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Upper gastrointestinalbleeding
Dr. AsfarAzimee
J.N Medical CollegeAligarh
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CLASSIFICATION OF G I B LEEDIN G
UPPER GI BLEEDLOWER GI BLEED
ACUTE or CHRONIC BLEEDING
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DIFFERENCE B ETWEEN UG I B AND L G I B
bleeding above and below ligament of trieitz
respectivelyUGIB presents with hematemesis andmelena
UGIB may presnt with haematochezia alsoUGIB presents with hyperactive bowel soundand raised blood urea nitrogenLGIB presents with hematochezia
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C auses of Upper G I Bleed (UG I B)
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
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CAU
SES 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,dieoulfaeoylesion ) 8%stress ulcer 1%
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C linical F eatures:
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
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CLINICALP
RESENTATION
Clinical manifestations of GI bleedingdepends upon extent & ratePostural hypotension suggests acutehemorrhage & intravascular volume
depletionFatigue & exertional dyspnea typicalsymptoms with slow, chronic blood loss
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PHYSICAL
examinationOrthostatic changes in pulse & BP
CardiopulmonarySkinExamine oral cavityLymph nodesAbdomen
Digital rectal
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General I nve stig a tio n s i n
c a s e of G I B leed
1. Hb, PCV 2. TLC,DLC 3. Bld glucose4. Platelets, coagulation profile5. Urea, creatinine, electrolytes6. Liver biochem.7. Acid-base state
8. Imaging: chest & abd. radiography, US, CT
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FIRST STE P S IN M ANE G E M ENT OF UPP ER G I B LEED
1 AIRWAY PROTECTION
airway monitoringendotracheal intubation
2 HAEMODYNAMIC STABILIZATIONlarge bore iv canulationiv fluids(crystalloids and colloids),packed RBC transfusion,
fresh frozen plasma, plateletsconsider erythropoietin
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ASSES MENT OF B LOOD LOSS IN G I B LEED
GIVE A FLUID CHALLENGE INITIALYWITH 20ml/kg THEN WITH 40ml/kg
1. IF BP RETURNS AND STABLIZESLOSS 15 TO 3 0%
2. IF BP RISES BUT FALLS AGAIN LOSS
OF 3 0 TO 40%3 . IF BP CONTINUES TO FALL BLOODLOSS MORE THAN 40%
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Estimation of blood loss
Estimated Fluid and Blood Losses in Shock
Class 1 Class 2 Class 3 Class 4
Blood Loss,mL Up to 750 750-1500 1500-2000 >2000
Blood Loss,%blood volume Up to 15% 15-30% 30-40% >40%
Pulse Rate,bpm 100 >120 >140
BloodPressure Normal Normal Decreased Decreased
RespiratoryRate
Normal orIncreased Decreased Decreased Decreased
UrineOutput,mL/h
14-20 20-30 30-40 >35
CNS/MentalStatus
Slightlyanxious
Mildlyanxious
Anxious,confused
Confused,lethargic
FluidReplacement,3-for-1 rule
Crystalloid Crystalloid Crystalloidand bloodCrystalloidand blood
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RISK FACTOR
FOR
DEAT
HAdvance age >60 yr
Shock on admission PR>100 BP10times mortality
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P E P TIC U LCER DISEASE
y
RISK FACTORH.pylori infectionNSAID use
y
MANEGEMENT1. H2 receptor antagonist2. Proton pump inhbitor
3 . Endoscopic hemostasis(thermal or laser)
4. Surgical
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V ARICEALH
AEM
ORRAG
E
CAUSE IS PORTAL HYPERTENTION DUE
TOcirrhosisschistosomiasis
DIAGNOSIS USUALLY MADE WITH
ESOPHAGO GASTRO DUODENOSTOMY
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M ANA G E M ENTy MEDICAL MANAGEMENT1. V asopressin (0.4 U bolus followed by 0.4to 1U/min
infusion) combine with nitroglycerine 10 to 50 mic/min2 . O ctreotide 50 mics bolus followed by 50mics/h iv
infusion for 5 days
3 . N onselective b eta b locker (propranolol , nadolol)y B ALLON TAMPONADE
ETI and sedation essential before placement of tubey ENDOSCOPY1. Sclerotherapy2. Variceal band ligation
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INVASIVEINTERVENTION
TIPS(intrahepaticconduit b/w portaland hepatic vein)
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y Gastroscopy image of esophageal variceswith prominent redwale spots.
Esophagealvarices seven dayspost banding ,
showing ulcerationat the site of banding.
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STRESSU
LCER
Acute, superficial inflammatory lesions of thegastric mucosa induced when an individualis subjected to abnormally elevated
physiological demands.Stress ulcers are Multiple and there is Lackof chronic Inflammation and most of the
times are asymptomatic
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Pathogenesis of S tress Ulcers
y Ischemia-Primary : promotes insufficient mucosalperfusion
1. Intramural acidosis2. Free radicals3 . Increased cell permeability4. Decreased bicarb.
5. Decreased acid-buffering capacity6. Decreased mucus production7. H.pylori plays no role
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C riteria for C linically- R ele v ant
O v ert Gastric- S tress BleedingDrop at least 2 gm% Hgb concentration
Need for transfusion of 2 units of packedRBCsSystolic BP < 90 mm Hg (shock) for more than 3 hoursDrop > 20 mm Hg in systolic BP
compared to prebleeding values
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Management: Prophylaxisv s. T reatmentProphylaxis:
AntacidsH-2 receptor antagonists
Proton pump inhibitorsSucralfateNutrition
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AD V ANTA G ES OF STRESS U LCER
P RO PHY LAXIS IN IC U P ATIENTS W H O ARE ON S U CRALFATE
1. Respiratory rate infection weresignificantly less frequent.2. The selection of drugs today depends not
only on efficacy but also on possibleadverse effects and on costs. In thisregard, the most cost-effective drug issucralfate.
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T reatment
Primary ABCs
Oxygen This should be given by facemask to allpatients in shock.
Close monitoring
Immediate resuscitation, 2 wide bore IV cannula
NG tube in all patients with significant bleeding
Consider blood transfusion if no improvementafter 2L of crystalloid or Hb < 10 gm/dL
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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
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Balloon TamponadeSengstaken-Blakemore tube can control varicealhemorrhage in 40 80% patientsInflate gastric balloon first, the esophagealballoon if no improvement
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Surgery
if all other interventions are ineffective endoscopic haemostasis fails to stop active
bleeding
rebleeding occurs on one occasion in an elderlyor frail patient, or twice in younger, fit patients
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Prognosis:Mortality following a diagnosis of acute upper gastrointestinal bleeding is approximately 10%.
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RISK FACTORS FOR DEAT H IN P ATIENTS WIT H AC U TE U G I H AE MORR H A G E
F actor Comments1. Increasing age: Risk increases over age 60 and
especially in very elderly2 . Comorbidity: Advanced malignancy; renal andhepatic failure
3. Shock: Def as pulse > 100/min, BP < 1004. Diagnosis: Varices and cancer have theworst prognosis
5. Endoscopic findings: Active bleeding and a non-bleeding visible vessel at endoscopy6. Rebleeding Associated with 10-fold rise in mortality
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TRIA G E W H O M TO AD M IT TO
IC U?y 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 BP1.5 times of normal
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CONCL U SSIONy THE CORNERSTONE OF
MANEGEMENT OF GI BLEED
INVOVES1. Protection of airway2. Volume resucitation3 . Correction of coagulation disorder 4. Determination of site of bleeding
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M ANE G E M ENT IS MU LTIDICI P LINAR Y AND IN V OL V ES
EMERGENCY ROOM PHYSICIAN
GASTROENTEROLOGISTSURGEONINTENSIVISTINTERVENTIONAL RADIOLOGIST
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THANKS !