Clinical Evaluation of Aortic Aneurysms


The vast majority of aortic aneurysms are asymptomatic, accounting for a much higher disease prevalence than hospitalization and mortality statistics would suggest (see Chapter 35 ). These data underscore the central challenge in aortic aneurysmal disease: a common clinical problem that is silent until rupture and death. Aortic aneurysms typically increase in size slowly over years or decades, with few warning signs. The management of aortic aneurysmal disease, therefore, requires suspicion and diligence to avoid adverse outcomes. This chapter will focus on the history, physical examination, and diagnostic tests important to clinical evaluation of aortic aneurysms.

Clinical history

Thoracic Aortic Aneurysms

Thoracic aortic aneurysms (TAA) typically produce no symptoms, but a variety of symptom complexes may arise related to aneurysm size and location within the thorax.

Patients with aneurysmal dilation of the ascending thoracic aorta may develop clinical manifestations of congestive heart failure (CHF) as a consequence of aortic valvular regurgitation. Enlargement of the sinuses of Valsalva may cause myocardial ischemia or infarction due to direct compression of the coronary arteries or coronary arterial thromboembolism. Right ventricular (RV) outflow tract obstruction and tricuspid regurgitation may result from aneurysmal deformation of the noncoronary sinus. Aneurysms of the sinuses of Valsalva may rupture directly into the RV cavity, right atrium, or pulmonary artery, causing heart failure associated with a continuous murmur. Chest pain may occur when the aneurysm compresses surrounding structures or erodes into adjacent bone such as the ribs or sternum. Compression of the superior vena cava may produce venous congestion of the head, neck, and upper extremities. Symptoms are frequently a harbinger of rupture or death. Rupture may occur into the left pleural space, pericardium, pulmonary artery, or superior vena cava.

Aneurysms of the aortic arch may produce symptoms by compression of contiguous structures, but most are asymptomatic. Dyspnea or cough may be caused by compression of the trachea or mainstem bronchi, dysphagia by compression of the esophagus, or hoarseness secondary to left vocal cord paralysis related to compression of the left recurrent laryngeal nerve. The superior vena cava syndrome and pulmonary artery stenosis result when these vessels are compressed. Chest pain, related either to compression of adjacent structures or to erosion of ribs or vertebrae, is typically positional. Aneurysms of the aortic arch may rupture into the mediastinum, pleural space, tracheobronchial tree (causing hemoptysis), or esophagus (causing hematemesis). Arteriovenous fistulas (AVFs) may result from rupture into the superior vena cava or pulmonary artery. Tuberculous aneurysms, akin to other causes of TAA, may present with pain but are commonly asymptomatic or may present with hypovolemic shock as a consequence of rupture.

Symptoms of descending TAAs include chest pain from compression of surrounding soft tissues or erosion of vertebrae. Irritation of the recurrent laryngeal nerve may produce hoarseness. Dyspnea may result from bronchial compression, and hemoptysis from direct erosion into the lung parenchyma. Dysphagia and hematemesis are features of esophageal compression or erosion. Rupture may occur into the mediastinum or left pleural space.

Thoracoabdominal Aortic Aneurysms

Although most patients with thoracoabdominal aortic aneurysms (TAAA) are asymptomatic, discomfort occasionally develops in the epigastrium or left upper quadrant of the abdomen. Back or flank pain may occur when the patient lies in left lateral decubitus position. Erosion of the anterior surfaces of the vertebral bodies may occur, leading to radiculopathy. Visceral artery occlusion may occur, but frank ischemia and infarction are infrequent. Patients who complain of claudication also may have occlusive atherosclerotic disease of the aorta, iliac, or more distal arteries. Because mural thrombosis is so common in atherosclerotic aneurysms, they may be the source of peripheral atheroembolism, causing occlusion of distal vessels. Rupture of the thoracic component of these aneurysms generally occurs into the left pleural space, producing a hemothorax; the abdominal component may rupture into the retroperitoneum, inferior vena cava, or duodenum.

Abdominal Aortic Aneurysms

Most patients with abdominal aortic aneurysms (AAAs) are asymptomatic, yet symptoms may take the form of abdominal discomfort or back pain; some patients become aware of abdominal pulsation. Less frequently, pain may occur in the legs, chest, or groin; anorexia, nausea, vomiting, constipation, or dyspnea may develop. Compression of the left iliac vein may cause left leg swelling, just as compression of the left ureter may cause hydronephrosis, or compression of testicular veins may cause varicocele. As the aneurysm expands and compresses vertebrae and lumbar nerve roots, pain may develop in the lower back and radiate to the posterior aspects of the legs. Flank pain radiating to the anterior left thigh or scrotum may reflect compression of the left genitofemoral nerve. Nausea and vomiting may occur as the aneurysm compresses the duodenum. Bladder compression may cause urinary frequency or urgency.

Occasionally, nascent or frank rupture occurs and causes symptoms indicating a life-threatening emergency. The mortality of patients with AAA rupture is 60%; patients with symptoms suggestive of rupture require emergent surgical referral. The classical triad associated with AAA rupture includes hypotension, back pain, and a pulsatile abdominal mass; however, fewer than 50% of patients have all components of this triad. Diverticulitis, renal colic, and gastrointestinal hemorrhage represent common disorders in the differential diagnosis in these patients.

In the absence of patient complaints, physicians must intuit the presence of aneurysm based on the clinical characteristics of the patient. Risk factors for aortic aneurysm disease (see Chapter 35 ) can be used to guide directed physical examination and, if necessary, diagnostic testing.

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