Cushing ulcer, which can form in the stomach, duodenum, or esophagus, is a complication of traumatic brain injuries. It develops very quickly (possibly within hours) following trauma. It is often discussed in the context of stress ulcers [1] and manifestations of stress gastritis (originally called neurogenic gastritis), but it has some characteristics not shared by other stress ulcers. Stress ulcers in general manifest as a number of superficial lesions in the gastric mucosa, whereas Cushing ulcer is usually solitary and deep, and therefore carries a high risk of perforation. Another distinguishing feature of Cushing ulcers is that it is associated with increased levels of gastrin and pepsin [2]. The pathophysiology of the condition is not completely clear but is likely to be due to the effects of elevated intracranial pressure following brain injury [1] with consequent increased gastric acid production due to stimulation of the vagus nerve [3].

The three patients described in the original 1932 paper of Cushing [4] [5] had cerebellar tumors and died after surgery due to perforative peritonitis. They had symptoms of bloating and abdominal sensitivity, or severe abdominal pain, or brown vomit. The occurrence of ulcers in patients with an intracranial disease was observed almost a century earlier by Rokitansky, hence the disease is often referred to as Rokitansky-Cushing ulcer. Presentation with sudden fever, leukocytosis, and volume contraction in the presence of increased intracranial pressure and high-dose corticosteroid administration were suggested as diagnostic clues for perforated stress ulcer by Walsh et al. [6] for aphasic patients. The lesions have about a 17% risk of bleeding [1] [7].

Acute stress gastritis following brain injury has been on the decline since the introduction of prophylaxis using antacids and histamine-2 receptor antagonists [4] [8]. Nevertheless, the condition still occurs for various reasons, one of which is a large number of head injuries due to traffic accidents [1]. Cushing ulcer sometimes develops in spite of ulcer prophylaxis, as in the case of an 8-month old infant with medulloblastoma who became afflicted with the condition once a preoperative dexamethasone treatment was initiated [9].

Perforation of a Cushing ulcer should be anticipated in patients with brain injuries [6].

Upper gastrointestinal endoscopy is the most sensitive technique for the detection of gastric and duodenal ulcers. Endoscopy can also be used to obtain biopsy samples for cytological examination, or for testing for Helicobacter pylori infection. Radiography is useful for the detection of free air in the abdomen, an indication of perforation; however, the absence of free air does not exclude the possibility of perforation [6]. Angiography is used in patients who have massive bleeds. Various laboratory parameters are performed, for example, serum gastrin levels.

Treatment of Cushing ulcers focuses on managing the underlying cause and preventing complications. Proton pump inhibitors (PPIs) or H2-receptor antagonists are commonly used to reduce stomach acid and promote healing. In cases of significant bleeding, endoscopic interventions or surgery may be necessary. Addressing the primary neurological condition is also crucial to prevent further ulcer development.

The prognosis for patients with Cushing ulcers depends on several factors, including the severity of the ulcer, the patient's overall health, and the effectiveness of treatment for the underlying brain injury. With appropriate management, many patients can recover without significant complications. However, severe cases with extensive bleeding may have a more guarded prognosis.

Cushing ulcers are primarily caused by severe physiological stress, particularly in the context of brain injuries. The exact mechanism involves increased intracranial pressure leading to vagal nerve stimulation, which in turn causes increased gastric acid secretion. This excessive acid can damage the stomach lining, resulting in ulcer formation.

Cushing ulcers are relatively rare and are most commonly seen in patients with significant brain injuries. They can occur in individuals of any age but are more frequently observed in adults. The incidence of Cushing ulcers has decreased with the widespread use of prophylactic acid-suppressing medications in at-risk patients.

The pathophysiology of Cushing ulcers involves a complex interplay between neurological and gastrointestinal systems. Increased intracranial pressure from brain injuries stimulates the vagus nerve, leading to excessive gastric acid production. This acid can erode the protective mucosal lining of the stomach, duodenum, or esophagus, resulting in ulcer formation and potential bleeding.

Preventing Cushing ulcers involves managing the underlying brain injury and reducing gastric acid production. Prophylactic use of acid-suppressing medications, such as PPIs or H2-receptor antagonists, is common in patients at high risk. Close monitoring and early intervention in patients with brain injuries can also help prevent the development of these ulcers.

Cushing ulcers are stress-induced gastric lesions associated with brain injuries. They can lead to significant gastrointestinal bleeding and require prompt diagnosis and treatment. Management involves acid suppression and addressing the underlying neurological condition. With appropriate care, many patients can recover without major complications.

For patients and their families, understanding Cushing ulcers can be challenging. These ulcers are a type of stomach injury that can occur when someone has a serious brain injury. They can cause symptoms like vomiting blood or having very dark stools. Doctors use special tests to look inside the stomach and treat the ulcers with medications that reduce stomach acid. It's important to treat both the ulcer and the brain injury to help the patient recover.

1. Alain BB, Wang YJ. Cushing’s ulcer in traumatic brain injury. Chin J Traumatol. 2008;11:114–119.
2. Silen W, Merhav A, Simson JNL. The pathophysiology of stress ulcer disease. World J Surg 1981;5:165–174.
3. Kemp WJ, Bashir A, Dababneh H, Cohen-Gadol AA. Cushing's ulcer: Further reflections. Asian J Neurosurg. 2015 Apr-Jun;10(2):87-94.
4. Wijdicks EF. Cushing's ulcer: the eponym and his own. Neurosurgery. 2011 Jun; 68(6):1695-1698.
5. Cushing H. Peptic ulcer and the interbrain. Surg Gynec Obst. 1932;55:1-34
.
6. Walsh TJ, Raine T, Chamberlin WH, Rice CL. Occult duodenal perforation complicating cerebral infarction: new problems in diagnosis of Cushing's ulcer. Am J Gastroenterol. 1982 Sep;77(9):608-610.
7. Kamada T, Fusamoto H, Kawano S, et al. Gastrointestinal bleeding following head injury: a clinical study of 433 cases. J Trauma. 1977;17(1):44-47.
8. Stollman N, Metz. DC Pathophysiology and prophylaxis of stress ulcer in intensive care unit patients. J Crit Care. 2004;20:35–45.
9. Sivakumar W, Spader HS, Scaife E, Bollo RJ. A case of Cushing ulcer in an 8-month-old patient with medulloblastoma. Transl Pediatr. 2016 Apr;5(2):85-89.