Umbilical artery Doppler velocimetry (UADV) has become an important clinical tool in obstetrical practice. UADV examines the impedance to blood flow in the placenta, and therefore is a test of the placental stages. The umbilical arteries are easy to sample because they are long, nonbranching, and surrounded by amniotic fluid.
Anatomy of the Umbilical Arteries
The umbilical arteries are branches of the internal iliac artery, which have a pelvic segment around the fetal bladder (Figure 11-1). Thereafter, the umbilical arteries have an upward trajectory inside the fetal abdomen as they travel to the umbilicus to become part of the umbilical cord. The vessels travel in the umbilical cord until the insertion of the placenta. An anastomosis of the umbilical arteries located approximately 3 cm from the placental insertion, acting as a pressure-equalizing system between umbilical arteries, can be demonstrated with ultrasound and is called "Hyrtl anastomosis."1,2
Two umbilical arteries surrounding the fetal bladder.
The umbilical cord contains 2 arteries and 1 vein. The arteries carry deoxygenated blood from the fetus to the placenta. Such blood is enriched with oxygen in the villous tree, and then returns to the fetus through the umbilical vein. Therefore, the umbilical arteries contain blood with a lower Po2 and pH than that in the umbilical vein.
Physiology of the Umbilical Arteries
The umbilical circulation is a low-resistance vascular bed. Blood flow to the placenta increases with advancing gestational age, and this is accomplished by a decrease in vascular resistance of the placenta. Umbilical vessels and placental vessels lack innervation, and they do not respond to vasoconstrictors.
Doppler signals can be obtained in any segment that is visible: around the fetal bladder, in the abdominal insertion of the umbilical cord, in a free loop, or in the placental insertion of the umbilical cord. There is evidence that Doppler indices vary depending upon where the Doppler signal is obtained.3,4,5, and 6 In general, Doppler indices are higher in the abdominal insertion of the umbilical cord than in the placental insertion.5,6 Although the difference is not large, a standard recommendation is that the same site be used for sampling, in particular when serial studies are being performed in a fetus at risk.
In most cases, Doppler signals are obtained from a free loop of the umbilical cord because of the ease of acquisition. The placental insertion and the abdominal insertion have the disadvantages of depending upon location. For example, it would be difficult to sample the umbilical cord at the placental insertion site in posterior placentas. Similarly, the position of the fetus may be suboptimal to sample the umbilical cord at the entry into the abdomen (when the fetus is facing down). In contrast, the umbilical arteries can be reliably identified and sampled on both sides of the bladder. This allows exclusion of a single umbilical artery (Figure 11-2) and also standardization. However, because this requires a greater level of skill, the free loop continues to be used in practice.
Two-vessel cord. Axial section of the umbilical cord containing an umbilical vein and a single umbilical artery.
We obtain Doppler waveforms for analysis by placing the sample volume of a pulsed Doppler system in a manner that would include 1 umbilical artery and 1 vein (Figure 11-3A). However, when there is absence of end-diastolic velocities, we prefer to sample the umbilical artery alone to avoid missing reversal of flow.7 It is also important to remove the high-pass filter (wall thump filter), which eliminates low-frequency signals that are generated from the vessel wall. A well-known artifact is the generation of artifactual absent end-diastolic velocities, because the high-pass filter is on, suppressing the low end-diastolic signal (Figure 11-4A and B).
Umbilical artery waveforms. A: Normal. B: Absent end-diastolic flow. C: Reversed end-diastolic flow.
Umbilical artery waveform. A: High-pass filter off. B: High-pass filter on.
The number of waveforms to be obtained has been recommended to vary from 3 to 5.8,9, and 10 An important aspect is that the waveforms should be regular to obtain an accurate assessment of the vascular impedance to flow. Ideally, these waveforms should be obtained when the fetus is not breathing and not moving. Fetal breathing can cause changes in the waveform (Figure 11-5).10,11 Similarly, an irregular fetal heart rate can also generate artifactual Doppler signals.11,12,13,14,15,16, and 17 It is not necessary to correct Doppler indices for the fetal heart rate when this is within normal ranges.14 The flow velocity waveform of the umbilical artery is not subject to diurnal variability,18,19,20, and 21 nor it is affected by maternal exercise.22,23 A maternal supine position was reported to be associated with a significantly higher systolic-to-diastolic (S/D) ratio24; however, this finding has not been confirmed.18
Umbilical artery and vein waveform during fetal breathing.
In the past, Doppler signals were calculated manually or using a planimeter. Today, the AutoTrace function allows calculation to be based on several waveforms. Similarly, modern equipment provides the S/D ratio, resistance index (RI), and pulsatility index (PI). These indices are angle independent. Most clinicians now use the PI to analyze waveforms. The initial studies employed the S/D ratio because it was easy to calculate (did not require integration of the entire waveform), but this issue has now been solved with modern ultrasound equipment. One advantage of using the PI is that it can be calculated when there are absent end-diastolic velocities. Under such circumstances, neither the S/D ratio nor the RI can be calculated.
Morphology of the Umbilical Artery Waveform and Changes with Gestational Age
In early pregnancy, an absent end-diastolic velocity is a normal finding (Figure 11-6A and B)25,26; however, the presence of end-diastolic velocities is expected after 18 weeks of gestation.27 From this point onward the umbilical artery waveform is characterized by forward flow during the entire cardiac cycle. Moreover, end-diastolic velocities are high, and this is consistent with low resistance to flow.28,29
Umbilical artery and vein waveforms at 14 weeks gestation (A) and at 16 weeks (B). Note that the absence of end-diastolic velocity in the umbilical artery during the first trimester is a normal finding (A).
The placenta increases in size with advancing gestational age, and this is associated with an increased number of tertiary stem villi. As the placenta grows, the vascular resistance decreases. Therefore, the Doppler indices decrease as gestation progresses,18,20,27,30,31,32,33,34,35, and 36 and this is demonstrated in Figure 11-7 and in Table 11-1, which display the normal values for the PI of the umbilical artery.37 Longitudinal reference ranges are also available for the blood velocity and PI at the intraabdominal portion, and fetal and placental ends of the umbilical artery.6
Table 11-1REFERENCE LIMITS (5TH, 50TH, AND 95TH CENTILES) FOR THE UMBILICAL ARTERY PULSATILITY INDEX BASED ON A CROSS-SECTIONAL STUDY OF 1556 LOW-RISK PREGNANCIES ||Download (.pdf) Table 11-1 REFERENCE LIMITS (5TH, 50TH, AND 95TH CENTILES) FOR THE UMBILICAL ARTERY PULSATILITY INDEX BASED ON A CROSS-SECTIONAL STUDY OF 1556 LOW-RISK PREGNANCIES
| ||Percentile |
|Gestational Age (wk) ||5th ||50th ||95th |
|20 ||1.04 ||1.54 ||2.03 |
|21 ||0.98 ||1.47 ||1.96 |
|22 ||0.92 ||1.41 ||1.90 |
|23 ||0.86 ||1.35 ||1.85 |
|24 ||0.81 ||1.30 ||1.79 |
|25 ||0.76 ||1.25 ||1.74 |
|26 ||0.71 ||1.20 ||1.69 |
|27 ||0.67 ||1.16 ||1.65 |
|28 ||0.63 ||1.12 ||1.61 |
|29 ||0.59 ||1.08 ||1.57 |
|30 ||0.56 ||1.05 ||1.54 |
|31 ||0.53 ||1.02 ||1.51 |
|32 ||0.50 ||0.99 ||1.48 |
|33 ||0.48 ||0.97 ||1.46 |
|34 ||0.46 ||0.95 ||1.44 |
|35 ||0.44 ||0.94 ||1.43 |
|36 ||0.43 ||0.92 ||1.42 |
|37 ||0.42 ||0.92 ||1.41 |
|38 ||0.42 ||0.91 ||1.40 |
|39 ||0.42 ||0.91 ||1.40 |
|40 ||0.42 ||0.91 ||1.40 |
|41 ||0.42 ||0.92 ||1.41 |
|42 ||0.43 ||0.93 ||1.42 |
Pulsatility index of the umbilical artery. The 5th, 50th, and 95th percentiles are plotted against gestational age. (Reproduced with permission from: Arduini A, Rizzo G. J Perinat. Med 1990;18:165-172.)
The Physiologic Significance of an Abnormal Umbilical Artery Waveform
Mathematical modeling of the placental circulation indicates that 50% to 60% of terminal arterial vessels must be obliterated for the PI to increase beyond its normal range. It is interesting that there is a steep increase of the PI after 80% of fractional terminal vessels are obliterated.38 Therefore, an abnormal umbilical artery velocimetry reflects substantial pathology of the placental vascular territory. It is noteworthy, according to the results of mathematical modeling, that the same rate of obliteration of the vessels has a stronger effect on the PI in a smaller placenta than in a larger placenta. The effect of obliteration appears to be greater in early gestation when the placenta is smaller, rather than in the third trimester when the placenta is larger.38
Patients with high Doppler indices have a significantly lower modal number of arterioles in the tertiary stem villi than that in a normal control group (7 to 8 arteries per field in the control group and 1 to 2 arteries per high-power field in the abnormal Doppler group). The pathologic lesion considered to be responsible for this is vascular sclerosis with obliteration of the small muscular arteries of the tertiary stem villi.39,40, and 41 Other vascular lesions associated with abnormal Doppler velocimetry of the umbilical arteries include fetal thrombotic vasculopathy, chronic villitis, and fetal vascular necrosis.42,43 It is important to note that an abnormal umbilical artery Doppler waveform reflects placental disease and not fetal disease.
Trudinger et al have demonstrated that fetuses with abnormal umbilical artery Doppler velocimetry have evidence of higher red blood cell count and hemoglobin concentration,44 endothelium activation,45 platelet activation (which promotes thrombosis),46 and platelet consumption.47 In addition, these fetuses have an atherogenic lipoprotein profile48 and evidence of intravascular inflammation.49 This may be important in relating placental vascular disease, detected by umbilical artery Doppler velocimetry, to the risk for adult cardiovascular disease.45 In other words, the fetus with abnormal umbilical artery Doppler velocimetry has similar changes to those observed in adults with atherosclerosis.
Clinical Correlations of Abnormal Umbilical Artery Doppler Velocimetry
Pregnancies with abnormal umbilical artery Doppler velocimetry are at increased risk for (1) perinatal death, (2) SGA, (3) congenital anomalies, and (4) admission to a neonatal intensive care unit. These conclusions are based on the pioneering and classic studies of Professor Trudinger in a large number of patients who had umbilical artery Doppler velocimetry because they were at risk for adverse pregnancy outcome based upon clinical indications or assessment.7,50
Meta-analysis of randomized clinical trials in which UADV was used for the management of patients has indicated that the use of this tool results in a reduction of perinatal morbidity of approximately 38%, and therefore UADV is no longer considered an investigational tool. It is clinically indicated when the diagnosis of SGA is made, there is a history of a fetal demise, or there are obstetrical or medical complications that increase the risk of perinatal morbidity and mortality, such as preeclampsia, chronic hypertension, thrombophilic states, lupus, and other complications of pregnancy.51,52,53, and 54
Small for Gestational Age
UADV is performed serially in SGA fetuses. Abnormalities of the umbilical artery waveform reflect the presence of placental rather than fetal disease. Therefore, absence or reversal of flow during the diastolic period is not by itself an indication for delivery, but rather an indication for increased surveillance to prevent in utero death.
The spectrum of abnormalities detectable in the waveforms evolves from a progressive reduction in the end-diastolic velocities (reflected by an elevated PI for gestational age), followed by the absence of the end-diastolic flow (AEDF) and, in extreme cases, the occurrence of reverse end-diastolic flow (REDF; see Figure 11-3B, and C).35,55,56,57,58, and 59
There is an association between abnormalities of UADV and the fetal acid–base status (lower pH, lower Po2, acidemia).60,61,62,63,64,65,66, and 67 When there is an umbilical artery PI greater than 1.5, lactate concentrations in umbilical venous blood increase sharply.66 Moreover, SGA fetuses with abnormal UADV are more likely to experience fetal distress,68,69 longer neonatal intensive care unit stays, and have a higher perinatal mortality.50,70,71, and 72 An abnormal UADV precedes the development of an abnormal fetal heart tracing by 2 to 4 weeks.70,73
Abnormalities in the UADV in fetuses who are not SGA should raise the suspicion of whether or not there is an undetected fetal congenital anomaly (anatomical or chromosomal).74,75,76,77, and 78 The spectrum of abnormalities described in association with abnormal umbilical artery Doppler indices is wide.75 The tertiary villi of placentas from fetuses with karyotype abnormalities often display a reduction in the total vessel count, in the small muscular artery number, and in the small muscular artery to villus ratio.77,79 This under-vascularization may represent placental immaturity as a result of arrested or delayed angiopoiesis,79 and may predispose to the Doppler abnormalities in the umbilical artery.80,81, and 82
Abnormalities of the umbilical artery Doppler velocimetry, such as a sudden increase in vascular resistance and appearance of a dicrotic notch, have been described in the presence of placental abruption.83
Persistent Discordant Flow Velocity Waveforms in the 2 Umbilical Arteries
Reproducibility studies show that the waveforms obtained from the 2 umbilical arteries are usually very similar.19 These vessels are joined just before entering the placenta by a wide transverse anastomosis (Hyrtl anastomosis) and placenta pathology is usually diffuse, with consequences in the territory of distribution of both vessels. Persistently discordant waveforms recorded in the 2 arteries, with elevated vascular resistance in one vessel but not in the other one is an unusual finding, suggesting the presence of asymmetrical placental damage, such as a placental infarction84 or placental abruption.85
Umbilical Artery Doppler Velocimetry during Labor
Uterine contractions, artificial rupture of the membranes, and oxytocin infusion do not change the umbilical artery flow velocity waveform.86,87 Whether administration of epidural anesthesia is associated with changes in the umbilical artery Doppler velocimetry is a subject of debate, with some investigators reporting no changes,88 whereas others claim a reduction of the umbilical artery Doppler waveform indices.24 A role for catecholamine has been proposed to explain such changes.89