AJR 2005; 185:541-549
© American Roentgen Ray Society
Remnants of Fetal Circulation: Appearance on MDCT in Adults
Elmar M. Merkle1 and
Robert C. Gilkeson2
1 Department of Radiology, Duke University Medical Center, Duke North, Rm. 1417,
Erwin Rd., Durham, NC 27710.
2 Department of Radiology, University Hospitals of Cleveland/Case Western
Reserve University, Cleveland, OH 44106-5056.
Received September 9, 2004;
accepted after revision November 8, 2004.
Address correspondence to E. M. Merkle.
Abstract
OBJECTIVE. The objective of our study was to describe the appearance
of the remnants of the fetal circulation in adults on MDCT.
CONCLUSION. The use of MDCT allows frequent visualization of the
remnants of the umbilical vein, ductus venosus, foramen ovale, ductus
arteriosus, and umbilical arteries.
Introduction
The peculiarities of the fetal vascular system and their variants are well
known (Fig. 1) and are often
visualized on prenatal sonography. However, remnants of the fetal circulation
may be overlooked on cross-sectional imaging in adults. Recognition of their
morphology and associated abnormalities and diseases improves the knowledge of
mediastinal, abdominal, and pelvic anatomy and may help to better understand
pathologic conditions. The use of MDCT allows more frequent visualization of
the remnants of the umbilical vein, ductus venosus, foramen ovale, ductus
arteriosus, and umbilical arteries. These remnants will be discussed in the
order that blood circulates from the placenta to and through the fetus.
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Fig. 1 —Schematic representation shows fetal circulation. Bright-red
blood vessels carry oxygenated blood, and blue vessels carry deoxygenated
blood. 1 = umbilical vein, 2 = ductus venosus, 3 = foramen ovale, 4 = ductus
arteriosus, 5 = umbilical arteries, 6 = main portal vein, 7 = left portal
vein, 8 = left hepatic vein, 9 = inferior vena cava, 10 = abdominal aorta, 11
= umbilicus, 12 = urinary bladder, 13 = placenta, 14 = liver.
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Review of Fetal Circulation
Fetal oxygenated blood is returned from the placenta to the fetus by the
umbilical vein. This vein enters the abdomen at the umbilicus and passes
upward to the liver. At the porta hepatis, it divides into two branches: Of
these, the large branch is joined by the portal vein and enters the right
lobe, and the small branch continues upward under the name of the ductus
venosus and joins the inferior vena cava. Therefore, the oxygenated blood that
traverses the umbilical vein passes to the inferior vena cava in two ways. A
considerable quantity of oxygenated blood circulates through the liver with
the portal venous blood before entering the inferior vena cava by the hepatic
veins; the remaining oxygenated blood (40–60%) passes directly into the
inferior vena cava through the ductus venosus.
In the inferior vena cava, the blood carried by the ductus venosus and
hepatic veins becomes mixed with that returning from the lower extremities. It
enters the right atrium and passes through the foramen ovale into the left
atrium where it mixes with a small quantity of blood returned from the lungs
by the pulmonary veins. From the left atrium, the blood passes into the left
ventricle and from the left ventricle into the aorta by means of which it is
distributed almost entirely to the head and upper extremities. From there, the
blood is returned by the superior vena cava to the right atrium where it mixes
with a small portion of the blood from the inferior vena cava. From the right
atrium it descends into the right ventricle and then passes into the main
pulmonary artery. Because the lungs of a fetus are inactive, only a small
quantity of the blood of the pulmonary artery is distributed to them by the
right and left pulmonary arteries; it is then returned by the pulmonary veins
to the left atrium. The greater part of the blood ejected from the right
ventricle passes through the ductus arteriosus into the aorta where it mixes
with a small quantity of the blood transmitted by the left ventricle into the
aorta. Through the aorta it descends and is in part distributed to the lower
extremities and the viscera of the abdomen and pelvis, but the greater amount
is conveyed by the umbilical arteries back to the placenta.
Ligamentum Teres Hepatis: Remnant of the Umbilical Vein
Fetal blood is returned from the placenta to the fetus by the umbilical
vein. This vein enters the fetal abdomen at the umbilicus and passes cephalad
to the posteroinferior surface of the liver as the sinus venosus where it
drains into the left portal vein (Fig.
1). After birth, the blood in the umbilical vein clots. Between
the second and fifth postnatal days, the umbilical vein is usually completely
occluded. After obliteration over the next several months, the umbilical vein
becomes the ligamentum teres hepatis, which usually measures between 10 and 20
cm (Fig. 2).
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Fig. 2 —52-year-old woman with normal findings on MDCT of abdomen and
pelvis. Curved planar reconstruction image shows ligamentum teres hepatis
(straight white arrows), which courses in free margin of falciform
ligament from umbilicus (curved white arrow) to left portal vein
(straight black arrow). Also, note right (curved black
arrow) and main (asterisk) portal veins.
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Occasionally, radiologists in training confuse the falciform ligament and
the ligamentum teres hepatis. The falciform ligament is a double fold of
peritoneum and is a true extra-hepatic ligament. It evolves from the right and
left triangular ligaments and extends from the anterosuperior surface of the
liver to the umbilicus. The falciform ligament is normally not seen on MDCT
scans, but can easily be detected when free air or fluid outlines the linear
structure anterior to the liver. The ligamentum teres hepatis on the other
hand is commonly seen on MDCT scans in the fissure of the ligamentum teres
hepatis as a round or linear structure and in the free margin of the falciform
ligament (Fig. 3).
Running adjacent to the ligamentum teres hepatis are small paraumbilical
vessels that may represent vasa vasorum and that connect the veins around the
umbilicus to the portal vein. Formerly, visualization of a patent blood vessel
in the free margin of the falciform ligament was called a
"reopened" or "recanalized" umbilical vein. Such
dilated veins are seen in approximately 25% of patients with portal
hypertension [1,
2]. However, the umbilical vein
never reopens after obliteration. It has been proven angiographically and
histologically that these vessels actually are enlarged paraumbilical veins
and not recanalized umbilical veins
[3].
On MDCT, dilated paraumbilical veins appear as circular or tubular
structures more than 2 mm in diameter and are seen in the fissure of the teres
ligament or along the free margin of the falciform ligament
[4]
(Fig. 4). In approximately 25%
of patients with dilated paraumbilical veins, unusual pathways are seen with
the vein arising from the left portal vein and passing through the hepatic
parenchyma [5].
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Fig. 4 —48-year-old man with cirrhosis and portal venous
hypertension. Curved planar reconstruction image of MDCT data set shows
dilated paraumbilical vein coursing in fissure of ligamentum teres hepatis
(black arrow) along free margin of falciform ligament (white
arrow).
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The finding of dilated paraumbilical veins is usually incidental, with
fewer than 10 cases having been reported in patients who presented with
symptoms of clinical significance attributable to these dilated paraumbilical
veins [6]. Symptomatic patients
usually present with either intraperitoneal or external hemorrhage significant
enough to cause hemodynamic instability
[6,
7]. Hemostasis is usually
achieved with compression bandages (if external) or surgically.
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Fig. 5 —53-year-old man with variant of hepatic arterial blood
supply. Contrast-enhanced axial MDCT image shows accessory left hepatic artery
(arrows) originating from left gastric artery and coursing in fissure
of ligamentum venosum.
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Ligamentum Venosum: Remnant of the Ductus Venosus
The ductus venosus emanates from the left portal vein opposite the entry of
the umbilical vein (Fig. 1) and
ends at its junction with the inferior vena cava. Just before this point, it
usually receives the left hepatic vein. Functionally, the ductus venosus is an
important vessel within the fetal circulation because it provides a means for
oxygenated umbilical vein blood to bypass the sinusoids of the liver.
Postnatal closure of the ductus venosus starts during the first minute
after birth but is not completed until days 15–20 postpartum. The
mechanism of closure is not clear, but it may be related to a decrease in
pressure within the portal venous system after cessation of umbilical vein
flow [8]. Of note, the ductus
venosus closes sooner after birth in neonates of greater gestational age or
higher birth weight [9].
The ligamentum venosum is an extrahepatic fibrous remnant of the fetal
ductus venosus and runs in a craniocaudal direction. It is only a few
centimeters long and usually is not seen within the fissure of the ligamentum
venosum on axial MDCT images. It should not be misconstrued for other
structures running in this fissure, such as a replaced or accessory left
hepatic artery originating from the left gastric artery, a normal variant of
the hepatic arterial blood supply (Fig.
5).
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Fig. 6A —45-year-old woman with patent ductus venosus. (Reprinted from
[14]) Contrast-enhanced axial
CT scan reveals abnormal vein (arrow) connecting large left portal
vein to inferior vena cava through fissure of ligamentum venosum.
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Fig. 7B —64-year-old woman with lipomatous hypertrophy of interatrial
septum. Axial contrast-enhanced CT image obtained inferior to A shows
mild aneurysm of prominent fossa ovalis (arrow), embryonic remnant of
foramen ovale.
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Like the umbilical vein, the ductus venosus never reopens after
obliteration. However, in very rare cases, the ductus venosus fails to
obliterate and persists as a left-sided extrahepatic portosystemic shunt.
Fewer than 30 cases of a patent ductus venosus have been reported in adults,
with a male-to-female ratio of 4:1
[10,
11]. Interestingly, two
separate scientific reports suggest a genetic basis for patent ductus venosus
as an autosomal recessive trait
[12,
13].
The clinical presentation of patients with a patent ductus venosus varies
from asymptomatic with or without hyperammonemia to encephalopathy;
hypergalactosemia; hypoglycemia; and, rarely, hypoxemia. Over time,
hypoperfusion and hepatic atrophy may occur in response to portal venous blood
shunting [10]. The incidence
of hepatic focal nodular hyperplasia may also be increased
[10,
12].
On MDCT, an abnormal vein can be seen between the left portal vein and the
left hepatic vein or inferior vena cava (Fig.
6A,
6B). This shunt usually courses
through the fissure of the ligamentum venosum with reported vein diameters
ranging from 10 to 40 mm [10,
11].
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Fig. 9 —62-year-old woman with left atrial mass. Axial CT image shows
lobulated left atrial mass (arrowhead). Note close relationship of
mass to fossa ovalis (arrow). At surgery, left atrial myxoma
originating at fossa ovalis was confirmed.
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Treatment options in symptomatic patients include medical treatment,
endovascular coiling of the left portal vein or patent ductus venosus, and
surgical division of the shunt
[8,
10,
13,
14]. Extreme care must be
taken to prevent severe portal hypertension in the postoperative period
secondary to intrahepatic portal vein hypoplasia
[8,
13]. Surgical banding of the
shunt with polytetrafluoroethylene tape has also been suggested to avoid this
life-threatening complication
[13].
Foramen Ovale
In utero, the patent foramen ovale is an interatrial communication that
allows blood to pass directly from the right atrium to the left atrium. The
septum primum provides a valve that helps closure of the patent foramen ovale.
The fossa ovalis, an oval depression of the septal wall, represents the
remnant of the closed foramen ovale (Fig.
7A,
7B). Aneurysms of the fossa
ovalis can be a source of paradoxic emboli
(Fig. 8), so patients with
these findings should be treated aggressively for the risk of recurrent
thromboemboli [15].
Identification of the fossa ovalis can be helpful in the differentiation of
left atrial masses. Atrial myxomas classically arise at the level of the fossa
ovalis, an imaging feature that helps differentiate these tumors from left
atrial thrombi [16]
(Fig. 9).
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Fig. 11 —64-year-old man with stroke. Sagittal
maximum-intensity-projection image confirms thrombus (arrow) crossing
into left atrium via patent foramen ovale (arrowhead). These findings
were confirmed at transesophageal echocardiography.
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Fig. 12A —72-year-old woman with pulmonary hypertension and
echocardiographic findings suspicious for patent ductus arteriosus. Sagittal
volume-rendered MDCT image shows heavily calcified patent ductus arteriosus
(arrow). LPA = left pulmonary artery.
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Fig. 12B —72-year-old woman with pulmonary hypertension and
echocardiographic findings suspicious for patent ductus arteriosus. Axial MDCT
image obtained during dynamic contrast study at level of patent ductus
arteriosus shows jet of unopacified blood from aorta entering main pulmonary
artery (arrow).
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The incidence of a persistent patent foramen ovale is estimated to be
between 15% and 30%, with significant variability in size and physiologic
significance. It is clearly an important risk factor in patients who present
with stroke. Steiner et al.
[17] reported a patent foramen
ovale in 33% of the patients who presented with cryptogenic stroke. In
patients with cerebral infarction shown on CT, 45% had a patent foramen ovale
and the size of the stroke correlated with the size of the patent foramen
ovale [17]. Numerous cases of
paradoxical air, tumor emboli, and fat emboli due to a previously undiagnosed
patent foramen ovale have also been described in the literature
[18].
Evaluation of the patent foramen ovale is important in patients with
unexplained dyspnea. Patients with a patent foramen ovale may present with
orthodeoxia, in which there is desaturation when the patient is in the upright
position due to shunting across the patent foramen ovale. Recent work in
patients undergoing CT evaluation of pulmonary embolism has shown an increased
prevalence of patent foramen ovale in patients with suboptimal CT angiograms
for the evaluation of pulmonary embolism
[19]. In that population, it
was postulated that visualization of the pulmonary arteries during suspended
inspiration was suboptimal because of right-to-left shunting. Patients with
proven deep venous thrombosis and patent foramen ovale are at increased risk
for systemic thromboembolic disease (Figs.
10A,
10B and
11).
Ligamentum Arteriosum: Remnant of the Ductus Arteriosus
The ductus arteriosus is a normal fetal structure that allows blood to
bypass the fetal lungs in utero by shunting blood from the left pulmonary
artery to the descending thoracic aorta
(Fig. 1). Typically, the patent
ductus arteriosus presents as a communication between the anterior aspect of
the left pulmonary artery and the inferior aspect of the aortic arch distal to
the left subclavian artery. The morphologic characterization of patent ductus
arteriosus has been established angiographically by Krichenko et al.
[20].
Diagnosis of a patent ductus arteriosus can be difficult in adults and is
often delayed. The traditional method of diagnosis in these patients is
echocardiography, MRI, or both
[21]. MRI has been a powerful
imaging tool for the diagnosis of patent ductus arteriosus, and flow
quantification with phase-contrast MRI correlates well with catheter
angiography [22]. However, the
use of MRI is limited in patients with claustrophobia, cardiac pacemakers, or
significant dyspnea.
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Fig. 12C —72-year-old woman with pulmonary hypertension and
echocardiographic findings suspicious for patent ductus arteriosus. Axial MDCT
image obtained inferior to B shows jet of unopacified blood
(arrow) from aorta runs into enhanced pulmonary artery, which is
confirmatory of patent ductus arteriosus.
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Fig. 13A —74-year-old woman who presented for preoperative assessment
of aortic calcification. Coronal (A) and sagittal (B)
reconstruction images of unenhanced MDCT data set show small residual patent
ductus arteriosus (arrows).
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Fig. 13B —74-year-old woman who presented for preoperative assessment
of aortic calcification. Coronal (A) and sagittal (B)
reconstruction images of unenhanced MDCT data set show small residual patent
ductus arteriosus (arrows).
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Newer MDCT techniques have markedly improved the assessment of patent
ductus arteriosus. In a recent article, Morgan-Hughes et al.
[23] described the CT findings
in five adult patients with patent ductus arteriosus. In that article, the
authors defined the ability of MDCT for volumetric anatomic assessment while
evaluating the degree of calcification of the patent ductus arteriosus. The
assessment of calcification with CT is superior to MRI, catheter angiography,
and echocardiography. Patent ductus arteriosus calcification in adult patients
is an important feature because the degree of patent ductus arteriosus
calcification defines those patients at high surgical risk. Transcatheter
coiling or aortic stent placement is preferred in the adult patient with a
heavily calcified patent ductus arteriosus
[24].
Postprocessing techniques including volume rendering and virtual angioscopy
enable anatomic perspectives not possible with catheter angiography. Shorter
imaging times made possible with MDCT enable dynamic assessment that can be
diagnostic of a patent ductus arteriosus (Fig.
12A,
12B,
12C). Although
contrast-enhanced images are important, the multiplanar capabilities of MDCT
can suggest the diagnosis even in the absence of IV contrast administration
(Fig. 13A,
13B).
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Fig. 14A —49-year-old man with abdominal pain who presented for MDCT of
pelvis. Volume-rendered sagittal reconstruction image shows median umbilical
ligament (thin arrows) as remnant of urachus coursing from urinary
bladder (asterisk) to umbilicus (thick arrow).
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Fig. 14B —49-year-old man with abdominal pain who presented for MDCT of
pelvis. Volume-rendered axial reconstruction image shows left medial umbilical
ligament (dashed arrows) as remnant of left umbilical artery coursing
from left internal iliac artery (thin straight arrow) to umbilicus.
Also, note anterior portion of right medial umbilical ligament (curved
arrow) and median umbilical ligament as remnant of urachus (thick
straight arrow).
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Bilateral Medial Umbilical Ligaments: Remnants of the Umbilical Arteries
The umbilical arteries arise from the internal iliac arteries and run along
the sides of the urinary bladder and then run upward and medially along the
undersurface of the anterior abdominal wall to the umbilicus
(Fig. 1), pass out of the
abdomen, and continue in the umbilical cord to the placenta. They convey the
fetal blood to the placenta. Postnatal closure of the umbilical arteries
begins soon after birth and is completed within a few days.
The various umbilical ligaments and folds can be confusing. The single
median umbilical ligament is an approximately 10-cm-long fold of parietal
peritoneum over the urachus, which courses in the midline from the dome of the
urinary bladder to the umbilicus (Fig.
14A,
14B). The two medial umbilical
ligaments are approximately 15- to 25-cm-long folds of parietal peritoneum
over the umbilical arteries. These ligaments course from the internal iliac
arteries to the umbilicus. Finally, for the sake of completeness, the two
lateral umbilical ligaments are folds of peritoneum over the inferior
epigastric arteries. Of note, all the umbilical ligaments are easier to see
when surrounded by fat.
Although the two medial umbilical ligaments were rarely seen in the era of
incremental CT, they are now visualized on a regular basis with MDCT
[25]. They appear as bilateral
linear structures that course from the internal iliac arteries along the sides
of the urinary bladder and then run medially and upward to the umbilicus (Fig.
14A,
14B). Of note, the two
umbilical ligaments produce an important radiographic finding in patients with
pneumoperitoneum: the inverted-V sign
[26].
The two medial umbilical ligaments never reopen, to the best of our
knowledge, and no pathologic conditions are known to be related to these
remnants of fetal circulation. However, fetuses with a single umbilical artery
(and therefore a single medial umbilical ligament) have a higher incidence of
anomalies, and some of these babies presumably survive to adulthood
[27].
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Abstract
Introduction
