Stress Ulcer Prophylaxis

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Stress ulcer is a broad spectrum of the pathologic condition of the acute, erosive, inflammatory change on the upper gastrointestinal tract (UGIT) which is associated with critical illness. Stress ulcer is also called stress-related mucosal damage (SRMD) Stress ulcer can cause profound upper gastrointestinal bleeding (UGIB) which result in death, thus now stress ulcer prophylaxis (SUP) become the standard care in the intensive care unit (ICU). The author tried to retrace the historical concept regarding stress ulcer.At 1842, Curling reported 8 patients who died from UGIB during hospital stay ranged from few days to nearly one month. They initially admitted with a major burn. Upper GI tract ulceration (especially in the duodenum) was found at postmortem examination. At 1867, Billroth reported a fatal peptic hemorrhage after a thyroid operation. Till, 1950, similar autopsy reports were followed continuously.

At 1950, Hans Selye used the term “stress ulcer” at first and this term became popular. Although the cause of a stress ulcer was not clear, the association between adrenocortical axis adaptation against stress and UGIT ulcer was suggested by H.Selye. At 1966, Fogelman reported 88 cases with stress ulcer, and the mortality was 58% (51/88) [surgery (n = 30), mortality 53%, trauma (n = 20), mortality 45%, and miscellaneous (n = 38), mortality 68%)]. Until then, the surgical approach was regarded as the primary treatment considering that most stress ulcers were single site ulcers.At 1969, Skillman collected the data of 150 consecutive ICU patients, wherein 8 patients (5.3%) experienced the massive hemorrhage because of the acute multiple gastric ulcers. In addition, gastric secretory studies indicated that increased acid secretion may be an important cause for the stress ulcer evolution. Followed studies also showed the similar results with excessive gastrin stimulation of parietal cells.

At 1978, Hastings and Skillman performed a randomized controlled trial (RCT) whether neutralization of gastric acid by the use of H2 receptor blocker or antacid drugs prevent stress ulcer or not. Significant UGIB was 4% (2/51) among the intervention group while it was 25% (12/49) among the control group.However, because gastric acidity is a defensive mechanism to pathogenic organisms, acid-suppressive treatment may be associated with increased pathologic colonization in the UGIT. This implies the increased chance for the nosocomial infection. Especially, hospital-acquired pneumonia (HAP) and C.difficile infection have become the major concerns. Gastric acid is an important defense against the acquisition of C.difficile spores. Herzig reported that acid-suppressive medication is associated with HAP occurrence [4.9% in 32,922 acid-suppression group vs. 2.0% in 30,956 no acid–suppression group, propensity-matched odd ratio.