Acute aortic dissection

Acute aortic dissection is a dramatic situation in which the intima wall of the aorta suffers a tear and blood leeks through the other layers, creating a hematoma that can expand, dissecting the aorta and structures and vessels attached to it on the way, or rupture leading to shock and death. It is one of the deadliest causes of chest pain. The incidence is between 2.5-3.5 cases/100.000 person years.

Risk factors include hypertension, genetic collagen defects, previous aortic aneurysm, bicuspid aortic valve, previous instrumentation of the aorta, aortic coarctation, vasculitis and trauma.


There are two major classifications of aortic injuries according to the area affected: the Stanford classification and the DeBakey classification.

Stanford classifies the dissection in type A (involves the ascending aorta) or type B (does not involve the ascending aorta). The DeBakey system classifies the injuries in type I (originates in the ascending aorta and extends), type II (originates and remains on the ascending aorta) or type III (originates on the descending aorta.


Depending on the extension and the area affected the symptoms may be different.

Chest pain is often present (90%) as an intense, sudden, sharp/stabbing pain that may radiate to the back.

Shortness of breath may be present due to complications (hemothorax, myocardial infarction, pericardial tamponade), as well as reduced breathing sounds or heart sounds.

A murmur of aortic regurgitation (diastolic decrescendo murmur) may be present.

Signs and symptoms of stroke or carotid dissection (e.g. Horner syndrome) may also be evident.

Abdominal pain (e.g mesenteric ischemia) may be present.

Limb pain or claudication can also be present due to ischemia. Difference in pulses may be observed as well.


A suggestive history (e.g. acute intense sharp chest pain) and physical examination (e.g. difference in pulses and blood pressure between limbs) should prompt the investigation of aortic dissection as a potential diagnosis.

As in any patient with chest pain, quick monitoring (O2 Sat and cardiac), venous access and oxygen should be provided.

ECG and chest radiograph (may show mediastinal widening) should be obtained.

The D-dimer may be elevated in patients with aortic dissection but it is often also elevated in pulmonary embolism and other situations. For that reason an elevated result does not confirm the condition, but lower number (<500ng/mL) may be useful to rule it out.

Other tests like CBC, CMP, coagulation studies and myocardial damage panel should be obtained.

Patients that are stable should undergo CT angiography (chest and abdomen) to confirm or exclude the diagnosis. Unstable patients may benefit from a transesophageal echocardiography instead, since it can often be performed quicker at the bedside.


The acute treatment should focus on reducing the rate of progression, control blood pressure, pain control and definitive treatment when appropriate.

The use of beta-blockers (e.g. labetalol – TRANDATE – 10-20mg over 1-2 minutes, may be repeated) reduce the aortic pulse which can help to reduce the rate of progression

Blood pressure should also be controlled, and additional anti-hypertensives may be used (e.g. nitroprusside IV 0.3-0.5mcg/kg/min). BP should be <120/80mmHg as long as the patient does not get confused or experience ischemic symptoms.

Emergency definitive treatment (surgery) is indicated for all Stanford type A aneurisms due to the risk of early complications (e.g. acute aortic regurgitation, myocardial infarction). The mortality in acute type A aneurism is 1-2% per hour, hence the need to quick intervention.

Patients with Stanford type B that are stable may be managed with medical treatment alone initially. If the development of end-organ hypoperfusion, refractory pain, aneurysmal dilation or lesion progression is visible, surgical intervention (open, endovascular or hybrid) becomes necessary. Patients with genetic conditions (e.g Marfan, Ehler Danlos) may benefit from early open intervention.

After surgery or after the acute stage in patients that will be observed the blood pressure should be controlled carefully with oral medications (e.g beta blockers, CCB). Postoperative patients may receive follow up imaging after 3, 6 and 12 months after (e.g. MRI).


  1. Nauta FJH et al. Update in the management of type B aortic dissection. Vascular Medicine. 2016. 1–13.
  2. The Task Force for the Diagnosis and Treatment of Aortic Diseases of the European Society of Cardiology (ESC). 2014 ESC Guidelines on the diagnosis and treatment of aortic diseases. European Heart Journal (2014) 35, 2873–2926.
  3. ACC/AHA. Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. March 2010.
  4. Khan IA, Nair CK. Clinical, Diagnostic, and Management Perspectives of Aortic Dissection. CHEST 2002; 122:311–328.