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Venous Doppler Sonography
toles can still be detected during the first weeks of life. A detail
fetal echocardiographic examination is recommended to exclude morphological cardiac abnormalities, which are present
in 1–8 % of cases. The cause of supraventricular extrasystoles is
an immaturity of the impulse formation and conduction system of the heart. When an extrasystole occurs, the action
potential arising from the sinus node (Keith–Flack node) encounters a still-refractory AV node (Aschoff–Tawara node),
leading to ventricular bradycardia. Increased atrial filling occurs during this bradycardiac phase, characterized by a
decrease in flow velocities and a rise of central venous pressure, especially during the subsequent atrial contraction (a)
(Fig. 16.
20). Because of the Frank–Starling mechanism, the in-
creased blood volume is handled in the next cardiac cycle by an
increase in the ventricular stroke volume. As a result of this
compensatory mechanism, the central venous pressure returns to normal, and even frequent runs of extrasystoles are
unable to produce cardiac failure or hydrops fetalis. It should
be noted, however, that extrasystoles may progress to paroxysmal supraventricular tachycardia in approximately 1–2% of
cases.
Supraventricular tachycardia. Fetal tachyarrhythmias, es-
16
pecially supraventricular tachyarrhythmias, atrial fibrillation,
and atrial flutter, may be associated with fetal heart failure and
the development of nonimmune fetal hydrops, polyhydramnios, and placental hydrops when they are of long duration.
Supraventricular tachycardia is marked by uncoordinated
electrical excitation processes in the heart (reentry circuits)
that disrupt the normal hemodynamics of ventricular filling
and emptying. It has been shown in animal studies that an
atrial rate of 300–320 bpm immediately causes monophasic,
bidirectional blood flow in the venous vessels, resulting in a
75% rise of venous pressures in the inferior vena cava
17
. Hydrops developed in these cases within 4–48 hours. The critical
heart rate in fetal sheep appears to be approximately 310 bpm.
Unlike the normal Doppler spectra in venous vessels, forward
diastolic flow is absent in supraventricular tachycardia owing
to the shortened diastolic phase, resulting in pulsatile, monophasic, holodiastolic reverse flow (Fig. 16.
21). This retrograde
flow correlates with the ventricular diastolic phase of the cardiac cycle, and its primary cause is not atrioventricular valvular
reflux during ventricular systole
15, 17
. Instead, the retrograde
flow appears to be caused by tachycardia-induced changes in
pressure and volume loads and a shortened relaxation phase
during diastole. Another factor appears to be a lack of coordination between atrial contraction and the opening of the atrioventricular valves, so that the blood volume propelled by the
atrial contraction encounters atrioventricular valves that are
essentially closed.
Development of hydrops fetalis. If supraventricular tachycar-
dia persists, there is a deterioration of myocardial perfusion,
which occurs mainly during ventricular diastole, and cardiomyopathy will eventually develop owing to a trophic and oxidative breakdown of the myocardial energy metabolism. The
cardiomyopathy leads to cardiomegaly with the development
of atrioventricular valve incompetence. If cardioversion cannot
be achieved with medication, the sustained tachycardia will
culminate in a generalized hydrops fetalis and possible intrauterine fetal death
pears to be 210bpm
14
. The critical heart rate for fetuses ap-
15
. If cardioversion is successful, the venous
waveforms quickly return to normal and the hydrops clears.
142
Fig. 16.20 Supraventricular bigeminal extrasystoles in a fetus. The
extrasystoles (ES) occur during ventricular systole.
Fig. 16.21 Monophasic, bidirectional Doppler spectrum of the inferior vena cava in a fetus with supraventricular tachycardia (220 bpm).
Fetal Anemia
Severe acute anemia in experimental animals induces vasoconstriction in the splanchnic and renal vascular beds, resulting in an increased oxygen supply to the brain, heart, and
adrenal glands. By contrast, fetuses with severe chronic anemia, due for example to blood group isoimmunization or a
fresh parvovirus B19 infection, are able to maintain an adequate oxygen supply for a certain period by means of specific
humoral, hemorheological, and cardiovascular adaptive
processes.
Hyperdynamic circulation. Although there is no evidence of
overall impedance changes in the fetoplacental vessels, the
anemic fetus responds with a progressive rise in cardiac output
and blood flow velocities
result from increased contractility of the heart and the low viscosity of the blood. This cardiovascular response to anemia is
also known as a “hyperdynamic circulation“
flow velocities can be measured in essentially all fetal vessels,
Doppler examinations of the middle cerebral artery, de-
scending aorta, and ductus venosus appear to be the most re-
warding (Fig. 16.
22). As in the arterial system, the pulsatility in
7,40, 41
. These hemodynamic changes
51
. While increased
Conclusion
Fig. 16.22 Doppler spectrum of the ductus venosus in a twin pregnancy (26 weeks 6 days) with a fresh parvovirus B19 infection. Note
the high maximum velocities and normal waveform pulsatility. The Hb
value determined by cordocentesis was 1.9 g/dl.
the venous vessels is not increased
26, 51
. Consequently, the resistance indices of the arterial vessels and the preload indices
of the venous vessels are not useful in predicting the degree of
anemia.
Development of hydrops fetalis. These findings are supported
by experimental studies in fetal lambs with induced chronic
anemia
7, 40
. It was shown, for example, that the right ventricular pressure does not rise in the presence of increasing anemia
and concomitant hydrops fetalis. Instead, there is an increase
in the right ventricular stroke volume and in myocardial blood
7
flow
. Thus, the hydrops does not appear to result primarily
from congestiveheart failure but more from changes in the colloid osmotic pressure, permeability changes, and hypoxemiainduced endothelial lesions of the fetal vessels. Cardiovascular
decompensation does not occur until the hematocrit falls
below 10%, at which point the dwindling cardiac stroke
volume and resulting high cardiac pressures lead to congestive
heart failure
7
. In the monitoring of intrauterine intravascular
blood transfusion, Doppler examination of the ductus venosus
can furnish information on hemodynamic changes during or
immediately after the transfusion
50
.
Fig. 16.23 Doppler spectrum of the ductus venosus in a hydropic
fetus with endocardial fibroelastosis. Note the extensive retrograde
flow during atrial contraction.
Other Diseases
Arteriovenous anastomoses. Abnormal venous Doppler spec-
tra recorded in fetuses with a sacrococcygeal teratoma or vein
of Galen aneurysm, for example, may be caused by the presence of arteriovenous anastomoses. Congestive heart failure
can develop in these cases as a result of the frequent high shunt
volumes.
Endocardial fibroelastosis. A progressive increase of pulsatility
in the venous vessels can also develop in the setting of endocardial fibroelastosis (Fig. 16.
the myocardium and the resultant loss of contractility lead to a
dwindling cardiac output and elevated central venous pressures. As cardiac compliance continues to decline, hydrops
fetalis develops with a poor prognosis.
Congenital heart disease. Abnormal venous flow patterns can
also be found in association with certain congenital heart defects, particularly those associated with anomalies of the
ventricular inflow or outflow tracts
fetalis may also correlate with agenesis of the ductus veno-
60
sus
.
23). The progressive stiffening of
45
. In rare cases, hydrops
Obstetric Ultrasound
Conclusion
In the hands of an experienced examiner, Doppler evaluation
of the venous vascular system is an important adjunct in the
surveillance and prognostic assessment of high-risk fetuses.
The use of venous preload indices permits a detailed evaluation of fetal cardiac function and its physiological and
pathophysiological changes.
143
Venous Doppler Sonography
144
References
1 Abithol MM, Rochelson BL, Monheit AG, Ryland SJ, Baumann AL, Stern
W: Use of an indwelling Doppler probe to study acute changes in
umbilical vein waveforms in the fetal sheep. Gynecol. Obstet. Invest.
34 (1992) 6–11
2 Baschat AA, Gembruch U, Reiss I, Gortner L, Dietrich K: Demonstration
of fetal coronary blood flow by Doppler ultrasound in relation to arterial and venous flow velocity waveforms and perinatal outcome—the
“heart-sparing effect”. Ultrasound Obstet. Gynecol. 9 (1997) 162–172
3 Baschat AA, Gembruch U: Triphasic umbilical venous blood flow with
prolonged survival in severe intrauterine growth retardation: a case
report. Ultrasound Obstet. Gynecol. 8 (1996) 201–205
4 Chan FY, Woo SK, Ghosh A, Tang M, Lam C: Prenatal Diagnosis of con-
genital fetal arrhythmias by simultaneous pulsed Doppler
Velocimetry of the fetal abdominal aorta and inferior vena cava. Obstet. Gynecol. 76 (1990) 200–204
5 Cohn HE, Sacks EJ, Heymann MA, Rudolph AM: Cardiovascular re-
sponses to hypoxemia and acidemia in fetal lambs. Amer. J. Obstet. Gynecol. 120 (1974) 817–824
6 Damron DP, Chaffin DG, Anderson CF, Reed KL: Changes in umbilical
arterial and venous blood flow velocity waveforms during late decelerations of the fetal heart rate. Obstet. Gynecol. 84 (1994) 1038–1040
7 Davis LE, Hohimer AR: Hemodynamics and organ blood flow in fetal
sheep subjected to chronic anemia. Amer. J. Physiol.261 (1991) R1542–
16
R1548
8 De Vore GR, Horenstein J: Ductus venosus index: a method for evaluat-
ing right ventricular preload in the second-trimester fetus. Ultrasound
Obstet. Gynecol. 3 (1993) 338–342
9 Edelstone DI, Rudolph AM: Preferential streaming of ductus venosus
blood to the brain and heart in fetal lambs. Amer. J. Physiol. 237 (1979)
H724–H729
10 Edelstone DI, Rudolph AM, Heymanm MA: Effects of hypoxemia and
decreasing umbilical flow on liver and ductus venosus blood flows in
fetal lambs. Amer. J. Physiol. 238 (1980) H656–H663
11 Eik-Nes SH, Brubakk AO, Ulstein MK: Measurement of human fetal
blood flow. BMJ (1980) 283–284
12 Erskine RLA, Ritchie JWK: Quantitative measurement of fetal blood
flow using Doppler ultrasound. Brit. J. Obstet. Gynecol. 92 (1985) 600–
604
13 Fitzgerald DE, Drumm DE: Non invasive measurement of human fetal
circulation using ultrasound: a new method. Brit. J. Obstet. Gynecol. 2
(1977) 1450–1451
14 Gembruch U, Redel DA, Bald R, Hansmann: Longitudinal study in 18
cases of fetal supraventricular tachycardia: Doppler echocardiographic findings and pathophysiologic implications. Am. Heart J. 125
(1993) 1290–1301
15 Gembruch U, Krapp M, Baumann P: Changes of venous blood flow
velocity waveforms in fetuses with supraventricular tachycardia. Ultrasound Obstet. Gynecol. 5 (1995) 394–399
16 Gembruch U, Baschat AA, Caliebe A, Gortner L: Prenatal diagnosis of
ductus venosus agenesis: a report of two cases and reviewof the literature. Ultrasound Obstet Gynecol 11 (1998) 185–189
17 Gest AL, Martin CG, Moise AA, Hansen TN: Reversal of venous blood
flow with atrial tachycardia and hydrops in fetal sheep. Pediatr. Res. 28
(1990) 223–226
18 Gill RW, Trudinger BJ, Gerrit WJ, Kossow G, Warren PS: Fetal umbilical
venous flow measured in utero by pulsed Doppler and B-mode ultrasound. Amer. J. Obstet. Gynecol. 139 (1981) 720–725
19 Gill RW, Kossoff G, Warren PS, Garrett WJ: Umbilical venous flow in
normal and complicated pregnancy. Ultrasound Med. Biol. 10 (1984)
349–363
20 Giles WB, Lingman G, Marsal K, Trudinger BJ: Fetal volume blood flow
and umbilical artery flow velocity waveform analysis: a comparison.
Brit. J. Obstet. Gynecol. 93 (1986) 461–465
21 Gonser M, Goelz R, Erz W, Mielke G: Dopplersonographie des Ductus
venosus bei Hochrisikoschwangerschaften zwischen 23 und 26 Wochen. Geburtshilfe Frauenheilkd 55 (1995) 661–663
22 Gudmundson S, Hutha JC, DC Wood, Tulzer G, Cohen AW, Weiner S:
Doppler ultrasonography in the fetus with nonimmune hydrops.
Amer. J. Obstet. Gynecol. 164 (1991) 33–37
23 Gudmundson S, Tulzer G, Hutha JC, Marsal K: Venous Doppler in the
fetus with absent end-diastolic flow in the umbilical artery. Ultrasound Obstet. Gynecol. 7 (1996) 262–267
24 Hecher K, Campbell S, Snijders R, Nicolaides K: Reference ranges for
fetal venous and atrioventricular blood flow parameters. Ultrasound
Obstet. Gynecol. 4 (1994) 381–390
25 Hecher K, Campbell S, Doyle P, Harrington K, Nicolaides K: Assessment
of fetal compromise by Doppler ultrasound investigation of the fetal
circulation. Arterial, intracardiac, and venous blood flow velocity studies. Circulation 91 (1995) 129 –138
26 Hecher K, Snijders R, Campbell S, Nicolaides K: Fetal venous, arterial,
and intracardiac blood flows in red blood cell isoimmunization. Obstet. Gynecol. 85 (1995) 122–128
27 Hecher K, Snijders R, Campbell S, Nicolaides K: Fetal venous, intra-
cardiac, and arterial blood flow measurements in intrauterine growth
retardation: Relationship with fetal blood gases. Amer. J. Obstet. Gynecol. 173 (1995) 10–15
28 Hecher K, Ville Y, Snijders R, Nicolaides K: Doppler studies of the fetal
circulation in twin-twin transfusion syndrome. Ultrasound Obstet.
Gynecol. 5 (1995) 318–324
29 Huisman TWA, Stewart PA, Wladimiroff JW: Flow velocity waveforms
in the fetal inferior vena cava during the second half of normal pregnancy. Ultrasound Med. Biol. 17 (1991) 379–382
30 Huisman TWA, Stewart PA, Wladimiroff JW: Ductus venosus blood
flow velocity waveforms in the human fetus – A Doppler study. Ultrasound Med. Biol. 18 (1992) 33–37
31 Huisman TWA, Gittenberger-De Groot AC, Wladimiroff JW: Recogni-
tion of a fetal subdiaphragmatic venous vestibulum essential for fetal
venous Doppler assessment. Pediatr. Res. 32 (1992) 338–341
32 Huisman TWA, van den Eijnde SM, Stewart PA, Wladimiroff JW:
Changes in inferior vena cava blood flow velocity and diameter during
breathing movements in the human fetus. Ultrasound Obstet. Gynecol. 3 (1993) 26–30
33 Indik J, Chen V, Reed KL: Association of umbilical venous with inferior
vena cava blood flow velocities. Obstet. Gynecol. 77 (1991) 551–557
34 Indik JH, Reed KL: Correlations in umbilical blood flow Doppler veloci-
ties in the human fetus during breathing. Ultrasound Obstet. Gynecol.
4 (1994) 361–366
35 Jouppila P, Kirkinen P: Umbilical vein blood flow in the human fetus in
cases of maternal and fetal anemia and uterine bleeding. Ultrasound
Med. Biol. 10 (1984) 365–370
36 Jouppila P, Kirkinen P: Umbilical vein blood flow as an indicator of fetal
hypoxia. Brit. J. Obstet. Gynecol. 91 (1984) 107–110
37 Kanzaki T, Chiba Y: Evaluation of the preload condition of the fetus by
inferior vena cava blood flow pattern. Fetal Diagn. Ther. 5 (1990) 168–
174
38 Kanzaki T, Murakami M, Kobayashi H, Chiba Y: Characteristic abnor-
mal blood flow patterns of the inferior vena cava in fetal arrhythmias.J.
Matern. Fetal. Invest. 1 (1991) 35–39
39 Karsdorp VHM, van Vugt JMG, Kostense PJ, Arduini D, Montenegro N,
Todros T: Clinical significance of absent or reversed end diastolic
velocity waveforms in umbilical artery. Lancet 344 (1994) 1664–1668
40 Kilby MD, Swarc R, Benson LN, Morrow RJ: Left ventricular hemody-
namics in anemic fetal lambs. J. Perinat. Med. 26 (1998) 5–12
41 Kirkinen P,Jouppila P: Umbilical vein blood flow in rhesus-isoimmuni-
zation. Brit. J. Obstet. Gynecol. 90 (1983) 640–643
42 Kiserud T, Eik-Nes SH, Blaas HG, Hellevik LR: Ultrasonographic
velocimetry of the fetal ductus venosus. Lancet 338 (1991) 1412–1414
43 Kiserud T, Eik-Nes SH, Blaas HG, Hellevik LR: Foramen ovale: An ultra-
sonographic study of its relation to the inferior vena cava, ductus venosus and hepatic veins. Ultrasound Obstet. Gynecol. 2 (1992) 389–
396
44 Kiserud T, Eik-NesSH, Hellevik LR, Blaas HG: Ductus venosus – a longi-
tudinal Doppler velocimetric study of the human fetus. J. Matern.
Fetal. Invest. 2 (1992) 5–11
References
45 Kiserud T, Eik-Nes SH, Hellevik LR, Blaas HG: Ductus venosus blood
velocity changes in fetal cardiac diseases. J. Matern. Fetal. Invest. 3
(1993) 15–20
46 Kiserud T, Eik-Nes SH, Blaas HG, Hellevik LR, Simensen B: Ductus veno-
sus blood velocity and the umbilical circulation in the seriously
growth-retarded fetus. Ultrasound Obstet. Gynecol. 4 (1994) 109–114
47 Künzel W: Das fetale Schocksyndrom. Z. Geburtsh. u. Perinat. 190
(1986) 177–184
48 Mari G, Uerpairojkit B, Copel JA: Abdominal venous system in the nor-
mal fetus. Obstet. Gynecol. 86 (1995) 729–733
49 Nakai Y, Miyazaki Y, Matsuoka Y: Pulsatile umbilical venous flow and
its clinical significance. Brit. J. Obstet. Gynecol. 99 (1992) 977–980
50 Oepkes D, Vanderbussche FP, van Bel F, Kanhai HHH: Fetal ductus ve-
nosus blood flow velocities before and after transfusion in red-cell alloimmunized pregnancies. Obstet. Gynecol. 82 (1993) 237–241
51 Oepkes D, Brand R, Vandenbussche FP, Meerman RH, Kanhai HHH: The
use of ultrasonography and Doppler in the prediction of fetal haemolytic anaemia: a multivariate analysis. Brit. J. Obstet. Gynecol. 101
(1994) 680–684
52 Ozcan T, Sbracia M, Dáncona RL, Copel JA, Mari G: Arterial and venous
Doppler velocimetry in the severely growth-restricted fetus and associations with adverse perinatal outcome. Ultrasound Obstet. Gynecol.
12 (1998) 39–44
53 Pennati G, Bellotti M, Ferrazzi E, Rigano S, Garberi A: Hemodynamic
changes across the human ductus venous: a comparison between
clinical findings and mathematical calculations. Ultrasound Obstet.
Gynecol. 9 (1997) 183–391
54 Reed KL, Appleton CP, Anderson CF, Shenker L, Sahn DL: Doppler stud-
ies of vena cava flows in human fetuses. Circulation 81 (1990) 498–505
55 Reed KL, Chaffin DG, Anderson CF: Umbilical venous Doppler velocity
pulsations and inferior vena cava pressure elevations in fetal lamb. Obstet. Gynecol. 87 (1996) 617–620
56 Reed KL, Chaffin DG, Anderson CF, Newman AT: Umbilical venous
velocity pulsations are related to atrial contraction pressure
waveforms in fetal lambs. Obstet. Gynecol. 89 (1997) 953–956
57 Reuss ML, Rudolph AM, Dae MW: Phasic blood flow patterns in the su-
perior and inferior venae cavae and umbilical vein of fetal sheep. Amer.
J. Obstet. Gynecol. 145 (1983) 70–78
58 Rizzo G, Arduini D, Romanini C: Umbilical vein pulsations: A physio-
logic finding in early gestation. Amer. J. Obstet. Gynecol. 167 (1992)
675–677
59 Rizzo G, Arduini D, Caforio L, Romanini C: Effects of sampling sites on
inferior vena cava flow velocity waveforms. J. Matern. Fetal. Invest. 2
(1992) 153–156
60 Rizzo G, Arduini D, Romanini C: Inferior vena cava flow velocity
waveforms in appropriate- and small-for-gestational-age fetuses.
Amer. J. Obstet. Gynecol. 166 (1992) 1271–1280
61 Rizzo G, Capponi A, Arduini D, Romanini C: Ductus venosus velocity
waveforms in appropriate and small for gestational age fetuses. Early
Hum. Develop. 39 (1994) 15–26
62 Rizzo G, Capponi A, Talone PE, Arduini D, Romanini C: Doppler indices
from inferior vena cava and ductus venosus in predicting pH and oxygen tension in umbilical blood at cordocentesis in growth-retarded fetuses. Ultrasound Obstet. Gynecol. 7 (1996) 401–410
63 Saling E: Die O
Frauenheilk. 26 (1966) 413–419
64 van Splunder IP, Huisman TWA, StijnenT, Wladimiroff JW: Presence of
pulsations and reproducibility of waveform recording in the umbilical
and left vein in normal pregnancies. Ultrasound Obstet. Gynecol. 4
(1994) 49–53
65 Wladimiroff JW, Huisman TW, Stewart PA: Normal fetal Doppler infe-
rior vena cava, transcuspid, and umbilical artery flow velocity
waveformsbetween 11
necol. 166 (1992) 921–924
66 Zikulnig L, Hecher K, Bregenzer T, Bäz E, Hackelöer BJ: Doppler sono-
graphy and prognostic factors in severe twin-twin transfusion syndrome with endoscopic laser therapy. Ultrasound Obstet. Gynecol.
12(Suppl.1) (1998) 9
-Sparschaltung des fetalen Kreislaufes. Geburtsh. u.
2
th
and 16thweek’sgestation. Amer.J. Obstet. Gy-
Obstetric Ultrasound
145
Specific Obstetric Problems
Color Doppler Sonography in the Diagnosis
17
of Nuchal Cord
A. K. Ertan, H. J. Hendrik, and W. Schmidt
Importance of Nuchal Cord
Possible sequelae of nuchal cord. Umbilical cord complications
are by far the most common cause of severe intrapartum fetal
hypoxic states
neck (nuchal cord, NC) is observed in 20–33 % of all
deliveries
Rare but serious complications of NC are an increased incidence of acidosis
normalities of neurological development
also be a cause of intrauterine fetal death
dystocic problems in the form of prolonged cervical dilatation
17
and hypotonic labor
Number of loops. Birnholz
increased risk of asphyxia-induced prenatal brain injury and
that the degree of risk increases with the number of entangling
loops. There are varying reports on the incidence of multiple
18
. Looping of the umbilical cord around the fetal
1, 42
and in up to 48% of breech-presenting fetuses7.
2, 10, 24
, neonatal hypovolemic shock42, and ab-
10
(Table 17.1).
1
notes that NC is associated with an
1
. Ultimately, NC can
1, 17
. It can also lead to
Table 17.1 Possible complications of nuchal cord
앫 More frequent occurrence of variable decelerations, FHR
changes
앫 Prolonged dilation period, hypotonic labor
앫 Higher rate of neonatal asphyxia
앫 Hypovolemic shock
앫 Neurologic abnormalities
앫 Intrauterine fetal death
FHR = fetal heart rate.
cord loops
cidence of double loops, a 2.5% incidence of triple loops, and a
0.1% incidence of quadruple loops
reports of up to nine cord loops
19, 20
. Kan-Pun-Shui and Eastman16found a 20.6% in-
16
. There have been isolated
22
.
148
Color Doppler Study on the Diagnosis of Nuchal Cord
Until recently, the only methods available for the diagnosis of
NC were B-mode ultrasound imaging
rate (FHR) monitoring
creasing reports on the use of pulsed Doppler ultrasound in the
diagnosis of NC
A prospective study was conducted at the Department of
Obstetrics and Gynecology, Homburg/Saar University, to assess
the role of high-resolution color Doppler sonography in the antenatal diagnosis of NC. A series of 254 pregnant women underwent ultrasound examinations on admission and for a suspicious fetal heart rate to check for NC. The prenatal ultrasound
results were then compared with the intrapartum and postpartum findings. All the examinations were performed with
high-resolution real-time color Doppler units (Acuson Computed Sonography 128 XP/10 with a 5 MHz curved array, Picker
CS 192 Integral Color Doppler, and Siemens Elegra with a
3.5 MHz curved array). Videotape and video hard-copy documentation were used. When fetal biometry was completed, the
fetal neck region was imaged and systematically scanned with
a color Doppler probe to check for signals from umbilical vessels. All results were entered on a documentation sheet. Positional drawings were made in special situations, such as when
ultrasound showed umbilical cord signals near the fetal neck
but did not show definite cord encirclement.
1,29, 31
23
. In recent years there have been in-
.
4, 6, 7, 11, 33, 36
and fetal heart
Examination Technique
Longitudinal scan. First the fetal neck region was examined
with conventional B-mode (gray-scale) ultrasound for the
presence of umbilical vessels. This was followed by a color
Doppler examination. Longitudinal scanning of the fetal neck
provides a cross-sectional view of the umbilical vessels
(Fig. 17.
plored in sagittal sections (dorsoanterior or dorsoposterior lie)
or coronal sections (fetal spine to the right or left). If a suspected umbilical cord signal is found near the fetal neck, the diagnosis can be confirmed in equivocal cases by identifying
typical frequency shifts in the umbilical arteries and veins with
pulsed Doppler.
Transverse scan. A definitive diagnosis of NC can be made only
by demonstrating direct encirclement of the fetal neck by the
umbilical cord with color Doppler. This view of the umbilical
vessels is obtained by imaging the neck region in transverse
section (Fig. 17.2
loop of cord around the neck, especially near term (owing to
oligohydramnios, a low presenting part, etc.). For this reason,
at least the anterior and lateral portions of the neck should be
closely scrutinized (Fig. 17.
false presumptive diagnosis of NC in cases where a “tangle” of
tortuous umbilical cord is seen abutting the side of the neck.
1). Depending on the fetallie, the neck region can be ex-
a). Often it is not possible to define a complete
2b). This is the only way to avoid a
Color Doppler Study on the Diagnosis of Nuchal Cord
Results
We achieved a 97% sensitivity rate in the diagnosis of NC by
antepartum color Doppler examination, with a 6% false-positive rate and a 1.5% false-negative rate. The specificity was 88%.
The positive predictive value was 89%, the negative predictive
value 96 %. The efficiency was 93%.
Sources of error. Using color flow alone, it is easy to obtain a
false-positive impression of NC owing to the close proximity of
the maternal pelvic vessels. The fetal and maternal vessels can
be differentiated, however, by their distinctive frequency-shift
patterns. NC is also difficult to diagnose in the presence of
oligohydramnios, where it is almost impossible to make a correct diagnosis by B-mode imaging alone.
Fig. 17.1 Umbilical cord signals in a longitudinal color Doppler scan
of the fetal neck.
a
b
FHR monitoring. In 21% of cases, an abnormal antepartum FHR
trace provided the indication for targeted color Doppler imaging. In the group with an antenatal diagnosis of NC, variable
heart rate decelerations were noted in 72% of cases, early
decelerations in 7%, and late decelerations in 21%. In the remaining cases without NC, half of the cases showed late decelerations, two cases had variable decelerations, and three cases
had early decelerations.
An abnormal intrapartum FHR trace was recorded in approximately one-fourth of all the cases examined. The percentage of spontaneous deliveries was 61%. A primary cesarean
delivery was performed in 17% of the cases, a secondary cesarean delivery in 10%. Twelve percent of the patients had an
operative vaginal delivery. In the cases that had an indication
for operative delivery, the percentage of abnormal FHR traces
(impending intrauterine asphyxia) was significantly higher in
the group with NC (43%) than in the group without NC (8 %, p ⬍
0.001).
Doppler examination of fetal vessels. Doppler velocimetry of
the fetal aorta was abnormal (S/D ratio ⬎ 7) in 30% of the cases
diagnosed with NC. There was an 11.3% rate of abnormal findings in the umbilical arteries (S/D ratio ⬎ 4) in the NC cases. In
12% of the cases with NC, the Doppler velocimetry findings deteriorated over the course of the pregnancy.
Specific Obstetric Problems
Fig. 17.2 Umbilical cord signals in a transverse color Doppler scan of
the fetal neck.
a Umbilical cord signals encircling the neck.
b Cord segments abutting the front and sides of the neck.
Umbilical cord length. Postpartum umbilical cord length was
measured in all patients (minimum 28 cm, maximum 101cm).
The average umbilical cord length in the group with NC was 65
⫾ 10 cm, versus 54 ⫾ 9 cm in the group without NC (p ⬍ 0.01).
Excessive umbilical cord length, defined as ⬎70 cm (⬎90th
percentile), was 7 times more prevalent in the group with NC
than in newborns without NC (Table 17.
Table 17.2 Distribution of umbilical cord length in groups with and
without nuchal cord
Umbilical cord length With nucal
35–70 cm (normal) 79% 97%
⬎ 70 cm (too long) (p ⬍ 0.001) 21% 3 %
cord
2).
Without
nucal cord
149
Color Doppler Sonography in the Diagnosis of Nuchal Cord
Importance of Nuchal Cord Diagnosis in the Biophysical (ABCD) Profile
Doppler sonography, especially color Doppler sonography, has
gained an important and established role in pregnancy surveillance using biophysical methods. The antepartum detection of
fetal compromise can be significantly improved by combining
Doppler ultrasound with other biophysical methods of examination (see Chronic Placental Insufficiency, Chapter 18)
Comparison of Doppler velocimetry and other biophysical parameters. We did another prospective study to determine the
importance of the diagnosis of fetal NC with prenatal Doppler
within the context of the biophysical(ABCD) profile. We particularly wanted to determine how the other biophysical parameters behaved in relation to Doppler velocimetry findings and
assess the impact of NC on perinatal outcome in the complex
biophysical evaluation. In 380 evaluations of the ABCD profile,
NC was detected by color Doppler in 128 cases (34%)
cases (57%) the pregnancy had no additional clinical risk factors. This group was compared with 144 pregnancies without
NC and without additional clinical risk factors (Table 17.
17
ABCD profile. The ABCD profile consists of extended fetal biometry, the amniotic fluid index (AFI or EFI), kinetocardiotocography (KCTG), and Doppler examination of the fetal aorta and
umbilical artery. Only singleton pregnancies were evaluated.
Comparing the biophysical profile variables in groups with
and without NC in the absence of other clinical risk factors, we
find only marginal differences with regard to biometry, amniotic fluid volume, and Doppler velocimetry (Table 17.
13
12
4).
.
.In73
3).
Similarly, we find no significant differences in individual
KCTG criteria between the groups. At most, the number of accelerations was lower in the cases with NC than in the cases
without NC (Table 17.
5). Fetal heart rate parameters based on
the Fischer score were the same in both groups.
A differentiated analysis of Doppler velocimetry findings
showed a slight decrease of perfusion in the aorta and umbili-
cal artery and no differences in the middle cerebral artery
(Table 17.
Table 17.4 ABCD profile findings in groups with and without a Dopp-
ler diagnosis of nuchal cord
Biometry
Amniotic fluid volume
Doppler velocimetry
Movements (mean block length)
FHR (Fischer score)
Table 17.5 Kinetocardiotocography findings associated with nuchal
cord
6).
Without
nuchal
cord
Normal 72% 79 % NS
Abnormal 28 % 21 %
Normal/increased 88 % 92% NS
Reduced 12% 8 %
Normal 75% 70 % NS
Abnormal 25 % 30 %
Normal 83% 78 % NS
Shortened 17% 22 %
⬎ 7 96 % 96% NS
ⱕ 74%4%
With
nuchal
cord
p
150
Table 17.3 Relationship of ABCD profile to fetal outcomes with and
without nuchal cord
Without
nuchal
cord
Cases n = 144 n =73
Weeks’ gestation at delivery 39 40
Birthweight in g (mean value, SD) 3204 (366) 3296 (240)
Mode of delivery
Spontaneous 82 % 75%
Primary cesarean section 11% 9 %
Secondary cesarean section 7 % 8 %
Operative vaginal – 8 %
Apgar score 1 min**
⬍ 72%16%
ⱖ 7 98% 84 %
Apgar score, 5 min
⬍ 70%0%
ⱖ 7 100% 100%
Umbilical cord arterial pH (mean, SD) 7.28 (0, 8) 7.28 (0, 9)
Intrapartum complications
No 76% 64 %
Yes 24 % 36%
** p ⬍ 0.01
With
nuchal
cord
% Movements
(mean value, SD)
Mean block length
(mean value, SD)
Number of accelerations
(mean value, SD)
Fischer score
8–10 96% 96% NS
5–7 4% 4%
Table 17.6 Individual color Doppler findings in the ABCD profile in
cases with and without nuchal cord
Vessel Evaluation Without
Aorta Normal 94% 78 % ⬍ 0.1
Umbilical artery Normal 75% 70 % ⬍ 0.1
Middle cerebral
artery
Without
nuchal
cord
18 (9,9) 18 (8,3) NS
5.77 (2.6) 5.06 (1.2) NS
8.6 (5.5) 6.0 (4.8) ⬍ 0.05
nuchal
cord
Abnormal/
borderline
Abnormal 25% 30%
Normal 84 % 82% NS
Abnormal 16% 15%
6% 22%
With
nuchal
cord
With
nuchal
cord
p
p
Role of Doppler Sonography in NC
Perinatal outcome. In pregnancies with no additional clinical
risk factors, there were no significant differences in perinatal
outcomes between the groups with and without NC. The cases
with NC had a slightly increased percentage of vaginal operative deliveries. The 1-minute Apgar score was markedly poorer
than in the cases with NC, but the 5-minute scores were the
same in both groups. There was no difference in arterial
umbilical cord pH. Overall intrapartum complications were
12% more frequent in cases with an antepartum diagnosis of
NC.
Role of Doppler Sonography in NC
Nuchal cord can have a variety of antepartum and intrapartum
complications ranging from sporadic, variable FHR decelerations to intrauterine fetal death
High diagnostic accuracy. In a prospective study,we found that
NC could be diagnosed prenatally with a 97% sensitivity by
using high-resolution real-time color Doppler sonography. The
89% positive predictive value, 97% negative predictive value,
and 93% efficiency confirm the high diagnostic accuracy of this
method. Especially with findings that are equivocal by B-mode
and color-flow imaging, the use of pulsed Doppler velocimetry
can further increase the detection rate based on the typical
frequency shift patterns that are observed in the umbilical arteries and vein.
Umbilical cord length. Little attention has been paid to the
issue of umbilical cord length. The mean reported umbilical
cord length in term deliveries is 50–60 cm. It is generally acknowledged that NC may be more common in pregnancies
where the umbilical cord is too long. This contrasts with the effects of a short umbilical cord, which is associated with constrained fetal movements and abnormalities of central nervous
system development. As early as 1750, Smellie reported cases
of intrauterine fetal death caused by too short an umbilical
38
cord
. Besides a “relatively” short umbilical cord (e.g., caused
by looping around the fetal neck), there may be an “absolute”
short cord whose length is less than 35 cm
short cord is present in 0.43–0.78 % of pregnancies and appears
to correlate with chromosome abnormalities including Down
syndrome
5
.
The frequent occurrence of excessive umbilical cord length
in newborns with NC was confirmed in our study. A cord length
⬎70 cm was 7 times more common in cases with NC than in
cases without NC (21% versus 3%, p ⬍ 0.001).
Correlation with FHR trace. According to Kubli and Schmidt
peracute fetal hypoxic states occur without prior warning,
probably as a result of occult umbilical cord compression, in
approximately 0.1–0.2% of all deliveries
abnormal prenatal FHR trace is an important indication for antenatal NC screening. Abnormal antepartum and intrapartum
heart rate changes are found more commonly in fetuses with
10, 26, 28
NC
. For example, Goldkrand et al.9found a 74% incidence
of variable FHR decelerations in cases with certain umbilical
cord abnormalities such as knotted cord and nuchal cord,
1,10, 14, 15, 17, 25, 35,37, 40
8, 30, 32
18
. This means that an
.
. Reportedly, a
18
Interpretation. In summary, we may conclude that NC is of
minor importance in the complex biophysical evaluation of
uncomplicated pregnancies. The perfusion values in the fetal
vessels are mildly impaired without causing a significant longterm perfusion deficit. The fetal outcome does show the typical
effects of acute changes caused by NC, but these are easily recognized and treated within the framework of ordinary obstetric management.
41
while Tejani et al.
found an 89% incidence. In our study using
the biophysical profile, NC in the absence of other clinical risk
factors was manifested only by a decreased number of accelerations in the FHR. The presence of NC did not affect the
Fischer scores or quantitative motion analysis by kinetocardiotocography.
It is generally accepted that variable decelerations in the
FHR can be caused by a fetal vagal reflex. Umbilical cord compression appears to be a factor in this process both before and
during delivery
43
.
Perinatal findings. Twenty-one percent of our study patients
were selected for antenatal NC screening based on abnormal
antenatal FHR findings. By contrast, the FHR abnormalities detected in the group without NC were due chiefly to other factors (e.g., suspected intrauterine growth retardation). The
mean Apgar score and umbilical cord pH values were also significantly lower in infants with NC, and the Pco
higher. The incidence of neonatal asphyxia was significantly
higher in cases with repeated variable decelerations than in
cases without (Apgar score ⬍ 7, 35.3% versus 3.8 %; and pH
⬍ 7.20, 44.1% versus 6.5 %). It is reported in the literature that
greenish amniotic fluid is 3–4 times more common in NC
and it was three times more common in the patients that we
examined.
Prevention of neuromotor deficits. The current main focus of
obstetric efforts, besides lowering prenatal mortality, is the
prevention of perinatal morbidity with the potential risk of
permanent neuromotor deficits
18
. As a general rule, the FHR
trace, by monitoring a single functional quantity (the fetal
heart rate), cannot cover all aspects of a potentially multifactorial disturbance, and the antenatal FHR trace offers no typical
warning signs that would indicate a subsequent impairment of
cerebral development
,
test whose ultimate goal is the early prediction of subsequent
34
. FHR monitoring is more a screening
(intrapartum) compromise of the fetal circulation, which is al-
ways stressed by the delivery. Greater attention is now being
given to prenatal abnormalities as distinguished from intra-
partum insults
27,34
. Mallard et al.21found that isolated umbilical cord occlusion for 10 minutes (in fetal sheep) caused severe
transient asphyxia in addition to hypotension, bradycardia,
and increased cortical impedance (EEG), but the principal effect was a loss of neurons in the hippocampus
21
. Hippocampal
damage in humans is manifested chiefly by memory deficits.
levels were
2
Specific Obstetric Problems
39
,
151