41
Vascular Disorders
Kimberly Day
http://evolve.elsevier.com/Lewis/medsurg/
CONCEPTUAL FOCUS
Glucose Regulation
Perfusion
Tissue Integrity
LEARNING OUTCOMES
1.Relate the etiology and pathophysiology of peripheral
artery disease (PAD) to the major risk factors.
2.Describe the clinical manifestations and interprofessional
and nursing management of the patient with PAD of the
lower extremities
3.Plan appropriate nursing and interprofessional management
for the patient with acute arterial ischemic disorders
4.Distinguish the pathophysiology, clinical manifestations,
and nursing and interprofessional management of the
patient with thromboangiitis obliterans (Buerger disease)
and Raynaud phenomenon.
5.Distinguish the pathophysiology, clinical manifestations,
and interprofessional and nursing management of patients
with different types of aortic aneurysms.
6.Select appropriate nursing interventions for a patient
undergoing an aortic aneurysm repair.
7.Describe the pathophysiology, clinical manifestations, and
interprofessional and nursing management of the patient
with aortic dissection.
8.Evaluate the patient’s risk factors for developing
superficial vein thrombosis or venous thromboembolism
(VTE).
9.Distinguish between the clinical characteristics of
superficial vein thrombosis and VTE.
10.Outline the interprofessional and nursing management of
patients with superficial vein thrombosis and VTE.
11.Prioritize the key aspects of nursing management for the
patient receiving anticoagulant therapy.
12.Relate the pathophysiology and clinical manifestations
to the interprofessional care of patients with varicose
veins, chronic venous insufficiency, and venous leg
ulcers.
KEY TERMS
acute arterial ischemia
aneurysm
aortic dissection
chronic venous insufficiency (CVI)
critical limb ischemia
deep vein thrombosis (DVT)
intermittent claudication
peripheral artery disease (PAD)
post-thrombotic syndrome (PTS)
superficial vein thrombosis
thromboangiitis obliterans (Buerger disease)
varicose veins
venous thromboembolism (VTE)
venous thrombosis
Virchow’s triad
Vascular system problems include disorders of the arteries, veins,
and lymphatic vessels. These problems can result in decreased
perfusion and ischemia of the peripheral tissues. Patients often
have pain and difficulties with mobility and activities of daily
living. Education is a key part of management. Proper nutrition,
smoking cessation, and exercise are important health promotion behaviors. Following measures to promote safety, especially
for those on anticoagulant therapy, is critical.
We classify arterial disorders as atherosclerotic, aneurysmal,
and nonatherosclerotic vascular diseases. Atherosclerotic vascular
disease is divided into coronary, cerebral, peripheral, mesenteric,
and renal artery disease.1 This chapter discusses peripheral artery
disease, aortic aneurysm and dissection, and venous diseases.
932
PERIPHERAL ARTERY DISEASE
Peripheral artery disease (PAD) involves thickening of artery
walls. This results in a progressive narrowing of the arteries of
the upper and lower extremities. PAD prevalence increases with
age. It typically becomes symptomatic between ages 50 and 70
CHAPTER 41
years. In people with diabetes, PAD occurs earlier. In the United
States, about 8.5 million people over age 40 have PAD. The prevalence is highest in Blacks.2,3
PAD is strongly related to other types of cardiovascular disease
(CVD) and their risk factors. Patients with PAD have a significantly higher risk for general mortality, CVD mortality, major
coronary events, and stroke.3 PAD is a marker of advanced systemic atherosclerosis. Patients with PAD are more likely to have
coronary artery disease (CAD) and/or cerebral artery disease.
Unfortunately, many people in the United States are unaware
of PAD and its risk factors. PAD remains underdiagnosed and
undertreated.
Etiology and Pathophysiology
The leading cause of PAD is atherosclerosis. It is a gradual thickening of the intima (the innermost layer of the arterial wall) and
media (middle layer of the arterial wall). This results from cholesterol and lipids deposited within the vessel walls, leading to
narrowing of the artery (see Fig. 37.1). Although we do not know
the exact cause of atherosclerosis, inflammation and endothelial
injury play a major role (see Chapter 37). Atherosclerosis often
affects certain segments of the arterial tree. These include the
coronary, carotid (see Chapter 62), and lower extremity arteries.
Symptoms occur when vessels are 60% to 75% blocked.
Other risk factors for PAD are similar, but not identical, to
those for CAD. Key risk factors for PAD are tobacco use (most
important), diabetes, hypertension, high cholesterol, and age
over 60 (Box 41.1).2 Having multiple risk factors dramatically
increases the risk for PAD.
BIOLOGIC SEX
CONSIDERATIONS
BOX 41.1
Vascular Disorders
Men
• Thromboangiitis obliterans (Buerger disease) occurs most often in men
younger than 40 years of age
• Abdominal aortic aneurysms (AAAs) and aortic dissections are more common in men
• Men with AAAs are more likely to undergo endovascular aneurysm repair
or open aneurysm repair
• Sexual problems are common after aortic surgery.
Women
• Women with PAD have poorer social functioning and higher rates of
depression than men with PAD4
• Women with PAD have faster functional decline and greater mobility loss
than men with PAD
• Raynaud’s phenomenon occurs mainly in women between 15 and 40 years
of age.
• Risk for VTE is greater in women over age 35 who use tobacco and oral contraceptives or oral hormone therapy, are pregnant or postpartum, or have a
family history of VTE
• Primary varicose veins are more common and more symptomatic in women
• Women with AAAs are at higher risk for rupture
• In-hospital mortality is higher in women undergoing revascularization
• Women have more graft thrombosis and amputation after lower extremity
bypass surgery
Vascular Disorders
933
PERIPHERAL ARTERY DISEASE OF THE LOWER
EXTREMITIES
Lower extremity PAD may affect the iliac, femoral, popliteal,
tibial, or peroneal arteries, or any combination of these arteries
(Fig. 41.1). The femoral popliteal area is the most common site
in patients without diabetes. Those with diabetes tend to develop
PAD in the arteries below the knee. Those with advanced PAD
often have multiple arterial occlusions.
Clinical Manifestations
The severity of PAD symptoms depends on the site and extent of
the blockage and the amount of collateral circulation. The classic
symptom of lower extremity PAD is intermittent claudication.
This ischemic muscle pain is caused by exercise, resolves within
10 minutes or less with rest, and is reproducible. The pain is due
to the buildup of lactic acid from anaerobic metabolism. Once
the patient stops exercising, the lactic acid clears, and the pain
subsides. PAD of the iliac arteries causes pain in the buttocks
and thighs. Calf pain occurs with femoral or popliteal artery
involvement.
As many as one-third of patients with PAD have classic
symptoms. Others have no symptoms or present with atypical leg symptoms (e.g., burning, heaviness, pressure, soreness,
tightness, weakness) in atypical locations (e.g., ankle, foot, hamstring, hip, knee, shin). PAD involving the internal iliac arteries
may result in erectile dysfunction.
Paresthesia (numbness or tingling) in the toes or feet may
result from nerve tissue ischemia. True peripheral neuropathy
occurs more often in patients with diabetes and in those with
long-standing ischemia. Neuropathy causes severe shooting
Superior
mesenteric
artery
Abdominal
aorta
Internal
iliac
artery
Celiac artery
Renal artery
Common
iliac artery
External
iliac artery
Deep
femoral artery
Superficial
femoral artery
Popliteal
artery
Anterior
tibial artery
Peroneal artery
Posterior
tibial artery
Fig. 41.1 Common anatomic locations of atherosclerotic lesions
(shown in yellow) of the abdominal aorta and lower extremities.
934
SECTION 8
Problems of Oxygenation: Perfusion
or burning pain in the extremity. It does not follow particular
nerve roots and may be present near ulcerated areas. Gradual,
reduced blood flow to neurons causes loss of sensation to pressure and deep pain. So, patients may not notice lower extremity
injuries.
The limb’s appearance gives vital information about reduced
blood flow. The skin becomes thin, shiny, and taut. The lower
legs lose their hair. Pedal, popliteal, or femoral pulses are
decreased or absent. Pallor (blanching of the foot) develops
when the leg is elevated (elevation pallor). Conversely, reactive
hyperemia (redness of the foot) develops when the limb is in a
dependent position (dependent rubor) (Table 41.1).
As PAD progresses and involves multiple arterial segments,
continuous pain develops at rest. Rest pain most often occurs in
the foot or toes. It is worse with limb elevation. Rest pain occurs
when blood flow does not meet basic metabolic needs of the
distal tissues. It occurs more often at night because cardiac output tends to drop during sleep and the limbs are at heart level.
Patients often try to relieve pain by gravity. They dangle the leg
over the side of the bed or sleep in a chair.
Critical limb ischemia (CLI) is a condition characterized by
chronic ischemic rest pain lasting more than 2 weeks, nonhealing arterial leg ulcers, or gangrene of the leg from PAD. Patients
with PAD who have diabetes, heart failure (HF), and a history
of a stroke have a higher risk for CLI.3
Comparison of Peripheral
Artery and Venous Disease
Diagnostic Studies
TABLE 41.1
Characteristic
Ankle-brachial
index
Capillary refill
Dermatitis
Edema
Hair
Peripheral Artery
Disease
Venous Disease
≤0.90
>0.90
>3 sec
Rarely occurs
Absent unless leg constantly
in dependent position
Loss of hair on legs, feet, toes
<3 sec
Often occurs
Lower leg edema
Nails
Pain
Thickened, brittle
Intermittent claudication or
rest pain in foot
Ulcer may or may not be painful
Peripheral pulses Decreased or absent
Pruritus
Skin color
Rarely occurs
Dependent rubor, elevation
pallor
Skin temperature Cool, temperature gradient
down the leg
Thin, shiny, taut
Skin texture
Ulcer
• Location
• Margin
• Drainage
• Tissue
Tips of toes, foot, or lateral
malleolus
Rounded, smooth, looks
“punched out”
Minimal
Black eschar or pale pink
granulation
Hair may be present
or absent
Normal or thickened
Dull ache or heaviness
in calf or thigh
Ulcer often painful
Present, may be hard to
palpate with edema
Often occurs
Bronze-brown
pigmentation
Varicose veins may be
visible
Warm, no temperature
gradient
Skin thick, hardened,
and indurated
Near medial malleolus
Irregularly shaped
Moderate to large
amount
Yellow slough or
dark red, “ruddy”
granulation
Complications
Lower extremity PAD progresses slowly. Prolonged ischemia
leads to atrophy of the skin and underlying muscles. Minor
trauma to the feet (e.g., stubbing one’s toe, blister from shoes)
can result in delayed healing, wound infection, and tissue
necrosis, especially in the patient with diabetes. Arterial (ischemic) ulcers most often occur over bony prominences on the
toes, feet, and lower legs (Table 41.1). Nonhealing arterial ulcers
and gangrene are the most serious complications. If PAD develops over an extended period, collateral circulation may prevent
gangrene.
Amputation may be needed if adequate blood flow is not
restored or if severe infection occurs. Uncontrolled pain and
severe, spreading infection are indicators for amputation in
people who are not candidates for revascularization.
Various tests assess blood flow and the vascular system (Table
41.2). Doppler ultrasound with duplex imaging maps blood
flow throughout an entire arterial region. It can determine the
degree of blood flow when we have difficulty palpating a peripheral pulse due to severe PAD.
Segmental BPs are obtained using Doppler ultrasound and a
sphygmomanometer at the thigh, below the knee, and at ankle
level while the patient is supine. A drop in segmental BP of
greater than 30 mm Hg suggests PAD. Angiography and magnetic resonance angiography show the location and extent of
PAD (see Table 35.10).
The ankle-brachial index (ABI) is a PAD screening tool. It is
done using a hand-held Doppler. Calculate the ABI for each leg
by dividing the ankle systolic BP (SBP) by the higher of the brachial SBPs. PAD guidelines recommend uniform reporting of
ABI results (Table 41.3).3 Calcified and stiff arteries in patients
who are older or have diabetes often show a falsely elevated ABI.
Interprofessional Care
Table 41.2 outlines the interprofessional care for a patient with
PAD.
Risk Factor Modification
The first treatment goal for patients with PAD is to reduce CVD
risk factors. This may require both lifestyle changes and drug
therapy (see Tables 37.2 to 37.6). Hypertension is a well-known
risk factor for PAD progression. Encourage reducing sodium
intake and following the dietary approaches to stop hypertension (DASH) or Mediterranean diet. Chapter 36 discusses
hypertension.
Tobacco cessation is essential to reduce the risk for CVD
events, PAD progression, and death. This is a difficult process
with a high incidence of relapse. Suggest tobacco cessation strategies (see Tables 11.3–11.6).
CHAPTER 41
TABLE 41.2 Interprofessional Care
Peripheral Artery Disease
Diagnostic Assessment
• Health history and physical assessment, including palpation of peripheral pulses
• Doppler ultrasound studies
• Segmental BPs
• ABI (Table 41.3)
• Duplex imaging
• Angiography
• Magnetic resonance angiography
Management
• CVD risk factor modification
• Tobacco cessation
• Regular physical exercise
• Achieve or maintain ideal body weight
• Follow Dietary Approaches to Stop Hypertension (DASH) diet or Mediterranean diet
• Tight glucose control with diabetes, including Hb A1C monitoring
• Tight BP control
• Treatment of hyperlipidemia and hypertriglyceridemia (see Table 37.6)
• Antiplatelet agent (aspirin, clopidogrel [Plavix])
• ACE inhibitors (see Table 36.6)
• Treatment of claudication symptoms
• Structured walking or exercise program
• Cilostazol or pentoxifylline
• Nutrition therapy
• Physical/occupational therapy
• Proper foot care (see Table 53.23)
Surgical Therapy
• Percutaneous transluminal balloon angioplasty with or without stent
• Percutaneous transluminal atherectomy
• Percutaneous transluminal cryoplasty
• Peripheral artery bypass surgery
• Patch graft angioplasty, often in conjunction with bypass surgery
• Endarterectomy (for localized stenosis; rarely done as a stand-alone procedure)
• Thrombolytic therapy or mechanical clot extraction therapy (for acute
ischemia only)
• Sympathectomy (for pain management only)
• Amputation
TABLE 41.3
Index Results
Interpreting Ankle-Brachial
(ABI
Clinical Significance
>1.30
1.00–1.30
0.91–0.99
≤0.90
Noncompressible arteries
Normal ABI
Borderline ABI
Abnormal ABI
Classification of PAD Severity
0.90–0.71
Mild PAD
0.70–0.41
Moderate PAD
≤0.40
Severe PAD
Diabetes is a major risk factor for PAD. It increases the risk
for amputation. Patients with diabetes should maintain a glycosylated hemoglobin (A1C) below 7.0%.5 Chapter 53 discusses
diabetes.
Vascular Disorders
935
Support aggressive lipid management for all patients with
PAD. Both diet interventions and drug therapy are needed.
Statins (e.g., simvastatin) and a fibric acid derivative (gemfibrozil) may be used (see Table 37.6).
Drug Therapy
Angiotensin-converting enzyme (ACE) inhibitors (e.g., ramipril) can reduce PAD symptoms. Antiplatelet agents are
critical to reduce the risks for CVD events and death. Oral
antiplatelet therapy should include low-dose aspirin therapy.
Aspirin-intolerant patients may take clopidogrel (Plavix) daily.
Combination antiplatelet therapy with aspirin and clopidogrel
may be used by select high-risk patients. Anticoagulants (e.g.,
warfarin) are not recommended for preventing CVD events in
patients with PAD.
DRUG ALERT
Clopidogrel (Plavix) and Omeprazole (Prilosec)
• Taking omeprazole with clopidogrel reduces the antiplatelet effect by half.
• This reduced effect increases the risk for myocardial infarction (MI) and
stroke.
Two drugs are available to treat intermittent claudication:
cilostazol and pentoxifylline. Cilostazol—a phosphodiesterase
inhibitor—inhibits platelet aggregation and increases vasodilation. Pentoxifylline—a synthetic dimethylxanthine derivative—improves the flexibility of RBCs and decreases fibrinogen
concentration, platelet adhesiveness, and blood viscosity. It is
not as effective as cilostazol. Most take cilostazol less than 3
months due to side effects.3
DRUG ALERT
Cilostazol
• Contraindicated in patients with HF.
Exercise Therapy
A supervised exercise program is recommended as part of the
initial treatment for all patients with intermittent claudication. The patient should exercise for 30 to 45 min/day, at least
3 times/week, for a minimum of 3 months. Although we most
often prescribe walking, other modes of exercise (e.g., cycling)
improve walking ability and quality of life.3
Encouraging exercise is especially important for women,
because they have faster functional decline and greater mobility loss than men with PAD. Overall, patients with PAD who
have higher levels of daily physical activity have better survival
rates.3,4
Nutrition Therapy
Teach patients with PAD to maintain a body mass index (BMI)
less than 25 kg/m2 and a waist circumference less than 40 inches
for men and less than 35 inches for women. Even modest, sustained weight loss of 3% to 5% yields important reductions in
triglycerides, glucose, A1C, and the risk for developing type 2
936
SECTION 8
Problems of Oxygenation: Perfusion
diabetes. Greater weight loss has greater benefits. Recommend a
diet reduced in calories and salt for obese or overweight persons.
Care of the Patient With Critical Limb Ischemia
Optimal therapy for the patient with CLI is revascularization via
bypass surgery using an autogenous (native) vein. An alternative is percutaneous transluminal angioplasty (PTA).3 Patients
with CLI who are not candidates for surgery or PTA may receive
IV prostanoids (e.g., iloprost [Ventavis]).6,7 However, the FDA
has not approved this drug for CLI treatment. Patients with CLI
should continue optimal drug therapy (e.g., statin, antiplatelet,
ACE inhibitor, β-blocker) to reduce the risk for a CVD event.
Conservative management includes protecting the extremity
from trauma, decreasing ischemic pain, preventing and controlling infection, and improving perfusion. Carefully inspect,
cleanse, and lubricate feet to prevent skin cracking and infection.
Avoid lubrication between the toes and soaking the patient’s feet
to prevent skin maceration (or breakdown). Keep the affected
foot clean and dry. Cover any ulcers with a dry, sterile dressing.
We use a variety of wound care products to treat deep ulcers.
Healing is unlikely without increasing the blood flow.
Encourage the patient to wear soft, roomy, and protective footwear and avoid extremes of heat and cold. Keep the patient’s heels
free of pressure. Place a pillow under the calves so that the heels
are off the mattress or use a heel protection device. Giving analgesics and placing the bed in the reverse Trendelenburg position
may control pain and increase perfusion to the lower extremities.
Spinal cord stimulation may help manage pain for patients
with CLI. Other promising strategies include growth factors
and gene and stem cell therapy to stimulate blood vessel growth
(angiogenesis). Unfortunately, almost half of the patients with
CLI will die within 5 years.7
Interventional Radiology Catheter-Based Procedures
Interventional radiology catheter-based procedures are alternatives to surgery for treating lower extremity PAD. These
procedures take place in a catheterization. They are similar to
angiography in that they involve inserting a specialized catheter
into the femoral artery. The PTA procedure uses a catheter with
a balloon at the tip. The tip of the catheter is moved to the narrowed (stenotic) area of the artery. The balloon is then inflated,
compressing the atherosclerotic intimal lining.3
Stents—expandable metallic devices—are placed within the
artery after the balloon angioplasty. The stent holds the artery
open. Angioplasty balloons and peripheral stents may be coated
with a drug (e.g., paclitaxel) to limit new tissue growth in the
treated area and improve long-term patency rates.3
Atherectomy is the removal of the obstructing plaque. A directional atherectomy device uses a high-speed cutting disk that cuts
long strips of the atheroma. Laser atherectomy uses ultraviolet
energy to break up the atheroma. Another type of atherectomy catheter has a diamond-coated tip that rotates at a high speed like a drill.
Cryoplasty combines PTA and cold therapy. A specialized
balloon is filled with liquid nitrous oxide, which changes to gas
as it enters the balloon. Expansion of the gas results in cooling to 14°F (−10°C). The cold temperature limits restenosis by
reducing smooth muscle cell activity.
A
Bypass graft
using
autogenous
(native) vein
Bypass graft using
synthetic graft
Superficial
femoral
artery
Popliteal
artery
Superficial
femoral
artery
Popliteal
artery
Anterior
tibial artery
Anterior
tibial artery
Peroneal
artery
Posterior
tibial artery
Peroneal
artery
Posterior
tibial artery
B
Fig. 41.2 (A) Femoral-popliteal bypass graft around an occluded superficial femoral artery. (B) Femoral–posterior tibial bypass graft around
occluded superficial femoral, popliteal, and proximal tibial arteries.
Nursing care is the same as for diagnostic angiography (see
Tables 35.10 and 35.12). Antiplatelet agents are given afterwards
to reduce the risk for restenosis. Long-term, low-dose aspirin
therapy or clopidogrel is recommended.
Surgical Therapy
Various surgical approaches are used to improve blood flow
beyond a blocked artery. When possible, peripheral artery
bypass surgery is done with an autogenous vein to bypass (carry
blood around) the lesion (Fig. 41.2). Synthetic grafts are used
for long routes, such as an axillary-femoral bypass. When a
person’s own vein is not available, a human umbilical vein or
a composite sequential bypass graft (native vein plus synthetic
graft) can be used.3 PTA with stenting may be done in combination with bypass surgery.
Other options include endarterectomy (opening the artery
and removing the obstructing plaque) and patch graft angioplasty (opening the artery, removing plaque, and sewing a
patch to the opening to widen the lumen). In-hospital mortality is higher in women undergoing revascularization than men,
regardless of disease severity or surgical procedure.4
Amputation may be needed if tissue necrosis is extensive,
gangrene or osteomyelitis develops, or all major arteries in the
limb are blocked. Preserving as much of the limb as possible
improves rehabilitation potential. Amputation is discussed in
Chapter 67.
NURSING MANAGEMENT: LOWER EXTREMITY
PERIPHERAL ARTERY DISEASE
Assessment
Table 41.4 presents subjective and objective data that you should
obtain from a patient with PAD.
CHAPTER 41
TABLE 41.4 NURSING ASSESSMENT
Peripheral Artery Disease
Subjective Data
Important Health Information
Health history: Tobacco use, diabetes, hypertension, hyperlipidemia, hypertriglyceridemia, hyperuricemia, impaired renal function, obesity. ↑ High-sensitivity C-reactive protein, homocysteine, or lipoprotein (a) [Lp(a)] levels.
Positive family history, sedentary lifestyle, stress
Functional Health Patterns
Health perception–health management: Family history of CVD. Tobacco use,
including exposure to environmental smoke
Nutritional-metabolic: High sodium, saturated fat, and cholesterol intake. Elevated Hb A1C
Activity-exercise: Exercise intolerance
Cognitive-perceptual: Buttock, thigh, or calf pain that is precipitated by exercise and that subsides with rest (intermittent claudication) or progresses
to pain at rest. Burning pain in feet and toes at rest. Numbness, tingling,
sensation of cold in legs or feet. Progressive loss of sensation and deep
pain in extremities
Sexuality-reproductive: Erectile dysfunction
Objective Data
Cardiovascular
Decreased or absent peripheral pulses. Feet cool to touch. Capillary refill >3 s.
Bruits may be present at pulse sites
Neurologic
Impaired mobility or sensation
Skin
Loss of hair on legs and feet. Thick toenails. Pallor with elevation. Dependent
rubor. Thin, cool, shiny skin with muscle atrophy. Skin breakdown and arterial ulcers, especially over bony areas. Gangrene
Possible Diagnostic Findings
Arterial stenosis evident with duplex imaging, ↓ Doppler pressures, ↓ ABI, angiography shows peripheral atherosclerosis
Clinical Problems
Clinical problems for the patient with PAD may include:
• Activity intolerance
• Impaired tissue integrity
• Inadequate tissue perfusion
• Musculoskeletal problem
• Pain
Additional information on clinical problems and interventions for the patient with PAD of the lower extremities is
presented in eNursing Care Plan 41.1 on the website for this
chapter.
Planning
Nursing care focuses on the priority problems of poor tissue
perfusion and pain. The overall goals for the patient who has
lower extremity PAD include (1) adequate tissue perfusion; (2)
pain relief; (3) increased exercise tolerance; (4) intact, healthy
skin on the extremities; and (5) knowledge of disease and treatment plan.
Vascular Disorders
937
Implementation
Health Promotion
Assess the patient for and provide instructions on how to control CVD risk factors (see Table 37.2). Teach diet modification
to reduce cholesterol, saturated fat, and salt (see Tables 37.4 and
37.5). Teach proper foot care and injury prevention. Encourage
patients with positive family histories of cardiac, diabetes, or
vascular disease to obtain regular follow-up care.
Acute Care
After surgical or radiologic intervention, observe the patient in
a recovery area. Check the operative extremity every 15 minutes initially and then hourly. Assess color, temperature, capillary refill, peripheral pulses, and sensation and movement.
Immediately notify the HCP of any loss of palpable pulses or
change in the Doppler sound over a pulse. We do not obtain
postoperative ABI measurements as they place the patient at
risk for graft thrombosis. Compare assessment findings with the
patient’s baseline and with findings in the opposite limb.
PAD patients with a history of chronic ischemic rest pain
may have tolerance to opioids. Thus, aggressive pain management may be needed after surgery.
After the patient leaves the recovery area, continue to monitor extremity perfusion. Assess for complications, such as bleeding, hematoma, thrombosis, embolization, and compartment
syndrome. A dramatic increase in pain, loss of previously palpable pulses, extremity pallor or cyanosis, numbness or tingling,
or a cold extremity suggests graft or stent blockage. Report these
findings to the HCP at once.
CHECK YOUR PRACTICE
You are caring for a 74-year-old male patient who is recovering from left femoral-popliteal bypass graft surgery. When you respond to the patient’s call
bell, the patient reports severe pain in the operative leg. On assessment, you
cannot palpate the dorsalis pedis and posterior tibial pulses. The foot is cold
to touch.
• What are your next actions?
Do not place the patient in a knee-flexed position except
for exercise. Turn the patient and position frequently with pillows to support the incision. On postoperative day 1, assist the
patient out of bed several times. Walking even short distances
is desirable. A walker may be helpful, especially for frail, older
patients. Discourage prolonged sitting with legs lowered, since it
may cause pain and edema, increase the risk for venous thrombosis, and place stress on the suture lines. Graduated compression stockings may help control leg edema. If edema develops,
position the patient supine, and elevate the leg above heart level.
Surgical site infection (SSI) is a serious complication. Careful
postoperative assessment and wound care are important. SSIs
are associated with early graft loss, longer hospitalization, reoperation, and sepsis.
Ambulatory Care
Assess for CVD risk factors and teach health promotion strategies. Continued tobacco use dramatically decreases the patency
rates of grafts and stents and increases the risk for an MI or stroke.
938
SECTION 8
Problems of Oxygenation: Perfusion
Long-term antiplatelet therapy with aspirin or clopidogrel is
used after surgery. Patients having distal peripheral bypass surgery (i.e., below the knee) using synthetic graft materials receive
dual antiplatelet therapy (clopidogrel plus aspirin) for 1 to 3
months, followed by lifelong single antiplatelet therapy.
Encourage supervised exercise training after revascularization. Explain that exercise decreases CVD risk factors, including hypertension, hyperlipidemia, obesity, and glucose levels.
Foot care is especially important in the patient with diabetes
and PAD (see Table 53.21). Diabetic neuropathy increases the
patient’s risk for injury. Tell patients to inspect their legs and feet
daily for changes in skin color or texture. Show patients how to
palpate pulses and check skin temperature and capillary refill.
Stress reporting any changes or the presence of ulceration or
inflammation to the HCP.
Thick or overgrown toenails and calluses are potentially
serious and need regular attention by an HCP (e.g., podiatrist).
Patients who have poor eyesight, back problems, obesity, or
arthritis may need help with foot care. Encourage patients to wear
clean, all-cotton or all-wool socks and comfortable shoes with
rounded (not pointed) toes and soft insoles. Tell patients to lace
shoes loosely and to break in new shoes gradually (Table 41.5).
TABLE 41.5 PATIENT & CAREGIVER
TEACHING
Peripheral Artery Bypass Surgery
Include the following information in the teaching plan for a patient undergoing
peripheral artery bypass surgery and the patient’s caregiver:
1.Reduce risk factors by stopping tobacco use, controlling blood glucose
levels with diabetes, controlling BP, lowering cholesterol and triglyceride levels, achieving or maintaining ideal body weight, and exercising
­regularly.
2.Provide teaching about the basic mechanism of action (why prescribed
for patient), side effects, and safety precautions for drugs such as
antiplatelets, antihypertensives, lipid-lowering therapy, and pain
­medication.
3.Eat healthy—it is essential to recovery. Drink plenty of fluids, eat a
well-balanced diet (e.g., foods high in protein, vitamins C and A, and zinc;
high-fiber foods; fresh fruits and vegetables), eat fewer high-fat foods,
and reduce salt intake.
4.Take part in a supervised exercise program or take a daily walk. In the
beginning, take several short walks a day and rest between activities.
Gradually increase your walking to 30 to 40 min/day, 3 to 5 days/week.
5.Care for feet and legs. Inspect feet and wash them daily. Wear clean
cotton or wool socks and well-fitting shoes. File toenails straight across.
Avoid sitting with legs crossed, extreme hot and cold temperatures, and
prolonged standing.
6.Follow routine postoperative wound care that includes keeping incision
clean and dry; do not disturb Steri-Strips (if present).
7.Monitor for signs and symptoms of impaired healing or infection of the
leg incision, and notify HCP if any of the following occur:
•Prolonged drainage or pus from the incision
•Increased redness, warmth, pain, or hardness along incision
•Separation of wound edges
•Temperature >100°F (37.8°C)
8.Keep all follow-up appointments with HCP.
9.Notify HCP at once of increased leg or foot pain or a change in the color
or temperature of leg or foot.
Evaluation
The expected outcomes are that a patient with PAD of the lower
extremities will have
• Adequate peripheral tissue perfusion
• Increased activity tolerance
• Effective pain management
• Knowledge of disease and treatment plan
ACUTE ARTERIAL ISCHEMIC DISORDERS
Etiology and Pathophysiology
Acute arterial ischemia is a sudden interruption in the arterial
blood supply to a tissue, an organ, or an extremity that—if left
untreated—can result in tissue death. It is caused by embolism,
thrombosis of an atherosclerotic artery, or trauma. Embolization
of a thrombus from the heart is the most frequent cause of
acute arterial occlusion. Heart conditions in which thrombi
can develop include infective endocarditis, mitral valve disease,
atrial fibrillation, cardiomyopathies, and prosthetic heart valves.
Noncardiac sources of emboli include aneurysms, ulcerated
atherosclerotic plaque, recent endovascular procedures, and
venous thrombi.
Thrombi that originate in the left side of the heart may dislodge and travel anywhere in the systemic circulation. Most
emboli block an artery of the leg where vessels branch (e.g.,
iliofemoral, popliteal, tibial) or narrow. Sudden local thrombosis
may occur at the site of an atherosclerotic plaque. Hypovolemia
(e.g., shock), hyperviscosity (e.g., polycythemia), and hypercoagulability (e.g., chemotherapy) predispose a person to thrombotic arterial occlusion.
Traumatic injury to an extremity may cause partial or total
arterial blockage. Acute arterial occlusion may develop from
arterial dissection in the carotid artery or aorta or from a procedure-related arterial injury (e.g., after angiography).
Clinical Manifestations
Manifestations of acute arterial ischemia include the 6 Ps: pain,
pallor, pulselessness, paresthesia, paralysis, and poikilothermia
(adaptation of the limb to the environmental temperature, most
often cool). If you detect these signs, immediately notify the
HCP. Without immediate intervention, ischemia may progress
to tissue necrosis and gangrene within a few hours.
Paralysis is a late sign of acute arterial ischemia and signals
the death of nerves supplying the extremity. Foot drop occurs
from nerve damage. Because nerve tissue is very sensitive to
hypoxia, limb paralysis or ischemic neuropathy may persist
even after revascularization.
Interprofessional Care
Early diagnosis and treatment are essential to keep the affected
limb viable during acute arterial ischemia. Anticoagulant therapy with IV unfractionated heparin (UH) is started to prevent
thrombus growth and inhibit further embolization. In patients
undergoing embolectomy, UH should be followed by long-term
anticoagulation.
To restore blood flow, the thrombus is removed as soon as possible. Options consist of surgical thrombectomy (recommended
CHAPTER 41
procedure), percutaneous catheter-directed thrombolytic therapy, percutaneous mechanical thrombectomy with or without
thrombolytic therapy, or surgical bypass.7
Percutaneous catheter-directed thrombolytic therapy using
alteplase or urokinase is recommended for acute arterial ischemia of less than 14 days. The HCP inserts a catheter into the
femoral artery and moves it to the site of the clot. The thrombolytic drug is continuously infused. Thrombolytics work by
directly dissolving the clot over a period of 24 to 48 hours.
(Chapter 37 discusses thrombolytic therapy.) Close monitoring
is required to make sure the catheter does not move and the
patient does not bleed from the catheter insertion site.
Surgical revascularization may be used in a patient with
trauma (e.g., lacerated artery) or with significant arterial blockage. Amputation is done for patients with ischemic rest pain
and tissue loss in those whom limb salvage is not possible. If
the patient is at risk for further embolization from a persistent
source (e.g., chronic atrial fibrillation), long-term anticoagulation is recommended.
THROMBOANGIITIS OBLITERANS
Thromboangiitis obliterans (Buerger’s disease) is a nonatherosclerotic, segmental, recurrent inflammatory disorder
of the small and medium arteries and veins of the arms and
legs. Cerebral, coronary, mesenteric, pulmonary, and/or renal
arteries are rarely involved. The disease occurs mostly in men
younger than 45 years of age with a long history of tobacco and/
or marijuana use without other CVD risk factors (e.g., hypertension, hyperlipidemia, diabetes).8
In the acute phase of Buerger disease, an inflammatory
thrombus blocks the vessel. Over time, the thrombus becomes
more organized and the inflammation in the vessel wall subsides.8 During the chronic phase, thrombosis and fibrosis in the
vessel cause tissue ischemia.
The symptoms of Buerger disease often are confused with
PAD and other autoimmune diseases (e.g., scleroderma).
Patients may have intermittent claudication of the feet, hands,
or arms. As the disease progresses, rest pain and ischemic ulcerations develop. Other signs and symptoms may include color
and temperature changes of the limbs, paresthesia, superficial
vein thrombosis, and cold sensitivity.
There are no laboratory or diagnostic tests specific to
Buerger disease. The diagnosis is based on age of onset; history;
symptoms; involvement of distal vessels; presence of ischemic
ulcerations; and exclusion of autoimmune disease, diabetes,
thrombophilia (inherited tendency to clot) and other sources of
emboli, such as atherosclerosis and aneurysm.8
The main treatment is the complete cessation of tobacco and
marijuana use in any form. Use of nicotine replacement products is contraindicated. Conservative management includes
avoiding limb exposure to cold temperatures, a supervised
walking program, antibiotics to treat any infected ulcers, and
analgesics to manage the ischemic pain. Teach patients to avoid
trauma to the extremities.
IV iloprost (Ventavis)—a prostaglandin analog that promotes
vasodilation—is used to manage rest pain, promote healing
Vascular Disorders
939
of ischemic ulcers, and decrease the need for amputation.8
Surgical options include lumbar sympathectomy (transection of
a nerve, ganglion, and/or plexus of the sympathetic nervous system), implanting a spinal cord stimulator, and bypass surgery.8
Sympathectomy and a spinal cord stimulator can improve distal
blood flow, reduce pain, and decrease the rate of amputation.
Neither alters the inflammatory process. Bypass surgery may be
used in select patients with severe ischemia. Stem cell therapy
promotes ulcer healing, new blood vessel formation, and nerve
cell regeneration.8
Painful ulcerations may require finger or toe amputations.
Amputation below the knee may be needed in severe cases. The
rate of amputation in those who continue tobacco or marijuana
use after diagnosis is much higher than in those who stop.
RAYNAUD’S PHENOMENON
Raynaud’s phenomenon is an episodic vasospastic disorder of
small cutaneous arteries, most often involving the fingers and
toes. It occurs more often in women, especially those between
15 and 40 years of age. The pathogenesis of Raynaud phenomenon is due to abnormalities in the vascular, intravascular, and
neuronal mechanisms that cause vasodilation.9,10
Raynaud’s phenomenon may occur in isolation (primary
Raynaud phenomenon) or with an underlying disease (e.g., thyroid conditions, scleroderma, systemic lupus erythematosus)
(secondary Raynaud phenomenon). Other contributing factors
include the use of vibrating machinery or work in cold environments, exposure to heavy metals (e.g., lead), and high homocysteine levels.
Diagnosis is based on persistent symptoms for at least 2
years. Patients with Raynaud phenomenon should have routine
follow-up to monitor for development of connective tissue or
autoimmune diseases.
Raynaud phenomenon is characterized by vasospasm-induced color changes (white, blue, and red) of fingers, toes, ears,
and nose. Decreased perfusion results in pallor (white). The
digits then appear cyanotic (bluish purple) (Fig. 41.3). These
changes are followed by rubor (red), a hyperemic response when
blood flow is restored. The patient usually describes coldness
Fig. 41.3 Raynaud’s phenomenon. (From James WD, Elston DM, Dirk
M: Andrews’ diseases of the skin clinical atlas, St Louis, 2018, Elsevier.)
940
SECTION 8
Problems of Oxygenation: Perfusion
and numbness in the vasoconstrictive phase. This is followed by
throbbing, aching pain, tingling, and swelling in the hyperemic
phase. An episode usually lasts only minutes but may last for
several hours. Triggers include cold exposure, emotional upsets,
tobacco use, and caffeine.
After frequent, prolonged attacks, the skin may become
thickened and the nails brittle. Complications include punctate
(small hole) lesions of the fingertips and superficial gangrenous
ulcers.
Patient teaching about preventing episodes is the focus of
nursing care. Tell patients to avoid temperature extremes and
wear loose, warm clothing as protection from the cold, including gloves when handling cold objects. Immersing hands in
warm water often decreases the vasospasm. The patient should
stop using all tobacco products and avoid caffeine and other
drugs that have vasoconstrictive effects (e.g., amphetamines,
ergotamine, pseudoephedrine). Suggest appropriate stress management strategies.
Sustained-release calcium channel blockers (e.g., nifedipine
[Procardia]) are the first-line drug therapy. They relax smooth
muscles of the arterioles by blocking the influx of calcium into
the cells. This reduces the frequency and severity of vasospastic attacks. If symptoms persist, other vasodilators (e.g., phosphodiesterase-5 inhibitors [sildenafil]) or topical nitroglycerin
2% ointment may be used.10 Calcium channel blockers can be
taken with nitroglycerin topical ointment. Phosphodiesterase-5
inhibitors are not used with topical nitroglycerin due to risk for
hypotension.
Prompt intervention is needed for patients with digital ulceration or critical ischemia. Treatment options include prostacyclin infusion therapy (e.g., iloprost), antibiotics, analgesics, and
surgical debridement of necrotic tissue. Botulinum toxin A
and statins may lessen the severity of Raynaud phenomenon.9
Sympathectomy is done only in severe cases refractory to medical treatment when digit survival is threatened.
important modifiable risk factor.11 The larger the aneurysm, the
greater is the risk for rupture.
Genetic Link
Both aortic aneurysm and aortic dissection have a strong
genetic component. The familial tendency is related to several
congenital anomalies. Examples include bicuspid aortic valve,
coarctation of the aorta, Turner syndrome, autosomal dominant
polycystic kidney disease, specific collagen defects (e.g., EhlersDanlos syndrome), and premature breakdown of vascular elastic tissue (e.g., Marfan syndrome).11
Classification
Aneurysms are classified as true or false aneurysms (Fig.
41.5A–C). A true aneurysm is one in which the wall of the artery
forms the aneurysm, with at least 1 vessel layer still intact. True
aneurysms are subdivided into fusiform and saccular types. A
fusiform aneurysm is circumferential and relatively uniform in
shape. A saccular aneurysm is pouchlike with a narrow neck
connecting the bulge to 1 side of the arterial wall.
A false aneurysm, or pseudoaneurysm, is not an aneurysm.
It is a disruption of all arterial wall layers with bleeding that
is contained by surrounding anatomic structures. False aneurysms may result from trauma, infection, peripheral artery
bypass graft surgery (at the site of the graft-to-artery anastomosis), or arterial leakage after removal of a cannula (e.g., femoral
artery catheter, intraaortic balloon pump).
Clinical Manifestations
Thoracic aortic aneurysms (TAAs) are often asymptomatic.
When present, symptoms include deep, diffuse chest pain that
may extend to the interscapular area. Ascending aorta and aortic arch aneurysms can cause (1) angina from decreased blood
flow to the coronary arteries; (2) transient ischemic attacks from
decreased blood flow to the carotid arteries; and (3) coughing,
AORTIC ANEURYSMS
The aorta is the largest artery. It supplies O2, nutrients, and blood
to all vital organs. One of the most common problems affecting
the aorta is an aneurysm, which is a permanent, localized outpouching or dilation of the vessel wall. Aneurysms occur more
often in men and in whites. The incidence increases with age.11
Aneurysms may occur in more than 1 location.
Etiology and Pathophysiology
Aortic aneurysms may involve the aortic arch and thoracic and/
or abdominal aorta. Three-fourths of aortic aneurysms occur in
the abdominal aorta (Fig. 41.4). Most abdominal aortic aneurysms (AAAs) occur below the renal arteries.
A variety of disorders are associated with aortic aneurysms.
The main causes are classified as degenerative, congenital, infectious, mechanical (e.g., penetrating or blunt trauma), or inflammatory (e.g., aortitis). Risk factors for aortic aneurysms include
age, male gender, hypertension, CAD, family history, tobacco
use, high cholesterol, lower extremity PAD, carotid artery
disease, previous stroke, and obesity. Tobacco use is the most
Fig. 41.4 Angiography showing fusiform abdominal aortic aneurysm. Note
calcification of the aortic wall (arrows) and extension of the aneurysm into
the common iliac arteries. (Courtesy Jo Menzoian, Boston, MA.)
CHAPTER 41
Fusiform area
Artery
Sacculated area
B
Ruptured area
Clot
Blood flow
C
Torn intima
D
941
resuscitation and immediate surgical repair are needed. For
patients admitted to the hospital with a ruptured AAA, in-hospital mortality is high at 53%.11
Artery
A
Vascular Disorders
Blood flow
Fig. 41.5 (A) True fusiform abdominal aortic aneurysm. (B) True saccular
aortic aneurysm. (C) False aneurysm, or pseudoaneurysm. (D) Aortic
dissection.
shortness of breath, hoarseness, and/or difficulty swallowing
from pressure on the laryngeal nerve. If the aneurysm presses
on the superior vena cava, decreased venous return can result
in jugular venous distention and edema of the face and arms.
AAAs are often asymptomatic. They are often found during
routine physical assessment or evaluation for another problem
(e.g., abdominal x-ray, CT scan). A pulsatile mass in the periumbilical area slightly to the left of the midline may be present.
Bruits may be auscultated over the aneurysm. Physical findings
may be hard to detect in obese persons.
AAA symptoms may mimic pain associated with abdominal
or back disorders. Compression of nearby anatomic structures
and nerves may cause symptoms, such as back pain, epigastric
discomfort, altered bowel elimination, and intermittent claudication. Sometimes, aneurysms spontaneously embolize plaque,
causing “blue toe syndrome” (patchy mottling of the feet and
toes in the presence of palpable pedal pulses).
Complications
Aneurysm rupture is more likely to occur in people who smoke
tobacco.11 If rupture occurs into the retroperitoneal space,
bleeding may be controlled by surrounding anatomic structures, preventing exsanguination and death. In this case, the
patient often has severe back pain. Back or flank bruising (Grey
Turner sign) may be present.
If rupture occurs into the thoracic or abdominal cavity,
patients can die from massive hemorrhage. The patient who
reaches the hospital will be in hypovolemic shock with tachycardia, hypotension, pale clammy skin, decreased urine output, altered level of consciousness, and abdominal tenderness.
Shock is discussed in Chapter 42. In this situation, simultaneous
Diagnostic Studies
Chest x-rays may reveal abnormal widening of the thoracic
aorta. An abdominal x-ray may show calcification within the
aortic wall. An ECG may rule out MI, since thoracic aneurysm
or dissection symptoms can mimic angina. Echocardiography
assesses the function of the aortic valve. Ultrasound is useful
for aneurysm screening and to monitor aneurysm size. A CT
scan or MRI can diagnose and assess the location and severity
of aneurysms. Angiography gives helpful information by using
contrast imaging to map the entire aortic system (see Table
35.10).
Interprofessional Care
The main goal of care is to prevent the rupture of an aneurysm. Early detection and prompt treatment are essential.
Conservative medical therapy of small, asymptomatic AAAs
(less than 5.4 cm) is the best practice.11 This consists of risk
factor modification (ceasing tobacco use, decreasing BP, optimizing lipid profile, gradually increasing physical activity).11
Patients should receive management for hypertension, hyperlipidemia, diabetes, and other CVD risk factors. A statin and
an ACE inhibitor may be prescribed. Those with small aneurysms—4.0 to 5.4 cm—should have monitoring of aneurysm
size using ultrasound or CT every 6 to 12 months. Ultrasound
monitoring every 3 years is done for patients with AAAs smaller
than 4.0 cm in diameter.
Surgical repair is recommended in patients with asymptomatic aneurysms 5.5 cm in diameter or larger. Surgical intervention may occur sooner if the patient has a genetic disorder (e.g.,
Marfan, Ehlers-Danlos syndrome), the aneurysm expands rapidly, the patient becomes symptomatic, or the risk for rupture
is high. A careful review of body systems is needed to identify
any comorbidities that affect the patient’s surgical risk. Existing
carotid or coronary artery blockages may be corrected before
aneurysm repair.
Surgical Therapy
For elective aneurysm repair surgery, the patient should be well
hydrated with normal electrolytes, coagulation, and hematocrit.
If the aneurysm ruptures, emergent surgery is required.
Open aneurysm repair (OAR) involves a large abdominal incision through which the surgeon (1) cuts into the diseased aortic
segment, (2) removes any thrombus or plaque, (3) sutures a synthetic graft to the aorta proximal and distal to the aneurysm, and
(4) sutures the native aortic wall around the graft to act as a protective cover (Fig. 41.6). For iliac artery aneurysms, a bifurcated
graft replaces the entire diseased segment. With saccular aneurysms, it may be possible to excise only the bulbous lesion and
repair the artery by primary closure (suturing the artery together)
or applying an autogenous or synthetic patch graft.
All OARs require aortic cross-clamping proximal and distal to the aneurysm. Most resections are done in 30 to 45 minutes. Then the clamps are removed, and blood flow is restored.
942
SECTION 8
Problems of Oxygenation: Perfusion
The risk for postoperative complications, such as acute kidney
injury, increases in patients who have OAR of AAAs above the
level of the renal arteries.
Endovascular graft procedure. Minimally invasive endo­
vascular aneurysm repair (EVAR) is an alternative to OAR for
select patients. EVAR involves the placement of a sutureless
aortic graft into the abdominal aorta inside the aneurysm via
the femoral artery. Grafts are made of various materials, such as
a Dacron cylinder consisting of several sections, and supported
with multiple rings of flexible wire. Eligibility criteria include
iliofemoral vessels that allow for safe graft insertion and vessels of
sufficient length and width to support the graft.11
The main section of the graft is bifurcated. It is delivered
through a femoral artery catheter. The second part of the graft is
inserted through the opposite femoral artery. When all graft components are in place, they are deployed against the vessel wall by
balloon inflation. The blood then flows through the endovascular
graft, preventing further expansion of the aneurysm (Fig. 41.7).
Angiography is done afterward to check for leaks and to
confirm patency of all stent-graft components. The aneurysmal
wall shrinks over time because the blood is diverted through
the endograft. EVAR is less invasive than OAR and requires a
shorter hospital stay. EVAR also has fewer complications, such
as paraplegia and death.
Complications. The most common complication of
AAA repair is endoleak, the seepage of blood back into the
old aneurysm. This may result from an inadequate seal at
either graft end, a tear through the graft fabric, or leakage
between overlapping graft segments. Repair may require coil
embolization (insertion of beads) for hemostasis.
Other complications include aneurysm growth above or
below the graft, aneurysm rupture, aortic dissection, bleeding,
renal artery occlusion caused by stent migration, graft thrombosis, incisional site hematoma, and incisional infection. Patients
undergoing EVAR need periodic imaging for the rest of their
lives to monitor for an endoleak, assess stability of the aneurysm, and determine the need for surgery.
A
B
C
Fig. 41.6 Surgical repair of an abdominal aortic aneurysm. (A) Incising
the aneurysmal sac. (B) Insertion of synthetic graft. (C) Suturing native
aortic wall over synthetic graft.
Renal artery
A
B
D
C
E
Fig. 41.7 Bifurcated (2-branched) endovascular stent grafting of an aneurysm. (A) Insertion of a woven polyester graft covered by a tubular metal web (stent). (B) The stent graft is inserted through a large blood vessel
(e.g., femoral artery) using a delivery catheter. The catheter is positioned below the renal arteries in the area
of the aneurysm. (C) The stent graft is slowly released into the blood vessel. When the stent comes in contact
with the blood vessel, it expands to a preset size. (D) A second stent graft can be inserted in the opposite
vessel, if needed. (E) Fully deployed bifurcated stent graft.
CHAPTER 41
A potentially lethal complication in an emergency repair of a
ruptured AAA is the development of intraabdominal hypertension (IAH) with associated abdominal compartment syndrome.
Persistent IAH reduces blood flow to the viscera. Abdominal
compartment syndrome refers to the impaired organ perfusion
caused by IAH and resulting multisystem organ failure. IAH is
confirmed by measuring the patient’s intraabdominal pressure
indirectly through a catheter and transducer system.
Treatment goals include controlling situations that lead to
IAH. Interventions include open (surgical) decompression, percutaneous drainage, and percutaneous drainage combined with
a thrombolytic infusion. Conservative measures, such as intubation, ventilation, patient positioning, gastric decompression,
cautious fluid resuscitation, pain management, and temporary
hemofiltration, are used.
NURSING MANAGEMENT: AORTIC
ANEURYSMS
Assessment
Begin by doing a thorough history and physical assessment.
Because atherosclerosis is a systemic disease, look for signs of
coexisting cardiac, pulmonary, cerebral, and lower extremity
vascular problems. Monitor the patient for signs of aneurysm
rupture. These include diaphoresis; pallor; weakness; tachycardia; hypotension; abdominal, back, groin, or periumbilical pain;
changes in level of consciousness; or a pulsating abdominal
mass.
Obtain baseline data to compare with later assessments. Pay
special attention to the character and quality of the patient’s
peripheral pulses and renal and neurologic status. Before surgery, mark pedal pulse sites (dorsalis pedis, posterior tibial)
with a marker. Note any skin lesions on the lower extremities.
Planning
The overall goals for a patient undergoing aortic surgery include
(1) normal tissue perfusion; (2) intact motor and sensory function; and (3) no complications related to surgical repair, such as
thrombosis, infection, or rupture.
Implementation
Health Promotion
To promote overall health, encourage the patient to reduce
CVD risk factors (see Table 37.2). These include controlling BP,
ceasing tobacco use (see Chapter 11), and maintaining normal
body weight and serum lipid levels. These measures also help
ensure continued graft patency after surgical repair. Counsel the
patient about taking part in moderate physical activity.
Acute Care
Before surgery, provide emotional support and teaching to the
patient and caregiver (see Chapter 18). In general, aortic surgery patients have a bowel preparation and skin cleansing with
an antimicrobial agent the day before surgery. They are NPO
after midnight the day of surgery and receive IV antibiotics
before the first incision. Patients with a history of CVD should
receive a β-blocker (e.g., metoprolol).
Vascular Disorders
943
After surgery, patients typically go to an ICU for 24 to 48 hours
for close monitoring. When the patient arrives in the ICU, various devices are in place. These include an endotracheal tube for
mechanical ventilation, an arterial line, a central venous pressure
(CVP) catheter, peripheral IV lines, an indwelling urinary catheter, and a nasogastric (NG) tube. The patient needs continuous
ECG and pulse oximetry monitoring. If the thorax is opened
during surgery, chest tubes will be in place. The patient may have
a lumbar catheter draining cerebrospinal fluid to prevent neurologic problems. Pain medication is given via subcutaneous infusion into incision site (e.g., On-Q pain pump), epidural catheters,
or IV patient-controlled analgesia (PCA).
In addition to the usual goals of care for a postoperative
patient (e.g., maintaining adequate respiratory function, fluid
and electrolyte balance, and pain control [see Chapter 20]),
check for graft patency and renal perfusion. Watch for and intervene to limit or treat cardiac ischemia, dysrhythmias, infections,
VTE, and neurologic complications. eNursing Care Plan 41.2
for the patient with an aneurysm repair or other aortic surgery
is available on the website for this chapter.
Graft patency. An adequate BP is important to maintain
graft patency. Prolonged low BP may result in graft thrombosis.
Give IV fluids and blood components as ordered to maintain
adequate blood flow. Monitor CVP or PA pressures and urine
output hourly in the immediate postoperative period to assess
the patient’s hydration and perfusion status.
Avoid severe hypertension which may stress the arterial
anastomoses. This can result in leakage of blood or rupture at
the suture lines. Drug therapy with IV diuretics (e.g., furosemide) or IV antihypertensive agents (e.g., labetalol, hydralazine,
sodium nitroprusside) may be indicated.
Cardiovascular status. Myocardial ischemia or infarction may
occur in the perioperative period from decreased myocardial
O2 supply or increased myocardial O2 demands. Dysrhythmias
may occur because of electrolyte imbalances, hypoxemia,
hypothermia, or myocardial ischemia. Maintain continuous ECG
monitoring. Administer O2 per protocol. Other care includes
frequent electrolyte and arterial blood gas determinations and
giving IV antidysrhythmics, antihypertensives, and electrolytes
as needed. Provide adequate pain control.
Infection. A prosthetic vascular graft infection is a rare but
potentially life-threatening complication. Nursing interventions
to prevent infection include giving a broad-spectrum antibiotic
as prescribed (see Table 15.8). Assess temperature regularly,
and promptly report fever. Monitor laboratory results for a
high WBC count, which may be the first sign of an infection.
Ensure adequate nutrition. Assess the surgical incision for signs
of infection (e.g., redness, swelling, drainage). Keep surgical
incisions clean and dry and perform wound care as prescribed.
Use good hand-washing and strict aseptic technique in the
care of all peripheral, arterial, and CVP catheter insertion sites.
These are ports of entry for bacteria. Meticulous perineal care
for the patient with an indwelling urinary catheter and early
catheter removal are essential to minimize the risk for urinary
tract infection.
Gastrointestinal status. After OAR, postoperative ileus may
develop because of anesthesia and the handling of the bowel
944
SECTION 8
Problems of Oxygenation: Perfusion
during surgery. The intestines may become swollen and bruised.
Peristalsis ceases for variable intervals. A retroperitoneal
surgical approach decreases the risk for bowel complications.
An NG tube may be present and connected to low, intermittent suction to decompress the stomach, prevent aspiration of
stomach contents, and decrease pressure on suture lines. Record
the amount and character of the NG output. While the patient
is NPO, provide frequent oral care. Ice chips or lozenges can
help soothe a dry or irritated throat. Assess for bowel sounds
every 4 hours. Note the passing of flatus as it signals returning
bowel function. Encourage early ambulation to help the return
of bowel function. A postoperative ileus rarely lasts beyond the
fourth postoperative day.
If the blood supply to the bowel is disrupted during surgery,
ischemia or infarction (death) of intestinal tissue may result.
Manifestations of this rare, but serious, complication include
absent bowel sounds, fever, abdominal distention and pain,
diarrhea, and bloody stools. If bowel infarction occurs, immediate reoperation is needed to restore blood flow and resect the
infarcted area of bowel.
Neurologic status. Neurologic complications can occur after
aortic surgery. When the ascending aorta and aortic arch are
involved, assess the patient’s level of consciousness, pupil size
and response to light, facial symmetry, tongue position, speech,
upper extremity movement, and quality of hand grasps. When
the descending aorta is involved, perform a neurovascular
assessment of the lower extremities. Record all assessments and
report changes from baseline to the HCP immediately.
Peripheral perfusion status. The location of the aneurysm
determines the type of peripheral perfusion assessment. Check
and record all peripheral pulses hourly for several hours and
then routinely (based on agency policy). When the ascending
aorta and aortic arch are involved, assess the carotid, radial,
and temporal artery pulses. For surgery of the descending
aorta, assess the femoral, popliteal, posterior tibial, and dorsalis
pedis pulses (see Fig. 35.6). You may need a Doppler to assess
peripheral pulses. Check skin temperature and color, capillary
refill time, and sensation and movement of the extremities.
Sometimes, lower extremity pulses may be absent for a short
time after surgery because of vasospasm and hypothermia. A
decreased or absent pulse together with a cool, pale, mottled,
or painful extremity may indicate embolization or graft occlusion. Report these findings to the HCP at once. Graft occlusion
requires reoperation if identified early. It is essential to compare
your findings with the preoperative status to determine the
cause of a decreased or absent pulse and the proper treatment.
In some patients, pulses may have been absent before surgery
because of coexistent PAD.
Renal perfusion status. The patient will have an indwelling
urinary catheter after surgery. In the immediate postoperative
period, record hourly urine output. Further evaluate renal
function by monitoring daily BUN and serum creatinine levels.
CVP pressures give vital information about hydration status.
Maintain accurate fluid intake and output and record daily
weights until the patient resumes a regular diet.
Decreased renal perfusion can occur from embolization of
an aortic thrombus or plaque to either or both renal arteries.
Hypotension, dehydration, prolonged aortic clamping during
surgery, or blood loss can lead to kidney ischemia. Irreversible
renal failure may occur after surgery, particularly in high-risk
people (e.g., patients with diabetes).
Ambulatory Care
Teach the patient and caregiver to gradually increase activities.
They should avoid heavy lifting for 6 weeks. Fatigue, poor appetite, and irregular bowel patterns are common.
Teach the patient and caregiver to look for changes in color
or warmth of the extremities. They can learn to palpate peripheral pulses to assess changes in pulse quality. Report any redness, swelling, increased pain, drainage from incisions, or fever
greater than 100°F (37.8°C) to the HCP.
Sexual problems in male patients are common after aortic
surgery. A referral to a urologist and counseling may be useful if
erectile dysfunction occurs.
Evaluation
Expected outcomes are that the patient who undergoes aortic
surgery will have:
• Patent arterial graft with adequate distal perfusion
• Adequate urine output
• No signs of infection
AORTIC DISSECTION
Aortic dissection, often called “dissecting aneurysm,” is not a
type of aneurysm. Rather, dissection results from the creation
of a false lumen between the intima (inner lining) and the
media (middle layer) of arterial wall (Figs. 41.5D and 41.8). We
classify aortic dissection based on the location of the dissection
and duration of onset. Type A dissection affects the ascending
Tear in
aortic wall
Ascending
aorta
Aortic
dissection
Descending
aorta
Fig. 41.8 Aortic dissection.
CHAPTER 41
aorta and arch, requiring emergency surgery. Type B dissection
begins in the descending aorta, allowing for potential conservative management.12 Dissections are acute (first 14 days), subacute (14 to 90 days), or chronic (greater than 90 days) based on
symptom onset.
Etiology and Pathophysiology
Nontraumatic aortic dissection is caused by weakened elastic
fibers in the arterial wall. Chronic hypertension hastens this
process. In aortic dissection, a tear develops in the inner layer of
the aorta. Blood surges through this tear into the middle layer of
the aorta, causing the inner and middle layers to separate (dissect). If the blood-filled channel ruptures through the outside
aortic wall, aortic dissection is often fatal.
As the heart contracts, each pulsation increases the pressure
on the damaged area and worsens the dissection. Extension of
the dissection may cut off blood supply to the brain, kidneys,
spinal cord, and extremities. The false lumen may remain patent, become thrombosed (clotted), rejoin the true lumen by way
of a distal tear, or rupture.
Men have a higher risk for developing aortic dissection than
women.13 Women who develop aortic dissection are older and
more likely than men to present with HF, coma, or altered mental status.13 Hypertension is the most important risk factor for
aortic dissection.12,13 Other risk factors include age, aortic diseases (e.g., aortitis, coarctation, arch hypoplasia), atherosclerosis, blunt trauma, tobacco use, cocaine or methamphetamine
use, congenital heart disease (e.g., bicuspid aortic valve), connective tissue disorders (e.g., Marfan’s syndrome), family history, history of heart surgery, and pregnancy.
Clinical Manifestations
About 80% of patients with an acute type A aortic dissection
report an abrupt onset of severe anterior chest or back pain.
Patients with acute type B aortic dissection are more likely to
report pain in their back, abdomen, or legs. Pain location may
overlap between type A and B dissections. The pain may be
described as “sharp” and “worst ever,” or as “tearing,” “ripping,”
or “stabbing.” As the dissection progresses, pain may follow the
path of the dissection. Older patients are less likely to have an
abrupt onset of pain and more likely to have hypotension and
vague symptoms. Some patients have a painless aortic dissection, emphasizing the importance of the physical assessment.
If the aortic arch is involved, the patient may have neurologic problems. These include altered level of consciousness,
weakened or absent carotid and temporal pulses, dizziness, and
syncope. Type A aortic dissection usually disrupts blood flow
in the coronary arteries and causes aortic valve insufficiency.
When either subclavian artery is involved, the radial, ulnar, and
brachial pulse quality and BP readings may be different between
the left and right arms. As the dissection progresses down the
aorta, the abdominal organs and lower extremities show evidence of decreased tissue perfusion.
Complications
A severe and life-threatening complication of an acute ascending aortic dissection is cardiac tamponade. This occurs when
blood from the dissection leaks into the pericardial sac.
Vascular Disorders
945
TABLE 41.6 Interprofessional Care
Aortic Dissection
Diagnostic Assessment
• Health history and physical assessment
• ECG
• Chest x-ray
• CT scan
• Transesophageal echocardiogram
• MRI
Management
• Bed rest
• Pain relief with opioids
• Blood transfusion (if needed)
Drug Therapy (see Table 36.6)
• IV β-blockers
• IV calcium channel blockers
• ACE inhibitors
Surgical Therapy
• Endovascular aortic dissection repair
• Open surgical repair
Manifestations of tamponade include hypotension, narrowed
pulse pressure, jugular venous distention, muffled heart sounds,
and pulsus paradoxus (see Chapter 40).
An aorta weakened by dissection may rupture. Hemorrhage
may occur into the mediastinal, pleural, or abdominal cavities.
Aortic rupture typically results in exsanguination and death.
Aortic dissection can lead to occlusion of the blood supply to vital organs. Spinal cord ischemia leads to weakness and
decreased sensation. Rarely, lower extremity paralysis may occur.
Renal ischemia can lead to renal failure. Abdominal (mesenteric)
ischemia can occur and cause abdominal pain, decreased bowel
sounds, altered bowel function, and bowel necrosis.
Diagnostic Studies
Diagnostic studies to detect aortic dissection are similar to
those for suspected aneurysms (Table 41.6). An ECG can help
rule out cardiac ischemia. A chest x-ray may show a widening
of the mediastinum and pleural effusion. MRI, 3D CT scanning,
and transesophageal echocardiography (TEE) are equally reliable for diagnosing acute aortic dissection. A CT scan or MRI
can give detailed information on the severity of the dissection
and related complications (e.g., pericardial effusions, carotid
dissection). TEE is preferred in very unstable patients or those
with contraindications to CT or MRI (e.g., those with metal
implants, allergies to contrast material).
Interprofessional Care
Patients with acute aortic dissection are managed in the ICU.
The initial goals of therapy for acute aortic dissection without
complications are heart rate (HR) and BP control and pain
management. Lowering HR and BP reduces aortic wall stress
by decreasing SBP and myocardial contractility (Table 41.6).
This limits extension of the dissection. An IV β-blocker (e.g.,
esmolol) is titrated to a target HR under 60 beats/min or SBP
between 100 and 110 mm Hg. A calcium channel blocker (e.g.,
946
SECTION 8
Problems of Oxygenation: Perfusion
diltiazem) can be used to lower HR if a β-blocker is contraindicated. Morphine decreases sympathetic nervous system stimulation and relieves pain. Supportive treatment for an acute
aortic dissection is a bridge to surgery.
Conservative Therapy
The patient with an acute or chronic Type B aortic dissection
without complications can be treated conservatively. Treatment
includes pain relief, HR and BP control, and CVD risk factor
modification with close surveillance imaging with CT or MRI.
Endovascular Dissection Repair
Endovascular repair is a treatment option for acute type B aortic
dissections with complications (e.g., hemodynamic instability)
and chronic type B aortic dissection with complications (e.g.,
peripheral ischemia).14 Thoracic endovascular aortic repair
(TEVAR) is similar to EVAR. Fewer postsurgical complications
occur with TEVAR. However, TEVAR does not prevent the risk
for renal failure, paraplegia, or stroke.14 If a lumbar spinal drain
is inserted to help decrease or prevent neurologic complications, strict aseptic technique is used to prevent infection.
Surgical Therapy
An acute type A aortic dissection is a surgical emergency.
Mortality rate is 50% within 48 hours of symptom onset.
Otherwise, surgery is indicated when conservative therapy is
ineffective or when complications (e.g., HF) occur. Open surgical repair is recommended for patients with a chronic dissection
who have a connective tissue disorder or an aneurysm greater
than 5.5 cm. 12,14
The aorta is fragile after dissection. Surgery is delayed, when
possible, to allow time for edema to decrease and to permit
blood clotting in the false lumen. Surgery involves resection of
the aortic segment with the intimal tear and replacement with
a synthetic graft. Even with prompt surgical intervention, the
in-hospital mortality is high.14 Causes of death include aortic
rupture, mesenteric ischemia, MI, sepsis, stroke, and multiorgan failure.
NURSING MANAGEMENT: AORTIC DISSECTION
Preoperatively, keep the patient in bed in a semi-Fowler’s position and maintain a quiet environment. Manage pain and anxiety, giving opioids and sedatives as prescribed. These measures
help to keep the HR and SBP at the lowest possible level that
maintains vital organ perfusion (typically HR less than 60 beats/
min; SBP between 100 and 120 mm Hg).
Titrating IV antihypertensive agents requires careful super­
vision. Maintain continuous ECG and arterial BP monitoring.
Monitor vital signs frequently, sometimes as often as every 2 to
3 minutes, until target HR and BP are reached. Look for changes
in peri­pheral pulses and signs of increasing pain, restlessness,
and anxiety.
Postoperative care is similar to that after OAR. In preparation for discharge, focus on patient and caregiver teaching.
Help patients understand that they need to take antihypertensive drugs daily for the rest of their lives. β-Blockers are used to
control HR and BP and decrease myocardial contractility. ACE
inhibitors (e.g., lisinopril) are given if the patient cannot tolerate β-blockers. It is important that patients understand the drug
regimen and side effects (e.g., dizziness, depression, fatigue,
erectile dysfunction). Tell the patient to discuss any side effects
with the HCP before stopping any medication.
Follow up with regularly scheduled MRIs or CTs is essential. The most common cause of death in long-term survivors
is aortic rupture from redissection or aneurysm formation. Tell
patients that if the pain or other symptoms return, they should
activate the emergency response system (ERS) for immediate
care.
ACUTE AND CHRONIC VENOUS DISORDERS
PHLEBITIS
Phlebitis is an acute inflammation of the walls of small, cannulated veins. Manifestations include pain, tenderness, warmth,
redness, swelling, and a palpable cord. Risk factors are mechanical irritation from an IV catheter, infusion of irritating drugs,
and IV catheter location in an area of flexion (e.g., wrist and
antecubital area). Avoid IV catheter insertion in these areas
whenever possible.
Phlebitis is rarely infectious. It usually resolves quickly after
catheter removal. If edema is present, elevate the extremity
to promote fluid reabsorption. Apply warm, moist heat and
give oral NSAIDs (e.g., ibuprofen) or topical NSAIDs (e.g.,
diclofenac gel) to relieve pain and inflammation.
VENOUS THROMBOSIS
Venous thrombosis involves the formation of a thrombus (blood
clot) with vein inflammation. It is the most common disorder of
the veins. We classify it as either superficial vein thrombosis or
deep vein thrombosis. Superficial vein thrombosis is the formation of a thrombus in a superficial vein, usually the greater or
lesser saphenous vein. Deep vein thrombosis (DVT) involves
a thrombus in a deep vein, most often the iliac and/or femoral
veins. Venous thromboembolism (VTE) is the preferred terminology. It represents the spectrum from DVT to pulmonary
embolism (PE) (Table 41.7). Chapter 30 discusses PE.
Superficial vein thrombosis is serious. Nearly 25% of patients
with superficial vein thrombosis have a DVT or PE at the time
of diagnosis.15 These patients are at risk for developing recurrent VTE.
Etiology
The 3 key factors (called Virchow triad) that cause venous
thrombosis are (1) venous stasis, (2) damage of the endothelium
(inner lining of the vein), and (3) hypercoagulability (Fig. 41.9).
The patient at risk for developing VTE usually has predisposing
conditions to these 3 factors (Table 41.8).
Venous Stasis
Normal venous blood flow depends on the action of muscles in
the extremities and the function of venous valves, which allow
CHAPTER 41
flow in one direction. Venous stasis occurs when the valves are
dysfunctional or the muscles of the extremities are inactive.
Venous stasis occurs most often in people who are obese or
pregnant, have chronic HF or atrial fibrillation, have been traveling on long trips without regular exercise, have a prolonged
surgical procedure, or are immobile for long periods (e.g., spinal cord injury, fractured hip, limb paralysis).
Comparison of Superficial Vein
Thrombosis and Venous Thromboembolism
TABLE 41.7
Superficial Vein
Thrombosis
Usual
location
Clinical
findings
Sequelae
Venous
Thromboembolism (VTE)
Typically, superficial leg
Deep veins of arms (e.g., axillary,
veins (e.g., varicosities).
subclavian), legs (e.g., femoral),
Sometimes superficial
pelvis (e.g., iliac), vena cava,
arm veins.
and pulmonary system.
Tenderness, itchiness,
Tenderness to pressure over
redness, warmth, pain,
involved vein, induration of
inflammation, and
overlying muscle, venous
induration along the
distention. Edema. May have
course of superficial
mild to moderate pain, deep
vein. Vein appears as a
reddish color to area caused by
palpable cord. Edema
venous congestion. Some have
rarely occurs.
no obvious physical changes in
the affected extremity.
If untreated, clot may
Embolization to lungs (PE) may
extend to deeper veins
occur and may result in death.
and VTE may occur.
Pulmonary hypertension and
post-thrombotic syndrome with
or without venous leg ulceration
may develop.
Vascular Disorders
Endothelial Damage
Damage to the endothelium may be caused by direct (e.g., surgery, intravascular catheterization, trauma, burns, prior VTE) or
indirect (chemotherapy, diabetes, sepsis) injury. Damaged endothelium stimulates platelet activation and starts the coagulation
cascade. This predisposes the patient to thrombus development.
Hypercoagulability of Blood
Blood hypercoagulability occurs with many problems. These
include severe anemias, polycythemia, cancers (e.g., breast,
brain, pancreas, GI tract); nephrotic syndrome; high homocysteine levels; and protein C, protein S, and antithrombin
deficiency. A patient with sepsis is predisposed to hypercoagulability because of endotoxins released from bacteria. Some
drugs (e.g., corticosteroids, estrogens) predispose a patient to
thrombus formation.
Women who use tobacco, take estrogen-based oral contraceptives, are postmenopausal on oral hormone therapy, are over
35 years old, and have a family history of VTE have a very high
risk for VTE.15 Women who take oral contraceptives and use
tobacco double their risk. Smoking causes hypercoagulability
by increasing plasma fibrinogen and homocysteine levels and
activating the intrinsic coagulation pathway.
Pathophysiology
Localized platelet aggregation and fibrin entrap RBCs, WBCs,
and more platelets to form a thrombus. A frequent site of
thrombus formation is the valve cusp of a vein, where venous
stasis occurs. As a thrombus enlarges, increased numbers of
blood cells and fibrin collect behind it. This makes a larger clot
with a “tail” that eventually blocks the lumen of the vein.
PATHOPHYSIOLOGY MAP
Virchow’s triad
Venous stasis
• Dysfunctional vein valves
• Inactive extremity muscles
• Change in unidirectional blood flow
947
Endothelial damage
• Release of clotting factors
• Activation of platelets
Blood hypercoagulability
• Imbalance in clotting mechanism
→ coagulation
• Increase in fibrin production
• Platelets aggregate (especially at vein valve cusps)
• Clotting factors stimulated to produce fibrin
• Fibrin entraps RBCs, WBCs, and platelets and
begins to adhere to vein wall
Thrombus formation
Clinical manifestations
• Unilateral leg edema, pain, and erythema
• Chronic venous insufficiency
• Embolism of thrombotic fragments
Fig. 41.9 Pathophysiology of VTE.
948
SECTION 8
TABLE 41.8
Problems of Oxygenation: Perfusion
Risk Factors for VTE
Endothelial Damage
• Abdominal and pelvic surgery (e.g., gynecologic, urologic surgery)
• Caustic or hypertonic IV drugs
• Pelvis, hip, or leg fractures
• History of VTE
• Indwelling, peripherally inserted central vein catheter
• IV drug use
• Trauma
Venous Stasis
• Advanced age
• Atrial fibrillation
• Bed rest
• Chronic heart failure
• Fractured leg or hip
• Long trips without adequate exercise
• Obesity
• Orthopedic surgery (especially hip or lower extremity)
• Pregnancy and postpartum period
• Prolonged immobility
• Spinal cord injury or limb paralysis
• Stroke
• Varicose veins
Hypercoagulability of Blood
• Antiphospholipid antibody syndrome
• Antithrombin III deficiency
• Cancer (especially breast, brain, hepatic, pancreatic, GI)
• Dehydration or malnutrition
• Elevated (clotting) factor VIII or lipoprotein (a)
• Erythropoiesis-stimulating drugs (e.g., epoetin alfa [Procrit])
• High altitudes
• Hormone therapy
• High homocysteine levels
• Nephrotic syndrome
• Oral contraceptives, especially in women older than 35 years who use
tobacco
• Polycythemia vera
• Pregnancy and postpartum period
• Protein C deficiency
• Protein S deficiency
• Sepsis
• Severe anemias
• Tobacco use
If a thrombus only partially blocks the vein, endothelial
cells cover the thrombus and stop the thrombotic process. If
the thrombus does not become detached, it undergoes lysis
or becomes firmly organized and adherent within 5 to 7 days.
The organized thrombus may detach and result in an embolus.
Turbulent blood flow is a major factor in embolization. The
thrombus can become an embolus that flows through the
venous circulation to the heart and lodges in the pulmonary circulation, becoming a PE.
Superficial Vein Thrombosis
Clinical Manifestations
The patient with superficial vein thrombosis may have a palpable, firm, subcutaneous cordlike vein (Table 41.7). The area
surrounding the vein may be itchy, painful to the touch, reddened, and warm. A mild temperature elevation and leukocytosis may be present. Extremity edema may occur. Lower
extremity superficial vein thrombosis often involves varicose
veins.
Risk factors include increased age, pregnancy, obesity, cancer, recent fracture(s), estrogen therapy, recent sclerotherapy
(e.g., treatment for varicose veins), recent surgery or long-distance travel, hypercoagulability, and a history of chronic venous
insufficiency (CVI), superficial vein thrombosis, or VTE. It
can occur in people with endothelial problems (e.g., Buerger
disease).
Interprofessional Care
Ultrasound can confirm the diagnosis (clot 5 cm or larger) and
rule out clot extension to a deep vein. If the superficial vein
thrombosis affects a very short vein segment (less than 5 cm)
and is not near the saphenofemoral junction, anticoagulants
may not be needed. Oral NSAIDs can ease symptoms. Other
interventions include telling the patient to wear graduated compression stockings or bandages, apply warm compresses, elevate the affected limb above the level of the heart, apply topical
NSAIDS, and perform mild exercise, such as walking.
Venous Thromboembolism
Clinical Manifestations
The patient with lower extremity VTE may have unilateral
leg edema, pain, tenderness with palpation, dilated superficial
veins, a sense of fullness in the thigh or the calf, paresthesias,
warm skin, redness, or a systemic temperature greater than
100.4°F (38°C) (Table 41.7). If the inferior vena cava is involved,
both legs may be edematous and cyanotic. About 10% of VTEs
involve the upper extremity veins. They may extend into the
internal jugular vein or superior vena cava. If the superior vena
cava is involved, similar symptoms may occur in the arms, neck,
back, and face.
Complications
The most serious complications of VTE are PE, chronic thromboembolic pulmonary hypertension, post-thrombotic syndrome, and phlegmasia cerulea dolens. Post-thrombotic
syndrome (PTS) occurs in 8% to 70% of patients. It results
from chronic inflammation and chronic venous hypertension.
Chronic venous hypertension is caused by vein wall and vein
valve damage (from acute inflammation and thrombus reorganization), venous valve reflux, and persistent venous (outflow)
obstruction.
Symptoms include pain, aching, fatigue, heaviness, sensation
of swelling, cramps, pruritus, tingling, paresthesia, bursting pain
with exercise, and venous claudication. Manifestations include
persistent edema, spider veins (telangiectasia), venous dilation
(ectasia), redness, cyanosis, increased pigmentation, eczema,
pain during compression, atrophie blanche (white scar tissue),
and lipodermatosclerosis (Fig. 41.10). Venous ulceration can
occur with severe PTS. Signs of PTS typically begin within a few
months to a few years of a VTE. Risk factors include persistent
leg symptoms 1 month after VTE, proximal VTE location (e.g.,
CHAPTER 41
Vascular Disorders
TABLE 41.9
VTE
Diagnostic Studies
Study
Description and Abnormal Findings
949
Blood Laboratory Studies
ACT, aPTT, INR,
bleeding time, Hgb,
Hct, platelet count
D-dimer
Fibrin monomer
complex
Fig. 41.10 Lipodermatosclerosis. The leg becomes tapered like an
“inverted bottle.” Skin becomes scarred and leathery with brown discoloration and changes in pigmentation. (From Larocca C, Phillips TJ,
et al: Treatment of skin disease: comprehensive therapeutic strategies,
St Louis, 2018, Elsevier.)
near the iliofemoral junction), extensive VTE, recurrent VTE
on the same side, asymptomatic VTE, and residual thrombus.
Other factors include obesity, older age, poor INR control, daily
tobacco use before pregnancy, increased D-dimer levels, elevated inflammatory markers, and varicose veins.
Phlegmasia cerulea dolens (swollen, blue, painful leg) is a rare
complication of severe lower extremity VTE. It involves the major
leg veins, causing near-total occlusion of venous outflow. Patients
typically have sudden, massive swelling; deep pain; and intense
cyanosis of the extremity. If untreated, the venous obstruction
causes arterial occlusion and gangrene, requiring amputation.
Diagnostic Studies
Diagnosis of an initial VTE is based on the assessment combined with D-dimer testing and/or ultrasound. Table 41.9 presents the diagnostic studies used to determine the site or location
and extent of a VTE.
Interprofessional Care
Prevention. All health care team members have important
roles in VTE prevention. VTE prevention is a core measure
of high-quality health care in high-risk hospitalized patients
developed by The Joint Commission (TJC) and the National
Quality Forum. TJC recommends that hospitals have a policy that
addresses VTE prevention on admission of all adult patients. In
patients at risk for VTE, interventions used are based on bleeding
and thrombosis risk, medical history, current drugs, medical
diagnoses, scheduled procedures, and patient preferences.
Early and aggressive mobilization is the easiest and most
cost-effective method to decrease VTE risk. Patients on bed rest
should change position at least every 2 hours. Unless contraindicated, teach patients to flex and extend their feet, knees, and
hips at least every 2 to 4 hours while awake. Patients who are
able should be out of bed in a chair for meals and walk at least
4 to 6 times per day. Teach the patient and caregiver about the
importance of these measures. Early and frequent ambulation is
sufficient prophylaxis for patients at very low risk for VTE who
Altered if patient has underlying blood dyscrasia
(e.g., increased Hgb and Hct in patient with
polycythemia).
Fragment of fibrin formed from fibrin degradation
and clot lysis. High results suggest VTE.
Normal results: <250 ng/mL (<250 mcg/L)
Forms when concentration of thrombin exceeds
that of antithrombin. Presence is evidence of
thrombus formation and suggests VTE.
Normal results: <6.1 mg/L
Noninvasive Venous Studies
Combination of compression ultrasound with
Duplex ultrasound
spectral and color flow Doppler. Veins examined
for compressibility and intraluminal filling defects
to help determine location and extent of thrombus
(most widely used test to diagnose VTE).
Venous compression Evaluation of deep femoral, popliteal, and
posterior tibial veins
ultrasound
Normal finding: Veins collapse with application of
external pressure.
Abnormal finding: Veins do not collapse with
application of external pressure. Failure to
collapse suggests a thrombus.
Invasive Venous Studies
Uses spiral CT to evaluate veins in the pelvis,
Computed
thighs, and calves after injection of contrast
tomography
material. May be done simultaneously with CT
venography (CTV)
angiography of pulmonary vessels for patients
being evaluated for VTE.
Contrast venography X-ray determination of location and extent of clot
using contrast media to outline filling defects.
(phlebogram)
Identifies the presence of collateral circulation.
Once the gold standard, but now rarely done.
Magnetic resonance Uses MRI with specialized software to evaluate
blood flow through veins. Can be done with or
venography
without contrast. Highly accurate for pelvic and
proximal veins. Less accurate for calf veins. Can
distinguish acute and chronic thrombus.
ACT, Activated clotting time.
had minor surgical procedures. Anticoagulation and mechanical prophylaxis are not recommended for acutely ill medical
patients at low risk for VTE.
Graduated compression stockings (e.g., thromboembolic
deterrent [TED] hose) are a part of VTE prevention in hospitalized patients. VTE prevention is enhanced if the stockings are
used along with anticoagulation. Proper stocking use means any
toe hole is under the toes, the heel patch is over the heel, a thigh
gusset is on the inner thigh (thigh length only), and there are no
wrinkles. The stockings should not be rolled down, cut, or otherwise altered. Stockings that are not fitted and worn correctly
impede venous return. This can cause arterial ischemia, edema,
skin breakdown, and VTE. Stockings are not recommended if
the patient already has a VTE.15
950
SECTION 8
Problems of Oxygenation: Perfusion
Intermittent pneumatic compression devices (IPCs) use inflatable
sleeves or boots to compress the calf and thigh and/or foot and
ankle to improve venous return. The sleeves apply external pressure
through an electric pump. IPCs may be used with graduated compression stockings. Ensure correct fit of IPCs by accurately measuring the extremities. IPCs will not be effective if they are not applied
correctly, if the fit is incorrect, or if the patient does not wear the
device continuously while at rest. The IPCs can be removed for
bathing, skin assessment, and ambulation. IPCs are not worn when
a patient has an active VTE because of the risk for PE.
Drug therapy. Anticoagulants are used routinely for VTE
prevention and treatment. The regimen depends on the patient’s
VTE risk. The goal of anticoagulant therapy for VTE prevention
is to prevent clot formation. The goals for treatment of a
confirmed VTE are to prevent new clot development, spread of
the clot, and embolization.
The 3 major classes of anticoagulants available are (1) vitamin K antagonists (VKAs), (2) thrombin inhibitors (both indirect and direct), and (3) factor Xa inhibitors (Table 41.10).15,16
Anticoagulant therapy does not dissolve the clot. Clot lysis
TABLE 41.10 Drug Therapy
Anticoagulant Therapy
Drug
Route of
Administration
Thrombin Inhibitors: Indirect
Low-Molecular-Weight Heparin (LMWH)
dalteparin (Fragmin) enoxaparin
Subcutaneous
(Lovenox)
Unfractionated Heparin (UH)
heparin sodium
Continuous IV
Intermittent IV
Subcutaneous
Factor Xa Inhibitors
apixaban (Eliquis)
betrixaban (Bevyxxa)
edoxaban (Savaysa)
fondaparinux (Arixtra)
rivaroxaban (Xarelto)
PO
PO
PO
Subcutaneous
PO
Thrombin Inhibitors: Direct
Hirudin Derivatives
bivalirudin (Angiomax)
IV
desirudin (Iprivask)
Subcutaneous
Synthetic Thrombin Inhibitors
argatroban (Acova)
IV
dabigatran (Pradaxa)
PO
Vitamin K Antagonists (VKA)
warfarin (Coumadin)
PO
Considerations
Routine coagulation tests typically not needed.
Monitor CBC count at regular intervals.
Do not expel air bubble from prefilled syringe. If giving subcutaneously, inject deep into
subcutaneous tissue (preferably into the abdominal fatty tissue or above the iliac crest), inserting
the entire length of the needle. Hold skinfold during injection but release before removing needle.
Do not aspirate. Do not inject IM. Do not rub site after injection. Rotate sites.
Reduced dosage needed in patients with renal problems. Use extreme caution in patients with a
history of HIT.
Antidote: Protamine reverses the effects of LMWH.
Therapeutic effects measured at regular intervals by the aPTT or ACT.
Monitor CBC counts at regular intervals and titrate according to parameters.
Follow administration guidelines for LMWH if giving subcutaneously.
IV given as an adjunct for existing blood clots.
SQ given prophylactically to prevent the development of clots.
Antidote: Protamine reverses the effect of UH.
All approved for VTE prevention and treatment.
Routine coagulation tests not needed. Monitor CBC and creatinine at regular intervals.
May cause thrombocytopenia.
Do not expel air bubble before giving fondaparinux. Follow administration guidelines as described
for subcutaneous LMWHs.
Antidote: Andexanet alfa (Andexxa) reverses the effects of all Factor Xa inhibitors.
Therapeutic effect measured by ACT or aPTT. Used in patients with HIT who need anticoagulation.
Antidote: None.
Argatroban therapeutic effect measured by aPTT. No routine coagulation tests needed for dabigatran.
Used in patients at risk for or with HIT, for VTE prevention in joint replacement surgery, stroke
prevention in nonvalvular atrial fibrillation.
Antidote: Idarucizumab (Praxbind) reverses the effect of dabigatran only.
INR used to monitor therapeutic levels.
Give at the same time each day.
Variations of certain genes (e.g., CYP2CP, VKORC1) may influence response to drug.
Antidote: Vitamin K. For VKA-related bleeding, treatment with prothrombin complex concentrate
(human) (Kcentra), IV vitamin K and/or fresh frozen plasma is recommended.
ACT, Activated clotting time; HIT, heparin-induced thrombocytopenia.
CHAPTER 41
TABLE 41.11
Blood Coagulation Tests
Normal
Value
Therapeutic
Value
Activated Clotting Time (ACT)
• Hirudin derivatives (e.g., bivalirudin
[Angiomax])
• Synthetic thrombin inhibitors (e.g.,
argatroban [Acova])
• Unfractionated heparin (e.g., heparin
[Hep-Lock])
70–120 sec*
>300 sec
Activated Partial
­Thromboplastin Time (aPTT)
• Hirudin derivatives
• Synthetic thrombin inhibitors
• Unfractionated heparin
30–40 sec
46–70 sec
Test and Drugs Monitored
Anti-Factor Xa
• Factor Xa inhibitors (e.g., fondaparinux 0 units/mL
0 units/mL
[Arixtra], rivaroxaban [Xarelto])
• Low-molecular-weight heparin (e.g.,
enoxaparin [Lovenox])
International Normalized
Ratio (INR)
• Vitamin K antagonists (e.g., warfarin
[Coumadin])
0.75–1.25
0.6–1.0 units/mL
0.2
1.5 units/mL
2–3
aVaries based on type of system and test reagent or activator used.
begins naturally through the body’s intrinsic fibrinolytic system
(see Chapter 33).
Vitamin K antagonists. The oral anticoagulant for long-term
or extended anticoagulation is warfarin, a VKA. Warfarin inhibits
activation of the vitamin K–dependent coagulation factors II,
VII, IX, and X and the anticoagulant proteins C and S. See the
list of clotting factors in Table 33.2. Fig. 33.4 shows the clotting
pathways. Warfarin begins to take effect in 48 to 72 hours and
achieves maximum effect several days later. Thus, an overlap of
a parenteral anticoagulant (e.g., UH or low-molecular-weight
heparin [LMWH]) and warfarin typically is required for 5 days.
We monitor the level of anticoagulation daily using the INR. The
INR is a standardized system of reporting prothrombin time (PT)
(Table 41.11).
Take a careful history before starting warfarin. Do not give antiplatelet drugs or NSAIDs with warfarin as these increase bleeding
risk.16 Many other drugs, vitamins, minerals, and herbal supplements interact with warfarin. A diet that varies in vitamin K intake
(e.g., green leafy vegetables) can make it hard to achieve and maintain a target INR level. Genetic variants in the genes VKORC1 and
cytochrome P450 2C9 (CYP2C9) may influence how some people
respond to warfarin. See Table 13.5 and Fig. 13.7.
Thrombin inhibitors. There are 2 major classes of indirect
thrombin inhibitors: UH and LMWHs. UH (e.g., heparin) affects
both the intrinsic and common pathways of blood coagulation by
way of the plasma antithrombin. Antithrombin inhibits thrombinmediated conversion of fibrinogen to fibrin by affecting factors II
(prothrombin), IX, X, XI, and XII (see Fig. 33.4).
Heparin can be given subcutaneously for VTE prevention or
by continuous IV infusion for VTE treatment. IV heparin use
Vascular Disorders
951
requires frequent monitoring of clotting status by measuring
activated partial thromboplastin time (aPTT) (Table 41.11).
One serious side effect of heparin is heparin-induced thrombocytopenia (HIT). An immune reaction to heparin causes a
severe, sudden decrease in the platelet count along with a paradoxical increase in venous or arterial thrombosis. We diagnose
HIT by measuring the presence of heparin antibodies in the
blood. Treatment includes immediately stopping heparin therapy. If further anticoagulation is needed, we give a non-heparin anticoagulant (e.g., fondaparinux).16 Another side effect of
long-term heparin therapy is osteoporosis.
LMWHs (e.g., enoxaparin [Lovenox]) are derived from UH.
They have more predictable dose responses, longer half-lives, and
fewer bleeding complications than UH. LMWHs are less likely
to cause HIT and osteoporosis. LMWHs typically do not require
ongoing anticoagulant monitoring and dose adjustment. Their
antiinflammatory properties may help prevent PTS and venous
ulcer development. Protamine reverses the effect of LMWH.
Direct thrombin inhibitors are classified as hirudin derivatives or synthetic thrombin inhibitors. Hirudin is made using
recombinant deoxyribonucleic acid (DNA) technology. It
binds specifically with thrombin and directly inhibits its function without causing plasma protein and platelet interactions.
Hirudin derivatives (e.g., bivalirudin [Angiomax]) are given by
continuous IV infusion. Bivalirudin is given to patients with or
at risk for HIT having a percutaneous coronary intervention.
Anticoagulant activity is monitored using aPTT or activated
clotting time (ACT) (Table 41.11). If bleeding occurs, there is
no antidote for hirudin derivatives.
Argatroban—a synthetic direct thrombin inhibitor—hinders
thrombin. Like bivalirudin, it is an alternative to heparin for
the prevention and treatment of HIT and for patients with or at
risk for HIT needing percutaneous coronary interventions. The
effect of argatroban is not reversible. Its anticoagulant effect is
monitored using aPTT or ACT.
Dabigatran (Pradaxa) is an oral direct thrombin inhibitor.
It is used for VTE prevention after elective joint replacement,
for stroke prevention in nonvalvular atrial fibrillation, and as
a treatment for VTE. Dabigatran has 5 major advantages compared to warfarin: rapid onset, no need to monitor anticoagulation, few drug-food interactions, lower risk for major bleeding,
and predictable dose response.
Factor Xa inhibitors. Factor Xa inhibitors inhibit factor Xa
directly or indirectly, producing rapid anticoagulation. These
include fondaparinux (Arixtra), rivaroxaban (Xarelto), apixaban
(Eliquis), and edoxaban (Savaysa). All are used for both VTE
prevention and treatment. Fondaparinux is contraindicated
in patients with severe renal disease. Although coagulation
monitoring or dose adjustment is not needed, anticoagulant
activity can be measured using anti-Xa assays (Table 41.11).
Anticoagulant therapy for VTE prevention. For VTE
prevention in the hospitalized medical patient at risk for
thrombosis who is not bleeding, low-dose UH, LMWH, or
fondaparinux is used. If the patient is at low VTE risk, drug
prophylaxis is not needed. Patients with moderate VTE risk
(e.g., general, gynecologic, urologic surgery) should receive
either UH or LMWH. Patients with high VTE risk (e.g., trauma)
should receive UH or LMWH until discharge. Patients having
952
SECTION 8
Problems of Oxygenation: Perfusion
abdominal or pelvic surgery for cancer or major orthopedic
surgery (e.g., total knee or hip replacement) should receive VTE
prophylaxis.15
Anticoagulant therapy for VTE treatment. Patients with
confirmed VTE should receive initial treatment with either
LMWH, UH, or an oral factor Xa drug. Oral VKA therapy may
be an option. A therapeutic INR is maintained between 2.0 and
3.0 if VKA therapy is used. Active treatment of VTE should
continue for at least 3 months.
Patients with multiple co-morbidities, complex medical
issues, or a very large VTE usually are hospitalized for parenteral UH administration. Depending on the presentation and
home situation, patients may be safely managed as outpatients.
Thrombolytic therapy for VTE treatment. Another
treatment option for patients with a thrombus is catheterdirected admi­nistration of a thrombolytic drug (e.g., urokinase,
tPA). It dis­
solves the clot(s), reduces the acute symptoms,
improves deep venous flow, reduces valvular reflux, and may
help to decrease the incidence of PTS. Catheter-directed
thrombolysis is an option for patients who have a low risk of
bleeding and present with an acute, extensive, symptomatic,
proximal VTE. Systemic anticoagulation is needed before,
during, and after catheter-directed thrombolysis. (Chapter 37
discusses thrombolytic therapy.)
CHECK YOUR PRACTICE
Your 55-year-old female patient is admitted with an extensive VTE in her right
leg. She is receiving weight-based IV heparin per agency protocol: 18 units/kg/
hr. You receive the following critical laboratory result: aPTT 122 s.
• Describe your next actions.
Surgical and interventional radiology therapies. A few patients
with extensive, acute, proximal VTE who are not candidates for
catheter-directed thrombolysis and/or interventional radiology
therapies (due to bleeding risk) may have surgery.3,15 Surgical
options include open venous thrombectomy and inferior vena
cava interruption. Venous thrombectomy involves the removal
of a clot through a vein incision. Anticoagulant therapy is used
after venous thrombectomy.
Vena cava interruption devices (e.g., Greenfield, Vena Tech,
TrapEase filters) can be placed percutaneously through the
right femoral or right internal jugular veins. The filter device is
opened, and the spokes penetrate the vessel walls (Fig. 41.11).
The filters act as a “sieve-type” device. They filter clots without
interrupting blood flow. Complications after the insertion are
rare but include air embolism, improper placement, migration
of the filter, and perforation of the vena cava with retroperitoneal bleeding. Over time, clots can clog the filter and completely
block the vena cava, requiring filter removal and replacement. A
filter device is recommended with acute PE or proximal VTE of
the leg in patients with active bleeding or if anticoagulant therapy is contraindicated or ineffective.
Percutaneous endovascular interventional radiology procedures can be used along with catheter-directed thrombolytic
therapy, especially for severely symptomatic patients with iliocaval or iliofemoral obstruction. The procedures are like those
used in the treatment of lower extremity PAD. The difference is
Nose
Leg
Blood clot
Hook
Blood flow
Fig. 41.11 Inferior vena cava interruption technique using Greenfield
stainless-steel filter to prevent pulmonary embolism. As blood travels
up the vena cava, clots are trapped in the filter.
accessing an occluded vein instead of an artery. Options include
mechanical thrombectomy, pharmacomechanical devices,
post-thrombus extraction, angioplasty, and/or stenting.15
Anticoagulation therapy is recommended after an iliofemoral
interventional radiology procedure. Post procedure nursing
care focuses on (1) maintaining catheter systems (if continuous infusions); (2) monitoring for bleeding, embolization, and
impaired perfusion; and (3) VTE prevention teaching.
NURSING MANAGEMENT: VENOUS
THROMBOEMBOLISM
Assessment
Table 41.12 presents the subjective and objective data to obtain
from a patient with VTE.
Clinical Problems
Clinical problems for the patient with VTE include:
• Inadequate tissue perfusion
• Pain
• Impaired tissue integrity
• Impaired respiratory function
• Musculoskeletal problem
Planning
The overall goals for the patient with VTE include (1) pain
relief, (2) decreased edema, (3) increased knowledge of disorder
and treatment plan, (4) no skin ulceration, (5) no bleeding complications, and (6) no evidence of PE.
Nursing Implementation
Acute Care
Focus your nursing care for the patient with VTE on preventing
thrombi and reducing inflammation (Table 41.13). Review with
the patient any drugs, vitamins, minerals, and herbal supplements that may interfere with anticoagulant therapy. Depending
on the anticoagulant ordered, monitor INR, aPTT, ACT,
anti-factor Xa levels, complete blood count (CBC), creatinine,
factor X levels, hemoglobin, hematocrit, platelet levels, and/or
liver enzymes. Monitor platelet counts for patients getting UH
CHAPTER 41
TABLE 41.12 NURSING ASSESSMENT
VTE
Subjective Data
Important Health Information (Table 41.8)
Health history: Trauma to vein, intravascular catheter (e.g., peripherally
inserted central catheter), varicose veins, pregnancy or recent childbirth,
bacteremia, obesity, prolonged bed rest, irregular heartbeat (e.g., atrial
fibrillation), COPD, HF, cancer, coagulation disorders and hypercoagulable
states, systemic lupus erythematosus, MI, spinal cord injury, stroke, prolonged travel, recent bone fracture, dehydration
Medications: Use of estrogens (including oral contraceptives, hormone therapy), tamoxifen, raloxifene (Evista), corticosteroids, excessive amounts of
vitamin E, erythropoiesis-stimulating drugs
Surgery or other treatments: Any recent surgery, especially orthopedic, gynecologic, GI, or urologic. Previous surgery involving veins. Central venous
catheter
Functional Health Patterns
Health perception–health management: IV drug abuse, tobacco use, obesity
Activity-exercise: Inactivity
Cognitive-perceptual: Pain in area on palpation or ambulation
Objective Data
Cardiovascular
Distention and warmth of superficial veins in affected area. Edema and cyanosis of extremities, neck, back, and face (if superior vena cava involvement)
General
Fever, anxiety, pain
Skin
Increased size of extremity when compared with other side. Taut, shiny, warm
skin, redness, tender to palpation. No physical changes in the affected
extremity in some patients
Possible Diagnostic Findings
Leukocytosis, abnormal coagulation, anemia or ↑ hematocrit and RBC count,
↑ D-dimer level, positive venous compression on duplex ultrasound study;
positive CT venogram, magnetic resonance venogram, or contrast venogram
study
TABLE 41.13
Vascular Disorders
MANAGEMENT
953
NURSING
Caring for the Patient With VTE
•Assess patients for VTE risk and monitor for VTE in at-risk patients (see
Table 41.8).
•Teach patients at risk for VTE about preventive measures, including leg
exercise and ambulation, using graduated compression stockings and intermittent pneumatic compression devices (IPCs), avoiding nicotine, and taking
anticoagulant drugs.
•Measure patients for graduated compression stockings and/or IPCs.
•Assess for the use of medications and substances that may affect the coagulation status.
•Give prescribed oral, subcutaneous, and IV anticoagulants.
•Evaluate the effect of anticoagulant drugs by monitoring appropriate laboratory results and side effects of therapy (Table 41.11).
•Titrate doses of unfractionated heparin (UH), warfarin, and direct thrombin
inhibitors based on results of blood studies and agency protocols.
•
Assess for complications of VTE, including PE and chronic venous
­insufficiency.
•Teach the patient and caregiver the manifestations of PE and the need to
contact the emergency response system if these occur.
•Provide discharge teaching about use of graduated compression stockings,
diet, laboratory testing, and anticoagulant therapy (Table 41.15).
•Supervise the AP:
•Reposition patients who are on bed rest at least every 2 hr.
•Remind patients about the need to flex and extend the legs and feet at
least every 2 hr while in bed.
•Help ambulatory patients to walk at least 4 to 6 times daily.
•Help patients with putting on graduated compression stockings.
•Apply IPCs.
•Collaborate with the physical therapist:
•Assess patient’s mobility status.
•Develop exercise/muscle strengthening program as needed.
•Collaborate with the dietitian:
•Assess patient’s diet and nutrition status.
•Provide diet teaching as needed.
DRUG ALERT
or LMWH to assess for HIT. Direct thrombin inhibitors may
need adjustment for patients with renal or liver disease. Check
the results of pertinent tests before starting, giving, or changing
anticoagulant therapy.
Monitor for and reduce the risk for bleeding with anticoagulant therapy (Table 41.14). Bleeding risk is greater in people
receiving LMWH or UH with an active gastroduodenal ulcer,
prior bleeding history, low platelet count, hepatic or renal failure, rheumatic disease, cancer, or age greater than 85 years.
Patients receiving warfarin with an INR of 5.0 or more have a
higher risk for bleeding. In case of anticoagulation above target
goals, give reversal agents (e.g., protamine, vitamin K) or make
dosage adjustments as prescribed.
Early ambulation does not increase the short-term risk of
a PE in patients with VTE. In addition, early ambulation after
acute VTE results in a more rapid decrease in edema and limb
pain, fewer PTS symptoms, and better quality of life. Teach the
patient and caregiver the importance of physical activity. Help
the patient ambulate several times a day. For patients with acute
Anticoagulant Therapy
• Observe closely for any signs of bleeding: hypotension, tachycardia, hematuria, melena, hematemesis, petechiae, bruising, oozing or visible bleeding
from trauma site or surgical incision.
• Tell patients to report bleeding: black or bloody stools, bleeding gums,
bloody urine or sputum, coffee-ground or bloody vomit, excessive bruising,
nosebleeds, excessive menstrual bleeding.
• Assess for mental status changes, especially in the older patient, since this
may indicate cerebral bleeding.
• Tell patients to avoid taking aspirin, NSAIDs, fish oil supplements, garlic
supplements, ginkgo biloba, and certain antibiotics (e.g., sulfamethoxazole
and trimethoprim [Bactrim]).
VTE with severe edema and limb pain, bed rest with limb elevation may initially be prescribed.
Ambulatory Care
Focus discharge teaching on modifying VTE risk factors,
monitoring laboratory values, diet and drug instructions, and
954
SECTION 8
Problems of Oxygenation: Perfusion
TABLE 41.14 NURSING MANAGEMENT
Patient Receiving Anticoagulants
Assessment
•Monitor vital signs as indicated.
•Examine urine and stool for overt and occult signs of blood.
•Inspect skin often, especially under any splinting devices.
•Evaluate platelet count for signs of heparin-induced thrombocytopenia.
•Evaluate appropriate laboratory coagulation tests for target therapeutic levels.
•Evaluate lower extremity for bruising or hematoma development if intermittent pneumatic compression device used.
•Perform assessments frequently for signs and symptoms of bleeding (e.g.,
hypotension, tachycardia) or clotting.
•Notify the HCP of any abnormalities in assessments, vital signs, or laboratory values.
Injections
•Avoid IM injections.
•Minimize venipunctures.
•Use small-gauge needles for venipunctures, unless therapy requires a
larger gauge.
•Apply manual pressure for at least 10 min (or longer if needed) on venipuncture sites.
Patient Care
•Avoid restrictive clothing.
•Humidify any supplemental O2.
•Apply moisturizing lotion to skin.
•Use electric razors, not straight razors.
•Perform physical care in a gentle manner.
•Tell patient not to forcefully blow nose.
•Avoid removing or disrupting established clots.
•Use soft toothbrushes or foam swabs for oral care.
•Reposition the patient carefully at regular intervals.
•Limit tape application. Use paper tape as appropriate.
•Give stool softeners to avoid hard stools and straining.
•Use support pads, mattresses, bed cradles, and therapeutic beds as indicated.
•Apply graduated compression stockings or intermittent pneumatic compression devices (if ordered) with attention to proper size, application, and use.
•Perform risk for fall and skin breakdown assessments per agency policy and
implement safety and preventive measures as needed.
guidelines for follow-up. Recommend the patient stop smoking and avoid all nicotine products. Teach the patient to avoid
constrictive clothing. Tell women with a history of VTE to stop
oral contraceptives or hormone therapy. Teach patients to limit
standing or sitting in a motionless, leg-dependent position.
When traveling long distances, tell patients to frequently
exercise the calf muscles, take short walks, and maintain hydration with nonalcoholic, noncaffeinated beverages. For those at
high risk for VTE who are planning a long trip, recommend
properly fitted, knee-high graduated compression stockings
during travel to decrease edema and VTE risk. Aspirin or anticoagulant use is not suggested for long-distance travelers. Teach
the patient and caregiver to contact ERS for signs and symptoms
of PE, such as sudden onset of dyspnea, tachypnea, and pleuritic
chest pain.
Review drug dosage, actions, and side effects, the need for
routine blood tests, and what symptoms need immediate medical
TABLE 41.15 PATIENT & CAREGIVER
TEACHING
Anticoagulant Therapy
Include the following information in the teaching plan for a patient receiving
anticoagulant therapy and the patient’s caregiver:
1.Give reasons for and action of anticoagulant drug and how long therapy
will last.
2.Take drug at the same time each day (preferably in afternoon or evening).
3.Depending on drug prescribed, obtain blood tests to assess therapeutic
effect and whether change in dosage is needed.
4.Contact emergency response system immediately for any of the following adverse side effects of drug therapy:
•Blood in urine or stool; or black, tarry stools
•Vomiting blood, coffee-grounds emesis
•Unusual bleeding from gums, skin, or nose, or heavy menstrual bleeding
•Severe headaches or stomach pain
•Chest pain, shortness of breath, palpitations (heart racing)
•Weakness, dizziness, mental status changes
•Cold, blue, or painful feet
5.Avoid activities with a high risk for injury that may cause bleeding (e.g.,
vigorous brushing of teeth, contact sports, rollerblading, use of straight
razor).
6.Avoid all aspirin-containing drugs and NSAIDs.
7.Limit alcohol intake to small to moderate amounts (12 oz beer, 4 oz wine,
1 oz hard liquor/day).
8.Wear a Medic Alert device saying the anticoagulant drug being taken.
9.If taking warfarin (Coumadin), avoid frequent or dramatic changes in
eating foods high in vitamin K (e.g., broccoli, spinach, kale, greens). Do
not take supplemental vitamin K.
10.Consult with HCP before beginning or stopping any drug, vitamin, mineral, or dietary or herbal supplement.
11.Inform all HCPs, including dentist, of anticoagulant therapy.
12.Correct dosing is essential. Provide supervision if patient has confusion
or cognitive problems.
13.Implement safety precautions to prevent falls (e.g., avoid use of throw
rugs).
14.Apply pressure for 10 to 15 min if bleeding occurs (e.g., nosebleed).
attention (Table 41.15). Devices are available for home monitoring of INR. Teach patients taking LMWH or fondaparinux
and their caregivers how to give the drug subcutaneously. A
well-balanced diet is important. Teach patients taking warfarin to follow a consistent diet of foods containing vitamin K.
They should avoid any supplements containing vitamin K (e.g.,
vitamins, green tea). Tell the patient to avoid excess amounts
of vitamin E and alcohol. Encourage proper hydration to prevent hypercoagulability of the blood, which may occur with
dehydration.
The overweight patient needs implement a diet plan and
increase physical activity to achieve and maintain desired
weight. Exercise may help patients with VTE and PTS and
improves the patient’s quality of life. Help the patient develop
an exercise program with an emphasis on leg strength training
and aerobic activity.
Graduated compression stockings reduce swelling in patients
with a proximal VTE.15 Alternatively, IPCs may be used for
patients with significant edema and moderate to severe PTS.
CHAPTER 41
The long-term use of graduated compression stockings may not
prevent PTS development.
Evaluation
The expected outcomes are that the patient with VTE will have:
• Minimal to no pain
• Intact skin
• Increased knowledge of disorder and treatment plan
• No signs of hemorrhage or occult bleeding
VARICOSE VEINS
Varicose veins, or varicosities, are dilated (3 mm or larger in
diameter), tortuous superficial veins. They are often found
in the saphenous vein system. Varicosities may be small and
harmless or large and bulging. Primary varicose veins (idiopathic) due to a weakness of the vein walls are more common
in women. Secondary varicose veins result from direct injury,
a previous VTE, or excessive vein distention. Secondary
varicose veins may occur in the esophagus (esophageal varices), vulva, spermatic cords (varicoceles), and anorectal
area (hemorrhoids), and as abnormal arteriovenous (AV)
connections.
Congenital varicose veins result from chromosomal
defects that cause abnormal development of the venous system. Reticular veins are smaller varicose veins that appear
flat, less tortuous, and blue-green in color. Telangiectasias
(often called spider veins) are small visible vessels (generally
less than 1 mm in diameter) that appear bluish black, purple,
or red.
Etiology and Pathophysiology
Superficial veins in the lower extremities become dilated and
tortuous in response to backward (retrograde) blood flow and
increased venous pressure. Risk factors include family history
of chronic venous disease, weak vein structure, female gender,
tobacco use, increasing age, obesity, multiparity, history of VTE,
venous obstruction resulting from extrinsic pressure by tumors,
thrombophilia, phlebitis, previous leg injury, and occupations
that require prolonged standing or sitting.
In primary varicose veins, weak vein walls allow the vein valve
ring to enlarge, so the leaflets no longer fit together properly (incompetent). Incompetent vein valves allow backward blood flow, particularly when the patient is standing. This results in increased
venous pressure and further venous distention. High pressure in
the superficial veins can be caused by vein valve dysfunction in the
deep veins or perforator veins (veins that perforate the deep fascia
of muscles to connect the superficial veins to the deep veins).
Clinical Manifestations and Complications
Discomfort from varicose veins varies among people. It tends
to be worse after episodes of superficial vein thrombosis.
Symptoms affect women more often than men. The most common symptoms include a heavy, achy feeling or pain after prolonged standing or sitting. Walking or limb elevation relieves
pain. Some patients feel pressure or an itchy, burning, tingling,
Vascular Disorders
955
throbbing, or cramp-like leg sensation. Swelling, restless or tired
legs, fatigue, and nocturnal leg cramps may occur.
Superficial venous thrombosis is the most frequent complication of varicose veins. It may occur spontaneously or after
trauma, surgery, or pregnancy. Rare complications include rupture of the varicose veins resulting in external bleeding and skin
ulcerations.
Diagnostic Studies and Interprofessional Care
Superficial varicose veins often can be diagnosed by physical assessment. Duplex ultrasound imaging is the gold standard to evaluate venous anatomy, valvular competence, and
venous obstruction.17 Conservative treatment involves rest
with limb elevation; graduated compression stockings; leg
strengthening exercise, such as walking; and weight loss, if
indicated.
Drug Therapy
Venoactive drugs work by stimulating release of chemicals
within the vein walls to strengthen the circulation and reduce
inflammation and edema. Several natural and synthetic venoactive agents have been used to treat varicose veins and advanced
chronic venous disease. These include micronized purified
flavonoid fraction, rutosides (e.g., horse chestnut seed extract
[Aesculus hippocastanum]), proanthocyanidins (from grapes
and apples), and Ruscus (butcher’s broom).16
Therapeutic benefits of venoactive drugs include pain relief,
edema reduction, and decreased leg cramping and restless legs.
These drugs are widely used in Europe. They are not approved
by the FDA. However, many are available over the counter as
diet or herbal supplements.
DRUG ALERT
Horse Chestnut Seed Extract (Aesculus
hippocastanum)
• May interact with lithium and antidiabetic, antiplatelet, and anticoagulant
drugs.
• Should not be taken by persons with liver or kidney disease or with a latex
allergy.
Interventional and Surgical Therapies
Sclerotherapy involves the direct IV injection of a liquid or
foam sclerosing substance (e.g., hypertonic saline, polidocanol,
glycerin) that chemically ablates (destroys) the treated veins.
Sclerotherapy can be used on telangiectasias, perforator veins,
reticular veins, smaller varicose veins, and venous malformations (Fig. 41.12). This procedure is done in an office setting and
causes minimal discomfort.
The most common complications of sclerotherapy are residual pigmentation, matting (new telangiectasias develop in the
area), thrombophlebitis, and ulcers.17 After injection, a graduated compression stocking or bandage is worn. Patients should
not travel long distances during the first week after sclerotherapy to minimize the risk for a VTE.
956
SECTION 8
A
Problems of Oxygenation: Perfusion
B
Fig. 41.12 (A) Lateral aspect of varicose veins before treatment. (B)
Lateral aspect of varicose veins 2 years after initial treatment with
sclerotherapy. (From Goldman MP, Guex JJ, Weiss RA: Sclerotherapy:
treatment of varicose and telangiectatic leg veins, ed 5, Philadelphia,
2011, Mosby.)
Other noninvasive options include transcutaneous laser
therapy for telangiectasias and high-intensity pulsed-light therapy for reticular veins. Transcutaneous laser or light therapy is
used for patients in whom sclerotherapy is contraindicated or
has been ineffective. Vascular lasers work by heating the hemoglobin in the vessels, resulting in vessel sclerosis. Complications
of these therapies include pain, blistering, hyperpigmentation,
and superficial erosions.
A minimally invasive treatment option for saphenous vein
reflux is endovenous ablation using thermal energy from
radiofrequency or laser therapy. The HCP inserts a catheter into the vein to heat the vein wall, which then causes the
vein to collapse. Complications include bruising, skin burns,
hyperpigmentation, infection, paresthesia, superficial or deep
vein thrombosis, and PE. Graduated compression stockings
or bandages are worn afterwards. Endovenous thermal ablation may be done in combination with surgical ligation or
phlebectomy.
Surgical intervention is needed for recurrent superficial
venous thrombosis or when symptoms cannot be controlled
with other therapy. The traditional surgical intervention involves
ligation of the entire vein (usually the greater saphenous vein)
and removal of its incompetent branches. An alternative but
time-consuming technique is ambulatory phlebectomy. This
involves pulling the varicosity through a “stab” incision followed
by excision of the vein. Transilluminated powered phlebectomy
involves the use of a tissue resector to destroy clusters of varicosities and removes the pieces via aspiration. Complications
include bleeding, bruising, and infection.
NURSING MANAGEMENT: VARICOSE VEINS
Prevention is a key factor related to varicose veins. Tell the
patient to avoid sitting or standing for long periods, maintain ideal body weight, take precautions against injury to the
extremities, avoid wearing constrictive clothing, and walk daily.
After vein ligation surgery, encourage the patient to deep
breathe, which promotes venous return. Check the extremities
regularly for color, movement, sensation, temperature, edema,
and quality of pedal pulses. Some bruising and discoloration
are normal. Elevate the legs 15 degrees to limit edema. Remove
graduated compression stockings or bandages every 8 hours for
short periods and then reapply them.
Long-term management is directed toward improving circulation and appearance, relieving discomfort, and avoiding
complications. Varicosities can recur in other veins after surgery. Teach the patient the proper use and care of custom-fitted graduated compression stockings. The patient should apply
stockings in bed before rising in the morning.
Emphasize the importance of periodic positioning of the
legs above the heart. The overweight patient may need help with
weight loss. The patient with a job that requires long periods of
standing or sitting needs to frequently flex and extend the hips,
legs, and ankles and change positions.
CHRONIC VENOUS INSUFFICIENCY AND
VENOUS LEG ULCERS
Chronic venous insufficiency (CVI) describes abnormalities of the venous system that result in advanced signs and
symptoms, such as edema, skin changes, and/or venous leg
ulcers.17 CVI can lead to venous leg ulcers (also called venous
stasis ulcers or varicose ulcers). Although CVI and venous leg
ulcers are not life-threatening diseases, they are painful, slow
to heal, debilitating, and costly conditions that adversely affect
patients’ quality of life. They are a common problem in older
adults.
Etiology and Pathophysiology
Both long-standing primary varicose veins and PTS can progress to CVI. Ambulatory venous hypertension causes serous fluid
and RBCs to leak from the capillaries and venules into the tissue.
This causes edema and chronic inflammatory changes. Enzymes
in the tissue eventually break down RBCs. This releases hemosiderin, which causes a brownish skin discoloration. Over time,
fibrous tissue replaces the skin and subcutaneous tissue around
the ankle. This results in thick, hardened, contracted skin.
Although the causes of CVI are known, the exact pathophysiology of venous leg ulcers is unknown.
Clinical Manifestations and Complications
In patients with CVI, the skin of the lower leg is leathery, with
a characteristic brownish or “brawny” appearance from the
hemosiderin deposition. Edema usually has been persistent for
a prolonged period. Eczema with itching and scratching is often
present (see Table 41.1).
Venous ulcers classically occur above the medial malleolus
(Fig. 41.13). The ulcer is often quite painful, particularly when
edema or infection is present. Pain may be worse when the leg
is in a dependent position. If the venous ulcer is untreated,
the wound becomes wider and deeper, increasing the risk for
infection.
CHAPTER 41
Interprofessional and Nursing Care
Compression is essential for venous ulcer healing and preventing venous ulcer recurrence. A variety of options are available
for compression therapy. These include custom-fitted graduated
compression stockings, elastic tubular support bandages, a Velcro
wrap (CircAid), IPCs, and multilayer (3 or 4) bandage systems
(e.g., Profore). Evaluate the patient when choosing a compression
method. Before starting compression therapy, assess the arterial
status to make sure that PAD is not present. An ABI of 0.4 or
less suggests severe PAD, and the patient should not have any
type of compression therapy.3 Show how to correctly apply the
compression therapy and have the patient “show back” the skill.
Stockings should be worn daily to prevent recurrent leg ulcers.
Tell the patient to replace stockings every 4 to 6 months.
Discuss activity guidelines and proper limb positioning. Tell
patients with CVI to avoid standing or sitting for long periods, which decreases blood return from the lower extremities.
Teach patients to frequently elevate their legs above the level of
the heart to reduce edema. Encourage patients to begin a daily
walking program once an ulcer heals. Tell the patient and caregiver to avoid trauma to the limbs. Teach proper foot and leg
care to avoid more skin trauma.
Moist environment dressings are the basis of wound care. A
variety of dressings are available. These include transparent film
dressings, hydrocolloids, hydrogels, foams, alginates, gauze, and
combination dressings. Dressing decisions should be based on
wound characteristics, cost, best evidence, and clinician judgment. Chapter 12 and Table 12.14 discuss dressings.
Evaluate the patient’s nutrition status. A balanced diet with
adequate protein, calories, and nutrients is essential. Foods high
in protein (e.g., meat, beans, cheese, tofu), vitamin A (green
leafy vegetables), vitamin C (citrus fruits, tomatoes, cantaloupe),
Vascular Disorders
957
and zinc (meat, seafood) are most important for healing. For
patients with diabetes, maintaining normal blood glucose levels
aids the healing process.
Though venous leg ulcers are colonized by bacteria, routine
use of antibiotics is not indicated. Signs of infection include
change in quantity, color, or odor of the drainage; pus; redness
of the wound edges; change in sensation around the wound;
and warmth around the wound. There may be increased local
pain, edema, or both; dark-colored granulation tissue; induration around the wound; delayed healing; and cellulitis. If signs
of infection occur, obtain a wound culture. Culture results guide
antibiotic therapy. The usual treatment for infection is wound
debridement, wound excision, and systemic antibiotics.
If the ulcer does not heal with conservative therapy, drug
therapy should be considered. Pentoxifylline is recommended
with compression therapy to improve healing. Pentoxifylline
minimizes WBC activation and adhesion to capillary endothelium and decreases oxidative stress.
Other treatments are considered for large venous leg ulcers
that do not respond to standard therapy after 4 to 6 weeks. These
include coverage with a skin replacement or substitute, such
as split-thickness skin grafts or artificial bioengineered skin.
Chapter 26 discusses skin grafting. Although grafts help with
healing, they do not replace the need for lifelong compression
therapy.
Patients with CVI have dry, flaky, itchy skin. Daily moisturizing decreases itching and prevents skin cracking. Contact
dermatitis may result from contact with sensitizing products.
These include such as topical antimicrobial agents (e.g., gentamicin); additives in bandages or dressings (e.g., adhesives);
ointments containing lanolin, alcohols, or benzocaine; and
over-the-counter creams or lotions with fragrance or preservatives. Assess wounds for signs of infection with each dressing
change (Table 41.16).
TABLE 41.16
NURSING MANAGEMENT
Caring for the Patient With Chronic Venous
Insufficiency
Fig. 41.13 Venous leg ulcer. (From Quick C, Biers SM: Essential surgery: problems, diagnosis, and management, St Louis, 2020, Elsevier.)
•Assess the patient for increases in edema, eczema, and venous leg ulcers.
•Assess diet and nutrition status and make referrals as needed.
•Assess for the use of venoactive diet supplements or herbs that may
adversely affect co-morbid conditions and/or prescription drugs.
•Choose best options for compression therapy and wound care.
•Give prescribed analgesics, antibiotics, or other drugs.
•Apply compression therapy.
•Provide wound care for venous leg ulcers.
•
Evaluate for the effectiveness of therapies and need for alternative
approaches.
•Teach patient and caregiver about the manifestations, complications, and
treatment of venous insufficiency.
•Supervise the AP:
•Aid patients in elevating legs to reduce edema and pain.
•Apply graduated compression stockings.
•Collaborate with the dietitian:
•Assess diet and nutrition status.
•Provide diet education as needed.
958
SECTION 8
Problems of Oxygenation: Perfusion
Case Study
Peripheral Artery Disease
Patient Profile
S.J., a 73-year-old man, is admitted to the hospital with rest
pain in both legs and a nonhealing ulcer of the big toe on the
right foot.
(© IPGGutenbergUKLtd/
iStock/
Thinkstock.)
Subjective Data
• History of a MI, stroke, hypertension, HF, type 1 diabetes
• Underwent a left femoral-popliteal bypass 5 years ago
• Has a 45-pack-year history of tobacco use
• Has been using insulin for 30 years
• Reports sudden, intense increase in right foot pain for past 2 hr
• Has slept in recliner with right leg in dependent position for
several months to decrease leg pain
Current Medications
• Furosemide (Lasix) 40 mg/day PO
• Isosorbide dinitrate/hydralazine hydrochloride (BiDil) 1 tablet every 8 hr
• Aspart (NovoLog) insulin with meals (sliding scale)
• Glargine insulin 50 units/day subcutaneously
• Diltiazem sustained release (Cardizem LA) 240 mg/day PO
• Aspirin 325 mg/day PO
• Fish oil daily (self-prescribed)
Objective Data
Physical Assessment
• BP 148/92 mm Hg, irregular apical HR 90/min, respiratory rate 22/min, temp
97.9°F (36.6°C)
• Alert and oriented, anxious, with no apparent physical or mental deficits from stroke
• Has 1+ right femoral pulse, popliteal pulse by Doppler only, posterior tibial
pulse by Doppler only, and dorsalis pedis pulse absent (not palpable or present by Doppler). Left leg pulses are 1+
• Right leg ABI: 0.20. Left leg ABI: 0.68
• Has a 2-cm necrotic ulcer on tip of right big toe
• Has thickened toenails. Shiny, thin skin on legs. No hair on both lower legs
• Right foot is very cool, pale, and mottled in color with decreased sensation
• No peripheral edema
• Bedside glucose measurement 298 mg/dL (last meal 4 hr before admission)
Discussion Questions
1. Recognize: What risk factors do you identify that led to S.J. having PAD?
2. Analyze: What are the important findings from S.J.’s assessment?
3. Plan: What treatment options are possible?
4. Prioritize: What is the important thing the team can do for S.J.?
5. Act: What role do APs have in providing care?
6. Evaluate: What do you need to continually monitor?
7. Safety: What safety precautions should we consider?
Answers available at http://evolve.elsevier.com/Lewis/medsurg.
B R I D G E T O N C L E X E X A M I N A T I O N
The number of the question corresponds to the same-numbered
outcome at the beginning of the chapter.
1.A 50-year-old woman who weighs 95 kg has a history of
high blood pressure, high sodium intake, tobacco use, and
sedentary lifestyle. Which is the most important risk factor
for peripheral artery disease (PAD) to address in the nursing plan of care?
a. Salt intake
b. Tobacco use
c. Excess weight
d. Sedentary lifestyle
2.Which information would the nurse include when explaining the cause of rest pain with PAD?
a. Vasospasm of cutaneous arteries in the feet
b. Decrease in blood flow to the nerves of the feet
c. Increase in retrograde venous perfusion to the lower
legs
d. C onstriction in blood flow to leg muscles during
­exercise
3.A patient with infective endocarditis develops sudden left
leg pain with pallor, paresthesia, and a loss of peripheral
pulses. Which action would the nurse take first?
a. Notify the HCP of the change in perfusion.
b. Start anticoagulant therapy with IV heparin.
c. Elevate the leg to improve the venous return.
d. Position the patient in reverse Trendelenburg.
4.Which clinical manifestations can the nurse expect to see
in both patients with Buerger disease and patients with
Raynaud phenomenon? (select all that apply)
a. Intermittent low-grade fevers
b. Sensitivity to cold temperatures
c. Gangrenous ulcers on fingertips
d. Color changes of fingers and toes
e. Episodes of superficial vein thrombosis
5.A patient is admitted to the hospital with a diagnosis of
abdominal aortic aneurysm. Which signs and symptoms
would suggest that the aneurysm has ruptured?
a. Rapid onset of shortness of breath and hemoptysis
b. Sudden low back pain and bruising along the flank
c. Patchy blue mottling on feet and toes and rest pain
d. Gradually increasing substernal chest pain and diaphoresis
6.Which nursing interventions are the priority 8 hours after
an abdominal aortic aneurysm repair?
a. Assessing nutrition status and diet preferences
b. Starting IV heparin and monitoring anticoagulation
c. Administering IV fluids and watching kidney function
d. Elevating the legs and applying compression stockings
7.Which goal is the first priority of interprofessional care for
a patient with a suspected acute aortic dissection?
a. Reduce anxiety
b. Monitor chest pain
c. Control blood pressure
d. Increase myocardial contractility
CHAPTER 41
REFERENCES
* 1.Creager MA, Belkin B, Bluth EI, et al.: 2012 ACCF/AHA/ACR/
SCAI/SIR/STS/SVM/SVN/SVS key data elements and definitions
for peripheral atherosclerotic vascular disease: a report of the
ACCF/AHA Task Force on Clinical Data Standards, Circ 125:395,
2012. (Classic).
2.Centers for Disease Control and Prevention: Peripheral arterial
disease (PAD) fact sheet. Retrieved from https://www.cdc.gov/
heartdisease/pad.htm.
*3.Gerhard-Herman M, Gornick H, Barrett C, et al.: 2016 AHA/
ACC guideline on the management of patients with lower extremity peripheral artery disease: Executive summary, Circ 135:e686,
2017. (Classic).
*4.Patel T, Baydoun H, Patel NK, et al.: Peripheral arterial disease in
women: the gender effect, CRM 21:404, 2019.
*5.Fan Y, Shen Y, Zhou J, et al.: Visit-to-visit hemoglobin A1c variability is associated with the risk of lower-extremity amputation
in patients with Type 2 diabetes, Diabetes Care 43:e178, 2020.
*6.Meini S, Dentali F, Melillo E: Prostanoids for critical limb ischemia: a clinical review and consideration of current guideline
recommendations, Angioplasty 7:226, 2020.
959
d. Arrange to have blood drawn twice a week to check drug
effects.
12.The nurse is planning care and teaching for a patient with
venous leg ulcers. Which patient action is the most important in healing and control of this condition?
a. Following activity guidelines.
b. Using moist environment dressings.
c. Taking horse chestnut seed extract daily.
d. Applying graduated compression stockings.
1. b; 2. b; 3. a; 4. b, c, d; 5. b; 6. c; 7. c; 8. b; 9. b, d; 10. d; 11. a; 12. d.
8.Which patient is at highest risk for venous thromboembolism (VTE)?
a. a. A 62-year-old man with spider veins who is having
arthroscopic knee surgery
b. b. A 32-year-old woman who smokes, takes oral contraceptives, and is planning a long flight
c. A 26-year-old woman who is 3 days postpartum and recei­
ved maintenance IV fluids for 12 hours during her labor
d. d. An active 72-year-old man at home recovering from
transurethral resection of the prostate for benign prostatic hyperplasia
9.Which clinical findings would the nurse expect in a person
with an acute lower extremity VTE? (select all that apply)
a. Pallor and coolness of foot and calf
b. Mild to moderate calf pain and tenderness
c. Grossly decreased or absent pedal pulses
d. Unilateral edema and induration of the thigh
e. Palpable cord along a superficial varicose vein
10.Which treatment would the nurse anticipate for an otherwise healthy person with an initial VTE?
a. IV argatroban as an inpatient
b. IV unfractionated heparin as an inpatient
c. Subcutaneous unfractionated heparin as an outpatient
d. Subcutaneous low-molecular-weight heparin as an outpatient
11.Which instruction is a key aspect of teaching for the patient
on anticoagulant therapy?
a. Monitor for and report any signs of bleeding.
b. Do not take acetaminophen (Tylenol) for a headache.
c. Decrease your dietary intake of foods containing vitamin K.
Vascular Disorders
For rationales to these answers and even more NCLEX review
questions, visit http://evolve.elsevier.com/Lewis/medsurg.
EVOLVE WEBSITE/RESOURCES LIST
http://evolve.elsevier.com/Lewis/medsurg
Review Questions (Online Only)
Key Points
Answer Keys for Questions
• Rationales for Bridge to NCLEX Examination Questions
• Answer Guidelines for Case Study
Student Case Studies
• Patient With Abdominal Aortic Aneurysm
• Patient With Chronic Peripheral Artery Disease
Nursing Care Plans
• eNursing Care Plan 41.1: Patient With Peripheral Artery
Disease of the Lower Extremities
• eNursing Care Plan 41.2: Patient After Surgical Repair of
the Aorta
Conceptual Care Map Creator
Audio Glossary
Content Updates
* 7.Haghighat L, Ionescu C, Regan C, et al.: Review of the current
basic science strategies to treat critical limb ischemia, Vasc Endovasc Surg 53:316, 2019.
8.Qaja E, Muco E, Hashmi M: Buerger disease. Retrieved from
https://www.ncbi.nlm.nih.gov/books/NBK430858/.
9.Herrick A, Wigley F: Raynaud’s phenomenon, Best Pract Res
Clin Rheumatol 34, 2020.
10.Pauling J, Hughes M, Pope J: Raynaud’s phenomenon: an update
on diagnosis, classification and management, Clin Rheumatol
38:3317, 2019.
*11.Chaikof EL, Dalman RL, Eskandari MK, et al.: The Society of
Vascular Surgery practice guidelines on the care of patients with
an abdominal aortic aneurysm, J Vasc Surg 67:2, 2018.
12.Kaji S: Acute medical management of aortic dissection, Gen
Thorac Cardiovasc Surg 67:203, 2019.
*13.Rylski B, Georgieva N, Beyersdorf F, et al.: Gender-related differences in patients with acute aortic dissection type A, J Thorac
Cardiovasc Surg, 2019.
*14.Boufi M, Patterson B, Loundou A, et al.: Endovascular versus
open repair for chronic type B dissection treatment: a meta-analysis, Ann Thorac Surg 107:1559, 2019.
*15.Ortel T, Neuman I, Ageno W, et al.: American Society of Hematology 2020 guidelines for management of venous thrombo-
960
SECTION 8
Problems of Oxygenation: Perfusion
embolism: treatment of deep vein thrombosis and pulmonary
embolism, Blood Adv 4:4693, 2020.
16.Burcham JR, Rosenthal LD: Lehne’s pharmacology for nursing
care, ed 10, St. Louis, 2019, Elsevier.
17.Youn Y, Lee J: Chronic venous insufficiency and varicose veins
of the lower extremities, Korean J Intern Med 34:269, 2019.
*Evidence-based information for clinical practice.