Approach to Management of Upper Gastrointestinal (GI) Bleeding


Approach to Upper GI Bleed
Seminar – November 30th 2015
Presenter: Dr.Arun Vasireddy

Case Senario
 A 73 yr old man presented to the ER with 5 day H/O passing black tarry
stools and abdomen pain.
 C/o postural dizziness since 1 week. c/o Indigestion
 Stools are normal coloured, c/o constipation intermittently
 H/o weight loss since 1 yr (6 kg loss)
 Pt had PVD since 2 yrs for which he takes aspirin daily.
 Consumes 30-40 units alcohol/week.
 In the ER, the Pt had giddiness and had vomited dark stained material
looking like coffee grounds.

 Vitals: bp- 90/60 mm hg (postural drop of 30mm hg)
HR-120/min , Moderated dehydration +, conjunctival pallor+
 CVS – Loud ejection systolic murmer radiating to carotids
 RS – B/l airway clear
 PA – epigastric tenderness+ no organomegaly/palpable mass
 Rectal exam revealed enlarged prostrate & fresh melaena + , no
fresh rectal bleeding
 EKG – sinus tachycardia with LVH, no evidence of ischemia
 Diagnosis…..?

Overview
 Definition & Classification
 Epidemiology
 Etio-pathogenesis
 Clinical features
 Complications
 Screening & Diagnosis
 Management & Prevention of complications
 Prognosis

Definition
 Loss of blood anywhere into the
gastrointestinal tract.
 Depending on location of Ligament of
treitz
 UGIB
 LGIB

Epidemiology
 UGIB vs LGIB= 5:1
 Incidence: 170 patients/ 1,00,000 population /year.
 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.
 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.

Classification
Ulcer disease 38 %
Esophagitis 13
Gastritis/erosions 8
Erosive duodenitis 7
Upper gastrointestinal tract tumor 7
Vascular ectasias 6
Portal Hypertensive Gastropathy 4
Mallory weiss tear 4
Obscure UGIB 12
Variceal bleed Non variceal bleed
Oesophageal varices &
Gastric varices
16%

Causes of UGIB
Esophageal causes
Esophageal varices
Esophagitis
Esophageal cancer
Esophageal ulcers
Mallory-Weiss tear
Cameron’s Lesions (linear ulcers
or erosions within large hiatal
hernia)
Gastric causes
Gastric ulcer
Gastritis
Gastric cancer
Gastric varices
Dieulafoy's lesions
Gastric Antral Vascular Ectasia
(watermelon stomach)
Portal Hypertensive Gastropathy
Hereditary hemorrhagic
telangiectasia
Duodenal causes
Duodenal ulcer
Vascular malformation including
aorto-enteric fistulae
Hematobilia, or bleeding from the
biliary tree
Hemosuccus pancreaticus, or
bleeding from the pancreatic duct
(ruptures pseudoaneurysm,
neoplasm, trauma/surgery)
Severe superior mesenteric artery
syndrome
Periampullary carcinoma

Causes
 Congenital
 Acquired –
 drug induced,
 Surgical history,
 Alcohol abuse,
 H.Pylori
 Physiological stress

Peptic Ulcers
 PATHOGENESIS:
 Infection/irritation leads to disruption of the mucous barrier and has
a direct inflammatory effect on gastric and duodenal mucosa.
 As the ulcer burrows deeper into the gastroduodenal mucosa,
weakening and necrosis of the arterial wall, development of a
pseudoaneurysm. weakened wall ruptures, hemorrhage
H.PYLORI: NSAIDS:
* involves antrum * gastric ulcers > common
*duodenal ulcers * 15-45% patients develop
* 25% indians have ulcers on regular use
lifetime risk of peptic ulcer

III (clean base)II-b (adherent clot)
II-a (visible vessel)I-b (oozing)
II-c (flat pigmentation)
I-a (arterial jet )
Forrest and Finlayson’s Classification

MALLORY WEISS SYNDROME /TEARS
 Mucosal or sub-mucosal lacerations that occur
at the gastro-esophageal junction and usually
extend distally into a hiatal hernia .
 Typically have a history of recent non-bloody
vomiting with excessive retching followed by
hematemesis..
 Endoscopy usually reveals a single tear that
begins at the gastro-esophageal junction and
extends several millimeters distally into a hiatal
hernia sac/within cardiac portion of stomach.

HAEMORRAGIC OR EROSIVE GASTRITIS
 Stress related mucosal injury
 Occur mostly in extremly sick patients
 Major Trauma
 Post Major Surgery
 3rd Degree burns
 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.

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.
 Usually, patients with severe PHG present with chronic blood
loss, but they occasionally can present with acute bleeding.

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 is 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.

Gastric AntralVascular 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 .

 Etiology unknown.
 GAVE is most commonly reported in older women and also
seems to be more common in patients with end-stage renal
disease
 GAVE has been associated with cirrhosis and scleroderma.
 Patients with GAVE who do not have portal hypertension
demonstrate linear arrays of angiomas (classic GAVE).
 Pts with portal hypertension have more diffuse antral
angiomas.

Aortoenteric fistula
 Bleeding is usually acute and massive, with a high mortality rate(30-
100%).
 The A-E 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.
 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.

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
 Consequence of Portal HTN.
 The initial factor in portal HTN is the increase in vascular resistance to portal
blood flow.
 This will lead to structural distortion (underlying disease) and active
contraction of portal/septal cells (hepatic cells,myofibroblasts) in portal
venules. (the dynamic component).
 This will lead to development of porto-systemic collaterals (possibly from
influence of angiogenic factors, VEGF) will cause shunting of blood around liver.

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 .
Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition

Clinical features
• HEMATEMESIS Vomiting of fresh or old blood
Proximal to Treitz ligament
Bright red blood = significant bleeding
Coffee ground emesis = no active bleeding
• MELENA Passage of black & foul-smelling stools
Usually upper source – may be right colon
• HEMATOCHEZIA Passage of bright red blood from rectum
If brisk & significant → UGI source
• OCCULT BLEEEDING Bleeding not apparent to patient
May lead to dyspnea, AP & even MI

Bleeding etiology Leading History
Mallory -Weiss tear Multiple Emesis before hematemesis, alcoholism, retching
Esophageal ulcer Dysphagia, Odynophagia, GERD
Peptic ulcer Epigastric pain, NSAID or aspirin use
Stress gastritis Patient in an ICU, gastrointestinal bleeding occurring
after admission,respiratory failure,multiorgan failure,coagulopathy
Varices, portal
gastropathy
Alcoholism, Cirrhosis of liver
Gastric antral
vascular ectasia
Renal failure, cirrhosis
Malignancy Recent involuntary weight loss, dysphagia, cachexia,
early satiety
Angiodysplasia Chronic renal failure, hereditary hemorrhagic
telangiectasia
Aortoenteric fistula Known aortic aneurysm, prior abdominal aortic
aneurysm repair
Clues regarding the cause of acute UGI bleeding

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, tachycardia
 BP = hypotension or orthostatic haemodynamic changes
 tachypnoea
 SKIN changes
 Cirrhosis – Palmar- 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

Approach to a Patient with UGIB
Immediate Initial Assessment
Stabilization of haemodynamic status
Identify bleed source
Stop active bleed
Treat underlying cause
Prevent recurrence of bleeding

Initial Assessment & triage
 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
Complete Rockall Score:
Clinical Rockall score +
endoscopic findings.
* Correlates well with mortality
& risk of rebleeding.

 Blood Urea Nitrogen(mmol/L)
6.5 – 7.9 2
8 – 9.9 3
10 – 24.9 4
≥25 6
 Haemoglobin (g/dL) for men
12-12.9 1
10-11.9 3
<10 6
 Haemoglobin (g/dL) for
women
10-11.9 1
<10 6
 Systolic BP (mm Hg)
◦ 100–109 1
◦ 90–99 2
◦ <90 3
•Other markers
Pulse ≥100 (per min) 1
Presentation with melena 1
Presentation with syncope 2
Hepatic disease 2
Cardiac failure 2
•Score from 0 to 23
•Scores ≥ 6 - 50% risk of needing an
intervention.
Score is"0" if :
•Hemoglobin level
>12.9 g/dl(men) or
>11.9 g/dl(women)
•Systolic blood pressure >109 mm Hg
•Pulse <100/minute
•BUN level <6.5 mmol/L
•No melena or syncope
•No liver disease or heart failureBlatchford O, Murray WR, Blatchford M: Lancet 2000; 356:1318-21.

ROCKALL SCORE
Rockall, Lancet 1996
• For Risk of Rebleeding and Death After Admission to the Hospital
for Acute GI Bleeding

Rockall’s score>8=High risk of death
50% Patients will rebleed.
Rockall’s score<3=excellent prognosis
Lower risk of hemorrhage.
Rockall score
Cumulativepatientswithrebleeding

Management as per risk
 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.
 Intermediate risk(3-5)
 same Tt + Hospitilisation for at least 72 hrs.
 High risk(>5%)
 Same Tt+ Hospitilisation in I.C.U.

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

Acute UGIB
HB%, PLT, PT, LFT, RFT,
Cross matching
(repeat Hb again after 72
hrs)
Check
Airway and
Spo2
• 2 large bore IV access
• NG tube
• Urinary catheter
• CVP line (if high risk)
Airway not protected
or SPO2 <90% after
max FiO2 by mask
Arrange
blood as
needed
RSI
Hypotension & poor
tissue perfusion
Transfuse 2-4 pints whole
blood or blood products until
haemodynamically stable &
HCT > 25%, CVP> 6-12cm
Persistant Hypotension
• Infuse Synthetic colloid or
crystalloid 1-2 lts with pressure
bag & proceed with volume
replacement until blood arrives
• Tranexamic acid 1g IV over I hour
then 500mg TID (if required)
• PPI – Pantoprazole 80mg IV stat
& continue Infusion
Inotrope support
Emergency OGD
(preferably within 4-24 hrs)
Blood
unavailable
Haemodynamically
Stable

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

ENDOSCOPIC MODALITIES AVAILABLE FORTHE
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
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

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 diseases eg. CHF, CRF,
IHD,COPD)
 20-25% in younger pt
 25-28% in portal HTN
 administration of vit k
 In symptomatic thrombocytopenia (<50000 )infused platelets.
 FFP transfusion 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.

Hematocrit values before & after bleeding

Medical Management
 Proton pump inhibitors-
 its use is widely adopted and is mandatory in all UGIB.
 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 continuous infusion 8mg/hr ,and
the need for endoscopic therapy has reduced.
 PPI+ Endotherapy shown the best results in terms of rebleeding,
morbidity and mortality.
 ? H2 antagonist /Sucralfate has not been shown to be effective in UGIB

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

DRUG DOSE
TRIPLE THERAPY(14 days) for H.Pylori
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

Medical Management
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 2010; 127:1062-71)
• The use of octerotide should be considered in pts who have persistent
bleeding even on optimal medical management.
Acute upper gastrointestinal bleeding in adults. Author. John R Saltzman,:current gastroenterology
updates 2014

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.

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

Upper GI Endoscopy
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.
:Acute upper gastrointestinal bleeding in adults. Author. John R Saltzman,:current
gastroenterology updates 2013

 Endoscopy can offer therapeutic options including: injections,
cautery , placement of endoclips or a combination of therapies
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

UTILITY OF ENDOTHERAPY
 Diagnostic & 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.

OPTIMIZING ENDOSCOPICVISUALIZATION
 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
:Acute upper gastrointestinal bleeding in adults. Author. John R
Saltzman,:current gastroenterology updates 2013

METHODSTO 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

INJECTIONTHERAPY
* 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
modalities of monotherapies.

CONTACTTHERMALTHERAPY
 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 involved
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 thermo coagulation technique.
* Combination therapy appears to provide durable control of bleeding than
monotherapies

Medical Management OfVariceal 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.

ENDOSCOPIC BAND LIGATION
 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.

 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 hemorrhage 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 presence 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. Severe 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 2014 API

Recurrent Gastrointestinal bleeding
Initial Control
Endoscopic
therapy
Permanent Control
Rebleeding
Endoscopic
therapy
Rebleeding
Surgery Angiography
Permanent
Control
80-90%
50%

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 tears:
 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.
Portal Gastropathy:
 β-adrenergic receptor blockers.
 TIPS procedure.
 Endoscopic management has no role unless an obvious focal
bleeding site is identified.
 The best treatment is liver transplantation.

 Gastric Antral Vascular Ectasia:
 Endoscopic therapy with argon plasma coagulation
has been shown to be equally (80%) effective in
cirrhotic and noncirrhotic patients with GAVE.
 Aorto-Enteric Fistula:
 Surgical treatment is required to remove the infected graft.
 Therapeutic endoscopy plays no role in the management of
bleeding from an aortoenteric fistula.

Obscure UGIB
Obscure Occult
UGIB
Stool OBT +, no frank
bloodloss
5-100ml/day loss
For diagnosis
1.Barium Meal follow
through
2.Enteroclysis (10-20%)
OGIB diagnosed
3.Technetium labelled
nuclear scan (70-80%)
4.Helical CT angiogram
(72%)
5.Capsule Endoscopy
(70-80%) 2 images per
sec
Diagnosis &
management
1.Angiography(40-80%)
2.Push Enteroscopy(30-
50%)
3.Intra-operative
enteroscopy(50-100%)
4.Double balloon
enteroscopy (80-90%)
Obscure Overt
UGIB
Clinically evident
persistant bleed not
identifiable after OGD
with blood loss
>100ml/day

Prevention
 Primary Prevention: to reduce ulcer incidence
 PPIs or misoprostol therapy is advised in Pts taking NSAIDs
 H.Pylori eradication
 Prophylactic PPI therapy in InPatients with physiologic stress
 Pts with cirrhosis, non selective beta blockers & endoscopic band
ligation reduces bleeding risk (compared to placebo)
 Secondary Prevention:
 Reduce risk of rebleeding - IV PPI therapy in Pts with PUD with high
risk stigmata.
 IV Octreotide therapy – reduces esophageal variceal rebleeding.

TAKE HOME MESSAGE
 Early Resuscitation.
 Nasogastric wash + look for GH.
 High dose PPI therapy for at least 72 hrs.
 Urgent Endoscopic therapy for mod to severe UGI bleeding.

TAKE HOME MESSAGE
 Nonvariceal bleeding should be treated with either:
 Combination therapy using an injection of dilute epinephrine
combined with a thermo coagulation OR
 Endoclip (with or without injection therapy)
 Combination therapy preferred along with medical
management.
 Relook endoscopy should be preferred only for mod to severe
bleeding.
 Pt should also be treated for specific cause/disease.


References:
 API Medicine Update 2014
 MayoClinicGastroenterology Board Review 5th Ed
 Mount Sinai Expert Guides: Gastroenterology 2015
 Guidelines Sources –
• American college of gastroenterology 2012 guidelines
• American society of gastrointestinal endoscopy 2015 guidelines

Approach to Management of Upper Gastrointestinal (GI) Bleeding

Recomendados

Recomendados

Más contenido relacionado

La actualidad más candente

La actualidad más candente (20)

Similar a Approach to Management of Upper Gastrointestinal (GI) Bleeding

Similar a Approach to Management of Upper Gastrointestinal (GI) Bleeding (20)

Más de Arun Vasireddy

Más de Arun Vasireddy (13)

Último

Último (20)

Approach to Management of Upper Gastrointestinal (GI) Bleeding

Notas del editor