Diabetes mellitus is a group of common metabolic disorders manifested by hyperglycemia resulting from a complex interaction of genetic and environmental factors. It is a public health problem and it currently affects more than 170 million people worldwide and will affect an estimated 366 million by 2030, with the most rapid growth and in low and middle income countries, among populations of working age (WHO, 2005).
Chronic hyperglycemia is the primary factor leading to the development of diabetic retinopathy and other complications of the disease. In major clinical trials, tight control of blood glucose and blood pressure has been demonstrated to reduce the risk of retinopathy and associated blindness. A range of ocular diseases is also associated with diabetes, such as cataract, glaucoma, retinal vein occlusions and artery occlusions, ischemic optic neuropathy, cranial nerve palsy, which may lead to vision loss and ocular misalignment.
Diabetic retinopathy is a leading cause of visual impairment and blindness among individuals between 25 and 74 years of age in the industrialized world. The progress of diabetic retinopathy can be classified into four stages: mild Non-proliferative Retinopathy (NPDR), moderate NPDR, severe NPDR and proliferative DR (PDR). Patients may need to be educated about the glucose test, the great importance of maintaining good control, and the possible consequences of poor control. Good glycaemic control is important in development and progression of DR. In addition, patients should be reminded that other modifiable risk factors for retinopathy progression, including hypertension, lipid abnormalities, early renal failure, and anemia, are also important. Regular retinal screening can prevent sight loss due to diabetic retinopathy as it provides early detection and treatment.
Most of the eye problems caused by diabetes can be treated, but it is vital that these problems are picked up as soon as possible, as treatment is more effective when given early. If the results show no retinopathy or some background retinopathy, patient will normally be invited back for another retinal screening in a year. If the results show signs that retinopathy could affect the sight, patient will be invited back sooner for treatment. If the patient is pregnant and has gestational diabetes, she will have retinal screenings more often during her pregnancy and after baby is born.
Cataract is a major cause of vision impairment in people with diabetes. The risk of cataract increases with increasing diabetes duration and severity of hyperglycemia. Deposition of advanced glycation end products in the lens has been postulated as one possible pathogenic mechanism for diabetic cataract. Cataract surgery is the standard treatment for patients with cataract and significant vision impairment. In individuals with diabetes, cataract occurs at a younger age and progresses more rapidly, resulting in higher rates of cataract surgery at a relatively young age. While the overall outcomes of cataract surgery are excellent, patients with diabetes may have poorer vision outcomes than those without diabetes, and the worst outcomes may occur in operated eyes with active proliferative retinopathy and/or preexisting macular edema. To improve cataract surgical outcomes in patients with diabetes, adequate control of diabetic retinopathy with laser treatment before cataract surgery is necessary.
The most devastating postoperative complication of cataract surgery is endophthalmitis, a severe intraocular infection, with several studies showing that patients with diabetes have an increased risk of developing this complication resulting in poorer outcomes. Management of endophthalmitis consists of a combination of intravitreal antibiotics injection and topical antibiotics and steroids and possibly ocular surgery. In patients with diabetes, treatment may need to be more aggressive, with surgery performed earlier rather than later.
Glaucoma is a progressive optic neuropathy associated with typical optic disc changes and visual field defects. Patients with diabetes are at risk of two major types of glaucoma: primary glaucoma and neovascular glaucoma. Several large epidemiological studies have reported positive associations between diabetes with primary open angle glaucoma. Microvascular damage from diabetes could impair blood flow to the anterior optic nerve, resulting in optic nerve damage. Diabetes also impairs the autoregulation of posterior ciliary circulation, which may exacerbate glaucomatous optic neuropathy. Neovascularization of the iris, an early precursor of neovascular glaucoma, is commonly seen in patients with long-standing poorly controlled diabetes. Hypoxia in the retina and other ocular tissue causes an increased expression of vascular endothelial growth factor (VEGF), which stimulates new vessel formation in the iris or in the anterior chamber angle. Studies have shown a consistent association between diabetes and neovascular glaucoma, with proliferative retinopathy the leading cause of this type of secondary glaucoma. Between 32 and 43% of neovascular glaucoma cases are caused by proliferative diabetic retinopathy. Neovascular glaucoma requires aggressive intervention to lower intraocular pressure with medication, followed by surgery. Regression of neovascularization following pan-retinal laser photocoagulation can occur if treated early.
In patients with diabetes, diabetic microvascular disease affecting the anterior part of the optic nerve is thought to cause the ischemia. Anterior ischemic optic neuropathy (AION) is an acute vascular condition of the optic nerve. Studies suggest that up to 25% of patients with AION have a history of diabetes. Patients with AION usually present with moderate loss of vision upon awakening, presumably related to nocturnal systemic hypotension. Visual acuity is better than 20/200 in 60% of cases at presentation. There are no proven treatments for AION, and the Ischemic Optic Neuropathy Decompression Trial revealed no benefit of optic nerve decompression surgery. There is no proven prophylaxis for AION, and the evidence for the efficacy of aspirin therapy is limited.
Retinal vein occlusion (RVO) is a retinal vascular condition characterized by dilated tortuous retinal veins with retinal hemorrhages, cotton wool spots, and macular edema. Central RVO occurs at the optic disc, whereas branch RVO occurs at retinal venular branches, usually at the site of arterio-venous crossing. Central RVO may be subdivided further into non ischemic and ischemic types, the latter associated with poorer vision prognosis. Diabetes is thought to be a major risk factor for RVO. The importance of RVO in patients with diabetes is that the retinal signs (e.g., hemorrhages or cotton wool spots) may “mimic” diabetic retinopathy. Thus, when patients with diabetes present with acute vision loss and asymmetric signs of “diabetic” retinopathy, RVO should be considered.
The two major complications of RVO are secondary neovascular glaucoma and macular edema. Pan-retinal laser photocoagulation has been shown to prevent neovascular glaucoma. No treatment has proven effective for macular edema in patients with central RVO, although focal laser treatment may be useful in patients with macula edema and branch RVO. The vision prognosis with central RVO, particularly ischemic central RVO, is poor, but that of branch RVO is relatively good, with nearly half of patients maintaining visual acuity better than 20/40.
Retinal arteriolar emboli are discrete plaque-like lesions lodged in the lumen of retinal arterioles. The majority of emboli are asymptomatic and transient, although patients infrequently present with episodes of sudden, painless, monocular blindness (amaurosisfugax), a transient ischemic attack, or stroke. Once an embolus has been detected, a full cardiovascular and cerebrovascular risk assessment is recommended, including carotid artery ultrasound and echocardiography to assess the source of the emboli. The hallmark of RAO is sudden, unilateral, painless loss of vision associated with a visual field defect. Patients with central RAO usually present with a dramatic loss of vision, an afferent pupillary defect, diffuse retinal whitening, and the resultant classic “cherry spot” on the macula. There is clear evidence that patients with diabetes are at higher risk of RAO. However, the prevalence of diabetes among patients with RAO has been reported to be as high as 21%, which is higher than in the general population of the same age. Patients with RAO should be referred immediately to an ophthalmologist for management. In the acute phase (within 24 h), ocular massage (to dislodge the embolus) and intravenous acetazolamide injection (to lower intraocular pressure) might help. It is important for physicians to measure the erythrocyte sedimentation rate and CRP to exclude giant cell arteritis. Regardless of treatment, however, the vision prognosis of central RAO is poor.
Ocular ischemic syndrome (OIS) is an uncommon vascular problem that results from chronic hypo-perfusion of the eye, most commonly caused by ipsilateral internal carotid or ophthalmic artery occlusion. Patients with OIS typically present with vision loss and dull ocular pain. The prevalence of diabetes in patients with OIS is higher than in the general population, with one study reporting that more than 50% of patients with OIS have diabetes. Diabetes is a major risk factor for carotid artery stenosis and plaque formation, the underlying causes of OI.
Among ischaemic cranial nerve palsies, isolated pupil sparing complete CN III and V1 palsy are most common and they can present with acute and isolated in patients over 50 years of age with known vascular risk factors (diabetes, hypertension or hyperlipidaemia). It usually resolves within 6 months. Of note, pain is commonly associated in CNIII palsy of microvascular cause. Whether or not neuroimaging is required at the time of diagnosis is controversial in isolated nerve palsy with known microvascular risk factors.
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