PAD is strongly related to other types of cardiovascular disease (CVD) and their risk factors.
Patients with PAD have a significantly higher risk of mortality (in general), CVD mortality, major coronary events, and stroke.
PAD is a marker of advanced systemic atherosclerosis.
Common anatomic locations of atherosclerotic lesions (shown in yellow) of the abdominal aorta and lower extremities.
Atherosclerosis more commonly affects certain segments of the arterial tree. These include the coronary (see Chapter 33), carotid (see Chapter 57), and lower extremity arteries.
Clinical symptoms occur when vessels are 60% to 75% blocked.
The risk for PAD increases with age and individuals usually become symptomatic in the sixth to eighth decades of life. In persons with diabetes mellitus, PAD occurs much earlier. PAD prevalence is higher in those of lower socioeconomic status, women and African Americans.
Nicotine is a vasoconstrictor and tobacco smoke impairs transport and cellular use of oxygen, and increases blood viscosity and homocysteine levels.
Other risk factors include elevated C-reactive protein, family history, hypertriglyceridemia, increasing age, hyperhomocysteinemia, hyperuricemia, obesity, sedentary lifestyle, and stress.
The femoral popliteal area is the most common site in nondiabetic patients.
The patient with diabetes tends to develop PAD in the arteries below the knee.
In advanced PAD, multiple levels of occlusions are found.
The ischemic pain is a result of the buildup of lactic acid resulting from anaerobic metabolism. Once the patient stops exercising, the lactic acid is cleared and the pain subsides.
PAD of the iliac arteries produces claudication in the buttocks and thighs, whereas calf claudication indicates femoral or popliteal artery involvement.
As many as one third of patients with PAD report classic claudication symptoms.
The remaining either 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). Older women experience classic claudication less often than men.
Paresthesia results from nerve tissue ischemia.
True peripheral neuropathy occurs more often in patients with diabetes (see Chapter 48) and in those with long-standing ischemia. Neuropathy produces severe shooting or burning pain in the extremity.
Gradual, reduced blood flow to neurons produces loss of both pressure and deep pain sensations. Thus patients may not notice lower extremity injuries.
True peripheral neuropathy occurs more often in patients with diabetes (see Chapter 48) and in those with long-standing ischemia. Neuropathy produces severe shooting 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 produces loss of both pressure and deep pain sensations. Thus patients may not notice lower extremity injuries.
Pallor (blanching of the foot) develops in response to leg elevation (elevation pallor).
Conversely, reactive hyperemia (redness of the foot) develops when the limb is in a dependent position (dependent rubor).
As PAD progresses and involves multiple arterial segments, continuous pain develops at rest. Rest pain most often occurs in the foot or toes and is aggravated by limb elevation.
Patients often try to achieve pain relief by dangling the leg over the side of the bed or sleeping in a chair to allow gravity to maximize blood flow.
Patients with PAD who also have diabetes, heart failure, and a history of a stroke are at increased risk for critical limb ischemia.
Arterial (ischemic) ulcers most often occur over bony prominences on the toes, feet, and lower legs (Table 37-1).
If PAD is present for an extended period, collateral circulation may prevent gangrene of the extremity.
Uncontrolled pain and severe, spreading infection are indicators that an amputation is needed in individuals who are not candidates for revascularization.
When palpation of a peripheral pulse is difficult because of severe PAD, the Doppler can determine the degree of blood flow.
A palpable pulse and a Doppler pulse are not equivalent, and the terms are not interchangeable.
Segmental blood pressures (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.
The ABI is calculated by dividing the ankle systolic BPs by the higher of the left and right brachial systolic BP.
A normal ABI is 0.91 to 1.30 and indicates adequate BP in the extremities. An ABI between 0.71 and 0.90 indicates mild PAD, between 0.41 and 0.70 indicates moderate PAD, and <0.40 indicates severe PAD.
Angiography and magnetic resonance angiography delineate the location and extent of PAD.
Table 37-2 summarizes the interprofessional care for a patient with PAD.
Because of the high risk for MI, ischemic stroke, and CVD-related death, the first treatment goal is to aggressively modify CVD risk factors in all patients with PAD regardless of the severity of symptoms.
• (Tables 10-4 to 10-6 discuss smoking cessation strategies.)
Diabetes is a major risk factor for PAD and increases the risk of amputation in these patients. It is recommended that diabetic patients maintain a glycosylated hemoglobin (A1C) below 7.0% and, optimally, as near as possible to 6.0%.
Aggressive lipid management is essential for all PAD patients. To manage lipids, both dietary interventions and drug therapy are needed. Statins (e.g., simvastatin [Zocor]) lower LDL and triglyceride levels and reduces CVD morbidity and mortality risks.
In PAD patients with coexistent diabetes mellitus or renal insufficiency, BP <130/80 mm Hg is recommended.
Angiotensin-converting enzyme (ACE) inhibitors (e.g., ramipril [Altace]) are used for symptomatic patients with PAD. Lifestyle changes are encouraged and include reducing dietary sodium and following the Dietary Approaches to Stop Hypertension (DASH) diet.
Guidelines for oral antiplatelet therapy recommend aspirin (75-325 mg daily).
Aspirin intolerant patients may take clopidogrel (Plavix) 75 mg daily.
DRUG ALERT—Clopidogrel (Plavix) and Omeprazole (Prilosec)
Antiplatelet effect of clopidogrel is reduced by about half when given with omeprazole.
This increases the risk of myocardial infarction and stroke.
Drug Alert: Cilostazol (Pletal)
• Contraindicated in patients with heart failure of any severity.
A supervised exercise program is recommended as an initial treatment modality for all patients with intermittent claudication.
Exercise should be performed for 30 to 45 min/day, 3 times/week, for a minimum of 3 months.
Although walking is the most commonly prescribed exercise for PAD patients, alternative modes of exercise (e.g., cycling) also improve walking ability and quality of life in patients with PAD.
Overall, patients with PAD who have higher levels of daily physical activity also have better survival rates.
Even modest, sustained weight loss of 3% to 5% yields important reductions in triglycerides, glucose, A1C, and the risk of developing type 2 diabetes. Greater weight loss produces greater benefits.
Patients taking antiplatelet agents, nonsteroidal antiinflammatory agents (NSAIDs) (e.g., ibuprofen [Motrin]), and anticoagulants (e.g., warfarin) should consult with their health care provider before taking any dietary or herbal supplements due to potential interactions and bleeding risks.
Critical limb ischemia is a condition characterized by chronic ischemic rest pain lasting longer than 2 weeks, arterial leg ulcers, and/or gangrene of the leg due to PAD.
Optimal therapy for the patient with critical limb ischemia is revascularization via bypass surgery using an autogenous (native) vein.
If this is not feasible, percutaneous transluminal angioplasty (PTA) is recommended.
Patients with CLI who are not candidates for surgery or PTA may be treated with IV prostanoids (e.g., iloprost [Ventavis]). These drugs may decrease rest pain and improve ulcer healing.
Spinal cord stimulation may be helpful in managing pain and preventing amputation in patients with CLI.
Growth factors and gene and stem cell therapy may be used to stimulate blood vessel growth (angiogenesis).
Carefully inspect, cleanse, and lubricate feet to prevent cracking of the skin and infection.
If ulceration is present, keep the affected foot clean and dry. Cover any ulcers with a dry, sterile dressing to maintain cleanliness.
Deep ulcers can be treated with a variety of wound care products, but healing is unlikely without increased blood flow. Systemic antibiotics are used in patients with CLI, skin ulcerations, and limb infection.
Encourage the patient to select soft, roomy, and protective footwear and avoid extremes of heat and cold.
These procedures take place in a catheterization laboratory rather than in an operating room. Determining which intervention to use depends on blockage location along with lesion type and severity.
Pre- and post-procedure nursing care is the same as for a diagnostic angiography. Antiplatelet agents are needed post-procedure to reduce the risk of restenosis. Long-term, low-dose aspirin therapy or clopidogrel is recommended.
Stents, expandable metallic devices, are positioned within the artery immediately after the balloon angioplasty is done. The stent acts as a scaffold to keep the artery open.
Both angioplasty balloons and peripheral stents may be coated with a drug-eluting agent (e.g., paclitaxel) to reduce restenosis. These drugs work by limiting the growth of new tissue in the treated stenotic area and improve long-term patency rates.
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.
Other types of atherectomy catheters have a diamond-coated tip that rotates at a high speed (similar to a dentist drill).
The specialized balloon is filled with liquid nitrous oxide that changes from liquid 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.
Surgery is indicated in patients with long areas of stenosis or severely calcified arteries.
(See next slide for figure.)
When possible, peripheral artery bypass surgery should be done with an autogenous vein to bypass (carry blood around) the lesion.
Synthetic grafts typically are used for long bypasses, such as an axillary-femoral bypass. When a person’s own vein is not available, human umbilical vein or a composite sequential bypass graft (native vein plus synthetic graft) is an alternative.
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.
Endarterectomy involves opening the artery and removing the obstructing plaque.
Patch graft angioplasty is opening the artery, removing plaque, and sewing a patch to the opening to widen the lumen.
Amputation may be required if tissue necrosis is extensive, gangrene or osteomyelitis develops, or all major arteries in the limb are blocked, precluding the possibility of successful surgery.
(Amputation is discussed in Chapter 62.)
Ineffective peripheral tissue perfusion related to deficient knowledge of contributing factors
Activity intolerance related to imbalance between oxygen supply and demand
Chronic pain related to ischemia, inflammation, and swelling
Ineffective health management related to lack of knowledge of disease and self-care measures
Assess the patient for CVD risk factors and provide instructions on how to control them (see Tables 33-2, 33-3, and 33-4).
Teach diet modification to reduce the intake of cholesterol, saturated fat, and refined sugars; proper care of the feet; and avoidance of injury to the extremities.
Encourage patients with positive family histories of cardiac, diabetic, or vascular disease to obtain regular follow-up care.
Check the operative extremity every 15 minutes initially and then hourly for color, temperature, capillary refill, presence of peripheral pulses, and sensation and movement.
Loss of palpable pulses and/or a change in the Doppler sound over a pulse requires immediate notification of the HCP and prompt intervention.
After the patient leaves the recovery area, you will continue to monitor perfusion to the extremities and will assess for potential complications, such as bleeding, hematoma, thrombosis, embolization, and compartment syndrome.
A dramatic increase in pain, loss of previously palpable pulses, extremity pallor or cyanosis, decreasing ABIs, numbness or tingling, or a cold extremity suggests blockage of the graft or stent.
Discourage prolonged sitting with leg dependency as it may cause pain and edema, increase the risk of venous thrombosis, and place stress on the suture lines.
If edema develops, position the patient supine and elevate the leg above heart level.
Walking even short distances is desirable. The use of a walker may be helpful, especially in frail, elderly patients.
Continued tobacco use dramatically decreases the long-term patency rates of grafts and stents, and increases the risk of an MI or stroke.
Long-term antiplatelet therapy with aspirin or clopidogrel is recommended for patients after surgery.
Explain that exercise decreases CVD risk factors, including hypertension, hyperlipidemia, obesity, and glucose levels.
Teach foot care to all patients with PAD. Meticulous foot care is especially important in the diabetic patient with PAD.
Tell patients to inspect their legs and feet daily for mottling, changes in skin color or texture, and reduction in hair growth.
Show patients how to check skin temperature and capillary refill and to palpate pulses.
Stress that they must report any changes in these findings or the development of ulceration or inflammation to their HCP.
Percutaneous catheter-directed thrombolytic therapy with alteplase or urokinase preferred if arterial ischemia is less than 14 days old
Thrombolytic dissolves clot over 24 to 48 hours
Requires close monitoring or catheter position and bleeding at insertion site
Surgical revascularization—trauma or arterial blockage
Amputation—ischemic rest pain and tissue loss
Long-term anticoagulation recommended if risk for further embolization exists.
Venous stasis: Dysfunctional valves, Inactive extremity muscles
At risk: Obese, Pregnant, Chronic HF or atrial fibrillation, Traveling on long trips without exercise, Prolonged surgery, Prolonged immobility
Hypercoagulability: Occurs with many disorders: Anemia, polycythemia, Cancer, Nephrotic syndrome, High homocysteine levels, Coagulation disorders, Sepsis, Drugs: corticosteroids, estrogens, Smoking
Very high risk—women who:
Use tobacco
Smoking increases plasma fibrinogen, homocysteine levels and activates intrinsic coagulation pathway
Are childbearing age and take estrogen-based oral contraceptives
Are postmenopausal and take oral hormone therapy
Are over age 35
Have family history of VTE
Inferior vena cava
Legs edematous and cyanotic
Superior vena cava
Similar symptoms of arms, neck, back and face
Some patients are asymptomatic
Post-thrombotic syndrome (PTS) : 8% to 70% of patients, Chronic inflammation and venous hypertension; damage to vein walls and valves, venous valve reflux, and persistent venous obstruction
Symptoms:Pain, aching, fatigue, heaviness, swollen sensation, cramps, pruritus, tingling, paresthesia, pain with exercise, and venous claudication
Manifestations
Persistent edema, spider veins, venous dilation, redness, cyanosis, increased pigmentation, eczema, pain during compression, white scar tissue, and lipodermatosclerosis (Fig 37-10)
Venous ulceration with severe PTS
Signs may occur in a few months or years
Risk factors:
Persistent leg symptoms for more than 1 month after VTE
VTE: Proximal location, extensive, or recurrent
Residual thrombus
Other: obesity, old age, poor INR control, tobacco use, increased D-dimer, increased inflammatory markers, varicose veins, and asymptomatic VTE
Post-thrombotic syndrome (PTS) : 8% to 70% of patients, Chronic inflammation and venous hypertension; damage to vein walls and valves, venous valve reflux, and persistent venous obstruction
Symptoms:Pain, aching, fatigue, heaviness, swollen sensation, cramps, pruritus, tingling, paresthesia, pain with exercise, and venous claudication
Manifestations
Persistent edema, spider veins, venous dilation, redness, cyanosis, increased pigmentation, eczema, pain during compression, white scar tissue, and lipodermatosclerosis (Fig 37-10)
Venous ulceration with severe PTS
Signs may occur in a few months or years
Risk factors:
Persistent leg symptoms for more than 1 month after VTE
VTE: Proximal location, extensive, or recurrent
Residual thrombus
Other: obesity, old age, poor INR control, tobacco use, increased D-dimer, increased inflammatory markers, varicose veins, and asymptomatic VTE
Early and aggressive mobilization: Bed rest—reposition every 2 hours, Flex and extend feet, knees and hips every 2 to 4 hours while awake, OOB to chair, Walk 4 to 6 times/day
Intermittent pneumatic compression devices (IPCs) - increased venous return
External pressure from electric pump inflates sleeves or boots to compress calf or thigh and/or foot and ankle
Use with graduated compression stockings
Fit and apply correctly; wear continuously except for bathing, skin assessment, and ambulation
Do not use with active VTE; risk of PE
Warfarin : Do not give with antiplatelet drugs or NSAIDS
Many interactions:
Avoid vitamin K in diet; alters INR - Green leafy vegetables and enetic variants may alter response
Dabigatran (Pradaxa)—oral
Indications: VTE prevention after elective joint replacement, for stroke prevention in nonvalvular atrial fibrillation, and as a treatment for VTE
Antidote: idarucizumab
Advantages over warfarin
Rapid onset, no monitoring, few drug-food interactions, decreased risk of bleeding, predictable response
Hirudin derivative—bivalirudin (Angiomax)
Binds with thrombin and inhibits function
Continuous IV infusion
Synthetic (Argatroban)—
Hinders thrombin
Both:
Indications: patients with or at risk for HIT having a percutaneous coronary intervention
Monitor aPTT or ACT (Table 37-11)
No antidote
Recommended for acute PE or proximal VTE of leg with active bleeding, or if anticoagulation contraindicated or ineffective
Complications: air embolism, improper placement, filter migration, perforation of vena cava with retroperitoneal bleeding, clogged filter
Dietary and Exercise Instructions
Vitamin K and warfarin
Obtain and maintain desired weight
Guidelines for follow-up
Report/call EMS:
Bleeding (urine, stool, vomit, nose, gums, skin)
Severe headache, stomach pain, chest pain, palpitations, dyspnea, mental status changes
Inform all HCP and dentist of anticoagulation
VTE risk factors
Smoking, hormone therapy, travel, prolonged sitting, signs/symptoms of PE
Drug doses, actions, side effects and routine blood tests; wear medic-alert ID
Avoid falls and trauma
Apply pressure to bleeding sites for 10-15 minutes
No ASA or NSAIDs; limit alcohol
Evaluation
Expected outcomes:
Minimal to no pain
Intact skin
Increased knowledge of disorder and treatment plan
No signs of hemorrhage or occult bleeding
Dilated (greater than or equal to 3mm in diameter), tortuous superficial veins
Primary—weakness of vein walls
Secondary—direct injury, previous VTE, or excessive dilation
Congenital—chromosomal defects
Reticular—flat, less tortuous, blue-green
Telangiectasias—(spider veins) small (smaller than 1 mm) blue-black, purple, or red
Antioxidants from plant extracts stimulate release of chemicals to strengthen the circulation and reduce inflammation and edema
Not FDA approved; available OTC and as herbal or dietary supplements
Micronized purified flavonoid fraction
Rutosides (horse chestnut seed extract—see Drug Alert)
Proanthocyanidins (apples and grapes)
Ruscus (butcher’s broom)
Sclerotherapy—ablates vein by direct injection of sclerosis agent (Fig. 37-12)
Complications: residual pigmentation, matting, thrombophlebitis, and ulcers
Wear compression stocking and limit travel
Transcutaneous laser therapy or high-intensity pulsed light therapy
Complications: pain, blistering, hyperpigmentation, and superficial erosions
Endovenous ablation—radiofrequency or laser therapy
Complications: bruising, burns, hyperpigmentation, infection, paresthesia, superficial or deep vein thrombosis, and PE
Graduated compression stockings after