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    Normal Fetal Development & Growth: Obstetrics

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    Fetal development is dependent on the transfer of nutrients and oxygen across the placenta from the mother. Factors that can affect normal fetal growth include the mother's weight, height, age, ethnicity, and medical conditions as well as fetal sex, genetic defects, infections, and placental function. Restricted fetal growth is associated with higher rates of complications like mortality and morbidity. The fetus has distinct circulatory, respiratory, immune, and other body systems that allow for development and adaptation to the in utero environment.

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    Normal Fetal Development & Growth: Obstetrics

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    Fetal development is dependent on the transfer of nutrients and oxygen across the placenta from the mother. Factors that can affect normal fetal growth include the mother's weight, height, age, ethnicity, and medical conditions as well as fetal sex, genetic defects, infections, and placental function. Restricted fetal growth is associated with higher rates of complications like mortality and morbidity. The fetus has distinct circulatory, respiratory, immune, and other body systems that allow for development and adaptation to the in utero environment.

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    Fetal development is dependent on the transfer of nutrients and oxygen across the placenta from the mother. Factors that can affect normal fetal growth include the mother's weight, height, age, ethnicity, and medical conditions as well as fetal sex, genetic defects, infections, and placental function. Restricted fetal growth is associated with higher rates of complications like mortality and morbidity. The fetus has distinct circulatory, respiratory, immune, and other body systems that allow for development and adaptation to the in utero environment.

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    63 views6 pages

    Normal Fetal Development & Growth: Obstetrics

    Uploaded by

    api-3829364
    Fetal development is dependent on the transfer of nutrients and oxygen across the placenta from the mother. Factors that can affect normal fetal growth include the mother's weight, height, age, ethnicity, and medical conditions as well as fetal sex, genetic defects, infections, and placental function. Restricted fetal growth is associated with higher rates of complications like mortality and morbidity. The fetus has distinct circulatory, respiratory, immune, and other body systems that allow for development and adaptation to the in utero environment.

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    of 6

    Obstetrics

    Dr. Hana Lec: -1-


    7-Oct-06

    Normal fetal development & growth

    Fetal growth & maturation

    Determinants of birth weight are multi-factorial


    Fetal growth is dependent on adequate transfer of nutrients & oxygen across the
    placenta.

    Factors affecting normal fetal growth

    A- Physiological variables affecting normal fetal growth include

    1- pre-pregnancy weight & maternal booking weight


    2-maternal height
    3-maternal age & parity
    4- ethnic group
    5- fetal sex
    6paternal height

    B-Other factors affecting intrinsic growth potential\

    • Reduced fetal growth potential

    1- chromosome defects,e.g.trisomy 18, tiploidy


    2- single gene defects,e.g. seckl` s syndrome.
    3-structural abnormalities ,e.g. renal agenesis.
    4- infections ,e .g , CMV, toxoplasmosis.

    Reduced fetal growth support

    A- maternal factors

    Under nutrition ,e .g, poverty. Eating disorders


    Maternal hypoxia ,e .g, altitude, cyanotic heart disease
    Drugs ,e .g, cigarette smoking, alcohol, cocaine.

    1
    Placental factors

    Reduced uteroplacental perfusion


    Inadequate trophoblastic invasion, APS, diabetes mellitus, sickle cell disease, multiple
    gestation.
    Reduced feto-placental perfusion ,e.g., single umbilical artery , twin pregnancy.
    3-fetal hormones
    1-insulin-like growth factors (IGFs)
    2- insulin
    3- thyroid hormone
    4-cortisol

    In developed countries , the average birth weight is about 3.5 kg at the end of a
    normal pregnancy lasting an average of 40 weeks.

    Growth- restricted fetuses have significantly


    • *Higher perinatal mortality & morbidity rate
    *hypoxia/asphyxia
    * stillborn
    *HIE
    *hypothermia
    *hypoglycaemia
    * infection & necrotizing entercolitis
    * in adulthood they are at great risk of hypertension, IHD, DM.

    Cardiovascular system

    the fetal circulation is quite different from that of the adult.


    Its distinctive features are as follow .
    1-oxygenation occurs in the placenta not the lungs
    2- the right & the left ventricles work in parallel rather than in series
    3- the heart , brain & upper body receive blood from the left ventricle, while the
    placenta &the lower body receive blood from both right & left ventricles.
    Modifications in fetal vascularity ensure that the best , oxygenated blood from the
    placenta is delivered to fetal brain.
    1- the ductus venosus
    2- the foramen ovale
    3-the ductus arteriosus

    2
    Respiratory system

    Full differentiation of capillary & canalicular elements of the fetal lung is apparent
    by 20 weeks gestation.
    Alveoli develop after 24 weeks.
    The lung alveoli are lined by a group of phospholipids known collectively as
    surfactant.
    Surfactant prevents the collapse of small alveoli during expiration by lowering surface
    tension. it is continually replaced by synthesis from type 2 alveolar cells.
    The predominant phospholipids (80%) is phosphotidylcholine (lecithin), the
    production of lecithin is enhanced by cortisol, growth restriction & prolonged rupture
    of the membrane. its production is delayed by diabetes.
    Other phospholipids ,is phosphotidylglycerol

    Normal lung development requires an adequate amniotic fluid volume & fetal
    breathing movement

    Causes of pulmonary hypoplasia


    1- oligohydramnios
    2- decreased intrathoracic space (e.g. ,diaphragmatic hernia )
    3-chest wall deformities
    Respiratory distress syndrome
    It is specific to babies born prematurely& is associated with surfactant deficiency.

    3
    Complications
    1-hypoxia & asphyxia
    2-intraventricular haemorrhage
    3- necrotizing entercolitis

    Prevention
    The incidence &severity of RDS can be reduced by administering steroids antenatally
    to mothers at risk of preterm delivery.
    Fetal blood
    The bone marrow starts to produce red cells at 7-8 weeks & is the predominant source
    of red cells from 26 w gestation.
    Most Hb in the fetus is fetal Hb (HbF) , which has two gamma chains. This differs
    from the adult Hb (Hb A & Hb A2).
    At term the ratio of Hb F/ Hb A is 80/20.after 6 months only 1% of Hb F persists.
    Thalassaemia are a group of genetic haematological disorders characterized by
    reduced or absent production of one or more of the globin chains of Hb.
    B thalassaemia
    Alpha thalassaemia

    Immune system

    The fetus enquire an effective immune system to resist intrauterine & perinatal
    infection.
    Lymphocytes appear from 8 w & by the middle of the second TM all phagocytes ,T
    &B cells &complement are available to mount a response.
    IgG originates mostly from the maternal circulation & cross the placenta to provide
    passive immunity.
    The fetus normally produces only small amounts of IgM & IgA which do not cross
    the placenta
    General immunological defenses include
    Amniotic fluid (lysosomes, IgG)
    The placenta (lymphoid cells ,phagocytes, barrier).
    Granulocytes from liver
    Interferon from lymphocytes

    Skin & homeostasis

    Fetal skin protects & facilitates homeostasis. A stratum corneum forms in the fifth
    month & after approximately 23 w the appearance of the skin approaches that of the
    adult epidermis.`
    During the last weeks , skin is covered by vernix, which consists of desquamated skin
    cells ,cholesterol & glycogen.
    Preterm babies have no vernix &thin skin, this allows a proportionately large amount
    of insensible loss.
    Thermal control in cool , ambient temperatures is limited by a large surface-to-body-
    weight ratio&poor thermal insulation.
    Heat may be conserved by peripheral vasoconstriction & can be generated by brown
    fat catabolism.
    The response to warm ambient temperature is also poor ,due to poor response of
    eccrine gland & can result in overheating of the infant.

    4
    Alimentary system & energy stores

    The primitive foregut & hind gut are present by the end of the fourth week &at this
    stage the intestine is almost a straight tube , suspended by the mesentery from the
    dorsal body wall . the midgut herniates into the base of the umbilical cord during the
    sixth week .re-entering the abdominal cavity by 12 weeks
    Failure of this process will result in development of an omphalocele.
    The fetus continually & increasingly swallows amniotic fluid. Up to approximately 20
    ml/h at term.
    Peristalsis in the intestine occurs from the second TM. The large bowel is filled with
    meconium at term.
    While the body water content gradually diminishes , glycogen & fat stores increase
    about five fold in the last TM.
    Preterm infants have virtually no fat ,poorly developed alimentary system therefore
    are more prone to hypoglycemia within the early neonatal period.

    Fetal liver & gallbladder

     The primitive liver appears at about the 8th day of embryonic life as
    adiverticulum arising from the duodenum.
     The large portion of this diverticulum gives rise to paranchymal cells &
    hepatic ducts, while the smaller portion gives rise to the gallbladder.in utero
    ,the normal metabolic functions of the liver are performed by the placenta .
     The fetal liver has a reduced ability to conjugate bilirubin because of relative
    deficiencies in glucuronyl transferase.

    The loss of placental route of excretion of unconjugated bilirubin, particularly in the


    premature infant, may result in transient unconjugated hyperbilirubinaemia
    (physiological jaundice).
    Fetal liver play an important role in haemopoiesis, which starts at 6 w, peak at 12-16
    w continues until approximately 36 w.
    Glycogen is stored within the liver in small quantities in the1st TM ,but storage is
    maximum at 3rd TM.

    Kidney &urinary tract

    After regression of Wolffian duct, the metanephros forms the renal collecting
    system(ureter, pelvis, calyces & collecting ducts)& induces the formation of the renal
    secretary system (glomeruli, convoluted tubes ,loops of henle)from the mesenchyme
    of the nephrogenic cord. Nephrogenesis is complete by 36 w,but the maturation of the
    excretory &concentrating ability of the fetal kidneys is gradual.
    Fetal urine forms much of the amniotic fluid, which is a protein free, sugar free
    hypotonic ultra-filtrate of fetal plasma. Fetal urine production rises gradually with
    fetal maturation reaching about 38 ml/h at 40 w
    Renal agenesis therefore result in sever reduction or absence of amniotic fluid
    (oligohydramnios)

    5
    Fetal behavior

    Quickening can 1st be perceived by the mother at 18 w in primigravida & two weeks
    earlier in multigravida
    1F is similar to quiet sleep (non REM ), with an absence of eye &body movement.
    2F periodic eye &body movement(REM) sleep
    3F has eye movement but no body movements(I,e.equivalent to quiet wakefulness)
    4F is an active phase with ongoing eye movement & fetal activity.

    Amniotic fluid

    The A.F is initially secreted by the amnion, but by the 10th w it is mainly a transudate
    of the fetal serum via the skin & umbilical cord. From 16 w gestation, the fetal skin
    becomes impermeable to water &the net increase in AF is through a small imbalance
    between the contributions of fluid through the kidneys & lung fluid& removal by fetal
    swallowing .AF increases progressively reaching about 1000 cc at 38 w,but there is a
    rapid fall in volume (at 40 w = 350 ml)
    Function of AF is to
    1-protect the fetus from mechanical injury
    2-permit movement of the fetus while preventing limb contructure
    3-prevent adhesions between fetus &amnion
    4- permit fetal lung maturation
    Oligohydramnios, caused by renal agenesis, cystic kidneys, IUGR.
    Polyhydramnios caused by anencephaly, esophageal/ duodenal atresia

    Written By:
    Rand Aras Najeeb

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