Management of Acute Bleeding from a Peptic Ulcer

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Management of Acute Bleedingfrom a Peptic Ulcer

• N Engl J Med 2008359928-37

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Epidemiology

• The vast majority of acute episodes of UGI
  bleeding (80 to 90) have nonvariceal causes,
  with peptic ulcer accounting for the majority of
  lesions.
• The annual incidence of bleeding from a peptic
  ulcer may be decreasing worldwide ( the incidence
  is 60 per 100,000 population)
• an increasing proportion of episodes related to
  the use of aspirin and NSAID
• Peptic ulcer bleeding is seen predominantly among
  the elderly
• 68 gt 60Y/O and 27 gt80Y/O
• Mortality associated with peptic ulcer bleeding
  remains high at 5 to 10

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Management of Acute Bleeding from a Peptic Ulcer,
According to Clinical Status and Endoscopic
Findings
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The first priority in treatment is
correctingfluid losses and restoring hemodynamic
stability.
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Initial Management

• Assess hemodynamic status
• Tachycardia (pulse, 100 beats per minute)
• Hypotension (systolic blood pressure, lt100 mm
  Hg),
• postural changes (an increase in the pulse of 20
  beats per minute or a drop in systolic blood
  pressure of 20 mm Hg on standing)
• Mucous membranes, neck veins, urine output
• Obtain CBC, electrolytes, BUN/Cr,
• PT INR/ APTT, blood type, and cross-match

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Initial Management

• Initiate resuscitation with crystalloid
  intravenous fluids with the use of large-bore
  IV-access catheters
• two peripheral catheters of 16 to 18 gauge
• a central catheter if peripheral access is not
  available
• PRBC
• If tachycardia or hypotension is present
• If the hemoglobin level is less than 10 g per
  deciliter.
• Oxygen
• correction of coagulopathy

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The insertion of a NG tube

• The presence of red blood in the NG aspirate is
  an adverse prognostic sign
• 15 of patients without bloody or coffee-ground
  material in NG aspirates are found to have
  high-risk lesions on endoscopy
• The use of a large-bore OG tube with gastric
  lavage
• improve visualization of the gastric fundus on
  endoscopy
• not improve the outcome.
• No role for occult-blood testing of aspirate

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Initial Management

• Consider giving a single 250-mg IV dose of
  erythromycin 30 to 60 minutes before endoscopy
• promote gastric motility and substantially
  improve visualization of the gastric mucosa on
  initial endoscopy.
• not improve the diagnostic yield of endoscopy
  substantially or to improve the outcome
• Consider initiating treatment with an IV PPI
  (80-mg bolus dose plus continuous infusion at 8
  mg/hr) while awaiting early endoscopy
• down-staging of endoscopic lesions
• not have an effect on outcomes
• The cost- effectiveness remains controversial
• No role for H2 blocker

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Risk-Stratification Tools for Upper
Gastrointestinal Hemorrhage

• The Rockall score
• Used clinical and endoscopic criteria
• The scale ranges from 0 to 11 points, with higher
  scores indicating higher risk.

Blatchford scores from 0 to 23, with higher
scores indicating higher risk
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Early endoscopy

• The cornerstone of treatment
• performed within 24 hours
• Improve certain outcomes
• the number of units of blood transfused
• the length of the hospital stay
• Determine the cause of bleeding, ascertain
  prognosis, and administer endoscopic therapy.
• Treatment recommendations have focused on the
  first 72 hours after presentation and endoscopic
  evaluation and therapy, since this is the period
  when the risk of rebleeding is greatest (90 )

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Forrest classification
Forrest grade IA
Forrest grade IB
Forrest grade IIA
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High-risk Forrest grade IA, IB, or IIA

• Perform endoscopic hemostasis
• contact thermal therapy
• mechanical therapy ( hemoclips )
• epinephrine injection, followed by contact
  thermal therapy or by injection of a second
  injectable agent.
• Epinephrine injection as definitive hemostasis
  therapy is not recommended
• The endoscopist should use the most familiar
  hemostasis technique

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High-risk Forrest grade IA, IB, or IIA

• Admit the patient to a monitored bed or ICU
  setting(for the first 24 hours of what is usually
  at least a 3-day hospital stay)
• Treat with an IV PPI (80-mg bolus dose plus
  continuous infusion at 8 mg per hour) for 72
  hours after endoscopic hemostasis
• No role for H2 blocker, somatostatin, or
  octreotide.
• Initiate oral intake of clear liquids 6 hours
  after endoscopy in patients with hemodynamic
  stability
• Transition to oral PPI after completion of IV
  therapy.
• Perform testing for Helicobacter pylori initiate
  treatment if the result is positive.

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Effect of Proton-Pump Inhibition in Peptic-Ulcer
Bleeding
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Effect of Proton-Pump Inhibition in Peptic-Ulcer
Bleeding

• Gastric acid impairs clot formation, promotes
  platelet disaggregation, and favors fibrinolysis
• Inhibiting gastric acid and raising the
  intragastric pH to 6 or more and maintaining it
  at that level may promote clot stability, thus
  decreasing the likelihood of rebleeding.
• Although data from clinical trials support the
  use of a bolus followed by a continuous infusion
  of proton-pump inhibitors, recent studies from
  North America show that even a high-dose,
  continuous infusion of proton-pump inhibitors may
  not sustain an intragastric pH of 6 or more.
• The reduction in mortality appears to occur only
  among patients with high-risk stigmata who have
  first undergone endoscopic therapy, a finding
  that supports the use of medical therapy as an
  adjunct to but not a replacement for endoscopic
  hemostasis..
• Intravenous bolus loading followed by continuous
  infusion of proton-pump inhibitors is more
  effective than bolus dosing alone in decreasing
  the rates of rebleeding and the need for surgery

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High-dose oral PPI

• The use of high-dose oral PPI in peptic-ulcer
  bleeding has been shown in Asian populations
  reductions
• the risk of rebleeding
• the need for surgery
• the risk of death
• These results may not be completely generalizable
  to North American or European populations

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Second-look endoscopy

• Planned, second-look endoscopy that is performed
  within 24 hours after initial endoscopic therapy
  has not been recommended.
• It provided only a limited reduction in the rate
  of rebleeding. (Two meta-analyses)
• It may not be cost-effective when medical therapy
  leading to profound acid suppression is used.
• Repeat endoscopy may be considered on a
  case-by-case
• if there are clinical signs of recurrent bleeding
  
• if there is uncertainty regarding the
  effectiveness of hemostasis during the initial
  treatment.

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Forrest classification
Forrest grade IIB
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High-risk Forrest grade IIB

• Consider endoscopic removal of adherent clot,
  followed by endoscopic hemostasis if underlying
  active bleeding or nonbleeding visible vessel is
  present.
• Admit the patient to a monitored bed or ICU
  setting.
• Treat with IV PPI (80-mg bolus dose plus
  continuous infusion at 8 mg per hour) for 72
  hours after endoscopy, regardless of whether
  endoscopic hemostasis was performed
• No role for H2 blocker, somatostatin, or
  octreotide
• Initiate oral intake of clear liquids 6 hours
  after endoscopy in patients with hemodynamic
  stability
• Transition to an oral PPI after completion of IV
  therapy.
• Perform testing for H. pylori initiate treatment
  if the result is positive.

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Forrest classification
Forrest grade IIC
Forrest grade III
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Low-risk Forrest grade IIC or III

• Do not perform endoscopic hemostasis.
• Consider early hospital discharge after endoscopy
  if the patient has an otherwise low clinical risk
  and safe home environment.
• Treat with an oral PPI.
• Initiate oral intake with a regular diet 6 hours
  after endoscopy in patients with hemodynamic
  stability.
• Perform testing for H. pylori initiate treatment
  if the result is positive.

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Predictors of failure of endoscopic treatment

• History of peptic ulcer disease
• Previous ulcer bleeding
• The presence of shock at presentation
• Active bleeding during endoscopy
• Large ulcers (gt2 cm in diameter)
• Large bleeding vessel (2 mm in diameter)
• Ulcers located on the lesser curve of the stomach
  or on the posterior or superior duodenal bulb

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After endoscopy

• If there is clinical evidence of ulcer
  rebleeding, repeat endoscopy with an attempt at
  endoscopic hemostasis,obtain surgical or
  interventional radiologic consultation for
  selected patients.
• For selected patients, discuss the need for
  ongoing use of NSAIDs, antiplatelet agents, and
  concomitant therapy with a gastroprotective agent.

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Thanks a lot!