If your patient maintains better blood glucose control, her pain and other symptoms may decrease. As nerve cells regenerate with improved blood glucose levels, your patient’s pain may worsen initially, but it will decrease over time.To prevent foot complications, your patient may need to use lamb’s wool padding to protect her feet from trauma. The physician may also refer her to a podiatrist, who will assess her feet regularly and gently file any callused areas, if necessary. Your patient may also need a referral to an orthotic or other foot care specialist to fit her for custommade shoes, molded insoles, or other orthotic devices to protect her feet. In some cases, your patient may require bed rest or crutches. Some patients with foot ulcers have casts applied so that they can walk while the ulcers heal. The cast redistributes foot pressure so that the ulcerated area bears much less weight than it would normally.

For pain associated with peripheral neuropathy, the physician may prescribe:

• a nonnarcotic analgesic, such as ibuprofen or sulindac
• tramadol hydrochloride
• phenytoin or carbamazepine
• a tricyclic antidepressant, such as amitriptyline, alone or with a phenothiazine derivative
• mexiletine
• topical capsaicin 0.075%.

Narcotic analgesics usually aren’t prescribed because peripheral neuropathy is a chronic condition, and the patient would risk developing an addiction. However, other therapeutic options may include transcutaneous electrical nerve stimulation therapy or referral to a pain control clinic.

Curing Steps for Patients

If your patient experiences painful paresthesia, especially at night, tell her to stretch gently or to get up and walk around. Also, teach her how to safely massage her feet and legs, and explain that this sometimes helps to block pain sensations. If appropriate, teach your patient how to safely use the TENS unit. Teach her about guided imagery, meditation, progressive relaxation techniques, exercise, and therapeutic massage.

Teach your patient the importance of foot care, and review safety measures she can take to prevent trauma. For instance, advise her to avoid prolonged standing and strenuous weight-bearing exercises. Tell her to wear well-cushioned, properly fitting shoes and to walk in well-lit areas where the ground is smooth.

If your patient has decreased temperature sensation, advise her to prevent severe burns by checking the water temperature with a part of her body that’s sensitive to temperature, such as forearm. If she experiences abnormal cold sensations, advise her to wear thin gloves in the spring or fall. When temperatures drop, she should wear heavier, insulated gloves. Tell her that mittens may be warmer than gloves. If cold feet are a problem, tell her to wear comfortable insulated socks with her shoes.

Review with your patient the name, dosage, action, and adverse effects of all her prescribed drugs. If she’s using topical capsaicin, tell her to wear gloves when she applies it, avoid contact with her eyes, and wash her hands immediately after application. Also, warn her that she may experience transient burning of the affected area after applying capsaicin.

Encourage your patient to avoid drinking alcohol. Explain that alcohol abuse may contribute to the progression of peripheral neuropathy. If appropriate, refer your patient to a counselor or to Alcoholics anonymous. If she smokes, encourage her to stop. Explain that cigarette smoking can worsen her condition and that stopping may slow its progress.

Explain that your patient should have her feet inspected at least four times a year and that a physician should perform a thorough physical examination and neurologic assessment at least once a year.

The early signs and symptoms of hypoglycemia tend to be autonomic. Neuroglycopenic signs and symptoms generally appear later.

Autonomic Signs and Symptoms

• nervousness
• tremors
• palpitations
• diaphoresis
• anxiety
• pallor
• irritability
• hunger
• paresthesia

Neuroglycopenic Signs and Symptoms

• dizziness
• headache
• lack of coordination
• difficulty concentrating
• mental dullness
• severe lethargy
• slurred speech
• blurred vision
• mood changes
• seizures
• coma

Acarbose, an Intestinal Alpha-Glucosidase Inhibitor, decreases postprandial hyperglycemia by inhibiting the digestion and absorption of carbohydrates. It achieves this by inhibiting the enzymes responsible for the digestion of starches and other carbohydrates in the brush border of the small intestine.The peak action of acarbose occurs within 1 hour of ingestion. The drug is metabolized by intestinal bacteria and digestive enzymes. Because the half-life for acarbose is only about 2 hours, the drug should be taken three times a day.

A physician will begin acarbose therapy at 25 mg three times a day. She will adjust dosages every 4 to 8 weeks based on 1-hour postprandial blood glucose levels and on tolerance until an effective dose is achieved. The maximum recommended dosage is 50 mg three times a day for patients who weigh 60 kg or less. For those who weigh more than 60 kg, the maximum dosage is 100 mg three times a day.

Indications and Contraindications

Acarbose is used with stable Type 2 patients as an adjunct to diet and exercise to reduce blood glucose levels. This drug benefits patients who can’t achieve near-normal blood glucose levels with sulfonylureas or metformin.

Because acarbose increases gas formation in the intestine, it’s contraindicated for anyone with inflammatory bowel disease, ulcerations of the colon, or intestinal obstruction. The drug is also contraindicated for patients with chronic intestinal diseases that alter digestion or absorption. Acarbose is contraindicated during pregnancy or breast-feeding. Patients with kidney dysfunction, DKA, or a hypersensitivity to the drug also shouldn’t take it.

Adverse Effects and Interactions

The most common reactions to acarbose are GI signs and symptoms. Patients may complain of abdominal pain, diarrhea, and flatulence caused by undigested carbohydrates in the intestines. These signs and symptoms tend to subside with time. At doses of 100 mg, acarbose may cause an asymptomatic, reversible increase in serum transaminase levels, especially in women.

The action of acarbose decreases with the concurrent use of charcoal, an intestinal adsorbent, and digestive enzyme preparations that contain carbohydrate-splitting enzymes, such as amylase and pancreatin. Hyperglycemia may result if a patient takes acarbose with thiazide and other diuretic drugs, beta-blockers, corticosteroids, phenothiazines, thyroid preparations, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers, or isoniazid. Acarbose can be taken with a sulfonylurea or insulin, but these combinations may cause hypoglycemia. However, acarbose can help to prevent weight gain associated with sulfonylurea therapy.

Advise your patients to take acarbose with meals. Because the goal is to prevent the absorption of intestinal glucose, they should take the drug along with the first bite of food. No food interactions occur.

Blood Tests

Blood tests used to diagnose diabetes include the fasting blood glucose test, the 2-hour oral glucose tolerance test, and the random blood glucose test.

The glycosylated hemoglobin test is used to monitor the effectiveness of a patient’s therapy.

Blood tests used to detect and monitor the progression of diabetic complications include a fasting lipid profile for cardiovascular disease and serum creatinine and blood urea nitrogen (BUN) tests for renal disease.

Diagnostic Tests

A physician may order diagnostic tests to diagnose diabetes, detect diabetic complications, or monitor the effectiveness of a patient’s therapy. Of course, a patient should also perform self-monitoring to check the effectiveness of her therapy.

Early detection of diabetic complications allows for early treatment, which can minimize their destructive effects. Tests that help diagnose a complication can be repeated to monitor its progress

Begin the review of body systems by asking your patient about her general well-being. Commonly, a patient with diabetes will say that she doesn’t feel as well as she used to, and she’ll attribute her fatigue and weakness to growing older.Ask your patient about her weight history. A recent weight loss that’s not attributed to diet or a recent illness is a typical symptom of diabetes, especially Type 1 diabetes. People with Type 2 diabetes are usually obese. No one is sure why. Some researchers speculate that obesity is a factor in the development of Type 2 diabetes because fat cells require more insulin per cell than nonfat cells do. This leads to substandard insulin production as the pancreas works overtime to meet the obese patient’s insulin demands. Other researchers believe that obesity is actually an early sign of Type 2 diabetes.

Ask your patient about any skin conditions. One common symptom is dry, itchy skin, which develops because of mild dehydration associated with hyperglycemia. The itchiness is caused by glucose pooling under the skin. Such pooling also creates an ideal environment for skin infections, another common complaint of patients with diabetes. Patients may also report skin discoloration and chronic skin conditions, such as ulcers that don’t heal.

Next, ask your patient about visual disturbances. As glucose levels rise, glucose molecules cause blood vessels in the eyes to become congested and vision to blur. If your patient has prolonged hyperglycemia, she may report that she has trouble reading. She also may tell you that she sees dark spots, rings around lights, or flashing lights. Find out how often she has her eyes examined, when she last had them examined, and whether an ophthalmologist performed the examination. A patient with diabetes requires frequent eye examinations because the disease is one of the major causes of new cases of blindness diagnosed each year. Because of the complexity of diabetic retinopathy, a common complication associated with diabetes, an ophthalmologist should perform all eye examinations on a patient with diabetes.

Ask your patient about any history of periodontal disease or oral infections. These problems are common in patients with diabetes because of glucose pooling in gum tissue, which leads to frequent infections and destruction of delicate oral tissues.

Diabetes is also a major risk factor for arteriosclerosis, so ask your patient if she has any of the signs or symptoms of cardiovascular or peripheral vascular abnormalities: heart problems, chest pain, shortness of breath, hypertension, elevated cholesterol and triglyceride levels, cold feet, pain that occurs with walking, or leg or foot ulcers. Arteriosclerosis that affects the cerebral arteries may cause the patient to report transient ischemic attacks-brief episodes of dizziness, loss of sight, slurred speech, or feelings of numbness or weakness in one arm or leg.

Neuropathy, which may occur because of excessive glucose coating of the nerves, results from prolonged hyperglycemia. History findings that suggest peripheral neuropathy include a pins­and-needles sensation, sharp stabbing pains, and numbness in the hands or feet. Some patients may report leg pain that occurs only at night and is relieved by walking. Complaints that suggest autonomic neuropathy include nausea and vomiting, abdominal bloating, and nocturnal diarrhea, all of which are typical signs and symptoms of gastroparesis.

Some patients may complain of dizziness when changing position (suggesting orthostatic hypotension), an irregular pulse rhythm, or a fixed heart rate despite exercise (suggesting an electrical dysfunction of the heart).

Prolonged hyperglycemia may also lead to diabetic nephropathy, which is usually well ad­vanced before the patient experiences any symptoms. Ask your patient whether she has ever been told that she has protein in her urine. Also, ask her if she has ever had urinary tract or kidney infections. If she has, take a detailed history of the infections including the frequency, signs and symptoms, and treatment.

Ask your patient about reproductive abnormalities. Sexual dysfunction, including loss of li­bido, commonly develops in patients with diabetes. Impotence may develop in men with diabetes because of both blood vessel disease and neuropathy caused by chronic hyperglycemia. Women with diabetes may report frequent vaginal infections.

Peripheral neuropathy, a common complication of diabetes, causes sensory loss in the arms and legs. Such sensory loss in the feet increases the patient’s risk of developing foot ulcers that could ultimately lead to amputation.Usually, sensory loss is diagnosed by an examiner touching different areas of the patient’s foot with a pin. Unfortunately, this technique isn’t reliable. An examiner may not exert the same amount of pressure on each area, and some examiners are more heavy-handed than others. In fact, the same examiner may be heavy-handed one day and have a lighter touch the next, making comparisons difficult.

Filament testing with a monofilament device alleviates these problems. The device places exactly 10 grams of force on a small area of the skin . To assess sensory loss in the feet, an examiner uses the device at 10 sites on each foot.

The test result is normal if the patient feels the filament in all 10 spots on each foot. The result is abnormal if she doesn’t feel it in one or more spots.

Filament testing can be used to monitor the progression of a patient’s sensory loss and to help in tailoring an ulcer prevention program for her.

Nursing Considerations

Have the patient lie down on the examination table and instruct her to say yes each time she feels the filament.

Have her keep her eyes closed to avoid an invalid response. After the test, develop an ulcer prevention program for your patient .

To help confirm a diagnosis of DKA and guide treatment, the physician may order laboratory measurements of:

• blood glucose
• blood bicarbonate
• blood urea nitrogen (BUN)
• hematocrit
• urine specific gravity
• blood osmolality
• white blood cell (WBC) count
• blood phosphate
• blood potassium and sodium
• pH.

The blood glucose level may range from 300 to 800 mg/dl. The blood bicarbonate level may drop below 15 mEq/L. Dehydration causes BUN levels,hematocrit, and urine specific gravity to rise. Blood osmolality may soar as high as 330 mOsm/L.

The WBC count may be high from hemoconcentration or infection. If the WBC count remains high after DKA has been treated, the patient probably has an infection. The blood phosphate level may be low. Blood potassium and sodium levels may be high, normal, or low, reflecting shifts between intracellular and extracellular fluid. The total body potassium generally is depleted. As ketones accumulate in the blood, the patient’s pH drops below 7.3.

Many people with diabetes aren’t physically fit, lead sedentary lives, and have microvascular, macrovascular, or neuropathic complications. However, they can still benefit from exercise that’s modified for their needs.If your patient has peripheral vascular disease, an assessment of arterial circulation is essential. Her exercise regimen may be modified to include interval training, such as walking with frequent rest periods. If your patient has only limited use of her legs because of claudication, chair or upper body exercise is a good alternative.

Your patient with retinopathy should avoid isotonic exercises, which provoke straining and cause blood pressure to rise rapidly, either of which can precipitate a hemorrhage of the vitreous humor. For this patient, aerobic exercises shouldn’t jar her head or require a headdown position.

Patients with nephropathy and those receiving hemodialysis tend to have low hemoglobin levels and hematocrit and impaired cardiac function. All these conditions contribute to an extremely low capacity for exercise. These patients should begin exercising slowly for short periods and increase gradually. In patients with renal osteodystrophy, weight-bearing exercise may improve bone density.

Although exercise can’t reverse sensorimotor neuropathy, it can improve the effects of disuse. Because patients with sensorimotor neuropathy have decreased sensation, they should perform stretching exercises gently and avoid highimpact exercises. Instead, they should use low-impact exercises such as walking, bicycling and swimming. Range-of-motion exercises can prevent or minimize joint contractures. Because of her decreased sensation, instruct your patient to inspect her feet daily for blisters, redness, fissures and ulcerations.

Patients with autonomic neuropathy and those taking beta-blockers may have an impaired counterregulatory response that fixes the heart rate at 80 to 90 beats per minute even when they’re exercising. The result is limited exercise tolerance. Exlain to your patient that sudden death or a silent myocardial infarction can occur when her heart fails to respond to nerve impulses. If your patient with autonomic neuropathy doesn’t have a fixed heart rate, her target heart rate should start low and then gradually increase over several exercise sessions. Advise her to avoid sudden changes in body position and significant changes in heart rate and blood pressure.

Most of the pancreas is made up of exocrine tissue, which is arranged in small saclike structures called acini. The cells of these acini release secretions into tiny ducts that eventually unite with the pancreatic duct, which extends from the tail to the head of the pancreas. The pancreatic duct gets larger as it passes through the pancreas. This duct joins the common bile duct and then empties into the duodenum at the ampulla of Vater. The accessory pancreatic duct, also known as the duct of Santorini, extends from the head of the pancreas into the duodenum.When food enters the stomach, the intestinal mucosa releases the hormone secretin into the bloodstream. Secretin in turn stimulates the acinar cells and ducts to secrete pancreatic juice. An alkaline solution, the pancreatic juice consists of water, bicarbonate, electrolytes, and enzymes for food digestion. These pancreatic enzymes fall into three categories- proteolytic enzymes (trypsin and chymotrypsin), which break down proteins, pancreatic lipase, which helps digest fat and pancreatic amylase, which helps digest carbohydrates. The digestive enzymes and the other components of the pancreatic juice pass from the microscopic ducts into the pancreatic duct and then enter the duodenum. In the duodenum, the pancreatic juice neutralizes the acidic chyme from the stomach.

The pancreas protects itself from these digestive enzymes by secreting them in inactive forms. They don’t become active until they reach the digestive tract, where activating enzymes convert them. For example, trypsin is released from the pancreas as the zymogen trypsinogen, which is then converted to active trypsin by enterokinase in the intestine.