Ugi bleeding muneshwar

UPPER
GASTROINTESTINAL
(UGI) BLEEDING
Dr . Muneshwar sah
MD resident, NAMS

Gastrointestinal Bleeding (GIB) Categorized
By Site Of Bleeding
• Upper GI bleed (UGIB)  (esophagus, stomach, duodenum;
bleeding proximal to the ligament of Treitz)
• Lower GI bleed (LGIB)  (colonic, anorectum)
• obscure bleeding1 ( the small intestine).
1. Sleisenger and Fordtrans Gastrointestinal and Liver disease 11th edition

Severe GI bleeding1 :
• documented GI bleeding(hematemesis, melena,
hematochezia, or positive NG lavage)
• accompanied by shock or orthostatic hypotension,
• a 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
(RBCs).

Causes of UGI Bleeding1

Cause Associated signs and
symptoms
Associated
conditions or risk
factors
Endoscopic findings
Duodenal
and/or gastric
ulcer
Gastroduoden
al artery / left
gastric artery
•Upper abdominal
pain
•Pain associated with
eating (worse when
eating suggests
gastric ulcer,
improvement with
eating suggests
duodenal ulcer)
•Dyspepsia
•Infections:
Helicobacter
pylori
CMV
HSV
•NSAIDs
•Stress ulcer (eg,
in patients who
are critically ill)
•Excess gastric
acid production
(ZES)
•Idiopathic
•Ulcer with smooth,
regular, rounded edges;
ulcer base often filled
with exudate
•Examination of the
ulcer may reveal:
Active bleeding or
oozing
Nonbleeding visible
vessel
Adherent clot
Flat pigmented spot
Clean ulcer base

cause Clinical
presentations
Associated conditions Endoscopic features
Esophago
gastric
varices
Lower
esophage
al veins
(coronary
veins )
stigmata of chronic
liver disease,
signs of portal
hypertension
(splenomegaly,
ascites,
thrombocytopenia)
Portal hypertension from:
•Cirrhosis
•Portal vein thrombosis
•Cryptogenic cirrhosis
(NCPH)
Vascular structures that
protrude into the esophageal
and/or gastric lumen
Findings associated with an
increased risk of hemorrhage:
•Longitudinal red streaks on the
varices (red wale marks)
•Cherry-colored spots that are
flat and overlie varices
•Raised, discrete red spots
(hematocystic spots)
Esophageal varices: (SIZE)
F1: Small, straight varices
F2: Enlarged, tortuous varices
that occupy less than one-third
of the lumen
F3: Large, coil-shaped varices
that occupy more than one-
third of the lumen
Gastric varices:(sarin
classification)
GOV1(70%):Gastroesophag
eal varices along the lesser
curvature of the stomach
GOV2: Gastroesophageal
varices along the greater
curvature of the stomach
IGV1: Isolated gastric
varices in the fundus
IGV2: Isolated gastric
varices at other loci in the
stomach
Bleeding risk:
(IGV1(78%)>GOV2>GOV1),

Cause Clinical
presentation
Associated condition Endoscopic findings
Esophagitis •Dysphagia/odyn
ophagia
•Retrosternal pain
•Food impaction
•Gastroesophageal
reflux disease(GERD)
•Medications that
may cause "pill
esophagitis":
Erythromycin
Tetracycline
Doxycycline
Clindamycin
Trimethoprim-
sulfamethoxazole
NSAIDs
Oral
bisphosphonates
•Infections:
HSV
CMV
Candida albicans
HIV
Peptic esophagitis:
The ulcerations are usually
irregularly shaped or linear,
multiple, and distal; may be
accompanied by Barrett's
esophagus
Pill-induced:
Ulcerations are usually
singular and deep,
occurring at points of stasis
(especially near the carina),
with sparing of the distal
esophagus

causes Clinical findings Associated
conditions
Endoscopic
findings
Ectopic varices
Stigmata of chronic
liver diseaseΔ, in
particular, signs of
portal
hypertension (sple
nomegaly, ascites,
thrombocytopenia)
Portal hypertension
from:Cirrhosis ,
Portal vein
thrombosis ,
Cryptogenic
cirrhosis (NCPH)
Vascular structures
that protrude into
areas of the
gastrointestinal
tract lumen other
than the
esophagus or
stomach (eg, small
bowel, rectum)
Portal hypertensive
gastropathy
Mosaic-like pattern
that gives the
gastric mucosa a
"snakeskin"
appearance

VASCULAR
LESIONS
CLINICAL FINDING ASSOCIATED
CONDITIONS
ENDOSCOPIC FINDINGS
Vascular
Ectasias
slow intestinal blood loss and
occur either in a sporadic
fashion or in a well-defined
pattern of distribution e.g.,
gastric antral vascular ectasia
[GAVE] or “watermelon
stomach”) , Cecal ,rectal
ectasia
chronic renal
failure and
with
hereditary
hemorrhagic
telangiectasia
flat mucosal vascular
Anomalies
Rx.
1.local endoscopic
ablative therapy, such as
argon plasma
coagulation
2. device-assisted
enteroscopy with
endoscopic therapy
or pharmacologic
treatment with
octreotide or
estrogen/progesterone

Causes Clinical findings Associated conditions Endoscopic findings
Mallory-Weiss
syndrome
Left gastric artery
Epigastric pain
Back pain
Spontaneously stops in 80-
90% (submucosal tear ) ,
recurs in only 1-10%
( cardia → LES)
•Vomiting/retching (often
related to alcohol
consumption)
•Straining at stool or
lifting
•Coughing
•Seizures
•Blunt abdominal trauma
•Hiatal hernia may
increase the risk of
developing a tear
•Hyperemesis gravidarum
•Tear in the
esophagogastric
junction (LES)
•Usually singular and
longitudinal, but may be
multiple
•Visualization may
require retroflexion of
the gastroscope in the
cardia
•Can be difficult to
identify at endoscopy
because of the
intermittent nature of
the bleeding of the
stomach
Cameron lesions Linear erosions or
ulcerations in the proximal
stomach at the end of a
large hiatal hernia near the
diaphragmatic pinch
Caused by mechanical
trauma and local ischemia as
the hernia moves
Hiatal hernia
Reflux esophagitis
•Linear ulcers or
erosions on the mucosal
folds of a hiatal hernia
at the diaphragmatic
impression

Vascular lesions Clinical findings Associated conditions Endoscopic findings
Angiodysplasia Hematemesis
Hematochezia
•End-stage kidney
disease
•Aortic stenosis
•Left ventricular assist
device
•Hereditary
hemorrhagic
telangiectasia
•von Willebrand disease
•Radiation therapy
•Idiopathic
small (5 to 10 mm), flat,
cherry-red lesions, often
with a fern-like pattern
of arborizing, ectatic
blood vessels radiating
from a central vessel
Dieulafoy's
lesion
A Dieulafoy’s Lesion is
dilated aberrant
submucosal vessel
that erode the
overlying epithelium
in the absence of
primary ulcer usually
located in gastric
fundus, within 6 cm of
GE junction
Etiology unknown
Bleeding may be
associated with NSAIDs,
cardiovascular disease,
hypertension, chronic
kidney disease,
diabetes, or alcohol
abuse
May have active arterial
spurting from the mucosa
without an associated ulcer
or mass
If the bleeding has stopped,
there may be a raised nipple
or visible vessel without an
associated ulcer
Endoscopic ultrasound may
help confirm the diagnosis

causes Clinical findings Associated conditions Endoscopic findings
Upper GI tumors •Weight loss
•Anorexia
•Nausea/vomiting
•Early satiety
•Epigastric pain
•Dysphagia (for tumors in
the esophagus or proximal
stomach)
•Gastric outlet obstruction
•Palpable mass
•Paraneoplastic
manifestations:
Diffuse seborrheic
keratoses
Acanthosis nigricans
Membranous
nephropathy
Coagulopathy
•Virtually any tumor
type may bleed
•Benign tumors:
Leiomyoma
Lipoma
Polyp (hyperplastic,
adenomatous,
hamartomatous,
inflammatory)
•Malignant tumors:
Adenocarcinoma
GI stromal tumors
Lymphoma
Kaposi sarcoma
Carcinoid
Melanoma
Metastatic tumors
Ulcerated mass in the
esophagus, stomach,
or duodenum

Causes Clinical
findings
Associated conditions Endoscopic conditions
Hemobilia
( most
common cause
– iatrogenic )
•Biliary colic
•Jaundice
(obstructive)
•Sepsis (biliary)
•Past history of liver or
biliary tract
instrumentation and/or
injury, including the
following:
Liver biopsy
Lap.Cholecystectomy
ERCP
Endoscopic biliary
biopsies or stenting
CholangioCa ,Klatskin
Tumor
TIPS placement
Angioembolization
Blunt or penetrating
abdominal trauma
Blood or clot
emanating from the
ampulla (a side-
viewing duodenoscope
may be required to
visualize the ampulla)
IOC : angiography
Rx: gel embolization
Harrison's Principles of Internal Medicine, 20edition
Sleisenger and Fordtrans Gastr.ointestinal and Liver disease 11th edition
A.K.Dutta ,Essenntials of Human Anatomy,9th edition
UpToDate 2022

APPROACH TO PATIENTS
WITH UGI BLEEDING

INITIAL EVALUATION
•Initially evaluated on the basis of History, Physical
Examination, Laboratory test and sometimes NG
tube.
GOAL OF EVALUATION-
1)Assess the severity of bleeding
2)Identify potential source of bleed
3)Identify comorbid condition that may affect
subsequent managemant

presentation of The Patients OF UGI Bleeding
As either overt or occult bleeding
Overt GIB manifested as;
• Hematemesis :proximal to ligament of treitz
• Frankly blood: moderate to severe bleeding
• Coffee-ground: more limited bleeding
• Melena (black tarry stool) - bleeding proximal to the ileo-caecal valve.
• seen in as little as 50 ml of blood
• Blood has to be present in the GI tract for at least 7h and as long as
14days
• Hematochezia: (red or maroon blood in the stool)2
• usually due to LGI bleeding ,Can occur with massive UGIB
(associated with orthostatic hypotension) : >1000 ml1
UpToDate2022 , hutinchsons24 edition, 1.CMDT2022

Occult GIB1 manifested as:
•Symptoms of blood loss or anemia
•Iron deficiency anemia.
• Positive fecal occult blood test on routine testing
• Other clues of UGIB:
• Hyperactive bowel sounds
• an elevated BUN (volume depletion and blood proteins
absorbed in small intestine
Obscure GI bleeding2 - bleeding from a site that is not
apparent after routine endoscopic evaluation with EGD (upper
endoscopy),and colonoscopy, and possibly push enteroscopy.
1.Uptodate2022,
2. Sleisenger and Fordtran's Gastrointestinal and Liver Disease ,11th edition

HISTORY
• Number of episodes, duration and last episode of
hematemesis
• Colour of blood/content in vomitus
• History suggestive of dysphagia/odynophagia/early
satiety/weight loss.
• History of multiple episodes of retching/vomiting preceding
UGIB.
• Colour of stool.

• Past Medical History:
Varices or portal hypertensive
Aorto-enteric fistula
Angiodysplasia
Peptic ulcer disease
Marginal ulcers (ulcers at an anastomotic site)
• Medication history:
NSAID, aspirin, antiplatelet, OAC.
Drug causing pill oesophagitis like doxycycline, oral
bisphosphonates
Bismuth, Iron (can turn stool black).
Uptodate2022

Physical Examination
• Vital Signs(Tachycardia,Hypotension,Tachypnoea)
• 1Signs of hypovolemia:
• Mild to moderate <15% of blood volume loss: Resting tachycardia
• Loss of at least 15%: Orthostatic hypotension
• At least 40%: Supine hypotension
• Icterus, clubbing and Oedema-LIVER DISEASE(possible varices bleed)
• Lymphadenopathy- Virchow’s node suggesting GI Malingnancy, possible
Ca Stomach
• Presence of abdominal pain if severe and a/w rebound tenderness or
involuntary guarding, raises concern for perforation
Uptodate2022

• Abdomen:
 surgical scars, tenderness, and masses.
Signs of chronic liver disease include spider
telangiectasias, palmar erythema, gynecomastia,
ascites, splenomegaly, caput medusae, and
Dupuytren contracture.
Sister Mary Joseph nodules
The skin, lips, and buccal mucosa:
 telangiectasias, which are suggestive of HHT, Or
Osler-Weber-Rendu disease.
Subungual telangiectasias (scleroderma )- GAVE or
UGI
telangiectasias

Pigmented lip lesions may suggest Peutz-Jeghers
syndrome.
Purpuric skin lesions may suggest Henoch-
Schönlein
purpura.
Acanthosis nigricans may suggest underlying
malignancy,
especially gastric cancer.
P/R examination :
Blood, Malena, Blumer’s Shelf

Laboratory Data
• CBC(Hb and Platelets),-Initially HB level checked two-eight
hourly depending upon the condition of the patients
• Blood grouping and cross matching
• LFT-To detect underlying liver disease
• RFT-To detect renal compromise
• (PT/INR)-To look for coagulopathy.
• PBS-
 Acute bleeding: Normocytic RBC
Microcytic RBC or IDA  chronic bleeding
Uptodate2022

• Acute UGIB typically have an elevated BUN to Cr or Urea: Cr
ratio ( >36:1 or >100:1 respectively)
The higher the ratio: more likely is from an upper GI source
Due to decreased renal perfusion and blood is absorbed as it
passes through the small bowel.
• Stool Occult blood test
• Iron Profile(Decreased S.Iron and S.Ferritin And Increase TIBC-
suggestive of IDA).
• Gastrin level-Increase in Zollinger Ellision Syndrome.
Uptodate2022

• ECG if patients complains of chest pain to look for ongoing
angina in setting of UGI bleed.
• NASOGASTRIC LAVAGE-
If History of UGI bleed is doubtful then NG aspirate showing
presence of red blood or coffee ground material conforms
UGI Bleed.
• USG-to look for features suggestive of cirrhosis And mass
lesion
Uptodate2022

General Management
patients presenting to the emergency department with upper
gastrointestinal bleeding (UGIB)
very low risk - risk assessment score with ≤1% ( false negative
rate for the outcome of hospital-based intervention or death
(e.g., Glasgow-Blatchford score = 0–1) → discharged with
outpatient follow-up
The American College of Gastroenterology ,2021

Glasgow-Blatchford score
• hepatic disease as
known history, or clinical and
laboratory evidence, of chronic
or acute liver disease
• cardiac failure as known
history, or clinical and
echocardiographic
evidence, of cardiac failure
The American College of
Gastroenterology ,2021

Modified Glasgow Blatchford Score - GBS
Calculated using only the blood urea nitrogen, Hb, systolic
blood pressure, and pulse
• The score ranges from 0 to 16

HEMODYNAMICALLY UNSTABLE PATIENTS (shock,
orthostatic hypotension)
GENERAL SUPPORT @ ABC
• Closely monitor airway, clinical status, vital signs, cardiac rhythm, urine
output, nasogastric output
• Do NOT give patient anything by mouth
• Establish two large bore IV lines (16 gauge or larger)
• Provide supplemental oxygen (goal oxygen saturation ≥94% for patients
without COPD)
• Treat hypotension initially with rapid, bolus infusions of isotonic crystalloid
(eg, 500 to 1000 mL per bolus.
Uptodate2022

• If fluid resuscitation is unable to increase MAP to 65-70mm
of Hg
• Vasopressors are used
NOREPINEPHRINE-initial dosing of 8-12mcg/min IV and
titrated for the desired BP and
Epinephrine Initial Dose of 100-200mcg/min IV and titrated
according to desired BP.

Blood Product Transfusion
Restrictive RBC transfusion
• threshold of 7 g/dL in hospitalized hemodynamically stable
patients, including critical care patients
• threshold of 8 g/dL in those undergoing orthopedic or cardiac
surgery and those with existing cardiovascular disease
• Threshold of > 8 g/dl in acute coronary syndrome .
• hemoglobin levels in hypotensive patients will be lower after
fluid resuscitation even in the absence of further bleeding,
transfuse hypotensive patients before hemoglobin levels reach
7 g/dL.

restrictive” transfusion 1 “liberal” transfusion
1. Initiating PRBC transfusion
at a hemoglobin threshold
of 7 g/dL and maintaining it at
7-9 g/dl.
2.Significantly lower early
rebleeding and mortality rates
1.Initiating PRBC transfusion
at a hemoglobin threshold of
9 g/dL and maintaining it at 9-
11 g/dL
 Massive transfusion protocol (MTP)2 -Three units of
red blood cells over one hour or any four blood
components in 30 minutes
1.AASLD 2017
2. UpToDate2022

• For severe, ongoing bleeding, immediately transfuse blood
products in 1:1:1 ration of RBCs, plasma, and platelets, as for
trauma patients
• For hemodynamic instability despite crystalloid resuscitation,
transfuse 1 to 2 units RBCs
• Avoid over-transfusion with possible variceal bleeding1
• platelets for thrombocytopenia (platelets <50,000) or platelet
dysfunction (eg, chronic aspirin therapy) or after transfusing four
units of RBCs.
• Correcting INR by the use of fresh frozen plasma or factor VIIa is
not recommended.2
• Coagulopathy not due to cirrhosis with INR >2 transfused with FFP.
1.Uptodate2022,
2.AASLD 2017

• More rapid reversal of anticoagulation can be achieved by use of
Prothrombin complex-concentrate infusion and preferred method
in life threatening /serious bleeding.
• patients taking warfarin, anticoagulation with active bleeding and
INR greater than 2.5, either fresh frozen plasma or four factor
prothrombin complex may be administered
• Endoscopy and hemostatic treatment is done when INR is <2.5
• Can Perform Endoscopy if platelet is >20,000, however if active
bleeding platelets should be >50,000/ml for UGIE.
CMDT2022
Uptodate2022

Endoscopy for UGIB
• patients admitted or under observation in hospital with
overt UGIB, whether predicted to be at low risk or high risk
of further bleeding and death, undergo upper endoscopy
within 24 hours of presentation.
• no benefit of very early endoscopy in high-riskpatients
(resuscitation and attention to other active comorbidities
should be undertaken as necessary before endoscopy )
• Hemodynamically stable patients without severe
comorbidities
(endoscopy as soon as possible within routine hours )
The American College of Gastroenterology

The American College of
Gastroenterology

High dose PPI therapy : defined as > 80 mg daily for > 3 days, given
continuously or intermittently.
• Continuous therapy should be 80-mg bolus followed by 8-mg/hr
infusion.
• intermittent oral or intravenous therapy is 80-mg bolus followed by
40 mg 2–4 times daily.
• Oral administration seems to produce a pharmacodynamic effect
similar to that of equivalent doses of intravenous PPI.
Standard PPI therapy (e.g., oral PPI once-daily) has been
recommended
PPIs promote hemostasis – neutralization of gastric acid leads to the
stabilization of blood clots .
The American College of Gastroenterology,2021

endoscopic therapy in patients with UGIB due
to ulcers.
• endoscopic hemostatic therapy :
1. bipolar electrocoagulation, heater probe, or injection of absolute
ethanol ( strong recommendation )
2. clips, argon plasma coagulation, or soft monopolar
electrocoagulation ( moderate recommendation )
3. epinephrine in combination with another hemostatic modality.
4. powder spray TC-325 ( expensive )
5. Recurrent bleeding after previous successful endoscopic
hemostasis:
over-the-scope clips
repeat endoscopy and endoscopic therapy → If failure
transcatheter arterial embolization (TAE)
surgery
The American College of Gastroenterology.,2021

Endoscopic hemostatic therapy followed by short-term high-dose
PPI therapy in hospital continue on twice-daily PPI therapy until 2
weeks after index endoscopy. (The American College of
Gastroenterology)

The Forrest classification1
(bleeding peptic ulcers )
endoscopic risk stratification
Type I: Active bleeding:
Ia: Spurting hemorrhage
Ib: Oozing hemorrhage
Type II: Stigmata of recent hemorrhage:
IIa: Non-bleeding visible vessel (NBVV )
IIb: Adherent clot
IIc: Flat pigmentation
Type III: Clean-base ulcers

Formation of collaterals and oesophageal varices
and bleeding
In normal condition
Anatomical communication between portal and systemic
circulation are not functional
Development of PHTN
HVPG>10 mm of hg(CSPH)
Portal pressure greater than systemic pressure

Reversal of blood flow from portal circulation to the
systemic venous circulation
Formation of the collaterals and the varices
Thus varices is formed in order to decompress the hypertensive
portal vein and return of blood to the systemic circulation.
HVPG>12mm of hg
Variceal Bleeding

PORTAL HTN AND COMPLICATIONS
•Portal hypertension is a pathological increase in the
pressure gradient between the portal vein and the
hepatic veins.
•hepatic vein pressure gradient(HVPG) more than 5 mm
of Hg is PHTN.
•Variceal haemorrhage, cause of 70% of all upper GI
bleeding events in patients with portal hypertension
•Second most frequent decompensating event after
ascites
•Child A patients – 42% , Child B/C patients – 72% have
gastro-oesophageal varices .
EASL 2018

Portal hypertension (portal pressure > 5mm Hg )
•Normal HVPG is 3-5mm Hg.
•HVPG > 5 but < 10mm Hg – Mild PH
•HVPG > 10mm Hg - CSPH
•HVPG > 12mm Hg - Bleeding
•HVPG > 16mm Hg - high risk of death
•HVPG > 20mm Hg- failure to control bleeding,
early rebleeding, and death HVPG 20mm Hg
predicts .
AASLD 2017

Endoscopic grading of esophageal varices (Japanese
Research Society for Portal Hypertension).
Predictors of the risk of variceal hemorrhage
1. LOCATION OF THE VARICES-
• The esophageal varices in the GEJ have the thinnest layer of the
supporting tissue and more likely to rupture and bleed.
• Bleeding from the isolated gastric varices in the fundus(IGV1)
occurred more frequently than either GOV or isolated varices at
other loci in the stomach(IGV2)

Gastric varices:
• GOV1: Gastroesophageal varices along
the lesser curvature of the stomach
• GOV2: Gastroesophageal varices along
the greater curvature of the stomach
• IGV1: Isolated gastric varices in the
fundus
• IGV2: Isolated gastric varices at other
loci in the stomach
• Bleeding risk:
• (IGV1>GOV2>GOV1),

2. SIZE OF THE VARICES
• The risk of variceal haemorrhage is independently related with
the size of the varices;
 F1(Grade1)-small straight varices
F2(Grade2)-Enlarged tortuous varices that occupy less than
1/3rd of lumen
F3(Grade3)-Large, coil shaped varices that occupy more than
1/3rd of the lumen.
• The management of F2 and F3 varices are same.
• Thus now it is classified as Small varices(<5mm in
diameter)and Large(>5mm in diameter)

3. APPEARANCE OF THE VARICES-
• Increased risk of the
haemorrhage.
RED WALE MARKS; are
longitudinal whip like red
streaks on varices that
resemble red corduroy wales.
CHERRY RED SPOTS(2-3mm or
less in diameter)
HEMATOCYSTIC SPOTS(Blood
filled blister 4mm or more in
diameter)
 DIFFUSE ERYTHEMA

Ectopic varices: Vascular structures that protrude into areas of the
gastrointestinal tract lumen other than the esophagus or stomach (eg, small
bowel, rectum)
Diulafoys lesion : May have active arterial spurting from the
mucosa without an associated ulcer or mass.
A persistent caliber artery is present in the gastric submucosa,
immediately beneath the mucosa.

• Mallory-Weiss Tear 2 : linear mucosal rent near or across the
gastroesophageal junction that is often associated with
retching or vomiting.
• Endoscopy is the best method for diagnosis.
• Portal hypertensive gastropathy 1: Mosaic-like pattern that
gives the gastric mucosa a "snakeskin" appearance
• Hemobilia: Blood or clot emanating from the ampulla of vater.
1.Sleisenger and Fordtrans Gastr.ointestinal and Liver disease 11th edition
2.Harrison's Principles of Internal Medicine, 20edition

Risk Stratification
• Endoscopic, clinical and lab features may be useful for risk
stratification of UGIB
• Factors associated with rebleeding identified in a meta-analysis
included
Hemodynamic instablilty (SBP <100, HR>100)
Hb <10 g/dl
Active bleeding at time of endoscopy
Large ulcer size (greater than 1 – 3 cm)
Ulcer location (posterior duodenal bulb or high lesser gastric
curvature)

The Rockall Score
The most commonly used postendoscopy scoring system is
the Complete Rockall Score
Consists of two parts:
• Pre-endoscopy, also known as clinical Rockall score
• Post-endoscopy, which is called the Rockall risk score
• Score after endoscopic therapy correlates well with
mortality
A score of 0-2 is associated with a low risk of further
bleeding or death
Risk Scores

The Rockall Score

AIMS65
Uses data available prior to endoscopy:
• 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
• High accuracy for predicting inpatient mortality BUT less
sensitive than Blatchford and pre endoscopic Rockall score for
identifying low-risk patients.
• 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

Endoscopic Treatment Methods
• Injection therapy is most commonly performed with a sclerotherapy
needle and submucosal injection (dilute epinephrine  local
tamponade and vasospasm)
• Thermal contact probes physically tamponade a blood vessel to stop
bleeding and interrupt underlying blood flow; thermal energy is then
applied to seal the underlying vessel
• Endoscopic hemoclips (or clips) serve to apply mechanical pressure to a
bleeding site
• Hemostatic spray is a proprietary inorganic powder with clotting
abilities that can create a mechanical barrier that adheres to and covers
a bleeding site

Second-look Endoscopy
• The 2010 International Consensus Recommendations for the
management of patients with non-variceal upper gastrointestinal
bleeding do not recommend routine use of second-look
endoscopy
• Situations that might warrant a second-look endoscopy include:
If visualization during the initial endoscopy was limited by blood
or debris
If there is concern on the part of the endoscopist that the prior
endoscopic therapy was suboptimal
• If active bleeding / non bleeding visible vessel present 
endoscopic therapy performed

High-risk varices
• medium/large varices - varices that do not collapse with
insufflation at endoscopy
• Small varices with red signs
• Small Varices in Child C
Screening Endoscopy should be repeated every year if
decompensation continues.
Without secondary prophylaxis, rebleeding occurs in approximately
60% to 70% of patients, usually within one to two years of the index
haemorrhagic event.
EASL 2018

Primary prophylaxis :
•Non selective B blocker for patients with cirrhosis
who have high-risk varices. ( NSBB > EBL)
•High doses of NSBB should be avoided in severe or
refractory ascites
•Progressive hypotension (systolic BP <90 mmHg),
bleeding, sepsis, SBP or AKI, NSBBs should be
discontinued.
•If intolerant to NSBB → EBL recommended.

Ballon occluded retrograde
transvenous obliteration

acute variceal hemorrhage
Goals of therapy:
• control of bleeding
• Prevention of early recurrence
• prevention of six-week mortality
 Must be suspected in any cirrhotic patient presenting
with upper acute GI bleeding (up to 30% of cirrhotic
patients bleed from non-variceal causes )1
Mortality 2 - patient with cirrhosis presents with VH
 isolated decompensating event (20%)
complications of cirrhosis (ascites or encephalopathy;
over 80%).
1.EASL 2018
2.AASLD 2017

Management of acute GIB in patients with cirrhosis
EASL 2018

DRUG THERAPY :
Analogues of somatostatin (octreotide, vapreotide)
•Longer half life than somatostatin
•Given as iv infusion of 50 mcg/h, after an iv bolus of 50 mcg,
up to 5 days
• Octreotide is not recommended for routine use in patients
with acute non-variceal upper GI bleeding
Terlipressin :
•Induces marked splanchnic vasoconstriction and increase
intrarterial pressure
•recommended dose of terlipressin is 2 mg/4 h during the first 48
h, followed by 1 mg/4 h thereafter (total 5 days )
EASL 2018

Drug Recommended Dose Duration
Octreotide
(SMT
analogue)
Initial IV bolus of 50 micrograms (can be
repeated in first hour if ongoing bleeding)
Continuous IV infusion of 50 mg/hr
2-5 days
Terlipressin
(VP analogue)
Initial 48 hours: 2mg IV every 4 hours until
control of bleeding
Maintenance: 1mg IV every 4 hours to prevent
rebleeding
2-5 days
SMT Initial IV bolus 250 mg (can be repeated in the
first hour if ongoing bleeding)
Continuous IV infusion of 250-500 mg/h
2-5 days
AASLD 2017

Antibiotic prophylaxis
• it reduces the incidence of infections and improves control
of bleeding and survival.
• Bacterial infections are observed in more than 50% of
patients and may already be present at the time of bleeding.
• Independent predictor of failure to control bleeding and
death.
• the first choice is Ceftriaxone (1 g/24 h) for up to seven days.
• Oral quinolones (norfloxacin 400 mg b.i.d) can be used.
Proton pump inhibitors (PPIs) have not shown efficacy for
the management of AVH.
EASL 2018

ENDOSCOPY IN AVH
• upper endoscopy should be performed, as soon as possible
within the first 12 h after admission.
• Erythromycin should be considered before emergency
endoscopy (250 mg i.v., 30–120 min before)- improves
visibility.
• The combination of endoscopic therapy ( EBL & glue ) and
vasoactive drugs is currently considered the standard of
care.
• persistent bleeding or early rebleeding – TIPS should be
considered as the rescue therapy of choice.
• early TIPS should be considered in patients with Child-Pugh
class C, with a score <14.
• Balloon tamponade in case of massive bleeding , can be
instituted and for a maximum of 24 hr.(Bridge )
EASL2018

Secondary prophylaxis :
•Combination therapy of NSBBs (propranolol/
nadolol) + EBL
•If intolerant to NSBB, covered TIPS placement
•Patients who have a TIPS placed successfully during
the acute episode do not require NSBBs or EVL.
•The use of carvedilol can not be recommended at
present recommended
EASL 2018

(Gastric varices- 20% )gastro-oesophageal varices
type 2 or isolated gastric varices type 1 /
(cardiofundal varices)/ (GOV 2 & IGV1)
• More frequent in patients with portal vein and/or splenic
vein thrombosis.
• NSBBs are suggested for primary prevention.
• Cyanoacrylate (glue ) is the recommended endoscopic
haemostatic treatment.
• TIPS with potential embolisation efficiently controls
bleeding.
EASL 2018

Transjugular Intrahepatic Portosystemic Shunt (TIPS)
• An expandable metal stent is placed via percutaneous insertion
between the hepatic and intrahepatic portal veins
• Effective for short term control of bleeding gastroesophageal
varices (those that fail endoscopic therapy) and Long term
prevention of rebleeding
• Recommended in recurrent and refractory ascites.
• Problems:
1. Hepatic encephalopathy, which can occur in up to 50% of
patients.
2. TIPS dysfunction - stent thrombosis and stenosis can develop in
up to 80% of cases
reduced with the use of polytetrafluoroethylene (PTFE)-covered
stent grafts of 8 mm.
EASL 2018

Tranexamic Acid
•An antifibrinolytic agent
•associated with an increase in venous
thromboembolic events (deep vein thrombosis,
pulmonary embolism) and seizures compared with
placebo
•no role for tranexamic acid in the treatment of
upper GI bleeding.
UpToDate 2022

Ugi bleeding muneshwar

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