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Upper Gastrointestinal Bleeding Treatment & Management

  • Author: Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF; Chief Editor: BS Anand, MD  more...
 
Updated: Mar 21, 2016
 

Approach Considerations

The goal of medical therapy in upper gastrointestinal bleeding (UGIB) is to correct shock and coagulation abnormalities and to stabilize the patient so that further evaluation and treatment can proceed. High doses of proton pump inhibitirs may reduce the need for endoscopic therapy (see Treatment with proton pump inhibitors).

Various methodologies have been proposed to quantitate rebleeding risk (eg, Rockall score, Baylor score).[40] These remain somewhat controversial in their application.

The 2008 Scottish Intercollegiate Guidelines Network (SIGN) guideline on the management of acute upper and lower gastrointestinal bleeding recommends that an initial (pre-endoscopic) Rockall score be calculated for all patients presenting with an acute UGIB. In patients with an initial Rockall score >0, endoscopy is recommended for a full assessment of bleeding risk.[35]

Resuscitation of a hemodynamically unstable patient begins with assessing and addressing the ABCs (ie, airway, breathing, circulation) of initial management. (Baradarian et al demonstrated that early, aggressive resuscitation can reduce mortality in acute UGIB.[41] )

Patients presenting with severe blood loss and hemorrhagic shock present with mental status changes and confusion. In such circumstances, patients cannot protect their airway, especially when hematemesis is present. In these cases, patients are at an increased risk for aspiration, which is a potentially avoidable complication that can significantly affect morbidity and mortality. This situation must be recognized early, and patients should be electively intubated in a controlled setting.

Intravenous access must be obtained. Bilateral, 16-gauge (minimum), upper extremity, peripheral intravenous lines are adequate for volume resuscitative efforts. Poiseuille’s law states that the rate of flow through a tube is proportional to the fourth power of the radius of the cannula and is inversely related to its length.[22] Thus, short, large-bore, peripheral intravenous lines are adequate for rapid fluid infusion.

According to the 2008 SIGN guideline, either colloid or crystalloid solutions may be used to attain volume restoration prior to administering blood products.[35] A rough guideline for the total amount of crystalloid fluid volume needed to correct the hypovolemia is the 3-for-1 rule. Replace each milliliter of blood loss with 3 mL of crystalloid fluid. This restores the lost plasma volume. Patients with severe coexisting medical illnesses, such as cardiovascular and pulmonary diseases, may require pulmonary artery catheter insertion to closely monitor hemodynamic cardiac performance profiles during the early resuscitative phase.

Once the ABCs have been addressed, assess the patient's response to resuscitation, based on evidence of end organ perfusion and oxygen delivery.

Consultation with a surgeon should be considered for all patients with gastrointestinal hemorrhage.

A study published by Kaplan et al indicated that skin temperature on physical examination in combination with serum bicarbonate levels correlated well with the level of systemic perfusion.[42]

Pulmonary artery catheters may be helpful to guide therapy. Foley catheter placement is mandatory to allow a continuous evaluation of the urinary output as a guide to renal perfusion. This labor-intensive management should be performed only in an ICU setting.

Once the maneuvers to resuscitate are underway, insert a nasogastric tube and perform an aspirate and lavage procedure. This should be the first procedure performed to determine whether the GI bleeding is emanating from above or below the ligament of Treitz. If the stomach contains bile but no blood, UGIB is less likely. If the aspirate reveals clear gastric fluid, a duodenal site of bleeding may still be possible.

In a retrospective review of 1190 patients, Luk et al found that positive nasogastric-tube aspirate findings were 93% predictive of an upper GI source of bleeding.[43]

According to a study performed by the ASGE, however, a nasogastric-tube aspirate finding can be negative even in the setting of a large duodenal bleeding ulcer. The study compared nasogastric-tube aspirate findings with endoscopic findings of the bleeding source.[26] The investigation revealed that 15.9% of patients with a clear nasogastric-tube aspirate, 29.9% of patients with coffee-ground aspirate, and 48.2% of patients with red blood aspirate had an active upper GI source of bleeding at the time of endoscopy.

A study correlated mortality with the color of the fluid from the nasogastric-tube aspirate and the color of the stool.[2] As shown in the following table, the color of the nasogastric-tube aspirate can be a prognostic indicator.

Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB Mortality Rate (Open Table in a new window)

Nasogastric Aspirate Color Stool Color Mortality Rate, %
Clear Brown or red 6
Coffee-ground Brown or black 8.2
  Red 19.1
Red blood Black 12.3
  Brown 19.4
  Red 28.7

Go to Pediatric Gastrointestinal Bleeding for complete information on this topic.

Surgery

Primary surgical intervention should be considered in patients with a perforated viscus (eg, from perforated duodenal ulcer, perforated gastric ulcer, or Boerhaave syndrome). In patients who are poor operative candidates, conservative treatment with nasogastric suction and broad-spectrum antibiotics can be instituted. Endoscopic clipping or sewing techniques have also been used in such patients.

Emergency surgery in UBIG typically entails oversewing the bleeding vessel in the stomach or duodenum (usually preoperatively identified by endoscopy), vagotomy with pyloroplasty, or partial gastrectomy. Angiographic obliteration of the bleeding vessel is considered in patients with poor prognoses.

Treatment-related contraindications and precautions

Contraindications to upper endoscopy include an uncooperative or obtunded patient, severe cardiac decompensation, acute myocardial infarction (unless active, life-threatening hemorrhage is present), and perforated viscus (eg, esophagus, stomach, intestine).

Contraindications to emergency surgery include impaired cardiopulmonary status and bleeding diathesis.

Esophagogastroduodenoscopy may be more difficult or impossible if the patient has had previous oropharyngeal surgery or radiation therapy to the oropharynx.

The presence of a Zenker diverticulum can make intubation of the esophagus more difficult.

Patients with Down syndrome are more sensitive to conscious sedation and should receive much less sedation, or they should be monitored by an anesthesiologist and/or intubated prophylactically prior to the procedure.

Hypotension may be exacerbated by sedation; therefore, patients who are unstable should be given less sedation.

Patients with massive bleeding should be considered for intubation to reduce the increased risk of aspiration. Such patients should be treated in an intensive care setting.

Ideally, the patient should be stabilized prior to endoscopy and abnormalities in coagulation should be corrected. When this is not possible, the judgment of an experienced endoscopist is vital.

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PPIs

The relative efficacy of the PPIs may be due to their superior ability to maintain a gastric pH at a level above 6.0, thereby protecting an ulcer clot from fibrinolysis.[44] Considering the available data, the ideal pharmacologic therapy for patients with acute ulcer bleeding appears to be an intravenous PPI whether the patient is NPO or not. This is confirmed in the 2008 SIGN guidelines, which recommend high-dose intravenous PPIs in patients with major peptic ulcer bleeding or nonbleeding visible vessels after endoscopic bleeding control.[35] Pantoprazole, lansoprazole, and esomeprazole are the only PPIs available as an intravenous formulation in the United States; intravenous omeprazole is used in other countries.

Lao et al have demonstrated that high-dose intravenous omeprazole can accelerate the resolution of stigmata of recent hemorrhage and reduce the need for endoscopic therapy.[45]

The suggested dosing of intravenous pantoprazole and esomeprazole is 80-mg bolus followed by 8-mg/h infusion. The infusion is continued for 48-72 hours. This therapy has been shown to be cost-effective by Barkun et al.[46] Laine et al have demonstrated that intravenous high-dose lansoprazole, as well as orally administered high-dose lansoprazole, can maintain the intragastric pH above 6.[47]

A meta-analysis of 24 randomized controlled trials that evaluated PPIs for bleeding ulcers (with or without endoscopic therapy) found a significant reduction in the risk of rebleeding, the need for repeat endoscopic hemostasis, and surgery. An improvement in mortality was also seen in Asian trials and in patients with active bleeding or nonbleeding visible vessels.[48]

The 2010 international consensus guidelines on UGIB recommended the use of intravenous PPIs in all patients with high-risk lesions post-endoscopic therapy; PPI therapy might downgrade the lesion if given pre-endoscopy.[49] The 2008 SIGN guideline agrees that PPIs should not be used pre-endoscopy in patients presenting with acute UGIB.[35]

High-dose oral PPIs may be used in patients who do not have active bleeding or other high-risk stigmata for recurrent bleeding (eg, a visible vessel, adherent clots); in such patients, the risk of recurrent bleeding is low. The goal of treatment in these patients (following resuscitation) should be directed at healing the ulcers and at eliminating precipitating factors (eg, H pylori, NSAIDs).

The 2008 SIGN guideline recommends taking biopsy samples to test for H pylori at the initial endoscopy procedure before starting PPI therapy. Biopsy specimens should be histologically evaluated when the rapid urease test is negative.[35]

A combined analysis of 5 studies that evaluated oral dosing with PPI (with or without endoscopic therapy) found a significant reduction in the risk of rebleeding and surgery.[50]

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Therapeutic Endoscopy

Since the late 1980s, endoscopic techniques to achieve hemostasis for bleeding ulcers and varices have continued to evolve. Endoscopy is now the method of choice for controlling active ulcer hemorrhage.[3]

Several randomized clinical trials and meta-analyses have demonstrated and supported the idea that early endoscopic hemostatic therapy significantly reduces the rates of recurrent bleeding, the need for emergent surgery, and mortality in patients with acute nonvariceal upper gastrointestinal bleeding (UGIB).

In the early history of endoscopy for UGIB, multiple published studies questioned the cost-effectiveness of endoscopy in this setting, because it was unclear whether the outcome was changed. In a setting in which 80% of patients respond to conservative medical management, studies were hampered by type 2 errors because of the large number of patients needed to demonstrate statistical significance.

In 1989, a National Institutes of Health (NIH) consensus conference on UGIB concluded that effective therapy was needed in the presence of active bleeding or a visible vessel. The conference affirmed that the treatment, when performed by an experienced endoscopist using 1 of 4 techniques (ie, injection of epinephrine or sclerosants, heater-probe coagulation, bipolar electrode coagulation, laser coagulation), was proven effective by the published evidence.

Three other techniques have since been developed: (1) endoscopic application of clips, (2) use of banding devices, and (3) argon plasma coagulation. Aside from ulcer hemorrhaging, other causes of gastrointestinal bleeding, including mucosal tears in the esophagus or upper stomach due to vomiting (Mallory-Weiss tears), venous blebs, and vascular ectasias, can also be treated with endoscopic coagulation.

The bleeding from gastric cancers and ulcers in leiomyomas does not usually respond to endoscopic therapy; surgical or radiologic intervention is needed.

Much debate has focused on the significance of the nonbleeding visible vessel (ie, color, size, diagnostic characteristics, risk of rebleeding) in ulcer hemorrhage. These matters became clarified after the characteristics and significance of the visible vessel in the ulcer crater were defined and the evidence for endoscopic therapy was established, demonstrating that patients requiring therapy to control bleeding or rebleeding could be diagnosed and treated at the time of the upper endoscopy.

Patients should be considered for upper endoscopy if blood loss from the upper gastrointestinal tract is suspected.

The patient should undergo upper endoscopy prior to any operative intervention in order to diagnose and localize the bleeding site. Most patients (85-90%) respond to endoscopic therapy.

During the endoscopy, the patient is monitored according to analgesia and sedation guidelines formulated by the American Society of Anesthesiology. The characteristics of the bleeding lesion are noted, and appropriate therapy is applied when necessary for high-risk lesions or active bleeding.

Urgent endoscopy

Urgent endoscopy is indicated when patients present with hematemesis, melena, or postural changes in blood pressure. Cooper et al have demonstrated a lower rate of rebleeding and shorter length of stay when endoscopy is performed within 24 hours of admission.[43, 51]

Early endoscopy

Cooper et al studied the effectiveness of performing an early endoscopy within the first 24 hours of an acute UGIB episode and found it to be associated with reductions in the length of hospital stay, rate of recurrent bleeding, and the need for emergent surgical intervention.[51]

According to the 2010 international consensus on nonvariceal upper gastrointestinal bleeding, early endoscopy (within 24 hours of presentation) is appropriate for most patients with UGIB.[52] In a retrospective review involving more than 30,000 cases, Yavorski et al showed that the mortality rates were more than twice as high in patients who did not undergo an early endoscopic procedure than for those who did undergo the procedure early on (11.1% vs 5.2%, respectively).

Endoscopic techniques

The following endoscopic techniques have been developed for achieving hemostasis[10] :

  • Injection of epinephrine or sclerosants
  • Bipolar electrocoagulation
  • Band ligation [53]
  • Heater probe coagulation
  • Constant probe pressure tamponade
  • Argon plasma coagulator
  • Laser photocoagulation
  • Rubber band ligation
  • Application of hemostatic materials, including biologic glue
  • Application of hemoclips or endoclips
  • Application of nanopowder (experimental) [54]

Treatment using a combination of endoscopic therapies has become more common. For example, injection therapy can be applied first to better clarify the bleeding site, especially in the actively bleeding patient, followed by the application of heater probe or bipolar (gold) probe coagulation. Injection therapy can also be performed prior to endoscopic placement of hemoclips.

According to the 2008 SIGN guideline, combinations of endoscopy with an injection of at least 13 mL of 1:10,000 adrenaline, coupled with either a thermal or mechanical treatment, are more effective than single modalities.[35]

The 2010 international consensus guidelines on UGIB recommended the use of endoscopic clips or thermal therapy for high-risk lesions.[52] As another example, injection therapy is useful prior to laser therapy to reduce the heat sink effect of rapidly flowing blood prior to laser coagulation.

Heater probe coagulation

The heater probe consists of a resistor electrode enveloped by a titanium capsule and covered by Teflon (to reduce sticking to the mucosa by the probe). The probe temperature rises to 250°C (482°F).

Bipolar electrocoagulation

The bipolar probe consists of alternating bands of electrodes producing an electrical field that heats the mucosa and the vessel. The electrodes are coated with gold to reduce adhesiveness. The probes are stiff in order to allow adequate pressure to be applied to the vessel to appose the walls and thus produce coaptive coagulation when the electrical-field energy is transmitted. Careful technique is required to heat-seal the perforated vessel.

Injection therapy

Injection therapy involves the use of several different solutions injected into and around the bleeding lesion. The different solutions available for injection are epinephrine, sclerosants, and clot-producing materials, such as fibrin glue.

The epinephrine used for injection is diluted (1:10,000) and injected as 0.5- to 1-mL aliquots. Debate continues over whether the hemostatic effect of epinephrine is due to induced vessel vasoconstriction and subsequent platelet aggregation or to the tamponade effect produced by injecting the volume of drug into the tissue surrounding the bleeding lesion.

Epinephrine injection is often used to reduce the volume of bleeding so that the lesion can be better localized and then treated with a coaptive technique (ie, heater probe, gold probe).

Combining epinephrine injections with human thrombin (600-1000 IU) reduces the risk of bleeding.[6]

Although the epinephrine administered in injection therapy is absorbed into the systemic circulation, this does not appear to have any adverse effects on the hemodynamic status.

Injecting a volume of sterile isotonic sodium chloride solution and providing a tamponade effect also leads to hemostasis, although not as effectively as does epinephrine.[6]

The sclerosant solutions used today include ethanol, polidocanol, and sodium tetradecyl sulfate.

The sclerosants create hemostasis by inducing thrombosis, tissue necrosis, and inflammation at the site of injection. When large volumes are injected, the area of tissue necrosis can produce an increased risk of local complications, such as perforation. Combining the various agents into a single injection has not been shown to be more beneficial than single-agent therapy alone.[6]

The use of fibrin glue in injection therapy has been shown to be successful, with results similar to those of epinephrine injections.[55]

Laser therapy

Laser phototherapy uses an Nd:YAG laser to create hemostasis by generating heat and direct vessel coagulation. This is a noncontact thermal method. It is not as effective as coaptive coagulation, because it lacks the use of compression to create a tamponade effect.[6] An additional deterrent to its use is expense.

To perform laser coagulation, the area near the vessel is first injected with epinephrine to reduce blood flow (reducing the heat-sink effect); then, the laser is applied around the vessel, producing a wall of edema. Caution must be observed to avoid drilling into the vessel with the laser, causing increased bleeding.

Hemostatic clips and endoclips

Hemostatic clips are available in the United States.

Modification of the delivery system has made clip placement much easier than it was in the original model. With careful placement of the clip, closing the defect in the vessel is possible. Usually, multiple clips are applied. They vary in the size and the strength of the clip. Four models of hemoclips are available: QuickClip2, which is rotatable; Resolution Clip, which can be reopened after closure; TriClip, which has 3 prongs; and InScope, which is a multiclip applier with 4 endoclips. The Resolution Clip seems to be the current clip of choice by experienced endoscopists.

Considering the available data, the efficacy of hemoclips is similar to that of thermal coagulation methods.

One report, concerning 113 patients with major stigmata of ulcer hemorrhage, found no difference between the use of hemoclips and photocoagulation with regard to hemostasis, 30-day mortality, and the need for emergency surgery.[56] Patients randomized to the endoclip group had significantly lower rebleeding rates (2% vs 21%). However, only 60% of active bleeders were successfully treated with the heater probe, a rate much lower than in previous reports.

A study of 80 patients found a higher rate of control of initial bleeding with the heater probe compared with the Olympus endoclip (100% vs 85%).[57] Rebleeding rates were not significantly different.

No significant differences in procedure duration, initial hemostasis, or rebleeding rates were found in a study of 47 patients comparing combination therapy with epinephrine injection plus monopolar electrocoagulation versus hemoclips.[58]

There are some clinical settings in which endoclips may be preferred over other hemostatic methods. These include the treatment of ulcers in patients who are coagulopathic or who require ongoing anticoagulation; in such patients, electrocoagulation will increase the size, depth, and healing time of treated lesions. Endoclips may also be preferable in the retreatment of lesions that rebleed after initial thermal hemostasis.

Ulcers on the lesser curvature, the posterior duodenum, or the cardia increase the difficulty of clip deployment and clip failure rates.

Larger endoclips have advantages over smaller hemoclips for the hemostasis of chronic ulcers and the closure of larger lesions.

Argon plasma coagulation

Argon plasma coagulation is a technique in which a stream of electrons flows along a stream of argon gas. The coagulation is similar to monopolar cautery, with the current flow going from a point of high current density (the point of contact of the gas with the mucosa) to an area of low current density (the conductive pad on the patient's body). The current flows through the body in an erratic path to the pad.

This monopolar cautery technique is similar to the laser technique in that energy is delivered to the vessel for coagulation with apposition of the vessel walls. This technique was found not to be effective for visible vessels larger than 1 mm. No animal models have been used for ulcer hemorrhage to validate this technique.

Nanopowder

Nanopowder has been found to be effective in a small study using a porcine model of arterial bleeding.[54] Further trails are awaited.

Endoscopic treatment decisions

The choice of treatment modality is influenced by the size of the vessel. Animal studies have demonstrated that the heater probe and bipolar probe are effective for vessels as large as 2 mm in diameter.

Other techniques (eg, clips, band ligation) or a combination of techniques are needed for larger vessels or vessels that are not approachable by the heater probe or bipolar probe. (Surgical intervention should be considered when dealing with vessels larger than 2 mm in diameter, discounting an enlargement due to the development of pseudoaneurysm.)

The 2008 SIGN guidelines recommend variceal band ligation in patients with confirmed esophageal variceal hemorrhage. It can be combined with a beta blocker as secondary prevention for esophageal variceal hemorrhage. For patients in whom band ligation is not suitable, a combination of nonselective beta blocker and nitrate is recommended as secondary prevention.[35]

Ulcers with an overlying clot

In the patient who has an ulcer with an overlying clot, attempting to remove the clot by target washing is critical. Endoscopic removal of the clot by washing or cold snare has been demonstrated to be effective in reducing the recurrence of bleeding.[59] (Cutting away the adherent clot is somewhat controversial but is recommended based on study results from experienced centers.)

The findings under the clot (eg, bleeding vessel, visible vessel, clean base, examples of which are seen in the images below) help to determine the therapy needed and improve efficacy by allowing treatment to be applied directly to the vessel. (See the table below.)

Ulcer with active bleeding. Ulcer with active bleeding.
Ulcer with a clean base. Ulcer with a clean base.
Diagram of an ulcer with a clean base. Diagram of an ulcer with a clean base.
Ulcer with an overlying clot. Ulcer with an overlying clot.
Ulcer with a visible vessel. Ulcer with a visible vessel.
Diagram of an ulcer with a visible vessel. Diagram of an ulcer with a visible vessel.

Table 5. Ulcer Characteristics and Correlations (Open Table in a new window)

Ulcer Characteristics Prevalence Rate, % Rebleeding Rate, % Surgery Rate, % Mortality Rate, %
Clean base 42 5 0.5 2
Flat spot 20 10 6 3
Adherent clot 17 22 10 7
Visible vessel 17 43 34 11
Active bleeding 18 55 35 11

If the clot cannot be removed by washing, then cutting away the clot using a cold snare can be considered by experienced endoscopists.

Vigorous washing of the clot formed after therapy is useful in determining the adequacy of coagulation. A combination of injection with heater probe or bipolar coaptive coagulation is often used and has been shown to be more effective in patients with active bleeding.

The patient is monitored under the protocol for conscious sedation, also called analgesia and sedation (ie, per the American Society of Anesthesiologists and the American Society for Gastrointestinal Endoscopy guidelines).

Active bleeding and rebleeding

Attempting to control active bleeding using the recommended techniques with the appropriate equipment or instituting appropriate therapy for a high-risk lesion is important. The large-channel therapeutic endoscope should be used so that the 10-French thermal probe can be employed for adequate coaptation.

Endoscopists should use the technique with which they have the most familiarity. The endoscopy should not be started unless the endoscopist is equipped for any potential lesions (eg, ulcer, varix, angioectasia, tear, tumor). The patient should be monitored for recurrent bleeding and treated a second time if appropriate. A surgical consultation should be considered for all patients with gastrointestinal hemorrhage.

The 2008 SIGN guidelines urge the consideration of transjugular intrahepatic portosystemic stent shunts (TIPS) to prevent esophageal variceal rebleeding for patients in whom endoscopy is contraindicated or has failed, and/or who are intolerant to pharmacological therapy,[35]

Rebleeding occurs in 10-30% of endoscopically treated patients. A second attempt at endoscopic control is warranted. Some authorities have concerns about the perils of a second esophagogastroduodenoscopy, which may result in delayed surgery, perforation, and increased morbidity and mortality rates. However, this approach has been validated in a large, randomized, controlled trial that showed decreased morbidity and mortality rates.[49]

Specific characteristics at endoscopy can predict rebleeding. Rebleeding occurs in 55% of patients who have active bleeding (pulsatile, oozing), in 43% who have a nonbleeding visible vessel, in 22% who have an ulcer with an adherent clot, and in 0-5% who have an ulcer with a clean base.

At endoscopy, the prevalence rate for a clean base is 42%, for a flat spot is 20%, for an adherent clot is 17%, for a visible vessel is 17%, and for active bleeding is 18%. (See the images below.)

Freeman et al have described a pale, visible vessel that appears to have a very high risk for rebleeding.[60] This must be differentiated from the presence of a clean ulcer base.

Good visualization is important. The uncleared fundal pool may obscure an ulcer, mucosal tear, gastric varices, portal gastropathy, or tumor (eg, leiomyoma, adenocarcinoma, lymphoma). Endoscopic therapy is recommended for ulcers at increased risk for rebleeding.

According to the 2008 SIGN guidelines, TIPS should be considered to prevent gastric variceal rebleeding.[35]

Using a combination of techniques is prudent when re-treating the ulcer site because the first therapy may have produced necrosis and weakening of the intestinal wall. Ulcers on the anterior surface of the stomach and duodenum are at an increased risk for perforation. Using injection as the first step increases the thickness of the submucosal layer, thus providing an extra margin of safety.

Even operative techniques can have a significant rebleeding rate with significant mortality, as noted in the study of Poxon et al. In this investigation, the rebleeding rate was 10% (80% mortality for rebleeders) in patients who underwent a conservative surgical technique in which the ulcer base was undersewn.[61] This more conservative approach was compared with the standard surgical technique (ie, vagotomy and pyloroplasty or partial gastrectomy). The comparison of the conservative approach with a standard gastrectomy resulted in similar mortality rates, ie, 26% versus 19%, respectively, with no rebleeding after partial gastrectomy.

Postendoscopic monitoring

Postoperatively, the patient is monitored for recovery from conscious sedation after endoscopy and from general anesthesia after abdominal surgery. Monitor the patient's mental status, vital signs, chest, cardiac, and abdominal findings to ascertain that the patient's clinical status has stabilized and that no complications (eg, aspiration, perforation, recurrent bleeding, myocardial infarction due to hypotension) have occurred. Monitor the hemoglobin level.

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Bleeding Peptic Ulcer Treatment

Upper GI endoscopy is the most effective diagnostic tool for PUD and has become the method of choice for controlling active ulcer hemorrhage. Failure of endoscopy to maintain hemostasis is one of the indications to initiate surgical intervention, especially in high-risk patients.

In a randomized, prospective trial that included 92 patients with recurrent peptic ulcer bleeding after initial endoscopic therapy for hemostasis, patients who underwent a second endoscopic attempt to control bleeding were found to have decreased transfusion requirements, 30-day mortality rates, and duration of ICU stay in comparison with the surgical group.[62]

With the exception of a patient in shock who has a life-threatening recurrent hemorrhage, this study supports attempting another trial of endoscopy to control a bleeding ulcer.

Regardless of the endoscopic therapy, however, 10-12% of patients with acute ulcerous hemorrhage require an operation as the definitive procedure to control the bleeding ulcer. In most circumstances, the operation is performed emergently, and the associated mortality rate is as high as 15-25%.

Medical therapy used in conjunction with endoscopy involves PPI administration. PPIs decrease rebleeding rates in patients with bleeding ulcers associated with an overlying clot or visible, nonbleeding vessel in the base of the ulcer.[63, 64] Consider transcatheter angiographic embolization in patients who are poor surgical candidates. Because of the extensive collateral circulation of the upper GI tract, ischemic complications are rare.

Surgical treatment

If 2 attempts at endoscopic control of the bleeding vessel are unsuccessful, avoid further attempts (ie, because of increased rebleeding and mortality rates) and pursue surgical intervention. The indications for surgery in patients with bleeding peptic ulcers are as follows:

  • Severe, life-threatening hemorrhage not responsive to resuscitative efforts
  • Failure of medical therapy and endoscopic hemostasis with persistent recurrent bleeding
  • A coexisting reason for surgery, such as perforation, obstruction, or malignancy
  • Prolonged bleeding, with loss of 50% or more of the patient's blood volume
  • A second hospitalization for peptic ulcer hemorrhage

The operative treatment options for a bleeding duodenal ulcer historically include vagotomy, gastric resection, and drainage procedures. Each specific operative option is associated with its own incidence of ulcer recurrence, postgastrectomy syndrome, and mortality (as seen in the table below). When making an intraoperative judgment on how to best manage the bleeding ulcer, it is extremely important for the surgeon to be aware of these differences.[16]

Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for Duodenal Ulcer (Open Table in a new window)

Original Operation Recurrence Rate, % Postgastrectomy Syndrome Rate, % Mortality Rate, %
Proximal gastric vagotomy 10 5 0.1
Truncal vagotomy and drainage 7 20-30 < 1
Truncal vagotomy and antrectomy



Billroth I or Billroth II



1 30-50 0-5
Truncal vagotomy and antrectomy



Roux-en-Y



5-10 50-60 0-5

The 3 most common operations performed for a bleeding duodenal ulcer are as follows[10] :

  • Truncal vagotomy and pyloroplasty with suture ligation of the bleeding ulcer
  • Truncal vagotomy and antrectomy with resection or suture ligation of the bleeding ulcer
  • Proximal (highly selective) gastric vagotomy with duodenostomy and suture ligation of the bleeding ulcer

The purpose of the vagotomy is to divide the nerves to the acid-producing body and fundus of the stomach. This inhibits acid production that occurs during the cephalic phase of gastric secretion. Although acid secretion is controlled, gastric motility and gastric emptying is affected, as indicated in the following table.[16]

Table 7. Effects of Operations for PUD on Gastric Emptying and Motility (Open Table in a new window)

Operation Antral Innervation Liquid Emptying Solid Emptying
Proximal gastric vagotomy Preserved Fast Normal
Truncal vagotomy Divided Fast Slow
Truncal vagotomy and drainage Divided Fast Fast
Truncal vagotomy and antrectomy Divided Fast Fast

Proximal vagotomy abolishes gastric receptive relaxation and impairs storage in the proximal stomach. As a result, a more rapid gastric emptying of liquids occurs. A drainage procedure is not required, because the innervation of the antrum and pylorus is still intact. Because of this, the gastric emptying of solid food is not altered. The antropyloric mechanism still functions normally and continues to prevent duodenogastric reflux.

In addition to having the same effects as a highly selective vagotomy in the proximal stomach, a truncal vagotomy also has marked effects on distal gastric motor function. It weakens distal gastric peristalsis, thus requiring the creation of a pyloroplasty to decrease the resistance to outflow from the stomach.

Truncal vagotomy and suture ligation of a bleeding ulcer is a frequently used operation for treating upper gastrointestinal bleeding (UGIB) in elderly patients with life-threatening hemorrhage and shock. The procedure can be performed rapidly, minimizing the time spent in the operating room under general anesthesia.

The principles of suture ligation of a duodenal bleeding ulcer that involves the gastroduodenal artery require the use of the 3-point ligation technique.

The gastroduodenal artery is ligated proximally and distally to the arterial bleeding site. The third suture is a horizontal mattress placed to control hemorrhage from the transverse pancreatic branch of the gastroduodenal artery. Failure to place this third stitch may result in recurrent bleeding that requires another emergent laparotomy of the abdomen. Vagotomy with antrectomy is reserved for patients whose conditions have failed to respond to more conservative attempts at surgical intervention and for those with aggressive and recurrent duodenal ulcer diathesis, such as gastric outlet obstruction.

When performing a highly selective vagotomy, the duodenostomy or the pyloroduodenostomy is closed anatomically, preserving the normal pyloric sphincter muscle. Most commonly, this operation is reserved for young, stable, low-risk patients. Although long-term follow-up care is still necessary, the recurrent ulcer rate is less than 10% at a mean follow-up of 3.5 years.[10]

Much of what is now known about the operations performed for bleeding duodenal ulcers came from the era before the etiologic role for H pylori and NSAIDs in the development of peptic ulcers was understood. Reducing gastric acidity has been proven to be beneficial, with lower rebleeding rates when using high-dose omeprazole.[6] Although PPIs seem to have an advantage, they have no affect on mortality.

The diagnosis of H pylori infection is important in the management of patients with a complicated bleeding peptic ulcer. If a patient with a bleeding ulcer requires surgery, then knowledge of the patient's H pylori status becomes pertinent, because it may help guide the decision to choose a particular surgical procedure (eg, simply oversewing the ulcer as opposed to performing an antiulcer operation). Many studies support the decision to manage the bleeding ulcer in conjunction with eradication of H pylori.

The 2008 SIGN guideline recommends testing for H pylori in patients with peptic ulcer bleeding and a 1-week course of therapy prescribed for those who test positive. Three weeks of continuous treatment should be given. In those who use NSAIDs, maintenance antisecretory therapy should not persist after successful healing of the ulcer and H pylori eradication.[35]

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Bleeding Gastric Ulcer Treatment

The surgical management of bleeding gastric ulcers is slightly different from that of duodenal ulcers, but the concepts are identical. The 3 most common complications of a gastric ulcer that mandate emergent surgical intervention are hemorrhage, perforation, and obstruction. The goals of surgery are to correct the underlying emergent problem, prevent recurrent bleeding or ulceration, and exclude malignancy.

A bleeding gastric ulcer is most commonly managed by a distal gastrectomy that includes the ulcer, with a gastroduodenostomy or a gastrojejunostomy reconstruction.

The common operations for the management of a bleeding gastric ulcer include (1) truncal vagotomy and pyloroplasty with a wedge resection of the ulcer, (2) antrectomy with wedge excision of the proximal ulcer, (3) distal gastrectomy to include the ulcer, with or without truncal vagotomy, and (4) wedge resection of the ulcer only.

Types of gastric ulcers

The choice of operation for a bleeding gastric ulcer depends on the location of the ulcer and the hemodynamic stability of the patient to withstand an operation. Five types of gastric ulcers occur, based on their location and acid-secretory status.

Type 1 gastric ulcers are located on the lesser curvature of the stomach, at or near the incisura angularis. These ulcers are not associated with a hypersecretory acid state.

Type 2 ulcers represent a combination of 2 ulcers that are associated with a hypersecretory acid state. The ulcer locations occur in the body of the stomach in the region of the incisura. The second ulcer occurs in the duodenum.

Type 3 ulcers are prepyloric ulcers. They are associated with high acid output and are usually within 3 cm of the pylorus.

Type 4 ulcers are located high on the lesser curvature of the stomach and (as with type 1 ulcers) are not associated with high acid output.

Type 5 ulcers are related to the ingestion of NSAIDs or aspirin. These ulcers can occur anywhere in the stomach.

Surgical management according to ulcer type

A vagotomy is added to manage type 2 or type 3 gastric ulcers.

Patients who are hemodynamically stable but have intermittent bleeding requiring blood transfusions should undergo a truncal vagotomy and distal gastric resection to include the ulcer for type 1, 2, and 3 ulcers.

In patients who present with life-threatening hemorrhage and a type 1, 2, or 3 ulcer, biopsy and oversew or excision of the ulcer in combination with a truncal vagotomy and a drainage procedure should be considered.

Patients with type 4 ulcers usually present with hemorrhage. The left gastric artery should be ligated, and a biopsy should be performed on the ulcer. Then, the ulcer should be oversewn through a high gastrotomy.

Rebleeding rates for the procedures that keep the ulcer in situ range from 20-40%.[16]

Gastric bleeding in the immediate postoperative period from recurrent PUD is initially best managed by endoscopic or angiographic means. If reoperation is required, gastric resection is usually indicated, because a repeat vagotomy is not reliable. A more definitive solution is warranted.

According to the 2008 SIGN guidelines, patients with confirmed gastric variceal hemorrhage require endoscopic therapy, preferably with cyanoacrylate injection.[35]

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Stress Gastritis Treatment

Knowledge of the predisposing conditions for stress ulceration allows the clinician to identify patients at risk for developing gastritis and GI bleeding. Treatment in this group of high-risk patients should focus on prevention. This is best accomplished by treating the underlying causes of ulceration.

Aggressive support of hemodynamic parameters ensures adequate mucosal blood flow. In addition, several strategies have evolved to treat gastric luminal acidity. Histamine receptor antagonists (HRAs) have proven to be effective at controlling stomach pH. Proton pump inhibitors (PPIs) are superior to the HRAs at suppressing acid; however, their role in stress ulceration prophylaxis is still being studied.[17]

Stress-related bleeding usually occurs 7-10 days after the initial insult but may manifest sooner. Initially, endoscopy is the most important diagnostic tool. The acute superficial erosions are multiple, begin in the fundus, and progress toward the antrum. Ninety percent of patients stop bleeding with conservative medical therapy that includes NGT lavage and gastric acid–controlling medications to maintain the gastric luminal pH above 5.0.[18]

Endoscopic hemostasis is attempted using electrocoagulation, laser, or injection therapy. Selective angiographic catheterization of the left gastric artery may be attempted with selective infusion of vasopressin (48-72 h) or embolization using Gelfoam, coils, or autologous clot to embolize the left gastric artery. Regardless of the angiographic technique used, it is often unsuccessful because of the rich and extensive submucosal plexus and collateral circulation within the stomach.

Surgical treatment

Surgical intervention becomes necessary if nonoperative therapy fails and blood loss continues. The goals of operative treatment are to control bleeding and to reduce recurrent bleeding and mortality. These patients are at extremely high risk, and the most expeditious procedure is the best option.

Simply oversewing an actively bleeding erosion is sometimes effective enough to control the bleeding. In the setting of life-threatening hemorrhage not amenable to endoscopic control, gastric resection with or without vagotomy with reconstruction may be necessary.

The type of gastric resection depends on the location of the gastric erosions, ie, whether they are proximal or distal. The options are antrectomy and subtotal, near total, or total gastrectomy. Operative mortality rates range from 4-17%.[65] The choice of the initial operation must be made with an understanding of the patient's condition, the amount and location of gastric disease, and an accurate assessment of one's technical ability to rapidly and safely perform a gastric resection. The trend has been to perform less surgery in general and to minimalize the type of surgical procedure performed.[66]

Managing the underlying insult causing the gastric stress ulcerations is also important. This involves supportive measures to maintain acceptable hemodynamic parameters, to provide adequate nutritional support in the critically ill patient, and to treat sepsis (if present).

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Mallory-Weiss Syndrome Treatment

Distinguishing Mallory-Weiss syndrome from Boerhaave syndrome is critical. Although both entities share a common pathogenesis, their management is completely different.

Boerhaave syndrome represents a full-thickness transmural laceration with perforation of the esophagus. A Gastrografin swallow helps to confirm the presence of the perforation in most cases, and prompt surgical intervention is necessary to prevent mediastinitis and sepsis.

On the other hand, surgical intervention in Mallory-Weiss syndrome is required to achieve hemostasis in only 10% of cases.[18] The bleeding from a Mallory-Weiss tear spontaneously ceases in 50-80% of patients by the time endoscopy is performed.[18]

For patients in whom bleeding is visualized at endoscopy, the endoscopic treatment options are electrocoagulation, heater-probe application, hemoclips, epinephrine injection, or sclerotherapy.

In a series published by Bataller et al, hemostasis was achieved in 100% of patients with Mallory-Weiss tears by using endoscopic sclerotherapy with epinephrine (1:10,000) and 1% polidocanol. Other nonoperative therapies are reserved for cases in which endoscopic attempts at creating hemostasis have failed.

Other available options are angiographic intra-arterial infusion of vasopressin and transcatheter embolization of branches of the left gastric artery using Gelfoam. Avoid the balloon tamponade technique using the Sengstaken-Blakemore tube in this particular circumstance, because this apparatus may extend the mucosal laceration into a transmural laceration with perforation.[18]

Surgical intervention is indicated in patients with continued bleeding after failed attempts at nonoperative therapies.

Bleeding from the gastroesophageal junction is visualized through an anterior gastrotomy. Once the tear is localized, the bleeding is controlled by oversewing the lesion.

The overall mortality rates for patients who require emergent surgery is 15-25%, in contrast to a mortality rate of 3% or less for patients whose bleeding stops by the time of the initial endoscopy.[18]

Go to Mallory-Weiss Tear for complete information on this topic.

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Dieulafoy Lesion Treatment

The initial endoscopic management of this lesion can be highly successful. In a report by Norton et al describing their experience with 90 Dieulafoy lesions, endoscopic management achieved primary hemostasis in 96% of cases.

Contact thermal ablation with a heater probe is the most effective technique, with or without the combined use of epinephrine to slow or stop the bleeding prior to applying the heater probe. No studies have been performed that compare surgical and endoscopic therapy for Dieulafoy lesions.

Although surgical intervention may be required after failed endoscopic therapy, endoscopy is still an important adjunct for management, because a nonbleeding Dieulafoy lesion may be undetectable through a gastrotomy.

Because of this potential problem, a combined endoscopic and surgical approach has been adopted. The vascular malformation can be marked with India ink through the endoscope.

Rebleeding after endoscopic therapy occurs in 11-15% of cases, with most cases of rebleeding controlled at repeat endoscopy.[21] (Repeat endoscopy in patients who have rebleeding has been validated in controlled studies of endoscopy and surgery.)

The 30-day mortality rate from the study by Norton et al was 42%, which is a reflection of the severe comorbid conditions associated with patients who have bleeding from a Dieulafoy lesion.

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Angiodysplasia Treatment

Bleeding from angiodysplasias can range from occult blood loss to life-threatening hemorrhage. Because the lesions are small and superficial, endoscopic therapy is highly successful. Endoscopic treatments and devices used for hemostasis include lasers, contact heat probes, electrocoagulation, and injection therapy.

The contact probe coagulators have been the most common form of endoscopic treatment because of their proven success and ability to target a bleeding lesion tangentially.

Recurrent bleeding can occur from the mucosal injury caused by the coagulation. To overcome the possibility of a delayed hemorrhage, endoscopic band ligation has been applied for hemostasis in nonvariceal GI bleeding, including angiodysplasias.[67]

When endoscopic techniques fail, surgical resection becomes necessary. When pangastric involvement is the source of bleeding, a total gastrectomy may be required; however, this is extremely rare. Available nonsurgical options include angiography with catheter-directed vasopressin. Combined hormonal therapy with estrogen and progesterone for patients in whom the diagnosis is unknown and vascular lesions are suggested has not been demonstrated to be effective.

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Aortoenteric Fistula

Patients with an aortoenteric fistula most often present with a self-limiting sentinel hemorrhage that is then followed by an exsanguinating, massive GI bleed. For the warning lesser sentinel bleed in a patient with a history of an abdominal aortic aneurysm repair or a known aortic aneurysm, the possibility of a graft-enteric fistula should be considered.

An upper endoscopy is the procedure of choice to help diagnose the fistula. It should be performed to the ligament of Treitz. Upper endoscopy findings also help to exclude other sources of UGIB.

Once the diagnosis of aortoenteric fistula is confirmed or seriously considered, emergency surgical intervention is required. In most instances, the aortic graft is removed after debridement and closure of the duodenum, followed by an extra-anatomic vascular bypass in order to bypass the ligated aorta and revascularize the lower extremities.

The perioperative mortality rate is 22-75%,[68] and major complications are common. Published opinions state that graft excision is not necessary as long as no gross contamination and purulence are present at the time of laparotomy.[69] Under these circumstances, antibiotics are administered long-term.

Another option emerging in the surgical literature is the use of endovascular stents to repair the fistula.[70, 71] Endovascular stent management is technically feasible and may be used as a bridge to more definitive treatment after hemodynamic stabilization in high-risk surgical patients.

Stent grafting controls hemorrhage immediately; however, because the device is placed in an infected field, adjunctive measures, such as long-term antibiotic use, percutaneous drainage, and bowel diversion, may be required.[72]

According to the 2010 ACR UGIB guidelines, variceal UGIB that does not respond to endoscopic management should be treated with a transjugular intrahepatic portosystemic stent shunt (TIPS).[37] The 2008 SIGN guidelines consider TIPS to be the treatment of choice for uncontrolled variceal bleeding.[35] Primary and secondary TIPS patency rates have greatly improved with the use of covered stents in lieu of the bare metal stents. Doppler ultrasonography of the liver is useful for TIPS monitoring, and both Doppler ultrasonography and CT may be useful for planning TIPS insertion.[37] Although endovascular stents have been shown to be effective in treating aortoenteric fistulas, case reports are emerging describing aortoenteric fistulas in patients with abdominal aortic aneurysm treated initially with stent grafts as well.[73]

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Treatment Complications

Complications of endoscopic therapy include aspiration pneumonia and perforation (1% for the first endoscopic therapy, 3% for the second). Bleeding can be caused by drilling into the vessel with the laser, by perforating the vessel with an injection, or by removing the clot with failure to coagulate the vessel.

Tseng et al investigated the cardiovascular effects of emergency endoscopy for UGIB in patients with stable coronary artery disease (CAD)[74] and found that the patients commonly experienced, primarily on a subclinical level, ventricular arrhythmias and myocardial ischemia. The authors' results were as follows:

  • Incidence of ventricular arrhythmias during endoscopy - 42% (patients with CAD) versus 16% (controls)
  • Frequency of ventricular arrhythmias during endoscopy - 1.19 events per minute (patients with CAD) versus 0.12 events per minute (controls)
  • Number of patients with ischemic ST changes - 9 patients with CAD versus 1 control

Complications from emergency abdominal surgery include ileus, sepsis, poor wound healing, and myocardial infarction.

Salvage surgery is associated with a high mortality rate, reflecting the comorbidities of patients who rebleed or continue to bleed.

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Posttreatment Monitoring and Care

The 2010 international consensus guidelines on UGIB state that selected low-risk patients may be discharged immediately following endoscopy, but high-risk patients should remain hospitalized for at least 72 hours.[52]

According to the 2008 SIGN guideline, patients with a post-endoscopic Rockall score of less than 3 have a low risk of rebleeding or death and are candidates for early discharge and outpatient follow up.[35]

The goal is to maintain the intragastric pH above 6 to maintain the clot. This is most easily achieved by intravenous proton pump inhibitor (PPI) therapy. After the acute phase, 72 hours, the coagulated vessel should be stable and the patient can be switched to oral therapy. If the patient rebleeds or has ongoing bleeding, repeat of endoscopic therapy would be considered. If this is not successful, interventional radiology is performed to clot the bleeding vessel. If this fails, surgery would be considered.

In the subsequent 48-72 hours after endoscopic therapy, the patient should receive acid-suppressive therapy to maintain a high gastric pH (above 6). A high gastric pH can be achieved by a continuous infusion of high-dose intravenous PPI therapy.

Patients who do not require endoscopic therapy and do not have other comorbidities should be considered for discharge.

Patients who did not require endoscopic treatment should receive routine, oral dosing of a PPI, ie, daily dosing prior to breakfast. Whether high-dose intravenous PPI therapy is advantageous in this setting remains controversial.

Oral PPI therapy can be used with any of the oral PPI preparations.

Patients should be tested for H pylori either by histology of gastric biopsy specimens taken on initial upper endoscopy or by serologic tests. If positive, H pylori therapy should be instituted after the patient has been discharged and is in stable condition. Moreover, H pylori eradication should be confirmed 4-6 weeks later in patients with UGIB. This can be done by checking the stool for the H pylori antigen.

Tachyphylaxis may develop within 24 hours if H2-receptor antagonists are administered.

Data on acid suppression via oral PPI therapy in order to produce a reduction in rebleeding are limited. High-dose intravenous PPI therapy appears to reduce rebleeding, but PPIs are not currently approved by the US Food and Drug Administration (FDA) for such treatment. The patient may be fed after recovery from local and intravenous anesthesia.

Some patients may require further endoscopic therapy. If repeat endoscopic therapy is needed, the stomach will empty liquids without residue within 3 hours. The 2008 SIGN guideline recommends repeat endoscopy and endotherapy within 24 hours when initial endoscopic treatment is deemed suboptimal or in patients in whom rebleeding will likely be life threatening.[35]

If the patient remains stable, the patient can then be started on therapy for ulcer healing.

The patient should continue oral therapy for ulcer disease noted on endoscopy or for ulcers caused by cautery techniques during endoscopic therapy. The greatest risk for perforation is usually within the first 48 hours after endoscopic therapy. Long-term acid suppression therapy should be offered with either full-dose H2-receptor antagonists or low-dose PPIs to prevent ulcer recurrence or its complications.[75]

Aspirin and NSAID therapies should be avoided in view of their adverse effect on platelet aggregation and ulcer healing. However, according to the 2010 international consensus guidelines, resumption of aspirin therapy in patients who require anticlotting prophylaxis should not be delayed as cardiovascular risks outweigh the risk of rebleeding.[52]

The 2008 SIGN guidelines state that patients with healed bleeding ulcers who are negative for H pylori require concomitant PPI therapy at the usual daily dose if NSAIDs, aspirin, or COX-2 inhibitors are indicated.[35]

If patients must remain on NSAIDs or low-dose aspirin, secondary prophylaxis against NSAID-induced ulcers should be given. According to the 2010 international consensus guidelines on UGIB, postdischarge use of aspirin or NSAIDs requires cotherapy with PPI.[52]

Only lansoprazole (15 mg or 30 mg daily),[76] esomeprazole (20-40 mg daily), and misoprostol (200 µg 4 times daily)[77] are approved by the FDA for prophylaxis against NSAID-induced ulcers.

The patient's hemoglobin value should be monitored to assess the efficacy of iron therapy as an outpatient; further improvement should be noted. Erythropoietin analogues have been shown to be effective in increasing the rate of hemoglobin production after ulcer hemorrhage.

Repeat endoscopy should be done in a few weeks in patients with gastric ulcers to document ulcer healing and to exclude cancer.[78]

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Deterrence and Prevention of UGIB

Antibiotic therapy should be given if H pylori is present in the setting of any history of ulcer disease. Eradication of H pylori has been demonstrated to reduce the risk of recurrent ulcers and, therefore, recurrent ulcer hemorrhages.

NSAIDs should be avoided. If not possible, they should be used at the lowest dose and duration.

PPI or misoprostol cotherapy should be used along with NSAIDs.

The use of cyclooxygenase-2 inhibitors has been shown to reduce the risk of ulcer hemorrhage, although only when not combined with aspirin therapy. Concerns have been raised about an increase in myocardial infarction and stroke in patients taking selective cyclooxygenase-2 inhibitors.

As demonstrated in the study by al-Assi et al, the combination of H pylori infection and NSAID use may increase the risk of ulcer hemorrhage; however, the treatment of H pylori in patients who are taking NSAIDs remains controversial.[1]

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Contributor Information and Disclosures
Author

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF Associate Professor of Clinical Medicine, Albert Einstein College of Medicine of Yeshiva University; Associate Professor of Clinical Medicine, Hofstra Medical School

Maurice A Cerulli, MD, FACP, FACG, FASGE, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, New York Society for Gastrointestinal Endoscopy, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Coauthor(s)

Shahzad Iqbal, MD Advanced Endoscopy Fellow, Department of Gastroenterology, Columbia University Medical Center

Shahzad Iqbal, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Acknowledgements

James de Caestecker, DO Instructor, Department of Surgery, MCP Hahnemann University

James de Caestecker, DO is a member of the following medical societies: American College of Surgeons

Disclosure: Nothing to disclose.

Michael A Grosso, MD Consulting Staff, Department of Cardiothoracic Surgery, St Francis Hospital

Michael A Grosso, MD is a member of the following medical societies: American College of Surgeons, Society of Thoracic Surgeons, and Society of University Surgeons

Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, FACG, AGAF Chief of Hepatology, Hunter Holmes McGuire Department of Veterans Affairs Medical Center; Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine

Douglas M Heuman, MD, FACP, FACG, AGAF is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association

Disclosure: Novartis Grant/research funds Other; Bayer Grant/research funds Other; Otsuka Grant/research funds None; Bristol Myers Squibb Grant/research funds Other; Scynexis None None; Salix Grant/research funds Other; MannKind Other

Alex Jacocks, MD Program Director, Professor, Department of Surgery, University of Oklahoma School of Medicine

Disclosure: Nothing to disclose.

Jason Straus, MD Staff Physician, Department of Surgery, Wright State University School of Medicine

Jason Straus, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, and Society of American Gastrointestinal and Endoscopic Surgeons

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Ulcer with active bleeding.
Ulcer with a clean base.
Diagram of an ulcer with a clean base.
Ulcer with an overlying clot.
Ulcer with a visible vessel.
Diagram of an ulcer with a visible vessel.
Table 1. Probable Source of GI Bleeding Within the Gut
Clinical Indicator Probability of Upper GI Source Probability of Lower GI Source
Hematemesis Almost certain Rare
Melena Probable Possible
Hematochezia Possible Probable
Blood-streaked stool Rare Almost certain
Occult blood in stool Possible Possible
Table 2. Estimated Fluid and Blood Losses in Shock
  Class 1 Class 2 Class 3 Class 4
Blood Loss, mL Up to 750 750-1500 1500-2000 >2000
Blood Loss,% blood volume Up to 15% 15-30% 30-40% >40%
Pulse Rate, bpm < 100 >100 >120 >140
Blood Pressure Normal Normal Decreased Decreased
Respiratory Rate Normal or Increased Decreased Decreased Decreased
Urine Output, mL/h >35 30-40 20-30 14-20
CNS/Mental Status Slightly



anxious



Mildly



anxious



Anxious,



confused



Confused,



lethargic



Fluid Replacement, 3-for-1 rule Crystalloid Crystalloid Crystalloid and blood Crystalloid and blood
Table 3. Effect of Number of Packed Erythrocyte Transfusions on Need for Surgery and Mortality from UGIB
Number of Units Transfused Need for Surgery, % Mortality Rate, %
0 4 4
1-3 6 14
4-5 17 28
>5 57 43
Table 4. Effect of the Color of the Nasogastric Aspirate and of the Stool on UGIB Mortality Rate
Nasogastric Aspirate Color Stool Color Mortality Rate, %
Clear Brown or red 6
Coffee-ground Brown or black 8.2
  Red 19.1
Red blood Black 12.3
  Brown 19.4
  Red 28.7
Table 5. Ulcer Characteristics and Correlations
Ulcer Characteristics Prevalence Rate, % Rebleeding Rate, % Surgery Rate, % Mortality Rate, %
Clean base 42 5 0.5 2
Flat spot 20 10 6 3
Adherent clot 17 22 10 7
Visible vessel 17 43 34 11
Active bleeding 18 55 35 11
Table 6. Recurrent Ulcer and Postgastrectomy Syndromes After Operations for Duodenal Ulcer
Original Operation Recurrence Rate, % Postgastrectomy Syndrome Rate, % Mortality Rate, %
Proximal gastric vagotomy 10 5 0.1
Truncal vagotomy and drainage 7 20-30 < 1
Truncal vagotomy and antrectomy



Billroth I or Billroth II



1 30-50 0-5
Truncal vagotomy and antrectomy



Roux-en-Y



5-10 50-60 0-5
Table 7. Effects of Operations for PUD on Gastric Emptying and Motility
Operation Antral Innervation Liquid Emptying Solid Emptying
Proximal gastric vagotomy Preserved Fast Normal
Truncal vagotomy Divided Fast Slow
Truncal vagotomy and drainage Divided Fast Fast
Truncal vagotomy and antrectomy Divided Fast Fast
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