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RATIONALE: Crush injury involves severe trauma to bone, soft tissue, nerve, and vascular structures. Acute traumatic ischemia occurs when there is a severe injury to a limb and the circulation of the extremity becomes compromised. This ischemic compromise may be severe enough to place the entire extremity at risk of necrosis and amputation. Secondary complications such as infection, nonhealing wounds, and nonunion of bones are frequently observed. Ischemia can result either from injury to the macrosized blood vessels, as in open fractures with interruption of major arteries, or at the microcirculation level, as in severe crush injuries and skeletal muscle compartment syndromes. The immediate threat to the limb is whether perfusion is sufficient to maintain viability of the tissues. Posttraumatic edema, which is associated with traumatic injuries, and ischemia further reduce oxygen availability to tissues. When tissue oxygen tensions fall below 30 mmHg, the host responses to infection and ischemia are compromised. Specifically, white blood cell killing becomes defective or nonexistent and host repair processes such as fibroblast secretion of collagen are arrested. Without a collagen matrix in the wound, neovascularization and wound healing cannot occur. The primary rationale for using HBO2 is that it increases tissue oxygen tensions to levels, which make it possible for the host responses to become functional. At 2 ATA, the blood oxygen content is increased by 25% whereas plasma and tissue oxygen tensions increase tenfold (i.e. 1000%). The net effect is that oxygen diffusion through tissue fluids is increased by a threefold factor. Sufficient oxygen becomes physically dissolved in the plasma to keep tissues alive despite inadequate hemoglobin-borne oxygen. Edema reduction secondary to vasoconstriction is another effect of hyperoxygenation. This mechanism reduces blood flow by 20%. The benefit of vasoconstriction is a concomitant (i.e. 20%) reduction in posttraumatic vasogenic edema. In effect, HBO2 maintains oxygen delivery while blood flow is improved in the microcirculation by the edema reducing effect of vasoconstriction. Thus, the immediate effects of HBO2 are threefold in acute traumatic ischemia: a) enhanced oxygenation at the tissue level, b) increased oxygen delivery per unit of blood flow, and c) edema reduction. Therapy should be initiated within 48 hours after the injury; however, to be most effective, treatment should be started within the first 4 to 6 hours. Source: Hyperbaric Oxygen Therapy: A Committee Report. Undersea and Hyperbaric Medical Society. 1996 Revision Telephone: Email: Chico Hyperbaric Center Web Site Developed & Hosted by Access Now 2000. Copyright © 1999-2001. All Rights Reserved. # |