Upper gastrointestinal

bleeding

Dr. Asfar Azimee

J.N Medical College
Aligarh
 CLASSIFICATION OF GI BLEEDING

• UPPER GI BLEED
• LOWER GI BLEED
• ACUTE or CHRONIC BLEEDING
DIFFERENCE BETWEEN
UGIB AND LGIB
• bleeding above and below ligament of trieitz
respectively
• UGIB presents with hematemesis and
melena
• UGIB may presnt with haematochezia also
• UGIB presents with hyperactive bowel sound
and raised blood urea nitrogen
• LGIB presents with hematochezia
UPPER GI BLEED
• incidence increases with age
• m>f around 2:1
• mortality ranging from 6% to 10%
• comorbidities such as renal or hepatic
failure, disseminated malignancy causes
high mortality rate
• 80% of ugib remit spontaneously and 90%
with endoscope but still there are 20%
chance of rebleeding
Causes of Upper GI Bleed (UGIB)
• Peptic Ulcer Disease (60% cases of UGIB)
• Erosive Gastritis(10-20%)
• Esophagitis (10%)
• Esophageal and Gastric Varices (2-9%)
• Mallory-Weiss Syndrome(5%)
• Malignancy(2%)
• Others
– Stress ulcer, arteriovenous malformation, Aorto-
duodenal Fistula, corrosive poisoning
 CAUSES OF UPPER GI BLEED
• peptic ulcer 55%
• gastric or oesophageal varix 14%
• angioma 6%
• mallory weiss tear 5%
• neoplasm 5%
• gastric erosion 4%
• esophagitis 4%
• others (mallory- weiss tear,dieoulfaeoy’lesion) 8%
• stress ulcer 1%
Clinical Features:
• History: Often misleading
– Usually presents with obvious complaints (melaena,
hematemesis, etc.)
– may present with more subtle signs (hypotension,
tachycardia, etc)
– Hematemesis,Melaena,Hematochezia
• H/o NSAIDs, Alcohol abuse, corrosive intake
• Weight loss/change in bowel habit (malignancy)
• Vomiting/retching followed by hematemesis
(Mallory-Weiss)
Clinical Features:
• Physical Exam
– Hypotension, tachycardia
– Skin: cool, clammy, jaundice, spider angioma and
other stigmata of Chronic Liver Disease
– Lymph node
– Abdomen: tenderness, mass, ascites,
hepatosplenomegaly
– PR Exam: blood
CLINICAL PRESENTATION
• Clinical manifestations of GI bleeding
depends upon extent & rate
• Postural hypotension suggests acute
hemorrhage & intravascular volume
depletion
• Fatigue & exertional dyspnea typical
symptoms with slow, chronic blood loss
PHYSICAL examination
• Orthostatic changes in pulse & BP
• Cardiopulmonary
• Skin
• Examine oral cavity
• Lymph nodes
• Abdomen
• Digital rectal
General Investigations in case of GI
Bleed

1. Hb, PCV
2. TLC,DLC
3. Bld glucose
4. Platelets, coagulation profile
5. Urea, creatinine, electrolytes
6. Liver biochem.
7. Acid-base state
8. Imaging: chest & abd. radiography, US, CT
FIRST STEPS IN MANEGEMENT
OF UPPER GI BLEED

1 AIRWAY PROTECTION
airway monitoring
endotracheal intubation

2 HAEMODYNAMIC STABILIZATION
large bore iv canulation
iv fluids(crystalloids and colloids),
packed RBC transfusion,
fresh frozen plasma, platelets
consider erythropoietin
3 NASOGASTRIC AND ORAL MANEGEMENT
gastric lavage

4 CLINICAL AND LABORATORY MONITORING

monitor vital signs,BP,pulse oximetry
haemogram,coagulation profile,LFT
ECG must in>50 yr

5 ENDOSCOPIC EXAMINATION AND THERAPY

diagnostic
therapeutic
ASSESMENT OF BLOOD LOSS IN
GI BLEED

GIVE A FLUID CHALLENGE INITIALY WITH

20ml/kg THEN WITH 40ml/kg

1. IF BP RETURNS AND STABLIZES LOSS 15

TO 30%
2. IF BP RISES BUT FALLS AGAIN LOSS OF 30
TO 40%
3. IF BP CONTINUES TO FALL BLOOD LOSS
MORE THAN 40%
Estimation of blood loss
Estimated Fluid and Blood Losses in Shock

Class 1 Class 2 Class 3 Class 4

Blood Loss,
Up to 750 750-1500 1500-2000 >2000
mL

Blood Loss,%
Up to 15% 15-30% 30-40% >40%
blood volume

Pulse Rate,
<100 >100 >120 >140
bpm

Blood
Normal Normal Decreased Decreased
Pressure

Respiratory Normal or
Decreased Decreased Decreased
Rate Increased

Urine
Output, 14-20 20-30 30-40 >35
mL/h

CNS/Mental Slightly Mildly Anxious, Confused,

Status anxious anxious confused lethargic

Fluid
Crystalloid Crystalloid
Replacement, Crystalloid Crystalloid
and blood and blood
3-for-1 rule
RISK FACTOR FOR DEATH
• Advance age >60 yr
• Shock on admission PR>100 BP<90
• Co morbidity hepatic or renal failure, disseminated
malignancy.
• Advance upper GI malignancy
• Endoscopicaly (spurting hemorrhage ,large
varices)
• Rebleeding >10times mortality
PEPTIC ULCER DISEASE
RISK FACTOR
H.pylori infection
NSAID use

MANEGEMENT
1. H2 receptor antagonist
2. Proton pump inhbitor
3. Endoscopic hemostasis (thermal or
laser)
4. Surgical
VARICEAL HAEMORRAGE
CAUSE IS PORTAL HYPERTENTION DUE
TO
 cirrhosis
 schistosomiasis

DIAGNOSIS USUALLY MADE WITH

ESOPHAGO GASTRO DUODENOSTOMY
MANAGEMENT
 MEDICAL MANAGEMENT
1. Vasopressin (0.4 U bolus followed by 0.4to 1U/min
infusion) combine with nitroglycerine 10 to 50 mic/min
2. Octreotide 50 mics bolus followed by 50mics/h iv
infusion for 5 days
3. Nonselective beta blocker (propranolol , nadolol)
 BALLON TAMPONADE
ETI and sedation essential before placement of tube
 ENDOSCOPY
1. Sclerotherapy
2. Variceal band ligation
• INVASIVE
INTERVENTION

• TIPS(intrahepatic
conduit b/w portal
and hepatic vein)
Sengstaken-Blackmore
tube
 • Esophageal
Gastroscopy image of varices seven days
esophageal varices post banding,
with prominent red showing ulceration
wale spots. at the site of
banding.
STRESS ULCER

• Acute, superficial inflammatory lesions of the

gastric mucosa induced when an individual
is subjected to abnormally elevated
physiological demands.
• Stress ulcers are Multiple and there is Lack
of chronic Inflammation and most of the
times are asymptomatic
Pathogenesis of Stress Ulcers

Ischemia-Primary :promotes insufficient mucosal

perfusion
1. Intramural acidosis
2. Free radicals
3. Increased cell permeability
4. Decreased bicarb.
5. Decreased acid-buffering capacity
6. Decreased mucus production
7. H.pylori plays no role
Risk Factors

• Multiple trauma, age > 65, corticosteroids,

• NSAIDs, major surgery, resp. failure, renal
failure, hepatic failure, mult. organ failure,
• Head injury, sepsis, burns > 30-35% BSA
• Coagulopathy, mech. ventilation, high dose
corticosteroids only independent risk
factors
Criteria for Clinically-Relevant
Overt Gastric-Stress Bleeding

• Drop at least 2 gm% Hgb concentration

• Need for transfusion of 2 units of packed
RBCs
• Systolic BP < 90 mm Hg (shock) for
more than 3 hours
• Drop > 20 mm Hg in systolic BP
compared to prebleeding values
Management: Prophylaxis
vs. Treatment

Prophylaxis:
• Antacids
• H-2 receptor antagonists
• Proton pump inhibitors
• Sucralfate
• Nutrition
ADVANTAGES OF STRESS ULCER
PROPHYLAXIS IN ICU PATIENTS
WHO ARE ON SUCRALFATE

1. Respiratory rate infection were

significantly less frequent.
2. The selection of drugs today depends not
only on efficacy but also on possible
adverse effects and on costs. In this
regard, the most cost-effective drug is
sucralfate.
SOME CONTRADICTION TO
STRESS ULCER PROPHYLAXIS
• The most important prophylactic measure is an
optimized resuscitation and ICU regime aiming to
improve oxygenation and microcirculation
• All patients receiving clinical treatment including
maintenance of adequate tissue perfusion (with low dose
inotropes and vasodilators) were not having stress ulcer,
• There is a lack of consensus regarding stress ulcer
prophylaxis in trauma patients
• Stress ulcer prophylaxis is indicated only in patients at
risk, and not in every ICU patient.
Treatment
• Primary
– ABCs
– Oxygen This should be given by facemask to all
patients in shock.
– Close monitoring

– Immediate resuscitation, 2 wide bore IV cannula

– NG tube in all patients with significant bleeding

– Consider blood transfusion if no improvement

Therapeutic Endoscopy
– Early treatment indicated when significant upper GI bleed
– Sclerotherapy or band ligation used to treat varices
– thermal modality 'heater probe‘
– injection of dilute adrenaline (epinephrine) into the bleeding
point
– application of metallic clips.
Drug Therapy
– Intravenous proton pump inhibitor infusions
reduce rebleeding
– Somatostatin and octreotide effective for reduction of acute
variceal bleeding
Balloon Tamponade
• Sengstaken-Blakemore tube can control variceal
hemorrhage in 40 – 80% patients
• Inflate gastric balloon first, the esophageal
balloon if no improvement
Surgery –
– if all other interventions are ineffective
– endoscopic haemostasis fails to stop active
bleeding
– rebleeding occurs on one occasion in an elderly
or frail patient, or twice in younger, fit patients
Prognosis:
• Mortality following a diagnosis of acute upper
gastrointestinal bleeding is approximately 10%.
RISK FACTORS FOR DEATH IN PATIENTS
WITH ACUTE U GI HAEMORRHAGE
Factor Comments
1. Increasing age: Risk increases over age 60 and
especially in very elderly
2. Comorbidity: Advanced malignancy; renal and
hepatic failure
3. Shock: Def as pulse > 100/min, BP < 100
4. Diagnosis: Varices and cancer have the
worst prognosis
5. Endoscopic findings: Active bleeding and a non-
bleeding visible vessel at endoscopy
6. Rebleeding Associated with 10-fold rise in mortality
TRIAGE WHOM TO ADMIT TO ICU?

While presenting in hospital patient are to be

stratified into high risk or low risk group.
PATIENT WITH ANY ONE OR MORE
FOLLOWING CRITERION ARE STRATIFIED AS
HIGH RISK
1. Systolic BP<100 on presentation
2. Severe comorbid
disease(cardiac,renal,pulmonary)
3. Evidence of ongoing GI bleed
4. Prothrombin thme >1.5 times of normal
CONCLUSSION
THE CORNERSTONE OF
MANEGEMENT OF GI BLEED
INVOVES
1. Protection of airway
2. Volume resucitation
3. Correction of coagulation disorder
4. Determination of site of bleeding
MANEGEMENT IS
MULTIDICIPLINARY AND
INVOLVES
• EMERGENCY ROOM PHYSICIAN
• GASTROENTEROLOGIST
• SURGEON
• INTENSIVIST
• INTERVENTIONAL RADIOLOGIST
THANKS !