upper G I Bleed (non variceal)

Dr. Balvir Singh
Professor
P. G. Deptt. Of medicine
S.N. Medical College ,Agra

UGI BLEED
 It is defined as bleeding from gastrointestinal tract proximal to
ligament of Trietz.
 It usually manifests as hematemesis or melena, and when severe,
may even lead to hematochezia.
 Clinical guidelines are recommended to predict out -come,
including rebleeding, and mortality.
 Stigmata of a recent hemorrhge are endoscopic finding that
predict outcome.
 Endoscopy can provide the diagnosis,prognosis,
and the potential for therapy. Medicine update 2013
API

Features Hemoptysis Haematemesis
Definition Coughing out of blood Vomiting out of blood
Symptoms Symptoms of pulmonary
and CVS disease
Symptoms of upper GI
tract diseases
Content & colour Mixed with sputum &
bright red in colour
Mixed with food particles
& coffee-ground in colour
Premonitory symptoms Cough, salty sensation in
throat
Nausea , vomiting,
retching, abdominal
discomfort.
Melaena Does not occur Usually followed by
melaena the next day
Amount Relatively less Huge in amount
Reaction Alkaline(Blue litmus
remain unchanged)
Acidic(Blue litmus
remains unchanged

UGI BLEED
 Upper vs Lower GI bleeding = 5:1
 Incidence: 170 patients/ 100,000 population /year(usa data).
 40% due to peptic ulcer(Most common).
 80% are self-limited.
 Pts on anti platelet therapy has two fold increase in bleed as compared to normal
ones(annual UGI Bleed incidence-.13%).
 20% of pts of moderate to high risk, who have recurrent bleeding (within 48-72 hrs)
have poor prognosis.
 The mortality rate is 5% to 10% for severe UGI bleed. (Barkun A, Sabbah S, Enns R, et al:Am J
Gastroenterol 2004; 99:1238-46)
Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition
:(Acute upper gastrointestinal bleeding in adults. Author. John R
Saltzman,:current gastroenterology updates 2013)

Clinical Features
1)Features due to blood loss :
1.Haemetemesis,malena or haematochezia , Hyperactive bowel sound.
2.H/O CLD presenting with shock.
3. H/O ESRD with sudden derange RFTs.
4. Features of co-morbid illnesses - IHD, COPD, CHF,SEPTICEMIA,PT ON
VENTILLATORY SUPPORT.
O/E:
1. Anemia
2.Orthostatic changes of BP and HR
3.Shock
Other Clues
-Raised BUN (Due to volume depletion and absorption of blood
protein)

b ) Features due to underlying cause:
Cause Features
Peptic ulcer Epigastric burning pain
Varices Vague right upper quadrant pain, fever, nausea,
vomiting, ascites, edema.
Features of hepatic failures
Oesophagitis Heartburn, regurgitation, chest pain,
dysphagia, odynophagia, and globus sensation.
Mallory weiss tear Excessive retching,Vomiting, or coughing
preceding hematemesis after alcohol intake.

CAUSES OF SEVERE UGI BLEED
Peptic ulcer 38 %
Esophagitis 13
No cause found 8
Upper gastrointestinal tract tumor 7
Angioma 6
Mallory weis tear 4
Erosions 4
Dieulafoy’s lesion 2
Other 2
Variceal bleed Non variceal bleed
Oesophageal varices
& Gastric varices
16%
Barkun A, Sabbah S, Enns R, et al Am J Gastroenterol 2004; 99:1238-46

Uncommon Causes of non variceal bleed (< 5%)
 Gastroesophageal reflux disease
 Trauma from foreign body
 Esophageal ulcer
 Cameron lesion
 Stress ulcer
 Drug induced erosions
 Angioma
 Watermelon stomach
 Portal hypertensive gastropathy
 Aorta-enteric Fistula
 Radiation telangiectasis/ Enteritis
 Benign tumours
 Malignant tumour
 Blue rubber bleb nevus syndrome
 Osler-Weber-Rendu syndrome
 Haemobilia
 Hemosuccus pancreatitis
 Infections(CMV,HSV)
 Stomal ulcer
 Zollinger-ellison syndrome
:Acute upper gastrointestinal bleeding in adults. Author. John R
Saltzman,:current gastroenterology updates 2013

DIAGNOSIS
HISTORY EXAMINATION
EMERGENCY ENDOSCOPY???

 History
 Helpful to find out the site and cause
 History suggestive of acid – peptic disease
 Alcoholic liver diseases / chronic hepatitis / Cirrhosis
 History of anticoagulant / anti platelets / NSAIDS /
Alcohol binge intake / steroids
 History of Coagulation disorder / Blood Dyscrasias
 History of Epistaxis or Hemoptysis to rule out the GI
source of bleeding
 Patients of CVA, BURN, Sepsis, Head Trauma may
have stress ulcers

ON EXAMINATION
 VITALS
 Pulse = Thready,BP = Orthostatic Hypotension
 SKIN changes
 Cirrhosis – Palmer- erythema, spider angioma
 Bleeding diasthasis – Purpura /Echymosis
 Coagulation Disorder – Haemarthrosis, Muscle
Hematoma
 ENT :- Look for clots (To rule out epistaxis P.N BLEED)
 P/A :-
 Liver , Spleen, Caput Medusa = Cirrhosis
 Epigastric Tenderness = APD/ Ulcer
 Respiratory, CVS, CNS  For comorbid diseses

Diagnostic Workup
 CBC
 Bleeding &Coagulation profile
(BT, CT,PT, a PTT)
 Liver Function Test
 Complete S. Biochemistry
 Relevant lab test for underlying
disease
BLOOD INV. ENDOSCOPY RADIO-IMAGING
• Barium Meal F.T.
• Arteriography
• USG/ Doppler USG
• Radio nucleotide study
(Tagged RBC scan)

RISK FACTORS AND RISK
STRATIFICATION
-To identify patients with nonvariceal UGI bleeding
at greatest risk for mortality and rebleeding.
-Pts may be categorised as low, intermediate and high risk
Pre-endoscopy scoring systems Postendoscopy scoring
system
Blatchford Score: BP,BUN level, Hb,
Heart rate , syncope, Melena ,liver
disease , Heart failure
Clinical Rockall Score: Patient’s age ,
shock & coexisting illnesses
Artificial neural network score: 21
variables
Complete Rockall Score:
Clinical Rockall score +
endoscopic findings.
* Correlates well with mortality
& risk of rebleeding.

Blatchford scoring system( pre
endoscopic assesment)
Variables Points
* SBP(mm Hg)
100-109 1
90-99 2
<90 3
* BUN (mg/dl)
39.0-47.4 2
48.0-59.4 3
60.0-149.4 4
>150 6
* Hb(men;g/dl)
12.0-12.9 1
10.0-11.9 3
<10.0 6
* Other variables
pulse >100 1
Presentation with melena 1
Hepatic disease 2
Cardiac failure 2
Most patients need
intervention if
their score is 6 or
higher.
Blatchford O, Murray WR, Blatchford M: Lancet 2000; 356:1318-21.

ROCKALL SCORING SYSTEM
Variable Points
0 1 2 3
Age(yr) <60 60-79 >80 -
Pulse rate <100 >100 - -
Systolic BP Normal >100 <100 -
Comorbidity None - IHD, Cardiac
failure.
Renal failure,
hepatic failure
, metastatic
cancer.
Diagnosis Mallory Weiss
tear or no lesion
observed
All other
diagnosis
Malignant
lesions
-
Endoscopic
stigmata
No stigmata or
dark spot in
ulcer base
- Blood in UGI
tract , visible
vessel etc
-
Rockall TA, Logan RF, Devlin HB, Northfield TCGut 1996; 38:316-21.

Total score Mortality rate(%) Rebleeding rate(%
0 0 4.9
1 0 3.4
2 0.2 5.3
3 2.9 11.2
4 5.3 14.1
5 10.8 24.1
6 17.3 32.9
7 27.0 43.8
≥8 41.1 41.8
Risk category:
High (> 5)
Intermediate (3–5)
Low (0–2)
Rockall TA, Logan RF, Devlin HB, Northfield TCGut 1996; 38:316-21.

Management as per risk
 1- Low risk(0-2)-Usually 80 % of the pt recovers
spontaneously with medical Tt( PPI)+ Hospitalisation
for 24 hrs and may be discharge if uneventful.
 2-Intermediate risk(3-5)- same Tt + Hospitilisation for
atleast 72 hrs.
 3- High risk(>5%)- Same Tt+ Hospitilisation in I.C.U.

Objectives in Acute GI bleeding:
Immediate Assessment
Stabilization of hemodynamic status
Identify the source of bleeding
Stopping the active bleeding
Treat the underlying
Prevent recurrent bleeding

Management of UGIB
GENERAL MEDICAL
MANAGEMENT
TYPE OF BLEEDING
VARICEAL
BLEEDING
NON VARICEAL
BLEEDING
MEDICAL ENDOTHERAPY
SURGICAL
INERVENTION
PRESSURE
TECHNIQUES

ENDOSCOPIC MODALITIES AVAILABLE FOR THE
MANAGEMENT OF U.G.I. BLEED
 INJECTION
 Adrenalin
 Fibrin glue
 Human Thrombin
 Sclerosants
 Alcohol
 THERMAL
 Heater Probe
 Bicap Probe
 Gold Probe
 Argon plasma
coagulation
 Laser therapy
 MECHANICAL
 Haemoclips
 Banding
 Endoloops
 Staples
 Sutures

NON VARICEAL
BLEED Mt
ENDOSCOPIC
MANAGEMENT
1.INJ.EPINEPHRINE
2.HAEMOCLIPS
3.LOOP LIGATION
4.CAUTERY :
• MONOPOLAR
• BIPOLAR
• APC
OTHERS
1.INTERVENTIONAL
RADIOLOGICAL PROCEDURES
2.TRANS CATHETRAL ARTERIAL
EMBOLISATION
Ripoll C, Banares R, Beceiro I, et al
2004; 15:447-50 :
3.SURGICAL INTERVENTION
• WITH ENDOSCOPE
• WITHOUT ENDOSCOPE

AUGIB
Rapid Assessment
Monitor Hemodynamic Status
Fluid Resuscitation
Ryle;s tube for Gastric Lavage
Self Limited Hemorrhage (80%) Continued bleeding (10-25%)
Urgent endoscopy
Recurrent Hemorrhage
Elective Endoscopy
(With in 24 – 48 hours)
Definitive Therapy
(If Necessary)
Site not localized Localized
Further Assessment
(Extended EGD,
Radio-isotope scan,
Arteriography,
Exploratory
Laprotomy)
Definitive
Therapy

 FLUID RESUSCITATION
 Vitals are monitored
 Assessment of severity of blood loss :- An orthostatic decrease of 20 mm Hg
in systolic blood pressure or increases in the pulse of 20 beats / min.
indicate – 10% blood loss, if pt is pulsless and in shock- > 20% loss.
 Order hemoglobin, hematocrit, BUN, grouping and cross matching of
blood.
 Insertion of central venous line may be beneficial to measure adequacy of
fluid replacement and perfusion of vital organ .
 Monitor urine output.
 Fluid resuscitation is done by crystalloids such as normal saline or RL if
hypoalbuminemia is detected use colloids.
 Placing the patient in trendelenburg position to maintaine cerebral blood
flow.
General Management

General Management
1.Oxygen support to prevent hypoxia of tissues
2.IV route - Crystaloid solution/Colloids|blood.
3. Blood transfusion:
 maintain Hct at 30% in the elderly, esp. with comorbid deseases eg. CHF,
CRF, IHD,COPD)
 20-25% in younger pt
 25-28% in portal HTN
 administration of vit k
4.In symptomatic thrombocytopenia (<50000 )infused platelets.
5.FFP-The transfusion of plasma should not be based solely on the patient’s
abnormal INR and/or PTT.
The decision to transfuse should be based on the patient’s clinical
condition. Wong et alBCMJ, Vol. 49, No. 6, July, August 2007, page(s) 311-319 Articles

A. MEDICAL THERAPY
 H2B vs PPI
 H2 blockers are not as effective as PPI
*Proton pump inhibitors-
-its use is widely adopted and is mandatory in all UGIBleed.
-PPIs are the only drugs that can maintain a gastric
pH >6 and thus prevent fibrinolysis of clot
- In patients initially treated with a bolus infusion
of omeprazole/ pantaprazole 80 mg followed by a continous
infusion 8mg/hr ,and the need for endoscopic therapy has
reduced.
- PPI+ Endotherapy shown the best results in terms of
rebleeding, morbidity and mortality.(Sung JJ, Mossner J, Barkun A, et alAliment
Pharmacol Ther 2008; 27:666-77. : )

- OMEPRAZOLE/PANTOPRAZOLE- 80 mg bolus followed
by 8 mg/h infusion for 72 hrs.(Khuroo MS, Yattoo GN, Javid G, et al: N Engl J
Med 1997; 336:1054-8.)
- ? H2 antagonist /Sucralfate has not been shown to be
effective in UGI bleed
* Octreotide/Somatostatin:
-A meta-analysis has suggested that intravenous
administration of somatostatin or its long-acting form
octreotide decreases the risk of rebleeding from peptic
ulcers when compared with placebo or an H2 receptor
blocker.(A meta-analysis. Ann Intern Med 1997; 127:1062-71)
 The use of octerotide should be considered in pts who have
persistent bleeding even on optimal medical management.
-
(Collins R, Langman M: Treatment with histamine H2 antagonists N
Engl J Med 1985; 313:660-6).

Identify bleeding source
(Pre- requisites for endoscopy):
Bloody endoscopy field
1. Naso-gastric tube(RT. esp. Wide bore) –
 coffee coloured/clots/fresh blood
 aspirate may categorize these pts- Low/ Intermediate/High
2. Gastric Lavage –
 saline with or without H2O2
 prokinetic(erythromycin, metchlopromide) agents may be used.
 color and rapidity of clearing: clear fluid indicates absence of GH
and pt may be subjected for endoscopy.
3. Risk of aspiration (insure airway/ E.T tube).

NASOGASTRIC LAVAGE
 Benefits of lavage :
 Better visualization during endoscopy.
 Give crude estimation of rapidity of bleeding.
 Prevent the development of porto systemic encephalopathy in
cirrhosis.
 Increases PH of stomach and hence decreases clot
desolution due to gastric acid dilution
 During gastric lavage use saline and not use large volume of
to avoid water intoxication.
 Gastric lavage should be done in alert and cooperative
patient to avoid broncho-pulmonary aspiration

NASOGASTRIC LAVAGE
 If gastric aspirate either is grossly bloody or yields
coffee ground effort should be made to lavage the
stomach before proceeding to diagnostic or
therapeutic endoscopy.
 The presence of bloody gastric aspirate confirms UGI
Bleed.
 A negative aspirate (16%) does not exclude an upper
bleeding. For Example in case of duodenal ulcer due to
absence of duodenogastric reflux aspirate is clear

B. Endoscopic therapy
1. Urgent vs elective endoscopy: < 12 hrs
2. Studies have not found overall advantage of early
endoscopy (<12 hrs) in terms of rebleeding, need for
surgery or mortality.
3. However persistent active bleeding may recquire
urgent endotherapy.
4. Elective endoscopy: Within 24-48 hrs of bleeding.

 Endoscopy can offer therapeutic options including:
injections , cautery , placement of endoclips or a
combination of therapies.
1. ENDOSCOPIC STIGMATAS OF RECENT
bhhaahahahhhHHAEMMHEMORRHAGE:Stigmata Risk of rebleeding (%) Mortality(%) Prevalence (%)
Active arterial bleeding 55-90 11 10
Non bleeding visible
vessel
40-50 11 25
Adherent clot 20-35 7 10
Oozing 10-25 NA 10
Flat spot <10 3 10
Clean ulcer base <5 2 35
HAEMORRHAGE

 2.UTILITY OF ENDOSCOPIC THERAPY
 Must for diagn.&therapeutic
* Endoscopic therapy resulted in a significant
improvement in:
Hemostasis , number of units of blood transfused , no. of
emergency interventions, hospital stay & hospital costs.
* In the managment of adherent clots ,endoscopic therapy show
improvement when compared with PPIs
* Mortality rate is lower in group treated with endoscopic
therapy + PPI as compared to alone. .(Sung JJ, Mossner J, Barkun A, et al Aliment
Pharmacol Ther 2008; 27:666-77. : )

 3.OPTIMIZING ENDOSCOPIC VISUALIZATION
* Visualization of blood within the GI tract is a
challenge in managing patients with GI bleed.
* This problem can be overcome by using:
- double channel or large channel endoscopes,
which allow for vigorous aspiration.
- i.v erythromycin(250mg bolus) can be used as a
prokinetic drug to clear the stomach of blood, it
is given 30-120 minutes prior to endoscopy

 4. METHODS TO CONTROL BLEEDING
Current endoscopic modalities are:
* Injection therapies (primarily with dilute epinephrine)
* Contact thermal therapies – heater probes,mono &
bipolar cautery.
* Noncontact thermal methods (argon plasma coagulation)
* Mechanical treatments- endoclips,loop/ band ligation
techniques.
* Combination of above treatment modalities

 INJECTION THERAPY
* Reduce blood flow by local tamponade.
* Use of vasoconstricting agents, eg epinephrine
further reduce blood flow.
(inject 0.5- to 1.0-mL aliquots of epinephrine (1 : 20,000) via a sclerotherapy
needle into four quadrants of the ulcer within 1 to 2 mm of the bleeding site )
* Other agents used – sclerosants like ethanolamine
& thrombogenic agents( less efficacious).
* injection therapy not as efficacious as other modalaties of
monotherapies.

 CONTACT THERMAL THERAPY
monopolar cautery – currently not in use
* Bipolar cautery - Thermal modality used most
extensively.
* It has the advantage over heater probes as it can be
used perpendicularly or tangentially.
* Bleeding vessel is compressed and then coagulated.
* Low wattage (10-15 watts in duodenum; 15-20 in
stomach) is used for a prolonged time (8-12 second
pulses) .
* End point of treatment is when involoved vessel
flattens out & there is no bleeding.

 MECHANICAL TREATMENT
- therapy of choice in obvious arterial bleeding.
* Endoscopic hemoclips are widely used.
* Has theoretical advantage over cautery of not
causing further tissue damage.
* Rebleeding rates are reduced with endoclips
 COMBINATION THERAPIES
* Typically involve injection therapies with
thermocoagulation technique.
* Combination therapy appears to provide durable
control of bleeding than monotherapies

 SECOND LOOK ENDOSCOPY
* Routine second-look endoscopy is not recommended for
most patients with peptic ulcer bleeding.
* Typically done 24 hours after the initial endoscopy.
* Any persistent stigmata of haemorrhage are treated.
* It is beneficial in certain circumstances, especially
after injection monotherapy.
Barkun A, Bardou M, Marshall JK: Ann Intern Med 2003; 139:843-57.

Impact of anticoagulation on rebleeding
 Anticoagulation should be stopped immediately.
 The prescence of mild to mod anticoagulation(INR 1.3-
2.7) did not appear to alter the outcomes of endoscopic
therapy.(wolf AT,Wasan SK,saltzman JR 2004;99:1238-1246)
 Patients who require an antiplatelet medication and
have a history of ulcer bleeding will have less chance of
recurrent bleeding if they take aspirin 81 mg and a PPI
daily compared with clopidogrel alone.
Chan FK, Ching JY, Hung LC, et al: Clopidogrel versus aspirin and esomeprazole N Engl J
Med 2005; 352:238-44

Adverse prognostic factor in UGIB
1. Age over 60
2. Shock(SBP<100mmhg), pulse >100
3. Malignancy or varices as bleeding source.
4. Sever coagulopathy
5. Comorbid medical illness
6. Continued or recurrent bleeding
7. Severe active Bleeding (Hypotension, multiple
transfusion, bright red nasogastric aspirate)
8. Endoscopically identified arterial bleeding or visible vessel
9. Ulcer location
10. Emergency surgery if surgical complication
Medicine update 2013
API

Treatment of Pt with recurrent Gastrointestinal
bleeding
Initial Control
Endoscopic
therapy
Permanent
Control
Rebleeding
Endoscopic
therapy
Rebleeding
Surgery Angiography
Permanent
Control
80-90%
50%

TAKE HOME MESSAGE
 Early Resucitation.
 Nasogastric wash + look for GH.
 High dose PPI therapy for at least 72 hrs.
 Urgent Endoscopic therapy for mod to severe UGI bleeding.
 Nonvariceal bleeding should be treated with either:
- Combination therapy using an injection of dilute
epinephrine combined with a thermocoagulation
OR
- Endoclip (with or without injection therapy)
 Combination therapy preffered along with medical management.
 Relook endoscopy should be preffered only for mod to severe
bleeding.
 Pt should also be treated for specific cause/disease.

PEPTIC ULCER
 PATHOGENESIS:
Due to decrease in mucosal defense mechanism:
aspirin, other NSAIDS, H.Pylori or both.
H.PYLORI: NSAIDS:
* involves antrum * gastric ulcers > common
*duodenal ulcers * 15-45% patients develop
* 3%(USA) & 25%(Japan) ulcers on regular use
lifetime risk of peptic ulcer

PEPTIC ULCER
SOURCE PREVALENCE
DUODENAL ULCER 24.3%
GASTRIC EROSIONS 23.4%
GASTRIC ULCER 21.3%
MALLORY-WEISS TEAR 7.3%
ESOPHAGITIS 6.3%
EROSIVE DUODENITIS 5.8%
:American society for gastrointestinal
endoscopy bleeding survey of 2225 pts

 Endoscopic risk stratification: (FORREST
classification)-
IA: Active spurting bleeding
IB: Oozing bleeding
IIA: Pigmented protuberance
IIB: Adherent clot
IIC: Flat pigmented spot
III: Clean based ulcer

Gastric antral ulcer with a clean base

Duodenal ulcer with flat pigmented
spots

Duodenal ulcer with a dense
adherent clot

Duodenal ulcer with active spurting
(arrow)

 High risk of rebleeding :
*active arterial bleeding(90%)
*nonbleeding visible vessel(50%)
*adherent clot(33%)
 Lower Risks:
1. flat red or black spot
2. clean based ulcer

 Doppler Probe Ultrasound :
* passed through working channel of endoscope .
* used to determine if blood flow is present beneath
a stigma in the ulcer base.
* preferred cost minimizing strategy over
conventional endoscopic therapy

(b) Adherent clots:
--endoscopic therapy (5% rebleeding rate) :
epinephrine rotatable cold snare to guillotine the
clot
-- medical therapy (upto 35% rebleeding rate).
(c) Clean –based ulcers:
--after target irrigation have rebleeding rate of <5%
-- do not require endoscopic therapy.
-- biopsies should be considered to exclude
malignancy

ALOGRITHM FOR MANAGEMENT OF ULCERS AND ACUTE
GASTROINTESTINAL BLEEDING
ULCER
OVERLYING
CLOT
IRRIGATE
ADHERENT
CLOT
CLOT
REMOVAL
ACTIVE BLEEDING
OR VISIBLE VESSEL DARK/PIG
MENTED
RED SPOT
CLEAN
BASE
MEDICAL
THERAPY
ENDOSCOPIC
INTERVENTION
SUCCESSFUL
NOT
SUCCESSFUL
ICU 1 DAY
HOSPITAL
FOR 3 DAYS
ANGIOGRAM
OR SURGERY
REBLEEDING
MEDICAL
THERAPY
EPINEPHRINE INJ
/ CLOT REMOVAL
:American society for gastroenterology 2001;53:853-

PHARMACOLOGICAL THERAPY
DRUG TYPE EXAMPLES DOSE
ACID SUPPRESSING DRUGS
a ) Antacids Mylanta, Tums 100-140 meq/l
b ) H2 receptor antagonists Cimetidine 400 mg bid
Ranitidine 300 mg hs
Famotidine 40 mg hs
Nizatidine 300mg hs
c) PPIs Omeprazole 20mg/d
Lansoprazole 30mg/d
Rabeprazole 20mg/d
Pantoprazole 40mg/d
Esmoprazole 20mg/d
MUCOSAL PROTECTIVE AGENTS
a) Sucralfate Sucralfate 1g qid
b) Prostaglandin analogue Misoprostol 200µg qid
c) Bismuth –containing compounds BSS
Harrison's™ PRINCIPLES OF INTERNAL MEDICINE Eighteenth Edition

Regimens for Eradication of H. Pylori Infection
DRUG DOSE
TRIPLE THERAPY(14 days)
1.BISMUTH SUBSALICYLATE PLUS 2 TAB. qid
• METRONIDAZOLE PLUS 250 mg qid
• TETRACYCLINE 500mg qid
2.RANITIDINE BISMUTH CITRATE PLUS 400mg bid
• TETRACYCLINE PLUS 500mg bid
• CLARITHROMYCIN OR
METRONIDAZOLE
500mg bid
3.OMEPRAZOLE PLUS 20 mg bid
CLARITHROMYCIN PLUS 250 or 500 mg bid
METRONIDAZOLE OR 500mg bid
AMOXICILLINE 1gm bid
QUADRUPLE THERAPY(7-10 days)
OMEPRAZOLE(LANSOPRAZOLE) 20mg(30mg) od
BISMUTH SUBSALICYLATE 2 tab. qid
METERONIDAZOLE 250 mg qid
TETRACYCLINE 500mg qid
Harrison's™ PRINCIPLES OF INTERNAL MED
18th Edition

ANGIOGRAPHY & SURGERY
Indications:
* Pt having large ulcer(>2cm) or ulcers in a location associated
with large arteries.
* Recurrent bleeding despite two sessions
of endoscopic hemostasis.
* Exsanguinating bleeding
* If the endoscopist does not feel comfortable
treating a large pulsating visible vessel
* Locally confined bleeding malignant
ulcerated mass.
SURGERY
Angiographic
interventions/surgery

MALLORY WEISS SYNDROME / TEARS
 Mallory-Weiss tears are mucosal or submucosal
lacerations that occur at the gastroesophageal junction
and usually extend distally into a hiatal hernia .
 Patients generally present with hematemesis or coffee-
ground emesis after alcohol intake.
 Typically have a history of recent nonbloody vomiting
with excessive retching followed by hematemesis..
 Endoscopy usually reveals a single tear that begins at the
gastroesophageal junction and extends several millimeters
distally into a hiatal hernia sac/within cardiac portion of
stomach.
Sleisengerand Fordtran's Gastrointestinal and Liver
Disease Ninth Edition

Mallory-Weiss tear at the
gastroesophageal junction.

 Occasionally, more than one tear is seen.
 The bleeding stigmata of Mallory-Weiss tears can
include a clean base, oozing, or active spurting.
 Bleeding stop spontaneously in 80 – 90% of the
patients
 In 0 – 5% of the patient bleeding recurs
 Endoscopic electro-coagulation of the tears
 Angiography therapy with intra arterial infusion of
vasopressin or embolisation.
 Operative therapy with oversewing of tear.

HAEMORRAGIC OR EROSIVE GASTRITIS
 Stress related mucosal injury
 Occur only in extremly sick patients
 Ex. Serious trauma
 Major Surgery
 Burn Covering > 1/3 of Surface area
 Major intracranial disease
 Severe medical illness (Ventilator dependence, coagulopathy)
 Significant bleeding probably does not develop unless
ulceration occurs.
 Intravenous H2-receptor antagonist is the treatment of
choice. Sucralfate also effective
 Aspirin and NSAIDS
 Half of the patient who chronically ingest NSAIDS have
Erosions. (15 – 30% have Ulcers)
 Most Frequently and severely affected site is gastric antrum.

Treatment of NSAID-Related Mucosal Injury
CLINICAL SETTING RECOMMENDATION
Active ulcer
NSAID discontinued H2 receptor antagonist or PPI
NASAID continued PPI
Prophylactic therapy Misoprostol, PPI,
H.Pylori infection Eradication if active ulcer prresent or
there is a past history of peptic ulcer
disease.
The approach to primary prevention has included avoiding the agent, using
NSAIDs that are theoretically less injurious, and/or the use of concomitant
medical therapy to prevent NSAID-induced injury.
Several nonselective NSAIDs that are associated with a lower likelihood of GI
toxicity include diclofenac, aceclofenac, and ibuprofen.Harrison's™ PRINCIPLES OF INTERNAL MEDICINE

PORTAL GASTROPATHY
 On endoscopic examination mucosa is engorged and friable.
 Portal hypertensive gastropathy (PHG) is caused by increased
portal venous pressure and severe mucosal hyperemia that
results in ectatic blood vessels in the proximal gastric body and
cardia and oozing of blood.
 Less severe grades of PHG appear as a mosaic or snake skin
appearance and are not associated with bleeding.
 Watermellon stomach.

 Usually, patients with severe PHG present with
chronic blood loss, but they occasionally can present
with acute bleeding.
TREATMENT:
 β-adrenergic receptor blockers.
 TIPS or surgical portacaval shunt.
 Endoscopic management has no role unless an
obvious focal bleeding site is identified.
 The best treatment is liver transplantation.

Dieulafoy's lesion
 It is a large (1- to 3-mm) submucosal artery that protrudes
through the mucosa.
 It is not associated with a peptic ulcer, and can cause
massive bleeding.
 It usually is located in the gastric fundus, within 6 cm of the
gastroesophageal junction.
 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 ultrasound has been used to help
identify a Dieulafoy's lesion that is not visualized on
endoscopy.
 If a Dieulafoy's lesion is found and treated, the site be
marked with submucosal injection of ink to tattoo the
area in case of rebleeding and the need for retreatment.
 Endoscopic hemostasis of a Dieulafoy's lesion can be
performed with injection therapy, a thermal probe, or
clip device or by band ligation.
 Rebleeding after successful hemostasis appears to be
rare.

Actively spurting jejunal Dieulafoy's
lesion

Esophagitis
 8% of all UGI bleeding was caused by erosive
esophagitis.
 independent risk factors for bleeding esophagitis were
grade 3 or 4 (moderate to severe) esophagitis.
 A history of heartburn was obtained in only 38% of
patients.
 Severe bleeding from gastroesophageal reflux–
induced esophagitis is treated medically with a PPI

 Upper endoscopy is critical to diagnosing severe erosive
esophagitis.
 endoscopic therapy generally has no role unless a focal
ulcer with a stigma of recent hemorrhage is found.
 These patients should be treated with a daily PPI for 8
to 12 weeks and undergo repeat endoscopy to exclude
underlying Barrett's esophagus

Upper Gastrointestinal Malignancy
 Malignancy accounts for 1% of severe UGI bleeds.
 The tumors are usually large, ulcerated masses in the
esophagus, stomach, or duodenum.
 Endoscopic hemostasis with Monopolar electro cautary,
laser, injection therapy, or hemoclips can temporarily
control acute bleeding.
 Angiography with embolization should be considered for
patients with severe UGI bleeding caused by malignancy.
 External beam radiation can provide palliative hemostasis
for patients with bleeding from advanced gastric or
duodenal cancer
Sleisenger and Fordtran's Gastrointestinal and Liver

Gastric Antral Vascular Ectasia
 Gastric antral vascular ectasia (GAVE), also described
as watermelon stomach.
 characterized by rows or stripes of ectatic mucosal
blood vessels that emanate from the pylorus and
extend proximally into the antrum .
 The cause is uncertain.
 GAVE is most commonly reported in older womenand
also seems to be more common in patients with end-
stage renal disease Sleisenger and Fordtran's Gastrointestinal and Liver

 GAVE has been associated with cirrhosis and
scleroderma.
 Patients with GAVE who do not have portal
hypertension demonstrate linear arrays of angiomas
(classic GAVE).
 whereas those with portal hypertension have more
diffuse antral angiomas.
 Endoscopic therapy with argon plasma coagulation
has been shown to be equally (80%) effective in
cirrhotic and noncirrhotic patients with GAVE.

Gastric Antral Vascular Ectasia

Aortoenteric fistula
 Bleeding is usually acute and massive, with a high mortality
rate(30-100%).
 A primary aortoenteric fistula is a communication between
the native abdominal aorta (usually an atherosclerotic
abdominal aortic aneurysm) and, most commonly, the
third portion of the duodenum.
 Often, a self-limited herald bleed occurs hours to months
before a more severe, exsanguinating bleed.
 On endoscopy obscure site of bleeding.

 Demonstration of an aortic aneurysm and fistulous track on
abdominal CT angiogram.
 Secondary aortoenteric fistula between the third portion of
the duodenum and the proximal end of the graft but may
occur elsewhere in the GI tract.
 The fistula usually forms between three and five years after
graft placement.
 Surgical treatment is required to remove the infected graft.
 Therapeutic endoscopy plays no role in the management of
bleeding from an aortoenteric fistula.

Cameron's lesions
 Cameron's lesions are 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.
 May present as slow GI bleeding and iron deficiency
anemia.
 The long-term medical management is usually with iron
supplements and an oral PPI.

Varices:
 Hepatic venous pressure
gradient > 12 mmHg.
 In esophageal varices ,
prefer variceal ligation
(with multiband ligator)
over endoscopic
sclerotherapy.
 In gastric varices, injection
with a glue will be more
beneficial .

Medical Management Of Variceal
Bleeding
Vasoconstrictors
 Vasopresin -0.1 0.5 units/minute for 4 to 12hrs(up to
48hrs) with short acting Nitrates.
 Terlipressin-2mg bolus followed by 1mg every 4-6 hrly for
3- 5 days.
 somatostatin -250ug bolus then 250ug/hr infusion
 Octeotride-50ug bolus then 50ug/hr infusion for 5 days

Pressure techniques
 Esophageal balloon
• Sengstaken blakemore tube,
• Minnesota tube
• Linton Nicholas tube
 Balloon should be inflated for less than 24 hrs.
75% rebleeding rate after balloon deflation.
 Most reports suggest that balloon tamponade
provides initial control of bleeding in 85% to 98%
of cases.

 variceal rebleeding recurs soon after the balloon is deflated
in 21% to 60% of patients.
 The major problem with tamponade balloons is a 30% rate
of serious complications, such as aspiration pneumonia,
esophageal rupture, and airway obstruction.
 Clinical studies have not shown a significant difference in
efficacy between vasopressin administration and balloon
tamponade.(Pitcher JL: Safety and effectiveness of the modified Sengstaken-Blakemore tube:
A prospective study. Gastroenterology )

ENDOSCOPIC SCLEROTHERAPY
 Various sclerosants used are
 Na. morrhuate
 Ethanolamine
 Polidocanol(3%)
 Na tetradecyl sulphate
 Tissue adhesive glue – N – Butyrl – 2 – cyanoacrylate -
prefered in fundal varices.

 Hemostasis can be achieved in 85% to 95% of cases, with a
rebleeding rate of 25% to 30%.
 Complications include esophageal ulcers, which can bleed
or perforate, esophageal strictures, mediastinitis, pleural
effusions, aspiration pneumonia.
 Band ligation is the preferred endoscopic therapy for
variceal bleeding.

 A rubber band is placed over a varix, which subsequently
undergoes thrombosis, sloughing, and fibrosis.
 Place two bands on each esophageal variceal column,
one distally near the gastroesophageal junction and
another 4 to 6 cm proximally.
 Acute hemostasis generally can be achieved in 80% to
85% of cases, with a rebleeding rate of 25% to 30%.
 Band ligation is associated with fewer local
complications, especially esophageal strictures, and
requires fewer endoscopic treatment sessions than
sclerotherapy.

 A meta-analysis has reported that variceal band
ligation reduces the rates of rebleeding, overall
mortality, and death from bleeding compared with
sclerotherapy.
 Band ligation + sclerotherapy combination has
got better results for rebleeding.

Surgical Management
 TIPS (transjugular intrahepatic porto-systemic
shunt): transjugular approach connect portal v.
and hepatic v.  reduce portal v. pressure gradient
to < 12-15 mmHg
 A relook endoscopy should be done to evaluate for
an alternative source of bleeding.
 Complications include: bleeding, dye-induced
renal failure, hemolysis, stent migration, and
puncture of the gallbladder or other organs
adjacent to the liver.

upper G I Bleed (non variceal)

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