Stress and the acute gastric mucosal lesion.

Abstract

Gastric erosions which occur in the clinical setting of physical or thermal trauma, shock, sepsis, or head injury have through common usage been called "stress ulcers" (1). While this terminology serves to dramatize the clinical environment in which such lesions occur, it has done little to identify factors which lead to their occurrence. Four important facts have emerged from a wealth of clinical and laboratory investigation of the problem: (1) Only a small number of patients at risk demonstrate clinical evidence of stress erosions, (2) hydrochloric acid is a critical requisite for their formation, (3) disruption of the mucosal barrier (as evidenced by increased back-diffusion of hydrogen ions) is not an essential component of the pathologic process, and (4) disturbance in gastric mucosal perfusion probably plays an important etiologic role. The numerous physiologic and biochemical events which accompany injury have obscured definition of the precise role of stress. It is clear, however, that the occurrence of gastric erosions under the conditions enumerated above is more than a chance association. The following remarks will attempt to sort out those factors which relate to the mechanism of erosion formation, with emphasis on variables which are unique to the stressed subject.