New vessel growth on the iris (rubeosis iridis – also in response to ischemia) (Figure 15.17) can close the drainage angle and cause acute glaucoma. This condition is called rubeotic glaucoma; it is acutely painful and can occasionally occur following cataract surgery or vitrectomy if there is active proliferative retinopathy. Treatment is unsatisfactory and the end result is often a painful blind eye.
Cataract is common and can occur acutely and diffusely with newly diagnosed diabetes (so-called snowstorm cataract) or, more commonly, posterior subcapsular and cortical cataracts, which occur after several years duration (Figure 15.18). The 10-year cumulative incidence of cataract surgery in the WESDR study was 8% and 25% for patients with type 1 and type 2 diabetes respectively. The underlying cause for snowstorm cataract is probably acute fluid shift due to hyperglycemia and hyperosmolality. Linear or central cataract probably results from non-enzymatic glycation and subsequent cross-linkage of lens crystallins. Sorbitol accumulation secondary to activation of the polyol pathway may also contribute. Extraction and replacement with a plastic implant is the treatment of choice. The results are generally good but active proliferative retinopathy should be treated first.
Anterior ischemic optic neuropathy is caused by microvascular disease of the anterior optic nerve. Patients present with painless loss of vision upon wakening. The condition usually remains stable but there is no known effective treatment.
A related problem of acute disc edema and moderate visual loss can occur and is termed diabetic papillopathy. This usually improves spontaneously but it may take up to 12 months. It can be confused with papilledema.
Other associated ocular conditions are listed in Box 15.1.
Factors associated with the development of retinopathy
Many of these have been identified from epidemiological studies and are therefore associations (Box 15.2), but most have been confirmed from intervention trials such as the DCCT and UKPDS.
Many of these factors are co-related, for example hyperglycemia (as estimated from HbA1c levels and thus severity of protein glycation) and duration of diabetes (being a measure of exposure to the hyperglycemic insult). Other factors are less intuitive; in pregnancy, many women rapidly improve glycemic control in order to minimize fetal risk of malformation. This can precipitate rapid worsening of retinopathy; perhaps by reducing blood flow through an already ischemic retina and causing a sudden release of growth factors. This phenomenon can also occur with too rapid correction of glycaemia in non-pregnant patients (e.g. commencing CSII). Careful retinal surveillance is needed in these situations (see below).