Because neither the human cornea nor a soft contact lens (SCL) is of constant thickness, corneal oxygenation varies locally. To quantify the importance of cornea/SCL thickness variations on oxygen demand, we develop a quasi-2-dimensional (2D) respiration model that accounts for aerobic and anaerobic metabolism and bicarbonate buffering.
Because metabolism is critical to oxygen demand, we extend the 1-dimensional (1D), 6-layer oxygen metabolic model of Chhabra et al. Lateral diffusion is shown to be negligible. Accordingly, we adopt the 1D reactive-diffusion metabolic model but apply it locally along the cornea/lens extent. This “quasi-2D” approximation permits 2D assessment of oxygen consumption, including the effects of carbon dioxide, glucose, and lactate, bicarbonate, and hydrogen ions. We use both an oxygen deficiency factor and an excess lactate factor to gauge corneal health after accounting for both cornea and contact lens thickness variations.
The quasi-2D respiration model provides quantitative spatial resolution of corneal oxygenation with minimal expenditure of computation time. When only aerobic oxygen loss is included, our quasi-2D approach is in excellent agreement with the fully 2D results of Alvord et al. However, the quasi-2D model predicts 2D concentration profiles of glucose, lactate ions, bicarbonate ions, hydrogen ions, and carbon dioxide, as well as oxygen. Neglect of metabolic reactions and/or thickness variations leads to inaccurate prediction of oxygen demand, especially near the lens periphery.
The quasi-2D respiration model indicates that lateral thickness variations and respiration kinetics are critical for assessing on-eye physiologic performance of an SCL. We find that oxygen deficiency factor and excess lactate factor are useful indices to gauge corneal hypoxia. A user-friendly computer program of the quasi-2D respiration model is available for lens design.