The Case against Stress Ulcer Prophylaxis in 2007

Abstract

This feature examines the impact of pharmacologic interventions on the treatment of the critically ill patient — an area of health care that has become increasingly complex. Recent advances in drug therapy (including evolving and controversial data) for adult intensive care unit patients will be reviewed and assessed in terms of clinical, humanistic, and economic outcomes. Direct questions or comments to Zachariah Thomas, PharmD at zachariah.thomas@gmail.com or Sandra Kane-Gill, PharmD, MSc, at kanesl@upmc.edu.

Emergency Management of Curling Ulcers: Exploring Strategies for Timely Diagnosis and Intervention in Critical Care Settings

“…Exponentialrelease of catecholamines and glucocorticoids, central mediators of the stress response, leads to peripheral vasoconstriction and hemodynamic redistribution that compromises the blood perfusion to the gastrointestinal mucosa, generating an environment of hypoxia and ischemia, which results in a decrease of synthesis and release of gastroprotective prostaglandins, responsible for maintaining the integrity of the mucosal barrier, thereby resulting in decreased production of bicarbonate and mucus [3]. Gastrointestinal microcirculation and the mucus layer normally maintain the integrity of the gastric mucosa by providing nourishment, eliminating hydrogen ions, oxygen radicals, and other toxic substances, and increasing bicarbonate secretion to neutralize hydrogen ions [4][5][6]. Ulceration occurs when the mucosal barrier is compromised and can no longer block the detrimental effects of hydrogen ions and oxygen radicals [4].…”

“…Simultaneously, tissue ischemia and hypoxia promote the excessive release of free radicals and reactive oxygen species, which perpetuates oxidative stress and causes direct cellular damage. Cell membrane injury and the activation of the complement system incites a progressive and exacerbated inflammatory response, characterized by the dysregulated release of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukins, which in turn contributes to tissue damage and a mucosal barrier breakdown [6]. The exacerbated inflammatory response also promotes the activation of immune system cells, such as neutrophils, which infiltrate the damaged mucosa and release proteolytic enzymes, such as matrix metalloproteinases (MMPs), that degrade the extracellular matrix and accentuate mucosal damage [1].…”