INTRODUCTION — Aortic dissection is relatively uncommon and often presents acutely as a catastrophic illness with severe tearing chest or back pain and acute hemodynamic compromise. Early and accurate diagnosis and treatment are crucial for survival.
Death from aortic dissection can be related to rupture of a proximal dissection into the pericardium precipitating cardiac tamponade or bleeding into the pleural space, dissection into the aortic valvular annulus leading to severe aortic regurgitation, obstruction of the coronary artery ostia leading to myocardial infarction, or end-organ failure due to abdominal aortic branch vessel obstruction [1,2]. The International Registry of Acute Aortic Dissection (IRAD) has provided a contemporary perspective of clinical features from the worldwide accrual of patients into a prospective database. Mortality related to aortic dissection is high; however, advances in surgical and endovascular techniques have lowered mortality rates overall for those who are diagnosed and treated in a timely fashion [3,4].
The clinical manifestations and diagnosis of acute aortic dissection will be reviewed here. Medical and surgical management are discussed separately.
PATHOPHYSIOLOGY — The primary event in aortic dissection is a tear in the aortic intima (image 1). Degeneration of the aortic media, or cystic medial necrosis, is felt to be a prerequisite for the development of nontraumatic aortic dissection. Blood passes into the aortic media through the tear, separating the intima from the surrounding media and/or adventitia and creating a false lumen. It is uncertain whether the initiating event is a primary rupture of the intima with secondary dissection of the media or hemorrhage within the media and subsequent rupture of the overlying intima . (See "Overview of acute aortic dissection and other acute aortic syndromes".)
Fifty to 65 percent of aortic intimal tears originate in the ascending aorta within the sinotubular junction and extend to involve remaining portions of the thoracoabdominal aorta . Approximately 20 to 30 percent of intimal tears will originate in the vicinity of the left subclavian artery and extend into the descending thoracic and thoracoabdominal aorta . The commonality of these two predominant locales for development of the aortic tear is hypothesized to be related to higher shear forces (dP/dT) in these regions [6-8].
The dissection can propagate proximally to involve the aortic valve and enter the pericardial space or distally to involve branch vessels . Such propagation is responsible for many of the ischemic clinical manifestations, including aortic regurgitation (figure 1), cardiac tamponade, or ischemia (coronary, cerebral, spinal, or visceral). Patients with involvement of the ascending aorta have imminent risk for aortic rupture. The intimal tear with type B dissection can spiral into a cleavage plane within the media of the aorta along the posterolateral descending thoracic aorta, leaving the celiac artery, superior mesenteric artery, and right renal artery, typically originating in the true lumen, with the left renal artery deriving false lumen flow . Variations in anatomy of the dissection are typical and underscore the critical need for proper axial imaging. In addition, multiple communications may form between the true lumen and the false lumen.
Immediately following dissection, there is "intrinsic true lumen collapse" to a variable degree, and false lumen dilation, thus increasing the aortic cross-sectional area . The increase of the false lumen area correlates with blood pressure, the size of the entry tear into the false lumen, the depth of the dissection plane within the media, and the percentage of aortic circumference involved. Because the outer wall of the false lumen is thinned, it expands to generate the necessary wall tension to accommodate aortic pressure. The true lumen collapses as a result of the pressure differential between the true and false lumens and may be exacerbated by the intrinsic recoil of the muscular elements within the dissection flap .
Malperfusion of aortic branch vessels may occur due to the extension of the dissection throughout the thoracoabdominal aorta. Malperfusion of a vascular bed can occur in one or more branch territories simultaneously. The standard nomenclature of the mechanisms of malperfusion of aortic branch vessels is termed "dynamic obstruction" (figure 2 and movie 1) and "static obstruction" (figure 3) . Malperfusion syndromes may occur in 30 to 45 percent of descending dissections and correlate with early mortality [3,13-16].
INCIDENCE AND ASSOCIATED CONDITIONS — The incidence of acute aortic dissection in the general population is estimated to range from 2.6 to 3.5 per 100,000 person-years [17-20]. Seasonal variation in the incidence of aortic dissection has been described, with winter months associated with higher admission rates for aortic dissection [21,22].
Patients with acute aortic dissection tend to be 60- to 80-year-old males [3-5,23-25]. In a review of 4428 patients from the International Registry of Acute Aortic Dissection (IRAD), 66.0 percent were male and the mean age was 63 years . Females presenting with aortic dissection are generally older than males (mean 67 years of age) and have a more delayed presentation [4,26].
There are some important differences between older adult patients and younger patients with dissections involving the ascending aorta. In an IRAD review, 32 percent of patients were ≥70 years of age and were significantly more likely to have atherosclerosis, prior aortic aneurysm, iatrogenic dissection, or intramural hematoma . In a review of patients under age 40, only 34 percent had a history of hypertension and only 1 percent had a history of atherosclerosis . Marfan syndrome is present in 8.5 percent of the younger patients (mean age 55 years) and was not seen in any older adult patient .
In a separate review, familial dissections also occurred in significantly younger patients compared with degenerative aortic dissection (54 versus 63 years of age) .
High-risk conditions — High-risk conditions commonly associated with aortic dissection include the following [30-32]:
●Hypertension – The most important predisposing factor of acute aortic dissection is systemic hypertension [4,5,23,33,34]. In the IRAD review, 76.6 percent had a history of hypertension . Hypertension was more common in those with a distal (type B) dissection compared with a type A dissection (70 versus 36 percent) [3,35].
An abrupt, transient, severe increase in blood pressure has been associated with acute aortic dissection through various mechanisms. Crack cocaine, which may cause transient hypertension due to catecholamine release, accounted for 37 percent of dissections in a report of an urban population . The mean duration from last cocaine use to the onset of symptoms was 12 hours. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse" and "Cocaine: Acute intoxication".)
High-intensity weight lifting or other strenuous resistance training can also cause a transient elevation in blood pressure and has been reported as an antecedent . Hypertension is also the postulated mechanism when energy drinks  or ergotism [39,40] have been associated with aortic dissection.
●Genetically mediated connective tissue disorders (eg, Marfan syndrome, Ehlers-Danlos syndrome) – In an IRAD review, Marfan syndrome was present in 50 percent of those under age 40, compared with only 2 percent of older patients . Most patients with Marfan syndrome (image 2) and aortic dissection have a family history of dissection. There may also be an association between Marfan syndrome and aortic dissection in the third trimester of pregnancy . (See "Genetics, clinical features, and diagnosis of Marfan syndrome and related disorders".)
●Preexisting aortic aneurysm – In an IRAD review, 13 percent of patients had a known aortic aneurysm prior to dissection . The ascending aorta was more often the site of origin of the dissection than the aortic arch or descending aorta. Such a history was more common in patients under age 40 (19 percent). In a later IRAD review, known aortic aneurysm was present in 20.7 percent of patients identified to have descending aortic dissection and 12.7 percent of those with ascending aortic dissection . (See "Clinical manifestations and diagnosis of thoracic aortic aneurysm" and "Clinical features and diagnosis of abdominal aortic aneurysm".)
●Preexisting variant of aortic dissection – Several anatomic variants of aortic dissection are described, including intimal tear without hematoma and aortic intramural hematoma. These variants are felt to be precursors to aortic dissection. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Definition and pathophysiology'.)
●Bicuspid aortic valve – In an IRAD review, 9 percent of patients under age 40 with aortic dissection had a bicuspid valve, compared with 1 percent of those over age 40  and 1 percent in the general population. Aortic dissection in patients with a bicuspid valve always involves the ascending aorta, usually with severe loss of elastic fibers in the media . The predisposition to dissection may reflect a genetic cause for the defect in the aortic wall, as enlargement of the aortic root and/or ascending aorta is frequently associated with bicuspid aortic valves, even those that function normally, independent of their function [43,44]. (See "Clinical manifestations and diagnosis of bicuspid aortic valve in adults".)
●Aortic instrumentation or surgery – Cardiac surgery or catheterization for coronary or valvular disease can be complicated by aortic dissection [28,45-47]. Cardiac catheterization, particularly with femoral artery access, with or without coronary intervention was reported to cause 14 of 723 dissections (2 percent) in a report from IRAD . Ascending aortic dissection is a rare complication of coronary artery bypass grafting (CABG), occurring with both conventional on-pump CABG and, perhaps more often, with minimally invasive off-pump CABG [49-52]. In a review from a single institution, ascending aortic dissection occurred in 1 of 2723 patients (0.04 percent) treated with conventional CABG and 3 of 308 undergoing off-pump CABG (1 percent) . (See "Early noncardiac complications of coronary artery bypass graft surgery", section on 'Aortic dissection' and "Off-pump and minimally invasive direct coronary artery bypass graft surgery: Clinical use".)
Although rare, other procedures that manipulate the aorta, including carotid or other great vessel interventions and thoracic or abdominal aortic repair (open or endovascular), can also be complicated by aortic dissection.
●Aortic coarctation – Aortic dissection can occur in patients with an aortic coarctation when surgery leaves behind abnormal para coarctation aorta that has intrinsic medial faults, or when balloon dilatation of native coarctation mechanically damages the inherently abnormal para coarctation aorta. (See "Clinical manifestations and diagnosis of coarctation of the aorta".)
●Familial TAAD – Familial thoracic aortic aneurysm and dissection (TAAD) refers to patients who have thoracic aortic disease associated with a family history of aneurysmal disease but who do not meet strict criteria for known connective tissue syndromes. The ascending thoracic aorta is predominantly involved. (See "Epidemiology, risk factors, pathogenesis, and natural history of thoracic aortic aneurysm and dissection", section on 'Familial TAAD'.)
●Turner syndrome – Aortic dissection or rupture, often occurring with coarctation, is an increasingly recognized cause of death in females with Turner syndrome. In a survey of 237 patients, at least 15 (6.3 percent) had aortic dilation: all involved the ascending aorta, 12 had an associated risk factor such as hypertension or another cardiovascular malformation (eg, coarctation), and two had a dissection [53,54]. (See "Clinical manifestations and diagnosis of Turner syndrome".)
●Inflammatory diseases – Inflammatory diseases that cause vasculitis (giant cell arteritis, Takayasu arteritis, rheumatoid arthritis, syphilitic aortitis) are associated with thoracic aortic aneurysm/dissection [55,56]. (See "Overview of and approach to the vasculitides in adults" and "Clinical manifestations of giant cell arteritis", section on 'Large vessel involvement'.)
●Trauma – Trauma rarely causes a classic dissection but can induce a localized tear in the region of the aortic isthmus (image 3). More commonly, chest trauma from acute deceleration (as in a motor vehicle accident) results in aortic rupture or transection . (See "Clinical features and diagnosis of blunt thoracic aortic injury".)
●Pregnancy and delivery – Pregnancy and delivery are independent risk factors for aortic dissection; however, the presence of other conditions (eg, bicuspid aortic valve, Marfan syndrome) may compound the risk [41,58-61]. In one review, postpartum aortic dissection occurred in 2 of 31 Marfan pregnancies . A cohort study of administrative claims data in several states from 2005 through 2013 found a rate of aortic complications of 5.5 per million patients during pregnancy and the postpartum period. Pregnancy was associated with a significantly increased risk of aortic dissection or rupture compared with the control period one year later (incidence rate ratio 4.0; 95% CI 2.0-8.2) among females with and without documented inherited connective tissue diseases (eg, Marfan syndrome), although the risk was significantly greater in those with connective tissue diseases . The authors noted that the findings may reflect prevalent but undiagnosed or undocumented connective tissue disorders, or they may indicate that the physiologic changes of pregnancy can cause aortic injury even in otherwise healthy females.
●Fluoroquinolone use – Observational studies have suggested that fluoroquinolone use may be associated with an increased risk of aortic aneurysm or dissection . (See "Epidemiology, risk factors, pathogenesis, and natural history of thoracic aortic aneurysm and dissection", section on 'Rupture/dissection' and "Epidemiology, risk factors, pathogenesis, and natural history of abdominal aortic aneurysm", section on 'Fluoroquinolone use'.)
Etiologic classification — Based on the etiology, aortic dissection can be classified as:
●Degenerative/sporadic – Aortic dissection that has a degenerative etiology is not associated with any known genetically mediated syndromes.
●Genetically mediated – Genetically mediated TAAD can be part of a syndrome (ie, syndromic), such as Marfan syndrome (table 1), Loeys-Dietz syndrome, vascular Ehlers-Danlos syndrome, or Turner syndrome; or nonsyndromic, as with familial TAAD or bicuspid aortic valve.
●Traumatic – Traumatic aortic dissection can be related to a blunt injury mechanism or iatrogenic in nature related to instrumentation (eg, catheterization, dissection following aortic repair).
CLINICAL FEATURES — Aortic dissection is classified clinically in terms of the duration of time from its occurrence as acute (hyperacute, acute, subacute) or chronic, and by clinical features, including the absence or presence of symptoms and whether disease becomes complicated. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Classification'.)
During the acute phase, particularly in the first two weeks, life-threatening complications due to branch involvement or aortic rupture are more likely to occur compared with a later timeframe [7,64]. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Duration'.)
Although acute aortic dissection can occur at any time of the day, the onset of symptoms more commonly occurs during waking hours. In a review that included 1827 patients, 25 percent of events occurred between 08:00 and 12:00 (8 am to 12 pm) . A lower incidence was seen in the late evening/early morning hours (22:00 to 02:00; 11pm to 2am). These may follow established patterns of blood pressure elevation and reduction throughout the day. Daytime physical activity has also been linked to onset of acute aortic dissection, particularly in younger patients .
Symptoms and signs — The symptoms and signs of acute aortic dissection depend upon the extent of the dissection and the affected cardiovascular structures (table 2). Pain is the most common symptom, occurring in over 90 percent of patients, most commonly in the chest or back [4,35]. Although painless dissection has been reported, it is relatively uncommon (6.4 percent in one retrospective review) . Patients with painless dissection were older (mean age 67 versus 62 years) and more often had ascending aortic dissection (75 versus 61 percent). A prior history of diabetes, aortic aneurysm, or cardiovascular surgery was more common in patients with painless dissection. Presenting symptoms of syncope, heart failure, or stroke were seen more often in this group. In another review, up to 10 percent of patients presented with neurologic symptoms but without chest pain .
Hypertension is present in 70 percent of type B dissections but only in 25 to 35 percent of type A dissections. The presence of hypotension complicating a type B dissection is rare, seen in less than 5 percent of patients, and usually implies rupture of the aorta. By contrast, hypotension may be present in 25 percent of dissections that involve the ascending aorta, potentially as a result of aortic valve disruption leading to severe aortic regurgitation and/or extravasation into the pericardial space leading to cardiac tamponade [3,4]. Malperfusion of brachiocephalic vessels by the dissection may falsely depress brachial cuff pressures, usually by involving the left subclavian artery origin in the type B dissection patient.
Acute pain — The most common presenting symptom is pain occurring in over 90 percent of patients, with 85 percent noting the onset to be abrupt [3,4,23,35,69,70]. Typically the pain is severe and sharp/knife-like, causing the patient to seek medical attention within minutes to hours of onset, and categorically unlike any pain experienced before. Pain can occur in isolation or be associated with syncope, a cerebrovascular accident, acute coronary syndrome, heart failure, or other clinical symptoms or signs.
While the pain is typically described as anterior chest in location in ascending (type A) dissection, for descending (type B) dissection, the pain is more often experienced in the back [3,4]. In an International Registry of Acute Aortic Dissection (IRAD) review, chest pain was significantly more common in patients with type A dissections (79 versus 63 percent in type B dissections) , while both back pain (64 versus 43 percent ) and abdominal pain (43 versus 22 percent ) were significantly more common with type B dissections. The pain can radiate anywhere in the thorax or abdomen [3-5]. Unlike the classic description of the character of pain in aortic dissection as ripping or tearing (50 percent), pain is more often described as sharp (68 percent), and less often as migratory (19 percent) [3,4,35]. Typical symptoms and signs were less common among those >70 years of age, which represented almost one third of patients . Older patients were significantly less likely to have an abrupt onset of pain compared with younger patients (77 versus 89 percent) .
The localization of pain to the abdomen was reported by 21 percent of patients in type A dissection and 43 percent of patients in type B dissection . In such patients, a high index of suspicion for mesenteric vascular compromise is warranted [9,71-73]. (See "Overview of intestinal ischemia in adults" and "Acute mesenteric arterial occlusion" and "Renal infarction" and "Ischemic hepatitis, hepatic infarction, and ischemic cholangiopathy".)
Pulse deficit — The presence of impaired or absent blood flow to peripheral vessels is manifest as a pulse deficit, defined as a weak or absent carotid, brachial, or femoral pulse resulting from the intimal flap or compression by hematoma. A considerable variation (>20 mmHg) in systolic blood pressure may be seen when comparing the blood pressure in the arms. In International Registry of Acute Aortic Dissection (IRAD) reviews, females were less likely to have a pulse deficit compared with males . Compared with younger patients, older adult patients (>70 years) were significantly less likely to have any pulse deficit (24 versus 33 percent) .
In those with aortic arch and/or thoracoabdominal aorta involvement, pulse deficits are common and occur in 19 to 30 percent of patients compared with 9 to 21 percent with a descending aortic dissection [3,35,74,75]. In the IRAD population, the involvement of the brachiocephalic trunk was noted in 14.5 percent of patients, the left common carotid artery in 6.0 percent, the left subclavian artery in 14.5 percent, and the femoral arteries in 13.0 to 14.0 percent . Patients presenting with pulse deficits more often had neurologic deficits, coma, and hypotension. Carotid pulse deficits, not surprisingly, were strongly correlated with fatal stroke, consistent with prior observations .
The number of pulse deficits was also clearly associated with increased mortality. Within 24 hours of presentation, 9.4 percent of patients with no deficits died, 15.8 percent of patients with one or two deficits died, and 35.3 percent of patients with three or more deficits died .
With respect to isolated lower extremity pulse deficits, mortality from lower extremity ischemia or its sequelae was uncommon . Nonetheless, leg ischemia caused by acute dissection is a marker of extensive dissection and may be accompanied by other compromised vascular territories. The clinical course of the peripheral ischemia can be quite variable, and up to one-third of this group may demonstrate spontaneous resolution of their pulse deficits .
Patients with a pulse deficit have a higher rate of in-hospital complications and mortality compared with those without a pulse deficit . A rapid bedside pulse examination can provide important information in the diagnosis of acute aortic dissection and those at risk for complications. In a previous report of patients treated during the 1990s, those with peripheral branch obstruction had a mortality rate of 23 percent compared with 16 percent for those without obstruction . In contrast to the IRAD findings, the presence of peripheral vascular complications did not increase mortality . This finding was thought to be due to a more timely diagnosis, prompt initiation of therapy, and the recognition of the importance and appropriate treatment of peripheral vascular complications.
Heart murmur — Aortic dissection that propagates proximal to the initial tear can involve the aortic valve (figure 1) . A new diastolic murmur in association with severe acute chest pain is a sign of acute aortic regurgitation. Characteristically, it is a diastolic decrescendo murmur associated with a wide pulse pressure, hypotension, and/or heart failure. Acute aortic valve regurgitation occurs in one-half to two-thirds of ascending dissections [3,77]. The murmur of aortic regurgitation related to aortic dissection is most commonly heard along the right sternal border, as compared with the left sternal border for aortic regurgitation due to primary aortic valve disease. The duration of the diastolic murmur may be quite short due to rapid ventricular filling and early equilibration of aortic and left ventricular diastolic pressures. (See "Auscultation of cardiac murmurs in adults" and "Acute aortic regurgitation in adults".)
In one IRAD review, patients older than 70 years were significantly less likely to have a murmur of aortic regurgitation compared with younger patients (29 versus 47 percent) .
Focal neurologic deficit — Focal neurologic deficits are due to propagation of the dissection proximally or distal to the initial tear involving branch arteries, or due to mass effects as the expanding aorta compresses surrounding structures .
●Stroke or altered consciousness can be from direct extension of the dissection into the carotid arteries or diminished carotid blood flow. Alterations of consciousness are more common in female patients compared with males.
●Horner syndrome is from compression of the superior cervical sympathetic ganglion.
●Hoarseness is from vocal cord paralysis due to compression of the left recurrent laryngeal nerve.
●Acute paraplegia is from spinal cord ischemia. Spinal cord ischemia from the interruption of intercostal vessels is clearly more common with type B aortic dissections than with type A dissections, and it may occur in 2 to 3 percent of all patients [3,78].
Hypotension — Syncope, hypotension, and/or shock at initial presentation are more common in patients with ascending aortic dissection, whereas hypertension is more common in patients with descending aortic dissection . Hypotension/shock may be related to rupture of the aorta, or propagation of the dissection via the following mechanisms:
●Acute myocardial ischemia or myocardial infarction (MI) due to coronary occlusion. The right coronary artery is most commonly involved and, in infrequent cases, leads to complete heart block. (See 'Electrocardiogram' below.)
●Hemothorax or hemoperitoneum, and possibly exsanguination if the dissection extends through the adventitia in the thoracic or abdominal aorta.
Syncope — Syncope occurs in 5 to 10 percent of patients and often indicates the development of cardiac tamponade or involvement of the brachiocephalic vessels . Overall, patients in the IRAD study presenting with syncope were more likely to have a type A dissection than a type B dissection (19 versus 3 percent), and more likely to have cardiac tamponade (28 versus 8 percent). Similarly, they were more likely to have a stroke (18 versus 4 percent) and more likely to die in the hospital (34 versus 23 percent). Although patients presenting with syncope had a higher rate of severe complications (tamponade, stroke, death), almost one-half of syncope patients had none of the aforementioned complications to explain their loss of consciousness .
Electrocardiogram — Electrocardiography (ECG) is often obtained in the initial evaluation of patients with chest pain. Aortic dissection that does not involve coronary ostia can usually be distinguished from acute coronary syndrome by the nature and location of the chest pain and the absence of ECG changes characteristic of ischemia. (See "Evaluation of the adult with chest pain in the emergency department", section on 'Electrocardiogram'.)
However, the ECG is less helpful when dissection leads to coronary ischemia. Data from IRAD further suggest that involvement of a coronary artery in an aortic dissection may not manifest changes in the electrocardiogram . In a review of 4428 patients, the ECG was normal in 30 percent, showed nonspecific ST and T wave changes in 42 percent (commonly, left ventricular hypertrophy and strain patterns associated with hypertension), showed ischemic changes in 15 percent, and, among patients with an ascending (type A) aortic dissection, showed evidence of an acute myocardial infarction in 5 percent .
Chest radiograph — Plain chest films are also commonly obtained to help rapidly differentiate the various causes of chest pain (eg, pneumothorax). (See "Evaluation of the adult with chest pain in the emergency department", section on 'Chest radiograph'.)
The most common abnormality seen in aortic dissection is widening of the aortic silhouette, appearing in 60 to 90 percent of cases [3,80]. The IRAD review of 464 patients found that mediastinal widening was present in 63 percent with type A dissections, while 11 percent of patients had no abnormality on chest radiography . The comparable values in patients with type B dissections were 56 and 16 percent.
Radiographic evidence of a pleural effusion was found in 19 percent of dissections; this finding is more common in females compared with males (26 versus 15 percent) . Other findings, which are less specific for dissection but have been described, include widening of the aortic contour, displaced calcification, aortic kinking, and opacification of the aorticopulmonary window . Hemothorax may be seen if the dissection extends through the adventitia, with hemorrhage into the pleural space, which can lead to exsanguination.
However, because of the limited sensitivity of the chest radiograph, especially in type B dissections, additional imaging studies are obtained in almost all patients (98 percent in data from IRAD) [3,75,80]. (See 'Cardiovascular imaging' below.)
Laboratory studies — Serum markers for acute aortic dissection are emerging as a diagnostic option, particularly in screening patients in the setting of differentiating chest pain where the cost of widespread cardiovascular imaging would be prohibitive.
D-dimer — D-dimer is a degradation product of cross-linked fibrin and reflects activation of the extrinsic pathway of the coagulation cascade by tissue factor exposed in the aortic media by the intimal tear. As such, D-dimer has emerged as a potential serum biomarker for acute dissection . However, as a nonspecific indicator of intravascular coagulation, D-dimer can be elevated in many conditions (table 3). D-dimer appears to be a useful screening tool to identify patients who do not have acute aortic dissection using a cutoff of 500 ng/mL. A level below this value is highly predictive for excluding dissection .
A systematic review identified seven studies that used assays for plasma D-dimer to screen patients for acute aortic dissection and included a control group . For D-dimer <500 ng/mL, the pooled estimate of the sensitivity was 97 percent, specificity was 56 percent, and negative predictive value was 96 percent. This study and others have concluded that patients with a D-dimer <500 ng/mL are not likely to benefit from further aortic imaging [81,83-91]. However, caution should be exercised in the application of D-dimer levels as some authors have reported up to 18 percent of patients with confirmed aortic dissection may have levels <400 ng/mL . However, in a later prospective multicenter study that included 1850 patients, 8 patients (0.4 percent) with acute aortic syndrome had a negative D-dimer . A D-dimer <500ng/mL may be more useful for ruling out acute aortic dissection when combined with low-probability acute aortic dissection risk score (ADD-RS 0 or 1). (See 'Aortic dissection detection risk score (ADD-RS)' below.)
While D-dimer testing carries a sensitivity of 90 to 95 percent, a meta-analysis suggests that its very low specificity, a lack of standardized testing protocols, and the variability of levels from the time since onset of symptoms should limit its usage to patients at low risk for having aortic dissection but in whom there remains a clinical diagnostic uncertainty .
Other experimental tests — Other experimental tests include measurements of smooth muscle myosin heavy chain, soluble ST2, soluble elastin fragments, high-sensitivity C-reactive protein, fibrinogen, and fibrillin fragments [94-99].
A rapid 30-minute immunoassay for the serum concentration of smooth muscle myosin heavy chain has been evaluated in patients suspected of having an aortic dissection [97,98]. The sensitivity and specificity of this assay in the first three hours were similar and possibly superior to those of transthoracic echocardiogram, conventional computed tomography (CT), and aortography but were lower compared with transesophageal echocardiogram, helical CT, or magnetic resonance imaging. The utility of this test needs further evaluation.
ST2 is an interleukin–1 receptor family member with transmembrane and soluble isoforms. Soluble ST2 (sST2) may be useful for discriminating acute aortic dissection from other conditions that present with acute chest pain . In one clinical study, at a cutoff level of 34.6 ng/mL, the sensitivity, specificity, positive predictive value, and negative predictive value of sST2 for acute aortic dissection were 99.1, 84.9, 68.7 and 99.7 percent, respectively.
DIAGNOSIS — The diagnosis of acute aortic dissection may be suspected clinically based upon the presence of high-risk clinical features (see 'Symptoms and signs' above and 'High-risk clinical features' below), but confirmation of the diagnosis requires cardiovascular imaging that demonstrates the dissection flap separating a false lumen from the true lumen (image 1 and image 4). (See 'Cardiovascular imaging' below.)
A high index of suspicion is important for identifying patients with acute aortic dissection to avoid a missed or delayed diagnosis [100-102]. In an autopsy study that included 388 patients over a 60-year period, 63 percent of patients under medical care were not diagnosed prior to death . In this study, risks for dissection included prior cardiovascular surgery, bicuspid aortic valve, connective tissue disease, and left ventricular hypertrophy suggestive of hypertension. In two other reviews, initial misdiagnosis occurred in nearly 40 percent of patients [101,102]. In one of these, acute coronary syndrome was the most common misdiagnosis and resulted in inappropriate treatments (eg, antiplatelet therapy, anticoagulation, fibrinolytic therapy). Exposure to these treatments was associated with higher rates of bleeding complications and a trend toward increased in-hospital mortality .
It is important to rapidly distinguish acute ascending thoracic aortic dissection, which is a cardiac surgical emergency, from acute descending thoracic aortic dissection, which is managed medically in hemodynamically stable patients who do not have malperfusion or other complications. In general, definitive vascular imaging studies should not be performed until the patient can be initially stabilized. (See 'Ascending versus descending aortic involvement' below.)
High-risk clinical features — Many studies have sought to identify which of the clinical features presented above are most reliable for predicting aortic dissection to avoid a missed or delayed diagnosis [50,101-107].
Clinical triad — In an analysis of 250 patients with acute chest and/or back pain (128 with a dissection), 96 percent of acute aortic dissections could be identified based upon three clinical features :
●Abrupt onset of thoracic or abdominal pain with a sharp, tearing, and/or ripping character
●A variation in pulse (absence of a proximal extremity or carotid pulse) and/or blood pressure (>20 mmHg difference between the right and left arm)
●Mediastinal and/or aortic widening on chest radiograph
The probability of a dissection related to the presence or absence of these three were:
●Isolated pulse or blood pressure differential, or any combination of the three: ≥83 percent
●Presence of mediastinal widening: 39 percent
●Pain alone: 31 percent
However, the absence of these clinical features does not exclude aortic dissection. In this review, all three features were absent in 7 percent . In a review 68 patients, the absence of a pulse deficit or an absence of a widened mediastinum on chest radiography increased the risk for a missed diagnosis (odds ratio [OR] 35.8, 95% CI 3.7-345.3; OR 33.16, 95% CI 5.7-191.5, respectively).
Factors associated with more accurate diagnosis in one systematic review included more comprehensive history-taking and increased use of imaging . Factors related to misdiagnosis included symptoms and features associated with other diseases (eg, acute coronary syndrome, stroke, pulmonary embolism), absence of typical features (such as widened mediastinum on chest radiograph), or concurrent conditions such congestive heart failure. In this review, among 1663 patients with aortic dissection, one-third of patients were initially misdiagnosed.
Aortic dissection detection risk score (ADD-RS) — The Aortic Dissection Detection Risk Score (ADD-RS) is based on the presence of one or more of the following:
●High-risk condition such as Marfan syndrome, family history of aortic disease, known aortic valve disease, known thoracic aortic aneurysm, or previous aortic manipulation, including cardiac surgery. (See 'High-risk conditions' above.),
●Pain in the chest, back, or abdomen described as abrupt, of severe intensity, or a ripping/tearing sensation. (See 'Acute pain' above.)
●Physical examination findings of perfusion deficit, including pulse deficit, systolic blood pressure difference, or focal neurologic deficit, or with aortic diastolic murmur and hypotension/shock. (See 'Pulse deficit' above and 'Heart murmur' above and 'Focal neurologic deficit' above and 'Hypotension' above.)
The presence of ≥1 marker within each of these groups is given a score of 1 with a maximum cumulative score of 3 if all three are present. In a review from the IRAD registry, high ADD-RS effectively stratified the risk for acute aortic dissection .
ADD-RS plus D-dimer — Initial studies suggested that the addition of D-dimer to ADD-RS may improve diagnostic performance compared with each of these when used alone for ruling out acute aortic dissection, or other acute aortic syndromes (ie, aortic intramural hematoma, penetrating aortic ulcer, ruptured aorta) [109,110]. The Aortic Dissection Detection Risk Score (ADD-RS) Plus D-Dimer in Suspected Acute Aortic Dissection (ADvISED) study used a combination of the ADD-RS and D-dimer as a diagnostic tool for acute aortic syndrome (AAS; ie, aortic dissection, penetrating aortic ulcer, aortic intramural hematoma, aortic rupture) . This multicenter study included 1850 patients for whom AAS was considered a possibility. The combination of ADD-RS (0 to 1) and negative d-dimer (<500 mg/dL) effectively ruled out AAS with a failure rate of less than 1 in 300 patients. Based on these results, about 60 percent of patients with a low probability for AAS might be spared from unnecessary conclusive vascular imaging. For ADD-RS>1, D-dimer was not discriminatory, requiring conclusive imaging. Although this initial experience appears promising, additional validation in a broader patient population is needed before routine use of this combination as a diagnostic tool can be recommended. (See 'Cardiovascular imaging' below.)
The details of this study for each risk group are as follows:
●Among 341 patients with high probability ADD-RS (2 or 3), 133 (39 percent) had an acute aortic syndrome (ie, aortic dissection, aortic rupture, aortic intramural hematoma, penetrating aortic ulcer). Among 113 with a negative D-dimer, 5 (4 percent) had an acute aortic syndrome.
●Among 1509 patients with a low probability ADD-RS (0 or 1), 108 (7.2 percent) had an acute aortic syndrome. Among the 924 patients with a negative D-dimer, 3 (0.3 percent) had an acute aortic syndrome. The overall sensitivity and specificity of ADD-RS (0 or 1) and negative D-Dimer for ruling out acute aortic syndrome was 98.8 and 57.3 percent, respectively.
●Among the 438 patients with an ADD-RS of 0, 12 (2.7 percent) had an acute aortic syndrome. Among 294 patients with a negative D-dimer, 1 (0.3 percent) had an acute aortic syndrome. The overall sensitivity and specificity of ADD-RS (0) and negative D-Dimer for ruling out acute aortic syndrome was 99.6 and 18.2 percent, respectively.
Ascending versus descending aortic involvement — Management of aortic dissection depends on the level or aortic involvement and etiology (table 4), and thus distinguishing between these is important. (See "Management of acute type A aortic dissection" and "Management of acute type B aortic dissection".)
Certain clinical features suggest involvement of the ascending versus descending aorta (table 2).
●Ascending aorta: Pain is located in the chest more so than in the back or abdomen [3,4]. Other clinical features include acute aortic valve regurgitation, acute coronary syndrome, cardiac tamponade, hemothorax, focal neurologic deficits related to cerebrovascular ischemia, and upper extremity pulse deficit [9,23]. Since most type A dissections include a distal extent to the abdomen, descending aortic manifestations may also be included.
●Descending aorta: Pain is located in the posterior chest/upper back and may radiate to the abdomen [3,4]. Other clinical features include evidence of malperfusion syndromes such as abdominal pain from visceral ischemia, renal insufficiency, lower extremity ischemia, and focal neurologic deficits related to spinal ischemia [9,75,111].
Cardiovascular imaging — Our recommendations for cardiovascular imaging are generally in agreement with multidisciplinary consensus guidelines [30,32,112,113]. Multiple imaging modalities can be used to demonstrate the dissection, including chest magnetic resonance (MR) angiography, computed tomographic (CT) angiography, and multiplane transesophageal echocardiography (TEE) . Each has its advantages and disadvantages, and one may be more appropriate for selected patient populations as an initial study. CT is the most common initial choice due to its widespread availability, particularly in the emergency department setting.
More than one study is often needed to obtain all the necessary information to fully guide treatment. In one International Registry of Acute Aortic Dissection (IRAD) review, patients had an average of 1.6 studies per patient . The initial study was CT in 61 percent, TEE in 33 percent, aortography in 4 percent, and MR in 2 percent. The availability of some studies may be limited, and accuracy depends upon the performance and interpretation of the test by skilled individuals, and as such, the studies chosen may differ from institution to institution.
The diagnosis of aortic dissection is based on the presence of an intimal flap separating a false lumen from a true lumen, and associated imaging findings or complications [9,115-119]:
●True and false lumen (image 7A-B)
●Involvement of the ascending aorta (image 8)
●Enlargement of the aorta
●The extent of dissection and the sites of entry and reentry
●Thrombus in the false lumen
●Branch vessel involvement
●Coronary artery involvement
●Aortic valve regurgitation
Hemodynamically unstable — For hemodynamically unstable patients or those with clinical features suggestive of ascending aortic involvement, we suggest transesophageal echocardiography (TEE) as an initial study in patients with suspected aortic dissection, wherever available. TEE is a portable procedure that yields a diagnosis within minutes and is easily performed in the emergency department . The sensitivity of TEE has been reported to be as high as 98 percent, and the specificity ranges from 63 to 96 percent [121,122]. The ascending aorta is typically assessed at approximately 130-degree orientation while the arch and descending thoracic aorta are assessed at 0 degrees. Biplane imaging may be useful.
The advantages of TEE include generally wide availability, ease of use, and bedside capability. In addition, TEE can detect entry tear sites, false lumen flow/thrombus, involvement of the arch or coronary arteries, degrees of aortic valvular regurgitation, and pericardial effusions. The addition of color flow Doppler patterns may decrease false positives by recognizing differential flow velocities in the true and false lumens that may assist in the diagnosis of malperfusion syndromes.
A disadvantage of TEE is that it requires esophageal intubation, which usually requires procedural sedation, which may have untoward effects in hemodynamically unstable patients. TEE requires the availability of experienced operators (both physicians and technicians) to ensure accurate results. As such, it is often not attainable on a "stat" basis in many centers. The theoretical technical limitation of TEE is the anatomic "blind spot" in the distal ascending aorta and proximal arch secondary to the air-filled trachea and left main stem bronchus, and inability to document dissection extension beyond the diaphragm that may be causing malperfusion of abdominal aorta branches. Despite these shortcomings, TEE can be particularly useful in delineating acute dissection and relevant surgical pathology in the ascending aorta, and therefore, it is chiefly applied in this territory. Moreover, in the unstable patient with a suspected acute dissection in the ascending aorta, TEE may be performed in the operating room to expedite diagnosis and definitive therapy. In the IRAD review, TEE was employed second most frequently (after CT) in the diagnosis and workup of an acute aortic dissection .
The following findings may be seen on TEE in patients with aortic dissection [46,119,120]:
●Intimal dissection flaps can be identified with high spatial resolution (image 6 and movie 2). The use of M-mode echocardiography may improve diagnostic accuracy by demonstrating a lack of relation between movement of the intimal flap and the aortic wall .
●The true and false lumens can be identified. They may not be distinguishable without color Doppler imaging or identification of the proximal border of the dissection. However, in some cases, the false lumen can be seen to surround the true lumen (movie 3 and movie 4). Color Doppler permits clear identification of flow within and between the true and false lumens (image 6 and movie 5). The presence of flow does not absolutely distinguish the true lumen from the false lumen. The true lumen has an endothelial lining and is contiguous with the aortic valve.
●Thrombosis in the false lumen, pericardial effusion, concomitant aortic regurgitation, and the proximal coronary arteries can be readily seen.
●The 135 degree long axis view from TEE can define the severity and mechanism of aortic regurgitation that complicates acute type A dissection . Patients with an intrinsically normal valve who have aortic regurgitation due to a correctable aortic lesion (incomplete leaflet closure, leaflet prolapse, or dissection flap prolapse) can undergo aortic valve repair (movie 6). By contrast, abnormalities that cannot be repaired (eg, Marfan syndrome, bicuspid valve, aortitis) will require valve replacement. (See "Management of acute type B aortic dissection".)
A less favorable alternative to TEE is transthoracic echocardiography (TTE), which can sometimes identify proximal ascending aortic dissection with the assistance of color flow Doppler and echo contrast but is particularly valuable for identifying complications associated with dissection (eg, aortic valve integrity/regurgitation, hemopericardium) (movie 7 and movie 8) [45,120,124]. The primary disadvantage with TTE is its inability to adequately and fully visualize the mid- and distal ascending, transverse arch, and descending aorta, or the presence of other complications in a substantial number of patients. Furthermore, the sensitivity and specificity of TTE are inferior to CT angiography, MR angiography, and TEE.
Hemodynamically stable — For hemodynamically stable patients without clinical features suggesting ascending aortic involvement, we obtain CT angiography as an initial study in patients with suspected aortic dissection, particularly in the emergency department setting where other studies are less available. Most patients with suspected acute aortic dissection should be evaluated with dynamic contrast-enhanced fine-cut CT scanning of the chest and abdomen (ie, CT angiography). In comparison with other modalities, CT angiography is the least operator dependent, provides useful anatomic correlates for surgical and endovascular therapy, and collects information for follow-up analysis and measurement. Most importantly, three-dimensional CT scan reconstructions can aid treatment planning, and axial imaging affords the best opportunity to detect topographic relationships of the true and false lumens and potential aortic branch compromise.
Conventional CT scanning has a reported sensitivity of 83 to 95 percent and specificity of 87 to 100 percent for the diagnosis of acute aortic dissection [120,125]. The chief limitation of imaging is the ascending aorta, where the sensitivity may drop to <80 percent, as contrast enhancement can depend upon timing of the injection. As an example, a CT scan to evaluate for initially suspected pulmonary embolus as a source of chest pain may or may not time correctly for assessment of the ascending aorta. The accuracy of CT is substantially improved with spiral (helical) CT [126-130]. Spiral CT may be more accurate than MR or TEE for the detection of aortic arch vessel involvement . A potential limitation is a spiral CT artifact that can simulate an aortic dissection flap in patients if performed without echocardiogram (ECG) gating [131-133]. Thus, ECG-gated scanning is recommended, when available. Advantages of CT include ready availability at most hospitals, even on an emergency basis, and identification of intraluminal thrombus and pericardial effusion. Two disadvantages of standard CT are that the intimal flap is seen in less than 75 percent of cases and that the site of entry is rarely identified . In addition, potentially nephrotoxic iodinated contrast is required, and there is no capability to assess for aortic insufficiency. If the CT is equivocal or if further delineation of the dissection is needed, MR angiography or TEE is indicated.
The diagnosis of aortic dissection by CT requires the identification of two distinct lumens; the intimal flap may or may not be demonstrated. In most cases, the true lumen may be localized by its continuity with an undissected proximal or distal segment of the aorta. The presence of intraluminal thrombus is a good marker of the false lumen, but in patients with a concomitant degenerative aneurysm, thrombus may be present in the true lumen. In the majority of cases, the false lumen is larger than the true lumen . A compressed true lumen is the key radiographic finding, which should substantially raise the index of suspicion for renal/visceral/lower extremity malperfusion syndrome. Curving of the dissection flap into the true lumen is seen in 63 percent of acute type B dissections but only 25 percent of chronic dissections . Indeed, it may be appropriate, if open surgical intervention is chosen as the revascularization procedure, to proceed directly to surgery after CT alone in circumstances where the clinical and/or laboratory signs dictate the need for urgent revascularization, as in evidence of bowel ischemia or vascular rupture.
For hemodynamically stable patients, MR angiography is an alternative to CT angiography, depending on availability [133,135]. Although less commonly used, MR angiography is highly accurate for diagnosing aortic dissection . Gadolinium-enhanced MR angiography has an overall sensitivity and specificity to diagnose aortic dissection of 95 to 100 percent . In a prospective trial of 110 patients, MR angiography had 85 percent sensitivity for identifying the site of entry . MR angiography can also detect differential flow between the true and false lumens. Additional suggestive findings include widening of the aorta with a thickened wall and thrombosis of the false lumen. The chief advantage of MR angiography is avoiding excess radiation exposure in the long term given the serial studies required in the standard surveillance of type B dissection patients. MR is safe in adequately monitored patients with aortic dissection, and MR contrast agents have a more favorable safety profile than iodinated contrast agents. Noncontrast MR angiography is another option. Other advantages of MR include the ability to assess branch vessels, although it may be less sensitive than spiral CT , and to assess for aortic insufficiency. The main disadvantages of MR imaging are inconvenience (patients are required to remain motionless with relatively limited access for more than 30 minutes) and limited applicability (MR imaging cannot be performed in patients with claustrophobia, pacemakers, or certain types of aneurysm clips or metallic ocular/auricular implants). MR is also not readily available on an emergency basis at many institutions, and there are concerns about patient monitoring and relative patient inaccessibility during prolonged scanning. Gadolinium administration for contrast-enhanced MR imaging in patients with moderate-to-severe kidney disease (particularly dialysis patients) should be avoided. The accuracy of noncontrast MR angiography for aortic dissection has been less well defined. (See "Nephrogenic systemic fibrosis/nephrogenic fibrosing dermopathy in advanced kidney disease".)
Role of aortography — Formerly the gold standard for the diagnosis of aortic dissection, aortography has largely yielded to CT angiography in the initial diagnosis of aortic dissection. In the endovascular management of dissection, it is used mainly as a component of an interventional treatment strategy. However, for patients in whom the suspicion for ascending aortic dissection is very strong but noninvasive imaging is unavailable or inconclusive, digital subtraction aortography should be performed. Aortography involves the injection of iodinated contrast media into the aortic lumen, permitting identification of the site of dissection, the relationship between the dissection and the major branches of the aorta, and the communication site between the true and false lumen (image 9) .
Findings on aortography considered supportive of a diagnosis of aortic dissection include distortion of the normal contrast column, flow reversal or stasis into a false channel, failure of major branches to fill, and aortic valvular regurgitation. Most contemporary diagnostic algorithms have deemphasized the role of aortography, especially when assessing for malperfusion syndromes. Furthermore, pressurized contrast injections into either lumen in the presence of aortic dissection can, in fact, lead to diagnostic confusion with respect to malperfusion syndromes by altering the hemodynamic gradients between lumens (during the hydraulically powered injections) that are causing malperfusion. Evaluation for aortic regurgitation, and coronary angiography, when indicated (suspected ascending aortic aneurysm and prior history or angina or myocardial infarction [MI], age >60 years of age, multiple risk factors for coronary disease) can also be performed during the same procedure .
Aortography is only moderately sensitive for the diagnosis of thoracic aortic dissection . In a review of 164 patients (82 had a dissection), aortography had a sensitivity of 88 percent and a specificity of 94 percent; the positive and negative predictive values were 96 and 84 percent, respectively . Lower values for sensitivity (77 percent) and accuracy (87 percent) were noted in other reports [140,141]. However, false negative results may be obtained when there is simultaneous opacification of the true and false lumen so that the intimal flap between them is not visible, when thrombosis of the false lumen results in lack of opacification with contrast, or when there is an intramural hematoma with noncommunicating dissection [139,140,142,143]. Also, intimal tears associated with only a minimal amount of blood in the dissected aortic wall that may not have been seen with noninvasive imaging will be demonstrated. In one study of 181 patients who underwent repair of the ascending aorta or aortic arch, nine (5 percent) had a subtle aortic dissection that was not diagnosed preoperatively despite the use of three or more imaging techniques .
Anatomic classification — Anatomic classifications used to describe aortic dissection are the DeBakey and Stanford (Daily) systems and the later Society for Vascular Surgery (SVS) and Society for Thoracic Surgery (STS) classification systems [9,145-147]. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Location of entry tear'.)
●The Stanford system (figure 4) is widely used and classifies dissections that involve the ascending aorta (and may also involve the arch or descending aorta) as type A, regardless of the site of the primary intimal tear. All other dissections are classified as type B.
●By comparison, the DeBakey system is based upon the site of origin, with type 1 originating in the ascending aorta and propagating to at least the aortic arch, type 2 originating in and confined to the ascending aorta, and type 3 originating in the descending aorta and extending distally or proximally, but not past the left subclavian artery.
•Type A aortic dissection is classified as an entry tear in zone 0, and the distal extent can range from zone 1 to 12.
•Type B has an entry tear in a zone >1, and the proximal and distal extent are noted.
Type A aortic dissections are almost twice as common as type B aortic dissections. The right lateral wall of the ascending aorta is the most common site . In patients with an ascending aortic dissection, aortic arch involvement occurs in up to 30 percent .
Isolated abdominal aortic dissection is reported and can be due to iatrogenic, spontaneous, or traumatic mechanisms (image 10) . The infrarenal abdominal aorta is more commonly involved than the suprarenal aorta. In one review of 52 reported cases, the entry site for spontaneous isolated abdominal aortic dissections most commonly occurred between the renal arteries and inferior mesenteric artery . A concomitant abdominal aortic aneurysm was identified in 40 percent of patients and indicated the need for repair. (See "Management of symptomatic (non-ruptured) and ruptured abdominal aortic aneurysm".)
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of acute aortic dissection includes other entities associated with acute chest or back pain, pulse deficit, and neurologic deficits, which includes both nonvascular and vascular pathologies . Nonvascular pathologies include acute coronary syndrome, pulmonary embolus, spontaneous pneumothorax, aortic regurgitation without dissection, esophageal rupture, pericarditis, and pleuritis, among others (table 5). Artifact on echocardiography can also mimic the appearance of a dissection flap . (See "Evaluation of the adult with chest pain in the emergency department".)
Vascular pathologies include other acute aortic pathologies such as aortic intramural hematoma without dissection, aortic aneurysm, aortic injury without dissection, peripheral artery disease, and chronic aortic dissection . These may be suspected by risk factors and patient history, but cardiovascular imaging distinguishes these from aortic dissection. In patients with new symptoms and chronic dissection, detailed comparison with existing/prior imaging data are necessary to distinguish dissection extension from other causes of their symptoms. (See "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Differential diagnosis'.)
Lower extremity ischemia in the absence of typical chest or back pain can also occur and can lead to a missed or delayed diagnosis . The clinical features of acute extremity ischemia are discussed separately. (See "Clinical features and diagnosis of acute lower extremity ischemia".)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Aortic dissection and other acute aortic syndromes".)
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SUMMARY AND RECOMMENDATIONS
●Acute aortic dissection – Acute aortic dissection is a relatively uncommon, though catastrophic, acute illness. The inciting event in aortic dissection is a tear in the aortic intima, causing severe pain. Propagation of the dissection can occur proximal (retrograde) or distal (antegrade) to the initial tear, involve the aortic valve, or branches of the thoracic and/or abdominal aorta. Propagation of the dissection is responsible for other clinical manifestations that can include aortic regurgitation, cardiac tamponade, and end-organ ischemia (coronary, cerebral, spinal, or visceral, extremity). (See 'Pathophysiology' above.)
●Risk factors – Risk factors for acute aortic dissection include older age, male sex, systemic hypertension, preexisting aortic aneurysm or variant of aortic dissection and risk factors for atherosclerosis. Seasonal variation in the incidence of aortic dissection has been noted. For those under age 40, these risk factors are less common, but other predisposing factors are often present, such as connective tissue disorders, vasculitis, bicuspid aortic valve, aortic coarctation, Turner syndrome, prior aortic valve surgery, vascular instrumentation, trauma, high intensity weightlifting or other exercise, and cocaine use. (See 'Incidence and associated conditions' above.)
●Clinical presentation – Acute aortic dissection typically presents with anterior chest pain in ascending aortic dissection or severe, sharp, or "tearing" posterior chest or back pain when the dissection progresses distal to the left subclavian artery. Pain can be an isolated symptom or associated with syncope, symptoms or signs of stroke, myocardial infarction (MI), heart failure, or other clinical signs of end-organ ischemia (visceral ischemia, renal insufficiency, extremity ischemia, spinal cord ischemia). Hypertension upon initial clinical presentation is more common with descending thoracic aortic dissection than with ascending thoracic aortic dissection. (See 'Clinical features' above.)
●Diagnosis – A diagnosis of acute aortic dissection depends upon demonstration of the dissection on imaging studies, which defines the extent of aortic involvement and identifies sites of entry and reentry, branch vessel involvement, aortic insufficiency, and pericardial effusion. No one study is capable of obtaining all the information that is needed to fully evaluate aortic dissection, and thus a combination of studies is often obtained. (See 'Diagnosis' above and 'Cardiovascular imaging' above.)
•D-dimer – D-dimer may become a useful screening tool in the setting of chest pain where the cost of widespread imaging would be prohibitive. A D-dimer <500 ng/mL may indicate a subset of patients who are not likely to benefit from aortic imaging. D-dimer levels may be most appropriate for patients with a low risk for aortic dissection but in whom there remains a clinical diagnostic uncertainty. (See 'D-dimer' above.)
•Vascular imaging – The initial imaging study of choice depends upon the hemodynamic status of the patient and institutional resources. It is important to rapidly distinguish acute ascending thoracic aortic dissection, which is a cardiac surgical emergency, from descending thoracic aortic dissection, which is managed medically in hemodynamically stable patients without end-organ complications.
-Hemodynamically stable patients – Computed tomographic (CT) angiography is generally used as the initial screening study in hemodynamically stable patients with suspected aortic dissection because of its widespread availability and speed of image acquisition, particularly for those presenting to the emergency department. If CT is equivocal or if further delineation of the dissection is necessary, imaging may involve transesophageal echocardiography (TEE), magnetic resonance (MR) angiography, or digital subtraction aortography, which may also be indicated when there is a strong suspicion for ascending aortic dissection.
-Hemodynamically unstable patients – For patients with chest pain suspected of having acute aortic dissection who are hemodynamically unstable, we suggest multiplanar TEE at the bedside or in the emergency department (or operating room) to establish the diagnosis and evaluate the location of the dissection.
●Classification – Based on the location of the intimal tear, aortic dissection is commonly classified as type A for as those that involve the ascending aorta, regardless of the site of the primary intimal tear, and type B for all other dissections (Stanford system (figure 4)). The Society for Vascular Surgery and Society for Thoracic Surgery classification system is similar to the Stanford system, distinguishing type A from B by level of involvement, but it also specifies the distal extent of the dissection (figure 5). Type A aortic dissections are almost twice as common as type B aortic dissections. Isolated abdominal aortic dissection can also occur. (See 'Anatomic classification' above and 'Pathophysiology' above.)
ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledges Emile R Mohler, III, MD, now deceased, who contributed to an earlier version of this topic review. UpToDate also acknowledges Dr. Mohler's work as our Section Editor for Vascular Medicine.
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