Intrauterine growth restriction: A contemporary review Answers to Multiple Choice Questions for Vol. 23, No. 6




1. (a) T (b) T (c) F (d) F (e) T


Explanations:


Many studies have demonstrated that umbilical artery Doppler stratifies risk of small-for-gestational age fetuses. The prevailing opinion is to classify small-for-gestational age fetuses according to their umbilical artery Doppler status. There is substantial evidence that the use of umbilical artery Doppler results in an improvement of a number of perinatal outcomes, with a reduction of 30% in perinatal mortality, in high-risk pregnancies. Further analyses have demonstrated that this benefit is mainly relevant in pregnancies with intrauterine growth restriction. Mathematical and experimental models of chronic placental embolization have demonstrated that more than a 30% of placental damage is required before the umbilical artery Doppler becomes abnormal. Thus, umbilical artery Doppler has low sensitivity for the prediction of adverse outcome, especially at term, when most instances of adverse outcome occurs in fetuses with normal umbilical artery. Observational studies have reported that this pattern, which reflects the end of the spectrum of placental damage, is associated with adverse outcome independently of gestational age at delivery and indeed birth weight.


2. (a) T (b) F (c) F (d) T (e) T


Explanations:


The reduction in the number of functional arterioles in the tertiary villi leads to a decrease in the PO 2 in the umbilical vein. This event sets into motion the phenomenon of circulatory redistribution principally characterized by the centralization of blood flow. The better oxygenated blood goes toward the most vital organs (brain, heart, adrenals), whilst vasoconstriction limits the blood’s arrival at the organs considered less indispensable (digestive system, lungs, skin, skeleton, etc.). The evaluation of the middle cerebral artery has become a standard in the antenatal assessment of the small fetuses. Studies by cordocentesis have demonstrated a good correlation between middle cerebral artery pulsatility index with hypoxemia but not with acidaemia. It has been claimed that the relationship between the umbilical and cerebral flow provides a more sensitive tool to discriminate between constitutional SGA and IUGR. In fact, animal models have demonstrated that this ratio is better correlated with hypoxia than its individual components. Furthermore, it has also been extensively reported that the prediction of adverse outcome is improved using umbilical and cerebral parameters in a combined ratio, with sensitivities of about 70%. Near-term, some observational studies have demonstrated that even in the presence of a normal umbilical artery, middle cerebral artery Doppler identifies a subgroup of babies at risk for adverse perinatal outcome.


3. (a) F (b) F (c) T (d) T (e) T


Explanations:


Most series have demonstrated that gestational age is the strongest predictor of adverse outcome in preterm growth restricted fetuses. A multicentre randomized trial, the Growth Restriction Intervention Trial (GRIT), found that early delivery prompted by umbilical artery reversed end-diastolic flow does not improve the mortality rate or the neurological outcome in preterm IUGR fetuses. Secondary to severe tissue hypoxia, anaerobic metabolism is required for energy production. Chronically, this anaerobic metabolism leads to metabolic academia and acidosis. The fetal myocardium responds to this acidosis with myocardial cell necrosis phenomena, with replacement by fibroid tissue, which affects the myocardial compliance and therefore increase telediastolic pressure at both ventricles. The increased concentrations of troponin-T in neonates with pulsatile umbilical vein suggests that myocardial cell destruction is the underlying cause of precordial vein flow abnormalities, with a decrease in velocities during atrial contraction and a consequent increase in pulsatility indices. Longitudinal studies have demonstrated that precordial vein flow waveforms become abnormal in advanced stages of fetal compromise. The temporal relation with other acute markers is variable: whereas in about a 50% of cases abnormal ductus venosus precedes the loss of short-term variability in the fetal heart rate, this later sign is the first to become abnormal in the other cases. In about 90% of cases, the ductus venosus become abnormal only 48–72 h before the biophysical profile. Observational studies have reported that Doppler ultrasonography and biophysical profile effectively stratify IUGR fetuses into risk categories, but Doppler and biophysical profile results do not show a consistent relationship with each other.


4. (a) F (b) F (c) T (d) T (e) F


Explanations:


Infants with symmetric IUGR have reduced growth measurements from early in pregnancy, a normal ponderal index, brain growth proportional to body size and low risks for perinatal asphyxia and neonatal hypoglycaemia. Conversely, those with asymmetric IUGR have late onset growth failure, a low ponderal index, brain sparing and increased risks for perinatal asphyxia and neonatal hypoglycaemia. At birth these 2 forms of IUGR can be distinguished by measuring weight, length and head circumference and plotting them on customised growth charts. With asymmetric IUGR there is relative brain sparing so that head circumference will plot on a higher percentile than either weight or length. With symmetric IUGR all 3 measurements will be below the 10th percentile. Infants with IUGR often have suffered from chronic fetal hypoxia which may result in fetal death and the perinatal mortality rate of IUGR infants is 5 to 20 times that of appropriately grown infants. Mortality is especially high in infants of less than 29 weeks’ gestation who weigh less than the 2nd percentile and this has been proposed as a “viability centile”. Therefore infants who present with both prematurity and IUGR are likely to suffer from the effects of both insults and have poorer short-term and long-term outcomes. Congenital infections are relatively uncommon but are a well-recognised cause of IUGR. The mnemonic TORCH stands for toxoplasmosis, rubella, cytomegalovirus and Herpes simplex infections. Infants with TORCH infections are generally SGA, and in addition they may have rashes, hepatitis, chorioretinitis and central nervous system abnormalities. There is no specific treatment for congenital rubella. Acquired toxoplasmosis is treated with sulphadiazine, pyrimethamine and folic acid. Spiramycin has been used to reduce the effects of maternal infection on the fetus but there is doubt about its effectiveness. There is no effective treatment for established CMV infection although drugs such as gangciclovir have been tried to reduce ocular lesions. For Herpes simplex infections intravenous acyclovir or adenosine arabinoside may be helpful but mortality and morbidity remain high. Another cause of congenital infection is syphilis and in this case penicillin in high doses may be helpful. Although many textbooks suggest that there is an association between the presence of a single umbilical artery and IUGR a recent publication disputes this. In this retrospective case-control study of 84 singleton pregnancies which resulted in the birth of an infant with an isolated single umbilical artery compared to those with 3-vessel umbilical cords the prevalence of SGA was 7.1% and 4.8% respectively, a difference that was not statistically significant. The authors concluded that fetuses with an isolated single umbilical artery are at similar risk for SGA compared with fetuses with 3-vessel umbilical cords.


5. (a) T (b) T (c) T (d) F (e) T


Explanations:


Perinatal asphyxia and its sequelae are the most important immediate problems of IUGR infants. Uterine contractions may add an additional hypoxic stress on the chronically hypoxic fetus with placental insufficiency. As a result there is acute on chronic fetal hypoxia with acidosis and cerebral and myocardial depression which at its worst leads to perinatal death. The IUGR infant may need prompt and effective resuscitation to prevent the combination of intrapartum and neonatal asphyxia which places the infant at double jeopardy for a continuum of cerebral and myocardial insult. The sequelae of perinatal asphyxia include multiple organ system failure characterised by encephalopathy, ischaemic heart failure, meconium aspiration (in the mature fetus), persistent fetal circulation, acute tubular necrosis with renal failure and gastrointestinal problems.


Hypoglycaemia, especially when fasting, occurs more commonly in IUGR infants than in any other group, apart from the infant of the poorly controlled diabetic mother. The greatest risk for hypoglycaemia is during the first 3 days of life but it may persist for many weeks. The major cause is reduced hepatic glycogen stores since glycogenolysis is the predominant source of glucose for the newborn immediately after birth. SGA infants also have impaired gluconeogenesis, most likely because of inactive enzymes and cofactors, rather than substrate unavailability. Blood glucose levels should be maintained above 2.6 mmol/L and this implies that frequent monitoring is necessary especially in the first 3 days of life. Early feeding with expressed breast milk or an intravenous infusion of glucose at up to 8 mg/kg/minute is recommended. Infants at greatest risk of hypoglycaemia are those with perinatal asphyxia and those with the most severe growth restriction indicated by a ponderal index of less than 2. Polycythaemia with hyperviscosity is also a risk in IUGR infants who have higher plasma volumes than non-growth restricted infants after birth. After 12 h the plasma volumes are similar but IUGR infants have increased red cell masses and with increased erythropoietin levels excessive red cell production. Raised haematocrits (above 65 or 70%) are associated with hyperviscosity increasing the risks of necrotising enterocolitis and thrombosis, for example renal vein thrombosis. Hypoxia and hypoglycaemia should be corrected and occasionally a partial exchange transfusion with albumin or plasma is needed to reduce the haematocrit by 10 to 15%. Physical examination may suggest a chromosomal or other abnormality if there are obvious dysmorphic features such as abnormal facies, unusual feet and hands, single palmar creases, cleft lip and/or palate, anterior abdominal wall defects, spina bifida, hydrocephalus or skin defects. Infants with congenital infection may have hepatosplenomegaly, jaundice, blueberry muffin rash, cataracts, cloudy corneas or other ocular disorders. Hypothermia is common in infants with IUGR for a number of reasons including reduced heat production and increased heat losses due to a relatively large surface area to body weight ratio. Temperature control is an essential component of resuscitation and stabilisation of any newborn infant but especially one with IUGR. Heat loss should be prevented by use of radiant warmers, warm towels and also polythene bags if the infant is also very preterm. Chronic fetal hypoxia with hepatic underperfusion may lead to disordered coagulation in IUGR infants. This state will be worsened after birth if there is persistent hypoxia, hypothermia and hypoglycaemia. Raised nucleated red blood cell counts have been associated with severe cerebral and pulmonary haemorrhages in severely growth restricted infants. Coagulopathy is usually short lived and responds to simple corrective measures. Occasionally severe bleeding such as pulmonary haemorrhage occurs and this requires aggressive treatment including endotracheal intubation and positive pressure ventilation. Hypoxia, hypothermia and hypoglycaemia should be corrected in addition to the specific measures to combat the coagulation disorder.


6. (a) F (b) F (c) T (d) F (e) T


Explanations:


Although most SGA infants show catch-up growth by 2 years about 10% do not. It is increasingly recognised that these infants are at risk of developing metabolic disease in later life. Reduced fetal growth is associated with increased risk of insulin resistance, obesity, cardiovascular disease and type 2 diabetes mellitus in later childhood and adulthood. There is evidence that some of the metabolic consequences of IUGR may be mitigated by ensuring early appropriate catch-up growth whilst avoiding excessive weight gain. This provides a dilemma for the neonatologist, paediatrician and dietician providing aftercare for these IUGR infants. The neonatologist is faced with the problem that on the one hand it is known that poor postnatal growth increases the risk of poor neuro-developmental outcome but on the other hand promotion of faster weight gain in SGA infants may increase blood pressure in later life possibly increasing long-term cardiovascular disease risk. Cerebral palsy is a disorder of aberrant control of movement or posture that appears early in life and leads to lifelong disability. It is the most common physical disability in childhood being present in about 2 per 1000 live births. An association between cerebral palsy and IUGR has been suspected for some time but has only recently been confirmed. In a population-based case control study using customised birth weight percentiles term infants with severe SGA had a five to seven-fold increased risk of developing cerebral palsy. Severe SGA was defined as being below the first customised growth percentile. The risk of developing cerebral palsy was linked to the severity of growth restriction at birth only in term infants as in babies born preterm there were no differences between cases and controls. Other studies found associations between cerebral palsy and IUGR in preterm infants at 34 to 36 weeks and at gestations below 32 weeks. The largest population study to date, the European collaborative study, also found that being large for gestational age was a risk factor for cerebral palsy but it assessed birth weight against general population norms rather than using a matched control group. About 10% of children born SGA will remain less than 2 standard deviations below the mean for height throughout childhood and adolescence into adulthood. It has been proposed that a child born SGA whose height remains more than 2 standard deviations below the mean at 2–3 years of age could become a candidate for growth hormone (GH) therapy. However, treatment with GH is indicated only when other causes of short stature, such as chronic disease, endocrine disorders, emotional deprivation, syndromes associated with poor growth and long-term steroid treatment have been excluded. The decision to start GH treatment must be taken by a paediatric endocrinologist after discussion with the child’s parents as there is an inherent risk of obesity and later insulin resistance in SGA children who show catch-up growth either spontaneously or after therapy with GH.


7. (a) T (b) F (c) F (d) T (e) F


Explanations:


The UK CEMACH (Confidential Enquiries into Maternal and Child Health) Perinatal Mortality Report 2007 shows a stillbirth rate of 5.2–5.7 per 1000 total births i.e. about 1 in 200 for the years 2000-2007. Stilbirth is associated with fetal growth restriction in about half of cases. Various reports give rates of 40–60% depending on how stillbirths are classified. According to a systematic review of randomized controlled trials, routine third trimester ultrasound has not be shown to be associated with a reduction in stillbirth rate or overall perinatal mortality rate. Routine antenatal care has been introduced to detect maternal and fetal complications of pregnancy to identify mothers or fetuses at risk and optimize maternal and baby outcomes. Congenital defects/malformations are present in less than 10% of unexpected stillbirths.


8. (a) F (b) T (c) F (d) T (e) T


Explanations:


There is no evidence from randomized trials that offering routine third trimester ultrasound confers any benefit for mother and/or baby. It seems logical that routine ultrasound may be of benefit but i) there are concerns that it may result in more and often unnecessary intervention; ii) it is unclear when and how often to scan and iii) it is unclear what parameters should be measured or assessed and what the cut off limits for normality are. Evidence from randomized trials shows that routine ultrasound in the third trimester does not reduce antenatal intervention. Antenatal admission rates and induction of labour rates from these trials are the same in intervention and control groups, but there is a suggestion that its use may result in increased Caesarean section rates. The only trial which has shown a reduction in stillbirth rates was a small single centre trial to compare concealed vs revealed placental textural assessment and while the trial was too small (2000 participants) and not designed to address this question, given the findings, it is recommended that future research should evaluate placental textural assessment/grading as a parameter in routine third trimester ultrasound. A number of fetal structural abnormalities may not manifest with ultrasound features at the routine mid-trimester anatomy scan which later evolve and become apparent on scan in the third trimester, for example cranio-spinal abnormalities such as hydrocephalus and microcephaly, gastrointestinal abnormalities such as duodenal or other bowel atresias, urinary tract abnormalities such as hydroneprhosis and skeletal dysplasias such as achondroplasia.


9. (a) F (b) T (c) T (d) T (e) T


Explanations:


This has not been shown in vivo but rather in vitro in laboratory studies. In vivo demonstration of ultrasound heat propagation is not possible as it would need to be invasive and would interfere with heat propagation. Follow up studies in Norway of children exposed to ultrasound in utero vs. those not exposed to ultrasound has shown an increased incidence of non-right handedness. The significance of this is unknown but it has raised some theoretical concerns about the effect of ultrasound on neurological pathway development. In a trial published in 1993 where women were randomized to serial ultrasound and Doppler ultrasound vs only clinically indicated ultrasound in the third trimester, there was an unexpected finding of a greater risk of intrauterine growth restriction (IUGR) in the intensive ultrasound screened group. The authors stressed that although this may have been a chance finding, further investigation of the effects of frequent ultrasound exposure is warranted. Depending on where, different countries/groups of countries have different regulators. The Medicines and Healthcare products Regulatory Agency (MHRA) regulates medical devices in the UK under European legislation. In the EU, all medical devices must be identified with the CE mark. Ultrasound falls under the medium risk category. The Federation of Societies of Ultrasound in Medicine and Biology (EFSUMB) also addresses safety and has produced safety guidelines (through the European Committee for Ultrasound Radiation Safety). The World Federation (WFUMB) held safety symposia in 1991 (on thermal issues) and 1996 (thermal and non-thermal issues), at which recommendations were proffered. Following review, these were published in 1992 and 1998 as guidelines. Manufacturers adhere to these standards and the safety advice. The European Federation of Societies for Ultrasound in Medicine and Biology (EFSUMB) Watchdog Committee recommend that all sonographers are aware of the theoretical risks of thermal injury and that to reduce these risks consideration should be given to dwell time (time spent in one place), overall scan time and aiming to use the lowest power output to achieve an optimal image and satisfactory examination.


10. (a) T (b) F (c) T (d) T (e) T


Explanations:


Irregular or uncertain information about the last menstrual period is very common compared to the increased risk of growth-restriction in this group of women. Very early onset growth restriction is well documented and therefore it is good practice to offer a further growth scan in the third trimester. It is worthwhile to search for more clues for the correct gestational age since an early start of growth restriction is possible and ultrasound thus notoriously will underestimate gestational age.


11. (a) F (b) T (c) T (d) T (e) T


Explanations:


It is common to regard the growth that follows a centile of the reference chart to be the expected normal growth pattern. But it is not correct. The growth trajectory of a physiologically small fetus runs more in parallel with the 50th centile of the background population. The correct assessment of serial measurement is not to do two independent cross-sectional evaluations but to calculate conditional reference ranges based on the first assessment.


12. (a) F (b) T (c) F (d) T (e) F


Explanations:


Appropriately constructed longitudinal charts for growth are suitable both for single measurements and for serial measurements. A true longitudinal assessment, however, is not carried out unless the conditional ranges have been calculated and exposed. Using SD-scores does not change this. Longitudinal growth charts and conditional terms for individual fetuses can also be customised i.e. adjusted for maternal and fetal factors, the fetal gender being the most important.


13. (a) T (b) T (c) F (d) T (e) T


Explanations:


The upper extreme limit of reference ranges represents the additive effect of extreme biological variation and extreme measurement error. We assume that the true fetal weight has not changed one minute later when we repeat the measurement. Random error, however, is symmetrically distributed around zero and it is unlikely that the next assessment will have the same degree and direction of random error. Thus the probability is high that the next measurement will be less. In serial measurements we therefore expect the normal weight development to move more parallel to the population mean than the centiles for the entire population. When sticking to the method of using the average of three measurements random error is reduced correspondingly. If that is the same technique as was used for constructing the reference ranges then false positive results are kept to a minimum. If you have chosen good reference ranges, they will have narrow 95% CI around the extreme limits and you know you will be more accurate in your diagnosis of growth deviation.


14. (a) F (b) F (c) T (d) F (e) T


Explanations:


The data about marijuana and risk of SGA are conflicting. The majority of papers suggest that marijuana does not result in increased SGA after adjustment for other confounding factors. Women who smoke at 8 weeks gestation can be divided into 2 groups: those who will continue to smoke beyond 15 weeks gestation (increased risk of SGA) and those who cease smoking by 15 weeks (risk of SGA is not different to that in non-smokers). This answer is therefore false as it does not allow for those who quit smoking, after 8 weeks but by 15 weeks gestation, who do not have elevated risk of SGA. Short and light women have increased rates of babies SGA by population centiles. A number of these babies are likely to be constitutionally small normal babies. A recent meta-analysis found that intake of 1 unit of alcohol daily in early pregnancy did not increase the risk of SGA. Cocaine use in pregnancy has been found to increase the risk of SGA after adjustment for confounders.


15. (a) F (b) F (c) F (d) T (e) F


Explanations:


Fish oil supplementation may reduce the risk of spontaneous preterm birth but does not modify the risk of SGA. The data about caffeine intake and risk of SGA are conflicting. Some data suggest that high intake of caffeine may be associated with increased SGA. A single coffee daily is unlikely to be harmful unless the mother has a very high caffeine intake from other sources. Several studies have found a positive (not inverse) relationship between milk intake and infant birthweight. The Cochrane systematic review reported that women treated with multiple-micro nutrient supplementation had a reduced risk of SGA babies. In the trials which compared multiple micro nutrients with iron and folic acid supplementation, no significant reductions were found for either SGA or low birthweight babies. The Cochrane systematic review of anti-oxidants (high dose vitamin C and E) for prevention of preeclampsia did not show any effect of treatment on risk of SGA (RR 0.83, 95% CI 0.62 to 1.11; five trials, 5271 babies).


16. (a) F (b) F (c) F (d) T (e) T


Explanations:


Population studies show that, as a group, women with chronic hypertension have increased risk of SGA. This risk is more marked in those who subsequently develop superimposed preeclampsia and perhaps in those with severe hypertension in early pregnancy. High rates of SGA persist in women with anti-phospholipid syndrome in spite of maternal treatment. There are no good data about risk of SGA in women with hypothyroidism. Malaria is one of the most important causes of SGA in Africa. This risk is reduced by anti-malarial prophylaxis in pregnancy which is an important public health priority. A recent systematic review found that pregnant women with congenital heart disease did not have increased SGA unless they had cyanotic heart disease or Eisenmenger’s syndrome.


17. (a) F (b) F (c) F (d) T (e) F


Explanations:


Zinc supplementation does not seem to have a significant effect on the number of small for gestational age babies, however there may be an effect on preterm birth. The most cost effective and sustainable means of ensuring adequate iodine intake is through universal salt iodization, although in areas where this is not possible, supplementation may be necessary. Multiple micronutrient supplementation does reduce the number of small for gestational age babies, although this effect is not seen when compared to folate supplementation alone. The lack of these 3 nutrients pose a significant risk to the health of women and children in low – income countries but are not the main causes of growth restriction.


18. (a) F (b) F (c) T (d) T (e) T


Explanations:


Malaria infection in pregnancy contributes to poor fetal growth via maternal anaemia which then impacts on fetal growth. Anti-malarial drugs and insect treated nets only reduce low birthweight babies in women in their first or second pregnancies as these are the women who are at most risk of infection. The risks to the mother and fetus are very high with untreated malaria and therefore it is almost always a positive benefit: risk analysis in endemic areas.


19. (a) T (b) F (c) T (d) F (e) F


Explanations:


Aspirin consistently produces a reduction in both small-for-gestational-age babies and pre-eclampsia, when given to women at risk for hypertensive disorders of pregnancy and related conditions. However calcium and antioxidants do not produce less growth restricted babies when examined in systematic reviews. Anti-hypertensive medication has only been proved to be useful for maternal end-organ protection and is not known to reduce fetal problems.


20. a) F b) F c) F d) F e) T


Explanations:


Bed rest, calcium channel blockers and maternal nutrient supplementation are not beneficial and may in some cases (e.g. glucose supplementation) cause harm to the baby. Exercise while in keeping with a healthy lifestyle has not been linked with an improvement in SGA incidence. As intrauterine treatments to date seem to offer limited benefit to the baby with fetal growth restriction, the key to management of a pregnancy with such a diagnosis is likely to be optimising the condition at delivery and minimising neonatal morbidity.


21. (a) F (b) F (c) T (d) F (e) T


Explanations:


It is mainly determined by maternal size. Recent studies have suggested that the role of fetal genes encoding Insulin like growth factor is important in controlling fetal growth. Uterine blood volume is 50% more than the minimal requirements of fetal oxygenation and is a safety measure to protect against minor fluctuations.


22. (a) F (b) T (c) T (d) T (e) T


Explanations:


The Ductus venosus bypasses the liver. b), c) and d) have all shown to be true. Uterine blood volume is indeed 50% more than the minimal requirements of fetal oxygenation.


23. (a) F (b) T (c) T (d) F (e) F


Explanations:


Maternal genes tend to restrain fetal growth. IGF-II does promote fetal growth and is over-expressed in Beckwith-Wiedemann syndrome resulting in macrosomia and under-expressed in IGF-II in Silver-Russell Syndrome resulting in IUGR. Growth restriction starting before mid-gestation can be asymmetrical sometimes.


24. (a) F (b) T (c) T (d) T (e) F


Explanations:


Placental mass may be a reflection of uterine size rather than the cause. Antiphospholipid antibodies can lead to IUGR through vascular microthrombosis and subsequent infarction. Fetal growth can be affected both ways even in patients with reliable and seemingly well controlled sugars. Reduction in global bodyweight is a later change in IUGR.


25. (a) F (b) T (c) F (d) F (e) T


Explanations:


The blood flow through the ductus venosus is increased in haemodynamic compromise.


In IUGR, the cerebral blood flow is indeed increased by 2–3 fold as seen when redistribution occurs. Until now, there are no interventions to reverse intrauterine programming. IUGR can have long term effects on adolescent and adult life such as the development of diabetes and hypertension.


26. (a) F (b) T (c) F (d) F (e) F


Explanations:


IUGR has been studied intensively, however, many questions are still unanswered, both regarding the underlying pathophysiological processes, responses of the fetus to developing hypoxia, and the clinical management. Not many clinical management protocols are evidence-based, especially not those concerning IUGR in very preterm fetuses. Clinical practice often differs between countries and between peri-natal centres.


27. (a) T (b) T (c) T (d) T (e) T


Explanations:


An ultrasonically estimated value that is below the chosen cut-off level, e.g. fetal weight below the 10th percentile, indicates SGA. When using the 10th percentile, a large proportion of SGA fetuses will be fully healthy, with normal growth rate and with a normally functioning placenta. To use the 3rd or 5th percentile to define SGA might be more rational as the risk group will be smaller with a higher prevalence of IUGR. In Sweden, the SGA fetal weight or birth weight is traditionally defined as weight below the mean of the standard population minus 2 standard deviations (SD). The detection of SGA fetuses enables the initiation of further evaluation, exclusion of healthy SGA fetuses, and surveillance of fetal health in pregnancies with true IUGR. In a large register study, it was shown that SGA fetuses (birth weight below the mean minus 2 SD of the standard growth curve) undetected before birth had a four fold-increased risk of severe adverse pregnancy outcome (hypoxic ischemic encephalopathy, 5-minute Apgar score <4, neonatal convulsions, acidosis, cerebral palsy, perinatal or infant death) as compared with SGA fetuses identified prior to birth and submitted to a structured antenatal surveillance program. Moreover, the magnitude of risk increase was related to the degree of growth restriction.


28. (a) F (b) F (c) T (d) T (e) F


Explanations:


In the absence of large prospective studies evaluating the benefits of antenatal detection of SGA fetuses, the Malmö retrospective study gives convincing support to screening for small fetuses. 3D-ultrasound techniques has raised expectations of a more accurate estimation of fetal weight. However, so far, the 3D-method has not proved superior to the 2D-method. Besides, the 3D-method requires more expensive equipment, specially trained operators and it is more time consuming than the 2D-method. At present, ultrasound estimation of fetal weight is the most reliable method for clinical practice. Many formulae have been presented utilizing various ultrasonically measured fetal variables, the most commonly used being the formulae based on fetal biparietal diameter and abdominal circumference, or using fetal head circumference, abdominal circumference and femur length. In Sweden, the most common formula uses the mean abdominal diameter instead of abdominal circumference.


29. (a) T (b) T (c) F (d) T (e) F


Explanations:


It was recognized early on that the waveform pattern of doppler shift signals recorded from the blood flow in the umbilical artery reflect the resistance to flow in the placenta and that the waveform changes correlate with the fetal condition and outcome of pregnancy. For practical use in a case of an SGA fetus, it is therefore reasonable to consider the finding of abnormal umbilical artery doppler velocimetry as proof of IUGR of placental origin. In cases with severely abnormal blood velocity waveforms with absent or reverse end-diastolic flow, the perinatal mortality is increased 4 and 10.6 times, respectively. The above described empirical findings have initiated application of umbilical artery doppler velocimetry for fetal surveillance in high risk pregnancies; it has been shown in randomized controlled trials that the use of doppler velocimetry leads to a decrease in perinatal mortality rate, number of antenatal admissions and inductions of labour. This effect was still more pronounced when only studies including pregnancy complications mainly due to placental dysfunction, like pre-eclampsia and IUGR, were considered. On the contrary, in uncomplicated pregnancies, randomized studies showed that use of umbilical artery doppler velocimetry as a screening for IUGR is not justified.


30. (a) T (b) T (c) T (d) T (e) T


Explanations:


When a fetus is very preterm and growth restricted with abnormal blood flow at doppler examination it should be delivered usually by Caesarean Section as the method of choice. Two recently published studies reported the caesarean section rate in such groups of fetuses delivered before 30 weeks of gestation to be 100% and 88%, respectively. The IUGR fetus in labour, whether induced or spontaneous, should indeed be continuously monitored as it is prone to developing fetal distress. It has been shown in many studies that SGA newborns often have suboptimal postnatal development. In IUGR newborns that have had abnormal intrauterine flow, neurological and cognitive development was found to be impaired up to the young adult age.

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Nov 9, 2017 | Posted by in OBSTETRICS | Comments Off on Intrauterine growth restriction: A contemporary review Answers to Multiple Choice Questions for Vol. 23, No. 6
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