The challenge in managing acute aortic syndrome, especially dissection, is an appropriate clinical suspicion and action in pursuing rapid diagnosis and therapy60,76.
Typical features of dissection are the acute onset of chest and/or back pain of blunt, severe, and sometimes radiating and migrating nature. A history of or signs of chronic hypertension are common if obvious signs of connective tissue disorders are absent. Clinical manifestations of acute aortic dissection are often dominated by the anatomicopathological characteristics of specific malperfusion syndrome from dissection-related sidebranch obstruction. Up to 20% of patients with acute aortic dissection may present with syncope without a history of typical pain or neurological findings4,10-13,60,76. Cardiac tamponade may result in hypotension and syncope2,62. Syncope may also result from severe pain, obstruction of cerebral vessels, or activation of aortic baroreceptors. After an initial dominance of chest or back pain, cardiac failure may become the main symptom and is usually related to severe aortic regurgitation2,60,62. Cerebrovascular manifestations and limb ischemia with pulse deficits are caused by involvement of a sidebranch orifice into the dissection or obliteration of the true lumen by an expanding false lumen61,66. Paraplegia may emerge if too many pairs of intercostal arteries are separated from the aortic truelumen.
Recurrent abdominal pain, elevation of acute phase proteins, and increase of lactate dehydrogenese are indicators of involvement of either the celiac trunk observed in about 8% or the mesenteric artery in 8-13%. Involvement of the renal arteries may result in oliguria or anuria76,77. Further propagation of the dissection will usually result in repetitive bouts of acute pain often along with a deteriorating clinical picture3. Dissection from trauma, after valve replacement or from iatrogenic causes, is usually obvious; however, dissection after aortic (valve) surgery is less frequent and easily overlooked63,78.
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