ENGLISH IN NURSING GASTROINTESTINAL SYSTEM DIARRHEA PEDIATRIC

By: 6th Group A-12/A-2 Zeinidar Auliyaun N. Ria Fitriani Sevina Ramahwati Nurul Istiqomah Ayu Priyanti Elfrida Kusuma Putri Jen Riko Dewantoro Dimas Hadi Prayoga (131211132024) (131211132026) (131211132054) (131211133002) (131211133010) (131211133018) (131211133026) (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 1.2.2 1.2.3 1.2.4 Hows the anatomy and physiology of Gastrointestinal (GI)? How do the types and classification of Diarrhea? What is the etiology of Diarrhea? What is the clinical appearances of Diarrhea?

1.3 1.3.1 1.3.2 1.3.3 1.3.4

Purpose of Problems To know the anatomy and physiology of Gastrointestinal To describe the types and classification of Diarrhea To describe the etiology of Diarrhea 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 (Peyers 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 fecaloral 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 travelers diarrhea. 5. Enterohemorrhagic E.coli (O157:H7) can be associated with a mild, selflimited 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, toxinproducing, 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 . mikroorganis mme Enter to the GI System Intestine mucos cell damaged rusak Change intestine capacity intestine function in absorbtion fluid and electrolyte disorder Secretion fluid qand increase electrolite Diarrhea

Figure2.4 patofisilogy mechanisme factor infeksi of 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 . Absorbtion failed Increased water and elektrolit enter to intestine cavity

Increased content of intestine cavity Diarrhea eee 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 . Toxins in the food Bad absorbtion Increased peristaltic intestine decreased food absorbtion 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

Web Of Caution (WOC) IInfection(viruses , bacteresi, parasites) enter to the GI system Malabsorbtio n factor Physicologi factor Dietary factor

Increased osmotic pressure

Increased permeability intestine

Stimulus Simpatic nerve

Enter to the GI System Production enterotoksin and neurotoksin

Interference intestine motility

Productionelifer otoksin

Increased Peristaltic intestine

damaged intestine mucus

Increased Secretion water and electrolyte

Irritation intestine mucus Hipersecretion fluid Osmolarity disorder

Increased intestine cavity pressure

hiperperistaltic Move to intestine

Less Absorbtion content of intestine

Absorbsition disorder

Inceased intestine cavity volume Respons to out

DIARRHEA

MK: less fluid volume

MK: pain b.d infection

MK: skin Integrity disorder

MK: intolerance activity

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 selflimiting, 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 1. Emotional stress (anxiety, fatigue) 2. Intestinal infection (bacteria [E. Coli, Salmonella, Shigella], Viral [Human Rotavirus, enteric Bowel Manifestation 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 intolerance of new (lactose, food, 6. Inflammation and ulceration of intestinal walls; reduces absorption of fluid; increased intestinal

adenovirus], fungal overgrowth) 3. Food sensivity (Gluten, Cows milk) 4. Food

introduction overfeeding)

5. Medication (iron, antibiotics) 6. Colon disease (colitics, necrotizing enterocolitis, enterocolitis) 7. Surgical alterations ( short bowel syndrome)

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 Marys 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 selflimiting. Laboratory tests are indicated for children who are severely dehydrated and receiving intravenous (IV) therapy. Diarrhea that develops after the introduction of cows 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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