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Causes of cell damage in connection with cataract surgery

01.01.2014

After cataract surgery, damage to endothelial cells located on the internal side of the cornea is observed in the majority of patients. The causes of this cell damage have not yet been fully clarified; this can affect the corneal dehydration for which these cells are responsible. The – in this case – reduced performance of the endothelial cells leads to a temporary swelling of the cornea in the affected patients. In the case of very rare previous illnesses or previous ophthalmologic surgery, there is, however, a risk of corneal clouding and thus of an irreversible blindness of the patient. Within the scope of an interdisciplinary research project in which ophthalmologists were involved, new findings with regard to the possible cause of this cell damage could be achieved at PTB.

Every year in Germany, approx. 800,000 persons are treated for cataracts, a disease which is related to age and in which the lens has become clouded and must be removed to be replaced with an artificial lens [1]. Such a surgical intervention for cataract treatment is among the most frequent ones in Germany and is, for the major part, carried out as an outpatient treatment. In the standard method, which is called "phacoemulsification", an ultrasonic instrument – the so-called "phacoemulsification probe" – is introduced into the eye; it disintegrates the eye lens inside the capsular bag and aspirates it via an aspiration/irrigation mechanism which ensures a constant liquid flow.

Different processes – such as friction around the phacoemulsification probe which oscillates forth and back at an ultrasonic frequency of approx. 42 kHz – generate heat and lead to a temperature rise inside the eye during surgery, which could cause thermal damage to the cells of the corneal endothelium. In order to check experimentally whether the increased temperatures really represent a risk for the endothelium, the temperature evolution was measured in porcine eyes within the scope of various surgery scenarios and at different settings of the instruments used. The cell damage to these same eyes could then be quantified by means of different methods (see Fig. 1), and a possible correlation with the previously measured temperature values was assessed. The experiments have shown that the instrument settings used in general practice only lead to moderate temperature rises of the endothelium of max. 2.5 °C. In addition, no correlation between the cell damage and the temperatures measured could be established. In fact, it turned out that there is a connection between cell damage and the ultrasonic power input used.

Under extreme – i.e. in practice only exceptionally occurring – conditions, however, high temperatures in the range between 40 °C and 50 °C, which is critical for cells, could be detected. However, a lack of understanding about the process of heat generation has, to date, prevented concrete operating instructions from being developed for physicians in order to avoid such situations. The first mathematical description of these processes within the scope of this project allowed the heat sources to be localized and quantified and the thermal distribution inside the eye to be numerically simulated, taking the extremely complex flow conditions into account (see Fig. 2). After the numerical simulation had been successfully validated by means of the experimental data, the thermal distribution was then simulated at different instrument settings and compared with each other from the viewpoint of the thermal stress of the cells. Based on these results, concrete safety recommendations have been formulated which, if complied with, prevent temperatures exceeding 40 °C from occurring in practice and contribute to reducing the thermal stress of the corneal endothelium to a degree that can be considered as being non-critical. To explain the cell damage encountered at lower temperature rises of less than 2.5 °C, other damaging mechanisms have to be focused on.

Figure 1: Example of damage to the corneal endothelium of a porcine eye.

Figure 2: Time-dependent temperature evolution in a sectional plane through the eye and the phacoemulsification probe. The animation shows the temperature evolution in real time for the case in which the phacoemulsification probe is switched on inside the eye for 5 seconds at settings that are typical for such operations. The simulation is in agreement with the experiments and shows very moderate temperature rises at the corneal endothelium which cannot be the cause of the cell damage observed. Such a simulation of the temperature distribution is possible for any imaginable instrument setting.

References:

[1] Wille, E. & Popp, M.: Die Bewertung von Kataraktoperationen aus gesundheitsökonomischer Sicht. BDOC Bundesverband Deutscher Ophtalmochirurgen e.V., 2012 [in German]

Contact person:

Steffen Buschschlüter, Dept. 1.6, WG 1.62, e-mail: steffen.buschschlueter@ptb.de