The present status of research in burn toxins.
Modern intensive care combined with current improvements in the specific, systemic and local therapy of burns has delayed the mortal effects of severe burns. Nor has there been any significant improvement in this mortality during the last decade. The occurrence of uncontrollable infection and sepsis due to gram-negative bacteria or fungi as the basic cause of death was not a satisfactory explanation. So, progress should only be expected from a new concept in burn treatment. This new concept should be to view the burn disease as being caused by toxic factors induced by thermal injury to the skin. Electron-microscope studies in mice and rats have revealed similar mitochondrial alterations in hepatocytes after either a sublethal controlled burn injury or an intraperitoneal application of an equivalent dose, of a cutaneous burn toxin. The intraperitoneal injection of different amounts of the burn toxin indicated, that the extent of the mitochondrial changes correlated directly with the dose of toxin. Investigations of liver metabolism suggested an inhibition of the oxygenation chain. The incubation of isolated liver cells together with the burn toxin demonstrated by scanning electron microscopy a direct cytotoxic effect of the burn toxin. In animal tests the pathogenic effect of the burn toxin could be prevented by treatment with an antitoxic IgG generated in sheep. The fatal sepsis of severely burned patients is the consequence of a decreased host defence against infections, which is caused by a primary and general toxic alteration of the whole organism. One important aspect of treatment should therefore be the elimination of burn toxins. To achieve this management should include primary excision of the burns, local application of nonabsorbable protein-complex-binding substances and specific passive immunotherapy with an antitoxic IgG.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D000818:Animals; D002056:Burns / Q000378:metabolism* / Q000628:therapy; D005947:Glucose / Q000096:biosynthesis; D006003:Glycogen / Q000096:biosynthesis; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007773:Lactates / Q000378:metabolism; D008099:Liver / Q000378:metabolism / Q000648:ultrastructure; D051379:Mice; D051381:Rats; D012867:Skin / Q000378:metabolism*; D014118:Toxins, Biological / Q000096:biosynthesis / Q000276:immunology / Q000633:toxicity*; D014508:Urea / Q000378:metabolism
D000596:Amino Acids; D007074:Immunoglobulin G; D007773:Lactates; D014118:Toxins, Biological; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D014508:Urea; D006003:Glycogen; D005947:Glucose