Mesentric ischemia
- 1. MESENTERIC ISCHEMIA DR. WALID GANOD NOV. 2019
- 2. ANATOMY: Celiac Artery : T12, L1 - Three branches : left gastric , Splenic . Common hepatic A - 25% true trifurcation , 65-75% left gasric branch first - Presence of fourth branch : dorsal pancreatic , middle colic 5-10% - 18-20 % of hepatic branches originating from SMA - Common hepatic A from SMA 2.5% - Accessory or replaced right or left hepatic artery from SMA 14-18%
- 3. SMA & IMA marginal A of drummond # meandaring A. (arc of riolan )
- 4. CLINICAL ANATOMY • Typicaly SMA embolus ludges just beyond first few jejunal branches as SMA tapers ----------------Sparing of proximal jejunum from ischemia • In acute thrombotic occlusion usually involve the origin of SMA –widespread ischemia
- 5. CLASSIFICATION OF MI • Arterial : (most common) - Occlusive MI • Acute: (surgical emergency) Embolic 40-50% or thrombotic 20-35% • Chronic Atherosclerotic 90% or non atherosclerotic - Non occlusive MI : colonic ischemia after aortoiliac surgery and abdominal compartment syndrome • MI due to Venous thrombosis
- 6. ACUTE MESENTERIC ARTERIAL EMBOLISM • Most emboli originate from the cardiac • associated with atrial fibrillation, myocardial dysfunction, poor ejection fraction, or cardiac valves due to endocarditis. • Occasionally emboli generated from an atherosclerotic aorta. • The majority of emboli lodge 3 to 10 cm distal to the origin of the SMA • classically sparing the proximal jejunum and colon. • 20% of emboli to the SMA are associated with concurrent emboli to another arterial bed including the spleen, or kidney.
- 7. ACUTE MESENTERIC ARTERIAL THROMBOSIS • occurs at areas of severe atherosclerotic narrowing, (origin of the SMA) named osteal stenosis • ischemia usually develops from the proximal jejunum to the mid- transverse colon • Dehydration, low cardiac output and hypercoagulable states are major contributing factors to thrombosis as patient had good collateral. • SMA thrombosis may also occur due to vasculitis, mesenteric dissection, or a mycotic aneurysm.
- 8. CHRONIC MESENTERIC ISCHEMIA • Atherosclerosis is the most common cause of CMI, • Patient H/O smoking, hypertension, and hyperlipidemia. • PMH : coronary, cerebrovascular, renal, aortoiliac, and other peripheral arteries disease • Non atherosclerotic CMI as vasculitis, lupus, Buerger disease, and radiation arteritis. • Median arcuate ligament syndrome
- 9. MESENTERIC VENOUS THROMBOSIS • 5 to 15% of cases of mesenteric ischemia • -------impaired venous outflow--------visceral edema, mucosal sloughs, hemorrhage and abdominal pain. • primary ( idiopathic) thrombosis • Secondary : 90% of cases are related to thrombophilia, trauma, or local inflammatory changes ( pancreatitis, diverticulitis, inflammation or infection in the biliary system), obesity or hypercoagulable state. • Patients typically have a response to anticoagulation (usually for life) in combination with treatment for the underlying local or systemic processes. • Surgical intervention is reserved for patients who are critically ill or whose condition is deteriorating.
- 10. THE THREE CLINICAL PHASES OF ACUTE EMBOLIC MI Phase 1 is the hyper-peristaltic phase: severe abdominal pain and minimal abdominal findings, forceful bowel emptying (vomiting and/or diarrohea) and the presence of a source of embolus (e.g. atrial fibrillation). Phase 2 is the paralytic phase Bowels distended and silent abdomen. The pain intensity often decreases. Phase 3 is the peritonitis phase continuous pain, peritonitis, rapid general deterioration and acidosis.
- 11. CLINICAL PRESENTATION • Classically, the pain is out of proportion to the findings on physical • examination. • Other late findings include fever, oliguria, dehydration, confusion, tachycardia, and shock • Metabolic abnormalities can include leukocytosis, metabolic acidosis, hyperamylasemia, elevated liver function values, and lactic acidemia.
- 12. patients with NOMI • critically ill, hospitalized, intubated patients who experience a sudden deterioration in their clinical condition. These patients are often administered intravenous vasopressors, worsening mesenteric vasoconstriction and thus decreasing splanchnic perfusion patients with MVT, • fever, abdominal pain and distention, nausea/vomiting, and bloody stools are most common findings. • nonspecific, normal D-dimer levels may help rule out MVT.
- 13. CMI • Postprandial abdominal pain and Progressive weight loss are the most common symptoms • Pain is often described as dull and crampy located in the mid epigastric region. • Pain often occurs 15 to 45 minutes after a meal, Patients typically develop “food fear” • Weight loss can help to distinguish CMI from other functional bowel disorders • Changes in bowel habits, nausea, and vomiting are less common findings. • CMI is seen more frequently in elderly women 70%
- 14. LABORATORY EVALUATION • AMI cause many laboratory changes but non specific • Most times associated with persistent leukocytosis >15000 , and heamoconcentration • Elevation of Intestinal fatty acid binding protein offer some promise as diagnostic tool • albumin, transthyretin, transferrin, and C-reactive protein, are the only studies of value in cases of chronic mesenteric ischemia,
- 15. NON INVASIVE STUDY • Pain x-ray : in late stage , free air , small bowal obstruction • Duplex U/S : need fasting well prepared patient and long time with pressure on abd. So reserved for evaluation of patients with CMI and for monitoring after intervention. • CT angio : failure of proximal mesenteric vessel to opacify, bowel edema , stranding in mesentery, pneumatosis are clue to diagnosis with 95 to 100% accuracy
- 16. INVASIVE EVALUATION • Conventional angiography remains the “gold standard” with Anteroposterior and lateral views of the visceral aorta • Selective catheterization of the celiac trunk, SMA, and IMA, provide the most accurate and specific localization of stenotic and occlusive lesions. • Therapeutic alternatives such as balloon angioplasty, stenting, and thrombolysis and percutaneous thrombus extraction can all be used to restore luminal visceral blood flow.
- 17. MANEGMENT : • The goal of therapy for patients with mesenteric ischemia is the prompt restoration of blood flow to the visceral organs not resection of ischemic visceral ONLY. • Medical treatment alone is not effective in patients with symptomatic mesenteric ischemia.
- 18. MEDICAL MANEGMENT : Before Operation • invasive monitoring, aggressive fluid resuscitation with restoration of adequate urine output is required, • Electrolyte abnormalities and metabolic acidosis should also be corrected. • Broad-spectrum intravenous antibiotics with aggressive fluid resuscitation can lead to decreased mortality in these patients. • Treatment against gram-negative and anaerobic organisms is especially important. • Patients are also started and maintained on palvix, aspirin and high dose statins indefinitely.
- 19. Endovascular Therapeutic Options In Acute Or Chronic Mesenteric Ischaemia • In those with short segment stenoses, cardiac and pulmonary co-morbidities, prior abdominal surgery, coagulopathy, or malnutrition, endovascular therapy is often favored • Balloon angioplasty and stenting has favored than open surgery as the dominant method of revascularization for CMI ACCE SS TO THE SMA • via the femoral and brachial routes, although sometimes local exposure of the SMA in • the abdomen is also needed. Brachial access may be preferable.
- 20. ASPIRATION EMBOLECTOMY OF SMA • Endovascular aspiration embolectomy is a treatment option in patients without peritonitis. LOCAL SMA THROMBOLYSIS • In cases of incomplete aspiration embolectomy or distal embolization, local thrombolysis is a viable treatment alternative in patients without peritonitis. RECANALIZATION & STENTIN G OF THE SMA after removal of a thrombotic clot by aspiration or thrombolysis.
- 21. CASE 1 • A patient with acute on chronic mesenteric ischaemia who had first undergone an exploratory laparotomy and resection of the distal small bowel and proximal large bowel due to mesenteric ischaemia. • Post-operative CT angiography identified a 7 cm long thrombotic occlusion from the origin of the SMA. • The arrow indicates the calcified SMA mixed with thrombotic clots (a).
- 22. • Recanalization and stenting of the proximal part of the occlusive SMA lesion was performed but was complicated by a long dissection (multiple black arrows) ending up with an occlusion of the distal part of the SMA • Re-exploratory laparotomy was performed and the entire small bowel was ischemic.
- 23. • A peripheral arterial SMA branch was punctured and a guidewire entered the true lumen up to the aorta and snared with devices from a transfemoral approach, creating a through-and-through access. • The long dissection was stented extensively from the true lumen from the aorta into a non-dissected site in the ileocolic artery • The patient is still alive and has been asymptomatic during the 4 years of follow-up with repeated CT angiographies.
- 24. SURGICAL THERAPY A.Exploration and define the cause • Confirm the cause and extent of mesenteric occlusion • Assessment of bowel viability by inspection • If no frank necrosis or perforation, start by revascularization before resection, otherwise resect of affected part without contamination
- 25. B. REVASCULARIZATION 1- SMA embolectomy 2- SMA bypass - supra celiac aorta inflow - Infra renal aorta inflow - Iliac artery inflow
- 26. C. Determine of intestinal viability D. Second look surgery E. Mangment of short bowal syndrome
- 27. THANKS