Chapter 15: Ocular Disorders Associated With Systemic Diseases
METABOLIC DISORDERS
DIABETES MELLITUS
Diabetes mellitus is a complex metabolic disorder that also involves the small blood vessels, often causing widespread damage to tissues, including the eyes.
The ocular complications occur approximately 20 years after onset despite apparently adequate diabetic control. Improved treatment measures (eg, improved insulins, antibiotics) that have lengthened the life span of diabetics have actually resulted in a marked increase in the incidence of retinopathy and other ocular complications. The visual outlook for adult (maturity-onset) diabetics is considerably better than for juvenile diabetics.
The possibility of diabetes should be considered in all patients with unexplained retinopathy, cataract, extraocular muscle palsy, optic neuropathy, or sudden changes in refractive error. Absence of glycosuria or a normal fasting blood glucose level does not exclude a diagnosis of diabetes.
Diabetic Retinopathy (Figures 15-17, 15-18, 15-19 and 15-20)
Diabetic retinopathy is a common cause of blindness and now accounts for almost one-fourth of blind registrations in the western world.
The presence and degree of retinopathy seem to be more closely related to the duration of the disease than to its severity. Good diabetes control retards the development of retinopathy and other diabetic complications.
The juvenile diabetic develops a severe form of retinopathy within 20 years in 60-75% of cases even if under good control. The retinopathy is usually proliferative. In older diabetic patients, retinopathy is more often nonproliferative, with the risk of severe central visual loss from maculopathy.
The details of characteristics and treatment of diabetic retinopathy are presented in Chapter 10.
Lens Changes
A. True Diabetic Cataract (Rare):
Bilateral cataracts occasionally occur with a rapid onset in severe juvenile diabetes. The lens may become completely opaque in several weeks.
B. Senile Cataract in the Diabetic (Common):
Typical senile nuclear sclerosis, posterior subcapsular changes, and cortical opacities occur earlier and more frequently in diabetics.
C. Sudden Changes in the Refraction of the Lens:
Especially when diabetes is not well controlled, changes in blood glucose levels cause changes in refractive power by as much as 3 or 4 diopters of hyperopia or myopia. This results in blurred vision. Such changes do not occur when the disease is well controlled.
Iris Changes
Glycogen infiltration of the pigment epithelium and sphincter and dilator muscles of the iris may cause diminished pupillary responses. The reflexes may also be altered by the autonomic neuropathy of diabetes.
Rubeosis iridis is a serious complication of the retinal ischemia that is also the stimulus to retinal neovascularization in severe diabetic retinopathy. Numerous small intertwining blood vessels develop on the anterior surface of the iris. Spontaneous hyphema may occur. The formation of peripheral anterior synechiae is aided by the vascularization of anterior chamber structures, eventually blocking aqueous outflow sufficiently to cause secondary glaucoma.
Extraocular Muscle Palsy (Figure 15-21)
This common occurrence in diabetes is manifested by a sudden onset of diplopia caused by paresis of an extraocular muscle. This may be the presenting sign and is due to infarction of the nerve. When the third nerve is involved, pain may be a prominent symptom. Differentiation from a posterior communicating aneurysm is important; in diabetic third nerve palsy, the pupil is usually spared. Recovery of ocular motor function begins within 3 months after onset and usually is complete. The fourth and sixth nerves may be similarly involved.
Optic Neuropathy
Visual loss is usually due to infarction of the optic disk or nerve. A characteristic telangiectatic pattern is visible at the optic disk in some younger diabetics with sudden visual loss.
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10.1036/1535-8860.ch15