Hiatal Hernia: Clinical Guidelines

List of Abbreviations

HH – hiatal hernia

GERD – gastroesophageal reflux disease

CT – computed tomography

HC – healthcare organization

MRI – magnetic resonance imaging

US – ultrasound examination

EGD – esophagogastroduodenoscopy

Terms and Definitions

A hernia is the protrusion of internal organs covered by peritoneum through natural or artificial openings (resulting from trauma or surgical interventions) in the abdominal wall, pelvic floor, or diaphragm beneath the outer integuments of the body or into another cavity.

Hernial ring – congenital or acquired defect in the musculoaponeurotic layer of the abdominal wall and/or diaphragm.

Hernia sac – a portion of the parietal peritoneum protruding through the hernial ring. The contents of the hernia sac may be represented by any abdominal organ.

Hiatal hernia – a disease associated with the displacement of the abdominal esophagus, cardia, upper stomach (in advanced cases - the entire stomach), as well as other organs, most frequently intestinal loops, through an enlarged esophageal hiatus into the thoracic cavity, causing compression and displacement of organs and structures of the posterior mediastinum.

Recurrent hiatal hernia – a hernia that appears in the area of a previously performed hernioplasty.

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Hiatal hernia (HH) is a condition associated with the displacement of the abdominal esophagus, cardia, upper stomach (in advanced cases, the entire stomach), and other organs—most commonly intestinal loops—through an enlarged esophageal hiatus into the thoracic cavity, causing compression and displacement of the organs and structures of the posterior mediastinum.

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

HH can be either congenital or acquired. Congenital HH is based on embryological developmental anomalies. Congenital short esophagus ("thoracic stomach") is an anomaly of the embryonic formation of the cardiac part of the digestive tract due to delayed esophageal growth in early embryogenesis. According to S.Ya. Doletsky's theory (1960), children are often born with moderately pronounced non-descended stomach, but the stomach subsequently migrates into the abdominal cavity. If reflux esophagitis develops concurrently, accompanied by scarring, the esophagus may become fixed in the mediastinum, thus forming a congenital HH.

A number of authors (B.P. Pokrovsky, N.N. Kanshin, et al.) believe that all cases of HH in childhood should be considered congenital.

Acquired HH develops in adulthood, although their occurrence in childhood cannot be ruled out.

According to one theory of HH pathogenesis (V.Ya. Barakov, 1957; V.I. Sobolev, 1957), the development of hernia in adults is associated with partial atrophy of muscle fibers, which becomes more pronounced in older age. As a result of atrophy, intermuscular connections weaken, the diaphragm lowers, and consequently, the esophageal hiatus enlarges. Muscle atrophy at a younger age is promoted by insufficient physical activity. This explains the fact that HH frequently develops in patients who do not engage in physical labor and do not lead an active lifestyle. Pulmonary emphysema also contributes to the descent of the diaphragm.

In addition to the enlargement of the esophageal hiatus, impairment of the fascial connections of the esophagus and stretching of the phrenoesophageal membrane play a role in the development of HH. This is linked, on the one hand, to a genetic predisposition in the form of so-called "connective tissue weakness." This explains why HH is frequently combined with hernias in other locations, flat feet, lower extremity varicose veins, and hemorrhoids. On the other hand, significant weight gain or rapid weight loss leads to stretching of the phrenoesophageal membrane [21].

The enlargement of the esophageal hiatus and relaxation of the phrenoesophageal membrane create anatomical prerequisites for the development of HH, while the triggering factor is an increase in the pressure gradient between the abdominal and thoracic cavities. Elevated intra-abdominal pressure promotes the "pushing" of the stomach into the chest. The second factor leading to the development of HH is considered to be the upward pulling of the cardia due to intense contraction of the longitudinal muscles of the esophagus. Bergmann first proposed this theory in the 1930s after observing, in experiments on dogs by stimulating the cervical vagus nerve, a jerky upward elevation of the stomach with simultaneous sharp longitudinal contraction of the esophagus. This mechanism can explain the development of HH in comorbid conditions accompanied by vagus nerve irritation, such as cholelithiasis, penetrating ulcers of the pancreas, etc. Proponents of this theory believe that all diseases that somehow lead to vagus nerve irritation contribute to the development of axial sliding HH.

Traumatic HH was first described by Stoianoff (1900). In 1962, Marchard first described several clinical cases of HH symptom onset in patients following closed abdominal trauma. At the same time, such HH cannot be called post-traumatic since there was no rupture of the diaphragm. Thus, it is believed that closed abdominal trauma can contribute to the development of HH in the presence of appropriate anatomical prerequisites.

Gastric and diaphragmatic surgeries can also lead to the development of HH. Furthermore, previously asymptomatic HH may become clinically manifest following these surgeries. The cause is the reflux of small bowel contents into the esophagus.

It is believed that a short esophagus forms as a result of reflux esophagitis, which develops due to concomitant gastroesophageal reflux disease (GERD) in sliding axial HH. Reflux esophagitis leads to inflammatory longitudinal cicatricial shortening of the esophagus. Another theory regarding the origin of esophageal shortening is based on the aforementioned experiments by Bergmann and is associated with longitudinal spastic contraction of the esophagus. According to this theory, spastic contractions of the smooth muscle of the esophagus are succeeded by the development of scar tissue, meaning there is a transition from a functional stage of the disease to an organic one. In this process, axial sliding HH develops secondarily as a result of esophageal spasm, while concomitant GERD and reflux esophagitis lead to the development of a short esophagus.

1.3 Epidemiology of the Disease or Condition

HH is a widespread condition: it occurs in 5% of the total adult population, with 50% of patients having no clinical manifestations and therefore remaining undiagnosed.

According to the Chief Surgeon of the Russian Ministry of Health, 4,680 elective surgeries for HH were performed in the Russian Federation in 2023. Laparoscopic procedures predominated (85.9%). Postoperative mortality was 0.18% [111].

1.4 Features of Coding the Disease or Condition

K44.0 Diaphragmatic hernia with obstruction, without gangrene

K44.1 Diaphragmatic hernia with gangrene

K44.9 Diaphragmatic hernia without obstruction or gangrene

1.5 Classification of the disease or condition

There is currently no universally accepted classification of HH.

Below are the HH classifications most widely used in domestic literature, which can be applied individually in clinical practice. It is advisable to adhere to the international classification, supplementing it with the B.V. Petrovsky and N.N. Kanshin classification of the short esophagus (1962), since if a patient has a short esophagus, its degree must be reflected in the diagnosis.

I. Anatomo-radiological classification of HH (the most common classification in Russia):

1. Sliding (axial) hernia - characterized by the fact that the abdominal esophagus, cardia, and fundus of the stomach can freely pass through the enlarged esophageal hiatus into the thoracic cavity and return back into the abdominal cavity (upon changing the patient's position).

2. Paraesophageal hernia - the terminal part of the esophagus and cardia remain below the diaphragm, but a portion of the gastric fundus penetrates the thoracic cavity and lies adjacent to the thoracic esophagus (paraesophageally).

3. Mixed hernia variant - a combination of axial and paraesophageal hernias.

II. Classification of HH based on the extent of gastric penetration into the thoracic cavity, rooted in radiological manifestations of the disease (I.L. Tager, A.A. Lipko, 1965):

Grade I HH: the abdominal esophagus is located in the thoracic cavity (above the diaphragm), the cardia is at the level of the diaphragm, and the stomach is elevated and directly adjacent to the diaphragm.

Grade II HH: the abdominal esophagus is located in the thoracic cavity, and a portion of the stomach lies directly in the area of the esophageal hiatus.

Grade III HH: the abdominal esophagus, cardia, and a portion of the stomach (fundus and body, and in severe cases the antrum) are located above the diaphragm.

III. Clinical classification of V.Kh. Vasilenko and A.L. Grebenev (1978), which is often presented in an abbreviated version:

• fixed or non-fixed hernias (for axial and paraesophageal hernias);

• axial hernia: esophageal, cardiofundic, subtotal and total gastric;

• paraesophageal hernia (fundic, antral);

• congenital short esophagus with "thoracic stomach" (developmental anomaly);

• other types of hernias (small bowel, omental, etc.).

When applying the classification of V.Kh. Vasilenko and A.L. Grebenev (1978), the diagnosis should be formulated in accordance with the full version of the classification:

1. Hernia type:

   • fixed or non-fixed (for axial and paraesophageal hernias);

   • axial: esophageal, cardiofundic, subtotal and total gastric;

   • paraesophageal (fundic, antral);

   • congenital short esophagus with "thoracic stomach" (developmental anomaly);

   • other types of hernias (small bowel, omental, etc.).

2. Complications:

   • reflux esophagitis (morphological characteristics: catarrhal, erosive, ulcerative);

   • peptic ulcer of the esophagus;

   • inflammatory cicatricial stenosis and/or shortening of the esophagus (acquired esophageal shortening), their severity grade;

   • acute or chronic esophageal (esophagogastric) hemorrhage;

   • retrograde prolapse of the gastric mucosa into the esophagus;

   • invagination of the esophagus into the hernia sac;

   • esophageal perforation;

   • reflex angina pectoris;

   • strangulated hernia (in paraesophageal hernias).

3. Causative factor:

   • digestive tract dyskinesia;

   • increased intra-abdominal pressure;

   • age-related weakening of connective tissue structures, etc.

4. Mechanism of hernia formation:

   • pulsion;

   • traction;

   • mixed.

5. Comorbidities.

6. Severity grades of reflux esophagitis:

   • mild grade (mild symptoms, sometimes absent; in this case, esophagitis is diagnosed based on esophageal X-ray, esophagoscopy, and targeted biopsy);

   • moderate grade (pronounced symptoms of the disease, deterioration of general well-being, and decreased performance);

   • severe grade (pronounced symptoms of esophagitis and the development of complications, primarily peptic strictures and cicatricial shortening of the esophagus).

IV. Petrovsky and N.N. Kanshin Classification of Hiatal Hernias (1962):

I. Sliding (axial) hiatal hernias:

1. esophageal hiatal hernia;

2. cardiac hiatal hernia;

3. cardiofundic hiatal hernia.

II. Paraesophageal hiatal hernias:

1. fundic hiatal hernia;

2. antral hiatal hernia;

3. intestinal hiatal hernia (small bowel and large bowel);

4. combined enterogastric hiatal hernia (combination of an intestinal hernia with one or another form of large gastric hernias);

5. omental hiatal hernia.

III. Giant hiatal hernias:

1. subtotal gastric hiatal hernia;

2. total gastric hiatal hernia.

IV. Short esophagus (brachyoesophagus) grades 1 and 2:

1. acquired short esophagus;

2. congenital short esophagus (thoracic stomach).

Grade 1 was defined by the authors as a short esophagus where the cardia is fixed no higher than 4 cm above the diaphragm. Grade 2: the cardia is located 4 cm or more above the diaphragm.

V. Modern anatomical classification adopted by consensus of most European countries and the USA (Types I-IV hiatal hernias):

Type I - sliding hiatal hernias, where the gastroesophageal junction is displaced above the diaphragm. The stomach is in its normal longitudinal position, and the gastric fundus remains below the gastroesophageal junction.

Type II - paraesophageal hernias; the gastroesophageal junction remains in its normal anatomical position, but part of the fundus adjacent to the esophagus herniates through the diaphragmatic hiatus.

Type III is a combination of types I and II: both the gastroesophageal junction and the fundus herniate through the esophageal hiatus of the diaphragm. The gastric fundus is located above the gastroesophageal junction.

Type IV: type III + other abdominal organs (colon, spleen, pancreas).

1.6 Clinical presentation of the disease or condition

The main symptoms of Type I hiatal hernias are manifestations of gastroesophageal reflux, the development of which is primarily associated with the widening of the angle of His and, consequently, flattening of Gubarev's valve. Hiatal hernias are accompanied by GERD in 80–90% of cases [54], with about 60% of patients with hiatal hernias complaining of gastroesophageal reflux [64]. Thus, not all Type I hiatal hernias are accompanied by gastroesophageal reflux, which explains the existence of so-called "asymptomatic" hiatal hernias. In patients with decreased gastric acidity, reflux is not accompanied by symptoms. It is generally accepted that the clinical manifestations of hiatal hernias are always caused by the presence of reflux esophagitis.

Hiatal hernia is a risk factor for the development of erosive reflux esophagitis [103].

It should be noted that the absence of macroscopic signs of esophagitis during EGD does not rule out its presence. As early as 1958, V.I. Saveliev, who studied the development of esophagitis in dogs after the formation of esophagogastric anastomoses, proved that histological preparations revealed esophageal mucosa damage more frequently than macroscopy did. The absence of macroscopic changes in the esophageal mucosa in long-standing gastroesophageal reflux is explained by varying individual resistance of the mucosa to hydrochloric acid. The state of esophageal innervation plays a significant role in this.

The most frequent symptom of hiatal hernia is pain, localized predominantly in the epigastric region, but it can also be retrosternal, and in the right or left hypochondrium. The pain is often burning in nature. Radiation of pain can vary, most often upwards (retrosternally, into the cardiac region, scapula, left shoulder, neck), but also into the left hypochondrium, both hypochondria, and even the lower back. In most patients, pain occurs some time after eating, especially in the supine position. Pain also frequently develops during physical exertion associated with bending the torso, physical or psycho-emotional stress. Pain syndrome cannot always be unequivocally linked to a hiatal hernia. Therefore, if the pain manifestation is not typical for reflux esophagitis, there is a high probability that the pain has another cause.

Reflux esophagitis is characterized by burning pain at the level of the xiphoid process behind the sternum, which intensifies after eating and in the horizontal position, and is accompanied by other typical symptoms of gastroesophageal reflux.

The second most frequent symptom in hiatal hernias is heartburn.

Regurgitation, which often reaches the oropharynx, is a consequence of gastroesophageal reflux, occurs suddenly in the horizontal position or when bending the torso, and is not accompanied by nausea. The suddenness of regurgitation causes aspiration, which induces a coughing fit and/or an unpleasant sensation of a "scratchy" throat, and sometimes leads to voice loss resulting from the chemical effect of the regurgitated fluid on the vocal cords.

Regurgitation, heartburn, and eructation are signs of cardiac incompetence, but all three symptoms rarely occur simultaneously in the same patient.

Nausea and vomiting are rare symptoms of hiatal hernias.

Dysphagia is most often associated with esophageal narrowing due to the development of a peptic stricture against the background of reflux esophagitis, or with oncology. Dysphagia directly related to hiatal hernia is rare and as a rule is mild, appears periodically, and often intensifies with anxiety and eating in a rush. Clinically, patients describe food getting stuck at the level of the xiphoid process in hiatal hernias.

The development of dysphagia can also be associated with the incarceration of paraesophageal hernias. In this case, dysphagia develops acutely and is accompanied by intense pain syndrome.

Shortness of breath and difficulty breathing in hiatal hernias occur predominantly in the horizontal position.

So-called "reflex angina pectoris" may develop in hiatal hernias.

Anemia in hiatal hernias can develop for various reasons. The first cause is reflux esophagitis. Bleeding can occur both from erosions of the esophageal mucosa and directly from the mucosa itself via diapedesis. Such bleedings are usually minor and lead to anemia in cases of long-term persistence. However, bleedings in erosive reflux esophagitis can also be profuse. The second cause is bleeding from the gastric mucosa. In particular, in cardioseptal/cardiofundic hiatal hernias, a significant part of the stomach is located above the diaphragm, and as a result of some compression of the organ at the level of the esophageal hiatus, venous outflow is impaired. At the same time, superficial erosions and ulcers easily form in the compression zone due to mechanical damage. Anemia in hiatal hernias is most often hypochromic, which can be associated both with bleeding and impaired iron absorption by the body. According to one theory, chronic trauma to the stomach wall (especially in large hiatal hernias) reduces its secretion, which in turn can negatively affect the body's iron absorption.

Some authors note the development of splenomegaly in hiatal hernias, which is associated with compression and thrombosis of the splenic vein.

Giant hiatal hernias often manifest as impaired evacuation of ingested food from the stomach. In clinical practice, this symptom is associated with the incarceration of the stomach in the hernia ring, which is not entirely correct, since the actual cause lies in the volvulus (torsion) of the stomach within the hernia sac. In English-language literature, the term "upside-down stomach" is used. The stomach twists by 180°, with the greater curvature facing right and the lesser curvature facing left. During exacerbation periods, the clinical picture resembles symptoms of pyloric stenosis, but with superimposed symptoms associated with the location of the expanded, fluid-filled stomach in the chest cavity rather than the abdominal cavity. Blood admixtures are often found in the vomit of such patients.

In an acquired short esophagus, GERD symptoms are usually pronounced and frequently combined with a peptic stricture.

2. Diagnostics, medical indications and contraindications for diagnostic methods

The diagnosis is established based on the detection of a hiatal hernia using one of the following methods: esophagogastroduodenoscopy (EGD), esophagography (barium swallow), or computed tomography.

2.1 Complaints and Anamnesis

• When interviewing a patient with hiatal hernia (HH), it is recommended to pay attention to complaints associated with the displacement of organs into the posterior mediastinum and complaints related to gastroesophageal reflux [1, 13, 21, 36, 59].

GCP BLoE 2Grade of Recommendation – B (Level of Evidence – 2).

Commentary. Complaints associated with the HH itself and those associated with gastroesophageal reflux differ. The anamnesis already makes it possible to suspect the presence of a large HH in a patient. Patients with sliding axial HHs present with complaints related to gastroesophageal reflux: burning pain without regurgitation of ingested food. Patients with paraesophageal HHs and mixed forms are more troubled by food regurgitation, postprandial pain, a sensation of retrosternal pressure, and respiratory symptoms. The presence of Cameron syndrome leads to the development of clinical symptoms of gastric bleeding and anemia, which is a frequent symptom in large HHs [101].

The development of Barrett's esophagus is often associated with HH [1, 51]. A meta-analysis published by Eusebi L.H. et al. (2021) revealed a correlation between the development of Barrett's esophagus and alcohol consumption, especially in patients with HH [51].

2.2 Physical Examination

• All patients with HH are recommended to undergo a physical examination (inspection, percussion, palpation, auscultation of the thoracic and abdominal cavities) with mandatory assessment of nutritional status [13, 15, 19, 24].

GCP CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Commentary. During the physical examination, attention must be paid not only to various clinical manifestations of HH, including nutritional deficiency, but also to the presence of disease complications.

2.3 Laboratory Diagnostics

Laboratory tests are of no diagnostic value in uncomplicated HH. They are ordered when preparing the patient for surgery. The scope of laboratory tests depends on the patient's comorbidities, the proposed type of anesthesia, and the surgical treatment method.

2.4 Instrumental Diagnostics

• Chest X-ray - is not recommended as a diagnostic method for HH [31, 45, 54].

GCR CLEL 5Grade of Recommendation — C (Level of Evidence — 5).

Commentary. A chest X-ray may suggest the presence of an HH in cases where the hernial protrusion is large and fixed in the posterior mediastinum. In such cases, there is soft tissue opacity in the chest with or without a fluid level. The presence of a retrocardiac fluid level on a chest X-ray is a pathognomonic sign of a paraesophageal hiatal hernia. A gas bubble in the chest is observed when the content of the HH consists of loops of the large intestine.

• As the primary diagnostic method for HH in patients with an established diagnosis and suspected HH, barium swallow X-ray of the esophagus and stomach is recommended [70, 81, 86, 88].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

Commentary. Barium swallow X-ray of the esophagus and stomach provides information on the size of the HH, the type of HH, the presence/absence of esophageal motility disorders, GERD-induced peptic stricture/stenosis, and also confirms or rules out a short esophagus and clarifies its degree [86]. Most published research results indicate that barium swallow X-ray remains an important method in the diagnosis of HH [70]. According to Siegal S.R. et al. (2017), HH can be diagnosed using this method if the size of the axial hernia is greater than 2 cm [88]. It is recommended to record a video esophagram, which provides additional information on the passage of the contrast agent through the esophagus [81].

• Computed tomography (CT) of the chest combined with CT of the abdomen is recommended for giant HHs, suspected incarceration of a paraesophageal HH, and in all unclear clinical situations, as well as to detect concomitant pathology [47, 86].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

Commentary. CT (A06.09.005 and A06.30.005) is not routinely recommended. CT is performed to obtain additional information about the location and type of HH when it is large. HH is frequently discovered incidentally during CT performed for other indications [86]. Dallemagne et al. (2018) recommend performing CT to rule out perforation, pneumoperitoneum, or pneumomediastinum [47]. CT is also indicated when HH incarceration is suspected [86].

• All patients with suspected HH or a confirmed diagnosis of HH are recommended to undergo esophagogastroduodenoscopy (EGD) [28, 46, 61, 86].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

Commentary. Following the collection of complaints, anamnesis, and physical examination, the baseline invasive diagnostic tool for HH is EGD, which allows visualization of the esophagogastric junction and exclusion of malignancy. In addition, EGD provides crucial information on the presence/absence of GERD, the severity of which must be described according to generally accepted classifications (e.g., the Los Angeles classification), Barrett's esophagus, Cameron ulcers, and lesions suspicious for malignancy [28, 46]. Displacement of the esophagogastric junction above the Z-line with intestinal metaplasia (Barrett's esophagus) must be described according to the Prague classification of Barrett's esophagus (2004) [61]. Roman S. et al. (2016) note that excessive air insufflation into the stomach during endoscopic examination can lead to an increase in hernia size [86].

2.5 Other Procedures

• In patients undergoing antireflux surgery for type I HH, it is recommended to perform 24-hour intraesophageal pH monitoring and high-resolution esophageal manometry to rule out esophageal motility disorders, such as achalasia [3, 28, 48, 64, 81, 83, 86, 106].

ACR BLEL 1Recommendation Readiness Level – B (Level of Evidence – 1).

Commentary. Functional esophageal surgery entails differential gastroesophageal diagnostics. 24-hour pH monitoring and high-resolution esophageal manometry are essential components for deciding on surgical treatment in patients with GERD combined with HH, typically type I. 24-hour pH monitoring is not a mandatory diagnostic method for HH, but it is important for the quantitative analysis of reflux episodes [81]. Prior to antireflux surgery in patients with type I HH, esophageal motility disorders associated with conditions such as achalasia must be ruled out [3, 28, 64, 83]. Esophageal motility can be assessed using high-resolution manometry (HRM) as it provides real-time pressure recording [86, 106]. However, catheter placement for manometry is quite challenging, and Dallemagne et al. (2018) reported that the method is effective in less than 50% of cases [48].

• In patients with symptomatic HH (types II, III, IV), routine 24-hour esophageal pH monitoring and high-resolution esophageal manometry are not recommended [24, 28, 31, 72, 94].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

Commentary. To detect gastroesophageal reflux, multichannel intraluminal impedance-pH monitoring is used, which in most cases allows the detection of acidic or weakly acidic gastroesophageal reflux, as well as recording gastric gas regurgitation [24, 28, 31].

In symptomatic HH (types II, III, IV), surgical indications are often determined by other criteria, therefore 24-hour pH monitoring and high-resolution esophageal manometry may be omitted [72, 94].

Magnetic resonance imaging (MRI) is recommended to be used in HH only for dynamic follow-up of operated patients to assess the position of the mesh implant when clinically indicated [72, 94].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

3.1. Conservative management

• Treatment of HH can only be surgical. There is no conservative treatment [1, 15, 24, 28, 31, 89].

Commentary. Conservative treatment consists of managing concomitant GERD and its complications, primarily reflux esophagitis [89].

3.2. Surgical treatment

Commentary. The goal of antireflux surgery in type I HH is to construct a fundoplication wrap in the lower third of the esophagus and thereby eliminate gastroesophageal reflux, whereas in symptomatic type II–IV HHs, the goal is to correct the abnormal position of the stomach and other organs displaced into the chest. The presence or absence of GERD in these patients is irrelevant in this context [102].

• Surgical treatment for patients with type I HH in the absence of GERD complications is not recommended [25, 33, 37, 49].

ACR BLEL 1Recommendation Readiness Level – B (Level of Evidence – 1).

• Surgical treatment is recommended for patients with type I hiatal hernia in the presence of GERD complications, as well as in cases of conservative GERD treatment failure for 6 months, or if the patient refuses long-term conservative therapy [6, 16, 17, 22, 23, 24, 27, 77, 101].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Comment. The indication for surgery for type I hiatal hernia is GERD [16, 17]. During surgery for GERD, fundoplication is mandatory and the hiatal hernia itself is repaired.

Indications for surgical treatment have changed little over the past years [6, 77, 111]. The first indication is the progression of GERD manifested by typical symptoms (heartburn, regurgitation), functional defects (cardioesophageal junction incompetence, hiatal hernia) and/or GERD complications (reflux esophagitis, Barrett's esophagus), as well as the need to increase drug doses due to the ineffectiveness of conservative treatment [22, 23, 24, 27].

The second indication is the presence of non-acid-related symptoms despite medical therapy, such as recurrent aspirations, "volume reflux", or regurgitation.

The third indication is the recurrence of symptoms upon attempting to discontinue medical therapy. Antireflux surgery is an alternative to long-term medical therapy, for example, in case of individual drug intolerance or patient refusal of conservative therapy [77, 111].

• Barrett's esophagus is recommended not to be considered a contraindication for surgical treatment of hiatal hernia [1, 2, 4, 26, 45, 60, 98].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Comment. The presence of Barrett's esophagus is not a contraindication for surgery in hiatal hernia [1, 2, 4, 26, 98]. At the same time, it has not been proven that surgical treatment with an antireflux component (fundoplication) in Barrett's esophagus prevents the development of malignancy [45, 98]. In this case, antireflux surgery serves to control and improve the clinical situation [60].

• Elective surgical treatment is recommended for patients with type II, III, and IV hiatal hernias [18, 31, 41, 47, 52, 75, 80, 109, 110].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Comment. Paraesophageal hiatal hernia is an indication for surgery, as confirmed by numerous studies [31, 41, 47, 75, 80, 109, 110]. The rationale is the gradual increase in hernia size with an increased risk of strangulation, which is associated with a high probability of complications and mortality in emergency surgeries [18]. However, the watchful-waiting concept is justified in some cases, since the risk of strangulation in paraesophageal hiatal hernia is 1.4% according to the literature [52]. Indications for surgery in type IV hiatal hernia are determined taking into account the high perioperative risk (pneumothorax, pneumonia, intrathoracic hemorrhage, empyema formation).

Surgical treatment of hiatal hernia must achieve the following goals: 1) tension-free reduction of the stomach from the mediastinum into the abdominal cavity; 2) functional reconstruction of the esophageal hiatus of the diaphragm without damaging the anterior and posterior vagus nerves; 3) elimination of gastroesophageal reflux on the one hand, while preventing the development of postoperative dysphagia following the creation of a partial or total fundoplication wrap on the other.

• Patients with hiatal hernia are recommended to undergo surgery via a laparoscopic approach [19, 31, 41, 47, 52, 75, 80, 109, 110].

GGR CLEL 4Grade of Recommendation – C (Level of Evidence – 4).

Comment. The laparoscopic approach in hiatal hernia surgery is currently the gold standard [19, 31, 41, 47, 52, 75, 80, 109, 110].

• The use of robotic-assisted systems in the treatment of patients with hiatal hernia is recommended at the discretion of the operating surgeon [9, 11, 42, 85].

GGR BLEL 3Grade of Recommendation – B (Level of Evidence – 3).

Comment. The use of robotic-assisted systems in hiatal hernia surgery demonstrates comparable outcomes to the laparoscopic approach, while surgical indications and methodology remain identical [9, 11, 42, 85].

• A laparotomy approach in the surgical treatment of patients with hiatal hernia is recommended in emergency situations when intraoperative complications develop, as well as in cases of peritonitis or gastric necrosis [7, 8, 12, 23, 25, 31].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Comment. Surgical conversion is sometimes necessary due to bleeding, splenic injury, or severe adhesions. Surgeons performing these operations laparoscopically must have the appropriate skills required for surgical conversion [7, 8, 12, 23, 25, 31].

• During esophageal mobilization in hiatal hernia surgery, both in laparoscopic and robot-assisted approaches, it is recommended to preserve the vagus nerve [1, 8, 95, 80, 82].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

Comment. During esophageal mobilization and creation of the fundoplication wrap, it is necessary to preserve the anterior and posterior trunks of the vagus nerve due to the risk of postoperative diarrhea, dumping syndrome, and bloating, as well as the long-term risk of cholecystolithiasis [1, 8, 95, 80, 82].

• During hiatal hernia surgery, both in laparoscopic and robot-assisted approaches, it is recommended to separate the hernial sac from mediastinal structures and then completely or partially excise it to facilitate the creation of the fundoplication wrap [50, 68, 99, 105].

GGR CLeD 4Grade of Recommendation – C (Level of Evidence – 4).

Comments. The mediastinally located hernial sac must be dissected during hiatal hernia surgery [68].

The results of scientific studies comparing complete and incomplete dissection of the hernial sac showed no differences in postoperative complications, except for early recurrence [50, 99, 105].

• During the mobilization of the greater curvature of the stomach and its fundus in hiatal hernia surgery, both in laparoscopic and robot-assisted approaches, short gastric vessels are not recommended to be routinely ligated and divided if fundoplication can be performed without tension [65, 66, 74].

ACR BLEL 1Recommendation Readiness Level – B (Level of Evidence – 1).

Comment. Complete division of all Vasa gastricae breves is accompanied by prolonged operative time and subsequent deterioration of the barrier function of the fundoplication wrap. On the other hand, complete division of Vasa gastricae breves along the greater curvature of the stomach facilitates the tension-free creation of a complete circular Nissen-Rossetti wrap [65, 66, 74].

• During the mobilization of the lesser curvature of the stomach in hiatal hernia surgery, both in laparoscopic and robot-assisted approaches, it is recommended to preserve aberrant or accessory hepatic arteries [96].

GGR BLeD 3Grade of Recommendation – B (Level of Evidence – 3).

Comment. During mobilization of the stomach along the lesser curvature, it is recommended to preserve aberrant or accessory hepatic arteries, which originate from the left gastric artery in 12% of cases [96].

• The choice of anterior or posterior crurorraphy is recommended at the discretion of the operating surgeon.

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Comment. When performing hiatal reconstruction, crural repair is of critical importance. Numerous publications on this topic demonstrate comparable results of anterior or posterior crural repair [74, 99]. Crural repair must not lead to narrowing of the esophageal hiatus to avoid the development of dysphagia. While a tight fundoplication wrap can be corrected using balloon dilation, a narrow esophageal hiatus will not respond to this intervention [48]. Standard routine esophageal stenting using a large-caliber gastric tube (32Ch) is described by many authors [48], but can be omitted given sufficient experience of the operating surgeon.

• Alloplasty of the esophageal hiatus with a mesh implant during hiatal hernia surgery—both in laparoscopic and robot-assisted approaches in patients with type II, III, and IV hiatal hernias—is recommended to be chosen on an individual basis [20, 25, 33, 34, 35, 37, 57, 58, 59, 68, 69, 77, 79, 87, 90, 92, 102, 104, 107].

GGR ALeD 1Grade of Recommendation – A (Level of Evidence – 1).

Comments. Since the first description of mesh repair for hiatal hernia by Kuster and Gilroy in 1993 [69], numerous variations of hiatal herniorrhaphy with mesh reinforcement have been published [20, 25, 57, 58, 79, 87, 107].

International clinical guidelines for the treatment of inguinal and incisional hernias recommend always using mesh implants, except in certain specific situations [34, 35, 77, 90, 104]. Conversely, routine mesh reinforcement for hiatal hernia remains controversial. Specifically, the Society of American Gastrointestinal and Endoscopic Surgeons (SAGES) considers the low recurrence rate to be an advantage of mesh repair in hiatal hernias. However, due to the limited number of evidence-based studies on this topic and the relatively high risk of mesh-related complications (such as dysphagia and esophageal perforation), SAGES does not recommend routine mesh reinforcement [68].

The pathogenesis of hiatal hernias, like other hernias, is multifactorial. It is generally accepted that elevated intra-abdominal pressure contributes to hernia development. While circular, tension-free, large-pore, structurally stable monofilament mesh implants extending well beyond the hernia defect margins are used in other hernia repairs, debates on this topic continue in hiatal hernia surgery [37, 104].

If a specific defect size and the condition of the surrounding soft tissues preclude tension-free primary closure, mesh use is recommended. Details such as the type of mesh, surgical access, and the required overlap of the hernia defect remain subjects of debate [33, 34, 37, 68, 77, 78, 90, 104].

First, it is necessary to standardize the defect size that serves as an indication for mesh reinforcement. Second, the technique for mobilizing the crura at the esophageal hiatus must be standardized. Third, a safe and appropriate type of mesh implant for hiatoplasty should be selected [58, 59]. MRI allows for the documentation of the mesh implant status during postoperative patient follow-up. Preliminary results from a single-center study showed a 6% hiatal hernia recurrence rate 2 years after mesh repair, with no mesh-related complications [102].

Evidence indicates the superiority of mesh repair over primary suture cruroplasty in terms of postoperative recurrence rates for large or paraesophageal hiatal hernias and in patients with GERD. Further clinical trials are needed to standardize the hernia defect size indicating mesh implantation, the mesh type and shape, and the technique for securing it to the defect. Additionally, long-term postoperative follow-up is required to identify specific complications associated with mesh reinforcement in hiatal hernia surgery.

A meta-analysis by Müller-Stich et al. (2015) demonstrated that mesh reinforcement should be performed routinely during laparoscopic repair of paraesophageal hiatal hernias [79].

Some experts recommend using biological implants for reinforcement. However, these recommendations are generally based on the authors' personal experience [92].

• In patients with type II, III, and IV hiatal hernias when a hernia protrusion (separation of the crura) greater than 5 cm in size is detected during surgery, whether via laparoscopic approach or robotic-assisted technologies, it is recommended to perform hiatal hernia repair with mesh reinforcement [15, 23, 53, 58, 68, 76, 80, 87].

GGR ALeD 1Grade of Recommendation – A (Level of Evidence – 1).

Comment. For large hiatal hernias (>5 cm), SAGES clinical guidelines recommend mesh repair due to lower recurrence rates [68]. There is a lack of long-term postoperative follow-up data after mesh repair, which precludes definitive conclusions regarding its safety concerning specific mesh-related complications. For example, 6–12 month follow-up data indicate hiatal hernia recurrence rates of 22–26% with primary sutures versus 0–8.6% with mesh repair [15, 23, 53, 58, 80]. A meta-analysis published by Memon et al. (2016) showed no difference between mesh repair and primary sutures, except for a lower recurrence rate with mesh [76]. Similar results were obtained in a meta-analysis by Sathasivam R et al. (2018) [87].

• Routine mesh reinforcement during antireflux surgery in patients with type I hiatal hernia is not recommended [15, 23, 53, 58, 80].

ACR BLEL 2Recommendation Readiness Level – B (Level of Evidence – 2).

Comment. Hiatal hernia repair combined with cruroplasty and fundoplication is highly effective in treating GERD [80]. When type I hiatal hernia is combined with GERD, the esophageal hiatus is usually only mildly widened, and tension-free primary closure without mesh is feasible in almost all cases.

• In patients with any type of hiatal hernia, following the reduction of the hernia protrusion and cruroplasty, additional fundoplication is strongly recommended as a mandatory step [5, 30, 32, 37, 39, 40, 43, 49, 58, 62, 73, 76, 84].

GCR ALEL 1Grade of Recommendation – A (Level of Evidence – 1).

Comment. Fundoplication should be performed during hiatal hernia repair regardless of the presence of GERD. A prospective study by Granderath FA et al. (2007) demonstrated that surgical outcomes in patients undergoing hiatal hernia mesh repair combined with fundoplication were superior compared to those who underwent mesh repair combined with cardiophrenicopexy [58].

Despite ongoing discussions, literature data demonstrate comparable results between partial (180°, 270°) and total (360°) fundoplication wraps.

Thus, a meta-analysis by Broeders et al. (2013) showed comparable outcomes between partial and total fundoplications, with a lower incidence of postoperative dysphagia in partial fundoplication [37]. A meta-analysis by Chrysos E. et al. encompasses 5 randomized controlled trials from 2004 to 2015 [32, 39, 40, 43, 84] and one randomized controlled trial translated from Chinese [49]. A comparative analysis was conducted between 266 patients with total fundoplication (360°) and 265 patients with a 180° fundoplication wrap. Postoperatively, no statistically significant differences in outcomes were found, except that the partial fundoplication group had a higher rate of reoperations due to GERD recurrence. The total fundoplication group had a higher incidence of dysphagia that did not require reoperation. Given these findings, the authors see no definitive advantage between the two types of fundoplication wraps, especially since patient satisfaction rates were high in both groups (94.2% and 89.4%).

Since this meta-analysis showed a higher incidence of dysphagia in the total fundoplication group, the feasibility of performing a 270° Toupet fundoplication instead of a total fundoplication has been discussed. However, this has not been statistically proven [36, 49, 73].

A meta-analysis by Memon et al. (2015) showed that gastroesophageal reflux occurs more frequently after anterior fundoplication, but with a lower incidence of dysphagia. However, only anterior versus posterior partial fundoplications were compared, and a fundamental advantage of partial over total fundoplication has not been proven [76].

There is a lack of clinical studies comparing 360° vs. 270° fundoplication wraps in the surgical treatment of type III–IV hiatal hernias [5, 30, 62]. The only single-center retrospective study on long-term outcomes of type III/IV hiatal hernia repair showed comparable results between the groups. Patient satisfaction was higher in the total fundoplication group [62].

• Gastropexy is not recommended as a standalone procedure in patients with type I–IV hiatal hernias and should be used only as an adjunct to the main surgical technique in certain clinical scenarios at the operating surgeon's discretion [32, 39, 40, 43, 84].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

Comment. Some authors have described hernia reduction and gastropexy without crurorrhaphy or excision of the hernial sac, particularly in patients with severe symptoms. Mortality and complications were low, but radiological recurrence was detected in 22% at 3 months. The outcomes of this surgical approach are inferior to standard surgical techniques, and therefore gastropexy alone should not be the primary goal of the operation [32, 39, 40, 43, 84].

• In the event of HH recurrence, reoperation is recommended only for patients with symptoms of HH and/or GERD [7, 8, 10, 12, 13, 38, 48, 55, 56, 71, 91, 97, 108].

GGR BLeD 3Grade of Recommendation – B (Level of Evidence – 3).

Comment. There is no standardized definition of recurrence following surgical treatment of HH [7, 8, 10, 12]. Recurrence may be based solely on radiological findings, but often the patient is asymptomatic and therefore has no recurrent symptoms. Lidor A.O. et al. (2015) compared symptoms with radiological findings on barium esophagram. They determined that radiologically recurrent hernias >2 cm correlate with worsening symptoms and thus defined a recurrent hernia as vertical extension of the gastric mucosa above the diaphragm >2 cm [71]. If fundoplication was not performed, a more general definition of recurrence is any new evidence of paraesophageal hernia or proximal migration of the cardia on contrast barium study or CT [48]. As part of the follow-up workup for radiologically confirmed HH recurrence, it is advisable to perform 24-hour pH monitoring, which makes it possible to detect GERD recurrence in so-called "asymptomatic" recurrences.

Indications for reoperation in the presence of confirmed HH recurrence may include recurrent gastroesophageal reflux; dysphagia; disruption or displacement of the fundoplication wrap into the chest through the diaphragmatic hiatus defect; displacement of more than 30% of the stomach into the chest (i.e., paraesophageal HH); medically refractory gas-bloat syndrome; and pain.

When deciding on reoperation, it should be taken into account that outcomes following reoperation for paraesophageal hernia are worse than after primary surgery [56]. Following primary surgery, symptoms are absent in 85–90% of cases, whereas after reoperation this figure is only 70% [97]. The rate of surgical conversion is higher in reoperation (up to 33%) [38, 55, 91]. The duration of surgery and hospital stay is also greater in reoperation [38, 108].

The rate of intraoperative complications during reoperation is higher: one study reports 13.1% esophageal or gastric injuries and 3.4% pneumothorax [56]. In the setting of reoperation, the risk of vagus nerve injury increases dramatically [56]. In the event of vagus nerve injury, pyloroplasty may be performed. If HH recurrence is accompanied by the clinical presentation of bilateral vagus nerve injury that occurred during the primary HH surgery (confirmed impaired gastric passage, pronounced gastroptosis detected during pre-reoperation evaluation), distal gastric resection, preferably Roux-en-Y, may be added to fundoplication. Making a decision to perform a resection based solely on data obtained by the surgeon intraoperatively during reoperation is not justified. Performing gastric resection for HH recurrences may also be justified if the patient has biliary duodenogastric reflux [97, 108].

Quality of life scores differ when comparing primary and repeat operations [13, 38, 97, 108]. One study showed that patients who underwent reoperation reported worse quality of life scores regarding criteria such as a feeling of fullness, belching, nausea, reflux, and overall gastrointestinal status compared to patients who underwent primary surgery [38]. However, another study found no difference in postoperative quality of life between primary and repeat operations using several quality of life questionnaires [97].

Reoperation should be performed only by experienced surgeons in high-volume medical centers. Reoperation should be offered only to patients with HH symptoms and objective evidence of prior surgical failure [108].

Patients should be informed prior to surgery that reoperation may not lead to complete resolution of symptoms. A thorough preoperative evaluation to determine the likely cause of initial failure and a comprehensive analysis of the patient's current condition is crucial.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

Rehabilitation is carried out in specialized care departments (Phase I), inpatient medical rehabilitation departments (Phase II), and outpatient rehabilitation departments, day hospital rehabilitation departments, and sanatorium rehabilitation departments (Phase III).

Rehabilitation is organized by a multidisciplinary rehabilitation team consisting of: a surgeon, a physical therapy physician, a medical psychologist, an occupational therapist, a physical rehabilitation specialist, and a gastroenterologist. During Phase I, the attending physician is a surgeon (thoracic surgeon), and all rehabilitation measures are coordinated with them and with the anesthesiologist-intensivist (while the patient is in the ICU). Other specialists may be involved if necessary. There is no evidence of the superiority of specific physiotherapy methods in HH; physiotherapy may be considered as an alternative and adjunctive technique to baseline care.

• Medical rehabilitation is recommended for all patients with HH; the choice of the optimal rehabilitation method depends on each specific case of the disease [2, 8, 47, 103].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

• Medical rehabilitation for patients with HH is recommended to be started as early as possible and carried out concurrently with treatment [4, 28, 55, 103].

GGR CLEL 5Grade of Recommendation – C (Level of Evidence – 5).

• On the first day after surgery, in addition to pain relief with non-narcotic analgesics (in accordance with the ATC system: N02B other analgesics and antipyretics), early mobilization, breathing exercises, and slow walking within the ward are recommended for all patients [17, 49, 74].

CGR CLOE 5Level of Recommendation Credibility – C (Level of Evidence – 5).

• Sanatorium-and-spa treatment is recommended for patients after completing treatment for HH [4, 8, 103].

GCP CLoE 5Recommendations Grade C (Level of Evidence – 5).

5. Prevention and Dispensary Observation

There are no reliable methods for preventing HH, as there are no ways to influence the predisposing causes of the disease.

To prevent hernia recurrence in the postoperative period, smoking cessation, limitation of prolonged and heavy physical labor, and the prevention and treatment of COPD and constipation are recommended for patients [2, 8, 10, 40, 103].

CGR CLOE 5Level of Recommendation Credibility – C (Level of Evidence – 5).

• Dispanserization (clinical follow-up) is recommended for non-operated patients with HH who have severe comorbid conditions or in case of refusal of surgical intervention [10, 55, 106].

CGR CLOE 5Level of Recommendation Credibility – C (Level of Evidence – 5).

Comments. Given the high risk of recurrence, operated patients with recurrent hernias may constitute a special follow-up group [10, 55, 106].

• A follow-up clinical examination by a surgeon of a patient after surgery for HH is recommended at 3 months and 12 months, and then at least once a year for 3 years [2, 47, 74, 106].

CGR CLOE 5Level of Recommendation Credibility – C (Level of Evidence – 5).

• Follow-up barium swallow esophagogastroduodenoscopy is recommended to be performed in patients at 3 months and 12 months after surgery, and thereafter only as indicated if there is a suspicion of HH recurrence [10, 58, 84].

CGR CLOE 5Level of Recommendation Credibility – C (Level of Evidence – 5).

6. Organization of Medical Care

The organization of medical care for patients with HH is carried out in accordance with the Procedure for Providing Medical Care to the Adult Population Profile "Surgery" (Order of the Ministry of Health of the Russian Federation No. 922n dated November 15, 2012).

Primary specialized health care is provided by a surgeon. If a hiatal hernia (HH) is suspected or detected in a patient, general practitioners, district general practitioners, family physicians, medical specialists, and mid-level medical personnel shall refer the patient in the established manner for a consultation with a surgeon to receive primary specialized health care. If medical care cannot be provided within the framework of primary health care and there are medical indications, the patient is referred to a medical organization providing specialized medical care in the profile of «surgery».

Specialized medical care is provided by surgeons and thoracic surgeons in inpatient settings and includes the prevention, diagnosis, and treatment of diseases and conditions requiring the use of special methods and complex medical technologies, as well as medical rehabilitation.

Surgical treatment of patients with HH in emergency situations (incarceration) can be performed in surgical and thoracic surgery departments of medical organizations at all levels. Elective surgical treatment of HH should preferably be performed in surgical or thoracic surgery departments of level III medical organizations. In complex cases of HH (type III and IV HH, recurrent HH, in patients with concomitant diseases, including cardiovascular and respiratory systems, diabetes mellitus, or when there are indications for simultaneous surgeries), surgical treatment should preferably be performed in level III medical organizations or federal centers specializing in the treatment of this category of patients.

Indications for planned hospitalization:

• Type II HH;

• Type III HH;

• Type IV HH;

• HH recurrence;

• Type I HH with GERD complications, as well as in the absence of effect from conservative GERD treatment for 6 months or patient refusal of long-term conservative GERD therapy.

Indications for emergency hospitalization:

Presence of a diagnosis of incarcerated HH for emergency surgical intervention.

Indications for patient discharge from the hospital:

Patient mobilization after surgery, absence of complications from the postoperative wound, internal organs, and body systems.

7. Additional Information

The outcome of the disease or condition may be influenced by:

• polyvalent allergy;

• history of leukemia, oncological diseases, tuberculosis, or a positive test for HIV infection, hepatitis B and C, syphilis;

• pronounced congenital defects confirmed by medical history and/or physical examination, leading to impaired normal life activity and requiring correction (congenital malformations of the heart, gastrointestinal tract, urogenital system, skeleton; Marfan syndrome, Klinefelter syndrome, Edwards syndrome, Opitz syndrome, Goldenhar syndrome, and others);

• cardiovascular diseases: post-infarction cardiosclerosis, silent myocardial ischemia, pericarditis, aortic aneurysm, grade III hypertension, effort angina, unstable angina, Prinzmetal angina;

• clinically significant rhythm and conduction disturbances (atrial fibrillation/flutter, frequent ventricular extrasystole of the bi(tri)geminy type, ventricular tachycardia, complete left bundle branch block, trifascicular block, ventricular fibrillation, sinoatrial block greater than degree I, atrioventricular block degree II-III, Fredericks syndrome);

• chronic heart failure grade III - IV according to NYHA;

• chronic cor pulmonale in the stage of decompensation;

• bronchial asthma;

• pulmonary embolism;

• acute myocardial infarction;

• acute cerebrovascular accident;

• transient ischemic attack;

• acute pneumonia, pleurisy;

• systemic connective tissue diseases according to medical history – systemic scleroderma, systemic lupus erythematosus, systemic vasculitis, antiphospholipid syndrome, dermatomyositis, sarcoidosis, rheumatism, and others;

• type I and II diabetes mellitus;

• obesity with a body mass index greater than 40;

• acute renal failure;

• chronic kidney disease with a glomerular filtration rate of less than 30 ml/min;

• gastric and duodenal ulcers in the acute stage, liver cirrhosis;

• multiple sclerosis and other demyelinating diseases;

• any history of psychiatric disorders;

• any history of hematological disorders;

• history of drug addiction or chronic alcoholism;

• pregnancy/lactation period.

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Allakhverdyan Alexander Sergeevich - Doctor of Medical Sciences, Professor, Head of the Department of Thoracic Surgery, Russian University of Medicine of the Russian Ministry of Health

2. Anipchenko Alexey Nikolaevich – Doctor of Medical Sciences, Deputy Chief Medical Officer for Surgical Care, City Clinical Hospital named after M.P. Konchalovsky of the Moscow City Health Department

3. Anischenko Vladimir Vladimirovich – Doctor of Medical Sciences, Professor, Head of the Department of Surgery, Novosibirsk State Medical University

4. Gallyamov Eduard Abdulhaevich - Doctor of Medical Sciences, Associate Professor, Head of the Department of General Surgery, I.M. Sechenov First Moscow State Medical University of the Russian Ministry of Health (Sechenov University)

5. Gankov Viktor Anatolyevich – Doctor of Medical Sciences, Associate Professor, Professor of the Department of General Surgery, Operative Surgery and Topographic Anatomy of the Faculty of General Medicine, Altai State Medical University of the Russian Ministry of Health

6. Puchkov Konstantin Viktorovich – Doctor of Medical Sciences, Professor

7. Sazhin Alexander Vyacheslavovich – Doctor of Medical Sciences, Professor, Corresponding Member of the RAS, Head of the Department of Faculty Surgery No. 1 of the Faculty of General Medicine, Pirogov Russian National Research Medical University of the Russian Ministry of Health

8. Starkov Yury Gennadievich – Doctor of Medical Sciences, Professor, Head of the Surgical Endoscopic Department, A.V. Vishnevsky National Medical Research Center of Surgery of the Russian Ministry of Health

9. Cherkasov Denis Mikhailovich – Doctor of Medical Sciences, Professor of the Department of Surgical Diseases No. 2, Rostov State Medical University of the Russian Ministry of Health

Appendix A2. Methodology for Developing Clinical Guidelines

The purpose of these guidelines is to provide practitioners with modern concepts of the etiology and pathogenesis of hiatal hernias, to familiarize them with modern algorithms for the diagnosis and treatment of the main clinical variants of this disease, but they do not constitute a universal and comprehensive protocol of care.

In situations not described in these guidelines, as well as in critical situations and/or under conditions of limited resources, it is advisable to proceed from the provisions of other consensus documents, decisions of local ethics committees and medical boards, personal experience and common sense.

Target audience of these clinical guidelines: surgeons, thoracic surgeons, anesthesiologists-resuscitators, gastroenterologists, cardiologists, emergency medicine doctors, emergency department doctors, general practitioners, district general practitioners, family physicians, radiologists, ultrasound diagnostics physicians, functional diagnostics physicians.

Table 1. Scale for grading the levels of evidence (LE) for diagnostic methods (diagnostic interventions)

Table 2. Scale for grading levels of evidence certainty (LEC) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions)

Table 3. Scale for grading grades of recommendation (GR) for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, and rehabilitative interventions)

Procedure for updating clinical guidelines

The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.

Appendix A3. Reference Materials

These clinical guidelines were developed taking into account the following regulatory legal documents:

1. Federal Law No. 323-FZ dated November 21, 2011 "On the Fundamentals of Protecting the Health of Citizens in the Russian Federation", Articles 37 and 79;

2. Decree of the Government of the Russian Federation No. 1968 dated November 17, 2021 (as amended on March 14, 2024) "On Approval of the Rules for the Phased Transition of Medical Organizations to the Provision of Medical Care Based on Clinical Guidelines Developed and Approved in Accordance with Parts 3, 4, 6-9 and 11 of Article 37 of the Federal Law 'On the Fundamentals of Protecting the Health of Citizens in the Russian Federation'";

3. Order of the Ministry of Health of the Russian Federation No. 922n dated November 15, 2012 "On Approval of the Procedure for Providing Medical Care to Adults in the Profile 'Surgery'";

4. Order of the Ministry of Health of the Russian Federation No. 203n dated May 10, 2017 "On Approval of Criteria for Assessing the Quality of Medical Care".

Appendix B. Physician Action Algorithms

Appendix C. Patient Information

Possible complications and consequences of surgical treatment of hiatal hernia.

When performing surgical treatment for hiatal hernia, there is a risk of developing the following complications: bleeding, intraoperative damage to adjacent organs and structures, and infectious complications. In all surgeries at the esophagogastric junction, there is a risk of vagus nerve injury, which can lead to delayed gastric emptying of ingested food in the postoperative period. In very rare cases, due to adhesion fixation of the stomach to the diaphragm, damage to the gastric wall may occur during surgery. According to the literature, the incidence of the aforementioned complications in hiatal hernia surgeries is 10-20%.

When laparoscopic surgeries for hiatal hernia are performed, long-term postoperative treatment results are quite favorable. Within the first three years after surgery, 8-12% of operated patients develop a recurrence, i.e., the hiatal hernia returns. However, among patients with recurrent hiatal hernias, no more than 10% require re-operation. The remaining patients are free from hiatal hernia symptoms for a long time.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

No.