Diabetic cataract is a general term for lens opacification that occurs in association with diabetes. It is broadly classified into two types.
True diabetic cataract (typical) occurs in relatively young individuals with persistently poor glycemic control. It is characterized by bilateral snowflake-like fine opacities appearing in the anterior and posterior subcapsular cortex of the lens, presenting a saucer-shaped posterior subcapsular opacity.
Modified age-related cataract associated with diabetes is the most common type of diabetic cataract. There are no characteristic opacities, and it may be difficult to distinguish from age-related cataract, especially in patients with type 2 diabetes.
| Type | Age of onset | Characteristic findings | Bilaterality |
|---|---|---|---|
| True diabetic cataract | Relatively young patients | Snowflake opacities, saucer-shaped posterior subcapsular opacities | Bilateral |
| Modified form of age-related cataract | Middle-aged and elderly | No characteristic findings (cortical/posterior subcapsular opacities predominant) | Often bilateral |
Cataracts are more common in diabetic patients than in non-diabetic patients, with a notable difference in prevalence across age groups, especially up to the early 60s. True diabetic cataract is very rare, occurring in about 1% of 600 pediatric diabetes cases.
Diabetes is considered the greatest risk factor for cortical and posterior subcapsular cataracts1). Diabetes, hypertension, obesity, and metabolic syndrome are associated with an increased risk of cataracts or cataract surgery1).
Cataracts develop earlier in diabetic patients compared to non-diabetic patients, with a clear difference in prevalence, especially up to the early 60s. Diabetes is considered the greatest risk factor for cortical and posterior subcapsular cataracts. Poor glycemic control, long disease duration, and retinopathy further increase the risk. Regular eye examinations are important.
Slit-lamp microscopy reveals opacities in the anterior and posterior subcapsular regions of the lens. It is not difficult to infer the presence of diabetes from lens findings. In cases with concurrent retinopathy, cataracts tend to be more advanced.
Early Stage
Findings: Numerous water clefts (water clefts containing granules) are seen from the equator.
Features: Water clefts in the superficial cortex are characteristic early changes in diabetic patients. Visual impairment is often mild at this stage.
Advanced Stage
Findings: Spoke-like opacities in the superficial cortex develop from the entire lens circumference. Combined posterior subcapsular opacities and retrodots cause severe visual impairment.
Features: Posterior subcapsular opacities are located on the visual axis, so they tend to cause early decreases in visual acuity and contrast sensitivity.
Advanced Stage
Snow flaky opacities characteristic of true diabetic cataract are fine white opacities scattered in the anterior and posterior subcapsular cortex, which may rapidly progress to mature cataract.
Because posterior subcapsular opacity tends to occur early, opacity on the visual axis appears earlier than in ordinary nuclear cataract. Compared to nuclear cataract, photophobia, glare, and decreased contrast sensitivity are more prominent. Progression may be rapid, requiring regular observation.
Multiple mechanisms are involved in the development of diabetic cataract.
Using a slit lamp microscope, observe opacities in the anterior and posterior lens capsule, and confirm characteristic opacity patterns (snow flaky, saucer-shape, water clefts). Checking blood glucose and HbA1c levels and evaluating for diabetic retinopathy are essential.
Patients with diabetic retinopathy have a significantly higher risk of macular edema (odds ratio 5.91, 95% confidence interval 2.72–12.84) and retinopathy progression (odds ratio 5.28, 95% confidence interval 3.05–9.14) after cataract surgery2). Accurate identification of diabetic retinopathy before surgery is essential for predicting postoperative visual outcomes2).
| Evaluation Item | Examination Method | Purpose |
|---|---|---|
| Fundus status and retinopathy stage | Fundus examination and fluorescein angiography | Assessment of postoperative progression risk and need for preoperative intervention |
| Presence of macular edema | OCT | Prediction of postoperative visual acuity prognosis |
| Cases with poor fundus visualization | Ultrasound tomography (B-mode) / electroretinography | Exclusion of posterior pole diseases |
| Blood glucose and HbA1c | Blood test | Assessment of long-term glycemic control |
| Systemic complications | Medical evaluation | Evaluation of cardiac, renal, and vascular complications |
In addition to standard preoperative cataract tests (axial length measurement, corneal curvature measurement, anterior chamber depth measurement, etc.), fundus examination and OCT evaluation of retinopathy stage and macular edema are essential. If the fundus is difficult to visualize, use ultrasonography or electroretinography to exclude posterior pole disease. Also check HbA1c and blood glucose levels, and perform systemic evaluation for cardiac, renal, and vascular complications.
Cataract surgery is considered in diabetic patients when visual impairment due to cataract is present, or when the fundus is difficult to observe and interferes with the management of retinopathy. Evaluation of ocular complications and systemic condition is necessary for determining indications.
Long-term stable glycemic control is most important. Lowering blood glucose only immediately before surgery is meaningless; conversely, rapidly correcting blood glucose levels in the short term before surgery may worsen retinopathy and macular edema. Patients with long-term poor glycemic control are more likely to have worsening of retinopathy after surgery.
Phacoemulsification and aspiration (PEA) with intraocular lens (IOL) implantation is the standard procedure. The small-incision self-sealing wound technique is recommended for the following reasons.
| Patient Category | Recommended Management |
|---|---|
| Diabetic patients without diabetic retinopathy | Combination of steroid eye drops and NSAID eye drops (CME prevention) 2) |
| Patients with diabetic retinopathy | Steroid eye drops + NSAID eye drops + subconjunctival triamcinolone injection at end of surgery (significantly reduces CME. PREMED study) 3) |
| Prophylactic administration of anti-VEGF drugs (e.g., intravitreal bevacizumab 1.25 mg) | Evidence is inconsistent; routine use is not recommended 2) |
When using steroid depot, postoperative intraocular pressure monitoring is essential2).
The PREMED study (Wielders et al.) showed that subconjunctival injection of triamcinolone at the end of surgery in patients with diabetic retinopathy significantly reduces the incidence of postoperative CME3).
During the first six months to one year after surgery, the onset and progression of retinopathy and macular edema are accelerated. Patients with long-term poor glycemic control are more likely to worsen postoperatively. The risk of postoperative retinopathy progression in patients with diabetic retinopathy is significantly higher, with an odds ratio of 5.28 (95% confidence interval 3.05–9.14)2). Careful postoperative fundus examination (OCT, fluorescein angiography) is essential.
In cataract surgery for diabetic patients with ischemic heart disease or cerebral infarction, it is not always necessary to discontinue anticoagulants or antiplatelet agents; continued administration is acceptable.
It can be safely performed with appropriate preoperative evaluation and long-term stable blood glucose control. However, rapid preoperative correction of blood glucose is contraindicated as it may worsen retinopathy and macular edema. Postoperatively, the risk of developing or progressing retinopathy and macular edema increases, so careful fundus follow-up for 6 months to 1 year is necessary.
Increased osmotic pressure due to polyol metabolism is frequently reported as a cause of diabetic cataract. The mechanism is as follows.
In a hyperglycemic environment, glucose covalently binds to lens proteins (crystallins) via the Maillard reaction, leading to accumulation of advanced glycation end products (AGEs). Accumulation of AGEs causes the following changes.
In diabetic patients, the oxygen level in the vitreous is low, which is thought to suppress the development of nuclear cataracts. This is considered the mechanism by which cortical and posterior subcapsular opacities are predominant and nuclear opacity is relatively less in diabetic cataracts.
