Gastric and Duodenal Ulcers (Gastroduodenal Ulcers): Symptoms, Etiology, Diagnosis, and Treatment

Gastroduodenal ulcer is a defect in the wall of the stomach or duodenum, penetrating deeper than the submucosal layer.

Relevance

In developed countries, this pathology reaches 15% of the adult population. The highest mortality rate is observed in Japan and Portugal, the lowest – in the USA and Canada. The incidence of duodenal ulcers is 5-7 times more frequent than gastric ulcers, and the ratio of men to women is 3-4 to 1.

Anatomy

The stomach is located in the upper floor of the abdominal cavity. The stomach is kept in its position by being held in place by the esophagus and duodenum, and by being held in place by a number of ligaments:

• With liver;
• Pancreas;
• Spleen;
• Transverse colon.

At the point of transition of the stomach to the duodenum is the pyloric stomas.

The gastric wall has serous, muscular, submucosal and mucosal layers. In the muscular layer, the fibers have multidirectional layers:

• Longitudinal;
• Slant;
• Circular.

The gastric mucosa is 0.5 to 1.5 mm thick and has a complex structure (folds and gastric fossae are formed) and structure (mucocytes, tubular glands).

The structure of the glands of the stomach differs in different parts of the organ:

• Cardiac compartment – intermediate, mucoid and argentophilic cells;
• Body and fundus – cladding cells (synthesize hydrochloric acid), supplementary cells (mucoid, synthesize mucus) and chief cells (synthesize pepsinogen);
• Pyloric section – the glands are composed mainly of mucoid and lining cells.

Endocrine cells (HITS) are located throughout the gastric mucosa.

The cells of the stomach are constantly renewing – on average, the epithelium is renewed every 3-5 days.

The blood supply to the stomach is from branches of the primal trunk:

• Left and right gastric arteries;
• Left and right gastric-salvic arteries;
• Short arteries of the fundus of the stomach.

Innervation is carried out by the vagus nerve and branches of the solar plexus, there are 3 main nerve plexuses in the wall of the stomach:

• Subserosal;
• Intermuscular;
• Submucosal.

The stomach produces up to 2 liters of gastric juice per day – the latter, in addition to hydrochloric acid, contains proteolytic enzymes and mucus.

The duodenum is an extension of the stomach, beginning at the pyloric junction and ending at the duodeno-jejunal junction (at the site of the ligament of Treitz).

The intestinal wall is made up of 3-4 layers:

• Serous (at mesoperitoneal sites);
• Muscular;
• Submucosal;
• Slimy.

The muscle sheath also has layers:

• The outer longitudinal layer (is an extension of the gastric layer, which provides continuity of the peristaltic wave);
• Inner Circular Layer.

The mucosa of the duodenum forms intestinal villi (up to 40 villi per 1 mm), the villi are covered with enterocytes. The mucosa also contains mucin-producing bocaloid cells and endocrine cells (diffusely located).

There are parts of the DIC that stand out:

• Upper horizontal (the bulb of the WPC);
• Top-down;
• Bottom horizontal;
• Rising.

The descending branch of the duodenum opens through the greater duodenal papilla (Fater nipple):

• Common bile duct;
• Wirsung’s duct

and through the small duodenal papilla – the accessory duct of the pancreas (Santorini’s duct).

The blood supply to the duodenum is from branches of the superior mesenteric artery:

• Anterior superior pancreaticoduodenal artery;
• Posterior superior pancreaticoduodenal artery;
• Anterior inferior pancreaticoduodenal artery;
• Posterior inferior pancreaticoduodenal artery.

Classification of gastric and duodenal ulcer disease

By localization

• Gastric ulcers (cardiac, subcardiac ulcers, gastric body ulcers (major and minor curvature), pyloric and antral ulcers);
• Ulcers of the 12-peritoneum (ulcers of the bulb of the duodenum, postbulbar ulcers).

By stage of ulcer development

• Active stage;
• Healing stage;
• Scarring stage (red scar, white scar).

By severity of course

• Latent;
• Lightweight;
• Medium severity;
• Severe course.

By etiologic factor

• True ulcers on the background of peptic ulcer disease;
• Acute ulcers (result of dietary errors, consumption of corrosive media);
• Symptomatic ulcers (as a result of the course of another disease – atherosclerosis, uremia, taking NSAIDs and others).

By size

• Small (up to 5 mm);

• Medium (5-10 mm);

• Large: 11-29 mm for the stomach and 11-19 mm for the duodenum;

• Giant: for the stomach 30 mm or more, for the duodenum 20 mm or more.

By number

• Singles;
• Plural.

Classification by A.G. Johnson (1990)

• Type I chronic ulcers are small curvature ulcers;
• Type II chronic ulcers – combined with duodenal ulcer, including healed duodenal ulcer;
• Type III chronic ulcers are prepyloric ulcers;
• Type IV chronic ulcers are acute superficial ulcers;
• Type V chronic ulcers – due to Zollinger-Elisson syndrome.

Forrest’s classification

• Type FI is active bleeding:

• Ia – pulsating jet;
• Ib is a flux.

• Type FII – signs of recent bleeding:

• IIa is a visible (non-bleeding) vessel;
• IIb – fixed clot thrombus;
• IIc – flat black spot (black bottom of the ulcer).

• Type FIII is an ulcer with a clear (white) fundus.

Classification of gastric and duodenal ulcer disease

Predisposing factors for the development of peptic ulcer disease

• Heredity: the predisposition is transmitted predominantly through the male line, the incidence in first-line heirs is 3 times more frequent than without aggravated heredity.
• Alcohol: in high concentrations has a direct damaging effect, disrupts the protective mucinous layer, stimulates the glands of the stomach, thereby increasing the production of hydrochloric acid.
• Smoking: nicotine leads to vasoconstriction of the stomach, stimulates the production of hydrochloric acid, provokes gastroduodenal reflux, while reducing the secretion of bicarbonates (worsening the protective properties of the mucosa).
• Eating habits: spicy food, excessively hot or excessively cold food, coarse food that can physically traumatize the GI wall.
• Irregular feeding: starvation hypersecretion and acid-peptic damage to the mucosa.
• Taking a number of medications: NSAIDs, glucocorticosteroids, anticoagulants, aspirin, alendronate.
• Prolonged or regular stress: development of stress ulcers.

Etiology of ulcers

In the development of gastroduodenal ulcers, the main causative factor is the predominance of aggression factors over the protective properties of the gastric and duodenal mucosa, which over time leads to the development of mucosal defects, and in the absence of treatment – the formation of complications (the so-called “Shoy scales”).

Aggression factors include:

• Excess production of hydrochloric acid: increased activity of gastric gland lining cells, hypertonicity of the vagus nerve, increased secretion of gastrin;
• Helicobacter pylori: secrete the enzyme mucinase, which disrupts the protective properties of the mucosa, secrete catalase and urease, which directly lead to the death of epitheliocytes, the mere presence of the microorganism in the submucosal layer causes an inflammatory reaction in the gastric wall;
• Gastroduodenal reflux: bile with pancreatic juice thrown in this condition destroys the protective layer of the stomach wall, leading to further direct damage to the cells of the mucosa;
• Hypergastrinemia (Zollinger-Ellison syndrome);
• Cytomegalovirus infection;
• Radiation therapy and chemotherapy;
• Crohn’s disease.

Protective factors include:

• Mucosal (mucinous) barrier: located directly on the mucosal layer and closely associated with it, consists of mucopolysaccharides and glycoproteins, prevents the penetration of aggression factors to epithelial cells;
• Continuous highly active epithelial regeneration: as mentioned above, gastric mucosal cells are renewed every 3-5 days, which promotes rapid repair of mucosal damage.

Clinical picture

• Pain syndrome. It is localized in the upper abdomen (in the epigastrium on the right side in duodenal ulcer or pyloric ulcer, in the epigastrium on the left side or behind the sternum in cardiac ulcer, in pyloric ulcer – pain irradiates to the back). Pain is due to both direct irritation of nerve endings acidic content, and spasm of the muscle layers of the stomach wall. Gastric ulcers are characterized by hunger pains, which are relieved after taking food or antacid medication.
• Heartburn. Pain and burning behind the sternum due to reflux of acidic contents from the stomach into the esophagus. This reflux is due to impaired gastric motility due to the irritating effect of the ulcer on the muscles of the organ.
• Nausea and vomiting. They occur against the background of reflex irritation and contraction of the stomach. It may also result from the development of stenosis of the outlet of the stomach.
• Decreased or lack of appetite (reflex genesis).
• Pain on palpation of the abdomen – in the projection of the ulcer, there may also be defans of the muscles of the anterior abdominal wall. It is possible to detect pain on percussion of the abdomen in the projection of the ulcer – Mendel’s symptom.
• It should be noted the possibility of asymptomatic course of peptic ulcer disease (according to some authors up to 30%).

Diagnosis of gastric and duodenal ulcer disease

• Examination of gastric secretion (basal acid production and maximum acid production). Maximum acid production is determined after stimulation of gastric secretion (histamine, pentagastrin).
• pH-metry. Normally, the acidity of gastric contents is 1.6-2.0. Duodenal ulcer is characterized by increased acidity in the pyloric duct and duodenum.
• Diagnosis of Helicobacter infection (breath test, blood test, stool analysis).
• Radiography is the main diagnostic method in confirming a perforating ulcer – free gas under the dome of the diaphragm.
• Fluoroscopy. The main symptom is the “niche” symptom: when the ulcer crater is filled with contrast agent, a characteristic depression (“niche”) appears. Symptom of convergence of folds – radially located folds of the stomach with the ulcer located in the center. It also often reveals impaired gastric peristalsis, retrograde flow of food into the esophagus. The effectiveness of this method is greatest in the diagnosis of impaired evacuation function and the development of stenosis of the outlet section of the stomach. Relaxation duodenoscopy is used for diagnostics of duodenal pathology (before the study, maximum relaxation and expansion of duodenal muscles are achieved (metacian, aeron)) for complete filling of all parts of the intestine and visualization of its contours.
• Endoscopic examination(FEGDS) – the “gold standard” of diagnostics at the modern stage – visualization of ulcer defect, the stage of the process, its localization, the presence of complications, biopsy, diagnosis of Helicobacter infection, the possibility of endoscopic manipulations in case of complications (hemostasis, clipping defects, argon plasma coagulation, endosutures).
• ULTRASOUND. At the current level of development of this technology, it is possible to detect ulcer infiltrate and defect of the stomach wall, the presence of complications of peptic ulcer disease (stenosis, perforation, cancer).
• OBP CT – combines the advantages of fluoroscopy and ultrasound – it is possible to diagnose both the ulcer defect itself and the development of complications (perforation, stenosis, penetration, cancer).

Complications and treatment in gastric and duodenal ulcer disease

1. Perforation or perforation

This complication according to a number of different sources makes from 3 to 30% of all complications in gastroduodenal ulcers. Males account for 95% of these complications. Pyloroduodenal ulcers account for 75%. The combination of perforated ulcer and bleeding reaches 10%.

In the clinical picture of a perforated ulcer, 3 periods are distinguished:

• First 4-6 hours (primary abdominal shock);
• 6-12 hours (period of perceived well-being);
• More than 12 hours (peritonitis stage).

In the case of perforation, the onset of pain is acute and sudden (“dagger pain”), the pain is localized in the first hours in the upper abdomen, then spreads to the right lateral canal and then throughout the abdomen.

In the first hours from the time of the perforation takes place:

• Bradycardia (due to vagus nerve irritation);
• Dry tongue;
• Possible phrenicus syndrome (irradiation of pain to the right clavicle, scapula due to irritation of the right diaphragmatic nerve);
• On percussion, hepatic bluntness may be absent (due to free gas in the abdominal cavity);
• Pain at rectal examination(Kulenkampf’s symptom).

As mentioned above, free gas is detected on the radiograph (in 70-80% of cases). To clarify the diagnosis it is possible to perform FEGDS, and if there is still doubt about the presence of a perforation – repeat radiography for the presence of free gas (in this case, the percentage of diagnostic value is higher).

Against the background of further progression of the disease leading symptoms of intoxication and peritonitis:

• Tachycardia;
• Decreased BP;
• Abdominal bloating;
• Intestinal paresis;
• Leukocytosis is on the rise.

Atypical forms of perforation (up to 4-6% of cases) include:

• Perforation of the posterior wall of the stomach (into the omental pouch);
• Perforation of the posterior wall of the duodenum (into the retroperitoneal tissue);
• Perforation of high ulcers of the cardiac part of the stomach at the border with the esophagus;
• Covered Perforations.

In these cases, the course of the clinical picture is blurred, without vivid main symptoms.

Treatment of perforated ulcers is exclusively operative (suturing of the ulcer, gastric resection).

The most common procedure is suturing the ulcer:

• Simple suturing with knotted sutures;
• Suturing by tamponade with omentum according to Oppel-Polikarpov (performed in the presence of a large perforation and impossibility of resection);
• Ulcer excision with pyloroduodenoplasty.

Indications for gastric resection are:

• Callous ulcer;
• Gastric ulcers;
• Perforation of multiple ulcers;
• Combination of perforation and stenosis of the outlet of the stomach.

There are many types of gastric resections, but the most applicable are:

• Bilroth 1 and Bilroth 2 resection (in Hofmeister-Finsterer modification);
• Roux resection;
• Balfour resection.

After surgical treatment of a perforated ulcer, a full course of anti-ulcer treatment is mandatory.

2. Bleeding

This complication develops in 10-15% of patients. Males up to 70%. The number of duodenal ulcers is up to 80%. Lethality in this pathology is up to 7-10%.

Bleeding develops at arrosion (destruction) of the wall of a large vessel in the bottom of the ulcer against the background of disease progression. The severity of the clinical picture is characterized by the amount of blood loss:

• From negligible (less than 20% of circulating blood volume);
• To severe – over 40% of the ODC.

The severity of bleeding determines the variability of clinical manifestations:

• Tachycardia;
• Tachypnoea;
• Hypotension;
• Decreased diuresis;
• A disturbance in the level of consciousness;
• Psycho-neurological symptoms (anxiety, agitation, hallucinations, delusions);
• Pale skin.

Of the symptoms of this complication, the most common are:

• Vomiting (vomiting blood – hematomesis or like “coffee grounds” – brown-black color gives vomit masses hematin as a result of oxidation of hemoglobin by hydrochloric acid of the stomach);
• Degestational stools (melena – black and purple stools, unformed consistency, this color stool acquires as a result of the action of digestive enzymes and microorganisms on hemoglobin with degradation and color change of the spilled blood).

Bergman’s symptom is characteristic – a decrease in ulcer pain at the onset of a bleeding episode.

The gold standard of diagnosis is FEGDS. This pathology requires mandatory hospitalization in a surgical hospital.

In case of moderate and severe blood loss, patients are transported to the operating room, where all diagnostic manipulations and intensive care are performed.

Conservative treatment consists of hemostatic therapy:

• Fresh frozen plasma;
• Cryoprecipitate or thromboconcentrate;
• Activators of thromboplastin formation (ethamsylate);
• Inhibitors of fibrinolysis (aminocaproic acid, hemostad, tranexam);
• Vitamin K (vicasol);
• Calcium chloride;
• Local hypothermia;
• Correcting anemia (red blood cells);
• Correction of hypovolemia (crystalloid solutions);
• Anti-ulcer treatment (proton pump inhibitors, H2-histaminoblockers, antacids);
• Symptomatic therapy.

On the background of the treatment, an emergency FEGDS with clarification of ulcer localization and endoscopic hemostasis is performed.

In case of ineffectiveness of these measures and continued bleeding, surgical intervention is performed. The type of surgical intervention is determined depending on the localization and nature of the ulcer, as well as the patient’s condition.

Thus, the most justified pathogenetically is the resection of 2/3 of the stomach (elimination of ulcer and hypersecretion of hydrochloric acid). However, due to the severity of the condition, age and comorbidity, not all patients can undergo such a volume of surgery – in such situations, a reduced volume of assistance is performed:

• Ulcer excision with gastric or duodenal plasty;
• If the patient is extremely severe, stitching of the ulcer defect to stop bleeding is limited.

3. GI tract obstruction

Gastrointestinal permeability disorders (gastric outlet stenosis, pyloroduodenal stenosis) can be compensated, subcompensated and decompensated.

This complication can wear:

• Temporary character (against the background of ulcer exacerbation due to edema and tissue infiltration with the development of narrowing of the lumen of the GI tract);
• And permanent (against the background of scar deformation after healed ulcers).

Against the background of the disturbed exit of the stomach contents, the latter stretches, increases in volume, against which the food in it stagnates and there is regurgitation of the contents. Due to the described pathogenesis, the main clinical picture of the disease develops:

• Burping a rotten odor;
• Vomiting “stale” food eaten (vomiting brings relief);
• Intermittent pain in the upper abdomen and a feeling of fullness in the stomach even after a small meal;
• Progressive weight loss (due to lack of nutrient intake into the gut);
• Constipation.

With further progression of the disease and lack of treatment, electrolyte disturbances increase, which can lead to:

• Neurological disorders;
• Muscle dysfunction;
• Hypochloremic coma.

As described above, the gold standard for diagnosing this pathology is a fluoroscopic examination – makes it possible to establish the degree of stenosis.

FEGDS can also reveal the presence of stenosis, but the degree of compensation is extremely difficult to specify and can only indirectly by the patency of the narrowing for the endoscope:

• The normal diameter is 2.5 cm;
• In compensated stenosis – 1.5 cm;
• In the subcompensated stage, 0.5-1.5 cm;
• In decompensation, less than 0.5 cm.

Treatment at the initial stages is conservative in order to differentiate temporary and scar constriction. Thus, in the process of conservative treatment within 7-10 days against the background of healing of the ulcer defect and elimination of inflammatory reaction in case of temporary stenosis the patency of the outlet part of the stomach is restored, while in case of organic scar constriction there is no improvement.

In permanent stenosis, treatment is exclusively surgical: after preoperative preparation for correction of electrolyte and protein disorders, gastric resection is performed (more often in the volume of 2/3).

4. Penetrating ulcer

Penetration of the ulcer is the penetration of the bottom of the ulcer defect into the neighboring organs (hepatoduodenal ligament, liver, pancreas, less often into the mesentery and wall of the colon, gallbladder, small omentum).

The main difference of this complication in the clinical picture is a change in the nature of the pain syndrome – the pain becomes localized, has a constant character, regardless of food intake.

There may be a clinic of lesions of the organ into which penetration has occurred:

• Pancreatitis;
• Cholecystitis;
• Reactive hepatitis;
• Mechanical jaundice;
• Omentite;
• Formation of inflammatory infiltrates of the abdominal cavity.

Diagnosis is the same as outlined above:

• FEGDS (deep ulcer with undermined edges, in the bottom can sometimes be visualized penetrated organ);
• Fluoroscopy (deep “niche”, fixed, not displaced by changes in body position);
• Ultrasound (infiltrates, inflammation of adjacent organs);
• CT of OPD (visualization of ulcer, infiltrate).

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5. Malignization

Against the background of a long-term chronic inflammatory process occurs dysplasia of epithelial cells with the development of malignant degeneration and tumor formation.

Diagnosis:

• FEGDS with visualization of the process and biopsy;
• C.T. SCAN OF THE OBP.

Treatment is surgical only, followed by specific oncologic treatment.