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Approach to gastrointestinal bleeding

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Approach to gastrointestinal bleeding

  1. 1. Approach to gastrointestinal bleeding Samir Haffar M.D. Associated Professor of Gastroenterology
  2. 2. Clinical Presentation of GI bleeding • 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
  3. 3. Assessing the severity of bleeding First step Bleeding severity Vital Signs Blood loss (%) Minor Normal < 10 % Moderate Postural (Orthostatic hypotension) 10 – 20 % Massive Shock (Resting hypotension) 20 – 25 %
  4. 4. Resuscitation Proportional to bleeding severity • 2 large-bore IV catheters: Normal saline – Ringer lactate • Oxygen by nasal cannula or facemask • Monitoring of vital signs & urine output • Blood Transfusion: Ht raised to Elderly: 30 % Young: 20 – 25 % PHT: 27 – 28 % • Fresh frozen plasma & platelet transfusion If transfusion of > 10 units of packed red blood cells
  5. 5. History • Elderly Diverticula - Angiodysplasia - Cancer • Young Peptic ulcer – Varices – Esophagitis • < 30 years Meckel diverticula • Previous bleeding Bleeding from similar causes • Aortic surgery Aortoenteric fistula • Known liver disease Esophageal or gastric varices • NSAIDs • Retching Mallory-Weiss tear • Non GI sources Especially from nasopharynx
  6. 6. Physical examination • PHT Spider naevi – caput medusa … • Acanthosis nigricans Underlying cancer • Pigemnted lip lesions Peutz-Jeghers syndrome • Cutaneous lesions Neurofibromatosis • Purpura Henoch-Schonlein purpura • Splenomegaly PHT - portal vein thrombosis • Telangiectasia Osler-Weber-Rendu disease
  7. 7. Spider Naevi Central arteriole Blanch if occluded with pinhead SVC Chest above nipple Face Arms Hands DD Childhood Pregnancy Chronic liver disease
  8. 8. Direction of blood flow in anterior abdominal wall PV obstruction S Sherlock & J Dooley. Diseases of the Liver & Biliary System – 2002. IVC obstruction
  9. 9. Collateral circulation Vein dilatation & tortuosity in abdominal wall of a cirrhotic patient suffering from ascites & jaundice
  10. 10. Caput Medusa Portal hypertension Seen much less frequently
  11. 11. Occlusion of the IVC
  12. 12. Gynecomastia in cirrhosis Seen in cirrhotic males Spironolactone is frequent cause Absent hair body Associated diminished libido Associated testicular atrophy
  13. 13. Palmar erythema Exagereted red flushing of palms Fades on pressure Specially Thenar eminence Hypothenar eminence Bases of fingers DD Pregnancy Thyrotoxicosis Bronchial carcinoma Genetically determined
  14. 14. White nails • Congenital • Cirrhosis: Present in most patients Due to hypoalbuminemia
  15. 15. Bruising Clotting disorder Around venepuncture site From intramuscular injection
  16. 16. Acanthosis nigricans Pigmentation of Axilla Groins Angles of mouth Hands Malignant disease Gastric carcinoma Pancreatic carcinoma Bronchial carcinoma
  17. 17. Hereditary telangiectasia Rendu-Osler-Weber disease Stomach Tongue
  18. 18. Peutz-Jeghers Syndrome
  19. 19. Neurofirmatosis “von Recklinghausen’s Disease” “Café au lait” spots Neurofibromas
  20. 20. Henoch-Scholein purpura Age Prepubertal boys (6 m – 6 years) Can occurs in adults Tetrad Purpuric rash: feet – buttocks – legs Colicky abdominal pain - bloody diarrhea Arthralgia Glomerulonephritis Prognosis Self-limited Complications Rapidly progressive renal failure GI hemorrhage
  21. 21. Henoch-Scholein Purpura Extenseor surfaces of legs Buttocks
  22. 22. Thyphoid fever Rose spots Frequency: 10 – 90 % During second week Erythematous macules (2 – 4 mm) Upper abdomen & anterior thorax Occur in small numbers Blanch on pressure Lasts 2 – 3 days
  23. 23. Laboratory evaluation • Hematocrit May not reflect blood loss accurately • Elevated BUN Not correlated to creatinine level Breakdown of blood proteins to urea Mild reduction of GFR • Iron deficiency anemia • Low MCV • Low ferritin level
  24. 24. Hematocrit values before & after bleeding
  25. 25. Diagnostic test in GI bleeding • Upper GI endoscopy • Colonoscopy • Small bowel endoscopy • Capsule endoscopy & double balloon enteroscopy • Barium radiograph • Radionuclide imaging • Angiography • Miscellaneous tests: abdominal US or CT
  26. 26. Causes of UGI bleeding Common Peptic ulcer Varices Mallory-Weiss Less Frequent Dieulafoy’s lesion Vascular ectasia Watermelon stomach Gastric varices Neoplasia Esophagitis Rare Esophageal ulcer Erosive duodenitis Hemobilia Crohn’s disease Aorto-enteric fistula
  27. 27. Causes & associations of PU Sleisenger & Fordtran’s Gastrointestinal & Liver Disease -1998 Common forms of PU (95%) HP-associated NSAID-associated Stress ulcer Uncommon forms of P U (5%) Acid hypersecretion :ZES – mastocytosis Other infections: HSV type 1 – CMV Duod obstruction: bands-annular pancreas Radiation-induced lesions Chemotherapy-induced lesions Idiopathic
  28. 28. Predisposing factors to bleeding PU • Acid Most prominent factor • Helicobacter pylori • NSAIDs • Biphosphnate alendronate • Chronic pulmonary disease • Cirrhosis • Anticoagulants • Ethanol
  29. 29. Bleeding peptic ulcer • Most frequent cause of UGI bleeding (50%) • Especially high on gastric lesser curvature or postero-inferior wall of duodenal bulb • Most ulcer bleeding is self-limited (80%)
  30. 30. Forrest’s classification for PU bleeding Stage Characteristics Rebleeding I a Jet arterial bleeding 90 % Ib Oozing 50 % IIa Visible Vessel 25 - 30 % IIb Adherent clot 10 - 20% IIc Black spot in ulcer crater 7 - 10% III Clean base ulcer 3 - 5 %
  31. 31. Forrest’s classification for PU bleeding III (clean base)II-b (adherent clot) II-a (visible vessel)I-b (oozing) II-c (black spot) I-a (arterial jet )
  32. 32. GI side effects of NSAIDs Organ Side Effects Esophagus Esophagitis – Ulcer – Stricture Stomach & duodenum Subepithelial hemorrhage – Erosion – Ulcer Small Intestine Ulcers – Strictures – NSAID enteropathy Colon No pre-existing colonic disease: Ulcerations – Stricture – Diaphragm – Colitis Pre-existing colonic disease: ↑ Complications of diverticular disease Activate IBD Ano-rectum Inflammation – Ulcer – Stricture
  33. 33. Highest risk Azapropazone Tolmetin Ketoprofen Piroxicam GI safety of non-selective NSAIDs RR of different NSAIDs could differ 10-fold Lowest risk Ibuprofen * Diclofenac * Risk at higher doses (> 1.5 –2.4 g/d) comparable to others NSAIDs Br Med J 1996 ; 312 : 1563 – 1566. Longer half-time Moderate risk Indomethacin Naproxen Sulindac Aspirin
  34. 34. Prevention of GI toxicity due to NSAIDs
  35. 35. Patients at increased risk for NSAIDs CV toxicity High risk Patients with risk factors for CV disease often receive prophylactic aspirin Arbitrarily defined as requirement for low-dose aspirin for prevention of serious CV events Low risk No risk factors
  36. 36. Patients at increased risk for NSAIDs GI toxicity High risk 1. History of complicated ulcer especially recent 2. Multiple (> 2 risk factors) HP is independent & additive risk factor & addressed separately ACG guidelines for prevention of NSAID-related ulcer complications . Am J Gastroenterol 2009 ; 104: 728 – 738. Moderate risk (1 – 2 risk factors) 1. Age > 65 years 2. High dose NSAID therapy 3. Previous history of uncomplicated ulcer 4. Concurrent use of aspirin 5. Concurrent use of corticosteroids 6. Concurrent use of anticoagulants Low risk No risk factors
  37. 37. Prevention of NSAID-related ulcer complications Naproxen may have some cardioprotective properties Patients with ulcer history: search for HP & if present eradicated ACG guidelines for prevention of NSAID-related ulcer complications. Am J Gastroenterol 2009 ; 104: 728 – 738. NSAID alone (least ulcerogenic at lowest dose) NSAID + PPI/misoprostol Alternative therapy or Coxibs + PPI/misoprostol Naproxen + PPI/misoprostol Naproxen + PPI/misoprostol Avoid NSAIDs & coxibs Use alternative therapy High GI riskModerate GI riskLow GI risk Low CV risk High CV risk
  38. 38. Treatment of bleeding PU • Pharmacological PPI 80 mg IV bolus 8mg / hr / 72 hours IV infusion • Endoscopic Injection (epinephrine 1/10.000) Monopolar coagulation Bipolar coagulation Heater probe Hemoclips Argon plasma coagulation • Surgical When endoscopic treatment fails
  39. 39. Summary of therapy of bleeding PU • Patients must be adequately resuscitated • UGI endoscopy is the primary diagnostic modality • Intubation if severe bleeding or altered mental status • Endoscopic therapy indicated in high risk lesions Combine 2 methods of endoscopic treatment • IV PPI should be used in high risk patients
  40. 40. Classification of esophageal varices Grade 1 Small Minimally elevated veins above surface AASLD practice guidelines: prevention & management of gastroesophageal varices. Hepatology 2007 ; 46 : 922 – 938. Grade 2 Medium Tortuous veins occupying < 1/3 of esophageal lumen Grade 3 Large Occupying > 1/3 of esophageal lumen
  41. 41. New classification of esophageal varices • Small Varices: < 5 mm • Large Varices: > 5 mm
  42. 42. Classification of gastric varices Yamada T et all. Yamada’s textbook of gastroenterology. Blackwell Publishing, West Sussex, UK, 5th edition, 2009. Gastro-Oesophageal Varices Type I Along lesser curve Type II To gastric fundus Isolated Gastric Varices Type I Fundal Type II Ectopic
  43. 43. Predictive factors for risk of bleeding North Italian Endoscopic Club Index • Variceal size Best predictor of bleeding • Severity of liver disease Expressed by Child-Pugh • Red signs On the varices NIEC. N Engl J Med 1988 ; 319 : 983 – 989.
  44. 44. Child-Pugh score Category 1 2 3 Bilirubin (mg/dl) < 2 2 - 3 > 3 Albumin (g/l) > 35 28 – 35 < 28 Ascites Absent Mild- Moderate Severe Encephalopathy 0 I – II III – IV INR < 1.7 (70%) 1.7 – 2.3 (40 – 70%) > 2.3 (< 40%) Class A: 5 – 6 Class B: 7 – 9 Class C: 10 – 15
  45. 45. MELD Score 0.957 x Loge (creatinine mg/dL) + 0.378 x Loge (bilirubin mg/dL) + 1.120 x Loge (INR) + 0.643∗ Multiply score by 10 & round to nearest whole number Laboratory values < 1.0 are set to 1.0 Maximum creatinine within MELD score: 4.0 mg/dl Dialysis twice/week prior to creatinine test: creatinine 4.0 mg/dl * 0.643 for etiology to make score comparable to previous published data
  46. 46. Score 3 month mortality ≥ 40 100% 30 – 39 83% 20 – 29 76% 10 – 19 27% < 10 4% Interpretation of MELD score The maximum score given for MELD is 40 All values > 40 are given a score of 40 www.unos.org/resources/MeldPeldCalculator
  47. 47. Treatment of acute variceal bleeding Recommendations - 1 • Best approach is combined use of: - Pharmacological agent started from admission & - Endoscopic procedure • Terlipressin & somatostatin preferable if available Octreotide, vasopressin + nitroglycerin may be used • Drug therapy maintained for at least 48 h 5 day therapy recommended to prevent early rebleeding
  48. 48. Treatment of acute variceal bleeding Recommendations - 2 • Bleeding EV Band ligation is the endoscopic treatment of choice Sclerotherapy may be used • Bleeding GV Obturation with cyanoacrylate • TIPS Rescue procedure if medical & endoscopic tt fails Bleeding from GV may require earlier decision for TIPS
  49. 49. • Shunt surgery Mesocaval graft shunts or traditional portacaval shunts may be an alternative to TIPS in Child A patients • Blood transfusion Done cautiously using packed red cells (Ht: 25 – 28 %) Plasma expanders to maintain hemodynamic stability • Prophylaxis of infection Given to all patients (norfloxacin 400 mg /12 hours) Treatment of acute variceal bleeding Recommendations - 3
  50. 50. Esophageal varices Endoscopic view of esophageal varices Varix endoscopically ligated with a band
  51. 51. TIPS
  52. 52. Transjugular Intrahepatic Portosystemic Shunt Technique Metallic stent between branch of PV & HV Under sedation with local anesthesia US guidance essential during the procedure Time of procedure: 1 – 2 hours Difficult (skilled interventional radiologist) Indications Control of bleeding from EV or GV Medical & endoscopic tt given before TIPS Results Bleeding control 90 % Mortality < 1 %
  53. 53. General results of surgical shunts Bleeding Prevented or at least decreased Varices disappear in 6 – 12 months Complications Post-operative jaundice Increase cardiac output & failure Hepatic encephalopathy May be transient Chronic changes in 30 – 40 % Increase with the size of shunt More common in older patients Mortality 5 % in good-risk patients 50 % in poor-risk patients
  54. 54. Side-to side porto-caval shunt
  55. 55. Distal spleno-renal shunt Veins feeding varices ligated: coronary-rt gastric-rt gastroepiploic Spleen is preserved
  56. 56. Distal spleno-renal shunt Mortality similar to non-selective shunts Hepatic encephalopathy similar to non-selective shunts Better results in non-alcoholic patients & in gastric varices Does not interfere with subsequent liver transplant Technically difficult (fewer surgeons willing to perform it)
  57. 57. Causes of bleeding in PHT • Esophageal varices • Gastric varices • Ectopic varices • Portal hypertensive gastropathy
  58. 58. Portal gastropathy Mosaic-like mucosal pattern Snake-skin appearance
  59. 59. Endoscopic images of PHT gastropathy New Italian Endoscopic Club • Mosaic-like mucosal pattern (snake-skin appearance) • Red point lesions Small (<1 mm), red, flat, point-like marks • Cherry-red spots Large (>2 mm), round, red-colored, protruding lesions • Black–brown spots Irregular black & brown flat spots not fading upon washing Might represent intramucosal hemorrhage Primignani M et al. Gastroenterology 2000 ; 119 : 181 – 187.
  60. 60. PHT gastropathy – Four main findings Mild (pink) Moderate (red) Mosaic-like pattern Snake-skin appearance Black-brown Brown spot Black–brown spots Red point lesions Small (<1 mm) Cherry-red spots Large (>2 mm) Gastroenterology 2000;119:181-187.
  61. 61. Mallory-Weiss syndrome Retroflexed view 5- 10 % of UGI bleeding Typically in gastric mucosa Stop spontaneously in 80-90% Not bleeding: discharge promptly Active bleeding: injection – banding
  62. 62. LA classification system of esophagitis Grade A One (or more) mucosal break, no longer than 5 mm, that does not extend between tops of 2 mucosal folds
  63. 63. One (or more) mucosal break, more than 5 mm long, that does not extend between tops of two mucosal folds LA classification system of esophagitis Grade B
  64. 64. One (or more) mucosal break continuous between tops of > 2 mucosal folds, but which involves < 75% of circumference LA classification system of esophagitis Grade C
  65. 65. One (or more) mucosal break that involves at least 75% of the esophageal circumference LA classification system of esophagitis Grade D
  66. 66. Barrett’s esophagus Endoscopic view of distal esophagus from a patient with GERD Tongue of Barrett’s mucosa (b) & Schatzki’s ring(s) (arrow)
  67. 67. Esophageal candidiasis Multiple small white plaques of Candida seen on background of abnormally reddened esophageal mucosa
  68. 68. Herpes Simplex in the esophagus Appearance not diagnostic of HSV infection It could be due to drug-induced lesion (K supplement) Presence of vesicles in mucosa virtually diagnostic of HSV Small volcano-like ulcers due to HSV
  69. 69. CMV esophagitis Solitary deep well-circumscribed ulcer at gastroesophageal junction
  70. 70. Cancer of gastroesophageal junction Large malignant mass at GE junction
  71. 71. Watermelon stomach Gastrointest Endosc 2005; 61 : 631 - 633.
  72. 72. Ampulloma Endoscopic view
  73. 73. Hemobilia Blood clot protruding from the ampulla Corresponding ERCP
  74. 74. Causes of lower GI bleeding Common Diverticula Vascular ectasia Less Frequent Neoplasia IBD Colitis: ischemia – radiation Hemorrhoids Small bowel source UGI source Rare Dieulafoy’s lesion Colonic ulceration Rectal varices
  75. 75. Diverticular disease of the colon Wide-mouthed openings to diverticula are present They were seen throughout the sigmoid colon in this patient
  76. 76. Mucosal telangiectasia of the colon The patient presented with hematochezia The lesion was subsequently cauterized endoscopically
  77. 77. Telangiectasia Telangiectasia in duodenum in patient with microcytic anemia Treatment with APC (Argon Plasma Coagulation)
  78. 78. Endoscopic polypectomy Snare passed through endoscope & positioned around polyp (P) Cautery applied & polyp resected leaving clean mucosal defect
  79. 79. Ulcerative colitis Colonic mucosa in a patient with idiopathic ulcerative colitis, showing a friable mucosa, extensive ulceration, and exudates.
  80. 80. Ulcerative colitis Air contrast barium enema demonstrating luminal narrowing & loss of haustra in sigmoid & descending colon in UC
  81. 81. Crohn’s disease Aphthous ulcers in the rectum in a patient with Crohn’s disease Lee YJ et al. Endoscopy 2006; 38 : 592 – 597.
  82. 82. Crohn’s disease Longitudinal ulcers & cobblestone appearance in a patient with Crohn’s disease Lee YJ et al. Endoscopy 2006; 38 : 592 – 597.
  83. 83. Crohn’s disease of the ileum Luminal narrowing Mucosal ulceration Separation of barium-filled loops (thickening of bowel wall) Small bowel follow-through in ileal Crohn’s disease
  84. 84. NSAIDs-induced colitis Endoscopically nonspecific findings Histologically nonspecific DD: infections, IBD, ischemia, vasculitis
  85. 85. Radiation proctitis Radiation proctitis in a patient with hematochezia Extensive neovascularization of the mucosa
  86. 86. Rectal Dieulafoy’s lesion Gastrointest Endosc 2004 ; 60 : 796. Endoscopic appearance During ligation After ligation
  87. 87. Classification of hemorrhoids Degree Description First degree Project a short way into anal canal Only symptom is bleeding Second degree Prolapse during defecation Reduce spontaneously Third degree Must be reduced manually Fourth degree Irreducible
  88. 88. Internal hemorroids Seen with the proctoscope
  89. 89. Prolapse of 3 mains hemorrhoidal piles
  90. 90. Preferences for treatment of hemorrhoids Degree or Grade Treatment 1 Sclerosing injections Infrared coagulation 2 Infrared coagulation Rubber band ligation 3 Rubber band ligation 4 Hemorrhoidectomy
  91. 91. Sclerosing injection
  92. 92. Infrared photocoagulation
  93. 93. Rubber band ligation
  94. 94. Rubber band ligation
  95. 95. Anal fissure
  96. 96. Meckel’s divertculum Isotope scan with Tc99m
  97. 97. Approach to lower GI bleeding • Less common than UGI bleeding • Usually less hemodynamicaly significant • Most common cause of severe bleeding: diverticula • Most common cause of minor bleeding: hemorrhoids • Controversial best diagnostic approach if severe: Urgent colonoscopy – RBC scintigraphy – angiography
  98. 98. Thank You