London Hyperbaric

In all of these conditions trauma causes tissue damage, hypoxia and oedema. Secondary effects, which damage tissue, include stasis in the microcirculation, reperfusion injury and infection, all of which can result in non-healing. It is worth noting that during the early phases of healing tissue metabolic demand can increase by a factor of over 20.

Following the primary insult, reperfusion of the tissue will occur, at this stage the first oxygen available is converted into oxygen free radicals, which are generated from neutrophils sequestrated on the capillary endothelium. These oxygen free radicals cause damage to the venules which results in low blood flow to the site of injury. Reperfusion also causes arteriole vasodilatation followed by vasoconstriction which again results in low blood flow to the site of injury.

Role of HBO:

HBO causes hyperoxygenation by dissolving oxygen in the plasma. At 2.4 ATA sufficient oxygen is dissolved in plasma to meet resting tissue oxygen requirements. When there is stasis of the microcirculation such as in ATPI, haemoglobin-borne oxygen cannot flow through the microcirculation however plasma will continue to flow and the oxygen dissolved in plasma will remain available to the tissue. HBO also causes vasoconstriction, which can reduce bleeding in the damaged area of tissue and reduce oedema. As the oedema reduces the microcirculation will improve. Further benefits of HBO include maintaining the tissue oxygen tensions at levels where tissues are able to heal (>30mmHg) and inhibiting the growth of anaerobic bacteria and slowing the growth of other organisms (e.g streptococci, pneumococci, candida and mycobacteria).

See other sections on the individual conditions for more information.