Rationale for use of hyperbaric oxygen in acute traumatic ischemia

Clinical and experimental evidence indicates, that HBO therapy used as an adjunct for management of acute traumatic ischemia may improve outcome. The appreciation of the potential applications in management of trauma cases requires an understanding of the mechanisms of potential action and of oxygen effects on various types of tissues.

The immediate effect of HBO therapy is hyperoxygenation. The effects of HBO therapy result from the increased amount of physically dissolved oxygen in plasma under hyperbaric conditions. Oxygen dissolves in plasma in direct proportion to the partial pressure of oxygen in the inspired gas. Oxygen is thus delivered to all perfused tissues of the body via systemic circulation. Under HBO treatment this supplement of the oxygen-carrying mechanism of haemoglobin becomes most important when stasis of cellular elements restricts red blood cell flow through the microcirculation.

In most cases trauma patients are treated at a pressure of 240 to 280 kPa. A patient breathing 100% oxygen at that pressure is exposed to pO2 of approx. 1600 mmHg. This increase of partial pressure of oxygen supports gas diffusion for a much greater distance than under normobaric conditions. Thus hyperbaric oxygen allows oxygenation of tissues even when the blood flow is disturbed.

A considerable elevation of the arterial pO2 provides protection against the vicious circle created by ischemia, hypoxia and oedema. The oedema reducing effect of hyperbaric oxygen was demonstrated in limb muscle after 3 hours of ischemia13. In the same model Nylander et al14 showed, that repeated hyperbaric oxygen in the early postischemic phase stimulated the aerobic metabolism resulting in higher levels of adenosine triphosphate (ATP) and phosphocreatinine and lower lactate levels than in untreated ischemic animals. Haapaniemi15 from the same working group found that repeated hyperbaric oxygen treatment had positive effects for at least 48 hours after severe ischemic injury. HBO erased the levels of high energy phosphate compounds, indicating stimulation of aerobic oxidation in the mitochondria. They found a diminished degree of skeletal muscle injury 48 hours after the ischemic insult which was explained by restoration of energy content, maintaining the transport of ions and molecules across the cell membrane and optimizing the possibilities of preserving the muscle cell structure.

Sufficient oxygen becomes dissolved in plasma while breathing pure oxygen at 240 kPa to meet almost normal tissue oxygen requirements. Under these conditions compromised tissues can stay alive without haemoglobin bound oxygen only by oxygen dissolved in plasma. This effect is important when microcirculation is compromised by stasis of cellular elements restricting red blood cell flow. Oxygenation of the tissues is restored by high levels of plasma dissolved oxygen. (Ten fold increment at 240 kPa).

The consequence of this systemic hyperoxygenation is a threefold increase of diffusion distance of oxygen through the tissues. Thus even cells suffering from ischemia (as result of impairment of the microcirculation) are able to survive. This anti-ischemic effect can prevent further evolution towards tissue necrosis.

Injured but viable cells in the penumbra have increased oxygen needs. At a time when oxygen delivery is decreased by impairment of the microcirculation survival of the cells is directly dependant on oxygen tension. However hyperbaric oxygen therapy can help ischemic tissue to survive only if an effective arterial flow persists in order that oxygen transport to the cells is maintained.

Tissue hypoxia caused by decreased blood flow and thrombosis of microvessels leads to undesirable swelling. If severe oedema occurs the diffusion distance of oxygen from the vessels to the injured area is increased. Both cytogenic and vasogenic oedema results in increased interstitial pressure. Retarded venous outflow along with continued or even increased arterial inflow causes further fluid transudation at the capillary level. Even vessels that are not directly damaged may alter their permeability and contribute to oedema formation and further ischemia. As a result of this secondary injury, tissues completely remote and unaffected by the primary injury are at risk of necrosis.

Compartment syndrome is the classic example of this pathologic process of secondary injury. HBO induces vasoconstriction in hyperoxygenated tissues that reduces blood flow by 20%, leading to oedema reduction16. This effect would seem to be undesirable especially in relative ischemic tissue, but the high oxygen content of the blood flow more than compensates for any blood flow reduction. Since resorption of extracellular fluid continues the net-effect is oedema reduction and improved oxygenation of tissues.

The vasoconstricting effect seems to be induced by direct action of the increased pO2 in blood vessel walls17. In an animal model hyperbaric oxygen reduced the formation of the oedema by approximately 20% in injured muscle tissue18. The anti-oedematic effect explains the efficacy of HBO in compartment syndrome. The oedema reduction in treating compartment syndrome is only effective when HBO therapy is started early. This explains the importance of the time factor in starting HBO therapy after crush injuries.

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