 NF

  • The exact pathogenesis of type 1 necrotizing fasciitis is not fully understood.
  • It is thought that type 1 NF is caused by polymicrobial species that work synergistically to enhance the spread of infection.
  • Synergistic NF is comparatively slow process evolving over days.
  • It usually develops in the area where gut flora breaches the mucosa, entering the tissue planes.

Type 2 NF

  • Group A streptococcus is the most common causative agent of type 2 NF.[6][7]
  • Type 2 NF is initially insidious in onset but progress more rapidly.[8]
  • The disease may appear spontaneously with no obvious focus. Hematogenous infection from many foci such as skin, throat, ascending vaginitis, primary peritonitis reaches the fascial layer or seeds vimentin exposed by muscle damage.
  • Direct inoculation of GAS through wounds or associated surgery is less common.
  • The pathogenesis of type 2 NF is the result of the following process:
  • Nerves supplying the necrotizing areas of skin die, the central areas become anaesthetic and peripheral areas remain tender
  • In later stages, infection from deeper layers ascends, producing edema of epidermal and dermal layers (peau d'orange) and a woody firmness of the tissues
  • The fascial and nerve destruction results in sensory and motor deficits, which causes progression of hemorrhagic bulae to cutaneous gangrene

Recurrent necrotizing fasciitis

Recurrent NF is seen in following conditions:[10]

Gross pathology

On gross pathology the characteristic findings of necrotizing fasciitis include:[11]

Microscopic Pathology

On microscopic histopathological analysis, the characteristic findings of necrotizing fasciitis are[11]

  • Early stages
  • Late stages

References

  1. 1.0 1.1 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.
  2. Lynch CM, Pinelli DM, Cruse CW, Spellacy WN, Sinnott JT, Shashy RG (1997). "Maternal death from postpartum necrotizing fasciitis arising in an episiotomy: a case report". Infect Dis Obstet Gynecol. 5 (5): 341–4. doi:10.1155/S1064744997000598. PMC 2364577. PMID 18476182.
  3. Morgan MS (2010). "Diagnosis and management of necrotising fasciitis: a multiparametric approach". J Hosp Infect. 75 (4): 249–57. doi:10.1016/j.jhin.2010.01.028. PMID 20542593.
  4. Stamenkovic I, Lew PD (1984). "Early recognition of potentially fatal necrotizing fasciitis. The use of frozen-section biopsy". N Engl J Med. 310 (26): 1689–93. doi:10.1056/NEJM198406283102601. PMID 6727947.
  5. Elliott DC, Kufera JA, Myers RA (1996). "Necrotizing soft tissue infections. Risk factors for mortality and strategies for management". Ann Surg. 224 (5): 672–83. PMC 1235444. PMID 8916882.
  6. Leitch HA, Palepu A, Fernandes CM (2000). "Necrotizing fasciitis secondary to group A streptococcus. Morbidity and mortality still high". Can Fam Physician. 46: 1460–6. PMC 2144855. PMID 10925760.
  7. Shiroff AM, Herlitz GN, Gracias VH (2014). "Necrotizing soft tissue infections". J Intensive Care Med. 29 (3): 138–44. doi:10.1177/0885066612463680. PMID 23753218.
  8. McHenry CR, Piotrowski JJ, Petrinic D, Malangoni MA (1995). "Determinants of mortality for necrotizing soft-tissue infections". Ann Surg. 221 (5): 558–63, discussion 563-5. PMC 1234638. PMID 7748037.
  9. Chelsom J, Halstensen A, Haga T, Høiby EA (1994). "Necrotising fasciitis due to group A streptococci in western Norway: incidence and clinical features". Lancet. 344 (8930): 1111–5. PMID 7934492.
  10. Miller LG, Perdreau-Remington F, Rieg G, Mehdi S, Perlroth J, Bayer AS; et al. (2005). "Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles". N Engl J Med. 352 (14): 1445–53. doi:10.1056/NEJMoa042683. PMID 15814880.
  11. 11.0 11.1 Librae pathology(2015) https://librepathology.org/wiki/Necrotizing_fasciitis Accessed on September 2,2016

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