Esophageal hiatal hernia
Overview.
The esophagus enters the abdominal cavity from the posterior mediastinum through a hole in the posterior part of the diaphragm; this hole is called the esophageal hiatus. The passage of the cardia and the ventral segment of the esophagus or abdominal viscera into the thoracic cavity through this foramen and its parietal protrusion is called hiatal hernias. It is important to recognize and distinguish between hiatal hernias and reflux esophagitis, which can exist simultaneously or separately.
Etiology Sun Chaoyong, Center for Gastroesophageal Reflux Disease, General Hospital of the Chinese People’s Liberation Army Rocket Force
The etiology of esophageal hiatal hernia is still controversial. A few patients with the onset of the disease in early childhood have congenital developmental disorders that result in a large esophageal hiatal hole and weak tissue around the hole; in recent years, it is mostly believed that acquired factors are the main ones, related to obesity and chronic intra-abdominal pressure elevation. The physiological role of the esophagogastric junction is still not well understood. When the esophagogastric junction is functional, it has an active flap, and liquids or solids are swallowed into the stomach without reflux, and only when hiccups or vomiting occur can a small amount of reflux occur. The factors that ensure this normal function are: (1) the clamping effect of the diaphragm on the esophagus; (2) the role of the mucosal folds in the esophagogastric junction; (3) the anatomically sharp angle between the esophagus and the fundus; (4) the involvement of the intra-abdominal esophageal segment in the valvular action of the lower esophagus; and (5) the role of the internal sphincter in the physiologically high pressure area of the lower esophagus. Most people consider the 5th of the above factors as the main factor in preventing reflux, which is supported by the normal anatomical relationships in the vicinity. The prevention of gastric reflux is governed by the vagus nerve, and this effect disappears after removal of the vagus nerve. When the pressure in the stomach increases, gastric juice tends to flow back into the esophagus. The squamous epithelium of the esophageal mucosa is not resistant to gastric acid, and long-term erosion by refluxed gastric acid can cause reflux esophagitis, with mucosal edema and congestion in mild cases and superficial ulcers in heavy cases, with patchy distribution or fusion, submucosal tissue edema, mucosal damage and pseudomembrane coverage, and easy bleeding. Inflammation can penetrate into the muscular layer and fibrous epithelium, and even involve the mediastinum, thickening the tissue, becoming brittle, and enlarging the nearby lymph nodes. In the later stages, the esophageal wall becomes fibrotic, scarred and narrowed, and the esophagus becomes shorter. In some cases, the diaphragmatic esophagus membrane may be found to be stretched below the aortic arch up to the level of the 9th thoracic vertebra. The severity of reflux esophagitis can vary depending on the following factors: the amount of gastric juice returned, the acidity of the reflux, the length of time present and individual differences in resistance. Most of the pathological changes in reflux esophagitis are reversible, and repair of mucosal lesions is possible after correction of esophageal hiatal hernia.
Symptoms
Patients come to the clinic with complaints of typical symptoms such as heartburn and acid reflux, or atypical symptoms such as foreign body sensation in the larynx, hoarseness, hysteria, acid vomiting, chest pain, and paroxysmal cough. Asthma and aspiration pneumonia and other non-ulcer dyspeptic symptoms should be considered for the diagnosis of reflux esophagitis. If antacid therapy given relieves the symptoms, the diagnosis is generally confirmed. To confirm the diagnosis, esophagoscopy and 24h pH monitoring should be performed. X-ray examination: endoscopy is the main method to diagnose hiatal hernia of the esophagus. Barium meal examination is most commonly used, but requires manual assistance to reveal the hernia. When the stomach is filled with barium, the abdomen is compressed by hand and the patient is forced to exhale. The following signs of hiatal hernia can be seen: the subdiaphragmatic esophageal segment (ventral segment) becomes shorter and wider or disappears, the cardia shows curtain-like upward traction, the gastric sac is visible on the diaphragm, and the esophagogastric stenosis ring (Schatzki annular stenosis), which corresponds to the junction of squamous and columnar epithelium, appears on the diaphragm. In the presence of esophageal stricture, the mucosa is deformed and the lumen is narrowed. In the case of short esophagus, there is a thick gastric mucosa on the diaphragm and the esophagogastric junction may rise to the level of the 9th thoracic vertebra due to scar contraction. When making barium meal examination, among the techniques used to stimulate reflux, Muller’s technique is more effective (closing the voice box after exhalation, then inhaling forcefully to increase the negative intrathoracic pressure, prompting the barium in the stomach to reverse into the esophagus); some people use the “drinking water” method; let the patient drink water into the stomach, mix with the barium, and then squeeze the abdomen. In hospitals that are in a position to do so, the upper gastrogram should be made into a videotape for repeated examination. Most people believe that there is not necessarily a sign of reflux on X-ray when there is a hiatal hernia; and there is not necessarily a hiatal hernia when there is a sign of reflux. There is disagreement as to whether the diagnosis of a hiatal hernia is made in those with curtain traction. A normal esophageal potbelly should not be mistaken for a hiatal hernia, and diffuse esophageal spasm can occur with hiatal hernia and signs of gastric reflux. Lack of peristaltic function of the esophagus in scleroderma and achalasia should also be distinguished from a hiatal hernia. If mechanical constriction of the esophagus is found, multiple observations should be made. To distinguish neoplastic, ulcerative benign constriction or esophageal dynamic disease, it is generally accepted that the radiologist’s report on the cause of constriction should only be used as a reference for diagnosis and a histological diagnosis must be available for each patient.
X-ray barium imaging of esophageal hiatal hernia: curtain-like traction of the gastric mucosa Esophageal hiatal hernia X-ray barium imaging: diaphragmatic view of the gastric capsule Esophageal hiatal hernia X-ray barium meal imaging: upward displacement of the Schatzki ring and upward traction of the gastric mucosa Endoscopy is second only to radiology in the diagnosis of esophageal hiatal hernia. Fiberoptic gastroscopy is safer and less painful than metal rigid tubeoscopy during examination and allows simultaneous examination of the stomach and duodenum to exclude factors causing elevated gastric pressure, and can be used multiple times for easy examination. In case of hiatal hernia, the lower esophageal sphincter is seen to be relaxed and open during both expiration and inspiration. The esophagogastric junction point drops during normal inspiration, but does not change position if there is a hernia, and the level of gastric juice appears higher than normal in the esophagoscope. In case of reflux esophagitis, erythema, number of ulcers, attempt and their arrangement, ulcer bleeding, mucosal erosion and shrinkage through can be observed through gastroscopy. If the cardia is open after the respiratory cycle, this is another indication of reflux. If the patient’s complaint is mainly difficulty in swallowing, applying the “ding” technique and observing the cardia from below may rule out the presence of early cancer in this area, and backing off the gastroscope to the esophagus. Careful step-by-step examination is very important. If esophageal constriction and severe esophagitis are found, or if Barrett’s columnar epithelium is suspected, multiple biopsies should be performed; esophageal ulcers can also become malignant. When cancer cannot be ruled out, a deep biopsy using a metal hard microscope is performed to clarify the diagnosis. In some cases of esophageal constriction, the diagnosis can be further clarified and the efficacy of dilatation can be observed during the initial endoscopy. If reflux is suspected, or if a hiatal hernia is found without signs of reflux and radiography does not show signs of reflux, functional esophageal examination should be considered. When the patient’s chief complaint is dysphagia, barium meal imaging and endoscopy are superior to esophageal function test; when dysphagia is not a main symptom and barium meal examination is double negative, esophageal function test should be considered first, and endoscopy may be avoided after a clear diagnosis. Esophageal function tests can be done on an outpatient basis and include esophageal manometry, standard acid reflux tests, acid clearance tests and acid perfusion tests using pH electrodes placed in the esophagus. In more complicated cases, hospitalization for long 24h pH monitoring and continuous manometry can be performed to provide more information.
Esophageal manometry: Esophageal intraluminal pressure can provide esophageal motility parameters when measured simultaneously in different planes. In recent years, multi-conductor micro-balloon manometry has been developed in China, which is easier, safer and reusable. In esophagitis, the lower segment of esophagus has low peristaltic amplitude, no peristalsis or abnormal peristalsis, and 2.67kPa (20mmHg) is the high too band when normal, and gastric reflux is likely to occur when it is lower than 1.33kPa (10mmHg). Pressure measurement can identify atypical pain caused by myocardial infarction and biliary tract disease. Standard acid reflux test: inject 150-300 ml of 0.1 mol/L HCL into the stomach and pull the electrode slowly. The electrode was placed 5 cm above the hypertensive area of the lower esophagus. The pH was measured at different points 5, 10 and 15 cm. Simultaneously with Valsala maneuver (acoustic closure to forcefully exhale to increase intrathoracic pressure) and Muller maneuver 9 exhalation followed by acoustic closure to forcefully inhale to increase negative intrathoracic pressure and change of position to induce gastroesophageal reflux), pH <4 for more than 5 min was considered positive. This test is helpful when the diagnosis is not exact by other clinical methods. The pH value in the stomach is 1~4 when correct, and the pH value in the esophagus is 5~7 in the high pressure area. If the pH value changes from 2~2.4 to 6.5~7.0 within 2cm from the stomach to the lower esophageal sphincter when measured with the pH electrode, it indicates normal cardia function. Acid clearance test: pH electrode was still placed 5cm above the high pressure area, 15cmml 0.1mol/L HCL was injected into the mid esophagus through the proximal end of the catheter, and the patient was asked to swallow every 30s to eliminate the acid in the esophagus, and the number of swallows required for the pH meeting to rise above 5 was recorded. In normal subjects, it is under 10 swallows. This method does not confirm the presence or absence of gastric reflux, but only indicates the severity of esophagitis. Acid perfusion test: This method can be used if reflux symptoms are not obvious. The catheter is still placed in the middle part of the esophagus and its proximal end is placed behind the patient, and two intravenous fluid bottles are connected by a Y-shaped tube. One bottle contains 0.1 mol/L HCL fluid and the other bottle contains saline. Each bottle was perfused separately for about 10 min, and the patient's response to the perfusion was recorded by the observer. If the acid infusion caused spontaneous reflux symptoms, while saline did not respond. A positive acid perfusion test indicates that the patient's symptoms are caused by acid reflux and not by esophageal motility disorders.
Long term pH monitoring: 24h continuous pH monitoring can provide valuable diagnostic information for patients who have had previous esophageal surgery, who have other comorbidities, who are suspected of having aspiration pneumonia due to reflux, or who are suffering from “angina pectoris”. After a series of standard esophageal function tests, the pH electrode is left 5 cm above the distal esophageal hypertensive area, connected to a strip chart meter, and recorded by a pH meter. 24 h of patient activity and symptoms are recorded. During this time the patient eats normally but restricts water and food variety to pH > 5. The number of reflux episodes can be quantitatively measured in both supine and upright positions, depending on the frequency and duration of the episodes. When the pH is higher than 7, it can be designated as alkaline reflux. Currently, 24h pH monitoring is considered the most reliable and sensitive method to diagnose gastroesophageal reflux. Changes in esophageal pH can be recorded continuously for 10, 12 and 24h. The test indexes are: ① the number of 24h pH <4; ② the percentage of pH <4 in the total time; ③ the number of pH <4 more than 5min; ④ the longest acid exposure time. These measured values can be compared with normal subjects to make the diagnosis of GERD. The latest generation of 24h esophageal pH and pressure synchronization record only, the subject is completely in a normal physiological state, now the domestic development and production. In recent years, ultrasound examination of the cardia of the esophagus and measurement of the length of the ventral segment of the esophagus are more effective than barium meal X-ray for the diagnosis of smaller hiatal hernia. Examination of paraesophageal hernia with magnetic resonance can determine the nature of the hernia content more clearly.
Examination: physical examination findings: no special.
Auxiliary examination: mainly rely on x-ray examination to confirm the diagnosis. Routine chest fluoroscopy and chest plain film pay attention to the presence of gas-containing cystic cavity and gas-fluid planes on the posterior side of the heart or on both sides of the heart shadow, pay attention to the presence of supradiaphragmatic hernia sac and the appearance of gastric mucosal shadow inside the hernia sac during barium swallow examination, and observe the appearance of supradiaphragmatic esophagogastric ring. If one or more of the above signs appear on barium meal examination, the diagnosis of sliding hiatal hernia can be basically established. Endoscopy can be used to exclude esophageal ulcers, inflammation, strictures, and occupying lesions, etc., which can be seen as an upward shift of the dentate line.
Differentiation: This type is the most common, accounting for approximately 90% of all hiatal hernia cases. However, if not combined with a slight enlargement of the diameter of the opening of the gastroesophageal hiatus, the diaphragmatic esophageal membrane elongates and thins, allowing the gastric cardia to slide upward into the hiatus and subsequently into the thoracic cavity. There is no defect or fissure in the intra-abdominal muscular membrane covering the fissure and extending into the esophageal wall, so the hernia does not have a true hernia sac. In most cases of this hernia found on barium meal examination, the diaphragmatic esophageal membrane extending into the submucosa of the esophageal wall remains in its normal position, i.e. 3-4 cm above the esophagogastric junction (at the junction of squamous and columnar epithelial cells), and thus there are no symptoms of gastroesophageal reflux. In larger sliding hiatal hernias, a gastric sac >3 cm protrudes into the thoracic cavity, often with no degree of gastroesophageal reflux per time sign, which can be detected on barium meal examination when the patient is at rest. The diaphragmatic esophagus membrane can be found in these cases during surgery, and its extension into the esophageal wall is closer to the gastroesophageal junction than normal. It is unclear whether such a low extension is due to congenital or acquired factors. This hernia is less common, accounting for approximately 2% of all hiatal hernias, but is clinically significant because of the herniation of intra-abdominal organs into the thoracic cavity. This hernia has a defect in the diaphragmatic esophagus, usually anterior to the left of the hiatal hernia and occasionally posterior to the right. The presence of this defect allows the peritoneum to pass through this defect into a true hernia sac and the adjacent stomach to herniate into the thoracic cavity through the defect in this fascia. Since the diaphragmatic esophagus membrane is unable to restrain the upwardly displaced stomach for a long period of time, and since the thoracic pressure is lower than the abdominal pressure part of the time, this defect must progressively enlarge. In later stages, the entire stomach can herniate into the thoracic cavity, while the cardia remains partially fixed in place by the diaphragmatic esophagus membrane and the pylorus has moved closer to it, the stomach can rotate, twist, obstruct and narrow, and the thoracic stomach can dilate and rupture, and any of these complications can lead to death if the diagnosis and treatment are delayed. Because of these reasons, early surgery should be considered even in paraoesophageal hernias that do not yet have obvious symptoms. Paraesophageal hernia Figure 5 Paraesophageal hernia with full gastric herniation into the thoracic cavity As type II hernia increases in size, the diaphragmatic esophageal membrane usually thins and the dilated stomach continues to deform, dragging the gastric cardia upward, and once it is made to herniate out of the esophageal hiatus and reach above the diaphragm, it is called mixed esophageal hiatus hernia (type III). It is believed that when multiple abdominal organs, such as the colon and small intestine, enter the paraesophageal hernia sac at the same time, it should be called a multi-organ hiatal hernia (type IV). Mixed type hiatal hernia esophageal hiatal hernia is mostly seen in men and at older age, and its clinical symptoms are due to complications of gastroesophageal reflux or hernia. Sliding hiatal hernia (type I) rarely causes symptoms, but only when combined with pathological reflux; paraesophageal hernia can cause symptoms without reflux, and symptoms are caused by complications. The clinical manifestations of patients with paraesophageal hernia vary depending on the content of the hernia, but the common clinical features are premature infection with fullness during feeding, vomiting after heavy feeding, epigastric discomfort, dysphagia, and chest crepitations. Difficulty in swallowing is caused by the herniated viscus pressing on the esophagus from the outside. The herniated viscus squeezing the lung and occupying a part of the thoracic cavity can cause coughing and dyspnea after meals. If complicated by obstruction, stenosis, necrosis or perforation of the hernia contents, the patient has symptoms of shock and gastrointestinal obstruction, which can often be fatal in severe cases. Gastric reflux manifests as retrosternal discomfort and acid reflux, with discomfort from the subxiphoid process to the pharynx, and a burning sensation when severe. The symptoms may be aggravated by playing, lifting weights, or straining to defecate, and relieved by eating or taking antacids. The sensation of epigastric pain is often atypical and may be caused by an acute esophageal contracture. The nature of the pain is similar to that of peptic gastric and duodenal ulcers, biliary colic, and angina pectoris, and should be distinguished. The pain of hiatal hernia radiates to the lower back and even to the upper extremities and jaw, can be triggered by swallowing activities and aggravated by hot drinks or alcohol consumption. If angina cannot be excluded, the patient should first be admitted to the monitoring room for further examination. Gastric reflux can also cause sore throat, burning sensation in the mouth, and even irritation of the vocal cords resulting in hoarseness. Difficulty in swallowing is a common symptom of gastric reflux. In some patients there may be no esophagitis and dysphagia may be due to varying degrees of esophageal spasm or poor esophageal contraction. In patients with esophagitis, when significant constriction develops, dysphagia is only found when eating hard foods, and the burning sensation can be aggravated by eating hot foods, drinking cold beverages, or drinking alcohol. As the narrowing of the esophagus worsens, the amount of gastric juice returning to the esophagus becomes less and less, and the heartburn sensation gradually decreases. Dysphagia caused by diffuse esophageal spasm is different from that caused by constriction. The former is paroxysmal and is often misdiagnosed as hysterical globus, regardless of whether it is a case of motor dysfunction of eating solid or liquid food, with difficulty in swallowing or feeling a lump in the neck from gastric juice reflux. In a few patients, dysphagia is dripping due to food obstruction in the esophagus. Misaspiration caused by gastric reflux is common in patients with a nocturnal supine reflux pattern, usually forcing the patient to awaken due to coughing misaspiration. Severe aspiration can cause lung abscess, recurrent pneumonia, and bronchiectasis. Morning hoarseness is another symptom of nocturnal misaspiration. Gastric reflux occasionally causes asthma, and the issue of citation is debated. However, an asthmatic patient can have more frequent attacks due to gastric reflux. Bleeding due to reflux esophagitis is uncommon. Bleeding in ulcerative esophagitis can be chronic for hours with positive fecal occult blood, which can lead to anemia, or acute with massive bleeding, vomiting blood or black stools, leading to hemorrhagic shock. Most of the bleeding in the stool out of the enemy state is due to a diffuse ulcer in the esophagus or due to a penetrating ulcer in the gastric mucosal region arranged in the distal esophagus, and these patients are in urgent need of surgical treatment.
Treatment.
Most sliding esophageal hiatal hernias have minimal symptoms, and mild to moderate esophagitis is common in the country. These patients should be treated internally first. Measures can be taken such as taking acid suppressants, regulating diet, avoiding activities with elevated abdominal pressure, and sleeping in a high pillow position and left side lying. If reflux esophagitis has progressed to grade III, surgery should be considered to avoid esophageal stricture. Paraesophageal hernia should be treated with surgery early regardless of symptoms; mixed hiatal hernia should also be treated with surgery to avoid complications of gastric obstruction and striae narrowing. Regarding the medical treatment of reflux esophagitis, such as antacids, alginate or antacid combination drugs can relieve the symptoms and reduce the inflammation, but most of them use H2 receptor blockers, which have more certain efficacy. In severe cases, omeprazole (Loxacol) is superior to regular doses of ranitidine. All antacids, despite their recent efficacy, do not alter the natural course of the disease and have a high recurrence rate after discontinuation. Therefore, surgical treatment with hernia repair and antacid is eventually required.
Surgical treatment of esophageal hiatal hernia mainly takes into account the anatomical defect itself. Paraesophageal hernias, mixed hiatal hernias and multi-organ hiatal hernias may be complicated by clamping or strangulation of the gastric wall or other herniated intra-abdominal organs, and early surgery is indicated due to compression of the lungs by the massive hernia contents, despite the absence of obvious symptoms. Asymptomatic sliding hiatal hernias are followed only in portal rash and do not require surgery. Sliding hiatal hernia with reflux esophagitis should be considered for surgery when it progresses to ulcerative esophagitis, esophageal constriction or hemorrhage, or when it causes recurrent pulmonary infections due to reflux. Regarding the columnar epithelium-covered esophagus. Surgery has also been advocated to prevent cancer. Contraindications to surgery: Cases with acute infection, severe cardiopulmonary failure and hepatic and renal impairment and patients with advanced cancer are contraindicated. Age itself is not a contraindication to surgery, unless there are obvious signs of aging.
Surgical options Surgery for hiatal hernia and reflux esophagitis should include several steps to repair the relaxed esophageal hiatus, lengthen and fix the subdiaphragmatic esophageal segment, and reconstruct the anti-reflux valve mechanism. There are many approaches to treat reflux esophagitis and its complications, and the choice of procedure depends on the specific patient and surgeon. Factors that must be considered before choosing a surgical approach include: whether a thoracic or abdominal approach is unfavorable; whether the patient has a history of anti-reflux surgery; whether an esophageal resection or myotomy is required; and what is the patient’s physical condition? Surgical practice suggests that in patients with extensive and severe esophagitis, the thoracic approach facilitates the freeing of the esophagus and facilitates fundoplication; patients who have previously undergone antirheumatic surgery that failed to free the esophagus and require reoperation should be treated with the thoracic approach. In obese cases, the transperineal incision is more adequately exposed and is more likely to deal with combined pulmonary or mediastinal disease. In patients with controlled esophagitis and less obesity, the abdominal route may be used for the first antacid operation. A transabdominal approach is also possible in the presence of co-morbid abdominal disease requiring surgery. Repair of paraesophageal hernias is mostly done via the chest or abdominal route. Regarding sutures, absorbent sutures and acid-resistant absorbent sutures have been used previously. Currently, most surgeons use nonabsorbable sutures and noninvasive nonabsorbable sutures. Currently, the operations performed to repair sliding esophageal hiatal hernia and to correct gastroesophageal reflux are fundoplication, partial fundoplication, anatomic repair and repair using ligament flap.
Fundoplication: In 1956, Nissen reported fundoplication and reported its early results in 1963, and in 1973 Rossetti reported his modified fundoplication. Nissen called his fundoplication “valvuloplasty”. The fundus is completely wrapped around the lower esophagus and sutured to the right side of the lesser curvature of the esophagus. In this way, positive pressure from the stomach is transmitted to this new “collar” around the esophagus and compresses the esophagus. This unidirectional valve function allows food to enter the stomach from the esophagus but not to flow back into the esophagus from the stomach when the pressure inside the stomach is applied. This procedure resulted in the disappearance of symptoms in 875 patients, with an operative mortality rate of 0.6% and a recurrence rate of about 1% for postoperative hernia and reflux esophagitis.