acute diarrhea
DESCRIPTION
diareTRANSCRIPT
ENGLISH IN NURSING
GASTROINTESTINAL SYSTEM
“DIARRHEA PEDIATRIC”
By:
6th Group A-12/A-2
Zeinidar Auliyaun N. (131211132024)
Ria Fitriani (131211132026)
Sevina Ramahwati (131211132054)
Nurul Istiqomah (131211133002)
Ayu Priyanti (131211133010)
Elfrida Kusuma Putri (131211133018)
Jen Riko Dewantoro (131211133026)
Dimas Hadi Prayoga (131211133034)
NURSING STUDY PROGRAM
FACULTY OF NURSING
AIRLANGGA UNIVERSITY
SURABAYA
2013
PREFACE
Praise be to Allah, The cherisher and sustainer of the worlds; God who has been
giving His blessing and mercy to the writer to complete the paper entitled
"Gastrointestinal System DIARRHEA in PEDIATRIC." This papers is submitted to
fulfill one of the task of English In Nursing subject in Faculty of Nursing. In finishing
this paper, the writer really gives his regards and thanks for people who has given
guidance and help; they are:
1. Nuzul Q, S.Kep., Ns., M.Ng , as the English lecture. who have teached us
and given detail information.
2. Our Parents who has always pray for us.
3. And all of my friends who has given support to us and help us.
Finally, the writer realizes there are unintended errors in writing this paper. She
really allows all readers to give their suggestion to improve its content in order to be
made as one of the good examples for the next paper.
Surabaya, Desember th 2013
Writer
Background of Problem
The infant mortality rate in Indonesia from 2003 to 2012 has decreased
very slowly or stagnant, that is from the birth of 1,000 babies, about 32 babies
died. This condition may occur due to lack of coverage of exclusive breastfeeding.
Based on data of Riskesdas 2010 only about 15% of infants who received breast
milk intake. The same thing occurs in infants, which is about 46 of the 1,000
infants died. The biggest cause of death of infants and toddlers is diarrhea.
Exclusive breastfeeding is the minimum intake is a major cause diarrhea in infants.
While deaths in infants are more affected because immediate treatment of diarrheal
diseases. The data says that only about 35% of infants who received treatment in
the form of oral rehydration salts (Riskesdas, 2010).
From the data above, we choose the theme of diarrhea in children. It
aims to provide information on diarrhea, diarrhea causes and treatment of diarrhea
in children.
Formulation of this Problems
1.2.1 How’s the anatomy and physiology of Gastrointestinal (GI)?
1.2.2 How do the types and classification of Diarrhea?
1.2.3 What is the etiology of Diarrhea?
1.2.4 What is the clinical appearances of Diarrhea?
1.3 Purpose of Problems
1.3.1 To know the anatomy and physiology of Gastrointestinal
1.3.2 To describe the types and classification of Diarrhea
1.3.3 To describe the etiology of Diarrhea
1.3.4 To describe the clinical appearances of Diarrhea
CHAPTER II
DISCUSSION
2.1 Anatomy and Physiology of Gastrointestinal System
The digestive or gastrointestinal system prepares food for use by hundreds
millions of body cells. Food when eaten cannot reach cells because it cannot pass
through the intestinal walls to the bloodstream and, if could not be useful chemical
state. The gut modifies food physically and chemically and disposes of unusable
waste. Physical and chemical modification (digestion) depends on exocrine and
endocrne secretions and controlled movement of food through the gastrointestinal
tract. Exocrine secretions prepare food for absorption by diluting it to the osmolality
of plasma (isotonic), altering the pH for hydrolysis, and hydrolyzing complex foods.
The exocrine secretions also protect the mucosa from physical and chemical irritants.
Endocrine secretions play a major role in the control and coordination of secretory
and motor activities involved in the digestion and absorption of food. The
gastrointestinal system consists of the mouth, pharynx, esophagus, stomach,small and
large intestines, rectum and anus. Accessory organs include liver, gallbladder, and
pancreas. The accessory organs found in the mouth are the teeth and salivary glands.
Picture. Gasrointestinal System
2.1.1 Small Intestine
Jejenum (8 feet) and ileum (12 feet) continue degenerative process. Surface
area increased by plica circulares (circular folds) carrying villi, cells of villi cary
microvilli. Each villus has a capillary and a lacteal (lymphatic capillary). Absorption
of digested foodstuffs is via these to the rich venous and capillary drainaged of the
gut. Towards the end of the small intestine accumulations of lymphoid tissue (Peyer’s
patches) more common. Undigested residue of food is rich in bacteria.
2.1.2 Large Intestine
Jejenum terminates at cecum. Cecum is small sac like evagination, important
in some animals as a repository for bacteria/other organism able to digest cellulose. A
blind ending appendix may give trouble (appendictis) if infected. The large intestine
has three longitudinal muscle bands (taenia coli) with bulges in the wall (haustra)
between them. These may evaginate in the elderly to become diverticuli and infected
in diverticulitis. The large intestine resorbs water then eliminates drier residues as
feces. Regions recognized are the ascending colon, from appendix in right groin up to
a flexure at the liver, transverse colon, liver to spleen, descending colon, spleen to left
groin, then sigmoid (S-shaped) colon back to midline and anus. Anus has voluntary
and involuntary sphincter and ability to distinguish whether contents are gas or solid.
No villi in large intestine, but many goblet cells secreting lubricative mucus.
2.1.3 Rectum
The rectum is the final straight organ of the large intestine, terminating in the
anus. The human rectum is about 12 cm long. The rectum intestinum acts as a
temporary storage facility for feces. As the rectal walls expand due to the materials
filling it from within, stretch receptors from the nervous system located in the rectal
walls stimulate the desire to defecate. If the urge is not acted upon, the material in the
rectum is often returned to the colon where more water absorbed. If defecation is
delayed for a prolonged period, it will result constipation and harderned feces. When
the rectum becomes full the increase in intrarectal pressure forces the walls of the
anal canal apart allowing the fecal matter to enter the canal. The rectum shortens as
material is forced in to the anal canal and peristaltic waves propel the feces out of the
rectum. The internal and external sphincter allow the feces to be passed by muscles
pulling the anus up over the exiting feces.
2.1.4 Anus
In anatomy, anus or bottom hole is an opening from rectum to the outside of
body. Opening and closing of anus is arranged by sphincter muscle. Feces is thrown
away from body although defecation process, which is the main function of anus. In
anus, feces is pulled out. This is a final digestive process.
2.1.5 Accessory Digestive Organs
1. Salivary glands
Three pairs, parotid, submandibular, sublingual. Mumps begins as infective
parotitis in the parotid glands in the cheek. The others open into the floor of the
mouth. Saliva is a mixture of mucus and serous fluids, each produced to various
extents in various glands. Also contains salivary amylase, (start to break down starch)
lysozyme (antibacterial) and IgA antibodies.
2. Pancreas
Endocrine and exocrine gland. Exocrine part produces many enzymes which
enter the duodenum via the pancreatic duct. Endocrine part produces insulin, blood
sugar regulator.
3. Liver and Gallbladder
Bile, a watery greenish fluid is produced by the liver and secreted via the
hepatic duct and cystic duct to the gall bladder for storage, and thence on
demand via the common bile duct to an opening near the pancreatic duct in the
duodenum. It contains bile salts, bile pigments (mainly billirubin, essentially the
non-iron part of haemoglobin) cholesterol and phospholipids. Bile salt and
phospholipids emulsify fats, the rest are just being excreted. Gallstones are
usually cholesterol based, may block the hepatic or common bile ducts causing
pain, jaundice.
2.2 Definition Acute Diarrhea (Gastroenteritis)
Gastrointeritis is an inflammation of the stomach and intestines that may be
accompanied by vomiting and diarrhea. It can affect any part of the GI tract.
Diarrhea is a common problem in children, accounting for 13% of
hospitalizations in children less than 5 years of age (Van Niel, Feudtner,
Garrison& Christakis, 2002). It may be an acute problem, caused by viral,
bacterial, or parasitic infections, or a cronic problem . Rotavirus is the leading
caused of gastroenteritis in children (Hsu et al., 2005). Acute gastroenteritis
affect proximately 30 million children per year in United State (Reeves,
Shannon, & Fleisher, 2002). Children under age 5 years average approximately
two episode of gastroenteritis each year. Infants and small children with
gastroenteritis or diarrhea can quickly become dehydrated and are at risk for
hipovolemic shock if fluid and electrocyte losses are not replaced.
2.3 Etiologi and Classification
Four types of diarrhea are recognize (Limbos,2005)
1. Osmotic diarrhea results when osmotically active particles in the intestine draw
excess fluid into the stool, this condition occurs with dumping syndrome,
lactase deficiency, overfeeding, and malabsorption syndromes.
2. Secretory diarrhea occurs because there is active secretion of water and
electrolyte from mucosal crypt cells in the small intestine into the bowel lumen.
There tends to be large volumes of watery diarrhea even if the child is not being
fed.
3. Motility disorders cause diarrhea but not malabsorption. Bile salt and pancreatic
enzyme deficiency can cause diarrhea by deletion or inhibition of the normal
absorption process.
4. Inflammatory processes, such as bacterial invasion, celiac sprue, or surgical
procedures can change the anatomy and functional ability of the intestine.
Acute diarrhea can be caused by various viruses, bacteria, and parasites.
Viral causes of acute diarrhea include :
1) Rotavirus affect children 4 to 24 months old, cause half of all cases of
acute gastroenteritis, occur mostly in the cooler months, and can cause
significant dehydration.
2) Adenoviruses are the second most common type of viral diarrhea. This
illness does not generally include the high fever or respiratory symptoms
associated with nonenteric adenovirus (Dennehy, 2005).
3) Noroviruses cause most of the diarrhea in industrialized countries
(Dennehy, 2005). Fifty percent of food-borne out-breaks of diarrhea
caused by noroviruses. Norovirus infection usually start with nausea,
vomiting, watery, nonbloody diarrhea, and abdominal cramping and last
about 24 to 60 hours.
4) Invasion of the GI tract by pathogens result in increased intestinal
secretion as a result of enterotoxins, cytotoxic mediators, or decreased
intestinal absorption secondary to intestinal damage or inflammation.
Enteric pathogens attach to the mucosal calls and form a cuplike
pedestal on which the bacteria rest. The pathogenesis of the diarrhea
depends on whether the organism remains attached to the cell surface,
resulting in a secretory toxin (noninvasive, toxin-producing,
noninflammatory type diarrhea), or penetrates to mucosa (systemic
diarrhea). Noninflammatory diarrhea is the most common diarrheal
illness, resulting from the action of enterotoxin that is released after
attachment to the mucosa (Ramaswamy and Jacobson, 2001). The most
serious and immediate physiologic disturbances associated with severe
diarrheal disease are (1) dehydration, (2) acid-base imbalance with
acidosis, and (3) shock that occurs when dehydration progresses to the
point that circulatory status is seriously impaired.
Bacterial diarhea, which is much less common, can be cused by:
1. Campylobacter jejuni is gram-negative rod found mostly in raw or
undercooked poultry or meat. It is transferred person to person by the
fecal-oral route and has a low infective dose (one drop of raw chicken
juice) (Dinolfo, 2005). Shedding of the bacteria can persist for 2 to 3
weeks. It is most common in the summer months. Symptoms include
diarrhea, abdominal pain, malaise, and fever. in neonates bloody diarrhea
may be the only symtom (Dennehy, 2005)
2. Salmonella is a gram-negative rod found in contaminated, improperly
cooked poultry, eggs, dairy product, and sausage. It is spread by human to
human contact. Salmonella is most common in children younger than 4
years old. The peak incidence is in the first months of life (AAP, 2003).
Invasive disease is more common in children with underlying chronic
illness or who are immunocompromised.
3. Shigella is gram-negative rod found in contaminated food and water.
Human are the host and reservoir, and the organism is spread by the fecal-
oral route. The organism multiplies and releases cytotoxin, which causes
epithelial damage and ulceration. There is usually a high spiking fever and
bloody diarrhea. Shigella is most common inchildren 6 months to 3 years
old.
4. Enteroadherent and enterotoxigenic strains of E.coli usually cause mild
traveler’s diarrhea.
5. Enterohemorrhagic E.coli (O157:H7) can be associated with a mild, self-
limited diarrhea that causes bloody stool and abdominal cramping,
hemorrhagic colitis, hemolytic-uremic syndrome, and postdiarrheal
idiophatic thrombocytopenic purpura. E.coli o157:H7 is the prototype and
can cause mild to severe, profuse, and bloody diarrhea. Incubation is from
10 hours to 6 days; E.coli O157:H7 infection usually last 3 to 4 days and
can be fatal. The bacteria are shed in cow feces and can be found in
undercooked ground beef, contaminated water, raw fruits and vegetables,
and unpasteurized milk and can be transmitted from infected persons.
Outbreaks are linked to unpasteurized fruit juice, ground beef, petting
zoos, salami, yoghurt, spinach, lettuce and contaminated drinking water.
6. Yesrinia enterocolitica is a gram-negative rod found in contaminated food
(e.g., uncooked pork and unpasturized milk) and water. It produces an
enterotoxin that causes secretion of fluid and electrolytes in to the bowel.
Y.Enterocolitica causes dhiarrea in children of all ages.
7. C. Difficiles is a gram-positive anaerobic bacillius. Asymtomatic carriers
of C. Defficile who take antibiotic (ussually ampicilin,clindamycin, and
cephalosporis) experience increased growth of the organism. C.difficile
intestinal colonization rate in healty neonates and young infants can be as
high as 50%.but are usually less than 5% in children older than 2 years
and adults (AAP,2006).Illnes caused by C.difficile is generaly mild, but
can be severe and cause death ,especialy with an emerging more virulent
strain (McDonald e al,2005).
There are nongastrointestinal ,reffered to as parenteral ,causes of acute
diarrhea in children including other infectious processes(e.g otitis
media ,UTI,Pneumonia, and meningitis) ,
endochrinopatie ,neoplasms,antibiotic use and allergic disorders (e.g.,milk
soy ,foods).
Acute diarrhea accounts for approximately 20%of acute care visits
children younger more than 2 years old.It is causes of 8 in 1000
hospitalizations in children younger than 1 years old and is the reason for
10% of preventable dheats in teh U.S. Acute diarrhea responsible for 500
deaths per year in the U.S. among children 1 to 4 years old. Poor asses to
care and proverty are correlated with with increased mortality rates from
diarrhea.
2.4 Pathophysiology
Invasion of the GI tract by pathogens result in increased intestinal secretion as
a result of enterotoxins, cytotoxic mediators, or decreased intestinal absorption
secondary to intestinal damage or inflammation. Enteric pathogens attach to
the mucosal calls and form a cuplike pedestal on which the bacteria rest. The
pathogenesis of the diarrhea depends on whether the organism remains
attached to the cell surface, resulting in a secretory toxin (noninvasive, toxin-
producing, noninflammatory type diarrhea), or penetrates to mucosa (systemic
diarrhea). Noninflammatory diarrhea is the most common diarrheal illness,
resulting from the action of enterotoxin that is released after attachment to the
mucosa (Ramaswamy and Jacobson, 2001). The most serious and immediate
physiologic disturbances associated with severe diarrheal disease are (1)
dehydration, (2) acid-base imbalance with acidosis, and (3) shock that occurs
when dehydration progresses to the point that circulatory status is seriously
impaired
2.5 Risk Factor
According to Hidayat (2006 ) , the occurrence of diarrhea can be caused by a
variety of possible factors, including :
a. factors infection
This factor can be initiated microorganisms ( germs ) which enter the digestive
tract which later evolved in the gut and intestinal mucosal cell damage that can
reduce the surface area of the intestine . Furthermore, a change in bowel capacity
which ultimately resulted in impaired intestinal function absorbs fluids and
electrolytes . Or also said the presence of bacterial toxins will lead to an active
transport system in the intestine so that the irritated mucous cell secretion of fluid
and electrolyte then be increased
.
Figure2.4 patofisilogy mechanisme factor infeksi of diarrhea
mikroorganis
Enter to the GI System
Intestine mucos cell damaged
Change intestine capacity
intestine function in absorbtion fluid and electrolyte disorder
Secretion fluid qand increase electrolite
Diarrhea
b. factors malabsorption
Is a failure to perform absorption resulting in increased osmotic pressure resulting in a
shift of water and electrolytes into the intestinal cavity which can increase the contents
of the intestinal cavity so there was diarrhea .
Gambar 2.5 Patophysiology mechanism malabsorbsi factor of diarrhea
c. dietary factors
May occur if there are no toxins that can be absorbed properly . Resulting in increased
intestinal peristalsis resulting in a decrease in the chance to absorb the food which then
causes diarrhea .
Gambar 2.6 patophisiology mechanism diatery factor of diarrhea
d. Psychological factors
Can affect the increase in intestinal pristaltik ultimately affect the absorption of food can
cause diarrhea
Absorbtion failed
Increased
water and elektrolit enter to intestine cavity
Increased content of intestine cavity
Diarrheaeee
Toxins in the food
Bad absorbtion
Increased peristaltic intestine
decreased food absorbtion
Diarrhea
Physicologi factor
IInfection(viruses, bacteresi, parasites)
Malabsorbtion factor
Dietary factor
damaged intestine mucus
Productioneliferotoksin
Increased intestine cavity pressure
Irritation intestine mucus
enter to the GI system
Hipersecretion fluid
Osmolarity disorder
Increased osmotic pressure
Increased Secretion water and electrolyte
Increased permeability
intestine
Move to intestine
Absorbsition disorder
Stimulus Simpatic nerve
Increased Peristaltic intestine
hiperperistaltic
Less Absorbtion content of intestine
Enter to the GI System
Production enterotoksin
and neurotoksin
Interference intestine motility
Inceased intestine cavity volume
Respons to out
DIARRHEA
MK: less fluid volume
MK: pain b.d infection
MK: intolerance activity
MK: skin Integrity disorder
Web Of Caution (WOC)
2.6 Clinical Manifestation
Diarrhea may be mild, moderate, or serve. In mild diarrhea, stools are
slightly in creased in number and have a more liquid consistency. In moderate
diarrhea the child has several loose or watery stools. Other symptoms include
Irritability, anorexia, nausea and vomiting. Moderate diarrhea is usually self-
limiting, resolving without treatment within 1 or 2 days. In severe diarrhea,
watery stools are continous. The child exhibits symptoms of fluid and
electrolyte imbalance, has cramping, and is extremely irritable and difficult to
console.
CAUSES OF DIARRHEA IN CHILDREN
Etiology Bowel Manifestation
1. Emotional stress (anxiety, fatigue)
2. Intestinal infection (bacteria [E.
Coli, Salmonella, Shigella], Viral
[Human Rotavirus, enteric
adenovirus], fungal overgrowth)
3. Food sensivity (Gluten, Cow’s
milk)
4. Food intolerance (lactose,
introduction of new food,
overfeeding)
5. Medication (iron, antibiotics)
6. Colon disease (colitics, necrotizing
enterocolitis, enterocolitis)
7. Surgical alterations ( short bowel
syndrome)
1. Incrased motility
2. Inflammation in mucosa; increased
mucus secretion in colon
3. Decreased digestion of food
4. Incrased motility; increased mucus
secretion in colon
5. Irritation and suprainfection
6. Inflammation and ulceration of
intestinal walls; reduces absorption
of fluid; increased intestinal
motility
7. Reduces size of colon; decreased
absorption surface
2.7 MANAGEMENT
The following steps are taken:
1. Restore and maintain hydration. Oral rehydration with an oral electrolyte
solution should be attempted. Appropriate rehydration solutions include pedialyte
and invalyte. It is in appropriate to use fliud juices, kool – aid, sprots drinks, or
soda. If the child is not vomiting, oral rehydration can be accomplished quickly
(less than 4 hours). For formula-fed infants, returning to full strength formula as
quickly as possible is recommended. If the child is unable to tolerate full strength
formula, a diluted formula (one fouth to half strength) can be used for a short time
(4 to 6 hours) as tolerate. The child regular formula can be used initially as look
as it is tolerated. If not tolerate use soy or hydrolisate formula. Breastfed infant
should continue to breastfeed more frequently for shorter period.
2. Resume early refeeding because contens of the bowel stimulate the growth.
Enterocyte and help to facilitate mucosal repair following injury. The resumption
of a regular diet once rehydretion has been accomplished or continouing with a
regular diet despite the diarrhea has been shown to shorten the duration of the
disease. There is no additional benefit to the BRAT diet; a diet tolerated by the
child is recommended.
3. Administer parenteral hydration if necessary for the following:
a. Impaired circulation and possible shock
b. Weigh less than 4 to 5 kg or a child younger than 3 months old
c. Intractable diarrhea, lethargy anatomic anomalies
d. Failure to gain weigh or continued weigh loss despite oral fluid
4. Prescribe medication as indicated
5. Anti diarrheals are not generally recommended because the offending
organism must be excreted. Most over the counter products intended for diarrhea
now contain salicylates, and there is cocern for reye sindrom. If diarrhea persist
beyond the initial infection, cautious use of those agents without salicylates in
older children is acceptable.
6. Lactobacillus given early in a viral diarrheal illness or antibiotic associated
diarrhea can shorten the duration of the diarrhea and lessen the number of stooles
per day (banks, 2004; Szajewska et all, 2006). Lactobacillus is most effective if a
dose above threshold (10 billion colony forming units) is given during the first 24
to 48 hours of diarrhea.
7. Dioctahedral smectite, an adsorbend clay, has been found to protect the
intestinal mucosa by absorbin viruses, bacterial, and bacterial toksin with few site
effect. (Szajewska et all, 2006; Yen & Lai, 2006)
2.8 COMPLICATION
Acute diarrhea can cause dehydration, metabolic asidosis, cardiovascular colaps,
possible death.
1. Rotavirus has been linked to bacteremia in children with recurrent fever or
new onset of fever in children who had know fever associated with the initial
diarrhea illness (lowenthal et all, 2006)
2.9 PREVENTION
Preventive measures include the following:
1. Good hand washing by the child and care providers. Liquid soap ang paper
towels are recommended at day care center.
2. Good sanitation and appropriate removal of soiled clothing and deepers.
Diapering area should be cleaned after changing each baby at day care center.
3. Avoiding contamined soures; meat should be properly cooked.
4. With shigella, culture all symptomatic contacs and treat those with positive
stool cultures.
5. Avoid unnecessary antibiotics usage.
CHAPTER III
CASE STUDY
A mother brings her 8-month-old infant, Mary, to the primary care clinic. The
mother reports that Mary has had a “cold” for about 2 days, and this morning she
began to vomit and has had diarrhea for the past 8 hours. The mother states that
Mary is still breastfeeding, but that she is not taking as much fluid as usual, and she
is having three times as many stools as usual (the stools are watery in consistency).
When the nurse practitioner examines Mary, she notes that her temperatures is 380 C
(100.40 F) her pulse and blood pressure are in the normal range, her mucous
membranes are moist, and she has tears when she cries. The nurse practitioner also
note that Mary’s weight has decreased from what it was when she was seen in the
clinic 2 weeks ago for her well-child visit.
Identity:
Name: Mary
Age : 8 months
Sex : Female
Assessment:
Subjective data:
a) cold for about 2 days
b) not taking as much fluid as usual
c) the stools are watery in consistency
d) vomit and has had diarrhea for the past 8 hours
Objective data:
a) The temperature is 380 C
b) had diarrhea for the past 8 hours
c) Pulse and blood pressure is normal
d) Mucous membranes are moist
e) Has tears when she cry
f) Lossing weight
Clinical findings
History . the following should be included:
1. Pattern of diarrhea : when diarrhea began ,nube of stools,frequency, and quality of
stools.
2. Signs and symptoms associated wit infectious diarrhea: bloody stool ,abdominal
pain , vomiting , or fever.
3. Number of wet diapers in the past 24 hours and approximate time of last void.
4. Dietary record , changes in a diet that might correlate with increased stooling.
5. Family members with similiar illnes or others GI diseases.
6. Day care or schol illnes patterns and contacts.
7. Travel history.
8. Most recent weight and previous growth pattern.
Physical Examination . Assess the following :
1. Complete physical examminations including vital sign ,assessment of
behaviour ,and evaluation of anterior fontanelle , if it is still open.
2. Assesment of dehydration . Steiner and colleagues (2004) ,found that CRT ,skin
turgor, tacypnea ,when consideret together, were the most helpful in the
determination of dehydration. Normal CRT is less than 2 seconds. Research has
shown that a CRT of 2 to 2.9 seconds corresponds to a 50-to 90-ml/kg loss, 3 to
3.5 seconds corresponds to a 90- to 110-ml/kg loss, 3.5 to 3.9 corresponds to a
110- to 120-ml/kg loss, and more tahan 4 seconds corresponds to a 150-ml/kg loss
(Findberg, 2002).
Diagnostic Studies. Most diarrheal ilness does not require any lab testing. The
following are ordered as indicated:
1. Stool examination (Color, consistency, blood, mucus, pus, odor, volume).
2. Stool pH, clinitest, and heme test.
3. Stool cultures should be considered for bloody or prolonged diarrhea ,suspected
food postioning,or recent travel aboard(Banks,2004)
4. Specific laboratory findings .
5. Rotavirus is diagnosed using enzyms immunosasy and later agglutination for
group A rotavirus antigen in the stool ,electron microscopy, and reverse
transcriptase PCR ( Dennehy,2005).
6. Adenoviruses are diagnoses by antigen detection by immunoassay.
7. Noroviruses are diagnosed via reverse transcriptase.
8. Campylobacter is diagnosed by stool culture.
9. E.Coli O157:H7 is diagnosed using MacConkey agar with sorbitol.
10. The following are criteria to culture stool for C.Difficile :
-Test patients who are older than 1 year. C.Defficile is commonly found in
asymtomatic children less than 1 year old.
-Severe diarrhea lasting at least 2 days.
-The presence of other GI symtoms (cramping,abdominal pain).
11. If intravenous fluids are necessary, serum bicarbonate will help establish the
severity of the dehydration. Other serum electrolytes and glucose may help to
evaluated complicated diarrhea (banks , 2004)
Diferrential diagnosis
Numerous causes, including infection (bacterial or viral) , medication ingestion ,
parasitic infestation ,anatomic abnormalities,dietary intolerances and appendicities
, may be responsible for accute diarrhea .
Collaborative Care
Diagnosis is based on the history, physical examination and laboratory
findings . athrough history may help identify the cause. Ask parents about
recent exposure to illnesses, use of antibiotics, travel, food and formula
preparation, food sensitives or allergies, and whether the child attends childcare.
Physical examination provides to guide the severity of dehydration . the stool
can be examinate for the presence of ova, parasites infectious organism, viruses,
fat and undigested sugars. Laboratory evaluation of serum and urine helps
identify electrolyte imbalances and other deficiencies.
Medical management depends on the severity of the diarrhea and fluid
and electrolyte imbalances. The goal of treatment is to correct the fluid and
electrolyte imbalances. For mild dehydration the child is rehydrated with oral
rehydration therapy. This may be accomplished at home or in the short-stay
observation unit in a hospital with oral rehydration solutions such as pedialyte,
infalyte, and rehydralyte. Carbonated and very sugary beverages should not be
given. Fermentation of sugar in the GI tract causes increased gas, abdominal
distension, and an increased frequency of diarrhea. For moderate and severe
dehydration, rehydration is accomplished by intravenous infusion ith a solution
chosen to correct the specific imbalances.
If the diarrhea is caused by bacteria or parasites, antimicrobial therapy may be
prescribed. Antiemetics and antidiarrheals are generally not used in young
children since they can mask the signs and symptoms of more serious illness
(thielman&guerrant, 2004).
Diagnostic Evaluation
Evaluation of the child with acute gastroenteritis begins with a careful history that
seeks to discover the possible cause of diarrhea, to assess the severity of symptoms
and the risk of complication, and to elicit information about current symptoms
indicating other treatable illnesses that could be causing the diarrhea. The history
should include question about recent travel, exposure to untreated drinking or washing
water sources, contact with animals or birds, daycare center attendance, recent
treatment with antibiotics, or recent diet changes. History question should also
explore the presence or absence of other symptoms such as fever and vomiting,
frequency and character of stools, urinary output, dietary habits, and recent food
intake.
Extensive laboratory evaluation is not indicated in children who have uncompleted
diarrhea and no evidence of dehydration, since most diarrheal illnesses are self-
limiting. Laboratory tests are indicated for children who are severely dehydrated and
receiving intravenous (IV) therapy. Diarrhea that develops after the introduction of
cow’s milk, fruits, or cereal may be related to enzyme deficiency or protein
intolerance. Neutrophils or red blood cells in the stool indicate bacterial gastroenteritis
or IBD. The presence of eosinophils suggests protein intolerance or parasitic
infection. Stool cultures should be performed only when blood, mucus, or
polymorphonuclear leukocytes are present in the stool, when symptoms are severe,
when there is a history of travel to a developing country, and when a specific
pathogen is suspected. Gross blood or occult blood may indicate pathogens such as
Shigella, Campylobacter, or hemorrhagic Eschericia coli strains. When the bacterial
and viral cultures are negative and when diarrhea persists for more than a few days,
stools should be examined for ova and parasites. A stools specimen with a pH of less
than 6 and the presence of reducing substances may indicate carbohydrate
malabsorption or secondary lactase deficiency. Stool electrolyte measurement may
help identify children with secretory diarrhea.
Urine specific gravity should be determined if dehydration is suspected. A complete
blood count (CBC, Serum electrolytes kreatinine, and blood urea nitrogens (PON)
should be obtain in the child who requires hospitalization. The hemogblobin
hematokrit, kreatinin, and BUN levels are usually elevated in acute diarrhea and
should normalize with rehydration.
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Leifer.2011.Introduction to maternity and pediatric nursing.USA: EL
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Jane,Ball W.Bindler,Ruth.2008.Pediatric nursing caring for children.USA:
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Hockenberry,Marilyn J.Wilson,David.2009.Wong’s Essentials of Pediatric
nursing Ed.8.USA: EL SEVIER SAUNDERS
Burns,Chaterine E.2009.Pediatric Primary care.USA: EL SEVIER
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Sodikin.2011. Asuhan keperawatan anak gangguan system gastrointestinal
dan Hepatobilier.Jakarta:Salemba Medika