eMedicine Specialties > Gastroenterology > Esophagus

Hiatal Hernia

Author: Waqar A Qureshi, MD, Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Aug 24, 2009

Introduction

Background

A hiatal hernia occurs when a portion of the stomach prolapses through the diaphragmatic esophageal hiatus. Although the existence of hiatal hernia has been described in earlier medical literature, it has come under scrutiny only in the last century or so because of its association with gastroesophageal reflux disease (GERD) and its complications. There is also an association between obesity and the presence of hiatal hernia. By far, most hiatal hernias are asymptomatic and are discovered incidentally. On rare occasion, a life-threatening complication, such as gastric volvulus or strangulation, may present acutely.

Pathophysiology

The esophagus passes through the diaphragmatic hiatus in the crural part of the diaphragm to reach the stomach. The diaphragmatic hiatus itself is approximately 2 cm in length and chiefly consists of musculotendinous slips of the right and left diaphragmatic crura arising from either side of the spine and passing around the esophagus before inserting into the central tendon of the diaphragm. The size of the hiatus is not fixed, but narrows whenever intra-abdominal pressure rises, such as when lifting weights or coughing.

The lower esophageal sphincter (LES) is an area of smooth muscle approximately 2.5-4.5 cm in length. The upper part of the sphincter normally lies within the diaphragmatic hiatus, while the lower section normally is intra-abdominal. At this level, the visceral peritoneum and the phrenoesophageal ligament cover the esophagus. The phrenoesophageal ligament is a fibrous layer of connective tissue arising from the crura, and it maintains the LES within the abdominal cavity. The A-ring is an indentation sometimes seen on barium studies, and it marks the upper part of the LES. Just below this is a slightly dilated part of the esophagus, forming the vestibule. A second ring, the B-ring, may be seen just distal to the vestibule, and it approximates the Z-line or squamocolumnar junction. The presence of a B-ring confirms the diagnosis of a hiatal hernia. Occasionally, the B-ring also is called the Schatzki ring.

Any sudden increase in intra-abdominal pressure also acts on the portion of the LES below the diaphragm to increase the sphincter pressure. An acute angle, the angle of His, is formed between the cardia of the stomach and the distal esophagus and functions as a flap at the gastroesophageal junction and helps prevent reflux of gastric contents into the esophagus (see Media file 1 or below).

Hiatal hernia. Figure 1 shows the normal relation...

Hiatal hernia. Figure 1 shows the normal relationship of the gastroesophageal junction, stomach, esophagus, and diaphragm. Figure 2 shows a sliding hiatal hernia where the stomach immediately below the gastroesophageal junction is seen to prolapse through the diaphragmatic hiatus into the chest. Figure 3 shows a paraesophageal hernia in which the cardia or fundus of the stomach prolapses through the diaphragmatic hiatus, leaving the gastroesophageal junction within the esophageal cavity.

Hiatal hernia. Figure 1 shows the normal relation...

Hiatal hernia. Figure 1 shows the normal relationship of the gastroesophageal junction, stomach, esophagus, and diaphragm. Figure 2 shows a sliding hiatal hernia where the stomach immediately below the gastroesophageal junction is seen to prolapse through the diaphragmatic hiatus into the chest. Figure 3 shows a paraesophageal hernia in which the cardia or fundus of the stomach prolapses through the diaphragmatic hiatus, leaving the gastroesophageal junction within the esophageal cavity.


The gastroesophageal junction acts as a barrier to prevent reflux of contents from the stomach into the esophagus by a combination of mechanisms forming the antireflux barrier. The components of this barrier include the diaphragmatic crura, the LES baseline pressure and intra-abdominal segment, and the angle of His. The presence of a hiatal hernia compromises this reflux barrier not only in terms of reduced LES pressure but also reduced esophageal acid clearance. Patients with hiatal hernias also have longer transient LES relaxation episodes particularly at night time. These factors increase the esophageal mucosa acid contact time predisposing to esophagitis and related complications. 

Frequency

United States

Hiatal hernias are more common in Western countries. The frequency of hiatus hernia increases with age, from 10% in patients younger than 40 years to 70% in patients older than 70 years.

International

Burkitt et al suggest that the Western, fiber-depleted diet leads to a state of chronic constipation and straining during bowel movement, which could explain the higher incidence of this condition in Western countries.1

Mortality/Morbidity

Paraesophageal hernias generally tend to enlarge with time, and sometimes the entire stomach is found within the chest. The risk of these hernias becoming incarcerated, leading to strangulation or perforation, is approximately 5%. This complication is potentially lethal, and surgical intervention is necessary. Because of the high mortality associated with this condition, elective repair often is advised wherever a paraesophageal hernia is found.3,2

Sihvo et al examined the mortality associated with adult paraesophageal hernia in a Finnish retrospective, population-based study.3  Five hundred sixty-three patients received surgical intervention and 67 received conservative treatment for paraesophageal hernia. Death occurred in 32 patients, of whom 29 had concomitant diseases.

Of the 563 patients in the surgical group, the overall mortality was 2.7% (15 patients), of whom 3 died following elective repair.3 Of the 67 patients in the conservative treatment group, 16.4% (11 patients) died; 13% (4 patients) of the deaths might have been avoided with elective surgical intervention. Of the 32 patients who died, over half had type III (16 patients; 50%) or type IV (9 patients; 28.1%) had hiatal hernias; 4 patients (12.5%) had had type II hiatal hernias, with the remaining 3 deceased having an unknown type. The causes of death were primarily from incarceration (24 patients; 75%), followed by surgical complications (6 patients; 18.8%) and bleeding ulcer (2 patients; 6.2%).3

Sihvo et al recommended of the paraesophageal hernia, at least in symptomatic patients, except for those at high surgical risk.3

In a Swiss study, Larusson et al investigated the predictive factors for postoperative morbidity and mortality in patients undergoing laparoscopic hernia repair.2 Of 354 laparoscopic paraesophageal hernia repairs, age at 70 years or older was significantly associated with postoperative morbidity (24.4%) and mortality (2.4%) relative to those younger than 70 years (10.1% postoperative morbidity, P = 0.001; 0% mortality, P = 0.045). Similar age findings were noted with gastropexy but not with fundoplication.2 In addition, high-risk patients had significantly higher morbidity but not mortality.

Larusson et al concluded that age, American Society of Anesthesiologists (ASA) score, and type of operation are significant predictive factors in patients undergoing laparoscopic paraesophageal hernia repair.2 The investigators advised caution in balancing surgical indications with each patient's comorbidities, age, symptoms, and potentially life-threatening complications. 2

Sex

Hiatal hernias are more common in women than in men. This might relate to the intra-abdominal forces exerted in pregnancy.

Age

Muscle weakening and loss of elasticity as people age is thought to predispose to hiatus hernia, based on the increasing prevalence in older people. With decreasing tissue elasticity, the gastric cardia may not return to its normal position below the diaphragmatic hiatus following a normal swallow. Loss of muscle tone around the diaphragmatic opening also may make it more patulous.

Clinical

History

Hiatal hernias are relatively common and, in themselves, do not cause symptoms. For this reason, most people with hiatal hernias are asymptomatic. Hiatal hernias may predispose to reflux or worsen existing reflux in a minority of individuals. Physicians should resist the temptation to label hiatal hernia as a disease.

Patients can have reflux without a demonstrable hiatal hernia. When a hernia is present in a patient with symptomatic GERD, the hernia may worsen symptoms for several reasons, including the hiatal hernia acting as a fluid trap for gastric reflux and increasing the acid contact time in the esophagus. In addition, with a hiatal hernia, episodes of transient relaxation of the LES are more frequent and the length of the high-pressure zone is reduced. The main symptoms of a sliding hiatal hernia are those associated with reflux and its complications.

No clear correlation exists between the size of a hiatal hernia and the severity of the symptoms. A very large hiatal hernia may be present with no symptoms at all. Some complications are specific for a hiatal hernia.

  • Esophageal complications
    • By far, the majority of hiatal hernias are asymptomatic.
    • Often, patients are left with the impression that they have a disease when a hiatal hernia is diagnosed.
    • In rare cases, however, a hiatal hernia may be responsible for intermittent bleeding from associated esophagitis, erosions (Cameron ulcers), or a discrete esophageal ulcer, leading to iron-deficiency anemia. The prevalence of large hiatal hernias in patients with iron deficiency anemia is 6-7%. This particular complication is more likely in patients who are bed-bound or those who take nonsteroidal anti-inflammatory drugs. Massive bleeding is rare.
  • Nonesophageal complications
    • Incarceration of a hiatal hernia is rare and is observed only with paraesophageal hernia.
    • When this occurs, it can present abruptly, with a sudden onset of vomiting and pain, sometimes requiring immediate operative intervention.

Physical

The physical examination usually is unhelpful. Certain conditions predispose to the development of hiatus hernia. These include obesity, pregnancy, and ascites.

Causes

  • Predisposing factors include the following:
    • Muscle weakening and loss of elasticity as people age is thought to predispose to hiatus hernia, based on the increasing prevalence in older people. With decreasing tissue elasticity, the gastric cardia may not return to its normal position below the diaphragmatic hiatus following a normal swallow. Loss of muscle tone around the diaphragmatic opening also may make it more patulous.
    • Hiatal hernias are more common in women. This may relate to the intra-abdominal forces exerted in pregnancy.
    • Burkitt et al suggest that the Western, fiber-depleted diet leads to a state of chronic constipation and straining during bowel movement, which might explain the higher incidence of this condition in Western countries.
    • Obesity predisposes to hiatus hernia because of increased abdominal pressure.
    • Conditions such as chronic esophagitis may cause shortening of the esophagus by causing fibrosis of the longitudinal muscles and, therefore, predispose to hiatal hernia. However, which comes first, the hiatal hernia worsening the reflux or the reflux-induced shortening of the esophagus, remains unknown.
    • The presence of abdominal ascites also is associated with hiatal hernias.
  • Diaphragmatic hernias may be congenital or acquired. Acquired hiatal hernias are divided further into nontraumatic and traumatic hernias. The most common types of hernias are those acquired in a nontraumatic fashion. Hernias acquired in a nontraumatic fashion are divided into 2 types, (1) sliding hiatal hernia and (2) paraesophageal hiatal hernia. A mixed variety with coexisting sliding and paraesophageal components is possible.
    • Sliding hiatal hernia by far is the most common type of hiatal hernia. It occurs when the gastroesophageal junction, along with a portion of the stomach, migrates into the mediastinum through the esophageal hiatus (see Media file 1). The majority of patients with demonstrated hiatal hernias are asymptomatic. This type of hernia interferes with the reflux barrier mechanism in several ways. As the LES moves into the chest, it no longer is exposed to positive intra-abdominal pressure and, therefore, is less effective as a sphincter. In fact, the sphincter moves into an area of low pressure, which interferes with the sphincter activity. In addition, the widening hiatus affects the competence of the diaphragmatic crura. The angle of His is lost, making regurgitation of gastric contents more likely. These changes not only predispose to reflux of gastric contents into the esophagus, but also prolong the acid contact time with the epithelium of the esophagus.
    • In paraesophageal hernia, also called rolling-type hiatal hernia, the widened hiatus permits the fundus of the stomach to protrude into the chest, anterior and lateral to the body of the esophagus; however, the gastroesophageal junction remains below the diaphragm (see Figure 3 of Media file 1). This causes the stomach to rotate in a counter-clockwise direction. As the hiatus widens, increasing amounts of the greater curvature of the stomach and, sometimes, the gastric-colic omentum, follow. The fundus eventually comes to lie above the gastroesophageal junction, with the pylorus being pulled towards the diaphragmatic hiatus. In this type of hernia, the anatomic relation of the stomach to the lower end of the esophagus (angle of His) tends to remain unchanged, so gross acid reflux does not occur.

More on Hiatal Hernia

Overview: Hiatal Hernia
Differential Diagnoses & Workup: Hiatal Hernia
Treatment & Medication: Hiatal Hernia
Follow-up: Hiatal Hernia
Multimedia: Hiatal Hernia
References
Further Reading

References

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Further Reading

Related eMedicine topics

Clinical Trials

Clinical Guideline

  • Hernia. Work Loss Data Institute - Public For Profit Organization. 2003 (revised 2008 Mar 10). 43 pages. NGC:006559

Keywords

hiatal hernia, hernias, paraesophageal hernias, paraesophageal hiatal hernia, esophageal hernia, hernia surgery, gastroesophageal reflux disease, GERD, gastric volvulus, hiatus herniaSchatzki ring, phrenoesophageal ligament, esophagitis, Cameron ulcers, sliding hiatal hernia, regurgitation

Contributor Information and Disclosures

Author

Waqar A Qureshi, MD, Associate Professor of Medicine, Chief of Endoscopy, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine and Veterans Affairs Medical Center
Waqar A Qureshi, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Medical Editor

Vivek V Gumaste, MD, Associate Professor of Medicine, Mt Sinai School of Medicine; Adjunct Clinical Assistant, Mt Sinai Hospital; Director, Division of Gastroenterology, City Hospital Center
Vivek V Gumaste, MD is a member of the following medical societies: American College of Gastroenterology and American Gastroenterological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
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