Abdominal aortic aneurysm repair

🧬 The Widening Wall

• Focal aortic dilation > 3.0 cm or >50% of normal diameter; typically infrarenal.
• Pathophysiology: Chronic inflammation → ↑Matrix Metalloproteinases (MMPs) → degradation of elastin & collagen → wall weakening.
• Key Risks: Smoking (strongest), male sex, age >65, family history, atherosclerosis.

⭐ Law of Laplace ($T \propto P \times r$): As AAA radius (r) increases, wall tension (T) increases, driving further expansion and ↑ rupture risk.

🛡️ Pathophysiology - Wall Under Siege

• Chronic Inflammation: Infiltration of macrophages & T-cells into the aortic wall.
• Proteolytic Degradation: ↑ Matrix Metalloproteinases (MMPs) & elastases degrade elastin and collagen.
• Structural Failure: Leads to smooth muscle cell apoptosis and loss of wall integrity.
• Law of Laplace: Wall tension $T \propto P \times r$. As radius (r) ↑, tension (T) ↑, promoting expansion.

⭐ Location: Most AAAs are infrarenal, likely due to reduced vasa vasorum supply, leading to relative ischemia and wall weakness.

🤫 Clinical Manifestations - The Silent Killer

• Asymptomatic (Most Common):

  • Usually an incidental finding on imaging.
  • May present as a palpable, pulsatile abdominal mass.

• Symptomatic (Non-ruptured):

  • Constant, gnawing abdominal, flank, or back pain.
  • Suggests rapid expansion or impending rupture.

• Ruptured AAA (Classic Triad):

  • Sudden, severe pain.
  • Hypotension/shock.
  • Pulsatile mass.

⭐ The classic triad of rupture (pain, hypotension, pulsatile mass) is present in only ~50% of patients.

📏 Diagnosis - Sizing Up the Threat

• Initial Test & Screening: Abdominal Ultrasound (US).
• Pre-op Planning (Gold Standard): CT Angiography (CTA).
  • Defines anatomy: diameter, length, neck morphology, renal/iliac artery involvement.
• 💡 Aortic diameter > 3.0 cm is defined as an aneurysm.

⭐ Repair is indicated for aneurysms > 5.5 cm in men, > 5.0 cm in women, or those with rapid growth (>0.5 cm in 6 months or >1 cm/year).

🔪 Management: Open Repair vs. EVAR

⭐ > EVAR's primary long-term complication is endoleak: persistent blood flow into the aneurysm sac outside the stent-graft. Type II is most common (from lumbar/IMA back-bleeding) and often observed. Type I (inadequate seal) requires urgent intervention.

💥 Complications - The Aftermath

• Early (<30d): MI (most common cause of death), AKI, colon ischemia (IMA ligation), graft thrombosis, limb ischemia.
• Late (>30d): Aortoenteric fistula (herald bleed → massive GI bleed), graft infection (S. aureus), anastomotic pseudoaneurysm.
• EVAR-Specific: Endoleak (persistent blood flow into aneurysm sac), graft migration.

⭐ Bowel ischemia classically presents with bloody diarrhea and abdominal pain post-op, often involving the sigmoid colon (watershed area of IMA).

⚡ Biggest Takeaways

• Screening is a one-time ultrasound for men 65-75 who have ever smoked.
• Repair is indicated for diameter >5.5 cm, rapid growth (>0.5 cm/6 mo), or symptoms.
• The classic triad of rupture is hypotension, a pulsatile abdominal mass, and severe back/flank pain.
• EVAR has lower perioperative mortality but requires surveillance for endoleaks.
• Open repair risks include ischemic colitis (early) and aortoenteric fistula (late).
• Myocardial infarction is the leading cause of death post-operatively.