Chronic mesentric ischemia.,classification,presentation,managmentpptx

Chronic mesentric ischemia.,classification,presentation,managment

1. CHRONIC MESENTERIC ISCHEMIA (INTESTINAL ANGINA ) Dr. Vijay K.C. DM resident G astroenterology C oms

2. Introduction A ccounts for <5% of intestinal ischemic disorders Etiology: mesenteric atherosclerosis (35% to 75%), median arcuate ligament syndrome, collagen vascular disease, and inflammatory vasculopathy are known. A subset of patients with CMI have NOMI incidence of CMI was estimated to be 5-6 per 100,000, with a prevalence of 30 per 100,000. 1 1.Kolkman JJ, Geelkerken RH. Diagnosis and treatment of chronic mesenteric ischemia: an update. Best Pract Res Clin Gastroenterol 2017;31:49–57.

3. CMI is caused by either occlusive mesenteric ischaemia or non-occlusive mesenteric ischaemia (NOMI)  Occlusive chronic mesenteric ischaemia can be caused by atherosclerosis, median arcuate ligament syndrome (MALS), vasculitis or by mesenteric venous thrombosis (MVT).  chronic NOMI patients experience gradually increasing symptoms, such as postprandial pain, fear of eating, weight loss, nausea and diarrhoea . Acute NOMI, in contrast, is characterised by more severe ischaemia . at risk of developing acute-on-chronic mesenteric ischaemia , e.g. in cases with a ruptured atherosclerotic plaque

4. Risk factors The presence of mesenteric artery stenosis (MAS) does not imply that abdominal pain or other GI symptoms is due to CMI symptomatic CMI have involvement of at least 2 vessels. Risk factors: female ,hypertension, hyperlipidemia, diabetes, smoking and obesity . Age group: 50-70 yrs Abdominal pain - most typical symptom is likely caused by ischemia of the small intestine.

5. Pathophysiology Blood flow through these arteries increases within an hour after eating due to an increase in metabolic demand of the intestinal mucosa. Diffuse atherosclerosis, usually occurring at the origin of these vessels Chronic occlusion of a single vessel allows collateral blood flow to compensate, thus symptoms do not typically present until at least two primary vessels are occluded. Less common causes include vasculitis, fibromuscular dysplasia, and radiation

6. Clinical Features -CMI cardinal feature: abdominal cramping or discomfort that starts within 30 minutes after eating, gradually increases in severity then slowly resolves over 1 to 3 hours. Abdominal pain : > 90% of patients A bdominal pain progressively increases in severity over weeks to months.

7. Clinical Features -CMI Intestinal angina Early in the course , pain occurs only after eating or during a meal. Later, pain occurs earlier in the meal, lasts longer, is more severe and can become continuous. Classical triad: postprandial abdominal pain, weight loss and abdominal bruit. pain with meals leads to fear of eating ( sitophobia )➡︎weight loss. H/O angina, transient ischemic attacks/cerebrovascular accidents, or lower extremity claudication. Diarrhea:7% to 35% of patients , sign of end-stage CMI . abdominal bruit may be audible in up to 50% One study found that 100% of patients with CMI presented with some abdominal pain, 78% of which was postprandial; 68% had weight loss with a mean loss of 23 ± 12 pounds; 13% had nausea and vomiting; 13% had constipation or diarrhea; and 8% presented with LGIB

8. Diagnosis -CMI Abdominal plain films and CT scans usually normal ± vascular calcification Endoscopy-normal radionuclear emptying tests -delayed gastric emptying. CTA is now the imaging modality of choice Arterial digital subtracted angiography (DSA) is the gold standard  Combination of the imaging with clinical presentation -essential for accurate diagnosis Duplex US -identify splanchnic artery stenoses Angiography should show occlusion of 2 or more splanchnic arteries to allow the diagnosis of CMI postprandial L-lactate and D-dimer ↑

9. Diagnosis -CMI functional testing to determine the adequacy of blood flow (1) Visible light spectroscopy (VLS): VLS uses white light delivered by an endoscopic fiberoptic probe to measure intramucosal O2 saturation. (2) Gastric tonometry exercise testing (GTET) GTET uses a specialized tonometric balloon catheter and peripheral arterial catheter or needle stick to obtain gastric juice and arterial blood respectively from a fasting patient who has been pretreated with acid-suppression medication and then undergoes a standard exercise protocol. Determination is made of the gastric-arterial PCO2 gradient before, during, and after exercise. An increase in the gradient after exercise is an indicator of GI ischemia.

10. Algorithm for the management of chronic mesenteric ischemia .

11. CMI- Treatment Surgical revascularization percutaneous transluminal mesenteric angioplasty (PTMA) alone or with stent insertion Open revascularization :antegrade inflow (aortomesenteric or aortoceliac bypass) or retrograde inflow (from the iliac artery), with either a vein or prosthetic conduit.

12. Surgical revascularization surgical intervention group: better primary and secondary patency rates The major complications of surgical revascularization included : acute renal failure (11%),bowel infarction requiring resection (8%), cardiac arrest (6%), respiratory complications (5%), myocardial infarction (5%), and GI hemorrhage (3%).

13. percutaneous transluminal mesenteric angioplasty (PTMA) less-invasive technique ,increasingly used Following stent placement, patients usually require clopidogrel and aspirin for 1 to 3 months The main complications : thrombosis, dissection, and hemorrhage. Postoperative complications, 30-day morbidity, and mortality did not differ with surgical intesrvention . lower efficacy for sustained symptomatic improvement compared with surgical management. A review of 43 articles including 1795 patients over 25 years showed that perioperative length of hospital stay, morbidity, and mortality were lower in those who underwent endovascular therapy, with no difference in survival

14. Vasculitis and angiopathy of the splanchnic circulation Inflammation and necrosis can affect splanchnic blood vessels of all sizes: arteries, arterioles, the vasa rectae , veins, and venules Symptoms depend on the size of the involved vessel ischemic injury typically involves short segments of the intestine. Abdominal pain, fever, GI bleeding, diarrhea, and obstruction are common HSP involve digestive tract -90% of affected patients. Polyarteritis nodosa, allergic granulomatous angiitis (Churg-Strauss syndrome), and SLE have GI involvement in up to 50% of patients. 30% of those with Behçet syndrome manifest GI involvement Takayasu arteritis, GPA (formerly Wegener granulomatosis), vasculitis associated with RA, and giant cell arteritis affect the digestive tract <15% of pts.

15. Allergic Granulomatous Angiitis (Eosinophilic Granulomatosis With Polyangiitis, or Churg-Strauss Syndrome) asthma, glomerulonephritis, eosinophilia, and granulomatous inflammation associated with ANCA. This necrotizing vasculitis – small and medium sized vessels involves the GI tract in almost 50 % of patients. small bowel being involved most Classic symptoms: abdominal pain, diarrhea, GI bleeding, and rarely perforation Glucocorticoid therapy usually is effective immunosuppressive therapy is first-line treatment. High dose IVIG is an altenativ e

16. Behçet Syndrome oral and genital ulcers, recurrent iritis or chorioretinitis, and skin lesions. Eastern Mediterranean men. Small-vessel vasculitis a/w large-vessel involvement GI involvement is rare ≅ 0.7% of 8763 patients ileocecal region: most commonly involved (61%) and large oval ulcerations. Abdominal pain (87%) and diarrhea (48%) 32% acute abdomen, 42% with massive bleeding, and 58% luminal perforations. ℞:oral 5-ASA derivatives, azathioprine, infliximab, or adalimumab

17. Thromboangiitis Obliterans ( Buerger Disease) medium-sized and small peripheral arteries and veins, especially infrapopliteal vessels foot claudication and rubor are its most common symptoms. Men with smoking habit with age of onset before 50 yrs No other atherosclerotic risk factors involvement of small intestine. Intestinal involvement usually requires resection.

18. Cogan Syndrome rare disorder of young people characterized by vasculitis of the conjunctiva, cornea, and cochlea. higher incidence in patients with IBD. vasculitis usually is localized hypersensitivity reaction to an unknown viral agent, 3%-10% of patients develop GI symptoms, with diarrhea and bloody stools. High-dose glucocorticoids, and cytotoxic agents Vascular surgery may be needed after inflammation is controlled .

19. Fibromuscular Dysplasia rare angiopathy that is neither related to atherosclerosis nor to inflammation. genetic factors might play a role A/W cigarette smoking and hypertension. R enal arteries most commonly affected, followed by the carotid and vertebral arteries and then mesenteric arteries. Splanchnic involvement can manifest with symptoms of AMI or CMI. mimic other chronic GI diseases such as Crohn disease . CT angiography :“string-of-beads” appearance is typical of only the medial type of FMD, whereas aneurysms and dissection may complicate all types. Therapy : PTMA, surgical revascularization, and resection of necrotic bowel.

20. Henoch-Schönlein Purpura affects children 4 - 7 years of age and preceded by an URTI. IgA immune complexes deposited within the small vessels of the skin, GI tract, joints, and kidneys. clinical triad: palpable purpura (usually below the waist), arthritis (knees and ankles), and abdominal pain GI tract -90% of patients. Colicky abdominal pain and GI bleeding a submucosal hematoma may be the lead point of an intussusception. Rarely, bowel perforation can occur. D uodenum and terminal ileum affected most often. self-limited disease less favorable in adults

21. Hypersensitivity Vasculitis uncommonly involves the splanchnic vasculature Etilogy : infection ( Streptococcus , Staphylococcus , HBV, influenza virus, cytomegalovirus, mycobacteria, and rickettsiae ), drugs, and chemicals. Treatment of the underlying disease or triggers.

22. Kawasaki Disease also called infantile febrile mucocutaneous lymph node syndrome necrotizing vasculitis of medium- sized arteries. It usually manifests in infants and children fever, palmar and solar rash, desquamation, conjunctival congestion, strawberry tongue, and cervical lymphadenopathy. GI involvement is rare, most commonly affecting the mouth and esophagus C/F: nausea, vomiting, abdominal pain, diarrhea, ileus, small bowel obstruction bleeding, and perforation. Death from coronary artery aneurysms and myocardial infarction. A spirin for the acute phase and large IV Ig for coronary artery aneurysms alternative treatments : corticosteroids and infliximab

23. Köhlmeier-Degos Disease (Malignant Atrophic Papulosis) rare form of progressive occlusive vascular disease of young men affects the small- and medium-sized arteries Typically, skin lesions of porcelain-white punctate atrophic scars with erythematous borders are found on the trunk and upper extremities, abdominal pain and spontaneous intestinal perforation-recurrent. no known therapy for this disease G enerally fatal when Gi tract involved

24. Polyarteritis Nodosa necrotizing vasculitis of medium-sized and small arteries -aneurysms at branch points. GI involvement is seen in up to 50% of patients. Abdominal pain, nausea, vomiting, diarrhea, and melena typify a benign course, GI bleeding, perforation, infarction and/ or pancreatitis are seen with severe disease. Involvement of the small intestine is most common CT angio : aneurysms up to 1 cm in diameter involving the renal, mesenteric, and hepatic vasculature. Induction therapy : high-dose glucocorticoids or cyclophosphamide Maintainance therapy: azathioprine or methotrexate for maintenance.

25. HBV Vasculitis (Formerly Hepatitis B–Associated Polyarteritis Nodosa) Vasculitis resembling polyarteritis also is a/w HBV infection. Approx 25% of patients PAN infected with hepatitis B deposition of antigen-associated immune complexes in the vessel wall. C/F similar to PAN but with more frequent GI involvement. better prognosis than those with polyarteritis nodosa. Treat infectious hepatitis. antiviral agent(s) + glucocorticoid and plasma exchange.

26. Rheumatoid Vasculitis develops after 10 to 15 years of erosive arthropathy. 10% to 38% have involvement of the GI tract. abdominal pain, bleeding, perforation, and gangrene. catastrophic, ischemic ulcers, bowel infarction, and pancolitis. with GI involvement, mortality ≅25% within 5 years Glucocorticoids and cyclophosphamide for severe RV

27. SLE affects the GI system in about half of cases abdominal pain, but diarrhea, pseudo-obstruction, constipation, peritonitis, pancreatitis, protein-losing enteropathy, and ascites are not infrequent. Vasculitis typically involves the SMA causing FSI and GI bleeding of the jejunum or ileum Thromboses of the mesenteric vasculature due to an associated coagulopathy. CT : evaluate the bowel wall and vasculature. Mesenteric vasculitis responds well to glucocorticoids and complete bowel rest. Cyclophosphamide ± glucocorticoid therapy. Perforation or necrosis : surgical repair and resection

28. Takayasu Disease an idiopathic chronic inflammatory disorder that most often affects the aorta and its branches in young asian women It is unusual that splanchnic vessels are involved CT angio : 25% had stenotic or occlusive lesions of the celiac axis or SMA. rarely has been associated with Crohn disease and UC Treatment : large doses of glucocorticoids + immunosuppressant such as an anti-TNF agent. Reconstructive surgery or PTMA is indicated in those with symptomatic celiac or MAS.

29. Thank you!