[2] Apart from the stomach, ulcers may also develop in the proximal duodenum and distal esophagus.
The mechanism of development of Cushing ulcers is thought to be due to direct stimulation of vagal nuclei as a result of increased intracranial pressure.
[3] Efferent fibers of the vagus nerve then release acetylcholine onto gastric parietal cell M3 receptors, causing insertion of hydrogen potassium ATPase vesicles into the apical plasma membrane.
As Cushing ulcers have a higher incidence of developing after shock, sepsis or trauma, diagnosis should include recent medical history evaluation.
[4] Most episodes of Cushing ulceration resolve on medical intervention, consisting primarily of rinsing the area with saline and the administration of antacids.