intra uterine growth retardation

Intra Uterine Growth Intra Uterine Growth RetardationRetardation

Dr. Waffa FageehDr. Waffa Fageeh

(Consultant and assistant (Consultant and assistant professor King Abdulaziz professor King Abdulaziz University Hospital)University Hospital)

INTRODUCTIONINTRODUCTION

Fetal growth restriction (FGR) is the term Fetal growth restriction (FGR) is the term used to designate a fetus that has not used to designate a fetus that has not reached its growth potential because of reached its growth potential because of genetic or environmental factors. This term is genetic or environmental factors. This term is an inaccurate label when used to describe an inaccurate label when used to describe the constitutionally small and otherwise the constitutionally small and otherwise healthy fetus.healthy fetus.

FGR is a major focus of Prenatal care, FGR is a major focus of Prenatal care, because there is an inverse relationship because there is an inverse relationship between the fetal/neonatal weight percentile between the fetal/neonatal weight percentile and parental morality.and parental morality.

DEFINITIONDEFINITION

Intrauterine growth restriction (IUGR), fetal growth Intrauterine growth restriction (IUGR), fetal growth restriction (FGR), small for gestational age (SGA), and restriction (FGR), small for gestational age (SGA), and low birth weight (LBW) are all terms used to describe low birth weight (LBW) are all terms used to describe small babies. The most common definition of fetal small babies. The most common definition of fetal growth restriction refers to a weight below the 10growth restriction refers to a weight below the 10thth percentile for gestational age.percentile for gestational age.

As many as 70 percent of fetuses who are estimated As many as 70 percent of fetuses who are estimated to weigh below the 10to weigh below the 10thth percentile for gestational age percentile for gestational age are small simply due to constitutional factors such as are small simply due to constitutional factors such as female sex or maternal ethnicity, parity, or body mass female sex or maternal ethnicity, parity, or body mass index; they are not at high risk of perinatal mortality index; they are not at high risk of perinatal mortality and morbidity.and morbidity.

Normal GrowthNormal Growth

Is compromised of three consecutive and somewhat Is compromised of three consecutive and somewhat overlapping phasesoverlapping phases

The first phase is referred to as cellular hyperplasia The first phase is referred to as cellular hyperplasia (the first 16 weeks of gestation)(the first 16 weeks of gestation)

The second phase, known as the phase of concomitant The second phase, known as the phase of concomitant hyperplasia and hypertrophy (between the 16hyperplasia and hypertrophy (between the 16thth and and 3232ndnd weeks) increases in cell size and number. weeks) increases in cell size and number.

The third phase, the phase of cellular hypertrophy The third phase, the phase of cellular hypertrophy (between the 32(between the 32ndnd week and term) rapid increase in week and term) rapid increase in cell size.cell size.

Quantitatively, normal singleton Quantitatively, normal singleton fetal growth increases from fetal growth increases from approximately approximately 5g/day at 14 to 5g/day at 14 to 15 week of gestation to 15 week of gestation to 10g/day at 20 weeks and 30-10g/day at 20 weeks and 30-35g/day at 32 to 34 weeks35g/day at 32 to 34 weeks, , after which the growth rate after which the growth rate decreases.decreases.

The median growth rate in The median growth rate in multiple gestations is lowermultiple gestations is lower than that of singletons during the than that of singletons during the 33rdrd trimester. trimester.

Abnormal growthAbnormal growth

Abnormal growthAbnormal growth Symmetric FGR :Symmetric FGR : comprises 30 percent of FGR, (all comprises 30 percent of FGR, (all

fetal organs are decreased proportionally) due to fetal organs are decreased proportionally) due to impairment of early fetal cellular hyperplasia.impairment of early fetal cellular hyperplasia.

Asymmetric FGRAsymmetric FGR : : comprises 70 percent of FGR is comprises 70 percent of FGR is characterized by a relatively greater decrease in characterized by a relatively greater decrease in abdominal size (eg. Liver volume and subcutaneous abdominal size (eg. Liver volume and subcutaneous fat tissue) then head circumference. It results from the fat tissue) then head circumference. It results from the capacity of the fetus to adapt to a hostile environment capacity of the fetus to adapt to a hostile environment by redistributing blood flow in favor of vital organs by redistributing blood flow in favor of vital organs (eg. Brain, heart, placenta) at the expense of non-vital (eg. Brain, heart, placenta) at the expense of non-vital fetal organs (eg. Abdominal viscera, lungs, skin, fetal organs (eg. Abdominal viscera, lungs, skin, kidneys).kidneys).

FETAL ETIOLOGIESFETAL ETIOLOGIES

GeneticGenetic Congenital anomalyCongenital anomaly Multiple gestationMultiple gestation


Genetic: contributes to Genetic: contributes to approximately 40 percent of the approximately 40 percent of the variation in birth weight, most variation in birth weight, most likely of symmetric type.likely of symmetric type.


Congenital anomaly: 22 percent Congenital anomaly: 22 percent of anomalous infants were growth of anomalous infants were growth restricted.restricted.


Multiple gestations: fetal growth in multiple Multiple gestations: fetal growth in multiple gestations has a direct relationship to the gestations has a direct relationship to the number of fetuses present;number of fetuses present;

The type of placentation also plays a role.The type of placentation also plays a role. Growth is similar to that of singletons until Growth is similar to that of singletons until

28-30 weeks28-30 weeks And then slows (15-20 percent less than that And then slows (15-20 percent less than that

of singletons of the same gestational age)of singletons of the same gestational age)

PLACENTAL PLACENTAL ETIOLOGIESETIOLOGIES Placental sizePlacental size: which is a gross measure of : which is a gross measure of

placental capacity, is 24 percent lower in placental capacity, is 24 percent lower in growth restricted infants than in normally grown growth restricted infants than in normally grown infants when adjustments are made for infants when adjustments are made for gestational agegestational age

Gross placental structural anomalies: Gross placental structural anomalies: includes single umbilical artery, velamentous includes single umbilical artery, velamentous umbilical cord insertion, placental hemangioma, umbilical cord insertion, placental hemangioma, and possibly placenta previa. However, there is and possibly placenta previa. However, there is no single uteroplacental or villous pathalogical no single uteroplacental or villous pathalogical lesion that consistently results in FGR.lesion that consistently results in FGR.

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES

1.1. Poor nutritionPoor nutrition

2.2. HypoxiaHypoxia

3.3. Prothrombotic disordersProthrombotic disorders

4.4. Hypertension and vascular diseaseHypertension and vascular disease

5.5. Infection Infection

6.6. Substance abuseSubstance abuse

7.7. toxintoxin

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES Poor nutrition-Poor nutrition- severe maternal starvation during severe maternal starvation during

pregnancy ex (the pregnancy ex (the Dutch populationDutch population suffered severe suffered severe famine during the winter of 1944-45; mean maternal famine during the winter of 1944-45; mean maternal {caloric intake fell from 750 to 450 kcal/day}{caloric intake fell from 750 to 450 kcal/day} average infant birth weight during this period decreased average infant birth weight during this period decreased by by 250 grams250 grams). Similarly, the average ). Similarly, the average birth weight birth weight fell by more than 500 gramsfell by more than 500 grams in in Leningrad Leningrad during during the world war 2 German siege, which resulted in a the world war 2 German siege, which resulted in a longer a more profound starvation period (down to longer a more profound starvation period (down to 300 300 kcal of mostly carbohydrateskcal of mostly carbohydrates and no proteins). and no proteins).

Modest degrees of nutritional deficiency also have an Modest degrees of nutritional deficiency also have an effect on birth weight, women who are underweight at effect on birth weight, women who are underweight at the start of the pregnancy or have poor weight gain the start of the pregnancy or have poor weight gain during the pregnancy are at higher risk of delivering an during the pregnancy are at higher risk of delivering an infant weighing less than 2500 grams.infant weighing less than 2500 grams.

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES Chronic maternal hypoxia due to Chronic maternal hypoxia due to

pulmonary disease, cyanotic heart pulmonary disease, cyanotic heart disease and sever anemia (as with disease and sever anemia (as with sickle cell anemia) are often sickle cell anemia) are often associated with FGR, as an example.associated with FGR, as an example.

Residing at high altitudes also results Residing at high altitudes also results in a chronic hypoxemia state and in a chronic hypoxemia state and lower birth weight.lower birth weight.

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES Hematological and immunological Hematological and immunological

disorders:disorders: that cause thrombosis of the that cause thrombosis of the intervillous space and thus decreases intervillous space and thus decreases uteroplacental perfusion (eg, uteroplacental perfusion (eg, antiphospholipid syndrome)antiphospholipid syndrome)

Hypotension and vascular disease: Hypotension and vascular disease: maternal medical disorders (eg, maternal medical disorders (eg, nephropathy, collagen vascular disease) and nephropathy, collagen vascular disease) and obstetrical complications (eg, preclampsia) obstetrical complications (eg, preclampsia) associated with vasculopathy and diminished associated with vasculopathy and diminished uteroplacental perfusionuteroplacental perfusion

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES Infection: viruses and parasitesInfection: viruses and parasites (eg, rubella, (eg, rubella,

toxoplasmosis, cytomegalovirus, varicella-zooster, toxoplasmosis, cytomegalovirus, varicella-zooster, malaria) (to the fetus transplacentally or across the malaria) (to the fetus transplacentally or across the membranes) mainly early in pregnancy. There is membranes) mainly early in pregnancy. There is less less evidence implicating bacterial infectionevidence implicating bacterial infection as an as an etiology for FGR, although maternal infection with etiology for FGR, although maternal infection with listeria, TB, Chlamydia, and mycoplasma have been listeria, TB, Chlamydia, and mycoplasma have been reported to increase the risk of FGR. reported to increase the risk of FGR.

Substance abuse-Substance abuse- including cigarette smoking, alcohol including cigarette smoking, alcohol consumption and elicit drug abuse can cause FGR direct consumption and elicit drug abuse can cause FGR direct or indirectly from related variables such as inadequate or indirectly from related variables such as inadequate nutrition. nutrition. Smoking during the 3Smoking during the 3rdrd trimester appears trimester appears to have the greatest impact on birth weight, and to have the greatest impact on birth weight, and women who quit smoking by the 3women who quit smoking by the 3rdrd trimester have trimester have birth weights similar to those of nonsmokers.birth weights similar to those of nonsmokers.

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES Toxins:Toxins: Toxic exposures,Toxic exposures, for various medications such as for various medications such as

warfarinwarfarin, anticonvulsants, antineoplastic agents, and , anticonvulsants, antineoplastic agents, and folic acidfolic acid antagonist, can produce FGR with specific antagonist, can produce FGR with specific dismorphic features, dismorphic features, antihypertensiveantihypertensive medications, medications, high high caffine caffine consumption (>300 mg/day) unclear.consumption (>300 mg/day) unclear.

Environmental tobacco smoke Environmental tobacco smoke (ETS) and infant (ETS) and infant birth weight. Most studies showed and increased risk birth weight. Most studies showed and increased risk of low birth weight in women with ETSof low birth weight in women with ETS

MATERNAL MATERNAL ETIOLOGIESETIOLOGIES Sociodemographic variables:Sociodemographic variables: include include

racerace, pregnancy at the , pregnancy at the extremes of extremes of reproductive lifereproductive life, and , and previous FGR previous FGR neonate.neonate.

Chronic maternal stress:Chronic maternal stress: is an active area is an active area of investigation. It is associated with elevated of investigation. It is associated with elevated corticotrophin-releasing hormone (CRH) corticotrophin-releasing hormone (CRH) levels, which > FGR and preterm birth.levels, which > FGR and preterm birth.

Paternal factors have less effects on birth Paternal factors have less effects on birth weight than maternal.weight than maternal.

Initial Diagnostic Initial Diagnostic EvaluationEvaluation Diagnosis of FGR is based upon Diagnosis of FGR is based upon

sonographic findings, which are sonographic findings, which are discussed in details separately.discussed in details separately.

A complete hx and physical examination A complete hx and physical examination is performed to detect risk factors.is performed to detect risk factors.

Fetal karyotyping is suggested if FGR is Fetal karyotyping is suggested if FGR is early (< 32 weeks), severe (> 3early (< 32 weeks), severe (> 3rdrd percentile), or accompanied by percentile), or accompanied by polyhydramnios (suggestive of trisomy polyhydramnios (suggestive of trisomy 18) or structural.18) or structural.

Initial diagnosis and Initial diagnosis and managementmanagement

When there is a clinical suspection of viral When there is a clinical suspection of viral infection maternal serum should be infection maternal serum should be examined for evidence of seroconversion. examined for evidence of seroconversion. Specific amniotic fluid viral DNA testing Specific amniotic fluid viral DNA testing can also be performed, sonographic can also be performed, sonographic markers for viral infection are often non-markers for viral infection are often non-specific but include echogenecity and specific but include echogenecity and classification of brain and liver and classification of brain and liver and hydrops.hydrops.

Assessment for congenital and acquired Assessment for congenital and acquired thrombophilic disorders maybe considered.thrombophilic disorders maybe considered.

SUBSEQUENT OBSTETRICAL SUBSEQUENT OBSTETRICAL MANAGEMENTMANAGEMENT

Periodic asessment :Periodic asessment : once or twice weekly once or twice weekly from the age of viability, using (BBP) and from the age of viability, using (BBP) and Doppler velocimentry is acceptable. To Doppler velocimentry is acceptable. To identify those fetuses who are at highest risk identify those fetuses who are at highest risk of utero demise and thus may benefit from of utero demise and thus may benefit from intervention by preterm delivery.intervention by preterm delivery.

UltrasoundUltrasound evaluation of fetal growth. evaluation of fetal growth. Serial examinationsSerial examinations should be performed should be performed

with the frequency based upon the severity with the frequency based upon the severity of findings (once to seven times per week) or of findings (once to seven times per week) or fetal growth (ever 2-4 weeks).fetal growth (ever 2-4 weeks).

Antenatal Antenatal corticosteroidscorticosteroids The efficiency of antenatal The efficiency of antenatal corticosteroids corticosteroids in the in the

management of the preterm growth restricted fetus management of the preterm growth restricted fetus remains controversial.remains controversial.

Fetal blood sampling-Fetal blood sampling- Antipartum fetal hypoxemia Antipartum fetal hypoxemia and acidemia are not associated with neonatal cerebral and acidemia are not associated with neonatal cerebral disfunction if fetal cardiovascular compensation with disfunction if fetal cardiovascular compensation with increased cerebral bloodflow occuring. However, if increased cerebral bloodflow occuring. However, if asphyxia persists, brain damage and death may occurasphyxia persists, brain damage and death may occur

Fetal blood sampling (FBS) for in severly growth Fetal blood sampling (FBS) for in severly growth restrictesd fetuses to assist in the identification of the restrictesd fetuses to assist in the identification of the optimal timing for delivery. However, fetal loss may optimal timing for delivery. However, fetal loss may

occur.occur.

Medical interventionsMedical interventions

Antenatal treatment for the growth Antenatal treatment for the growth restricted fetus is benifitial. Nutritional restricted fetus is benifitial. Nutritional suplementation, plasma volume suplementation, plasma volume expansion, low-dose expansion, low-dose aspirinaspirin, , heparinheparin, bed , bed rest, maternal rest, maternal oxygen therapyoxygen therapy, and beta-, and beta-mimetics/calcium channel blockers were mimetics/calcium channel blockers were used to improve blood flow to the used to improve blood flow to the placenta. placenta. None have consistantly None have consistantly been shown to be of value.been shown to be of value.

Antihypertensive therapy of hypertensive Antihypertensive therapy of hypertensive gravidus doesn't improve fetal growthgravidus doesn't improve fetal growth

Intapratum Intapratum managementmanagement Labour with careful intrapartum Labour with careful intrapartum

monitroing and vaginal delivery is monitroing and vaginal delivery is a reasonable approach in the a reasonable approach in the presence of normal antenatal presence of normal antenatal testing. The clinician should be testing. The clinician should be prepared for rapid intervention if prepared for rapid intervention if there is any evidence of fetal there is any evidence of fetal intolerance to labourintolerance to labour

Recurrence RiskRecurrence Risk

The tendancy to repeat SGA or The tendancy to repeat SGA or low birth weight deliveries in low birth weight deliveries in succesive pregnancies are around succesive pregnancies are around 9 and 29 percent, respectively.9 and 29 percent, respectively.

intra uterine growth retardation

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