Upper Gastrointestinal Bleeding 2007

8/14/2019 Upper Gastrointestinal Bleeding 2007

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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 !

Upper Gastrointestinal Bleeding 2007

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