In patients admitted to hospital because of UGI hemorrhage the prognosis depends on age, underlying diseases, hemodynamic status, and the persistence or recurrence of bleeding. The causes of bleeding were not relevant to the prognosis.

We tested a variety of antioxidants as possible therapeutic agents in an acute CCl4 mouse model of hepatotoxicity. Liver damage, gauged by the amount of serum aminotransferase released into the blood, morphological changes, lethal dose response, and presence of thiobarbituric acid-reactive substances (TBARS), were significantly inhibited in a dose-dependent manner by liposomes containing vitamin E (LVE) or by Rocavit E, a water-soluble emulsion of alpha-tocopherol. Serum aminotransferase levels in LVE- or Rocavit E-treated animals were always > 10-fold lower than levels in corresponding CCl4 controls. Other liposome-associated antioxidants, butylated hydroxytoluene, vitamin E succinate, catalase, desferoxamine, superoxide dismutase, and ascorbic acid 6-palmitate, were also able to elicit a decrease in damage; however, they were substantially less effective. Intravenous therapy with LVE decreased mortality by nearly 90% when a lethal dose of CCl4 was given. When the biodistribution of the liposomes was examined, it was determined that the vast majority were localized in the Kupffer cell population. This approach of delivering nontoxic therapeutic agents selectively to the liver offers a variety of clinical applications in humans.

Secondary hemorrhage is associated with an increased mortality, which is related to the underlying diseases and not to a difference in the causes of bleeding.

Age > or = 80 years is an independent determinant of esophagitis, a major cause of UGI bleeding in the elderly.

This paper describes a rare complication of enteral feeding, esophageal obstruction due to feeding formula bezoar, and reviews the published cases. An attempt to re-insert the nasogastric tube in a chronically ventilated 80-year-old female fed via a nasogastric tube with Jevity(®) failed. An esophagogastroduodenoscopy revealed an 18 cm-long concretion of the feeding formula, filling most of the esophageal lumen, which was removed endoscopically. Forty-two cases of feeding formula esophageal bezoars have been reported in the literature. The formation of feeding formula bezoars is triggered by acidic gastroesophageal reflux. The acidic pH in the esophagus causes clotting of the casein in the formula. Predisposing factors for bezoar formation are: mechanical ventilation, supine position, neurological diseases, diabetes mellitus, hypothyroidism, obesity and history of partial gastrectomy. Diagnosis and removal of the bezoar is done endoscopically. Feeding in a semi-recumbent position, administration of prokinetic agents and proton pump inhibitors may prevent this complication.