VOMITING IN CHILDREN

Mentor :
dr. Pulung M. Silalahi, Sp. A

Written by :
Astri Faluna 1102009044

Faculty of Medicine Yarsi

Pediatric Department
Rumah Sakit Bhayangkara tk.I R.S. Sukanto-Jakarta
Periode: 1 Desember 2014 30 January 2015

FOREWORD

Praise and gratitude we say to Allah SWT

upon completion referat

entitled vomiting in children.

This academc writing is given as a part of clinical practice duty as a CoAss in RS Bhayangkara Tingkat 1 Raden Said Sukanto, in the Pediatrics
department.
The sources that I use for the writing contain information from textbooks,
journals and online references.
The author would like to give special mention to mentor, dr Pulung M.
Silalahi, Sp. A, for guiding author throughout the entire writing process.
I hope that this writing can be a positive use to the readers, be it as an
additional information or future references. I realize that the writing is still lacking
in many areas but I hope the readers can give critical remarks so that further
improvement can be made in the future.

Jakarta, Desember 2014

author

TABLE OF CONTENTS
FOREWORD......................................................................................................... i
TABLE OF CONTENTS...................................................................................... ii
CHAPTER I INTRODUCTION......................................................................... 1
1.1 Background....................................................................................................... 1
1.2 Purpose of Writing............................................................................................ 2
1.3 Problems........................................................................................................... 2
1.4 Benefits of the article........................................................................................ 2

CHAPTER II LITERATURE REVIEW............................................................ 3

2.1 Definition.......................................................................................................... 3
2.2 Etiology............................................................................................................. 3
2.3 Pathophysiology.............................................................................................. 11
2.4 Classification...................................................................................................16
2.5 Clinical Manifestations.................................................................................. 17
2.6 Diagnosis........................................................................................................ 18
2.7 Treatment........................................................................................................ 19
2.8 Complication.................................................................................................. 24
2.9Prognosis.. 24
2.10 Prevention...24

CHAPTER III CONCLUSION......................................................................... 25

3.1 Conclusion...................................................................................................... 25
ACKNOWLEDGEMENTS............................................................................... 26

CHAPTER I
INTRODUCTION
Background
Digestive tract can be likened to a group of funnel-shaped organs that are
interconnected and form a tube that is covered by muscles; from the mouth to the
anus. Based on the difference in diameter and its characteristic function, the
channel can be divided into the esophagus, stomach, small intestine, large
intestine (colon), rectum, anus. The liver and spleen are other organs that play a
role in the digestive process by secreting fluid into the gastrointestinal tract. One
of the most common clinical manifestations exhibited by a child due to a
disturbance in the digestive tract is vomiting. This situation can be a clinical
manifestation of a state that is not dangerous, but it can also be a sign of an illness
'serious'. Vomiting is not a single disease but is one of the clinical manifestations
of the disease. Therefore the diagnosis and management approach vomiting varies
depending on the alleged cause.1,2,3
Two organs of the digestive tract are the most involved in the process of
vomiting is the esophagus and stomach. Therefore, understanding the anatomy
and physiology of the two organs is important.
Physiology of swallowing.
Sendiritelah ingestion occurs when the fetus. Swallowing will lead to a peristaltic
movement that starts from the pharynx, next to the latitude and smooth muscle fibers of
the esophagus and gastric cardia end on. In the early swallow esophageal sphincter
relaxation top will cause the food / drinks can be entered into the esophagus. Upper
esophageal sphincter is an important part, prevents regurgutasi from the esophagus into
the oral cavity and larings. Once the food / drinks into the esophagus, esophageal
sphincter closes upper and esophageal peristaltic movement occurs. Lower esophageal
sphincter relaxation also suffered during the swallowing process progresses and kept open
until the peristaltic movement reaches the bottom esophageal sphincter. At the time of
swallowing are also aimed at encouraging secondary peristaltic materials reflux back into
the stomach. Secondary peristaltic can also occur when there is food in the esophagus that
are not driven by the primary peristaltic into the stomach. The vagus nerve plays a role in

the process of swallowing by adjusting the muscle movements of the mouth, pharynx,
and smooth muscle contraction. At the time of swallowing, lower esophageal sphincter
pressure decreases so that similar pressure hull 2.

Purpose of Writing
Provide further and detailed understanding of vomiting in children starting
from definition, classification, etiology, pathophysiology, clinical manifestation,
treatment and complication in a thorough review.
Problems

Definition, epidemiology, and risk factor of vomiting in children

Etiology, pathogenesis, and clinical manifestations of vomiting in children
Diagnosis, treatment, and prevention of vomiting in children

Benefits of the article

In order to present a detailed information and knowledge for other for readers

targeted as fellow health workers

To provide an adequate information to be used for subsequent academic
writing purposes

CHAPTER II
LITERATURE REVIEW
2.1 Definition
Clinically, sometimes

difficult

to

distinguish

between

vomiting,

gastroesophageal reflux (RGE), with regurgitation. Vomiting was defined as the

release of stomach contents through the mouth through oral expulsive contractions
with the help of the abdominal muscles. Attempts to remove the contents of the
stomach looks as kontrksi abdominal muscles. While gastroesophageal reflux was
defined as the return of stomach contents into the esophagus without visible
presence of child business, may be caused by the lower esophageal sphincter
hypotonia or solid gastric emptying. Regurgitation material is removed from the
mouth of the stomach. Antiperistaltik regurgitation caused by movement of the
esophagus. While rumination that food expenditure consciously to chew then
swallow back1
2.2 Etiology
The causes of vomiting in children varies greatly and depends on age.
Some circumstances can be a trigger vomiting, such as stomach or intestinal
disorders (infection, irritation food, trauma), disturbance in the inner ear
(dizziness and motion sickness), abnormalities in the central nervous system
(trauma, infection) or due to excessive eating . Although rare, intestinal
obstruction is the cause of vomiting in infants2.
The causes of vomiting vary with age and range from relatively benign to
potentially life threatening. Vomiting is a protective mechanism that provides a
means to expel potential toxins; however, it can also indicate serious disease (eg,
intestinal obstruction). Bilious vomiting indicates a high intestinal obstruction
and, especially in an infant, requires immediate evaluation2.
Infants: Infants normally spit up small amounts (usually < 5 to 10 mL)
during or soon after feedings, often when being burped. Rapid feeding, air
swallowing, and overfeeding may be causes, although spitting up occurs even
without these factors. Occasional vomiting may also be normal, but repeated
vomiting is abnormal.

The most common causes of vomiting in infants and neonates include the
following2 :

Acute viral gastroenteritis

Gastroesophageal reflux disease
Other important causes in infants and neonates include the following :

Pyloric stenosis
Intestinal obstruction (eg, meconium ileus, volvulus, intestinal atresia,

stenosis)
Intussusception (typically in infants aged 3 to 36 mo)

Less common causes of recurrent vomiting include sepsis and food intolerance.
Metabolic disorders (eg, urea cycle disorders, organic acidemias) are uncommon
but can manifest with vomiting.
Older children: The most common cause is:
Acute viral gastroenteritis
Non-GI infections may cause a few episodes of vomiting. Other causes to
consider include serious infection (eg, meningitis, pyelonephritis), acute
abdomen (eg, appendicitis), increased intracranial pressure secondary to a
space-occupying lesion (eg, caused by trauma or tumor), and cyclic vomiting.
In adolescents, causes of vomiting also include pregnancy, eating disorders,
and toxic ingestions

Some Causes of Vomiting in Infants, Children, and Adolescents

Cause*

Suggestive Findings

Diagnostic Approach

Vomiting in infants

Viral gastroenteritis

Usually with diarrhea

Clinical evaluation

Sometimes fever and/or contact Sometimes rapid immunoassays

with a person who has similar

for viral antigens (eg, rotavirus,

symptoms

adenovirus)

Gastroesophageal reflux disease Recurrent fussiness during or

Empiric trial of acid suppression

after feedings
Possibly poor weight gain,

Bacterial enteritis or colitis

Sometimes upper GI contrast

arching of the back, recurrent

study, a milk scan, esophageal

respiratory symptoms (eg,

pH monitoring and/or

cough, stridor, wheezing)

impedance study, or endoscopy

Usually with diarrhea (often

bloody), fever, crampy
abdominal pain, distention

Clinical evaluation
Sometimes stool examination for
WBC and culture

Often contact with a person who

has similar symptoms
Pyloric stenosis

Recurrent projectile vomiting

immediately after feeding in

Ultrasonography of pylorus
Upper GI contrast study if

neonates aged 212 wk,

ultrasonography is unavailable

infrequent stools

or uncertain

May be emaciated and

dehydrated
Sometimes palpable olive in
right upper quadrant
Congenital atresias or stenosis Abdominal distention

Abdominal x-ray

Bilious emesis in first 2448 h of Upper GI series or contrast

life (with lesser degrees of

enema depending on findings

stenosis, vomiting can be

delayed)
Sometimes polyhydramnios
during pregnancy, Down
syndrome, jaundice
Intussusception

Colicky abdominal pain,

inconsolable crying, lethargy,
drawing of legs up to chest
Later, bloody ("current jelly")
stool

Abdominal ultrasonography
If ultrasonography is positive or
nondiagnostic, air or contrast
enema (unless patient has signs
of peritonitis or perforation)

Typically age 336 mo, but can

be outside this range
Hirschsprung disease

In neonates, delayed passage of Abdominal x-ray

meconium, abdominal

Contrast enema

distention, bilious emesis

Malrotation with volvulus

In neonates, bilious emesis,

Rectal biopsy
Abdominal x-ray

abdominal distention and pain Contrast enema or upper GI

Bloody stool
Sepsis

Fever, lethargy, tachycardia,

tachypnea
Widened pulse pressure,
hypotension

Food intolerance

series
Cell counts and cultures (blood,
urine, CSF)
Chest x-ray if pulmonary
symptoms are present

Abdominal pain, diarrhea

Elimination diet

Possibly eczematous rash or

Sometimes skin testing and/or

urticaria

radioallergosorbent testing
(RAST)

Metabolic disorders

Poor feeding, failure to thrive,

Electrolytes, ammonia, liver

lethargy, hepatosplenomegaly,

function tests, BUN, creatinine,

jaundice

serum glucose, total and direct

Sometimes unusual odor,

cataracts

bilirubin, CBC, PT/PTT

Neonatal metabolic screening
Further specific tests based on
findings

Vomiting in children and adolescents

Viral gastroenteritis

Usually with diarrhea

Clinical evaluation

Sometimes fever, contact with a Sometimes rapid immunoassays

Bacterial enteritis or colitis

person who has similar

for viral antigens (eg, rotavirus,

symptoms, or history of travel

adenovirus)

Usually with diarrhea (often

bloody), fever, crampy
abdominal pain, distention,

Clinical evaluation
Sometimes stool for WBC,
culture

fecal urgency
Often contact with a person who
has similar symptoms or
history of travel
Non-GI infection

Fever

Clinical evaluation

Often localizing findings (eg,

Testing as needed for suspected

headache, ear pain, sore throat,

cervical adenopathy, dysuria,

cause

flank pain, nasal discharge)

depending on cause
Appendicitis

Initial general malaise and

Ultrasonography (preferred over

periumbilical discomfort

CT to limit radiation exposure)

followed by pain localizing to

right lower quadrant,
vomiting after pain
manifestation, anorexia, fever,
tenderness at McBurney point,
decreased bowel sounds
Serious infection

Fever, toxic appearance, back

pain, dysuria (pyelonephritis)
Nuchal rigidity, photophobia

Cell counts and cultures (blood,

urine, CSF) as indicated by
findings

(meningitis)
Listlessness, hypotension,
tachycardia (sepsis)
Cyclic vomiting

3 episodes of intense acute

Exclusion of metabolic, GI (eg,

nausea and unremitting

malrotation), or CNS (eg, brain

vomiting and sometimes

tumor) disorders

abdominal pain or headache

lasting hours to days
Intervening symptom-free
intervals lasting weeks to
months
Intracranial hypertension
(caused by tumor or trauma)

Chronic, progressive headache; Brain CT (without contrast)

nocturnal awakenings; morning
vomiting; headache worsened
by coughing or Valsalva
maneuver; vision changes

Eating disorders

Binge and purge cycles, erosion Clinical evaluation

of tooth enamel, weight loss or
gain
Sometimes skin lesions on hand
from inducing vomiting
(Russell sign)

Pregnancy

Amenorrhea, morning sickness, Urine pregnancy test

bloating, breast tenderness

History of unprotected sexual
activity
Toxic ingestions
(eg,acetaminophen

Often history of ingestion

Various findings depending on
ingested substance

Qualitative and sometimes

quantitative serum drug levels
(depending on substance)

, iron, ethanol)
Adverse drug reaction (eg, to

Exposure to a specific drug

chemotherapeutic drugs)
*Causes are listed in order of frequency.

Many adolescents do not admit to sexual activity.

Cause of Vomiting in Neonatus

Clinical evaluation

stomatch irritation to
amniotic fluid
Non
organik

metabolic
abnormalities:
galaktosemia,
hiperkalsemia
drug

Vomiting
in
Neonatus

Obstruksi

Intrinsik :
Atresia, polyps,
Lactobezoar,
Hirschsprung
disease
Ekstrinsik:
Anulare
pancreas, Cyst
mesebterium,
Hernia
diafragmatica

Non
Obstruksi

Chalasia, gastric
perforation.

Traktus
Gastrointestinal
is

Organik
Ekstragastrointesti
nal

Insufiiensi kidney,
urethral obstruction,
Adrenal Hyperplasia

SSP

Edema serebri,
increased intracranial
pressure, subdural
effusion.

Causes of Vomiting in Infants

posetting
Non
organik

feeding too
much
drugs/toxins

Vomiting
in Infants

Obstruksi

Web antral,
pyloric stenosis,
intussusception,
hiatus hernia,
intestinal
duplication

Non Obstruksi

short esophagus,
peptic ulcer
disease coleiac,
GER, appendicitis,
peritonitis

Traktus
Gastrointestinalis

Organik

Ekstragastrointesti
nal

pertusis,
tonsilofaringitis,
OMA, Uremia,
Asidosis, Inborn
errors of
metabolism

SSP

Meningitis,
Ensefalitis,
increased
intracranial
pressure

Cause Vomiting in Child

Non organik

Vomiting in
child

anxiety, fear,
suggestion, post
nasal drip,
motion sickness

Obstruksi

intussuscepti
on, intestinal
obstruction

Non Obstruksi

appendicitis

Traktus
Gastrointestinalis

Organik
Ekstragastrointestin
al

SSP

tonsilofaringitis,
pertussis, OMA,
pyelonephritis,
testicular torsion,
uremia, acidosis

hidrosefalus,
increased intracranial
pressure, abdominal
epilepsy.

2.3 Pathophysiology
Vomiting is a somatic reflex responses are perfectly coordinated because
of various stimuli, involving the activity of respiratory muscles, abdominal
muscles, and the muscles diaragma4.
Vomiting process consists of three phases, namely nausea, retching and
expulsion.
1. Phase Nausea
A psychic sensation due to the stimulation of the visceral organs, and
emotional labyrinth. Not always continues with retching and expulsion. This
condition is characterized by a desire to vomit felt in the throat or stomach, often

accompanied by symptoms of hypersalivation, pale, sweating, tachycardia, and

anorexia.
During periods of nausea, decreased tone greater curvature, corpus and
fundus. Antrum and duodenum to contract again and again, while the bulb
duodeni relaxation resulting in reflux of gastric fluid into the duodenum. In this
phase has not happened peristaltic nausea active.
Vomiting caused by increased intracranial pressure and obstruction of the
gastrointestinal tract is not preceded by a phase of nausea.
2. Phase Retching
Retching can occur without vomiting followed.
In phase retching breathing cessation of spasms and repetitive, while the
closed glottis. Pernfasan and daifragma muscle contraction causes the
intrathoracic pressure becomes negative. At the same time there was a contraction
of the abdominal muscles and stomach, dilated fundus antrum and pylorus while
contracting. Lower esophageal sphincter opens, but the upper esophageal
sphincter still menututp cause chymemasuk into the esophagus. At the end of
retching phase occurs diding muscle relaxation phase stomach and the stomach so
that the chime that had been entered into the esophagus back kelambung. This
phase can last for several cycles.
3. Expulsive Phase (vomiting)
If retching peaked and is supported by the contraction of the abdominal
muscles and diaphragm, will continue to be vomiting if the pressure can overcome
the anti-reflux mechanism of the LSE.
In this expulsion pylorus and antrum and fundus contract while sofagus
relaxation and an open mouth. This phase also changes in intrathoracic and intraabdominal pressure, as well as the contraction of the diaphragm. In a single
episode of expulsion occurs intra thoracic negative pressure and positive intraabdominal pressure, and at the same time the rapid contraction of the diaphragm
which presses the fundus resulting in reflux of stomach contents into the

esophagus. If expulsion is already happening, intrathoracic pressure and

diaphragm positive return back to the normal position.
The process of nausea and vomiting as well as retching regulated by the central
nervous system in two areas in the medulla.
1. Vomiting center located in the medulla called Nucleus Salitarius.
2. Section adjacent to the lateral retikulariss formation in the medulla
oblongata. These centers are adjacent to the central respiratory, vasomotor
center, the nucleus, salitarius, nucleusvestibularis and bulbo fascilitatory
and inhibitory system.
Vomiting center is activated by stimuli from:
1. Cortex: the vestibular system through the vestibular nucleus VIII
2. Channel gastrointestinal (posterior pharynx, liver, kidney, pancreas, heart
and lungs) through efferent parasympathetic (vagal nuclei) and
sympathetic.
3. "Supraneuron": olfactory nerve efferent nerves, N.Optikus and central
nervous system (increased intracranial pressure, emotions).
Vomiting center in the medulla can also be activated by stimulation of the
second center called chemo receptive trigger zone (CTZ) located diarea post rema
floor ventricular 4. Region is very sensitive to various chemicals contained in the
blood, and can work when the center vomiting intact. The materials which react
directly on this region is an exogenous substance (opiate, ipecac, digoxin,
cytotoxic agents) and endogenous materials (enkafalin, adrenaline, urea,
ammonia, ketones and materials that are endogenous emetic agent that causes
stimulation of humoral on the CTZ. vomiting that occurs in diseases such as
meningitis beyond gastrointestinal, tonsillitis, otitis media, pneumonia, urinary
tract infections and others, whose pathophysiology is unclear, it is likely occurs
through the stimulation of endogenous emetic this agent5.
Efferent fibers associated with vomiting are transmitted through the
phrenic nerve, spinal nerves and efferent vagus to specifically from striated
muscle (voluntary muscle) in the pharynx and larings.

The vomiting centre of the brain The fourth ventricle of the brain hosts the
vomiting centre. The floor of the fourth ventricle contains an area called the
chemoreceptor trigger zone (CTZ). It is also called the area postrema. When the
CTZ is stimulated, vomiting may occur.
The

CTZ

contains

receptors

for

dopamine,

serotonin,

opioids,

acetylcholine and the neurotransmitter substance P. When stimulated, each of

these receptors gives rise to pathways leading to vomiting and nausea. Present in
high concentrations in the vomiting centre, Substance P seems to be involved in
the final common pathways that give rise to vomiting.
The CTZ lies outside the blood-brain barrier (BBB). Normally, the BBB
controls substances that affect the brain. Medications and chemicals in the blood
have selective access to the brain when protected by the BBB. As the CTZ,
however, lies outside the BBB, drugs and medications are capable of stimulating
this area to trigger vomiting. Medications that control or are used to treat vomiting
may inhibit this area to prevent vomiting3.
Inputs to the vomiting centre in the brain The CTZ in the brain is
stimulated by various inputs from different parts of the body and this leads to
vomiting. Some of the inputs to the CTZ include5:

Inputs from the vestibular system of the inner ear. These travel via the eighth
cranial nerve or the vestibulocochlear nerve and are involved in motion
sickness causing nausea and vomiting. There is an abundance of the H1 type
of histamine receptors in this system that can be suppressed by the H1 type of
antihistaminics to control vomiting induced by motion sickness.

The tenth cranial nerve or the vagus nerve carries signals to the CTZ when the
back of the throat or pharynx is irritated or stimulated. This is called the gag
reflex.

The nervous system around the gut or the enteric nervous system also
transmits signals to the brain via the vagus nerve. It is via this system that
radiation therapy, chemotherapy and gastroenteritis activate the 5-HT3
receptors leading to vomiting.

Dopamine receptors are activated by stress and several psychiatric conditions,

leading to vomiting.

The process of vomiting involves several phases and steps. These include5:

Stimulation of the CTZ leading to activation of the motor, parasympathetic

and sympathetic nervous system

Stimulation of the parasympathetic nervous system leading to increased
salivation

Deep breathing preceding the actual vomiting to protect the lungs from
aspiration

Heaving or retching before the actual vomiting

Relaxation of the pyloric sphincter that guards the lower end of the stomach to
bring up content from the gut

The pressure within the abdomen rises and the pressure within the chest or
thorax is lowered. The abdominal muscles contract to expel the contents of the
stomach

Activation of the sympathetic nervous system leads to sweating, palpitation

and rapid heart rate

2.4 Classification
Vomiting can be classified according to its nature and cause as well as by
the character of the vomitus. The nature of the vomiting may be projectile or non
projectile. Projectile vomiting refers to forceful vomiting and may indicate
increased intracranial pressure, especially if it occurs early in the morning.
Projectile vomiting also is a classic feature of pyloric stenosis. Non projectile
vomiting is seen more commonly in gastroesophageal reflux. These somewhat
arbitrary descriptions are not definitive in establishing a diagnosis6.
Emesis often is classifiedbased on its quality. The vomitus may be bilious,
bloody, or non bloody and non bilious. Emesis originating from the stomach
usually is characterized as being clear or yellow and often contains remmants of
previously ingested food. Emesis that is dark green is referred to 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
emptics. The presence of blood in the emesis, also know as hematemesis,
indicates acute bleeding from the upper portion of the GI tract, as can occur with
gastritis, Mallory-Weiss tears, or peptic ulcer disease. Coffee ground like material
often is representative of and old GI hemorrhage because blood darkens to a black
or dark brown color when exposed to the acidity of the gastric secretions. The
more massive or proximal the bleeding, the more likely is it to be bright red6.

2.5 Clinical Manifestations

Vomiting in children is usually a sign of infection . Vomiting in a child
who has an infection is usually accompanied by fever , nausea , abdominal pain or
diarrhea . This situation will usually stop 6-48 hours . If vomiting continues need
contemplated the existence of a more serious condition . Children have a greater
factor to become dehydrated , especially if accompanied by diarrhea . Vomiting
and fever is more often caused by viral or bacterial infection than the parasite .
Peptic disease should be considered when vomiting occurs immediately after a
meal , while vomiting caused by food poisoning usually occurs 1-8 hours after
eating . Vomiting due to food borne disease such as Salmonella require a longer
time to cause clinical symptoms because it takes time for incubation . Oral
candidiasis is often a cause of vomiting in infants8.
Non - bilious projectile vomiting over and over on the baby can be a sign
of obstruction of the gastrointestinal tract , such as stenosis of the pylorus .
Stenosis of the pylorus is often found in the second week after birth . Persistent
vomiting in neonates that occur at night to think about the possibility of a hiatal
hernia .
One important also to be understood in a child who is experiencing
vomiting is to determine abnormalities requiring immediate surgery . These
disorders are generally classified into groups of acute abdominal disease . There
are some clues that can be used as markers of suspicion against these disorders ,
namely :
1. Abdominal pain arising preceded by vomiting and / or lasts for more
than 3 hours .

2. Vomiting mixed with gall .

3. abdominal distension .
Volvulus in neonates showed green vomit arising in the first days of life
and followed signs of obstruction of the gastrointestinal tract and the high location
of peritonitis .
Vomiting can also be caused by disorders outside the gastrointestinal tract
such as respiratory tract infections or urinary tract . Some medications can also as
the originator of vomiting in children , such as histamine , phenytoin , ( antiepilepsy drugs ) , chemotherapy , aspirin , and some antibiotics . Vomiting after
mild head trauma was found in 15 % of children and most have a history of
recurrent headaches and motion sickness , and other cernafungsional tract
disorders ( such as abdominal pain , defecation disorders ) . When complaints are
like behavior behavior disorder anorexia or bulimia nervosa should be considered
the presence of psychiatric disorders .
Broadly speaking, the approach to the diagnosis of vomiting in children
can be summarized as follows 9:
Establish / remove sebgai infectious disease that causes vomiting ( otitis
media , diarrhea , intracranial infections , urinary tract infections or
breath , sepsis , or hepatitis . )
Establish / remove organic gastrointestinal disorders ( atresia of the
esophagus , gastroesophageal reflux , stenosis of the pylorus ,
Hirschsprung 's disease , peptic disease . )
Find the possibility of problems in food ( lactose intolerance , food
allergies , overeating , engineering feeding / drinking is wrong )
Look for a possible influence of drugs , psychological
disorders and metabolic disorders .
2.6 Diagnosis
Approach to the identification of very important issues, including:
1. Age and sex
2. Decide in advance what is encountered: vomiting or other
3. How the nutritional state of children
4. Is there a predisposing factor
5. Is there a disease that strikes children interkuten

6. What form (content) vomit, whether as milk / food origin (the sign of the
esophagus), or have a milk clot (stomach contents), containing bile
(duodenal contents) or is there blood
7. Do you currently associated with vomiting when eating or drinking.
8. What changes in body position affects vomiting
9. Information Diet: quality, quantity, and frequency of meals (especially for
small children)
10. What techniques of drinking
11. How psychosocial conditions at home
Investigations carried out to assist the diagnosis approach. Examination of
selected types sesuasi with alleged diagnosis based on history and clinical
manifestations. Investigations may include blood tests, radiological with or
without contrast, ultrasound, endoscopy, esophageal pH monitoring (pH-metri),
hydrogen breath test, biopsy gastrointestinal mucosa.
Green vomit in neonates either accompanied or not accompanied by
abdominal distension can be an early sign of gastrointestinal obstruction .
Nasogatrik pipe must be installed to decompress the stomach . Examination of the
stomach smooth muscle that showed dilated bowel and air-fluid levels showed a
gastrointestinal obstruction requiring surgery . Radiological examination using
contrast can differentiate their duodeni atresia , midgut malrotation , volvulus ,
jejunal atresia , or ileus which is the cause of obstruction of the gastrointestinal
tract are most often in neonates .7
Clinical suspicion of stenosis of the pylorus Adaiah can be proved by
barium meal examination or ultrasound which showed a typical picture .
Gastroesophageal reflux ( RGE ) can be proved by esophageal pH monitoring for
24 hours ( pH - metri ) . Reflux index above 5 % showed the presence of
pathological gastroesophageal reflux . Esophagitis and peptic disease ( erosion ,
ulcers ) can be proved by endoscopy and biopsy examination of the
gastrointestinal mucosa . Suspicion of lactose intolerance is proved by the breath
hydrogen test . Penginkatan H2 breath above 20 ppm in the 60-120 minutes after
drinking a lactose solution showed the presence of lactose malabsorption , while
the increase in the 30th minute show bacteria overgrowth . Examination of blood
gas and electrolyte analysis performed when alleged to have occurred
complications of metabolic disorders or otherwise of the suspicion that the
underlying metabolic disorders such complaints.9
2.7 Treatment
The main therapeutic vomiting shown to find and fix the cause , while
supportive therapy is required to prevent a worse situation and overcome the
complications that have occurred . Some of the instructions below can be used as
initial therapy for vomiting in children , namely :
prevent dehydration and electrolyte balance disorders
Stop suspected drugs can irritate the stomach and make vomiting increased
( aspirin , aspirin , corticosteroids )
Provide food that is easily digested so it helps the healing process of the
gastrointestinal tract .

 After 3 hours of no vomiting , can be given a drink by the glass ( child ) or

bottle ( baby ) with a number that increased gradually
After 6 hours of no vomiting , the baby can be given bananas , cereal and
apple juice , while older children can be given bread , honey , potatoes ,
chicken soup or rice .
Anti-vomiting drugs are not used routinely in children , but only in
children who refuse to drink after vomiting , or vomiting lasts more than 24 hours
so in fear of the situation will lead to complications in the form of dehydration
and electrolyte balance disorders and blood gas
On motion sickness occurs vestibular system disorders , the class of
anticholinergics ( scopolamine ) is the drug of choice . Class of antihistamines
( hyocine hydrobromide , promethazine ) who worked on the ' vomiting center '
can be used in these circumstances . Class of serotonin receptor antagonists
( ondansentron ) who worked on the CTZ is very effective in the case of
chemotherapy and radiotherapy .
In the gastrointestinal tract such as an infection , class of dopamine
receptor antagonists ( metoclopramide and domperidone ) who works at the center
( CTZ ) and peripheral ( gastrointestinal ) is the drug of choice . Metoclopramide
has the effect of inhibiting the dopamine receptors in the CTZ , thereby reducing
nausea and vomiting . A variety of symptoms such as anxiety , tremor , dystonia .
Domperidone is widely used as an anti- vomiting drugs because the effect
is positive . And minor side effects . This drug inhibits dopamine receptors other
than in the CTZ , also dopamine receptors in the peripheral ( gastrointestinal
tract ) . The recommended dose in children is 0.2-0.4 mg / kg / day peroral.11
Management:
1. General
Local effects.
Mallory-Weiss tear usually only cause minor bleeding so that no action
was necessary. Instead rips esophagus require radical action.
Metabolic Effects
In patients with recurrent and prolonged vomiting can occur fluid and
electrolyte balance disorders that require fluid and electrolyte replacement
(Ringer lactate) followed by administration of fluids and electrolytes for
maintenance7
Aspiration
Apirasi massive gastric contents require anibiotika and sometimes
corticosteroids. On inhalation of gastric contents in the form of milk in
small amounts at a time can lead to sensitization to cow's milk protein
causing allergic bronchitis.

 The effect of nutrition

Explaining shown to parents about how making techniques drinks / food
and eating. And last but not least is someone who emphasizes the
harmonious relationship between the baby with the mother and father. If
vomiting continuously and is expected to lead to malnutrition or vomiting
healing will be long, sometimes required parenteral nutrition.
2. Symptomatic
Drug Antiemetic
Although the main purpose of management of vomiting is to eliminate the
specific movement, but symptomatic management to reduce or eliminate
symptoms of vomiting often needs to be done first. Keep in mind that the
state of acute and severe vomiting, anti-vomiting drug is only useful if the
drug can be absorbed in sufficient amounts. Stop eating / drinking for a
few hours can help reduce the terrible vomiting allowing oral
administration of drugs.
Capture Point Anti-Vomiting Drug Action
Capture point anti-vomiting drug action can be located in several parts of
the body, such as chemical receptors mainly influenced by group
fenotiasin, antihistamines and dopamine antagonist. Vomiting center
directly affected by anti kholinergik group. Receptors in the vestibule by a
group of antihistamines, while the peripheral receptors are affected
differently by groups fenotiasin, dopamine antagonists, betanekhol, an
increase of acetylcholine by group metoclopramide, domperidone and
cicaprid. In general it can be said, especially good antihistamine used for
anti-drunk (motion sickness), dopamine antagonists for gastrointestinal
motility and phenothiazines to the side effects of the drug sitostatica,
radiation and uremia7.

Antiemetic Drug Classes

Anticholinergics

: Hyosine, buskopan, holopon, atropine.

Antihistamines

: Dimenhydrinate (Dramamin, Antimo),

Meclozine (Tavegyl), promethazine (Fenergan, Avropeg).

Phenothiazines
: Proklorperazine (Stenetil). Pervanazine

(Avomit) Tietilperazine maleate (Torecan).

Dopamine antagonist
: Metoclopramide (Vomitrol), Domperidone

(Motilium)
Increasing acetylcholine : Metoclopramide (Vomitrol).
Direct on muscarinic receptors: Bethanecol.
Based on intestinal motility, a drug commonly given as symptomatic

medication for vomiting can be divided into two groups9:

Category I
Gastrointestinal

stimulant

class

motors

are

materials

(often

neurotransmitter or similar) which enhances smooth muscle activity. In addition to

stimulating motility also stimulates the secretion is not confined to the intestine
only. example:Bethanechol, which in children is only used at RGE
(gastroesophageal reflux)
Category II
Prokinetic drug classes10.
This drug normalizes muscle motility disorders that have a nature to
improve the coordination of peristaltic activity. The prototype of this class is
Metoclopramide that have the effect of dopamine receptor antaginis (antagonist
against motoric inhibition by dopamine) which is not only limited to
gastriptointestinal level, but also has an influence on the level of the central
nervous arrangement that can occur neurologic side effects.
Drugs Domperidone (Motilium) is said to have the same effect but without
affecting the central nervous system, although not specific.
Both of these dopamine antagonist drugs prokinetiknya power is a way
antagonistic to inhibi motoric by dopamine.
Lately produced drugs that have a prokinetic no antagonistic effects, has a
direct effect asetilkolinsecara physiological stimulate spending in myenteric
plexus, and thus has a specific effect on the level motoric distal intestine.

Drugs that affect intestinal motility.

mechanisms of action
Direct effect on

motility stimulants
muscarinic Betanechol

prokinetic drugs
-

receptors
Antagonis reseptor dopamine

Metoklopramid,

Increasing acetylcholine

Domperidon
Metoklopramid, Cisaprid

A drug often used to treat vomiting and gastric motility disorders11.

1. Metoclopramide
Quite effective, way of working is the blockade of dopamine receptors
in the CTZ, so it can control nausea and vomiting both centrally. Keep in
mind, these drugs can cause a reaction in dystonia and dikinetik okulogirik
crisis.
2. Domperidone
Can be said to be more secure. The workings of the blockade of
dopamine receptors in the CTZ and intestines either. Can be administered
orally or suppository. Bioavaibility low because experiencing rapid
metabolism in the intestinal wall and liver, and only slightly into the brain. To
prevent nausea and vomiting in sitostatica treatment, oral doses of
1mg/kg.bb/day (more effective than metoclopramide 0.5 mg/kg.bb/ay) Dosage
in children 0.2-0.4 mg/kg.bb/day orally, 4-8 hour intervals.
3. Cisapride
New prokinetic drug, increased spending physiologically selective
acetylcholine at the level of post-ganglionic nerves in myenteric plexus. Do
not have the nature of the blockade of dopamine receptors, but the increase
peristaltic gastroduodenal.
Pad children are also effective in preventing reflux and repair material
klerens of reflux in the esophagus. Dose 0,2-0,4mg/kg.bb/day.

4. Betanekhol
A selective kholinester with the workings of the muscarinic receptor,
its effect is quite long. In children RGE used for therapy, a dose of 0.6
mg/kg.bb/day, divided into 3 doses, orally 0.15 to 0.2 mg/kg.bb/day subcutaneous.
2.8 Complications
Loss of fluids and electrolytes , aspiration of gastric contents , malnutrition
and failure to thrive , Mallory - Weiss syndrome ( tear in epithelial
gastroesophageal junction due to repeated vomiting ) , Boerhave syndrome
( rupture of the esophagus ) , and peptic esophagitis.
2.7 Prognosis
The prognosis of patients with symptoms of vomiting depends on the degree
of dehydration and treatment of dehydration, the etiology of the disease which
causes vomiting, as well as complications of vomiting itself.
2.8 Prevention
Prevention is meant here is the prevention of complications due to vomiting ,
such as fluid and electrolyte balance disorders ( dehydration , acidosis / metabolic
alkalosis , hypokalemia , hyponatremia ) , aspiration , nutritional disorders , peptic
esophagitis , Mallory - Weiss syndrome . The situation can be prevented by
following the instructions or the treatment of vomiting in children as described
previously .12

CHAPTER III
CONCLUSION
Conclusion
Vomiting is one of the most common clinical manifestations shown by a child
with disorders of the digestive tract and out of the digestive tract . The causes of
vomiting in children vary widely , therefore the introduction of specific clinical
manifestations of each disease as the cause of vomiting that often needs to be
understood by a physician . Proper approach and speedy diagnosis would lead to
optimal management . Anti- vomiting drug use is not a primary option vomiting
cases , but in some circumstances , anti- vomiting drug effective and safe is
needed.

ACKNOWLEDGEMENTS
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1998.
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3. Fitzgerald JF,Clark JH, 1988; Manual of pediatric gastroenterology. Churchill
livingstones p 25-32.
4. Tamaela L, Kartono D. Muntah pada bayi baru lahir. Dalam: Naskah lengkap
Pendidikan Tembahan Berkala IKA FKUI. Jakarta: Balai Penerbit FKUI, 1985;2844..
5. Orensteins SR,1993; Dysphagia and vomiting .In Pediatric Gastroeintestinal
Disease. Pathophysiology, Diagnosis, Management Edited by Willy R, Hyams JS.
WB Saunders Comp. 135-150.
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Jilid I. Cetakan Ketiga. Jakarta: Badan Penerbit IDAI
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Edited by Walter,Durie, Hmilton, Walkersmith, Watkins. Black and Decker Inc. p
97-115.
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Dalam: Contituining Education IKA FK Unair. Surabaya, IDAI Jatim, 1991;8592.
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10. Markum AH, Ismael S., Alatas H dkk. Muntah. Dalam: Buku Ajar Ilmu
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of pediatrics. 15th ed Philadelphia . WB Saunders; 1996:1033.