Corneal swelling and recovery following wear of thick hydrogel contact lenses in insulin‐dependent diabetics

Abstract

SummaryThick, 0.34 mm, 38% water hydrogel lenses were fitted, under a pressure patch, no one eye of 18 type I diabetic patients (aged 18–40 years) to assess the acute response to hypoxia and hypercapnia; the response was compared with that in 18 healthy, aged‐matched non‐diabetic subjects; the closed‐eye lens wear was started mid‐morning. Pre‐lens wear assessments were made of acuity, intraocular pressure (IOP), central corneal thickness (CCT) and corneal appearance by biomicroscopy. The mean duration of the diabetes was 13 ± 7 years and the average fasting blood glucose was 8.7 ± 3.3 mM l−1. Baseline CCT values were marginally greater in diabetic patients (600 ± 33 μm) compared with a group of non‐diabetic control subjects (584 ± 26 μm; P > 0.5). A 7.7 ± 2.1% increase in CCT was measured after 3 h lens wear in the diabetic patients while an average 10.6 ± 2.4% increase in CCT was measured in the control subjects (P < 0.05). The recovery of corneal thickness to baseline values in diabetic patients was slower (at 44.8 ± 2.0% per hour) than the control subjects (53.9 ± 2.1 per hour; P < 0.05) although recovery of corneal thickness occurred in both groups within 2.5–3 h. IOP values (non‐contact tonometry) were higher in the diabetic patients than in the controls (14.5 ± 2.9 vs 12.4 ± 1.7 mmHg; P < 0.01). Overall, those corneas with greater baseline CCT values tended to swell less than those with lower baseline CCT values (r = 0.582). Positive correlations were also found between corneal thickness and IOP and blood glucose. The diabetic patients thus tended to have slightly thicker corneas (but this could be related to blood glucose or IOP rather than true corneal disease) and also had corneas that tended to swell less with a contact lens stress test (but this could be constitutively due to the slight oedema already present). The different corneal response in diabetic patients may thus be the result of physical determinants such as initial oedema and IOP and not the result of a disease of the cornea itself.