LECTURE No. 9. Diseases of the digestive tract. Diseases of the esophagus. Esophagitis and peptic ulcer of the esophagus

1. Acute esophagitis

Acute esophagitis is an inflammatory lesion of the mucous membrane of the esophagus lasting from several days to 2-3 months.

Etiology and pathogenesis. Etiological factors: infectious diseases, injuries, burns, poisoning, allergic reactions, nutritional errors.

Of the infectious agents, the most characteristic of acute esophagitis are diphtheria, scarlet fever, typhoid and typhus, influenza, parainfluenza, adenovirus infection, mumps.

Physical and chemical damaging factors are represented by ionizing radiation, chemical burns, hot and very cold food, and spices.

Classification. There is no single classification. It is possible to use a working classification of acute esophagitis.

Morphologically, the listed types of acute esophagitis are distinguished: catarrhal, edematous, erosive, pseudomembranous, hemorrhagic, exfoliative, necrotic, phlegmonous.

By etiology: infectious, chemical, physical, alimentary.

By endoscopic stages: 1st - edema and hyperemia of the mucosa, 2nd - the appearance of single erosions on the tops of the edematous mucosal folds, 3rd - significant edema and hyperemia of the mucosa with foci of eroded and bleeding mucous membranes, 4th - "weeping "- diffusely eroded mucous membrane, bleeds at the slightest touch of the endoscope.

clinical picture. Catarrhal esophagitis is the most common form of acute esophagitis. It occurs against the background of errors in nutrition: when eating spicy, cold, hot foods, with minor injuries, alcohol burns.

It is clinically manifested by burning and pain behind the sternum, forcing patients to refuse food for several days.

Endoscopically noted esophagitis I-II degree, x-ray - hyperkinesia of the esophagus.

Erosive esophagitis occurs with infectious diseases (finn, typhus, sepsis, fungal processes) and allergies. It also appears with chemical burns and injuries of the esophagus. In fact, this form of esophagitis is a phase of the evolution of catarrhal esophagitis. The main clinical picture consists of the symptoms of the underlying disease.

Clinical symptoms are similar to those of catarrhal esophagitis: significant pain in the chest during the passage of food; heartburn, belching, hypersalivation, putrid odor from the mouth (cacosmia). Endoscopically ascertain signs of esophagitis II-III degree. Histological examination revealed hyperemia, mucosal edema, hemorrhage, erosion. An X-ray examination shows an abundance of mucus in the esophagus, a restructuring of the relief with the formation of flat depots of barium of a longitudinal shape up to 1 cm long, and hyperkinesia of the walls of the esophagus.

Hemorrhagic esophagitis is a rare clinical form of erosive esophagitis. The etiology is the same as in erosive esophagitis. Intense pain syndrome and hematemesis are clinically typical.

Endoscopy reveals grade III-IV inflammation with a predominance of the hemorrhagic component. There is a detachment of the bleeding mucous membrane in the form of narrow thin strips. Fibrinous (pseudomembranous) esophagitis. Etiological factors in it are scarlet fever, diphtheria, blood diseases, fungal diseases, the effects of radiation therapy.

The clinic is dominated by dysphagia and intense pain, aggravated after eating, nausea, vomiting. With vomit, fibrin films are released, there may be hemoptysis.

Endoscopically, on the affected areas of the mucosa, gray and yellow-gray fibrinous plaques are found, formed by layers of fibrin and detritus covering the surface of the mucosa. With the rejection of pseudomembranes, flat slowly healing erosions are formed, sometimes bleeding ulcers. After a severe infectious process, membranous stenoses remain in the esophagus, which disappear after repeated bougienage. Membranous (exfoliative) esophagitis by etiology is chemical (burns of the esophagus), infectious (causes are sepsis, shingles, smallpox, generalized herpes infection).

The clinic of the disease is variable - from mild forms, diagnosed endoscopically, to severe ones. In the clinic of severe membranous esophagitis, intoxication, dysphagia and pain syndrome prevail. Possible bleeding, perforation of the esophagus, mediastinitis, which, as a rule, end in death. In endoscopic examination, damage to all layers of the esophagus is observed, the epithelium of which is rejected by layers. When the underlying disease subsides, symmetrical and asymmetric membranous or rough cicatricial stenoses sometimes remain in the esophagus.

Necrotizing esophagitis is a rare form of acute inflammation of the esophagus. Its development is facilitated by reduced immunity in such serious diseases as sepsis, typhoid fever, candidiasis, end-stage renal failure.

The clinic is characterized by painful dysphagia, vomiting, general weakness, bleeding, frequent development of mediastinitis, pleurisy, pneumonia. After the treatment of the underlying disease, strictures remain in the esophagus, diagnosed as facultative precancerous changes.

Septic esophagitis is a rare local or diffuse inflammation of the walls of the esophagus of streptococcal etiology or occurs when the mucosa is damaged by a foreign body, with burns, ulcerations, and can pass from neighboring organs. Sometimes acute phlegmonous esophagitis occurs as a complication of any form of acute esophagitis, leading to purulent fusion of the walls of the esophagus. The collapse of the walls is accompanied by a breakthrough of pus into the tissue of the mediastinum, the development of mediastinitis, pleurisy, purulent bronchitis, pneumonia, spondylitis, rupture of the aorta or other great vessels. Accession of an anaerobic infection can lead to mediastinal emphysema or spontaneous pneumothorax.

The clinical picture is characterized by severe intoxication, high fever, pain behind the sternum and in the neck, vomiting. On examination, there is swelling in the neck, mobility in this part of the spine is limited. The position of the head is forced, with an inclination to one side. The disease often transforms into purulent mediastinitis.

In blood tests - hyperleukocytosis, accelerated ESR.

Instrumental examination (X-ray, endoscopic) in the acute stage is not indicated. During the period of scarring, an x-ray examination is mandatory due to the risk of developing gross deformities and cicatricial stenosis of the esophagus.

Treatment. Principles of treatment of acute esophagitis: etiotropic, pathogenetic and symptomatic.

Etiotropic treatment - treatment of the underlying disease. In infectious diseases complicated by acute esophagitis, antibiotics are used (parenterally). With pronounced necrotic and hemorrhagic changes in the esophagus, it is recommended to refrain from eating for 2-3 weeks. During this period, parenteral nutrition, intravenous administration of protein hydrolysates, mixtures of amino acids, intralipid, vitamins, and detoxification therapy are indicated. After reducing inflammation, thermally and chemically sparing foods are prescribed: warm milk, cream, vegetable soups, liquid cereals. To reduce local symptoms of inflammation - inside solutions of tannin 1%, collargol - 2%, novocaine - 1-2% before meals. Astringents are taken in a horizontal position with the head of the bed lowered low. In the absence of the effect of local administration of astringent preparations, non-narcotic analgesics are prescribed parenterally.

To reduce the effects of esophageal dyskinesia, prokinetic drugs (cerucal, raglan, cisapride) are used orally before meals. With multiple erosions, bismuth preparations (denol, vikair), injections of solcoseryl are indicated.

With hemorrhagic esophagitis, complicated by bleeding, aminocaproic acid preparations, vikasol, dicynone are used. With massive bleeding, a blood or plasma transfusion is prescribed. With purulent, necrotic esophagitis, the patient should be on parenteral nutrition for a long time, massive therapy with several antibiotics is used, and the abscess is drained.

Esophageal strictures are corrected by bougienage. In rare cases, a gastrostomy is placed.

Forecast. The prognosis for catarrhal and erosive esophagitis is favorable. Spontaneous disappearance of the symptoms of esophagitis is possible provided that the underlying disease is adequately corrected. The prognosis of pseudomembranous, ecfoliative, and phlegmonous esophagitis is serious. In all cases, subject to recovery from the underlying disease, esophagitis ends with the formation of scar strictures, which subsequently require correction. Patients with severe forms of esophagitis complicated by esophageal strictures are unable to work.

Prevention of acute esophagitis consists in adequate and timely diagnosis and treatment of the underlying disease.

2. Chronic esophagitis

Chronic esophagitis is a chronic inflammation of the mucous membrane of the esophagus lasting up to 6 months. The most common variant is peptic esophagitis (reflux esophagitis), which can be complicated by peptic ulcer of the esophagus.

Etiology and pathogenesis. The main cause of the disease is constant reflux of gastric contents into the esophagus, sometimes bile and intestinal contents, i.e. peptic esophagitis is an aseptic burn of the esophagus by stomach acid.

In the pathogenesis of reflux esophagitis, regurgitation of acidic contents and a violation of the purification and emptying of the esophagus from it are important. The rate of clearance of the esophagus from chemical irritation is called esophageal clearance. With normal clearance, single reflux of aggressive secretions does not cause reflux esophagitis. Hot food, alcohol, smoking and other exogenous factors reduce the clearance of the esophagus. These factors include fast food, in which a significant amount of air is swallowed along with food. The quality of food also matters: fatty meat, lard, pasta, spicy spices help delay the evacuation of food from the stomach, followed by the reflux of the contents into the esophagus. Drugs significantly reduce the tone of the lower esophageal sphincter and promote reflux: calcium antagonists, nitrates, narcotic analgesics, anticholinergic drugs, theophylline and its analogues, drugs from the prostaglandin group. There are five criteria for the pathogenicity of reflux in the genesis of peptic esophagitis: frequency, volume, regurgitation, chemical composition, condition of the esophageal mucosa and sensitivity to a chemical factor (inflammation of the walls reduces sensitivity), emptying rate (clearance), which depends mainly on active peristalsis, alkalizing action saliva and mucus.

The occurrence of reflux esophagitis is promoted by hernia of the esophageal opening of the diaphragm, duodenal ulcer, post-gastroresection disorders, and allergies. Allergic predisposition also matters.

Morphological examination of patients with peptic esophagitis reveals edema, hyperemia of the mucosa, infiltration of the submucosa of the supradiaphragmatic segment of the esophagus. There are two options for the spread of chronic inflammation - total and local reflux esophagitis. With involvement in the process of more than 2/3 of the esophageal mucosa, the development of reflux tracheitis, reflux bronchitis is possible.

At the top of the esophageal folds, erosions, small ulcers occur (in places of maximum irrigation with gastric contents). Chronic inflammation of the esophagus leads to spastic contracture and shortening of the organ.

clinical picture. Typical signs of reflux esophagitis include a burning sensation behind the sternum, heartburn, regurgitation, which worsens when lying down, dysphagia, and the positive effect of taking antacids. Pain in the chest may occur after eating, reminiscent of angina pectoris.

The occurrence of pain in reflux esophagitis is associated with peptic irritation of the esophageal wall and its spasms during regurgitation of acidic gastric contents, as well as with infringement of the prolapsed mucosa. Distinctive features of this pain: its long, burning character, localization in the xiphoid process, irradiation along the esophagus, less often to the left half of the chest, no noticeable effect from taking antacids, antispasmodics, increased in a horizontal position, especially after eating.

Particular attention in clinical diagnosis should be given to minor symptoms of dysphagia, such as a feeling of a lump behind the sternum, a feeling of hot food passing through the esophagus. A sign of gradually beginning esophagitis may be salivation and the habit of drinking water with food.

Physical examination of patients with reflux esophagitis does not provide diagnostically significant information.

The complications of reflux esophagitis include bleeding, ulceration, strictures, shortening of the esophagus, and malignancy. Chronic reflux esophagitis can lead to the development of axial hiatal hernia.

Diagnosis and differential diagnosis. The most valuable research method for this pathology is endoscopy, during which hyperemia, edema, and thickening of the folds of the mucous membrane are noted. A whitish coating covering the mucous membrane is reliable, which in the initial stages of the disease can be thin, barely noticeable, but with a long process - massive white or dirty gray. In some areas, against a background of white plaque, the bright red mucous membrane of the esophagus is often visible. In some cases, erosive and ulcerative defects in the form of stripes are detected. Changes in the mucous membrane can correspond to any of the four stages of esophagitis: from hyperemia to “crying” mucous membrane. With severe esophagitis, a lot of saliva and mucus accumulate in the lumen. pH-metry, unlike endoscopy, makes it possible to more objectively assess esophageal clearance. X-rays reveal gastroesophageal reflux.

It is necessary to differentiate reflux esophagitis with peptic ulcer of the stomach and duodenum, coronary heart disease, chronic cholecystitis and pancreatitis. The leading symptom in the differential diagnosis is pain. Differentiation with peptic ulcer is helped by the absence of late and "hungry" pains in esophagitis, as well as data obtained from endoscopy of the esophagus and stomach. Coronary pain, in contrast to esophagitis, is characterized by a connection with physical and emotional stress, the effect of nitrates, signs of ischemia on the ECG, including those according to bicycle ergometry. Ultrasound data of the abdominal organs help to exclude the pathology of the gallbladder and pancreas as the cause of the pain syndrome.

Treatment. Therapy for reflux esophagitis includes treatment of the diseases that caused it and the prescription of antireflux therapy.

Patients are advised to avoid lifting weights, bending over. It is necessary to take the correct position during rest and sleep (the headboard is raised by 15-20 cm, at an angle of 30-50 °). It is recommended to normalize body weight, eat fractionally (the last meal - 3 hours before bedtime). Alcohol and spicy foods are excluded from the diet.

Assign adsorbents and alkalizing drugs that have a protective effect on the mucous membrane. These substances include Venter, which is administered orally at a dose of 1 g (preferably in the form of a suspension) 30-40 minutes before meals 3 times a day and the 4th time on an empty stomach at bedtime. The course of treatment is 8-10 weeks. Almagel, phosphalugel, maalox, gastal have a similar effect. These drugs are used in the interdigestive period (1/2-2 hours after meals and at night) until complete remission occurs. Phosphalugel and Maalox are prescribed 1-2 packets 2-3 times a day, gastal - 2-3 tablets a day. Tea soda, a mixture of Bourget, white clay due to insufficient efficiency is not advisable to use. Enveloping and astringent action has bismuth nitrate 1 g 3-4 times a day. A high antireflux activity of a new antacid, topalkan, was noted. Mineral waters - "Borjomi", "Essentuki No. 4", "Jermuk", "Smirnovskaya" have an alkalizing effect.

To reduce acidic gastric secretion, H blockers are prescribed.₂histamine receptors (cimetidine, ranitidine, famotidine), Ka-K-ATPase inhibitors (omeprazole), a selective blocker of M-cholinergic receptors of parietal cells, its analogue buscopan. Cimetidine is prescribed 400 mg 2 times a day, ranitidine - 300 mg and famotidine - 40 mg once in the evening after dinner. Omeprazole is recommended for resistant forms of erosive and ulcerative reflux esophagitis. It is prescribed at 30-40 mg per day for 3-4 weeks. To normalize motor-evacuation disorders in reflux disease, metoclopramide (cerucal, raglan, perinorm, biomral), prepulsid (sizepride, motilium, domperidone, coordinax) are prescribed. Metoclopramide and its 2nd generation analogues increase the tone of the lower esophageal sphincter, reduce intragastric pressure, and accelerate evacuation from the stomach. Assign metoclopramide 1 tablet 3-4 times a day before meals or 2 ml intramuscularly 2 times a day. The drug is usually well tolerated. When using it, dry mouth, drowsiness, tinnitus are possible, which decrease after eating.

Sizepride is a novel gastrointestinal prokinetic agent. It increases the tone of the lower esophageal sphincter, improves esophageal clearance, enhances the motor-evacuation function of the digestive tract, and suppresses pathological refluxes (gastroesophageal and duodenogastric). The drug, unlike metoclopramide, does not block donamine receptors, is not a direct stimulant of anticholinergic receptors, and is devoid of side effects inherent in cerucal and its analogues. It is prescribed orally at 5 or 10 mg 2-3 times a day. The course of treatment lasts from 2-3 weeks to 2-3 months. Cesapride with reflux esophagitis can be used as a monotherapy.

Prognosis and prevention. The prognosis for life and work is favorable. In complicated cases, the prognosis is determined by the timeliness and quality of medical care. Patients with severe disease are assigned a disability group. Patients with chronic reflux esophagitis should be under the supervision of a gastroenterologist. Endoscopic and morphological studies are indicated at least 2 times a year due to the possibility of malignancy.

3. Peptic ulcer of the esophagus

Peptic ulcer of the esophagus is an acute or chronic disease characterized by ulceration of the mucosa of the distal segment of the esophagus under the influence of active gastric juice.

Etiology and pathogenesis. Chronic peptic ulcers of the esophagus are complications of reflux esophagitis and hiatal hernia. Their occurrence is facilitated by an internal short esophagus, focal metaplasia of the mucosa, heterotopia of the gastric mucosa into the esophagus, reflux disease with cardia insufficiency, diseases accompanied by frequent vomiting (post-vagotomy syndrome, afferent loop syndrome, chronic alcoholism).

Acute ulcers of the esophagus are possible with pathological dryness of the esophageal mucosa (xerosis), drug allergies, the use of NSAIDs, fungal infections, viral infections, skin burns and diseases of the central nervous system. These ulcers are considered symptomatic.

clinical picture. Some patients have a combined ulcerative lesion of the mucous membrane of the esophagus and gastroduodenal zone. Symptoms of a peptic ulcer of the esophagus resemble the clinical picture of peptic esophagitis: persistent heartburn, worsening after eating, when bending the body, in a lying position, regurgitation, pain when swallowing, and impaired passage of solid food occur. Complications typical of esophageal ulcers: perforation, bleeding, penetration, stricture. Bleeding is manifested by hematemesis, melena, hypochromic anemia, and a decrease in cardiac activity. Perforation of the esophagus is diagnosed extremely rarely.

The clinical symptoms of perforation are indistinguishable from the symptoms of acute penetrating and non-penetrating mechanical injury by foreign bodies. Approximately 14% of esophageal ulcers penetrate into the surrounding tissues.

Diagnosis and differential diagnosis. It is extremely difficult to suspect a peptic ulcer based on clinical symptoms. The diagnosis is verified during instrumental and laboratory studies. The most informative is x-ray and endoscopic examination. Radiologically, the ulcer appears as a niche in the supracardiac esophagus with slight perifocal edema of the mucous membrane. The esophagus in the area of ​​the ulcer is spastically contracted, and a slight suprastenotic expansion is detected above it. The ulcer is accompanied by signs of hyperkinesia and reflux esophagitis, and symptoms of hiatal hernia are very common. Sometimes the ulcer resembles a small epiphrenic diverticulum, but the latter does not have a typical clinical course and is not combined with cardial insufficiency, hernia, or esophagitis.

It is more difficult to distinguish a peptic ulcer of the esophagus from ulcerated endophytic cancer, which is accompanied by rigidity of the walls and relief of the mucous membrane, and an asymmetric shaft, by radiological signs.

The most reliable information in the verification of peptic ulcer of the esophagus is provided by endoscopy and multiple biopsy from the edges of the ulcer. When advancing the endoscope to the peptic ulcer, signs of stage I-IV esophagitis, motor dysfunction of the esophagus, perifocal edema and hyperemia of the mucous membrane are revealed. An acute ulcer is usually round or oval, with steep edges, covered with a whitish or green coating. A chronic ulcer has a flat bottom with dense and uneven walls, gentle edges, purulent-fibrinous deposits, foci of granulations and cicatricial overlays. To exclude malignancy, 4-6 biopsies are taken from the edges of the ulcer. Endoscopic examination reveals single peptic defects, elongated along the axis of the esophagus. Their length varies within 1-10 cm, but more often does not exceed 1 cm. The ulcer is often shallow, its bottom is covered with a whitish coating. Hyperemia, mucosal edema and single erosions often reflect a moderate perifocal inflammatory reaction.

After healing of a peptic ulcer, a rough linear or stellate scar or a rough diverticulum-like deformity of the wall and narrowing of the lumen remain in the esophagus.

It is necessary to differentiate peptic ulcers of the esophagus with ulcerations of a specific nature (with tuberculosis, syphilis). In these situations, specific serological tests, the results of histological and bacteriological studies significantly help. The combination of the pathology of the esophagus with damage to the lungs and other organs makes it necessary to purposefully examine the patient in relation to a specific process.

Treatment. Treatment includes a diet: mechanically and chemically gentle food is recommended, which is taken in small portions 5-6 times a day. To prevent reflux of contents from the stomach into the esophagus, the patient's position in bed should be with the head of the bed elevated. Medicines are taken lying down. Monotherapy is prescribed with a drug from one of the following pharmacological groups: antisecretory, including antacids and adsorbents, stimulants of the motor-evacuation function of the stomach (prokinetics), drugs - mucus simulators. Therapy is carried out for a long time - 1,5-3 months.

Indications for surgical treatment - lack of healing within 6-9 months, complicated course (perforation, penetration, stenosis, bleeding).

Prognosis and prevention. The course of the disease is relapsing. The prognosis for life and work is favorable. Periodic (1-2 times a year) examination on an outpatient basis by a gastroenterologist using endoscopy and biopsy is recommended.

Seasonal (spring - autumn) prevention of reflux esophagitis is carried out.

Author: Mostovaya O.S.

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