CHAPTER I

INTRODUCTION

Diarrhea is the passage of unusually loose or watery stools, usually at least three times in
a 24 hour period. However, it is the consistency of the stools rather than the number that is
most important. Frequent passing of formed stools is not diarrhea16.

Diarrheal episodes are classically distinguished into acute and chronic (or persistent)
based on their duration. Acute diarrhea is thus defined as an episode that has an acute onset
and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that
lasts longer than 14 days. The distinction, supported by the World Health Organization
(WHO), has implications not only for classification and epidemiological studies but also from
a practical standpoint because protracted diarrhea often has a different set of causes, poses
different problems of management, and has a different prognosis8.

In the year 2000, diarrheal diseases claimed an estimated 1.4 to 2.5 million lives, they are
among the leading causes of death in children in developing countries. Both the incidence
and the risk of mortality from diarrheal diseases are greatest among children younger than 1
year of age, and thereafter rates decline incrementally. Other direct consequences of diarrhea
in children include malnutrition, diminished growth, and impaired cognitive development in
resource-limited countries1.

During the past three decades, factors such as the widespread distribution and use of oral
rehydration solutions (ORS), improved rates of breastfeeding, improved nutrition, better
sanitation and hygiene, and increased coverage of measles immunization have contributed to
a consistent decline in the mortality rate in developing countries1.

CHAPTER II
1
 THEORY

2.1 Definition
Although the term " gastroenteritis" is commonly used synonymously with "diarrhea",
the former term is a misnomer. The term gastroenteritis implies inflammation of both the
stomach and the small intestine, whereas, in reality, gastric involvement is rarely if ever seen
in acute diarrhea (including diarrhea with an infectious origin); enteritis is also not
consistently present8. Diarrhea is the passage of unusually loose or watery stools, usually at
least three times in a 24 hour period. However, it is the consistency of the stools rather than
the number that is most important. Frequent passing of formed stools is not diarrhea 8.
Diarrhea describes loose, watery stools that occur more frequently than usual 4. Diarrhea is a
condition with increase weight of feces (>200 mg/day) which can be assosiate with
abnormally high fluid content in the stool, frequency of stool, uncomfort in perianal and urge
to passage stool with or without fecal incontinentia 13. Diarrhea is an alteration in a normal
bowel movement characterized by an increase in the water content, volume, or frequency of
stools. A decrease in consistency (i.e., soft or liquid) and an increase in frequency of bowel
movements to >3 stools per day have often been used as a definition for epidemiological
investigations2.

2.2 Epidemiology
In the year 2000, diarrheal diseases claimed an estimated 1.4 to 2.5 million lives; they
are among the leading causes of death in children in developing countries. Both the incidence
and the risk of mortality from diarrheal diseases are greatest among children younger than 1
year of age, and thereafter rates decline incrementally. Other direct consequences of diarrhea
in children include malnutrition, diminished growth, and impaired cognitive development in
resource-limited countries1.

In industrialized countries, relatively few patients die from diarrhea, but it continues to
be an important cause of morbidity and incurs substantial health-care costs (Table 2.1).

2
 2.1

Data from Indonesians health profile in 2002 showed that morbidity rate based on
province has decline from 1999 2001. In the 1999, the morbidity rate is 25,63 per 1000
persons and decline in to 22,69 per 1000 persons in 2000 and become 12,00 per 1000 persons
in 2001. Otherwhile, based on data from Indonesians health profile in 2003 that showed the
frequency of diarrhea is 92 cases with 3865 patients, 113 patients died, dan Case Fatality
Rate (CFR) 2,92%18.

During the past three decades, factors such as the widespread distribution and use of oral
rehydration solutions (ORS), improved rates of breastfeeding, improved nutrition, better
sanitation and hygiene, and increased coverage of measles immunization have contributed to
a consistent decline in the mortality rate in developing countries (Table 2).

Table 2.2 Estimates of mortality from diarrheal diseases among children in developing
countries1
Publication Year of Year of Deaths per year
estimate publication ( 1 000 000)
Rohde JE. Selective primary health care: 1976 1984 5
strategies for control of disease in the
developing world. XV. Acute diarrhea. Rev
Infect Dis 1984;6:84054.
Snyder JD, Merson MH. The magnitude of 1982 1982 4.6
the global problem of acute diarrheal disease:
a review of active surveillance data. Bull
World Health Organ 1982;60:60513.

3
Institute of Medicine. The prospects of 1986 1986 3.5
immunizing against rotavirus. In: New
vaccine development: diseases of importance
in developing countries, vol. 2. Washington,
DC: National Academy Press, 1986: D13-11-
12.
Martines J, Phillips M. Diarrheal diseases. 1990 1990 3.2
In: Jamison D, Mosley W, Measham A,
Bobadilla J, editors. Disease control priorities
in developing countries. New York: Oxford
University Press, 1993: 91116.
Bern C, Martines J, Glass RI. The magnitude 1992 1992 3.3
of the global problem of diarrheal disease: a
ten-year update. Bull World Health Organ
1992;70:70514.
World Bank. World development report: 1993 1993 2.5
investing in health. New York: World Bank,
1993.
Murray CJ, Lopez AD. Global mortality, 1997 1997 2.42.9
disability, and the contribution of risk factors.
Global Burden of Disease Study. Lancet
1997;349:143642.
Kosek M, Bern C, Guerrant RL. The global 2000 2003 2.14.7
burden of diarrheal disease, as estimated from
studies published between 1992 and 2000.
Bull World Health Organ 2003;81:197204.
Parashar U, Hummelman E, Bresee J, et al. 2000 2003 1.73.0
Global illness and deaths caused by rotavirus
disease in children. Emerg Infect Dis
2003;9:56572.
World Health Organization. Global burden of 2001 2002 1.4
disease estimates 2001. Geneva: WHO, 2002.
Murray C, Lopez A, Mathers C, et al. The
Global Burden of Disease 2000 project: aims,
methods, and data sources. Geneva: World
Health Organization, 2001.

4
World Health Organization. World health 2002 2003 1.6
report 2003: shaping the future. Geneva:
World Health Organization, 2003.

The morbidity from diarrhea has remained relatively constant during the past two
decades, with each child under 5 years of age experiencing an average of three annual
episodes. ORS and nutritional improvements probably have a greater impact on mortality
rates than the incidence of diarrhea (Fig. 2.1). Interventions such as breastfeeding and
improved sanitation are expected to affect mortality and morbidity simultaneously1.

Fig. 2.1 Inverse association between coverage rates of oral rehydration solution (ORS) use
and rates of mortality from diarrhea in various countries.

2.3 Etiology
Although infectious agents are by far the most common cause for sporadic or endemic
episodes of acute diarrhea, one should not dismiss other causes that can lead to the same
presentation8.

Causes of diarrhea with acute onset include the following:

Infections
Enteric infections (including food poisoning)

Extraintestinal infections

Drug-induced

Antibiotic-associated

Laxatives

Antacids that contain magnesium

Opiate withdrawal

Other drugs
5

Food allergies or intolerances

Cow's milk protein allergy

Soy protein allergy

Multiple food allergies

Olestra

Methylxanthines (caffeine, theobromine, theophylline)

Disorders of digestive/absorptive processes

Glucose-galactose malabsorption

Sucrase-isomaltase deficiency

Late-onset (adult-type) hypolactasia, resulting in lactose intolerance

Chemotherapy or radiation-induced enteritis

Surgical conditions

Acute appendicitis

Intussusception

Vitamin deficiencies

Niacin deficiency

Folate deficiency

Vitamin toxicity

Vitamin C

Niacin, vitamin B3

Ingestion of heavy metals or toxins (eg, copper, tin, zinc)

Ingestion of plants (eg, hyacinths, daffodils, azalea, mistletoe, Amanita species

mushrooms
Infectious causes of acute diarrhea in developed countries

Viruses

Rotavirus - 25-40% of cases

Norovirus - 10-20% of cases

Calicivirus - 1-20% of cases

Astrovirus - 4-9% of cases

Enteric-type adenovirus - 2-4% of cases

Bacteria

Campylobacter jejuni - 6-8% of cases

Salmonella - 3-7% of cases

E. Coli - 3-5% of cases
6

Shigella - 0-3% of cases

Y. enterocolitica - 1-2% of cases

C. difficile - 0-2% of cases

Vibrio parahaemolyticus - 0-1% of cases

V. cholerae - Unknown

Aeromonas hydrophila - 0-2% of cases

Parasites

Cryptosporidium - 1-3% of cases

G. lamblia - 1-3% of cases8

2.4 Classification
It is most practical to base treatment of diarrhea on the clinical type of the illness, which
can easily be determined when a child is first examined. Laboratory studies are not needed.
Four clinical types of diarrhea can be recognized, each reflecting the basic underlying
pathology and altered physiology:
1. Acute watery diarrhea (including cholera), which lasts several hours or days: the main
danger is dehydration; weight loss also occurs if feeding is not continued;
2. Acute bloody diarrhea, which is also called dysentery: the main dangers are damage of
the intestinal mucosa, sepsis and malnutrition; other complications, including
dehydration, may also occur;
3. Persistent diarrhea, which lasts 14 days or longer: the main danger is malnutrition and
serious non-intestinal infection; dehydration may also occur;
4. Diarrhea with severe malnutrition (marasmus or kwashiorkor): the main dangers are
severe systemic infection, dehydration, heart failure and vitamin and mineral deficiency16.

2.5 Physiology of stool fluid balance

Normally, 2 litres (or more) of water are ingested per day, which, added to the 7 litres of
secretions from salivery glands, stomach, bile and pancreas, totals 9 litres per day passing
into the small intestine. 7.5 litres are absorbed by the small intestine, leaving just over 1 litre
to be absorbed by the colon. This represents approximately 20% of total body water and so it
can be readily seen that minor imbalances in this system can rapidly lead to profound
dehydration. Sodium movement across the luminal border of the small intestine controls
water movement by osmosis. Na+ absorption from the lumen facilitates glucose absorption,
while K+ diffuses back into the lumen. This explains why diarrhea can lead to hypokalaemia
7
and why sodium and glucose replacement is effective in treating hypovolaemia following
diarrhea12.

Actually, the large intestine can absorb a maximum of 5 to 8 liters of fluid and
electrolytes each day. When the total quantity entering the large intestine through the
ileocecal valve or by way of large intestine secretion exceeds this amount, the excess appears
in the feces as diarrhea The feces normally are about three-fourths water and one-fourth solid
matter that itself is composed of about 30 per cent dead bacteria, 10 to 20 per cent fat, 10 to
20 per cent inorganic matter, 2 to 3 per cent protein, and 30 per cent undigested roughage
from the food and dried constituents of digestive juices, such as bile pigment and sloughed
epithelial cells. The brown color of feces is caused by stercobilin and urobilin, derivatives of
bilirubin. The odor is caused principally by products of bacterial action; these products vary
from one person to another, depending on each person's colonic bacterial flora and on the
type of food eaten. The actual odoriferous products include indole, skatole, mercaptans, and
hydrogen sulfide17.

2.6 Pathogenesis
In this case report, we will explain some of the pathogenesis based on etiology.
1. Rotavirus
Rotavirus causes patchy damage to the epithelium of the small intestine, resulting in the
blunting of the villi. There is some reduction in the activity of lactase and other
dissacharidases, resulting in reduced absorption of carbohydrates, but this is usually of no
clinical significance. The intestinal morphology and absorptive capacity return to normal
within 2-3 weeks16, 11.

8
 Fig. 2.2 pathogenesis of diare caused by rotavirus11

2. ETEC ( Enterotoxigenic E. Coli)

Two important virulent factors of ETEC are: (1) colonisation factors that allow ETEC to
adhere to enterocytes of the small bowel, and (2) enterotoxins. ETEC produce heat-labile
(LT) and/or heat stable (ST) enterotoxins that cause secretion of fluid and electrolytes,
resulting in watery diarrhea. ETEC do not destroy the brush border or inade the mucosa11.

Fig. 2.3 pathogenesis of diare caused by ETEC11

3. EIEC (Enteroinvasive E. Coli)

EIEC are similar to Shigella both biochemically and serologically. Like Shigella, EIEC
penetrate and multiply within the colonic epithelial cells16.

9
4. EHEC (Enterohaemorargic E. Coli)
EHEC produce a Shigalike toxin that may be responsible for oedema and diffuse bleeding
in the colon, as well as the haemolytic-uraemic syndrome that sometimes develops in
children16.

5. Shigella
Shigella invade and multiply within colonic epithelial cells, causing cell death and
mucosal ulcers. Shigella occasionally invade the bloodstream. The virulence factors
include: a smooth lipopolysaccharide cell-wall antigen, antigens that promote cell
invasion, and Shiga toxin which is cytotoxic, neurotoxic and perhaps also causes watery
diarrhea16.

Fig. 2.4 pathogenesis of diare caused by shigella11

6. Vibrio Cholera
V. cholerae adhere to and multiply on the mucosa of the small intestine where they
produce an enterotoxin which causes the diarrhea. Cholera toxin is closely related to the
heat-labile toxin (LT) of ETEC16.

7. Salmonella
Salmonella invade the ileal epithelium. An enterotoxin causes watery diarrhea. When
mucosal damage occurs, diarrhea may be bloody. Bacteraemia may occur and can lead to
localized infection in other tissues, such as bone and meninges16.

8. Giardia duodenalis
G. duodenalis infects the small bowel; the pathogenic mechanism is unclear. Flattening of
the intestinal epithelium is seen in severe cases. Giardia infections are foodborne,

10
 waterborne, or spread by faecal-oral route; the latter occurs particularly in children living
in crowded circumstances or attending day-care centres16.

9. Entamoeba Histolitica
E. histolytica invades the mucosa of the large intestine, where it is thought to elaborate
neurohumoral substances that cause intestinal secretion and damage, resulting in an
inflammatory type of diarrhea16.

2.7 Pathophysiology
Base on the pathophysiology, diare can be explained in four type of diarrhea.

A. Osmotic diarrhea
As stool leaves the colon, fecal osmolality is equal to the serum osmolality, ie,
approximately 290 mosm/kg. Under normal circumstances, the major osmoles are Na +,
K+, Cl, and HCO3. The stool osmolality may be estimated by multiplying the stool (Na++
K+) x 2. The osmotic gap is the difference between the measured osmolality of the stool
(or serum) and the estimated stool osmolality and is normally less than 50 mosm/kg. An
increased osmotic gap (> 125 mosm/kg) implies that the diarrhea is caused by ingestion
or malabsorption of an osmotically active substance. The most common causes are
disaccharidase deficiency (lactase deficiency), laxative abuse, and malabsorption
syndromes (current medical). Osmotic diarrheas resolve during fasting. Nonabsorbed
substances are osmoticall active in the small intestine and therefor suck water into the
lumen. (H2O secretion; B, left). In malabsorption of carbohydrates (B right) the reduced
Na+ absorption in the upper small intestine (diminished Na+ symport with glucose and
galactose) leads to reduced water absorption. The osmotic activity of the nonabsorbed
carbohydrate additionally results in water secretion. However, bacteria in the large
intestine can metabolize up to 80 g/d (divided over four meals) of nonabsorbed
carbohydrates into organic acids useful for providing energy that together with water are
absorbed in the colon (B). It is only the large amounts of marked gas produced
(flatulence) that provide evidence of carbohydrate malabsorption. However, if > 80 g/d
(i.e., > 14 of normal carbohydrate supply) is not absorbed or the intestinal bacteria are
decimated by antibiotics, diarrhea occurs3.

11
 Fig.2.5 Malabsorption of Carbohydrates3

B. Secretory Diarrhea
Secretory diarrhea (in the narrow sense) occurs when Cl secretion of the small intestinal
mucosa is activated (C). Within the mucosal cells Cl is secondarily actively enriched by
a basolateral Na+-K+-2 Cl symport carrier and is secreted via luminal Cl channels.
These open more frequently when the intracellular concentration of cAMP rises. cAMP is
formed in greater amounts in the presence of, for example, certain laxatives and bacterial
toxins (Clostridium difficile, Vibrio cholerae). Cholera toxin causes massive diarrhea (up
to 1000 mL/h) that can rapidly become life-threatening because of the loss of water, K+,
and HCO3 (hypovolemic shock, hypokalemia, nonrespiratory acidosis)3.

Fig. 2.6 Raised Cl secretions3

12
C. Malabsorption
The major causes of malabsorption are small mucosal intestinal diseases, intestinal
resections, lymphatic obstruction, small intestinal bacterial overgrowth, and pancreatic
insufficiency. Its characteristics are weight loss, osmotic diarrhea, steatorrhea, and
nutritional deficiencies. Significant diarrhea in the absence of weight loss is not likely to
be due to malabsorption (current medical). There are several reasons why diarrhea occurs
after resection of the ileum and of part of the colon. Bile salts, normally absorbed in the
ileum, cause accelerated passage through the colon (reduced water absorption). In
addition, the nonabsorbed bile salts are dehydroxylated by the bacteria in the colon. The
resulting bile salt metabolites stimulate the secretion of NaCl and H2O in the colon.
Finally, there is also a lack of active absorption of Na+ in the resected intestinal
segments3.

Fig.2.7 Partial Intestinal Resection3

D. Inflammatory/exudative diarrhea
Gut inflammation disrupts the integrity of the mucosa resulting in fluid loss into the
lumen. There may also be a secretory element because inflammatory mediators may also
stimulate secretion12.

E. Dysmotility diarrhea
Abnormal gut motility may also cause diarrhea because decreased transit times allow
insufficient time for adequate fluid absorption. This alone may cause diarrhea but is
unlikely to cause increased stool weights; however, dysmotility often coexists with other
mechanisms for diarrhea production12.

13
 Table 2.3. Mechanisms of Diarrhea and Major Specific Causes5
Mechanisms of Specific Causes
Diarrhea
Osmotic Disaccharidase deficiencies (eg, lactase deficiency)
Glucose-galactose or fructose malabsorption
Mannitol, sorbitol ingestion
Lactulose therapy
Some salts (eg, magnesium sulfate)
Some antacids (eg, Maalox)
Generalized malabsorption
Secretory Enterotoxins
Tumor products (eg, VIP, serotonin)
Laxatives
Bile acids
Fatty acids
Congenital defects
Malabsorption Pancreatic enzyme deficiency
Pancreatic enzyme inactivation (eg, by excess acid)
Defective fat solubilization (disrupted enterohepatic
circulation or defective bile formation)
Ingestion of nutrient-binding substances
Bacterial overgrowth
Loss of enterocytes (eg, radiation, infection, ischemia)
Lymphatic obstruction (eg, lymphoma, tuberculosis)
Motility disorder Diabetes mellitus
Postsurgical
Inflammatory Inflammatory bowel disease
Infection (eg, shigellosis)
exudation

2.8 Diagnosis
A child with diarrhea should be assessed for dehydration, bloody diarrhea, persistent
diarrhea, malnutrition and serious non-intestinal infections, so that an appropriate treatment
plan can be developed and implemented without delay. The information obtained when
assessing the child should be recorded on a suitable form16:

History
Ask the mother or other caretaker about (annex 1):
presence of blood in the stool;
duration of diarrhea;
number of watery stools per day;
number of episodes of vomiting;
14
 presence of fever, cough, or other important problems (e.g. convulsions, recent measles);
pre-illness feeding practices;
type and amount of fluids (including breastmilk) and food taken during the illness;
drugs or other remedies taken;
Knowledge of the characteristics of consistency, color, volume, and frequency of stool
can be helpful in determining whether the source is from the small or large bowel. Table
2.4 outlines these characteristics and demonstrates that an index of suspicion can be easily
generated for a specific set of organisms16.

Table 2.4 Stool Characteristics and Determining Their Source8

Stool Characteristics Small Bowel Large Bowel
Appearance Watery Mucoid and/or bloody
Volume Large Small
Frequency Increased Highly increased
Blood Possibly positive but never gross Commonly grossly bloody
blood
pH Possibly <5.5 >5.5
Reducing substances Possibly positive Negative
WBCs <5/high power field Commonly >10/high power
field
Serum WBCs Normal Possible leukocytosis,
bandemia
Organisms Viral Invasive bacteria
Rotavirus
Adenovirus Escherichia Coli
Calicivirus (enteroinvasive,
Astrovirus enterohemorrhagic)
Shigella species
Norovirus Salmonella species
Campylobacter species
Yersinia species
Aeromonas species

Plesiomonas species
Enterotoxigenic bacteria Toxic bacteria
E coli Clostridium difficile
Klebsiella
Clostridium perfringens
Cholera species

Vibrio species

15
 Parasites Parasites
Giardia species Entamoeba organisms

Cryptosporidium species

Physical examination
First, check for signs and symptoms of dehydration.
Look for these signs:
General condition: is the child alert; restless or irritable; lethargic or unconscious?
Are the eyes normal or sunken?
When water or ORS solution is offered to drink, is it taken normally or refused, taken
eagerly, or is the child unable to drink owing to lethargy or coma?
Feel the child to assess:
Skin turgor. When the skin over the abdomen is pinched and released, does it flatten
immediately, slowly, or very slowly (more than 2 seconds)?
Then, check for signs of other important problems. Look for these signs:
Does the child's stool contain red blood?
Is the child malnourished? Remove all upper body clothing to observe the shoulders,
arms, buttocks and thighs, for evidence of marked muscle wasting (marasmus). Look
also for oedema of the feet; if this is present with muscle wasting, the child is severely
malnourished. If possible, assess the child's weight-for-age, using a growth chart, or
weight-for-length. Alternatively, measure the mid-arm circumference.
Is the child coughing? If so, count the respiratory rate to determine whether breathing
is abnormally rapid and look for chest indrawing.
Take the child's temperature:
Fever may be caused by severe dehydration, or by a non-intestinal infection such as
malaria or pneumonia16.

Table 2.5 Diagnosis of moderate or severe malnutrition10

16
 Use the chart in Table 2.5 to determine the degree of dehydration and select the
appropriate plan to treat or prevent dehydration. The signs typical of children with no signs of
dehydration are in column A, the signs of some dehydration are in column B, and those of
severe dehydration are in column C. If two or more of the signs in column C are present, the
child has "severe dehydration". If this is not the case, but two or more signs from column B
(and C) are present, the child has "some dehydration". If this also is not the case, the child is
classified as having "no signs of dehydration"10.

Table 2.6 Assessment of diarrhea patients for dehydration16

Children with some dehydration or severe dehydration should be weighed without

clothing, as an aid in estimating their fluid requirements. If weighing is not possible, a child's
age may be used to estimate the weight16.
Treatment should never be delayed because a scale is not readily available.
A child's fluid deficit can be estimated as follows:

Diagnose other important problems16

Diagnose dysentery: if the stool contains red blood or the mother says she saw blood.
Diagnose persistent diarrhea: if diarrhea began at least 14 days ago (and any period
without diarrhea has not exceeded two days).
17
 Diagnose malnutrition: if weight-for-length or weight-for-age, using the child's weight
after rehydration, indicate moderate or severe malnutrition; or there is oedema with
muscle wasting; or the child has obvious marasmus.
Diagnose a serious non-intestinal infection: based, for example, on signs of pneumonia or
sepsis; in areas with falciparum malaria, fever or a history of recent fever is sufficient to
suspect and treat malaria. If sepsis or meningitis are suspected, the child should be
referred to the hospital. After dehydration has been treated following Plan B or C, the
patient should continue treatment at home with Plan A.

Table 2.7 Organisms and Frequency of Symptoms8

Organism Incubation Duration Vomiting Fever Abdominal
Pain
Rotavirus 1-7 d 4-8 d Yes Low No
Adenovirus 8-10 d 5-12 d Delayed Low No
Norovirus 1-2 d 2d Yes No No
Astrovirus 1-2 d 4-8 d +/- +/- No
Calicivirus 1-4 d 4-8 d Yes +/- No
Aeromonas species None 0-2 wk +/- +/- No
Campylobacter 2-4 d 5-7 d No Yes Yes
species
C difficile Variable Variable No Few Few
C perfringens Minimal 1d Mild No Yes
Enterohemorrhagic 1-8 d 3-6 d No +/- Yes
E coli
Enterotoxigenic 1-3 d 3-5 d Yes Low Yes
E coli
Plesiomonas species None 0-2 wk +/- +/- +/-
Salmonella species 0-3 d 2-7 d Yes Yes Yes
Shigella species 0-2 d 2-5 d No High Yes
Vibrio species 0-1 d 5-7 d Yes No Yes
Y enterocolitica None 1-46 d Yes Yes Yes
Giardia species 2 wk 1+ wk No No Yes
Cryptosporidium 5-21 d Months No Low Yes
species
Entamoeba species 5-7 d 1-2+ wk No Yes No
Rotavirus 1-7 d 4-8 d Yes Low No
Adenovirus 8-10 d 5-12 d Delayed Low No

18
Norovirus 1-2 d 2d Yes No No
Astrovirus 1-2 d 4-8 d +/- +/- No
Calicivirus 1-4 d 4-8 d Yes +/- No
Aeromonas species None 0-2 wk +/- +/- No
Campylobacter 2-4 d 5-7 d No Yes Yes
species
C difficile Variable Variable No Few Few
C perfringens Minimal 1d Mild No Yes
Enterohemorrhagic 1-8 d 3-6 d No +/- Yes
E coli
Enterotoxigenic 1-3 d 3-5 d Yes Low Yes
E coli
Plesiomonas species None 0-2 wk +/- +/- +/-
Salmonella species 0-3 d 2-7 d Yes Yes Yes
Shigella species 0-2 d 2-5 d No High Yes
Vibrio species 0-1 d 5-7 d Yes No Yes
Y enterocolitica None 1-46 d Yes Yes Yes
Giardia species 2 wk 1+ wk No No Yes
Cryptosporidium 5-21 d Months No Low Yes
species
Entamoeba species 5-7 d 1-2+ wk No Yes No
Laboratory Studies8
The following may be noted in patients with diarrhea:
In patients with diarrhea, a stool pH level of 5.5 or less or presence of reducing
substances indicates carbohydrate intolerance, which is usually secondary to viral illness
and transient in nature.
Enteroinvasive infections of the large bowel cause leukocytes, predominantly neutrophils,
to be shed into stool. Absence of fecal leukocytes does not eliminate the possibility of
enteroinvasive organisms. However, presence of fecal leukocytes eliminates consideration
of enterotoxigenic E coli, Vibrio species, and viruses.
Examine any exudates found in stool for leukocytes. Such exudates highly suggest colitis
(80% positive predictive value). Colitis can be infectious, allergic, or part of
inflammatory bowel disease (Crohn disease, ulcerative colitis).
Many different culture mediums are used to isolate bacteria. With stool not cultured
within 2 hours of collection, refrigerate at 4C or place in a transport medium. Although
stool cultures are useful when positive, yield is low.

19
 Always culture stool for Salmonella, Shigella, and Campylobacter organisms and Y
enterocolitica in the presence of clinical signs of colitis or if fecal leucocytes are found.
Look for C difficile in persons with episodes of diarrhea characterized by colitis and/or
blood in the stools. Remember that acute-onset diarrheal episodes associated with C
difficile may also occur without a history of antibiotic use.
Bloody diarrhea with a history of ground beef ingestion must raise suspicion for
enterohemorrhagic E coli. If E coli is found in the stool, determine if the type of E coli is
O157:H7. This type of E coli is the most common, but not only, cause of HUS.
History of raw seafood ingestion or foreign travel should prompt additional screening for
Vibrio and Plesiomonas species.
Rotavirus antigen can be identified by enzyme immunoassay and latex agglutination
assay of the stool. The false-negative rate is approximately 50%, and false-positive results
occur, particularly in the presence of blood in the stools.
Adenovirus antigens can be detected by enzyme immunoassay. Only serotypes 40 and 41
are able to induce diarrhea.
Examination of stools for ova and parasites is best for finding parasites. Perform stool
examination every 3 days or every other day.
The leukocyte count is usually not elevated in viral-mediated and toxin-mediated
diarrhea. Leukocytosis is often but not constantly observed with enteroinvasive bacteria.
Shigella organisms cause a marked bandemia with a variable total white blood cell count.
At times, a protein-losing enteropathy can be found in patients with extensive
inflammation in the course of enteroinvasive intestinal infections (eg, Salmonella species,
enteroinvasive E coli). In these circumstances, low serum albumin levels and high fecal
alpha1-antitrypsin levels can be found.

Other Tests8
Because the pathogenesis of diarrhea can be either osmolar (due to the presence of an
excess of unabsorbed substrates in the gut lumen) or secretory (due to active anion secretion
from the enterocytes), the anion gap in the stools is occasionally used to ascertain the nature
of the diarrhea. The stool anion gap is calculated according to the formula: 290 - [(Na+K) X
2]. If the value is more than 100, osmolar diarrhea can be assumed to be present. If the value
is less than 100, the diarrhea has a secretory origin.

2.9 Differential Diagnosis8

20
 Table 2.8 Differential diagnosis of diarrhea
Appendicitis Intussusception
Carcinoid Tumor Irritable Bowel Syndrome
Congenital Microvillus Atrophy Malabsorption Syndromes
Crohn Disease Meckel Diverticulum
Cystic Fibrosis Protein Intolerance
Giardiasis Shigella Infection
Glucose-galactose malabsorption Short Bowel Syndrome
Hyperthyroidism Ulcerative Colitis
Intestinal Enterokinase Deficiency
Intestinal Protozoal Diseases

2.10 Treatment
Replacement of fluid and electrolytes is the most important to treat diarrhea. If there are
no sign of dehydration, we treat the patient based on treatment of dehydration plan A (annex
2). If there are sign of some dehydration, we treat the patient based on treatment of
dehydration plan B (annex 3). If there are sign of severe dehydration, we treat the patient
based on treatment of dehydration plan C (annex 4)10, 16.

In the treatment of dehydration plan A, we must teach mother to choose the suitable
fluids for rehydration. Most fluids that a child normally takes can be used. It is helpful to
divide suitable fluids into two groups:
1. Fluids that normally contain salt, such as:
ORS solution
salted drinks (e.g. salted rice water or a salted yoghurt drink)
vegetable or chicken soup with salt.
Teaching mothers to add salt (about 3g/l) to an unsalted drink or soup during diarrhea is
also possible, but requires a sustained educational effort.
A home-made solution containing 3g/l of table salt (one level teaspoonful) and 18g/l of
common sugar (sucrose) is effective but is not generally recommended because the recipe
is often forgotten, the ingredients may not be available or too little may be given16.

2. Fluids that do not contain salt, such as:

plain water
water in which a cereal has been cooked (e.g. unsalted rice water)
unsalted soup
yoghurt drinks without salt

21
 green coconut water
weak tea (unsweetened)
unsweetened fresh fruit juice.
Unsuitable fluids, a few fluids are potentially dangerous and should be avoided during
diarrhea. Especially important are drinks sweetened with sugar, which can cause osmotic
diarrhea and hypernatraemia. Some examples are:
commercial carbonated beverages
commercial fruit juices
sweetened tea.
Other fluids to avoid are those with stimulant, diuretic or purgative effects, for example:
coffee
some medicinal teas or infusions16.

For more than 25 years WHO and UNICEF have recommended a single formulation of
glucose-based ORS to prevent or treat dehydration from diarrhea irrespective of the cause or
age group affected. This product has contributed substantially to the dramatic global
reduction in mortality from diarrheal disease during this period. Despite this success, research
to develop an improved ORS has continued. This would be an ORS that would be at least
as safe and effective as standard ORS for preventing or treating dehydration from all types of
diarrhea, but would, in addition, reduce stool output or have other important clinical benefits.
One approach has been to reduce the osmolarity of ORS solution to avoid possible adverse
effects of hypertonicity on net fluid absorption. This was done by reducing the solutions
glucose and salt (NaCl) concentrations16.

The studies that evaluated this approach showed that the efficacy of ORS solution for
treatment of children with acute non-cholera diarrhea was improved by reducing the sodium
concentration to 75 mEq/l, the glucose concentration to 75 mmol/l, and the total osmolarity to
245 mOsm/l. The need for unscheduled supplemental IV therapy in children given this
solution was reduced by 33% when compared with standard ORS (311 mOsm/l). In a
combined analysis of this study and studies with other reduced osmolarity ORS solutions
(osmolarity 210-268 mOsm/l, sodium 50-75 mEq/l) stool output was also reduced by about
20% and the incidence of vomiting by about 30%. The 245 mOsm/l solution also appeared to
be as safe and at least as effective as standard ORS for use in children with cholera10.

22
 Based on the greater efficacy of reduced osmolarity ORS solution, especially for children
with acute, non-cholera diarrhea, WHO and UNICEF now recommend that countries use and
manufacture the following formulation in place of the previously recommended standard
ORS solution10.
Table 2.9 Composition by weight and molar concentrations
of reduced (low) osmolarity ORS solution16

When prepared and given correctly, ORS solution provides sufficient water and
electrolytes to correct the deficits associated with acute diarrhea. Potassium is provided to
replace the large potassium losses associated with acute diarrhea, especially in infants, thus
preventing serious hypokalaemia. Citrate is provided to prevent or correct base deficit
acidosis. Glucose is essential because, when it is absorbed, it promotes the absorption of
sodium and water in the small intestine. This is true irrespective of the cause of the diarrhea.
Without glucose, ORS solution would be ineffective16.

In the treatment of dehydration plan B and C, we need an IV solution. A number of

solutions are available for IV solutions. Most, however, do not contain appropriate amounts
of the electrolytes required to correct the deficits associated with acute diarrhea. Early
provision of ORS solution and early resumption of feeding help to ensure adequate
electrolyte replacement. Table 2.10 shows the composition of IV fluids that can be used16.

Table 2.10. Ionic composition of intravenous infusion solutions16

23
Preferred solutions16
Ringer's Lactate Solution (also called Hartmann's Solution for Injection) is the best
commercially available solution. It supplies an adequate concentration of sodium and
sufficient lactate (which is metabolized to bicarbonate) for the correction of acidosis. The
concentration of potassium is low and there is no glucose to prevent hypoglycaemia. It
can be used in all age groups for the initial treatment of severe dehydration caused by
acute diarrhea of any etiology.
Ringer's Lactate Solution with 5% dextrose has the added advantage of providing glucose
to help prevent hypoglycaemia. If available, it is preferred to Ringer's Lactate Solution
without dextrose.

Acceptable solution16
Normal saline (0.9% NaCl; also called isotonic or physiological saline) is often available.
It does not contain a base to correct acidosis and does not replace potassium losses.

Diarrheal diseases have been the object of numerous forms of treatment, both dietetic
and pharmacologic, for centuries. However, the evidence is now clear that, in most cases, the
best option for treatment of acute-onset diarrhea is the early use of oral rehydration therapy
(ORT). Pharmacological treatment is rarely of any use, and antidiarrheal drugs are often
harmful (see table 2.11)16.
24
 Antimotility drugs (e.g. loperamide hydrochloride, diphenoxylate with atropine, tincture
of opium, camphorated tincture of opium, paregoric, codeine). These opiate or opiate like
drugs and other inhibitors of intestinal motility may reduce the frequency of stool passage in
adults. However, they do not appreciably decrease the volume of stool in young children.
Moreover, they can cause severe paralytic ileus, which can be fatal, and they may prolong
infection by delaying elimination of the causative organisms. Sedation may occur at usual
therapeutic doses and fatal central nervous system toxicity has been reported for some agents.
None of these agents should be given to infants or children with diarrhea16.

Bismuth subsalicylate decreases the number of diarrhea stools and subjective complaints
in adults with travellers' diarrhea. When given every four hours, it is reported to decrease
stool output in children with acute diarrhea by about 30%. This treatment schedule is,
however, rarely practical16.

Many products combine adsorbents, antimicrobials, antimotility drugs or other agents.

Manufacturers may claim that these formulations are appropriate for various diarrheal
diseases; however, such combinations are irrational and their cost and side effects are
substantially higher than for individual drugs. They have no place in the treatment of diarrhea
in children16.

Zinc can be given as a syrup or as dispersible tablets, whichever formulation is available

and affordable. By giving zinc as soon as diarrhea starts, the duration and severity of the
episode as well as the risk of dehydration will be reduced. By continuing zinc
supplementation for 10 to 14 days, the zinc lost during diarrhea is fully replaced and the risk
of the child having new episodes of diarrhea in the following 2 to 3 months is reduced. In
some dehydration, begin to give supplemental zinc, as in Treatment Plan A, as soon the child
is able to eat following the initial four hour rehydration period16.

Diarrhea reduces the absorption of, and increases the need for, vitamin A. In areas where
bodily stores of vitamin A are often low, young children with acute or persistent diarrhea can
rapidly develop eye lesions of vitamin A deficiency (xerophthalmia) and even become blind.
This is especially a problem when diarrhea occurs during or shortly after measles, or in
children who are already malnourished. In such areas, children with diarrhea should be
25
examined routinely for corneal clouding and conjunctival lesions (Bitot's spots). If either is
present, oral vitamin A should be given at once and again the next day: 200 000 units/dose for
age 12 months to 5 years, 100 000 units for age 6 months to 12 months, and 50 000 units for
age less than 6 months. Children without eye signs who have severe malnutrition or have had
measles within the past month should receive the same treatment. Mothers should also be
taught routinely to give their children foods rich in carotene; these include yellow or orange
fruits or vegetables, and dark green leafy vegetables. If possible, eggs, liver, or full fat milk
should also be given16.

The infant usual diet should be continued during diarrhea and increased afterwards. Food
should never be withheld and the child's usual foods should not be diluted. Breastfeeding
should always be continued. The aim is to give as much nutrient rich food as the child will
accept. Most children with watery diarrhea regain their appetite after dehydration is
corrected, whereas those with bloody diarrhea often eat poorly until the illness resolves.
These children should be encouraged to resume normal feeding as soon as possible. When
food is given, sufficient nutrients are usually absorbed to support continued growth and
weight gain. Continued feeding also speeds the recovery of normal intestinal function,
including the ability to digest and absorb various nutrients. In contrast, children whose food is
restricted or diluted lose weight, have diarrhea of longer duration, and recover intestinal
function more slowly16.

Recently, some strains of probiotics (lactic acid bacteria or mycetes thought to benefit
the host in some circumstances when ingested in adequate doses) have been found to be
effective as an adjunct when treating children with acute diarrhea. Data from well-conducted
randomized controlled trials on efficacy of probiotics in children with diarrhea are definitely
positive. They consistently show a statistically significant benefit and moderate clinical
benefit of a few, now well-identified probiotic strains (mostly Lactobacillus GG and
Saccharomyces boulardii but also Lactobacillus reuteri) in the treatment of acute watery
diarrhea (primarily rotaviral) in infants and young children in developed countries8.

Such a beneficial effect seems to result in a reduction of the duration of diarrhea of little
more than one day and seems to be exerted mostly on rotaviral diarrhea, with lack of
evidence of efficacy in invasive bacterial diarrhea. The effect is not only strain-dependent but

26
also dose-dependent, with doses of at least 5 billion/d. Shortening the duration of diarrhea by
one day may not appear to be hugely beneficial. However, in consideration of the high
morbidity of the infection, even a reduction of this order is indeed desirable because it affords
considerable savings in terms of loss of working days and direct health costs 8.

Currently, estimates suggest that rotavirus infections cause over 50,000 hospital
admissions annually in the United States alone. Furthermore, probiotics may reduce the risk
of spreading rotavirus infection by shortening diarrhea duration and volume of watery stool
output and by reducing the fecal shedding of rotavirus8.

Table 2.11. Antimicrobials used to treat spesific causes of diarrhea16

27
2.11 Preventions
Water, sanitation, and hygiene:
Safe water
Sanitation: houseflies can transfer bacterial pathogens
Hygiene: hand washing1.
Safe food:
Cooking eliminates most pathogens from foods
Exclusive breastfeeding for infants
Weaning foods are vehicles of enteric infection1.
Micronutrient supplementation: the effectiveness of this depends on the childs overall
immunologic and nutritional state; further research is needed1.

28
Vaccines
Salmonella typhi: two typhoid vaccines currently are approved for clinical use. No
available vaccine is currently suitable for distribution to children in developing countries1.
Shigella organisms: three vaccines have been shown to be immunogenic and protective in
field trials. Parenteral vaccines may be useful for travelers and the military, but are
impractical for use in developing countries. More promising is a single-dose live-
attenuated vaccine currently under development in several laboratories1.
V. cholerae: oral cholera vaccines are still being investigated, and their use is
recommended only in complex emergencies such as epidemics. Their use in endemic
areas remains controversial. In travelers diarrhea, oral cholera vaccine is only
recommended for those working in refugee or relief camps, since the risk of cholera for
the usual traveler is very low1.
ETEC vaccines: the most advanced ETEC vaccine candidate consists of a killed whole
cell formulation plus recombinant cholera toxin B subunit. No vaccines are currently
available for protection against Shiga toxinproducing E. coli infection1.
Rotavirus: in 1998, a rotavirus vaccine was licensed in the USA for routine immunization
of infants. In 1999, production was stopped after the vaccine was causally linked to
intussusception in infants. Other rotavirus vaccines are being developed, and preliminary
trials are promising. Currently, two vaccines have been approved: a live oral vaccine
(RotaTeq) made by Merck for use in children, and GSKs Rotarix1.
Measles : in baby, 1 7 % of diarrhea assosiated with measles. Babies who have diarrhea
in measles have more severe and prolonged manifestation and tendency to become
chronic because there is an destruction in intestinal epithelial. t has been estimated that
measles vaccination in 45 90 % babies ( 9 11 months) can prevent 40 60 %
measles, 0,6 3,8 % diarrhea, and 6 25 % death because of diarrhea in babies19.

2.12 Complications8
Common complications include the following:
Aeromonas caviae - Intussusception, gram-negative sepsis, hemolytic-uremic syndrome
(HUS) .
Campylobacter species -Bacteremia, meningitis, cholecystitis, urinary tract infection,
pancreatitis, Reiter syndrome (RS).
C difficile - Chronic diarrhea.

29
 C perfringens serotype C - Enteritis necroticans.
Enterohemorrhagic E coli - Hemorrhagic colitis.
Enterohemorrhagic E coli O157:H7 HUS.
Plesiomonas species Septicemia.
Salmonella species - Seizures, HUS, perforation, RS.
Vibrio species - Rapid dehydration.
Y enterocolitica - Appendicitis, perforation, intussusception, peritonitis, toxic megacolon,
cholangitis, bacteremia, RS.
Rotavirus - Isotonic dehydration, carbohydrate intolerance.
Giardia species - Chronic fat malabsorption.
Cryptosporidium species - Chronic diarrhea.
Entamoeba species - Colonic perforation, liver abscess.

Enteric fever is caused by S typhi. This syndrome has an insidious onset of malaise,
fever, abdominal pain, and bradycardia. Diarrhea and rash (rose spots) appear after 1 week of
symptoms. Bacteria may have disseminated at that time, and treatment is required to prevent
systemic complications such as hepatitis, myocarditis, cholecystitis, or GI bleeding.

2.13 Prognosis8
In developed countries, with proper management, prognosis is very good.
Death is caused predominantly by dehydration and secondary malnutrition from a
protracted course. Severe dehydration must be managed with parenteral fluids. Once
malnutrition from secondary malabsorption begins, prognosis turns grim unless the
patient is hospitalized and supplemental parenteral nutrition is started. Neonates and
young infants are at particular risk of dehydration, malnutrition, and malabsorption
syndromes.
Even though the mortality rate is low in developed countries, children can die from
complications; however, prognosis for children in countries without modern medical care
and children with comorbid conditions is more guarded.

CHAPTER 3
CASE REPORT

OBJECTIVE
30
 The objective of this paper is to report a case of gastroenteritis with mild-moderate
dehydration in a 7-months-old girl that was admitted at the infectious unit of Haji Adam
Malik General Hospital.

CASE
A, a 7-months-old girl, with the body weight and body height of 7 kg and 70 cm
respectively, was admitted to the infectious unit of Haji Adam Malik General Hospital on
February 13th 2011 at 09.15 pm with the chief complaint of diarrhea. This complaint was
experienced by the patient for about 3 days ago, the frequency is 10 times in a day, the
volume glass every time diarrhea, in feces the water is more than the dregs, mucus was
found in the feces and blood was not found.

The patient are also complained of vomiting, the frequency is 3 times in a day, the
volume 20 cc for each time vomiting, the contents of vomite is that what she ate and drank.

The patient has fever since one week ago, high temperature. Fever lowered with
antipyretic. Seizure and shiver was not found. History of recurrent fever (+) since birth.

Weight loss was found, one month ago patient's weight is 8 kg.

The last urination at 05.00 pm, the volume is an adequate, the color is brown.

Worms infection history was not found.

Patient was born spontaneously, aided by a midwife, cried immediately at birth, cyanosis
was not found.

History of maternal conditions: fever (-), hypertension (-), diabetes mellitus(-), drugs(-),
used the herbal medicine while two months pregnancy. The herbal medicine are used for
abortion. Patient is the fifth child. Her mother age is 32 years old during their give birth.

Ate history : Breast feed and cow milk was giving during 0-2 months. Two month until
now are giving breast feed, cow milk and porridge.

31
 History of immunization: BCG (+), Polio (three times), Hepatitis B (two times), DPT
(two times).

PHYSICAL EXAMINATION

Generalized Status:
Body weight (BW) : 7 kg Body height (BH) : 70 cm
BW/ BH : 82,3% (mild malnutrition)
Sensorium : Compos Mentis Body Temperature : 38,2 oC
The patient was not anemic, icteric, cyanotic, oedem or dyspnoe.

Localized Status:
Head : On eye examination was found light reflexes on both eyes, pupils were
isochoric, pale on inferior palpebrals conjunctival, sunken eyes was found.
Examination of the ear, nose and mouth cannot be found any abnormalities.
Neck : Lymph node enlargement was not found.
Chest : The chest was symmetrical fusiform.
Heart rate was 132 beats per minute, regular, no murmur was found.
Respiratory rate was 40 times per minute, regular, no ronchi was found.
Abdominal : Soft and tenderness, peristaltic was increased, the liver and spleen was
unpalpable, turgor slow to return.
Extremities : Pulse was 132 beats per minute, regular, pressure and volume were normal,
acral was warm. Blood pressure was 90/60 mmHg in both upper and lower
extremities.
Urogenital : Female. No abnormalities.

Laboratorium Findings (December 13th 2010) from Patology Clinic

Adam Malik General Hospital
Test Result Normal Value

32
 Complete Blood Count
Hemoglobin (Hb) 10.50 g% 11.1-14.4
Erytrocyes (RBC) 4.82 x 106/mm3 3.71-4.25
Leucocytes (WBC) 11.00 x 103/ mm3 6.0-17.5
Hematocrit 33.20 % 35-41
Thrombocyte (PLT) 456 x 103/ mm3 217-497
MCV 68.80 fL 82-100
MCH 21.80 pg 24-30
MCHC 31.70 g% 28-32
RDW 15.70 % 14.9-18.7

Cell Count
Neutrophil 37.80 % 37-80
Lymphocyte 47.10 % 20-40
Monocyte 12.90 % 2-8
Eosinophil 0.12 % 1-6
Basophil 2.040 % 0-1

Electrolit
Sodium 133 135-155
Potassium 3,4 3.6-5.5
Chloride 90 96-106

Carbohydrate metabolism
Ad random glucose 104.00 mg\dl < 200

Working Diagnosis : Gastroenteritis with mild-moderate dehydration.

Management :
IVFD RL 75cc/kgBW/4hours 130 cc 130 gtt/i micro

33
 Paracetamol 3 x 100 mg (pulv)
Breast feed + porridge diet of 700 ccal with 96 gram of protein

Investigation Plan :
Complete Blood Count
Electrolit
Ad random glucose
Renal function test
Liver function test

Follow Up Date 14/2/2011

S : Diarrhea (+), the frequency is 7 times in a day, in feces the water is more than the dregs
O: Consciousness: Compos Mentis T: 37.7oC, BW: 7kg, BH: 70cm, BW/ BH: 82,3%
Head : Eyes: Light reflexes(+/+), isochoric pupil, pale inferior palpebrals conjunctiva
(-/-), Ears and Nose: no abnormalities, Mouth: dry mouth (+)
Neck : Lymph node enlargement (-)
Chest : Symmetrical fusiformic, retraction (-),
HR: 126 bpm, regular, murmur (-)
RR: 38 tpm, regular, ronchi(-).
Abdomen : Soft and terderness, normal peristaltic. No liver and spleen enlargement.
Extremities : Pulse 125 bpm, regular, Pressure/Volume: adequate, warm acral
BP: 90/60 mmHg
Urogenital : Female, no abnormalitites
A: Gastroenteritis without dehydration.
P : IVFD D5% NaCl 0.225%: 30 gtt/i micro
Paracetamol 3 x100 mg (pulv)
porridge 700 ccal with 14 gram of protein

Follow Up Date 15/2/2011

S : Diarrhea (+), the frequency is 3 times in a day, the volume 20 cc everytime diarrhea ,in
feces the water is more than the dregs
O: Consciousness: Compos Mentis T: 36.8oC BW: 8kg, BH: 70cm, BW/ BH: 94.12%

34
Head : Eyes: Light reflexes(+/+), isochoric pupil, pale inferior palpebra conjunctiva
(-/-), Ears, Nose and Mouth: no abnormalities.
Neck : Lymph node enlargement (-)
Chest : Symmetrical fusiformic, retraction (-),
HR: 140 bpm, regular, murmur(-).
RR: 40 tpm, regular, ronchi(-).
Abdomen : Soft and terderness, normal peristaltic. No liver and spleen enlargement
Extremities : Pulse 140 bpm, regular, Pressure/Volume: adequate, warm acral
BP: 90/60 mmHg
Urogenital : Female, no abnormalitites
A: Gastroenteritis without dehydration
P : IVFD D5% NaCl 0.225%: 30 gtt/i micro
Paracetamol 3 x100 mg (pulv)
Zink 1x20 mg
porridge 700 ccal with 14 gram of protein

Follow Up Date 16/2/2011

S : Diarrhea (+), the frequency is 4 times in a day, the volume 20 cc every ,in feces the
water is more than the dregs
O: Consciousness: Compos Mentis T: 37.4oC BW: 8kg, BH: 70cm, BW/ BH: 94.12%
Head : Eyes: Light reflexes(+/+), isochoric pupil, pale inferior
palpebra conjunctiva (-/-), sunken eyes (-). Ears and Nose: no abnormalities,
Mouth: dry mouth (+)
Neck : Lymph node enlargement (-)
Chest : Symmetrical fusiformic, retraction (-),
HR: 132 bpm, regular, murmur(-),
RR: 52 bpm, regular, ronchi(-).
Abdomen : Soft and terderness, normal peristaltic. No liver and spleen enlargement.
Turgor fast return (+).
Extremities : Pulse 132 bpm, regular, Pressure/Volume: adequate, warm acral
BP: 100/60 mmHg
Urogenital : Female, no abnormalitites
A: Gastroenteritis without dehydration.
P : IVFD D5% NaCl 0.225% 30 gtt/i micro
35
 Paracetamol 3 x100 mg (pulv)
Zink 1x20 mg
porridge 700 ccal with 14 gram of protein
Oralit 50-100 cc/each time diarrhea.

Follow Up Date 17/2/2011

S : Diarrhea (+), the frequency is 4 times in a day, in feces the water and dregs were the same,
mucus (-), blood (-).
O: Consciousness: Compos Mentis T: 38oC BW: 8kg, BH: 70cm, BW/ BH: 94.12%
Head : Eyes: Light reflexes(+/+), isochoric pupil, pale inferior
palpebra conjunctiva (-/-), sunken eyes (-), tears (+).
Ears, Nose and Mouth: no abnormalities.
Neck : Lymph node enlargement (-)
Chest : Symmetrical fusiformic, retraction (-),
HR: 152 bpm, regular, murmur(-),
RR: 40 tpm, regular, ronchi(-).
Abdomen : Soft and terderness, normal peristaltic. No liver and spleen enlargement.
Turgor fast return.
Extremities : Pulse 152 bpm, regular, Pressure/Volume: adequate, warm acral, CRT < 3
Urogenital : Female, no abnormalitites.
A: Gastroenteritis without dehydration.
P : IVFD D5% NaCl 0.225% 30 gtt/i micro
Paracetamol 3 x100 mg (pulv)
Zink 1x20 mg
porridge 700 ccal with 14 gram of protein
Oralit 50-100 cc/each time diarrhea.
Investigational Plan: - Complete Blood Count
- Electrolit
- Ad random glucose
- Anal swab
- RFT
- LFT

Laboratorium Findings (December 17th 2010) from Patology Clinic

36
 Adam Malik General Hospital
Test Result Normal Value
Complete Blood Count
Hemoglobin (Hb) 8.80 g% 11.1-14.4
Erytrocyes (RBC) 3.97 x 106/mm3 3.71-4.25
Leucocytes (WBC) 9.21 x 103/ mm3 6.0-17.5
Hematocrit 26.30 % 35-41
Thrombocyte (PLT) 404 x 103/ mm3 217-497
MCV 56.20 fL 82-100
MCH 22.20 pg 24-30
MCHC 33.50 g% 28-32
RDW 17.40 % 14.9-18.7

Cell Count
Neutrophil 23.80 % 37-80
Lymphocyte 53.50 % 20-40
Monocyte 20.20 % 2-8
Eosinophil 1.80 % 1-6
Basophil 0.700 % 0-1

Electrolit
Sodium 137 135-155
Potassium 2.0 3.6-5.5
Chloride 108 96-106

Carbohydrate metabolism
Ad random glucose 86.80 mg\dl < 200
Liver function test
Total bilirubin 0.23 mg/dl <1
Direct bilirubin 0.09 mg/dl 0-0.2
ALP 83 U/L < 462
SGOT 24 U/L < 32
SGPT 10 U/L < 31

37
 Renal function test
Ureum 8.00 mg/dl < 50
Creatinine 0.23 mg/dl 0.17-0.42
Uric acid 1.7 mg/dl < 5.7

Anal swab
Color Yellow
Consistency Watery
Blood Negative Negative
Mucus Negative Negative
Worm egg Negative Negative
Amoeba Negative Negative
Red blood cells 0-1
White blood cells 0-1

CHAPTER 4
DISCUSSION & SUMMARY

4.1 Discussion
A, a 7-months-old girl, with the body weight and body height of 7 kg and 70 cm
respectively, was admitted to the infectious unit of Haji Adam Malik General Hospital on
February 13th 2011 at 09.15 pm with the chief complaint of diarrhea. This complaint was
experienced by the patient for about 3 days ago, the frequency is 10 times in a day, the
38
volume glass every time diarrhea, in feces the water is more than the dregs, mucus was
found in the feces and blood was not found. The patient are also complained of vomiting, the
frequency is 3 times in a day, the volume 20 cc for each time vomiting, the contents of
vomite is that what she ate and drank. The patient has fever since one week ago, high
temperature. Fever lowered with antipyretic. Seizure and shiver was not found. History of
recurrent fever (+) since birth. Weight loss was found, one month ago patient's weight is 8
kg.The last urination at 05.00 pm, the volume is an adequate, the color is brown. Worms
infection history was not found.

Patient was born spontaneously, aided by a midwife, cried immediately at birth, cyanosis
was not found. History of maternal conditions: fever (-), hypertension (-), diabetes
mellitus(-), drugs(-), used the herbal medicine while two months pregnancy. The herbal
medicine are used for abortion. Patient is the fifth child. Her mother age is 32 years old
during their give birth.

Diarrhea is the passage of unusually loose or watery stools, usually at least three times in
a 24 hour period. However, it is the consistency of the stools rather than the number that is
most important. Frequent passing of formed stools is not diarrhea 8. In this case, the patient
was admitted with chief complain diarrhea and the frequency is 10 times in a day with the
water is more than the dregs.

Diarrheal episodes are classically distinguished into acute and chronic (or persistent)
based on their duration. Acute diarrhea is thus defined as an episode that has an acute onset
and lasts no longer than 14 days; chronic or persistent diarrhea is defined as an episode that
lasts longer than 14 days. In this case, the patient has acute diarrhea because he has diarrhea
for 7 days (February 10th 2011 - February 17th 2011).

A child with diarrhea should be assessed for dehydration. In some dehydration, we must
look at the condition (restless, irritable), sunken eyes, thirsty and eagerly to drink, and feel
the skin pinch that goes back slowly. In this case, the patient was restless, has sunken eyes,
thirsty and eagerly to drink.

39
 This patient, general supportive care should include IVFD RL 75cc/kgBW/4hours.
Decided treatment for this patient with diarrhea is dictated based on the weight and clinical
status of the patient that has some dehydration. The patient also has fever with high
temperature, so we gave paracetamol. The children usual diet should be continued during
diarrhea and increased afterwards. Food should never be withheld and the child's usual foods
should not be diluted. Breastfeeding should always be continued. The aim is to give as much
nutrient rich food as the child will accept. The patient continued to has breastfeeding addition
with porridge diet of 700 ccal with 96 gram of protein. On February 15th 2011, the patient got
zinc for the first time. By giving zinc as soon as diarrhea starts, the duration and severity of
the episode as well as the risk of dehydration will be reduced.

The prognosis for this patient is good with use of oral rehydration solutions (ORS),
improved rates of breastfeeding, improved nutrition, better sanitation and hygiene have
contributed to a consistent decline in the mortality rate in developing countries.

4.2 Summary
It has been reported that a case of a 7-months-old girl diagnosed as gastroenteritis with
mild-moderate dehydration. The diagnosis was established based on history taking, clinical
manifestation, and laboratory finding. The treatment of this patient are IVFD D5% NaCl
0.225%, Paracetamol, Zink, Oralit, and diet (porridge) 700 ccal with 14 gram of protein. The
patient has been recovered after get medication for 4 days in Adam Malik General Hospital
and was controlled at Adam Malik General Hospital gastroentererology polyclinic.

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4. Mayo Clinic Staff. Diarrhea. Available from:
http://www.mayoclinic.com/health/diarrhea/ds00292 [ Accesed 23 February 2011].

40
5. McPhee et al. Current Medical Diagnosis and Treatment 2009. San Francisco: McGraw-
Hills, 2009.
6. Putra DS. Diare Akut pada Anak. Ilmu Kesehatan Anak RSUD Arifin Achmad/FK UNRI,
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