Aortic Dissection and Aneurysm

Non-modifiable / structural

• Age and male sex: cumulative elastin fragmentation and medial degeneration; abdominal aortic aneurysm (AAA) is several-fold more common in men, and both dissection and AAA incidence rise steeply after age 60
• Heritable thoracic aortic disease: Marfan syndrome (FBN1/fibrillin-1, loss of TGF-β sequestration), Loeys-Dietz (TGFBR1/2), vascular Ehlers-Danlos (COL3A1), and familial nonsyndromic TAA — all produce cystic medial necrosis and root/ascending disease at young ages. The 2022 ACC/AHA Aortic Disease Guideline recommends genetic testing and screening imaging of first-degree relatives
• Congenital valvulo-aortic lesions: bicuspid aortic valve, coarctation, Turner syndrome — abnormal flow plus intrinsic medial abnormality dilates the ascending aorta
• Family history of aneurysm or dissection: independent risk factor even without a syndromic diagnosis

Modifiable

• Hypertension: the single most common risk factor for dissection; raises dP/dt and wall shear stress. Poorly controlled hypertension is the classic stem detail
• Smoking: the dominant modifiable driver of AAA growth and rupture via elastolysis and inflammation; underlies USPSTF one-time ultrasound screening of men 65–75 who have ever smoked
• Atherosclerosis/dyslipidemia: chiefly descending thoracic and abdominal disease
• Stimulants: cocaine and amphetamines cause abrupt catecholamine-driven pressure surges; also extreme isometric straining

Acquired and situational

• Inflammatory aortitis: Takayasu (young women, arch), giant cell arteritis, IgG4-related disease
• Infectious: syphilitic aortitis (obliterative endarteritis of vasa vasorum → tree-bark intima, ascending aorta/root); mycotic aneurysm from Salmonella or Staphylococcus seeding a diseased wall
• Trauma and iatrogenic: rapid deceleration injury tears at the aortic isthmus near the ligamentum arteriosum; cardiac catheterization, cross-clamping, and prior cardiac surgery cause iatrogenic dissection
• Pregnancy: third trimester/peripartum dissection, especially in Marfan or bicuspid valve
• Distractor: diabetes is inversely associated with AAA — do not treat it as a risk factor.

Aortic Dissection Mechanisms

• Intimal tear with blood penetration: High shear stress (typically from uncontrolled hypertension or aortic wall weakness) causes disruption of the intimal layer, allowing blood from the true lumen to dissect between the intima and media, creating a false lumen that may re-enter the true lumen distally (re-entry tear)
• Medial degeneration and weakening: Cystic medial necrosis (loss of elastic fibers and smooth muscle in the media) predisposes to dissection; occurs in conditions like Marfan syndrome, Ehlers-Danlos syndrome, Loeys-Dietz syndrome, and with advancing age and chronic hypertension
• Increased wall stress: Hypertension, aortic stenosis, and hypercontractile states (pregnancy, cocaine use) increase dP/dt (rate of pressure change) and wall shear stress, precipitating intimal disruption
• Propagation dynamics: The dissection plane extends along tissue planes of weakness; proximal extension may compromise aortic root and coronary ostia; distal extension may occlude branch vessels (subclavian, carotid, renal, iliac arteries)
• False lumen hemodynamics: The false lumen may remain patent, thrombose, or rupture; a patent false lumen with bidirectional flow has worse prognosis than a thrombosed false lumen

Aortic Aneurysm Mechanisms

• Degenerative loss of elastic fibers: Breakdown of elastin and collagen in the media leads to loss of elastic recoil and progressive dilation; smoking, atherosclerosis, and chronic inflammation accelerate this process
• Inflammatory and enzymatic degradation: Increased metalloproteinase activity degrades structural proteins; elevated inflammatory cytokines promote smooth muscle apoptosis and weakening
• Hemodynamic stress and Laplace's Law: Wall tension = (Pressure × Radius) / (2 × Wall thickness); as radius increases, tension increases exponentially, promoting further dilation in a vicious cycle
• Genetic predisposition: Connective tissue disorders, family history, and specific genetic mutations (fibrillin-1, collagen mutations) increase aneurysm risk and may cause early-onset disease
• Smoking and atherosclerotic damage: Nicotine-induced vascular inflammation, increased oxidative stress, and atherosclerotic plaque formation weaken the aortic wall

Aortic Dissection

• Sudden-onset severe chest pain (80-90% of cases): Typically described as "tearing," "ripping," or "knife-like"; maximum intensity at onset (unlike MI which crescendos); often radiates to the back, particularly the interscapular region; may migrate as dissection propagates
• Hypertension and pulse deficits: Elevated blood pressure is present in ~60% of cases (though hypotension suggests rupture or tamponade); blood pressure differential >20 mmHg between arms is a classic sign; diminished or absent pulse in one or more extremities may occur if dissection compromises branch vessels
• Neurological symptoms: Depends on branch vessel involvement—stroke (carotid involvement), spinal cord ischemia (paraplegia from intercostal/lumbar artery compromise), Horner's syndrome (left-sided dissection affecting sympathetic fibers)
• Cardiac complications: Acute aortic regurgitation (if proximal dissection extends to aortic root), myocardial infarction (if dissection involves right or left main coronary artery ostium), acute heart failure
• Visceral malperfusion: Mesenteric ischemia (abdominal pain, bloody diarrhea), renal infarction (flank pain, hematuria), limb ischemia
• Syncope or altered mental status: Suggests aortic rupture, tamponade, or stroke
• Important pearl: Absence of chest pain does NOT rule out dissection; up to 10% present without severe pain, particularly in elderly patients, those with diabetes, or after cardiac surgery

Aortic Aneurysm

• Often asymptomatic: Many AAAs are discovered incidentally on imaging for unrelated complaints; asymptomatic AAAs may grow silently for years
• Abdominal or back pain: Occurs when aneurysm expands or approaches rupture; pain is typically steady, differs from dissection's maximal onset
• Pulsatile abdominal mass: Palpable on exam if aneurysm is large; but absence does not exclude disease
• Rupture presentation: Hypotension, flank pain, pulsatile abdominal mass, syncope (classic triad); mortality approaches 80-90% if transport to OR is delayed
• Distal embolization: Small thrombi from aneurysmal wall may lodge in distal vessels, causing acute limb ischemia ("trash foot")

Aortic Dissection

• CT angiography (CTA) with IV contrast: Gold standard diagnostic test with sensitivity and specificity >95%; visualizes the intimal flap, true and false lumens, and extent of dissection; should include imaging from arch to iliac bifurcation; rapidly obtained and widely available
• Transesophageal echocardiography (TEE): Excellent for proximal aorta (ascending aorta and aortic root); sensitivity 85-98%, specificity 85-90%; particularly useful intraoperatively for surgical patients; less useful for distal descending aorta
• MRI/MRA: Highest sensitivity and specificity (>98%) but time-consuming and not suitable for unstable patients; gold standard for follow-up of chronic dissection
• Chest X-ray: Nonspecific; may show widened mediastinum, left pleural effusion, or displacement of trachea; not diagnostic but may increase suspicion
• ECG: Typically normal or shows LVH; may show inferior MI if right coronary artery is involved; helps distinguish from ACS
• D-dimer: Elevated in nearly all acute dissections; high negative predictive value makes it useful as a screening tool when clinical suspicion is low; however, should NOT delay imaging if clinical suspicion is high
• Classification systems: Stanford system (Type A = involvement of ascending aorta regardless of origin; Type B = descending aorta only) is most clinically relevant; determines whether surgery is needed; DeBakey system (Type I = entire aorta; Type II = ascending aorta only; Type III = descending aorta) is less commonly used clinically

Aortic Aneurysm

• Abdominal ultrasound: First-line screening modality for AAA; sensitivity 95-100%, specificity 98-100%; measures maximum anteroposterior diameter; used in screening programs
• CT angiography: Most accurate for size, extent, and surgical planning; evaluates relationship to renal arteries and other branch vessels; required before surgical repair
• MRA: Useful for follow-up in patients with renal insufficiency (avoid iodinated contrast); also assess for other vascular pathology
• Size criteria: Aneurysm defined as >3 cm diameter; risk of rupture increases dramatically when >5.5 cm in diameter; growth rate >0.6 cm per 6 months indicates higher rupture risk

Aortic Dissection

• Immediate blood pressure and heart rate reduction: Goal is to reduce dP/dt (rate of pressure change) to minimize shear stress on the aortic wall
• Beta-blockers: Start first-line (e.g., IV labetalol 10-20 mg, repeat every 10-20 minutes to target

Dissection — emergencies (all Stanford type A until proven otherwise)

• Hemopericardium with tamponade: rupture of the false lumen into the pericardial sac; hypotension, JVD, muffled heart sounds, pulsus paradoxus, electrical alternans. Pericardiocentesis is generally avoided — definitive treatment is emergency operative repair per the 2022 ACC/AHA Aortic Disease Guideline
• Acute aortic regurgitation: annular distortion or flap prolapse; new early diastolic decrescendo murmur with wide pulse pressure and flash pulmonary edema
• Coronary ostial involvement: most often the right coronary → inferior ST elevation. This is why an inferior MI pattern plus tearing back pain must not be sent for thrombolysis
• Rupture into pleura/mediastinum: hemothorax (usually left), widened mediastinum, shock
• Malperfusion syndromes: stroke or Horner syndrome (carotid/sympathetic), paraplegia (intercostal/lumbar segmental arteries), mesenteric ischemia with pain out of proportion and lactic acidosis, renal infarction, acute limb ischemia — a complicated type B dissection and an indication for intervention rather than medical therapy alone
• Late: aneurysmal degeneration of a patent false lumen, recurrent dissection, chronic pain

Aneurysm

• Rupture (emergency): Laplace's law failure; retroperitoneal bleed with hypotension, back/flank pain, pulsatile mass — no imaging delay if unstable
• Aortoenteric fistula: erosion into duodenum (classically after graft repair); herald bleed then massive GI hemorrhage
• Aortocaval fistula: continuous abdominal bruit, high-output heart failure, leg edema
• Mural thrombus embolization: trash foot, livedo, blue toes
• Inflammatory/retroperitoneal fibrosis variant: ureteral entrapment with hydronephrosis

Treatment-related

• Vasodilator before beta blockade: nitroprusside alone causes reflex tachycardia and increased dP/dt — beta blocker first
• Spinal cord ischemia after TEVAR/open thoracic repair: segmental artery sacrifice; managed with CSF drainage and blood pressure augmentation
• Endoleak, graft infection, retrograde type A dissection after TEVAR; ischemic colitis after AAA repair (bloody diarrhea, left colon), contrast nephropathy, and abdominal compartment syndrome

• The buzzword triad: abrupt tearing/ripping pain maximal at onset, radiating interscapularly, with a >20 mmHg inter-arm blood pressure differential or pulse deficit. MI pain crescendos; dissection pain peaks instantly
• Single best next step: hemodynamically stable with high suspicion → CT angiography of the whole aorta; unstable/cannot leave the resuscitation bay → TEE at bedside. The 2022 ACC/AHA Aortic Disease Guideline supports immediate imaging over serial biomarkers
• Stanford drives management: type A = emergency open surgical repair; uncomplicated type B = medical therapy (beta blocker first for dP/dt, then vasodilator), with TEVAR for malperfusion, rupture, or refractory pain/hypertension
• The association examiners test: young tall patient with arachnodactyly, lens subluxation, and a new diastolic murmur = Marfan syndrome (FBN1) with root dilation and cystic medial necrosis. Beta blockers or ARBs slow root growth, and repair thresholds are lower than in degenerative aneurysm
• Screening: USPSTF recommends a one-time abdominal ultrasound in men 65–75 who have ever smoked; it recommends against routine screening in women who have never smoked and have no family history
• Repair thresholds: infrarenal AAA at about 5.5 cm in men (or rapid interval growth or symptoms) per Society for Vascular Surgery/ACC-AHA; ascending aortic aneurysms are repaired at smaller diameters in heritable thoracic aortic disease and at experienced centers
• Distractors to reject: aspirin, heparin, or fibrinolytics for the "inferior MI" that is really a type A dissection; nitroprusside or hydralazine before beta blockade (reflex tachycardia worsens shear); pericardiocentesis for tamponade from type A dissection; and calling absent chest pain reassuring — painless dissection occurs, especially in the elderly
• Two drug-safety facts: avoid fluoroquinolones in known aneurysm or connective tissue disease (FDA aortic warning), and pursue aggressive smoking cessation, the only intervention shown to slow AAA expansion