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.
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,
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.
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.
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.
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.
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.
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
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)
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.