Today’s science bit comes courtesy of our overview document. More specifically the chapter which covers aspects of the above title, but also thanks to the Undersea and Hyperbaric Medical Society (UHMS) themselves, and their article entitled: “Arterial Inefficiencies: Central Retinal Artery Occlusion”.
But before a finger gets pointed for misquoting anyone, the UHMS publication linked at the bottom of this post refers to Central Retinal Artery Occlusion only. This condition is approved by the Food & Drug Administration in the US for treatment with hyperbaric oxygen therapy (HBOT). Its one of the main 14 indications globally accepted for the commissioning of HBOT. Except for in the UK of course. The NHS doesn’t currently commission HBOT for Central Retinal Occlusion. As this article develops however it will become clear as to why this UHMS publication is linked-in and included.
In short, all of the above conditions involve some measure of vascular compromise and subsequent local hypoxia in the central retina which can, and very often does result in permanent loss of sight.
While the pathologies differ somewhat in as much as different blood supplies are affected, and the mechanical cause of this localised lack of oxygen to the retinal tissue differs, the result is the same. Either premature cell death, or cell ischemia. Both leading to potential loss of sight. Certainly in cases of cell death sight is irreparably lost. The same is not always true for ischemia though. It’s the ischemia that is of greatest interest to us.
Contrary to what some HBOT practitioners may advocate, cells which have completely died cannot be saved and cannot be rejuvenated. There is no silver bullet cure here. Don’t be mislead. Ischaemic cells however can be rejuvenated in the eye just as they can be in the brain. Ischemia is defined as follows:
Ischemia or ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive). Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue.
Its dysfunction that interests us. Ischemic cells are not necessarily dead cells but may still be alive, but without sufficient oxygen cannot function in their intended capacity. Not quite alive, but also not quite dead.
This ischemia is present in all of the conditions discussed here. And it is present because of compromised vascularistaion, (blood supply). As we know from previous articles and multiple studies, including studies accepted by the UHMS, HBOT is a powerful upregualtor of angiogenesis, or more simply put, the formation of new blood vessels. (For references see the overview reference section). What better way to restore oxygen supply to an area of compromised blood supply than to grow new blood vessels into the area, or to restore the adequate function of existing blood supplies.
In Ocular Occlusion (retinal vessel occlusion), it is the obstruction of the ophthalmic artery (or vein as the case may be), that causes this interruption in blood (and oxygen supply) to the central retina. In cases of Age Related Macular Degeneration(AMD), specifically wet AMD, or Neovascular AMD as it is medically known, it is the smaller capillaries in the central retina which grow abnormally and begin leaking which causes this problem. Similarly in cases of diabetic retinopathy, the smallest of capillaries in the retina begin to break down as persistently high blood glucose begins to stick to and degrade the internal walls of the capillaries, compromising blood and oxygen delivery to the area resulting in loss of sight and ultimately, blindness. AMD is considered the leading cause of blindness in people aged 55 and over and a great many diabetics who fail to adequately control blood glucose levels throughout their lives.
It is already established by studies, and accepted by the UHMS that Retinal Occlusion can benefit from hyper-oxygenation (HBOT). (See the linked publication below). So it seems superfluous to ‘re-invent the wheel’ so to speak by repeating their findings which can be read by following the link to their website and the publication. The attached publication details how HBOT can restore sight to ischaemic cells, provided those cells have not already been irreparably damaged .
It is our belief that the same can be said for AMD and Diabetic Retinopathy which essentially conclude in the same pathology; Hypoxia in the retina resulting in cell and tissue loss along with sight. Simply, caused by problems further down stream than Ocular Occlusion in vascular terms.
Included below is an excerpt from the Overview which is available for download on the files and resources page. It addresses our hypothesis regarding wet AMD specifically and Diabetic Retinopathy.
We hope to publish case studies in this regard in the future.
Macular Degeneration and Diabetic Retinopathy: Pg 69
Hyperbaric Oxygen Therapy and Treatment
An Overview
Hayden Dunstan
March 2018
Copyright 2018 ©
…Another condition close to my heart is macular degeneration or better described as “Age Related Macular Degeneration (AMD)”. Specifically, the version of this described as Wet (neovascular) AMD. Since this is the more serious of the two kinds I will address this here.
Dry AMD occurs because of a thinning of the macular over time following the build-up of small white or yellowish drusen deposits. Dry AMD occurs in 9 out of 10 AMD sufferers, and can progress to wet AMD over time, however is a slower progressing condition than wet AMD and is perhaps a topic for another discussion.
Wet AMD is an age-related degenerative condition of the central retina and the far more serious of the two with vision loss sometimes occurring in days. The macular area of the central retina begins to exhibit poor capillary quality resulting in leaky vessels forming a lump on the macular as a result of a collection of fluid under the macular epithelium. This fluid leaking from the choroid collects between the choroid and a thin layer called the retinal pigment epithelium. This is what causes loss of vision in the central field. Vision is interfered with by the growing of abnormal blood vessels from the choroid into the macular (choroidal neovascularization). This is the layer of vessels between the retina and the sclera, (outer firm coat of the eye). These abnormal vessels then leak into the macular compromising retinal function. (We’ve discussed leaking fluid where fluid shouldn’t be leaking).
Surely it stands to reason then that, when considering the inflammatory response detailed above, as more fluid leaks into the macular, inflammation perpetuates the inflammatory response cycle and opening of the blood/tissue barrier, further compromising the capillary structures, allowing yet more
fluid to leak, causing cell death or cell ischemia as a result of poor oxygenation of those cells? This reasonably then leads to bacterial infection as well which would of course trigger the deconstruction of those damaged cells by neutrophils.
Further consideration must be given to the argument that as the blood/tissue barrier opens, red blood cells leak out and as the red blood cells degrade in the tissue this causes the iron to breakdown into the worst of the free radicals. Again, resulting in cell death.
A similar end is of concern to diabetics who suffer from diabetic retinopathy. While the pathology causing the damage to capillaries differs in diabetes, the result is largely the same, vision loss and potential blindness. In uncontrolled diabetes, glucose sticks to the internal linings of capillaries damaging them and preventing oxygen transport, this results in leakage also. This is screened annually in diabetics by way of retinal photographic screening which looks for tiny signs of leakage in retinal capillaries. A test I know all too well myself.
The important point of this being, that cells either become ischemic or die completely following fluid leakage from retinal capillaries in both conditions.
This is where HBOT seems paradoxically contra-indicated again. Current treatments make use of drugs called “anti vascular endothelial growth factor” drugs, or “Anti-VEGF” drugs. Drugs such as Avastin and Eylea are routinely used around the world to retard the growth of these abnormal capillaries and close them down, stopping the leakage and halting the progression of the condition.
That’s all very well, fantastic drugs they are, with applications extending into cancer treatment of tumours with a similar anti VEGF function which compromises tumour blood vessel recruitment. But while it may prevent further deterioration, and even regain a little of some patient’s vision, it does nothing to revive cells which haven’t died just yet, i.e. the ischemic cells in the macular, which could very well constitute a considerable share of the affected tissues. It stands to reason then, that before cells die they become ischemic in a low oxygen environment.
As we have discussed, HBOT up-regulates neovascularisation by up-regulating the vascular endothelial growth factor protein (VEGF). Anti-VEGF drugs injected into the eye shut down the local VEGF function preventing further leakage. It seems contrary to suggest that stimulating the VEGF would help. But it may. Because it stimulates healthy growth and normal vessel structures.
Surely it is reasonable to hypothesize that HBOT could stabilise the condition of the capillaries by stimulating the growth of healthy vessels, which replace the unhealthy ones, thus preserving tissue and vision loss. Why shut them down when healthy growth can be restored? Furthermore, it is reasonable to hypothesize that any tissue and cells that haven’t yet died off completely, (ischemic cells and tissues), could be rejuvenated in the presence of healthy blood flow and oxygenation, leading to a restoration of at least some vision. Ischemic cells being described as cells getting enough oxygen to exist as cells, but not necessarily perform the function of cells as they are meant to.
Ischemic tissue rejuvenation is not a new concept. It is the basis for much research into the benefit of HBOT on the brain and degenerative brain conditions as well as mild and traumatic brain injury as studied by, among many others, Dr Shai Efrati at the SAGOL centre for research and hyperbaric medicine in Tel Aviv.
To add an aside to the above paragraphs, the UHMS article below states:
“In CRAO, the inner retinal layers (ganglion cell layer and inner nuclear layer), which are normally served by the retinal circulation, may obtain enough oxygen via diffusion from the choroidal circulation to function normally if the individual is exposed to elevated partial pressures of oxygen.”
This means that oxygen doesn’t strictly need the ophthalmic artery to reach the central retina. An therein, the punchline. Oxygen can diffuse into the retina from other unaffected blood supplies. diffusion also occurs in body fluids other than blood. This diffusion can very likely sustain cells long enough to prevent cell death while new blood vessels grow to restore oxygen to affected areas. It is even conceivable , as implied in the article, that under hyperbaric conditions these cells could become sufficiently oxygenated to function normally during the course of a treatment. Even if only while in the chamber, it would indicate the presence of ischemic cells which are recoverable and could extend the recovery period long enough to sustain these cells while healthy blood flow and oxygen transport is restored. The impact of restoring some, or all sight in ischemic cells while under hyperbaric conditions is nothing less than monumental. Can you imagine? getting even just some of your site back?
The UHMS publication can be found here:
cumbria-hyperbaric.org 
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