CASE REPORT

ENTRY: DIARRHEA

ANDRE ELTON HERYANTO

1306388162
Group A1

Supervisor:
dr. Lilis Diah Hendrawati, Sp.A

MODUL KESEHATAN ANAK DAN REMAJA

DEPARTEMEN ILMU KESEHATAN ANAK
FAKULTAS KEDOKTERAN UNIVERSITAS INDONESIA
JAKARTA 2018
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 STATEMENT OF ORIGINALITY

I hereby acknowledge that the research report is my original work and that all the resources,
whether cited or referred to, has been stated accordingly

Name : Andre Elton Heryanto

NPM : 1306388162

Signature :

Date : 9 February 2018

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 TABLE OF CONTENT

STATEMENT OF ORIGINALITY ......................................................................... 2

TABLE OF CONTENT ........................................................................................... 3

CHAPTER 1. CASE ILLUSTRATION............................................................... 5

1.1 Patient's Identity ............................................................................................. 5
1.2 Anamnesis ...................................................................................................... 5
1.3 Physical Examination ..................................................................................... 6
1.4 Laboratory Examination................................................................................. 8
1.5 List of Problems ........................................................................................... 12
1.6 Plans ............................................................................................................. 13
1.7 Prognosis ...................................................................................................... 13

CHAPTER 2. LITERATURE REVIEW ........................................................... 14

2.1 Normal Physiology of Intestines .................................................................. 14
2.1.1 Neural Control ..................................................................................... 14
2.1.2 Fluid Absorption and Excretion .......................................................... 14
2.1.3 Defecation ........................................................................................... 15
2.2 Diarrhea ........................................................................................................ 16
2.2.1 Definition ............................................................................................ 16
2.2.1 Epidemiology ...................................................................................... 16
2.3 Acute Diarrhea ............................................................................................. 17
2.3.1 Mode of Transmission......................................................................... 17
2.3.2 Risk Factors ......................................................................................... 17
2.3.3 Etiology ............................................................................................... 18
2.3.4 Pathophysiology .................................................................................. 19
2.3.4.1 Absorption Problem or Osmotic Diarrhea ................................. 19
2.3.4.2 Malabsorption ............................................................................ 19
2.3.4.3 Secretory Diarrhea...................................................................... 20
2.3.4.4 Peristaltic Problems and Inflammation ...................................... 20
2.3.4.5 Immunology Associated Diarrhea .............................................. 21
2.3.5 Clinical Manifestations and Complications ........................................ 21
2.3.6 Diagnosis ............................................................................................. 22
2.3.6.1 Anamnesis .................................................................................. 22
2.3.6.2 Physical Examination ................................................................. 22
2.3.6.3 Laboratory Examination ............................................................. 22
2.3.7 Management ........................................................................................ 23
2.3.7.1 Oral Rehydration Therapy.......................................................... 23
2.3.7.2 Zinc............................................................................................. 23
2.3.7.3 Breastmilk and Nutritional Support ........................................... 24
2.3.7.4 Antibiotics .................................................................................. 24
2.3.7.5 Education .................................................................................... 24

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 2.3.7.6 Management of Dehydration ...................................................... 25

CHAPTER 3. DISCUSSION .............................................................................. 27

CHAPTER 4. CONCLUSION ............................................................................ 29

REFERENCES ..................................................................................................... 30

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 CHAPTER I
CASE ILLUSTRATION

1.1 Patient’s Identity

• Name : Carissa Putri
• Age : 1 year, 2 months, and 19 days.
• Gender : Female
• Date of Birth : 17 November 2016
• Address : Cipinang Baru Bunder No.40, Rt 09, Rw 01.
• Religion : Islam
• Insurance : Badan Penyelenggara Jaminan Sosial (BPJS)
• Medical Record Number : 2317514

1.2 Anamnesis
(Hetero-anamnesis: with the mother’s patient is conducted on 5 February 2018, time: 9:30 PM)
• Main Complaint:
High fever and frequent defecation in the last 3 days before admission to hospital.
• History of the Current Disease:
The mother’s patient complaints of high fever and frequent defecation in the patient for the
last 3 days before admission to hospital. The fever was recorded by the mother and said to
reach 39-oC. Paracetamol was used to relieve the fever but was unable to do so. The fever
occurred for the whole day and no sweat was found in the toddler. Frequent defecation was
also complained and said to reach 10 times within 24 hours, with watery stools and green
mucus as the presentation of the stools described by the mother. No other complaints were
mentioned regarding the frequent defecation. The mother also mentioned vomits during
fever and often occurred during breastfeeding. Seizure and dyspnea were not present in the
patient. As the patient was admitted to the hospital, the patient experienced a few times of
productive cough with white phlegm and common cold with white mucus.
• Past Medical History:
No significant past medical history admitted by the mother of the patient.

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 • History of Pregnancy and Birth:
The patient’s mother conceived the patient for 39 weeks and proceeded the vaginal
delivery. The birth weight is 3 Kg in the absence of cyanosis, icteric, and bleeding.
Antenatal care was performed once every month.
• Growth and Development:
The patient can walk on her own, and spell 1 word at a time.
• Nutrition History:
Exclusive breastfeeding was given for 6 months, followed with complementary feeding
like the food that the other family members consumed. The mother mentioned vegetables
and rice.
• Immunization Status:
Immunization was said to be complete up to the age of a year, which is for the measles.
• Family History of Disease:
None of the family members were experiencing similar condition as the patient at that
moment. No other significant family history of diseases mentioned.
• Socio-Economic Status:
Patient lived with her both of her parents, grandfather, and grandmother. The grandfather
was a smoker. In the neighborhood, none of the them had experiences similar to the
condition of the patient.

1.3 Physical Examination

(Performed on 6 February 2018, time: 9:20 AM)

• Conscious : Compos mentis, GCS 15 (E4M6V5).

• General Condition : Not in pain.
• Blood Pressure : Not performed (several attempts performed but cuff size too big).
• Pulse Rate : 136 times/minute, regular rhythm, vessel fill adequate.
• Body Temperature : 35.6-oC.
• Respiratory Rate : 32 times/minute, regular rhythm, thoraco-abdominal pattern.

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General Status
• Head: Symmetric, absent of deformities.
• Hair: equal distribution, not easily pulled.
• Eye: Conjunctiva not pale, sclera not icteric, absent of sunken eyes, isochoric pupil,
direct and indirect pupillary light reflex +/+.
• Nose: no nasal flaring, no septum deviation, nasal cavity adequate, enlargement and
hyperemia of nasal concha is absent, secretions -/-, no pain on nasal sinuses palpation
• Ear: earlobe normal, secretion -/-.
• Lips: not dry, not cyanotic.
• Mouth: mucosa hydrated, no oral thrush, incomplete teeth, no deviation and fasciculation
of tongue.
• Throat: Uvula in the middle, pharyngeal arch symmetric, pharynx is not hyperemia.
• Neck: Trachea is symmetric, no enlargement of thyroid, no mass in the lymph nodes of
submental, submandibular, preauricular, postauricular, occipital, cervical anterior,
cervical posterior, supraclavicular, and infraclavicular.
• Thorax:
o Inspection: Chest expansion symmetric, no chest retraction.
o Palpation: no pain elicited by palpation, ictus cordis palpable at 5th intercostal
space in the left midclavicular line.
o Percussion: Not performed.
o Auscultation: Heart sound I-II regular, murmur -, gallop -, vesicular +/+, rhonchi -
/-, wheezing -/-.
• Abdomen:
o Inspection: No mass observed, no signs of inflammation, no rash.
o Palpation: no mass palpated, no pain elicited through palpation, skin turgor
normal (goes back spontaneously), right lobe and left lobe of liver are not
palpable, spleen not palpable.
o Percussion: Not performed.
o Auscultation: Abdominal bruits 6 times/minute.
• Extremities: Extremities are warm, CRT <2 seconds, no edema.

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 • Anthropometry: Since age < 5 years, WHO charts are used.
o Body weight (BW) : 7.7 Kg
o Body height (BH) : 72 cm
o Head circumference (HC) : 43.5 cm
o Upper arm circumference (UAC) : 14 cm
BW/Age : 7.7/9.4 (-2<Z<median)  Body weight adequate
BH/Age : 72/76.4 (-2<Z<median)  Body stature adequate
Age based on Actual Height : 10 months
BW/BH : 7.7/8.6 (-2<Z<median)  Nutritional status normal
HC/Age : 43.5/45.4 (-2<Z<median)  Normocephalic
UAC/Age : 14/14.3 (97.90%)  Nutritional status normal

1.4 Laboratory Examination

• Hematology: (30-01-2018)
Component Result Unit Standard Range
Hemoglobin 11.2 g/dL 10.5-14.0
Hematocrit 34.4 % 32.0-42.0
Erythrocyte 5.24 10^6/µL 3.70-5.30
MCV/VER 65.6 fL 72.0-88.0
MCH/HER 21.4 pg 24.0-30.0
MCHC/KHER 32.6 g/dL 32.0-36.0
Thrombocyte 290 10^3/µL 150-400
Leukocyte 15.47 10^3/µL 6.00-14.00
Basophil 0.2 % 0-1
Eosinophil 0.0 % 1-3
Neutrophil 59.8 % 52.0-76.0
Lymphocyte 31.9 % 20-40
Monocyte 8.1 % 2-8
RDW-CV 15.4 <16.5

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• Stool Analysis: (31-01-2018)
Component Result Unit Standard Range
Macroscopic
Color Green Yellow
Consistency Thick Soft
Mucus Positive Negative
Blood Negative Negative
Pus Negative Negative
Microscopic
Leucocyte 5-7 /LPB
Erythrocyte 2-4 /LPB
Worm’s egg Not found Negative
Amoeba Positive Negative
Others Negative
Digestive System
Fat Negative Negative
Fiber Negative Negative
Muscle tissues Negative Negative
Faint blood feces Positive Negative

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• Urine Analysis: (31-01-2018)
Component Result Unit Standard Range
Color Light yellow Yellow
Clarity Clear Clear
Leukocyte 0-1 /LPB
Erythrocyte 0-1 /LPB
Cylinder Negative
Epithelial cells +1
Crystal Negative
Bacteria Negative Negative
Density 1.005 1.005-1.030
pH 6.5 4.5-8
Albumin Negative Negative
Glucose Negative Negative
Ketone Negative Negative
Blood/Hb Negative Negative
Bilirubin Negative Negative
Urobilinogen 3.4 µmol/L 3.4-17.0
Nitrite Negative Negative
Leucocyte esterase Negative Negative

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• Stool Analysis: (03-02-2018)
Component Result Unit Standard Range
Macroscopic
Color Green Yellow
Consistency Soft Soft
Mucus Negative Negative
Blood Negative Negative
Pus Negative Negative
Microscopic
Leucocyte 0-2 /LPB
Erythrocyte 0-1 /LPB
Worm’s egg Not found Negative
Amoeba Negative Negative
Digestive System
Fat Negative Negative
Fiber Positive Negative
Muscle tissues Negative Negative
Faint blood feces Negative Negative

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 • Hematology: (04-02-2018)
Component Result Unit Standard Range
Hemoglobin 11.3 g/dL 10.5-14.0
Hematocrit 33.5 % 32.0-42.0
Erythrocyte 5.22 10^6/µL 3.70-5.30
MCV/VER 64.2 fL 72.0-88.0
MCH/HER 21.6 pg 24.0-30.0
MCHC/KHER 33.7 g/dL 32.0-36.0
Thrombocyte 341 10^3/µL 150-400
Leukocyte 14.26 10^3/µL 6.00-14.00
Basophil 0.6 % 0-1
Eosinophil 3.0 % 1-3
Neutrophil 30.5 % 52.0-76.0
Lymphocyte 59.2 % 20-40
Monocyte 6.7 % 2-8
RDW-CV 15.5 <16.5

1.5 List of Problems

1. Acute diarrhea with mild-moderate dehydration.
2. Amoebiasis.
3. Leukocytosis.

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1.6 Plans
Therapeutic Management:
• 30 January 2018:
o KAEN-3B 15 drops/minute.
o Paracetamol drop 4X0.8 ml.
o Zinc syrup 1X20 g.
• 31 January 2018:
o Metronidazole injection 3X75 mg.
• 5 February 2018:
o Metronidazole syrup 3X5 ml.

1.7 Prognosis
Ad Vitam : Bonam
Ad Functionam : Dubia ad sanam
Ad Sanationam : Bonam

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 CHAPTER II
LITERATURE REVIEW

2.1 Normal Physiology of Intestines

2.1.1 Neural Control

The small intestine and the colon are the two main organs responsible for the regulation of
secretion and absorption of water and electrolytes as well as the storage and transport of nutrients.
They have intrinsic and extrinsic innervation. The intrinsic innervation, also known as enteric
nervous system, consist of the myenteric, submucosal, and mucosal neuronal layers. The myenteric
plexus regulates smooth-muscle function and the submucosal plexus controls the secretion,
absorption, and mucosal blood flow. The extrinsic innervations are part of the autonomous nervous
system that also control the motor and secretory functions.1

2.1.2 Fluid Absorption and Excretion

9 L of fluid enter the gastrointestinal tract on an average day and around 1 L of residual fluid
reaches the colon. Stool excretion also excretes some fluids at the rate of 0.2 L per day. The colon
has great capacity to reabsorb fluids up to 4 times of the average fluid recovery of 0.8 L/day.
Hence, the colon can compensate the fluid reabsorption if the intestine has absorption or secretory
disorder. In the colon, sodium absorption is mainly through electrogenic that takes place at the
apical membrane of the intestine and compensated by a basolateral sodium pump.1

During food intake, small intestines produces irregular, mixing contractions with low amplitude
except at the distal ileum where there is powerful contraction for bolus transfer. The distal ileum
functions as a reservoir that intermittently remove the contents through bolus movement and this
movement provides time to reabsorb the content. In the colon, haustra facilitates mixing, retention
of the residue and is responsible for the solid stool appearance. Resident bacteria in the colon

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digests unabsorbed carbohydrates that will be used as nutrients for the mucosa. Moreover, the
bacteria also keep pathogenic bacteria level at bay. The ascending and transverse regions of the
colon act as reservoirs (15 hours of transit), while the descending colon functions as conduit
(average transit only 3 hours). Colon is efficient in the absorption of sodium and water that is
crucial at times of sodium-depleted conditions where the small intestines cannot maintain the
balance.1

2.1.3 Defecation

During defecation, sacral parasympathetic nerves relax puborectalis muscle that leads to the
straightening of the anorectal angle by at least 15 degrees from the normal angle of 80-110 degrees.
The distention of the rectum causes transient relaxation of the internal anal sphincter via intrinsic
and reflex sympathetic innervation. There is also voluntary relaxation of the external anal sphincter
(innervated by the pudendal nerve) in response to the sensation produced by distention permits the
evacuation of feces.1

Fig 1. Schematic illustration of the anorectum (A) at rest and (B) during defecation.1

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2.2 Diarrhea

2.2.1 Definition

Diarrhea is defined as the passage of three or more loose or liquid stools within 24 hours.2, 3
Frequent solid stools are not classified as diarrhea, along with loose stools formed by breastfed
babies.2 Classification of diarrhea can be based on the duration and etiology. Diarrhea that occurs
less than 2 weeks is categorized as acute diarrhea, persistent if it last for 2-4 weeks, and chronic of
diarrhea last for more than 4 weeks.1, 4 Acute diarrhea is commonly associated with infection in
public heath setting, while chronic diarrhea is often due to non-infectious etiologies such as protein
intolerance in cow/donkey milk, celiac disease, and cystic fibrosis.5, 6

2.2.2 Epidemiology

According to the World Health Organization (WHO), diarrhea is the second leading cause of death
in children under five years old. Each year, an estimate of 525,000 children under five died due to
diarrhea and around 1.7 billion cases of diarrhea in children found annually on a global scale. This
has made diarrhea as a huge contributing factor in causing malnutrition in children under five.3
From all the cases in children, around 78% are from Africa and Southeast Asia.7

From the Ministry of Health Republic of Indonesia in 2013, the highest incidence and prevalence
of diarrhea occurred in Papua (6.3% and 14.7% respectively), followed by South Sulawesi (5.2%
and 10.2% respectively), and Aceh (5.0% and 9.3% respectively).8 Based on the population’s
characteristic, toddlers had the highest number of diarrhea cases among other characteristics.8
When categorized in terms of work group, farmers had the highest proportion of diarrhea cases
(7.1%).8 However, gender showed relatively equal proportion and hence showed no correlation in
the incidence of diarrhea.8 In 2015, there were 18 diarrhea outbreaks reported across 18 districts
with a case fatality rate of 2.47%, which was more than the expected number of less than 1%.9
Norovirus is one of the etiologies of diarrhea that caused one-fifth of all infectious diarrhea cases
and has resulted in 200,000 deaths every year in developing countries. Historically, rotavirus is

16
the leading cause of severe diarrhea in children globally. For chronic diarrhea, the main causes are
inflammatory bowel disease, Crohn’s disease, and ulcerative colitis.10

2.3 Acute Diarrhea

2.3.1 Mode of Transmission

Acute diarrhea is commonly caused by infections that is often though fecal-oral route.6 Infectious
organisms that include viruses, bacteria, protozoa, and helminths, are transmitted from the stool of
an individual to another’s mouth (fecal-oral transmission).11 Ingestion of food and drinks as well
as direct contact through hands or non-living things are the possible route for infections. Indirect
transmission also can occur through flies that could potentially contaminate foods that will be
ingested. In summary, it can be described as 4F, which are finger, flies, fluid, and field.6

2.3.2 Risk Factors

There are several risk factors that increases the likelihood of transmission. Some of the factors are
not breastfeeding infants for the first 4-6 months of life, no clean water reservoir, water
contamination by stools, poor sanitation, poor personal and environment hygiene, unhygienic
storage and serving of foods, low maternal education, and shorter boiling time of water.6, 12 Other
factors that are owned by individuals also contribute the risk of getting infected, such as poor
nutrition, immunodeficient, lack of gastric acidity, decrease of intestine motility, infected with
measles within the last 4 weeks and genetic factors.6

Most of the cases occur in children in their first 2 years of life with the highest incidence during
the age of 6-11 months. At the age of 6-11 months, the baby starts to receive other foods than
breastmilk with the combination of decrease in passive immunity from the mother’s
immunoglobulin.6 Asymptomatic infection can also occur, mostly in children at the age of 2 or
more since their immune system has developed. These kinds of people do not show symptoms of

17
infections, but their stools contain the enteropathogens that can infect other people.6 Seasons also
can affect the infection rate. In tropical area such as Indonesia, diarrhea cause by rotavirus can
happen along the year with an increase in dry season and bacterial infections increases during the
rainy season.6

2.3.3 Etiology

In the rapid development in the field of medicine, around 80% pathogens have been identified in
health facilities and around 50% mild cases in the community. Around 25 types of microorganism
have been identified to cause diarrhea in children and infants. The main causative groups are from
virus, bacteria, and parasite. It can further be divided into non-inflammatory and inflammatory
which is due to the mechanism of how the disease develops.6

Non-inflammatory diarrhea develops through the production of enterotoxin by bacteria,

attachment by bacteria or parasite, and destruction of cell surface villi by virus. On the contrary,
inflammatory diarrhea often caused by bacteria penetrating the intestines or through the production
of cytotoxin.5 In developing countries, the most common pathogens to infect children are rotavirus,
Enterotoxigenic Escherichia coli, Shigella, Campylobacter jejuni and Cryptosporidium.6

Fig 2. Three types of enteric infections and their respective causative agents.6

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2.3.4 Pathophysiology

Diarrhea can occur if the fluid content in the colon is beyond its capacity to reabsorb, which can
be caused by a lower absorption or increase excretion in the small intestine. If the small intestine
is working normally, the problem rises from the colon either due to a decrease in the absorption or
increase in the secretions.6

2.3.4.1 Absorption Problem or Osmotic Diarrhea

A decrease in absorption can be due to several causes such as consumption of magnesium

hydroxide and sucrase-isomaltase deficiency.6 Magnesium produces laxative effect due to the
poorly absorbable magnesium ions in the intestinal lumen exerting osmotic pressure that causes
water and sodium to be retained in the intestinal lumen.6, 13 Sucrase-isomaltase are glycoprotein in
the brush border of the small intestine villi. Isomaltase digest dextrin, while sucrase digests
sucrose, maltose, and short linked glucose oligomers. Deficient of these enzymes lead to
undigested sugars to stay in the lumen that exert osmotic pressure that leads to watery, osmotic
diarrhea.14

2.3.4.2 Malabsorption

Malabsorption in the intestine can be due to changes in the brush border, or other organs that are
responsible in the digestion of the content. Destruction of cell linings in the intestines can be due
to virus or other pathogenic agents that leads to villi atrophy, rendering its ability to absorb
nutrients form the lumen. Some pathogens, such as E. coli, cause malabsorption by altering the
physiology of the brush border without changing the anatomical structure. Insufficient exocrine
secretion of the pancreas causes proteins, carbohydrates, and triglyceride to be improperly digested
and therefore leads to malabsorption as well.6

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2.3.4.3 Secretory Diarrhea

Several conditions that cause secretory diarrhea are crypt hyperplasia and luminal secretagogue.
Any diseases that cause crypt hyperplasia will lead to secretion in the intestine and secretory
diarrhea, and often accompanied with villi atrophy.6 Bacterial enterotoxins and chemicals such as
bile acids or laxatives also causes secretory diarrhea.15 Enterotoxins mainly work by increasing
intracellular cAMP, cGMP, or Ca2+ that cause the activation of protein kinase.6 Activated protein
kinase will lead to Cl- to be excreted into the lumen. Sodium will be pulled out as well due to the
Cl- along with water that leads to diarrhea. Some laxatives also work by increasing intracellular
cAMP and increasing intestinal permeabilities, or even cellular destruction.6

Secretory diarrhea in children of developing countries often caused by enterotoxin E. coli or

Cholera. In developed countries, secretory diarrhea is considered rare and often associated with
drugs or cancers. This often causes changes in the mucosa of the intestines that leads to excessive
secretion of water and minerals into the lumen.6

2.3.4.4 Peristaltic Problems and Inflammation

Peristaltic problem is rarely associated with diarrhea, but either an increase or a decrease can lead
to diarrhea. Although a decrease in motility will give more time for the intestine to absorb, bacteria
will also have time to colonize in the intestine that leads to diarrhea. Watery diarrhea is caused by
hypermotility of irritable colon in babies. A static intestine can cause inflammation that results in
deconjugation of bile acids and causes malabsorption.6

Inflammation also causes destruction of tight junction and epithelial cells that increases
permeability of the cells, which will cause movement of water, electrolyte, and other capillaries
content into the lumen of the intestine due to hydrostatic pressure in the capillaries.6

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2.3.4.5 Immunology Associated Diarrhea

Diarrhea associated with immunology is often in the cases of hypersensitivity type 1, III, and IV.
Type I is a reaction between mast cell and IgE with food allergen, type III is like a condition in
gastroenteropathy, and type IV in Coeliac disease and protein loss enteropathies. Different
mechanism for each type of allergies but ultimately leads to destruction of cells in the intestines
that stimulates the secretion of chlorides followed by sodium and water.6

2.3.5 Clinical Manifestations and Complications

Clinical manifestation for acute diarrhea can be from gastrointestinal, such as frequent defecation,
stomach cramps, and vomits. However, signs and symptoms in general are dependent on the
etiology of the disease. Stools will often contain several electrolytes such as sodium, chlorides,
and bicarbonate. Vomits and fever can also be present in infectious diarrhea of will contribute
complications such as dehydration, metabolic acidosis, and hypokalemia.6

Fig 3. Association between causative and its clinical features in acute infectious diarrhea.1

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2.3.6 Diagnosis

2.3.6.1 Anamnesis

In the anamnesis, things to be asked are duration of diarrhea, the frequency, volume, consistency
of the stool, the color and smell of the stool, and presence of mucus or blood in the stool. Other
symptoms may involve vomits with information on the volume and frequency. Urination should
also be disclosed along with the volume, frequency, and asked the patient if they have urinated
within 6-8 hours. Dietary information should also be asked to the patients. Fever is often well
associated with infections and can occur in patients with infectious diarrhea. Ask about fever or
any other symptoms such as cough and cold. It is crucial to ask what countermeasures that have
been taken to resolve the diarrhea, such as the medications or hospital visits. In children, it is
prudent to also ask the immunization history.6

2.3.6.2 Physical Examination

It is essential to start physical examination with body weight, body temperature, pulse rate,
respiratory rate, blood pressure. Signs of dehydration should be assessed, such as conscious, skin
turgor, tongue, eye, mouth, and sunken fontanelle in infants.6

2.3.6.3 Laboratory Examination

Laboratory examination should be conducted based on the etiology of the diarrhea, but there are
some examinations that are non-specific and still can be done. Most common lab examinations
that are performed in patients with diarrhea are:6
• Complete blood count: serum electrolytes, blood gas analysis, blood glucose, blood culture,
and antibiotic resistant testing.
• Urine: Culture and antibiotic resistant testing.
Stool examination can be done for macroscopic and microscopic examination. Macroscopic
examination (color, consistency, presence of mucus or blood) is performed in all diarrhea patients.

22
Watery diarrhea without mucus or blood is often caused by enterotoxin virus, protozoa, or
infections outside the gastrointestinal tract. Stool with the presence of mucus or blood might be
caused by bacterial infection that secretes cytotoxin, enteroinvasive that cause inflammation of
mucosa, or parasites in the intestines (E. histolytica, Balantidium coli, and T. trichiora). Stools that
smell rotten present in infections caused by Salmonella, Giardia, Cryptosporidium and
Strongyloides. In microscopic, leukocytes, eggs and the parasites are the main points for lookout
to determine the etiology of the diarrhea.6

2.3.7 Management

There are 5 important things for the management of diarrhea, which are rehydration using oral
rehydration salts, zinc for 10 consecutive days, breast feeding or sufficient nutrients, antibiotic
based on etiology, and education to the parents.6 Dehydration in patients with diarrhea should also
be intervened as well.6

2.3.7.1 Oral Rehydration Therapy

Oral rehydration salts are given every defecation with the criteria as follow: children less than 2
years old will be given 50-100 ml for every defecation, and children with an age of 2 years old or
above will be given 100-200 ml for every defecation. The package can be given to parents and a
pack of oral rehydration salts diluted in 1 L of clean water. The solution can only be used 24 hours
after the mixing with clean water.6

2.3.7.2 Zinc

Zinc has numerous functions, such as cell growth and division, antioxidant, cellular immunity, and
appetite. It also increases water and electrolytes absorption, increasing regeneration of epithelial
cells of intestines, increasing the number of apical brush border, and increases the appetite of the

23
patients.6 Zinc also reduces the volume and frequency of defecation and hence reduces the risk of
dehydration. The administration of zinc for 10-14 days significantly reduces the morbidity and
mortality of patients and should continuously be given even if the patients have recovered. Dosage
for children under 6 months old is 10 mg (half a tablet) per day and for children above 6 months
with 20 mg (1 tablet) per day. For babies, zinc tablet can be dissolved in clean water, breast milk,
or the oral rehydration solution.6

2.3.7.3 Breastmilk and Nutritional Support

Nutritional intake should be given like healthy children according to the age to prevent weight loss
and replace the nutritional loss. In dysentery, appetite often reduced and an increase in the appetite
indicates recovery phase.6

2.3.7.4 Antibiotics

Antibiotics are often not recommended unless there are evidences for infections. Irrational use of
antibiotics can harm the normal flora in the intestines, causes antibiotic resistance.6

2.3.7.5 Education

Advice the mother if the children experiencing fever again will be required to return to the hospital.
Additional symptoms that require admission of hospital are bloody stools, recurrent diarrhea, loss
of appetite, thirsty, or did not improve within 3 days.6

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2.3.7.6 Management of Dehydration

The criteria for dehydration is in Fig 4. Initially assessment of dehydration is important to prevent
undesired complications. In case of patients without dehydration, they are required to have
adequate fluid intake from home to prevent dehydration, such as soup, water with sweetener, etc.
Volume of fluid to be administered is 10 ml/Kg Body weight or for children less than 1 year is 50-
100 ml, 1-5 years is 100-200 ml, 5-12 years is 200-300 ml, and for adults is 300-400 ml every time
they defecate.6

Fig 4. Category of dehydration and the respective management by WHO 2014.4

In patients with dehydration the management can be summarized as:6

• Mild-moderate: 75 cc/Kg Body weight of oral rehydration therapy in the first 3 hours. If
still thirsty, fluid should be given again. If it is not possible through oral, using nasogastric
at a rate of 20 ml/Kg Body weight/hour. The contents of the oral rehydration fluid in

25
 mmol/L are 90 sodium, 20 potassium, 80 chlorides, 30 bases, and 111 glucoses. Evaluate
every 3 hours.6
• Severe: Must be managed in hospitals or medical facilities. 100 ml/Kg body weight of
ringer lactate is used for to manage severe dehydration. For less than 1-year old patients,
30 cc/Kg body weight is given for the first hour, followed by 70 cc/Kg body weight on the
next 5 hours. For more than 1-year old patients, 30 cc/Kg body weight is given on the first
½ an hour, followed by 70 cc/Kg body weight for 2 ½ hours.6

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 CHAPTER III
DISCUSSION

Carissa Putri, a girl, age 1 year 2 months, came with complains of with high fever and frequent
defecation for 3 days before admission to hospital. High fever accompanied with frequent
defecation of 10 times/day are symptoms directing the working diagnosis to infectious diarrhea,
that is often acute. Mode of transmission is through oral and often occur in infants who started to
eat complimentary food besides breastfeeding. The patient receives complimentary foods starting
at the age of 6 months, which further add to the suspicion that the diarrhea might come from the
complimentary foods. The other family members do not suffer the same condition as the patient
since adult’s immune system is better than children at the age of 1 year old. Breastfeeding portion
also reduced due to complimentary food and hence less passive immunity from the mother.
Physical examination on admission to hospital is not performed, only after the treatment on the
day of discharge (7 February 2018).

From the laboratory results, there was a slight leukocytosis and reduction of mean corpuscular
volume (MCV) and mean corpuscular hemoglobin (MCH) from the lab test conducted on 30
January 2018. The leukocytosis indicates infections, low MCV indicating smaller erythrocytes,
and lower MCH indicates slight lower hemoglobin content in red blood cells. However, the mean
corpuscular hemoglobin concentration (MCHC), which is based on the hemoglobin content per
unit volume of red blood cells, is normal, and hemoglobin is normal, vascular problems should not
be prioritized at the moment. From the urine analysis performed on 31 January 2018, none of the
results showed abnormalities. From the stool examination conducted on 31 January 2018, the color
of the stool was green, with thick consistency, and positive of mucus. There was also a positive
faint of blood and for amoeba. This shows positive infection for Amoeba infections, often caused
by Entamoeba histolytica.6 It is a parasite infection that leads to destruction of tissue in the
intestines and cause dysentery.

Invasive amebiasis such as E. histolytica start of from the motile form trophozoite that lives in the
lumen of the large intestine. After attachment, it multiplies and differentiates into the cyst, which

27
is the resistant form and the one responsible for the transmission to other vectors via stool that can
contaminate food and water. The parasite will excyst in the terminal ileum and emerge as
quadrinucleate trophozoite and further developed into 8 uninucleated trophozoites. These
trophozoites will start to invade the colonic mucosa and cause bleeding, which is shown as
dysentery as one of the symptoms. It also can invade the bloodstream and infect other organs,
causing extra-intestinal lesions that mainly occur in liver, leading to liver abscesses.16

Since it can spread through the blood stream, the clinical manifestations depend on which organs
are affected. There are 4 types of invasive intestinal amebiasis, which are dysentery, fulminating
colitis, amebic appendicitis, and ameboma of the colon. However, 90% of intestinal amebiasis
cases are the dysentery-diarrhea type. The often have 3-5 defecations per day, moderate colic pain
preceding discharge, and rectal tenesmus. The stool is often to be liquid and stained with blood.16

From the findings, the patient is diagnosed as acute diarrhea with mild-moderate dehydration,
leukocytosis, and amoebiasis. Initial management of the patient is administering
• 30 January 2018:
o KAEN-3B 15 drops/minute.
o Paracetamol drop 4X0.8 ml.
o Zinc syrup 1X20 g.
• 31 January 2018:
o Metronidazole injection 3X75 mg.
• 5 February 2018:
o Metronidazole syrup 3X5 ml.
After the treatment, Stool analysis was conducted again on 3 February 2018. The color of the stool
was still green, but the consistency changed from thick to soft, mucus was not present, amoeba
changed from positive to negative, and not more faint blood present. Fiber was detected during the
examination. From the hematology examination on 4 February 2018, leukocyte is still slightly
above the normal standard range, while MCV and MCH were still below normal. The patient was
discharged on 6 February 2018 and were planned to return for control on 9 February 2018.

28
 CHAPTER IV
CONCLUSION

Carissa Putri, a girl, aged 1 year and 2 months came to the hospital with complaints of high fever
and frequent defecation in the last 3 days before admission to hospital. From the anamnesis,
physical examination, and laboratory examinations, the patient is diagnosed with acute diarrhea
and mild-moderate dehydration with blood stain on stool and can be referred as intestinal
amebiasis. Immunization is complete, growth and development are according to age, and the
nutritional status is good. There are no other clinical signs suggesting other morbidities. For
management, the patient is given KAEN-3B, paracetamol to manage the fever, zinc to manage the
diarrhea, and metronidazole to treat the parasitic infections. The patient condition improved and is
discharged on 6 February 2018. The patient is asked to return for control on 9 February 2018. For
prognosis, ad vitam bonam, ad functionam dubia ad sanam, ad sanationam bonam.

29
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