Causes of Upper GI Hemorrhage
Causes of upper GI hemorrhage can be divided into variceal and nonvariceal bleeding (Table 11-2), of which the latter is more common. Nonvariceal bleeding is also more common than variceal bleeding in patients with portal hypertension; however, the higher morbidity and mortality of variceal bleeding means that this should be excluded before bleeding is attributed to any other source.
Table 11-2: Causes of Upper GI Bleeding ||Download (.pdf)
Table 11-2: Causes of Upper GI Bleeding
|Nonvariceal||Peptic ulcer disease||40|
|upper GI||Mallory-Weiss tears||15–20|
|upper GI||Portal hypertensive||Rare|
Peptic Ulcer Disease and Bleeding.
Numerous studies demonstrated a worldwide reduction in the incidence of peptic ulcers between 1958 and 1999, attributable to the introduction of H. pylori eradication therapy and PPIs. A reduction was also noted in the rate of operation and mortality from peptic ulcer disease; however, the overall incidence of peptic ulcer bleeding did not show a significant decrease over the same period.12 Peptic ulcer bleeding still carries a mortality rate of 5–10%,11,54 and in-hospital care costs more than $2 billion annually in the United States.55
Nonvariceal bleeding accounts for 80–90% of acute upper GI bleeding, the majority of which is due to gastroduodenal peptic ulceration,11 which accounts for 40% of all nonvariceal upper GI bleeding.24 A large proportion of this is associated with use of aspirin and NSAIDs, and the majority of cases occur in the elderly (68% of patients are >60 years of age and 27% >80 years of age).56 At some point during the course of the disease, 10–15% of ulcers will bleed. Patients with bleeding ulcers commonly present with hematemesis and/or melena, and require early and aggressive fluid resuscitation to replace any existing losses. History, examination, and investigations should proceed as outlined previously (Fig. 11-2). Both duodenal and gastric ulcers can bleed profusely; however, this predilection is higher in gastric compared to the more common duodenal ulcers. Bleeding is most significant when involving an artery such as branches of the gastroduodenal or left gastric arteries.
An algorithm for the management of peptic ulcer bleeding.
Several risk stratification scores have been developed to assist in identification of patients who require close monitoring and are at risk of rebleeding. The two most commonly used tools are the Rockall score and the lesser used Blatchford score (Table 11-3). The Rockall score utilizes clinical as well as endoscopic findings to risk-stratify patients. The score ranges from 0 to 11; a higher score is associated with greater risk of rebleeding or death.57 The Blatchford score uses hemoglobin, blood urea nitrogen, systolic blood pressure, pulse, melena, syncope, hepatic disease, or cardiac failure to produce a maximum score of 23; again higher scores indicate higher likelihood of rebleeding or death.58
Table 11-3: Comparison of the Blatchford and Rockall Scores ||Download (.pdf)
Table 11-3: Comparison of the Blatchford and Rockall Scores
|Criteria of the Blatchford Score||Criteria of the Rockall Score|
|Systolic blood pressure||Age|
|Blood urea nitrogen||Shock|
|Melena||Endoscopic stigmata of recent hemorrhage|
The endoscopic appearance of a bleeding ulcer alone can also be used to stratify the risk of rebleeding using the Forrest criteria (Table 11-4).59 High-grade lesions are those that are actively spurting or oozing blood, or have a nonbleeding visible vessel or adherent clot.
Table 11-4: Forrest Classification for Endoscopic Findings and Risk of Rebleeding in Peptic Ulcer Disease ||Download (.pdf)
Table 11-4: Forrest Classification for Endoscopic Findings and Risk of Rebleeding in Peptic Ulcer Disease
|Classifi cation (Grade)||Endoscopic Finding||Risk of Rebleeding|
|Ia||Active, pulsatile bleeding||High|
|Ib||Active, nonpulsatile bleeding||High|
|IIa||Nonbleeding visible vessel||High|
|IIc||Ulcer with flat, pigmented spot||Low|
|III||Clean, nonbleeding ulcer bed||Low|
Stop Any Causes (Eg, Drugs).
All ulcerogenic medication such as salicylates, NSAIDs, and SSRIs should be stopped and nonulcerogenic alternatives prescribed. Cyclooxygenase-2 (COX-2) inhibitors, which initially showed promise as a gastroprotective alternative to NSAIDs have recently been shown to demonstrate cardiotoxicity without significant benefit on gastric mucosal protection and are therefore infrequently used.60
Eradication of H. Pylori and Long-Term Acid Suppression.
The association of bleeding with H. pylori infection is not as strong as the association reported for perforated ulcers, with H. pylori infection reported in only 60–70% of bleeding ulcers. However, recent data show that treating patients positive for H. pylori with eradication therapy reduces the risk of rebleeding and obviates the need for long-term acid suppression61; hence H. pylori eradication is recommended in all bleeders infected with H. pylori.
Gastric acid has been shown to impair clot formation, promote platelet disaggregation, and increase fibrinolysis. In keeping with this, PPIs have been shown to significantly reduce the risk of ulcer rebleeding, the need for urgent surgery, and, in patients with high-risk stigmata who have undergone endoscopic therapy, mortality.62,63
Patients with high-risk stigmata on endoscopy (active bleeding or nonbleeding visible vessel) require haemostatic intervention, such as injection, and thermal or mechanical therapy such as clips (Fig. 11-3). Addition of any one of these to adrenaline injection further reduces rebleeding rates, the need for surgery, and mortality.64–66
Metallic clips to arrest bleeding from a duodenal ulcer. (Used with permission from Dr Nicola Simmonds, Luton and Dunstable Hospital, UK.)
Several factors are predictors of failure of endoscopic therapy for peptic ulcer bleeding, including previous ulcer bleeding, shock and presentation, active bleeding during endoscopy, ulcers greater than 2 cm in diameter, a large underlying bleeding vessel greater than 2 mm in diameter, and ulcers on the lesser curve of the stomach or the posterior or superior duodenal bulb.67 Recent studies suggest that second-look endoscopy (within 24 hours of the initial endoscopic therapy) provides only a small reduction in the rate of rebleeding, is not cost-effective in the presence of acid-suppressing medication, and is overall not recommended.25,68,69 Repeat endoscopy should only be considered in cases of recurrent hemorrhage or unsuccessful first treatment.
Meta-analysis and surgical registry data show the rate of surgical intervention for bleeding peptic ulcers has decreased to 6.5–7.5%. An improved understanding of peptic ulcer disease as well as the development of newer pharmacologic and endoscopic treatments has meant that surgery is now employed not as first-line or curative treatment, but instead only when other modalities have failed.
There are no consensus guidelines on the appropriate indications for surgery; however in general, persistent blood loss with failure of endoscopic therapy and a blood transfusion requirement in excess of 6 units are often considered an indication for surgical intervention (Table 11-5). Similarly, hypovolemic shock associated with recurrent hemorrhage or a slow continuous blood loss requiring transfusion of more than 3 units per day is also considered indicative. Shock on admission, an elderly patient, severe comorbidity, a rare blood type, refusal of transfusion, and bleeding chronic gastric ulcer with a suspicion of malignancy are considered relative indications for surgery.
Table 11-5: Possible Indications for Surgical Intervention for Peptic Ulcer Bleeding ||Download (.pdf)
Table 11-5: Possible Indications for Surgical Intervention for Peptic Ulcer Bleeding
|Possible Indications for Surgery in Peptic Ulcer Bleeding|
Persistent blood loss refractory to endoscopic therapy
Shock with recurrent hemorrhage
Slow blood loss requiring >3 units blood
Shock on admission
Transfusion in excess of 6 units
Rare blood type/refusal of transfusion
Suspicion of malignancy in a gastric ulcer
In stable patients with evidence of rebleeding, a second attempt at endoscopic hemostasis is often as effective as surgery with fewer complications and is the recommended management.70 The aim of surgery in both gastric and duodenal ulcers is to arrest hemorrhage and perform an acid-reducing procedure if deemed necessary.
Operative Procedure for Duodenal Ulcers.
A longitudinal duodenotomy or duodenopyloromyotomy provides good exposure of bleeding sites in the duodenal bulb, the most common site of duodenal ulcers. Direct pressure provides temporary arrest of the bleeding, and it should be followed by suture ligation with a nonabsorbable suture such as Prolene. Four-quadrant suture ligation will achieve hemostasis in anterior ulcers. Posterior ulcers, particularly if involving the pancreaticoduodenal or gastroduodenal artery, will require suture ligation of the artery both proximal and distal to the ulcer for adequate control of hemorrhage, as well as placement of a U-stitch underneath the ulcer to control the pancreatic branches (Fig. 11-4).
Suture control of bleeding duodenal ulcers. A longitudinal pyloric incision is made and figure-of-eight sutures are placed at the cephalad and caudad aspects of the ulcer to occlude the gastroduodenal artery.
The use of an acid-reducing procedure in duodenal ulcers remains a topic of debate, as theoretically arrest of hemorrhage and H. pylori eradication is likely to be sufficient management. In the absence of trials and convincing data, however, it is hard to make any firm recommendations, and the decision is best left to the surgeon taking into account each patient's condition and their experience with such operations. Surgical options for acid reduction in bleeding duodenal ulcer management include pyloroplasty with truncal vagotomy, parietal cell vagotomy, or antrectomy with truncal vagotomy. The former is the most frequently used as it is facilitated by the longitudinal approach to the pylorus for arrest of hemorrhage. Parietal cell vagotomy is limited by surgeon inexperience. Antrectomy with truncal vagotomy may be suitable in patients refractory to conservative surgery but is a complex procedure that is unsuitable in the shocked patient. Ulcer surgery is covered in greater detail in Chap. 26.
Operative Procedure for Gastric Ulcers.
Management of the bleeding gastric ulcer also prioritizes arrest of the bleeding. However, because of the risk of rebleeding and the 10% risk of malignancy in gastric ulcers, gastrotomy and suture ligation are insufficient in these patients. Resection of the ulcer alone is associated with a 20% rebleeding rate; hence a distal gastrectomy is recommended for ulcers in the antrum and distal stomach. In patients who may be unfit for a distal gastrectomy, resection of the ulcer itself combined with an acid-reducing procedure in the form of a vagotomy and pyloroplasty may be an option. Management of bleeding ulcers at the cardioesophageal junction and the proximal stomach is more challenging. While optimal resection would involve a proximal or near-total gastrectomy, this results in increased morbidity and mortality in patients acutely bleeding. More conservative options may suffice, such as distal gastrectomy with resection of a tongue of proximal stomach to ensure excision of the ulcer, or a wedge resection of the ulcer or simple oversewing with a vagotomy and pyloroplasty.
The sensation of nausea is accompanied by closure of the pylorus, gastric distension, and retrograde propulsion of gastric contents toward the cardia. When this is followed by vomiting, the diaphragm moves abruptly upward, associated with rapid increase in intra-abdominal pressure that pushes the gastric cardia into the thorax through the diaphragmatic hiatus. With sufficient force, a longitudinal laceration of the esophagus or stomach can result.71 Hiatus hernias coexist in more than 75% of patients with Mallory-Weiss tears, and the amount of herniated stomach determines the point of maximal dilation (law of Laplace) and therefore the position of the tear.72,73 Large hiatus hernias are associated with more distal tears, while in patients with small or absent hiatus hernias, tears occur at or below the gastroesophageal junction. The majority of tears are situated within 2 cm of the gastroesophageal junction on the lesser curvature.
The highest incidence of Mallory-Weiss tears occurs in patients between 30 and 50 years of age and in men more than women. Some 40–75% of patients have a history of alcohol use74 and 30% a history of aspirin use.75 Patients typically present with a history of several episodes of vomiting or retching followed by hematemesis with fresh red blood. Ten percent of patients may present with only melena.
EGD usually identifies a single tear on the lesser curve of the cardia, or occasionally on the greater curvature of the cardia. Retroflexion during the endoscopic examination is an important maneuver in these patients to ensure the distal gastroesophageal junction and cardia are visualized. The majority of lesions heal spontaneously; hence management is largely supportive, with emphasis on antiemesis and acid suppression. Patients with persistent bleeding may require endoscopic injection or thermocoagulation, or angiographic embolization. Surgery may be required should these options prove unsuccessful, and hemorrhage can be arrested operatively by a high gastrotomy and suture of the mucosal laceration.
Stress-Related Mucosal Bleeding.
Critically ill patients are at risk for the development of diffuse mucosal injury of the stomach, resulting in upper GI bleeding with significant morbidity and mortality. This phenomenon, termed “stress-related mucosal bleeding” or occasionally “stress gastritis,” is a result of a combination of mucosal ischemia and reperfusion injury and impairment of host cytoprotective defenses, and ultimately results in a prolonged ICU stay in a vulnerable population of patients.65 While this phenomenon was previously common, the incidence of clinically significant bleeding in the critically ill population has now decreased to less than 3.5% with the use of prophylaxis.76
The most important risk factors for stress-related mucosal bleeding are prolonged mechanical ventilation (>48 hours) and coagulopathy. Other factors include shock, severe sepsis, neurologic injury/neurosurgery, greater than 30% burns, and multiorgan failure. Patients with these risk factors require prophylaxis with antacids, H2-receptor blockers, PPIs, or Carafate.
Acid suppression is often sufficient to control hemorrhage in stress-related mucosal bleeding. For persistent bleeding, options include selective infusion of octreotide or vasopressin via the left gastric artery, endoscopic measures, or angiographic embolization. Surgery is now rarely performed but, if necessary, involves vagotomy and pyloroplasty with oversewing of discrete regions of hemorrhage or subtotal gastrectomy.
In rare cases bleeding may originate in the esophagus and is then often due to esophagitis. Gastroesophageal reflux disease (GERD) repeatedly exposes the mucosa to irritant acidic gastric content, causing chronic inflammation and blood loss (Fig. 11-5). Occasionally ulceration may follow, presenting as occult bleeding with anemia or guaiac-positive stool. While GERD is the most common cause, other causes include Crohn's disease, certain drugs, and radiotherapy. Immunocompromised patients may have esophagitis of an infective etiology; causes most commonly include herpes simplex, Candida, and cytomegalovirus (CMV), but esophagitis can occasionally be due to ulceration directly induced by human immunodeficiency virus (HIV) or Epstein-Barr virus, or secondary involvement of the esophagus in mycobacterial infection of adjacent lymph nodes.77 Infective esophagitis is uncommon but may lead to torrential hemorrhage.
Gastroesophageal reflux disease (GERD) viewed on endoscopy.
Management, particularly of GERD-induced esophagitis, hinges on acid-suppressive therapy, occasionally requiring therapeutic endoscopy to arrest the bleeding. Treatment of the infective cause is often successful at managing the bleeding in immunocompromised infected patients.
Dieulafoy's lesions are an arterial vascular anomaly featuring abnormally large (“caliber persistent”) submucosal end arteries, likely congenital in origin, and with the potential for massive, potentially life-threatening hemorrhage upon erosion of the overlying gastric mucosa. These lesions are most commonly located in the stomach within 5–7 cm of the cardia but may present in small bowel, duodenum, and colon. These account for 1.5% of upper GI bleeding and are more commonly encountered in men.78
Dieulafoy's lesions appear as reddish-brown protrusions on endoscopy with no ulceration. Endoscopic therapy is often successful provided good visualization of the lesion is obtained; mechanical methods such as clipping or banding have been shown to work better than injections for control of hemorrhage.79,80 Angiographic embolization or surgery may be employed for endoscopic failures. Surgical intervention may require prior endoscopic tattooing to facilitate identification of the site, followed by wedge resection of the lesion.78
Gastric Antral Vascular Ectasia (Gave).
GAVE, or “watermelon stomach,” is so named for the dilated, tortuous mucosal capillaries and veins present in the antrum, converging onto the pylorus, and resembling the surface of a watermelon (Fig. 11-6). This condition is more common in women than in men and often presents with occult blood loss and iron deficiency anemia. APC is the treatment of choice for GAVE; treatment may need to be repeated for recurrences, and PPI cover is recommended for 1 month following treatment.78,81 Patients refractory to APC should be considered for surgical intervention in the form of an antrectomy.
Gastric antral vascular ectasia (GAVE) can be seen in the gastric antrum, giving the stomach a watermelon appearance. (Used with permission from Dr Nicola Simmonds, Luton and Dunstable Hospital, UK.)
Malignant upper GI lesions rarely present with overt significant hemorrhage and instead are more likely to present with hemoccult-positive stool or iron deficiency anemia. Endoscopy occasionally reveals a recurrent bleeding ulcer, a common feature of GI stromal tumors, which characteristically appear as a submucosal tumor with central umbilication and ulceration (discussed further in Chap. 24), and on occasion leiomyomas and lymphomas (Fig. 11-7). Surgery is necessary as the rate of rebleeding in these malignant lesions is high, and may involve full curative resections or in unfit patients, palliative wedge resections for hemorrhage control.
A gastrointestinal stromal tumor (GIST) of the stomach on endoscopy. (Used with permission from Dr Nicola Simmonds, Luton and Dunstable Hospital, UK.)
Aortoenteric fistula is an important clinical condition, often presenting with torrential GI hemorrhage. Primary fistulae are rare; most commonly fistulation occurs following a previous abdominal aortic aneurysm (AAA) repair and is seen in approximately 1% of these cases. The pathophysiology behind this is likely to be infective in origin, leading to the development of a pseudoaneurysm at the proximal suture line, resulting in fistulization into the duodenum (Fig. 11-8).
Intraoperative appearance of an aortoenteric fistula. The photograph demonstrates a large hole (black arrow) in the posterior aspect of the third part of the duodenum after it was medialized and peeled off of the graft. The photograph has been taken from left side of the table with the patient in supine position. (Used with permission from Neal Barshes, MD, MPH, Brigham and Women's Hospital, Boston, MA.)
Early diagnosis of this problem is critical but can be difficult. A high index of suspicion is required in all patients presenting with GI hemorrhage with known aortic aneurysms or a history of previous aortic aneurysm repair. Often, patients present with several smaller, self-limiting episodes of GI hemorrhage (“sentinel bleeds”). Urgent endoscopy at this stage is essential to preempt a subsequent torrential, often fatal bleed, and usually reveals bleeding at the third or fourth part of the duodenum (Fig. 11-9). CT with IV contrast is a useful adjunct in these patients, often demonstrating air within the aortic thrombus or around the graft (particularly in the context of an infected graft), and rarely a pseudoaneurysm or contrast within the duodenal lumen.
Endoscopic view of the aortoenteric fistula on EGD showing the fistulous track (black arrow) into the aneurysmal sac from the third part of the duodenum. (Used with permission from Neal Barshes, MD, MPH, Brigham and Women's Hospital, Boston, MA.)
Surgical repair involves extra-anatomic bypass grafting and aortic ligation for primary aortoenteric fistula. For secondary aortoenteric fistula, surgery involves excision of the graft with extra-anatomic bypass or in situ aortic reconstruction. By necessity these procedures are often performed in critically ill, severely exsanguinated, and septic patients and hence associated with high morbidity and mortality.
With the advent of endovascular stenting for primary AAA repair, various studies have been performed to determine the effectiveness of endovascular stenting for aortoenteric fistula. This has been associated with a high incidence of recurrent bleeding and infection, particularly in the presence of preprocedural infection.82
Hemobilia is a rare cause of GI bleeding. Causes include trauma, hepatic neoplasms, instrumentation of the biliary tree, percutaneous radiofrequency liver ablation, and following liver transplant. A high index of suspicion is required in patients with these risk factors, as the classic presentation of hemorrhage, right upper quadrant pain, and jaundice is only seen in a minority of patients. Endoscopy may reveal blood at the ampulla, but angiography and embolization remain the diagnostic and therapeutic modality of choice.
Bleeding from the pancreatic duct (hemosuccus pancreaticus) is another rare cause of upper GI bleeding, due to fistulation of a pancreatic pseudocyst into the splenic or other peripancreatic artery.83 A presentation of abdominal pain, hematemesis, and melena in patients with a previous history of pancreatitis should raise suspicion of hemosuccus pancreaticus. Angiography is again both diagnostic and therapeutic, although in some cases distal pancreatectomy may be employed.
Upper GI endoscopy or surgery is another cause of bleeding. Percutaneous gastrostomy is often necessary as a means of nutritional support in certain conditions but is accompanied by a 3% rate of GI hemorrhage. Bleeding may have tracked into the stomach from the incision site but may also be from the stomach mucosa; both causes can be managed endoscopically.
Endoscopic sphincterotomy is increasingly common as a means of accessing the biliary tree during an endoscopic retrograde cholangiopancreatography and facilitates endoscopic clearance of the common bile duct, but it is associated with a 2% risk of bleeding. Bleeding may occur after 48 hours but can often be arrested by local injection of epinephrine, rarely requiring surgical intervention. Bleeding following upper GI surgery may occur from suture or staple lines. This can occasionally be treated endoscopically, with minimal insufflation to avoid disruption of the anastomosis.
Variceal Bleeding and Portal Hypertension
Portal hypertension is a serious cause of upper GI bleeding, often the result of cirrhosis that is the end stage of chronic liver disease. The pathophysiology of portal hypertension is discussed further in Chap. 47 and hence is not covered here. Approximately 50% of patients with cirrhosis will develop gastroesophageal varices as a result of portal hypertension.84 Variceal bleeding occurs in 30% of patients and is one of the most important complications of hepatic cirrhosis. Variceal bleeding is associated with increased risk of rebleeding and transfusion requirement, greater length of hospital stay, and higher morbidity and mortality compared with nonvariceal bleeding.17,84
Gastroesophageal varices represent one site of portosystemic anastomosis, which is dilated as the portal circulation tries to decompress to the systemic circulation. Other sites of portosystemic collaterals are the stomach, the umbilical region (collateral formation leads to formation of caput medusae), and the distal rectum.
Factors that determine variceal bleeding include high variceal wall tension (determined by vessel diameter) and variceal pressure, in turn related to hepatic venous pressure gradient (HPVG). Patients with a HPVG of less than 12 mm Hg are unlikely to develop variceal bleeding.85
Isolated gastric varices (IGV) can occur in the absence of esophageal varices and are located along the gastric fundus (IGV1), or along the body, antrum, or pylorus (IGV2).84 Risk factors for gastric variceal bleeding include variceal size and the presence of a cherry-red spot (localized reddish mucosal area or spots on the mucosal surface of a varix).86
In addition to varices, portal hypertension can also cause the development of portal hypertensive gastropathy, diffuse dilation of the mucosal, and submucosal venous plexus of the stomach with overlying gastritis. The stomach develops a snake-skin appearance with cherry-red spots on endoscopy, and rarely may be the site of major hemorrhage (Fig. 11-10).
Endoscopic view of portal hypertensive gastropathy. Note the snake-skin appearance of the stomach and the associated cherry-red spots. (Used with permission from Dr Nicola Simmonds, Luton and Dunstable Hospital, UK.)
The management of variceal upper GI bleeding follows the same principles as those of nonvariceal upper GI bleeding, with emphasis on urgent resuscitation and therapeutic endoscopy because of the higher morbidity and mortality associated with variceal bleeds (Fig. 11-11).
An algorithm for the management of variceal bleeding. DSRS, distal splenorenal shunt; TIPS, transjugular intrahepatic portosystemic shunt.
EGD remains the gold standard for diagnosing variceal bleeding. The diagnosis of variceal hemorrhage is based on meeting one of the following criteria: active bleeding from a varix, a “white nipple” overlying a varix, clots overlying a varix, or varices with no other potential source of bleeding.87
Treatment of variceal bleeding requires a combination of medical and endoscopic management.
Somatostatin or its analogues octreotide or terlipressin should be administered as a bolus immediately in cases where there is a high index of suspicion, and continued for 3–5 days after endoscopic confirmation of diagnosis.84 Fluids and blood products should be administered judiciously to maintain a hemoglobin level of greater than 8 g/dL. Current recommendations are that any patients with cirrhosis and GI bleeding should be given up to 7 days of antibiotic prophylaxis, specifically a fluoroquinolone such as norfloxacin or ciprofloxacin.
Variceal bleeding should be diagnosed and treated by EGD, either with variceal ligation or sclerotherapy.84 In patients with variceal bleeding, endoscopy should be performed as soon as possible (within 12 hours of admission).88,89 This is of particular importance in patients with hemodynamic instability or features of cirrhosis. Early endoscopy also excludes nonvariceal causes of bleeding, which occur in 15% of patients with varices.90 Variceal ligation is the endoscopic treatment of choice as it has been shown to have lower rates of complications compared to sclerotherapy, which can cause perforation, mediastinitis, and stricture formation. Variceal ligation involves the placement of rubber bands on the varices to completely interrupt blood flow into the ligated varix and arrest hemorrhage acutely. The mucosa and submucosa develop ischemic necrosis and granulation and sloughing of the rubber rings, and necrotic tissue results in replacement of varices by scar tissue. Sequential treatments may be required, as many as three treatments over 24 hours, but will achieve control of hemorrhage in up to 90% of patients.
Mechanical tamponade devices may be useful in temporarily controlling bleeding from esophageal varices where endoscopy and medical management have failed. One example is the Sengstaken-Blakemore tube, which consists of a gastric tube with gastric and esophageal balloons. Inflation of the gastric and esophageal balloons compresses the esophagogastric venous plexus, arresting bleeding, but at the risk of ischemic necrosis and perforation. Deflation of the tube can be associated with recurrent bleeding in 50% of patients; hence this technique is reserved as a temporizing measure in massive hemorrhage before more definitive intervention is commenced.
Gastric varices should be managed initially by pharmacotherapy. Endoscopic therapy is not as successful in gastric varices because of the diffuse nature of portal hypertensive gastropathy. Patients with refractory bleeding should be referred early for decompressive therapy such as TIPS (transjugular intrahepatic portosystemic shunt) or shunting.
IGVs, without associated portal hypertension, can occur in the setting of splenic vein thrombosis, often associated with pancreatitis. Varices occur in the presence of normal central portal pressures due to left-sided hypertension, rerouted from the spleen to the short gastric vessels. Splenectomy may relieve the hypertension, but the risk of variceal bleeding in these patients is low and hence splenectomy should not be routinely undertaken.91
Prevention of Rebleeding.
Prevention of rebleeding is of the utmost importance in this patient population. Rebleeding may occur in up to 70% of patients within 2 months without further definitive therapy.92 The highest risk of rebleeding is in the first few days following the initial episode. A combination of nonselective beta-blockers with isosorbide mononitrate has been shown to be more effective than beta-blockers alone in preventing rebleeding.93 The addition of prophylactic endoscopic band ligation to combination pharmacotherapy did not reduce the risk of rebleeding but instead was associated with more adverse events in a recent randomized controlled trial.94
Radiologic or Surgical Portal Decompression.
In approximately 10% of cases of variceal bleeding, endoscopic management is unsuccessful, necessitating urgent decompression of the portal system. A TIPS procedure involves the creation of an artificial anastomosis between the hepatic and portal veins under fluoroscopic guidance with the use of a covered stent, shunting blood away from the hepatic sinusoids and relieving portal pressure.95 TIPS is, however, associated with a 30-day mortality of up to 30% in the emergency setting, usually a result of hepatic encephalopathy from diversion of blood away from the liver parenchyma.96 Rebleeding may occur in 20% of patients and is often due to occlusion of the anastomosis. Surgery is another therapeutic option for decompression of the portal system. Surgical shunts, such as the selective distal splenorenal shunt (DSRS), have lower rates of rebleeding compared to endoscopic therapy but do not demonstrate any difference in survival.97 DSRS patients have an in-hospital mortality of approximately 5%, a 5–8% rate of rebleeding, and a 75–80% 3-year survival.97 A recent randomized controlled trial comparing TIPS with DSRS in patients with failed medical or endoscopic therapy showed no significant difference in the rate of rebleeding, hepatic encephalopathy, or overall survival, but identified a need for close follow-up and a greater need for reintervention in patients subjected to TIPS, suggesting that in patients with relatively limited access to health care facilities, DSRS may be a more suitable therapeutic option.98 Further details on surgical decompression for portal hypertension are covered in Chap. 47.