The preceding two chapters address benign diseases of the esophagus, including the diagnosis, evaluation, and management of hiatal hernia, motility disorders, and gastroesophageal reflux disease (GERD). In commenting on these entities, we follow the structure of these chapters.
Hiatal hernia (HH), as common as it is, is truly idiopathic. While HH is rare in Asian and African populations, exact predisposing features are difficult to pin down. In a North American population, GERD is more common among middle-aged males,1 and giant hiatal hernias (often called paraesophageal hernias) are more common among elderly women.2 The predisposing conditions for development of these large hernias in elderly women include diaphragmatic stress during pregnancy (years earlier), loss of abdominal domain, kyphosis (as a result of degenerative spine disease),3,4 and greater longevity than their male counterparts. There may also be collagen ultrastructural defects responsible for hiatal hernia development, but there is insufficient evidence yet to confirm this hypothesis.5–8
The natural history of hiatal hernia may explain the changing symptoms seen in these patients. Early, small “sliding” hiatal hernias (type 1) predispose to GERD by separating the lower esophageal sphincter (LES) from the crural diaphragm, effacing the angle of His, and placing the LES in the thorax where negative intrathoracic pressure contributes to a reduced resting pressure relative to intra-abdominal pressure.9 Over the years, and as the hernia defect grows larger, type 1 hiatal hernia may evolve into type 3 (aka mixed paraesophageal hernia) where the gastric fundus again resumes a position cephalad to the GE junction. This progression will often re-create a GE junction flap valve, and the patients will notice that GERD markedly improves. Replacing the GERD symptoms are symptoms of early satiety, postprandial chest pain, and iron deficiency anemia (in 30%) as a result of visible or occult gastric bleeding by erosions or ulcers at the level of the diaphragm, known as Cameron's ulcers or erosions.10,11 Because of this natural progression, it is understandable why type 2 HH, in which the GE junction remains below the diaphragm, is distinctly rare and probably only occurs when the GE junction is so tightly anchored to the preaortic fascia that the development of a hiatal hernia only results in an attenuation of the phrenoesophageal ligament and cephalad displacement of the gastric fundus. An even rarer event is the parahiatal hernia, where a diaphragmatic defect adjacent to the hiatus allows cephalad migration of the fundus. This is so rare that a true incidence has not been determined, but it presents as a type 2 HH and may be encountered once or twice in an esophageal surgeon's career.
Despite evolving support for the strategy of “watchful waiting” for the asymptomatic hiatal hernia, the incidental detection of a giant HH will warrant questioning about upper GI symptoms. Close questioning reveals that most patients with this defect are either symptomatic or anemic. In either situation, repair is warranted. Far and ...