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Digestive system in children
Normal development, structure, and
function of digestive system
Major symptoms and signs of digestive
tract disorders in children
Normal digestive tract
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
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:
Digestion and absorption
85% of the gastric mucosa is lined by oxyntic
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
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
Carbohydrate, protein, and fat are normally
absorbed by the upper half of the small
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
Normal transport of nutrients and
electrolytes across the GI tract
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
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
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.
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
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
Toddler’s diarrhea
Intermittent loose stools occurs
commonly between 1 and 3 yr.
Drink excessive carbohydrate-containing
beverages and eat snacks throughout the
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
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
Common in neonates, especially in premature
Results form the inability of an immature liver to
conjugate bilirubin, leading to an elevated indirect
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
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
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.
Hunger and satiety centers are located in the
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 caused by obstruction of the GI is
probably mediated by intestinal visceral
afferent nerves stimulating the vomiting
If obstruction occurs below the second part of
the duodenum, vomiting is usually bile
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.
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
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
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
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
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
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.