AD Flashcards

1
Q

What is an aortic dissection?

A

Aortic dissection describes the condition when a separation has occurred in aortic wall intima, causing blood flow into a new false channel between the tunica intima and tunica media.

It is a potentially life-threatening surgical emergency.

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2
Q

What is the aetiology of AD?

A
  • Chronic hypertension
    • Pregnancy
  • Connective tissue disorders – Marfan’s, Ehlers-Danlos
  • Aneurysms
  • Infection
  • Atherosclerosis
  • Trauma – shearing stresses in RTA
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3
Q

What is the pathophysiology of AD?

A

Aortic dissection is a potentially life-threateningsurgical emergency.

It occurs when there is atear in the tunica intima, and blood then splits the vessel wall anddissects through the tunica media.

Consequently, afalse lumenis created as the blood in the media layer propagates both proximally and distally.

Abnormal flow through this false lumen can occlude flow through the branches of the aorta.

Blood penetrates the intima and enters the media layer.

  • Results from a tear in the intima
  • Blood flowing into media is under high pressure which creates a false lumen in the diseased media and splits it

Leads to occlusion of the branches of the aorta

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4
Q

What is the detailed pathophysiology of AD?

A

An aortic dissection is where there is a tear in part of the tunica intima of the aorta. High-pressured blood flowing through the aorta begins to tunnel between the tunica intima and the tunica media, separating the two layers.

As the high-pressured blood continues to shear more and more of the tunica intima off the tunica media, blood starts to pool between the two layers, increasing the outside diameter of the blood vessel. The area where blood collects between the tunica intima and the media is called a false lumen.

This most commonly occurs around the ascending aorta and aortic arch, but can affect any part of the aorta.

Hypertension is a key risk factor. In order for an aortic dissection to occur, an underlying condition also usually has to exist that weakens the aorta’s wall. Connective tissue disorders e.g. Marfan’s and Ehlers-Danlos syndrome can cause a dissection. Alternatively, aneurysms can be a cause of aortic dissection.

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5
Q

What is the epidemiology of AD?

A
  • Aortic dissection has a worldwide incidence of 0.5 to 2.95 per 100,000 people annually
  • Affects males more than females
    • M>F
  • Most common emergency affecting the aorta
  • Most common between the ages of 50-70 and is rare below 40
    • Common presentation 50-70
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6
Q

What are the symptoms of AD?

A

Abrupt onset of severe, tearing central chest pain radiating to the back and down arms.

  • Sudden onset, severe ‘tearing’ or ‘ripping’ chest pain that may radiate to the back
  • Syncope: red flag symptom
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7
Q

What are the signs of AD?

A
  • Signs
    • Absent peripheral pulses
      • Weak downstream pulses: radio-radial and/or radio-femoral delay
    • Unequal blood pressure in the left and right arm
      • A difference in blood pressure between two arms: >10 mmHg
    • Hypertension
    • Tachycardia and hypotension: as condition progresses
      • Poor prognostic features more commonly associated with a Type A dissection
    • Diastolic murmur: due to aortic regurgitation
    • Marfan syndrome signs
      • Tall
      • Arachnodactyly
      • Hypermobile joints
      • Narrow face
    • Ehlers-Danlos syndrome signs
      • Translucent skin
      • Easy bruising
      • Hypermobility of small joints
  • Neurological signs due to involvement of branch arteries
    • Involvement of specific arteries
      • Spinal arteries → paraplegia
      • Coronary arteries → angina
      • Distal aorta → limb ischaemia
  • Aortic regurgitation, cardiac tamponade
  • Compression of other arteries – renal, subclavian
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8
Q

What are the classification systems of AD?

A

There are two main classification systems for aortic dissection:StanfordandDeBakey.

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9
Q

What is the Stanford classification of AD?

A

Stanford:

  • Type A: dissection involves the ascending aorta with or without the involvement of the arch and descending aorta, occurringproximalto the left subclavian artery (⅔ of cases)
  • Type B: dissection doesnotinvolve the ascending aorta. Involves only the descending thoracic or the abdominal aorta, occurringdistalto the left subclavian artery (⅓ of cases)

Stanford Type A and Type B dissections. Remember, Type A occurs proximally to the left subclavian artery, whilst Type B occurs distal to it.

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10
Q

What is the debakey classification?

A

DeBakey:

  • Type I: originates in the ascending aorta and involves at least the aortic arch, but can extend distally
  • Type II: originates and confined to the ascending aorta
  • Type III: originates in the descending aorta and extends distally, but can extend proximally
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11
Q

What are the primary investigations of AD?

A
  • ECG:non-specific changes such as T-wave inversion or ST-segment depression. ST-segment elevation may be seen in the inferior leads in some patients
  • FBC:anaemia may be present, although Hb may be normal given the acute nature of a dissection
  • U&Es: required prior to a CT with contrast and to detect pre-renal acute kidney injury secondary to hypovolaemia
  • Group & save and crossmatch: all patients with suspected dissection should have blood crossmatched in case of a transfusion, with 4-6 units available for theatre as required
  • Chest X-ray:may demonstrate a widened mediastinum/aorta
  • Contrast-enhanced CT angiogram:gold-standard imaging. The thorax, abdomen and pelvis should ideally be visualised to determine the extent of aortic disease
    • TOE is an alternative = Show intima flap + false lumen Transesophageal cardiogram
  • CT/MRI angiography confirms diagnosis – contraindicated in patients with renal disease
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12
Q

What are some other investigations to consider?

A
  • Other investigations to consider
    • Transoesophageal echocardiogram
      • Echocardiogram (echo): a transthoracic or transoesophageal echo should be considered in a very unstable patient, with the latter being more accurate and able to confirm the diagnosis with the presence of an intimal flap.
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13
Q

What is the management for AD?

A

Type A and Type B managements

  • Type A dissection – surgical repair of ascending aortic dissection
    • Blood transfusion
    • Beta blocker e.g. IV labetalol: aim for a systolic blood pressure of 100-120 mmHg; high pressures are associated with extension of the dissection
    • Urgent surgical repair/ stenting: open surgery with replacement of the ascending aorta should be performed immediately upon diagnosis
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14
Q

What is the management for Type B AD?

A
  • Type B
    • Conservative management: bed rest and analgesia
    • Beta blocker e.g. IV labetalol: aim for a systolic blood pressure of 100-120 mmHg; patients are usually monitored closely on the high dependency or intensive care unit
    • Thoracic endovascular aortic repair (TEVAR): may be performed to reduce the risk of future dissection, although further studies are required before this is the standard of care in clinical practice
    • Surgical repair of descending aortic dissection
    • Antihypertensives to control blood pressure
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15
Q

What are the complications of AD?

A
  • Aortic valve damage (aortic regurgitation) or rupture into the lining around the heart (cardiac tamponade)
    • Aortic regurgitation:dissection extends proximally, leading to loss of support for valve leaflets
  • Myocardial infarction:occurs when dissection propagates proximally; inferior ST-elevation may be seen due to right coronary involvement
  • Stroke
  • Renal failure: blood could continue to tunnel between the tunica intima and the tunica media until it reaches another artery that branches off the aorta e.g. renal arteries. The blood in the false lumen can put pressure on this branching artery decreasing blood flow to the kidneys
  • Pericardial tamponade:blood from the false lumen leaks into pericardial space, and may cause tamponade
  • Haemorrhage and shock: blood flowing through the false lumen could puncture a hole through the tunica media and tunica externa and bleed into the mediastinum. This can result in rapid death
  • Death due to severe internal bleeding
  • Organ damage, such as kidney failure or life-threatening intestinal damage
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16
Q

What are the risk factors for AD?

A
  • Hypertension: the most important risk factor
    • Uncontrolled high blood pressure
  • Smoking
  • Family history of aortic aneurysm or dissection
    • Weakened and bulging artery (aortic aneurysm)
  • Bicuspid aortic valve
    • An aortic valve defect (bicuspid aortic valve)
  • Coarctation of the aorta: a narrowing of the aorta at birth (aortic coarctation)
  • Connective tissue disorders:Marfan
    • Marfan syndrome → This is a condition in which connective tissue, which supports various structures in the body, is weak.
  • Other connective tissue disorders.
    • This includes Ehlers-Danlos syndrome, a group of connective tissue disorders that involve loose joints and fragile blood vessels and Loeys-Dietz syndrome, which causes twisted arteries, especially in the neck.
  • Turner syndrome and Noonan syndrome
  • Trauma
  • Pregnancy: increased blood plasma volume
  • Syphilis
  • Hardening of the arteries (atherosclerosis)

Certain genetic diseases increase the risk of having an aortic dissection

17
Q

What is the prognosis for AD?

A
  • Anuntreated proximal aortic dissectionwill result in a false channel rupture with fatal haemorrhage in 50-60% of patients within 24 hours.
  • It is estimated that20% of patients die before reaching hospitaland a further30% die before reaching theatre.
  • However, the 5-year survivalafter surgeryfor Type A and B dissections is up to 80%.