bubble_chart Overview

Infantile diarrhea is the most common digestive tract syndrome in infants and young children in China. In 1982, the National Pediatric Diarrhea Collaborative Group discussed and adopted a classification method, dividing pediatric diarrhea into infectious and non-infectious types. Infectious diarrhea includes established names such as bacillary dysentery, amoebic dysentery, cholera, and Salmonella infections (e.g., typhoid fever), as well as infections caused by other bacteria (e.g., Escherichia coli, Campylobacter jejuni), viruses (e.g., rotavirus, astrovirus, Coxsackie virus), fungi, and some infections of unknown origin, all of which are diagnosed as pediatric enteritis.

bubble_chart Epidemiology

In the past, this condition was one of the most prevalent diseases in infants and young children and a major cause of infant mortality. After years of domestic and international research, enhanced prevention, and improved diagnosis and treatment, the incidence has decreased in recent years, and cases have become milder. However, it remains a common illness among infants and young children. From 1986 to 1988, the Capital Institute of Pediatrics conducted monthly diarrhea surveillance among 300,000 children across seven provinces and one municipality. The results showed that rural children under five years old had an average annual incidence rate of 2.01 episodes per child, while in Beijing, the rate was 0.45 episodes per child—lower than the Third World average of 3.3 episodes per child. The peak incidence occurred in July and August, with children under two years old accounting for three-fourths of cases. The mortality rate was 0.51% (compared to the Third World average of 6.5%). Nationwide statistics indicate that infant and child diarrhea accounts for approximately 12–24% of total pediatric hospital admissions, with higher incidence rates in rural areas than in cities. Deaths still occur in cases of delayed treatment or severe complications such as malnutrition or intestinal external infections. However, the general hospital fatality rate has now dropped to around 1%.

bubble_chart Etiology

1. Constitutional Factors The disease primarily occurs in infants and young children, with intrinsic characteristics including: ① Immature gastrointestinal development in infants, with lower enzyme activity, yet relatively high nutritional demands, placing a heavy burden on the gastrointestinal tract. ② During infancy, the nervous, endocrine, circulatory systems, as well as liver and kidney functions, are underdeveloped, resulting in poor regulatory capabilities. ③ The immune function of infants is also incomplete. Serum antibody titers against *Escherichia coli* are lowest from birth to 2 years of age, gradually increasing thereafter. Thus, infants and young children are susceptible to *E. coli* enteritis. Breast milk contains high titers of *E. coli* antibodies, particularly secretory IgA in colostrum, which is effective against pathogenic *E. coli*. Therefore, breastfed infants are less likely to contract the disease or experience milder symptoms. Similarly, due to low rotavirus antibody levels in young infants, they are more prone to infection during outbreaks. ④ The distribution of body fluids in infants differs from adults, with a higher proportion of extracellular fluid, vigorous water metabolism, and poor regulatory function, making them more susceptible to fluid and electrolyte imbalances. Infants are prone to rickets and malnutrition, which can lead to digestive dysfunction. At this time, insufficient secretory IgA in the intestines may result in prolonged diarrhea.

2. Infectious Factors These are divided into infections within the digestive tract and external infections of the digestive tract, with the former being predominant.

(1) Infections within the digestive tract: Pathogenic microorganisms can enter a child's digestive tract through contaminated food or water, making artificially fed infants more susceptible. If feeding utensils or food itself are not properly sterilized, infection may also occur. Viruses can also spread via the respiratory tract or water sources. Another route is transmission from adult carriers (of bacteria or viruses), such as when healthcare workers become asymptomatic intestinal carriers after outbreaks of bacterial (or viral) enteritis in wards, leading to pathogen spread.

(2) External infections of the digestive tract: Infections in organs or tissues outside the digestive tract can also cause diarrhea, commonly seen in otitis media, pharyngitis, pneumonia, urinary tract infections, and skin infections. Diarrhea is usually mild and more frequent in younger infants. The causes include digestive dysfunction triggered by external infections of the digestive tract, as well as infections by the same pathogen (mainly viruses) both inside and outside the intestines.

(3) Intestinal dysbiosis due to antibiotic misuse: Prolonged or excessive use of broad-spectrum antibiotics such as chloramphenicol, kanamycin, gentamicin, ampicillin, and various cephalosporins, especially when two or more are combined, can directly irritate the intestines or stimulate the autonomic nerves, accelerating intestinal motility, reducing glucose absorption, and lowering disaccharidase activity, leading to diarrhea. More severely, it can disrupt the intestinal microbiota. Normal intestinal *E. coli* may disappear or significantly decrease, while drug-resistant *Staphylococcus aureus*, *Proteus*, *Pseudomonas aeruginosa*, *Clostridium difficile*, or *Candida albicans* may proliferate excessively, causing enteritis that is difficult to control with medication.

3. Digestive Dysfunction

(1) Dietary factors; (2) Carbohydrate intolerance; (3) Food allergies; (4) Drug effects; (5) Other factors: Such as unclean environments, insufficient outdoor activities, sudden changes in daily routines, or abrupt shifts in external climate (referred to as "wind, cold, summer heat, and dampness diarrhea" in traditional Chinese medicine) can also easily trigger infant diarrhea.

bubble_chart Pathogenesis

The known pathogenesis of the disease is related to the pathogen, with bacterial and viral enteritis being distinctly different.

1. Bacterial

(1) Pathogenic nature of Escherichia coli enteritis: At the onset of the disease, EPEC specifically adheres to the mucosal epithelial cells of the small intestine. This adhesion is mediated by a special plasmid-transmitted fimbriae. These fimbriae are filamentous membrane proteins encoded by a specific plasmid and exhibit adhesiveness to cells with species-specific receptors. They can penetrate the gel layer covering epithelial cells through motility, forming colonies that result in injury to the microvilli of the small intestine's epithelial cells.

(2) Enterotoxigenic Escherichia coli (ETEC) enteritis: ETEC differs from EPEC in serotype, and its pathogenic mechanism involves two steps: ① Initial adhesion to the mucosal cells of the small intestine, followed by colonization and proliferation on their surface, primarily facilitated by the bacteria's specialized fimbriae; ② The second step involves the production of enterotoxins: one is heat-labile toxin (LT), which resembles cholera toxin in structure, pathogenic mechanism, and immunological properties. It consists of two subunits, A and B, with subunit B binding to GM1 gangliosides on small intestine epithelial cells. Subunit B facilitates the entry of subunit A into the cell, where it exerts its biological effect: activating adenylate cyclase on the cell membrane, converting ATP to cAMP, significantly increasing intracellular cAMP levels. This leads to excessive secretion of water and chloride in the intestines, inhibition of sodium reabsorption, increased intestinal fluid secretion, and heightened peristalsis, resulting in watery diarrhea. The other toxin is heat-stable toxin (ST), with its active components divided into STa and STb. The latter is the main component of the enterotoxin, stimulating guanylate cyclase to convert GTP to cGMP, increasing intracellular cGMP levels, reducing chloride absorption, and causing increased intestinal fluid secretion. Many ST-producing strains also produce LT, often leading to more severe diarrhea. The plasmid carrying the enterotoxin also carries genes for colonization factors. Known serotypes of Escherichia coli with colonization factors include: O₇₈:H₁₁, O₆:H₁₆, O₁₅₉:Hv, O₁₃₉:H₂₅, etc.

(3) Enteroinvasive Escherichia coli (EIEC) enteritis: EIEC is a Shigella-like Escherichia coli. Its primary characteristic is the ability to invade the mucosa of the large and small intestines, penetrate epithelial cells, dissolve cellular proteins, and proliferate within them, damaging the mucosal brush border and causing local ulcers or even bleeding. Thus, the clinical presentation resembles dysentery. Its invasiveness is controlled by a plasmid; eliminating this plasmid renders the bacteria non-invasive, and the plasmid can be transferred to non-virulent strains.

(4) Campylobacter jejuni enteritis: LT has been identified in Campylobacter jejuni, which increases intestinal cAMP levels. Other bacterial toxins are also involved, but the exact pathogenic mechanisms require further study.

2. Viral The mechanism of viral enteritis differs from bacterial enteritis, with no increase in cAMP or cGMP. Taking rotavirus enteritis as an example: after rotavirus infection, it first invades the epithelial cells of the small intestine mucosa, spreading extensively from the infected area to the surroundings until the entire small intestine is affected. Experimental rabbit models indicate that in the early stages of infection, the Peyer's patches in the small intestine are severely affected, suggesting this area as the entry point. Later, the villous epithelium of the small intestine is extensively damaged, while the crypt epithelium remains unaffected. Apart from the small intestine, neither the stomach nor the large intestine is infected. After the surface epithelium of the small intestine is damaged, the crypt epithelium rapidly proliferates, shedding the virus. The rapidly proliferating crypt epithelium expands outward from the crypts, covering the surface of the small intestinal lumen. These newly proliferated epithelial cells cannot differentiate quickly, thus lacking digestive and absorptive functions. As a result, a large amount of intestinal fluid accumulates in the intestinal lumen, leading to the excretion of watery stools. Norwalk virus also follows a similar pathogenic process in the small intestine as described above.

Pathophysiology

1. Disorders of fat, protein, and carbohydrate metabolism Due to reduced intestinal digestive function and hyperactive intestinal motility, the digestion and absorption of nutrients are impaired. During the course of the disease, protein assimilation is not significantly reduced. Some children with severe diarrhea can still digest and absorb considerable amounts of protein. Fat assimilation and absorption are more affected, with fat absorption typically at 50–70% of normal levels in general cases; in severe cases, only 20% of ingested fat is absorbed. During the convalescence stage, even after hyperactive intestinal motility has subsided for several days to weeks, fat balance tests reveal that fat assimilation remains low. Carbohydrate absorption is also impaired. The flat glucose tolerance test curve in affected children is related to carbohydrate malabsorption.

2. Water and electrolyte disturbances Diarrhea leads to significant loss of water and electrolytes, primarily due to the loss of large amounts of intestinal fluid, resulting in a series of clinical symptoms.

(1) Dehydration: Causes: ① Increased fluid loss from vomiting and diarrhea. According to observations from Beijing Children's Hospital, severe cases lose approximately 30 ml/kg of fluid daily through stool, with a maximum of 81 mg/kg, more than 10 times the normal amount. ② Reduced intake of food and fluids due to decreased appetite and severe vomiting, which is almost equivalent to fasting. ③ Loss of electrolytes such as sodium and potassium through diarrhea reduces the body's ability to retain water. Most children have fever and increased respiratory rate, and deep, rapid breathing during acidosis further increases insensible water loss, which can reach up to 80 mg/kg/day (normal: 30 mg/kg/day). It has been observed that for every 1°C increase in body temperature, water loss increases by 10–12 mg/kg/day.

Based on the proportion of water and electrolyte loss, dehydration can be classified into three types:

1) Isotonic dehydration: Domestic data show that isotonic dehydration accounts for 40–80% of dehydration cases in infants and young children with diarrhea. Serum sodium remains within the normal range (130–150 mmol/L). Cases with a shorter course, lower sodium content in stool, and better renal regulation often present as isotonic dehydration. Large intestine bacillus enteritis with a short course and normal nutritional status also frequently manifests as isotonic dehydration. The main feature of this type is extracellular fluid loss, with minimal intracellular fluid loss.

2) Hypotonic dehydration: Accounts for 20–50% of dehydrated children. Serum sodium concentration decreases (hyponatremia) to below 130 mmol/L. Diarrheal stools with higher sodium content, such as those from large intestine bacillus enteritis with a slightly longer course, often contain 20–75 mmol/L of sodium or even higher. Severe diarrhea with a prolonged course, significant sodium loss, and excessive water intake with low electrolyte intake can easily lead to hypotonic dehydration. Malnourished children, who typically have low or borderline serum sodium levels, are also prone to hypotonic dehydration after diarrhea. The hallmark of this type is significant extracellular fluid loss, with some excreted and some entering cells, leading to intracellular fluid expansion. Thus, dehydration symptoms appear early, and circulatory volume decreases rapidly, increasing the risk of circulatory failure.

3) Hypertonic dehydration: Accounts for 1–12% of dehydrated children. Serum sodium concentration increases (hypernatremia) to above 150 mmol/L. This occurs when water loss is proportionally greater than sodium loss or when excessive salt is ingested. Children with good nutritional status, acute onset, high fever, short course, and low sodium content in stool, especially those with minimal reduction in food intake, are prone to hypertonic dehydration. In hot climates, excessive milk intake due to thirst, severe dehydration impairing renal function, or inappropriate use of sodium-containing fluids can also lead to hypertonic dehydration. The key feature is high extracellular osmotic pressure, causing intracellular fluid to shift outward, resulting in intracellular dehydration. Since extracellular fluid loss is less severe, clinical dehydration symptoms appear later, while neurological symptoms emerge due to brain cell dehydration.

(2) Acidosis: Dehydration is often accompanied by varying degrees of acidosis. Causes: ① Loss of large amounts of alkaline solutes in the stool; ② In grade II or higher dehydration, reduced blood volume and insufficient renal blood flow lead to decreased renal regulatory function, resulting in reduced exchange of Na⁺ and H⁺ in the distal convoluted tubule, decreased excretion of H⁺, and increased H⁺ in the body; ③ Hemoconcentration slows circulation, leading to tissue hypoxia and other effects, which increase the body's catabolic processes and elevate acidic metabolic products (organic and inorganic acids, etc.); ④ Hunger-induced hypoglycemia, insufficient liver glycogen, and reduced liver function cause ketone body accumulation, which the kidneys cannot excrete promptly. Thus, the acidosis is metabolic. The serum carbon dioxide combining power in affected children is often between 10–20 mmol/L (22–45 vol%), and in severe cases, it may drop to 5–10 mmol/L or lower. Acidosis in young infants is often more severe, but due to poor respiratory compensatory function, symptoms like deep breathing are usually absent, making early detection difficult. In cases of severe hypotonic dehydration, where extracellular fluid loss is significant and renal regulatory function is impaired, acidosis tends to be more severe.

(3) Hypokalemia: In diarrhea, the potassium concentration in watery stools is approximately 20–50 mmol/L. Due to reduced food intake, potassium intake is also low. During diarrhea, the loss of intracellular potassium is significant. The reasons for this loss include: ① In acidosis, hydrogen ions and sodium ions from the extracellular fluid enter the cells, displacing potassium ions, which are then excreted in urine. This occurs even when intracellular potassium is deficient. Therefore, during acidosis, intracellular potassium is deficient, but serum potassium levels may not be low and can even increase due to hemoconcentration. ② When serum potassium decreases, intracellular potassium ions move out of the cells, while sodium ions enter the cells. ③ When dehydration, hypoxia, or other factors impair cellular function, the sodium-potassium pump in the cell membrane is affected, reducing the movement of potassium into cells and sodium out of cells. Before fluid therapy, hemoconcentration and impaired renal function reduce urinary potassium excretion, so serum potassium levels are often not low, and symptoms of hypokalemia are rare. After fluid therapy, hemoconcentration is corrected, diluting serum potassium. As dehydration improves, urine output increases, and the exchange of sodium and potassium ions in the distal convoluted tubule becomes more active, leading to significant potassium excretion. The glucose provided during fluid therapy also fixes some potassium during glycogen synthesis (0.36 mmol of potassium is required for every 1 g of glycogen synthesized). Additionally, fasting during fluid therapy further reduces potassium intake.

(4) Changes in blood calcium and magnesium: In children with prolonged diarrhea or preexisting malnutrition or rickets, hypocalcemic tetany may occur after acidosis is corrected due to decreased ionized calcium levels. Symptoms of magnesium deficiency are rare and typically seen only in cases of chronic diarrhea or malnutrition. A pediatric research institute measured serum magnesium levels in 41 children: levels were normal at admission but decreased to varying degrees after fluid therapy, with an average reduction of 0.53–0.55 mmol/L. The decrease was more pronounced in cases of severe dehydration. Without magnesium supplementation during treatment, serum magnesium levels generally returned to normal during the convalescence stage in most cases, but recovery was limited in prolonged illness or severe dehydration. Symptoms of hypomagnesemia often appear after hyponatremia, hypokalemia, and hypocalcemia have been corrected.

bubble_chart Pathological Changes

The pathological changes are mild and disproportionate to the clinical symptoms. The main gross findings include intestinal distension, congestion of the small intestinal mucosa, and catarrhal inflammation. In a few cases, pneumatosis cystoides intestinalis is observed in the lower ileum and cecum, primarily in the submucosal layer. Some cases may show one or two shallow ulcers the size of a pinhead in the lower ileum. Occasionally, bloody stools are present in the intestinal lumen, but the bleeding site is often difficult to locate. Microscopically, aside from congestion, leukocyte infiltration, and occasional small ulcers, no other specific findings are noted. In chronic cases, signs of malnutrition may be observed. Fatty infiltration of the liver is relatively common. Rare instances of cerebral venous sinus thrombosis may occur. Common complications include bronchopneumonia and suppurative foci in the middle ear, renal pelvis, and other areas.

bubble_chart Clinical Manifestations

1. General Symptoms Vary depending on the severity of diarrhea.

(1) Mild diarrhea: Mainly characterized by increased frequency of bowel movements, ranging from several times to about 10 times a day. The stool is loose, sometimes with a small amount of water, appearing yellow or yellowish-green, mixed with a small amount of mucus. The volume per bowel movement is not large, often containing small white or pale yellow lumps, which are soap-like masses formed by the combination of calcium, magnesium, and fatty acids. Occasionally, there may be slight vomiting or milk regurgitation, decreased appetite, normal body temperature, or occasional low-grade fever. The complexion is slightly pale, but the child’s spirit remains relatively good, with no other systemic symptoms. Weight does not increase or may slightly decrease. Fluid loss is below 50ml/kg, and clinical dehydration symptoms are not obvious. The prognosis is relatively good, and the course of the illness lasts about 3–7 days. In children with rickets or malnutrition, although the diarrhea is mild, it often occurs 3–7 times a day, with yellow stools frequently containing mucus and a foul odor. A small number of white blood cells may be seen in stool examinations. The consistency and frequency of stools are unstable. If prolonged, nutritional status worsens, often leading to secondary infections in the urinary tract, middle ear, or other areas.

(2) Severe diarrhea: May develop from mild diarrhea. Bowel movements occur dozens to 40 times a day. At the onset of severe diarrhea, the stool becomes more watery, occasionally with mucus, appearing yellow or yellowish-green, with a foul, fishy odor and an acidic reaction. If diaper changes are insufficient, the skin around the buttocks may become eroded, red, and peeling. As the condition worsens and food intake decreases, the foul odor of the stool diminishes, fecal lumps disappear, and the stool becomes watery or like egg drop soup, lighter in color, mainly composed of intestinal fluid and a small amount of mucus, with an alkaline reaction. The volume of stool increases to 10–30ml per bowel movement, sometimes up to 50ml. Microscopic examination reveals fat droplets, motile bacteria, mucus, and in severe cases, occasional red blood cells, with white blood cells reaching about 10 per high-power field. The child’s appetite is poor, often accompanied by vomiting. Irregular low-grade fever is common, and in severe cases, high fever may occur. Weight drops rapidly, and the child becomes noticeably emaciated. If fluid replacement is insufficient, dehydration and acidosis gradually worsen. A few severe cases have a sudden onset, with high fever reaching 39–40°C, frequent vomiting, watery stools, and rapid development of symptoms of water and electrolyte imbalance. In recent decades, due to early medical intervention, severe cases of diarrhea have significantly decreased.

2. Symptoms of Water and Electrolyte Imbalance Mainly include dehydration and acidosis, sometimes with symptoms of hypokalemia and hypocalcemia.

(1) Dehydration: The child becomes thinner and loses weight rapidly, appears lethargic, has pale or even grayish skin with poor elasticity, sunken anterior fontanel and eye sockets, dry mucous membranes, a sunken abdomen, weak and rapid pulse, low blood pressure, and reduced urine output. Dehydration is classified into three grades: mild, moderate, and severe. ① Grade I dehydration: Fluid loss accounts for less than 5% of body weight. The child is slightly lethargic, complexion is somewhat pale, skin is slightly dry but elasticity is still good, eye sockets are slightly sunken, and urine output is slightly less than usual. ② Grade II dehydration: Fluid loss accounts for about 5–10% of body weight. The child is lethargic and intermittently dysphoric, with pale or grayish skin that is dry, loose, and has poor elasticity, not immediately flattening when pinched. The area around the mouth appears bluish, the anterior fontanel and eye sockets are noticeably sunken, lips and mucous membranes are dry, heart sounds are muffled, the abdomen is sunken, limbs are cold, and urine output is significantly reduced. ③ Grade III dehydration: Fluid loss accounts for 10–15% of body weight. The child is lethargic and apathetic, unresponsive to surroundings, with grayish skin and extremely poor elasticity, not easily flattening when pinched. The anterior fontanel and eye sockets are deeply sunken, eyes do not close, conjunctiva is dry, crying produces no tears, cornea is dull, lips are cyanotic, mucous membranes are dry and unclear, heart rate is rapid, blood pressure is difficult to measure, the abdomen is deeply sunken, limbs are cold, and urine output is minimal or absent.

When assessing the degree of dehydration, attention should be paid to the extent of sunken eye sockets and anterior fontanel. Hypotonic dehydration is more likely to cause reduced skin elasticity, while malnourished children already have poor skin elasticity, which should be noted.

Clinical symptoms also vary depending on the type of dehydration. In hypotonic dehydration, due to the significant loss of extracellular fluid, children exhibit early and severe dehydration symptoms, but thirst is milder while lethargy is more pronounced. In hypertonic dehydration, intracellular fluid shifts outward, resulting in relatively less loss of extracellular fluid. Children show obvious thirst, fever, dysphoria, increased muscle tone, and occasionally convulsions. The sunken eye sockets and anterior fontanel are less pronounced, hands and feet remain warm, and the pulse is palpable.

(2) Acidosis: Mainly manifested as lethargy and deep, sigh-like breathing. In severe cases, breathing may accelerate, even leading to unconsciousness. Newborns or young infants may not exhibit deep breathing or may show it later, primarily presenting as drowsiness, pallor, refusal to eat, and weakness. When assessing acidosis, the child's age must be taken into account.

(3) Hypokalemia: Significant hypokalemia often appears after more than a week of watery diarrhea, occurring earlier and more severely in children with pre-existing malnutrition. Generally, children rarely show hypokalemia symptoms before fluid therapy, but after receiving potassium-free fluids, symptoms gradually emerge as dehydration and acidosis are corrected: lethargy, decreased muscle tone, and dull first heart sounds. In more severe cases, abdominal distension and fullness, weakened or absent borborygmi, and diminished tendon reflexes may occur. If potassium is not promptly supplemented, severe hypokalemia can lead to muscle paralysis, even respiratory muscle paralysis, intestinal paralysis, bladder paralysis, absent tendon reflexes, slowed heart rate, arrhythmias, systolic murmurs at the cardiac apex, and cardiac enlargement, which can be life-threatening. Hypokalemia symptoms typically appear when serum potassium levels fall below 3.5 mmol/L.

(4) Hypocalcemia: Children with pre-existing malnutrition, rickets, or prolonged diarrhea often exhibit hypocalcemia symptoms such as dysphoria, restlessness, hand-foot convulsions, or even seizures after fluid therapy. Physical examination may reveal positive Chvostek's and Trousseau's signs.

(5) Hypomagnesemia: A few children may develop hypomagnesemia-induced hand-foot convulsions after correcting dehydration, acidosis, and calcium supplementation. Symptoms include hand-foot tremors, convulsions, irritability, crying, and difficulty sleeping. Some children may develop flushing on the forehead or skin folds.

bubble_chart Diagnosis

Pay attention to identifying the disease cause, excluding diarrhea caused by external contraction in the digestive tract. First, understand the feeding situation, history of unclean food, disease contact history, and disinfection status of food and utensils from the medical history to distinguish between infectious and non-infectious diarrhea. Secondly, note the season and region of onset. In northern China, diarrhea from March to July is mostly caused by large intestine bacilli, while cases from August to December are often viral. If conditions permit, stool culture, electron microscopy, or virus isolation should be performed.

Before fluid infusion, the degree and nature of dehydration should be analyzed and judged based on the medical history and signs. Detailed inquiries should include: feeding conditions before and during the illness, the amount of water intake and whether it contained salt; the number of days, daily frequency, and nature of diarrhea and vomiting; the number, type, and amount of fluid infusions before admission; urine output, color, and the time of the last urination before admission. Based on this, combined with sign findings, estimate the degree and nature of dehydration. For severe or difficult-to-judge cases, serum sodium, potassium, chloride, and blood gas analysis should be measured, or carbon dioxide combining power should be tested. Serum calcium can be measured if convulsions occur. Note that the analysis of water and electrolyte disturbances must be based on medical history and clinical manifestations, and fluid replacement should not be based solely on laboratory results to ensure accurate judgment. Electrocardiogram examination helps understand blood potassium levels. In hypokalemia, the T wave flattens, then inverts, the ST segment lowers, and a U wave often appears, sometimes merging with the T wave. Severe hypokalemia may lead to ventricular premature beats and ventricular tachycardia. In rare severe cases, ventricular fibrillation may occur. Differentiate the clinical characteristics of diarrhea caused by various pathogens to aid diagnosis.

1. Enteritis caused by large intestine bacilli: Occurs year-round but is most common from May to July. The onset is usually gradual, starting with mild diarrhea and no fever, rarely vomiting. It gradually worsens, with vomiting and low fever often appearing alongside dehydration. Stools are often egg-drop soup-like, pale yellow, sometimes with more mucus, occasionally with blood streaks, and have a foul odor. In cases of O111, O126, O127, and O128 enteritis, white pus may be present in the stool. O111 causes the most severe cases, while O55, O86, O26, and O44 cause milder ones. This type of enteritis often presents with isotonic or hypotonic dehydration. Enterotoxic large intestine bacilli enteritis produces large amounts of watery stool; invasive large intestine bacilli enteritis, due to bacterial invasion of the small intestine mucosa, can cause ulcers, and stools often contain small amounts of pus or blood.

2. Viral enteritis: Mainly caused by rotavirus. In Beijing, it mostly occurs from August to December, peaking in October and November. It predominantly affects children under 2 years old. The incubation period is 1–3 days. The onset is acute, with early vomiting and often accompanying upper respiratory infection symptoms. Body temperature typically ranges from 38–40°C. Abdominal distension and fullness are more pronounced. Watery stools begin within 1–2 days of onset, thin and pale, sometimes resembling white rice water or clear water, with little mucus and rarely a foul odor. Severe thirst and dysphoria are common. Dehydration is mostly grade I or grade II isotonic or hypertonic, rarely hypotonic. Antibiotics are ineffective, and most cases resolve naturally within 5–7 days. Rare critical cases may develop cyanosis in the late stage, possibly related to microcirculation disorders or heart failure, leading to fatality.

3. Campylobacter jejuni enteritis: Cases are gradually increasing. The average incubation period is 3–5 days; if the infection dose is small, the incubation period may be longer. Before diarrhea, fever, abdominal pain, and other prodromal symptoms may occur, and severe complications like sepsis or meningitis may rarely appear. The seasonal pattern of this disease is unclear, and it is most common in children aged 1–3. Stools often contain blood, and white blood cells may be seen under microscopy. Diagnosis relies on bacteriological examination, with a significant rise in serum antibodies during the convalescence stage.

4. Yersinia enteritis: Yersinia can cause acute or chronic gastroenteritis in children, though it is rare domestically. The main symptoms are diarrhea, fever, and abdominal colicky pain. About 25% of affected children have bloody stools. Although a few cases may persist, most are self-limiting and resolve within a few days.

5. Staphylococcus aureus enteritis is rarely primary and often secondary to the oral administration of broad-spectrum antibiotics. The symptoms and course of the disease are usually related to the degree of dysbiosis, and sometimes it occurs secondary to chronic dysentery. The main manifestations include vomiting, fever, and diarrhea. Vomiting often appears 1–5 days before fever. In the initial stage of diarrhea, the stool is yellow-green, and after 3–4 days, it often turns into dark green watery stool with a foul odor, occurring 10–20 times or more per day. Fluid loss is greater than in enteritis caused by coliform bacteria, and symptoms of dehydration and electrolyte imbalance are severe, even leading to shock. Gray-white pseudomembranous patches are commonly seen in the stool (placing a small amount of stool in saline allows the pseudomembrane to float on the water), which aids clinical diagnosis. A mucus smear of the stool reveals numerous pus cells and Gram-positive cocci. Culture shows growth of Staphylococcus aureus.

6. Fungal Enteritis Mostly occurs as a complication of other infections, such as persistent large intestine bacillary enteritis. Most patients have a history of long-term use of broad-spectrum antibiotics. Stool frequency is 3–4 times per day or slightly more, with yellow, watery stools, occasionally resembling bean curd residue, sometimes greenish with more foam and mucus. Microscopic examination of stool reveals fungal spores and hyphae. Guangxi once reported 3 fatal cases of mucormycosis enteritis, with a disease course of 6 days to 3 months, presenting with yellow-green watery stools occasionally containing mucus, and red and white blood cells observed under microscopy. Autopsy revealed large amounts of mucor in intestinal blood vessels and surrounding tissues.

bubble_chart Treatment Measures

1. The principles are: ① Provide appropriate rest for the digestive tract after diarrhea begins; ② Control external contraction infections in the intestines; ③ Correct typical edema and electrolyte imbalances; ④ Provide good nursing care.

2. Dietary therapeutics: Initially, provide appropriate rest for the digestive tract. For mild and moderate cases, reduce food intake to about half the usual amount for 4–6 hours; for severe cases, reduce for 6–12 hours. During reduced food intake, fluid supplementation is necessary: for mild and moderate cases, prepare and administer "initial rehydration solution" orally. For viral enteritis, due to glucose-induced sodium transport impairment, the oral glucose solution concentration should not exceed 2%, and the sodium concentration should not exceed 50 mmol/L; severe cases require intravenous fluid therapy. When resuming feeding, breastfed infants should have reduced feeding duration per session; formula-fed infants can start with rice water, diluted lotus rhizome node powder, or diluted milk (or yogurt). The amount of milk and added sucrose should be gradually increased, starting from small quantities and diluted concentrations. Except for cases of poor appetite or severe vomiting, increasing milk intake should not be a concern, as post-diarrhea, the child's body has significant nutritional depletion. Although stool frequency may increase with increased food intake, intestinal absorption is proportional to intake. Prolonged fasting or overly slow calorie increase can lead to malnutrition. Generally, sufficient calories should be provided within 48 hours of treatment, with normal diet restored in about 5 days.

3. Fluid therapy

(1) Oral rehydration salts (ORS): Since 1971, the World Health Organization (WHO) has promoted the use of ORS-prepared beverages for acute diarrhea in children of different ages and etiologies worldwide. Since 1980, ORS has been widely used in various provinces and cities in China with good results. To prepare 1 liter of ORS solution, the following are needed: NaCl 3.5g, NaHCO₃ 2.5g, KCl 1.5g, and glucose 20g. The electrolyte concentrations are: Na 90 mmol/L, K 20 mmol/L, Cl 80 mmol/L, HCO₃ 30 mmol/L, and glucose 111 mmol/L. Since children with viral enteritis often have isotonic or hypertonic dehydration, ORS should be diluted by 1/3–1/2 before oral administration, reducing Na to 45–60 mmol/L, K to 10–13.3 mmol/L, Cl to 40–53.4 mmol/L, HCO₃ to 15–20 mmol/L, and glucose to 56–74 mmol/L, while maintaining a glucose concentration that still promotes water and sodium absorption in the digestive tract. On the first day, the ORS dosage is: Grade I dehydration, 50–60 ml/kg, to be consumed within 4 hours; Grade II dehydration, 70–100 ml/kg, to be consumed within 4–6 hours. Potassium and calcium should also be supplemented as described later. Recently, WHO has recommended replacing sodium bicarbonate in the original formula with potassium citrate, as the latter is more stable and less prone to moisture absorption. Clinical applications have confirmed the advantages of this substitution. Additionally, WHO advocates replacing the 20g glucose in the ORS formula with 30g rice flour or other cereal flour, as cereal-based preparations are more palatable, better accepted by children, cause less vomiting, and lead to faster stool formation. Clinical practice has proven its efficacy in promoting water and electrolyte absorption. The Pediatrics Department of West China Medical University once replaced the 20g glucose in the original formula with 50g rice flour, which effectively prevented dehydration and outperformed the original ORS formula. For children who have difficulty taking ORS orally or those with Grade III dehydration and circulatory failure, intravenous rehydration is necessary first. In rural areas where intravenous infusion is inconvenient, ORS can also be administered via gastric tube. If dehydration does not improve after oral or gastric tube administration of ORS, intravenous fluid therapy should be arranged.

(2) Parenteral rehydration: For children with vomiting, difficulty in oral rehydration, or grade III dehydration, treatment should be carried out step by step according to the principles of parenteral fluid therapy outlined in the previous volume. First, rapidly restore circulating volume and replenish cumulative losses, then more slowly replace ongoing losses and physiological consumption. Over the past decade, there has been an international trend toward reducing the total volume of rehydration fluids and the amount of sodium-containing fluids administered.

1) Total fluid replacement volume: The fluid replacement volume for the first 24 hours of treatment should include: cumulative loss volume, ongoing loss volume, and physiological consumption volume. The total replenishment volume should be 120–200 ml/kg based on the degree of dehydration (Grade I dehydration: 120–150 ml/kg, Grade II dehydration: 150–180 ml/kg, Grade III dehydration: 180–200 ml/kg). For most cases, feeding can begin 4–12 hours later (milk volume is included in the aforementioned fluid volume). If diarrhea remains severe, some cases may still require intravenous fluids on the second day. Hypertonic dehydration should be corrected slowly over 2–3 days. After dehydration is corrected, the daily fluid volume only needs to replenish ongoing losses and physiological consumption, approximately 100–120 ml/kg per day.

2) Fluid composition: The fluid composition for the first day of rehydration includes isotonic electrolyte solution (containing Na⁺ and K+) and non-electrolyte solution (glucose solution). The ratio of the total daily volume is determined by the nature of dehydration: - Isotonic dehydration: 1:1 (equivalent to 1/2 tonicity electrolyte solution). - Hypotonic dehydration: 2:1 (equivalent to 2/3 tonicity electrolyte solution). - Hypertonic dehydration: The ratio should be adjusted to 1:1 to 1:2 (total concentration equivalent to 1/3 tonicity electrolyte solution) depending on the severity of hypertonicity, to avoid excessively rapid reduction in serum sodium concentration, which may lead to relative water intoxication. In 1990, Ronald Kallen proposed the following average daily sodium concentration recommendations:

For milder cases, children with good kidney function, or when conditions are limited, normal saline alone may be used as the electrolyte solution. However, in cases of obvious acidosis, "2:1 solution" (2 parts normal saline + 1 part 1/6 mol sodium bicarbonate or sodium lactate) should be used as the sodium-containing solution. For patients with hypokalemia, after urination is confirmed during fluid therapy, potassium chloride (0.3%) should be added to the remaining fluid volume for infusion.

3) Steps and speed of fluid replacement: The principle is to administer the required fluids in order of sodium concentration, starting with higher concentrations and faster rates, then transitioning to lower concentrations and slower rates. Initial infusion: For isotonic and hypotonic dehydration, use "2:1" solution; for hypertonic dehydration, use "3:4:2" solution (3 parts glucose solution, 4 parts saline, 2 parts 1/6 mol sodium lactate) at 20 ml/kg, administered over half to one hour to restore circulating volume. Subsequently, gradually reduce the sodium concentration of the fluid and complete the total fluid replacement within 24 hours (48 hours for hypertonic dehydration). The general infusion rate is 8–10 ml/kg/hour, while for hypertonic dehydration, it is 5–8 ml/kg/hour. To prevent rapid shrinkage of brain cells in hypotonic dehydration, avoid administering hypertonic fluids. Kallen suggests the following fluid replacement schedule:

Cumulative rehydration volume (%)

4) Potassium supplementation: Generally, children should receive 2～4 mmol/kg·d of potassium (equivalent to 1.5～3 ml/kg·d of 10% KCl solution) orally after urination begins, divided into 3～4 doses per day. For those with significant hypokalemia, a slow intravenous infusion of 40 mmol/L (0.3%) KCl can be administered, with the total daily dose increased to 4～6 mmol/kg·d (equivalent to 2～3 ml/kg·d of 15% KCl). If all KCl must be administered intravenously (never by IV push or via the drip chamber), it should be evenly distributed throughout the day's IV fluids. A safer method is to add 100 mg/kg of KCl to the first batch of IV fluids after urination (0.3% KCl) for slow infusion. Hypokalemia usually improves, and the remaining required KCl can be supplemented orally in 3～4 divided doses. Excessive concentration or rapid IV administration of potassium can lead to hyperkalemia and sudden death, requiring special caution. Since foods are rich in potassium, potassium supplementation can be discontinued once the diet returns to half the normal amount.

5) Calcium and magnesium supplementation: During rehydration, if the child exhibits excessive excitability, convulsions, or spasms, 10 ml of 10% calcium gluconate can be diluted and administered intravenously, repeated if necessary. If oral intake is possible, 5～10 ml of 10% calcium chloride can be given 3～4 times daily. Such children often have rickets; after spasms subside, vitamin D2 200,000～300,000 units can be administered intramuscularly, followed by continued calcium supplementation. For severe dehydration, chronic diarrhea, or symptoms of hypomagnesemia, 25% magnesium sulfate 0.2～0.4 ml/kg/dose can be administered intramuscularly 2～3 times daily for 2～4 days.

6) Management of severe acidosis: Most cases of acidosis can be corrected with the above rehydration therapy once renal function recovers. For severe acidosis, the dosage of sodium lactate or sodium bicarbonate can be increased, replacing an equivalent amount of normal saline.

7) Blood transfusion or plasma: For severe diarrhea or cases accompanied by malnutrition, plasma transfusion is recommended at 25～50 ml per dose, repeated every 1～3 days as needed, for a total of 2～4 times. For anemia, whole blood transfusion may be substituted.

4. Chinese medicine therapy

5. Control of intestinal infection: Appropriate antibacterial agents should be used based on the pathogen, especially for severe cases.

(1) For Escherichia coli infections: Except for invasive strains, E. coli rarely invades tissues. The bacteria accumulate heavily in the intestines, so bactericidal drugs poorly absorbed by the intestines should be selected. If efficacy is poor, drug sensitivity testing should be performed to guide treatment. Commonly used drugs include:

1) Kanamycin; 2) Gentamicin; 3) Paromomycin; 4) Trimethoprim.

(2) For invasive large intestine bacillus infections: Non-absorbable intestinal bactericidal Yaodui has poor efficacy for such infections. Medications used to treat bacillary dysentery can be employed. Ampicillin shows better effectiveness, with a dose of 50mg/kg·d, administered intravenously in 4 divided doses.

(3) For mouse cold-damage disease infection: Antibiotics should be selected based on drug sensitivity tests. Before the results are available, ampicillin or compound formula sulfamethoxazole can be used.

(4) For secondary infections caused by Staphylococcus aureus, Pseudomonas aeruginosa, or Proteus after intestinal flora disturbance: If early signs of flora disturbance are detected, the original antibiotics should be discontinued promptly, and oral lactasin (0.3–0.9g, three times daily) should be administered. This helps restore the normal intestinal flora and suppress pathogenic transient bacteria. Additionally, compound vitamin B, vitamin C, and folic acid should be supplemented, which can correct intestinal flora disturbance within a few days, with symptoms improving accordingly. If improvement is not significant and stool smear shows a significant reduction in large intestine bacilli, 5–10g of normal infant stool can be suspended in saline and administered once daily as a rectal retention enema to accelerate recovery. For Staphylococcus aureus infections, choose from: erythromycin, new penicillin, gentamicin, vancomycin, or cefazolin. For Pseudomonas aeruginosa infections, use polymyxin B, carbenicillin, or gentamicin. For Proteus infections, use ampicillin, kanamycin, or cephalosporins.

(5) For rotavirus infection: Intramuscular injection of α-interferon (10u/dose, twice daily) for 3–5 days is highly effective in treating autumn diarrhea.

(6) For Campylobacter jejuni infection: Erythromycin is the first-line drug, at a dose of 25–50mg/kg/day, divided into 3–4 oral doses. It is also sensitive to gentamicin, neomycin, and furazolidone, but not to compound formula sulfamethoxazole.

(7) For Yersinia enterocolitica infection: Both neomycin and sulfonamides are effective.

(8) For fungal infections: Oral nystatin at a dose of 125,000–500,000 units, 2–4 times daily, should be administered while discontinuing the original antibiotics. If intestinal absorption is significantly impaired, injectable drugs such as amphotericin B should be considered.

bubble_chart Prognosis

The prognosis depends on the disease cause, nutritional status, and the timeliness of treatment. Diarrhea caused by drug-resistant bacteria or fungi in the large intestine has a poorer prognosis. Viral enteritis has a good prognosis. Children with malnutrition or rickets who develop diarrhea have a poorer prognosis due to their weakened regulatory functions. Severe cases, delayed treatment, and serious complications such as acute renal failure or severe secondary infections lead to a poor prognosis.

bubble_chart Prevention

Main methods: ① Encourage breastfeeding, especially during the first 4–6 months and the first summer, avoiding weaning in summer; ② For artificial feeding, pay attention to dietary hygiene and clean water sources. Rinse and scald feeding utensils with boiling water before each feeding, and sterilize them by boiling once daily; ③ Both breastfeeding and artificial feeding should introduce complementary foods on schedule, avoiding adding several complementary foods simultaneously; ④ For poor appetite or during the fever initial stage [first stage], reduce the intake of milk and other foods, replacing them with water, preferably using oral rehydration salts to prepare a drink for oral intake; ⑤ In hot summers, avoid overeating or consuming fatty foods. Infants have poor temperature regulation, so dress them lightly in summer and ensure good ventilation in living spaces; ⑥ For malnutrition, rickets, or intestinal external contraction infections, treat promptly to prevent complications like diarrhea; ⑦ Infectious diarrhea, especially caused by large intestine bacilli, mouse cold-damage disease, other Salmonella, or rotavirus, is highly pestilential and easily spreads widely in wards. Strict disinfection and isolation are necessary to prevent cross-infection in pediatric wards. The most effective disinfection method is fumigation with peracetic acid, followed by surface disinfection with new disinfectants and ultraviolet irradiation. Diarrhea wards should ideally undergo thorough peracetic acid fumigation monthly; ⑧ Children playing outdoors should wash their hands before meals and after using the toilet; ⑨ Medical staff should actively promote preventive measures for childhood diarrhea to prevent recurrence.

Rotavirus enteritis is highly prevalent, and vaccines are the ideal preventive method. There have been reports of oral vaccines for rotavirus with a protection rate of over 80%, but their long-term efficacy requires further study.

bubble_chart Complications

Diarrhea often leads to malnutrition, multiple vitamin deficiencies, and various infections.

1. Gastrointestinal external contraction infection: Gastrointestinal external contraction infection may be a disease cause of diarrhea, but it is also often due to systemic resistance decline after diarrhea. Common infections include skin pyogenic infections, urinary tract infections, otitis media, upper respiratory tract infections, bronchitis, pneumonia, phlebitis, and sepsis. Viral enteritis may occasionally complicate myocarditis.

2. Thrush: Children with prolonged illness or pre-existing malnutrition are prone to thrush, especially after long-term use of broad-spectrum antibiotics. If antibiotics are discontinued when deficient, fungi may invade the intestines or even cause systemic fungal disease.

3. Toxic hepatitis: Jaundice may occur during the course of diarrhea, particularly in children with pre-existing malnutrition. It may be caused by enteritis induced by large intestine bacilli, complicated by large intestine bacilli sepsis, leading to toxic hepatitis. After diarrhea, the condition worsens rapidly, and death may occur soon after jaundice appears. However, early detection and timely injection of polymyxin, ampicillin, or carbenicillin can often lead to a cure.

4. Malnutrition and vitamin deficiencies: Prolonged diarrhea, repeated fasting, or long-term caloric deficiency can easily lead to malnutrition, anemia, and vitamin A deficiency. Chronic diarrhea impairs liver function, reduces vitamin K absorption, and decreases prothrombin levels, resulting in bleeding.

5. Others: Severe dehydration may complicate acute renal failure. Other complications include toxic intestinal paralysis, intestinal hemorrhage, intestinal perforation, intussusception, and gastric dilation. Improper fluid therapy may also cause acute heart failure, hypernatremia or hyponatremia, or hyperkalemia. Poor nursing care for infants with vomiting around the clock may lead to suffocation.

bubble_chart Differentiation

1. Bacillary dysentery Infant dysentery often presents atypically. There is usually no pus or blood in the stool, and the clinical manifestations resemble general diarrhea, making it difficult to differentiate. Attention should be paid to the epidemic situation, as a contact history can often be elicited. Before defecation, the infant often cries, indicating tenesmus. Careful observation may reveal frequent bowel movements with small amounts each time, sometimes with watery stools mixed with pus and blood. Microscopic examination shows numerous pus cells, red blood cells, and phagocytes. In contrast, large intestine bacillary enteritis produces larger stool volumes each time, with some exceeding 20ml per bowel movement. Mucus is commonly seen in the stool, but thick pus is rare, and there may be occasional few white blood cells and red blood cells. Culture is necessary for differentiation.

2. Infant hemorrhagic enteritis The onset is indistinguishable from large intestine bacillary enteritis, but diarrhea persists and the condition worsens despite treatment, with significant abdominal distension and fullness, high fever, and frequent vomiting. In severe cases, coffee bean-like vomitus may occur. Early stools are watery with a negative occult blood test, later developing into typical dark red, jam-like stools. Severe dehydration may lead to early shock. In cases of severe toxicity, unconsciousness and convulsions may occur.

3. "Physiological diarrhea" Children with an exudative constitution may start passing yellowish-green loose stools shortly after birth, with frequent bowel movements but no vomiting. Appetite remains good, and weight gain is normal. Stools naturally return to normal after complementary foods are introduced.