1. Gastrointestinal Bleeding
Dr Shahid Aziz MBBS, MRCP, MRCEM, FRCP
Assistant Professor of Emergency Medicine

2. Learning Objectives To develop an understanding of the,
1- Pathophysiology of the disease
2- Important causes and differential diagnosis
3- Approach to patients with GIB including, history, physical examination, resuscitation, investigations and further management.

3. GIB should be considered as potentially life threatening until proven otherwise.

4. Epidemiology:
Gastrointestinal bleeding (GIB) accounts for more than 1 million hospitalizations annually in the United States, with significant morbidity, mortality, and economic burden.
UGIB accounts for more than 500,000 U.S. hospital admissions annually, with approximately 165 incidents per 100,000 patients.

5. Mortality rates have remained consistent at 13 to 14% over the past two decades despite advances in medical therapy, intensive care unit (ICU) management, endoscopy, and surgery.
An increasing proportion of elderly patients, who may die owing to comorbid conditions, and increases in the number of cirrhotic and variceal patients may contribute to the lack of change in mortality rates.
The incidence of LGIB in the United States is approximately 20.5 per 100,000 patients, with a mortality rate of 4%. Age greater than 70 years, intestinal ischemia, comorbid illness, coagulation defects, transfusion of packed red blood cells (RBCs), and male gender are the predictors of increased LGIB mortality.

6. Both UGIB and LGIB are more common in male population.

7. Definitions
Upper GI bleed – arising from the esophagus, stomach, or proximal duodenum
Mid-intestinal bleed – arising from distal duodenum to ileocecal valve
Lower intestinal bleed – arising from colon/rectum

8. For practical purposes, any bleeding above the ligament of Trietz is UGIB and below this ligament is LGIB.
Haematemesis: Vomiting of blood, suggests UGIB, Coffee ground vomitus refers to a particular appearance of vomit. Within organic heme molecules of red blood cells is the element iron, and when this iron has been exposed for some time to gastric acid, it becomes oxidized.

9. Guaiac positive stool Melena Hematochezia Occult blood in stool
Does not provide any localizing information
Indicates slow pace, usually low volume bleeding
Melena
Very dark, tarry, pungent stool
Usually suggestive of UGI origin (but can be small intestinal, proximal colon origin if slow pace)
Hematochezia
bright red blood, dark red, maroon
Usually suggestive of colonic origin (but can be UGI origin if brisk pace/large volume)

10. Causes
UGIB, Peptic ulcers (gastric more than duodenal)
Gastric erosion, Esophagogastric varices,
Mallory-Weiss tears, Esophagitis, Gastric cancer
50% due to peptic ulcer disease
LGIB, Diverticular disease, Angiodysplasia
Colitis (inflammatory, infectious, ischemic)
Anorectal sources, Neoplasm, Upper GI bleeding
Most common cause is diverticular disease and angiodysplasia

11. Differential Considerations
Epistaxis, dental bleeding, or red food coloring can mimic the appearance of hematemesis.
Bismuth-containing medications and iron supplements can create melanotic-appearing (but guaiac-negative) stools.
Vaginal bleeding, gross hematuria, and partially digested red foods (such as beets) can all be mistaken for hematochezia.
Unless an alternative diagnosis is clearly evident, the appropriate approach is to continue with the workup for GIB.

12. Approach to the patients with GIB- Case Discussion:
68 yo male presents with a chief complaint of a large amount of “bleeding from the rectum”

13. Case Discussion- HPI
Describes bleeding as large volume, very dark maroon colored stool
Has occurred 4 times over past 3 hours
He felt light headed and nearly passed out upon trying to get up to go the bathroom

14. Case Discussion- HPI
Denies abdominal pain, nausea, vomiting, antecedent retching
No history of heartburn, dysphagia, weight loss
No history of diarrhea or constipation/hard stools
No prior history of GIB
Screening colonoscopy 10 years ago – no polyps, (+) diverticulosis

15. Case Discussion– PMHx, Meds
Hepatitis C
CAD – h/o MI
PVD
AAA – s/p elective repair 3 years ago
HTN
Hypercholesterolemia
Lumbago
Medications:
Aspirin
Clopidogrel
Atorvastatin
Atenolol
Lisinopril

16. Case Discussion – Physical Exam
Physical examination:
BP 105/70, Pulse 100, (+) orthostatic changes
Alert and mentating, but anxious appearing
Anicteric
Mid line scar, benign abdomen, nontender liver edge palpable in epigastrium, no splenomegaly
Rectal examination – no masses, dark maroon blood

17. Case Discussion - Labs Labs Hct 21% (Baseline 33%) Plt 110K
BUN 34, Cr 1.0
Alb 3.5
INR 1.6
ALT 51, AST 76

18. Initial Considerations
Differential diagnosis?
What is most likely source?
What diagnosis can you least afford to miss?
How sick is this patient? (risk stratification)
Determines disposition
Guides resuscitation
Guides decision re: need for/timing of endoscopy

19. Differential Diagnosis – Upper GIB
Peptic ulcer disease
Gastroesophageal varices
Erosive esophagitis/gastritis/duodenitis
Mallory Weiss tear
Vascular ectasia
Neoplasm
Dieulafoy’s lesion
Aortoenteric fistula
Hemobilia, hemosuccus pancreaticus
Most common
Rare, but cannot afford to miss

20. Hemobilia, bleeding from biliary tract Hemosuccus Pancreaticus,
Pancreatitis, pancreatic tumor, splenic artery aneurysm

21. Differential Diagnosis – Lower GIB
Most common diagnosis
Diverticulosis
Angioectasias
Hemorrhoids
Colitis (IBD, Infectious, Ischemic)
Neoplasm
Post-polypectomy bleed (up to 2 weeks after procedure)
Dieulafoy’s lesion

22. History and Physical History Physical Examination
Localizing symptoms
History of prior GIB
NSAID/aspirin use
Liver disease/cirrhosis
Vascular disease
Valvular disease, chronic renal failure
AAA repair
Radiation exposure
Family history of GIB
Vital signs, orthostatics
Abdominal tenderness
Skin, oral examination
Stigmata of liver disease
Rectal examination
Objective description of stool/blood
Assess for mass, hemorrhoids
No need for guaiac test

23. History and Physical History Physical Examination
Localizing symptoms
History of prior GIB
NSAID/aspirin use
Liver disease/cirrhosis
Vascular disease
Valvular disease, chronic renal failure
AAA repair
Radiation exposure
Family history of GIB
Vital signs, orthostatics
Abdominal tenderness
Skin, oral examination
Stigmata of liver disease
Rectal examination
Objective description of stool/blood
Assess for mass, hemorrhoids
No need for guaiac test

24. Always get objective description of stool
Take Home Point # 1
Always get objective description of stool
Avoid noninformative terms such as “grossly guaiac positive”

25. Take Home Point #2
If you need a card to tell you whether there’s blood in the stool, it’s NOT an acute GIB

26. Narrowing the DDx: Upper or Lower Source?
Predictors of UGI source:
Age <50
Melenic stool
BUN/Creatinine ratio
If ratio ≥ 30, think upper GIB
J Clin Gastroenterol 1990;12:500
Am J Gastroenterol 1997;92:1796
Am J Emerg Med 2006;24:280

27. Utility of NG Tube
Most useful situation: patients with severe hematochezia, and unsure if UGIB vs. LGIB
Positive aspirate (blood/coffee grounds) indicates UGIB
Can provide prognostic info:
Red blood per NGT – predictive of high risk endoscopic lesion
Coffee grounds – less severe/inactive bleeding
Negative aspirate – not as helpful; 15-20% of patients with UGIB have negative NG aspirate
Ann Emerg Med 2004;43:525
Arch Intern Med 1990;150:1381
Gastrointest Endosc 2004;59:172

28. Take Home Point #3
Upper GI bleed must still be considered in patients with severe hematochezia, even if NG aspirate negative

29. Initial Assessment Always remember to assess A,B,C’s
Assess degree of hypovolemic shock
Class I
Class II
Class III
Class IV
Blood loss (mL)
750
>2000
Blood volume loss (%)
< 15%
15-30%
30-40%
>40%
Heart rate
<100
>100
>120
>140
SBP
No change
Orthostatic change
Reduced
Very low, supine
Urine output (mL/hr)
>30
20-30
10-20
<10
Mental status
Alert
Anxious
Aggressive/drowsy
Confused/unconscious

30. Resuscitation IV access: large bore peripheral IVs
Use crystalloids first
Anticipate need for blood transfusion
Threshold should be based on underlying condition, hemodynamic status, markers of tissue hypoxia
Should be administered if Hgb ≤ 7 g/dL
1 U PRBC should raise Hgb by 1 (HCT by 3%)
Remember that initial Hct can be misleading (Hct remains the same with loss of whole blood, until re-equilibration occurs)
Correct coagulopathy

31. Resuscitation
40%
20%
bleed
Time
IVFs
IV access: large bore peripheral IVs best (alt: cordis catheter)
Use crystalloids first
Anticipate need for blood transfusion
Threshold should be based on underlying condition, hemodynamic status, markers of tissue hypoxia
Should be administered if Hgb ≤ 7 g/dL
1 U PRBC should raise Hgb by 1 (HCT by 3%)
Remember that initial Hct can be misleading (Hct remains the same with loss of whole blood, until re-equilibration occurs)
Correct coagulopathy

32. Transfusion Strategy Randomized trial:
921 subjects with severe acute UGIB
Restrictive (tx when Hgb<7; target 7-9) vs. Liberal (tx when Hgb<9; target 9-11)
Primary outcome: all cause mortality rate within 45 days
NEJM 2013;368;11-21

33. Restrictive Strategy Superior
Liberal
P value
Mortality rate 5% 9%
0.02
Rate of further bleeding
10%
16%
0.01
Overall complication rate
40%
48%
Benefit seen primarily in Child A/B cirrhotics
NEJM 2013;368;11-21

34. Resuscitation
IV access: large bore peripheral IVs best (alt: cordis catheter)
Use crystalloids first
Anticipate need for blood transfusion
Threshold should be based on underlying condition, hemodynamic status, markers of tissue hypoxia
Should be administered if Hgb ≤ 7 g/dL
1 U PRBC should raise Hgb by 1 (HCT by 3%)
Remember that initial Hct can be misleading (Hct remains the same with loss of whole blood, until re-equilibration occurs)
Correct coagulopathy
Weigh risks and benefits of reversing anticoagulation
Assess degree of coagulopathy
Vitamin K – slow acting, long-lived
FFP – fast acting, short lived
- Give 1 U FFP for every 4 U PRBCs

35. Resuscitation Early intensive resuscitation reduces mortality
Consecutive series of patients with hemodynamically significant UGIB
First 36 subjects = Observation Group (no intervention)
Second 36 subjects = Intensive Resuscitation Group (intense guidance provided) – goal was to decrease time to correction of hemodynamics, Hct and coagulopathy
Am J Gastroenterol 2004;99:619

36. Early Intensive Resuscitation Reduces UGIB Mortality
Intervention: Faster correction of hemodynamics, Hct and coags.
Time to endoscopy similar
(groups are essentially the same)
Am J Gastroenterol 2004;99:619

37. Early Intensive Resuscitation Reduces UGIB Mortality
Observation group
5 MI
4 deaths
Intense group
2 MI
1 death (sepsis)
Am J Gastroenterol 2004;99:619

38. Causes of Mortality in Patients with Peptic Ulcer Bleeding
Patients rarely bleed to death
Prospective cohort study >10,000 cases of peptic ulcer bleed
Mortality rate 6.2%
80% of deaths not related to bleeding
Am J Gastroenterol 2010;105:84

39. Causes of Mortality in Patients with Peptic Ulcer Bleeding
Most common causes of non-bleeding mortality:
Terminal malignancy (34%)
Multiorgan failure (24%)
Pulmonary disease (24%)
Cardiac disease (14%)
Am J Gastroenterol 2010;105:84

40. Take Home Point #4
Early resuscitation and supportive measures are critical to reduce mortality from UGIB

41. Risk Stratification
Identify patients at high risk for adverse outcomes
Helps determine disposition (ICU vs. floor vs. outpatient)
May help guide appropriate timing of endoscopy

42. Factors associated with higher morbidity are,
Hemodynamic instability
Repeated hematemesis or hematochezia
Failure to clear with gastric lavage
Age older than 60 years
Coexistent organ system disease

43. Rockall Scoring System
Validated predictor of mortality in patients with UGIB
2 components: clinical + endoscopic
Variable 1 2 3
Age
<60
60-79
≥ 80
Shock No
SBP ≥ 100
P<100
Tachy-
P>100
Hypotension-
SBP <100
Comorbidity
No major
Cardiac failure, CAD, other major
Renal failure, liver failure, malignancy
Gut 1996;38:316

44. Endoscopic finding (evidence of bleeding):
None- 0 score
2 score for blood, adherent clot, spurting vessel
Diagnosis:
0 score- Mallory weiss tear
2 score- GI malignancy
1 score- all other dignosis

45. Clinical Rockall Score – Mortality Rates

46. AIMS65 Albumin <3.0 INR > 1.5 Mental status altered
Simple risk score that predicts in-hospital mortality, LOS, cost in patients with acute UGIB
Albumin <3.0
INR > 1.5
Mental status altered
Systolic BP <90
65+ years old
Gastrointest Endosc 2011;74:1215

47. AIMS65
Gastrointest Endosc 2011;74:1215

48. Blatchford Score Predicts need for endoscopic therapy
Based on readily available clinical and lab data
Can use UpToDate calculator
Lancet 2000;356:1318

49. Blatchford Score
Gastrointest Endosc 2010;71:1134

50. Blatchford Score BUN < 18 mg/dL Hgb > 13 (men), 12 (women)
Most useful for safely discriminating low risk UGIB patients who will likely NOT require endoscopic hemostasis
“Fast track Blatchford” – patient at low risk if:
BUN < 18 mg/dL
Hgb > 13 (men), 12 (women)
SBP >100
HR < 100

51. Pre-endoscopic Pharmacotherapy
For Non-Variceal UGIB
IV PPI: 80 mg bolus, 8 mg/hr drip
Rationale: suppress acid, facilitate clot formation and stabilization
Duration: at least until EGD, then based on findings

52. Pre-endoscopy PPI
Reduces the proportion of patients with high risk endoscopic stigmata (“downstages” lesion)
Decreases need for endoscopic therapy
Has not been shown to reduce rebleeding, surgery, or mortality rates
High risk
Low risk
Endoscopic treatment required:
Omeprazole – 19% (23% of PUD)
Placebo – 28% (37% of PUD)
N Engl J Med 2007;356:1631

53. Endoscopy - Nonvariceal UGIB
Early endoscopy (within 24 hours) is recommended for most patients with acute UGIB
Achieves prompt diagnosis, provides risk stratification and hemostasis therapy in high-risk patients
J Clin Gastroenterol 1996;22:267
Gastrointest Endosc 1999;49:145
Ann Intern Med 2010;152:101

54. ~80% bleeds spontaneously resolve
Endoscopic stigmata of recent hemorrhage
Stigmata
Continued/rebleeding rate
Active bleeding
55-90%
Nonbleeding visible vessel
40-50%
Adherent clot
Variable, depending on underlying lesion: 0-35%
Flat pigmented spot
7-10%
Clean base
< 5%
major

55. Major Stigmata – Active Spurting
Kelsey, PB (Dec ). Duodenum - Ulcer, Arterial Spurting, Treated with Injection and Clip. The DAVE Project. Retrieved Aug, 1, 2010, from

56. Major Stigmata - NBVV

57. Adherent Clot
Role of endoscopic therapy of ulcers with adherent clot is controversial
Clot removal usually attempted
Underlying lesion can then be assessed, treated if necessary

58. Low rebleeding risk – no endoscopic therapy needed
Minor Stigmata
Flat pigmented spot
Clean base
Low rebleeding risk – no endoscopic therapy needed

59. Endoscopic Hemostasis Therapy
Epinephrine injection
Thermal electrocoagulation
Mechanical (hemoclips)
Combination therapy superior to monotherapy
Kelsey, PB (Nov ). Stomach - Gastric Ulcer, Visible Vessel. The DAVE Project. Retrieved Aug, 1, 2010, from
Baron, TH (May ). Duodenum - Bleeding Ulcer Treated with Thermal Therapy, Perforation Closed with Hemoclips. The DAVE Project. Retrieved Aug, 1, 2010, from

60. Nonvariceal UGIB – Post-endoscopy management
Patients with low risk ulcers can be fed promptly, put on oral PPI therapy.
Patients with ulcers requiring endoscopic therapy should receive PPI IV x 72 hours
Significantly reduces 30 day rebleeding rate vs placebo (6.7% vs. 22.5%)
Note: there may not be major advantage with high dose over non-high dose PPI therapy
N Engl J Med 2000;343:310
Arch Intern Med 2010;170:751

61. Nonvariceal UGIB – Post-endoscopy management
Determine H. pylori status in all ulcer patients
Discharge patients on PPI (once to twice daily), duration dictated by underlying etiology and need for NSAIDs/aspirin
In patients with cardiovascular disease on low dose aspirin: restart as soon as bleeding has resolved
RCT demonstrates increased risk of rebleeding (10% v 5%) but decreased 30 day mortality (1.3% v 13%)
Ann Intern Med 2010;152:1

62. Nonvariceal UGIB – Post-endoscopy management
Determine H. pylori status in all ulcer patients
Discharge patients on PPI (once to twice daily), duration dictated by underlying etiology and need for NSAIDs/aspirin
In patients with cardiovascular disease on low dose aspirin: restart as soon as bleeding has resolved
RCT demonstrates increased risk of rebleeding (10% v 5%) but decreased 30 day mortality (1.3% v 13%)
Not dying is more important
than not rebleeding
Ann Intern Med 2010;152:1

63. Variceal Bleeding Occurs in 1/3 of patients with cirrhosis
1/3 initial bleeding episodes are fatal
Among survivors, 1/3 will rebleed within 6 weeks
Only 1/3 will survive
1 year or more

64. Predictors of large esophageal varices
Severity of liver disease (Child Pugh)
Platelet count < 88K
Palpable spleen
Platelet count/spleen diameter (mm) ratio <909
Gut 2003;52:1200
J Clin Gastroenterol 2010;44:146
J Gastroenterol Hepatol 2007;22:1909
Arch Intern Med 2001;161:2564
Am J Gastroenterol 1999;94:3103

65. VARICEAL Bleed Vasoconstrictor therapy Resuscitation Antibiotics
ICU level care
Endoscopy
ALternative/Rescue therapies
Beta blockade

66. Vasoconstrictor therapy
Goal: Reduce splanchnic blood flow
Terlipressin – only agent shown to improve control of bleeding and survival in RCTs and meta-analysis
Not available in US
Vasopressin + nitroglycerine – too many adverse effects
Somatostatin – not available in US
Octreotide (somatostatin analogue)
Decreases splanchnic blood flow (variably)
Efficacy is controversial; no proven mortality benefit
Standard dose: 50 mcg bolus, then 50 mcg/hr drip for 3-5 days
Gastroenterology 2001;120:946
Cochrane Database Syst Rev 2008;16:CD000193
N Engl J Med 1995;333:555
Am J Gastroenterol 2009;104:617

67. Antibiotics
Bacterial infection occurs in up to 66% of patients with cirrhosis and variceal bleed
Negative impact on hemostasis (endogenous heparinoids)
Prophylactic antibiotics reduces incidence of bacterial infection, significantly reduces early rebleeding
Ceftriaxone 1 g IV QD x 5-7 days
Alt: Norfloxacin 400 mg po BID
Hepatology 2004;39:746
J Korean Med Sci 2006;21:883
Hepatogastroenterology 2004;51:541

68. Resuscitation Promptly but with caution
Goal = maintain hemodynamic stability, Hgb ~7-8, CVP 4-8 mmHg
Avoid excessively rapid overexpansion of volume; may increase portal pressure, greater bleeding

69. Endoscopy
Should be performed as soon as possible after resuscitation (within 12 hours)
Endotracheal intubation frequently needed
Band ligation is preferred method
Layer, L. & Jaganmohan, S. & Raju, GS & DuPont, AW (Oct ). Esophagus - Band Ligation of Actively Bleeding Gastroesophageal Varices. The DAVE Project. Retrieved Aug, 2, 2010, from

70. ALternative/Rescue therapies
TIPS – Transjugular Intrahepatic Portosystemic Shunt
Early placement of shunt (within 24-72hrs) associated with improved survival among high-risk patients
Preferred treatment for gastric variceal bleeding (rule out splenic vein thrombosis first)
Fan, C. (Apr ). Vascular Interventions in the Abdomen: New Devices and Applications. The DAVE Project. Retrieved Aug, 2, 2010, from
Hepatology 2004;40:793
Hepatology 2008;48:Suppl:373A
N Engl J Med Jun 24;362:2370

71. TIPS+embolization of gastric varices

72. ALternative/Rescue therapies
Sengstaken-Blakemore Tube
Very effective for immediate, temporary control
High complication rate – aspiration, migration, necrosis + perforation of esophagus
Use as bridge to TIPS within 24 hours
Airway protection strongly recommended

73. ALternative/Rescue therapies
Self-Expanding Metal Stent
Specially designed covered metal stent
Tamponades distal esophageal varices
Removable; does not require airway protection
Very limited data
Gastrointest Endosc 2010;71:71

74. Beta blockade Reduces risk for recurrent variceal hemorrhage
Use nonselective beta blocker (e.g. Nadolol – splanchnic vasoconstriction, decrease cardiac output) and titrate up to maximum tolerated dose, HR 50-60
Start as inpatient, once acute bleeding has resolved and patient shows hemodynamic stability

75. Lower GI Bleed Bleeding arising from the colorectum
In patients with severe hematochezia, first consider possibility of UGIB
10-15% of patients with presumed LGIB are found to have upper GIB

76. Smaller volume, pain, diarrhea
Lower GI Bleed
Differential Diagnosis
Large volume, painless
- Diverticulosis (# 1 cause)
- Angioectasias
- Hemorrhoids
- Colitis (IBD, Infectious, Ischemic)
- Neoplasm
- Post-polypectomy
- Dieulafoy’s lesion
Smaller volume, pain, diarrhea

77. LGIB – Risk Stratification
0 factors: ~6% risk
1-3 factors: ~40%
>3 factors: ~80%
Predictors of severe* LGIB:
HR>100
SBP<115
Syncope
nontender abdominal examination
bleeding during first 4 hours of evaluation
aspirin use
>2 active comorbid conditions
* Defined as continued bleeding within first 24 hours (transfusion of 2+ Units, decline in HCT of 20+%) and/or recurrent bleeding after 24 hours of stability
Arch Intern Med 2003;163:838
Am J Gastroenterol 2005;100:1821

78. LGIB – Risk Factors for Mortality
Age
Intestinal ischemia
Comorbid illnesses
Secondary bleeding (developed during admission for a separate problem)
Coagulopathy
Hypovolemia
Transfusion requirement
Male gender
Clinical Gastro Hepatol 2008;6:1004

79. Role of Colonoscopy
Like UGIB, ~80% of LGIBs will resolve spontaneously; of these, ~30% will rebleed
Lack of standardized approach
Traditional approach:
elective colonoscopy after resolution of bleeding, bowel prep – low therapeutic benefit
Angiography for massive bleeding, hemodynamically unstable patient
Urgent colonoscopy approach
Similar to UGIB – identify stigmata of hemorrhage, perform therapy

80. Urgent Colonoscopy Within 6-12 hours of presentation
Requires rapid “purge” prep with 5-6 L Golytely administered 1L every minutes
Colonoscopy performed within 1 hour after clearance of stool, blood and clots
Need for bowel prep and risks of procedural sedation may be prohibitive in unstable patient

81. Endoscopic Therapy
Srinivasan, R. & Luthra, G. & Raju, GS (Jul ). Colon - Endoscopic Hemostasis of Diverticular Bleed. The DAVE Project. Retrieved Aug, 3, 2010, from

82. Urgent Colonoscopy
Limited high quality evidence of benefit
Establishes diagnosis earlier, shorter length of stay
“Landmark” study supporting urgent colonoscopy for diverticular bleed published in 2000
2 consecutive prospective, non-randomized studies
Group 1 (n=73): urgent colonoscopy, surgical therapy
Group 2 (n=48): urgent colonoscopy, endoscopic therapy
N Engl J Med 2000;342:78

83. Urgent Colonoscopy Group 1: 17 pts with definite diverticular bleed
9 had recurrent/persistent bleeding
6 required emergency surgery
Group 2: 10 pts with definite diverticular bleed
All 10 patients treated endoscopically
0 had recurrent bleed, complications, further transfusions, or surgery
N Engl J Med 2000;342:78

84. Standard Management Algorithm
Urgent Colonoscopy
Two RCTs published to date
Compared urgent colonoscopy (within 8 hours) vs. standard management
Standard Management Algorithm
Am J Gastroenterol 2005;100:2395

85. Urgent Colonoscopy – RCT#1
Definite bleeding source identified more frequently (42% vs 22%)
But no significant difference in important outcomes (but underpowered)
Am J Gastroenterol 2005;100:2395

86. Urgent Colonoscopy – RCT#2
85 patients with serious hematochezia (hemodynamically significant, Hgb drop > 1.5 g/dL, blood transfusion)
EGD performed within 6 hours
If EGD negative, randomized to urgent (<12 hr) or elective ( hr) colonoscopy
Primary endpoint= further bleeding
Am J Gastroenterol 2010;105:2636

87. Urgent Colonoscopy – RCT#2
EGD positive in 15%
No evidence of improved clinical outcomes with urgent colonoscopy – but prespecified sample size not reached
Am J Gastroenterol 2010;105:2636

88. Urgent Colonoscopy
In published series, endoscopic therapy is applied in 10-40% of patients undergoing colonoscopy for LGIB
Taken together, evidence suggests that colonoscopy should be performed within hours in stable patients
However, it is unclear how faster timing affects major clinical outcomes

89. Radiographic Studies
Tagged RBC scan
Noninvasive, highly sensitive ( ml/min)
Ability to localize bleeding source correctly only ~66%
More accurate when positive within 2 hours (95-100%)
Lacks therapeutic capability
Coordinate with IR so that positive scan is followed closely by angiography

90. (or have had colonoscopy with failure to localize/treat bleeding site)
Radiographic Studies
Angiography
Detects bleeding rates of ml/min
Therapeutic capability – embolization with microcoils, polyvinyl alcohol, gelfoam
Complications: bowel infarction, renal failure, hematomas, thromboses, dissection
Recommended test for patients with brisk bleeding who cannot be stabilized or prepped for colonoscopy
(or have had colonoscopy with failure to localize/treat bleeding site)

91. Multi-Detector CT (CT angio)
Radiographic Studies
Multi-Detector CT (CT angio)
Readily available, can be performed in ER within 10 minutes
Can detect bleeding rate of 0.5 ml/min
Can localize site of bleeding (must be active) and provide info on etiology
Useful in the actively bleeding but hemodynamically stable patient
Gastrointest Endosc 2010;72:402

92. Role of Surgery
Reserved for patients with life-threatening bleed who have failed other options
General indications: hypotension/shock despite resuscitation, >6 U PRBCs transfused
Preoperative localization of bleeding source important

93. Algorithmic Evaluation of Patient with Hematochezia
Assess activity of bleed
active
inactive
NG lavage
Prep for Colonoscopy
Positive
Negative
No risk for UGIB
Risk for UGIB
EGD
negative
Hemodynamically stable?
Treat lesion
positive

94. Algorithmic Evaluation of Patient with Hematochezia
Active Lower GIB
Hemodynamically stable?
Angiography
(+/- Tagged RBC scan) Or
Surgery if life-threatening
Consider “urgent colonoscopy” vs. traditional approach
Yes No

95. Take Home Points
Always get objective description of stool color (best way – examine it yourself)
Severe hematochezia can be from UGIB, even if NG lavage is negative

96. Take Home Points
All bleeding eventually stops (and majority of nonvariceal bleeds will stop spontaneously, with the patient alive)
Early resuscitation and supportive care are key to reducing morbidity and mortality from GIB
Multitasking- resuscitating, history, physical examination, plan further investigations.