Acute Peripheral Arterial Insufficiency

APAI is defined as the reduction of arterial arteriolar blood flow to a tissue other than the central nervous system.  The causes of injury can be a result of surgery, damage to an artery, or as a result of blockage from a clot or reperfusion injury.  The result is acute hypoxia of the ischemic tissues with cellular death.  Where no blood flow exists tissue death is inevitable, but in those areas with some perfusion.*  HBOT maximizes the oxygen content of the plasma and can save the threatened tissues.  HBOT elevates plasma oxygen to 2000% and has been shown to sustain life in a large mammal that has no hematocytes.

* the process of nutritive delivery (including oxygen) of arterial blood to a capillary bed in the body’s tissues.

Acute peripheral arterial insufficiency covers a range of diseases that includes acute traumatic and non-traumatic peripheral arterial insufficiency and acute crush injuries (with or without compartment syndrome).  Crush injuries are those that involve the stripping of the skin and underlying tissue from the bones, usually of the hands of feet as occurs in industrial accidents.

These injuries can compromise large vessels and the capillary beds.  The edema that follows often creates a vicious cycle causing complications such as compartment syndrome, a condition where pressure within a confined space in tissue causes ischemia and dysfunction.  Large vessels are repaired surgically, but the hypoxia resulting from the compromised capillary system may benefit from HBOT.

HBOT also helps preserve intracellular levels of ATP (adonine triphosphate, the mitochondrial energy produced by the cell that transports chemical energy for metabolism), reduces edema, and prevents reperfusion injury. HBOT also reduces the tendency of WBCs to adhere to the endothelium of injured tissue, believed to reduce secondary ischemia.  Edema can be reduced by 50% if HBOT is begun within about eight hours, if the large vessels have not been disrupted.

The first important effect of HBOT is to hyperoxygenate the tissues.  It also causes vasoconstriction.  A 20% reduction in blood flow reduces capillary leakage and therefore edema.  HBOT provides a direct antibacterial effect on certain anaerobes, and maintains the killing ability of leukocytes after phagocytosis.  Tissue oxygen levels are raised to the extent that fibroblasts can lay down collagen, angiogenesis can occur, and cellular growth can be supported.  HBOT also increases the effectiveness of the antibiotics in helping them across the cell walls.

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

The effectiveness of HBOT in clinical human studies is well documented.  Acute ischemias arising from surgery and trauma have been well studied.  HBOT not only increases tissue oxygenation but also, through an unknown mechanism, enables cells to better tolerate ischemia.  The best currently available technology for monitoring the usefulness of HBOT in ischemic areas is transcutaneous oxygen monitoring.