| Risk factors | • Chronic hypertension (strongest overall risk factor present in ≥70% of patients) • Underlying aortopathy (eg, Marfan syndrome) • Cocaine use • ‣ have increased risk • Pregnancy due to hormonal changes on aortic wall and hemodynamic stress of pregnancy and delivery • Athersclerosis • Male sex | | --- | --- | | Clinical presentation (complications section down ) | • Severe, tearing chest pain that radiates to the back or back pain, migratory pain may develop as dissection propagates • Maximal at onset
• ± Variation in SBP between arms >20 mm Hg or asymmetry of pulse due to involvement of the subclavian or between UL and LL due to involvement of iliac arteries
• Hypertension usually present but may have Hypotension on presentation suggesting aortic rupture or other complication (eg, cardiac tamponade, acute aortic regurgitation).
• Syncope occurs in approximately 10% of cases and may result from a pain-induced vasovagal response or an abrupt drop in brain perfusion due to a mechanical disruption of blood flow.
• Dissections can propagate proximally or distally causing ischemic symptoms in any organ | | Labs | • D-dimer elevation (sensitive but not specific) due to the presence of fibrin degradation products. | | Diagnosis | • ECG: normal or nonspecific ST-segment & T-wave changes depending on underlying comorbodities and wether coronary ostia are compromised or not. • Chest x-ray: mediastinal widening • CT angiography of the aorta (ie CT artorography) or TEE for definitive diagnosis→intimal flap and double aortic lumen. | | Treatment | • Pain control (eg, morphine) • Intravenous beta blockers (eg, esmolol) • ± Sodium nitroprusside (if SBP >120 mm Hg despite beta blockers) • Emergency surgical repair for ascending dissection (Type A) |
Stanford classification: Type A 60%
Dissections can propagate proximally or distally; therefore, a type B dissection may extend to involve the ascending portion, becoming a retrograde type A dissection.
intimal tears separating the true and false lumens of the ascending and descending aorta
<aside> 💡 Cocaine use is associated with aortic dissection in young patients
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<aside> 💡 Anterior chest pain occurs in less than half of patients with type B (descending) dissection, with back pain being more typical.
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Acute aortic dissection typically presents with sudden onset of tearing chest or back pain in the setting of severe hypertension. Upper extremity pulse deficits or differential blood pressure measurements are important clinical signs but are present only in a minority of patients; the absence of pain makes this diagnosis highly unlikely.
Sudden and transient increases in blood pressure—as can occur with cocaine use, power lifting, or intense coughing (eg, in the setting of an upper respiratory illness)—may encourage intimal tearing and initiation of aortic dissection.
In younger patients and those without hypertension, an underlying heritable disease of the aorta should be suspected (eg, Marfan syndrome, bicuspid aortic valve).
Fluid in the pleural space can occur due to hemothorax (as is likely in this patient with hypotension, suggesting blood resulting from rupture into the chest cavity) or from an inflammatory response in the adjacent pleura (pleural effusion).
Type A aortic dissection can sometimes extend into the carotid arteries and cause stroke; this is best evaluated using CT aortography.
Type A (ascending) aortic dissection is a surgical emergency with acute mortality rates of 1%-2% per hour after symptom onset.
The goals of initial therapy of aortic dissection regardless of type include:
Intravenous beta blockers (eg, labetalol, propranolol, esmolol) are preferred for initial therapy to reduce heart rate, SBP, and LV contractility. These effects lead to a decrease in the rate of rise in SBP (dP/dt) and in aortic wall stress.
Early identification of aortic dissection is essential because therapies for similarly presenting conditions (eg, aspirin and heparin for myocardial infarction; thrombolytics for pulmonary embolism or ischemic stroke) worsen outcomes and are contraindicated.
Anticoagulation should be avoided in aortic dissection because it may encourage extension of the dissection or aortic rupture.
CT angiography of the chest (CT aortography) is often the test of choice, but hypotensive patients are at risk of imminent cardiac arrest and cannot safely undergo prolonged imaging. For these patients, transesophageal echocardiography (TEE), often performed in the operating room while preparing for emergency surgery, is usually preferred. TEE allows for visualization of the dissection plane and confirms type A aortic dissection.
<aside> 💡 Type B dissections complicated by organ malperfusion benefit from urgent surgical or endovascular repair.
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Intraoperative transesophageal echocardiography is frequently performed to identify further abnormalities that may require intervention including aortic root/valve damage or tamponade.
Intravenous heparin, sometimes indicated in the treatment of PE or myocardial infarction, is contraindicated in aortic dissection due to concern for accelerating propagation of the dissection and increasing bleeding during operative repair.
Hyperlipidemia can result in the formation of plaque in the tunica intima of arterial walls. This plaque can contribute to the development of atherosclerosis, which increases the risk of aortic dissection. However, hyperlipidemia is not the strongest risk factor for this condition.