Ocular Consequences of Systemic Disease
Of all of the medical disorders that the nurse encounters, diabetes mellitus is one of the most common and one that can have dev-astating effects on the patient. Diabetes affects every system of the body in a deleterious way and consequently affects the patient’s family and society in general. Diabetes is the leading cause of new cases of blindness in people between 20 and 74 years of age in the United States today. Before the discovery of insulin in the 1920s, diabetic retinopathy was relatively rare. Most people with dia-betes did not survive for more than 1 or 2 years; however, with the use of insulin, more and more patients are able to survive and enjoy relatively normal life spans. They are also confronted with the complications of long-term diabetes. One of the most serious complications is retinopathy.
Many ophthalmic complications are associated with AIDS. On autopsy, up to 90% of patients have ocular lesions directly related to AIDS. Cytomegalovirus (CMV) is the most common cause of retinal inflammation in patients with AIDS. About 40% of pa-tients who have CMV retinitis lose their central vision in both eyes by the time of death.
Early symptoms of CMV retinitis vary from patient to patient. Some patients complain of floaters or a decrease in peripheral vision. Some patients have a paracentral or central scotoma, whereas others have a fluctuation in vision from macular edema. The retina often becomes thin and atrophic and susceptible to retinal tears and breaks.
CMV retinitis generally takes one of three forms: hemor-rhagic, brushfire, or granular. In the hemorrhagic type, large areas of white, necrotic retina may be associated retinal hemorrhage. The brushfire form appears to have a yellow-white margin, which begins at the edge of burned-out atrophic retina. This retinitis ex-pands and, if untreated, involves the entire retina. The granular form of CMV retinitis consists of white, granular lesions in the periphery of the retina that gradually expand. The white, feath-ery infiltration of the retina destroys sensory retina and leads to necrosis, optic atrophy, and retinal detachment.
Pharmacologic agents available for treatment of CMV retinitis include ganciclovir (Cytovene), foscarnet (Foscavir), and cido-fovir (Vistide).
Ganciclovir is administered intravenously, orally, or intra-vitreously in the acute stage of CMV retinitis. A surgically im-planted intraocular device has provided a new mode of effective ganciclovir administration. This enables a higher, more effective dose of medication to be administered and is well tolerated by pa-tients. This constant intraocular concentration of ganciclovir lasts for about 6 to 10 months before the inserts must be replaced. Once begun, ganciclovir must be given continuously. A study that combined the use of the intravitreous implant with oral gan-ciclovir demonstrated a reduction in the risk of new CMV dis-ease as well as a delay in the progression of the retinitis (Martin et al., 1999). This very potent medication, when administered systemically, can cause neutropenia, thrombocytopenia, anemia, and elevated serum creatinine levels. Although the surgically im-planted sustained release device enables higher concentrations of ganciclovir to reach the CMV retinitis, there are risks and com-plications associated with the devices, including endophthalmi-tis, retinal detachment, and hypotony.
Foscarnet inhibits viral DNA replication. It may be the medication of choice when ganciclovir is ineffective. It may be administered intravenously or locally by intravitreal injections. The combination of foscarnet and ganciclovir has been more ef-fective than either medication alone. Nephrotoxicity may occur with systemic foscarnet, and renal function must be monitored carefully.
Cidofovir impedes CMV replication. This medication is ad-ministered intravenously. Cidofovir has been shown to delay the progression of CMV retinitis significantly. Nephrotoxicity, pro-teinuria, and increased serum creatinine levels are significant side effects of its administration.
Hypertension, known as the silent killer, can shorten the life span by as many as 20 years. End-organ damage affects the heart, brain, kidney, and eye. Hypertension may be manifested in one of two forms: chronic or acute. This differentiation is determined by the rapidity in rise of the blood pressure as well as the degree of elevation. The retinal changes observed with each form are dif-ferent and have different consequences for the eye.
Chronic hypertension and atherosclerosis go hand in hand, and the associated retinal changes are evidenced by the develop-ment of retinal arteriolar changes, such as tortuousness, narrow-ing, and a change in light reflex. Funduscopic examination reveals a copper or silver coloration of the arterioles and venous com-pression (arteriovenous nicking) at the arteriolar and venous cross-ings. Intraretinal hemorrhages from hypertension appear flame shaped because they occur in the nerve fiber layer of the retina.
Acute hypertension can result from pheochromocytoma, acute renal failure, pregnancy-induced hypertension, and malignant essential hypertension. The retinopathy associated with these crisis states is extensive, and the manifestations include cotton-wool spots, retinal hemorrhages, retinal edema, and retinal exudates, often clustered around the macula.
The choroid is also affected by the profound and abrupt rise in blood pressure and resulting vasoconstriction, and ischemia may result in serous retinal detachments and infarction of theretinal pigment epithelium (RPE). Ischemic optic neuropathy and papilledema (ie, swelling of the optic disc due to increased IOP) may also result.
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