Practice nursing care for Clients with Vascular Problems

Practice nursing care for Clients with Vascular Problems



The leading cause of death in the United States is disease associated with atherosclerosis. Nearly 1 million people die of heart and blood vessel diseases each year in the United States (American Heart Association). Atherosclerosis is a common link between cardiovascular disease, cerebrovascular disease, and peripheral vascular disease (PVD). People with atherosclerosis have an increased risk of developing one or more of these diseases. Disorders of the vascular system cause many problems and may lead to complete shutdown of all body organs and eventually death. Although vascular disease can affect any portion of the human body, such as the heart, brain, and kidneys, the peripheral vascular system and its associated diseases are described here.




Arteriosclerosis is a thickening, or hardening, of the arterial wall. Atherosclerosis, a type of arteriosclerosis, involves the formation of plaque within the arterial wall. Atherosclerosis is the most common cause of arterial obstruction.


The exact pathophysiology of atherosclerosis is not known, but the condition is thought to occur in the following way (Figure 36-1).

A fatty streak appears on the intimal surface (inner lining) of the artery. At this stage, the fatty streak may appear flattened or elevated, but it generally does not affect the integrity of the arterial wall. Next, a fibrous plaque develops. This plaque is described as a white, glistening, fibrous elevation that covers a lipid core. At this stage, the plaque is elevated enough to partially or completely occlude the blood flow of an artery. In the final stage, the fibrous lesions become calcified, hemorrhagic, ulcerated, or thrombosed. The rate of progression of this process may be influenced by genetic factors; certain chronic diseases, such as diabetes mellitus; and lifestyle habits, including smoking, eating habits, and level of exercise.



The exact etiology of atherosclerosis is unknown, but several theories attempt to explain its cause. It is believed that an injury to the intimal layer of the artery may initiate the development of atherosclerosis. One popular theory, known as platelet aggregation, is that after the intimal injury has occurred, platelets form a cluster at the arterial wall and produce a peptide that stimulates the proliferation of the smooth muscle cells of the intima. Eventually, this proliferation can narrow the artery enough to compromise the flow of blood or completely occlude arterial blood flow.

Another theory, the lipid hypothesis, assumes that after an intimal injury, a group of blood lipids (fats) accumulate. Again, this accumulation can partially or completely occlude arterial blood flow. The principal lipids involved are cholesterol and triglyceride.

Many theorists believe that a combination of these two events provides the most appropriate explanation of the atherosclerotic process and that this process can occur in any arterial wall of the body. Usually the disease affects the larger arteries, such as the coronary artery beds, the major branches of the aorta, the visceral branches of the aorta, the terminal abdominal aorta, the carotid and vertebral arteries, or any combination of these.


Intimal injury of the major arteries of the body can be attributed to many factors. Hypertension can cause a mechanical injury, whereas elevated levels of low-density lipoproteins (LDLs) and decreased levels of high-density lipoproteins (HDLs) can cause chemical injuries to the intimal wall. Chemical injury can also be caused by elevated levels of toxins in the bloodstream, which may occur with renal failure or by carbon monoxide circulating in the bloodstream from cigarette smoking. The intimal wall can be weakened by the natural process of aging or by physiologic disorders, such as diabetes.

Genetic predisposition and diabetes have a fairly direct effect on the development of atherosclerosis. Some families demonstrate inherited hyperlipidemia, an elevation in levels of blood lipids. In these people the liver makes excessive cholesterol, which accounts for the development of atherosclerosis. In some people with hereditary atherosclerosis, however, the blood cholesterol level is normal. The reason for the development and progression of plaque in these people is not understood.

People with severe diabetes mellitus frequently have premature and severe atherosclerosis, often involving the microvasculature. This occurs because diabetes promotes an increase in LDL in plasma. In addition, intimal arterial damage may result from the effect of hyperglycemia.

Factors indirectly related to atherosclerosis include obesity, a sedentary lifestyle, and stress. Clients who are obese are at greater risk, most often because of concomitant elevations in cholesterol levels. Long-term physical activity is important in maintaining ideal body weight; it is also thought to help in maintaining optimal blood pressure and cholesterol levels and improved glucose tolerance. The effect of stress may be due to its effect on the sympathetic and parasympathetic release of catecholamines and an acute rise in blood pressure.


It is not known exactly how many people have atherosclerosis, but small plaques are almost always present in the arteries of young adults. The incidence can be better quantified by assessing diseases that result from this process. However, it is estimated that peripheral atherosclerosis affects 5% of Americans over 60 years of age and up to 25% of those over 75 years of age (Meyerson & Schwartz, 1999). It is predicted that these numbers will increase as a result of the increasing population of older adults.



VITAL SIGNS Because of the high incidence of hypertension in clients with atherosclerosis, the nurse assesses the blood pressure in both arms. The heart is also thoroughly assessed because concomitant cardiac disease is often present. The nurse may palpate pulses at all of the major sites on the body and note any differences. Carotid arteries are palpated separately because of the risk of inadequate cerebral perfusion. The nurse also palpates for temperature differences in the lower extremities and checks capillary filling. Prolonged capillary filling (>3 seconds in young to middle-aged adults; >5 seconds in older adults) generally indicates poor circulation. An extremity in a person with significant atherosclerotic disease may be cool or cold, with a diminished or absent pulse.

ASSESSMENT FOR BRUITS After palpating the pulses, the nurse may auscultate each large artery from the carotid to the dorsalis pedis with a stethoscope or a Doppler probe. Many clients with vascular disease have a bruit in the larger arteries.

A bruit is described as a turbulent, swishing sound, which can be soft or loud in pitch. The mere existence of a bruit is considered abnormal, but the role it plays in indicating the severity of vascular disease is not understood. The nurse should document the location of bruits. They often occur in the carotid, aortic, femoral, and popliteal arteries and usually indicate some degree of narrowing of the arterial wall. The rate and intensity of the pulse in each artery during auscultation is also noted. A decrease in intensity and audibility or a complete loss of a pulse may indicate an arterial occlusion.


Total serum cholesterol levels are often elevated in clients with atherosclerosis. Clients should keep their total serum cholesterol levels below 200 mg/dL.

The National Cholesterol Education Program has recommended screening guidelines based on the following:

Ø      Total serum cholesterol and high-density lipoprotein (HDL) cholesterol levels in individuals without evidence of cardiac or vascular disease

Ø     Total serum cholesterol and HDL cholesterol levels in individuals with risk factors (Table 36-1)

Elevated cholesterol levels must be validated by HDL and LDL determinations. Elevated LDL cholesterol levels indicate that a person is at an increased risk for atherosclerosis. Low or normal HDL cholesterol levels also indicate an increased risk. A desirable LDL level is one below 100 mg/dL for all individuals. A desirable HDL level is 35 mg/dL or above. In some people, particularly women, an elevated cholesterol level may be due to an elevated HDL level, which is not considered a risk.

Triglyceride levels may also be elevated with atherosclerosis. A level of 200 mg/dL or above indicates hypertriglyceridemia. Elevated triglyceride levels may not cause atherosclerosis, but an elevated triglyceride level is often associated with the condition.

Homocysteine is derived from dietary methionine and metabolized either by remethylation or transsulfuration. Homocysteine is an essential sulfur-containing amino acid derived from dietary protein. Research studies have shown that individuals with increased homocysteine levels are at greater risk for the premature development of peripheral vascular disease (PVD) and coronary artery disease (CAD). High serum levels of homocysteine have an adverse effect on the vascular endothelium. A serum homocysteine level greater than 15 |xmol/L is considered a risk factor. Recent studies have demonstrated that folic acid, usually 1 mg every day, can improve endothelial function and lower homocysteine levels. These actions assist in decreasing the risk for the development of PVD (Jacques et al., 1999).

 Interventions Atherosclerosis progresses for years before clinical manifestations are evident. Clients with or at risk for atherosclerosis can often be identified through cholesterol screening. Because of the high incidence of atherosclerosis in the United States, all people 20 years of age and older are advised to have their total serum cholesterol level evaluated.

 DIET THERAPY. New 2001 guidelines from the National Cholesterol Education Program focus on an aggressive approach to lowering low-density lipoprotein (LDL) values. Having an LDL value of less than 100 mg/dL is optimal; values of 100 to 129 mg/dL are near or above optimal. Clients with LDL values of 130 to 159 mg/dL (borderline high) are advised to follow a fat-modified diet. In collaboration with the dietitian, the nurse instructs clients with LDL values of 160 mg/dL or greater (high or very high) to follow a more structured diet aimed at decreasing saturated fat and cholesterol and, if appropriate, promoting weight loss. A decrease in fat, particularly saturated fat, is considered more important than simply decreasing the cholesterol number because saturated fat is one of the main determinants of cholesterol synthesis in the body.

In the United States, 37% of the total caloric intake in the diets of many people is made up of fat, and this overconsumption of fat and cholesterol leads to hypercholesterolemia, an elevated total blood cholesterol level. On the other hand, elevated cholesterol levels can often be decreased if fat in the diet is limited to no more than 30% of the caloric intake.

To assess what 30% of the caloric intake is, clients first need to determine their ideal daily caloric intake. They can then cal-  culate their fat limit in grams. In addition to tracking fat in grams, people need to assess the fatty acid content of foods.

STEP ONE DIET. The Step One diet of the American Heart Association, which is often recommended to decrease the serum cholesterol level, calls for a total fat intake of less than 30% of total calories, with less than 10% of total caloric intake coming from saturated fat, up to 10% of total calories coming from polyunsaturated fat, and 10% to 15% coming from monounsaturated fat. Cholesterol intake with this diet is limited to less than 300 mg daily. In collaboration with the dietitian, the nurse educates the client about the fat content of foods in terms of the total degree of fat and saturation. Meats and eggs contain mostly saturated fats. Because canola (rapeseed) oil is rich in monounsaturated fat and safflower and sunflower oil are rich in polyunsaturated oils, they are recommended over highly saturated oils, such as palm or coconut oil. Cholesterol is found only in animal sources, such as meat and eggs, which are also high in saturated fats.

STEP TWO DIET. The client's serum cholesterol levels are retested 6 and 12 weeks after the initial dietary intervention. If the cholesterol level has not significantly decreased, the client may be referred to a registered dietitian for instruction on a more restricted diet, such as the Step Two diet. The Step Two diet limits saturated fat to less than 7% of total calories and cholesterol to less than 200 mg/day. In addition to elevated LDL values, other variations of hyperlipidemias put clients at risk for atherosclerosis. A low-fat, low-cholesterol diet, however, can play a significant role in improving a lipid profile, regardless of the lipid alteration.

SMOKING CESSATION. Cigarette smoking lowers levels of high-density lipoprotein (HDL) cholesterol and dramatically increases the rate of progression of atherosclerosis. The nurse can play an important role in helping clients stop smoking. The nurse advises all clients who smoke to stop smoking and all clients to avoid secondhand smoke. The nurse describes the relationship of smoking to atherosclerosis and assesses the client's willingness to change this behavior. Nurses and other health care providers can refer to the Agency for Healthcare Research and Quality's Practice Guidelines on Smoking Cessation (formerly the Agency for Health Care Policy and Research). This reference provides strategies to assist clients in quitting smoking. A smoking cessation group, such as the American Cancer Society's Fresh Start, may help with this difficult process. Most formal programs encourage people to stop smoking "cold turkey." Johns Hopkins Hospital in Baltimore has developed a stage-of-readiness model that classifies clients into one of six stages (Stillman, 1995).

The nurse can assess the client's readiness to stop smoking using this model (Table 36-2).

Clients may consider using a nicotine patch (Nicoderm, Habitrol, Prostep), which helps relieve nicotine withdrawal symptoms. The patch is about 50% effective in helping clients to stop smoking and is available over the counter. The dose is determined by the client's weight and the extent to which he or she smokes. Clients are urged to stop smoking completely when the nicotine patch is initiated. The nurse informs clients that if they continue to smoke while using the patch, their risks for adverse effects are increased because the peak levels of nicotine are higher than those experienced from smoking alone. Serious cardiovascular effects, such as angina and dysrhythmias, may result from the patch, although the most common side effect is skin irritation. Many health insurance programs will not cover the costs associated with nicotine patches unless the client is enrolled in a smoking cessation program. Nicotine gum (Nicorette) also may be used if a client feels the need to smoke. Clients should not chew more than 30 pieces of gum per day. Some clients need an oral medication, such as bupropion (Wellbutrin, Zyban), to help decrease the urge to  smoke. Because these drugs depress the central nervous system, clients taking them are carefully monitored by a health care provider.


Some clients try other methods to help them stop smoking, including acupuncture, acupressure, hypnosis, and biofeedback.

EXERCISE. Regular exercise is recommended to promote optimal lipid levels and can actually prevent atherosclerosis. Exercise can also lead to regression of atherosclerotic plaque and the building of collateral circulation in people with atherosclerosis. The level of exercise required to provide protection from atherosclerotic disease has not been well established, but it is recommended that individuals get 30 minutes of moderate to vigorous exercise at least three to four times a week. The nurse should instruct clients with heart disease and other comorbid conditions, such as hypertension, vascular disease, or diabetes, to undergo an exercise tolerance (treadmill or stress) test before undertaking an exercise program (e.g., aerobics, walking, or running).

DRUG THERAPY. Clients with elevated total and LDL cholesterol levels that do not respond adequately to dietary intervention are started on a regimen of lipid-lowering agents (Chart 36-1).

Drug choice is dependent on the triglyceride levels. Because most of these drugs can produce major side effects, they are generally given only when nonpharmacologic management has been unsuccessful. Bile acid-binding resins, such as cholestyramine (Questran) or colestipol (Colestid), may be recommended initially because of their low toxicity. Medications such as lovastatin (Mevacor), simvastatin (Zocor), atorvastatin (Lipitor), and fluvastatin (Lescol) lower both LDL and triglyceride levels. These statins are contraindicated in clients with active liver disease or during pregnancy, since they can cause muscle myopathies and marked increases in liver function. Nicotinic acid lowers LDL and very low-density lipoprotein (VLDL) cholesterol levels and increases HDL cholesterol levels. It is used as a single agent or in combination with an acid-binding resin drug or a statin. Low doses (1.0 to 1.5 g/day) are generally well tolerated, but higher doses can result in an elevation of hepatic enzymes and various other side effects. Gemfibrozil (Lopid) raises HDL and lowers triglyceride and VLDL levels, but it is not as effective in lowering LDL levels.

GENE THERAPY. As the U.S. population continues to age, it is predicted that more people will need some type of vascular intervention. Ongoing clinical trials are examining the effectiveness of gene therapy in treating vascular disease. In addition, vascular endothelial growth factor (VEGF) is being used to stimulate new blood vessel growth through angiogenesis in clients with end-stage peripheral ischemia (Meyerson & Schwartz, 1999). As clinical research continues in this area, more options will be available for people with vascular disease.



Hypertension is generally defined as a systolic blood pressure greater than or equal to 140 mm Hg and/or a diastolic blood pressure greater than or equal to 90 mm Hg in individuals who do not have diabetes. In individuals with diabetes and/or renal impairment, hypertension is considered to be a systolic blood pressure of 130 mm Hg and/or a diastolic blood pressure of 85 mm Hg or higher (Joint National Committee, 1997). Generally, hypertension is determined by two separate readings (Figure 36-2).

 However, if the client has risk factors for hypertension, lifestyle changes can be recommended before the second evaluation. Hypertension is classified into three stages (Table 36-3).


The significance of this disease is that it is a major risk factor for coronary, cerebral, renal, and peripheral vascular disease. However, control of hypertension has resulted in significant decreases in cardiovascular morbidity and mortality. Although mortality rates have declined over the last 20 years, hypertension costs more than $500 million per year and accounts for the largest number of health care provider visits per year, as well as the largest consumption of prescription drugs (Eaton, Buck, & Catanzaro, 1996). To achieve the Healthy People 2010 objective of increased blood pressure control among clients with hypertension, nurses must be able to assess and intervene appropriately in their care.


The systemic arterial pressure is a product of the cardiac output and the total peripheral resistance (Figure 36-3). Cardiac output is determined by the stroke volume and heart rate. Control of peripheral resistance is maintained by the autonomic nervous system and circulating hormones, such as norepinephrine and epinephrine. Consequently, any factor producing an alteration in peripheral resistance, heart rate, or stroke volume affects the systemic arterial pressure.


Stabilizing mechanisms exist in the body to exert an overall regulation of systemic arterial pressure and to prevent circu latory collapse. Four control systems play a major role in maintaining blood pressure: the arterial baroreceptor system, regulation of body fluid volume, the renin-angiotensinaldosterone system, and vascular autoregulation.


The arterial baroreceptors are found primarily in the carotid sinus but also in the aorta and the wall of the left ventricle. These baroreceptors monitor the level of arterial pressure. The baroreceptor system counteracts a rise in arterial pressure through vagally mediated cardiac slowing and vasodilation with decreased sympathetic tone. Therefore reflex control of circulation elevates the systemic arterial pressure when it falls and lowers it when it rises. Why this control fails in hypertension is unknown. There is evidence for upward resetting of baroreceptor sensitivity so that pressure rises are inadequately sensed even though pressure decreases are not.


Changes in fluid volume also affect the systemic arterial pressure. If there is an excess of salt and water in a person's body, the blood pressure rises through complex physiologic mechanisms that change the venous return to the heart, producing a rise in cardiac output. If the kidneys are functioning adequately, a rise in systemic arterial pressure produces diuresis and a fall in pressure. Pathologic conditions that change the pressure threshold at which the kidneys excrete salt and water alter the systemic arterial pressure.


Renin, angiotensin, and aldosterone also regulate blood pressure (Figure 36-4). The kidney produces renin, an enzyme that acts on a plasma protein substrate to split off angiotensin I, which is converted by an enzyme in the lung to form angiotensin II.


 Angiotensin II has strong vasoconstrictor action on blood vessels and is the controlling mechanism for aldosterone release. The significance of aldosterone in hypertension is most evident in primary aldosteronism. By increasing the activity of the sympathetic nervous system, angiotensin II also appears to inhibit sodium excretion, resulting in an elevation in blood pressure. Inappropriate secretion of renin may cause increased peripheral vascular resistance in essential (primary) hypertension. In high blood pressure, renin levels should be expected to fall because the increased renal arteriolar pressure should inhibit renin secretion. In most people with essential hypertension, however, renin levels are normal.


The process of vascular autoregulation, which keeps perfusion of tissues in the body relatively constant, appears to be important in causing hypertension accompanying salt and water overload. This mechanism is poorly understood.


Sustained blood pressure elevation in clients with essential (primary) hypertension results in damage to blood vessels in vital organs. Essential hypertension produces medial hyperplasia (thickening) of the arterioles. As the blood vessels thicken and perfusion decreases, body organs are damaged; these changes can result in myocardial infarctions, strokes, PVD, or renal failure.

Malignant hypertension is a severe type of elevated blood pressure that is rapidly progressive. A person with malignant hypertension usually has symptoms such as morning headaches, blurred vision, and dyspnea and/or symptoms of uremia (accumulation in the blood of substances ordinarily eliminated in the urine). Clients are often in their 30s, 40s, or 50s. The systolic blood pressure is greater than 200 mm Hg. The diastolic blood pressure is greater than 150 mm Hg, or greater than 130 mm Hg when there are pre-existing complications. Unless intervention occurs promptly, a client with malignant hypertension may experience renal failure, left ventricular failure, or stroke.


Hypertension can be essential (primary) or secondary (Table 36-4). Essential hypertension accounts for 90% of all cases (Dumas, 1999).


Although there is no known cause for essential hypertension, several associated risk factors have been discovered on the basis of common characteristics of people with this disease:

Ø     Age greater than 60 years

Ø     A family history of hypertension

Ø     Excessive calorie consumption

Ø     Physical inactivity

Ø     Excessive alcohol intake

Ø     Hyperlipidemia

Ø     African-American ethnicity

Ø     High intake of salt or caffeine; reduced intake of potassium, calcium, or magnesium

Ø      Obesity

Ø     Smoking

Ø     Stress

36.4. Etiology of Hypertension


Ø      No known cause

Ø      Associated risk factors

Ø     Family history of hypertension

Ø     High sodium intake

Ø     Excessive calorie consumption

Ø     Physical inactivity

Ø     Excessive alcohol intake

Ø     Low potassium intake


Ø     Renal vascular and renal parenchymal disease

Ø     Primary aldosteronism

Ø     Pheochromocytoma

Ø     Cushing's disease

Ø     Coarctation of the aorta

Ø     Brain tumors

Ø     Encephalitis

Ø     Psychiatric disturbances

Ø     Pregnancy

Ø     Medications

Ø     Estrogen (e.g., oral contraceptives)

Ø     Glucocorticoids

Ø     Mineralocorticoids

Ø     Sympathomimetics


A family history of hypertension is a major risk factor. In families with hypertension, there may be a defect in renal secretion of sodium or a heightened sympathetic nervous system response to stress.

The stress of caregiving by family members can also accelerate the risk of hypertension. Shaw et al. (1999) found that hypertension was more common in spouses of clients with Alzheimer's disease when compared with similar subjects who did not have caregiving responsibilities. The researchers concluded that the chronic stress of caregiving contributed to the incidence of high blood pressure.


Specific disease states and medications can increase a person's susceptibility to hypertension; a person with this type of elevation in blood pressure has secondary hypertension.

DISEASES. Renal vascular and renal parenchymal diseases are two of the most common causes of secondary hypertension. Hypertension can develop when there is any sudden damage to the kidneys. Renovascular hypertension is associated with narrowing of one or more of the main arteries carrying blood directly to the kidneys. Renal parenchymal diseases are related to infection, inflammation, and changes in kidney structure and function. Dysfunction of the adrenal medulla or the adrenal cortex can cause secondary hypertension. Adrenal-mediated hypertension is due to primary excesses of aldosterone, cortisol, and catecholamines.

In primary aldosteronism, excessive aldosterone causes hypertension and hypokalemia (low potassium levels). Primary aldosteronism usually arises from benign adenomas of the adrenal cortex. Pheochromocytomas originate most commonly in the adrenal medulla and result in excessive secretion of catecholamines. In Cushing's syndrome, excessive glucocorticoids are excreted from the adrenal cortex. The cause of Cushing's syndrome may be either adrenocortical hyperplasia or adrenocortical adenoma.

Coarctation of the aorta is a congenital narrowing of the aorta that may cause hypertension. Occurring at any level of the thoracic or abdominal aorta, the narrowing restricts blood flow through the aortic arch, resulting in an elevated blood pressure above the constriction. After surgical repair, the elevation in blood pressure eventually subsides. Secondary hypertension is also associated with other neurogenic disturbances, such as brain tumors, encephalitis, and psychiatric disturbances.

MEDICATIONS. Medications that can cause secondary hypertension include estrogen, glucocorticoids, mineralocorticoids, sympathomimetics, cyclosporine, and erythropoietin. The use of estrogen-containing oral contraceptives is probably the most common cause of secondary hypertension in women. Discontinuation of medications capable of causing hypertension often reverses this problem.


It is estimated that 50 million Americans, or 1 in every 4 adults, have high blood pressure or are currently being treated for hypertension.




During history taking, the client's risk factors for hypertension are reviewed. The nurse ascertains the client's age; ethnic origin or race; family history of hypertension; average dietary intake of calories, sodium- and potassium-containing foods, and alcohol; and exercise habits. Any past and/or present history of renal or cardiovascular disease and current use of medications are also assessed.


When a diagnosis of hypertension is made, most clients have no symptoms; however, they may experience headaches, dizziness, or fainting as a result of the elevated blood pressure. The nurse obtains blood pressure readings in both arms. Two or more readings are taken at each visit, with the average of the readings used as the value for the visit. To detect postural (orthostatic) changes, the nurse should also take readings with the client in the supine (lying) or sitting position and at least 2 minutes later with the client standing. Funduscopic examination of the eyes is done by a skilled practitioner to observe vascular changes in the retina. The appearance of the retina can be a reliable index of the severity and prognosis of hypertension.

The Keith-Wagener (KW) classification of retinal changes in hypertension is commonly used to stage changes:

• Stage I is characterized by minimal arteriolar narrowing.

• Stage II involves more marked narrowing of arterioles and arteriovenous nicking (changes at the arteriovenous crossings).

• Stage III shows circular or flame-shaped hemorrhages and fluffy, "cotton wool" exudates.

• Stage IV, the most severe, is the same as stage III but with the addition of papilledema (malignant hypertension is always associated with papilledema).

Physical assessment is helpful in diagnosing several conditions that produce secondary hypertension. The presence of abdominal bruits is typical of clients with renovascular disease.

Tachycardia, sweating, and pallor suggest a pheochromocytoma or adrenal medulla tumor. Coarctation of the aorta is often characterized by elevation of blood pressure in the arms, with normal or low blood pressure in the lower extremities. Femoral pulses are also delayed or absent.


The nurse assesses for psychosocial stressors that can worsen hypertension and that may affect the client's ability to collaborate in treatment. Job-related, economic, and other life stressors are evaluated, as well as the client's response to these stressors. Some clients may have difficulty coping with the lifestyle changes needed to control hypertension. The nurse assesses the client's past coping strategies.


Although no laboratory tests are diagnostic of essential hypertension, several laboratory tests can assess possible causes of secondary hypertension. The presence of protein, red blood cells, pus cells, and casts in the urine; elevated levels of blood urea nitrogen (BUN); and elevated serum creatinine levels indicate renal disease. In clients with a pheochromocytoma (tumor of the adrenal medulla), urinary test results are positive for the presence of catecholamines. An elevation in levels of serum corticoids and 17-ketosteroids in the urine is diagnostic of Cushing's disease.


No specific x-ray studies can diagnose hypertension. Routine chest radiography may be of assistance in recognizing left ventricular hypertrophy that results from hypertension. Intravenous pyelography (IVP) is performed when clinical findings suggest renovascular hypertension. Renal arteriography is undertaken to establish the exact location and the extent of any lesions, the degree of obstruction, and the basic pathologic change in the renal arteries.

OTHER DIAGNOSTIC ASSESSMENT An electrocardiogram (ECG) is of value in determining the degree of cardiac involvement. Left atrial abnormality is the first ECG sign of cardiac involvement resulting from hypertension.



The following are common nursing diagnoses for clients with hypertension:

1. Deficient Knowledge related to information misinterpretation or unfamiliarity with information resources

2. Risk for Ineffective Therapeutic Regimen Management related to noncompliance with treatment


In addition to the common nursing diagnoses, clients with hypertension may have one or more of the following:

Ø     Ineffective Tissue Perfusion (Renal, Cerebral, Cardiopulmonary, and Peripheral) related to decreased blood flow

Ø     Imbalanced Nutrition: Risk for More Than Body Requirements related to learned eating behaviors, ethnic and cultural values, lack of social support for weight loss, and/or imbalance between the activity level and caloric intake

Ø     Fatigue related to altered body chemistry (medications)

Ø     Ineffective Sexuality Patterns related to effects of medical treatment (drugs)

Ø     Ineffective Coping related to effects of chronic illness and major changes in lifestyle

Ø     Risk for Noncompliance with treatment regimen

Ø     The following collaborative problems may also occur in some clients with hypertension:

Ø     Potential for Cerebrovascular Hemorrhage

Ø     Potential for Retinal Hemorrhage

Planning and Implementation



The client with hypertension is expected to verbalize an understanding of the management of hypertension.

INTERVENTIONS. For the client with essential hypertension, the nurse initially recommends the following lifestyle modifications:

Ø     Sodium restriction

Ø     Weight reduction

Ø     Moderation of alcohol intake

Ø     Exercise

Ø     Relaxation techniques

Ø     Tobacco avoidance

If these modifications, which are considered the foundation of hypertension control, are unsuccessful, the health care provider considers the use of antihypertensive drugs (see the Concept Map).

There is no surgical treatment for essential hypertension. However, surgery may be indicated for certain causes of secondary hypertension, such as renal vascular disease, coarctation of the aorta, and pheochromocytoma.

SODIUM RESTRICTION. In collaboration and consultation with the dietitian, the nurse advises all clients with hypertension to decrease their sodium chloride intake from the average of 150 mmol/L (150 mEq/L) to less than 100 mmol/L (100 mEq/L; less than 2.3 g of sodium) per day. To accomplish this goal, clients should avoid adding salt at the table, avoid cooking with salt, avoid adding seasonings that contain sodium, and limit consumption of canned, frozen, or other processed foods. The dietitian reviews a 3-day dietary recall with the client to identify whether sodium intake has been excessive. In collaboration with the dietitian, the nurse suggests spices, herbs, fruits, and other non-salt-containing substances, such as powdered garlic and onion, to enhance the flavor of meat, chicken, seafood, and snacks. The nurse and dietitian instruct clients to read the labels on processed foods and to avoid those that are high in sodium. Salt substitutes are an alternative to salt, but a physician's order is needed before using them. This order is necessary because salt substitutes are high in potassium, and the client may have hyperkalemia (high potassium levels) associated with a concomitant problem, such as renal impairment. Although hyperkalemia is unusual, it can also occur in clients who are taking potassium-sparing diuretics. Whereas salt is restricted, the client should include recommended daily allowances of potassium, calcium, and magnesium in the diet. Studies are not conclusive, but data suggest that low levels of these electrolytes are associated with high blood pressure.

WEIGHT REDUCTION. If a client's body mass index (BMI) is 27 or higher, the nurse and dietitian encourages weight loss. The dietitian discusses the rationale for reducing or maintaining weight and plans a weight reduction diet with the client. He or she may be referred to a group or organization for weight reduction. Because of the relationship of saturated fat and cholesterol to weight, a weight reduction plan is formulated with the following limits: Total fat: less than 30% of daily caloric intake Saturated fat: less than 10% Cholesterol: less than 300 mg/day Table 36-5 describes how to calculate grams of fat.

MODERATION OF ALCOHOL INTAKE. The nurse instructs clients to limit alcohol intake to no more than 1 ounce of ethanol (2 ounces of liquor, 8 ounces of wine, or 24 ounces of beer) daily. The client is taught that alcohol consumption may elevate arterial blood pressure and can add "empty" calories.   

 EXERCISE. With the physician's approval and in collaboration with the physical therapist, the nurse can help the client develop a regular exercise program. The therapist usually recommends regular aerobic exercise, such as brisk walking, running, cycling, swimming, or stair climbing, 30 to 45 minutes three to five times a week. The client should initiate exercise gradually and should stop and notify the physician if severe shortness of breath, fainting, or chest pain occurs. Clients should avoid muscle-building isometric exercise (weight lifting, wrestling, rowing) because it may raise the blood pressure to dangerous levels.

SMOKING CESSATION ASSISTANCE. Although cigarette smoking is not directly related to hypertension, it is a major risk factor for cardiovascular disease. Therefore the client who smokes is strongly urged to stop (Chart 36-2). With input from the nurse and physician, the client plans a smoking cessation program that best fits into his or her lifestyle. The nurse explains use of the nicotine patch and smoking cessation programs and implements follow-up to assess the client's plans for quitting.

COMPLEMENTARY AND ALTERNATIVE THERAPIES. In addition to exercise, complementary modalities are often used by clients to reduce stress and thus decrease blood pressure. Examples include yoga, massage, biofeedback, music therapy, and hypnosis. Information on these therapies is found in Chapter 4.

DRUG THERAPY. Drug therapy is individualized for each client, with consideration given to the client's culture, age, concomitant illness, severity of blood pressure elevation, and cost of drugs and follow-up. Treatment of hypertension generally begins with a single drug. Once-a-day drug therapy is best, because the more doses required each day, the higher the risk that a client will not follow the treatment regimen. Several classifications of medications are available to control hypertension. Examples of commonly used drugs for hypertension are listed in Chart 36-3.

DIURETICS. Three basic types of diuretics are used to decrease blood volume and lower blood pressure:

Thiazide diuretics, such as hydrochlorothiazide (HydroDiuril, Urozide), prevent sodium and water reabsorption in the distal tubules while promoting potassium excretion.

Loop (high-ceiling) diuretics, such as furosemide (Lasix, Furoside), depress sodium reabsorption in the ascending loop of Henle and promote potassium excretion.

Potassium-sparing diuretics, such as spironolactone (Aldactone, Novospiroton), act on the distal tubule to inhibit reabsorption of sodium ions in exchange for potassium, thereby retaining potassium.

Diuretics are the drugs of choice for clients who have asthma, chronic airway limitation, and chronic renal disease and for selected clients with congestive heart failure. They are particularly effective for African Americans.

Diuretics are relatively inexpensive, and adherence to the medication regimen is enhanced because the drug can usually be prescribed on a once-a-day or, at most, twice-a-day schedule.


However, the frequent voiding that occurs after a person takes a diuretic may interfere with daily activities. The most frequent side effect associated with diuretics is hypokalemia (low potassium levels). The nurse monitors the serum potassium level and assesses for signs and symptoms of irregular pulse and muscle weakness, which may indicate hypokalemia. Clients receiving potassium-depleting diuretics should eat foods high in potassium, such as bananas and orange juice. However, the client may need a potassium supplement to maintain adequate serum potassium levels. The nurse assesses for hypokalemia and hyperkalemia in clients taking potassiumsparing diuretics. Both of these electrolyte disturbances are characterized by weakness and an irregular pulse.

BETA-ADRENERGIC BLOCKING AGENTS. Beta blockers lower blood pressure by blocking beta receptors in the heart and peripheral vessels, reducing the cardiac rate and output. By blocking beta-adrenergic receptors in the heart, these drugs cause a decrease in the heart rate and decreased contractility. Bradycardia (slow heart rate) and heart failure may result. Beta blockers can also prohibit bronchodilation by blocking beta receptors in the lungs. Therefore clients with a history of asthma or bronchospasm are generally not given these drugs, and all clients taking these drugs must be monitored for shortness of breath and wheezing.

Common side effects of beta blockers include fatigue, weakness, depression, and sexual dysfunction, although the potential for side effects depends on the "selective" blocking effects of the drag. A variety of drags are available, and they differ from each other in terms of their cardioselectivity (primarily betai effects, with lesser beta2 effects), lipid solubility, and sympathomimetic activity throughout the body.

Clients with diabetes who take beta blockers may not have the usual signs and symptoms of hypoglycemia because the sympathetic nervous system is blocked. Counterregulatory responses to hypoglycemia, such as gluconeogenesis, may also be inhibited by certain beta blockers.

CALCIUM CHANNEL-BLOCKING AGENTS. Calcium channel blockers, such as verapamil hydrochloride (Calan), nifedipine (Procardia, Adalat), and diltiazem (Cardizem), lower blood pressure by interfering with the transmembrane flux of calcium ions, resulting in reduced vasoconstriction.

ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. Angiotensin-converting enzyme (ACE) inhibitors are also used as single or combination agents in the treatment of hypertension. The angiotensin-converting enzyme converts angiotensin I to angiotensin II, one of the most powerful vasoconstrictors in the body. ACE inhibitors include captopril (Capoten), enalapril (Vasotec), and lisinopril (Prinivil).

The client receiving an ACE inhibitor for the first time is instructed to stay in bed for 3 to 4 hours to avoid the severe hypotensive effect that can occur with initial use. The nurse monitors the blood pressure every 15 minutes after this first dose. Postural (orthostatic) hypotension may occur with subsequent doses, but it is less severe. Postural hypotension is assessed by taking the blood pressure when the client is lying, sitting, and standing. If there is a significant decrease in the systolic blood pressure (<20 mm Hg), the nurse notifies the physician.

ANGIOTENSIN II RECEPTOR ANTAGONISTS. Angiotensin II receptor antagonists make up a new group of drags that selectively block the binding of angiotensin II in the vascular and adrenal tissues by competing directly with angiotensin II but not inhibiting ACE. Examples of drags in this group are candesartan (Atacand), losartan (Cozaar), and telmisartan (Micardis). Angiotensin II receptor antagonists can be used alone or in combination with other antihypertensive drags. They are excellent options for clients who complain of cough associated with ACE inhibitors and for those with hyperkalemia. In addition, these drags do not require initial adjustment of the dose for older adults or for clients with renal impairment. However, these drugs may be less effective in African Americans (Dumas, 1999).

CENTRAL ALPHA AGONISTS. Central alpha agonists act on the central nervous system, preventing reuptake of norepinephrine, resulting in a lowering of peripheral vascular resistance and blood pressure. Common central alpha agonists include clonidine (Catapres) and methyldopa (Aldomet, Apo- Methyldopa). Methyldopa can cause unique side effects, such as hemolytic anemia and inflammatory disorders of the liver, although they happen rarely. Because of this potential, clonidine is the more commonly used central alpha agonist. Clonidine can also be given as a transdermal patch, providing control of blood pressure for as long as 7 days. Side effects common to clonidine and methyldopa include sedation, postural hypotension, and impotence.

VASODILATORS. Vasodilators lower blood pressure by relaxing vascular smooth muscle tone, thus reducing total peripheral resistance. Vasodilators include minoxidil (Loniten), nitroglycerin (Nitro-Bid), and nitroprusside (Nitropress).

ALPHA-ADRENERGIC RECEPTOR AGONISTS. Alpha-adrenergic agonists, such as prazosin (Minipress), dilate the arterioles and veins. These drugs can lower blood pressure quickly, but their use is limited because of frequent and bothersome side effects.


The Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (1997) has recommended that initial therapy for hypertension include either a diuretic or a beta blocker unless these drags are contraindicated or ineffective, or there are special indications for agents such as calcium antagonists or ACE inhibitors. If after 1 to 3 months blood pressure does not decrease adequately in response to initial therapy, the health care provider may increase the dose of the drug, substitute a drug from another class of antihypertensives, or add a second drug from another class. Because of changes in recommendations and the availability of more drug options and more information on drug tolerance, the nurse sees a variety of drug protocols used by the health care provider to meet the individual needs of clients with hypertension.



The client with hypertension is expected to adhere to the therapeutic regimen, thus minimizing the risk of target organ damage.

INTERVENTIONS. Clients who require pharmacologic treatment to control essential hypertension usually need to take medication for the rest of their lives. Frequently, however, clients stop taking antihypertensive medications because they have no symptoms. They may also discontinue medication because of cost or side effects. In collaboration with the pharmacist, the nurse and client discuss the goals of therapy, including potential side effects, to help identify potential problems. The nurse then assists the client in tailoring the therapeutic regimen to his or her activities of daily living (ADLs). Clients who do not comply with antihypertensive treatment are at great risk for target organ damage and hypertensive crisis (malignant hypertension). Clients in hypertensive crisis are admitted to critical care units, where they receive intravenous (IV) antihypertensive therapy, such as nitroprusside (Nitropress), nitroglycerin (Nitro-Bid IV, Tridil), labetalol (Normodyne), or diazoxide (Hyperstat IV), or sublingual nifedipine (Procardia, Adalat) (Chart 36-5).

 Hospitalization for complications of hypertension can be financially costly both in medical expenses and in lost income. Community-Based Care Clients who require pharmacologic treatment to control essential hypertension usually need to take medication for the rest of their lives. Studies have shown that within the first year of therapy, more than 50% of clients discontinue their treat- ment (Eaton, Buck, & Catanzaro, 1996). They often stop taking antihypertensive medications with the assumption that the hypertension is under control because they have no symptoms. Clients may assume that if their blood pressure returns to normal levels with antihypertensives, they no longer need them. They may also stop taking antihypertensives because of adverse side effects or cost.

HOME CARE MANAGEMENT If possible, the client should obtain a blood pressure monitor for use at home so that the pressure can be checked periodically. The nurse evaluates the client's ability to learn how to check his or her blood pressure. If the client cannot monitor the blood pressure, a family member or significant other may be taught how to perform this procedure. If weight reduction is a goal, the nurse suggests having a scale in the home for weight monitoring.

HEALTH TEACHING The client is instructed about sodium restriction, weight maintenance or reduction, alcohol restriction, stress management, and exercise (see Interventions [Arteriosclerosis and Atherosclerosis], p. 730). If necessary, the nurse also explains about the need to stop smoking. Older adults can also benefit from lifestyle modifications (Matteson, McConnell, & Linton, 1997). For clients taking medication for hypertension, the nurse provides oral and written information about the indications, dosage, times of administration, side effects, and drug interactions (see Chart 36-3). The nurse stresses that the medication must be taken as prescribed and that when all of it has been consumed, the prescription must be renewed on a continual basis. Abrupt discontinuation of medications such as beta blockers can result in angina (chest pain) or myocardial infarction. The nurse also urges clients to report unpleasant side effects, such as sexual dysfunction. In many instances, an alternative medication can be prescribed to minimize certain side effects. Hypertension is a chronic illness, and clients may not be prepared to accept this fact. The nurse allows clients to verbalize feelings about this disease and its treatment. They are advised that their involvement in the treatment can lead to control of this disease and can prevent complications.

 HEALTH CARE RESOURCES A home care nurse may be needed for follow-up to monitor the blood pressure. The nurse evaluates the ability of the client or the family to obtain accurate blood pressure measurements and assesses their compliance with treatment. If clients cannot purchase equipment to monitor their blood pressure, the American Heart Association, the Red Cross, or a local pharmacy may be used for free blood pressure checks.

 Evaluation: Outcomes

The nurse evaluates the care of the client with hypertension on the basis of the identified nursing diagnoses and collaborative problems. The expected outcomes are that the client will:

• Explain the rationale for treatment of hypertension

• Maintain a blood pressure of less than 130/85 mm Hg for clients with diabetes and less than 140/90 mm Hg for clients without diabetes

• Demonstrate no signs or symptoms of target organ damage, such as renal or heart disease



 OVERVIEW Peripheral vascular disease (PVD) includes disorders that alter the natural flow of blood through the arteries and veins of the peripheral circulation. PVD affects the lower extremities much more frequently than the upper extremities. Generally, a client with a diagnosis of PVD has arterial disease (peripheral arterial disease [PAD]) rather than venous involvement. Some clients have both arterial and venous disease.


PAD is a chronic condition in which partial or total arterial occlusion deprives the lower extremities of oxygen and nutrients. PAD of the lower extremities is sometimes referred to as lower extremity arterial disease (LEAD). Body tissues cannot live without an adequate oxygen and nutrient supply, and tissue eventually dies. Atherosclerosis is the most common cause of chronic altered blood flow. Fatty substances accumulate at the site of vessel wall injury and alter or totally occlude blood flow within the arteries. Tissue damage generally occurs below the arterial obstruction. Obstructions are classified as inflow or outflow, according to the arteries involved and their relationship to the inguinal ligament (Figure 36-5).

 Inflow obstructions involve the distal end of the aorta and the common, internal, and external iliac arteries. They are located above the inguinal ligament. Outflow obstructions involve infrainguinal arterial segments (the femoral, popliteal, and tibial arteries) and are below the superficial femoral artery (SEA). Gradual inflow occlusions may not cause significant tissue damage; gradual outflow occlusions typically do.  

Etiology Because atherosclerosis is the most common cause of chronic arterial obstruction, the risk factors for atherosclerosis apply to PAD as well. These include hypertension, hyperlipidemia, diabetes mellitus, cigarette smoking, obesity, and familial predisposition. Advancing age also increases the risk of disease related to atherosclerosis.

Incidence/Prevalence Approximately 8 million people in the United States have PAD. At least 10% of people over 70 years of age and 2% of people 37 to 69 years of age have symptomatic, chronic PAD (American Heart Association, 1999). PAD generally occurs in men older than 45 years of age and in postmenopausal women. The costs of vascular disease to society are astounding .



HISTORY The clinical course of chronic peripheral arterial disease (PAD) can be divided into four stages (Chart 36-6). Clients do not experience symptoms in the early stages of disease.

PAIN ASSESSMENT. Most clients initially seek treatment for a characteristic leg pain known as intermittent claudication (a term derived from a word meaning "to limp"). Usually they can walk only a certain distance before a cramping, burning muscle discomfort or pain forces them to stop. The pain subsides after rest. When they resume walking, they can walk the same distance before the pain returns. The pain is thus considered reproducible. As the disease progresses, clients can walk only shorter and shorter distances before pain recurs. Ultimately, pain may occur even while at rest. The nurse questions the client about the nature and characteristics of leg pain to determine whether the client may be experiencing intermittent claudication. Rest pain, which may begin while the disease is still primarily in the stage of intermittent claudication, is a numbness or burning, often described as feeling like a toothache, that is severe enough to awaken clients at night. It is usually located in the distal portion of the extremities—in the toes, the foot arches, the forefeet, and the heels, but rarely in the calves or ankles. Clients can sometimes achieve pain relief by keeping the limb in a dependent position. Clients with rest pain have advanced disease that may result in limb loss.


Clients with inflow disease experience discomfort in the lower back, buttocks, or thighs. Lower back or buttock discomfort indicates obstruction at or above the common iliac artery or abdominal aorta. Thigh discomfort indicates obstruction at or above the profunda femoris artery. Clients with mild inflow disease experience discomfort after walking about two blocks. This discomfort is not severe but causes the client to stop walking. It is relieved with rest. Clients with moderate inflow disease experience pain in these areas after walking about one or two blocks. The discomfort is described as being more like pain, but it subsides with rest most of the time. Severe inflow disease causes the client severe pain after walking less than one block. These clients usually have rest pain.

Clients with outflow disease describe burning or cramping in the calves, ankles, feet, and toes. Calf discomfort usually indicates arterial obstruction at or below the superficial femoral or popliteal artery. Instep or foot discomfort indicates an obstruction below the popliteal artery. Clients with mild outflow disease experience discomfort after walking about five blocks. This discomfort is relieved by rest. Clients with moderate outflow disease have pain after walking about two blocks. Intermittent rest pain may be present. Clients with severe outflow disease are usually unable to walk more than one-half block and usually experience rest pain. They may hang their feet off the bed at night for comfort. Clients with outflow disease complain more frequently of rest pain than do those with inflow disease.

PHYSICAL ASSESSMENT/CLINICAL MANIFESTATIONS Specific findings for PAD depend on the severity of the disease. The nurse may observe loss of hair on the lower calf, ankle, and foot; dry, scaly, dusky, pale, or mottled skin; and thickened toenails. With severe arterial disease, the extremity is cold and gray-blue (cyanotic) or darkened. Pallor may occur when the extremity is elevated; dependent rubor may occur when the extremity is lowered. Muscle atrophy can accompany prolonged chronic arterial disease. The nurse palpates all pulses in both legs. The most sensitive and specific indicator of arterial function is the quality of the posterior tibial pulse. The pedal pulse is not palpable in a small percentage of people. The strength of the pulse should be compared bilaterally. Several scales are available for grading pulse strength.

A popular system is presented in Table 36-6.

The nurse may also note early signs of ulcer formation or complete ulcer formation, a complication of PAD. Arterial and venous stasis ulcers differ from diabetic ulcers (Chart 36-7). Initially, arterial ulcers are painful and develop on the toes (often the great toe), between the toes, or on the upper aspect of the foot. With prolonged occlusion, the toe(s) can become gangrenous. Diabetic ulcers develop on the plantar surface of the foot, over the metatarsal heads, and on the heel anywhere that pressure is exerted. Diabetic ulcers may not be painful because of diabetic neuropathy. Venous stasis ulcers cause minimal pain and occur in the ankle area. The foot is warm, and distal pulses are palpable. The nurse notes discoloration of the lower extremity at the ulcer site. Skin lesions are discussed in further detail in Chapter 67.

RADIOGRAPHIC ASSESSMENT The most common x-ray study for PAD is arteriography of the lower extremities. Because arteriography involves injecting contrast medium into the arterial system, the risks, which include hemorrhage, thrombosis, embolus, and death, are serious. Arteriography is often performed before surgery to pinpoint the exact location of the occlusion. The nurse prepares the client for the procedure and carefully implements followup care.

OTHER DIAGNOSTIC ASSESSMENT The advent of noninvasive evaluation of arterial disease has become a popular method of diagnosis. Noninvasive testing provides information about the arterial system with minimal risk to the client.

SEGMENTAL SYSTOLIC BLOOD PRESSURE MEASUREMENTS. Segmental systolic blood pressure measurements of the lower extremities at the thigh, calf, and ankle are a noninvasive method of assessing PAD. Normally, blood pressure readings in the thigh and calf are higher than those in the upper extremities. With the presence of arterial disease, these pressures are lower than the brachial pressure.

With inflow disease, pressures taken at the thigh level indicate the severity of disease. Mild inflow disease may cause a difference of only 10 to 30 mm Hg in pressure on the affected side compared with the brachial pressure. Severe inflow disease can cause a pressure difference of greater than 40 to 50 mm Hg. The ankle pressure is normally equal to or greater than the brachial pressure.

To evaluate outflow disease, the nurse compares ankle pressure with the brachial pressure, which provides a ratio known as the ankle-brachial index (ABI). This value can be derived by dividing the ankle blood pressure by the brachial blood pressure. With mild outflow disease, the client has an ankle/brachial index of 0.8 to 1.0; pressures are decreased by about 10 to 30 mm Hg. The client with moderate outflow disease has an ankle/brachial index of 0.5 to 0.8, with pressure differences of 20 to 40 mm Hg. An ankle/brachial index of less than 0.5 indicates severe outflow disease.

EXERCISE TOLERANCE TESTING. Exercise tolerance testing (by stress test or treadmill) may give valuable information about clients who are experiencing claudication (muscle pain) without rest pain. The nurse or technician obtains resting pulse volume recordings and has the client walk on a treadmill until the symptoms are reproduced. At the time of symptom onset or after approximately 5 minutes, the nurse or technician obtains another pulse volume recording. Normally, there may be an increased waveform with minimal, if any, drop in the ankle pressure. In clients with arterial disease, the waveforms are decreased (dampened) and there is a decrease in the ankle pressure of 40 to 60 mm Hg for 20 to 30 seconds in the affected limb. If the return to normal pressure is delayed (longer than 10 minutes), the results suggest abnormal arterial flow in the affected limb.

PLETHYSMOGRAPHY. Plethysmography can also be performed to evaluate arterial flow in the lower extremities. This measurement provides graphs or tracings of arterial flow in the limb. If an occlusion is present, the waveforms are dampened to flattened, depending on the degree of occlusion.

Interventions The nurse first determines whether the altered tissue perfusion is of arterial or venous origin. An accurate assessment often provides this information, but in some people both conditions may exist. In this case, each disease must be considered separately when appropriate interventions are planned.

NONSURGICAL MANAGEMENT. The interventions of exercise, position changes, promotion of vasodilation, drug therapy, and invasive nonsurgical procedures are used to increase arterial flow to the affected limb.

EXERCISE. Exercise may improve arterial blood flow to the affected limb through buildup of the collateral circulation. (Collateral circulation provides blood to the affected area through smaller vessels that develop and compensate for the occluded vessels.) Exercise is individualized for each client, but people with severe rest pain, venous ulcers, or gangrene should not participate. Other clients with peripheral arterial disease (PAD) can benefit from exercise that is initiated gradually and is slowly increased; walking is an excellent exercise (Braun, Colucci, & Patterson, 1999). The nurse instructs the client to walk until the point of claudication, stop and rest, and then walk a little farther. Eventually, clients are able to walk longer distances as collateral circulation develops. The nurse collaborates with the health care provider and physical therapist in determining an appropriate exercise program.

POSITIONING. Positioning of the client to promote circulation has been somewhat controversial. Some clients have swelling in their extremities. Because swelling prevents arterial flow, they should elevate their feet at rest, but the nurse teaches them to refrain from raising their legs above the heart level. Extreme elevation slows arterial blood flow to the feet. In severe cases, clients with PAD and swelling may sleep with the affected limb hanging from the bed, or they may sit upright in a chair for comfort. The nurse instructs all clients with PAD to avoid crossing their legs, which may interfere with blood flow.


 Vasodilation can be achieved by providing warmth to the affected extremity and preventing long periods of exposure to cold. The nurse encourages the client to maintain a warm environment at home and to wear socks or insulated shoes at all times. The client is cautioned never to apply direct heat to the limb, such as with the use of heating pads or extremely hot water. Sensitivity is decreased in the affected limb, and the client may get burned without feeling it. The nurse encourages clients to prevent exposure of the affected limb to the cold because cold temperatures cause vasoconstriction (decreasing of the diameter of the blood vessels) and therefore decrease arterial blood flow. Emotional stress, caffeine, and nicotine also can cause vasoconstriction. The nurse emphasizes that complete abstinence from smoking or chewing tobacco is the most effective method of preventing vasoconstriction. The vasoconstrictive effects of each cigarette may last up to 1 hour after the cigarette is smoked.

DRUG THERAPY. For clients with chronic PAD, prescribed drugs include hemorheologic and antiplatelet agents. Pentoxifylline (Trental) is a hemorheologic agent that increases the flexibility of red blood cells; it decreases blood viscosity by inhibiting platelet aggregation and decreasing fibrinogen and thus increases blood flow in the extremities. Many clients report limited improvement in their daily lives after taking pentoxifylline. Moreover, clients with extremely limited endurance for walking have reported improvement to the point that they can perform some activities (e.g., walk to the mailbox or dining room) that were previously impossible.

Antiplatelet agents, such as aspirin (acetylsalicylic acid, Ancasal) and clopidogrel (Plavix), are commonly used for clients with PAD. Aspirin 325 or 81 mg/day is typically recommended for all clients with chronic PAD. In a trial of clopidogrel versus aspirin in patients at risk of /schemic events (CAPRIE), clopidogrel demonstrated improvement over aspirin for risk reduction for myocardial infarction, ischemic stroke, and vascular death, but the difference was slight. Therefore clients with peripheral vascular disease (PVD) with no contraindications to platelet therapy should receive either aspirin or clopidogrel. Controlling hypertension can improve tissue perfusion by maintaining pressures that are adequate to perfuse the periphery but not vasoconstrict the vessels. Nurses should make clients aware of the effect of blood pressure on the circulation and should instruct them in methods of control. For example, clients taking beta blockers may experience drug-related claudication or an exacerbation of their symptoms. The health care provider closely monitors clients with PAD who are receiving beta blockers.


Another nonsurgical but invasive method of improving arterial flow is percutaneous transluminal angioplasty (PTA) (Figure 36-6).

One or more arteries are dilated with a balloon catheter advanced through a cannula, which is inserted into or above an occluded or stenosed artery. When the procedure is successful, it opens the vessel lumen and improves arterial blood flow, creating a smooth inner-vessel surface. In addition, a stent (wirelike device) may be used along with the PTA to help keep the vessel open.

Clients who are candidates for PTA must have occlusions or stenoses that are accessible to the catheter. The physician often uses (PTA) for clients who are poor surgical candidates who cannot withstand general anesthesia or for whom amputation may be inevitable. Reocclusion may occur after this procedure, and the procedure may be repeated. Some clients are occlusion free for up to 3 to 5 years, whereas others may experience reocclusion within a year.

During PTA, intravascular stents may be placed to ensure adequate blood flow in a stenosed vessel. Candidates for this type of procedure are individuals with stenosis of the common or external iliac arteries. This type of procedure is costeffective and results in shorter hospital stays and earlier recoveries.

LASER-ASSISTED ANGIOPLASTY. Another invasive procedure is laser-assisted angioplasty. A laser probe is advanced through a cannula similar to that used for PTA. Laserassisted angioplasty is usually reserved for clients with smaller occlusions in the distal superficial femoral, proximal popliteal, and common iliac arteries. Heat from the laser vaporizes the arteriosclerotic plaque to open the occluded or stenosed artery. If significant stenosis remains after the artery is opened, a balloon catheter may be inserted to further dilate the artery.

Preparation of the client for PTA or laser-assisted angioplasty is similar to that for diagnostic angiography. The client must have nothing by mouth (NPO) after midnight. The surgeon may require that the client scrub the groin area with an antiseptic solution.

Postprocedure nursing care involves observing for bleeding at the puncture site. The nurse or assistive nursing personnel closely observes vital signs and frequently checks the distal pulses in both limbs. These clients are typically restricted to bedrest, with the limb straight for approximately 6 to 8 hours before ambulation. Many receive anticoagulant therapy, such as heparin, during the procedure and for a short time after the procedure. Some type of antiplatelet drug is provided for 1 to 3 months after the procedure. Clients usually take aspirin on a permanent basis.

ATHERECTOMY. The technique of mechanical rotational abrasive atherectomy is used to improve blood flow to ischemic limbs in people with PAD. The rotational atherectomy device (Rotablator) is a high-speed rotary, metal bur ranging in size from 1.25 to 4.5 mm in diameter. The distal half of the bur is embedded with fine abrasive bits, which at rotational speeds of 100,000 to 120,000 rotations per minute result in fine-particle destruction of tissue. The Rotablator is designed to preferentially scrape "hard" surfaces (such as plaque) while minimizing damage to the vessel surface.

SURGICAL MANAGEMENT. Clients with severe rest pain or claudication that interferes with the ability to work or threatens loss of a limb become surgical candidates. Arterial revascularization is the surgical procedure most commonly used to increase arterial blood flow in an affected limb.

Surgical procedures are classified as inflow or outflow. Inflow procedures involve bypassing arterial occlusions above the superficial femoral arteries (SFAs). Outflow procedures involve surgical bypassing of arterial occlusions at or below the SFAs. For clients who have both inflow and outflow problems, the inflow procedure (for larger arteries) is done before the outflow repair.

Inflow procedures include aortoiliac, aortofemoral, and axillofemoral bypasses. Outflow procedures include femoropopliteal and femorotibial bypasses. Inflow procedures are more successful, with less chance of reocclusion or postoperative ischemia. Outflow procedures are less successful in relieving ischemic pain and are associated with a higher incidence of reocclusion. Graft materials for the bypasses are selected on an individual basis. For outflow procedures the preferred graft material is an autogenous saphenous vein. However, these clients can experience systemic vascular disease and may need this vein for coronary artery bypass. When the saphenous vein is not usable, the cephalic or basilic arm veins may be used.

Grafts made of synthetic materials, such as polytetrafluoroethylene, Gore-Tex, and Dacron, have also been used when autogenous veins were not available. Although synthetic grafts have achieved adequate patency in arteries above the knee, they have failed to achieve satisfactory results in infrapopliteal outflow vessels. In addition, autogenous veins are often not long enough for use in these vessels. Composite grafts constructed from multiple vein segments offer even better patency to arteries below the knee.

PREOPERATIVE CARE. Preparing the client for surgery is similar to that described for general or epidural anesthesia (see Chapter 17). Documentation of vital signs and peripheral pulses provides a baseline of information for comparison during the postoperative phase. Depending on the surgical procedure, the client may have an intravenous (IV) line, urinary catheter, central venous catheter, and/or arterial line. To prevent postoperative infection, clients typically receive antibiotic therapy before the procedure.

OPERATIVE PROCEDURES. The anesthesiologist or nurse anesthetist places the client under general, epidural, or spinal anesthesia. Epidural or spinal induction is preferred for older adults to decrease the risk of cardiopulmonary complications in this age-group. If arterial bypass is to be accomplished by autogenous grafts, the surgeon excises the appropriate veins through an incision. The occluded artery is then exposed through an incision, and the conduit veins or synthetic graft material is sutured above and below the occlusion to facilitate blood flow around the occlusion. For aortoiliac and aortofemoral bypass surgery, the surgeon makes a midline incision into the abdominal cavity to expose the abdominal aorta, with additional incisions into each groin (Figure 36-7). Graft material is tunneled from the aorta to the groin incisions, where it is sutured in place. In an axillofemoral bypass (Figure 36-8), the surgeon makes an incision beneath the clavicle and tunnels graft material subcutaneously with a catheter from the chest to the iliac crest, into a groin incision, where it is sutured in place. Neither the thoracic nor the abdominal cavity is entered. For this reason, the axillofemoral bypass is used for high-risk clients who cannot tolerate a procedure requiring abdominal surgery.

POSTOPERATIVE CARE. Graft occlusion often occurs within the first 24 hours. Therefore astute nursing care is cru-    cial. The Client Care Plan below highlights the most important aspects of postoperative care.

Assessment for Graft Occlusion. The nurse monitors the patency of the graft by checking the extremity every 15 minutes for the first hour, then hourly, for changes in color, temperature, and pulse intensity. Warmth, redness, and edema of the affected extremity are often expected outcomes of surgery as a result of increased blood flow. Immediately postoperatively, the operating room or postanesthesia care unit (PACU) nurse marks the site where the distal (dorsalis pedis or posterior tibial) pulse is best palpated or heard by Doppler ultrasonography. The nurse communicates this information to the nursing staff on the unit where the client will be sent. Pain is frequently the first indicator of postoperative graft occlusion. Many people experience a throbbing pain caused by the increased blood flow to the extremity. This sensation is different from ischemic pain, and the nurse must assess the type of pain that the client is experiencing. If graft occlusion occurs, the client will experience a sharp increase in ischemic pain, described as similar to the pain felt before surgery. The nurse reports severe pain to the surgeon immediately.

Promotion of Graft Patency. To promote graft patency, the nurse monitors the client's blood pressure and notifies the surgeon if the pressure increases or decreases beyond normal limits. Hypotension may indicate hypovolemia, which can increase the risk of clotting. Range of motion of the affected limb is usually limited, with bending of the hip and knee contraindicated. The nurse consults with the surgeon on a caseby- case basis regarding limitations of movement, including turning. Clients are restricted to bedrest for at least 24 hours postoperatively. The nurse instructs all clients to cough and deep breathe every 1 to 2 hours and to use an incentive spirometer. Clients who have undergone aortoiliac or aortofemoral bypass are allowed nothing by mouth for at least 1 day postoperatively. Those who have undergone bypass surgery of the lower extremities not involving the aorta or abdominal wall (femoropopliteal or femorotibial bypass) may be on NPO status the night of surgery but are often allowed clear liquids the morning after surgery.

Treatment of Graft Occlusion. If manifestations of graft occlusion occur, the nurse notifies the surgeon immediately. Perfusion through the graft must be resolved promptly to avoid ischemic injury to the limb. Emergency thrombectomy (removal of the clot), which the surgeon may perform at the bedside, is the most common treatment for acute graft occlusion. Thrombectomy is associated with excellent results in prosthetic grafts but variable results in autogenous vein grafts, which often necessitate graft revision and even replacement. Local intra-arterial thrombolytic therapy with an agent such as tissue plasminogen activator (t-PA), or an infusion of a platelet inhibitor such as abciximab (ReoPro), may be used for acute graft occlusions in selected clients in settings where health care providers are experts on its use. The physician considers these therapies when the surgical alternative (e.g., thrombectomy with or without graft revision or replacement) carries high morbidity or mortality or when surgery for this type of occlusion has traditionally yielded poor results. When the physician uses thrombolytic therapy, the  nurse closely assesses the client for signs and symptoms of bleeding.

Monitoring for Compartment Syndrome. Compartment syndrome occurs when tissue pressure within a confined body space becomes elevated and restricts blood flow. The resultant ischemia can lead to tissue damage and eventually tissue death. The nurse assesses the motor and sensory function of the affected extremity. The extremity should also be assessed for worsening pain, fullness, swelling, and tenseness. These symptoms should be reported to the health care provider immediately. When compartment syndrome is suspected, the nurse continues to assess the extremity, removes or loosens the dressings, and places the extremity at the level of the heart.

 Assessment for Infection. Graft or wound infections can be life threatening and can endanger the client's limb. The nurse uses sterile technique when in contact with the incision and observes for symptoms of infection at or around the graft and incision sites. If the area over the graft becomes hard, tender, red, or warm, the client may have an infection. The nurse notifies the surgeon if any of these symptoms occur.

Community-Based Care

CASE MANAGEMENT Peripheral arterial disease (PAD) is a chronic, long-term problem with frequent complications. Clients with PAD may benefit from a case manager who can follow them across the continuum of care. The goal is to maintain the client in the home environment.

HOME CARE MANAGEMENT Managing the client at home often requires an interdisciplinary team approach. Chart 36-8 outlines the assessment highlights for home care clients with peripheral vascular disease (PVD). The clinical guide in Figure 36-9 shows how one home care agency documents care for homebound clients with PAD.

HEALTH TEACHING The nurse instructs all clients on methods to promote vasodilation. They are taught to avoid raising their legs above the level of the heart unless they also have venous stasis. The nurse provides written and oral instructions on foot care and methods to prevent injury and ulcer development for all clients (Chart 36-9).

 Clients who have had surgery require additional instruction on incision care. The nurse encourages all clients to avoid smoking and to limit dietary fat intake to less than 30% of the total daily calories. Clients with chronic arterial obstruction may fear recurrent occlusion or further narrowing of the artery. They often fear that they might lose a limb or become debilitated in other ways. Indeed, chronic PAD may worsen, especially in clients with diabetes mellitus. The nurse, however, reassures clients that their participation in prescribed exercise, diet, and pharmacologic therapy, along with cessation of smoking, can limit further formation of atherosclerotic plaques.


 HEALTH CARE RESOURCES Clients with arterial compromise may need assistance with activities of daily living (ADLs) if activity is limited by pain. They may need to limit or avoid stair climbing, depending on the severity of disease. Clients who have undergone surgery usually need temporary help with ADLs. Clients who must limit activity because of PAD may benefit from the assistance of a home care aide. Those who has undergone surgery may require a home care nurse to assist with incision care. The nurse or case manager arranges for home care resources before the client is discharged.

Acute Peripheral Arterial Occlusion

OVERVIEW Although chronic peripheral arterial disease (PAD) progresses slowly, the onset of acute arterial occlusions may be sudden and dramatic. An embolus is the most common cause of peripheral occlusions, although a local thrombus may be the cause. Occlusion may affect the upper extremities, but it is more common in the lower extremities. Emboli originating from the heart are the most common cause of acute arterial occlusions. Most clients with an embolic occlusion have had an acute myocardial infarction and/or atrial fibrillation within the preceding weeks.


 Assessment Clients with an acute arterial occlusion describe severe pain below the level of the occlusion that occurs even at rest. The affected extremity is cool or cold, pulseless, and mottled. Minute areas on the toes may be blackened or gangrenous.

Clients with acute arterial insufficiency often present with the "six P's" of ischemia: pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia (coolness) of the involved extremity.

 Interventions The health care provider must initiate treatment promptly to avoid permanent damage or loss of an extremity. Anticoagulant therapy with unfractionated heparin (UFH; Hepalean*) is usually the first intervention to prevent further clot forma tion. A bolus of up to 10,000 units may be ordered. The client may also undergo angiography.

A surgical thrombectomy or embolectomy with local anesthesia may be performed to remove the occlusion. The physician makes an incision, which is followed by an arteriotomy (a surgical opening into an artery). The physician then inserts a Fogarty catheter into the artery and retrieves the embolus. It may be necessary to close the artery with a patch graft.

Postoperatively, the nurse monitors the affected extremity for improvement in color, temperature, and pulse, as well as other extremities for signs and symptoms of new thrombi or emboli. Pain should significantly diminish after the surgical procedure, although mild incisional pain remains. The nurse watches closely for complications caused by reperfusing the artery after thrombectomy or embolectomy, which include spasms and swelling of the skeletal muscle. Swelling of the skeletal muscles is characterized by edema, pain on passive movement, poor capillary refill, numbness, and muscle tenseness. Fasciotomy (surgical opening into the tissues) may be necessary to prevent further injury and save the limb.

The use of systemic thrombolytic therapy for acute arterial occlusions has been disappointing because bleeding complications have outweighed the benefits obtained. Local intra-arterial thrombolytic therapy with alteplase (Activase) or t-PA and the use of platelet inhibitors, such as abciximab (ReoPro), have emerged as alternatives to surgical treatment in selected clients in settings where health care providers are familiar with their use and complications. When thrombolytics are given, the nurse monitors for signs and symptoms of bleeding, bruising, or hematoma. When a client receives abciximab (ReoPro), platelet counts need to be monitored for the first 3, 6, and 12 hours after the start of the infusion. If the platelet count decreases to below 100,000, the abciximab infusion needs to be readjusted or discontinued. If any of these complications occur, the nurse notifies the physician immediately.


OVERVIEW An aneurysm is a permanent localized dilation of an artery, which enlarges the artery to at least two times its normal diameter.

Types of Aneurysms An aneurysm may be described as fusiform (a diffuse dilation affecting the entire circumference of the artery) or saccular (an outpouching affecting only a distinct portion of the artery). Aneurysms may also be described as true or false. In true aneurysms the arterial wall is weakened by congenital or acquired problems. False aneurysms occur as a result of vessel injury or trauma to all three layers of the arterial wall.

Dissecting hematomas, traditionally called dissecting aneurysms, are more accurately described as aortic dissections (see the later discussion on p. 760). Aortic dissections differ from aneurysms in that they are formed when blood accumulates in the wall of an artery.

Aneurysms tend to occur at specific anatomic sites (Figure 36-10), most commonly in the abdominal aorta.

Aneurysms often occur at a point where the artery is not supported by skeletal muscles or on the lines of curves or flexion in the arterial tree.

Pathophysiologic Process An aneurysm forms when the middle layer (media) of the artery is weakened, producing a stretching effect in the inner layer (intima) and outer layers (adventitia) of the artery. As the artery widens, tension in the wall increases and further widening occurs, thus enlarging the aneurysm. Hypertension (high blood pressure) produces more tension and enlargement within the artery. As the aneurysm grows, the risk of arterial rupture increases.

Abdominal aortic aneurysms (AAAs) account for approximately 75% of all aneurysms. Most of these aneurysms are located between the renal arteries and the aortic bifurcation. Of all AAAs greater than 6 cm in diameter, 50% rupture within 1 year; of those aneurysms smaller than 6 cm in diameter, 15% to 20% rupture.

Thoracic aortic aneurysms account for approximately 25% of all aneurysms and are frequently misdiagnosed (McClarren- Curry & Shaughnessy, 1999). They commonly develop between the origin of the left subclavian artery and the diaphragm. They are located in the descending, ascending, and transverse sections of the aorta.

Aneurysms can cause symptoms by exerting pressure on surrounding structures or by rupturing. Rupture of an aneurysm is the most frequent complication and is life threatening be    cause abrupt and massive hemorrhagic shock occurs with the rupture. Thrombi within the wall of an aneurysm can also be the source of emboli in distal arteries below the aneurysm.

Atherosclerosis is the most common cause of all aneurysms, with hypertension and cigarette smoking being contributing factors. Syphilis (a sexually transmitted disease) and Ehlers-Danlos syndrome (a rare genetic disorder) are other causes of AAAs. The incidence of AAAs, estimated to be between 30 and 66 per 1000 persons, is increasing in the Western world. Approximately 15,000 people in the United States die annually from abdominal aneurysms, making it the thirteenth leading cause of death in the United States. Thoracic aortic aneurysms occur most often in older adults and have a 50% mortality rate even with surgical intervention (McClarren-Curry & Shaughnessy, 1999). AAAs are more common in men than in women (with a ratio of 4:1).


Assessment Most clients with abdominal or thoracic aneurysms are asymptomatic when their aneurysms are first discovered by routine examination or during radiographic study performed for another reason.

ABDOMINAL AORTIC ANEURYSMS Because there may be symptoms, the nurse assesses clients with a known or suspected abdominal aortic aneurysm (AAA) for abdominal, flank, or back pain. Pain related to an AAA is usually steady with a gnawing quality, is unaffected by movement, and may last for hours or days. A pulsation in the upper abdomen slightly to the left of the midline between the xiphoid process and the umbilicus may be present. A detectable aneurysm is at least 5 cm in diameter. The nurse auscultates for a bruit over the mass but avoids palpating the mass because it may be tender and there is a risk of rupture. Although some clients have symptoms when the aneurysm is intact, many are asymptomatic until the time of rupture. If expansion and impending rupture of an AAA are suspected, the nurse assesses for severe pain of sudden onset in the back or lower abdomen, which may radiate to the groin, buttocks, or legs. Clients with a rupturing AAA are critically ill and in hemorrhagic (hypovolemic) shock. Signs include hypotension, diaphoresis, mental obtundation, oliguria, and dysrhythmias. Retroperitoneal hemorrhage is manifested by hematomas in the flanks. Rupture into the abdominal cavity causes abdominal distention.

 THORACIC AORTIC ANEURYSMS When a thoracic aortic aneurysm is suspected, the nurse assesses the client for back pain and manifestations of compression of the aneurysm on adjacent structures. Signs include shortness of breath, hoarseness, and difficulty swallowing. Thoracic aneurysms are not often detected by physical assessment, but occasionally a mass may be visible above the suprasternal notch. The client with suspected rupture of a thoracic aneurysm is assessed for sudden and excruciating back or chest pain. Rupture of a thoracic aneurysm is also indicated by hemorrhagic shock.

RADIOGRAPHIC ASSESSMENT An abdominal x-ray film or a lateral x-ray film of the spine often shows an AAA. The "eggshell" appearance of the aneurysm is essentially diagnostic. Computed tomographic (CT) scanning is the standard tool for assessing the size and location of an abdominal or thoracic aneurysm. A thoracic aneurysm can be diagnosed by chest xray examination. Aortic arteriography is usually performed for clients who are to undergo surgical repair of a thoracic aneurysm.  

OTHER DIAGNOSTIC ASSESSMENT Ultrasonography is a noninvasive technique that provides an accurate diagnosis, as well as information about the size and location of an AAA.

Interventions The size of the aneurysm and the presence of symptoms are the most important parameters in the determination of treatment.

NONSURGICAL MANAGEMENT. The goal of nonsurgical management is to monitor the growth of the aneurysm and maintain the blood pressure at a normal level to decrease the risk of rupture. Because elevated blood pressure can increase the rate of aneurysmal enlargement, hypertension is an important risk factor for rupture. Clients with hypertension are treated with antihypertensives to decrease the rate of enlargement and the risk for early rupture. For clients with small or asymptomatic aneurysms, frequent CT scans are necessary to monitor the growth of the aneurysm. The nurse emphasizes the importance of following through with scheduled tests to monitor the growth. The nurse also explains the clinical manifestations of aneurysms that need to be promptly reported.

SURGICAL MANAGEMENT. Surgical management of an aneurysm may be an elective or an emergency procedure. For clients with either a rupturing abdominal aortic or a thoracic aneurysm, emergency surgery is performed. Clients with an abdominal aortic aneurysm (AAA) 6 cm in diameter or wider undergo elective surgery. Some surgeons favor surgical treatment for clients with aneurysms 4 to 6 cm in diameter if the client is in good health. Clients in good health with aneurysms smaller than 4 cm and clients in poor health with aneurysms 4 to 6 cm in diameter undergo istration of large volumes of intravenous IV fluids to maintain tissue perfusion.

Operative Procedure. The surgeon makes a midline abdominal incision from the xiphoid process to the symphysis pubis, or a wide transverse incision from flank to flank, to expose the aneurysm. Clamps are applied just above and just below the aneurysm, the aneurysm is excised, and a preclotted Dacron graft is sutured in an end-to-end fashion.

Postoperative Care. Immediately postoperatively, the client is typically admitted to a critical care unit for 24 to 48 hours, depending on his or her the age and condition. In addition to providing the routine postoperative care discussed in Chapter 19, the nurse assesses for and assists in prevention of the postoperative complications that can occur after an AAA repair. These complications include myocardial infarction, graft occlusion or rupture causing hemorrhage, hypovolemia and/or renal failure, respiratory distress, and paralytic ileus.

Myocardial Infarction. During the immediate postoperative period, the client's blood pressure is monitored with an arterial catheter. Continuous cardiac monitoring is used to detect any dysrhythmias. Using hemodynamic monitoring, the nurse monitors for low cardiac output and other findings consistent with an acute myocardial infarction. Other signs of myocardial infarction, include chest pain, shortness of breath, complaints of dyspnea, diaphoresis, anxiety, and restlessness.

Graft Occlusion or Rupture. The nurse or assistive nursing personnel assesses vital signs and circulation every 15 minutes for the first hour, then hourly, with assessment of pulses distal to the graft site (including the posterior tibial and dorsalis pedis pulses).

Signs of graft occlusion or rupture are reported, including the following:

 • Changes in pulses

• Cool to cold extremities below the graft

 • White or blue extremities or flanks

• Severe pain

• Abdominal distention

The nurse limits elevation of the head of the bed to 45 degrees to avoid flexion of the graft.

Hypovolemia or Renal Failure. Hypovolemia and renal failure may occur because of blood loss during surgery or before if rupture occurred. The nurse assesses urine output via a Foley catheter hourly. If urine output is less than 50 mL/hr, the nurse notifies the surgeon. Although advances in surgical technique have decreased the risk of renal failure after clamping during surgery, renal failure may occur. Renal failure caused by acute tubular necrosis is more common after emergency surgery. In addition to monitoring urine output, the nurse and physician monitor serum creatinine and blood urea nitrogen (BUN) levels daily.

Respiratory Distress. The nurse assesses the respiratory rate and depth every hour and auscultates breath sounds every 4 hours to monitor for respiratory complications. Often, the client is maintained on a ventilator at least overnight to facilitate respiratory exchange. Opioids are administered for pain, as ordered, and the client is turned and suctioned as needed. The nurse provides firm abdominal support of the incision with a pillow or bath blanket while the client is coughing to prevent the incision from separating. After the client is extubated, he or she should continue to turn, cough, and deep breathe every 1 to 2 hours, and increase his or her mobility as ordered.

Paralytic Ileus. Paralytic ileus after AAA repair is expected for 2 to 3 days. Clients have a nasogastric tube set to low sue nonsurgical treatment until the aneurysm reaches 6 cm. Clients with thoracic aortic aneurysms measuring 7 cm or more in diameter and clients with smaller aneurysms that are producing symptoms are advised to have elective surgery. Clients with aneurysms smaller than 7 cm in diameter that are not causing symptoms are treated nonsurgically until symptoms occur or the aneurysm enlarges to 7 cm. The most common procedure performed for clients with an AAA has traditionally been an AAA resection or repair (aneurysmectomy). The mortality rate for elective AAA resection is 2% to 5%. The mortality rate for emergency surgery for expanding AAAs is 5% to 15% and 50% for those that have ruptured. Newer technology, such as endothelial stent grafts, has improved mortality rates and shortened the hospital stay for selected clients who need aneurysm repair.

ABDOMINAL AORTIC ANEURYSM RESECTION. In an AAA resection, the physician excises the aneurysm from the abdominal aorta to prevent or repair the rupture. The goal is to secure stable aortic integrity and tissue perfusion throughout the body.

Preoperative Care. Interventions are similar to those for clients undergoing surgery with general anesthesia. A bowel preparation and emphasis on coughing and deep breathing are very important. Because significant blood loss often occurs during AAA resection, clients planning elective surgery may be advised to bank their blood for autologous (self) transfusions postoperatively. The nurse assesses all peripheral pulses to serve as a baseline for comparison postoperatively. The nurse may mark where the pulse is palpated or heard by Doppler ultrasonography to facilitate locating the pulse postoperatively. Clients with ruptured aneurysms are brought to the operating suite directly from the emergency department. Preoperative care of clients with ruptured aneurysms involves admin-  tion until bowel sounds return. The nurse listens for bowel sounds every 8 hours and reports their return to the physician. Prolonged absence of bowel sounds and distention may indicate a prolonged ileus or a bowel infarction.

THORACIC AORTIC ANEURYSM REPAIR. Repair of thoracic aneurysms is tailored to each client; the procedure depends on the type and location of the aneurysm. Total cardiopulmonary bypass (CPB) is necessary for excision of aneurysms in the ascending aorta, and partial bypass is often used during excision of aneurysms in the descending aorta.

Preoperative Care. The care of the client undergoing thoracic aneurysm resection is similar to that provided for the client having thoracic surgery.

Operative Procedure. The surgeon uses either a thoracotomy or a median sternotomy approach to enter the thoracic cavity. The surgeon exposes the aneurysm and excises it. After excising the aneurysm, the surgeon usually sews a Dacron graft or prosthesis onto the aorta. Saccular aneurysms, which have an outpouching from a distinct portion of the arterial wall, can sometimes be removed without resection of the aorta.

Postoperative Care. The care of a client who has undergone thoracic aneurysm repair is similar to that after other chest surgery. The nurse assesses for and assists in the prevention of postoperative complications that can occur after a thoracic aneurysm repair. These complications include hemorrhage, ischemic colitis, spinal cord ischemia resulting in paraplegia, respiratory distress, and cardiac dysrhythmias.

Hemorrhage. The nurse assesses vital signs at least hourly, reporting any signs of hemorrhage (e.g., a decrease in blood pressure, an increase in pulse rate, rapid respirations, diaphoresis) to the physician immediately. The nurse assesses for bleeding or separation at the graft site by noting significant increases in chest drainage from the chest tubes.

Paraplegia. Inadvertent interruption of the blood supply to the spinal cord during thoracic aneurysm repair can result in paraplegia. The nurse assesses the client hourly for sensation and motion in all extremities and reports deficits immediately.

Respiratory Distress. After thoracic aneurysm repair, clients are especially susceptible to respiratory distress from atelectasis or pneumonia. This problem occurs as a result of both CPB and incisional discomfort. Both atelectasis and pneumonia may cause shallow breathing and poor cough effort. These clients are often maintained on a ventilator, at least overnight, after surgery. For clients with a median sternotomy, the surgeon firmly splints the incision to prevent separation of the sternum. Cardiac

Dysrhythmias. The nurse assesses all clients recovering from thoracic aneurysm repair for cardiac dysrhythmias. The stress of the thoracic surgery, added to the increased incidence of arteriosclerosis in this group, may predispose these clients to a myocardial infarction, cardiac dysrhythmias, or heart failure.

ENDOVASCULAR REPAIR OF ABDOMINAL AORTIC ANEURYSMS. The repair of AAAs with endovascular stent grafts provides an alternative choice for some clients. Clients selected for endovascular repair of AAAs are generally at high risk for major abdominal surgery. However, some clients with AAAs may be referred for endovascular repair before the aneurysm reaches the recommended diameter for elective surgery.

There are different designs of endovascular stent grafts for use, depending on the anatomic involvement of the aneurysm. The stent graft is flexible with either Dacron or polytetrafluoroethylene (PTFE) material. It is inserted through a skin incision into the femoral artery by way of a catheter-based system. The catheter is advanced to a level above the aneurysm, away from the renal arteries. The graft is released from the catheter, and the stent graft is deployed into place with a series of hooks. A defined proximal and distal neck is needed for tight seating of the stent to prevent leakage. This procedure is done in collaboration with the vascular surgeon, interventional radiologist, operating room team, and at some centers, vascular medicine physician.

The endovascular repair of AAAs has decreased the length of hospital stay for clients requiring repair of abdominal aneurysms from 7 to 9 days to 5 to 6 days or less; however, the client needs to be closely monitored, in the hospital and at home, for the development of complications following the procedure. Expert nursing care is required to allow for early identification of problems and complications that can be resolved in a timely fashion. In addition, expert nursing skills are needed for the coordination and collaboration required for discharge planning and follow-up care for clients at home.

Endovascular stent repair is not without its complications. Complications include the need for conversion from an endovascular repair to open surgical repair of the aneurysm, bleeding, aneurysm rupture, peripheral embolization, and misdeployment of the stent graft. All of these complications require surgical interventions.

Community-Based Care Most clients are discharged to home after aneurysm repair. In rare instances, in the absence of family or other support systems, the postoperative client may be discharged to an extended (long-term) care facility for rehabilitation.

HOME CARE MANAGEMENT If discharged to home, the client must follow the instructions provided by the nurse regarding activity level and incisional care. Because stair climbing may be restricted initially, the client may need a bedside commode if the bathroom is inaccessible.

HEALTH TEACHING For clients who have not undergone surgical aneurysm repair, the teaching plan emphasizes the importance of compliance with the schedule of computed tomography (CT) scanning to monitor the size of the aneurysm. The nurse educates the client receiving treatment for hypertension about the importance of continuing to take prescribed medication. The client and family or significant others are instructed about signs and symptoms that they must promptly report to the health care provider:

• Clients with abdominal aortic aneurysms (AAAs) must report abdominal fullness or pain, or back pain.

• Clients with thoracic aneurysms must report chest or back pain, shortness of breath, difficulty swallowing, or hoarseness.

 The nurse teaches the client who has undergone repair of the aneurysm about activity restrictions, wound care, and pain management. Clients may not engage in activities that involve lifting heavy objects (usually more than 15 to 20 pounds [6.8 to 9.1 kg]) for 6 to 12 weeks postoperatively. The nurse advises them to use discretion in activities that involve pulling, pushing, or straining, such as vacuuming, changing bed linens, moving furniture, mopping or sweeping, raking leaves, mowing grass, and chopping wood. Clients should temporarily avoid such hobbies as tennis, swimming, horseback riding, and golf, although putting practice is allowed. Because of postoperative weakness, they are usually restricted from driving a car for several weeks after discharge.

Clients who have not undergone aneurysm repair may fear rupture and subsequent death. The nurse reinforces the rationales for CT monitoring of the size of the aneurysm and for controlling hypertension and encourages clients to verbalize their fears.

HEALTH CARE RESOURCES In collaboration with the case manager or social worker, the nurse assesses the availability of transportation to and from appointments for clients needing CT monitoring. Clients who have undergone surgery may require the services of a home care nurse for assistance with dressing changes. A home care aide may be needed to assist with activities of daily living (ADLs).

Aneurysms of the Peripheral Arteries

OVERVIEW Although femoral and popliteal aneurysms are relatively uncommon, they are often associated with an aneurysm in another location of the arterial tree. To detect a popliteal aneurysm, the nurse observes a pulsating mass in the popliteal space. To detect a femoral aneurysm, the nurse observes a pulsatile mass over the femoral artery. Both extremities are evaluated because more than one femoral or popliteal aneurysm may be present.

 COLLABORATIVE MANAGEMENT The client may exhibit symptoms of limb ischemia, including diminished or absent pulses, cool to cold skin, and pain. Pain may also be present if an adjacent nerve is compressed. The recommended treatment for either type of aneurysm, regardless of the size, is surgery because of the risk of thromboembolic complications associated with their presence. To treat a femoral aneurysm, the physician excises the aneurysm and restores circulation using a Dacron graft or an autogenous saphenous vein graft. Most surgeons prefer to bypass rather than resect a popliteal aneurysm. Postoperatively, the nurse monitors for lower limb ischemia. The nurse palpates pulses below the graft to assess graft patency. Often, Doppler ultrasonography is necessary to assess blood flow when pulses are not palpable. Sudden development of pain or discoloration of the extremity is reported immediately to the physician because it may indicate graft occlusion.


OVERVIEW Aortic dissection has traditionally been referred to as a dissecting aneurysm. However, because this condition is more accurately described as a dissecting hematoma, the term aortic dissection has gained favor. Aortic dissection is thought to be caused by a sudden tear in the aortic intima, opening the way for blood to enter the aortic wall. Degeneration of the aortic media might be a prerequisite for this condition, with hypertension an important contributing factor. Aortic dissection is a relatively common event, occurring in at least 2000 people in the United States annually. It is frequently associated with connective tissue disorders such as Marfan's syndrome. It also occurs in older people, peaking in adults in their 50s and 60s, and in women in their third trimester of pregnancy. Because the circulation of any major artery arising from the aorta can be impaired in clients with aortic dissection, this condition is highly lethal and represents an emergency situation.

Dissections are classified in various ways (Goldman & Braunwald, 1998).

Debakey's classification contains three groups:

Type 1: Characterized by an intimal tear in the ascending (proximal) aorta, with extension of the dissection into the descending (distal) aorta

Type 2: Originates in and is limited to the ascending (proximal) aorta

Type 3: Arises within the descending (distal) thoracic aorta and often progresses distally

Proximal dissections occur almost twice as often as distal dissections. Although the ascending aorta and descending thoracic aorta are the most common sites, dissections can also occur in the abdominal aorta and other arteries.


The most common presenting symptom of aortic dissection is pain, with painless dissection occurring rarely. The pain is described as "tearing," "ripping," and "stabbing" and tends to move from its point of origin. Depending on the site of dissection, the client may feel pain in the anterior chest, back, neck, throat, jaw, or teeth. Diaphoresis, nausea, vomiting, faintness, and apprehension are also common. Blood pressure is usually elevated unless complications, such as cardiac tamponade or rupture, have occurred. A decrease or absence of peripheral pulses is common, as is aortic regurgitation, which is characterized by a musical murmur better heard along the right sternal border. Neurologic deficits, such as an altered level of consciousness, paraparesis, and strokes, can also occur. Chest x-ray examination, Doppler echocardiogram, computed tomography (CT), and aortic angiography are commonly used to confirm the diagnosis.

The following are goals of emergency treatment:

• The elimination of pain

• A reduction of blood pressure to 100 to 120 mm Hg

• A decrease in the velocity of left ventricular ejection

The physician prescribes IV sodium nitroprusside (Nitropress) by continuous drip initially to lower the blood pressure. Cardene) may be used. Propranolol (Inderal, Apo-Propranolol) is given in increments of 1 mg intravenously to decrease left ventricular ejection. Subsequent treatment depends on the location of the dissection. Generally, clients receive continued medical treatment for uncomplicated distal dissections and surgical treatment for proximal dissections. For clients receiving long-term medical treatment, the systolic blood pressure must be maintained at or below 130 to 140 mm Hg. Beta blockers (propranolol) and calcium channel antagonists are indicated. Clients receiving surgical intervention for a proximal dissection always require cardiopulmonary bypass (CPB). The surgeon excises the intimal tear and obliterates entry in the false opening by suturing edges of the dissected aorta. Usually, a prosthetic graft is used.


OVERVIEW Buerger's disease (thromboangiitis obliterans) is a relatively uncommon occlusive disease limited to the medium and small arteries and veins. The distal upper and lower limbs are the most frequently affected. Typically, Buerger's disease is identified in young adult men who smoke. Larger arteries, such as the femoral and brachial, become involved in the late stages of the disease. The veins are less commonly involved. The disease often extends into the perivascular tissues, resulting in fibrosis and scarring that binds the artery, vein, and nerve firmly together. For people who have this disease, cessation of cigarette smoking usually arrests the disease process, but persistence in smoking causes occlusion in the more proximal vessels. The cause of Buerger's disease is unknown, although there is a strong association with tobacco smoking. A familial or genetic predisposition and autoimmune etiologic factors are also possible.


Assessment The first clinical manifestation of Buerger's disease is usually claudication (pain in the muscles resulting from an inadequate blood supply) of the arch of the foot. Intermittent claudication may occur in the lower extremities. The pain may be ischemic, occurring in the digits while the client is at rest. Often, there is an aching pain that is more severe at night. Paroxysmal shocklike pain can be the result of ischemic neuropathy. Clients often experience increased sensitivity to cold and complain of coldness and numbness. On physical examination, the nurse notes that the pulses are often diminished in the distal extremities, and the extremities are cool and red or cyanotic in the dependent position. A diagnosis of Buerger's disease is commonly based on a physical finding of peripheral ischemia, often in association with migratory superficial phlebitis. Ulcerations and gangrene may be seen in the digits. The ulcerations are usually sharply demarcated. The gangrenous lesion can be small or can affect the entire digit. Arteriograms can be useful in delineating the degree of disease in the arteries. Commonly, arteriography reveals multiple segmental occlusions in the smaller arteries of the forearm, hand, leg, and foot. Plethysmographic studies of the fingers or toes may be diagnostic of the disease in the early stages. These studies can also be useful in following the progression of the disease in more proximal arteries.

Interventions Nursing interventions are directed at:

• Preventing the progression of the disease

• Avoiding vasoconstriction

• Promoting vasodilation

" Relieving pain

• Treating ulceration and gangrene

To prevent the progression of Buerger's disease, complete abstinence from tobacco in all forms is essential. The client is instructed to avoid extreme or prolonged exposure to cold to prevent vasoconstriction. The nurse instructs the client about medications that are prescribed for vasodilation, such as nifedipine (Procardia, Adalat). The treatment of clients with Buerger's disease is similar to that for peripheral arterial disease (PAD).

Subclavian Steal

OVERVIEW Subclavian steal occurs in the upper extremities from a subclavian artery occlusion or stenosis. The result is altered blood flow and ischemia in the arm. Subclavian steal can occur in people at any age but is more common in those with risk factors for atherosclerosis. Symptoms include tiredness in the arm with exertion, paresthesias, dizziness, and exerciseinduced pain in the forearm when the arms are elevated.

COLLABORATIVE MANAGEMENT Physical examination usually reveals a significant difference in the blood pressures between the arms. A difference greater than 20 mm Hg is considered significant. Another important finding is a subclavian bruit, which can occur on the affected side. The subclavian pulse may be decreased on the occluded side compared with the opposite side. The client's arm may also be discolored or cyanotic; however, this finding generally occurs only in severe cases. Surgery is the recommended intervention when a client has cyanosis or pain. One of three procedures may be used: endarterectomy of the subclavian artery, carotid-subclavian bypass, or dilation of the subclavian artery with placement of a vascular stent. Nursing care encompasses postoperative care of the client and monitoring of the arterial flow in the affected arm. The nurse should check brachial and radial pulses frequently and observe for ischemic changes. The nurse also observes the arm for edema, redness, or any other signs.


 OVERVIEW Thoracic outlet syndrome is a compression of the subclavian artery at the thoracic outlet by anatomic structures, such as a rib or muscle. The arterial wall may be damaged, producing thrombosis or embolization to distal arteries of the arms.

The three common sites of compression in the thoracic outlet are as follows:

• The interscalene triangle

• Between the coracoid process of the scapula and the pectoralis minor tendon

• Most commonly, the costoclavicular space

COLLABORATIVE MANAGEMENT Thoracic outlet syndrome is more common in females and in people whose occupations require holding their arms up or leaning over, such as baseball players, golfers, or swimmers. It is also seen in clients who have had trauma such as whiplash or after clavicular fracture. Clients generally complain of neck, shoulder, and arm pain that may be intermittent. They may also have numbness and moderate edema of the extremity. The pain and numbness are worse when the arm is placed in certain positions, such as over the head or out to the side. Clients may have overdeveloped neck and shoulder muscles, and the affected arm may appear cyanotic. Treatment includes physical therapy, exercises, and avoiding aggravating positions, such as elevating the arms. Surgical treatment involves resection of the anatomic structure that is compressing the artery. Surgery is performed only if a client has severe pain, has lost hand function, or is responding poorly to conservative treatment.


OVERVIEW Raynaud's phenomenon is caused by vasospasm of the arterioles and arteries of the upper and lower extremities, usually unilaterally. Raynaud's disease occurs bilaterally. The two terms are sometimes used interchangeably, but although they are related, there are some differences. Raynaud's phenomenon usually occurs in people older than 30 years of age; Raynaud's disease can occur between the ages of 17 and 50 years. Raynaud's phenomenon can occur in either sex, but Raynaud's disease is more common in women. The pathophysiology is the same for both entities. The etiology is unknown. Clients often have an associated systemic connective tissue disease, such as systemic lupus erythematosus or progressive systemic sclerosis. As a result of vasospasm, the cutaneous vessels are constricted and blanching of the extremity occurs, followed by cyanosis. When the vasospasm is relieved, the tissue becomes reddened or hyperemic. The client's extremities are numb and cold, and he or she may complain of pain and swelling. Ulcers may also be present. These attacks are intermittent and can be aggravated by cold or stress. In severe cases, the attack lasts longer and gangrene of the digits can occur.

COLLABORATIVE MANAGEMENT Treatment involves relieving or preventing the vasoconstriction by drug therapy. Commonly prescribed drugs are nifedipine (Procardia), cyclandelate (Cyclospasmol), and phenoxybenzamine (Dibenzyline). These vasodilating agents may help to relieve the symptoms, but they can cause uncomfortable side effects, such as facial flushing, headaches, hypotension, and dizziness. For severe symptoms that cannot be alleviated by drugs, a lumbar sympathectomy can be performed. The physician cuts the sympathetic nerve fibers that cause vasoconstriction of blood vessels in the lower extremities. This method is effective when clients are experiencing foot symptoms. For the upper extremities, a similar procedure—sympathetic ganglionectomy— may provide symptom relief. The long-term effectiveness of these treatments is questionable. Education of the client is important in prevention of complications. The nurse explains methods to prevent vasoconstriction, such as minimizing exposure to cold and decreasing stress. The client is instructed to wear warm clothes, socks, or gloves when exposed to cool or cold temperatures. He or she should keep the homes at a comfortably warm temperature. The nurse helps the client to identify stressors and provides suggestions for reducing them. 


Popliteal entrapment causes ischemic symptoms in the affected leg or foot because of anatomic compression of the popliteal artery. Popliteal entrapment occurs in young people, most often in men complaining of intermittent claudication of one or both extremities. Physical examination may reveal ischemic changes of the affected extremity, with normal function of the unaffected limb. When the client is at rest, the nurse may note diminished distal pulses, although this is a rare finding. Diagnosis of popliteal entrapment is possible only after an accurate client history, physical examination, and arteriography. The recommended treatment is surgical repair of the anatomic compression. Reconstruction of the popliteal artery may be necessary to restore arterial blood flow to the limb. Nursing care involves preventing general postoperative complications and evaluating the patency of the graft or artery postoperatively. The nurse observes for ischemic changes and evaluates distal pulses frequently postoperatively.


To function properly, veins must be patent (unobstructed) with competent valves. Vein function also necessitates the assistance of the surrounding muscle beds to help pump blood toward the heart. If one or more veins are not operating efficiently, they become distended and clinical manifestations occur.

Two distinct phenomena alter the blood flow in veins:

• Thrombus formation (venous thrombosis) can lead to pulmonary embolism, a life-threatening complication

 • Defective valves lead to venous insufficiency and varicose veins, which are not life threatening but are problematic.

Venous Thrombosis

OVERVIEW Thrombus formation constitutes one of health care's greatest challenges. A thrombus (also called a thrombosis) is a blood clot believed to result from an endothelial injury, venous stasis, or hypercoagulability. The thrombosis may not be specifically attributable to one element, or it may involve all three elements. Thrombosis is often associated with an inflammatory process. When a thrombus develops, inflammation can occur around the thrombus, thickening the vein wall and consequently leading to embolization (the formation of an embolus).

Thrombophlebitis refers to a thrombus that is associated with inflammation; phlebothrombosis is a thrombus without inflammation. Thrombophlebitis can occur in superficial veins; however, it most frequently occurs in the deep veins of the lower extremities. Deep vein thrombophlebitis, commonly referred to as deep vein thrombosis (DVT), not only is more common but also is more serious than superficial thrombophlebitis because it presents a greater risk for pulmonary embolism (PE), in which a dislodged blood clot travels to the pulmonary artery. Clients with DVT account for up to 600,000 hospitalizations each year in the United States. Of these, between 50,000 and 200,000 clients experience PE, causing up to 25% of all hospital deaths (Church, 2000).

Thrombus formation has been associated with stasis of blood flow, endothelial injury, and/or hypercoagulability, known as Virchow's triad. The precise cause of these events remains unknown; however, a few predisposing factors have been identified. Thrombosis has commonly occurred in people undergoing certain surgical procedures. The highest incidence of clot formation occurs in clients who have undergone hip surgery or open prostate surgery. Other conditions that seem to promote thrombus formation are pregnancy, ulcerative colitis, and heart failure. Immobility can predispose a person to thrombosis. This can occur during prolonged bedrest, such as when a client is confined to bed during the perioperative period.

Phlebitis (vein inflammation) associated with invasive procedures, such as IV therapy, can predispose clients to thrombosis. Severe infections, systemic lupus erythematosus, polycythemia vera, oral contraceptives, and trauma have also been linked to thrombosis.


 Assessment Clients with DVT may have symptoms or may be asymptomatic. The classic signs and symptoms of DVT are calf or groin tenderness and pain, and sudden onset of unilateral swelling of the leg. Pain in the calf on dorsiflexion of the foot (positive Homan's sign) appears in only 10% of clients with DVT, and false-positive findings are common (Church, 2000). Therefore checking a Homan 's sign is not advised! The nurse examines the area described as painful, comparing this site with the contralateral limb. The nurse gently palpates the site, observing for warmth and edema. Signs and symptoms, however, may be absent with thrombophlebitis. Because there are often silent clinical findings, the nurse must have a high index of suspicion for this disorder when caring for clients at high risk.

Localized edema in one extremity may suggest thrombophlebitis. The nurse can measure and compare right and left calf and thigh circumferences for changes over time as an indicator of DVT or venous insufficiency. However, serial leg measurements may not be the most reliable indicator of DVT.

Although diagnostic tests for DVT are available, physical examination findings are often adequate for diagnosis. If a definitive diagnosis is lacking from physical examination alone, other diagnostic tests may be performed, such as contrast venography, duplex ultrasonography, Doppler flow studies, and impedance plethysmography.

Venography with contrast medium visualizes clot formation in approximately 95% of people with DVT. However, this study is generally not performed, because it may precipitate thrombosis and is very painful.

Duplex ultrasonographic scanning, a noninvasive test, is the preferred diagnostic test for DVT if a definitive diagnosis cannot be made by physical examination. Doppler flow studies may also be useful in the diagnosis of DVT, but they are more sensitive in detecting proximal rather than distal DVT. Normal venous circulation is characterized by audible signals, whereas thrombosed veins produce little or no flow. Impedance plethysmography assesses venous outflow and can detect more than 90% of DVTs that are located above the popliteal vein. However, it is not helpful in locating clots in the calf and is less sensitive than Doppler studies (Church, 2000).

 Interventions The focus of treatment for thrombophlebitis is to prevent complications, such as pulmonary emboli, and to prevent an increase in size of the thrombus. Deep venous thrombophlebitis (thrombosis) is the most common type of thrombophlebitis. Clients with deep vein thrombosis (DVT) are often hospitalized for treatment, although this practice is changing as a result of the use of newer drugs.

NONSURGICAL MANAGEMENT. DVT is most often treated medically, using a combination of rest, drug therapy, and preventive measures.

REST. Supportive therapy for DVT includes bedrest and elevation of the extremity. Some health care providers order intermittent or continuous warm, moist soaks to the affected area. All clients are evaluated for signs and symptoms of pulmonary embolism (PE), which include shortness of breath and chest pain. Emboli may also travel to the brain or heart, but these complications are not as common as PE.

DRUG THERAPY. Anticoagulants are the drugs of choice for a client with DVT and for clients at risk for DVT. The conventional treatment has been IV unfractionated heparin followed by oral anticoagulation with warfarin (Coumadin). However, unfractionated heparin can be problematic because each client's response to the drug is unpredictable, and hospital admission is usually required for laboratory monitoring and dose adjustments. Today the use of low-molecular weight heparin is changing the management of both DVT and PE.

Unfractionated Heparin Therapy. Many clients with a confirmed diagnosis of an existing blood clot are started on a regimen of IV unfractionated heparin (UFH; Hepalean) therapy. UFH is an anticoagulant agent that at low doses interacts with antithrombin III to produce selective inhibition of clotting factors Ila (thrombin) and Xa. At higher doses it inhibits practically all clotting factors. The ultimate result is inhibition of fibrin formation; the drug does nothing to the existing clot. The physician prescribes UFH to prevent the formation of other clots, which often develop in the presence of an existing clot, and to prevent enlargement of the existing clot. Over a long period of time, the existing clot is slowly absorbed by the body.

Before UFH administration the client requires a baseline prothrombin time (PT), activated partial thromboplastin time (aPTT), International Normalized Ratio (INR), complete blood count (CBC) with platelet count, urinalysis, stool for occult blood, and creatinine level.

UFH is initially given in a bolus IV dose of approximately 100 units/kg of body weight, followed by constant infusion. The infusion is regulated by a reliable electronic infusion device that protects against accidental free flow of solution. The physician or clinical pharmacist orders concentrations of UFH (in 5% dextrose in water) and the number of units or milliliters per hour needed to maintain a therapeutic aPTT. aPTTs are obtained daily, or more frequently, and are reported to the health care provider as soon as the results are available to allow adjustment of heparin dosage. Therapeutic levels of aPTTs are usually one to two times normal control levels. The nurse assesses clients for signs and symptoms of bleeding, which include hematuria, frank or occult blood in the stool, ecchymosis (bruising), petechiae, an altered level of consciousness, or pain.

UFH can also decrease platelet counts. Mild reductions are common and are resolved with continued heparin therapy. Severe platelet reductions, although rare, result from the development of antiplatelet bodies within 6 to 14 days after the beginning of treatment. Platelets aggregate into "white clots" that can cause thrombosis, usually in the form of an acute arterial occlusion (Simko & Lockhart, 1996). The provider discontinues heparin administration if severe heparin-induced thrombocytopenia and thrombosis (HITT) (> 100,000 mm3), or "white clot syndrome," occurs. An oral anticoagulant may then be substituted for heparin if necessary.

The nurse also ensures that protamine sulfate, the antidote for heparin, is available, if needed, for excessive bleeding. Chart 36-10 highlights information important to nursing care and client education associated with anticoagulant therapy.

To prevent DVT, heparin may be given in low doses subcutaneously for high-risk clients, especially after orthopedic surgery.

Other pharmacologic agents that may be used for prophylaxis are as follows:

Ø     Low-molecular weight heparin (e.g., enoxaparin [Lovenox])

Ø     Dextran, an IV plasma expander

Ø     Dihydroergotamine (DHE)

Ø     Warfarin (Coumadin, Warfilone)

Ø     Aspirin (ASA)

Prevention of DVT also includes early ambulation and mobilization, thigh-high graduated compression elastic stockings (such as TED stockings), and external intermittent or sequential compression devices (SCDs) (Church, 2000). The nurse ensures that the compression devices fit properly and do not restrict blood flow.

Low-Molecular Weight Heparin. Subcutaneous lowmolecular weight heparins (LMWHs), such as enoxaparin (Lovenox), dalteparin (Fragmin), and ardeparin (Normiflo), have a consistent action and are approved for prevention and treatment of DVT.

Danaparoid (Orgaran) is also classified as an LMWH but is actually a heparinoid. LMWHs bind less to plasma proteins, blood cells, and vessel walls, resulting in a longer half-life and more predictable response. Clients may be safely managed at home with daily visits from a home care nurse. They must be willing to learn self-injection or have a family member, friend, or home care nurse administer the subcutaneous injections.

Some health care providers place the client on a regimen of IV unfractionated heparin (UFH) for several days, then follow up with an LMWH. In this case, the UFH is discontinued at least 30 minutes before the first LMWH injection. The usual dose of enoxaparin is 1 mg/kg of body weight, not to exceed 90 mg, and is repeated every 12 hours. If the client's creatinine level is greater than 2 mg/dL (indicating renal insufficiency), the health care provider lowers the dose. Dalteparin can be given once a day at 200 units/kg of body weight and does not require dose adjustment for renal insufficiency. The usual dose of ardeparin is 50 units/kg of body weight and is given every 12 hours.

The nurse monitors the INR and stools daily for occult blood. aPTTs are not checked on an ongoing basis, because the doses of LMWH are not adjusted.

Warfarin Therapy. If the client is receiving continuous UFH, warfarin (Coumadin) is added at least 5 days later. Clients receiving LMWH are placed on a regimen of warfarin after the first dose. Warfarin works in the liver to inhibit synthesis of the four vitamin K-dependent clotting factors and takes 3 to 4 days before it can exert therapeutic anticoagulation. The heparin continues to provide therapeutic anticoagulation until this effect is achieved with warfarin. IV heparin is then discontinued at that time.

Therapeutic levels of warfarin are monitored by measuring prothrombin time (PT) and/or the International Normalized Ratio (INR). Because PTs are often inconsistent and misleading, the INR was developed. Most laboratories report both results. Most clients receiving warfarin for DVT should have an INR between 2.0 and 3.0 (Coyne, 1997).

Warfarin therapy should be started with low doses, at least 5 mg, and gradually titrated up according to the INR. Clients usually receive warfarin for 3 to 6 months after an episode of DVT.

Nursing assessment for bleeding is similar to that described for clients receiving heparin. The nurse ensures that vitamin K, the antidote for warfarin, is available in case of excessive bleeding (see Chart 36-10).

Thrombolytic Therapy. The use of systemic thrombolytic therapy for DVT is effective in dissolving thrombi quickly and completely. The greatest advantage is thought to be the prevention of valvular damage and consequential venous insufficiency, or "postphlebitis syndrome." However, thrombolytic therapy is contraindicated postoperatively, during pregnancy, and after childbirth, trauma, brain attacks, or spinal injuries. To be most effective, thrombolytic therapy must be initiated within 5 days after the onset of symptoms. Thrombolytic agents such as streptokinase and recombinant tissue plasminogen activator (t-PA), as well as platelet inhibitors such as abciximab (ReoPro), may be effective in dissolving a clot or preventing new clots during the first 24 hours. Nurses caring for clients receiving these agents must monitor closely for signs and symptoms of bleeding.

PREVENTION AND TREATMENT OF PERIPHERAL EDEMA. The client's legs should be elevated when in bed and when in a chair. To help prevent chronic venous insufficiency, clients with active and resolving DVT are often instructed to wear knee- or thigh-high compression or elastic stockings.

SURGICAL MANAGEMENT. A deep vein thrombus is rarely removed surgically unless there is a massive occlusion that does not respond to medical treatment and the thrombus is of recent (1 to 2 days) onset. Thrombectomy is the most common surgical procedure for removing the thrombus. Preoperative and postoperative care of clients undergoing thrombectomy are similar to that for clients undergoing arterial surgery (see earlier discussion under Acute Peripheral Arterial Occlusion, p. 755).

INFERIOR VENA CAVAL INTERRUPTION. For clients with recurrent deep vein thrombosis (DVT) or pulmonary emboli that do not respond to medical treatment and for clients who cannot tolerate anticoagulation, inferior vena caval interruption may be indicated to prevent pulmonary emboli. Preoperative care is similar to that provided for clients receiving local anesthesia.

If clients have recently been taking anticoagulants, such as warfarin (Coumadin, Warfilone) or heparin (Hepalean), the nurse consults with the physician about interrupting this therapy in the preoperative period to avoid hemorrhage. The surgeon inserts a filter device, or "umbrella," percutaneously into the inferior vena cava (Figure 36-12).

The device is meant to trap emboli in the inferior vena cava before they progress to the lungs. Holes in the device allow blood to pass through, thus not significantly interfering with the return of blood to the heart. Popular inferior vena caval filters include the bird's-nest filter and the Greenfield filter. Postoperatively, the nurse inspects the incision on the right side of the chest for bleeding and signs or symptoms of infection. Other postoperative nursing care is similar to that for any client undergoing surgery.

LIGATION OR EXTERNAL CLIPS. If an inferior vena caval filter is not successful in preventing pulmonary emboli, or if the filter becomes blocked with thrombi, the surgeon may perform ligation or insert external clips on the inferior vena cava to prevent pulmonary emboli. Preoperative care for clients undergoing ligation of the vena cava or placement of an external clip is similar to that for an abdominal laparotomy. If the client is receiving anticoagulation therapy, the nurse consults with the surgeon about temporary interruption of therapy. Ligation and insertion of external clips in the inferior vena cava are often performed by means of an abdominal laparotomy. In a ligation, the surgeon ties off the inferior vena cava to block emboli. Application of an external clip, such as the Adams-DeWeese clip, narrows the inferior vena cava to four serrated transverse slits, 3 to 5 mm in diameter. If laparotomy is performed, the external clip procedure is preferred because there are fewer hemodynamic or venous complications and a low frequency of recurrent pulmonary emboli associated with its use. Postoperative care for the client with inferior vena caval ligation or external clip placement is similar to that for an abdominal laparotomy.  Community-Based Care Clients recovering from thrombophlebitis or deep vein thrombosis (DVT) are usually ambulatory when they are discharged from the hospital. The primary focus of planning for discharge is to educate the client about the hazards of anticoagulation therapy (see Chart 36-10).  

HOME CARE MANAGEMENT The nurse helps the client identify situations and equipment that might cause trauma, such as the use of a straight-edged razor. The nurse helps the client and family or significant others to make arrangements to avoid hazardous situations and to procure alternative types of equipment if needed, such as an electric razor.

HEALTH TEACHING The nurse teaches clients recovering from DVT to stop or avoid smoking and to avoid the use of oral contraceptives to decrease the risk of recurrence. Most clients are discharged on a regimen of warfarin (Coumadin, Warfilone) or lowmolecular weight heparin (LMWH).

The nurse instructs clients and their families to avoid potentially traumatic situations, such as participation in contact sports. The nurse provides written and oral information about the signs and symptoms of bleeding. The client must report any of these manifestations to the health care provider immediately. The anticoagulant effect of warfarin may be reversed by the omission of one or two doses of the drug or by the administration of vitamin K. In case of injury, clients are directed to apply pressure to bleeding wounds and to seek medical assistance immediately. The nurse encourages them to carry an identification card or wear a medical alert bracelet that states that they are taking warfarin. The nurse also instructs clients to inform their dentist and other health care providers that they are taking warfarin before receiving treatment or prescriptions.

Prothrombin times are affected by many prescription and over-the-counter medications, such as antacids, antihistamines, aspirin, mineral oil, oral contraceptives, and large doses of vitamin C. The action of warfarin is also affected by high-fat and vitamin K-rich foods, such as cabbage, cauliflower, broccoli, asparagus, turnips, spinach, kale, fish, and liver. Clients are therefore instructed to eat a well-balanced diet and to avoid taking additional medications without consulting a health care provider. The nurse arranges for clients to have prothrombin time (PT) and International Normalized Ratio (INR) determinations made 1 to 2 weeks after discharge. Clients receiving subcutaneous LMWH injections at home need instruction on self-injection. If family members or friends are administering the injections, the nurse teaches the appropriate caregiver.

Clients who have experienced DVT may fear recurrence of a thrombus and may also be concerned about treatment with warfarin and the risk for bleeding. The nurse assures them that participation in the prescribed treatment frequently helps in resolving this problem and that ongoing assessment of PTs and INRs should minimize the risks of bleeding.

HEALTH CARE RESOURCES Clients discharged on a regimen of warfarin need access to a pharmacy to renew prescriptions and, if feasible, obtain a medical alert bracelet. They also need access to a laboratory for frequent monitoring of PTs and INRs.

Venous Insufficiency


Venous insufficiency occurs as a result of prolonged venous hypertension, which stretches the veins and damages the valves. This can lead to a backup of blood and further venous hypertension, resulting in edema. Edema occurs as the by products of red blood cells break down and infiltrate the surrounding tissues. Because the client cannot eliminate waste products, they accumulate within the tissues. With time, this stasis (stoppage) results in venous stasis ulcers, swelling, and cellulitis. Venous efficiency is altered when thrombosis occurs or when valves are not functioning correctly. Defective valves can result from prolonged venous hypertension, which stretches the veins and damages valves. This can occur in people who stand or sit in one position for long periods, such as teachers and office personnel. Pregnancy and obesity can also cause chronically distended veins, which lead to damaged valves. Thrombus formation can contribute to valve destruction. Chronic venous insufficiency often occurs in clients who have had thrombophlebitis.


 Assessment Clients with venous insufficiency may have edema in both extremities. There may be stasis dermatitis or discoloration along the ankles, extending up to the calf. In people with long-term venous insufficiency or stasis, ulcers often form. Ulcer formation can result from the edema or from minor injury to the limb. Venous ulcers typically occur over the malleolus, more often medially than laterally. The ulcer usually has irregular borders. Generally, these ulcers are chronic and difficult to heal. Many clients live with ulcers for years, and recurrence is common. Some may lose one or both limbs if ulcers are not controlled. • Interventions The focus of treating venous insufficiency is to decrease edema and promote venous return from the affected extremity. Clients are not usually hospitalized for venous insufficiency alone unless it is complicated by an ulcer or another disorder is occurring simultaneously.

NONSURGICAL MANAGEMENT. Treatment of chronic venous insufficiency is primarily nonsurgical, unless it is complicated by a venous stasis ulcer that requires surgical debridement. The goal of managing venous stasis ulcers is twofold: to heal the ulcer and to prevent stasis with recurrence of ulcer formation.

TREATMENT OF EDEMA. Clients with chronic venous insufficiency wear elastic or compression stockings, which fit from the middle of the foot to just below the knee or to the thigh. Clients should wear the stockings during the day and evening. The nurse instructs them to elevate their legs for at least 20 minutes four or five times per day and to avoid long periods of sitting or standing in place. When the client is in bed, the legs should be elevated above the level of the heart (Chart 36-11).

 The nurse and physician should also confer about the use of intermittent sequential pneumatic compression of the lower extremities for clients with past or present venous stasis ulcers. If the client is being treated for an open venous ulcer, the device is applied over a dressing such as an Unna boot. The nurse instructs the client to apply the pump as directed during the period of healing. Because of the high incidence of venous ulcer recurrence, clients with chronic venous insufficiency whose ulcers have healed are encouraged to continue compression therapy for life.

TREATMENT OF VENOUS STASIS ULCERS. Venous stasis ulcers are slightly more manageable than ulcers resulting from arterial disease. They are chronic in nature, with some clients manifesting the same ulcer for years. Ulcers often heal, only to recur in the same area. The client may have simultaneous ulcers for several years.

Dressings. Two types of occlusive dressings are used for venous stasis ulcers: oxygen permeable dressings and oxygen impermeable dressings. Because the role of atmospheric oxygen in wound healing is controversial, opinions vary with regard to which type of dressing is preferred. An oxygenpermeable polyethylene film and an oxygen-impermeable hydrocolloid dressing (e.g., DuoDerm) are common. Hydrocolloid dressings are left in place for a minimum of 3 to 5 days for best effect.

A cultured, bilayered human skin equivalent has recently become available for difficult-to-heal venous leg ulcers. This graft was approved first in Canada, and research on its success has been very promising (Dolynchuk et al., 1999).

If the client is ambulatory, an Unna boot may be used. This dressing is constructed of gauze that has been moistened with zinc oxide. The health care provider applies the boot to the affected limb, from the toes to the knee, after the ulcer has been cleaned with normal saline solution. Povidone-iodine (Betadine) and hydrogen peroxide are not used, because they destroy granulation tissue. The Unna boot is then covered with an elastic wrap and hardens like a cast; this promotes venous return and prevents stasis. The Unna boot also forms a sterile environment for the ulcer. The physician or advancedpractice nurse should change the boot approximately once a week. The nurse instructs the client about what to look for if arterial occlusion should occur from an Unna boot that is too tight.

Drug Therapy. The provider may prescribe topical agents, such as Accuzyme, to chemically debride the ulcer, eliminating necrotic tissue and promoting healing. If an infection or cellulitis develops, systemic antibiotics are necessary.

SURGICAL MANAGEMENT. Surgery for chronic venous insufficiency is not usually performed, because historically it has not been successful. Attempts at transplanting vein valves have had limited success. Surgical debridement of venous ulcers is similar to that performed for arterial ulcers

 Community-Based Care The goal for the client with chronic venous insufficiency is to be managed in the home. For clients with frequent acute complications and repeated hospital admissions, case management can help to meet appropriate clinical and cost outcomes.

HOME CARE MANAGEMENT The nurse helps clients with chronic venous insufficiency to plan for opportunities and facilities that allow for elevation of the lower extremities in and outside the home. In addition, clients with venous stasis ulcers need to plan for care of the ulcers.


The nurse instructs clients with chronic venous stasis to:

Ø     Avoid standing still if possible

Ø     Elevate their legs when sitting

Ø     Avoid crossing their legs

Ø     Avoid wearing tight girdles, tight pants, and narrowbanded knee-high socks

The physician prescribes support hose or antiembolism stockings. The nurse teaches clients to apply these stockings before they get out of bed in the morning and to remove them just before going to bed at night . The nurse also advises them that they will probably need to wear these stockings for the rest of their lives. To improve circulation and aid in weight reduction, the nurse prescribes an exercise program on an individual basis with health care provider input. The nurse encourages all clients to maintain an optimal weight and may consult with the dietitian to plan a weight reduction diet. The nurse instructs clients with venous stasis ulcers how to care for the ulcers at home. Clients with venous stasis disease, especially those with venous stasis ulcers, may require long-term emotional support to assist them in meeting chronic needs. They may also need assistance in coping with necessary lifestyle adjustments, such as changes in occupation.

HEALTH CARE RESOURCES Clients with venous stasis ulcers may need the assistance of a home care nurse to perform dressing changes. Clients with Unna boots need weekly transportation to their health care provider for dressing changes. The nurse arranges for a sequential compression device in the home if the health care provider prescribes one.

Varicose Veins

OVERVIEW Varicose veins are distended, protruding veins that appear darkened and tortuous. They can occur in anyone, but they are common in clients older than 30 years of age whose occupations require prolonged standing. Varicose veins are also frequently seen in pregnant women, clients with systemic problems (such as heart disease), obese clients, and clients with a family history of varicose veins. As the vein wall weakens and dilates, venous pressure increases and the valves become incompetent (defective). The incompetent valves enhance the vessel dilation, and the veins become tortuous and distended. The client may complain of pain, especially after standing, and may experience a fullness in the legs. Nursing assessment reveals distended, protruding veins. The Trendelenburg test assists with the diagnosis. The client is placed in a supine position with elevated legs. As the client sits up, the veins would normally fill from the distal end; however, if there are varicosities, the veins fill from the proximal end.

COLLABORATIVE MANAGEMENT Conservative measures are the treatment of choice. These involve wearing elastic stockings and elevating the extremities as much as possible. Clients who continue to have pain or unsightly veins, despite this treatment, may opt for either sclerotherapy or surgical removal of the vein.

Sclerotherapy is performed on small or a limited number of varicosities. The physician injects a solution, such as sodium tetradecyl, directly into the vein, or he or she may use a laser device. A pressure dressing may be applied over the sclerosed vein to keep vessels free of blood for 24 to 72 hours. The surgeon performs an incision and drainage of trapped blood in the sclerosed vein 14 to 21 days after injection, followed by application of a second pressure dressing for 12 to 18 hours.

Varicose veins are surgically removed when they are larger than 4 mm in diameter or are in clusters. The stab avulsion technique may be used if the saphenous veins are competent. The surgeon exposes varices through 2- to 3-mm stab incisions, grasping the veins with hooks, and dividing and avulsing each vein. The surgeon may need to strip (remove) affected veins if the saphenous vein is incompetent. The surgeon threads a long wire through an incision above an affected vein, pulling it down through the vein and out through an incision below with firm elastic (Ace) bandages. Postoperatively, the nurse assesses the groin and entire leg for bleeding through the elastic bandage. The nurse instructs the client to keep the legs elevated and to perform range-ofmotion exercises of the legs at least hourly. Clients are ambulatory and are often discharged from the hospital by the first postoperative day. At this time, the nurse instructs clients to continue to wear elastic stockings, walk, limit sitting, avoid standing in one place, and elevate their legs when sitting.

PHLEBITIS Phlebitis is an inflammation of the superficial veins caused by an irritant, such as IV therapy. The client has a reddened, warm area radiating up an extremity, commonly an arm. The client may also experience pain, soreness, and swelling of the extremity. Treatment involves application of warm, moist soaks, which dilate the vein and promote circulation. Sometimes a heating unit is used to keep the soaks warm. Rarely, ice packs are used. The nurse applies the soaks, making sure that the temperature is not hot enough to burn the client, and assesses for complications, such as tissue necrosis, infection, or pulmonary embolus. After a few days of conservative therapy, the inflammation usually subsides.


 OVERVIEW Many types of trauma can result in vascular injury. Injuries to the blood vessels in the upper and lower extremities account for approximately 70% of all vascular injuries to the human body. Vascular injuries to the blood vessels include punctures, lacerations, and transections. Acute blunt or penetrating trauma may result in a false aneurysm or hematoma. Arteriovenous fistulas may be seen after penetrating injuries. The more common causes of penetrating injuries to the blood vessels are gunshot and knife wounds. Blunt trauma, which is less common, can result from highspeed automobile accidents as a result of the shearing force of rapid deceleration. Vascular trauma can also occur during arterial puncture for arteriographic or hemodynamic studies in which a dissection, hematoma, or occlusive lesion occurs.

COLLABORATIVE MANAGEMENT The history and physical examination aid in establishing the diagnosis in the client with vascular injury. The nurse questions the client or family about the mechanism of injury, the site of injury, the amount of blood loss, and symptoms present after the injury.

The nurse assesses for circulatory, sensory, or motor impairment but is aware that, despite significant trauma, impairment may not be apparent, especially if deep vessels have been injured. Arteriography provides essential information about the vascular injury. Emergency or urgent surgical intervention is warranted for clients with ischemia to maximize successful revascularization.

Management of vascular injuries is often initiated in a hospital emergency department. Careful triage by the nurse is crucial. The most important principles in the management of vascular trauma are establishment of a patent airway, control of bleeding, and restoration of blood flow. The method of repair varies with the type of vascular injury. Techniques include vein bypass grafting, lateral suture repair, thrombectomy (excision of blood clot), resection with end-to-end anastomosis, and vein patch grafting.