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PATHOPHYSIOLOGY:

Essential hypertension is by far the most common risk factor, being present in approximately 70% of cases.

Marfan syndrome is likely to be present in 50% of cases of dissection presenting under the age of 40.

Location of primary aortic tear: 70% ascendng aorta, 15%descending, 5% Arch, 5% abdominal aorta.

CLINICAL PRESENTATION:

anterior chest pain 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.

‘Migratory pain’ which typically starts where the aortic tear is and progresses to a branch vessel e.g. 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

Presenting without pain

AAD may present without pain (5-15%) and occurs in the following circumstances:

• Syncope: this may be the presentation of acute dissection and the patient may remain confused or in 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.

INVESTIGATIONS:

D-dimer is typically elevated in patients with acute aortic dissection. Studies have looked at using D-dimer as a screening tool for AAD at a cut-off of 500ng/ml, where a positive D-dimer has been found to be around 96% sensitive for AAD.

The following ECG features are associated with AAD:

• 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)

Only 30% of patients with AAD will have a normal ECG.

CXR sensitivity for aortic dissection is generally estimated at around 60-90% in studies, though even where positive findings exist, these may be subtle and non-specific.

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

TTE is not a definitive test for AAD; it only has a sensitivity of approximately 80% for Type A and 50% for Type B dissections, so TTE may miss the dissection altogether. It may however have a role in some centres alongside CT scanning.

Aortic dissection is diagnosed on CT by identifying two distinct lumens with a visible intimal flap. It can also delineate branch vessel involvement, visualise the entire aorta and has a sensitivity approaching 100% but it is not yet 100%. It may miss a dissection if there is complete thrombosis of one lumen or if there is similar opacification of both the true and false lumens.

Also, intramural haematoma may be missed as the findings are often subtle and only evident on pre-contrast images.

However It is imperative that if there is a strong clinical suspicion of aortic dissection and the result of the first modality of imaging is normal, a second test should be performed.

MANAGEMENT:

Definitive treatment depends upon the type of dissection:

• Type A dissections require open surgery to prevent rupture into the pericardial sac
• 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 

In theory, we would like the systolic blood pressure to be the lowest it can be, whilst still maintaining adequate end organ perfusion. In clinical practice, a cut off target for systolic blood pressure of <120 mmHg is generally used.
 the target HR should be at least <80 bpm, though some publications advocate the more restrictive target of around 60 bpm.

Remember that the first step to controlling BP is often to provide adequate pain control, thereby reducing sympathetic stimulus. Opiate analgesia is normally indicated.

An intravenous β-blocker is generally the optimal first line anti-hypertensive. (Labetalol, Esmolol)

Would you drain a haemopericardium secondary to AAD ?

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 [6].

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.