AORTIC DISEASE - AORTIC ANEURYSMS
Aortic aneurysms, localized areas of increased aortic diameter, may occur in the ascending aorta, aortic arch, descending thoracic aorta, or abdominal aorta, depending on the etiology. For example, aneurysms of the sinuses of Valsalva may occur in Marian’s syndrome, syphilis, as a complication of infective endocarditis, or as a congenital lesion, while aneurysms of the ascending aorta or aortic arch occur in syphilis, aortic dissection, or cystic medial necrosis with or without Marian’s syndrome. Aneurysms of the descending thoracic aorta occur from syphilis, atherosclerosis, or dissection. Aneurysms just distal to the take-off of the left subclavian artery are commonly due to trauma. Abdominal aortic aneurysms are usually atherosclerotic but can be secondary to syphilis or extension of a dissection from above.
Arteriosclerotic aneurysms usually occur in the abdominal aorta, most often between the renal arteries and the aortic bifurcation, and are most common in males older than 50 years. Abdominal aortic aneurysms may cause back or epigastric pain but usually produce no symptoms. Their first manifestion may be rupture with severe pain and exsanguinating hemorrhage. Impending rupture of an aneurysm is often heralded by increasing abdominal or back pain, usually constant, “gnawing” in quality, and not affected by movement. Aneurysms may be tender to palpation. Some patients seek medical attention because of fullness or abnormal pulsations in their abdomen. A prominent abdominal aortic pulsation may be felt in normally thin people and be mistakenly diagnosed as an abdominal aortic aneurysm; on the other hand, an abdominal aortic aneurysm may not be palpable in patients who are obese or who have muscular abdominal walls. On occasion, manifestations of peripheral emboli secondary to debris from the aneurysm may be noted in the feet and toes. Bruits may be heard over the aneurysm, and associated occlusive peripheral vascular disease is often present. Aneurysms may rapture into the inferior vena cava producing an arteriovenous fistula, into the duodenum with acute massive gastrointestinal hemorrhage, into the retroperitoneal space manifested by flank or groin hematomas, or into the abdominal cavity causing abdominal distention.
The size of the aneurysm can be estimated from physical examination, routine chest x-ray if calcification of the aortic wall is present, abdominal ultrasound, CT scan, and aortography. The normal aorta is no more than 2 cm in diameter. Physical examination is the least accurate method for estimating abdominal aortic size; abdominal ultrasound is simple and very accurate. Angiography may be less accurate because mural clot may cause the lumen to appear smaller than it really is. If surgery is contemplated, however, aortography is necessary to assess the extent of aortic involvement and the status of the aortic branches.
Half of all aneurysms exceeding a 6-cm diameter rupture within one year, and surgical resection with prosthetic graft replacement is usually recommended. Aneurysms less than 6 cm also may rupture. In patients with relatively high surgical risk, aneurysms of 4 to 6 cm should be followed closely and surgery undertaken upon signs of expansion or impending rupture.
Three-fourths of atherosclerotic aneurysms are confined to the abdominal aorta. One-fourth also involve the thoracic aorta, most commonly the descending aorta. Thoracic aortic aneurysms may cause tracheal deviation with pulmonary complications, hoarseness due to recurrent laryngeal nerve compression, dysphagia from obstruction of the esophagus, Horner’s syndrome from compression of the sympathetic chain, or superior vena caval obstruction. Steady, gnawing pain may occur, and occasionally a visible aneurysmal pulsation can be noted in the sternum or in the suprasternal notch. Rupture of the aneurysm is associated with severe chest or back pain. Thoracic aortic aneurysms are usually visible on chest x-ray and must be differentiated from other mediastinal masses. The aneurysms can be identified by CT scan, but aortography usually is necessary before surgery. Larger thoracic aortic aneurysms, especially those exceeding 6 to 7 cm in diameter and those showing evidence of expansion or causing symptoms, should be resected and replaced with a vascular prosthesis if possible. Aortic valve surgery may be required if the aneurysm involves the ascending aorta, and reimplantation of the great vessels or coronary arteries is sometimes necessary. In patients who are poor surgical risks or in whom an extensive aneurysm obviates surgery, reduction of blood pressure and force of ventricular ejection with beta blockade is reasonable.
A dissecting aneurysm is caused by a tear of the aortic intima with formation of a false channel within the aortic media. Blood in the false channel may re-enter the true aortic channel via a second intimal tear or rupture through the adventitia into the periaortic tissues. Aortic dissections, probably not related to atherosclerosis of the aorta, tend to occur in middle-aged men with hypertension, Marfan’s syndrome, cystic medial necrosis, and coarctation of the aorta. They are also somewhat more common during pregnancy. They may be caused by trauma and may be a complication of aortic angiography. If the dissection travels retrogradely toward the aortic valve, severe aortic valvular regurgitation may occur. Involvement of the coronary, carotid, or spinal cord arteries may produce myocardial infarction, stroke, or paraplegia, respectively. Dissections can rupture into the pericardium and cause cardiac tamponade or renal impairment if the dissection extends to the renal arteries.
Most dissections arise either in the ascending aorta within several centimeters of the aortic valve or in the descending thoracic aorta just beyond the origin of the left subclavian artery in the region of the ligamentum arteriosum. Dissections have been classified into three types: type I begins in the proximal ascending aorta and extends to the descending aorta, type II is confined to the ascending aorta, and type III begins in the descending aorta and extends distally. Patients with proximal dissections tend to be younger and have a higher incidence of Marfan’s syndrome and cystic medial necrosis; distal dissections more commonly involve older patients with hypertension.
Dissecting aortic aneurysms are usually associated with chest pain radiating into the abdomen or the back. The pain is usually severe, sudden, maximal in intensity at its onset, and described as sharp or tearing. An occasional patient presents with aortic insufficiency and heart failure without the history of an acute painful episode. Physical examination may reveal hypertension/Pulses are often but not always asymmetrical. Abnormal pulsations may be felt in the region of the sternoclavicular joints. The electrocardiogram is usually nonspecific but may show evidence of complieating pericarditis or myocardial infarction. The chest x-ray often but not always reveals widening of the mediastinum.
CT scan with contrast injection is very accurate in diagnosing both ascending and descending dissecting aortic aneurysms. Echocardiography can sometimes demonstrate ascending aortic involvement. Angiography is necessary to identify the site of the intimal tear, to determine the full extent of aortic involvement, to evaluate the competency of the aortic valve, and to determine the relationship of the dissection to the aortic branches.
The prognosis is usually poor. Surgical therapy should be undertaken when a dissection involves the ascending aorta or arch, or the distal aorta when there is evidence of leaking or retrograde extension, impairment of cerebral or other vital circulations, inability to control pain or blood pressure, and when hypertension is absent and thought not to be the etiology of the dissection. Patients with distal dissections tend to be older, have more generalized atherosclerosis, and have more cardiopulmonary disease. Thus, surgery generally is indicated in type I and type II, while medical therapy may be the treatment of choice for uncomplicated distal dissection (type III). Medical therapy must be administered to surgical patients both during the preoperative stabilization period and chronically postoperatively to prevent the risk of progression or repeat dissection. Medical management involves control of hypertension and lessening the force of ventricular contraction. Potent antihypertensive agents such as intravenous sodium nitroprusside or trime-thaphan may be used. Trimethaphan has the advantage of also decreasing the force of myocardial ejection but exhibits both unpleasant side effects and tachyphylaxis. Therefore, sodium nitroprusside, combined with beta blockade to lessen the force of contraction, is usually the medical treatment of choice.
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