Health Articles

Carotid aneurysms are rare, occur in Ihe midneck area, and present as pulsatile masses. Rupture is rare, but they are a source of cerebral emboli. A carotid aneurysm must be distinguished from the much more common tortuosity and bending of a carotid artery, which lacks clinical consequence. Kinking, usually with a strong pulse just above the clavicle, more often on the right side, is common in the elderly. Ultrasonography is useful in distinguishing kinking from aneurysmal dilatation. Surgical repair is usually indicated for carotid arterial aneurysm.
accurately delineate the aortic calcification. It appears to be as sensitive as arteriography. If both echocardiography and CT scanning results are unequivocally negative, dissection has not occurred.
Transesophageal echocardiography is now the most sensitive and specific method of diagnosing aortic dissection. In fact, it delects very small intimal flaps from very limited dissections, many of which are asymptomatic.
Aortography, usually performed in retrograde fashion through a femoral artery, can be used to assess the extent of damage and to plan a surgical approach. The aortogram typically shows the false channel, the compression of major branches, and the site of intimal tear. II’ the false channel contains unclolted blood, il fills with contrast material. A false channel containing clotted blood does not opacify. This finding has prognostic value, since clotting is the first step in the healing process. However, if the catheter enters the false channel, pressure from the injected contrast material can cause perforation.
Treatment
Uncomplicated distal dissections can be treated medically. Systemic blood pressure must be treated to decrease the rising pressure against the aortic wall: immediate control should be obtained with a litrcitable agent administered by continuous IV infusion. Hither a sympathetic ganglionic blocking agent such as trimethaphan camsylate or an a- and β-adrenergic blocking agent such as labelalol can be used. At the same time, oral therapy is begun with a β-blocker and a diuretic. The dosage of oral agents is increased until the IV infusion is no longer needed. Pure vasodilators (eg. prazosin, nitroprusside, and hydralazine) and angiotensin converting enzyme inhibitors (eg, captopril and enalapril) should be avoided because they lead to increased left ventricular contraction-—producing increased pressure against the aorlic wall—and may do more harm than good. Centrally acting vasodilators (melhyldopa and clonidinethave lillleor no effect on cardiac output and can be used if necessary. If β-blockers are contraindicated. verapamil can be used.
Surgery must be considered if pain is not reduced within the first few hours of medical therapy and eliminated within the first 2 days. After discharge, patients should be followed up weekly for the first month and at least every 3 mo afterwards. Chest x-rays should be obtained after I mo and every 3 to 4 mo for the first 2 yr to look for development of a saccular aneurysm. Mortality rates after 3 and 5 yr for patients with uncomplicated distal dissections arc about the same, whether they are treated medically or surgically.
Proximal dissections are much more dangerous and tend to cause severe complications if treated only medically. Perforation rates are high, with pericardial tamponade being the most common cause of death. Hypertension should first be controlled with IV drugs if the patient is stable, and then surgery should be performed. Synthetic grafts that can be placed inside the thoracic aorta have simplified surgery and reduced mortality. A graft with tin attached aortic valve is also available for patients with severe aortic regurgitation. After graft insertion, the false channel can be obliterated into the true lumen. A distal saccular aneurysm or interference with blood flow through any major distal aortic branch mandates repair at the local site. Thus, a combined thoracoabdominal approach is often necessary.
The small, atypical intimal tears found only by transesophageal echocardiography should be treated medically.

Femoral aneurysms have a course similar to that of popliteal aneurysms, can be confirmed by ultrasonography, and require surgical repair.

A hemorrhage into the media after an initial intimcil tear.
Aortic dissection is often inappropriately called a dissecting aneurysm. The tear occurs because of medial necrosis or severe atrophy, often as a result of chronic, sustained hyperlension. Dissection secondary to Marfan’s syndrome is rare after age 55.
The initial intimal tear is almost always just distal to the aorlic valve (proximal type) or just beyond the left subclavian artery (distal type). Proximal dissections are reported more often, but the prevalence of distal dissections may be underestimated because clinical findings can be more subtle.
Symptoms and Signs
Symptoms are variable. Pain may be excruciating, radiating throughout the chest and back; mild and limited to one small area of the back or chest; or totally absent. The clinical findings reflect what happens to the hemaloma that forms in the media, which may do any of the following: (I) exlend distally along the aorta; (2) clot at any poinl along the aorta; (3) extend dislally inloany major aortic branch and compress the lumen; (4) become Ihe major blood-flow channel in any aortic branch; (5) reenter the aorta or a branch through a second, more distal intimal tear; or (6) perforate through the adventitia at any point.
Distal dissection: The dissection may cause mild back pain, but pain is often absent. The presenting complain! is often related to regional ischemia. Patients may have abdominal pain due to mesenteric ischemia, flank pain and hematuria secondary to renal infarction, paraplegia from anterior spinal artery involvement, or leg pain because of iliac artery occlusion. Ischemia may be promptly and spontaneously reversed if the dissecting hematoma reenlers the normal lumen; for example, femoral pulses that were missing may suddenly reappear. Many areas of acute ischemia should always suggest a possible aortic dissection.
Spontaneous healing of a dissection usually involves clotting of the hemaloma followed by fibrosis around it. However, the aortic wall remains weak, and a true saccular aneurysm can develop. Because there is little support to the wall, the aneurysm usually expands and soon thereafter ruptures. During acute dissection, rapid expansion of a saccular aneurysm portends imminent rupture. Expansion occurring weeks or months later is generally less dire, although Ihe aneurysm may rupture within days. A patient with a thoracic aorlic dissection may present with the symptoms of a sudden abdominal aortic aneurysm.
A distal dissection usually perforates near the initial tear, with blood tracking into the left pleural cavity. Frequently, an initial small perforation is sealed off by a clot. A small left pleural effusion on chest x-ray may be the only clue.
Proximal dissection: Because proximal dissections often involve the aortic valve ring, Ihe extracranial arteries, and the pericardium, they are more dangerous than distal dissections. A regurgitation murmur and a loud sound on aortic closure can usually be heard. Less frequently, hemodynamically significant acute aortic regurgitation results in low cardiac output, with pulmonary edema and hypotension. Rarely. silent dissection produces chronic aortic regurgitation, and the physician discovers cither an asymptomatic diastolic murmur or a murmur and left ventricular failure.
Neurologic symptoms (eg, hemiplegia and aphasia) are common presenting complaints. The disseciion may occlude both the innominate and left carotid arteries, lffocal neurologic signs are present, the corresponding carotid pulse should he either diminished or absent. A lower blood pressure in the right arm is expected with left hemiplegia, as compression of the innominate artery should affect both the subclavian and carotid arteries.
If the false channel is prominent in the transverse aortic wall, findings of mediastinal compression—hoarseness, unilateral external jugular venous distention, and a unilateral Homer’s syndrome—can occur. Death often results from rupture of the dissection into the pericardial space.
Diagnosis
Aortic dissection can be a great masquerader. with an onset that can be acute or insidious. Since the diagnosis is easily missed, cerlain constellations of findings should always trigger consideration of this entity
(sec TABLE 43-1).
Initially, chest x-ray is important for evaluation of the aortic shadow. The aorta almost always is somewhat prominent, especially in the elderly, but this finding is not specific to dissection. The aortic shadow is usually tortuous and uncoiled owing to long-standing hypertension, and sometimes it is very dilated. Aortic calcification not extending to Ihe shadow’s borders suggests i\ false channel and is specific for dissection only if a lateral view demonstrates a lack of calcium in the anterior or posterior wall.
If, after clinical evaluation and review of chest x-rays, the index of suspicion is not very high, echocardiography or contrast CT is indicated. Transthoracic two-dimensional echocardiography is useful only for proximal dissection. It can usually demonstrate the false channel and detect even subclinical desrees of aortic regurgitation. It may also demonstrate early mitral valve closure, which indicates acute aortic regurgitation. CT scanning can demonstrate the false channel and also Prognosis
Many studies confirm Ihe high mortality rate associated with unrepaired abdominal aortic aneurysms. The 5-yr survival rale varies from 14% to 37%. Complications of abdominal aortic aneurysms other than rupture occur infrequently. Mural thrombi may embolize to the legs. Rarely, consumption coagulopathy occurs, resulting in thrombocylope-nia, elevated thrombin time, fibrin split products in ihe blood, and a bleeding diathesis. An infection in Ihe aneurysm is even more rare, but if it occurs Salmonella is most often implicated. Patients with a recurrent Salmonella septicemia of unknown origin should be evaluated for an arterial aneurysm.
Surgical repair prolongs life. With an experienced surgical team, elective repair has an operative mortality rate of < 3%. even though most patients have other manifestations of atherosclerotic disease. Contraindications to surgery include recent transient ischemic attacks and unstable angina.
Treatment
Abdominal aortic aneurysms > 5 cm in diameter usually should be repaired. Repair of slightly smaller lesions might be considered, particularly if serial sonograms show progressive enlargement and if (he patient is otherwise healthy. 1′atients with small aneurysms can be followed up clinically and with ultrasonography every 6 mo.
Treatment of patients who have both coronary artery disease and an abdominal aneurysm is controversial. Some authorities advocale coronary angiography and bypass surgery as the first intervention, but most reserve this approach for patients with severe heart disease. Most surgeons forgo coronary angiography in patients with little or no angina and a good ejection fraction (as determined by radionuclide left ventricular cineangiography).
The management of patients with significant stable angina is open to question. One promising technique is the use of thallium scanning of the heart before and after IV injections of dipyridamole. Evidence of blood flow redistribution after dipyridamole adminislration is well correlated with postoperative myocardial infarction. Conventional sub-maximal stress tests and 48-h ambulatory ECG monitoring also can help to assess (he need for coronary bypass before aneurysm repair.
POPLITEAL ARTERIAL ANEURYSM
The popliteal artery is the second most common site of aneurysm formation. Knee movements subject the artery to trauma. In addition, compression of the artery as it leaves Hunter’s canal in the lower thigh leads to poststenotic dilatation, which is then exacerbated by the development of atherosclerosis. Most lesions are asymptomatic. Patients with patent aneurysms have pulsatile masses in the popliteal fossa, but an occluded aneurysm may be mistaken for a cyst. Ultrasonography is diagnostic.
Thromboembolism—either acute or as a series of small emboli to the foot—is the most common complication (16% of casesl and often necessitates amputation. Occasionally, the popliteal pulse disappears and reappears as Ihe thrombus changes position in the aneurysmal sac. Other complications include rupture (about 10% of cases), popliteal vein compression and thrombosis, and posterior tibial nerve compression with radiating pain or sensory loss in the calf.
Treatment
Occluded aneurysms do not require specific treatment: patients should be managed as for peripheral arterial occlusion (see PERIPHERAL ATHEROSCLEROSIS in Ch. 42). Patent aneurysms, however, are quite dangerous because of the high risk of rupture and thromboembolism. Surgery is required unless the patient is very debilitated or is expected to die shortly of another cause. Spinal or even local anesthesia can be used, if necessary. The aneurysm is not resected but is bypassed and separated from the circulation by proximal ligation. Other aneurysms should be sought; 50% of patients with popliteal aneurysms also have popliteal aneurysms in (he other leg, and 35% have abdominal aortic aneurysms.

The distal aorta is the site of the most common and most dangerous atherosclerotic aneurysms. They often involve the proximal common iliac arteries and rarely (< 2%) extend above the level of the renal arteries. These lesions almost always remain silent until they reach, or are close to. the point of rupture. An estimated 1 of 250 people > 50 yr die of a ruptured abdominal aortic aneurysm.
Symptoms, Signs, and Diagnosis
Most abdominal aneurysms can be detected by palpation. Thorough palpation of the abdominal aorta in the elderly is unQiiestionably one of the most important components of the physical examination. Typically, an aneurysm appears as an expansile mass that has both lateral and anterior pulsalions. However, often only a strong pulse is felt, making it difficult to distinguish the aneurysm from generalized ectasia and tortuosity. In persons of normal girth, the aortic pulse is generally palpable in the epigastrium. A strong pulse is normal in thin patients, whereas any pulse may signal an aneurysm in obese patients. About 50% of aneurysms are associated with a bruit.
Too often, the lesion is missed or is suspected only after an abdominal x-ray is taken for another reason. An anteroposterior view may indicate curvilinear aortic calcification near the midline, whereas a laleral film may outline ihe aneurysm’s calcified anterior and posterior walls.
Ultrasonography is the method of choice for confirming the diagnosis. It is virtually 100% accurate, providing precise information on the aneurysm’s size, shape, and location. The likelihood of rupture is directly related to the aneurysm’s transverse and anteroposterior diameters and inversely related to ils length. Rupture is not likely with diameters < 5 cm; thereafter, the rupture rate rises quickly. Abdominal aortic aneurysms have a much faster expansion rate than thoracic aortic aneurysms.
Initially, the rupture is usually a small perforation, blocked from leaking for hours or even days by pressure from a retroperitoneal blood clot. If it is diagnosed rapidly, lifesaving surgical repair may be possible. Unexplained abdominal or lower back pain with a prominent pulsation should suggest a ruptured aneurysm until proved otherwise. In an older obese patient, sudden pain suggests the diagnosis, even if a pulsation is undetectable.
In some cases, immediate exploratory laparotomy is indicated. However, if the index of suspicion is low and the onset of pain is recent, contrast CT of the abdomen can be performed. If the aneurysm has already ruptured, retroperitoneal swelling can usually be seen. Diagnosis of rupture is the only advantage a CT scan has over ultrasonography.

About 80% of thoracic aortic aneurysms are secondary to atherosclerosis associated with hypertension. Tertiary syphilis remains responsible for about 14%, and these are always located in the ascending aorta. Other causes include congenital factors, Marfan”s syndrome, and blunt trauma to the chest (1%).
Symptoms and Signs
Symptoms and signs are related to the site of the lesion. Dilatation of the ascending thoracic aorta rarely causes pain until the aneurysm ruptures. Examination may reveal a loud aortic closing sound and an early decrescendo diastolic murmur of aortic regurgitation secondary to dilalation of the aortic ring. The murmur, usually heard best in (he aortic area, may be accompanied by a louder systolic murmur. Palpating the chest of a thin person who is leaning forward may reveal a pulse along the righl slernal border.
Although asymptomatic when small, aneurysms of the transverse thoracic aorta may cause symptoms and signs of mediastinal compression—hoarseness secondary to compression of the recurrent laryngeal nerve, dysphagia, wheezing, and superior vena cava syndrome—as they enlarge. Since these aneurysms may resemble mass lesions on chest x-rays, they can easily be confused with bronchogenic carcinomas and mediastinal neoplasms.
Aneurysms of tho descending thoracic aorta are genei ally asymptomatic until very large, and they can even penetrate the spine without causing pain.
Diagnosis
Diagnosis is usually made coincidental^ upon review of rouline chest x-rays. Generally, good posleroanteriorand lateral views can distinguish the aorta from other mediastinal structures, and CT can confirm the diagnosis. If an aneurysm seems likely on chest x-ray, contrasl CT is recommended to verify its size and location and to distinguish it from a silent aortic dissection. Angiography should be performed only if surgical repair is considered.
Treatment
The decision to perform surgery is based on the aneurysm’s size and location, the presence of symptoms, and the patient’s general condition. Aneurysms < 5 cm in transverse diameter rarely rupture, but those > 10 cm often do. Pain or compression symptoms suggest an increased likelihood of rupture.
The transverse thoracic aorta is the most critical site for surgery because it requires not only total cardiopulmonary bypass but also rc-anaslomosis of the extracranial arteries into the graft. The descending thoracic aorta is less critical because only partial cardiopulmonary bypass is required to protect the kidneys and spinal cord. Lesions of the ascending thoracic aorta are of intermediate risk.
Surgery should not be considered for most older patients. Rather, they should have chest x-rays every 4 to 6 mo. Asymptomatic thoracic aortic aneurysms < 8 cm in size that are not expanding call for a conservative approach. Hypertension should be treated with drugs that do not increase cardiac stroke volume (which can stress the aortic wall). p-Blockers (nonvasodilator type) and calcium channel-bloekers arc the drugs of choice; methyldopa, clonidine. and diuretics can also be used. Vasodilators (eg. hydralazine, prazosin, and angiotensin converting enzyme inhibitors) should be avoided.

A localized dilatation of an artery secondary to loss of smooth muscle and elastic tissue in the media.
In the elderly, aneurysms are most likely to occur at branching points (eg, the terminal aorta) or at areas of stress (eg, the popliteal artery) and are almost always of atherosclerotic origin. Systemic hypertension is a major risk factor. When a local dilatation develops, blood flow velocity decreases, leading to increased pressure against the arterial wall. This in turn results in more dilatation and perpetuates a vicious circle that often terminates in rupture of the artery. Saccular aneurysms are more likely to rupture than fusiform aneurysms because Ihc total wall pressure is applied to a smaller area. Clinical findings and prognosis vary with the aneurysm’s location and size.