Hiatal hernia is a common condition found in approximately 10% of all adults age 40 and younger and 70% of all adults age 70 and older.1 The word ‘hernia’ refers to the protrusion of part of an organ through the wall of the cavity it's contained in. A hiatal hernia occurs when part of the stomach prolapses through the esophageal diaphragmatic hiatus. Most cases are of no clinical concern, and the patient is largely unaware of the condition. Unfortunately, some patients suffer from severe, recurrent complications of gastroesophageal reflux disease (GERD) that can complicate a hiatal hernia. These patients may develop reflux-associated pulmonary complications such as asthma, chronic cough, or aspiration pneumonia.1 If standard medical and pharmacologic treatment with a proton pump inhibitor aren't successful, these patients may benefit from elective surgery. One of the most popular surgical procedures used for managing GERD and correcting hiatal hernia is the Nissen fundoplication.
Types of hiatal hernia
Although hiatal hernias are common (they're much more common in women, perhaps as a result of childbearing), the incidence in the general population is unknown.1 Hiatal hernias are congenital or acquired, the latter of which are either traumatic or nontraumatic. Nontraumatic hernias are most often classified as Type I, or sliding hiatal hernia, and paraesophageal hiatal hernia, classified as Type II, III, or IV, is known as rolling hiatal hernia.2
Sliding hiatal hernias
The Type I, or sliding hiatal hernia, is the most common of all hiatal hernias. In a Type I hiatal hernia, the gastroesophageal junction and the cardia portion of the stomach move through the esophageal hiatus into the posterior mediastinum (see Types of hiatal hernias). This is due to a gradual widening and weakening of the diaphragmatic hiatus, which is why these hernias are considered somewhat of an age-related problem. The exact cause for this gradual weakening and widening is unknown and may simply be part of the aging process. It may also be due to a lack of fiber in the diets of many people living in western countries. This can cause chronic constipation and straining to defecate, which can increase intrathoracic pressure. Obesity is also associated with an increased risk of developing hiatal hernia.3
Most patients who have a Type I hiatal hernia are unaware of the condition because it causes no signs or symptoms. The defect is usually found during diagnostic tests for other problems. However, some patients with a Type I hiatal hernia may report heartburn, nausea, vomiting, postprandial fullness, dysphagia, or epigastric pain.
A Type I hiatal hernia affects the antireflux mechanisms that protect the esophagus from exposure to gastric acids by reducing the length and pressure of the lower esophageal sphincter (LES).2 For many years, there was controversy regarding the association of hiatal hernia and GERD, but it's now thought that the Type I hiatal hernia is associated with an increased incidence of GERD. Patients with GERD are at risk for increased exposure to gastric acid and an increased incidence of esophagitis and Barrett esophagus.4 Barrett esophagus is diagnosed via endoscopic visualization of columnar mucosa lining the distal esophageal epithelium and tissue biopsy confirming the presence of intestinal metaplasia with the characteristic goblet cells.4 Factors associated with the development of Barrett esophagus include male gender, older age (50 years and older), ethnicity (whites appear to be at a higher risk), and a longer duration and higher severity of GERD symptoms.4 Patients with Barrett esophagus are at an increased risk of developing esophageal adenocarcinoma.
Medical treatment options for GERD include lifestyle modifications and control of gastric acid secretions with pharmacologic agents such antacids and a histamine H2 -receptor antagonist (such as famotidine [Pepcid], nizatidine [Axid], or ranitidine [Zantac]), a proton pump inhibitor, or a promotility agent (such as metoclopramide [Reglan]).1 Pharmacologic management of Barrett esophagus focuses on managing reflux symptoms with the preferred agent, a proton pump inhibitor (such as omeprazole [Prilosec], lansoprazole [Prevacid], or esomeprazole [Nexium]).1,4 The proton pump inhibitors act by binding the proton pump in the parietal cells of the stomach. When this happens, gastric acid secretion is effectively stopped.
Figure. Types of hia...Image Tools
Paraesophageal/rolling hiatal hernias
A paraesophageal hiatal hernia occurs when the gastric fundus is herniated but the cardia portion of the stomach doesn't move. This hernia is considered a Type II. A Type III paraesophageal hiatal hernia combines elements of a Type I and a Type II paraesophageal hiatal hernia, and a Type IV paraesophageal hiatal hernia is characterized by a large defect in the diaphragmatic hiatus that allows other organs such as the colon, pancreas, spleen, or small intestine to herniate.2 Paraesophageal hiatal hernias usually cause more signs and symptoms than Type I hernias, and there are serious complications associated with this disorder such as bleeding, anemia, pulmonary complications (caused by aspiration of gastric contents), volvulus, perforation, and strangulation. The exact incidence of these complications is between 0.7% and 7%, and emergency surgery is needed in approximately 1% of cases.5 Patients with a paraesophageal hiatal hernia are less likely to develop GERD because there are no anatomic changes to the antireflux mechanisms.1
Most patients with Type I hiatal hernias will never need surgery, however, some can't tolerate or afford pharmacologic management of reflux symptoms. There are also patients with Type I hiatal hernias and GERD who suffer from serious complications of reflux, such as hemorrhagic esophagitis, asthma, chronic cough, strictures, aspiration pneumonia, or esophageal perforation. These patients will benefit from elective surgery. A final consideration is the patient's age and the cost of therapy. If the patient has a mechanically incompetent LES, is expected to live 10 years or longer and needs lifelong therapy, has good esophageal body function, and evidence via pH testing of abnormal acid exposure in the esophagus, surgery is an option.6
Generally, the procedure to treat hernias under these circumstances is the Nissen fundoplication. It's the most common surgical procedure performed on infants and children with GERD, and it's also frequently performed in adults with GERD.7 The procedure is designed to strengthen the LES, restore the intra-abdominal esophagus, reconstruct the diaphragmatic hiatus, and reinforce the LES.
The procedure can be performed laparoscopically or as an open procedure, and involves a 360-degree transabdominal fundoplication (fundoplication is suturing the fundus of the stomach around the esophagus; the word comes from fundus and the Latin word plico, which means "to fold"). The fundoplication (a) increases the resting pressure of the LES, (b) accentuates the angle of His (the angle of His is formed by the juncture of the cardia of the stomach and the distal esophagus and helps act as a flap at the gastroesophageal junction), (c) increases the intra-abdominal length of the sphincter, and (d) increases the rate of gastric emptying.8
The laparoscopic approach is generally preferred because when compared with the open technique, there's no difference in postoperative mortality, postoperative symptoms, or the need for reoperation because of failure. In addition, the laparoscopic approach offers lower operative morbidity and a shorter postoperative length of stay, decreased pain, and a quicker return to normal activities.8
The Nissen fundoplication is generally considered an effective procedure with a high success rate, low morbidity, and low mortality. The Nissen fundoplication was first performed by Dr. Rudolph Nissen in 1955, and two case reports were published in 1956. The procedure was refined by Nissen through the years, and by the 1970s, it was the most common antireflux surgical procedure.9
Most patients will be scheduled for the following preoperative tests/procedures: endoscopy with a biopsy, a barium swallow with fluoroscopy, 24-hour esophageal pH monitoring, manometry of the esophageal body and the LES, and gastric secretory or gastric emptying studies.8
The laparoscopic Nissen fundoplication is performed with the patient in a low lithotomy position at approximately 25 degrees. The particular technique described here is also called a left crus approach to a 360-degree wrap. The surgeon stands between the patient's legs, the camera operator is positioned on the patient's right, and another assistant is positioned on the left side of the patient. Five trocars (three 10 mm and two 5 mm) are placed so that two equilateral triangles share a common medial angle. The operation is performed via the two ports in the most cephalad position. An assistant works through the two ports in the most caudad position. The remaining port is used for the liver retractor.6
The abdomen is insufflated to 12 to 15 mm Hg, and a first assistant begins by retracting the greater curve and then the omentum. The left lateral segment of the liver is retracted in an anterior direction to expose the esophagus. A Babcock clamp is placed on the esophageal fat pad and retracted toward the patient's feet in order to release the gastrohepatic ligament and phrenoesophageal membrane. The surgeon then dissects the left crus (the crus is a tendinous portion of the diaphragm, a band of tissue that forms part of the hiatus) and the greater curve. The fundus is mobilized by dividing the short gastric vessels, and then dissecting the phrenoesophageal membrane that covers the left crus. The entire length of the left crus is then mobilized. Next, the lesser omentum is opened and the right crus is dissected. A Penrose drain is placed around the esophagus to allow for more dissection and to facilitate creation of the wrap, or the fundoplication.6
After the esophagus has been mobilized, the next step is to move both crura posteriorly using heavy sutures to make room for a 52-French bougie. When this is in place, the surgeon passes the posterior aspect of the fundus behind the esophagus from left to right. The wrap is created and sutured to the esophagus and to the right crus at the hiatus, and the bougie is removed. The wrap is further anchored, anteriorly and posteriorly, with additional sutures. The trocar sites are then fascially closed.6
The mortality for Nissen fundoplication is approximately 0% to 1%, the rate of complications is about 10% to 20%, and the failure rate is estimated at 5%.6,10 Intraoperatively, the most common complication is pneumothorax, which occurs in 5% to 8% of all patients. Some complications that may occur are common in many surgeries, such as ileus, urinary retention, infection, and venous thrombosis. Complications specific to the Nissen procedure include chest pain, persistent dysphagia, paraesophageal hernia, gas bloating, nausea, vomiting, postprandial fullness, diarrhea, and dumping syndrome. These complications may be due to persistent GERD, a disrupted or herniated wrap, or a wrap that's too tight.11 However, patients often report that these complications are more easily tolerated than the GERD symptoms, and a majority of patients are satisfied with the procedure.11
Laparoscopic Nissen fundoplication is a well-established treatment for GERD and repair of hiatal hernia. Nevertheless, there are still some issues regarding specific approaches to the procedure, which are controversial and haven't been resolved.
Although a majority of patients who have a Nissen fundoplication with a 360-degree wrap are satisfied with the quality of their lives after the procedure, there are some patients who have a high incidence of dysphagia, bloating, and other gastrointestinal symptoms after the surgery, which can be very troublesome. The new reflux barrier formed by the surgery may actually be more effective than the LES in normal patients, thus causing these problems. To avoid this, some surgeons use an anterior or posterior partial fundoplication. In this procedure, the surgeon performs hiatal dissection and repair, and sutures the anterior wall of the gastric fundus and the right lateral wall of the distal esophagus to the right hiatal pillar and the apex of the esophageal hiatus, thus covering the anterior aspect of the intra-abdominal esophagus with the gastric fundus.12 Some surgeons have found that this approach results in fewer adverse effects but a higher rate of reflux. Other surgeons have found no difference between the two techniques regarding the incidence of adverse effects.13
Some surgeons have modified the Nissen procedure using a technique called the floppy Nissen in order to prevent postoperative complications such as dysphagia. In this procedure, the short gastric vessels are divided, the gastric fundus is completely mobilized, an intraluminal bougie is placed to help gauge tightness of the wrap, and the subsequent wrap is made loose or floppy. The idea is to allow for more relaxation of the LES during swallowing and to reduce the incidence of dysphagia. However, randomized trials of the floppy Nissen haven't shown it to be any more effective at reducing postoperative complications than the standard technique.14 Using intraoperative manometry is a proposed method to make the floppy Nissen more effective.15
In the traditional Nissen fundoplication, the hiatus is closed posteriorly. Anterior closure has been proposed as an alternative to reduce postoperative complications, for example, dysphagia.16
A common problem after the Nissen fundoplication is movement of the wrap into the mediastinum. Some surgeons have reported that this problem can be prevented by reinforcing the hiatal crura closure with a polypropylene mesh.17 Problems associated with the use of mesh prosthesis include mesh erosion, ulceration, stricture, and dysphagia. These may be avoided by using a biologic graft, an absorbable biologic mesh called small intestinal submucosa.
Surgical management of paraesophageal hernia
Paraesophageal hernias account for a small percentage of all hiatal hernias, but the risk of developing acute symptoms and/or incarceration has been estimated at over 30%.18 Gastric volvulus, strangulation, perforation, and bleeding can also occur.
Patients with these complications clearly need surgery, but for patients with a paraesophageal hiatal hernia and no immediate, serious complications, there are no clear guidelines as to who should have surgery and when. For patients who need emergency surgery because of complications, a laparoscopic approach for repair of a pararesophageal hernia is the procedure of choice. This procedure is more difficult than repair of a Type I hiatal hernia and there are differences between the two, but it's still considered safe and effective.19
The patient is positioned and the ports are placed in the manner described for repair of a sliding hiatal hernia. The greater curve and the fundus of the stomach are mobilized, and the left crus are thus exposed. The hernia sac and the peritoneal sac are divided. Division of the peritoneal sac allows the stomach to be freed and delivered into the peritoneal cavity. The hernia sac must be transected circumferentially as much as possible at the hiatus, and this must be done carefully due to the close proximity of the esophagus and the anterior vagus nerve. After the hernia sac is dissected, the crura are dissected, the short gastric vessels are divided, and a fundoplication is performed.6,20
The success rate of this procedure is 90% to 100%, and morbidity and mortality are low. The average hospital stay is 36 to 48 hours, and most of the postoperative discomfort is from the incision. Oral intake starts with a liquid diet and progresses quickly, although meats and breads shouldn't be eaten for 2 to 3 weeks.20
Immediate postoperative care includes observation for and treatment of complications such as pneumothorax, esophageal tear, subcutaneous emphysema, infection, and pain. Occasionally, some patients will require another revision if they're having persistent dysphagia or reflux symptoms.8
Patients are placed initially on a liquid diet after a laparoscopic Nissen fundoplication, and must only eat pureed foods for 1 to 2 weeks after the surgery. Patients can then progress to soft foods and, in 4 to 6 weeks, return to their normal diet.
Before discharge, the nurse should review diet and activity restrictions (no heavy lifting for 4 weeks, chewing food thoroughly, avoiding carbonated beverages, gum, and smoking) and educate the patient that dysphagia, sore throat, and gas bloating are commonly experienced. Most patients can return to work in 2 weeks, and after the surgery, a majority of patients experience significant relief and are pleased with the long-term results.21,20,21
2. Kahrilas PJ, Kim HC, Pandolfino JE. Approaches to the diagnosis and grading of hiatal hernia. Best Pract Res Clin Gastenterol. 2008;22(4):601–616.
3. Anand G, Katz PO. Gastroesophageal reflux disease and obesity. Rev Gastroenterol Disord. 2008;8(4):233–239.
4. Wang KK, Sampliner RE. Practice Parameters Committee of the American College of Gastroenterology. Updated guidelines 2008 for the diagnosis, surveillance and therapy of Barrett's esophagus. The American College of Gastroenterology. Am J Gastroenterol. 2008;103(3):788–797
5. Shivo EL, Salo JA, Räsänen J, Rantanen TK. Fatal complications of adult paraesophageal hernia: a population-based study. J Thorac Cardiovasc Surg. 2009;137(2):419–424.
6. Maish MD. Esophagus. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL (eds.). Sabiston Textbook of Surgery. 18th ed. Philadelphia: Elsevier; 2008.
8. Aronson BS, Yeakel S, Ferrer M, Caffrey E, Quaggin C. Care of the laparoscopic Nissen fundoplication patient. Gastroenterol Nurs. 2001;24(5):231–236.
9. Stylopoulos N, Rattner DW. The history of hiatal hernia surgery: from Bowditch to laparoscopy. Ann Surg. 2005;241(1):185–193.
10. Mattioli S, Lugaresi ML, Pierluigi M, DiSimone MP, D'Ovidio F. Indications for anti-reflux surgery in gastroesophageal reflux disease (review article). Aliment Pharmacol Ther. 2001;17(suppl 2):60–67.
11. Connor F. Gastrointestinal complications of fundoplication. Curr Gastroenterol Rep. 2005;7:219–226.
12. Teixeira JP, Mosquera V, Flores A. Long-term outcomes of quality of life after laparoscopic Nissen fundoplication. Hepatogastroenterology. 2009;56:80–84.
13. Rice S, Watson DI, Lally CJ, Devitt PG, Game PA, Jamieson GG. Laparoscopic anterior 180 degree partial fundoplication: five-year results and beyond. Arch Surg. 2006;141:271–275.
14. Cai W, Watson DI, Lally CJ, Devitt PG, Game PA, Jamieson GG. Ten-year clinical outcome of a prospective randomized trial of laparoscopic Nissen versus anterior 180 degree partial fundoplication. Br J Surg. 2008;95:1501–1505.
15. O'Boyle CJ, Watson DI, Jamieson GG, Myers JC, Game PA, Devitt PG. Division of the short gastric vessels at laparoscopic Nissen fundoplication: a prospective double-blind randomized trial with 5-year follow up. Ann Surg. 2002;235(2):165–170.
16. Lei Y, Li JY, Jiang J, et al. Outcome of floppy Nissen fundoplication with intraoperative manometry to treat sliding hiatal hernia. Dis Esophagus. 2008;21:364–369.
17. Wijnhoven BP, Watson DI, Devitt PG, Game PA, Jamieson GG. Laparoscopic Nissen fundoplication with anterior versus posterior hiatal repair: long-term results of a randomized trial. Am J Surg. 2008;195:61–65.
18. Granderath FA, Kamolz T, Schweiger UM, Pointner R. Impact of laparoscopic Nissen fundoplication with prosthetic hiatal closure on esophageal body motility: results of a prospective randomized controlled trial. Arch Surg. 2007;141(7):625–632.
19. Bawahab M, Mitchell P, Church N, Debru E. Management of acute paraesophageal hernia. Surg Endosc. 2009;23:255–259.
20. Rogers MA, Cox JA. Laparoscopic paraesophgeal hernia repair with Nissen fundoplication. AORN J. 1998;67(3):536–551.
21. Mark LA, Okrainec A, Ferri LE, Feldman LS, Mayrand S, Fried GM. Comparison of patient-centered outcomes after laparoscopic Nissen fundoplication for gastroesophageal reflux disease or paraesophgeal hernia. Surg Endosc. 2008;22:343–347.
© 2010 Lippincott Williams & Wilkins, Inc.