LO WEEK 1 – NEURO

10 T antenatal
(T1-T14)
Berat badan pas kehamilan 0.5 kg per minggu mulai dari trimester ke-2
Bp 🡪 diantara 110/80 hingga 140/90
Tinggi fundus uteri (cek besar bayi)
Pemberian table Fe sebanyak 90 tablet selama kehamilan
Pemberian imunisasi tetanus toxoid
Pemeriksaan Hb
Pemeriksaan FDRL
Evaluasi perawatan payudara 🡪 senam payu dara & pijat tekan payudara (.)(.)
Pemeliharaan tingkat kebugaran 🡪 senam ibu hamil
Temu bicara dalam rangka persiapan rujukan (optional)
Pemeriksaan urin atas indikasi
Pemeriksaan reduksi urin atas indikasi
Pemberian kapsul yodium untuk daerah endemis gondok
Pemberian terapi anti malaria untuk daerah endemis malaria

Tetanus toxoid
Neonatal tetanus is a form of generalised tetanus that occurs in newborns. Infants
who have not acquired passive immunity from the mother having been immunised
are at risk. It usually occurs through infection of the unhealed umbilical stump,
particularly when the stump is cut with a non-sterile instrument. Neonatal tetanus
mostly occurs in developing countries, particularly those with the least developed
health infrastructure. It is rare in developed countries.
Tetanus is acquired through exposure to the spores of the bacterium Clostridium
tetani which are universally present in the soil. The disease is caused by the action of
a potent neurotoxin produced during the growth of the bacteria in dead tissues, e.g.
in dirty wounds or in the umbilicus following non-sterile delivery. People of all ages
can get tetanus. But the disease is particularly common and serious in newborn
babies. This is called neonatal tetanus. Most infants who get the disease die.
Neonatal tetanus is particularly common in rural areas where most deliveries are at
home without adequate sterile procedures.

Iron supplements
Iron supplements are particularly important for pregnant women who have anemia.
In women who have normal iron levels, taking iron supplements as a precautionary
measure probably doesn’t have any health benefits. They can get enough iron in
their diet.
Iron deficiency anemia can make you feel tired and exhausted. Severe anemia can
also lead to complications in pregnancy. For instance, it can weaken the mother’s
immune system and make infections more likely. It also increases the risk of the
baby weighing too little at birth (low birth weight).

https://www.ncbi.nlm.nih.gov/books/NBK235217/
Although some epidemiologic evidence suggests that anemia during pregnancy could
be harmful to the fetus, the data are far from conclusive.
The infant of an iron-depleted mother has surprisingly little evidence of anemia or
depletion of iron stores.

Iron Requirements for Pregnancy

The body iron requirement for an average pregnancy is approximately 1,000 mg.
Hallberg (1988) calculated that 350 mg of iron is lost to the fetus and the placenta
and 250 mg is lost in blood at delivery. In addition, about 450 mg of iron is required
for the large increase in maternal red blood cell mass. Lastly, basal losses of iron
from the body continue during pregnancy and amount to about 240 mg. Thus, the
total iron requirements of a pregnancy (excluding blood loss at delivery) average
about 1,040 mg. Permanent iron losses during pregnancy include loss to the fetus
and placenta, blood loss at delivery, and basal losses, which together total 840 mg.
The total iron needs of slightly more than 1,000 mg are concentrated in the last two
trimesters of pregnancy. This amount is equivalent to about 6 mg of iron absorbed
per day in a woman who starts pregnancy with absent or minimal storage iron. This
is a large amount of iron to accumulate over a 6-month period, especially when
compared with the average total body iron content of 2,200 mg and the 1.3 mg of
iron absorbed per day by nonpregnant women.
Although 450 mg of iron for red cell production must be supplied during pregnancy,
a large part of this can subsequently augment iron stores after a vaginal delivery,
when the red cell mass decreases. The result is analogous to a postpartum injection
of iron: serum ferritin levels will spontaneously increase within a few months after
delivery in most women who develop mild iron deficiency during late pregnancy
because of the iron that is released by the decline in red cell mass (Puolakka et al.,
1980b; Svanberg et al., 1976a; Taylor et al., 1982). Postpartum iron status is also
improved by the decreased iron loss during this period: less than 0.3 mg/day is lost
in human milk, and menstruation is rare in women during their first few months of
lactation.
The average blood loss during a cesarean delivery is almost twice that occurring with
the average vaginal delivery of a single fetus (Pritchard, 1965; Pritchard et al; 1962;
Ueland, 1976); the postpartum improvement in iron status may therefore be less
complete after a cesarean delivery.
Duration and Dose
An appropriate time to begin iron supplementation at a dose of 30 mg/day is after
about week 12 of gestation (the beginning of the second trimester), when the iron
requirements for pregnancy begin to increase. Iron administration at a dose of 60 to
120 mg/day (preferably in divided doses) is indicated if there is laboratory evidence
of an already established anemia at any stage of pregnancy. The dose should be
decreased to 30 mg/day when the hemoglobin concentration is within the normal
range for the stage of gestation
Compliance and Side Effects
One problem with supplement use during pregnancy is uncertainty about
compliance (Bonnar et al., 1969), particularly when poverty and certain ethnic beliefs
reduce the availability or acceptability of supplements. Early in pregnancy, morning
sickness probably contributes to reduced consumption of nutrient supplements. Late
in pregnancy, constipation and abdominal discomfort are frequent regardless of
whether supplements are used or not. Taking high doses of iron may increase these
problems and thus discourage supplement use. Iron appears to be best tolerated
when administered at bedtime.
Potential side effects of iron administration include heartburn, nausea, upper
abdominal discomfort, constipation, and diarrhea. The most careful studies that
focused on side effects involved double-blind administration of large therapeutic
doses of iron to large groups of blood donors (Hallberg et al., 1967b; Sölvell, 1970).
At a dosage of 200 mg of iron per day as ferrous sulfate divided into three doses per
day, approximately 25% of subjects had side effects, compared with 13% of those
who received a placebo. When the dose was doubled, side effects increased to 40%.
Constipation and diarrhea occurred with the same frequency at the two doses, but
nausea and upper abdominal pain were more common at the higher dose. The risk
of side effects is proportional to the amount of elemental iron in various soluble
ferrous iron compounds and therefore appeared to be primarily a function of the
amount of soluble iron in the small intestine. Little information is available about
side effects at doses below 200 mg, but it is reasonable to infer that side effects are
much less likely at 30 mg/day.

Clinical Applications
To prevent iron deficiency, the subcommittee recommends the routine use of 30 mg
of ferrous iron per day beginning at about week 12 of gestation, in conjunction with
a well-balanced diet that contains enhancers of iron absorption (ascorbic acid,
meat).
To enhance absorption, it is advisable to take supplemental iron between meals with
liquids other than milk, tea, and coffee.
Hemoglobin or hematocrit should routinely be determined at the first prenatal visit
in order to detect preexisting anemia. A hemoglobin level below 11.0 g/dl during the
first or third trimesters or below 10.5 g/dl during the second trimester is defined as
anemia. Anemia accompanied by a serum ferritin concentration of <12 µg/dl can be
presumed to be iron deficiency anemia and requires treatment with 60 to 120 mg of
ferrous iron daily. When the hemoglobin concentration becomes normal for the
stage of gestation, the dose can be decreased to 30 mg/day.

Effects
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4375689/
Impact of iron deficiency anemia
Throughout pregnancy, iron deficiency anemia adversely affects the maternal and
fetal well-being, and is linked to increased morbidity and fetal death. Affected
mothers frequently experience breathing difficulties, fainting, tiredness, palpitations,
and sleep difficulties.16 They also have an increased risk of developing perinatal
infection, pre-eclampsia, and bleeding. Post-partum cognitive impairment and
behavioral difficulties were also reported.17-19 Adverse perinatal outcomes include
intrauterine growth retardation, prematurity, and low birth weight, all with
significant mortality risks, particularly in the developing world.20-22 Iron deficiency
during the first trimester, has a more negative impact on fetal growth than anemia
developing later in pregnancy.23,24 This is also true for risk of premature labor.25
Poor socio-economic status contributes significantly to all aspects of these inter-
linked problems that are more commonly encountered in the developing world. Any
successful public prevention or treatment program should put into consideration all
these contributing and correlating factors.
Lowered iron stores of the newborn child may persist for up to one year and result in
iron deficiency anemia.26 Such a state should be identified and treated promptly
because of the possible long term consequences. Iron is essential for neural
metabolism and functioning. Iron deficiency anemia results in changes in energy
metabolism within the brain with defects in neurotransmitter function and
myelination.27 Therefore, infants and young children with iron deficiency anemia
are at risk of developmental difficulties involving cognitive, social-emotional, and
adaptive functions.28,29 Other studies have documented delays in both language
and motor development. Breastfeeding is usually protective, but not if the mother is
iron deficient. It has been noted that iron levels in breast milk fall as lactation
progresses over time.30 Careful monitoring and adequate supplementation is
therefore needed for infants at risk.

TORCH
TORCH refers to (T)oxoplasmosis, (O)ther Agents, (R)ubella (or German Measles),
(C)ytomegalovirus, and (H)erpes Simplex.
If a developing fetus is infected by a TORCH agent, the outcome of the pregnancy
may be:
Miscarriage
Stillbirth
Delayed fetal growth and maturation (intrauterine growth retardation) (retardasi
pertumbuhan intrauterin)
Early delivery.
In addition, newborns infected by any one of the TORCH agents may develop a
spectrum of similar symptoms and findings. These may include:
Listlessness (lethargy)
Fever
Difficulties feeding
Enlargement of the liver and spleen (hepatomegaly)
Decreased levels of the oxygen-carrying pigment (hemoglobin) in the blood
(anemia).
In addition, affected infants may develop areas of bleeding, resulting in reddish or
purplish spots or areas of discoloration visible through the skin (petechia or
purpura); yellowish discoloration of the skin, whites of the eyes, and mucous
membranes (jaundice); inflammation of the middle and innermost layers of the eyes
(chorioretinitis); and/or other symptoms and findings. Each infectious agent may
also cause additional abnormalities that may vary in degree and severity, depending
upon the stage of fetal development at time of infection and/or other factors.
Following is a more specific description of the TORCH agents.
Toxoplasmosis is an infectious disease caused by the microscopic parasitic organism
called Toxoplasma gondii. This parasitic infection, found worldwide, may be acquired
or transmitted to the developing fetus from an infected mother during pregnancy. In
some severely affected newborns, Toxoplasmosis may be associated with abnormal
smallness of the head (microcephaly), inflammation of the middle and innermost
layers of the eyes (chorioretinitis), calcium deposits in the brain (intracranial
calcifications), and/or other abnormalities.
Rubella is a viral infection characterized by fever, upper respiratory infection,
swelling of the lymph nodes, skin rash, and joint pain. Severely affected newborns
and infants may have visual and/or hearing impairment, heart defects, calcium
deposits in the brain, and/or other abnormalities.
Cytomegalovirus (CMV) Infection is a viral infection that may occur during
pregnancy, after birth, or at any age. In severely affected newborns, associated
symptoms and findings may include growth retardation, an abnormally small head
(microcephaly), enlargement of the liver and spleen (hepatosplenomegaly),
inflammation of the liver (hepatitis), low levels of the oxygen-carrying pigment in the
blood due to premature destruction of red blood cells (hemolytic anemia), calcium
deposits in the brain, and/or other abnormalities.
Neonatal Herpes is a rare disorder affecting newborns infected with the Herpes
simplex virus (HSV). This disorder may vary from mild to severe. In most cases, the
disorder is transmitted to an infant from an infected mother with active genital
lesions at the time of delivery. In the event that a mother has a severe primary
genital outbreak, it is possible that a mother may transmit the infection to the fetus.
After delivery, direct contact with either genital or oral herpes sores may result in
neonatal herpes. Severely affected newborns may develop fluid-filled blisters on the
skin (cutaneous vesicles), lesions in the mouth area, inflammation of the mucous
membrane lining the eyelids and whites of the eyes (conjunctivitis), abnormally
diminished muscle tone, inflammation of the liver (hepatitis), difficulties breathing,
and/or other symptoms and findings.
Toxo 🡪 macrocephali 🡪 ibu suka makan daging mentah / pelihara kucing
Cmv 🡪 microcephali

Interpretasi chart

Perkembangan anak per usia

1. A
2. A
3. A
4. A
5. A
6. A
7. A
 8. Hydrocephalus
Hydrocephalus refers to the abnormal enlargement of cerebral ventricles and/or subarachnoid
space as a result of excess cerebrospinal fluid (CSF) accumulation.
There are two types of true hydrocephalus:
 Communicating hydrocephalus
Occurs due to decreased CSF absorption or increased CSF production in absence of any CSF-

flow obstruction
 Non-communicating hydrocephalus
 Occurs due to the obstructed passage of CSF from the ventricles to the subarachnoidal space.

Both forms cause elevated intracranial pressure (ICP), which leads to headache, nausea, and/or
vomiting.
Specific clinical manifestations include changes in vital signs resulting
from brainstem compression and, in ocongenital hydrocephalus, macrocephaly.
Normal pressure hydrocephalus (NPH) is a chronic form of communicating
hydrocephalus that occurs in older individuals (> 60 years of age). NPH occurs due to
decreased CSF absorption and manifests with normal ICP because of effective compensation to the
slow CSF accumulation by ventricular dilation. This ventricular distension leads to the classic
presentation of urinary incontinence, dementia, and ataxic gait.
Hydrocephalus ex vacuo is the enlargement of the ventricles and subarachnoid space due to
loss of brain tissue (e.g., cerebral atrophy) and the subsequent filling of the void with CSF. It is not
considered a true hydrocephalus since ventricular enlargement does not result
from CSF accumulation and, accordingly, does not affect intracranial pressure or flow
of cerebrospinal fluid.
CT or MRI (and ultrasound for infants) are important diagnostic procedures for all types of
hydrocephalus. A CSF tap test confirms the diagnosis of NPH. Treatment involves surgical insertion of
a shunt, which drains excess CSF into another area of the body (usually the peritoneum).
9. Cutoff untuk macrocephaly :
Macrocephaly adalah kondisi dimana Head Circumference bayi berada
diatas 2 standard deviasi, yaitu diatas persentil 97.
 10. What are the possible problems in the baby according to the risk
factors in this case?

Penggunaan alkohol -> Berbahaya untuk dikonsumsi pada saat

kehamilan karena alkohol yang berada pada darah sang ibu akan
dialirkan ke janin melalui umbilical cord. Sedangkan metabolisme
alkohol pada janin lebih lambat daripada di dalam tubuh ibu, sehingga
mungkin terdapat kadar alkohol yang lebih tinggi yang akan bertahan
lebih lama di dalam darah janin -> hal ini terjadi karena janin memiliki
lebih sedikit alcohol dehydrogenase untuk melakukan metabolisme
alkohol.

Liver janin adalah salah satu organ yang belum akan berkembang
maksimal sampai bagian akhir kehamilan. Hal inilah yang
menyebabkan sang janin tidak bisa memproses alkohol sebaik ibunya.

Dapat menyebabkan beberapa hal yaitu:

 Keguguran
 Stillbirth (mati saat lahir)
 Kelainan pada fisik
 Perilaku yang abnormal
 Kelainan intelektual

Kelainan tersebut disebut sebagai Fetal Alcohol Spectrum Disorders

(FASDs).

Karakterisitik daripada FASD:

 Abnormalitas pada wajah seperti philtrum yang rata (diantara
hidung dan mulut)
 Ukuran kepala yang kecil
 Tinggi badan lebih pendek dari rata-rata
 Berat badan rendah
 Koordinasi yang buruk
 Hiperaktif
 Kesulitan untuk fokus
 Poor Memory
 Kesulitan di sekolah (terutama dengan matematika)
 Keterlambatan bicara (delayed speech)
 Cacat intelektual atau iq rendah
 Sleep and Sucking problems ketika bayi
 Masalah dalam melihat atau mendengar
 Kelainan pada jantung, ginjal, atau tulang.

Lack of prenatal checkup : The deprivation of prenatal care can lead to premature
pregnancy, intrauterine growth retardation, low weight at birth, and maternal and child
mortality as a result of infections in the perinatal and postnatal periods.
 1. Anatomi
Cranial fossa:
1. anterior cranial fossa
- frontal bone
- frontal lobes
- ethmoid bone
- olfactory enrves
- sphenoid lesser wing bone
2. middle cranial fossa
- temporal bone
- temporal lobes
- sphenoid greater wing bone
- pituitary gland
3. posterior cranial fossa
a. occipital fossa occipital bone & lobes
b. cerebellar fossa cerebellum
struktur anatomis yang pisahin occipital dari cerebellar fossa: tentorium cerebelli

Brain hemisphere
Superior view

Lateral
Ventricles

 Cerebrum terbagi jadi left & right cerebral hemispheres. Hemispheres punya folds &
convulitions di permukaan mereka. Ridges di antara convolutions disebut gyri.
Valleys (cekungan) antara gyri disebut sulci kalau sulci deep disebut fisura.
 Longitudinal fissure / fissure longitudinalis cerebri: belah R & L hemisphere
 Corpus callosum: sekumpulan nerve fibres yang gabungin otak kanan kiri
 Central sulcus of roland/ sulcus centralis rolandi: bagi precentral. & postcentral
gyrus.
 Precentral gyrus of the brain/ gyrus precentalis: lokasi untuk primary motor cortex,
tugas untuk jalankan voluntary movement
 Postcentral gyrus of the brain / gyrus postcentralis: lokasi primary somatosensory
cortex, main sensory receptive area buat sensasi sentuhan
 Lateral sulcus of sylvii: fisura yang pisahin frontal lobe & parietal lobe dengan
temporal lobe
Lobes
 Frontal lobe/lobus frontalis cerebri: atur cognitive skills / ekspresi emosi, problem
solving, memori, personalitas, kemampuan komunikasi
 Parietal lobe: proses info sensory: sentuhan, peraba, suhu
 Temporal lobe: proses input sensory meanings dengan appropriate retensi dari
visual memory, komprehensi Bahasa, emosi
 Osipital: visual
 Insula: deep di lateral sulcus, buat kesadaran, ad aperan emosi & homeostasis
Fisiologi Otak (cerebrum, cerebellum)
Brain terdiri dari 4 struktur utama: cerebrum, cerebellum, pons, medulla
Cerebrum: upper part brain dibagi jadi 2 hemispheres. Mengatur kesadaran & mental. Outer layer
disebut gray matter, dalemnya disebut white matter
Cerebral hemispheres dibagi jadi 4 sections / lobe:
1. Frontal: berpikir, making judgements, planning, decision making, conscious
emotions, attention, mood, personality, self awareness, social & moral reasoning.
Broca area terletak di frontal lobe & bertanggung jawab baut speaking & writing
skills.
2. Parietal: spatial computation, body orientation & attention, interpreting vision,
motor, sensory, memory function
3. Temporal: hearing, language, memory, understanding spoken & written language.
Proses retensi memori, bahasa emosi,
4. Occipital: visual processing

Cerebellum: bagian otak yang terletak di antara batang otak & belakang cerebrum. Atur koordinasi
otot & keseimbangan tubuh. (kalau tertekan CSF di 4th ventricle bisa bikin gangguan gait,
keseimbangan, masalah postural) Terdiri dari cerebellar cortex & deep cerebellar nuclei. Cerebellar
cortex terbentuk dari 3 layer (molecular, purkinje, granular). Cerebellum nyambung ke brainstem
oleh cerebellar peduncles. Fungsi utama: modulate koordinasi motor, posture, balance
Brainstem: terdiri dari midbrain, pons, medulla
Pons: di depan cerebellum, koordinasi aktivitas cerebrum & cerebellum dengan terima & kirim
impuls dari mereka ke spinal cord
Medulla: bagian brainstem di antara pons & spinal cord, atur nafas, heartbeat, vomit

Cellular
Grey matter: main komponen dari CNS. Consists of neuronal cell bodies, dendirt, myelinated &
unmyelinated axon, glial cells, sinapsis, kapiler. Membentuk cerebral cortex
2. Fisiologi cns
 Cerebrospinal fluid
Cerebrospinal fluid bentuknya cair/liquid yg clear, colorless dan berisi air yg tugasnya nge
protect brain dan spinal cord dari chemical dan physical injuries. Mengandung oxygen, glucose dan
chemicals lainnya yg dibutuhkan. CSF terus menerus bersirkulasi melalui cavities di brain dan spinal
cord disekitar brain dan di subarachnoid space nya spinal cord. Total volume CSF 80-150 mL kalo pd
orang dewasa. CSF jg mengandung glucose, proteins, lactic acid, urea, cations dan anions, ada jg
sedikit WBC.

CSF filled cavities di brain atau yg disebut ventricles ada 4. Ada satu lateral ventricle
di setiap hemisphere dari cerebrum (anggep aja ventricle 1 sama 2). Kalo dari anterior,
lateral ventricles ini dipisahin sama thin membrane yg namanya septum pellucidum. Kalo
yang 3rd ventricle itu bentuknya narrow slitlike cavity di midline superior sampe ke
hypothalamus dan antara thalamus kanan dan kiri. Kalo yg 4th ventricle ada diantara brain
stem dan cerebellum
Fungsi cerebrospinal fluid ada 3 :
1. Mechanical protection : CSF bekerja sebagai shock absorbing medium yg
melindungi jaringan di otak dan spinal cord.
2. Homostatic function : pH dari CSF mempengaruhi pulmonary ventilation dan
cerebral blood flow, jd penting untuk maintain homeostatic controls buat jaringan otak. CSF
jg bekerja sebagai transport systemnya polypeptide hormones yg disekresiin sama
hypothlamic neurons yg bekerja di remote sites di brain
3. Circulation : CSF merupakan medium untuk minor exchange dari nutrients dan
waste products antara blood dan adjacent nervous tissue
Ratarata CSF diproduksi oleh choroid plexuses yg merupakan kumpulan kapiler di
dinding ventricles. Ependymal cells yg disambungkan oleh tight junction mengelilingi kapiler
dari choroid plexuses. Substances tertentu (misalnya air) dari blood plasma yang difilt dari
kapiler kemudian disekresikan oleh ependymal cells untuk memproduksi cerebrospinal fluid.
Kapasitas sekresinya bidirectional dan menyebabkan CSF terus menerus diproduksi,
sementara juga ada perpindahan metabolites dari nervous tissue balik ke blood. Karena
adanya si tight junction diantara ependymal cells ini, nyebabin material yg masuk ke CSF dari
choroid capillary gabisa bocor. Karena gbs bocor, jdnya kalo mau masuk tu harus lewat
ependymal cells. Sementara blood cerebrospinal fluid barrier cuma ngizinin substances
tertentu aja yg masuk ke CSF karena buat menjaga brain dan spinal cord dari substances yg
berbahaya.
CSF dibentuk di choroid plexuses dr tiap lateral ventricle trus flow ke 3rd dan 4th
ventricle melalui interventricular foramina. CSF jumlahnya accumulate jadi banyak di 3rd
ventricle. Fluidnya trus flow melewati aqueductnya midbrain (cerebral aqueduct), yang
ngelewatin midbrain, trus masuk ke 4th ventricle. Choroid plexus di 4th ventricle
berkontribusi mengeluarkan lebh banyak fluid. CSF abis itu masuk ke subarachnoid space
melewati 3 openings di roof nya 4h ventricle, yaitu di single median aperture dan paired
lateral apertures di masing masing side. CSF kemudian bersirkulasi di central canal dari
spinal cord dan di subarachnoid space yg mengelilingi surface nya brain dan spinal cord. CSF
akan di reabsorb ke blood melalui arachnoid villi yg ada di arachnoid mater trs projects ke
superior sagittal sinus. (Cluster villi disebut arachnoid granulation. Karena rate sekresi dan
reabsorsi sama, jadinya balance.

Braxton Hicks Contraction :

Braxton Hicks contractions are sporadic contractions and relaxation of the uterine
muscle. Sometimes, they are referred to as prodromal or “false labor" pains. It is
believed they start around 6 weeks gestation but usually are not felt until the second
or third trimester of the pregnancy. Braxton Hicks contractions are the body's way of
preparing for true labor, but they do not indicate that labor has begun or is going to
start.

Braxton Hicks contractions are a normal part of pregnancy. They may be

uncomfortable, but they are not painful. Women describe Braxton Hicks contractions
as feeling like mild menstrual cramps or a tightening in a specific area of the
abdomen that comes and goes.

Braxton Hicks contractions can be differentiated from the contractions of true labor.
Braxton Hicks contractions are irregular in duration and intensity, occur infrequently,
are unpredictable and non-rhythmic, and are more uncomfortable than painful.
Unlike true labor contractions, Braxton Hicks contractions do not increase in
frequency, duration, or intensity. Also, they lessen and then disappear, only to
reappear at some time in the future. Braxton Hicks contractions tend to increase in
frequency and intensity near the end of the pregnancy. Women often mistake
Braxton Hicks contractions for true labor. However, unlike true labor contractions,
Braxton Hicks contractions do not cause dilatation of the cervix and do not
culminate(berujung) in birth.

Patof
Kontraksi Braxton Hicks diduga berperan dalam mengencangkan otot rahim untuk
persiapan proses kelahiran. Kadang-kadang kontraksi Braxton Hicks disebut sebagai
"latihan untuk persalinan". Kontraksi Braxton Hicks tidak menyebabkan dilatasi
serviks tetapi mungkin berperan dalam pelunakan serviks.

Kontraksi intermiten otot rahim juga dapat berperan dalam meningkatkan aliran
darah ke plasenta. Darah yang kaya oksigen mengisi ruang intervili rahim di mana
tekanannya relatif rendah. Adanya kontraksi Braxton Hicks menyebabkan darah
mengalir sampai ke chorionic plate di sisi janin plasenta. Dari sana darah yang kaya
oksigen memasuki sirkulasi janin.