Eur. Radiol.

(2001) 11: 509±512

Ó Springer-Verlag 2001 P E D IAT R I C

F. J. PØrez Fontµn Accessory spleen torsion: US, CT and

R. Soler
M. Santos MR findings
I. Facio

Received: 16 December 1999

Revised: 24 May 2000
Accepted: 24 May 2000
)
F. J. PØrez Fontµn ( ) ´ R. Soler ´
M. Santos
Department of Radiology,
Hospital Juan Canalejo, Xubias de Arriba,
84, 15006 La Coruæa, Spain
I. Facio
Department of Radiology,
Centro Oncológico, Avda Monserrat,
s/n, 15009 La Coruæa, Spain
Abstract Torsion of an accessory
spleen is a very unusual entity that
can appear with abdominal pain as-
sociated with the presence of an
avascular mass. We report the case
of a 13-year-old boy with torsion and
infarction of an accessory spleen
presenting as a painful abdominal
mass in which imaging examination
with US, CT and MR showed a large
avascular mass in the upper left ab-
domen.
Key words Spleen ´ Accessory
spleen ´ Torsion ´ CT ´ MR ´
Ultrasound

We describe the US, CT and MR examinations of an

Introduction
Accessory spleen is a congenital anomaly that consists
of ectopic splenic tissue separated from the main body
of the spleen. The spleen develops from mesenchymal
cells that migrate during fetal life into the dorsal me-
sogastrium and a failure in the fusion of splenic tissue
results in the formation of an accessory spleen [1, 2].
The frequency of accessory spleens is 3.1±3.7 % of CT
and US examinations [2, 3]; however, the frequency of
accessory spleen is difficult to estimate because it is
frequently asymptomatic and thus may be unrecog-
nized. Accessory spleens have been found as an inci-
dental finding in 10 % of autopsy series and in 33 % of
patients with hematologic diseases [3]. Occasionally, as
in our case, accessory spleen may appear with symp-
toms related to acute or recurrent torsion and infarc-
tion [4, 5]. Clinical presentation of torsioned accessory
spleen is usually heralded by abdominal pain without
any clinical or laboratory clue for the correct diagno-
sis.
accessory spleen with torsion and infarction in a teen-
ager with abdominal pain and vomiting.
Case report
A 13-year-old male patient with a history of intermittent abdomi-
nal pain of 1-month duration was admitted with severe left hypo-
chondrial pain and vomiting. Physical and laboratory examinations
were normal. Abdominal plain radiograph showed a soft tissue
mass over the left kidney silhouette. A ultrasound examination
was performed which revealed a homogeneous oval mass with
good sound transmission, measuring 10 cm in diameter (Fig. 1),
anterior to the aorta and independent of the kidney, pancreas and
spleen; a normal-size spleen could be seen in its normal position.
Unenhanced CT scan showed a well-defined soft tissue mass in the
upper left abdomen adjacent to the pancreatic tail and clearly
separated from the spleen, left kidney and left adrenal gland. The
mass was hypodense as compared with the spleen. After i. v. injec-
tion of contrast material, the mass remained hypodense with only a
thin peripheral rim enhancement (Fig. 2). Magnetic resonance im-
aging was performed on a 0.5-T unit and showed that the mass was
510
Fig. 1 Longitudinal US examination shows a well-defined, homo-
geneous hypoechogenic mass, anterior to the aorta
Fig. 2 Contrast-enhanced CT scan of upper abdomen shows an
intraperitoneal hypodense mass of 10 cm with a thin peripheral
enhanced rim and a small crescent of subcapsular fluid. A clear
cleavage plane is seen related to the neighbouring structures
hypointense with a thin peripheral hyperintense halo on T1-
weighted spin-echo images (TR/TE: 500/15 ms; Fig. 3) and became
homogeneously hyperintense on T2-weighted spin-echo (TR/TE:
2000/120 ms) sequences.
With the suggested diagnosis of congenital malformation of the
gut or mesentery, the patient was operated on and the lesion was
resected. Surgical exploration showed a rounded violet mass with a
twisted pedicle, located under the omentum, in the vicinity of the
colonic splenic flexure. Histological study revealed haemorrhagic
and infarcted splenic tissue.
Fig. 3 Sagittal T1-weighted image shows a hypointense mass with
a thin peripheral hyperintense rim (arrows) situated anterior to the
descendent colon. Normal spleen can be seen in the usual location
(asterisk)
Discussion
An accessory spleen is caused by the failure of splenic
anlage to fuse during embryogenesis [2]. The size varies
from a few millimetres up to 1.5±2 cm in diameter [3, 6],
but in patients with pathologic splenic findings or in
those who have previously undergone splenectomy, ac-
cessory spleens can hypertrophy and reach a size of 5 cm
or more [2]. Accessory spleens are most often located in
the vicinity of the splenic hilum, along the course of the
splenic vessels or omentum [6], but they may occur
anywhere in the abdomen and even in the left scrotum
[2, 4]. The vascular pedicle of an accessory spleen is
most commonly related to the splenic hilum but may
also be related to the tail of the pancreas, the gastros-
plenic ligament, the small bowel mesentery or to vessels
from the fundus of the stomach [7]. Although usually
accessory spleen appears as an isolated asymptomatic
abnormality, it can be associated with other anomalies
such as polysplenia and short pancreas [8].
Torsion and infarction of an accessory spleen is a
very rare process, with only a few previous reports
dealing with the radiological findings [4, 5, 7, 9, 10]. Pa-
tients range from infants to the elderly, but more than
 511

half of the reported cases were children [4]. The symp-
toms varied from vague abdominal pain in the case of a
wandering accessory spleen with intermittent torsion
[8], to fever, vomiting and acute onset of severe abdom-
inal pain in case of infarction [4, 5].
The diagnosis is usually established with the aid of
imaging. Abdominal plain radiographs may demon-
strate a soft tissue mass depending on the size of the le-
sion. In our case the accessory spleen was very large,
reaching 10 cm in diameter, and a mass effect could be
seen over the left kidney shadow. We agree with Valls
et al. [5] in thinking that probably so large a size of the
accessory spleen, in the absence of hematologic or liver
disease, can be due to venous congestion secondary to
twisting of the vascular pedicle.
The ultrasonographic descriptions of previously re-
ported cases include a hypoechoic well-encapsulated
oval mass in the left upper quadrant [4], a hypoechoic
mass behind the stomach [7], a hypoechoic mass with
central hyperechoic areas [9] and a nodular solid mass
below the splenic hilus and adjacent to the left kidney
[5]. In our case a well-delineated solid mass with good
sound transmission could be seen. In all these cases the
presence of the main spleen is in its normal position
discarding the possibility of a wandering spleen. Dop-
pler ultrasound can be used to evaluate the degree of
vascularization of an abdominal mass; however, the ab-
sence of flow does not allow differentiation between a
cystic mass or an ischaemic lesion such as a twisted ac-
cessory spleen.
On CT studies accessory spleen tissue tends to ex-
hibit the same pattern of contrast enhancement, as does
the spleen itself. In the few reports [4, 5] about a twisted
infarcted accessory spleen, and in our case, the CT
findings are similar to classical pattern reported in dif-
fuse splenic infarcts. Diffuse infarctions appear on CT as
massive hypodense lesions which involve the splenic
parenchyma with peripheral enhancement due to arte-
rial supply from capsular vessels [11]. The CT reports of
twisted wandering spleen have shown a whirled appear-
ance of the splenic pedicle and surrounding fat at the
splenic hilum, hyperdense splenic vessels corresponding
to acute thrombosis [12], or ascitis with low attenuation
of the pancreatic tail due to necrosis [13]. These findings
have not been reported in torsion of an accessory spleen
and were not seen in our case perhaps due to the small
size of the vascular supply and independence from the
pancreatic tail. The torsion of vascular pedicle produces
a spleen infarction which, on CT scan, has considerably
lower attenuation compared with normal spleen or liver.
When masses with these CT characteristics are found in
the abdomen, the differential diagnosis between mes-
enteric or omental cysts, intestinal duplication, pancre-
atic pseudocysts and abscesses should be considered
[12].
The MR imaging has been reported in two previous
cases. In the first case an infarcted accessory spleen
presented as a hypointense mass on T1- and T2-weight-
ed images containing low-signal structures which were
thought to be due to vessels. Three weeks later, the in-
farcted accessory spleen showed homogeneous high
signal intensity on T2-weighted images, whereas on T1-
weighted images, the signal intensity remained low ex-
cept for a peripheral rim of high signal intensity, pre-
sumably reflecting a combination of peripheral fibrosis
secondary to progressive inflammatory changes super-
imposed on infarction [4]. In the other case Jans et al.
suggested that T2-weighted images may help in the di-
agnosis of infarcted spleen by demonstrating the pres-
ence of haemorrhagic necrosis [10].
In our case MR examination was performed after a
month of intermittent abdominal pain and showed
findings similar to the previously reported case. Hyper-
intensity on T1-weighted images is usually related to fat
deposit or paramagnetic materials. Because we did not
find peripheral adhesions, fibrous tissue or fat deposits
in the pathological specimens of our case, we think that
the cause of the hyperintense peripheral rim was not
related to fibrosis as has been previously stated [4]. We
thought that a possible explanation for the peripheral
hyperintense rim on T1-weighted spin-echo sequence
could be the presence of haemoglobin degradation
product methemoglobin related to the evolution of in-
farcted areas or slow-flowing blood in residual capsular
or subcapsular vessels.
In conclusion, torsion of an accessory spleen implies
a diagnostic problem which derives from the fact that it
settles in a normal but inconstant structure. Torsion of
an accessory spleen should be considered in the differ-
ential diagnosis when an avascular intraperitoneal mass
is seen in a patient with acute or subacute abdominal
pain.

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BOOK RE VIEW
Orrison W. W. Jr. (Editor): Neuroimaging
(2 volume set). Philadelphia: WB Saunders,
2000, 1776 pages illustrated, £ 280.00, Set
ISBN 0-7216-6799-6
(continued from p. 505)
The first chapters of Section 2 concerns
normal brain imaging and normal variations
of the head. Chapters 19 and 20 deal with
intracranial tumours. There is some discre-
pancy between the chapter on intraaxial tu-
mours (28 pages, 96 references) and the
chapter on extraaxial and sellar tumours
(106 pages, 718 references). The chapter on
cerebrovascular disease is rather poorly re-
ferenced. The six remaining chapters of this
section include intracranial infection, white
matter disease, neurodegenerative disor-
ders, haemorrhage, head trauma and sei-
zure imaging. It is worth mentioning that the
chapter on haemorrhage includes a library
of illustrative cases.
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patient: imaging findings at CT, MRI
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80:229±230
Section 3 consists of head and neck, or-
bit and spine. It remains unclear why chap-
ters on spine imaging are included in this
section. It appears logical to dedicate a
separate section to spinal imaging in a neu-
roimaging textbook. The images of Chap-
ters 28 (temporal bone) and 29 (skull base)
were taken from the author's digital teach-
ing file. The other chapters concern the or-
bit, nasal cavity and paranasal sinuses,
pharynx and oral cavity, parapharyngeal
and masticator space, thyroid and para-
thyroid, salivary glands and lymph nodes,
temporomandibular joint imaging, larynx
and hypopharynx. The referencing in these
chapters is reasonable.
The last part of the textbook concerns
paediatric neuroimaging. First there is a
chapter on normal development. Chapters
follow on congenital malformations of the
brain and spine. Both chapters are unsatis-
factory from the point of view of both con-
tents and referencing (almost all references
date from 1993 or earlier). The remaining
chapters are concise and well referenced.
Metabolic diseases, anoxic ischaemic in-
jury, neurocutaneous syndromes and trau-
11. Balcar I, Seltzer SE, Davis S, Geller S
(1984) CT patterns of splenic infarction:
a clinical and experimental study. Radi-
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12. Raissaki M, Prassopoulos P, Daskalo-
giannaki M, Magkanas E, Gourtsoyian-
nis N (1998) Acute abdomen due to
torsion of a wandering spleen: CT diag-
nosis. Eur Radiol 8:1409±1412
13. López MenØndez C, Calvo J, López-
Negrete L, Prieto A, Luyando L (1995)
The wandering spleen. Eur J Radiol
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ma are discussed. One chapter is dedicated
to hydrocephalus and CSF flow and one
chapter reviews congenital abnormalities
of the face.
The editor points out himself that the
book is meant as a master file in the field of
neuroimaging, cataloguing and including
all aspects of the practice of neuroimaging.
The book suffers to some degree from the
drawbacks of a multi-author textbook.
Most chapters are excellent but there are a
few that are unsatisfactory from the point
of view of content and lack of recent refer-
ences. Spinal imaging is treated as the poor
relation since only 100 pages are dedicated
to this important part of neuroradiology
practice compared with more than 400 pa-
ges on head and neck imaging. Overall the
book is certainly recommended as one of
the possible choices when one has to decide
on buying a reference book on neurora-
diology. In fact the reader gets a book on
neuroimaging and head and neck imaging.
The high price will be a disadvantage.
P. Demaerel, Leuven