1. GASTRO-INTESTINAL BLEEDING

2. GIB 1-2% of acute hospital admissions. 5% mortality.
90% cease spontaneously.

3. Classification
Level of bleeding - Upper / Low. (above and below the ligament of Trietz).
Time - Acute / Chronic
Severity of blood loss

4. Clinical Presentation
Hematemesis - bloody vomiting
Coffee Ground vomiting
Melena- dark/black stool.(degradation of hemoglobin).
Hematochezia-Rectal bleeding

5. Evaluation of the bleeding patient
-Patient assessment: anamnesis and hemodynamic status.
-resusitation.
-dignosis: bleeding source.
-treatment.

6. Medical history
Characteristics of bleeding ( melena, coffee ground, rectal bleeding).
Symptoms reflect severity of bleeding. (syncope, dizziness, onset and frequency).
Symptoms associate possible etiologies. Dyspepsia, abdominal pain, weight loss, early satiety, liver disease, alcohol abuse. Antececedent vomiting. Dysphagia and reflux.

7. Cont- Constipation, bowel movements. Medications: NSAIDS, coumadin.
Coagulopathy.
History of aortic surgery.
Previous episodes.
Comorbidities. (ability to respond to hemorrhage).

8. Physical Examination
Determine degree of blood loss: pale, cold extremeties, sweating pulse, BP, orthostatism.
- consciousness.
Epigastric tenderness. Abdominal mass.
Signs of liver disease. (jaundices, ascites….)
Oropharynx (rare).

9. Cont- Rectal examination – quality of stool.
Nasogastric tube. ( blood, coffee ground, bile, gastric fluids)

10. Management and monitoring
Large bore IV lines (Haggen/Pousseleur low)
Fluids - Hartman’s solution (restoration of intravascular volume).
Oxygen (espicially in IHD pts).
Blood typing and cross matching .
Blood tests- CBC, PT PTT, LFT.

11. Cont-
Unstable pt- start packed cells, consider intubation(prevent aspiration in obtunded pts) .
Repair coagulation defects.
Consider central line cath (uaually not needed).
Urine output.

12. Level of bleeding-Upper/Low
Upper GI bleeding - the source is above the Treitz ligament
Lower GI bleeding – is below

13. Upper GI Bleeding - Diagnosis
Naso-gastric tube – blood or coffee ground
Melena in rectal exam
After stabilisation and primary treatment - upper GI endoscopy in first hours
Specific treatment: medical, antibiotics, endoscopy, angiography, surgery.

14. Low GI Bleeding-diagnosis
Rectal bleeding – blood on rectal exam.
Normal NGT contents.
Melena with normal upper GI endoscopy
After stabilization – rectoscopy , colonoscopy
Proffuse bleeding – lateralisation of bleeding site by angio or bleeding scan

15. Upper Gastrointestinal Bleeding

16. Upper GI Bleeding Erosive gastritis 15-30%. Esophageal Varices 10-20%.
Peptic disease – duodenal or gastric ulcer, 50%.
Erosive gastritis 15-30%.
Esophageal Varices 10-20%.
Gastrinoma – Zollinger-Ellison synd.
Mallory-Weiss tears 8-10%.
Malignancy- 3%.
Dieulafoy’s.
Esophagitis.
Osler weber rendu.
Hypertrophic gastritis – Menetrier disease or Water-Melon Stomach
Aorto-duodenal fistula (rare)

19. Peptic disease 5% - hemorrhage is presenting symptom.
20%- develop bleeding at least once.
Hemorrhage is the most lethal form of complicated ulcer dis.

20. Peptic disease- Pathogensis
Acid peptic erosions into submucosal or extraluminal vessels.
Helicobacter pylori. Most common etiology for duodenal ulcer.
NSAIDS. Damage to GI mucosa.
- inhibition of prostaglandin synthysis--> inhibition of mucos and bicarbonate production.
- delay ulcer healing.
- epithlial acidification.
- platelet dysfunction.
ZES. Gastrin secreting tumor.

21. Peptic dis- prognostic factors
Severity of bleeding, hemodynamic status.
Persistent or recurrent.
Transfusion requirements.
Nasogastric aspirate, blood, coffee groud.
Older pts.
Comorbidities.

22. Gastric ulcer- Classification
Type 1- distal lesser curvature.
Type 2- combined gastric and duodenal. High acid secretion.
Type 3- prepyloric. High acid secretion.
Type 4- proximal lesser curvature.
Type 5- secondary to NSAIDS.

23. Gastric ulcer 10% of gastric ulcers are malignant.
Most bleedind ulcers arise in incisura, antrum and distal body of stomach.

24. Duodenal ulcer 95% - secondary to Helicobacter pylori infection.
10% of pts with HP develop ulcer. 20% of pts with ulcer and HP bleed.
Bleeding DU, usually located on the posterior duodenal wall.

25. Peptic dis- Treatment NPO. Fluids. Stop NSAIDS.
Antisecretory agent. H2-rec blockers or proton pump inhibitors.
PPI may reduce rebleeding.
Endoscopy- diagnostic and therapeutic. within hours.
Anti H pylori treatment. Not immediatly.
Massive bleeding- consider emergent endoscopoy.

26. The Role of Adjunctive Pharmacological Therapy
Clot stabilization: at a pH of above 6.0 pepsin is inactivated and cannot lyse clots
Effective clotting may not occur at pH<6.
Antacids, iced saline gastric lavage and H2-blockers and other interventions are ineffective in reducing rebleeding.
PPI decreases the incidence of rebleeding.

27. Peptic dis- Endoscopy Rebleeding 10-20%. Consider re-endoscopy
Prognostic endoscopic findings for rebleed:
1) appearence -small clean ulcer base. 0%
- flat, pigmented 10%
- adherent clot. 20%
- visible vessel. 40%
- active bleeding.
2) size > 2cm.

28. Peptic Ulcer Endoscopic manipulation Coagulation
Injection of sclerosant or vasoconstricting agent.
Clip.

29. Peptic Ulcer Endoscopy

30. Endocliping of Bleeding Ulcer

31. Angiography- embolization
To consider in:
- high risk pts.
- rec bleeding.
Duodenum: gastroduodenal art.

32. Angioembolization of bleeding duodenal ulcer

33. Surgical therapy Indications:
-active bleeding not responsive to endoscopic treatment.
- significant rec bleeding after endoscopic treatment.
-ongoing transfusion requirment. 6 pc/d.
The goal of surgery: to control hemorrhage.
Acid reducing procedure is secondary, but important.

34. Surgery for bleeding ulcer
DU: Suturing of bleeding ulcer +/- vagotomy with or without drainage. Rebleeding<10%.
GU: Partial gastrectomy or wedge resection.
Antrectomy+truncal vagotomy

35. Vagotomy

36. Drainage Procedure

37. Gastrectomy

38. Bleeding ulcer in pts with HP
Eradication of HP decrease the incidence of rebleeding.
Only 0.2 % of ulcer pts with HP infection need surgery for bleeding peptic ulcer.

39. Erosive Gastritis
common source of bleeding in critically ill pts, elderly and NSAIDS treated pts.
Lesions distributed throught the gastric mucosa.
Pathogenesis- acid peptic injury and mucosal ischemia d/t hypoperfusion

40. Erosive gastritis
in critically ill pts- prophylaxis H2 rec antagonist is recommended.
Treatment- conservative+ treat the underlying dis.
PPI
In profuse bleeding :
- angiography- embolization.
- surgery- rarely indicated,
if single bleeding site gastrotomy, suturing of and vagotomy.
if multiple sitesnear/total gastrectomy

41. Esophageal varices
Dilated submucosal veins that communicate portocollateral circulation and the systemic venous system secondary to Liver cirrhosis or portal hypertension.
25-30% develop hemorrhage.
70% rebleeding.

42. Esophageal varices
Pathogenesis: elevated portal venous pressure. Hepatic pressure gradient>12 mmHg  varices.
Risk for hemorrhage:
size.
red color signs on endoscopy.
poor liver function.
active alcohol use.

43. Primary treatment B-blockers. Nitrate. Less common.
Endoscopy. Band ligation , sclerotherapy.

44. Treatment of acute hemorrhage
Vasoactive drugs:Vasopressin IV, empiric
Somatostatin IV.
effective 80-90%.
Emergent Endoscopy-ligation or sclerotherapy.
- Rule out other etiologies.
- decrease rebleeding and mortality.

45. Esophageal Varices Endoscopy

46. Endoscopic Ligation of Varices

47. Varices – acute hemorrhage
Blackmore tube insertion- massive bleeding

48. Varices-Treatment of rec bleeding
B-blocker. Decrease rebleed- 30%.
Repeated endoscopy.
TIPS: - nonselective shunt. decrease hepatic flow may induce encephlopathy.
- rebleeding-20%.
- thrombosis %.
- useful in acute hemorrhage.
-definitive or temporary treatment.
Surgical shunt.
Liver Tx.

49. Surgical porto-systemic shunt
High mortality rate as emergency procedures.
Nonselective- more effective in reduce hemorrhage.
- greater risk for encephalopathy.
- effective for ascites.
Selective- selective decompressing of left side portal system and esophageal varices.
-allow hepatic perfusionlower rate of encephlopathy.
Procedure of choice- distal splenorenal shunt.
Devascularization procedure- if shunt procedure not possible.

50. Mallory-Weiss Tears Tear in the gastric mucosa near GEJ.
Characterized by antecedent history of vomiting,retching or coughing.
Common- associated alcoholism, nsaids, hiatal hernia, age>60.

52. Mallory-Wiess treatment
90% stop spontaneously.
Endoscopy for diagnosis and treatment.
Rebleeding:pts with active bleeding in initial endoscopy, or pts with coagulation disorders.
Surgery rarely needed.(gastrotomy and oversewing of the mucosal tear).

53. Esophageal sources Esophagitis GERD. Barrett’s Malignancy.
Medications.
Radiation.
IBD.

54. Rare Source - Dieulafoy
Aberrant submucosal vessel m/p in the lesser curv.
Treatment- endoscopy / surgery.
Endoscopic diagnosis is difficult, no ulcerated lesion.
Rebleeding is common.

55. Hypertrophic Gastritis
Water-melon stomach or Menetrier syndrome

56. Zollinger-Ellison Syndrome
Bleeding from ulcers – duodenal and postbulbar origin
CT and EUS are diagnostic tools
Operation with complete resection or at least debulking is treatment of choice

58. Lower GI Tract Bleeding

59. LGIB Bleeding below ligament of Trietz. 97% colon 3% small bowel.
Incidence increases with age.
Slow bleeding may present as melena.
Shock is less common than in UGIB.
Usually intermittent.

60. LGIB- Etiology Diverticulosis of the colon
AV malformation or angiodysplasia
Colon Cancer
IBD-Ulcerative colitis/Crohn’s
Hemorrhoides and anorectal diseases.
Ischemic colitis.
Radiation injury.(proctitis)
Meckle’s diverticulum, or other small bowel diverticula.

61. Etiology by age group, in order of frequency
Adolescents and young adults
Adults to 55 y.o.
Adults over y.o.
- Meckel’s
diverticulum
- Inflammatory
bowel disease
- Polyps
Anorectal dis
Inflammatory
- Diverticulosis
- Malignancy
AVMs
Diverticulosis

62. Diagnostic procedures
Rigid proctoscopy- in the ER, for all pts.
Colonoscopy.
Nuclear scintigraphy.
Angiography.
Operative intervention.

63. proctoscopy
Rule out anorectal disease.

64. Colonoscopy
Useful in evaluating patients with: occult chronic GI bleeding Acute self limited hemorrhage that has stopped bleeding.(test of choice).
Use in patients with massive ongoing bleeding remains controversial.
PROS :Diagnostic and therapeutic tool.(laser, coagulation, Injection).
CONS:-Technical difficulty in not prepared pts.
-Complications, Perforation.

65. Nuclear scintigraphy
Bleeding scan- detect intraluminal extravasation of blood, utilize technetium sulfur colloid or technetium 99m-labeled red blood cells.
PROS:-Noninvasive.
-Detects bleeding as slow as 0.1 mL/min.
- repeated scans are possible up to 24h, it can detect intermittent bleeding.
CONS:-not therapeutic.
- delay in diagnosis.
-lateralization lt or rt , but not localization of bleeding.

66. Red blood cells bleeding scan

67. Angiography
Selective catheterization of mesenteric vessels and injection of contrast
Looking for extravasation and pooling of media within intestinal lumen
In absence of preangiographic localization catheterize SMA  IMA  Celiac.
Once site of hemorrhage found intra-arterial infusion of vasopressin arterial, venous, and bowel contraction  promotes thrombosis at bleeding site
--If patient an operative risk, transcatheter embolization with gel foam, wire coils, or autologous blot clots.(may be complicated with bowel infarction).

68. Angiography PROS:- localization of bleeding.
- visualize nonbleeding vascular malformations, neoplasms and other lesions.
- Detects bleeding as slow as 0.5 mL/min.
- therapeutic
- recently superselective embolization is optional .
- 85% effectiveness – identify and control hemorrhage.
CONS: - achieves temporary control before definitive surgical resection.
- Invasive.
- Complications: cardiac, visceral, and peripheral ishchemia (relative contraindication)
- Chance of rebleeding.

69. Angiography

70. Diverticulosis
Diverticular bleeding is the most common source of LGIB, 40-50%.
Diverticulosis Present in > 50% of population > 60 y.o.
Risk of bleeding 5% of pts.
Hemorrhage is not associated with diverticulitis.

71. Diverticulosis
Hemorrhage d/t weakening and erosion/rupture of vasa recta/branches of the marginal arteries,at the dome or the neck of the diverticulum, with decompression into bowel lumen.
Luminal traumatic factors lead to hemorrhage .
Hemorrhage tends to be massive d/t arterial source
The most common source of massive LGIB, from the lt colon.

72. Diverticulosis Most cases stop spontaneously.
Risk of rebleeding 25% at 4 years.
50% risk if patient has suffered two prior episodes of diverticular bleeding
10-20% bleeding continues in absence of intervention.
Colonoscopy- diagnostic and therapeutic.
Consider surgery for recurrent episodes.

73. Endoscopy of Diverticulosis

74. Angiodysplasia=AVM
Small ectatic vessels in the submucosa, arteriovenous malformation.
common in old cardiac pts, CRF, AS.
5-20% of LGIB.
The most common cause of hemorrhage from SB.
The most common cause of massive LGIB from rt colon.

75. Endoscopy of angiodyspasia

76. AVM- diagnosis
Occur primarily in cecum and ascending colon of elderly patients> 50%.
Recurrent intermittent bleeding.
Colonoscopy-most sensitive tool.
- diagnostic and therapeutic.
Angiographic criteria for identification of AVM
1) early and prolonged filling of draining vein
2) clusters of small arteries
3) visualization of vascular tufts

77. Colon Cancer Most common after AVM and diverticulosis. 5-10%.
Colonoscopy and biopsy is essential
massive bleeding uncommon.

78. Endoscopy of Colon Cancer

79. COLON CANCER
Proximal colonic tumors have high propensity for occult bleeding
Rectosigmoid tumors easily confused with hemorrhoidal bleeding
Treatment of hemorrhoids should be preceded by flexible sigmoidoscopy in patients > y.o.

80. Inflammatory Bowel Disease
bleeding more common in ulcerative colitis

81. IBD- UC
Minor and hemodynamically insignificant bleeding  conservative treatment directed at inflammatory disease
Hemodynamically significant bleeding  surgery
total abdominal colectomy
End ileostomy + Hartmann’s pouch

82. Anorectal disease
Small amounts of bright red blood on surface of stool and toilet tissue, hemodynamically insignificant
Precipitated by strained passage of hard stool
Hemorrhoids
Engorgement of venous plexi of rectum/anus with protrusion of mucosa
Anal Fissure
Tear in anal epithelium

83. Internal hemorrhoids

84. Colitis
Infectious
Ischemic

85. Obscure GI bleeding
Intermittent GI bleeding for which no source has been determined, despite rigorous endoscopic (gastroscopy+colonoscopy) and radiologic investigation.
Almost all are from small bowel.

86. Bleeding from obscure source
Angiodysplasia of small bowel, most common. 40%. Acquired lesions, may recur .
Polyps and neoplasms.
Meckel’s Diverticulum. Most common in young.
Submucosal lesion – lymphoma, stromal cell tumor etc.
Others.

87. Obscure GIB- Diagnostic modalities
-Enteroclysis or CT enterography:
Able to detect SB tumors (80%), but poor modality for superficial mucosal lesions as AVM.
Enteroscopy : can visualize through to the jejunum.
Arteriography: special attention to evidence of angiodysplasia. 60% sen
Meckel’s scan. Initial evaluation in young pts.
GI capsule- camera.
Laparotomy and intraopertive enteroscopy. (70%sen)
Provocative testing: arteriography + heparin or thrombolytics to precipitate acute bleeding

88. Obscure GI bleeding (cont.)
Operative exploration
Exploratory laparotomy with examination from GE junction to intraperitoneal rectum followed by:
Transillumination of bowel wall with fiberoptic light source
Intraoperative endoscopy
Vigorous hydrationaccentuates thin walled veins that constitute most AVMs
Treatment = resection of segment of SB or LB containing the offending lesion

89. Meckel’s Diverticulum
Rare, true diverticulum.
Gastric, pancreatic mucosa.
The origin of bleeding is ulceration of small bowel mucosa distally to the diverticulum.
Treatment: excision of diverticulum and segment of ileum to assure inclusion of adjacent ulceration.

90. Submucosal lesions
Lymphoma of small bowel – rare disease
Stromal cell tumor - GIST may be a reason of mucosal erosions and bleeding.

91. Operative intervention in massive unidentified bleeding source
Exploratory laparotomy :
Thorough examination of entire GI tract
Initial step: determine visually location of blood within GI tract
Next: careful inspection and gentle palpation of entire GI tract
Intraoperative upper endoscopy in absence of obvious bleeding source.

92. Operative intervention (cont.)
If bleeding site localized preoperatively:
Segmental bowel resection that includes offending lesion
Usually safe to perform primary anastomosis
End stoma + mucous fistula if patient hemodynamically unstable, malnourished

93. Operative intervention (cont.)
If bleeding site not localized preoperatively:
intraoperative colonoscopy followed by segmental colectomy.
if bleeding site still not identified: “blind” total colectomy is indicated.
repeat proctoscopy to definitely rule out rectal source of bleeding.
5% mortality rate.

94. Thank You !