Liquefaction necrosis

Incubation period is 6 hours to 1 day. Symptoms of exposure include the development of gas gangrene (anaerobic destruction of tissue with the production of gas) and myonecrosis (muscle destruction). Naturally-occurring gas gangrene usually involves rapid invasion, liquefaction (changing solids to liquids), and necrosis of muscles, with gas formation followed by clinical signs of toxicity. 

Abscess. A circumscribed collection of pus a cavity formed by liquefaction necrosis within the solid tissue. 

Figure 16.6. The four primary types of necrosis. (A) Coagulative. On the cut surface of this canine kidney, there is a dark red, wedge-shaped area of coagulative necrosis caused by blockage of the blood supply to the area (infarction). The pale areas are older infarcts. (B) Caseous. This bovine lymph node contains a large whitish, cheese-like area of caseous necrosis characterized by loss of the normal tissue architecture. (C) Liquefactive necrosis, equine brain. There are two large areas of liquefaction with extensive loss of brain tissue. (D) Fat necrosis, bovine abdominal fat. Necrotic fat is firm and chalky white and often becomes mineralized. See color insert.

Alkalies cause toxicity by liquefaction necrosis, meaning that the alkali destroys the cell membrane and cell integrity and thereby causes cell lysis. 

Alkali burns are, accordingly, also referred to as progressive burns. It should be noted that hydrofluoric acid is unique among acids, in that it, like alkalis, produces a liquefaction necrosis, making it perhaps the most dangerous acid for skin contact. 

Converted to ammonium hydroxide aerosol when mixed with water in mucous membranes (eyes, oral mucosa, airways), causing thermal and chemical liquefaction tissue necrosis... 

The primary and most immediate effect of ammonia exposure is bums to the skin, eyes, and respiratory tract. The topical damage caused by ammonia is probably due mainly to its alkaline properties. Its high water solubility allows it to dissolve in moisture on the mucous membranes, skin, and eyes, forming ammonium hydroxide, which causes liquefaction necrosis of the tissues (Jarudi and Golden 1973). Specifically, ammonium hydroxide causes saponification of cell membrane lipids, resulting in cell disruption and death. Additionally, it breaks down cell stmctural proteins, extracts water from the cells, and initiates an inflammatory response, which further damages the surrounding tissues (Amshel et al. 

The primary effects of ammonia in humans are due to its corrosive and irritative properties. Exposure to ammonia gas causes damage to the respiratory tract, eyes, and skin when the ammonia combines with water to become ammonium hydroxide, which results in liquefaction necrosis of the tissues, cell structural breakdown, and inflammatory damage (Amshel et al. 2000 Wibbenmeyer et al. 1999). Animal studies have indicated similar types of injuries of the respiratory tract (Coon et al. 1970 Kapeghian et al. 1982 Mayan and Merilan 1972 Richard et al. 1978a, 1978b Schaerdel et al. 1983 Stombaugh et al. 1969), eyes, and skin (Morgan 1997). 

B. In contrast, alkalis (eg, Drano) cause a liquefactive necrosis with saponification and continued penetration into deeper tissues, resulting in extensive damage. 

D. Injection of hydrocarbons into skin, subcutaneous tissue, or muscie may cause a severe local inflammatory reaction and liquefaction necrosis. 

Fig. 4.43 Ghostly aspect of epidermal cells during liquefaction necrosis...

The process of necrosis requires several hours before it becomes apparent. A current example is the yellowish pus formation consisting primarily of white blood cells having undergone necrosis of liquefaction during acute inflammatory response that moved in response to a bacterial infection. 

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