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Page 1: Lapkas anak campur

Chapter 1

Introduction

The term gastroenteritis denotes infections of the gastrointestinal (GI) tract caused by bacterial, viral, or parasitic pathogens Many of these infections are foodborne illnesses. The most common manifestations are diarrhea and vomiting,which can also be associated with systemic features such as abdominal pain and fever. The term gastroenteritis captures the bulk of infectious cases of diarrhea. The term diarrheal disorders is more commonly used to denote infectious diarrhea in public health settings, although several noninfectious causes of GI illness with vomiting and/or diarrhea are well recognized.

Diarrheal disorders in childhood account for a large proportion (18%) of childhood

deaths, with an estimated 1.5 million deaths per year globally, making it the second most

common cause of child deaths worldwide. The World Health Organization (WHO) and

UNICEF estimate that almost 2.5 billion episodes of diarrhea occur annually in children < 5

yr of age in developing countries, with more than 80% of the episodes occurring in Africa

and South Asia (46% and 38%, respectively). Global mortality may be declining, but the

overall incidence of diarrhea remains unchanged at about 3.6 episodes per child-year ( Fig.

332-1 ), and it is estimated to account for 13% of all childhood disabilityadjusted life years

(DALYs).

The relationship between infection and malnutrition is bidirectional. Infection

adversely affects nutritional status through reductions in dietary intake and intestinal

absorption, increased catabolism and sequestration of nutrients that are required for tissue

synthesis and growth.On the other hand, malnutrition can predispose to infection because of

its negative impact on the barrier protection afforded by the skin and mucous membranes and

by inducing alterations in host immune function

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Chapter 2

Literature Review

A. Definition

Gastroenteritis is a condition of wasting stool that is not normal or usual,

marked by increased volumes, dilution, as well as the frequency is more than 3

times and in neonates more than 4 times a day with or without mucus blood

(Hidayat, 2013: 12).

Gastroenteritis is a state of the frequency of bowel movements more than 4

times in infants and more than 3 times in children, watery stool consistency, can

be green or mixed with mucus and blood or mucus only (Ngastiyah, 2005: 224)

Gastroenteritis is inflammation of the stomach and intestines caused by a

variety of bacterial, viral, and parasitic pathogens (Wong, 2014: 492)

From some understanding of the above, it can be concluded that

gastroenteritis is a condition in which inflammation of the stomach and intestine

characterized by the frequency of bowel movements in neonates more than 4

times a day, and the child is more than 3 times a day with stool consistency

watery, with or without mucus and blood.

One complication of gastroenteritis is dehydration.

Classification according to the level of dehydration hidayat (2013) are:

1. Mild dehidration

If the loss of 2-5% of body weight, or an average of 25 ml / kg with

the clinical picture is less elastic skin turgor, hoarseness, the patient

has not fallen in a state of shock.

2. Moderate dehidration

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If the fluid loss of 5-8% of body weight, or an average of 75 ml / kg

with poor skin turgor clinical picture, hoarseness, patients falling

shock, rapid pulse and inside.

3. Severe dehidration

If the fluid loss of 8-10% of body weight or an average of 125 ml /

kg, in severe dehydration, blood volume is reduced resulting in

hypovolemic shock with symptoms of rapid heart rate, rapid pulse

and small, decreased blood pressure, patients are very tired,

awareness decreased (apathy, somnolence, sometime up

soporokomateus

B. Etiology

Factors causing diarrhea according ngastiyah (2009), namely:

1. Infection factors

Enteral infection is infection of the digestive tract are a major

cause of gastroenteritis in children. Covers enteral infection as

follows: a bacterial infection such as vibrio, E. coli, salmonella

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shigella, campylobacter, yersinia, Aeromonas, and so on; a viral

infection that enterovirus (ECHO virus, Coksakie, poliomyelitis,

Adenovirus, Rotavirus and others); Parasitic infections: worms

(Ascaris, trichuriasis, Oxyuris,Strongyloides), protozoa

(Entamoeba histolytica, Giardia lamblia, Trichomonas hominis

and fungi (Candida albicans)

2. Parenteral factors

Parenteral infection is an infection outside the digestive tract of

food such as: acute otitis media (AOM), tonsillitis /

tonsilofaringitis, bronchopneumonia, encephalitis and so on. This

situation is mainly found in infants and children under the age of

2 years.

3. Malabsorbtion factors

Malabsorption of carbohydrate, such as a disaccharide (lactose

intolerance, maltose and sucrose), monosaccharides (glucose

intolerance, fructose and galactose); Malabsorption of fat and

protein malabsorption.

4. Dietery Factors

Stale food, toxic, food allergies

5. Psychological factors

Fear and anxiety (rare, but can occur in older children)

C. Epidemiology

Diarrheal disorders in childhood account for a large

proportion(18%) of childhood deaths, with an estimated 1.5 million

deaths per year globally, making it the second most common cause

ofchild deaths worldwide. The World Health Organization (WHO)

and UNICEF estimate that almost 2.5 billion episodes of

diarrheaoccur annually in children < 5 yr of age in developing

countries, with more than 80% of the episodes occurring in Africa and

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South Asia (46% and 38%, respectively). Global mortality may be

declining, but the overall incidence of diarrhea remains unchanged at

about 3.6 episodes per child-year ( Fig. 332-1 ), and it is estimated to

account for 13% of all childhood disability adjusted life years

(DALYs). Although the exact etiologic fractions of diarrhea in

developing countries are a subject of much research, there are

indications that rates of various types of bacterial diarrhea may be

decreasing. There are indications that rates of hospitalization and

deaths due to Shigella infections, especially Shigella dysenteriae type

1, the most severe form of shigellosis, may be declining and account

for almost 160,000 deaths annually. Enterotoxigenic Escherichiacoli

(ETEC) may be responsible for 300,000-500,000 deaths among

children < 5 yr annually. Rotavirus infections (the most common

identifiable viral cause of gastroenteritis in all children) account for

527,000 deaths annually or 29% of all deaths due to diarrhea among

children < 5 yr of age. About 23% of deaths due to rotavirus disease

occurred in India; 6 countries (India, Nigeria, Congo, Ethiopia, China,

and Pakistan) accounted for > 50% of deaths due to rotavirus disease.

The decline in diarrheal mortality, despite the lack of significant

changes in incidence, is the result of preventive rotavirus

D. Risk Factor

Major risks include environmental contamination and increased exposure

to enteropathogens. Additional risks include young age, immunodeficiency,

measles, malnutrition, and lack of exclusive or predominant breast-feeding.

Malnutrition increases the risk of diarrhea and associated mortality, and moderate

to severe stunting increases the odds of diarrhea-associated mortality 1.6- to 4.6-

fold. The fraction of such infectious diarrhea deaths that are attributable to

nutritional deficiencies

E. Patophysiology

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Gastroenteritis is an increasing condition in dilution and frequency of

stool . Gastroenteritis may occur due to dissolved substances that can not be

absorbed in the stool, which is called osmotic diarrhea, or irritation of the

digestive tract.. The cause of irritation is the most common viral infection or

bacteria in the distal small intestine or large intestine. Gastroenteritis can be

transmitted through oral fecal route from person to person and some daily nursing

facilities also increases the risk of diarrhea. Transport activated by stimuli of

bacterial toxins against electrolytes into the small intestine, intestinal mucosal

cells become irritated and increase the secretion of fluids and electrolytes.

Microorganisms that enter will damage the intestinal mucosal cells thereby

reducing the intestinal surface area. Irritable bowel by a pathogen affects the

mucosal lining of the intestines, resulting in increased secretory products,

including mucous irritation by microbes also affect the muscle layer resulting in

increased motility.Increasing diarrhea cause a lot of wasted water and electrolytes

because the time available for absorption of substances in colon decrease

.Individual who experience severe diarrhea can die from hypovolemic shock and

electrolyte disturbances. Cholera toxin is transmitted through bacteria cholera is

an example of a material that is very stimulating motility and can directly lead to

the secretion of water and electrolytes into the colon so unsure- this important

element of the plasma which is wasted in large numbers. Absorption of fluid and

electrolyte disturbances can cause intestinal inflammation and reduce the ability

to absorb fluids and electrolytes. This happens because of malabsorption

syndrome intestinal increase intestinal motility motility and rapid discharge at the

disruption of intestinal absorption and secretion of electrolytes potassium and

sodium bicarbonate Fluid move from extra cellular cavity into feces, so Acute

gastroenteritis is characterized by vomiting and diarrhea related to loss of fluid

and electrolytes that causes dehydration and fluid and electrolyte balance

disorders. The main cause of diarrhea is a virus (adenovirus enteric and

robavirus) and parasites (biardia lambiachristopodium) these pathogens cause

disease by meninfeksi cells produce enterotoxin or kristotoksin attached to the

intestinal wall. Digestive tract that are impaired in patients with acute

gastroenteritis is the small intestine.

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F. Clinical Manifestation

Patients suffering from gastroenteritis, firsty experience whiny, fidgety,

increasing body temperature, decreased appetite or no possibility of liquid may arise

diare.Stools are accompanied by mucus or phlegm and the bloody stool . Feces color

turned into greenish because it is mixed with bile. Anus and the surrounding area arise

scratched by frequent defecation and fecal increasingly acidic as a result of the more

lactic acid derived from lactose in absorption by the small intestine during diarrhea.

Vomiting may occur after or before it can be caused due to diarrhea and stomach join

inflamed or due to disruption of acid-base and electrolyte balance. If the patient has a

lot of fluid and electrolyte loss, dehydration symptoms start appears, ie weight loss,

turgor decreases, the eye and the crown of a large sunken (in infants), the mucous

membranes of the lips and mouth and the skin looks dry

The frequency of defecation in infants more than 3 times a day and in neonates

more than 4 times a day, liquid form to defecate magnitude sometimes with mucus

and blood, appetite decreased, the color gradually becomes greenish because of mixed

bile, vomiting, thirst, malaise, the blisters on the area around the anus, feces are a lot

of lactic acid derived from lactose can not be absorbed by the intestine, is without

dehydration, can then occur diuresis reduced (oliguria up to anuria) or until the

happening of metabolic acidosis such as looking pale with respiratory kusmaul.

G. Diagnosis

The diagnosis of gastroenteritis is based on clinical recognition,an evaluation of its

severity by rapid assessment and by confi rmation by appropriate laboratory

investigations, if indicated

Clinical Evaluation of Diarrhea

The most common manifestation of GI tract infection in children is diarrhea,

abdominal cramps, and vomiting. Systemic manifestations are varied and associated

with a variety of causes. The evaluation of a child with acute diarrhea includes:

Assess the degree of dehydration and acidosis and provide rapid resuscitation and

rehydration with oral or intravenous fluids as required (Tables 332-8 and 332-9).

Obtain appropriate contact, travel, or exposure history. This includes information on

exposure to contacts with similar symptoms, intake of contaminated foods or water,

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child-care center attendance, recent travel of patient or contact with a person who

traveled to a diarrhea-endemic area, and use of antimicrobial agents. Clinically

determine the etiology of diarrhea for institution of prompt antibiotic therapy, if

indicated. Although nausea and vomiting are nonspecific symptoms, they indicate

infection in the upper intestine. Fever suggests an inflammatory process but also

occurs as a result of dehydration or co-infection (e.g., urinary tract infection, otitis

media). Fever is common in patients with inflammatory diarrhea. Severe abdominal

pain and tenesmus indicate involvement of the large intestine and rectum. Features

such as nausea and vomiting and absent or low-grade fever with mild to moderate

periumbilical pain and watery diarrhea indicate small intestine involvement and also

reduce the likelihood of a serious bacterial

infection.

This clinical approach to the diagnosis and management of diarrhea in young

children is a critical component of the integrated management of childhood illness

(IMCI) package that is being implemented in developing countries with high burden

of diarrhea mortality ( Fig. 332-6 ).

Stool Examination

Microscopic examination of the stool and cultures can yield important

information on the etiology of diarrhea. Stool specimens should be examined for

mucus, blood, and leukocytes.

Fecal leukocytes indicate bacterial invasion of colonic mucosa, although some

patients with shigellosis have minimal leukocytes at an early stage of infection, as do

patients infected with Shigatoxin-producing E. coli and E. histolytica.In endemic

areas, stool microscopy must include examination for parasites causing diarrhea, such

as G. lamblia and E. histolytica Stool cultures should be obtained as early in the

course of disease as possible from children with bloody diarrhea in whom stool

microscopy indicates fecal leukocytes, in outbreaks with suspectedhemolytic-uremic

syndrome (HUS), and in immunosuppressed children with diarrhea. Stool specimens

for culture need to be transported and plated quickly; if the latter is not quickly

available, specimens might need to be transported in special media. The yield and

diagnosis of bacterial diarrhea is improved by using molecular diagnostic procedures

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such as PCR. In most previously healthy children with uncomplicated watery

diarrhea, no laboratory evaluation is needed except for epidemiologic purposes.

H. Treatment

The broad principles of management of acute gastroenteritis in children

include oral rehydration therapy, enteral feeding and diet selection, zinc

supplementation, and additional therapies such as probiotics.

Oral Rehydration Therapy

Children, especially infants, are more susceptible than adults to dehydration

because of the greater basal fluid and electrolyte requirements per kg and because

they are dependent on others to meet these demands. Dehydration must be evaluated

rapidly and corrected in 4-6 hr according to the degree of dehydration and estimated

daily requirements. A small minority of children, especially those in shock or unable

to tolerate oral fluids, require initial intravenous rehydration, but oral rehydration is

the preferred mode of rehydration and replacement of ongoing losses. Risks

associated with severe dehydration that might necessitate intravenous resuscitation

include: age < 6 mo, prematurity, chronic illness, fever > 38 ° C if <3 mo or > 39 ° C

if 3-36 mo, bloody diarrhea, persistent emesis, poor urineoutput, sunken eyes, and a

depressed level of consciousness. Thelow-osmolality WHO oral rehydration solution

(ORS) containing 75 mEq of sodium and 75 mmol of glucose per liter, withtotal

osmolarity of 245 mOsm per liter, is more effective thanother formulations in

reducing stool output without the risk ofhyponatremia, and it is now the global

standard of care .Cereal-based oral rehydration fluids can also be advantageous in

malnourished children and can be prepared at home.Home remedies including

decarbonated soda beverages, fruit juices, and tea are not suitable for rehydration or

maintenance therapy because they have inappropriately high osmolalities and low

sodium concentrations. A clinical evaluation plan andmanagement strategy for

children with moderate to severe diarrhea is outlined in Figure 332-6 and Table 332-

9 . Oral rehydration should be given to infants and children slowly, especiallyif they

have emesis. It can be given initially by a dropper, teaspoon, or syringe, beginning

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with as little as 5 mL at a time. The volume is increased as tolerated. Replacement for

emesisor stool losses is noted in Table 332-9 . Oral rehydration can also be given by a

nasogastric tube if needed; this is not the usual route.Limitations to oral rehydration

therapy include shock, an ileus, intussusception, carbohydrate intolerance (rare),

severe emesis, and high stool output ( >10 mL/kg/hr). Ondansetron (oral mucosal

absorption preparation) reduces the incidence of emesis, thus permitting more

effective oral rehydration.

Enteral Feeding and Diet Selection

Enteral feeding in diarrhea aids in recovery from the episode, and a continued

age-appropriate diet after rehydration is the norm. Although intestinal brush border

surface and lumina lenzymes can be affected in children with prolonged diarrhea,

there is evidence that satisfactory carbohydrate, protein, and fat absorption can take

place on a variety of diets. Once rehydration is complete, food should be reintroduced

while oral rehydrationcan be continued to replace ongoing losses from emesis or

stools and for maintenance. Breast-feeding or nondiluted regular formula should be

resumed as soon as possible. Foods with complex carbohydrates (rice, wheat,

potatoes, bread, and cereals), lean meats, yogurt, fruits, and vegetables are also

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tolerated. Fattyfoods or foods high in simple sugars (juices, carbonated sodas) With

the exception of acute lactose intolerance in a small subgroup, most children with

diarrhea are able to tolerate milk and lactose-containing diets. Withdrawal of milk and

replacement with specialized (and expensive) lactose-free formulations are

unnecessary. Although children with persistent diarrhea are not lactose intolerant,

administration of a lactose load exceeding 5 g/kg/day may be associated with higher

purging rates and treatment failure. Alternative strategies for reducing the lactose load

while feeding malnourished children who have prolonged diarrhea include addition of

milk to cereals and replacement of milk with fermented milk products such as yogurt.

Rarely, when dietary intolerance precludes the administration of cow ’ s milk – based

formulations or milk it may be necessary to administer specialized milk-free diets

such as a comminuted or blenderized chicken-based diet or an elemental formulation.

Although effective in some settings, the latter are unaffordable in most developing

countries. In addition to rice-lentil formulations, the addition of green banana or

pectin to the diet has also been shown to be effective in the treatment of persistent

diarrhea. Figure 332-7 gives an algorithm for managing children with prolonged

diarrhea in developing countries.

Zinc Supplementation

There is strong evidence that zinc supplementation in children with diarrhea in

developing countries leads to reduced duration and severity of diarrhea and could

potentially prevent a largeproportion of cases from recurring. In addition to

improvingdiarrhea recovery rates, administration of zinc in community settings leads

to increased use of ORS and reduction in the inappropriate use of antimicrobials.

Although some studies have failed to demonstrate benefi cial effects of zinc

supplementation in young infants < 6 mo of age, WHO and UNICEF recommend that

all children with acute diarrhea in at-risk areas should receive oral zinc in some form

for 10-14 days during and after diarrhea (10 mg/day for infants < 6 mo of age and 20

mg/day for those > 6 mo).

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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 diminshes 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 thepotential 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 reducesall-cause childhood mortality by 21% and diarrhea-specifi c

mortality by 31% (95% CI, 17-42%)

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CHAPTER 3

CASE REPORT

Case

CS, 1 year and 3 month came with the main complaint of diarrhea that has been experienced since 3 days ago with the frequency of 6X/ day. The stool which consisted of diet and fluid, had ¼ volume of aqua cup. The patient also had vomiting since 3 days ago that consisted of diet and fluid consumed 1 day earlier . The patient had continuous high fever since 3 days ago with the temperature of 39 C and decreased by taking anti pyretic drugs.

The convulsion history (-), Diarrhea(-), Cough(-), Sneezing(-), Dysphagia(-),

Defecation (+) Normal, Urination (+) Normal,

Disease History: (-)

Drug History (-)

GestastionalHistory : when the mother giving birth, she was 34 and had frequently controlled her pregnancy to midwife. DM(-), Herbal drugs history (-).

Obstetric History: This patient was firstborn. she was born through normal laborand was crying during the labor. His birth bodyweight was 3000 gr with 45 cm in body length.

Immunization History: Completed until 9 month of age

Growth and developments status: According to age

Diet History: 0-6 mo: Exclusive breast feeding

7- till present: Breastmilk+ Cerelac instant meal ½ bowl

Physical Examination

General status

Body weight: 7.2 kg, Body length: 70 cm, Z scores in Height for age boys: -3<Z<-2Z scores in Weight for age boys: Z<-3 Z scores in weight for height boys : -3<Z<-2

Present status

Consciousness: GCS 15 (E4 V5 M6)

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Blood Pressure: 100/60 mmHgPulse: 140 x/iRespiratory Rate: 30 x/iBody Temperature: 38,8oC.Anemic (-).Icteric (-).Cyanosis (-).Edema (-).Dyspnea (-).

Local status

Head : Eyes : Isochoric pupil . Inferior palpebra conjunctiva pale (-/-).Icteric sclera (-/-). Light reflex (+/+). Face edema (-).Inferior and superior palpebral edema (-/-). Ears/ nose: Within normal limit, mouth mucosal: dry

Neck : Lymph node enlargement (-)Thorax :Symmetricfusiformis. Chest retraction (-). HR: 140x/i, regular,

murmur (-). RR: 30x/i, reguler, ronchi (-).Breath sound: vesicular. Additional sound (-).

Abdomen : Soepel, peristaltic (+), liver and spleen unpalpable, Skin pinch returns slowly , Shifting dullness (-), Ascites (-)

Extremities : Pulse 140x/i, regular, adequate pressure and volume, warm, CRT > 3”. Pitting edema(-).

Differential Diagnosis:

Working Diagnosis: Acute GE + Mild to moderate dehydration

Management:

- O2 ½ - 1 l/minute nasal canule- Initial: IVFD RL 0,45% 40 gtt/i macro/4h

Maintenance: IVFD RL 30 gtt/I micro- Zinc oral 1 x 20 mg- Paracetamol 3 x 60 mg- Diet with heavy food 720 Kkal + 14.4 gr protein

Diagnostic Planning:

- Complete Blood Test- Electrolyte- Random Blood glucose level

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Laboratory Finding: August 30th , 2015

Haematology Result NormalHb g/dl 11.3 12.0-14.1MCV fl 69.70 81-95MCH pg 25 25-29MCHC g% 35.90 29-31DiftelLimfosit % 50.50 20-40Monosit % 12.60 2-8-All component are normal except MCV which is 69,7 (N=81-95). In which, the morphology of eritrosite is hypochromic micrositer.

-Thus, this patient has anemiahipochromicmikrositer.

Laboratory Finding: April 30th 2015

Clinical ChemistryElectrolyte- Ca Mg/dl 6.9 8.4 – 10.4- Na mEq/l 137 135 – 155 - K mEq/l 3.0 3.6 – 5.5

From Electrolyte, we found that the result is hipokalemia

FOLLOW UP

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August, 30th 2015 (09.00am)

S Diarrhea (+), fever(+)

O Cons: alert, Temp: 38,2oC

Body weight: 7.6 kg, Body length: 70 cm.

Head :

Eyes : Isochoric pupil . Inferior palpebra conjunctiva pale (-/-). Icteric sclera (-/-). Light reflex (+/+). Face edema (-).Inferior and superior palpebraedema (-/-).

Ears/ nose/ mouth : Within normal limit

Neck :

Lymph node enlargement (-)

Thorax:

Symmetricfusiformis. Chest retraction (-). HR: 110 x/i, regular, murmur (-). RR: 26 x/i, reguler, ronchi (-).Breath sound: vesicular. Additional sound (-).

Abdomen:

Soepel, peristaltic (+) increased, liver and spleen unpalpable, Skin pinch returns quickly, Shifting dullness (-), Ascites (-)

Extremities:

Pulse 120 x/i, regular, adequate pressure and volume, warm, CRT < 3”. Pitting edema(-).

A Acute Gastroenteritis+ Mild to moderate dehydration

P Management:

- O2 ½ - 1 l/minute nasal canuleMaintenance: IVFD RL 0.5% 250 cc + D5% 250cc 30 gtt/I micro

- Zinc oral 1 x 20 mg- Paracetamol 3 x 60 mg- Diet with heavy food 720 Kkal + 14.4 gr protein

August, 30th 2015 (20.00 pm)

S Fever (+), diarrhea (-)

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O Cons: alert, Temp: 38,2oC, HR= 112 x/I, RR: 24x/I,

Body weight: 7.8 kg, Body length: 122 cm.

Head:

Eyes : Isochoric pupil . Inferior palpebra conjunctiva pale (-/-). Icteric sclera (-/-). Light reflex (+/+). Face edema (-).Inferior and superior palpebraedema (-/-).

Ears/ nose/ mouth : Within normal limit

Neck :

Lymph node enlargement (-)

Thorax:

Symmetric fusiformis. Chest retraction (-). HR: 112 x/i, regular, murmur (-). RR: 24 x/i, reguler, ronchi (-).Breath sound: vesicular. Additional sound (-).

Abdomen:

Soepel, peristaltic (+) normal, liver and spleen unpalpable, Skin pinch returns quickly, Shifting dullness (-), Ascites (-)

Extremities:

Pulse 112 x/i, regular, adequate pressure and volume, warm, CRT < 3”. Pitting edema(-).

A Acute Gastroenteritis+ Mild to moderate dehydration

P Management:

- O2 ½ - 1 l/minute nasal canuleMaintenance: IVFD 4:1 Nacl 0.225% + D5% 30 gtt/I micro/24h

- Zinc oral 1 x 20 mg- Paracetamol 3 x 60 mg- Diet with heavy food 720 Kkal + 14.4 gr protein

August, 31th2015 (06.00am)

S Fever (+), diarrhea (-)

O Cons: alert, Temp: 37,4oC, HR= 112 x/I, RR: 24x/I, T= 38.2

Body weight: 7.8 kg, Body length: 122 cm.

Head:

Eyes : Isochoric pupil . Inferior palpebra conjunctiva pale (-/-). Icteric sclera (-/-). Light reflex (+/+). Face edema (-).Inferior and superior palpebraedema (-/-).

Ears/ nose/ mouth : Within normal limit

Neck :

Lymph node enlargement (-)

Thorax:

Symmetric fusiformis. Chest retraction (-). HR: 112 x/i, regular, murmur (-). RR: 24 x/i, reguler, ronchi (-).Breath sound: vesicular. Additional sound (-).

Abdomen:

Soepel, peristaltic (+) normal , liver and spleen unpalpable, Skin pinch returns quickly, Shifting dullness (-), Ascites (-)

Extremities:

Pulse 110 x/i, regular, adequate pressure and volume, warm, CRT < 3”. Pitting edema(-).

A Acute Gastroenteritis+ Mild to moderate dehydration

P Management:

- O2 ½ - 1 l/minute nasal canuleMaintenance: IVFD 4:1 Nacl 0.225% + D5% 30 gtt/I micro/24h

- Zinc oral 1 x 20 mg- Paracetamol 3 x 60 mg- Diet with heavy food 720 Kkal + 14.4 gr protein- Routine Fecal examination

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August, 31th2015 (06.00am)

S Fever (+), diarrhea (-)

O Cons: alert, Temp: 37,2oC, HR= 112 x/I, RR: 24x/I,

Body weight: 7.8 kg, Body length: 122 cm

Head:

Eyes : Isochoric pupil . Inferior palpebra conjunctiva pale (-/-). Icteric sclera (-/-). Light reflex (+/+). Face edema (-).Inferior and superior palpebraedema (-/-).

Ears/ nose/ mouth : Within normal limit

Neck :

Lymph node enlargement (-)

Thorax:

Symmetric fusiformis. Chest retraction (-). HR: 112 x/i, regular, murmur (-). RR: 24 x/i, reguler, ronchi (-).Breath sound: vesicular. Additional sound (-).

Abdomen:

Soepel, peristaltic (+) normal, liver and spleen unpalpable, Skin pinch returns quickly, Shifting dullness (-), Ascites (-)

Extremities:

Pulse 110 x/i, regular, adequate pressure and volume, warm, CRT < 3”. Pitting edema(-).

A Acute Gastroenteritis+ Mild to moderate dehydration

P - O2 ½ - 1 l/minute nasal canule- Maintenance: IVFD 4:1 Nacl 0.225% + D5% 30 gtt/I micro/24h- Zinc oral 1 x 20 mg- Paracetamol tab 3 x 60 mg- Chicken porridge Diet - Routine Fecal examination

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CHAPTER 4

DISCUSSION AND

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SUMMARY

4.1. Discussion

This patient was first diagnosed with Acute Gastroenteritis with mild to moderate

dehydration when was admitted to Adam Malik General Hospital based on history taking and

physical examination. The findings showcased that the patient came with the main complaint

of diarrhea that has been experienced 6 times/day for 3 days and increasing frequency of

defecation and vomiting. Based on history taking that we have taken, This patient fulfill the

criteria for Acute Gastroenteritis because of the wasting stool that was marked by increased

volumes, dilution as well as the frequency more than 3 times a day with or without mucus

and blood. (Hidayat) The physical examinations findings complement with the sign and

symptoms of mild to moderate dehydration which involved dry mucosal mouth, skin pinch

returned slowly and CRT >3 s. This findings fulfilled the criteria for mild to moderate

dehydration.

Based on risk factors that caused acute gastroenteritis, This condition may be caused by

environmental contamination, increased exposure to enteropathogens, additional risk may

include young age, immunodeficiency, measles, malnutrition and lack of exclusive breast

feeding, malnutrition increases the risk of diarrhea-associated mortality 1.6-4.6 fold. The

fraction of such infectious diarrhea deaths that are attributable to nutritional deficiencies. In

this patient we found that the patient’s nutritional status was under nutrition ( Z scores in

height for age and weight for height was -3<Z<-2) . This condition may contribute in

elevating the risk of Acute Gastroenteritis in children., malnutrition can predispose to infection because of its negative impact on the barrier protection, the skin and mucous membranes by inducing alterations in host immune function. The groups in Guatemala and Bangladesh proceeded to explore the mechanisms whereby

diarrhea causes growth failure, focusing on dietary intake and intestinal malabsorption.

Martorell et al. (10) reported that fully weaned Guatemalan children reduced their energy

intake by 30% during acute infections, whereas Brown et al. (11) found that Bangladeshi

children who were still breastfeeding reduced their intakes by only about 7%, suggesting that

breastfeeding may protect against diarrhea-induced reductions in intake. During a subsequent

study in Peru (12), intakes of breast milk energy and non breast milk food sources were

examined separately; and this analysis of disaggregated data confirmed the foregoing

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hypothesis. Whereas intake of non breast milk energy declined by about 30% during illness,

there were no changes in breast milk consumption. Thus, the overall impact of illness on

energy intake was partially mitigated by breastfeeding. 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.

The management of this case was treated with Intravenous solution of Ringer lactate

for fluid replacement and maintenance therapy. Indeed from the result of electrolyte

examination, The result was hypokalemia and normal sodium level. This treatment was given

alongside with zinc supplement during the hospital stay. Intravenous rehydration is

considered for treating mild to moderate dehydration if the patients are unable to tolerate

ORS but oral rehydration is the preferred mode of rehydration and replacement of ongoing

losses. zinc supplementation in children with diarrhea in developing countries leads to

reduced duration and severity of diarrhea and could potentially prevent a large proportion of

cases from recurring. In addition to improving diarrhea recovery rates, administration of zinc

in community settings leads to increased use of ORS and reduction in the inappropriate use of

antimicrobials. Although some studies have failed to demonstrate benefi cial effects of zinc

supplementation in young infants < 6 mo of age, WHO and UNICEF recommend that all

children with acute diarrhea in at-risk areas should receive oral zinc in some form for 10-14

days during and after diarrhea (10 mg/day for infants < 6 mo of age and 20 mg/day for those

> 6 mo).

4.2. Summary

N, 1 year and 4 months old Indonesian girl was admitted on August, 30th 2015 with a chief

complaint of diarrhea (+) experienced by os since 3 days ago with the frequency of 6 times

per day, and additional symptoms such as vomiting(+) since 3 days ago with gastric content

and fever (+) since 3 days ago with temperature of 39 ̊C