Peripheral arterial insufficiency is predominantly a disease of
the lower extremities. Upper extremity arterial lesions are uncommon
and confined mostly to the subclavian arteries. Even when present,
upper extremity atherosclerosis rarely produces symptoms due to
abundant collateral pathways. In the lower extremities, however,
obstructive lesions are distributed widely, with lesions of the
superficial femoral and iliac arteries the most common (Figure 34–1). Symptoms are related
to the location and number of obstructions.
Common sites of stenosis and occlusion of the visceral
and peripheral arterial systems.
Peripheral arterial disease affects at least 20% of
individuals older than 70 years. Although most patients with this disorder
do not develop gangrene or require amputations, adverse outcomes
of systemic atherosclerosis, including death, are common. Even after
adjustment for known risk factors, individuals with peripheral arterial
disease exhibit a several-fold higher risk of mortality than the
nonaffected population. A low ankle-brachial index is one of the
strongest risk factors for all-cause mortality. Peripheral arterial disease
is more a marker of a more virulent form of atherosclerosis and
early death from cardiovascular or cerebrovascular disease than
an indicator of imminent limb loss; thus, identifying and treating
associated atherosclerotic risk factors is essential (Figure 34–2).
Odds ratios for risk factors for all-cause mortality.
ABI, ankle-brachial index; CAD, coronary artery disease. (Reproduced,
with permission, from TASC Working Group: Management of peripheral
arterial disease: epidemiology, natural history, risk factors. J
Vasc Surg 2000;31[1 Suppl]:S22. © 2000
Society for Vascular Surgery. Reprinted with permission from Elsevier.)
Intermittent claudication refers to pain in muscles of the lower
extremity associated with walking and relieved by rest. Because
tissue perfusion is adequate at rest, tissue loss is not present
and the risk of amputation is low unless there is progression of
disease. Claudication is derived from the Latin word meaning “to limp”;
therefore, the term should be used only for symptoms in the lower
extremities. The pain is a deep-seated ache usually in the calf
muscle, which gradually progresses until the patient is compelled
to stop walking. Patients occasionally describe “cramping” or “tiredness” in
the muscle. Typically, symptoms are completely relieved after 2–5
minutes of inactivity. Claudication is distinguished from other types
of pain in the extremities in that it does not occur at rest and
some period of exertion is always required before it appears, it
generally occurs after a relatively consistent distance traveled,
and it is relieved by cessation of walking. Relief of symptoms is
not dependent upon sitting or other positional change. The severity
of claudication is traditionally expressed in terms of city blocks.
Regardless of which arterial segment is involved, claudication
most commonly involves the calf muscles because of their high workload
with the mechanics of normal walking. Occlusions proximal to the
origin of the profunda femoris can extend the pain to involve the
thigh. Gluteal pain indicates lesions in or proximal to the hypogastric
arteries and is often accompanied by impotence. Leriche syndrome occurs
in men with aortoiliac disease and includes claudication of calf, thigh,
and buttock muscles; impotence; and diminished or absent femoral
pulses. Occasionally, patients describe transient numbness of the
extremity accompanying the pain and fatigue of claudication as nerves
as well as muscles become ischemic.
The two conditions that most often mimic claudication are osteoarthritis
of the hip or knee and neurospinal compression due to congenital
or osteophytic narrowing of the lumbar neurospinal canal (spinal
stenosis). Osteoarthritis can be differentiated from claudication
because pain occurs predominantly in joints, the amount of exercise
required to elicit symptoms varies, symptoms are characteristically worse
in the morning and upon initiating exercise, rest does not relieve
symptoms promptly, the severity of symptoms changes from day to
day, and anti-inflammatory agents may relieve the pain. Impingement
on the spinal canal or nerve root produces neurospinal compression
symptoms; therefore, the pain is typically burning in nature and
symptoms may occur with sitting or standing. Neurospinal pain may follow
a dermatomal distribution.
Uncommon conditions such as coarctation of the aorta, chronic
compartment syndrome, popliteal artery entrapment, and vasculitis
can mimic symptoms of atherosclerotic arterial insufficiency. Age
at presentation and associated findings may aid in diagnosing these
The correct diagnosis of vascular claudication should be easily
established by determining the location of pain with exercise (calf),
the quality of the pain (aching or cramping), the length of time
required for relief of symptoms after stopping exercise (immediate),
and the reproducibility of the distance walked before symptoms begin
(initial claudication distance).
With extensive disease, patients develop ischemic rest pain and/or
ulceration. Ischemic rest pain, a grave symptom caused by ischemic
neuritis, indicates advanced arterial insufficiency that carries
a risk of gangrene and amputation if arterial reconstruction cannot
be performed. The pain is severe and burning, usually confined to the
forefoot distal to the metatarsals. It may be localized to the vicinity
of an ischemic ulcer or pregangrenous toe. It is aggravated by elevation
of the extremity or by bringing the leg to the horizontal position.
Thus, it appears at bed rest (hence the name) and may prevent sleep.
Because gravity aids the delivery of arterial blood, classically,
the patient with rest pain can obtain relief by simply hanging the
leg over the side of the bed. This simple maneuver will not relieve
pain caused by peripheral neuropathy, the most common cause of foot
pain at rest. If the foot is constantly kept dependent to relieve
pain, the leg and foot may be swollen, causing some confusion in
diagnosis. The ischemic neuritis of rest pain is severe and resistant
to opioids for relief.
Patients with rest pain may give a history of claudication, but
rest pain also may occur de novo in diabetics with distal tibial
disease, embolic occlusion of the distal tibial arteries, and patients
whose walking is limited by other conditions. Differentiating ischemic
rest pain from neuropathy in diabetics may be difficult and require
Wounds or Ulcers
Patients with severe lower extremity arterial insufficiency often
develop ulcers or wounds on the feet even from seemingly trivial
trauma. These lesions are most commonly located on the distal foot and
toes, but on occasion they can be in the upper foot or ankle. Typically,
the wounds are excruciatingly painful, deep, and devoid of any evidence
of healing such as contraction or formation of granulation tissue.
Inability to attain or maintain an erection may be produced by
lesions that obstruct blood flow through both hypogastric arteries
and is commonly found in association with narrowing of the terminal
aorta or common iliac arteries. Vasculogenic erectile dysfunction
is less common than that due to other causes.
Although the patient may report numbness in the extremity, sensory
abnormalities are generally absent on examination. If decreased
sensation is found in the foot, peripheral neuropathy should be
Physical examination is of paramount importance in assessing
the presence and severity of vascular disease. The physical findings
of peripheral atherosclerosis are related to changes in the peripheral
arteries and to tissue ischemia.
Decreased amplitude of the pulse denotes proximal obstructions
to flow. The pulse examination can help localize disease. For example,
an absent femoral pulse usually signifies aortoiliac disease. It
is unusual for collateral flow to be sufficient to produce a pulse distal
to an occluded artery.
A bruit is the sound produced by dissipation of energy as blood
flows through a stenotic arterial segment. With extremely high flows,
the energy may vibrate the artery, creating a “thrill.” The
bruit or thrill is transmitted distally along the course of the
artery. Thus, when a bruit is heard through a stethoscope placed
over a peripheral artery, stenosis is present at or proximal to
that level. The pitch of the bruit rises as the stenosis becomes more
marked, until a critical stenosis is reached or the vessel becomes
occluded, when the bruit may disappear. Thus, absence of a bruit
does not indicate insignificant disease.
Exercise in a normal individual increases the pulse rate without
producing arterial bruits or reduction in pulse amplitude. In an
individual who complains of claudication, there may be minimal findings
at rest, but exercise will produce decreased pulse strength, distal arterial
pressure, and possibly an audible bruit unmasking a significant
stenosis. Exercise is best used in conjunction with noninvasive
Chronic ischemia commonly produces loss of hair over the dorsum
of the toes and foot and may be associated with thickening of the
toenails (onychomycosis) due to slowed keratin turnover. With more advanced
ischemia, there is atrophy of the skin and subcutaneous tissue so
that the foot becomes shiny, scaly, and skeletonized. Hence, a quick
glance at a foot usually can identify the presence or absence of
serious arterial insufficiency.
Pallor of the foot on elevation of the extremity with a complete
absence of capillary refill indicates advanced ischemia. Pallor
on elevation does not occur unless advanced ischemia is present.
When pallor is produced with elevation, the ischemia results
in maximum cutaneous vasodilation. When the extremity is returned
to a dependent position, blood returning to the dilated vascular
bed produces an intense red or possibly ruborous color in the foot,
called reactive hyperemia, and denotes advanced disease. The delay
in the appearance of color when the extremities return to a dependent
position is proportionate to the impairment in circulation.
In advanced atherosclerotic disease, the skin of the foot displays
a characteristic dark red/cyanotic color on dependency.
Because of low inflow, the blood in the capillary network of the
foot is relatively stagnant, oxygen extraction is high, and the
capillary blood becomes the color of the venous blood. The concurrent
vasodilation due to ischemia causes blood to suffuse the cutaneous
plexus, imparting a purple color to the skin. The purple discoloration due
to severe chronic venous insufficiency does not develop pallor on
With chronic ischemia, the temperature of the skin of the foot
decreases. Coolness can best be detected by palpation with the back
of the examiner’s hand with comparison to the contralateral
Ischemic ulcers are usually very painful and accompanied by rest
pain in the foot. They occur in toes or at a site where minor trauma
from a shoe or bedding can initiate the injury. The margin of the
ulcer is sharply demarcated or punched-out, and the base is devoid
of healthy granulation tissue. The surrounding skin is pale and mottled,
and signs of chronic ischemia are invariably present
Moderate to severe degrees of chronic ischemia produce gradual
soft tissue and muscle atrophy and loss of strength in the ischemic
zone. Joint mobility may be reduced in the forefoot as atrophy of
the muscles of the foot produces increasing prominence of the interosseous
spaces. Subsequent changes in foot structure and gait increase the possibility
of developing foot ulceration.
Tissue necrosis first becomes apparent in the most distal portions
of the extremity or at an ulcer site. Necrosis halts proximally
at a line where the blood supply is sufficient to maintain viability
and results in dry gangrene. If the necrotic portion is infected
(wet gangrene), necrosis may extend into tissues that would normally
Vascular Laboratory Tests
Noninvasive assessment is helpful to determine the severity of
hypoperfusion and the sites of hemodynamically significant stenoses
The ankle-brachial index (ABI) is a quick screening
test and the cornerstone of the diagnosis of peripheral vascular disease.
The ABI is determined by dividing the systolic pressure obtained
by Doppler insonation at the ankle by the brachial arterial pressure.
Normally, the ABI is 1.0 or greater; a value below 1.0 indicates
occlusive disease proximal to the point of measurement. The ABI
correlates roughly with the degree of ischemia (eg, claudication
occurs with a value less than 0.7 and rest pain usually appears
when the ratio is 0.3 or lower). Patients with diabetic vascular
disease may have artificially elevated ABI values due to calcified, noncompressible
arteries, and toe-to-brachial pressure ratios should be substituted.
Blood pressures can be measured at rest and after exercise in
the ankle, and the effect of exercise can be monitored. Exercise
testing confirms and quantitates the diagnosis of claudication.
To perform exercise testing, the patient walks on a treadmill at
a standard speed and grade until claudication pain is experienced
or a time limit is reached. With significant arterial occlusive
disease, there will be a decrease in the ABI with exercise, usually
measured 1 minute after cessation of walking. If the pain is not
due to arterial stenosis, no fall in pressure will occur. This test
is particularly useful in differentiating neurogenic pain with walking
Color duplex ultrasound imaging is a mainstay of
vascular imaging. It is a painless, relatively inexpensive, and
(in experienced hands) accurate method for acquiring anatomic and
functional information (eg, velocity gradients across stenoses).
Although the accuracy of this study is operator dependent, it can
supply sufficient information to permit intervention in selected
CT angiography (CTA) is useful for imaging the arterial tree
and has the advantage of visualizing cross sections of the vessel
lumen. In many instances, this allows for more accurate determination
of vessel diameter and stenosis severity than conventional angiography.
It does require the administration of nephrotoxic contrast dye,
and its images may be obscured by the presence of calcification
or metallic implants. MR angiography (MRA) also can
be used to obtain images similar in quality to angiography in most cases.
MRA does not show calcifications and gives better visualization
of tibial vessels than CTA. MRA also can reveal details of composition
of atherosclerotic plaque. Gadolinium-associated nephrogenic fibrosing
dermopathy limits its use in patients with renal insufficiency.
The integrated use of computer workstations with CT and MR image
data can provide 3D images that can be useful in visualizing patient
anatomy and planning interventional procedures.
Conventional arteriography provides detailed anatomic information
about peripheral arterial disease. It is reserved for patients warranting
invasive intervention such as percutaneous transluminal angioplasty
(often shortened to PTA) or vascular surgery. Complications of angiography
are related to technique and contrast media. Technical complications such
as puncture site hematomas, arteriovenous fistulas, and false aneurysms
are rare (1%). Contrast agents may precipitate allergic
reactions (0.1%). Patients with renal failure, proteinuria,
diabetes, and dehydration are at increased risk for contrast-induced
renal failure. Adequate hydration of patients before and after angiography,
acetylcysteine, and periprocedural infusions of sodium bicarbonate
infusions may reduce the incidence of this complication.
The objectives of treatment for lower extremity occlusive disease
are relief of symptoms, prevention of limb loss, and maintenance
of bipedal gait.
In general, patients with peripheral vascular disease have shortened
life expectancies because of their severe atherosclerotic disease.
Nondiabetic patients with ischemic disease of the lower extremity
have a 5-year survival rate of 70%. The survival rate is
60% in patients with associated ischemic heart disease
or cerebrovascular insufficiency. Patients with peripheral vascular
disease and renal failure have a 2-year survival rate of less than
50%. Most deaths are due to myocardial infarctions and
strokes. Only 20% of deaths are due to nonatherosclerotic
Nonoperative treatment consists of (1) medical management of
cardiovascular risk factors, (2) exercise rehabilitation, (3) foot
care, and (4) pharmacotherapy.
of Cardiovascular Risk Factors
See Table 34–1. Cigarette smoking
is the single most important risk factor for peripheral vascular
disease, and all patients should stop smoking. At high levels of
consumption, 2–3 packs per day, claudicants will experience
immediate improvement in walking distance.
Table 34–1. Summary of Risk Factor Modification in Peripheral
Vascular Disease. |Favorite Table|Download (.pdf)
Table 34–1. Summary of Risk Factor Modification in Peripheral
|Risk Factor||Therapy||Clinical Effect|
|Tobacco use||Counseling||Reduced overall mortality|
|Antiplatelet||Aspirin||Antiplatelet therapy gives > 20% reduction
in MI, stroke, or vascular death|
|Hyperlipidemia||Statin||20–30% reduction in cardiovascular
and all-cause mortality in CAD patients|
|Lipid goals in PAD patients: LDL <
|Hypertension||Target BP < 140/90 in PAD patients||Beta-blocker and ACE inhibitors each associated with
> 20% reduction in cardiovascular mortality|
|Diabetes||Goal hemoglobin A1c < 7%||Benefits in vascular disease unproven|
|Lifestyle||Daily aerobic exercise||Reduced lipid levels|
|Weight loss||Reduced cardiovascular events|
In the past, elevated lipids were not usually associated with
peripheral vascular disease. Hyperlipidemia, however, is often present,
especially in patients with early onset of disease. Elevated triglyceride
levels and low high-density lipoprotein (HDL) cholesterol levels
are more prevalent than elevated levels of low-density lipoprotein
(LDL) cholesterol. Reduction of elevated lipid levels is associated
with stabilization or regression of arterial plaques. Statins are
extremely effective in reducing LDL cholesterol, and goals of therapy for
patients with peripheral vascular disease are to maintain cholesterol
levels at less than 100 mg/dL (2.6 mmol/L). Statins
have other pleiotropic effects that may reduce inflammation, stabilize
plaques, and independently increase walking distance in claudicants.
Other antihyperlipidemic medications, including niacin and fibrates
(gemfibrozil), may be used to lower hypertriglyceridemia, which
can increase HDL cholesterol.
Both type 1 and type 2 diabetes increase the prevalence and severity
of cardiovascular disease. Intensive glycemic control reduces the
incidence of nephropathy, neuropathy, and retinopathy in diabetes,
but it does not correlate with the severity or progression of peripheral
arterial disease. In order to reduce all-cause mortality, however,
it is recommended that fasting blood sugars should be controlled
with hemoglobin A1c levels less than 7%.
For claudicants, exercise ranging from unsupervised walking to
formal supervised exercise on a treadmill significantly improves
walking ability. A 21-study meta-analysis of exercise programs showed
an average 180% increase in initial claudication distance
and a 120% increase in maximal walking distance achieved through
exercise. The precise mechanism behind this improvement is not firmly
established. Collateral development seems unlikely because ankle
pressures and limb flow do not increase substantially. Possible
explanations include improved metabolic capacity and conditioning
of the muscles.
Since patients with claudication are at a twofold to fourfold
greater risk of dying from complications of generalized atherosclerosis
than people without claudication, an additional benefit of exercise
in these patients is that an improvement in walking distance as
part of an aggressive risk factor modification regimen results in
an overall decrease in cardiovascular risk.
The feet of patients with neuropathy or with critical limb ischemia
should be inspected and washed daily and kept dry. Mechanical and
thermal trauma to the feet should be avoided. Toenails should be
trimmed carefully, and corns and calluses should be attended to
promptly. Even minor foot infections or injuries should be treated
aggressively. Educating the patient to understand neuropathy, peripheral
vascular insufficiency, and the importance of foot care is a central
aspect of treatment.
The Antiplatelet Trialists Collaboration found an overall 25% decrease
in fatal and nonfatal myocardial infarctions, strokes, and vascular
deaths in those treated with antiplatelet agents. Aspirin at dosages
ranging from 75 to 350 mg/d is the first-line antiplatelet
agent recommended, though clopidogrel, which blocks the activation
of platelets by adenosine diphosphate (ADP), may be useful in aspirin-intolerant
patients. Clopidogrel is also an important adjunctive therapy in
reducing thrombogenicity at locations of endovascular arterial treatment.
All patients with cardiovascular disease, whether symptomatic or
asymptomatic, should be considered for antiplatelet therapy to reduce
the risk of cardiovascular morbidity and mortality.
Two drugs have been approved by the FDA for treatment of intermittent
claudication. Pentoxifylline produces a small improvement in both
initial claudication distance (about 20%) and absolute
claudication distance (about 10%). Cilostazol is a phosphodiesterase
III inhibitor with vasodilator, antiplatelet, and antilipid activity.
Randomized, placebo-controlled, blinded trials have shown an increase
of about 50% in absolute claudication distance in patients
treated with cilostazol. Quality-of-life assessments also improved
significantly. Gene therapy for cardiovascular disease is being investigated,
but conclusions regarding safety and efficacy are premature.
Baigent C et al: Efficacy and safety of cholesterol-lowering treatment:
prospective meta-analysis of data from 90,056 participants in 14
randomised trials of statins. Lancet 2005;366:1267.
Clagett P et al: Antithrombotic therapy in peripheral arterial disease:
the seventh ACCP conference on antithrombotic and thrombolytic therapy.
Critchley JA, Capewell S: Mortality risk reduction associated
with smoking cessation in patients with coronary heart disease:
a systematic review. JAMA 2003;290:86.
Dormandy JA, Murray GD: The fate of the claudicant–a
prospective study of 1969 claudicants. Eur J Vasc Surg 1991;5:131.
Fowkes F, Lee A, Murray G: Ankle-brachial index as an independent
indicator of mortality in fifteen international population cohort
studies. ABI Collaboration. Circulation 2005;112:3704.
McCullough PA: Contrast-induced acute kidney injury. J Am Coll Cardiol
Rehring TF, Stolcpart RS, Hollis HW Jr: Pharmacologic risk factor
management in peripheral arterial disease: a vade mecum for vascular
surgeons. Society for Vascular Surgery. J Vasc Surg 2008;47:1108.
Stewart K et al: Exercise training for claudication. N Engl
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Yusuf S et al: Effects of an angiotensin-converting-enzyme inhibitor,
ramipril, on cardiovascular events in high-risk patients. Heart
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Interventional procedures, open or endovascular, are performed
both for limb salvage and for incapacitating claudication. The choice
of operative procedure depends on the location and distribution
of arterial lesions and the patient’s comorbidities. Recognition
of coexistent cardiopulmonary disease is particularly relevant,
because many patients with peripheral vascular disease also have
ischemic heart disease and/or chronic lung disease associated
with tobacco use. Preoperative cardiac functional assessment is
sometimes necessary, but preoperative myocardial revascularization
is not beneficial in patients with reasonable cardiac reserve. All patients
undergoing vascular surgery should have preoperative risk assessment.
Randomized trials have shown that perioperative beta-blocker, angiotensin-converting
enzyme (ACE) inhibitor, and statins may reduce cardiac morbidity
in patients undergoing vascular surgery. Evidence is also emerging
demonstrating the importance of maintaining statin therapy throughout
the perioperative period.
Endovascular therapy consists of image-guided techniques to treat
diseased arterial segments from within the lumen of the vessel.
Access to the arterial system is established by the insertion of
valved sheaths, usually percutaneously, into the access vessel,
often the common femoral artery. Steerable wires and catheters are
then passed through the vasculature under fluoroscopic guidance
to the target lesion (Figure 34–3).
Once the target lesion is accessed, therapeutic maneuvers, such
as angioplasty, or devices, such as stents, can be delivered. In
many arterial beds, endovascular therapy is more commonly utilized
than open surgical therapy because of its minimally invasive nature
and reduction of short-term morbidity and mortality. However, many
questions remain concerning the long-term durability of endovascular
repairs, and open surgery still plays a major role in the treatment
of patients with arterial disease.
Endovascular gear. A: Sheath. Inserted using
Seldinger technique into access vessel. Wires, catheters, and devices
pass through the sheath. Sheaths provide stable working access points
and protect artery. B: Catheter. Variable length, stiffness,
coating, and shape (examples: B.1, cobra; B.2, pigtail; B.3, mesenteric
selective). Catheters help steer wires through vasculature and also
maintain access in vessel. C: Guidewire. Variable diameter,
length, stiffness, and shape. Used to gain access into vasculature, cross
lesions, and deliver devices. D: Balloon catheter. E: Peripheral
stent graft. F: Peripheral nitinol self-expanding stent. G: Aortoiliac
stainless steel/Dacron stent-graft.
Percutaneous transluminal angioplasty, with or without
placement of an intravascular stent, is often the treatment of choice
when stenoses or even occlusions are relatively short and localized.
As the angioplasty balloon expands, it stretches the adventitia,
fracturing and compressing plaque, expanding the artery to widen
the lumen. Energy losses associated with a stenosis are inversely
proportionate to the fourth power of the radius; therefore, even
small increases in radius can result in substantial increases in
blood flow, although durability of the procedure is improved with
the reestablishment of a normal lumen. Concomitant stenting is frequently
performed to improve luminal expansion and the arteriographic appearance
of the lesion. Stent grafts (stents with fabric covering) may also
be used in selected cases or to repair the inadvertent rupture of
an artery during angioplasty (Figure 34–4).
Aortoiliac occlusive disease. A: Aorta. B: Severely
stenotic/occluded iliac arteries. B.1: Widely patent
iliac arteries following balloon angioplasty and stenting (C).
Both stents and stent grafts are commonly used from the aortic
bifurcation to the distal popliteal artery. Stenting is rarely performed
below the knee, but angioplasty of tibial disease is now common
with the use of small catheters and wires. Percutaneous mechanical
and laser atherectomy are other options in removing obstructing
lesions in lower extremity atherosclerotic occlusive disease. Mechanical
atherectomy removes plaque by shaving with a cutting or rotating
For short, stenotic segments in larger, more proximal vessels,
the results of endovascular therapies are good with 1-year success
rates of 85% in common iliac disease and 70% in
external iliac disease. The results with superficial femoral and
popliteal lesions are lower (Figure 34–5).
The success of endovascular therapy for lower extremity occlusive
disease is inversely related to the complexity of the lesion, defined
by the number and length of stenoses treated.
Superficial femoral artery occlusion, angioplasty and
stent-graft. A: Common femoral artery. B: Occluded
superficial femoral artery. B.1: Recannulized, stent-grafted
superficial femoral artery. C: Profunda femoris artery. D: Stent-graft.
Since disease may recur more frequently after angioplasty than
after bypass surgery, the patient should be closely followed up
using noninvasive tests. Repeat angioplasty or stenting may be indicated
for recurrent disease, but the improvement in morbidity and mortality
of endovascular interventions may be offset by the need for multiple
repeat procedures. In general, minimally invasive percutaneous treatment
of lower extremity occlusive disease is best used in patients of
high operative risk and severe, limb-threatening ischemia (Figure 34–6).
Comparison of outcomes for surgical and endovascular
intervention in lower extremity occlusive disease.
Open operations are indicated for aortoiliac occlusive disease
in younger patients with low operative risk or patients with severe
disease not amenable to endovascular therapy. To completely bypass
the aortoiliac segment, an inverted Y-shaped prosthesis
is interposed between the infrarenal abdominal aorta and the femoral
arteries, creating an aortofemoral bypass. The goal
of operation is restoration of blood
flow to the common
femoral artery or, when occlusive disease of the superficial femoral
artery is present, to the profunda femoris artery. The clinical
results of aortofemoral reconstruction are excellent, although the
mortality and morbidity clearly are higher than for endovascular
therapy. The operative death rate is 5%; early patency
rate, 95%; and late patency rate (5–10 years postoperatively),
about 80%. Late complications may be as high as 10% and
include graft-intestinal fistula formation, anastomotic aneurysm
formation, renal failure, and erectile dysfunction.
Lower risk procedures may be preferable in high-risk patients.
If the clinically important lesions are confined to one side, a
femoral-femoral or iliofemoral bypass graft can be used. A graft
from the axillary to the femoral artery (ie, axillofemoral graft)
can be used for bilateral disease. Unfortunately, these “extra-anatomic” methods
of arterial reconstruction are more prone to late occlusion than
are direct reconstructions.
When disease is confined to the femoropopliteal segment, femoropopliteal bypass is
used. The principal indication for these operations is limb salvage.
In patients with claudication alone, the indications for femoropopliteal
bypass are more difficult to define but must include substantial
disability from claudication. For limited lesions of the superficial
femoral artery, endovascular therapy is often attempted first, with
surgery reserved for extensive disease or angioplasty failure.
The best graft for femoropopliteal bypass is an autologous greater
saphenous vein. The saphenous vein may be left in situ or removed
and reversed. In the former instance, the venous tributaries are
ligated, and special instruments are used to render the valves incompetent.
Expanded polytetrafluoroethylene (PTFE) may also be used as a conduit,
particularly for bypass to the suprageniculate popliteal artery.
Below the knee, PTFE conduits produce much lower patency rates than
saphenous veins. Operative death rates are low (2%), and
5-year patency rates range from 60% to 80%. Limb
salvage rates are higher than graft patency rates.
The profunda femoris artery perfuses the thigh and acts as an
important source of collateral flow when the superficial femoral
artery is diseased. When there is a stenosis of the profunda, profundoplasty alone
can be performed for limb salvages with success rates of 80% when
the suprageniculate popliteal artery is patent and 40–50% when
the popliteal artery is occluded. Isolated profundoplasty is rarely
helpful for treating claudication.
Tibioperoneal Arterial Reconstruction
Reconstruction of tibial arteries (ie, distal bypass to
the tibial, peroneal, or pedal vessels) is performed only for limb salvage.
Advancing technology allows better endovascular therapy in the tibial
vessels, with decreased short-term morbidity and mortality, and
similar gains in limb salvage when compared to bypass surgery. However,
endovascular techniques are not as widely used in the tibial vessels,
and bypass still remains the primary mode of therapy for these patients.
Autogenous saphenous veins are preferred because prosthetic conduits
have high failure rates. Due to smaller vessel size, extensive disease,
and probably the length of the bypass conduit, these grafts are
not as durable as femoropopliteal bypass, so the limb salvage rate
is substantially higher than graft patency. The operative death rate
for these procedures is about 5%.
Amputation of the limb is necessary within 5–10 years
in only 5% of patients presenting with claudication. Amputation
is more common if patients continue to smoke cigarettes. Patients
with multiple risk factors for atherosclerosis and short-distance
claudication are also at increased risk for eventual limb loss.
Of patients who present with ischemic rest pain or ulceration, 5–10% require amputation
as initial therapy, and most eventually will require amputation
if not revascularized. Successful revascularization results in lower
costs than primary amputation and an infinite improvement in quality
of life. Occasionally, primary amputation may be preferable to revascularization if
the likelihood of successful bypass is low, extensive foot infection
is present, or the patient is nonambulatory. Amputation levels,
options, and the special needs of amputees are covered in the section
on Lower Extremity Amputation.
Hirsch AT et al: ACC/AHA 2005 guidelines
for the management of patients with peripheral arterial disease
(lower extremity, renal, mesenteric, and abdominal aortic): a collaborative
report from the American Association for Vascular Surgery/Society for
Vascular Surgery, Society for Cardiovascular Angiography and Interventions,
Society for Vascular Medicine and Biology, Society of Interventional
Radiology, and the ACC/AHA Task Force on Practice Guidelines
(Writing Committee to Develop Guidelines for the Management of Patients
with Peripheral Arterial Disease) endorsed by the American Association
of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung,
and Blood Institute; Society for Vascular Nursing; TransAtlantic
Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll
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