Introduction
Hyperbaric oxygen therapy (HBOT) is a medical treatment in which a person breathes nearly 100% oxygen inside a pressurized chamber (usually 1.5–3 times normal atmospheric pressure). This increases the amount of dissolved oxygen in the blood and tissues (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). HBOT has approved uses (like treating carbon monoxide poisoning or wound healing) and experimental uses in eye diseases, but its effects on glaucoma (a disease of the optic nerve) are not well established. Glaucoma involves progressive loss of retinal ganglion cells (the nerve cells in the back of the eye) and their axons, often associated with high eye pressure or poor blood flow (pmc.ncbi.nlm.nih.gov). In theory, raising oxygen levels in the retina and optic nerve head could help cells survive stress, but excess oxygen can also cause harm. This article explores how HBOT changes eye oxygen levels, blood flow, and cellular metabolism, and what that might mean for glaucoma – weighing the potential benefits and risks.
HBOT and Oxygen in the Eye
The retina (nerve layer lining the back of the eye) is extremely active metabolically and needs a lot of oxygen (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Under normal conditions, the inner retina (including ganglion cells) gets oxygen from the small retinal arteries, while the outer retina (photoreceptors) gets it from the choroid (a dense layer of blood vessels beneath the retina). When someone undergoes HBOT, the air they breathe has very high oxygen partial pressure. This dramatically increases the oxygen carried by the blood and dissolved in the eye’s fluids (pmc.ncbi.nlm.nih.gov). For example, HBOT can saturate the vitreous gel (inside the eye) and even replace nitrogen with oxygen, so that oxygen levels in the eye remain elevated for hours (pmc.ncbi.nlm.nih.gov). One review notes that “tissue oxygen level has been observed to remain high for up to 4 hours after therapy” (pmc.ncbi.nlm.nih.gov). In effect, the eye has an unusually large oxygen reserve.
For glaucoma, higher oxygen in the optic nerve head and retina might influence cell survival. In an oxygen-rich environment, cells may make more energy (ATP) via their mitochondria and resist low-oxygen damage. In animal models, HBOT has been shown to protect injured retinal neurons from programmed cell death (pmc.ncbi.nlm.nih.gov). By enhancing the diffusion of oxygen from the choroid into the deep retina, HBOT could especially help regions suffering poor blood flow (pmc.ncbi.nlm.nih.gov). However, these ideas are theoretical for glaucoma. The typical goal is that extra oxygen might “rescue” stressed ganglion cells. That said, oxygen also reacts in tissues: high oxygen can generate reactive oxygen species (ROS), which can damage cells if overwhelming. Thus, HBOT in the eye is a balance – it may relieve hypoxia, but also carries a risk of oxidative injury (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov).
Retinal Ganglion Cell Bioenergetics and Hyperoxia
Retinal ganglion cells (RGCs) are highly energy-demanding neurons. They rely on their mitochondria to perform oxidative phosphorylation (using oxygen to make ATP). During normal oxygen levels, mitochondria in RGCs generate most of the needed cellular energy. If oxygen is low (hypoxia), cells must switch to less efficient processes (glycolysis) and may starve for energy (pmc.ncbi.nlm.nih.gov). In glaucoma, one factor leading to RGC damage is thought to be poor oxygen supply (due to high eye pressure or vascular dysregulation), causing chronic low-oxygen stress (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Studies in experimental glaucoma show that RGCs exhibit signs of hypoxia (low oxygen) and energy impairment before they die (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov).
Breathing high oxygen through HBOT could boost the cells’ energy supply: with more oxygen available, mitochondria could produce more ATP and support normal axonal transport (the process that RGCs use to move materials up and down their long fibers). By helping RGCs meet their energy needs, hyperoxia might theoretically slow down glial stress pathways. Indeed, HBOT has been reported to improve survival of retinal ganglion cells in animal optic nerve injury models (pmc.ncbi.nlm.nih.gov). In practice, more oxygen can mean better cellular metabolism. For instance, supplemental oxygen after acute blockage of retinal arteries restored oxygen metabolism in animal studies (pmc.ncbi.nlm.nih.gov).
However, there is a flip side. Mitochondria also produce reactive oxygen species as a by-product of energy production. Excess oxygen can increase ROS formation (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Too much ROS can damage mitochondrial DNA and proteins, leading to oxidative stress. In glaucoma, oxidative damage is already suspected to harm both trabecular meshwork cells (eye’s drainage) and RGCs (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Thus, HBOT could conceivably add to that stress in susceptible eyes. One review cautions that “HBOT exposes the eye to increased oxygen concentration and the risk of oxidative damage”, especially if oxygen reaches the front of the eye (pmc.ncbi.nlm.nih.gov).
In summary, from a bioenergetics viewpoint HBOT may give RGCs more oxygen to make energy (a potential benefit), but may also raise oxidative stress (a potential risk) (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). The net effect likely depends on the individual balance of oxygen need versus antioxidant defenses.
Blood Flow and Vasoconstriction Effects
A major response of blood vessels to high oxygen levels is vasoconstriction. When retinal arteries sense elevated oxygen, they tend to narrow. This is a normal autoregulatory mechanism: if less blood flow is needed (because there is plenty of oxygen), the vessels tighten. Studies have shown that breathing pure oxygen causes retinal blood flow to decrease (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). For example, one report found “in the first 10 minutes after initiating HBOT, there is a considerable reduction in blood flow” in the retinal circulation (pmc.ncbi.nlm.nih.gov). Shortly after HBOT ends, vessels re-dilate (often due to a surge in nitric oxide) and flow returns to normal (pmc.ncbi.nlm.nih.gov).
How might this affect glaucoma? On one hand, lower blood flow could mean less fresh blood coming to the retina and optic nerve (a potential worry). On the other hand, because blood is now packed with more oxygen, the total oxygen delivery may still improve. Indeed, studies in ischemic retina models show that despite vasoconstriction, oxygen delivery (DO₂) and even metabolism (MO₂) can recover under hyperoxia (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). For example, in rats with blocked carotid arteries (reducing blood to the eye), a short burst of 100% oxygen restored inner retinal metabolism to near-normal (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov).
The choroid (the thick vascular layer under the retina) behaves differently under hyperoxia. Unlike retinal vessels, the choroid lacks strong oxygen autoregulation (pmc.ncbi.nlm.nih.gov). High oxygen does not strongly constrict choroidal vessels. In fact, choroidal blood continues to supply a steady flow of oxygen. During HBOT, extra oxygen dissolves in the choroidal blood, elevating oxygen levels that can diffuse into the retina (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). In practical terms, the retina may receive more oxygen from the choroid when retinal vessels constrict. One study notes that increased oxygen in under-perfused retinal regions (thanks to diffusion from the choroid) can improve retinal health, while the accompanying retinal vasoconstriction helps prevent fluid leakage and edema (pmc.ncbi.nlm.nih.gov).
Overall, the vasoconstriction effect of HBOT on the eye may reduce blood flow but simultaneously deliver more oxygen per blood unit. The net impact on glaucoma patients is not fully known. On one hand, less blood flow could be problematic if perfusion was already marginal. On the other, the reduced flow may lessen swelling and the extra oxygen might meet metabolic needs. Degree of perfusion pressure is also key: if intraocular pressure is high in glaucoma, even a small drop in blood flow could risk ischemia. These factors must be carefully weighed.
Intraocular Pressure and Translaminar Gradient
Intraocular pressure (IOP) is the fluid pressure inside the eye. Since glaucoma risk is tightly linked to IOP, it’s natural to ask: does HBOT change IOP? A human study did measure IOP during HBOT at 2.5 atmospheres. The finding: IOP dropped slightly during treatment and then returned to normal afterwards (www.researchgate.net). On average, pressure fell by about 2 mmHg in patients breathing 100% oxygen at 2.5 ATA (www.researchgate.net). This change was statistically significant but small. In healthy eyes, such a minor decrease is not clinically important (www.researchgate.net). No dramatic pressure spikes were reported. In practice, routine HBOT is not known to raise IOP. In fact, breathing oxygen (even at normal pressure) tends to lower IOP in many studies. Thus, HBOT would likely not worsen IOP; it might even transiently ease it.
Beyond IOP, glaucoma damage also depends on the translaminar pressure gradient – the difference between IOP (pressing outward on the optic nerve head) and the pressure behind the eye (typically cerebrospinal fluid pressure in the brain). If this gradient is high, more mechanical strain is placed on the delicate lamina cribrosa where the optic nerve fibers exit the eye. Hyperbaric conditions could alter this gradient in complex ways. For example, increasing ambient pressure (as in HBOT) tends to raise pressure everywhere in the body. This may raise venous and intracranial pressure. In a recent imaging study of healthy humans at 2.4 ATA, retinal and choroidal layers thickened, likely reflecting elevated intracranial venous pressure and reduced outflow (pmc.ncbi.nlm.nih.gov). If intracranial or orbital venous pressure goes up during HBOT, the pressure behind the eye might increase. Meanwhile IOP itself fell slightly (www.researchgate.net). Thus, the translaminar gradient (IOP minus brain pressure) might actually decrease. In theory, a smaller pressure difference across the lamina cribrosa could ease mechanical stress on optic nerve fibers.
However, the picture is nuanced. Elevated venous/brain pressure might also cause venous congestion at the back of the eye, as the study observed (pmc.ncbi.nlm.nih.gov). The lamina cribrosa is a sieve-like structure supporting the nerve fibers. If outside pressure rises (blood or cerebrospinal), it could deform the lamina differently than high IOP would. We have little direct data on how HBOT affects lamina biomechanics. It is plausible that HBOT might in some ways relieve lamina strain (due to reduced gradient), but it might also introduce other stresses (e.g. increased venous pressure against the nerve head). Until studied, the effect on glaucomatous damage from this mechanism remains speculative.
Potential Benefits and Risks
Putting it all together, HBOT may have both pros and cons for glaucoma:
-
Possible Benefits: HBOT could improve oxygen supply to retinal ganglion cells and the optic nerve head, potentially supporting their metabolism when blood flow is compromised (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). In eye conditions like acute retinal ischemia, HBOT has restored visual function when given promptly (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). By analogy, more oxygen might slow neurodegeneration in glaucoma by reducing chronic hypoxic stress. The transient IOP reduction seen in HBOT (www.researchgate.net) might also slightly unburden the optic nerve. In healthy volunteers, HBOT caused only mild, temporary changes in eye structure, suggesting it can be tolerated physiologically (www.researchgate.net) (pmc.ncbi.nlm.nih.gov).
-
Potential Risks: Extra oxygen comes with oxidative stress. Reviews warn that high oxygen levels in the eye angle could harm the trabecular meshwork (the tissue draining eye fluid) and promote damage (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). In practice, oxidative stress from HBOT might worsen glaucoma in susceptible individuals (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Other documented ocular side-effects of HBOT (though rare) include reversible nearsightedness (myopia) and lens changes. For example, patients often develop a transient myopic shift after multiple sessions, and prolonged HBOT has been linked to cataract formation (www.researchgate.net). The 2025 dive-study also found that hyperbaric exposure can thicken the choroid and inner retina (pmc.ncbi.nlm.nih.gov), hinting at possible fluid shifts that could affect vision. All treatments for glaucoma must be used with caution. In fact, experts recommend caution if a glaucoma patient ever needs HBOT for other reasons – monitoring should be strict (pmc.ncbi.nlm.nih.gov).
A balanced framework is needed. On one hand, HBOT conceptually could help by correcting oxygen deficits in the optic nerve. On the other hand, it could add oxidative injury or vascular stress. Currently, there is no solid clinical evidence that HBOT treats glaucoma; its use would be off-label and experimental. (pmc.ncbi.nlm.nih.gov) (pmc.ncbi.nlm.nih.gov). Given the lack of definitive studies, any benefit remains a hypothesis. Importantly, if considered at all, HBOT should be approached cautiously in glaucoma patients, with careful eye monitoring.
Conclusion
Hyperbaric oxygen therapy profoundly raises the oxygen levels in the eye, which can boost tissue metabolism but also trigger blood-vessel changes and oxidative stress. These effects have clear theoretical implications for glaucoma: better oxygen might support ganglion cell energy production, but guarding against oxidative damage and blood flow reduction is crucial. High ambient pressure can also alter the fluid pressures across the optic nerve head (translaminar gradient), potentially reducing mechanical load but possibly causing venous congestion. In summary, HBOT’s influence on glaucoma is biologically plausible but uncertain. It presents a mix of hypothesized benefits (improved nerve oxygenation, slight pressure relief) and risks (oxidative injury, drainage impairment, vascular strain). Until research clarifies this balance, HBOT cannot be recommended for glaucoma. Any consideration would require careful weighing of patient-specific factors and vigilant monitoring.