Studies in experimental traumatic shock. IV, Evidence of a toxic factor in wound shock / W.B. Cannon.

  • Walter Bradford Cannon
Date:
1922
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Licence: Public Domain Mark

Credit: Studies in experimental traumatic shock. IV, Evidence of a toxic factor in wound shock / W.B. Cannon. Source: Wellcome Collection.

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    as a consequence of wounds a reflex relaxation of blood vessels similar to that which occurs in fainting. Indeed, as Cowell*® has observed, fainting is, in fact, not infrequently observed after the reception of wounds. Vincent ® likewise has seen cases of this character; but in the only instance which he describes in detail (that of a man wounded in the abdomen, who, a few minutes after being hit, manifested the syndrome of shock), the blood pressure, at the end of forty-five minutes, had risen from 60 to 90 millimeters of mercury. It is possible, then, that there may be produced by a wound an effect similar in character to fainting or syncope, but persisting for a longer period than the usual fainting spell. British, French and American observers had occasion during the war to note that shock may begin to appear two or three hours after the wounding. It may be associated with continued bleeding, but commonly cannot be explained by hemorrhage or infection. Exposure to cold, lack of water, rough transportation, and the agitation of broken bones have been recognized as circumstances favorable to its development. These factors may later have their action increased by infection, especially by the bacilli of gas gangrene. This is secondary wound shock and was by far the most common form noted during the. war. An analysis of the theories which have been most commonly advocated in the past, such as inhibition,’® reduction of the carbon dioxid content of the blood (acapnia ™), fat embolism,’? exhaustion of nerve centers and of certain glands,’? shows that they do not offer an adequate explanation for the onset of delayed or secondary shock. Their chief and common defect is that they fail to account for the occurrence, both in clinical and in experimental shock, of a diminution of blood volume and either a local or a general concentration of blood corpuscles. A group of theories which do take these facts into con- sideration, namely, those which postulate a primary vasoconstriction with a consequent capillary congestion,’ fail in that they do not suggest how a vasoconstriction would occur, capable of bringing about a reduction of blood volume. What is required is a demonstra- 8. Cowell, E. M.: The Initiation of Wound Shock, J. A. M. A. 70:608 (March 2) 1918. 9. Vincent: Compt. rend. Soc. de biol. 81:887, 1918. 10. Meltzer, S.J.: The Nature of Shock, Arch. Int. Med. 1:578 (July 15) 1908. 11. Henderson: Am. J. Physiol. 21:128, 1908. 12. Porter: Harvey Lectures, Philadelphia, 1917-1919, p. 21. 13. Crile, G. W., and Lower, W. E.: Surgical Shock and the Shockless Operation Through Anoci-Association, Philadelphia, W. B. Saunders Company, 1920. — . 14. Malcolm: Tr. Med. Soc., London $2:274, 1909. Starling, E. H.: Arch. méd. belges 71:369 (Oct.) 1918. Erlanger, J.; Gessell, R., et al.: Am. J. Physiol. 49:90, 151, 345, 1919; Ibid. 50:31, 104, 119, 1919.
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