Burn injury results in decreased gastric acid production in the acute shock period.

Gastrointestinal complications including acute stress ulcerations occur after burn injury. The causes of acute gastric derangements are multiple, and tissue ischemia in the acute period of burn shock may promote breakdown of the gastric mucosal protective barrier. We compared gastric pH in mice after 25% total body surface area, full-thickness murine burn injury with that in unburned control animals. Animals were anesthetized with methoxyflurane and were resuscitated with 1 ml normal saline solution immediately after burn. Animals were killed at intervals up to 24 hours after burn injury, stomachs were removed and opened, and gastric mucosal pH was measured by use of a surface pH probe. In other animals mixed venous blood was obtained via direct inferior vena cava puncture, and blood gas analysis was performed at intervals up to 24 hours after burn injury. Unexpectedly, gastric mucosal pH increased in burned mice compared with that in controls. The peak difference, greater than one log pH unit, occurred at 3 hours after burn injury (pH 4.45 burn vs pH 3.34 control, p < 0.00001), and this difference was maintained through 12 hours (pH 4.88 burn vs pH 3.20 control, p < 0.005). In this model, shock was observed to begin as early as 1 hour after burn injury and reached its maximal period (base deficit, -27.8 mEq/L) at 12 hours after burn injury. In view of the higher gastric pH in burned mice with concomitant profound shock, gastric acid production appears to be impaired during this time, which suggests acute postburn gastrointestinal ulcerations may be primarily due to ischemia. Prevention of organ ischemia may play a key role in the prevention of acute gastric ulcerations after burn injury.