Cardiac, Thoracic, and Vascular: Vascular Surgery

Question 1

Aneurysms

Answer 1

• An aneurysm is an abnormal dilation of an artery.

Saccular aneurysms occur when a portion of the

artery forms an outpouching, or “mushroom.” Fusiform

aneurysms occur when the entire arterial diameter

grows. True aneurysms involve all layers of the arterial
wall: intima, media, and adventitia. An artery is con-

sidered aneurysmal if the diameter is greater than 1.5 times its normal size. Otherwise, an enlarged artery is considered

ectatic.

Question 2

Dissections

Answer 2

• occurs when a defect in

the intima allows blood to enter between layers of

the wall (Fig. 16-1). Blood pressure then causes the

layers of the wall to separate from one another. The

serious nature of aneurysms and dissections is due to

the weakened vessel wall and the potential for cata-

strophic events. In the case of an aneurysm, this includes

rupture or vascular compromise; dissections can result

in the occlusion of the ostia of visceral arteries or progress

into the heart and can affect the coronary circulation

or lead to tamponade.

Question 3

Abdominal Aortic Aneurysm: Anatomy

Answer 3

• The abdominal aorta lies below the diaphragm and

above the iliac arteries. Branches include the celiac trunk,

superior mesenteric artery, inferior mesenteric artery,

renal arteries, and gonadal arteries. Approximately

95% of abdominal aneurysms begin distal to the takeoff

of the renal arteries.

Question 4

Abdominal Aortic Aneurysm: Etiology

Answer 4

• Ninety-five percent of aneurysms of the abdominal

aorta are associated with atherosclerosis. Other causes

include trauma, infection, syphilis, and Marfan’s syn-

drome. Protease activity in the vessel wall is commonly

increased.

Question 5

Abdominal Aortic Aneurysm: Epidemiology

Answer 5

• Abdominal aortic aneurysms are responsible for

15,000 deaths per year. The incidence is approxi-

mately 0.05%, but in selected high-risk populations,

the incidence increases to 5%. Men are affected 10 times

more frequently than women, with an age of onset

usually between 50 and 70 years. Risk factors include

atherosclerosis, hypertension, hypercholesterolemia,

smoking, and obesity. The disease is associated with

peripheral vascular disease, heart disease, and carotid

artery disease.

Question 6

Abdominal Aortic Aneurysm: History

Answer 6

• Most aneurysms are asymptomatic. Pain usually signi-

fies a change in the aneurysm—commonly enlarge-

ment, rupture, or compromise of vascular supply—

and should therefore be considered an ominous

symptom. Pain may occur in the abdomen, back, or
flank. The legs could be involved if the aneurysm

includes the iliac arteries or if an embolic event occurs.

The pain is usually sudden in onset and does not

remit.

Question 7

Abdominal Aortic Aneurysm: Physical Examination

Answer 7

• Abdominal examination may reveal a pulsatile abdom-

inal mass.Enlargement, rupture, or compromise of

vascular supply may manifest by tenderness, hypoten-

sion, tachycardia, or a change in the location or inten-

sity of pain. In addition, the lower extremities may have

pallor, cool temperature or pulses that are diminished

or unequal.

Question 8

Abdominal Aortic Aneurysm: Diagnostic Evaluation

Answer 8

• Ultrasound is an accurate, noninvasive method to assess

the size of the aneurysm and the presence of clot within

the arterial lumen. Computed tomography (CT) or mag-

netic resonance imaging provides anatomic detail and

precise localization of the aneurysm. An aortogram may

be helpful in planning surgical intervention to demon-

strate involvement of other vessels, specifically the renal,

mesenteric, and iliac arteries.

Question 9

Abdominal Aortic Aneurysm: Treatment (Part 1)

Answer 9

• If the patient is asymptomatic, workup can proceed
  electively. Treatment of asymptomatic abdominal

aortic aneurysms depends on the size of the lesion,

which is directly proportional to its propensity to

grow, leak, or rupture. Aneurysms less than 4 cm in diameter

are unlikely to rupture, and medical management with

antihypertensives, preferably beta-blockers, is advocated.

When the aneurysm reaches approximately 4 to 5 cm,

two options are available: early operation or close follow-

up. A recent randomized trial suggests that mortality

is the same in both options. When the aneurysm

reaches 5 cm in diameter, the incidence of rupture is greater than 25% at 5 years, and repair is recommended, unless

he patient is at prohibitive operative risk. Table 16-1

lists rupture rates per year based on aneurysm size.

Question 10

Abdominal Aortic Aneurysm: Treatment (Part 2)

Answer 10

• Treatment options have recently expanded with the

advent of stent grafts that can be placed through the

femoral artery. In selected patients, these stents carry

less morbidity than traditional operative repair.

Concerns include stent migration and leaks around

the prosthesis, but in general, these complications can

be managed effectively. Technologic advances and

clinical experience are widening the versatility of

these stents, allowing the placement of fenestrated

stents with orifices for visceral vessels and stents with

limbs that can be placed at arterial bifurcations.

Any patient presenting on physical examination

with symptoms that suggest a catastrophic aortic

event should undergo emergent diagnostic workup or

intervention. Once the diagnosis of ruptured or leaking

abdominal aortic aneurysm is determined, arrangements

should be made for fluid resuscitation and immediate

operative intervention.

Question 11

Abdominal Aortic Aneurysm:

Repair of Abdominal Aortic Aneurysm:

The Operation

Answer 11

• Consistent with the size of the operation, preopera-

tive preparation includes large-bore intravenous lines,

central monitoring, and intravenous antibiotics.

Blood, either autologous or cross-matched, should be

available. Abdominal aortic aneurysms can be

approached via either a midline incision or an oblique

incision over the left 11th intercostal space. Using a

midline incision requires mobilization of the small

bowel to the patient’s right. Incision of the posterior

peritoneum to the left of the aorta allows exposure of

the entire aorta. The oblique incision is reserved for a

retroperitoneal approach, in which the entire con-

tents of the peritoneal cavity are mobilized to the

right, allowing exposure of the aorta. Proximal and

distal control around the aneurysm is obtained, and

heparin is administered before clamping. A graft is

placed using permanent sutures. If a transabdominal

approach is used, the peritoneum is closed over the

graft if possible (Fig. 16-2).

Question 12

Thoracic Aortic Aneurysm: Anatomy

Answer 12

• The thoracic aorta lies between the heart and the
  diaphragm. It gives rise to the brachiocephalic, left

common carotid, left subclavian, bronchial, esophageal,

and intercostal arteries.

Question 13

Thoracic Aortic Aneurysm: Etiology

Answer 13

• Thoracic aortic aneurysms are caused by cystic medial

necrosis, atherosclerosis, or, less commonly, trauma,

dissection, or infection.

Question 14

Thoracic Aortic Aneurysm: Epidemiology

Answer 14

• Males are affected three times as often as females.

Risk factors include atherosclerosis, smoking, hyper-

tension, and family history

Question 15

Thoracic Aortic Aneurysm: History

Answer 15

• Most aneurysms are asymptomatic. Rupture usually

presents with chest pain or pressure. Expansion of

the aneurysm can compress the trachea, leading to

cough, or erode into the trachea or bronchus, causing

massive hemoptysis. An aneurysm close to the aortic

valve can cause dilation of the annulus, resulting in

aortic valve insufficiency and chest pain, dyspnea, or

syncope.

Question 16

Thoracic Aortic Aneurysm: Physical Examination

Answer 16

• Hypotension and tachycardia may be present. If the

aneurysm involves the aortic annulus, it can lead to

aortic regurgitation and congestive heart failure. Pulse

examination may be abnormal if distal embolization

occurs.

Question 17

Thoracic Aortic Aneurysm: Diagnostic Evaluation

Answer 17

• Chest radiography may show a widened thoracic aorta.

Electrocardiography may demonstrate myocardial

ischemia, especially if the aneurysm compromises the

coronary supply. In the asymptomatic patient with a

thoracic aneurysm, CT or echocardiography is helpful

in establishing the diagnosis. Echocardiography can also

determine the extent of involvement of the aortic valve

and possible cardiac tamponade. Aortography may be

useful for planning operative intervention, because it

defines the aneurysm’s relation to a number of critical

structures.

Question 18

Thoracic Aortic Aneurysm: Treatment

Answer 18

• As with abdominal aortic aneurysms, operative

repair should be considered when the maximum

diameter approaches 5 cm. Symptomatic presentation

is an indication for immediate operative intervention.

As with abdominal aortic aneurysms, the indications

for stent grafts for thoracic aortic aneurysms are being

carefully evaluated.

Question 19

Aortic Dissection: Pathogenesis

Answer 19

• Dissections can be caused by hypertension, trauma,

Marfan syndrome, or aortic coarctation.

Question 20

Aortic Dissection: Epidemiology

Answer 20

• Aortic dissections are more common than either tho-

racic or abdominal aneurysms. Incidence increases

with age, and men are more commonly affected than

women

Question 21

Aortic Dissection: History

Answer 21

• Patients usually complain of the immediate onset of

severe pain, often described as tearing, usually in the

chest, back, or abdomen. Nausea or light-headedness

may also be present.

Question 22

Aortic Dissection: Physical Examination

Answer 22

• Patients may be hypotensive. Rales on chest ausculta-

tion or a new murmur suggest that the dissection

continues retrograde into the aortic root. Peripheral

pulses are diminished if distal blood flow is compro-

mised. If the dissection continues into the visceral

arteries, compromise of mesenteric vessels can pro-

duce abdominal pain, compromise of renal arteries

can cause oliguria, and compromise of spinal blood

supply can produce neurologic deficits.

Question 23

Aortic Dissection: Diagnostic Evaluation

Answer 23

• A chest radiograph may show a widened mediastinum.

CT may show the dissection or clot in the arterial

lumen. Diagnosis can be made with transesophageal

ultrasound, magnetic resonance imaging, or aortogram.

Dissections are classified according to the DeBakey

classification: type I involves both the ascending and

the descending aorta, type II involves only the ascend-

ing aorta, and type III involves only the descending

aorta.

Question 24

Aortic Dissection: Treatment

Answer 24

• Dissection of the ascending thoracic aorta usually

requires surgery, because of the potential for retro-

grade progression into the aortic root and subsequent

compromise of the coronary circulation or tampon-

ade from rupture into the pericardium. Eighty per-

cent of patients with involvement of the ascending

aorta die without treatment. Antihypertensive ther-

apy is used preoperatively in an attempt to halt the

progression of the dissection.

• In contrast, dissections limited to the descending

aorta are best managed medically, with antihyperten-

sives, including sodium nitroprusside and beta block-

ade. Invasive monitoring with fluid resuscitation

should be instituted immediately. Surgery is reserved

for lesions that progress or cause distal ischemia. Stent

grafts have been shown to be safe in selected patients.

Determination of who should receive a stent graft is

being studied.

Question 25

Carotid Artery Disease: Anatomy (Part 1)

Answer 25

• The common carotid artery on the right arises from

the brachiocephalic artery, and on the left, from the

aorta. The common carotid then bifurcates into

internal and external branches. The internal carotid

gives off the ophthalmic artery before continuing to

the circle of Willis to supply the brain. The area

around the bifurcation is clearly “high-rent” terri-

tory, which contains a number of vital structures

which can be injured during surgery. The marginal

mandibular branch of the facial nerve lies deep and

inferior to the horizontal ramus of the mandible. Injury

to this nerve during dissection results in lower lip

paralysis. Branches of the cervical plexus, including

the greater auricular nerve, may be at the cranial

aspect of the incision and should be avoided to pre-

serve sensation to the ear and the angle of the

mandible.

Question 26

Carotid Artery Disease: Anatomy (Part 2)

Answer 26

• Posterolateral to the carotid artery in the

carotid sheath lies the vagus nerve. Injury results in

vocal cord paralysis. One or two centimeters above

the carotid bifurcation is the hypoglossal nerve; injury

results in dysphagia and tongue deviation. In contrast,

the ansa cervicalis, which courses inferiorly from

the hypoglossal to innervate the strap muscles, can

be sacrificed as needed for exposure. Laterally and

deep to the carotid artery lies the

jugular vein, a branch of which, the facial vein, is generally divided to facilitate exposure of the carotid.

Question 27

Carotid Artery Disease: Pathogenesis

Answer 27

• Symptoms are the result of atherosclerosis. Mechanisms

of morbidity include plaque rupture, ulceration, hem-

orrhage, thrombosis, and low flow states. Because of

the rich collateralization of the cerebral circulation

through the circle of Willis, thrombosis and low flow

states may be asymptomatic.

Question 28

Carotid Artery Disease: Epidemiology

Answer 28

• Atherosclerotic occlusive disease of the carotid

artery is a major cause of stroke. In the United

States, 400,000 people are hospitalized for stroke

each year, and cerebrovascular events are the third

most common cause of death. The incidence of

stroke increases with age. Other risk factors include

hypertension, diabetes, smoking, and hypercholes-

terolemia. Markers for carotid disease include evi-

dence of other atherosclerotic disease and prior neu-

rologic events.

Question 29

Carotid Artery Disease: History

Answer 29

• Patients often relate previous neurologic events,

including focal motor deficits, weakness, clumsiness,

and expressive or cognitive aphasia. These could

occur as a transient ischemic attack, which resolves

in 24 hours; a reversible ischemic neurologic deficit,

which resolves in greater than 24 hours; or a fixed

neurologic deficit. One characteristic presentation

for carotid disease is amaurosis fugax, or transient

monocular blindness, usually described as a shade

being pulled down in front of the patient’s eye. This

is due to occlusion of a branch of the ophthalmic

artery.

Question 30

Carotid Artery Disease: Physical Examination

Answer 30

• Patients may exhibit a fixed neurologic deficit. Hollen-

horst plaques on retinal examination are evidence of

previous emboli. A carotid bruit is evidence of turbu-

lence in carotid blood flow, but the presence of a bruit

does not unequivocally translate into a hemodynam-

ically significant lesion, and the absence of a bruit

does not unequivocally indicate the absence of signif-

icant disease.

Question 31

Carotid Artery Disease: Diagnostic Evaluation

Answer 31

• Carotid duplex scanning is both sensitive and specific

for carotid disease. Conventional or magnetic reso-

nance angiography is more accurate for assessing the

degree of stenosis.

Question 32

Carotid Artery Disease: Treatment

Answer 32

• Treatment depends on the history, degree of stenosis,

and characteristics of the plaque. Antiplatelet therapy

with aspirin is effective in preventing neurologic

events. When dealing with an acute event, heparin

should be considered after head CT determines that

the event is not hemorrhagic. Indications for carotid

endarterectomy are controversial. Results of two large

randomized controlled trials—the Asymptomatic

Carotid Atherosclerosis Study (ACAS) and the North

American Symptomatic Carotid Endarterectomy

Trial (NASCET)—suggest surgery is best reserved for

the following patients: those with

75% stenosis, those

with 70% stenosis and symptoms, those with bilateral

disease and symptoms, or those with

50% stenosis

and recurring transient ischemic attacks despite aspirin

therapy. The role of stenting is controversial. Despite the

Systolic and Pulse Pressure Hemodynamic Impro-

vement by Restoring Elasticity (SAPPHIRE) trial, which

suggested stenting is not inferior to endarterectomy in

high-risk patients, there were problems with the study

design, and the procedure is still being evaluated as an

alternative to open surgery, which has low morbidity

and mortality in large centers.

Question 33

Carotid Artery Disease:

CAROTID ENDARTERECTOMY:

THE OPERATION

Answer 33

• Perioperative monitoring is surgeon-dependent.

Techniques include keeping the patient awake through

the procedure, using local or regional anesthesia, using

continuous electroencephalogram monitoring, or using

no monitoring at all. Administration of intravenous

antibiotics, usually a first-generation cephalosporin,

precedes the incision. After site verification, the neck is

extended, and an incision is made over the anterior

border of the sternocleidomastoid muscle. Dissection

continues through the platysma and along the stern-

ocleidomastoid. Ligation of the facial vein allows com-

plete exposure of the carotid, which lies just medial to

the jugular vein. Care is taken not to injure the

hypoglossal nerve at the superior aspect of the dissec-

tion or the spinal accessory nerve (Fig. 16-3). Proximal

and distal control of the carotid is obtained, the patient

is heparinized, and the artery is opened after clamps

are applied. Use of a stent may provide cerebral pro-

tection. Plaque is carefully dissected out of the artery,

and the artery is usually closed with a patch.

Question 34

Acute and Chronic Mesenteric Vascular Disease: Anatomy

Answer 34

• Acute and chronic mesenteric vascular disease includes

disease of the celiac axis, which is the arterial supply

to the liver, spleen, pancreas, and stomach; the superior

mesenteric artery, which supplies the pancreas, small

bowel, and proximal colon; and inferior mesenteric

artery, which supplies the distal colon and rectum. In

addition, thrombosis of the superior mesenteric vein

can cause visceral ischemia.

• The celiac axis arises from the aorta below the crus

of the diaphragm. It travels ventrally and is surrounded

by a dense network of nerves and connective tissue.

After a short distance, it gives rise to the splenic

artery, which travels to the left behind the pancreas

to the spleen; the common hepatic artery, which trav-

els to the right toward the hepatic hilum; and the

smaller left gastric artery, which travels cranial and

toward the left. The superior mesenteric artery

courses below the pancreas and slightly to the right

toward the mesentery of the bowel. The inferior

mesenteric artery arises below the renal arteries and

above the aortic bifurcation and travels to the left

toward the bowel. The superior mesenteric vein runs

above and to the right of the superior mesenteric

artery. Its location can be determined by palpating

the artery at the root of the mesentery in thin

patients. The vein then joins the splenic and inferior

mesenteric veins to form the portal vein.

Question 35

Acute and Chronic Mesenteric Vascular Disease: Pathogenesis

Answer 35

• Acute ischemia is caused by embolization, thrombo-

sis, nonocclusive ischemia, and mesenteric vein throm-

bosis. Embolization is associated with atherosclerotic

disease or mural cardiac thrombus. Acute thrombosis is

associated with atherosclerosis and hypercoagulable

states. Vasopressor agents can produce acute ischemia.

Chronic ischemia usually requires severe atheroscle-

rotic disease in at least two major arterial trunks among

the superior and inferior mesenteric arteries and the

celiac axis, because of the extensive collateralization.

Question 36

Acute and Chronic Mesenteric Vascular Disease: Epidemiology

Answer 36

• he incidence of acute mesenteric ischemia is estimated

at one in 1,000 hospital admissions, and mortality is greater than 50%. Prevalence of chronic ischemia increases with

age, and risk factors include hypertension, smoking,

hypercholesterolemia, and diabetes.

Question 37

Acute and Chronic Mesenteric Vascular Disease: History

Answer 37

• Patients with acute ischemia may have a history of

previous embolic events, atrial fibrillation, or conges-

tive failure. Abdominal pain is usually sudden in onset

and is severe, with diarrhea or vomiting. History in

chronic mesenteric ischemia usually reveals crampy

abdominal pain after eating. This results in decreased

oral intake and weight loss. Nausea, vomiting, consti-

pation, or diarrhea may occur. The disease can be mis-

taken for malignant disease or cholelithiasis.

Question 38

Acute and Chronic Mesenteric Vascular Disease: Physical Examination

Answer 38

• In episodes of acute ischemia, the classic finding is

“pain out of proportion to physical examination.” The

abdomen may be distended. Rectal examination often

reveals guaiac-positive stool. Atrial fibrillation may be

present. Physical findings in chronic ischemia include

abdominal bruits, guaiac-positive stool, and evidence

of peripheral vascular disease or coronary artery disease.

Question 39

Acute and Chronic Mesenteric Vascular Disease: Diagnostic Evaluation

Answer 39

• In acute ischemia, there could be an elevated white

blood cell count, metabolic acidosis, or an elevated

hematocrit as fluid is sequestered in the infarcting

bowel. Abdominal radiographs are often normal in

the early phase of the disease, but as the intestine

becomes edematous, “thumbprinting” of the bowel

wall occurs. Evaluation in chronic ischemia includes

selective visceral angiography to identify the site of

the lesion.

Question 40

Acute and Chronic Mesenteric Vascular Disease: Treatment

Answer 40

• Once the diagnosis of acute ischemia is made, laparot-

omy with examination and resection of any infarcted

bowel should be considered. In selected cases, angiog-

raphy can be therapeutic, as well as diagnostic, with

catheter-based therapies. Aggressive surgical interven-

tion should not be delayed if there is evidence sugges-

tive of dead bowel. Despite aggressive intervention,

mortality is extremely high. For chronic ischemia,

angiography can define the lesion and allow considera-

tion of surgical options. Acute mesenteric vein throm-

bosis is treated with anticoagulation and laparotomy

if necrotic bowel is suspected.

Question 41

Peripheral Vascular Disease: Anatomy

Answer 41

• Lesions may occur in the iliac, common and superficial

femoral, popliteal, peroneal, anterior tibial, and poste-

rior tibial arteries. The common iliac arteries arise at

approximately the level of the umbilicus. They course

in the retroperitoneal space and give rise to the inter-

nal iliac artery, which runs to the pelvis, and the exter-

nal, which becomes the femoral artery in the femoral

canal as it passes under the inguinal ligament. It enters

the adductor canal, below the Sartorius, and continues

through the adductor hiatus, where is becomes the

popliteal artery. Below the knee, the popliteal artery

branches into the anterior tibial, the posterior tibial,

and dorsalis pedis arteries, which supply the distal leg.

In general, of the three vessels that supply the distal

ankle and foot, a single direct arterial supply is ade-

quate to prevent limb loss and rest pain.

Question 42

Peripheral Vascular Disease: Pathogensis

Answer 42

• In acute disease, the most common cause is an embolus

that causes a sudden decrease in blood flow. The most

common sources are the aorta and the heart. Rarer

causes include acute arterial thrombosis, acute venous

thrombosis, and arterial spasm. In chronic disease, pro-

gressive atherosclerotic disease causes narrowing of the

arterial lumen and decreased blood flow. Pain occurs as

decreased blood flow is unable to meet the metabolic

and waste-removal demand of the tissue.

Question 43

Peripheral Vascular Disease: Epidemiology

Answer 43

• Acute disease occurs in patients with cardiac throm-

bus, atrial fibrillation, or atherosclerosis. Risk factors

for chronic disease include atherosclerosis, smoking,

diabetes, hypertension, and advanced age.

Question 44

Peripheral Vascular Disease: History

Answer 44

• Acute ischemia causes sudden and severe lower-

extremity pain and paresthesias. Patients with chronic

ischemia typically present with claudication, defined

as reproducible pain on exercise relieved by rest. The

site of claudication provides a clue to the level of dis-

ease. Buttock claudication usually indicates aortoiliac

disease, whereas calf claudication suggests femoral

atherosclerosis. Pain at rest is indicative of severe dis-

ease and a threatened limb. Slow or nonhealing ulcers

may be present.

Question 45

Peripheral Vascular Disease: Physical Examination

Answer 45

• In acute disease, the patient may exhibit pulselessness,

pallor, and poikilothermia (coolness). Taken together

with pain and paresthesia, these form the five P’s of

acute vascular compromise (Fig. 16-4). In chronic

disease, the lower extremity may reveal loss of hair,

pallor on elevation, rubor on placing the extremity in

a dependent position, wasting of musculature, thick

nails, and thin skin. The extremity may be cool to the

touch, and pulses may be diminished or absent.

Ulcers or frank necrosis may be present.

Question 46

Peripheral Vascular Disease: Diagnostic Evaluation

Answer 46

• Angiography is necessary in cases of acute ischemia to

identify the lesion. Evaluation for chronic ischemia

includes Doppler flow measurement of distal pulses.

The normal signal is triphasic; as disease progresses,

the signal becomes biphasic, monophasic, and then

absent. Ankle-brachial indices are calculated as the

systolic blood pressure at the ankle divided by the

systolic pressure in the brachial artery. A value of less than 0.5 is indicative of significant disease (Table 16-1).

Arteriography is the gold standard for defining the

level and extent of disease and for planning surgery.

Question 47

Peripheral Vascular Disease: Treatment

Answer 47

• Acute ischemic embolus can be treated with heparin,

thrombolysis, or embolectomy. For chronic ischemia,

patients with claudication have a low rate of limb

loss, and initial therapy is based on smoking cessation

and a graded exercise program. Success rates with non-

operative therapy are good. In patients with disabling

claudication, threatened limbs, nonhealing ulcers, or

gangrene, angioplasty or revascularization should be

considered (Table 16-2). It is always prudent to con-

sider amputation in selected patients with long-standing

acute ischemia or chronic ischemia, though this decision

is often a difficult one and requires experience and care-

ful discussions with the patient.

Question 48

Peripheral Vascular Disease:

PERIPHERAL BYPASS: THE OPERATION

Answer 48

• Patients usually have concurrent coronary artery dis-

ease, and preoperative evaluation and intraoperative

beta blockade should be considered. The entire leg is

usually prepped. Intravenous antibiotics are often a

first-generation cephalosporin, and central monitor-

ing should be considered. The most common tech-

niques for anesthesia include general and regional. If

the proximal vessels are open, inflow is usually from

the femoral artery, which is dissected via an infrain-

guinal incision directly over the artery. If the target is

the popliteal, it is isolated via an incision over the

medial aspect of the knee, at the level where the out-

flow will be targeted. If the target is the dorsalis pedis,

tibialis anterior, or peroneal, the incision is made

directly over the target. Above-knee popliteal recon-

struction can be accomplished with synthetic grafts,

but infrapopliteal reconstructions should use either in

situ or reversed saphenous vein.

Question 49

Venous Disease: Deep Venous Thrombosis

Answer 49

• First-line therapy for patients with deep venous

thrombosis or pulmonary embolism is systemic anti-

coagulation. In patients for whom this therapy is con-

traindicated (e.g., patients requiring a planned major

surgery, those with active bleeding, or those facing

significant complication of anticoagulation), filter

placement in the inferior vena cava may decrease the

short-term risk of pulmonary embolism. The use of

filters, though common, is generally not well sup-

ported by randomized controlled trials. They have

not been shown to decrease mortality and are associ-

ated with significant complications, including inferior

vena cava thrombosis, recurrent deep venous throm-

bosis, and postphlebitic syndrome. Recently, removable

filters increasingly are being used to try to decrease

the risk of long-term complications, but their use is still

being studied.

Question 50

Venous Disease: Varicose Veins

Answer 50

• This is an extremely common lesion, affecting up

to 15% of men and 25% of women. Over time,

the pressure of gravity in the lower extremity

may cause enlargement of the veins in the leg as

valves fail. In most cases, the lesions are of cosmetic

concern only, though they can become large and

painful and cause ulcers. In deep veins this can lead

to venous thrombosis. Treatment options include scle-

rotherapy, laser or catheter-based ablation, and vein

stripping.

Question 51

Vascular Surgery: Key Points

Answer 51

• Aneurysms and dissections can be rapidly fatal.
• Repair via open operation or stent graft should be

considered for asymptomatic aneurysms with

diameter >4 or 5 cm.

• Symptomatic aneurysms or dissections require

emergency diagnosis and treatment.

• Dissections that involve the ascending aorta usually

require surgery, whereas dissections that involve

the descending aorta are best managed medically.

• Carotid artery disease is a major cause of stroke in

the United States.

• Indications for operation include 75% stenosis, 70%

stenosis and symptoms, bilateral disease and symp-

toms, or >50% stenosis and recurring transient

ischemic attacks despite aspirin therapy.

• Stenting is an option for selected patients.
• Patients with acute mesenteric ischemia present with “pain out of proportion to examination,” and amechanism for embolic disease is usually present.
• Chronic mesenteric ischemia results in weight loss and abdominal pain and is frequently mistaken for malignant disease.
• Acute peripheral embolus is marked by the five P’s: pulselessness, pallor, poikilothermia, pain, and paresthesia.
• Symptoms of chronic peripheral vascular disease usually follow a well-defined progression.
• Operation should be considered only in patients with severe chronic peripheral vascular disease.