The Clinical Approach to the Most Frequent Acute Conditions in Abdominal SurgeryGI BleedingAdam Janiak

GI BleedingUpper GI bleedingLower GI bleeding

Upper GI BleedingProximal to the ligament of TreitzCauses:

peptic ulcer disease (1/2 2/3 UGI bleeding)esophageal varices (10 percent)hemorrhagic gastritisgastric varicesnose bleedMallory-Weiss tearsreflux esophagitisgastric neoplasmshematobilia

The most common causes of upper gastrointestinal bleeding are chronic duodenal ulcers, chronic gastric ulcers, esophageal varices, gastric varices, Mallory-Weiss tears, acute hemorrhagic gastritis, and gastric neoplasms. Less common causes include various other gastrointestinal conditions and certain hepatobiliary and pancreatic disorders

Presentations of UGI BleedingSevere bleedinghematemesis 25 % red blood hematemesiscoffee ground emesishematochezia 15 %hypotensionGradual bleedingmelena 25 % (50 100 cc of blood will render stool melenic)Occult bleedingpositive tests for blood in the stool

Upper gastrointestinal hemorrhage may present as severe bleeding with hematemesis, hematochezia, and hypotension; as gradual bleeding with melena; or as occult bleeding detected by positive tests for blood in the stool.

Initial Evaluation of UGI Bleeding 1Perceived rate of bleedingDegree of hemodynamic stabilityOutpatient basishemodynamically stableno evidence of active bleeding or comorbiditiesendoscopic findings favorableHospitalizationevidence of serious bleeding

The initial steps in the evaluation of patients with upper GI bleeding are based on the perceived rate of bleeding and the degree of hemodynamic stability. Hemodynamically stable patients who show no evidence of active bleeding or comorbidities and in whom endoscopic findings are favorable may be treated on an outpatient basis, whereas patients who show evidence of serious bleeding should be managed aggressively and hospitalized.

Initial Evaluation of UGI Bleeding 2ABCHistory of or current:hematemesismelenahematocheziaLab Tests:CBCblood chemistries (liver and renal function tests)prothrombin time (PT) and partial thromboplastin time (PTT)blood typing and crossmatching

Initial Evaluation of UGI Bleeding 3patient stable & no evidence of recent or active hemorrhage proceed with the workup. patient stable & shows evidence of recent or active bleeding large-bore IV line before workuppatient unstable immediate resuscitation

The airway, breathing, and circulation should be rapidly assessed, and the examiner should note whether the patient has a history of or currently exhibits hematemesis, melena, or hematochezia. Blood should be drawn for a complete blood count, blood chemistries (including tests of liver function and renal function), and measurement of the prothrombin time (PT) and the partial thromboplastin time (PTT). Blood should be sent to the blood bank for typing and crossmatching.If the patient is stable and shows no evidence of recent or active hemorrhage, the surgeon may proceed with the workup. If, however, the patient is stable but shows evidence of recent or active bleeding, a large-bore intravenous line should be placed before workup is begun; the presence of the line ensures immediate I.V. access should the patient subsequently become unstable. If the patient is unstable, resuscitation should be begun immediately.

Resuscitation in UGI Bleedingsecure airway for adequate ventilation (Oxygen as necessary) large-bore I.V. line for lactated Ringer solution urinary catheter for urine output monitoringblood infusion as necessarycoagulopathy correcion

It is all too easy to forget these basic steps in a desire to evaluate and manage massive GI hemorrhage!

patient unstable & continues to bleed intraoperative diagnosislaparotomy through an upper midline incisionanterior gastrotomypylorus-preserving duodenotomy

Resuscitation of an unstable patient is begun by establishing a secure airway and ensuring adequate ventilation. Oxygen should be given as necessary, either by mask or by endotracheal tube and ventilator. A large-bore I.V. line should then be placed, through which lactated Ringer solution should be infused at a rate high enough to maintain tissue perfusion. A urinary catheter should be inserted and urine output monitored. Blood should be given as necessary, and any coagulopathies should be corrected if possible. It is all too easy to forget these basic steps in a desire to evaluate and manage massive GI hemorrhage. If the patient remains unstable and continues to bleed despite supportive measures, he or she should be taken to the operating room for intraoperative diagnosis. The abdomen should be opened through an upper midline incision, and an anterior gastrotomy should be performed. If inspection does not reveal the source of the bleeding or if bleeding is observed beyond the pylorus, a duodenotomy is made, with care taken to preserve the pylorus if possible. Bleeding from the proximal stomach may be difficult to verify, but it should be actively sought if no other bleeding site is identified.

Clinical Evaluation of UGI BleedingHistory known causes of upper GI bleeding (e.g., ulcers, recent trauma or stress, liver disease, varices, alcoholism, and vomiting)use of medications that interfere with coagulation (e.g. NSAIDs, dipyridamole) or alter hemodynamics (e.g., beta blockers and antihypertensive agents)cardiac history for assessing ability to withstand anemia Physical Examination jaundiceascitestumor massbruit from an abdominal vascular lesion Nasogastric Aspirationbloody aspirate EGDclear, nonbilious aspirate bleeding site distal to the pylorusclear and bile-stained aspirate source of the bleeding is unlikely to be the stomach, the duodenum, the liver, the biliary tree, or the pancreas

HISTORY Only after the initial measures to protect the airway and stabilize the patient have been completed should an attempt be made to establish the cause of the bleeding. The history should focus on known causes of upper GI bleeding (e.g., ulcers, recent trauma or stress, liver disease, varices, alcoholism, and vomiting) and on the possible use of medications that interfere with coagulation (e.g., aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], and dipyridamole) or alter hemodynamics (e.g., beta blockers and antihypertensive agents). The cardiac history is particularly important for assessing the patient's ability to withstand varying degrees of anemia. PHYSICAL EXAMINATION The physical examination is seldom of much help in determining the exact site of bleeding, but it may reveal jaundice, ascites, or other signs of hepatic disease; a tumor mass; or a bruit from an abdominal vascular lesion. NASOGASTRIC ASPIRATION The next step is nasogastric aspiration. A bloody aspirate is an indication for esophagogastroduodenoscopy (EGD), as is a clear, nonbilious aspirate if a bleeding site distal to the pylorus has not been excluded. If the aspirate is clear and bile-stained, the source of the bleeding is unlikely to be the stomach, the duodenum, the liver, the biliary tree, or the pancreas. Nonetheless, if subsequent evaluation of the lower GI tract for the source of the bleeding is unrewarding, an upper GI site that had stopped bleeding when the nasogastric tube was passed or that was distal to the ligament of Treitz should still be considered.

Upper GI Endoscopy 1almost always reveals the source of UGI bleedingrequires considerable skillhematemesis emergency EGD (within 1 hour of presentation) melena urgent EGDendoscopic control of bleeding sites injectionthermal coagulationmechanical occlusion (clip application or variceal banding)

EGD almost always reveals the source of upper GI bleeding; its utility and accuracy have been well documented in the literature. This procedure requires considerable skill: identification of bleeding sites in a blood-filled stomach is far from easy. Hematemesis is an indication for emergency EGD, usually within 1 hour of presentation. If the rate of bleeding is high, saline lavage may be performed to clear the stomach of blood and clots. If the rate of bleeding is moderate or low, as is often the case in patients with melena, urgent EGD is indicated.EGD is not only an excellent diagnostic tool but also a valuable therapeutic modality. Indeed, most upper GI hemorrhages may be controlled endoscopically, though the degree of success to be expected in individual cases varies according to the expertise of the endoscopist and the specific cause of the bleeding. Therapeutic endoscopic maneuvers include injection, thermal coagulation, and mechanical occlusion of bleeding sites (by means of clip application or variceal banding). The choice of therapy depends on the cause, the site, and the rate of bleeding.

Upper GI Endoscopy 2

Ulcer Appearance and Prognosis

AppearancePrevalence %Rebleed %Mortality %Clean base4252Flat spot20103Clot17227Visible vessel174311Active bleeding185511

Other Testsenteroclysis + RTGTc tagged red cell scanarteriographyvideo capsule endoscopyintraoperative endoscopy

If endoscopic examination reveals no lesions in the stomach or the duodenum and bleeding has ceased, enteroclysis (direct introduction of BaSO4 into the small bowel) and roentgenography of the duodenum and the jejunum should be done next. This is probably a more sensitive radiologic test than a standard small bowel roentgenogram. Nonetheless, the absence of a lesion on this test does not rule out the small bowel as the source of the hemorrhage; not uncommonly, the x-ray is negative when a bleeding small bowel lesion is present. Tagged red cell scans may confirm the presence of an active bleeding site; however, scans are fairly nonspecific with respect to determining the anatomic location of the bleeding. Arteriography may demonstrate that a lesion is present, but it cannot reliably identify a bleeding site unless the bleeding is brisk (> 1 ml/min). Occasionally, arteriography reveals the cause of the bleeding even if the bleeding has stopped. Recurrent bleeding or bleeding that is suspected to be secondary to small bowel pathology may be evaluated by means of video capsule endoscopy, which is capable of localizing a variety of lesions (including arteriovenous malformations, ulcers, strictures, and malignancies) so as to direct surgical intervention. Video capsule endoscopy should be used with caution in patients exhibiting obstructive symptoms: if the capsule becomes trapped, complete obstruction may result. Intraoperative endoscopic exploration may also prove useful in this situation. Before the small bowel is manipulated, a pediatric colonoscope is introduced either orally or through a distal jejunal enterotomy; the latter method allows easier viewing of the entire small bowel. The mucosal detail is examined as the surgeon guides the scope through the small bowel. The bowel must be handled gently to avoid a mucosal injury, which could mimic a significant lesion.These tests, in conjunction with EGD, should allow the surgeon to establish the cause of upper GI bleeding at least 90% of the time.

Enteroclysis

Enteroclysis is a test performed to examine the small bowel. A tube is placed down the nose and throat, through the stomach into the small intestine. When in place, contrast dye is introduced and x-ray images are viewed on a fluoroscopic monitor to visualize how the contrast moves through the bowel structures. The enteroclysis test is the most complete means of demonstrating whether or not the small intestine is normal when abnormality is suspected.

Upper GI Tract Barium RTG

Tc Red Cell Scan

Celiac Arteriography

Video Capsule Endoscopy

Endoscopic Therapy in UGI bleedingEffectively reducesRebleedingNeed for SurgeryMortality (by meta-analysis)10 20 percent of patients have rebleeding after (initially successful) endoscopic therapy

The Role of Adjunctive Pharmacological TherapyClot stabilization: at a pH of above 6.0 pepsin is inactivated and cannot lyse clotsEffective clotting may not occur at a pH of 5.9 or lowerAntacids, iced saline gastric lavage and H2-blockers and other interventions are ineffective in reducing rebleeding rates

Proton Pump InhibitorsNEJM 1997: high dose oral omeprazole effective in reducing rebleeding rates. No endoscopic therapy performed in this study from IndiaTwo multicenter trials from Scandinavia showed benefit of high dose I.V. omeprazole (1997)Taiwanese study of 100 patients randomized between IV omeprazole and cimetidine. Intragastric pH was around 6.0 for first 24 hours in omeprazole group but only between 4.5 to 5.5 for cimetidine group. 12 pts in the cimetidine group and 2 pts in the omeprazole group rebled. No change in LOS, number of procedures, or mortality (1998)

Management of UGI Bleeding 1Chronic duodenal ulcerendoscopic controlPPIanti-HP antibiotherapysurgery (anterior gastrotomy, duodenotomy)Gastric ulcerendoscopic controlPPIanti-HP antibiotherapysurgery (ulcer excision, , hemigastrectomy, duodenotomy, vagotomy+pyloroplasty?)Esophageal or gastric varicesendoscopy (rubber banding, intravariceal sclerotherapy)balloon tamponade (four-port Minnesota tube, Sengstaken-Blakemore tube) somatostatin, octreotide (synthetic analogue of somatostatin)vasopressinsurgery (transjugular intrahepatic portosystemic shunt TIPS, distal splenorenal shunt, central portacaval shunt, Segura procedure)

CHRONIC DUODENAL ULCER The development of effective medical regimens for controlling uncomplicated duodenal ulcers has led to a drastic reduction in the number of elective surgical procedures performed for this purpose. Nevertheless, the incidence of bleeding from duodenal ulcers that is severe enough to necessitate emergency endoscopic or operative intervention has not decreased over the past decade. Once EGD has demonstrated that a duodenal ulcer is the source of the bleeding, the first question that must be addressed is whether active bleeding is present. If it is, an attempt should be made to control the hemorrhage endoscopically. Because ongoing blood loss eventually leads to coagulopathies, the surgeon must exercise good judgment in deciding how long to pursue endoscopic treatment before concluding that such treatment has failed and that surgical treatment is necessary. In general, substantial bleeding (four to six units or more) that is not easily controlled endoscopically is an indication for immediate surgical intervention. Likewise, ongoing hemorrhage in a hemodynamically unstable patient (especially an elderly one) calls for immediate surgical therapy. If bleeding is controlled endoscopically, then a proton pump inhibitor (PPI)such as pantoprazole, 40 mg/dayshould be given intravenously. In addition, antibiotic therapy directed against Helicobacter pylori (e.g., a 14-day course of metronidazole, 500 mg p.o., t.i.d.; omeprazole, 20 mg p.o., b.i.d.; and clarithromycin, 500 mg p.o., b.i.d.) should be considered if the organism is present; such therapy has been shown to decrease rebleeding rates after antacid medication has been stopped. Food need not be withheld unless the likelihood of rebleeding is high, in which case operation or repeat endoscopy would be necessary. Resumption of oral feeding does not appear to affect rebleeding rates. If bleeding continues despite medical and endoscopic therapy, it should be managed surgically. In addition, certain patients whose bleeding was controlled endoscopicallysuch as those with a visible gastroduodenal artery and a clot in the base of the ulcer, those who experience rebleeding despite medical and endoscopic therapy, and those with giant ulcersshould be strongly considered for surgical therapy. Surgical management may be accomplished either laparoscopically or via an open approach. The latter begins with an upper midline incision. The duodenum is mobilized and an anterior longitudinal duodenotomy performed over the site of the ulcer. The bleeding vessel, which is usually on the posterior wall of the first portion of the duodenum, is ligated with nonabsorbable sutures at sites proximal and distal to the bleeding point. A third stitch is placed posterior to the bleeding vessel. Pains must be taken to avoid injury to the common bile duct during the placement of these sutures. The duodenotomy is then closed. The role of vagotomy in the management of bleeding duodenal ulcers has been called into question. Previously, proximal gastric vagotomy was recommended for stable patients. It was considered preferable to truncal vagotomy because it is less likely to result in gastric atony, alkaline reflux gastritis, dumping, and diarrhea. In unstable patients, truncal vagotomy was typically performed in conjunction with pyloroplasty. Frozen section to confirm the presence of nerve tissue is helpful for ensuring that the vagotomy is complete. The recommendation for truncal vagotomy was based on data from studies done before PPI and anti-H. pylori therapy came into use. Subsequent studies that evaluated rebleeding rates with current medical regimens, however, demonstrated much lower rebleeding rates. Furthermore, it seems probable that long-term PPI therapy (e.g., omeprazole, 20 mg p.o., q.d.)the medical equivalent of vagotomyin conjunction with eradication of H. pylori and avoidance of NSAIDs, should decrease rebleeding rates significantly. Therefore, one may consider an alternative treatment approach in patients who had not been receiving ulcer therapy before the bleeding begannamely, ligation of the bleeding vessel, postoperative administration of PPIs, and anti-H. pylori therapy. This approach avoids the complications associated with truncal vagotomy. CHRONIC GASTRIC ULCER Initially, bleeding from a chronic gastric ulcer is managed in much the same way as that from a chronic duodenal ulcer (i.e., endoscopically) To prevent aggravation of the bleeding, early biopsy generally is not recommended; repeat endoscopy and biopsy are done at a later date. Emergency surgical indications for gastric ulcers are the same as those for duodenal ulcers. In addition, if a gastric ulcer does not resolve after 6 weeks of medical therapy, surgical excision is often indicated. In stable patients, surgical management of a nonhealing chronic gastric ulcer generally consists of a hemigastrectomy that includes the ulcer site; if the ulcer is located more proximally, it may be removed by means of wedge excision. Excision of the ulcer should be immediately followed by frozen section to rule out cancer. There is no need for a vagotomy in these instances. In unstable patients, hemigastrectomy should probably be avoided because of the increased morbidity and mortality that can follow it. Wedge excision should be combined with aggressive acid-suppressive therapy (PPIs or H2 receptor antagonists), followed by anti-H. pylori treatment. Truncal vagotomy with pyloroplasty is rarely indicated; however, it may be considered in a patient with previous complications from ulcer disease. ESOPHAGEAL VARICES The value of endoscopy in the diagnosis and management of variceal bleeding cannot be overemphasized. Even in patients with known varices, the site of bleeding is frequently nonvariceal; endoscopy is therefore essential. If bleeding varices are identified, rubber banding or intravariceal sclerotherapy with a sclerosing agent (1.5% sodium tetradecyl sulfate, ethanolamine, sodium morrhuate, or absolute alcohol) is performed [see Figure 2]. If these measures do not control the hemorrhage, balloon tamponade is indicated. Patients who are to undergo this procedure should have an endotracheal tube in place. The tube we prefer to use for balloon tamponade is the four-port Minnesota tube, although the Sengstaken-Blakemore tube is also acceptable. The Minnesota tube has a gastric balloon, an esophageal balloon, and aspiration ports for the esophagus and the stomach. The gastric balloon is inflated first and placed on traction. If the bleeding is not controlled, the esophageal balloon is then inflated. The pressure in the balloons should be released in 24 to 48 hours to prevent necrosis of the esophageal or the gastric wall. Successful balloon tamponade is followed by endoscopic variceal injection or variceal banding.

I.V. somatostatin (250 ug bolus, followed by infusion of 250 ug/hr) should be administered in conjunction with the above-mentioned steps. Vasopressin (10 U/hr) may also be given; however, it causes diffuse vasoconstriction, and nitroglycerin is required to alleviate cardiac side effects. Somatostatin has proved superior to placebo in controlling variceal hemorrhage when used in conjunction with endoscopic sclerotherapy. It is as effective as vasopressin while giving rise to fewer side effects. Octreotide, a synthetic analogue of somatostatin, shares many of the properties of somatostatin but perhaps not all. Both agents decrease secretion of gastric acid and pepsin; to date, however, the decreased gastric blood flow observed with somatostatin administration has not been reported with octreotide administration. Nevertheless, some clinicians in the United States elect to use octreotide (25 to 50 ug/hr) in place of I.V. somatostatin because the former tends to be more widely available in the United States. Multiple prospective, randomized trials showed that propranolol (40 mg b.i.d., p.o.) decreased the incidence of first-time variceal bleeding as well as the incidence of recurrent variceal bleeding. Propranolol should not be used during active bleeding but should be started once bleeding stops.

After the acute variceal bleeding has been controlled, any remaining varices should be subjected to injection sclerotherapy or banding at 2-week intervals until they too are obliterated.

The main indications for surgical intervention in patients with bleeding esophageal varices are uncontrolled hemorrhage and persistent rebleeding despite endoscopic and medical therapy. When surgical intervention is planned, it is essential to determine whether the patient is a transplant candidate. If so, operation should be avoided and bleeding managed by decompressing the portal venous system with a transjugular intrahepatic portosystemic shunt (TIPS). TIPS yields excellent short-term results with respect to stopping bleeding and providing time to locate a liver suitable for transplantation; however, it has not been shown to have the capacity to control hemorrhage by itself over the long term. Thus, its use in patients who are not transplant candidates is questionable.

If the patient is not a transplant candidate and is not actively bleeding, a distal splenorenal shunt is preferable. Arteriograms with views of the portal vein and the left renal vein are obtained. Alternatively, computed tomographic angiography with three-dimensional reconstruction may be performed. If the venous anatomy is suitablethat is, if the diameter of the splenic vein is greater than 0.75 cm (preferably greater than 1.0 cm) and the vein is within one vertebral body of the renal vein on venographya distal splenorenal shunting procedure should be feasible. If the venous anatomy is not suitable, then esophageal transection, a mesocaval venous graft, or a portacaval shunt is required.

In the emergency setting, we prefer a central portacaval shunt, usually in a side-to-side orientation or with a short polytetrafluoroethylene (PTFE) interposition graft. Esophageal transection is also a reasonable choice. This procedure is associated with a lower incidence of encephalopathy than a portacaval shunting procedure; however, it is associated with higher rates of rebleeding (particularly late rebleeding), and it can be difficult to perform when active bleeding is present. Suture ligation of the bleeding varices with devascularization (the Segura procedure) should also be considered.

In general, prognosis is related to the underlying liver disease. For example, patients with varices that are secondary to chronic extrahepatic portal venous or splenic venous occlusion generally have a much better prognosis than those whose portal hypertension is secondary to hepatic parenchymal causes. The severity of the cirrhosis also determines short-term and long-term survival and may influence the decision whether to perform a shunting procedure.

Varices in children are generally secondary to portal vein thrombosis. A conservative, nonoperative approach is preferred. If operation is required, either a portacaval shunt, a distal splenorenal shunt, or a devascularization procedure is performed. In children or adults with varices that are secondary to splenic vein thrombosis (sinistral portal hypertension), a splenectomy is usually curative; the procedure may be performed laparoscopically [see 3:19 Laparoscopic Splenectomy].

GASTRIC VARICES

Gastric varices are managed in much the same way as esophageal varices [see Figure 2], though they are less amenable to sclerotherapy. If sclerotherapy fails to control bleeding from gastric varices, surgical interventionin the form of distal splenorenal shunting, portosystemic shunting, or suture ligation with gastric devascularizationis indicated. If the patient is a suitable candidate, liver transplantation may be performed as an alternative to shunting.

MALLORY-WEISS TEARS

Mallory-Weiss tears are linear tears at the esophagogastric junction that are usually caused by vomiting. Any patient who presents with vomiting that initially is not bloody but later turns so should be suspected of having a Mallory-Weiss tear. As a rule, these lesions stop bleeding without therapy. If bleeding is substantial or persistent, however, endoscopic coagulation may be necessary. In rare instances, the tear will have to be oversewn at operation. This is accomplished via an anterior gastrotomy and direct suture ligation of the tear.

ACUTE HEMORRHAGIC GASTRITIS

Bleeding from gastritis is virtually always managed medically with H2 receptor blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if H. pylori is present. Somatostatin may be beneficial. Sometimes, administration of vasopressin via the left gastric artery is needed to control bleeding. In rare cases, total or near-total gastrectomy [see 3:13 Gastroduodenal Procedures] is required; however, the mortality associated with this operation in this setting is high. Stress ulcer prophylaxis in severely ill or traumatized patients is essential to prevent this problem. The gastric pH should be kept as close to neutral as possible. If the gastritis is relatively mild, a biopsy specimen should be obtained and tested for H. pylori. Treatment consists of acid reduction and anti-H. pylori therapy.

NEOPLASMS

Benign tumors of the upper GI tract (e.g., leiomyomas, hamartomas, and hemangiomas) bleed at times. Wedge excision of the offending lesion is the procedure of choice. Gastrointestinal stromal tumors run the gamut from benign to highly aggressive. They typically present as a submucosal mass that may cause bleeding as a result of mucosal ulceration. The bleeding may be treated with wedge excision of the tumor. Such excision can often be accomplished laparoscopically [see 3:13 Gastroduodenal Procedures].

Bleeding from malignant neoplasms, whether early stage or late stage, generally can be controlled initially by endoscopic means; however, rebleeding rates are high. If the lesion is resectable, it should be excised promptly once the patient is stable and any coagulopathies have been corrected. If disease is advanced, however, surgical options are limited, and a nonoperative approach, though necessarily imperfect, is preferable.

ESOPHAGEAL HIATAL HERNIA

Not infrequently, the source of chronic enteric blood loss is an esophageal hiatal hernia. Major bleeding is rare in this condition but may occur as a result of linear erosions at the level of the diaphragm (Cameron lesions), gastritis within the hernia, or torsion of a paraesophageal hernia. Endoscopy is generally diagnostic, though the sources of chronic blood loss are not always obvious. Recognition that the bleeding derives from a Cameron lesion should incline the surgeon toward operative intervention [see 3:9 Open Esophageal Procedures and 3:10 Minimally Invasive Esophageal Procedures]: this lesion is usually mechanically induced and therefore tends to be less responsive to antacid therapy.

Chronic bleeding from a sliding esophageal hiatal hernia should be treated initially with a PPI; anti-H. pylori therapy should be added if biopsy shows this organism to be present. Operation (i.e., laparoscopic Nissen fundoplication [see 3:10 Minimally Invasive Esophageal Procedures]) should be considered for fit patients who have complications associated with their hiatal hernia. A paraesophageal hernia should be repaired surgically; we prefer the laparoscopic approach when feasible.

DIEULAFOY LESION

A Dieulafoy lesion (also referred to as exulceratio simplex) is the rupturing of a 1 to 3 mm bleeding vessel through the gastric mucosa (usually in the proximal stomach) without surrounding ulceration. This lesion tends to be found high on the lesser curvature, but it can also occur in other locations. Histologic studies have not revealed any intrinsic abnormalities either of the mucosa or of the vessel.

Initial treatment consists of either coagulation of the bleeding vessel with a heater probe or mechanical control with clips or rubber bands; local injection of epinephrine may help control acute hemorrhage while this is being done. In skilled hands, endoscopic therapy has a 95% success rate, and long-term control is excellent. If endoscopic therapy fails, surgical options, including ligation or excision of the vessel involved, come into play. Arteriographic embolization may be employed in patients who are too ill to tolerate surgical intervention.

HEMOBILIA

Hemobilia should be suspected in all patients who present with the classic triad of epigastric and right upper quadrant pain, GI bleeding, and jaundice; however, only about 40% of patients with hemobilia present with the entire triad. Endoscopy demonstrating blood coming from the ampulla of Vater points to a source in the biliary tree or the pancreas (hemosuccus pancreaticus).

Arteriography may provide the definitive diagnosis: a bleeding tumor, a ruptured artery from trauma, or another cause. Arteriographic embolization of the affected portion of the liver is the preferred treatment option; hepatic artery ligation (selective if possible) or hepatic resection [see 3:17 Hepatic Resection] may be required.

HEMOSUCCUS PANCREATICUS

Bleeding into the pancreatic duct, generally from erosion of a pancreatic pseudocyst into the splenic artery, is signaled by upper abdominal pain followed by hematochezia. If endoscopy is performed when hematochezia is present, the bleeding site may not be seen; however, if endoscopy is performed when pain is first noted, blood may be seen coming from the ampulla of Vater. The combination of significant GI bleeding, abdominal pain, a history of alcohol abuse or pancreatitis, and hyperamylasemia should suggest the diagnosis. Angiography can be diagnostic and, at times, therapeutic. Distal pancreatectomy [see 3:18 Pancreatic Procedures], including excision of the pseudocyst and ligation of the splenic artery, is the preferred treatment and generally leads to cure.

AORTOENTERIC FISTULA

Aortoenteric fistulas may occur spontaneously as a result of rupture of an aortic aneurysm or perforation of a duodenal lesion; more often, they arise after aortic surgery. A common initial manifestation of an aortoenteric fistula is a small herald bleed that is followed a few days later by a massive hemorrhage. Patients often present with the triad of GI hemorrhage, a pulsatile mass, and infection; however, not all of these symptoms are invariably present. A high index of suspicion facilitates diagnosis. Endoscopy may show an aortic graft eroding into the enteric lumen, but this is an uncommon finding. CT scanning is the procedure of choice for diagnosis. The finding of air around the aorta or the aortic graft is diagnostic and is an indication for emergency exploration. The preferred surgical treatment is resection of the graft with extra-abdominal bypass. Some authorities, however, advocate resection of the graft with in situ graft replacement.

VASCULAR ECTASES

Vascular ectases (also referred to as vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and arteriovenous malformations) may bleed briskly. As a rule, gastric lesions are readily identified and the bleeding controlled by endoscopic means. Lesions that continue to bleed, either acutely or chronically, despite endoscopic measures should be excised. Some patients have multiple and extensive lesions that necessitate resection of large portions of the stomach or the small intestine. Pharmacotherapy and hormone therapy have been tried; the results have been mixed.

DUODENAL AND JEJUNAL DIVERTICULA

Duodenal and jejunal diverticula are rare causes of upper GI bleeding. Accurate identification of a bleeding site within a given diverticulum is difficult, but an attempt should be made to accomplish this by means of peroral enteroscopy or video capsule endoscopy. Excision is the preferred treatment and is accomplished by means of segmental resection. Great care must be taken in the treatment of duodenal diverticula in the region of the ampulla of Vater to ensure that the pancreatic duct and the bile ducts are not injured during excision.

JEJUNAL ULCER

Ulcerations of the jejunum are also rare. They may be secondary to medications (e.g., NSAIDs), infection, a gastrinoma, or idiopathic causes. Offending medications should be stopped, infections should be treated, and gastrinomas should be excised. If these measures do not control the hemorrhage, the bleeding segment of the jejunum should be excised.

Management of UGI Bleeding 2Mallory-Weiss Tears endoscopic coagulationsurgery (anterior gastrotomy and direct suture ligation of the tear) Acute hemorrhagic gastritis H2 receptor blockersPPIssucralfateantacidsantibioticssomatostatinvasopressinsurgery (total or near-total gastrectomy) Neoplasms Benign tumors wedge excision of the offending lesionMalignant neoplasmsendoscopysurgery (excision)Esophageal Hiatal Hernia PPIanti-H. pylori antibiotherapysurgery (i.e., laparoscopic Nissen fundoplication)

MALLORY-WEISS TEARS Mallory-Weiss tears are linear tears at the esophagogastric junction that are usually caused by vomiting. Any patient who presents with vomiting that initially is not bloody but later turns so should be suspected of having a Mallory-Weiss tear. As a rule, these lesions stop bleeding without therapy. If bleeding is substantial or persistent, however, endoscopic coagulation may be necessary. In rare instances, the tear will have to be oversewn at operation. This is accomplished via an anterior gastrotomy and direct suture ligation of the tear. ACUTE HEMORRHAGIC GASTRITIS Bleeding from gastritis is virtually always managed medically with H2 receptor blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if H. pylori is present. Somatostatin may be beneficial. Sometimes, administration of vasopressin via the left gastric artery is needed to control bleeding. In rare cases, total or near-total gastrectomy is required; however, the mortality associated with this operation in this setting is high. Stress ulcer prophylaxis in severely ill or traumatized patients is essential to prevent this problem. The gastric pH should be kept as close to neutral as possible. If the gastritis is relatively mild, a biopsy specimen should be obtained and tested for H. pylori. Treatment consists of acid reduction and anti-H. pylori therapy. NEOPLASMS Benign tumors of the upper GI tract (e.g., leiomyomas, hamartomas, and hemangiomas) bleed at times. Wedge excision of the offending lesion is the procedure of choice. Gastrointestinal stromal tumors run the gamut from benign to highly aggressive. They typically present as a submucosal mass that may cause bleeding as a result of mucosal ulceration. The bleeding may be treated with wedge excision of the tumor. Such excision can often be accomplished laparoscopically.Bleeding from malignant neoplasms, whether early stage or late stage, generally can be controlled initially by endoscopic means; however, rebleeding rates are high. If the lesion is resectable, it should be excised promptly once the patient is stable and any coagulopathies have been corrected. If disease is advanced, however, surgical options are limited, and a nonoperative approach, though necessarily imperfect, is preferable. ESOPHAGEAL HIATAL HERNIA Not infrequently, the source of chronic enteric blood loss is an esophageal hiatal hernia. Major bleeding is rare in this condition but may occur as a result of linear erosions at the level of the diaphragm (Cameron lesions), gastritis within the hernia, or torsion of a paraesophageal hernia. Endoscopy is generally diagnostic, though the sources of chronic blood loss are not always obvious. Recognition that the bleeding derives from a Cameron lesion should incline the surgeon toward operative intervention [see 3:9 Open Esophageal Procedures and 3:10 Minimally Invasive Esophageal Procedures]: this lesion is usually mechanically induced and therefore tends to be less responsive to antacid therapy. Chronic bleeding from a sliding esophageal hiatal hernia should be treated initially with a PPI; anti-H. pylori therapy should be added if biopsy shows this organism to be present. Operation (i.e., laparoscopic Nissen fundoplication [see 3:10 Minimally Invasive Esophageal Procedures]) should be considered for fit patients who have complications associated with their hiatal hernia. A paraesophageal hernia should be repaired surgically; we prefer the laparoscopic approach when feasible. HEMOBILIA Hemobilia should be suspected in all patients who present with the classic triad of epigastric and right upper quadrant pain, GI bleeding, and jaundice; however, only about 40% of patients with hemobilia present with the entire triad. Endoscopy demonstrating blood coming from the ampulla of Vater points to a source in the biliary tree or the pancreas (hemosuccus pancreaticus). Arteriography may provide the definitive diagnosis: a bleeding tumor, a ruptured artery from trauma, or another cause. Arteriographic embolization of the affected portion of the liver is the preferred treatment option; hepatic artery ligation (selective if possible) or hepatic resection may be required.

Management of UGI Bleeding 3Hemobilia Arteriographic embolizationSurgery (hepatic artery ligation or hepatic resection)Aortoenteric fistula air around the aorta or the aortic graft emergency exploration (resection of the graft with extra-abdominal bypass, resection of the graft with in situ graft replacement)Vascular ectases (vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and arteriovenous malformations)surgery (excision)Duodenal and jejunal diverticula surgery (excision)Jejunal ulcer (NSAIDs, infection, gastrinoma)medications stoppinginfections treatmentsurgery (excision of gastrinoma, resection of bleeding segment of the jejunum)

AORTOENTERIC FISTULA Aortoenteric fistulas may occur spontaneously as a result of rupture of an aortic aneurysm or perforation of a duodenal lesion; more often, they arise after aortic surgery. A common initial manifestation of an aortoenteric fistula is a small herald bleed that is followed a few days later by a massive hemorrhage. Patients often present with the triad of GI hemorrhage, a pulsatile mass, and infection; however, not all of these symptoms are invariably present. A high index of suspicion facilitates diagnosis. Endoscopy may show an aortic graft eroding into the enteric lumen, but this is an uncommon finding. CT scanning is the procedure of choice for diagnosis. The finding of air around the aorta or the aortic graft is diagnostic and is an indication for emergency exploration. The preferred surgical treatment is resection of the graft with extra-abdominal bypass. Some authorities, however, advocate resection of the graft with in situ graft replacement. VASCULAR ECTASES Vascular ectases (also referred to as vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and arteriovenous malformations) may bleed briskly. As a rule, gastric lesions are readily identified and the bleeding controlled by endoscopic means. Lesions that continue to bleed, either acutely or chronically, despite endoscopic measures should be excised. Some patients have multiple and extensive lesions that necessitate resection of large portions of the stomach or the small intestine. Pharmacotherapy and hormone therapy have been tried; the results have been mixed. DUODENAL AND JEJUNAL DIVERTICULA Duodenal and jejunal diverticula are rare causes of upper GI bleeding. Accurate identification of a bleeding site within a given diverticulum is difficult, but an attempt should be made to accomplish this by means of peroral enteroscopy or video capsule endoscopy. Excision is the preferred treatment and is accomplished by means of segmental resection. Great care must be taken in the treatment of duodenal diverticula in the region of the ampulla of Vater to ensure that the pancreatic duct and the bile ducts are not injured during excision. JEJUNAL ULCER Ulcerations of the jejunum are also rare. They may be secondary to medications (e.g., NSAIDs), infection, a gastrinoma, or idiopathic causes. Offending medications should be stopped, infections should be treated, and gastrinomas should be excised. If these measures do not control the hemorrhage, the bleeding segment of the jejunum should be excised.

Lower GI BleedingDistal to the ligament of TreitzCauses:Diverticulosis 60%Angiodysplasia 20%NeoplasiaIBDIschaemic colitisInfective colitisAno-rectal diseaseSmall intestinecoagulopathyUpper GI cause in 10-15%

Lower gastrointestinal bleeding is defined as abnormal hemorrhage into the lumen of the bowel from a source distal to the ligament of Treitz. In the majority of cases, lower GI bleeding derives from the colon; however, the small bowel is identified as the source of bleeding in as many as one third of cases,1,2 and the upper GI tract is identified as the source in as many as 11% of patients presenting with bright red blood per rectum.3 Lower GI bleeding is more common in men than in women. The incidence rises steeply with advancing age, exhibiting a greater than 200-fold increase from the third decade of life to the ninth. This increase is largely attributable to the various colonic disorders commonly associated with aging (e.g., diverticulosis and angiodysplasia).4-6 The exact incidence of lower GI bleeding is not known, because there is no standardized technique for localizing it. Several investigators, however, estimate the incidence to be in the range of 20 to 27 cases per 100,000 adults.4,7 A 1997 survey of GI bleeding from the American College of Gastroenterology found that lower GI hemorrhage accounted for 24% of all GI bleeding events.8 Another study published the same year found that 0.7% of 17,941 discharges from a Veterans Affairs Hospital were for patients who had had lower GI bleeding.

Management PrinciplesTreatment & evaluation should be instigated concurrentlyHaemodynamic assessment + directed history and examinationPR / proctoscopy essential to evaluate ano-rectum

Initial ManagementLarge bore IV access + crystaloid resucitationNGTX-match, coagulation profile, Blood film & count, routine biochemistry85% cease spontaneously

Localisation99mTc labelled RBC scanSelective mesenteric angiographyColonoscopy

Selective Mesenteric AngiographyOnce localised can treat bleeding with super selective embolisationVasopressin infusion superseeded due to cardiac and ischaemic complications

Management of LGI BleedingEndoscopythermal contact probeslaser photocoagulationelectrocauterizationinjection of vasoconstrictorsapplication of metallic clipsinjection sclerotherapyAngiographic therapy

ENDOSCOPIC THERAPY When colonoscopy identifies a bleeding source, endoscopic treatment may be an option. Endoscopic modalities used to treat lower GI bleeding include use of thermal contact probes, laser photocoagulation, electrocauterization, injection of vasoconstrictors, application of metallic clips, and injection sclerotherapy. The choice of a specific modality often depends on the nature of the offending lesion and on the expertise and resources available locally. A 1995 survey of members of the American College of Gastroenterology found that endoscopic therapy was used in 27% of patients presenting with lower GI bleeding.Diverticular hemorrhage can be difficult to treat endoscopically because of the high bleeding rate and the location of the bleeding point within the diverticulum. In 2000, one group of investigators reported their experience with endoscopic therapy for severe hematochezia and diverticulosis in a prospective series of 121 patients.48 In this series, none of the patients treated endoscopically with epinephrine injections, bipolar coagulation, or both required surgery and none experienced recurrent bleeding episodes. A 2001 study from another group, however, reported high rates of recurrent bleeding episodes in both the early and the late posttreatment periods.49 In the absence of prospective, randomized trials, it is difficult to draw definitive conclusions about the utility of endoscopic therapy in treating diverticular hemorrhage. Angiodysplasias resulting in GI hemorrhage typically are amenable to endoscopic treatment. That these lesions are frequently found in the right colon makes perforation a concern; this complication is reported in approximately 2% of patients.50 Good success rates have been reported with both injection and thermal methods.51 In one series, endoscopic fulguration was successful in 87% of patients, and no rebleeding episodes occurred over a 1- to 7-year follow-up period.51 Bleeding from multiple telangiectatic lesions in the distal colon resulting from radiation injury can be treated with thermal contact probes, lasers, or noncontact devices such as the argon plasma coagulator.52 Postpolypectomy hemorrhage can often be successfully treated by endoscopic means. Methods used include simple resnaring of the stalk while pressure is maintained53; electrocauterization, with or without epinephrine injection; endoscopic band ligation; and placement of metallic clips. For patients whose bleeding is attributable to benign anorectal causes, endoscopic therapy may include epinephrine injection, sclerosant injection, or band ligation of internal hemorrhoids.54 ANGIOGRAPHIC THERAPY Diagnostic use of angiography in patients with lower GI bleeding can often be followed by angiographic therapy. The two main angiographic treatment options are intra-arterial injection of vasopressin and transcatheter embolization.

Vasopressin acts to control bleeding by causing arteriolar vasoconstriction and bowel wall contraction.9 Once the bleeding site has been localized angiographically, the catheter is positioned in the main trunk of the vessel. Infusion of vasopressin is initiated at a rate of 0.2 U/min and can be increased to a rate of 0.4 U/min. Within 20 to 30 minutes, another angiogram is performed to determine whether the bleeding has ceased. If the bleeding is under control, the catheter is left in place and vasopressin is continuously infused for 6 to 12 hours. If the bleeding continues to be controlled, infusion is continued for an additional 6 to 12 hours at 50% of the previous rate. Finally, vasopressin infusion is replaced by continuous saline infusion, and if bleeding does not recur, the catheter is removed.55,56

The vasoconstrictive action of vasopressin can have deleterious systemic side effects, including myocardial ischemia, peripheral ischemia, hypertension, dysrhythmias, mesenteric thrombosis, intestinal infarction, and death.9,37 Occasionally, simultaneous I.V. administration of nitroglycerine is necessary to counteract these systemic effects. The reported success rate of vasopressin in controlling lower GI bleeding ranges from 60% to 100%, and the incidence of major complications ranges from 10% to 20%.57-60 Rebleeding rates as high as 50% have been reported.59,60

An alternative for patients with coronary vascular disease, severe peripheral vascular disease, or other comorbidities that prevent safe administration of vasopressin is transcatheter embolization. In this technique, a catheter is superselectively placed into the identified bleeding vessel and an embolizing agent (e.g., a gelatin sponge, a microcoil, polyvinyl alcohol particles, or a balloon) is injected. Several small series found this technique to be 90% to 100% successful at stopping bleeding.61-64 Equally impressive was the finding that the rebleeding rates in these series were 0%. The complication rates of this procedure are generally reasonable as well; however, intestinal infarction has been reported.37,65

SURGICAL THERAPY

Although there are no absolute criteria for surgery, there are several factorsincluding hemodynamic status, associated comorbidities, transfusion requirements, and persistent bleedingthat are instrumental in making an appropriate and timely decision whether to operate. In general, patients who require more than 4 units of blood in a 24-hour period to remain hemodynamically stable, whose bleeding has not stopped after 72 hours, or who experience rebleeding within 1 week of an initial episode should undergo surgery.9

If the patient's hemodynamic status permits, surgical treatment should be undertaken after accurate localization of the bleeding site. When possible, directed segmental resection is the procedure of choice: it is associated with rebleeding rates ranging from 0% to 14% and mortalities ranging from 0% to 13%.10,37,66 Blind segmental colectomy should never be performed: it is associated with rebleeding rates as high as 75% and mortalities as high as 50%.67 If hemodynamic compromise and ongoing hemorrhage make it necessary to perform surgical exploration before the bleeding site can be localized, every effort should be made to identify the source of bleeding intraoperatively before embarking on resection. Intraoperative options for bleeding site localization include colonoscopy (to allow for this option, patients should always be placed in the lithotomy position), EGD, and transoral passage of a pediatric colonoscope for enteroscopy with simultaneous intraperitoneal assistance for small bowel manipulation.9 If the bleeding site still cannot be accurately localized, subtotal colectomy is the procedure of choice. This procedure is associated with mortalities ranging from 5% to 33%,68,69 which underscores the importance of accurate preoperative localization of bleeding before surgical intervention.

Selective Mesenteric AngiographySuper selective embolisation into bleeding vessel (beyond marginal artery)Excellent control if technically feasible.Time consuming, risk of colonic infarction (0-20%), rebleeding (10-20%)?Role of check colonoscopy at 2-3days

Bandi R, Shetty P, Sharma R, Burke T, Burke M, Kastan D. Superselective arterial emboilization for the treatment of lower gastrointestinal hemorrhage. J Vasc Interv Radiol 2001; 12: 1399-1405

Colonoscopy 1Procedure of choice if bleeding has stopped or slowed significantlyReports of the use of colonoscopy in acute bleeds (+/- cleansing purge)Only consider in stable patient, abort if severe colitisLocalisation in 70-80%

Jensen D, Machicado G. Diagnosis and treatment of severe hematochezia: the role of urgent colonoscopy after purge. Gastroenterology 1988; 95: 1569-1574

Colonoscopy 2Heater probe or Argon / Nd:YAG laser can be used to treat angiodysplasia.Diverticular bleeding can also be treated with endoscopic therapyRebleed 10-50%, Perforation

Indications for SurgeryHD unstable despite resuscitationMore than 6-8 units PRBC requiredOngoing bleeding beyond 72 hoursSignificant early (

SurgeryOperative localisation (endoscopy, colotomies, transverse loop colostomy) are notoriously poorGastroscopy is essentialTreatment of choice is subtotal colectomy + IRAIf localised pre-operatively then segmental resection.Primary anastomosis is generally safe

ReferencesACS Surgery: Principles and Practice by Douglas W., Md. Wilmore (Editor), Laurence Y., Md. Cheung (Editor), Alden H., Md. Harken (Editor), James W., Md. Holcroft (Editor), Jonathan L., Md. Meakins (Editor), Nathaniel J., Md. Soper (Editor), Douglas W. Wilmore, Laurence Y. Cheung, Alden H. Harken, James W. Holcroft, Jonathan L. Meakins, Nathaniel J. SoperPublisher: WebMD Professional Publishing; 2nd edition (February 1, 2003)Sabiston Textbook of Surgery: the Biological Basis of Modern Surgical Practic. Courtney M. Townsend, Jr., editor-in-chief; associate editors, R. Daniel Beauchamp, B. Mark Evers, Kenneth L. Mattox. W.B. Saunders Company 2001Oxford Textbook of Surgery (3-Volume Set) 2nd edition (January 15, 2000): by Peter J. Morris (Editor), William C. Wood (Editor) By Oxford PressEssentials of Surgery: Scientific Principles and Practice 2nd edition (January 15, 1997): by Lazar J., Md. Greenfield (Editor), Michael W. Mulholland (Editor), Keith T. Oldham (Editor), Gerald B. Zelenock (Editor), Keith D. Lillimoe (Editor), Keit Oldham By Lippincott Williams & Wilkins PublishersCurrent Surgical Diagnosis and Treatment, 11th Ed 2003: Lawrence W. Way, Gerard M. Doherty By McGraw-Hill/Appleton & LangePrinciples of Surgery Seventh Edition Editor-in-Chief Seymour I. Schwartz, M.D. The McGraw-Hill Companies, Inc. 1999Vernava A, Moore B, Longo W, Johnson F. Lower gastrointestinal bleeding 1997. Dis Col Rectum; 40(7): 846-858

The most common causes of upper gastrointestinal bleeding are chronic duodenal ulcers, chronic gastric ulcers, esophageal varices, gastric varices, Mallory-Weiss tears, acute hemorrhagic gastritis, and gastric neoplasms. Less common causes include various other gastrointestinal conditions and certain hepatobiliary and pancreatic disordersUpper gastrointestinal hemorrhage may present as severe bleeding with hematemesis, hematochezia, and hypotension; as gradual bleeding with melena; or as occult bleeding detected by positive tests for blood in the stool.The initial steps in the evaluation of patients with upper GI bleeding are based on the perceived rate of bleeding and the degree of hemodynamic stability. Hemodynamically stable patients who show no evidence of active bleeding or comorbidities and in whom endoscopic findings are favorable may be treated on an outpatient basis, whereas patients who show evidence of serious bleeding should be managed aggressively and hospitalized.

The airway, breathing, and circulation should be rapidly assessed, and the examiner should note whether the patient has a history of or currently exhibits hematemesis, melena, or hematochezia. Blood should be drawn for a complete blood count, blood chemistries (including tests of liver function and renal function), and measurement of the prothrombin time (PT) and the partial thromboplastin time (PTT). Blood should be sent to the blood bank for typing and crossmatching.If the patient is stable and shows no evidence of recent or active hemorrhage, the surgeon may proceed with the workup. If, however, the patient is stable but shows evidence of recent or active bleeding, a large-bore intravenous line should be placed before workup is begun; the presence of the line ensures immediate I.V. access should the patient subsequently become unstable. If the patient is unstable, resuscitation should be begun immediately. Resuscitation of an unstable patient is begun by establishing a secure airway and ensuring adequate ventilation. Oxygen should be given as necessary, either by mask or by endotracheal tube and ventilator. A large-bore I.V. line should then be placed, through which lactated Ringer solution should be infused at a rate high enough to maintain tissue perfusion. A urinary catheter should be inserted and urine output monitored. Blood should be given as necessary, and any coagulopathies should be corrected if possible. It is all too easy to forget these basic steps in a desire to evaluate and manage massive GI hemorrhage. If the patient remains unstable and continues to bleed despite supportive measures, he or she should be taken to the operating room for intraoperative diagnosis. The abdomen should be opened through an upper midline incision, and an anterior gastrotomy should be performed. If inspection does not reveal the source of the bleeding or if bleeding is observed beyond the pylorus, a duodenotomy is made, with care taken to preserve the pylorus if possible. Bleeding from the proximal stomach may be difficult to verify, but it should be actively sought if no other bleeding site is identified. HISTORY Only after the initial measures to protect the airway and stabilize the patient have been completed should an attempt be made to establish the cause of the bleeding. The history should focus on known causes of upper GI bleeding (e.g., ulcers, recent trauma or stress, liver disease, varices, alcoholism, and vomiting) and on the possible use of medications that interfere with coagulation (e.g., aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], and dipyridamole) or alter hemodynamics (e.g., beta blockers and antihypertensive agents). The cardiac history is particularly important for assessing the patient's ability to withstand varying degrees of anemia. PHYSICAL EXAMINATION The physical examination is seldom of much help in determining the exact site of bleeding, but it may reveal jaundice, ascites, or other signs of hepatic disease; a tumor mass; or a bruit from an abdominal vascular lesion. NASOGASTRIC ASPIRATION The next step is nasogastric aspiration. A bloody aspirate is an indication for esophagogastroduodenoscopy (EGD), as is a clear, nonbilious aspirate if a bleeding site distal to the pylorus has not been excluded. If the aspirate is clear and bile-stained, the source of the bleeding is unlikely to be the stomach, the duodenum, the liver, the biliary tree, or the pancreas. Nonetheless, if subsequent evaluation of the lower GI tract for the source of the bleeding is unrewarding, an upper GI site that had stopped bleeding when the nasogastric tube was passed or that was distal to the ligament of Treitz should still be considered. EGD almost always reveals the source of upper GI bleeding; its utility and accuracy have been well documented in the literature. This procedure requires considerable skill: identification of bleeding sites in a blood-filled stomach is far from easy. Hematemesis is an indication for emergency EGD, usually within 1 hour of presentation. If the rate of bleeding is high, saline lavage may be performed to clear the stomach of blood and clots. If the rate of bleeding is moderate or low, as is often the case in patients with melena, urgent EGD is indicated.EGD is not only an excellent diagnostic tool but also a valuable therapeutic modality. Indeed, most upper GI hemorrhages may be controlled endoscopically, though the degree of success to be expected in individual cases varies according to the expertise of the endoscopist and the specific cause of the bleeding. Therapeutic endoscopic maneuvers include injection, thermal coagulation, and mechanical occlusion of bleeding sites (by means of clip application or variceal banding). The choice of therapy depends on the cause, the site, and the rate of bleeding.

If endoscopic examination reveals no lesions in the stomach or the duodenum and bleeding has ceased, enteroclysis (direct introduction of BaSO4 into the small bowel) and roentgenography of the duodenum and the jejunum should be done next. This is probably a more sensitive radiologic test than a standard small bowel roentgenogram. Nonetheless, the absence of a lesion on this test does not rule out the small bowel as the source of the hemorrhage; not uncommonly, the x-ray is negative when a bleeding small bowel lesion is present. Tagged red cell scans may confirm the presence of an active bleeding site; however, scans are fairly nonspecific with respect to determining the anatomic location of the bleeding. Arteriography may demonstrate that a lesion is present, but it cannot reliably identify a bleeding site unless the bleeding is brisk (> 1 ml/min). Occasionally, arteriography reveals the cause of the bleeding even if the bleeding has stopped. Recurrent bleeding or bleeding that is suspected to be secondary to small bowel pathology may be evaluated by means of video capsule endoscopy, which is capable of localizing a variety of lesions (including arteriovenous malformations, ulcers, strictures, and malignancies) so as to direct surgical intervention. Video capsule endoscopy should be used with caution in patients exhibiting obstructive symptoms: if the capsule becomes trapped, complete obstruction may result. Intraoperative endoscopic exploration may also prove useful in this situation. Before the small bowel is manipulated, a pediatric colonoscope is introduced either orally or through a distal jejunal enterotomy; the latter method allows easier viewing of the entire small bowel. The mucosal detail is examined as the surgeon guides the scope through the small bowel. The bowel must be handled gently to avoid a mucosal injury, which could mimic a significant lesion.These tests, in conjunction with EGD, should allow the surgeon to establish the cause of upper GI bleeding at least 90% of the time. Enteroclysis is a test performed to examine the small bowel. A tube is placed down the nose and throat, through the stomach into the small intestine. When in place, contrast dye is introduced and x-ray images are viewed on a fluoroscopic monitor to visualize how the contrast moves through the bowel structures. The enteroclysis test is the most complete means of demonstrating whether or not the small intestine is normal when abnormality is suspected.

CHRONIC DUODENAL ULCER The development of effective medical regimens for controlling uncomplicated duodenal ulcers has led to a drastic reduction in the number of elective surgical procedures performed for this purpose. Nevertheless, the incidence of bleeding from duodenal ulcers that is severe enough to necessitate emergency endoscopic or operative intervention has not decreased over the past decade. Once EGD has demonstrated that a duodenal ulcer is the source of the bleeding, the first question that must be addressed is whether active bleeding is present. If it is, an attempt should be made to control the hemorrhage endoscopically. Because ongoing blood loss eventually leads to coagulopathies, the surgeon must exercise good judgment in deciding how long to pursue endoscopic treatment before concluding that such treatment has failed and that surgical treatment is necessary. In general, substantial bleeding (four to six units or more) that is not easily controlled endoscopically is an indication for immediate surgical intervention. Likewise, ongoing hemorrhage in a hemodynamically unstable patient (especially an elderly one) calls for immediate surgical therapy. If bleeding is controlled endoscopically, then a proton pump inhibitor (PPI)such as pantoprazole, 40 mg/dayshould be given intravenously. In addition, antibiotic therapy directed against Helicobacter pylori (e.g., a 14-day course of metronidazole, 500 mg p.o., t.i.d.; omeprazole, 20 mg p.o., b.i.d.; and clarithromycin, 500 mg p.o., b.i.d.) should be considered if the organism is present; such therapy has been shown to decrease rebleeding rates after antacid medication has been stopped. Food need not be withheld unless the likelihood of rebleeding is high, in which case operation or repeat endoscopy would be necessary. Resumption of oral feeding does not appear to affect rebleeding rates. If bleeding continues despite medical and endoscopic therapy, it should be managed surgically. In addition, certain patients whose bleeding was controlled endoscopicallysuch as those with a visible gastroduodenal artery and a clot in the base of the ulcer, those who experience rebleeding despite medical and endoscopic therapy, and those with giant ulcersshould be strongly considered for surgical therapy. Surgical management may be accomplished either laparoscopically or via an open approach. The latter begins with an upper midline incision. The duodenum is mobilized and an anterior longitudinal duodenotomy performed over the site of the ulcer. The bleeding vessel, which is usually on the posterior wall of the first portion of the duodenum, is ligated with nonabsorbable sutures at sites proximal and distal to the bleeding point. A third stitch is placed posterior to the bleeding vessel. Pains must be taken to avoid injury to the common bile duct during the placement of these sutures. The duodenotomy is then closed. The role of vagotomy in the management of bleeding duodenal ulcers has been called into question. Previously, proximal gastric vagotomy was recommended for stable patients. It was considered preferable to truncal vagotomy because it is less likely to result in gastric atony, alkaline reflux gastritis, dumping, and diarrhea. In unstable patients, truncal vagotomy was typically performed in conjunction with pyloroplasty. Frozen section to confirm the presence of nerve tissue is helpful for ensuring that the vagotomy is complete. The recommendation for truncal vagotomy was based on data from studies done before PPI and anti-H. pylori therapy came into use. Subsequent studies that evaluated rebleeding rates with current medical regimens, however, demonstrated much lower rebleeding rates. Furthermore, it seems probable that long-term PPI therapy (e.g., omeprazole, 20 mg p.o., q.d.)the medical equivalent of vagotomyin conjunction with eradication of H. pylori and avoidance of NSAIDs, should decrease rebleeding rates significantly. Therefore, one may consider an alternative treatment approach in patients who had not been receiving ulcer therapy before the bleeding begannamely, ligation of the bleeding vessel, postoperative administration of PPIs, and anti-H. pylori therapy. This approach avoids the complications associated with truncal vagotomy. CHRONIC GASTRIC ULCER Initially, bleeding from a chronic gastric ulcer is managed in much the same way as that from a chronic duodenal ulcer (i.e., endoscopically) To prevent aggravation of the bleeding, early biopsy generally is not recommended; repeat endoscopy and biopsy are done at a later date. Emergency surgical indications for gastric ulcers are the same as those for duodenal ulcers. In addition, if a gastric ulcer does not resolve after 6 weeks of medical therapy, surgical excision is often indicated. In stable patients, surgical management of a nonhealing chronic gastric ulcer generally consists of a hemigastrectomy that includes the ulcer site; if the ulcer is located more proximally, it may be removed by means of wedge excision. Excision of the ulcer should be immediately followed by frozen section to rule out cancer. There is no need for a vagotomy in these instances. In unstable patients, hemigastrectomy should probably be avoided because of the increased morbidity and mortality that can follow it. Wedge excision should be combined with aggressive acid-suppressive therapy (PPIs or H2 receptor antagonists), followed by anti-H. pylori treatment. Truncal vagotomy with pyloroplasty is rarely indicated; however, it may be considered in a patient with previous complications from ulcer disease. ESOPHAGEAL VARICES The value of endoscopy in the diagnosis and management of variceal bleeding cannot be overemphasized. Even in patients with known varices, the site of bleeding is frequently nonvariceal; endoscopy is therefore essential. If bleeding varices are identified, rubber banding or intravariceal sclerotherapy with a sclerosing agent (1.5% sodium tetradecyl sulfate, ethanolamine, sodium morrhuate, or absolute alcohol) is performed [see Figure 2]. If these measures do not control the hemorrhage, balloon tamponade is indicated. Patients who are to undergo this procedure should have an endotracheal tube in place. The tube we prefer to use for balloon tamponade is the four-port Minnesota tube, although the Sengstaken-Blakemore tube is also acceptable. The Minnesota tube has a gastric balloon, an esophageal balloon, and aspiration ports for the esophagus and the stomach. The gastric balloon is inflated first and placed on traction. If the bleeding is not controlled, the esophageal balloon is then inflated. The pressure in the balloons should be released in 24 to 48 hours to prevent necrosis of the esophageal or the gastric wall. Successful balloon tamponade is followed by endoscopic variceal injection or variceal banding.

I.V. somatostatin (250 ug bolus, followed by infusion of 250 ug/hr) should be administered in conjunction with the above-mentioned steps. Vasopressin (10 U/hr) may also be given; however, it causes diffuse vasoconstriction, and nitroglycerin is required to alleviate cardiac side effects. Somatostatin has proved superior to placebo in controlling variceal hemorrhage when used in conjunction with endoscopic sclerotherapy. It is as effective as vasopressin while giving rise to fewer side effects. Octreotide, a synthetic analogue of somatostatin, shares many of the properties of somatostatin but perhaps not all. Both agents decrease secretion of gastric acid and pepsin; to date, however, the decreased gastric blood flow observed with somatostatin administration has not been reported with octreotide administration. Nevertheless, some clinicians in the United States elect to use octreotide (25 to 50 ug/hr) in place of I.V. somatostatin because the former tends to be more widely available in the United States. Multiple prospective, randomized trials showed that propranolol (40 mg b.i.d., p.o.) decreased the incidence of first-time variceal bleeding as well as the incidence of recurrent variceal bleeding. Propranolol should not be used during active bleeding but should be started once bleeding stops.

After the acute variceal bleeding has been controlled, any remaining varices should be subjected to injection sclerotherapy or banding at 2-week intervals until they too are obliterated.

The main indications for surgical intervention in patients with bleeding esophageal varices are uncontrolled hemorrhage and persistent rebleeding despite endoscopic and medical therapy. When surgical intervention is planned, it is essential to determine whether the patient is a transplant candidate. If so, operation should be avoided and bleeding managed by decompressing the portal venous system with a transjugular intrahepatic portosystemic shunt (TIPS). TIPS yields excellent short-term results with respect to stopping bleeding and providing time to locate a liver suitable for transplantation; however, it has not been shown to have the capacity to control hemorrhage by itself over the long term. Thus, its use in patients who are not transplant candidates is questionable.

If the patient is not a transplant candidate and is not actively bleeding, a distal splenorenal shunt is preferable. Arteriograms with views of the portal vein and the left renal vein are obtained. Alternatively, computed tomographic angiography with three-dimensional reconstruction may be performed. If the venous anatomy is suitablethat is, if the diameter of the splenic vein is greater than 0.75 cm (preferably greater than 1.0 cm) and the vein is within one vertebral body of the renal vein on venographya distal splenorenal shunting procedure should be feasible. If the venous anatomy is not suitable, then esophageal transection, a mesocaval venous graft, or a portacaval shunt is required.

In the emergency setting, we prefer a central portacaval shunt, usually in a side-to-side orientation or with a short polytetrafluoroethylene (PTFE) interposition graft. Esophageal transection is also a reasonable choice. This procedure is associated with a lower incidence of encephalopathy than a portacaval shunting procedure; however, it is associated with higher rates of rebleeding (particularly late rebleeding), and it can be difficult to perform when active bleeding is present. Suture ligation of the bleeding varices with devascularization (the Segura procedure) should also be considered.

In general, prognosis is related to the underlying liver disease. For example, patients with varices that are secondary to chronic extrahepatic portal venous or splenic venous occlusion generally have a much better prognosis than those whose portal hypertension is secondary to hepatic parenchymal causes. The severity of the cirrhosis also determines short-term and long-term survival and may influence the decision whether to perform a shunting procedure.

Varices in children are generally secondary to portal vein thrombosis. A conservative, nonoperative approach is preferred. If operation is required, either a portacaval shunt, a distal splenorenal shunt, or a devascularization procedure is performed. In children or adults with varices that are secondary to splenic vein thrombosis (sinistral portal hypertension), a splenectomy is usually curative; the procedure may be performed laparoscopically [see 3:19 Laparoscopic Splenectomy].

GASTRIC VARICES

Gastric varices are managed in much the same way as esophageal varices [see Figure 2], though they are less amenable to sclerotherapy. If sclerotherapy fails to control bleeding from gastric varices, surgical interventionin the form of distal splenorenal shunting, portosystemic shunting, or suture ligation with gastric devascularizationis indicated. If the patient is a suitable candidate, liver transplantation may be performed as an alternative to shunting.

MALLORY-WEISS TEARS

Mallory-Weiss tears are linear tears at the esophagogastric junction that are usually caused by vomiting. Any patient who presents with vomiting that initially is not bloody but later turns so should be suspected of having a Mallory-Weiss tear. As a rule, these lesions stop bleeding without therapy. If bleeding is substantial or persistent, however, endoscopic coagulation may be necessary. In rare instances, the tear will have to be oversewn at operation. This is accomplished via an anterior gastrotomy and direct suture ligation of the tear.

ACUTE HEMORRHAGIC GASTRITIS

Bleeding from gastritis is virtually always managed medically with H2 receptor blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if H. pylori is present. Somatostatin may be beneficial. Sometimes, administration of vasopressin via the left gastric artery is needed to control bleeding. In rare cases, total or near-total gastrectomy [see 3:13 Gastroduodenal Procedures] is required; however, the mortality associated with this operation in this setting is high. Stress ulcer prophylaxis in severely ill or traumatized patients is essential to prevent this problem. The gastric pH should be kept as close to neutral as possible. If the gastritis is relatively mild, a biopsy specimen should be obtained and tested for H. pylori. Treatment consists of acid reduction and anti-H. pylori therapy.

NEOPLASMS

Benign tumors of the upper GI tract (e.g., leiomyomas, hamartomas, and hemangiomas) bleed at times. Wedge excision of the offending lesion is the procedure of choice. Gastrointestinal stromal tumors run the gamut from benign to highly aggressive. They typically present as a submucosal mass that may cause bleeding as a result of mucosal ulceration. The bleeding may be treated with wedge excision of the tumor. Such excision can often be accomplished laparoscopically [see 3:13 Gastroduodenal Procedures].

Bleeding from malignant neoplasms, whether early stage or late stage, generally can be controlled initially by endoscopic means; however, rebleeding rates are high. If the lesion is resectable, it should be excised promptly once the patient is stable and any coagulopathies have been corrected. If disease is advanced, however, surgical options are limited, and a nonoperative approach, though necessarily imperfect, is preferable.

ESOPHAGEAL HIATAL HERNIA

Not infrequently, the source of chronic enteric blood loss is an esophageal hiatal hernia. Major bleeding is rare in this condition but may occur as a result of linear erosions at the level of the diaphragm (Cameron lesions), gastritis within the hernia, or torsion of a paraesophageal hernia. Endoscopy is generally diagnostic, though the sources of chronic blood loss are not always obvious. Recognition that the bleeding derives from a Cameron lesion should incline the surgeon toward operative intervention [see 3:9 Open Esophageal Procedures and 3:10 Minimally Invasive Esophageal Procedures]: this lesion is usually mechanically induced and therefore tends to be less responsive to antacid therapy.

Chronic bleeding from a sliding esophageal hiatal hernia should be treated initially with a PPI; anti-H. pylori therapy should be added if biopsy shows this organism to be present. Operation (i.e., laparoscopic Nissen fundoplication [see 3:10 Minimally Invasive Esophageal Procedures]) should be considered for fit patients who have complications associated with their hiatal hernia. A paraesophageal hernia should be repaired surgically; we prefer the laparoscopic approach when feasible.

DIEULAFOY LESION

A Dieulafoy lesion (also referred to as exulceratio simplex) is the rupturing of a 1 to 3 mm bleeding vessel through the gastric mucosa (usually in the proximal stomach) without surrounding ulceration. This lesion tends to be found high on the lesser curvature, but it can also occur in other locations. Histologic studies have not revealed any intrinsic abnormalities either of the mucosa or of the vessel.

Initial treatment consists of either coagulation of the bleeding vessel with a heater probe or mechanical control with clips or rubber bands; local injection of epinephrine may help control acute hemorrhage while this is being done. In skilled hands, endoscopic therapy has a 95% success rate, and long-term control is excellent. If endoscopic therapy fails, surgical options, including ligation or excision of the vessel involved, come into play. Arteriographic embolization may be employed in patients who are too ill to tolerate surgical intervention.

HEMOBILIA

Hemobilia should be suspected in all patients who present with the classic triad of epigastric and right upper quadrant pain, GI bleeding, and jaundice; however, only about 40% of patients with hemobilia present with the entire triad. Endoscopy demonstrating blood coming from the ampulla of Vater points to a source in the biliary tree or the pancreas (hemosuccus pancreaticus).

Arteriography may provide the definitive diagnosis: a bleeding tumor, a ruptured artery from trauma, or another cause. Arteriographic embolization of the affected portion of the liver is the preferred treatment option; hepatic artery ligation (selective if possible) or hepatic resection [see 3:17 Hepatic Resection] may be required.

HEMOSUCCUS PANCREATICUS

Bleeding into the pancreatic duct, generally from erosion of a pancreatic pseudocyst into the splenic artery, is signaled by upper abdominal pain followed by hematochezia. If endoscopy is performed when hematochezia is present, the bleeding site may not be seen; however, if endoscopy is performed when pain is first noted, blood may be seen coming from the ampulla of Vater. The combination of significant GI bleeding, abdominal pain, a history of alcohol abuse or pancreatitis, and hyperamylasemia should suggest the diagnosis. Angiography can be diagnostic and, at times, therapeutic. Distal pancreatectomy [see 3:18 Pancreatic Procedures], including excision of the pseudocyst and ligation of the splenic artery, is the preferred treatment and generally leads to cure.

AORTOENTERIC FISTULA

Aortoenteric fistulas may occur spontaneously as a result of rupture of an aortic aneurysm or perforation of a duodenal lesion; more often, they arise after aortic surgery. A common initial manifestation of an aortoenteric fistula is a small herald bleed that is followed a few days later by a massive hemorrhage. Patients often present with the triad of GI hemorrhage, a pulsatile mass, and infection; however, not all of these symptoms are invariably present. A high index of suspicion facilitates diagnosis. Endoscopy may show an aortic graft eroding into the enteric lumen, but this is an uncommon finding. CT scanning is the procedure of choice for diagnosis. The finding of air around the aorta or the aortic graft is diagnostic and is an indication for emergency exploration. The preferred surgical treatment is resection of the graft with extra-abdominal bypass. Some authorities, however, advocate resection of the graft with in situ graft replacement.

VASCULAR ECTASES

Vascular ectases (also referred to as vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and arteriovenous malformations) may bleed briskly. As a rule, gastric lesions are readily identified and the bleeding controlled by endoscopic means. Lesions that continue to bleed, either acutely or chronically, despite endoscopic measures should be excised. Some patients have multiple and extensive lesions that necessitate resection of large portions of the stomach or the small intestine. Pharmacotherapy and hormone therapy have been tried; the results have been mixed.

DUODENAL AND JEJUNAL DIVERTICULA

Duodenal and jejunal diverticula are rare causes of upper GI bleeding. Accurate identification of a bleeding site within a given diverticulum is difficult, but an attempt should be made to accomplish this by means of peroral enteroscopy or video capsule endoscopy. Excision is the preferred treatment and is accomplished by means of segmental resection. Great care must be taken in the treatment of duodenal diverticula in the region of the ampulla of Vater to ensure that the pancreatic duct and the bile ducts are not injured during excision.

JEJUNAL ULCER

Ulcerations of the jejunum are also rare. They may be secondary to medications (e.g., NSAIDs), infection, a gastrinoma, or idiopathic causes. Offending medications should be stopped, infections should be treated, and gastrinomas should be excised. If these measures do not control the hemorrhage, the bleeding segment of the jejunum should be excised. MALLORY-WEISS TEARS Mallory-Weiss tears are linear tears at the esophagogastric junction that are usually caused by vomiting. Any patient who presents with vomiting that initially is not bloody but later turns so should be suspected of having a Mallory-Weiss tear. As a rule, these lesions stop bleeding without therapy. If bleeding is substantial or persistent, however, endoscopic coagulation may be necessary. In rare instances, the tear will have to be oversewn at operation. This is accomplished via an anterior gastrotomy and direct suture ligation of the tear. ACUTE HEMORRHAGIC GASTRITIS Bleeding from gastritis is virtually always managed medically with H2 receptor blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if H. pylori is present. Somatostatin may be beneficial. Sometimes, administration of vasopressin via the left gastric artery is needed to control bleeding. In rare cases, total or near-total gastrectomy is required; however, the mortality associated with this operation in this setting is high. Stress ulcer prophylaxis in severely ill or traumatized patients is essential to prevent this problem. The gastric pH should be kept as close to neutral as possible. If the gastritis is relatively mild, a biopsy specimen should be obtained and tested for H. pylori. Treatment consists of acid reduction and anti-H. pylori therapy. NEOPLASMS Benign tumors of the upper GI tract (e.g., leiomyomas, hamartomas, and hemangiomas) bleed at times. Wedge excision of the offending lesion is the procedure of choice. Gastrointestinal stromal tumors run the gamut from benign to highly aggressive. They typically present as a submucosal mass that may cause bleeding as a result of mucosal ulceration. The bleeding may be treated with wedge excision of the tumor. Such excision can often be accomplished laparoscopically.Bleeding from malignant neoplasms, whether early stage or late stage, generally can be controlled initially by endoscopic means; however, rebleeding rates are high. If the lesion is resectable, it should be excised promptly once the patient is stable and any coagulopathies have been corrected. If disease is advanced, however, surgical options are limited, and a nonoperative approach, though necessarily imperfect, is preferable. ESOPHAGEAL HIATAL HERNIA Not infrequently, the source of chronic enteric blood loss is an esophageal hiatal hernia. Major bleeding is rare in this condition but may occur as a result of linear erosions at the level of the diaphragm (Cameron lesions), gastritis within the hernia, or torsion of a paraesophageal hernia. Endoscopy is generally diagnostic, though the sources of chronic blood loss are not always obvious. Recognition that the bleeding derives from a Cameron lesion should incline the surgeon toward operative intervention [see 3:9 Open Esophageal Procedures and 3:10 Minimally Invasive Esophageal Procedures]: this lesion is usually mechanically induced and therefore tends to be less responsive to antacid therapy. Chronic bleeding from a sliding esophageal hiatal hernia should be treated initially with a PPI; anti-H. pylori therapy should be added if biopsy shows this organism to be present. Operation (i.e., laparoscopic Nissen fundoplication [see 3:10 Minimally Invasive Esophageal Procedures]) should be considered for fit patients who have complications associated with their hiatal hernia. A paraesophageal hernia should be repaired surgically; we prefer the laparoscopic approach when feasible. HEMOBILIA Hemobilia should be suspected in all patients who present with the classic triad of epigastric and right upper quadrant pain, GI bleeding, and jaundice; however, only about 40% of patients with hemobilia present with the entire triad. Endoscopy demonstrating blood coming from the ampulla of Vater points to a source in the biliary tree or the pancreas (hemosuccus pancreaticus). Arteriography may provide the definitive diagnosis: a bleeding tumor, a ruptured artery from trauma, or another cause. Arteriographic embolization of the affected portion of the liver is the preferred treatment option; hepatic artery ligation (selective if possible) or hepatic resection may be required.AORTOENTERIC FISTULA Aortoenteric fistulas may occur spontaneously as a result of rupture of an aortic aneurysm or perforation of a duodenal lesion; more often, they arise after aortic surgery. A common initial manifestation of an aortoenteric fistula is a small herald bleed that is followed a few days later by a massive hemorrhage. Patients often present with the triad of GI hemorrhage, a pulsatile mass, and infection; however, not all of these symptoms are invariably present. A high index of suspicion facilitates diagnosis. Endoscopy may show an aortic graft eroding into the enteric lumen, but this is an uncommon finding. CT scanning is the procedure of choice for diagnosis. The finding of air around the aorta or the aortic graft is diagnostic and is an indication for emergency exploration. The preferred surgical treatment is resection of the graft with extra-abdominal bypass. Some authorities, however, advocate resection of the graft with in situ graft replacement. VASCULAR ECTASES Vascular ectases (also referred to as vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and arteriovenous malformations) may bleed briskly. As a rule, gastric lesions are readily identified and the bleeding controlled by endoscopic means. Lesions that continue to bleed, either acutely or chronically, despite endoscopic measures should be excised. Some patients have multiple and extensive lesions that necessitate resection of large portions of the stomach or the small intestine. Pharmacotherapy and hormone therapy have been tried; the results have been mixed. DUODENAL AND JEJUNAL DIVERTICULA Duodenal and jejunal diverticula are rare causes of upper GI bleeding. Accurate identification of a bleeding site within a given diverticulum is difficult, but an attempt should be made to accomplish this by means of peroral enteroscopy or video capsule endoscopy. Excision is the preferred treatment and is accomplished by means of segmental resection. Great care must be taken in the treatment of duodenal