Hyperbaric Oxygen Therapy and Associated Cataracts

Etiology

The exact cause of cataracts is not fully understood and is believed to be influenced by multiple factors. As individuals age, the lens undergoes changes, and patients experience increased amounts of oxidative damage to the lens over time.

• The weight and thickness of the lens increase, accompanied by a reduction in its accommodative power.

• Nuclear sclerosis occurs as new cortical layers are added, leading to the compression and hardening of the central nucleus.

• The diminished transparency of the lens is attributed to a decrease in lens epithelial cell density and aberrant differentiation of lens fiber cells.

• The rate at which water and potentially water-soluble low-molecular-weight metabolites can enter the cells of the lens nucleus via the epithelium and cortex decreases, leading to a subsequent reduction in the transport rate of water, nutrients, and antioxidants.

• Recent evidence suggests that the lifetime exposure to oxygen, and, particularly, the increased partial pressure of oxygen that reaches the lens with increasing age, are significant contributing factors to the development of cataracts. The patients undergoing HBOT develop nuclear cataracts and a reversible myopic shift, which suggests oxidative damage to lens proteins.

Factors that increase the risk of developing cataracts include increasing age, smoking, alcohol consumption, ultraviolet exposure, diabetes, prolonged steroid therapy, and malnutrition. 

Epidemiology

Numerous clinical reports describe the development of reversible myopia during a course of HBOT. Approximately 75% of patients experience this change.[5] The myopic shift appears more pronounced using a hood system than an oronasal mask.[5] Irreversible cataract changes are rarely reported, and when they are, they usually manifest after prolonged exposure to more than 100 treatment sessions. In a study involving 25 patients undergoing 150 or more hyperbaric treatments, 7 out of the 15 individuals with initially clear lenses developed cataracts. Notably, all 25 patients experienced transient myopia, as expected.[6]  Although this series involves an unusually high number of treatments, another study in which subjects only receive a more typical 40 treatments still reveals mild lens opacification changes.[7]

An ongoing randomized trial, not yet published, examining myopic shift in patients administered oxygen through a hood versus a mask will incidentally report the development of nuclear cataracts in approximately 2% of the 120 patients treated with 20 to 40 exposures. This implies that the actual incidence of cataracts may be underestimated. One potential explanation is that the myopic shift in many patients may endure for several weeks, and the failure to resolve may be overlooked by the hyperbaric treatment. Consequently, the diagnosis of cataracts may only be established much later. In addition, an informal belief exists that a course of HBOT could accelerate the maturation of an early cataract that was already present before the initiation of treatment.

Pathophysiology

Nuclear cataracts result from changes in the lens proteins called crystalline. Emerging evidence suggests that these changes likely result from oxidative damage, which nitric oxide pathways could mediate. Notably, the lens cannot eliminate its nonviable cells. These cells continue to compress into the center of the lens and begin to lose their transparency. The modifications in crystalline structures affect the lens's capacity to refract light, thereby decreasing visual acuity. This overall understanding of the pathophysiology of nuclear cataracts aligns with the observed increase in myopic changes and cataracts related to hyperbaric oxygen.

Toxicokinetics

An experiment in guinea pigs illustrates that hyperbaric oxygen induces the cross-linking of lens nuclear crystallins into substantial disulfide-bonded aggregates capable of scattering light. A similar process may be involved in the formation of human nuclear cataracts.[3]  

History and Physical

The routine assessment of patients undergoing HBOT includes obtaining an ocular history, specifically focusing on any history of cataracts or deterioration in visual acuity. Individuals with cataracts typically report a gradual decline in visual acuity and challenges with night and near vision. Key symptoms include reduced visual acuity, glare sensitivity in well-lit environments, and myopic shift due to cataract progression. Moreover, individuals may encounter monocular diplopia attributed to nuclear changes in the lens, resulting in a "lens within a lens" phenomenon. This diplopia is often uncorrectable with spectacles, prisms, or contact lenses.

Clinicians should assess visual acuity before initiating a course of HBOT and repeat the assessment after therapy, even without reported visual disturbances. Interim examinations and referral for specialist assessment may be warranted if patients complain of deteriorating vision or if a myopic shift persists 10 to 12 weeks after HBOT. A formal ocular refraction can detect changes in lens opacity, aiding in future treatment planning. An established cataract may present as a cloudy or yellowish lens during examination. However, in the context of hyperbaric oxygen, the gross appearance of the lens may appear normal despite potential underlying changes.

Evaluation

Although some authorities recommend formal refraction and visual acuity testing by an ophthalmologist, more often, patients undergo a simple measurement of visual acuity using a Snellen chart or similar tool before commencing HBOT. This is followed by repeated testing at the end of therapy or in the presence of visual complaints during treatment. Symptomatic patients undergo a nondilated fundal examination, which may reveal darkening, opacities, or obscuration within the red reflex. A more comprehensive ophthalmic examination is then conducted to assess the type and extent of lens opacity. Furthermore, a dilated fundus examination is performed to exclude other pathologies contributing to reduced vision or impede complete vision restoration after cataract surgery.

Formally diagnosing cataracts is exceedingly uncommon during or in the weeks following the completion of HBOT. However, clinicians should consider the possibility of cataracts if the myopic shift associated with HBOT persists beyond 2 to 3 months of treatment. Notably, all patients need to be aware that the late development of cataracts is a recognized but rare complication of HBOT.

Treatment / Management

The myopic shift following the cessation of HBOT should be managed expectantly. Temporary spectacles can be used to assist with daily activities during this period. If the changes are significant, an early referral for further examination is warranted. If visual acuity does not show improvement after 10 to 12 weeks, a thorough eye examination may reveal the presence of a cataract. Cataract extraction and replacement with an intraocular lens will be necessary in such cases. Before starting HBOT, healthcare professionals should inform patients about the possibility of experiencing myopic shifts and the potential development of cataracts. Patients with early cataracts should be aware that these may likely progress more rapidly during and after HBOT.[8][9][10](B3)

Differential Diagnosis

Clinicians should conduct a comprehensive evaluation during HBOT to explore alternative causes of visual acuity deterioration. Notably, a history of sudden acuity reduction within minutes or hours constitutes an ocular emergency. An ophthalmologist should rule out more prevalent causes of acute blindness, including retinal arterial occlusion, retinal venous occlusion, cerebral stroke, retinal detachment, and vitreous hemorrhage.

Complications

Complications arising from HBOT-induced cataracts primarily pertain to surgical challenges associated with lens replacement. The risk of uveitis and infectious and noninfectious endophthalmitis exist immediately postoperatively and during the delayed postoperative period.

Intraoperative Complications 

Intraoperative complications may include a shallow or flat anterior chamber, capsular rupture, suprachoroidal hemorrhage or effusion, expulsive choroidal hemorrhage, retained lens material, vitreous disruption, and incarceration into the wound, iridodialysis, and retinal light toxicity.

Immediate Postoperative Complications

Immediate postoperative complications include acute endophthalmitis, intraocular lens displacement or malposition, corneal and macular edema, toxic anterior segment syndrome, and hemorrhagic occlusive retinal vasculitis due to intraocular vancomycin use.

Notably, using vancomycin as prophylaxis against endophthalmitis in cataract surgery is generally not recommended. Additional complications may include a flat or shallow anterior chamber due to wound leak, choroidal detachment, pupillary and ciliary block, suprachoroidal hemorrhage, stromal and epithelial edema, hypotony, Brown-McLean syndrome, vitreocorneal adherence, delayed choroidal hemorrhage, hyphema, elevated intraocular pressure, and uveitis-glaucoma-hyphema syndrome.

Potential Late Postoperative Complications 

Potential late postoperative complications may include suture-induced astigmatism, retinal detachment, posterior capsule opacification, macular degeneration, pupillary capture, decentration, iris atrophy, chronic uveitis, chronic endophthalmitis, and the use of an incorrect power of intraocular lens.