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Prevention of Gi
bleedinG in the iCU
Waleed Th.Aletreby
ICU Registrar
King Saud Medical City
Riyadh, KSA
Stress Ulcers
• Also known as Stress Related Mucosal disease.
• Encompasses 2 types:
1. 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.
2.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.
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.
PATHOPHYSIOLOGY
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.
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.
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.
Critical illness
Decrease CO
Hypovolemiacatecholamines
vasoconstriction Proinflammatory
cytokines
Splanchnic hypoperfusion
Dec HCO3
Dec Mucosal
Blood flow
Dec motility
Acid
Back diffusion
Acute Stress Ulcer
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
Risk Factors
• In a landmark, prospective, multicenter cohort
investigation (N=2252),
• 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:
• 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.
Risk factors: Major
• Mechanical ventilation for more than 48 hours.
• Coagulopathy
platelet count of <50,000mm3
INR>1.5
PTT of >2 times the control
• Recent GI ulcers/bleeding Within 12 months.
Risk factors: Minor (2 or more)
• Sepsis or septic shock.
• ICU admission > 1 week.
• Burn >35%
• Head and spinal trauma.
• Multi-organ failure.
• High dose corticosteroids:
 Methylprednisolone ≥ 40 mg/day
 Hydrocortisone ≥ 250 mg/day
Prognosis
• Overt GI bleeding due to stress ulceration is
associated with increased mortality.
So, What to do ?
PREVENTION
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.
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. 2004;49:906-913.
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.
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; 23:313.
• Cook D, et al.Canadian Critical Care Trials Group. Crit Care
Med 1999;27:2812.
• 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.
• 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.
Pharmacological
prevention
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).
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.
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.
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)
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.
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.
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.
Proton pump inhibitors
• PPIs (particularly Omeprazole) delay clearence of:
warfarin, diazepam, phenytoin, digoxin,
theophylline, and carbamazepine.
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.
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. 1999;27:98-103.)
Which agent to choose ?
Comparative studies
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.
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.
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.
Level 2
• Aluminum containing compounds should not be
used in patients on dialysis.
• Prophylaxis should continue during mechanical
ventilation or intensive care unit stay.
Level 3
• Enteral feeding alone may be insufficient stress
ulcer prophylaxis.
• Prophylaxis should continue until able to tolerate
enteral nutrition.
Prevention of GIT bleeding in the icu

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Prevention of GIT bleeding in the 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: 1. 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. 2.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.
  • 3.
  • 4. 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.
  • 6. 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.
  • 9. Critical illness Decrease CO Hypovolemiacatecholamines vasoconstriction Proinflammatory cytokines 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 (N=2252), • 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:
  • 12. • 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.
  • 13. Risk factors: Major • Mechanical ventilation for more than 48 hours. • Coagulopathy platelet count of <50,000mm3 INR>1.5 PTT of >2 times the control • Recent GI ulcers/bleeding Within 12 months.
  • 14. Risk factors: Minor (2 or more) • Sepsis or septic shock. • ICU admission > 1 week. • Burn >35% • 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
  • 17. 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.
  • 18. 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. 2004;49:906-913.
  • 19. 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.
  • 20.
  • 21. 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; 23:313. • Cook D, et al.Canadian Critical Care Trials Group. Crit Care Med 1999;27:2812.
  • 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.
  • 23. • 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.
  • 25. 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.
  • 31. 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.
  • 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. 1999;27:98-103.)
  • 35. Which agent to choose ? Comparative studies
  • 36.
  • 37.
  • 38.
  • 39.
  • 40.
  • 41.
  • 42. 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.