Line Z. Catalog of fire alarm devices Z line above
Studies with long-term pH monitoring have shown that even in healthy people, short-term episodes of gastroesophageal reflux (GER) occur, usually after eating an excess meal.
Over the past 30 years, much experimental work has been carried out in the field of pathophysiology of reflux esophagitis. These studies proved the polyetiology and multifactorial nature of this disease. It is known that the pathogenesis of reflux esophagitis is based on cardia insufficiency and disruption of its valvular function. Most often, destruction of the antireflux mechanism of the cardia occurs with a sliding hiatal hernia (HHH), especially with a short esophagus - in this case, reflux esophagitis is most pronounced. Ulcerative pyloric stenosis, especially in combination with cardiac hernia of the pyloric hernia, significantly contributes to the development of reflux esophagitis. Gastric resection and gastroenterostomy lead to the reflux of bile into the stomach, in such cases the so-called “alkaline reflux esophagitis” can develop. Esophagitis easily occurs in some cases with severe vomiting (for example, after various operations, with toxicosis of pregnancy). Often, severe reflux esophagitis occurs as a result of prolonged tube drainage of the stomach, since a standing tube actually causes cardial failure. Reflux esophagitis develops after previous operations on the cardia, destroying its pneumo-valve mechanism.
According to the degree of severity, they are distinguished:
Mild esophagitis, which is macroscopically characterized by hyperemia and edema of the mucous membrane.
At moderate esophagitis these changes worsen, erosions appear on the mucous membrane.
Severe esophagitis characterized by gross changes in the form of ulcers covered with fibrin against the background of a sharply inflamed, easily bleeding mucous membrane, which in the distal esophagus can be completely destroyed or replaced by intestinal-type metaplastic columnar epithelium - the so-called. Barrett's esophagus. The same stage is also characterized by the development of a peptic (“round”) ulcer of the esophagus. Severe reflux esophagitis often ends in the formation of a cicatricial peptic stricture of the esophagus. Peptic strictures are usually localized in the lower third of the esophagus. This area is most exposed to aggressive gastric juice. The inflammatory process usually affects all layers of the wall of the esophagus, but pathological changes are most pronounced in its mucous membrane and submucosal layer.
Peptic strictures are divided into short (less than 3 cm) and long (most often from 3.5 to 6–7 cm in length).
Long-term inflammation leads to shortening of the esophagus, while the cardia of the stomach is further retracted into the posterior mediastinum (therefore the sliding hernia becomes fixed), and the anti-reflux mechanism of the cardia is increasingly destroyed - this is how a vicious circle is closed, when inflammation in the esophagus contributes to its shortening, and the short The esophagus supports reflux.
Barrett's esophagus or Barrett's syndrome is a pathological replacement of the squamous epithelium of the lower third of the esophagus with specialized (intestinal-type metaplastic) columnar epithelium. On endoscopic examination, lesions of Barrett's epithelium appear as tongues of bright red epithelium (visually indistinguishable from the epithelium of the gastric cardia) rising above the dentate (Z-line) line.
Figure - Endoscopic view of Barrett's esophagus
Normally, the Z-line tongues can rise 2-3 cm above the main level of the esophagogastric junction, so the so-called long Barrett's segment (more than 3 cm long). A special role is played by the detection of incomplete intestinal metaplasia and severe dysplasia in Barrett's epithelium, which is currently considered as an obligate precancer. The likelihood of developing adenocarcinoma in Barrett's esophagus increases almost 10-fold when foci of severe dysplasia occur in the Barrett's epithelium.
A muscular tube connecting the oropharynx to the stomach. It begins at the level of the lower edge of the cricopharyngeal muscle. The length of the esophagus is approximately 25 cm. Its upper third is formed by striated muscles, the rest is smooth. The inside of the muscular tube is lined with flat epithelium.
IN mediastinum esophagus surrounded by two trunks of the vagus nerve, trachea, aorta, and heart. Using a barium contrast X-ray on the esophagus, it is possible to detect impressions from the aorta and left bronchus, and not only the structure of the normal mucous membrane can be seen, but also a slight narrowing approximately 2 cm below the diaphragm; the expansion underneath is called the “ventricle” or “diaphragm ampulla”.
At X-ray examination this formation should not be confused with a hiatal hernia. The esophagus enters the stomach at the angle just below the diaphragmatic notch and approximately 40 cm from the edge of the incisors.
Food passes through the esophagus due to the coordinated contraction of its muscle layers. This wave of peristalsis is relatively slow: its speed towards the stomach is 2-6 cm/s. In response to chewing, primary peristalsis occurs, and secondary peristalsis begins below the subpharyngeal region in the absence of previous chewing movements. The barrier function of the esophagus depends on the functional state of the upper cricopharyngeal sphincter and lower esophageal sphincter (LES).
In area NPC the pressure is quite high (normally 15-35 mm Hg), along the lower 3-4 cm of the esophagus it has similar values; in this case there is no specific anatomical structure. Esophageal motility manometry is usually performed using a transnasal catheter. Normally, when swallowing, the cricopharyngeal sphincter relaxes until the bolus passes, its contraction occurs, and then peristaltic contractions occur along the body of the esophagus.
Endoscopic picture of the esophagus of a healthy person. Pale pink mucous membrane visible: 1 - normal mucous membrane
NPC relaxes only immediately before the wave of contractions reaches it, thus ensuring the passage of the bolus of food into the stomach. However, contraction of the LES alone is not enough to prevent gastroesophageal reflux - at the same time, compression of the subphrenic part of the esophagus occurs as a result of an increase in intragastric or intra-abdominal pressure. The entry of the esophagus into the stomach at an angle in this case plays the role of an additional protective factor.
Inside the esophagus pH usually reaches values of 5-7; prolonged low levels (less than 4) are considered abnormal. Acidity is best assessed using 24-hour pH monitoring.
Variant of the norm. Transition of squamous epithelium to columnar epithelium (Z-line): 1 - entrance to the stomach;
2 - columnar epithelium (mucous membrane of the “gastric” type);
3 - transition of squamous epithelium to cylindrical (Z-line);
4 - squamous epithelium of the esophageal mucosa
At endoscopy The esophagus looks like a smooth tube with visible vessels in the submucosal layer. At the junction of the esophagus with the stomach, the transition from the mucous membrane of one organ to the mucous membrane of another organ usually takes the form of an irregular circular stripe known as the Z-line, or gastric rosette. During examination, peristalsis waves can often be observed.
Esophageal lumen lined with non-keratinizing squamous epithelium. Papillae - protrusions of the lamina propria of the mucous membrane - penetrate a short distance into the epithelium. The lamina propria is separated from the submucosal layer by smooth muscle fibers, or the muscular lamina mucosa. The circular muscle fibers lie deeper than the submucosal layer, and the intermuscular nerve plexus runs between them and the external longitudinal muscles.
Esophagography for poorly differentiated cancer of the upper lobe of the right lung
Educational video on the anatomy of the esophagus and its narrowings
Other video lessons on the anatomy of the esophagus, including Professor V.A. Izranova are presented.When describing the endoscopic picture, it is most convenient to use the Brombart diagram of the segmental structure of the esophagus. Tracheal (supra-aortic) segment of the esophagus from its mouth to the aortic arch (8 - 9 cm). The aortic segment is equal to the diameter of the aortic arch (2.5 - 3 cm). The bronchial segment is at the level of the tracheal bifurcation. The aortic-bronchial segment is between the lower edge of the aortic arch and the upper edge of the left main bronchus. Subbronchial segment - from the bifurcation of the trachea to the left atrium. The retropericardial segment is located anteriorly from the wall of the left atrium to the descending aorta. The supradiaphragmatic segment occupies the epiphrenal space (3 - 4 cm). The intradiaphragmatic segment occupies the hiatus region, about 2 cm long. The abdominal segment occupies the lower part of the physiological cardia (3 - 4 cm).
The esophagoscopic picture is normal.
The entrance to the esophagus opens in the form of a rounded slit-like opening located in the frontal plane. The mucosa is pale pink in color, with a thin vascular pattern, with vaguely pronounced longitudinal folds of the mucosa, which straighten during insufflation. Rhythmic circular peristaltic contractions of the walls of the esophagus are visible. The transition to the stomach is clearly differentiated - the cardia, where the pale pink mucosa of the esophagus changes to the reddish mucosa of the cardia of the stomach. When passing through the cardia, slight resistance is felt.
Endoscopic semiotics of the esophagus.
Functional disorders of the esophagus are often expressed in hyperkinesia or hypokinesia.
Hyperkinesia of the esophagus is expressed in increased motility and tone of the walls of the esophagus. Endoscopic findings in case of esophageal hyperkinesia can be hiatus diaphragm, esophagitis, reflux esophagitis. With hyperkinesia, transverse folding of the esophageal mucosa is clearly visible.
Hypokinesia of the esophagus includes weakening of peristalsis and tone of the esophagus, gaping of the upper and lower sphincters of the esophagus. The endoscopic picture of peptic esophagitis often corresponds to its hypokinesia. Cardiac insufficiency in endoscopic practice occurs in 9.6% of the studied patients. With peptic esophagitis, the mucous membrane is smoothed and has a varnish-red color. Refluxate from the stomach contents is visible in the lumen of the esophagus.
Esophagitis is most often observed in the lower part of the esophagus. Various degrees of severity and distribution of hyperemia and mucous membrane. Inflammatory infiltrates are often visible in the form of separate areas. The mucous membrane is covered with a whitish or grayish coating, and as the process progresses, it is covered with a yellowish-gray fibrinous coating and bleeds easily.
Erosive esophagitis is characterized by the presence of an indeterminate shape, often longitudinal erosions, covered with a yellow-gray coating that is easily removed with endocontact. Erosive esophagitis occurs more often with reflux esophagitis.
With fibrinous esophagitis, the mucous membrane is whitish-gray in color, slightly displaceable, the walls of the esophagus are rigid. When air is pumped, the esophagus is difficult to straighten, which is accompanied by painful sensations. The relief of the mucous membrane is uneven, the cardiac ring is closed, the folds are rough, swollen, and thickened.
To characterize changes in the esophagus during reflux esophagitis, a classification of the degrees of change is used.
Degree (mild form): slight redness and moderate swelling of the mucous membrane of the esophagus in the lower third, often directly above the cardia and along the posterior wall, wide thickened folds, inconsistently gaping cardia, gastroesophageal reflux, moderate dilatation of the esophagus in the area of inflammation, z line saved.
Degree (moderate): severe redness and swelling of the mucous membrane in the lower third of the esophagus, expansion and thickening of the folds, pronounced expansion in the area of inflammation. The esophageal mucosa bleeds easily in the area of esophagitis upon contact with the endoscope, the cardia gapes, gastroesophageal reflux. Segmental spasm of the esophagus in the area of esophagitis, the z line is almost not visible.
Degree (severe form): severe hyperemia and swelling of the mucous membrane in the middle and lower 1/3 of the esophagus. The mucous membrane is covered with an easily removable fibrinous coating, under which eroded or ulcerated bleeding areas are often revealed. Alternating expansion and spasm in the area of esophagitis, constantly gaping cardia. Gastroesophageal reflux. The Z line (Z - line) is missing.
Forms of esophagitis: dyspeptic, mixed, algic Degrees of esophagitis: generalized, isolated ulcers, fusion of superficial ulcers in combination with inflammation of the deep layers of the esophageal wall, fibrinous necrosis - inflammation of all walls of the esophagus.
Criteria for esophagitis:
Diffuse hyperemia of the mucosa in the form of longitudinal stripes, hyperemia in the lower 1/3 makes the Z-line invisible;
The presence of erosion and ulcers;
Contact and spontaneous bleeding of the mucous membrane;
The presence of granular growths on the mucosa, thickening of the folds of the mucosa, insufficient straightening of the walls of the esophagus during insufflation;
The presence of leukoplakia in the esophagus (hyperplastic growths of the integumentary epithelium, the number of epithelial layers increases 5-6 times, epithelial cells acquire a cubic shape).
Peptic ulcer of the esophagus is often a complication of reflux esophagitis or axial hernia. Usually the ulcer is elongated along the axis of the esophagus, shallow, the bottom is covered with a whitish coating. Black spots indicate previous bleeding, and a dirty green hue indicates bile reflux. The mucous membrane is swollen, hyperemic, and isolated erosions are visible. After the ulcer heals, gross deformation and structure of the esophagus occurs. The scar is linear or star-shaped.
Candidomycosis of the esophagus is extremely rare in endoscopic practice, but its demonstrative endoscopic picture leaves no problems in diagnosis; in addition to the picture of esophagitis, “drops of sour cream” are visible in the form of smooth or wrinkled lesions up to 2 - 4 mm from white to brown, small areas of necrosis and pseudomembranous raids.
Insufficiency of the cardia is accompanied and causes esophagitis. Signs of cardia insufficiency: moderate gaping, easy straightening during insufflation, smoothness of the relief of the mucous membrane of the cardiac sphincter, the appearance of circular folds, gastroesophageal reflux.
Endoscopic signs of an axial hernia: shortening of the distance from the anterior incisors to the Z-line, gastroesophageal reflux, transhiatal prolapse of the gastric mucosa into the esophagus, the presence of refluxate in the lumen of the esophagus, free passage of the apparatus through the prolapsing segment. The hernial sac in an axial hernia is the parietal peritoneum, the hernial contents are the stomach. Example of a protocol: cardia rosette at a distance of 35 - 36 cm from the anterior incisors. There is no closure of the cardia, the mucous membrane of the esophagus in the lower third is swollen, the folds are thickened. In the hernial sac there are gastric contents and sharply swollen and hyperemic folds of the gastric mucosa, actively bleeding upon endocontact. The patient constantly regurgitates air.
Esophageal varicose veins (EVV) often have one to four trunks, from small convoluted collapsed veins to flask-shaped vein fragments hanging into the lumen of the esophagus. There are isolated nodes or total damage to the veins of the esophagus. Example: the entrance to the esophagus is oval-shaped, freely passable. Against the background of the smooth whitish-pink mucosa of the esophagus, bluish strands of various shapes and diameters are visible, spread out in the submucosal layer. There are single, network, stem, and mixed forms of VRVP. If there is severe inflammation with varicose veins of the esophagus, endoscopy should not be performed.
Esophageal diverticula are sac-like protrusions in the walls of the esophagus that end blindly. Diverticula of the esophagus are distinguished between congenital and acquired, true (with all the membranes of the esophageal wall) and false. Based on topographic characteristics, they are distinguished: proximal pharyngoesophageal diverticula, epibronchial and supradiaphragmatic diverticula. When diverticulitis occurs, the leading symptoms are: dysphagia, regurgitation, dysphonia, cough, halitosis. Surgical treatment is indicated. Endoscopically, with a diverticulum: the mucous membrane inside is hyperemic, food and mucus residues are visible in the sac, it is not completely emptied, the gates of the diverticulum are clearly differentiated. In 10% of cases, diverticulitis is complicated by esophagitis.
Malignant tumors of the esophagus
In 42% of cases, malignant tumors of the esophagus occur in the middle esophagus, in 12% - in the upper 1/3, in 26% - in the lower 1/3 of the esophagus. Cardioesophageal cancer occurs in 20%. According to the endoscopic picture, five types are distinguished (according to Stark).
Limited cancer infiltration (Stark-1):
one wall is affected in a limited area. During endoscopy, the mucous membrane in this area is pale, different from the surrounding area, the relief is rearranged, there is no folding, and peristalsis is not visible. The color of a limited area of the mucous membrane is dull; biopsy shows fragmentation. The lumen of the esophagus is not changed.
Ulcerated esophageal cancer (Stark-2):
affects one or two walls of the esophagus. Endoscopically, it appears as an irregularly shaped ulcer with unclear contours, a shallow bottom covered with fibrin. There is no inflammatory shaft around the ulcer, the lumen of the esophagus is not changed, there is no peristalsis. On instrumental palpation, the edges of the ulcer are rigid.
Parietal tumor (Stark-3):
plaque-like or polypoid, on one or two walls of the esophagus, tuberous in shape, grayish-red in color. Narrows the lumen of the esophagus. On palpation - contact bleeding. The consistency may be soft. Peristalsis at the tumor site is not visible.
Circular cancerous stricture of the esophagus (Stark-4):
the lumen of the esophagus is narrowed by 0.3 cm. The wall is lumpy, gray, stone-like, dull, moderately bleeds/during endopalpation and biopsy.
Cardioesophageal cancer of the esophagus (Stark-5):
the function of the cardia is always impaired, which contributes to the reflux of stomach contents into the lumen of the esophagus. The Z line is leveled. The mucous membrane is fine-grained, gray, dull, rigid, and bleeds. Differentiate with cardiospasm.
Early esophageal cancer affects the mucous and submucosal layers, spreading up to 5 cm along the length of the esophagus. Verified after. Most often there are no metastases. Endoscopic examinations and biopsies can detect esophageal cancer in 97% of cases.
Foreign bodies of the esophagus.
In the case of foreign bodies in the esophagus, it is important to follow a sequence of actions. If a foreign body is suspected, endoscopic examination is preceded by a qualified consultation. Esophagoscopy should be performed in a specialized department (thoracic) so that, excluding subsequent transportation of the patient, after the examination, full surgical assistance can be provided. The presence of a foreign body in the esophagus for 4 - 5 days leads to local necrosis of the walls of the esophagus. More often, foreign bodies get stuck at the mouth of the esophagus or in the thoracic region. With cicatricial lesions of the esophagus proximal to the stricture, food fragments get stuck, forming a conglomerate (esophagolithiasis). When removing foreign bodies from the esophagus, caution and certain experience are required, since perforation of the esophageal wall leads to serious complications: periesophagitis, subcutaneous emphysema,. For endoscopic removal of foreign bodies, the following are used: forecepts, loops, crocodile, rat teeth, tripod, fork, etc. grips. When removing foreign bodies that have invaded the opposite walls of the esophagus, a thorough visual assessment of the situation and extreme caution is required when removal of the blunt end of a foreign body (needle) into the lumen. Then the needle is removed from the other wall. After this, fixing the edge of the needle with one of the grips, the foreign body is removed along with the endoscope. To objectively assess the degree of damage to the walls of the esophagus, esophagoscopy is necessary after removing the foreign body.
The article was prepared and edited by: surgeon
Esophagoscopy is one of the most reliable research methods that allows one to study the mucous membrane of the esophagus and stomach based on visual examination data, as well as the results of histological and cytological examination of biopsy material obtained specifically through an endoscope. It should be noted that only relatively large hiatal hernias can be visually detected. The use of fibroesophagogastroscopy for hiatus hernia is more justified for the diagnosis of reflux esophagitis (Grigoriev P.Ya. et al., 1990,1996). The combination of a number of signs during endoscopic examination suggests the presence of a hiatal hernia in the patient. These signs are: a decrease in the distance from the incisors to the esophagogastric junction, the presence of a hernial orifice, the detection of a “funnel” during retrograde examination of the cardia, prolapse of the gastric mucosa into the esophagus (Kubyshkin V.A., Kornyak B.S., 1999).
\d In our work, we identify several endoscopic signs of hiatal hernia.
Endoscopic examination reveals various stages of the inflammatory process from catarrhal to necrotizing ulcerative esophagitis, most pronounced in the lower third of the esophagus. Usually normal
- -ring "A" - muscle ring; 2 - ring "B" - hiatal narrowing of the esophagus; 3 - hernial cavity; 4 - “second entrance” to the stomach
no resistance of the diaphragmatic ring is felt, and the esophagoscope falls into the stomach. You can observe the flow of gastric contents into the esophagus from the stomach.
Histologically, reflux esophagitis is characterized by inflammatory infiltration of the submucosal layer predominantly by plasma cells, neutrophilic leukocytes and lymphocytes, edema of the mucous and submucosal layers, vacuolar degeneration and ocanthosis of the epithelium. Along with this, sclerotic and cystic changes in the mucous membrane, desquamation and folding of the epithelium, venous stagnation, and microhematomas are detected. Changes in at least one biopsy specimen indicate esophagitis.
To unify and evaluate endoscopic examination data, the Savary-Miller classification of the severity of esophagitis is used, and four stages of the disease are distinguished:
- stage - round and longitudinal lesions that do not merge and spread from the Z-line to the mucous membrane of the esophagus (Fig. 11);
- stage - merging transient lesions in the Z-line area, not covering the entire surface of the mucous membrane (Fig. 12);
- stage - ulcerative lesions merging in the lower part of the esophagus and covering the entire surface of the mucous membrane (Fig. 13);
- stage - chronic ulcerative lesions of the esophagus, fibrous stenosis, shortening of the esophagus (Barrett's esophagus) (Fig. 14).
in 6.5% and grade 4 esophagitis (Barrett's esophagus) - in 1% of patients (Savary-Miller classification). Suspicion of the presence of a hiatal hernia arose in 67.3% of patients. Duodenal ulcer was diagnosed in 42.9% of patients in group 1 (open fundoplication according to Nissen), 39.3% in the second (laparoscopic fundoplication according to Nissen), in 17% and 34.4% of cases in group 3 (posterior partial Toupet fundoplication) and 4th (2-sided Toupet fundoplication) groups, respectively.
Today, in connection with changes in the concept of Barrett's esophagus, we should dwell on its definition and diagnosis.
It is currently believed that Barrett's esophagus is an acquired condition resulting from chronic damage to the mucous membrane of the distal esophagus due to reflux, in which columnar glandular epithelium, which contains specialized intestinal-type metaplastic cells, replaces stratified squamous epithelium in the distal section of the esophagus, regardless of the length of the metaplastic area. A synonym for the concept of “Barrett's esophagus” is “cylindrical metaplasia of the esophageal mucosa” (Dent J. et al., 1991; Armstrong D. et al., 1992; Kubyshkin V.A., Kornyak B.S., 1999). During endoscopic examination, Barrett's esophagus should be suspected if the transition from squamous to columnar epithelium (Z-line) does not coincide with the position of the cardia. The border can be clear and even, but more often it has the appearance of finger-like protrusions.
Since endoscopic signs of cylindrical metaplasia of the esophageal mucosa of the intestinal type may be absent, a biopsy is taken from 4 randomly selected points around the circumference of the esophagus with an interval of 1-2 cm along the entire length of the segment (Kubyshkin V.A., Kornyak B.S., 1999) . The diagnosis is made on
based on endoscopy data with biopsy, which makes it possible to identify intestinal metaplasia of the mucous membrane of the distal esophagus.
^ Endoscopic anatomy of the esophagogastric junction in gastroesophageal reflux disease
Among 370 patients with gastroesophageal reflux disease, the Z-line at the level of the cardia was determined only in 16.8% of cases, and in 81.3% - above the cardia rosette, of which from 10 to 40 mm - in 61.6%. In this group of subjects, patients appear with the Z-line located from 40 to 60 mm above the cardia (2.4%). Below the cardia rosette, the Z-line descends to 10 mm in 1.9% of cases.
A comparison of the levels of Z-line location under normal conditions and with gastroesophageal reflux disease is presented in Table 1.
^ Table No. 1 Comparison of the levels of location of the Z - line under normal and
for gastroesophageal reflux disease
| ^ Level of location of the Z-line in relation to the cardia (mm) | The junction line of the esophageal and gastric epithelium on anatomical preparations (normal) | Endoscopic anatomy (normal) |
|
| Fine | For gastroesophageal reflux disease |
||
| ^ Percentage of observations |
|||
| Percentage (%) | Percentage (%) | Percentage (%) |
|
| Higher by 40 – 60 | - | - | 2,4 |
| Higher by 20 - 39 | 7,1 | 10,0 | 27,0 |
| Higher by 10 – 19 | 27,1 | 30,0 | 34,6 |
| Higher by 5 – 9 | 28,6 | 31,8 | 17,3 |
| Cardia level | 24,3 | 20,0 | 16,8 |
| Below by 5 – 9 | 4,3 | 4,6 | 1,2 |
| Lower by 10 - 18 | 8,6 | 3,6 | - |
| Total: | 100,0 | 100 | 100,0 |
A symmetrical arrangement of the Z-line along all walls in relation to the rosette of the cardia was present in 78 (21.1%) of 370 patients; in other cases, at different levels.
In patients with gastroesophageal reflux disease, complex forms of the Z-line occur (tongue-like, complex, like a maple leaf, jagged, combinations of different forms) - in 51.8%, complex shapes of the figures that it forms - in 57.8%.
In these patients, complex forms of cardia predominate in the open (46.2%) and closed (53.2%) states.
^ Endoscopic manifestations of gastroesophageal reflux disease in the mucous membrane of the esophagogastric junction
Taking into account the variability and range of levels of the Z-line location, as well as the change in the level of the Z-line after passing the endoscope into the stomach, we were guided by the rules for examining the esophagogastric junction:
Assess the function of the cardia rosette and the level of the Z-line before passing the endoscope into the stomach and not reaching the cardia rosette 5.0 - 6.0 cm;
The reflux of gastric contents into the esophagus is considered reflux if there is no gag reflex;
For biopsies from the esophagus, forceps that were used for biopsies in the stomach or duodenum should not be used.
During endoscopic examination and description of the esophagogastric junction, attention was paid to:
cardia - its shape in the open and closed state, the completeness and rhythm of the closure of its walls;
walls of the esophagus (elasticity, symmetry and depth of peristalsis);
Z-line – (its shape, the severity of these forms along the entire circumference, the shape of the figure formed by the Z-line, its symmetry in relation to the “rosette” of the cardia;
mucous membrane above the Z-line: severity of vascular pattern, edema (focal, uniform), foci with columnar epithelium, defects, erosions, ulcers;
mucous membrane below the Z-line - swelling, hyperemia (uniform, in patches, in the form of stripes), looseness, vulnerability, granularity, the presence of “islands” of squamous epithelium;
presence and nature of refluxate (light gastric, bile-stained, bile).
When assessing the degree of esophagitis, we were guided by the Los Angeles classification, but we consider it advisable to take into account changes in the mucous membrane with columnar epithelium located within the esophagus.
When comparing endoscopic changes in the mucous membrane with columnar epithelium in the esophageal-gastric junction in patients with gastroesophageal reflux disease with and without Helicobacter pylori, it was found that for Helicobacter-positive patients in comparison with Helicobacter-negative patients the following are characteristic: edema (82.9% in comparison with 29.4%), focal hyperemia (58.6% compared with 19.1%), friability (62.2% compared with 6.8%), granularity, and the hemorrhagic component was present only in Helicobacter-positive patients .
Endoscopic and morphological studies made it possible to draw attention to the presence of preneoplastic complications of gastroesophageal reflux disease in less severe degrees of esophagitis. Significant is the frequent absence of visual signs of intestinal metaplasia, dysplasia, and sometimes intraepithelial adenocarcinoma, as indicated by E.A. Gogello and Yu.I. Gallinger (2001).
^ Study of the possibilities of laser-induced autofluorescence of normal and metaplastic epithelium
Currently, one of the important tasks of the diagnostic service is the timely recognition of preneoplastic complications of gastroesophageal reflux disease for the primary prevention of oncopathology of this part of the digestive system (A.S. Trukhmanov, 2002).
In the last decade, endoscopy has used such modern technology as optical spectroscopy and, in particular, local fluorescence spectroscopy, which was first used in 1996 for the diagnosis of severe dysplasia and adenocarcinoma of the esophagus (J. Haringsma, G. N. J. Tytgat, 2001). Although in subsequent years the diagnostic effectiveness of this method was studied in many scientific centers (J. Bourg-Heckly et al., 2000; I. Georgakoudi et. al., 2001; K. K. Wong, 2001), there are only two foreign publications in which the possibilities of autofluorescent detection of metaplastic epithelium of the mucous membrane of the esophagogastric junction were studied (K. Niepsuj, G. Niepsuj, W. Cebula et. al., 2003; L. M. Wong Kee Song, N. E. Marcon, 2001). All studies were carried out with autofluorescence excited by laser sources in the ultraviolet or blue spectral ranges. For the first time in Russia, we used a laser source in the green range of the spectrum to excite fluorescence.
Differences were identified in the autofluorescence spectra of normal columnar and intestinal-type metaplastic columnar epithelium of the esophagogastric junction when excited in the green region of the spectrum in 13 of 15 patients. The parameters of the autofluorescence spectra (fluorescence intensity and spectral fluorescence diagnostic parameter D f) of normal columnar, squamous and intestinal metaplastic columnar epithelium and adenocarcinoma of the esophagogastric junction were determined. Thus, local fluorescence spectroscopy with the excitation of autofluorescence during esophagoscopy in vivo in real time made it possible to obtain diagnostic information, which facilitated the taking of targeted biopsies and made it possible to minimize their number and carry out timely diagnosis and treatment.
^ Gastroesophageal reflux disease and Helicobacter pylori
One of the problems of gastroesophageal reflux disease is the participation of Helicobacter pylori infection in the development of the disease. Currently, the central role of Helicobacter pylori in the occurrence of gastritis, gastric and duodenal ulcers, as well as gastric carcinogenesis is generally recognized and proven (V.T. Ivashkin, F. Megro, T.L. Lapina, 1999; V.D. Pasechnikov et al., 2004), and the development of gastroesophageal reflux disease has not yet been clarified (A.A. Sheptulin, 1999; A.S. Trukhmanov, 2002; A.A. Sheptulin, V.A. Kiprianis, 2006). There are 3 opinions on the role of Helicobacter pylori in the development of gastroesophageal reflux disease: the presence of Helicobacter pylori reduces the risk of developing gastroesophageal reflux disease (M.A. Vinogradova et al., 1998; S.I. Rapoport, O.N. Lapteva, N.T. Raikhlin, 2000; I.V. Mayev, 2002; G. Holtmann, C.R. Cain, P. Malfertheiner, 1999), the presence of Helicobacter pylori plays a negative role in the development of the disease (P. Malfertheiner, S. Veldhuyzen van Zanten, 1998) and the presence or the absence of Helicobacter pylori does not affect the incidence of gastroesophageal reflux disease (F. Carbone, M. Neri, E. Zaterza et al., 1999). But this mainly concerns the presence of Helicobacter pylori in the stomach. The identification of Helicobacter pylori in the columnar epithelium of the esophagus is known (J.P. Gisbert, J.M. Pajares, 2002), but there have been no reports on the effect of Helicobacter pylori on preneoplastic transformations of the columnar epithelium in the esophagus.
For this purpose, we examined 485 adults and 210 children with gastroesophageal reflux disease. Preneoplastic complications in the mucous membrane with columnar epithelium of the esophagogastric junction were found in 13.2% of adults and 10.9% of children. Helicobacter pylori was detected in adults - in 35.2%, in children - in 31.4% of cases, and in patients with preneoplastic complications - in 79.1% and 82.6%, respectively. In 64 (13.2%) patients with preneoplastic complications, intestinal metaplasia was detected - in 56 (11.6%), atrophy - in 33 (6.8%), dysplasia - in 8 (1.7%), adenocarcinoma - in 2 (0.4%), and among patients with intestinal metaplasia, 18 (3.8%) had incomplete intestinal metaplasia, 38 (7.8%) had complete intestinal metaplasia. Moreover, more often these complications occurred against the background of grade A esophagitis - in 48 (75.0%).
Helicobacter pylori was detected in patients with incomplete intestinal metaplasia in 83.3%, and in patients with complete intestinal metaplasia in 81.6%. In patients with atrophy of the mucous membrane of this section - in a smaller percentage of cases - in 57.6%, with dysplasia - in 50.0%.
A comparison of the frequency of development of preneoplasia in the antrum, body and esophagus in 348 patients with gastroesophageal reflux disease revealed that atrophy in these sections is observed in decreasing order: 30.5% - 17.6% - 7.5%, as well as dysplasia: 1. 8% - 1.2% - 0.9%, intestinal metaplasia in the antrum - in 14.4%, in the body - in 8.3%, and in the esophagus - in 11.8%. Moreover, incomplete intestinal metaplasia in the structure of total intestinal metaplasia in the antrum is 32.0%, in the body - 17.2%, and in the esophagus - 36.6%.
In these patients, Helicobacter pylori was detected in metaplasia in the antrum in 66.7%, in the body - 66.2%, in the esophagus - 83.3%, in atrophy - in 56.4% - 55.6% and 52.9 %, i.e. The contamination of Helicobacter pylori in atrophic processes in the stomach and esophagus is lower than in intestinal metaplasia, but Helicobacter pylori is detected more often in intestinal metaplasia in the esophagus.
Thus, a parallelism was revealed between the high frequency of Helicobacter pylori contamination of the mucous membrane of the esophageal-gastric junction in patients with gastroesophageal reflux disease with preneoplastic complications in it.
Since the mucosa with the cylindrical epithelium of this section of the esophagus has significant morphological changes, in contrast to similar mucosa in the stomach, it can represent that favorable background against which, in the presence of Helicobacter pylori, acid or alkaline reflux, neoplastic processes develop.
It follows from this that anti-Helicobacter therapy is justified in the complex treatment of gastroesophageal reflux disease if this microorganism is detected in the stomach, and even more so in the mucous membrane of the esophagogastric junction, i.e. eradication of Helicobacter pylori may be one of the components of the prevention of preneoplasia and adenocarcinoma of the esophagus. Our opinion coincides with the conclusions of B.N. Khrennikova, E.E. Seregina (2004), V.D. Pasechnikova, S.Z. Chukova (2006), N.A. Wright (1998), P. Malfertheiner et al. (2005): in the absence of eradication of Helicobacter pylori, progression of neoplastic and inflammatory processes was noted, as well as D.M. Kadyrova et al. (2004), who note that after Billroth II gastrectomy, Helicobacter pylori reinfection and gastroesophageal reflux contribute to the development of inflammatory and atrophic processes, therefore eradication therapy is necessary to improve the functional rehabilitation of patients.
When determining the degree of activity of the inflammatory process in the mucous membrane with columnar epithelium of the esophageal-gastric junction in Helicobacter-positive patients, high and medium degrees of activity of the inflammatory process were detected in 51.9% and 39.4%, and low in 8.7%, and in Helicobacter-negative – predominantly (80.9%) low degree of inflammation.
The analysis of our studies draws attention to the fact of detection of preneoplastic complications of gastroesophageal reflux disease in less severe degrees of esophagitis: in 75.0% for grade A esophagitis and only in 15.9% and 9.1% for grade B and C esophagitis, respectively, and also does not depend on age: it occurs at the age of 20–30 years (17.2%) and in children (10.9%). Significant is the frequent absence of characteristic visual signs of intestinal metaplasia, dysplasia, and sometimes intraepithelial cancer in the mucosa with columnar epithelium in the esophagus.
A number of researchers have found that intestinal metaplasia, and especially specialized intestinal metaplasia, is associated with the risk of dysplasia and then adenocarcinoma (V.I. Chissov et al., 1998; L.I. Aruin et al., 1999; V.A. Kuvshinov, B.S. Kornyak, 1999; A.F. Chernousov et al., 2001; M.P. Korolev et al., 2002; G.N. Tytgod et al., 1985). Currently, the detection of Helicobacter pylori in the esophagus distal to the Z-line is known (J.P. Gisberg, J.M. Pajares, 2002). But there is no information about the use of antilysozyme activity of Helicobacter pylori for the diagnosis of preneoplastic processes in the esophagus. Considering that Helicobacter pylori has antilysozyme activity, and in tissues against the background of the development of a cancerous tumor the content of lysozyme increases (V.F. Vi; V.R. Huang, 1998), we attempted to determine the level of antilysozyme activity of Helicobacter pylori isolated from the mucous membrane with columnar epithelium in esophagus, with and without preneoplastic complications of gastroesophageal reflux disease. It was found that in patients with gastroesophageal reflux disease in the presence of intestinal metaplasia and dysplasia, the level of antilysozyme activity of Helicobacter pylori is equal to or more than 2 μg/ml (patent No. 2229712 dated May 27, 2004), which made it possible to use these results to identify preneoplastic complications of gastroesophageal reflux disease in the early stages.
^ Functional state of the gastrointestinal tract in patients with gastroesophageal reflux disease
The functional state of the gastrointestinal tract was assessed using 24-hour pH monitoring in the upper gastrointestinal tract.
As for daily pH-metry, there are works devoted to the equipment, the technique of the study itself, the main characteristics of pH-grams (E.Yu. Linar, 1988; Yu.Ya. Leya, 1996; A.V. Okhlobystin, 1996; S. Mantilla et al., 1988). There are many studies devoted to the pathogenesis and diagnosis of diseases of the upper gastrointestinal tract (most often diseases of the stomach and duodenum) in adults and children (M.A. Osadchuk, A.Yu. Kulidzhanov, 2005; O.A. Sablin et al. , 2002; P.L. Shcherbakov, 2002), identifying the effect of drugs on gastric secretion, on the healing of erosions in the esophagus (B.D. Starostin, G.A. Starostina, 2004; M.P. Williams et al., 1998; C. Birbara et al., 2000), the result of vagotomy surgery (Yu.M. Pantsyrev et al., 2005). I.V. Mayev (2000) offers 30-hour intraesophageal pH-metry to assess the effect of medications used in the treatment of patients with gastroesophageal reflux disease. S.S. Belousov, S.V. Muratov, A.M. Ahmad (2005), J.N. Tytgat (1998) compared the prevalence of gastroesophageal and duodenogastric reflux, average daily pH readings and Helicobacter pylori infection in the stomach. But among the large number of works, there were no studies that would indicate the possibility of using daily pH-metry in patients with gastroesophageal reflux disease to predict the degree of esophagitis and determine the prognosis of the disease.
For this purpose, we analyzed data from daily monitoring of intraesophageal pH in 63 patients with gastroesophageal reflux disease who had esophagitis A (50.8%), B (26.9%) and C (22.3%) degrees. Among them, 10 (15.9%) patients had intestinal metaplasia of columnar epithelium in the esophagus and 2 (3.2%) patients had dysplasia. The most significant indicators of pH-grams in the diagnosis of changes in the mucous membrane of the esophagus were: total acidification time (pH
Patients with gastroesophageal reflux disease with esophageal symptoms had variants I (100.0%) and II (88.2%), and with extraesophageal manifestations – III (100.0%), IV (84.2%) and V (90. 5%) pH gram options. Preneoplastic complications of gastroesophageal reflux disease are detected with a smaller total number of refluxes and with shorter duration of refluxes than grades B and C esophagitis, which corresponds to endoscopic and morphological relationships. Metaplasia and dysplasia of columnar epithelium in the esophagus were detected with less pronounced pH-gram values than leukoplakia of stratified squamous epithelium.
Rice. 4 - Patient M., 59 years old. Diagnosis: Chronic hyperacid Helicobacter-associated gastritis: ^ A – 24-hour pH-gram of the esophagus ( Ioption)
Rice. 5 - Patient K., 31 years old. Diagnosis: Gastroesophageal reflux disease. Esophagitis grade A: ^ II-option)
Rice. 6 - Patient G., 38 years old. Diagnosis: Gastroesophageal reflux disease. Esophagitis grade A. Barrett's esophagus: ^ A – 24-hour pH-gram of the esophagus ( III-option)
Rice. 7 - Patient P., 50 years old. Diagnosis: Gastroesophageal reflux disease. Esophagitis grade B: ^ A – 24-hour pH-gram of the esophagus ( IV- option)
Rice. 8 - Patient I., 45 years old. Diagnosis: Gastroesophageal reflux disease. Esophagitis grade C: ^ A – 24-hour pH-gram of the esophagus ( V-option)
Peripheral computer electrogastroenterography is a method that characterizes the motor-evacuation function of the gastrointestinal tract.
In recent years, due to its non-invasiveness and good tolerance by patients, electrogastroenterography is increasingly used for an in-depth study of the pathogenesis of diseases and for their diagnosis in adults (H.P. Nugaeva et al., 1998; S.L. Pilskaya et al., 2000; S.A. Vyskrebentseva et al., 2002; V.A. Stupin et al., 2005; W.K. Kauer, 1999; J. Lin et. al., 2001), and in children (A.M. Zaprudnov, A.I.A I. Volkov, 1995; L. N. Tsvetkova, P. L. Shcherbakov, V. A. Filin, 2000; E. E. Krasnova, 2005). G.N. Shlyakova points out the possibility of predicting relapse of peptic ulcer using electrogastroenterography. But there are few studies on gastroesophageal reflux disease (S.A. Vyskrezbentseva et al., 2002). Therefore, we set the task, using peripheral computer electrogastroenterography, to study some pathogenetic aspects of gastroesophageal reflux disease, as well as its capabilities in diagnosing the disease.
The motor function of the stomach, duodenum, jejunum, ileum and colon of patients with gastroesophageal reflux disease was assessed in the fasting (I) and feeding (II) phases according to the following indicators:
The level of electrical activity (Pi/Ps), which indicates the severity of blood supply to organs
The level of the ratio coefficient (or comparison coefficient), which indicates the coordination of work between departments (Pi/Ps+1).
Of 140 people with gastroesophageal reflux disease who underwent peripheral computed electrogastroenterography, 88 people (62.8%) had grade A esophagitis, 36 people (25.7%) had grade B esophagitis, and 16 people (11.5% ) with grade C esophagitis.
Of 140 patients with gastroesophageal reflux disease with varying degrees of esophagitis, 22 (15.7%) people had atypical electrogastroenterograms.
Based on the indicators of electrical activity and the ratio of various parts of the gastrointestinal tract in the fasting and feeding phases, disorders of the motor-evacuation function of the stomach, duodenum, small and large intestines were identified. By comparing the data of electrogastroenterography and endoscopy, it was possible to identify three types of electrogastroenterograms characteristic of each degree of esophagitis, which is schematically presented in Figures 9 and 10.
| Esophagitis | Electrical activity |
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| ^ Stomach (22.4±11.2) | duodenum (2.1± 1.2) | Jejunum (3.35±1.65) | Ileum (8.08±4.01) | Large intestine (64.0±32.01) |
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| Phase I | II phase | Phase I | II phase | Phase I | II phase | I phase | II phase | Phase I | II phase |
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| Grade A | Nmax | N |  | |||||||