Mesenteric Ischemia Medical Slides
Generate publication-quality mesenteric ischemia lecture slides in 30 seconds. AI-powered content structured for clinical education.
Generate Mesenteric Ischemia DeckWhy teach Mesenteric Ischemia?
Acute mesenteric ischemia (AMI) has an overall mortality of 60-80%, primarily due to delayed diagnosis. AMI accounts for approximately 1 in 1000 hospital admissions, with SMA embolism (50%), SMA thrombosis (25%), non-occlusive mesenteric ischemia (20%), and mesenteric venous thrombosis (5%) as the four etiologies. CTA has become the diagnostic standard with sensitivity >95%. The critical teaching point is the "pain out of proportion to physical examination" — early recognition before bowel necrosis develops is the primary determinant of survival.
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Mesenteric Ischemia Presentation FAQ
How should the four etiologies be differentiated in mesenteric ischemia teaching?
Present the clinical differentiation: SMA embolism — sudden onset, atrial fibrillation/recent MI, proximal SMA occlusion (usually distal to middle colic origin, sparing proximal jejunum). SMA thrombosis — more insidure onset over hours, history of chronic mesenteric ischemia (postprandial pain, food fear, weight loss), occlusion at SMA origin (diffuse ischemia). NOMI — occurs in critically ill/low-flow states (sepsis, post-cardiac surgery, pressors), diffuse spasm without occlusion, treated medically (papaverine infusion, optimize cardiac output). Mesenteric venous thrombosis — subacute onset over days, hypercoagulable states, CT shows portal/SMV thrombus + bowel wall edema, initially treated with anticoagulation. Each etiology has different treatment — accurate classification is essential.
What is the role of second-look laparotomy and when should it be taught?
Present the second-look concept: after initial revascularization and bowel resection, plan a mandatory re-exploration at 24-48 hours to reassess bowel viability — demarcation of viable from non-viable bowel is often unclear at the initial operation. Indications: any case where bowel viability is questionable after revascularization, extensive ischemia requiring damage control, or hemodynamic instability preventing definitive resection. Technique: assess color, peristalsis, arterial pulsation, and use adjuncts (fluorescein, ICG angiography) to evaluate perfusion. Additional resection performed as needed. Damage control approach: resect obviously necrotic bowel, leave questionable segments, staple bowel ends (no anastomosis — create stomas only at second look when viability is confirmed). This approach reduces short gut syndrome.
How should emerging endovascular options be presented alongside open surgery?
Present the evolving role: SMA embolism — endovascular aspiration thrombectomy or catheter-directed thrombolysis (urokinase/TPA) is appropriate for patients WITHOUT peritoneal signs (no necrosis yet). Success rates of 70-90% for SMA recanalization. If peritoneal signs present → laparotomy for embolectomy + bowel assessment (cannot evaluate bowel viability endovascularly). SMA thrombosis — endovascular stenting of underlying stenosis, combined with open assessment if bowel viability is uncertain. Hybrid approach (angiography suite + OR, or OR with intraoperative angiography) is ideal. Meta-analyses suggest lower mortality with endovascular-first in selected patients (43% vs 53% for open surgery), but selection bias is significant. Teaching message: endovascular is complementary to, not a replacement for, surgical exploration when bowel necrosis is suspected.
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