Hyperbaric oxygen (HBO) therapy is used in the treatment of a number of medical conditions, including decompression sickness, carbon monoxide poisoning, arterial gas embolism, anaerobic infections, and other disorders characterized by local ischemia. The patient breathes 100% oxygen at a pressure of 200 to 240 kPa in a hyperbaric chamber. HBO therapy has been shown to stimulate growth of capillaries, fibroblast proliferation, and collagen synthesis in ischemic tissue.
Temporary refractive changes toward increased myopia or reduced hypermetropia is a frequently reported ocular side effect in patients undergoing prolonged periods of daily HBO therapy. We present an atypical case in which a hypermetropic shift followed the myopic shift in a patient after each of two series of hyperbaric oxygen exposures.
DISCUSSION
A myopic shift is commonly described in HBO-treated patients. The myopic shift found in this patient was within the range of collated data from other patients treated with a standard HBO therapy protocol. After cessation of the hyperbaric oxygen exposure, the myopic shifts tend to revert to baseline values. Recently, a temporary hypermetropia (+2.00 D) was observed as an initial phenomenon in a single patient who recovered by 8 to 9 weeks after completed treatment. The patient in our case report showed relatively slow changes in refraction and terminated with a longlasting low-level hypermetropia, which is difficult to explain on an osmotic basis.
Sufficient changes in central corneal power, anterior chamber depth, and axial length of the eye or accommodative tonus have not been found to explain the degree of ocular refractive changes in HBO-treated patients. Although the exact mechanism remains obscure, the myopic shift has been attributed to refractive index change within the crystalline lens. Ultrasonographic measurements showed no change in total lens thickness.
Oxidative stress has been proposed to cause an aggregation of proteins in the lens nucleus with an implication of increased refractive index and a consequent myopic shift. Some support for this notion has been provided from studies on guinea pig lenses: in vivo treatment with HBO resulted in a decrease in the water-soluble and an increase in the insoluble protein proportion. However, it should be noted that increases in insoluble protein on extraction may not necessarily represent increased aggregation in the intact lens, because high levels of water-insoluble protein have been found in clear bovine lenses. The relatively high level of insoluble proteins extracted from older lenses is more likely to reflect an age-related increase in aggregation on extraction, because older proteins may be more vulnerable to abrupt changes in their immediate environment.
A manifestation of protein aggregation in the intact lens is opacification or loss of clarity and this has been reported after HBO treatment in human and guinea pig lenses. Recently, a study conducted by Bantseev et al. showed that HBO treatment of guinea pig lenses results in a decrease in sharp focusing of laser rays. This may result in a loss of optical quality but should not necessarily be interpreted as an increase in light scatter if, like in Bantseev et al.'s findings, all rays that are traced through the lens cross the optic axis at some point. Furthermore, results from guinea pig lenses may not reflect the situation in the human lens, because the former contains [zeta]-crystallin, a protein not found in its human counterpart.
If indeed, the refractive changes after HBO treatment are attributable to changes in the lens proteins, it is not clear how this may occur. The total amount of protein in the lens must remain the same so there cannot be any overall reduction or increase in protein concentration. Any change in response to HBO therapy would therefore have to relate to how the proteins and water interact and/or in their respective distributions. This would result in a change in the refractive index within the lens. Whether this change affects the entire lens or is restricted to cortical or nuclear regions is not known. The refractive index in the lens is relatively constant in the nuclear region and manifests as a gradient in the cortex. To contribute to the refractive shifts reported in this study, maximal amplitude of 3.00 D (range –1.37 D to +1.62 D) in the right eye and 2.75 D (range –1.25 D to +1.50 D) in the left eye, the fluctuation in nuclear refractive index would need to be around ±0.005 for nuclear refractive indices of 1.401 to 1.411. This would, according to the Gladstone-Dale formula, equate to changes in local protein concentration of around 3 mg. Given that there can be no overall loss or gain of protein but only a redistribution of protein and water in localized regions, these calculated values would be very likely to manifest as opacities by slit lamp examinations.
Because no such reduction in the clarity of the lens nucleus was found, any changes to the structure of the lens were most likely to have occurred in the cortex. A change in cortical refractive index would not require an overall increase or decrease in magnitude, but only very slight changes in the gradient sufficient to alter the refractive power to a measurable degree.
The underlying causes for the refractive changes reported in this study are not clear, and it is not possible to reach any conclusions from a single case. The long-term low hyperopic shift may simply be reflecting a progression that would have occurred without HBO therapy, because such changes in presbyopes are not uncommon. However, this is the first reported case in which a hypermetropic shift has immediately succeeded a myopic shift in a patient after each of two series of HBO treatments. Any explanation needs to take into account that significant increases and decreases in ocular refractive power can occur in patients treated with a standard HBO therapy protocol without causing clinically detectable loss of lens transparency or reduction in best-corrected visual acuity.
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