Diarrhea in the newborn - Causes, symptoms and treatment. MF.

Diarrhea( diarrhea) is a pathological condition in which there is an increase in defecation, and a change in the qualitative composition of the stool. Before talking about diarrhea in children, you need to know the normative indicators of childhood.

The first feces of a newborn is meconium, it is viscous and dark as resin. Meconium occurs within the first 24 hours and is gradually replaced by a normal newborn stool. Meconium is formed in utero, shortly before birth, when there is a spontaneous ingestion of the amniotic fluid. This is the norm.

Normal stool for newborns

	Breastfeeding children	Children with mixed and artificial feeding
No.	From 15 g at the first birthdays and reaches 50 grams per year	Also
Consistency	Unformed, mushy, medium viscous	Thick, paste-like consistency
Feces frequency	3-4 times a day up to 6 months, after 6 months - 1-2 times a day	Also, but may be susceptibility to constipation
Color	Bright yellow with greenish reed	Darker than withfeeding and color spectrum can be shifted to brown shade
Smell	Acid	Tart, sometimes noticeable odor, reminiscent of putrefactive

These rules are explained by the following facts:

1. Acid and pepsin formation in the stomach of newborns is at a low level, which causes a neutral environment, at which only 2 fractions of pepsin can function: chemosin and gastricin, suitable for the cleavage of only breast milk and adapted mixtures.
2. Functionality of the pancreas is at the stage of development, especially lipolytic and amylolytic activity, therefore in the process of digestion of milk fat an important role is played by the lipase of gastric juice and female milk.
3. Low excretion of bile acids.

As a result, due to the functional immaturity of the enzymatic system of the stomach and pancreas, most of the burden on oneself is taken by the intestine, so the slightest shifts in nutrition( including maternal, if the child is on natural feeding) can lead to dyspepsia, bloating, colic, diarrhea.

If you deviate from the norms, you can suspect a pathology. The most frequent reason is considered to be infectious and parasitic lesion, which in newborns is most likely mistaken if the sanitary and hygienic standards in which the child is kept are preserved. In the formation of diarrheal syndrome in the newborn participate 4 mechanisms of development: intestinal hypersecretion, increased osmotic pressure in the intestinal cavity, violation of transit of intestinal contents and intestinal hyperexcision. Below is a list of diseases targeted specifically at infancy, as the causes of diarrhea in newborns are much greater than in the adult period, and they are more insidious. Only after excluding the most probable causes and stability of the child's well-being, the problem can be considered solved.

Possible causes of diarrhea in newborns

Classification of causes is given by the level of damage, from subcellular structures and to the tissue level, with a predominance of diarrhea among the symptoms. The prevalence of these diseases is equal, and treatment for all is different.

1. Infectious and parasitic enteritis.

2. Infectious and inflammatory diseases in congenital immunodeficiencies( Bruton's disease, IgA deficiency, combined immunodeficiency, neutropenia, allergic enteropathies), lipodystrophy, autoimmune enteropathy.

3. Alimentary( illness of infants due to disparity in the volume or composition of food physiological capabilities of the child).

4. Endocrine pathology: insufficiency of exocrine pancreatic function.

5. Enzymopaic( enzymatic) pathology at the level of intestinal enzymes: violation of cavity, parietal or membrane digestion as a result of changes in the structure of intestinal enzymes.

6. Damage to carrier proteins in the assimilation of fat-soluble substances, vitamins, micronutrients.

7. Congenital disorders of the structure of enterocytes( structural unit of the intestine): atrophy, epithelialdysplasia, etc., lymphoid and vascular tissue.

8. Decreased absorption surface: short bowel syndrome, cecal syndrome.

9. Endocrinopathies, including hormone-producing tumors: vipoma, gastrinoma, somatostatinoma, carcinoid.

10. Difficultly classified pathologies( pathogenesis to the end has not been studied, but well suited to corrective treatment): Crohn's disease, celiac disease.

Predisposing factors of diarrhea in newborns:

- Decreased mucus-forming function of the intestine, which is a nonspecific protective barrier.
- High pH( acid-base balance) of gastric juice. Ie hydrochloric acid is not produced enough to "protect" the gastrointestinal tract( gastrointestinal tract) and participate in the activation of digestive enzymes.
- Reduction of secretory IgA( this immunoglobulin is the first line of protection of the gastrointestinal mucosa).
- Reduced immunity in the absence of breastfeeding( because the immune cells of the mother's memory, getting into the baby's body through milk, form passive immunity to the diseases that the mother got sick herself).
- Low stock of transport systems regulating the reabsorption( absorption) of Na /Cl/ Mg and other elements that, in diarrhea, causes their rapid loss and the formation of an imbalance.

Let's analyze each reason a little more.

Infectious and parasitic enteritis.

• Intestinal infections that directly cause diarrheal syndrome: shigellosis, salmonellosis, escherichiosis, intestinal forms of yersiniosis, pseudotuberculosis, cholera, rotavirus infection, typhoid fever, botulism.
• Intestinal infections caused by conditionally pathogenic microflora: proteosis, klebsiellosis infection, Pseudomonas aeruginosa, clostridiosis, campylobacteriosis.
• Parasitic infections: more often diarrheal syndrome causes certain classes - trematodes( opisthorchiasis), cestodes, nematodes( pinworms, ascarids).

One way or another, the presence of a foreign agent predetermines the development of infectious-toxic symptoms and changes in laboratory data.

Infectious and inflammatory diseases in congenital immunodeficiencies.

• Allergic enteropathy. Symptoms appear with the introduction of complementary foods, or pre-breastfeeding, there is an intestinal type of steatorrhea( fatty acids and soaps of fatty acids) + unstable stool character( constipation, followed by relaxation) + exudative enteropathy( loss of plasma protein through the intestinal wall, which eventually leads to edema,cardiovascular unsatisfaction, etc.).

• IgA deficiency ( syndrome of general variable unclassifiable immunodeficiency): the deficiency of IgA is isolated, therefore, in addition to diarrhea, dysbiosis always occurs. Symptoms are noted from the first days of life, as a result of an inadequate response to opportunistic and pathogenic colonies of the intestinal flora.

• Bruton's disease ( a violation of maturation of B-lymphocytes) is a genetically determined disease, the maturation of B-lymphocytes suffers, which means that the symptoms are much more diverse, although they start with the GI tract, but as you grow up, secondary infection is connected not only with intestinalmicroflora, but in general from the side of any gate infection - mucous membranes, respiratory tract, urinary system, CNS, etc.

• Lipodystrophy( Whipple's disease) - the disease develops more often in adults, but there are described variants in children. This disease is considered systemic with diarrhea + arthralgia + fever + various polymorphic clinic( heart, lung, CNS).

• Autoimmune enteropathy - in this case, activation of T-lymphocytes with autoimmune directivity against their own enterocytes takes place. Symptoms with a predominance of diarrheal syndrome, manifested in the first 2 months and characterized by a progressive chronic course.

When suspected of immune pathology, in addition to standard clinical and laboratory studies, it is necessary to take into account immunological markers( in particular, search for autoantibodies to structural elements of the gastrointestinal tract, etc.), the study of the morphology of the small intestine, as well as the genetic method. Consultation of an immunologist is necessary.

Endocrine pathology( insufficiency of exocrine pancreas function).

Malformations of the pancreas: ectopia, anular and bifurcated gland, hypoplasia. With this pathology, there is a violation of the "release" of pancreatic enzymes into the lumen of the duodenum, with the normal structure and secretion of the enzymes themselves, with the exception being hypoplasia. In the latter pathology, the qualitative and quantitative characteristics of the enzymatic system of the pancreas also suffer. Hypoplasia can be total, partial and congenital - depending on this, the variability of clinical symptoms is determined.

But one way or another, steatorea comes to the fore in different degrees, up to a constant leakage of fat from the anus.
Pancreatic dysfunction is considered to be the primary cause of the domibular species of malabsorption.

In order to confirm or refute the diagnosis, if there is a suspicion of a violation of the exocrine function of the pancreas, it is necessary to go from simple to complex: coprogram, pancreatic elastase - if necessary, biochemical blood test, antibodies to some parasitic infections in order to avoid obturation of the excretory duct,structural elements of the pancreas. Also do not forget about ultrasound methods. When deciding whether to implement diagnostic measures, you should consult a specialist to avoid unnecessary waste.

Enzymopathic pathology( at the level of the intestine).

Is another indicator of malbosorption syndrome. This type can include the following types of deficiency: disaccharidic( lactase, sugarazo-isomaltaznaya, trehalaznaya), enterokinase, duodenas.

When suspicion of disaccharidic insufficiency is suspected, several features should be considered:

- Maltose activity of the small intestinal mucosa is high in children of all ages, while its sucrose activity is much lower. The lactose activity of the mucous membrane, noted in the first year of life, gradually decreases with age, remaining at the minimum level in the adult.
- Enzyme activity, in some cases, is a hormone-dependent process - so lactose activators are thyroxine and glucocoricoids.

All this is important to know in order to track the cause of diarrheal syndrome, in order to avoid diag- nostic errors( for example: the introduction of an improper complementary supplement / supplement, the presence of endocrinopathy).

• Lactose insufficiency. During the course of this pathological process, the following symptoms come to the fore:

- Intestinal colic: incomplete cleavage of disaccharides occurs in the distal part of the intestine, fermentation occurs with the release of H +, this leads to gas formation and as a result - increased pressure in the intestine, which causespain and discomfort.
- Vomiting and regurgitation are explained by increased pressure in the abdominal cavity due to gas formation and weakness of the cardiac sphincter of the stomach.
- Diarrhea: due to the resulting fermentation, there is a shift in the acid-base balance to the acid side by fatty acids( lactic, propionic, oily, acetic) - these organic acids are osmoactive, so osmotic diarrhea occurs, after the corresponding saccharide.

Diagnostics:

1) Coprogram: reduced pH of the stool & lt; 5.5;fatty acids, iodophilic flora.
2) Load tests: the use of the sugar curve for giving lactose 1.5 g / kg( not more than 50 g) determine the fasting glucose concentration and after 15 /30/ for 60 min, so when the lacrimal insufficiency the glycemic curve has a flat appearance.

Treatment: Maintaining a food diary. Low-lactose mixtures( All-100, Low-Lactose Nutrilone, Omneo, etc.), in more severe cases - lactose-free mixtures based on soy proteins. Against the background of these mixtures, it is necessary to fill the content of Ca2 +.

• Sucrose-isomaltous insufficiency: is a genetically associated disease characterized by clinical signs - persistent watery diarrhea, intestinal colic, flatulence, refusal of sweet food. The diagnosis is based on extracellular starch in the stool, acidic pH, and the appearance of a flat sugar curve with a load.

Treatment of is to exclude sucrose and starch, and if symptoms persist in the background of diet therapy - add Sucraid.

Enterocellular insufficiency with impaired absorption(

intestinal damage) • Globose-galactose malabsorption is a genetic mutation that leads to a disruption in the structure of the transporter protein of membrane structures. Clinically, this genetic defect will be manifested in the form of watery excrements with an acidic odor, 10 to 20 times a day, resembling urine, containing in its composition a large amount of glucose and galactose, polyuria is noted because of the mellituria.

Treatment of in this case is reduced to the transfer to a mixture with fructose or a mixture based on protein hydrolysates, hereinafter - dairy-free diet and sugar substitution - fructose.

• Malabsorption of fructose. At the heart of the violation of the structure of the protein-carrier of fructose, there is a violation of one of the transport of glucose into the intestine( synthesis of glucose from fructose on the intestinal wall with subsequent absorption).Syndrome of diarrhea occurs after the consumption of juices and fruits, because unutilized osmoactive fructose causes osmotic diarrhea. The only exception among the products is a banana, because the content of glucose and fructose in it is the same.

As diagnostic , the maintenance of a diary and a glycemic curve with a load are the foreground. In this case, it will be direct. In this case, it is necessary to carry out differential diagnostics from fructoemia, at which there will be an increase in the liver, fructose in the urine, a decrease in the activity of the liver enzyme of fructose-1-phosphodolase.

Treatment: exclusion of fructose - oranges, apples, pears, peaches, cherries, sweet cherries.

• Primary malbosorption of bile salts. In this case, the underlying disease also has a genetic mutation leading to a disruption of the structure of the transporter protein in the ileum. In this case, enterohepatic circulation is disturbed and some of the bile acids are not absorbed back into the liver. Acquired species of this pathology can be with resection of the small intestine after Crohn's disease.

Symptoms: unboiled bile acids stimulate secretion and intestinal motility, resulting in diarrhea of ​​a secretory type that does not respond to treatment, which increases when transferred to artificial feeding. Because of the violation of absorption of fat-soluble vitamins, absorption of vitamin K is impaired, hemorrhagic eruptions and edema appear( up to the anosarcoma).

Diagnosis: steatorea due to fatty acids, hypocholesterinemia, hypoproteinemia, decreased complement.

Treatment: diet therapy - replacement of long-chain TAG, medium-chain( Portagen, Prigichstimil, Alfare, Izocal, Nutrizone).

• Enteropathic acrodermatitis. In this pathology zinc assimilation is disrupted. Symptoms arise and develop during the transfer of a child to artificial feeding, because female milk contains a binding Zn ligand( protein), which provides assimilation. The frequent liquid stool, steatorrhoea, erythroderma with desquamation of the epithelium( erythromatous / vesicullibullious / pustular dermatitis) in the perioral region, in the crotch, on the extremities comes to the fore, hair loss with the formation of allopecia, paronychia occurs. In the absence of treatment, secondary immunodeficiency is formed.

Diagnosis of is to determine and compare the level of [Zn] in blood and urine.

Treatment of is to transfer to unpasteurized donor milk. In the absence of donor milk and transfer to artificial mixtures, it is necessary to add aspartate Zn from the calculation of 2 mg / kg / day.

• Congenital chloride diarrhea. In this pathology, the ion exchange of Cl / HCO3 on the enterocytes is impaired as a result of a genetic defect.
Symptoms are characterized by: a decrease in the blood of ions Cl, K, Na;alkalosis( shift of the acid-base blood level to the alkaline side).Later [Na] is restored due to compensatory mechanisms. But as the concentration of electrolytes in the body decreases, the symptoms of the cardiovascular and central nervous system are added: changes in behavioral reactions, changes in the conductive and contractile capacity of the heart, and other accompanying pathologies. Already with prenatal diagnosis, intrauterine polyhydramnios( due to diarrhea before birth), absence of meconium are noted. After birth - increase in the size of the abdomen due to the paresis of the intestine, vomiting a fountain after each feeding, a liquid watery stool that looks like urine up to 20 times a day. Infusion therapy and the abolition of dairy nutrition are ineffective.

Diagnosis is based on an increase in Cl excretion with feces( more than 1 g / day), hypokalemia and hypochloraemia, severe alkalosis( blood pH 7.7).

Treatment of is based on parenteral artificial feeding and lifelong replacement of electorites with the selection of individual doses.

• Congenital sodium diarrhea is a genetic disorder characterized by a violation of the conformation of the transport protein Na, which leads to damage to Na / H metabolism, resulting in loss of Na, followed by water, diarrhea, complicated acidosis.

Diagnosis is based on monitoring the concentration of electrolytes in the blood and feces. Differential diagnostics is carried out: with the Soltering form of adrenogenital syndrome, therefore it is necessary to control [17-ketosteroids] in urine;Congenital Cl of diarrhea - in this case, in the stool of Cl & gt;Na and K;and with Na diarrhea - on the contrary.

Treatment of is reduced to the transfer to parenteral nutrition, with the appointment of citrate-Na, glucose-saline solutions for oral rehydration( Regidron / Oralit).

Congenital infringement of the structure of enterocytes

• Anomaly of intestinal microvilli: At the moment, the reasons for ovulation are not clear, but a genetic mutation is found in which the formation of the cytoskeleton of enterocytes occurs. As a result of this pathology, from the first days of life, secretory diarrhea is formed, resistant to standard methods of treatment.

• Intestinal epithelial dysplasia( beam enteropathy). In this case, abnormal sloughing of the intestinal epithelium is observed. This disease is common in the Middle East, the cause is a genetic mutation. With this disease, there is a change in the structure of the connection between the epithelial cells and the basal membrane. This explains the atrophy of the villi.

Symptoms: severe watery diarrhea, resistant to treatment.

Diagnosis: small intestine biopsy. But the changes can not always be registered, because the epilation of the epilation occurs very quickly.

Treatment of is ineffective, predictions are sad.

• Syndromic enteropathy - watery persistent diarrhea 50-100 ml / kg per day, occurring at the 1st month of life, there are delays at birth in terms of gestation, external anomalies of development are observed( prominent forehead, wide nose, hypertelorism, woolly hair), unclassifiable immunodeficiency. With this pathology occurs atrophy of microvilli. Treatment of is ineffective.

• Exudative enteropathy. This disease is characterized by the loss of plasma protein through the intestinal wall. This condition can be either the primary cause, ie an independent disease, as a result of malformations of the intestinal lymphocytes, and the result of the transferred disease, in this case they speak of Secondary pathology - Whipple's disease, Crohn's disease, food allergy, autoimmune enteropathy, etc.

In this disease there is a rupture of enlarged lymphocytes, accelerated rejection of the epithelium, a sharp change in pressure in the wall of the gut. High-molecular plasma proteins, when entering the lumen of the gut, attract water, diarrhea occurs, after a change in pressure, a breakthrough occurs, aggravating diarrhea. Along with low-molecular proteins( albumins), high-molecular proteins are lost, secondary immunodeficiency develops and secondary bacterial translocation develops with the development of intestinal sepsis. Ie the planned local immune defense becomes damaged and that flora that was acceptable and tolerant before the "breakdown" becomes dangerous. Symptoms are noted from the first months of life with classical symptoms and secondary vitamin deficiency( ie polymorphic clinic).

Diagnostics: is aimed at detecting the hidden form of the protein, determining α1-antitrypsin in feces, elastase-1 in the feces / blood, endoscopic examination of the upper and lower gastrointestinal tract using X-ray examination of the small intestine;To exclude retroperitoneal pathology of the small intestine, use the CT method, angiography, lymphography, ECHO-kg, ECG.

Treatment: administration of mixtures containing medium-chain TAGs, which, when mastered, pass the lymphoid tract - Portagen, Pregestamal, Alfare. Substitution therapy: plasma, albumins, reducing edema syndrome Veroshpironom, with the intercurrent infection, prescribe drugs Ig( Pentaglobin, Intraglobin).

Difficultly classified bowel diseases( with predominance of inflammatory morphological pattern), manifested by diarrhea syndrome, characterized by digestion and absorption disorders.

The following pathologies, except for celiac disease, are extremely rare in children, but in recent years have acquired relevance, since "rejuvenation" of these diseases is noted, and if earlier they were found only in adults, now they began to register in children.

• Celiac: is a chronic polysyndromic disease characterized by damage to the mucous membrane of the small intestine by gluten from cereals( wheat, rye, barley, oats).Pathogenesis to the end is not clear, but there are 4 theories - enzymatic, viral, patoreceptor, immunological.
The clinical picture of can be typical, atypical, latent. Symptoms occur more often after the introduction of complementary food semolina or oatmeal, and it does not immediately occur, and 1-4 months after the introduction of complementary foods. There is polyphecal( 2-5 times a day) mushy, abundant, frothy, offensive, with a greasy shine, poorly washable stool. An abdominal enlargement is noted. Polyclinic symptoms due to impaired absorption of other trace elements( Ca2 +, Mg, Zn, etc.) are characterized by ostealgia, early caries, dryness and thinning of the skin, violation of behavioral reactions, pigmentation of open skin areas and atrophic dermatitis, atrophic glossitis and stomatitis.

Diagnosis: Coprogram - intestinal steatorrhea( fatty acid and their soaps), extracellular starch. Colonoscopy with polyfocal biopsy and cytological examination. Immunological and genetic research with detection of haplotype HLA-A1-B8-DR3 and B44-DR7;also the most frequently associated alleles associated with the target are DQA1 * 0501, DQB1 * 0201, DRB1 * 04;the presence of Am to gluten, endomesia, reticulin, tissue transglutaminase.

• NUK( ulcerative colitis), cystic fibrosis and Crohn's disease occur on average around 240 cases per 100,000 population( globally, these data are not targeted at our country) and are constantly younger. Due to the rarity of the registration of these diseases, it is not yet possible to establish clear age criteria in pediatric practice, the only thing that is known about this issue is that the entire disease occurs before the patients reach 10 years of age. The causes of these diseases are not fully understood, therefore, preventive measures have not yet been developed. However, it is known that the diseases have polyfacorne aetiology( genetic, immunological, microbiotic and barrier).There are a number of classifications in terms of severity, level of damage and the clinical course of these diseases.

Symptoms: diarrhea syndrome, mainly at night, the degree of severity is variable, pathological impurities are noted - especially the admixture of blood. There is one characteristic contradictory feature - tenesmus( urge to defecate) in combination with constipation. This feature arises with limited distal forms of NNC.
Abdominal pain is a common symptom in Crohn's disease, for NUK this symptom is not typical.
Attachment of extraintestinal changes: immunological, malbosorption syndromes with consequent consequences( symptoms of hypovitaminosis, dysproteinemia, etc).

Diagnosis is based on clinical, laboratory, X-ray endoscopy and histological signs.

Treatment of is performed by immunocorrective drugs, anibioikoterapii, probiotics and prebiotics, glucocorticosteroids. With timely diagnostics, right-minded tactics of treatment and timely start of it, the prognosis can be favorable.

Let the given data be for somebody a guide / guide and will be able to prevent someone's misfortune.

Therapist doctor Shabanova I.Е.