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IUGR.pptx

This document provides information about intra-uterine growth retardation (IUGR). It begins with general and specific objectives of the topic. IUGR is defined as fetal growth restriction, and can be classified as symmetrical or asymmetrical based on onset and organ size. Causes include maternal, fetal, placental and unknown factors. Diagnosis involves ultrasound to measure head circumference, abdominal circumference, femur length and amniotic fluid. Complications for the fetus include hypoxia, acidosis, hypoglycemia and multi-organ failure. Long term risks include delayed development and metabolic syndrome in adulthood.

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INTRA–UTERINE GROWTH RETARDATION Presented by Ms Mamatha B.Sc Nursing
GENERAL OBJECTIVES The group will be able to gain knowledge regarding intra uterine growth retardation
SPECIFIC OBJECTIVES The group will be able to 1. To Introduce the topic IUGR 2. To Define IUGR 3. To Explain about SGA 4. To Explain about IUGR and its types. 5. To Enumerate the etiology of IUGR and its pathophysiology. 6. To enlist diagnostic evaluation and its management along complication.
Introduction Intra uterine growth retardation (IUGR) is when a fetus in the womb does not grow as expected. The fetus as not as big would be expected for the stage of the mother’s pregnancy due to poor maternal nutrition or lack of adequate oxygen supply to the fetus. It can occur in preterm, term or post-term babies.
Definition Intra uterine growth restriction or retardation is defined as to be present in those babies whose birth weight is below the 10th percentiles of the average for the gestational age. Or A condition where the fetus fails to achieve its genetic growth potential and consequently is at risk of increased perinatal morbidity and mortality.
Incidence In developed countries its over all incidence is about 2 - 8%. The incidence among the term babies is about 5% and that among the post term babies is about 15%. In India the incidence of IUGR has been found to be 6- 7%. Nomenclature Small for gestational age (SGA) and IUGR are too often used synonymously although there is a degree of overlap.
IUGR Vs SGA Characteristics IUGR SGA Definition Growth of a fetus is restricted or retarded while in the uterus Size of the fetus is small for gestational age. Appearance Babies always appear mal nourished. Babies appear small and do not always appear to be mal nourished Diagnosis Ultra sound and Doppler of blood flow, measurements of fundus to the pubic bone. Ultrasound and measurements of the fundus to the pubic bone. Measurement Measure is based on the change in growth over time. Measure is based on a one time measurement that falls below a statistical value. Growth rate in utero Always slower than normal Can be normal or slower than normal Birth weight q Sometimes lower than normal but not always Always lower than normal Pathological condition Always due to sort of problem or disorder Not always due to disorder or a problem, sometimes the cause is small- sized mother.
Small for Gestational Age (SGA) Intra Uterine Growth Retardation (IUGR)
Normal fetal growth 1. Cellular hyperplasia- upto 16 weeks 2. Hyperplasia and hypertrophy- 16 to 32 weeks 3. Hypertrophy – after 32 weeks. Most of fetal weight gain (23) occurs beyond 24th week of pregnancy.
Types Based on clinical evaluation and ultrasound examination Based on time of onset, relative size of their head, abdomen and femur 1.symmetrical 2. asymmetrical
Based on clinical evaluation and ultrasound examination 1. Fetuses who are small and healthy The birth weight is less than 10th centiles for their gestational age. They have normal ponderal index, normal subcutaneous fat and usually have uneventful neonatal course. 2. Fetuses where growth is restricted by pathological process(IUGR).
Based on time of onset, relative size of their head, abdomen and femur Difference between symmetrical and asymmetrical Symmetrical Asymmetrical 1. Affected from the noxious effect very early in the phase of cellular hyperplasia.- 20% 1. Affected in the later months during the face of cellular hypertrophy about 80% 2. Total cell number is less but the size of the cell is normal 2. Total cell number remains same but the size of cell is smaller. 3. Often caused by structural, chromosomal abnormalities or congenital infection(TORCH) (intrinsic to fetus) 3. Pathological process that too often results due to maternal diseases. (Extrinsic fetus) 4. Neonatal course is complicated with poor prognosis 4. Usually uncomplicated having good prognosis 5. HC: AC and FL: AC- are normal 5. Elevated.
Maternal Fetal Placental Unknown Etiology
Maternal 1. Constitutional 2. Maternal nutrition 3. Social deprivation 4. Maternal disease 5. Toxins 6. Antiphospholipid antibody syndrome 7. Extra uterine pregnancy 1. Constitutional • Small women, maternal genetic and racial background • Not at increased risk • Pre-pregnancy weight less than 100 pounds • Reduced intrauterine growth of the mother is a risk factor .
2. Maternal nutrition before and during pregnancy -Glucose, amino acids and oxygen are deficient during pregnancy 3. Social Deprivation effects of associated lifestyle factors such as smoking, alcohol or other substance abuse, and poor nutrition. 4. Maternal diseases Anemia(sickle cell disease, hereditary anemias), hypertension, thrombotic diseases, heart diseases, chronic renal disease, collagen vascular disease
5. Toxins Alcohol, smoking, cocaine, heroin, drugs 6. Antiphospholipid Antibody Syndrome maternal platelet aggregation and placental thrombosis. 7.Extrauterine Pregnancy
2. Fetal abnormalities: There is enough substrate in the maternal blood and also crosses the plecenta but it is not utilized by the fetus Fetal Substrate not utilized by fetus 1. Structural anomalies - cardiovascular, renal 2. Chromosomal abnormality - 8-12% growth retarded infants - Triploidy, aneuploidy - Trisomies( 13, 18, 21), Turner’s syndrome 3. Infection • TORCH and malaria 4. Multiple pregnancy Mechanical hindrance to growth and excessive fetal demand
3. Placental • Poor uterine blood flow to placental site for a long time • This leads to chronic placental insufficiency with inadequate substrate transfer • Placenta praevia, Abruption, circumvallate, infarction, mosaicism 4.Unknown- 40%
Pathophysiology • Reduced availability of nutrients in mother • Reduced transfer by placenta to fetus • Reduced utilisation by fetus Brain size (asymmetric) as well as cell no (symmetric) are reduced . Liver glycogen content is reduced Renal and pulmonary contribution to amniotic fluid are diminished due to reduced blood flow to these organs Oligohydramnios SGA fetus is at risk of intrauterine hypoxia and acidosis if severe Intra uterine fetal death.
Diagnosis Clinical • Palpation of uterus Fundal height Liqour volume Fetal mass • SFH Closely correlates with gestational age after 24 weeks Lag of 4 cm or more- IUGR Fairly sensitive (30-80%) Serial measurement is important • Maternal weight gain - stationary or falling during second half of pregnancy • Abdominal girth stationary or falling. Investigations Hemoglobin Blood group- ABO, Rh Urine- sugar, albumin, microscopy, culture and sensitivity HIV, STS TSH HbSAg OGTT.
Biophysical • First examination(16-20 weeks) should confirm gestational age, anomalies • USG • 2-3 weekly • 2.diagnosis of IUGR Sonographic predictive values that are commonly used are Head circumference (HC)  Abdominal circumference(AC) Femur length (FL) Amniotic Fluid Volume
Head circumference/ Abdominal circumference ratios 1-before 32 weeks Elevated- asymmetrical IUGR =1 - 32-34 weeks Normal – asymmetrical IUGR <1- after 34 weeks 85% IUGR fetuses are detected AC-Single most sensitive parameter 2-Femur length Not affected in asymmetric IUGR FL/AC =22 from 21 weeks to term FL/AC> 23.5- IUGR.
3-Amniotic fluid volume Vertical pocket of amniotic fluid <1 cm suggests IUGR Four quadrant technique –measuring vertical diameter of largest pockets of fluid found in each of 4 quadrants of uterus. The sum of results is AFI AFI 5 to 25 cm- normal AFI< 5 cm- oligohydramnios. 4-Anatomical survey: To exclude fetal abnormalities
Ultrasound Doppler parameters 1. Doppler velocimetry Elevated systolic or diastolic ratio, the resistance index(RI) and the pulsalioty (PI) indicate increased blood flow resistance and decrease in end diastolic velocity. It is associated with IUGR and Intra uterine fetal hypoxia. 2. Uterine Artery The presence of diastolic notch suggests incomplete invasion of placental trophoblasts to the uterine spinal arteries. It predicts possible development of pre-eclampsia. Normally the diastolic flow increases as pregnancy progress
3. Umbilical artery Decreased en diastolic velocity indicates increased placental vascular resistance. There is progressive decrease in the umbilical artery, end diastolic velocity – reduced fetomaternal O2 and nutrient exchange. 4. Umbilical artery Doppler study It should be primary surveillance tool in the IUGR fetus. It predicts, moderates acidosis and recommends delivery when there presence of AREDV
5. AREDV It indicates fetal jeopardy and poor perinatal outcome. 6. Umbilical venous pulsations Indicates inefficient cardiac output with rise in central venous pressure- impending cardiac failure. 7. Middle cerebral Artery (MCA) Method to assess the resistance to flow in the fetal brain circulation. Increased diastolic velocity (Brain sparing effect) is observed in IUGR due to cerebral vasodilatation in response to hypoxemia. 8. Biochemical markers A low level of PAPP-A in maternal serum in the first trimester of pregnancy is considered a marker of major risk factor for IGUR.
Complications 1. Fetal • Antenatal chronic fetal distress, fetal death, diminished amniotic fluid volume increases the likelihood of cord compression • Intranatal hypoxia, acidosis • After birth- immediate –late 2.Immediate • Asphyxia , bronchopulmonary dysplasia and RDS • Hypoglycemia due to shortage of glycogen reserve in liver because of chronic hypoxia • Meconium aspiration syndrome • Microcoagulation leading to DIC • Hypothermia
Complications • Pulmonary hemorrhage • Polycythaemia, anemia, thrombocytopenia • Electrolyte abnormalities , • Multiorgan failure • Increased perinatal mortality and morbidity 3. Late • Symmetrical growth retarded baby is likely to grow slowly after birth • Asymmetrical- catch up growth in early infancy
Long term complications: • retarded neurologic and intellectual development in infancy • Increased risk- metabolic syndrome in adult life: obesity, hypertension, diabetes, coronary heart disease • altered orexigenic mechanism that causes increased appetite and reduced satiety 4. Reduced no of nephrons- renal vascular hypertension • Maternal • Per se IUGR does not cause any harm to mother • Underlying disease process like pre-eclampsia, heart disease, malnutrition may be life threatening
Immediate neonatal mortality - 6 times more than normal newborn or even similar weight appropriate to shorter gestational age Most babies - die within 24 hours Morbidity rises to 50%. Management • Constitutionally small- no intervention • symmetric IUGR • investigated for anomalies, infections, genetic syndromes -No effective therapy • Placental disease or reduced placental blood flow May be given some treatment
General Antepatum evaluation Time of delivery Methods of delivery Care during vaginal delivery Immediate care of the baby after birth It includes
1.General No proven therapy for reversing IUGR once it has established • Adequate bed rest specially in left lateral position • Correct malnutrition by balanced diet- 300 extra calories per day • Appropriate therapy for complicating factors likely to produce IUGR • Avoidance of smoking, alcohol • Maternal hyperoxygenation at the rate of 2.5 mL/min by nasal prong ,for short term prolongation of pregnancy • Low dose aspirin (50 mg daily) in selected cases with history of thrombotic disease, hypertension, pre- eclampsia or IUGR 2. Antepartum evaluation Serial evaluations of fetal growth and assessment of well being should be done 1.USG: intervals of 3-4 weeks for assessment of BPD, HC/AC, fetal weight and AFI 2. Fetal well being kick count, NST, biophysical profile, amniotic fluid volume and cordocentesis for blood
1.General No proven therapy for reversing IUGR once it has established • Adequate bed rest specially in left lateral position • Correct malnutrition by balanced diet- 300 extra calories per day • Appropriate therapy for complicating factors likely to produce IUGR • Avoidance of smoking, alcohol • Maternal hyperoxygenation at the rate of 2.5 mL/min by nasal prong ,for short term prolongation of pregnancy • Low dose aspirin (50 mg daily) in selected cases with history of thrombotic disease, hypertension, pre- eclampsia or IUGR
2. Antepartum evaluation Serial evaluations of fetal growth and assessment of well being should be done 1.USG: intervals of 3-4 weeks for assessment of BPD, HC/AC, fetal weight and AFI 2. Fetal well being kick count, NST, biophysical profile, amniotic fluid volume and cordocentesis for blood gases 3 . Doppler ultrasound parameters
3. Time of delivery Factors to be considered: 1. Presence of fetal abnormality 2. Duration of pregnancy 3. Degree of growth restriction 4. Associated complicating factor 5. Degree of fetal compromise 6. Previous obstetric history 7. Availability of NICU Optimal time of delivery 1. Beyond 37 weeks Delivery should be done 2. Before 37 weeks a) Uncomplicated mild IUGR: General treatment Placental function may improve pregnancy is allowed to continue till at least 37 weeks
(b) Severe degree of IUGR • If lung maturation is achieved: Presence of phosphatidyl glycerol and L:S ratio at least 2 from amniotic fluid study termination • Lung maturation not yet achieved problems- prematurity, growth restriction Preterm IUGR requires highest level of NICU. Betamethasone therapy - <34 week Corticosteroid reduce risk of neonatal HMD and IVH
Methods of delivery Route and time decided considering: 1. Severity of IUGR 2. Maternal condition 3. Any other obstetric complication Low rupture of membranes followed by oxytocin • Beyond 34 weeks with favourable cervix and head is deep in pelvis • PGE2 gel when cervix unfavourable Intrapartum monitoring by clinical , continuous electronic and scalp blood sampling is needed as risk of intrapartum asphyxia is high Precautions Caesarean section without a trial of labour- when risks of vaginal delivery are more( fetal acidemia, absent or reversed diastolic flow in umbilical artery or unfavourable cervix)
Care during vaginal delivery • Equipped institution where intensive intranatal monitoring (clinical and electronic) is possible and having facilities for NICU. First stage • Ensure adequate fetal oxygenation by giving oxygen to mother by mask • Epidural analgesia is of choice • Labour carefully monitored preferably with continuous EFM Second stage • Birth should be gentle and slow to avoid rapid compression and decompression of head • Episiotomy may be done to minimise head compression • Tendency to delay is curtailed by low forceps • Cord is to be clamped immediately at birth Immediate care of the baby A pediatrician should be available at the time delivery The baby should be placed preferably in the neonatal intensive care unit.
Management protocol of IUGR •To confirm IUGR and type •To exclude cong malformation •To treat specific cause if found •Fetal surveillance • Daily fetal movement count • Cardiotocography, NST • Biophysical profile • Doppler USG parameters, umbilical vein
Management protocol of IUGR Pregnancy< 37 weeks Delivery Pregnancy >= 37 weeks Severe IUGR Mild IUGR •Increased rest •Folic acid •Increased fliud intake •General management •Fetal monitoring till 37 weeks Delivery Equipped centre Centre with limited facilities In utero transfer to a referral centre Fetal surveillance Reassuring Non reassuring fetal status fetal status Doppler after 1 week assess lung maturity Delivery
Assess lung maturity •L:S ratio •Phosphatidyl glycerol level Not mature Delivery Betamethasone therapy Delivery Mature
Presented by Ms Mamatha B.Sc Nursing