Oxygen has been shown to be harmful to many tissues in the body via the formation of oxygen free radicals through normal metabolic processes. The higher PO2 used in hyperbaric oxygen therapy is thought to increase production of these harmful, reactive species. The body has natural defense mechanisms to protect against free radical damage. Superoxide dismutase, a protective enzyme, acts to remove superoxide radicals and other reactive products of metabolism. Under hyperoxic conditions, it is thought that the increased production of these reactive species overwhelms the body's natural defense mechanisms which leads to oxygen toxicity and cellular damage.
The toxic effects of hyperbaric oxygen have damaging effects on the eye, particularly the lens. The most commonly reported symptoms are eyelid twitching, blurry vision, and visual-field disturbances. Many of the reported symptoms have been attributed to oxygen toxicity of the lens which leads to various complications such as myopia and the formation and progression of cataracts. The majority of ocular side effects are reversible, but some of the effects from prolonged therapy can be irreversible.
One of the most commonly observed side effects in patients receiving prolonged hyperbaric oxygen therapy is hyperoxic or hyperbaric myopia. Myopia, or "nearsightedness," is a refractive disorder of the eye. Myopia has two major causes: (1) the axial length of the eye when measured from the posterior cornea to the retina is too long to correctly focus the image, or (2) the refractive power of the lens or the cornea is too powerful. In both cases, the image becomes focused in front of the retina, causing blurry vision. The visual disturbance is more pronounced with distant images. While many cases of myopia are anatomic, acute myopic shifts in vision can have different etiologies. Acute myopic shifts often are seen in hyperosmolar states, medications causing miosis, and ciliary spasm. Myopic shifts also are common in the early stages of cataract development.
Progressive myopic changes to the eye are a complication of repetitive hyperbaric oxygen therapy. The exact mechanism is not fully understood, but it is thought that oxygen toxicity causes changes to the crystalline lens, hardening the lens and increasing its refractive power. The ultimate effect is a myopic shift and blurry vision reported by the patient. Most of the myopic changes are reversible after cessation of therapy. Many studies report this effect lasting from days to months. In a study by Lyne involving 26 patients undergoing hyperbaric therapy at 2.5 atm for greater one month, 18 patients developed myopic changes of 0.5 to 5.5 diopters. Reversal of myopia was rapid within the first few weeks and then progressed more slowly over months up to a year. The patients were examined with pretreatment and follow-up refraction studies, measurement of axial length, keratometry, fundus examination, and tonometry. The results of these examinations revealed no other effects of hyperbaric oxygen therapy and helped suggest that the myopic changes observed were due to changes within the lens.
Another study conducted by Palmquist et al. involved 25 patients with a range of 150-850 daily exposures at 2-2.5atm. Twenty-four out of 25 patients showed myopic changes; however, in this study, other ocular changes were observed. These other changes are discussed in the section regarding cataract formation. This study also showed a possible increase in the risk of irreversible refractive changes if the number of therapies exceeds 100. Normal hyperbaric therapy practiced in the United States utilizes 20 to 50 treatments.
A study conducted by Evanger et al. suggested that increased oxygen delivery across the cornea in addition to arterial circulation may be a major mechanism of the lenticular oxygen toxicity seen in hyperbaric oxygen therapy. This study looked at 20 patients receiving oxygen via hood versus 12 patients receiving oxygen via an oronasal mask. Those receiving oxygen by a hood with greater eye exposure to oxygen showed a higher incidence of myopia, greater refractive changes, and longer recovery time after cessation of therapy. Evidence also suggests that hyperbaric oxygen therapy at higher pressure may increase the incidence and severity of myopia.
Cataract Formation and Progression
Cataract formation and progression is a known but less common complication of hyperbaric oxygen therapy. A cataract is an opacity in the lens of the eye that causes blindness. Major risk factors contributing to cataract formation include increasing age, smoking, alcohol consumption, UV exposure, diabetes, prolonged steroid therapy, and malnutrition. Although exact mechanisms are not fully understood it is believed that cataracts form due to oxidative and toxic insults to the crystalline lens. Cataracts are less likely to form under the normal duration of hyperbaric treatment, but unfortunately, when cataracts do form or progress, the changes to the lens are irreversible and may require lens replacement surgery.
In the study previously mentioned by Palmquist et al., 15 of the patients had clear lenses with no evidence of cataract before therapy. Seven of these 15 patients developed nuclear cataracts with the first evidence appearing at 150 treatments. These changes were not fully reversible after cessation of these prolonged therapies.
It is thought that the formation of new cataracts only occurs in extreme cases of hyperbaric therapy. This is supported by many studies including the study by Lyne, where the patients underwent extensive examinations that revealed no formation of cataracts or progression of existing cataracts after greater than one month of treatments. As mentioned previously, most common hyperbaric regimen used in the United States typically last for a series of 20 to 50 treatments. Beyond normal treatment duration, the risk for permanent lenticular changes, such as cataract formation, increases. One case was an exception to this idea. A 49-year-old woman developed cataracts after only 48 treatment. The woman had no identifiable risk factors for cataract development, such as diabetes, prolonged UV exposure, or steroid therapy. This evidence suggests some patients have predisposing conditions that may contribute to early cataract formation within the normal treatment duration. Hyperbaric cataract formation could be considered a more severe presentation of oxygen toxicity on the same spectrum as the lenticular changes seen in hyperbaric myopia.
During the consent and before hyperbaric treatment has begun, patients should be provided information regarding the risk of temporary myopic changes in vision and permanent cataract formation. While there are no set guidelines, a baseline ophthalmologic exam could be considered to detect preexisting lenticular pathology and monitor the progression of visual disturbances. The examination may be more beneficial to patients at greater risk of cataract formation, such as diabetics, those greater than 50 years old, smokers, patients on steroid therapy, or those with previous radiation exposures.
A baseline examination of visual acuity and progressive monitoring can detect myopic changes. Patients should be made aware that these changes usually are reversible within days to months after cessation of therapy. Depending on the severity of myopia, most patients will not need prescription lenses. Cataract formation, however, is usually permanent and will likely require lens replacement surgery. With the high success rate of cataract surgery, this side effect is considered very manageable. Due to the relatively benign nature and manageability of these side effects, patients who are determined to have a clinical need for hyperbaric oxygen therapy medicine should not discontinue treatment if myopia or cataracts develop.