LEARNING OBJECTIVES - Weebly · 3131ChapterChapter Assessment and Management of Patients With...

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31Assessment andManagement of PatientsWith Vascular Disordersand Problems of Peripheral CirculationLEARNING OBJECTIVES

On completion of this chapter, the learner will be able to:1. Identify anatomic and physiologic factors that affect peripheral

blood flow and tissue oxygenation.2. Use appropriate parameters for assessment of peripheral circulation.3. Use the nursing process as a framework of care for patients with

circulatory insufficiency of the extremities.4. Compare the various diseases of the arteries, their causes, patho-

logic and physiologic changes, clinical manifestations, manage-ment, and prevention.

5. Describe the prevention and management of venous thrombosis.6. Compare the preventive management of venous insufficiency, leg

ulcers, and varicose veins.7. Use the nursing process as a framework of care for patients with

leg ulcers.8. Describe the relationship between lymphangitis and lymphedema.

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816 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION

Adequate perfusion oxygenates and nourishes body tissues anddepends in part on a properly functioning cardiovascular system.Adequate blood flow depends on the efficient pumping action ofthe heart, patent and responsive blood vessels, and adequate cir-culating blood volume. Nervous system activity, blood viscosity,and the metabolic needs of tissues influence the rate and adequacyof blood flow.

Anatomic and Physiologic OverviewThe vascular system consists of two interdependent systems. Theright side of the heart pumps blood through the lungs to the pul-monary circulation, and the left side of the heart pumps blood toall other body tissues through the systemic circulation. The bloodvessels in both systems channel the blood from the heart to the tis-sues and back to the heart (Fig. 31-1). Contraction of the ventriclesis the driving force that moves blood through the vascular systems.

Arteries distribute oxygenated blood from the left side of theheart to the tissues, whereas the veins carry deoxygenated bloodfrom the tissues to the right side of the heart. Capillary vessels, lo-cated within the tissues, connect the arterial and venous systemsand are the site of exchange of nutrients and metabolic wastes be-tween the circulatory system and the tissues. Arterioles and venulesimmediately adjacent to the capillaries, together with the capil-laries, make up the microcirculation.

The lymphatic system complements the function of the cir-culatory system. Lymphatic vessels transport lymph (a fluidsimilar to plasma), and tissue fluids (containing smaller pro-teins, cells, and cellular debris) from the interstitial space to sys-temic veins.

ANATOMY OF THE VASCULAR SYSTEMArteries and ArteriolesArteries are thick-walled structures that carry blood from theheart to the tissues. The aorta, which has a diameter of approxi-mately 25 mm (1 inch), gives rise to numerous branches, whichdivide into smaller arteries that are about 4 mm (0.16 inch) indiameter by the time they reach the tissues. Within the tissues,

Glossaryanastomosis: surgical junction of two

vesselsaneurysm: a localized sac or dilation of an

artery formed at a weak point in the vesselwall

ankle-brachial index (ABI) or ankle-armindex (AAI): ratio of the ankle systolicpressure to the arm systolic pressure; anobjective measurement of arterial diseasethat provides quantification of the degreeof stenosis

angioplasty: an invasive procedure that usesa balloon-tipped catheter to dilate astenotic area of a blood vessel

arteriosclerosis: diffuse process whereby themuscle fibers and the endothelial lining ofthe walls of small arteries and arteriolesthicken

atherosclerosis: disease process involvingthe accumulation of lipids, calcium, bloodcomponents, carbohydrates, and fibroustissue on the intimal layer of a large ormedium-sized artery

bruit: sound produced by turbulent bloodflow through an irregular, tortuous,stenotic, or dilated vessel

dissection: separation of the weakened elas-tic and fibromuscular elements in themedial layer of an artery

duplex ultrasonography: combines B-modegray-scale imaging of tissue, organs, andblood vessels with capabilities of estimat-ing velocity changes by use of a pulsedDoppler

intermittent claudication: a muscular,cramp-like pain in the extremities con-

sistently reproduced with the same degreeof exercise or activity and relieved by rest

international normalized ratio (INR):method of measuring anticoagulationlevels, such as warfarin (Coumadin);devised to bring a universal standard tomonitoring of anticoagulation achievedby oral medications

ischemia: deficient blood supplyrest pain: persistent pain in the foot or digits

when the patient is resting, indicating asevere degree of arterial insufficiency

rubor: reddish blue discoloration of the ex-tremities; indicative of severe peripheralarterial damage in vessels that remaindilated and unable to constrict

stenosis: narrowing or constriction of a vessel

Cranialcirculation

Superiorvena cava

Aorta

Pulmonaryartery

Leftpulmonary veins

Right atrium

Rightventricle

Hepaticcirculation

Renalcirculation

Systemiccirculation

Leftventricle

Leftatrium

Inferiorvena cava

Pulmonarycirculation

Pulmonarycirculation

Rightpulmonaryveins

FIGURE 31-1 Systemic and pulmonary circulation. Oxygen-rich bloodfrom the pulmonary circulation is pumped from the left heart into the aortaand the systemic arteries to the capillaries, where the exchange of nutrientsand waste products takes place. The deoxygenated blood returns to the rightheart by way of the systemic veins and is pumped into the pulmonary circu-lation. From Stedman’s Medical Dictionary (27th ed.). (2000). Philadelphia:Lippincott Williams & Wilkins.

Chapter 31 Assessment and Management of Patients With Vascular Disorders and Problems of Peripheral Circulation 817

the vessels divide further, diminishing to approximately 30 µmin diameter; these vessels are called arterioles.

The walls of the arteries and arterioles are composed of threelayers: the intima, an inner endothelial cell layer; the media, amiddle layer of smooth elastic tissue; and the adventitia, an outerlayer of connective tissue. The intima, a very thin layer, providesa smooth surface for contact with the flowing blood. The mediamakes up most of the vessel wall in the aorta and other large ar-teries of the body. This layer is composed chiefly of elastic andconnective tissue fibers that give the vessels considerable strengthand allow them to constrict and dilate to accommodate the bloodejected from the heart (stroke volume) and maintain an even,steady flow of blood. The adventitia is a layer of connective tis-sue that anchors the vessel to its surroundings. There is much lesselastic tissue in the smaller arteries and arterioles, and the mediain these vessels is composed primarily of smooth muscle.

Smooth muscle controls the diameter of the vessels by con-tracting and relaxing. Chemical, hormonal, and nervous systemfactors influence the activity of smooth muscle. Because arteriolescan alter their diameter, thereby offering resistance to blood flow,they are often referred to as resistance vessels. Arterioles regulatethe volume and pressure in the arterial system and the rate ofblood flow to the capillaries. Because of the large amount of mus-cle, the walls of the arteries are relatively thick, accounting for ap-proximately 25% of the total diameter of the artery. The walls ofthe arterioles account for approximately 67% of the total diame-ter of arterioles.

The intima and the inner third of the smooth muscle layer arein such close contact with the blood that the blood vessel receivesits nourishment by direct diffusion. The adventitia and the outermedia layers have a limited vascular system for nourishment andrequire their own blood supply to meet metabolic needs.

CapillariesCapillary walls, which lack smooth muscle and adventitia, arecomposed of a single layer of endothelial cells. This thin-walledstructure permits rapid and efficient transport of nutrients to thecells and removal of metabolic wastes. The diameter of capillar-ies ranges from 5 to 10 µm; this narrow channel requires redblood cells to alter their shape to pass through these vessels.Changes in a capillary’s diameter are passive and are influencedby contractile changes in the blood vessels that carry blood to andfrom a capillary. The capillary’s diameter also changes in responseto chemical stimuli. In some tissues, a cuff of smooth muscle,called the precapillary sphincter, is located at the arteriolar end ofthe capillary and is responsible, along with the arteriole, for con-trolling capillary blood flow.

Some capillary beds, such as in the fingertips, contain arte-riovenous anastomoses, through which blood passes directlyfrom the arterial to the venous system. These vessels are believedto regulate heat exchange between the body and the externalenvironment.

The distribution of capillaries varies with the type of tissue.For example, skeletal tissue, which is metabolically active, has adenser capillary network than does cartilage, which is less active.

Veins and VenulesCapillaries join to form larger vessels called venules, which jointo form veins. The venous system is therefore structurally analo-gous to the arterial system; venules correspond to arterioles, veinsto arteries, and the vena cava to the aorta. Analogous types of ves-

sels in the arterial and venous systems have approximately thesame diameters (see Fig. 31-1).

The walls of the veins, in contrast to those of the arteries, arethinner and considerably less muscular. The wall of the averagevein amounts to only 10% of the vein diameter, in contrast to 25%in the artery. The walls of a vein, like those of arteries, are com-posed of three layers, although these layers are not as well defined.

The thin, less muscular structure of the vein wall allows thesevessels to distend more than arteries. Greater distensibility andcompliance permit large volumes of blood to be stored in theveins under low pressure. For this reason, veins are referred to ascapacitance vessels. Approximately 75% of total blood volume iscontained in the veins. The sympathetic nervous system, whichinnervates the vein musculature, can stimulate the veins to con-strict (venoconstriction), thereby reducing venous volume andincreasing the volume of blood in the general circulation. Con-traction of skeletal muscles in the extremities creates the primarypumping action to facilitate venous blood flow back to the heart.

Some veins, unlike arteries, are equipped with valves. In gen-eral, veins that transport blood against the force of gravity, as inthe lower extremities, have one-way bicuspid valves that interruptthe column of blood to prevent blood from seeping backward asit is propelled toward the heart. Valves are composed of endo-thelial leaflets, the competency of which depends on the integrityof the vein wall.

Lymphatic VesselsThe lymphatic vessels are a complex network of thin-walled vesselssimilar to the blood capillaries. This network collects lymphaticfluid from tissues and organs and transports the fluid to the venouscirculation. The lymphatic vessels converge into two main struc-tures: the thoracic duct and the right lymphatic duct. These ductsempty into the junction of the subclavian and the internal jugularveins. The right lymphatic duct conveys lymph primarily from theright side of the head, neck, thorax, and upper arms. The thoracicduct conveys lymph from the remainder of the body. Peripherallymphatic vessels join larger lymph vessels and pass through re-gional lymph nodes before entering the venous circulation. Thelymph nodes play an important role in filtering foreign particles.

The lymphatic vessels are permeable to large molecules andprovide the only means by which interstitial proteins can returnto the venous system. With muscular contraction, lymph vesselsbecome distorted to create spaces between the endothelial cells,allowing protein and particles to enter. Muscular contraction ofthe lymphatic walls and surrounding tissues aids in propelling thelymph toward the venous drainage points.

FUNCTION OF THE VASCULAR SYSTEMCirculatory Needs of TissuesThe amount of blood flow needed by body tissues constantlychanges. The percentage of blood flow received by individual or-gans or tissues is determined by the rate of tissue metabolism, theavailability of oxygen, and the function of the tissues (Table 31-1).When metabolic requirements increase, blood vessels dilate to in-crease the flow of oxygen and nutrients to the tissues. Whenmetabolic needs decrease, vessels constrict, and blood flow to thetissues decreases. Metabolic demands of tissues increase withphysical activity or exercise, local heat application, fever, and in-fection. Reduced metabolic requirements of tissues accompanyrest or decreased physical activity, local cold application, and


cooling of the body. If the blood vessels fail to dilate in responseto the need for increased blood flow, tissue ischemia (ie, deficientblood supply to a body part) results. The mechanism by whichblood vessels dilate and constrict to adjust for metabolic changesensures that normal arterial pressure is maintained.

As blood passes through tissue capillaries, oxygen is removed,and carbon dioxide is added. The amount of oxygen extracted byeach tissue differs. For example, the myocardium tends to extractabout 50% of the oxygen from arterial blood in one pass throughits capillary bed, whereas the kidneys extract only about 7% ofthe oxygen from the blood that passes through them. The aver-age amount of oxygen removed collectively by all of the body tis-sues is about 25%. This means that the blood in the vena cavaecontains about 25% less oxygen than aortic blood. This is knownas the systemic arteriovenous oxygen difference. The value increaseswhen the amount of oxygen delivered to the tissues is decreasedrelative to their metabolic needs (see Table 31-1).

Blood FlowBlood flow through the cardiovascular system always proceeds inthe same direction: left side of the heart to the aorta, arteries, ar-terioles, capillaries, venules, veins, vena cavae, and right side ofthe heart. This unidirectional flow is caused by a pressure differ-ence that exists between the arterial and venous systems. Becausearterial pressure (approximately 100 mm Hg) is greater than ve-nous pressure (approximately 4 mm Hg) and fluid always flowsfrom an area of high pressure to an area of lower pressure, bloodflows from the arterial to the venous system.

The pressure difference (∆P) between the two ends of the ves-sel provides the impetus for the forward propulsion of blood. Im-pediments to blood flow offer the opposing force, which isknown as resistance (R). The rate of blood flow is determined bydividing the pressure difference by the resistance:

Flow rate = ∆P/R

This equation clearly shows that, when resistance increases, agreater driving pressure is required to maintain the same degreeof flow. In the body, an increase in driving pressure is accom-plished by an increase in the force of contraction of the heart. Ifarterial resistance is chronically elevated, the myocardium hyper-trophies (enlarges) to sustain the greater contractile force.

In most long smooth blood vessels, flow is laminar or stream-lined, with blood in the center of the vessel moving slightly fasterthan the blood near the vessel walls. Laminar flow becomes tur-bulent when the blood flow rate increases, when blood viscosityincreases, when the diameter of the vessel becomes greater thannormal, or when segments of the vessel are narrowed or con-stricted. Turbulent blood flow creates a sound, called a bruit, thatcan be auscultated with a stethoscope.

Blood PressureChapters 26 and 32 provide more information on the physiologyand measurement of blood pressure.

Capillary Filtration and ReabsorptionFluid exchange across the capillary wall is continuous. This fluid,which has the same composition as plasma without the proteins,forms the interstitial fluid. The equilibrium between hydrostaticand osmotic forces of the blood and interstitium, as well as cap-illary permeability, governs the amount and direction of fluidmovement across the capillary. Hydrostatic force is a driving pres-sure that is generated by the blood pressure. Osmotic pressure isthe pulling force created by plasma proteins. Normally, the hy-drostatic pressure at the arterial end of the capillary is relativelyhigh compared with that at the venous end. This high pressure atthe arterial end of the capillaries tends to drive fluid out of thecapillary and into the tissue space. Osmotic pressure tends to pullfluid back into the capillary from the tissue space, but this os-motic force cannot overcome the high hydrostatic pressure at thearterial end of the capillary. At the venous end of the capillary,however, the osmotic force predominates over the low hydro-static pressure, and there is a net reabsorption of fluid from thetissue space back into the capillary.

Except for a very small amount, fluid that is filtered out at thearterial end of the capillary bed is reabsorbed at the venous end.The excess filtered fluid enters the lymphatic circulation. Theseprocesses of filtration, reabsorption, and lymph formation aid inmaintaining tissue fluid volume and removing tissue waste anddebris. Under normal conditions, capillary permeability remainsconstant.

Under certain abnormal conditions, the fluid filtered out ofthe capillaries may greatly exceed the amounts reabsorbed and car-


ried away by the lymphatic vessels. This imbalance can result fromdamage to capillary walls and subsequent increased permeability,obstruction of lymphatic drainage, elevation of venous pressure,or decrease in plasma protein osmotic force. The accumulation offluid that results from these processes is known as edema.

Hemodynamic ResistanceThe most important factor that determines resistance in the vas-cular system is the vessel radius. Small changes in vessel radiuslead to large changes in resistance. The predominant sites ofchange in the caliber or width of blood vessels, and therefore inresistance, are the arterioles and the precapillary sphincter. Pe-ripheral vascular resistance is the opposition to blood flow pro-vided by the blood vessels. Poiseuille’s law provides the methodby which resistance can be calculated:

R = 8θL/πr4

where R = resistance, r = radius of the vessel, L = length of thevessel, θ = viscosity of the blood, and 8/π = a constant. This equa-tion shows that the resistance is proportional to the viscosity orthickness of the blood and the length of the vessel but is inverselyproportional to the fourth power of the vessel radius.

Under normal conditions, blood viscosity and vessel length donot change significantly, and these factors do not usually play animportant role in blood flow. A large increase in hematocrit, how-ever, may increase blood viscosity and reduce capillary blood flow.

Peripheral Vascular Regulating MechanismsBecause the metabolic needs of body tissues, even at rest, are con-tinuously changing, an integrated and coordinated regulatory sys-tem is necessary so that blood flow to individual areas is maintainedin proportion to the needs of that area. As might be expected, thisregulatory mechanism is complex and consists of central nervoussystem influences, circulating hormones and chemicals, and inde-pendent activity of the arterial wall itself.

Sympathetic (adrenergic) nervous system activity, mediated bythe hypothalamus, is the most important factor in regulating thecaliber and therefore the blood flow of peripheral blood vessels. Allvessels are innervated by the sympathetic nervous system except thecapillary and precapillary sphincters. Stimulation of the sympa-thetic nervous system causes vasoconstriction. The neurotransmit-ter responsible for sympathetic vasoconstriction is norepinephrine.Sympathetic activation occurs in response to physiologic and psy-chological stressors. Diminution of sympathetic activity by med-ications or sympathectomy results in vasodilation.

Other hormonal substances affect peripheral vascular resis-tance. Epinephrine, released from the adrenal medulla, acts likenorepinephrine in constricting peripheral blood vessels in mosttissue beds. In low concentrations, however, epinephrine causesvasodilation in skeletal muscles, the heart, and the brain. Angio-tensin, a potent substance formed from the interaction of renin(synthesized by the kidney) and a circulating serum protein, stim-ulates arterial constriction. Although the amount of angiotensinconcentrated in the blood is usually small, its profound vasocon-strictor effects are important in certain abnormal states, such asheart failure and hypovolemia.

Alterations in local blood flow are influenced by various circu-lating substances that have vasoactive properties. Potent vaso-dilators include histamine, bradykinin, prostaglandin, and certainmuscle metabolites. A reduction in available oxygen and nutrients

and changes in local pH also affect local blood flow. Serotonin, asubstance liberated from platelets that aggregate at the site of ves-sel wall damage, constricts arterioles. The application of heat toparts of the body surface causes local vasodilation, whereas theapplication of cold causes vasoconstriction.

PATHOPHYSIOLOGY OF THE VASCULAR SYSTEMReduced blood flow through peripheral blood vessels character-izes all peripheral vascular diseases. The physiologic effects of al-tered blood flow depend on the extent to which tissue demandsexceed the supply of oxygen and nutrients available. If tissue needsare high, even modestly reduced blood flow may be inadequate tomaintain tissue integrity. Tissues then fall prey to ischemia (defi-cient blood supply), become malnourished, and ultimately die ifadequate blood flow is not restored.

Pump FailureInadequate peripheral blood flow occurs when the heart’s pump-ing action becomes inefficient. Left ventricular failure causes anaccumulation of blood in the lungs and a reduction in forwardflow or cardiac output, which results in inadequate arterial bloodflow to the tissues. Right ventricular failure causes systemic ve-nous congestion and a reduction in forward flow (see Chap. 30).

Alterations in Blood and Lymphatic VesselsIntact, patent, and responsive blood vessels are necessary to de-liver adequate amounts of oxygen to tissues and to remove meta-bolic wastes. Arteries can become obstructed by atheroscleroticplaque, a thrombus, or an embolus. Arteries can become dam-aged or obstructed as a result of chemical or mechanical trauma,infections or inflammatory processes, vasospastic disorders, andcongenital malformations. A sudden arterial occlusion causesprofound and often irreversible tissue ischemia and tissue death.When arterial occlusions develop gradually, there is less risk forsudden tissue death because collateral circulation has an oppor-tunity to develop and the body adapts to the decreased blood flow.

Venous blood flow can be reduced by a thrombus obstructingthe vein, by incompetent venous valves, or by a reduction in theeffectiveness of the pumping action of surrounding muscles. De-creased venous blood flow results in increased venous pressure, asubsequent rise in capillary hydrostatic pressure, net filtration offluid out of the capillaries into the interstitial space, and sub-sequent edema. Edematous tissues cannot receive adequate nu-trition from the blood and consequently are more susceptible tobreakdown, injury, and infection. Obstruction of lymphatic ves-sels also results in edema. Lymphatic vessels can become ob-structed by tumor or by damage resulting from mechanical traumaor inflammatory processes.

Gerontologic Considerations

Aging produces changes in the walls of the blood vessels thataffect the transport of oxygen and nutrients to the tissues. Theintima thickens as a result of cellular proliferation and fibrosis.Elastin fibers of the media become calcified, thin, and fragmented,and collagen accumulates in the intima and the media. Thesechanges cause the vessels to stiffen, which results in increasedperipheral resistance, impaired blood flow, and increased leftventricular workload.


Circulatory Insufficiency of the ExtremitiesAlthough many types of peripheral vascular diseases exist, most re-sult in ischemia and produce some of the same symptoms: pain,skin changes, diminished pulse, and possible edema. The type andseverity of symptoms depend in part on the type, stage, and extentof the disease process and on the speed with which the disorderdevelops. Table 31-2 highlights the distinguishing features of ar-terial and venous insufficiency. In this chapter, peripheral vascu-lar disease is categorized as arterial, venous, or lymphatic disorders.

AssessmentHEALTH HISTORY AND CLINICAL MANIFESTATIONSA description of the pain and any precipitating factors, the skincolor and temperature, and the peripheral pulses are importantfor the diagnosis of arterial disorders.

Intermittent ClaudicationA muscular, cramp-type pain in the extremities consistently re-produced with the same degree of exercise or activity and relievedby rest is experienced by patients with peripheral arterial insuffi-ciency. Referred to as intermittent claudication, this pain iscaused by the inability of the arterial system to provide adequateblood flow to the tissues in the face of increased demands for nu-trients during exercise. As the tissues are forced to complete theenergy cycle without the nutrients, muscle metabolites and lacticacid are produced. Pain is experienced as the metabolites aggra-vate the nerve endings of the surrounding tissue. Usually, about50% of the arterial lumen or 75% of the cross-sectional area mustbe obstructed before intermittent claudication is experienced.When the patient rests and thereby decreases the metabolic needsof the muscles, the pain subsides. The progression of the arterialdisease can be monitored by documenting the amount of exerciseor the distance a patient can walk before pain is produced. Per-sistent pain in the forefoot when the patient is resting indicates asevere degree of arterial insufficiency and a critical state of is-chemia. Known as rest pain, this discomfort is often worse at

night and may interfere with sleep. This pain frequently requiresthat the extremity be lowered to a dependent position to improveperfusion pressure to the distal tissues.

The site of arterial disease can be deduced from the locationof claudication, because pain occurs in muscle groups below thedisease. As a general rule, the pain of intermittent claudicationoccurs one joint level below the disease process. Calf pain may ac-company reduced blood flow through the superficial femoral orpopliteal artery, whereas pain in the hip or buttock may resultfrom reduced blood flow in the abdominal aorta or the commoniliac or hypogastric arteries.

Changes in Skin Appearance and TemperatureAdequate blood flow warms the extremities and gives them a rosycoloring. Inadequate blood flow results in cool and pale extrem-ities. Further reduction of blood flow to these tissues, which oc-curs when the extremity is elevated, for example, results in aneven whiter or more blanched appearance (pallor). Rubor, areddish blue discoloration of the extremities, may be observedwithin 20 seconds to 2 minutes after the extremity is dependent.Rubor suggests severe peripheral arterial damage in which vesselsthat cannot constrict remain dilated. Even with rubor, the ex-tremity begins to turn pale with elevation. Cyanosis, a bluish tinton the skin, is manifested when the amount of oxygenated hemo-globin contained in the blood is reduced.

Additional changes resulting from a chronically reduced nutri-ent supply include loss of hair, brittle nails, dry or scaling skin,atrophy, and ulcerations. Edema may be apparent bilaterally orunilaterally and is related to the affected extremity’s chronically de-pendent position because of severe rest pain. Gangrenous changesappear after prolonged, severe ischemia and represent tissue necro-sis. In elderly patients who are inactive, gangrene may be the firstsign of disease. These patients may have adjusted their lifestyleto accommodate the limitations imposed by the disease, andmay not walk enough to develop symptoms of claudication. Cir-culation is decreased, but this is not apparent to the patient untiltrauma occurs. At this point, gangrene develops when minimalarterial flow is impaired further by edema formation resultingfrom the traumatic event.

CHARACTERISTIC ARTERIAL VENOUS

PainPulsesSkin characteristics

Ulcer characteristicsLocation

PainDepth of ulcerShapeUlcer base

Leg edema

Intermittent claudication to sharp, unrelenting, constantDiminished or absentDependent rubor—elevation pallor of foot, dry, shiny

skin, cool-to-cold temperature, loss of hair over toesand dorsum of foot, nails thickened and ridged

Tip of toes, toe webs, heel or other pressure areas ifconfined to bed

Very painfulDeep, often involving joint spaceCircularPale to black and dry gangrene

Minimal unless extremity kept in dependent positionconstantly to relieve pain

Aching, crampingPresent, but may be difficult to palpate through edemaPigmentation in gaitor area (area of medial and lateral

malleolus), skin thickened and tough, may be reddishblue, frequently with associated dermatitis

Medial malleolus; infrequently lateral malleolus oranterior tibial area

Minimal pain if superficial or may be very painfulSuperficialIrregular borderGranulation tissue—beefy red to yellow fibrinous in

chronic long-term ulcerModerate to severe

Table 31-2 • Characteristics of Arterial and Venous Insufficiency


PulsesDetermining the presence or absence, as well as the quality, ofperipheral pulses is important in assessing the status of peripheralarterial circulation (Fig. 31-2). Absence of a pulse may indicatethat the site of stenosis (narrowing or constriction) is proximalto that location. Occlusive arterial disease impairs blood flow andcan reduce or obliterate palpable pulsations in the extremities.Pulses should be palpated bilaterally and simultaneously, com-paring both sides for symmetry in rate, rhythm, and quality.


In elderly people, symptoms of peripheral arterial disease may bemore pronounced than in younger people because of the con-dition’s duration and coexisting chronic disease. Intermittentclaudication may occur after walking only a few short blocks orafter walking up a slight incline. Any prolonged pressure on thefoot can cause pressure areas that become ulcerated, infected,and gangrenous. The outcomes of arterial insufficiency in theelderly person include reduced mobility and activity and a lossof independence.

Diagnostic EvaluationIn identifying and diagnosing the various abnormalities affectingthe vascular structures (arteries, veins, and lymphatics), varioustests may be performed.

DOPPLER ULTRASOUND FLOW STUDIESPalpating pulses is subjective, and the examiner may mistake his orher own pulse for that of the patient. To prevent this, the examinershould use light touch and avoid using only the index finger for pal-pation, because this finger has the strongest arterial pulsation of allthe fingers. The thumb should not be used for the same reason.When pulses cannot be reliably palpated, use of a microphone-like,hand-held Doppler ultrasound device, called a transducer or probe,may be helpful in detecting and assessing peripheral flow.

A continuous-wave (CW) Doppler ultrasound device may beused to hear (insonate) the blood flow in vessels when pulses can-not be palpated. This hand-held device emits a continuous signalthrough the patient’s tissues. The signals are reflected by (echooff ) the moving blood cells and are received by the device. Thefiltered-output Doppler signal is then transmitted to a loudspeakeror headphones, where it can be heard for interpretation. BecauseCW Doppler emits a continuous signal, all vascular structures inthe path of the sound beam are insonated, and differentiating ar-terial from venous flow and detecting the site of a stenosis may bedifficult. The depth at which blood flow can be detected by Doppleris determined by the frequency (in megahertz [MHz]) it generates.The lower the frequency, the deeper the tissue penetration; a 5- to10-MHz probe may be used to evaluate the peripheral arteries.

To evaluate the lower extremities, the patient is placed in asupine position with the head of bed elevated 20 to 30 degrees; thelegs are externally rotated, if possible, to permit adequate access tothe medial malleolus. Acoustic gel is applied to the patient’s skin

FIGURE 31-2 Assessing peripheral pulses. (Left ) Popliteal pulse. (Right) Dorsalis pedis pulse. (Bottom) Posteriortibial pulse.


to permit uniform transmission of the ultrasound wave (electro-cardiogram gel is not used because it contains sodium, which maydissolve the epoxy that covers the transducer’s tip). The tip of theDoppler transducer is positioned at a 45- to 60-degree angle overthe expected location of the artery and angled slowly to identifyarterial blood flow. Excessive pressure is avoided because severelydiseased arteries can collapse with even minimal pressure.

Because the equipment can detect blood flow in advanced ar-terial disease states, especially if collateral circulation has devel-oped, identifying a signal documents only the presence of bloodflow. However, it is clinically relevant to notify the primary careprovider of the absence of a signal if one had been detected duringa previous examination.

CW Doppler (Fig. 31-3) is more useful as a clinical tool whencombined with ankle blood pressures, which are used to determinethe ankle-brachial index (ABI), also called the ankle-arm index(AAI). The ABI is the ratio of the ankle systolic blood pressure tothe arm systolic blood pressure. It is an objective indicator of arte-rial disease that allows the examiner to quantify the degree of ste-nosis. With increasing degrees of arterial narrowing, there is aprogressive decrease in systolic pressure distal to the involved sites.

The first step in determining the ABI is to have the patient restin a supine position (not seated) for at least 5 minutes. An ap-propriate-sized blood pressure cuff (typically, a 10-cm cuff) is ap-plied to the patient’s ankle above the malleolus. After identifyingan arterial signal at the posterior tibial and dorsalis pedis arteries,the systolic ankle pressures are obtained in both feet. Diastolicpressures cannot be measured with a Doppler. If pressure in thesearteries cannot be measured, pressure can be measured in the per-oneal artery, which can also be assessed at the ankle (Fig. 31-4).

Doppler ultrasonography is used to measure brachial pressuresin both arms. Both arms are evaluated because the patient mayhave an asymptomatic stenosis in the subclavian artery, causingbrachial pressure on the affected side to be 20 mm Hg or morelower than systemic pressure. The abnormally low pressure shouldnot be used for assessment.

To calculate ABI, the ankle systolic pressure for each foot isdivided by the higher of the two brachial systolic pressures;

FIGURE 31-3 Continuous-wave (CW) Doppler ultrasound detects bloodflow in peripheral vessels. Combined with computation of ankle or arm pres-sures, this diagnostic technique helps health care providers characterize thenature of peripheral vascular disease. Photo reprinted with permission fromCantwell-Gab, K. (1996). Identifying chronic PAD. American Journal ofNursing, 96(7), 40–46.

FIGURE 31-4 Location of peroneal artery; lateral malleolus. Photoreprinted with permission from Cantwell-Gab, K. (1996). Identifyingchronic PAD. American Journal of Nursing, 96(7), 40–46.

Chart 31-1 offers more information. The ABI can be computedfor a patient with the following systolic pressures:

Right brachial: 160 mm HgLeft brachial: 120 mm HgRight posterior tibial: 80 mm HgRight dorsalis pedis: 60 mm HgLeft posterior tibial: 100 mm HgLeft dorsalis pedis: 120 mm Hg

The highest systolic pressure for each ankle (80 mm Hg for theright, 120 mm Hg for the left) would be divided by the highestbrachial pressure (160 mm Hg).

Right: 80/160 mm Hg = 0.50 ABILeft: 120/160 mm Hg = 0.75 ABI

In general, systolic pressure in the ankle of a healthy person isthe same or slightly higher than the brachial systolic pressure,resulting in an ABI of about 1.0 (no arterial insufficiency). Pa-tients with claudication usually have an ABI of 0.95 to 0.50(mild to moderate insufficiency); patients with ischemic rest painhave an ABI of less than 0.50, and patients with severe ischemiaor tissue loss have an ABI of 0.25 or less.

EXERCISE TESTINGExercise testing is used to determine how long a patient can walkand to measure the ankle systolic blood pressure in response towalking. The patient walks on a treadmill at 1.5 mph with a 10%incline for a maximum of 5 minutes. Most patients can completethe test unless they have severe cardiac, pulmonary, or orthopedicproblems or are physically disabled. A normal response to the testis little or no drop in ankle systolic pressure after exercise. In a pa-tient with true claudication, however, ankle pressure drops. Com-bining this hemodynamic information with the walking timehelps the physician determine whether intervention is necessary.

DUPLEX ULTRASONOGRAPHYDuplex ultrasonography involves B-mode gray-scale imaging ofthe tissue, organs, and blood vessels (arterial and venous) and per-mits estimation of velocity changes by use of a pulsed Doppler


(Fig. 31-5). Color flow techniques, which can identify vessels,may be used to shorten the examination time. The procedurehelps determine the level and extent of disease and is universallyemployed to evaluate the venous system. The technique makes itpossible to image and assess blood flow, evaluate the runoff statusof the distal vessels, locate the disease (stenosis versus occlusion),and determine anatomic morphology and the hemodynamic sig-nificance of plaque causing stenosis. Duplex ultrasound findingshelp in planning therapy and monitoring its outcomes. More-over, the test is noninvasive and usually requires no patient prepa-ration. The equipment is portable, making it useful anywhere forinitial diagnosis or follow-up evaluations.

COMPUTED TOMOGRAPHYComputed tomography (CT) provides cross-sectional images ofsoft tissue and can identify the area of volume changes to an ex-tremity and the compartment where changes take place. CT of alymphedematous arm or leg, for example, demonstrates a char-acteristic honeycomb pattern in the subcutaneous tissue.

In spiral (also called volumetric) CT, the scan head moves cir-cumferentially around the patient as the patient passes throughthe scanner, creating a series of overlapping images that are con-nected to one another in a continuous spiral (Verta & Verta,1998). Scan times are short; however, the patient is exposed to

x-rays, and contrast agent usually must be injected to adequatelyvisualize the blood vessels. Using computer software, the slicelikeimages are reconstructed into three-dimensional images that canbe rotated and viewed from multiple angles.

COMPUTED TOMOGRAPHICANGIOGRAPHYIn computed tomographic angiography (CTA), a spiral CT scan-ner and rapid intravenous infusion of contrast agent are used toimage very thin (1-mm) sections of the target area; the results areconfigured in three dimensions so that the image closely resem-bles a regular angiogram (Verta & Verta, 1998). CTA shows theaorta and main visceral arteries better than it shows smaller branchvessels. Scan times are usually between 20 and 30 seconds. Thelarge volume of contrast agent required for CTA limits the useful-ness of this study in patients with allergy to the contrast agent orwith significantly impaired renal function.

MAGNETIC RESONANCE ANGIOGRAPHYMagnetic resonance angiography is performed with a standardMRI scanner but with image-processing software specifically pro-grammed to isolate the blood vessels. The images are reconstructedto resemble a standard angiogram, but because the images are re-assembled in three dimensions, they can be rotated and viewedfrom multiple angles. Because no contrast agent is necessary, thisstudy is useful in patients with poor renal function or allergy tocontrast agent. Scan time is long, and motion artifacts are com-mon, restricting the use of the test to relatively short segments ofthe vascular system (Verta & Verta, 1998).

ANGIOGRAPHYAn arteriogram produced by angiography may be used to confirmthe diagnosis of occlusive arterial disease when considering surgeryor other interventions. The procedure involves injecting a radio-paque contrast agent directly into the vascular system to visualizethe vessels. The location of a vascular obstruction or an aneurysm(abnormal dilation of a blood vessel) and the collateral circulationcan be demonstrated. Usually, patients experience a temporarysensation of warmth as the contrast agent is injected, and localirritation may occur at the injection site. Infrequently, a patient

FIGURE 31-5 Color flow duplex image of popliteal artery with normaltriphasic Doppler flow.

Avoiding Common Errors in Calculating Ankle-Brachial Index (ABI)

Take the following precautions to ensure an accurate ABI calculation:• Use the correctly sized blood pressure cuffs. To obtain accurate

blood pressure measurements, use a cuff with a bladderwidth at least 40% and length at least 80% of the limbcircumference.

• On the nursing plan of care, document the blood pressure cuffsizes used (for example, “12-cm BP cuff used for brachialpressures; 10-cm BP cuff used for ankle pressures”). Thisminimizes the risk of shift-to-shift discrepancies in ABIs.

• Use sufficient blood pressure cuff inflation. To ensure completeclosure of the artery and the most accurate measurements,inflate cuffs 20 to 30 mm Hg beyond the point at which thelast arterial signal is detected.

• Do not deflate blood pressure cuffs too rapidly. Try to maintaina deflation rate of 2 to 4 mm Hg/second for patients with-out dysrhythmias and 2 mm Hg/second or slower for pa-tients with dysrhythmias. Deflating the cuff more rapidlymay miss the patient’s highest pressure and result in record-ing an erroneous (low) blood pressure measurement.

• Be suspicious of arterial pressures recorded at less than 40 mm Hg.This may mean the venous signal has been mistaken for thearterial signal. If the arterial pressure, which is normally 120 mm Hg, is measured at less than 40 mm Hg, ask a col-league to double-check the findings before recording this asan arterial pressure.

• Suspect medial calcific sclerosis anytime an ABI is 1.3 orgreater or ankle pressure is more than 300 mm Hg. Medialcalcific sclerosis is associated with diabetes mellitus, chronicrenal failure, and hyperparathyroidism. It produces falselyelevated ankle pressures by hardening the medra of thearteries; making the vessels noncompressible.

(From Cantwell-Gab, K. [1996]. Identifying chronic PAD. AmericanJournal of Nursing, 96[1] 40–46, with permission.)

Chart31-1

Chart31-1


may have an immediate or delayed allergic reaction to the iodinecontained in the contrast agent. Manifestations include dyspnea,nausea and vomiting, sweating, tachycardia, and numbness of theextremities. Any such reaction must be reported to the physicianat once; treatment may include the administration of one or moreof epinephrine (adrenaline), antihistamines, or corticosteroids.Additional risks include vessel injury, bleeding, and CVA (brainattack, stroke).

AIR PLETHYSMOGRAPHYNamed for the standardized air chambers that fit around the lowerleg and that are calibrated after being filled with a standardamount of air, air plethysmography quantifies venous reflux andcalf muscle pump ejection. Changes in volume are measured withthe patient’s legs elevated, with the patient supine and standing,and after the patient performs toe-ups (patient extends ankle whilestanding; stands on tip-toes). Air plethysmography provides in-formation about venous filling time, functional venous volume,ejected volume, and residual volume. It is useful in evaluating pa-tients with suspected valvular incompetence or chronic venousinsufficiency.

CONTRAST PHLEBOGRAPHYAlso known as venography, contrast phlebography involves in-jecting radiographic contrast media into the venous systemthrough a dorsal foot vein. If a thrombus exists, the x-ray imagediscloses an unfilled segment of vein in an otherwise completelyfilled vein. Injection of the contrast agent may cause a brief butpainful inflammation of the vein. The test is generally per-formed if the patient is to undergo thrombolytic therapy, butduplex ultrasonography is now accepted as the gold standard fordiagnosing venous thrombosis.

LYMPHANGIOGRAPHYLymphangiography affords a means of detecting lymph node in-volvement that results from metastatic carcinoma, lymphoma, orinfection in sites that are otherwise inaccessible to the examinerexcept by surgery. In this test, a lymphatic vessel in each foot (orhand) is injected with contrast agent. A series of x-rays are takenat the conclusion of the injection, 24 hours later, and periodicallythereafter, as indicated. The failure to identify subcutaneous lym-phatic collection of contrast agent and the persistence of contrastagent in the tissue for days afterward help to confirm a diagnosisof lymphedema.

LYMPHOSCINTIGRAPHYLymphoscintigraphy is a reliable alternative to lymphangiogra-phy. A radioactively labeled colloid is injected subcutaneously inthe second interdigital space. The extremity is then exercised tofacilitate the uptake of the colloid by the lymphatic system, andserial images are obtained at preset intervals. No adverse reactionshave been reported.

Management of Arterial DisordersARTERIOSCLEROSISAND ATHEROSCLEROSISArteriosclerosis is the most common disease of the arteries; theterm means hardening of the arteries. It is a diffuse process wherebythe muscle fibers and the endothelial lining of the walls of small

arteries and arterioles become thickened. Atherosclerosis involvesa different process, affecting the intima of the large and medium-sized arteries. These changes consist of the accumulation of lipids,calcium, blood components, carbohydrates, and fibrous tissue onthe intimal layer of the artery. These accumulations are referred toas atheromas or plaques.

Although the pathologic processes of arteriosclerosis and ath-erosclerosis differ, rarely does one occur without the other, andthe terms are often used interchangeably. Because atherosclerosisis a generalized disease of the arteries, when it is present in the ex-tremities, atherosclerosis is usually present elsewhere in the body.

PathophysiologyThe most common direct results of atherosclerosis in arteries in-clude narrowing (stenosis) of the lumen, obstruction by throm-bosis, aneurysm, ulceration, and rupture. Its indirect results aremalnutrition and the subsequent fibrosis of the organs that thesclerotic arteries supply with blood. All actively functioning tis-sue cells require an abundant supply of nutrients and oxygenand are sensitive to any reduction in the supply of these nutrients.If such reductions are severe and permanent, the cells undergo is-chemic necrosis (death of cells due to deficient blood flow) and arereplaced by fibrous tissue, which requires much less blood flow.

Atherosclerosis can develop at any point in the body, but cer-tain sites are more vulnerable, typically bifurcation or branchareas. In the proximal lower extremity, these include the distal ab-dominal aorta, the common iliac arteries, the orifice of the super-ficial femoral and profunda femoris arteries, and the superficialfemoral artery in the adductor canal. Distal to the knee, athero-sclerosis occurs anywhere along the artery. There are no specificareas, such as arterial bifurcations, that are more vulnerable foratherosclerosis.

Although many theories exist about the development of ath-erosclerosis, no single theory fully explains the pathogenesis;however, parts of several theories have been combined into thereaction-to-injury theory. According to this theory, vascular en-dothelial cell injury results from prolonged hemodynamic forces,such as shearing stresses and turbulent flow, irradiation, chemi-cal exposure, or chronic hyperlipidemia in the arterial system. In-jury to the endothelium increases the aggregation of platelets andmonocytes at the site of the injury. Smooth muscle cells migrateand proliferate, allowing a matrix of collagen and elastic fibers toform. It may be that there is no single cause or mechanism for thedevelopment of atherosclerosis; rather, multiple processes may beinvolved (Moore, 2002).

Morphologically, atherosclerotic lesions are of two types: fattystreaks and fibrous plaque. Fatty streaks are yellow and smooth,protrude slightly into the lumen of the artery, and are composedof lipids and elongated smooth muscle cells. These lesions havebeen found in the arteries of people of all age groups, includinginfants. It is not clear whether fatty streaks predispose the personto the formation of fibrous plaques or if they are reversible. Theydo not usually cause clinical symptoms.

The fibrous plaque characteristic of atherosclerosis is composedof smooth muscle cells, collagen fibers, plasma components, andlipids. It is white to whitish yellow and protrudes in various de-grees into the arterial lumen, sometimes completely obstructingit. These plaques are found predominantly in the abdominalaorta and the coronary, popliteal, and internal carotid arteries.This plaque is believed to be an irreversible lesion (Fig. 31-6).Gradual narrowing of the arterial lumen as the disease processprogresses stimulates the development of collateral circulation


(Fig. 31-7). Collateral circulation consists of preexisting vesselsthat enlarge to reroute blood flow in the presence of a hemody-namically significant stenosis or occlusion. Collateral flow allowscontinued perfusion to the tissues beyond the arterial obstruction,but it is often inadequate to meet imposed metabolic demand,and ischemia results.

Risk FactorsMany risk factors are associated with atherosclerosis (Chart 31-2).Although it is not completely clear whether modification of theserisk factors prevents the development of cardiovascular disease,evidence indicates that it may slow the disease process. Some riskfactors, such as age or gender, cannot be modified. However, it isbelieved that genetic factors can be modified indirectly by alter-ing other risk factors (Moore, 2002).

Tobacco use may be one of the strongest risk factors in the de-velopment of atherosclerotic lesions. Nicotine decreases bloodflow to the extremities and increases heart rate and blood pressureby stimulating the sympathetic nervous system, causing vasocon-striction. It also increases the risk for clot formation by increasingthe aggregation of platelets. Carbon monoxide, a toxin producedby burning tobacco, combines more readily with the hemoglobinthan oxygen does, depriving the tissues of oxygen. The amountof tobacco use is directly related to the extent of the disease, andcessation of tobacco use reduces the risks. Many other factors

Fattystreak

Fibrousplaque

Complicated lesion: Hemorrhage Ulceration Calcification Thrombosis

Thrombus

Range of clinical symptoms

Infarct

Stroke

Gangrene

0 10 years 20 30 40 50 60 70

FIGURE 31-6 Schematic concept of the pro-gression of atherosclerosis. Fatty streaks constituteone of the earliest lesions of atherosclerosis. Manyfatty streaks regress, whereas others progress tofibrous plaques and eventually to atheroma, whichmay be complicated by hemorrhage, ulceration,calcification, or thrombosis and may producemyocardial infarction, stroke, or gangrene.

Lumbar

Inferiormesenteric

Superiorhemorrhoidal

Middlehemorrhoidal

Inferiorhemorrhoidal

Occlusion

Colon

Rectum

Right commoniliac artery

FIGURE 31-7 Development of channels for collateral blood flow in re-sponse to occlusion of the right common iliac artery and the terminal aorticbifurcation.

Chart 31-2Risk Factors for Atherosclerosis

ModifiableNicotine use (ie, tobacco smoking, chewing)Diet (contributing to hyperlipidemin)HypertensionDiabetes (which speeds the atherosclerotic process by thickening

the basement membranes of both large and small vessels)StressSedentary lifestyle

NonmodifiableAgeGender

such as obesity, stress, and lack of exercise have been identified ascontributing to the disease process.

PreventionIntermittent claudication is a sign of generalized atherosclerosisand may be a marker of occult coronary artery disease. Because ahigh-fat diet is suspected of contributing to atherosclerosis, it isreasonable to measure serum cholesterol and to begin preventionefforts. The American Heart Association recommends reducingthe amount of fat ingested in a healthy diet, substituting unsatu-rated fats for saturated fats, and decreasing cholesterol intake tono more than 300 mg daily to reduce the risk of cardiovasculardisease (Krauss et al., 2000).

Certain medications combined with dietary modification andexercise are being used to reduce blood lipid levels. There is limitedevidence that these medications can alter the course of peripheralarterial disease, but they may reduce the mortality rate from cardio-vascular disease. Several classes of medication are used to preventatherosclerosis: bile acid sequestrants (cholestyramine [Questran,Prevalite] or colestipol [Colestid]), nicotinic acid (niacin, B3, Nia-cor; Niaspan), statins (atorvastatin [Lipitor], lovastatin [Mevacor],pravastatin [Pravachol], simvastatin [Zocor]), fibric acids (gem-fibrozil [Lopid]), and lipophilic substances (probucol). Patients re-ceiving long-term therapy with these medications require closemedical supervision. Hypertension, which may accelerate the rateat which atherosclerotic lesions form in high-pressure vessels, canlead to cerebrovascular accident (CVA; brain attack, stroke), is-chemic renal disease, severe peripheral arterial disease, or coronaryartery disease. Results of large, randomized studies demonstrateddramatic reductions in myocardial infarction, stroke, and cardio-vascular death when blood pressure was decreased to at least140/90 mm Hg (Moser, 1999; McAlister et al., 2001).

Although no single risk factor has been identified as the pri-mary contributor to the development of atherosclerotic cardio-vascular disease, it is clear that the greater the number of riskfactors, the greater the likelihood of developing the disease. Elim-ination of all controllable risk factors, particularly tobacco use, isstrongly recommended.

Clinical ManifestationsThe clinical signs and symptoms resulting from atherosclerosisdepend on the organ or tissue affected. Coronary atherosclerosis(heart disease), angina, and acute myocardial infarction are dis-cussed in Chapter 28. Cerebrovascular diseases, including transientcerebral ischemic attacks and stroke, are discussed in Chapter 62.Atherosclerosis of the aorta, including aneurysm, and atheroscle-rotic lesions of the extremities are discussed later in this chapter.Renovascular disease (renal artery stenosis and end-stage renaldisease), including hypertension, is discussed in Chapter 45.

Medical ManagementThe traditional medical management of atherosclerosis involvesmodification of risk factors, a controlled exercise program toimprove circulation and increase the functioning capacity of thecirculation, medication, and interventional or surgical graftprocedures.

SURGICAL MANAGEMENTVascular surgical procedures are divided into two groups: inflowprocedures, which provide blood supply from the aorta into thefemoral artery, and outflow procedures, which provide blood sup-


ply to vessels below the femoral artery. Inflow surgical proceduresare discussed with diseases of the aorta and outflow procedureswith peripheral arterial occlusive disease.

RADIOLOGIC INTERVENTIONSSeveral interventional radiologic techniques are important ad-junctive therapies to surgical procedures. If an isolated lesion orlesions are identified during the arteriogram, angioplasty, alsocalled percutaneous transluminal angioplasty (PTA), may be per-formed. After the patient receives a local anesthetic, a balloon-tipped catheter is maneuvered across the area of stenosis. Exactlyhow PTA works is controversial. Some theorize that it improvesblood flow by overstretching (and thereby dilating) the elasticfibers of the nondiseased arterial segment, but most clinicians be-lieve that the procedure widens the arterial lumen by cracking andflattening the plaque against the vessel wall (see Chap. 28). Com-plications from PTA include hematoma formation, embolus,dissection (separation of the intima) of the vessel, and bleeding.To decrease the risk of reocclusion, stents (small, mesh tubesmade of nitinol, titanium, or stainless steel) may be inserted tosupport the walls of blood vessels and prevent collapse immedi-ately after balloon inflation (Fig. 31-8). A variety of covered wallstents and stent-grafts may be used for short-segment stenoses.Complications associated with stent or stent-graft use include dis-tal embolization, intimal damage (dissection), and dislodgment.The advantage of angioplasty, stents, and stent-grafts is the de-creased length of hospital stay required for the treatment; manyof the procedures are performed on an outpatient basis.

NURSING PROCESS: THE PATIENT WHO HAS PERIPHERALARTERIAL INSUFFICIENCY OF THE EXTREMITIESAssessmentThe nursing assessment includes a complete health and medica-tion history and identification of risk factors for peripheral arterydisease. Signs and symptoms detected during the nursing assess-ment may include claudication pain; rest pain in the forefoot;pallor, rubor, or cyanosis; weak or absent peripheral pulses; andskin breakdown or ulcerations.

Nursing DiagnosisBased on assessment data, major nursing diagnoses for the patientmay include the following:

• Ineffective peripheral tissue perfusion related to compro-mised circulation

• Chronic pain related to impaired ability of peripheral vesselsto supply tissues with oxygen

• Risk for impaired skin integrity related to compromisedcirculation

• Deficient knowledge regarding self-care activities

Planning and GoalsThe major goals for the patient may include increased arterialblood supply to the extremities, promotion of vasodilation, pre-vention of vascular compression, relief of pain, attainment or main-tenance of tissue integrity, and adherence to the self-care program.

Measures used by the patient and members of the health careteam to accomplish a single goal must be evaluated in terms of


equate clothing and warm temperatures protect the patient fromchilling. If chilling occurs, a warm bath or drink is helpful.

When heat is applied directly to ischemic extremities, the tem-perature of the heat source must not exceed body temperature.Even at lower temperatures, burn injuries can occur in ischemicextremities. Excess heat may increase the metabolic rate of the ex-tremities and increase the need for oxygen beyond that providedby the reduced arterial flow through the diseased artery.

Nicotine causes vasospasm and can thereby dramatically re-duce circulation to the extremities. Tobacco smoke also impairstransport and cellular use of oxygen and increases blood viscosity.Patients with arterial insufficiency who use tobacco (ie, smoke,chew) must be fully informed of the effects of nicotine on circu-lation and encouraged to stop using tobacco.

Emotional upsets stimulate the sympathetic nervous system,resulting in peripheral vasoconstriction. Although emotionalstress is unavoidable, it can be minimized to some degree byavoiding stressful situations when possible or by consistently fol-lowing a stress-management program. Counseling services or re-laxation training may be indicated for people who cannot copeeffectively with situational stressors.

Constrictive clothing and accessories such as tight socks, pantygirdles, and shoelaces impede circulation to the extremities andpromote venous stasis and therefore should be avoided. Cross-ing the legs should be discouraged because it compresses vesselsin the legs.

RELIEVING PAINFrequently, the pain associated with peripheral arterial insuffi-ciency is chronic and continuous. It limits activities, affects workand responsibilities, disturbs sleep, and alters patients’ sense ofwell-being. Patients are often depressed, irritable, and unable toexert the energy necessary to execute prescribed therapies, mak-ing pain relief even more difficult. Analgesics such as oxycodoneplus acetylsalicylic acid (Percodan) or oxycodone plus acetamin-

the positive and the negative effects these measures may have onthe simultaneous achievement of other goals. An overview of thecare of a patient with peripheral arterial problems is provided inthe Plan of Nursing Care: The Patient With Peripheral VascularProblems.

Nursing InterventionsIMPROVING PERIPHERAL ARTERIAL CIRCULATIONArterial blood supply to a body part can be enhanced by position-ing the part below the level of the heart. For the lower extremities,this is accomplished by elevating the head of the patient’s bed on15-cm (6-inch) blocks or by having the patient use a reclining chairor sit with the feet resting on the floor.

The nurse can assist the patient with walking or other moder-ate or graded isometric exercises that may be prescribed to pro-mote blood flow and encourage the development of collateralcirculation. The nurse instructs the patient to walk to the point ofpain, rest until pain subsides, and then resume walking so that en-durance can be increased as collateral circulation develops. Paincan serve as a guide in determining the amount of exercise appro-priate for an individual. The onset of pain indicates that the tis-sues are not receiving adequate oxygen, signaling the patient to restbefore continuing activity. However, a regular exercise programcan result in increased walking distance before the onset of clau-dication. The amount of exercise a patient can tolerate before theonset of pain is determined to provide a baseline for evaluation.

Not all patients with peripheral vascular disease should exercise.Before recommending any exercise program, the primary healthcare provider should be consulted. Conditions that worsen with ac-tivity include leg ulcers, cellulitis, gangrene, or acute thromboticocclusions.

PROMOTING VASODILATION AND PREVENTINGVASCULAR COMPRESSIONArterial dilation promotes increased blood flow to the extremitiesand is therefore a desirable goal for patients with peripheral arte-rial disease. However, if the arteries are severely sclerosed, inelas-tic, or damaged, dilation is not possible. For this reason, measuresto promote vasodilation, such as medications or surgery, may beonly minimally effective.

Nursing interventions may involve applications of warmth topromote arterial flow and instructions to the patient to avoid ex-posure to cold temperatures, which causes vasoconstriction. Ad-

NURSING ALERT Patients are instructed to test the temperatureof bath water and to avoid using hot-water bottles and heatingpads on the extremities. Applying a heating pad to the abdomencan cause reflex vasodilation in the extremities and is safer thandirect application of heat to affected extremities.

!

FIGURE 31-8 (A) Flexible stent. Courtesy of Medtronics, Peripheral Division, Santa Rosa, California. (B) Represen-tation of a common iliac artery with a Wallstent (Boston Scientific).

A B


Plan of Nursing CareThe Patient With Peripheral Vascular Problems

Nursing Interventions Rationale Expected Outcomes

1. Lower the extremities below the level ofthe heart (if condition is arterial in nature).

2. Encourage moderate amount of walkingor graded extremity exercises.

1. Dependency of lower extremities enhancesarterial blood supply.

2. Muscular exercise promotes blood flowand the development of collateralcirculation.

• Extremities warm to touch• Color of extremities improved• Experiences decreased muscle pain with

exercise

Nursing Diagnosis: Chronic pain related to impaired ability of peripheral vessels to supply tissues with oxygenGoal: Relief of pain

1. Promote increased circulation.

2. Administer analgesics as prescribed, withappropriate nursing considerations.

1. Enhancement of peripheral circulationincreases the oxygen supplied to themuscle and decreases the accumulation ofmetabolites that cause muscle spasms.

2. Analgesics help to reduce pain and allowthe patient to participate in activities andexercises that promote circulation.

• Uses measures to increase arterial bloodsupply to extremities

• Uses analgesics as prescribed

(continued)

Nursing Diagnosis: Ineffective peripheral tissue perfusion related to compromised circulationGoal: Increased arterial blood supply to extremities

Goal: Decrease in venous congestion

1. Elevate extremities above heart level (if condition is venous in nature).

2. Discourage standing still or sitting forprolonged periods.

3. Encourage walking.

1. Elevation of extremities counteracts gravi-tational pull, promotes venous return,and prevents venous stasis.

2. Prolonged standing still or sittingpromotes venous stasis.

3. Walking promotes venous return byactivating the “muscle pump.”

• Elevates lower extremities as prescribed• Decreased edema of extremities• Avoids prolonged standing still or sitting• Gradually increases walking time daily

Goal: Promotion of vasodilation and prevention of vascular compression

1. Maintain warm temperature and avoidchilling.

2. Discourage nicotine use.

3. Counsel in ways to avoid emotionalupsets; stress management.

4. Encourage avoidance of constrictiveclothing and accessories.

5. Encourage avoidance of leg crossing.

6. Administer vasodilator medications andadrenergic blocking agents as prescribed,with appropriate nursing considerations.

1. Warmth promotes arterial flow by pre-venting the vasoconstriction effects ofchilling.

2. Nicotine causes vasospasm, whichimpedes peripheral circulation.

3. Emotional stress causes peripheral vaso-constriction by stimulating the sympa-thetic nervous system.

4. Constrictive clothing and accessoriesimpede circulation and promote venousstasis.

5. Leg crossing causes compression of vessels with subsequent impediment ofcirculation, resulting in venous stasis.

6. Vasodilators relax smooth muscle;adrenergic blocking agents block theresponse to sympathetic nerve impulsesor circulating catecholamines.

• Protects extremities from exposure to cold• Avoids nicotine• Uses stress-management program to mini-

mize emotional upset• Avoids constricting clothing and accessories• Avoids leg crossing• Takes medication as prescribed

Nursing Diagnosis: Risk for impaired skin integrity related to compromised circulationGoal: Attainment/maintenance of tissue integrity

1. Instruct in ways to avoid trauma toextremities.

1. Poorly nourished tissues are susceptibleto trauma and bacterial invasion; healingof wounds is delayed or inhibited due topoor tissue perfusion.

• Inspects skin daily for evidence of injuryor ulceration

• Avoids trauma and irritation to skin


ophen (Percocet) may be helpful in reducing pain to the pointwhere the patient can participate in the therapies that can increasecirculation and ultimately relieve pain more effectively.

MAINTAINING TISSUE INTEGRITYPoorly nourished tissues are susceptible to damage and infec-tion. When lesions develop, healing may be delayed or inhib-ited because of the poor blood supply to the area. Infected,nonhealing ulcerations of the extremities can be debilitatingand may require prolonged and often expensive treatments. Am-putation of an ischemic limb may eventually be necessary. Mea-sures to prevent these complications must be a high priority andvigorously implemented.

Trauma to the extremities must be avoided. Advising the pa-tient to wear sturdy, well-fitting shoes or slippers to prevent footinjury and blisters may be helpful, as may be recommending neu-tral soaps and body lotions to prevent drying and cracking of skin.Scratching and vigorous rubbing can abrade skin and create a sitefor bacterial invasion; therefore, feet should be patted dry. Stock-ings should be clean and dry. Fingernails and toenails should becarefully trimmed straight across and sharp corners filed to followthe contour of the nail. If nails are thick and brittle and cannot betrimmed safely, a podiatrist must be consulted. Corns and callusesneed to be removed by a health care professional. Special shoe in-serts may be needed to prevent calluses from recurring. All signs ofblisters, ingrown toenails, infection, or other problems should be

reported to health care professionals for treatment and follow-up.Patients with diminished vision may require assistance in periodi-cally examining the lower extremities for trauma.

Good nutrition promotes healing and prevents tissue break-down and is therefore included in the overall therapeutic programfor patients with peripheral vascular disease. Eating a well-balanced diet that contains adequate protein and vitamins is nec-essary for patients with arterial insufficiency. Key nutrients playspecific roles in wound healing. Vitamin C is essential for colla-gen synthesis and capillary development. Vitamin A enhancesepithelialization. Zinc is necessary for cell mitosis and cell prolif-eration. Obesity strains the heart, increases venous congestion,and reduces circulation; therefore, a weight-reduction plan maybe necessary for some patients. A diet low in lipids may be indi-cated for patients with atherosclerosis.

PROMOTING HOME AND COMMUNITY-BASED CAREThe self-care program is planned with the patient so that activitiesthat promote arterial and venous circulation, relieve pain, and pro-mote tissue integrity are acceptable. The patient and family arehelped to understand the reasons for each aspect of the program andthe possible consequences of nonadherence. Long-term care of thefeet and legs is of prime importance in the prevention of trauma,ulceration, and gangrene. The Plan of Nursing Care describes nurs-ing care for patients with peripheral vascular disease. Chart 31-3provides detailed patient instructions for foot and leg care.

Plan of Nursing CareThe Patient With Peripheral Vascular Problems (Continued)

Nursing Interventions Rationale Expected Outcomes

2. Encourage wearing protective shoes andpadding for pressure areas.

3. Encourage meticulous hygiene; bathingwith neutral soaps, applying lotions, care-fully trimming nails.

4. Caution to avoid scratching or vigorousrubbing.

5. Promote good nutrition; adequate intakeof vitamins A and C, protein, and zinc;control of obesity.

2. Protective shoes and padding preventfoot injuries and blisters.

3. Neutral soaps and lotions prevent dryingand cracking of skin.

4. Scratching and rubbing can cause skinabrasions and bacterial invasion.

5. Good nutrition promotes healing andprevents tissue breakdown.

• Wears protective shoes• Adheres to meticulous hygiene regimen• Eats a healthy diet that contains adequate

protein and vitamins A and C

Nursing Diagnosis: Deficient knowledge regarding self-care activitiesGoal: Adherence to the self-care program

1. Include family/significant others in teach-ing program.

2. Provide written instructions about footcare, leg care, and exercise program.

3. Assist to obtain properly fitting clothing,shoes, stockings.

4. Refer to self-help groups as indicated,such as smoking cessation clinics, stressmanagement, weight management, andexercise program.

1. Adherence to the self-care program isenhanced when the patient receives sup-port from family and from appropriateself-help groups and agencies.

2. Written instructions serve as reminderand reinforcement of information.

3. Constrictive clothing and accessoriesimpede circulation and promote venousstasis.

4. Reducing risk factors may reducesymptoms or slow disease progression.

• Practices frequent position changes asprescribed

• Practices postural exercises as prescribed• Takes medications as prescribed• Avoids vasoconstrictors• Uses measures to prevent trauma• Uses stress management program• Accepts condition as chronic but

amenable to therapies that will decreasesymptoms


Chart 31-4Risk Factors for Peripheral Arterial Disease

NonmodifiableAgeGenderFamilial predisposition

ModifiableNicotine use (eg, tobacco

smoking, chewing)

HypertensionDiet (contributing to

hyperlipidemia)ObesitySedentary lifestyleStressDiabetes mellitus

EvaluationEXPECTED PATIENT OUTCOMESExpected patient outcomes may include:

1. Demonstrates an increase in arterial blood supply toextremitiesa. Exhibits extremities warm to touchb. Has improved color of extremities (ie, free of rubor or

cyanosis)c. Experiences decreased muscle pain with exercised. Demonstrates an increase in walking distance or duration

2. Promotes vasodilation; prevents vascular compressiona. Protects extremities from exposure to coldb. Avoids use of tobaccoc. Uses stress management strategies to minimize emo-

tional upsetd. Wears nonconstricting clothinge. Avoids leg crossingf. Takes medication as prescribed

3. Has decrease in severity and duration of pain4. Attains or maintains tissue integrity

a. Avoids trauma and irritation to skinb. Wears protective shoesc. Adheres to meticulous hygienic regimend. Eats a healthy diet that contains adequate protein, vita-

mins A and C, and zince. Performs self-care activities

PERIPHERAL ARTERIAL OCCLUSIVE DISEASEArterial insufficiency of the extremities is usually found in indi-viduals older than 50 years of age, most often in men. The legsare most frequently affected; however, the upper extremities maybe involved. The age of onset and the severity are influenced bythe type and number of atherosclerotic risk factors (Chart 31-4).In peripheral arterial disease, obstructive lesions are predomi-nantly confined to segments of the arterial system extending fromthe aorta below the renal arteries to the popliteal artery (Fig. 31-9).However, distal occlusive disease is frequently seen in patientswith diabetes mellitus and in elderly patients.

Chart 31-3Home Care Checklist • Foot and Leg Care in Peripheral Vascular Disease

At the completion of the home care instruction, the patient or caregiver will be able to:

• Demonstrate daily foot bathing: Wash between toes with mild soap and lukewarm water, then rinse thoroughly and pat rather than rub dry. ✓ ✓

• Recognize the dangers of thermal injury: ✓– Wear clean, loose, soft cotton socks (they are comfortable, allow air to circulate, and will absorb moisture)– In cold weather, wear extra socks in extra-large shoes.– Avoid heating pads, whirlpools, and hot tubs.– Avoid sunburn.

• Identify safety concerns: ✓ ✓– Inspect feet daily with a mirror for redness, dryness, cuts, blisters, etc.– Always wear soft shoes or slippers when out of bed.– Trim nails straight across after showering.– Consult podiatrist to trim nails if vision is decreased; also for care of corns, blisters, ingrown nails.– Clear pathways in house to prevent injury.– Avoid wearing thong sandals.– Use lamb’s wool between toes if they overlap or rub each other.

• Demonstrate comfort measures: ✓– Wear leather shoes with an extra-depth toebox. Synthetic shoes do not allow air to circulate.– If feet become dry and scaly, use cream with lanolin. Never put cream between toes.– If feet perspire, especially between toes, use powder daily and/or lamb’s wool between toes to promote drying.

• Demonstrate ability to decrease risk of constricting blood vessels: ✓– Avoid promoting circular compression around feet or knees—for example, by applying knee-high stockings or

tight socks.– Do not cross legs at knees.– Stop using nicotine (ie, tobacco smoking or chewing) because nicotine causes vasoconstriction and vasospasm.– Avoid applying tight, constricting bandages.– Participate in a regular walking exercise program to stimulate circulation.

• Recognize when to seek medical attention: ✓ ✓– Contact health care provider at the onset of skin breakdown such as abrasions, blisters, athlete’s foot, or pain.– Do not use any medication on feet or legs unless prescribed.– Avoid using iodine, alcohol, corn/wart-removing compound, or adhesive products before checking with health

care provider.

Patient Caregiver

Clinical ManifestationsThe hallmark is intermittent claudication. This pain may be de-scribed as aching, cramping, fatigue, or weakness that is consis-tently reproduced with the same degree of exercise or activityand relieved with rest. The pain commonly occurs in musclegroups one joint level below the stenosis or occlusion. As thedisease progresses, the patient may have a decreased ability towalk the same distance or may notice increased pain with am-bulation. When the arterial insufficiency becomes severe, the

patient begins to have rest pain. This pain is associated withcritical ischemia of the distal extremity and is persistent, aching,or boring; it may be so excruciating that it is unrelieved by opi-oids. Ischemic rest pain is usually worse at night and oftenwakes the patient. Elevating the extremity or placing it in a hor-izontal position increases the pain, whereas placing the extrem-ity in a dependent position reduces the pain. In bed, somepatients sleep with the affected leg hanging over the side of thebed. Some patients sleep in a reclining chair in an attempt to re-lieve the pain.

Chapter 31 Assessment and Management of Patients With Vascular Disorders and Problems of Peripheral 831

Popliteal

Aortic arch

Posteriorcommunicating

Anterior cerebral

Middle cerebral

Posterior cerebral

Internal carotid

Anterior spinal

External carotid

Vertebral

Common carotid

Left subclavian

Basilar

Rightcommon carotid

Vertebral

Right subclavian

Aortic arch

Celiac trunk

Rightrenal artery

Superiormesenteric Left common

iliac arteryInternal iliac

Superficial femoral

Anterior tibial

Posterior tibial

Deep femoral

Common femoral

FIGURE 31-9 Common sites of atherosclerotic obstruction in major arteries.


Assessment and Diagnostic Findings

A sensation of coldness or numbness in the extremities may ac-company intermittent claudication and is a result of the reducedarterial flow. When the extremity is examined, it may feel cool tothe touch and look pale when elevated or ruddy and cyanotic whenplaced in a dependent position. Skin and nail changes, ulcerations,gangrene, and muscle atrophy may be evident. Bruits may beauscultated with a stethoscope; a bruit is the sound produced byturbulent blood flow through an irregular, tortuous, stenotic vesselor through a dilated segment of the vessel (aneurysm). Peripheralpulses may be diminished or absent.

Examining the peripheral pulses is an important part of assess-ing arterial occlusive disease. Unequal pulses between extremitiesor the absence of a normally palpable pulse is a sign of peripheralarterial disease. The femoral pulse in the groin and the posteriortibial pulse beside the medial malleolus are most easily palpated.The popliteal pulse is sometimes difficult to palpate; the locationof the dorsalis pedis artery on the dorsum of the foot varies andis normally absent in about 7% of the population.

The presence, location, and extent of arterial occlusive diseaseare determined by a careful history of the symptoms and by phys-ical examination. The color and temperature of the extremity arenoted and the pulses palpated. The nails may be thickened andopaque, and the skin may be shiny, atrophic, and dry, with sparsehair growth. The assessment includes comparison of the right andleft extremities.

The diagnosis of peripheral arterial occlusive disease may bemade using CW Doppler and ankle-brachial indices (ABIs), tread-mill testing for claudication, duplex ultrasonography, or otherimaging studies previously described.

Medical ManagementGenerally, patients feel better with some type of exercise pro-gram. If this program is combined with weight reduction and ces-sation of tobacco use, patients often can improve their activitytolerance. Patients should not be promised that their symptomswill be relieved if they stop tobacco use, because claudication maypersist, and they may lose their motivation to stop using tobacco.

PHARMACOLOGIC THERAPYVarious medications are prescribed to treat the symptoms of pe-ripheral arterial disease. Pentoxifylline (Trental) increases ery-throcyte flexibility and reduces blood viscosity, and it is thereforethought to improve the supply of oxygenated blood to the mus-cle. Cilostazol (Pletal) works by inhibiting platelet aggregation,inhibiting smooth muscle cell proliferation, and increasing vaso-dilation. Antiplatelet aggregating agents such as aspirin, ticlopi-dine (Ticlid), and clopidogrel (Plavix) are thought to improvecirculation throughout diseased arteries or prevent intimal hyper-plasia leading to stenosis.

SURGICAL MANAGEMENTIn most patients, when intermittent claudication becomes severeand disabling or when the limb is at risk for amputation becauseof tissue loss, vascular grafting or endarterectomy is the treatmentof choice. The choice of the surgical procedure depends on thedegree and location of the stenosis or occlusion. Other importantconsiderations are the overall health of the patient and the lengthof the procedure that can be tolerated. It is sometimes necessaryto provide the palliative therapy of primary amputation ratherthan an arterial bypass. If endarterectomy is performed, an inci-sion is made into the artery, and the atheromatous obstruction is

removed. The artery is then sutured closed to restore vascular in-tegrity (Fig. 31-10).

Bypass grafts are performed to reroute the blood flow aroundthe stenosis or occlusion. Before bypass grafting, the surgeon de-termines where the distal anastomosis (site where the vessels aresurgically joined) will be placed. The distal outflow vessel must beat least 50% patent for the graft to remain patent. A higher by-pass graft patency rate is associated with keeping the length of thebypass as short as possible.

If the atherosclerotic occlusion is below the inguinal ligamentin the superficial femoral artery, the surgical procedure of choiceis the femoral-to-popliteal graft. This procedure is further classifiedas above-knee and below-knee grafts, referring to the location ofthe distal anastomosis.

Lower leg or ankle vessels with occlusions may also requiregrafts. Occasionally, the entire popliteal artery is occluded, andthere is only collateral circulation. The distal anastomosis may be

Braun, C. M., Colucci, A. M., & Patterson, R. B. (1999). Componentsof an optimal exercise program for the treatment of patients with claudi-cation. Journal of Vascular Nursing, 17(2), 32–36.

PurposeBecause patients with peripheral arterial claudication increasinglylimit activity because of pain, they become physically deconditioned.The patients and their families report decreased quality of life (QOL)because of the activity limitations. Traditional treatment for pe-ripheral arterial claudication has been surgical bypass. Exercise pro-grams are beginning to be offered as treatment for patients withperipheral arterial claudication. Little is known about the effec-tiveness of exercise in the treatment of this patient population. Thisstudy evaluated whether a supervised exercise and education programincreased pain-free walking distance and improved total fitness ofpatients with peripheral arterial claudication.

Study Sample and DesignThis study was a retrospective review of 96 patients who had expe-rienced symptoms of peripheral arterial claudication for longer than3 months. Patients participated in a cardiovascular conditioningand muscle training exercise program with education classes for12 weeks. Twenty-two patients were monitored for 2 years; data werecollected at 1 year and 2 years after the original 12-week program.

FindingsPatients’ walking distances increased threefold after participationin the 12-week program. The average maximum distance patientswere able to walk at the beginning of the program was 190 meters.After the 12-week program the average distance was 580 m. The22 patients followed for two years had an average maximum walk-ing distance of 882 m 1 year after the 12-week program and 731 m2 years after the 12-week program. The researchers concluded thatpatients were able to maintain and continue exercising after comple-tion of the 12-week program. Families reported improvement in gen-eral health and psychosocial behavior of the patients.

Nursing ImplicationsPatients with peripheral arterial claudication benefit from a su-pervised exercise program combined with education programs.Supervised exercise programs may enable patients with peripheralarterial claudication to increase the distance they can walk withoutsymptoms, improve their quality of life, and avoid or delay surgicalintervention.

Does Exercise Relieve Pain of PeripheralArterial Claudication?

NURSING RESEARCH PROFILE 31-1

made onto any of the tibial arteries (posterior tibial, anterior tib-ial, or peroneal arteries) or the dorsalis pedis or plantar artery. Thedistal anastomosis site is determined by the ease of exposure ofthe vessel in surgery and by which vessel provides the best flow tothe distal limb. These grafts require the use of native vein to en-sure patency. Native vein is autologous vein (the patient’s ownvein). The greater or lesser saphenous vein or a combination ofone of the saphenous veins and an upper extremity vein such asthe cephalic vein are used to meet the required length.

How long the graft remains patent is determined by several fac-tors, including the size of the graft, graft location, and develop-ment of intimal hyperplasia at anastomosis sites. Bypass grafts maybe synthetic or autologous vein. Several synthetic materials areavailable for use as a peripheral bypass graft: woven or knittedDacron, expanded polytetrafluoroethylene (ePTFE, such as Gore-Tex or Impra), collagen-impregnated, and umbilical vein. Infec-tion is a problem that threatens survival of the graft and almostalways requires removal of the graft.

If a vein graft is the surgical choice, care must be taken in theoperating room not to damage the vein after harvesting (removingthe vein from the patient’s body). The vein is occluded at oneend and inflated with a heparinized solution to check for leakageand competency. When this is done, the graft is placed in aheparinized solution to keep it from becoming dry and brittle.

Nursing ManagementMAINTAINING CIRCULATIONThe primary objective in the postoperative management of patientswho have undergone vascular procedures is to maintain adequatecirculation through the arterial repair. Pulses, Doppler assessment,color and temperature of the extremity, capillary refill, and sensoryand motor function of the affected extremities are checked, com-pared with those of the other extremity, and recorded every hour forthe first 8 hours and then every 2 hours for 24 hours. Doppler eval-uation of the vessels distal to the bypass graft should be performedfor all postoperative vascular patients, because it is more sensitivethan palpation for pulses. The ABI is monitored at least once every8 hours for the first 24 hours and then once each day until discharge(not usually assessed for pedal artery bypasses). An adequate circu-lating blood volume should be established and maintained. Disap-pearance of a pulse that was present may indicate thromboticocclusion of the graft; the surgeon is immediately notified.


MONITORING AND MANAGING POTENTIAL COMPLICATIONSContinuous monitoring of urine output (more than 30 mL/hour),central venous pressure, mental status, and pulse rate and volumepermit early recognition and treatment of fluid imbalances. Bleed-ing can result from the heparin administered during surgery orfrom an anastomotic leak. A hematoma may form as well.

Leg crossing and prolonged extremity dependency are avoidedto prevent thrombosis. Edema is a normal postoperative finding;however, elevating the extremities and encouraging the patient toexercise the extremities while in bed reduces edema. Elastic com-pression stockings may be prescribed for some patients, but caremust be taken to avoid compressing distal vessel bypass grafts. Se-vere edema of the extremity, pain, and decreased sensation of toesor fingers can be an indication of compartment syndrome.

PROMOTING HOME AND COMMUNITY-BASED CAREDischarge planning includes assessing the patient’s ability tomanage independently. The nurse determines if the patient has anetwork of family and friends to assist with activities of daily liv-ing. The patient may need to be encouraged to make the lifestylechanges necessary with a chronic disease, including pain man-agement and modifications in diet, activity, and hygiene (skincare). The nurse ensures that the patient has the knowledge andability to assess for any postoperative complications such as in-fection, occlusion of the artery or graft, and decreased blood flow.The nurse assists the patient in developing a plan to stop usingtobacco. The Plan of Nursing Care describes nursing care forpatients with peripheral vascular disease.

UPPER EXTREMITY ARTERIALOCCLUSIVE DISEASEArterial occlusions occur less frequently in the upper extremities(arms) than in the legs and cause less severe symptoms becausethe collateral circulation is significantly better in the arms. Thearms also have less muscle mass and are not subjected to the work-load of the legs.

Clinical ManifestationsStenosis and occlusions in the upper extremity result from ather-osclerosis or trauma. The stenosis usually occurs at the origin of

FIGURE 31-10 In an aortoiliac endarterectomy, the vascular surgeon (A) identifies the diseased area, (B) clamps off theblood supply to the vessel, (C) removes the plaque, and (D) sutures the vessel shut, after which blood flow is restored. Adaptedwith permission from Rutherford, R. B. (1999). Vascular surgery: Vol. 1 and 2 (5th ed.). Philadelphia: W. B. Saunders.

A B C D


the vessel proximal to the vertebral artery, setting up the vertebralartery as the major contributor of flow. The patient may developa “subclavian steal” syndrome characterized by reverse flow in thevertebral and basilar artery to provide blood flow to the arm. Thissyndrome may cause vertebrobasilar (cerebral) symptoms. Mostpatients are asymptomatic; however, some report vertigo, ataxia,syncope, or bilateral visual changes.

The patient typically complains of arm fatigue and pain withexercise (forearm claudication) and inability to hold or grasp ob-jects (eg, painting, combing hair, placing objects on shelves abovethe head). Some even notice difficulties driving.

Assessment and Diagnostic FindingsAssessment findings include coolness and pallor of the affected ex-tremity, decreased capillary refill, and a difference in arm bloodpressures of more than 20 mm Hg. Noninvasive studies performedto evaluate for upper extremity arterial occlusions include upper andforearm blood pressure determinations and duplex ultrasonographyto identify the anatomic location of the lesion and to evaluate thehemodynamics of the blood flow. Transcranial Doppler evaluationis performed to evaluate the intracranial circulation and to detectany siphoning of blood flow from the posterior circulation to pro-vide blood flow to the affected arm. If a surgical or interventionalprocedure is planned, an arteriogram may be necessary.

Medical ManagementIf a short, focal lesion is identified in an upper extremity artery, aPTA may be performed. If the lesion involves the subclavian arterywith documented siphoning of blood flow from the intracranial cir-culation, several surgical procedures are available: carotid–to–sub-clavian artery bypass, axillary–to–axillary artery bypass, andautogenous reimplantation of the subclavian to the carotid artery.

Nursing ManagementNursing assessment involves bilateral comparison of upper armblood pressures (obtained by stethoscope and Doppler); radial,ulnar, and brachial pulses; motor and sensory function; tempera-ture; color changes; and capillary refill every 2 hours. Disappear-ance of a pulse or Doppler flow that had been present may indicatean acute occlusion of the vessel, and the physician is notified immediately.

After surgery, the arm is kept at heart level or elevated, withthe fingers at the highest level. Pulses are monitored with Dopplerassessment of the arterial flow every hour for 8 hours and thenevery 2 hours for 24 hours. Blood pressure (obtained by stetho-scope and Doppler) is also assessed every hour for 8 hours andthen every 2 hours for 24 hours. Motor and sensory function,warmth, color, and capillary refill are monitored with each arte-rial flow (pulse) assessment.

Discharge planning includes assessing the patient’s ability tomanage independently. The nurse determines whether the pa-tient has a network of family and friends to assist with activitiesof daily living. The patient may need to be encouraged to makethe lifestyle changes necessary for a chronic disease, includingpain management and modifications in diet, activity, and hygiene

(skin care). The nurse ensures that the patient has the knowledgeand ability to assess for any postoperative complications such asinfection, reocclusion of the artery or occlusion of the graft, anddecreased blood flow. The patient is assisted in developing a planto stop using tobacco. The Plan of Nursing Care describes nursingcare for patients with peripheral vascular disease.

THROMBOANGIITIS OBLITERANS(BUERGER’S DISEASE)Buerger’s disease is characterized by recurring inflammation ofthe intermediate and small arteries and veins of the lower and (inrare cases) upper extremities. It results in thrombus formationand occlusion of the vessels. It is differentiated from other vesseldiseases by its microscopic appearance. In contrast to atheroscle-rosis, Buerger’s disease is believed to be an autoimmune diseasethat results in occlusion of distal vessels.

The cause of Buerger’s disease is unknown, but it is believedto be an autoimmune vasculitis. It occurs most often in men be-tween the ages of 20 and 35 years, and it has been reported in allraces and in many areas of the world. There is considerable evi-dence that heavy smoking or chewing of tobacco is a causative oran aggravating factor (Frost-Rude et al., 2000). Generally, thelower extremities are affected, but arteries in the upper extremi-ties or viscera can also be involved. Buerger’s disease is generallybilateral and symmetric with focal lesions. Superficial throm-bophlebitis may be present.


Although this condition is different from atherosclerosis, Buerger’sdisease in older patients may also be followed by atherosclerosisof the larger vessels after involvement of the smaller vessels. Thepatient’s ability to walk may be severely limited. Patients are athigher risk for nonhealing wounds because of impaired circulation.

Clinical ManifestationsPain is the outstanding symptom of Buerger’s disease. The pa-tient complains of foot cramps, especially of the arch (instep clau-dication), after exercise. The pain is relieved by rest; often, aburning pain is aggravated by emotional disturbances, nicotine,or chilling. Cold sensitivity of the Raynaud type is found in onehalf the patients and is frequently confined to the hands. Digitalrest pain is constant, and the characteristics of the pain do notchange between activity and rest.

Physical signs include intense rubor (reddish blue discoloration)of the foot and absence of the pedal pulse but with normalfemoral and popliteal pulses. Radial and ulnar artery pulses areabsent or diminished. Various types of paresthesia may develop.

As the disease progresses, definite redness or cyanosis of thepart appears when the extremity is in a dependent position. In-volvement is generally bilateral, but color changes may affect onlyone extremity or only certain digits. Color changes may progressto ulceration, and ulceration with gangrene eventually occurs.

Assessment and Diagnostic FindingsSegmental limb blood pressures are taken to demonstrate the dis-tal location of the lesions or occlusions. Duplex ultrasonographyis used to document patency of the proximal vessels and to visu-alize the extent of distal disease. Contrast angiography is per-formed to demonstrate the diseased portion of the anatomy.

NURSING ALERT Before and for 24 hours after surgery, thepatient’s arm is kept at heart level and protected from cold,venipunctures or arterial sticks, tape, and constrictive dressings.!

ManagementThe treatment of Buerger’s disease is essentially the same as thatfor atherosclerotic peripheral arterial disease. The main objectivesare to improve circulation to the extremities, prevent the pro-gression of the disease, and protect the extremities from traumaand infection. Treatment of ulceration and gangrene is directedtoward minimizing infection and conservative débridement ofnecrotic tissue. Tobacco use is highly detrimental, and patientsare strongly advised to stop using tobacco completely. Symptomsare often relieved by cessation of smoking and other uses oftobacco.

Vasodilators are rarely prescribed because these medicationscause dilation of only healthy vessels; vasodilators may divertblood away from the partially occluded vessels, making the situa-tion worse. A regional sympathetic block or ganglionectomy maybe useful in some instances to produce vasodilation and increaseblood flow.

SURGICAL MANAGEMENT OF COMPLICATIONSIf gangrene of a toe develops as a result of arterial occlusive dis-ease in the leg, it is unlikely that toe amputation or even trans-metatarsal amputation will be sufficient; usually, a below-kneeamputation or, occasionally, an above-knee amputation is nec-essary. The indications for amputation are worsening gangrene,especially if the infected area is moist, severe rest pain, or fulmi-nating sepsis.

NURSING MANAGEMENT OF COMPLICATIONSIf an amputation is performed, immediate postoperative care in-cludes elevating the stump for the first 24 hours to promote ve-nous return and minimize edema. The incision is monitored forsigns of hematoma (unapproximated suture line, discoloration orruddy color changes of the skin along the suture line, tendernesswith palpation, or oozing of dark blood from the suture line).The nurse assesses the fit of the elastic bandages and ensures theintegrity of the wrap and continued ability to fit two fingers be-tween layers of the wrap. Distal skin color and warmth are as-sessed, if accessible, and recorded. Elastic bandages are removedand reapplied as prescribed by the surgeon (eg, every 6 hours usingfigure-of-eight turns).

The patient may experience grief, fear, or anxiety related toloss of the limb. The patient is encouraged to discuss his or herfeelings. Spiritual advisors and other health care team membersare consulted as appropriate. Recovery and rehabilitation requireconsultation among health care providers (eg, physicians, physicaland occupational therapists, prosthetists, dietitians, nurses, dis-charge coordinators). The patient may decide to be fitted for andlearn to use a prosthetic device. Rehabilitation facilities, homecare, and outpatient therapy can assist the patient to adapt to thechanges in lifestyle.

Discharge planning includes assessing the patient’s ability tomanage independently. The patient is assisted in developing aplan to stop using tobacco and to manage pain. The patient mayneed to be encouraged to make the lifestyle changes necessarywith a chronic disease, including modifications in diet, activity,and hygiene (skin care). The nurse determines whether the pa-tient has a network of family and friends to assist with activitiesof daily living. The nurse ensures that the patient has the knowl-edge and ability to assess for any postoperative complicationssuch as infection and decreased blood flow. The Plan of NursingCare describes nursing care for patients with peripheral vasculardisease.


AORTITISThe aorta, which is the main trunk of the arterial system, is di-vided into the ascending aorta (5 cm [2 inches] in diameter, con-tained in the pericardium), the aortic arch (extending upward,backward, and downward), and the descending aorta. The tho-racic aorta is above the diaphragm; the abdominal aorta is belowthe diaphragm. The abdominal aorta is further designated assuprarenal (above renal artery level), perirenal level (at renal arterylevel), and infrarenal (below renal artery level).

Aortitis is inflammation of the aorta, particularly of the aor-tic arch. Two types are known to occur: Takayasu’s disease andsyphilitic aortitis. Takayasu’s disease, or occlusive thromboaor-topathy, is uncommon; today, syphilitic aortitis is rare.

Takayasu’s disease, a chronic inflammatory disease of the aor-tic arch and its branches, primarily affects young or middle-agedwomen and is more common in those of Asian descent. It isnonatherosclerotic; the exact pathologic mechanism is unknownbut thought to be immune complex mediated. It progresses froma systemic inflammation with localized arteritis to end-organ is-chemia because of large vessel stenosis or obstruction. Magneticresonance angiography, CT, duplex ultrasonography, or arteri-ography is used to diagnose and evaluate the lesions, which are typ-ically long, smooth areas of narrowing with or without aneurysms.In the early stages, the disease may respond to corticosteroids, andpatients may benefit from the addition of cytotoxic immuno-suppressive agents (Strider et al., 1996). Selective PTA and sur-gical revascularization may be performed after suppression of thesystemic vascular inflammation.

AORTOILIAC DISEASEIf collateral circulation has developed, patients with a stenosis orocclusion of the aortoiliac segment may be asymptomatic, or theymay complain of buttock or low back discomfort associated withwalking. Men may experience impotence. These patients mayhave decreased or absent femoral pulses.

Medical ManagementThe treatment of aortoiliac disease is essentially the same as thatfor atherosclerotic peripheral arterial occlusive disease. The sur-gical procedure of choice is the aortobi iliac graft. If possible, thedistal anastomosis is made to the iliac artery, and the entire sur-gical procedure can be performed within the abdomen. If the iliacvessels are diseased, the distal anastomosis is made to the femoralarteries (aortobifemoral graft). Bifurcated woven or knitted Dacrongrafts are preferred for this surgical procedure.

Nursing ManagementPreoperative assessment, in addition to the standard parameters(see Chap. 18), includes evaluating the brachial, radial, ulnar,femoral, posterior tibial, and dorsalis pedis pulses to establish abaseline for follow-up after arterial lines are placed and postoper-atively. Patient teaching includes an overview of the procedure tobe performed, the preparation for surgery, and the anticipatedpostoperative plan of care. Sights, sounds, and sensations that thepatient may experience are discussed.

Postoperative care includes monitoring for signs of thrombo-sis in arteries distal to the surgical site. The nurse assesses colorand temperature of the extremity, capillary refill time, sensoryand motor function, and pulses by palpation and Doppler everyhour for the first 8 hours and then every 2 hours for the first


24 hours. Any dusky or bluish discoloration, coolness, capillaryrefill time greater than 3 seconds, decrease in sensory or motorfunction, or decrease in pulse quality are reported immediately tothe physician.

Postoperative care also includes monitoring for urine outputgreater than or equal to 30 mL/hour. Renal function may be im-paired as a result of hypoperfusion from hypotension, involvementof the renal arteries during the surgical procedure, hypovolemia,or embolization of the renal artery or renal parenchyma. Vitalsigns, pain, and intake and output are monitored with the pulseand extremity assessments. Results of laboratory tests are moni-tored and reported to the physician. Abdominal assessment forbowel sounds and paralytic ileus is performed at least every 8 hours.Bowel sounds may not return before the third postoperative day.The absence of bowel sounds, absence of flatus, and abdominaldistention are indications of paralytic ileus. Manual manipulationof the bowel during surgery may have caused bruising, resultingin decreased peristalsis. Nasogastric suction may be necessary todecompress the bowel until peristalsis returns. A liquid bowelmovement before the third postoperative day may indicate bowelischemia, which may occur when the mesenteric blood supply(celiac, superior mesenteric, or inferior mesenteric arteries) is oc-cluded. Ischemic bowel usually causes increased pain and an el-evated white blood cell count (20,000 to 30,000 cells/mm3).

AORTIC ANEURYSMAn aneurysm is a localized sac or dilation formed at a weak pointin the wall of the aorta (Fig. 31-11). It may be classified by itsshape or form. The most common forms of aneurysms are sac-cular or fusiform. A saccular aneurysm projects from one side ofthe vessel only. If an entire arterial segment becomes dilated, afusiform aneurysm develops. Very small aneurysms due to local-ized infection are called mycotic aneurysms.

Historically, the cause of abdominal aortic aneurysm, the mostcommon type of degenerative aneurysm, has been attributed toatherosclerotic changes in the aorta. Other causes of aneurysmformation are listed in Chart 31-5. Aneurysms are serious becausethey can rupture, leading to hemorrhage and death.

Adventitia

Media

Intima

FIGURE 31-11 Characteristics of arterial aneurysm. (A) Normal artery. (B) False aneurysm—actually a pulsatinghematoma. The clot and connective tissue are outside the arterial wall. (C) True aneurysm. One, two, or all three lay-ers of the artery may be involved. (D) Fusiform aneurysm—symmetric, spindle-shaped expansion of entire circumfer-ence of involved vessel. (E) Saccular aneurysm—a bulbous protrusion of one side of the arterial wall. (F) Dissectinganeurysm—this usually is a hematoma that splits the layers of the arterial wall.

Etiologic Classification of Arterial Aneurysms

Congenital: Primary connective tissue disorders (Marfan’ssyndrome, Ehlers-Danlos syndrome) and other diseases (focal medial agenesis, tuberous sclerosis, Turner’s syndrome,Menkes’ syndrome)

Mechanical (hemodynamic): Poststenotic and arteriovenousfistula and amputation-related

Traumatic (pseudoaneurysms): Penetrating arterial injuries,blunt arterial injuries, pseudoaneurysms

Inflammatory (noninfectious): Associated with arteritis(Takayasu’s disease, giant cell arteritis, systemic lupus erythe-matosus, Behçet’s syndrome, Kawasaki’s disease) and peri-arterial inflammation (ie, pancreatitis)

Infectious (mycotic): Bacterial, fungal, spirochetal infectionsPregnancy-related degenerative: Nonspecific, inflammatory

variantAnastomotic (postarteriotomy) and graft aneurysms: Infec-

tion, arterial wall failure, suture failure, graft failure

Adapted with permission from Rutherford, R. B. (1999). Vascular surgery(Vols. 1 and 2, 5th ed.). Philadelphia: W. B. Saunders.

Chart31-5

Chart31-5

A B C D E F

THORACIC AORTIC ANEURYSMApproximately 85% of all cases of thoracic aortic aneurysm arecaused by atherosclerosis. They occur most frequently in menbetween the ages 40 and 70 years. The thoracic area is the mostcommon site for a dissecting aneurysm. About one third of pa-tients with thoracic aneurysms die of rupture of the aneurysm(Rutherford, 1999).

Clinical ManifestationsSymptoms are variable and depend on how rapidly the aneurysmdilates and how the pulsating mass affects surrounding intratho-racic structures. Some patients are asymptomatic. In most cases,pain is the most prominent symptom. The pain is usually con-stant and boring but may occur only when the person is supine.


Other conspicuous symptoms are dyspnea, the result of pressureof the sac against the trachea, a main bronchus, or the lung itself;cough, frequently paroxysmal and with a brassy quality; hoarseness,stridor, or weakness or complete loss of the voice (aphonia), re-sulting from pressure against the left recurrent laryngeal nerve;and dysphagia (difficulty in swallowing) due to impingement onthe esophagus by the aneurysm.

Assessment and Diagnostic FindingsWhen large veins in the chest are compressed by the aneurysm,the superficial veins of the chest, neck, or arms become dilated,and edematous areas on the chest wall and cyanosis are oftenevident. Pressure against the cervical sympathetic chain can resultin unequal pupils. Diagnosis of a thoracic aortic aneurysm is prin-cipally made by chest x-ray, transesophageal echocardiography,and CT.

Medical ManagementIn most cases, an aneurysm is treated by surgical repair. Generalmeasures such as controlling blood pressure and correcting riskfactors may be helpful. It is important to control blood pressurein patients with dissecting aneurysms. Systolic pressure is main-tained at about 100 to 120 mm Hg with antihypertensive med-ications (eg, hydralazine hydrochloride [Hydralazine], esmololhydrochloride [Brevibloc] or another beta-blocker such as atenolol[Tenormin] or timolol maleate [Timoptic]). Pulsatile flow is re-duced by medications that reduce cardiac contractility (eg, pro-

pranolol [Inderal]). The goal of surgery is to repair the aneurysmand restore vascular continuity with a vascular graft (Fig. 31-12).Intensive monitoring is usually required after this type of surgery,and the patient is cared for in the critical care unit. Repair ofthoracic aneurysms using endovascular grafts implanted (de-ployed) percutaneously in an interventional laboratory (eg, cardiaccatheterization laboratory) may decrease postoperative recoverytime and decrease complications compared with traditional sur-gical techniques.

ABDOMINAL AORTIC ANEURYSMThe most common cause of abdominal aortic aneurysm is athero-sclerosis. The condition, which is more common among Cau-casians, affects men four times more often than women and ismost prevalent in elderly patients (Rutherford, 1999). Most of these aneurysms occur below the renal arteries (infrarenalaneurysms). Untreated, the eventual outcome may be ruptureand death.

PathophysiologyAll aneurysms involve a damaged media layer of the vessel. Thismay be caused by congenital weakness, trauma, or disease. Afteran aneurysm develops, it tends to enlarge. Risk factors include ge-netic predisposition, smoking (or other tobacco use), and hyper-tension; more than one half of patients with aneurysms havehypertension.

Ascending aorticaneurysm

Surgical clampon aorta

Heart

Incision line

Surgical clampon aorta

Trimmed aorta,sutured

Heart

Ascending aorticaneurysm

Aortic graftimplant

Right coronary artery

Aortic valve sutureline; coronary arterybeing sutured tograft above valve

Surgical ties to holdedges of aneurysmout of operative field

FIGURE 31-12 Repair of an ascending aortic aneurysm and aortic valve replacement. (A) Incision into aorticaneurysm. (B) Aortic valve replacement with aortic graft implant to repair ascending aortic aneurysm. (C) Aorticaneurysm trimmed and closed over graft.

A B C


Clinical ManifestationsAbout two fifths of patients with abdominal aortic aneurysmshave symptoms; the remainder do not. Some patients complainthat they can feel their heart beating in their abdomen when lyingdown, or they may say they feel an abdominal mass or abdomi-nal throbbing. If the abdominal aortic aneurysm is associatedwith thrombus, a major vessel may be occluded or smaller distalocclusions may result from emboli. A small cholesterol, platelet,or fibrin emboli may lodge in the interosseous or digital arteries,causing blue toes.

Assessment and Diagnostic FindingsThe most important diagnostic indication of an abdominal aorticaneurysm is a pulsatile mass in the middle and upper abdomen.About 80% of these aneurysms can be palpated. A systolic bruitmay be heard over the mass. Duplex ultrasonography or CT isused to determine the size, length, and location of the aneurysm(Fig. 31-13). When the aneurysm is small, ultrasonography isconducted at 6-month intervals until the aneurysm reaches a sizeat which surgery to prevent rupture is of more benefit than thepossible complications of a surgical procedure. Some aneurysmsremain stable over many years of observation.


Most abdominal aneurysms occur in patients between the ages of60 and 90 years. Rupture is likely with coexisting hypertensionand with aneurysms wider than 6 cm. In most cases at this point,the chances of rupture are greater than the chance of death duringsurgical repair. If the elderly patient is considered at moderate riskfor complications related to surgery or anesthesia, the aneurysmis not repaired until it is at least 5 cm (2 inches) wide.

Medical ManagementAn expanding or enlarging abdominal aneurysm is likely to rup-ture. Surgery is the treatment of choice for abdominal aneurysmswider than 5 cm (2 inches) wide or those that are enlarging.

SURGICAL MANAGEMENTThe standard treatment for abdominal aortic aneurysm repair hasbeen open surgical repair of the aneurysm by resecting the vessel

and sewing a bypass graft in place. The mortality rate associatedwith elective aneurysm repair, a major surgical procedure, is re-ported to be 1% to 4%. The prognosis for a patient with a rup-tured aneurysm is poor, and surgery is performed immediately(Rutherford, 1999).

An alternative for treating an infrarenal abdominal aortic aneu-rysm is endovascular grafting. Endovascular grafting involves thetransluminal placement and attachment of a sutureless aortic graftprosthesis across an aneurysm (Fig. 31-14). This procedure can beperformed under local or regional anesthesia. Endovascular graft-ing of abdominal aortic aneurysms may be performed if thepatient’s abdominal aorta and iliac arteries are not extremely tor-tuous and if the aneurysm does not begin at the level of the renalarteries. Clinical trials are evaluating endograft treatment of ab-dominal aortic aneurysms at or above the level of the renal arteriesand the thoracic aorta. Potential complications include bleeding,hematoma, or wound infection at the femoral insertion site; distalischemia or embolization; dissection or perforation of the aorta;graft thrombosis; graft infection; break of the attachment system;graft migration; proximal or distal graft leaks; delayed rupture; andbowel ischemia.

Nursing ManagementBefore surgery, nursing assessment is guided by anticipating arupture and by recognizing that the patient may have cardiovas-cular, cerebral, pulmonary, and renal impairment from athero-sclerosis. The functional capacity of all organ systems should beassessed. Medical therapies designed to stabilize physiologic func-tion should be promptly implemented.

Signs of impending rupture include severe back pain or ab-dominal pain, which may be persistent or intermittent and is often

FIGURE 31-14 Ancure Endograft repair of an abdominal aortic aneurysm.

FIGURE 31-13 Duplex ultrasonic image of abdominal aortic aneurysmat the perirenal level. Cross-sectional image documents the location of rightand left renal arteries.


localized in the middle or lower abdomen to the left of the midline.Low back pain may also be present because of pressure of theaneurysm on the lumbar nerves. This is a serious symptom, usuallyindicating that the aneurysm is expanding rapidly and is about torupture. Indications of a rupturing abdominal aortic aneurysm in-clude constant, intense back pain; falling blood pressure; and de-creasing hematocrit. Rupture into the peritoneal cavity is rapidlyfatal. A retroperitoneal rupture of an aneurysm may result inhematomas in the scrotum, perineum, flank, or penis. Signs ofheart failure or a loud bruit may suggest a rupture into the venacava. Rupture into the vena cava results in the higher-pressure ar-terial blood entering the lower-pressure venous system and causingturbulence, which is heard as a bruit. The high blood pressure andincreased blood volume returning to the right heart from the venacava may cause the right heart to fail. The overall surgical mortal-ity rate associated with a ruptured aneurysm is 50% to 75%.

Postoperative care requires intense monitoring of pulmonary,cardiovascular, renal, and neurologic status. Possible complica-tions of surgery include arterial occlusion, hemorrhage, infection,ischemic bowel, renal failure, and impotence.

DISSECTING AORTAOccasionally, in an aorta diseased by arteriosclerosis, a tear de-velops in the intima or the media degenerates, resulting in a dis-section (see Fig. 31-11).

PathophysiologyArterial dissections (separations) are commonly associated withpoorly controlled hypertension; they are three times more com-mon in men than in women and occur most commonly in the50- to 70-year-old age group (Rutherford, 1999). Dissection iscaused by rupture in the intimal layer. A rupture may occurthrough adventitia or into the lumen through the intima, allow-ing blood to reenter the main channel and resulting in chronicdissection or occlusion of branches of the aorta.

As the separation progresses, the arteries branching from the in-volved area of the aorta shear and occlude. The tear occurs mostcommonly in the region of the aortic arch, with the highest mor-tality rate associated with ascending aortic dissection. The dissec-tion of the aorta may progress backward in the direction of theheart, obstructing the openings to the coronary arteries or produc-ing hemopericardium (effusion of blood into the pericardial sac) oraortic insufficiency, or it may extend in the opposite direction,causing occlusion of the arteries supplying the gastrointestinal tract,kidneys, spinal cord, and legs.

Clinical ManifestationsOnset of symptoms is usually sudden. Severe and persistent pain,described as tearing or ripping, may be reported. The pain is in theanterior chest or back and extends to shoulders, epigastric area, orabdomen. Aortic dissection may be mistaken for an acute myo-cardial infarction, which could confuse the clinical picture and ini-tial treatment. Cardiovascular, neurologic, and gastrointestinalsymptoms are responsible for other clinical manifestations, de-pending on the location and extent of the dissection. The patientmay appear pale. Sweating and tachycardia may be detected.Blood pressure may be elevated or markedly different from onearm to the other if dissection involves the orifice of the subcla-vian artery on one side. Because of the variable clinical pictureassociated with this condition, early diagnosis is usually difficult.

Assessment and Diagnostic FindingsArteriography, CT, transesophageal echocardiography, duplexultrasonography, and magnetic resonance imaging aid in thediagnosis.

Medical ManagementMedical or surgical treatment of a dissecting aneurysm dependson the type of dissection present and follows the general princi-ples outlined for the treatment of thoracic aortic aneurysms.

Nursing ManagementA patient with a dissecting aorta requires the same nursing care asa patient with an aortic aneurysm requiring surgical intervention,as described earlier in this chapter. Interventions described in thePlan of Nursing Care are also appropriate.

OTHER ANEURYSMSAneurysms may also arise in the peripheral vessels, most oftenas a result of atherosclerosis. These may involve such vessels asthe subclavian artery, renal artery, femoral artery, or (most fre-quently) popliteal artery. Between 50% and 60% of poplitealaneurysms are bilateral and may be associated with abdominalaortic aneurysms.

The aneurysm produces a pulsating mass and disturbs peripheralcirculation distal to it. Pain and swelling develop because of pres-sure on adjacent nerves and veins. Diagnosis is made by duplexultrasonography and CT to determine the size, length, and extentof the aneurysm. Arteriography may be performed to evaluate thelevel of proximal and distal involvement.

Surgical repair is performed with replacement grafts or endo-vascular repair using a stent-graft or wall graft, which is a Dacronor PTFE (polytetrafluroethylene) graft with external structuresmade from a variety of materials (nitinol, titanium, stainless steel)for additional support.

Nursing ManagementThe patient who has had an endovascular repair must lie supinefor 6 hours; the head of the bed may be elevated up to 45 degreesafter 2 hours. The patient needs to use a bedpan or urinal while onbed rest, or a Foley catheter may be used. Vital signs and Dopplerassessment of peripheral pulses are performed every 15 minutesfor four times, then every 30 minutes for four times, then everyhour for four times, and then as directed by the physician or unitstandards. The catheterization site is assessed when vital signs andpulses are monitored. The nurse assesses for bleeding, swelling,pain, and hematoma formation. Any changes in vital signs, pulsequality, bleeding, swelling, pain, or hematoma are reported to thephysician. The physician is also notified of persistent coughing,sneezing, vomiting, or systolic blood pressure above 180 mm Hgbecause of the increased risk for hemorrhage. Most patients areable to resume their preprocedure diet and are encouraged todrink fluids. An intravenous infusion may be continued until thepatient is able to drink normally. Fluids are important to main-tain blood flow through the arterial repair site and to assist thekidneys with excreting intravenous contrast agent and other med-ications used during the procedure. Six hours after the procedure,the patient may be able to roll side to side and may be able to am-bulate with assistance to the bathroom. After the patient is able to


take adequate fluids orally, the intravenous infusion may be dis-continued and the intravenous access converted to a saline lock.

ARTERIAL EMBOLISMAND ARTERIAL THROMBOSISAcute vascular occlusion may be caused by an embolus or acutethrombosis. Acute arterial occlusions may result from iatrogenicinjury, which can occur during insertion of invasive catheterssuch as those used for arteriography, PTA or stent placement, oran intra-aortic balloon pump. Other causes include trauma froma fracture, crush injury, and penetrating wounds that disrupt thearterial intima. The accurate diagnosis of an arterial occlusion asembolic or thrombotic in origin is necessary to initiate appropri-ate treatment.

PathophysiologyArterial emboli arise most commonly from thrombi that developin the chambers of the heart as a result of atrial fibrillation, myo-cardial infarction, infective endocarditis, or chronic heart failure.These thrombi become detached and are carried from the left sideof the heart into the arterial system, where they lodge in and ob-struct an artery that is smaller than the embolus. Emboli may alsodevelop in advanced aortic atherosclerosis because the atheroma-tous plaques ulcerate or become rough. Acute thrombosis fre-quently occurs in patients with preexisting ischemic symptoms.

Clinical ManifestationsThe symptoms of arterial emboli depend primarily on the size ofthe embolus, the organ involved, and the state of the collateral ves-sels. The immediate effect is cessation of distal blood flow. Theblockage can progress above and below the obstruction. Secondaryvasospasm can contribute to the ischemia. The embolus can frag-ment or break apart, resulting in occlusion of distal vessels. Em-boli tend to lodge at arterial bifurcations and areas narrowed byatherosclerosis. Cerebral, mesenteric, renal, and coronary arteries areoften involved in addition to the large arteries of the extremities.

The symptoms of acute arterial embolism in extremities withpoor collateral flow are acute, severe pain and a gradual loss ofsensory and motor function. The six Ps associated with acute ar-terial embolism are pain, pallor, pulselessness, paresthesia, poi-kilothermia (coldness), and paralysis. Eventually, superficial veinsmay collapse because of decreased blood flow to the extremity.The part of the extremity below the occlusion is markedly colderand paler than the part above the occlusion because of ischemia.

Arterial thrombosis can also acutely occlude an artery. Athrombosis is a slowly developing clot that usually occurs wherethe arterial wall has become damaged, generally as a result of ath-erosclerosis. Thrombi may also develop in an arterial aneurysm.The manifestations of an acute thrombotic arterial occlusion aresimilar to those described for embolic occlusion. However, treat-ment is more difficult with a thrombus because the arterial oc-clusion has occurred in a degenerated vessel and requires moreextensive reconstructive surgery to restore flow than is requiredwith an embolic event.

Assessment and Diagnostic FindingsAn arterial embolus is usually diagnosed on the basis of the suddennature of the onset of symptoms and an apparent source for theembolus. Two-dimensional echocardiography or transesophageal

echocardiography, chest x-ray, and electrocardiography may re-veal underlying cardiac disease. Noninvasive duplex and Dopplerultrasonography can determine the presence and extent of un-derlying atherosclerosis, and arteriography may be performed.

Medical ManagementManagement of arterial thrombosis depends on its cause. Man-agement of acute embolic occlusion usually requires surgery be-cause time is of the essence. Because the onset of the event isacute, collateral circulation has not developed, and the patientquickly moves through the list of six Ps to paralysis, which is themost advanced stage. Heparin therapy is initiated immediately toprevent further development of emboli and to hamper the exten-sion of existing thrombi. Typically, an initial bolus of 5,000 to10,000 units is administered intravenously, followed by a con-tinuous infusion of 1,000 units per hour until the patient is ableto undergo surgery.

SURGICAL MANAGEMENTEmergency embolectomy is the procedure of choice only if theinvolved extremity is viable (Fig. 31-15). Arterial emboli are usuallytreated by insertion of an embolectomy catheter. The catheter ispassed through a groin incision into the affected artery and ad-vanced past the occlusion. The balloon is inflated with sterile salinesolution, and the thrombus is extracted as the catheter is withdrawn.This procedure involves incising the vessel and removing the clot.

PHARMACOLOGIC THERAPYWhen the patient has collateral circulation, treatment may in-clude intravenous anticoagulation with heparin, which can preventthe thrombus from spreading and reduce muscle necrosis. The useof intra-arterial thrombolytic medications helps to dissolve theembolus. Fibrin-specific thrombolytic medications (eg, tissue plas-minogen activator [t-PA, alteplase, Activase] and single-chainurokinase-type plasminogen activator [scu-PA, pro-urokinase])avoid systemic depletion of circulating fibrinogen and plasmino-gen, which prevents the development of systemic fibrinolysis.

FIGURE 31-15 Extraction of an embolus by balloon-tipped embolec-tomy catheter. The deflated balloon-tipped catheter is advanced past the em-bolus, inflated and then gently withdrawn, carrying the embolic materialwith it. Adapted with permission from Rutherford, R. B. (1999). Vascularsurgery: Vol. 1 and 2 (5th ed.). Philadelphia: W. B. Saunders.

sult from a defect in basal heat production that eventually decreasesthe ability of cutaneous vessels to dilate. Episodes may be triggeredby emotional factors or by unusual sensitivity to cold. The diseaseis most common in women between 16 and 40 years of age, and itoccurs more frequently in cold climates and during the winter.

The term Raynaud’s phenomenon is used to refer to localized,intermittent episodes of vasoconstriction of small arteries of thefeet and hands that cause color and temperature changes. Gener-ally unilateral and affecting only one or two digits, the phenom-enon is always associated with underlying systemic disease. It mayoccur with scleroderma, systemic lupus erythematosus, rheuma-toid arthritis, obstructive arterial disease, or trauma.

The prognosis for Raynaud’s disease varies; some patients slowlyimprove, some become progressively worse, and others show nochange. Ulceration and gangrene are rare; however, chronic dis-ease may cause atrophy of the skin and muscles. With appropri-ate patient teaching and lifestyle modifications, the disorder isgenerally benign and self-limiting.

Clinical ManifestationsThe classic clinical picture reveals pallor brought on by suddenvasoconstriction. The skin then becomes bluish (cyanotic) due topooling of deoxygenated blood during vasospasm. As a result ofexaggerated reflow (hyperemia) due to vasodilation, a red color isproduced (rubor) when oxygenated blood returns to the digits afterthe vasospasm stops. The characteristic sequence of color changeof Raynaud’s phenomenon is described as white, blue, and red.Numbness, tingling, and burning pain occur as the color changes.The involvement tends to be bilateral and symmetric.

Medical ManagementAvoiding the particular stimuli (eg, cold, tobacco) that provokevasoconstriction is a primary factor in controlling Raynaud’s dis-ease. Calcium channel blockers may be effective in relievingsymptoms. Studies indicate that nifedipine (Procardia, Adalat) isan effective calcium channel blocker for treating an acute episodeof vasospasm (Kaufman et al., 1996). Sympathectomy (inter-rupting the sympathetic nerves by removing the sympatheticganglia or dividing their branches) may help some patients.

Nursing ManagementThe nurse teaches patients to avoid situations that may be stress-ful or unsafe. Stress management classes may be helpful. Expo-sure to cold must be minimized, and in areas where the fall andwinter months are cold, the patient should remain indoors asmuch as possible and wear layers of clothing when outdoors. Hatsand mittens or gloves should be worn at all times when outside.Fabrics specially designed for cold climates (eg, Thinsulate) arerecommended. Patients should warm up their vehicles before get-ting in so that they can avoid touching a cold steering wheel ordoor handle, which could elicit an attack. During summer, asweater should be available when entering air-conditioned rooms.

Concerns about serious complications, such as gangrene andamputation, are common among patients. However, these con-sequences are uncommon. Patients should avoid all forms ofnicotine; the nicotine gum or patches used to help people quitsmoking may induce attacks.

Patients should be careful about safety. Sharp objects shouldbe handled carefully to avoid injuring the fingers. Patients shouldbe informed about the postural hypotension that may result


Other thrombolytic medications are reteplase (r-PA, Retavase),tenecteplase (TNKase), and staphylokinase (Moore, 2002). Al-though these agents differ in their pharmacokinetics, they areadministered in a similar manner. A catheter is advanced underx-ray visualization to the clot, and the thrombolytic agent is infused.

Thrombolytic therapy should not be used when there areknown contraindications to therapy or when the extremity can-not tolerate the several additional hours of ischemia that it takesfor the agent to lyse (disintegrate) the clot. Contraindicationsto thrombolytic therapy include active internal bleeding, CVA(brain attack, stroke), recent major surgery, uncontrolled hyper-tension, and pregnancy.

Nursing ManagementBefore surgery, the patient remains on bed rest with the extremitylevel or slightly dependent (15 degrees). The affected part is keptat room temperature and protected from trauma. Heating andcooling pads are contraindicated because ischemic extremities areeasily traumatized by alterations in temperature. If possible, tapeand electrocardiogram electrodes should not be used on the ex-tremity; sheepskin and foot cradles are used to protect the legfrom mechanical trauma.

If the patient is treated with thrombolytic therapy, she or heis accurately weighed in kilograms, and the dose of thrombolytictherapy is determined based on the patient’s weight. The patientis admitted to a critical care unit for continuous monitoring. Vitalsigns are taken every 15 minutes for 2 hours, then every 30 min-utes for the next 6 hours, and then every hour for 16 hours.Bleeding is the most common side effect of thrombolytic therapy,and the patient is closely monitored for any signs of bleeding. Thenurse also minimizes the number of punctures for inserting in-travenous lines, avoids intramuscular injections, prevents anypossible tissue trauma, and applies pressure at least twice as longas usual after any puncture that is performed. If t-PA is used forthe treatment, heparin is usually administered to prevent anotherthrombus from forming at the site of the lesion. The t-PA acti-vates plasminogen on the thrombus more than circulating plas-minogen, but it does not decrease the clotting factors as much asother thrombolytic therapies, so patients receiving t-PA are ableto make new thrombi more easily than with some of the otherthrombolytics.

During the postoperative period, the nurse collaborates withthe surgeon about the patient’s appropriate activity level basedon the patient’s condition. Generally, every effort is made to en-courage the patient to move the leg to stimulate circulation andprevent stasis. Anticoagulant therapy may be continued aftersurgery to prevent thrombosis of the affected artery and to di-minish the development of subsequent thrombi at the initiatingsite. The nurse assesses for evidence of local and systemic hemor-rhage, including mental status changes, which can occur whenanticoagulants are administered. Pulses, Doppler signals, ABI,and motor and sensory function are assessed every hour for thefirst 24 hours, because significant changes may indicate reocclu-sion. Metabolic abnormalities, renal failure, and compartmentsyndrome may be complications after an acute arterial occlusion.

RAYNAUD’S DISEASERaynaud’s disease is a form of intermittent arteriolar vasocon-striction that results in coldness, pain, and pallor of the fingertipsor toes. The cause is unknown, although many patients with thedisease seem to have immunologic disorders. Symptoms may re-


from medications, such as calcium channel blockers, used to treatRaynaud’s disease. The nurse also discusses safety precautionsrelated to alcohol, exercise, and hot weather.

Management of Venous DisordersVENOUS THROMBOSIS,DEEP VEIN THROMBOSIS (DVT),THROMBOPHLEBITIS,AND PHLEBOTHROMBOSISAlthough the terms venous thrombosis, deep vein thrombosis(DVT), thrombophlebitis, and phlebothrombosis do not necessarilyreflect identical disease processes, for clinical purposes, they areoften used interchangeably.

PathophysiologySuperficial veins, such as the greater saphenous, lesser saphenous,cephalic, basilic, and external jugular veins, are thick-walled mus-cular structures that lie just under the skin. Deep veins are thinwalled and have less muscle in the media. They run parallel to ar-teries and bear the same names as the arteries. Deep and su-perficial veins have valves that permit unidirectional flow back tothe heart. The valves lie at the base of a segment of the vein that isexpanded into a sinus. This arrangement permits the valves toopen without coming into contact with the wall of the vein, per-mitting rapid closure when the blood starts to flow backward.Other kinds of veins are known as perforating veins. These vesselshave valves that allow one-way blood flow from the superficialsystem to the deep system.

Although the exact cause of venous thrombosis remains un-clear, three factors, known as Virchow’s triad, are believed to playa significant role in its development: stasis of blood (venous sta-sis), vessel wall injury, and altered blood coagulation (Chart 31-6). At least two of the factors seem to be necessary for thrombosisto occur. Venous stasis occurs when blood flow is reduced, as inheart failure or shock; when veins are dilated, as with some med-ication therapies; and when skeletal muscle contraction is reduced,as in immobility, paralysis of the extremities, or anesthesia.Moreover, bed rest reduces blood flow in the legs by at least 50%.Damage to the intimal lining of blood vessels creates a site for clotformation. Direct trauma to the vessels, as with fractures or dis-location, diseases of the veins, and chemical irritation of the veinfrom intravenous medications or solutions, can damage veins. In-creased blood coagulability occurs most commonly in patientswho have been abruptly withdrawn from anticoagulant medica-tions. Oral contraceptive use and several blood dyscrasias (ab-normalities) also can lead to hypercoagulability.

Formation of a thrombus frequently accompanies thrombo-phlebitis, which is an inflammation of the vein walls. When athrombus develops initially in the veins as a result of stasis or hy-percoagulability but without inflammation, the process is referredto as phlebothrombosis. Venous thrombosis can occur in anyvein but occurs more in the veins of the lower extremities. Thesuperficial and deep veins of the extremities may be affected.

Upper extremity venous thrombosis is not as common as lowerextremity thrombosis. However, upper extremity venous throm-bosis is more common in patients with intravenous catheters orin patients with an underlying disease that causes hypercoagula-bility. Internal trauma to the vessels may result from pacemakerleads, chemotherapy ports, dialysis catheters, or parenteral nutri-

tion lines. The lumen of the vein may be decreased as a result ofthe catheter or from external compression, such as by neoplasms oran extra cervical rib. Effort thrombosis of the upper extremity iscaused by repetitive motion, such as experienced by competitiveswimmers, tennis players, and construction workers, that irritatesthe vessel wall, causing inflammation and subsequent thrombosis.

Venous thrombi are aggregates of platelets attached to the veinwall, along with a tail-like appendage containing fibrin, whiteblood cells, and many red blood cells. The “tail” can grow or canpropagate in the direction of blood flow as successive layers of thethrombus form. A propagating venous thrombosis is dangerousbecause parts of the thrombus can break off and produce an em-bolic occlusion of the pulmonary blood vessels. Fragmentation ofthe thrombus can occur spontaneously as it dissolves naturally,or it can occur in association with an elevation in venous pressure,as occurs when a person stands suddenly or engages in muscularactivity after prolonged inactivity. After an episode of acute deepvein thrombosis, recanalization of the lumen typically occurs.The time required for complete recanalization is an important de-terminant of venous valvular incompetence, which is one com-plication of venous thrombosis (Meissner et al., 2000). Othercomplications of venous thrombosis are listed in Chart 31-7.

Clinical ManifestationsA major problem associated with recognizing deep vein throm-bosis is that the signs and symptoms are nonspecific. The excep-tion is phlegmasia cerulea dolens (massive iliofemoral venousthrombosis), in which the entire extremity becomes massivelyswollen, tense, painful, and cool to the touch. Despite this vari-ability, clinical signs should always be investigated.

DEEP VEINSWith obstruction of the deep veins comes edema and swelling ofthe extremity because the outflow of venous blood is inhibited.

Chart 31-6Risk Factors for Deep Vein Thrombosis(DVT) and Pulmonary Embolism

Endothelial damageTraumaSurgeryPacing wiresCentral venous cathetersDialysis access cathetersLocal vein damageRepetitive motion injury

Venous stasisBed rest or immobilizationObesityHistory of varicositiesSpinal cord injuryAge (>65 yr)

CoagulopathyCancerPregnancyOral contraceptive usePresence of congenital proteins C and SPresence of anticardiolipin antibodyAntithrombin III deficiencyPolycythemiaSepticemia


The amount of swelling can be determined by measuring the cir-cumference of the affected extremity at various levels with a tapemeasure and comparing one extremity with the other at the samelevel to determine size differences. If both extremities are swollen,a size difference may be difficult to detect. The affected extremitymay feel warmer than the unaffected extremity, and the superficialveins may appear more prominent.

Tenderness, which usually occurs later, is produced by in-flammation of the vein wall and can be detected by gently pal-pating the affected extremity. Homans’ sign (pain in the calf afterthe foot is sharply dorsiflexed) is not specific for deep vein throm-bosis because it can be elicited in any painful condition of the calf.In some cases, signs of a pulmonary embolus are the first indica-tion of deep vein thrombosis.

SUPERFICIAL VEINSThrombosis of superficial veins produces pain or tenderness, red-ness, and warmth in the involved area. The risk of the superficialvenous thrombi becoming dislodged or fragmenting into emboliis very low because most of them dissolve spontaneously. Thiscondition can be treated at home with bed rest, elevation of theleg, analgesics, and possibly anti-inflammatory medication.

Assessment and Diagnostic FindingsCareful assessment is invaluable in detecting early signs of venousdisorders of the lower extremities. Patients with a history of vari-cose veins, hypercoagulation, neoplastic disease, cardiovasculardisease, or recent major surgery or injury are at high risk. Otherpatients at high risk include those who are obese or elderly andwomen taking oral contraceptives.

When performing the nursing assessment, key concerns in-clude limb pain, a feeling of heaviness, functional impairment,ankle engorgement, and edema; differences in leg circumferencebilaterally from thigh to ankle; increase in the surface tempera-ture of the leg, particularly the calf or ankle; and areas of tender-ness or superficial thrombosis (ie, cordlike venous segment).Homans’ sign (pain in the calf as the foot is sharply dorsiflexed)has been used historically to assess for DVT. It is not a reliable orvalid sign for DVT and has no clinical value in the assessment ofa patient for DVT.

PreventionVenous thrombosis, thrombophlebitis, and DVT can be pre-vented, especially if patients who are considered at high risk areidentified and preventive measures are instituted without delay.

Preventive measures include the application of elastic compres-sion stockings, the use of intermittent pneumatic compressiondevices, and special body positioning and exercise (discussed laterin the section on nursing management). A further method toprevent venous thrombosis in surgical patients is administrationof subcutaneous unfractionated or low molecular weight heparin.

Medical ManagementThe objectives of treatment for deep vein thrombosis are to pre-vent the thrombus from growing and fragmenting (risking pul-monary embolism) and to prevent recurrent thromboemboli.Anticoagulant therapy (administration of a medication to delaythe clotting time of blood, prevent the formation of a thrombusin postoperative patients, and forestall the extension of a throm-bus after it has formed) can meet these objectives, although anti-coagulants cannot dissolve a thrombus that has already formed.

ANTICOAGULATION THERAPYMeasures for preventing or reducing blood clotting within thevascular system are indicated in patients with thrombophlebitis,recurrent embolus formation, and persistent leg edema fromheart failure. They are also indicated in elderly patients with a hipfracture that may result in lengthy immobilization.

Unfractionated Heparin. Unfractionated heparin (heparin) is ad-ministered subcutaneously to prevent development of deep veinthrombosis, or by intermittent intravenous infusion or continuousinfusion for 5 to 7 days to prevent the extension of a thrombusand the development of new thrombi. Oral anticoagulants, suchas warfarin (Coumadin), are administered with heparin therapy.Medication dosage is regulated by monitoring the partial throm-boplastin time, the international normalized ratio (INR), andthe platelet count.

Low-Molecular-Weight Heparin. Subcutaneous low-molecular-weight heparin (LMWH) is an effective treatment for some casesof deep vein thrombosis. It has a longer half-life than unfrac-tionated heparin, so doses can be given in one or two subcuta-neous injections each day. Doses are adjusted according to weight.LMWH prevents the extension of a thrombus and developmentof new thrombi and is associated with fewer bleeding complica-tions than unfractionated heparin. Because there are several prepa-rations, the dosing schedule must be based on the product usedand the protocol at each institution. The cost is higher than forunfractionated heparin; however, LMWH may be used safely inpregnant women, and the patients may be more mobile and havean improved quality of life.

Thrombolytic Therapy. Unlike the heparins, thrombolytic (fibri-nolytic) therapy causes the thrombus to lyse and dissolve in 50%of patients. Thrombolytic therapy (eg, tissue plasminogen acti-vator [t-PA, alteplase, Activase], reteplase [r-PA, Retavase],tenecteplase [TNKase], staphylokinase, urokinase, streptokinase)is given within the first 3 days after acute thrombosis. Therapyinitiated beyond 5 days after the onset of symptoms is signifi-cantly less effective (Moore, 2002). The advantages of throm-bolytic therapy include less long-term damage to the venousvalves and a reduced incidence of postthrombotic syndrome andchronic venous insufficiency. However, thrombolytic therapy re-sults in approximately a threefold greater incidence of bleedingthan heparin. If bleeding occurs and cannot be stopped, thethrombolytic agent is discontinued.

Complications of Venous Thrombosis

Chronic venous occlusionPulmonary emboli from dislodged thrombiValvular destruction

Chronic venous insufficiencyIncreased venous pressureVaricositiesVenous ulcers

Venous obstructionIncreased distal pressureFluid stasisEdemaVenous gangrene

Chart31-7

Chart31-7


SURGICAL MANAGEMENTSurgery is necessary for deep vein thrombosis when anticoagulantor thrombolytic therapy is contraindicated (Chart 31-8), thedanger of pulmonary embolism is extreme, or the venous drainageis so severely compromised that permanent damage to the ex-tremity will probably result. A thrombectomy (removal of thethrombosis) is the procedure of choice. A vena cava filter may beplaced at the time of the thrombectomy; this filter traps largeemboli and prevents pulmonary emboli (see Chap. 23).

Nursing ManagementIf the patient is receiving anticoagulant therapy, the nurse mustfrequently monitor the partial thromboplastin time, prothrom-bin time, hemoglobin and hematocrit values, platelet count, andfibrinogen level. Close observation is also required to detectbleeding; if bleeding occurs, it must be reported immediately andanticoagulant therapy discontinued.

ASSESSING AND MONITORING ANTICOAGULANT THERAPYTo prevent inadvertent infusion of large volumes of heparin,which could cause hemorrhage, continuous intravenous infusionby electronic infusion device is the preferred method of adminis-tering unfractionated heparin. Dosage calculations are based onthe patient’s weight, and any possible bleeding tendencies aredetected by a pretreatment clotting profile. If renal insufficiencyexists, lower doses of heparin are required. Periodic coagulationtests and hematocrit levels are obtained. Heparin is in the effec-tive, or therapeutic, range when the partial thromboplastin timeis 1.5 times the control.

Intermittent intravenous injection is another means of ad-ministering heparin; a dilute solution of heparin is administeredevery 4 hours. Administration may be facilitated by using a hep-arin lock, an intravenous catheter or a small, butterfly-type scalpvein needle with an injection site at the end of the tubing.

Oral anticoagulants, such as warfarin, are monitored by theprothrombin time or INR. Because their effect is delayed for 3 to

5 days, they are usually administered with heparin until desiredanticoagulation has been achieved (ie, when the prothrombintime is 1.5 to 2 times normal or the INR is 2.0 to 3.0).

MONITORING AND MANAGING POTENTIAL COMPLICATIONS

Bleeding. The principal complication of anticoagulant therapyis spontaneous bleeding anywhere in the body. Bleeding from thekidneys is detected by microscopic examination of the urine andis often the first sign of anticoagulant toxicity from excessivedosage. Bruises, nosebleeds, and bleeding gums are also early signs.To reverse the effects of heparin promptly, intravenous injectionsof protamine sulfate may be administered. Reversing the effectsof warfarin, a coumarin derivative, is more difficult, but effectivemeasures that may be prescribed include vitamin K and possiblytransfusion of fresh frozen plasma.

Thrombocytopenia. Another complication of therapy may beheparin-induced thrombocytopenia (decrease in platelets), whichmay develop in patients who receive heparin for more than 5 daysor on readministration after a brief interruption of heparintherapy. Beginning warfarin concomitantly with heparin canprovide a stable INR or prothrombin time by day 5 of heparintreatment.

The use of LMWH is less frequently associated with heparin-induced thrombocytopenia. The thrombocytopenia is thought toresult from an immunologic mechanism that causes aggregationof platelets. This serious complication results in thromboembolicmanifestations, and the prognosis is extremely guarded.

Prevention of thrombocytopenia depends on regular moni-toring of platelet counts. Early signs of thrombocytopenia are afalling platelet count to less than 100,000/mL, a decrease in plateletcount exceeding 25% at one time, the need for increasing dosesof heparin to maintain the therapeutic level, thromboembolic orhemorrhagic complications, and a history of heparin sensitivity(Stevens, 2000). If thrombocytopenia does occur, platelet aggre-gation studies are conducted, the heparin is discontinued, andprotamine sulfate is administered to reverse heparin’s effects.

Drug Interactions. Because oral anticoagulants interact withmany other medications and herbal and nutritional supplements,close monitoring of the patient’s medication schedule is neces-sary. Medications and supplements that potentiate oral anticoag-ulants include salicylates, anabolic steroids, chloral hydrate,glucagon, chloramphenicol, neomycin, quinidine, phenylbuta-zone (Butazolidin), coenzyme Q10, dong quai, garlic, gingko,ginseng, green tea, and vitamin E; those that decrease the antico-agulant effect include phenytoin, barbiturates, diuretics, estrogen,and vitamin C. It is advisable to identify medication interactionsfor patients taking specific oral anticoagulants. Contraindicationsto anticoagulant therapy are summarized in Chart 31-8.

PROVIDING COMFORTBed rest, elevation of the affected extremity, elastic compressionstockings, and analgesics for pain relief are adjuncts to therapy.They help to improve circulation and increase comfort. Depend-ing on the extent and location of a venous thrombosis, bed restmay be required for 5 to 7 days after diagnosis. This is approxi-mately the time necessary for the thrombus to adhere to the veinwall, preventing embolization.

Warm, moist packs applied to the affected extremity reducethe discomfort associated with deep vein thrombosis, as do mildanalgesics prescribed for pain control. When the patient beginsto ambulate, elastic compression stockings are used. Walking is

Chart 31-8 • PHARMACOLOGYContraindications to Anticoagulation Therapy

Lack of patient cooperationBleeding from the following systems:

GastrointestinalGenitourinaryRespiratoryReproductive

Hemorrhagic blood dyscrasiasAneurysmsSevere traumaAlcoholismRecent or impending surgery of:

EyeSpinal cordBrain

Severe hepatic or renal diseaseRecent cerebrovascular hemorrhageInfectionsOpen ulcerative woundsOccupations that involve a significant hazard for injuryRecent delivery of a baby


better than standing or sitting for long periods. Bed exercises,such as dorsiflexion of the foot, are also recommended.

APPLYING ELASTIC COMPRESSION STOCKINGSElastic compression stockings usually are prescribed for patientswith venous insufficiency. These stockings exert a sustained,evenly distributed pressure over the entire surface of the calves,reducing the caliber of the superficial veins in the legs and result-ing in increased flow in the deeper veins. The stockings may beknee-high, thigh-high, or panty hose. Thigh-high stockings aredifficult for the patient to wear, because they have a tendency toroll down. The roll of the stocking further restricts blood flowrather than the stocking providing evenly distributed pressure overthe thigh.

When the stockings are off, the skin is inspected for signs ofirritation, and the calves are examined for possible tenderness.Any skin changes or signs of tenderness are reported. Stockingsare contraindicated in patients with severe pitting edema becausethey can produce severe pitting at the knee.


Because of decreased strength and manual dexterity, elderly pa-tients may be unable to apply elastic compression stockings prop-erly. If such is the case, a family member or friend should betaught to assist the patient to apply the stockings so that they donot cause undue pressure on any part of the feet or legs.

USING INTERMITTENT PNEUMATIC COMPRESSION DEVICESThese devices can be used with elastic compression stockings toprevent deep vein thrombosis. They consist of an electric con-troller that is attached by air hoses to plastic knee-high or thigh-high sleeves. The leg sleeves are divided into compartments, whichsequentially fill to apply pressure to the ankle, calf, and thigh at35 to 55 mm Hg of pressure. These devices can increase bloodvelocity beyond that produced by the stockings. Nursing measuresinclude ensuring that prescribed pressures are not exceeded andassessing for patient comfort.

POSITIONING THE BODY AND ENCOURAGING EXERCISEWhen the patient is on bed rest, the feet and lower legs should beelevated periodically above the level of the heart. This position al-lows the superficial and tibial veins to empty rapidly and to re-main collapsed. Active and passive leg exercises, particularly thoseinvolving calf muscles, should be performed to increase venousflow. Early ambulation is most effective in preventing venous sta-sis. Deep-breathing exercises are beneficial because they produceincreased negative pressure in the thorax, which assists in empty-ing the large veins. Once ambulatory, patients are instructed toavoid sitting for more than 2 hours at a time. The goal is to walk atleast 10 minutes every 1 to 2 hours. Patients are also instructedto perform active and passive leg exercises when they are not able toambulate as frequently as necessary, such as during long car, train,and plane trips.

• Take the anticoagulant at the same time each day, usually be-tween 8:00 and 9:00 AM.

• Wear or carry identification indicating the anticoagulant beingtaken.

• Keep all appointments for blood tests.• Because other medications affect the action of the anticoagulant,

do not take any of the following medications or supplementswithout consulting with the primary health care provider: vita-mins, cold medicines, antibiotics, aspirin, mineral oil, andanti-inflammatory agents, such as ibuprofen (Motrin) and sim-ilar medications or herbal or nutritional supplements. The pri-mary health care provider should be contacted before takingany over-the-counter drugs.

• Avoid alcohol, because it may change the body’s response to ananticoagulant.

• Avoid food fads, crash diets, or marked changes in eatinghabits.

• Do not take warfarin (Coumadin) unless directed.• Do not stop taking Coumadin (when prescribed) unless directed.• When seeking treatment from physician, a dentist, a podiatrist,

or another health care provider, be sure to inform the caregiverthat you are taking an anticoagulant.

• Contact your primary health care provider before having den-tal work or elective surgery.

• If any of the following signs appear, report them immediatelyto the primary health care provider:

Faintness, dizziness, or increased weaknessSevere headaches or abdominal painReddish or brownish urineAny bleeding—for example, cuts that do not stop bleedingBruises that enlarge, nosebleeds, or unusual bleeding from

any part of the bodyRed or black bowel movementsRash

• Avoid injury that can cause bleeding.• For women: Notify the primary health care provider if you sus-

pect pregnancy.

Chart 31-9 • PATIENT EDUCATIONTaking Anticoagulant Medications

PROMOTING HOME AND COMMUNITY-BASED CAREIn addition to teaching the patient how to apply elastic compres-sion stockings and explaining the importance of elevating the legsand exercising adequately, the nurse teaches about the medica-tion, its purpose, and the need to take the correct amount at thespecific times prescribed (Chart 31-9). The patient should alsobe aware that blood tests are scheduled periodically to determinewhether a change in medication or dosage is required. If the pa-tient fails to adhere to the therapeutic regimen, continuation ofthe medication therapy should be questioned. A person who re-fuses to discontinue the use of alcohol should not receive anti-coagulants because chronic alcohol use decreases their effectiveness.In patients with liver problems, the potential for bleeding may beexacerbated by anticoagulant therapy.

CHRONIC VENOUS INSUFFICIENCYVenous insufficiency results from obstruction of the venousvalves in the legs or a reflux of blood back through the valves.Superficial and deep leg veins can be involved. Resultant venoushypertension can occur whenever there has been a prolonged in-crease in venous pressure, such as occurs with deep venous throm-bosis. Because the walls of veins are thinner and more elastic than

NURSING ALERT Any type of stocking, including the elastictype, can inadvertently become a tourniquet if applied incorrectly(ie, rolled tightly at the top). In such instances, the stockings pro-duce stasis rather than prevent it. For ambulatory patients, elasticcompression stockings are removed at night and reapplied beforethe legs are lowered from the bed to the floor in the morning.

!


the walls of arteries, they distend readily when venous pressure isconsistently elevated. In this state, leaflets of the venous valvesare stretched and prevented from closing completely, allowing abackflow or reflux of blood in the veins. Duplex ultrasonographyconfirms the obstruction and identifies the level of valvularincompetence.

Clinical ManifestationsWhen the valves in the deep veins become incompetent after athrombus has formed, postthrombotic syndrome may develop(Fig. 31-16). This disorder is characterized by chronic venous sta-sis, resulting in edema, altered pigmentation, pain, and stasis der-matitis. The patient may notice the symptoms less in the morningand more in the evening. Obstruction or poor calf muscle pump-ing in addition to valvular reflux must be present for the develop-ment of severe postthrombotic syndrome, which includes stasisulceration (Caps et al., 1999). Superficial veins may be dilated. Thedisorder is long-standing, difficult to treat, and often disabling.

Stasis ulcers develop as a result of the rupture of small skinveins and subsequent ulcerations. When these vessels rupture, redblood cells escape into surrounding tissues and then degenerate,leaving a brownish discoloration of the tissues. The pigmentationand ulcerations usually occur in the lower part of the extremity,in the area of the medial malleolus of the ankle. The skin becomesdry, cracks, and itches; subcutaneous tissues fibrose and atrophy.The risk of injury and infection of the extremities is increased.

ComplicationsVenous ulceration is the most serious complication of chronic ve-nous insufficiency and can be associated with other conditionsaffecting the circulation of the lower extremities. Cellulitis or der-matitis may complicate the care of chronic venous insufficiencyand venous ulcerations.

ManagementManagement of the patient with venous insufficiency is directedat reducing venous stasis and preventing ulcerations. Measuresthat increase venous blood flow are antigravity activities, such aselevating the leg, and compression of superficial veins with elasticcompression stockings.

Elevating the legs decreases edema, promotes venous return,and provides symptomatic relief. The legs should be elevatedfrequently throughout the day (at least 15 to 30 minutes every2 hours). At night, the patient should sleep with the foot of thebed elevated about 15 cm (6 inches). Prolonged sitting or standingstill is detrimental; walking should be encouraged. When sitting,the patient should avoid placing pressure on the popliteal spaces,as occurs when crossing the legs or sitting with the legs danglingover the side of the bed. Constricting garments such as pantygirdles or tight socks should be avoided.

Compression of the legs with elastic compression stockings re-duces the pooling of venous blood and enhances venous returnto the heart. Elastic compression stockings are recommended forpeople with venous insufficiency. The stocking should fit so thatpressure is greater at the foot and ankle and then gradually de-clines to a lesser pressure at the knee or groin. If the top of thestocking is too tight or becomes twisted, a tourniquet effect is cre-ated, which worsens venous pooling. Stockings should be appliedafter the legs have been elevated for a period, when the amountof blood in the leg veins is at its lowest.

Extremities with venous insufficiency must be carefully pro-tected from trauma; the skin is kept clean, dry, and soft. Signs ofulceration are immediately reported to the health care providerfor treatment and follow-up.

LEG ULCERSA leg ulcer is an excavation of the skin surface that occurs wheninflamed necrotic tissue sloughs off. About 75% of all leg ulcersresult from chronic venous insufficiency. Lesions due to arterialinsufficiency account for approximately 20%; the remaining 5%are caused by burns, sickle cell anemia, and other factors (Gloviczki& Yao, 2001).

PathophysiologyInadequate exchange of oxygen and other nutrients in the tissueis the metabolic abnormality that underlies the development ofleg ulcers. When cellular metabolism cannot maintain energy bal-ance, cell death (necrosis) results. Alterations in blood vessels atthe arterial, capillary, and venous levels may affect cellularprocesses and lead to the formation of ulcers.

Clinical ManifestationsThe clinical appearance and associated characteristics of leg ulcersare determined by the cause of the ulcer. Most ulcers, especiallyin an elderly patient, have more than one cause. The symptomsdepend on whether the problem is arterial or venous in origin (seeTable 31-2). The severity of the symptoms depends on the extentand duration of the vascular insufficiency. The ulcer itself appearsas an open, inflamed sore. The area may be draining or coveredby eschar (dark, hard crust).

ARTERIAL ULCERSChronic arterial disease is characterized by intermittent claudica-tion, which is pain caused by activity and relieved after a few min-utes of rest. The patient may also complain of digital or forefootpain at rest. If the onset of arterial occlusion is acute, ischemicpain is unrelenting and rarely relieved even with opioid analgesics.Typically, arterial ulcers are small, circular, deep ulcerations onthe tips of toes or in the web spaces between toes. Ulcers oftenoccur on the medial side of the hallux or lateral fifth toe and maybe caused by a combination of ischemia and pressure (Fig. 31-17).

FIGURE 31-16 Competent valves showing blood flow patterns when thevalve is open (A) and closed (B), allowing blood to flow against gravity. (C) Withfaulty or incompetent valves, the blood is unable to move toward the heart.

A B C


Arterial insufficiency may result in gangrene of the toe (digi-tal gangrene), which usually is caused by trauma. The toe isstubbed and then turns black (see Fig. 31-17). Usually, patientswith this problem are elderly people without adequate circulationto provide revascularization. Débridement is contraindicated inthese instances. Although the toe is gangrenous, it is dry. Man-aging dry gangrene is preferable to débriding the toe and causingan open wound that will not heal because of insufficient circula-tion. If the toe were to be amputated, the lack of adequate circu-lation would prevent healing and might make further amputationnecessary—a below-knee or an above-knee amputation. A higher-level amputation in the elderly could result in a loss of indepen-dence and possibly institutional care. Dry gangrene of the toe inan elderly person with poor circulation is usually left undisturbed.The nurse keeps the toe clean and dry until it separates (withoutcreating an open wound).

VENOUS ULCERSChronic venous insufficiency is characterized by pain describedas aching or heaviness. The foot and ankle may be edematous.Ulcerations are in the area of the medial or lateral malleolus(gaiter area) and are typically large, superficial, and highly exuda-tive. Venous hypertension causes extravasation of blood, whichdiscolors the gaiter area (see Fig. 31-17). Patients with neuropa-thy frequently have ulcerations on the side of the foot over themetatarsal heads. These ulcers are painless and are described infurther detail in Chapter 41.

Assessment and Diagnostic FindingsBecause ulcers have many causes, the cause of each ulcer needs tobe identified so appropriate therapy can be prescribed. The his-tory of the condition is important in determining venous or arte-rial insufficiency. The pulses of the lower extremities (femoral,popliteal, posterior tibial, and dorsalis pedis) are carefully exam-ined. More conclusive diagnostic aids are Doppler and duplexultrasound studies, arteriography, and venography. Cultures ofthe ulcer bed may be necessary to determine whether the infect-ing agent is the primary cause of the ulcer.

Medical ManagementPatients with ulcers can be effectively managed by advanced prac-tice nurses or certified wound care nurses in collaboration withphysicians. All ulcers have the potential to become infected.

PHARMACOLOGIC THERAPYAntibiotic therapy is prescribed when the ulcer is infected; thespecific antibiotic is selected on the basis of culture and sensitiv-ity test results. Oral antibiotics usually are prescribed because top-ical antibiotics have not proven to be effective for leg ulcers.

DÉBRIDEMENTTo promote healing, the wound is kept clean of drainage andnecrotic tissue. The usual method is to flush the area with nor-mal saline solution. If this is unsuccessful, débridement may benecessary. Débridement is the removal of nonviable tissue fromwounds. Removing the dead tissue is important, particularly ininstances of infection. Débridement can be accomplished byseveral different methods:

• Sharp surgical débridement is the fastest method and can beperformed by a physician, skilled advanced practice nurse, orcertified wound care nurse in collaboration with the physician.

• Nonselective débridement can be accomplished by apply-ing isotonic saline dressings of fine-mesh gauze to the ulcer.When the dressing dries, it is removed (dry), along with thedebris adhering to the gauze. Pain management is usuallynecessary.

• Enzymatic débridement with the application of enzyme oint-ments may be prescribed to treat the ulcer. The ointment isapplied to the lesion but not to normal surrounding skin.Most enzymatic ointments are covered with saline-soakedgauze that has been thoroughly wrung out. A dry gauze dress-ing and a loose bandage are then applied. The enzymaticointment is discontinued when the necrotic tissue has beendébrided and an appropriate wound dressing is applied.

• Débriding agents can be used. Dextranomer (Debrisan)beads are small, highly porous, spherical beads (0.1 to 0.3 mmin diameter) that can absorb wound secretions. Bacteria andthe products of tissue necrosis and protein degradation areabsorbed into the bead layer. When the beads are satu-rated, they take on a grayish yellow color, at which pointtheir cleansing action stops. They are then flushed from thewound with normal saline, and a fresh layer is applied.

• Calcium alginate dressings can also be used for débridementwhen absorption of exudate is needed. These dressings arechanged when the exudate seeps through the cover dressingor at least every 7 days. The dressing can also be used on areasthat are bleeding, because the material helps stop the bleed-ing. As the dry fibers absorb exudate, they become a gel thatis painlessly removed from the ulcer bed. Calcium alginatedressings should not be used on dry or nonexudative wounds.

A

B C

FIGURE 31-17 (A) Ulcers resulting from arterial emboli. (B) Gangrene ofthe toes resulting from severe arterial ischemia. (C) Ulcer from venous stasis.

TOPICAL THERAPYA variety of topical agents can be used in conjunction with cleans-ing and débridement therapies to promote healing of leg ulcers.The goals of treatment are to remove devitalized tissue and to keepthe ulcer clean and moist while healing takes place. The treatmentshould not destroy developing tissue. For topical treatments to besuccessful, adequate nutritional therapy must be maintained.

WOUND DRESSINGAfter the circulatory status has been assessed and determined tobe adequate for healing (ABI of more than 0.5), surgical dressingscan be used to promote a moist environment. The simplestmethod is to use a wound contact material (eg, Tegapore) next tothe wound bed and cover it with gauze. Tegapore maintains amoist environment, can be left in place for several days, anddoes not disrupt the capillary bed when removed for evaluation.Hydrocolloids (eg, Comfeel, DuoDerm CGF, Restore, Tegasorb)are also available options to promote granulation tissue and re-epithelialization. They also provide a barrier for protection becausethey adhere to the wound bed and surrounding tissue. However,deep wounds and infected wounds are often more appropriatelytreated with other dressings.

Knowledge deficit, frustration, fear, and depression can resultin the patient’s and family’s decreased compliance with the pre-scribed therapy; therefore, patient and family education is neces-sary before beginning and throughout the wound care program.

STIMULATED HEALINGTissue-engineered human skin equivalent along with therapeuticcompression has been developed by Apligraf; it is a skin productcultured from human dermal fibroblasts and keratinocytes. Whenapplied, it seems to react to factors in the wound and may inter-act with the patient’s cells to stimulate the production of growthfactors. Application is not difficult, no suturing is involved, andthe procedure is painless.

NURSING PROCESS: THE PATIENT WHO HAS LEG ULCERSAssessmentA careful nursing history and assessment of symptoms are im-portant. The extent and type of pain are carefully assessed, asare the appearance and temperature of the skin of both legs. Thequality of all peripheral pulses is assessed, and comparisons aremade of the pulses in both legs. The legs are checked for edema.If the extremity is edematous, the degree of edema is determined.Any limitation of mobility and activity that results from the vas-cular insufficiency is identified. The patient’s nutritional status isassessed, and a history of diabetes, collagen disease, or varicoseveins is obtained.

DiagnosisNURSING DIAGNOSESBased on the assessment data, major nursing diagnoses for thepatient may include:

• Impaired skin integrity related to vascular insufficiency• Impaired physical mobility related to activity restrictions of

the therapeutic regimen and pain• Imbalanced nutrition: less than body requirements, related

to increased need for nutrients that promote wound healing

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONSBased on the assessment data, potential complications that maydevelop include:

• Infection• Gangrene

Planning and GoalsThe major goals for the patient may include restoration of skinintegrity, improved physical mobility, adequate nutrition, andabsence of complications.

Nursing InterventionsThe nursing challenge in caring for these patients is great,whether the patient is in the hospital, in a long-term care facility,or at home. The physical problem is often a long-term one thatcauses a substantial drain on the patient’s physical, emotional,and economic resources.

RESTORING SKIN INTEGRITYTo promote wound healing, measures are used to keep the areaclean. Cleansing requires very gentle handling, a mild soap, andlukewarm water. Positioning of the legs depends on whether theulcer is of arterial or venous origin. If there is arterial insuffi-ciency, the patient should be referred to be evaluated for vascularreconstruction. If there is venous insufficiency, dependent edemacan be avoided by elevating the lower extremities. A decrease inedema promotes the exchange of cellular nutrients and wasteproducts in the area of the ulcer, promoting healing.

Avoiding trauma to the lower extremities is imperative in pro-moting skin integrity. Protective boots may be used (eg, the RookeVascular boot, Lunax Boot, Bunny Boot); they are soft and pro-vide warmth and protection from injury. If the patient is on bedrest, it is important to relieve pressure on the heels to preventpressure ulcerations. When the patient is in bed, a bed cradle canbe used to relieve pressure from bed linens and to prevent any-thing from touching the legs. When the patient is ambulatory, allobstacles are moved from the patient’s path so that the patient’slegs will not be bumped. Heating pads, hot-water bottles, or hotbaths are avoided. Heat increases the oxygen demands and thusthe blood flow demands of the tissue, which in this case are al-ready compromised. The patient with diabetes mellitus suffersfrom neuropathy with decreased sensation, and heating pads mayproduce injury before the patient is aware of being burned.

IMPROVING PHYSICAL MOBILITYGenerally, physical activity is initially restricted to promote heal-ing. When infection resolves and healing begins, ambulationshould resume gradually and progressively. Activity promotesarterial flow and venous return and is encouraged after the acutephase of the ulcer process. Until full activity resumes, the patientis encouraged to move about when in bed, to turn from side toside frequently, and to exercise the upper extremities to maintainmuscle tone and strength. Meanwhile, diversional activities thatinterest the patient are encouraged. Consultation with an occu-pational therapist may be helpful if a prolonged period of limitedmobility and activity is anticipated.

If pain limits the patient’s activity, analgesics may be prescribedby the physician. The pain of peripheral vascular disease, whetherit is arterial or venous, is typically chronic. Analgesics may be takenbefore scheduled activities to help the patient participate morecomfortably.



PROMOTING ADEQUATE NUTRITIONNutritional deficiencies are determined from the patient’s reportof usual dietary intake. Alterations in the diet are made to remedythese deficiencies. A diet that is high in protein, vitamins C andA, iron, and zinc is encouraged in an attempt to promote healing.

Many patients with peripheral vascular disease are elderly.Their caloric intake may need to be adjusted because of their de-creased metabolic rate and level of activity. Particular considerationshould also be given to their iron intake, because many elderlypeople are anemic.

After a diet plan has been developed that meets the patient’snutritional needs and promotes healing, diet instruction is pro-vided to the patient and family. The nurse and patient design thediet plan to be compatible with the lifestyle and preferences of thepatient and family.

PROMOTING HOME AND COMMUNITY-BASED CAREThe self-care program is planned with the patient so that activitiesto promote arterial and venous circulation, relieve pain, and pro-mote tissue integrity will be used. Reasons for each aspect of theprogram are explained to the patient and family. Leg ulcers areoften chronic and difficult to heal; they frequently recur, evenwhen patients rigorously follow the plan of care. Long-term careof the feet and legs to promote healing of wounds and prevent re-currence of ulcerations is the primary goal. Leg ulcers increase thepatient’s risk for infection, may be painful, and limit mobility, ne-cessitating life-style changes. Participation of family members andhome-health providers may be necessary for treatments such asdressing changes, reassessments, and evaluation of the plan ofcare. Regular follow-up with a primary health care provider isnecessary.

EvaluationEXPECTED PATIENT OUTCOMESExpected patient outcomes may include:

1. Demonstrates restored skin integritya. Exhibits absence of inflammationb. Exhibits absence of drainage; negative wound culturec. Avoids trauma to the legs

2. Increases physical mobilitya. Progresses gradually to optimal level of activityb. Reports that pain does not impede activity

3. Attains adequate nutritiona. Selects foods high in protein, vitamins, iron, and zincb. Discusses with family members dietary modifications

that need to be made at homec. Plans, with the family, a diet that is nutritionally sound

VARICOSE VEINSVaricose veins (varicosities) are abnormally dilated, tortuous,superficial veins caused by incompetent venous valves (see Fig. 31-16). Most commonly, this condition occurs in the lowerextremities, the saphenous veins, or the lower trunk; however,it can occur elsewhere in the body, such as esophageal varices(see Chap. 39).

It is estimated that varicose veins occur in up to 60% of theadult population in the United States, with an increased inci-dence correlated with increased age ( Johnson, 1997). The condi-tion is most common in women and in people whose occupationsrequire prolonged standing, such as salespeople, hair stylists, teach-

ers, nurses, ancillary medical personnel, and construction workers.A hereditary weakness of the vein wall may contribute to the de-velopment of varicosities, and it is not uncommon to see this con-dition occur in several members of the same family. Varicoseveins are rare before puberty. Pregnancy may cause varicosities.The leg veins dilate during pregnancy because of hormonal effectsrelated to distensibility, increased pressure by the gravid uterus,and increased blood volume which all contribute to the develop-ment of varicose veins ( Johnson, 1997).

PathophysiologyVaricose veins may be considered primary (without involvement ofdeep veins) or secondary (resulting from obstruction of deep veins).A reflux of venous blood in the veins results in venous stasis. Ifonly the superficial veins are affected, the person may have nosymptoms but may be troubled by the appearance of the dilatedveins.

Clinical ManifestationsSymptoms, if present, may take the form of dull aches, musclecramps, and increased muscle fatigue in the lower legs. Ankle edemaand a feeling of heaviness of the legs may occur. Nocturnal crampsare common. When deep venous obstruction results in varicoseveins, patients may develop the signs and symptoms of chronicvenous insufficiency: edema, pain, pigmentation, and ulcerations.Susceptibility to injury and infection is increased.

Assessment and Diagnostic FindingsDiagnostic tests for varicose veins include the duplex scan, whichdocuments the anatomic site of reflux and provides a quantitativemeasure of the severity of valvular reflux. Air plethysmographymeasures the changes in venous blood volume. Venography is notroutinely performed to evaluate for valvular reflux. When it isused, however, it involves injecting an x-ray contrast agent intothe leg veins so that the vein anatomy can be visualized by x-raystudies during various leg movements.

PreventionThe patient should avoid activities that cause venous stasis, suchas wearing tight socks or a constricting panty girdle, crossing thelegs at the thighs, and sitting or standing for long periods. Chang-ing position frequently, elevating the legs when they are tired, andgetting up to walk for several minutes of every hour promote cir-culation. The patient should be encouraged to walk 1 or 2 mileseach day if there are no contraindications. Walking up the stairsrather than using the elevator or escalator is helpful in promotingcirculation. Swimming is also good exercise for the legs.

Elastic compression stockings, especially knee-high stockings,are useful. Patients are more likely to use knee-high stockings thanthigh-high stockings. The overweight patient should be encour-aged to begin a weight-reduction plan.

Medical ManagementSurgery for varicose veins requires that the deep veins be patentand functional. The saphenous vein is ligated and divided. Thevein is ligated high in the groin, where the saphenous vein meetsthe femoral vein. Additionally, the vein may be removed (stripped).After the vein is ligated, an incision is made in the ankle, and a


metal or plastic wire is passed the full length of the vein to thepoint of ligation. The wire is then withdrawn, pulling (removing,“stripping”) the vein as it is removed (Fig. 31-18). Pressure andelevation keep bleeding at a minimum during surgery.

SCLEROTHERAPYIn sclerotherapy, a chemical is injected into the vein, irritating thevenous endothelium and producing localized phlebitis and fibro-sis, thereby obliterating the lumen of the vein. This treatmentmay be performed alone for small varicosities or may follow veinligation or stripping. Sclerosing is palliative rather than curative.After the sclerosing agent is injected, elastic compression ban-dages are applied to the leg and are worn for approximately 5 days.The health care provider who performed sclerotherapy removesthe first bandages. Elastic compression stockings are then wornfor an additional 5 weeks.

After sclerotherapy, patients are encouraged to perform walk-ing activities as prescribed to maintain blood flow in the leg.Walking enhances dilution of the sclerosing agent.

Nursing ManagementSurgery can be performed in an outpatient setting, or patients canbe admitted to the hospital on the day of surgery and dischargedthe next day, but nursing measures are the same as if the patientwere hospitalized. Bed rest is maintained for 24 hours, afterwhich the patient begins walking every 2 hours for 5 to 10 min-utes. Elastic compression stockings are used to maintain com-pression of the leg. They are worn continuously for about 1 weekafter vein stripping. The nurse assists the patient to perform ex-ercises and move the legs. The foot of the bed should be elevated.Standing still and sitting are discouraged.

PROMOTING COMFORT AND UNDERSTANDINGAnalgesics are prescribed to help patients move affected extremi-ties more comfortably. Dressings are inspected for bleeding, par-ticularly at the groin, where the risk of bleeding is greatest. Thenurse is alert for reported sensations of “pins and needles.” Hyper-

sensitivity to touch in the involved extremity may indicate a tem-porary or permanent nerve injury resulting from surgery, becausethe saphenous vein and nerve are close to each other in the leg.

Usually, the patient may shower after the first 24 hours. Thepatient is instructed to dry the incisions well with a clean towelusing a patting technique rather than rubbing. Application of skinlotion is to be avoided until the incisions are completely healedto decrease the chance of developing an infection.

If the patient underwent sclerotherapy, a burning sensation inthe injected leg may be experienced for 1 or 2 days. The nurse mayencourage the use of a mild analgesic (eg, propoxyphene napsylateand acetaminophen [Darvocet N], oxycodone and acetaminophen[Percocet], oxycodone and acetylsalicylic acid [Percodan]) as pre-scribed by a physician or nurse practitioner and walking to pro-vide relief.

PROMOTING HOME AND COMMUNITY-BASED CAREPatients require long-term elastic support of the leg after dis-charge, and plans are made to obtain adequate supplies of elas-tic compression stockings or bandages as appropriate. Exercisesof the legs are necessary; the development of an individualizedplan requires consultation with the patient and the health careteam.

CellulitisPathophysiology and Clinical ManifestationsCellulitis is the most common infectious cause of limb swelling.Cellulitis can occur as a single isolated event or a series of recur-rent events. It is often misdiagnosed, usually as recurrent throm-bophlebitis or chronic venous insufficiency. Cellulitis occurs whenan entry point through normal skin barriers allows bacteria toenter and release their toxins in the subcutaneous tissues. Theacute onset of swelling, localized redness, and pain is frequentlyassociated with systemic signs of fever, chills, and sweating. Theredness may not be uniform and often skips areas. Regional lymphnodes may also be tender and enlarged.

Femoralvein

Greatsaphenous

vein

Greatsaphenous

vein

Smallsaphenousvein

Alternateincision

Veinstripper

FIGURE 31-18 Ligation and strippingof the great and the small saphenous veins.(A) The tributaries of the saphenous veinhave been ligated at the saphenofemoraljunction. (B) The vein stripper has beeninserted from the ankle superiorly to thegroin. The vein is removed (“stripped”)from above downward. A number of al-ternate incisions may be needed to re-move separate varicose masses. (C) Thesmall saphenous vein is stripped from itsjunction with the popliteal vein to a pointposterior to the lateral malleolus.

A B C


Medical ManagementMild cases of cellulitis can be treated on an outpatient basis withoral antibiotic therapy. If the cellulitis is severe, the patient is hos-pitalized and treated with intravenous antibiotics for at least 7 to14 days. The key to preventing recurrent episodes of cellulitis liesin adequate antibiotic therapy for the initial event and in identify-ing the site of the bacterial entry. The most commonly overlookedareas are the cracks and fissures that occur in the skin between thetoes. Other possible locations are drug use injection sites, contu-sions, abrasions, ulcerations, ingrown toenails, and hangnails.

Nursing ManagementThe patient is instructed to elevate the affected area above heartlevel and apply warm, moist packs to the site every 2 to 4 hours.Individuals with sensory and circulatory deficits, such as diabetesand paralysis, should use caution when applying warm packsbecause burns may occur; it is advisable to use a thermometer orhave a caregiver ensure that the temperature is not more thanlukewarm. Education should focus on preventing a recurrentepisode. The patient with peripheral vascular disease or diabetesmellitus should receive education or re-education about skin andfoot care.

Management of Lymphatic DisordersThe lymphatic system consists of a set of vessels that spreadthroughout most of the body. These vessels start as lymph capil-laries that drain unabsorbed plasma from the interstitial spaces(spaces between the cells). The lymphatic capillaries unite to formthe lymph vessels, which pass through the lymph nodes and thenempty into the large thoracic duct that joins the jugular vein onthe left side of the neck.

The fluid drained from the interstitial space by the lymphaticsystem is called lymph. The flow of lymph depends on the in-trinsic contractions of the lymph vessels, the contraction of mus-cles, respiratory movements, and gravity. The lymphatic systemof the abdominal cavity maintains a steady flow of digested fattyfood (chyle) from the intestinal mucosa to the thoracic duct. Inother parts of the body, the lymphatic system’s function is re-gional; the lymphatic vessels of the head, for example, empty intoclusters of lymph nodes located in the neck, and those of the ex-tremities empty into nodes of the axillae and the groin.

LYMPHANGITIS AND LYMPHADENITISLymphangitis is an acute inflammation of the lymphatic channels.It arises most commonly from a focus of infection in an extrem-ity. Usually, the infectious organism is a hemolytic Streptococcus.The characteristic red streaks that extend up the arm or the legfrom an infected wound outline the course of the lymphatic vesselsas they drain.

The lymph nodes located along the course of the lymphaticchannels also become enlarged, red, and tender (acute lym-phadenitis). They can also become necrotic and form an abscess(suppurative lymphadenitis). The nodes involved most often arethose in the groin, axilla, or cervical region.

Because these infections are nearly always caused by organismsthat are sensitive to antibiotics, it is unusual to see abscess forma-tion. Recurrent episodes of lymphangitis are often associated withprogressive lymphedema. After acute attacks, an elastic compres-

sion stocking or sleeve should be worn on the affected extremityfor several months to prevent long-term edema.

LYMPHEDEMA AND ELEPHANTIASISLymphedemas are classified as primary (congenital malforma-tions) or secondary (acquired obstructions). Tissue swelling oc-curs in the extremities because of an increased quantity of lymphthat results from obstruction of lymphatic vessels. It is especiallymarked when the extremity is in a dependent position. Initially,the edema is soft, pitting, and relieved by treatment. As the con-dition progresses, the edema becomes firm, nonpitting, and un-responsive to treatment. The most common type is congenitallymphedema (lymphedema praecox), which is caused by hy-poplasia of the lymphatic system of the lower extremity. This dis-order is usually seen in women and first appears between ages 15and 25.

The obstruction may be in the lymph nodes and the lymphaticvessels. Sometimes, it is seen in the arm after an axillary node dis-section (eg, for breast cancer) and in the leg in association withvaricose veins or chronic thrombophlebitis. In the latter case, thelymphatic obstruction usually is caused by chronic lymphangitis.Lymphatic obstruction caused by a parasite (filaria) is seen fre-quently in the tropics. When chronic swelling is present, theremay be frequent bouts of acute infection characterized by highfever and chills and increased residual edema after the inflamma-tion has resolved. These lead to chronic fibrosis, thickening of thesubcutaneous tissues, and hypertrophy of the skin. This condition,in which chronic swelling of the extremity recedes only slightlywith elevation, is referred to as elephantiasis.

Medical ManagementThe goal of therapy is to reduce and control the edema and pre-vent infection. Active and passive exercises assist in moving lym-phatic fluid into the bloodstream. External compression devicesmilk the fluid proximally from the foot to the hip or from thehand to the axilla. When the patient is ambulatory, custom-fittedelastic compression stockings or sleeves are worn; those with thehighest compression strength (exceeding 40 mm Hg) are required.When the leg is affected, strict bed rest with the leg elevated mayaid in mobilizing the fluids.

PHARMACOLOGIC THERAPYAs initial therapy, the diuretic furosemide (Lasix) is prescribed asneeded to prevent the fluid overload that can result from the mo-bilization of extracellular fluid. Diuretics have also been used pal-liatively for lymphedema in conjunction with elevating the legand wearing elastic compression stockings or sleeves. However,the use of diuretics alone has little benefit because their mainaction is to limit capillary filtration by decreasing the circulatingblood volume. If lymphangitis or cellulitis is present, antibiotictherapy is initiated. The patient is taught to inspect the skin forevidence of infection.

SURGICAL MANAGEMENTSurgery is performed if the edema is severe and uncontrolled bymedical therapy, if mobility is severely compromised, or if infec-tion persists. One surgical approach involves the excision of theaffected subcutaneous tissue and fascia, with skin grafting to coverthe defect. Another procedure involves the surgical relocation of su-perficial lymphatic vessels into the deep lymphatic system by meansof a buried dermal flap to provide a conduit for lymphatic drainage.


Nursing ManagementAfter surgery, the management of skin grafts and flaps is the sameas when these therapies are used for other conditions. Prophylacticantibiotics may be prescribed for 5 to 7 days. Constant elevationof the affected extremity and observations for complications areessential. Complications may include flap necrosis, hematoma orabscess under the flap, and cellulitis. The nurse instructs the patientor caregiver to inspect the dressing daily. Unusual drainage or anyinflammation around the wound margin may suggest infectionand should be reported to the physician. The patient is informedthat there may be a loss of sensation in the skin graft area. Thepatient is also instructed to avoid the application of heating padsor exposure to sun to prevent burns or trauma to the area.

Haimovici, H. (1996). Vascular surgery principles and techniques (4th ed.).Cambridge, MA: Blackwell Science.

Jarvis, C. (1999). Physical examination and health assessment (3rd ed.).Philadelphia: W. B. Saunders.

Lynn-McHale, D. J. (2000). AACN procedure manual for critical carenurses (4th ed.). St. Louis: Mosby.

Moore, W. S. (2002). Vascular surgery: A comprehensive review (6th ed.).Philadelphia: W. B. Saunders.

Parodi, J. C., Veith, F. J., & Marin, M. (1999). Endovascular graftingtechniques. Baltimore: Williams & Wilkins.

Rutherford, R. B. (1999). Vascular surgery (5th ed., Vols. I and II).Philadelphia: W. B. Saunders.

Strandness, D. E. (2002). Duplex scanning in vascular disorders (3rd ed.).Philadelphia: Lippincott Williams & Wilkins.

White, R. A., & Fogarty, T. J. (1999). Peripheral endovascular interven-tions (2nd ed.). New York: Singer-Verlag.

Yao, J. T. & Pearce, W. H. (1999). Practical vascular surgery. Stamford,CT: Appleton & Lange.

JournalsBeckey, N. P. (1999). Outpatient management of patients on warfarin.

Lippincott’s Primary Care Practice, 3(3), 280–289.Berdejo, G. L., Lyon, R. T., Ohki, T., Sanchez, L. A., Wain, R. A.,

del Valle, W. N., et al. (1998). Color duplex ultrasound evaluationof transluminally placed endovascular grafts for aneurysm repair.Journal of Vascular Technology, 22(4), 201–207.

Bryant, J. L., & Turkoski, B. B. (1999). Relieving intermittent claudi-cation: A nursing approach. Journal of Vascular Nursing, 16(4),81–85.

Caps, M. T., Meissner, M. H., Tullis, M. J., Polissar, N. L., Manzo, R. A.,Zierler, B. K., et al. (1999). Venous thrombus stability during acutephase of therapy. Vascular Medicine, 4(1), 9–14.

Finkelmeier, B. A. (1997). Dissection of the aorta: A clinical update.Journal of Vascular Nursing, 15(3), 88–93.

Frost-Rude, J. A., Nunnelee, J. D., & Spaner, S. (2000). Buerger’s dis-ease. Journal of Vascular Nursing, 18(4), 128–130.

Gramse, C. A., Hingorani, A., & Ascher, E. (2001). Postoperative anti-coagulation in vascular surgery: Part 1. A retrospective comparisonof clinical outcomes for unfractionated heparin versus low-molecular-weight heparin. Journal of Vascular Nursing, 19(2), 42–49.

Hirsch, A. T., Criqui, M. H., Treat-Jacobson, D., Regensteiner, J. G.,Creager, M. A., Olin, J. W., et al. (2001). Peripheral arterial diseasedetection, awareness, and treatment in primary care. Journal of theAmerican Medical Association, 286(11), 1317–1324.

Johnson, M. T. (1997). Treatment and prevention of varicose veins.Journal of Vascular Nursing, 15(3), 97–103.

Kaufman, M. W., & All, A. C. (1996). Raynaud’s disease: Patient edu-cation as a primary nursing intervention. Journal of Vascular Nursing,14(2), 34–39.

Kowallek, D. L., & DePalma, R. G. (1997). Venous ulceration: Activeapproaches to treatment. Journal of Vascular Nursing, 15(2), 50–57.

Krauss, R. M., Eckel, R. H., Howard, B., Appel, L. J., Daniels, S. R.,Deckelbaum, R. J., et al. (2000). AHA dietary guidelines. Revision2000: A statement for healthcare professionals from the NutritionCommittee of the American Heart Association. Circulation, 102(18),2284–2299.

Lacey, K. O. (1996). Subclavian steal syndrome: A review. Journal ofVascular Nursing, 14(1), 1–7.

Lombardo, K. M. (1997). Endovascular grafting of abdominal aorticaneurysms. Journal of Vascular Nursing, 15(3), 83–87.

Mawhorter, S. D. (2000). Nonhealing cellulitis in a 54-year-old man withdiabetes mellitus. Cleveland Clinic Journal of Medicine, 67(1), 21–24.

McAlister, F. A., Levine, M., Zarnke, K. B., Campbell, N., Lewanczuk, R.,Leenen, F., et al. (2001). The 2000 Canadian recommendations forthe management of hypertension: Part 1. Therapy. Canadian Journalof Cardiology, 17(5), 543–559.

Meissner, M. H., Caps, M. T., Zierler, B. F., Bergelin, R. O., Manzo,R. A., Stradnes, D. E., Jr. (2000). Deep venous thrombosis andsuperficial venous reflux. Journal of Vascular Surgery, 32(1), 48–56.

Critical Thinking Exercises

1. Your patient has been diagnosed with an enlarging ab-dominal aortic aneurysm (AAA). The physician gives thepatient two surgical options: repair of the AAA using anendovascular graft or open surgical repair. What factorswould you include in discussing the surgical options, post-operative care, continuing care, and home care? If thepatient is taking warfarin (Coumadin) for atrial fibrillationand insulin for diabetes, how would you incorporate thesefactors into the plan of care?

2. Your 96-year-old patient presents with a 1-year historyof experiencing symptoms of claudication after walking fouror five blocks. The patient lives alone, six blocks from thelocal shopping area, and no longer drives a vehicle. Thepatient does not wish to undergo surgery at this time andwants to continue living at his current location. Whatoptions would you discuss with the patient? If this patientalso had a nonhealing foot wound and had smoked twopacks of cigarettes each day for the past 80 years, how wouldyour plan of care change?

3. Your patient has been diagnosed with deep vein throm-bosis of a calf. The physician gives the patient two treatmentoptions: hospitalization with intravenous sodium heparintherapy or home treatment with LMWH. What factorswould you include in discussing the treatment options withthe patient?

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REFERENCES AND SELECTED READINGS

BooksBickely, L. S., & Szilagyi, P. G. (2003). Bates’ guide to physical examina-

tion and history taking (8th ed.). Philadelphia: Lippincott Williams& Wilkins.

Bullock, B., & Henze R. (1999). Focus on pathophysiology (4th ed.).Philadelphia: Lippincott Williams & Wilkins.

Coleman, R. W., Hirsch, J., Marder, V. J., Clowes, A. W., George, J. N.(2000). Hemostasis and thrombosis: Basic principles and clinical prac-tice (4th ed.). Philadelphia: Lippincot Williams & Wilkins.

Fahey, V. (1999). Vascular nursing (3rd ed.). Philadelphia: W. B. Saunders.Gloviczki, P., & Yao, J. T. (2001). Handbook of venous disorders—

Guidelines of the American Venous Forum (2nd ed.). New York:Oxford University Press.

Guyton, A., & Hall, J. (2000). Textbook of medical physiology (10th ed.).Philadelphia: W. B. Saunders.

Moser, M. (1999). World Health Organization-International Society ofHypertension guidelines for the management of hypertension—Dothese differ from the U.S. recommendations? Which guidelinesshould the practicing physician follow? Journal of Clinical Hyper-tension, 1, 48–54.

O’Connor, C. M. (2001). Raynaud’s phenomenon. Journal of VascularNursing, 19(3), 87–92.

Phillips, L. (2000). Putting a damper on cellulitis. Nursing, 30(12),52–53.

Rudolph, D. (2001). Standards of care for venous leg ulcers: Compres-sion therapy and moist wound healing. Journal of Vascular Nursing,19(1), 20–27.

Stevens, S. L. (2000). Heparin-induced thrombocytopenia. Journal ofVascular Nursing, 18(2), 54–58.

Strider, D., Robinson, T., Guarini, J., Ivey, J. (1996). Challenges withTakayasu’s arteritis: A case study. Journal of Vascular Nursing, 14(1),12–17.

Verta, K. F., & Verta, M. J. (1998). Alternative imaging techniques invascular surgery. Journal of Vascular Nursing, 16(4), 78–83.

Vogeley, C. L., & Coeling, H. (2000). Prevention of venous ulcerationby use of compression after deep vein thrombosis. Journal of VascularNursing, 18(4), 123–127.

Zierler, R. E. (1999). Vascular surgery without arteriography: use ofDuplex ultrasound. Cardiovascular Surgery, 7(1), 74–82.

RESOURCES AND WEBSITES

Agency for Healthcare Research and Quality, Public Health Service,U.S. Department of Health and Human Services, National GuidelineClearinghouse, P.O. Box 8547, Silver Spring, MD 20907; 1-800-358-9295; http://www.ahrq.gov and http://www.guideline.gov.

American Venous Forum, 13 Elm Street, Manchester, MA 01944; 978-526-8330; http://www.venous-info.com.

National Heart, Lung, and Blood Institute, Health Information Center,P.O. Box 30105, Bethesda, MD 20824-0105; 301-592-8573; http://www. nhlbi.nih.gov.

Society for Vascular Surgery, 13 Elm Street, Manchester, MA 01944-1314; 978-526-8330; http://www.vascularweb.org.

Society of Vascular Nursing, 7794 Grow Drive, Pensacola, FL 32514;888-536-4786; http://www.svnnet.org.

Society of Vascular Ultrasound, 4601 Presidents Drive, Suite 260,Lanham, MD 20706-4831; 301-459-7550; http://www.svtnet.org.

Vascular Disease Foundation, 3333 S. Wadsworth Boulevard, #B104-37,Lakewood, CO 80227; 1-866-723-4636; http://www.vdf.org.


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