GI%20bleeds:%20what

1
GI bleeds whats old, whats new?

• Grand Rounds, Department of Emergency Medicine
• April 15, 2004
• Christine Hall MSc MD FRCPC

2
Outline

• Upper GI bleeds overall summary
• PUD
• Drinkers and non drinkers
• Variance
• NSAIDs
• Upper GI bleeds specific physiology
• NSAIDs
• Upper GI bleed Rx issues
• PPIs
• EGD
• Discharge criteria
• Variceal bleeds
• Lower GI bleeds
• Patient disposition

3
Introduction

• GI bleeding
• 2 of all US hospital admissions
• 5 of admissions originating in the ED
• Majority of bleeds are UGI

4
UGI bleeding incidence

• 103/100,00 adult per year in UK
• incidence 23/100,00 in age under 30 to 485/100,00
  in over 75
• men more than double women except in elderly
• 14 occurred in inpatients already in hospital
  for some other reason
• 27 of cases (37 female, 19 male) patients were
  aged over 80.

Rockall TA, Logan RF, Devlin HB, Northfield TC.
Gastrointest Endosc. 2002 Jan55(1)1-5.
5
UGI Bleeding mortality

• Overall mortality 14
• 11 in emergency admissions
• 33 in inpatients
• In the emergency admissions
• 65 of deaths in pts under 80 associated with
  malignancy or organ failure at presentation
• Mortality for patients under 60 in the absence of
  malignancy or organ failure at presentation was
  0.8.

Rockall TA, Logan RF, Devlin HB, Northfield TC.
Gastrointest Endosc. 2002 Jan55(1)1-5.
6
UGI bleeds in drinkers

• From August 1, 1990 through September 9, 1994.
  Prospective.
• Pts referred to GI (selection bias)
• subnormal hematocrit on or within 12 h of
  admission or a fall of at least 5 points from
  previous
• Upper GI endoscopy was performed in all patients
  within 48 h of admission
• Alcohol use was quantitated as chronic (80 g or
  more per day for at least 1 month), binge,
  occasional, or none.

7
UGI bleeds in drinkers

• 727 pts 212 (29) chronic alcohol users
• Peptic ulcer disease was most common cause of
  bleeding (60).
• Gastropathy etiological in only 32 patients (4)
• portal hypertension in 22 patients
• NSAID induced gastropathy in 5
• Alcohol induced gastropathy in 5 pts
• bleeding was mild and self-limited.

Wilcox CM, Alexander LN, Straub RF, Clark WS Am
J Gastroenterol. 1996 Jul91(7)1343-7
8
UGI bleeds in drinkers

• Causes of bleeding were compared between drinkers
  and nondrinkers
• drinkers were more likely to bleed from varices
  (p 0.024)
• portal hypertension-related causes (p lt 0.01),
• Peptic ulcer was more common in nondrinkers
  compared with chronic ETOH
• (67 vs 53 p lt 0.01)
• Esophagitis (p 0.95) and Mallory-Weiss tear (p
  0.15) were NS between the two groups.

Wilcox CM, Alexander LN, Straub RF, Clark WS Am
J Gastroenterol. 1996 Jul91(7)1343-7
9
UGI bleed variance

• Qiu, YJ. Zhonghua Hu Li Za Zhi. 1987
  Jun22(6)269-70.
• Relation between hemorrhage and the waxing or
  waning of the moon
• Unfortunately in Chinese so not available for
  today

10
Upper GI bleeds pathophysiology

• Esophagitis
• Candidal
• Non candidal
• bisphosphonates
• Esophageal tears
• Gastritis
• Thats all well say about the benign causes

11
UGI bleed diagnosis to OG or not to OG?

• Not great evidence for confirming UGI bleed by
  putting in NG or OG
• Practice discouraged by most GIs
• Can confound UGI bleed re trauma of insertion
• Relative contraindication in variceal bleed
  although this is witchcraftmore about that later

12
PUD Causation
13
H. Pylori

• Serology never becomes negative once positive
• Even if H. Pylori is eradicated
• Complicates repeat breath tests or biopsies
• PPIs are antimicrobial for h.pylori despite poor
  initial performance in development as an
  antibiotic

14
Current Rx for H. Pylori Eradication
15
NSAID induced ulcers
16
NSAIDS whats the problem?

• Toxic effects of NSAIDs thought to be due to
  Cox-1 inhibition
• launch of the cyclooxygenase-2 (COX-2) selective
  NSAIDs was based on 2 hypotheses
• the major adverse effects limiting the
  usefulness of nonselective NSAIDs are
  gastrointestinal in nature
• COX-2 selective NSAIDs are associated with fewer
  gastrointestinal adverse effects than
  nonselective NSAIDs.

17
The CLASS Trial

• To determine whether celecoxib, a COX-2-specific
  inhibitor, is associated with a lower incidence
  of significant upper GI toxic effects and other
  adverse effects compared with conventional
  NSAIDs.
• double-blind, randomized controlled trial
  conducted from September 1998 to March 2000
• Three hundred eighty-six clinical sites in the
  United States and Canada

18
The CLASS trial

• 8059 patients gt/18 years old, OA or RA, 7968
  received at least 1 dose of study drug.
• 4573 patients (57) received treatment for 6
  months
• Random assign
• celecoxib, 400 mg twice per day (2 and 4 times
  the maximum RA and OA dosages, respectively
• n 3987
• ibuprofen, 800 mg 3 times per day (n 1985)
• diclofenac, 75 mg twice per day (n 1996).
• ASA for CV prophylaxis (lt/325 mg/d) was
  permitted.

19
CLASS Trial

• Incidence of prospectively defined symptomatic
  upper GI ulcers and ulcer complications
  (bleeding, perforation, and obstruction) and
  other adverse effects during the 6-month
  treatment period.
• Overall annual incidence rates of UGI ulcer
  complications alone 0.76 vs 1.45 with NSAIDs
  (p0.09)
• Overall annual incidence rate of UGI ulcer
  complications plus symptomatic ulcers 2.08 vs
  3.54 , p0.02
• Pts not on ASA
• UGI complication alone 0.44 vs 1.27, p0.04
• UGI complication plus symptoms 1.40 vs 2.91, p
  .02
• For patients onASA
• UGI complications alone 2.01 vs 2.12,l p0.92
• UGI complications plus symptomatic ulcers 4.70
  vs 6.00 (P .49).

20
CLASS conclusions

• Fewer celecoxib-treated patients than
  NSAID-treated patients experienced chronic GI
  blood loss, GI intolerance, hepatotoxicity, or
  renal toxicity.
• No difference was noted in the incidence of
  cardiovascular events between celecoxib and
  NSAIDs, irrespective of aspirin use.
• CONCLUSIONS Celecoxib, at big doses, was
  associated with a lower incidence of symptomatic
  ulcers and ulcer complications combined, as well
  as other clinically important toxic effects,
  compared with NSAIDs at standard dosages (800 mg
  tid).
• The decrease in upper GI toxicity was strongest
  among patients not taking aspirin concomitantly.

JAMA. 2000 Sep 13284(10)1247-55.
21
The VIGOR trial

• clinical upper gastrointestinal events occur in 2
  to 4 percent of patients who are taking
  nonselective NSAIDs
• Is rofecoxib associated with a lower incidence of
  clinically important upper gastrointestinal
  events than Naproxen among patients with
  rheumatoid arthritis
• randomly assigned 8076 RA patients who were at
  least 50 years of age (or at least 40 years of
  age and receiving long-term glucocorticoid
  therapy)
• received either 50 mg of rofecoxib daily or 500
  mg of naproxen twice daily
• primary end point was confirmed clinical upper
  gastrointestinal events (gastroduodenal
  perforation or obstruction, upper
  gastrointestinal bleeding, and symptomatic
  gastroduodenal ulcers)

22
VIGOR Trial

• Rofecoxib and naproxen had similar efficacy
  against rheumatoid arthritis.
• median follow-up of 9 months
• 2.1 per 100 pt years confirmed gastrointestinal
  events with refecoxib
• 4.5 per 100 pt-years with naproxen
• relative risk, 0.5 CI 0.3 to 0.6 Plt0.001
• The respective rates of complicated confirmed
  events (perforation, obstruction, and severe
  upper gastrointestinal bleeding)
• 0.6 per 100 patient-years refecoxib
• 1.4 per 100 patient-years naproxen
• relative risk, 0.4 CI 0.2 to 0.8 P0.005

23
VIGOR trial

• The incidence of myocardial infarction
• lower among patients in the naproxen group than
  among those in the rofecoxib group
• 0.1 percent vs. 0.4 percent
• relative risk, 0.2 CI 0.1 to 0.7
• the overall mortality rate and the rate of death
  from cardiovascular causes were similar in the
  two groups.

Bombardier C, Laine L, Reicin A, Shapiro D,
Burgos-Vargas R, Davis B, Day R, Ferraz MB,
Hawkey CJ, Hochberg MC, Kvien TK, Schnitzer TJ
N Engl J Med. 2000 Nov 23343(21)1520-8
24
So.

• increased incidence of total and
  nongastrointestinal serious adverse events with
  the COX-2 selective NSAIDs remains a major
  concern
• increased morbidity may be a manifestation of the
  COX-2 selectivity or the supramaximal doses of
  these drugs used in the trials
• proof that the increased harm was not caused by
  the COX-2 selectivity of the drugs depends on a
  randomized controlled trial of COX-2 selective
  NSAIDs at usual doses vs. nonselective NSAIDs
• Thus far, no such trial
• What about Cox-2s plus PPIIs?...no trial

25
Rx of UGI bleed

• Shots in the dark?

26
Upper GI bleeds

• Coagulation and fibrinolysis are dependent on
  intragastric pH
• When pH is below 6, platelet aggregation is
  abolished
• When pH is below 4, fibrin clots are digested by
  gastric pepsin
• In UGI bleed, need to raise gastric pH and keep
  it there for 72 hours

27
PUD H2 blockers

• H2 receptor antagonists inhibit gastric acid
  production
• Little if any evidence of improved outcome in
  active GI bleed
• Insufficient acid suppression
• Rapid drug tolerance

28
Proton Pump Inhibitors

• More profound and sustained acid suppression
• Binds irreversibly to HKATPase (proton pump)
  inhibiting actively secreting parietal cells
• Predictable t1/2 1 hr but effect 24 hrs
• No tolerance developed
• Excellent safety profile, no dose reduction in
  renal failure/cirrhosis
• IV Omeprazole released in 1991

29
PPIs in PUD

• IV Proton pump inhibitors
• Lau et al NEJM 2000 Aug 3 343 (5) 310-16
• After endoscopic Rx, bleed recurs in 15-20
• Assess whether use of high dose PPI decreased
  recurrence within 30 days
• Dbl blind rand to Omeprazole bolus and infusion
  vs placebo
• All got Omeprazole orally x 2 weeks post infusion

30
PPIs in PUD (Lau, ctd)

• 240 patients, recur in 6.7 of omeprazole vs
  22.5 of placebo
• Most recurrent bleed occurs in first three days
• Only evidence for IV infusion is in acute bleed
  with ulcer with high risk stigmata (i,.e visible
  vessel)
• But, EGD was done within 1 hour 24/7

31
Waiting for EGD
32
PPIs while waiting for EGD

• R. Enns C. Andrews, UBC, Can J Gastro 2003
  Aliment Pharmacol Ther 2003.
• To evaluate cost effectiveness of IV PPI while
  awaiting EGD compared with EGD alone
• Probabilities of rebleeding and surgery taken
  into account
• In a hypothetical cohort of 1000 patients, IV PPI
  utilization while awaiting EGD mean savings of
  20,700 Canadian
• Using PPI pre EGD averted 37 rebleeds
• Use of PPI while awaiting EGD is cost effective
• Finidngs do not apply to low risk stigmata,
  variceal bleeds, lower GI bleeds

33
PUD RUGBE

• Canadian Registry of patients with Upper GI
  Bleeding Undergoing Endoscopy
• Pt char and Rx from 1999 on
• J. Romagnolo is local PI
• Protective effect of PPI use and EGD in specific
  patient subgroups
• Meta-analysis supports high dose IV PPIs leads to
  improvement when coupled with EGD
• Optimum dose, timing, and subgroup analysis needs
  further work

34
PPIs the local challenge

• CHR Pharmanews
• Vol 28 Issue 3 Revised November 2003
• Kaplan Gf, Bates D, McDonald D, Romagnulo J.
• Inappropriate Prescribing Leading to Rapidly
  Escalating Costs of IV PPI in the Calgary Health
  Region

35
PPIs the local cost
Year FMC PLC RGH Total
1999 56K 35K 9K 100K
2000 149K 86K 73K 308K
2001 207K 96K 121K 425K
2002 168K 94K 123K 386K
36
PPIs Local guidelines

• Ideally withold PPIs until EGD but case by case
  adaptationi.e. night
• IV Omeprasole 80 mg bolus and 8mg/hr infusion for
  max of 72 hours
• Pts with HRS on EGD (arterial or venous active
  bleed, visible vessel, adherent clot) should have
  endo Rx and then 72 hr infusion
• No HRS stop infusion
• Inpts who are NPO get bid dosing not infusion

37
PPIs Local guidelines ctd

• Clinical equivalence between IV PPI and oral PPI
  in GERD
• Clinical equivalence between IV PPI and NG PPI
• 40 mg PPI IV 13.70
• 40 mg PPI po 0.45

38
Can UGI bleeds go home?

• Selection of patients for early discharge or
  outpatient care after acute UGI haemorrhage.
  National Audit of Acute Upper GI Haemorrhage
• Attempted to identify patients who had negligible
  risk of further bleeding or death and for whom
  early discharge or even outpatient management
  would be possible with no adverse effect on
  standards of care.

39
UGI bleed and discharge

• Used a validated risk scoring system based on
• age (score 0-2)
• presence of shock (0-2)
• comorbidity (0-3)
• diagnosis (0-2)
• endoscopic stigmata of recent haemorrhage (0-2)
• maximum possible score was 11.

40
Rockalls Scoring System
VARIABLE 0 1 2 3
Age lt60 60-79 gt 80 ----
Shock HRlt100 HRgt100, SBP gt100 HRgt100, SBPlt100 ----
Comorbidity None ---- CHF, IHD, any major dx Renal failureLiver failureMets
Dx post OGD MW tear All other dx UGI malig, Blood in UGI ----
Major SRH None or dark spot ---- Adherent clot, vis vessel ----
41
UGI bleed and discharge

• 2531 patients who underwent endoscopy after an
  acute admission
• 744 (29.4) of the 2531 patients scored 2 or less
  on the risk score
• Of these
• 32 or 4.3 rebled 95 Cl 3.0-6.0
• 1 or 0.1 died 95 CI 0.006-0.75
• Conclusions the risk score identifies patients
  at low risk of rebleeding or death
• Median hospital stay increased with risk score
• Within low risk score categories of 5 or less
• trend of increasing hospital stay as the time
  between admission and endoscopy increased

Lancet. 1996 Apr 27347(9009)1138-40 Rockall TA,
Logan RF, Devlin HB, Northfield TC.
42
UGI bleed and discharge

• Three year prospective validation of a PRE-EGD
  risk stratification in patients with acute UGI
  hemorrhage
• To assess the accuracy of a risk stratification
  used at initial assessment (does not rely on EGD)
• To identify groups with increased risk of
  mortality and requirement for urgent treatment
  intervention
• Prospective assessment of risk stratification in
  consecutive patients with acute
  upper-gastrointestinal haemorrhage.

43
UGI risk stratification

• 3-year period, 1349 consecutive patients, risk
  stratified and followed up for 2 weeks
• Two-week, all-cause mortality, re-bleeding, and
  need for urgent treatment intervention.

44
UGI bleed and discharge without EGD?

• Stratification within the high-risk group
  predicted a significant increased risk of 2-week,
  all-cause mortality (P lt 0.001)
• Hi risk 11.8
• Intermediate risk 3
• Low risk 0
• High risk strata significantly higher re-bleeding
  (P lt 0.001)
• Hi risk 44.1
• Intermediate 2.3
• Low risk 0
• High risk strata significantly higher need for
  urgent treatment intervention (P lt 0.001)
• Hi risk 71
• Intermediate risk 40.6
• Low risk 2.6

Cameron EA, Pratap JN, Sims TJ, Inman S, Boyd D,
Ward M, Middleton SJ. Eur J Gastroenterol
Hepatol. 2002 May14(5)497-501.
45
So, who admits?

• Physician specialty and variations in the cost of
  treating patients with acute upper
  gastrointestinal bleeding.
• Pts stratified into three groups based on a
  validated risk score
• Length of stay and hospital costs compared
• primarily cared for by internists, surgeons, and
  gastroenterologists
• Median length of stay (2 days) if admitted to GI
• Significantly shorter than admitted under other
  physicians (P lt 0.05)
• Median hospitalization cost (2856) if admitted
  to GI
• Significantly lower than other services (P lt
  0.01)
• No differences in the time to endoscopy among
  services.

Quirk DM, Barry MJ, Aserkoff B, Podolsky
DK Gastroenterology. 1997 Nov113(5)1443-8
46
Now for some risky business
47
Variceal bleeding

• Esophageal and/or gastric varices account for
  about 20 of all GI bleeds
• Most dramatic and life threatening presentation
  of portal hypertension
• 25-50 of bleeds in cirrhotic pts is non variceal
• Dave P et al, Clin Gastroenterol 5113, 1983
• After 1 bleeding episode, risk of a second is 70
• Accounts for 50 of all deaths from cirrhosis

48
Variceal bleeding

• Risk of mortality from each bleeding episode is
  20-84
• Risk depends on etiology of portal hypertension,
  hepatic reserve of the pt., duration of
  hemorrhage prior to presentation

49
IV Octreotide

• Octreotide or Somatostatin is a potent
  nonselective vasoconstrictor
• Should be routine in known or strongly suspected
  variceal bleed
• Can be used alone or in conjunction with
  sclerotherapy/banding
• No role in non variceal UGI bleeds

50
Balloon tamponade

• Originated in the 1930s, first filled with water
  not air
• 1950 Sengstaken and Blakemore invented double
  lumen balloon
• Modified by Linton, Nachlasm, Boyce and Edlich
• Currently have
• Blakemore 3 lumens gastric, esoph and gastric
  suction
• Linton as above with esoph aspiration port as
  well

51
Balloon tamponade

• Roberts still recommends NG insertion in all GI
  bleed..no real evidence for itnice in flight or
  if ongoing vomiting
• There is no evidence to support passage of an NG
  tube increases variceal bleed
• Meeroff et al Mangement of massive UGI bleed
  Hosp Practice, 1984
• Management of varices is substantially different
  from other causes

52
Balloon tamponade

• Used when sclerotherapy not available
• Used when vasoconstrictor therapy is not adequate
• Can control bleeding in up to 80 of cases
• In the absence of endoscopy indications
• pt with known portal hypertension
• prior variceal bleed
• not responding to vasoconstrictor Rx

53
Balloon Tamponade of Varices

• Use of GEBT has serious/lethal complications
• Overall complication rate higher than most other
  ED procedures
• Clear indications and complete understanding of
  placement is essential
• best placed by the individual most familiar with
  technique (which is usually no-one including GI
  guys)

54
GEBT

• Patient at risk re uncooperative, or hepatic
  encephalopathy
• If patient is not awake, alert and fully
  cooperative should be intubated
• Roberts, Procedures in emergency medicine
• Patients at extremely high risk for regurg and
  aspiration
• Threshold for intubation should be lower than
  usual

55
GEBT Procedure

• Unfamiliar to most docs
• Gastric balloon holds 500 to 700 mL, test both
  balloons for patency
• Patient at 45 degrees or in left lateral
• Anesthetize nose and post pharynx if necessary
• Deflate balloons and lock off, lubricate tube

56
GEBT procedure

• Pass through mouth is preferred (especially in
  intubated) but nose can be used
• Pass tube to at least 50 cm mark or max depth
  allowed by tube length
• Suction to esoph and gastric ports to minimize
  aspiration risk even further prior to inflation
• Confirm radiographically prior to inflation

57
GEBT procedure

• Once markers seen can begin to inflate gastric
  balloon
• Should monitor pressure in balloon as inflated
• Use AIR not water
• Repeat radiograph once inflated
• Clamp air ports on tube and gently pull back on
  tube to snug up to GE junction

58
Indications to inflate the esophageal balloon

• If continuous bloody aspirate from gastric
  suction
• Absolutely must be done with manometer guidance
• Pressure at lowest level that stops bleeding and
  should not exceed 45 mm Hg
• If ongoing bleeding with both balloons up, likely
  gastric and NOT esophageal source

59
GEBT traction

• Use if inflation of balloons has been done and
  active gastric bleeding persists
• External traction on the tube
• Foam rubber block often included in the kit
• Various traction mechanisms

60
GEBT Complications

• Occur in 8-16 of patients
• Mortality considered in about 3
• Variceal hemorrhage itself carries 40-80
  mortality
• One study reported GEBT directly casued death in
  22 of pts in which it was used

61
GEBT complications

• Major occur in 8-16
• Mortality around 3
• Common
• Aspiration pneumonia
• Asphyxiation (balloon migration, cut the tubes)
• Esophageal necrosis
• Uncommon
• Esophageal perforation (overinflation or duration
  tube)
• Duodenal rupture
• Tracheobronchial rupture
• Periesophageal abcess
• mediastinitis

62
GEBT Complications

• Minor
• Common
• Gastroesophageal ulceration
• Regurgitation
• Chest discomfort
• Back pain
• Pressure necrosis re traction
• Uncommon
• Epistaxis
• Pharyngeal erosions
• Pressure necrosis of tongue
• hiccups

63
Problems at the bottom end
64
Lower GI bleeds

• defined as blood loss that originates from a
  source distal to the ligament of Treitz
• results in hemodynamic instability or symptomatic
  anemia
• approximately 10 to 15 of patients presenting
  with acute severe hematochezia have an upper
  gastrointestinal source of bleeding
• most common causes of lower gastrointestinal
  bleeding are diverticulosis, hemorrhoids,
  ischemic colitis, and angiodysplasia
• lower gastrointestinal bleeding ceases
  spontaneously in most cases

65
LGI bleed, does colonoscopy affect outcome?

• management of lower-GI hemorrhage remains
  controversial largely because outcomes data are
  lacking
• Hypothesized that clinical factors, such as
  comorbidity, hemodynamic instability, and timing
  of colonoscopy, are associated with hospital
  lengths of stay
• Retrospective review of LGI hospitalized, 1993 to
  2000 (selection bias)
• regression model was constructed to explore
  associations between time to discharge (i.e.,
  length of stay) and clinical parameters.

66
LGI, colonoscopy continued

• 565 hospitalizations, mean length of stay was 6.7
  days
• Colonoscopy was performed during 415
  hospitalizations
• 1/3 discharged within 48 hours after colonoscopy
• Regression model, decreased likelihood of
  discharge if
• hemodynamic instability
• higher comorbidity
• performance of a tagged red blood cell nuclear
  scan
• surgery for hemostasis
• Colonoscopy at any timepoint associated with an
  increased likelihood of being discharged
• hazard ratio 1.5 95 CI 1.2, 1.8.
• Mean lengths of stay for colonoscopy within 24
  hours of hospitalization was shorter
• 5.4 vs. 7.2 days plt0.008

Early colonoscopy for acute lower GI bleeding
predicts shorter hospital stay a retrospective
study of experience in a single
center.Schmulewitz N, Fisher DA, Rockey DC.
67
Predictors of severe LGI bleed

• Harvard group
• Goal to determine risk factors for severe acute
  LIB
• 252 consecutive patients admitted with acute LIB
• Data were collected on 24 clinical factors
  available in the first 4 hours of evaluation
• outcome was severe bleeding, which was defined
  as
• continued bleeding within the first 24 hours of
  hospitalization documented by transfusion of gt or
  2 units of blood and/or hematocrit decrease of
  gt or 20)
• recurrent bleeding after 24 hours of stability
  (additional transfusions, further hematocrit
  decrease of gt or 20, or readmission for LIB
  within 1 week of discharge)
• Severe LGI bleeding occurred in 123 pts (49)

68
Predictors of Severe LGI bleed

• Independent correlates of severe bleeding were as
  follows
• Heart rate, gt 100/min
• OR 3.67 (1.78-7.57)
• Systolic blood pressure, lt 115 mm Hg
• OR 3.45 (1.54-7.72)
• Syncope
• OR 2.82 (1.06,7.46)
• Nontender abdominal examination
• OR 2.43 (1.22-4.85)
• Bleeding per rectum during the first 4 hours of
  evaluation
• OR, 2.32 (1.28-4.20)
• Aspirin use
• OR, 2.07 (1.12-3.82)
• More than 2 active comorbid conditions
• OR, 1.93 (1.08-3.44)

Strate LL, Orav EJ, Syngal S. Arch Intern Med.
2003 Apr 14163(7)838-43.
69
So, who can be discharged from the ED?

• Lit search 0 papers, so we are adrift on this
  one

70
Questions?
71
Can you differentiate based on stool color?

• Now, here was a fun trial.
• Subjective reporting of the color of blood passed
  per rectum has been used to predict the location
  of gastrointestinal bleeding
• validity of this clinical approach has never been
  evaluated systematically
• this study determined the spectrum of patient and
  physician descriptors used to characterize the
  color of blood passed per rectum
• evaluated prospectively if an objective test of
  stool color would correlate with or improve upon
  subjective descriptions in predicting bleeding
  locations
• I know you can hardly wait for the results...

72
Stool color continued (hows that breakfast
going?)

• objective test employed was a card containing
  five numbered colors that typify the spectrum of
  stool blood colors
• 120 pts used 23 different descriptors or terms to
  verbalize the color of blood they passed per
  rectum
• in 22 of cases there was a seeming discrepancy
  between their verbalized color and the color they
  pointed to on the test card

73
Stool color results

• Pts pointing to black card resulted in closer
  matching to an upper bleeding source than
  physicians using terminology such as melena or
  tarry stools, p lt0.02
• Pts picking the brightest red colors resulted in
  closer matching to a coloanorectal bleeding
  source than physicians using the terms
  hematochezia or bright red blood per rectum, p
  lt0.02
• PPV of the black card for UGI bleed was very high
  both when patients pointed to this color or when
  it was determined from the available stool (0.95
  and 0.98, respectively)
• PPV of brightest red card for LGI bleed was 100
  when patients picked it than and 0.83 if stool
  was directly compared.
• Anyone want to order cards?

74
Hematochezia vs melena and outcome

• Consecutive patients in Atlanta
• August 1, 1990 - September 31, 1994
• Prospective
• Vital signs and stool color were recorded on
  admission to ED
• Endoscopy was performed in all patients, usually
  within 48 h of admission
• Cause of bleeding determined by endoscopy,
  surgery, or autopsy.

75
Hematochezia results

• 727 pts
• 104 (14) presenting with hematochezia (18 with
  bright red blood and 86 with maroon blood).
• In those with hematochezia most common causes of
  bleeding were duodenal ulcer (44) and gastric
  ulcer (20)
• Hematochezia vs melena patients with
  hematochezia were older (55 vs 50 yr, p lt 0.01)
  and more likely to present with duodenal ulcer
  bleeding (43 vs 25, p lt 0.01)
• No differences in vital signs, including
  prevalence of shock, or admission Hb
  concentration were found b/t hematochezia vs
  melena.

76
Conclusions

• Transfusion requirements
• 5.4 vs 4.0 units, p 0.01
• Need for surgery
• 11.7 vs 5.7, p 0.03
• Mortality
• 13.6 vs 7.5, p 0.05
• All significantly higher in patients with
  hematochezia than in those with melena

Wilcox CM, Alexander LN, Cotsonis G Am J
Gastroenterol. 1997 Feb92(2)231-5