Stress Gastritis: Stress Ulceration, Stress Erosive Gastritis

What is Stress Gastritis?

Stress gastritis is also known as stress ulceration, stress erosive gastritis, or hemorrhagic gastritis. It is characterized by multiple small superficial erosions which are non-ulcerating in nature. Stress gastritis usually begins in the acid-secreting part, which is the proximal part of the stomach. The presence of luminal acid makes it a prerequisite for the development of stress

ulcers. The Proximal part has a maximum concentration of parietal cells. These parietal cells secrete acid and then progress distally. Stress gastritis occurs in patients after physical trauma, shock, sepsis, hemorrhagic failure, or respiratory failure. These patients with stress ulcers can develop life-threatening gastric bleeding.

Cushing and Curling Ulcer

The Cushing ulcer is seen in patients with head injuries. Head injury increases intracranial pressure, which leads to vagal nerve stimulation and results in increased acid secretion.

Stress gastritis related to Cushing ulcer is due to increased acid secretion.

Curling ulcer is seen in patients after thermal burns. Burns lead to hypovolemia and ischemia. As a result, there is decreased production of defense factor or deficiency of defense factor. This can cause stress and gastritis. However, all patients with thermal burn injuries do not develop a curling ulcer. Patients in whom more than 30% of body surface area is involved in the burn develop a curling ulcer.

Stress gastritis lesions change with time. Early lesions of stress gastritis have multiple shallow discrete areas of erythema with focal hemorrhage or an adherent clot. Whereas in late lesions, there is the presence of regenerating mucosa around healing gastric ulcer.

Pathophysiology

Stress gastritis has multifactorial causes. It is mainly due to an imbalance between acid production and mucosal protection. In stress gastritis, there is an impaired mucosal protection

defense mechanism against luminal acid. This can be a result of a reduction in blood flow, reduction of mucus, decreased production of bi-carbonate secretion, or decreased endogenous Prostaglandins. Stress is considered when a patient has hypoxia, sepsis, or organ failure.

Mucosal ischemia due to stress is the main factor responsible for the breakdown of the mucosal defense mechanism, and the presence of luminal acid is a prerequisite for stress gastritis to evolve. Both these factors lead to stress gastritis.

Clinical Features

• Stress gastritis develops within 1-2 days after traumatic events in more than 50-75% of patients.
• Sometimes, the only clinical sign of stress gastritis is painless upper GI bleeding. In most patients there is slow and intermittent bleeding. But occasionally, there is profound upper

GI hemorrhage that leads to hematemesis and hypotension.

Diagnosis

Endoscopy is performed as the first investigation in patients with upper GI bleeding to confirm the diagnosis of stress gastritis and to differentiate stress gastritis from other sources of GI hemorrhage.

Prophylaxis

Prophylaxis for stress gastritis is usually not required in all patients. Only high-risk patients should be treated prophylactically. The two strongest risk factors for developing significant

bleeding from stress ulcers are coagulopathy and respiratory failure requiring prolonged mechanical ventilation requiring 48 hours. Apart from coagulopathy and respiratory failure, the other significant risk factors for GI bleeding are the history of peptic ulcer disease or GI bleeding in the past year, head, or CNS injury, burn injury, or sepsis. 

Enteral nutrition reduces the risk of stress ulcer formation. It should be initiated as soon as possible in the patients. The Prophylaxis drug indicated for stress ulcers is PPI rather than the H2 receptor and sucralfate. Prophylaxis should be limited to high-risk patients only because using PPI suppresses gastric acid secretion. Gastric acid suppression is associated with an increased risk of nosocomial pneumonia and Clostridium difficile infection.

Treatment

In patients with significant upper GI bleeding, treatment is started with fluid resuscitation followed by correction of any coagulation or platelet abnormalities. Then, a nasogastric tube is inserted. Intravenous PPI therapy is given to all patients, and urgent endoscopy is performed for both diagnosis as well as treatment.

Vasopressin is administered in the left gastric artery. Precautions should be taken while administering vasopressin. It should not be used in cardiac and liver disease patients as vasopressin causes intense vasoconstriction.

Surgery

Surgery in stress gastritis is indicated for hemodynamically unstable patients with uncontrollable GI bleeding and patients requiring persistent transfusion. Long anterior gastrotomy is performed as the stress ulcer is located in the proximal part of the stomach or fundus. After surgery, bleeding areas were stitched with a figure of 8 stitches and taken deep within the gastric walls.

However, most of the superficial lesions are not actively bleeding. Hence, do not require ligation unless a blood vessel is visible.

In stable patients, surgery is completed by closing the anterior gastrotomy with truncal vagotomy pyloroplasty to reduce acid secretion. Alternative surgery performed in such patients is partial gastrectomy with vagotomy. Whereas total gastrectomy is performed rarely in patients who are at risk of developing life-threatening hemorrhage and refractory to other forms of treatment.

Also read: Super Speciality in Surgical Gastroenterology

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