Persistent diarrhea refers to a course of illness between 2 weeks and 2 months; chronic diarrhea refers to a course of illness longer than 2 months. Abroad, both are collectively referred to as persistent diarrhea (persistent diarrhea). The diagnosis of refractory diarrhea is based on: ① Small age of onset, commonly seen in infants under 3 months old; ② Course of illness longer than 2 weeks; ③ Concurrent malnutrition and growth and development disorders; ④ No effect after general treatment; ⑤ Poor prognosis, high mortality rate.
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Persistent and chronic diarrhea in children
- Table of Contents
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1. What are the causes of persistent and chronic diarrhea in children
2. What complications can persistent and chronic diarrhea in children lead to
3. What are the typical symptoms of persistent and chronic diarrhea in children
4. How to prevent persistent and chronic diarrhea in children
5. What laboratory tests should be done for children with persistent and chronic diarrhea
6. Diet taboos for children with persistent and chronic diarrhea
7. Conventional methods for the treatment of persistent and chronic diarrhea in children according to Western medicine
1. What are the causes of persistent and chronic diarrhea in children?
First, the cause of disease
1. Host factors
(1) Age: Persistent diarrhea often occurs within the first year of life, and refractory diarrhea often occurs within the first three months.
(2) Malnutrition is prone to lead to persistent diarrhea, and persistent diarrhea can further promote malnutrition, forming a vicious cycle. (3) A low immune function was observed in 29 children with persistent and chronic diarrhea by the Pediatric Research Institute of Capital Medical University. It was found that the fecal SIgA was significantly lower than normal; CD4 decreased, CD8 increased, and the CD4/CD8 ratio decreased. This indicates a decrease in both humoral and cellular immune functions. Indian research shows that the incidence of persistent diarrhea in children switching from breast milk to animal milk feeding increases by 2-3 times within one month, which may be due to the reduction of protective factors in breast milk and the ease of contamination in animal milk.
2. The role of intestinal microbiota
Vibrios and viruses (including rotavirus) do not cause persistent diarrhea. In addition, various pathogens that cause acute diarrhea have been detected in the stool of persistent diarrhea, as reported abroad. They can be divided into 2 groups:
(1) Pathogens with equal isolation rates in acute and persistent diarrhea: Such as Shigella, Salmonella, enterotoxigenic Escherichia coli, Campylobacter jejuni, Yersinia, Clostridium difficile, etc. After treatment with the corresponding antibiotics, persistent diarrhea is difficult to eliminate, which may be related to the low immune function of the host.
(2) Pathogens with a high isolation rate in persistent diarrhea: They include adherent Escherichia coli (EAEC), pathogenic Escherichia coli (EPEC), and Cryptosporidium. These are considered important pathogens of persistent diarrhea. Observations of persistent diarrhea in Chinese children show a low isolation rate of pathogens, mainly due to the incomplete recovery of intestinal digestive function, leading to persistent diarrhea. Therefore, it is best not to use antibiotics blindly before obtaining the pathogen.
3. Continuous damage to the intestinal mucosa
The Affiliated Children's Hospital of Zhejiang Medical University used jejunal mucosal biopsy, 15 cases were scanned by scanning electron microscopy, and 11 cases were examined by transmission electron microscopy. All had ultrastructural abnormalities, manifested as villous atrophy, severe surface necrosis, damage to small intestinal epithelial cells, cytoplasmic effusion, and cell shedding. 17 cases showed damage to the surface microvilli of the absorptive epithelial cells and loss of glycocalyx, indicating a reduction in the absorptive area of the intestinal cells, and factors causing mucosal injury and absorption disorders include microbial invasion, disaccharide absorption disorders (especially lactose), and protein allergy. Due to intestinal mucosal injury and incomplete barrier function, the absorption of a considerable amount of antigenic intact proteins triggers the immune mechanism and damages the mucosa. Bile contains bile acids, which function to emulsify fat particles in food, making them easily absorbable. When intestinal bacteria overgrow, bile acids are decomposed, thereby affecting fat absorption and causing steatorrhea. Additionally, intestinal bacteria can convert bile acids to dihydroxybile acid and transform undigested fats in food to hydroxyfatty acids. Once these metabolic products enter the colon, they promote excessive colonic secretion and cause diarrhea.
4. Delayed mucosal repair
Animal experiments have confirmed that protein-energy malnutrition delays the repair of the intestinal mucosa, and deficiencies in trace elements such as zinc and iron, vitamin A, B12, and folic acid also affect the repair of the intestinal mucosa.
II. Pathogenesis
1. Pathogenesis of infectious diarrhea
(1) Pathogens adhere to the intestinal mucosal surface: However, they do not invade or damage the mucosa, and mainly cause secretory diarrhea in the host by producing enterotoxins or cytotoxins. The intestinal mucosal epithelial cells are not damaged, the intestinal mucosa is intact, the stool is watery, and no leukocytes are found under the microscope. Diarrhea of this type is represented by cholera (including O139 type cholera), enterotoxigenic Escherichia coli (ETEC) enteritis, Staphylococcus aureus enteritis, gas-forming Clostridium perfringens, non-agglutinating Vibrio, Bacillus cereus, and certain proteobacteria, etc., all of which cause diarrhea belong to this category.
The mechanism of diarrhea caused by enterotoxins is most thoroughly studied in cholera. These enterotoxins initiate a series of pathological mechanisms by activating adenylate cyclase (AC). AC can convert adenosine triphosphate (ATP) in the cell into cyclic adenosine monophosphate (cAMP), which then promotes a series of enzyme reactions inside the cell, leading to increased secretion function of intestinal cells, excessive excretion of water and electrolytes, and clinical manifestations of excessive loss of intestinal fluid and severe diarrhea.
In diseases dominated by secretory diarrhea, in addition to cholera toxin, Escherichia coli (ETEC), and Salmonella toxins, vasoactive intestinal peptide (VIP), prostaglandins (PG) can all bind to mucosal cell receptors, activate the aforementioned adenylate cyclase-cAMP system, increase the concentration of cAMP, and cause excessive secretion of intestinal fluid and clinical diarrhea.
In addition to infectious diarrhea, vascular active peptide tumors (VIP tumors), VIP released by the tumor can activate the adenylate cyclase of the intestinal mucosa, stimulate the large secretion of the small intestine, and appear as cholera-like severe diarrhea, also known as 'pancreatic cholera'. There are also gastric secretion tumors, medullary thyroid tumors, certain ganglioneuromas, malignant carcinoid syndromes, and secretory villous adenomas that are considered to be diseases causing secretory diarrhea. These non-infectious diseases are initiated by the increased secretion of VIP, kinins, and prostaglandins, thus activating the adenylate cyclase-cAMP system, increasing cAMP, and causing excessive secretion of intestinal fluid and diarrhea.
(2) Direct invasion of epithelial cells by pathogens: and reproduction, destruction, and then entering the lamina propria to continue reproduction, and causing inflammatory reactions in the intestines, leading to diffuse edema, congestion of the intestinal mucosa, mucous blood exudates in the intestinal lumen, mucosal necrosis, and superficial ulcers. Clinical manifestations include abdominal pain, diarrhea, urgency, and mucous pus blood stools, characterized by bacterial dysentery. Other diseases belonging to this type of diarrhea include salmonella enteritis, campylobacter enteritis, yersinia enteritis, invasive Escherichia coli (EIEC) enteritis, hemorrhagic Escherichia coli (EHEC) enteritis, and amebic dysentery, etc.
(3) Destruction of intestinal villus epithelial cells: Diarrhea caused by pathogens primarily through the destruction of intestinal villus epithelial cells. This type of pathogen mainly invades the villus epithelial cells of the small intestine, causing intestinal epithelial cells to deform and become irregular, forming villus vacuoles, epithelial cell shedding, and the new intestinal epithelial cells to be functionally incomplete, leading to digestive and absorptive dysfunction and malabsorption. The characteristics of this type of diarrhea are: ①Starvation can alleviate diarrhea. ②The osmotic pressure in the intestinal lumen is higher than that of plasma. ③The osmotic pressure in the feces is formed by the unabsorbed electrolytes and other substances. The feces may contain a large amount of fat. This type of diarrhea is mainly characterized by watery stools. Diseases belonging to this type of diarrhea include diarrhea caused by rotavirus, enteric adenovirus, norovirus, and other pathogens. In addition, enteritis caused by pathogenic Escherichia coli (EPEC), cryptosporidium enteritis, and other enteritis also belong to this category.
Infectious diarrhea has a complex pathogen and varied clinical manifestations, so the pathogenesis is not single. Many diseases cause diarrhea through several mechanisms at the same time.
2. Pathogenesis of non-infectious diarrhea
Osmotic diarrhea (osmotic diarrhea): It refers to the absorption disorder of a soluble substance that can be absorbed, leading to increased osmotic pressure in the distal small intestine and colon, causing an increase in the reflux of fluid from plasma to the intestinal lumen, resulting in an increase in the volume of intestinal contents, intestinal dilation, and acceleration of intestinal peristalsis, which leads to diarrhea. This condition is common in malabsorption of carbohydrates. Normally, if the food intake is hypertonic, the fluid will quickly cross the duodenal epithelial cells and reflux into the intestinal lumen when the chyme reaches the Treitz ligament, making it isotonic. This part of the fluid must be reabsorbed in the distal small intestine. The proximal small intestine has high permeability to water and various ions, and Na, Cl- are continuously secreted along the concentration gradient in the distal small intestine and colon. Due to the reduced permeability, and the osmotic pressure formed by the unabsorbed carbohydrates can resist the normal reabsorption of water driven by the active transport of Na, Cl-, causing a large amount of fluid to reflux into the intestinal lumen. By the time it reaches the distal small intestine, Na, Cl- are actively reabsorbed, while the unabsorbed carbohydrates are not reabsorbed, which leads to a significantly lower Na concentration in the intestinal lumen than in the plasma. The unabsorbed carbohydrates can also be further metabolized into short-chain fatty acids, such as propionate, butyrate, H2, CO2, and methane, forming additional osmotic load, further aggravating diarrhea. Another characteristic of osmotic diarrhea is a relatively large osmotic gap (osmotic gap), generally greater than 50. The osmotic gap can be calculated using the following formula: [Na (mmol/L) K (mmol/L)] × 2 = measured fecal osmolality (osmolality) mmol/L. If there is no malabsorbed solute in the food, the sum of the Na and K concentrations measured is equal to 290. During osmotic diarrhea, if the concentration of electrolytes in the feces decreases, it indicates that there are other osmotic substances in the isotonic fecal fluid excreted from the colon. Another characteristic of osmotic diarrhea is that the undigested carbohydrates in the small intestine of infants are fermented by bacteria, forming small molecular organic acids such as lactic acid, formic acid, etc., which lowers the pH of the feces, generally pH < 5.5. In summary: Osmotic diarrhea has the following common characteristics: ① Diarrhea stops after fasting. ② The feces contain a large amount of undigested and decomposed food or drug components. ③ The osmotic pressure in the intestinal lumen exceeds the plasma osmotic pressure. ④ The content of electrolytes in the feces is not high. ⑤ The acidity and alkalinity of the feces decrease (pH < 5.5).
Osmotic diarrhea is mostly caused by incomplete digestion and decomposition of food. Fats, proteins, and carbohydrates in food must be digested and absorbed by enzymes in the intestines. If there is a congenital enzyme deficiency, insufficient pancreatic secretion, or reduced secretion or obstruction of bile汁 from the liver and gallbladder, the undigested chyme becomes non-absorbable solutes, causing the osmotic pressure in the intestinal lumen to be higher than that of plasma, thus leading to osmotic diarrhea. For example, congenital sucrose-isomaltase deficiency or primary delayed lactase deficiency in adults and older children. In addition, laxatives such as lactulose or milk of magnesia can also cause osmotic diarrhea.
Secretory diarrhea (secretory diarrhea): The net difference between intestinal absorption and secretion is the absorption of water and electrolytes. However, in general, normal people absorb more than they secrete. If the gastrointestinal secretion increases significantly beyond the normal absorption capacity, the excessive water and electrolytes in the intestines cause diarrhea. This type of diarrhea is called secretory diarrhea. Some people believe that all intestinal absorption cells have both absorption and secretion functions. Others believe that the mucosal crypt cells are the basic anatomical units with secretion functions, while absorption relies on the epithelial cells on the surface of the intestinal villi. When the villi of the epithelial cells are extensively damaged, absorption decreases, and increased secretion leads to secretory diarrhea. However, many cases of secretory diarrhea can occur in patients with completely normal small intestinal morphology. The mechanism of secretory diarrhea involves various factors, including enterotoxins, vasoactive intestinal peptide (VIP), calcitonin, prostaglandins, serotonin, and the high secretion of the stomach and pancreas, bile acids, fatty acids, and laxatives, which stimulate secretion. Among them, the mechanism of enterotoxins through the activation of cAMP and the stimulation of a large amount of intestinal fluid secretion has been studied relatively clearly. Congenital chloride diarrhea also belongs to secretory diarrhea. Secretory diarrhea has the following characteristics: ① The excretion of a large amount of watery or rice gruel-like feces, which can reach about 5 liters per day. ② The feces contain a large amount of electrolytes with the same osmotic pressure as plasma. ③ There is no pus and blood or fat in the feces. ④ There is usually no abdominal pain. ⑤ The histological examination of the intestinal mucosal tissue is basically normal. ⑥ Diarrhea does not stop even after fasting. Simple secretory diarrhea is rare, and most cases of diarrhea often manifest a combination of secretory, inflammatory, osmotic diarrhea, and intestinal dysfunction.
(3) Malabsorption diarrhea: Intestinal malabsorption is one of the important pathogenic mechanisms of diarrhea. Normally, 98% of the fluid in the digestive tract is reabsorbed, which requires the digestive tract to have sufficient area and healthy absorption function. Any disease that can damage the absorption area of the digestive tract and affect its absorption function can affect the reabsorption of intestinal fluid and lead to diarrhea. Malabsorption diarrhea can be roughly divided into the following situations:
① Abnormal mucosal permeability: This is due to the deformation and atrophy of villi or microvilli in the intestinal mucosal cells, which reduces the effective absorption area of the small intestine, causing a decrease in the permeability of water and electrolytes. This type of diarrhea is seen in children with chylous disease, tropical and nontropical steatorrhea (tropical and nontropical celiac disease), and other conditions.
② Decreased absorption area: For example, resection of the distal small intestine can affect the absorption of bile salts and cause excessive entry into the colon. Bile salts stimulate the intestinal mucosa, leading to malabsorption of fat and severe watery diarrhea.
③ Congestion of the intestinal mucosa: Congestion and edema of the intestinal mucosa caused by various reasons can affect the absorption of nutrients, thus causing diarrhea.
④ Excessive bacterial proliferation: Toxins secreted by bacteria affect the action of digestive enzymes, and their decomposition products can bind bile salts, causing fats to lose the ability to form micelles, thereby hindering the digestion and absorption of food, causing steatorrhea and diarrhea.
⑤ Inhibition of absorption: Certain causes can lead to inhibition of absorption by the intestinal mucosa.
⑥ Lymphatic obstruction: Lymphatic obstruction can occur due to lymphoma, tuberculosis, malignant histiocytosis, primary intestinal lymphatic dilation, or metastasis of cancer to mesenteric lymph nodes or chyle pool, leading to malabsorption of fat and diarrhea.
(4) Diarrhea caused by intestinal motility disorders: Diarrhea can be caused by bacterial overgrowth due to weakened and stagnated intestinal motility. Increased intestinal peristalsis can reduce the time for food to pass through, affect water absorption, and also cause diarrhea. Diarrhea caused by abnormal colonic motility is seen in infants with colonic irritability syndrome. In addition, diarrhea can also be seen after vagotomy, gastrectomy, hyperthyroidism, and other diseases. Peritonitis, abdominal and pelvic inflammation can also reflexively increase intestinal motility and cause diarrhea. The characteristics of diarrhea caused by increased intestinal motility are: ① Soft or watery stools. ② Rare inflammatory cells in stool examination. ③ Marked hyperactive bowel sounds. ④ Often accompanied by abdominal pain. Diarrhea caused by intestinal motility disorders generally has no specific clinical manifestations and should be considered after excluding other types of diarrhea.
2. What complications are easy to cause in children with protracted and chronic diarrhea
Concurrent symptoms such as abdominal pain, vomiting, dehydration, acidosis, and shock should be considered for corresponding diagnoses. General fever is often associated with various infections; abdominal pain and invasive diarrhea, as well as secretory diarrhea, are closely related; vomiting should be considered more often due to gastric and small intestinal lesions; dehydration, acidosis, and shock are related to the degree of diarrhea-related fluid loss and electrolytes; severe diarrhea such as cholera, and severe infections such as toxic dysentery, are often accompanied by dehydration and shock.
3. What are the typical symptoms of persistent and chronic diarrhea in children?
1, Persistent diarrhea
Increased frequency of stools, ≥4 times a day, changes in stool characteristics,呈水样便、黏液或脓血便, the course of diarrhea ≥2 weeks.
2, Refractory diarrhea
The onset age is younger, more common in infants under 3 months of age, the course of diarrhea exceeds 2 weeks, combined with malnutrition and growth and development disorders, general treatment is ineffective, the prognosis is severe.
3, The manifestations directly caused by malabsorption
Weight loss, delayed growth and development, pale complexion, may have glossitis, abdominal distension, and increased flatus causing discomfort. There is often diarrhea, if it is malabsorption of fat, the stool is pale, soft, oily, foamy, large in amount, has an unpleasant odor, and this type of stool often sticks to the toilet, and it is not easy to flush off.
4, The manifestations of various deficiencies secondary to malabsorption
The scope and severity of malnutrition are related to the severity of the primary disease and the area and size of the gastrointestinal tract involved. There may be deficiencies in vitamin D and calcium, leading to convulsions, tetany, and delayed development of bones and teeth. Poor absorption of fat-soluble vitamin K can cause a decrease in prothrombin, leading to purpura and a tendency to bleed. Deficiency of riboflavin can cause glossitis and cheilitis. Poor protein absorption can lead to hypoproteinemic edema, usually seen in the lower limbs.
5, The relationship between persistent diarrhea and nutrition
During diarrhea, growth and development may slow down or stop, especially when diet is restricted, weight loss may occur.
4. How to prevent persistent and chronic diarrhea in children?
Advocate breastfeeding, rational feeding, prevent malnutrition, and promote the growth and development of children. Pay attention to dietary hygiene, prevent gastrointestinal infectious diseases, and for children with (acute) diarrhea, master the principles of treatment, rational medication, adjust diet, prevent the prolongation of the course of the disease, adopt a combination of traditional Chinese and Western medicine, promote the recovery of children, and strengthen supportive treatment if necessary, prevent the occurrence of persistent and chronic diarrhea.
5. What laboratory tests are needed for children with persistent and chronic diarrhea?
One, Stool examination
At high magnification (400x), if there are more than 15 white blood cells and a small number of red blood cells, clinical diagnosis of bacillary dysentery can be made; if the white blood cell count is ≤15, it is diagnosed as enteritis. The microscope can also detect worm eggs, and smears can detect amebic trophozoites and Vibrio cholerae.
Two, Serum immunological examination
Various antigen-antibody immunological tests are helpful for the etiological diagnosis of various infectious diarrhea, such as the Widal reaction for the confirmation of typhoid and paratyphoid fever.
Three, X-ray examination
Under fluoroscopy, X-rays can dynamically observe the motility, morphology, the presence of ulcers, and space-occupying lesions of the esophagus, stomach, duodenum, small intestine, large intestine, and anus, which have important diagnostic value for the entire digestive tract.
Four, Ultrasonic examination
Abdominal ultrasound provides morphological diagnostic evidence for the morphology, space-occupying lesions, and other aspects of the gastrointestinal tract, liver, and gallbladder.
Five, Magnetic Resonance Imaging (MRI)
MRI is very meaningful for the differential diagnosis of liver tumors, especially malignant liver tumors and cystic lesions. It can also be used for the diagnosis of inflammatory bowel disease, necrotizing enterocolitis, lymphoma, and post-traumatic intestinal wall hematoma.
Six, CT Examination
It plays an important role in the differential diagnosis of pediatric abdominal diseases, mainly used for the diagnosis and differential diagnosis of abdominal masses, peritoneal abscesses, trauma, liver, pancreas, and other diseases.
Seven, Fiberoptic Gastroscopy, Fiberoptic Colonoscopy Examination, and Laparoscopic Examination
Upper gastrointestinal endoscopy includes three types: fiberoptic endoscopy, electronic endoscopy, and passive small bowel endoscopy. These endoscopes have clear imaging, can take photos, record videos, perform biopsies, and are convenient for treatment, and have been widely used in pediatric clinical practice. Laparoscopic examination can be performed under direct vision or take living tissue for pathological examination to clarify the diagnosis.
Eight, Pathological Examination
Biopsy tissue pathological examination is of decisive significance for the diagnosis of diarrhea. Through histological examination, pathological diagnosis is provided for the diagnosis of the disease.
Nine, Breath Test
Due to its simplicity, non-invasiveness, and suitability for patients of all age groups, it can be widely used in clinical gastroenterology and has become one of the effective means for diagnosing gastrointestinal diseases.
1, Hydrogen breath test
(1) Lactose hydrogen breath test (lactose hydrogen breath test):
Used for the diagnosis of lactose malabsorption.
(2) Sucrose hydrogen breath test:
Used for the diagnosis of primary sucrose-isomaltose deficiency.
(3) Hydrogen breath test for the diagnosis of excessive growth of bacteria in the small intestine:
It can be used to diagnose excessive growth of bacteria in the small intestine.
2, Carbon dioxide breath test
(1) Detection of fat absorption:
The 14C-labeled triglyceride breath test is a simple and reliable method for detecting poor fat absorption.
(2) Detection of sugar absorption:
The application of a natural rich in 13C-lactose breath test can diagnose lactose malabsorption.
(3) Diagnosis of excessive growth of bacteria in the small intestine:
The 14C-glycocholate test can be used to diagnose excessive growth of bacteria in the small intestine.
(4) Urea breath test:
Used for the detection of Helicobacter pylori. In addition to diagnosis, it can also be used for follow-up checks after antibacterial treatment, and this test can accurately reflect the negative conversion, recurrence, and reinfection of Helicobacter pylori, so it can be an important means for determining efficacy and screening effective drugs.
6. Dietary taboos for children with protracted and chronic diarrhea
Children with protracted and chronic diarrhea are mostly caused by a lack of corresponding enzymes in the body. Children with a deficiency of disaccharidase have severe diarrhea when eating foods containing disaccharides (including sucrose, maltose, and lactose), with watery stools and a decrease in pH. Due to the stimulation of acidic stools, urinary cloth dermatitis is prone to occur. The diagnosis can be determined by measuring the content of disaccharides in the stool. These children can consume diets without disaccharides, such as soy milk (i.e., fresh soy milk with 10% or 15% glucose). Since human milk and cow's milk contain a high amount of lactose, children with a lactose enzyme deficiency cannot consume human milk or cow's milk. If human milk or cow's milk is made into yogurt, the lactose content decreases and it can be consumed.
Children with celiac disease cannot eat wheat foods, as all wheat foods contain gliadin, and should be replaced with animal milk, rice, eggs, lean meat, and legumes.
Children with milk allergy are better to switch to breast milk, because almost all children can tolerate breast milk and there is no need to worry about milk allergy. Milk allergy can be naturally relieved, so after stopping breast milk for 6 months, breast milk can be tried again, and this can determine whether the milk allergy has disappeared.
7. The conventional method of Western medicine for the treatment of pediatric persistent and chronic diarrhea
First, treatment
Children with persistent and chronic diarrhea should be treated in the hospital.
1. Fluid therapy
Actively do a good job in fluid therapy, prevent dehydration, correct water and electrolyte, and acid-base balance disorders.
2. Nutritional therapy
Most of these patients have nutritional disorders, so continuing to eat is a necessary treatment measure, and fasting is harmful.
(1) Continue breastfeeding.
(2) For artificial feeding, the diet should be adjusted. For infants under 6 months old, mix milk with an equal amount of rice gruel or water to dilute, feed for 2 days and then gradually return to normal diet, or use yogurt, or also use a milk-grain mixture, feed 6 times a day to ensure sufficient calories. Children over 6 months old can use the accustomed daily diet, choose thick porridge, noodles, and add some cooked vegetable oil, vegetables, minced meat, or fish, but need to start from less to more.
(3) Parenteral nutrition: In a few severe cases, oral nutrients cannot be tolerated, and supportive therapy should be added. If conditions permit, parenteral nutrition can be adopted. The plan is: 10% fat emulsion 2-3g/kg per day, compound crystalline amino acids 2-2.5g/kg per day, glucose 12-15g/kg per day, electrolytes and various vitamins in appropriate amounts, liquid 12-15ml/kg per day, calories 209-376kJ/kg (50-90kcal/kg) per day, administered through peripheral vein. The total fluid volume should be evenly infused within 24 hours (it is best to use a computer infusion pump to control the speed), and then switch to oral intake after improvement.
3. Drug therapy
Antibiotics should be used with caution, and only used for children with specific pathogens isolated, and should be selected based on the results of drug sensitivity tests. Supplement trace elements and vitamins zinc, vitamin A, C, B, B12, and folic acid, and at the same time, microecological therapy should be given.
(1) Enteric mucosal protective agent: double octahedral montmorillonite powder. It is suitable for acute watery diarrhea (viral or toxin-producing bacterial) and persistent diarrhea. The drug can adsorb pathogens, fix toxins, and then be excreted out of the body with feces, and can also strengthen the gastrointestinal mucosal barrier function and promote the repair of the intestinal mucosa.
Commonly used is the double octahedral montmorillonite (Simida), which has good efficacy. Now there is also domestic double octahedral montmorillonite powder that can be tried. Each bag contains 0.3g, the dose is: 3 years old, 1 bag per time, 3 times a day.
(2) Probiotic preparations: The purpose is to supplement the normal intestinal flora, restore the microecological balance, and reconstruct the natural biological barrier protection function of the intestines.
Commonly used probiotics include Bifidobacterium, Lactobacillus, Streptococcus faecalis, Bacillus cereus, etc. Effective varieties include: Oral Bifidobacterium Triple Live Bacteria Preparation (Peifengkang), Bifidobacterium (Lizhu肠乐), Bifidobacterium/Eosinophilic Lactobacillus/Streptococcus faecalis (Jinshuang), Probiotics, Lichenspora (Chengchangsheng), Lactase, etc. Among them, the probiotic preparations such as Oral Bifidobacterium Triple Live Bacteria Preparation (Peifengkang), Bifidobacterium (Lizhu肠乐), Bifidobacterium/Eosinophilic Lactobacillus/Streptococcus faecalis (Jinshuang) are Bifidobacterium (the main strain of intestinal microecology), listed as the preferred choice. These preparations must maintain a sufficient number of viable bacteria; preparations without viable bacteria are ineffective. The immediate astringent effect of probiotic preparations is not good, and they should not be used as routine applications for acute diarrhea. They are suitable for children with prolonged and chronic diarrhea accompanied by obvious intestinal flora disorder.
In summary, the best treatment for infantile diarrhea is the integration of traditional Chinese and Western medicine, with reasonable medication, which can accelerate the cure of diarrhea.
4. Treatment of non-infectious diarrhea
(1) Food-induced diarrhea: Adjust diet, continue breastfeeding. For children with mixed feeding or artificial feeding, feed with diluted milk or dairy products for two days, then return to normal diet, and children adopt semi-liquid easy-to-digest food, then return to normal diet.
(2) Symptomatic diarrhea: Actively treat the primary disease.
(3) Sugar-induced diarrhea: Some are due to congenital lactase deficiency, and most are due to acute enteritis causing large areas of damage to the small intestinal microvilli during acute enteritis, resulting in a lack of disaccharidase, especially lactase, so that the lactose ingested cannot be digested, forming a high osmotic substance in the intestine, causing osmotic diarrhea, causing diarrhea to persist. At this time, a lactose-free diet can quickly cure the child.
Lactose-free diet: There are lactose-free milk powder or lactose-free soy milk powder; a simple method is to use soy milk feeding, 100ml soy milk plus 5-10g glucose, instead of cow's milk or breast milk feeding.
(4) Allergic diarrhea: Some children may still have diarrhea after applying a sugar-free diet, and protein allergy should be considered, and other protein-containing diets should be used.
5. Traditional Chinese medicine treatment
Chinese traditional Chinese medicine has accumulated rich experience in the treatment of infantile diarrhea with good effects, and commonly used differentiated formula and medicine are as follows:
(1) Damp-heat diarrhea: More common in summer and autumn, suitable for acute watery diarrhea, viral or toxin-producing bacterial infection.
Symptoms: Acute onset, frequent diarrhea, loose or watery stools, red and burning anal mucosa, fever, restlessness, thirst, desire for drinking, nausea and vomiting, decreased appetite, yellow and less urine, red tongue, yellow greasy coating, slippery and rapid pulse.
Treatment principle: Clear heat and promote diuresis, separate and astringe diarrhea. Formula: Modified Gegen Qin Lian Decoction.
Commonly used drugs: Radix Puerariae, Scutellaria baicalensis, Coptis chinensis, Prepared licorice, Poria, Plantago asiatica, Atractylodes macrocephala, etc.
Severe fever: Add Huoxiang, Bupleurum chinense, and Gypsum fibrosum.
Vomiting: Add Pinellia ternata and ginger.
Prescription drugs include: Radix Puerariae and Scutellaria baicalensis Granule, Atractylodes and Poria Astringent Oral Liquid, Bupleurum and Poria Astringent Oral Liquid, etc.
(2) Spleen and stomach deficiency cold diarrhea: Suitable for the prolonged and chronic diarrhea after acute diarrhea.
Symptoms: Course longer than 2 weeks, varying from mild to severe, loose stools, light color and no smell, poor appetite, sallow complexion, pale tongue, thin white fur, fine and slippery pulse.
Treatment principle: Warming the middle Jiao, strengthening the spleen, and astringing and stopping diarrhea. Prescription: Modified Shenling Baizhu Powder combined with Taohua Decoction.
Commonly used drugs: Dangshen, Cangzhu, Baizhu, Fuling, Shanyao, Roukou, Dingxiang, Chishizhi, Shiliu pi, Jinenjin, Wumei, etc.
(3) Spleen and kidney deficiency cold diarrhea: Suitable for severe refractory diarrhea. Commonly seen in infants under 3 months of age with severe malnutrition.
Symptoms: Chronic diarrhea, not cured for a long time, frequent diarrhea, light-colored stools with no smell, emaciated, pale complexion, cold limbs, pale tongue with little fur, weak pulse.
Treatment principle: Warming and tonifying the spleen and kidney, astringing and stopping diarrhea. Prescription: Modified Fuzi Lishen Decoction.
Commonly used drugs: Chuanxiong (decocted first), Hongshenren (decocted first), Cangzhu, Gancao, 4g of Ganshaoyao, Chishizhi, Fuling, Shanyao, etc.
(4) Spleen deficiency diarrhea: Suitable for diarrhea after birth or diarrhea accompanied by illness.
Symptoms: Chronic course, varying from mild to severe, intermittent onset and cessation, loose stools, milk residue or undigested food, light color and no smell, poor appetite, listless and exhausted, emaciated or虚胖, pale tongue, thin white fur, slow and weak pulse.
Treatment principle: Strengthening the spleen and replenishing Qi, astringing and stopping diarrhea. Prescription: Modified Shenling Baizhu Powder.
Commonly used drugs: Dangshen, Fuling, Baizhu, Cangzhu, Shanyao, Chenpi, Jiaosanshan, Jinenjin, Chishizhi.
Proctoptosis: Add Huangqi, Shengma.
Prescription drugs: There are Qipi Pill, Xiangju Dan.
(5) Food-induced diarrhea: Diarrhea caused by improper diet.
Symptoms: Abdominal distension and fullness, pain, desire to defecate when in pain, pain reduced after defecation, loose stools with milk residue, indigestion, sour and smelly taste, poor appetite, nausea and vomiting, impatience and crying, restless sleep at night, pale and red tongue, white and thick greasy or light yellow greasy fur, slippery and rapid pulse.
Treatment principle: Eliminate food stagnation and guide the flow, regulate Qi and relieve pain. Prescription: Modified Baohuo Pill.
Commonly used drugs: Huoxiang, Chenpi, Jiaosanshan, Lai LVZI, Fuling, Banxia, Muxiang, Baishao, Yuanhu, Jinenjin, etc.
Prescription drugs: There are Zhibao Pill, Bai Shou Dan for children, Pizhengxin, etc.
II. Prognosis
Actively investigate the cause of the disease and adopt comprehensive treatment plans. Most cases can alleviate the condition and gradually recover, but the mortality rate is high if there is severe infection or refractory diarrhea. Nowadays, most diarrhea deaths are due to persistent and refractory diarrhea diseases.
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