Acute aortic dissection Flashcards

1
Q

How would you define an aortic dissection?

A
  • An aortic dissection occurs following a tear in the aortic intima with subsequent separation of the tissue within the weakened media by the propagation of blood.
  • At the point of dissection, the aorta is not aneurysmal and the term dissecting aneurysm is incorrect and may be misleading.
  • A ruptured or leaking abdominal aneurysm is a different disease and requires immediate surgery with only occasional need for any imaging. This can be performed in most hospitals by a vascular surgeon and does not require the use of cardiopulmonary bypass.
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2
Q

What is the Standford classification of acute aortic dissection?

A
  • Type A: Involves the ascending aorta and/or the arch

- Type B: involve only the descending aorta and occur distal to the left subclavian artery

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3
Q

What is the DeBakey’s classification of Acute aortic dissection?

A
  • Type 1: Involve the entire aorta
  • Type 2: Involve the ascending aorta and/or the arch of the aorta
  • Type 3: Involve only the descending aorta
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4
Q

What is the Reul and Cooley classification of Acute aortic dissection?

A

Reul and Cooley further subdivided DeBakey’s classification into subtypes IIIa and IIIb. In IIIa the dissection involves the aorta just distal to the left subclavian artery but extends proximal or distal to this but is largely above the diaphragm. In IIIb the dissection occurs only distal to the left subclavian artery and may extend below the diaphragm.

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5
Q

What is Svensson’s classification of Acute aortic dissection?

A
  • Class 1: Classic dissection with a flap between the true and false aneurysm and clot in the false lumen
  • Class 2: Intramural hematoma
  • Class 3: Limited intimal tear with an eccentric bulge at the tear site
  • Class 4: Penetrating atherosclerotic ulcer with surrounding hematoma, usually subadventitial
  • Class 5: Iatrogenic or traumatic dissection illustrated by coronary catheter causing dissection
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6
Q

What are the predisposing factors for aortic dissection?

A
  • Hypertension
  • Marfan syndrome
  • Ehlers-Danlos syndrome
  • Annuloaortic ectasia and familial aortic dissection
  • Bicuspid aortic valve
  • Coarctation of the aorta
  • Pregnancy
  • Turner syndrome
  • Cocaine abuse
  • Giant cell arteritis
  • Iatrogenic
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7
Q

Where does the majority of aortic dissections occur?

A

The ascending aorta (70%)

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8
Q

Where could an aortic dissection rupture in the ascending aorta and what would happen if this were to occur?

A
  • Haemopericardium (syncope and/or sudden death)

- Right haemothorax (invariably sudden death)

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9
Q

Where could an aortic dissection rupture in the arch of the aorta and what would happen if this were to occur?

A
  • Mediastinal haematoma
  • Interatrial septal haematoma (cardiac conduction defects)
  • Compression of pulmonary trunk/artery
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10
Q

Where could an aortic dissection rupture in the descending aorta and what would happen if this were to occur?

A
  • Left haemothorax (sudden death)

- Rarely into oesophagus (profuse haematemesis)

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11
Q

Where could an aortic dissection rupture in the abdominal aorta and what would happen if this were to occur?

A
  • Retroperitoneal haemorrhage (back pain with shock)

- Rarely intraperitoneal haemorrhage (shock and acute abdomen)

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12
Q

What are the consequences if the coronary vessels were occluded by the AAD?

A

ST-elevation myocardial infarction

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13
Q

What are the consequences if the common carotid arteries were occluded by the AAD?

A

Any type of stroke

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14
Q

What are the consequences if the subclavian arteries were occluded by the AAD?

A

An acutely ischaemic upper limb

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15
Q

What are the consequences if the coeliac/ mesenteric vessels were occluded by the AAD?

A

Ischaemic bowel

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16
Q

What are the consequences if the renal vessels were occluded by the AAD?

A

Frank haematuria

17
Q

What are the consequences if the spinal arteries were occluded by the AAD?

A

Sudden onset painless paraplegia

18
Q

What is the most common presenting symptom of AAD?

A

Pain occurs in 80-90% of patients.

19
Q

What are the typical features of the presentation of pain for AAD?

A
  • Abruptness in onset: usually patients can state exactly what they were doing at the onset of pain
  • Often maximal at the time of onset
  • Commonly sharp in nature although a ‘tearing pain’ is often described
  • Occurs in the anterior chest in 70-80% of patients with Type A dissection
  • Upper back pain is experienced in about 50% of patients and more commonly in patients with a Type B dissection
20
Q

What are the less common presenting features of the pain of AAD?

A
  • Sudden abdominal pain occurs in a minority of patients although this is much more likely to be due to ruptured abdominal aortic aneurysm (AAA), perforated hollow viscus or ischaemic bowel
  • Sudden radiation of pain to the neck, throat or jaw
    ‘Migratory pain’ which typically starts where the aortic tear is and progresses to a branch vessel for example chest pain to arm pain (subclavian involvement); back pain to leg pain (common or external iliac involvement). This is often unilateral and occurs in approximately 20% of patients
  • Short duration of pain. This may occur if the dissection process has stopped or if there has been a re-entry tear into the true lumen with the relief of intra-luminal pressure
21
Q

What percentage of AAD presents without pain?

A

5-15%

22
Q

When does AAD present without pain?

A
  • Syncope: this may be the presentation of acute dissection and the patient may remain confused or in a coma
  • Stroke: the neurological deficit in these patients occurs almost simultaneously with the primary aortic tear so no pain is experienced at all, or the pain may not be expressed (e.g. if dysphasic)
  • Acute cardiac failure: this is usually due to sudden aortic annular dilatation with immediate severe aortic regurgitation or coronary artery dissection with complete vessel occlusion and consequent cardiogenic shock
  • Paraplegia: occurs when the dissection occludes the origin(s) of the spinal arteries. This is typically painless
  • The elderly: in the very old, pain perception is sufficiently reduced that the dissection process does not cause a noxious stimulus
23
Q

What signs should be sought specifically in a patient whom you suspect has AAD?

A
  1. Signs of haemopericardium
    - Faint or absent heart sounds
    - Pulsus paradoxus
    - Distended neck veins
    - Presence of shock
  2. Signs of branch vessel occlusion
    - A difference of >20 mmHg in the blood pressure of -each arm
    - A weaker central or peripheral pulse compared to the contralateral side
    - A palpable thrill or audible bruit over any of the pulses or the abdominal aorta
  3. Signs of aortic root dilatation
    - A wide pulse pressure
    - A diastolic murmur over the aortic valve area
24
Q

What are the causes of hypotension in patients with AAD?

A
  1. Hypovolaemia:
    - Massive haemothorax
    - Loss of blood into an extensive aortic wall false lumen
    - Bowel ischaemia with or without haematemesis/melaena
    - Retroperitoneal haemorrhage
  2. Pump failure:
    - Haemopericardium with cardiac tamponade
    - Left ventricular dysfunction secondary to STEMI (coronary artery dissection/occlusion)
    - Complete heart block following haemorrhage into the interatrial septum
  3. Neurogenic shock:
    - Spinal cord ischaemia or infarction
25
Q

What are the ECG features associated with AAD?

A
  • Non-specific ST segment and T wave changes (40% of patients)
  • Acute ischaemic changes (15% of patients)
  • ST-elevation myocardial infarction pattern (occurs in 3% of patients due to extension of the dissection process into a coronary ostium)
26
Q

What radiological signs must be sought in a CXR of an AAD?

A
  • A widened mediastinum
  • An abnormal aortic contour
  • A soft tissue shadow peripheral to a calcified aortic annulus
  • A globular heart suggesting a large haemopericardium
  • A pleural effusion
27
Q

Out of transthoracic echocardiography and transoesophageal echocardiography, which is more definitive?

A

Transoesophageal echocardiography (TOE) is an ideal test because it can be performed in the resuscitation room. It has a sensitivity of 90-98% and can easily delineate the extent of the dissection and can visualise the aortic root and valve

28
Q

What is the advantage of CT over other modalities of aortic imaging?

A

CT has a distinct advantage over other modalities of aortic imaging in that currently most hospitals in the UK are able to transfer these images to a regional cardiothoracic centre if required.

This gives the surgeons adequate information on whether to transfer the patient and allows them to plan the type of surgery required prior to patient arrival.

29
Q

What would you do if the scan was normal but the clinical suspicion was high?

A

None of the individual imaging modalities for AAD is perfect. One study created a decision model to determine the 30-day survival of patients who did, and did not, have a second test performed (not including TTE) when the clinical probability of acute dissection was high (>15%).

This review concluded that the 30-day survival of patients with a high probability of dissection was significantly improved when a second test was performed after the first test was negative.

30
Q

What is the treatment for type A dissections?

A

require open surgery to prevent rupture into the pericardial sac.

31
Q

What is the treatment for type B dissections?

A

Type B dissections are managed medically but may require endovascular stenting if the patient has persistent pain, a rapidly expanding aortic diameter, or malperfusion of branch vessel organs.

It is important that patients with a Type B dissection are still managed in a High Dependency Unit and referred to a vascular interventional team if complications arise

32
Q

How is blood pressure controlled in AAD?

A

It is vital that patients with suspected or proven dissection should have their blood pressure actively reduced if higher than a systolic of 110 mmHg otherwise the dissection process may progress.

In order to facilitate this, an arterial line must be placed; intravenous labetalol is the ideal agent to be used in this setting. Labetalol is both an alpha and beta-blocker and should be given as an initial bolus and then as an infusion with invasive arterial monitoring used to guide the actual dose.

Vasodilators and β-blockers must not be used on their own. If a vasodilator is used it will cause a reflex increase in contractility of the left ventricle which will potentially worsen the dissection. A β-blocker may cause unopposed alpha-receptor stimulation with increased peripheral vasoconstriction. These agents can, however, be used to good effect if administered together.

33
Q

What are the drugs used to manage hypertension in AAD?

A
  • Labetalol
  • Esmolol
  • Metoprolol
  • Glyceryl trinitrate
  • Sodium nitroprusside
34
Q

Would you drain a haemopericardium secondary to AAD?

A

No. In patients with haemopericardium, it is imperative that pericardiocentesis is not performed as a number of case series have demonstrated that rapid decompression of the pericardium can restart fresh bleeding with rapidly fatal consequences.

It is thought that the pressure gradient between the false lumen and the pericardial sac is suddenly increased when pericardiocentesis is performed thereby causing sudden and catastrophic bleeding into the pericardial sac.

As a result of several case reports highlighting this problem, the recommendations of the Task Force on Aortic Dissection also discourage pericardiocentesis in this context