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Necrosis (in Greek Νεκρός = "dead") is the name given to unnatural death of cells and living tissue. It begins with cell swelling, chromatin digestion, and disruption of the plasma membrane and organelle membranes. Late necrosis is characterized by extensive DNA hydrolysis, vacuolation of the endoplasmic reticulum, organelle breakdown, and cell lysis. The release of intracellular content after plasma membrane rupture is the cause of inflammation in necrosis.
In contrast to apoptosis, cleanup of cell debris by phagocytes of the immune system is generally more difficult, as the disorderly death generally does not send cell signals which tell nearby phagocytes to engulf the dying cell. This lack of signaling makes it harder for the immune system to locate and recycle dead cells which have died through necrosis than if the cell had undergone apoptosis.
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Causes
There are many causes of necrosis including prolonged exposure to injury, infection, cancer, infarction, poisons, and inflammation. Severe damage to one essential system in the cell leads to secondary damage to other systems, a so-called "cascade of effects." Necrosis can arise from lack of proper care to a wound site. Necrosis is accompanied by the release of special enzymes, that are stored by lysosomes, which are capable of digesting cell components or the entire cell itself. The injuries received by the cell may compromise the lysosome membrane, or may initiate a disorganised chain reaction which causes the release in enzymes. Unlike apoptosis, cells that die by necrosis may release harmful chemicals that damage other cells. In biopsy, necrosis is halted by fixation or freezing. Many species of viper (e.g. rattlesnakes or Bothrops) produce venom which causes severe necrosis in snake-bite victims. Additionally, some spiders (eg the brown recluse) contain venom which may cause significant cutaneous injuries with tissue loss and necrosis.
Morphologic patterns
There are seven distinctive morphologic patterns of necrosis:
- Coagulative necrosis is typically seen in hypoxic environments (e.g. myocardial infarction, infarct of the spleen). Cell outlines remain after cell death and can be observed by light microscopy.
- Liquefactive necrosis is usually associated with cellular destruction and pus formation (e.g. pneumonia). This is typical of bacterial or, sometimes, fungal infections because of their ability to stimulate an inflammatory reaction. Curiously, ischemia (restriction of blood supply) in the brain produces liquefactive rather than coagulative necrosis, this is due to the lack of any substantial supportive stroma.
- Gummatous necrosis is restricted to necrosis involving spirochaetal infections (e.g. syphilis).
- Haemorrhagic necrosis is due to blockage of the venous drainage of an organ or tissue (e.g. in testicular torsion).
- Caseous necrosis is a specific form of coagulation necrosis typically caused by mycobacteria (e.g. tuberculosis), fungi, and some foreign substances. It can be considered a combination of coagulative and liquefactive necroses.
- Fatty necrosis results from the action of lipases on fatty tissues (e.g. acute pancreatitis, breast tissue necrosis).
- Fibrinoid necrosis is caused by immune-mediated vascular damage. It is marked by deposition of fibrin-like proteinaceous material in arterial walls, which appears smudgy and eosinophilic on light microscopy.
Arachnogenic necrosis
Spider bites are cited as causing necrosis in some areas. These claims are widely disputed. In the US at least, only the bites of spiders in the genus Loxosceles or brown recluse have been proven to consistently cause necrosis.[2] Many other spider species are claimed to cause necrosis but in most cases firm evidence is lacking, partially because the early bite is often painless and the spider species seldom identified and because a common reaction by doctors to a possible necrotic spider bite is to remove the flesh pre-emptively.
Several species of spiders possess toxins proven to cause necrosis:
- Loxosceles spiders, including the brown recluse in the midwestern United States and the Chilean recluse in South America[3][4]
Spiders suspected of, but not shown to cause necrosis:
- White-tailed spiders in Australia and New Zealand[5]
- Hobo spider in northwestern USA[6]
- Sac spider in United States and Australia[7]
Treatment
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Please help improve this section by expanding it. Further information might be found on the talk page or at requests for expansion. (October 2008) |
The standard therapy of necrosis (wounds, bedsores, burns etc.) is surgical debridement of necrotic tissue. Another option for removal of necrotic tissue would be use of an enzymatic debriding.
In selected cases special maggot therapy has been utilized with good results.
See also
External links
- Necrosis causes, details and definition
- Undersea and Hyperbaric Medical Society. "Necrotizing Soft Tissue Infections". Retrieved on 2008-07-25.
References
- ^ Norris R. 2004. Venom Poisoning in North American Reptiles. In Campbell JA, Lamar WW. 2004. The Venomous Reptiles of the Western Hemisphere. Comstock Publishing Associates, Ithaca and London. 870 pp. 1500 plates. ISBN 0-8014-4141-2.
- ^ Atkins J, Wingo C, Sodeman W (1957). "Probable cause of necrotic spider bite in the Midwest". Science 126 (3263): 73. doi:. PMID 13442644.
- ^ Maynor ML, Moon RE, Klitzman B, Fracica PJ, Canada A (March 1997). "Brown recluse spider envenomation: a prospective trial of hyperbaric oxygen therapy". Acad Emerg Med 4 (3): 184–92. PMID 9063544.
- ^ Maynor ML, Abt JL, Osborne PD (19892). "Brown Recluse Spider Bites: Beneficial Effects of Hyperbaric Oxygen". J. Hyperbaric Med 7 (2): 89–102. ISSN 0884-1225. Retrieved on 2008-07-25.
- ^ Isbister G, Gray M (2003). "White-tail spider bite: a prospective study of 130 definite bites by Lampona species.". Med J Aust 179 (4): 199–202. PMID 12914510.
- ^ Vetter R, Isbister G (2004). "Do hobo spider bites cause dermonecrotic injuries?". Ann Emerg Med 44 (6): 605–7. doi:. PMID 15573036.
- ^ Vetter R, Isbister G, Bush S, Boutin L (2006). "Verified bites by yellow sac spiders (genus Cheiracanthium) in the United States and Australia: where is the necrosis?". Am J Trop Med Hyg 74 (6): 1043–8. PMID 16760517.
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