Upper Gastro intestinal Bleeding. .

A ppt on Uppet GI bleed made by Monika Pathania

1. UPPER GIT BLEEDING Dr Monika Pathania MD,Medicine .

2. Question : A 35-year-old man with chronic alcoholism is evaluated because of bright-red hematemesis and syncope. At 11 PM his pulse rate is 100/min and his blood pressure is 100/60 mm Hg, and there is red-tinged irrigant present in the nasogastric tube. The patient has multiple, vascular spider angiomata and a distended abdomen with shifting dullness. He has received 2 L of normal saline solution, and an octreotide drip. His vital signs have stabilized. What is the optimal management for this patient? ( A ) endoscopy ( B ) medical therapy ( C ) Portocaval shunt surgery ( D ) Transjugular intrahepatic portosystemic shunt (TIPS)

3. Definitions Hematemesis V omitus of red blood or "coffee-grounds" material. Represents an upper GI bleed.  Hematochezia T he passage of bright red or maroon blood from the rectum. Represents lower GI bleeds (90%) or severe upper GI bleeds (10%)

4. Definitions Melena B lack, tarry , foul-smelling stool resulting from digested blood (at least 100 ml) Usually indicates upper GI bleed with blood prsent in the GI tract for at least 14 hrs

5. Black Stool Non-GIB causes of black stool include: Bismuth subsalicylate Iron Spinach Charcoal Dark beers Swallowed blood from nose bleeding

6. Introduction Upper GI bleeds are considered medical emergency, and require admission to hospital for urgent diagnosis and management. Proximal bleeding to Ligament of Treitz .

7. Ligament of Treitz Ligament of Treitz: a fibrous band by which the duodenojejunal junction is fixed to posterior wall of abdominal cavity, usually at the level of L1. Upper GIB – Bleeding arising proximal to the ligament of Treitz Lower GIB – Bleeding arising distal the ligament of Treitz

8. Epidemiology Incidence 150/100,000 population per year. Overall mortality 10% in those admitted to hospital. Mortality 30 % in the elderly.

9. Etiology

10. Peptic Ulcer Disease half of major UGIB mortality of 6-10%. Chronic ulcers, caused by exposure to acid & pepsin Usually solitary Size ranges from ~ 0.6 - 4 cm Most common in duodenum and antrum Ratio of duodenal:gastric ~ 4 : 1

11. Peptic Ulcer Disease Clinical: epigastric pain 1-3 hours after meals & is worse at night; nausea; vomiting; belching, weight loss Complications: Hemorrhage - 25% of ulcer deaths Perforation – 66% of ulcer deaths Obstruction Malignant transformation

12. Risk Factors for peptic ulcers H. pylori NSAIDS Stress Gastric Acid

13. Benign gastric ulcer

14. Cardia carcinoma

15. H. Pylori Transmitted fecal-oral Disrupts mucous layer, liberating enzymes and toxins causing mucosal damage Assoc. w/ gastric cancer and non-Hodgkin’s gastric lymphoma Eradication should be sought-PPI, Clarithromycin and amoxicillin

16. Duodenal ulcer

17. NSAIDS Inhibition of prostaglandins Most of these ulcers are asymptomatic and uncomplicated Implicated as an important factor for non-healing ulcers

18. Gastritis produced by aspirin and other nonsteroidal anti-inflammatory drugs

19. Stress related ulcers Stress is able to stimulate the limbic system in the CNS which in turn activates hypothalamic and medullary systems Leads to gastric acid hypersecretion , disturbances in GI motility, and production of cathecholamines , glucocorticoids , and histamine In extremely sick patients wd serious trauma,or burn>1/3 bsa,cva etc

20. Gastritis endoscopically visualized subepithelial hemorrhages and erosions mucosal lesions, thus do not cause major bleeding. Rarely causes UGIB (5%) more commonly results in chronic blood loss Common causes: ingestion of NSAIDs 50% of patients who chronically ingest NSAIDs. Alcohol 20% of actively drinking alcoholic patients stress (severe medical or surgical illness).

21. Endoscopic erosive gastritis

22. Gastric Acid Rarely is hyperacidity the only contributor to peptic ulcer formation Hyperacidity coupled with H. pylori, NSAIDS, stress leads to increased permeability to back diffusion of hydrogen ions resulting in ulceration

23. Portal Hypertension Bleeding from varices (2 nd MCC of UGI Bleeding): esophageal rarely gastric or duodenal Usually stops spontaneously -50% Mortality rate near 70-80% for those with continued bleeding Untreated 50% will rebleed during hospitalization Tx: propanolol or nadolol can decrease risk of rebleeding or endoscopic variceal ligation for high risk patients

24. Large esophageal varices

25. Mallory-Weiss Tears Hemorrhage induced by vomiting, usually in alcoholics Tearing occurs when the cardia has been forced into the thorax Morphology: irregular longitudinal tear in the esophago-gastric junction. May involve only the mucosa, or may rarely penetrate the wall. 5-10% of UGI bleeding

26. Mallory-Weiss tear Tears usually on GASTRIC side Stops spontaneously 80-90% pts

27. Boerhaave’s Tears When a Mallory-Weiss tear penetrates all layers of the wall, it is called Boerhaave’s syndrome. Boerhaave’s tears may cause mediastinitis or peritonitis.

28. Vascular Anomalies Found throughout the GI tract; chronic or acute bleeding 7% of UGIB. Examples: Vascular ectasias (angiodysplasias) bright red stellate appearance. Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu) gastric antral vascular ectasia ("watermelon stomach“) CREST syndrome Incidence increased in chronic renal failure

29. Watermelon Stomach Gastric Antral Vascular Ectasia Cause unknown primarily in older women iron-deficient anemia, which is usually manageable with iron supplementation. In extreme cases, endoscopic thermal therapy or surgical antrectomy may be necessary

30. Erosive Esophagitis Severe erosive esophagitis due to chronic GERD may rarely cause UGIB. Other Predisposing Factors: Infections (esp. in immunosuppressed patients- candida, herpes, bacteria) Ingestion of irritants: alcohol, hot tea, smoking Uremia Cancer chemotherapy, radiation therapy Prolonged gastric intubation

31. Two ulcers in the mid oesophagus

32. 1% of UGIB. Risk Factors: 1. Diet: Nitrites (from food preservatives), smoked and salted foods. 2. Host Factors: chronic gastritis (autoimmune & H. pylori), adenomatous polyps, partial gastrectomy. 3. Genetic Factors: <4% of pt’s w/ gastric CA have a family Hx. Types: 95% are Gastric Adenocarcinoma High prevalence in Japan 5% Lymphoma, Leiomyosarcoma, Carcinoid, and Sarcoma Gastric Neoplasm

33. Other Causes Aortoenteric fistulas (complicates 2% of abd aortic graft or can occur in untreated aneurysm). Hemobilia: presence of blood in bile (from hepatic tumor, angioma, penetrating trauma) and hemosuccus pancreaticus (bleeding from the bile duct or pancreatic duct). Dieulafoy’s lesion

34. Dieulafoy’s lesion Uncommon cause of major GIB. Aberrant arteriole that protrudes through a tiny mucosal defect causing a single small ulcer usually within 6 cm of the gastroesophageal junction on the lesser curvature Can occur in distal esophagus, small intestine, colon, and rectum.

35. How to approach?

36. Patient assessment Patient resuscitation Risk assessment Upper Endoscopy Low risk lesion High risk lesion Surgery Endoscopic Rx Medical Rx Rebleed

37. Initial patient assessment Initial approach to the patient with acute upper gastrointestinal bleeding should include near simultaneous completion of the following: Patient resuscitation and stabilization. Brief clinical history. Limited physical examination. Both a gastroenterologist and a surgeon should be promptly notified of all patients with severe acute UGI bleeding.

38. Patient resuscitation and stabilization Check vital signs Assess airway and breathing Assess circulatory status (postural hypotension) Obtain intravenous access Replace volume Transfuse blood (if necessary) Measure urine output

39. Airway & Breathing Inspect airway Clear airway Check ventilation Supplemental oxygen Endotracheal intubation: Intubation and mechanical ventilation should be considered for the following patients: in shock from massive bleeding. on going hematemesis , especially if the bleeding is torrential. severe agitation. depressed sensorium . depressed respiratory status.

40. Circulation A quick assessment of the circulatory status should be made by: pulse rate. measuring the supine blood pressure checking for pallor and agitation patients with normal supine blood pressure should be checked for postural hypotension.

41. Circulation Intravenous access At least two large bore (14 to 18 gauge) peripheral intravenous lines should be inserted for access and volume replacement. Central Venous Catheter (CVC) A CVC is usually not indicated because volume can easily be replaced with large bore peripheral IV lines. However a CVC may be useful in the following conditions: failure to establish peripheral IV access patients who have an unstable cardiac disease or cirrhosis, in whom measurement of left ventricular filling pressure is necessary to accurately assess volume status.

42. Volume replacement: Volume should be replaced using crystalloids, such as 0.9% NaCl solution (normal saline) or Ringer's lactate, as rapidly as the patient's cardiopulmonary status will allow, to stabilize vital signs

43. Guidelines for transfusion of blood and blood products in Upper GI Bleed Symptoms related to poor tissue oxygenation (e.g. angina). If there is continued acute bleeding despite therapy. If the patient is clinically shocked despite crystalloids. If the hematocrit is low (in elderly, high risk patient Hct <30%, and in young, otherwise healthy patients <20%). If there is coagulopathy (INR>1.5) or thrombocytopenia (<50,000/ microL ) , then fresh frozen plasma and platelets transfusion should be given, respectively.

44. Nasogastric tube Patients with definite or suspected acute upper gastrointestinal bleeding should have a nasogastric (NG) tube inserted. There is no contraindication to NG tube placement in patients suspected to have esophageal or gastric varices . Once the NG tube has been placed, the stomach should be lavaged with tap water or normal saline at room temperature and then the tube should be connected to a gravity bag

45. Brief History Previous history of an upper gastrointestinal bleeding, if so what was the cause. Symptoms or previous history of peptic ulcer disease. Use of NSAID's, aspirin or anticoagulants. Previous history of liver disease. Risk factors for liver disease (e.g. alcohol consumption, h/o blood transfusion, h/o hepatitis or jaundice). Recent history of vomiting or retching.

46. Brief History History of heartburn. Abdominal pain. Any previous surgeries, especially recently. Any co morbid illnesses (e.g. cardiac, pulmonary or neurological illness, bleeding disorders, etc). abdominal aortic aneurysm (AAA), or abdominal aortic vascular graft → aortoenteric fistula Melena . Hematochezia .

47. Laboratory investigations CBC PT (INR), aPTT Type and cross match blood Creatinine , urea, Liver function tests HBSag and anti-HCV if liver disease is suspected ECG in patients over 50 years of age or h/o cardiac disease ( boz they are more pron to develop M.I.)

48. Risk assessment Mild to Moderate /low risk Upper GI Bleeding The patient is < 60 years of age, and has no chronic medical illness. There is no sign of hemodynamic instability. Hematocrit is > 30%.

49. Risk assessment Severe/ high risk Upper GI Bleeding The patient is > 60 years old. There are signs of hemodynamic instability (Pulse >100/min, SBP < 100 or postural hypotension). There is active bleeding (bright red hematemesis , bright red blood in NG tube or hematochezia with hypotension). Drop in hematocrit of 6% or more. There is severe co morbid disease (liver, cardiac, pulmonary or renal)

50. Endoscopic diagnosis & treatment   Upper Endoscopy ALL pts when hemodynamically stable continued active bleeding require more urgent endoscopic evaluation. Upper Endoscopy is the procedure of choice .

51. Other diagnostic tests  For acute UGI bleeding include angiography and a tagged red blood cell scan, which can detect active bleeding. UGI barium studies are contraindicated in the setting of acute UGI bleeding because they will interfere with subsequent endoscopy, angiography, or surgery.

52. TREATING THE CAUSE OF BLEEDING

53. Acute Pharmacologic Therapies 1. Acid inhibitory therapy: IV PPI Omeprazole or pantoprazole , 80 mg bolus, followed by 8mg/h continuous infusion for 72hrs Reduces the risk of rebleeding in pts w/ peptic ulcers w/ high risk features after endoscopic tx . High doses of oral PPI Give for suspected peptic ulcer bleeding while pending the results of endoscopic exam.

54. Acute Pharmacologic Therapies 2. Octreotide: IV 100ug bolus, followed by 50-100ug/h Reduces splanchnic blood flow and portal bp Effective initial control of bleeding related to portal htn All UGIB and evidence of liver disease or portal HTN until the source of bleeding can be determined by endoscopy

55. Varices - treatment: Hepatic venous pressure gradient > 12 mmHg. In esophageal variceal , prefer variceal ligation (with multiband ligator ) over endoscopic sclerotherapy . In gastric varices , injection with a sclerosing agent will be more beneficial than band ligation.

56. Varices: Medical therapy (could combine endoscopy): 1. Vasopressin: side effect-- Myocardial infarction 25%. Combine with NTG. 2. Octreotide (somatostatin analog) 3. Nonselective ß-blockers, (haldolol or propranolol) decreased rebleeding rate. 4. ß-blockers with nitrates in stable pt.

57. Transvenous intrahepatic portosystemic shunts (TIPS): Performed percutaneously through the jugular vein and involves the creation of a permanent intrahepatic shunt between the hepatic and portal veins, easing portal hypertension. Indicated in pts in whom endoscopy has failed to control acute variceal bleeding. TIPS decreases rebleeding more effectively than endoscopic therapy.

58. Varices: TIPS ( transjugular intrahepatic porto -systemic shunt): transjugular approach  connect portal v. and hepatic v.  reduce portal v. pressure gradient to < 12-15 mmHg. Complications include: bleeding, dye-induced renal failure, hemolysis , stent migration, and puncture of the gallbladder or other organs adjacent to the liver.

59. Varices: Balloon tamponade: 1. Intubation 2. Gastric balloon 3. Esophageal balloon Balloon should be inflated for less than 24 hrs. 75% rebleeding rate after balloon deflation. Antibiotic prophylaxis for cirrhosis pt: norfloxacin, ciprofloxacin. Maintain Hct at 25-28 %.

60. Balloon Tamponade Sengstaken-Blakemore tube can control variceal hemorrhage in 40 – 80% patients Inflate gastric balloon first, the esophageal balloon if no improvement

61. Preventing recurrent bleeding: Predictors of Rebleeding : 1. Older age 2. Shock/hemodynamic instability/ orthostasis 3. Comorbid disease states (e.g., coronary artery disease, congestive heart failure, renal and hepatic diseases, cancer) 4. Specific endoscopic diagnosis (e.g., GI malignancy) 5. Use of anticoagulants/ coagulopathy 6. Presence of a high-risk lesion (e.g., arterial bleeding, nonbleeding , visible vessel and clot)

62. Case 1 U r an intern on duty and sister calls“The patient is vomiting blood!” You arrive on the floor to find a middle-aged male in bed, well awake, vomiting bright red blood into a basin. What is your next step?

63. Always First thing : ABC Vitals: He is afebrile, blood pressure is 90/60 , pulse is 120/min , sats 96% on room air Then review the chart or discuss with the patient the different medical problems…

64. The nurse tells you that this is a 56-year old male with history of alcoholism and IV drug abuse admitted for pneumonia.

65. What else are you looking for on history? What are you looking for on physical exam? What is the differential diagnosis? What will you order? How will you initially manage the patient?

66. What else are you looking for on history? History of liver disease/ portal hypertension (cirrhotic with variceal bleed) Anticoagulation (warfarin/heparin drip) Use of NSAIDs, Plavix, ASA, Steroids. Multiple episodes of vomiting (Mallory Weiss Tear…)/ nausea Melena ,hematokezia. History of AAA repair Signs of hypovolemia (dizziness, SOB, CP, syncope…)

67. What are you looking for on physical exam? Vital signs: hypotension/ tachycardia eyes: conjunctival colors (pale/icteric..), JVD Skin color: pale, lesion, itching signs… Chest: telangiectasia, gynecomastia, hair loss Heart: tachycaria Abdomen: ascitis, caput medusae, prominent umbilicus, rectal exam (important to assess bleeding and prostate…) Extremities: edema, pulse Neuro : oriented, asterixis

68. What will you order? NPO 2 big IV lines PPI drip Stat CBC/INR/type and cross/BUN Octreotide drip (if cirrhotic) Antibiotics (if cirrhotic) To consider ICU admission Naso-gastric lavage not always needed Correct coagulopathy if needed (high INR give FFP)

69. Laboratory CBC – in rapid blood loss the initial Hct may not accurately reflect the amount of blood loss as equilibration of the extravascular fluid may take several hours. PTT, PT/INR, LFTs Type and cross BUN, Creatinine – ratio >10:1 suggestive of a UGIB. Occurs as a result of breakdown of blood proteins by bacteria to urea and re-uptake of this from the gut Very important to repeat lab values in several hours to follow clinical course

70. Thank you