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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