Definition and Causes

A traumatic ischemia is a condition of inadequate supply of blood to organs and body tissues as a result of a severe physicial injury. Crush injuries and compartment syndrome are traumatic ischemias associated with complex wounds resulting from such traumatic injuries.

Great weight, severe blows, gunshots, or automobile and other accidents may cause crush injuries, which are compressions of the extremities or other parts of the body. Crush injuries commonly cause muscle swelling and neurologic problems. Cellular damage and damaged blood vessels are also typical. Complications include infections, nonhealing bone fractures, and amputation.

Note: crush injuries, which effect a portion of the body such as a leg, are different from crush syndrome, in which the local compression injury is accompanied by a systemic problem such as shock or kidney failure.

In anatomical terms, a compartment is a section of the body containing muscles and nerves which is surrounded by connective tissue (fascia). The arms and legs each have an upper and lower compartment.

Acute compartment syndrome is a medical emergency in which serious injury causes severe high pressure within the anatomical compartment, disrupting the blood flow in the compartment. Nerve and muscle death may result from the inadequate blood supply (ischemia) if acute compartment syndrome is untreated. Surgery is usually required.

"Chronic exertional compartment syndrome is a condition in which blood flow is restricted (ischemia) in muscles as a result of extreme pressure within the muscles brought on by repetitive exercises like running or cycling. Chronic exertional comparment syndrome is typically relieved by ceasing the exercise activity, although persistent symptoms may indicate the need for medicine or surgery."



The immediate justifications for using HBO2 in crush injuries and compartment syndromes are twofold:

First, HBO2 supplements oxygen availability to hypoxic tissues during the early post-injury period when perfusion is most likely to be inadequate.

Second, HBO2 increases tissue oxygen tensions to sufficient levels for the host responses mentioned above to function. Hyperbaric oxygen exposures at two atmospheres absolute (ATA) increase the blood oxygen content (the combination of hemoglobin and plasma carried oxygen) by 125 percent.

The oxygen tensions in plasma as well as tissue fluids is increased 10-fold (1000 %). Sufficient oxygen can be physically dissolved in plasma under HBO2 conditions to keep tissues alive without hemoglobin-borne oxygen. Increased tissue oxygen tensions result in a three-fold "driving force" (mass effect) for oxygen to diffuse through tissue fluids.This helps to compensate for the hypoxia resulting from the increased oxygen diffusion distance from the capillary to the cell through the surrounding edema.

Edema reduction is a secondary effect of tissue hyperoxygenation. Hyperbaric oxygen induces vasoconstriction which reduces blood flow by 20 percent. Since inflow is decreased by 20 percent through vasoconstriction while outflow is maintained, the net effect is edema reduction of 20 percent.

Edema reduction occurs because of decreased filtration of fluid from the capillary to the extracellular space as a consequence of vasoconstriction while resorption of fluid at the capillary level is maintained. Hyperoxygenation of the plasma maintains oxygen delivery to tissues in the presence of HBO2-induced vasoconstriction. Another consequence of decreasing the interstitial fluid pressure through edema reduction is improved blood flow through the microcirculation. The reason for this is that once the interstitial fluid pressure is reduced below the capillary perfusion pressure, the collapsed microcirculation can again open-up and allow perfusion to resume. By reducing edema while supplementing tissue oxygenation, HBO2 interrupts the self-perpetuating, edema-ischemia "vicious circle" cycle to prevent progression of the injury.

Mitigation of the reperfusion injury is another effect of HBO2 for crush injuries and compartment syndromes. It interrupts the interactions between toxic oxygen radicals and cell membrane lipids by perturbing lipid peroxidation of the cell membrane and inhibiting the sequestration of neutrophils on post-capillary venules.

The biochemical mechanism that accounts for this latter effect is that HBO2 interferes with the adherence of neutrophils elaborated through the Beta2 integrin (Cluster-Designation-11) on the sensitized capillary endothelium.

The result is interruption of the superoxide anion interaction with nitric oxide that produces the highly reactive peroxynitrite radical. Another benefit of HBO2 for reperfusion injury is the help in providing an oxygenated environment for the generation of oxygen radical scavengers (such as superoxide dismutase, catalase, peroxidase and glutathione) that detoxify reactive oxygen species.