Acute aortic syndromes encompass a number of life-threatening aortic emergencies. These include aortic dissection, penetrating atherosclerotic ulcer, intramural hematoma, and aortic aneurysmal leakage or ruptured abdominal aortic aneurysm (see chapter 60, Aneurysmal Disease).

Acute aortic syndromes are uncommon but frequently fatal. The incidence ranges from 2.9 to 4.7 cases per 100,000 people per year.^1,2,3,4 The 1-year, 5-year, and 10-year actuarial survival rates are 92%, 77%, and 57%, respectively, for operative patients.⁴ Twenty-two percent of cases are undiagnosed prior to death.⁵ The most common cardiovascular complication of Marfan’s syndrome is aortic root disease and type A dissection (ascending aorta). The identification of gene mutations associated with Marfan’s syndrome, such as TGFBR2 and FBN1, combined with regular follow-up can reduce fatal outcomes.⁶

Acute aortic syndromes occur in the setting of chronic hypertension and other factors that lead to degeneration of the media of the aortic wall. Bicuspid aortic valve, Marfan’s syndrome, Ehlers-Danlos syndrome, and familial history of aortic dissection all predispose to aortic syndromes. Chronic cocaine or amphetamine use accelerates atherosclerosis, increasing the risk for dissection.⁷ Prior cardiac surgery is another risk factor for aortic dissection. All mechanisms involve weakening of the medial layer and intimal wall stress. Response to stress may include aortic dilation, aneurysm formation, development of a penetrating ulcer, intramural hemorrhage, aortic dissection, and aortic rupture.

Aortic dissection occurs after a violation of the intima allows blood to enter the media and dissect between the intimal and adventitial layers. The dissecting column of blood forms a false lumen and may extend proximally, distally, or in both directions. Blood may dissect and reenter the intima, and this may clinically suggest a spontaneous cure. Alternatively, the blood may dissect through the adventitia, which nearly always proves rapidly fatal.

Aortic dissection has a bimodal age distribution.⁴ The first peak involves younger patients with specific predisposing conditions such as connective tissue disorders. The second peak includes those aged >50 years with chronic hypertension. Other atherosclerotic risk factors appear to be only minor contributors to pathogenesis of acute aortic syndromes.

Aortic dissections are classified using two separate systems, the Stanford and DeBakey systems. The Stanford classification considers any involvement of the ascending aorta a type A dissection. Stanford type B dissections are restricted to only the descending aorta. DeBakey type 1 dissections simultaneously involve the ascending aorta, the arch, and the descending aorta. DeBakey type 2 dissections involve only the ascending aorta, and type 3 involve only the descending aorta.

An aortic intramural hematoma results from infarction of the aortic media, usually from injury to the vasa vasorum.⁸ An intramural hematoma may resolve spontaneously or may lead to dissection.⁹ Penetrating atherosclerotic ulcer can lead to intramural hematoma, aortic dissection, or perforation of the aorta.^8,10

HISTORY

The site of initial intimal disruption predicts the initial symptoms.¹¹ Symptoms may change as the dissection extends along the aorta or involves other arteries or organs. Classically, dissection presents with abrupt and severe pain in the chest that radiates to an area between the scapulae and may be accompanied by a feeling of impending doom. In a case series of 464 dissections,⁵ 60% of patients had anterior chest pain (more common in Stanford type A); abdominal pain is more common in Stanford type B. Most patients describe the pain as severe or the worst they have ever experienced. Sixty-four percent describe it as sharp pain and 50% as tearing or ripping pain. Syncope occurs almost 10% of the time (more common in Stanford type A). Twenty-two percent of dissections occur in patients with prior cardiac surgery.⁵

Dissection in or near a carotid artery may present as a classic stroke, and 20% of patients with type A dissection display neurologic findings, which predicts a poorer prognosis.^12,13 Interruption of blood supply to the spinal cord may lead to paraplegia. Further distal dissection may present as back, flank, or abdominal pain. A proximal dissection to the aortic root may lead to cardiac tamponade and is generally fatal.

PHYSICAL EXAMINATION

For most patients with aortic dissection, examination findings are relatively normal. An aortic insufficiency murmur may occur (32%), and a pulse deficit in radial arteries or femoral arteries can be found (15%).⁹ Hypertension is common (49%), but hypotension occurs in 18% to 25% and worsens prognosis.^5,9,14 Aneurysmal dilation of the aorta may compress regional structures such as the esophagus, the recurrent laryngeal nerve, or the superior cervical sympathetic ganglion, causing dysphagia, hoarseness, or Horner syndrome.

Using retrospective data from the International Registry of Acute Aortic Dissection,^15,16 three clinical categories (underlying condition; pain quality and location; examination findings) were parsed into 12 features^15,16 associated with acute aortic dissection (Table 59-1).

The large differential diagnosis for chest pain plus the many end-organ ischemic manifestations associated with aortic dissections make the diagnosis challenging. The most important differential diagnoses are listed in Table 59-2.

Ischemic manifestations may change with time (as the dissection progresses), and this may distract the physician from making the correct diagnosis. Rupture of the dissection into the true aortic lumen may cause a cessation of symptoms, and the correct diagnosis may then be inappropriately dismissed. History, physical examination, and chest radiography can suggest the diagnosis, but only if one is alert to aortic dissection as one of the diagnostic possibilities in a patient with acute chest pain, syncope, or acute focal neurologic signs. Factors associated with misdiagnosis include walk-in mode of admission, normal mediastinal width/aortic contour on chest radiograph, absent extremity pulse amplitude differences, and nonspecific symptoms.^17,18,19

ECG

It may be difficult to differentiate aortic dissection from acute coronary syndromes on ECG, because both conditions are associated with ECG changes; dissection may limit or obstruct coronary artery blood flow. Abnormal ECG findings include new Q waves or ST-segment elevation in 3% to 4%, ST depression in 15% to 22%, and nonspecific ST and T-wave changes in 41% to 62%.^5,9,20 The ECG is normal in only 19% to 31% of patients.^5,20

BIOMARKERS

Several potential biomarkers have been investigated for their utility to identify or exclude aortic dissection.²¹ D-Dimer

Related posts:

Emergency Medical Services Bioterrorism Bomb, Blast, and Crush Injuries Chronic Pain Postrepair Wound Care Puncture Wounds and Bites

Stay updated, free articles. Join our Telegram channel

Join