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Doppler Sonography of the Fetal Venous Circulation
3
Fig. 18.15 Abnormal blood flow in the DV with reduced ES blood flow and RF in marked placental insufficiency.
Knowledge of the underlying disease is important and decisive in the interpretation of the venous flow curve, for, as explained above, both a raised cardiac preload and a cardiac afterload due to severe placental insufficiency lead to an increase in A blood flow; the impairment in cardiac function is more severe in the latter case.
In our own studies of the RHV we added the calcula­tion of ES blood flow (Hofstaetter et al. 1996), and we found that there was also a significant decrease in ES blood flow with increasing cardiac afterload. This was due to marked placental insufficiency, especially in myocardial dysfunction based on hypoxia. When the load on the heart was simply due to increased volume,
18.18).
ES flow was not impeded (
At this time Doppler ultrasound of the fetal v.’s is used to monitor premature fetuses with advanced placental insufficiency, i.e., with ES blood flow
Fig.
164
Fig. 18.16 Abnormal blood flow in the hepatic v.’s in a case of cardiac malformation with cardiac insufficiency and hydrops fetalis.
Fig. 18.18 Abnormal blood flow in the hepatic v.’s with nega­tive ES blood flow and increased A blood flow.
Fig. 18.17 Abnormal blood flow in the DV of an acceptor twin
in a twin-to-twin transfusion syndrome (TTTS).
throughout diastole or reverse flow in the umbilical a. Experience so far has shown that the hearts especially of fetuses younger than 30 completed weeks of gesta­tion can withstand this fragile situation for some time. Deterioration of venous blood flow indicates that such a heart-sparing effect has come to an end and ante­dates an abnormal cardiotocogram(CTG) by one to two days.
A fetus older than 31 weeks of gestation can decom­pensate much more rapidly and should be delivered prematurely if there is reverse flow in the umbilical a., while venous Doppler readings and the CTG remain normal. This is especially true since the risks of pre­maturity are meanwhile much diminished (Hecher et al. 1995).
In cases of right heart overload due to hypervolemia Doppler sonography of the venous system is helpful in monitoring and also allows the prognosis for the preg­nancy to be assessed. Here, too, the decision regarding how to manage the pregnancy must be made individu­ally on a case by case basis.
The application of Doppler sonography of the veins is much simpler in cardiac arrhythmias. Since the pre­cordial v.’s reflect the filling and emptying of the heart, the extra contractions of the atrium and ventricles eli­cit characteristic changes in venous blood flow.
In supraventricular extrasystoles (SVES) the atrium contracts prematurely during ventricular systole. Since the AV valve is closed, blood in the veins is turned back and flow reversal becomes evident during the pro­longed S blood flow. Because the whole cardiac cycle is prolonged, this reverse flow, i.e., A blood flow, intensi-
18.19).
fies during atrial contraction (
In ventricular extrasystoles (VES), by contrast, for-
ward flow to the heart remains unimpeded during
ventricular systole and early diastole, while A blood flow increases. The premature ventricular contraction takes place while the AV valves are still open and the atria are contracting, thus the increase in right atrial
volume leads to a stronger reverse flow into the veins.
Supraventricular tachycardia (SVT) is associated
with a biphasic venous blood flow, the forward flow being broader, while the reverse flow is narrower, but intensified (Fig. 18.20).
In bradycardia atrial filling time is prolonged, lead­ing to a somewhat intensified reverse flow, while AV block shows variable intervals between S blood flow and D blood flow.
Fig.

Summary

Fig. 18.19 Alteration of a venous blood flow curve by SVES.
Advanced Topics
Fig. 18.20 Alteration of a venous blood flow curve by SVT.
Summary
Venous Doppler ultrasound is a useful complement to arterial Doppler ultrasound in selected cases of fetal distress, for example, in marked placental insufficiency
with circulatory centralization and increased volume load on the heart, or in arrhythmias.
The procedure offers an effective and fascinating in­sight into the physiology and pathophysiology of the fetal heart and circulatory regulation. Every case, often every examination, is instructive, but it takes years of experience to evaluate the exact role and significance of venous blood flow.
165
3
166
19 Seven Cases Illustrating the Use of Doppler Ultrasound in
Obstetrics

1—Fetal Growth Restriction

Patient A, gestational age: 29 weeks 5 days
Clinical findings: First presentation for growth
retardation of three weeks; symmetrical; mild proteinuria.
Age 36; gravida 1, para 0; blood pressue (BP) normal range; cardiotocogram (CTG) normal.
Ultrasound findings: No evidence for malformation;
estimated weight by ultra­sound 1000 g (ideal weight 1400 g).
Doppler findings: Zero flow in umbilical a. (UA),
with control (Fig. 19.1a, b);
19.1c);
zero flow in aorta ( brain sparing (Fig. 19.1d); bi­lateral uterine a. notch and ab­normally raised pulsatility index (PI) (Fig. 19.1e, f).
Assessment: Early fetal growth restriction
with impaired uteroplacental perfusion and consequent feto-
Fig.
Course: Hospitalized with bed rest
Result: Girl, 980 g; Apgar 5−8−8 (1−5−
placental perfusion impair­ment, centralization of fetal circulation; still compensated.
until 30 weeks 4 days; BP intermittently to 160/100. At 30 weeks 6 days increas­ingly silent CTG showing decelerations without uterine contractions. In view of unripe cervix, pri­mary section was performed.
10minutes) UA pH 7.23; base
excess (BE) −4.5 mmol/L. Development good with rapid weight increase on neonatal intensive care.
Jaundice, phototherapy. Dis-
charge after seven weeks weighing 2550 g.
Advanced Topics
abc
def
Fig. 19.1a−f Doppler ultrasound find­ings in a case of impaired uteroplacental perfusion with consequent impairment of fetoplacental perfusion and centrali-
zation of the fetal circulation due to
early fetal growth restriction. The condi­tion is still compensated.
a Zero flow in the UA. b Zero flow in the UA (control). c Zero flow in the aorta.
d Brain sparing. e Right uterine a. with notch and ab-
normally elevated PI.
f Left uterine a. with notch and abnor-
mally elevated PI.
167
3
Seven Cases Illustrating the Use of Doppler Ultrasound in Obstetrics

2—Extreme Fetal Growth Restriction Due to Endarteritis Obliterans

Patient B, gestational age: 28 weeks 3 days
Clinical findings: Age 22, gravida 2, para 0, sta-
tus post intrauterine death at 18th week of pregnancy two
years ago. Initial presentation for oligohydramnios; CTG shows silent oscillations.
Ultrasound findings: Extreme growth retardation of
six to seven weeks, anhydram­nios, estimated weight by ul­trasound 300 g; mild peri­cardial effusion.
Doppler findings: Zero to reverse flow in the UA
ig.
F
19.2a); zero flow in the
( aorta (Fig. 19.2b); brain sparing (Fig. 19.2c); abnormal flow in the inferior vena cava (IVC) (Fig. 19.2d); uteroplacental flow unremarkable (Fig. 19.2e).
Assessment: Unfavorable prognosis due to
extreme maldevelopment. No clear obstetric basis for decision concerning the child. Consultation included mother and pediatrician, consensus re-
garding expectant treatment.
Course: After three days intrauterine
death confirmed; prostaglan­din induction.
Result: Spontaneous delivery 290 g; no
malformation; placenta shows severe endarteritis obliterans.
ab
c
d
Fig. 19.2a−e Doppler ultrasound find­ings in extreme growth restriction with poor prognosis.
a Zero and reverse flow in the UA. b Zero flow in the aorta. c Brain sparing. d Abnormal flow in the IVC. e No abnormal finding in utero-
placental flow.
168
e

3—Exclusion of Potter Syndrome

Patient C, gestational age: 26 weeks 4 days
Clinical findings: Age 26, gravida 1, para 0.
First presentation for sus­pected Potter syndrome due to decreased amniotic fluid.
Ultrasound findings: Anhydramnios, disproportional
growth restriction, head diameters appropriate to ge­stational age, thorax retarded by two weeks, weight esti­mated by ultrasound 800 g; kidneys were displayed by color Doppler bilaterally (Fig. 19.3a, b).
Doppler findings: Reverse flow in the UA
ig.
F
19.3c); reverse flow in the
( aorta (Fig. 19.3d); brain sparing (Fig. 19.3e); abnormal utero­placental perfusion bilaterally
with notch (Fig. 19.3f, g).
Evaluation: No Potter syndrome; severe
uteroplacental and fetoplacen­tal perfusion impairment with centralization of the circulation.
3—Exclusion of Potter Syndrome
Course: Evening CTG showed “bird’s wing”
pattern (i.e., CTG looks like the sil­houette of birds flying as seen from a distance; a typical CTG pattern correlated to fatal hypoxia) with silent oscillation and spontaneous contractions (Fig. section with biopsy of the placental bed (i.e., uterine tissue adjacent to placental insertion).
Result: 760g, no malformations (Fig. 19.3i).
Apgar 4 (1 minute): primary intuba­tion UA pH 7.18, BE −10 mmol/L. Placenta 80 % infarcted, with old and recent infarcts. Placental bed biopsy showed pre­dominantly eccentric narrowing and occlusion of the lumen of the spiral aa., with hypertrophy of the media and fibroblastic proliferation (Fig. 19.3k).
19.3h). Emergency
Advanced Topics
abc
def
Fig. 19.3a−k Fndings in severe impair­ment of uteroplacental and fetoplacen­tal perfusion with centralization of the circulation.
a Sonographic image of a fetal kidney. b Color Doppler image of renal arter-
ies.
c Reverse flow in the UA. d Reverse flow in the aorta.
g
e Brain sparing. f Abnormal perfusion with notch in
the right uterine a.
g Abnormal perfusion with notch in
the left uterine a.
169
3
Seven Cases Illustrating the Use of Doppler Ultrasound in Obstetrics
fi
j
k
Fig. 19.3h CTG. “Bird’s wing” pattern
with silent oscillation
i Newborn infant, 760 g, Apgar 4, pri-
mary intubation required.
j Placenta showing old and more re-
cent infarctions, in total 80 % in­farcted.
k Placental bed biopsy histology shows
predominantly eccentric narrowing
of the lumen and occlusion of the spiral arteries, media hypertrophy, and proliferation of fibroblasts.
170

4—Closely Coordinated Preventive Care for High-Risk Patients

4—Closely Coordinated Preventive Care for High-Risk Patients
Patient D, gestational age: 638 weeks History: Age 32, gravida 3, para 2
Status post stillbirth at 33
weeks of gestation with severe
growth restriction and placen­tal insufficiency. Status post cesarean section for severe preeclampsia at 27
weeks. Infant was severely
growth restricted and soon died. Intense desire for a living child.
Advice: Closely coordinated preventive
pregnancy monitoring, course followed by Doppler. Acetyl­salicylic acid (ASA) from 6th
week of pregnancy.
Doppler findings: Uteroplacental perfusion was
Course: ASA discontinued at 36th week
Result: Infant 2870 g, continued good
appropriate and adapted to ge­stational age 6th to 38th week
Fig.
of pregnancy (
19.4a−f).
(risk of cerebral hemorrhage in the infant). At 38 weeks sec­ondary cesarean section for dystocia.
development, normal dis­charge.
Advanced Topics
Fig 19.4a−f Doppler ultrasound dis­play of the right uterine a. during
timely and normal adaptation of
uteroplacental perfusion from the 6th
to 38th weeks of gestation.
a Gestational age: 6 weeks 5 days. b Gestational age: 9 weeks 5 days. c Gestational age: 13 weeks 6 days. d Gestational age: 17 weeks 6 days. e Gestational age: 20 weeks 3 days.
f Gestational age: 38 weeks 4 days.
a
c
b
d
171
e
f
Seven Cases Illustrating the Use of Doppler Ultrasound in Obstetrics

5—Patient with Antiphospholipid-Antibody Syndrome

Mrs. T.M., age 31, gravida 4, para 4, status post three stillbirths (24 weeks, 700 g, 25 weeks of gestation, weight unknown), with known antiphospholipid-anti­body syndrome. From the beginning of pregnancy patient received 100 mg ASA daily and metoprolol tab
1 q.d. Outpatient ultrasonic monitoring was performed
at two-week intervals. Because of the significant his­tory the patient was admitted from the 28th week of pregnancy. Initially growth was normal by ultrasound, but from the 30th week of pregnancy growth began to
Fig.
19.5a, b). The uteroplacental Doppler find-
3
slow ( ings were always abnormal, showing notches. The notches were more marked from the 28th week on. The resistance indices of the UA and the aorta were in the upper normal range until the 32nd week of gesta­tion, after which the aorta exhibited a block and the umbilical a. a very high resistance index (RI). The RI of the middle cerebral a. (MCA) declined continuously, a sign of centralization (Figs. 19.6−19.11). There was no tricuspid incompetence and there were no abnormal flow readings in the course of the pregnancy (Fig. 19.12). The increasing centralization led to the decision to perform a primary section at 33 weeks 4 days.
Infant male, 1680 g (normal) Apgar values 9−10−10, UA pH 7.29. The infant was kept on inpatient care for about four weeks and was discharged in good general condition.
The mother’s immediate postoperative course was unremarkable, and she was discharged on the 13th postoperative day. Ten days after discharge the patient spiked a fever of 100 °F with pleuropneumonia at the left base. Further examination revealed a deep vein thrombosis of the pelvis and leg veins and necrosis of the thigh consequent on thrombocytopenia type II as­sociated with heparin (HIT-II). Excision of necrotic tissue from the left thigh and a mesh graft were re­quired. The patient was discharged four months after delivery.
12
10
8
6
+
BPD cm
FL cm
+
4
2
0
12 16 20 24 28 32 36 40
a
12
10
8
6
4
2
0
12 16 20 24 28 32 36 40
b
Fig. 19.5a Biparietal diameter (BPD) and femur length (FL)
throughout the course of pregnancy.
Fig. 19.5b Abdominal diameter (AD) throughout the course
of pregnancy
Weeks of gestation
Weeks of gestation
AD cm
+
172
5—Patient with Antiphospholipid-Antibody Syndrome
Fig. 19.6a−d Doppler ultrasound readings through the course of preg­nancy.
a RI of the UA. b RI of the MCA. c Placental−cerebral ratio (PCR) (RI
umbilical a./RI middle cerebral a.)
d RI of the uterine a. (UT).
1.0
1.0
+
+
0.5
0
24 27 30 36 39 42
RI of UA
a
1.5
33
Weeks of gestation
0.5
0
b
RI of MCA
3324 27 30 36 39 42
+
1.0
1.0
+
0.5
0
PCR
cd
3324 27 30 36 39 42
Weeks of
gestation
0.5
0
3324 27 30 36 39 4215 18 21
RI of UT
Weeks of
gestation
Advanced Topics
Weeks of
gestation
Fig. 19.7a−e Doppler sonographic display of the right uterine a. through
the course of pregnancy: PI values
tend to increase, notch intensity in­creases, an additional (double notch) systolic notch appears as the preg­nancy progresses. a Gestational age: 22 weeks 5 days,
minimal postsystolic notch, PI:
1.05.
b Gestational age: 25 weeks 0 days,
minimal postsystolic notch, PI:
1.22.
c Gestational age: 27 weeks 2 days,
minimal postsystolic notch, PI:
1.53, systolic notch (double notch).
d Gestational age: 32 weeks 3 days,
minimal postsystolic notch, PI:
1.30, systolic notch.
e Gestational age: 33 weeks 3 days,
very marked postsystolic notch, PI
1.45, systolic notch.
ab
cd
173
d