October 1981

Defects in Peripheral Oxygen Utilization Following Trauma and Shock

Author Affiliations

From the Samuel R. Powers Trauma Center, Departments of Surgery (Drs Shah, Newell, and Saba) and Physiology (Dr Saba), Albany (NY) Medical College.

Arch Surg. 1981;116(10):1277-1281. doi:10.1001/archsurg.1981.01380220029005

• Following shock and trauma, there may be capillary block or stasis that sets up a neurohumoral response, causing further capillary constriction and ischemia. This ischemia may not result in tissue hypoxia, as functioning capillaries may still exist near the damaged areas. Following resuscitation, however, a reperfusion syndrome causing massive tissue edema, endothelial swelling, and further capillary block may lead to tissue hypoxia. We used isolated canine hind limb as a model of the peripheral circulation in a series of experiments that showed that interstitial edema alone did not reproduce the defect in peripheral oxygen utilization. On the other hand, both reperfusion syndrome and microembolization were able to reproduce this response. Hypertonic mannitol and imidazole reversed this defect following either reperfusion syndrome or microembolization, respectively. These data suggest that resuscitated posttrauma patients suffer from defects in peripheral oxygen utilization probably owing to microembolization, reperfusion, and tissue edema, which may be treated by specific therapy.

(Arch Surg 1981;116:1277-1281)