Cicatricial pyloric obstruction caused by gastric and duodenal ulcers occurs due to recurrent ulcers in the pylorus, pyloric canal, or duodenal bulb, leading to scar formation and stenosis. This is often accompanied by pyloric spasm and edema.
Etiology and Pathology
The causes of pyloric obstruction associated with ulcers include spasm, edema, and scarring, which often coexist. When scar formation has not yet caused significant narrowing of the gastric outlet, symptoms may be reversible once localized spasm and inflammatory edema subside. However, severe narrowing caused by scarring eventually requires surgical intervention. In the early stages of pyloric obstruction, gastric peristalsis increases and the gastric wall thickens as it works to overcome the obstruction. In later stages, the tension of the gastric wall weakens, leading to gastric dilation. Vomiting or gastric decompression through a nasogastric tube during obstruction results in loss of gastric contents, and if fluid and electrolytes are not replenished in time, dehydration, electrolyte imbalances, acid-base disturbances, and nutritional deficiencies may ensue.
Clinical Manifestations
Key manifestations include abdominal pain and recurrent vomiting. Patients initially report symptoms such as bloating, intermittent upper abdominal pain, belching, and nausea. As the condition progresses, more prominent abdominal pain and vomiting develop. Vomitus typically consists of undigested food lacking bile, with a foul, sour odor. When dehydration occurs, signs include dry and wrinkled skin, reduced skin elasticity, sunken eyes, decreased urinary output, and dark-colored urine. Visible gastric distention may be observed, and "succussion splash" sounds may be detected on abdominal examination.
Diagnosis and Differential Diagnosis
The diagnosis is often straightforward based on a history of chronic peptic ulcer disease along with classic symptoms and physical findings. A nasogastric tube can generally aspirate large amounts of gastric fluid containing undigested food. However, in some cases, undigested food may obstruct the nasogastric tube, making it difficult to aspirate gastric contents, but this does not preclude the diagnosis.
It is critical to distinguish between edematous and cicatricial pyloric obstruction. Edematous obstruction may resolve after inflammation subsides with standard medical management for peptic ulcers, avoiding the need for surgery. Evaluation involves gastric decompression, gastric lavage using warm hypertonic saline, electrolyte replenishment, maintenance of acid-base balance, and nutritional support, followed by observation of symptom improvement. Additionally, differentiation is needed to exclude obstruction caused by tumors in the stomach, descending duodenum, or pancreatic head. These conditions can be identified using endoscopy, CT, or MRI. If gastrointestinal contrast imaging is performed, water-soluble contrast agents are preferable to barium agents.
Treatment
Treatment begins with conservative measures, including nasogastric decompression to reduce gastric pressure. Gastric lavage with warm hypertonic saline is conducted to alleviate gastric wall edema. Intravenous fluid administration is undertaken to correct acid-base imbalances and support basic nutritional needs. If symptoms persist despite conservative treatment, surgical intervention may be indicated. Preoperatively, efforts focus on alleviating gastric wall edema, correcting water and electrolyte imbalances and anemia, and improving the patient’s overall condition. The aim of surgery is to relieve obstruction and address the underlying cause, with partial gastrectomy being the primary surgical option.