Pyloric Obstruction

Pyloric obstruction, also referred to as gastric outlet obstruction, is a condition characterized by narrowing or blockage at the pylorus—the muscular valve regulating the flow of stomach contents into the duodenum. When this passage becomes impaired, the stomach cannot effectively empty its contents into the small intestine. This disruption leads to a range of gastrointestinal symptoms, including early satiety, bloating, epigastric pain, postprandial nausea, persistent vomiting, and unintentional weight loss.

Etiology

The causes of pyloric obstruction are broadly classified as non-cancerous or cancerous.

Non-cancerous causes include:

• Chronic peptic ulcer disease, where inflammation and scarring gradually narrow the pyloric canal.
• Gastric bezoars, which are compact masses of undigested material that can block the outlet.
• Crohn’s disease and eosinophilic gastroenteritis which can thicken the stomach wall and constrict the passage.
• Postsurgical scarring and caustic ingestion may also cause non-cancerous obstruction.

Cancerous causes include:

• Gastric or duodenal carcinoma can directly invade or compress the pylorus.
• Extrinsic compression from cancers such as pancreatic adenocarcinoma, which can press on the gastric outlet without direct invasion.

Pathophysiology

Pathophysiologically, impaired gastric emptying leads to the retention of ingested material, which progressively distends the stomach. Initially, individuals may better tolerate liquids than solids, but as the obstruction worsens, even fluids may become poorly tolerated. Vomiting becomes frequent and may involve undigested food from previous meals. Over time, the stomach may lose its ability to contract, further exacerbating the stasis.

Complications include dehydration and electrolyte imbalances, such as hypochloremic and hypokalemic metabolic alkalosis, resulting from repeated vomiting. Chronic obstruction can also lead to malnutrition, especially in patients with concurrent malignancy.

Additionally, prolonged retention of gastric contents raises the risk of aspiration pneumonia, particularly in individuals with compromised airway protection. Timely identification of the underlying cause is critical for effective treatment, as management varies significantly between structural and functional etiologies.