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A hiatal hernia is an abnormal protrusion of the stomach or other abdominal structures through the esophageal hiatus into the thoracic cavity. Normally, the gastroesophageal junction is anchored below the diaphragm by the phrenoesophageal membrane and diaphragmatic crura. These supporting structures weaken with age or increased intra-abdominal pressure from pregnancy, heavy lifting, or coughing, enlarging the hiatus and allowing herniation.

Type I (sliding hernia), the most common, involves upward movement of the gastroesophageal junction. Type II (paraesophageal hernia) occurs when the gastric fundus herniates beside the esophagus. Type III (mixed hernia) combines both features. Type IV (complex hernia) is most severe, involving herniation of additional organs like the colon or small intestine through a large defect.

Herniation disrupts the anti-reflux barrier, which includes the lower esophageal sphincter, crural diaphragm, intra-abdominal esophagus, and angle of His. The hernia lowers sphincter pressure, shortens the intra-abdominal esophagus, and flattens the angle of His, promoting acid reflux. Increased transient relaxations and reduced acid clearance elevate esophageal acid exposure.

Hiatal hernias promote gastroesophageal reflux disease and its complications, including esophagitis, Barrett's esophagus, and esophageal adenocarcinoma. Type II hernias carry additional risks of volvulus and ischemia due to the fundus herniating beside the esophagus. Chronic acid exposure from disrupted anti-reflux mechanisms drives these serious complications.

The phrenoesophageal membrane, diaphragmatic crura, and connective tissues supporting the gastroesophageal junction weaken due to aging and congenital defects like a short esophagus. Sustained increases in intra-abdominal pressure from pregnancy, obesity, coughing, and heavy lifting also contribute to structural weakening and hiatal enlargement.

Type II paraesophageal hernia occurs when the gastric fundus herniates beside the esophagus while the gastroesophageal junction remains in place. This configuration carries a risk of volvulus, where the herniated stomach twists, and ischemia, where blood supply is compromised. Type I sliding hernias, by contrast, involve simple upward movement without these mechanical complications.

Sustained increases in intra-abdominal pressure enlarge the esophageal hiatus by stressing the supporting structures. Activities like heavy lifting, pregnancy, obesity, and chronic coughing generate this pressure. Over time, the phrenoesophageal membrane and diaphragmatic crura weaken and stretch, allowing the gastroesophageal junction and stomach to herniate upward into the thoracic cavity.