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  • Timely diagnosis of aortic dissection has more life-saving potential than almost any other diagnosis in medicine.

  • Diagnosis can be difficult, requiring high clinical suspicion and quick, efficient use of diagnostic modalities.

  • Clinical clues are the typical pain, incongruous poor tissue perfusion despite hypertension, or evidence of aortic branch occlusion.

  • Emergent control or support of blood pressure and pain is imperative.

  • Urgent CT angiogram or transesophageal echocardiography are preferred means to confirm the diagnosis and detect complications.

  • Distinguishing type A (ascending aorta involved) versus type B (only descending aorta involved) guides definitive treatment.

  • Type A dissection requires emergency cardiac surgical repair.

  • Uncomplicated type B dissection is managed medically.

  • Complicated type B dissection is usually managed with endostenting: surgery is rarely performed.

  • Long-term surveillance and strict control of hypertension are important to identify the need for late intervention and maximize long-term survival.


Aortic dissection occurs much more frequently than previously appreciated and is the most common catastrophe affecting the aorta, occurring two to three times more commonly than acute abdominal aortic aneurysm rupture.1–3 Although the diagnosis is sometimes obvious, the majority of cases are not clear-cut and the patient’s survival will depend on a high index of suspicion by the physician despite myriad clinical presentations. Time is of the essence as the mortality rate is 50% for the first 48 hours without treatment and 85% to 90% over 3 months. The typically hypertensive patient must have blood pressure and pain controlled quickly, followed by rapid diagnosis with definitive imaging and immediate therapy (emergency surgery, endostenting, or medical management).


Previously, aortic dissections were referred to as dissecting aneurysms, as originally coined by Laënnec. This is a misnomer in that the pathology is a dissecting hematoma that separates the intima and inner layers of the media from the outer medial and adventitial layers (Fig. 41-1B). The intima is not aneurysmal, and is, if anything, narrowed. Blood invades the media through a tear in the intima and proceeds ante- or retrogradely through the aortic wall, forming a false lumen that is usually much bigger than the true lumen (Fig. 41-1).4 In type A dissections (originating in the ascending aorta), the hematoma commonly spirals around the right and posterior aspects of the ascending aorta, supraposteriorly along the arch, and then down the left and posterior aspects of the descending aorta. The hematoma may then produce several serious sequelae (Fig. 41-1D). It may rupture into the pericardial space, causing tamponade, or into the pleural space with exsanguinating hemorrhage, especially in type B dissections (those beginning after the left subclavian artery). This occurs less frequently than expected because the adventitial layer represents 66% of the overall strength of the aortic wall. It may also cause occlusion of aortic branch arteries or prolapse of one or more of the aortic ...

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