Overview of Acute Aortic Syndromes

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Overview of acute aortic syndromes
Authors: Warren J Manning, MD, James H Black, III, MD

Section Editors: Gabriel S Aldea, MD, Edward Verrier, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jun 2017. | This topic last updated: Sep 29, 2016.
INTRODUCTION Acute aortic syndromes include a spectrum of life-threatening aortic conditions. By convention, acute disease is distinguished from
chronic disease at an arbitrary time point of two weeks from initial clinical presentation (<24 hours hyperacute, 1 to 14 days acute, 14 to 90 days subacute,
and >90 days chronic) and is typically manifest with symptoms. Acute aortic dissection is the most familiar and is defined by a separation of the layers of
the aortic wall by an inciting intimal injury. Intimal tear without hematoma, penetrating aortic ulcer, aortic intramural hematoma, and periaortic hematoma
are variants of the classically described aortic dissection (figure 1) [1-3]. The changes associated with these are more localized, though they are similar to
those of aortic dissection, with penetration and weakening of the aortic wall that predisposes to aortic rupture, which may manifest as a contained
periaortic hematoma or free rupture into the chest or abdomen [2]. Each of these conditions can affect the thoracic aorta, abdominal aorta, and, in some
cases, both.
An overview of the clinical features, classification, diagnosis, and approach to treatment of acute aortic syndromes including acute aortic dissection, which
is also discussed in detail elsewhere, aortic intramural hematoma, and penetrating aortic ulcer are reviewed here. (See "Clinical features and diagnosis of
acute aortic dissection" and "Management of acute aortic dissection".)
DEFINITION AND PATHOPHYSIOLOGY
Acute aortic dissection Acute aortic dissection is defined as a separation of the layers of the aortic wall due to an intimal tear (figure 1). For
spontaneous dissection, it is uncertain whether the initiating event is a primary rupture of the intima with secondary dissection of the media or primary
hemorrhage within the media and subsequent rupture of the overlying intima [4]. The initial intimal tear can occur in the ascending aorta or descending
aorta and occasionally can originate in the abdominal aorta. Blood at high pressure passes through the tear and separates the intima from the media
and/or adventitia, creating a true lumen and a false lumen. The dissection can propagate proximally or distally from the initial tear to involve the aortic
valve, coronary arteries, or branches of the thoracic or abdominal aorta [5]. Such propagation is responsible for many of the associated clinical features of
aortic dissection (acute chest or back pain, neurologic symptoms). A higher mean pressure in the false lumen can cause dynamic or static compression
and occlusion of the true lumen with malperfusion of the branches of the aorta, resulting in end-organ ischemia (coronary, cerebral, spinal, extremity,
visceral) [6]. Aortic regurgitation, coronary ischemia, and cardiac tamponade can occur if the dissection progresses proximally to involve the aortic valve or
the pericardial sac. In addition, multiple communications may form between the true lumen and the false lumen. (See "Clinical features and diagnosis of
acute aortic dissection", section on 'Clinical features'.)
Abdominal aortic dissection can occur as an extension to a thoracic aortic dissection with the intimal flap located in the proximal or descending thoracic
aorta, or it can occur in isolation [7-13]. Isolated abdominal aortic dissection is reported occasionally and can be due to spontaneous, iatrogenic, or
traumatic mechanisms [14]. 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 (SIAADs) most commonly occurred between the renal arteries and inferior mesenteric
artery [15]. A concomitant abdominal aortic aneurysm was identified in 40 percent of patients and indicated the need for repair. (See "Management of
asymptomatic abdominal aortic aneurysm".)
Intimal tear without hematoma Intimal tear without hematoma (figure 1) is an uncommon variant of aortic dissection that is characterized by a
stellate or linear intimal tear associated with exposure of the underlying aortic media or adventitia. There is no separation of the medial layers or
progression [3].
Iatrogenic or traumatic dissection Aortic dissection that does not occur spontaneously can be due to instrumentation or trauma. Traumatic tears
typically involve the descending thoracic aorta just distal to the subclavian artery and are reviewed in detail elsewhere [16]. Iatrogenic or traumatic injury
(eg, intra-aortic balloon pump placement, motor vehicle accident) was responsible for 6 percent of cases of aortic intramural hematoma in one review [17].
(See "Blunt thoracic aortic injury" and "Surgical and endovascular repair of blunt thoracic aortic injury".)
Penetrating aortic ulcer Penetrating aortic ulcer refers to a region of the aorta (ulcer-like projection) where the aortic intima is denuded with the lesion
progressing through a variable amount of the aortic wall, over which there may or may not be overlying thrombus [18,19]. Penetrating aortic ulcers are
typically associated with atherosclerotic changes of the adjacent aortic wall [19].
Penetrating aortic ulcer may be associated with hematoma within the media and may progress to perforation or aortic dissection [2,19-21]. Penetrating
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ulcer is the initiating lesion in <5 percent of all aortic dissections (image 1) [20,22].
Aortic intramural hematoma Aortic intramural hematoma is defined as a hematoma confined within the medial layer of the aorta in the absence of a
detectable intimal tear, although microtears may be present (figure 1). The absence of an intimal lesion distinguishes aortic intramural hematoma from the
hematoma that may be associated with a penetrating aortic ulcer, for which there is a clear break in the intima. Aortic intramural hematoma can be a
precursor to acute aortic dissection [2]. In different series, aortic intramural hematoma accounted for 5 to 20 percent of patients with symptoms consistent
with an aortic dissection (eg, acute aortic syndrome) [16,17,23-25].
The mechanism by which an intramural hematoma is created is not certain. Two mechanisms have been described: rupture induced by a penetrating
atherosclerotic ulcer and spontaneous rupture [2]. Spontaneous rupture of the vasa vasorum as a pathogenesis has not been proven [26,27]. In this
scenario, the false lumen originates from spontaneous rupture of the vasa vasorum into the media of the aortic wall. Because there is no continuous flow,
the blood contained within the wall quickly thromboses (picture 1).
Some believe that intramural hematoma represents acute aortic dissection with thrombosis of the false lumen and that an intimal tear is always present
whether or not it is identified [28]. Intimal defects have been identified surgically and radiographically in approximately 70 percent of cases initially
diagnosed as an intramural hematoma [29,30]. However, there appears to be a difference in the affected plane of the aortic media. For intramural
hematoma, the outer media (toward the adventitia) is thinner, which may explain the higher risk of rupture for intramural hematoma compared with acute
dissection [31-34]. Between 8 and 16 percent will evolve into aortic dissection [32,34,35].
Periaortic hematoma Periaortic hematoma represents a contained aortic rupture, due to slow oozing from the damaged aorta at or near the site of
aortic injury (figure 1). Periaortic hematoma is more common in aortic intramural hematoma compared with acute aortic dissection. In a review of 971
patients with acute dissections from the International Registry of Acute Aortic Dissections (IRAD), 227 (23 percent) had a periaortic hematoma [36]. Not
surprisingly, patients with periaortic hematoma had higher rates of shock, cardiac tamponade, and altered consciousness/coma and had a significantly
higher mortality rate compared with those without a periaortic hematoma (33 versus 20 percent).
CLASSIFICATION Acute aortic syndromes are classified according to the location and extent of involvement of the aorta. Acute aortic syndromes are
further classified by clinical features, including the absence or presence of symptoms and whether disease becomes complicated. The nature of the
complications differs for each variant, but each has the potential to cause life-threatening or limb-threatening complications. (See 'Clinical features' below.)
For aortic dissection, two different anatomic classification systems, the DeBakey and Daily (Stanford) systems, have been used (figure 2) [37,38]. The
Stanford system is the more widely used of these and will be used in this review. The variants of aortic dissection, intimal tear without hematoma,
penetrating aortic ulcer, aortic intramural hematoma, and periaortic hematoma can be described in a similar manner based upon the location of the aortic
abnormality.
The Stanford system classifies aortic dissections that involve the ascending aorta as type A, regardless of the site of the primary intimal tear, and all
other dissections as type B [2,5,37,38].
The DeBakey system is based upon the site of the origin of the tear, 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 [3,39,40].
Ascending aortic dissections are almost twice as common as descending dissections [32,35,41]. The right lateral wall of the ascending aorta is the most
common site [4]. In patients with an ascending aortic dissection, aortic arch involvement is seen in up to 30 percent [42].
Aortic intramural hematoma more commonly involves the descending aorta [17,32,35,41,43]. For some patients, the lesion in the ascending aorta
represents the early stage of an acute aortic dissection [16,25].
Most penetrating aortic ulcers are located in the descending thoracic aorta (85 to 95 percent), but they can also occur in the ascending aorta or arch
[21,22,44-47].
EPIDEMIOLOGY AND RISK FACTORS The overall incidence of acute aortic syndromes ranges from 2 to 4 cases per 100,000 individuals. Acquired or
genetically mediated conditions can weaken the aortic wall tissues, predisposing to acute aortic syndromes [4].
Acute aortic dissection comprises the majority of acute aortic syndromes [48-52]. Risk factors associated with acute aortic dissection include hypertension,
atherosclerosis, prior cardiac surgery, known aneurysm, known connective tissue disorder (eg, Marfan syndrome, Loeys-Dietz syndrome), bicuspid aortic
valve, and prior aortic surgery [39,52]. Acute aortic dissection is more common in men (65 percent in an International Registry of Acute Aortic Dissections
[IRAD] review), while women tend to be older at presentation (67 versus 60 years) [1,52]. Systemic hypertension, which increases the stress on the aortic
wall, is the most important factor precipitating acute aortic dissection [4,52,53]. In a review of the IRAD data, 72 percent had a history of hypertension, and
31 percent had a history of atherosclerosis [52]. These factors are less important in young patients; in a separate review, in patients under age 40, only 34
percent had a history of hypertension, and only 1 percent had a history of atherosclerosis [54]. (See "Clinical features and diagnosis of acute aortic
dissection", section on 'Incidence and associated conditions'.)
Aortic intramural hematoma accounts for 5 to 20 percent of patients with symptoms consistent with acute aortic syndrome, although the incidence may be
higher [16,17,23-25]. In a review of 1010 patients in the IRAD registry, intramural hematoma was present in 58 patients (5.7 percent). Among 51 patients
with only aortic intramural hematoma at the initial diagnosis, eight (16 percent) progressed to aortic dissection on serial imaging studies [35]. Compared
with acute aortic dissection, patients with intramural hematoma are older and more commonly present with aortic aneurysm, and fewer have Marfan
syndrome [31-33,41]. None of the 58 patients with intramural hematoma had Marfan syndrome in the IRAD review [35]. Also distinguishing intramural
hematoma from aortic dissection is the higher prevalence of females that are affected [34,41]. But like aortic dissection, aortic intramural hematoma is
most often associated with longstanding hypertension [17,35,43]. In a meta-analysis of 143 reported cases, approximately half were hypertensive [17]. In
another series of 94 patients, 79 (84 percent) of aortic intramural hematomas were associated with hypertension [43]. In addition, the proportion of acute
aortic syndromes that are diagnosed as aortic intramural hematoma is greater in Asian patients compared with American and European patients (28 to 32
percent versus 4 to 11 percent) [35,41,55-57].
Penetrating aortic ulcers account for 2 to 7 percent of acute aortic syndromes [44]. Patients with penetrating aortic ulcers are older (over 70 years) and
have risk factors that are associated with atherosclerosis, including hypertension, hyperlipidemia, coronary artery disease, tobacco use, and infrarenal
abdominal aortic aneurysm [21,45-47]. As discussed below, the presence of a penetrating atherosclerotic ulcer is associated with a higher likelihood of
disease progression with medical therapy alone [21]. (See 'Management' below.)
CLINICAL FEATURES In the authors experience, acute aortic syndromes are rarely identified as incidental findings with minimal symptoms on
advanced imaging studies, although this has been reported [58-60]. Although very similar, there are some differences in the clinical manifestations of acute
aortic dissection and those of other acute aortic syndromes.
The acute onset of severe chest or back pain occurs in 80 to 90 percent of patients with acute aortic dissection [53]. The pain is described as severe,
sharp, or "tearing" and is located in the anterior chest pain for type A aortic dissection and in the posterior chest or back pain for type B aortic dissection.
Other symptoms or signs can be related to progression of the dissection and end-organ malperfusion (eg, shock, syncope, acute congestive heart failure,
myocardial ischemia, stroke, paraplegia, extremity ischemia, mesenteric ischemia) [39,50,52,53,61]. A complete discussion of the symptoms and signs of
acute aortic dissection is provided separately. (See "Clinical features and diagnosis of acute aortic dissection".)
Pain is also common with intramural hematoma [31,32,35], but since patients with intramural hematoma are more likely to have type B aortic lesions
compared with acute aortic dissection (eg, 60 versus 35 percent in the International Registry of Acute Aortic Dissections review), patients are more likely
to present with upper or lower back pain [17,35,62]. Other manifestations seen with type A aortic dissections, such as myocardial infarction, stroke, aortic
regurgitation, and syncope, are relatively infrequent with type A intramural hematomas [17,35,43,63]. In one series, cardiogenic shock was present on
admission in only 14 percent of patients, mostly associated with type A aortic intramural hematoma [43]. On the other hand, type A aortic intramural
hematoma is more often associated with pericardial tamponade and periaortic hematoma [30,32,34,41,55]. Several studies have noted a higher risk of
rupture for acute intramural hematoma compared with acute aortic dissection (26 percent versus 8 percent) [32-34]. Pericardial effusion occurs in 60 to 70
percent of type A aortic intramural hematoma and is much more common than with acute aortic dissection [31,32,35,41]. Malperfusion and aortic valve
regurgitation is less common with aortic intramural hematoma.
Symptomatic penetrating aortic ulcers present similarly to other acute aortic syndromes, primarily with pain, the location of which depends upon the
location of the ulcer.
No biomarkers are available to provide a diagnosis of acute aortic syndrome; however, for acute aortic dissection, a low D-dimer (less than 500 mcg/L)
may help exclude the diagnosis among those who present with chest pain [64]. (See "Clinical features and diagnosis of acute aortic dissection", section on
'Laboratory studies'.)
Although certain radiographic features, such as a widened mediastinum, may raise suspicion for aortic disease, plain films are not sensitive for a diagnosis
of acute aortic syndromes but are also often not completely normal [35,65]. (See "Clinical features and diagnosis of acute aortic dissection", section on
'Chest radiograph' and "Clinical features and diagnosis of acute aortic dissection", section on 'Diagnosis'.)
DIAGNOSIS Acute aortic syndromes cannot be distinguished from each other clinically, and imaging confirmation is necessary to determine the type of
acute aortic syndrome, classify the location and extent of the pathology, and identify any anatomic complications [16,17,63,66]. (See "Clinical features and
diagnosis of acute aortic dissection".)
Computed tomographic (CT) angiography is the diagnostic imaging modality of choice in hemodynamically stable patients. It is highly sensitive and
specific for imaging aortic pathology. The study should include the entire aorta, including the iliac and femoral vessels. Other imaging modalities such as
transthoracic echocardiography (TTE) or transesophageal echocardiography (TEE) may be useful in hemodynamically unstable patients. Both TTE and
TEE can identify aortic valve regurgitation, hemorrhagic pericardial effusions and tamponade, and regional wall motion abnormalities. However, the view of
the aorta is limited with TTE. TTE and TEE may not be diagnostic for intramural hematoma. Magnetic resonance imaging (MRI) is seldom used due to the
wider availability of CT in the emergency department; catheter-based arteriography is rarely necessary [67].
The imaging diagnosis of aortic dissection by CT scanning requires the identification of two distinct lumens; the intimal flap may or may not be
demonstrated. The presence of intraluminal thrombus is a good marker of the false lumen. In the majority of cases, the false lumen is larger than the true
lumen. (See "Clinical features and diagnosis of acute aortic dissection".)
Absence of an intimal flap is a prerequisite for the imaging diagnosis of aortic intramural hematoma [41]. In one review of 143 cases of aortic intramural
hematoma, 81 percent were diagnosed by CT scan, and the remaining patients by MRI and/or TEE [17]. The main finding on CT or magnetic resonance
(MR) angiography is a crescentic or circular high attenuation area along the aortic wall that does not enhance with contrast, absence of an intimal flap, and
absence of compression of the patent lumen (image 2). However, the appearance of an aortic intramural hematoma and an acute dissection with complete
thrombosis of the false lumen is similar, and an aortic intramural hematoma may be difficult to identify correctly. On TEE, findings include regional
thickening of the aortic wall of more than 7 mm in a crescentic (nontraumatic) or circular shape (traumatic) and/or evidence of intramural accumulation of
blood (image 3) [16]. In one series of 49 patients in whom the diagnosis of aortic intramural hematoma was confirmed by surgery or follow-up changes, the
sensitivity and specificity of TEE were 100 and 91 percent, respectively [63].
These same imaging modalities also identify a penetrating aortic ulcer (image 4 and image 5). Radiographic imaging of penetrating aortic ulcers show a
lesion that penetrates the aortic wall to varying degrees, causing hematoma formation within the media, pseudoaneurysm, or rupture (image 6 and image
7). Penetrating atherosclerotic ulcer without medial thrombosis is more common in the ascending aorta [21]. Identification of penetrating aortic ulcer may
have prognostic importance, as it is associated with a much higher rate of disease progression [21]. (See 'Progression and subsequent treatment' below.)
Differential diagnosis The differential diagnosis of acute aortic syndromes includes other entities associated with acute chest or back pain, pulse
deficit, and neurologic deficits, which includes both nonvascular and vascular pathologies [68]. Nonvascular pathologies include acute coronary syndrome,
pulmonary embolus, spontaneous pneumothorax, aortic regurgitation without dissection, esophageal rupture, pericarditis, and pleuritis, among others
(table 1).
Triple rule-out CT (TRO-CT) is a modified coronary CT angiography protocol with extended thoracic coverage that may have advantages for identifying
life-threatening causes of chest pain beyond coronary artery disease, such as pulmonary thromboembolism or acute aortic syndromes [69]. Artifact on
echocardiography can also mimic the appearance of a dissection flap [70]. (See "Evaluation of the adult with chest pain in the emergency department".)
Vascular pathologies include other acute aortic pathologies such as aortic aneurysm, chronic aortic disease with new symptoms, and complications of prior
aortic repair (eg, endoleak, pseudoaneurysm) [71]. These may be suspected by risk factors and patient history, but cardiovascular imaging distinguishes
these from the acute aortic syndromes discussed here. In patients with new symptoms and chronic pathologies, detailed comparison with existing/prior
imaging data is necessary to distinguish dissection extension from other causes of their symptoms.
MANAGEMENT
Treatment overview The general principles of the treatment of acute aortic syndromes are similar. A crucial aspect of early therapy is ensuring a
correct diagnosis so that the appropriate treatment can be instituted in a timely fashion.
Acute medical management of acute aortic syndromes includes controlling pain and anti-impulse therapy by controlling the blood pressure to
minimize the likelihood of rupture or progression, unless hypotension is present. These should be initiated immediately for all patients once the
diagnosis has been made but should not interfere with the timely transfer to the operating room for those with indications for immediate aortic repair.
(See 'Acute medical management' below.)
The treatment of type A acute aortic syndromes is surgical, with ongoing medical management of type A lesions reserved for patients who would not
survive surgery. By contrast, type B acute aortic syndromes can generally be managed medically, with surgery reserved for those experiencing
complications or progressive symptoms. (See 'Ascending aorta (type A)' below and 'Descending aorta (type B)' below.)
The association of intramural hematoma and penetrating ulcer may imply a more malignant course, particularly in the ascending aorta, and surgery
should be considered [21]. Type B penetrating aortic ulcer may also have a more aggressive course, even when identified incidentally, and may merit
early intervention.
In general, type A aortic pathologies are repaired using open surgical techniques, while an initial endovascular approach is appropriate for most type B
aortic pathologies provided the patients anatomy is suitable for endograft placement. (See 'Open surgical and endovascular techniques' below and
"Overview of open surgical repair of the thoracic aorta" and "Endovascular repair of the thoracic aorta".)
Acute aortic syndromes are associated with significant mortality, even when treated surgically. In an International Registry of Acute Aortic Dissections
(IRAD) review, the in-hospital mortality rates for acute aortic dissection and aortic intramural hematoma were 24 and 21 percent, respectively.
Acute medical management Patients with suspected acute aortic syndromes should be admitted to an intensive care unit as rapidly as possible after
confirmation of the diagnosis for pain control with morphine and anti-impulse therapy to reduce systolic blood pressure to the lowest level tolerated,
typically using beta blockers [2,68]. Patients generally require blood pressure monitoring with an arterial line to facilitate rapid management of changes in
blood pressure. Patients who are hemodynamically unstable or with airway compromise should be intubated. Acute medical therapies should not interfere
with timely transfer to the operating room for those in whom immediate surgery is indicated. An experienced cardiovascular surgeon should be consulted
early in the course to discuss any decision for surgery and its timing, which must be individualized taking into account the patients comorbidities (eg, prior
stroke), age, and patient and family wishes.
Before fluid volume is administered, hypotensive patients should be evaluated to determine if the cause is hemopericardium with tamponade, valvular
dysfunction, or left ventricular systolic dysfunction. In patients with cardiac tamponade, percutaneous pericardiocentesis can accelerate bleeding and
shock [72].
Anti-impulse therapy Systolic blood pressure should be reduced to the lowest level that is tolerated without compromising mentation or urine
output, generally between 100 and 120 mmHg. Although there are no randomized trials in patients with acute aortic syndromes, observational studies
suggest that lowering blood pressure reduces the rate of progression, and this is typically accomplished using intravenous beta blockers [73,74]. These
act by reducing both the systolic pressure and the rate of rise in systolic pressure, thereby diminishing aortic wall stress [75]. Inotropic agents should be
avoided since they will increase aortic wall shear stress and may lead to progression. (See 'Progression and subsequent treatment' below.)
Initial treatment consists typically of an intravenous beta blocker to reduce the heart rate below 60 beats/minute. Either propranolol (1 to 10 mg load,
followed by 3 mg/hour) or labetalol can be used. Labetalol can be given as a bolus (20 mg initially, followed by 20 to 80 mg every 10 minutes to a total
dose of 300 mg) or as an infusion (0.5 to 2 mg/minute). Esmolol has advantages in the acute setting due to its short half-life and ability to titrate to effect. It
is also advantageous in patients who might be intolerant of beta blockers due to asthma or heart failure, for example [2]. Verapamil or diltiazem are
alternatives in patients who cannot tolerate beta blockers [2]. (See "Drugs used for the treatment of hypertensive emergencies".)
If after beta blockade the systolic blood pressure remains elevated, nitroprusside can be added, if needed, to achieve a systolic blood pressure of 100 to
120 mmHg. The initial dose of nitroprusside is 0.25 to 0.5 mcg/kg per minute. Nitroprusside should not be used without first controlling heart rate with beta
blockade since vasodilation alone induces reflex activation of the sympathetic nervous system, leading to enhanced ventricular contraction and increased
aortic shear stress. Patients receiving nitroprusside should be continuously monitored, preferably using an intra-arterial cannula from the arm with the
highest auscultatory pressure. While nitroprusside is the preferred second-line agent, angiotensin converting enzyme (ACE) inhibitors or intravenous
nicardipine, verapamil, or diltiazem may also be effective in lowering blood pressure [2,72]. Other direct vasodilators, such as hydralazine, should be
avoided, since they increase aortic wall shear stress and provide less accurate and reversible control of the blood pressure.
Pain control Means to provide pain control other than antihypertensive therapies are warranted. This may include intravenous opioids as needed or
patient-controlled analgesia (PCA) as would be administered to a postoperative patient, in the absence of contraindications. (See "Management of acute
perioperative pain".)
Pain refractory to optimal medical management has been associated with worse outcomes in patients with aortic dissection [73]. However, recurrence of
pain may not always be associated with failure of medical therapy. In a study of 34 patients who experienced recurrent pain after diagnosis of type B aortic
dissection [74], repeat imaging studies revealed no change in aortic diameter and no radiographic evidence of worsening. Overall, only 2 of the 34 patients
had a complicated hospital course. On the basis of these observations, the authors concluded that among patients with early recurrent pain after type B
aortic dissection, in the absence of clinical or radiographic signs of anatomic changes such as effusion, dilation, or refractory hypertension, a conservative
strategy of continued medical management is a reasonable approach [74].
Progression and subsequent treatment Intervention for acute aortic syndromes depends upon the location of the involved aorta and the presence of
complications. In general, type A lesions are treated with early surgery, whereas in many cases type B lesions can be treated with ongoing medical care
[2,5,17,24,62]. (See "Management of acute aortic dissection".)
In general, type A aortic pathologies are repaired using open surgical techniques, while an initial endovascular approach is appropriate for most type B
aortic pathologies, provided the patients anatomy is suitable for endograft placement. (See "Overview of open surgical repair of the thoracic aorta" and
"Endovascular repair of the thoracic aorta".)
Ascending aorta (type A) Patients with acute aortic syndromes affecting the ascending aorta (type A) should be referred for emergent surgical
evaluation and treatment. (See "Overview of open surgical repair of the thoracic aorta", section on 'Indications for open repair'.)
Type A aortic dissection is a surgical emergency. Rupture of the dissected aorta is fortunately uncommon but is an ominous complication with certain
mortality unless prompt surgical intervention can be undertaken. The development of malperfusion in type A aortic dissection is associated with mortality
rates up to 44 percent [75-77]. In one IRAD study, 87 to 90 percent of patients with acute type A aortic dissections were able to initially be treated
surgically. Among patients with acute type A aortic dissection who are treated with medical management alone, mortality progressively increases with time
(20, 30, 40, and 50 percent at 1, 2, 7, and 30 days, respectively) [52]. In spite of other improvements in patient care, the in-hospital mortality rate for type A
aortic dissection has remained at approximately 20 percent over the past 20 years. Repair of type A aortic dissection involves replacement of the
ascending aorta, resection of intimal tears and aneurysmal aorta, and either restoring the competency of or replacing the aortic valve. (See "Management
of acute aortic dissection", section on 'Ascending (type A) aortic dissection'.)
The treatment of type A penetrating aortic ulcer is also emergent surgery owing to its natural history and predilection for rupture. Even asymptomatic acute
ascending or arch penetrating aortic ulcers should generally be managed operatively as these do not appear to follow a benign course [21,34,45,47]. The
risk of rupture of a type A penetrating aortic ulcer may be as high as 33 to 40 percent [34,45]. Graft replacement of the ascending aorta is the standard
treatment of a penetrating aortic ulcer of the ascending aorta. Transverse arch penetrating aortic ulcers can be managed by open graft replacement or by
using endovascular techniques, often with brachiocephalic vessel debranching.
Similarly, treatment of type A aortic intramural hematoma is aggressive to prevent progression to aortic dissection or rupture [32,33,55,57]. Among
medically treated patients, mortality rates range from 33 to 40 percent [32,33,55]. In a multicenter study of 66 patients who were admitted to the hospital
within 48 hours after the onset of symptoms, 39 patients (59 percent) showed evidence of progression to dissection, rupture, or aneurysm within 30 days;
most of these patients had ascending lesions [62]. In a review of 143 patients with aortic intramural hematoma, patients with lesions of the ascending aorta
had a lower mortality with surgery than medical treatment (14 versus 36 percent) [17]. Mortality for surgically treated intramural hematoma is similar to that
of aortic dissection [32,33,41,55]. Among those patients with type A aortic intramural hematoma for whom surgery is deemed too high a risk because of
advanced age or other comorbid conditions, mortality rates are lower with medical treatment compared with similar patients with type A aortic dissection (6
versus 58 percent with classic dissections, in one study [25]).
It has also been suggested that good outcomes can be achieved in type A intramural hematomas when therapy is guided by specific patient
characteristics and only those deemed at high risk for complications are taken for surgery. A maximum aortic diameter 50 mm on initial computed
tomography (CT) may identify patients who are more likely to progress [78]. However, progression also occurs in patients with smaller lesions [62]. In one
series of 41 patients, only 11 (27 percent) underwent early surgical intervention, in each case because of cardiac tamponade or aortic rupture [43]. Among
the remaining patients, who were managed conservatively, nine (22 percent) subsequently required surgery for progression of the aortic intramural
hematoma. In another study, the three-year survival rate was 78 percent. However, such good outcomes have not been noted in other reports [79]. Until
more data are available, surgery should remain the preferred approach for type A aortic intramural hematomas [80].
There is evidence to suggest that type A aortic intramural hematomas in Korean and Japanese patients may be best managed medically, with surgical
intervention reserved for those who develop complications [41,57]. However, over 30 percent of Japanese and Korean patients treated medically will
eventually require surgery [35]. In one study, overall hospital mortality with this strategy was 7.9 percent, which was less than that associated with acute
dissection at 17.2 percent [81]. There was no difference in mortality between the patients who did not have complicating features of the aortic intramural
hematoma and who continued with medical therapy compared with those who required surgery (6.1 versus 8.8 percent). The proportion of patients who
eventually required urgent surgery was 32 percent, which was similar to other reported series [41,56,57]. Risk factors for death, rupture, or conversion to
aortic dissection in medically treated patients include aortic diameter (>50 to 55 mm) and thickness of the aortic intramural hematoma (>10 to 16 mm)
[41,57]. Interestingly, medical management of aortic intramural hematoma in Chinese patients has similar outcomes to that of American and Europeans
patients, high mortality (32 percent) and high risk of adverse outcomes (40 percent) [82].
Descending aorta (type B) Most lesions associated with acute aortic syndromes affecting the descending aorta (type B) respond well to medical
management. Intervention (surgical or endovascular) is reserved for patients who have persistent severe hypertension, persistent or recurrent or pain,
progression (to dissection or propagation of dissection), aneurysmal expansion, malperfusion leading to end-organ ischemia, or rupture [2]. An exception
may be penetrating aortic ulcer associated with intramural hematoma, for which earlier intervention may be needed to prevent complications. The mortality
associated with such complications can exceed 60 percent. The rapid evolution of the use of endovascular treatments mandates their immediate
availability in the acute phase or the transfer of the patient to a regional medical center with such resources.
Progression of type B aortic dissection (early or late) in medically managed patients occurs in approximately one-third of patients, necessitating
intervention. (See "Management of acute aortic dissection", section on 'Efficacy of medical management' and "Management of acute aortic dissection",
section on 'Descending (type B) aortic dissection'.)
Patients with aortic intramural hematoma are more likely to have type B lesions compared with those who present with aortic dissection (60 versus 35
percent in the IRAD review) [35]. Many patients with type B aortic intramural hematoma respond well to medical therapy with resolution of the aortic
abnormality over time [5,24,41,43,83,84]. In a review of 143 patients with type B aortic intramural hematoma, mortality rates were similar for medical
versus surgical treatment (14 versus 20 percent) [17]. As many as 10 percent of aortic intramural hematoma may completely resolve with medical therapy
[32,34,35]. Predictors of progression, which occurs in 8 to 16 percent of patients with type B intramural hematoma (defined as aortic rupture, hematoma
expansion, or dissection) in spite of adequate medical management, include maximum aortic diameter 40 mm, maximum aortic thickness 10 mm on CT
scan [85], age >70 years, and presence of a penetrating atherosclerotic ulcer [17,83]. Late progression can also occur in patients with aortic intramural
hematoma who survive the initial episode [62,83]. Patients who progress are less likely to have been treated with a beta blocker compared with those who
were treated (49 versus 7 percent) [62]. One study evaluated 53 patients with a type B aortic intramural hematoma and 57 with a type B aortic dissection,
all of whom were initially treated medically [83]. At three years, 77 percent of intramural hematomas had regressed or disappeared. Survival at five years
was significantly better for patients with aortic intramural hematoma compared with aortic dissection (97 versus 79 percent). However, a similar analysis
found similar survival for patients with type B aortic intramural hematoma and type B aortic dissection (85 versus 89 percent) [86].
Aortic intramural hematoma associated with penetrating atherosclerotic ulcer has a higher rate of progression with medical therapy [21,87]. This was
illustrated in a series of 65 symptomatic patients with aortic intramural hematoma, 34 (52 percent) of whom had an associated penetrating atherosclerotic
ulcer, almost all of whom (31 patients) had a type B hematoma [21]. Progression with medical therapy (defined as aortic rupture, hematoma expansion, or
dissection) occurred significantly more often in patients with a penetrating aortic ulcer compared with those who did not (48 versus 8 percent).
Among patients with a penetrating atherosclerotic ulcer associated with aortic intramural hematoma or persistent pain, early endovascular intervention has
been proposed as a less invasive alternative to treat these lesions and prevent complications. In a small series of 26 patients, all had successful device
deployment [88]. Three patients died within 30 days and two had an early endoleak (leakage of blood around the graft within the aortic lumen). Actuarial
survival estimates at one, three, and five years were 85, 76, and 70 percent, respectively.
Open surgical and endovascular techniques Type A lesions are treated using an open surgical approach, although some hybrid approaches may be
available for a limited number of focal lesions. For most patients with type B lesions, an endovascular approach is appropriate; however, patients with
genetically mediated thoracic aortic aneurysm/dissection who have complications should be managed using open surgical techniques. Open surgical and
endovascular methods for treating thoracic aortic lesions are reviewed separately. (See "Management of acute aortic dissection", section on 'Ascending
(type A) aortic dissection' and "Management of acute aortic dissection", section on 'Descending (type B) aortic dissection' and "Overview of open surgical
repair of the thoracic aorta" and "Endovascular repair of the thoracic aorta".)
SUMMARY AND RECOMMENDATIONS
Acute aortic syndromes include a spectrum of life-threatening aortic conditions including acute aortic dissection, which is the most familiar to
clinicians, but also aortic intramural hematoma, penetrating aortic ulcer, intimal tear without hematoma, and periaortic hematoma. (See 'Introduction'
above and 'Definition and pathophysiology' above.)
Aortic dissection is defined as a separation of the layers of the aortic wall due to an intimal tear. Acute aortic dissection comprises the majority of
acute aortic syndromes. Ascending aortic dissections are almost twice as common as descending aortic dissections.
Intimal tear without hematoma is characterized by a stellate or linear intimal tear associated with exposure of the underlying aortic media or
adventitia.
Penetrating aortic ulcer is a region where the aortic intima is denuded with the lesion progressing through a variable amount of the aortic wall.
Most penetrating aortic ulcers are located in the descending thoracic aorta.
Aortic intramural hematoma is defined as a collection of blood confined within the medial layer of the aorta in the absence of a detectable intimal
tear. It can be a precursor to acute aortic dissection and may be associated with penetrating aortic ulcer. Aortic intramural hematoma can also be
due to aortic injury, which may be iatrogenic (eg, intra-aortic balloon pump) or traumatic (eg, auto accident). Aortic intramural hematoma more
commonly involves the descending aorta.
Periaortic hematoma represents a contained aortic rupture.
Acute aortic syndromes are classified according to the location and extent of involvement of the aorta (figure 2). The Stanford system, which is the
more widely used, classifies aortic dissections that involve the ascending aorta as type A, regardless of the site of the primary intimal tear, and all
other dissections as type B. The variants of aortic dissection, intimal tear without hematoma, penetrating aortic ulcer, aortic intramural hematoma, and
periaortic hematoma can be described in a similar manner. (See 'Classification' above.)
Chest pain is the most common presenting symptom of acute aortic syndromes. Anterior chest pain is more typical of ascending (type A) lesions,
while upper or lower back pain is more common with descending (type B) lesions. Other manifestations seen with type A aortic dissections, such as
myocardial infarction, stroke, aortic regurgitation, syncope, and paraplegia, are less common manifestations of the other acute aortic syndromes. (See
'Clinical features' above.)
Since clinical manifestations are nonspecific, the diagnosis of acute aortic syndromes relies on imaging studies to define the aortic abnormality,
classify the location and extent, and identify any anatomic complications. A crucial aspect of early therapy is ensuring a correct diagnosis so that the
appropriate management scheme can be instituted in a timely fashion. Imaging modalities that can be used to make the diagnosis include computed
tomography (CT) or magnetic resonance (MR) angiography of the chest (with or without contrast) and transesophageal echocardiography. Exclusion
of an intimal flap is a prerequisite for the radiologic diagnosis of aortic intramural hematoma. Imaging may also identify a penetrating atherosclerotic
ulcer as the etiology of aortic intramural hematoma. (See 'Diagnosis' above.)
The general principles of medical treatment of acute aortic syndromes are similar and include pain control and anti-impulse therapy to reduce the rate
of progression, which should be initiated for all patients unless hypotension is present but should not interfere with the timely transfer to the operating
room for those with indications for immediate aortic repair. (See 'Management' above.)
Intravenous beta blockers (eg, propranolol, labetolol) are typically used as initial anti-impulse therapy. Intravenous sodium nitroprusside can be
added if the systolic blood pressure remains above 100 mmHg, provided mentation and renal function are intact. Nitroprusside should not be
used without beta blockade since vasodilation induces reflex activation of the sympathetic nervous system, leading to enhanced ventricular
contraction and aortic shear stress. (See 'Acute medical management' above.)
For type A acute aortic syndromes, the definitive treatment is surgical. Surgery may not be feasible in patients of advanced age or other comorbid
conditions, and these patients are managed medically. Compared with patients with classic ascending aortic dissection who are treated
medically, patients with type A aortic intramural hematoma have a better prognosis. For Japanese or Korean patients with type A aortic intramural
hematoma, conservative medical management may be the preferred initial approach. (See 'Ascending aorta (type A)' above and "Management of
acute aortic dissection", section on 'Ascending (type A) aortic dissection'.)
For type B acute aortic syndromes, the treatment is generally medical with surgery reserved for those experiencing complications or refractory or
progressive symptoms. For most patients with complicated type B lesions, we suggest an initial endovascular approach, rather than open
surgery, provided the patients anatomy is suitable for endograft placement (Grade 2C). Perioperative morbidity and mortality is lower for an
endovascular compared with open surgical approach. However, patients with genetically mediated thoracic aortic aneurysm/dissection affecting
the descending thoracic aorta who have complications should be managed using open surgical techniques. (See 'Descending aorta (type B)'
above and "Management of acute aortic dissection", section on 'Descending (type B) aortic dissection'.)
Use of UpToDate is subject to the Subscription and License Agreement.
Topic 8178 Version 11.0
GRAPHICS
Acute aortic syndromes
Class I Classic dissection with separation of intima/media and dual lumens; there is a
flap between true and false aneurysm and clot in false lumen.
Class II Intramural hematoma with separation of intima/media but no intraluminal tear
or flap on imaging.
Class III Limited intimal tear without hematoma and eccentric bulge at tear site (limited
dissection).
Class IV Atherosclerotic ulcer penetrating to adventitia with surrounding hematoma that
is usually subadventitial.
Class V Iatrogenic or traumatic dissection (eg, due to a cardiac catheterization).
Modified from:
1. Lahey Clinic, Burlington, MA.
2. Svensson LG, Lalsib JB, Eisenhauer AC, et al. Intimal tear without hematoma: an important
variant of aortic dissection that can elude current imaging techniques. Circulation 1999;
99:1331.
Graphic 62132 Version 6.0
Aortic dissection complicating penetrating ulcer on CT
An axial CT scan performed five days following identification of a penetrating ulcer with hematoma (arrowhead) now shows an aortic dissection (arrow).
Image B shows an intimal flap (arrows) involving the ascending aorta and hemopericardium (asterisk). Image C shows the intimal flap in the descending
aorta (arrows).
CT: computed tomography.
https://bdbib.javerianacali.edu.co:2118/contents/overview-of-acuteearch_result&search=acute%20aortic%20syndrome&selectedTitle=1~150 Pgina 10 de 21
Pathology aortic intramural hematoma
Autopsy specimen from a patient with an intramural hematoma of the ascending aorta.
Left panel: Transverse section through the aorta shows the surrounding the aortic intima
(*); the intima itself is intact. Right panel: Longitudinal section through the aorta.
From Maraj R, Rekpattanapipat P, Jacobs LE, et al. Am J Cardiol 2000; 86:664, with permission
from Excerpta Medica, Inc.
http://www.elsevier.com/locate/jacc
http://www.sciencedirect.com
Classification of aortic dissection
In the DeBakey classification of aortic dissection:

Type I involves the ascending aorta, arch, and descending thoracic aorta and may
progress to involve the abdominal aorta.
Type II is confined to the ascending aorta.
Type IIIa involves the descending thoracic aorta distal to the left subclavian artery and
proximal to the celiac artery.
Type IIIb dissection involves the thoracic and abdominal aorta distal to the left
subclavian artery.
In the Stanford classification of aortic dissection:
Type A involves the ascending aorta and may progress to involve the arch and
thoracoabdominal aorta.
Type B involves the descending thoracic or thoracoabdominal aorta distal to the left
subclavian artery without involvement of ascending aorta.
Aortic intramural hematoma on TEE and CT
Representative transesophageal echocardiograms (panels A and B) and

computed tomograms (panels C and D) of a section of the descending aorta
in a patient with intramural hemorrhage. Panels A and C reveal a crescentic
thickening of the aortic wall without any evidence of flow communication or
intimal tear (arrows). Panels B and D show complete normalization at follow-
up.
TEE: transesophageal echocardiogram; CT: computed tomography.
With permission from Song, JK, Kang, DH, Lim, TH, et al. Am J Cardiol 1999;
83:937.
http://www.elsevier.com/locate/jacc
http://www.sciencedirect.com
Penetrating atherosclerotic ulcer of the thoracic aorta on CT
An axial CT scan through the descending thoracic aorta shows a penetrating ulcer extending into the wall of the aorta (arrow). Image B is a
magnified view and shows the mouth of the ulcer, which then extends into and expands the wall of the aorta (arrowheads).
Aortic ulcer on CT scan
An axial CT scan through the mid chest shows an aortic ulcer (arrow) with a wide mouth (arrowhead). Bilateral pleural effusions are
present (asterisks). Image B is a magnified view and shows an aortic ulcer (arrow) with a wide mouth (arrowhead).
Pentrating ulcer with hematoma on radiography and CT scan
A frontal chest radiograph (A) shows an enlarged aortic knob (arrow) and a prominent aorto-pulmonary window (arrowhead). A computed
tomography scan (B) through the aortic arch shows a penetrating ulcer with a mural hematoma (arrowhead).
Penetrating ulcer with mural hematoma and aortic rupture
A magnified view of the abdominal aorta (A) shows a wide mouthed penetrating ulcer (asterisk) with a mural hematoma (arrows). Image B shows a large
high density mural hematoma (arrows), high density hematoma in the right psoas muscle (asterisk), and extension of the bleed into the surrounding soft
tissues (arrowheads).
Penetrating ulcer with mural hematoma on CT
An axial CT scan through the arch of the aorta (A) shows a penetrating ulcer (arrowhead).
Image B is a magnified view and shows a penetrating ulcer (arrowhead) and a small mural
hematoma (arrow). Image C is a coronal reconstruction, magnified in D, and shows a focal
penetrating ulcer (arrowhead), with a small mural hematoma (D, arrow).
Differentiation of life-threatening causes of chest pain
Additional
Examination Chest Additional
Diagnosis Historical features Electrocardiogram important
findings radiograph tests
information
Acute Substernal/left-sided chest Nonspecific ST segment Nonspecific Troponin Assume

coronary pressure or tightness is May detect signs of elevations, Q waves, May show evidence and/or CK-MB symptoms of ACS
syndrome common HF new left bundle branch of HF elevations within days or a
Onset is gradual block are evidence of diagnose AMI few weeks of PCI
AMI Single set of or CABG is from
Pain radiating to shoulders
Single ECG is not biomarkers is an occluded artery
or pain with exertion
sensitive for ACS not sufficiently or graft
increases relative risk
Prominent R waves sensitive to
"Atypical" symptoms (eg,
with ST segment rule out AMI
dyspnea, weakness) more
common in older adults, depressions in V 1 and
women, diabetics V 2 strongly suggests
posterior AMI
Older adults can present
with dyspnea, weakness,
syncope, or MS alone
Aortic Sudden onset of sharp, Absent upper Ischemic changes in Wide mediastinum Can mimic many
dissection tearing, or ripping pain extremity or carotid 15 percent or loss of normal diseases
Maximal severity at onset pulse is suggestive Nonspecific ST and T aortic knob contour is depending on
Discrepancy in changes in 30 percent common (up to 76 branch arteries
Most often begins in
systolic BP >20 percent) involved (eg, AMI,
chest, can begin in back
mmHg between right 10 percent have stroke)
Can mimic stroke, ACS,
and left upper normal CXR
mesenteric ischemia, kidney
extremity is
stone
suggestive
Up to 30 percent
with neurologic
findings
Findings vary with
arteries affected
Pulmonary Many possible No finding is Usually abnormal but Great majority are A high-
embolism presentations, including sensitive or specific nonspecific normal sensitivity D-
pleuritic pain and painless Extremity exam Signs of right heart May show dimer is useful
dyspnea generally normal strain suggestive (eg, atelectasis, elevated to rule out PE
Often sudden onset RAD, RBBB, RAE) hemidiaphragm, only when
Lung exam
pleural effusion negative in
Dyspnea often dominant generally
low-risk
feature nonspecific; focal
patients
wheezing may be
present; tachypnea
is common
Tension Often sudden onset Ipsilateral Demonstrates air in

pneumothorax Initial pain often sharp diminished or absent pleural space
and pleuritic breath sounds
Dyspnea often dominant Subcutaneous

feature emphysema is
uncommon
Pericardial Pain from pericarditis is Severe tamponade Decreased voltage and May reveal Ultrasound
tamponade most often sharp anterior creates obstructive electrical alternans can enlarged heart reveals
chest pain made worse by shock and causes appear with significant pericardial
inspiration or lying supine jugular venous effusions effusion with
and relieved by sitting distension, pulsus Diffuse PR segment tamponade
forward paradoxus depressions and/or ST
Dyspnea is common Pericardial effusion segment elevations can
can cause friction appear with acute
rub pericarditis
Mediastinitis Forceful vomiting often Ill-appearing; Large majority

(esophageal precedes esophageal shock; fever have some
rupture) rupture May hear abnormality:
Recent upper endoscopy (Hamman's) crunch pneumomediastinum,
pleural effusion,
or instrumentation increases over mediastinum pneumothorax

risk of perforation
Odontogenic infection is
possible cause
Coexistent respiratory and
gastrointestinal complaints
may occur
MS: altered mental status; ACS: acute coronary syndrome; AMI: acute myocardial infarction; BP: blood pressure; CABG: coronary artery bypass graft; CK-MB:
creatine kinase-MB; CXR: chest radiograph; ECG: electrocardiogram; HF: heart failure; PCI: percutaneous coronary intervention; PE: pulmonary embolism; RAD: right
axis deviation; RAE: right atrial enlargement; RBBB: right bundle branch block.

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Overview of acute aortic syndromes - UpToDate 17/07/17 9:11 p.m.

Official reprint from UpToDate

Authors: Warren J Manning, MD, James H Black, III, MD

DEFINITION AND PATHOPHYSIOLOGY

SUMMARY AND RECOMMENDATIONS

Periaortic hematoma represents a contained aortic rupture.

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 8178 Version 11.0

Acute aortic syndromes

Graphic 62132 Version 6.0

Aortic dissection complicating penetrating ulcer on CT

CT: computed tomography.

Graphic 101396 Version 1.0

Pathology aortic intramural hematoma

Classification of aortic dissection

In the DeBakey classification of aortic dissection:

Graphic 100115 Version 4.0

Aortic intramural hematoma on TEE and CT

Representative transesophageal echocardiograms (panels A and B) and

TEE: transesophageal echocardiogram; CT: computed tomography.

Penetrating atherosclerotic ulcer of the thoracic aorta on CT

CT: computed tomography.

Graphic 101394 Version 1.0

Aortic ulcer on CT scan

CT: computed tomography.

Graphic 101580 Version 2.0

Pentrating ulcer with hematoma on radiography and CT scan

CT: computed tomography.

Graphic 101578 Version 3.0

Penetrating ulcer with mural hematoma and aortic rupture

Graphic 101397 Version 1.0

Penetrating ulcer with mural hematoma on CT

CT: computed tomography.

Graphic 101395 Version 1.0

Differentiation of life-threatening causes of chest pain

Acute Substernal/left-sided chest Nonspecific ST segment Nonspecific Troponin Assume

Tension Often sudden onset Ipsilateral Demonstrates air in

Dyspnea often dominant Subcutaneous

Mediastinitis Forceful vomiting often Ill-appearing; Large majority

or instrumentation increases over mediastinum pneumothorax

Graphic 54629 Version 3.0

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