paraesophageal hernia

Hiatal hernias are classified into four types. Type I (sliding, ~95%) involves upward displacement of the gastroesophageal (GE) junction and cardia through the esophageal hiatus. Types II–IV are 'true' paraesophageal hernias: Type II is a pure paraesophageal hernia where the GE junction stays fixed below the diaphragm but the gastric fundus herniates next to the esophagus; Type III is a combined sliding and paraesophageal hernia (most common of the true PEHs) where both the GE junction and fundus herniate; Type IV involves herniation of the stomach plus another organ (colon, spleen, small bowel) into the chest.

Pathophysiology involves widening of the diaphragmatic hiatus and laxity of the phrenoesophageal ligament, allowing the stomach to migrate into the mediastinum. Risk factors include obesity, advancing age, chronic increased intra-abdominal pressure, and prior esophageal surgery.

Clinical presentation varies from asymptomatic (often incidental finding on imaging) to symptoms such as postprandial chest pain, dysphagia, early satiety, GERD symptoms, or chronic occult GI bleeding from a Cameron lesion (linear gastric erosions at the diaphragmatic hiatus) leading to iron deficiency anemia. A key complication is gastric volvulus, which can present emergently with Borchardt's triad: severe epigastric pain, retching without ability to vomit, and inability to pass a nasogastric tube—a surgical emergency due to risk of strangulation and perforation.

Diagnosis is via upper GI barium swallow (classic finding: retrocardiac air-fluid level or 'stomach in the chest'), CT scan, or upper endoscopy.

Management: Type I hernias are typically managed conservatively unless refractory GERD symptoms occur. Types II–IV, given the risk of strangulation/volvulus, generally warrant surgical repair (often elective, but urgent in symptomatic or complicated cases) via laparoscopic reduction of the hernia, excision of the hernia sac, crural repair, and often fundoplication.