Rutherford's 133: Acute Mesenteric Ischemia: Epidemiology, Pathophysiology, Clinical Evaluation, Rx скачать в хорошем качестве

Rutherford's 133: Acute Mesenteric Ischemia: Epidemiology, Pathophysiology, Clinical Evaluation, Rx

#AcuteMesentericIschemia #AMI #VascularSurgery #BowelIschemia #CTA #Embolism #Thrombosis #NOMI #Diagnosis #Treatment #SecondLookSurgery #DrGregoryWeir #RutherfordChapters This summary is based on excerpts from a YouTube transcript discussing Acute Mesenteric Ischemia (AMI) from Rutherford's Vascular and Endovascular Therapy 10th Edition. AMI is a critical condition where blood flow to the intestines is suddenly cut off or severely reduced. Historically, mortality was very high (70-90%), improving to around 50% with angiography and surgery, but still remains significant (17-21% in-hospital mortality with revascularization today). AMI is relatively rare, affecting less than one in a thousand hospital admissions. It is seen more often in older patients with multiple health problems and is notably three times more common in women than men, though the reason is not specified. The main causes are: 1. *Arterial Embolism:* A clot travels from elsewhere (often the heart, e.g., AFib) and blocks a mesenteric artery, frequently the superior mesenteric artery (SMA). This often causes sudden, severe pain. 2. *Arterial Thrombosis:* A clot forms directly in a mesenteric artery already narrowed by atherosclerosis (plaque buildup). This may be more common now and can have a slower onset due to existing collateral vessels. 3. *Non-occlusive Mesenteric Ischemia (NOMI):* Caused by severe vasospasm (artery narrowing) without a physical blockage. This accounts for about 20% of cases and has the highest mortality, typically occurring in critically ill patients with shock or severe low blood pressure. Regardless of the cause, the result is bowel ischemia, insufficient blood flow to the intestines. The gut has some reserve capacity but prolonged ischemia leads to damage, starting with the inner lining (mucosa). Symptoms are often vague initially, like general abdominal pain, nausea, or vomiting, and there may be pain out of proportion to physical findings. Diagnosis can be delayed in up to 60% of cases, which significantly impacts survival. Laboratory tests are not definitive but can indicate severity (e.g., high white blood cell count, acidosis, high lactate). Imaging is crucial. CT Angiography (CTA) is now the cornerstone for diagnosis due to its speed, accuracy, and ability to show arteries, veins, bowel wall changes, and rule out other causes. MRA is an alternative but less practical acutely. Traditional angiography is used more for intervention or diagnosing NOMI spasm patterns. Plain x-rays and ultrasound have limited roles acutely. Treatment focuses on rapid restoration of blood flow (revascularization) and managing bowel damage. Immediate steps include resuscitation, fluids, broad-spectrum antibiotics, and heparin. For NOMI, treating the underlying critical illness is primary. Revascularization for embolism or thrombosis can be achieved through open surgery (embolectomy or bypass) or increasingly, endovascular procedures (thrombolysis, mechanical thrombectomy, angioplasty, stenting). A hybrid approach called ROMs is also used. After restoring flow, assessing bowel viability is essential. Surgeons inspect the bowel and aim to conserve tissue. A planned second look operation (returning to surgery later) is crucial to identify what bowel recovered and what definitively needs removal, helping prevent devastating short gut syndrome. Long-term surveillance, often with Duplex ultrasound, is needed to check for graft or stent problems. A multidisciplinary approach guided by algorithms is key for managing this complex and serious condition. Progress has improved outcomes, but it remains a major challenge.