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EDUCATION EXHIBIT
67
Where There Is Blood,
There Is a Way: Unusual
Collateral Vessels in Superior and Inferior Vena
Cava Obstruction1
Online-Only
CME
See www.rsna
.org/education
/rg_cme.html
LEARNING
OBJECTIVES
After reading this
article and taking
the test, the reader
will be able to:
■■List
the common
collateral pathways
in patients with
SVC or IVC obstruction.
■■Discuss
the uncommon collateral
pathways in patients
with SVC or IVC
obstruction.
■■Describe
the imaging features of the
uncommon collateral pathways in SVC
or IVC obstruction.
Sangita Kapur, MD • Eugene Paik, MD • Ario Rezaei, MD
Doan N.Vu, MD
Obstruction of the superior vena cava (SVC) or inferior vena cava (IVC)
is most commonly an acquired condition, typically caused by malignancy, benign conditions such as mediastinal fibrosis, and iatrogenic
causes such as venous catheterization. In the event of chronic occlusion, collateral pathways must develop to maintain venous drainage.
The major collateral pathways seen with SVC or IVC obstruction are
well described and include the azygos-hemiazygos, internal and external
mammary, lateral thoracic, and vertebral pathways. In addition, several
unusual collateral pathways may be seen with SVC or IVC obstruction;
these include systemic-to-pulmonary venous, cavoportal, and intrahepatic collateral pathways. In patients with systemic-to-pulmonary venous
collateral vessels, the systemic veins drain directly into the left side of
the heart, resulting in a right-to-left shunt. The collateral veins consist of
mediastinal connections between the innominate veins and the superior
pulmonary veins through bronchial venous plexuses around the airways,
hilar vessels, and pleura. The cavoportal collateral pathways consist of
collateral formation between the SVC or IVC and a tributary to the portal system. They include the caval-superficial-umbilical-portal pathway,
caval-mammary-phrenic–hepatic capsule–portal pathway, caval-mesenteric-portal pathway, caval-renal-portal pathway, caval-retroperitonealportal pathway, and intrahepatic cavoportal pathway. These types of
collateral pathways may result in unusual enhancement patterns in the
liver. An understanding of these unusual collateral pathways is essential
in a patient with caval occlusion who presents with signs and symptoms
of a right-to-left shunt or has unusual enhancing lesions in the liver.
©
RSNA, 2010 • radiographics.rsna.org
Abbreviations: IVC = inferior vena cava, SVC = superior vena cava
RadioGraphics 2010; 30:67–78 • Published online 10.1148/rg.301095724 • Content Code:
From the Department of Radiology, University of Cincinnati Medical Center, 234 Goodman Street, Cincinnati, OH 45267-0761 (S.K., A.R., D.N.V.);
and the Department of Radiology, Christ Hospital, Cincinnati, Ohio (E.P.). Received April 3, 2009; revision requested May 29 and received July 31; accepted September 15. All authors have no financial relationships to disclose. Address correspondence to S.K. (e-mail: [email protected]).
1
The Editor has no relevant financial relationships to disclose.
©
RSNA, 2010
68 January-February 2010
Introduction
Obstruction of the superior vena cava (SVC) or
inferior vena cava (IVC) is typically an acquired
condition. SVC syndrome is most commonly
associated with metastatic pulmonary or mediastinal malignancy (1). Benign causes include
infection, idiopathic mediastinal fibrosis, retrosternal thyroid, aortic aneurysm, benign tumors,
mediastinal hematoma, sarcoidosis, radiation
fibrosis, and iatrogenic causes (2–5). Thrombosis
of the SVC is a well-known complication of central venous catheter placement (2,3).
Thrombosis is a major cause of IVC obstruction and often results from superior extension of
lower extremity or pelvic deep venous thrombosis
(6). Causes such as dehydration, sepsis, pelvic
inflammatory disease, coagulopathy, congestive
heart failure, trauma, immobility, severe exertion,
or iatrogenic causes (eg, placement of an IVC
filter) may also result in IVC thrombosis. Other
less common causes of IVC obstruction include
tumor invasion, extrinsic compression, and intrinsic caval disease, (eg, congenital membranes
or primary caval tumors) (6).
In the event of chronic occlusion, collateral
pathways must develop to maintain venous drainage (1,2,5,6) The pattern of collateral pathways
can be predicted on the basis of the level of
obstruction. The following four major collateral
pathways are commonly reported in SVC or IVC
obstruction (1,2,5,6).
1. The azygos-hemiazygos pathway includes the
azygos, hemiazygos, intercostal, and lumbar veins.
2. The internal and external mammary pathway includes the internal mammary, superior
epigastric, and inferior epigastric veins and superficial veins of the thorax.
radiographics.rsna.org
3. The lateral thoracic pathway uses the lateral
thoracic, thoracoepigastric, superficial circumflex,
long saphenous, and femoral veins to collateralize
to the IVC.
4. The vertebral pathway uses the innominate,
vertebral, intercostal, lumbar, and sacral veins to
collateralize to the azygos and internal mammary
pathways.
The azygos-hemiazygos pathway predominates unless it is poorly developed or obstruction
blocks the azygos vein confluence with the SVC
(2,6,7). In addition, gonadal and periureteric
veins can also function as collateral vessels in
infrarenal IVC obstruction (Fig 1) (6).
Certain unusual collateral circulations may
also develop with SVC or IVC obstruction. In
this article, the systemic-to-pulmonary venous
collateral pathway, cavoportal collateral pathway,
and intrahepatic collateral pathway are discussed.
Unusual Collateral Pathways
Systemic-to-Pulmonary
Venous Collateral Pathway
The systemic-to-pulmonary venous collateral
pathway is an uncommon result of SVC obstruction (1,2,5,8–11). The presence of such collateral
vessels results in a right-to-left shunt, subsequently leaving the patient susceptible to stroke,
brain abscess, and a high cardiac output state (4).
This pathway is usually the result of SVC obstruction from malignant causes, but it may rarely
be caused by benign conditions (8). The pathway
consists of mediastinal connections between the
innominate veins and the superior pulmonary
veins via the bronchial venous plexuses around
the airways, hilar vessels, and pleura (8) (Fig 2).
These shunts may be further categorized as anatomic, congenital, or acquired (8).
Teaching
Point
Teaching
Point
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Kapur et al 69
Figure 1. Cavocaval collateral vessels in a 61-year-old woman with a primary leiomyosarcoma of the IVC. The
leiomyosarcoma produced obstruction below the level of the renal veins and resulted in cavocaval collateralization
through the left gonadal vein. (a–c) Axial (a, b) and coronal (c) contrast material–enhanced computed tomographic
(CT) images (a obtained at a higher level than b) show a large IVC mass (arrowheads) that causes IVC obstruction.
A large left gonadal vein (arrows) acts as a collateral vessel between the IVC below the mass and the IVC above the
mass. (d, e) Images from venography performed with a right common femoral approach show the IVC obstruction
(arrowheads in d) and unnamed small collateral vessels (arrowheads in e) between the right common iliac vein and
the left gonadal vein (arrows). LIV in e = left common iliac vein.
70 January-February 2010
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Figure 2. Systemic-to-pulmonary collateral vessels in a 37-year-old woman with a history of end-stage renal
disease and multiple placements of dialysis catheters. She underwent CT pulmonary angiography because of shortness of breath. There was poor opacification of the pulmonary vasculature. (a, b) CT images show collateral
vessels around the left pulmonary artery (arrow in a) and the left main-stem bronchus (arrow in b). (c) Coronal
multiplanar reformation image shows systemic-to-pulmonary collateral vessels (arrows) surrounding the left pulmonary artery and left main-stem bronchus with opacification of the left superior pulmonary vein (arrowhead).
(d) Coronal maximum intensity projection image shows stenosis of the left brachiocephalic vein (arrow) and collateral vessels at the left pulmonary hilum (arrowhead). (e) Volume-rendered image shows collateral vessels at the
left pulmonary hilum (arrow) and a pericardiophrenic collateral vessel (arrowhead).
1. In an anatomic shunt, the bronchial and
pulmonary veins are connected through preexisting bronchial venous plexuses. These plexuses
drain predominantly into the right atrium, with
approximately one-third of their flow directed
into the left atrium through pulmonary veins.
Normally, pleurohilar bronchial veins are also
connected to the azygos-hemiazygos system with
intervening valves. If systemic venous pressure
rises, as in caval obstruction, the valves can become incompetent with resultant reversal of flow
and a right-to-left shunt.
2. There are three types of congenital systemic-to-pulmonary venous collateral pathways.
These consist of (a) anomalous pulmonary venous return, with reversed flow; (b) an embryologic remnant connecting the posterior cardinal
venous system with the pulmonary veins; and
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Kapur et al 71
Figure 3. Spontaneous cavoportal collateral vessel in a 45-year-old man. Axial (a) and coronal (b,
c) contrast-enhanced CT images show a spontaneous collateral vessel (white arrow in c), which connects the IVC circulation (arrowheads in c) with
the inferior mesenteric vein (ie, portal) circulation
(black arrows).
(c) a persistent left SVC, which may occasionally be a thin channel that drains into the left
superior pulmonary vein or left atrium.
3. The acquired type of systemic-to-pulmonary
venous collateral system is inflammatory in origin
and results in newly formed vessels bridging
subpleural pulmonary veins and intercostal veins
through pleural adhesions. The formation of this
systemic-to-pulmonary shunt is theorized to arise
from adhesions between the chest wall and lung,
allowing bridging veins to develop across the pleural space (8,9). Fibrosing mediastinitis, adhesions,
radiation fibrosis, and chronic inflammation have
been postulated as contributing factors (9–12).
Methods for depicting right-to-left shunts
include scintigraphy (eg, technetium 99m [99mTc]
macroaggregated albumin scanning), venography,
and helical CT. CT venography has recently been
explored for depiction of such shunts (9), as multidetector CT and three-dimensional reformation
can aid in delineation and diagnosis of this complex anatomy (Fig 2). CT can also help identify
the underlying cause of obstruction, its exact level,
and other potential collateral pathways. Keys to
visualization of these vessels at cross-sectional
imaging include presence of extensive obstruction,
use of dynamic high-contrast spiral CT technique,
and abundant collateral vessels (11).
Cavoportal Collateral Pathway
Another unusual but important collateral pathway is the cavoportal collateral pathway, whereby
flow is directed from the vena cava to the portal
vein (13). In contradistinction, portocaval collateral vessels are frequently visualized with portal
hypertension, where blood flow is hepatofugal
(13). On occasion, cavoportal collateral vessels
may form spontaneously (Fig 3).
72 January-February 2010
Teaching
Point
A brief review of the developmental embryology will facilitate a better understanding of these
collateral pathways. The developing visceral veins
consist of the right and left vitelline veins from
the yolk sac and the right and left umbilical veins
from the placenta. These veins open into corresponding horns of the sinus venosus.
The vitelline veins anastomose with each
other around the developing duodenum and pass
through the septum transversum (the primitive
liver) to the sinus venosus. In the primitive liver,
these veins are broken up into sinusoids. The left
vitelline vein disappears, and blood is redistributed to a now enlarged right vitelline vein. The vitelline system gives rise to the suprahepatic IVC,
the hepatic veins, and the portal vein (14,15).
The umbilical veins carry oxygenated blood
to the embryo. The right umbilical vein and the
portion of the left umbilical vein between the
liver and the sinus venosus degenerate. The remainder of the left umbilical vein then carries all
the blood from the placenta to the fetus. A large
channel known as the ductus venosus develops
in the liver and connects the umbilical vein with
the IVC, bypassing the sinusoidal circulation of
the liver (14,15).
The complicated development of the cardinal
system and the close relationship of its development with that of the vitelline and umbilical veins
may explain the occurrence of congenital portosystemic anastomoses (14).
The normal existence of portosystemic connections was observed by Ruysch in 1738 (16).
Madden identified preexisting portosystemic connections in 50% of normal individuals after death
(17). Two embryologic hepatofugal collateral
channels were observed by McIndoe (17).
1. One is at the site of the obliterated fetal
circulation in the falciform ligament comprising
the umbilical and paraumbilical veins.
2. Another is at areas where the gastrointestinal
tract becomes retroperitoneal developmentally (ie,
where the bare areas come in contact with somatic
tissues): the duodenum, pancreas, spleen, colon,
and liver. The presumed basis for intrahepatic portosystemic shunts is a persistent communication
between the vitelline veins of the omphalomesenteric system and the sinus venosus owing to a focal
absence of sinusoid formation (14).
radiographics.rsna.org
Figure 4. Caval-superficial-umbilical-portalpathway. Diagram shows SVC or IVC obstruction and cavoportal collateral pathways. The
epigastric venous tributaries of the caval circulation anastomose with a recanalized paraumbilical vein, which in turn drains into the left portal
vein. EMV = external mammary vein, EV =
epigastric vein, IEV = inferior epigastric vein,
IMV = internal mammary vein, SEV = superior
epigastric vein.
The term downhill varices was used by Felson
and Lessure (18) to describe a type of cavoportal
collateral pathway in the case of SVC obstruction. The lower part of the esophageal venous
plexus communicates with the coronary vein of
the portal system inferiorly, while superiorly it
communicates with the azygos system. Thus, the
lower esophageal veins join the azygos system
with the portal system. In patients with SVC obstruction below the azygos vein entry, this communication can divert blood to the portal system,
with the flow directed toward the portal system
or “downhill” (18).
Four cavoportal collateral pathways have been
identified.
1. Caval-superficial-umbilical-portal pathways
may be seen with either SVC or IVC obstruction
(Fig 4). The superficial, superior, and inferior epigastric veins anastomose with external or internal
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Kapur et al 73
Figure 5. Cavoportal collateral vessels in a 21-yearold woman with end-stage renal disease and a history
of multiple placements of dialysis catheters. (a) Contrast-enhanced CT image shows wedge-shaped hyperenhancement of segment IV of the liver, prominent
collateral vessels in the anterior abdominal wall (arrowheads), and a recanalized paraumbilical vein (arrow).
(b) Contrast-enhanced CT image shows the recanalized paraumbilical vein communicating with a portal
vein branch (arrowhead). (c) Contrast-enhanced CT
image shows reflux of contrast material into hepatic
veins (arrow). (d) Multiple images from the perfusion
portion of a 99mTc macroaggregated albumin ventilation-perfusion study show increased uptake in segment
IV of the liver (arrow). LAO = left anterior oblique, L
lat = left lateral, LPO = left posterior oblique, RAO =
right anterior oblique, RPO = right posterior oblique,
Rt lat = right lateral.
fashion into the left portal vein (13). The presence of such a pathway may result in a hot spot
at hepatic segment IV during nuclear medicine
studies, such as 99mTc sulfur colloid scanning or
99m
Tc lung scintigraphy, or in hyperenhancement
at venography or CT (Fig 5) (4,5,7,12,19–22).
mammary veins. These superficial collateral veins
then communicate with a recanalized paraumbilical vein, which in turn drains in a hepatopetal
74 January-February 2010
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Figure 6. Caval-mammary-phrenic–hepatic
capsule–portal pathway. Diagram shows
SVC obstruction. There is collateral formation between the internal mammary vein
(IMV) and hepatic capsular veins, which ultimately drain into the portal venous system.
2. Caval-mammary-phrenic–hepatic capsule–
portal pathways are seen with SVC obstruction.
In this pathway, blood flows from the internal
mammary vein to the inferior phrenic vein.
The inferior phrenic vein then communicates
with hepatic capsular veins, which in turn drain
into the intrahepatic portal tributaries (Fig 6).
A focal hot spot may be visualized on nuclear
medicine scans along the anterior and superior
aspect of the liver, near the bare area. Focal contrast enhancement along the superior aspect of
the liver and enlarged inferior phrenic veins and
hepatic capsular collateral vessels can be seen at
CT (13).
3. Caval-mesenteric-portal pathway: In IVC
obstruction, venous blood may drain from the
internal iliac veins to the hemorrhoidal plexus.
From there, blood flow can ascend through the
inferior mesenteric vein to the portal vein (Fig 7).
Thus, the pathway is located between the superior rectal branches of the inferior mesenteric
vein and the middle and inferior rectal branches
of the internal iliac veins (13). This pathway may
be visualized with CT (Fig 8), magnetic resonance imaging, or angiography (Fig 9).
Figure 7. Caval–inferior mesenteric–portal
pathway. Diagram shows IVC obstruction and
collateral vessels from the caval system (internal
iliac vein [IIV]) and the hemorrhoidal venous
plexus, which drain into the portal venous system. IMV = inferior mesenteric vein, SMV =
superior mesenteric vein.
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Kapur et al 75
Figure 8. Caval–inferior mesenteric–portal pathway in a 35-year-old man with testicular cancer, retroperitoneal
adenopathy, IVC thrombosis, and formation of cavoportal collateral vessels. (a) Longitudinal ultrasonographic
image of the right testicle shows a mass (arrow) and a dystrophic calcification (arrowhead). (b) Contrast-enhanced CT image shows retroperitoneal adenopathy (arrow). (c) Contrast-enhanced CT image shows unopacified blood from the inferior mesenteric vein (arrowhead) draining into the splenic vein (arrow). (d) Contrastenhanced CT image shows unopacified blood in the inferior mesenteric vein (arrow). (e) Contrast-enhanced
CT image shows the hemorrhoidal vein and collateral vessels (arrow). (f) Contrast-enhanced CT image shows
hemorrhoidal collateral vessels (arrow).
76 January-February 2010
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Figure 9. Caval–inferior mesenteric–portal pathway in a 45-year-old woman with occlusion of the
proximal IVC and cavoportal collateral vessels.
Venography was performed with a left common
iliac approach. (a, b) Venograms show superior
hemorrhoidal collateral vessels (arrow in a), which
drain into the inferior mesenteric vein (arrow in b).
(c) Venogram shows the inferior mesenteric vein
draining into the splenic vein (portal system) (arrow). Arrowhead = occlusion of the proximal IVC.
(d) Delayed venogram shows hepatic enhancement (arrow), which was due to the cavoportal
collateralization.
Figure 10. Caval-retroperitoneal-portal pathway. Diagram shows IVC obstruction
and formation of retroperitoneal collateral vessels between
the IVC and the superior
mesenteric vein (SMV). RV =
renal vein.
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Kapur et al 77
Figure 11. Intrahepatic collateral vessels in a 60-year-old man who underwent venography for evaluation for filter placement. (a) Venogram shows IVC occlusion by a web (white arrow) and an inferior
hepatic vein (black arrow). (b) Venogram shows opacification of the IVC superior to the obstruction
(white arrow). The opacification is due to intrahepatic collateralization between the inferior hepatic vein
(arrowheads) below the level of the obstruction and the right and middle hepatic veins (black arrow).
The flow in the inferior hepatic vein is retrograde, as evidenced by the higher opacity of the contrast
material within it. The opacity of the contrast material in the right and middle hepatic veins is lower because they fill by means of collateral flow.
Teaching
Point
4. Caval-renal-portal and caval-retroperitonealportal pathways have mainly been reported with
mid-IVC occlusion (13). In IVC obstruction, as in
portal hypertension, the left renal vein can develop
connections to the splenic vein via an inferior
phrenic vein and the epiploic veins of the stomach. Other tributaries of the portal system such
as duodenal, jejunal, and pancreatic veins may
communicate with retroperitoneal branches of the
renal or lumbar veins. These in turn are tributaries of the IVC and azygos system (Fig 10). The
establishment of this collateral pathway may result
in duodenal varices (13).
As mentioned earlier, the cavoportal collateral pathway may result in enhancement abnormalities in the liver and hot spots during nuclear
medicine studies (13). Two methods may be used
to differentiate the commonly seen portocaval
collateral vessels from the uncommon cavoportal collateral vessels: (a) Knowledge of the site
of venous obstruction, whether caval or portal,
can help determine the direction of flow within
the collateral vessel. (b) The opacity or attenuation of contrast material in the collateral vessels
is an important determinant, as the opacity or
attenuation of contrast material in the collateral
vessel matches the venous system from where the
blood flows. Therefore, the opacity or attenuation
of contrast material in the collateral vessel will
match the cava in the case of cavoportal collateral
vessels and will match the portal circulation in
the case of portocaval collateral vessels (Figs 1,
8). It is also important to note the site of contrast
material injection, whether the upper or lower
extremity, as this will also determine whether
the collateral vessel will enhance. Therefore, the
degree of enhancement of the collateral veins, in
conjunction with knowledge of the site of injection, can provide important information about
flow direction in the collateral circulation (4).
Intrahepatic Collateral Pathway
Intrahepatic communications between the
hepatic veins can be demonstrated at hepatic
venography or in anatomic or autopsy studies.
This pathway is unique in that it is seen only
with obstruction of the intrahepatic cava or occlusion of the right or left hepatic venous orifice.
Over time, patients with intrahepatic IVC obstruction will develop collateralization between
the hepatic vein branch that drains into the IVC
proximal to the obstruction and the hepatic vein
branch distal to the obstruction (23,24). The
blood from the IVC below the obstruction can
then drain into the right atrium (Fig 11). The
blood flow in the hepatic venous branch proximal to the obstruction is retrograde (23,24).
These collateral vessels are usually insufficient
to prevent Budd-Chiari syndrome (23).
78 January-February 2010
Conclusions
Teaching
Point
The presence of systemic-to-pulmonary or
cavoportal collateral vessels suggests SVC or IVC
obstruction. Evidence of a right-to-left shunt and
focal characteristic enhancement in the liver
(pseudolesion) may be detected at contrastenhanced CT. Because the preferential collateral
pathway is the azygos-hemiazygos pathway, that
focal liver enhancement pattern is not commonly
seen. If such focal liver enhancement is visualized at CT or a focal hot spot is seen on a nuclear
medicine scan, a search for possible obstruction
of the SVC or IVC should be made (7). The
existence of collateral vessels and caval obstruction allows differentiation of these enhancement
abnormalities from enhancement due to liver
masses (13,17). If the shunting is considerable,
the hepatic perfusion abnormality may also be
demonstrated at angiography (12). From a practical point of view, care should be taken when
interpreting a defect in segment IV of the liver at
CT, especially in the presence of known or potential SVC or IVC obstruction.
References
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3.Madan AK, Allmon JC, Harding M, Cheng SS,
Slakey DP. Dialysis access-induced superior vena
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CT findings when the superior vena cava, brachiocephalic vein, or subclavian vein is obstructed. AJR
Am J Roentgenol 1996;167(6):1457–1463.
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13.Dahan H, Arrive L, Monnier-Cholley L, Le Hir P,
Zins M, Tubiana JM. Cavoportal collateral pathways
in vena cava obstruction: imaging features. AJR Am
J Roentgenol 1998;171(5):1405–1411.
14.Gallego C, Miralles M, Marín C, Muyor P, González
G, García-Hidalgo E. Congenital hepatic shunts. RadioGraphics 2004;24(3):755–772.
15.Singh IB, Pal GP. Cardiovascular system. In: Human embryology. 7th ed. Chennai, India: Macmillan
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17.Fleming RJ, Seaman WB. Roentgenographic demonstration of unusual extra-esophageal varices. Am
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This article meets the criteria for 1.0 AMA PRA Category 1 Credit TM. To obtain credit, see www.rsna.org/education
/rg_cme.html.
RG
Volume 30
Number 1
January-February 2010
Kapur et al
Where There Is Blood, There Is a Way: Unusual Collateral
Vessels in Superior and Inferior Vena Cava Obstruction
Sangita Kapur, MD, et al
RadioGraphics 2010; 30:67–78 • Published online 10.1148/rg.301095724 • Content Code:
Page 68
The presence of such collateral vessels results in a right-to-left shunt, subsequently leaving the patient
susceptible to stroke, brain abscess, and a high cardiac output state (4).
Page 68
The pathway consists of mediastinal connections between the innominate veins and the superior
pulmonary veins via the bronchial venous plexuses around the airways, hilar vessels, and pleura (8)
(Fig 2).
Page 72
The complicated development of the cardinal system and the close relationship of its development
with that of the vitelline and umbilical veins may explain the occurrence of congenital portosystemic
anastomoses (14).
Page 77
The opacity or attenuation of contrast material in the collateral vessels is an important determinant,
as the opacity or attenuation of contrast material in the collateral vessel matches the venous system
from where the blood flows.
Page 78
Because the preferential collateral pathway is the azygos-hemiazygos pathway, that focal liver
enhancement pattern is not commonly seen. If such focal liver enhancement is visualized at CT or a
focal hot spot is seen on a nuclear medicine scan, a search for possible obstruction of the SVC or IVC
should be made (7).