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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 accompanying vomiting, is not universally associated with it and does not have an
obvious physical mechanism. It is an uncomfortable feeling known to be
relieved by vomiting.1
Vomiting itself results from the activation of protective physiological
mechanisms that exist in order to eliminate toxins from the body. Therefore,
an understanding of pathophysiology and pharmacology are fundamental to
management, as it needed to be recognized as early as possible to prevent any
complication that could happen, such as dehydration and electrolyte
imbalance. 4

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
ones body, both acute and chronic disorder, such as gastrointestinal tract
disease or extraintestinal disease, such as high intracranial pressure, etc. 1
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

the small intestine. Additionally, there is often reverse peristalsis in the


proximal small intestine.6
Retching ("dry heaves") refers to spasmodic respiratory movements
conducted with a closed glottis. This effort can be seen as preparation to
vomit. While this is occurring, the antrum of the stomach contracts and the
fundus and cardia relax. This condition consists of diaphragm, both costal and
crural, and abdominal muscle contraction. At the same time, the lower
esophageal sphincter (LES) also relaxes and pulled up by the contraction of
upper longitude esophageal muscle. During 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 back into the stomach which results from the
presence of esophagus peristaltic. Thus, in the retching event, the gastric
content is not expulsed out from the stomach to the mouth. This is what
differs retching and vomiting. 1

CHAPTER II
CONTENT
c. Physiology

Vomiting is a protective response to eliminate toxin within the humans


body. The physiology of vomiting cannot be separated from an area in the
brainstem called the central vomiting center (CVC), which always involved in
the presence of vomiting. The other one is Chemoreceptor Trigger Zone
(CTZ), both of which are located in medullary structure on the brain called
area postrema. (Fig 1). These two areas have receptors, which then activated
by some proemetic chemicals within the blood circulation or cerebrospinal
fluid resulting in vomiting. The central vomiting center contains of
muscarinic receptors, while the chemoreceptor trigger zone contains of 5-HT
receptors and Dopamine-2 receptors.3 It also receives impulses from
exogenous substances that circulate in the body which are mostly drugs,
uremia, radiation, chemotherapy, toxins, hormones and peptides. As well as
opiates,

digitalis

or

aspirin

via

Canaboid,

Substance

P,

and

Hydroxytryptamine receptors. These receptors are activated by some factors


which then initiate vomiting. 5

Figure 1. Area postrema


There are several pathways involved which are able to induce vomiting :
1. Gastrointestinal 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.
2. Extra-gastrointestinal tract the vomiting signals can also arise from nongastrointestinal sources, including :
a. Higher center of the brain, which send impulses directly to the
b.

vomiting center of the brain


Heart and genitalia, through vagus and sympathetic route directly to
the vomiting center.

c.

Blood vessels, which contain endogenous and exogenous substances

d.

send impulses to the CTZ.


The 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 CTZ and to the vomiting center at the end. 7

Figure 2. Vomiting physiology

Figure 3. Factors influencing vomiting

Mechanism of vomiting
The vomiting center within the medulla acts as the incident commander
for vomiting. This area processes incoming stimuli from vomiting triggers
outside and inside the brain. It is also thought to be the area where nausea is
controlled.2
Afferent impulses due to any stress on any of the areas will shoot and
impulse going to the vomiting center which generates efferent impulses either
mild causing nausea or mild causing retching or severe causing vomiting.
Due to mild impulses, the duodenal and jejunal muscle will contract
while the gastric tone decreases, causing reflux of intestinal contents to the
stomach along with tachycardia, hypersalivation and repetitive swallowing,
which now completes a nausea phase depending on the strength of the
stimulus.4
When impulses are moderate and had much time to act, the vomiting
center starts to send impulses through the phrenic nerve (innervate the
diaphragm), vagus nerve which then send signals to the esophagus, stomach,
and duodenum, the spinal nerves going to the abdominal and intercostal
muscles.3
A rhythmic synchronized movement of contractions of the diaphragm,
abdominal and intercostal muscles, and closure of the glottis due to all the
impulses begins. It causes the intraabdominal pressure to rise and the
intrathoracic pressure to decrease, pushing contents up to the esophagus
against the glottis. This is called retching phase. The retching phase is not
always followed by the vomiting phase. 1
When severe and continuous impulses are prolonged, the abdominal
muscles contract and the hiatal part of the diaphragm relaxes, while the
stomach squeezes and contracts and the cardia and fundus parts are relax.
This will cause relaxation of the upper and lower esophageal sphincters,

which will then allow the gastric contents that under severe pressure to be
pushed through the esophagus and then pass out of the mouth.9
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). These signals begin in a series of
coordinated events that lead to the coordinated and complex act of vomiting.5

Pathogenesis
True vomiting can be divided into two broad categories: nonbilious and
bilious. Bilious vomiting occurs when bile is purged along with the gastric
contents. Although some small intestinal reflux into the stom- ach is common
with all vomiting, in nonbilious vomiting, antegrade intestinal flow is preserved,
and the majority 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. Conditions leading to bilious vomiting involve
either a disorder of motility or physical blockage to this antegrade flow of
proximal intestinal contents distal to the ligament of Treitz.1
Gastroesophageal reflux (GER), although not true vomiting, fre- quently is
included in discussions of vomiting. In contrast to the mechanism of true
vomiting dis- cussed previously, GER occurs as a result of failed normal
esophageal function. Normally, the lower eso- phageal sphincter (LES) relaxes
with swallowing and propagation of esophageal peristalsis, allowing a food
bolus to enter the stomach. Its basal contraction prevents food from re-entering
the esophagus from the stomach. Transient relaxation of the LES predisposes to

GER and is the major mechanism in infants who have GER. The LES is aided by
sur- rounding structures, especially the crural diaphragm, and disruption of these
structures, as with a hiatal her- nia, contributes to the GER in some patients.
Nicotine, alcohol, caffeine, and some medications can increase relaxation of the
LES, contributing to GER in some individuals. GER also is distinguished from
true vom- iting by its symptoms; the emesis of GER is effortless and generally
not associated with retching or auto- nomic symptoms.8

d. Types of vomiting
Vomiting can be classified according to its nature and cause, as well as by
the character of the vomiting itself.
According to the nature, vomiting can be classified as :
1. Projectile.
Projectile vomiting refers to a forceful vomiting and may indicate an
elevated intracranial pressure, especially if it occurs early in the morning.
2. Non-projectile.
Non-projectile vomiting are seen more commonly in gastroesophageal
reflux disease and other disorder.1
Vomiting also classified according to its duration of symptoms :
1. Acute vomiting occurring less than or within 1 week. Usually
associated with obstruction, ischemic, toxic, metabolic, infectious,
neurological, and post-operative reasons.
2. Chronic vomiting occurring for more than 1 month, usually due to
partial obstruction, motility disorder, neurological chronic conditions,
pregnancy or functional reasons.
3. Cyclic 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
4. Recurrent vomiting
Causes of Vomiting
Although 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

(Table 1). Targeted studies help identify the cause of the illness.

A. Non Bilious Infectious/inflammatory


Acute 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. The most common viral
agent in infants is rotavirus. Bacterial pathogens include
Salmonella, Shigella, Campylobacter, and Escherichia coli.
Bacterial infections are associated more commonly with bloody diarrhea and high
fevers than are viral infections. Enterohemorrhagic E coli 0157:H7 can cause
hemorrhagic colitis and may be complicated by the development of hemolyticuremic syndrome. Clostridium difficile is a bacterial pathogen that frequently is
associated with the recent use of antibiotics. It causes a pseudo- membranous colitis,
often with bloody diarrhea and associated with abdominal pain and vomiting.
Giardia lamblia is a protozoan commonly associated with contaminated water and
attendance at child care centers.5 It may cause watery diarrhea and vomiting.
Diagnosis is made with stool bacterial cultures, rotazyme analysis for rotavirus,
detection of C difficile toxin, and detection of ova and parasites
for G lamblia. Sepsis, central nervous system infections, urinary
tract infections, and pneumonia all can present with or involve
vomiting, usually in addition to other symptoms.
Labyrinthitis and pancreatitis both cause vomiting. Dizziness
usually is associated with labyrin- thitis and abdominal pain with
pancreatitis.3
Inflammatory conditions of the intestinal tract, such as
inflammatory bowel disease, also tend to involve vomiting. In
these conditions, the vomiting frequently is related to altered
motility with abnormal or dysfunctional swallowing, gastric
emptying, or peristalsis.9

1. Metabolic/endocrinologic
Both inborn errors of metabolism and endocrinologic disorders can cause vomiting
(Table 2). The inborn errors of metabolism gener-ally present in early infancy, and
the vomiting is associated with symptoms of lethargy, hypo- or hypertonia, seizures,
or coma. The constellation of symptoms is similar to that seen in sepsis, necessitating a high index of suspicion in the evaluation of these patients. The presence or
absence of meta- bolic acidosis, hypoglycemia, hyper- ammonemia, or ketosis and a
family history that includes possible con- sanguinity can help to determine
the diagnosis. One endocrinologic condition associated with vomiting is diabetes
mellitus. Vomiting can complicate acute ketoacidosis or occur in patients who have
had long-stand- ing diabetes and consequent gastro- paresis. Slowed gastric motility
usually presents after diabetes mellitus has been present for approximately 10 years.
Early satiety and a sense of fullness frequently precede the onset of vomiting in
diabetic gastroparesis.10
Vomiting as a consequence of food-related sensitivity always should be considered.
The variants encountered most commonly in pediatric patients are cow milk and soy
protein intolerance, type I (IgE-mediated) food allergy, and celiac disease. Cow milk
protein intolerance affects 2% to 7% of infants, with approximately 20% of these
also sensitive to soy protein. In addition to vomiting, the patients usually have
diarrhea that frequently is guaiac-positive. Celiac disease occurs only in children
who eat gluten-containing foods. Patients typically suffer from wasting, irri- tability,
and diarrhea, but vomiting also can occur.5

2. Neurologic
Vomiting occurs in any neurologic condition that involves increased intracranial
pressure (ICP) (Table 3). Additionally, patients who have seizures,
autonomic disorders (Riley-Day syndrome), and con- ditions
affecting the floor of the fourth ventricle without increased ICP
frequently have their condition worsened with vomiting.
Cyclic vomiting is a unique entity that must be considered
separately. Onset occurs typically at early school age, and it is

characterized by acute-onset periodic episodes of nausea and vomiting interspersed


with conspicuous periods of wellness. Approximately 77% of patients can identify
precipitating events, usually intense emotional states. These patients have an
increased incidence of migraine headaches and prevalence of epilepsy and irritable
bowel syndrome. Because no diagnostic test or specific clinical identifying feature
distinguishes cyclic vomiting syndrome from other potentially life-threatening
conditions, the diagnosis can be made only after time has elapsed and upon exclusion
of other diagnoses.7

3. Psychological
Behavioral or psychological causes of vomiting can be problematic in the pediatric
age group. Some children induce vomiting to seek attention in environments in
which personal attention is lacking. The extreme of this behavior is rumination.
Rumination is a serious condition that occurs in infants when there is a failure in
reciprocal interaction between the infant and caregiver. The purposes of rumination
are self-stimulation and satisfaction of needs. Rumination also is seen in older
children, especially those who are severely mentally retarded.8
Classically, the infant (older than 3 months) learns to bring up gastric contents into
the mouth, frequently by inserting a hand into the back of the throat or simply
through rhythmic contractions of the pharynx, tongue, and abdominal muscles. The
oral contents then are reswallowed, although spillage does occur. Not only do these
patients suffer social deprivation, but the chronic emesis can lead to inanition and
growth failure. The failure to thrive does not improve with traditional medical
intervention, but rather requires sensitive and interactive nurturing. A mothersubstitute who is empathic with and observant of both the parents and infants needs
is required to help the parent establish more nurturing skills. More formal
psychotherapeutic help frequently is needed for the parents.
Bulimia, characterized by secretive binge-eating episodes followed by self-induced
vomiting, is a cause of vomiting especially among teenagers.6

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4. Anatomic
The 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 Treitz (Table 4). Whereas congenital anomalies usually
present in the newborn period, acquired lesions can present at any
age. Any 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).4
An easy and rapid test to evaluate possible esophageal atresia is the
ability to pass a nasogastric tube easily into the stomach. After 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. Any 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 to
prevent aspiration of pooled esophageal secretions. Contrast studies are the standard
for the diagnosis of these conditions. 9

B. Bilious

Although not absolute, anatomic conditions causing luminal


obstruction distal to the ligament of Treitz usually cause bilious
vomiting. Bilious vomiting is an ominous sign that mandates
immediate evaluation (Table 5).
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. After the diagnosis has been established

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radiographically, the gastrointestinal tract should be decompressed with a nasogastric


tube, food and drink withheld, and the patient supported with intravenous fluids until
definitive surgical intervention can be undertaken.4

e. Clinical manifestation
Vomiting in children usually indicate a sign of infection. Fever, nausea,
abdominal pain, or diarrhea become symptoms accompanying the vomiting that
already existed in infected children. This condition will stop within 6-48 hours.
When vomiting remains, concerns any other serious conditions. Children are in
higher risk 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. Peptic ulcer needs to be in mind when vomiting comes
right after having meal, while in food poisoning vomiting occurs about 1-8 hours
after meals. Vomiting et causa food borne disease such as Salmonella needs
more time to develop symptoms due to its incubation period. Another cause of
vomiting in children is also oral candidiasis.10
Projectile non-billous type of vomiting in babies is a probable sign of
gastrointestinal obstruction, such as pyloric stenosis. Pyloric stenosis usually
found in the second week of birth, but rarely found at birth. Persistent vomiting
in neonates which usually happen at night has a possibility of any hiatal hernia.
Causes of this abnormality are often viral infection, drugs induced, and trauma.
Another symptoms beside vomit are epigastric pain and left upper quadrant
which at some point look alike gastritis but unresponsive to antagonist receptor
H2 treatment. 1
Physician needs to rule out any surgical abnormalities immediately in
children with vomiting. There are some clues that can be used to eliminate all
the possibilities, such as (1) stomach pain which occurs before the vomit and/or
continuous for more than 3 hours, (2) bile liquid among the vomiting fluid, and
(3) 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. Almost 90% of children
with volvulus presents vomiting and 80% of them complains about stomachache.
2

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


example respiratory tract infection or urinary tract infection. Some medicines
like histamines, phenytoin, chemotherapy agents, aspirins, and some antibiotics.
can also induce vomiting.3
Vomiting after mild head injury found in 15% children and most of them
have a history of recurrent headache and motion sickness. Therefore, vomiting in
mild head injury associates with individual intrinsic factor. Vomiting due to
functional disorder mostly found in children 2-7 years of age with migrain,
motion sickness, and gastrointestinal tract disorder such abdominal pain and
defecation disorder. Sometimes, anorexia nervosa of bulimia might be stay in
mind for any possibilities of psychiatry disorder. 6
Based on its quality, vomiting can be classified as bilious, bloody, nonbilious and non-bloody. Vomiting that comes from stomach is usually yellow
or clear and contains remnants of previously ingested food.10
When the vomiting is dark green, it may referred as bilious because it
indicates the presence of bile. Bilious vomiting frequently is pathologic
because it may be a sign of an underlying abdominal problem such as
intestinal obstruction beyond the duodenal ampulla of Vater, where the
common bile duct empties.9
The presence of blood in the emesis, also known as hematemesis,
indicates acute bleeding from the upper portion of the GI tract, as can occur wit
gastritis, Mallory-Weiss tears, or peptic ulcer disease. Coffee ground-like
material often is representative of an old GI hemorrhage because blood darkens
to a black or dark-brown color when exposed to the acidity of the gastric

13

secretions. The more massive or proximal the bleeding, the more likely it is to be
bright red. 1

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f. Differential diagnosis
There are a large number of conditions, which indicated by vomiting as
the main and/or other symptom. Etiology of vomiting may vary according to
each systems of the body.

Common causes of vomiting in infancy :


1. GER and GERD
Gastroesophageal reflux (GER) is the effortless and nonprojectile passage of stomach
contents into the esophagus and can be a normal physiologic process. It is common
in healthy term infants, children, and adults. Regurgitation is often used
interchangeably with GER. Peaks at 3 to 4 months (67% of infants), gradually
decreases to 14% at 7 months, and decreases to less than 5% by 12 to 14 months.
Common symptoms associated with this are feeding refusal, irritability, fussiness,
cough, apnea, and wheezing. Appropriate weight for age is a good marker that does

15

not warrant additional investigation. GER can be confirmed by monitoring


esophageal pH for 24 hours (pH-meter) . Reflux index > 5% shows pathologic GER
(GERD). Parental education about the natural course of infantile GER is the key to
successful management. Mostly resolve by 12 months of age. 10 If symptoms persist
past 18 months of age the child warrants an evaluation. GERD symptoms : frequent
heartburn (>2 times a week), chest pain, regurgitation of partially digested food into
the back of the throat, trouble swallowing, breathing difficulties similar to asthma,
coughing, sore throat, a sour taste in the back of the mouth. GERD risk factors :
genetics, injury and trauma to the esophagus, hiatal hernia, diabetes, connective
tissue disorders that weaken the LES, Zollinger- Ellison syndrome. 3
2. Pyloric Stenosis
Occurs in 2 to 3 infants per 1000 live births. More common in males, with a male-female ratio of 4:1 to 6:1. Typical presentation: a 3- to 6-week-old infant with
progressive or intermittent vomiting after feeding (often projectile). Physical
examination : an olivelike mass in the right midepigastrium, mostly after emesis.
Visible gastric peristalsis is seen with feeding. Diagnosis is usually made by
abdominal USG. 9

3. Intestinal Atresia
Occurrence of 2.8 per 10,000 live births. Duodenal atresia (49%), jejunal atresia
(36%) and ileal atresia (14%). Infants present with bilious vomiting, abdominal
distension, and failure to pass meconium. History of maternal polyhydramnios.
Abdominal radiographs show the pathognomonic double bubble. 1

Common causes of vomiting beyond infancy :


1. Acute Gastroenteritis

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Although may occur in infants, acute gastroenteritis is the most common reason for
vomiting beyond infancy. Viruses (Rotavirus) are the most common cause, followed
by bacteria and parasites. Typical presentation is acute onset of vomiting followed by
diarrhea. Vomiting is a self-protective process that may reduce the load of the
infectious organisms and associated toxins or irritants that cause the vomiting.
Rehydration (oral, enteral, or intravenous) is key to successful management of acute
gastroenteritis.8
Initial care in the emergency department should focus on correction of dehydration.
The 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 drink, or other culturally appropriate fluid) should be
given at a rate of approximately 500 mL/day for children younger than 2 years, 1000
mL/day for children aged 2-10 years, and 2000 mL/day for children older than 10
years.
In addition, ongoing fluid losses should be replaced with 10 mL/kg body weight of
additional ORS for each loose stool and 2 mL/kg body weight of additional ORS for
each episode of emesis (both for breastfed and nonbreastfed children).10

Mild-to-moderate dehydration
Children should be given 50-100 mL/kg of ORS over a 2- to 4-hour period to replace
their estimated fluid deficit, with additional ORS given to replace ongoing losses (10
mL/kg body weight for each stool and 2 mL/kg body weight for each episode of

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


maintenance fluids as described above.3
ORS should be given slowly by the parent using a teaspoon, syringe, or medicine
dropper at the rate of 5 mL every 1-2 minutes. If tolerated by the patient, the rate of
ORS delivery can be increased slowly over time.
For patients who do not tolerate ORS by mouth, nasogastric (NG) feeding is a safe
and effective alternative. Multiple clinical trials have found NG rehydration to be as
efficacious as IV rehydration, but more cost effective and with fewer adverse events.
Patients should be reassessed frequently by the clinician to ensure adequacy of oral
intake and resolution of the various signs and symptoms of dehydration.1
Severe dehydration
Severe dehydration constitutes a medical emergency requiring immediate
resuscitation with IV fluids. IV access should be obtained and patients should be
administered a bolus of 20-30 mL/kg lactated Ringer (LR) or normal saline (NS)
solution over 60 minutes. If pulse, perfusion, and/or mental status do not improve, a
second bolus should be administered. After this, the patient should be given an
infusion of 70 mL/kg LR or NS over 5 hours (children < 12 months) or 2.5 hours
(older children). If no peripheral veins are available, an intraosseous line should be
placed. Serum electrolytes, bicarbonate, urea/creatinine, and glucose levels should be
tested.
Once resuscitation is complete and mental status returns to normal, rehydration
should continue with ORS as described above, as it has been shown to decrease the
rate of hyponatremia and hypernatremia when compared with IV rehydration. 7
Type of ORS
A large Cochrane meta-analysis confirmed several earlier studies showing that
reduced-osmolarity ORS (osmolarity< 250 mmol/L) is associated with fewer
treatment failures, lower stool output, and less frequent vomiting compared with
standard-osmolarity ORS for patients with noncholera gastroenteritis.7 Patients with

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cholera, however, appear to have higher rates of hyponatremia with reducedosmolarity ORS compared with standard-osmolarity ORS, without any of the added
benefits seen in patients with noncholera gastroenteritis.5
Multiple preparations of reduced-osmolarity ORS are available in the United States,
including Pedialyte, Infalyte, and Naturalyte. Available formulations in Europe
include Dioralyte and Diocalm Junior. In developing countries, clinicians can use
WHO ORS sachets or a homemade solution of 3 g (1 tsp) salt and 18 g (6 tsp) sugar
added to 1 liter of clean water.6
New research suggests that polymer-based ORS, made from complex carbohydrates
such as rice, wheat, or maize, may reduce stool output and length of diarrhea
compared with glucose-based ORS. With these solutions, carbohydrates are slowly
digested in the small intestine, releasing glucose to facilitate sodium uptake without
adding a significant osmotic load to bowel contents. Although not widely available in
the United States currently, polymer-based ORS may become the preferred solution
for oral rehydration of children with diarrhea in the future.1
Feeding and nutrition
In general, children with gastroenteritis should be returned to a normal diet as rapidly
as possible. Early feeding reduces illness duration and improves nutritional outcome.
Breastfed infants should continue to breast feeding throughout the rehydration and
maintenance phases of acute gastroenteritis. Formula-fed infants should restart
feeding at full strength as soon as the rehydration phase is complete (ideally in 2-4
hours). Weaned children should restart their normal fluids and solids as soon as the
rehydration phase is complete. Fatty foods and foods high in simple sugars should be
avoided.
For the majority of infants, clinical trials have found no benefit of lactose-free
formulas over lactose-containing formulas. Similarly, highly specific diets, such as
the BRAT (bananas, rice, applesauce, and toast) diet, have not been shown to
improve outcomes and may provide suboptimal nutrition for the patient.7

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Assesment of dehydration using the Dhaka method

2. Acute intestinal obstruction after infancy


Typical presentations : abdominal pain, nausea, vomiting (often bilious), abdominal
distension, and signs of peritonitis if the obstruction has been present for a prolonged
period. Bilious vomiting is characteristic of intestinal obstruction distal to the
ampulla of Vater.
Differential diagnosis of intestinal obstruction
1. Intussusception
2. Malrotation with or without midgut volvulus
3. Incarcerated hernias
4. Strictures (eg, Crohn disease, nonsteroidal anti-inflammatory drugs, and
irradiation)
5. Adhesions
6. Bezoars
7. Superior mesenteric artery syndrome
8. Small intestinal tumors
Initial management of intestinal obstruction :
-Bowel rest is key in the management of intestinal obstruction.
-Gastric decompression via a nasogastric tube to prevent further episodes of emesis
and minimize the risk of aspiration.
-Determine & manage the degree of dehydration.
-Appropriate management of electrolyte abnormalities.
-Symptomatic control of nausea, vomiting, and pain.
-Appropriate radiologic studies to confirm and determine the site of obstruction.
-Plain abdomen radiograph
- Barium study of the upper GI tract: most helpful in the evaluation for small bowel
obstruction.
-Barium enema : for evalution of obstruction in lower GI tract.
-Pediatric surgery consultation is mandated when intestinal obstruction is suspected.

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CHAPTER III
WORKUP

g. Diagnosis
Generally diagnostic approach of vomiting in children can be concluded as
followed 3:
- Ruled in / out infection as the cause of vomiting (e.g : otitis media, diarrhea,
intracranial infection, urinary or respiratory tract infection, sepsis, or hepatitis)
- Ruled in / out gastrointestinal organic disorder, such as esophagus atresia,
GERD, pyloric stenosis, Hirschprung disease, peptic disease.
- Look for any possibilities of food disorder, for example lactose intolerance,
food allergy, excessive food intake, inappropriate feeding technic.
- Look for any possibilities of drugs side effects, psychological disorder, or
metabolic disorders.

Approach to problem identification is very important, including :


1. Age and gender
2. Define first what is happening, whether it is vomiting or any other problems
3. Determine children nutritional status

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4. Is there any predisposition factor


5. Any intercurrent disease affecting children
6. Content of vomiting, any milk or food appearance (sign of esophageal
content), or appear like thick milk (gastric content), or is it bile containing
(duodenal content) or any blood within
7. Was vomiting associated with meal or drinking time, before or after
8. Was vomiting associated with body position
9. Diet information : quality, quantity, and feeding frequency (particularly in
children)
10. Water intake technique
11. Determine psychosocial condition at home
Laboratory investigations are done to provide the diagnosis. Types of
investigations may vary according to differential diagnosis related to history taking
and clinical manifestation. Laboratory investigation can be blood test, radiology with
or without contrast, ultrasonography, endoscopy, esophageal pH observation (pHmeter), hydrogen breath test, or gastrointestinal mucosa biopsy.
Green vomiting in neonates which accompanied by or without abdominal
distention may be the first sign of gastrointestinal obstruction. Nasogastric tube has
to be attached for gastric decompression. Dilated intestines and air fluid level on
abdominal plain radiography showing bowel obstruction and needed surgical
intervention. Radiology investigation using contrast can differs any duodenal atresia,
midgut malrotation, volvulus, jejunal atresia, or ileus, which become the most
common cause of bowel obstruction in neonates. 9
Pyloric stenosis can be proven by barium meal or ultrasonography showing a
classical picture. Gastroesophageal reflux disease (GERD) is proven by observing
esophageal pH in 24 hours (pH-meter). Reflux index above 5% showing any
pathologic GERD. Esophagitis and peptic ulcer can be evidenced with endoscopy
and mucosal biopsy of gastrointestinal. Hydrogen breath test may be done in any

22

suspicion of lactose intolerance and overgrowth bacteria. Increase in H2 level on


breath above 20 ppm on the 60th 120th minutes after drink a lactose solution
showing lactose intolerance, while increase in 30th minutes shows any bacteria
overgrowth. Peripheral blood test and urine are essential to see any possibility of
infection that underlined the cause of complaint, while arterial blood gas
investigation and electrolyte are done when there is any suspicion of metabolic
disorder or in reverse, there is any suspect of metabolic disorder that underlined the
cause of complaint.10

Condition

History and Physical


Diagnostic approach
Diarrhea (usually), history of
Gastroenteritis
infectious contact, fever
Clinical evaluation
(sometimes)
Fussiness after feeding, poor
Empiric trial of acid
GERD
weight gain
suppression
Recurrent projectile vomiting in
Pyloric stenosis
neonates aged 3-6 weeks,
Ultrasound
emaciated and dehydrated
Congenital atresia
Abdominal distension, bilious
Abdominal X ray
or stenosis
emesis in first 24-48 hours of life
Contrast enema
Abdominal X ray
Bilious emesis, abdominal
Upper GI series with
Malrotation
distention, abdominal pain, bloody
contrast under
stool
fluoroscopy
Fever, lethargy, tachycardia,
CBC,
Sepsis
tachypnea, widening pulse
Cultures (blood,
pressure, hypotension
urine, CSF)
Abdominal pain, urticarial,
Food intolerance
Elimination diet
eczematous rash
Electrolytes,
ammonia, liver
Poor feeding, failure to thrive, function tests, BUN,
hepatosplenomegaly, jaundice,
creatinine, serum
Metabolic disorders
dysmorphic features,
glucose, total and
developmental delays, unusual direct bilirubin, CBC,
odors
PT/PTT
Further specific tests
based on findings
Non-GI infection
Fever, localized findings (sore
Clinical evaluation
throat, dysuria, flank pain)
Further tests if

23

depending on source
Meningitis
photophobia, nuchal
rigidity, headaches
Serious infection
Pyelonephritis
fever, back pain, dysuria
At least 3 self-limited episodes of
vomiting lasting 12 h,
7 days
Cyclic vomiting
between episodes,
no organic
cause of vomiting
Nocturnal wakening, progressive
recurrent headache made worse by
Intracranial
coughing or Valsalva maneuver,
hypertension
nuchal rigidity, visual changes,
weight loss, photophobia
Body dysmorphism, teeth erosions,
Eating disorders
skin lesions on hand (Russells
sign), binge eating behavior
Amenorrhea, morning sickness,
breast tenderness, bloating, history
Pregnancy
of sexual activity and improper
contraception use
History of ingestion, findings vary
Toxic ingestion
depending on substance and
pattern of ingestion

needed
CBC, Cultures (CSF,
blood, urine) gram
stains
CBC, Cultures (urine,
blood)
Diagnosis of
exclusion

Brain CT (without
contrast)

Clinical evaluation

Urine pregnancy test


Varies depending on
substance

24

CHAPTER IV
MANAGEMENT

h. Treatment
Main goal of vomiting therapy is to found and solve the causes, while
supportive therapy is needed to prevent a worse condition and relieve any
complications happened.
Some of the following may be used as the first line therapy to manage
vomiting in children 6:
- If there is no sign of gastrointestinal tract obstruction, vomiting
-

usually will recover within 6-48 hours.


Correct and prevent dehydration and electrolyte imbalance
Bed rest until there is no more vomiting within 6 hours and the

child feels better.


Stop any drugs which may irritate gastric and increasing vomiting ,

such as aspirin, asetosal, corticosteroid, macrolyte antibiotics.


Do not give any solid food within the first 6 hours and comfort

children within this period (eg : slowing down the temperature)


Give easily digestable food to improving gastrointestinal healing
Fruit juice should be given (except orange and grapes because its
acidic nature), syrup, or honey (for children above 1 year of age)
gradually every 15-20 minutes in 1-2 tea spoons. Other fluid that can
be given such as chicken broth or ORS.

After the 1st hour, the patient can be given drink in a more quantity (24 tea spoons every 15-20 minutes) gradually and then raised up twice
every 1 hour. If vomit occurs, patient should be given drink in a lesser
quantity. Giving drink ad libitum on children and baby causing

vomiting in higher risk to recur.


After 3 hours where there is no more vomiting, patient can be given

25

drink by glass (children) or bottle (baby) with gradually increased


-

quantity as well.
After 6 hours without vomiting, babies can be given bananas, cereals,
apple juice, while in older children can be given breads, crackers,
honey, chicken soup, potatoes, or rice. Types and quantities are given
gradually. Normal diet usually can be given after 24 hours. Activities

should be prevented after food intake.


Antiemetic drugs are given necessarily. Administrating these drugs
have to consider the advantages and disadvantages. Drugs are given
when the children refuse to drink after vomiting or vomiting lasts for
more than 24 hours.

Antiemetic drugs are not used routinely in children, but only for the children
who refuse to drink after vomiting or vomiting has last for more than 24 hours, so
that it is concerned the complications might occur, either dehydration or electrolyte
imbalance and blood gas. Antiemetic drugs can be given directly in chemotherapy or
radiotherapy cases. The most important thing is to make sure that there is no bowel
obstruction.2
Variety of drugs has been reported as antiemetic agents for example
dopamine receptor antagonist, anticholinergic, antihystamine, and serotonin receptor
antagonist. Those drugs are selected based on of which the vomiting pathophysiology
occur. In motion sickness, there is vestibular disturbance, so that anticholinergics,
such as scopolamine, become the drug of choice. Antihistamines, such as hyoscine
hydrobromide, promethazine, which works at the vomiting center can also be used in
such condition. While serotonin receptor antagonists which work on the Central
Trigger Zone are highly effective on patients with chemotherapy and radiotherapy. 6
For any disorder in gastrointestinal tract as happened in infection, dopamine
receptor antagonist which works at the central trigger zone (central) and the
gastrointestinal itself (peripheral) could be the drug of choice. From those category,
metoclopramide and domperidone are used the most as antiemetic drugs.
Metoclopramide has a dopamine-receptor blocker effect on the CTZ, therefore
reducing nausea and vomiting. Many symptoms as anxiety, tremor, dystonia, and
dyskinetic have been reported on patients using this drug. 8

26

Domperidone has been widely used as antiemetic drugs because of its positive
effect and little side effects (0.5%). This drug is not only blocking the dopamine
receptor on the CTZ, but also dopamine receptor on the peripheral, especially on
gastrointestinal in this case. Positive effects shown after giving domperidone
includes increasing lower esophageal sphincter pressure, increasing gastric
contractility, improving antroduodenal coordination, and accelerating gastric
emptying. Domperidone has a low bioavailability because it is metabolized quickyly
within the intestinal wall and liver. Domperidone is more tolerated and has smaller
extrapiramidal effect compared to metoclopramide because of its small ability to pass
the blood brain barrier. Recommended doses for children is 0.2 0.4 mg/kgBW/day
per oral. 10

Anti emetic drugs action mechanism

i. Complication
Vomiting can results in a number of sequelae, some of which are listed below.8
1. Aspiration

27

Vomiting in a patient with altered mental status, low or depressed level


of consciousness, or one that suffers from extremely repetitive cycles will
most likely have bad epiglottic control or non for that matter, which in term
will lead to aspiration of gastric contents whatever they are to the respiratory
tract and lung causing aspiration pneumonia.
The results will almost be disturbing and can be a serious condition in
many cases especially if the contents were of chemical or highly irritating to
the respiratory tract causing airway compromise.
2. Electrolyte imbalance
Mainly hypokalemia due to a very complex reflex due to volume
depletion which will cause hyperaldosteronism, leading to increased reabsorption of sodium and increased excretion of large amounts of potassium
in the urine.
3. Hypovolemia
Occurs due to a lot of vomiting, high water volume vontent and
sodium and chloride will be lost from the body, which will cause contraction
of the extra cellular fluid space leading to activation of the Reninangiotensin-aldosterone system.
4. Mallory Weiss syndrome
This syndrome occurs due to severe and repetitive retching and
vomiting a partial tear of the mucosa and sub-mucosa in the stomach and
gastroesophageal junction will form, which may lead to bleeding which most
likely will be minimal and self limiting, but it can proceed to a more
catastrophic form.
5. Boerhaves Syndrome (esophagus rupture)
This happens commonlyt due to repetitive, extreme prolonged both of
retching and vomiting, causing a full tear of all the layers of the esophagus,
mainly and most commonly the posteriolateral lower part of the esophagus
which is by itself a lethal medical emergency.

6. Hypochloremic metabolic alkalosis

28

It occurs in the setting of continuous large amount of vomiting for


more than 3 days with a series of event : loss of H+ from HCl, low volume
concentration, hypokalemia, chloride depletion, high aldosteron, shifting of
H+ from extra to intra cellular. All gathers up and causing severe metabolic
alkalosis due to extreme high frequency of vomiting.
7. Malnutrition and failure to thrive
Failure to thrive in childhood is a state of undernutrition due to
inadequate caloric intake, inadequate caloric absorption, or excessive caloric
expenditure. Some diseases can cause frequent vomiting, such as metabolic
disorder, food insensitivities, or malabsorption, like celiac disease, chronic
diarrhea, or protein-losing enteropathy, therefore the body has inadequate caloric
absorption and if the condition remains for long time, it can cause failure to
thrive.10

j. Conclusion
Vomiting is one the most common clinical manifestation shown by children
who suffering disorder either in the gastrointestinal or outside the
gastrointestinal system. The cause of vomiting varies, therefore knowing and
recognizing the specific and classical clinical manifestation from each disease is
essential for a physician. An appropriate and prompt diagnostic approach will
result in an optimal and appropriate management. The use of antiemetic agents is
not the main choice, but in several conditions, effective and safe antiemetic
agents are very necessary.

29

Bibliography

1. Chandran, Latha. Chitkara, Maribeth. Vomiting in Children:


Reassurance, Red Flag, or Referral? Pediatrics in Review
2008;29;183. DOI: 10.1542/pir.29-6-183
2. Buku Ajar Gastroenterologi-Hepatologi IDAI. 2009.
3. Freedman, Stephen B. et al. Oral Ondansetron for Gastroenteritis in a Pediatric
Emergency Department. 2006. The New England Journal of Medicine. N Engl J Med
354;16
4. Cole, Sarah Z., Lanham, Jason S. Failure to Thrive : An Update. Am Fam
Physician. 2011 Apr 1;83(7):829-834.
5. Bowen, R. Physiology of Vomiting. 1996.
http://arbl.cvmbs.colostate.edu/hbooks/pathphys/digestion/stomach/vomiting.html
6. F D Brown, J Brown, T F Beattie. Why do children vomit after minor head injury?
J Accid Emerg Med 2000;17:268271.
7. Leung, Alexander KC. Robson, Wm Lane M. 2008. In children with vomiting
related to acute gastroenteritis, are antiemetic medications an effective adjunct to
fluid and electrolyte therapy? Paediatric Child Health Vol 13 No 5 May/June 2008.

30

8. The North Italian Endoscopic Club for the Study ant Treatment of Esophageal
Varices. Prediction of the first variceal hemorrhage in patients with cirrhosis of the
liver and esophageal varices. N Engl J Med. 1988; 319: 983-9.
9. Al-Amri, Nawaf. Emergency Medicine Approach To Nausea & Vomiting. 2011.
http://www.slideshare.net/NawafAlAmri/nausea-vomiting-10620984#
10. Jurnalis, Yusri Dianne., et al. Malrotasi dan Volvulus pada Anak.
http://jurnal.fk.unand.ac.id

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