Optom Vis Sci. 2016 Jul; 93(7):772-8.
Transient Ocular Wavefront Data in Type 1 Diabetes Mellitus.
Blendowske R, Kalb M.
University of Applied Sciences, Optical Technologies and Image Processing, Department of Mathematics and Natural Sciences, D 64295 Darmstadt, Germany.
We report transient ocular wavefront and blood glucose data for one patient with acute type 1 diabetes mellitus after the treatment with insulin has been initiated.
The wavefront data for both eyes of a 34-year-old male patient were examined by a Hartmann-Shack wavefront sensor. Refraction data and higher-order aberrations were recorded during 130 days for eyes in natural conditions, without cycloplegia. At the beginning, we sampled data every 3 to 4 days and enlarged the intervals, when values settled. In total, we report 20 measurements and 1 baseline entry. Blood glucose levels were recorded at least six times a day during the complete period. For the equivalent sphere, we recorded a bilateral hyperopic shift of 5 D from -2.75 DS to +2.25 DS, followed by a reverse myopic shift of the same amount. The equivalent sphere peaked about 15 to 18 days after the treatment with insulin had begun. Cylinder values kept remarkably stable. Higher-order aberrations are dominated by the spherical aberration. The Zernike coefficient c12 for both eyes changed substantially from OD 0.036 μm and OS 0.062 μm to OD 0.24 μm and OS 0.22 μm (5 mm pupil diameter) following the time pattern of the equivalent sphere. About 60 days after they had reached their peak, all refraction values and higher-order aberrations stabilized at their baseline levels. The baseline was defined by records taken 4 years before the treatment with insulin was commenced.
Wavefront aberrometry gives quantitative insights in the transient alteration and recovering of the eye’s optics whilst the therapy of acute type 1 diabetes mellitus is being initiated. The data of this case support the assumption that variations in the crystalline lens, most probably the modification of its refractive gradient index, as a cause for the transient behavior. An explanation is still missing.
Diabetes Mellitus is often accompanied by strong effects on vision (1,2). The disruptive change in blood glucose levels caused by the onset of insulin treatment is most important. The patients eyes undergo a refractive shift of some diopters in the hyperopic direction. In our case study, the blood glucose level declined from 17 mMol/ml to a normal level in the first 8 days after beginning of the treatment. We measured a maximum of +5 diopters in both eyes, which built up in some 20 days after the first insulin intake. This means a rate of 0.25 diopters per day. After this surge, both eyes slowly come back to normal values in a time span of 60 days, a much slower rate of 0,083 D per day. Because the rates for the increase and the decrease of the hyperopic shift are so different (by a factor of 3), the underlaying processes have to be quite different. It is important to bear in mind the time delay between the first intake and the maximum refractive shift amounts to 2 to 3 weeks. Therefore, early clinical measurement directly after the beginning of the insulin treatment will not show significant changes in the refraction values. Additionally, follow-up measurements two or three months later will neither show significant changes. So far many clinical reports fall outside the time window, where the changes take place.
It is of great advantage for the patient to inform her / him beforehand about the transitional changes in vision that will appear with the insulin treatment. This includes the instruction that after two to three months vision will be back to normal. There is little use of fitting normal spectacle lenses during the transition period. Instead quickly adaptable lenses, like trial lenses or adjustable focus lenses (e.g. Alvarez lenses), are of great help, because they can be adjusted on a daily basis.
Beside the refractive shift, we observed a synchronized movement of an aberration called spherical aberration. This type is characterized by a rotational symmetry and clearly hints to the eye lens as the origin of the refractive shift. Optical calculations (3, 4) indicate that the gradient index structure of the lens is the only reasonable source which can explain the great refractive modification of the eye’s optics. A retinal causation is highly un-probable.
A speculation about the mechanism of the refractive shift is shown in Figure 1. The patient starts with a hyperglycemia, where after a sufficient long time glucose is all over the place, including the eye lens. The insulin treatment quickly decreases the glucose level outside, but not inside the lens. The interior of the lens shows nearly no metabolism and changes in the concentration of glucose are quite slow. Due to the osmotic pressure difference water enters the lens, the volume increases and hence the refractive index decreases. This effect leads to the hyperopic shift and the spherical aberration.
Slowly, the glucose disappears out of the eye lens and the status quo ante is restored to a very high precision. However, the nature of the disappearance of the glucose inside the eye lens remains unclear. An experimental test of this scenario would be the measurement in a patient, which already had an intraocular lens implanted. We would expect, that the material of the intraocular lens would not absorb much glucose and, therefore, the whole process, if at all, would take place on a much smaller scale. The refractive shift and the spherical aberration should be much smaller in such patients.
Importance of the study: We emphasize two fundamental observations. First, spherical aberration was the dominant higher-order aberration in our case of acute Diabetes Mellitus transition phenomena. This finding supports the assumption that changes in refractive gradient index structure plays a major role. Second, after 80 days both eyes recovered the original baseline data to an impressive degree. This is true not only for refraction data but also for higher-order aberrations as well.
Prof. Dr. Ralf Blendowske,
Optical Technologies and Image Processing
Department of Mathematica and Natural Sciences
University of Applied Sciences
D 64295 Darmstadt
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Figure 1: Speculation about the mechanism of the refractive shift caused by the eye lens. The patient starts with a hyperglycemia, where glucose is all over the place, including the eye lens. The insulin treatment quickly decreases the glucose level outside the lens. Due to the osmotic pressure difference water enters the lens, the volume increases and the refractive index decreases. This effect leads to the hyperopic shift and the spherical aberration. Slowly, the glucose disappears out of the eye lens and the status quo ante is restored.