UGI Bleed

1. Risk Stratification And
Management Of UGI Bleeding
Dr Rajesh K Mandal
MD Internal Medicine
NAMS,Bir Hospital,Nepal

2. Epidemiology
• The annual rate of hospitalization for any
type of GI hemorrhage in the United States
is estimated to be 350 hospital
admissions/100,000 population.
 Approximately 50% of admissions for GI
bleeding are for upper GI bleeding
40% are for lower GI bleeding
10% are for obscure bleeding

3. • The mortality rate is 5% to 10% for severe
UGI bleeding.
• Bleeding is self-limited in 80% of patients
with UGI hemorrhage even without specific
therapy.
• Of the remaining 20% who continue to
bleed or rebleed, the mortality rate is 30%
to 40%.

4. Clinical Presentations
• Hematemesis: vomitus of red blood or “coffee-ground”
material
• Melena: black, tarry, foul-smelling stool
• Hematochezia: passage of bright red or maroon blood
from the rectum.
• Occult GIB in patients with symptoms of blood loss or
anemia when routine diagnostic evaluation reveals iron
deficiency anemia or a positive fecal occult blood test.

5. Sources of Bleeding

6. causes of severe upper gi bleeding in UCLA CURE database

15. RISK STRATIFICATION
• Endoscopic
• clinical
• laboratory feature
• may be useful for risk stratification of patients
who present with acute upper GI bleeding

16. Pre-endoscopy scoring systems for
nonvariceal bleeding include :
• Clinical Blatchford Score,
• Clinical Rockall Score,
• artificial neural network score
• AIMS65 score.
• T Score
Risk Scores

17. Postendoscopy scoring system:
• Complete Rockall Score.
• Baylor Scoring System.
 Cedars-Sinai Bleeding Index.
(scoring systems are better at determining
mortality than rebleeding)

18. • The Blatchford score (also known as the Glasgow
Blatchford score)it does not take endoscopic data into
account and thus can be used when the patient first
presents .
• The score ranges from zero to 23 and the risk of requiring
endoscopic intervention increases with increasing score
• Low scores (2 or less) are associated with a very low
risk of adverse outcome.
The Blatchford Score:

20. When to use
• Use for adult patients being considered for
hospital admission due to upper GI bleeding.
• Do NOT use in pediatric patients or patients
with suspected small bowel or lower GI
bleeding.
• Its use is controversial for patients already
admitted

21. Pitfalls of Blatchford
• The Glasgow-Blatchford Bleeding Score (GBS) helps identify
which patients with upper GI bleeding (UGIB) may be safely
discharged from the emergency room.
• Any of the 9 variables, if present, increase the priority for
admission (and likelihood of need for acute intervention).
• Scores range from 0-23, with higher scores corresponding
to increasing acuity and mortality.
• A score of 0 suggests low risk of complications (0.5%) and
these patients may likely not need to be admitted for
workup.
• Scores >0 do not imply that the patient must be admitted.

22. • Points to keep in mind:
• Clinicians must use their best judgment in assessing whether the
patient has heart failure or liver disease. For example, a mild
elevation in liver enzymes or steatosis is not considered hepatic
failure; likewise, mild diastolic dysfunction was not considered
heart failure in the model. History of coffee-ground emesis is NOT
counted in the tool as it has a low risk of case fatality (likelihood
ratio 0.5).
• Its use is controversial for patients already admitted
• Variables such as age, creatinine, coagulopathy, mental status, and
comorbidities like malignancy or pulmonary disease are not a part
of this calculator, although they may impact medical decision
making.
• Other risk assessment tools like the Rockall and AIMS65 Scores
account for these variables.

23. Why use
• Easy and quick to calculate.
• Doesn’t rely on endoscopic findings.
• Aids in efficient resource utilization.
• Spares the use of NG lavage.
• Scores correlate with cost and length of stay, need for blood
transfusion, endoscopic treatment, surgery, and mortality.
• Well-validated in numerous populations.
• Has been found to be superior to the AIMS65 in predicting
need for intervention (transfusion, endoscopic treatment,
IR, or surgery) or rebleeding, although the AIMS65 remains
a better predictor of mortality (Stanley 2017)

25. Modified Glasgow Blatchford score, is
calculated using only the blood urea nitrogen, Hb,
systolic blood pressure, and pulse.
• The score ranges from 0 to 16.
• A prospective study of the modified score found
that it performed as well as the full Blatchford
score and that it outperformed the Rockall score
with regard to predicting the need for clinical
intervention, rebleeding, and mortality

26.  AIMS65 is another scoring system that uses data
available prior to endoscopy.
 Studies suggest it has high accuracy for
predicting inpatient mortality among patients
with upper GI bleeding
AIMS65 score less than 2 is associated with a lower
risk of mortality, length of stay, and cost of
hospitalization than a score of 2 or more.
AIMS65:

27. • ●Albumin less than 3.0 g/dL (30 g/L)
• ●INR greater than 1.5
• ●Altered Mental status (Glasgow coma score
less than 14, disorientation, lethargy, stupor,
or coma)
• ●Systolic blood pressure of 90 mmHg or less
• ●Age older than 65 years

28. • In the validation cohort, the mortality rate
increased significantly as the number of risk
factors present increased:
• ●Zero risk factors: 0.3 percent
• ●One risk factor: 1 percent
• ●Two risk factors: 3 percent
• ●Three risk factors: 9 percent
• ●Four risk factors: 15 percent
• ●Five risk factors: 25 percent

29. • The Rockall score is based upon age, the presence of shock,
comorbidity, diagnosis, and endoscopic stigmata of recent
hemorrhage.
• This score consists of two parts: pre-endoscopy, also known as
clinical Rockall score, and post-endoscopy, which is called the
Rockall risk score .
• The Rockall Score after endoscopic therapy correlates well
with mortality.
• A score of 2 or less is associated with a low risk of further
bleeding or death.
The Rockall Score:

32. T Score
• T-score system was designed based on the
clinical status of UGIB patients before
performing endoscopy

34. • A score <6 indicates high-risk status (T1),
• A score between 7 and 9 shows moderate-risk
status(T2),
• And a score of ¸ 10 reveals low-risk status
(T3).
• Good clinical conditions include a patient
without weakness or orthostatic hypotension
who have 1comorbidity

35. Artificial
neural
network
score

36. Baylor bleeding score (BBS)
• They designed it for predicting the risk of re-
bleeding in patients with UGIB

38. Patients with a score < 3 can be discharged
from ED and others need hospitalization. These patients are
re-evaluated after 24-72 hours based on endoscopy results.

42. Approach to a patient
• History
• Physical examination
• Laboratory study
• Resuscitation
• Diagnostic approach

43. The goal of the evaluation is to assess:
 the severity of the bleed,
identify potential sources of the bleed
and
determine if there are conditions
present that may affect subsequent
management.

44. History
• Bleeding manifestations —
Hematemesis suggests bleeding
proximal to the ligament of Treitz.
• The presence of frankly bloody emesis
suggests moderate to severe bleeding
that may be ongoing
• whereas coffee-ground emesis suggests
more limited bleeding.

45. • The majority of melena originates proximal to
the ligament of Treitz (90 percent), though it
may also originate from the small bowel or
right colon .
• 60 to 80ml blood for melena.
• Hematochezia is usually due to lower GI
bleeding. However, it can occur with massive
upper GI bleeding , which is typically
associated with orthostatic hypotension.

46. Past medical history —
• Patients should be asked about prior
episodes of upper GI bleeding, since up
to 60 percent of patients with a history
of an upper GI bleed are bleeding from
the same lesion

47. Medication history-
• Particular attention paid to drugs that:
• Predispose peptic ulcer disease- Aspirin,
NSAIDs
• a/w pill esophagitis
• Promote bleeding- antiplatelets, anticoagulant
• May alter the clinical presentation- bismuth
and iron (turn stool black)

48. Suspected source of UGI bleeding by history

49. Suspected source of UGI bleeding by history

50. Physical examination
• Signs of Hypovolemia:
Mild to moderate hypovolemia: resting
tachycardia
Blood volume loss of atleast 15%: orthostatic
hypotension
Blood volume loss of atleast 40%: Supine
hypotension

51. • Accompanied by shock or
• Orthostatic hypotension
– decrease in the hematocrit value by at
least 6% (or a decrease in the
hemoglobin level of at least 2 g/dl) or
– transfusion of at least 2 units of
packed red blood cells
Severe UGI Bleed

52. Laboratory
• Hematology
• Renal chemistry
• Liver biochemical
• Coagulation studies and for typing and cross
matching for packed red blood cells.

53. Nasogastric lavage :
• Whether all patients with suspected acute
upper GI bleeding require nasogastric tube
(NGT) placement is controversial.
• if a patient has ongoing bleeding and thus
might benefit from an early endoscopy.
• Nasogastric tube lavage can be used to
remove particulate matter, fresh blood, and
clots from the stomach to facilitate
endoscopy.

54. Resuscitation
• Resuscitation efforts should be initiated at
the same time as initial assessment in the
emergency department and continue
during the patient’s hospitalization.
• At least 1 large-bore (14- or 16-gauge)
catheter should be placed intravenously,
and 2 should be placed when the patient
has ongoing bleeding.

55. • Normal saline is infused as fast as needed to keep
the patient’s systolic blood pressure higher than
100 mm Hg and pulse lower than 100/min.
• Transfuse packed red blood cells if Hb less than
7gm/dL, platelets if count 50,000/mm3, and fresh
frozen plasma if prothrombin time less than 15
seconds.
• Patients with heart failure or valvular disease may
benefit from pulmonary catheter monitoring to
minimize the risk of fluid overload.

56. • approach is to initiate blood transfusions if the hemoglobin
is <7 g/dL (70 g/L) for most patients (including those with
stable coronary artery disease)
• Hemoglobin at a level of ≥9 g/dL (90 g/L) for patients at
increased risk of suffering adverse events in the setting of
significant anemia, such as those with unstable coronary
artery disease.
• patients should have a goal hemoglobin of
≥9 g/dL (90 g/L), and instead base the decision on the
patient's comorbid conditions.
• However, patients with active bleeding and hypovolemia
may require blood transfusion despite an apparently
normal hemoglobin

57. • restrictive transfusion strategy were at lower risk than
those assigned to a liberal transfusion strategy for
mortality and rebleeding
• There were no differences between patients with cirrhosis
and those with non-variceal bleeding.
• With regard to mortality, there were trends toward a higher
risk of mortality with a restrictive transfusion strategy
among patients with ischemic heart disease and a lower
risk of mortality among patients without ischemic heart
disease .
• With regard to rebleeding, the risk was similar between
those with and without ischemic heart disease
respectively)

58. Transfer to ICU
• Patients who require admission to the
intensive care unit and early involvement of
both a gastroenterologist and a surgeon
include the following:
1. Patients in shock.
2. Patients with continuous active bleeding.
3. Patients at high risk, such as patients with serious
co-morbidities, those needing multiple blood
transfusions, or those with an acute abdomen.

59. Initial Medical Therapy
• Administration of a PPI is useful for reducing
rebleeding rates in patients with PUD
• Patients with a strong suspicion of portal
hypertension and variceal bleeding should be
started empirically on intravenous octreotide
(bolus followed by infusion) which can reduce
the risk of rebleeding to a rate similar to that
following endoscopic therapy.

60. Endoscopy
• GI endoscopy will identify the bleeding site
and permit therapeutic hemostasis in most
patients with GI bleeding. Endoscopy should
be done only when it is safe to do so and
when the information obtained from the
procedure will influence patient care.

61. Endoscopy:
• Ideally, the patient should be hemodynamically
stable, with HR<100/min and a systolic blood
pressure >100 mm Hg.
• Respiratory insufficiency, altered mental status,
or ongoing hematemesis indicates the need for
endotracheal intubation before emergency upper
endoscopy to stabilize the patient and protect the
airway.
• Coagulopathy and thrombocytopenia should be
corrected with transfusions prior to endoscopy.

62. Endoscopy:
• Patients with active hemorrhage should
undergo emergency endoscopy soon after
medical resuscitation.
• Patients suspected of having cirrhosis or an
aortoenteric fistula or who rebleed in the
hospital should undergo emergent
endoscopy, usually within 6 hours of
admission or rebleeding.
• Patients who are hemodynamically stable
without evidence of ongoing bleeding can
undergo urgent endoscopy (within 12
hours)

63. Endoscopy:
• In the rare patient with massive bleeding and
refractory hypotension, endoscopy can be
performed in the operating room, with the
immediate availability of surgical management,
if necessary.
• In patients with severe UGI bleeding:
Intravenous administration of a gastric
prokinetic medication (e.g., erythromycin or
metoclopramide) 30 to 90 minutes is advisable.

64. Endoscopic Hemostasis
• Thermal contact probes have been the mainstay
of endoscopic hemostasis since the 1970s.
• Contact probes can physically tamponade a
blood vessel to stop bleeding and interrupt
underlying blood flow; thermal energy is then
applied to seal the underlying vessel (coaptive
coagulation).
• The most commonly used probe is a multipolar
electrocoagulation (MPEC) probe, also referred
to as a bipolar electrocoagulation probe.

65. Endoscopic Hemostasis:
• Injection therapy is most commonly performed with a
sclerotherapy needle and submucosal injection of
epinephrine, diluted to a concentration of 1 : 10,000 or 1 :
20,000, into or around the bleeding site or stigma of
hemorrhage.
• The advantages are its wide availability, relatively low cost,
safety in patients with a coagulopathy, and lower risk of
perforation and thermal burn damage than thermal
techniques
• Performed with a sclerosant, such as ethanolamine or
alcohol, but these agents are associated with increased
tissue damage and other risk.

66. Endoscopic Hemostasis
• Endoscopic hemoclips (or clips) serve to
apply mechanical pressure to a bleeding
site.
• Hemoclips are especially useful for
patients with malnutrition or
coagulopathy.

67. Endoscopic Hemostasis
• With band ligation, mucosal (with or without
submucosal) tissue is suctioned into a cap placed
on the end of the endoscope, and a rubber band
is rolled off the cap and over the lesion to
compress its base.
• This technique is widely used for the treatment of
esophageal varices and occasionally can be used
for other bleeding lesions.

68. OTHER METHODS:
• Hemostatic spray is a proprietary inorganic
powder with clotting abilities that can create a
mechanical barrier that adheres to and covers
a bleeding site.
• In small clinical studies the technique has
been used successfully to control oozing of
blood from peptic ulcers, tumors, and other
lesions.

69. Peptic Ulcer Disease
• Burning epigastric pain exacerbated by fasting
and improved with meals is a symptom
complex associated with peptic ulcer
disease(PUD).
• PUD includes ulcerations and erosions in
stomach and duodenum from various causes
• Peptic term: pepsin,proteolytic enzyme at
acidic pH,major role in mucosal break.

70. • Ulcers are defined as disruption of the mucosal integrity of
stomach/duodenum leading to local defect or excavation
due to active inflammation.
• Ulcer: 5mm or larger with depth to submucosal extention:
• less than 5mm:erosion
• 4 million individuals (new cases and recurrences) affected
per year.
• Lifetime prevalence of PUD in the United States is ~12% in
men and 10% in women
• Helicobacter pylori and NSAIDs are the most common risk
factors for PUD

71. Peptic Ulcer:
• Peptic ulcer, most commonly gastric or
duodenal ulcer, accounts for 50% of UGI
bleeds and approximately 100,000
hospitalizations/year in the United States.
 The mortality rate associated with peptic
ulcer bleeding is 5% to 10%

72. • Peptic ulcers are most commonly caused by a
decrease in mucosal defense mechanisms
attributable to aspirin or other NSAIDs, Hp
infection, or both
• Prevalence of Hp infection over 80% (developing
countries); 20-50% (industrialized countries)
• 15-45% of patients taking NASAIDs develop ulcers

73. • Those at high risk of recurrent bleeding and consequent death should be
offered urgent endoscopy and a higher level of monitoring:

74. Endoscopic Risk Stratification:
The Forrest classification is used to categorize findings during
endoscopic evaluation of bleeding peptic ulcers as follows:
Type I: Active bleeding:
Ia: Spurting hemorrhage
Ib: Oozing hemorrhage
Type II: Stigmata of recent hemorrhage:
IIa: Nonbleeding visible vessel
IIb: Adherent clot
IIc: Flat pigmentation
Type III: Clean-base ulcers

78. Acid Suppression Medication:
• In vitro studies have shown that a luminal gastric
pH higher than 6.8 is required for normal
clotting function (platelet aggregation and fibrin
formation) and that a pH less than 5.4 almost
abolishes platelet aggregation and plasma
coagulation .
• Platelet aggregates lyse at an acidic pH, an effect
that is enhanced by the presence of pepsin.
• Reducing the risk of acute bleeding and
rebleeding from a peptic ulcer is theoretically
possible by maintaining a gastric pH higher than
6.

79. • Several studies have shown that in normal
subjects, intravenous administration of a PPI
can consistently keep gastric PH higher than 4
(and often 6) over a 72-hour infusion
• Trials of intravenous H2 receptor antagonists
for the prevention of recurrent ulcer bleeding
have shown no definite benefit.

80. • The optimal effective PPI dose after endoscopic
hemostasis is uncertain, with a meta-analysis
finding no difference between high-dose
intravenous continuous infusion of a PPI (80 mg
bolus followed by 8 mg/hr for 3 days) and non–
high-dose intermittent or oral administration (for
3 days).
• The increase in intragastric pH with high-dose
oral PPI administration is almost identical
(although delayed by 1 hour) to that with
intravenous PPI administration.

83. VARICEAL BLEED
MEDICAL THERAPY:
• Somatostatin and its long-acting analog,
octreotide, cause selective splanchnic
vasoconstriction and lower portal pressure
without causing the cardiac complications seen
with vasopressin (even in combination with
nitroglycerin)
• A meta-analysis has shown that vasoactive drugs
(e.g., octreotide, somatostatin, terlipressin) are
as effective as sclerotherapy for controlling
variceal bleeding and cause fewer adverse
events.

84. • No studies have shown a survival benefit
to vasopressin or somatostatin in patients
with variceal bleeding.
• The dose of octreotide for acute variceal
hemorrhage is a 50 to 100-μg bolus
followed by a continuous infusion of 25 to
50 μg/hr for up to 5 days.

85. • Administration of an antibiotic to cirrhotic
patients with variceal bleeding is associated with a
decrease in the rates of mortality and bacterial
infections.
commonly prescribed antibiotics are:
 norfloxacin oral (400 mg twice daily),
 ciprofloxacin iv (400 mg every 12 hours),
 levofloxacin iv (500 mg every 24 hours), and
 ceftriaxone iv 1 g every 24 hours, administered
for 7 days.

86. SCLEROTHERAPY:
• The most commonly used sclerosants are
ethanolamine oleate, sodium tetradecyl
sulfate, sodium morrhuate, and ethanol.
• Prospective randomized trials suggest
improved immediate hemostasis and a
reduction in acute rebleeding with
sclerotherapy compared with medical
therapy alone for bleeding esophageal
varices,

87. Endoscopic band ligation:
• Acute hemostasis achieved in 80% to 85% of cases.
• Band ligation is associated with fewer local complications,
especially esophageal strictures, and requires fewer endoscopic
treatment sessions than sclerotherapy.
• A metaanalysis has reported that variceal band ligation reduces the
rates of rebleeding, overall mortality, and death from bleeding
compared with sclerotherapy.
• Band ligation, however more technically difficult to perform than
sclerotherapy during active variceal bleeding
TIPS is effective for short term control of bleeding gastroesophageal
varices, especially those that fail endoscopic therapy

89. AFTER ACUTE BLEED:

90. Other Nonvariceal Causes:
Esophagitis:
• severe erosive esophagitis can present with
hematemesis or melena
• Severe bleeding from gastroesophageal reflux–
induced esophagitis is treated medically with a PPI .
• Upper endoscopy is essential for diagnosing severe
erosive esophagitis.
• Treated with a daily PPI for 8 to 12 weeks and
undergo repeat endoscopy to exclude underlying
Barrett’s esophagus,Infections or pill induced
esophagitis.
• Endoscopy with biopsies and brushings is critical for
making these diagnoses and determining the
appropriate pharmacologic therapy.

91. Dieulafoy’s Lesion:
• It usually is located in the gastric fundus, within 6 cm
of the gastroesophageal junction, although lesions in
the duodenum, small intestine, and colon have been
reported.
• Dieulafoy’s lesion can be difficult to identify at
endoscopy because of the intermittent nature of the
bleeding; the overlying mucosa may appear normal if
the lesion is not bleeding.
• Endoscopic Doppler US has been used to help identify
a Dieulafoy’s lesion not visualized on endoscopy.
 Endoscopic hemostasis of a Dieulafoy’s lesion can be
performed with injection therapy, a thermal probe, or
clip device
or by band ligation.

92. Mallory-Weiss Tears:
• Mucosal or submucosal lacerations that occur at
the gastroesophageal junction and usually extend
distally into a hiatal hernia.
• The tear is thought to result from increased intra-
abdominal pressure, possibly in combination with
a shearing effect caused by negative intrathoracic
pressure above the diaphragm, which is often
related to vomiting in patients with a history of
alcohol abuse.
• Bleeding stigmata of Mallory-Weiss tears can
include a clean base, oozing, or active spurting

93. • Usually- bleeding is selflimited and mild, but
occasionally it can be severe.
• Mucosal (superficial) Mallory-Weiss tears can start
healing within hours and can heal completely within 48
hours.
• Although approximately 50% of patients hospitalized
with UGI bleeding from a Mallory-Weiss tear receive
blood transfusions.
• Patients with active bleeding from a Mallory-Weiss tear
should undergo endoscopic therapy, which can be
performed successfully with epinephrine injection,
hemoclip placement, or band ligation.

94. Cameron’s Lesions:
• Linear erosions or ulcerations in the proximal
stomach at the end of a large hiatal hernia
near the diaphragmatic pinch.
• Cameron’s lesions are thought to be caused by
mechanical trauma and local ischemia as the
hernia moves against the diaphragm and only
secondarily by acid and pepsin.

95. • They can be a source of acute UGI bleeding
but more commonly may present as slow GI
bleeding and iron deficiency anemia.
• Long-term medical management is usually
with iron supplements and an oral PPI
.Occasionally surgical repair of the hiatal
hernia may be needed.

96. Hemobilia:
• Occur in patients who have experienced liver trauma,
undergone a liver biopsy or manipulation of the
hepatobiliary system (ERCP, percutaneous transhepatic
cholangiography, or TIPS), or have hepatocellular
carcinoma or a biliary parasitic infection.
• The diagnosis can be confirmed by using a side-viewing
duodenoscope to identify bleeding from the ampulla .
• Ongoing or recurrent bleeding is treated with arterial
embolization via arteriography.

97. Portal Hypertensive Gastropathy:
• patients with severe PHG present with chronic
blood loss, but they occasionally can present with
acute bleeding.
• Severe PHG with diffuse bleeding is treated by
measures that decrease portal pressure, usually
with β-adrenergic receptor blockers or possibly
with placement of a TIPS or surgical portacaval
shunt.
• Endoscopic management has no role unless an
obvious focal bleeding site is identified.
• The best treatment is liver transplantation.

98. Upper GI Malignancy
• 1% of severe UGI bleeds
• Endoscopic hemostasis with MPEC, laser,
injection therapy, or hemoclips can
temporarily control acute bleeding in most
patients and allow time to determine the
appropriate long-term management.

99. Ulcer Hemorrhage in Hospitalized Patients
• The classic cause is stress related mucosal
injury (SRMI, or stress ulcers), characterized by
diffuse bleeding from erosions and superficial
ulcers.
• The second category is inpatient ulcers, which
are large, focal, chronic-appearing ulcers that
are painless and present with severe UGI
hemorrhage manifested by hematochezia,
melena, or bloody emesis.

100. • Therapy with an H2 receptor antagonist has
been shown to decrease the rate of clinically
significant bleeding in ICU patients at high risk
of SRMI.
• Generally, if a patient with SRMI or an
inpatient ulcer is supported hemodynamically
and medically, the lesion will heal as the
patient’s overall medical status improves.

101. Summary
• Peptic ulcer disease is the most common cause of
upper GI bleeding.
• Usually presented with hematemesis, melena or
hematochezia.
• Resuscitation should be done along with the
investigation of causes of upper GI bleeding.
• UGI endoscopy should be done once the patient
is hemodynamically stable.
• If peptic ulcer is suspected intravenous PPI should
be given and if varices is suspected then
somatostatin analogue should be given.

102. THANK YOU
REFERENCES:
• UPTODATE
• Sleisenger`s Gastrointestinal and Liver diseases
10th ed.
 Harrison’s principle of internal medicine 19th
edition
 American college of gastroenterology
 The official journal of Emergrncy department-
SBMU, www.jemerg.com