DISCUSSION RESULT REPORT

GROWTH AND DEVELOPMENT MODULE

SECOND CASE

3rd Discussion Group :

Melvy Purwanti

I1011131038

Tri Sandra

I1011141001

Muhammad Deni Kurniawan

I1011141010

Adinda Gupita

I1011141013

Vini Apriyanti

I1011141022

Teresa Asali

I1011141044

Mirantika Audina

I1011141045

Kristian Wilson

I1011141047

Maudy Nadya

I1011141064

Anton Lius

I1011141077

MEDICAL EDUCATION STUDY PROGRAM

FACULTY OF MEDICINE
UNIVERSITY OF TANJUNGPURA
PONTIANAK
2015
CHAPTER I
OVERVIEW

1.1.Case
Seven- month old infant was brought to you because she didnt respond to
sound, even loud sound like thunder. She cant roll over and sit unsupported. Her
mother noticed the girl has white colour in the pupil since birth. The girl was
aterm and her birth weight was 2700 grams. You found microcephaly, cataracts,
and persistent ductus arteriosus in the infant. There rubella antibody is positive of
on laboratory finding. You planned to do further hearing testing for the infant.
1.2.Clarification and Definition
1. Microcephaly: A rare neurological condition in which an infant head is
significantly smaller than the head of other children of the same age and
sex.
2. Cataracts: A clouding or loss of transparency of the lens in the eye as a
result of tissue breakdown and protein clumping.
3. Persistent Ductus Arteriosus: One of the most frequently occurring
abnormalities of the great vessels (8/100000 births) especially in
premature infants, either maybe an isolated abnormality or may
accompany other heart defect.
4. Rubella: An acute, usually benign infectious disease caused by viruses of
genus Rubivirus, a togavirus, affecting, most often children and nonimmune young adult.
1.3.Keywords
1. She didnt respond to sound
(thunder)
2. 7 month old infant
3. She cant roll over and sit
unsupported
4. The girl has white colour in

5. Persistent ductus arteriosus

6. Positive Rubella antibody
7. Birth weight was 2700 grams
8. Microcephaly
9. Cataracts
10. Hearing testing

pupil since birth

11.
12. 1.4. Problems Case

13.

Seven month old infant didnt respondto sound even like

thunder, cant roll over, and sit unsupported, has white colour in the pupil
since birth also experience microcephaly, cataracts, persistent ductus
arteriosus with rubella antibody is positive.
14.
15. 1.5. Problems Analyze
16.

Seven-month old infant

Aterm
Birth weight 2700 gr

17.
18.
19.
Physical Examination

Condition

20.

21.Microcephaly

Deafness

22.Cataracts
23.

Lab Examination
Further Examination

Cant roll over

Positive Rubella Antibody
Hearing test

PDA

Sit unsupported

24.
25. 1.6. Hypotheses
26.

Growth and developments defect that occur in that seven-

month old infant is caused by rubella virus.

27.
28. 1.7. Learning Issue
1.
2.
3.
4.
5.
6.

The basic needs for better growth and development

Eye development
Ear development
Immunization
Infants Microcephaly
Infants cataract

7. Heart congenital
8. Milestone score of 0-2 years old infants
9. Measurement of childs growth
10. Mechanism of intrauterine infection
11. Transitional circulation of neonate
12. What are the virus that can cause the congenital defect?
13. Rubella Disease
14. Congenital Rubella Syndrome
15. Hearing testing
16. Red flags
29.
30.
31.
32.
33.
34. CHAPTER II
35. EXPLANATION
36.
37.
2.1.The Basic Needs for Better Growth and Development
38.

The field of pediatrics is dedicated to optimizing the growth

and development of each child. Pediatricians require knowledge of normal

growth, development, and behavior in order to effectively monitor
childrens progress, identify delays or abnormalities in development,
obtain needed services, and counsel parents and caretakers.
1. Biological Needs
1.1. Nutrition (breastfeed exclusively)
39.
The American Academy of Pediatrics (AAP) and World
Health Organization (WHO) have declared breastfeeding and the
administration of human milk to be the normative practice for infant
feeding and nutrition. Breastfeeding has documented short- and long-term
medical and neurodevelopmental advantages and rare thus the decision to
breastfeed should be considered a public health issue and not only a

lifestyle choice. The AAP and the WHO recommend that infants should be
exclusively breastfed or given breast milk for 6 months. Breastfeeding
should be continued with the introduction of complementary foods for 1
year or longer, as mutually desired by mother and infant. The success of
breastfeeding initiation and continuation depends on multiple factors, such
as education about breastfeeding, hospital breastfeeding practices and
policies, routine and timely follow-up care, and family and societal
support.1
40. 1.2 Immunization
41.
Immunization is the process of inducing immunity against a
specific disease. Immunity can be induced either passively through
administration of antibody-containing preparations or actively by
administering a vaccine or toxoid to stimulate the immune system to
produce a prolonged humoral and/or cellular immune response. As of
2015, infants, children, and adolescents in the United States routinely are
immunized

against

16

diseases:

diphtheria,

tetanus,

pertussis,

poliomyelitis, H. influenzae type b (Hib) disease, hepatitis A, hepatitis B,

measles, mumps, rubella, rotavirus, varicella, pneumococcal disease,
meningococcal disease, influenza, and human papillomavirus (HPV)
infection.1
42. 1.2.1 Passive Immunity
43.
Passive immunity is achieved by administration of preformed
antibodies to induce transient protection against an infectious agent. Products
used include:1
a. Immunoglobulin (Ig) administered intramuscularly (IM)
b. Specific or hyper immune immunoglobulin preparations administered IM
c. Intravenous immunoglobulin (IVIG)
d. Specific or hyper immunoglobulin preparations administered IV
e. Subcutaneous (SC) human immunoglobulin, which has been
f. licensed to treat patients with primary immunodeficiency
g. Antibodies of animal origin
h. Monoclonal antibodies
44. 1.2.2 Active Immunization
45.
Vaccines are defined as whole or parts of microorganisms
administered to prevent an infectious disease. Vaccines can consist of whole

inactivated microorganisms (e.g., polio and hepatitis A), parts of the organism
(e.g., a cellular pertussis, HPV, and hepatitis B), polysaccharide capsules (e.g.,
pneumococcal and meningococcal polysaccharide vaccines), polysaccharide
capsules conjugated to protein carriers (e.g., Hib, pneumococcal, and
meningococcal conjugate vaccines), live attenuated microorganisms (measles,
mumps, rubella, varicella, rotavirus, and live-attenuated influenza vaccines),
and toxoids (tetanus and diphtheria) .1
46. Sources : IDAI.org

47. 1.2.3 Hygiene

48.
1.2.3.1 Hand Hygiene
49.
The most important tool in any infection control program is
good hand hygiene. Although much attention is directed at the type of
cleansing agent employed, the most important aspect of hand washing is
placing the hands under water and using friction with or without soap.
Studies show that a 15 sec scrub removes the majority of transient flora
but does not alter hand permanent flora. A variety of hand gels and rubs
can be used in place of hand washing. Waterless hand hygiene products

increase hand hygiene compliance and save time; these agents are the
preferred agents for routine hand hygiene when hands are not visibly
soiled. These products are effective in killing most microbes but do not
remove dirt or debris. However, they are ineffective against C. difficile
spores, requiring the use of other cleansing products during hospital C.
difficile outbreaks. Hands should be cleaned before and after every patient
encounter. In hospital hand washing compliance studies, physicians are
usually the least-compliant group studied, and compliance programs must
pay special attention to this group of caregivers. Meals, vegetables, fruit,
water, snack are must be hygiene. The danger environment agent must be
avoid from baby in order to keep healthty.1
50. 1.2.4 Sleep
51.
Six behavioral states have been described. Initially, sleep and
wakefulness are evenly distributed throughout the 24 hr. Neurologic maturation

accounts for the consolidation of sleep into blocks of 5 or 6 hour at night, with
brief awake, feeding periods. Learning also occurs; infants whose parents are

consistently more interactive and stimulating during the day learn to

concentrate their sleeping during the night.1
52.
2. Psychosocial & Emotional Needs:
53. 2.1 Family Systems and the Ecologic Model
54.
Contemporary models of child development recognize the critical
importance of influences outside of the motherchild dyad. Fathers play
critical roles, both in their direct relationships with their children and in
supporting mothers. As traditional nuclear families become less dominant, the
influence of other family members (grandparents, foster and adoptive parents,
same-sex partners) becomes increasingly important. Children are increasingly
raised by unrelated caregivers while parents work or while they are in foster
care.

55.

Families function as systems, with internal and external

boundaries, subsystems, roles, and rules for interaction. In families with

rigidly defined parental subsystems, children may be denied any decisionmaking, exacerbating rebelliousness. In families with poorly defined parent
child boundaries, children may be required to take on responsibilities beyond
their years, or may be recruited to play a spousal role.
56.
Family systems theory recognizes that individuals within systems
adopt implicit roles. One child may be the troublemaker, whereas another is
the negotiator and another is quiet. Birth order may have profound effects on
personality development, through its influence on family roles and patterns of
interaction. Families are dynamic. Changes in one persons behavior affect
every other member of the system; roles shift until a new equilibrium is found.
The birth of a new child, attainment of developmental milestones such as
independent walking, the onset of nighttime fears, and the death of a
grandparent are all changes that require renegotiation of roles within the
family and have the potential for healthy adaptation or dysfunction.
57.
The family system, in turn, functions within the larger systems of
extended family, subculture, culture, and society. Bronfenbrenners ecologic
model depicts these relationships as concentric circles, with the parentchild
dyad at the center (with associated risks and protective factors) and the larger
society at the periphery. Changes at any level are reflected in the levels above
and below. The shift from an industrial economy to one based on service and
information is an obvious example of societal change with profound effects on
families and children.1
58.
59.
60. 2.2 Developmental Domains and Theories of Emotion and Cognition
61.
Child development can also be tracked by the childs
developmental progress in particular domains, such as gross motor, fine motor,
social, emotional, language, and cognition. Within each of these categories are
developmental lines or sequences of changes leading up to particular
attainments. Developmental lines in the gross motor domain, leading from

rolling to creeping to independent walking, are obvious. Others, such as the

line leading to the development of conscience, are more subtle. 1
62.
The concept of a developmental line implies that a child passes
through successive stages. Several psychoanalytic theories are based on stages
as qualitatively different epochs in the development of emotion and cognition.
In contrast, behavioral theories rely less on qualitative change and more on the
gradual modification of behavior and accumulation of competence.1
63.
2.2.1 Psychoanalytic Theories
64.
At the core of Freudian theory is the idea of bodycentered (or, broadly, sexual) drives; the emotional health of both the
child and the adult depends on adequate resolution of these conflicts.
Although Freudian ideas have been challenged, they opened the door to
subsequent theories of development.
65.
Erikson recast Freuds stages in terms of the emerging
personality. The childs sense of basic trust develops through the
successful negotiation of infantile needs. As children progress through
these psychosocial stages, different issues become salient. It is predictable
that a toddler will be preoccupied with establishing a sense of autonomy,
whereas a late adolescent may be more focused on establishing meaningful
relationships and an occupational identity. Erikson recognized that these
stages arise in the context of Western European societal expectations; in
other cultures, the salient issues may be quite different.
66.
Eriksons work calls attention to the intrapersonal
challenges facing children at different ages in a way that facilitates
professional intervention. Knowing that the salient issue for school-age

10

children is industry vs inferiority, pediatricians inquire about a childs

experiences of mastery and failure and (if necessary) suggest ways to
ensure adequate successes.
67.
2.2.2 Cognitive Theories
68.
Cognitive development is best understood through the work
of Piaget. A central tenet of Piagets work is that cognition changes in
quality, not just quantity. During the sensorimotor stage, an infants
thinking is tied to immediate sensations and a childs ability to manipulate
objects. The concept of in is embodied in a childs act of putting a block
into a cup. With the arrival of language, the nature of thinking changes
dramatically; symbols increasingly take the place of objects and actions.
Piaget described how children actively construct knowledge for
themselves through the linked processes of assimilation (taking in new
experiences according to existing schemata) and accommodation (creating
new patterns of understanding to adapt to new information). In this way,
children are continually and actively reorganizing cognitive processes
69.
Piagets basic concepts have held up well. Challenges have
included questions about the timing of various stages and the extent to
which context may affect conclusions about cognitive stage. Childrens
understanding of cause and effect may be considerably more advanced in
the context of sibling relationships than in the manipulation and perception
of inanimate objects. In many children, logical thinking appears well
before puberty, the age postulated by Piaget. Of undeniable importance is
Piagets focus on cognition as a subject of empirical study, the universality
of the progression of cognitive stages, and the image of a child as actively
and creatively interpreting the world.
70.
Piagets work is of special importance to pediatricians for 3
reasons: (1) Piagets observations provide insight into many puzzling
behaviors of infancy, such as the common exacerbation of sleep problems
at 9 and 18 months of age. (2) Piagets observations often lend themselves
to quick replication in the office, with little special equipment. (3) Open-

11

ended questioning, based on Piagets work, can provide insights into

childrens understanding of illness and hospitalization.
71.
Based on cognitive development, Kohlberg developed a theory of
moral development in 6 stages, from early childhood through adulthood.
Preschoolers earliest sense of right and wrong is egocentric, motivated by
externally applied controls. In later stages, children perceive equality,
fairness, and reciprocity in their understanding of interpersonal
interactions through perspective-taking. Most youth will reach stage 4,
conventional morality, by mid to late adolescence. The basic theory has
been modified to distinguish morality from social conventions. Whereas
moral thinking considers interpersonal interactions, justice, and human
welfare, social conventions are the agreed-on standards of behavior
particular to a social or cultural group. Within each stage of development,
children are guided by the basic precepts of moral behavior, but also may
take into account local standards, such as dress code, classroom behavior,
and dating expectations. Additional studies have even demonstrated some
protomorality in infants.1
72.
2.2.3 Behavioral Theory
73.
This theoretical perspective distinguishes itself by its lack
of concern with a childs inner experience. Its sole focus is on observable
behaviors and measurable factors that either increase or decrease the
frequency with which these behaviors occur. No stages are implied;
children, adults, and, indeed, animals all respond in the same way. In its
simplest form, the behaviorist orientation asserts that behaviors that are
positively reinforced occur more frequently; behaviors that are negatively
reinforced or ignored occur less frequently. The strengths of this position
are its simplicity, wide applicability, and conduciveness to scientific
verification. A behavioral approach lends itself to interventions for various
common problems, such as temper tantrums, aggressive preschool
behavior, and eating disorders in which behaviors are broken down into
discrete units. In cognitively limited children and children with autism
spectrum disorders, behavioral interventions using applied behavior

12

analysis approaches have demonstrated their ability to teach new, complex

behaviors. Applied behavior analysis has been particularly useful in the
treatment of early-diagnosed autism. However, in cases in which
misbehavior is symptomatic of an underlying emotional, perceptual, or
family problem, an exclusive reliance on behavior therapy risks leaving
the cause untreated. Behavioral approaches can be taught to parents to
apply at home.1
3. Stimulation Needs
74.
Stimulation needs consist of sensory, motoric, cognitive,
communication

language,

socio-emotional,

self-help,

creativity,

cooperation and leadership, spiritual etc. through repetitive experiences

include parents sounds, music, movement, touch, speak, singing, act, play,
brain gym, write, draw. The repetitive experiences stimulates complicity
connection (synapse) between brain cells.2
75.

2.2.Eye development
76.

The eyes begin to develop as a pair of outpocketings that

will become the optic vesicles on each side of the forebrain at the end of
the fourth week of development. The optic vesicles contact the surface
ectoderm and induce lens formation. When the optic vesicle begins to
invaginate to form the pigment and neural layers of the retina, the lens
placode invaginates to form the lens vesicle. Through a groove at the
inferior aspect of the optic vesicle, the choroid fissure, the hyaloids artery
(later the central artery of the retina) enters the eye. Nerve fibers of the eye
also occupy this groove to reach the optic areas of the brain. The cornea is
formed by (a) a layer of surface ectoderm, (b) the stroma, which is
continuous with the sclera, and (c) an epithelial layer bordering the
anterior chamber PAX6, the master gene for eye development, is expressed
in the single eye fi eld at the neural plate stage. The eye field is separated
into two optic primordia by SHH, which up regulates PAX2 expression in
the optic stalks while down regulating PAX6, restricting this genes
expression to the optic cup and lens. Epithelial mesenchymal interactions

13

between prospective lens ectoderm, optic vesicle, and surrounding

mesenchyme then regulate lens and optic cup differentiation.3
77.
2.3.Ear development
78.

In the adult, the ear forms one anatomic unit serving both

hearing and equilibrium. In the embryo, however, it develops from three

distinctly different 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.
a. Internal Ear
79.

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.

14

80.

Figure 2.3.1 A. An embryo at the end of the fourth week of development

showing the otic and optic vesicles. B. Region of the rhombencephalon

showing the otic placodes in a 22-day embryo1
81.

These thickenings, the otic placodes, invaginate rapidly and form

the otic or auditory vesicles (otocysts).

82.
83.

84.
85.

Figure 2.3.2 AC. Transverse sections through the region of the

rhombencephalon showing formation of the otic vesicles. A. 24 days. B. 27

days. C. 4.5 weeks. Note the statoacoustic ganglia1
86.

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.

15

87.

88.

Figure 2.3.3 A,B. Development of the otocyst showing a dorsal

utricular portion with the endolymphatic duct and a ventral saccular portion.
CE. Cochlear duct at 6, 7, and 8 weeks, respectively. Note formation of the
ductus reuniens and the utriculosaccular duct1
89.
On the development of the scala tympani and scala vestibuli the
cochlear duct is surrounded by a cartilaginous shell. During the 10th week,
large vacuoles appear in the cartilaginous shell. The cochlear duct (scala
media) is separated from the scala tympani and the scala vestibuli by the
basilar and vestibular membranes, respectively. Note the auditory nerve fi
bers and the spiral (cochlear) ganglion.

16

90.

91.

Figure 2.3.4 Development of the semicircular canals. A. 5 weeks. B. 6

weeks. C. 8 weeks. DF. Apposition, fusion, and disappearance, respectively,

of the central portions of the walls of the semicircular outpocketings. Note the
ampullae in the semicircular canals1
92.
Together, these epithelial structures form the membranous labyrinth.
b. Middle Ear
93.
The tympanic cavity, which originates in the endoderm, is derived
from the fi rst 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.
94.

17

95.

96.

Figure 2.3.5 A. Transverse section of a 7-week embryo in the

region of the rhombencephalon, showing the tubotympanic recess, the first

pharyngeal

cleft,

and

mesenchymal

condensation,

foreshadowing

development of the ossicles. B. Middle ear showing the cartilaginous

precursors of the auditory ossicles. Thin yellow line in mesenchyme indicates
future expansion of the primitive tympanic cavity. Note the meatal plug
extending from the primitive auditory meatus to the tympanic cavity1
97.

The malleus and incus are derived from cartilage of the fi rst

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. The
supporting ligaments of the ossicles develop later within these mesenteries.

18

98.

99.

Figure 2.3.6 Ear showing the external auditory meatus, the middle

ear with its ossicles, and the inner ear1

100. 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.
101.

19

102.

Figure 2.3.7 A. Derivatives of the first three pharyngeal arches.

Note the malleus and incus at the dorsal tip of the first arch and the stapes at
that of the second arch. B. Middle ear showing the handle of the malleus in
contact with the eardrum. The stapes will establish contact with the
membrane in the oval window. The wall of the tympanic cavity is lined with
endodermal epithelium
103.

During late fetal life, the tympanic cavity expands dorsally by

vacuolization of 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. Expansion of infl ammations of the middle
ear into the antrum and mastoid air cells is a common complication of middle
ear infections.
c. External Ear
104. The external auditory 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 plate, 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.
105. 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 intermediate 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.

20

106.

Figure 2.3.8 A. Drawing of a 6-week-old embryo showing a lateral

view of the head and six auricular hillocks surrounding the dorsal end of the
first pharyngeal cleft. B. Six-week-old human embryo showing a stage of
external ear development similar to that depicted in A. Note that hillocks 1, 2,
and 3 are part of the mandibular portion of the first pharyngeal arch and that
the ear lies horizontally at the side of the neck. At this stage, the mandible is
small. As the mandible grows anteriorly and posteriorly, the ears, which are
located immediately posterior to the mandible, will be repositioned into their
characteristic location at the side of the head. CE. Fusion and progressive
development of the hillocks into the adult auricle
107.

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 defi nitive auricle . As fusion of
the auricular hillocks is complicated, developmental abnormalities of the
auricle are common. Initially, the external ears are in the lower neck region,
but with development of the mandible, they ascend to the side of the head at
the level of the eyes.3
108.
2.4.Immunization
109. Immunization of children have managed to reduce the impact of
communicable diseases. Active immunization induces immunity by vaccination

21

with either vaccine or toxoid (inactivated toxin). While passive immunization

include transplacental transfer of antibodies from mother to baby, and the
provision of antibodies, both in the form of immunoglobulin or monoclonal
antibodies.
110.

Vaccines can be derived from a virus which is attenuated

(polio vaccine, measles, mumps, glubela, varicella and influenza nasal), a

virus that switched off or inactivated (polio vaccine injections, hepatitis A
and influenza intramuscular), recombinant products (hepatitis B, human
papillomavirus) , reassortant viruses (rotavirus) or immunogenic
components of bacteria (pertussis, Haemophilus influenza type B and
streptococcus pneumoniae), and the group toxoid (diphtheria, tetanus).
Many purified polysaccharides are T-independent antigens that stimulate
proliferation of B cells without involving lymphocytes T CD4 but less
immunoglobulin in children less than 2 years.
111. Most vaccines are given by intramuscular or subcutaneous
injection. The recommended location is part of the anterolateral thigh in
infants and the deltoid in children and adults. Multiple vaccinations can be
administered simultaneously at separate anatomical locations (extremity
different or separate locations more than 1 inch), this does not diminish the
immune response. Vaccines against measles, mumps and rubella (MMR measles, mump, and rubella) and varicella vaccine (chickenpox) can be
administered simultaneously or separately at an interval of more than 30
days.4
112.

Hepatitis

B vaccine
114.
Polio
Vaccine

113.

Given within 12 hours after birth.

115.

Given at the first visit. Babies born in RB / RS

OPV vaccine is given when the baby is discharged in order

to avoid transmission of the vaccine virus to infants others.
Next to polio 1, polio-2-3 can be administered polio

116.

BCG

Vaccine

vaccine OPV or IPV

117.
Optimal given at age 2-3 months. If the BCG
vaccine will be given after the age of 3 months, needs to be

22

done tuberculin test, if the pre-BCG tuberculin test is not

possible, BCG can be given but must be observed within 7
days. If there is a local reaction quickly injected
(accelerated local reaction) need further evaluation
118.

DTP

vaccine
120.

Measles

vaccine
122.
Pneumoc
occal vaccine
124.

Rotaviru

s vaccine

(diagnostic TB)
119.
Given at age 6 weeks. DTwP or can be given in
combination with DTaP or Hepatitis B or Hib. Repeat DTP
at the age of 18 months and 5 months.
121.
Measles vaccine given at the age of 9 months, the
booster vaccine is given at age 5-7 years.
123.
Can be given to the age of 2, 4, 6, 12-15 months. At
the age of 7-12 months are given two times at intervals of 2
months.
125.
Monovalent (Rotarix) given 2 times, pentavalent
rotavirus vaccine (RotaTeq) given 3 times. I monovalent
rotavirus vaccine doses given 6-14 weeks of age, the 2nd
dose given at intervals of at least 4 weeks. Instead finished
monovalent rotavirus vaccine administered before age 16
weeks and not beyond the age of 24 weeks. Pentavalent
rotavirus vaccine: 1 dose given 6-12 weeks of age, dosing
interval of the 2nd and 3rd weeks 4-10, the dose given on

126.

Varisela

vaccine

the 3rd age <32 weeks (minimum interval of 4 weeks).

127.
Can be administered after age 12 months, the best
in the age before entering elementary school. When given
at age> 12 years, need two doses with an interval of at least

128.

MMR

vaccine
130.

Influenza

vaccine
132.

HPV

4 weeks.
129.
Can be administered after the age of 12 months, if
it has not received measles vaccine 9 months of age.
Furthermore repeat MMR given at age 5-7 years.
131.
Given at age> 6 months, every year. For primary
immunization children 6 months - <9 years was given 2
times with a minimum interval of 4 weeks.
133.
Can be given from the age of 10 years. Schedule

23

vaccine

vaccine HPV (Human Papilloma Virus) bivalent 0, 1, 8

months. HPV vaccine is tetravalent 0, 2, 6 months.

134.
135.
2.5.Infants Microcephaly
a. Definition
136.
A situation where the size of the circumference of the head is
smaller than normal for age and gender.
b. Pathogenesis
137.
Benign primary microcephaly associated with genetic factors.
These include genetic microcephaly due to familial and chromosome aberration.
Microcephaly due to the closure of the sutures (craniosynostosis). This type of
microcephaly result in an abnormal head shape, but in most cases there is no
obvious cerebral anomalies.
138.
Cerebrum will begin to be seen as a structure that can be recognized at 28
days gestation the embryo, while the anterior end of the neural tube to experience
a globular ekspensi, presensefalon. In the next few ari, prosensefalon splitting into
two lateral expansion which is the origin hemisfrum cerebral and lateral
ventricles. Ventricular wall at this stage is formed by a layer of seed active
neuroblasts divide. Formed neuroblasts migrate from the ventricular wall to
hemisferium primitive surface, accumulate and form the cerebral cortex. The first
entrants to form the bottom layer of the cortex, later entrants pass through these
layers, forming layers above. Differentiation of neuroblasts forming neuron cell
extensions that grew longer and eventually formed axons with ventricular lumen
through cell extensions that grew longer and eventually formed axons alba
subcortical substance. Axons crossing from 1 hemisferium to hemisferium other
to form the corpus callosum, fully formed, in the 5th. At this time the surface was
akorteks began to show progressive identity formed during the last trimester, so
that at term, cycles and major gyrus has been demarcated.1
139.
Brain term infants have the entire complement of adult neurons,
but weighs only about a third of the adult brain. Postnatal weight gain is due to the
subcortical white matter myelination, the full development of neural processes,
both dendrites and axons as well as an increase in glia cell.

24

140.

In general the effect of abnormal before the 6th month of

pregnancy tends to affect the growth of macroscopic structure of the brain and
reduce the total number of neurons. Effect of pathological changes in the perinatal
period tend to be mild, such as delays myelination and reduced the formation of
dendrites. The loss of the substance of the brain due to destructive lesions can
occur at the end of fetal life and early infancy, either separately or with other
developmental disabilities. 1
141.
Primary autosomal recessive microcephaly (MCPH) or Autosomal
Recessive Microcephaly Primer is a congenital disorder characterized by mental
retardation and brain size small without additional severe brain malformations.
Several genes underlying primary microcephaly have been identified. Although
the proteins encoded have diverse functions, previous studies have shown that
there is interference with the process of mitotic division of cortical structures
during embryonic development. During the early stages of cortical development,
progenitor cells that have the ability symmetrically cleavage is essential for cells
to produce sufficient quantities and jointly serve as the core of an ongoing process
of neurogenesis. Proliferation and differentiation processes is particularly the case
in the ventricles and subventrikular zone lining the brain cavity. Asymmetric
neural progenitor cell portion produce stem cells and children with different
results. Disruption from the symmetrical division can cause the depletion of core
neural progenitor cells, further decline in the rate of proliferation and neuronal
levels can reduce cell production. The end result is a brain smaller than usual and
microcephaly. Severe brain malformations are usually not found in MCPH.
142.
Microcephaly secondary to cerebral atrophy. Secondary
microcephaly can be caused by intrauterine infections such as cytomegalic
inclusion disease, rubella, syphilis, toxoplasmosis, and herpes simplex; radiation,
systemic hypotension maternal, placental insufficiency; anoxia; maternal systemic
diseases such as diabetes mellitus, chronic renal disease, phenylketonuria; and
perinatal and postnatal disorders such as asphyxia, infections, trauma, chronic
heart defects, as well as disorders of the lungs and kidneys. This type of
microcephaly associated with mental retardation in a range tingkat.17
Development of the nervous system begins with the formation of the neural tube

25

is the induction of dorsal region that occurs in week 3 of gestation. Any

interruption during this period resulted in congenital abnormalities such as
kranyosksis, totalis, etc. The next phase of a proliferation of neurons that occurs
during gestation. Disturbances in this period can cause microcephaly.
143.
Syphilis infects its way through direct contact with lesions. Caused
by the bacterium Treponema malibu through intact mucous membranes / skin
lesions then enter the bloodstream and all organs in the body (one of the brain) to
the fetus. Rubella infects the embryo to first 3 months of pregnancy. Causing
malformations of the eye, the inner ear, heart and teeth
144.
Herpes infects infants born vaginally (mother herpes) that infants be
infected. Cytomegalovirus is an organism that is where and essentially infect most
humans, evidence of fetal infection is found in between 0.5 -2% of all newborns.
After the primary infection is usually asymptomatic, 10% of fetal infection
causing symptomatic at birth and 5-25% leaving squeal. In some countries CMV
infection is 1% obtained in ultra-infection and 10-15% in the prenatal period. The
virus becomes latent and there are periodic reactivation with the release of the
virus even though there are antibodies in the serum. Humoral antibodies are
produced, but the immunity in mediated by cells appears to be the primary
mechanism for the recovery, and the state of impaired immune either occurring
naturally or as a result of drug use would increase the tendency of the incidence of
serious cytomegalovirus infection. It is estimated that the reduction in immune
surveillance mediated by cells, causing the baby fetuses are in a high risk for the
occurrence of squeal to this infection. Meanwhile, Rubeinstein-Taybi Syndrome
occurs because absence of the gene that causes abnormalities in binding proteins
CREB.5
145.

2.6.Infants cataract
146.

A cataract is any opacity of the lens some are clinically

unimportant; others significantly affect visual function. The incidence of

infantile cataracts is approximately 2-13/10,000 live births. An
epidemiologic study of infantile cataracts published in 2003 suggests that
approximately 60% of cataracts are an isolated defect; 22% are part of a

26

syndrome; and the remainder are associated with other unrelated major
birth defects. Cataracts are more common in low birth weight infants.
Infants who weigh at or below 2,500 g have 3-4fold increased odds of
developing infantile cataracts. Some cataracts are associated with other
ocular or systemic diseases.1
147.

Congenital cataract cause the lens to become opaque during intra

uterine life. Although this anomaly is usually geneticallyy determined, many

children born to mothers who had Rubella (German measles) between the fourth
and seventh weeks of pregnancy cataracts.
148.
If the mother is infected after the seventh week of pregnancy, the
lens escape damage, but the child may have hearing loss as a result of cochlea
abnormalities. Because of the MMR vaccine, CRS has been nearly eradicated in
USA.3
149.
2.7.Heart congenital
150.
Atrial Septal Defect (ASD) is a congenital heart abnormality with
an incidence of 6.4/10,000 births and with a 2:1 prevalence in female to male
infants. One of the most significant defects is the ostium secuncum defect,
characterized by a large opening between the left and right atria.
151.
Endocardial cushion of the atrioventricular canal not only divide
this canal into a right and left orifice, but also participate in formation of the
membranous portion of the intervetricular septum and in closure of the ostium
prinum.
152.

Ebstein abnormaly is a condition where the sricuspid valve is

displaced toward the apex of right ventricle.3

153. .
2.8.Milestone score of 0-2 years old infants1
1. BIRTH3 MO
154.

Startles to loud sounds

155.

Makes pleasure sounds

(cooing, gooing)
156.

Quiets or smiles when

spoken to

157.

Cries differently for

different needs

27

158.

Seems to recognize your

159.

Smiles when sees you

voice and quiets if crying

160.

Increases or decreases

sucking behavior in response to

161.

sound
162.

46 MO

163.

Moves eyes in direction

of sounds

164.

Babbling sounds more

speech-like, with many

different sounds, including p, b,
and m

165.

Responds to changes in

tone of your voice

167.

Notices toys that make

sounds

166.

Vocalizes excitement

and displeasure
168.

Makes gurgling sounds

when left alone and when

playing with you

169.

Pays attention to music

171.

7 MO1 YR

172.

Enjoys games such as

peekaboo and pat-a-cake

170.

173.

Babbling has both long

and short groups of sounds,

such as tata upup bibibibi.

174.

Turns and looks in

direction of sounds

175.

Uses speech or

noncrying sounds to get and

keep attention

176.

Listens when spoken to

177.

Imitates different speech

sounds
178.

Recognizes words for

179.

Has 1 or 2 words (bye-

common items, such as cup,

bye, Dada, Mama), although

shoe, and juice

they may not be clear

180.

Begins to respond to

181.

requests (Come here.Want

28

more?)
182.

12 YR

183.

Points

to a few body parts

184.

when asked
185.

Follows simple

Says more words every

month
186.

Uses some 12 word

commands and understands

questions (Where kitty? Go

simple questions (Roll the ball.

bye-bye? your shoe?)

Kiss the baby.)

187.

Listens to simple stories,

188.

songs, and rhymes

Puts 2 words together

(more cookie, no juice, mommy

book)

189.

Points to pictures in a

190.

book when named

Uses many different

consonant sounds at the

beginning of words

191.
192.
2.9.Measurement of childs growth
193.
1.

Normal growth of child, include:

Average birth weight for most full-term infants is between 2.5 and

4.5 kg with a gestation of between 37 and 42 weeks duration.

2.
3.
194.

Weight loss of ten percent in the first week of life is normal.

Birth weight is usually regained by 10-14 days.6
Table 2.9. Average weight gain from birth to five years of age
195.
Child's age
0-3 months
3-6 months
6-12 months
Between birth & 1 year
1-2 years

196.

Average weight gain

150-200 g / week
100-150 g / week
70-90 g / week
Birth weight doubles (or more)
2-3 kg / year (40-50 g / week)

197.
198.
199.
200.
201.
202.
203.
204.
205.
206.
207.
208.
2.10. Mechanism of intrauterine infection
209.
Intrauterine infection is a result of clinical or subclinical maternal
infection with a variety of agents (cytomegalovirus [CMV], Treponema pallidum,

29

Toxoplasma gondii, rubella virus, varicella virus, parvovirus B19) and

hematogenous transplacental transmission to the fetus. Transplacental infection
may occur at any time during gestation, and signs and symptoms may be present
at birth or may be delayed for months or years. Infection may result in early
spontaneous abortion, congenital malformation, intrauterine growth restriction,
premature birth, still birth, acute or delayed disease in the neonatal period, or
asymptomatic persistent infection with squeal later in life. In some cases, no
apparent effects are seen in the newborn infant.
210.
The timing of infection during gestation affects the outcome. Firsttrimester infection may alter embryogenesis, with resulting congenital
malformations (congenital rubella). Third-trimester infection often results in
active infection at the time of delivery (toxoplasmosis, syphilis). Infections that
occur late in gestation may lead to a delay in clinical manifestations until
sometime after birth (syphilis).
211.
Maternal infection is a necessary prerequisite for transplacental
infection. For some etiologic agents (rubella), maternal immunity is effective and
antibody is protective for the fetus. For other agents (CMV), maternal antibody
may ameliorate the outcome of infection or may have no effect. Even without
maternal antibody, transplacental transmission of infection to a fetus is variable
because the placenta may function as an effective barrier.1
212.
2.11. Transitional circulation of neonate
213. Changes in the vascular system at birth are caused by cessation of
placental blood flow and the beginning of respiration. Since the ductus arteriosus
loses by muscular contraction of its wall, the amount of blood flowing through the
lung vessels increases rapidly. This, in turn, raises pressure in the left atrium.
Simultaneously, pressure in the right atrium decreases as a result of interruption of
placental blood flow. The septum primum is then opposed to the septum
secundum, and functionally, the oval foramen closes. To summarize, the following
changes occur in the vascular system after birth.
214. Closure of the umbilical arteries, accomplished by contraction of
the smooth musculature in their walls, is probably caused by thermal and
mechanical stimuli and a change in oxygen tension. Functionally, the arteries

30

close a few minutes after birth, although the actual obliteration of the lumen by
fibrous proliferation may take 2 to 3 months. Distal parts of the umbilical arteries
form the medial umbilical ligaments, and the proximal portions remain open as
the superior vesical arteries.
215. Closure of the umbilical vein and ductus venosus occurs shortly
after that of the umbilical arteries. Hence, blood from the placenta may after
obliteration, the umbilical vein forms the ligamentum teres hepatis in the lower
margin of the falciform ligament. The ductus venosus, which courses from the
ligamentum teres to the inferior vena cava, is also obliterated and forms the
ligamentum venosum.
216. Closure of the ductus arteriosus by contraction of its muscular
wall occurs almost immediately after birth; it is mediated by bradykinin,a
substance released from the lungs during initial infl ation. Complete anatomical
obliteration by proliferation of the intima is thought to take 1 to 3 months. In the
adult, the obliterated ductus arteriosus forms the ligamentum arteriosum.
217.
Closure of the oval foramen is caused by an increased pressure in
the left atrium, combined with a decrease in pressure on the right side. The first
breath presses the septum primum against the septum secundum. During the fi rst
days of life, however, this closure is reversible. Crying by the baby creates a shunt
from right to left, which accounts for cyanotic periods in the newborn. Constant
apposition gradually leads to fusion of the two septa in about 1 year. In 20% of
individuals, however, perfect anatomical closure may never be obtained (probe
patent foramen ovale).3

31

218.
219.
220.
2.12. What are the virus that can cause the congenital defect?
2.12.1 Toxoplasmosis (Toxoplasma gondii)
a. Congenital Toxoplasmosis
221.

Transmission to the fetus usually follows acquisition of primary

infection by an immunologically normal pregnant woman during gestation.

Congenital transmission from mothers infected before pregnancy is extremely
rare except for immunocompromised women who are chronically infected. The
incidence of congenital infection in the United States ranges from 1 in 1,000 to
1 in 8,000 live births. The incidence of infection among pregnant women
depends on the general risk for infection in the specific locale and the
proportion of the population that has not been infected previously.
222.
When a mother acquires infection during gestation, organisms may
disseminate hematogenously to the placenta. Infection may be transmitted to
the fetus transplacentally or during vaginal delivery. Of untreated maternal
infections acquired in the 1st trimester, approximately 17% of fetuses are
infected, usually with severe disease. Of untreated maternal infection acquired
in the 3rd trimester, approximately 65% of fetuses are infected, usually with

32

disease that is more mild or in apparent at birth. These different rates of

transmission and outcomes are most likely related to placental blood flow,
virulence, inoculum of T. gondii, and immunologic capacity of the mother and
fetus to limit parasitemia.
223.
Examination of the placenta of infected newborns may reveal
chronic inflammation and cysts. Tachyzoites can be seen with Wright or
Giemsa stains but are best demonstrated with immunoperoxidase technique.
Tissue cysts stain well with periodic acidSchiff and silver stains as well as
with the immunoperoxidase technique. Gross or microscopic areas of necrosis
may be present in many tissues, especially the CNS, choroid and retina, heart,
lungs, skeletal muscle, liver, and spleen. Areas of calcification occur in the
brain. Almost all congenitally infected individuals who are not treated manifest
signs or symptoms of infection, such as chorioretinitis, by adolescence. Some
severely involved infants with congenital infection appear to have Toxoplasma
antigenspecific cell-mediated anergy, which may be important in the
pathogenesis of disease.1
2.12.2 Cytomegalovirus
a. Congenital Infection
224.

Congenital infection with CMV can present with symptomatic

infections in approximately 10% of infected newborns, whereas 90% of

infected infants will have no clinical manifestations of infection in the newborn
period. Severe multiorgan disease is infrequent and occurs in less than 5% of
infants with congenital CMV infections. The clinical findings of infants with
symptomatic congenital CMV infections can include hepatosplenomegaly,
petechial rashes, jaundice, and in some cases microcephaly. These findings
were utilized for natural history studies to classify infants as having
symptomatic or asymptomatic infections; however, several authors have
included intrauterine growth restriction as a finding of symptomatic congenital
CMV infection. Laboratory findings include direct hyperbilirubinemia,
elevation of hepatic transaminases, thrombocytopenia, anemia, and abnormal
findings on cranial ultrasonography. If cerebrospinal fluid is obtained, there can
be evidence of encephalitis with elevation of mononuclear cell number and in

33

some cases, elevation of cerebrospinal fluid protein. A small number of

symptomatically infected infants (<10%) will be found to have chorioretinitis.
Finally, because hearing loss is the most common long-term sequela associated
with congenital CMV infection, the failure of an infant to pass a newborn
hearing screening exam should raise the possibility of congenital CMV
infection. Hearing loss in the older infant and young child should also alert the
clinician to the possibility of congenital CMV infection, as approximately 50%
of infants with hearing loss associated with congenital CMV infection will pass
an initial hearing screening exam but develop hearing loss in later infancy and
early childhood.
225.
An organized plan for follow-up is an important aspect in the
clinical management of infants with congenital CMV infection. Because
permanent sequelae are limited to disorders of the nervous system, long-term
follow-up should include appropriate assessment of development and
neuromuscular function in infected infants, with referral to specialized care if
necessary. Hearing loss will develop in approximately 11% of infected infants,
and in some infants hearing loss will progress during infancy. Thus, audiologic
testing and follow-up are mandatory in these patients. Other sequelae such as
vision loss are infrequent, but vision testing and comprehensive eye
examinations should be included in the care plan.1
b. Perinatal Infection
226.

Perinatal infections can be acquired

during birth or following ingestion of CMV-containing breast milk. In almost

all cases, perinatal infections are not associated with any clinical
manifestations of infection and, perhaps more importantly, have not been
associated with any long-term sequelae. In rare cases, such as is seen in breast
milk transmission of CMV to extremely premature infants or infants born to
nonimmune women, perinatal infection can result in severe, disseminated
infections associated with end-organ disease and death. These more severe
infections are thought to develop in infants who lack transplacentally acquired

34

antiviral antibodies either secondary to extreme prematurity or being the

product of a mother lacking anti-CMV antibodies.1
2.12.3 Herpes Simplex Virus
a. Perinatal Infections
227.

HSV infection may be acquired in utero, during the birth process,

or during the neonatal period. Intrauterine and postpartum infections are well
described but occur infrequently. Postpartum transmission may be from the
mother or another adult with a nongenital (typically HSV-1) infection such as
herpes labialis. Most cases of neonatal herpes result from maternal infection
and transmission, usually during passage through an infected birth canal of a
mother with asymptomatic genital herpes. Transmission is well documented in
infants delivered by cesarean section. Fewer than 30% of mothers of an infant
with neonatal herpes have a history of genital herpes. The risk for infection is
higher in infants born to mothers with primary genital infection (>30%) than
with recurrent genital infection (<2%). Use of scalp electrodes may also
increase risk. There also have been rare cases of neonatal herpes associated
with Jewish ritual circumcisions, but only with ritual oral contact with the
circumcision site.
228.
Neonatal HSV infection is thought to never be asymptomatic. Its
clinical presentation reflects timing of infection, portal of entry, and extent of
spread. Infants with intrauterine infection typically have skin vesicles or
scarring, eye findings including chorioretinitis and keratoconjunctivitis, and
microcephaly or hydranencephaly that are present at delivery. Few infants
survive without therapy, and those who do generally have severe sequelae.
Infants infected during delivery or the postpartum period present with 1 of the
following 3 patterns of disease: (1) disease localized to the skin, eyes, or
mouth; (2) encephalitis with or without skin, eye, and mouth disease; and (3)
disseminated infection involving multiple organs, including the brain, lungs,
liver, heart, adrenals, and skin.
229.
Infants with skin, eye, and mouth disease generally present at 511 days of life and typically demonstrate a few small vesicles, particularly on
the presenting part or at sites of trauma such as sites of scalp electrode

35

placement. If untreated, skin, eye, and mouth disease in infants may progress to
encephalitis or disseminated disease.
230.
Infants with encephalitis typically present at 8-17 days of life with
clinical findings suggestive of bacterial meningitis, including irritability,
lethargy, poor feeding, poor tone, and seizures. Fever is relatively uncommon,
and skin vesicles occur in only approximately 60% of cases. If untreated, 50%
of infants with HSV encephalitis die and most survivors have severe
neurologic sequelae.
231.
Infants with disseminated HSV infections generally become ill at
5-11 days of life. Their clinical picture is similar to that of infants with
bacterial sepsis, consisting of hyperthermia or hypothermia, irritability, poor
feeding, and vomiting. They may also exhibit respiratory distress, cyanosis,
apneic spells, jaundice, purpuric rash, and evidence of central nervous system
infection; seizures are common. Skin vesicles are seen in approximately 75%
of cases. If untreated, the infection causes shock and disseminated intravascular
coagulation; approximately 90% of these infants die, and most survivors have
severe neurologic sequelae.
232.
Infants with neonatal herpes whose mothers received antiherpes
antiviral drugs in the weeks prior to delivery may present later than their
untreated counterparts; whether the natural history of the infection in these
infants is different is an unanswered question.1

36

233.
234.
235.
2.13. Rubella Disease
a. Definition
236.
Rubella (German measles or 3 day measles) is a mild, often
exanthematous disease of infants and children that is typically more severe
and associated with more complications in adults. Its major clinical
significance is transplacental infection and fetal damage as part of the
congenital rubella syndrome (CRS).1
237.
238.
b.

Etiology
239.
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.1

37

c. Epidemiology
240. In the prevaccine era, rubella appeared to occur in major epidemics
every 6-9 yr, with smaller peaks interspersed every 3-4 yr, and was most
common in preschool-age and school-age children. During the rubella
epidemic of 1964-1965 there were an estimated 12.5 million cases of rubella
associated with 2,000 cases of encephalitis, more than 13,000 abortions or
perinatal deaths, and 20,000 cases of CRS. Following introduction of the
rubella vaccine in 1969, the incidence of rubella fell 78% by 1976 and CRS
cases fell 69%). Further decline in rubella and CRS cases occurred when
certain at-risk populations were added to those for whom rubella
immunization is indicated, including adolescents and college students. After
years of decline, a resurgence of rubella and CRS cases occurred during
1989-1991 in association with the epidemic of measles during that period.
Subsequently, a 2 dose recommendation for rubella vaccine was implemented
and resulted in a decrease in incidence of rubella from 0.45 per 100,000
population in 1990 to 0.1 per 100,000 in 1999 and a corresponding decrease
of CRS, with an average of 6 infants with CRS reported annually from 19922004. Mothers of these infants tended to be young, Hispanic, or foreign born.
The number of reported cases of rubella continued to decline through the
1990s and first decade of this century. The endemic spread of rubella has been

38

eliminated in the United States; elimination of transmission of rubella in the

Americas also may have been achieved. However, cases of rubella continue
to be imported into the United States from countries where it remains
endemic. From 2004-2012 there were 79 cases of rubella and 6 cases of CRS,
all of which were imported cases of unknown source. Three of the CRS cases
were acquired in Africa. Between January 1 and May 1, 2013, 5,442 cases of
rubella and 10 cases of CRS were reported, demonstrating that the
elimination of rubella internationally has not been achieved and continued
vigilance and maintenance of high levels of immunity in the United States are
necessary.1
d.
Pathology
241.
Little information is available on the pathologic findings in rubella
occurring postnatally. The few reported studies of biopsy or autopsy material
from cases of rubella revealed only nonspecific findings of lymphoreticular
inflammation and mononuclear perivascular and meningeal infiltration. The
pathologic findings for CRS are often severe and may involve nearly every
organ system.1
e. Pathogenesis
242. The viral mechanisms for cell injury and death in postnatal or
congenital rubella are not well understood. Following infection, the virus
replicates in the respiratory epithelium and then spreads to regional lymph
nodes. Viremia ensues and is most intense from 10-17 days after infection.
Viral shedding from the nasopharynx begins approximately 10 days after
infection and may be detected up to 2 week following onset of the rash. The
period of highest communicability is from 5 days before to 6 days after the
appearance of the rash. The most important risk factor for severe congenital
defects is the stage of gestation at the time of infection. Maternal infection
during the 1st 8 week of gestation results in the most severe and widespread
defects. The risk for congenital defects has been estimated at 90% for
maternal infection before 11 week of gestation, 33% at 11-12 week, 11% at
13-14 week, and 24% at 15-16 wk. Defects occurring after 16 wek of
gestation are uncommon, even if fetal infection occurs. Causes of cellular and

39

tissue damage in the infected fetus may include tissue necrosis due to
vascular insufficiency, reduced cellular multiplication time, chromosomal
breaks, and production of a protein inhibitor causing mitotic arrests in certain
cell types. The most distinctive feature of congenital rubella is chronicity.
Once the fetus is infected early in gestation, the virus persists in fetal tissue
until well beyond delivery. Persistence suggests the possibility of ongoing
tissue damage and reactivation, most notably in the brain.1
f. Clinical Manifestation
243. Postnatal infection with rubella is a mild disease not easily
discernible from other viral infections, especially in children. Following an
incubation period of 14-21 days, a prodrome consisting of low-grade fever,
sore throat, red eyes with or without eye pain, headache, malaise, anorexia,
and lymphadenopathy begins. Suboccipital, postauricular, and anterior
cervical lymph nodes are most prominent. In children, the first manifestation
of rubella is usually the rash, which is variable and not distinctive. It begins
on the face and neck as small, irregular pink macules that coalesce, and it
spreads centrifugally to involve the torso and extremities, where it tends to
occur as discrete macules. About the time of onset of the rash, examination of
the oropharynx may reveal tiny, rose-colored lesions (Forchheimer spots) or
petechial hemorrhages on the soft palate. The rash fades from the face as it
extends to the rest of the body so that the whole body may not be involved at
any one time. The duration of the rash is generally 3 days, and it usually
resolves without desquamation. Subclinical infections are common, and 2540% of children may not have a rash.1
g. Laboratory Findings
244. Leukopenia, neutropenia, and mild thrombocytopenia have been
described during postnatal rubella.1
h. Diagnoses

40

245.
rubella

A specific diagnosis of
is

important

for

reasons,

for

epidemiologic

diagnosis of infection in pregnant

women, and for confirmation of
the

diagnosis

rubella.
diagnostic

The

of

congenital

most

test

is

common
rubella

immunoglobulin (Ig) M enzyme

immunosorbent assay. As with
any serologic test, the positive
predictive

value

of

testing

decreases in populations with

low prevalence of disease. Tests should be performed in the context of a
supportive history of exposure or consistent clinical findings. The relative
sensitivity and specificity of commercialkits used in most laboratories range
from 96-99% and 86-97%, respectively. A caveat for testing of congenitally
infected infants early in infancy is that false-negative results may occur owing
to competing IgG antibodies circulating in these patients. In such patients, an
IgM capture assay, reverse transcriptase polymerase chain reaction test, or
viral culture should be performed for confirmation.1
i. Differential Diagnoses
246. Rubella may manifest as distinctive features suggesting the
diagnosis. It is frequently confused with other infections because it is
uncommon, similar to other viral exanthematous diseases, and demonstrates
variability in the presence of typical findings. In severe cases, it may
resemble measles. The absence of Koplik spots and a severe prodrome as well
as a shorter course allow for differentiation from measles. Other diseases
frequently confused with rubella include infections caused by adenoviruses,
parvovirus B19 (erythema infectiosum), Epstein-Barr virus, enteroviruses,
and Mycoplasma pneumoniae.1
j. Complications

41

247.
infrequent

Complications following postnatal infection with rubella are

and

generally

not

life-threatening.

Postinfectious

thrombocytopenia occurs in approximately 1 in 3,000 cases of rubella and

occurs more frequently among children and. in girls. It manifests about 2 wk
following the onset of the rash as petechiae, epistaxis, gastrointestinal bleeding,
and hematuria. It is usually self-limited.
248. 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.
249. Encephalitis is the most serious complication of postnatal rubella.
It occurs in 2 forms: a postinfectious syndrome following acute rubella and a
rare progressive panencephalitis manifesting as a neurodegenerative disorder
years following rubella. Postinfectious 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.
250. Progressive rubella panencephalitis (PRP) is an extremely rare
complication of either acquired rubella or CRS. It has an onset and course
similar to those of the subacute sclerosing panencephalitis associated with
measles. Unlike in the post infectious form of rubella encephalitis, however,
rubella virus may be isolated from brain tissue of the patient with PRP,
suggesting an infectious pathogenesis, albeit a slow one. The clinical
findings and course are undistinguishable from those of sub-acute sclerosing
panencephalitis and transmissible spongiform encephalopathies. Death occurs

42

2-5 yr after onset. Other neurologic syndromes rarely reported with rubella
include Guillain-Barr syndrome and peripheral neuritis. Myocarditis is a rare
complication.1
251.
2.14. Congenital Rubella Syndrome
252.

In 1941, an ophthalmologist first described a syndrome of

cataracts and congenital heart disease that he correctly associated with

rubella infections in the mothers during early pregnancy. Shortly after the
first description, hearing loss was recognized as a common finding often
associated with microcephaly. In 1964-1965 a pandemic of rubella
occurred, with 20,000 cases reported in the United States, leading to more
than 11,000 spontaneous or therapeutic abortions and 2,100 neonatal
deaths. From this experience emerged the expanded definition of CRS that
includes numerous other transient or permanent abnormalities.
253. Nerve deafness is the single most common finding among
infants with CRS. Most infants have some degree of intrauterine growth
restriction. Retinal findings described as salt-and-pepper retinopathy are
the most common ocular abnormality but have little early effect on vision.
Unilateral or bilateral cataracts are the most serious eye finding, occurring
in about a third of infants. Cardiac abnormalities occur in half of the
children infected during the 1st 8 week of gestation. Patent ductus
arteriosus is the most frequently reported cardiac defect, followed by
lesions of the pulmonary arteries and valvulardisease. Interstitial
pneumonitis leading to death in some cases has been reported. Neurologic
abnormalities

are

common

and

may

progress

following

birth.

Meningoencephalitis is present in 10-20% of infants with CRS and may

persist for up to 12 mo. Longitudinal follow-up through 9-12 yr of infants
without initial retardation revealed progressive development of additional
sensory, motor, and behavioral abnormalities, including hearing loss and
autism. PRP has also been recognized rarely after CRS. Subsequent
postnatal growth retardation and ultimate short stature have been reported

43

in a minority of cases. Rare reports of immunologic deficiency syndromes

have also been described.
254. A variety of late-onset manifestations of CRS have been
recognized. In addition to PRP, they include diabetes mellitus (20%),
thyroid dysfunction (5%), and glaucoma and visual abnormalities
associated with the retinopathy, which had previously been considered
benign.1
a. Treatment
255.
There is no specific treatment available for either acquired rubella
or CRS.
b. Supportive Care
256. Postnatal rubella is generally a mild illness that requires no care
beyond antipyretics and analgesics. Intravenous immunoglobulin or
corticosteroids can be considered for severe, non-remitting thrombocytopenia.
257. Management of children with CRS is more complex and requires
pediatric, cardiac, audiologic, ophthalmologic, and neurologic evaluation and
follow-up because many manifestations may not be readily apparent initially
or may worsen with time. Hearing screening is of special importance, because
early intervention may improve outcomes in children with hearing problems
caused by CRS.1
c. Prognosis
258. Postnatal infection with rubella has an excellent prognosis. Longterm outcomes of CRS are less favorable and somewhat 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.
259. Reinfection with wild virus occurs postnatal in both individuals
who were previously infected with wild-virus rubella and in vaccinated
individuals. Reinfection is defined serologically as a significant increase in Ig
G antibody level and/or an Ig M response in an individual who has a
documented preexisting rubella-specific Ig G above an accepted cutoff.
Reinfection may result in an anamnestic Ig G response, an Ig M and Ig G

44

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.1
d. Prevention
260. Patients with postnatal infection should be isolated from
susceptible individuals for 7 days after onset of the rash. Standard plus
droplet precautions are recommended for hospitalized patients. Children with
CRS may excrete the virus in respiratory secretions up to 1 yr of age, so
contact precautions should be maintained for them until then, unless repeated
cultures of urine and pharyngeal secretions have negative results. Similar
precautions apply to patients with CRS with regard to attendance in school
and out-of-home childcare.
261. Exposure of susceptible pregnant women poses a potential risk to
the fetus. For pregnant women exposed to rubella, a blood specimen should
be obtained as soon as possible for rubella Ig G-specific antibody testing; a
frozen aliquot also should be saved for later testing. If the rubella antibody
test result is positive, the mother is likely immune. If the rubella antibody test
is negative, a 2nd specimen should be obtained 2-3 week later and tested
concurrently with the saved specimen.
262.
If both of these test negative, a 3rd specimen should be obtained 6
week after exposure and tested concurrently with the saved specimen. If both
the 2nd and 3rd specimens test negative, infection has not occurred. A
negative 1st specimen and a positive test result in either the 2nd and 3rd
specimen indicate that second version has occurred in the mother, suggesting
recent infection. Counseling should be provided about the risks and benefits
of termination of pregnancy. The routine use of immunoglobulin for
susceptible pregnant women exposed to rubella is not recommended and is
considered only if termination of pregnancy is not an option because of
maternal preferences. In such circumstances, immunoglobulin 0.55 mL/kg IM
may be given with the understanding that prophylaxis may reduce the risk for
clinically apparent infection but does not guarantee prevention of fetal
infection.1

45

263.

Ongoing surveillance for all cases of rubella and of CRS is a vital

component of a prevention program. Patients with illnesses that are

compatible with rubella or measles should have a serum rubella and measles
immunoglobulin (Ig) M serology requested. In low-prevalence situations, in
the absence of clear epidemiological links or travel history to endemic areas,
Ig M serology has a low positive predictive value for both measles and
rubella. Thus, additional laboratory testing such as paired acute and
convalescent Ig G serology (to look for a fourfold or greater rise in titre)
and/or virus detection is necessary to confirm measles and rubella infections.
This is not only important for surveillance purposes, but is critical for the
laboratory investigation of suspected rubella in pregnant women where
important patient management decisions must be made. In this situation of
suspected rubella in a pregnant woman, rubella Ig G avidity testing has been
shown to be a very useful laboratory test for differentiating primary infection
(with a high risk of CRS) from past infection (low risk of CRS). Infants with
unexplained microcephaly, cataracts, glaucoma, pigmentary retinopathy,
hearing

impairment,

patent

ductus

arteriosus,

hepatosplenomegaly,

thrombocytopenia or radiolucent bone densities should be evaluated for CRS

with the appropriate investigations depending on the age of the child.
264.
To prevent CRS:
1) Continued universal infant immunization to protect recipients and to
decrease circulation of the virus;
2) Use of the MMR vaccine rather than the monovalent measles vaccine as
the immunizing agent in all immunization programs for measles
worldwide to expedite the elimination of rubella;
3) Screening of all pregnant women to determine the need to confirm
seropositivity and to enable postpartum immunization of all women found
to be susceptible on prenatal screening. Standing orders on the postpartum
ward should be implemented (similar to the RhoGam [Ortho-Clinical
Diagnostics Inc., USA] standing order in the postpartum period) because
they will expedite postpartum immunization. Breastfeeding is not a
contraindication to immunization;

46

4) Screening for immunity and vaccination, if necessary, of all health care

personnel, including students in training;
5) Immunizing all non-pregnant immigrant and refugee women at their first
encounter with the Canadian health care system unless they have
documentation of effective vaccination or natural immunity; and
6) Fully investigating and reporting every case of possible rubella or CRS.8
e. Vaccination
265. Rubella vaccine in the United States consists of the attenuated
Wistar RA 27/3 strain that is usually administered in combination with
measles and mumps (MMR) or also with varicella (MMRV) in a 2 dose
regimen at 12-15 months and 4-6 year of age. It theoretically may be effective
as post exposure prophylaxis if administered within 3 days of exposure.
Vaccine should not be administered to severely immunocompromised patients
(e.g., transplant recipients). Patients with HIV infection who are not severely
immunocompromised may benefit from vaccination. Fever is not a
contraindication, but if a more serious illness is suspected, immunization
should be delayed. Immunoglobulin preparations may inhibit the serologic
response to the vaccine. Vaccine should not be administered during
pregnancy. If pregnancy occurs within 28 days of immunization, the patient
should be counseled on the theoretical risks to the fetus. Studies of more than
200 women who had been inadvertently immunized with rubella vaccine
during pregnancy showed that none of their offspring developed CRS.
Therefore, interruption of pregnancy is probably not warranted. Following a
single dose of rubella RA 27/3 vaccine, 95% of persons 12 months of age and
older develop serologic immunity, and after 2 doses 99% have detectable
antibody. Rubella RA 27/3 vaccine is highly protective as 97% of those
vaccinated are protected from clinical disease after 1 dose. Detectable
antibodies remain for 15 year in most individuals vaccinated following 1
dose, and 91% to 100% had antibodies after 12-15 yearafter 2 doses.
Although antibody levels may wane, especially after 1 dose of vaccine,
increased susceptibility to rubella disease does not occur.

47

266.

Adverse reactions to rubella vaccination are uncommon in

children. MMR administration is associated with fever in 5-15% of vaccines

and with rash in approximately 5% of vaccines. Arthralgia and arthritis are
more common following rubella vaccination in adults. Approximately 25% of
post pubertal women experience arthralgia, and 10% experience arthritis.
Peripheral neuropathies and transient thrombocytopenia may also occur.
267. As part of the worldwide effort to eliminate endemic rubella virus
transmission and occurrence of CRS, maintaining high population immunity
through vaccination coverage and high-quality integrated measles-rubella
surveillance have been emphasized as being vital to its success.1
268.
2.15. Hearing testing
269.

Currently, hearing screening in newborns is performed via

otoacoustic emission (OAE) and automated auditory brainstem response

(AABR) testing. These physiological, noninvasive, automated screening
tests can be performed at the bedside in term and pre-term infants.
Depending on the screening protocol, they may be performed singly (OEA
or AABR) or sequentially. Both the OAE and AABR tests are automated
screening adaptations of more detailed diagnostic tests for hearing loss.
270.
OAEs are forms of energy, measured as sound, generated
by the outer hair cells of the human cochlea, in response to received
auditory input. First described by a geophysicist in the middle 1940s, the
screening test was developed in 1978 by David Kemp. Based on the
natural phenomenon of sound echoes, a sound stimulus is sent to the
newborns auditory system via ear-specific probes placed in the external
ear canal. The probe simultaneously records emissions returning from the
outer hair cells of the cochlea via the middle ear. OAEs can be recorded in
99% of normally hearing ears. The response is generally absent in ears
with a hearing loss of 30 dB or greater.
271.
The AABR test records brainstem electrical activity in
response to sounds presented to the infant via earphones. In contrast to the
OAE test, the AABR evaluates the auditory pathway from the external ear

48

to the level of the brainstem, enabling diagnosis of auditory neuropathy,

which is a less common cause of hearing impairment.7
272.
2.16. Red flags
273.

Red flag is an informal term that, in this context, simply

implies that some aspect of the childs development has been noticed as at
risk for falling outside the range deemed typical. A red flag may be
discovered during a standardized developmental screening or through the
ongoing, daily interactions between the infant/toddler caregiver and child.
In essence, a red flag is a signal to pay increased attention to the aspect of
concern in a childs development, and to be even more intentional in
documenting observations and providing opportunities for the child to
acquire the skill.
274. Red flags guidliness (6-24 months):
1) 6 month of age
a. Fine motor: Infant is unable to hold or grasp an adult finger or a toy/object
for a short period of time, persistence of grasp reflex, and consistently
ignores or has difficulty using one side of body; or uses one hand
exclusively
b. Gross motor: Does not pull up to sit or does not roll over, baby is unable to
hold head in the middle to turn and look left and right and asymmetry (i.e.
a difference between two sides of body or body too stiff or too floppy)
c. Vision: Turning or tilting head to use only one eye to look at things,
Holding toys close to eyes, or no interest in small objects and constant
jiggling or moving of eyes side-to-side
d. Speech and language: Early babbling stops, Does not respond when called
and a lot of colds and ear infections
e. Cognitive : Unable to follow moving objects with his/her eyes and will not
reach out to explore/touch objects
f. Social : Unresponsive to a familiar voice, no eye contact, unresponsive to
social situations (i.e., flat affect), not smiling socially
g. Emotional: Unresponsive to familiar caregivers, Extreme irritability and
unresponsive to social situations
2) 12 month of age

49

a. Fine motor: Consistently ignores or has difficulty using one side of body
or uses one hand exclusively
b. Gross motor: Baby is unable to hold head in the middle to turn and look
left and right and asymmetry (i.e. a difference between two sides of body
or body too stiff or too floppy)
c. Vision: Unusually short attention span; will only look at you if he or she
hears you, turning or tilting head to use only one eye to look at things,
eyes that cross, turn in or out, move independently, no interest in small
objects and pictures, and constant jiggling or moving of eyes side-to-side
(roving)
d. Speech and language: Lost vocalization
e. Cognitive : Does not make sounds to get attention, does not search for
dropped or hidden objects and child does not respond to caregiver
interactions
f. Social : Will not show interest or participate in social situations,not
laughing in playful situations,hard to console, stiffens when approached
g. Emotional: Will not seek comfort when upset
3) 18 month of age
a. Fine motor: Infant is unable to hold or grasp an adult finger or a toy/object
for a short period of time, unable to use hands in a variety of ways,
turning, twisting, throwing, etc and unconsistently ignores or has difficulty
using one side of body, or uses one hand exclusively
a. Gross motor: Baby is unable to hold head in the middle to turn and look
left and right and asymmetry (i.e. a difference between two sides of body
or body too stiff or too floppy)
b. Vision: Eyes that itch or burn; sensitivity to bright light and sun, unusually
short attention span; will only look at you if he or she hears you,
avoidance of tasks with small objects, turning or tilting head to use only
one eye to look at things, eyes that cross, turn in or out, move
independently, and constant jiggling or moving of eyes side-to-side
c. Speech and language: Failure to do what they may to do
d. Cognitive: Does not imitate simple actions, does not show any
understanding of cause and effect. does not search for objects when moved
from within sight to out of sight

50

e. Social : Does not explore the environment, very passive responses, does
not show preferences and dislikes, child ignores, avoids or is hostile with
caregiver after separation, and shows little fear towards a new room or
stranger
f. Emotional: Facial expression shows little variation, child shows few
emotions, does not seek comfort in a person or object when distressed
4) 12 month of age
a. Fine motor: Unable to use hands in a variety of ways, turning, twisting,
and throwing.
b. Gross motor: Unable to walk with heels down
c. Vision: Eyes that itch or burn; sensitive to bright light and sun, avoidance
of tasks with small objects, turning or tilting head to use only one eye to
look at things
d. Speech and language: Lack of face to face or eye contact and loss of
speech
e. Cognitive : Misses small objects when reaching for them and does not use
trial and error to solve problems
f. Social : Does not make face to face contact during play or any interactions,
does not show affection for familiar people or objects, child kicks, bites
and scream easily and without provocation, and rocks back and forth
g. Emotional: Failure to talk about feelings, show preferences of likes and
dislikes, show pride and pleasure at new accomplishments and express
negative feelings. 9
275.
276.
277.
278.

281.

CHAPTER III
CONCLUSION
279.
280.
The sign of the symptoms that are appeared on the infant

indicates the suffered Congenital Rubella Syndrome which cause by the

infection.
282.
283.
284.

51

285.
REFERENCES
286.
287.
1. Kliegman M. Robert, Stanton F. Bonita, St Geme III W. Joseph, Schor F.
Nina, Behrman E. Richard. Nelson Textbook of Pediatrics. International
Edition. Twentieth Edition. Canada : Elsevier, Inc ; 2015
2. Usman Ali, Kosim Sholeh, Yunanto Ari, Dewi Eizalya, Sarosa Gatot
Irawan. Buku Ajar Neonatologi. Penerbit Ikatan Dokter Anak Indonesia ;
2009
3. Sadier, TW. 2012. Langmans Medical Embryology 12th Edition. Lippincott
Williams and Wilkins, a Wolter Kluwer Business
4. Melnick & Adelbergs, Jawetz. 2010. Medical Microbiology 25th Edition.
Mc Graw Hill.
5. Wollnik, Bernd. A Common Mechanism for Microcephaly. Nature Genetics.
2010, p.42(11): 923-4.
6. http://www.education.vic.gov.au/childhood/professionals/support/pages/chi
ldgrowth.aspx, accessed on September 17th 2015
7. Patel H, Feldman M. Universal newborn hearing screening. Pediatrics &
Child Health. 2011;16(5):301-305.
8. McLean HQ, Fiebelkorn AP, Temte JL, Wallace GS. Centers for Disease
Control and Prevention. Prevention of measles, rubella, congenital rubella
syndrome, and mumps. 2013: summary recommendations of the advisory
committee

on

immunization

practices

(ACIP) MMWR

Recomm

Rep. 2013; 62: 134.

9. Department of Maternal and Child Health. 2010. Infant/Toddler
Development, Screening, and Assessment. Chapel Hill : The University of
North Carolina
288.
290.

289.

52