Stenosis of the pylorus and duodenum

Peptic ulcer of the stomach and duodenum is complicated by stenosis of the pylorus or the initial department of the duodenum in 6-15% of cases. There are organic and functional pyloroduodenal stenosis. Organic - is due to post-ulcer cicatricial changes, functional - edema and spasm of the pyloroduodenal zone. A characteristic feature of functional (dynamic) stenosis is that it develops during peptic ulcer exacerbation and disappears after carefully conducted treatment and relief of exacerbation.

Organic stenosis of the pylorus and stenosis of the duodenum have an identical clinical picture and are combined by the term pyloroduodenal stenosis. There are three stages of its flow: compensated, subcompensated and decompensated.

[1], [2], [3], [4], [5], [6], [7], [8]

Compensated pyloroduodenal stenosis

Compensated pyloroduodenal stenosis is characterized by moderate constriction, hypertrophy of the stomach muscles, increased motor activity. This leads to the fact that the evacuation of food from their stomach occurs at regular intervals or is slowed down slightly. For compensated pyloroduodenal stenosis, the following symptoms are characteristic:

• after eating, there is a feeling of overcrowding in the epigastric region;
• often repeated heartburn caused by gastroesophageal reflux. To stop heartburn, patients repeatedly take soda during the day;
• often there is an eructation of sour and vomiting food, which brings relief;
• with the radiographic examination of the stomach, a highly-initiated, intensified segmenting peristalsis of the stomach is defined, but there is no significant slowing of its emptying.

The duration of the compensated stage can vary from a few months to several years.

Compensated pyloroduodenal stenosis

Compensated stenosis is characterized by the following main manifestations:

• the most important feature is abundant vomiting, which brings the patient considerable relief, it allows him to get rid of a very painful and painful feeling of stomach eruption. Often the patient himself causes vomiting to ease his own well-being. Vomit masses contain food eaten on the eve or even in the evening;
• very characteristic of belching rotten;
• quite often they are concerned about significant pain and feeling of bursting in the epigastrium even after taking a small amount of food;
• there is a progressive weight loss of the patient, but at the beginning of the subcompensated stage it is not pronounced sharply;
• when examining the abdomen in the projection of the stomach, peristaltic waves visible from left to right are visible;
• with percussion palpation of the upper abdomen in accordance with the location of the stomach (especially in the antrum section), a pronounced splashing sound is determined several hours after eating and even on an empty stomach. The lower border of the stomach is determined much lower than the navel, indicating a widening of the stomach;
• Radiologically there is a significant amount of gastric contents on an empty stomach, a moderate expansion of it, initially lively, intensified, but then rapidly weakening peristalsis. The most characteristic radiographic evidence is a violation of the evacuation function of the stomach: the contrast substance remains in the stomach for 6 or more hours, and sometimes more than a day.

The duration of the subcompensated stage ranges from several months to 1.5-2 years.

[9], [10], [11]

Decompensated pyloroduodenal stenosis

Decompensated pyloroduodenal stenosis is due to an increasingly weakening motor-evacuation function and an increase in the degree of stenosis. Often this is exacerbated peptic ulcer. The characteristic signs of decompensated pyloroduodenal stenosis are:

• frequent vomiting, almost no longer bringing relief to the patient, since it does not completely relieve the stomach from stagnant contents;
• constant eructations are rotten;
• a painful feeling of constant overflow of the stomach;
• painful thirst due to the fact that the patient loses fluid during vomiting and when washing the stomach;
• periodic muscle twitching caused by electrolyte disorders, and with very pronounced electrolyte shifts convulsive seizures ("gastric" tetany);
• complete lack of appetite;
• progressive depletion of the patient;
• sharp decrease in turgor and elasticity of the skin;
• sharpened facial features;
• the protrusion of contours of the distended stomach in the epigastric region through the thinned anterior abdominal wall and the disappearance of the peristaltic waves defined in the subcompensated stage;
• the constantly determined splash noise even with a slight jerky poklachivanie on the front abdominal wall;
• very low situated lower gastric boundary, sometimes lower than l. Bilias (on the noise of splashing);
• the need for regular gastric lavage, which allows freeing the stomach and alleviating the condition of the patient;
• a sharp widening of the stomach, a decrease in its propulsive capacity, a large amount of contents (all these signs are well revealed in fluoroscopy of the stomach).

With frequent vomiting, a large number of electrolytes, fluid and a hypochloremic coma may develop.

[12], [13], [14]

Laboratory data and electrocardiography

• General analysis of blood: possible development of normo- or hypochromic anemia (due to a decrease in intake and absorption in the intestines of the main components of food and trace elements (particularly iron) .After the progression of pyloroduodenal stenosis with the onset of multiple vomiting and dehydration, an increase in the number of erythrocytes and hemoglobin due to the thickening of the blood.) The increase in ESR is also characteristic.
• Biochemical blood test: decrease in the total protein and albumin content; with repeated vomiting and dehydration, electrolyte disturbances occur-hyponatremia, hypokalemia, hypochloraemia, hypocalcemia; possible reduction in iron content. Sharply expressed hypochloremia is accompanied by the development of hypochloremic alkalosis and an increase in the urea blood content.
• ECG. Expressed diffuse changes in the myocardium - a decrease in the amplitude of the T wave in many leads. When the electrolyte blood composition is disturbed, characteristic ECG changes appear:
  • at a hypocalcemia - a progressing elongation of an electric systole of ventricles - interval QT, less often shortening of an interval PQ and depression of amplitude of a wave T;
  • with hypokalemia - a decrease in the amplitude of the T wave or the formation of a two-phase (±) or negative asymmetric T wave; an increase in the amplitude of the tooth U; elongation of ventricular systole - QT interval; horizontal displacement of the ST segment below the isoline.