Digestive system in children 浙江大学医学院附属儿童医院 江米足 Contents Normal development, structure, and function of digestive system Major symptoms and signs of digestive tract disorders in children Normal digestive tract phenomena Gastrointestinal function varies with maturity 12 wk gestation: A fetus can swallow amniotic fluid 34 wk gestation: Nutritive sucking in neonates first the first few months of infants: coordinated oral and pharyngeal movements for swallowing solids 1 mo: show preferences for sweet and salty foods. 4 mo: Infants’ interest in solids increases. The current recommendation to begin solids at 6 mo of age is based on nutritional concepts rather than maturation of the swallowing process Esophagus Hollow muscular tube, separated from the pharynx above and the stomach below by tonically closed sphincters. To convey ingested material from the mouth to the stomach No active role in digestion lacking digestive glands and enzymes The length is 2.5 mm in 11 wk embryo, is 810 cm at birth, and doubles during the first 23 yr, reaching 25 cm in an adult. Stomach and intestines The primitive gut is recognizable by the 4th wk of gestation and is composed of the foregut, midgut, and hindgut. Foregut: esophagus, stomach, and duodenum Midgut: small bowel and large bowel to the mid-transverse colon Hindgut: the remainder of the colon and upper anal canal The structure of digestive tract The wall of the stomach, small bowel, and colon consists of four layers: mucosa submucosa muscularis serosa Digestion and absorption 85% of the gastric mucosa is lined by oxyntic glands contain cells that secrete hydrochloric acid, pepsinogen, intrinsic factor, and mucous endocrine cells that secrete peptides. Pepsinogen is a precursor of the proteolytic enzyme pepsin, and intrinsic factor is required for the absorption of vitamin B12. Pyloric glands are located in the antrum and contain gastrin-secreting cells. Acid secretion Acid production and gastrin levels are inversely related to each other except in pathologic secretory states. Acid secretion is low at birth but increases dramatically by 24 hr. Acid and pepsin secretion peak during the first 10 days and decrease from 10-30 days after birth. Intrinsic factor secretion rises slowly during the first 2 wk Small intestine The small bowel is approximately 270 cm in length at birth in a term neonate and grows to an adult length of 450-550 cm by 4 yr. The mucosa of the small intestine is composed of villi, which are finger-like projections of the mucosa into the bowel lumen that significantly expand the absorptive surface area. The mucosal surface is further expanded by a brush border containing digestive enzymes and transport mechanisms for monosaccharides, amino acids, dipeptides and tripeptides, and fats. The cells of the villi originate in adjacent crypts and become functional as they migrate from the crypt up to the villus. The small bowel mucosa is completely renewed in 4-5 days, providing a mechanism for rapid repair after injury, but in young infants or malnourished children the process may be delayed. Crypt cells also secrete fluid and electrolytes. Small intestine The villi are present by 8 wk gestation in the duodenum and by 11 wk in the ileum. Disaccharidase activities are measurable at 12 wk, but lactase activity does not reach maximal levels until 36 wk. Mechanisms to digest and absorb protein are in place by the 20th wk of gestation including pancreatic enzymes and mucosal mechanisms to transport amino acids and dipeptides and tripeptides. Carbohydrate, protein, and fat are normally absorbed by the upper half of the small intestine The distal segments represent a vast reserve of absorptive capacity. Most of the sodium, potassium, chloride, and water are absorbed in the small bowel. Bile salts and vitamin B12 are selectively absorbed in the distal ileum, and iron is absorbed in the duodenum and proximal jejunum Normal transport of nutrients and electrolytes across the GI tract Jejunum Ileum Colon The glucose-sodium cotransporter, requires the presence of a sodium gradient across the brush border membrane (Na+- K+ATPase). The electroneutral NaClcoupled pathway that involves the double exchange mechanism by the Na+-H+ exchanger (NHE) and the Cl-HCO3- exchanger located at the apical membrane. The number, color, and consistency of stools Vary greatly in the same infant and between infants of similar age. The earliest stools after birth consist of meconium, a dark, viscous material that is normally passed within the first 48 hr of life. With the onset of feeding, meconium is replaced by green-brown transition stools, often containing curds, and by yellow-brown milk stools after 4-5 days. The color of stools Little significance except for the presence of blood or absence of bilirubin products (white-gray rather than yellow-brown) The presence of vegetable matter, such as peas or corn, in the stool of an older infant or toddler ingesting solids is normal and suggests poor chewing and not malabsorption Stool frequency Extremely variable in normal infants and may vary from none to seven per day. Breast-fed infants may have frequent small, loose stools early (transition stools) and then after 2-3 wk may have very infrequent soft stools. It is possible for a nursing infant not to pass any stool for 1-2wk and then to have a normal soft bowel movement. The characteristic of digestive tract symptoms in children A symptom that might be abnormal at an older age, such as regurgitation, is normal in an infant. Regurgitation The result of GER in the first year of life Effortless regurgitation may dribble out of an infant’s mouth but also may be forceful Volumes of emesis are commonly about 15-30ml, but may occasionally be larger Remains happy, although possibly hungry, after an episode of regurgitation Episodes may occur from less than one to several times per day. Resolves in 80% of infants by 6 mo and in 90% by 12 mo Complication: failure to thrive, pulmonary disease, and esophagitis Protuberant abdomen Often noted in infants and toddlers, especially after large feedings. Weak abdominal musculature, relatively large abdominal organs, and lordotic stance. In the first year of life, it is common to palpate the liver 1 to 2 cm below the right costal margin. The normal liver is soft in consistency and percusses to normal size for age A soft spleen tip may also be palpable as a normal findings Toddler’s diarrhea Intermittent loose stools occurs commonly between 1 and 3 yr. Drink excessive carbohydrate-containing beverages and eat snacks throughout the day Stools typically occur during the day and not overnight. Blood loss Blood loss from the GI tract is never normal, but swallowed blood may be misinterpreted as GI bleeding Maternal blood may be ingested at the time of birth or later by a nursing infant if there is bleeding near the mother’s nipple Nasal or oropharyngeal bleeding is occasionally mistaken for GI bleeding Red dyes in foods or drinks may turn the stool red but do not produce a positive test result for occult blood Jaundice Common in neonates, especially in premature infants, Results form the inability of an immature liver to conjugate bilirubin, leading to an elevated indirect component. Persistent elevation of indirect bilirubin levels in nursing infants may be a result of breast milk jaundice, which is usually a benign entity in full-term infants Elevated direct bilirubin is never normal and suggests liver disease, although in infants with extrahepatic infection Indirect hyperbilirubinemia, which occurs commonly in normal newborns, tends to tint the sclerae and skin golden yellow, whereas direct hyperbilirubinemia produces a greenish yellow hue. Major symptoms and signs of digestive tract disorders Dysphagia Regurgitation Anorexia Vomiting Diarrhea Constipation Abdominal pain GI hemorrhage Abdominal distention and abdominal masses Dysphagia (difficulty swallowing) Structural defect: Cause a fixed impediment to the food bolus arise from narrowing within the esophagus, such as a stricture, web, or tumor, vascular ring Cause more problems swallowing solids than liquids. Motility disorder Oropharynx or esophagus motility abnormalities Swallowing is a complex process When dysphagia is associated with a delay in passage through the esophagus, a child may be able to point to the level of the chest where the delay occurs. Anorexia Hunger and satiety centers are located in the hypothalamus Satiety is stimulated by distention of the stomach or upper small bowel, transmitted by sensory afferents, which are especially dense in the upper gut. Chemoreceptors in the intestine, influenced by the assimilation of nutrients, also affect afferent flow to the appetite centers. Impulses reach the hypothalamus from higher centers, possibly influenced by pain or the emotional disturbance of an intestinal disease. Other regulatory factors include hormones, leptin, and plasma glucose, which in turn reflect intestinal function. Vomiting Vomiting caused by obstruction of the GI is probably mediated by intestinal visceral afferent nerves stimulating the vomiting center. If obstruction occurs below the second part of the duodenum, vomiting is usually bile stained. With repeated vomiting in the absence of obstruction, however, duodenal contents are refluxed into the stomach and the emesis may become bile stained. Nonobstructive lesions of the digestive tract can also cause vomiting Most diseases of the upper bowel, pancreas, liver, or biliary tree are capable of provoking emesis. CNS or metabolic derangements may lead to severe, persistent emesis. Constipation Relative and depends on stool consistency, stool frequency, and difficulty in passing the stool A normal child may have a soft stool only every 2nd or 3rd day without difficulty A hard stool passed with difficulty every 3rd day should be treated as constipation A nursing infant may have very infrequent stools of normal consistency True constipation in the neonatal period is most likely secondary to hirschsprung disease, intestinal pseudoobsturction, or hypothyroidism Abdominal pain Individual children differ greatly in their perception of and tolerance for abdominal pain. This is one reason the evaluation of chronic abdominal pain is difficult. A child with functional abdominal pain may be as uncomfortable as one with an organic cause. Normal growth and physical examination are reassuring in a child who is suspected of having functional pain. Painful stimuli originating in the liver, pancreas, biliary tree, stomach, or upper bowel are felt in the epigastrium; Pain from the distal small bowel, cecum, appendix, or proximal colon is felt at the umbilicus; Pain from the distal large bowel, urinary tract, or pelvic organ is usually suprapubic. In the gut, the usual stimulus provoking pain is tension or stretching. Inflammatory lesions may lower the pain threshold, but the mechanisms producing pain of inflammation are not clear. Tissue metabolites released near nerve endings probably account for the pain caused by ischemia. Psychologic factors are particularly important GI hemorrhage Bleeding may occur anywhere along the GI tract and identification of the site may be challenging Small intestine, which is most difficult to study, is the least likely site of bleeding The only exception is the painless bleeding of a Meckel diverticulum. Erosive damage to the mucosa of the GI is the most common cause of bleeding, although variceal bleeding secondary to portal hypertension Vascular malformations are a rare cause in children When bleeding originates in the esophagus, stomach, or duodenum, it may cause hematemesis When exposed to gastric or intestinal juices, blood quickly darkens to resemble coffee grounds；massive bleeding is likely to be red Red or maroon blood in stools, hematochezia, signifies either a distal bleeding site or massive hemorrhage above the distal ileum. Moderate to mild bleeding from sites above the distal ileum tends to cause blackened stools of tarry consistency (melena); major hemorrhages in the duodenum or above can cause melena. Abdominal distention and abdominal masses Enlargement of the abdomen can result from diminished tone of the wall musculature or from increased content: fluid, gas, or solid. Ascites, the accumulation of fluid in the peritoneal cavity, distends the abdomen both in the flanks and anteriorly when it is large in volume. This fluid shifts with movement of the patient and conducts a percussion wave. Ascitic fluid is usually a transudate with a lowprotein concentration resulting from reduced plasma colloid osmotic pressure of hypoalbuminemia, from raise portal venous pressure, of from both. In cases of portal hypertension, the fluid leak probably occurs from lymphatics on the liver surface and from visceral peritoneal capillaries, but ascites does not usually develop until the serum albumin level falls. An abdominal organ may enlarge diffusely or be affected by a discrete mass. Such discrete masses may occur in the lumen, in the wall, or in the mesentery. In a constipated child, mobile, nontender fecal masses are often found. Anomalies, cysts, or inflammatory disease can affect the wall of the gut. Gut wall neoplasms are extremely rare in children The liver may enlarge diffusely in response to many disorders.