This document provides information on upper gastrointestinal bleeding (UGIB), including its definition, epidemiology, causes, clinical presentation, diagnostic evaluation, and management. Some key points: - UGIB is 5 times more common than lower GI bleeding and is most often caused by peptic ulcers (duodenal more than gastric). - Clinical presentation depends on the rate of bleeding, ranging from chronic anemia to hypovolemic shock. - Initial management involves resuscitation, blood transfusion, and early endoscopy for diagnosis and treatment. - Endoscopy allows for diagnosis in 80% of cases and treatment of high-risk stigmata like active bleeding or non-bleeding visible

2.  Done by Yasmeen Eljamhawi
Definition
Epidemiology
LGIB vs UGIB
Blood supply and venous drainage
The most common cause
The least common cause
Classification
The clinical approach ( history and
physical examination )

3. ■ The upper GI bleeding is a bleeding
derived from a source proximal to
ligament of Tretiz
■ Significant morbidity
and mortality so need
early intervention to
improve this
■ The upper GI bleeding
is 5 times as common
as bleeding from lower
GI

4.  UGIB vs LGIB = 5 :1
 The most common cause peptic ulcer
(duodenal ulcer more common then the gastric
ulcer )
 80% are self limiting
 Anti platelet therapy has two fold increase in
bleed
 The patients who have recurrent bleeding
within 48-72 hours have poor prognosis
 The mortality rate 5-10% for severe UGIB
 More in male than female
 The incidence increase with age
 Using NSAIDs increase the risk of bleeding

5.  Age
 Evidence of co-morbidity, e.g. cardiac failure,
ischemic heart disease, renal disease and
malignant disease
 Presence of the classical clinical features of
shock (pallor, cold peripheries, tachycardia and
low blood pressure)
 Endoscopic diagnosis, e.g ulcer with active
bleeding or endoscopic stigmata of recent
bleeding
 Clinical signs of chronic liver disease

8.  The upper third (cervical
esophagus ):
Supplied by branches from
the inferior thyroid artery
 The middle third
( thoracic esophagus ) :
Supplied by branches from
the descending thoracic aorta
and bronchial arteries
 the lower third (abdominal
esophagus ):
Supplied by branches from
the left gastric artery

9.  The venous from the
upper third drain into
the inferior thyroid
veins
 The vein from the
middle third drain into
the azygos veins
 The vein from the
lower third drain into
the left gastric vein , a
tributary of the portal
vein

11.  The lesser curvature supplied by
the left gastric artery (branch
from celiac artery ) and right
gastric artery(branch from
common hepatic artery)
 The greater curvature supplied by
the left gastro-omental (or gastro-
epiploic )artery ( from splenic
artery )and right gastro-omental
artery ( from gastroduodenal
artery )
 The fundus and upper part of the
body supplied by the short and
posterior gastric artery ( from
splenic artery )
 The pylorus is supplied by the
gastroduodenal artery (from the
common hepatic artery )

12.  Veins drain into the portal circulation
 Left and right gastric veins drain directly into
portal vein
 Short gastric vein and left gastroduodenal veins
join splenic vein
 Right gastroepiploic vein join the superior
mesenteric vein

13.  the upper half is supplied by the superior
pancreaticoduodenal artery ( branch of
gastroduodenal artery )
 The lower half is supplied by the inferior
pancreaticoduodenal artery ( branch of superior
mesenteric artery )

14.  pancreaticoduodenal veins drains
into superior mesenteric vein then to
portal vein

17.  Peptic ulcer diasease (62%)
 Idiopathic (10%)
 Gastroduodenitis (8%)
 Esophageal varices (6%)
 Mallory – weiss tear ( 4%)

18. Esophagus causes Stomach causes Duodenum causes
• Esophageal varices
(the most common
cause )
• Esophagitis
• Esophageal cancer
• Esophageal ulcer
• Mallory – weiss tear
(the most common
cause )
• Gastric ulcer (the
most common
cause )
• Gastric cancer
• Gastritis
• Gastric varices (the
most common
cause )
• Dieulafoy’s lesion
• Duodenal ulcer (the
most common
cause )
• Aorto-enteric fistula
• (vascular
malformation)
• Severe superior
mesenteric artery
syndrome

19. How to approach
upper gastrointestinal
bleeding

20. Airway
Breathing
Circulation

21. Secure to prevent aspiration
Endotracheal tube and give oxygen if needed
Support respiratory function
2 large bore i.v cannula
Take blood for hemoglobin, urea, electrolytes, liver
biochemistry, coagulation screen, blood grouping and
crossmatch
Normal saline is given until the blood becomes available
A central venous catheter is considered when there are
signs of cardiovascular instability.
Bladder catheterization for monitoring urine output
Insertion of a nasogastric tube to confirm wither there is
blood in the stomach

22. Transfusion must be monitored to avoid overload
leading to heart failure. The pulse rate and venous
pressure are the best guides to adequacy of
transfusion
If the Hb is less than 10 g/dL and the patient has
either bled recently or is actively bleeding,
transfusion is usually necessary
Indications for blood transfusion are:
1.Shock (pallor, cold peripheries, systolic BP
below 100 mmHg, pulse > 100/min)
2.Hemoglobin < 10 g/dL in patients with recent
or active bleeding

23.  Hematamesis : vomiting of blood ( red blood or
“coffee-grounds” material)
 Melena : tarry, shiny , semi solid , black stool with
distinctive odor containing partly digested blood
 Hematochezia : passage of fresh blood through
the anus ( in massive bleeding )
 Abdominal pain / epigastric pain
 Odynophagia , dysphagia
 Retching
 symptoms of blood loss : shock , anemia
,syncope
 Non specific symptoms : dyspepsia , weight loss
, anorexia

24. Drug history :
NSAIDs , aspirin , corticosteroid ,
anticoagulants
Past medical history :
DM , coronary artery disease , chronic liver
disease , chronic renal disease , H. pylori
and previous upper GI bleed
Past surgery history :
Previous abdominal surgery
Family history
Social history
Smoking

25. Inspection Palpation percussion
Auscultation
Digital rectal
examination

26.  Pale
 Lymph node swelling
 Feature of chronic liver disease **
 Cyanosis
 Abdominal distension
 Dilated vein
 Visible peristalsis
 Sign of dehydration (dry tongue ,
sunken eyes)

28. Ascites caput medusae gynecomastia
Palmar erythema spider naevi leukonychia

29.  Tenderness
 Abdominal mass
 Shifting dullness
 Absent bowel sound
 Bruit
 Hemorrhoid
 Fresh blood
 fissures

30.  Full blood count
 Hematocrit ( PCV decrease only after 24
hours to 72 hours after bleeding )
 Coagulation profile
 Liver function test
 Renal function test
 Blood urea nitrogen ratio
 Blood grouping and cross matching
 Stool occult blood test

31.  Red blood …. Current bleeding
 Coffee ground …. Recent bleeding
 Continuous aspiration …. Severe
active bleeding

32.  Adolph Kussmaul of
Germany succeeded in
taking a look inside the
stomach of a living human
body for the first time in
1868.
 The endoscope using for
diagnosis and therapeutic if
needed
› ‘Gold Standard’
› URGENT
› More sensitive than contrast
radiography

33.  After adequate
resuscitation, urgent
endoscopy should be
performed in patients
with shock, suspected
varices or with
continued bleeding
 Endoscopy can detect
the cause of the
hemorrhage in 80% or
more of cases
 At endoscopy, Varices
should be treated,
usually with banding

34. • Professor Tim Rockall, who was the main investigator and
first author of the studies that led to its formulation
• Assessing the risk of death and re-bleeding in patients with
UGI hemorrhage
• A score less than 3 carries good prognosis but total score
more than 8 carries high risk of mortality

35. Bleeding
peptic ulcer
disease

36. Peptic ulcer disease
definition :
PUD is the discontinuation of the mucosa of the gastrointestinal
tract that extends deep into the muscularis propria layer of the
gastric mucosa caused by the corrosive action of pepsin and
hydrochloric acid , ulcers usually range between 3 mm and
several centimeters in diameter . It usually occurs in the stomach
and the proximal duodenum and it can involve the lower
esophagus , distal duodenum or jejunum .
 Types:
1. Gastric ulcer (mostly in the antrum , most susceptible part to
bleed is the lesser curvature )
2. Duodenal ulcer ( Duodenal bulb , the posterior wall is the most
common site for bleeding )

37.  Peptic ulcer is the primary cause of non-variceal upper
gastrointestinal bleeding occurring in 50-70 %of
patients. However, bleeding is the presenting
symptom in only 10% of patients with peptic ulcers ,
hypovolemic shock or its consequences is a major
cause of mortality in acute setting .
 Recent studies show that bleeding out of peptic ulcers
either duodenal or gastric (Bleeding from duodenal
ulcers is four times more common than from gastric
ulcers) remain by far the most common complication
of annual incidence ranging from 0.02 % to 0.06% in
general population .
 This complication occurs as the PUD remains
untreated for a period of time .

38. Source of bleeding in Peptic ulcers ?
In case of gastric ulcers the most common site
that is susceptible to bleed due to erosion in the
lesser curvature out of the left gastric artery .
While in duodenal ulcers , the posterior wall of
the duodenal bulb ( the first part of duodenum
closest to the pylorus ) is the most common site
bleeding out of the gastroduodenal artery .

39. Presentation of a patient with bleeding PUD
:
It depends on the rate of bleeding :
Symptoms
-The ulcer can either bleed slowly and chronically which
makes it go unnoticed , as the symptoms will be similar to
that of anemia :
1.Pallor of skin and mucous membranes
3. Shortness of breath and lack of energy
3. Fatigue
4. Lightheadedness
- Or the bleeding occurs heavily and profusely that cause :
1.Melena
2. Hematemesis
3. Hematochezia

40. Signs
1 general signs (anemia if bleeds slowly
and chronically and hypovolemic shock
if bleeds heavily and profusely )
1.Tachycardia
2. Hypotension
3. Little or no urine output
4. Loss of consciousness or confusion
2 local signs (epigastric
tenderness )

41. General Management :
Resuscitation ( mentioned in the previous slides )
1 endoscopy
2 SMA angiography
3 CBCand KFTS
After the patient becomes stabilized :
Endoscopy ( EGD) is the preferred diagnostic and
therapeutic tool in suspected bleeding peptic ulcers due
to low complications and the high accuracy in decreasing
the risk of rebleeding , need for surgery and mortality . It
is recommended to be performed as soon as possible (
up to 24 hours after presentation is considered early
endoscopy ) especially in high risk patients .

42. Data are limited in the literature on the
use of CT-scan in the evaluation of
Upper GI bleeding. Given the
assumption that gastroscopy is the first
diagnostic step, in patients where it is
negative or not feasible, CT-scan may be
a valuable tool to detect the site and the
degree of the bleeding

43. High risk : active bleeding (spurting , oozing )
or non-bleeding visible vessel (Forrest grade
IA , IB or IIA )
Perform endoscopic hemostasis using contact thermal therapy
alone , mechanical therapy using clips , or injection with
vasoconstrictive properties (epinephrine, vasopressin)
epinephrine injection , followed by contact thermal therapy or by
injection of a second injectable agent .
Dual therapy is preferred .
Epinephrine injection as definitive hemostasis therapy is not
recommended
. Admit the patient to a monitored or ICU setting
. Treat with Intravenous PPI (80mg bolus dose +continuous
infusion at 8mg /hour ) for 72 hours after endoscopic hemostasis .
.initiate oral intake of clear liquids 6 hours after endoscopy in
patients with hemodynamic stability
.Transition to oral PPI after completion of intravenous therapy .
. Perform testing for H.pylori ; initiate treatment if the result is
positive

45. High risk : Adherent clot ( Forrest grade IIB )
Consider endoscopic removal of the adherent clot followed by
endoscopic hemostasis ( as mentioned in the previous slide ) If
underlying active bleeding or non-bleeding visible vessel is
present.
.Admit the patient to a monitored bed or ICU setting
.Treat with an intravenous PPI for 72 hours after endoscopy ,
regardless of whether endoscopic hemostasis was performed .
. Initiate oral intake of clear liquids 6 hours after endoscopy in
patients with hemodynamic stability .
. Transition to oral PPI after completion of intravenous therapy .
. Perform testing for H.pylori ; initiate treatment if the result is
positive .

47. Low risk : Flat pigmented (hematin ) spot or clear base (
Forrest grade IIC or III )
.Do not perform endoscopic hemostasis , consider early
hospital discharge after endoscopy if the patient has an
otherwise low clinical risk and safe home environment
.Treat with an oral PPI
. Initiate oral intake with a regular diet 6 hours after endoscopy
in patients with hemodynamic stability .
. Perform testing for H.pylori ; initiate treatment if the result is
positive

49. After endoscopy :
If there is clinical evidence of ulcer rebleeding
,the guideline is o repeat endoscopy with an
attempt at endoscopic hemostasis , for selected
patients it is recommended to obtain surgical or
interventional radiologic consultation.

50. Predictors of failure of endoscopic
treatment:
1.History of peptic ulcer disease
2. Previous ulcer bleeding
3. Presence of shock at presentation
4. Active bleeding during endoscopy
5. Large ulcers ( >2cm in diameter )
6. Large underlying bleeding vessel ( 2mm in diameter )
7. Ulcers located on the lesser curvature , posterior or superior
duodenal bulb .

51. When should endoscopy be repeated ?
It is considered on recurrent bleeding or if there is uncertainty
regarding the effectiveness of hemostasis during the initial
treatment .
Planned second-looked endoscopy that is performed within 24
hours after initial endoscopic therapy is generally not
recommended .

52. Surgery
The decision for surgery should be made early in the first 48-72 hours
as the results of the late surgery are poor with high mortality .
*Patient should have more than one IV line open and running .
Indications :
A. Absolute indications :
1. Patient under adequate medical therapy and bleeds
2. Severe bleeding from the start of about 2L or more ( >4 units of blood needed
for correction )
3. Continuous bleeding ( as evidenced by the need to transfuse 1000 ml of blood
/day to maintain stability )
4. If bleeding recurs while patient is in the hospital
B. Relative indications :
1. Old patient due atherosclerosis
2. Associated with serious diseases ( the risk of surgery is far less than the risk
of bleeding )
3. Long history of ulcer disease
.

53. The preferred operative approach to a peptic
ulcer will depend on the location of the ulcer,
and for this reason it is important for the
surgeon caring for the patient to be present
during upper GI endoscopy to obtain precise
information on the location of the ulcer.

54. 1.Bleeding gastric ulcer : is generally the excision of the ulcer
and repair of the gastric defect . Excision or biopsy of the ulcer
is important, as 4–5% of benign appearing ulcers are actually
malignant ulcers
. For ulcers along the greater curvature of the stomach, antrum or
body of the stomach wedge excision of the ulcer and closure of the
resulting defect can easily be achieved in most cases without
causing significant deformation of the stomach.
. For ulcers in the lesser curvature , due to the rich arcades of the
left gastric artery , wedge excision would leave a stomach
deformation with increased incidence of gastric volvulus and luminal
obstruction . So distal gastrectomy with Bilroth I or Bilroth II as a
reconstruction surgery to resume GI continuity .

55. 2.Bleeding duodenal ulcer
Dissection is carried out to expose the pylorus and first part of the
duodenum. An anterior longitudinal duodenotomy is made
extending through the pyloric channel to the distal stomach.
Bleeding from the GDA complex is controlled with a three-vessel
ligation technique.. A Heineke Mikulicz closure of the
duodenotomy is then performed by closing the horizontal incision in
a vertical fashion and truncal vagotomy

56. Interventional Radiology
Angiography ( can be diagnostic and
therapeutic ) with transcatheter
embolization is reserved for patients in
whom endoscopic therapy has failed ,
especially if such patients are high risk
surgical candidates .
Primary rates of technical success range
from 52% to 94% , with recurrent
bleeding requiring repeated embolization
procedures in approximately 10% of
patients .

58. Reference :
.The New England Journal of Medicine,
.Endoscopy Campus Magazine ,
.Johns Hopkins Gastroenterology and Hepatology department
Done by : Rahaf Qubelat

59. 59
Done by :
DIMA MAHER RAHHAL

60.  ANATOMY
 DEFINATION
 ETIOLOGY
 RISK FACTOR
 CLINICAL MANIFISTATION
 DIAGNOSIS EVALUATION
 MANAGEMENT
60

61. 61
The esophagus is a 25
cm long fibromuscular
tube extending from the
pharynx (C6 level) to the
stomach (T11 level).

62.  ESOPHAGUS is mainly studied in 3 parts:
All anatomical features, pathologies, surgical
approach and management options are specific to
each of these parts.
62

63. Oesophageal varices are abnormal dilated,
elongated , and tortuous veins .
They are prone to rupture and often are the
sources of massive haemorrhage from the
upper gastro-intestinal tract.
63

64. 64
Portal hypertension:
*DEFIITION:
Elevation of portal venous pressure above 12mmHg
*ETIOLOGY :
*pathophysiology :
Portal vein is formed by union of superior mesentric &splenic vein so portal
hypertension leads to :
1- spleen congesion 2- intestinal congestion 3- porto-systemic shunt
SUPRA HEPATIC HEPATIC INFRA HEPATIC
CARDIAC CIRRHOSIS
(RSHF – TR – IVC obstruction –
Budd chiari syndrome )
Liver cirrhosis
Schistosomiasis
Congenital fibrosis
Portal vein thrombosis
Extrinsic compression

65. 65

66. Normal HVPG = 5 mm Hg
** Portal hypertension
> 5 mm Hg
** Esophageal hemorrhage
Only with HVPG > 12 mm Hg
66

67. Severe liver scarring (cirrhosis)
Blood clot (thrombosis) A blood clot in the
portal vein or in a vein that feeds into the portal
vein (splenic vein) can cause esophageal varices.
Parasitic infection. Schistosomiasis is a
parasitic infection found in parts of Africa, South
America. The parasite can damage the liver, as
well as the lungs, intestine, bladder and other
organs
67

68. High portal vein pressure. The risk of
bleeding increases with the amount of pressure in the
portal vein (portal hypertension).
Large varices. The larger the varices, the more
likely they are to bleed.
68

69.  Red marks on the varices. When viewed through an
endoscope passed down your throat, some varices show long, red
streaks or red spots. These marks indicate a high risk of bleeding.
 Severe cirrhosis or liver failure. Most often, the more
severe your liver disease, the more likely varices are to bleed.
alcohol. Your risk of variceal bleeding is far greater if you
continue to drink than if you stop, especially if your disease is
alcohol related.
69

70. Before rupture :
1- asymptomatic (silent)
2- dysphagia (rare)
At rupture :
1- hematemesis
2- melena
70

71. 71
Ascites
Splenomegaly Jaundice

72. 1- Upper gastrointestinal endoscopy
is the most commonly used method to detect varices.
• Detect early varices .
• Detect sign of impending rupture (red sign ) .
• Detect active bleeding and its site .
* In patients in whom no varices are detected on initial
endoscopy, endoscopy to look for varices should be
repeated in 2 to 3 years.
* If small varices are detected on the initial endoscopy,
endoscopy should be repeated in 1 to 2 years.
72

73. .
73
2- Imaging by CT or MRI scan:
The pictures created by CT or MRI show the esophagus,
the liver and the portal and splenic veins. They give
the physician more information about the liver’s
health than endoscopy alone.
3- CBC
4- LIVER FUNCTION TEST
5- KIDNEY FUNCTION TEST

74. 74
DURING
BLEEDING
SILENT
VARICES

75.  Bleeding from esophageal varices is an emergency
that requires immediate treatment.
75
A- initial resuscitation
a- 2 wide bore venous cannulas(IV LINE)
are inserted, one for installing fluids and one
for drawing blood for CBC, coagulation profile,
urea and electrolytes and cross-matching.
- VASOPRESSIN
- SEDATIVE
b- Bladder catheterization
For follow up of urine output for fear of ARF
C- Insertion of a nasogastric tube
monitor the bleeding and prevent aspiration.
B- MONITORING
:
1- Pulse
2- HR
3- RR
4- Urine output
5- BP
6- Temperature

76. vasoconstrictor therapy
1- VASOPRESSIN
2- SOMATOSTATIN
3- TERLIPRESSIN
4- OCTREOTIDE
76

77. 77

78. The technique involves injection of a
sclerosant into (intravariceal) or adjacent
to(paravariceal) a varix.
78

79. Esophageal varices are ligated with endoscopically placed
small elastic O-rings
*is the preferred endoscopic modality.
* Variceal ligation is simpler to perform than injection sclerotherapy.
* Endoscopic variceal ligation is associated with fewer complications
than sclerotherapy
79

80. When there is failure of vasopressin or
endoscopy
Control active bleeding in > 90%
Serious complication :
Esophageal rupture
Aspiration pneumonia
Perform endotracheal intubation before placing these tubes
Airway obstruction
80
.Pressure techniques

81. Severe hemorrhage unresponsive to initial
resuscitation
 Unavailable or failure of endoscopic therapy
 Coexisting 2nd indication to operations such
as perforation, obstruction orsuspicious of
malignancy
81

82. *TIPS reduces elevated portal pressure by creating a
communication between the hepatic vein and an
intrahepatic branch of the portal vein.
*Therapy of choice for acute variceal bleeding after
failure of drug and endoscopic therapy
-Indication :
-When endoscopic or drug treatments have failed
-Poor surgical risks
82

83. 83

84.  Synonyms of Mallory Weiss Syndrome
• Gastroesophageal Laceration-Hemorrhage
• Mallory-Weiss Laceration
• Mallory-Weiss Tear 84
Mallory Weiss Syndrome

85.  DEFINITION
 EPIDEMEOLOGY
 CAUSES
 SIGNS AND SYMPTOMS
 DIAGNOSTIC MEASURES
 DD
 MANAGEMENT
85

86. Mallory-Weiss syndrome refers to a tear or
laceration of the mucous membrane, most
commonly at the point where the
esophagus and the stomach meet
(gastroesophageal junction)..
86

87. * it occurs more frequently in
individuals with alcoholism.
*MWS appears to affect more males
then females.
*The ages of those affected varies
considerably, with a peak at ages 40
through 60. However, some cases
have been reported in children.
87

88. 1- severe vomiting
2- chronic alcoholism
3- a severe trauma to the chest or
abdomen
4- inflammation of the lining of the
stomach (gastritis) or esophagus
(esophagitis)
5- hiatus hernia, convulsions
6 - CPR (cardiopulmonary
resuscitation).
7- Cancer patients undergoing
88

89. abdominal pain
a history of severe vomiting,
vomiting of blood (hematemesis),
and the strong involuntary effort
to vomit (retching). The blood is
often clotted and has the
appearance of “coffee grounds”.
The stools may be as dark as tar
(melenic).
89

90. *endoscopic examination of the esophagus
membrane.
90

91.  In many cases, bleeding caused by Mallory-Weiss
syndrome will stop without treatment.
 In cases where the bleeding persists, treatment
may include sealing the lesion by applying heat or
chemicals (cauterization) or high frequency
electrical current (electrocoagulation).
 Blood transfusions and/or the use of the
vasopressive drug, pitressin, may be required.
 Direct pressure may also be used by inserting a
catheter which is surrounded by a balloon. The
balloon is then inflated (balloon tamponade) to
stop the bleeding.
 Surgery is usually not necessary unless the
bleeding cannot be controlled by conservative
measures.
 Other treatment is symptomatic and supportive.
 Embolization (may be necessary as a treatment
for massive uncontrolled bleeding of the
esophagus. This procedure consists of inserting a
91

92.  Zollinger-Ellison Syndrome
 Chronic Erosive Gastritis
 Esophagus Perforation
 Peptic Ulcer
 Esophageal Varices
92

93. 93