You are on page 1of 50

CHAPTER I

PRELIMINARY

Case II
Seven month old infant was brought to you because she didn't respond to
sound, even loud sound like thunder. She can't roll over and sit unsupported. Her
mother noticed the girls has white color, in the pupil since birth. The girl was
aterm and her birth weight was 2700 grams. You found microcepal, cataract,and
persisten ductus arteriosus in infant . There rubella antibody is positive of on
laboratory finding. You planned to do further hearing testing for the infant.

1. Clarification and Definition


a. Microcephaly
Microcephaly is an abnormal small head dut to failure of brain
growth.
b. Antibody
Antibody is molecules (also called immunoglobulins) produced by
a B cell in response to an antigen. When an antibody attaches to an
antigen , it helps the body destroy or inactive the antigen.
c. Cataract
Cataract is opacities in the lens of the eye and capsule.
d. Rubella
Rubella (German measles; 3-day measles) is an acute febrile illness
characterized by a rash and lymphadenopathy that affects children
and young adults. It is the mildest of common viral exanthems.
2. Keywords
 Seven month old infant
 She didn’t respond to sound
 She can't roll over and sit unsupported
 White color in the pupil since birth
 Aterm

33
 Birth weight was 2700 grams
 Microcephaly
 Cataract
 Persisten ductus arteriosus in infant
 Rubella antibody is positive
3. Problem
Seven month old infant didn’t respond to sound, she can’t roll over
and sit, has white color in the pupil since birth and also can find
microcephaly,cataract, persisten ductus arteriosus in infant and the result
of laboratory eximination showed Rubella antibody is positive.
4. Probelm Analyzed
Seven month
old

Aterm, but the


Did not Can’t roll over and sit White colours in
weight was 2700 grams
respond the sound unsupported pupil

Found microcephaly,
Rubella antibody was
cataracs, and persisten ductus
possitive
arteriosus

Rubella infection

Etiology Phatogenesis Treatment Prevetion

Different diagnosis Clinical


manifestation 33
5. Hypothesis
The baby was born with congenital rubella syndrom, if mother is
infected with the rubella virus in the 1st trimester.
6. Learning issue
1. What is congenital infection?
2. Congenital Rubella Syndrom :
a. Etiology
b. Patogenesis
c. Prevention
d. Clinical Manifestation
e. Complication and Prognosis
f. Treatment
g. Diagnosis
3. How about the state of immunity after the attack Rubella virus?
4. How about milestone the growth and development?
5. How about physiology of development baby
a. Eye
b. Ear
c. Cardiovascular
d. Immune System
6. What is developmental disorder in infant?
7. How about the growth and development neurology of the infant?
8. What is mental retardation?
9. What the definition of teratogen?
10. What the teratogen factor from intrauterine?
11. How about intrauterine growth restriction?
12. What is TORCH?
13. How about five basic of vaccine during pregnancy?

33
CHAPTER II
DISCUSSION

1. Definition of congenital infection1


Congenital infection is an infection acquired transplacentally
during gestation is a congenital infection. Numerous pathogens that
produce mild or subclinical disease in older infants and children can cause
severe disease in neonates who acquire such infections prenatally or
perinatally.
Congenital infections include a well-known group of fungal,
bacterial, and viral pathogens ; toxoplasmosis, rubella, cytomegalovirus
(CMV), herpes simplex virus (HSV), varicella- zoster virus, congenital
syphilis, parvovirus, human immunodeficiency virus (HIV), hepatitis B,
Neisseria gonorrhoeae, Chlamydia, and Mycobacterium tuberculosis.
2. Congenital Rubella Syndrome
a) Etiology1
Rubella virus is a member of the family Togaviridae and is
the only species of the genus Rubivirus. It is a single-stranded
RNA virus with a lipid envelope and 3 structural proteins,
including a nucleocapsid protein that is associated with the nucleus
and 2 glycoproteins, E1 and E2, that are associated with the
envelope. The virus is sensitive to heat, ultraviolet light, and
extremes of pH but is relatively stable at cold temperatures.
Humans are the only known host.
b) Phatogenesis and Pathology2
Maternal viremia associated with rubella infection during
pregnancy may result in infection of the placenta and fetus. Only a
limited number of fetal cells become infected. The growth rate of
infected cells is reduced, resulting in fewer numbers of cells in
affected organs at birth. The infection may lead to deranged and

33
hypoplastic organ development, resulting in structural anomalies in
the newborn.
Timing of the fetal infection determines the extent of
teratogenic effect. In general, the earlier in pregnancy infection
occurs, the greater the damage to the fetus. Infection during the
first trimester of pregnancy results in abnormalities in the infant in
about 85% of cases, whereas detectable defects are found in about
16% of infants who acquired infection during the second trimester.
Birth defects are uncommon if maternal infection occurs after the
20th week of gestation.
Inapparent maternal infections can produce these anomalies
as well. Rubella infection can also result in fetal death and
spontaneous abortion. Intrauterine infection with rubella is
associated with chronic persistence of the virus in the newborn. At
birth, virus is easily detectable in pharyngeal secretions, multiple
organs, cerebrospinal fluid, urine, and rectal swabs. Viral excretion
may last for 12–18 months after birth, but the level of shedding
gradually decreases with age.
c) Prevention3
 In people who are vulnerable, passive protection from
disease or weakening variation can be given by intramuscular
injection of immune serum globulin (GIS) given in large doses
(0.25 to 0.50 mL / kg or 0.12 to 0.20 mL / lb ) in 7-8 days after
exposure.
 The effectiveness of immune globulin can not be fore seen. Seems
to depend on the levels of antibody products used and the
unknown factor. GIS benefits has been questioned due to several
circumstances prevented rash and clinical manifestations no or
minimal even if the live virus can be demonstrated in the blood.
 Vaccination or immunization program is a prevention against
rubella.

33
 Rubella immunization should be given to post-pubertal women
who are vulnerable to virus
 Vaccination since childhood or before pregnancy. For protection
against rubella virus vaccine has been available in the form of a
combination vaccine that also is used to prevent measles and
mumps infection, known as MMR (Mumps, Measles, Rubella).
Rubella vaccine is given at age 15 months. After it should have a
repeat at the age of 4-6 years. When you do not get a repeat at the
age of 4-6 years, should be given 11-12 years of age, even
teenagers. The vaccine can not be given to women who are
already pregnant.
 Detection of the immune status before pregnancy. Before
pregnancy should check immunity against Rubella, as well as to
other TORCH infections. If anti-Rubella IgG positive only,
meaning you ever been infected or vaccinated against Rubella.
You may not be exposed to Rubella again, and the fetus is 100%
safe. If anti-Rubella IgM are positive or anti-Rubella IgM and
anti-Rubella IgG positive, it means you are infected with Rubella
new or newly vaccinated against Rubella. Your doctor will advise
you to postpone pregnancy until IgM became negative, ie for 3-6
months.
 If anti-Rubella IgG and anti-Rubella IgM negative means that you
do not have immunity to rubella. If you are not pregnant, the
doctor will give the vaccine Rubella and postpone pregnancy for
3-6 months. If you can not get the vaccine, do not want to delay
pregnancy or are already pregnant, which can be done is to
prevent you exposed to rubella. When you are pregnant though not
immune, forced learns to avoid contracting rubella in the
following way : Do not approach the sick with a fever, do not go
to where many children congregate, such as kindergarten and
elementary school Playgroup.Do not go to day care.Unfortunately,

33
this can not be 100% implemented because of circumstances or
because someone else gets Rubella do not necessarily show
symptoms of fever. Rubella immunity against re-examined again
the age of 17-20 weeks. When women experience Rubella, blood
check what really hit Rubella. If the pregnant mother has a fever
accompanied by rash, be sure to check whether the correct Rubella
IgG Rubella and IgM after 1 week. When IgM positive, it means
completely new Rubella infection.

d) Clinical Manifestation1
The incubation period for postnatal rubella is typically 16
to 18 days (range, 14 to 21 days). The mild catarrhal symptoms of
the prodromal phase of rubella may go unnoticed. The
characteristic signs of rubella are retroauricular, posterior cervical,
and posterior occipital lymphadenopathy accompanied by an
erythematous, maculopapular, discrete rash. The rash begins on the
face and spreads to the body, lasting for 3 days and less prominent
than that of measles. Rose-colored spots on the soft palate, known
as Forchheimer spots, develop in 20% of patients and may appear
before the rash. Other manifestations of rubella include mild
pharyngitis, conjunctivitis, anorexia, headache, malaise, and low-
grade fever. Polyarthritis, usually of the hands, may occur,
especially among adult females, but usually resolves without
sequelae. Paresthesias and tendinitis may occur.
e) Complication and prognosis
 Complication4
Complications are relatively uncommon in childhood.
Encephalitis similar to that seen with measles occurs in about 1
in 6,000 cases. The severity is highly variable, and there is an
overall mortality rate of 20%. Symptoms in survivors usually
resolve within 1-3 week without neurologic sequelae.

33
Thrombocyt openic purpura occurs at an overall rate of 1 in
3,000 cases of rubella and occurs more frequently among
children and in girls. It manifests about 2 week following the
onset of the rash as petechiae, epistaxis, gastrointestinal
bleeding, and hematuria. It is usually self-limited.
Arthritis following rubella occurs more commonly among
adults, especially women. It begins within 1 wk of onset of the
exanthem and classically involves the small joints of the hands.
It also is self-limited and resolves within weeks without
sequelae. There are anecdotal reports and some serologic
evidence linking rubella with rheumatoid arthritis, but a true
causal association remains speculative.
Encephalitis is the most serious complication of postnatal
rubella. It occurs in two forms : a post infectious syndrome
following acute rubella and a rare progressive panencephalitis
manifesting as a neuro degenerative disorder years following
Rubella.
Post infectious encephalitis is uncommon, occurring in 1 in
5,000 cases of rubella. It appears within 7 days after onset of
the rash, consisting of headache, seizures, confusion, coma,
focal neurologic signs, and ataxia. Fever may recrudesce with
the onset of neurologic symptoms. Cerebrospinal fluid may be
normal or have a mild mononuclear pleocytosis and or elevated
protein concentration. Virus is rarely, if ever, isolated from
cerebrospinal fluid or brain, suggesting a noninfectious
pathogenesis. Most patients recover completely, but mortality
rates of 20% and long-term neurologic sequelae have been
reported.
 Prognosis4
Post natal infection with rubella has an excellent prognosis.
Long-term outcomes of CRS are less favorable and some what

33
variable. In an Australian cohort evaluated 50 year after
infection, many had chronic conditions but most were married
and had made good social adjustments. A cohort from New
York from the mid-1960s epidemic had less-favorable
outcomes, with 30% leading normal lives, 30% in dependent
situations but functional, and 30% requiring institutionalization
and continuous care.
Reinfection with wild virus occurs postnatally in both
individuals who were previously infected with wild-virus
rubella and in vaccinated individuals. Reinfection is defined
serologically as a significant increase in IgG antibody level
and/or an IgM response in an individual who has a documented
preexisting rubella-specific IgG above an accepted cutoff.
Reinfection may result in an anamnestic IgG response, an IgM
and IgG response, or clinical rubella. There are 29 reports of
CRS following maternal reinfection in the literature.
Reinfection with serious adverse outcomes to adults or children
is rare and of unknown significance.
f) Treatment
There is no specific treatment for congenital rubella. It can
be prevented by childhood immunization with rubella vaccine to
ensure that women of childbearing age are immune.2
g) Diagnosis5
Diagnosis is based on clinical symptoms arise, and from
blood tests in the laboratory to see the levels of IgG and IgM
antibodies to rubella her. Diagnosis is by serology. IgM will
quickly respond after exit rash and then will decline and disappear
within 4-8 weeks, IgG also responds after being out of rash and
remain high throughout life. Diagnosis is confirmed with a 4-fold
increase in titer of hemagglutination-inhibiting (HAI) antibody
from serum obtained two twice an interval of 2 weeks or after the

33
IgM. Rubella diagnostics can also be enforced through the culture
and isolation of the virus in the acute phase. The discovery of the
blood placenta IgM or IgG in neonates or infants 6 months to
support the diagnosis of Rubella infection.
10-15% of adult women are susceptible to Rubella
infection. Course of the disease is not affected by pregnancy and
pregnant women may or may not show any symptoms of the
disease. The degree of the mother's disease had no impact on the
risk of fetal infection. Infections that occur in the first trimester
have a major impact on the fetus. Rubella infections occurred in
danger when a young pregnant woman, because it can lead to
abnormalities in the baby (Arsa, 2010).
When pregnant women are not immune to rubella virus
during pregnancy of less than 4 months, there will be a variety of
severe defects in the fetus. Most babies will have cataracts in the
lens of the eye, hearing loss, heart leaking, even brain damage.
Rubella infection in pregnancy can cause miscarriage,
stillbirth or disruption to the fetus The trouble, as much as 50%
more women who suffer Rubella do not feel anything. Others have
a fever, aching bones, glands behind the ears enlarged and
somewhat painful. After 1-2 days appear red blotches all over the
body correct itself after a few days. Not all fetuses will be infected.
If a pregnant woman is infected at the age of pregnancy <12 weeks
the fetus risk of contracting 80-90 percent. If the infection of the
mother at the age of 15-30 weeks of pregnancy, the risk of fetal
infection is 10-20 percent drop. However, the risk of fetal infected
rising to 100 percent if the mother is infected during pregnancy >
36 weeks. Fortunately,Congenital Rubella syndrome usually occurs
only when the mother is infected during gestation is still less than 4
months.When it passed 5 months, rare infection. In addition, babies

33
are also at greater risk for developing diabetes mellitus, thyroid
disorders,gastrointestinal disorders and neurological disorders.
3. The state of immunity after the attack
Rubella virus after the attack Rubella usually occurs long-
term immunity. Reinfection can occur but usually not accompanied
by clinical signs and symptoms. Subclinical reinfection can occur
at elevated levels of IgM antibodies. When a mother who suffered
reinfection Rubella during pregnancy .It is less likely that the baby
suffered from Congenital Rubella .6
Normally, maternal rubella antibody in the form of IgG is
transferred to infants and is gradually lost over a period of 6
months. Demonstration of rubella antibodies of the IgM class in
infants is diagnostic of congenital rubella. As IgM antibodies do
not cross the placenta, their presence indicates that they must have
been synthesized by the infant in utero. Children with congenital
rubella exhibit impaired cell-mediated immunity specific for
rubella virus.2
4. Milestone1
Age Gross motor Fine motor- Personal Languange Other
adaptive social cognitive
2wk Move hide Regards face Alert to bell
side to side

2mo Lifts shoulder Tracks past Smiles Cooing


while prone midline responsively
Search for
sound with
eyes
Lifts uphands Reaches for Looks at hand Laughs and
object aqueals

33
Rolls front to Raking grasp Begin to work
back toward toy
If pulled to sit
from supine,
no head lag

6mo Sit a lone Transfers object Feed self Babbles


hand to hand

Hold bootle Says dada and


mama but no
spesific

9mo Pulls to stands Starting to Waves bye- Two-syllable


get into sitting pincer grasp bye play pat-a sounds
position Bangs two cake
blocks together
12mo Walks stoops Puts block in Drinks drom a Says mama
and stands cup cup imitates and dada,
others spesific says
one to two
other words
15 Walks Scribbles stack Uses spoon Says three to
mo backwards two blocks and fork helps six words
in housework follows
commands

18 Runs Stacks four Removes Says at least


mo blocks kicks a garmeny”feeds six words
ball ” doll

33
2yr Walks up and Stacks six Washes and Put two words Understan
down stairs. blocks , copies dries together point ds concept
Throws line hands,brushes to pictures of today
overhans teeth, puts on knows body
clothes parts
3yr Walk step Stacks eight Use spoon Names Understan
alternating blocks, wiggle well, spilling pictures, ds concept
feet, broad thumb little , puts on speech of
jump t-shirt understands to tommorow
stranger 75%, and
says three- yesterday
wordsentences
4yr Balance well Copies O, Brushes teeth Names colors,
on eachfoot , maybe +, draw without help, understand
hops on one person with dresses adjective
foot three parts without help
5yr Skips , heel- Copies□ Counts,
to-toe walks understand
opposite
6yr Balances on Copies ∆, draws Defines words Begins to
each foot 6sec persong with six understand
parts right and
left
5. a.Phisiology developemnt of Eye
Optic cup and lens vesicle7
The developing eye appears in the 22-day embiyo as a pair
of shallow grooves on the sides of the forebrain . With dosure of
the neural tube, these grooves form out pocketings of the forebrain,
the optic vesicles. These vesicles subsequently come in contact
with the surface ectoderm and induce changes in the ectoderm
necessary for lens formation. Showing there after, the optic vesicle

33
begins to invaginate and forms the double-walled optic cup. The
inner and outer layers of this cup are initially separated by a lumen,
the intraretinal space, but soon this lumen disappears, and the two
layers appose each other.

33
33
Invagination is not restricted to the central portion of the
cup but also involves a part of the inferior surface that forms the
choroid fissure. Formation of this fissure allows the hyaloid artery
to reach the inner chamber of the eye .
During the seventh week, the lips of the choroid fissure
fiise, and the mouth of the optic cup becomes a round opening, the
future pupil. During these events, cells of the surface ectoderm,
initially in contact with the optic vesicle, begin to elongate and
form the lens placode . This placode subsequently invaginates and
develops inte the lens vesicle. During the fifth week, the lens
vesicle loses contact with the surface ectoderm and lies in the
mouth of the optic cup
Retina,Iris and Ciliary Body7
The outer layer of the optic cup, which is characterized by
small pigment granules, is known as the pigmented layer of the
retina . Development of the inner (neural) layer of the optic cup is
more complicated.
The posterior four-fifths, the pars óptica retinae, contains
cells bordering the intraretinal space that differentiate into the
photoreceptive rods and cones. Rods are more numerous (120
million) and more sensitive than cones (6 to 7 million) but do not
detect color like the cones.
Adjacent to this photoreceptive layer is the mantle layer,
which, as in the brain, gives rise to neurons and supporting cells,
including the outer nuclear layer, inner nuclear layer, and ganglion
cell layer.
On the surface is a fibrous layer that contains axons of
nerve cells of the deeper layers. Nerve fibers in this zone converge
toward the optic stalk, which develops inte the optic nerve. Hence,
light impulses pass through most layers of the retina before they
reach the rods and cones.

33
The anterior fifth of the inner layer, the pars ceca retinae,
remainsone cell layer thick. It later divides into the pars iridica
retinae, which forms the inner layer of the iris, and the pars ciliaris
retinae, which participates in formation of the cliary body.
Meanwhile, the región between the optic cup and the overlying
surface epithelium is filled with loose mesenchyme. The sphincter
and dilator pupillae muscles form in this tissue. These muscles
develop from the underlying ectoderm of the optic cup. In the
adult, the iris is formed by the pigment-containing external layer,
the unpigmented internal layer of the optic cup, and a layer of
richly vascularized connective tissue that contains the pupillary
muscles.The pars ciliaris retinae is easily recognized by its marked
folding . Externally, it is covered by a layer of mesenchyme that
forms the ciliary muscle; on the inside, it is connected to the lens
by a network of elastic fibers, the suspensory ligament or zonula.
Contraction of the ciliary muscle changes tensión in the ligament
and Controls curvature of the lens.

33
33
Lens7
Shortly after formation of the lens vesicle cells of the
posterior wall begin to elongate anteriorly and form long fibers that
gradually fill the lumen of the vesicle. By the end of the seventh
week, these primary lens fibers reach the anterior wall of the lens
vesicle. Growth of the lens is not finished at this stage, however,
because new (secondary) lens fibers are continuously added to the
central core..
Choroid, Sclera, and Cornea7
At the end of the fifth week, the eye primordium is
completely surrounded by loose mesenchyme. This tissue soon
differentiates into an inner layer comparable with the pia mater of
the brain and an outer layer comparable with the dura mater. The
inner layer later forms a highly vascularized pigmented layer
known as the choroid; the outer layer develops into the sclera and
is continuous with the dura mater around the optic nerve.
Differentiation of mesenchymal layers overlying the anterior
aspect of the eye is diíferent. The anterior chamber forms through
vacuolization and splits the mesenchyme into an inner layer in
front of the lens and iris, the iridopupillary membrane, and an outer
layer continuous with the sclera, the substantia propria of the
cornea. The anterior chamber itself is lined by fiattened
mesenchymal cells. Hence, the cornea is formed by (1) an
epithelial layer derived from the surface ectoderm, (2) the
substantia propria or stroma, which is continuous with the sclera,
and (3) an epithelial layer, which borders the anterior chamber. The
iridopupillary membrane in front of the lens disappears completely.
The posterior chamber is the space between the iris anteriorly and
the lens and ciliary body posteriorly.
The anterior and posterior chambers communicate with
each other through the pupil and are filled with fluid called the

33
aqueous humor produced by the ciliary process of the ciliary body.
The clear aqueous humor circulates from the posterior chamber
into the anterior chamber providing nutrients for the avascular
cornea and lens. From the anterior chamber, the fluid passes
through the scleral venous sinus (canal of Schlemm) at the
iridocorneal angle where it is resorbed into the bloodstream.
Blockage of the flow of fluid at the canal of Schlemm is one cause
of glaucoma.
Vitreous Body7
Mesenchyme not only surrounds the eye primordium from
the outside but also invades the inside of the optic cup by way of
the choroid fissure. Here, it forms the hyaloid vessels, which
during intrauterine life supply the lens and form the vascular layer
on the inner surface of the retina. In addition, it forms a delicate
network of fibers between the lens and retina. The interstitial
spaces of this network later ñll with a transparent gelatinous
substance, forming the vitreous body. The hyaloid vessels in this
región are obhterated and disappear during fetal life, leaving
behind the hyaloid canal.
Optic Nerve7
The optic cup is connected to the brain by the optic stalk,
which has a groove, the choroid físsure, on its ventral surface. In
this groove are the hyaloid vessels. The nerve fibers of the retina
returning to the brain lie among cells of the inner wall of the stalk.
During the seventh week, the choroid fissure closes, and a narrow
tunnel forms inside the optic stalk. As a result of the continuously
increasing number of nerve fibers, the inner wall of the stalk
grows, and the inside and outside walls of the stalk fuse. Cells of
the inner layer provide a network of neuroglia that supports the
optic nerve fibers. The optic stalk is thus transformed into the optic
nerve. Its center contains a portion of the hyaloid artery, later

33
called the central artery of the retina. On the outside, a continuation
of the choroid and sclera, the pia arachnoid and dura layer of the
nerve, respectively, surround the optic nerve.

Molecular Regulation Of Eye Development7


PAX6 is the key regulatory gene for eye development. It is a
member of the PAX (paired box) family of transcription factors and
contains two DNA-binding motifs that include a paired domain and a
paired-type homeodomain. Initially, this transcription factor is expressed
in a band in the anterior neural ridge of the neural píate before neurulation
begins. At this stage, there is a single eye field that later separates into two
optic primordia.
The signal for separation of this field is SONIC HEDGEHOG
(SHH) expressed in the prechordal píate. SHH expression upregulates
PAX2 in the center of the eye field and downregulates PAX6. Later, this
pattern is maintained so that PAX2 is expressed in the optic stalks and
PAX6 is expressed in the optic cup and overlying surface ectoderm that
forms the lens. As development proceeds, it appears that PAX6 is not
essential for optic cup formation. Instead, this process is regulated by
Interactive signáis between the optic vesicle and surrounding mesenchyme
and the overlying surface ectoderm in the lens-forming region. Thus,
fibroblast growth factors (FGFs) from the surface ectoderm promote
differentiation of the neural (inner layer) retina, whereas transforming
growth factor (3 (TGF-P), secreted by surrounding mesenchyme, directs
formation of the pigmented (outer) retinal layer. Downstream from these
gene producís, the transcription factors M ITF and CHXIO are expressed
and direct differentiation of the pigmented and neural layer, respectively.
Thus, the lens ectoderm is essential for proper formation of the optic cup,
such that without a lens placode, no cup invagination occurs.
Differentiation of the lens depends on PAX6, although the gene is not
responsible for inductive activity by the optic vesicle. Instead, PAX6 acts

33
in the surface ectoderm to regúlate lens development. This expression
upregulates the transcription factor S0X2 and also maintains PAX6
expression in the prospective lens ectoderm. In turn, the optic vesicle
secretes BMP4, which also upregulates and maintains S0X2 expression as
well as expression of LMAF, another transcription factor. Next, the
expression of two homeobox genes, SIX3 and PROXI is regulated by
PAX6. The combined expression of PAX5, S0X2, and LMAF initiates
expression of genes responsible for lens crystallin formation, including
PROXl. SIX3 also acts as a regulator of crystallin production by inhibiting
the crystallin gene. Finally, PAX6, acting through F0X3, regulates cell
proliferation in the lens.7

33
b. Phisiology Developmental of Ear
In the adult, the ear forms one anatomic unit serving both hearing
and equilibrium. In the embryo, however, it develops from three distinctly
diíferent parts: ( 1) the external ear, the sound-collecting organ; (2) the
middle ear, a sound conductor from the external to the internal ear; and (3)
the internal ear, which converts sound waves into nerve impulses and
registers changes in equilibrium.7
INTERNAL EAR7
The first indication of the developing ear can be found in embryos
of approximately 22 days as a thickening of the surface ectoderm on each
side of the rhombencephalon. These thickenings, the otic placodes,
invaginate rapidly and form the otic or auditory vesicles (otocysts). Cells
from the otocyst differentiate and form ganglion cells for the statoacoustic

33
(vestibulocochlear) ganglia. During later development, each vesicle
divides into (1) a ventral component that gives rise to the saccule and
cochlear duct and (2) a dorsal component that forms the utricle,
semicircular canals, and endolymphatic duct. Together, these epithelial
structures form the membranous labyrinth. Saccule, Cochiea, and Organ of
Corti In the sixth week of development, the saccule forms a tubular
outpocketing at its lower pole. This outgrowth, the cochlear duct,
penetrates the surrounding mesenchyme in a spiral fashion until the end of
the eighth week, when it has completed 2.5 turns.

33
In the seventh week, cells of the cochlear duct diíferentiate into the
spiral organ of Corti that transduces sound vibrations into electrical signáis
for hearing. A connection between the cochlear duct and the remaining
portion of the saccule is maintained but confined to a narrow pathway, the
ductus reuniens.
Mesenchyme surrounding the cochlear duct soon differentiates into
cartilage. In the l0th week, this cartilaginous shell undergoes
vacuolization, and two perilymphatic spaces, the scala vestibuli and scala
tympani, are formed. The cochlear duct is then separated from the scala
vestibuli by the vestibular membrana and from the scala tympani by the
basilar membrane. The lateral wall of the cochlear duct remains attached
to the surrounding cartilage by the spiral ligament, whereas its median
angle is connected to and supported by a long cartilaginous process, the
modiolus, the fiiture axis of the bony cochlea. Initially, epithelial cells of
the cochlear duct are alike. With further development, however, they form
two ridges: the inner ridge, the future spiral limbus, and the outer ridge.
The outer ridge forms one row of inner and three or four rows of outer hair
cells, the sensory cells of the auditory system. They are covered by the
tectorial membrane, a fibrillar gelatinous substance attached to the spiral

33
limbus that rests with its tip on the hair cells. The sensory cells and
tectorial membrane together constitute the organ of Corti. Impulses
received by this organ are transmitted to the spiral ganglion and then to the
nervous system by the auditory fibers of cranial nerve VIII.

33
Utricle and SemicircuEar Canals During the sixth week of
development,semicircular canals appear as flattened outpocketings of the
utricular part of the otic vesicle. Central portions of the walls of these
outpocketings eventually appose each other and disappear, giving rise to
three semicircular canals . Whereas one end of each canal dilates to form
the crus ampullare, the other, the crus nonampullare, does not widen.
Because two of the latter type fuse, however, only five crura enter the
utricle, three with an ampulla and two without. Cells in the ampullae form

33
a crest, the crista ampullaris, containing sensory cells for maintenance of
equilibrium. Similar sensory areas, the maculae acusticae, develop in the
walls of the utricle and saccule. Impulses generated in sensory cells of the
cristae and maculae as a result of a change in position of the body are
carried to the brain by vestibular ñbers of cranial nerve VIII. During
formation of the otic vesicle, a small group of cells breaks away from its
wall and forms the statoacoustic ganglion. Other cells of this ganglion are
derived from the neural crest. The ganglion subsequently splits into
cochlear and vestibular portions, which supply sensory cells of the organ
of Corti and those of the saccule, utricle, and semicircular canals,
respectively.
MIDDLE EAR7
Tympanic Cavity and Auditory Tube
The tympanic cavity, which originates in the endoderm, is
derived from the first pharyngeal pouch. This pouch expands in a
lateral direction and comes in contact with the floor of the first
pharyngeal cleft. The distal part of the pouch, the tubotympanic
recess, widens and gives rise to the primitive tympanic cavity, and
the proximal part remains narrow and forms the auditory tube
(eustachian tube) through which the tympanic cavity
communicates with the nasopharynx. Ossicles The malleus and
incus are derived from cartilage of the first pharyngeal arch, and
the stapes is derived from that of the second arch. Although the
ossicles appear during the first half of fetal life, they remain
embedded in mesenchyme until the eighth month when the
surrounding tissue dissolves . The endodermal epithelial lining of
the primitive tympanic cavity then extends along the wall of the
newly developing space. The tympanic cavity is now at least twice
as large as before. When the ossicles are entirely free of
surrounding mesenchyme, the endodermal epithelium connects
them in a mesentery-like fashion to the wall of the cavity.

33
The supporting ligaments of the ossicles develop later
within these mesenteries. Because the malleus is derived from the
first pharyngeal arch, its muscle, the tensor tympani, is innervated
by the mandibular branch of the trigeminal nerve. The stapedius
muscle, which is attached to the stapes, is innervated by the facial
nerve, the nerve to the second pharyngeal arch. During late fetal
life, the tympanic cavity expands dorsally by vacuolization of

33
surrounding tissue to form the tympanic antrum. After birth, the
epithelium of the tympanic cavity invades the bone of the
developing mastoid process, and epithelium-lined air sacs are
formed (pneumatization). Later, most of the mastoid air sacs come
in contact with the antrum and tympanic cavity. Expansión of
inflammations of the middle ear into the antrum and mastoid air
cells is a common complication of middle ear infections.
EXTERNAL EAR
External Audítory Meatus7
The external audítory meatus develops from the dorsal
portion of the first pharyngeal cleft. At the beginning of the third
month, epithelial cells at the bottom of the meatus proliferate,
forming a solid epithelial píate, the meatal plug. In the seventh
month, this plug dissolves, and the epithelial lining of the floor of
the meatus participates in formation of the definitive eardrum.
Occasionally, the meatal plug persists until birth, resulting in
congenital deafness. Eardrum or Tympanic Membrane The
eardrum is made up of (1) an ectodermal epithelial lining at the
bottom of the auditory meatus, (2) an endodermal epithelial lining
of the tympanic cavity, and (3) an intermedíate layer of connective
tissue that forms the fibrous stratum. The major part of the eardrum
is firmly attached to the handle of the malleus , and the remaining
portion forms the separation between the external auditory meatus
and the tympanic cavity. Auricle The auricle develops from six
mesenchymal proliferations at the dorsal ends of the first and
second pharyngeal arches, surrounding the first pharyngeal cleft.
These swellings (auricular hillocks), three on each side of the
external meatus, later fuse and form the definitive auricle. Because
formation and fusion of the auricular hillocks is complicated,
developmental abnormalities of the auricle are common.
Furthermore, because the hillocks are derived from neural crest

33
cells, external ear defects are often associated with malformations
in other organs derived from neural crest cells, such as the face,
skull, and heart. Initially, the external ears are in the lower neck
region, but growth of the mandible posteriorly and cranially,
moves the external ears to the side of the head at the level of the
eyes.
HEARING7
Hearing is dependent on sound waves that cause vibrations
in the tympanic membrane, which is held tightly like the surface of
a drum by the tensor tympani muscle. If too loud a sound, causing
potentially damaging vibrations, occurs, the tensor tympani
together with the stapedius muscle stretches the membrane even
tighter to prevent it from vibrating too forcefully. Once the
tympanic membrane vibrates, it causes movement of the ear
ossicles, the malleus, incus, and stapes that serve to amplify the
forcé of the sound wave and to transmit the pressure of the wave to
the cochlea through the oval window.
Amplification results from two factors: (1) The large size
difFerence between the tympanic membrane (55 mm^) and the
oval window (3.2 mm^), where the stapes attaches, results in
greater energy produced by the membrane to be transferred and
amplified at the oval window; (2) because of its shape, the malleus
acts like a lever to increase the force received by the stapes.
Pressure produced by movement of the stapes at the oval window
ereates a fluid wave in the cochlea that is balanced by movement of
the round window. The fluid wave moves small regions of the
basilar membrane and the location of these regions is determined
in part by the amplitude (loudness) and frequency (pitch) of the
wave. Near the oval window, the basilar membrane is attached by
shorter stiffier fibers to the side of the cochlea; farther along the
cochlea, the fibers are longer and more flexible. Based on these

33
fiber characteristics and the frequency of the wave, the wave
reaches a point where it resonates with the fibers and moves the
basilar membrane. This movement is sensed by adjacent hair cells
that send impulses back through nerve fibers of the acoustic
segment of the statoacoustic nerve. High frequencies (high pitch)
are heard near the oval window where fibers connecting the basilar
membrane are shorter and stiffer; lower frequencies are heard
farther up the cochlea where the fibers are longer and more
flexible.

33
c. Phisiology Developmental of Cardiovascular
Cardiovascular system experienced a significant change
after birth.Foramen ovale,ductus arteriosus, and the ductus venosus
closes. umbilical artery and hepatic artery into the ligament.8
The first breath of newborns who do make the lungs to
flow.Decreased pulmonary pressure. Chain and this great event is a
major mechanism that causes the right arterial pressure decreased.
Increased pulmonary blood flow back to the heart and into the
heart of the left, so that the left atrial pressure increases. This
change causes the foramen ovale closes during the first few days of
life, a baby's cry can restore blood flow through the foramen ovale
for a while and resulted in mild cyanosis.8
Baby heart rate average of 140 times per minute at birth,
with variations ranging between 120 until160 times per minute.
when babies sleep frequency different from the frequency when the
baby wakes up. At the age of one week, the baby's heart rate on
average 128 times per minute during sleep and 163 times per
minute. at the age of one month frequency of 138 times per minute
during sleep and 167 times per minute while awake. Sinus
arrhythmia (irregular heart beats) at this age can be perceived as a
physiological phenomenon and as an indication of good heart
function. Systolic blood pressure of newborns is 78 and the
average diastolic blood pressure 42. vary from day to day during
the first month of pregnancy. Systolic blood pressure decreases the
baby frequently (approximately 15 mmHg) during the first hour
after birth. crying and moving normally lead to an increase in
systolic blood pressure. newborn blood volume varies from 80 to
110 ml / kg during the first few days and doubled at the end of the
first year.9
Transition Circulation Neonatal

33
The left picture is circulation blood prenatal (Fetus) , The
right picture is circulation blood postnatal (Neonatus) In the picture
most different each other. The circulatory system of the fetus
different from the adult circulatory system, because the fetus lungs
haven’t develop so that oxygen is taken from the placenta .9
d. Phisiology Developmental of Immune System
The process of the development of the immune system in
humans began during pregnancy. During pregnancy, there is a
natural imbalance in the immune system of our body, in which the
immune asistem more developed is the Th2-directed immunity
than Th1-directed immunity. Th2 cytokines contained on-directed
immunity would suppress cellular immunity in Th1-directed
immunity, so there is no aggression between the components of a
father and mother to the fetus components. If the natural imbalance
is not the case, where Th1-directed immunity is more dominant or
balanced with Th2-directed immunity, it is likely there will be a
miscarriage.10
After birth, the concentration of Th2 began to decrease, and
the more developed immune system is Th1-directed immunity.
Natural imbalance that occurs when in the womb shifts toward the

33
point of balance between Th1 and Th2-directed immunity-directed
immunity. This allows the baby's body in order to be better
prepared to fight pathogens from outside. 10
At the time in the womb, the fetus showed low specific
immune response against food antigens and inhalants. T
lymphocytes appear at 13 weeks gestation. T cell precursors begin.
The activated at 18-22 weeks gestation. Increased maternal IgG
antibodies and transferred to the fetus at 20 weeks gestation and
above.9
The table of the stages of development of the immune system
during pregnancy.10

The age innate immunity humoral immunity cellular immunity Passive


of immunity
The fetus
(week)
5-6 Form macrophages Form T cell
in the liver and precursors in liver
blood
9-10 Commencement Form B cell Form T cell
synthesis precursors in Liver precursors in
complement thymus
12-14 Form macrophages B cell precursors T cells are formed Commencment
in lymph nodes and equipped with CD4 + and CD8 + maternal IgG
APC MHC class 2 IgD, IgG, and IgA in liver and spleen transfer
to fetus

16-17 Macrophages in the B cells are formed T cells are formed


liver already mature amounts great in the blood and
and circulating spleen, blood, and lymphoid tissue,
neutrophils bone marrow preparation

33
throughout the body back receptors
Macrophages in the T cells
liver

20-30 B cells begin Enhancement Enhancement


Secreting antibody Gradually T-cell gradually IgG
lymphocytes transport
produce
lymphokines

At birth, the baby has a naive immune system that require


exposure to foreign antigens in order to develop normally.
Immunity acquired from the mother can not provide a protective
effect against all infections and only lasted a few moments. This
concept is used in vaccination.9
In term infants born to mothers with good conditions,
specific antibodies can be generally persist up to 18 months. In
preterm infants, the development of the immune system is waiting
for the maturation of the immune system, can not be accelerated.
Therefore, the immune response in preterm infants in contrast to
term infants, depending on the gestational age at the time the baby
is born.10

6. Example Growth and Development Disorders1


 Psychological Disorders
a. Vegetative disorders
1. Disruption of mastication
2. Pica
3. Eneuresis
4. Enkopresis
5. Sleep disturbance

33
b. Habit disorders
c. Anxiety disorders
d. Mood Disorders
1. Major Depression
2. Interference Distimik
3. Bipolar Disorders
e. Suicide and attempted suicide
f. Disorderly conduct disorder
g. Attention deficit hyperactivity disorder
h. Sexual behavior and its variations
1. Disruption and gender identity
2. Homosexuality
i. Psychosisin childhood
1. Infantile Autism
2. Pervasive developmental Disorders
3. Psychosis start-slow
4. Personality disorder threshold
j. Neuro developmental dysfunction
 Social Issues
 Nutrition Disorders
 Disorders of body fluids
 Acute Pain
 Genetic
 Metabolic Diseases
 Infection

7. The growth and development neurology of the fetus


Growth and brain development begins with the formation of
neural plate (neural plate), the embryo is about the 16th day which is then
rolled up to form the neural tube (neural tube) on day 22. On the 5th week
began to look forerunner of big brains at the end of the neural tube.

33
Further formed brain stem, cerebellum and other parts. Brain development
requires a series of complex developmental processes comprising: forming
tube neural, then the neurons (nerve cells) proliferate in the region are
different, the migration of neurons from the formation to a permanent
place, followed by aggregation of cells that form parts of the brain, then
neurons immature differentiated, and formed relationships between
neurons (synapses) , the next stage occurs in cell death and selective
elimination, enhanced myelination (myelin formation).1
8. Mental Retardation11
Mental retardation (MR) is a genetic disorder mainfested in
significantly below average overall intellectual functioning and deficits in
adaptive behaviour. Mental retardation is a particular state of functioning
that begins in childhood and is characterized by decreased intelligence and
adaptive skills and also is the mostcommon developmental disorder.
Causes Of Mental Retardation-Etiology
 Genetics conditions
A number of single-gene disorders result in mental
retardation.Many of these are associated with atypical or
dysmorphic physical characteristics. Such conditions include
fragile X syndrome, neurofibromatosis, tuberous sclerosis,
Noonan's syndrome and Cornelia de Lange's syndrome.
 Prenatal problems
Mental disability can result when the fetus does not
develope inside the mother properly.
Moreover, prenatal causes include congenital infections
such as cytomegalovirus, toxoplasmosis,herpes,syphilis,rubella
and human immunodeficiency virus; prolonged maternal fever
in the first trimester; exposure to anticonvulsants or alcohol;
and untreated maternal phenylketonuria (PKU).
 Perinatal problems

33
Perinatal causes involve late pregnancy (complications
of pregnancy, diseases in mother such us heart and kidney
disease and diabetes and placental dysfuction), during delivery
(labour) (severe prematurity, very low birth weight, birth
asphyxia, difficult and complicated delivery and birth trauma),
neonatal (first 4 weeks of life) (septicaemia, severe jaundice,
hypoglycemia).

Teratogen Congenital Malformations


Infection agent
Rubella Virus Cataracts, Glaucoma, Heart defects,
Deafness , Tooth disorder
Cytomegalovirus Microcephaly, Blindness, Mental
retardation , Fetal death

Herpes simplex Virus Microphthalmia, Microcephaly,


Retinal dysplasia
Varicella Virus Hypoplastic extremities,
Mental retardation , Atrophy
HIV Microcephaly , Growth retardation
Toxoplasma Hydrocephalus ,Cerebral
calcification microphthalmia
Syphilis Mental retardation , Deafness

Physical agents

X-Ray Microcephaly , Spina bifida ,


The sky - the sky cleft palate,
Limb defects

33
Hypertermia Anencephaly , Spina bifida , Mental
retardation , Facial deformities,
Heart defects, Omphalocele,
Limb defects

Chemical material

Talidomid Limb defects , Heart melformasi


Aminopterin Anencephaly , Hydrocephalus, Lips
and sky – cleft
Difenilhidentoin Fetal hydantoin syndrome,Facial
(feniton) deformities , Mental retardation
Valproate Acid Neural tube defects, Cardiac
anomaly / craniofacial / limb
Trimetadion Sky - cleft palate,Heart defects,
Urogenital abnormalities and bone
Litium Cardiac malformations
Amfetamin Lips and sky - cleft palate, Heart
Defects
Warfarin Condrodisplasia, Microcephaly
Inhibitor ACE Growth retardation, Death fetus

Cocaine Growth retardation, Microcephaly,


Abnormal behavior, Gastroschisis.
Alcohol Fetal alcohol syndrome, Short
palpebral fissures, Maxillary
hypoplasia, Heart defects, Mental
retardation.
Isotretinon (vit A) Embryopathy vitamin A, Small ears
and Abnormal shape, Hypoplasia of
mandibular, Sky cleft palate, Heart

33
defects
Solvents industry Low birth weight,
Craniofacial defects and Neural tube
Mercury organic Neurological symptoms similar to
those caused by cerebral palsy.
Lead Growth retardation,
Neurological disorders
Hormon
Androgenic Masculinization of female genitalia,
substance(etisteron, Fused labia, Clitoris hypertrophy.
norethisterone)
Dietilstilbestrol Malformations of the uterus, Uterine
(DES) tubes, and upper vagina, Vaginal
cancer : testicular malformation.
Diabetes from mother Various malformations : the most
common cardiac and neural tube
defects, Heart defects, Omphalocele.

 Postnatal problems (in infancy and childhood)


Postnatal problems include infancy and childhood.
It is involved brain infections such as tuberculosis, Japanese
encephalitis, bacterial meningitis. As well as head injury,
chronic lead exposure, severe and prolonged malnutrition and
gross understimulation.

33
9. Definition of teratogen
Teratogen is an agent that exposes the mother during pregnancy
that can lead to birth defects. The causes include radiation, infection, drugs
and chemicals.4
10. Teratogen factors 12
Teratogens work through pathways or mechanism specific to the
cells and growing network to trigger abnormal embryogenesis or
pathogenesis . This mechanism may involve inhibitors of the biochemical
or molecular specified ; pathogenesis may involve cell death , reduction in
cell proliferation, phenomena other cells. Which in the process of
determining how much the capacity of an agent to cause birth defects ,
there are several factors, such as :
 Susceptibility to teratogenesis dependent on the genotype of the
conceptus and the way it interacts with the genetic composition of
the environment.
 Vulnerability to teratogens vary according to the stage of
development when exposure . Especially at week - 3-8 / period of
embryogenesis . The dose and duration of exposure to the fetus
teratogen.

11. Intrauterine Growth Restriciton 13


Intrauterine growth restriction is a problem faced by obstetrical
care providers on a daily basis. Neonatal mortality in both term and pre-
term neonates is signifcantly increased in those diagnosed antenatally with
IUGR. Despite the importance of the topic, there is a paucity of level I
evidence. The purpose of this guideline is to provide summary statements
and recommendations and to establisha framework for screening,
diagnosis, and management of pregnancies affected with IUGR. A
previously published review (Lausman et al., 2012) provides further
background.

33
IUGR is present when fetal growth stops and, over time, declines
to less than the 5th percentile of growth for gestational age or when
growth proceeds slowly, but absolute size remains less than the 5th
percentile. Growth restriction may result from fetal conditions that reduce
the innate growth potential, such as fetal rubella infection, primordial
dwarfing syndromes, chromosomal abnormalities, and congenital
malformation syndromes. Reduced fetal production of insulin and insulin-
like growth factor I is associated with fetal growth restriction. Placental
causes of IUGR include villitis (congenital infections), placental tumors,
chronic abruptio placentae, twin-to-twin transfusion syndrome, and
placental insufficiency. Maternal causes include severe peripheral vascular
diseases that reduce uterine blood flow (chronic hypertension, diabetic
vasculopathy, and preeclampsia/eclampsia), reduced nutritional intake,
alcohol or drug abuse, cigarette smoking, and uterine constraint (noted
predominantly in mothers of small stature with a low prepregnancy
weight) and reduced weight gain during pregnancy. The outcome of IUGR
depends on the cause of the reduced fetal growth and the associated
complications after birth.
IUGR is a problem associated with signifcant perinatal morbidity
and mortality. Level 1 evidence to direct clinicians in practice does exist,
but is limited to a few high quality trials. Several demographic factors,
including advanced maternal age, assisted conception technologies,and
pregnancy with maternal comorbidities, interact to steadily increase the
risk of IUGR and stillbirth in the third trimester. More effective use of
current evidence may reduce this risk, but further studies, especially to
evaluate the role of systematic screening of placental function in the
second trimester, are needed to improve the perinatal prognosis of IUGR
due to placental insuffciency. Since IUGR has many additional causes,
when it is suspected, a detailed fetal anatomical ultrasound examination
should be performed including further testing when fetal abnormalities are

33
suspected, soft markers are seen, or there is no apparent supportive
evidence of underlying placental insuffciency.
In uncomplicated IUGR attributed to placental insuffciency, no
pharmacological interventions are of proven beneft, although the
accumulated data from several trials and meta-analyses of low-dose
aspirin demonstrate some preventive beneft. By contrast, no evidence
currently exists to support the preventive use of the parenteral
anticoagulant drug heparin for either the prevention or treatment of IUGR.
After 36 weeks of gestation, IUGR due to suspected placental insuffciency
can be managed equally effectively by early delivery or delayed delivery
with increased fetal surveillance.Further research is needed to defne
optimum management of early-onset IUGR. Following delivery,
pathological examination of the placenta may provide key insights into the
underlying cause and form the basis of an effective postpartum counselling
visit to discuss that cause. Since the events leading up to and following
delivery of an infant with severe IUGR may trigger signifcant emotional
stress, a review of mental health status and family circumstances at this
visit is prudent.
12. TORCH
TORCH [Toxoplasma gondii, Rubella virus, Cytomegalovirus
(CMV), Herpes simplex virus (HSV)] and others agents like Chlamydia
trachomatis, Treponema pallidum, Neisseria gonorrhoeae, HIV, etc.
These pathogens usually cause only asymptomatic or mild infection in
mother, but can cause much more serious consequences in fetus.14
13. Five basic of vaccine during pregnancy 15
There are three kinds of vaccinations are recommended during
pregnancy is safe, is not recommended during pregnancy and specific
recommendations .Vaksinasi are not recommended because it is derived
from an attenuated live microorganisms. These microorganisms can grow
and cause disease in the host. Hence, contraindications to BCG
vaccination, MMR, Varicella in pregnant women. Recommended

33
vaccinations safe namely TT, Diftheri, influenza, rabies and meningitis.
Influenza vaccination is usually given in a country like the United States
and Europe that have 4 seasons. Influenza season usually occurs in
October-December, so that the month-on-month increase demand for
vaccination and pandemic influenza. Indonesia is a tropical country so
there is no influenza season. Specifically recommended vaccinations are
usually used to endemic areas or pregnant women who travel to where the
disease is endemic or high-risk jobs have to be infected with the disease.
In consideration of the risk of the disease is more dangerous than the side
effects of the vaccination is recommended in particular. Vaccine Tetanus
Toxoid (TT) in Indonesia advisable given during antenatal care because of
the incidence of neonatal tetanus in Indonesia is very high.
1. Tetanus Toxoid (TT)
Tetanus vaccine is effective for the prevention of tetanus as
a dangerous disease. Most deaths are caused by neonatal tetanus
are in countries that birth in a health facility and TT is low, such as
India and Nigeria. Neonatorum Tetanus is an acute illness
characterized not have the ability to suck, followed by neck
stiffness and muscle spasms. The disease is caused by clostridium
tetani entering through the umbilical cord. Most (90%) of cases of
neonatal tetanus develops during the first 3-14 days of birth,
especially 6-8 days, the mortality rate is very high because of this
case.
2. Diphtheria
Diphtheria is an infection of the nose, pharynx, larynx, or
infection of the mucous membranes that may cause neuritis,
myocarditis, thrombocytopenia and ascending paralysis. Diptheria
vaccine is recommended for pregnant women because there is no
scientific evidence showing that the teratogenic diphtheria vaccine.
3. Influenza

33
Advantages of this vaccine that protects against the
increased risk of influenza in pregnancy. Some research shows
antibody response to influenza vaccine is similar in pregnant and
nonpregnant women. The antibody response was measured in 15
pregnant women 4-6 weeks, then followed after vaccination in the
second and third trimesters titer results are the same as in non-
pregnant women were vaccinated.
4. Rabies
Not identified an association between vaccination with
rabies fetal abnormality. Consideration of potential risks for both
mother and fetus of untreated rabies. As a guideline should be done
prophylaxis in pregnant and nonpregnant women.
5. Meningitis
Research in Gambia with a control study in which the
vaccination is given in the last trimester of pregnancy. All women
have a good response to the immunization and antibody increased
during labor. Maternal immunization may provide protection to
infants from meningococcal disease only during the first few
months of birth.15

33
CHAPTER III
CONCLUSION

The baby was born with congenital rubella syndrome , because the mother
is infected with Rubella virus in trimester period of pregnancy.

33
REFERENCES
1. Kliegman R.M., Marcdante K.J., and Behrman R.E.2015. Nelson
Essentials of Pediatric. 5th ed. Philadelphia: Elsevier Saunders.
2. Jawetz, Melnick, & Adelberg's.2007. Medical Microbiology, 24th
Edition.Unites States of America : The McGraw-Hill Companies.
3. Mason WH. Rubella. In Kliegman RM, Berhamn RE, jenson HB,
Stanton BF, eds. Nelson Textbook of Pediatrics. 18th ed. Philadelphia,
Pa: Saunders Elsevier;2007: chap 244.
4. Nelson, Woldo E. 2015. Ilmu Kesehatan Anak, Edisi 20 Vol.1. Editor
Bahasa Indonesia A. Jamik Wahab. Jakarta: EGC.
5. Arsa, Mudi.2010.Symptoms of Congenital Rubella (congenital) Based
Inspection And Rna Virus Serology. Faculty of Medicine Airlangga
University; Surabaya.
6. Soedarmo, Sumarmo S.Poorwo,dkk.2012. Buku Ajar Infeksi &
Pediatri Tropis 2th ed. Jakarta ; Ikatan Dokter Anak Indonesia.
7. Sadler,T.W.2015. Langmans Medical Embryology 13th edition.China;
Wolters Kluwer Health.
8. Muttaqin, Arif.2010. Nursing care clients with disorders of the
cardiovascular system. Jakarta. Publisher: Salemba Medika.
9. Evans, R. J., Evans, M. K., Brown, Y. M. R., & Orshan, S. A. (2010).
Canadian Maternity, Newborn, & Women’s Health Nursing (1st Ed.).
Philadelphia, PA: Lippincott Williams & Wilkins.
10. Dr.Nia Kurniati,Sp.A (K).2014. Immunology Pattern in Infant Born
with Small for Gestational Age. Indonesia : Nestle Nutrition Institute.
11. Armatas, V. 2009. Mental retardation: definitions, etiology,
epidemiology and diagnosis. Journal of Sport and Health Research.
1(2):112-122.
12. Sadler TW. Langman’s Medical Embriology. 12th ed. Philadelphia:
Lippincott Williams & Wilkins; 2012.

33
13. Ayala DE, Ucieda R, Hermida RC. Chronotherapy with Low-Dose
Aspirin For Prevention of Complications in Pregnancy. Chronobiol Int
2013;30:260-79.
14.Seroprevalence of TORCH Infections and Adverse Reproductive
Outcome in Current Pregnancy with Bad Obstetric History. 2013;62.
14. Frierson J: The yellow fever vaccine: a history. Yale journal of biology
and medicine 2010; 83: 77-85.

33
33