1	"Thomas S" Thomas S. Huber, MD, PhD Professor of Surgery Department of Surgery University of Florida College of Medicine
2	Outline Introduction. Chronic mesenteric ischemia. Acute mesenteric ischemia. Colon ischemia.
3	Introduction Mesenteric ischemia – inadequate blood flow to the intestine. Clinical presentation – acute, chronic. Clinical concerns. CMI - postoperative MOD. AMI - diagnosis and postoperative MOD.
4	Pathophysiology of CMI Failure to achieve normal postprandial hyperemic intestinal arterial flow.
5	Pathophysiology of CMI Resting intestinal blood flow modest – increases markedly postprandial. Hyperemic response varies with the size and composition of the meal. Majority of hyperemic flow increase in the small bowel and pancreas. Hyperemic changes are maximal 30 - 90 minutes postprandial.
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7	Pathophysiology of CMI Symptoms usually do not occur unless 2/3 major vessels diseased. Symptoms may occur with single vessel disease in the absence of collaterals. SMA involvement most worrisome. CMI unusual with uninvolved SMA.
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10	Etiology of Visceral Occlusion Atherosclerosis.* Fibromuscular disease. Neurofibromatosis. Visceral artery dissection. Buerger’s disease. Radiation injury. Rhematologic disorders. Drug induced - cocaine/ergots.
11	Visceral Atherosclerosis 5 - 10% of autopsy series with one visceral vessel with > 50% stenosis. Prevalence increases with age Associated with systemic disease. Same atherosclerotic risk factors.
12	Clinical Presentation of CMI Characteristic patient – middle aged/female/smoker. Abdominal pain. Postprandial pain → persistent. Non-specific. Food avoidance → weight loss.
13	Diagnostic Evaluation for CMI Evaluation for abdominal pain/weight loss → malignancy workup. Ultrasound. EGD/colonoscopy. CT scan. Visceral artery occlusions. Mesenteric duplex → screening. CT arteriography. Catheter-based arteriography
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15	Treatment CMI All patients require revascularization. Natural history of untreated CMI. Death from inanition. Death from acute mesenteric ischemia. No role for total parenteral nutrition. Endovascular treatment has emerged as first option.
16	Endovascular Treatment for CMI Decreased mortality rate. Decreased complication rate. Decreased LOS. Decreased patency rates. Recurrent stenosis ≠ recurrent symptoms.
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19	Open Treatment for CMI Reserved for patients that are not endovascular candidates. Endovascular failures. Flush SMA occlusion. Long-segment SMA occlusion.
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22	Postoperative - Open Profound IR injury. Activation of inflammatory mediators. Pulmonary injury/ARDS common. Multisystem organ dysfunction common. Prolonged ileus. Graft thrombosis (AMI) vs IR injury.
23	MOD - Open Revascularization
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26	Postoperative - Open Support individual organ systems. Standard ventilator wean. Expectant management of coagulopathy/thrombocytopenia. Total parenteral nutrition. Assessment of graft patency with changes in clinical status.
27	Long-term Outcome 5-yr graft patency rates 75% for open. 5-yr patency rates < 75% endo. 5-yr survival 75%. Patients resumed preoperative weight. Small percentage with refractory diarrhea.
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30	Acute Mesenteric Ischemia Mesenteric embolus – 50%. In situ thrombosis – 25%. Non-occlusive mesenteric ischemia – 20%. Mesenteric venous thrombosis – 5%. Other.
31	Pathophysiology of AMI Impaired perfusion → mucosal compromise. Release of intracellular contents and influx of substances with bowel lumen. Activation of inflammatory response → local/distant organ injury.
32	AMI Embolus Pathophysiology Emboli lodge in SMA (macro emboli). Cardiac source – MI, atrial fibrillation, ventricular aneurysm. Frequently have other emboli. Extent of bowel ischemia/infarction Duration (6 – 12 hour window). Collaterals. Pattern.
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34	AM Presentation (Embolus) Acute abdominal pain – “pain out of proportion” to examination. No specific features – peritoneal signs late Examination confound by critical illness. Laboratory signs non-specific. Index of suspicion – MI, ESRD, CABG.
35	AMI Diagnosis (Embolus) CT arteriography (no oral contrast). “Meniscus sign” in SMA. Bowel wall thickening. Organ infarction. Hepatic/portal venous gas. Catheter arteriography. Laparoscopy. Laparotomy.
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37	AMI Embolus Treatment *Emergent open revascularization. Preoperative medical management. Anticoagulation. Antibiotics. Volume resuscitation.
38	AMI Embolus Treatment - Bowel Resect all obvious dead bowel → proximal and distal stomas. Reassess ischemic bowel after revascularization. Role of second-look (24 – 48 hrs). Decision at time of initial procedure. Clinical judgment best predictor.
39	Postoperative – AMI (Embolus) Similar to CMI with IR injury – higher incidence of organ dysfunction. Abdominal compartment syndrome. Broad spectrum antibiotics. Lifetime anticoagulation.
40	Outcome – AMI (Embolus) Mortality rate 70% (all causes). Stable rate historically. Lead cause of death MOD. Breakdown by etiology. Mesenteric venous – 32%. Embolus - 54%. NOMI – 74%. In situ thrombosis – 77%.
41	AMI in Situ Thrombosis Mechanism similar to CMI – 50% with symptoms consistent with CMI. Presentation, diagnosis, treatment, and postoperative care similar to AMI. Diagnosis of embolus/in situ thrombosis may be confusing – history. Management of isolated bowel infarct.
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43	AMI NOMI Pathophysiology Paradoxical vasoconstriction with loss of autoregulation. Shock → vasoconstriction to maintain cerebral/cardiac perfusion. Persistent vasoconstriction → NOMI. Etiology – any factor that causes shock.
44	AMI NOMI Presentation/Dx Critically ill patient – physical examination/laboratory studies consistent with intra-abdominal process. Catheter arteriography. Segmental stenosis of SMA (“string of beads”) Spasm of mesenteric arcades. Impaired filling of intramural branches.
45	AMI/NOMI Treatment Correct the underlying condition. Volume resuscitation. Wean vasopressors. Antibiotics. Anticoagulation. Catheter arteriography and intra-arterial vasodilators. Expectant management of bowel.
46	AMI MVT Pathophysiology Similar to venous thrombosis in other beds – stasis/hypercoagulable/injury. Bowel edema → third space loss. Bowel infarction less common – contingent upon collaterals.
47	AMI MVT Presentation/Dx Prolonged prodrome of vague, non-specific, mild pain. CT scan diagnostic study of choice. Thrombus within mesenteric veins. Bowel edema.
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49	AMI MVT Treatment Aggressive anticoagulation. Hypercoagulable workup. Expectant management of bowel. Long-term anticoagulation even in the absence of identifiable condition.
50	Colon Ischemia Isolated colon ischemia can occur after open AAA, EVAR, shock states. Incidence (contingent upon modality). Elective open repair 2 – 14% Ruptured open repair 25 – 40%.
51	Colon Ischemia Presentation/DX Blood diarrhea early postoperative. Suspect in AAA patients with MOD, thrombocytopenia, “failure to thrive.” Diagnosis confirmed with endoscopy.
52	Colon Ischemia Treatment Treatment based on endoscopic findings and clinical setting. Difficulty differentiating mucosal ischemia from full thickness necrosis. Colectomy for presumed infarction. Expectant management for ischemia. Antibiotics. Serial endoscopy.
53	Summary/Conclusions CTA diagnostic study for CMI/AMI. Etiology of AMI can usually be determined by history, clinical setting. Clinical concerns for AMI is to reverse the underlying condition, salvage bowel. AMI from embolus/in situ thrombosis require emergent revascularization. Expectant operative management for NOMI and MVT.
54	Summary/Conclusions Mesenteric revascularization is associated with severe IR injury. Immediate postoperative course after revascularization complicated by MOD. Optimal treatment for postoperative MOD is supportive care.
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