ANEURYSMS AND DISSECTIONS
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 considered aneurysmal if the diameter is >1.5 times its normal size. Otherwise, an enlarged artery is considered ectatic.
In contrast, a dissection 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 catastrophic 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.
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Figure 16-1 • Aneurysms and dissections. |
ABDOMINAL AORTIC ANEURYSM
Anatomy
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.
Etiology
Ninety-five percent of aneurysms of the abdominal aorta are associated with atherosclerosis. Other causes include trauma, infection, syphilis, and Marfan's syndrome. Protease activity in the vessel wall is commonly increased.
EPIDEMIOLOGY
Abdominal aortic aneurysms are responsible for 15,000 deaths per year. The incidence is approximately 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.
HISTORY
Most aneurysms are asymptomatic. Pain usually signifies a change in the aneurysm–-commonly enlargement, 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.
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Physical Examination
Abdominal examination may reveal a pulsatile abdominal mass. Enlargement, rupture, or compromise of vascular supply may manifest by tenderness, hypotension, tachycardia, or a change in the location or intensity of pain. In addition, the lower extremities may have pallor, cool temperature or pulses that are diminished or unequal.
Diagnostic Evaluation
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 magnetic resonance imaging provides anatomic detail and precise localization of the aneurysm. An aortogram may be helpful in planning surgical intervention to demonstrate involvement of other vessels, specifically the renal, mesenteric, and iliac arteries.
Treatment
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 <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 >25% at 5 years, and repair is recommended, unless the patient is at prohibitive operative risk. Table 16-1 lists rupture rates per year based on aneurysm size. 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.
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TABLE 16-1 Ankle-Brachial Index |
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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.
Repair of Abdominal Aortic Aneurysm: The Operation
Consistent with the size of the operation, preoperative 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 contents 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
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approach is used, the peritoneum is closed over the graft if possible (Fig. 16-2).
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Figure 16-2 • Aneurysm, aortic: abdominal aneurysm of the descending aorta. LifeART image copyright (c) 2006 Lippincott Williams & Wilkins. All rights reserved. |
THORACIC AORTIC ANEURYSM
Anatomy
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.
Etiology
Thoracic aortic aneurysms are caused by cystic medial necrosis, atherosclerosis, or, less commonly, trauma, dissection, or infection.
EPIDEMIOLOGY
Males are affected three times as often as females. Risk factors include atherosclerosis, smoking, hypertension, and family history.
History
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.
Physical Examination
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.
Diagnostic Evaluation
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.
Treatment
As with abdominal aortic aneurysms, operative repair should be considered when the maximum diameter approaches 5 cm. Symptomatic presentation
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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.
AORTIC DISSECTION
PATHOGENESIS
Dissections can be caused by hypertension, trauma, Marfan syndrome, or aortic coarctation.
Epidemiology
Aortic dissections are more common than either thoracic or abdominal aneurysms. Incidence increases with age, and men are more commonly affected than women.
History
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.
Physical Examination
Patients may be hypotensive. Rales on chest auscultation or a new murmur suggest that the dissection continues retrograde into the aortic root. Peripheral pulses are diminished if distal blood flow is compromised. If the dissection continues into the visceral arteries, compromise of mesenteric vessels can produce abdominal pain, compromise of renal arteries can cause oliguria, and compromise of spinal blood supply can produce neurologic deficits.
Diagnostic Evaluation
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 ascending aorta, and type III involves only the descending aorta.
Treatment
Dissection of the ascending thoracic aorta usually requires surgery, because of the potential for retrograde progression into the aortic root and subsequent compromise of the coronary circulation or tamponade from rupture into the pericardium. Eighty percent of patients with involvement of the ascending aorta die without treatment. Antihypertensive therapy 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 antihypertensives, including sodium nitroprusside and beta blockade. 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.
CAROTID ARTERY DISEASE
ANATOMY
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" territory, 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 preserve sensation to the ear and the angle of the mandible. 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
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of which, the facial vein, is generally divided to facilitate exposure of the carotid.
PATHOGENESIS
Symptoms are the result of atherosclerosis. Mechanisms of morbidity include plaque rupture, ulceration, hemorrhage, 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.
Epidemiology
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 hypercholesterolemia. Markers for carotid disease include evidence of other atherosclerotic disease and prior neurologic events.
History
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.
PHYSICAL EXAMINATION
Patients may exhibit a fixed neurologic deficit. Hollen-horst plaques on retinal examination are evidence of previous emboli. A carotid bruit is evidence of turbulence in carotid blood flow, but the presence of a bruit does not unequivocally translate into a hemodynamically significant lesion, and the absence of a bruit does not unequivocally indicate the absence of significant disease.
DIAGNOSTIC EVALUATION
Carotid duplex scanning is both sensitive and specific for carotid disease. Conventional or magnetic resonance angiography is more accurate for assessing the degree of stenosis.
TREATMENT
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.
CAROTID ENDARTERECTOMY: THE OPERATION
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 sternocleidomastoid. Ligation of the facial vein allows complete 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 dissection or the spinal accessory nerve (Fig. 16-3). Proximal and distal control of the carotid is obtained, the patient
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is heparinized, and the artery is opened after clamps are applied. Use of a stent may provide cerebral protection. Plaque is carefully dissected out of the artery, and the artery is usually closed with a patch.
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Figure 16-3 • Carotid endarterectomy: pertinent anatomical structures. |
ACUTE AND CHRONIC MESENTERIC VASCULAR DISEASE
ANATOMY
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 travels 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.
PATHOGENESIS
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
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associated with atherosclerosis and hypercoagulable states. Vasopressor agents can produce acute ischemia. Chronic ischemia usually requires severe atherosclerotic disease in at least two major arterial trunks among the superior and inferior mesenteric arteries and the celiac axis, because of the extensive collateralization.
EPIDEMIOLOGY
The incidence of acute mesenteric ischemia is estimated at one in 1,000 hospital admissions, and mortality is >50%. Prevalence of chronic ischemia increases with age, and risk factors include hypertension, smoking, hypercholesterolemia, and diabetes.
HISTORY
Patients with acute ischemia may have a history of previous embolic events, atrial fibrillation, or congestive 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, constipation, or diarrhea may occur. The disease can be mistaken for malignant disease or cholelithiasis.
PHYSICAL EXAMINATION
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.
DIAGNOSTIC EVALUATION
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.
TREATMENT
Once the diagnosis of acute ischemia is made, laparot-omy with examination and resection of any infarcted bowel should be considered. In selected cases, angiography can be therapeutic, as well as diagnostic, with catheter-based therapies. Aggressive surgical intervention should not be delayed if there is evidence suggestive of dead bowel. Despite aggressive intervention, mortality is extremely high. For chronic ischemia, angiography can define the lesion and allow consideration of surgical options. Acute mesenteric vein thrombosis is treated with anticoagulation and laparotomy if necrotic bowel is suspected.
PERIPHERAL VASCULAR DISEASE
ANATOMY
Lesions may occur in the iliac, common and superficial femoral, popliteal, peroneal, anterior tibial, and posterior 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 internal iliac artery, which runs to the pelvis, and the external, 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 adequate to prevent limb loss and rest pain.
PATHOGENESIS
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, progressive 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.
EPIDEMIOLOGY
Acute disease occurs in patients with cardiac thrombus, atrial fibrillation, or atherosclerosis. Risk factors
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for chronic disease include atherosclerosis, smoking, diabetes, hypertension, and advanced age.
HISTORY
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 disease. Buttock claudication usually indicates aortoiliac disease, whereas calf claudication suggests femoral atherosclerosis. Pain at rest is indicative of severe disease and a threatened limb. Slow or nonhealing ulcers may be present.
PHYSICAL EXAMINATION
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.
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Figure 16-4 • Signs and symptoms of acute embolus. |
DIAGNOSTIC EVALUATION
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 <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.
TREATMENT
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 nonoperative 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 consider amputation in selected patients with long-standing acute ischemia or chronic ischemia, though this decision is often a difficult one and requires experience and careful discussions with the patient.
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TABLE 16-2 Progression of Peripheral Vascular Disease |
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PERIPHERAL BYPASS: THE OPERATION
Patients usually have concurrent coronary artery disease, 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 monitoring should be considered. The most common techniques for anesthesia include general and regional. If the proximal vessels are open, inflow is usually from the femoral artery, which is dissected via an infrainguinal 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 outflow 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 reconstruction can be accomplished with synthetic grafts, but infrapopliteal reconstructions should use either in situ or reversed saphenous vein.
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VENOUS DISEASE
DEEP VENOUS THROMBOSIS
First-line therapy for patients with deep venous thrombosis or pulmonary embolism is systemic anticoagulation. In patients for whom this therapy is contraindicated (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 supported by randomized controlled trials. They have not been shown to decrease mortality and are associated with significant complications, including inferior vena cava thrombosis, recurrent deep venous thrombosis, 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.
VARICOSE VEINS
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 sclerotherapy, laser or catheter-based ablation, and vein stripping.
KEY POINTS