Iugr obs

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Iugr obs

  1. 1. Intrauterine Growth Restriction Prof. M.C.Bansal MBBS,MS,MICOG,FICOG Professor OBGY Ex-Principal & Controller Jhalawar Medical College & Hospital Mahatma Gandhi Medical College, Jaipur.
  2. 2. Definitions IUGR: A condition where the fetus fails to achieve its genetic growth potential and cosequently is at risk of increased perinatal morbidity & mortality. SGA: Infant with weight < 10th percentile of those born at the same gestational age or > 2 SDs below mean for Gestational Age.
  3. 3. Easiest way to think about these terms are IUGR: is a term used by Obstetrician to describe a pattern of growth over a period of time. SGA: is a term used by Pediatrician to describe a single point on a growth curve.
  4. 4. Incidence 3 - 5% of all pregnancies. 20 % of stillborns are growth retarded. 1/3 of infants with BW < 2750 gms are growth retarded and not premature. Only 20-30% of growth restricted fetuses are small due to pathological restriction of growth. Perinatal mortality is 8 - 10 times higher for these fetuses.
  5. 5. Normal Intrauterine Growth pattern Stage I (Hyperplasia) - 4 to 20 weeks - Rapid mitosis - Increase of DNA content Stage II (Hyperplasia & Hypertrophy) - 20 to 28 weeks - Declining mitosis. - Increase in cell size.
  6. 6. Normal Intrauterine Growth pattern Stage III ( Hypertrophy) - 28 to 40 weeks - Rapid increase in cell size. - Rapid accumulation of fat, muscle and connective tissue. 95% of fetal weight gain occurs during last 20 weeks of gestations.
  7. 7. Classification Based on evaluation & USG examination small fetuses are divided into two categariesHealthy SGA or True IUGRorConstitutionally small Pathologically growthrestricted Type –I Type –II Symmetrical IUGR Asymmetrical
  8. 8. Symmetrical IUGR(20-30%)
  9. 9. Symmetrical IUGR Etiology- Structural Congenital malformation Chromosomal Intrauterine Infection -Toxoplasma,Rubella,Cytomegalovirus,Herpes simplex Toxins & DrugsNeonatal course- Complicated with poor prognosis
  10. 10. Asymmetrical IUGR(70-80%)
  11. 11. Asymmetrical IUGR Etiology- Maternal Diseases - Chronic hypertention Renal diseases Vasculopathy Placental Insufficiency Neonatal course- Uncomplicated and good prognosis
  12. 12. Comparison between PFGR and Normal SGANormal, Small for gestation Pathological GrowthAge RestrictionBirth weight <10% Birth weight usaully <10% but may be <25%Birth weight <2500gms Birth weight usaully <2500gms but may be largerNormal Ponderal Index Low Ponderal IndexNormal subcutaneous fat Decreased subcutaneous fatNormal nucleated blood red Elevated nucleated blood redcells & thrombocytopenia cells & thrombocytopeniaUneventful neonatal period Complicated neonatal periodusually
  13. 13. Etiology1) Fetal factors: Genetic Factors: - Race, ethnicity, nationality - sex ( male weigh 150 -200 gm more than female ) -genetic disorders ( Achondroplasia, Russell - silver syn.) Chromosomal anomalies: - Chromosomal deletions - Trisomies 13,18 & 21
  14. 14. Etiology Congenital malformations: Anencephaly, GI atresia, potter’s syndrome, and pancreatic agenesis. Fetal Cardiovascular anomalies Congenital Infections: mainly TORCH infections. Inborn error of metabolism: - Transient neonatal diabetes - Galactosemia - PKU
  15. 15. Etiology2) Maternal Factors: Decrease Uteroplacental blood flow: - Pre eclampsia / eclampsia - chronic renovascular disease - Chronic hypertension Maternal malnutrition Multiple pregnancy Drugs - Cigarettes, alcohol, heroin, cocaine - Teratogens, antimetabolites and therapeutic agents such as trimethadione, warfarin, phenytoin
  16. 16. Etiology Maternal hypoxemia - Hemoglobinopathies - High altitudes• Others - Short stature - Younger or older age (<15 and >45) - Low socioeconomic class - Primiparity - Grand multiparity - Low pregnancy weight - Previous h/o preterm IUGR baby - Chronic illness ( DM, renal failure, cyanotic heart
  17. 17. Etiology3) Placental Factors: Placental insufficiency ( most imp in 3rd trimester) Anatomic problems: – Multiple infarcts – Aberrant cord insertions – Umbilical vascular thrombosis & hemangiomas – Premature placental separation – Small Placenta
  18. 18. DiagnosisClinical Biophysical Biochemical Ultrasonography MSAFP & hCG in 2nd trimester Erythropoietin level in cord blood is high in IUGR
  19. 19. Diagnosis- Clinically Maternal weight gain- Stationary or falling during second half of pregnancy Palpation of uterus-  Symphysio Fundal Height-Normally increases by 1 cm per week between 14 – 32 wks - A lag in fundal height of 4 wks s/o moderate IUGR and over 6 wks s/o severe IUGR
  20. 20. ComplicationsFETAL Antepartum-  Oligohydroamnios  Fetal distress  Fetal death Intrapartum-  Fetal Acidosis  Fetal Hypoxia
  21. 21.  MATERNAL-Per se fetal growth restriction does not causeany harm to mother. But underlying disease progress like pre- eclampsia, heart diseases, malnutrition may be life threatening. A woman with a growth restricted infant , risk of having another is two fold.
  22. 22. Prevention Strategies include – prenatal care modalities for high risk screening – protein/energy supplementation – vitamin/mineral supplementation – fish oil supplementation – prevention and treatment of  Hypertensive disorders  Infection  Anemia
  23. 23. Prevention Strong evidence of benefit only for the following interventions: – balanced protein/energy supplementation & maternal volume expansion – strategies to reduce maternal smoking – antibiotic administration to prevent urinary tract infections and – antimalarial prophylaxis. Few statistically significant reductions in the risk of IUGR have been demonstrated with other interventions.
  24. 24. Antenatal Fetal Surveillance The purpose is to identify further progression of the disease process that would jeopardize the foetus to a point that it would be better to be delivered than to remain in utero. There are four testing modalities which are helpful –Daily fetal movement count,Non- Stress Test, Amniotic Fluid Index, Doppler of the Umbilical Artery & Biophysical Profile, each of which addresses different aspects of surveillance. Combination of tests are better than an isolated test.
  25. 25.  Some more complex protocols have been also proposed like— Kramer & Weiner suggested that UmA doppler is more reliable because severely abnormal doppler findings can precede an abnormal FHR by several weeks. Harman & Baschat suggested a different strategy which includes multiple venous & arterial doppler and Biophycal profile
  26. 26. MANAGEMENT Suspect IUGR clinically Confirm IUGR & Type of IUGRSymmetrical Asymmetrical-Screening for TORCH Management dependsupon-USG to r/o cong.malformation -Complicatingfactor-Fetal blood sampling to r/o -Previous obshistory- Chromosomal abnormality -Gestational Age
  27. 27. TreatmentIUGR has many causes, therefore, thereis not one treatment that always works.
  28. 28. Treatment Although there are many causes of IUGR, the treatment consists of either delivery or remaining in utero and improving blood flow to the uterus. When blood flow is improved, the delivery of oxygen and other nutrients to the foetus occurs. If the foetus is lacking in these substances, their increased availability may result in improved growth and development.
  29. 29. Treatment 1.Maternal Bed RestThis is the initial approach for thetreatment of IUGR.Adequate bed rest in left lateral positionresults in increased blood flow to theuterus & placenta.
  30. 30. Treatment
  31. 31. Treatment 2. Aspirin Therapy(1- 2mg/kg/day) The use of aspirin to treat fetuses with IUGR is still controversial. If aspirin is used, it may be advantageous if given to patients before 20 weeks of gestation. It is minimal to limited benefit if given at the time of diagnosis (third trimester). The Maternal-Fetal Medicine Network randomized 3135 women to receive 60mg/d aspirin or placebo
  32. 32. Aspirin Therapy(1- 2mg/kg/day) However it is benificial in cases with history of thrombotic disease, hypertension, pre-eclampsia.
  33. 33. Treatment 3.Hyperoxygenation Fetal oxygenation is crucial for fetal growth . A positive response to maternal oxygen therapy found by decreased resistance in placental circulation is marker of good prognosis and lack of response is an indication of poor outcome. (Bilardo et al 1991)
  34. 34. Treatment Other forms of treatment that have been studied are maternal hyperalimantation by aminoacids,nutritional supplementation, zinc supplementation, fish oil and hormones. Maternal volume expansion may be helpful in improving placental perfusion. Limited studies are available regarding the use of these modalities in the treatment of IUGR.
  35. 35. Judge Optimum Time Of DeliveryRISK OF PREMATURITY RISK OF IUDDifficult extra uterine Hostile intra uterine existence environment
  36. 36. Management according to Gestational Age Less than 24 weeks of gestational age Antenatal surveillance with Umbilical & Ductus venosus doppler study is reliable. If UmA diastolic flow +nt If UmA –RDF DV – Uninterrupted DV– Interrupted forward flow forward flow Fetal Acidosis& Hypoxia Expectant Management Imminent Fetal Death Termination
  37. 37. Less than 24 weeks of gestational age There is no evidence that corticosteroids accelerate the fetal pulmonary maturity or prevent the development of Intraventricular haemorrhage. On the other hand, there is evidence that the use of steroids in severe IUGR may cause hemodynamic decompensation (Simchen et al 2004).
  38. 38. 26 to 34 weeks Gestational Age Antenatal surveillance with NST and Umbilical A, Middle cerebral A, Ductus venosus doppler. 1. NST-Reactive UmA Doppler-Reassuring Repeat in 1wk UmA Doppler-Non reassuring Ductus venosus Doppler Reassuring--Repeat in1wk Non reassuring—Deliver
  39. 39. 2. NST-Non reactive UmA Doppler—follow as above Or Biophysical profile ≥8 UmA doppler ≤4 Deliver 6 Repeat in 6-24hrs wait till ≥36wks Deliver
  40. 40. 34 to 37 weeks Gestational AgeAntenatal surveillance with FHR monitoring by NST and Color doppler velocimery.1. Both the tests reassuring Repeat in 1wk Test for lung maturity Immature Mature Repeat in 1 wk Deliver2.Either test non reassuring Deliver
  41. 41. Delivery of Pathological Growth Restricted Fetus The full term fetus has a large capacity to tolerate the hypoxic stress of labour which is substantially reduced in PGRF due to marked depletion of energy stores in liver & subcutaneous tissue. Thus, intrapartum asphyxia is the major cause of perinatal morbidity & mortality in
  42. 42.  Therefore, when umbilical doppler shows Absent flow or Reverse flow Fetal aciosis & hypoxia is more common Delivery by cesarean section is indicated
  43. 43.  Now ,the question is how to deliver the PGRF with lesser degrees of doppler or FHR abnormalities. Skinner et al (1998) and Li et al (2003)Conclusion- Vaginal delivery is notcontraindicated in patients with resistance inUmA velocimetry but cesarean delivery shouldbe anticipated in a large number of them. Indications for LSCS in IUGR pregnancies1. Established fetal acidosis2. Absent or Reverse flow in UmA doppler3. Unfavourable cervix
  44. 44. Precautions to be taken during delivery Delivery should be in an equipped institution with Intensive intranatal monitoring & neonatal intensive care facilities. Continous FHR monitoring Amnioinfusion in early stage of labour if amniotic fluid volume is decreased. Second stage of labour requires special attention. Second stage should not be prolonged > 2 hrs in nulliparous and 1 hr in multiparous . Placenta needs careful examination as in many cases it will provide evidence about the etiology of the problem (Rayburn et al 1989).
  45. 45. Amnioinfusion Amnioinfusion refers to the instillation of fluid into the amniotic cavity. This procedure is typically performed during labor through an intrauterine pressure catheter introduced transcervically after rupture of the fetal membranes. Alternatively, fluid can be infused through a needle transabdominally, the reverse process of amniocentesis.
  46. 46. Randomised trial of amnioinfusion during labour with meconium stained amniotic fluid (BJOG Jan 2002) Conclusion- Amnioinfusion in an under resourced labour ward decreases caesarean section rates and fetal morbidity
  47. 47. TH YA ON UK

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