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- 1. Intra Uterine Growth Retardation Prof.Surendra Nath Panda, M.S. Dept.of Obstetrics & Gynecology M.K.C.G.Medical College Berhampur, Orissa, INDIA
- 2. Intra Uterine Growth Retardation Intra Uterine Growth Restriction Small for gestational age (SGA) Foetal growth restriction 'wasted' and 'stunted' Please also see notes pages for more details in most of the slides
- 3. Definition Intrauterine growth retardation (IUGR) occurs when the unborn baby is at or below the 10th weight percentile for his or her age (in weeks). The foetus is affected by a pathologic restriction in its ability to grow. Low birth weight (LBW) means a baby with a birth weight of less than 2500Gms, which could be due to IUGR or Prematurity Please also see notes pages for more details in most of the slides
- 4. Classification Symmetricl the baby's head and body are proportionately small. may occur when the foetus experiences a problem during early development. Asymmetrical baby's brain is abnormally large when compared to the liver. may occur when the foetus experiences a problem during later development In a normal infant, the brain weighs about three times more than the liver. In asymmetrical IUGR, the brain can weigh five or six times more than the liver.
- 5. Classification Newer Classification: 1. Normal small fetuses- have no structural abnormality, normal umbilical artery & liquor but wt., is less.They are not at risk and do not need any special care. 2. Abnormal small fetuses- have chromosomal anomalies or structural malformations. They are lost cases and deserve termination as nothing can be done. 3. Growth restricted fetuses- are due to impaired placental function.Appropriate & timely treatment or termination can improve prospects.
- 6. Aetiology The foetal growth is dependent on multiple factors. IUGR resulting in SGA babies can result from many factors known and unknown either acting alone or in conjunction or in association . The aetiologic determinants of IUGR have two measures of effect: relative risk and etiologic fraction. Most of the evidence on aetiologic determinants is based on observational studies and systematic overviews or meta-analyses of such studies. In a majority of cases (40%) the cause is unknown– probably due to placental insufficiency (idiopathic).
- 7. Aetiology 1. General- Racial / Ethnic origin, Small maternal / paternal height / weight, Foetal sex. 2. 3. 4. 5. Maternal causes. Foetal causes. Placental causes. Idiopathic- In a majority of cases (40%) the cause is unknown– probably due to placental insufficiency.
- 8. Maternal Risk Factors Has had a previous baby who suffered from IUGR. Extremes of age. Is small in size (Ht & Wt). Has poor weight gain and malnutrition during pregnancy. Is socially deprived. Uses substances (like tobacco, narcotics, alcohol) that can cause abnormal development or birth defects. Has a low total blood volume during early pregnancy.
- 9. Maternal Risk Factors Is pregnant with more than one baby. High altitude. Drugs like anticoagulants, anticonvulsants. Has a cardio-vascular disease-preeclampsia, hypertension, cyanotic heart disease, cardiac disease Gr III & IV, diabetic vascular lesions. Chronic kidney disease Chronic infection- UTI, Malaria, TB, genital infections Has an antibody problem that can make successful pregnancy difficult (antiphospholipid antibody syndrome, SLE).
- 10. Fetal Risk Factors Exposure to an infection-German measles (rubella), cytomegalovirus, herpes simplex, tuberculosis, syphilis, or toxoplasmosis, TB, Malaria, Parvo virus B19. A birth defect (cardiovascular, renal, anencephally, limb defect, etc). A chromosome defect- trisomy-18 (Edwards’ syndrome),21(Down’s syndrome), 16, 13, xo (turner’s syndrome. A primary disorder of bone or cartilage. A chronic lack of oxygen during development (hypoxia). Developed outside of the uterus. Placenta or umbilical cord defects.
- 11. Placental Factors Uteroplacental insufficiency resulting from -. Improper / inadequate trophoblastic invasion and placentation in the first trimester. Lateral insertion of placenta. Reduced maternal blood flow to the placental bed. Foetoplacetal insufficiency due to-. Vascular anomalies of placenta and cord. Decreased placental functioning mass-. » Small placenta, abruptio placenta, placenta previa, post term pregnancy.
- 12. Diagnosis Intrauterine IUGR can be difficult to diagnose. Presence of risk factors. Inadequate growth detected by serial measurement of Wt., abdominal girth and fundal Ht. Ultrasound to evaluate the foetal growth. Inadequate foetal growth. Reduced AFI. Placental calcification.
- 13. Diagnosis Neonatal Low ponderal index (Wt./Fl). Decreased subcutaneous fat. Presence / appearance of – Hypoglycemia, Hyperbilirubinemia, Narcotizing enterocolitis, Hyper viscosity syndrome
- 14. Neonate and Placenta in IUGR Normal & IUGR Newborn babies Normal & IUGR Placentas
- 15. Prevention Strategies include prenatal care modalities, protein/energy supplementation, treatment of anaemia, vitamin/mineral supplementation, fish oil supplementation prevention and treatment of » hypertensive disorders, » foetal compromise » infection.
- 16. Prevention Strong evidence of benefit only for the following interventions: balanced protein/energy supplementation, 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.
- 17. Surveillance Unless delivery occurs, once treatment begins the foetus must undergo surveillance. The purpose - 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 -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.
- 18. Surveillance Non- Stress Test (NST) This simplest to perform test should b used first in the surveillance of IUGR foetuses. With the help of a heart rate monitor, the changes in the foetal heart rate with foetal movement are to be determined. If the heart rate increases more than 15 beats for more than 15 seconds, this is considered to be a reactive test. If the heart rate does not accelerate, remains flat, or decreases, then this is an abnormal test. The problem with this test is that it changes late in the course of the disease and is not an early predictor of adverse outcome.
- 19. Surveillance Amniotic Fluid Index (AFI) The vertical depth of four pockets of amniotic fluid are measured by USG, to obtain a total AFI. This method allows for comparison of changes in amniotic fluid with time. In the normal foetus the AFI remains relatively constant. In the foetus with IUGR, it may decrease slowly, or decrease abruptly with time. A decrease in AFI may occur before there are changes in the non-stress test.
- 20. Surveillance Amniotic Fluid Index (AFI) The current recommendations are that if the AFI decreases below 8 after 35 weeks, then delivery should occur.
- 21. Surveillance Doppler of the Umbilical Artery When IUGR is diagnosed, the value of sequential studies of the umbilical artery Doppler waveform is to determine if the Resistance Index is increasing or decreasing. If it is increasing, then this signifies a deteriorating condition.
- 22. Surveillance Biophysical Profile This test combines the NST and the AFI with foetal movement, breathing, and muscle tone. If each of the tests are normal they are given a score of 2. If abnormal, a score of 0. A score of 6 or less suggests the foetus is at risk for adverse outcome. While the biophysical profile is an useful test, when it becomes abnormal the foetus may have already suffered some damage
- 23. Treatment IUGR has many causes, therefore, there is not one treatment that always works.
- 24. 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. If IUGR is caused by a problem with the placenta and the baby is otherwise healthy, early diagnosis and treatment of the problem may reduce the chance of a serious outcome. There is no treatment that improves foetal growth, but IUGR babies who are at or near term have the best outcome if delivered promptly.
- 25. Treatment Maternal bed rest This is the initial approach for the treatment of IUGR. The benefit of bed rest is that it results in increased blood flow to the uterus. Studies have shown, however, that in most cases bed rest at home is just as effective as bed rest in the hospital environment.
- 26. Treatment Maternal bed rest
- 27. Treatment Aspirin Therapy The use of aspirin to treat foetuses 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). At the present time it is not recommended as a form of prevention for low risk patients.
- 28. Treatment Other Forms of Treatment Other forms of treatment that have been studied are nutritional supplementation, zinc supplementation, fish oil, hormones and oxygen therapy. Limited studies are available regarding the use of these modalities in the treatment of IUGR.
- 29. Treatment Judge Optimum Time Of Delivery RISK OF PREMATURITY DIFFICULT EXTRA UTERINE EXISTENCE RISK OF IUD HOSTILE INTRA UTERINE ENVIRONMENT
- 30. Short Term Risks of IUGR Increased perinatal morbidity and mortality. Intra uterine / Intrapartum death. Intrapartuum foetal acidosis characterized by-. » » » » Late deceleration. Severe variable deceleration. Beat to beat variability. Episodes of bradicardia. Intrapartum foetal acidosis may occur in as many as 40 % of IUGR, leading to a high incidence of LSCS. IUGR infants are at greater risk of dying because of neonatal complications- asphyxia, acidosis, meconium aspiration syndrome, infection, hypoglycemia, hypothermia, sudden infant death syndrome. IUGR infants are likely to be susceptible to infections because of impaired immunity
- 31. Long term Prognosis Babies who suffer from IUGR are at an increased risk for death, low blood sugar, low body temperature, and abnormal development of the nervous system. These risks increase with the severity of the growth restriction. The growth that occurs after birth cannot be predicted with certainty based on the size of the baby when it is born. Infants with asymmetrical IUGR are more likely to catch up in growth after birth than are infants who suffer from prolonged symmetrical IUGR. If IUGR is related to a disease or a genetic defect, the future of the infant is related to the severity and the nature of that disorder.
- 32. Long term Prognosis IUGR infants are more likely to remain small than those of normal birth weight. They will need the special attention of primary health, nutrition and social services during infancy and early childhood. Implication of IUGR can be life long affecting: Body size growth, composition and physical performance. Immunocompetence. It appears to predispose to adult adult-onset, degenerative diseases like maturity onset diabetes and cardiovascular diseases. Each case is unique. Can not reliably predict an infant's future progress.
Hinweis der Redaktion
- Current available estimates confirm that intrauterine growth retardation (IUGR) is a major public health problem world-wide. The prevalence of IUGR in most developing countries is above the international cut-off point for triggering public health action, and population-wide strategies are therefore urgently needed. Being born small for gestational age (SGA), which is usually defined as having a birth weight below the 10th centile of an accepted reference, is often used as a proxy for IUGR. SGA and IUGR are not synonymous, however. Some SGA infants may merely represent the lower tail of the 'normal' fetal growth distribution, while other infants who have been affected in utero by an inadequate nutritional milieu or other growth-inhibiting influences may nevertheless have a birth weight that is 'appropriate' for gestational age (AGA). Variations in fetal growth over the entire distribution of birth weight may have both etiologic and prognostic importance. In individual cases, however, it is usually very difficult to determine whether an observed birth weight that is low for gestational age is the result of true in utero growth restriction or represents a 'normally small' infant. Classification of IUGR is therefore based on the established cut-off for SGA. The higher the prevalence of low birth weight (LBW) in a given population, the greater the likelihood that the majority are a result of IUGR.
- Because classification of LBW as due to preterm birth or IUGR requires valid estimates of gestational age (GA), attention is required to improving the availability and quality of GA estimates on a population-wide basis in developing countries. This includes, where feasible, recording early in pregnancy the mother's recall of the date her last normal menstrual period began and the training of birth attendants (traditional birth attendants, midwives, nurses, and physicians) in the physical assessment of the newborn (Dubowitz, Ballard, or Capurro scores). In developed countries, early (< 20 weeks) ultrasound examination has improved the validity and reliability of GA assessment, although evidence from randomized trials does not demonstrate improvement in maternal or fetal/infant outcomes with routine early ultrasound. An international fetal growth reference curve should be developed based on pooled data from countries in different geographic regions where fetal growth is believed optimal. Care should be taken to ensure that such a reference fits with the new infant growth reference currently being developed under WHO auspices. Further research is needed to identify those determinants of fetal growth that influence mortality, morbidity, and performance independently of their effects on growth. Although it is quite clear that the use of sex-specific reference curves is justifiable, additional research is needed using large populations and ultrasound confirmation of GA to assess whether infants of different races born at a particular weight for gestational age are at substantially different risks for important health outcomes. Similar research is needed to determine whether infants who are born small because their mothers are primiparous or of short stature or living at high altitude are at the same risk for adverse sequelae as those of equivalent size who are small because, for example, their mothers have pre-eclampsia or smoke cigarettes. Until this information is available, the use of a single, sex-specific international reference has much to recommend it.
- Description There are standards or averages in weight for unborn babies according to their age in weeks. When the baby's weight is at or below the 10th percentile for his or her age, it is called intrauterine growth retardation or fetal growth restriction. These babies are smaller than they should be for their age. How much a baby weighs at birth depends not only on how many weeks old it is, but the rate at which it has grown. This growth process is complex and delicate. There are three phases associated with the development of the baby. During the first phase, cells multiply in the baby's organs. This occurs from the beginning of development through the early part of the fourth month. During the second phase, cells continue to multiply and the organs grow. In the third phase (after 32 weeks of development), growth occurs quickly and the baby may gain as much as 7 ounces per week. If the delicate process of development and weight gain is disturbed or interrupted, the baby can suffer from restricted growth.
- Application of the international foetal growth reference curve will vary according to its specific clinical and public health uses or purposes. Criteria for diagnosis of foetal growth restriction (e.g., SGA) should be related to evidence of increased risk for perinatal mortality and/or other indices of adverse outcomes. The new reference should provide percentiles [(e.g., 3rd, 5th, 10th, 15th, 25th, 50th (median), 75th, 85th, 90th, 95th, and 97th)] as well as z-scores [(e.g., -3, -2, -1, 0 (mean), 1, 2, and 3 SD)], so that health planners and practitioners can use the most appropriate cut off based on local circumstances. Proportionality at birth may be related to adverse outcomes. Thus there is a need to develop reference data for birth length and head circumference in relation to GA, and for birth weight in relation to birth length. Because the concepts of 'wasting' and 'stunting' have proven useful for categorizing undernourished infants and older children, an attempt should be made to quantify the mortality and morbidity risks associated with 'wasted' and 'stunted' newborns and to develop indicators for their classification.
- The etiologic determinants of IUGR must be considered with respect to two measures of effect: the relative risk (the ratio of the risk of IUGR in women exposed to the determinant to the risk in those who are unexposed) and the etiologic fraction (the proportion of IUGR in a given population that is attributable to the determinant). From a clinical perspective, relative risk is the more important measure, because it allows an estimate of an individual woman's risk of delivering a growth-retarded infant. But from a public health perspective, the etiologic fraction is the effect measure of major interest and, because it depends on the prevalence of the determinant in the population, it will differ substantially from one population to another. Thus, the importance of a given determinant will vary between developed and developing countries and between the rich and the poor within countries. Most of the evidence on etiologic determinants is based on observational studies and systematic overviews or meta-analyses of such studies. In developing countries, the major determinants of IUGR are nutritional: low gestational weight gain (primarily due to inadequate energy intake), low pre-pregnancy BMI (reflecting chronic maternal undernutrition), and short maternal stature (principally due to undernutrition and infection during childhood). Gastroenteritis, intestinal parasitosis, and respiratory infections are prevalent in developing countries and may also have an important impact. Malaria is a major determinant in countries where that disease is endemic. Cigarette smoking is an increasingly important factor in some settings
- In developed countries, cigarette smoking is far and away the most important etiologic determinant, but low gestational weight gain and low pre-pregnancy BMI are also determinants. The etiologic roles of pre-eclampsia, short stature, genetic factors, and alcohol and drug use during pregnancy are well-established but quantitatively less important. Socioeconomic disparities in IUGR risk within developed countries are largely attributable to socioeconomic gradients in smoking, weight gain and maternal stature. In poor urban areas where cocaine abuse is highly prevalent, this may also be important. The etiologic role of micronutrients in IUGR remains to be clarified. The best evidence concerning their importance derives from randomized trials and from systematic overviews of those trials contained in the Cochrane Collaboration Pregnancy and Childbirth database. Unfortunately, there are few supplementation or fortification trials in developing country settings where deficiencies in these micronutrients are prevalent. Trials are required to define the possible etiologic roles of iron, calcium, vitamin D, and vitamin A, especially in developing countries. The evidence concerning folate, magnesium, and zinc also looks sufficiently promising to justify further investigation.
- The physiologic and molecular mechanisms by which nutritional or other determinants affect fetal growth are incompletely understood. Growth is determined not only by substrate availability but also by the integrity of physiologic processes necessary to ensure transfer of nutrients and oxygen to the developing fetus. Expansion of maternal plasma volume, maintenance of uterine blood flow, and development of adequate placentation are key physiologic mechanisms required for optimal fetal growth. All substances used by the fetus are transported by the placenta: some (like oxygen and most other gases) by passive diffusion, others by facilitated transport proteins (e.g., Glut 1 for glucose), and still others (e.g., amino acids) by active energy-dependent transport processes. Insulin-like growth factors (IGFs) are important mediators of substrate incorporation into fetal tissue. IGF1 appears to induce cell differentiation, including (perhaps) oligodendrocyte development in the brain, whereas IGF2 may function to stimulate mitosis. It remains uncertain whether these physiologic and molecular mechanisms are merely the final common pathways for genetic or environmental determinants of IUGR, or whether they themselves vary (favorably or pathologically) independently of those determinants.
- Most of the evidence on etiologic determinants is based on observational studies and systematic overviews or meta-analyses of such studies. In developing countries, the major determinants of IUGR are nutritional: low gestational weight gain (primarily due to inadequate energy intake), low pre-pregnancy BMI (reflecting chronic maternal undernutrition), and short maternal stature (principally due to undernutrition and infection during childhood). Gastroenteritis, intestinal parasitosis, and respiratory infections are prevalent in developing countries and may also have an important impact. Malaria is a major determinant in countries where that disease is endemic. Cigarette smoking is an increasingly important factor in some settings. In developed countries, cigarette smoking is far and away the most important etiologic determinant, but low gestational weight gain and low pre-pregnancy BMI are also determinants. The etiologic roles of pre-eclampsia, short stature, genetic factors, and alcohol and drug use during pregnancy are well-established but quantitatively less important. Socioeconomic disparities in IUGR risk within developed countries are largely attributable to socioeconomic gradients in smoking, weight gain and maternal stature. In poor urban areas where cocaine abuse is highly prevalent, this may also be important.
- The etiologic role of micronutrients in IUGR remains to be clarified. The best evidence concerning their importance derives from randomized trials and from systematic overviews of those trials contained in the Cochrane Collaboration Pregnancy and Childbirth database. Unfortunately, there are few supplementation or fortification trials in developing country settings where deficiencies in these micronutrients are prevalent. Trials are required to define the possible etiologic roles of iron, calcium, vitamin D, and vitamin A, especially in developing countries. The evidence concerning folate, magnesium, and zinc also looks sufficiently promising to justify further investigation. The physiologic and molecular mechanisms by which nutritional or other determinants affect fetal growth are incompletely understood. Growth is determined not only by substrate availability but also by the integrity of physiologic processes necessary to ensure transfer of nutrients and oxygen to the developing fetus. Expansion of maternal plasma volume, maintenance of uterine blood flow, and development of adequate placentation are key physiologic mechanisms required for optimal fetal growth. All substances used by the fetus are transported by the placenta: some (like oxygen and most other gases) by passive diffusion, others by facilitated transport proteins (e.g., Glut 1 for glucose), and still others (e.g., amino acids) by active energy-dependent transport processes. Insulin-like growth factors (IGFs) are important mediators of substrate incorporation into fetal tissue. IGF1 appears to induce cell differentiation, including (perhaps) oligodendrocyte development in the brain, whereas IGF2 may function to stimulate mitosis. It remains uncertain whether these physiologic and molecular mechanisms are merely the final common pathways for genetic or environmental determinants of IUGR, or whether they themselves vary (favorably or pathologically) independently of those determinants.
- The etiologic role of micronutrients in IUGR remains to be clarified. The best evidence concerning their importance derives from randomized trials and from systematic overviews of those trials contained in the Cochrane Collaboration Pregnancy and Childbirth database. Unfortunately, there are few supplementation or fortification trials in developing country settings where deficiencies in these micronutrients are prevalent. Trials are required to define the possible etiologic roles of iron, calcium, vitamin D, and vitamin A, especially in developing countries. The evidence concerning folate, magnesium, and zinc also looks sufficiently promising to justify further investigation. The physiologic and molecular mechanisms by which nutritional or other determinants affect fetal growth are incompletely understood. Growth is determined not only by substrate availability but also by the integrity of physiologic processes necessary to ensure transfer of nutrients and oxygen to the developing fetus. Expansion of maternal plasma volume, maintenance of uterine blood flow, and development of adequate placentation are key physiologic mechanisms required for optimal fetal growth. All substances used by the fetus are transported by the placenta: some (like oxygen and most other gases) by passive diffusion, others by facilitated transport proteins (e.g., Glut 1 for glucose), and still others (e.g., amino acids) by active energy-dependent transport processes. Insulin-like growth factors (IGFs) are important mediators of substrate incorporation into fetal tissue. IGF1 appears to induce cell differentiation, including (perhaps) oligodendrocyte development in the brain, whereas IGF2 may function to stimulate mitosis. It remains uncertain whether these physiologic and molecular mechanisms are merely the final common pathways for genetic or environmental determinants of IUGR, or whether they themselves vary (favorably or pathologically) independently of those determinants.
- IUGR can be difficult to diagnose and in many cases doctors are not able to make an exact diagnosis until the baby is born. A mother who has had a growth restricted baby is at risk of having another during a later pregnancy. Such mothers are closely monitored during pregnancy. The length in weeks of the pregnancy must be carefully determined so that the doctor will know if development and weight gain are appropriate. Checking the mother's weight and abdomen measurements can help diagnose cases when there are no other risk factors present. Measuring the girth of the abdomen is often used as a tool for diagnosing IUGR. During pregnancy, the healthcare provider will use a tape measure to record the height of the upper portion of the uterus (the uterine fundal height). As the pregnancy continues and the baby grows, the uterus stretches upward in the direction of the mother's head. Between 18 and 30 weeks of gestation, the uterine fundal height (in cm.) equals the weeks of gestation. If the uterine fundal height is more than 2-3 cm below normal, then IUGR is suspected. Ultrasound is used to evaluate the growth of the baby. Usually, IUGR is diagnosed after week 32 of pregnancy. This is during the phase of rapid growth when the baby should be gaining more weight. IUGR caused by genetic factors or infection may sometimes be detected earlier.
- IUGR can be difficult to diagnose and in many cases doctors are not able to make an exact diagnosis until the baby is born. A mother who has had a growth restricted baby is at risk of having another during a later pregnancy. Such mothers are closely monitored during pregnancy. The length in weeks of the pregnancy must be carefully determined so that the doctor will know if development and weight gain are appropriate. Checking the mother's weight and abdomen measurements can help diagnose cases when there are no other risk factors present. Measuring the girth of the abdomen is often used as a tool for diagnosing IUGR. During pregnancy, the healthcare provider will use a tape measure to record the height of the upper portion of the uterus (the uterine fundal height). As the pregnancy continues and the baby grows, the uterus stretches upward in the direction of the mother's head. Between 18 and 30 weeks of gestation, the uterine fundal height (in cm.) equals the weeks of gestation. If the uterine fundal height is more than 2-3 cm below normal, then IUGR is suspected. Ultrasound is used to evaluate the growth of the baby. Usually, IUGR is diagnosed after week 32 of pregnancy. This is during the phase of rapid growth when the baby should be gaining more weight. IUGR caused by genetic factors or infection may sometimes be detected earlier.
- A systematic review of 126 available randomized controlled trials (RCTs) has been carried out to summarize the efficacy of 36 prenatal interventions aimed at reducing IUGR. Strategies include prenatal care modalities, protein/energy supplementation, treatment of anemia, vitamin/mineral supplementation, fish oil supplementation, and prevention and treatment of hypertensive disorders, fetal compromise, and infection. Based on this review, few statistically significant reductions in the risk of IUGR have been demonstrated with these interventions. However, the point estimate (average effect) associated with some interventions suggests a potential effect of considerable magnitude; these interventions should be further evaluated by targeting populations at risk for IUGR, increasing sample size, and addressing coexisting factors limiting growth. Studies should be conducted in developed as well as developing countries.
- A systematic review of 126 available randomized controlled trials (RCTs) has been carried out to summarize the efficacy of 36 prenatal interventions aimed at reducing IUGR. Strategies include prenatal care modalities, protein/energy supplementation, treatment of anemia, vitamin/mineral supplementation, fish oil supplementation, and prevention and treatment of hypertensive disorders, fetal compromise, and infection. Based on this review, few statistically significant reductions in the risk of IUGR have been demonstrated with these interventions. However, the point estimate (average effect) associated with some interventions suggests a potential effect of considerable magnitude; these interventions should be further evaluated by targeting populations at risk for IUGR, increasing sample size, and addressing coexisting factors limiting growth. Studies should be conducted in developed as well as developing countries.
- Systematic reviews provide strong evidence of benefit only for the following interventions: balanced protein/energy supplementation, strategies to reduce maternal smoking, and antimalarial prophylaxis. In Jamaica, antibiotic administration to prevent urinary tract infections further reduced an already low prevalence of IUGR. Improvement of maternal nutrition should be a priority, especially in developing countries. Unless maternal undernutrition is severe, the effect of balanced protein/energy supplementation on birth weight is likely to be modest » 100 g). Reduction in maternal smoking should be encouraged, both by individual clinicians (using behavioral modification techniques, for example) and by policy makers (e.g., taxes on cigarettes and other tobacco products). Antimalarial chemoprophylaxis should be provided in endemic areas, particularly to primigravidae, although more research is needed to elucidate the ideal timing of treatment, combination of agents, and safety for the fetus.
- The effectiveness of other interventions has not been demonstrated, but further research is required based on limited, suggestive results from RCTs. 'Packages' of combined interventions and community-based (cluster randomization) approaches should be explored. Potentially adverse effects of these interventions also require careful assessment. Maternal supplementation of iron, zinc, folate, and magnesium should be rigorously evaluated, as these interventions may affect fetal growth, as well as preterm delivery and necrologic outcomes. It is important to target women deficient in the nutrient of interest to maximize the chance of detecting a beneficial effect. In this regard, the possibility of coexisting nutrient deficiencies limiting fetal growth must be considered. Two trials of iron supplementation conducted in developed countries have shown no effect on IUGR; it remains to be seen whether routine iron supplementation affects IUGR in populations with a high prevalence of anemia. A RTC the effect of vitamin A supplementation during pregnancy is currently under way in Nepal. Unlike food fortification with vitamin A, however, supplementation might have adverse safety implications, and caution is required to avoid teratogenic or other adverse effects. In countries where multiple deficiencies and pathologies exist, it may be difficult to demonstrate a significant effect with a single intervention. For example, malaria and other parasitic infections, malnutrition, and anemia coexist in many developing countries. An appropriate combination of anti-anemic (iron-folate) and antimicrobial/antiparasitic agents tested in population-based trials may have a greater chance of showing a reduction in IUGR. Antibiotic treatment of genito-urinary tract infections appears to be a promising area for perinatal research, although the impact may be greater for preterm delivery than for impaired fetal growth. The efficacy and safety of drug treatment remain to be demonstrated. A few older and methodologically weaker trials of abdominal decompression have reported large reductions in IUGR. In selected developed country settings, strategies to improve blood flow to the uterus may merit further testing.
- RCTs aimed at other putative causes of IUGR have been disappointing. For example, efforts to prevent and treat hypertensive disorders have not significantly reduced IUGR. Trials using antiplatelet agents in high-risk women have yielded only modest benefits, while trials of betablockers have suggested a potential for harm. Prenatal care and nutritional education interventions have not heretofore been shown to impact significantly on IUGR, but better approaches are required (e.g., community-wide interventions to promote optimal weight gain and discourage 'eating down'). Future research in the prevention and treatment of IUGR should be based on sound epidemiologic and other scientific evidence. Rigorous randomization procedures (including concealment of treatment allocation) and efforts to minimize losses to follow-up fare required to ensure high methodological quality. Without randomization there is a high risk of bias due to confounding. Sample sizes should be planned with sufficient power to detect significant impacts on IUGR and other fetal/infant outcomes. Study designs should also include practical measures to assess gestational age, as well as potential obstetric complications or other adverse outcomes. Lastly, while systematic reviews of RCTs represent the most objective way to evaluate the effectiveness of health care interventions, the available data are limited. Moreover, there are problems related to the size of the trials, their heterogeneity, settings, and methodologic quality. Findings from observational studies should not be totally discounted, but rather tested in RCTs whenever possible.
- This is an example of a foetus at risk for IUGR in which the amniotic fluid index was measured but the nurses and physician did not understand the principles of an abnormal reading. The foetus was allowed to remain in utero and developed cerebral palsy from oxygen deprivation. The family sued the hospital and the physician and was awarded 9.7 million dollars which was the largest malpractice award in the state of Utah This is the amniotic fluid index in the above case. The blue represents the normal range. At 35 weeks the fluid measurement was 16. Four days later it dropped to 6.3. This sudden drop was ignored by the nurses and physician caring for the patient. A few days later the fetus was damaged because the umbilical cord was compressed, resulting in cerebral palsy.
- A systematic review of 126 available randomized controlled trials (RCTs) has been carried out to summarize the efficacy of 36 prenatal interventions aimed at reducing IUGR. Strategies include prenatal care modalities, protein/energy supplementation, treatment of anemia, vitamin/mineral supplementation, fish oil supplementation, and prevention and treatment of hypertensive disorders, fetal compromise, and infection. Based on this review, few statistically significant reductions in the risk of IUGR have been demonstrated with these interventions. However, the point estimate (average effect) associated with some interventions suggests a potential effect of considerable magnitude; these interventions should be further evaluated by targeting populations at risk for IUGR, increasing sample size, and addressing coexisting factors limiting growth. Studies should be conducted in developed as well as developing countries.
- Systematic reviews provide strong evidence of benefit only for the following interventions: balanced protein/energy supplementation, strategies to reduce maternal smoking, and antimalarial prophylaxis. In Jamaica, antibiotic administration to prevent urinary tract infections further reduced an already low prevalence of IUGR. Improvement of maternal nutrition should be a priority, especially in developing countries. Unless maternal undernutrition is severe, the effect of balanced protein/energy supplementation on birth weight is likely to be modest 100 g). Reduction in maternal smoking should be encouraged, both by individual clinicians (using behavioral modification techniques, for example) and by policy makers (e.g., taxes on cigarettes and other tobacco products). Antimalarial chemoprophylaxis should be provided in endemic areas, particularly to primigravidae, although more research is needed to elucidate the ideal timing of treatment, combination of agents, and safety for the fetus. The effectiveness of other interventions has not been demonstrated, but further research is required based on limited, suggestive results from RCTs. 'Packages' of combined interventions and community-based (cluster randomization) approaches should be explored. Potentially adverse effects of these interventions also require careful assessment.
- Maternal supplementation of iron, zinc, folate, and magnesium should be rigorously evaluated, as these interventions may affect fetal growth, as well as preterm delivery and necrologic outcomes. It is important to target women deficient in the nutrient of interest to maximize the chance of detecting a beneficial effect. In this regard, the possibility of coexisting nutrient deficiencies limiting fetal growth must be considered. Two trials of iron supplementation conducted in developed countries have shown no effect on IUGR; it remains to be seen whether routine iron supplementation affects IUGR in populations with a high prevalence of anemia. A RTC the effect of vitamin A supplementation during pregnancy is currently under way in Nepal. Unlike food fortification with vitamin A, however, supplementation might have adverse safety implications, and caution is required to avoid teratogenic or other adverse effects. In countries where multiple deficiencies and pathologies exist, it may be difficult to demonstrate a significant effect with a single intervention. For example, malaria and other parasitic infections, malnutrition, and anemia coexist in many developing countries. An appropriate combination of anti-anemic (iron-folate) and antimicrobial/antiparasitic agents tested in population-based trials may have a greater chance of showing a reduction in IUGR.
- Antibiotic treatment of genito-urinary tract infections appears to be a promising area for perinatal research, although the impact may be greater for preterm delivery than for impaired fetal growth. The efficacy and safety of drug treatment remain to be demonstrated. A few older and methodologically weaker trials of abdominal decompression have reported large reductions in IUGR. In selected developed country settings, strategies to improve blood flow to the uterus may merit further testing. RCTs aimed at other putative causes of IUGR have been disappointing. For example, efforts to prevent and treat hypertensive disorders have not significantly reduced IUGR. Trials using antiplatelet agents in high-risk women have yielded only modest benefits, while trials of betablockers have suggested a potential for harm. Prenatal care and nutritional education interventions have not heretofore been shown to impact significantly on IUGR, but better approaches are required (e.g., community-wide interventions to promote optimal weight gain and discourage 'eating down').
- Future research in the prevention and treatment of IUGR should be based on sound epidemiologic and other scientific evidence. Rigorous randomization procedures (including concealment of treatment allocation) and efforts to minimize losses to follow-up fare required to ensure high methodological quality. Without randomization there is a high risk of bias due to confounding. Sample sizes should be planned with sufficient power to detect significant impacts on IUGR and other fetal/infant outcomes. Study designs should also include practical measures to assess gestational age, as well as potential obstetric complications or other adverse outcomes. Lastly, while systematic reviews of RCTs represent the most objective way to evaluate the effectiveness of health care interventions, the available data are limited. Moreover, there are problems related to the size of the trials, their heterogeneity, settings, and methodologic quality. Findings from observational studies should not be totally discounted, but rather tested in RCTs whenever possible.
- Babies who suffer from IUGR are at an increased risk fordeath, low blood sugar, low body temperature, and abnormal development of the nervous system. These risks increase with the severity of the growth restriction. The growth that occurs after birth cannot be predicted with certainty based on the size of the baby when it is born. Infants with asymmetrical IUGR are more likely to catch up in growth after birth than are infants who suffer from prolonged symmetrical IUGR. However, as of 1998, doctors cannot reliably predict an infant's future progress. Each case is unique. Some infants who have IUGR will develop normally, while others will have complications of the nervous system or intellectual problems like learning disorders. If IUGR is related to a disease or a genetic defect, the future of the infant is related to the severity and the nature of that disorder.