G a s t r o i n t e s t i n a l I m a g i n g • R ev i ew

Fong et al.
Abdominal Vascular Compression Syndromes

Gastrointestinal Imaging
Review
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Imaging Findings and Clinical

FOCUS ON:

Features of Abdominal Vascular

Compression Syndromes
Jeffrey Kah Keng Fong1 OBJECTIVE. This article describes the typical imaging findings and clinical features
Angeline Choo Choo Poh that are associated with four abdominal vascular compression syndromes. We explain the
Andrew Gee Seng Tan underlying pathophysiology that results in these clinical syndromes so that the patient subset
Ranu Taneja who will benefit from treatment can be identified.
CONCLUSION. The abdominal vascular compression syndromes discussed here are un-
Fong JKK, Poh ACC, Tan AGS, Taneja R common and are potentially easily missed on a cursory review of radiologic examinations, par-
ticularly in a nonspecific and vague clinical setting. Hence, knowledge of the typical imaging
findings and associated clinical symptoms is essential so that the they can be carefully sought
and excluded. However, because these findings may also exist in healthy individuals as anatom-
ic variants, it is important to correlate radiologic findings with clinical symptoms to identify the
subset of patients who will benefit from treatment.

Keywords: abdomen, compression, CT, syndrome,
vascular
DOI:10.2214/AJR.13.11598
Received July 22, 2013; accepted after revision
September 26, 2013.
1 
All authors: Department of Radiology, Changi General
Hospital, 2 Simei St 3, 529889, Singapore. Address
correspondence to J. K. K. Fong (jeffrey.fong@mohh.com.sg).
This article is available for credit.
AJR 2014; 203:29–36
0361–803X/14/2031–29
© American Roentgen Ray Society
T
he world of medicine is full of
eponymous conditions, an im-
mortal catalog to the legacies of
past pioneers. In this article,
three eponymous conditions are presented
along with a more generically named disease
under the common theme of “abdominal vas-
cular compression syndromes.”
The underlying pathophysiology that ac-
counts for these clinical syndromes, patient
demographics and clinical presentation, and
typical imaging findings for each condition
are described. A thorough understanding of
these disease processes will enable the accu-
rate diagnosis of disease in the small subset
of patients who require treatment and the ex-
clusion of individuals with anatomic findings
associated with these syndromes but who are
asymptomatic and do not require treatment.
Nutcracker Syndrome
Background
The term “nutcracker syndrome” is at-
tributed to de Schepper [1] and describes
compression of the left renal vein (LRV)
between the aorta and superior mesenter-
ic artery (SMA). This condition is also re-
ferred to as “anterior nutcracker syndrome.”
Less commonly, a circumaortic (up to 17%)
or completely retroaortic (3%) LRV may be
compressed between the aorta and vertebral
body, which is termed “posterior nutcracker
syndrome” [2].
Theories about the cause of nutcracker
syndrome include posterior renal ptosis, an
abnormally high course of the LRV, and an
abnormal SMA branching from the aorta [3].
Compression of the LRV predisposes to
venous hypertension and the formation of
periureteric varices [1].
Demographics and Clinical Features
The exact prevalence of nutcracker syn-
drome is unknown, likely because of the
variable presenting features [3]. However, it
is estimated to be relatively more common in
females and usually presents in the 3rd or 4th
decade of life [4].
The severity of nutcracker syndrome is
variable, and affected individuals may be
completely asymptomatic or, in the most
extreme cases, experience severe pelvic
congestion [5].” However, the most com-
mon presenting symptom is micro- or mac-
roscopic hematuria. Hematuria has been
attributed to hemorrhage into the calyce-
al fornices from the thin-walled varices,
which develop secondary to renal venous
hypertension [6]. Other symptoms or com-
plications that may occur include left flank

AJR:203, July 2014 29

 Fong et al.
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A B

C D E
Fig. 1—Contrast-enhanced CT images of 69-year-old woman who presented with history of repeated hospital admissions for undiagnosed abdominal pain.
A, CT image shows beak sign (arrow), which is narrowing of left renal vein (LRV) between aorta and superior mesenteric artery (SMA) (arrowhead).
B, Ratio of more than 4.9 of anteroposterior diameter of LRV at aortomesenteric (left arrowhead and short line) and hilar (right arrowhead and long line) regions is
considered 100% specific for nutcracker syndrome.
C, Oblique sagittal reformation image with SMA and aorta in same plane shows aortomesenteric angle (lines) of 35°; value of less than 41° is 100% sensitive for
diagnosing nutcracker syndrome.
D, Beak angle obtained by intersection of line from points A and C, which is drawn from anterior wall of LRV where it passes deep to SMA to point of LRV narrowing, and
intersection of line from points B and D, which is drawn from posterior renal wall to point of narrowing. In this case, beak angle is 35°. Value of more than 32° is diagnostic
of nutcracker syndrome.
E, Oblique coronal image shows dilated tortuous collateral vein (arrowheads) between LRV (arrow) and inferior vena cava.

pain, pelvic discomfort, varicocele, or ovar-
ian vein syndrome [7].
Radiologic Findings
On CT, the beak sign (Fig. 1A) is an abrupt
narrowing of the LRV between the aorta and
SMA, with proximal dilatation of the LRV.
This sign has a sensitivity of 91.7% and spec-
ificity of 88.9% in the diagnosis of nutcrack-
er syndrome. Also, a ratio of the LRV diam-
eters at the hilar and aortomesenteric regions
of more than 4.9 (i.e., a dilated proximal LRV;
Fig. 1B) has a sensitivity of 66.7% and specific-
ity of 100% for this condition. An aortomes-
enteric angle (between the superior mesenteric
artery [SMA] and aorta; Fig. 1C) of less than
41° is 100% sensitive and 55.6% specific [8] for
nutcracker syndrome; a normal aortomesen-
teric angle measures approximately 90° [4]. A
beak angle measurement may also be obtained
but is cumbersome to perform. It is obtained by
drawing two lines along the anterior and pos-
terior walls of the LRV where it passes under-
neath the SMA to the point of narrowing of the

30 AJR:203, July 2014

 Abdominal Vascular Compression Syndromes

LRV lumen (Fig. 1D). A measured beak angle
of more than 32° has a diagnostic sensitivity of
83.3% and specificity of 88.9% [8].
Classic retrograde venography with a
renocaval pressure gradient measurement of
more than 3 mm Hg is considered the refer-
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tive management have been suggested [3].
Various surgical approaches, ranging from a
straightforward LRV bypass to the more rad-
ical option of nephrectomy, have been de-
scribed [3]. Recently, endovascular stenting
has been used as a less invasive alternative

ence standard for the diagnosis of nutcracker
syndrome but has the inherent drawback of
being invasive [4, 9].
On ultrasound, measurements of both an-
teroposterior diameter and peak velocity of the
LRV at the renal hilum and the aortomesenter-
ic junction should be obtained. A ratio of more
than 5 for both is suggestive of nutcracker syn-
drome [10]. Dilated tributaries to the LRV (left
gonadal, left adrenal, and lumbar veins) may
be seen if the internal valves are incompetent
(Fig. 1E). Alternatively, collateral formation, in
which the LRV is decompressed and nondis-
tended, may be a feature. Color Doppler ultra-
sound to look for flow away from the LRV has
a diagnostic sensitivity of 78% and specificity
of 100% for nutcracker syndrome [9].
Management
Because 44% of asymptomatic patients
were found to have mild narrowing of the
LRV without the beak sign [8], it is important
to correlate radiologic findings with the pa-
tient’s clinical condition to determine wheth-
er further management is needed. There is no
consensus about which symptoms are suffi-
ciently severe to warrant definitive manage-
ment, but severe pain, gross hematuria, renal
insufficiency, and 2 years of failed conserva-
with good outcomes, but it does have inherent
drawbacks such as the potential complications
Aorta
of stent migration, fracture, or occlusion [11].
Superior Mesenteric Artery SMA
Syndrome (Wilkie Syndrome)
Background
First described comprehensively by
Wilkie in 1927 [12], this syndrome is Adipose
known more commonly as SMA syndrome
as opposed to its eponymous namesake.
SMA syndrome is caused by vascular com- Duodenum
pression of the third part of the duodenum
between the aorta and SMA.
The duodenum is normally surrounded
by mesenteric adipose tissue as it traverses
the aortomesenteric plane (Fig. 2). This tis-
sue functions as a natural fatty cushion and Fig. 2—Illustration shows duodenum surrounded
by adipose tissue. Loss of this fatty cushion
prevents extrinsic compression [13]. Hence, results in narrowing of aortomesenteric angle.
marked weight loss (e.g., weight loss caused by Angle measurement of less than 22° is diagnostic
a chronic debilitating disease or an acute cata- of superior mesenteric artery (SMA) syndrome.
bolic state) and a low body mass index (BMI (Drawing by Fong JKK)
[weight in kilograms divided by the square of
height in meters]) are risk factors [14]. Relative Demographics and Clinical Features
lengthening of the spine after corrective scolio- The prevalence of SMA syndrome based
sis surgery is also a known risk factor for SMA on fluoroscopy studies is estimated to be
syndrome, probably because superior displace- 0.013–0.3% [14], whereas other sources
ment of the SMA origin alters the aortomesen- quote a prevalence of 0.0965% in a chronic
teric angle between the aorta and SMA [15]. hospital setting versus 0.00108–0.0052% in

A B
Fig. 3—Asthenic 17-year-old girl with symptoms of abdominal distention and vomiting.
A, Obliquely oriented sagittal reconstruction of superior mesenteric artery (SMA) obtained from contrast-enhanced CT scan shows
aortomesenteric angle (lines) of 15°.
B, Axial image from same study as A shows stomach is grossly dilated and duodenum abruptly narrows as it travels under SMA.
Aortomesenteric distance measures 5 mm (arrowhead and line).
(Fig. 3 continues on next page)

AJR:203, July 2014 31

 Fong et al.
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C D

Fig. 3 (continued)—Asthenic 17-year-old girl with symptoms of abdominal distention and vomiting.
C and D, Posteroanterior (C) and left lateral decubitus (D) views from barium meal study show abrupt vertical compression of mucosal folds
and proximal dilatation of duodenum and stomach from vascular compression.

an acute general hospital setting [16]. This
syndrome is rare. There is a slight female
preponderance (64–66%), with 75% of cas-
es occurring in individuals who range in age
from 10 to 39 years [13, 17].
The typical symptoms of SMA syndrome
are postprandial or intermittent abdominal
pain and features of bowel obstruction such
as vomiting, nausea, and anorexia [17]. Ma-
neuvers such as lying prone or adopting the
left lateral decubitus position are described
as reducing the pain [18]. Patients are often
underweight, with a reported median BMI at
diagnosis of 17.4 [13].
Radiologic Findings
On CT, the two key signs of SMA syn-
drome are an aortomesenteric angle of less
than 22° (Fig. 3A) and an aortomesenter-
ic distance of less than 8 mm. The former
sign has a sensitivity of 42.8% and speci-
ficity of 100% for SMA syndrome, whereas
the sensitivity and specificity of the latter
are 100% [19]. The normal aortomesenter-
ic distance is typically between 10 and 28
mm and is measured at the level of the du-
odenum as it travels between the aorta and
SMA [19, 20] (Fig. 3B). Ancillary features
include a dilated stomach and duodenum up
to the aortomesenteric space followed by a
sharp narrowing as the duodenum travels
underneath the SMA [21].
There is a wide variation in the aortomes-
enteric angle values that have been reported
as “normal”; originally, a normal aortomes-
enteric angle was described as between 38°
and 56° [22], whereas newer studies claim
a 90° aortomesenteric angle in control sub-
jects is a more accurate value for normal
[23]. Nevertheless, it should be understood
that simple sagittal reconstructions may be
insufficient for assessing the aortomesenteric
angle because of the normal slight anterolat-
eral angulation of the SMA; an obliquely ori-
ented sagittal reconstruction provides more
accurate measurements [24].
Fluoroscopy was the previous mainstay
of diagnosing SMA syndrome. The classic
(but nonspecific) feature is a dilated prox-
imal duodenum with an abrupt termina-
tion at the third part of the duodenum with
or without gastric distention (Figs. 3C and
3D). Other features include abrupt verti-
cal compression of the mucosal folds at the
third part of the duodenum, antiperistaltic
flow of contrast material proximal to the ob-
struction (resulting in a forward-backward
“rocking” flow of barium), and relief of ob-
struction when the patient is in a prone or
left lateral decubitus position [14]. Howev-
er, a recent study using CT as the primary
diagnostic modality found a ­false-negative
rate of 18.6% for barium studies [13].
Management
The initial management of SMA syn-
drome is conservative, particularly in the
acute setting of less than 1 month. Manage-
ment includes insertion of a nasogastric tube
to decompress the stomach and duodenum as
well as to provide enteral feeding, hopefully
restoring a normal aortomesenteric distance
and relieving the obstruction [14].
If conservative management fails in a pa-
tient with severe symptoms, surgery is indi-
cated; the primary choice was traditionally
open duodenojejunostomy, with good opera-
tive results being reported in 79–100% of the
cases [14]. However, a review of nine arti-
cles found laparoscopic duodenojejunostomy
to be a safe and effective treatment with a
100% success rate [25].
Median Arcuate Ligament Syndrome
(“Dunbar Syndrome”)
Background
In a report of dissection findings from a
study of 83 cadavers, Lipshutz [26] noted that
the celiac axis “is not infrequently partly cov-
ered at its origin by the diaphragm.” The me-

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 Abdominal Vascular Compression Syndromes
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A B
dian arcuate ligament (MAL) is a fibrous arch
that connects the diaphragmatic crura to form
the anterior margin of the aortic hiatus. How-
ever, the location of the MAL is “exceedingly
variable” and the celiac artery origin was ei-
ther at or superior to the MAL in 33% of a 75-
case autopsy study [27]. The MAL may indent
upon the celiac trunk and cause downward an-
gulation, but this appearance may be a mere
anatomic variant that is nonobstructive [28].
However, in certain individuals, compres-
sion of the celiac trunk resulting in mesen-
teric ischemia can occur. It was first Harjola
[29] (1963) in a case study and then Dunbar
et al. [30] (1965) in a larger case series of 15
subjects who linked the anatomic anomaly
with clinical symptoms of intestinal angina.
The syndrome is also known as celiac artery,
axis, or trunk compression syndrome.
Demographics and Clinical Features
In a retrospective study of aortograms of
1500 patients discovered compression of the
celiac artery severe enough to cause symp-
toms in approximately 1% of the patients [31].
However, the exact incidence of MAL syn-
drome in the general population is unknown
[31]. A retrospective study of 14 patients with
MAL syndrome found a mean age of 28.4
years and 71% female preponderance [32].
The common complaint of patients with
MAL syndrome is of vague intermittent ab-
dominal pain, typically epigastric and usu-
ally postprandial. Given the association
with eating, weight loss is a common fea-
ture. Associated symptoms include nausea
AJR:203, July 2014 33
Fig. 4—63-year-old woman.
A and B, Sagittal arterial
phase CT image (A) and
volume-rendered 3D
reconstruction from
abdominal aortogram
(B). Hooked appearance
of proximal celiac axis
(arrows) with poststenotic
dilatation is being caused
by median arcuate ligament
indenting upon superior
aspect of artery.
and diarrhea. Examination usually reveals
mild epigastric tenderness, with an occa-
sional finding of a midabdominal systolic
bruit on auscultation [30].
Radiologic Findings
On modern MDCT with its superior spa-
tial resolution, the MAL may be visible; a
thickness of more than 4 mm is considered
abnormal [33]. The definitive finding for the
diagnosis of MAL syndrome is focal nar-
rowing of the proximal celiac axis with a
characteristic hooked appearance caused by
the inferior displacement of the celiac ar-
tery by the MAL (Fig. 4). Stenosis of the
celiac artery is more obvious on its superior
aspect where it indented upon by the MAL.
On the other hand, atherosclerosis results
in stenosis without the hooked appearance.
The sagittal axis is optimal for visualizing
the “hooking” of the proximal celiac trunk,
and this finding may be extremely subtle
and not visible on axial sections. Associ-
ated findings include poststenotic dilata-
tion or collateral vessel formation from the
SMA branches [34].
CT and MRI studies for diagnosing MAL
syndrome should ideally be performed in
the end-inspiratory phase. Because the
MAL attaches to the diaphragmatic crura,
its position and, hence, compression of the
celiac axis change during respiration [35].
True compression persists during end-inspi-
ration, whereas transient compression may
be seen only during end-expiration as the
diaphragm ascends in healthy individuals.
Therefore, CT and MRI studies performed
in the end-expiratory phase would show a
greater degree of compression in individu-
als with the syndrome but will also be pre-
disposed to false-positive results [36]. If a
patient in whom this syndrome is suspected
is unable to follow breathing instructions,
ancillary signs such as poststenotic dilata-
tion and collateral vessel formation should
be assessed.
Percutaneous angiography is the reference
standard for the diagnosis of MAL syndrome
and shows findings similar to CT such as su-
perior indentation, hooking, and poststenotic
dilatation of the celiac axis. A useful addi-
tional finding on angiography is the ability
to assess the stenosis in both end-inspiration
and end-expiration [33]. Compression is con-
sidered severe if it persists on end-inspiration
and if poststenotic dilatation and retrograde
filling of the celiac axis from the SMA and
pancreaticoduodenal arcade are present [34].
However, CT has the advantages of being
widely available, accurate, and noninvasive.
Furthermore, postprocessing techniques that
are useful for planning further intervention,
such as multiplanar and 3D volume-rendered
reconstructions, are available with CT [37].
Doppler ultrasound is a useful noninva-
sive alternative for diagnosing MAL syn-
drome. A peak systolic velocity of greater
than 200 cm/s has a reported sensitivity and
specificity of 75% and 89%, respectively,
in detecting a stenosis of at least 70% [38].
Given the inherent dynamic nature of ultra-
sound examination, flow turbulence, which
is accentuated during the expiratory phase,
can also be assessed [38].
Management
The existence of MAL syndrome is con-
troversial; the ideal treatment options are de-
bated because imaging of 13–50% of healthy
asymptomatic individuals may show com-
pression of the celiac artery during expira-
tion and the exact pathophysiology of MAL
syndrome remains indeterminate [34, 39]. If
surgical treatment is attempted, it will usu-
ally be celiac decompression via ligation of
the offending MAL, which can be performed
laparoscopically [39]. A novel approach is
laparoscopic release of the MAL using intra-
operative duplex ultrasound for guidance. If
the celiac artery flow abnormality on Dop-
pler ultrasound persists after MAL release,
angioplasty and stenting are advocated [40].
Surgical management is best reserved for
patients in the 40- to 60-year-old age group

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Fig. 5—Axial CT images of 53-year-old woman with history of tense, swollen left lower limb.
A, Left common iliac vein is compressed by overlying right common iliac artery (arrow).
B, There is also thrombus of left common iliac vein (arrow) distal to vascular compression.
with clinical symptoms of postprandial pain
and significant weight loss (20 lb [9 kg]), and
with radiologic features of poststenotic dila-
tation and collateral vessels [41].
May-Thurner Syndrome
Background
In 1957, May and Thurner [42] joint-
ly first described this syndrome in which
the left common iliac vein was compressed
by the right common iliac artery against
the lumbar vertebra in 22% of 430 cadav-
ers. However, this syndrome was allud-
ed to more than a century earlier by Vir-
chow [43] in his observation that deep vein
thrombosis (DVT) was five times more
likely to occur in the left lower limb. Cock-
ett, a British vascular surgeon, and Thomas
[44] also reported this condition in 1965,
so this syndrome is also known as “Cockett
syndrome.” An alternative nomenclature is
the more descriptive “iliac vein compres-
sion syndrome” [44].
The inferior vena cava is located to the
right of the spine, and the left common il-
iac vein emerges at a sharp angle, crossing
the midline where the natural convexity of
the lumbar vertebrae is most prominent [45].
May and Thurner [42] proposed the pathol-
ogy as intimal “spurs” developing from in-
timal hypertrophy of the left iliac vein wall
consequential to it suffering mechanical
compression and arterial pulsation by the
overlapping right common iliac artery [42].
These “spurs” are proposed to increase the
risk of thrombosis.
34 AJR:203, July 2014
Fong et al.
A B
Demographics and Clinical Features
May-Thurner syndrome tends to occur
in women (72% of the cases) in the 2nd–
4th decades [46]. Although the exact preva-
lence is unknown [47], a study of 44 patients
with isolated left lower limb DVT found that
27 patients had physiologic findings consis-
tent with May-Thurner syndrome [48]. May-
Thurner syndrome may be underdiagnosed
because many patients initially diagnosed
with DVT on ultrasound do not undergo fur-
ther investigative workup [47].
The typical features of May-Thurner syn-
drome overlap with those of DVT such as leg
pain, swelling, venous claudication, and var-
icose veins [45]; the complications of chron-
ic disease include venous eczema, hyper-
pigmentation, and ulcers [45]. Patients may
alternatively present with persistent painless
left lower limb edema [47].
Radiologic Findings
There is no consensus about specific radi-
ologic signs that are diagnostic of May-
Thurner syndrome. However, the most useful
finding is of compression of the left common
iliac vein by the right common iliac artery
(Fig. 5A). In one study, the mean diameter
of the left common iliac vein origin was 3.5
mm (range, 1.0–8.5 mm) in patients with
May-Thurner syndrome versus 11.5 mm in
a control group (range, 6.3–16.1 mm) [45].
Tortuous venous collaterals crossing the pel-
vis to drain into the contralateral veins [47]
and thrombus formation (Fig. 5B) are also
suggestive features.
Conventional venography is considered
the reference standard but is invasive and
is also suboptimal for visualizing the cen-
tral veins. Doppler ultrasound is most often
used in screening for DVT because of the
ease of availability and convenient bedside
examination [45]. However, it is often diffi-
cult to visualize the pelvic veins particularly
if the patient is obese or if bowel gas inter-
venes [49]. CT is widely available, is simple
to perform, and is useful to rule out the pres-
ence of an external mass compressing the
left common iliac vein.
Management
May-Thurner physiology is found in as
many as 22–32% of cadavers, although the
incidence of lower limb DVT approximates
a mere 100 cases per 100,000 individuals
(0.1%). Given the significant difference in
indicence of May-Thurner physiology and
that of lower limb DVT, the anatomic find-
ing alone does not represent an increased
risk of DVT [46]. One can have compres-
sion of the left common iliac vein by the
right common iliac artery and remain as-
ymptomatic. Therefore, the term “May-
Thurner physiology” should be used to de-
scribe the anatomy, whereas “May-Thurner
syndrome” should be reserved for cases of
venous stasis and resultant thrombus forma-
tion resulting from compression [50].
Treatment of DVT is typically antico-
agulation therapy. However, it may be in-
sufficient in patients with May-Thurner
syndrome because it does not relieve the un-
 Abdominal Vascular Compression Syndromes
derlying mechanical compression. The pa-
tient may therefore be at risk for recurrent
DVT or postthrombotic syndrome. Hence, a
carefully selected small subset of lower limb
DVT patients with diagnosed May-Thurn-
er syndrome will benefit from endovascular
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stenting to achieve long-term patency [51].
Summary
The four abdominal vascular compression
syndromes discussed here are uncommon
and are potentially easily missed on a cur-
sory review of radiologic examinations, par-
ticularly in a nonspecific and vague clinical
setting. Hence, knowledge of the typical im-
aging findings and associated clinical symp-
toms is essential so that they can be careful-
ly sought and excluded. However, because
these findings may also exist in healthy indi-
viduals as anatomic variants, it is important
to correlate radiologic findings with clinical
symptoms to identify the subset of patients
who will benefit from treatment.
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36 AJR:203, July 2014