Chronic enteritis - Symptoms.

The symptoms of chronic enteritis consist of two symptom complexes that should be considered as manifestations of functional disorders associated with changes in the structure of the small intestinal mucosa. One of them, the local enteral syndrome, is caused by a disorder in the processes of parietal (membrane) and cavity digestion (maldigestion); the other, the general enteral syndrome, is caused by a disorder in the absorption of food ingredients (malabsorption), which results in disorders of all types of metabolism and changes in the general condition of the body.

Chronic enteritis of the first degree of severity is characterized by intestinal symptoms, II - a combination of intestinal symptoms with a mild disturbance of metabolic processes, III - severe metabolic disorders with the occurrence of often irreversible changes in internal organs. The symptoms of chronic enteritis in its late stage are practically no different from the symptoms of other diseases occurring with malabsorption syndrome - gluten enteropathy, exudative hypoproteinemic enteropathy, Crohn's disease, Whipple's disease, etc. Therefore, it is necessary to examine patients with chronic enteritis of the third degree of severity especially carefully to exclude these diseases.

Local enteral syndrome. It is characterized by the following intestinal manifestations: flatulence, abdominal pain, mainly in the middle part, bloating (the abdomen is shaped like a cap), loud rumbling, diarrhea, less often constipation, or their alternation. Palpation reveals pain in the middle part of the abdomen, as well as on the left and above the navel at the level of the 12th thoracic - 1st lumbar vertebrae (Porges symptom), "splashing noise" in the area of the cecum (Obraztsov symptom). The feces have a clayey appearance, polyfecalia is typical.

The following clinical symptoms are characteristic of local enteral syndrome.

Bowel disorders

Chronic enteritis is most characterized by diarrhea, the frequency of stool fluctuates from 4-6 to 20 times a day. Sometimes patients note a violent urge to defecate immediately after eating, while the stool is abundant and watery. Defecation may be accompanied by general weakness, hand tremors, tachycardia, and decreased blood pressure.

The amount of feces in chronic enteritis is increased (polyfecalia), the feces are liquid or mushy, light yellow in color, contain pieces of undigested food, muscle fibers (creatorrhea). The presence of blood and mucus in the feces is uncharacteristic. With a high fat content (steatorrhea), the feces become gray, clayey, shiny, and ointment-like. The predominance of putrefactive processes causes a foul odor and alkaline reaction of the feces. With fermentation processes in the intestines, the feces are foamy, with gas bubbles, and have an acidic reaction.

The appearance of diarrhea in chronic enteritis is caused by:

• intestinal hypersecretion;
• increased osmotic pressure in the small intestine;
• intestinal exudation;
• acceleration of the passage of intestinal contents;
• insufficient absorption of bile acids in the small intestine.

In mild and moderate forms of chronic enteritis, diarrhea is caused mainly by increased exudation; in severe forms of the disease, by intestinal hypersecretion and increased osmotic pressure in the small intestine.

The occurrence of diarrhea in chronic enteritis is associated with intestinal hypersecretion, increased osmotic pressure in the small intestine, disorder of its motor function, resulting in acceleration of the passage of intestinal contents, intestinal hyperexudation, and in patients with chronic enteritis of I and II severity, diarrhea predominates, caused mainly by increased exudation, grade III - more often by intestinal hypersecretion and increased osmotic pressure in the intestinal cavity. The study of the pathogenesis of diarrhea at the molecular level made it possible to establish that in the "brush" border of the mucous membrane of the small intestine there are two enzymes with anion-stimulated ATPase activity: Na ⁺, HCO3 - ATPase and the newly isolated NaCl/HCO ^- - ATPase, which apparently also participate in ensuring the active transfer of ions from cells to the intestinal lumen.

Flatulence

Flatulence is most pronounced in the afternoon (at the height of intestinal digestion), accompanied by moderate abdominal pain of a diffuse nature, which intensifies after eating and decreases after the passage of gases and defecation. With flatulence, the abdomen increases in size, the patient is hampered by a belt, a strap, and feels difficulty breathing. Percussion of the abdomen reveals widespread tympanitis. Flatulence is often accompanied by pain in the heart, palpitations, and sometimes paroxysmal tachycardia. Flatulence often intensifies after taking sweet milk and dishes containing it.

Stomach ache

Abdominal pain in chronic enteritis is not the leading symptom, but is observed quite often. It is localized around the navel (with predominant damage to the jejunum), in the right iliac region (with predominant damage to the ileum); often the pain spreads throughout the abdomen.

With chronic enteritis, the following types of abdominal pain are possible:

• spastic;
• due to flatulence;
• mesenteric;
• consequence of ganglionitis;
• of mixed nature.

Spastic pain is caused by spastic contractions of the small intestine and is paroxysmal in nature, localized around the navel.

Pain due to flatulence is usually of a constant nature, associated with bloating of the intestines with gases and decreases after the passage of gases and defecation.

Mesenteric pain is caused by the development of non-specific mesadenitis. These pains are constant, are not related to food, are not relieved by anticholinergics, antispasmodics, and do not disappear after defecation and gas discharge. The pains are located along the mesentery of the small intestine in the direction: right iliac region - umbilical region - left hypochondrium. When the mesentery of the small intestine is involved in the inflammatory process, palpation pain is felt at the following points:

• Perges point - to the left and above the navel at the level of the 12th thoracic and 1st lumbar vertebrae;
• Sternberg points - 1 - in the ileocecal region, 2 - above the navel on the right at the level of the second lumbar vertebra.

In addition, with the development of mesoadenitis, a cross Sternberg symptom appears. The method for determining the symptom is as follows. Using deep sliding palpation with the right hand, feel the cecum and move it outward and slightly downward. Without releasing the right hand, feel the right iliac region medially to the displaced cecum with the left hand. With inflammation of the mesenteric lymph nodes, there is clear pain here. If the pain is caused by inflammation of the cecum, then there is no pain medially from it.

Pain due to ganglionitis. In chronic enteritis, the ganglia of the autonomic nervous system may be involved in the pathological process. In this case, the pain is of a peculiar burning nature, it is constant, does not decrease after defecation and gas emission, as well as after the use of antispasmodics.

Mixed pains are caused by a combination of causes that cause abdominal pain. Most often, this is a combination of spasmodic pains and pains caused by flatulence.

Characteristic local manifestations of chronic enteritis are rumbling in the stomach, intolerance to sweet milk, which manifests itself as flatulence, diarrhea after taking milk and dishes containing it. This is caused by either an allergy to milk or a deficiency of lactase in the intestine (congenital or acquired), which breaks down milk sugar - lactose.

During an objective examination of the patient, the following characteristic manifestations of local enteral symptoms can be identified:

• a grayish-white coating on the tongue;
• bloating, mainly in the central parts (with severe flatulence) or depression in various parts of the abdomen (with severe diarrhea).

V. P. Obraztsov pointed out in his lectures the following characteristic signs of chronic enteritis:

• loud rumbling when palpating the cecum, which is caused by the entry of liquid contents of the small intestine into the cecum; this is especially pronounced in case of ileocecal valve insufficiency. Normally, the cecum does not rumble when palpated, because the contents in it are quite thick;
• rumbling on palpation of the terminal section of the ileum;
• spastic contractions of the terminal ileum.

General enteral syndrome. It is characterized primarily by protein metabolism disorders, which can be associated with other metabolic shifts and changes in a number of organs and systems, such as endocrine, hematopoietic, and hepatobiliary.

General enteral syndrome develops in moderate and severe forms of the disease and is caused by the development of maldigestion (digestive disorder in the small intestine) and malabsorption (impaired intestinal absorption) syndromes.

Patients complain of general weakness, malaise, decreased performance, irritability, poor appetite, memory impairment, headaches, and dizziness. Many patients develop functional dumping syndrome (characteristic of enteritis with predominant damage to the ileum). It consists in the fact that after eating food, especially rich in carbohydrates, due to the rapid passage of food through the intestine, rapid absorption of carbohydrates, and irritation of the insular apparatus, hyperinsulinism phenomena occur: sweating, hand tremors, palpitations.

Patients with chronic enteritis have dry, flaky, pale or grayish skin, reduced turgor and elasticity, pigment spots on the face and neck, dull, brittle nails, sometimes like "watch glasses", hair that falls out easily. The tongue has teeth marks along the edges, sometimes crimson-red, cracked, the papillae are atrophied ("varnished tongue").

In connection with malabsorption and maldigestion syndromes, all types of metabolic disorders develop.

Protein metabolism disorders

Protein metabolism disorders are manifested by the following symptoms:

• progressive weight loss;
• muscle atrophy, decreased muscle strength;
• hypoproteinemia (the content of total protein and albumin in the blood is sharply reduced); with a sharp drop in protein in the blood, hypoproteinemic edema develops;

The causes of protein metabolism disorders in chronic enteritis are:

• decreased activity in the mucous membrane of the small intestine of enzymes involved in protein hydrolysis (glycine-leucine dipeptidase and other peptide hydrolases, enterokinase and other enzymes);
• amino acid malabsorption;
• exudative enteropathy syndrome with increased loss of protein into the lumen of the gastrointestinal tract.

Disorders of fat metabolism

The small intestine plays a major role in lipid metabolism: it synthesizes cholesterol, triglycerides, absorbs fats, transports exogenous triglycerides (neutral fats) in the form of chylomicrons, and endogenous low-density lipoproteins. Some lipids are excreted in feces.

Disorders of fat metabolism have the following characteristic symptoms:

• weight loss, disappearance of subcutaneous fat;
• steatorrhea (increased excretion of fat in the feces);
• changes in the lipid spectrum of blood serum (decrease in the content of cholesterol, phospholipids, triglycerides).

The main causes of lipid metabolism disorders:

• decreased activity of lipase in the jejunum, which ensures the initial stages of triglyceride hydrolysis;
• disturbance of digestion and absorption of fat.

Disorders of carbohydrate metabolism

Disorders of carbohydrate metabolism in chronic enteritis are observed less frequently than disorders of protein and lipid metabolism, are expressed much less and are manifested by the following symptoms:

• fermentative intestinal dyspepsia (bloating, rumbling, transfusions, severe flatulence, diarrhea). These symptoms are caused by the fermentation of absorbed carbohydrates under the influence of intestinal flora;
• a tendency to decrease blood glucose levels; pronounced hypoglycemic manifestations are not often observed;
• milk intolerance (caused by a deficiency of the enzyme lactase);
• flat glycemic curve after glucose load.

The causes of carbohydrate metabolism disorders are:

• decreased activity of enzymes that break down carbohydrates: deficiency of lactase (in 70-85% of patients), sucrase (in 45-50%), maltase (in 55% of patients), as well as a-amylase produced by the pancreas and g-amylase produced by enterocytes;
• impaired absorption of carbohydrates in the small intestine.

Disorders of mineral metabolism

Disturbances in mineral metabolism are extremely characteristic of severe malabsorption syndrome.

Hypocalcemia develops in 87% of patients with a disease duration of more than 10 years. The main manifestations of calcium deficiency:

• decreased calcium levels in the blood;
• increased neuromuscular excitability (convulsions of the arms and legs, trunk; muscle pain; positive Chvostek's symptom - convulsive contraction of the facial muscles and the corresponding half of the face when tapping at the tragus of the auricle, at the exit of the facial nerve; positive Trousseau's symptom - air is pumped into the cuff of the tonometer, placed on the shoulder area, and when the pressure in it reaches a value exceeding systolic blood pressure, a convulsive contraction of the hand occurs in the form of an "obstetrician's hand");
• osteoporosis (in severe cases of malabsorption syndrome).

The main reason for the development of calcium deficiency is a violation of its absorption in the intestine.

Disruption of the exchange of other electrolytes, microelements and water-salt metabolism.Due to the disruption of the intestinal absorption function in patients with chronic enteritis, there is a tendency for the content of sodium and potassium in the plasma to decrease, as well as a decrease in the blood level of magnesium, phosphorus, and trace elements: manganese, copper, lead, chromium, strontium, and vanadium.

Certain changes occur in the water-salt balance, which is caused by the development of secondary hyperaldosteronism as a compensatory-adaptive reaction of the body in response to a decrease in sodium reabsorption in the intestine and the loss of sodium and water during diarrhea. Violation of the water-salt balance is manifested by weakness, muscle pain, decreased muscle tone, nausea, vomiting, extrasystolic arrhythmia, and decreased blood pressure.

Of great clinical significance is iron deficiency, which is caused by impaired iron absorption and has the following manifestations:

• iron deficiency hypochromic anemia;
• dry skin and mucous membranes;
• dysphagia due to atrophic changes in the esophageal mucosa;
• changes in nails (nails lose their natural shine, become brittle, a spoon-shaped depression appears on the surface of the nail - koilonychia);
• hair fragility and loss;
• perversion of taste and smell;
• atrophic changes in the gastric mucosa, decreased secretory function of the stomach;
• decreased iron levels in the blood.

Vitamin metabolism disorders

Polyhypovitaminosis of varying degrees of severity occurs in almost all patients with severe and moderate chronic enteritis.

Vitamin C deficiency manifests itself in increased bleeding of the gums, nosebleeds, and the appearance of hemorrhagic rash on the skin (with severe vitamin C deficiency) due to pronounced capillary permeability.

Deficiency of vitamin B ₁₂ and folic acid manifests itself as B ₁₂ (folic acid) deficiency anemia, the characteristic symptoms of which are:

• hyperchromic macrocytic anemia;
• the appearance of hypersegmented neutrophils in the leukocyte formula;
• atrophic gastritis and absence of free hydrochloric acid in gastric juice;
• damage to the nervous system in the form of funicular myelosis.

Deficiency of vitamin PP (nicotinic acid) is characterized by pigmentation of the skin of exposed areas of the body, dermatitis, taste disturbance, tingling sensation and reddening of the tongue with smoothing of its papillae (polished "raspberry" tongue); with severe deficiency of vitamin PP, dementia may develop (with prolonged deficiency) and increased diarrhea.

Vitamin A deficiency manifests itself as dry skin and deterioration of evening and night vision (“night blindness”).

_{Vitamin B1} deficiency is characterized by a burning and tingling sensation in the legs, "crawling ants", weakness in the legs, and decreased tendon reflexes (polyneuropathy syndrome).

A deficiency of vitamin B2 _causes angular stomatitis (cheilitis in the corners of the mouth), cheilitis (inflammation of the red border of the lips), dermatitis in the area of the wings of the nose and nasolabial folds.

Deficiency of fat-soluble vitamin K leads to decreased prothrombin synthesis and bleeding phenomena.

Vitamin D deficiency disrupts the absorption of calcium in the intestines, leading to hypocalcemia.

Dysfunction of endocrine glands

Endocrine changes of varying severity are observed in 35-40% of patients with chronic enteritis, mainly in moderate and severe forms of the disease. As a rule, clinical and laboratory or only laboratory signs of damage to several endocrine glands are observed, less often - to one gland.

Hypothalamic-pituitary insufficiency is manifested by weakness, loss of appetite, thirst, frequent urination, increasing cachexia, arterial hypotension, pronounced pallor of the skin, atrophy of the genitals, and a sharp decrease in their function.

Hypothyroidism is manifested by facial swelling, chills, dry skin, memory loss, constipation, hoarseness, bradycardia, hair loss, and decreased levels of thyroxine and triiodothyronine in the blood.

With hypofunction of the adrenal cortex, skin pigmentation appears, body weight decreases, arterial hypotension, hypoglycemia, hyponatremia, hypochloremia develop, and the level of cortisol in the blood decreases.

The development of hypofunction of the sex glands is characteristic .

Damage to the endocrine glands contributes to the worsening of anemia in patients with chronic enteritis.

The symptoms of endocrine diseases are described in detail in the relevant section of this guide.

Damage to other digestive organs

With prolonged and severe chronic enteritis, damage to other organs of the digestive system occurs - chronic gastritis, reactive hepatitis, chronic pancreatitis, aggravating the course of chronic enteritis.

Severity of clinical course

Depending on the severity of local and general enteral syndromes, three degrees of severity of chronic enteritis are distinguished.

• The mild form (grade I) is characterized by the predominance of local intestinal symptoms, increased fatigue and slight weight loss (up to 5 kg).
• In moderate severity of the disease (grade II), a more pronounced weight loss is observed in conditions of adequate nutrition (up to 10 kg), general disorders become more pronounced (trophic disorders, electrolyte shifts), although they do not dominate the clinical picture.
• The severe form (grade III) is characterized by progressive weight loss, dystrophic changes in the skin, nails, hair, symptoms of hypovitaminosis, pain in the calf muscles, bones, hypoproteinemia, anemia, hypotension, edema, menstrual irregularities in women, and sexual weakness in men.

Mild forms of chronic enteritis are characterized by a latent monotonous course, moderate and severe forms are characterized by a recurrent and continuously recurring course. Latent course occurs in secondary forms of chronic enteritis that has developed in connection with other chronic diseases of the digestive organs. Monotonous course is characterized by scarcity, episodicity of the appearance of enteral symptoms without a tendency to intensification. Recurrent course occurs with a clear alternation of periods of exacerbation and remission, vivid clinical manifestations of the disease during the exacerbation, the frequency of the latter is no more than 3 times a year. Continuously recurring course differs from recurrent by the short duration of clear intervals (on average from 2 to 4 weeks) between periods of improvement and deterioration, the absence of complete elimination of clinical symptoms of the disease.

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