Sucralfate is a basic nonabsorbable aluminum salt of sucrose octasulfate. Despite weak antacid properties, the protective effect of sucralfate is not mediated by acid suppression or neutralization, but by a mucosal protective effect on the gastric mucosa. The mucosal protection afforded by sucralfate is mediated by several mechanisms, including formation of a protective barrier, stimulation of gastric mucosal blood flow, prostaglandin-mediated increase in mucus and bicarbonate secretion, and by the stimulation of a variety of growth factors that have been implicated in ulcer healing.
Despite this theoretical benefit, the role of sucralfatein the prophylaxis of clinically significant stress-related erosive syndrome hemorrhage is controversial. Although some studies suggest that sucralfate is an effective prophylactic agent with a benign side effect profile that possibly includes a lower incidence of nosocomial pneumonia, in many of the studies reviewed, sucralfate was not statistically superior to the control group in preventing stress-related erosive syndrome hemorrhage.
In a large study by Cook and colleagues (1998), including 1,200 mechanically ventilated patients, sucralfate was inferior to ranitidine in the prevention of upper gastrointestinal bleeding, and there was no significant differences in the rates of ventilator-associated pneumonia between the two agents. Sucralfate (Carafate) is available as tablets or as liquid slurry that is administered 1 g orally or by nasogastric tube every 4 to 6 hours. Although usually well tolerated, constipation occurs in 2 to 4% of patients receiving sucralfate, and aluminum toxicity has occurred in patients with chronic renal failure.
Despite some theoretical advantages of sucralfate, including its ease of use, lack of need for monitoring, lack of need for supplemental antacid therapy, and cost effectiveness, this agent cannot be recommended as the drug of choice in stress-related erosive syndrome because of discordant study results.
Despite the promise demonstrated in earlier trials, synthetic prostaglandin derivatives, such as misoprostol (Cytotec) have not been shown to be effective in the prophylaxis of stress-related erosive syndrome. Synthetic prostaglandin analogues exert a cytoprotective effect at low doses and have been demonstrated to protect the gastric mucosa from a variety of agents. Given the relatively high cost and major side effects associated with their use, it is unlikely that any large scale randomized clinical trial will be performed to investigate the role of prostaglandin analogues in stress-related erosive syndrome hemorrhage; therefore, the use of these agents in the prophylaxis of SERS cannotbe recommended.