Hiatal Hernia

 A hiatal hernia is a type of hernia in which abdominal organs (typically the stomach) slip through the diaphragm into the middle compartment of the chest. (1,2) This may result in gastroesophageal reflux disease (GERD) or laryngopharyngeal reflux (LPR) with symptoms such as a taste of acid in the back of the mouth or heartburn. (ibid) Other symptoms may include trouble swallowing, chest pains and shallow breathing. (Ibid) Complications may include iron deficiency anemia, volvulus, or bowel obstruction. (1)

In other words, a hiatal hernia occurs when the upper part of the stomach pushes through an opening in the diaphragm and into the chest cavity. The diaphragm is the thin muscle wall that separates the chest cavity from the abdomen. The opening in the diaphragm is where the esophagus and stomach join. The esophagus sphincter muscle normally closes tightly. With a hiatal hernia, the sphincter’s new position may keep it from completely closing and becomes bulgy. The back flow of digestive juices can damage the esophagus to the point of triggering an esophagial cancer.

Signs and symptoms

Hiatal hernia has often been called the “great mimicker” because its symptoms can resemble many disorders. Among them, a person with a hiatal hernia can experience dull pains in the chest, shortness of breath (caused by the hernia’s effect on the diaphragm), heart palpitations (due to irritation of the vagus nerve), and swallowed food “balling up” and causing discomfort in the lower esophagus until it passes on to the stomach. In addition, hiatal hernias often result in heartburn but may also cause chest pain or pain with eating. (Ibid).

In most cases however, a hiatal hernia does not cause any symptoms. The pain and discomfort that a patient experiences is especially due to the reflux of gastric acid, air, and-or bile.  Bitter or sour taste in the back of the throat can ensue, as well as bloating and belching.

In newborns, the presence of Bochdalek hernia can be recognised (3) from symptoms such as difficulty breathing fast respiration, increased heart rate. (4,5)


Some of the most common risk factors are obesity and older age. (Ibid.) Other risk factors include major trauma, scoliosis, and certain types of surgery, (1), to which can be added bowel and nutritional dysfunction.

Pathophysiology (Causes)

Although there appears to be a link between hiatal hernia and GERD, one condition does not seem to cause the other. Many people have a hiatal hernia without having GERD, and others have GERD without having a hiatal hernia. Hence, correlation is not necessarily causation.

On the other hand, the following are potential causes of a hiatal hernia. Increased pressure within the abdomen caused by: Heavy lifting. Frequent or hard coughing. Hard sneezing Violent vomiting Straining during defecation (i.e., the Valsalva maneuver) Obesity and age-related changes to the diaphragm are also general risk factors. (6)

From the up to date evidence, it would appear that the most common cause of a hiatal hernia is an increase in pressure in the stomach and abdominal cavity. (The abdomen consists of the lower part of the esophagus, stomach, small intestine, colon, rectum, liver, gallbladder, pancreas, spleen, kidneys, and bladder.)

Stomach Pressure

Pressure in the stomach can occur in conjunction with several common conditions, including indigestion and constipation. Indigestion is usually caused by an imbalance and-or insufficient of acid in the stomach. It’s typically accompanied by belching heartburn and feeling of fullness in the stomach.  Heartburn or  GERD is most often caused by too little hydrochloric acid being secreted by the stomach.  (Source)

Pressure in the stomach or abdomen may be caused by a backup of fecal matter. Daily bowel movements are key.  Constipation can be caused by: dehydration, lack of fiber and plant based foods, medication, injury lack of physical activity and stress.

Overeating can cause pressure in the stomach. This is due to the stomach stretching to accommodate the food that is ingested. And stress can cause any number of deleterious reactions within including indigestion.

Premenstrual syndrome can be another factor. PMS symptoms can include stomach pressure, cramping, or tightness. A growing baby can also cause physical pressure within the stomach as inflammatory bowel disease, pancreatitis and other auto immune conditions. (Source)


Incidence of hiatal hernias increases with age; approximately 60% of individuals aged 50 or older have a hiatal hernia. (16). Of these, 9% are symptomatic, depending on the competence of the lower esophageal sphincter (LES). 95% of these are “sliding” hiatal hernias, in which the LES protrudes above the diaphragm along with the stomach, and only 5% are the “rolling” type (paraesophageal), in which the LES remains stationary, but the stomach protrudes above the diaphragm. Hiatal hernias are most common in North America and Western Europe and rare in rural African communities. (18) A few studies Some have proposed that insufficient dietary fiber and the use of a high sitting position for defecation may increase the risk. (ibid)


The diagnosis of a hiatal hernia is typically made through an upper GI series, endoscopy or high resolution manometry

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Four types of esophageal hiatal hernia are identified. (8)

Type I: A type A hernia is also known as a sliding hiatal hernia. There is a widening of the muscular hiatal tunnel and circumferential laxity of the phrenoesophageal ligament, allowing a portion of the gastric cardia to herniate upward into the posterior mediastinum. The clinical significance of type I hernias is in their association with reflux disorder. Sliding hernias are the most common type and account for 95% of all hiatal hernias. (9)

Type II: A type B hernia results from a localized defect in the phrenoesophageal ligament while the gastroesophageal junction remains fixed to the pre aortic fascia and the median arcuate ligament. The gastric fundus then serves as the leading point of herniation. Although type II hernias are associated with reflux disease, their primary clinical significance lies in the potential for mechanical complications.

Type III: Type C hernias have elements of both types I and II hernias. With progressive enlargement of the hernia through the hiatus, the phrenoesophageal ligament stretches, displacing the gastroesophageal junction above the diaphragm, thereby adding a sliding element to the type II hernia.

Type IV: Type D hiatus hernia is associated with a large defect in the phrenoesophageal ligament, allowing other organs, such as colon, spleen, pancreas and small intestine to enter the hernia sac.

The end stage of type I and type II hernias occurs when the whole stomach migrates up into the chest by rotating 180° around its longitudinal axis, with the cardia and pylorus as fixed points. In this situation the abnormality is usually referred to as an intrathoracic stomach.

Conventional Treatment

In the great majority of cases, hiatal hernia sufferers experience no life-altering discomfort. If there is pain or discomfort, 3 or 4 sips of room temperature good quality water will usually relieve the pain. Symptomatic patients should elevate the head of their beds and avoid lying down directly after meals

If the condition has been brought on by stress, stress reduction techniques may be prescribed, or if overweight, weight loss may be indicated. Antisecretory drugs like proton pump inhibitors and H2 receptor blockers are used in conventional medicine, but have significant drawbacks as does acid inhibitors. Medications that reduce the lower esophageal sphincter (LES) pressure should be avoided.

If symptoms from such a hernia are severe for example if chronic acid reflux threatens to severely injure the esophagus or is causing Barrett’s esophagus, conventional medicine recommends surgery. However surgery has its own risks including death and disability, so that even for large or paraesophageal hernias, watchful waiting may on balance be safer and cause fewer problems than surgery. (10) Complications from surgical procedures to correct a hiatal hernia may include gas bloat syndrome, dysphagia (trouble swallowing), dumping syndrome, excessive scarring, and, inter alia,  achalasia.[10] Surgical procedures sometimes fail over time, requiring a second surgery to make repairs.

One surgical procedure used is called Nissen fundoplication. In fundoplication, the gastric fundus (upper part) of the stomach is wrapped, or plicated, around the inferior part of the esophagus, preventing herniation of the stomach through the hiatus in the diaphragm and the reflux of gastric acid. The procedure is now commonly performed laparoscopically. (11-15)

Holistic Medicine

Holistic medicine uses naturopathic and innovative techniques that get to the root causes of the hiatal hernia, while relieving pain and indigestion with gentle and innovative interventions.

To learn about the cutting edge holistic techniques to better control and reverse hiatal hernia, schedule a consult-coaching.

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  1. Roman, S; Kahrilas, PJ (23 October 2014). “The diagnosis and management of hiatus hernia”. BMJ (Clinical research ed.). 349: g6154. doi:10.1136/bmj.g6154.
  2.  “Hiatal Hernia”. PubMed Health. Archived from the original on 28 April 2017. Retrieved 6 May 2017.
  3.  Chang SW, Lee HC, Yeung CY, Chan WT, Hsu CH, Kao HA, Hung HY, Chang JH, Sheu JC, Wang NL (2010). “A twenty-year review of early and late-presenting congenital Bochdalek diaphragmatic hernia: are they different clinical spectra?”. Pediatr Neonatol. 51 (1): 26–30. doi:10.1016/S1875-9572(10)60006-X. PMID 20225535.
  4.  Ganeshan DM, Correa AM, Bhosale P, Vaporciyan AA, Rice D, Mehran RJ, Walsh GL, Iyer R, Roth JA, Swisher SG, Hofstetter WL. “Diaphragmatic hernia after esophagectomy in 440 patients with long-term follow-up”. Ann Thorac Surg. 96: 1138–45. doi:10.1016/j.athoracsur.2013.04.076.
  5. Alam, A; Chander, B.N. (July 2005). “Adult bochdalek hernia”. MJAFI. 61 (3): 284–6. doi:10.1016/S0377-1237(05)80177-7.
  6. https://www.mayoclinic.org/diseases-conditions/hiatal-hernia/symptoms-causes/syc-20373379
  7.  “UOTW #39 – Ultrasound of the Week”. Ultrasound of the Week. 25 February 2015. Archived from the original on 9 May 2017. Retrieved 27 May 2017.
  8.  Kahrilas, Peter J.; Kim, Hyon C.; Pandolfino, John E. “Approaches to the diagnosis and grading of hiatal hernia”. Best Practice & Research Clinical Gastroenterology. 22 (4): 601–616. doi:10.1016/j.bpg.2007.12.007.
  9. Dennis Kasper; Anthony Fauci; Stephen Hauser; Dan Longo; J. Larry Jameson; Joseph Loscalzo. Harrison’s Principles of Internal Medicine, 19e (19 ed.). McGraw-Hill Global Education. p. 1902. ISBN 978-0071802154.
  10. Stylopoulos N, Gazelle GS, Rattner DW. “Paraesophageal hernias: operation or observation?”. Ann Surg. 236: 492–500. doi:10.1097/01.SLA.0000029000.06861.17.
  11. Migaczewski M, Pędziwiatr M, Matłok M, Budzyński A (2013). “Laparoscopic Nissen fundoplication in the treatment of Barrett’s esophagus — 10 years of experience”. Wideochir Inne Tech Maloinwazyjne. 8 (2): 139–45. doi:10.5114/wiitm.2011.32941.  23837098.
  12. Witteman BP, Strijkers R, de Vries E, Toemen L, Conchillo JM, Hameeteman W, Dagnelie PC, Koek GH, Bouvy ND (2012). “Transoral incisionless fundoplication for treatment of gastroesophageal reflux disease in clinical practice”. Surg Endosc. 26 (11): 3307–15. doi:10.1007/s00464-012-2324-2. PMC 3472060. PMID 22648098.
  13.  Ozmen V, Oran ES, Gorgun E, Asoglu O, Igci A, Kecer M, Dizdaroglu F (2006). “Histologic and clinical outcome after laparoscopic Nissen fundoplication for gastroesophageal reflux disease and Barrett’s esophagus”. Surg Endosc. 20 (2): 226–9. doi:10.1007/s00464-005-0434-9. 16362470.
  14. Abbas AE, Deschamps C, Cassivi SD, Allen MS, Nichols FC, Miller DL, Pairolero PC (2004). “Barrett’s esophagus: the role of laparoscopic fundoplication”. Ann. Thorac. Surg. 77 (2): 393–6. doi:10.1016/S0003-4975(03)01352-3.
  15. “Journal Index PDF (fee for article)” (PDF). Lange Current Medical Diagnosis & Treatment 2006. Archived (PDF) from the original on 27 February 2015.
  16.  Goyal Raj K, “Chapter 286. Diseases of the Esophagus”. Harrison’s Principles of Internal Medicine, 17e.
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  18. ^ Sontag S (1999). “Defining GERD”. Yale J Biol Med. 72 (2–3): 69–80. 2579007..

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