Approach to Management of Upper Gastrointestinal (GI) Bleeding

Upper gastrointestinal bleeding is gastrointestinal bleeding in the upper gastrointestinal tract, commonly defined as bleeding arising from the esophagus, stomach, or duodenum. Blood may be observed in vomit (hematemesis) or in altered form in the stool (melena). Depending on the severity of the blood loss, there may be symptoms of insufficient circulating blood volume and shock. As a result, upper gastrointestinal bleeding is considered a medical emergency and typically requires hospital care for urgent diagnosis and treatment. Upper gastrointestinal bleeding can be caused by peptic ulcers, gastric erosions, esophageal varices, and some rarer causes such as gastric cancer.

The initial assessment includes measurement of the blood pressure and heart rate, as well as blood tests to determine hemoglobin concentration. In significant bleeding, fluid replacement is often required, as well as blood transfusion, before the source of bleeding can be determined by endoscopy of the upper digestive tract with an esophagogastroduodenoscopy. Depending on the source, endoscopic therapy can be applied to reduce rebleeding risk. Specific medical treatments (such as proton pump inhibitors for peptic ulcer disease) or procedures (such as TIPS for variceal hemorrhage) may be used. Recurrent or refractory bleeding may lead to need for surgery, although this has become uncommon as a result of improved endoscopic and medical treatment.

1. Approach to Upper GI Bleed Seminar – November 30 t h 2015 Presenter: Dr.Arun Vasireddy

2. 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.

3. 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 …..?

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

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

6. 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.

7. 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%

8. 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

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

10. 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

11. 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

12. MALLORY WEISS SYNDROME / TEARS M ucosal 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.

13. HAEMORRAGIC OR EROSIVE GASTRITIS Stress related mucosal injury Occur mostly in extremly sick patients Major Trauma Post Major Surgery 3 rd Degree burns Major intracranial disease Severe medical illness (Ventilator dependence, coagulopathy ) Significant bleeding probably does not develop unless ulceration occurs. Intravenous H 2 -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 .

14. 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.

15. 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.

16. 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.

17. Gastric Antral Vascular Ectasia Gastric antral vascular ectasia (GAVE), also described as watermelon stomach. C haracterized by rows or stripes of ectatic mucosal blood vessels that emanate from the pylorus and extend proximally into the antrum .

18. 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 .

19. 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.

20. 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.

21. 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.

22. 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

23. 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

24. 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

25. 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

26. 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

27. Approach to a Patient with UGIB

28. 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 .

29. 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 BLATCHFORD SCORE 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 S cores ≥ 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 failure Blatchford O, Murray WR, Blatchford M:  Lancet   2000; 356:1318-21 .

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

31. 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

32. 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.

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

34. 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

35. 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

36. ENDOSCOPIC MODALITIES AVAILABLE FOR THE 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 Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition

37. 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

38. 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.

39. Hematocrit values before & after bleeding

40. 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

41. 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

42. 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 400 mg 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

43. 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 H 2 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

44. 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.

45. 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).

46. 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

47. 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

48. 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

49. 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

50. UTILITY OF ENDOTHERAPY D iagnostic & 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.

51. OPTIMIZING ENDOSCOPIC VISUALIZATION 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

52. METHODS TO 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

53. INJECTION THERAPY * 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.

54. CONTACT THERMAL THERAPY M onopolar 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.

55. 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

56. Medical Management Of Variceal 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. S omatostatin -250ug bolus then 250ug/hr infusion Octeotride-50ug bolus then 50ug/hr infusion for 5 days Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition

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

58. 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  )

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

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

61. 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.

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

63. 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 .

64. 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

65. Adverse prognostic factor in UGIB Age over 60 Shock(SBP<100mmhg), pulse >100 Malignancy or varices as bleeding source. Severe coagulopathy Comorbid medical illness Continued or recurrent bleeding Severe active Bleeding (Hypotension, multiple transfusion, bright red nasogastric aspirate) Endoscopically identified arterial bleeding or visible vessel Ulcer location Emergency surgery if surgical complication Medicine update 2014 API

66. R ecurrent Gastrointestinal bleeding Initial Control Endoscopic therapy Permanent Control Rebleeding Endoscopic therapy Rebleeding Surgery Angiography Permanent Control 80-90% 50%

67. 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 Sleisenger and Fordtran's Gastrointestinal and Liver Disease Ninth Edition Angiographic interventions/surgery

68. Angioembolization

69. 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.

70. 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.

71. 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 .

72. 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.

73. 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.

74. References: API Medicine Update 2014 Mayo Clinic Gastroenterology Board Review 5 th Ed Mount Sinai Expert Guides: Gastroenterology 2015 Guidelines Sources – American college of gastroenterology 2012 guidelines American society of gastrointestinal endoscopy 2015 guidelines