Approach to Upper GI Tract Bleed (UGI Bleed).pptx

Surgical Approach

1. Approach to UGI Bleed Dr. Akshay Sarraf 2nd Year Resident Dept. of General surgery

2. Objectives Introduction Acute Management- Initial Evaluation Localisation Risk Stratification Causes- Nonvariceal Variceal bleeding Treatment

3. Introduction Upper gastrointestinal haemorrhage remains a major medical problem. Classified as any blood loss from a gastrointestinal source above the ligament of Treitz.  Incidence of over 100/1,00,000 per year. Incidence increases with age. 

4. May present in a subtle way as a diagnosis of unexplained microcytic anemia. Can manifest as hematemesis, hematochezia, or melena. Strongly associated with NSAID use.  Estimated mortality rates between 2% to 15%. - Upper Gastrointestinal Bleeding: Etiologies and Management. Mayo Clin Proc. 2019 Apr;94(4):697-703. Rises to 33% when bleeding is first observed in patients who are hospitalized for other reasons. 

5. Etiology - Acute Upper Gastrointestinal Bleeding in a Tertiary Care Centre of Nepal. Journal of Nepal Medical Association, 56(206).

6. Approach Initial Management- Rapid triage of hemorrhaging patients while localizing the areas of blood loss is essential. (IV) access with two large-bore (14- or 16- gauge) catheters should be obtained. Central access with resuscitative lines is needed in massively hemorrhaging patient. Assessment should adhere to the ABCDEs.

7. Severe hematemesis or decreased mental status from shock or hepatic encephalopathy may compromise oxygenation, ventilation, and airway protective reflexes. Tachypnea, tachycardia, hypotension, agitation, and mental status changes are all quick indicators of a severe degree of hemorrhage. Hypotension is a harbinger of death- SBP <90 mm Hg do not typically manifest until a patient has experienced a 30% to 40% blood loss. These signs may be absent or subtle in well-compensated hosts, or patients taking beta blockers or those patients who are at the extremes of age.

8. Priorities- obtaining a type and crossmatch, complete blood count, metabolic panel, coagulation profile, and liver function tests. Serum lactate can be utilized as an endpoint of resuscitation when elevated. Serum hematocrit is not a reliable marker of the amount of blood loss. The strategy for fluid resuscitation should be guided by the severity of hemorrhage. Important to distinguish massively hemorrhaging patients from stable patients.

9. Severity of hypovolemic shock should be assessed. Start with a warm isotonic crystalloid solution of 30 ml/kg body weight, infused rapidly to restore tissue perfusion quickly.(~1 L of crystalloid in 10 to 15 minutes) - Surviving Sepsis Campaign Guidelines 2021: highlights for the practicing clinician. Pol Arch Intern Med. 2022 Aug 22;132(7-8)

10. In large volume loss, utilization of massive transfusion protocols. Universal donor blood products rapidly available in prespecified ratios. One unit fresh-frozen plasma per two units of packed red blood cells [RBCs] administered. - Should all massively transfused patients be treated equally? An analysis of massive transfusion ratios in the nontrauma setting. Crit Care Med. 2017;45:1311–1316. Normalization of prothrombin time, partial thromboplastin time, fibrinogen levels, and platelet count are important adjuncts.

11. Often require admission to the intensive care unit and urgent intervention to localize and control hemorrhage. Adequacy of resuscitation- mental status, radial pulse pressure, SBP of 90 mm Hg, with endpoints of resuscitation, such as lactate clearance and urine output. Restrictive transfusion strategy should be employed in stable patients. Villanueva Trial- compared a restrictive transfusion threshold of a hemoglobin level of 7 to 9 g/dL to a liberal threshold of 9 to 11 g/dL. This randomized controlled trial found lower rates of mortality, rebleeding, and other adverse outcomes with the restrictive strategy of 7 g/dL. - Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368:11–21.

12. Localization- Runs parallel and equally important as the active resuscitation. History and physical exam guide the assessment. C haracteristic of the blood loss, is helpful for determining an upper versus lower source.

13. Hematemesis is the emesis of blood or coffee ground gastric secretions, most commonly from a UGIB. Melena, a malodorous, black stool with a tar-like quality, is also indicative of a proximal source of bleeding in 90%. - Initial management of acute upper gastrointestinal bleeding: from initial evaluation up to gastrointestinal endoscopy. Med Clin North Am. 2008;92:491– 509, xi. Hematochezia, the passage of bright red blood from the anus in brisk UGIB with swift transit through the intestinal tract; is an important etiology to rule out upon evaluation.

14. An exsanguinating or moribund patient with unlocalized bleed should proceed to a hybrid room for visceral angiography and/or operative intervention. Hemodynamically stable patient for further workup, the multidetector computed tomography angiogram (CTA). The sensitivity and specificity of CTA approaches 100% and over 90%, respectively. Can detect bleeding rates as low as 0.3 mL/min.

15. T echnetium-99-m-labeled RBC scintigraphy can detect bleeding as low as 0.04 mL/min. Sacrifices the precision of hemorrhage localization. Multiphase CT enterography can be superior to capsule endoscopy in detecting bleeding from tumors. Double-balloon endoscopy is quickly gaining favor in the diagnosis and treatment of small bowel lesions. Capable of examining the entire small bowel, with successful identification of 77% to 85% of occult bleeding sources.

16. Obscure Bleed Often a common lesion that is missed on initial evaluation. Repeated endoscopy may identify lesions in up to 35% of patients. Tagged RBC scan and angiography require ongoing hemorrhage.

17. Small bowel Ct Enteroclysis can identify gross lesions such as small bowel tumors and inflammatory conditions. Cannot visualize angiodysplasias, the main cause of obscure small bowel hemorrhage. Provocative angiographic testing, has been employed in small series with favorable results. Surgical backup to salvage the patient is essential to the planning of such a procedure.

18. Risk Stratification Identify patients at high risk for adverse outcomes. Helps determine disposition (ICU vs. floor vs. outpatient). May help guide appropriate timing of endoscopy.

19. Rockall Score For the assessment of rebleeding and death after upper gastrointestinal haemorrhage .  Pre-endoscopy format for safe early discharge. Post endoscopy, can accurately predict rebleeding and death. 

20. - Risk assessment after acute upper gastrointestinal haemorrhage . Gut, 38(3), 316–321.

21. AIMS65 Score -A simple risk score accurately predicts in-hospital mortality, length of stay, and cost in acute upper GI bleeding. Gastrointestinal endoscopy, 74(6), 1215–1224.

22. Glassgow-Blatchford Score Designed to discriminate between patients who needed clinical intervention and admission. Does not rely on endoscopic findings. Predicts need for endoscopy. Relies on clinical data and laboratory studies.

23. - A risk score to predict need for treatment tor uppergastrointestinal h aemorrhage . 356(9238), 0-1321. A GBS greater than zero suggests a “High Risk” GI bleed Likely to requires medical intervention: transfusion, endoscopy, or surgery. A higher GBS also correlates with a higher likelihood of needing intervention Scores ≥6 are associated with >50% risk of needing intervention.

24. Non Variceal Causes Peptic Ulcer Disease- Responsible for up to two-thirds of UGIBs. 10% to 15% of patients with PUD will develop bleeding. Results from an imbalance between mucosal barriers and other aggravating factors. Major etiologic factors in PUD are H. pylori and NSAIDs. Up to 77% of duodenal ulcers are associated with H. pylori infection.

25. Causes an inflammatory reaction within the mucosa that impairs mucosal defense and allows ulcer formation. NSAIDs inhibit cyclooxygenases, thus impairing prostaglandin synthesis, enhancing neutrophil adherence and subsequent mucosal injury. Erosion of the mucosal surface leads to injury, ulceration, and chronic blood loss. Can be further exacerbated by antiplatelet agents, anticoagulants, and SSRIs. Most significant hemorrhage occurs when duodenal or gastric ulcers penetrate branches of the gastroduodenal or left gastric arteries, respectively.

26. Management- B egins with effective prophylaxis. Aggressive treatment of H. pylori, reduction of NSAIDs, and the use of alternative NSAIDS. After initial resuscitation, patients should undergo esophagogastroduodenoscopy (EGD). PPIs have become a mainstay in the treatment.

27. While awaiting EGD, patients should be treated with a PPI. Those with high clinical risk should undergo EGD within 12 hours of presentation. -Upper gastrointestinal bleeding due to a peptic ulcer. N Engl J Med. 2016;374:2367–2376. Prokinetics like erythromycin prior to endoscopy has shown to reduce the need for second endoscopy, amount of blood transfusion, and hospital length of stay. - Pre-endoscopic erythromycin administration in upper gastrointestinal bleeding: an updated meta-analysis and systematic review. Ann Gastroenterol. 2016 Jul-Sep;29(3):312-7. ~25% of patients undergoing EGD for UGIB will require an endoscopic intervention.

28. Forrest Classification Developed to assess the risk of rebleeding based on endoscopic findings and groups patients into high, intermediate, and low risk of rebleeding. - Management of non-variceal upper gastrointestinal bleeding: where are we in 2018?. Frontline gastroenterology, 10(1), 35–42.

29. Endoscopic therapy is recommended for ulcers with active bleeding as well as those with a visible ulcer (Forrest I– IIa ). In cases with an adherent clot (Forrest IIb), the clot is removed and the ulcer evaluated. Ulcers with a clean base or black spot secondary to hematin deposition (Forrest IIc –III) do not require endoscopic treatment and are managed medically. If the endoscopy is unable to achieve hemostasis, angiography should be performed. Surgery is the next step if angiography fails or is not available.

30. Medical Management All patients with confirmed peptic ulcer bleed should receive PPI therapy. Preendoscopic high-dose IV PPI therapy has been associated with decreased frequency of high-risk findings on endoscopy (Forrest Ia – IIa ). If PPI has not been started prior to endoscopy, a bolus of 80 mg should be given, followed by an infusion at 8 mg an hour for 72 hours. Continuing PPI therapy postendoscopy also has been associated with reduced risk of further bleeding, need for surgery, and mortality.

31. Eradication of H. pylori infection results in less rebleeding. All ulcerogenic medications should be discontinued. A double-blind trial showed that COX-2 inhibitors plus PPI has a much lower rebleed risk as compared to COX-2 selective NSAIDs alone (0% vs. 8.9%). - Combination of a cyclo-oxygenase-2 inhibitor and a proton-pump inhibitor for prevention of recurrent ulcer bleeding in patients at very high risk: a double-blind, randomised trial. Lancet. 2007;369:1621–1626. A randomized controlled trial studied the benefits of low dose aspirin in primary prevention of cardiovascular events. - Effect of aspirin on cardiovascular events and bleeding in the healthy elderly. N Engl J Med. 2018;379:1509–1518.

32. Endoscopic Management- Includes injection, thermal coagulation, plasma argon coagulation, mechanical clips, and fibrin glue. Recommended approach is to use thermal coagulation or clips, with or without epinephrine injection generally, 0.2 to 2 mL is injected in each quadrant. Heat or mechanical therapy is usually added and together can achieve initial hemostasis in up to 90% of bleeding ulcers. Hemoclips are less effective than thermal therapy, but are advantageous in dealing with a spurting vessel for immediate control of hemorrhage. Sclerosant injection, such as absolute alcohol are less commonly used.

33. Angiographic Management Diagnostic as well as therapeutic. Should be considered if a patient has failed endoscopic management or if the bleeding has not been localized. Access is obtained through the common femoral artery. Celiac artery and its branches are interrogated first if UGIB is suspected from gastric or duodenal ulcers. Transcatheter s uperselective embolization allows control of bleeding while maintaining adequate collateral flow to prevent bowel infarct. Embolic agents include coils, polyvinyl alcohol particles, Gelfoam , glue, and plugs.

34. Surgical Management Approximately 10% of patients with bleeding ulcers require surgical intervention. Endoscopic factors associated with increased risk of rebleeding are Active bleeding at time of endoscopy, Large ulcer size (i.e., >2 cm), Posterior duodenal wall ulcer, and Lesser gastric curve ulcer. Clinical judgment and local expertise must play a critical role in decision for surgical management.

35. Relative Indication Rare blood type or difficult crossmatch Refusal of transfusion Shock on presentation Advanced age Severe comorbid disease Bleeding chronic gastric ulcer for which malignancy is a concern

36. Duodenal Ulcer Most of these lesions are in the duodenal bulb. Controlled initially with pressure and then stay sutures are placed on either side of a longitudinal duodenotomy or duodenopyloromyotomy . Anterior ulcers can be directly ligated. More commonly, a posterior ulcer erodes into the pancreaticoduodenal or gastroduodenal artery proximal and distally, typically in a superior and inferior orientation. Omental buttressing of the suture line may assist in healing.

37. Gastric Ulcers- Begins with a gastrotomy and suture ligation- alone associated with 30% risk of rebleeding. Ulcer resection is generally indicated due to the 10% incidence of malignancy- a/w rebleeding in ~20% of patients, so distal gastrectomy is generally preferred. Ulcer excision combined with vagotomy and pyloroplasty may be considered in high-risk patients. Proximal or near-total gastrectomies are associated with a particularly high mortality in bleeding ulcers of the proximal stomach near the GE-junction.

38. Esophagitis Infrequent site of nonvariceal hemorrhage. Secondary to repeated exposure of the esophageal mucosa to the acidic gastric secretions in gastroesophageal reflux disease. Results in chronic blood loss. Ulceration may accompany esophagitis and is manifested as anemia or guaiac-positive stools.

39. Other causes of esophageal bleeding include infectious agents in the immune-compromised host, medications, Crohn disease, and radiation. Treatment- Acid suppressive therapy. Endoscopic control of the hemorrhage, usually with electrocoagulation or heater probe. Targeted therapy in infectious cause. Surgery is seldom necessary.

40. Gastritis Characterized by multiple superficial erosions of the entire stomach, most commonly in the body. Results from the combination of acid and pepsin injury due to decreased mucosal protection from hypoperfusion, NSAIDs, chemotherapy, or other agents. Commonly afflicts the critically ill. Decreased due to improvements in the management of shock and prophylactic use of acid suppression in high-risk patients.

41. Acid suppressive therapy is often successful in controlling the hemorrhage. O n failure- administration of octreotide or vasopressin, endoscopic therapy, or angiographic embolization. Surgical choices included vagotomy and pyloroplasty with oversewing of the hemorrhage or near-total gastrectomy. Carried mortality rates as high as 60% and seldom required these days.

42. Mallory-Weiss Tear- Partial-thickness tears of the mucosa and submucosa that occur near the GE junction. Accounts for 5% to 10% of cases of UGIB. Classically develop in alcoholic patients after a period of intense retching and vomiting following binge drinking Mechanism- forceful contraction of the abdominal wall against an unrelaxed cardia, resulting in mucosal laceration of the cardia as a result of the increased intragastric pressure. Diagnosed by history, and endoscopy is used to confirm the diagnosis.

43. Most tears occur along the lesser curvature and can extend into the esophagus. Acid suppression therapy is successful in 90% of bleeding episodes, the mucosa often healing within 72 hours. In s evere ongoing bleeding, endoscopic therapy with injection or electrocoagulation may be effective. Angiographic embolization, usually with absorbable material such as a gelatin sponge High gastrotomy and suturing of the mucosal tear

44. Gastric Antral V a scular Ectasia Characterized by a collection of dilated venules that appear as a linear red streak converging on the antrum, giving the appearance of a watermelon. Severe hemorrhage is rare, most patients present with persistent, iron deficiency anemia from continued occult blood loss. Endoscopic therapy is indicated for persistent anemia or transfusion- dependent bleeding. Endoscopic therapy failure- should be considered for antrectomy

45. Dieulafoy Lesions- Vascular malformations found primarily along the lesser curve of the stomach within 6 cm of the gastroesophageal junction. Erosion of the gastric mucosa overlying these sizable submucosal vessels (1 to 3 mm) leads to bleeding. No associated ulcer, hence difficult to identify. Bleeding can be massive due to large size of the underlying artery

46. Application of thermal or sclerosant therapy is effective in 80% to 100% of cases. Angiographic coil embolization in failed. Surgical intervention post endoscopic tattooing or clipping can facilitate the procedure. Gastrotomy with oversewing of bleeder. In cases in which the bleeding point is not identified, a partial gastrectomy may be necessary.

47. Hemobilia Difficult diagnosis to make. It is typically associated with- trauma, recent instrumentation of the biliary tree, or hepatic neoplasms. Increasing in incidence with expanded use of advanced endoscopy and other minimally invasive hepatopancreaticobiliary procedures. should be suspected in those with right upper quadrant pain and/or jaundice.

48. CT with angiography is the preferred modality for diagnosis. Endoscopy can demonstrate bloodxat the ampulla or other biliary abnormalities suggestive of hemobilia and can offer numerous therapeutic options. If angiographic embolization is performed, the portal vein must be verified to be patent. Surgical intervention when all other therapies have failed, for infected pseudoaneurysms or compression of surrounding vascular structures.

49. Malignancy associated with chronic anemia or hemoccult-positive stool manifested as ulcerative lesions that bleed persistently- most characteristic of the GI stromal tumor (GIST). Endoscopic therapy is often successful in controlling these bleeds . Rebleeding rate is high-therefore, when a malignant neoplasm is diagnosed, surgical resection is indicated. Depend on stage and the hemodynamic stability of the patient.

50. Aortoenteric Fistula Classified as primary or secondary. Most often involve the duodenum. usually fatal as they represent free rupture of the aorta into the bowel. Primary form due to aortic aneurysm compressed against the bowel. Secondary fistulas(m/c) are the result of an aortic graft-enteric erosion in up to 0.4% to 4% of aortic graft cases.

51. Should be considered in all bleeding patients with a known abdominal aortic aneurysm or any prior aortic reconstruction. often massive and fatal unless immediate surgical intervention is undertaken. present first as a selfl imited episode that heralds the subsequent massive and often fatal hemorrhage. If the suspicion for an aortoenteric fistula is high, CTA should be the first-line study. bleeding in the distal duodenum on EGD in a patient at risk for an aortoenteric fistula should be considered diagnostic.

52. Treatment Ligation of the aorta proximal to the graft, removal of the infected prosthesis with debridement of surrounding tissue, and extra-anatomic bypass. treatment should include long-term antibiotics. Endovascular repair may be used as a bridge to definitive open repair.

53. Hemosuccus Pancreaticus Bleeding from the pancreatic duct through ampulla of vater is one of the rarest causes. most typically from a pancreatic malformation, ductal wall ulceration, or a pancreatic pseudocyst that erodes into a pseudoaneurysm. Angiography is the diagnostic gold standard and first therapeutic line of action due to high efficacy (75%–100%) and low-associated mortality. Surgery- required to treat the pseudocyst- procedures such as pancreatic resection and/or arterial ligation.

54. Variceal Bleeding GI can occur due to prehepatic (portal or splenic vein thrombus), intrahepatic (cirrhosis) or posthepatic (Budd-Chiari) pathology. m/c cause of variceal hemorrhage is portal hypertension from the sinusoidal fibrosis associated with cirrhosis. defined as a hepatic venous pressure gradient of more than 5 mm Hg. Increased resistance to flow of the portal vein and its tributaries leads to engorgement of portacaval collaterals in the esophagus, stomach, and the hemorrhoidal plexus.

55. Exacerbated by the hyperaldosteronism and expanded plasma volume, as well as splanchnic vasodilatation Catastrophic bleeding can occur with disruption of the overlying mucosa, associated with 6-week mortality of 10% to 20% Management begins with prevention. Liver stiffness measured by transient elastography values of more than 15 to 20 kPa suggests compensated advanced chronic liver disease- EGD Patients without varices should be surveyed every 2 years, whereas those with small varices should be scoped annually.

56. Patients with red wale marks (longitudinal red streaking), may benefit from starting a nonselective beta blocker. Medium or large varices benefit from treatment with nonselective beta blockade (propranolol, nadolol, and carvedilol) or prophylactic banding. In acute hemorrhage, attention to the ABCDEs of resuscitation is of utmost importance Often brisk and complicated by coagulopathy and thrombocytopenia. Transfusions target Hb between 7 and 8 g/dL is generally recommended to minimize increasing the hepatic venous pressure gradient

57. An INR less than 2 and platelet count greater than 50,000 should be attempted. Vasoactive drugs such as terlipressin , somatostatin, octreotide, and vapreotide should be used prior to endoscopic evaluation and continued for up to 5 days. Antibiotics should be administered to guard against infection and spontaneous bacterial peritonitis. (oral fluoroquinolones or IV Ceftriaxone) Mechanical tamponade in severe instable patient to prevent imminent exsanguination. Temporary measures reserved for pronounced hemodynamic instability as a bridge to more definitive therapy.

58. S engstaken-Blakemore tube

59. Recent trials using self-expanding esophageal stents to control massive variceal hemorrhage have been encouraging Endoscopic venous ligation is preferred over sclerotherapy for acute esophageal bleeding. Definitive long-term management- Early transjugular intrahepatic portosystemic shunt (TIPS) should be performed within 24 to 72 hours high risk patient populations.

60. Contraindication Hepatocellular carcinoma (relative), Heart failure, Pulmonary hypertension, Tricuspid regurgitation Failure predicted by- Venous pressures greater than 20 mm Hg Model for End-Stage Liver Disease (MELD) score greater than 20 Child-Pugh class C cirrhosis Active bleeding at the time of intervention.

61. Surgical decompression- effective, superior, long-term therapy a/w with a mortality rate >50%. Shunts Operations- Nonselective shunt- decompress the entire portal tree. Distal splenorenal shunt- selectively decompress the GE varices while leaving the superior mesenteric and portal veins intact. Non Shunt Operations- Esophageal transection -distal esophagus is transection with delayed stapled after varices ligation. Sugiura procedure- devascularization of the gastroesophageal junction and splenectomy.

62. References 1. Bailey & Love’s Short Practice of Surgery, 28 th Edition. 2. Sabiston Textbook of Surgery, 21 st Edition. 3. Schwartz’s Principles of Surgery, 11 th Edition. 65

63. THANK YOU 66