RECAPEM

Acute aortic syndromes

July 29, 2020, by Shahriar Lahouti

CONTENTS:

Preface

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Acute aortic syndromes include a wide range of life-threatening aortic conditions with high probability of misdiagnosis1 ,which requires immediate diagnosis and management. It encompasses aortic dissection (AD), intramural haematoma (IMH), penetrating atherosclerotic ulcer (PAU) and traumatic aortic injury (TAI),aortic rupture, and ruptured aortic aneurysm.2

AAA has its unique pathophysiology, presentation and management as such is not included in this post (More to come on this).

Anatomy

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The gross anatomy of the aorta is divided into the following segments2: (1) aortic root; (2) sinotubular junction; (3) ascending aorta; (4) aortic arch; (5) isthmus and descending (thoracic) aorta; and (6) abdominal aorta.

  1. The aortic root (Light blue bellow picture) is intrapericardial and consists of three rounded dilations (sinuses) at the aortic valve leaflet level that allows the aortic valve leaflets to open appropriately3. Normally, the left coronary ostium arises from the superior left coronary sinus, and the right coronary ostium arises from the superior right coronary Sinus. Aortic root can be involved in a variety of pathologic conditions. In aortic dissection with root involvement, following consequences are possible:
    1. Disruption of aorta and rupture into pericardial sac resulting in hemopericardium.
    2. Dynamic obstruction of coronary ostium, most commonly on the right side, resulting in ACS.
    3. Dilation of the root leads to reduced suspension of the leaflets resulting in acute aortic valve insufficiency.

Photo from, Hutchison, Stuart J. Aortic diseases: clinical diagnostic imaging atlas. Clinical diagnostic imaging atlas, Philadelphia, Saunders, Elsevier, 2009

2. The ascending aorta is the segment of the aorta from the sinotubular junction to the first great arch vessel. This segment is also intrapericardial and frequently involved with the same pathologic processes as the aortic root.

3. Aortic arch is the transverse portion of the aorta from the first arch vessel to the left subclavian artery Ostium and is mostly extrapericardial.

4. Isthmus: a short portion of the aorta after the left subclavian artery to the present or former ductus arteriosus.

5. Descending aorta: the vertically oriented portion of the aorta continuing from the isthmus to the level of the diaphragm. Branch vessels include intercostal, spinal, and bronchial arteries. Rupture of the descending aorta is either into the mediastinum or into the large left pleural cavity, which is catastrophic

6. Abdominal aorta: is the infradiaphragmatic segment down to the aortic bifurcation. Branch vessels include:

  • Inferior phrenic arteries
  • Celiac artery branches (hepatic artery, gastroepiploic artery, and splenic artery)
  • Renal arteries
  • Superior mesenteric artery
  • Inferior mesenteric artery
  • Lumbar and spinal arteries
  • iliac arteries (internal iliac artery: anterior division [obturator artery, inferior gluteal artery, internal pudendal artery, and visceral branches] and posterior division [superior gluteal artery, iliolumbar artery, and lateral sacral arteries]; and external iliac artery).

The predominant disease processes involving the abdominal aorta include: atherosclerosis and aneurysms.

Normal diameter of different segments of aorta is shown below: 4

The basic components of the aorta are the intima, media, and adventitia.5 Each contributes to specific properties of aorta as the major conduit in the body, and their functional alteration during pathologic processes result in certain pathophysiological features shown in following table.3

Pearl: Calcification of atherosclerotic plaque, a subtype of atheroma complication, increases with each decade of advancing age, until it is present in the vast majority of elderly in their 80s. There’s a twofold increase in cardiovascular death if atherosclerotic calcification of the aorta is present before 65 years old. In individuals younger than 70 years old, risk of cardiovascular events e.g. CAD, Stroke; approximates the plaque burden of aorta { > 4mm plaque are 90% sensitive for significant CAD).3

On imaging, calcified aortic intimal atheroma is a marker of intimal location radiographically, and can helpto distinguish certain disease states (below, diagnostic findings in imaging).

Pathophysiology and Definitions

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Acute aortic syndromes, defined as life threatening conditions with similar clinical features involving the aorta. It encompasses aortic dissection, intramural hematoma (IMH), ruptured aneurysm, penetrating atherosclerotic ulcer (PAU).6

  1. Aortic dissection: It could be spontaneous or iatrogenic / traumatic. In spontaneous form, intramural bleeding causes disruption of the medial layer which results in formation of a false lumen (FL) partitioned from true lumen(TL) by an intimal flap. In most cases the inciting event is intimal tear or an ulcer, but sometimes the rupture of vasa vasorum causes a bleed within the media. The dissection can propagate proximally or distally from intimal tear to involve the aortic root (aortic valve, coronary arteries), side branches of aortic arch and descending aorta.7

  1. Aortic intramural hematoma (IMH): defined as hematoma within the medial layer of the aorta, in the absence of detectable intimal tears. Recent studies show that ‘microscopic’ tears in the intima is the possible mechanism of bleeding into the media layer of the aorta. Therefore, there’s no imaging evidence of intimal flap or false lumen within the aorta. Presence of blood within the media layer, provokes an inflammatory response. This weakens the components of the aortic wall, and consequently it may lead to aortic rupture.

  1. Penetrating aortic ulcer(PAU): refers to the region of the aorta where the aortic intima is denuded with the lesion progressing through a variable depth of the aortic wall, over which there may or may not be overlying thrombus. Penetrating aortic ulcers are typically associated with atherosclerotic changes of the adjacent aortic wall. It may be associated with thrombus formation within the media (IMH), or may progress through the adventitia to form pseudoaneurysm, and finally perforation or aortic dissection may happen.

  1. Periaortic hematoma: represents a ‘contained aortic rupture’ due to slow oozing from the damaged aorta at or near the site of aortic injury.

Relationship among the entities grouped under the acute aortic syndrome is shown below:

Anatomic classification

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Acute aortic syndromes are classified based on their location and extent of involvement. There are two different anatomic classification systems:

  1. DeBakey system: is based upon the site of the origin of the tear, whereas 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 proximal to the left subclavian artery
  2. 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

Other classifications

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Aortic dissection can also be classified according to the disease phase (acute, subacute and chronic phases), to the status of blood flow in the FL (communicating and non-communicating types), or to the presence of associated complications (complicated vs. uncomplicated)

By convention, acute disease is distinguished from chronic disease at an arbitrary time point of two weeks from initial clinical presentation. A new classification system by the International Registry of Acute Aortic Dissection (IRAD) takes into account that the morbidity and mortality

associated with acute dissection are highest in the first 2 weeks, especially the first 24 to 48 hours. The IRAD classification includes hyperacute (<24 hours), acute (2 to 7 days), subacute (8 to 30 days), and chronic (>30 days).8

Complete ‘FL’ thrombosis (absence of flow and presence of thrombus within the FL) is the key to long-term clinical success and long-term survival.9

The mortality of acute aortic syndromes is a consequence of its complications. Aortic dissection as the prototype of this syndromes can give rise to a variety of organ dysfunction either by rupture or via malperfusion. The latter may be dynamic, static or mixed.

  • Dynamic malperfusion is the most common and results from the overpressurized false lumen pushing the septum toward the true lumen, leading to collapse of the true lumen and obstruction of branch vessels.
  • Static malperfusion results from stenosis or occlusion of a branch artery caused by the dissection flap, hematoma, embolism, or thrombosis.

  • Pearl:
    • Presence of blood within the aortic wall layer can cause localized inflammation. This inflammatory response not only weakens the aortic wall which leads to rupture, pseudoaneurysm, fistula formation with adjacent structures; but also may provoke inflammatory reaction within adjacent anatomic structures such as in pleura (causing pleural effusion), pericardium (causing pericarditis).

  • IMH: Can complicate into:
    • Aortic dissection: about 8% to 16% evolves into aortic dissection.
    • Rupture: risk of rupture is more than aortic dissection as the outer adventitia is thinner.
    • Periaortic hematoma: more common in IMH relative to aortic dissection.

  • PAU: Can complicate into:
    • IMH
    • Rupture (Rare)
    • Aortic dissection

Epidemiology and Risk Factors

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The overall incidence of acute aortic syndromes ranges from two to four cases per 100,000 individuals, with most cases being ‘acute aortic dissection’. Aortic dissection is the most common form of aortic catastrophe and twice that of abdominal aortic aneurysm rupture.

Aortic intramural hematoma accounts for 5 to 20 percent of patients with symptoms consistent with acute aortic syndrome, while penetrating aortic ulcers account for 2 to 7 percent of acute aortic syndromes.10

Aortic dissection has a bimodal age distribution. The first peak involves younger patients with specific predisposing conditions such as connective tissue disorders or crack cocaine use. The second peak occurs in those aged > 50 years with chronic hypertension and/or ischemic heart disease.

Risk factors associated with aortic dissection include:

  1. Hypertension: most important risk factor
  2. Atherosclerosis
  3. Gender: more common in men than women
  4. Known aneurysm
  5. Congenital diseases: Bicuspid aortic valve, coarctation of aorta, tetralogy of fallot.
  6. Connective tissue disorder, e.g. Marfan syndrome.
  7. Substance abuse e.g. cocaine, methamphetamine.
  8. Inflammation/infectious diseases: Giant cell arteritis, Takayasu arteritis, Behçetdisease, Syphilis.
  9. Pregnancy: Possibly attributed to hemodynamic and hormonal milieu changes during pregnancy
  10. Trauma, blunt or iatrogenic e.g. cardiac, or aortic surgery

AD more frequently occurs between 6 a.m. and 12 p.m., peaking at 9 a.m., and during the winter months, with a peak in January

Clinical Presentation

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The clinical presentation of acute aortic syndromes depends upon the extent of dissection and the affected cardiovascular structures

  • Pain
    • Location: Chest/back/abdomen. In the presence of abdominal pain, have a high index of suspicion for mesenteric vascular compromise.
    • Onset: abrupt onset, with maximal intensity at its inception
    • Severity: It’s severe (in 90% of patients)
    • Other features:
      • May be accompanied by a ‘sense of doom
      • Quality of pain is often described as sharp, severe, or stabbing and adjectives such as tearing or ripping are less commonly used.
      • Pain is migratory (17% of patients) and tends to follow the pathway of dissection through the aorta.
    • Pitfalls:
      • Pain may lessen or resolve which makes diagnosis even more challenging.
      • In some patients, the symptoms related to complication dominate and pain is not mentioned or is downplayed.
      • The description of pain is not universal, because patients may also present with a more gradual onset of mild pain that is similar in description to musculoskeletal conditions of the thorax, back, or groin.
      • Painless AD more likely to present with neurological symptoms.11
  • Syncope: 5 to 10% of patients with aortic dissection present with syncope. It’s more common in type A rather than type B aortic dissection. Syncope happens either due to development of cardiac tamponade or involvement of the brachiocephalic vessels, and carries an increased mortality rate.12 13
  • Focal neurologic deficit
    • Acute paraplegia
    • Ischemic stroke and altered consciousness (6%)13
    • Horner syndrome
    • Hoarseness
  • Cardiac arrest and sudden death

Physical findings

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Physical findings are highly variable and range from virtually unremarkable to full cardiac arrest secondary to tamponade or rupture. The findings may signify complications related to dissection. The presence of these findings must raise clinical suspicion for aortic dissection, but their absence

does not exclude dissection and should not deter pursuit of the diagnosis when suspected.

  • Hypotension:14 Presence of hypotension in type B signifies rupture; while hypotension especially in type A aortic dissection should prompt you to consider the following:
    • Acute aortic valve insufficiency (<10%)13
    • Cardiac tamponade: most common cause of death. More common in women.15
    • Hemothorax: can happen on both sides, though more commonly it occurs on the left side.
    • Hemoperitoneum
    • Acute Coronary syndrome(1-2%): more commonly involves RCA, though left sided STEMI is not uncommon. Virtually any patient with STEMI, is not safe from ‘AD’-induced myocardial infarction. Aortic dissection may not be suspected as a cause of coronary ischemia, and misdiagnosis may lead to inappropriate therapy and delays in treatment.
    • Pseudo-hypotension: the dissection flap has cut off the limb perfusion.
      • Troubleshooting: switch the BP cuff to the other side.

  • Hypertension (70%): more common in patients with descending ‘AD’. The underlying pathophysiology could be attributed to either hyperadrenergic response to pain, or renal arterial occlusion, renal ischemia.14
  • Pulse deficit: a pulse deficit is reported in 31% of type A dissections and 19% of type B dissections.
  • Aortic regurgitation (41%-76%): Is a key diagnostic feature of type A dissection.
  • Neurologic findings related to ischemic stroke (6%), TIA, spinal cord ischemia, ischemic neuropathy, and hypoxic encephalopathy, seizure. Coma and cerebral malperfusion are associated with poor outcomes.

Differential diagnosis of acute aortic dissection

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  • Clinical DDx:
    • ACS
    • Pulmonary embolism
    • Pneumothorax
    • Aortic regurgitation without dissection
    • Esophageal rupture
    • Tamponade
    • Pericarditis
    • Peripheral arterial disease
  • Imaging DDx:16
    • Artifacts
      • Aortic pulsation ‘motion artefact’ (typically left anterior and right posterior aspects of ascending aorta)
      • Contrast streaks on CECT
      • Reverberation artifacts in ascending aorta on TEE
    • Adjacent atelectasis
    • Pericardial recess
    • Innominate vein
    • Remnant of a nonpatent PDA
    • IMH
    • Periaortic fat and hemiazygos sheath may mimic IMH
    • Mural thrombus within aneurysm
    • PAU
    • Prior surgery of aorta
    • Atheromatous plaque
    • Aortitis

Lab evaluation

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In patients admitted to the hospital with chest pain and suspicion of AD, the following laboratory tests, are required for differential diagnosis or detection of complications:

  • RBC count: to detect blood loss, anemia.
  • Troponin: almost 18% of patients with ‘AD’ have elevated troponin. Chest pain with an elevated troponin does not rule out ‘AD’.
  • Renal function test: to detect signs of renal failure (existing or developing).
  • Liver function test: to scan for signs of liver ischemia, liver disease.
  • Serum lactate: in contrast to traditional belief holding that elevated serum lactate is a marker of organ hypoperfusion (anaerobic metabolism); several studies (in patients with septic shock) show that this is not true.17, 18
    • Elevated serum lactate represents endogenous catecholamine release, stimulating beta-2 receptors. This stimulation upregulates glycolysis, generating more pyruvate than can be used by mitochondria by TCA cycle. Excess pyruvate is converted into lactate.
  • Tox screen in young patients without apparent clinical risk factor for stimulant drugs abuse. The results of toxicology screening may alter the pharmacological agents chosen for acute medical management.
  • D-dimer:
    • Within the context of acute aortic syndromes, a positive D-dimer possibly signifies activation of extrinsic coagulation cascade within the aortic media.
    • Disadvantages of D-dimer as a diagnostic tool:
      • Very low specificity: For D-dimer <500 ng/mL, the pooled estimate of the sensitivity 97%, specificity 56%, and negative predictive value 96% was reported. A positive D-dimer can be seen in a variety of conditions.19
      • Lack of standardized testing protocols.
      • Variability of levels from the time since onset of the symptoms.
    • In a recent prospective multicenter study that included 1850 patients, 8 patients (0.4%) with acute aortic syndrome had a negative D-dimer.20
    • its usage may be limited to patients at low risk for having aortic dissection but in whom ‘AD’ remains a clinical diagnostic uncertainty.21
    • ACEP Clinical Guidelines have issued a Level C recommendation cautioning physicians not to rely on the D-dimer assay alone to exclude a diagnosis of acute AD.22
  • Type and screen with crossmatch: Essential for operative management and should be collected in the ED.

ECG

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Presence of ECG findings consistent with acute myocardial infarction, do not rule out acute aortic dissection, as ‘AD’ can cause myocardial ischemia/infarction.

‘AD’ is notorious to cause right sided STEMI/ischemia; However it’s not true in the sense that left sided events can happen.23 Virtually no one with STEMI, is safe from AD-induced STEMI.

Other findings such as evidence of left heart strain is seen in patients with uncontrolled HTN.24

Imaging modalities and diagnostic performances

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The diagnosis of acute aortic syndromes may be suspected clinically, based on high risk clinical features (discussed below), but confirmation of the diagnosis, and determining the type of acute aortic syndromes, as well as the the location and extent of the pathology and finally delineating any anatomic complications require cardiovascular imaging. Multiple imaging modalities are available, however each has its advantages and disadvantages.

  • CT angiography of the aorta is the diagnostic imaging modality of choice in hemodynamically stable patients.

  • Advantages include: availability, accuracy (roughly 100% sensitive, and specific) , ability to depict rupture, and ability to identify differential diagnostic concerns e.g. PAU, IMH, PE.
  • Disadvantages include: inability to identify cardiac complications of AAS, e.g. AR, and impracticable to perform in patients impending to crash.

  • TTE: applicable in unstable patients and can identify AR, hemorrhagic pericardial effusion and tamponade, as well as regional wall motion abnormalities. However a negative TTE cannot rule out aortic dissection due to its insensitivity.
    • ACEP Clinical Guidelines recommend not relying on an abnormal bedside TTE for the definitive diagnosis of thoracic AD (ACEP Clinical Guidelines, Level B). However, the guidelines do provide a consensus recommendation that if an AD is identified on limited bedside ultrasound, then surgical consultation and/or transfer to a higher level of care capable of definitively managing AD should occur (ACEP Clinical Guidelines, Level C).

  • TEE: despite having reasonable sensitivity (86% -100%) and specificity (90%-100%), it requires specialized equipment, experienced clinician and sedation.

  • MRA: Highly sensitive and specific, however it can cause a delay in diagnosis due to its limited availability as well as longer image acquisition time.

Diagnostic findings on imaging:

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Diagnosis of acute aortic syndrome requires cardiovascular imaging, therefore it is important to recognize the imaging signs of acute aortic syndromes and be capable of distinguishing imaging findings from artifacts.

Imaging considerations on artifacts:3

  • The aortic root and ascending aorta move about 1.5 cm per cardiac cycle, conferring to motion artifact to nongated imaging with low temporal resolution. High-resolution imaging of the ascending aorta requires either high temporal resolution (e.g. multidetector computed tomography [MDCT]) or electrocardiography (ECG) gating.
  • High-attenuation streak artifacts from concentrated contrast dye in the adjacent SVC, brachiocephalic veins are common and clinically important problems because these streak artifacts can contaminate the depiction of the ascending aorta, and arch respectively. Pacemaker leads in the SVC, and brachiocephalic vein may also project artifacts across the ascending aorta, and arch correspondingly.
  • Descending and abdominal aorta are less subject to motion artifacts

Diagnostic findings for acute aortic dissection:25

The diagnosis of AD is based on the presence of an intimal flap separating a false lumen (FL) from a true lumen (TL) , and imaging signs of associated findings or complications such as:

  • Thrombus in FL
  • Aortic regurgitation (on echo)
  • Pericardial effusion
  • Branched vessel involvement
  • Aortic enlargement

Pearl: It is important to identify and differentiate ‘TL’ from ‘FL’, since in a situation where intervention is warranted, placing the stent within the ‘FL’ is devastating!

‘TL’ is the one, which is smaller’ , has ‘outer wall calcification’ , and gives rise to the origin of celiac trunk, superior mesenteric artery and right renal artery.

FL has the following radiographic features:

  • ‘FL’ is larger (due to higher systolic pressure within the FL).
  • Has no outer wall calcification.
  • On NECT: FL appears darker due to more slower blood flow.
  • On CECT: often appear as a lower density due to delayed enhancement i.e. opacification.
  • May contain thrombus (more common in chronic AD). Thrombus appears as a low density on NECT.
  • Beak sign: Wedges around the ‘TL’.
  • Cobwebs: Collagenous media remnants.
  • Circular configuration (due to persistent systolic pressure).
  • Forms outer curve of the aortic arch.
  • Origin of the left renal artery is usually from the ‘FL’.
  • Surround ‘TL’ in type A aortic dissection.
  • On color doppler it shows flow in acute AD, while in chronic AD may lack flow due to the formation of thrombus.
  • ‘FL’ is at risk of rupture due to reduced elastic recoil and dilation.

Echocardiographic findings in acute AD:16

  1. Recognizing direct evidence of AD:

  • The diagnostic hallmark of AD is a mobile dissection flap that separates the true and false lumens. Important features of the dissection flap include:
    • Oscillation or motion that is independent of the aorta itself.
    • Visualization in more than one view.
    • Clear distinction of the flap from reverberations from other structures, such as a calcified aortic wall, catheter in the right ventricular outflow tract, pacemaker wire, or pericardial fluid in the transverse oblique sinus.
  • Other main direct evidence of AD include,e.g. identifying ‘TL’ vs. ‘FL’(below table).

B. Identifying indirect evidence of ‘AD’ (complications of AD):

  • Dilatation of the aorta.
  • Compression of the left atrium.
  • AR
  • Pericardial and/or pleural effusion.
  • Involvement of the coronary arteries.

The following table summarizes main diagnostic finding on echo in ‘AD’

Pearls:

  • Use the high right/left parasternal long axis views to achieve a better window of the ascending aorta.
  • Substernal view gives valuable information regarding involvement of aortic arch and branched vessels.
  • A short-axis view of the descending aorta can be imaged posteriorly to the left atrium in the parasternal long-axis view.
  • The use of M-mode echo may improve diagnostic accuracy by demonstrating a lack of relation between movement of the intimal flap and the aortic wall.
  • Scanning the neck vessels (carotid artery) can be informative especially in those with neurological findings.
  • Remember that the hallmark of ‘AD’ is detection of undulating linear echoes of an intimal flap.
  • Artifacts mimicking intimal flaps are common in ascending aorta and are a potential diagnostic challenge. There are two types of artifacts:

  • Side lobe artifact: A curvilinear echodensity along a sector arc which is Not Undulating. It is caused by calcification of aortic root, aortic valve, and sinotubular junction.
  • Reverberation artifact: It’s the duplication of a linear echo signal along the pathway of ultrasound beam. It may originate from the left atrial wall, Rt pulmonary artery.
  • Linear artifacts are more common when aortic root diameter is > left atrium.
  • These Artifacts c/b easily recognized by using M-mode to assess their movement and color flow doppler to assess their flow characteristics on either sides of the linear echodensity.
    • M-mode proves that the artifact has the same motion as its originating structure.
    • Color flow doppler proves presence of homogenous color flow on both sides of the curvilinear echodensity without communicating jets.

Parasternal long axis: Enlarged aortic root, intimal flap © British Society of Echocardiography.2019

Type B dissection diagnosed by colour Doppler TEE showing a turbulent flow through a secondary tear from the true lumen to false lumen © British Society of Echocardiography.2019

Direct signs of aortic dissection, e.g. intimal flap are not always appreciated. Watch for indirect signs of aortic dissection such as dilated aortic root and aortic regurgitation, as are present in this clip. Courtesy to THE POCUS ATLAS

Quien, MM, Saric, M. Ultrasound imaging artifacts.Echocardiography. 2018.26

Diagnostic findings for IMH:27

The diagnosis of IMH is based on:

  • Focal crescentic thickening of the aortic wall of ≧5 mm in aortic wall with a smooth inner surface.
  • Displaced intimal calcification inwardly.
  • Absence of flap, intimal Tear, or flow within the hematoma.
  • NCECT: a hyperattenuating rim or crescent along the curvature of an aortic wall.
  • CECT: non-enhancing low attenuation rim.

Echocardiographic signs for diagnosis of IMH:16

  • Areas of echolucency within the aortic wall and no intimal flap or flow in the aortic wall28
  • Focal thickening of the aortic wall:
    • Normal aortic wall thickness is < 3mm. Wall thickness must be > 5-7mm to be diagnostic for IMH.
    • Presence of mixed echogenicity within the aortic wall (predominantly echodense with scattered internal echo lucencies).
  • Absence of intimal flap, and false lumen.
  • Absence of detectable internal flow: employment of color doppler flow is important to differentiate IMH from AD, as the TL of AD will demonstrate systolic flow, and variable flow patterns m/b present in the ‘FL’, which tends to expand in size during diastole.
  • The luminal surface in IMH tends to be smooth and continuous.

Diagnostic findings on imaging for PAU:16

  • Extensive atherosclerosis with severe intimal calcifications and atherosclerotic plaques.
  • Focally displaced and separated intimal calcifications.
  • Crater and/or contrast extravasation.
  • Focal IMH, with longitudinal spread limited by media fibrosis.
  • Possibly enhancing an aortic wall.

Objectives

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  • Identify critically ill patients.
  • Employ simultaneous diagnostic and resuscitative measures.
  • Identify and distinguish acute aortic syndromes from other potential life threatening diseases.
  • Recognize and differentiate type A from type B in AAS.
  • Identify presence of end-organ malperfusion.

Diagnostic approach

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AAS encompases potentially life threatening conditions which can happen in patients without apparent risk factors and can present with a wide variety of clinical pictures from virtually unremarkable to cardiac arrest. The large differential diagnosis for the complaint of chest pain plus the many end-organ ischemic manifestations associated with aortic dissections make the diagnosis challenging.

It is frequently mistaken for other etiologies that cause chest pain; most commonly ACS. The incidence of misdiagnosis has been reported of up to 40% especially when the ascending aorta is involved.29 30

Such errors in diagnosis, not only delay timely treatment of aortic catastrophe, but also can lead to using inappropriate treatments (e.g. antithrombotic agents) which increase the risk of bleeding and other serious complications in such patients.

Factors associated with delay in diagnosis have been reported as female gender, transfer from another hospital, fever, and normal BP.31

It is significantly important to rapidly identify situations where emergent cardiac surgery is warranted:

  1. Identifying type A (which calls for emergent surgical procedures), vs. type B (which often can be managed medically in hemodynamically stable patients).
  2. Recognition of end-organ complication, upon which cardiac surgery is required, regardless of the anatomic type of aortic dissection.

Proposed diagnostic approach: 2 32

  • Step 1: Identify patients at risk for acute AD
  • Collect information by taking medical history, exam, ECG.
    • Consider Acute AD in all patients presenting with:
      • Chest/back/abdominal pain
      • Syncope
      • Symptoms consistent with perfusion deficit i.e. CNS, mesenteric, myocardial, limb ischemia.

  • Step 2: Bedside risk assessment (pretest risk): The Aortic Dissection Detection Risk Score (ADD-RS) is based on the presence of one or more of the following high-risk features:

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.33

  • Step 3: Risk-based diagnostic evaluation
  • Employ the ADD-RS score to direct your diagnostic evaluation, management accordingly (see following algorithm).

Diagnostic Pathway for Acute Aortic Dissection

The Aortic Dissection Detection Risk Score Plus D-dimer (ADD-RS Plus D-dimer)study:34

  • Used a combination of the ADD-RS and D-dimer as a diagnostic tool for acute aortic syndromes.
  • 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% 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.
  • However additional validation in a broader patient population is required before routine use of this combination as a diagnostic tool.
  • See more on D-dimer for aortic dissection: the evidence (First10EM blog)

Treatment

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General Principles of treatment are:

  • Treatment strategy for acute ‘AD’ and ‘IMH’ depends on the type, location, presence of complication (end-organ ischemia), and progression or rupture.
  • Make sure the patient is NPO.
  • Place two large bore IVs.
  • Monitor HR, and BP continuously, preferentially using an arterial line to adequately titrate antihypertensive medications (put your arterial line on the side with stronger pulse).
  • Provide analgesia to control the pain.
  • Control HR and BP: Keep HR < 60 bpm and SBP between 100-120 mmHg.
  • Place foley catheter for monitoring urine output and renal perfusion.
  • Surgical consultation (cardiothoracic, vascular surgery) as soon as diagnosis is strongly suspected or confirmed (regardless of location).
  • Stanford Type A aortic dissection: is a cardiac surgical emergency.
  • Stanford Type B aortic dissection: can be managed medically in the ICU. Urgent aortic stent-grafting or surgery is warranted in the presence of following conditions:
    • Evidence of end-organ malperfusion
    • Rupture or impending to rupture, e.g. periaortic hematoma
    • Hemorrhagic pleural effusion
    • Refractory hypertension
    • Refractory pain
    • Aneurysmal dilation (>55 mm)
    • Rapid increase in diameter
    • Recurrent symptoms
  • If appropriate surgical services are not available, initiate emergent transfer to the nearest available cardiovascular center (the most expeditious means is encouraged i.e. air).
  • If sudden cardiac arrest occurs, perform POCUS to evaluate for likely etiologies such as tamponade, hemothorax. Despite that pericardiocentesis is technically difficult in tamponade due to aortic dissection (as often blood clots), draining even a small amount of fluid (e.g. even 4cc!) may potentially be associated with ROSC.

  • IMH: The mortality rate is similar in patients with IMH compared to patients with aortic dissection. Therefore, they should be treated in a fashion similar to an individual with a true AD at the level of the hematoma, that is to say:
    • Stanford Type A IMH: is a cardiac surgical emergency.
    • Stanford Type B IMH: can be managed medically in the ICU. Surgical or endovascular treatment is considered in the presence of the following situations:
      • Hemodynamic instability
      • Persistence of chest pain despite medical management
      • Signs of aortic rupture e.g. periaortic hematoma, enlarging pleural effusion
      • Presence of a large ulcer-like projection (Depth > 10 mm}
      • Maximal aortic diameter > 55 mm
      • Rapid aortic diameter growth during in-hospital stay

Pain control:

Pain induces sympathetic system response, resulting to hyperadrenergic state, which could potentiate progression of AAS. Adequate analgesia is of paramount importance.

Preferred choice: Fentanyl

Pain refractory to optimal medical management has been associated with worse outcomes in patients with aortic dissection. In patients with recurrent pain despite optimal medication, request for radiographic studies, as it may be due to progression of the disease (rupture,effusions,etc.).

Anti-impulse therapy

The aortic root and ascending aorta move about 1.5 cm per cardiac cycle. Anti-impulse therapy aims to reduce the velocity of left ventricular contraction, thereby decreasing pulse pressure-related shear stress (Δp/Δt) and minimizing lesion progression. Tree goals are deserved:

  1. ↓HR
  2. ↓Intopry
  3. ↓Afterload

This is usually accomplished first’ by administering intravenous selective beta blockers.

  • Beta blockade: Initial treatment consists of IV beta blocker to reduce HR < 60 bpm. Beta blocker use has been associated with improved survival in the International Registry of Acute Aortic Dissection database.
    • Caution: If there is evidence of acute aortic insufficiency, significant caution must be used when initiating beta blockers, because this intervention may blunt the patient’s compensatory tachycardia, leading to cardiovascular collapse.32
    • Esmolol: 250 to 500 mcg/kg loading dose over one minute, then infuse at 25 to 50 mcg/kg/minute; maximum of 300 mcg/kg/minute. Notice that prior to each upward dose titration, a re-bolus should be given.
      • Advantages include: Short half-life, ability to titrate to the effect perfectly, controls both cardiac HR, and inotropy, clearance is not dependent on renal or hepatic function.
      • Disadvantages: Nausea, flushing, bronchospasm,bradycardia,first-degree heart block,infusion site pain; and half-life prolongation in the setting of anemia.
    • Labetalol: 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).
      • Disadvantage: It’s predominantly a negative inotropy, but not a great chronotropic agent, and despite its alpha blocking properties, it’s not a great afterload reducer either. It’s not a perfectly titratable agent.
      • Advantages: it’s a combined alpha and beta-blockade that may enable management with a single agent.

  • Antihypertensive medications (add-on to beta blockade): If after beta blockade the SBP remains elevated, adding an antihypertensive (to ↓afterload) medication is warranted, preferential medications are listed below in sequence as:
    • Clevidipine IV initial dose 1-2 mg/h IV infusion, titrate up by doubling the dose at 90-s intervals initially; once approaching target blood pressure, increase by less than double dose and lengthen dose interval to 5-10 min, to a max of 32 mg/h.
      • Advantages: Perfectly titratable to the effect, short time to onset of action, its a pure afterload reducer without any effects on heart rate and inotropy (the same as for nicardipine), and clearance is not dependent on renal or hepatic function.
      • Disadvantages: lipid contains potential allergens (eg, soy, egg), atrial fibrillation, nausea.
    • Nicardipine IV 5 mg/h; may titrate up by 2.5 mg/h every 5-15 min to a max of 15 mg/h.
    • Sodium nitroprusside IV 0.25 to 0.5 mcg/kg per minute to a maximum of 10 mcg/kg per minute for a maximum duration of 10 minutes.
      • Disadvantages: a tiny dose adjustment leads to massive BP change, making titration very difficult, definitely needs an arterial line for BP monitoring, has deleterious effects on cerebral perfusion pressure, cyanide and thiocyanate toxicity, nausea, vomiting, muscle spasm, flushing, and sweating.
    • Nitroglycerin: IV infusion at 5 to 200 mcg/minute.
      • Advantages: m/b useful in patients with acute pulmonary edema, coronary ischemia, available in most centers.
      • Disadvantages:tachycardia (reflex sympathetic activation), headache, vomiting, flushing, methemoglobinemia, tolerance with prolonged use.

  • Caution: avoid other direct vasodilators like hydralazine as they increase aortic wall shear stress and provide less accurate and reversible control of the BP.

Intubation:

Consider the same way as you intubate the patients with high ICP/high BP

  • If you choose to intubate the patient (e.g. when deciding to transfer the patient to another facility, in the presence of any deterioration in mental status), follow the hemodynamically safe intubation, that is bringing HR and BP down to the safe range with aforementioned medications, and only then proceeding to intubation, perfectly using video-guided approach.
  • For more comprehensive lecture on this, see: Neurocritical Care Intubation (EMCrit RACC)

Cocaine intoxication

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  • Cocaine toxicity results from central monoamine reuptake inhibition, and its sodium channel blockade properties. Decreasing central-mediated sympathetic tone is achieved by administration of benzodiazepines. Non-selective beta blockers are generally avoided in such patients as it ‘may’ lead to unopposed alpha stimulation and worsening the situation. However for patients with acute ’AD’, antihypertensive medications are usually started before the Tox screen results become available and as such, many patients do receive beta blockers. In an IRAD review of cocaine-related dissection, there were No differences in the type of treatment received comparing cocaine and non-cocaine users, including beta blocker therapy.35 However, when more than one antihypertensive agent was used, it was not stated which medication was used first.
  • Management:
    • BZD: diazepam (5 mg IV) or lorazepam (1 mg IV); may repeat q 5 minutes until sedated
    • Selective beta blockers such as esmolol or mixed agents like labetalol may be reasonable for treating patients with acute aortic syndrome when needed. When additional antihypertensive medication is needed, nitroglycerin or calcium channel blockers can be considered.

Prognosis of AAS

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  • Mortality is estimated to increase by 1% to 2% per hour following the onset of symptoms, calling for a timely diagnosis and intervention.
  • Poor prognostic indicators for Stanford Type A ADs include:
    • previous history of aortic valve replacement
    • migrating chest pain
    • presenting in shock or with tamponade physiology
    • limb ischemia
    • hypotension
  • Poor prognostic indicators for Stanford Type B ADs include:
    • Older age
    • Presence of mesenteric ischemia
    • Presenting with hypotension or shock
    • Acute renal failure
    • an aorta diameter larger than 5.5 cm
    • Periaortic hematoma
    • Limb ischemia

Recap

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  • Remember that chest pain with an elevated troponin does not rule out ‘AD’.
  • Patients with ‘AD’ can present with neurologic deficit, chest pain etc. that may initially make you think about ischemic CVA, type 1 STEMI. Be cautious! Have a low threshold for ‘AD’ when patients present with weird symptoms like neurologic deficit plus abdominal pain. Do not give antithrombotic meds until appropriate diagnostic imaging is performed (which is variable in different circumstances).
  • By enlarge; do not rely on the D-dimer assay alone to exclude a diagnosis of acute AD. A negative D-dimer may have diagnostic utility in patients with low probability of ‘AD’.
  • Artifacts on CECT and echo, can mimik imaging findings of ‘AAS’.
  • Analgesics and anti-impulse therapy are the cornerstone of medical management of patients with ‘AAS’.
  • The knee jerk response to development of hypotension in patients with suspected or confirmed diagnosis of aortic dissection is to perform POCUS, looking for possible tamponade, hemorrhagic complications,catastrophic aortic regurgitation, all of which can be appreciated by bedside ultrasound.

Going further:

  1. Aortic Dissection (Core ultrasound)
  2. Aortic Dissection (EM:RAP)
  3. Aortic Dissection Live from The EM Cases Course (Emergency Medicine Cases)
  4. The ADvISED Trial: A Novel Clinical Algorithm for the Diagnosis of Acute Aortic Syndromes (REBELEM)

Top image: Case courtesy of Assoc Prof Frank Gaillard, Radiopaedia.org, rID: 9068

Post Peer Reviewed By: Mojtaba Chardoli. MD, Darab Zohri. MD

 

  1. Zhan, S., Hong, S., Shan-Shan, L., Chen-Ling, Y., Lai, W., Dong-Wei, S., Chao-Yang, T., Xian-Hong, S., & Chun-Sheng, W. (2012). Misdiagnosis of Aortic Dissection: Experience of 361 Patients. Journal of Clinical Hypertension, 14(4), 256–260. https://doi.org/10.1111/j.1751-7176.2012.00590.x
  2. Erbel, R., Aboyans, V., Boileau, C., Bossone, E., Di Bartolomeo, R., Eggebrecht, H., Evangelista, A., Falk, V., Frank, H., Gaemperli, O., Grabenwöger, M., Haverich, A., Iung, B., Manolis, A. J., Meijboom, F., Nienaber, C. A., Roffi, M., Rousseau, H., Sechtem, U., … Vlachopoulos, C. (2014). 2014 ESC guidelines on the diagnosis and treatment of aortic diseases. European Heart Journal, 35(41), 2873–2926. https://doi.org/10.1093/eurheartj/ehu281
  3. Hutchison, Stuart J. Aortic diseases: clinical diagnostic imaging atlas. Clinical diagnostic imaging atlas, Philadelphia, Saunders, Elsevier, 2009
  4. Evangelista, A., Flachskampf, F. A., Erbel, R., Antonini-Canterin, F., Vlachopoulos, C., Rocchi, G., Sicari, R., Nihoyannopoulos, P., Zamorano, J., Pepi, M., Breithardt, O. A., & Płońska-Gościniak, E. (2010). Echocardiography in aortic diseases: EAE recommendations for clinical practice. European Journal of Echocardiography, 11(8), 645–658. https://doi.org/10.1093/ejechocard/jeq056
  5. Mussa, F. F., Horton, J. D., Moridzadeh, R., Nicholson, J., Trimarchi, S., & Eagle, K. A. (2016). Acute aortic dissection and intramural hematoma a systematic review. JAMA – Journal of the American Medical Association, 316(7), 754–763. https://doi.org/10.1001/jama.2016.10026
  6. Erbel, R., Alfonso, F., Boileau, C., Dirsch, O., Eber, B., Haverich, A., Rakowski, H., Struyven, J., Radegran, K., Sechtem, U., Taylor, J., Zollikofer, C., Klein, W. W., Mulder, B., & Providencia, L. A. (2001). Diagnosis and management of aortic dissection: Recommendations of the Task Force on Aortic Dissection, European Society of Cardiology. European Heart Journal, 22(18), 1642–1681. https://doi.org/10.1053/euhj.2001.2782
  7. Nienaber, C. A., & Eagle, K. A. (2003). Aortic dissection: New frontiers in diagnosis and management. Part I: From etiology to diagnostic strategies. Circulation, 108(5), 628–635. https://doi.org/10.1161/01.CIR.0000087009.16755.E4
  8. Booher, A. M., Isselbacher, E. M., Nienaber, C. A., Trimarchi, S., Evangelista, A., Montgomery, D. G., Froehlich, J. B., Ehrlich, M. P., Oh, J. K., Januzzi, J. L., O’Gara, P., Sundt, T. M., Harris, K. M., Bossone, E., Pyeritz, R. E., & Eagle, K. A. (2013). The IRAD classification system for characterizing survival after aortic dissection. American Journal of Medicine, 126(8), 730.e19-730.e24. https://doi.org/10.1016/j.amjmed.2013.01.020
  9. Valente, T., Rossi, G., Lassandro, F., Rea, G., Marino, M., Muto, M., Molino, A., & Scaglione, M. (2016). MDCT evaluation of acute aortic syndrome (AAS). British Journal of Radiology, 89(1061), 1–19. https://doi.org/10.1259/bjr.20150825
  10. Evangelista, A., Isselbacher, E. M., Bossone, E., Gleason, T. G., Di Eusanio, M., Sechtem, U., Ehrlich, M. P., Trimarchi, S., Braverman, A. C., Myrmel, T., Harris, K. M., Hutchinson, S., O’Gara, P., Suzuki, T., Nienaber, C. A., & Eagle, K. A. (2018). Insights from the international registry of acute aortic dissection: A 20-year experience of collaborative clinical research. Circulation, 137(17), 1846–1860. https://doi.org/10.1161/CIRCULATIONAHA.117.031264
  11. Imamura, H., Sekiguchi, Y., Iwashita, T., Dohgomori, H., Mochizuki, K., Aizawa, K., Aso, S. ichi, Kamiyoshi, Y., Ikeda, U., Amano, J., & Okamoto, K. (2011). Painless acute aortic dissection -Diagnostic, prognostic and clinical implications -. Circulation Journal, 75(1), 59–66. https://doi.org/10.1253/circj.CJ-10-0183
  12. Nallamothu, B. K., Mehta, R. H., Saint, S., Llovet, A., Bossone, E., Cooper, J. V., Sechtem, U., Isselbacher, E. M., Nienaber, C. A., Eagle, K. A., & Evangelista, A. (2002). Syncope in acute aortic dissection: Diagnostic, prognostic, and clinical implications. American Journal of Medicine, 113(6), 468–471. https://doi.org/10.1016/S0002-9343(02)01254-8
  13. Hagan, P. G., Nienaber, C. A., Isselbacher, E. M., Bruckman, D., Karavite, D. J., Russman, P. L., Evangelista, A., Fattori, R., Suzuki, T., Oh, J. K., Moore, A. G., Malouf, J. F., Pape, L. A., Gaca, C., Sechtem, U., Lenferink, S., Deutsch, H. J., Diedrichs, H., Marcos y Robles, J., … Eagle, K. A. (2000). The International Registry of Acute Aortic Dissection (IRAD). Jama, 283(7), 897. https://doi.org/10.1001/jama.283.7.897
  14. Pape, L. A., Awais, M., Woznicki, E. M., Suzuki, T., Trimarchi, S., Evangelista, A., Myrmel, T., Larsen, M., Harris, K. M., Greason, K., Di Eusanio, M., Bossone, E., Montgomery, D. G., Eagle, K. A., Nienaber, C. A., Isselbacher, E. M., & O’Gara, P. (2015). Presentation, diagnosis, and outcomes of acute aortic dissection: 17-year trends from the international registry of acute aortic dissection. Journal of the American College of Cardiology, 66(4), 350–358. https://doi.org/10.1016/j.jacc.2015.05.029
  15. Nienaber, C. A., Fattori, R., Mehta, R. H., Richartz, B. M., Evangelista, A., Petzsch, M., Cooper, J. V., Januzzi, J. L., Ince, H., Sechtem, U., Bossone, E., Fang, J., Smith, D. E., Isselbacher, E. M., Pape, L. A., & Eagle, K. A. (2004). Gender-related differences in acute aortic dissection. Circulation, 109(24), 3014–3021. https://doi.org/10.1161/01.CIR.0000130644.78677.2C
  16. Goldstein, S. A., Evangelista, A., Abbara, S., Arai, A., Asch, F. M., Badano, L. P., Bolen, M. A., Connolly, H. M., Cuéllar-Calàbria, H., Czerny, M., Devereux, R. B., Erbel, R. A., Fattori, R., Isselbacher, E. M., Lindsay, J. M., McCulloch, M., Michelena, H. I., Nienaber, C. A., Oh, J. K., … Schepens, M. (2015). Multimodality imaging of diseases of the thoracic aorta in adults: From the American society of echocardiography and the european association of cardiovascular imaging: Endorsed by the society of cardiovascular computed tomography and society for cardiova. Journal of the American Society of Echocardiography, 28(2), 119–182. https://doi.org/10.1016/j.echo.2014.11.015
  17. Garcia-Alvarez, M., Marik, P., & Bellomo, R. (2014). Sepsis-associated hyperlactatemia. Critical Care, 18(5), 1–11. https://doi.org/10.1186/s13054-014-0503-3
  18. Adeva-Andany M, López-Ojén M, Funcasta-Calderón R, et al. Comprehensive review on lactate metabolism in human health. Mitochondrion. 2014;17:76-100. doi:10.1016/j.mito.2014.05.007
  19. Suzuki, T., Distante, A., Zizza, A., Trimarchi, S., Villani, M., Uriarte, J. A. S., De Luca Tupputi Schinosa, L., Renzulli, A., Sabino, F., Nowak, R., Birkhahn, R., Hollander, J. E., Counselman, F., Vijayendran, R., Bossone, E., & Eagle, K. (2009). Diagnosis of acute aortic dissection by D-dimer: The international registry of acute aortic dissection substudy on biomarkers (IRAD-bio) experience. Circulation, 119(20), 2702–2707. https://doi.org/10.1161/CIRCULATIONAHA.108.833004
  20. Nazerian, P., Mueller, C., De Matos Soeiro, A., Leidel, B. A., Salvadeo, S. A. T., Giachino, F., Vanni, S., Grimm, K., Oliveira, M. T., Pivetta, E., Lupia, E., Grifoni, S., Morello, F., Capretti, E., Castelli, M., Gualtieri, S., Trausi, F., Battista, S., Bima, P., … Soeiro, A. M. (2018). Diagnostic accuracy of the aortic dissection detection risk score plus D-dimer for acute aortic syndromes the ADvISED prospective multicenter study. Circulation, 137(3), 250–258. https://doi.org/10.1161/CIRCULATIONAHA.117.029457
  21. Marill, K. A. (2008). Serum D-Dimer is a Sensitive Test for the Detection of Acute Aortic Dissection: A Pooled Meta-Analysis. Journal of Emergency Medicine, 34(4), 367–376. https://doi.org/10.1016/j.jemermed.2007.06.030
  22. Diercks, D. B., Promes, S. B., Schuur, J. D., Shah, K., Valente, J. H., & Cantrill, S. V. (2015). Clinical policy: Critical issues in the evaluation and management of adult patients with suspected acute nontraumatic thoracic aortic dissection from the american college of emergency physicians clinical policies subcommittee (writing committee) on thorac. Annals of Emergency Medicine, 65(1), 32-42.e12. https://doi.org/10.1016/j.annemergmed.2014.11.002Lentini S, Perrotta S. Aortic dissection with concomitant acute myocardial infarction: From diagnosis to management. J Emerg Trauma Shock. 2011;4(2):273-278. doi:10.4103/0974-2700.82221
  23. Kawahito, K., Adachi, H., Murata, S. I., Yamaguchi, A., & Ino, T. (2003). Coronary Malperfusion Due to Type A Aortic Dissection: Mechanism and Surgical Management. Annals of Thoracic Surgery, 76(5), 1471–1476. https://doi.org/10.1016/S0003-4975(03)00899-3
  24. Lentini S, Perrotta S. Aortic dissection with concomitant acute myocardial infarction: From diagnosis to management. J Emerg Trauma Shock. 2011;4(2):273-278. doi:10.4103/0974-2700.82221
  25. McMahon, M. A., & Squirrell, C. A. (2010). Multidetector ct of aortic dissection: A pictorial review. Radiographics, 30(2), 445–460. https://doi.org/10.1148/rg.302095104
  26. Quien, M. M., & Saric, M. (2018). Ultrasound imaging artifacts: How to recognize them and how to avoid them. Echocardiography, 35(9), 1388–1401. https://doi.org/10.1111/echo.14116
  27. Gutschow, S. E., Walker, C. M., Martínez-Jiménez, S., Rosado-de-Christenson, M. L., Stowell, J., & Kunin, J. R. (2016). Emerging concepts in intramural hematoma imaging. Radiographics, 36(3), 660–674. https://doi.org/10.1148/rg.2016150094
  28. Chao, C. P., Walker, T. G., & Kalva, S. P. (2009). Natural history and CT appearances of aortic intramural hematoma. Radiographics, 29(3), 791–804. https://doi.org/10.1148/rg.293085122
  29. Chua, M., Ibrahim, I., Neo, X., Sorokin, V., Shen, L., & Ooi, S. B. S. (2012). Acute aortic dissection in the ED: Risk factors and predictors for missed diagnosis. American Journal of Emergency Medicine, 30(8), 1622–1626. https://doi.org/10.1016/j.ajem.2011.11.017
  30. Hansen, M. S., Nogareda, G. J., & Hutchison, S. J. (2007). Frequency of and Inappropriate Treatment of Misdiagnosis of Acute Aortic Dissection. American Journal of Cardiology, 99(6), 852–856. https://doi.org/10.1016/j.amjcard.2006.10.055
  31. Nienaber, C. A., & Clough, R. E. (2015). Management of acute aortic dissection. The Lancet, 385(9970), 800–811. https://doi.org/10.1016/S0140-6736(14)61005-9
  32. Hiratzka, L. F., Bakris, G. L., Beckman, J. A., Bersin, R. M., Carr, V. F., Casey, D. E., Eagle, K. A., Hermann, L. K., Isselbacher, E. M., Kazerooni, E. A., Kouchoukos, N. T., Lytle, B. W., Milewicz, D. M., Reich, D. L., Sen, S., Shinn, J. A., Svensson, L. G., Williams, D. M., Jacobs, A. K., … Yancy, C. W. (2010). 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM guidelines for the diagnosis and management of patients with thoracic aortic disease: Executive summary: A report of the american college of cardiology foundation/american heart association task force on practice guidelines, american association for thoracic surgery, american college of radiology, american stroke association. Circulation, 121(13), 266–369. https://doi.org/10.1161/CIR.0b013e3181d4739e
  33. Rogers, A. M., Hermann, L. K., Booher, A. M., Nienaber, C. A., Williams, D. M., Kazerooni, E. A., Froehlich, J. B., O’Gara, P. T., Montgomery, D. G., Cooper, J. V., Harris, K. M., Hutchison, S., Evangelista, A., Isselbacher, E. M., & Eagle, K. A. (2011). Sensitivity of the aortic dissection detection risk score, a novel guideline-based tool for identification of acute aortic dissection at initial presentation: Results from the international registry of acute aortic dissection. Circulation, 123(20), 2213–2218. https://doi.org/10.1161/CIRCULATIONAHA.110.988568
  34. Nazerian, P., Mueller, C., De Matos Soeiro, A., Leidel, B. A., Salvadeo, S. A. T., Giachino, F., Vanni, S., Grimm, K., Oliveira, M. T., Pivetta, E., Lupia, E., Grifoni, S., Morello, F., Capretti, E., Castelli, M., Gualtieri, S., Trausi, F., Battista, S., Bima, P., … Soeiro, A. M. (2018). Diagnostic accuracy of the aortic dissection detection risk score plus D-dimer for acute aortic syndromes the ADvISED prospective multicenter study. Circulation, 137(3), 250–258. https://doi.org/10.1161/CIRCULATIONAHA.117.029457
  35. Dean, J. H., Woznicki, E. M., O’Gara, P., Montgomery, D. G., Trimarchi, S., Myrmel, T., Pyeritz, R. E., Harris, K. M., Suzuki, T., Braverman, A. C., Hughes, G. C., Kline-Rogers, E., Nienaber, C. A., Isselbacher, E. M., Eagle, K. A., & Bossone, E. (2014). Cocaine-related aortic dissection: Lessons from the international registry of acute aortic dissection. American Journal of Medicine, 127(9), 878–885. https://doi.org/10.1016/j.amjmed.2014.05.005

 

Shahriar Lahouti

Founder, Chief Editor
I am Shahriar Lahouti and RECAP EM is my primary FOAMed project. The philosophy of RECAP EM is to promote critical thinking and enlightening the mindsets with most rational, current evidence towards a safer practice.

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