I. U .G.R.SignificanceI.U.G.R. is a major cause of neonatal morbidity & mortality. Certain adult diseases including hypertension & diabetes are related to I.U.G.R.
DefinitionI.U.G.R. Is defined as failure of the fetus to acheive its genetic growth potential . S.G.A.: fetus or neonate is below a certain defined centile of weight or size for a particular gestational age ( below 3 rd or 5 th centile ) ,and SGA are constitutionally small due to normal genetic influences. While IUGR indicates that a particular pathological process is operating to modify the intrinsic growth potential of the fetus by reducing its growth rate .
Recent definition of IUGR■Early ‐onset growth restriction < 32 weeks. ■AC or EFW <3rd centile or absent EDF in the umbilical artery ■or ■1) AC/EFW <10th centile combined with ■2) Uterine artery PI >95th centile and/or ■3) Umbilical artery PI >95th centile ■Late ‐onset growth restriction > 32 weeks.
Incidence of IUGR 3-5%Aetiology1-Reduced fetal growth potential (intrinsic) A-chromosome defect e.g trisomy 18 , triploidy. B-single gene defects e.g seckel’s synd. C-structional abn. e.g renal agenesis D-infection e.g TORCH
Aetiology2-Reduced fetal growth support (extrinsic) A- maternal factors : 1.Undernutrition e.g poverty , eating disorders . 2.Maternal hypoxia e.g altitude , cyanotic heart disease . 3.drugs:cigarette smoking , alcohol, cocaine , warfarin, phenytoin, cytotoxic drugs.
1-Reduced utero –placental perfusion: e.g inadequate trophoblast invasion ( e.g HT, PET ), Antiphospholipid syn. ,D.M with vascular lesions advanced ), sickle cell disease , multiple pregnancy .
2-Reduced feto – placental pefrusionA-single umbelical artery. B- twin – twin trasfusion syn.
ComplicationsAntepartum complications 1- stillbirth (fetal death in IUGR more frequent after 35 weeks of gestation ) . 2- oligohydramnios ( in severe IUGR due to vasoconstriction in the fetal kidney results in impaired urine production ). 3- Antepartum fetal distress.
Intrapartum complicationsIntrapartum fetal hypoxia & acidosis Increased incidence of c/s Due to marked depletion of energy stores in the liver & subcutaneous tissues .
Neonatal complications1- Related to perinatal asphyxia & acidosis : Persistent fetal circulation , meconium aspiration syn. ,hypoxic – ischemic encephalopathy . 2- Metabolic alterations : hypoglycemia , hypocalcemia , hyperviscosity syn. ,hyperbilirubinemia, hypothermia .
Neon atal complications 3- Related to the specific cause of IUGR Infection , cong. Malformations , chromosomal abn.
Classifications1- Intrinsic IUGR (symmetric ) : due to fetal condition e.g infection , chromosomal abn. 2-Extrinsic (Asymmetric) : due to element outside fetus ( placental condition or maternal disease ) . 3- Combined IUGR (both intrinsic & extrinsic factors ). 4- Idiopathic IUGR.
Comparison of symmetric & Asymm. IUGRSymmetric Asymmetric 1-symmetrically small 1-head larger than abdomen 2-Normal ponderal index 2-Low ponderal PI=8 ±2 index PI<7 3-Normal head/abd. 3-Elevated head / & femur /abd. Ratio abd.& femur/abd. ratio.
4-Genetic disease , infection . 4-placental vascular insuffiency 5-complicated neonatal 5-benign Course neonatal course Poor prognosis
Diagnosis1-clinical diagnosis: A-medical & obs. History Chronic HT , PET, Ch. Renal disease, twin pregnancy, advanced DM, prior history of delivery of IUGR . B-Decrease maternal weight gain during pregnancy ( insensitive sign ). C- Uterine fundal height :is most common method used .
Symphysis–fundal height■symphysis–fundal height (SFH), the distance ■from the symphysis pubis to the uterine fundus, is measured ■at each midwife or antenatal attendance from 24 weeks’ gestation. ■As a guide, the SFH in centimetres is equal to the ■number of weeks of gestation plus or minus 2 cm. ■After 36 weeks, the acceptable difference increases to 3 cm.
Diagnosis2- u/s biometry BPD, head circumference, abd. Circumference,femur length. Amount of liquor :oligohydramnios.
Diagnosis3- Doppler waveform analysis During pregnancy:umbilical & uterine artery have low resistance & low S/D ratio . In IUGR : decreased or absent diastolic flow or reversed diastolic blood flow.
■the concept of ‘brainsparing’ ■involves redistribution of blood by dilatation of the cerebral vessels, thus increasing substrate and oxygen supply to the brain, in response to fetal chemoreceptor or baroreceptor stimulation. ■ results in ■ a reduction in fetal MCA PI. ■this is associated with increasing impedance in the ■umbilical artery.
Cerebroplacental ratio■By using the ratio of MCA to umbilical artery Doppler PI – ■ the cerebroplacental ratio. ■Reduced CPR in IUGR
Diagnosis4- Amniocentesis Every week after 36 weeks for fetal lung maturation. 5- Cordocentesis Umbilical cord blood sampling (rarely indicated ). For rapid determination of fetal karyotype when chromosomal defect is suspected .
(a) Normal uterine artery Doppler waveforms(b) abnormal uterine artery Doppler waveforms. The waveform in (b) has reduced diastolic flow velocities and an early diastolic notch.
Umbilical artery Doppler waveforms: (a) normal; (b) absent end ‐diastolic flow; (c) reversed end ‐diastolic flow.
Management 1.At present no accepted treatment available for growth restriction related to placental dysfunction . 2.Obvious adverse factors :smoking, alcohol &drug abuse should be stopped. 3.Health of the mother should be maximized (optimal control of DM, thyroid dysfunction, HT ). 4.When growth restriction is severe & the fetus is considered too immature to be delivered :bed rest in hospital is advised to
to maximize placental blood flow. 5. Antepartum assesment of fetal wellbeing By fetal biometry every 2 weeks , Doppler u/s & fetal cardiotocography (NST). Absence of blood flow in the umbilical artery or reversed flow (i.e back towards the heart requires delivery in the near future or when NST is non- reactive .
NST daily in severe cases . Less severe cases : NST weekly or twice weekly .No effective drug therapy for IUGR has yet been found .Small studies suggested aspirin , nitric oxide donors , or anti- oxidants may be helpful in some cases . These drugs may act by reducing platelet activation in the utero- placental circulation , or may be acting directly as vasodilators.
Labour■Because of the high incidence of hypoxia & acidosis , labour & delivery should be aggresively managed . ■Continuous fetal heart monitoring ( scalp monitoring electrode & uterine pressure catheter . ■Shorten the second stage of labour by forceps . ■Epidural anesthesia is the method of choice for pain relieve .
Labour■Pediatrician should be present at delivery . ■Placenta need careful examination by pathologist :for cause of IUGR .
Prognosis1.The length of the insult seems to be more important than its severity in terms of both somatic growth & neurologic development .so the earlier in pregnancy that IUGR is detected the greater the probability of developmental problems later in life . 2. The probability of developmental problems is lower when there is catch – up growth during the first 6 months of life .
Prognosis3. The worst prognosis is for babies with IUGR caused by congenital infections or chromosomal defects . 4. A link between IUGR & the adult incidence of both hypertension & DM has now been established .