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    CHAPTER I

    INTRODUCTION

    a. Introduction

    Vomiting (emesis) is a symptom which often occurs in children

    indicating a large number of conditions inside the body, many of which are

    results from disorder in the gastrointestinal tracts. It can be seen really often

    as a common symptom in the clinical practice. Vomiting is a generally

    unpleasant activity that results in the expulsion of stomach contents through

    the mouth. It is a physical act that has clearly associated gastrointestinal

    motor activity. Nausea, on the other hand, although frequently accompa

    nying vomiting, is not universally associated with it and does not have an

    obvious physical mechanism. It is an uncomfortable feeling !nown to be

    relieved by vomiting."

    Vomiting itself results from the activation of protective physiological

    mechanisms that exist in order to eliminate toxins from the body. #herefore,an understanding of pathophysiology and pharmacology are fundamental to

    management, as it needed to be recogni$ed as early as possible to prevent any

    complication that could happen, such as dehydration and electrolyte

    imbalance. %

    b. Definition

    Vomiting involves a protective reflexive process, which contribute the

    forceful expulsion of gastric content that is highly coordinated. Vomiting

    itself is a symptom which occurs as a manifestation of many conditions inside

    one&s body, both acute and chronic disorder, such as gastrointestinal tract

    disease or extraintestinal disease, such as high intracranial pressure, etc. "

    Vomiting usually preceded by nausea and retching and then the whole

    series events are executed by vomiting.

    Nausea is an unpleasant and difficult to describe experience in humans. It

    is typically associated with decreased gastric motility and increased tone in

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    the small intestine. 'dditionally, there is often reverse peristalsis in the

    proximal small intestine.

    etching (*dry heaves*) refers to spasmodic respiratory movements

    conducted with a closed glottis. #his effort can be seen as preparation to

    vomit. +hile this is occurring, the antrum of the stomach contracts and the

    fundus and cardia relax. #his condition consists of diaphragm, both costal and

    crural, and abdominal muscle contraction. 't the same time, the lower

    esophageal sphincter (-) also relaxes and pulled up by the contraction of

    upper longitude esophageal muscle. /uring the retching event, the gastric

    content pushed in by the esophagus due to intraabdominal pressure and the

    presence of elevated negative intrathoracal pressure, after that the whole

    gastric content will be pushed bac! into the stomach which results from the

    presence of esophagus peristaltic. #hus, in the retching event, the gastric

    content is not expulsed out from the stomach to the mouth. #his is what

    differs retching and vomiting. "

    CHAPTER II

    CONTENT

    c. Physiology

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    Vomiting is a protective response to eliminate toxin within the humans&

    body. #he physiology of vomiting cannot be separated from an area in the

    brainstem called the central vomiting center (0V0), which always involved in

    the presence of vomiting. #he other one is 0hemoreceptor #rigger 1one

    (0#1), both of which are located in medullary structure on the brain called

    area postrema.(2ig "). #hese two areas have receptors, which then activated

    by some proemetic chemicals within the blood circulation or cerebrospinal

    fluid resulting in vomiting. #he central vomiting center contains of

    muscarinicreceptors, while the chemoreceptor trigger $one contains of 34#

    receptors and /opamine5 receptors.6

    It also receives impulses fromexogenous substances that circulate in the body which are mostly drugs,

    uremia, radiation, chemotherapy, toxins, hormones and peptides. 's well as

    opiates, digitalis or aspirin via 0anaboid, ubstance 7, and

    4ydroxytryptamine receptors. #hese receptors are activated by some factors

    which then initiate vomiting. 3

    2igure ". 'rea postrema

    #here are several pathways involved which are able to induce vomiting 8

    ". 9astrointestinal tract : lead to be the main cause and the most common

    disorder present at the clinical practice, mainly the stomach. It is going

    via vagus and sympathetic route to the vomiting center and will send and

    afferent impulses via serotonin receptors.

    5. -xtragastrointestinal tract : the vomiting signals can also arise from non

    gastrointestinal sources, including 8

    a. 4igher center of the brain, which send impulses directly to the

    vomiting center of the brain

    b. 4eart and genitalia, through vagus and sympathetic route directly to

    the vomiting center.

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    c. ;lood vessels, which contain endogenous and exogenous substances

    send impulses to the 0#1.

    d. #he vestibular system as it control coordination and balance system

    of the body, send impulses via the vestibular nuclei in the brainstem

    and then to the 0#1 and to the vomiting center at the end.

    It then sends out signals to the vagus nerve (to the esophagus, stomach

    and duodenum), the phrenic nerve (to the diaphragm) and spinal nerves (to

    the intercostals and abdominal rectus). #hese signals begin in a series of

    coordinated events that lead to the coordinated and complex act of vomiting.3

    Pathogenesis

    #rue vomiting can be divided into two broad categories8 nonbilious and

    bilious. ;ilious vomiting occurs when bile is purged along with the gastric

    contents. 'lthough some small intestinal reflux into the stom ach is common

    with all vomiting, in nonbilious vomiting, antegrade intestinal flow is preserved,

    and the ma=ority of the bile drains into the more distal portions of the intestine. If

    an obstruction is present, nonbilious vomiting implies that the obstruction is

    proximal to the ampulla of Vater. 0onditions leading to bilious vomiting involve

    either a disorder of motility or physical bloc!age to this antegrade flow of

    proximal intestinal contents distal to the ligament of #reit$."

    9astroesophageal reflux (9-), although not true vomiting, fre quently is

    included in discussions of vomiting. In contrast to the mechanism of true

    vomiting dis cussed previously, 9- occurs as a result of failed normal

    esophageal function. Normally, the lower eso phageal sphincter (-) relaxes

    with swallowing and propagation of esophageal peristalsis, allowing a food

    bolus to enter the stomach. Its basal contraction prevents food from reentering

    the esophagus from the stomach. #ransient relaxation of the - predisposes to

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    9- and is the ma=or mechanism in infants who have 9-. #he - is aided by

    sur rounding structures, especially the crural diaphragm, and disruption of these

    structures, as with a hiatal her nia, contributes to the 9- in some patients.

    Nicotine, alcohol, caffeine, and some medications can increase relaxation of the

    -, contributing to 9- in some individuals. 9- also is distinguished from

    true vom iting by its symptoms? the emesis of 9- is effortless and generally

    not associated with retching or auto nomic symptoms.@

    d. Ty#es of "o!iting

    Vomiting can be classified according to its nature and cause, as well as by

    the character of the vomiting itself.

    'ccording to the nature, vomiting can be classified as 8

    ". 7ro=ectile.

    7ro=ectile vomiting refers to a forceful vomiting and may indicate an

    elevated intracranial pressure, especially if it occurs early in the morning.

    5. Nonpro=ectile.

    Nonpro=ectile vomiting are seen more commonly in gastroesophageal

    reflux disease and other disorder."

    Vomiting also classified according to its duration of symptoms 8

    1. 'cute vomiting occurring less than or within " wee!. Asually

    associated with obstruction, ischemic, toxic, metabolic, infectious,

    neurological, and postoperative reasons.

    2. 0hronic vomiting occurring for more than " month, usually due to

    partial obstruction, motility disorder, neurological chronic conditions,

    pregnancy or functional reasons.

    3. 0yclic vomiting refers to vomiting of which onset is repetitice but

    interrupted cycles of high frequency vomiting, followed by an

    asymptomatic phase usually due to viral

    %. ecurrent vomiting

    Causes of $o!iting

    'lthough the causes of vomiting in children are many, a thorough his tory of

    the nature of the vomiting and any associated signs or symp toms as well as a

    complete physical examination generally helps narrow the differential diagnosis

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    (#able "). #argeted studies help identify the cause of the illness.

    A. Non %ilious Infectious&infla!!atory

    'cute gastroenteritis is the most common cause of vomiting in

    children. It is usually associated with diarrhea and abdominal

    pain, and viruses are common etiologic agents, although bacterial

    patho gens also must be considered. #he most common viral

    agent in infants is rotavirus. ;acterial pathogens include

    Salmonella, Shigella, Campylobacter, andEscherichia coli.

    ;acterial infections are associated more commonly with bloody diarrhea and high

    fevers than are viral infections. -nterohemorrhagicE coli B"3

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    '. etabolic&endocrinologic

    ;oth inborn errors of metabolism and endocrinologic disorders can cause vomiting

    (#able 5). #he inborn errors of metabolism generally present in early infancy, and

    the vomiting is associated with symptoms of lethargy, hypo or hypertonia, sei$ures,

    or coma. #he constellation of symptoms is similar to that seen in sepsis, neces

    sitating a high index of suspicion in the evaluation of these patients. #he presence or

    absence of meta bolic acidosis, hypoglycemia, hyper ammonemia, or !etosis and a

    family history that includes possible con sanguinity can help to determine

    the diagnosis. Cne endocrinologic condition associated with vomiting is diabetes

    mellitus. Vomiting can complicate acute !etoacidosis or occur in patients who have

    had longstand ing diabetes and consequent gastro paresis. lowed gastric motility

    usually presents after diabetes mellitus has been present for approximately "B years.

    -arly satiety and a sense of fullness frequently precede the onset of vomiting in

    diabetic gastroparesis."B

    Vomiting as a consequence of foodrelated sensitivity always should be considered.

    #he variants encountered most commonly in pediatric patients are cow mil! and soy

    protein intolerance, type I (Ig-mediated) food allergy, and celiac disease. 0ow mil!protein intolerance affects 5D to

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    characteri$ed by acuteonset periodic episodes of nausea and vomiting interspersed

    with conspicuous periods of wellness. 'pproximately

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    *. Anato!ic

    #he anatomic and, thus, the generally surgical causes of nonbilious

    vomiting are those that affect the intestinal tract proximal to the

    point of bilious drainage (ampulla of Vater), which is proximal to the

    ligament of #reit$ (#able %). +hereas congenital anomalies usually

    present in the newborn period, acquired lesions can present at any

    age. 'ny infant who exhibits persistent nonbilious vomiting, with or

    without feeding, in the immediate newborn period must be suspected

    of having an intestinal atresia or a luminally obstructing lesion

    (pyloric stenosis, luminal band, web) proximal to the point of bile

    drainage (ampulla of Vater).%

    'n easy and rapid test to evaluate possible esophageal atresia is the

    ability to pass a nasogastric tube easily into the stomach. 'fter the

    tube has been passed, it is important to obtain a radiograph to assure

    that the tube is in the stomach and not coiled in an atretic esophagus. 'ny resistance

    to passage of the tube is an indication for evaluation by contrast radio graph for an

    obstruction. If an obstruction is present, nasoesophageal tube drainage is important toprevent aspiration of pooled esophageal secretions. 0ontrast studies are the standard

    for the diagnosis of these conditions. >

    %. %ilious

    'lthough not absolute, anatomic conditions causing luminal

    obstruction distal to the ligament of #reit$ usually cause bilious

    vomiting. ;ilious vomiting is an ominous sign that mandates

    immediate evaluation (#able 3).

    In the newborn period, intestinal atresias and stenosis and

    malrotation with or without volvulus need to be ruled out

    immediately. In the older child, malrotation with volvulus also is a

    surgical emergency that is diagnosed relatively easily by

    gastrointestinal contrast study. 'fter the diagnosis has been established

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    radiographically, the gastrointestinal tract should be decompressed with a nasogastric

    tube, food and drin! withheld, and the patient supported with intravenous fluids until

    definitive surgical intervention can be underta!en.%

    e. Clinical !anifestation

    Vomiting in children usually indicate a sign of infection. 2ever, nausea,

    abdominal pain, or diarrhea become symptoms accompanying the vomiting that

    already existed in infected children. #his condition will stop within %@ hours.

    +hen vomiting remains, concerns any other serious conditions. 0hildren are in

    higher ris! to develop dehydration, particularly when accompanied by diarrhea.

    Viral infections become the most common cause compared to other pathogens.

    Vomiting accompanied by fever are more common caused by bacteries rather

    than virus or parasites. 7eptic ulcer needs to be in mind when vomiting comes

    right after having meal, while in food poisoning vomiting occurs about "@ hours

    after meals. Vomiting et causa food borne disease such as almonella needs

    more time to develop symptoms due to its incubation period. 'nother cause of

    vomiting in children is also oral candidiasis."B

    7ro=ectile nonbillous type of vomiting in babies is a probable sign of

    gastrointestinal obstruction, such as pyloric stenosis. 7yloric stenosis usually

    found in the second wee! of birth, but rarely found at birth. 7ersistent vomiting

    in neonates which usually happen at night has a possibility of any hiatal hernia.

    0auses of this abnormality are often viral infection, drugs induced, and trauma.

    'nother symptoms beside vomit are epigastric pain and left upper quadrant

    which at some point loo! ali!e gastritis but unresponsive to antagonist receptor

    45 treatment. "

    7hysician needs to rule out any surgical abnormalities immediately in

    children with vomiting. #here are some clues that can be used to eliminate all

    the possibilities, such as (") stomach pain which occurs before the vomit andFor

    continuous for more than 6 hours, (5) bile liquid among the vomiting fluid, and

    (6) abdominal distention. Volvulus in neonates occurs to be some episodes of

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    greenish vomiting in few days after birth and followed by any signs of

    obstruction in gastrointestinal system also peritonitis. 'lmost >BD of children

    with volvulus presents vomiting and @BD of them complains about stomachache.5

    Vomiting can also be caused by any disorder from extraintestinal, for

    example respiratory tract infection or urinary tract infection. ome medicines

    li!e histamines, phenytoin, chemotherapy agents, aspirins, and some antibiotics.

    can also induce vomiting.6

    Vomiting after mild head in=ury found in "3D children and most of them

    have a history of recurrent headache and motion sic!ness. #herefore, vomiting in

    mild head in=ury associates with individual intrinsic factor. Vomiting due to

    functional disorder mostly found in children 5< years of age with migrain,

    motion sic!ness, and gastrointestinal tract disorder such abdominal pain and

    defecation disorder. ometimes, anorexia nervosa of bulimia might be stay in

    mind for any possibilities of psychiatry disorder.

    ;ased on its quality, vomiting can be classified as bilious, bloody, non

    bilious and nonbloody. Vomiting that comes from stomach is usually yellow

    or clear and contains remnants of previously ingested food."B

    +hen the vomiting is dar! green, it may referred as bilious because it

    indicates the presence of bile. ;ilious vomiting frequently is pathologic

    because it may be a sign of an underlying abdominal problem such asintestinal obstruction beyond the duodenal ampulla of Vater, where the

    common bile duct empties.>

    #he presence of blood in the emesis, also !nown as hematemesis,

    indicates acute bleeding from the upper portion of the 9I tract, as can occur wit

    gastritis, Eallory+eiss tears, or peptic ulcer disease. 0offee groundli!e

    material often is representative of an old 9I hemorrhage because blood dar!ens

    to a blac! or dar!brown color when exposed to the acidity of the gastric

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    secretions. #he more massive or proximal the bleeding, the more li!ely it is to be

    bright red. "

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    f. Differential diagnosis

    #here are a large number of conditions, which indicated by vomiting as

    the main andFor other symptom. -tiology of vomiting may vary according to

    each systems of the body.

    0ommon causes of vomiting in infancy 8

    ". 9- and 9-/9astroesophageal reflux (9-) is the effortless and nonpro=ectile passage of stomach

    contents into the esophagus and can be a normal physiologic process. It is common

    in healthy term infants, children, and adults. egurgitation is often used

    interchangeably with 9-. 7ea!s at 6 to % months (

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    not warrant additional investigation. 9- can be confirmed by monitoring

    esophageal p4 for 5% hours (p4meter) . eflux index G 3D shows pathologic 9-

    (9-/). 7arental education about the natural course of infantile 9- is the !ey to

    successful management. Eostly resolve by "5 months of age. "B If symptoms persist

    past "@ months of age the child warrants an evaluation. 9-/ symptoms 8 frequent

    heartburn (G5 times a wee!), chest pain, regurgitation of partially digested food into

    the bac! of the throat, trouble swallowing, breathing difficulties similar to asthma,

    coughing, sore throat, a sour taste in the bac! of the mouth. 9-/ ris! factors 8

    genetics, in=ury and trauma to the esophagus, hiatal hernia, diabetes, connective

    tissue disorders that wea!en the -, 1ollinger -llison syndrome.6

    5. 7yloric tenosis

    Cccurs in 5 to 6 infants per "BBB live births. Eore common in males, with a male

    female ratio of %8" to 8". #ypical presentation8 a 6 to wee!old infant with

    progressive or intermittent vomiting after feeding (often pro=ectile). 7hysical

    examination 8 an oliveli!e mass in the right midepigastrium, mostly after emesis.

    Visible gastric peristalsis is seen with feeding. /iagnosis is usually made by

    abdominal A9. >

    6. Intestinal 'tresia

    Cccurrence of 5.@ per "B,BBB live births. /uodenal atresia (%>D), =e=unal atresia

    (6D) and ileal atresia ("%D). Infants present with bilious vomiting, abdominal

    distension, and failure to pass meconium. 4istory of maternal polyhydramnios.

    'bdominal radiographs show the pathognomonic Hdouble bubble. "

    0ommon causes of vomiting beyond infancy 8

    ". 'cute 9astroenteritis

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    'lthough may occur in infants, acute gastroenteritis is the most common reason for

    vomiting beyond infancy. Viruses (otavirus) are the most common cause, followed

    by bacteria and parasites. #ypical presentation is acute onset of vomiting followed by

    diarrhea. Vomiting is a selfprotective process that may reduce the load of the

    infectious organisms and associated toxins or irritants that cause the vomiting.

    ehydration (oral, enteral, or intravenous) is !ey to successful management of acute

    gastroenteritis.@

    Initial care in the emergency department should focus on correction of dehydration.

    #he type and amount of fluid given should reflect the degree of dehydration in the

    child.

    Minimal or no dehydration

    No immediate treatment is required. If the child is breastfed, the mother should be

    encouraged to breastfeed more frequently than usual and for longer at each feed. If

    the child is not exclusively breastfed, then oral maintenance fluids (including clean

    water, soup, rice water, yogurt drin!, or other culturally appropriate fluid) should be

    given at a rate of approximately 3BB mFday for children younger than 5 years, "BBB

    mFday for children aged 5"B years, and 5BBB mFday for children older than "B

    years.

    In addition, ongoing fluid losses should be replaced with "B mF!g body weight of

    additional C for each loose stool and 5 mF!g body weight of additional C for

    each episode of emesis (both for breastfed and nonbreastfed children). "B

    Mild-to-moderate dehydration

    0hildren should be given 3B"BB mF!g of C over a 5 to %hour period to replace

    their estimated fluid deficit, with additional C given to replace ongoing losses ("B

    mF!g body weight for each stool and 5 mF!g body weight for each episode of

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    emesis). 'fter the initial rehydration phase, patients may be transitioned to

    maintenance fluids as described above.6

    C should be given slowly by the parent using a teaspoon, syringe, or medicine

    dropper at the rate of 3 m every "5 minutes. If tolerated by the patient, the rate of

    C delivery can be increased slowly over time.

    2or patients who do not tolerate C by mouth, nasogastric (N9) feeding is a safe

    and effective alternative. Eultiple clinical trials have found N9 rehydration to be as

    efficacious as IV rehydration, but more cost effective and with fewer adverse events.

    7atients should be reassessed frequently by the clinician to ensure adequacy of oral

    inta!e and resolution of the various signs and symptoms of dehydration."

    Severe dehydration

    evere dehydration constitutes a medical emergency requiring immediate

    resuscitation with IV fluids. IV access should be obtained and patients should be

    administered a bolus of 5B6B mF!g lactated inger () or normal saline (N)

    solution over B minutes. If pulse, perfusion, andFor mental status do not improve, asecond bolus should be administered. 'fter this, the patient should be given an

    infusion of

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    cholera, however, appear to have higher rates of hyponatremia with reduced

    osmolarity C compared with standardosmolarity C, without any of the added

    benefits seen in patients with noncholera gastroenteritis.3

    Eultiple preparations of reducedosmolarity C are available in the Anited tates,

    including 7edialyte, Infalyte, and Naturalyte. 'vailable formulations in -urope

    include /ioralyte and /iocalm Kunior. In developing countries, clinicians can use

    +4C C sachets or a homemade solution of 6 g (" tsp) salt and "@ g ( tsp) sugar

    added to " liter of clean water.

    New research suggests that polymerbased C, made from complex carbohydrates

    such as rice, wheat, or mai$e, may reduce stool output and length of diarrhea

    compared with glucosebased C. +ith these solutions, carbohydrates are slowly

    digested in the small intestine, releasing glucose to facilitate sodium upta!e without

    adding a significant osmotic load to bowel contents. 'lthough not widely available in

    the Anited tates currently, polymerbased C may become the preferred solution

    for oral rehydration of children with diarrhea in the future."

    eeding and nutrition

    In general, children with gastroenteritis should be returned to a normal diet as rapidly

    as possible. -arly feeding reduces illness duration and improves nutritional outcome.

    ;reastfed infants should continue to breast feeding throughout the rehydration and

    maintenance phases of acute gastroenteritis. 2ormulafed infants should restart

    feeding at full strength as soon as the rehydration phase is complete (ideally in 5%

    hours). +eaned children should restart their normal fluids and solids as soon as the

    rehydration phase is complete. 2atty foods and foods high in simple sugars should be

    avoided.

    2or the ma=ority of infants, clinical trials have found no benefit of lactosefree

    formulas over lactosecontaining formulas. imilarly, highly specific diets, such as

    the ;'# (bananas, rice, applesauce, and toast) diet, have not been shown to

    improve outcomes and may provide suboptimal nutrition for the patient..

    6. 2reedman, tephen ;. et al. Cral Cndansetron for 9astroenteritis in a 7ediatric

    -mergency /epartment. 5BB. The !e" England #ournal of Medicine.N -ngl K Eed

    63%?"

    %. 0ole, arah 1., anham, Kason . 2ailure to #hrive 8 'n Apdate.$m am

    %hysician.5B"" 'pr "?@6(@6%.

    3. ;owen, . 7hysiology of Vomiting. ">>.

    http8FFarbl.cvmbs.colostate.eduFhboo!sFpathphysFdigestionFstomachFvomiting.html

    . 2 / ;rown, K ;rown, # 2 ;eattie. +hy do children vomit after minor head in=uryO

    #$ccid Emerg Med 5BBB?'/85@:5

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    @. #he North Italian -ndoscopic 0lub for the tudy ant #reatment of -sophageal

    Varices. 7rediction of the first variceal hemorrhage in patients with cirrhosis of the

    liver and esophageal varices. N -ngl K Eed. ">@@? 6">8 >@6>.

    >. 'l'mri, Nawaf. -mergency Eedicine 'pproach #o Nausea L Vomiting. 5B"".http8FFwww.slideshare.netFNawaf'l'mriFnauseavomiting"B5B>@%Q

    "B. Kurnalis, Rusri /ianne., et al. Ealrotasi dan Volvulus pada 'na!.

    http8FF=urnal.f!.unand.ac.id

    http://www.slideshare.net/NawafAlAmri/nausea-vomiting-10620984http://jurnal.fk.unand.ac.id/http://www.slideshare.net/NawafAlAmri/nausea-vomiting-10620984http://jurnal.fk.unand.ac.id/