Ischemic bowel disease


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Ischemic bowel disease

  1. 1. IschemIcboweldIseaseLecture 11, 12Vascular disorders
  2. 2. Vascular disorders•Ischemic Bowel Disease•Angiodysplasia•Hemorrhoids
  3. 3. DefinitionIschemic bowel disease results frominadequate flow of oxygenatedblood to the intestines.• The extent of ischemic bowel disease can rangefrom mild to severe based on the amount ofdamage from lack of oxygenated blood.
  4. 4. • Ischemic lesions may be restricted to the•Small intestine mesenteric ischemia•Large intestine ischemic colitis or•Both enterocolitis
  5. 5. Blood Supply• The majority of the GI tract is supplied by theceliac, superior mesenteric, andinferior mesenteric arteries.• As they approach the intestinal wall the superiorand inferior mesenteric arteries ramifyinto the mesentericarcades.
  6. 6. • Interconnections between arcades, as well ascollateral supplies from the proximal celiacand distal pudendal and iliac circulations,make it possible for the small intestine andcolon to tolerate slowly progressive loss ofthe blood supply from one artery.• In contrast, acute compromise of any majorvessel can lead to infarction of severalmeters of intestine.
  7. 7. Levels of infarction• Transmural infarction involving all layers of the gut.• Mural infarction– mucosa & submucosa• Mucosal infarction- mucosaMural-Of Wall
  8. 8. • Transmural infarction is caused by acuteocclusion of a major mesenteric artery.• Mural or mucosal infarction more often resultsfrom either physiologic hypoperfusion or morelocalized anatomic defects and may beacuteor chronic.
  9. 9. Predisposing conditions1. Arterial thrombosis2. Arterial embolism Occlusive3. Venous thrombosis- less frequentcause4. Nonoclusive ischemia5. Miscellaneous}
  10. 10. Arterial thrombosis• Severe atherosclerosis• Systemic vasculitis• Dissecting aneurism An aneurysm in which the wall of an artery rips (dissects) longitudinally• Angiographic procedures• Aortic reconstructive surgery• Surgical accidents• Hypercoagulable states• Oral contraceptives
  11. 11. Arterial embolism•Cardiac vegetation An abnormal growth of tissue around a valve, composed of blood platelets, bacteria, and a protein involved in clotting.•Angiographic procedures•Aortic atheroembolism
  12. 12. Venous thrombosis• Hypercoagulable states induced, for example, by oral contraceptive or antithrombin III deficiency,• intraperitoneal sepsis,• the postoperative state,• vascular invasive neoplasm (particularly hepatocellular carcinoma),• cirrhosis,• abdomina trauma.
  13. 13. Nonoclusive ischemia• Cardiac failure• Shock• Dehydration• Vasoconstrictive drugs
  14. 14. Miscellaneous• Radiation injury• Volvulus• Stricture• Internal & external herniation
  15. 15. Causes• Ischemic bowel disease occurs when an artery thatsupplies blood becomes blocked or narrowed.There are several possible causes of ischemic boweldisease, including:• Blockage in the arteries due to a tumor or bloodclot• Narrowing of the arteries supplying blood to thebowel from atherosclerosis• Obstruction in the colon (large intestine)
  16. 16. Risk Factors• Advanced age• Shock induced by conditions such as bloodstream infection and blood loss• Recent heart attack• Sustained abnormal heart beat• Congestive heart failure• Peripheral vascular disease• Coronary artery bypass surgery or other vascularsurgeries
  17. 17. • Colon cancer• Certain medications that cause arteries to narrow• Diabetes• Hemodialysis• Sickle cell disease• Dehydration• Pregnancy
  18. 18. Pathophysiology• Arterial sources v.s. venous sources:proximately 9:1. Similarly, arterial occlusivedisease occurs more frequently thannonocclusive disease approximately 9:1• The SMA and IMA, and their branches, aremore frequently than the celiac artery.
  19. 19. Pathophysiology (a. source)Acute:1.atheromatous plaque with intimal calcifications2.embolic from cardiac disease3. abdominal aortic aneurysms with dissection intoSMA4. hypoperfusion secondary to hypovolemic shock orlow-flow cardiac failure.
  20. 20. Pathophysiology (a. source)Chronic :1.atherosclerosis2.fibromuscular dysplasia3.vasculitis.Both occlusive and nonocclusive subtypes can occur .
  21. 21. Pathophysiology (v. source)• are less frequently.• In these cases, bowel ischemia results fromdecreased mesenteric outflow ofdeoxygenated blood rather than from decreasedperfusion of oxygen-rich blood• Mortality rates generally are low.• SMV is involved more often than the IMV.
  22. 22. 3.Nonocclusive mesenteric ischemia– more frequently in older patients than otherforms and often already in an ICU setting .– Symptoms typically develop over several days,and may have had a prodrome of malaise andvague abdominal discomfort.– When infarction occurs, increased pain associatedwith vomiting,hypotensive and tachycardic, withloose bloody stool.
  23. 23. 4.Mesenteric venous thrombosisin a much younger patient population than other types .– acute or subacute abdominal pain involvement of thesmall intestine rather than the colon.– The symptoms are frequently less dramatic. 27% havesymptoms for >30 d.– Many patients have a history of the risk factors forhypercoagulability. include oral contraceptive use, deepvein thrombosis (DVT), liver disease, tumor, or portocavalsurgery.
  24. 24. PathogenesisIntestinal responses to ischemia occur in twophases.I. The initial hypoxic injury occurs at the onsetof vascular compromise. While some damageoccurs during this phase, the epithelial cellslining the intestine are relatively resistant totransient hypoxia.
  25. 25. II. The second phase, reperfusion injury, is initiatedby restoration of the blood supply and it is at thistime that the greatest damage occurs.In severe cases this may triggermultiorgan failure.While the underlying mechanisms of reperfusioninjury are incompletely understood, they involvefree radical production, neutrophil infiltration, andrelease of inflammatory mediators, such ascomplement proteins and TNF.
  26. 26. • Activation of intracellular signalingmolecules and transcription factors,including hypoxia-inducible factor 1 (HIF-1)and NF-κB(nuclear factor kappa-light-chain-enhancer of activated B cells) is a protein complex thatcontrols the transcription of DNA) also contribute to intestinalischemia-reperfusion injury
  27. 27. • The severity of vascular compromise,• the time frame during which it develops, and• the vessels affectedare the major variables inischemic bowel disease.
  28. 28. • Two aspects of intestinal vascular anatomy alsocontribute to the distribution of ischemic damage.1. Intestinal segments at the end oftheir respective arterial suppliesare particularly susceptible toischemia.Tail enders
  29. 29. • These watershed zones include thesplenic flexure, where the superiorand inferior mesenteric arterial circulationsterminate, and, to a lesser extent,• the sigmoid colon and rectum whereinferior mesenteric, pudendal, and iliac arterialcirculations end.
  30. 30. • Generalized hypotension or hypoxemia cantherefore cause localized injury, and ischemicdisease should be considered in thedifferential diagnosis of focal colitis of thesplenic flexure or• rectosigmoid colon.
  31. 31. 2. Intestinal capillaries run alongside the glands,from crypt to surface.
  32. 32. •This allows oxygenatedblood to supply crypts butleaves the surface epitheliumvulnerable to ischemic injury.• This anatomy protects the crypts, which containthe epithelial stem cells that are necessary torepopulate the surface.
  33. 33. • Thus, surface epithelial atrophy,or even necrosis and sloughing,with normal orhyperproliferative cryptsis a morphologic signature of ischemicintestinal disease.
  34. 34. MorphologyTransmural Intestinal Infarction-may involve a short or long segment, depending onthe particular vessel affected and the patency ofthe anastomotic supply. Whether the occlusion isarterial or venous, the infarctionalways has adark red hemorrhagic appearance (RedInfarction).
  35. 35. • The ischemic injury usually begins in themucosa and extends outwards;within 18 to 24 hours.• There is a thin, fibrinous exudateover the serosa.
  36. 36. • With arterial occlusion the demarcationfrom adjacent normal bowel is fairly sharplydefined, but• with venous occlusion the margins are lessdistinct.
  37. 37. • Affected foci may or may not be visiblefrom the serosal surface, because bydefinition the ischemia does not affect theentire thickness of the bowel.• When the bowel is opened, hemorrhagicedematous thickening of the mucosa,sometimes with superficial ulcerations, isseen.
  38. 38. EHNEHistologic features are those ofacute injury:Edema, hemorrhage, and outright necrosis ofthe affected tissue layers.Inflammation develops at the margins of thelesions, and an inflammatory fibrin-containingexudate (pseudomembrane), usuallysecondary to bacterial superinfection, maycoat the affected mucosa.
  39. 39. • Alternatively, Chronic vascular insufficiency mayproduce achronic inflammatory and ulcerative condition,mimicking idiopathic inflammatory bowel disease.
  40. 40. •Lecture12
  41. 41. Morphology –Transmural infarction• Histologically, the changes are typical of ischemicdamage with• marked edema,• interstitial hemorrhage,• necrosis and sloughing of the mucosa.• Within 24 hours intestinal bacteria produceoutright gangrene and sometimes perforation ofthe bowel.
  42. 42. Mural & mucosal infarctions-are recognised by multifocal lesionsinterspersed with spared areas.Their location depends in part onthe extent of preexisting atherosclerotic narrowing ofthe arterial supply;lesions can be scattered over large regions of thesmall or large intestines.Patchy lesions(Necrosis)
  43. 43. Symptoms• Cramping and abdominal pain• Bloody stools• Frequent urge to defecate• Diarrhea• Nausea or vomiting• Abdominal distension
  44. 44. Ischemia bowel• acute or chronic.• arterial or venous• occlusive or nonocclusive.
  45. 45. Acute transmural infarctiontypically presents withsudden, severe abdominal paintenderness (more sudden with mesenteric embolism),sometimes accompanied bynausea,vomiting,bloody diarrhea, orgrossly melanotic stool.
  46. 46. Patients may progress to shock and vascular collapse within hours as a result of bloodloss. Peristaltic sounds diminish or disappear, andmuscular spasm createsboard-likerigidity of theabdominal wall.
  47. 47. Because these physical signs overlap with those ofother abdominal emergencies, includingacute appendicitis,perforated ulcer, andacute cholecystitis,the diagnosis of intestinal necrosis may bedelayed or missed,with disastrous consequences.
  48. 48. As the mucosal barrier breaks down, bacteria enter the circulation andsepsiscan develop;mortality may exceed 50%.The overall progression of ischemic enteritis depends on the underlyingcause and severity of injury.
  49. 49. • The mortality rate with infarction ofthe bowel approaches 90%, largelybecausethe window of time between onsetof symptoms and perforationcaused by gangrene is so small.
  50. 50. Mucosal and mural infarctionsby themselves may not be fatal. However, these may progress to more extensiveinfarctionif the vascular supply is not restored by correction of theinsultor,in chronic disease, by development of adequatecollateral supplies.
  51. 51. • The diagnosis of nonocclusive ischemic enteritis andcolitis can be particularly difficult because there may be a confusing array ofnonspecific abdominal symptoms, includingintermittent bloody diarrheaand•intestinal pseudo-obstruction.
  52. 52. ,Chronic ischemia may masquerade asinflammatory bowel disease, with episodes ofbloody diarrhea interspersed with periods of healing.
  53. 53. Diagnosis• X-ray of abdomen• CT Scan or MRI of the abdomen• Colonoscopy—a procedure where a longflexible tube is inserted through the rectum toinspect the colon and rectum.• Angiography—an x-ray test used to view thearteries supplying the bowel
  54. 54. DifferentialAppendicitisTraumaPseudomembranous colitis AdenocarcinomaDiverticulitisCrohn DiseaseNecrotizing EnterocolitisPneumatosis IntestinalisTyphlitisUlcerative Colitis
  55. 55. TreatmentSupportive Care• Bowel rest and intravenous fluids are given in mildcases without significant progressed damage to thebowel.• Antibiotics• Antibiotics are administered to minimize infection,which can quickly complicate an ischemic bowel.• Surgery• In more severe cases, surgery is required to removethe ischemic colon.
  56. 56. Complications• Bowel necrosis (requiring bowel resection)• Septic shock• Death• Patients in whom the diagnosis is missed until infarctionoccurs have a mortality rate of 90%. Even with goodtreatment, up to 50-80% of patients die.• Survivors of extensive bowel resection face lifelong disability.
  57. 57. Prevention• Stay well hydrated.• Reduce your risk of cardiovascular diseasethrough regular exercise and a balanced dietlow in fat and calories.• Consume plenty of fresh fruits, vegetables,and fiber, which may reduce your risk of coloncancer.
  58. 58. Major Causes ofIntestinalObstruction
  59. 59. Major Causes of Intestinal ObstructionMechanical Obstruction:• Hernias• Adhesions• Intussuception• Volvulus 80%
  60. 60. Intestinal obstruction. The four major causes of intestinal obstruction are (1)herniation of a segment in the umbilical or inguinal regions, (2) adhesion betweenloops of intestine, (3) volvulus, and (4) intussusception.
  61. 61. Other less frequent conditions• Tumors & Infarction 10-15 %• Inflammatory strictures• Obstructive gall stones, fecaliths, foreign bodies• Congenital Strictures, atresias• Congenital bands• Meconium in cystic fibrosis• Imperforate anus