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Title: Prevention of GI bleeding in ICU


1
Prevention of GI bleeding in the ICU
  • Waleed Th.Aletreby
  • ICU Registrar
  • King Saud Medical City
  • Riyadh, KSA

2
Stress Ulcers
  • Also known as Stress Related Mucosal disease.
  • Encompasses 2 types
  • Stress related injury, which is diffuse,
    superficial mucosal damage, that cause oozing of
    blood from superficial capillary beds. In the
    fundus and body of stomach, antrum, duodenum, or
    distal esophagus.
  • Discrete stress ulcers, which are deep focal
    lesions that penetrate the submucosa, most often
    in the body and fundal parts of the stomach. And
    cause massive hemorrhage or rarely perforation.

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Epidemiology
  • Within 24 hrs of ICU admission, 75 to 100 of
    critically ill patients have some endoscopic
    evidence of gastroduodenal lesions.
  • Overt GI bleeding range from 1.5 to 8.5 among
    all ICU patients.
  • And as high as 15 among patients who do not
    receive stress ulcer prophylaxis.
  • Clinically significant bleeding (hemodynamic
    compromise, need for blood transfusion, need for
    surgery) occurs in approximately 2 to 6 of ICU
    patients.

5
Pathophysiology
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Normally
  • The integrity of the gastric mucosa is maintained
    by the microcirculation and the mucus layer.
  • which nourishes the mucosa and eliminates
    hydrogen ions, oxygen radicals, and other
    potentially toxic substances.
  • The mucus layer protects the epithelial mucosal
    surface from hydrogen ions (including acid) and
    other potentially harmful substances.
  • It traps bicarbonate ions secreted by the mucosa
    to neutralize hydrogen ions.

7
Normally
  • At normal levels, nitric oxide synthase enhances
    gastric mucosal integrity by maintaining blood
    flow and perfusion in the gastric mucosa.
  • The buffering effect of bicarbonate and the mucus
    layer keep pH neutral even though the pH in the
    gastric lumen is often between 1.5 and 2.0.

8
In critically ill patients
  • The major factors of SRMD recognized include
    reduced blood flow, mucosal ischemia,
    hypoperfusion, and reperfusion injury.
  • Gastric hypoperfusion causes the release of
    nitric oxide, production of oxygen radicals, and
    reduction of prostaglandin synthesis.
  • Additionally, upper GIT motility is slowed,
    leading to prolonged exposure of the poorly
    defended mucosa to gastric acid.

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Critical illness
Hypovolemia
catecholamines
Decrease CO
Proinflammatory cytokines
vasoconstriction
Splanchnic hypoperfusion
Dec HCO3
Dec Mucosal Blood flow
Dec motility
Acid Back diffusion
Acute Stress Ulcer
10
Risk Factors
  • Deborah J. Cook
  • Professor, Department of Medicine,
  • Clinical Epidemiology Biostatistics
  • Joint Member, Dept of Clinical Epidemiology
    Biostatistics
  • Academic Chair, Critical Care Medicine, McMaster
    University
  • Co-Chair, Critical Research Interest Group

11
Risk Factors
  • In a landmark, prospective, multicenter cohort
    investigation (N2252),
  • Cook et al. studied the risk factors for stress
    ulceration in the ICU and the incidence of
    clinically important GIT bleeding.
  • Clinically important bleeding was defined as
    overt bleeding complicated by one of the
    following within 24 hours after the onset of
    bleeding

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  • Spontaneous decrease in SBP of 20 mm Hg or more.
  • Increase in heart rate more than 20 beats per
    minute.
  • Decrease in SBP more than 10 mm Hg on sitting up.
  • Decrease in hemoglobin level more than 2 g/dL and
    subsequent transfusion of blood after which
    hemoglobin levels do not increase by a value
    defined as the number of units transfused minus 2.

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Risk factors Major
  • Mechanical ventilation for more than 48 hours.
  • Coagulopathy
  • platelet count of lt50,000mm3
  • INRgt1.5
  • PTT of gt2 times the control
  • Recent GI ulcers/bleeding Within 12 months.

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Risk factors Minor (2 or more)
  • Sepsis or septic shock.
  • ICU admission gt 1 week.
  • Burn gt35
  • Head and spinal trauma.
  • Multi-organ failure.
  • High dose corticosteroids
  • Methylprednisolone 40 mg/day
  • Hydrocortisone 250 mg/day

15
Prognosis
  • Overt GI bleeding due to stress ulceration is
    associated with increased mortality.

16
So, What to do ?
  • PREVENTION

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Non Pharmacological
  • High risk patients should be aggressively
    monitored and treated.
  • Frequently assessed for signs of
    hypoperfusion(blood pressure, skin color and
    warmth, and mental status).
  • Laboratory investigations (hemoglobin, hematocrit
    ,WBC, and serum electrolyte levels).
  • Local irritants (NSAID or aspirin) should be
    avoided.
  • Restrict the use of vasopressors when possible
    because they worsen ischemia of the GIT.

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Non Pharmacological
  • Peripheral oxygen saturation levels are not an
    indication of gastromucosal perfusion.
  • In one study, critically ill patients with sepsis
    who required mechanical ventilation had
    approximately 50 less blood flow in the upper
    GIT than controls. Both groups, however, had
    normal peripheral oxygen saturation.
  • Spirt MJ, Guth PH, Randall G, Leung FW.
    Gastroduodenal perfusion and mortality in
    mechanical ventilation-dependent patients with
    systemic inflammatory response syndrome. Dig Dis
    Sci. 200449906-913.

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Non Pharmacological
  • Gastric tonometry the measurement of the carbon
    dioxide level inside the stomach in order to
    assess the degree of blood flow to the stomach
    and bowel.

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Enteral nutrition
  • Enteral feedings initiated within 12 hours of
    trauma were as effective as H2RA.
  • The risk of clinically important gastric bleeding
    was reduced in patients receiving enteral
    feedings.
  • Raff T, et al.Burns 1997 23313.
  • Cook D, et al.Canadian Critical Care Trials
    Group. Crit Care Med 1999272812.

22
  • Surgical Critical Care and Medical Critical Care
    Services at Orlando Regional Medical Center
    recommend considering discontinuing prophylaxis
    therapy in all patients when full enteral feeding
    is tolerated except for mechanically ventilated
    patients.
  • A meta-analysis published in 2010 included 17
    randomized, controlled trials that enrolled a
    total of 1836 patients (Marik P et al), showed
    that Stress ulcer prophylaxis did not decrease
    the risk for GI bleeding in the patients that
    were fed enterally.

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  • The gastroprotective effect of enteral feedings
    is an area of continued debate.
  • Overall, studies in which the effects of enteral
    nutrition on gastric bleeding risk were evaluated
    have had numerous shortcomings.
  • Including inadequate statistical power,
    concurrent use of pharmacological prophylaxis,
    lack of a consistent enteral nutrition regimen,
    and variable definitions of bleeding.

24
Pharmacological prevention
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1) Histamine2 Receptor Agonists
  • Act by decreasing gastric acid secretion through
    reversible, competitive inhibition of histamine
    stimulated acid secretion and are effective in
    reducing basal acid production.
  • cimetidine, ranitidine , famotidine , nizatidine.
  • Significantly lower rates of clinically important
    GIT bleeding among patients who received
    ranitidine than among patients who received
    sucralfate (cook et al 1998).

26
Histamine2 Receptor Agonists
  • They can be given orally, via NGT, or
    intravenously, and well tolerated.
  • Continuous IV infusion is more effective than
    bolus IV at controlling gastric pH, but not in
    preventingclinically significant GI bleeding.
  • Incidence of thrombocytopenia is rare.
  • Ranitidine 50mg IV Q8h, 150mg PO Q12h.

27
Histamine2 Receptor Agonists
  • Gastrin and acetylcholine provide alternative
    pathways to the stimulation of acid secretion,
    acid suppression with H2RA is incomplete.
  • Dosing can be difficult because of the nonlinear
    kinetics and short duration of action.
  • Tolerance develops with H2RA as early as 72 hours
    after administration.
  • Decrease clearance of warfarin, theophylline,
    phenytoin, lidocaine, and clarithromycin (mainly
    cimetidine). Ranitidine interactions, though less
    frequent, can occur with nifedipine and
    cyclosporine.

28
2) Sucralfate
  • Sucralfate is a sulfated polysaccharide complexed
    with aluminum hydroxide .
  • It exerts its effects by coating and protecting
    the gastric mucosa, without altering gastric acid
    secretion or significantly buffering acid.
  • Administered orally or via NGT at a dose of 1
    gram four times per day.
  • H2RA and sucralfate have comparable effectiveness
    for preventing stress ulcers, at 10-25 and at
    15-40, respectively (Darlong V 2003, Kantorova
    I 2004)

29
Sucralfate
  • Since it does not inhibit or neutralize gastric
    acid, it does not favor growth of gram-negative
    organisms in stomach or increase risk of
    nosocomial pneumonia.

30
Sucralfate
  • Sucralfate decreases the absorption of
    ciprofloxacin, norfloxacin, theophylline,
    tetracycline, phenytoin, cimetidine, ranitidine,
    l-thyroxine, ketoconazole, and digoxin.
  • Use of sucralfate should be avoided in patients
    with compromised renal function to avoid aluminum
    accumulation and poisoning.

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3) Proton pump inhibitors
  • Block acid secretion by irreversibly binding to
    and inhibiting the hydrogen-potassium ATPase pump
    that resides on the luminal surface of the
    parietal cell membrane.
  • omeprazole , lansoprazole , rabeprazole ,
    pantoprazole , esomeprazole.
  • They can be given orally, via NGT, or
    intravenously.
  • Rapid onset of action, linear kinetics, longer
    duration of action, and lack of observed
    tolerance.
  • Not renally eliminated.
  • Omeprazole 40 mg/24 hrs orally, or NGT.

32
Proton pump inhibitors
  • PPIs (particularly Omeprazole) delay clearence
    of warfarin, diazepam, phenytoin, digoxin,
    theophylline, and carbamazepine.

33
4) Antacids
  • Antacids neutralize gastric acid and protect the
    gastric mucosa.
  • Administered every one to two hours at a dose of
    30 to 60 mL either orally or via nasogastric
    tube.
  • Side effects include hypermagnesemia,
    hypercalcemia, hypophosphatemia, constipation,
    and diarrhea.
  • Level 1 recommendation that antacids should not
    be used as stress ulcer prophylaxis.
  • diarrhea, flatulence, headache, nausea, hepatic
    dysfunction, electrolyte abnormalities,
    constipation, and altered drug absorption.

34
5) Prostanoids
  • Misoprostol , inhibit gastric acid secretion by
    selectively reducing the ability of the parietal
    cell to generate cyclic AMP in response to
    histamine.
  • Exert a cytoprotective effect by enhancing
    mucosal defense mechanisms.
  • Rarely used in ICU due to the lack of data
    regarding their impact on clinically important
    outcomes.
  • Found ineffective in stress ulcer prophylaxis by
    some authors (Lam NP, National survey of stress
    ulcer prophylaxis.Crit Care Med. 19992798-103.)

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Which agent to choose ?
  • Comparative studies

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Which agent to choose ?
  • Agents that reduce the frequency of overt GI
    bleeding in ICU patients most effectively (H2
    blockers and PPIs) might be associated with more
    frequent nosocomial pneumonia.
  • In contrast, a less effective prophylactic agent
    ( sucralfate ) may be associated with fewer
    nosocomial pneumonias.
  • Thus, clinicians need to consider whether
    prevention of overt GI bleeding or minimizing the
    incidence of nosocomial pneumonia is of greater
    clinical importance.

43
Which agent to choose ?
  • Cost Choosing less expensive prophylactic
    agents or administering prophylaxis only to
    patients who are at high risk for stress
    ulceration can diminish the cost of stress ulcer
    prophylaxis.

44
Level 1
  • Prophylaxis is recommended for all high risk
    patients.
  • There is no difference between H2 antagonists,
    cytoprotective agents, and some proton pump
    inhibitors.
  • No recommendation regarding duration of
    prophylaxis.

45
Level 2
  • Aluminum containing compounds should not be used
    in patients on dialysis.
  • Prophylaxis should continue during mechanical
    ventilation or intensive care unit stay.

46
Level 3
  • Enteral feeding alone may be insufficient stress
    ulcer prophylaxis.
  • Prophylaxis should continue until able to
    tolerate enteral nutrition.

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