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FETAL GROWTH RESTRICTION (1).pptx management in pregancy antenatal care

Obstetrics fgr management guidelines scan antepartum management delivery

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FETAL GROWTH RESTRICTION PRESENTED BY DR MANASA.G (1ST YR PG) MODERATOR NAMES: DR.SUCHITRA DR.PADMASREE DR.MANISREE DR.SREELEKHA
Normal fetal growth  May be divided into 3 phases:  The initial phase - first 16 wks - Hyperplasia  Second phase - upto 32 wks – Hyperplasia & Hypertrophy  Third phase - > 32 wks – Hypertrophy  Corresponding fetal growth rates during these phases are: 5 g/d at 15 wks , 15 g/d at 24 wks , 30 g/d at 34 wks.  Symphysiofundal height (SFH) measured from upper border of symphysis pubis to uterine fundus increases by approx. 1cm/wk between 14 to 36wks.  Abdominal girth increases on average of 1inch/wk after 30wks(30 inches at 30wks in average built women)
Definition  FGR is a pathological condition in which a fetus has not achieved his genetic growth potential regardless of fetal size.  FGR & Small for Gestational Age (SGA) are not synonymous.  A fetus does not need to be small to be growth restricted.
 SGA is defined as an EFW or AC < 10th centile  Severe SGA as EFW or AC < 3rd centile  FGR is defined as SGA with abnormal Doppler indices such as Umbilical artery PI >95th centile (or) mean Uterine artery PI >95th centile (or) CPR <5th centile for gestational age >32 wks.  Classification of FGR:
Delphi concensus criteria: • Gestational age <32 wks • AC/EFW <3rd centile or the AEDF in Umbilical artery • AC/EFW <10th centile combined with Uterine artery PI >95th centile and/or Umbilical art PI >95th centile Early FGR • Gestational age >32 wks • AC/EFW <3rd centile (or) • Atleast 2 of the following- .AC/EFW <10th centile, .AC/EFW crossing centiles >2 quartiles on growth centiles(noncustomised centiles), .CPR <5th centile or Umbilical artery PI >95th centile. Late FGR
parameters Early onset FGR Late onset FGR Placental disease Severe Mild Umbilical art Doppler- abnormal Umbilical art Doppler- normal High assoc. with PE Low assoc. with PE Hypoxia Present May be present/absent Fetal maturity Immature with high tolerance to hypoxia Mature with low tolerance to hypoxia Morbidity & Mortality High Low(but common cause of late still birth)
Risk factors  Maternal :  Previous history of FGR  Previous still births  Previous PE  Extremes of reproductive age  Low socioeconomic status  Low pre pregnancy weight  Poor gestational weight gain  Poor nutrition  Short inter pregnancy interval  Smoker,substance abuse  Drugs & teratogens  Medical conditions like-chr HTN,PE,gestational Diabetes,SLE,Anti Phospholipid sundrome,asthma,cyanotic cong heart ds,vascular & renal ds,chrons ds  Anemia,beta thalassemia  Mullerian anomalies  Maternal infections  Fetal:  Genetic abnormalities  Multifetal gestation,  Congenital malformations  Drugs & teratogens  Infections- viral(rubella,CMV,herpes,varicella,herpes zoster,HIV),parasitic(toxoplasmosis,syphilis,malar ia)  Placental:  Placental & cord abnormalities  Placental insufficiency  Maternal medical conditions  Multifetal gestation  infections
Causes of smallness  4 reasons:  1.error in pregnancy dating  2.SGA:constitutionally small  3.SGA:fetal disease/anamoly/infection(non placental mediated smallness)  4.SGA:Placental insufficiency
Error in pregnancy dating:  If pregnancy is dated inappropriately a fetus can be misclassified as SGA.  Pregnancy should be dated acc to crown rump length until 13+6 wks gestation,or acc to head circumference from 14+0 wks.  Symmetry-  means that all fetal segments(head,abdomen,long bones) are small and that centiles of their measurements are comparable.  Asymmetry-  Related to more accentuated reduction of the abdomen,compared to other fetal segments.
 Constitutionally small fetuses:  These fetuses are small because they are genetically programmed to be so.  A)they are small from 2nd trimester  B)symmetrically small  C)have low 1st trimester risk for aneuploidy,low/normal placental hormones(PAPP-A,hcg)  D)maintain their growth velocity across gestation  E)have Normal fetoplacental Doppler patterns.  Structural or chromosomal abnormality:  Another group of small fetuses  Trisomy 18 MC(chromosomal abnormality)- usually assoc with multiple structural abnormalities visible on scan.  One example of structural abnormality-Gastroschisis(abd wall defect),abdominal measurement is smaller.  A)small from early second trimester  B)symmetrical/asymmetrical  C)have high 1st trimester risk for aneuploidy and low placental hormones  D)Maintain or reduce their growth velocity  E)have normal fetoplacental Doppler patterns.
 Fetal infection:  Several viral & parasitic pathogens are assoc to SGA.(unrelated to placental insufficiency)  When passed from mother to fetus,these pathogens lead to placental inflammation,lesions vascular endothelium,fetal viraemia,with direct inhibition of cellular multiplication,obliterating angiopathy and cytolysis.  This group has  A)small fetus since infected  B)usually asymmetrically small  C)low 1st trimester risk of aneuploidy and normal placental hormones  D)shows deceleration in growth velocity unless the infection is cured  E) usually normal fetoplacental Doppler patterns.
 placental insufficiency:  Interactions between maternal & fetal circulations in the placenta are fundamental for adequate exchange of nutrients and oxygen,by continuous physiological process called ‘waves of trophoblast migration’.  Inadequate placentation is consequent to the absence of muscle destruction and elastic portion of spiral arteries in trophoblast migration.  It leads to territory with high resistance to blood flow and decreased nutrition of intervillous space.  This is assoc with greater frequency of PE and SGA.  A)may start from 2nd trimester  B)asymmetrically small  C)has low 1st trimester risk for aneuploidy ,but low placental hormones(particularly PAPP-A)  D)progressive deceleration in growth velocity  E)likely to show abnormal fetoplacental Doppler patterns.
Diagnosis  The first step in the diagnosis of FGR is to identify women who are at high risk of developing FGR based on history & co morbid conditions.  Women with one or more risk factors should have a uterine art doppler assessment at 20-24 wks.  If ut.a doppler is abnormal with a PI >95th centile and/or diastolic notching, these women should be monitored with serial ultrasound from 26-28 wks of gestation.  Determination of gestational age is of utmost importance for the diagnosis of FGR.
Clinical examination:  women are routinely weighed at every antenatal visit. .Poor weight gain during pregnancy may be assoc with FGR. .Pre pregnancy weight or booking weight is an important independent indicator besides total weight gain in pregnancy.  The first line screening tool to assess fetal growth is abdominal palpation & assessment of fundal height. .Fundal height or symphysiofundal height is measured by tape from upper border of pubic symphysis to uterine fundus. .It usually corresponds in centimeters to gestational age between 20-36 wks. .FGR can be suspected if difference between expected & observed values in fundal height is 3cm or more.
Sonographic evaluation  Fetal biometry:  To assess BPD,HC,AC,FL & EFW.  AC & EFW are most accurate ultrasound parameters for the diagnosis of FGR.  AC/EFW <10th centile should be considered high risk for FGR.  Serial assessments of fetal biometry can identify the worsening of growth velocity in fetuses dignosed as SGA.  Placental morphology:  The placenta is graded from 0 to 3.  Placental changes are not specific for FGR but acceleration of placenta maturation may occur with FGR & PIH.
 Amniotic fluid volume:  Amniotic fluid volume reflects how the fetus has been coping during the previous 2-3wks.  FGR usually assoc with oligohydramnios,which indicates chronic fetal hypoxia.  Measured by Single deep pocket(SDP) & Amniotic fluid index(AFI).  SDP-normal values 2-8cm,<2cm – oligo.  AFI-normal values 8-25cm,<5cm – oligo. (after 20 wks gestation)  Interpretation of amniotic fluid volume is based on single deep vertical pocket over AFI.
Doppler paramaters Fetal maternal doppler assessment is gold standard to assess placental development & function.  Uterine art doppler:  UtA doppler reflects trophoblastic invasion that is completed at 23-24 wks gestation & placental development.  Measured at 11-14 wks and repeated in 2nd trimester.  Presence of U/L or B/L Uterine artery notching, indicates risk of PE,placental failure & FGR.  UtA PI >95th centile,assoc with AC/EFW <10th centile used to diagnose early onset FGR.  Normal UtA doppler may rule out FGR in high risk women.
 Umbilical artery doppler:  UA doppler reflects placental function and degree of placental insufficiency.  High UA PI (>95th centile)  with Positive EDF->50% placental insufficiency,  with Absent EDF ->70% placental insufficiency,  with Reverse EDF ->90% placental insufficiency.  UA doppler has an important role in differentiating early & late onset FGR.
 Middle cerebral artery doppler:  Reflects fetal response to placental insufficiency.  Cerebral vasodilatation,also known as ‘Brain sparing effect’,is a response of fetus to chronic hypoxemia.(inc in diastolic flow & dec in pulsatality)  Results in reduced MCA PI & reduced CPR (MCA/UA PI ratio) – are early signs of fetal hypoxia in SGA fetuses.  Brain sparing effect may develop in 2 scenarios- A)in early onset FGR,where UA was already abnormal bz of worsening of placenta function, B)in late onset FGR,UA is typically normal bz fetal metabolic needs are greater than placental capacity(small placenta)  Development of brain sparing effect is considered for timing of delivery in late onset FGR where UA is normal.  CPR is a marker of failure to reach growth potential at term and could help in identifying the at risk fetuses.  Normal CPR- >1,almost constant in last 10wks of pregnancy.  Pathological CPR -<1,FGR,neonatal acidosis,low birth weight.
 Ductus venosus doppler:  Reflects atrial pressure volume changes during cardiac cycle.  Normally,flow in DV is forward.moving towards heart.  Increased PI and absent or reverse a-wave in DV reflects onset of overt cardiac compromise.  DV PI >95th centile-high risk of fetal hypoxia.  Absent or reverse a-wave – fetal survival of longer than 1wk is unlikely.  Decision to deliver fetus is considered after giving steroids for lung maturity and magnesium sulphate for neuroprotection.
 Tests for maternal & fetal infections:  MC pathogens to be reported are CMV,toxoplasma,syphilis,& malaria.  Tuberculosis also assoc with fetal growth.  Malaria is known to be a significant cause of preterm birth and LBW worldwide.  Serological screening for CMV,toxoplasma sld be offered.  Test for malaria ,syphilis must be considered in high risk populations.  If screening results are positive ,the only way to assess fetal infection is C reactive protiene of amniotic fluid.  Different USG findings can be suggestive of fetal infections,but not diagnostic.(hydrops,ascites,placental enlargement,echogenic bowel,cataract,shortening of long bones,bone deformity,hepatosplenomegaly,ventriculomegaly etc.)
 Invasive antenatal diagnosis considered for chromosomal abnormalities.  Karyotype should be offered in severe SGA.
Management  Mainly includes monitoring fetal wellbeing and the decision of when and how to deliver the fetus to prevent neurological injury and stillbirth.
 Pharmacological:  Antiplatelet agents during pregnancy are assoc with consistent reductions in relative risk in PE,birth before 34 wks,SGA and other adverse outcomes.  Aspirin when started before 16 wks – showed reduced incidence in PE & SGA.  When started after 20 wks – no reduction observed.  Smoking cessation by 15 wks shown recuced incidence of LBW.
 Steroids,  Single course of antenatal glucocorticoids to accelerate fetal lung maturity,to reduce incidence of respiratory distress syndrome,intraventricular hemorrhage and death in FGR.  All patients with FGR who are planned for delivery between 24-34 wks gestation should receive steroids.  ACOG recommends extended steroid coverage between 34+0 to 36+6 wks of gestation.  RCOG recommends till 35+6 wks gestation.
 Magnesium sulphate,  A portion of growth restricted fetuses will be delivered preterm and are at high risk for cerebral palsy.  Maternal magnesium sulphate administration – shown to have neuroprotection & to reduce incidence of cerebral palsy in preterm infants.  Patients who are planned to deliver before 32 wks gestation should receive magnesium sulphate for neuroprotection.  RCOG recommends between 24+0 to 29+6 wks gestation.
Fetal surveillance: Early onset FGR Minimum surveillance frequency UA doppler PI >95th centile, No other testing abnormalities Every 2wks doppler, Weekly BPS or cCTG Low MCA PI or CPR Weekly doppler with BPS or cCTG UA AEDF Consider admission twice weekly doppler with BPS or cCTG UA REDF, Increased DV, Oligohydramnios(sdp<2) Admission 3times weekly doppler with BPS,daily cCTG Absent or reversed a-wave in DV Daily doppler with BPS or cCTG In preparation to delivery Late onset FGR Minimum surveillance frequency UA doppler PI >95th centile, No other testing abnormalities Weekly doppler with BPS Low MCA PI or CPR Doppler 2-3 times weekly with BPS
 Timing of delivery:  Timing of delivery remains the critical issue.  Delivery timing balances Risks of prolonging the pregnancy (i.e stillbirth)with the risks due to prematurity.  GA is critical in decision making.  As a thumb rule neonatal risk decreases with increasing GA.  Other critical issues in decision making is the interpretation of surveillance tests used to predict perinatal outcomes are sequence of doppler changes,BPP,cCTG
 Mode of delivery:  Mode of delivery depends primarily on the gestational age and any evidence of acidaemia.  Vaginal delivery can be allowed as long as there is no obstetric indication for caesarean and FHR pattern is normal.  Fetuses with major anomalies incompatible with life should be delivered vaginally.  In all case of FGR with features of acidosis– elective caesarean section should be performed without trail of labour.
 For near term fetus,  Delivery of a suspected growth restricted fetus with normal UA doppler , normal AFI and reassuring fetal testing can likely be deferred until 37-38 wks gestation.  If oligohydramnios present , delivery between 36+0 and 37+6 wks is recommended.  With normal FHR pattern vaginal delivery is planned.  Notably some of the fetuses cannot tolerate labor.
 Fetus remote from term,  If growth restriction is identified before 34 wks,with normal AFI,normal fetal surveillance findings – Observation is recommended.  As long as interval fetal growth and fetal surveillance test results are normal,pregnancy is allowed to continue.  Fetal growth Reassessment is typically made no sooner than 3 wks later.
Fetal & Neonatal problems associated with FGR  Fetal hypoxia and acidosis (repetitive late deccelerations,poor BPP,reversal of EDF in UA,abnormal venous doppler,blood gas analysis showing acidic pH)  Stillbirth  Oligohydramnios (common finding)  Neonatal complications (signs of soft tissue wasting,thin skin,little s/c fat,abdomen is scaphoid,protruberant ribs,reduced muscle mass,umbilical cord is thin & limp,frequently meconium stained,birth wt < 10th centile,thrombocytopenia,elevated nucleated rbc count)  Respiratory distress syndrome  Meconium aspiration syndrome
 Persistant fetal circulation (frequent sequel to hypoxia & acidosis,pulm hypertension develops,blood flow ductus arteriosis persists even after birth,rt to lt shunting with no structural heart defect)  Intraventricular haemorrhage  Newborn encephalopathy (cerebral edema,intracranial bleed or infarct,cerebral palsy)  Hypoglycemia  Hypocalcemia  Hyperviscosity syndrome (high hematocrit,polycythemia,lead to sluggish blood flow,thrombosis,congestive heart failure,pulmonary edema)
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