Although the underlying cause of diabetic retinopathy isn’t fully understood, chronic hyperglycemia, blood platelet abnormalities, and blood vessel narrowing are thought to cause retinal capillary damage. The disease usually occurs in both eyes, but the severity may differ in each eye. Diabetic retinopathy is classified by stage as non proliferative, preproliferative, or proliferative.

You’ll see nonproliferative (or background) retinopathy more commonly than any other stage of the disease. In this stage, the retinal capillaries undergo several changes that impair their ability to transport essential oxygen and nutrients to the retina . This is what happens: The retinal capillary walls thicken, and capillary fluid leaks through them into the interstitial spaces, causing retinal edema. Eventually, this fluid forms thick yellow deposits, or hard exudates, which can be seen on ophthalmoscopic examination. Also, the retinal capillaries begin to become occluded, and microaneurysms form in the capillary walls. All of these changes cause the capillary walls to bleed easily, resulting in blot hemorrhages in the retina, which are visible on ophthalmoscopic examination.

If the micro aneurysms leak into or near the macular area of the retina, macular edema may result. This may cause blurred vision because the macula is the part of the retina that provides the most acute vision. Macular edema, which can occur at any stage of retinopathy, is the most common cause of decreased vision in nonproliferative retinopathy.

Preproliferative retinopathy involves further deterioration and obstruction of the retinal capillaries. Poor capillary perfusion may lead to retinal ischemia and infarction. More hemorrhages occur during this stage, but patients may have no symptoms.

Proliferative retinopathy, the most severe stage of diabetic retinopathy, involves the retina and vitreous cavity. As retinal capillaries become occluded, new blood vessels form to supply blood to the retina (a process called neovascularization). Over time, these new capillaries become fibrous and rupture easily, producing bleeding into the vitreous humor and contraction of the vitreous cavity wall. When blood enters the vitreous humor, light can’t reach the retina. Your patient may report seeing red or black spots or lines.

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The new fibrous tissue may stick to the cell layer surrounding the vitreous humor. Then the contraction of the fibrous tissue may pull on the vitreous cell layer and the retina, causing your patient to develop tractional retinal detachment. And if the macula is involved, she’ll have a complete vision loss.

Inside The Eye

This cross section shows you the internal structures of the eye. The sclera-the white, opaque outside coat of the eye-helps maintain the eye’s shape. The transparent cornea-the anterior, avascular portion of the sclerapermits light to enter the eye. The cornea lies over the pupil and the iris, the colored part of the eye. The aqueous humor, a clear liquid, fills the anterior chamber. The canal of Schlemm, a ring-shaped venous sinus located at the base of the cornea, drains the aqueous humor away from the anterior chamber and into the blood-stream. The avascular lens refracts and focuses images onto the retina.

The choroid, or middle coat, is made up of many arteries and veins. The retina, the innermost coat of the eyeball, is rich in neurons, including the rods and cones, which serve as visual receptors. The retina is connected to the optic nerve, which conducts visual information to the brain. The vitreous humor-a thick, gelatinous material-fills the space behind the lens. It maintains the shape of the eye­ball and placement of the retina.

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To localize an occlusion, blood pressure readings are taken at the thigh, calf, and ankle of the affected leg during Doppler ultrasonography. If the systolic blood pressure at one of these sites is more than 20 mm Hg lower than the brachial systolic blood pressure, arterial occlusion probably exists at or near the site.

Plethysmography detects blood volume and pressure in a limb using a plethysmograph (a pulse volume recorder). It’s especially useful when blood vessels are calcified. During plethysmography, blood pressure is measured at the thigh, calf, and ankle. If the systolic blood pressure at one of these sites is more than 20 mm Hg lower than the brachial systolic blood pressure, arterial occlusion probably exists at or near the site. While blood pressure is measured, the plethysmograph displays the blood flow as sound waves on a strip, similar to an ECG tracing. Decreased amplitude in the sound waves indicates arterial occlusion

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Complications of laser therapy depend on the type and number of treatments. Some patients experience discomfort. Others complain of a slight loss of vision, a decrease in peripheral vision, or impaired night vision.

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In patients who have diabetes and peripheral vascular disease, hyperglycemia, uncontrolled hypertension, or other factors can lead to atherosclerotic changes in the peripheral arteries. These changes may include capillary basement membrane thickening and increased platelet adhesion. They may lead to arterial occlusion, which diminishes the oxygen supply to the tissues, and subsequent muscle tissue ischemia and pain. Unfortunately, the diabetic patient’s poor tissue perfusion and impaired small vessels may reduce her ability to develop good collateral circulation to bypass the occlusion.

If your diabetic patient has hyperlipidemia, she’s at even greater risk for developing peripheral vascular disease. If she smokes, she’ll experience further compromised circulation. Smoking increases the progression of atherosclerosis by increasing LDL and triglyceride levels and decreasing HDL levels. It also raises the blood pressure, which can damage the arterial endothelium. The nicotine in cigarettes induces vasospasm and increases blood viscosity and clotting factor concentrations, which helps diminish arterial circulation.

If peripheral vascular disease is untreated, your patient may develop infections or even gangrene in her legs, which may lead to amputation. More than half of all nontraumatic amputations of the lower leg are caused by peripheral vascular disease in patients with diabetes.

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The exact cause of kidney destruction in diabetic nephropathy isn’t known. What’s known is that kidney damage occurs in the glomerulus, which consists of tufts of capillaries in the renal corpuscle, which is surrounded by Bowman’s capsule. The glomerular capillaries are made up of three layers of cells: the endothelium, basement membrane, and visceral epithelium. Mesangial cells lie between and support the capillaries.

Normally, blood enters the glomerulus through the afferent arteriole and exits by the efferent arteriole. As blood passes through the glomerulus, water, electrolytes, creatinine, urea nitrogen, and glucose filter across the capillary basement membrane into Bowman’s capsule. This filtrate is similar to blood plasma, but it doesn’t normally contain proteins. After the filtrate enters Bowman’s capsule, it flows through the tubules of the kidney and is eventually excreted from the body.

In diabetic nephropathy, kidney destruction results from gradual structural changes in the glomerulus. First, the glomerulus enlarges. Then glomerulosclerosis-the replacement of normal glomerular tissue with fibrous scar tissue occurs. In diffuse glomerulosclerosis, the more common type, the basement membrane of the glomerular capillaries thickens and eventually leaks capillary fluid. Also, the mesangial matrix (the spongy network surrounding the mesangial cells) thickens. In nodular glomerulosclerosis, hyaline nodules (hard masses of glassy, eosinophilic substances) form in the mesangial part of the glomerulus. In both types of glomerulosclerosis, the sclerotic changes disrupt the function of increasing numbers of glomeruli, slowly impairing the patient’s renal function.

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Glucose Control

Tight blood glucose control-maintaining glucose levels as close to normal as possible without increasing the frequency or severity of hypoglycemic episodes-can help delay the onset and slow the progression of nephropathy. Tight blood glucose control also can reverse microalbuminuria in some patients. However, tight blood glucose control doesn’t affect the course of advanced nephropathy.

Antihypertensive Drug Therapy

Aggressive antihypertensive therapy may slow the progression of diabetic nephropathy. Certain antihypertensive drugs, such as angiotensin­converting enzyme (ACE) inhibitors and calcium channel blockers, may be used to treat hypertension. They also inhibit diabetic nephropathy in hypertensive patients and in normotensive patients with microalbuminuria.

However, ACE inhibitors may cause hyperkalemia and should be used cautiously if your patient has renal failure. Expect to avoid thiazide diuretics and beta-lockers because thiazide diuretics may worsen hyperlipidemia and hyperglycemia, and beta-blockers may mask or alter the symptoms of hypoglycemia.

Protein Restriction

Restricting your patient’s protein intake can reduce the rate of urine albumin excretion and kidney deterioration. The typical dietary protein intake in the United States is 1.2 to 1.4 g/kg/day. The physician may prescribe a diet that limits protein intake to 0.8 g/kg/day or less. For example, if your patient weighs 143 lb (65 kg), she may be limited to 52 grams of protein per day.

Therapy for Urinary Tract Infections

If your patient develops a UTI, her risk of renal dysfunction increases. If she has signs and symptoms of a UTI, such as dysuria (burning on urination), urinary frequency or urgency, or foul­smelling urine, the physician may request a urine sample for culture and sensitivity testing. And if your patient has an infection, the physician will prescribe an antibiotic. Before administering the antibiotic, however, check a current drug reference to determine if the drug is contraindicated or requires cautious use in a patient with a kidney disease, such as nephropathy.

Nephrotoxic Drug and Dye Restrictions

Your patient may be taking nephrotoxic drugs, such as an aminoglycoside or a nonsteroidal anti-inflammatory drug (NSAID). If so, the physician will monitor her kidney function by testing her serum creatinine levels. If your patient has impaired kidney function, the physician may adjust her drug dosage based on her GFR or creatinine clearance or prescribe a less nephrotoxic drug.

Radiographic dyes also are nephrotoxic. If your patient must undergo a test that requires radiographic dye, the physician may prescribe I.V. mannitol to be given 1 hour before the test to induce osmotic diuresis and minimize nephrotoxic effects.

Dialysis and Transplantation

A patient with end-stage renal disease may need hemodialysis or peritoneal dialysis, or she may be a candidate for a kidney transplant. Many patients who undergo hemodialysis develop sclerotic blood vessels from the numerous needle punctures at the dialysis access site. Eventually, they may have no more access sites to continue hemodialysis. These patients may be good candidates for peritoneal dialysis or kidney transplant.A donor kidney for a transplant can be obtained from a living relative, a living unrelated person, or a cadaver. A transplanted kidney has a 75% to 80% chance of functioning for at least 5 years. However, kidney transplants have many drawbacks:

• Donor kidneys are in short supply. Depending on your patient’s blood type and whether she has certain proteins or antibodies, she may never be offered a kidney.
• The risk of organ rejection is high, especially in the first year after the transplant.
• Expensive, long-term therapy with immunosuppressants is needed to help prevent organ rejection.
• Immunosuppression may lead to infection or malignancy .
• Immunosuppression makes tight glucose control more difficult.

Patients who test positive for the human immunodeficiency virus or who have a malignancy aren’t candidates for kidney transplant. Those with psychosis, active infection, severe neuropathies, or inoperable cardiovascular disease may not be approved for the procedure. Transplant complications include thrombosis, infection, anastomotic leaks (usually at the ureters), bleeding, and adverse effects of immunosuppression.

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If your patient develops constipation, treatment includes adequate fluid intake; increased physical activity; increased fiber intake; stool softeners, such as psyllium; judicious use of laxatives; and drugs, such as metoclopramide or cisapride, to stimulate gastric motility.

If your patient has diarrhea, her physician may prescribe drugs to slow intestinal motility, including loperamide, codeine, or diphenoxylate hydrochloride with atropine. The physician also may prescribe a high-fiber diet and psyllium to increase stool bulk and consistency. If your patient has diarrhea related to overgrowth of intestinal bacteria, her physician may prescribe a broad-spectrum antibiotic with anaerobic coverage, such as tetracycline or metronidazole. Your patient may benefit from biofeedback, relaxation, and bowel training, so discuss these treatment options with the physician.

A patient with diarrhea may benefit from a liquid, low-fat diet consisting of several small meals a day. This diet is effective when used with drugs taken one-half hour before eating. If your patient has severe diarrhea, the physician may prescribe total parenteral nutrition or jejunostomy tube feedings.

If your patient has orthostatic hypotension, treatment includes increasing her venous pressure by using supportive elastic body stockings applied while she’s lying down. Hypovolemia can be corrected by good blood glucose control, adequate salt intake, or fludrocortisone. The physician may prescribe a drug, such as ephedrine, to increase the heart rate and blood pressure through vasoconstriction.

No treatment is available for cardiac denervation. However, if the patient has periods of sustained sinus bradycardia or heart block that produce life-threatening symptoms, such as severe hypotension, she may need a permanent pacemaker. The physician may prescribe theophylline and terbutaline to increase the patient’s resting heart rate.

For a patient with bladder dysfunction, treatment focuses on improving bladder function and preventing UTls. Specific interventions may include treatment with antibiotics for UTIs or a parasympathomimetic drug, such as bethanechol, to improve bladder nerve contraction.

More Facts

Your teaching topics depend on your patient’s specific treatment. For GI dysfunction, teach her about her diet and meal planning. Advise her to check her blood glucose levels frequently, and reinforce the importance of using blood glucose levels to detect hypoglycemia and hyperglycemia. To promote optimal GI function, instruct your patient to consume enough fluid and fiber to prevent constipation. Also, advise her to use laxatives judiciously. Teach her relaxation exercises and biofeedback techniques.

Teach your patient with a dysfunctional bladder to schedule urination every 2 hours to help keep her bladder empty and to reduce the risk of UTI. Review the signs and symptoms of UTI, such as dysuria, fever, and chills, and tell her to contact her physician immediately if she experiences them. Teach her Crede’s method to help empty her bladder: She should place a cupped hand directly over her bladder, push in and down, and then massage her bladder to empty it. Also, teach her to palpate her bladder to check for fullness. If your patient must perform self-catheterization, teach her clean technique.

If your patient doesn’t have a prescription for glucagon, talk with the physician. Make sure the patient’s family and friends know how and when to administer glucagon and when to call for help.

Advise your patient with abnormal pupillary response to use a night-light and keep a flash­light by her bed in case she needs to get up during the night. Also tell her to avoid driving at night. Inform her that her abnormal pupil response and decreased peripheral sensation may cause her to lose her sense of balance easily. Advise her to keep her environment well lit and free from clutter.

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