[Normal Digestive Tract Phenomena

Gastrointestinal function varies with maturity; what is a physiologic event in a newborn

or infant might be a pathologic symptom at an older age. A fetus can swallow amniotic fluid
as early as 12 wk gestation, but nutritive sucking in neonates 1st develops at about 34 wk
gestation. The coordinated oral and pharyngeal movements necessary for swallowing solids
develop within the 1st few months of life. Before this time, the tongue thrust is upward and
outward to express milk from the nipple, instead of a backward motion, which propels solids
toward the esophageal inlet. By 1 mo of age, infants appear to show preferences for sweet
and salty foods. Infants' interest in solids increases at about 4 mo of age. The
recommendation to begin solids at 6 mo of age is based on nutritional and cultural concepts
rather than maturation of the swallowing process (see Chapter 42 ). Infants swallow air
during feeding and burping is encouraged to prevent gaseous distention of the stomach.
Jaundice is common in neonates, especially among premature infants, and usually
results from the inability of an immature liver to conjugate bilirubin, leading to an elevated
indirect component (see Chapter 102.3 ). 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. An elevated direct bilirubin is not normal and suggests liver disease,
although in infants it may be a result of extrahepatic infection (urinary tract infection) or
pooling of blood with an excessive load of bilirubin being released into the circulation
(intracranial hemorrhage). The direct bilirubin fraction should account for no more than 15
20% of the total serum bilirubin. Elevations in direct bilirubin levels can following indirect
hyperbilirubinemia as the liver converts excessive indirect to direct bilirubin and the ratelimiting step in bilirubin excretion shifts from the glucuronidation of bilirubin to excretion of
direct bilirubin into the bile canaliculus. 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.
Sumber : From Kliegman RM, Greenbaum LA, Lye PS (eds): Practical Strategies in

Pediatric Diagnosis and Therapy, 2nd ed. Philadelphia, Elsevier, 2004,

Complications of dierrhea
Complications may result from diarrhea of any etiology. Fluid loss with consequent
dehydration, electrolyte loss (Na, K, Mg, Cl), and even vascular collapse sometimes occur.
Collapse can develop rapidly in patients who have severe diarrhea (eg, patients with cholera)
or are very young, very old, or debilitated. HCO 3 loss can cause metabolic acidosis.
Hypokalemia can occur when patients have severe or chronic diarrhea or if the stool contains
excess mucus. Hypomagnesemia after prolonged diarrhea can cause tetany.
Sumber :

TABLE 303-4 -- Complications of Vomiting

COMPLICATION PATHOPHYSIOLOGY

HISTORY, PHYSICAL
EXAMINATION, AND
LABORATORY STUDIES

Metabolic

Fluid loss in emesis

Dehydration

HCl loss in emesis

Alkalosis;hypochloremia

Na, K loss in emesis

Hyponatremia;hypokalemia

Alkalosis
Na into cells
HCO3 loss in urine

Urine pH 78

Na and K loss in urine

Urine Na , K

Hypochloremia Cl conserved Urine Cl

by kidneys
Nutritional

Emesis of calories and nutrients Malnutrition;failure to thrive

Anorexia for calories and
nutrients

Mallory-Weiss tear Retching tear at lesser curve Forceful emesis hematemesis

of gastroesophageal junction
Esophagitis

Chronic vomiting esophageal Heartburn;hemoccult + stool

acid exposure

Aspiration

Aspiration of vomitus,
especially in context of
obtundation

Shock

Severe fluid loss in emesis or in Dehydration (accompanying diarrhea

accompanying diarrhea
can explain acidosis?)
Severe blood loss in
hematemesis

Pneumonia;neurologic dysfunction

Blood volume depletion

From Kliegman RM, Greenbaum LA, Lye PS (eds): Practical Strategies in Pediatric
Diagnosis and Therapy, 2nd ed. Philadelphia, Elsevier, 2004, p 318.
Cl, chloride; HCl, hydrogen chloride; HCO3, bicarbonate; K, potassium; Na, sodium.

Normal giving MPASI infant

The dramatic growth of infants during the 1st yr of life (a 3-fold increase in weight; a
50% increase in length) and continued growth, albeit at lower rates, from 1 yr of age through
adolescence impose unique nutritional needs.

Reference intakes of most nutrients have been established, and these appear to support
normal growth of the infant and young child. The recommendations of the Food and
Nutrition Board, National Academy of Sciences, for infants, children, and adolescents are
summarized in Tables 41-1 to 41-3 [1] [2] [3].
TABLE 41-1 -- Dietary Reference Intakes (DRIs): Recommended Intakes for
Individuals, Macronutrients (Food and Nutrition Board, Institute of Medicine, National
Academies)[*]
LIFE
STAG
TOTA
E
TOTAL
L
FAT LINOLEI LINOLENI
GROU WATER[ CARBOHYDRA FIBER (g/day C ACID C
ACID PROTEI
]
P
(L/day) TE (g/day)
(g/day) )
(g/day)
(g/day)
N (g/day)
INFANTS
06
mo

0.7[*]

60[*]

ND

31[*]

4.4[*]

0.5[*]

9.1[*]

712
mo

0.8[*]

95[*]

ND

30[*]

4.6[*]

0.5[*]

11.0

13 yr 1.3[*]

130

19[*]

ND

7[*]

0.7[*]

13

48 yr 1.7[*]

130

25[*]

ND

10[*]

0.9[*]

19

2.4[*]

130

31[*]

ND

12[*]

1.2[*]

34

1418 3.3[*]
yr

130

38[*]

ND

16[*]

1.6[*]

52

1930 3.7[*]
yr

130

38[*]

ND

17[*]

1.6[*]

56

2.1[*]

130

26[*]

ND

10[*]

1.0[*]

34

1418 2.3[*]
yr

130

26[*]

ND[*] 11[*]

1.1[*]

46

1930 2.7[*]
yr

130

25[*]

ND

12[*]

1.1[*]

46

175

28[*]

ND

13[*]

1.4[*]

71

CHILDREN

MALES
913
yr

FEMALES
913
yr

PREGNANCY
1418 3.0[*]
yr

LIFE
STAG
TOTA
E
TOTAL
L
FAT LINOLEI LINOLENI
GROU WATER[ CARBOHYDRA FIBER (g/day C ACID C
ACID PROTEI
]
P
(L/day) TE (g/day)
(g/day) )
(g/day)
(g/day)
N (g/day)
1930 3.0[*]
yr

175

28[*]

ND

13[*]

1.4[*]

71

1418 3.8[*]
yr

210

29[*]

ND

13[*]

1.3[*]

71

1930 3.8[*]
yr

210

29[*]

ND

13[*]

1.3[*]

71

LACTATION

Based on 0.8 g/kg body weight for the reference body weight.

ND, not determined.

TABLE 41-2 -- Dietary Reference Intakes (DRIs): Recommended Intakes for
Individuals, Vitamins (Food and Nutrition Board, Institute of Medicine, National
Academies)[*]
VIT
VIT VIT VIT AM
LIFE AM AM AMI IN
STAG IN A IN N D E
E
(g/ C
(g/d (mg/
GRO day) (mg/ ay)[] day)
[]
[]
UP
day) []

VIT
AM
IN
K
(g/
day)

THI
AM
IN
(mg/
day)

RIBO
FLAV
IN
(mg/d
ay)

NIA
CIN
(mg/
day)
[]

VIT
AM
IN
B6
(mg/
day)

FO
LA
TE
(g/
day)
[#]

VIT
AM
IN
B12
(g/
day)

PANT
OTHE
NIC
ACID
(mg/da
y)

BI
OT
IN
(g
/da
y)

CHO
LINE
[**]

(mg/d
ay)

INFA
NTS
06
mo

400[ 40[*] 5[*]

4[*]

*]

2.0[* 0.2[* 0.3[*]

]

712 500[ 50[*] 5[*]

*]
mo

5[*]

0.1[* 65[*] 0.4[* 1.7[*]

]

2.5[* 0.3[* 0.4[*]

]

2[*]

4[*]

0.3[* 80[*] 0.5[* 1.8[*]

]

5[*] 125[*]

6[*] 150[*]

CHIL
DRE
N
13
yr

300 15

5[*]

30[*] 0.5

0.5

0.5

150 0.9

2[*]

8[*] 200[*]

48
yr

400 25

5[*]

55[*] 0.6

0.6

0.6

200 1.2

3[*]

12[* 250[*]

MAL
ES

VIT VIT
LIFE AM AM
STAG IN A IN
E
(g/ C
GRO day) (mg/
[]
UP
day)

VIT
VIT AM
AMI IN
ND E
(g/d (mg/
ay)[] day)
[]

[]

913 600 45
yr

5[*]

11

14
18 yr

900 75

5[*]

19
30 yr

900 90

VIT
AM
IN
K
(g/
day)

THI
AM
IN
(mg/
day)

60[*] 0.9

RIBO
FLAV
IN
(mg/d
ay)

NIA
CIN
(mg/
day)

0.9

12

[]

VIT
AM
IN
B6
(mg/
day)

FO
LA
TE
(g/
day)

1.0

300 1.8

[#]

VIT
AM
IN
B12
(g/
day)

PANT
OTHE
NIC
ACID
(mg/da
y)

BI
OT
IN
(g
/da
y)

4[*]

20[* 375[*]

CHO
LINE
[**]

(mg/d
ay)

15

75[*] 1.2

1.3

16

1.3

400 2.4

5[*]

25[* 550[*]
]

5[*]

15

120[ 1.2

1.3

16

1.3

400 2.4

5[*]

*]

30[* 550[*]
]

FEM
ALES
913 600 45
yr

5[*]

14
18 yr

700 65

5[*]

19
30 yr

700 75

11

60[*] 0.9

0.9

12

1.0

300 1.8

4[*]

20[* 375[*]
]

15

75[*] 1.0

1.0

14

1.2

400 2.4

5[*]

25[* 400[*]
]

5[*]

15

90[*] 1.1

1.1

14

1.3

400 2.4

5[*]

30[* 425[*]
]

PRE
GNA
NCY
14
18 yr

750 80

19
30 yr

770 85

5[*]

15

75[*] 1.4

1.4

18

1.9

600 2.6

6[*]

30[* 450[*]
]

5[*]

15

90[*] 1.4

1.4

18

1.9

600 2.6

6[*]

30[* 450[*]
]

LAC
TATI
ON
14
18 yr

1,20 115 5[*]

0

19

19
30 yr

1,30 120 5[*]

0

19

75[*] 1.4

1.6

17

2.0

500 2.8

7[*]

35[* 550[*]
]

90[*] 1.4

1.6

17

2.0

500 2.8

7[*]

35[* 550[*]
]

TABLE 41-3 -- Dietary Reference Intakes (DRIs): Recommended Intakes for

Individuals, Elements (Food and Nutrition Board, Institute of Medicine, National
Academies)[*]

LI
FE
ST
AG CA CHR
E LCI OMI
GR UM UM
OU (mg/ (g/d
P day) ay)

CO
PP FLU
ER ORI
(g/ DE
day (mg/
)
day)

IO
DI
NE
(g
/da
y)

IR
ON
(m
g/d
ay)

MAG MAN MOL

NESI GAN YBDE
UM ESE NUM
(mg/d (mg/d (g/da
ay) ay) y)

PHO
SPH
ORU
S
(mg/d
ay)

SEL
ENI
UM
(g/
day)

ZI
NC
(m
g/d
ay)

POT
ASSI
UM
(g/da
y)

SO CHL
DI ORI
UM DE
(g/d (g/da
ay) y)

INFANTS
0 210[ 0.2[*] 200 0.01[ 11 0.2 30[*]
[*]
*]
6 *]
0[*] 7[*]
mo

0.003 2[*]

7 270[ 5.5[*] 220 0.5[*] 13 11 75[*]

[*]
12 *]
0[*]
mo

0.6[*] 3[*]

275[*] 20[*] 3

0.7[*] 0.3 0.57[

7[*] *]

1.2[*] 17

460

3.0[*] 1.0[ 1.5[*]

[*]

100[*] 15[*] 2[*] 0.4[*] 0.1 0.18[

2[*] *]

CHILDREN
1 500[ 11[*] 340 0.7[*] 90 7
3 *]
yr
4 800[ 15[*] 440 1[*]
8 *]
yr

80

20

*]

90 10 130

1.5[*] 22

500

30

3.8[*] 1.2[ 1.9[*]

*]

MALES
9 1,30 25[*] 700 2[*]
13 0[*]
yr

12 8
0

14 1,30 35[*] 890 3[*]

0[*]
18
yr

15 11 410
0

2.2[*] 43

19 1,00 35[*] 900 4[*]

0[*]
30
yr

15 8
0

400

2.3[*] 45

9 1,30 21[*] 700 2[*]

13 0[*]
yr

12 8
0

240

14 1,30 24[*] 890 3[*]

0[*]
18
yr

15 15 360
0

240

1.9[*] 34

1,250 40

4.5[*] 1.5[ 2.3[*]

*]

1,250 55

11 4.7[*] 1.5[ 2.3[*]

*]

700

55

11 4.7[*] 1.5[ 2.3[*]

*]

FEMALES
1.6[*] 34

1,250 40

4.5[*] 1.5[ 2.3[*]

*]

1.6[*] 43

1,250 55

4.7[*] 1.5[ 2.3[*]

*]

LI
FE
ST
AG CA CHR
E LCI OMI
GR UM UM
OU (mg/ (g/d
P day) ay)

CO
PP FLU
ER ORI
(g/ DE
day (mg/
)
day)

19 1,00 25[*] 900 3[*]

0[*]
30
yr

IO
DI
NE
(g
/da
y)

IR
ON
(m
g/d
ay)

MAG MAN MOL

NESI GAN YBDE
UM ESE NUM
(mg/d (mg/d (g/da
ay) ay) y)

15 18 310
0

1.8[*] 45

14 1,30 29[*] 1,0 3[*]

0[*]
00
18
yr

22 27 400
0

2.0[*] 50

19 1,00 30[*] 1,0 3[*]

0[*]
00
30
yr

22 27 350
0

2.0[*] 50

14 1,30 44[*] 1,3 3[*]

0[*]
00
18
yr

29 10 360
0

2.6[*] 50

19 1,00 45[*] 1,3 3[*]

0[*]
00
30
yr

29 9
0

2.6[*] 50

PHO
SPH
ORU
S
(mg/d
ay)

SEL
ENI
UM
(g/
day)

ZI
NC
(m
g/d
ay)

POT
ASSI
UM
(g/da
y)

700

55

4.7[*] 1.5[ 2.3[*]

SO CHL
DI ORI
UM DE
(g/d (g/da
ay) y)
*]

PREGNANCY
1,250 60

12 4.7[*] 1.5[ 2.3[*]

*]

700

60

11 4.7[*] 1.5[ 2.3[*]

*]

LACTATION

310

1,250 70

13 5.1[*] 1.5[ 2.3[*]

*]

700

70

12 5.1[*] 1.5[ 2.3[*]

*]

SOURCES: Dietary Reference Intakes for Calcium, Phosphorous, Magnesium, Vitamin D,

and Fluoride (1977); Dietary Reference Intakes for Thiamin, Riboflavin, Niacin, Vitamin B6,
Folate, Vitamin B12, Pantothenic Acid, Biotin, and Choline (1988); Dietary Reference
Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); Dietary Reference
Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron,
Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc (2001);and Dietary
Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate (2004). These reports
may be accessed at
Pathophysiology E.coli
In contrast to the essential and beneficial role of most E coli isolates in the human intestine,
pathogenic E coli are responsible for a broad spectrum of human disease.E coli has emerged
as an important cause of diarrheal illness, with diverse phenotypes and pathogenic

mechanisms. Hemolytic-uremic syndrome (HUS) is a potentially devastating consequence of

enteric infection with specific E coli strains.E coli is also a commonly identified cause
of urinary tract infections (UTIs), as well as neonatal sepsis and meningitis.
Uropathogenic E coli (UPEC) has the ability to colonize the uroepithelium by means of
surface fimbriae. Although only partially understood, UPEC has been suggested to cause
either direct cellular damage or direct invasion of the renal epithelial cells.[1]
Five pathotypes have of diarrheagenic E coli have been recognized; each pathotype has a
distinct pathogenesis. The pathotypes are as follows:

Enterotoxigenic E coli (ETEC)

Enterohemorrhagic E coli (EHEC)

Enteropathogenic E coli (EPEC)

Enteroinvasive E coli (EIEC)

Enteroaggregative E coli (EAEC)

ETEC adheres to the small bowel mucosa by means of several different fimbrial

colonization factor antigens (CFAs). Once colonization is achieved, one or both of the
enterotoxins are released (ie, heat labile toxin [LT] and heat stable toxin [ST]). These toxins
draw fluid and electrolytes from the small bowel mucosa. ST is reportedly the more virulent
of the toxins.[1] LTs are closely related in structure and function to the enterotoxin expressed
by Vibrio cholerae. Immunity develops to ETEC surface antigens, confining most disease to
immunologically nave travelers and weaning infants.
EHEC, also known as Shiga-toxin producing E coli (STEC), induces an attaching and
effacing (AE) lesion in the large bowel. Once established in the colon, EHEC releases one or
more toxins known as Shiga-like toxin (Stx). Stx is related to the Shiga toxin of Shigella
dysenteriae and is cytotoxic to the vascular endothelium. The systemic circulation of Stx
accounts for the potential development of HUS but is not required for EHEC hemorrhagic
colitis to occur. E coli O157:H7 is the most virulent of the EHEC.[2, 1]
HUS consists of the triad of microangiopathic hemolytic anemia, thrombocytopenia, and
renal insufficiency. HUS typically develops in the second week of illness (range, 2-14 d),
often after the diarrhea has resolved. Patients present with pallor, weakness, irritability, and
oliguria or anuria.
EPEC also produce AE lesions; however, it does so in the absence of Shiga toxin
production. The pathogenesis includes colonization of the small intestine, followed by the
formation of AE lesions and a subsequent net secretory state.[2, 1]

The pathogenesis of EIEC mimics that of the Shigella species. The EIEC invades the
large bowel epithelial cells, producing secretogenic enterotoxins and subsequent colonic
epithelial cell death. These enterotoxins are typically lactose nonfermenting and are
responsible for the local colonic inflammatory response. [2, 1]Invasiveness derives from a
virulence plasmid closely related to that possessed byShigella species.
EAEC adheres to the small and large bowel by means of aggregative adherence fimbriae
(AAFs), and colonization ensues. This colonization produces enterotoxins and cytotoxins,
which, in turn, damages the intestinal mucosa.[2, 1]
Systemic infections caused by E coli are frequently seen in neonates either by means of
vertical or horizontal transmission. The characteristic serotype of this pathogenic E
coli displays the K1 antigen, which is responsible for 40% of the cases of bacteremia and
80% of the cases of meningitis caused by E coli.[2] The virulent activity of the K1 antigen
reduces the ability of the host to develop an antibody specific response and to activate the
alternative complement system. In addition, S fimbriae have been associated with many of
the E coli of patients with CNS infections. S fimbriae enhance the ability of E coli to adhere
to vascular epithelium as well as the spread of the bacterium within the CNS.[1]
1. Nataro JP. Escherichia coli. Long S, Pickering LK, Prober CG (Editors). Principles
and Practice of Pediatric Infectious Diseases. 3rd Edition. Orlando, Fl: Churchill
Livingstone; 2008.
2. Escherichia coli diarrhea. Pickering LK, Baker CJ, Overturf GD, Prober CG
(Editors). American Academy of Pediatricians Report of the Committee on Infectious
Diseases. Red Book. 2008. 291-6.