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UPPER
GASTROINTESTINAL
BLEEDING
Dr. Rishabh Handa
M.S. (General Surgery)
INTRODUCTION
• Potentially life-threatening abdominal emergency that
remains a common cause of hospitalization.
• Defined as bleeding derived from a source proximal to
the ligament of Treitz.
Annual incidence - 170 cases/100,000 adults (increases steadily
with advancing age)
Slightly more common in men than women.
Accounts for almost 80% of significant GI hemorrhage.
Common Causes of Upper Gastrointestinal
hemorrhage
Non Variceal Bleed
Peptic ulcer disease 30%-50%
Mallory-Weiss tears 15%-20%
Gastritis or duodenitis 10%-15%
Esophagitis 5%-10%
Arteriovenous malformations
5%
Tumors 2%
Others 5%
Portal hypertensive bleeding
Gastroesophageal varices
>90%
Hypertensive portal
gastropathy, <5 %
Isolated gastric varices,
rare
General approach to the patient
with acute GI hemorrhage.
Risk Stratification
Not all patients with GI bleeding require hospital
admission or emergent evaluation.
Several prognostic factors have been associated with
adverse outcomes including the need for emergent
operation and death.
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
Criteria of the Blatchford
Score
Systolic blood pressure
Blood urea nitrogen
Hemoglobin
Pulse
Melena
Syncope
Hepatic disease
Cardiac failure
Criteria of the Rockall Score
Age
Shock
Coexisting illness
Endoscopic diagnosis
Endoscopic stigmata of
recent hemorrhage
Resuscitation
More severe the bleeding, the more aggressive the
resuscitation.
Intubation and ventilation should be initiated early if
there is any question of respiratory compromise.
Unstable patients should receive a 2-liter bolus of
crystalloid solution, usually lactated Ringer’s,
The response to the fluid resuscitation should be noted.
Routine blood investigations, grouping and cross matching
A Foley catheter should also be inserted for assessment of end-
organ perfusion.
In older patients and patients with significant cardiac, pulmonary,
or renal disease - central venous or pulmonary artery catheter
The oxygen-carrying capacity of the blood can be
maximized by administering supplemental oxygen.
Frequently, these patients benefit from early admission to
and management in the ICU.
Blood transfusion
The decision to transfuse blood depends on
the response to the fluid challenge,
age of the patient,
whether concomitant cardiopulmonary disease is present,
and
whether the bleeding continues.
The initial effects of crystalloid infusion and the patient’s
ongoing hemodynamic parameters should be the primary
criteria.
In general, the hematocrit should be maintained
above 30% in older adults and
above 20% in young, otherwise healthy patients.
Packed red blood cells are the preferred form of
transfusion
Whole blood, preferably warmed, may be used in scenarios
of massive blood loss.
Defects in coagulation and platelets should be replaced
as they are detected.
Patients who require more than 10 U of blood should
receive fresh-frozen plasma, platelets, and calcium
empirically.
History and Physical Examination
Once the severity of the bleeding is assessed and
resuscitation initiated, attention is directed to the history
and physical examination.
The time of onset, volume, and frequency are important
in estimating blood loss.
The medical history may provide clues to the diagnosis.
Antecedent vomiting - Mallory-Weiss tear
Weight loss in malignancy.
Past history of GI disease, bleeding, or operation.
Antecedent epigastric distress in peptic ulcer
Previous aortic surgery - aortoenteric fistula.
history of liver disease prompts a consideration of variceal
bleeding.
Medication use – NSAIDS and SSRIs
The physical examination may also be revealing
The oropharynx and nose can occasionally simulate
symptoms from a more distal source and should always be
examined.
Epigastric tenderness - gastritis or peptic ulceration.
The stigmata of liver disease, including jaundice, ascites,
palmar erythema, and caput medusae, may suggest
bleeding related to varices,
Localization
Subsequent management of the patient with acute GI
hemorrhage depends on localization of the site of the
bleeding.
Algorithm for the
diagnosis of acute GI
hemorrhage
Nonvariceal
Bleeding
Peptic Ulcer Disease
Most frequent cause of upper GI hemorrhage, accounting for
approximately 40% of all cases.
Approximately 10% to 15% of patients with PUD develop bleeding
at some point in the course of their disease.
Bleeding is the most frequent indication for operation and the
principal cause for death in PUD.
Bleeding develops as a consequence of peptic acid
erosion of the mucosal surface.
The most significant hemorrhage occurs when duodenal
or gastric ulcers penetrate into branches of the
gastroduodenal artery or left gastric arteries, respectively.
Forrest Classification for endoscopic Findings and
rebleeding risks in peptic Ulcer Disease
Algorithm for the diagnosis
and management of non-
variceal upper GI bleeding.
Medical Management
STOP All ulcerogenic medications ; nonulcerogenic alternatives
prescribed.
ERADICATION OF H. PYLORI AND LONG-TERM ACID
SUPPRESSION. –
• H. pylori infection reported in only 60–70% of bleeding ulcers.
• 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 sup- pression;
• hence H. pylori eradication is recommended in all bleeders infected
with H. pylori.
Proton Pump Inhibitors (PPIs)
• reduce the risk of rebleeding and
• the need for surgical intervention.
• Therefore, patients with a suspected or confirmed
ulcer should be started on a PPI.
Endoscopic Management
Timing - patients with clinical evidence of a GI bleed
should receive an endoscopy within 24 hours and, while
awaiting this procedure, they should be treated with a
PPI.
Techniques :
1. Injection techniques
2. Thermal techniques
3. Mechanical therapy
Injection techniques
Primary mechanism – tamponade, resulting from a volume
effect
Commonest injection fluid - Epinephrine (1 : 10,000)
injected in all four quadrants of the lesion, optimum
injection volume – 30ml
Epinephrine alone is associated with a high rebleeding
rate; therefore used in combination with thermal
therapy
Thrombin, Fibrin and Cyanoacrylate glue – used to
create a primary tissue seal at the bleeding site
Ethanolamine, sodium tetradecyl sulphate and absolute
alcohol – high risk of mucosal perforation and necrosis
Thermal techniques
Include
• Heater probes
• Neodymium Yttrium Aluminium Garnet laser
• Argon Plasma coagulation –primarily used for superficial
lesions such as vascular abnormalities
• Electrocautery (monopolar or bipolar) – for bleeding
ulcers
Mechanical therapy
Use of device that causes physical tamponade of the
bleeding site e.g.
• Haemoclips and
• bands
May be particularly effective when dealing with a
spurting vessel because they provide immediate control
of hemorrhage.
Metallic clips to arrest bleeding from a duodenal ulcer.
Which endoscopy therapy?
Choice of the endoscopic modality remains largely
personal, based on availability, training and experience
A combination of injection with thermal therapy
achieves hemostasis in 90% of bleeding PUDs.
Second look endoscopy
Defined as preplanned systematic second endoscopy
performed 16-24 hours after the initial endoscopy.
In those who rebleed, the role of a second attempt at
endoscopic control has been controversial but has been
validated.
Most clinicians now encourage a second attempt at
endoscopic control before subjecting the patient to surgery.
Post endoscopy PPIs
Post endoscopy high dose IV PPI infusion is effective in
reducing rebleeding and the need for surgery.
Regimen – Omeprazole or Pantoprazole 80mg bolus,
followed by an 8mg/hr infusion for 72 hours
Rebleeding following endoscopic therapy
Percutaneous angio-embolization or transarterial
embolization can be considered as an alternative to
surgery in case of persistent or recurrent bleeding
refractory to endoscopic therapy
Percutaneous angio-embolization
For the management of TPH (hemobilia and pancreatic
duct haemorrhage), embolization is emerging as the
first line of intervention.
Materials used for embolization-
• Coils
• Polyvinyl alcohol particles,
• Gel-foam,
• Iso-butyl cyanoacrylate,
• ethibloc
One of the above is more effective and has decreased
rebleeding rates
Complications – uncommon; include bowel ischaemia,
gastric, splenic and hepatic infarction
Surgical Management
Indications for Surgery in Peptic Ulcer Bleeding
Absolute indications
• Persistent blood loss refractory to endoscopic
therapy
• Shock with recurrent hemorrhage
• Slow blood loss requiring >3 units blood Shock on
admission
Relative indications
• Transfusion in excess of 6 units
• Elderly patient
• Severe comorbidity
• Rare blood type/refusal of transfusion
• Suspicion of malignancy in a gastric ulcer
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
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.
OPERATIVE PROCEDURE FOR GASTRIC ULCERS
Although it may initially require gastrotomy and suture
ligation, this alone is associated with a high risk of
rebleeding of almost 30%.
In addition, because of a 10% incidence of malignancy,
gastric ulcer resection is generally indicated.
Simple excision alone is associated with rebleeding in as
many as 20% of patients so distal gastrectomy is
generally preferred, although excision combined with
vagotomy and pyloroplasty may be considered for the
high-risk patient.
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 mortality in the setting of acute
hemorrhage.
Options include distal gastrectomy combined with
resection of a tongue of proximal stomach to include the
ulcer, and vagotomy and pyloroplasty combined with
wedge resection or simple oversewing of the ulcer.
Mallory-Weiss tears
Mucosal and submucosal tears that occur near the
gastroesophageal junction.
Usually develop in alcoholic patients after a period of intense
retching and vomiting following binge drinking, but can occur
in any patient who has a history of repeated emesis.
Mechanism(proposed by Mallory and Weiss in 1929)-forceful
contraction of the abdominal wall against an unrelaxed
cardia, resulting in mucosal laceration of the cardia as a result
of the increase intragastric pressure.
5% to 10% of cases of upper GI bleeding.
Diagnosis :
• usually based on history.
• Endoscopy - to confirm the diagnosis - important to perform
a retroflexion maneuver and view the area just below the
gastroesophageal junction. Most tears occur along the lesser
curvature and less commonly on the greater curve.
Treatment :
• 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.
• Angiographic embolization, usually with an absorbable
material such as a gelatin sponge, has been successfully used
in cases of failed endoscopic therapy.
• If these maneuvers fail, high gastrotomy and suturing of the
mucosal tear is indicated.
Stress Gastritis
Characterized by the appearance of multiple superficial
erosions of the entire stomach, most commonly in the
body.
Thought to result from the combination of acid and
pepsin injury in the context of ischemia from
hypoperfusion states, although NSAIDs produce a similar
appearance.
If associated with major burns, these lesions are
referred to as Curling’s ulcers.
Significant bleeding from such lesions is rarely encountered.
In those that develop significant bleeding, acid suppressive
therapy is often successful in controlling the hemorrhage.
In rare cases, when this fails, consideration should be given to
administration of octreotide or vasopressin selectively via the
left gastric artery, endoscopic therapy, or even angiographic
embolization.
Esophagitis
 Esophagus - infrequent source for significant hemorrhage.
 Most commonly the result of esophagitis. Seen in -
• Gastroesophageal reflux disease (GERD). Ulceration may
accompany this but the superficial mucosal ulcerations
generally do not bleed acutely
• Infectious agents may also cause esophagitis, particularly in the
immunocompromised host. With infection, hemorrhage can
occasionally be massive.
 Other causes of esophageal bleeding include medications, Crohn’s
disease, and radiation.
Treatment:
• Acid suppressive therapy
• Endoscopic control of the hemorrhage, usually with
electrocoagulation or a heater probe, is often
successful.
• In patients with an infectious cause, targeted therapy
is appropriate.
• Surgery is seldom necessary.
Bleeding esophageal ulcer secondary to
herpes esophagitis
Gastroesophageal reflux disease (GERD)
viewed on endoscopy.
Dieulafoy’s Lesion
 They are vascular malformations found primarily along the lesser
curve of the stomach within 6 cm of the gastroesophageal junction,
although they can occur elsewhere in the GI tract.
 They represent rupture of unusually large vessels (1 to 3 mm) found
in the gastric submucosa.
 Erosion of the gastric mucosa overlying these vessels leads to
hemorrhage.
 The mucosal defect is usually small (2 to 5 mm) and may be difficult
to identify. Bleeding can be massive
Treatment:
• Initially – endoscopic thermal or sclerosant therapy
• In cases that fail endoscopic therapy, angiographic coil
embolization can be successful.
• If these approaches are unsuccessful, surgical intervention
may be necessary. A gastrostomy is performed and
attempts are made at identifying the bleeding source. The
lesion can then be oversewn.
• In patients in whom the bleeding point is not identified, a
partial gastrectomy may be necessary.
Bleeding Dieulafoy’s lesion of the stomach.
Gastric Antral Vascular Ectasia
Also known as watermelon stomach.
Characterized by a collection of dilated venules
appearing as linear red streaks converging on the antrum
in a longitudinal fashion, giving it the appearance of a
watermelon.
Acute severe hemorrhage is rare in GAVE.
Most patients present with persistent iron deficiency
anemia from continued occult blood loss.
Treatment:
• Endoscopic therapy is indicated for persistent, transfusion-
dependent bleeding and has been reportedly successful in up
90% of patients.
• The preferred endoscopic therapy is APC (Argon Plasma
coagulation)
• Patients failing endoscopic therapy should be considered for
antrectomy.
Malignancy
Malignancies of the upper GI tract are usually associated
with chronic anemia or hemoccult-positive stool rather
than episodes of significant hemorrhage.
Occasionally they may present as ulcerative lesions that
bleed persistently.
Most characteristic of the GI stromal tumor (GIST),
although it may occur with other lesions, including
leiomyomas and lymphomas.
Treatment:
• Although endoscopic therapy is often successful in
controlling these bleeds, the rebleeding rate is high;
• Therefore, when a malignancy is diagnosed, surgical
resection is indicated.
Aortoenteric Fistula
Primary aortoduodenal fistulas are rare lesions.
They typically develop in the setting of a previous abdominal
aortic aneurysm repair.
Although, they may occur as a result of an inflammatory or
infectious aortitis, and they may develop in up to 1% of
aortic graft cases.
The median interval between surgery and hemorrhage is
approximately 3 years.
 Typically, patients will present first with a sentinel bleed. Self-
limited episode - heralds the subsequent massive, and often
fatal, hemorrhage.
 Diagnosis : EGD and CT scan
 Therapy includes
• ligation of the aorta proximal to graft,
• removal of the infected prosthesis, and
• an extra-anatomic bypass.
• defect in the duodenum is often small and can be repaired
primarily.
Hemobilia
Difficult diagnosis to make.
Typically associated with trauma, recent instrumentation of
the biliary tree, or hepatic neoplasms.
Should be suspected in anyone who presents with
hemorrhage, right upper quadrant pain, and jaundice.
This triad is seen in less than 50% of patients.
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.
Hemosuccus pancreaticus
Another rare cause of upper GI bleeding is bleeding from
the pancreatic duct.
This is often caused by erosion of a pancreatic
pseudocyst into the splenic artery.
Presents with abdominal pain and hematochezia.
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 patients amenable to a distal pancreatectomy, the
procedure often results in cure.
Iatrogenic Bleeding
Percutaneous transhepatic procedures
Endoscopic sphincterotomy
Percutaneous endoscopic gastrostomy (PEG)
Bleeding Related
to Portal
Hypertension
Hemorrhage related to portal hypertension is usually the
result of bleeding from 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.
They are most common in the distal esophagus and can
reach sizes of 1 to 2 cm.
As they enlarge, the overlying mucosa becomes increasingly
tenuous, excoriating with minimal trauma.
Grading of esophageal varices
Assessing the Risk of Bleeding
Algorithm for diagnosis and
management of GI
hemorrhage related to
portal hypertension.
Management of variceal bleeding
Pharmacologic modalities
 Non selective beta blockers
• Decrease blood flow in the splanchnic circulation
• Propranolol 20mg BD or 60mg/day (max. upto
160mg/day)
• Nadolol 40mg/day (max. upto 80mg/day)
 Vasopressin analogues
• Vasopressin – given as IV infusion due to short half life
• Terlipressin – longer half life, can be given every 4-6 hours
safer.
 Somatostatin analogues
• Somatostatin – can be used only in acute control because of
its short half life. Given as IV infusion in a dose of
250microgram IV bolus followed by 250microgram/hr
• Octreotide (synthetic analogue) – 50microgram IV bolus
followed by 50microgram/hr infusion
 Drugs that decrease intrahepatic resistance to portal
flow
• Nitrates (isosorbide mononitrate)
• Prazosin
• Carvedilol
• Angiotensin receptor blockers
Endoscopic techniques
 Endoscopic sclerotherapy
• Cyanoacrylate is used for gastric varices
• Polymerizes and hardens within seconds after coming
into contact with blood
 Endoscopic variceal ligation
 Modality of choice for endoscopic treatment of
esophageal varices
 Multiple sessions at 3-4 week intervals are needed to
achieve complete obliteration of varices (2-4 sessions
on an average)
Interventional radiology
 Transjugular intrahepatic portosystemic stent shunt
(TIPSS)
• Indicated in uncontrolled and refractory variceal
haemorrhage
• Involves cannulation of the right heatic vein via the right
internal jugular venous approach under digital subtraction
fluoroscopy
 Balloon occluded retrograde obliteration of gastric
varices
 Coil embolization of varices
 Surgeries
• Portosystemic shunts
• Selective (distal splenorenal) shunts
• Non selective (portocaval or mesocaval) shunts
• Non shunt procedures
• Devascularization(sugiura procedure)
• spenectomy
Treatment Before the First Bleed
 The prognosis depends more on the degree of hepatic insufficiency
rather than on the severity of the varices.
 Mild varices do not require treatment
 Pronounced varices with a high bleeding risk can be treated
medically with propranolol, which may be combined with 40-80
mg/day isosorbide mononitrate.
Spironolactone in a dose of 100−200 mg/day can be
considered as an alternative to beta-blockers.
No endoscopic, operative or TIPS insertion treatment
required
Treatment During the First Bleed
Pharmacological
Terlipressin plus nitrate
Balloon tamponade
Sengstaken−Blakemore tube (for esophageal varices)
Linton−Nachlas tube (for fundic varices)
Endoscopic
Sclerotherapy with Polidocanol and Histoacryl
Rubber band ligation
TIPSS
Operative treatment
Treatment After the First Bleed
Esophageal varices are ligated or sclerosed with polidocanol or
Histoacryl.
An initial second look is scheduled approximately four days after
successful hemostasis.
Further follow- ups are scheduled at 3 weeks, 3 months, and 6
months.
If the varices persist, sclerotherapy or ligation is
continued at 2-4 week intervals with the goal of complete
eradication.
Small residual varices following primary ligation can be
sclerosed.
Propranolol may also be given as an adjunct.
THANK YOU

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Upper GI bleeding

  • 2. INTRODUCTION • Potentially life-threatening abdominal emergency that remains a common cause of hospitalization. • Defined as bleeding derived from a source proximal to the ligament of Treitz.
  • 3. Annual incidence - 170 cases/100,000 adults (increases steadily with advancing age) Slightly more common in men than women. Accounts for almost 80% of significant GI hemorrhage.
  • 4. Common Causes of Upper Gastrointestinal hemorrhage Non Variceal Bleed Peptic ulcer disease 30%-50% Mallory-Weiss tears 15%-20% Gastritis or duodenitis 10%-15% Esophagitis 5%-10% Arteriovenous malformations 5% Tumors 2% Others 5% Portal hypertensive bleeding Gastroesophageal varices >90% Hypertensive portal gastropathy, <5 % Isolated gastric varices, rare
  • 5. General approach to the patient with acute GI hemorrhage.
  • 6. Risk Stratification Not all patients with GI bleeding require hospital admission or emergent evaluation. Several prognostic factors have been associated with adverse outcomes including the need for emergent operation and death.
  • 7.
  • 8. 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
  • 9. Criteria of the Blatchford Score Systolic blood pressure Blood urea nitrogen Hemoglobin Pulse Melena Syncope Hepatic disease Cardiac failure Criteria of the Rockall Score Age Shock Coexisting illness Endoscopic diagnosis Endoscopic stigmata of recent hemorrhage
  • 10. Resuscitation More severe the bleeding, the more aggressive the resuscitation. Intubation and ventilation should be initiated early if there is any question of respiratory compromise. Unstable patients should receive a 2-liter bolus of crystalloid solution, usually lactated Ringer’s, The response to the fluid resuscitation should be noted.
  • 11. Routine blood investigations, grouping and cross matching A Foley catheter should also be inserted for assessment of end- organ perfusion. In older patients and patients with significant cardiac, pulmonary, or renal disease - central venous or pulmonary artery catheter
  • 12. The oxygen-carrying capacity of the blood can be maximized by administering supplemental oxygen. Frequently, these patients benefit from early admission to and management in the ICU.
  • 13.
  • 14. Blood transfusion The decision to transfuse blood depends on the response to the fluid challenge, age of the patient, whether concomitant cardiopulmonary disease is present, and whether the bleeding continues. The initial effects of crystalloid infusion and the patient’s ongoing hemodynamic parameters should be the primary criteria.
  • 15. In general, the hematocrit should be maintained above 30% in older adults and above 20% in young, otherwise healthy patients. Packed red blood cells are the preferred form of transfusion Whole blood, preferably warmed, may be used in scenarios of massive blood loss.
  • 16. Defects in coagulation and platelets should be replaced as they are detected. Patients who require more than 10 U of blood should receive fresh-frozen plasma, platelets, and calcium empirically.
  • 17. History and Physical Examination Once the severity of the bleeding is assessed and resuscitation initiated, attention is directed to the history and physical examination. The time of onset, volume, and frequency are important in estimating blood loss.
  • 18. The medical history may provide clues to the diagnosis. Antecedent vomiting - Mallory-Weiss tear Weight loss in malignancy. Past history of GI disease, bleeding, or operation. Antecedent epigastric distress in peptic ulcer Previous aortic surgery - aortoenteric fistula. history of liver disease prompts a consideration of variceal bleeding. Medication use – NSAIDS and SSRIs
  • 19. The physical examination may also be revealing The oropharynx and nose can occasionally simulate symptoms from a more distal source and should always be examined. Epigastric tenderness - gastritis or peptic ulceration. The stigmata of liver disease, including jaundice, ascites, palmar erythema, and caput medusae, may suggest bleeding related to varices,
  • 20. Localization Subsequent management of the patient with acute GI hemorrhage depends on localization of the site of the bleeding.
  • 21. Algorithm for the diagnosis of acute GI hemorrhage
  • 23. Peptic Ulcer Disease Most frequent cause of upper GI hemorrhage, accounting for approximately 40% of all cases. Approximately 10% to 15% of patients with PUD develop bleeding at some point in the course of their disease. Bleeding is the most frequent indication for operation and the principal cause for death in PUD.
  • 24. Bleeding develops as a consequence of peptic acid erosion of the mucosal surface. The most significant hemorrhage occurs when duodenal or gastric ulcers penetrate into branches of the gastroduodenal artery or left gastric arteries, respectively.
  • 25. Forrest Classification for endoscopic Findings and rebleeding risks in peptic Ulcer Disease
  • 26. Algorithm for the diagnosis and management of non- variceal upper GI bleeding.
  • 27. Medical Management STOP All ulcerogenic medications ; nonulcerogenic alternatives prescribed. ERADICATION OF H. PYLORI AND LONG-TERM ACID SUPPRESSION. – • H. pylori infection reported in only 60–70% of bleeding ulcers. • 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 sup- pression; • hence H. pylori eradication is recommended in all bleeders infected with H. pylori.
  • 28. Proton Pump Inhibitors (PPIs) • reduce the risk of rebleeding and • the need for surgical intervention. • Therefore, patients with a suspected or confirmed ulcer should be started on a PPI.
  • 29. Endoscopic Management Timing - patients with clinical evidence of a GI bleed should receive an endoscopy within 24 hours and, while awaiting this procedure, they should be treated with a PPI. Techniques : 1. Injection techniques 2. Thermal techniques 3. Mechanical therapy
  • 30. Injection techniques Primary mechanism – tamponade, resulting from a volume effect Commonest injection fluid - Epinephrine (1 : 10,000) injected in all four quadrants of the lesion, optimum injection volume – 30ml Epinephrine alone is associated with a high rebleeding rate; therefore used in combination with thermal therapy
  • 31. Thrombin, Fibrin and Cyanoacrylate glue – used to create a primary tissue seal at the bleeding site Ethanolamine, sodium tetradecyl sulphate and absolute alcohol – high risk of mucosal perforation and necrosis
  • 32. Thermal techniques Include • Heater probes • Neodymium Yttrium Aluminium Garnet laser • Argon Plasma coagulation –primarily used for superficial lesions such as vascular abnormalities • Electrocautery (monopolar or bipolar) – for bleeding ulcers
  • 33. Mechanical therapy Use of device that causes physical tamponade of the bleeding site e.g. • Haemoclips and • bands May be particularly effective when dealing with a spurting vessel because they provide immediate control of hemorrhage.
  • 34. Metallic clips to arrest bleeding from a duodenal ulcer.
  • 35. Which endoscopy therapy? Choice of the endoscopic modality remains largely personal, based on availability, training and experience A combination of injection with thermal therapy achieves hemostasis in 90% of bleeding PUDs.
  • 36. Second look endoscopy Defined as preplanned systematic second endoscopy performed 16-24 hours after the initial endoscopy. In those who rebleed, the role of a second attempt at endoscopic control has been controversial but has been validated. Most clinicians now encourage a second attempt at endoscopic control before subjecting the patient to surgery.
  • 37. Post endoscopy PPIs Post endoscopy high dose IV PPI infusion is effective in reducing rebleeding and the need for surgery. Regimen – Omeprazole or Pantoprazole 80mg bolus, followed by an 8mg/hr infusion for 72 hours
  • 38. Rebleeding following endoscopic therapy Percutaneous angio-embolization or transarterial embolization can be considered as an alternative to surgery in case of persistent or recurrent bleeding refractory to endoscopic therapy
  • 39. Percutaneous angio-embolization For the management of TPH (hemobilia and pancreatic duct haemorrhage), embolization is emerging as the first line of intervention. Materials used for embolization- • Coils • Polyvinyl alcohol particles, • Gel-foam, • Iso-butyl cyanoacrylate, • ethibloc
  • 40. One of the above is more effective and has decreased rebleeding rates Complications – uncommon; include bowel ischaemia, gastric, splenic and hepatic infarction
  • 41. Surgical Management Indications for Surgery in Peptic Ulcer Bleeding Absolute indications • Persistent blood loss refractory to endoscopic therapy • Shock with recurrent hemorrhage • Slow blood loss requiring >3 units blood Shock on admission
  • 42. Relative indications • Transfusion in excess of 6 units • Elderly patient • Severe comorbidity • Rare blood type/refusal of transfusion • Suspicion of malignancy in a gastric ulcer
  • 43. 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.
  • 44. 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
  • 45. 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.
  • 46. OPERATIVE PROCEDURE FOR GASTRIC ULCERS Although it may initially require gastrotomy and suture ligation, this alone is associated with a high risk of rebleeding of almost 30%. In addition, because of a 10% incidence of malignancy, gastric ulcer resection is generally indicated.
  • 47. Simple excision alone is associated with rebleeding in as many as 20% of patients so distal gastrectomy is generally preferred, although excision combined with vagotomy and pyloroplasty may be considered for the high-risk patient. Bleeding ulcers of the proximal stomach near the gastroesophageal junction are more difficult to manage.
  • 48. Proximal or near-total gastrectomy is associated with a particularly high mortality in the setting of acute hemorrhage. Options include distal gastrectomy combined with resection of a tongue of proximal stomach to include the ulcer, and vagotomy and pyloroplasty combined with wedge resection or simple oversewing of the ulcer.
  • 49. Mallory-Weiss tears Mucosal and submucosal tears that occur near the gastroesophageal junction. Usually develop in alcoholic patients after a period of intense retching and vomiting following binge drinking, but can occur in any patient who has a history of repeated emesis. Mechanism(proposed by Mallory and Weiss in 1929)-forceful contraction of the abdominal wall against an unrelaxed cardia, resulting in mucosal laceration of the cardia as a result of the increase intragastric pressure.
  • 50. 5% to 10% of cases of upper GI bleeding. Diagnosis : • usually based on history. • Endoscopy - to confirm the diagnosis - important to perform a retroflexion maneuver and view the area just below the gastroesophageal junction. Most tears occur along the lesser curvature and less commonly on the greater curve. Treatment : • Supportive therapy is often all that is necessary because 90% of bleeding episodes are self- limited and the mucosa often heals within 72 hours.
  • 51. • In rare cases of severe ongoing bleeding, local endoscopic therapy with injection or electrocoagulation may be effective. • Angiographic embolization, usually with an absorbable material such as a gelatin sponge, has been successfully used in cases of failed endoscopic therapy. • If these maneuvers fail, high gastrotomy and suturing of the mucosal tear is indicated.
  • 52. Stress Gastritis Characterized by the appearance of multiple superficial erosions of the entire stomach, most commonly in the body. Thought to result from the combination of acid and pepsin injury in the context of ischemia from hypoperfusion states, although NSAIDs produce a similar appearance. If associated with major burns, these lesions are referred to as Curling’s ulcers.
  • 53. Significant bleeding from such lesions is rarely encountered. In those that develop significant bleeding, acid suppressive therapy is often successful in controlling the hemorrhage. In rare cases, when this fails, consideration should be given to administration of octreotide or vasopressin selectively via the left gastric artery, endoscopic therapy, or even angiographic embolization.
  • 54. Esophagitis  Esophagus - infrequent source for significant hemorrhage.  Most commonly the result of esophagitis. Seen in - • Gastroesophageal reflux disease (GERD). Ulceration may accompany this but the superficial mucosal ulcerations generally do not bleed acutely • Infectious agents may also cause esophagitis, particularly in the immunocompromised host. With infection, hemorrhage can occasionally be massive.  Other causes of esophageal bleeding include medications, Crohn’s disease, and radiation.
  • 55. Treatment: • Acid suppressive therapy • Endoscopic control of the hemorrhage, usually with electrocoagulation or a heater probe, is often successful. • In patients with an infectious cause, targeted therapy is appropriate. • Surgery is seldom necessary.
  • 56. Bleeding esophageal ulcer secondary to herpes esophagitis Gastroesophageal reflux disease (GERD) viewed on endoscopy.
  • 57. Dieulafoy’s Lesion  They are vascular malformations found primarily along the lesser curve of the stomach within 6 cm of the gastroesophageal junction, although they can occur elsewhere in the GI tract.  They represent rupture of unusually large vessels (1 to 3 mm) found in the gastric submucosa.  Erosion of the gastric mucosa overlying these vessels leads to hemorrhage.  The mucosal defect is usually small (2 to 5 mm) and may be difficult to identify. Bleeding can be massive
  • 58. Treatment: • Initially – endoscopic thermal or sclerosant therapy • In cases that fail endoscopic therapy, angiographic coil embolization can be successful. • If these approaches are unsuccessful, surgical intervention may be necessary. A gastrostomy is performed and attempts are made at identifying the bleeding source. The lesion can then be oversewn. • In patients in whom the bleeding point is not identified, a partial gastrectomy may be necessary.
  • 59. Bleeding Dieulafoy’s lesion of the stomach.
  • 60. Gastric Antral Vascular Ectasia Also known as watermelon stomach. Characterized by a collection of dilated venules appearing as linear red streaks converging on the antrum in a longitudinal fashion, giving it the appearance of a watermelon. Acute severe hemorrhage is rare in GAVE. Most patients present with persistent iron deficiency anemia from continued occult blood loss.
  • 61. Treatment: • Endoscopic therapy is indicated for persistent, transfusion- dependent bleeding and has been reportedly successful in up 90% of patients. • The preferred endoscopic therapy is APC (Argon Plasma coagulation) • Patients failing endoscopic therapy should be considered for antrectomy.
  • 62.
  • 63. Malignancy Malignancies of the upper GI tract are usually associated with chronic anemia or hemoccult-positive stool rather than episodes of significant hemorrhage. Occasionally they may present as ulcerative lesions that bleed persistently. Most characteristic of the GI stromal tumor (GIST), although it may occur with other lesions, including leiomyomas and lymphomas.
  • 64. Treatment: • Although endoscopic therapy is often successful in controlling these bleeds, the rebleeding rate is high; • Therefore, when a malignancy is diagnosed, surgical resection is indicated.
  • 65. Aortoenteric Fistula Primary aortoduodenal fistulas are rare lesions. They typically develop in the setting of a previous abdominal aortic aneurysm repair. Although, they may occur as a result of an inflammatory or infectious aortitis, and they may develop in up to 1% of aortic graft cases. The median interval between surgery and hemorrhage is approximately 3 years.
  • 66.  Typically, patients will present first with a sentinel bleed. Self- limited episode - heralds the subsequent massive, and often fatal, hemorrhage.  Diagnosis : EGD and CT scan  Therapy includes • ligation of the aorta proximal to graft, • removal of the infected prosthesis, and • an extra-anatomic bypass. • defect in the duodenum is often small and can be repaired primarily.
  • 67.
  • 68. Hemobilia Difficult diagnosis to make. Typically associated with trauma, recent instrumentation of the biliary tree, or hepatic neoplasms. Should be suspected in anyone who presents with hemorrhage, right upper quadrant pain, and jaundice. This triad is seen in less than 50% of patients.
  • 69. 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.
  • 70. Hemosuccus pancreaticus Another rare cause of upper GI bleeding is bleeding from the pancreatic duct. This is often caused by erosion of a pancreatic pseudocyst into the splenic artery. Presents with abdominal pain and hematochezia. High index of suspicion in patients with abdominal pain, blood loss, and a past history of pancreatitis.
  • 71. Angiography is diagnostic and permits embolization, which is often therapeutic. In patients amenable to a distal pancreatectomy, the procedure often results in cure.
  • 72. Iatrogenic Bleeding Percutaneous transhepatic procedures Endoscopic sphincterotomy Percutaneous endoscopic gastrostomy (PEG)
  • 74. Hemorrhage related to portal hypertension is usually the result of bleeding from 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. They are most common in the distal esophagus and can reach sizes of 1 to 2 cm. As they enlarge, the overlying mucosa becomes increasingly tenuous, excoriating with minimal trauma.
  • 76.
  • 77. Assessing the Risk of Bleeding
  • 78.
  • 79. Algorithm for diagnosis and management of GI hemorrhage related to portal hypertension.
  • 80. Management of variceal bleeding Pharmacologic modalities  Non selective beta blockers • Decrease blood flow in the splanchnic circulation • Propranolol 20mg BD or 60mg/day (max. upto 160mg/day) • Nadolol 40mg/day (max. upto 80mg/day)
  • 81.  Vasopressin analogues • Vasopressin – given as IV infusion due to short half life • Terlipressin – longer half life, can be given every 4-6 hours safer.  Somatostatin analogues • Somatostatin – can be used only in acute control because of its short half life. Given as IV infusion in a dose of 250microgram IV bolus followed by 250microgram/hr • Octreotide (synthetic analogue) – 50microgram IV bolus followed by 50microgram/hr infusion
  • 82.  Drugs that decrease intrahepatic resistance to portal flow • Nitrates (isosorbide mononitrate) • Prazosin • Carvedilol • Angiotensin receptor blockers
  • 83. Endoscopic techniques  Endoscopic sclerotherapy • Cyanoacrylate is used for gastric varices • Polymerizes and hardens within seconds after coming into contact with blood
  • 84.  Endoscopic variceal ligation  Modality of choice for endoscopic treatment of esophageal varices  Multiple sessions at 3-4 week intervals are needed to achieve complete obliteration of varices (2-4 sessions on an average)
  • 85. Interventional radiology  Transjugular intrahepatic portosystemic stent shunt (TIPSS) • Indicated in uncontrolled and refractory variceal haemorrhage • Involves cannulation of the right heatic vein via the right internal jugular venous approach under digital subtraction fluoroscopy
  • 86.  Balloon occluded retrograde obliteration of gastric varices  Coil embolization of varices
  • 87.  Surgeries • Portosystemic shunts • Selective (distal splenorenal) shunts • Non selective (portocaval or mesocaval) shunts • Non shunt procedures • Devascularization(sugiura procedure) • spenectomy
  • 88. Treatment Before the First Bleed  The prognosis depends more on the degree of hepatic insufficiency rather than on the severity of the varices.  Mild varices do not require treatment  Pronounced varices with a high bleeding risk can be treated medically with propranolol, which may be combined with 40-80 mg/day isosorbide mononitrate.
  • 89. Spironolactone in a dose of 100−200 mg/day can be considered as an alternative to beta-blockers. No endoscopic, operative or TIPS insertion treatment required
  • 90. Treatment During the First Bleed Pharmacological Terlipressin plus nitrate Balloon tamponade Sengstaken−Blakemore tube (for esophageal varices) Linton−Nachlas tube (for fundic varices)
  • 91. Endoscopic Sclerotherapy with Polidocanol and Histoacryl Rubber band ligation TIPSS Operative treatment
  • 92. Treatment After the First Bleed Esophageal varices are ligated or sclerosed with polidocanol or Histoacryl. An initial second look is scheduled approximately four days after successful hemostasis. Further follow- ups are scheduled at 3 weeks, 3 months, and 6 months.
  • 93. If the varices persist, sclerotherapy or ligation is continued at 2-4 week intervals with the goal of complete eradication. Small residual varices following primary ligation can be sclerosed. Propranolol may also be given as an adjunct.