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Intrauterine Growth Retardation obstetrics and gynecology

Detailed presentation on Intrauterine Growth Retardation covering definition, types, risk factors, etiology, clinical features, diagnostic methods including ultrasound Doppler, and management strategies.

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INTRAUTERINE GROWTH RETARDATION
CONTENT • DEFINITION • RISK FACTORS • ETIOLOGY • TYPES • PATHOPHYSIOLOGY • CLINICAL MANIFESTATION • prediction and diagnosis • Management • Nursing diagnosis
• FGR is a syndrome where fetus fails to reach its growth potential due to several underlying disorders related to maternal, fetal or placental. • Small for Gestational Age (SGA) is defined as an estimated fetal weight below the 10th percentile for the gestational age. • Fetal Growth Restriction (FGR) is defined on a combination of measures of fetal size percentile and Doppler abnormalities. • FGR may be with early onset (<32 weeks) or late onset (>=32 weeks). • Growth restriction can occur in preterm, term or post term babies. DEFINITION
DEFINITION • If a baby is under-grown and below the 10th centile for weight, historically there has been for some an automatic assumption that as a fetus the baby has experienced intrauterine growth restriction (IUGR) • Wilkins-Haug and Heffner (2012) define IUGR as a rate of fetal growth that is less than the normal growth potential for a specific baby. • However, this does not mean that all SGA babies are small as a result of IUGR. • Some small babies are genetically small because they have small parents or grandparents and this familial factor determines their smallness. They are well, healthy babies who need to be treated accordingly.
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INCIDENCE FGR comprises about one-third of low birth weight babies. In high income group countries, its overall incidence is about 2-8%. The incidence among the term babies is about 5% and that among the post-term babies is about 15%.
TYPES • IUGR that begins early in the first trimester caused by a combination of intrinsic (transplacental infections or chromosomal/ genetic defects) and extrinsic factors, results in symmetrical fetal growth • Onset: Early pregnancy (1st or early 2nd trimester) • Features: Proportionate reduction in head circumference, length, and weight • Cause: ↓ Cell number • Common causes: • Chromosomal abnormalities (e.g., trisomies) • Congenital infections (TORCH) • Severe maternal malnutrition • Prognosis: Poorer (often permanent growth deficit) • IUGR that begins in the last trimester, caused by extrinsic factors, results in asymmetrical fetal growth • Onset: Late pregnancy (3rd trimester) • Features: Disproportionate growth • Head circumference relatively normal • Abdominal circumference reduced • ↑ Head-to-abdomen ratio (head-sparing) • Cause: ↓ Cell size • Common causes: • Uteroplacental insufficiency • Maternal hypertension / preeclampsia • Prognosis: Better (catch-up growth common) Symmetrical IUGR Asymmetrical IUGR
RISK FACTORS • Maternal age more than 35 years; • IVF singleton pregnancy; • Nulliparity; • BMI <20 or >35; • Previous pre-eclampsia; • Pregnancy interval <6 or >60 months. : • Maternal age >40 years; • Previous SGA baby; • Previous stillbirth; • Maternal SGA; • Chronic hypertension; • Diabetes with vascular disease; • Renal impairment; • Antiphospholipid syndrome; • Heavy bleeding similar to menses and Minor risk factors: Major risk factors:
ETIOLOGY
• Constitutional: Small women, slim, maternal genetic and racial background. • Age >40 years; • Maternal BMI ( <20 or >35}; • IVF singleton pregnancy; • Nulliparity; • Poor weight gain during pregnancy; • Anemia, • malnutrition; • Hypoxemia (lung disease}; • Smoking, alcohol, drugs; • Previous pre-eclampsia, SGA, stillbirth; • Pregnancy interval <6 or 􀂾60 months 1. MATERNAL • Pregnancy-induced hypertension, pre- eclampsia, to include HELLP syndrome • Congenital and acquired heart disease, to include chronic hypertension • Diabetes mellitus • Undernutrition, to include obesity. Underweight mother/small stature. Eating disorders • Drugs: therapeutic (anticancer, thyroid medication), recreational (narcotic, prescription) • Renal disease, collagen disorders, anaemia, thyroid disorders and epilepsy • Genetic diseases such as maternal phenylketonuria and cystic fibrosis
• Abruptio placenta • Placenta praevia • Chorioamnionitis • Abnormal cord insertion • Oligohydramnios • Poor uterine blood flow (maternal vascular malperfusion); • Infarction (5%}, abruption, • Diabetes with vascular disease; • Antiphospholipid syndrome; • Placental inflammation ( villitis) 2. FETAL • Structural anomalies • Congenital infection (CMY, TORCH} • Teratogen exposure (drugs) • Multiple pregnancy • Chromosomal/genetic abnormality (particularly trisomy conditions), including inborn errors of metabolism, dwarf syndromes • Intrauterine infection: toxoplasmosis, rubella, cytomegalovirus, herpes simplex (ToRCH) and syphilis 3. Placental
ETIOLOGY • Increased cord length; • Single umbilical artery; • Velamentous cord insertion; • Cord knot (true). 4. Cord Factors 5. UNKNOWN
PATHOPHYSIOLOGY
CLINICAL FEATURES At birth:- Low birth weight for gestational age (<10th percentile) -Thin, emaciated appearance (“wasted baby”); Appearance described as “old man look” -Dry, wrinkled skin due to Decreased subcutaneous fat -Loose, wrinkled skin -Relatively large head compared to body (head-sparing, especially in asymmetric IUGR) -Thin umbilical cord -Scaphoid (sunken) abdomen reduced subcutaneous fat -Thin, meconium-stained vernix caseosa -Pinna with cartilaginous ridges -Well-defined plantar creases Anthropometric findings :-Reduced weight most affected -Length mildly reduced -Head circumference relatively preserved (asymmetric IUGR) -All parameters reduced proportionally in symmetric IUGR Metabolic and systemic problems:-Hypoglycemia -Hypothermia -Hypocalcemia -Polycythemia → hyperviscosity -Meconium aspiration -Birth asphyxia Organ system manifestations :Respiratory distress -Poor feeding -Increased risk of necrotizing enterocolitis -infections Long-term consequences:-Postnatal growth failure -Neurodevelopmental delay (especially symmetric IUGR) Increased risk of adult diseases: hypertension, type 2 diabetes, ischemic heart disease (Barker hypothesis)
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PREDICTION AND DIAGNOSIS • CLINICAL : • Clinical palpation of the uterus for the fundal height, liquor volume and fetal mass may be used for screening. It is simple, safe and inexpensive. But it is less sensitive. • Symphysis Fundal Height (SFH): A lag of 3 cm or more suggests growth restriction. • Maternal weight gain remains stationary or, at times, falling during the second-half of pregnancy. • Measurement of the abdominal girth showing stationary or falling values. • BIOPHYSICAL: • Head Circumference (HC) and Abdominal Circumference (AC) ratios: If the fetus is affected by asymmetric FGR, the HC remains larger. The HC/ AC is then elevated. In symmetric FGR, both the HC and AC are reduced. The HC/ AC ratio remains normal. • AC is the single most sensitive parameter to detect FGR • Femur Length (FL) : not affected in asymmetric FGR. The FL/AC ratio is 22 at all gestational ages from 21 weeks to term. FL/AC ratio greater than 23.5 suggests FGR. • Amniotic fluid volume: Vertical pocket of amniotic fluid <1cm suggests iugr • Anatomical survey: To exclude fetal anomalies by sonography (aneuploidy, structural defects).
ULTRASOUND DOPPLER PARAMETERS • Doppler velocimetry: Elevated Systolic/Diastolic (SID) ratio, the Resistance Index (RI) and the Pulsatility Index (PI) indicate increased blood flow resistance and decrease in end diastolic velocity. These are associated with FGR and intrauterine fetal hypoxia. • Umbilical Artery (UA) Doppler study : should be the primary surveillance tool in the FGR fetus (RCOG). Reduced or Absent or Reversed End-Diastolic Velocity (AREDV) in the umbilical artery indicates fetal jeopardy and poor perinatal outcome. • Uterine Artery (UtA): The presence of diastolic notch suggests the possible development of pre-eclampsia IUGR and fetal demise. • Middle Cerebral Artery (MCA) Doppler: Reflects fetal adaptation (brain-sparing effect); ↓ MCA PI; ↑ Diastolic flow due to cerebral vasodilatation and Indicates chronic hypoxia • Cerebroplacental Ratio (CPR) = MCA PI / UA PI; Normal: > 1.0–1.1; Abnormal: < 1 → early marker of fetal compromise and is the Best single predictor of adverse outcome • Ductus venosus Doppler study can predict fetal acidemia and adverse perinatal outcome (still birth). It is used when UA Doppler study is abnormal • Ponderal index (PI): The degree of fetal wasting is judged by fetal Pl. PI below 10th centiles is taken as FGR.
ULTRASOUND DOPPLER PARAMETERS • Biochemical markers: • Maternal serum markers : • ↑MSAFP(Maternal Serum Alpha-Fetoprotein) and • ↑ hCG in the second trimester are the markers for IUGR by 5-10 fold. • Placental dysfunction markers: • ↓ PAPP-A (Pregnancy-Associated Plasma Protein-A) :Low in 1st trimester, Strongly associated with IUGR & preeclampsia • ↓ PlGF (Placental Growth Factor): Reflects impaired placental angiogenesis, Low levels → placental insufficiency
MANAGEMENT Fetuses that are constitutionally small (70%) require no intervention. • General • Rest, especially in left lateral position; • Improve nutritional status by balanced diet: 300 extra calories per day are to be taken; • To institute appropriate therapy for the associated complicating factors likely to produce growth restriction; • Avoidance of smoking, tobacco and alcohol; • Maternal hyperoxygenation at the rate of 2.5 L/min by nasal prong, for short-term prolongation of pregnancy; • Low-dose aspirin (75-150 mg daily) since 12 weeks may be helpful in very selected cases with history of thrombotic disease, hypertension, pre-eclampsia, or recurrent FGR; • Maternal hyperalimentation by amino acids can improve fetal growth if it was due to maternal malnutrition. Maternal hyperalimentation is only helpful when IUGR is due maternal malnutrition. It is not helpful when placental function is deficient; • Maternal circulatory volume expansion may be helpful in improving placental perfusion.
MANAGEMENT Antepartum evaluation: Serial evaluations of fetal growth and assessment of wellbeing should be done once the diagnosis is made • Ultrasound examination should be done at an interval of 1-2 weeks for the assessment of BPD, HC/ AC, fetal weight and AFI for high risk fetus (based on history, biochemistry, UtA Doppler or single SFH measurement <10th centile or serial measurements indicative of FGR). • Fetal wellbeing is assessed by • Kick count, • NST, • Biophysical profile, • Amniotic fluid volume • Monitoring • CTG • Monitoring frequency: CTG/ NST twice weekly. • Doppler ultrasound parameters are to be studied. • At present, there is no effective treatment to improve FGR. There is no proven treatment for FGR • Timing of delivery is a critical issue. This is to balance the risk of prematurity against the risk of continued pregnancy. Unless carefully judged, continued pregnancy may end in IUFD or organ damage due to hypoxia. • TIMING OF DELIVERY: • The factors to be considered are: (1) Presence of fetal abnormality; (2) Duration of pregnancy; (3) Onset ofFGR; (4) Associated complicating factor; (5) Underlying pathology (if known); (6) Results of antenatal fetal surveillance; and (7) Availability of neonatal intensive care unit (NICU).
DELIVERY • Delivery timing beyond 37 weeks is recommended • Before 37 weeks, • for uncomplicated mild IUGR: • General treatment applied • Placental function may improve • Pregnancy can continue until at least 37 weeks • Severe iugr: • If lung maturation is achieved : presence of phosphatidyl glycerol and L:S ratio ≥ 2 in amniotic fluid → consider delivery • If lung maturation is not achieved: • Risks include prematurity and growth restriction and Preterm IUGR infants need highest level NICU care • Betamethasone therapy recommended before 34 weeks gestation: Corticosteroids reduce risk of neonatal hyaline membrane disease (HMD) and intraventricular hemorrhage (IVH) • When delivery is to be done before 32 weeks, magnesium sulfate should be given ( additional) to the mother for fetal and neonatal neuroprotection. • Absolute indications for delivery: Irrespective of gestational age are: CTG/NST abnormalities: Reduced variability, repetitive late deceleration, severe PE with end-organ damage.
DELIVERY • Delivery method and timing depend on: • Severity of Intrauterine Growth Restriction (IUGR) • Maternal health status • Presence of other obstetric complications • Labor induction options: • Low rupture of membranes followed by oxytocin if beyond 34 weeks, cervix is favorable, and fetal head is low in pelvis • Prostaglandin E2 (PGE2) gel if cervix is unfavorable • Intrapartum monitoring includes: • Clinical assessment • Continuous electronic fetal monitoring • Scalp blood sampling • High risk of intrapartum asphyxia necessitates close monitoring • Opt for Caesarean section without trial of labour if vaginal delivery risks are high, such as fetal acidemia, absent or reversed diastolic flow in the umbilical artery, or an unfavourable cervix
NURSING DIAGNOSIS 1. Ineffective placental tissue perfusion related to vasospasm secondary to preeclampsia, hypercoagulable state due to APLA positivity as evidenced by stage 2 intrauterine growth restriction (IUGR), maternal hypertension, abnormal fetal growth parameter 2. Excess fluid volume related to: endothelial damage and capillary leakage secondary to preeclampsia as evidenced by edema, elevated blood pressure, proteinuria 3. Anxiety related to: high-risk pregnancy, fear of fetal loss or preterm delivery ,complex medical conditions and frequent monitoring as evidenced by: verbalization of concern, restlessness, difficulty concentrating 4. Deficient knowledge related to: complex pregnancy management, anticoagulation therapy, blood glucose monitoring, warning signs of preeclampsia 5. Disturbed sleep pattern related to: anxiety, hospital environment, physical discomfort (edema, headache) 6. Risk for fetal injury related to: reduced uteroplacental blood flow, maternal hypertension, hypercoagulability (APLA positive), poor glycemic control (prediabetes) 7. Risk for maternal injury related to: severe preeclampsia (risk of eclampsia), thromboembolic complications associated with APLA 8. Risk for unstable blood glucose level related to: insulin resistance during pregnancy, prediabetic state, stress response associated with high-risk pregnancy 9. Risk for impaired maternal–fetal attachment related to: prolonged hospitalization, fear of poor pregnancy outcome, emotional stress related to IUGR diagnosis
NURSING MANAGEMENT • Antenatal nursing management • Identify high-risk mother • PIH, anemia, diabetes, malnutrition, smoking • Monitor fetal well-being • Daily fetal movement count • Assist with USG & Doppler follow-up • Non-stress test (NST) / BPP • Maternal care • Encourage adequate nutrition & rest • Left lateral position → improves uteroplacental flow • Administer prescribed iron, folic acid, antihypertensives • Prepare for preterm delivery • Assist with antenatal corticosteroids • Counseling regarding NICU care • Intrapartum nursing management • Continuous fetal monitoring (CTG) • Observe for fetal distress & meconium • Maintain maternal oxygenation & hydration • Prepare for: • Operative delivery if fetal compromise • Neonatal resuscitation at birth • Postnatal nursing management • Thermoregulation • Prevent hypothermia • Warm chain, radiant warmer, skin-to- skin (KMC) • Glucose monitoring • Frequent blood sugar checks • Early feeding / IV glucose if needed • Prevent hypoglycemia • Feeding • Early, frequent feeds • Expressed breast milk preferred • Gavage feeding if weak suck
COMPLICATION • After birth: Immediate: Asphyxia, bronchopulmonary dysplasia and RDS; • Hypoglycemia due to shortage of glycogen reserve in the liver; • Meconium aspiration syndrome; • Microcoagulation leading to DIC; • Hypothermia; • Pulmonary hemorrhage; • Polycythemia, anemia, thrombocytopenia; • Hyperviscosity-thrombosis; • necrotizing enterocolitis; • Intraventricular hemorrhage (IVH); • Electrolyte abnormalities: hypocalcemia (due to hypoparathyroidism), hyponatremia, hyperphosphatemia (due to tissue break down), hypokalemia due to impaired renal function; • Multiorgan failure; • Increased perinatal morbidity and mortality. • Late: Asymmetrical FGR babies tend to catch up normal growth in early infancy • retarded neurological and cognitive function, delayed intellectual development in infancy • Other long-term complications are: • Increased risk of metabolic syndrome in adult life: obesity, hypertension, diabetes and Coronary Heart Disease (CHD). • LBW infants have an altered orexigenic mechanism that causes increased appetite and reduced satiety. • Reduced number of nephrons-causes renal vascular hypertension. Fetal: (A) Antenatal- (A) chronic fetal distress, (B) fetal death, (C) preterm birth; (B) Intrapartum-hypoxia and acidosis;
Intrauterine Growth Retardation obstetrics and gynecology