1. Presenter: Dr. Abdulaziz Almusallam Moderator: Dr. Maher Morris
Upper GI Bleeding
Presenter: Dr. Abdulaziz Almusallam
Moderator:
Dr. Maher Morris

2. Objectives
To Know:
The Definition
Causes
Management Plan

3. Upper GI bleeding
Bleeding that arises from the GI tract proximal to the ligament of Treitz.
Accounts for nearly 80% of significant GI hemorrhage.

4. The causes of upper GI bleeding
Best categorized as:
Nonvariceal Bleeding Or
Bleeding related to portal hypertension

5. The nonvariceal causes account for about 80% of such bleeding
PUD is the most common cause.
In the remaining 20% of patients, most of them have cirrhosis and portal hypertension
which can lead to the development of:
- Gastroesophageal varices,
-Isolated gastric varices,
-Hypertensive portal gastropathy,
All can be the source of an acute upper GI bleed.

6. The patients with cirrhosis are at high risk for developing variceal bleeding,
Even in these patients, nonvariceal sources account for most of the episodes of GI hemorrhage.[
Because of the greater morbidity and mortality of variceal bleeding,
Patients with cirrhosis is generally assumed to have variceal bleeding and appropriate therapy initiated

7. Common Causes of Upper Gastrointestinal Hemorrhage
NONVARICEAL BLEEDING (80%)
PORTAL HYPERTENSIVE BLEEDING (20%)
Peptic ulcer disease 30-50%
Mallory-Weiss tears 15-20%
Gastritis or duodenitis %
Esophagitis 5-10%
Arteriovenous malformations 5%
Tumors 2%
Other 5%
Gastroesophageal varices >90%
Hypertensive portal gastropathy <5%
Isolated gastric varices Rare
Common Causes of Upper Gastrointestinal Hemorrhage

8. Upper GI Endoscopy
The foundation of diagnosis and management of patients with an upper GI bleed is an EGD.
Multiple studies have demonstrated that early EGD (within 24 hours) results in:
Reductions in blood transfusion requirement
Decrease in the need for surgery
Shorter length of hospital stay

9. Upper GI Endoscopy
Endoscopic identification of the source of bleeding also permits:
Estimate the risk for subsequent or persistent hemorrhage
Facilitating operative planning
20% to 35% of patients undergoing EGD will require a therapeutic endoscopic intervention.
5% to 10% will eventually require surgery.

10. Although the best tool for localization of the bleeding source is an EGD
1% to 2% of patients the source cannot be identified
Excessive blood impair visualization of the mucosal surface.
Aggressive lavage of the stomach with room temperature normal saline solution before the procedure can be helpful.

11. Recent evidence has suggested that a single bolus injection of intravenous erythromycin, stimulates gastric emptying, and can significantly improve visualization.
If identification of the source is still not possible:
Angiography may be appropriate in the reasonably stable patient

12. Although operative intervention must be seriously considered if the blood loss is extreme or the patient hemodynamically unstable.
Tagged RBC scan is seldom necessary with a confirmed upper GI bleed.
Contrast studies are usually contraindicated because they will interfere with subsequent maneuvers.

13. Specific Causes of Upper Gastrointestinal Hemorrhage
Nonvariceal Bleeding

14. Peptic Ulcer Disease
PUD is the most frequent cause of upper GI hemorrhage.
Accounting for about 40% of all cases.
About 10% to 15% of patients with PUD develop bleeding at some point in the course of their disease.
Bleeding develops as a consequence of acid-peptic erosion of the mucosal surface.

15. Peptic Ulcer Disease
Although chronic blood loss is common with any ulcer,
Significant bleeding results when there is involvement of an artery:
Either of the submucosa
Or, penetration of the ulcer a larger vessel.

16. Peptic Ulcer Disease Duodenal ulcers are more common
But gastric ulcers bleed more commonly
The most significant hemorrhage occurs when:
duodenal or gastric ulcers penetrate into branches of the gastroduodenal artery or left gastric artery.

17. Management
Management Strategies depend on the appearance of the lesion at endoscopy.
Endoscopic therapy is instituted if:
Bleeding is active
Bleeding has already stopped but there is a significant risk for rebleeding.

18. The ability to predict the risk for rebleeding permits:
Prophylactic therapy
Closer monitoring
Earlier detection of hemorrhage in high- risk patients.
The Forrest classification assess the risk based on endoscopic findings, and stratify the patients into low-, intermediate-, and high-risk groups

19. Forrest Classification of Endoscopic Findings and Rebleeding Risks in Peptic Ulcer Disease
Grade Ia: Active, pulsatile bleeding
Grade Ib: Active, nonpulsatile bleeding
Grade IIa: Nonbleeding visible vessel
Grade IIb: Adherent clot
Grade IIc: Ulcer with black spot
Grade III: Clean, nonbleeding ulcer bed
High
Intermediate
Low

20. Algorithm for the diagnosis and management of nonvariceal upper GI bleeding

21. Endoscopic therapy Recommended in: 1)active bleeding
2)visible vessel (Forrest I to IIa).
In cases of an adherent clot (Forrest IIb): the clot is removed and the underlying lesion evaluated.

22. Endoscopic therapy
Ulcers with a clean base or a black spot, secondary to hematin deposition, are generally not treated endoscopically.

23. Medical Management In cases of an acute peptic ulcer bleed
PPIs:
reduce the risk for rebleeding
the need for surgical intervention
patients with a suspected or confirmed bleeding ulcer are started on a PPI.

24. Association between H. pylori infection and bleeding
Unlike perforated ulcers, which are commonly associated with H. pylori infection,
the association between H. pylori infection and bleeding is less strong.
Only 60% to 70% of patients with a bleeding ulcer test positive for H. pylori.

25. Association between H. pylori infection and bleeding
This has generated some controversy as to the importance of H. pylori treatment in patients with a bleeding peptic ulcer. However,
several studies and a large meta-analysis have shown that H. pylori treatment and eradication, in patients who test positive for the infection, results in decreased rebleeding.

26. Importantly After the H. pylori has been eradicated:
No need for long-term acid suppression.
No increased risk for further bleeding.

27. Patients taking ulcerogenic medications
Such as NSAIDs or SSRIs,
Who present with a bleeding GI lesion
These medications are stopped, and
The patient is started on a nonulcerogenic alternative.

28. Endoscopic options Available endoscopic options include:
Epinephrine injection
Heater probes and coagulation
Application of hemoclips.

29. Epinephrine injection
Epinephrine injection (1:10,000) to all four quadrants of the lesion is very successful in controlling the hemorrhage.
It has been shown that large-volume injection (>13 mL) is associated with better hemostasis,
This suggesting that the endoscopic injection works in part by compressing the bleeding vessel and inducing tamponade.

30. Combination therapy
Epinephrine injection alone is associated with a high rebleeding rate
The standard practice is to provide combination therapy.
This usually means the addition of thermal therapy to the injection.

31. The thermal energy
A combination of injection with thermal therapy achieves hemostasis in 90% of bleeding PUD cases.
The sources of thermal energy can be heater probes, monopolar or bipolar electrocoagulation, laser, or argon plasma coagulator.

32. The thermal energy The most commonly used therapies are :-
Electrocoagulation for bleeding ulcers
Argon plasma coagulator for superficial lesions.

33. Hemoclips The role of hemoclips is less clear
Several studies have reported mixed results.
Hemoclips, which can be difficult to apply, may be particularly effective when dealing with a spurting vessel because they provide immediate control of hemorrhage.

34. Rebleeding of an ulcer
Rebleeding of an ulcer is associated with a significant increase in mortality
Careful observation of patients at high risk for rebleeding is important.

35. Second Endoscopy
In those that rebleed, the role of a second attempt at endoscopic control has been controversial but recently validated.
Recent study demonstrated that a second attempt at endoscopic hemostasis is successful in 75% of patients. Although this will fail in 25% of patients who will then require emergent surgery
There is no increase in morbidity or mortality. Therefore, most clinicians would now encourage a second attempt at endoscopic control before surgical intervention.

36. Surgical Management
Despite significant advances in endoscopic therapy, about 10% of patients with bleeding ulcers still require surgical intervention for effective hemostasis
several clinical and endoscopic parameters have been employed to identify patients at high risk for failed endoscopic therapy

37. Indications for Surgery in Gastrointestinal Hemorrhage
Hemodynamic instability despite vigorous resuscitation (>6 units transfusion)
Failure of endoscopic techniques to arrest hemorrhage
Recurrent hemorrhage after initial stabilization (with up to two attempts at obtaining endoscopic hemostasis)
Shock associated with recurrent hemorrhage
Continued slow bleeding with a transfusion requirement exceeding 3 units/day

38. Surgical Management
The first priority at operation is control of the haemorrhage.
Then
A decision must be made regarding the need for a definitive acid-reducing procedure.

39. Surgical Management (Duodenal Ulcer)
The first step in the operation for duodenal ulcer is exposure of the bleeding site.
Because most of these lesions are in the duodenal bulb, longitudinal duodenotomy or duodenal pyloromyotomy is performed.
Hemorrhage can typically be controlled initially with pressure and then direct suture ligation with nonabsorbable suture.

40. Surgical Management (Duodenal Ulcer)
When ulcers are positioned anteriorly, typically four-quadrant suture ligation suffices.
A posterior ulcer eroding into the pancreaticoduodenal or gastroduodenal artery may require suture ligature of the vessel proximal and distal to the ulcer.

41. Surgical Management (Duodenal Ulcer)
After the bleeding has been addressed, a definitive acid-reducing operation is considered.
With the identification of the role of H. pylori infection in the pathogenesis of duodenal ulcers
There is an argument that simple closure and subsequent treatment for H. pylori is sufficient to prevent recurrence.

42. Surgical Management (Duodenal Ulcer)
At the present time an acid-reducing procedure still appears appropriate in most patients.
The choice between various operative procedures has been based on the hemodynamic condition of the patient and whether there is a long- standing history of refractory ulcer disease.

43. Surgical Management (Duodenal Ulcer)
As the pylorus has often been opened in a longitudinal fashion to control the bleeding,
Closure as a pyloroplasty combined with truncal vagotomy is the most frequently used operation for bleeding duodenal ulcer.

44. Truncal vagotomy

45. Surgical Management (Duodenal Ulcer)
There is some evidence to suggest that parietal cell vagotomy may represent a better therapy for a bleeding duodenal ulcer in the stable patient
Surgeon experience with this procedure may be the determining factor.

46. Surgical Management (Duodenal Ulcer)
In a patient who has a known history of refractory duodenal ulcer disease or who has failed more conservative surgery, antrectomy with truncal vagotomy may be more appropriate.
This procedure is more complex and is rarely undertaken in a hemodynamically unstable patient.

47. Surgical Management (Bleeding gastric ulcers)
Similar to bleeding duodenal ulcers, control of bleeding is the immediate priority
This may require gastrotomy and suture ligation, which, if no other procedure is performed, is associated with about a 30% risk for rebleeding.
In addition, because of the approximate 10% incidence of malignancy, gastric ulcer resection is generally indicated.

48. Surgical Management (Bleeding gastric ulcers)
Simple excision alone is associated with rebleeding in as many as 20% of patients,
so that distal gastrectomy is generally preferred,
although excision combined with vagotomy and pyloroplasty may be considered in the high-risk patient.

49. Surgical Management (Bleeding gastric ulcers)
Bleeding ulcers of the proximal stomach near the gastroesophageal junction are more difficult to manage.
Proximal or near-total gastrectomy is associated with a particularly high morbidity in the setting of acute hemorrhage.

50. Surgical Management (Bleeding gastric ulcers)
Options include:
Distal gastrectomy combined with resection of a tongue of proximal stomach to include the ulcer Or
Vagotomy and pyloroplasty combined with either wedge resection or simple oversewing of the ulcer.

51. Mallory-Weiss tears
Mucosal and submucosal tears that occur near the gastroesophageal junction.
Classically, these lesions develop in alcoholic patients after a period of intense retching and vomiting after binge drinking,
Can occur in any patient who has a history of repeated emesis.

52. Mallory-Weiss tears
The mechanism, proposed by Mallory and Weiss in 1929, is forceful contraction of the abdominal wall against an unrelaxed cardia, resulting in mucosal laceration of the proximal cardia as a result of the increase in intragastric pressure.
Account for 5% to 10% of cases of upper GI bleeding

53. Mallory-Weiss tears Usually diagnosed based on history.
Endoscopy is frequently employed to confirm the diagnosis. To avoid missing the lesion.
Important to perform a retroflexion maneuver and view the area just below the gastroesophageal junction.
Most tears occur along the lesser curvature.

54. Mallory-Weiss tears

55. Mallory-Weiss tears
Supportive therapy is often all that is necessary because 90% of bleeding episodes are self-limited, and the mucosa often heals within 72 hours.
In rare cases of severe ongoing bleeding, local endoscopic therapy with injection or electrocoagulation may be effective.

56. Mallory-Weiss tears
Angiographic embolization, with absorbable material such as gelatin sponge, has been successfully employed
If these maneuvers fail, high gastrotomy and suturing of the mucosal tear is indicated.
It is important to rule out the diagnosis of variceal bleeding.
Recurrent bleeding from a Mallory-Weiss tear is uncommon.

57. Stress- gastritis
Stress-related gastritis is characterized by the appearance of multiple superficial erosions of the entire stomach, most commonly in the body.
It is thought to result from the combination of acid and pepsin injury in the context of ischemia from hypoperfusion states, although NSAIDs produce a very similar appearance.

58. Stress- gastritis
In the 1960s and 1970s, it was a commonly encountered lesion in critically ill patients, with significant morbidity and mortality from bleeding.
Today, with improvements in the management of shock and sepsis, as well as widespread use of acid-suppressive therapy, significant bleeding from such lesions is rarely encountered

59. Esophagitis
The esophagus is infrequently the source of significant hemorrhage. When it does occur, it is most commonly the result of esophagitis.
Esophageal inflammation secondary to repeated exposure of the esophageal mucosa to the acidic gastric secretions in gastroesophageal reflux disease (GERD) leads to an inflammatory response, which can result in chronic blood loss.

60. Esophagitis
Ulceration may accompany but the superficial mucosal ulcerations generally do not bleed acutely, but rather present as anemia or guaiac-positive stools.
A variety of infectious agents may also cause esophagitis, particularly in the immunocompromised host .
With infection, hemorrhage can occasionally be massive.

61. Esophagitis
Other causes of esophageal bleeding include medications, Crohn's disease, and radiation.
Treatment typically includes acid- suppressive therapy.
Endoscopic control of the hemorrhage, usually with electrocoagulation or heater probe, is often successful.

62. Esophagitis
In patients with an infectious etiology, targeted therapy is appropriate.
Operation is seldom necessary.

63. Dieulafoy's Lesion
Dieulafoy's lesions are vascular malformations found primarily along the lesser curve of the stomach within 6 cm of the gastroesophageal junction

64. Dieulafoy's Lesion Can occur elsewhere in the GI tract
They represent rupture of unusually large vessels (1-3 mm) that are found in the gastric submucosa.
Erosion of the gastric mucosa overlying these vessels leads to hemorrhage.
The mucosal defect is usually small (2-5 mm) and may be difficult to identify.

65. Dieulafoy's Lesion
Given the large size of the underlying artery, bleeding from a Dieulafoy's lesion can be massive.
Initial attempts at endoscopic control are often successful.
Application of thermal or sclerosant therapy is effective in 80% to 100% of cases.

66. Dieulafoy's Lesion
In cases that fail endoscopic therapy, angiographic coil embolization can be successful.
If these approaches fail, surgical intervention may be necessary.
Because of the difficulties in visualization and palpation of these lesions, prior endoscopic tattooing can facilitate the procedure.

67. Dieulafoy's Lesion
A gastrotomy is performed, and attempts are made at identifying the bleeding source.
In cases in which the bleeding point is not identified, a partial gastrectomy may be necessary.

68. Gastric Antral Vascular Ectasia
Also known as “watermelon stomach,”
Gastric antral vascular ectasia (GAVE) is characterized by a collection of dilated venules appearing as linear red streaks converging on the antrum in longitudinal fashion, giving it the appearance of a watermelon.

69. Gastric Antral Vascular Ectasia
Acute severe hemorrhage is rare in GAVE
Most patients present with persistent, iron deficiency anemia from continued occult blood loss.

70. Gastric Antral Vascular Ectasia
Endoscopic therapy is indicated for persistent, transfusion-dependent bleeding and has been reportedly successful in up to 90% of patients.
The preferred endoscopic therapy is argon plasma coagulation.
Those failing endoscopic therapy are considered for antrectomy.

71. Malignancy
Malignancies of the upper GI tract are usually associated with chronic anemia or hemoccult-positive stool rather than episodes of significant hemorrhage.
On occasion, malignancies present as ulcerative lesions that bleed persistently.
This is perhaps most characteristic of the GI stromal tumor (GIST)

72. Malignancy
Bleeding may occur with a variety of other lesions, including leiomyomas and lymphomas.
Although endoscopic therapy is often successful in controlling hemorrhage, the rebleeding rate is high.
Therefore, when a malignancy is diagnosed, surgical resection is indicated.

73. Malignancy
The extent of resection is dependent on the specific lesion and on whether the resection is curative or palliative.
Palliative resections for control of bleeding usually entail wedge resections.
Standard cancer operations are indicated when possible, although this may depend on the hemodynamic stability of the patient.

74. Aortoenteric Fistula
Primary aortoduodenal fistulas are rare lesions developing in up to 1% of aortic graft cases.
They typically develop in the setting of a previous abdominal aortic aneurysm repair.
May occur as a result of an inflammatory or infectious aortitis.

75. Aortoenteric Fistula
The interval between surgery and hemorrhage can be days to years.
The median interval is about 3 years.
The sequence is thought to involve development of a pseudoaneurysm at the proximal anastomotic suture line in the setting of an infection,
With subsequent fistulization into the overlying duodenum.

76. Aortoenteric Fistula
Aortoenteric fistula is considered in all patients with GI hemorrhage with a known abdominal aortic aneurysm or a previous prosthetic aneurysm repair.
Hemorrhage is often massive and fatal unless immediate surgical intervention is undertaken.

77. Aortoenteric Fistula
Typically, patients with bleeding from an aortoenteric fistula will present first with a “sentinel bleed.”
This is a self-limited episode that heralds the subsequent massive, and often fatal, hemorrhage.
This prompts urgent EGD because diagnosis at this stage can be lifesaving.

78. Aortoenteric Fistula
Any evidence of bleeding in the distal duodenum (3rd or 4th portion) is considered diagnostic.
CT scan with IV contrast will demonstrate air around the graft (suggestive of an infection),
Possible pseudoaneurysm,
Rarely the presence of IV contrast in the duodenal lumen.

79. Aortoenteric Fistula

80. Aortoenteric Fistula Therapy includes :
Ligation of the aorta proximal to the graft.
Removal of the infected prosthesis.
Extra-anatomic bypass.
The defect in the duodenum is often small and can be repaired primarily.
This is a complex and often morbid procedure.

81. Hemobilia Difficult diagnosis to make.
Typically associated with trauma, recent instrumentation of the biliary tree, or hepatic neoplasms.
Unusual cause of GI bleeding.
Suspected in anyone who presents with hemorrhage, right upper quadrant pain, and jaundice.
Unfortunately, this triad is seen in less than half of patients

82. Hemobilia
Endoscopy can be helpful by demonstrating blood at the ampulla.
Angiography is the diagnostic procedure of choice.
If diagnosis is confirmed:
Angiographic embolization is the preferred treatment.

83. Hemosuccus Pancreaticus
Rare cause of upper GI bleeding.
Bleeding from the pancreatic duct, or hemosuccus pancreaticus.
Typically caused by erosion of a pancreatic pseudocyst into the splenic artery.
Presents with abdominal pain and hematochezia.

84. Hemosuccus Pancreaticus
Difficult diagnosis to make and requires a high index of suspicion.
In patients with abdominal pain, blood loss, and a past history of pancreatitis.
Angiography is diagnostic and permits embolization, which is often therapeutic.
In cases that are amenable to a distal pancreatectomy, this procedure often results in cure.

85. Iatrogenic Bleeding
Upper GI bleeding may follow therapeutic or diagnostic procedures.
Hemobilia may be iatrogenic in nature, particularly after percutaneous transhepatic procedures.
Another common cause of iatrogenic bleeding is endoscopic sphincterotomy. This can occur in up to 2% of cases.

86. Iatrogenic Bleeding
Percutaneous endoscopic gastrostomy (PEG) placement is an increasingly common procedure.
Bleeding rates of up to 3% have been reported.
This can often be controlled endoscopically.

87. Iatrogenic Bleeding
Upper GI bleeding can also be seen in patients who have recently undergone upper GI surgery.
In cases in which a resection and anastomosis have been performed, the source of the bleeding may be the suture or the staple line.
It is safe to perform a diagnostic or even therapeutic EGD

88. Bleeding Related to Portal Hypertension

89. Bleeding Related to Portal Hypertension
Upper GI bleeding is a serious complication of portal hypertension.
Most often in the setting of cirrhosis.
Hemorrhage related to portal hypertension is most commonly the result of bleeding from varices.

90. The Varices
These dilated submucosal veins develop in response to the portal hypertension.
Providing a collateral pathway for decompression of the portal system into the systemic venous circulation.
Most common in the distal esophagus.
May develop in the stomach and the hemorrhoidal plexus of the rectum.

91. The Varices They can reach sizes of 1 to 2 cm.
As they enlarge, the overlying mucosa becomes increasingly tenuous and bleeding occurring with minimal trauma.

92. Portal hypertensive gastropathy
Diffuse dilation of the mucosal and submucosal venous plexus of the stomach associated with overlying gastritis.
Incompletely understood entity.
Endoscopically, the stomach acquires a snakeskin-like appearance with cherry-red spots.
This entity uncommonly produces major hemorrhage.

93. Gastroesophageal varices
Develop in about 30% of patients with cirrhosis and portal hypertension.
30% in this group develop variceal bleeding.
Compared with nonvariceal bleeding, variceal hemorrhage is associated with :
Increased risk for rebleeding
Increased need for transfusions
increased hospital stay, and mortality

94. Gastroesophageal varices
Hemorrhage is frequently massive, accompanied by hematemesis and hemodynamic instability.
The hepatic functional reserve, estimated by Child's criteria.
Despite improvements in the medical management of these patients, the 6-week mortality rate after the first hemorrhage is about 20%.

95. Gastroesophageal varices

96. Algorithm for diagnosis and management of GI hemorrhage related to portal hypertension. EGD, esophagogastroduodenoscopy; TIPS, transjugular intrahepatic portosystemic shunt.

97. Medical Management For Bleeding GE varices
In patients with cirrhosis:
pharmacologic therapy to reduce portal hypertension even while preparing for emergent EGD.
Vasopressin produces splanchnic vasoconstriction but also cardiac vasoconstruction and can lead to MI.
Somatostatin or its synthetic analogue, Octreotide, is now the vasoactive agent of choice without cardiac side effects.
Studies have demonstrated its efficacy in controlling variceal bleeding.

98. Endoscopic Management For Bleeding GE varices
Early EGD is critical to evaluate the source of bleeding.
If bleeding esophageal varices are identified:
Both sclerotherapy and variceal banding have been shown to control hemorrhage effectively.
Banding appears to have a lower complication rate and, when expertise is available, is the therapy of choice

99. Endoscopic Management For Bleeding GE varices
Endoscopic approaches, sometimes with as many as three treatments over 24 hours, control the hemorrhage in up to 90% of patients with esophageal varices.
Unfortunately, gastric varices are not effectively managed by endoscopic techniques.

100. Actively bleeding varices. And Effective control after variceal banding.

101. Other Management For Bleeding GE varices
In cases in which pharmacologic or endoscopic therapies fail to control the hemorrhage:
Tamponade can be successful in temporizing the hemorrhage.
The Sengstaken-Blakemore tube consists of a gastric tube with esophageal and gastric balloons. The Sengstaken-Blakemore tube consists of a gastric tube with esophageal and gastric balloons.

102. Other Management For Bleeding GE varices
The gastric balloon is inflated, and tension is applied to the gastroesophageal junction.
If this does not control the hemorrhage, the esophageal balloon is inflated as well. compressing the venous plexus between them.
These tubes are associated with a high rate of complications with both aspiration and inappropriate placement with esophageal perforation.

103. Other Management For Bleeding GE varices
Hemorrhage recurs on deflation in up to 50% of patients.
Currently, balloon tamponade is reserved for patients with massive hemorrhage to permit more definitive therapies.
In cases of severe variceal bleeding that cannot be controlled endoscopically, emergent portal decompression is indicated.

104. percutaneous transjugular intrahepatic portosystemic shunt (TIPS)
Required in about 10% of patients with variceal bleeding.
TIPS procedure can be lifesaving in patients who are hemodynamically unstable from refractory variceal bleeding.
Associated with significantly less morbidity and mortality than surgical decompression.

105. percutaneous transjugular intrahepatic portosystemic shunt (TIPS)
Studies have shown that TIPS can control bleeding in 95% of cases.
Rebleeding occurs in up to 20% within the first month, usually related to occlusion.
In cases in which TIPS is not available or fails, emergent surgical intervention is indicated.

106. Isolated gastric varices
Managed in much the same way as esophageal varices, although endoscopic therapy tends to be less successful.
Pharmacotherapy is primarily indicated, but when this fails, portal decompression by means of TIPS or a surgical shunt is recommended.

107. Isolated gastric varices
Rarely, isolated gastric varices occur after splenic vein thrombosis.
Most commonly seen in the setting of pancreatitis.
portal pressures are normal, but left-sided hypertension, decompressed from the spleen through the short gastric vessels, produces the varices.
splenectomy was routinely recommended, recent data suggest that the incidence of variceal bleeding is low (4%)
splenectomy is not routinely undertaken now.

108. Portal hypertensive gastropathy
Unlike variceal hemorrhage, bleeding from portal hypertensive gastropathy is not amenable to endoscopic treatment.
Because of the diffuse nature of the mucosal abnormalities. The underlying pathology involves elevated portal venous pressures;
Therefore, pharmacologic therapies aimed at reducing portal venous pressure are indicated.
If pharmacologic therapy fails to control acute bleeding, TIPS is considered.

109. Thank you