NECROTIC encyclopedia topics

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. 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

Spiders suspected of, but not shown to cause necrosis:

White-tailed spiders in Australia and New Zealand
Hobo spider in northwestern USA
Sac spider in United States and Australia

Treatment

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.