January 2008

Section 5 Gastrointestinal Tract and Abdomen

Despite recent advances in therapeutic endoscopy and the widespread use of antisecretory medications, upper gastrointestinal bleeding (UGIB)—defined as bleeding that occurs proximal to the ligament of Treitz—continues to be one of the more common reasons for surgical consultation. It also remains a significant source of mortality for both emergency admissions (11%) and inpatients (33%).¹ The most common causes of UGIB are esophageal (varices and Mallory-Weiss tears), gastric (acute hemorrhagic gastritis, varices, ulcers, and neoplasms), and duodenal (ulcers) [see Management of Specific Sources of Upper GI Bleeding, below]. Less common causes include various other GI conditions and certain hepatobiliary and pancreatic disorders.

Upper gastrointestinal hemorrhage may present as severe bleeding with hematemesis, hematoche zia, 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 UGIB 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,² 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, short, large-bore intravenous lines should be placed before workup is begun to ensure that immediate I.V. access is possible should the patient subsequently become unstable.

If the patient is unstable, he or she should be taken to an intensive care unit and resuscitated immediately. Resuscitation of an unstable patient is begun by establishing a secure airway and ensuring adequate ventilation.^3,4 Oxygen should be given, with a low threshold for endotracheal intubation. Much as in trauma resuscitation, either short, large-bore peripheral I.V. lines or a single-lumen 8 French catheter in the femoral vein should then be placed, through which lactated Ringer solution or 0.9% normal saline should be infused at a rate high enough to maintain tissue perfusion. A urinary catheter should be inserted and urine output monitored. Blood products should be given as necessary, and any coagulopathies should be corrected. It is all too easy to forget these basic steps in a desire to evaluate and manage massive GI hemorrhage.

Every effort should be made to resuscitate and stabilize the patient sufficiently to allow clinical evaluation and esophagogastroduodenoscopy (EGD) to help determine the cause of the bleeding and direct subsequent care. Only if the patient remains unstable and continues to bleed despite maximal supportive measures should he or she be taken to the operating room for intraoperative diagnosis as a last resort. In such cases, 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. Intraoperative endoscopy should be considered in this situation.

EGD [see 5:18 Gastrointestinal Endoscopy] almost always reveals the source of UGIB; its utility and accuracy have been well documented in the literature.^5,6 Performance of 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 (clip application or variceal banding). The choice of therapy depends on the cause, the site, and the rate of bleeding.

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.⁷ 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. Angiography may also be considered as a therapeutic modality for high-risk surgical patients.⁸ These tests, in conjunction with EGD, should allow the surgeon to establish the cause of upper GI bleeding more than 90% of the time.

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.⁹

Figure 1. Management of bleeding ulcers

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 [see Figure 1].¹⁰ 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 (six units or more) or bleeding that is not controlled endoscopically is an indication for surgical intervention. Likewise, ongoing hemorrhage in a hemodynamically unstable patient (especially an elderly one) calls for immediate surgical therapy. In addition, certain patients whose bleeding is controlled endoscopically (e.g., those with a visible vessel, active bleeding, or an adherent clot,¹¹ as well as those with giant ulcers) should be strongly considered for surgical therapy.

If bleeding is controlled endoscopically, then a proton pump inhibitor (PPI), such as pantoprazole, should be given intravenously, either in a bolus twice daily or by continuous infusion.¹² 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 reduce rebleeding rates after antacid medication has been stopped.¹³ Food need not be withheld unless the likelihood of rebleeding is high, because resumption of oral feeding does not appear to affect rebleeding rates.¹⁴ If bleeding recurs despite medical and endoscopic therapy, a second attempt at endoscopic control should be made. Repeat endoscopic treatment reduces the need for surgery without increasing the risk of death and is associated with fewer complications than surgery is.¹⁵

Surgical management may be accomplished either laparoscopically or via an open approach [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease]. 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 non-absorbable 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. If a truncal vagotomy is to be performed, the duodenotomy should extend through the pylorus and closed transversely to perform a pyloroplasty. Frozen section to confirm the presence of nerve tissue is helpful for ensuring that the vagotomy is complete.

The recommendation for truncal vagotomy is based on data from studies done before PPIs and H. pylori therapy came into use. Subsequent studies and a 2004 Cochrane review that evaluated rebleeding rates with current medical regimens demonstrate much lower rebleeding rates.¹⁶ Furthermore, it seems probable that long-term PPI therapy (the medical equivalent of vagotomy), in conjunction with eradication of H. pylori and avoidance of NSAIDs, should reduce rebleeding rates significantly. Studies from the United States⁹ and the United Kingdom¹⁷ have shown that a vagotomy is performed less than 50% of the time during surgical treatment of an acute bleeding duodenal ulcer. Therefore, although there are no prospective, randomized studies to support it, one may consider an alternative treatment approach in patients who have not been receiving ulcer therapy before the bleeding began—namely, ligation of the bleeding vessel, postoperative administration of PPIs, and H. pylori therapy. This approach avoids the complications associated with truncal vagotomy.

Another option for preventing postvagotomy symptoms when operating on stable patients for bleeding duodenal ulcer is to perform a highly selective vagotomy (HSV) [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease]. This procedure is considered preferable to truncal vagotomy because of the decreased incidence of gastric atony, alkaline reflux gastritis, dumping, and diarrhea; however, HSV is associated with a higher recurrence rate than truncal vagotomy is.¹⁸

Bleeding is less common than with duodenal ulcers, but initial management of a bleeding gastric ulcer is the same as that of a duodenal ulcer (i.e., endoscopic control) [see Figure 1]. To prevent aggravation of the bleeding, early biopsy generally is not recommended; repeat endoscopy and biopsy are done at a later date. The indications for emergency surgical intervention for gastric ulcers are the same as those for duodenal ulcers.

Bleeding gastric ulcers that necessitate operative intervention should be treated with resection. For type I ulcers, wedge resection is typically performed. For type II and III ulcers, the usual approach consists of antrectomy with Billroth I reconstruction and truncal vagotomy [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease]. Type IV ulcers can pose a technical challenge as a consequence of their close proximity to the esophagogastric junction. A distal gastrectomy with a tongue-shaped extension upward along the lesser curvature to incorporate the ulcer, followed by a Roux-en-Y reconstruction (the Csendes procedure), is often required.¹⁹ Another option is ligation of the left gastric artery, followed by biopsy and oversewing of the ulcer.

Esophageal Varices

Figure 2. Management of bleeding 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.²⁰ 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].^21,22 If these measures do not control the hemorrhage, balloon tamponade is indicated.²³ Patients who are to undergo this procedure require an endotracheal tube. The preferred tube 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.

Intravenous somatostatin (250 µg bolus, followed by infusion of 250 µg/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.²⁴ 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; 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 µg/hr) in place of I.V. somatostatin because the former tends to be more widely available. 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.^25–27 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 per sistent rebleeding despite endoscopic and medical therapy. When such intervention is considered, 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) [see 5:10 Portal Hypertension]. TIPS significantly reduces rebleeding rates, but it poses a risk of encephalopathy.²⁸

If the patient is not a transplant candidate and is not actively bleeding, a distal splenorenal shunt (DSRS) is preferable.²⁹ 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 suitable—that 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 venography—a DSRS 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, a central portacaval shunt, usually in a side-to-side orientation or with a short polytetrafluoroethylene (PTFE) interposition graft, may be placed. 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 Sugiura procedure) [see 5:10 Portal Hypertension] 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. For varices that are secondary to splenic vein thrombosis (sinistral portal hypertension), splenectomy is usually curative; the procedure may be performed laparoscopically [see 5:25 Splenectomy].³⁰

Gastric varices are managed in much the same way as esophageal varices [see Figure 2], though they are less amenable to sclerotherapy.³¹ Other endoscopic treatments (e.g., ligation or sclerotherapy plus ligation) and interventional radiologic treatments (e.g., TIPS or intravascular balloon occlusion) should be considered before surgical management (i.e., DSRS, portosystemic shunting, or suture ligation with gastric devascularization). If the patient is a suitable candidate, liver transplantation may be performed as an alternative to shunting.

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 injection, clipping, banding, or coagulation may be necessary.^32,33 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.

Bleeding from gastritis is virtually always managed medically with H₂ blockers, PPIs, sucralfate, or antacids (either alone or in combination), along with antibiotics if H. pylori is present.³⁴ 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 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease] 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.³⁵ 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 H. pylori therapy.

Benign tumors of the upper GI tract (e.g., gastrointestinal stromal tumors [GISTs], hamartomas, and hemangiomas) occasionally bleed [see 5:8 Tumors of the Stomach, Duo denum, and Small Bowel]. Wedge excision of the offending lesion is the procedure of choice. GISTs (previously classified as leiomyomas or leiomyosarcomas) 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, which can be challenging when the GIST is located in the gastric cardia. Such excision can often be accomplished laparoscopically [see 5:20 Procedures for Benign and Malignant Gastric and Duodenal Disease] or even through a laparoscopic intragastric approach.³⁶ Some surgeons now perform full-thickness wedge resections endoscopically with the use of a flexible stapler.³⁷

Bleeding from malignant neoplasms, whether early stage or late stage, generally can be controlled initially by endoscopic means; however, rebleeding rates are high.³⁸ If the lesion is resectable, it should be excised promptly once the patient is stable (provided that it has been appropriately staged). If disease is advanced, however, surgical options are limited, and a nonoperative approach, though necessarily imperfect, is preferable.³⁹

Not infrequently, the source of chronic enteric blood loss is a 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),⁴⁰ 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 4:7 Open Esophageal Procedures and 4:8 Minimally Invasive Esophageal Procedures]; this lesion is usually mechanically induced and therefore tends to be less responsive to antacid therapy.

Chronic bleeding from a type I hiatal hernia should be treated initially with a PPI. H. pylori therapy should be added if biopsy shows this organism to be present. Operative management (i.e., laparoscopic Nissen fundoplication [see 4:5 Minimally Invasive Esophageal Procedures]) should be considered for fit patients who have complications associated with their hiatal hernia and for all symptomatic patients with type II, III, or IV hiatal hernias (laparoscopic paraesophageal hernia repair).⁴¹

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.⁴² Having the endoscopist mark the site with India ink is helpful for localization.

Arteriography may provide the definitive diagnosis: a bleeding tumor, a ruptured artery from trauma, or another cause.⁴³ Arteriographic embolization of the affected portion of the liver is the preferred treatment option; hepatic artery ligation (selective if possible) or hepatic resection [see 5:23 Hepatic Resection] may be required.⁴⁴

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.⁴⁵ 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. If there are no pancreatitis-related indications for surgery, angiographic embolization can be definitive treatment.⁴⁶ If there are pancreatitis-related indications for operation, angiographic embolization may allow an elective operative procedure based on the structural changes observed in the pancreas. If embolization fails, pancreatic resection is usually required, often on an emergency basis [see 5:24 Procedures for Benign and Malignant Pancreatic Disease].

Aortoenteric fistulas may occur spontaneously as a result of rupture of an aortic aneurysm or perforation of a duodenal lesion (primary); more often, they arise after aortic surgery (secondary).⁴⁷ 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.⁴⁸ Some now advocate endovascular stent repair for high-risk patients without evidence of infection.⁴⁹

Vascular ectasias (also referred to as vascular dysplasia, angiodysplasia, angiomata, telangiectasia, and arteriovenous malformations) may bleed briskly. As a rule, gastric lesions can be readily identified and the bleeding controlled by endoscopic means.⁵⁰ 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. Pharmacotherapy and hormone therapy have been tried; the results have been mixed.

Duodenal diverticula are rare causes of UGIB. Accurate identification of a bleeding site within a given diverticulum is difficult, but an attempt should be made to accomplish this by means of per oral enteroscopy or video capsule endoscopy. Excision is the preferred treatment and is accomplished by means of segmental resection.⁵¹ 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.