Introduction

Cataract is the clouding of the lens of the eye that results in loss of visual acuity, often progressing to incapacitating blindness. Nuclear cataracts of old age (affecting the central part of the lens) are the most common type of cataract. Hyperbaric oxygen therapy (HBOT) is the administration of 100% oxygen at pressures greater than one-atmosphere absolute pressure (1 ATA) for a therapeutic purpose. HBOT thus involves a patient being confined within an air-tight vessel and compressed to pressures above ambient and the administration of 100% oxygen to breathe. Oxygen may be supplied through compression in a 100% oxygen environment (most often in a monoplace chamber) or the use of an oxygen delivery system (usually a mask or a hood) delivered in a larger multiplace chamber. There are potential side-effects of HBOT, one of which is the development of cataracts. This is a rare event, but may be both unrecognized and under-reported. The cause of cataract remains to be fully elucidated, but evidence is emerging that points to one major precipitating factor: the lifetime exposure to oxygen, particularly the increased partial pressure of oxygen that reaches the lens as the vitreous humor deteriorates with increasing age.[1][1][2]

The development of both nuclear cataracts and a reversible myopic shift in hyperbaric patients strongly suggests that oxidative damage to lens proteins is responsible. In an experiment using guinea pigs exposed to hyperbaric oxygen, the average apparent diameter of proteins in the nucleus of lenses in HBO-treated animals was nearly twice that of the control animals and was similar to the of aggregates found in human nuclear cataracts. The authors concluded that molecular oxygen in vivo could induce the cross-linking of lens nuclear crystallins into large disulfide-bonded aggregates capable of scattering light. A similar process may be involved in the formation of human nuclear cataracts, and may be the end-stage of the much more commonly described "myopic shift" that is detectable in the majority of hyperbaric patients who have a course of 20 to 30 treatments.[4][3]

Etiology

The cause of cataract remains to be fully elucidated, but the evidence is emerging that one major precipitating factor is the lifetime exposure to oxygen, and in particular the increased partial pressure of oxygen that reaches the lens as the vitreous humor deteriorates with increasing age. The development of both nuclear cataracts and a reversible myopic shift in hyperbaric patients strongly suggests that oxidative damage to lens proteins is responsible. In an experiment using guinea pigs exposed to hyperbaric oxygen, the average apparent diameter of proteins in the nucleus of lenses in HBO-treated animals was nearly twice that of the control animals and was similar to the of aggregates found in human nuclear cataracts. The authors concluded that molecular oxygen in vivo could induce the cross-linking of lens nuclear crystallins into large disulfide-bonded aggregates capable of scattering light. A similar process may be involved in the formation of human nuclear cataract.[4][5]

Epidemiology

Numerous clinical reports describe the development of reversible myopia during a course of HBOT, but the development of irreversible changes in the form of cataract is rarely reported and usually after prolonged exposure (> 100 treatment sessions). A yet to be published randomized trial investigating myopic shift in patients given oxygen in a hood versus a mask (Bennett) will incidentally report the development of nuclear cataract in approximately 2% of 120 patients treated with 20 to 40 exposures, suggesting the true incidence of cataract may be under-recognized. A likely reason is that in many patients the myopic shift may persist for many weeks and a failure to resolve may be missed by the hyperbaric team, with the diagnosis of cataract only made much later. Informally, there is a wide belief that a course of HBOT will lead to more rapid maturing of an early cataract present before treatment.

Pathophysiology

Nuclear cataracts are the product of changes in the lens proteins known as crystallins. Evidence is emerging that these changes are likely due to the effect of oxidative damage, probably through a nitric oxide-mediated pathway. Cataracts can be thought of as a chronic oxidative injury of aging. The changes in crystallins alter the lens' ability to refract light and therefore decrease visual acuity. This general view of the pathophysiology of nuclear cataract is concordant with the increase in myopic changes and cataracts reported in relation to hyperbaric oxygen.

History and Physical

The routine assessment of hyperbaric patients will include taking an ocular history and, in particular, any history of cataract or deterioration in visual acuity. An assessment of visual acuity should be made before commencing a course of hyperbaric oxygen therapy and at the completion of that course, even in the absence of complaints of visual disturbance. Interim examinations and referral for specialist assessment may be appropriate in response to complaints of deteriorating vision or a failure of a myopic shift to resolve over eight to ten weeks after completion of a course of hyperbaric oxygen. Formal ocular refraction will pick up changes in lens opacity that may assist in planning further treatment in the future. On examination, the lens may appear cloudy or yellowish with established cataract, but in the context of hyperbaric oxygen, the gross appearance of the lens may be normal.

Evaluation

While some authorities advocate formal refraction and visual acuity testing by an optometrist, the more usual practice is for simple measurement of visual acuity using a Snellen chart or similar tool before commencing HBOT, followed by repeated testing at the end of therapy or if there are any complaints of worsening vision during treatment. The formal diagnosis of cataract is diminishingly rare during or in the weeks following the completion of a course of HBOT but should be borne in mind if the myopic shift associated with HBOT does not resolve within two to three months of treatment. All patients should be warned that the late development of cataract is a known but rare complication of HBOT.

Treatment / Management

Myopic shift should be treated expectantly following the cessation of HBO. During this time, temporary spectacles will assist in daily living. If changes are pronounced, early referral for further examination is justified. If visual acuity is not improving after 10 to 12 weeks, formal assessment of the eye may reveal the presence of a cataract. If present, these will require extraction and replacement with an intraocular lens as for other causes of cataract, at the discretion of an ophthalmic surgeon. Patients assessed before commencing HBOT should be forewarned of the high possibility of myopic shifts and the possibility of developing cataracts. Patients with early cataracts should be warned these are likely to progress more rapidly during and after HBOT.[6][7][8]

Differential Diagnosis

Deterioration in visual acuity during a course of HBOT should be evaluated thoroughly and consideration given to alternative causes. In particular, a history of a sudden reduction in acuity over minutes or hours should be treated as an emergency and the more common causes of acute blindness excluded by referral to an ophthalmologist. Such causes include retinal arterial or venous occlusion, cerebral stroke, retinal detachment, and vitreous hemorrhage.

Enhancing Healthcare Team Outcomes

There have been reports that HBO therapy may induce cataract formation.This may be true after chronic therapy but there is no evidence that a single session of HBO can affect vision. Patients who undergo multiple HBO treatments and complain of visual changes persisting for more than two to three months after completion of the HBO course, should be seen by an ophthalmologist to assess vision and diagnose the cause of any impairment.