Points
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Acute aortic syndromes (AAS) include aortic dissection (AoD), intramural hematoma (IMH), and penetrating atherosclerotic ulcer (PAU).
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AoD is the most prevalent, accounting for 85%-95% of AAS; IMH 5%-25%; and PAU 2%-7%.
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The mortality rate of AoD is 1%-2% per hour after onset of symptoms; untreated, mortality is 90% at 3 months.12
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The Stanford classification system is the most used, with type A (proximal) affecting the ascending aorta and type B (distal) affecting the descending aorta. See Figure 1 and Table 1 for other classifications.
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Two-thirds of patients who present with AoD are males aged 50 to 70 years.
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AoD patients aged <40 years are more likely to have a bicuspid aortic valve, Marfan syndrome or other connective tissue disorder, or have had prior aortic surgery.
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Marfan syndrome, Loeys-Dietz syndrome, and Ehlers-Danlos syndrome type IV are connective tissue disorders associated with AoD.
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Half of patients presenting with AoD will be hypertensive and tachycardic. (See Table 3 for occurrence of examination findings in AoD.)
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Hypotension on presentation (8%) usually indicates complications such as tamponade, contained rupture, or myocardial ischemia.4
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The ADD-RS (Aortic Dissection Detection Risk Score) is a set of 12 clinical markers of AoD for low to moderate risk patients when AoD is on the differential.
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D-dimer has low sensitivity and specificity when used alone; a positive D-dimer necessitates further imaging, but a negative D-dimer should be interpreted with caution.
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Electrocardiogram has not been shown to be sensitive or specific in detection of AAS, though it may suggest a cardiac etiology. In patients with high-risk features, further testing is needed.
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Transesophageal echocardiography (TEE) is more accurate than transthoracic echocardiography (TTE) for identifying and ruling out acute proximal AoD.
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TTE is recommended for patients with aortic regurgitation, pericardial effusion, cardiac tamponade, and wall motion abnormalities.
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CT is the preferred initial imaging modality for evaluation of aortic disease.9
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The incidence of true contrast-induced nephropathy is lower than traditionally believed, and guidelines recommend that, in the setting of AoD, contrast should not be withheld.58
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Admit all AAS patients to the ICU.
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Ascending type A dissections almost uniformly require surgical intervention.
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Cardiothoracic surgery consult should be obtained for patients with IMH and PAU.
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When resources for operative intervention for AoD with tamponade are limited, controlled pericardial drainage may be used. See “Management of Patients in Shock”.
Pearls
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The most common presenting symptom of AAS is sudden and severe chest pain.
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Type A dissection: anterior chest pain that radiates to back, neck, and abdomen.
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Type B dissection: posterior chest pain that radiates to abdomen.
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Other presenting symptoms include syncope (13%), neurologic deficits (17%), apparent stroke, STEMI (3%), coma, weakness, flank pain (5%), and back pain. The symptoms typically relate to the location of the dissection.
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Contrary to classical teaching, pain migration has been associated with only 17% of cases.24
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The goal of ED management is stabilization, primarily through control of systolic blood pressure (SBP) and heart rate.
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A rapidly titratable beta blocker is preferred for rate control. (See Table 4.)
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Once heart rate is controlled, SBP should be maintained at 100-220 mm Hg.4,5
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