الفهرس 
ANATOMY OF THE AORTAOnly 14 pages are availabe for public view
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Abstract
Aortic dissection occurs when a tear in the aortic intima exposes the underlying media to the hydrodynamic forces of blood within the aortic lumen leading to dissection within the media. A false lumen is created by blood filling the space within the media between the intimal flap and the adventitia.
The documented incidence is approximately 2.9 per 100,000 per year. The peak incidence of aortic dissection is in the sixth and seventh decades of life, with a mean age of 62 years. Overall, men are affected twice as often as women (68% vs. 32%).
Aortic dissection is classified as acute or chronic based upon the duration of symptoms at presentation. Frist the Stanford classification of aortic dissection distinguishes between type A and type B; Type A means the dissection includes the ascending aorta and Type B dissection does not involve the ascending aorta. While the De Bakey classification subdivides the dissection process in Type I dissection involving the entire aorta, Type II dissection involving only the ascending aorta and Type III dissection sparing the ascending aorta and the arch.
All mechanisms that weaken the aortic wall lead to higher wall stress, which can induce aortic dilatation and aneurysm formation, eventually resulting in aortic dissection or rupture as hypertension, which is the most common clinical predisposing factor for aortic dissection, also, three major inherited connective tissue disorders are currently known to affect the arterial walls: (1) Marfan’s syndrome, (2) Ehlers-Danlos syndrome, and (3) familial forms of thoracic aneurysm and dissection.
The diagnosis of acute aortic dissection requires high index of suspicion. The most common initial symptom of acute aortic dissection is severe migrating back or chest pain (up to 96% of cases). Dyspnea, orthopnea and dysphagia may also be presnt. Neurological symptoms such as transient syncope or stroke are often dramatic and may dominate the clinical picture and mask the underlying condition. Pulse deficits on physical examination are important clues for diagnosis.
Chest radiography and ECG do not have a definitive role in suspected aortic dissection because they are often nonspecific. Transthoracic/transoesophageal echocardiography, contrastenhanced CT, MRI and aortography are currently used to confirm the diagnosis.
All patients in whom acute aortic dissection is strongly suspected should immediately be placed in an acute-care setting for monitoring of blood pressure, cardiac rhythm and urine output. Initial therapeutic aims include elimination of pain and reduction of systolic blood pressure to 120 mm Hg or less, or the lowest level commensurate with adequate vital organ (cardiac, cerebral, renal) perfusion, by the use of intravenous β-blockers.
Type A dissection is a surgical emergency. The aims of definitive surgery usually include resection of the most severely damaged segment of the aorta, excision of the intimal tear, and obliteration of entry to the false lumen by suturing the edges of the dissected aorta both proximally and distally. After resection of the segment containing the intimal tear (typically a segment of the ascending aorta in proximal dissection or of the proximal descending aorta in distal dissection), aortic continuity is eventually re-established by interposition of a prosthetic sleeve graft.
In uncomplicated type B dissection medical treatment in the form of beta blockers, aiming at optimal blood pressure control is the treatment of choice.
Endovascular techniques, more recently, intraluminal stent-grafts placed percutaneously via a transfemoral catheter have been introduced in patients with type B dissection as a potential alternative to surgical repair or medical therapy alone. The aim of this procedure is to close the site of entry to the false lumen using a tube-like nitinol grid covered with a Dacron shell, and induce complete thrombosis of the false lumen followed by remodelling of the aortic wall.