Acute Peripheral Arterial Insufficiency 2015-11-15T15:54:19+00:00

Acute peripheral arterial insufficiency covers a spectrum of disease that includes acute traumatic and non-traumatic peripheral arterial insufficiency and acute crush injuries (with or without compartment syndrome). Sudden occlusion of the peripheral arterial blood supply occurs with each condition. So does concomitant hypoxia of the involved tissues. Tissue ischemia produces two primary effects: a reduction of the oxygen supply to the involved area; and retention of CO2 and other byproducts of tissue metabolism. Following acute ischemia in a limb, the microcirculation changes, producing interference with the flow of blood and transport of essential nutrients. The integrity of membranes separating intravascular and extravascular spaces is impaired. Such impairment leads to extravasation of intravascular fluids into the tissues and ultimately to edema. Even when circulation is restored, edema may persist or worsen.

Trauma produces intensive tissue destruction with damage to bone and muscle along with acute arterial and venous insufficiency. Several factors affect survival of a limb. First, anatomical reconstruction of severed vessels may be required, and second, the period of time between injury and repair is critical.

During the early injury phase of healing and infection control, the metabolic needs of tissues increase by a factor of 20 or more. Without increased blood flow, these new metabolic demands will not be met. Infection, non-healing wounds, or both can result from insufficient blood supply. Swelling of the traumatized tissues increases the distance that oxygen must diffuse from the capillary to supply the injured tissue. Edema also causes collapse of capillaries, and causes microcirculation to cease. As the tissue pressure from the edema increases, compartment syndrome may result.

The first physiologic effect of hyperbaric oxygen therapy (HBOT) is hyperoxygenation of the tissues affected by acute arterial insufficiency. The effect is not linear but logarithmic, and enough oxygen is physically dissolved in plasma at usual treatment pressures to raise arterial PO2 by a factor of 10 to 15. Because of this increase, the oxygen diffusion distance from capillary to tissue increases three to four times.

Hyperbaric oxygen also causes a vasoconstriction due to the effect of high arterial oxygen tensions in chemoreceptors. This 20 percent reduction in blood flow reduces capillary leakage and diapedesis, thereby reducing edema. Because there is increased oxygen physically dissolved in plasma, this vasoconstriction occurs at no risk to the oxygenation of tissues, and tissue oxygen levels are high. Thirdly, hyperbaric oxygen beneficially affects factors involved with infection control. HBOT offers a direct antibacterial effect on certain anaerobes, and maintains the killing ability of leukocytes after phagocytosis. HBOT supplies the leukocytes with needed oxygen. HBOT also raises tissue oxygen tension above the level necessary for fibroblasts to lay down collagen, for angiogenesis to occur, and for cellular growth to be supported in healing. Additionally, HBOT increases the effectiveness of the antibiotics that require active transport across the cell wall.

Hyperbaric oxygen theoretically protects tissues from reperfusion injury. HBOT confers this effect either by maintaining the cell’s ability to produce scavengers that detoxify free radicals or by preventing lipid peroxidation in cell membranes.

Experimental clinical experience with HBOT in acute ischemias verifies these postulates. In an animal model, Strauss (1983) showed that HBOT lowered pressures in compartment syndrome. Moreover, animals treated with HBOT tolerated much higher compartment pressures without necrosis than untreated animals. In a review of over 700 cases, the likelihood of successful treatment of the syndrome was related to the frequency of HBOT treatments.

Management of crush injuries is two fold. Surgical and orthopedic intervention (debridement, repair of severed vessels, bony fixation, and tissue repair) is required in the acute phase of injury. Also, dealing with or protection from the secondary effects of the injury is necessary. This includes optimizing perfusion with fluid and/or blood therapy, appropriate antibiotics, and maintenance of oxygenation. It is in this arena that HBOT is useful as an adjunct. Timing of the HBOT therapy is an important factor and will be discussed under “therapy.”

Acute peripheral arterial insufficiency is defined as the traumatic or atraumatic reduction of arterial or arteriolar blood flow to a tissue other than the central nervous system. The mechanisms of injury can be iatrogenic (“trash foot”), traumatic damaging of the artery, or vascular occlusion from a clot or reperfusion injury. The result is acute hypoxia of the ischemic tissues with cellular death. Often there is collateral flow to the ischemic site, but this is rarely sufficient to provide adequate oxygen levels for tissue survival and healing. In an area where no flow exists, tissue death is inevitable; but in those areas with some perfusion, the use of HBOT maximizes the oxygen content of the serum phase of the blood and can save the threatened tissues. HBOT elevates serum PO2 up to 2000 percent. This effect is sufficient to sustain even marginal flow in areas served by tortuous collateral circulation that prevents the adequate transit of hematocytes. Using animal models, HBOT has been shown to provide sufficient oxygen delivery to sustain life in a large mammal that has no hematocytes, Boerema, (1960).

Animal and human studies support these findings. All cells require oxygen for aerobic metabolism and cellular energy production. Hunt and Van Winkle showed that a minimum PO2 of 30 mm Hg is required by cells for functioning. Hunt and Pai demonstrated that collagen synthesis for maintenance and healing is oxygen dependent, with an optimal PO2 of at least 50 to 100 mm Hg. Sheffield showed that HBOT can provide PO2 levels in excess of 1,000 mm Hg in ischemic areas. Nemiroff et al., in a randomized, prospective animal study of ischemic flaps, demonstrated markedly greater survival of ischemic tissue when treated with HBOT (p<0.05). Kihara et al., in their controlled study of ischemic neuropathy, demonstrated that “hyperbaric oxygenation will effectively rescue fibers from ischemic fiber degeneration” (p<0.05). The effectiveness of hyperbaric oxygen in clinical human studies is well documented, with acute ischemias arising from surgery and trauma having been particularly well studied. Bowersox et al., showed the effectiveness of HBOT in a large series of patients with ischemic flaps and grafts, as has Perrins. Shupak et al., demonstrated a doubling of the survival rate of ischemic limbs using HBOT. Hill et al., showed that even complex tissues, such as the ear, can survive severe post traumatic ischemia using HBOT. Strauss and Hart showed that HBOT not only increases the tissue oxygenation, but through an unknown mechanism, enables cells to better tolerate ischemia. Zamboni has shown that HBOT is particularly effective in reducing the damage of tissue reperfusion and in preventing the “no-reflow phenomenon.” Finally, Strauss showed the cost effectiveness of using HBOT when salvaging limbs damaged as a result of ischemia.

We believe that the use of HBOT is appropriate in the treatment of acute peripheral arterial insufficiency. However, because HBOT requires adequate circulation to be effective, documentation of blood flow to the affected area should be required if this condition is treated with HBOT. The best currently available technology for indicating the potential usefulness of HBOT in most ischemic areas is transcutaneous oxygen monitoring. We suggest that if the transcutaneous PO2 of the ischemic tissue does not reach at least 100 mm Hg during the initial hyperbaric treatment, the use of HBOT is not warranted. On those regions where, for technical reasons, the oxygen sensor cannot be applied, then clinical documentation of improvement of hypoxia (as a consequence of treatment) should be supplied.



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