ISCHEMIC COMPRESSION SHOCK, WITH AN ANALYSIS OF LOCAL FLUID LOSS

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Abstract
An ischemic trauma was produced by application of rubber tubes in the form of a tight continuous spiral bandage from the ankle to the groin of both hind legs of dogs anesthetized with morphine and sodium pentobarbital. Upon release of the tubes after 6 or more hrs. compression, death occurred in 24 of a first group of 25 minimally anesthetized dogs which were free to move about their cages and in all of a 2d group of 14 dogs anesthetized for longer intervals and restricted to animal boards in a supine position. The dogs of the 1st group survived 0.8-50 hrs. after release of the rubber tubes, with an avg. survival of 11.8 hrs. The dogs of the 2d group survived 2.0-20 hrs. with an avg. survival of 7.9 hrs. Following the release of the rubber tubes the mean arterial pressure in the dogs of the 2d group fell rapidly from around 170-180 mm. Hg to around 120-150 mm. Hg accompanied by a marked rise in heart rate, and a reduction of blood flow in the forepaws, as indicated by subcut. temp. records. The mean arterial pressure then declined more slowly to about 50-60 mm. Hg, after which death from respiratory or cardiovascular failure ensued within a relatively few mins. Collapse of the peripheral veins was noted during the period of declining arterial pressure. The hematocrit reading rose rapidly during the 1st hr. after removab of the rubber tubes and continued to rise slightly during the ensuing hrs. Depression of activity and sluggish response to stimulation were seen in the lightly anesthetized dogs after release of the limb compression. The accumulation of fluid in the traumatized extremities was measured by immersion of the legs separately in a suitable tall narrow vessel before applying the rubber tubes and again after death. After allowing 5 ml./kg. of dog/extremity for shrinkage of the legs with death and after allowing for the fact that immersion may-measure only 91% of the true edema the estimated maximum vol. of edema still ranged from 15-56 with an avg. of 41.3 ml./kg. of body wt. in the dogs of the 1st group and from 3.3-33 with an avg. of 17.6 ml./kg. of body wt. in the 2d group of expts. One leg only was traumatized in 7 dogs. Three of these died with an estimated maximum vol. of edema of 33, 33 and 55 ml./kg. The remaining 4 were killed at approx. 20 hrs. The estimated maximum edema in these dogs was 20-47 ml./kg. of dog. The above observations are not explainable on the basis of a reactive hyperemia in the traumatized legs alone. Accumulation of fluid in the legs is apparently an important factor in the induction of the shock state, but in many of the expts. the vol. of edema appears to be insufficient of itself to explain the death. If the operation of humoral or nervous factors are not subsequently demonstrated to play a part in the induction of this type of shock, estimates may have to be revised downward of the quantity of local edema neces-Bary to induce shock, especially in the absence of hemorrhage into the traumatized tissues. The somewhat shorter survival and lesser edema in the 2d group of dogs demonstrates the importance of prolonged anesthesia and of restriction of activity in contributing to the ease with which shock with fatal outcome may be induced. Evidence is presented which suggests that dogs studied in the spring resist shock better than do dogs studied during the winter mos.

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