Comparative newborn anthropometric data in symmetric versus asymmetric intrauterine growth retardation

Comparative newborn anthropometric data in symmetric versus asymmetric intrauterine growth retardation

Comparative newborn anthropometric data in symmetric versus asymmetric intrauterine growth retardation JAMES P. CRANE, M.D. 1\.,f 1v.1. l!f\D'T~t\ n...

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Comparative newborn anthropometric data in symmetric versus asymmetric intrauterine growth retardation JAMES P. CRANE, M.D. 1\.,f 1v.1.

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St. Louis, Missouri Autopsy studies have shown that the fetal liver is more severely affected than the brain in asymmetric fetal intrauterine growth retardation (IUGR). This "brain-sparing" concept has led to the suggestion that ultrasonic measurements of biparietal diameter (BPD) are of limited value in detecting IUGR since the BPD is an indirect reflection of head and brain size. This study compares the effects of asymmetric and symmetric IUGR on newborn anthropometric measurements, including head circumference (HC), birth weight (BW), length (L), and ponderal index (PI) in 33 growth-retarded infants divided into two groups, asymmetric (uteroplacental failure) and symmetric (maternal smoking, drug exposure, congenital anomalies, intrauterine infection), on the basis of the etiology of the IUGR. The percentage reduction in size from mean values for the same gestational age was calculated for each parameter. None of the newborn parameters were useful in distinguishing between infants with asymmetric and those with symmetric IUGR. Particularly noteworthy is the fact that the percentage decrease in HC was similar in both groups. Therefore, the concept of absolute "brain sparing" in asymmetric IUGR is erroneous, and ultrasonic measurements of BPD should be of value in detecting this form of IUGR. (AM. J. OesTET. GYNECOL. 138:518, 1980.)

AUTOPSY studies!. 2 in small-for-gestational-age (SGA) infants have revealed two basic patterns of IUGR (intrauterine growth retardation). One of these is designated "symmetric" IUGR because all body organs tend to be proportionately reduced in size. Etiologic factors responsible for symmetric growth retardation include intrauterine infections, such as rubella and cytomegalovirus, chromosome abnormalities, other congenital anomalies, maternal malnutrition, and smoking. Ultrasonically, the symmetric SGA fetus demonstrates a "reduced growth potential" pattern of biparietal diameter (BPD) growth which begins prior to the third trimester. Although BPD size increases from one examination to the next, absolute values consistently fall below -2 SD on the normal growth curve. 3 • 4 The other type of IUGR is "asymmetric" in nature, From the Perinatal Division, Department of Obstetrics and Gynecology, Washington University School of Medicine. Received for publication May 8, 1980. Acceptedjuly 17, 1980. Reprint requests: James P. Crane, M.D., Department of Obstetrics and Gynecology, 4911 Barnes Hospital Plaw, St. Louis, Missouri 63110.

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with some body organs more affected than others. For example, the fetal liver tends to be disproportionately small in comparison to the fetal brain.'· 2 Asymmetric growth retardation is due to uteroplacental insufficiency and is commonly seen in pregnancies complicated by chronic hypertension, preeclampsia, and advanced diabetes. Ultrasonically, biparietal growth is essentially normal in these fetuses until some point in the third trimester, when abnormal slowing and eventual total arrest of BPD growth is observed. 3 • 4 Many studies have evaluated the reliability of ultrasonic measurements of BPD in detecting IUGR.5- 8 Accuracy rates from as low as 56% to as high as 93% have been reported. The reason for the high percentage of undetected cases of I UGR in some studies is unclear. One common explanation is that in asymmetrically growth-retarded fetuses the brain is preferentially spared at the expense of the body. Since the biparietal diameter is a reflection of head size and, indirectly, brain size, abnormal slowing of, or reduction in, BPD growth might not always occur in this form of IUGR. This "brai,n sparing" theory is based upon experiments in rats, where ligation of the uterine artery that supplied one horn of a bicornuate uterus resulted 0002-9378/80/210518+05$00.50/0

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1980 The C. V. Mosby Co.

Symmetric versus asymmetric IUGR

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Table II. Predisposing factors in 20 infams with asymmetric IliGR Factor Chronic hypertension Preeclampsia Cardiac disease Diabetes Unknown Total

6 :I I

Table III. Predisposing factors in I :3 infants with symmetric IUGR

31 WEEK OF GESTATION

Fig. I. Birth weights in 3~1 newborn infants with symmetric and asymmetric growth retardation (plotted on Colorado Intrauterine Growth Curve 15 ). UP!: Uteroplacental insufficiency. R(;p; Reduced growth potential.

Table I. Parameters of fetoplacental status in 20 SGA infants with uteroplacental insufficiency Abnormal Parameter Abnormal estriol pattern

Low human placental lactogen

Antepartum meconium Positive contraction stress test +lor late deceleration in labor Abnormal placental histologic features

patients tested

No.

I%

12 )9

8 10 10 18

67 100 50 95

8

6

75

No.

of

10 20

in asymmetric fetal growth retardation in which the brain was minimally affected. 9 Acute ablation of the blood supply to a portion of the placenta has produced similar results in monkeys. 10 However, comparison of growth retardation in human fetuses with that in subhuman primate models may not be appropriate, since the brain of the rhesus monkey is more advanced in maturation and development than that of the human fetus. Nevertheless. this ''brain sparing" concept has become quite popular in the obstetric literature5 • 11 - 14 and has Jed many investigators to suggest that ultrasonic cephalometry is of limited value in the detection of IUGR. The purpose of this study was to test this hypothesis by examining the effects of symmetric and asymmetric IUGR on head circumference as well as other anthropometric parameters in newborn infants. Material and methods

The study population consisted of 33 consecutive SGA infants evaluated in the Perinatal Laboratory. Twenty of the infants suffered from asymmetric

Maternal smoking Drug addiction Maternal leukemia and chemotherapy during pregnancy Maternal red cell aplasia with severe anemia Congenital cytomegalovirus infection Multiple congenital anomalies Trisomy 13 Total

6 I I

2 I

13

Table IV. Comparative anthropometric data among infants with symmetric and those with asymmetric IUGR

Parameter

S_ymmetrir

Asymmetric

IUGR-1 1

IUGR-20

mfants ( %J

Mean % durmse in: Birth weight Body length* Head circumference Infants with ponderal index
31

6.8 6.3

54

infants ('}t) 37 10.6 8.5 50

*Statistically significant, p < 0.0 I.

growth retardation due to uteroplacental insufficiencv, as confirmed by multiple parameters of placental function (Table 1). Complications of pregnancv in this group are listed in Table II. Thirteen infants were classified as symmetrically growth retarded on the basis of: (I) the existence of factors known to predispose to this form of IUGR (Table Ill), (2) the absence of fetal distress during labor, and (3) a "reduced growth potential" type of biparietal growth pattern on ultrasonography. Newborn anthropometric measurcmenb, including birth weight, body length. and head circumference values, as well as ponderal indices, were obtained on all infants and plotted by gestational age on Colorado Intrauterine Growth Curves.'" The observed measurements were compared with mean values for the same gestational age, and the percentage differt"nce was calculated for each parameter.

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WEEK OF GESTATION Fig. 3. Head circumference values in 33 newborn infants with symmetric and asymmetric growth retardation (plotted on Colorado Intrauterine Growth Curve 15 ).

WEEK OF GESTATION Fig. 2. Body lengths in 33 newborn infants with symmetric and asymmetric growth retardation (plotted on Colorado Intrauterine Growth Curve 15 ).

Results Body weight. All infants in both the symmetric and asymmetric groups plotted below the tenth percentile for gestational age (Fig. 1). The effect on body weight was not significantly different (p = 0.10) in symmetric versus asymmetric IUGR (Table IV). Among asymmetrically growth-retarded infants, body weight was reduced by an average of 37% when compared to mean values for infants of similar gestational age. The average reduction in body weight among symmetrically growth-retarded infants was 31%. Body lens..h. Fifteen (75%) of the 20 asymmetrically growth-retarded newborn infants plotted below the tenth percentile for gestational age, and the other five fell between the tenth and twenty-fifth percentiles (Fig. 2). The average reduction in body length as compared to AGA infants of similar gestational age was 10.6% (Table IV). Six (46%) of the 13 symmetrically growth-retarded infants plotted below the tenth percentile (Fig. 2). Five fell between the tenth and twenty-fifth percentiles, and two between the twenty-fifth and fiftieth percentiles. The average reduction in body length compared

to mean values for AGA singletons of similar gestational age was 6.8% (Table IV). Head circumference. Fifteen (75%) of the 20 asymmetrically growth-retarded infants had head circumference values at or below the tenth percentile for gestational age (Fig. 3). The other five newborn infants plotted between the tenth and twenty-fifth percentiles. The average reduction in head circumference compared to mean values for AG"A. singletons matched for gestational age was 8.5%. Head circumferences in nine (69%) of the 13 symmetrically growth-retarded newborn infants plotted at or below the tenth percentile, and four fell between the tenth and twenty-fifth percentiles (Fig. 3). There was an average decrease in head circumference of 6.3% below mean values for AGA infants of similar gestational age. When the symmetric and asymmetric SGA groups were compared, the percentage decrease in head circumference was not found to be significantly different (p = 0.10) (Table IV). Ponderal index. Ten (50%) of the 20 asymmetrically growth-retarded infants had ponderal indices below the tenth percentile for gestational age (Fig. 4). Three infants plotted between the tenth and twenty-fifth percentiles, four fell between the twenty-fifth and fiftieth percentiles, and three plotted above the fiftieth percentile. Ponderal indices below the tenth percentile for gestational age were observed in seven (54%) of the 13 infants with symmetric growth retardation (Fig. 4). Five infants were between the tenth and twenty-fifth percentiles, and one plotted at the fiftieth percentile.

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Comment None of the newborn anthropometric parameters measured in this study were useful in distinguishing between infants with symmetric and those with asymmetric I UGR. Approximately equal percentages of infants in each group had ponderal indices below the tenth percentile for gestational age, and the mean reductions in birth weight, body length. and head circumference were also similar (Table IV). Particularly noteworthy is the fact that the percentage decrease in head circumference was approximately 8.5% in asymmetrically growth-retarded newborn infants. Therefore, the concept of absolute "brain sparing" in asymmetric IUGR is erroneous. This finding is supported by the autopsy data of 1'\aeye and co-workers, 1• 16 • 17 who compared the brain weights of symmetric and asymmetric SGA neonates to those of AGA infants of similar gestational age. The mean reduction in brain weight among asymmetric SGA fetuses who suffered from uteroplacental insufficiency was 18%. Among symmetricaiiy growthretarded infants with rubella and Down's syndrome, the average decreases in brain weight were 2 i% and 19%. respectively. Although the absolute reductions in brain weight were similar in both forms of IUGR, other body organs did tend to be more severely affected in the asymmetric group. For example, asymmetric SGA infants demonstrated mean reductions in liver and spleen weights of 53% and 57%, respectively, as compared to only an 18% decrease in brain weight. In contrast, all bodv organs tended to be proportionately reduced in size in the symmetrically retarded infants. For example, among infants with congenital rubella, the mean reductions in brain, liver, and spleen weights were 21%. 2~~%,, and 28%, respectively. Therefore, use of the terms "symmetric" and "asymmetric" is justified on this basis. but the concept of absolute Hbrain sparing" in asymmetric IUGR is incorrect and misleading. Since brain size and head circumference are reduced in asymmetric I U GR, ultrasonic measurement of the biparietal diameter should be of value in the prenatal detection of this form of growth retardation. Indeed, the major problem with the use of biparietal measurements has been "overdiagnosis" and not "underdiagnosis" of IUGRY This is because inadequate growth of the head from one examination to the next

REFERENCES I. N aeye, R. L., Kelly ,J. A.: Judgment of fetal age. III. The pathologist's evaluation. Pediatr. Clin. North Am. 13:849, 1966. 2. Gruenwald. P.: Chronic fetal distress and placental insufficiency. Bioi. Neonate 5:215, 1963. 3. Crane.]. P .. Kopta, M. M., Welt, S.l., and Sauvage,]. P.:

30 34 38 WEEK OF GESTATION

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Fig. 4. Pondera! indices in 33 newborn infants with symmetric and asymmetric growth retardation (plotted on Colorado Intrauterine Growth Curve' 5 ).

can be related to other factors, such as technical error in correctly identifving and measuring the true biparietal diameter. Another problem may be related to normal biologic variation in cranial morphology. The biparietal diameter reflects onlv one dimension of head size, so that less than average biparietal growth need not always correlate with IUGR. \ arious techniques have been proposed to overcome this problem, including ultrasonic measurement of fetal head circumference, 1 ~ endocranial volume. 20 and ratio of head to abdominal circumference. 2 t. 22 The latter technique is based upon the fact that the liver is more severely _rr __ . __ l L'--- .L_ 1 • • __ • · aueueu utan ute urarn Ill asynuuernc 11 •t.,K. I.A>nsequently, the abdominal circumference measured at the level the umbilical vein may be disproportionately small in comparison to fetal head circumference when true asyn1n1etric I liGR exists. In summary, the average decrease in brain size is approximately lH% in asynunetnl I LH ~R. 'rhis i~ reflected by an average 8.5% decrease in fetal head circumference for gestational age. The fetal brain is not spared in asymmetric IUGR, and ultrasonic measurement of the biparietal diameter can be of value in detecting this form of I UGR. 1r1r~.--..

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Abnormal fetal growth patterns-UltrasoniC diagnosis and management, Obstet. Gynecol. 50:205, 1977. 4_ Campbe!!, S.: Fetal growth. C!in. Obstet. (~yneco1. 1:41, 1974. 5. Dewhurst, C.J., Beasley,]. M., and Campbell, S.: Assessment of fetal n1aturity and dysmaturity. AM. j. OssTET. GYNECOL. 113:141, 1972.

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6. Queenan, J. T., Kubarych, S. F., Cook, L. N ., Anderson, G. D., and Griffin, L P.: Diagnostic ultrasound for detection of intrauterine growth retardation, AM. J. 0BSTET. GYNECOL. 124:865, 1976. 7. rv1ann, L. I., Tejani, i"~. A., and '\Veiss, R. R.: Antenatal diagnosis and management of the small-for-gestational age fetus, AM. J. 0BSTET. GYNECOL. 120:995, !974. H. Whetham, J. C. G., Muggah, H., and Davidson, S.: Assessment of intrauterine growth retardation by diagnostic ultrasound. AM. 1. 0BSTET. GvNECOL. 125:577. 1976. 9. Wiggleswo~th, J.JS.: Experimental growth reta~dation in the fetal rat, J. Pathol. 88: I, 1964. 10. Hill, D. E., Myers, R. E., Holt, A. B., Scott, R. E., and Cheek, D. B.: Fetal growth retardation produced by experimental placental insufficiency in the rhesus monkey, Bioi. Neonate 19:68, 1971. II. Gohari, P., Berkowitz, R. L., and Hobbins, J. C.: Prediction of intrauterine growth retardation by determination of total intrauterine volume, AM. ]. 0BSTET. GYNECOL. 127:255, 1977. 12. Wladimiroff,]. W., Bloemsma, C. A., and Wallenburg, H. C. S.: Ultrasonic assessment of fetal head and body sizes in relation to normal and retarded fetal growth, AM. j. 0BSTET. GYNECOL. 131:857, i978. l:l. Hobbins, J. C., Be!'kowitz, R. L., and Grannum, P. A.: Diagnosis and antepartum management of intrauterine gro~th retardation:]. Reprod. Med. 21:319, 1978. 14. Levine, S.C., Filly, R. A., and Creasy, R. K.: Identification of fetal gro\vth retardation by u!trasonographic estima-

November I, l!JHO

Am.]. Obstet. Gynecol.

15. 16. 17. 18. 19. 20.

21.

22.

tion of total intrauterine volume, J. Clin. Ultrasound 7:21, 1979. Lubchenco, L. 0., Hausman, C., and Boyd, E.: Intrauterine growth as estimated from liveborn birth weight data al 24 to 42 weeks' gestation, Pediatfics 32:i93, i 963. Naeye, R. L.: Malnutrition-Probable causes of fetal growth retardation, Arch. Pathol. Lab. Med. 79:284, 1965. Naeye, R. L., and Blanc, W.: Pathogenesis of congenital rubella,J.A.M.A 194:!277, 1965 Sabbagha, R. E.: Intrauterine growth retardation-Antenatal diagnosis by ultrasound, Obstet. Gynecol. 52:252. 1978. Jordaan, H. V., Sattar, F. A., Shah, P .. and Makarachi, A.: Simplified method of determining fetal brain weight in utero, Obstet. Gynecol. 55:673, 1980. Martinez, D. A., and Barton, ]. L.: Estimation of fetal body and head volumes: Description of technique and nomograms for 18 to 41 weeks of gestation, AM. J. 0BSTET. GYNECOL. 137:78, 1980. Crane, J.P., and Kopta, M. M.: Prediction of intrauterine growth retardation via ultrasonically measured head: abdominal circumference ratios, Obstet. Gyneco\. 54:597, i979. Campbell, S., and Thoms, A.: Ultrasound measurement of the fetal head to abdomen circumference ratio in the assessment of growth retardation, Br. ]. Obstet. Gynaeco\. 84:165, !977.