8 successful has often been aligned with the use of systemic or intravesical agents such as hyaluronic acid, aminocaproic acid, formalin or prostaglandins (14) which often present with limited success . Pathology of CHC and RHC Radiation and cyclophosphamide-induced HC is a severe and potentially life-threatening complication of certain radiation treatment modalities. The management thereof can be highly challenging with well-known urological treatment options and the number of these are expected to increase during the (15) next decades . This is expected to parallel a rise in complications and side effects, such as RHC, oedema, ulceration, neovascularisation, and haemorrhagic necrosis are an acute reaction as an inammatory response in both CHC and RHC causing urothelial damage. Since the 1970s the prophylactic application of Mesna has been applied as a standard protocol for prevention of haemorrhagic complications. Mesna neutralises acrolein and its toxic effects to the urothelium, decreasing CHC urotoxicity (caused directly by renal excretion of acrolein, metabolites of oxazaphosphorine alkylated (15) drugs) . In RHC however, urothelial damage is caused by radiolysis of water. The concentration of highly reactive free oxygen radicals increases which causes cell membrane injury by lipid peroxidation, precipitating immediate cell death. Delayed cell death through replication failures is perpetuated directly (by radiation energy) and indirectly (by (8) oxygen radicals) through DNA damage . This DNA damage is dose related. This acute reaction can escalate with progressive endarteritis and vascular rarefaction (hypovascular) resulting in critical ischaemia with a reduction in oxygen concentration of up to 70-80%. This ischaemia of the mucosal tissue leads to necrosis and shedding of cells because of impaired healing capacity. In this case compensatory teleangiectasia develops and causes persistent haematuria and impaired bladder (17,18) capacity through brotic repair . These processes can occur as late as 20 years post-radiation (19) therapy . Hyperbaric Oxygen Therapy Hyperbaric oxygen therapy (HBOT) is a wellestablished treatment for several validated conditions (13 Class A evidence). Hyperbaric oxygen therapy is performed in a hyperbaric chamber, which increases and maintains the atmosphere absolute (ATA) pressure as the chamber is pressurised with either pure 100% oxygen (monoplace chamber) or air (multiplace chamber). The pressure may vary between centres but is usually only effective from 2.4 ATA. For most on label treatments, patients lie in the hyperbaric chamber daily (5-6 days a week), for a duration of 60 to 90minutes for up to 30 to 45 sessions. Studies on the indications of HBOT have demonstrated positive effects in the treatment of hypoxia, oxidative stress, inammation-induced brain damage, stroke, Alzheimer's disease, and chronic (15) Lyme disease, and cancer complications . Monoplace chambers deliver oxygen to the patient's tissues utilising the respiratory and vascular systems through direct breathing of 100% volume concentration (v/v) of oxygen used to pressurise the chamber. Multiplace chambers, pressurised with air (21% v/v) deliver 100% v/v oxygen to the patient's tissues through the respiratory and vascular systems via a breathing aid such as a mask or hood. In addition to the gas concentration of the chamber, the temperature and humidity are managed in accordance to the change in pressure in the chamber (when the pressure rises, the temperature and humidity also rise). It is therefore important for the chamber operator to measure the changing pressure and maintain the temperature and humidity. The only disadvantage of HBOT may be the logistical difculties of a patient attending a hospital or centre with South African Undersea and Hyperbaric Medicine Association (SAUHMA) registered pressured (16,17,18,19) oxygen chamber on a daily basis . The Effect Hyperbaric Oxygen on Irradiated Tissues Hyperbaric oxygen therapy (HBOT) is a promising but still extremely under-utilised treatment option for patients suffering with RHC, CHC and HC in whom standard management has proven unsuccessful. A cause and consistent manifestation of radiation injury (24,25) is vascular obliteration and stromal brosis . Stimulating angiogenesis is an important mechanism of HBOT which makes this an effective treatment modality for radiation injury. Hyperbaric Oxygen therapy induces neovascularization in hypoxic tissues(20) and has been proven to enhance vascularity and cellularity in heavily radiated tissues(21). The use of HBOT for radiation cystitis is based on the fact that radiation causes cellular hypoxia of the bladder tissues. With the administration of 100% v/v oxygen under high pressures, the pathophysiology of radiation cystitis can be reversed. As an indirect demonstration of vascular improvement, it has been demonstrated that HBOT patients often demonstrate an increase in transcutaneous oxygen measurements as well as (22) increased vascular density . Since HBOT has been proven to be cancer neutral, it was proven that prophylactic HBOT can also reduce the effect of brosis through pre-radiation injury application(23, 24, 25). Hyperbaric oxygen therapy has been demonstrated to induce broblast proliferation, neovascularisation and therefore angiogenesis, granulation tissue formation, and optimisation of the (17,18,19) cellular immune functions Tissue oxygenation occurs principally via diffusion of oxygen from the capillaries. The application of as little as 2.4 ATA (1 ATA sea level + 1.4 ATA / 13-15 meters of sea water (MSW)) has been proven to increase dissolved oxygen in the plasma. At 2.4 ATA this is a 1015-fold increase in O2 available to the tissues promoting capillary angiogenesis thus increasing the regeneration of damaged urothelium with success (26,27,28,29) rates of 73 to 96% . The increase in the pO2, encourages and mediates the repair processes of macrophages, broblasts and granulocytes, as well as induces neo-angiogenesis, achieving 80% of the UROLOGY, URO-ONCOLOGY AND SEXOLOGY UPDATE
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