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Severely Abnormal Doppler Findings and Perinatal Abnormalities
the pathophysiology leading to reverse flow is still uncertain.
Because of small case numbers, adequate epidemiological data
have not yet been published on reverse flow. Nearly all authors
studied fewer than 30 cases and usually analyzed the data on
AEDF and reverse flow together (“ARED“ = absent or reverse
end-diastolic flow), without differentiating between them. An
exceptionis the study byKarsdorp et al., who analyzed the data
from nine perinatal centers
26
(Table 19.4).
Many factors that can affect fetal and maternal hemody-
namics alter the flow pattern in the umbilical artery or fetal
8
aorta
. Absent and/or reverse end-diastolic flow is significantly
more common in pregnancies with intrauterine growth retardation (IUGR) (odds ratio 3.1), with PIH, or with IUGR and PIH
(odds ratio 7.4)
5, 13, 26, 45,64
. In our study, we found that cases
with IUGR were at high risk for the development of reverse
flow (odds ratio 22.6). In cases with severe IUGR, we found
either a small placenta or massive intervillous fibrin deposits
in the placenta. This could account for the occurrence of abnormal flow patterns.
Pregnancy-induced hyper tension. Patients diagnosed with PIH
in our study had an increased risk for end-diastolic reverse
flow (odds ratio 3.8). A number of authors suggest that a close
19
correlation exists b etween severely abnormal Doppler
waveforms and PIH
13, 64
. An increased production of prostacyclin and/or endothelium-derived relaxing factors has b een detected in patients with PIH. This is believed to decrease placental blood flow due to the reduction of active renin and angiotensin II in the peripheral circulation or to increased activity of
the renin–angiotensin system in the uteroplacental circulation. In turn, this leads to local hypoxemia in the placenta and
also induces the production of oxygen free radicals, which are
known to mediate local vasoconstriction of the placental ves-
sels in PIH. Apparently this could explain the increased placen-
tal vascular resistance that is found in patients with PIH.
Nicotine abuse. An increased incidence of reverse flow was
also documented in women who smoke more than 10 cigarettes per day (odds ratio 9.4). These results conflict with those
reported in the literature. Karsdorp et al. found no relationship
between the risk of reverse flow and maternal smoking hab-
26
its
. Another study found that nicotine did not affect hemodynamics prior to the appearance of vascular damage with morphological changes
20
. Nicotine can induce the vasoconstriction
of placental vessels, however, causing a reduction of uteroplacental blood flow. These changes are well documented by
the available literature on placental studies
25, 42
.
Intrauterine fetal death. The increased incidence of in-
trauterine death is a problem in fetuses with reverse
flow
5, 8, 45, 58
. Seven authors in the literature reported an average
incidence of 47%, meaning that almost half of fetuses with
reverse flow died in utero (Table 19.
5). The interval from initial
diagnosis to fetal death ranged from one day to several days. In
our own study, intrauterine death occurred in 40% of the fetuses with reverse flow. The average interval between the detection of reverse flow and the occurrence of intrauterine fetal
death was only 2.5 days. Overall, 92% of the intrauterine fetal
deaths occurred within one week after diagnosis.
Todros et al. reported that absent or reverse end-diastolic
flow had a high predictive value for an adverse fetal outcome.
They therefore consider that a definitive diagnosis of ARED is
an indication for immediate delivery.
172
Table 19.4 Review of the literature on mortality rates associated with reverse end-diastolic flow
Authors Year Cases Gestational
age at delivery
(weeks)
Brar 1988 12 30 + 1 50 33 50 18
Illyes 1988 5 32 + 2 100 100 100 –
Schmidt 1991 4 30 + 4 100 75 50 25
Fouron 1993 5 28 +3 60 60 – –
Valcamonico 1994 5 30 + 1 – 20 40 20
Karsdorp (multicenter study) 1994 67 29 + 0 75 24 – 51
Zelop 1996 24 29 +1 – 17 33 –
Average values for all studies 17 30 77 47 55 29
Our results 1998 30 30 + 6 53 40 27 22
IUFT = intrauterine fetal death
Cesarean
section rate
(%)
IUFD
(%)
Perinatal
mortality
Postpartum
mortality
Table 19.5 Comparison of perinatal abnormalities
Summary
Perinatal abnormalities Reverse flow
(authors = 8)
Total cases 152 1062 560
Average values Median Average values Median Average values Median
Cases 19 9 51 30 35 32
Gestational age at delivery (weeks) 30.1 30.1 31.9 31.6 31.2 31.2
Total mortality 73.0 67.5 32.2 34 43.9 40
Perinatal mortality 50.0 45 28.7 22 35.4 38
Neonatal mortality 27.1 22 19.4 20 20.0 10
IUFD (%) 46.0 36.5 16.7 11 25.1 16
Anomalies (%) 21.8 23 18.2 15 21 21
IUGR (%) 100 100 88.3 91 90 94
Birthweight (g) 997 983 1337 1225 1114 1037
Cesarean delivery (%) 93 96 72.7 80 74.4 75
1-min Apgar ⱕ 7 (%) 84.3 78 63.8 66 68.5 72
pH ⱕ 7.2 (%) 41.5 41.5 19.0 19 26.0 26
IUFD = intrauterine fetal death.
IUGR = intrauterine growth retardation.
AEDF
(authors = 21)
Reverse flow/AEDF
(authors = 16)
Specific Obstetric Problems
Summary
Prognostic factor for high-risk pregnancies. Doppler
velocimetry is an important method in perinatal diagnosis for
the evaluation of high-risk pregnancies. Since severely abnormal findings are often noted in the initial Doppler examination, high-risk pregnancies should undergo Doppler evaluation
as early as possible. A severelyabnormal Doppler finding in the
fetal vessels, such as absent end-diastolic flow (AEDF) or
reverse flow, appears to be a significant additional prognostic
factor for the high-risk pregnancy.
Absent and reverse flow. Because of small case numbers, absent and reverse end-diastolic flow haveof ten been assigned to
a common group in the previous literature (“ARED flow”). This
practice should be discontinued in the future. If we define “hypovascularization of the placenta” as the underlying cause of
these flow patterns, we must regard both phenomena as the
end points on a continuum of placental malperfusion. Generally the clinical consequences of AEDF are more “benign”
than in cases with reverse flow.
Doppler sonography and ABCD profile. It is essential that we
continue to research the underlying principles of placental
malperfusion. We should also direct our efforts toward learning to assess the dynamics of placental insufficiency in order to
prevent antenatal intrauterine insults to the maturing organs,
as these insults appear to be chiefly responsible for long-term
morbidity. Proficient Doppler scanning of the fetomaternal
vessels will continue to be the principal instrument for making
this assessment. It may also be necessary to apply further biophysical tests within the context of a biophysical profile (ABCD
profile)
22, 23
to meet this important clinical challenge.
Therapeutic implications. There are occasional cases in which
end-diastolic flow can be improved with appropriate treatment in fetuses who manifest absent or reverse flow. This
means that immediate delivery may be unnecessary in some
fetuses that have a severely abnormal flow pattern but receive
optimum, intensive perinatal care. A prompt cesarean delivery
is unavoidable in many cases, however.
Postnatal development. These children have markedly increased mortality and serious morbidity in the neonatal period
as well as a markedlyincreased risk of later neuromotor abnormalities compared with children of comparable gestational
age with normal prenatal Doppler findings.
Long-term sequelae can also result from hypoxia-induced
intracerebral hemorrhage, which is common in cases with a
brain-sparing redistribution of blood flow. Fetuses that are
delivered in a compromised condition (abnormal umbilical
cord pH, abnormal Apgar score) have a markedly higher risk of
hemorrhage than fetuses that have received optimum perinatal management. Optimum management includes early referral to a perinatal center, where the timing of the delivery
and perinatal management can be decided in close cooperation with a neonatologist and tailored to the individual situation following a detailed consultation with the parents.
173
Severely Abnormal Doppler Findings and Perinatal Abnormalities
174
References
1 Adiotomre PN, Johnstone FD, Laing IA: Effect of absent end diastolic
flow velocity in the fetal umbilical artery on subsequent outcome.
Arch. Dis. Child Fetal Neonatal. 76(1) (1997) 35–38
2 Arabin B, Saling E: Die „Sparschaltung“ des fetalen Kreislaufs
dargestellt anhand von eigenen quantitativen Doppler-Blutflussparametern. Z. Geburtshilfe Perinatol. 191 (1987) 213–218
3 Arduini D, Rizzo G: Prediction of fetal outcome in small for gesta-
tional age fetuses: Comparision of Doppler measurements obtained
from different fetal vessels. J. Perinat. Med. 20 (1992) 29–38
4 Ariyuki Y, Hata T, Kitao M: Reverse end-diastolic umbilical artery
velocity in a case of intrauterine fetal death at 14 weeks' gestation.
Amer. J. Obstet. Gynecol. 169(6) (1993) 1621–1622
4a Babajan A: Die intrauterine fetale Wachstumsretardierung; Ätiologie
und Diagnostik. Dissertationsschrift, Universität des Saarlandes 1998
5 Battaglia C, Artini PG, Galli PA, D'ambrogio G, Droghini F, Genazzani
AR: Absent or reversed end-diastolic flow in umbilical artery and severe intrauterine growth retardation. Acta. Obstet. Gynecol. Scand. 72
(1993) 167–171
6 Bekedam DJ, Visser GHA, van der Zee AGJ, Snijders RJM, Poelmann-
Weesjes G: Abnormal velocity waveforms of the umbilical artery in
growth-retarded fetuses: Relationship to antepartum late heart rate
decelerations and outcome. Early Hum. Dev. 24 (1990) 79–89
7 Bjerre F, Hansen E: Psychomotor development and school adjustment
19
of 7-year-old children with low birthweight. Acta. Paediatr. Scand. 65
(1976) 88–96
8 Brar HS, Platt LD: Reverse end-diastolic flow velocity on umbilical
artery velocimetry in high-risk pregnancies: An ominous finding
with adverse pregnancy outcome. Amer. J. Obstet. Gynecol. 159
(1988) 559–561
9 Chandran R, Serra-Serra V, Sellers SM, Redman CWG: Fetal middle
cerebral artery flow velocity waveforms – a terminal pattern. Brit. J.
Obstet. Gynaecol. 98 (1991) 937–938
10 Chaoui R, Hoffmann H. Zienert A, Bollmann R, Halle H, Grauel EL:
Klinische Bedeutung und fetal outcome beim enddiastolischen
Flowverlust in der A. umbilicalis und/oder fetale Aorta: Analyse von
51 Fällen. Geburtsh. u. Frauenheilk. 51 (1991) 532–539
11 Comas C, Carrera M, Devesa R et al.: Early detection of reversed dias-
tolic umbilical flow: should we offer karyotyping? Ultrasound Obstet.
Gynecol. 10 (1997) 400–402
12 Edelstone DI: Fetal compensatory response to reduced oxygen
delivery. Sem. Perinat. 8 (1984) 184–191
13 Ertan AK, He JP, Tossounidis I, Schmidt W: Einfluss der EPH-Gestose
auf perinatale Faktoren bei Fällen mit „Reverse Flow“ bzw. „enddiastolischem Block“ in den fetalen Gefäßen. In Künzel W (ed.), Arch. Gynecol. Obstet. 258 (1996) 113
14 Ertan AK, Jost W, Mink D, Schmidt W: Neuromotoric development of
children after ARED-Flow during pregnancy. In Kurjak A, Latin V,
Rippmann E (eds.): Advances on the pathophysiology of pregnancy.
CIC Edizioni internazionali 1995, 55–62
15 Ertan AK, Jost W, Hendrik J, Lauer S, Uhrmacher S, Schmidt W: Peri-
natal events and neuromotoric development of children with zero
flow in the fetal vessels during the last trimester. In Cosmi EV, Di
Renzo GC: 2 nd World Congress of Perinatal Medicine. Monduzzi Editore 1993, 1049–1052
16 Erz W, Gonser, M: Dopplersonographie der fetalen Arteria cerebri
media: Präfinale Normalisierung des zerebralen Blutflusses? Geburtshilfe Frauenheilkd. 55 (1995) 407–409
17 Fitzgerald DE, Drumm JE: Non-invasive measurement of human fetal
circulation using ultrasound: a new method. Brit. Med. J. 2 (1977)
1450–1451
18 Göschen K: Überwachung der Schwangerschaft aus forensischer
Sicht. Gynäkologe 27 (1994) 197–207
19 Gudmundsson S, Tulzer G, Huhta JC, Marsal K: Venous Doppler in the
fetus with absent end-diastolic flow in the umbilical artery. Ultrasound Obstet. Gynecol. 7(4) (1996) 262–267
19a He JP: Reverse Flow; perinatologische Auffälligkeiten. Dissertations-
schrift, Universität des Saarlandes 1998
20 He JP, Ertan AK, Reitnauer K, Mink D, Schmidt W: Pathomorpholo-
gische Veränderungen der Endzotten: Vergleich bei Fällen mit
„Reverse Flow“ / enddiastolischem Block bzw. mit normalen Doppler-Flow-Befunden in den fetalen Gefäßen. Im Druck 2000
21 Hellbrügge T, Lajosi F, Menara D, Schamberger R, Rautenstrauch T:
Münchner Funktionelle Entwicklungsdiagnostik. Erstes Lebensjahr.
Hansisches Verlagskontor, Lüb eck 1978
22 Hendrik H-J, Ertan AK, Schmidt W: Die Überwachung der
Risikoschwangerschaft mit einem neuen biophysikalischen Profil
(ABCD-Profil). Im Druck 2000
23 Hendrik H-J, Tossounidis I, Boos R, Schmidt W: Neuentwicklung eines
fetalen biophysikalischen Profils unter Verwendung verschiedener
sonographischer Parameter, Doppler-Flow und der Kinetocardiotokographie. Ultraschalldiagnostik, Dreiländertreffen, Bildgebung/
Imaging 61(Suppl. 2) (1994) 92
23a Hitschold T, Ulrich S, Kalder M, Müntefering H, Berle P: Blut-
strömungsprofile der A. umbilicalis. Korrelation zur Plazentamorphologie und zu klinisch-geburtshilflichen Daten im Rahmen der
Präeklampsie. Z. Geburtsh. u. Neonat. 199 (1995) 8–12
24 Jouppila P, Kirkinen P: Increased vascular resistance in the de-
scending aorta of the human fetus in hypoxia. Brit. J. Obstet. Gynaecol. 91 (1984) 853–856
25 Karsdorp VH, Dirks BK, van der Linden JC, van Vugt JM, Baak, JP, van
Geijn HP: Placenta morphology and absent or reversed end diastolic
flow velocities in the umbilical artery: a clinical and morphometrical
study. Placenta 17 (1996) 393 –399
26 Karsdorp VH, van Vugt JM, van Geijn HP et al.: Clinical significance of
absent or reversed end diastolic velocity waveforms in umbilical
artery. Lancet 17(344) (1994) 1664–1668
27 Kingdom JC, Kaufman P: Oxygen and placental villous development:
origins of fetal hypoxia. Placenta 18 (1997) 613–621
28 Köhler G, Egelkraut H: Münchner Funktionelle Entwicklungsdiagnos-
tik für das zweite und dritte Lebensjahr. Eigenverlag der Aktion Sonnenschein 1984
29 Krebs C, Macara LM, Leiser R, Bowman AWF, Greer IA, Kingdom JCP:
Intrauterine growth restriction and absent diastolic flow velocity in
umbilical artery is associated with maldevelopment of the terminal
placental villous tree. Amer. J. Obstet. Gynecol. 175 (1996) 1534–1542
30 Kubli F, Schmidt W: Zustandsdiagnostik des Feten. In Bachmann KD,
Ewerbeck H, Kleihauer E, Rossi E, Stalder G (eds.): Pädiatrie in Klinik
und Praxis. Bd. 1.Thieme, Stuttgart (1987) 79–94
31 Kurkinen-Raty M, Kivela A, Jouppila P: The clinical significance of an
absent end-diastolic velocity in the umbilical artery detected before
the 34 th week of pregnancy. Acta. Obstet. Gynecol. Scand. 76 (1997)
398–404
31a Lauer S: Enddiastolischer Block und neuromotorische Entwicklung.
Dissertationsschrift, Universität des Saarlandes 1997
32 Low JA, Handley-Derry MH, Burke SO et al.: Association of in-
trauterine fetal growth retardation and learning deficits at age of 9 to
11
years. Amer. J. Obstet. Gynecol. 167 (1992) 1499–1505
33 Manning FA, Morrison I, Lange IR: Fetal biophysical profile scoring. A
prospective study in 1184 high-risk patient. Amer. J. Obstet. Gynecol.
140 (1981) 289–293
34 Marlow N, Hunt LP, Chiswick ML: Clinical factors associated with ad-
verse outcome for babies weighing 2000 g or less at birth. Arch. Dis.
Child 63 (1988) 1131–1136
35 Matilainen R, Heinonen K, Siren-Tiusanen H, Jokela V, Launiala K:
Neurodevelopmental screening of in utero growth-retarded prematurely born children before school age. Eur. J. Pediatr.146 (1987) 453–
457
36 Nickel RE, Bennett FG, Lawson FN: School performance of children
with birthweightsof 1000 g or less. Amer. J. Dis. Child 136(1982) 105–
110
37 Poulain P, Palaric JC, Milon J et al.: Absent end diastolic flow of umbili-
cal artery Doppler: pregnancy outcome in 62 cases. Eur. J. Obstet. Gynecol. Reprod. Biol. 53(2) (1992) 115–119
References
38 Richter T, Lietz R, Beyreiss K: Gewichts- und Längenentwicklung ehe-
mals hypotroph geborener Kinder in Abhängigkeit vom Schweregrad
der intrauterinen Retardierung. Kinderärztl. Praxis 59 (1991) 341–
345
39 Riegel K: Die Entwicklung des Kindes nach Schwangerschafts- und
Geburtsrisiken. Diagnostik 14 (1981) 493–500
40 Rizzo G, Pietropoll-Li A, Capponi A, Arduini D, Romanini C: Chromo-
somal abnormalities in fetuses with absent end-diastolic velocity in
umbilical artery: analysis of risk factors for an abnormal karyotype.
Amer. J. Obstet. Gynecol. 171(3) (1994) 827–831
41 Rochelson B: The clinical significance of absent end-diastolic velocity
in the umbilical artery waveforms. Clin. Obstet. Gynecol. 32 (1989)
692–702
42 Salafia CM, Pezzullo JC, Minior VK, Divon MY: Placental pathology of
absent and reversed end-diastolic flow in growth-restricted fetuses.
Obstet. Gynecol. 90(5) (1997) 830–836
43 Scherjon SA, Smolders-De Haas H, Kok JH, Zondervan HA: The “brain-
sparing” effect: Antenatal cerebral Doppler findings in relation to
neurologic outcome in very preterm infants. Amer. J. Obstet. Gynecol.
169 (1993) 169–175
44 Schmidt W, Ertan AK: Dopplersonographie in der Geburtsmedizin.
Geburtshilfliches Management bei hochpathologischen DopplerFlow-Befunden. In Hillemans HG (ed.): Geburtshilfe – Geburtsmedizin. Eine umfassende Bilanz zukunftsweisender Enwicklungen
am Ende des 20. Jahrhunderts. Springer, Heidelberg 1995, 317–325
45 Schmidt W, Ertan AK, Rühle W, von Ballestrem CL, Gnirs J, Boos R:
Dopplersonographie: „Enddiastolischer Block bzw. Reverse Flow“ –
Perinatologische Daten und geburtshilfliches Management. Jahrbuch
der Gynäkologie und Geburtshilfe. Biermann Verlag, Zülpich 1991,
99–106
46 Schmidt W, Graf-von-Ballestrem CL, Ertan AK, Rühle W, Gnirs J, Boos
R: Pathologische Doppler-Flow-Befunde und kardiotokographische
Ergebnisse. Geburtsh. u. Frauenheilk. 51 (1991) 523–531
47 Schmidt W, Gnirs J: Fetale Bewegungsaktivität und akustische Stimu-
lation. Gynäkologe 23 (1990) 289–297
48 Schmidt W, Kubli F, Garoff L et al.: Diagnose der intrauterinen
Wachstumsretardierung – Vergleich von Klinik, Gesamtöstrogenbestimmung aus dem 24 h Urin und Ultraschallbiometrie (Distanzmessungen, biparietaler Kopfdurchmesser, thorako-abdominaler Querdurchmesser) unter Berücksichtigung des antepartalen und subpartalen CTGs. Geburtshilfe Frauenheilkd. 42 (1982)
49 Schmidt W, Rühle W, Ertan AK, Boos R, Gnirs J: Doppler-Sonographie
– Perinatologische Daten bei Fällen mit enddiastolischem Block bzw.
Reverse Flow. Geburtshilfe Frauenheilkd. 51 (1991) 288–292
50 Schulman H, Fleischer A, Stern W, Farmakides G, Jagani N, Blattner P:
Umbilical velocity wave ratios in human pregnancy. Amer. J. Obstet.
Gynecol. 148 (1984) 985–990
51 Taylor DJ, Howie PW: Fetal growth achievement and neu-
rodevelopmental disability. Brit. J. Obstet. Gynaecol. 96 (1989) 789–
794
52 Trudinger BJ, Cook CM, Giles WB, Connelly A, Thompson RS: Umbili-
cal artery flow velocity waveforms in high-risk pregnancy. Randomised controlled trial. Lancet 1 (1987) 188–190
53 Ulrich S, Ernst JP, Kalder M, Weiss E, Berle P: Neurologische Spät-
morbidität von Frühgeburten mit intrauterin diagnostiziertem Nulloder Negativflow der Nabelarterien. Z. Geburtshilfe Perinatol. 198
(1994) 100–103
54 Ulrich S, Weiss E, Kalder M, Hitschold T,Berle P: Doppler sonographic
flow measurements of the middle cerebral artery in end-diastolic
zero flow in the umbilical arteries in relation to fetal outcome. Z. Geburtsh. Neonatol. 200(1) (1996) 21 –24
55 Vohr B, Oh W: Growth and development in preterm infants small for
gestational age. J. Pediatr. 103 (1983) 941–944
56 Vohr B, Garcia-Coll C: Neurodevelopmental and school performance
of very low-birthweight infants: a seven year longitudinal study. Pediatrics 76 (1985) 345–350
57 Vyas S, Nicolaides KH, Bower S, Campbell S: Middle cerebral artery
flow velocity waveforms in fetal hypoxaemia. Brit. J. Obstet. Gynecol.
97 (1990) 797–803
58 Wang KG, Chen CP, Yang JM, Su TH: Impact of reverse end-diastolic
flow velocity in umbilical artery on pregnancy outcome after the
28 th gestational week. Acta. Obstet. Gynecol. Scand. 77(5) (1998)
527–531
59 Weiner Z, Farmakides G, Schulman H, Penny B: Central and peripheral
hemodynamic changes in fetuses with absent enddiastolic velocity in
umbilical artery: Correlation with computerized fetal heart rate pattern. Amer. Obstet. Gynecol. 170 (1994) 509–515
60 Weiss E, Berle P: Clinical management of fetuses with diastolic zero
or reverse flow of the umbilical arteries: Duration of clinical surveillance and fetal outcome. Z. Geburtsh. Perinat. 195 (1991) 37–42
61 Weiss E, Hitschold T, Müntefering H, Berle P: Dopplersonographie der
Art. umbilicalis: Differenzierte Diagnostik bei der intrauterinen Mangelentwicklung. Geburtsh. u. Frauenheilk. 49 (1989) 466–471
62 Weiss E, Ulrich S, Berle P: Condition at birth of infants with previously
absent or reverse umbilical artery end-diastolic flow velocities. Arch.
Gynecol. Obstet. 252 (1982) 37–43
63 Woo JSK, Liang ST, Lo RLS: Significance of an absent or reversed end
diastolic flow in doppler umbilical artery waveforms. J. Ultrasound
Med. 6 (1987) 291–297
64 Zelop CM, Richardson DK, Heffner LJ: Outcomes of severely abnormal
umbilical artery doppler velocimetry in structurally normal singleton
fetuses. Obstet. Gynecol. 87(3) (1996) 434–438
Specific Obstetric Problems
175
20 Fetal Doppler Findings in Late Pregnancy
K. Vetter
Physiological Findings in Late Pregnancy
Late pregnancy and delivery are characterized by a constant
rise in fetal demand with very little concomitant growth of the
placental supply organ.
Uterine artery blood flow. The blood flow rate in the uterine arteries rises steadily during the course of pregnancy, increasing
from about 190 ml/min before pregnancy to approximately
680 ml/min in late pregnancy
uterine artery expands from 1.6 mm before pregnancy to
3.7 mm near term. The ratio of the peak systolic velocity to the
20
maximum end-diastolic velocity—a measure of flow impedance—decreases from a mean value of 5.3 (RI = 0.81) before
pregnancy to 2.3 (RI = 0.57) near term
Placental weight and blood flow. The mass of the placenta
grows steadily from approximately 6 g at 6 weeks menstrual
age to more than 500 g at term
bly faster than the placenta. As a result, the placental-to-fetal
weight ratio of 1.16 at 16 weeks menstrual age declines to
0.13at term
placental blood flow increases during the course of pregnancy
from approximately 100 ml/min at 22 weeks to a maximum of
more than 320 ml/min at 37–38 weeks. It then falls to about
300 ml/min during the final two weeks. The rate of placental
blood flow relative to fetal weight is a constant 120 (ml/
min)/kg at 36–37 weeks. This may decline to 90 (ml/min)/kg
during the final weeks
from 0.6 at 28 weeks to 0.5 at term
The amniotic fluid volume dwindles as term approaches,
and finally the vernix caseosa disappears from the fetal skin as
a sign of decreased placental nutrition.
40
. Very early Doppler data show that the mean
13
1, 35
. The mean diameter of the
35
.
3, 40
. The fetus grows considera-
. Meanwhile the resistance index falls
26
.
aorta, and one of the first reported quantitative Doppler findings was a flow rate of 185 ⫾ 7.6 (ml/min)/kg estimated fetal
weight in the descending aorta
Values during the course of pregnancy. In subsequent years,
various groups of authors determined and published values
during the course of pregnancy
blood flow velocity (TASAV= temporal average of spatial average velocity) in the aorta ranged from 26.5 to 34.6 cm/s, with a
median value of 29.0 cm/s. The relative mean blood flow was
between 169 and 246 (ml/min)/kg, with a median value of
220 (ml/min)/kg. The peak systolic velocity (Mv
tween 70 and 118 cm/s, with a median value of 100 cm/s. The
reported mean aortic stroke volume at term was 5.4 ⫾ 1.6 ml,
with a relative stroke volume of 1.8 ⫾ 0.5 ml/kg. The mean systolic diameter of the aorta was 7.3 ⫾ 1.1mm; the mean diastolic
diameter was 6.3 ⫾ 1.1 mm. The averageeffective aortic diameter (determined by echo tracking) was 7.0 ⫾ 1.1 mm
In a study of blood flow in the descending aorta by the
author, the values showed the greatest development between
24 weeks and delivery,with a considerable rangeof variation
It is notable that the quantitative assessment of blood flow
shows substantial variability in both normal and abnormal
pregnancies. One reason for this is the difficulty of accurately
measuring fetal vascular diameters with ultrasound. Clinicians
were disappointed when Doppler ultrasound did not provide
the accuracy of blood flow measurements that they had hoped
for.
7, 8
.
9–11,15–17,20, 21, 24, 36,37
. The mean
) was be-
max
19
.
38
Aorta: Qualitative Analysis
.
176
Maternal adaptation. The signs of maternal adaptation to pregnancy gradually regress: the hematocrit rises again, the maternal blood pressure returns to its original level, AT-II sensitivity
returns to normal, and pregnancy-related edema may clear.
These are the boundary conditions for the responses of the
fetal circulation: a relative reduction in the amount of placental tissue available for nutrient supply and gas exchange, and
an absolute decrease in fetoplacental blood flow.
Aorta: Quantitative Analysis
In the early years of obstetric Doppler ultrasound, quantitative
blood flow measurements were performed on the uteroplacentofetal unit. The largest easily accessible vessel is the fetal
Waveform analysis. Analysis of the envelope curve of the
Doppler spectrum, either alone or as an adjunct to quantitative
measurements, has provided an effective impetus for prenatal
Doppler scanning. Flow impedance and pulse-wave reflections
have become more important in the interpretation of Doppler
sonograms than comparisons of flow volumes. Despite technical advances, qualitative results are easier to obtain than quantitative data—one reason being that they are more or less independent of the insonation angle. Qualitative waveform analysis has made it possible to evaluate blood flow even in small
vessels. Over time, therefore, the focus of Doppler scanning has
shifted away from the fetal aorta and more toward the cerebral
arteries in addition to other peripheral vessels such as the renal
arteries.
Fetal Doppler Findings in Late Pregnancy
300
38–42 Weeks’ gestation
28–32 Weeks’ gestation
250
200
150
100
50
Mean frequency in percent
0
0 0.16 0.24 0.32 0.400.08
Mean value
Seconds
Fig. 20.1 Frequency index profile (FIP). Nomogram ⫾ 2 SD for normalized descending aorta waveforms in the early and late third
trimester. A deepening notch appears in the late third trimester as
compared with the early third trimester. (From Griffin et al. 1983
Indices. Numerous methods have been devised for analyzing
the Doppler spectrum of the aorta. Most analyses in the literature are based on two-value indices: the S/D ratio (Stuart
and the resistance index RI (Pourcelot
satility index PI (Gosling
14
) was occasionally used by virtue of
28
). The three-value pul-
its greater sensitivity to waveform changes between the maximum and minimum. The frequency index profile (FIP
very interesting but complicated analytical method (Fig. 20.
Values during the course of pregnancy. A longitudinal study of
blood flow in the thoracic aorta during the third trimester of
pregnancy showed no significant changes in relation to gestational age: the peak velocity was 115.6 ⫾ 19.0 cm/s, the pulsatility index 1.96⫾ 0.31,the acceleration time percentage 19.2
⫾ 2.2 %, the rising slope 25.7 ⫾ 5.6, and the descending slope
4.5 ⫾ 0.9. The values in the abdominal aorta showed a similar
lack of change: peak velocity 99.7 ⫾ 18.8 cm/s, pulsatility index
1.68 ⫾ 0.28, acceleration time percentage 19.1 ⫾ 2.2 %, rising
slope 29.9 ⫾ 4.9, and descending slope 5.3 ⫾ 0.9
21
.
The mean blood flow velocity in the aorta shows a definite
increase from week 17 to week 32 of gestation, remains constant until the due date, and then falls again until week 42
The PI in the aorta remains constant throughout the pregnan-
4
cy
. The most important quantitative and qualitative indices of
aortic blood flow after 24 weeks’ gestation are reviewed in
Table 20.
1.
15
.)
33
6
)isa
1).
4, 38
Table 20.1 Quantitative and qualitative blood flow indices in the
fetal descending aorta after 24 weeks in five gestational-age groups
Parameter Unit Weeks of gestation
26 30 34 38 ⬎ 40
Heart rate beats/min 146 143 142 145 145
TASAV cm/s 26 30 31 30 28
Diameter mm 3.9 5.2 5.8 6.6 7.4
Blood flow ml/min 204 400 480 638 694
MV
max
RI 0.77 0.80 0.79 0.77 0.79
PI 1.73 1.77 1.62 1.59 1.66
TASAV = temporal average of spatial average velocities = ?????
= peak systolic velocity
Mv
max
cm/s 78 91 97 100 92
scanners with integrated Doppler make these vessels much
easier to interrogate—especially the middle cerebral artery,
which can usually be scanned at an optimum beam–vessel
angle that approaches 0⬚.
Common carotid artery. The flow velocity in the common
carotid artery increases throughout the pregnancy. The PI
)
shows a sharp decline after 32 weeks’ gestation
4
Middle cerebral artery. The Doppler velocity waveforms of the
middle cerebral artery (MCA) typically show a biphasic pattern
with continuous forward flow during diastole. The RI values
show a significant decrease at the end of pregnancy (Fig.
18, 31
20.
2)
. In another study, the S/D ratio showed a significant
decline from 6.89 ⫾ 1.48at 25 weeks to 4.23 ⫾ 0.67 at term
Renal Arteries
The PI of the renal arteries shows a linear decline between 18
and 42 weeks’ gestation, decreasing from an average of 3 to
2. This reflects a substantial decrease in impedance and may
therefore signal an increase in renal perfusion
41
Femoral Arteries
.
Unlike most other arterial sonograms during pregnancy, the PI
of the femoral arteries shows a linear rise from 1.8at 15 weeks
to 5.0 at 42 weeks
sidered a normal finding in the third trimester.
23
. Reverse flow in the femoral arteries is con-
Specific Obstetric Problems
.
42
.
.
Cerebral Arteries
The brain is a very important region in terms of the blood flow
conditions that prevail there. The common carotid artery, internal carotid artery, circle of Willis arteries, and the anterior,
middle and posterior cerebral arteries are accessible to sonographic evaluation. With the offset Doppler scanners that were
originally used, it was much easier to analyze the carotid ar-
25
teries
than the circle of Willis arteries. Today, however, sector
177
Fetal Doppler Findings in Late Pregnancy
100
95
90
85
80
75
70
65
60
RI in the middle cerebral artery
55
50
25–28 28–32 33 –36 37–40 41–42
Weeks’ gestation
Changes in Findings at Term and in Postterm Pregnancies
20
90th percentile
10th percentile
Fig. 20.2 Resistance indices (RI values) of
fetal intracranial arterial waveforms in nor-
mal pregnancies. A box plot (25th, 50th
and 75th percentiles) and whiskers plot
(10th and 90th percentiles) is shown for
each gestational age. (From Kirkinen et al.
18
198 7
.)
A variety of changes occur in the fetal circulation when the
pregnancy reaches term. As noted in a recent publication, “we
conclude that postterm pregnancy may mimic a mild fetal
growth restriction“
Fetoplacental blood flow. The first report challenging the
traditional view of a continuous progression of fetal values
during pregnancy was published in 1981. It was observed that
fetoplacental blood flow in the umbilical artery increased until
36 weeks, was maximal between 37 and 38 weeks, and then
decreased during the last two weeks of pregnancy. The blood
flow relative to fetal weight was constant until 36–37 weeks of
pregnancy, when a reduction occurred (Fig. 20.
2
.
13
3)
.
500
n = 47
400
Term Effect
Fetal aorta. When blood flow in the fetal descending aorta was
evaluated with pulsed Doppler ultrasound, it was found that
the flow showed a steady decline after term, with very little
concomitant change in the RI
velocity, we observed a very sharp velocity drop in late systole,
which in some cases was so pronounced that a notch appeared
in the Doppler velocity waveform. This phenomenon occurred
about two weeks before the start of spontaneous delivery (Fig.
20.
4). Significant dilatation of the fetal aorta was noted at the
same time
showed that notching of the aortic waveform was a normal
39
. A later study of pregnancies carried beyond term
90th percentile
29
. Besides a decreased mean flow
Fig. 20.3 Fetal umbilical cord blood flow
in normal pregnancies as a function of gestational age. The 10th and 90th percentile
values are shown. (From Gill et al. 1981
13
.)
178
300
200
100
0
Umbilical artery blood flow (ml/min)
22 24 26 28 30 32 34 36 38 40
Weeks’ gestation
50th percentile
10th percentile
cm/s
100
3–4 weeks before delivery
1– 2 weeks before delivery
Changes in Findings at Term and in Postterm Pregnancies
Table 20.2 Doppler ultrasound findings at term and in postterm
pregnancies
앫 Decreased placental blood flow
앫 Unchanged or decreased impedance in the umbilical arteries
앫 Increased impedance in the femoral arteries
앫 Decreased impedance in the renal arteries
앫 Decreased mean blood flow velocity in the dilated aorta
앫 Increased pulsatility with a notch in the descending aorta
(normal finding)
앫 Decreased impedance in the aorta
앫 Reverse diastolic flow in the aortic arch and elevated balance
index (BI)
앫 Increased diastolic flow velocities in the cerebral arteries
0
1/2 2/3
Fig. 20.4 The term effect. Median values of the fetal descending
aorta waveform recorded 3–4 weeks before delivery compared with
the median values recorded during the last two weeks before delivery.
The arrow indicates the postsystolic notch. (From Vetter et al. 1989
MinimumMaximum
39
cm/s
100
0
1 second
before any significant changes appear in the umbilical artery
waveforms. The aortic isthmus waveform was used to calculate
an index called the balance index (BI), equal to S–D divided by
the difference between the forward-and reverse-flow velocity
integrals. The BI increased slowly throughout gestation. It
.)
could be shown by color Doppler that the reverse flow ob-
Specific Obstetric Problems
served late in gestation in the aortic isthmus was coming from
the ductus arteriosus
Table 20.
2 reviews the hemodynamic situation at term and
12
.
beyond term as it may be demonstrated by Doppler scanning
of the large fetal vessels.
Circulatory Balance
In a simplified scheme, pulsatile blood flow reflects the driving
forces of the heart on the one hand and the moderating forces
of peripheral vascular resistance on the other. Several inter-
vening factors are also present:
➤
Vessel wall compliance
➤
Effects of branching vessels
➤
Differences of impedance and flow resistance in the vascular
regions supplied by the examined vessel
Fig. 20.5 Postterm pregnancy. The waveform of the fetal descending
aorta exhibits a notch in early diastole. (From Malcus et al. 1991
22
.)
finding in prolonged pregnancies (Fig. 20.5)22. The compliance
of the aorta appears to decrease around term on the basis of increased pulse-wave velocities determined by measurements
using an echo-tracking technique
in the aorta as the “term effect“
32
. We refer to these changes
39
.
Aortic isthmus. It a Doppler study of the aortic isthmus, forward flow was recorded throughout the cardiac cycle before 20
weeks’ gestation, and the diastolic deceleration phase was
gradual and smooth. After 20 weeks, a notch appeared at endsystole that progressively increased, and by 30 weeks’ gestation a brief phase of reverse diastolic flow was consistently recorded. Experimental and clinical observations have shown
that an increase of resistance in the fetoplacental circulation
initially causes changes in the waveforms of the aortic isthmus
Thus, the Doppler sonogram of a vessel represents the balance
of all these factors.
Redistribution of blood flow. In a normal pregnancy, the region
with the lowest flow resistance is the placenta, followed by the
cerebral arteries. Assuming a stable combined cardiac output,
the differential distribution of the blood follows the path of
least resistance. For this reason, most of the blood is directed
into the placenta. At the end of the pregnancy, the requirements of the brain increase both absolutely and in relation to
other organs. One way to redistribute the blood flow (in this
case, to meet the increased cerebral demand) is to open up
circulatory channels to the brain. This is accomplished by lowering the flow resistance in the cerebral arteries. The increased
supply to the brain must not occur at the expense of the
placenta, however. Because blood flow to the placenta cannot
be directly regulated, another way to redistribute the flow (to
the placenta in this case) is to close some peripheral channels
by raising their flow resistance. This is illustrated by the signifi-
179
Fetal Doppler Findings in Late Pregnancy
cant rise of impedance that occurs in the lower extremity arteries. Both mechanisms—the opening of some channels and
the closing of others—can be observed near term. The result is a
redistribution of blood flow that favors the brain without
diminishing the placental supply.
Changes in the aortic arch. These redistribution mechanisms
lead to significant changes in the vascular connections between the parallel circulatory systems that are perfused by the
left and right cardiac ventricles
systems is located in the aortic arch
shed (Fig. 20.
27
6)
. Under normal circumstances, blood flows
forward through the aortic arch, but near term it is not uncommon to see notches in the Doppler waveform or periods of
reverse flow. These partial or complete shifts follow either an
increased peripheral resistance in the vascular bed of the aorta
or decreased resistances in the cerebral circulation—or both.
Interpretation of Doppler findings near term. Many changes
take place within a few days as the pregnancy reaches term.
Some findings can mimic serious pregnancy
making it more difficult to interpret the Doppler sonogram.
Not all changes occur synchronously, despite isolated reports,
20
and therefore the overall result is extremely difficult to predict
in any given case. Our present knowledge appears to be too
limited to draw simple conclusions from individual unexpected findings, especially with regard to changes in the aorta.
Thus, before definitive conclusions are drawn from Doppler ultrasound findings, all available information should be gathered
together and interpreted on the basis of broad physiological
and pathophysiological knowledge. The major difference between the physiological changes that occur near term and abnormal placental changes is the continuation of normal fetoplacental blood flow at term in the normal pregnancy.
5
. The “link” between the two
34
and functions as a water-
complications
ab
2
,
cd
Fig. 20.6 Diastolic flow patterns in the aortic isthmus associated
with various degrees of resistance to placental blood flow.
a Normal resistance.
b Slight increase.
c Moderate increase.
d Severe increase.
(From Teyssier et al. 1993
34
.)
180
Summary
A redistribution of blood flow can occur at the end of pregnancy to correct for the discrepancy that may arise between
fetal demand and placental supply. Flow to the placenta is increased by an elevation of peripheral resistance in the lower
half of the body, while flow to the brain is augmented by a fall
of impedance in the cerebral vessels. The ef fects of these mech-
anisms can be seen either in the affected vascular territories or
in the central vessel, the aorta, where they can be observed in
all segments. Thus, the term effect in the fetal aorta is the net
result of all the redistribution mechanisms that occur in the arteries of the extremities, kidneys, and brain.
References
References
1 Adamsons K, Myers RE: Circulation in the intervillous space; obstetri-
cal considerations in fetal deprivation. In Grünwald P (ed.): The
placenta and its maternal supply line. MT Press, Lancaster 1975, 158–
177
2 Battaglia C, Artini PG, Ballestri M et al.: Hemodynamic, hematological
and hemorheological evaluation of post-term pregnancy. Acta. Obstet.
Gynecol. Scand. 74 (1995) 336–340
3 Benirschke K, Kaufmann P: Pathology of the human placenta. Springer,
New York 1995
4 Bilardo CM, Campb ell S, Nicolaides KH: Mean blood velocities and
flow impedance in the fetal descending thoracic aorta and common
carotid artery in normal pregnancy. Early Hum. Dev. 18 (1988) 2–3
5 Bonnin P, Fouron JC, Teyssier G, Sonesson SE, Skoll A: Quantitative
assessment of circulatory changes in the fetal aortic isthmus during
progressive increase of resistance to umbilical blood flow. Circulation
88 (1993) 216–222
6 Campbell S, Diaz-Recasens J, Griffin DR et al.: New Doppler technique
for assessing uteroplacental blood flow. Lancet 32 (1983) 675–677
7 Eik-Nes SH, Marsál K, Brubakk AO, Kristofferson K, Ulstein M: Ultra-
sonic measurement of human fetal blood flow. J. biomed. Engng. 4
(1982) 28–36
8 Eik-Nes SH, Maršál K, Kristofferson K, Vernersson E: Noninvasive Mes-
sung des fetalen Blutstromes mittels Ultraschall. Ultraschall 2 (1981)
226–231
9 Eldridge MW, Berman W Jr, Greene ER: Serial echo-Doppler measure-
ments for human fetal abdominal aortic blood flow. J. Ultrasound Me d.
4 (1985) 453–458
10 Erskine RL, Ritchie JW: Umbilical artery blood flow characteristics in
normal and growth-retarded fetuses. Brit. J. Obstet. Gynaecol. 92
(1985) 605–610
11 Fendel H, Fendel M, Warnking R: Fehlermöglichkeiten der gepulsten
Dopplermethode zur Blutflußmessung am Feten. Z. Geburtsh. u. Perinat. 187 (1983) 83–87
12 Fouron JC, Zarelli M, Drblik SP, Lessard M: Flow velocity profile of the
fetal aortic isthmus through normal gestation. Amer. J. Cardiol. 74
(1994) 483–486
13 Gill RW, Trudinger BJ, Garrett WJ, Kossoff G, Warren PS: Fetal umbilical
venous flow measured in utero by pulsed Doppler and B-mode ultrasound. I. Normal pregnancies. Amer. J. Obstet. Gynecol. 139 (1981)
720–725
14 Gosling R, Dunbar G, King DH et al.: The quantitative analysis of occlu-
sive peripheral arterial disease by a non-intrusive ultrasonic technique. Angiology 22 (1971) 52–55
15 Griffin D, Cohen Overbeek T, Campbell S: Fetal and utero-placental
blood flow. Clin. Obstet. Gynaecol. 10 (1983) 565–602
16 Jouppila P, Kirkinen P: Blood velocity waveforms of the fetal aorta in
normal and hypertensive pregnancies. Obstet. Gynecol. 67 (1986)856–
860
17 Kaesemann H, Trenkel K: Kombinierte B-Bild-Doppler-Sonographie –
Messungen am In-vitro-Modell und in fetalen Gefäßen. Z. Geburtsh. u.
Perinat. 190 (1986) 43–48
18 Kirkinen P, Müller R, Huch R, Huch A: Blood flow velocity waveforms in
human fetal intracranial arteries. Obstet. Gynecol. 70 (1987) 617–621
19 Lingman G, Gennser G, Maršál K: Ultrasonic measurements of the
blood velocity and pulsatile diameter changes in the fetal descending
aorta. In Rolfe P (ed.): Fetal physiological measurements. Vol. 56. Butterworths, London 1986, 206 –210
20 Lingman G, Maršál K: Fetal central blood circulation in the third
trimester of normal pregnancy – A longitudinal study. I. Aortic and
umbilical blood flow. Early Hum. Dev. 13 (1986) 137–150
21 Lingman G, Maršál K: Fetal central blood circulation in the third
trimester of normal pregnancy – A longitudinal study. II. Aortic blood
velocity waveform. Early Hum. Dev. 13 (1986) 151–159
22 Malcus P,Maršál K, Persson P-H:Fetal and uteroplacental blood flow in
prolonged pregnancies. Ultrasound Obstet. Gynecol. 1 (1991) 40–45
23 Mari G: Arterial blood flow velocity waveforms of the pelvis and lower
extremities in normal and growth-retarded fetuses. Amer. J. Obstet.
Gynecol. 165 (1991) 143–151
24 Maršál K, Lindblad A, Lingman G, Eik-Nes SH: Blood flow in the fetal
descending aorta; intrinsic factors affecting fetal blood flow, i.e. fetal
breathing movements and cardiac arrhythmia. Ultrasound Med. Biol.
10 (1984) 339–348
25 Maršál K, Lingman G, Giles WB: Evaluation of the carotid, aortic and
umbilical blood velocity waveforms in the human fetus. XIth Annual
Conference of the Society for the Study of Fetal Physiology. Oxford
1984; C33
26 Pal A, Kurjak A: Examination of the blood flow in the umbilical artery
by ultrasound. Zentralbl. Gynäkol. 108 (1986) 724–729
37 Patton DJ, Fouron JC: Cerebral arteriovenous malformation: Prenatal
and postnatal central blood flow dynamics. Pediatr. Cardiol. 16 (1995)
141–144
28 Pourcelot L: Applications cliniques de l'éxamen Doppler transcutane.
INSERM Colloq. 34 (1974) 213–240
29 Rightmire DA, Campbell S: Fetal and maternal Doppler blood flow pa-
rameters in postterm pregnancies. Obstet. Gynecol. 69 (1987) 891–
894
30 Rudolph AM: Distribution and regulation of blood flow in the fetal and
neonatal lamb. Circ. Res. 57 (1985) 811
31 Satoh S, Koyanagi T, Hara K, Shimokawa H, Nakano H: Developmental
characteristics of blood flow in the middle cerebral artery in the
human fetus in utero, assessed using the linear-array pulsed Doppler
method. Early Hum. Dev. 17 (1988) 2–3
32 Stale H, Gennser G, Maršál K: Blood flow velocity and pulsatile diame-
ter changes in the fetal descending aorta: A longitudinal study.Amer. J.
Obstet. Gynecol. 163 (1990) 26–29
33 Stuart B, Drumm J, FitzGerald DE, Duignan NM: Fetal blood velocity
waveforms in normal pregnancy. Brit. J. Obstet. Gynaecol. 87 (1980)
780–785
34 Teyssier G, Fouron JC, Maroto E, Sonesson S-E, Bonnin P: Blood flow
velocity profile in the fetal aortic isthmus: A sensitive indicator of
changes in systemic peripheral resistances. I. Experimental studies. J.
Mat. Fetal Invest. 3 (1993) 213 –218
35 Thaler I, Manor D, Itskovitz J et al.: Changes in uterine blood flow
during human pregnancy. Amer. J. Obstet. Gynecol. 162 (1990) 121–
125
36 Tonge HM, Stewart PA, Wladimiroff JW: Fetal blood flow measure-
ments during fetal cardiac arrhythmia. Early Hum. Dev. 10 (1984) 1–2
37 Van Lierde M, Oberweis D, Thomas K: Ultrasonic measurement of aor-
tic and umbilical blood flow in the human fetus. Obstet. Gynecol. 63
(1984) 801–805
38 Vetter K: Dopplersonographie in der Schwangerschaft. VCH Verlags-
gesellschaft, Weinheim 1991
39 Vetter K, Favre Y, Suter T, Huch R, Huch A: Doppler-sonographisch er-
mittelte spezifisch hämodynamische Veränderungen im Kreislauf von
Feten in den letzten 4 Wochen vor Geburt. Z. Geburtsh. u. Perinat. 193
(1989) 215–218
40 Vogel M: Atlas der morphologischen Plazentadiagnostik. Springer,
Berlin 1992
41 Vyas S, Nicolaides KH, Campbell S: Renal artery flow-velocity
waveformsin normal and hypoxemic fetuses. Amer. J. Obstet. Gynecol.
161 (1989) 168–172
42 Woo JSK, Liang ST, Lo RLS, Chan FY: Middle cerebral artery Doppler
flow velocity waveforms. Obstet. Gynecol. 70 (1987) 613–616
Specific Obstetric Problems
181