TABLE OF CONTENT

Table of Content .................................................................................................................... 1

Section I - Case Report ......................................................................................................... 2
Identity ....................................................................................................................... 2
Anamnesis .................................................................................................................. 2
Physical Examination ................................................................................................. 5
Laboratory Investigation ............................................................................................ 9
Working Diagnosis ..................................................................................................... 10
Management ...............................................................................................................10
Prognosis ....................................................................................................................10
Follow Up ...................................................................................................................10
Section II – Literature of Review ........................................................................................ 15
Definition ................................................................................................................... 15
Epidemiology ............................................................................................................. 15
Etiology ...................................................................................................................... 15
Patoghenesis.... ........................................................................................................... 16
Patophysiology............................................................................................................ 22
Clinical Manisfestation .............................................................................................. 22
Diagnosis .................................................................................................................... 26
Differential Diagnosis ................................................................................................ 27
Treatment ................................................................................................................... 28
Complication .............................................................................................................. 39
Prognosis .................................................................................................................... 40
Prevention .................................................................................................................. 40
Section III – Conclusion ....................................................................................................... 42
References ............................................................................................................................. 43

1
 SECTION I
CASE REPORT

IDENTITY
Patient
Name : Child P
Birth Date : Oct 30th, 2014
Age : 22 months
Gender : Male
Address : Kp. Makasar cililitan
Nationality : Indonesian
Religion : Moslem
MR No. : 8278**
Date of admission : August 20 th, 2016
Date of examination : August 25th, 2016

Parents
Father Mother
Name Mr. M Mrs. M
Age 40 years old 38 years old
Job Private employees Housewife
Nationality Indonesian Indonesian
Religion Moslem Moslem
Education High school High school
Earning/month Rp 3.000.000,- -
Address Kampung makassar Cililitan

ANAMNESIS
The anamnesis was taken on August 21th 2016 using alloanamnesis method. It was taken at
room No. 5 Anggrek 2 Ward, RS Bhayangkara tk.I R. Said Sukanto, Jakarta.
Main complaint : Fever since 2 days prior to admission to hospital.
Additional complaint : Watery stools ≥ 10x/day since 3 days before admission to hospital,
dregs (+), foam (+), acid odor, blood (-), mucous (+), the color is
yellow. Vomiting after drinking and eating, frequency ≥5x/day.
History of Present Illness
A 22 months old boy with body weight 11,5 kg came to RS Bhayangkara tk.I R. Said
Sukanto Emergency Room at August, 20th 2016 on 5 am with a main complaint of fever
since 2 days ago. Since 2 days ago, the patient has gotten fever. The fever high constantly and
wasn’t measured. His mother gave sanmol syrup to decrease the temperature but it did not go
down well.

2
 His mother also complained that her son got diarrhea since 2 days ago after fever.
frequency ≥ 10x/days, consistency liquid, with a little dregs, foam positive, no blood, acid
odor, the colour is yellow. Other than that, the patient stomach was bloated, his mother says
the patient was vomiting, frequency ≥5x every after drinking dan eating, yellow liquid.
History of Past Illness
History of Past Illness
Pharyngitis/Tonsilitis -
Bronchitis -
Pneumonia -
Morbilli -
Varicella -
Diphteria -
Malaria -
Polio -
Enteritis -
Bacillary Dysentry -
Amoeba Dysentry -
Diarrhea -
Thypoid -
Worms -
Surgery -
Brain Concussion -
Fracture -
Drug Reaction -
Febril seizure -

Allergic History
The patient didn’t have allergy to medicine
The patient didn’t have allergy to food
The patient didn’t have allergy to weather and pollen
Birth History
Mother’s Pregnancy History
The mother routinely checked her pregnancy at local clinic with a doctor since she
knew she got pregnant and every months until she gave birth. She also said that she
consumed vitamins, iron supplement, and folic acid during pregnancy.
Child’s Birth History
- Labor : Hospital
- Birth attendants : Doctor
- Mode of delivery : Normal
- Gestation : 38 weeks
- Infant state : Healthy
- Birth weight : 3500 grams
- Body length : 51 cm

3
 - According to the mother, the baby started to cry, the baby’s skin is red, and no
congenital defects were reported.
Development History
- Psychomotor development
 Raised his head : 2 months
- Conclution : growth and developmental is still in the normal limits and was
appropriate according to the patient’s age.
Post Natal History
After birth, the baby checked at local doctor and the infant state is healthy.
History of Eating
- Breast milk : + until now
- Formula milk : + (chilkid)
- Baby biscuits : + (milna, sun)
- Fruit and vegetables :+
- Solid food and side dishes: -
Immunization History
Immunization Frequency Time
BCG 1 time 2 month
Hepatitis B 2 time 0 month
DPT 4time 2,4,6 months
Polio 4 time 0,2,4,6 month
Campak - -

Family History
- Patient’s father is healthy
- Patient’s mother is healthy
History of Sibling
No. Age Gender Childbirth Age Died Sumption Died
1 5 years old Male Normal - -

- The patient is the second child of the family

- The patient has 1 brother
- Born died : (-)
- Child dies : (-)
- Miscarriage : (-)
History of Disease in Other Family Members / Around the House
- None

4
PHYSICAL EXAMINATION (August 20th, 2016)
General Status
- General condition : Mildly ill
- Consciousness : Compos Mentis
- Pulse : 111 x/min, regular, strong
- Breathing rate : 24 x/min
- Temperature : 38,7°C per axilla
Anthropometry Status
- Weight : 11,5 kg
- Height : 84 cm
Nutritional Status based on NCHS (National Center for Health Statistics) year 2000 :
WFA (Weight for Age) : 11,5/12,3 x 100 % = 93 % (good nutrition)
HFA (Height for Age) : 84/85.3 x 100 % = 98 % (good noutrition)
WFH (Weight for Height) : 11,5/12,3 x 100 % = 93 % (good noutrition)

Conclution : The patient has good noutritional status.

5
 P. A

84
22 11,5
cm
mo
kg

6
Head to Toe Examination
- Head
Normocephal, hair (black, normal distribution, not easily removed), sign of
trauma (-), large fontanelle closed, fontanel concave (+)
- Eyes
Icteric sclera -/-, pale conjungtiva -/-, hyperaemia conjungtiva -/-, Tears +/+
sunken eyes +/+, pupils 3mm/3mm isokor, direct and indirect light response
++/++.
- Ears
Normal shape, no wound, no bleeding, secretion or serumen.
- Nose
Normal shape, midline septum, secretion +/+.
- Mouth
Lips : dry
Teeth : caries (+)
Mucous : watery
Tongue : clean
Tonsils : T1/T1, no hyperemia
Pharinx : no hyperemia
- Neck
Lymph node enlargement (-), scrofuloderma (-).
- Thorax
Inspection : Symmetric when breathing, retraction (-), ictus cordis is not
visible, rash (+), brething distress (-)
Palpation : Fremitus tactile +/+ symmetric, mass (-)
Percussion : Sonor on both lungs
Auscultation : Cor : S1-S2 regular, murmur (-), gallop (-)
Pulmo : vesicular +/+, ronchy -/-, wheezing -/-
- Abdomen
Inspection : Convex, epigastric retraction (-), spider nevi (-), rash (-)
Palpation : Supple, abdominal mass (-), liver and spleen not palpable,
acites (-)
Percussion : tympanic abdomen on the entire field, shifting dullness (-),
bloated (+)
Auscultation : bowel sound increase, bruit (-)
- Vertebra
There weren’t appear scoliosis, kyphosis, lordosis, and any massa long the
vertebral line.
- Ekstremities
Warm, capillary refill time <2 second, edema (-)
- Skin
Turgor slowly, rash (-), dry skin (-)
- Genitalia
Anus Hyperemis (+)

7
Neurogical Examination
Meningeal Sign
- Nuchal rigidity (-)
- Kernig sign (-)
- Lasegue sign (-)
- Brudzinski I (-)
- Brudzinski II (-)
Motoric Examination
Power
- Hand 5555/5555
- Feet 5555/5555
Tonus
- Hand Normotonus / Normotonus
- Feet Normotonus / Normotonus
Trophy
- Hand Normotrophy / Normotrophy
- Feet Normotrophy / Normotrophy
Physiologic Reflex
Upper extremities
- Biceps +/+
- Triceps +/+
Lower extremities
- Patella +/+
- Achilles +/+
Pathologic Reflex
Upper extremities
- Hoffman -/-
- Trommer -/-
Lower extremities
- Babinsky -/-
- Chaddock -/-
- Oppenheim -/-
- Gordon -/-
- Schaeffer -/-
Clonus
- Patella -/-
- Achilles -/-

Autonom Examination
Defecation Diarrhea (frequency 10 times daily)
Urination Normal (4-5 times daily)
Sweating Normal

8
LABORATORY INVESTIGATION
Hematology (August, 20th, 2016)
Hematology Results Normal Value
Hemoglobin 11,8 13 – 16 g/dl
Leukocytes 13.600 5.000 – 10.000 u/l
Hematocrits 34 40 – 48 %
Thrombocytes 265.000 150.000 – 400.000 /ul

Complete urin (August, 20th, 2016)

Results Normal Value
Color Yellow
Purity Clear
Ph 7.0 5 – 8.5
Specific Weight 1.010 1.000 – 1.030
Protein - Negative
Bilirubin - Negative
Glukosa - Negative
Keton - Negative
Blood/ Hb - Negative
Nitrite - Negative
Urobilinogen 0,1 0,1 – 1,0 IU
Leucocytes - Negative
Sedimen :
*Leucocytes 1–2 0 – 5 /LPB
*Erythrocytes 0–2 1 – 3 /LPB
*Epitel Cell -
*Silinder - /LPK
*Crystal -
Others -

Complete feces (August, 20th 2016)

Results Normal Value
Macroscopic
Color Green
Consistency Liquid
Mucous +
Blood -
Microscopic
Leucocytes 0-1/LPB
Eritrocytes 2-3/LPB
Worm eggs
Ascaris Sp -
Anchilostoma Sp -

9
 Trichuris Sp -
Oxyuris Sp -
Others -

WORKING DIAGNOSIS
Acute Diarrhea with mild-moderate dehydration
MANAGEMENT
- IVFD Kaen 3B 1050 cc/ 24 hours (32 tpm)
- Paracetamol 4x1cc per oral
- Lacto B 3x1 sachet
- Zinkkid syr 1x10mg
PROGNOSIS
- Quo ad vitam : dubia ad bonam
- Quo ad functionam : dubia ad bonam
- Quo ad sanactionam : dubia ad bonam
FOLLOW UP
May, 21st 2016, second day of hospitalization, 4th day of illness
Fever (+)
Defecation (+) frequency 8x, consistency liquid, green color, acid odor, foam(+)
S
dregs (+)mucous (-)blood (+)
Bloated (+)
Consciousness : Compos Mentis
General condition : Midly ill
Temperature : 38,5°C
Pulse : 111 x/min
Respiratory rate : 2 x/min
Head : Normocephal, fontanel concave (+)
Eyes : Pale conjungtiva (-), icteric sklera (-), hyperemia
conjungtiva (-), sunken eyes +/+ tears +?+
Mouth : Dry lips, dry mucous, tonsils T1/T1,hyperemiapharinx
Pulmonary : Vesiculer +/+, ronchi -/-, wheezing -/-
O Cardio : S1/S2 normal regular, murmur (-), gallop (-)
Abdomen : Distention (+), bowel sound (+) increase, bloated (+)
Skin : dry (+)
Turgor : Slowly
Akral : Warm
Anus : Hyperemis (+)

10
 Laboratory Investigation
Kimia clinic (August,21st 2016)
Electrolite Results Normal Value
Natrium 133 135-145 mmol/l
Kalium 2,3 3,5-5,0 mmol/l
Chlorida 101 98-108 mmol/l

A Acute Diarrhea with mild-moderate dehydration and hypokalemia

IVFD KAEN 3B 1100 cc/24 hours
Paracetamol 3x1cc per oral
Inj. Cefotaxime 2x500mg
P
Lacto B 3x1 sachet
Zinkkid 1x10mg
KCL 10 mEq/ kolf

August, 22nd 2016, third day of hospitalization, 5thday of illness

Fever (↑↓)
S Defecation (+) frequency 5x, consistency liquid, yellow to green color, acid
odor, foam(-) dregs (+) mucous (+) blood (-)
Consciousness : Compos Mentis
General condition : Midly ill
Temperature : 38 °C
Pulse : 110 x/min
Respiratory rate : 24 x/min
Head : Normocephal, fontanel concave (-)
Eyes : Pale conjungtiva (-), icteric sklera (-), hyperemia
conjungtiva (-) sunken eye +/+, tears +/+
Mouth : Dry lips, dry mucous, tonsils T1/T1,hyperemia pharinx
Pulmonary : Vesiculer +/+, ronchi -/-, wheezing -/-
Cardio : S1/S2 normal regular, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) increase, bloated (+),
abdominal pain (-)
O Skin : dry (+)
Turgor : Slowly
Anus : Hyperemis (+)
Akral : Warm

Hematology (August, 22nd 2016)

Hematology Results Normal Value
Hemoglobin 9,1 13 – 16 g/dl
Leukocytes 12,400 5.000 – 10.000 u/l
Hematocrits 25 40 – 48 %
Thrombocytes 354.000 150.000 – 400.000 /ul

A Acute diarrhea with mild-moderate dehydration

11
 IVFD KAEN 3B 1100 cc/24 hours
Paracetamol 3x1cc per oral
Inj. Cefotaxime 2x500mg
P
Lacto B 3x1 sachet
Zinkkid 1x10mg
KCL 10 mEq/ kolf

August,23rd 2016, fourth day of hospitalization, 6th day of illness

Fever (↑↓)
S Defecation (+) frequency 5x, consistency liquid, yellow to green color, acid
odor, foam(-) dregs (+) mucous (+) blood (+)
Consciousness : Compos Mentis
General condition : Midly ill
Temperature : 37,2 °C
Pulse : 108 x/min
Respiratory rate : 24 x/min
Head : Normocephal, fontanel concave (-)
Eyes : Pale conjungtiva (-), icteric sklera (-), hyperemia
conjungtiva (-)tears +/+
O Mouth : Dry lips, dry mucous, tonsils T1/T1
Pulmonary : Vesiculer +/+, ronchi +/+, wheezing -/-
Cardio : S1/S2 normal regular, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) normal, bloated (+)
Skin : dry (+)
Turgor : Slowly
Anus : Hyperemis (+)
Akral : Warm

Acute diarrhea with improvements

A
Hypokalemia
IVFD KAEN 3B 1100 cc/24 hours
Paracetamol 3x1cc per oral
Inj. Cefotaxime 2x500mg
P Lacto B 3x1 sachet
Zinkkid 1x10mg
KCL 10 mEq/ kolf
Micozaf zalf

12
August, 24th2016, fifth day of hospitalization, 7th day of illness
Fever (-)
Defecation (+) frequency 3x, consistency liquid, yellow color, acid odor, foam(-)
S
dregs (+) mucous (+) blood(-)

Consciousness : Compos Mentis

General condition : Midly ill
Temperature : 36,8 °C
Pulse : 112 x/min
Respiratory rate : 30 x/min
Head : Normocephal, fontanel concave (+)
Eyes : Pale conjungtiva (-), icteric sklera (-), hyperemia
conjungtiva (-) tears +/+
Mouth : Dry lips, dry mucous, tonsils T1/T1
Pulmonary : Vesiculer +/+, ronchi -/-, wheezing -/-
Cardio : S1/S2 normal regular, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) normal, abdominal
pain
(-), bloated (+)
Skin : dry (+)
Turgor : Slowly
Anus : hyperemis (+)
Akral : Warm

Laboratorium
Haematology (August, 22nd 2016)
O Hematology Results Normal Value
Hemoglobin 10,0 13 – 16 g/dl
Leukocytes 7.400 5.000 – 10.000 u/l
Hematocrits 29 40 – 48 %
Thrombocytes 193.000 150.000 – 400.000 /ul
Count of Leukocytes type
Basofil 0 0-13 %
Eosinofil 1 1-3 %
Rod 1 2-6 %
Segmen 52 50-70%
Limfocytes 35 20-40%
Monocytes 11 2-8%
LED 47 <15mm/hour
Eritrocytes 3,60 Milyar/ul

Kimia Clinic (August, 22nd 2016)

Electrolite Results Normal Value
Natrium 134 135-145 mmol/l
Kalium 4,3 3,5-5,0 mmol/l
Chlorida 101 98-108 mmol/l

A Acute diarrhea with improvements

13
 IVFD KAEN 3B 1100 cc/24 hours
Paracetamol 3x1cc per oral
Inj. Cefotaxime 2x500mg
P Lacto B 3x1 sachet
Zinkkid 1x10mg
KCL 10 mEq/ kolf
Micozalf zalf

August, 25th2016, fifth day of hospitalization, 8st day of illness

fever (-)
S Defecation (+) frequency 2x, consistency liquid, yellow color, no odor, foam(-)
dregs (+) no mucous nor blood
Consciousness : Composmentis
General condition : Midly ill
Temperature : 36,5 °C
Pulse : 110 x/min
Respiratory rate : 24 x/min
Head : Normocephal, fontanel concave (-)
Eyes : Pale conjungtiva (-), icteric sklera (-), hyperemia
conjungtiva (-) tears+/+
O Mouth : dry lips, wet mucosa, tonsils T1/T1
Pulmonary : Vesiculer +/+, ronchi -/-, wheezing -/-
Cardio : S1/S2 normal regular, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) normal, bloated (-)
Turgor : Normal
Anus : Hyperemis (-)
Akral : warm

A Acute diarrhea with improvements

IVFD KAEN 3B 1100 cc/24 hours
Paracetamol 3x1cc per oral
P Lacto B 3x1 sachet
Zinkkid 1x10mg
Micozalf zalf

14
 SECTION II

LITERATURE OF REVIEW

ACUTE DIARRHOEA

DEFINITION

Diarrhoea is defined as an increase in the frequency and fluidity of stools. Acute

infectious diarrhoea (usually lasting less than 7 days) is a common reason for consulting a
general practitioner and for admission to hospital in Australian children. Parents or carers
consult a GP in up to 75% of cases of childhood gastroenteritis, while advice is sought from
accident and emergency departments in about 50% and from pharmacists in about 5% of
cases.1

Diarrhea is the passage of loose or watery stools at least 3 times in a 24- hour period.
However, it is the consistency of the stools rather than the number that is most important.
Acute diarrhea may be caused by different viruses, bacteria, and parasites. Rotavirus and
Norwalk-like virus are the most common agents, causing up to 50% of acute diarrhea cases
during the high-incidence seasons. It is most practical to base the treatment of diarrhea on the
clinical type of the illness, which is easy to establish when a child is first examined. Usually
there is no need for laboratory tests.2

EPIDEMIOLOGY

In 1998–1999, the Australian Institute of Health and Welfare identified 22709

children under the age of 15 years who were admitted to hospital with gastroenteritis,
including three children under the age of 4 years who died of gastroenteritis. These figures
underestimate the true burden of the disease in the community. A National Health Survey in
1995, using selfreported data, estimated that each year in the community there were around
4056 episodes of diarrhoea per 1000 children under 15 years. Rotavirus infection is thought
to account for half of all hospital admissions for severe diarrhoea. In New South Wales alone
about 3700 children are admitted to hospital each year with rotavirus infection, at a cost to
the health system of nearly $5 million. While the cost of hospitalisation for rotavirus
infection is estimated at around $1700 per episode per child, the cost of care in the
community (at $441 per child) is also significant. To both of these costing estimates must be

15
added significant costs to the family, including time lost at work and missed schooling.
Indigenous children have increased rates of gastroenteritis, more frequent and longer hospital
admissions, and higher rates of dehydration, acidosis and comorbidity, than non-Indigenous
children.1

ETIOLOGY

Viral pathogens account for approximately 70% of episodes of acute infectious

diarrhoea in children, and rotaviruses are most commonly implicated (Case study and Box 1).
Bacterial infections account for about 15% of episodes and occur less often indeveloped than
in developing communities. Overall, Campylobacter and Salmonella species are the most
commonly reported bacterial infections in Australia, although atypical enteropathogenic
Escherichia coli are emerging as important pathogens. Infections with Shiga-toxin-producing
E. coli are rare in Australia, but may be complicated by the haemolytic–uraemic
syndrome(HUS). Increasingly, E. coli infection, typhoid and shigellosis are reported in
Australian children who have travelled abroad.1

PATHOGENESIS

Pathogenesis and severity of bacterial disease depend on whether organisms have

preformed toxins (S. aureus, Bacillus cereus), produce secretory (cholera, E. coli, Salmonella,
Shigella) or cytotoxic (Shigella, S. aureus, Vibrio parahemolyticus, C. difficile, E. coli, C.
jejuni) toxins or are invasive and on whether they replicate in food. Enteropathogens can lead
to either an inflammatory or noninflammatory response in the intestinal mucosa (Table 332-
5).

16
 Enteropathogens elicit noninflammatory diarrhea through enterotoxin production by
some bacteria, destruction of villus (surface) cells by viruses, adherence by parasites, and
adherence and/or translocation by bacteria. Inflammatory diarrhea is usually caused by
bacteria that directly invade the intestine or produce cytotoxins with consequent fluid,
protein, and cells (erythrocytes, leukocytes) that enter the intestinal lumen. Some
enteropathogens possess >1 virulence property. Some viruses, such as rotavirus, target the
microvillus tips of the enterocytes and can enter the cells by direct invasion or calcium-
dependent endocytosis. This can result in villus shortening and loss of enterocyte absorptive
surface through cell shortening and loss of microvilli (Fig. 332-2).

Most bacterial pathogens elaborate

enterot oxins; the rotavirus protein NSP4
acts as a viral enterotoxin. Bacterial
enterotoxins can selectively activate enterocyte intracellular signal transduction and can also
affect cytoskeletal rearrangements with subsequent alterations in the water and electrolyte
fluxes across enterocytes. In toxigenic
diarrhea enterotoxin produced by
Vibrio cholerae, increased
mucosal levels of cAMP inhibit
electroneutral NaCl absorption but
have no effect on glucose-
stimulated Na+ absorption. In
inflammatory diarrhea (e.g., Shigella

17
spp. or Salmonella spp.) there is extensive histologic damage, resulting in altered cell
morphology and reduced glucose-stimulated Na+ and electroneutral NaCl absorption. The
role of 1 or more cytokines in this inflammatory response is critical. In secretory cells from
crypts, Cl-secretion is minimal in normal subjects and is activated by cyclic adenosine
monophosphate (cAMP) in toxigenic and inflammatory diarrhea (Fig. 332-3).

ETEC colonizes and adheres to enterocytes of the small bowel via its surface fimbriae
(pili) and induces hypersecretion of fluids and electrolytes into the small intestine through 1
of 2 toxins: the heat-labile enterotoxin (LT) or the heat-stable enterotoxin. LT is structurally
similar to the V. cholerae toxin, and activates adenylate cyclase, resulting in an increase in

intracellular cyclic guanosine monophosphate (cGMP) (Fig. 332-4).

18
 In contrast, Shigella spp. cause gastroenteritis via a superficial invasion of colonic
mucosa, which they invade through M cells located over Peyer patches. After phagocytosis, a
series of events occurs, including apoptosis of macrophages, multiplication and spread of
bacteria into adjacent cells, release of inflammatory mediators (interleukin [IL]-1 and IL-8),
transmigration of neutrophils into the lumen of the colon, neutrophil necrosis and

degranulation, further breach of the epithelial barrier, and mucosal destruction (Fig. 332-5).3

19
The pathogenesis of diarrhea in systemic infections is not well understood because basic data
on the mechanisms that lead to diarrhea are lacking.

Several cytokines have been shown to have a role in the pathogenesis of diarrhea. For
example, interferon-gamma (IFN-γ), interleukin (IL)-6 and IL-10 concentrations were
elevated in the sera of children with diarrhea caused by rotaviruses.[3] The level of IL-6 was
higher in those patients with fever, and increased tumor necrosis factor alpha (TNF-α) levels
also correlated with the presence of fever and the number of diarrheal episodes.[3] TNF-α is a
central mediator of intestinal inflammation and also known to be involved in chloride
secretion by intestinal epithelial cells.[4

Polyclonal T-cell activation with an anti-CD3 antibody in mice leads to a release of

cytokines such as TNF-α, IFN-γ, IL-2, IL-3, IL-4 and IL-6 into the circulation, which results
in a severe but self-limiting syndrome consisting of diarrhea, hypothermia and
hypomotility.[5] The expression of the proinflammatory cytokine IL-8 can be stimulated by
the flagella proteins of various bacteria,[6] and has been shown to predict the severity of
enterocolitis in pediatric oncology patients.[7] IL-8 is strongly chemoattractant for CD8+
intraepithelial lymphocytes and a strong inducer of CD4+ T cells; it probably has a role in the

20
generation of the mucosal immune response to rotavirus infection.[8] The anti-inflammatory
cytokine IL-10 was recently shown to protect IL-10 knockout mice from severe diarrhea and
the loss of intestinal villi induced by T-cell activation through administration of anti-CD3
monoclonal antibodies.[9] These cytokines might be of particular interest as an explanation
of gastrointestinal symptoms in systemic infections.

In addition to the cytokine and humoral alterations, diarrhea-causing factors in

systemic infections might include direct invasion of gut epithelial cells by various pathogens,
inflammation of the lamina propria and other layers of the intestinal wall (including elements
of the enteric nervous system), and rosetting and sequestration of red blood cells, which
causes ischemia, endothelial apoptosis, increased permeability of the gut microvasculature
and edema (Figure 1). In the following sections we describe the mechanisms that lead to
diarrhea whenever data are available.

PATOPHISIOLOGY

Diarrhea is the reversal of the normal net absorptive status of water and electrolyte
absorption to secretion. Such a derangement can be the result of either an osmotic force that
acts in the lumen to drive water into the gut or the result of an active secre-tory state induced
in the enterocytes. In the former case, diarrhea is osmolar in nature, as is observed after the
ingestion of nonabsorbable sugars such as lactulose or lactose in lactose malabsorbers.
Instead, in the typical active secretory state, enhanced anion secretion (mostly by the crypt
cell compartment) is best exemplified by enterotoxin--induced diarrhea.

In osmotic diarrhea, stool output is proportional to the intake of the unabsorbable

substrate and is usually not massive; diarrheal stools promptly regress with discontinuation of
the offending nutrient, and the stool ion gap is high, exceeding 100 mOsm/kg. In fact, the
fecal osmolality in this circumstance is accounted for not only by the electrolytes but also by
the unabsorbed nutrient(s) and their degradation products. The ion gap is obtained by
subtracting the concentration of the elec-trolytes from total osmolality (assumed to be 290
mOsm/kg), according to the formula: ion gap = 290 – [(Na + K) × 2].

In secretory diarrhea, the epithelial cells’ ion transport processes are turned into a
state of active secretion. The most common cause of acute-onset secretory diarrhea is a

21
bacterial infection of the gut. Several mechanisms may be at work. After colonization, enteric
pathogens may adhere to or invade the epithelium; they may produce enterotoxins (exotoxins
that elicit secretion by increasing an intracellular second messenger) or cytotoxins. They may
also trigger release of cytokines attracting inflammatory cells, which, in turn, contribute to
the acti-vated secretion by inducing the release of agents such as prostaglandins or platelet-
activating factor. Features of secretory diarrhea include a high purg-ing rate, a lack of
response to fasting, and a normal stool ion gap (ie, 100 mOsm/kg or less), indicating that
nutrient absorption is intact.

CLINICAL MANIFESTATION

Most of the clinical manifestations and clinical syndromes of diarrhea are related to
the infecting pathogen and the dose orinoculum. Additional manifestations depend on the
development of complications (e.g., dehydration and electrolyte imbalance) and the nature of
the infecting pathogen. Usually the ingestion of preformed toxins (e.g., those of S. aureus) is
associated with the rapid onset of nausea and vomiting within 6 hr, with possible fever,
abdominal cramps, and diarrhea within 8-72 hr. Watery diarrhea and abdominal cramps after
an 8-16 hr incubation period are associated with enterotoxin-producing C. perfringens and B.
cereus. Abdominal cramps and watery diarrhea after a 16-48 hr incubation period can be
associated with noroviruses, several enterotoxin-producing bacteria, Cryptosporidium, and
Cyclospora and have also been a notable feature of influenza virus H1N1 infections. Several
organisms, including Salmonella, Shigella, C. jejuni, Yersinia enterocolitica, enteroinvasive
or hemorrhagic (Shigatoxin-producing) E. coli, and V. parahaemolyticus, produce diarrhea
that can contain blood as well as fecal leukocytes in association with abdominal cramps,
tenesmus, and fever; these features suggest bacterial dysentery and fever. Bloody diarrhea
and abdominal cramps after a 72-120 hr incubation period are associated with infections due
to Shigella and also Shigatoxin-producing E. coli, such as E. coli O157:H7. Organisms
associated with dysentery or hemorrhagic diarrhea can also cause watery diarrhea alone
without fever or that precedes a more complicated course that results in dysentery. Although
many of the manifestations of acute gastroenteritis in children are nonspecific, some clinical
features can help identify major categories of diarrhea and allow rapid triage for antibiotic or
specific dietary therapy. There is considerable overlap in the symptomatology. The positive
predictive values for the features of dysentery are very poor; the negative predictability for
bacterial pathogens is much better in the absence of signs of dysentery. If warranted and if
facilities and resources permit, the etiology can be verified by appropriate laboratory testing.3

22
 Clinical features sometimes provide a clue to the cause. Diarrhea caused by small
intestine disease is typically high volume, watery, and often associated with malabsorption.
Dehydration is frequent. Diarrhea caused by colonic involvement is more often associated
with frequent small-volume stools, the presence of blood, and a sensation of urgency.

Important factors in evaluating acute diarrhea include travel and animal exposure
history, sources of water (e.g., well water), recent food intake, history of profuse diarrheal
episodes, history of recent antibiotic treatment, dehydration, fever, hematochezia, nausea,
vomiting, and abdominal pain. Important clinical features include: abrupt versus gradual
onset of symptoms, symptom duration, including bowel movement frequency, stool
quantities, dysentery with fever, tenesmus, hematochezia or pus in the stool, signs of volume
depletion (including thirst, tachycardia,and orthostasis), decreased urine output, skin turgor,
and lethargy or confusion.

Patients ingesting toxins or those with toxigenic infection typically have nausea and
vomiting as prominent symptoms, along with watery diarrhea but rarely have a high fever.
Vomiting that begins within 6 hours of ingesting a food should suggest food poisoning
caused by preformed toxin from bacteria such as S. aureus or B. cereus. If diarrhea disease
begins within 8-14 hours of food ingestion, C. perfringens should be suspected. When the
incubation period is longer than 14 hours and vomiting is also a significant symptom,
accompanied by diarrhea, viral agents should be considered. Parasites that do not invade the
intestinal mucosa, such asGiardia lamblia and Cryptosporidium, usually cause only mild
abdominal discomfort. Giardiasis may be associated with mild steatorrhea, gaseousness, and
bloating.

Infection with invasive bacteria such as Campylobacter, Salmonella,

and Shigella spp., and organisms that produce cytotoxins, such as C. difficile and
enterohemorrhagic E. coli (serotype O157:H7), often result in abdominal pain, and low-grade
fever; occasionally, peritoneal signs may suggest a surgical abdomen.Yersinia organisms
often infect the terminal ileum and cecum and manifest with right lower quadrant pain and
tenderness suggesting acute appendicitis.

Hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura can occur in

infections with enterohemorrhagic E. coli and Shigella organisms, particularly in young

23
children and older adults. Yersinia infection and other enteric bacterial infections may be
accompanied by Reiter's syndrome (arthritis, urethritis, and conjunctivitis), thyroiditis,
pericarditis, or glomerulonephritis. Enteric fever, caused by Salmonella typhi or Salmonella
paratyphi, is a severe systemic illness manifested initially by prolonged high fevers,
prostration, confusion, and respiratory symptoms, followed by abdominal tenderness,
diarrhea, and rash.

Epidemiologic risk factors should be investigated for certain diarrheal diseases and
their spread. These risk factors include: recent travel to an underdeveloped area, daycare
center exposure, consumption of raw meat, eggs, shellfish, and unpasteurized milk products,
contact with reptiles or pets with diarrhea, a history of other ill people in a shared dormitory
facility, recent antibiotic use, and a history of HIV or medically induced immunosuppression.
In cases of homosexual males, in addition to immunosuppression, there are two other disease
transmission routes that lead to an increased susceptibility to infectious agents that cause
diarrhea. These include an increased rate of fecal-oral transmission of all infectious agents
spread by this route, including Shigella, Salmonella, Campylobacter, and intestinal protozoa
and anal intercourse. Anal intercourse can lead to a direct rectal inoculation, resulting in
proctitis associated with rectal pain, tenesmus, and passage of small-volume, bloody, mucous
stoolsClinical features sometimes provide a clue to the cause. Diarrhea caused by small
intestine disease is typically high volume, watery, and often associated with malabsorption.
Dehydration is frequent. Diarrhea caused by colonic involvement is more often associated
with frequent small-volume stools, the presence of blood, and a sensation of urgency.

Important factors in evaluating acute diarrhea include travel and animal exposure
history, sources of water (e.g., well water), recent food intake, history of profuse diarrheal
episodes, history of recent antibiotic treatment, dehydration, fever, hematochezia, nausea,
vomiting, and abdominal pain. Important clinical features include: abrupt versus gradual
onset of symptoms, symptom duration, including bowel movement frequency, stool
quantities, dysentery with fever, tenesmus, hematochezia or pus in the stool, signs of volume
depletion (including thirst, tachycardia,and orthostasis), decreased urine output, skin turgor,
and lethargy or confusion.

Patients ingesting toxins or those with toxigenic infection typically have nausea and
vomiting as prominent symptoms, along with watery diarrhea but rarely have a high fever.

24
Vomiting that begins within 6 hours of ingesting a food should suggest food poisoning
caused by preformed toxin from bacteria such as S. aureus or B. cereus. If diarrhea disease
begins within 8-14 hours of food ingestion, C. perfringens should be suspected. When the
incubation period is longer than 14 hours and vomiting is also a significant symptom,
accompanied by diarrhea, viral agents should be considered. Parasites that do not invade the
intestinal mucosa, such asGiardia lamblia and Cryptosporidium, usually cause only mild
abdominal discomfort. Giardiasis may be associated with mild steatorrhea, gaseousness, and
bloating.

Infection with invasive bacteria such as Campylobacter, Salmonella,

and Shigella spp., and organisms that produce cytotoxins, such as C. difficile and
enterohemorrhagic E. coli (serotype O157:H7), often result in abdominal pain, and low-grade
fever; occasionally, peritoneal signs may suggest a surgical abdomen.Yersinia organisms
often infect the terminal ileum and cecum and manifest with right lower quadrant pain and
tenderness suggesting acute appendicitis.

Hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura can occur in

infections with enterohemorrhagic E. coli and Shigella organisms, particularly in young
children and older adults. Yersinia infection and other enteric bacterial infections may be
accompanied by Reiter's syndrome (arthritis, urethritis, and conjunctivitis), thyroiditis,
pericarditis, or glomerulonephritis. Enteric fever, caused by Salmonella typhi or Salmonella
paratyphi, is a severe systemic illness manifested initially by prolonged high fevers,
prostration, confusion, and respiratory symptoms, followed by abdominal tenderness,
diarrhea, and rash.

Epidemiologic risk factors should be investigated for certain diarrheal diseases and
their spread. These risk factors include: recent travel to an underdeveloped area, daycare
center exposure, consumption of raw meat, eggs, shellfish, and unpasteurized milk products,
contact with reptiles or pets with diarrhea, a history of other ill people in a shared dormitory
facility, recent antibiotic use, and a history of HIV or medically induced immunosuppression.
In cases of homosexual males, in addition to immunosuppression, there are two other disease
transmission routes that lead to an increased susceptibility to infectious agents that cause
diarrhea. These include an increased rate of fecal-oral transmission of all infectious agents
spread by this route, including Shigella, Salmonella, Campylobacter, and intestinal protozoa

25
and anal intercourse. Anal intercourse can lead to a direct rectal inoculation, resulting in
proctitis associated with rectal pain, tenesmus, and passage of small-volume, bloody, mucous
stools.

DIAGNOSIS

The most important diagnostic step is clinical assessment of the degree of

dehydration. The further diagnostic evaluation concerns the potential complications or
differential diagnoses that may lie behind the clinical presentation of infectious enteritis.
Good history-taking and physical examination is the foundation of the diagnostic evaluation.
In severe cases, when complications arise, or when the diagnosis is in doubt, further studies
must be performed.

History

History-taking should follow a structured procedure, as the information obtained will

largely determine the further diagnostic and therapeutic measures to be taken. It helps, for
example, to use a questionnaire of the type developed at the Dr. von Hauner Children's
Hospital in Munich (Box), which is filled out in the walk-in emergency service either by the
parents themselves or else by the physician on the basis of their verbal responses. The most
important pieces of information concern the onset and frequency of diarrhea and vomiting,
the intake offluids and food, urine production, and fever. The parents are asked about the
child's intake of medications, any preexisting illnesses (e.g., metabolic or intestinal conditions
or disorders of immunity), and any possible exposures resulting from recent travel abroad,
hospitalization, or contact with ill persons. If the patient has bloody stool and there is
suspicion of a bacterial infection, particularly one caused by enterohemorrhagic E. coli
(EHEC), the parents should be asked about the consumption of unpasteurized milk or
uncooked meat and possible contact with cows.

Physical examination

Every child should be examined and weighed with clothes off. The extent of
dehydration and fluid loss can be estimated (Table).

Further diagnostic testing

Astool sample should be sent for culture only if the findings will have clinical
consequences. This is not the case for most children with infectious enteritis in Germany. The

26
yield of positive determinations is low, while thecost of such studies is high. The
demonstration of viruses and most types of bacteria causing enteritis would be of no
therapeutic consequence for the individual patient. The results of a stool culture are often not
available until two to three days after the sample is obtained, by which time the diarrhea has
usually improved or resolved. Nonetheless, a search for the causative organism by culture,
direct demonstration of an antigen or toxin, or molecular genetic methods is recommended in
the following situations:

- Nosocomial infection in hospitalized patients, i.e., onset of diarrhea more than three
days after admission
- Severe course, with an estimated loss of more than 9% of total body weight
- Bloody diarrhea
- Recent travel to high-risk countries (Africa, Asia, Central and South America)
- Congenital or acquired immune deficiency or immunosuppressive therapy
- Suspected Clostridium difficile colitis or hemolyticuremic syndrome
- Infants under 4 months of age, particularly prematurely born infants
- Other ill persons in the child's environment, with suspicion of food poisoning
- Persistent diarrhea (for more than two weeks), if a positive result might lead to the
administration of antibiotics.

Blood tests are generally not necessary in cases of mild or moderate dehydration,
because the results do not influence the treatment (oral rehydration and feeding). Viral and
bacterial causation cannot be distinguished from each other reliably on the basis of
inflammatory parameters such as the C-reactive protein and the erythrocyte sedimentation
rate. Blood tests are indicated for severely dehydrated patients and/or those who will undergo
IVrehydration. These should include a complete blood count, acid-base status, glucose,
electrolytes, creatinine, and blood urea nitrogen. The urine output should be monitored in all
patients with severe dehydration, impaired renal function, or suspected infection with
enterohemorrhagic E. coli (EHEC).

DIFFERENTIAL DIAGNOSIS

- Appendicitis
- Carcinoid Tumor
- Giardiasis
- Glucose-galactose malabsorption

27
 - Intestinal Enterokinase Deficiency
- Intestinal Protozoal Diseases
- Intussusception
- Meckel Diverticulum Imaging
- Microvillus Inclusion Disease
- Pediatric Crohn Disease
- Pediatric Hyperthyroidism
- Pediatric Irritable Bowel Syndrome
- Pediatric Malabsorption Syndromes
- Pediatric Short Bowel Syndrome
- Protein Intolerance
- Shigella Infection
- Sinonasal Manifestations of Cystic Fibrosis
- Ulcerative Colitis Imaging6

TREATMENT

Treatment Plan A

Home therapy to prevent dehydration and malnutrition

Children with no signs of dehydration need extra fluids and salt to replace their losses
of water and electrolytes due to diarrhoea. If these are not given, signs of dehydration may
develop. Mothers should be taught how to prevent dehydration at home by giving the child
more fluid than usual, how to prevent malnutrition by continuing to feed the child, and why
these actions are important. They should also know what signs indicate that the child should
be taken to a health worker. These steps are summarized in the four rules of Treatment Plan
A:

Rule 1: Give the child more fluids than usual, to prevent dehydration

Many countries have designated recommended home fluids. Wherever possible, these
should include at least one fluid that normally contains salt. Plain clean water should also be
given. Other fluids should be recommended that are frequently given to children in the area,
that mothers consider acceptable for children with diarrhoea, and that mothers would be
likely to give in increased amounts when advised to do so.

28
 Most fluids that a child normally takes can be used. It is helpful to divide suitable
fluids into two groups:

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 diarrhoea 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 given.

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
- Green coconut water
- Weak tea (unsweetened)
- Unsweetened fresh fruit juice.

A few fluids are potentially dangerous and should be avoided during diarrhoea. Especially
important are drinks sweetened with sugar, which can cause osmotic diarrhoea 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 infusions.

29
The general rule is: give as much fluid as the child or adult wants until diarrhoea stops. As a
guide, after each loose stool, give:

- Children under 2 years of age: 50-100 ml (a quarter to half a large cup) of fluid;
- Children aged 2 up to 10 years: 100-200 ml (a half to one large cup);
- Older children and adults: as much fluid as they want.

Rule 2: Give supplemental zinc (10 - 20 mg) to the child, every day for 10 to 14 days Zinc
can be given as a syrup or as dispersible tablets, whichever formulation is available and
affordable. By giving zinc as soon as diarrhoea 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 diarrhoea is fully replaced and the risk of the child having
new episodes of diarrhoea in the following 2 to 3 months is reduced.

Rule 3: Continue to feed the child, to prevent malnutrition The infant usual diet should be
continued during diarrhoea 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
diarrhoea regain their appetite after dehydration is corrected, whereas those with bloody
diarrhoea 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 diarrhoea of longer duration, and recover intestinal
function more slowly.

What foods to give This depends on the child's age, food preferences and pre-illness feeding
pattern; cultural practices are also important. In general, foods suitable for a child with
diarrhoea are the same as those required by healthy children. Specific recommendations are
given below.

Milk

- Infants of any age who are breastfed should be allowed to breastfeed as often and as
long as they want. Infants will often breastfeed more than usual; this should be
encouraged.

30
 - Infants who are not breastfed should be given their usual milk feed (or formula) at
least every three hours, if possible by cup. Special commercial formulas advertised for
use in diarrhoea are expensive and unnecessary; they should not be given routinely.
Clinically significant milk intolerance is rarely a problem.
- Infants below 6 months of age who take breastmilk and other foods should receive
increased breastfeeding. As the child recovers and the supply of breastmilk increases,
other foods should be decreased. (If fluids other than breastmilk are given, use a cup,
not a bottle.) This usually takes about one week. If possible, the infant should become
exclusively breastfed.

There is no value in routinely testing the stools of infants for pH or reducing substances. Such
tests are oversensitive, often indicating impaired absorption of lactose when it is not clinically
important. It is more important to monitor the child's clinical response (e.g. weight gain,
general improvement). Milk intolerance is only clinically important when milk feeding
causes a prompt increase in stool volume and a return or worsening of the signs of
dehydration, often with loss of weight.

Other foods

If the child is at least 6 months old or is already taking soft foods, he or she should be given
cereals, vegetables and other foods, in addition to milk. If the child is over 6 months and such
foods are not yet being given, they should be started during the diarrhoea episode or soon
after it stops.

Recommended foods should be culturally acceptable, readily available, have a high content
of energy and provide adequate amounts of essential micronutrients. They should be well
cooked, and mashed or ground to make them easy to digest; fermented foods are also easy to
digest. Milk should be mixed with a cereal. If possible, 5-10 ml of vegetable oil should be
added to each serving of cereal7. Meat, fish or egg should be given, if available. Foods rich in
potassium, such as bananas, green coconut water and fresh fruit juice are beneficial.

How much food and how often

Offer the child food every three or four hours (six times a day). Frequent, small feedings are
tolerated better than less frequent, large ones.

31
After the diarrhoea stops, continue giving the same energy-rich foods and provide one more
meal than usual each day for at least two weeks. If the child is malnourished, extra meals
should be given until the child has regained normal weight-for-height.

Rule 4: Take the child to a health worker if there are signs of dehydration or other problems

The mother should take her child to a health worker if the child:

- Starts to pass many watery stools;

- Has repeated vomiting;
- Becomes very thirsty;
- Is eating or drinking poorly;
- Develops a fever;
- Has blood in the stool; or
- The child does not get better in three days.5

Treatment Plan B

Oral rehydration therapy for children with some dehydration

Children with some dehydration should receive oral rehydration therapy (ORT) with
ORS solution in a health facility following Treatment Plan B, as described below. Children
with some dehydration should also receive zinc supplementation as described above.

32
 If the child's weight is known, this should be used to determine the approximate
amount of solution needed. The amount may also be estimated by multiplying the child's
weight in kg times 75 ml. If the child's weight is not known, select the approximate amount
according to the child's age.

The exact amount of solution required will depend on the child's dehydration status.
Children with more marked signs of dehydration, or who continue to pass frequent watery
stools, will require more solution than those with less marked signs or who are not passing
frequent stools. If a child wants more than the estimated amount of ORS solution, and there
are no signs of over-hydration, give more.

Oedematous (puffy) eyelids are a sign of over-hydration. If this occurs, stop giving
ORS solution, but give breastmilk or plain water, and food. Do not give a diuretic. When the
oedema has gone, resume giving ORS solution or home fluids according to Treatment Plan
A.

A family member should be taught to prepare and give ORS solution. The solution
should be given to infants and young children using a clean spoon or cup. Feeding bottles
should not be used. For babies, a dropper or syringe (without the needle) can be used to put
small amounts of solution into the mouth. Children under 2 years of age should be offered a
teaspoonful every 1-2 minutes; older children (and adults) may take frequent sips directly
from the cup.

Vomiting often occurs during the first hour or two of treatment, especially when
children drink the solution too quickly, but this rarely prevents successful oral rehydration
since most of the fluid is absorbed. After this time vomiting usually stops. If the child vomits,
wait 5-10 minutes and then start giving ORS solution again, but more slowly (e.g. a spoonful
every 2-3 minutes).

Monitoring the progress of oral rehydration therapy Check the child from time to time
during rehydration to ensure that ORS solution is being taken satisfactorily and that signs of
dehydration are not worsening. If at any time the child develops signs of severe dehydration,
shift to Treatment Plan C.

After four hours, reassess the child fully, following the guidelines in Table 1. Then decide
what treatment to give next:

33
 - If signs of severe dehydration have appeared, intravenous (IV) therapy should be
started following Treatment Plan C. This is very unusual, however, occurring only in
children who drink ORS solution poorly and pass large watery stools frequently
during the rehydration period.
- If the child still has signs indicating some dehydration, continue oral rehydration
therapy by repeating Treatment Plan B. At the same time start to offer food, milk and
other fluids, as described in Treatment Plan A, and continue to reassess the child
frequently.
- If there are no signs of dehydration, the child should be considered fully rehydrated.
When rehydration is complete:
 the skin pinch is normal;
 thirst has subsided;
 urine is passed;
 the child becomes quiet, is no longer irritable and often falls asleep.

Teach the mother how to treat her child at home with ORS solution and food
following Treatment Plan A. Give her enough ORS packets for two days. Also teach her the
signs that mean she should bring her child back.

Meeting normal fluid needs While treatment to replace the existing water and electrolyte
deficit is in progress the child's normal daily fluid requirements must also be met. This can be
done as follows:

- Breastfed infants: Continue to breastfeed as often and as long as the infant wants,
even during oral rehydration.
- Non breastfed infants under 6 months of age: If using the old WHO ORS solution
containing 90 mmol/L of sodium, also give 100-200ml clean water during this period.
However, if using the new reduced (low) osmolarity ORS solution containing
75mmol/L of sodium, this is not necessary. After completing rehydration, resume full
strength milk (or formula) feeds. Give water and other fluids usually taken by the
infant.
- Older children and adults: Throughout rehydration and maintenance therapy, offer as
much plain water to drink as they wish, in addition to ORS solution.

If oral rehydration therapy must be interrupted If the mother and child must leave before
rehydration with ORS solution is completed:

34
 - show the mother how much ORS solution to give to finish the four-hour treatment at
home;
- give her enough ORS packets to complete the four hour treatment and to continue oral
rehydration for two more days, as shown in Treatment Plan A;
- show her how to prepare ORS solution;
- teach her the four rules in Treatment Plan A for treating her child at home.

When oral rehydration failS, With the previous ORS, signs of dehydration would persist
or reappear during ORT in about 5% of children. With the new reduced (low) osmolarity
ORS, it is estimated that such treatment “failures” will be reduced to 3%, or less. The usual
causes for these “failures” are:

- continuing rapid stool loss (more than 15-20 ml/kg/hour), as occurs in some children
with cholera;
- insufficient intake of ORS solution owing to fatigue or lethargy;
- frequent, severe vomiting.

Such children should be given ORS solution by nasogastric (NG) tube or Ringer's Lactate
Solution intravenously (IV) (75 ml/kg in four hours), usually in hospital. After confirming
that the signs of dehydration have improved, it is usually possible to resume ORT
successfully.

Rarely, ORT should not be given. This is true for children with:

- abdominal distension with paralytic ileus, which may be caused by opiate drugs (e.g.
codeine, loperamide) and hypokalaemia;
- glucose malabsorption, indicated by a marked increase in stool output when ORS
solution is given, failure of the signs of dehydration to improve and a large amount of
glucose in the stool when ORS solution is given.

In these situations, rehydration should be given IV until diarrhoea subsides; NG therapy

should not be used.

Begin to give supplemental zinc, as in Treatment Plan A, as soon the child is able to
eat following the initial fourhour rehydration period.

Giving food Except for breastmilk, food should not be given during the initial four-
hour rehydration period. However, children continued on Treatment Plan B longer than four

35
hours should be given some food every 3-4 hours as described in Treatment Plan A. All
children older than 6 months should be given some food before being sent home. This helps
to emphasize to mothers the importance of continued feeding during diarrhoea.

Treatment Plan C

For patients with severe dehydration

The preferred treatment for children with severe dehydration is rapid intravenous
rehydration, following Treatment Plan C. If possible, the child should be admitted to hospital.
Guidelines for intravenous rehydration are given in Table 3.

Children who can drink, even poorly, should be given ORS solution by mouth until
the IV drip is running. In addition, all children should start to receive some ORS solution
(about 5 ml/kg/h) when they can drink without difficulty, which is usually within 3-4 hours
(for infants) or 1-2 hours (for older patients). This provides additional base and potassium,
which may not be adequately supplied by the IV fluid.

Patients should be reassessed every 15-30 minutes until a strong radial pulse is
present. Thereafter, they should be reassessed at least every hour to confirm that hydration is
improving. If it is not, the IV drip should be given more rapidly.

When the planned amount of IV fluid has been given (after three hours for older
patients, or six hours for infants), the child's hydration status should be reassessed fully, as
shown in Table 1.

Look and feel for all the signs of dehydration:

36
 - If signs of severe dehydration are still present, repeat the IV fluid infusion as outlined
in Treatment Plan C. This is very unusual, however, occurring only in children who
pass large watery stools frequently during the rehydration period.
- If the child is improving (able to drink) but still shows signs of some dehydration,
discontinue the IV infusion and give ORS solution for four hours, as specified in
Treatment Plan B.
- If there are no signs of dehydration, follow Treatment Plan A. If possible, observe the
child for at least six hours before discharge while the mother gives the child ORS
solution, to confirm that she is able to maintain the child's hydration. Remember that
the child will require therapy with ORS solution until diarrhoea stops.

If the child cannot remain at the treatment centre, teach the mother how to give treatment
at home following Treatment Plan A, give her enough ORS packets for two days and teach
her the signs that mean she should bring her child back.

If IV therapy is not available at the facility, but can be given nearby (i.e. within 30
minutes), send the child immediately for IV treatment. If the child can drink, give the mother
some ORS solution and show her how to give it to her child during the journey.

If IV therapy is not available nearby, health workers who have been trained can give ORS
solution by NG tube, at a rate of 20 ml/kg body weight per hour for six hours (total of 120
ml/kg body weight). If the abdomen becomes swollen, ORS solution should be given more
slowly until it becomes less distended.

If NG treatment is not possible but the child can drink, ORS solution should be given
by mouth at a rate of 20 ml/kg body weight per hour for six hours (total of 120 ml/kg body
weight). If this rate is too fast, the child may vomit repeatedly. In that case, give ORS
solution more slowly until vomiting subsides.

Children receiving NG or oral therapy should be reassessed at least every hour. If the
signs of dehydration do not improve after three hours, the child must be taken immediately to
the nearest facility where IV therapy is available. Otherwise, if rehydration is progressing
satisfactorily, the child should be reassessed after six hours and a decision on further
treatment made as described above for those given IV therapy.

If neither NG nor oral therapy is possible, the child should be taken immediately to the
nearest facility where IV or NG therapy is available.

37
Electrolyte disturbances

Knowing the levels of serum electrolytes rarely changes the management of children
with diarrhoea. Indeed, these values are often misinterpreted, leading to inappropriate
treatment. It is usually not helpful to measure serum electrolytes. The disorders described
below are all adequately treated by ORT with ORS solution.

Hypernatraemia

Some children with diarrhoea develop hypernatraemic dehydration, especially when

given drinks that are hypertonic owing to their excessive content of sugar (e.g. soft drinks,
commercial fruit drinks, too concentrated infant formula) or salt. These draw water from the
child's tissues and blood into the bowel, causing the concentration of sodium in extra-cellular
fluid to rise. If the solute in the drink is not fully absorbed, the water remains in the bowel,
causing osmotic diarrhoea.

Children with hypernatraemic dehydration (serum Na >150 mmol/l) have thirst that is
out of proportion to other signs of dehydration. Their most serious problem is convulsions,
which usually occur when the serum sodium concentration exceeds 165 mmol/l, and
especially when IV therapy is given. Seizures are much less likely when hypernatraemia is
treated with ORS solution, which usually causes the serum sodium concentration to become
normal within 24 hours.

Hyponatraemia

Children with diarrhoea who drink mostly water, or watery drinks that contain little
salt, may develop hyponatraemia (serum Na <130 mmol/l). Hyponatraemia is especially
common in children with shigellosis and in severely malnourished children with oedema.
Severe hyponatraemia can be associated with lethargy and, less often, seizures. ORS solution
is safe and effective therapy for nearly all children with hyponatraemia. An exception is
children with oedema for whom ORS solution provides too much sodium.

Hypokalaemia

Inadequate replacement of potassium losses during diarrhoea can lead to potassium

depletion and hypokalaemia (serum K+ <3 mmol/l), especially in children with malnutrition.
This can cause muscle weakness, paralytic ileus, impaired kidney function and cardiac
arrhythmia. Hypokalaemia is worsened when base (bicarbonate or lactate) is given to treat

38
acidosis without simultaneously providing potassium. Hypokalaemia can be prevented, and
the potassium deficit corrected, by using ORS solution for rehydration therapy and by giving
foods rich in potassium during diarrhoea and after it has stopped.5

COMPLICATION

- 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
- 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.

HUS is caused by damage to vascular endothelial cells by verotoxin (released by

enterohemorrhagic E coli and by Shigella organisms). Thrombocytopenia, microangiopathic
hemolytic anemia, and acute renal failure characterize HUS. Symptoms usually develop one
week after onset of diarrhea, when the organism may be absent.

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RS can complicate acute infections and is characterized by arthritis, urethritis, conjunctivitis,
and mucocutaneous lesions. Individuals with RS usually do not demonstrate all features.

Carrier states are observed after some bacterial infections.

- After diarrhea caused by Salmonella organisms, 1-4% of individuals with nontyphoid

and enteric fever infections become carriers. The carrier stage
forSalmonella organisms is more likely for females, infants, and individuals with
biliary tract disease.
- Asymptomatic C difficile carriage may be observed in as many as 20% of hospitalized
patients receiving antibiotics and in 50% of infants.
- Rotavirus is excreted asymptomatically in feces of children who were previously
infected, typically for as long as 1-2 weeks.

PROGNOSIS

In developed countries, with proper management, prognosis is very good. However, data
show an increase in diarrhea-associated deaths among US children from the mid-1980s
through 2006. During 2005-2007, 1087 diarrhea-associated infant deaths were reported with
86% of deaths occurring among low birthweight (< 2500g) infants. Risk factors for these
infants included male sex, black race, and low 5-minute Apgar score (< 7).

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.6

PREVENTION

In many developed countries, diarrhea due to pathogens such as C. botulinum, E. coli

O157:H7, Salmonella, Shigella, V. cholerae, Cryptosporidium, and Cyclospora is a notifiable
disease and, thus, contact tracing and source identification is important in preventing
outbreaks.

40
 Many developing countries struggle with huge disease burdens of diarrhea where a
wider approach to diarrhea prevention may be required. Preventive strategies may be of
relevance to both developed and developing countries.

Promotion of Exclusive Breast-feeding

Exclusive breast-feeding (administration of no other fluids or foods for the 1st 6 mo

of life) is not common, especially in many developed countries. Exclusive breast-feeding
protects very young infants from diarrheal disease through the promotion of passive
immunity and through reduction in the intake of potentially contaminated food and water.
Breast milk contains all the nutrients needed in early infancy, and when continued during
diarrhea, it also diminishes the adverse impact on nutritional status. Exclusive breast-feeding
for the first 6 mo of life is widely regarded as one of the most effective interventions to
reduce the risk of premature childhood mortality and the potential to prevent 13% of all
deaths of children <5 yr of age. Improved Complementary Feeding Practices There is a
strong inverse association between appropriate, safe complementary feeding and mortality in
children age 6-11 mo; malnutrition is an independent risk for the frequency and severity of
diarrheal illness. Complementary foods should be introduced at 6 mo of age, and breast-
feeding should continue for up to 1 yr (longer period for developing countries).
Complementary foods in developing countries are generally poor in quality and often are
heavily contaminated, thus predisposing to diarrhea. Contamination of complementary foods
can be potentially reduced through caregivers’ education and improving home food storage.
Improved vitamin A status has been shown to reduce the frequency of severe diarrhea.
Vitamin A supplementation reduces all-cause childhood mortality by 21% and diarrhea-
specific mortality by 31% (95% CI, 17-42%).

Rotavirus Immunization

Most infants acquire rotavirus diarrhea early in life; an effective rotavirus vaccine
would have a major effect on reducing diarrhea mortality in developing countries. In 1998, a
quadrivalent Rhesus rotavirus-derived vaccine was licensed in the United States but
subsequently withdrawn due to an increased risk of intussusception. Subsequent development
and testing of newer rotavirus vaccines have led to their introduction in most developed
countries and approval by the WHO in 2009 for widespread use in developing countries.
Emerging evidence indicates that the introduction of these vaccines is associated with a

41
significant reduction in severe diarrhea and associated mortality. The institution of large-scale
rotavirus vaccination programs has led to major reduction in the burden of disease and
associated mortality. In an evaluation of large-scale rotavirus vaccine introduction, coverage
rate of 74% was achieved in infants <12 mo of age, with 41% reduction (95% CI, 36-47%) in
diarrhearelated mortality. In an evaluation of the vaccine in Africa, overall protective efficacy
against rotavirus gastroenteritis ranged from 49% to 61%, with 30% protective efficacy
against all-cause severe gastroenteritis in infancy. Vaccine (live virus) associated rotavirus
infection has been reported in children with severe combined immunodeficiency disease.
Other vaccines that could potentially reduce the burden of severe diarrhea and mortality in
young children are vaccines against Shigella and ETEC.

Improved Water and Sanitary Facilities and Promotion of Personal and Domestic
Hygiene

Much of the reduction in diarrhea prevalence in the developed world is the result of
improvement in standards of hygiene, sanitation, and water supply. Strikingly, an estimated
88% of all diarrheal deaths worldwide can be attributed to unsafe water, inadequate
sanitation, and poor hygiene. Improved sanitation across a range of studies has been shown to
reduce the incidence of diarrhea by 36%. In addition, routine handwashing with plain soap in
the home can reduce the incidence of diarrhea in all environments. Behavioral change
strategies through promotion of handwashing indicate that handwashing promotion and
access to soap reduces the burden of diarrhea in developing countries.

Improved Case Management of Diarrhea

Improved management of diarrhea through prompt identification and appropriate

therapy significantly reduces diarrhea duration, its nutritional penalty, and risk of death in
childhood. Improved management of acute diarrhea is a key factor in reducing the burden of
prolonged episodes and persistent diarrhea. The WHO/ UNICEF recommendations to use
low-osmolality ORS and zinc supplementation for the management of diarrhea, coupled with
selective and appropriate use of antibiotics, have the potential to reduce the number of
diarrheal deaths among children. A recent estimate indicated that 22% of all deaths of
children <5 yr of age could be prevented by optimal use of ORS, zinc supplements, and
antibiotics for dysentery.3

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 SECTION III
CONCLUTION

Diarrhea is the passage of loose or watery stools at least 3 times in a 24 hour period.
However, it is the consistency of the stools rather than the number that is most important.
Acute diarrhea may be caused by different viruses, bacteria, and parasites. It is most practical
to base the treatment of diarrhea on the clinical type of the illness, which is easy to establish
when a child is first examined. Usually there is no need for laboratory tests.

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1. Koletzko, Sibylle., Stephanie Osterrieder. 2009. Acute Infectious Diarrhea in

Children. Deutsches Ärzteblatt International; 106(33): 539–48
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Diagnosis and treatment of severely malnourished children with diarrhoea. Journal of
Paediatrics and Child Health 51 (2015) 387–395.
3. Yu, Clifton., Douglass llougee., Jorge R. Murno. Diarrhea and Dehydration. Module
6.
4. Robert Kliegman, Bonita Stanton, Joseph St. Geme, Nina Schor. Nelson Textbook
of Pediatrics, 2-Volume Set, 20th Edition from
5. Elliott, Elizabeth J., Jacqueline R Dalby-Payne. 2004. Acute infectious diarrhoea and
dehydration in children Volume 181.
6. Stefano Guandalini, MD. 2015. Diarrhea Follow-up. From :
http://emedicine.medscape.com/article/928598-followup#e5
7. MB Peddle MD. 2008. Clinical corner. Paediatr Child Health Vol 13 No 5.

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