|Year : 2015 | Volume
| Issue : 2 | Page : 69-79
Management of Upper Gastrointestinal Bleed
V Jain, PN Agarwal, R Singh, A Mishra, A Chugh, M Meena
Department of Surgery, Maulana Azad Medical College and Lok Nayak Hospital, New Delhi, India
|Date of Web Publication||1-Jun-2015|
Dr. V Jain
72, Anupam Apartments, B 13 Vausundhara Enclave, New Delhi - 110 096
Source of Support: None, Conflict of Interest: None
Upper gastrointestinal bleed (UGIB) causes significant morbidity and mortality the world over. The two main causes have been due to increasing nonsteroidal anti-inflammatory drug use along with the high prevalence of Helicobacter pylori infection in patients with peptic ulcer and bleeding from gastroesophageal varices due to portal hypertension. Other causes of esophageal tears, gastrointestinal malignancy, and arteriovenous malformations also contribute to the morbidity and motality. Rapid assessment, resuscitation, and early endoscopy form the basis of early management of patients with severe bleeding. Risk stratification is based on clinical assessment and endoscopic findings. Early Upper gastrointestinal endoscopy (UGIE) (within 24 h of presentation) confirms the diagnosis and allows for targeted endoscopic treatment, which results in reduced morbidity, hospital stay, the risk of recurrent bleeding, and need for surgery. Despite successful endoscopic therapy, re-bleeding remains a risk and a second attempt at endoscopic therapy is recommended in most. Arteriography with embolization can serve as an extremely useful therapeutic option. Thanks to excellent medical and endoscopic control, surgery for UGIB is rarely required nowadays.
Keywords: Endoscopy, ulcer bleeding, upper gastrointestinal hemorrhage, variceal bleed
|How to cite this article:|
Jain V, Agarwal P N, Singh R, Mishra A, Chugh A, Meena M. Management of Upper Gastrointestinal Bleed. MAMC J Med Sci 2015;1:69-79
|How to cite this URL:|
Jain V, Agarwal P N, Singh R, Mishra A, Chugh A, Meena M. Management of Upper Gastrointestinal Bleed. MAMC J Med Sci [serial online] 2015 [cited 2020 Apr 6];1:69-79. Available from: http://www.mamcjms.in/text.asp?2015/1/2/69/157913
| Introduction|| |
Acute gastrointestinal (GI) bleeding is a potentially life-threatening emergency that remains a common cause of hospitalization the world over. With early recognition and appropriate management protocols, morbidity and mortality can be significantly reduced.
The incidence of upper gastrointestinal bleed (UGIB) is approximately 100 cases/100,000 population per year.  The incidence of UGIB is two-fold greater in males than in females, in all age groups; however, the death rate is similar in both sexes. 
Bleeding from the upper gastrointestinal tract (GIT) is approximately 4 times as common as bleeding from the lower GIT and is a major cause of morbidity and mortality. Mortality rates from UGIB are 6-10% overall. 
The population with UGIB due to peptic ulcer has become progressively older, with a concurrent increase in significant comorbidities that increase mortality. This has chiefly been due to increased overall life expectancy along with the availability of effective "over the counter" medication allowing symptomatic relief of ulcer pain, but inadequate healing. Mortality increases with older age (>60 years) in males and females.  In patients with UGIB, age-related co-morbid illness often complicates the UGIB process and is the major cause of death rather than the bleed itself. In UGIB due to varices, the underlying liver disease with resultant portal hypertension also contributes to morbidity and mortality.
| Relevant Anatomy|| |
On embryologic grounds, the foregut extends from the pharynx till the major papilla in the duodenum. From the point of view of GI bleeding, however, the demarcation between the upper and lower GIT is the duodenojejunal junction or the attachment of the ligament of Treitz. Bleeding proximal to the ligament of Treitz is called UGIB.
| Etiology|| |
Obscure gastrointestinal bleeding (OGIB) is defined as occult or overt bleeding of unknown origin that persists or recurs after an initial negative endoscopic evaluation including colonoscopy and esophago-gastro-duodenoscopy (EGD). Overt OGIB is defined as visible GI bleeding (i.e., melena or hematochezia) and can be categorized further as active (evidence of ongoing bleeding) versus inactive bleeding. OGIB is designated as occult when there is no evidence of gross bleeding (unexplained iron deficiency anemia suspected to be caused by GI blood loss). OGIB may occur anywhere throughout the GIT. Prior to the evaluation of the small bowel, upper, and lower GIT endoscopies are often repeated in patients with OGIB because substantial initial endoscopic miss rates have been reported. Newer endoscopic evaluation techniques for the small bowel include video capsule endoscopy and deep enteroscopy. EGD is indicated for the initial evaluation of a suspected upper GI source of bleeding. Early endoscopic intervention has been associated with lower hospital cost; however, optimal timing after an episode of bleeding and the impact of early endoscopy on diagnostic yield have not been rigorously studied.  Repeat examination may yield a source even when the initial EGD is negative. Examples of missed lesions in the upper GIT include Cameron's erosions, peptic ulcerations, angiectasis, Dieulafoy's lesions, hemosuccus pancreaticus, and gastric antral vascular ectasias (GAVEs). Factors associated with an increased yield of repeat EGD include large hiatal hernias, hematemesis, and a history of nonsteroidal anti-inflammatory drug (NSAID) use [Table 1] and [Table 2].
There have been a number of definitions for the severity of hemorrhage in terms of volume. Various definitions for massive GI hemorrhage have ranged from relatively objective ones such as, one causing a loss of total circulating red cell mass to <60% of normal to more subjective ones like hemorrhage endangering life. Another way to define the severity of hemorrhage is in terms of volume of required blood transfusion:
- Massive hemorrhage requires transfusion of 5 or more units of packed red blood cells (RBCs)
- Moderately severe requires transfusion of <5 units
- Minor hemorrhage does not require any packed RBC transfusion.
Of major concern is the management of patients presenting with a moderately severe massive upper GI hemorrhage, and in this article we will outline a management strategy for the same.
| Management Approach|| |
The goal of therapy in massive UGIB is to correct shock and coagulation abnormalities and to stabilize the patient so that further evaluation and treatment can proceed. In slower and more chronic bleeds, patient has a less dramatic presentation, and allows sufficient time and opportunity for a more systematic initial work up [Figure 1].
Resuscitation of a hemodynamically unstable patient begins with assessing and addressing the ABCs (i.e., airway, breathing, circulation) of initial management.
Threshold for elective intubation must be low. Initial intravenous access must be obtained using at least two 16-gauge (minimum), upper extremity, peripheral intravenous lines which are adequate for volume resuscitative efforts. A rough guideline for the total amount of crystalloid fluid volume needed to correct the hypovolemia is the 3-for-1 rule (3 ml of crystalloid for every 1 ml intravascular volume to be replaced).
Once the ABCs have been addressed, assess the patient's response to resuscitation, based on evidence of end-organ perfusion and oxygen delivery by monitoring pulse rate, blood pressure (BP) along with oxygen saturation. Foley catheter placement is mandatory for measurement of the urinary output as a guide to renal perfusion.
Once resuscitation is underway, insert a nasogastric tube and perform an aspirate and lavage procedure. 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.  The contents of the naso-gastric aspirate serve as a guide to the presence or absence of an UGIB but must be interpreted with caution, as the absence of blood or the presence of bile does not necessarily rule out bleeding and may simply imply a bleed at a location more distal to the ligament of Treitz, and therefore, warrants a more detailed investigation.
The presentation of bleeding depends on the amount and location of hemorrhage. Patients with upper GI hemorrhage often present with hematemesis, melena or hematochezia.
- Vomiting of blood is common when bleeding originates from stomach or esophagus
- Coffee-ground when gastric acid converts heme to brown colored acid hematin.
- Passage of black tarry stools are common when there is bleeding from any part of upper GIT
- The black color of melenic stool is caused by iron sulfide, formed by the action of by-products from colonic bacteria on heme iron.
- It is defined as passage of bright-red blood from the rectum
- Common in bleeding from colon, rectum, and anus
- In case of brisk bleeding in the upper GIT, Bright-red blood may come out unchanged in the stool.
- Patients may also present with symptoms of iron deficiency anemia or hypovolemic shock including chest pain, syncope, fatigue, and shortness of breath.
Patients may have a history of dyspepsia, ulcer disease, early satiety, and NSAID or aspirin use. A history of chronic alcohol use of more than 50 g/day or chronic hepatitis (B or C) may suggest the presence of chronic liver disease with portal hypertension, thereby increasing the risk of variceal hemorrhage, GAVE or portal gastropathy.
The finding of subcutaneous emphysema in the neck, with a history of vomiting is suggestive of Boerhaave syndrome (esophageal perforation) and requires prompt consideration of surgical therapy.
Few of the most common clinical presentations in patients with an UGIB are: 
- Hematemesis - 40-50%
- Melena - 70-80%
- Hematochezia - 15-20%
- Either hematochezia or melena - 90-98%
| Physical Examination|| |
The primary and urgent goal of general physical examination in a patient with a massive UGIB is to evaluate for shock and blood loss.
Assessment of Hemorrhagic Shock
Patients who present in hemorrhagic shock have a mortality rate of up to 30%.  Worrisome clinical signs and symptoms of hemodynamic compromise include tachycardia >100 beats/min, systolic BP <90 mmHg, cool extremities, syncope, and other obvious signs of shock, such as ongoing brisk hematemesis or the occurrence of maroon or bright-red stools, which requires rapid blood transfusion.
Postural changes in pulse rate and BP indicate an acute blood loss of approximately 20% or more. Unless the patient has evidence of shock, orthostatic testing should be performed to assess and document a hypovolemic state. The mortality rate when orthostatic changes are present is 13.6%, compared to 8.7% when they are absent. 
Abdominal examination is necessary for detecting obvious signs of liver failure or portal hypertension such as caput medusa, ascites, splenomegaly, jaundice, spider angioma, and hepatic encephalopathy. A nodular liver, an abdominal mass, and enlarged and firm lymph nodes indicate a malignancy and have a poor prognosis.
Despite the availability of a wide array of available investigations, all investigations are not required in most patients. Resuscitation of the patient takes precedence over any diagnostic investigation. By and large, investigations must be conducted once the patient is hemodynamically stable or once resuscitation measures are underway in the hemodynamically unstable patients.
Hemoglobin Level and Type and Crossmatch Blood
The patient should be crossmatched for 2-6 units, based on the rate of active bleeding. The hemoglobin level should be monitored serially in order to follow the trend.
The patient's prothrombin time, activated partial thromboplastin time, and international normalized ratio should be checked to document the presence of a coagulopathy. The coagulopathy may be consumptive and associated with thrombocytopenia or may even be an indicator of deranged synthetic function of the liver in the setting of cirrhotic portal hypertension.
A platelet count of <50,000/cumm with active hemorrhage requires a platelet transfusion and fresh frozen plasma in an attempt to replete lost clotting factors.
This procedure may confirm recent bleeding (coffee ground appearance), possible active bleeding (red blood in the aspirate that does not clear) or a lack of blood in the stomach (active bleeding less likely but does not exclude an upper GI lesion).
It is the first choice in a case of upper GI bleed, and is discussed in detail later.
A gastrin level in a detailed work-up can be used to establish the etiology in patients with gastrinoma as the cause of multiple ulcers and UGIB.
Chest radiographs should be ordered to exclude esophageal perforation where history might be suggestive. It may also show signs of aspiration pneumonia, effusion resulting as a consequence of aspiration of gastric contents and esophageal perforation respectively. It would be significant for anesthetic fitness in case the patient requires operative intervention.
Computed tomography scanning
Limited role in active UGIB in emergency setting. The 2010 American College of Radiology (ACR) criteria state that computed tomography (CT) is particularly useful for localizing obscure UGIB and for evaluating a patient with UGIB and a history of aortic reconstruction or pancreaticobiliary procedure. 
Nuclear medicine scanning
The 2010 ACR criteria state that Tc-99 m-labeled erythrocyte scans are of limited value in the routine evaluation of UGIB, but continue to be useful in certain cases of obscure UGIB.  It can detect bleeding at rates as low as 0.1-0.5 mL/min.
May be useful as a diagnostic cum therapeutic procedure if bleeding persists and endoscopy fails to identify a bleeding site. According to the 2010 ACR guidelines, angiography along with transcatheter arterial embolization should be considered for all patients with a known source of arterial UGIB that does not respond to endoscopic management or to diagnose and treat a patient with active bleeding and a negative endoscopy.  To be detectable angiography requires active bleeding (1 mL/min).
When medical and endoscopic treatments fail, angiographic embolization serves as an invaluable therapeutic modality. It can also be used in recurrent bleeding after surgery. There are no absolute contraindications because angiography and embolization may be needed as lifesaving procedures.
Improvements in catheter-based therapy, interventional devices, embolic materials, and wider availability of skilled interventional radiologists have increased the utility of embolization procedures in the management of nonvariceal UGI bleeding.
Capsule endoscopy is a method for mainly evaluating the small bowel. Its role is for diagnosis of obscure overt or occult GI bleeding, wherein patient presents with signs or symptoms suggesting an ongoing bleed but no source is identified after upper GI endoscopy.
| Diagnostic Protocol Summary|| |
| Specific Therapy|| |
Proton pump inhibitors
The relative efficacy of the proton pump inhibitors (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. 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 supported in the 2008 Scottish Intercollegiate Guidelines Network (SIGN) guidelines, which recommend high-dose intravenous PPIs in patients with major peptic ulcer bleeding or non-bleeding visible vessels after endoscopic bleeding control. 
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.
The 2010 international consensus guidelines on UGIB recommend 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. 
Endoscopy has provided clinicians with the ability for simultaneous diagnostic and therapeutic approaches to bleeding from the GIT. Endoscopic examination of the upper GIT provides useful information regarding the source and site of bleeding.
The 2008 SIGN guidelines on the management of acute upper and lower GI bleeding recommends that an initial (pre-endoscopic) Rockall score be calculated for all patients presenting with acute UGIB. In patients with an initial Rockall score >0, endoscopy is recommended for a full assessment of bleeding risk  [Table 3].
Apart from the Rockall score there are other scoring systems that determine the need for hospital admission and intervention. One popular scoring system is the Glasgow-Blatchford scoring system (GBS) which utilizes parameters such as blood urea, hemoglobin, systolic BP, pulse rate, symptomatology, and co-morbid illness. Advantages of the GBS over the Rockall score, which assesses the risk of mortality in patients with UGIB, include a lack of subjective variables such as the severity of systemic diseases and the lack of a need for EGD to complete the score, a feature unique to the GBS.
Endoscopy is able to diagnose the cause and identify the source of bleeding in the majority of the cases. In a survey by Silverstein et al. findings on endoscopy in terms of etiology of UGI bleed are summarized below: 
The 2010 ACR appropriateness criteria for UGIB recommend upper endoscopy as the initial diagnostic examination for all patients presumed to have UGIB. 
| Nonvariceal Bleeding|| |
Since the late 1980s, endoscopic techniques to achieve hemostasis for bleeding ulcers have continued to evolve. Several randomized clinical trials and meta-analyses have demonstrated and supported the idea that early endoscopic hemostatic therapy significantly reduces rates of recurrent bleeding, the need for emergency surgery, and mortality in patients with acute nonvariceal UGIB. Endoscopy is the method of choice for controlling active ulcer hemorrhage.
According to the 2010 international consensus on nonvariceal UGIB, early endoscopy (within 24 h of presentation) is appropriate for most patients with UGIB.  In a retrospective review involving more than 30,000 cases, Yavorski et al. showed that the mortality rates were more than twice as high for 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).
The following endoscopic techniques are available for achieving hemostasis: 
- Injection of epinephrine or sclerosants
- Bipolar electrocoagulation
- Heater probe coagulation
- Application of hemoclips or endoclips
- Argon plasma coagulator
- Laser photocoagulation
- Application of hemostatic materials including biologic glue.
Treatment using a combination of the above has become more common. The 2010 international consensus guidelines on UGIB recommend the use of endoscopic clips or thermal therapy for high-risk lesions. 
Nowadays there is an ongoing debate regarding the use of octreotide as a splanchnic vasoconstrictor in nonvariceal hemorrhage as well. It seems reasonable to believe that in patients who are unwell and not responding adequately to other measures may sometimes benefit by the use of octreotide.
A minority of patients experience recurrent bleeding after endoscopic therapy, and these cases are usually associated with risk factors for rebleeding. These factors include age older than 60 years, the presence of shock upon admission, coagulopathy, active pulsatile bleeding, and the presence of cardiovascular disease (the appearance of the ulcer at the time of endoscopy provides important information regarding the risk of rebleeding). These circumstances are associated with a poorer prognosis and a higher mortality rate. 
Forrest et al. were the first to classify the stigmata of hemorrhage from peptic ulcers. Based on these classifications, the risk of recurrent bleeding can be predicted [Table 4].
By and large rebleeding occurs in 10-30% of endoscopically treated patients. A second attempt at endoscopic control is warranted. This approach has been validated in a large, randomized, controlled trial that showed decreased morbidity and mortality rates. Using a combination of techniques is prudent when re-treating the ulcer site because the first therapy may have produced partial necrosis and weakening of the stomach wall.
Bleeding peptic ulcer: Surgical management
Regardless of the endoscopic therapy, 10-12% of patients with acute ulcer 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%.
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 (two attempts) with persistent or 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 after previous intervention
- The three most common operations performed for a bleeding duodenal ulcer are as follows 
- Truncal vagotomy and pyloroplasty with suture ligation of the bleeding ulcer
- Truncal vagotomy and antrectomy with resection or suture ligation of the bleeding ulcer
- Highly selective vagotomy with duodenotomy and suture ligation of the bleeding ulcer
- 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 2008 SIGN guideline recommends testing for Helicobacter pylori in patients with peptic ulcer bleeding and a 2-week course of therapy prescribed for those who test positive. 
Bleeding gastric ulcer: Surgical management
The surgical management of bleeding gastric ulcers is slightly different from that of duodenal ulcers, but the concepts are identical. The goals of surgery are to correct the underlying emergent problem, prevent recurrent bleeding or ulceration, and exclude malignancy by excising the ulcer containing segment and subjecting it to a histopathological examination.
The common operations for the management of a bleeding gastric ulcer include:
- Truncal vagotomy and pyloroplasty with a wedge resection of the ulcer
- Antrectomy with wedge excision of the proximal ulcer
- Distal gastrectomy to include the ulcer, with or without truncal vagotomy, and
- Wedge resection of the ulcer only.
| Variceal Bleeding|| |
After initial resuscitation as described earlier, octreotide, a somatostatin analogue, is administered as soon as variceal hemorrhage is identified. It is given as an initial 50 µg bolus followed by a continuous infusion of 25-50 µg/h. It acts as a direct splanchnic vasoconstrictor. Once initiated, octreotide should be maintained for 2-5 days. Vasopressin, a posterior pituitary hormone is a potent vasoconstrictor that will also reduce portal pressure. It also increases systemic vasoconstriction and has been associated with myocardial infarction and small bowel necrosis. Terlipressin is a long-acting safer analogue of vasopressin that can reduce mortality from variceal hemorrhage.  Terlipressin has been shown to be safer than vasopressin and is also known to stimulate kidney function and to prolong survival time in patients with bleeding esophageal varices. Terlipressin is administered as an IV bolus 6-hourly. For acute variceal bleeding, the dose is 2 mg 6 hourly for the first 24 h, reducing to 1 mg 6 hourly for the second 24 h if bleeding has stabilized. If bleeding has ceased after 48 h then terlipressin can be stopped.
Balloon tamponade with a Linton-Nachlas or Sengstaken-Blakemore or Minnesota tube can be a bridge to endoscopic therapy or as a temporizing measure in bleed that cannot be controlled after an initial endoscopic attempt in massive variceal hemorrhage. Care should be taken to prevent insufflation of the gastric balloon within the esophagus [Figure 2].
Urgent endoscopy should typically be completed within 12 h of onset of bleeding. Endoscopic therapies for varices aim to reduce variceal wall tension by obliteration of the varix. The two principal methods available for esophageal varices are endoscopic sclerotherapy (EST) and band ligation.
Endoscopic sclerotherapy consists of the injection of a sclerosing agent into the variceal lumen or adjacent to the varix, inducing thrombosis of the vessel and inflammation of the surrounding tissues.
The main objective was to target the lower esophagus near the gastroesophageal (GE) junction. In the acute setting, the paravariceal injection cannot be easily accomplished because of the ongoing bleeding and it is mostly reserved for elective sclerotherapy. Intra-variceal injection is practiced in such situations.
The advantages of EST are that it is cheap and easy to use and it can be quickly assembled. In addition, there is a rapid thrombosis and arrest of bleeding.
However, several local and systemic complications may arise after EST. The reported frequency of complications of sclerotherapy varies greatly between series and is critically related to the experience of operators and the frequency and completeness of follow-up examinations. Minor complications occurring within the first 24-48 h and not requiring treatment such as low-grade fever, retrosternal chest pain, temporary dysphagia, asymptomatic pleural effusions, and other nonspecific transient chest radiographic changes are very common. 
Endoscopic variceal ligation (EVL) consists of the placement of rubber rings on variceal columns, which are sucked into a plastic hollow cylinder attached to the tip of the endoscope. EVL obliterates varices by causing mechanical strangulation with rubber bands. Owing to its action on the suctioned, entrapped varices, the main reaction is usually limited over the superficial esophageal mucosa. The ligation induced-ulcers are shallower have a greater surface area and heal more rapidly than those caused by EST. 
Villanueva et al. found that the use of variceal ligation instead of sclerotherapy had a lower failure rate (4% vs. 15%; P = 0.02), and a lower transfusion requirement (P = 0.05). No statistically significant difference was found in mortality. Adverse effects (e.g., aspiration pneumonia, esophageal bleeding, ulceration, and chest pain) occurred in 28% of patients receiving sclerotherapy and 14% with ligation (risk ratios, 1.9; 95% confidence interval: 1.1-3.5; P = 0.03).  In another similar but smaller study, Sarin et al. found that the rate of rebleeding was lower in the EVL group (n = 47) than in the sclerotherapy group (n = 48) (6.4% vs. 20.8%; P < 0.05).  EVL is the recommended form of therapy for acute esophageal variceal bleeding, although sclerotherapy may be used in the acute setting if ligation is technically difficult. Endoscopic treatments are best used in combination with pharmacologic therapy, which preferably should be started before endoscopy. The American Association for Study of Liver Diseases Practice Guidelines Committee and the Practice Parameters Committee of American College of Gastroenterology on the Prevention and management of GE varices and variceal hemorrhage in cirrhosis recommend that for the control and management of acute hemorrhage, the combination of vasoconstrictive pharmacologic therapy and variceal ligation is the preferred approach. 
Other options for endoscopic hemostasis in variceal bleeding
Argon plasma coagulation and hemoclip application have been used successfully in the combination of band ligation and sclerotherapy. Tissue adhesives n-butyl-2-cyanoacrylate (histoacryl) and isobutyl-2-cyanoacrylate (bucrylate) have been used to treat esophageal and gastric varices. When injected into esophageal or gastric varices, almost immediate obliteration of the vessel was achieved in (84-100%) of esophageal varices and in (58-100%) of gastric varices. , Rate of rebleeding was found to be 28% in esophageal varices and 0-40% in gastric varices. ,
Uncontrolled bleeding, defined as continued bleeding at 24 h, is uncommon when band ligation and octreotide are used. If bleeding continues, repeat banding or placement of a transjugular intrahepatic portosystemic shunt (TIPSS or TIPS) or surgical shunting should be considered.
Wherever endoscopy is available, surgery has no role in primary prophylaxis. Its role in acute variceal bleeding is exceedingly limited, because therapy with endoscopic treatment controls bleeding in 90% of patients. A TIPSS is a viable option and is less invasive for patients whose bleeding is not controlled. However, if TIPS is not available, then surgery is required.
Surgical interventions include the following:
- Decompressive shunts (including TIPS)
- Devascularization procedures.
Transjugular intrahepatic portosystemic shunt (TIPS)
TIPS is the percutaneous formation of a tract between the hepatic vein and the intrahepatic segment of the portal vein in order to reduce the portal venous pressure.
According to the 2010 ACR UGIB guidelines, variceal UGIB (caused due to sinusoidal or postsinusoidal causes of portal hypertension) that does not respond to endoscopic management should be treated with a TIPS. 
In the emergency setting, a portocaval shunt is used because it rapidly and effectively decompresses the portal venous circulation. However, the decision on whether or not to perform a shunt procedure, and which shunt procedure would be best suited should be based on the cause or pathology of portal hypertension and also the status of the liver function in relation to the implication of diverting hepatic portal blood flow. In conditions, where bleeding has temporarily been controlled by pharmacotherapy or balloon tamponade and where liver function is already compromised a more complex and selective distal splenorenal shunt may be more appropriate.
Surgical shunts provide better control of rebleeding when compared to the combination therapy of beta-blocker and EVL. However, these shunts are associated with higher incidence of hepatic encephalopathy and should be reserved for failure of TIPSS placement, hemorrhage from gastric varices or portal hypertensive gastropathy, Child-Pugh class A patients with recurrent bleeding despite adequate combination therapy.
Devascularization is rarely performed but may have a role in patients with portal and splenic vein thrombosis who are not suitable candidates for shunt procedures and who continue to have variceal bleeding despite the endoscopic and pharmacologic treatment.
Devascularization procedures target the lover portion of the esophagus, upper two-third of the stomach or the splenic circulation. The incidence of hepatic encephalopathy is less since the portal blood flow is maintained, however, these procedures are only rarely performed in selected patients as a salvage procedure.
Various procedures include the historical Sugiura procedure, stapler transection of lower esophagus, and in some cases, even a splenectomy. The Sugiura procedure (esophagogastric devascularization with splenectomy and preservation of the coronary and para-esophageal veins) had a rebleeding rate of <10% in a Japanese series. , The Sugiura procedure is especially useful for patients who are unable to undergo shunting because of extensive portal, splenic, and superior mesenteric vein thrombosis. It was originally developed as a two-step operation, but has been modified numerous times by many surgeons since its original creation. Modifications of this procedure have not been as successful in North America, likely due to a difference in the proportion of patients with alcoholic cirrhosis.  One common modification uses a single abdominal operation to achieve GE devascularization. A splenectomy is initially performed and is followed by devascularization of the distal esophagus through the diaphragm hiatus and the superior two-thirds of the major and lesser gastric curve taking careful consideration to not ligate the left gastric vein. To ensure complete separation of the azygous vein system from the intramucosal venous plexus, an end-to-end anastomosing stapling device transects and anastamoses a region of the esophagus 4-6 cm above the GE junction. This anastomosis can then be reinforced with vicryl suture. A pyloroplasty is routinely followed to facilitate gastric emptying, since the associated vagotomy causes pylorospasm. Early experience with the Sugiura procedure demonstrated an operative mortality of 32% and overall morbidity occurred in 33% of the patients.  Significant causes of morbidity and mortality were related to complications of the esophageal transection as anastomotic leakage occurred in 8.6% of patients undergoing emergent surgery versus 4.8% in elective cases. All patients who developed an esophageal leak died.  For this reason, modification of the original procedure was introduced to avoid the risk of perioperative mortality due to esophageal transection.
Secondary prophylaxis following variceal hemorrhage
Secondary prophylaxis is used to prevent rebleeding. Variceal hemorrhage has a 2 year recurrence rate of approximately 80%. Overall mortality from rebleeding is 30% and is more frequent with large varices, initial severe hemorrhage, and decompensated liver disease. 
Propranolol and nadolol significantly reduce the risk of rebleeding and are associated with prolongation of survival.
Usually performed at weekly intervals. Approximately 4-5 sessions are required for the eradication of varices, which is achieved in nearly 70% of patients.
Endoscopic variceal ligation
Endoscopic variceal ligation is considered the endoscopic treatment of choice in the prevention of rebleeding. Sessions are repeated at 7- to 14-day intervals until variceal obliteration (which usually requires 2-4 sessions). This procedure is associated with lower rebleeding rates and a lower frequency of esophageal strictures.
| Other Causes|| |
Stress induced and erosive gastritis
Stress ulceration is a phenomenon commonly seen in chronically ill and patients admitted to intensive care units. Its pathogenesis revolves around the altered gastric mucosal blood flow and protection imparted by it. These have occasionally been seen in patients with severe burns and with head injury and have been named as Curling and Cushing ulcers, respectively. Other important causes of gastritis include the widespread use of NSAIDs and consumption of alcohol and cigarette smoking.
Removal of the inciting agents and correction of deranged physiology remains central to the management of stress 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 have proven to be the most effective in controlling stomach pH.  Endoscopic hemostasis may be attempted using electrocoagulation, laser, or injection therapy. Selective angiographic catheterization with vasopressin infusion or embolization may also be tried. Surgical intervention becomes necessary if nonoperative therapy fails and blood loss continues.
Mallory-Weiss and Boerhaave syndrome
Distinguishing Mallory-Weiss syndrome More Details 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 since it is a mucosal tear only. The bleeding from a Mallory-Weiss tear More Details spontaneously ceases in 50-80% of patients by the time endoscopy is performed. 
These are vascular malformation of the proximal stomach, usually within 6 cm of the GE junction along the lesser curvature of the stomach. However, it can occur anywhere along the GIT. This lesion accounts for 2-5% of acute UGIB episodes. 
Endoscopically, the lesion appears as a large submucosal vessel that has become ulcerated. Because of the large size of the vessel, bleeding can be massive and brisk. The vessel rupture usually occurs in the setting of chronic gastritis, which may induce necrosis of the vessel wall. Alcohol consumption is reportedly associated with the Dieulafoy lesion.
Initial endoscopic therapy remains the mainstay of management. 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. In cases of failed endoscopic therapy, angiography, and embolization may be tried. Occasionally surgical intervention in the form of gastrotomy with wide wedge resection or even gastrectomy may be required, which may be completed through conventional open approach or via minimally invasive techniques.
In patients with prior aortic surgery like aneurysmal graft repair, aortoenteric fistula is also a possible cause of upper GI hemorrhage. An aortoenteric fistula results from the erosion of the aortic graft into the bowel lumen, usually the third or fourth portion of the duodenum. The result is a direct communication between the aortic graft lumen and the bowel lumen. Most aortoenteric fistulas involve the proximal aortic anastomotic suture line. This often presents as an initial minor sentinel bleed followed by a massive GI hemorrhage. In patients with history of prior aortic surgery, this possibility must always be considered. An UGIE is the procedure of choice to help diagnose the fistula. It should be performed to the ligament of Treitz. UGIE findings also help to exclude other sources of UGIB. Alternatively a contrast enhanced CT scan may also diagnose the condition.
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. Endovascular treatment options are also an option where expertise is available and condition of the patient permits.
This is a rare cause of hemorrhage in the GIT. It is caused by a bleeding source in the pancreas, pancreatic duct or structures adjacent to the pancreas, such as the splenic artery that bleed into the pancreatic duct, which is connected with the bowel at the duodenum. It is usually associated with pancreatitis, pancreatic cancer and aneurysms or pseudoaneurysms of the splenic artery. The condition may be diagnosed by upper GI endoscopy, where fresh blood may be seen from the pancreatic duct. Alternatively, angiography may be used to identify the bleeding source and also be used to arrest bleeding by embolization of the feeding vessel. Occasionally a distal pancreatectomy may be required to arrest hemorrhage.
| Summary|| |
Upper gastrointestinal bleed is a significant problem dealt with routinely by physicians and surgeons. The two most common causes are peptic ulcer disease and variceal bleed due to portal hypertension. An acute bleed requires prompt and effective resuscitation measures followed by emergent management, whereas chronic bleeds may be dealt with using more detailed investigations and choosing an elective management strategy. The management of acute upper gastrointestinal hemorrhage is now centred on endoscopy, for both diagnostic as well as therapeutic purpose and is considered an essential service in any emergency department. The availability of a wide variety of endoscopic techniques has been revolutionary in the management of upper GI bleeding and has greatly decreased the requirement of surgical procedures for the same. It is however, essential to understand the limitations of a certain therapeutic option and the decision to switch to a more suitable option should always be a timely one [Figure 3].
Other causes of upper GI bleeding such as gastric erosions, Mallory Weiss tears, vascular malformations and bleeding tumours must always be kept in mind, and once diagnosed they also may be given an attempt at endoscopic management, before considering a surgical procedure.
Overall timely diagnosis and appropriate management is the key to decreasing mortality related to upper gastrointestinal haemorhage.
| References|| |
Fallah MA, Prakash C, Edmundowicz S. Acute gastrointestinal bleeding. Med Clin North Am 2000;84:1183-208.
Yavorski RT, Wong RK, Maydonovitch C, Battin LS, Furnia A, Amundson DE. Analysis of 3,294 cases of upper gastrointestinal bleeding in military medical facilities. Am J Gastroenterol 1995;90:568-73.
Pilotto A, Maggi S, Noale M, Franceschi M, Parisi G, Crepaldi G, et al.
Development and validation of a new questionnaire for the evaluation of upper gastrointestinal symptoms in the elderly population: A multicenter study. J Gerontol A Biol Sci Med Sci 2010;65:174-8.
Lee JG. Endoscopy-based triage significantly reduces hospitalization rates and costs of treating upper GI bleeding: A randomized controlled trial. Gastrointest Endosc 1999;50:755-61.
Luk GD, Bynum TE, Hendrix TR. Gastric aspiration in localization of gastrointestinal hemorrhage. JAMA 1979;241:576 -8.
Al-Assi MT, Genta RM, Karttunen TJ, Graham DY. Ulcer site and complications: Relation to Helicobacter pylori
infection and NSAID use. Endoscopy 1996;28:229-33.
Kauvar DS, Lefering R, Wade CE. Impact of hemorrhage on trauma outcome: An overview of epidemiology, clinical presentations, and therapeutic considerations. J Trauma 2006;60 Suppl: S3-11.
Silverstein FE, Gilbert DA, Tedesco FJ, Buenger NK, Persing J. The national ASGE survey on upper gastrointestinal bleeding. II. Clinical prognostic factors. Gastrointest Endosc 1981;27:80-93.
Schenker MP, Majdalany BS, Funaki BS, Expert Panel on Vascular Imaging and Interventional Radiology. ACR appropriateness criteria® upper gastrointestinal bleeding. Reston, VA: American College of Radiology (ACR); 2010.
Scottish Intercollegiate Guidelines Network (SIGN). Management of acute upper and lower gastrointestinal bleeding. A national clinical guideline.(SIGN publication; no. 105). Edinburgh, Scotland: Scottish Intercollegiate Guidelines Network (SIGN); 2008.
Barkun AN, Bardou M, Kuipers EJ, Sung J, Hunt RH, Martel M, et al.
International consensus recommendations on the management of patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med 2010;152:101-13.
Stabile BE, Stamos MJ. Surgical management of gastrointestinal bleeding. Gastroenterol Clin North Am 2000;29:189-222.
Elmunzer BJ, Young SD, Inadomi JM, Schoenfeld P, Laine L. Systematic review of the predictors of recurrent hemorrhage after endoscopic hemostatic therapy for bleeding peptic ulcers. Am J Gastroenterol 2008;103:2625-32.
Ioannou GN, Doust J, Rockey DC. Systematic review: Terlipressin in acute oesophageal variceal haemorrhage. Aliment Pharmacol Ther 2003;17:53-64.
de Franchis R, Primignani M. Endoscopic treatments for portal hypertension. Semin Liver Dis 1999;19:439-55.
Lo GH. The role of endoscopy in secondary prophylaxis of esophageal varices. Clin Liver Dis 2010;14:307-23.
Villanueva C, Piqueras M, Aracil C, Gómez C, López-Balaguer JM, Gonzalez B, et al.
A randomized controlled trial comparing ligation and sclerotherapy as emergency endoscopic treatment added to somatostatin in acute variceal bleeding. J Hepatol 2006;45:560-7.
Sarin SK, Govil A, Jain AK, Guptan RC, Issar SK, Jain M, et al.
Prospective randomized trial of endoscopic sclerotherapy versus variceal band ligation for esophageal varices: Influence on gastropathy, gastric varices and variceal recurrence. J Hepatol 1997;26:826-32.
Maluf-Filho F, Sakai P, Ishioka S, Matuguma SE. Endoscopic sclerosis versus cyanoacrylate endoscopic injection for the first episode of variceal bleeding: A prospective, controlled, and randomized study in Child-Pugh class C patients. Endoscopy 2001;33:421-7.
Sarin SK, Jain AK, Jain M, Gupta R. A randomized controlled trial of cyanoacrylate versus alcohol injection in patients with isolated fundic varices. Am J Gastroenterol 2002;97:1010-5.
Idezuki Y, Kokudo N, Sanjo K, Bandai Y. Sugiura procedure for management of variceal bleeding in Japan. World J Surg 1994;18:216-21.
Selzner M, Tuttle-Newhall JE, Dahm F, Suhocki P, Clavien PA. Current indication of a modified Sugiura procedure in the management of variceal bleeding. J Am Coll Surg 2001;193:166-73.
Jin G, Rikkers LF. Transabdominal esophagogastric devascularization as treatment for variceal hemorrhage. Surgery 1996;120:641-7.
Barbot DJ, Rosato EF. Experience with the esophagogastric devascularization procedure. Surgery 1987;101:685-90.
Gouge TH, Ranson JH. Esophageal transection and paraesophagogastric devascularization for bleeding esophageal varices. Am J Surg 1986;151:47-54.
Garcia-Pagán JC, Bosch J. Endoscopic band ligation in the treatment of portal hypertension. Nat Clin Pract Gastroenterol Hepatol 2005;2:526-35.
Stollman N, Metz DC. Pathophysiology and prophylaxis of stress ulcer in intensive care unit patients. J Crit Care 2005;20:35-45.
Cameron JL, editor. Current Surgical Therapy. 5 th
ed. St. Louis, Mo: Mosby-Year Book; 1995. p. 4.
Larson G, Schmidt T, Gott J, Bond S, O′Connor CA, Richardson JD. Upper gastrointestinal bleeding: Predictors of outcome. Surgery 1986;100:765-73.
[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3], [Table 4]