Aortic dissection occurs when a tear in the intimal layer (innermost) of the aortic wall causes blood to flow between the layers of the wall of the aorta, splitting the layers apart.
It can be defined as acute (when diagnosed ≤14 days) or chronic (when diagnosed >14 days).
In this article, we shall look at the classification, clinical features and management of aortic dissection.
Aortic dissections from the initial intimal tear can progress distally, proximally, or in both directions from the point of origin. Anterograde dissections propagate towards the iliac arteries, and retrograde dissections propagate towards the aortic valve (at the root of the aorta)*.
*Retrograde dissections can result in prolapse of the aortic valve, bleeding into the pericardium and cardiac tamponade.
Thoracic aortic dissections are classified anatomically by two systems, Stanford and DeBakey.
The DeBakey classification groups aortic dissections anatomically (Fig. 2):
- Type I – originates in the ascending aorta and propagates at least to the aortic arch
- They are typically seen in patients under 65 and carry the highest mortality
- Type II – confined to the ascending aorta
- Classically in elderly patients with atherosclerotic disease and hypertension
- Type III – originates to the left of the subclavian artery in the descending aorta
- Further subdivided into IIIa which extends distally to the diaphragm and IIIb which extends beyond the diaphragm into the abdominal aorta
The Stanford classification divides aortic dissection into two groups, A and B:
- Group A – includes DeBakey Types I and II and involves the ascending aorta, aortic arch and can propagate to the descending aorta; the tear can originate anywhere along this path.
- Group B – dissections do not involve the ascending aorta and include DeBakey Type III.
There are certain factors associated with an increased risk of developing an aortic dissection:
- Atherosclerotic disease
- Connective tissue disorders
- Most commonly Marfan’s syndrome or Ehler’s-Danlos syndrome
- Biscuspid aortic valve
As a general rule, younger cases often have associated connective tissue disorders, whilst older patients are more likely to have underlying hypertension or atherosclerosis.
The characteristic presentation of an aortic dissection is of a tearing or stabbing chest pain, which can radiate depending on the anatomy of the dissection, particularly to the back. However, the diagnosis can be difficult to establish acutely and may prove to be a more subtle presentation
The most common clinical signs include tachycardia, hypotension*, a new aortic regurgitation murmur, or signs of end-organ hypoperfusion (such as reduced urine output or deteriorating conscious level). They may also have neurological sequelae of the dissection, such as paraplegia.
*Secondary to hypovolaemia from blood loss into the dissection or cardiogenic from severe aortic regurgitation or pericardial tamponade
Thoracic aortic dissection will often present as chest pain, a presenting problem that has multiple differential diagnoses:
- Myocardial infarction – classically crushing and central chest pain, with signs of cardiac ischaemia on ECG and / or raised serum Troponin levels.
- Pulmonary embolism – dyspnoea will be a prominent feature and ABG will show hypoxia, confirm with CTPA or V/Q scan.
- Pericarditis – classically pleuritic chest pain, with the ECG showng diffuse ST elevation as well as potential pericardial rub on auscultation.
- Musculoskeletal back pain – the patient will not present with systemic signs of shock and will be tender to palpation of the chest wall or paraspinal muscles.
Baseline blood tests (FBC, U&Es, LFTs, troponin, coagulation) with a crossmatch of at least 6 units, with an ABG to aid initial assessment. An ECG is essential to exclude any cardiac pathology.
A computed tomography (CT) angiogram is recommended to diagnose aortic dissection as first line imaging (Fig. 3). This will also allow classification, establish the anatomy of the dissection, and assist surgical planning.
A transoesophogeal ECHO can also provide useful information about the thoracic aorta but is operator dependent.
Urgent initial assessment is required, as for any other critcially ill surgical patient. Start high flow oxygen, gain IV access (x2 large bore cannulas) and fluid resuscitation; the target systolic pressure in these patients should be 100-120mmHg (termed ‘permissive hypotension’). Catheterise the patient and start a fluid balance.
Stanford Type A dissections should be managed surgically in the first instance, if possible, and carry a worse prognosis than Type B dissections. Any uncomplicated Type B dissections can usually be managed medically.
Type A Dissections
Type A dissections carry a high mortality if left untreated and these cases should be discussed urgently with a cardiac or vascular surgeon. They will most likely require transfer to a cardiothoracic centre.
The surgery involves removal of the ascending aorta (with or without the arch) and replacement with synthetic graft. If the dissection has damaged the suspensory apparatus of the aortic valve, this will also require repair.
Any additional branches of the aortic arch that are involved will require reimplanation into the graft (i.e. brachiocephalic artery, left common carotid artery, left subclavian artery), with long Type A dissections involving the descending and possibly abdominal aorta may require staged procedures with both open and endovascular treatment.
Type B Dissections
Uncomplicated Type B dissections are best managed medically, with good survival rates. First line treatment is management of any hypertension with beta blockers (or calcium channel blockers as second line therapy).
Research is ongoing as to the benefit of endovascular repair in these patients and medical management remains gold standard. Surgical intervention in Type B dissections will be determined on the basis of complications, such as visceral or limb ischemia, refectory pain, or uncontrollable hypertension. Any surgical repair attempted is usually endovascular with a stent graft.
Type B dissections can go on to be chronic, with continued leakage into the dissection, even if a stent has been placed. The most common complication of chronic disease is the formation of an aneurysm. These present further surgical problems, with open repair being complex and endovascular repair offering a better survival chance.
Long Term Management
All patients need lifelong antihypertensive therapy and surveillance imaging, due to the high risk of developing further dissection or other complications. Imaging would usually be at one, three and 12 months after discharge, with further scans at 6-12 month intervals depending on the size of the aorta.
Any complications that arise depend on the site and spread of the dissection into the aortic branches, damaging end organs. Consequently, complications that can occur include:
- Aortic rupture
- Aortic regurgitation
- Myocardial ischaemia
- Secondary to coronary artery dissection
- Cardiac tamponade
- Stroke or paraplegia
- Secondary to cerebral artery or spinal artery involvement
Mortality remains high, with over 20% of cases dying before reaching hospital, however early diagnosis, intervention, and blood pressure control significantly improves the prognosis
- An aortic dissection occurs following a tear in the intimal layer of the aortic wall causing blood to flow between the layers of the aortic wall
- Patients will classically present with a ‘tearing’ central chest pain
- A computed tomography (CT) angiogram is the gold-standard first line investigation
- Type A dissections should be managed surgically whilst uncomplicated Type B dissections can be managed medically