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Upper GI Bleeding Presenter: Dr. Abdulaziz Almusallam Moderator: Dr. Maher Morris Slide 2 Objectives To Know: The Definition Causes Management Plan Slide 3 Upper GI bleeding Bleeding that arises from the GI tract proximal to the ligament of Treitz. Accounts for nearly 80% of significant GI hemorrhage. Slide 4 The causes of upper GI bleeding Best categorized as: Nonvariceal Bleeding Or Bleeding related to portal hypertension Slide 5 The nonvariceal causes account for about 80% of such bleeding PUD is the most common cause. In the remaining 20% of patients, most of them have cirrhosis and portal hypertension which can lead to the development of: - Gastroesophageal varices, -Isolated gastric varices, -Hypertensive portal gastropathy, All can be the source of an acute upper GI bleed. Slide 6 The patients with cirrhosis are at high risk for developing variceal bleeding, Even in these patients, nonvariceal sources account for most of the episodes of GI hemorrhage. [ [ Because of the greater morbidity and mortality of variceal bleeding, Patients with cirrhosis is generally assumed to have variceal bleeding and appropriate therapy initiated Slide 7 Common Causes of Upper Gastrointestinal Hemorrhage NONVARICEAL BLEEDING (80%) PORTAL HYPERTENSIVE BLEEDING (20%) Peptic ulcer disease 30-50% Mallory-Weiss tears 15-20% Gastritis or duodenitis 10- 15% Esophagitis 5-10% Arteriovenous malformations 5% Tumors 2% Other 5% Gastroesophageal varices >90% Hypertensive portal gastropathy Epinephrine injection Epinephrine injection (1:10,000) to all four quadrants of the lesion is very successful in controlling the hemorrhage. It has been shown that large-volume injection (>13 mL) is associated with better hemostasis, This suggesting that the endoscopic injection works in part by compressing the bleeding vessel and inducing tamponade. Slide 30 Combination therapy Epinephrine injection alone is associated with a high rebleeding rate The standard practice is to provide combination therapy. This usually means the addition of thermal therapy to the injection. Slide 31 The thermal energy A combination of injection with thermal therapy achieves hemostasis in 90% of bleeding PUD cases. The sources of thermal energy can be heater probes, monopolar or bipolar electrocoagulation, laser, or argon plasma coagulator. Slide 32 The thermal energy The most commonly used therapies are :- Electrocoagulation for bleeding ulcers Argon plasma coagulator for superficial lesions. Slide 33 Hemoclips The role of hemoclips is less clear Several studies have reported mixed results. Hemoclips, which can be difficult to apply, may be particularly effective when dealing with a spurting vessel because they provide immediate control of hemorrhage. Slide 34 Rebleeding of an ulcer Rebleeding of an ulcer is associated with a significant increase in mortality Careful observation of patients at high risk for rebleeding is important. Slide 35 Second Endoscopy In those that rebleed, the role of a second attempt at endoscopic control has been controversial but recently validated. Recent study demonstrated that a second attempt at endoscopic hemostasis is successful in 75% of patients. Although this will fail in 25% of patients who will then require emergent surgery There is no increase in morbidity or mortality. Therefore, most clinicians would now encourage a second attempt at endoscopic control before surgical intervention. Slide 36 Surgical Management Despite significant advances in endoscopic therapy, about 10% of patients with bleeding ulcers still require surgical intervention for effective hemostasis several clinical and endoscopic parameters have been employed to identify patients at high risk for failed endoscopic therapy Slide 37 Indications for Surgery in Gastrointestinal Hemorrhage Hemodynamic instability despite vigorous resuscitation (>6 units transfusion) Failure of endoscopic techniques to arrest hemorrhage Recurrent hemorrhage after initial stabilization (with up to two attempts at obtaining endoscopic hemostasis) Shock associated with recurrent hemorrhage Continued slow bleeding with a transfusion requirement exceeding 3 units/day Slide 38 Surgical Management The first priority at operation is control of the haemorrhage. Then A decision must be made regarding the need for a definitive acid-reducing procedure. Slide 39 Surgical Management (Duodenal Ulcer) The first step in the operation for duodenal ulcer is exposure of the bleeding site. Because most of these lesions are in the duodenal bulb, longitudinal duodenotomy or duodenal pyloromyotomy is performed. Hemorrhage can typically be controlled initially with pressure and then direct suture ligation with nonabsorbable suture. Slide 40 Surgical Management (Duodenal Ulcer) When ulcers are positioned anteriorly, typically four-quadrant suture ligation suffices. A posterior ulcer eroding into the pancreaticoduodenal or gastroduodenal artery may require suture ligature of the vessel proximal and distal to the ulcer. Slide 41 Surgical Management (Duodenal Ulcer) After the bleeding has been addressed, a definitive acid-reducing operation is considered. With the identification of the role of H. pylori infection in the pathogenesis of duodenal ulcers There is an argument that simple closure and subsequent treatment for H. pylori is sufficient to prevent recurrence. Slide 42 Surgical Management (Duodenal Ulcer) At the present time an acid-reducing procedure still appears appropriate in most patients. The choice between various operative procedures has been based on the hemodynamic condition of the patient and whether there is a long- standing history of refractory ulcer disease. Slide 43 Surgical Management (Duodenal Ulcer) As the pylorus has often been opened in a longitudinal fashion to control the bleeding, Closure as a pyloroplasty combined with truncal vagotomy is the most frequently used operation for bleeding duodenal ulcer. Slide 44 Truncal vagotomy Slide 45 Surgical Management (Duodenal Ulcer) There is some evidence to suggest that parietal cell vagotomy may represent a better therapy for a bleeding duodenal ulcer in the stable patient Surgeon experience with this procedure may be the determining factor. Slide 46 Surgical Management (Duodenal Ulcer) In a patient who has a known history of refractory duodenal ulcer disease or who has failed more conservative surgery, antrectomy with truncal vagotomy may be more appropriate. This procedure is more complex and is rarely undertaken in a hemodynamically unstable patient. Slide 47 Surgical Management (Bleeding gastric ulcers) Similar to bleeding duodenal ulcers, control of bleeding is the immediate priority This may require gastrotomy and suture ligation, which, if no other procedure is performed, is associated with about a 30% risk for rebleeding. In addition, because of the approximate 10% incidence of malignancy, gastric ulcer resection is generally indicated. Slide 48 Surgical Management (Bleeding gastric ulcers) Simple excision alone is associated with rebleeding in as many as 20% of patients, so that distal gastrectomy is generally preferred, although excision combined with vagotomy and pyloroplasty may be considered in the high-risk patient. Slide 49 Surgical Management (Bleeding gastric ulcers) Bleeding ulcers of the proximal stomach near the gastroesophageal junction are more difficult to manage. Proximal or near-total gastrectomy is associated with a particularly high morbidity in the setting of acute hemorrhage. Slide 50 Surgical Management (Bleeding gastric ulcers) Options include: Distal gastrectomy combined with resection of a tongue of proximal stomach to include the ulcer Or Vagotomy and pyloroplasty combined with either wedge resection or simple oversewing of the ulcer. Slide 51 Mallory-Weiss tears Mucosal and submucosal tears that occur near the gastroesophageal junction. Classically, these lesions develop in alcoholic patients after a period of intense retching and vomiting after binge drinking, Can occur in any patient who has a history of repeated emesis. Slide 52 Mallory-Weiss tears The mechanism, proposed by Mallory and Weiss in 1929, is forceful contraction of the abdominal wall against an unrelaxed cardia, resulting in mucosal laceration of the proximal cardia as a result of the increase in intragastric pressure. Account for 5% to 10% of cases of upper GI bleeding Slide 53 Mallory-Weiss tears Usually diagnosed based on history. Endoscopy is frequently employed to confirm the diagnosis. To avoid missing the lesion. Important to perform a retroflexion maneuver and view the area just below the gastroesophageal junction. Most tears occur along the lesser curvature. Slide 54 Mallory-Weiss tears Slide 55 Supportive therapy is often all that is necessary because 90% of bleeding episodes are self-limited, and the mucosa often heals within 72 hours. In rare cases of severe ongoing bleeding, local endoscopic therapy with injection or electrocoagulation may be effective. Slide 56 Mallory-Weiss tears Angiographic embolization, with absorbable material such as gelatin sponge, has been successfully employed If these maneuvers fail, high gastrotomy and suturing of the mucosal tear is indicated. It is important to rule out the diagnosis of variceal bleeding. Recurrent bleeding from a Mallory-Weiss tear is uncommon. Slide 57 Stress- gastritis Stress-related gastritis is characterized by the appearance of multiple superficial erosions of the entire stomach, most commonly in the body. It is thought to result from the combination of acid and pepsin injury in the context of ischemia from hypoperfusion states, although NSAIDs produce a very similar appearance. Slide 58 Stress- gastritis In the 1960s and 1970s, it was a commonly encountered lesion in critically ill patients, with significant morbidity and mortality from bleeding. Today, with improvements in the management of shock and sepsis, as well as widespread use of acid-suppressive therapy, significant bleeding from such lesions is rarely encountered Slide 59 Esophagitis The esophagus is infrequently the source of significant hemorrhage. When it does occur, it is most commonly the result of esophagitis. Esophageal inflammation secondary to repeated exposure of the esophageal mucosa to the acidic gastric secretions in gastroesophageal reflux disease (GERD) leads to an inflammatory response, which can result in chronic blood loss. Slide 60 Esophagitis Ulceration may accompany but the superficial mucosal ulcerations generally do not bleed acutely, but rather present as anemia or guaiac-positive stools. A variety of infectious agents may also cause esophagitis, particularly in the immunocompromised host. With infection, hemorrhage can occasionally be massive. Slide 61 Esophagitis Other causes of esophageal bleeding include medications, Crohn's disease, and radiation. Treatment typically includes acid- suppressive therapy. Endoscopic control of the hemorrhage, usually with electrocoagulation or heater probe, is often successful. Slide 62 Esophagitis In patients with an infectious etiology, targeted therapy is appropriate. Operation is seldom necessary. Slide 63 Dieulafoy's Lesion Dieulafoy's lesions are vascular malformations found primarily along the lesser curve of the stomach within 6 cm of the gastroesophageal junction Slide 64 Dieulafoy's Lesion Can occur elsewhere in the GI tract They represent rupture of unusually large vessels (1-3 mm) that are found in the gastric submucosa. Erosion of the gastric mucosa overlying these vessels leads to hemorrhage. The mucosal defect is usually small (2-5 mm) and may be difficult to identify. Slide 65 Dieulafoy's Lesion Given the large size of the underlying artery, bleeding from a Dieulafoy's lesion can be massive. Initial attempts at endoscopic control are often successful. Application of thermal or sclerosant therapy is effective in 80% to 100% of cases. Slide 66 Dieulafoy's Lesion In cases that fail endoscopic therapy, angiographic coil embolization can be successful. If these approaches fail, surgical intervention may be necessary. Because of the difficulties in visualization and palpation of these lesions, prior endoscopic tattooing can facilitate the procedure. Slide 67 Dieulafoy's Lesion A gastrotomy is performed, and attempts are made at identifying the bleeding source. In cases in which the bleeding point is not identified, a partial gastrectomy may be necessary. Slide 68 Gastric Antral Vascular Ectasia Also known as watermelon stomach, Gastric antral vascular ectasia (GAVE) is characterized by a collection of dilated venules appearing as linear red streaks converging on the antrum in longitudinal fashion, giving it the appearance of a watermelon. Slide 69 Gastric Antral Vascular Ectasia Acute severe hemorrhage is rare in GAVE Most patients present with persistent, iron deficiency anemia from continued occult blood loss. Slide 70 Gastric Antral Vascular Ectasia Endoscopic therapy is indicated for persistent, transfusion-dependent bleeding and has been reportedly successful in up to 90% of patients. The preferred endoscopic therapy is argon plasma coagulation. Those failing endoscopic therapy are considered for antrectomy. Slide 71 Malignancy Malignancies of the upper GI tract are usually associated with chronic anemia or hemoccult-positive stool rather than episodes of significant hemorrhage. On occasion, malignancies present as ulcerative lesions that bleed persistently. This is perhaps most characteristic of the GI stromal tumor (GIST) Slide 72 Malignancy Bleeding may occur with a variety of other lesions, including leiomyomas and lymphomas. Although endoscopic therapy is often successful in controlling hemorrhage, the rebleeding rate is high. Therefore, when a malignancy is diagnosed, surgical resection is indicated. Slide 73 Malignancy The extent of resection is dependent on the specific lesion and on whether the resection is curative or palliative. Palliative resections for control of bleeding usually entail wedge resections. Standard cancer operations are indicated when possible, although this may depend on the hemodynamic stability of the patient. Slide 74 Aortoenteric Fistula Primary aortoduodenal fistulas are rare lesions developing in up to 1% of aortic graft cases. They typically develop in the setting of a previous abdominal aortic aneurysm repair. May occur as a result of an inflammatory or infectious aortitis. Slide 75 Aortoenteric Fistula The interval between surgery and hemorrhage can be days to years. The median interval is about 3 years. The sequence is thought to involve development of a pseudoaneurysm at the proximal anastomotic suture line in the setting of an infection, With subsequent fistulization into the overlying duodenum. Slide 76 Aortoenteric Fistula Aortoenteric fistula is considered in all patients with GI hemorrhage with a known abdominal aortic aneurysm or a previous prosthetic aneurysm repair. Hemorrhage is often massive and fatal unless immediate surgical intervention is undertaken. Slide 77 Aortoenteric Fistula Typically, patients with bleeding from an aortoenteric fistula will present first with a sentinel bleed. This is a self-limited episode that heralds the subsequent massive, and often fatal, hemorrhage. This prompts urgent EGD because diagnosis at this stage can be lifesaving. Slide 78 Aortoenteric Fistula Any evidence of bleeding in the distal duodenum (3rd or 4th portion) is considered diagnostic. CT scan with IV contrast will demonstrate air around the graft (suggestive of an infection), Possible pseudoaneurysm, Rarely the presence of IV contrast in the duodenal lumen. Slide 79 Aortoenteric Fistula Slide 80 Aortoenteric Fistula Therapy includes : Ligation of the aorta proximal to the graft. Removal of the infected prosthesis. Extra-anatomic bypass. The defect in the duodenum is often small and can be repaired primarily. o This is a complex and often morbid procedure. Slide 81 Hemobilia Difficult diagnosis to make. Typically associated with trauma, recent instrumentation of the biliary tree, or hepatic neoplasms. Unusual cause of GI bleeding. Suspected in anyone who presents with hemorrhage, right upper quadrant pain, and jaundice. Unfortunately, this triad is seen in less than half of patients Slide 82 Hemobilia Endoscopy can be helpful by demonstrating blood at the ampulla. Angiography is the diagnostic procedure of choice. If diagnosis is confirmed: Angiographic embolization is the preferred treatment. Slide 83 Hemosuccus Pancreaticus Rare cause of upper GI bleeding. Bleeding from the pancreatic duct, or hemosuccus pancreaticus. Typically caused by erosion of a pancreatic pseudocyst into the splenic artery. Presents with abdominal pain and hematochezia. Slide 84 Hemosuccus Pancreaticus Difficult diagnosis to make and requires a high index of suspicion. In patients with abdominal pain, blood loss, and a past history of pancreatitis. Angiography is diagnostic and permits embolization, which is often therapeutic. In cases that are amenable to a distal pancreatectomy, this procedure often results in cure. Slide 85 Iatrogenic Bleeding Upper GI bleeding may follow therapeutic or diagnostic procedures. Hemobilia may be iatrogenic in nature, particularly after percutaneous transhepatic procedures. Another common cause of iatrogenic bleeding is endoscopic sphincterotomy. This can occur in up to 2% of cases. Slide 86 Iatrogenic Bleeding Percutaneous endoscopic gastrostomy (PEG) placement is an increasingly common procedure. Bleeding rates of up to 3% have been reported. This can often be controlled endoscopically. Slide 87 Iatrogenic Bleeding Upper GI bleeding can also be seen in patients who have recently undergone upper GI surgery. In cases in which a resection and anastomosis have been performed, the source of the bleeding may be the suture or the staple line. It is safe to perform a diagnostic or even therapeutic EGD Slide 88 Bleeding Related to Portal Hypertension Slide 89 Upper GI bleeding is a serious complication of portal hypertension. Most often in the setting of cirrhosis. Hemorrhage related to portal hypertension is most commonly the result of bleeding from varices. Slide 90 The Varices These dilated submucosal veins develop in response to the portal hypertension. Providing a collateral pathway for decompression of the portal system into the systemic venous circulation. Most common in the distal esophagus. May develop in the stomach and the hemorrhoidal plexus of the rectum. Slide 91 The Varices They can reach sizes of 1 to 2 cm. As they enlarge, the overlying mucosa becomes increasingly tenuous and bleeding occurring with minimal trauma. Slide 92 Portal hypertensive gastropathy Diffuse dilation of the mucosal and submucosal venous plexus of the stomach associated with overlying gastritis. Incompletely understood entity. Endoscopically, the stomach acquires a snakeskin-like appearance with cherry-red spots. This entity uncommonly produces major hemorrhage. Slide 93 Gastroesophageal varices Develop in about 30% of patients with cirrhosis and portal hypertension. 30% in this group develop variceal bleeding. Compared with nonvariceal bleeding, variceal hemorrhage is associated with : Increased risk for rebleeding Increased need for transfusions increased hospital stay, and mortality Slide 94 Gastroesophageal varices Hemorrhage is frequently massive, accompanied by hematemesis and hemodynamic instability. The hepatic functional reserve, estimated by Child's criteria. Despite improvements in the medical management of these patients, the 6-week mortality rate after the first hemorrhage is about 20%. Slide 95 Gastroesophageal varices Slide 96 Algorithm for diagnosis and management of GI hemorrhage related to portal hypertension. EGD, esophagogastroduodenoscopy; TIPS, transjugular intrahepatic portosystemic shunt. Slide 97 Medical Management For Bleeding GE varices In patients with cirrhosis: pharmacologic therapy to reduce portal hypertension even while preparing for emergent EGD. Vasopressin produces splanchnic vasoconstriction but also cardiac vasoconstruction and can lead to MI. Somatostatin or its synthetic analogue, Octreotide, is now the vasoactive agent of choice without cardiac side effects. Studies have demonstrated its efficacy in controlling variceal bleeding. Slide 98 Endoscopic Management For Bleeding GE varices Early EGD is critical to evaluate the source of bleeding. If bleeding esophageal varices are identified: Both sclerotherapy and variceal banding have been shown to control hemorrhage effectively. Banding appears to have a lower complication rate and, when expertise is available, is the therapy of choice Slide 99 Endoscopic Management For Bleeding GE varices Endoscopic approaches, sometimes with as many as three treatments over 24 hours, control the hemorrhage in up to 90% of patients with esophageal varices. Unfortunately, gastric varices are not effectively managed by endoscopic techniques. Slide 100 Actively bleeding varices. And Effective control after variceal banding. Slide 101 Other Management For Bleeding GE varices In cases in which pharmacologic or endoscopic therapies fail to control the hemorrhage: Tamponade can be successful in temporizing the hemorrhage. The Sengstaken-Blakemore tube consists of a gastric tube with esophageal and gastric balloons. The Sengstaken-Blakemore tube consists of a gastric tube with esophageal and gastric balloons. Slide 102 Other Management For Bleeding GE varices The gastric balloon is inflated, and tension is applied to the gastroesophageal junction. If this does not control the hemorrhage, the esophageal balloon is inflated as well. compressing the venous plexus between them. These tubes are associated with a high rate of complications with both aspiration and inappropriate placement with esophageal perforation. Slide 103 Other Management For Bleeding GE varices Hemorrhage recurs on deflation in up to 50% of patients. Currently, balloon tamponade is reserved for patients with massive hemorrhage to permit more definitive therapies. In cases of severe variceal bleeding that cannot be controlled endoscopically, emergent portal decompression is indicated. Slide 104 percutaneous transjugular intrahepatic portosystemic shunt (TIPS) Required in about 10% of patients with variceal bleeding. TIPS procedure can be lifesaving in patients who are hemodynamically unstable from refractory variceal bleeding. Associated with significantly less morbidity and mortality than surgical decompression. Slide 105 percutaneous transjugular intrahepatic portosystemic shunt (TIPS) Studies have shown that TIPS can control bleeding in 95% of cases. Rebleeding occurs in up to 20% within the first month, usually related to occlusion. In cases in which TIPS is not available or fails, emergent surgical intervention is indicated. Slide 106 Isolated gastric varices Managed in much the same way as esophageal varices, although endoscopic therapy tends to be less successful. Pharmacotherapy is primarily indicated, but when this fails, portal decompression by means of TIPS or a surgical shunt is recommended. Slide 107 Isolated gastric varices Rarely, isolated gastric varices occur after splenic vein thrombosis. Most commonly seen in the setting of pancreatitis. portal pressures are normal, but left-sided hypertension, decompressed from the spleen through the short gastric vessels, produces the varices. splenectomy was routinely recommended, recent data suggest that the incidence of variceal bleeding is low (4%) splenectomy is not routinely undertaken now. Slide 108 Portal hypertensive gastropathy Unlike variceal hemorrhage, bleeding from portal hypertensive gastropathy is not amenable to endoscopic treatment. Because of the diffuse nature of the mucosal abnormalities. The underlying pathology involves elevated portal venous pressures; Therefore, pharmacologic therapies aimed at reducing portal venous pressure are indicated. If pharmacologic therapy fails to control acute bleeding, TIPS is considered. Slide 109 Thank you