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6.2 · Visceral andRetroperitoneal Veins
. Fig. 6.39 Inammatory abdominal aortic aneurysm (AAA). Trans-
verse (left) and longitudinal (right) images show inammatory wall
thickening with a wall thickness of 9mm. Here, the intima appears
bright due to the presence of atherosclerotic plaque (arrow) and
allows dierentiation of vascular pathology on the luminal side from
processes external to the intima. In this case, wall thickening involves
the outer layers of the vessel wall. Thus, the relationship to the intima
distinguishes inammatory vessel wall thickening from thrombotic
deposits, which would be seen to extend into the lumen from the inner
side of the intima. The patent lumen is 31mm in width
435
6.2 Visceral andRetroperitoneal Veins
6.2.1 Vascular Anatomy
6.2.1.1 Vena Cava
e inferior vena cava ascends parallel to the course of the
aorta and to the right of the vertebral column. It is a capacitance vessel with an elliptical cross section and may vary in its
anteroposterior diameter from 0.5 to 2.5cm during the respiratory cycle. It is formed by the junction of the common iliac
veins at the L4/L5 level slightly below the aortic bifurcation.
Variants and anomalies of the inferior vena cava are
present in 1.5–4.0% of the population and are typically
detected incidentally. ey result from errors in the complex
embryonic development with a disturbance in the transition
from the symmetric venous system to the predominantly
right-sided, asymmetric secondary system. e congenital
anomalies were classied by Chuang etal. as early as 1974
(. Table6.8).
Vena cava anomalies typically involve the segment below
the renal vein entries. Duplication (0.2–3%) and transposition
(0.2–0.5%) are the most common anomalies. In both cases,
the inferior vena cava, which runs to the le of the aorta,
6
. Fig. 6.40 a Retroperitoneal brosis (Ormond’s disease) histologically proven by core biopsy. A thickened aortic wall as in vasculitis can be dif-
ferentiated from retroperitoneal brosis by the course of the inferior mesenteric artery (<A.M.INF). The abnormal retroperitoneal tissue pushes the
inferior mesenteric artery toward the aorta. The inferior mesenteric artery thus appears closer to the aortic lumen than in vasculitis. b Aortic wall
thickening in giant cell arteritis (power mode images in longitudinal orientation on the left and transverse orientation on the right). The course of
the inferior mesenteric artery at its origin conrms disease of the aortic wall as the artery pierces the thickened wall directly as it arises from the
aorta rather than being pushed toward the aortic wall, as in brosis. The CT scan (rightmost image) shows circumferential wall thickening due to
giant cell arteritis. Both ultrasound and CT additionally show plaque on the thickened wall in the lumen (Courtesy of K.Amendt)
Chapter 6 · Visceral andRetroperitoneal Vessels
436
. Table 6.8 Classication of congenital anomalies of the
inferior vena cava (According to Chuang etal. 1974)
Level Segment Description
Disturbed embryonic development may result in an atypical
retroaortic course of the le renal vein.
6.2.1.3 Portal Venous System and
Hepatic Veins
I Postrenal
Type A Persistence of right posterior cardinal
vein (retro- or circumaortic ureter)
Type B Persistence of right supracardinal vein
(normal inferior vena cava)
Type C Persistence of left supracardinal vein
(left-sided inferior vena cava)
6
Type BC Persistence of both supracardinal
veins (duplicated inferior vena cava)
II Renal Persistence of renal venous ring
(circumaortic ureter)
III Prerenal or
hepatic
Absence of hepatic segment (azygos
or hemiazygos vein continuation)
crosses the aorta together with or as part of the le renal vein
to then continue on its course on the right side of the aorta
(see . Fig.6.42).
6.2.1.2 Renal Veins
e right renal vein courses anterior to the renal artery, and
aer 3–4cm it empties into the vena cava at the level of
the L1 vertebra. e le renal vein runs anterior and somewhat superior to the renal artery to then curve between the
aorta and superior mesenteric artery and posteroinferior
to the head of the pancreas on its way to the inferior vena
cava. e le renal artery receives the ovarian or spermatic
vein, which empty directly into the vena cava on the right
(. Fig.6.1).
Variants include duplication of the renal veins and atypi-
cal terminations, for example, in the common iliac vein.
e portal vein is a thick trunk, normally 6–8 cm long,
and has a transverse, anteroposterior elliptical diameter of
8–12mm, rarely up to 16mm, with wide physiologic variation. It passes through the hepatoduodenal ligament behind
the proper hepatic artery and ascends to the porta hepatis,
taking an oblique lateral course. Intrahepatically, it follows
the branches of the hepatic artery and the bile ducts. e
branching pattern of the portal vein provides the basis for
the anatomic segmentation of the liver. e branches of the
hepatic veins are intersegmental vessels.
e splenic vein passes behind the pancreas from the
hilum of the spleen to the head of the pancreas, where it
joins the superior mesenteric vein to form the portal vein
(
. Fig.6.41). e conuence of the two veins is situated to the
le of and behind the pancreatic head, somewhat lateral and
inferior to the origin of the mesenteric artery. e superior
mesenteric vein courses to the right of the superior mesenteric artery and anterior to the aorta.
Blood is drained from the liver through the segmental
branches into the three major veins, which empty directly
into the inferior vena cava.
6.2.2 Examination Technique
6.2.2.1 Vena Cava
e aorta can serve as a landmark when examining the vena
cava. When assessing the lower extremity vessels for thrombosis or when assessing patients with pulmonary embolism,
the course of the vena cava is followed aer evaluation of
the pelvic and leg veins. Evaluation in the transverse plane
is followed by longitudinal scanning for spectral Doppler
. Fig. 6.41 a Transverse diagram showing the course of the splenic vein from right to left, where it joins the superior mesenteric vein to form
the portal vein, below the head of the pancreas. b Course of the splenic vein (V.L), posterior to the pancreas (P) and anterior to the superior
mesenteric artery (A.M.S), terminating in the portal vein (V.P)
6.2 · Visceral andRetroperitoneal Veins
437
6
Right renal
vein
a
c
Vena cava
Left renal vein
Ovarian vein
Left-sided vena cava
b
. Fig. 6.42 a Cardiac modulation of the vena cava waveform (W-shaped). b Anatomic variant of the vena cava seen in transverse orientation on
the left and longitudinal orientation on the right. The transverse image shows the infrarenal vena cava (V.C) to the left of the aorta (A). The transposed vena cava ascends to the left of the aorta, is joined by the left renal vein (V.R.L., longitudinal image), crosses the aorta, and then continues
on its normal course, i.e., to the right of the aorta (A.R.L, left renal artery). c Diagram illustrating this anatomic variant: the transposed inferior vena
cava ascends to the left of the aorta and, after receiving the left renal vein, crosses the aorta. The further ascent is orthotopic, i.e., to the right of
the aorta
measurement. e conuence of the iliac veins at the level of
the umbilicus can be identied using the aortic bifurcation at
about the same level or slightly above for orientation.
In pelvic vein thrombosis, possible extension of the
thrombus into the vena cava must be identied and the end
of the thrombus evaluated for the presence of surrounding
ow signals. e respiratory variation in vena cava diameter
is determined in transverse or longitudinal images. Diameter
variation is absent in thrombosis.
Compression ultrasound is unreliable in the abdomen
(where compressibility is limited by anatomy), which is why
(color) duplex ultrasound is necessary to exclude thrombosis.
Only in slender patients is it possible to reliably compress the
vena cava. e ow velocity determined from the Doppler
waveform is likewise aected by respiratory phasicity and
increasing cardiac pulsatility toward the heart (. Fig.6.42a).
Below the kidneys, the liver can be used as an acoustic window with the portal vein being located anterior to the vena
cava at the hilum of the liver.
e hepatic veins join the vena cava shortly before it
passes through the diaphragm.
6.2.2.2 Renal Veins
e renal veins are scanned from the ank beginning at
the renal hilum and following their course proximally (see
. Fig. 6.6). While the shorter right vein can be visualized
from this position throughout its course to the inferior
vena cava, the le vein (. Fig.6.43) must be scanned from
a medial approach in transverse orientation to visualize the
segment between the aorta and superior mesenteric artery
and its termination.
e superior mesenteric artery can serve as a landmark
to avoid confusion of the le renal vein with the slightly more
anterocranial splenic vein. e le renal vein runs posterior to
the superior mesenteric artery, that is, between the latter and
the aorta; the splenic vein courses anterior to it and then crosses
over the superior mesenteric artery to enter the portal vein.
When searching for renal vein thrombosis or intravas-
cular tumor extension in the B-mode, the examiner must
look for the absence of respiratory diameter uctuations and
the presence of echogenic intraluminal material dilating the
vein. e absence of ow in the spectral Doppler recording is
diagnostic of thrombosis.
Chapter 6 · Visceral andRetroperitoneal Vessels
438
6
. Fig. 6.43 a The left renal vein (V.R.L) courses from the left renal hilum, between the aorta (A) and superior mesenteric artery (A.M.S), to the
vena cava (V.C). Transverse epigastric image. b With the transducer on the right ank (left image), the right renal vein (V.R.) can easily be evaluated
from the hilum (K) to the vena cava (V.C). With a slightly more medial transducer position (right image), the liver can be used as an acoustic window, and the renal vein can be seen deep to the liver (L) from the renal hilum (K) to the vena cava (V.C), coursing anterior to the renal artery (A.R.)
SMV
SMA
Ao
a
. Fig. 6.44 a In the subcostal oblique image (right upper abdomen), the portal vein formed by the conuence of the superior mesenteric and
splenic veins posterior to the pancreatic head (right image) is seen anterior to the vena cava (V.C) on its course through the hepatoduodenal ligament to the liver hilum (left margin of left image). b Diagram of the course of the superior mesenteric vein (SMV; SMA, superior mesenteric artery;
Ao, aorta). c The transverse upper abdominal image (left) shows the vena cava (V.C) to the left of the aorta (landmark); the portal vein (V.P) courses
inside the hepatoduodenal ligament deep to the liver (L). The longitudinal image (right) shows the superior mesenteric vein (V.M.S.) coursing
anterior to the vena cava (V.C, landmark) and terminating in the portal vein (V.P.) posterior to the pancreatic head
6.2.2.3 Portal Vein andSuperior
Mesenteric Vein
e course of the portal vein from below the pancreatic head
to the liver hilum is most easily accessible from a subcostal
approach in an oblique plane through the right upper abdomen
(. Fig.6.44). If visualization is impaired by overlying bowel
gas, the liver hilum can be identied and the portal vein followed distally from an intercostal position (right ank) using
the liver as an acoustic window. Portal vein thrombosis is suggested by the presence of echogenic material in the lumen and
absent respiratory diameter variation in the B-mode image,
and is subsequently conrmed by (color) duplex imaging.
Suspected portal hypertension is easily demonstrated
sonographically by the identication of portal vein collaterals. e evaluation for collateral circulation comprises the
following steps:
5 Flow in the portal vein: to-and-fro ow, retrograde ow,
or reduced ow velocity (unreliable sign; augmentation
maneuver may be necessary, which will elicit a less
marked increase in ow).
b
5 Flow direction in the splenic vein.
5 Visualization of the falsiform ligament and reopening of
the collapsed umbilical vein with hepatofugal ow (Cruveilhier–Baumgarten syndrome).
5 Dilated le gastric vein (in longitudinal plane, arising
from portal vein at the site of mesenteric vein termination).
5 Varicose dilatation in the gallbladder wall.
5 Identication of dilated gastroepiploic veins postero-
lateral to the le hepatic lobe and of splenorenal and
splenogastric collaterals at the upper and lower poles of
the kidney.
e
superior mesenteric vein courses to the right of the
superior mesenteric artery with a position to the le suggesting malrotation. e criteria for diagnosing thrombosis are the same as in the portal vein. If mesenteric vein
thrombosis
is suspected, the vein should be traced to the
level of the jejunal branches, the ileocolic vein, and right
colic vein. is is most easily accomplished in transverse
c
6.2 · Visceral andRetroperitoneal Veins
439
6
orientation with slight angulation of the transducer in the
color duplex mode.
6.2.3 Clinical Role ofDuplex Ultrasound
6.2.3.1 Renal Veins
Acute renal vein thrombosis may be asymptomatic or present
with pain and hematuria. e presentation depends on the
extent of retroperitoneal collateralization, and based on this
variability, it is assumed that renal vein thrombosis actually
occurs more frequently than it is diagnosed. romboembolic complications are rare. Renal vein thrombosis can occur
in patients with renal diseases such as nephrotic syndrome
and glomerulonephritis, external compression of the renal
vein by tumor or retroperitoneal lymphoma, and systemic
conditions including clotting disorders and intra-abdominal
inammatory conditions such as acute pancreatitis or sepsis.
e severity of renal impairment (from normal to acute renal
failure) varies with the degree of thrombotic obstruction and
the extent of retroperitoneal collateral ow (through capsular and suprarenal veins). is is why a duplex ultrasound
examination of the renal vein is indicated not only in patients
with clinical signs and symptoms but also in patients with a
retroperitoneal tumor, so that prompt anticoagulation treatment can be initiated.
Renal vein evaluation is mandatory before surgery for a
retroperitoneal tumor and especially before nephrectomy for
renal cell carcinoma. e presence of tumor thrombus in the
vein is especially important for the surgical approach in renal
cell carcinoma; it has been shown that 20–40% of patients
with a large renal tumor have tumor thrombus in the renal
vein, among them 5–10% with extension of the thrombus
into the vena cava (Goncharenko etal. 1979; Levine 1990).
6.2.3.2 Portal Venous System
In patients with chronic hepatic dysfunction, the examination focuses on parenchymal damage, ranging all the way
to cirrhosis. It also includes damage of the vascular system,
in particular portal hypertension, which typically develops
secondary to cirrhosis. Portal hypertension can result from
obstruction at dierent levels: sinusoidal obstruction (typical
in cirrhosis); presinusoidal obstruction in schistosomiasis,
Wilson’s disease, and myeloproliferative diseases; prehaptic
thrombosis or occlusion of the portal vein; postsinusoidal
hepatic vein occlusion; compression of the vena cava; and
severe right ventricular insuciency.
In patients with
suspected cirrhosis, evaluation of por-
tal hypertension is important for the interpretation of the
clinical ndings and the patient’s prognosis. Gray-scale
ultrasound criteria are highly specic for liver cirrhosis,
but sensitivity is very poor compared with liver biopsy and
intraoperative ndings. However, if portal hypertension is
present and other underlying causes can be ruled out, then
even with an inconclusive gray-scale examination, cirrhosis
can be assumed. Criteria on gray-scale images include macroscopic and microscopic nodules, primarily identiable
as liver contour irregularities, and an increase in attenuation and echogenicity. Shrinkage of the right hepatic lobe
with enlargement of the caudate lobe (caudate-to-right lobe
ratio>0.65) was found to be 90–100% specic for cirrhosis
but with a poor sensitivity of only 43% (Harbin etal. 1980;
Giorgio et al. 1986). Splenomegaly is common in portal
hypertension but is also not very specic. Duplex imaging
allows adequate evaluation of blood ow in the portal vein
and in the splenic and mesenteric veins in 93–95% of patients
(Patriquin etal. 1987; Yeh etal. 1996). e ultrasound criteria described below do not allow reliable exclusion of portal
hypertension or cirrhosis.
6.2.4 Normal Findings
6.2.4.1 Vena Cava andRenal Veins
e normal vena cava has an average diameter of 1.5–3.0cm
with a maximum blood ow velocity of 40–100cm/s. Intraindividually, the
respiration
diameter varies from 0.5 to 2.5cm with
. is variation is reected in the Doppler waveform. Additional cardiac phasicity due to pressure changes
in the right atrium results in an M-shaped ow prole. e
rst peak reects the tricuspid valve movement during systole, followed by a decrease in ow velocity with increasing
atrial lling and a second ow acceleration upon opening of
the tricuspid valve, which produces the second peak. During
atrial contraction, ow again becomes faster, sometimes with
a short retrograde component.
e normal renal vein diameter is 4–10 mm with a
maximum ow velocity of 20–40cm/s. e renal veins, in
particular the right one, also show respiratory blood ow
uctuation
, which is reected in the Doppler waveform by
an increase in ow velocity during inspiration and a decrease
during expiration. e le renal vein typically exhibits pulsatile variation due to brief compression of the vein during
systole in the narrow passageway between the aorta and
superior mesenteric artery. e le renal vein occasionally takes an atypical retroaortic course, and rarely multiple
branches are present on the le (4% versus approx. 20% on
the right). If the le renal vein is not depicted between the
aorta and superior mesenteric artery, the examiner should
look for it behind the aorta at about the level of the origin of
the le renal artery.
e major branches of the hepatic venous system and the
right renal vein have the same ow character as the vena cava
(cardiac (atrial) pulsatility and respiratory phasicity).
6.2.4.2 Portal Venous System
e normal portal vein is depicted by gray-scale sonography with an anechoic, smoothly delineated lumen below
the liver and shows less marked respiratory caliber variation
than the vena cava (usually 8–13 mm, larger caliber during deep inspiration). e (color) duplex mode depicts ow
toward the liver with respiratory variation. Maximum ow
velocity (V
) is 15–35 cm/s with a mean velocity (V
max
mean
)
of 10–25cm/s (Seitz and Kubale 1988; Moriyasu etal. 1986;
Chapter 6 · Visceral andRetroperitoneal Vessels
440
Gaiani etal. 1989). Postprandially, ow velocity may exceed
35cm/s. Altogether, ow velocities in the portal system are
characterized by wide interindividual variation and also
increase aer a meal as in the mesenteric circulation (two- to
threefold increase in ow volume in the superior mesenteric
artery and vein). In fasting individuals, the normal superior
mesenteric vein diameter is 4–12mm with a maximum ow
velocity of 10–45cm/s, while the normal splenic vein diameter is 5–10mm with a maximum ow velocity of 10–25cm/s.
Rare variants and atypical courses of the individual
vessels are identied and dierentiated from retroperitoneal
lymph nodes in the color duplex mode (. Fig.6.45). Compression of the vena cava is most commonly due to retroperitoneal
lymph nodes or tumors, aortic aneurysm, or retroperitoneal
brosis. Rare venous leiomyomas or leiomyosarcomas may
also arise from the smooth muscle layer of the vena cava.
Since compression ultrasound is of limited use in demonstrating thrombosis of the retroperitoneal and visceral veins,
duplex imaging and above all color-coded duplex imaging
come in handy. However, there also exist B-mode criteria for
6.2.5 Documentation
6
Documentation of ndings in the retroperitoneal veins as in
the portal venous system depends on the clinical question
to be answered. In addition to the B-mode ndings and the
Doppler waveform from the vein of interest, the perivenous
ndings should be documented as well. Specically, vein
compression and the extent of thrombotic changes must be
recorded as well as collateral pathways in case of disturbed
venous drainage, for example, retroperitoneal and splenorenal shunts in renal vein thrombosis and gastric or umbilical
shunts in portal hypertension (liver cirrhosis, Cruveilhier–
Baumgarten syndrome).
thrombosis of the intra-abdominal or retroperitoneal veins.
Thrombus may be visualized directly as a hyperechoic
structure. In addition, thrombosis is suggested if the respiratory caliber variation typical of the larger retroperitoneal veins,
in particular the vena cava, is lost. is nding is unspecic,
and dilatation of the vena cava with reduced or absent caliber
uctuation may also occur in right ventricular failure. rombosis should always be ruled out by color duplex imaging with
a low pulse repetition frequency and high gain or by obtaining
a Doppler waveform. Apart from thrombosis, venous drainage may be obstructed by tumor compression, tumor inltration, or intravascular tumor growth (
. Fig.6.45).
e clinical symptoms of thrombosis depend on its
site, temporal course, and collateralization. ere is a risk of
embolism, especially in pelvic vein and vena cava throm-
6.2.6 Abnormal Ultrasound Findings,
Measurement Parameters, and
Diagnostic Role
bosis
. e latter is typically caused by an ascending thrombus from the pelvic and leg veins, less commonly by local
obstruction (external tumor compression or inltration),
thrombus or tumor extension from the renal veins (renal
6.2.6.1 Vena Cava
e complex embryonic development of the venous system
gives rise to numerous variants and malformations, all of
which are rare. e vena cava can show the whole range of
anomalies from aplasia to duplication (. Fig.6.42).
cell carcinoma), or extension of hepatic vein thrombosis in
Budd-Chiari syndrome.
Acute ascending thrombus is typically hypoechoic and
may be dicult to identify on gray-scale ultrasound in obese
patients. Over time, the thrombus undergoes hyalinization
. Fig. 6.45 a Transverse (left) and longitudinal image (right) of vena cava (V.C) thrombus due to ascending thrombosis from the common iliac
artery (V.I.C). Vena cava thrombus must be dierentiated from caval wall tumors and vena cava compression by outside structures. b Tumor of
the vena cava wall (histologically diagnosed as leiomyoma) posterior to the liver hilum causes circumscribed luminal narrowing with aliasing (see
. Fig. 3.36). Sonomorphologically, a wall tumor cannot be dierentiated from vena cava compression due to posteriorly located retroperitoneal
tumors. Among the external tumors that can compress the vena cava, the relationship to the vena cava dierentiates a retroperitoneal connective
tissue tumor (sarcoma) from lymphoma, which is characterized by its paracaval or para-aortic position lateral or anterior to the vena cava
6.2 · Visceral andRetroperitoneal Veins
441
6
and becomes inhomogeneous. rombus organization with
invasion of cells from the vessel wall and retraction of brin
bers results in increasing echogenicity and poorer delineation from the wall. Very old thrombi may undergo partial
mural calcication.
Because a variety of collateral pathways exist, even
occlusion of the vena cava may occasionally cause only a
few clinical symptoms. Venous return occurs predominantly
through the paravertebral plexus, the ascending lumbar and
azygos venous systems, the supercial veins of the abdominal
wall, and the portal collateral route. Color duplex scanning
enables good evaluation of the collateral pathways in vena
cava or pelvic vein thrombosis, though the ndings have no
clinical relevance in most cases.
Disturbed drainage of the pelvic and leg veins demon-
strated by spectral Doppler (continuous ow without respiratory phasicity) may be due to central vena cava thrombosis
caused by thrombus or tumor extension from the renal veins
or compression of the vena cava by a retroperitoneal tumor
or aortic aneurysm. erefore, the examiner must carefully
look for these possible causes. If the spectral waveform from
the vena cava or pelvic veins shows pulsatile ow, a thorough
search must be undertaken for an AV stula, which may be
caused by trauma, idiopathically, perforating aneurysm, or
iatrogenically aer surgery or puncture.
Tricuspid insuciency or right ventricular failure
aects caval blood ow, causing dilatation and changes in the
Doppler waveform. Regurgitation into the right atrium in
tricuspid insuciency extends into the proximal vena cava,
where it becomes apparent in the waveform by a reux component during systole.
6.2.6.1.1 Membranous Vena Cava Obstruction
Congenital membranous structures can cause narrowing of
the vena cava below the diaphragm (membranous stenosis) or
at the termination of the le common iliac vein (venous spur).
While oen clinically asymptomatic, vena cava narrowing
may give rise to descending thrombosis. In patients with good
insonation conditions, color duplex imaging will demonstrate
a slit-shaped stenosis with circumscribed ow acceleration.
e xed nature of the stenosis can be conrmed by a provocative test (Valsalva’s maneuver with respiratory excursions).
6.2.6.2 Renal Veins
Just as in the inferior vena cava, thrombosis and central
tumor thrombus of the renal veins can be identied sonog-
raphically in patients with adequate insonation conditions.
erefore, preoperative color duplex imaging of the renal
veins is sucient prior to tumor nephrectomy. Venography
has a similar diagnostic yield only if it is performed as venacavography with compression or provocative maneuvers. For
this reason, contrast-enhanced CT is the primary alternative
imaging modality in the routine clinical setting.
e nephrotic syndrome associated with glomerulonephritis is the most common cause of renal vein throm-
bosis
. Other factors promoting renal vein thrombosis
include antithrombin III deciency, sepsis, pregnancy, oral
contraceptives, corticoid therapy, collagen diseases, and
amyloidosis. Secondary renal vein thrombosis can be caused
by obstruction due to retroperitoneal tumors, aortic aneurysm, or caval thrombosis as well as intravenous extension
of renal tumors.
Unspecic features of renal vein thrombosis, detectable
by gray-scale ultrasound, are enlargement of the kidney and
reduced echogenicity of the renal parenchyma. In patients
with an adequate acoustic window, the thrombus will be identied as a hypoechoic and partially inhomogeneous structure
within the lumen of the dilated vein (
sis is conrmed by the absence of ow in color duplex images
or in the Doppler waveform. A partially occlusive thrombus
may be seen as a defect in the color coding with a decrease
or complete loss of cardiac pulsatility and respiratory phasicity of ow in the Doppler waveform. If there is good venous
drainage through capsular veins and the suprarenal vein,
venous ow may be detectable in the renal hilum even if
there is complete occlusion of the renal vein.
An
indirect sign of acute renal vein thrombosis is a
marked reduction or even transient reversal of diastolic ow
in the waveform from the renal artery. is is due to reex
vasoconstriction, and the ow pattern resembles that seen in
rejection of a kidney transplant.
Apart from an increased peripheral resistance reected in
the waveform from the renal artery, acute renal vein thrombosis can also cause kidney enlargement. e magnitude of
these changes depends on the extent of collateral pathways of
the thrombosed renal vein, which may involve splenorenal
shunts or retroperitoneal routes such as venous connections
to the adrenal gland. Recanalization aer acute renal vein
thrombosis is seen on color duplex as meander-like ow in
an otherwise dilated and echogenic lumen.
Markedly slower ow in the renal vein with loss of
cardiac pulsatility and respiratory phasicity is also seen in
obstruction of the proximal inferior vena cava by a tumor or
thrombosis or in right ventricular failure (acute: pulmonary
embolism; chronic: tricuspid insuciency).
Prior to tumor nephrectomy, sonographic evaluation
of the renal veins is necessary to plan the extent of surgery
according to the
5 Stage I is characterized by a button-like protrusion of
tumor from the renal vein into the vena cava (see
. Fig.6.107).
5 In stage II the tumor extends farther into the vena
cava but the upper margin is still below the level of the
hepatic vein termination.
5 In stage III the tumor extends to the level of the hepatic
veins.
5 In stage IV there is tumor extension into the atrium.
Adequate sonographic evaluation of venous thrombus or
tumor thrombus is impaired by superimposed bowel gas
and by ow phenomena, especially when examining obese
patients, resulting in adequate duplex evaluation of the renal
veins in only 50–80% cases (Schwerk etal. 1994; Didier etal.
1987; Dubbins 1986; London et al. 1989). When there is a
stage of venous tumor extension:
. Fig.6.106). rombo-
442
Chapter 6 · Visceral andRetroperitoneal Vessels
6
. Fig. 6.46 a Occlusive thrombosis of the superior mesenteric vein (V.M.S): the lumen is dilated, slightly echogenic, and homogeneous. The
vein can be identied adjacent to the superior mesenteric artery (A.M.S), which serves as a landmark. b Thrombosis of the portal vein (PV) with
ow signals along the thrombus but no respiratory modulation (ow obstruction) and reduced ow velocity. There is ow displayed in red in the
hepatic artery (A.H) and in venous collaterals in the liver hilum, particularly around the gallbladder
good acoustic window, ultrasound has 95–100% accuracy in
detecting tumor thrombus. Because detailed evaluation of
the renal veins by ultrasound is not always possible, contrast-
enhanced computed tomography and magnetic resonance
imaging
are more accurate in preoperatively dening the
extent of tumor thrombus in the renal vein and beyond and
in planning the surgical resection. Given the importance of
this information, these two imaging modalities should be used
liberally as supplements to duplex ultrasound before surgery.
6.2.6.3 Superior Mesenteric Vein
andSplenic Vein
Mesenteric vein thrombosis is a rare cause of intestinal
necrosis. erefore, duplex imaging performed to rule out
mesenteric artery occlusion in patients presenting with the
respective clinical symptoms should also include the mesenteric vein to exclude thrombosis there as well (. Fig.6.46).
Edematous thickening of the intestinal walls is a conspicuous
nding and will already be seen in the gray-scale image.
Causes of mesenteric vein thrombosis include hematologic diseases, clotting disorders, abscess or sepsis, and
tumor occlusion. Apart from acute thrombosis presenting
with acute symptoms of intestinal necrosis, there may be
chronic thrombosis with unspecic ndings such as fever,
leukocytosis, or thrombocytosis.
An abnormal course of the superior mesenteric vein suggests
malrotation, which is conrmed if the superior mes-
enteric vein lies to the le of the superior mesenteric artery.
If the vein is anterior to the artery, malrotation is present in
one third of the cases. ese indirect signs of malrotation are
easily detected by duplex ultrasound.
e clinical severity of mesenteric vein thrombo-
sis
depends on the extent and site of the thrombus (see
. Figs. 6.99 and 6.100 (both Atlas)) and collateralization.
Partial thrombosis of the superior mesenteric vein, for
instance, may be fairly asymptomatic and present with clinical signs of enteritis only. Conversely, patients with extensive central mesenteric vein thrombosis may present with
. Table 6.9 Mesenteric vein thrombosis
Criterion Parameter
Risk factors Portal hypertension
Sepsis
Diverticulitis
Paraneoplastic syndrome
Autoimmune disease
Clotting disorder
Clinical
presentation
Duplex
ultrasound
ndings
From unspecic symptoms to acute abdomen
(depending on the extent of collateralization)
Hyperechoic thrombus
Dilated vein
No intraluminal ow signals
Diastolic ow in the superior mesenteric artery
may be reduced
Thickening of bowel loops in gray-scale image
an acute abdomen due to intestinal necrosis. Early diagnosis with initiation of anticoagulation therapy is essential
for preventing progression. erefore, the mesenteric vein
should be included in the diagnostic workup of all patients
with unspecic symptoms and intestinal wall thickening on
B-mode images. e criteria for thrombosis of the superior
mesenteric vein are the same as in other vascular territories: dilatation of the vein, absence of respiratory diameter
variation, possibly depiction of the thrombus as an echogenic
intraluminal structure on the B-mode image, and absence of
ow signals or only residual ow signals near the wall surrounding a central thrombus on (color) duplex imaging
. Fig.6.99 (Atlas)). Apart from intestinal wall thicken-
(see
ing, another indirect sonographic sign, which can be seen
in extensive mesenteric vein thrombosis, is an increase in
pulsatility in the arterial waveform (see . Fig.6.100 (Atlas))
(. Table6.9).
e left gastric vein (coronary vein) and the inferior
mesenteric vein
play no role in routine clinical examinations
of the abdomen; however, they can be recruited as collaterals
6.2 · Visceral andRetroperitoneal Veins
443
6
in portal hypertension. If this is the case, the veins become
enlarged, and sonographic demonstration of ow reversal is
indicative of portal hypertension.
6.2.6.3.1 Splenic Vein Thrombosis
e splenic vein is part of the collateral pathway in portal
hypertension and thus rarely thrombosed in these patients.
More common causes of splenic vein thrombosis, besides
systemic factors, include pancreatitis and pancreatic tumors.
Clinical symptoms tend to be mild and the sonographic
ndings are the same as in other thrombosed veins. e
thrombosed splenic vein is seen as a wormlike structure of
low echogenicity posterior to the pancreas. Other ndings
include splenomegaly and absent or reduced ow (in partial
thrombosis) on color duplex imaging.
Abnormalities of the splenic vein (such as thrombosis)
are negligible, both clinically and in terms of their therapeutic consequences, because extensive collateral routes exist.
However, the splenic vein should be included in the examination of patients with cirrhosis and portal hypertension,
where it plays a role as a collateral.
6.2.6.4 Portal andHepatic Veins
Atresia and hypoplasia of the portal vein are rare, as are
anatomic variants and malformations. In individuals with
a congenital extrahepatic portocaval shunt, portal venous
blood from the mesentery and spleen drains directly into
the inferior vena cava. As a result of this direct communication of the splenic and superior mesenteric veins with the
vena cava (gray-scale scan), the cardiac pulsatility of venous
return in the vena cava is transmitted to the mesenteric vein
and reected in the Doppler waveform from the latter.
Aneurysm of the portal vein is also rare and must be differentiated from pseudocysts of the pancreas, choledochal
cysts, and liver cysts by the demonstration of ow in the
color duplex mode.
6.2.6.4.1 Portal Vein Thrombosis
Portal vein thrombosis is diagnosed using the same sonomorphologic criteria as for other sites: dilatation of the lumen,
absent respiratory diameter variation, and no ow signals or
only residual ow signals around the thrombus on (color)
duplex images.
Acute portal vein thrombus tends to be hypoechoic and
is clearly delineated from perivascular structures, whereas
older thrombi contain more inhomogeneous and hyperechoic portions and their contours become blurred, resulting in poorer sonographic discrimination of the thrombotic
vein. e Doppler waveform sampled with an adequate angle
will show absence of ow or owing blood characterized by
higher-frequency signals and loss of respiratory phasicity
around a central thrombus.
Acute portal vein thrombosis (. Fig.6.103 (Atlas)), like
acute proximal mesenteric vein thrombosis, presents with
acute symptoms. However, collateralization in portal vein
thrombosis is more extensive if the superior mesenteric vein
is not involved; the collateral vessels in this case include
the splenic vein and gastric veins. e veins recruited as
collaterals are expanded and can be detected by duplex
ultrasound.
e causes of portal vein thrombosis include liver cirrhosis, paraneoplasia, clotting disorders, and sepsis. Other
causes of thrombotic changes in the portal venous system
are:
5 Acute pancreatitis
5 Chronic pancreatitis (may be associated with pseudocyst)
5 Cancer (hepatocellular carcinoma, metastasis, pancreatic
carcinoma)
5 Idiopathic
5 Abdominal infections
5 Collagen diseases
5 Myeloproliferative syndrome
5 Trauma
5 Status post splenectomy
5 Pregnancy
5 Medications
5 Liver disease, cirrhosis, thrombocytosis
5 Antiphospholipid antibody syndrome
5 Deciency of AT3, protein C, protein S.
Similar to portal hypertension in liver cirrhosis, acute
portal vein thrombosis is associated with widening of the
veins recruited as collaterals (splenic vein, esophagogastric
vessels) and ascites. ese features are detectable sonographically as secondary signs of portal vein thrombosis.
Ultrasound detects portal vein thrombosis with 89–100%
sensitivity and 95–100% specicity, which is comparable to
its accuracy in the detection of deep leg vein thrombosis
(Zwiebel 2000). Very slow ow in severe portal hypertension
with to-and-fro ow is dicult to detect sonographically and
may pose a diagnostic problem.
As with older thrombosis in other territories,
portal vein thrombosis
distended vessel, seen as an inhomogeneous, more hyperechoic thrombus within the lumen. In contradistinction to
acute portal thrombosis, clinical signs and symptoms are
relatively unspecic and mild, in particular when chronic
portal thrombosis occurs secondary to liver cirrhosis.
e formation of collateral pathways in the liver hilum
and partial recanalization of the thrombotic portal vein, so-
cavernous transformation, results in a worm-like
called
meshwork of tortuous tubular structures, among which the
former portal vein (with connective tissue structures) is at
times dicult to identify by color duplex imaging. e sonographic appearance with meandering venous channels and a
mosaic of colors, reecting changing ow directions relative
to the transducer, in and around the portal vein bed is pathognomonic (. Fig.6.104 (Atlas)). However, despite recanalization in the form of cavernous transformation, many patients
will have some kind of residual portal hypertension.
6.2.6.4.2 Portal Hypertension
Portal hypertension can be caused by obstruction of the
portal venous system at dierent levels (. Fig.6.47a) and is
associated with complex circulatory changes. e pressure
in the portal vein is typically 2–4mmHg above that in the
leads to shrinkage of the initially
chronic
Superior vena cava Azygos vein
Chapter 6 · Visceral andRetroperitoneal Vessels
444
Central
vein
Drainage to
inferior vena
cava
Sinus
C
B
2
B
1
6
Artery
Portal branch
A
Paraumbilical
vein (Medusa’s
head)
Rectal
a
plexus
Portal
vein
Esohageal varices
Splenogastrorenal
anastomoses
Stomach (cut)
Inferior mesenteric vein
Superior mesenteric vein
Spleen
Kidney
b
c
d
. Fig. 6.47 a Portal venous system: Causes of portal hypertension and collateral circulation (From Droste 1989). Portal hypertension (>15cm H2O
in portal venous system) can be caused by: A Prehepatic obstruction: thrombosis of portal or splenic vein, tumor of adjacent organ (e.g., pancreas,
stomach, duodenum, gallbladder). B Intrahepatic obstruction: B1 Presinusoidal: schistosomiasis, Wilson’s disease, myeloproliferative diseases (intrasinusoidal: chronic hepatitis, fatty liver); B2 Postsinusoidal obstruction: liver cirrhosis (cause of portal hypertension in 90% of cases), cytostatics and other
medications. C Posthepatic obstruction: hepatic vein occlusion (Budd-Chiari syndrome), compression of inferior vena cava, constrictive pericarditis.
b–d Cruveilhier-Baumgarten syndrome (due to portal hypertension). b Portal hypertension in Child C cirrhosis with the portal vein dilated to 15mm.
There is continuous blood ow in the portal vein (loss of respiratory phasicity) with a maximum ow velocity of 29cm/s (which is relatively high for
portal hypertension; see collateral pathways in a). c The high ow velocity in the portal vein is due to supply from the widely patent umbilical vein (V) in
Cruveilhier-Baumgarten syndrome. d The vein connecting the portal vein (PV) and patent umbilical vein (V) runs in the ligament. It is dilated and ow
velocity is high (26cm/s)