CHAPTER XVII 

 INFLAMMATION 



The studies that have been made in recent years which deal with 

 the healing of wounds and the factors that favor or retard bacterial 

 growth in wounds have added much to our understanding of the 

 fundamentals of local infection and resistance. 



We must keep in mind the following facts. Injured tissue con- 

 tused burned fragmented or altered to such a degree that its cir- 

 culation is markedly interfered with is a twofold source of intoxica- 

 tion. As it becomes necrotic even though sterile it produces protein 

 split products which are profoundly toxic to the organism and cause 

 either a febrile reaction if relatively small in amount, or complete 

 prostration and shock if larger in amount. Very likely the mere 

 liberation of tissue (cell) juices without digestion can bring about 

 similar effects; in animal experimentation the toxicity of the tissue 

 extracts is, of course, well known, where their effect on the coagulation 

 mechanism usually brings about an acute shock picture and death. 

 Nageli has emphasized the importance of tissue necrosis, even when 

 aseptic, in general pathological problems. Experimentally it has been 

 found that the products of tissue contusion can kill an animal and 

 the investigations on the production of shock made during the recent 

 war by a number of American investigators have also served to focus 

 our attention on this practical problem. Nageli, among other experi- 

 ments, took small pieces of tissue, permitted them to autolyze for 24 

 hours aseptically and found that on reimplantation the animal died 

 as a result of the absorption of the toxic split products from the auto- 

 lyzing material. Even sterile blood (autogenous) will, when free in 

 the tissues, cause a considerable leukocytosis (Dold), and Freund 

 has recently published interesting studies that demonstrate the forma- 

 tion of toxic substances from blood. Secondly, the altered tissue per- 

 mits the establishment of bacterial invasion against which normal 

 tissues would be amply able to protect themselves. 



For the first twelve or twenty-four hours following injury (the 

 so-called preinflammatory stage) infecting organisms are confined to 

 the surface of such wounds. If during this period the injured tissue 

 is excised (debridement) we remove the potential sources of intoxica- 

 tion as well as the opportunity for infection, and healing by primary 

 intention is the rule. 



When once this pre-inflammatory stage has been passed and bac- 



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