Stress ulcer evidence
and management of stress ulcers in the ICU
of overt and clinically important bleeding in ICU patients can be achieved
with H2 receptor antagonists
who are not mechanically ventilated, are not coagulopathic, are enterally
fed and have no major organ failure may not require prophylaxis
are currently reserved for treatment of bleeding or prevention of rebleeding
erosions, which may sometimes extend deeper into the submucosa, of the upper
gastrointestinal tract. Usually multiple.
found in the fundus or acid secreting parts of the stomach.
experimentally with different types of stress
The upper GIT is a digestive organ. In particular, H+ ions
play a central role in the digestion of proteins, both by a direct action and by
facilitating the role of Pepsin. H+ ions are secreted by parietal
cells in the gastric mucosa as a result of stimulation of acetylcholine, gastrin
and histamine receptors (Fig 1). Autodigestion is prevented by a series of
defense mechanisms. These include the production of a mucous gel layer by mucous
secreting cells in the gastric mucosa, secretion of bicarbonate ions into the
gel and maintenance of an “unstirred” relatively pH neutral layer of
protection for gastric mucosal cells. Mucosal cells are rapidly replaced in the
crypts by proliferation and migrate to damaged surfaces by the process of
restitution. Prostaglandins play an important role in maintaining these
defenses. Good regional blood supply and perfusion is needed to support the
intense metabolic activity required to maintain these processes.
studies demonstrate that the severity of stress ulceration is associated with
the degree of stress induced decrease in gastric blood flow. Prevention of
decreases in gastric blood flow with agents such as NO donors can protect
experimental animals from stress ulceration.
of gastric acid and mucosal injury
reduce & treat stress ulceration
Based on pathophysiology, the following preventive measures
and treatments are used clinically.
of haemodynamic stability
and/or regional stability of perfusion pressure and flow.
sedation, analgesia, communication
preventive medical therapies decrease morbidity and mortality from stress
are the best medical preventive therapies?
every ICU patient require preventive therapy?
of stress ulceration is low and decreasing with time and routinely using
prophylaxis in all patients is probably not cost effective.
mortality from stress ulcer bleeding is probably very low (< 0.1%)
patients need stress ulcer prophylaxis?
bleeding stress ulcer
acid suppression and rebleeding
pH >6 for at least 3 to 4 days in patients with acute GI bleed.
At this pH the effects of acid on platelet function and clot digestion are
pump inhibitors (eg omeprazole) reduce recurrence
of acute bleeding in high risk ulcers and re-bleeding rate following
successful endoscopically treated ulcers. However no mortality
advantage. A similar strategy is probably useful for stress ulcers
of PPIs is short and proton pumps are continuously being synthesized
the actively secreting pumps with a bolus dose
prevent pH lowering by newly synthesized pumps with a continuous
of omeprazole or pantoprazole is 80 mg intravenous bolus followed by
continuous infusion of 8 mg/h
receptor antagonists are unable to consistently achieve gastric pH >6 and
tachyphylaxis occurs after 24 h. There is no good evidence that they
decrease the rebleeding rate.
©Gavin Joynt, September 2003