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This document provides an overview of the approach to upper GI bleeding. It begins with definitions of terms like hematemesis, melena, and hematochezia. It then discusses the causes of upper GI bleeding, which can be variceal or non-variceal. For patients presenting with upper GI bleeding, the summary provides that history, physical exam, and investigations like endoscopy are important to determine the cause and guide management. Management may involve treating any active bleeding, administering PPIs for non-variceal causes, or using vasoactive agents, balloon tamponade, or endoscopic therapies for variceal bleeding.

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APPROACH TO UPPER GI BLEEDING By :- Dr. NITESH PANSARI MEDICINE UNIT –A RNT MEDICAL COLLEGE , UDAIPUR
SYNOPSIS • Definition & Presentation • Causes of UGI bleeding • History & Physical Examination • Investigations • Management of acute episode • Variceal bleeeding & management • Nonvariceal bleeding & management • High risk Factors • Scoring systems • Indication of surgical intervention
DEFINITION • Upper GI bleeding is defined as bleeding from a source proximal to the Ligament of Treitz
Hematemesis • Vomiting of red blood or coffee- grounds material when gastric acid converts hemoglobin into methemoglobin . • Differentiate from :- Hemoptysis. Bleeding from Pharynx , nasal passage.
Patient with hematemesis usually requires a bucket; whereas patient with hemoptysis usually requires a small bowl. Is It Hematemesis?
Melena • Passage of black tarry stools. • Blood loss between 50-100 ml /day will produce melena. • The black color of melenic stools is caused by Hematin, the product of oxidation of Heme by intestinal and bacterial enzymes. • Can be seen in LGI bleed also (10%). • Non GI bleed – swallowed blood from epistaxis • Blood for 14 hrs in the GI tract • Oral iron and bismuth mimics melena.
Hematochezia • It is defined as passage of bright-red or maroon blood from the rectum. • Common in bleeding from colon, rectum and anus. • In case of brisk bleeding in the upper git, bright red blood may come out unchanged in the stool. • 10% of UGI bleed Occult GI bleeding • Absence of overt bleeding • Fecal occult blood test - +ve • Suspected in patients with iron deficiency anemia • Normally 2.5 ml of blood is lost per day. • OBT detects amount between 10-50 ml/d. Symptoms of blood loss or anemia • Light headedness, syncope, angina, or dyspnea
UPPER GI BLEEDING VARICEAL BLEEDING NON VARICEAL BLEEDING
Esophageal causes • Esophageal varices • Esophagitis • Esophageal cancer • Esophageal ulcers • Mallory-Weiss tear Gastric causes • Gastric ulcer • Gastric cancer • Gastritis • Gastric varices • Dieulafoy's lesions • Gastric Antral Vascular Ectasia • Portal Hypertensive Gastropathy 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 • Severe superior mesenteric artery syndrome CAUSES
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
• Previous Episodes Of GI Bleed • H/O Instrumentation • H/O Head Injury • Co-morbid Conditions o Liver Disease o Renal Disease o Cardiovascular Disease o Chronic Respiratory Conditions • H/O Abdominal Surgery Personal History • Alcoholism , Smoking , Tobacco Abuse • Cocaine Abuse • Weight Loss, Anorexia Past History
Drug History • Salicylates/ NSAIDS • Anticoagulants (warfarin / Heparin) • Corticosteroids • Oral Iron , Bismuth ( Mimic Melena )
• Pallor , signs of dehydration , Shock • Icterus • Clubbing • Oedema }Liver disease PHYSICAL EXAMINATION
Lymphadenopathy Virchow’s Node (Troisier’s sign) Vital signs Tachycardia Hypotension Tachypnea
SIGNS OF LIVER CELL FAILURE
• Ascites • Spider naevi • Palmar erythema • Dupuytren’s contracture
• Leuconychia • Gynecomastia • Bleeding manifestations • Scars of previous surgery
• Splenomegaly • Caput medusae • Parotid Swelling • Fetor hepaticus • Asterixis • Testicular atrophy • Acanthosis nigricans • Alopecia • Glossitis • Loss of Axillary hair • Loss of Pubic Hair
INSPECTION Distention , Dilated Veins Swelling Visible peristalsis PALPATION Tenderness HSM, secondary metastasis Sister Mary Joseph nodules Mass PERCUSSION Shifting dullness HSM AUSCULTATION Absent Bowel sound Bruit Cruveilhier-Baumgarten venous hum ABDOMEN EXAMINATION
PR EXAMINATION • Hemorroids • Melena , blood • Blumer’s shelf
LAB ASSESSMENT • Full Blood Count- Hb, Platelet count • PCV* • Coagulation Profile • Liver Function tests • Serum electrolytes • Blood urea nitrogen ratio > 30 sensitivity of 68% and a specificity of 98% • Blood Grouping & Cross matching. • Serial ECG • Stool Occult Blood Test • HIV, HbsAg , Anti HCV Markers INVESTIGATIONS
• Renal Function Tests • Gastrin level • Nasogastric aspiration 1. Red blood-current bleeding 2. Coffee ground-recent bleeding 3. Continuous aspiration-severe active bleed Lavage not +ve- i) bleeding has stopped ii) beyond pylorus • PCV* : decreased only by 24 to 72hrs, after bleed  CHEST XRAY  USG
ESOPHAGOGASTRODUODENOSCOPY • Most important component of investigation. • 90% accuracy in diagnosis if done with in 24 hours. ENDOSCOPY
•Examination of whole bowel possible •Indicated in GI bleeding of obscure source Video capsule endoscopy
•PUSH ENTEROSCOPY •DEEP ENTEROSCOPY  SINGLE OR DOUBLE BALLOON ENDOSCOPY  SPIRAL ENDOSCOPY
RADIOLOGIC IMAGING • ANGIOGRAPHY :- bleeding rate at least 0.5 mL/min. • RADIONUCLIDE IMAGING :- bleeding at a rate of 0.04 mL/min Technetium pertechnetate–labeled red blood cell scans >>> Technetium sulfur colloid scans • CT enterography and CT angiography • Barium radiography is not indicated (and contraindicated if endoscopy or angiography is planned) in the emergency setting.
Airway: • Secure to prevent aspiration • Endotracheal tube & give oxygen Breathing: • support respiratory function Circulation: • Expand circulatory volume • 2 large bore i.v. cannula • RBC transfusion with the goal of maintaining the hematocrit value to 30% or hemoglobin to 8 g/dL. • Normal saline may be infused intravenously until packed red blood cells are available for transfusion. • Maintain systolic B.P. at equal or greater than 90mmHg • Pressure agents like dopamine 2.5 to 10 mcg/kg/min, and dobutamine 2.5 to 10 mcg/kg/min as infusion, Noradrenalin 3mg. /h as infusion may be required, as a last resort, to maintain peripheral perfusion.
• Correct any coagulopathy with :- 10 - 15 ml/kg of FFP (if PT INR > 1.5) and/or platelet transfusions (if platelet count < 50,000/cu.mm) • Monitor:  Skin color, peripheral temperature  Pulse Rate, BP  Respiratory Rate, O2 saturation of blood  Urine output (Foley’s Catheter) TREATMENT OF SUSPECTED PEPTIC ULCER BLEEDING: • Start High dose , constant infusion IV PPIs (Omeprazole 80 mg bolus and 8mg/ h infusion for 72 h)
TREATMENT OF SUSPECTED VARICEAL HEMORRHAGE  Antibiotic prophylaxis • To prevent bacteremia and spontaneous bacterial peritonitis • Intravenous ceftriaxone, 1 g every 24 hours for 7 days ; or • Norfloxacin, 400 mg orally twice daily for 7 days, is the preferred choice. • Intravenous ciprofloxacin, 400 mg every 12 hours; or • Intravenous levofloxacin, 500 mg every 24 hours  Pharmacological therapy • Pharmacological therapy (somatostatin or its analogues octreotide and vapreotide; terlipressin) should be initiated and continued for 3-5 days after diagnosis is confirmed.  Inj. Vit K.  Correct Hepatic encephalopathy by lactulose and phosphate enemas.  Avoid Sedatives.  If tense ascites is present , paracentesis may be done and iv albumin and spironolactone may be used .
VARICEAL BLEEDING AND MANAGEMENT
VARICEAL BLEEDING ESOPHAGEAL VARICES GASTRIC VARICES ECTOPIC VARICES
ESOPHAGEAL VARICES • Present in approximately 40% of patients with cirrhosis and in 60% of patients with cirrhosis and ascites. • Up to 25% of patients with newly diagnosed varices will bleed within two years. • Approximately one half of patients with a variceal bleed stop bleeding spontaneously. • The risk of bleeding in patients with varices:-  less than 5 mm in diameter is 7% by two years.  greater than 5 mm in diameter is 30% by two years. • The risk of death with acute variceal bleeding is 5% to 8% at one week and about 20% at six weeks.
GRADING OF ESOPHAGEAL VARICES Japanese Research Society for Portal Hypertension • Esophageal varices may be :- • Grade I: small and straight • Grade II : tortuous and occupying less than one third of the esophageal lumen • Grade III : large and occupying more than one third of the esophageal lumen
Risk of bleeding is higher with a) Large varices – Grade III > Grade I / II b) Red Wale sign c) Child Pugh Turcotte Score – C>B>A
PRIMARY PROPHYLAXIS OF ESOPHAGEAL VARICEAL HEMORRHAGE
• INDICATIONS:-  All Patients with Class C cirrhosis who have small varices.  All patients with large varices (diameter greater than 5 mm). • In patients who do not bleed during therapy and who do not experience side effects, treatment should be continued indefinitely. • The goal of treatment is to reduce the HVPG to <12 mm Hg or by ≥20%. • The usual starting dose of -  Long-acting Propranolol is 60 mg once daily (Start as 20 mg BD).  Nadolol is 20 mg once daily.. • The dose of propranolol or nadolol can be increased gradually every three to five days until the target heart rate of 25% below baseline or 55 to 60 beats per minute or the maximum tolerated dose is reached, provided that the systolic blood pressure remains above 90 mm Hg. • In patients on pharmacologic therapy, follow-up endoscopy is unnecessary unless gastrointestinal bleeding occurs.
MANAGEMENT OF ACUTE BLEEDING ESOPHAGEAL VARICES.
VASOACTIVE AGENTS • Vasopressin with Nitroglycerin 50-400 µg/min • Terlipressin( triglycyl-lysine-vasopressin) : 2mg iv every 6 h for 48 h ; may be continued 1 mg every 4-6 h for further 3 days. • Somatostatin : 250 or 500 µg iv bolus f/b infusion of 6 mg/24 h for 120 h. • Somatostatin analogs : • Octreotide 50 µg iv bolus & 50µg /h infusion for 2-5 days. • Lanreotide and vapreotide. • Pharmacologic treatment should be continued for up to five days to prevent early rebleeding.
BALL00N TAMPONADE Sengstaken Blakemore Tube Minnesota four-lumen tube • Balloon tamponade should be used as a temporizing measure (maximum 24 hours) in patients with uncontrollable bleeding for whom a more definitive therapy (e.g., TIPS or endoscopic therapy) is planned.
ENDOSCOPIC METHODS ENDOSCOPY METHODS ENDOSCOPIC VARICEAL LIGATION ENDOSCOPIC SCLEROTHERAPY Inj. CYANOACRYLATE GLUE OGD, performed within 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage, either with EVL or sclerotherapy.
ENDOSCOPIC VARICEAL LIGATION (EVL) • Mechanical strangulation of varices by a rubber band. • Multiple bands are applied. • Fall away in 1 to 10 days. • Sloughing produces ulcers which are shallow and heal faster as compared to EST. • Frequency of application of EVL  Varies from 2wks to 2months.  The preferred interval is 4wks. • Complications :  Esophageal ulcers, laceration, perforation.  Transient dysphagia, chest pain.  Bacteremia (EST>10times EVL)
ENDOSCOPIC SCLEROTHERAPY (EST) • Induces inflammation and thrombosis of varix which leads to fibrosis and obliteration of varices. • Used where poor visualisation of varices is present. SOLUTION FOR EST  Polidocanol 1-3%  Sodium morrhuate  1% Sodium Tetradocyl sulphate  Absolute alcohol  5% Ethanolamine oleate COMPLICATIONS  Post esophageal ulcers  Bacteremia – seen in 35%.  Esophageal stenosis – 2 -10%  Esophageal perforation – rare. Can occur early or late  Mortality – 2%. Due to recurrent bleed, perforation, sepsis
REBLEED • Approximately 33% will rebleed within the next 6 weeks. • Of all rebleeding episodes, approximately 40% will take place within 5 days of the initial bleed. • Predictors of rebleeding include :- active bleeding at emergency endoscopy, bleeding from gastric varices, hypoalbuminemia, renal insufficiency, HVPG greater than 20 mm Hg
Prevention of recurrent variceal bleeding (secondary prophylaxis)
• Combined therapy with endoscopic variceal ligation and a nonselective beta blocker is the preferred treatment. • If goals are not achieved, isosorbide mononitrate may be added. • Isosorbide mononitrate-an initial starting dose of 30 mg/day. • Patients with a CTP score of 7 or greater also should be evaluated for liver transplantation.
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT (TIPS) • TIPS is indicated in patients in whom hemorrhage from esophageal varices cannot be controlled or in whom bleeding recurs despite combined pharmacological and endoscopic therapy. • Does not prolong the survival of patients with variceal bleeding.
GASTRIC VARICES • In contrast with esophageal varices, bleeding from gastric varices has been described with an HVPG less than 12 mm Hg. • If endoscopic and pharmacologic therapies fail to control gastric variceal bleeding, then a Linton- Nachlas tube, which has a 600- mL balloon, may be passed as a temporizing measure. • Occurs with splenic vein thrombosis and pancreatitis or pancreatic cancer.
SARIN CLASSIFICATION
 Type 1 : Gastroesophageal varices (GOV1) extend 2 to 5 cm below the gastroesophageal junction and are in continuity with esophageal varices; Type 2 : Gastroesophageal varices (GOV2) are in the cardia and fundus of the stomach and in continuity with esophageal varices; Type 3 : Isolated gastric varices type 1 (IGV1) that occur in the fundus of the stomach in the absence of esophageal varices; Type 4 : Isolated gastric varices type 2 (IGV2) that occur in the gastric body, antrum , or pylorus. SARIN CLASSIFICATION
Management of bleeding gastric varices
Management of bleeding from ectopic varices
Snake skin appearance • One fourth of all cases of bleeding (acute and chronic) in patients with portal hypertension . • The more common presentation is one of chronic, slow bleeding and anemia. • A characteristic mosaic-like pattern of the gastric mucosa. • Development of PHG correlates with the duration of cirrhosis but not necessarily the degree of liver dysfunction. PORTAL HYPERTENSIVE GASTROPATHY
Management Of Chronic Bleeding From Portal Hypertensive Gastropathy
NON VARICEAL BLEEDING AND MANAGEMENT
• Most frequent cause of upper GI Bleed (31- 67% of all cases) Duodenal Ulcer-gastroduodenal A. PUD Gastric ulcer-left gastric A. PEPTIC ULCER DISEASE
Modified Johnson classification for gastric ulcer
– Ia: Active Spurting Bleeding – Ib: Non spurting Active oozing – IIa: Non bleeding visible vessel (NBVV) – IIb: Non bleeding ulcer with adherent clot – IIc: Ulcer with hematin covered base(Flat pigment) – III: Clean base ulcer ground Minor SRH Major SRH 62/81 FORREST CLASSIFICATION FOR BLEEDING PEPTIC ULCER
ENDOSCOPIC CHARACTERISTIC FREQUENCY (%) FURTHER BLEEDING (%) SURGERY (%) MORTALITY (%) Clean base (type III) 42 5 0.5 2 Flat pigmentation (type IIc) 20 10 6 3 Adherent clot (type IIb) 17 22 10 7 Nonbleeding visible vessel (type IIa) 17 43 34 11 Active bleeding (type I) 18 55 35 11
Modalities for endoscopic therapy Two sessions of endoscopic hemostasis Angiographic embolization Surgical therapy
PUD (GU OR DU) H. Pylori Related NSAID Related If symptoms remain , refer to Gastroenterologist After 4 weeks Eradication Test Triple therapy for 14 days + H2 blockers or PPI for 4-6 weeks Active Ulcer NSAID Discontinued → H2 blocker Or PPI NSAID Continued→ PPI Prophylaxis Misoprostol PPI COX 2 Inhibitor
• H.Pylori Treatment- TRIPLE THERAPY • 30mgBD 500mgBD 1000 mg BD
• Mallory-Weiss syndrome refers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting. • Mallory-Weiss tears account for 5% to 10% of cases Mallory-Weiss Tears
Mallory-weiss tears • Supportive therapy:- 90% episodes are self limiting. Mucosa heals within 72hrs. • Ongoing bleeding-local endoscopic therapy
• Appearance of multiple superficial erosions of the entire stomach, most commonly in the body.  Respiratory failure  Coagulopathy  NSAID users  Sepsis  Hemodynamic instability  Head injuries with I.C.T (Cushing ulcer)  Burn injuries (Curling ulcer)  Multiple trauma Stress Gastritis decrease splanchnic mucosal blood flow altered gastric luminal acidity STRESS GASTRITIS
PROPHYLACTIC THERAPY •Routine uses of stress ulcer prophylaxis in the intensive care unit is not recommended unless the patient has a coagulopathy or is receiving mechanical ventilation. •Maintain the luminal gastric pH above 4. PPIS,,, H2 Antagonists.. Sucralfate..
• PERSISTENT CALIBER ARTERY • Vascular malformations along the lesser curve of the stomach within 6 cm of the GEJ • Represents rupture of unusually large vessels (1-3 mm) in the gastric submucosa. • Erosion of the gastric mucosa overlying these vessels leads to hemorrhage. • Endoscopic therapy DIEULAFOY’S LESION
• “Watermelon stomach” • Collection of dilated venules appearing as linear red streaks converging on the antrum in longitudinal fashion, giving it the appearance of a watermelon. • GAVE is related to liver failure, rather than to portal hypertension. GASTRIC ANTRAL VASCULAR ECTASIA
Management of chronic bleeding from gastric vascular antral ectasia (GAVE)
• Usually associated with chronic anemia or hemoccult-positive stool • Occasionally, malignancies present as ulcerative lesions that bleed persistently. • Most characteristic of the GIST • Also occur with leiomyomas and lymphomas. MALIGNANCY
Aortoenteric fistula • Primary aortoenteric fistula is a communication between the abdominal aorta and most commonly, the third portion of the duodenum. • Secondary aortoenteric fistulas usually occur between the small intestine and an infected abdominal aortic surgical graft. • CT with intravenous contrast • Surgical treatment
• Typically associated with liver trauma, liver biopsy, recent instrumentation of the biliary tree, or hepatic neoplasms. • Suspected in anyone who presents with hemorrhage, right upper quadrant pain, and jaundice • Angiographic embolisation HAEMOBILIA
• Bleeding from the pancreatic duct. • In patients with acute pancreatitis, chronic pancreatitis, pancreatic pseudocyst, or pancreatic cancer or after ERCP • Also result from rupture of a splenic artery aneurysm into the pancreatic duct. • Presents with abdominal pain and hematochezia • Angiographic embolization or Distal pancreatectomy Haemosuccus Pancreaticus
• May follow therapeutic or diagnostic procedures. • Common causes of iatrogenic bleeding – Endoscopic sphincterotomy. Percutaneous transhepatic procedures. • 2% of cases. • It is often mild and self-limited. • Percutaneous endoscopic gastrotomy. IATROGENIC BLEEDING
1. Advanced AGE >65 years 2. SHOCK on admission(pulse rate >100 beats/min; systolic blood pressure < 100mmHg) 3. COMORBIDITY (particularly hepatic or renal failure , DM , HTN and disseminated malignancy) 4. Diagnosis (worst PROGNOSIS for advanced upper gastrointestinal malignancy) 5. ENDOSCOPIC FINDINGS (active, spurting hemorrhage from peptic ulcer; non-bleeding visible vessel) 6. RECURRENT BLEEDING (increases mortality 10 times) 7. Where there is simultaneous upper and lower GI bleeding. 8. On steroids or NSAIDs 9. Alcoholic or tobacco smoker 80/81 UPPER GI BLEED: HIGH RISK FACTORS
SCORING SYSTEM 1. Glasgow-Blatchford Score 2. AIMS 65 3. THE ROCKALL SCORE
 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 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 failure
AIMS 65 High accuracy for predicting inpatient mortality among patients with upper GI bleeding. • Albumin less than 3.0 g/dL (30 g/L) • INR greater than 1.5 • Altered Mental status (Glasgow coma score less than 14, disorientation, lethargy, stupor, or coma) • Systolic blood pressure of 90 mmHg or less • Age older than 65 years The mortality rate increased significantly as the number of risk factors present increased: ●Zero risk factors: 0.3 percent ●One risk factor: 1 percent ●Two risk factors: 3 percent ●Three risk factors: 9 percent ●Four risk factors: 15 percent ●Five risk factors: 25 percent
THE ROCKALL SCORE Rockall, Lancet 1996 • For Risk of Rebleeding and Death After Admission to the Hospital for Acute GI Bleeding
Risk category Rockall’s score>8=High risk of death 50% Patients will rebleed. Rockall’s score<3=excellent prognosis Lower risk of hemorrhage. Rockall score Cumulative patients with rebleeding
Who can be sent home from the emergency room? Gralnek, NEJM, 2008 These patients represent up to 20-40% of all patients presenting with PUB
SURGICAL MANAGEMENT
• Hemodynamic instability despite vigorous resuscitation (>6 units transfusion) • Failure of endoscopy • Recurrent hemorrhage after initial stabilization (with up to two attempts of endoscopy) • Shock associated with recurrent hemorrhage • Continued slow bleeding with a transfusion exceeding 3 units/day  Oneofthecriteriausedtodeterminetheneedforsurgicalinterventionis thenumberofunitsoftransfusedbloodrequiredtoresuscitatethepatient. Themoreunitsrequired,thehigherthemortalityrate(Larson,1986). Operativeinterventionisindicatedoncethebloodtransfusionnumber reachesmorethan5units,asnotedinthefollowingtable(Larson,1986). NumberofUnits Transfused Needfor Surgery,% Mortality Rate,% 0 4 4 1-3 6 14 4-5 17 28 >5 57 43 Indications for Surgery in Gastrointestinal Hemorrhage :-
Relative Indications • Rare blood type or difficult crossmatch • Refusal to transfusion • Shock at presentation • Advanced age • Severe comorbid diseases • Bleeding chronic gastric ulcer where malignancy is a possibility
PRIORITIES •Control Hemorrhage !! • Definitive procedure for the underlying pathology
uppergibleeding-150402032909-conversion-gate01.pdf

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In this document
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Overview of upper GI bleeding, its definition, causes, and initial management approach.

Defining upper GI bleeding and differentiating types: hematemesis, melena, hematochezia.

Types of upper GI bleeding categorized as variceal and non-variceal, with associated causes.

Important historical aspects and potential causes linked to various types of upper GI bleeding.

Examination findings for assessing patients with upper GI bleeding, including signs of liver disease.

Diagnostic tests used in evaluating upper GI bleeding including blood tests and imaging.

Endoscopic techniques and imaging methods essential for diagnosing sources of upper GI bleeding.

Immediate treatment measures including volume resuscitation and stabilization protocols.

Specific management strategies for variceal bleeding focusing on pharmacological and endoscopic treatments. Ongoing management to prevent rebleeding, with interventions like TIPS and medication adjustments.

Focus on common causes like peptic ulcers, stress gastritis, and their respective management protocols.Identification of high-risk indicators and implementation of scoring systems for assessing patient prognosis.

Criteria for surgical intervention in upper GI bleeding cases and the importance of controlling hemorrhage.

uppergibleeding-150402032909-conversion-gate01.pdf

  • 1.
    APPROACH TO UPPERGI BLEEDING By :- Dr. NITESH PANSARI MEDICINE UNIT –A RNT MEDICAL COLLEGE , UDAIPUR
  • 2.
    SYNOPSIS • Definition &Presentation • Causes of UGI bleeding • History & Physical Examination • Investigations • Management of acute episode • Variceal bleeeding & management • Nonvariceal bleeding & management • High risk Factors • Scoring systems • Indication of surgical intervention
  • 3.
    DEFINITION • Upper GIbleeding is defined as bleeding from a source proximal to the Ligament of Treitz
  • 4.
    Hematemesis • Vomiting ofred blood or coffee- grounds material when gastric acid converts hemoglobin into methemoglobin . • Differentiate from :- Hemoptysis. Bleeding from Pharynx , nasal passage.
  • 5.
    Patient with hematemesisusually requires a bucket; whereas patient with hemoptysis usually requires a small bowl. Is It Hematemesis?
  • 6.
    Melena • Passage ofblack tarry stools. • Blood loss between 50-100 ml /day will produce melena. • The black color of melenic stools is caused by Hematin, the product of oxidation of Heme by intestinal and bacterial enzymes. • Can be seen in LGI bleed also (10%). • Non GI bleed – swallowed blood from epistaxis • Blood for 14 hrs in the GI tract • Oral iron and bismuth mimics melena.
  • 7.
    Hematochezia • It isdefined as passage of bright-red or maroon blood from the rectum. • Common in bleeding from colon, rectum and anus. • In case of brisk bleeding in the upper git, bright red blood may come out unchanged in the stool. • 10% of UGI bleed Occult GI bleeding • Absence of overt bleeding • Fecal occult blood test - +ve • Suspected in patients with iron deficiency anemia • Normally 2.5 ml of blood is lost per day. • OBT detects amount between 10-50 ml/d. Symptoms of blood loss or anemia • Light headedness, syncope, angina, or dyspnea
  • 8.
  • 9.
    Esophageal causes • Esophagealvarices • Esophagitis • Esophageal cancer • Esophageal ulcers • Mallory-Weiss tear Gastric causes • Gastric ulcer • Gastric cancer • Gastritis • Gastric varices • Dieulafoy's lesions • Gastric Antral Vascular Ectasia • Portal Hypertensive Gastropathy 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 • Severe superior mesenteric artery syndrome CAUSES
  • 11.
    Bleeding etiology LeadingHistory 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
  • 12.
    • Previous EpisodesOf GI Bleed • H/O Instrumentation • H/O Head Injury • Co-morbid Conditions o Liver Disease o Renal Disease o Cardiovascular Disease o Chronic Respiratory Conditions • H/O Abdominal Surgery Personal History • Alcoholism , Smoking , Tobacco Abuse • Cocaine Abuse • Weight Loss, Anorexia Past History
  • 13.
    Drug History • Salicylates/NSAIDS • Anticoagulants (warfarin / Heparin) • Corticosteroids • Oral Iron , Bismuth ( Mimic Melena )
  • 14.
    • Pallor ,signs of dehydration , Shock • Icterus • Clubbing • Oedema }Liver disease PHYSICAL EXAMINATION
  • 15.
    Lymphadenopathy Virchow’s Node (Troisier’s sign) Vitalsigns Tachycardia Hypotension Tachypnea
  • 16.
    SIGNS OF LIVERCELL FAILURE
  • 17.
    • Ascites •Spider naevi • Palmar erythema • Dupuytren’s contracture
  • 18.
    • Leuconychia •Gynecomastia • Bleeding manifestations • Scars of previous surgery
  • 19.
    • Splenomegaly • Caputmedusae • Parotid Swelling • Fetor hepaticus • Asterixis • Testicular atrophy • Acanthosis nigricans • Alopecia • Glossitis • Loss of Axillary hair • Loss of Pubic Hair
  • 20.
    INSPECTION Distention , DilatedVeins Swelling Visible peristalsis PALPATION Tenderness HSM, secondary metastasis Sister Mary Joseph nodules Mass PERCUSSION Shifting dullness HSM AUSCULTATION Absent Bowel sound Bruit Cruveilhier-Baumgarten venous hum ABDOMEN EXAMINATION
  • 21.
    PR EXAMINATION • Hemorroids •Melena , blood • Blumer’s shelf
  • 22.
    LAB ASSESSMENT • FullBlood Count- Hb, Platelet count • PCV* • Coagulation Profile • Liver Function tests • Serum electrolytes • Blood urea nitrogen ratio > 30 sensitivity of 68% and a specificity of 98% • Blood Grouping & Cross matching. • Serial ECG • Stool Occult Blood Test • HIV, HbsAg , Anti HCV Markers INVESTIGATIONS
  • 23.
    • Renal FunctionTests • Gastrin level • Nasogastric aspiration 1. Red blood-current bleeding 2. Coffee ground-recent bleeding 3. Continuous aspiration-severe active bleed Lavage not +ve- i) bleeding has stopped ii) beyond pylorus • PCV* : decreased only by 24 to 72hrs, after bleed  CHEST XRAY  USG
  • 24.
    ESOPHAGOGASTRODUODENOSCOPY • Most importantcomponent of investigation. • 90% accuracy in diagnosis if done with in 24 hours. ENDOSCOPY
  • 25.
    •Examination of wholebowel possible •Indicated in GI bleeding of obscure source Video capsule endoscopy
  • 26.
    •PUSH ENTEROSCOPY •DEEP ENTEROSCOPY SINGLE OR DOUBLE BALLOON ENDOSCOPY  SPIRAL ENDOSCOPY
  • 27.
    RADIOLOGIC IMAGING • ANGIOGRAPHY:- bleeding rate at least 0.5 mL/min. • RADIONUCLIDE IMAGING :- bleeding at a rate of 0.04 mL/min Technetium pertechnetate–labeled red blood cell scans >>> Technetium sulfur colloid scans • CT enterography and CT angiography • Barium radiography is not indicated (and contraindicated if endoscopy or angiography is planned) in the emergency setting.
  • 30.
    Airway: • Secure toprevent aspiration • Endotracheal tube & give oxygen Breathing: • support respiratory function Circulation: • Expand circulatory volume • 2 large bore i.v. cannula • RBC transfusion with the goal of maintaining the hematocrit value to 30% or hemoglobin to 8 g/dL. • Normal saline may be infused intravenously until packed red blood cells are available for transfusion. • Maintain systolic B.P. at equal or greater than 90mmHg • Pressure agents like dopamine 2.5 to 10 mcg/kg/min, and dobutamine 2.5 to 10 mcg/kg/min as infusion, Noradrenalin 3mg. /h as infusion may be required, as a last resort, to maintain peripheral perfusion.
  • 31.
    • Correct anycoagulopathy with :- 10 - 15 ml/kg of FFP (if PT INR > 1.5) and/or platelet transfusions (if platelet count < 50,000/cu.mm) • Monitor:  Skin color, peripheral temperature  Pulse Rate, BP  Respiratory Rate, O2 saturation of blood  Urine output (Foley’s Catheter) TREATMENT OF SUSPECTED PEPTIC ULCER BLEEDING: • Start High dose , constant infusion IV PPIs (Omeprazole 80 mg bolus and 8mg/ h infusion for 72 h)
  • 32.
    TREATMENT OF SUSPECTED VARICEALHEMORRHAGE  Antibiotic prophylaxis • To prevent bacteremia and spontaneous bacterial peritonitis • Intravenous ceftriaxone, 1 g every 24 hours for 7 days ; or • Norfloxacin, 400 mg orally twice daily for 7 days, is the preferred choice. • Intravenous ciprofloxacin, 400 mg every 12 hours; or • Intravenous levofloxacin, 500 mg every 24 hours  Pharmacological therapy • Pharmacological therapy (somatostatin or its analogues octreotide and vapreotide; terlipressin) should be initiated and continued for 3-5 days after diagnosis is confirmed.  Inj. Vit K.  Correct Hepatic encephalopathy by lactulose and phosphate enemas.  Avoid Sedatives.  If tense ascites is present , paracentesis may be done and iv albumin and spironolactone may be used .
  • 34.
  • 35.
  • 36.
    ESOPHAGEAL VARICES • Presentin approximately 40% of patients with cirrhosis and in 60% of patients with cirrhosis and ascites. • Up to 25% of patients with newly diagnosed varices will bleed within two years. • Approximately one half of patients with a variceal bleed stop bleeding spontaneously. • The risk of bleeding in patients with varices:-  less than 5 mm in diameter is 7% by two years.  greater than 5 mm in diameter is 30% by two years. • The risk of death with acute variceal bleeding is 5% to 8% at one week and about 20% at six weeks.
  • 37.
    GRADING OF ESOPHAGEALVARICES Japanese Research Society for Portal Hypertension • Esophageal varices may be :- • Grade I: small and straight • Grade II : tortuous and occupying less than one third of the esophageal lumen • Grade III : large and occupying more than one third of the esophageal lumen
  • 38.
    Risk of bleedingis higher with a) Large varices – Grade III > Grade I / II b) Red Wale sign c) Child Pugh Turcotte Score – C>B>A
  • 39.
    PRIMARY PROPHYLAXIS OFESOPHAGEAL VARICEAL HEMORRHAGE
  • 40.
    • INDICATIONS:-  AllPatients with Class C cirrhosis who have small varices.  All patients with large varices (diameter greater than 5 mm). • In patients who do not bleed during therapy and who do not experience side effects, treatment should be continued indefinitely. • The goal of treatment is to reduce the HVPG to <12 mm Hg or by ≥20%. • The usual starting dose of -  Long-acting Propranolol is 60 mg once daily (Start as 20 mg BD).  Nadolol is 20 mg once daily.. • The dose of propranolol or nadolol can be increased gradually every three to five days until the target heart rate of 25% below baseline or 55 to 60 beats per minute or the maximum tolerated dose is reached, provided that the systolic blood pressure remains above 90 mm Hg. • In patients on pharmacologic therapy, follow-up endoscopy is unnecessary unless gastrointestinal bleeding occurs.
  • 41.
    MANAGEMENT OF ACUTEBLEEDING ESOPHAGEAL VARICES.
  • 42.
    VASOACTIVE AGENTS • Vasopressinwith Nitroglycerin 50-400 µg/min • Terlipressin( triglycyl-lysine-vasopressin) : 2mg iv every 6 h for 48 h ; may be continued 1 mg every 4-6 h for further 3 days. • Somatostatin : 250 or 500 µg iv bolus f/b infusion of 6 mg/24 h for 120 h. • Somatostatin analogs : • Octreotide 50 µg iv bolus & 50µg /h infusion for 2-5 days. • Lanreotide and vapreotide. • Pharmacologic treatment should be continued for up to five days to prevent early rebleeding.
  • 43.
    BALL00N TAMPONADE Sengstaken BlakemoreTube Minnesota four-lumen tube • Balloon tamponade should be used as a temporizing measure (maximum 24 hours) in patients with uncontrollable bleeding for whom a more definitive therapy (e.g., TIPS or endoscopic therapy) is planned.
  • 44.
    ENDOSCOPIC METHODS ENDOSCOPY METHODS ENDOSCOPIC VARICEAL LIGATION ENDOSCOPIC SCLEROTHERAPY Inj. CYANOACRYLATE GLUE OGD, performedwithin 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage, either with EVL or sclerotherapy.
  • 45.
    ENDOSCOPIC VARICEAL LIGATION(EVL) • Mechanical strangulation of varices by a rubber band. • Multiple bands are applied. • Fall away in 1 to 10 days. • Sloughing produces ulcers which are shallow and heal faster as compared to EST. • Frequency of application of EVL  Varies from 2wks to 2months.  The preferred interval is 4wks. • Complications :  Esophageal ulcers, laceration, perforation.  Transient dysphagia, chest pain.  Bacteremia (EST>10times EVL)
  • 46.
    ENDOSCOPIC SCLEROTHERAPY (EST) •Induces inflammation and thrombosis of varix which leads to fibrosis and obliteration of varices. • Used where poor visualisation of varices is present. SOLUTION FOR EST  Polidocanol 1-3%  Sodium morrhuate  1% Sodium Tetradocyl sulphate  Absolute alcohol  5% Ethanolamine oleate COMPLICATIONS  Post esophageal ulcers  Bacteremia – seen in 35%.  Esophageal stenosis – 2 -10%  Esophageal perforation – rare. Can occur early or late  Mortality – 2%. Due to recurrent bleed, perforation, sepsis
  • 47.
    REBLEED • Approximately 33%will rebleed within the next 6 weeks. • Of all rebleeding episodes, approximately 40% will take place within 5 days of the initial bleed. • Predictors of rebleeding include :- active bleeding at emergency endoscopy, bleeding from gastric varices, hypoalbuminemia, renal insufficiency, HVPG greater than 20 mm Hg
  • 48.
    Prevention of recurrentvariceal bleeding (secondary prophylaxis)
  • 50.
    • Combined therapywith endoscopic variceal ligation and a nonselective beta blocker is the preferred treatment. • If goals are not achieved, isosorbide mononitrate may be added. • Isosorbide mononitrate-an initial starting dose of 30 mg/day. • Patients with a CTP score of 7 or greater also should be evaluated for liver transplantation.
  • 51.
    TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT(TIPS) • TIPS is indicated in patients in whom hemorrhage from esophageal varices cannot be controlled or in whom bleeding recurs despite combined pharmacological and endoscopic therapy. • Does not prolong the survival of patients with variceal bleeding.
  • 52.
    GASTRIC VARICES • Incontrast with esophageal varices, bleeding from gastric varices has been described with an HVPG less than 12 mm Hg. • If endoscopic and pharmacologic therapies fail to control gastric variceal bleeding, then a Linton- Nachlas tube, which has a 600- mL balloon, may be passed as a temporizing measure. • Occurs with splenic vein thrombosis and pancreatitis or pancreatic cancer.
  • 53.
  • 54.
     Type 1: Gastroesophageal varices (GOV1) extend 2 to 5 cm below the gastroesophageal junction and are in continuity with esophageal varices; Type 2 : Gastroesophageal varices (GOV2) are in the cardia and fundus of the stomach and in continuity with esophageal varices; Type 3 : Isolated gastric varices type 1 (IGV1) that occur in the fundus of the stomach in the absence of esophageal varices; Type 4 : Isolated gastric varices type 2 (IGV2) that occur in the gastric body, antrum , or pylorus. SARIN CLASSIFICATION
  • 55.
    Management of bleedinggastric varices
  • 56.
    Management of bleedingfrom ectopic varices
  • 57.
    Snake skin appearance •One fourth of all cases of bleeding (acute and chronic) in patients with portal hypertension . • The more common presentation is one of chronic, slow bleeding and anemia. • A characteristic mosaic-like pattern of the gastric mucosa. • Development of PHG correlates with the duration of cirrhosis but not necessarily the degree of liver dysfunction. PORTAL HYPERTENSIVE GASTROPATHY
  • 58.
    Management Of ChronicBleeding From Portal Hypertensive Gastropathy
  • 59.
  • 60.
    • Most frequentcause of upper GI Bleed (31- 67% of all cases) Duodenal Ulcer-gastroduodenal A. PUD Gastric ulcer-left gastric A. PEPTIC ULCER DISEASE
  • 61.
  • 62.
    – Ia: ActiveSpurting Bleeding – Ib: Non spurting Active oozing – IIa: Non bleeding visible vessel (NBVV) – IIb: Non bleeding ulcer with adherent clot – IIc: Ulcer with hematin covered base(Flat pigment) – III: Clean base ulcer ground Minor SRH Major SRH 62/81 FORREST CLASSIFICATION FOR BLEEDING PEPTIC ULCER
  • 63.
    ENDOSCOPIC CHARACTERISTIC FREQUENCY (%) FURTHER BLEEDING (%) SURGERY(%) MORTALITY (%) Clean base (type III) 42 5 0.5 2 Flat pigmentation (type IIc) 20 10 6 3 Adherent clot (type IIb) 17 22 10 7 Nonbleeding visible vessel (type IIa) 17 43 34 11 Active bleeding (type I) 18 55 35 11
  • 65.
    Modalities for endoscopictherapy Two sessions of endoscopic hemostasis Angiographic embolization Surgical therapy
  • 66.
    PUD (GU ORDU) H. Pylori Related NSAID Related If symptoms remain , refer to Gastroenterologist After 4 weeks Eradication Test Triple therapy for 14 days + H2 blockers or PPI for 4-6 weeks Active Ulcer NSAID Discontinued → H2 blocker Or PPI NSAID Continued→ PPI Prophylaxis Misoprostol PPI COX 2 Inhibitor
  • 67.
    • H.Pylori Treatment-TRIPLE THERAPY • 30mgBD 500mgBD 1000 mg BD
  • 68.
    • Mallory-Weiss syndromerefers to bleeding from tears (a Mallory-Weiss tear) in the mucosa at the junction of the stomach and esophagus, usually caused by severe retching, coughing, or vomiting. • Mallory-Weiss tears account for 5% to 10% of cases Mallory-Weiss Tears
  • 69.
    Mallory-weiss tears • Supportivetherapy:- 90% episodes are self limiting. Mucosa heals within 72hrs. • Ongoing bleeding-local endoscopic therapy
  • 70.
    • Appearance ofmultiple superficial erosions of the entire stomach, most commonly in the body.  Respiratory failure  Coagulopathy  NSAID users  Sepsis  Hemodynamic instability  Head injuries with I.C.T (Cushing ulcer)  Burn injuries (Curling ulcer)  Multiple trauma Stress Gastritis decrease splanchnic mucosal blood flow altered gastric luminal acidity STRESS GASTRITIS
  • 71.
    PROPHYLACTIC THERAPY •Routine usesof stress ulcer prophylaxis in the intensive care unit is not recommended unless the patient has a coagulopathy or is receiving mechanical ventilation. •Maintain the luminal gastric pH above 4. PPIS,,, H2 Antagonists.. Sucralfate..
  • 72.
    • PERSISTENT CALIBER ARTERY •Vascular malformations along the lesser curve of the stomach within 6 cm of the GEJ • Represents rupture of unusually large vessels (1-3 mm) in the gastric submucosa. • Erosion of the gastric mucosa overlying these vessels leads to hemorrhage. • Endoscopic therapy DIEULAFOY’S LESION
  • 73.
    • “Watermelon stomach” •Collection of dilated venules appearing as linear red streaks converging on the antrum in longitudinal fashion, giving it the appearance of a watermelon. • GAVE is related to liver failure, rather than to portal hypertension. GASTRIC ANTRAL VASCULAR ECTASIA
  • 74.
    Management of chronicbleeding from gastric vascular antral ectasia (GAVE)
  • 75.
    • Usually associatedwith chronic anemia or hemoccult-positive stool • Occasionally, malignancies present as ulcerative lesions that bleed persistently. • Most characteristic of the GIST • Also occur with leiomyomas and lymphomas. MALIGNANCY
  • 76.
    Aortoenteric fistula • Primaryaortoenteric fistula is a communication between the abdominal aorta and most commonly, the third portion of the duodenum. • Secondary aortoenteric fistulas usually occur between the small intestine and an infected abdominal aortic surgical graft. • CT with intravenous contrast • Surgical treatment
  • 77.
    • Typically associated withliver trauma, liver biopsy, recent instrumentation of the biliary tree, or hepatic neoplasms. • Suspected in anyone who presents with hemorrhage, right upper quadrant pain, and jaundice • Angiographic embolisation HAEMOBILIA
  • 78.
    • Bleeding fromthe pancreatic duct. • In patients with acute pancreatitis, chronic pancreatitis, pancreatic pseudocyst, or pancreatic cancer or after ERCP • Also result from rupture of a splenic artery aneurysm into the pancreatic duct. • Presents with abdominal pain and hematochezia • Angiographic embolization or Distal pancreatectomy Haemosuccus Pancreaticus
  • 79.
    • May followtherapeutic or diagnostic procedures. • Common causes of iatrogenic bleeding – Endoscopic sphincterotomy. Percutaneous transhepatic procedures. • 2% of cases. • It is often mild and self-limited. • Percutaneous endoscopic gastrotomy. IATROGENIC BLEEDING
  • 80.
    1. Advanced AGE>65 years 2. SHOCK on admission(pulse rate >100 beats/min; systolic blood pressure < 100mmHg) 3. COMORBIDITY (particularly hepatic or renal failure , DM , HTN and disseminated malignancy) 4. Diagnosis (worst PROGNOSIS for advanced upper gastrointestinal malignancy) 5. ENDOSCOPIC FINDINGS (active, spurting hemorrhage from peptic ulcer; non-bleeding visible vessel) 6. RECURRENT BLEEDING (increases mortality 10 times) 7. Where there is simultaneous upper and lower GI bleeding. 8. On steroids or NSAIDs 9. Alcoholic or tobacco smoker 80/81 UPPER GI BLEED: HIGH RISK FACTORS
  • 81.
    SCORING SYSTEM 1. Glasgow-BlatchfordScore 2. AIMS 65 3. THE ROCKALL SCORE
  • 82.
     Blood UreaNitrogen(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 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 failure
  • 83.
    AIMS 65 High accuracyfor predicting inpatient mortality among patients with upper GI bleeding. • Albumin less than 3.0 g/dL (30 g/L) • INR greater than 1.5 • Altered Mental status (Glasgow coma score less than 14, disorientation, lethargy, stupor, or coma) • Systolic blood pressure of 90 mmHg or less • Age older than 65 years The mortality rate increased significantly as the number of risk factors present increased: ●Zero risk factors: 0.3 percent ●One risk factor: 1 percent ●Two risk factors: 3 percent ●Three risk factors: 9 percent ●Four risk factors: 15 percent ●Five risk factors: 25 percent
  • 84.
    THE ROCKALL SCORE Rockall,Lancet 1996 • For Risk of Rebleeding and Death After Admission to the Hospital for Acute GI Bleeding
  • 85.
    Risk category Rockall’s score>8=Highrisk of death 50% Patients will rebleed. Rockall’s score<3=excellent prognosis Lower risk of hemorrhage. Rockall score Cumulative patients with rebleeding
  • 86.
    Who can besent home from the emergency room? Gralnek, NEJM, 2008 These patients represent up to 20-40% of all patients presenting with PUB
  • 87.
  • 88.
    • Hemodynamic instability despitevigorous resuscitation (>6 units transfusion) • Failure of endoscopy • Recurrent hemorrhage after initial stabilization (with up to two attempts of endoscopy) • Shock associated with recurrent hemorrhage • Continued slow bleeding with a transfusion exceeding 3 units/day  Oneofthecriteriausedtodeterminetheneedforsurgicalinterventionis thenumberofunitsoftransfusedbloodrequiredtoresuscitatethepatient. Themoreunitsrequired,thehigherthemortalityrate(Larson,1986). Operativeinterventionisindicatedoncethebloodtransfusionnumber reachesmorethan5units,asnotedinthefollowingtable(Larson,1986). NumberofUnits Transfused Needfor Surgery,% Mortality Rate,% 0 4 4 1-3 6 14 4-5 17 28 >5 57 43 Indications for Surgery in Gastrointestinal Hemorrhage :-
  • 89.
    Relative Indications • Rareblood type or difficult crossmatch • Refusal to transfusion • Shock at presentation • Advanced age • Severe comorbid diseases • Bleeding chronic gastric ulcer where malignancy is a possibility
  • 90.
    PRIORITIES •Control Hemorrhage !! •Definitive procedure for the underlying pathology