Aortic Dissection

Imaging makes the diagnosis - CT aortography or TEE identifies the intimal tear, establishes the Stanford class, and detects valve or branch involvement. An acute infarct pattern is on the ECG in 8% of dissections, and absence of a widened mediastinum on chest radiograph does not exclude it.

TEE when the patient is unstable - TEE is the recommended modality in instability, and also in renal insufficiency or contrast allergy. It doubles as intraoperative visualization.

Both arms, every time - More than 20 mmHg of inter-arm systolic difference raises suspicion for dissection, so a single-arm pressure cannot be trusted as the perfusion number.

Rate and pressure targets - A short-acting IV beta blocker to a heart rate near 60 reduces aortic wall tension and limits extension. If systolic pressure remains elevated, nitroprusside is added for a systolic goal of 100 to 120 mmHg, held there only as long as mentation and urine output are preserved. Esmolol, labetalol, and diltiazem are alternatives, and non-dihydropyridine calcium channel blockers cover a beta blockade contraindication.

Caution with acute aortic regurgitation - Beta blockade removes the compensatory tachycardia that is maintaining forward flow.

Do not reach for an inotrope - Inotropes increase the force and rate of ventricular contraction and worsen aortic wall stress. Treat hypotension with IV fluid first; vasopressors can be added to maintain perfusion but may propagate the false lumen.

Analgesia is hemodynamic therapy - Morphine is preferred because it lowers sympathetic output as well as treating the pain.

Lines and endpoints - Arterial line and central venous catheter for monitoring, plus a Foley to follow urine output as a perfusion endpoint.

Baseline neurologic exam - Neurologic deficits are present in one fifth of patients at presentation, and syncope is common. Document what is there before induction.

Hypotension is a grave sign - In a dissection it most likely indicates rupture.

Know which repair you are in - Ascending dissection is a surgical emergency: excision of the intimal tear, obliteration of the proximal false lumen entry, and interposition graft, often with aortic valve replacement. Descending dissection is repaired only for a complicated course, increasingly by TEVAR, and carries a risk of paraplegia.

Painless presentations exist - About 10% of dissections are painless, more commonly in Marfan syndrome.

Aortic dissection starts with a tear in the intima. Blood enters the intima-media space under pressure and splits the wall, creating a false lumen that is usually larger than the true lumen and that propagates antegrade, retrograde, or both. Most tears begin in the ascending aorta at the right lateral wall, where shear force is greatest, and ascending dissections are almost twice as common as descending ones.

Chronic hypertension is the single most important risk factor, damaging the aortic media directly and stiffening the wall. Aging, connective tissue disease such as Marfan, Ehlers-Danlos, Loeys-Dietz, and Turner syndromes, and congenital lesions including bicuspid aortic valve and coarctation also weaken the media. Propagation is what kills: branch occlusion produces coronary, cerebral, spinal, or visceral ischemia, and a proximal dissection can cause acute aortic regurgitation, cardiac tamponade, or rupture.