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DOI: 10.1148/radiol.2343030695
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(Radiology 2005;234:728-732.)
© RSNA, 2005


Diagnosis Please

Case 80: Splenosis1

Giuseppe Brancatelli, MD, Valérie Vilgrain, MD, Magali Zappa, MD and Roberto Lagalla, MD

1 From the Department of Radiology, Hôpital Beaujon, Clichy, France (G.B., V.V., M.Z.); and Department of Radiology, Università di Palermo, Italy (G.B., R.L.). Received April 30, 2003; revision requested July 11; revision received July 25; accepted August 25. Address correspondence to G.B., Via Villaermosa 29, 90139 Palermo, Italy (e-mail: gbranca@yahoo.com).


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A 38-year-old woman was examined at our institution because a liver mass was suspected. The patient had been in excellent health until 24 months earlier, when she developed fever and acute severe pain in the right lower quadrant of the abdomen. An appendectomy was performed at a different institution. Abdominal ultrasonography (US) (not shown) was performed preoperatively to evaluate right lower quadrant pain and raised suspicion of a liver mass. This mass was confirmed with contrast material–enhanced magnetic resonance (MR) imaging (not shown), performed within 7 days of abdominal US. Since the patient was otherwise healthy, a decision was made to conservatively follow up the mass, as it was believed to be benign.

The patient’s medical history was otherwise unremarkable, except for appendectomy at 36 years of age and emergency splenectomy at 6 years of age after a motor vehicle accident.

The patient had used oral contraceptives for several years; however, the exact number of years was not specified. Vital signs and the results of a physical examination were normal. Contrast-enhanced computed tomography (CT) and contrast-enhanced MR imaging were performed. MR imaging characteristics and the size of the mass had not changed in comparison to those seen at MR imaging 2 years earlier at a different institution.


    IMAGING FINDINGS
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Contrast-enhanced CT of the upper abdomen demonstrated a 5-cm lesion originating from or in close contact with the left hepatic lobe, adjacent to the anterior part of the left hemidiaphragm. The lesion showed strong and slightly inhomogeneous enhancement during the arterial phase (Fig 1a), with diminished enhancement in the portal venous phase (Fig 1b). A 5-cm well-defined solid enhancing mass was identified on MR images. The mass was hyperintense on images obtained with the T2-weighted fast spin-echo MR sequence (Fig 2a). On both CT and MR images, the lesion appeared to indent the surface of the liver. This configuration supported a mass of extrahepatic origin. A smaller mass of similar intensity was noted in the left upper quadrant. The breath-hold T1-weighted gradient-echo MR sequence (Fig 2b) demonstrated a mass of low signal intensity. Strong slightly inhomogeneous enhancement of the mass was present during the arterial phase of the dynamic gradient-echo sequence (Fig 2c), with diminished enhancement in the portal phase (Fig 2d).



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Figure 1a. Transverse helical CT scans (5-mm collimation) obtained through the liver during the (a) arterial and (b) portal phases after administration of a 150-mL bolus of intravenous contrast material. In a, note the strong slightly inhomogeneous enhancement of a well-defined hepatic lesion (arrow). In b, the lesion (arrow) is slightly hypoattenuating to adjacent liver parenchyma.

 


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Figure 1b. Transverse helical CT scans (5-mm collimation) obtained through the liver during the (a) arterial and (b) portal phases after administration of a 150-mL bolus of intravenous contrast material. In a, note the strong slightly inhomogeneous enhancement of a well-defined hepatic lesion (arrow). In b, the lesion (arrow) is slightly hypoattenuating to adjacent liver parenchyma.

 


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Figure 2a. (a) Transverse T2-weighted fast spin-echo abdominal MR image (repetition time msec/echo time msec, 1600/70; matrix, 307 x 512; one signal acquired). The lesion (oblique arrow) is of high signal intensity. A 2-cm splenic implant (vertical arrow) of similar intensity is noted in the left upper quadrant. (b) Transverse T1-weighted breath-hold gradient-echo abdominal MR image (146/2.3; flip angle, 80°; matrix, 155 x 256; two signals acquired). The lesion (arrow) is hypointense to the liver parenchyma. Transverse T1-weighted breath-hold gradient-echo abdominal MR image obtained during the (c) arterial and (d) portal phases after intravenous administration of a 10-mL bolus of gadopentate dimeglumine (223/5.3; flip angle, 80°; matrix, 180 x 256; one signal acquired). In c, early strong slightly inhomogeneous enhancement of the lesion (arrow) is noted. In d, the lesion (arrow) is isointense to the liver parenchyma.

 


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Figure 2b. (a) Transverse T2-weighted fast spin-echo abdominal MR image (repetition time msec/echo time msec, 1600/70; matrix, 307 x 512; one signal acquired). The lesion (oblique arrow) is of high signal intensity. A 2-cm splenic implant (vertical arrow) of similar intensity is noted in the left upper quadrant. (b) Transverse T1-weighted breath-hold gradient-echo abdominal MR image (146/2.3; flip angle, 80°; matrix, 155 x 256; two signals acquired). The lesion (arrow) is hypointense to the liver parenchyma. Transverse T1-weighted breath-hold gradient-echo abdominal MR image obtained during the (c) arterial and (d) portal phases after intravenous administration of a 10-mL bolus of gadopentate dimeglumine (223/5.3; flip angle, 80°; matrix, 180 x 256; one signal acquired). In c, early strong slightly inhomogeneous enhancement of the lesion (arrow) is noted. In d, the lesion (arrow) is isointense to the liver parenchyma.

 


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Figure 2c. (a) Transverse T2-weighted fast spin-echo abdominal MR image (repetition time msec/echo time msec, 1600/70; matrix, 307 x 512; one signal acquired). The lesion (oblique arrow) is of high signal intensity. A 2-cm splenic implant (vertical arrow) of similar intensity is noted in the left upper quadrant. (b) Transverse T1-weighted breath-hold gradient-echo abdominal MR image (146/2.3; flip angle, 80°; matrix, 155 x 256; two signals acquired). The lesion (arrow) is hypointense to the liver parenchyma. Transverse T1-weighted breath-hold gradient-echo abdominal MR image obtained during the (c) arterial and (d) portal phases after intravenous administration of a 10-mL bolus of gadopentate dimeglumine (223/5.3; flip angle, 80°; matrix, 180 x 256; one signal acquired). In c, early strong slightly inhomogeneous enhancement of the lesion (arrow) is noted. In d, the lesion (arrow) is isointense to the liver parenchyma.

 


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Figure 2d. (a) Transverse T2-weighted fast spin-echo abdominal MR image (repetition time msec/echo time msec, 1600/70; matrix, 307 x 512; one signal acquired). The lesion (oblique arrow) is of high signal intensity. A 2-cm splenic implant (vertical arrow) of similar intensity is noted in the left upper quadrant. (b) Transverse T1-weighted breath-hold gradient-echo abdominal MR image (146/2.3; flip angle, 80°; matrix, 155 x 256; two signals acquired). The lesion (arrow) is hypointense to the liver parenchyma. Transverse T1-weighted breath-hold gradient-echo abdominal MR image obtained during the (c) arterial and (d) portal phases after intravenous administration of a 10-mL bolus of gadopentate dimeglumine (223/5.3; flip angle, 80°; matrix, 180 x 256; one signal acquired). In c, early strong slightly inhomogeneous enhancement of the lesion (arrow) is noted. In d, the lesion (arrow) is isointense to the liver parenchyma.

 

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In this patient, the imaging finding of multiple intraabdominal enhancing masses coupled with the history of emergent splenectomy after a motor vehicle collision 32 years earlier allowed the diagnosis of splenosis to be assigned. The contrast-enhanced CT scan of the upper abdomen (Fig 3a) obtained during the arterial phase at a lower level than that of Figures 1 and 2 showed strong and homogeneous enhancement of a 2-cm mass in the left upper quadrant. A contrast-enhanced CT scan obtained during the arterial phase (Fig 3b) at a lower level than that of Figure 3a showed strong and homogeneous enhancement in another 2-cm mass. An anterior planar image obtained by means of splenic scintigraphy with technetium 99m (99mTc) sulfur colloid (Fig 4) showed radionuclide uptake in the left upper quadrant, which is consistent with locations of the masses (splenic implants) on CT scans.



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Figure 3a. Transverse helical CT scans (5-mm collimation) obtained after intravenous administration of a 150-mL bolus of contrast material. (a) CT scan obtained through the liver during the arterial phase demonstrates strong and homogeneous enhancement of a 2-cm lesion, which is a splenic implant (arrow). (b) CT scan obtained at a lower level than that of a shows a well-defined 2-cm nodule (arrow), which is another splenic implant.

 


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Figure 3b. Transverse helical CT scans (5-mm collimation) obtained after intravenous administration of a 150-mL bolus of contrast material. (a) CT scan obtained through the liver during the arterial phase demonstrates strong and homogeneous enhancement of a 2-cm lesion, which is a splenic implant (arrow). (b) CT scan obtained at a lower level than that of a shows a well-defined 2-cm nodule (arrow), which is another splenic implant.

 


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Figure 4. Anterior 99mTc sulfur colloid planar scintigram shows radionuclide uptake in the liver and left upper quadrant (arrows). This finding is consistent with locations of splenic implants.

 
Given the age and sex of the patient, the enhancement pattern at multiphasic CT and MR imaging, and the patient’s use of oral contraceptives for several years, a diagnosis of either hepatic adenoma or focal nodular hyperplasia was considered initially (1). However, these diagnoses would not have explained the smaller lesion in the left upper quadrant, which was isointense to the large lesion seen on T2-weighted fast spin-echo MR images (Fig 2a). Hepatocellular carcinoma would have been unlikely in a young woman who lacked a history of chronic liver disease, and hepatocellular carcinoma in a noncirrhotic liver generally appears as a larger mass, with marked inhomogeneous enhancement in all phases (2). Moreover, the lesion size in this patient was unchanged over 2 years. Fibrolamellar hepatocellular carcinoma is usually larger and markedly heterogeneous, with large scars and fibrous septa. Central calcifications and abdominal lymphadenopathy are noted in 65% of patients. Biliary and vascular invasion are commonly seen. None of these features were observed in this patient (3). Finally, liver metastases secondary to neuroendocrine tumors can appear as hypervascular lesions with strong hyperintensity on T2-weighted images, as in the present case; however, a primary tumor was not apparent in this patient.

Splenosis is defined as the autotransplantation of splenic tissue resulting from the spillage of cells from the pulp of the spleen after splenic injury or splenectomy. As in this patient, splenic implants are generally numerous, can be located anywhere in the peritoneal cavity, are supplied by arteries from the surrounding tissue rather than a hilar artery, have no particular shape, and have neither a hilus nor a normal capsule. Splenic implants located in the peritoneal cavity may be confused with renal neoplasms (4), abdominal lymphomas (5), and endometriosis (5). If splenic rupture is associated with a diaphragmatic tear, the implants may seed the pleural cavity or pericardium (6), which causes intrathoracic splenosis.

In this case, given the strong slightly inhomogeneous enhancement and the history of oral contraceptive use for several years, we could not rule out the diagnosis of liver adenoma for the large mass in close contact with the anterior surface of the liver. When the patient was informed of the potential for a hepatic adenoma to bleed, she requested further workup. In this case, 99mTc sulfur colloid scintigraphy (Fig 4) revealed multiple areas of increased activity in the left abdomen. Functional imaging of the spleen may also be obtained with denaturated blood cell scintigraphy, which is considered more sensitive than 99mTc sulfur colloid scintigraphy and allows imaging of the splenic tissue independent of imaging of the liver. Labeled red blood cell studies may be particularly useful if there is overlap of the liver and spleen at 99mTc sulfur colloid imaging (7). Moreover, single positron emission computed tomography allows for direct correlation with other imaging techniques (8). In this patient, there was still a possibility that the lesion anterior to the liver represented a liver mass and not a splenic implant; therefore, the diagnosis was confirmed with a percutaneous core biopsy sample obtained from the largest mass located anterior to the left lobe of the liver. Histologic examination of the lesion demonstrated white and red pulp, which proved that the lesion consisted of healthy splenic tissue.


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  1. Gruen DR, Gollub MJ. Intrahepatic splenosis mimicking hepatic adenoma. AJR Am J Roentgenol 1997; 168:725-726.[Free Full Text]
  2. Winston CB, Schwartz LH, Fong Y, Blumgart LH, Paniceck DM. Hepatocellular carcinoma: MR imaging findings in cirrhotic livers and noncirrhotic livers. Radiology 1999; 210:75-79.[Abstract/Free Full Text]
  3. Ichikawa T, Federle MP, Grazioli L, Madariaga J, Nalesnik M, Marsh W. Fibrolamellar hepatocellular carcinoma: imaging and pathologic findings in 31 recent cases. Radiology 1999; 213:352-361.[Abstract/Free Full Text]
  4. Kiser JW, Fagien M, Clore FF. Splenosis mimicking a left renal mass. AJR Am J Roentgenol 1996; 167:1508-1509.[Free Full Text]
  5. Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises: case 29–1995—a 65-year-old man with mediastinal Hodgkin’s disease and a pelvic mass. N Engl J Med 1995; 333:784-791.[Free Full Text]
  6. White CS, Meyer CA. General case of the day: thoracic splenosis. RadioGraphics 1998; 18:255-257.[Medline]
  7. Massey MD, Stevens JS. Residual spleen found on denaturated red blood cell scan following negative colloid scan. J Nucl Med 1991; 32:2286-2287.[Abstract/Free Full Text]
  8. Gunes I, Ylmazlar T, Sarikaya I, Akbunar T, Irgil C. Scintigraphic detection of splenosis: superiority of tomographic selective spleen scintigraphy. Clin Radiol 1994; 49:115-117.[CrossRef][Medline]

Congratulations to the 154 individuals who submitted the most likely diagnosis (splenosis) for Diagnosis Please, Case 80. The names and locations of the individuals, as submitted, are as follows:
Gholamali Afshang, MD, Tinley Park, Ill
Dr Jorge Ahualli, Tucuman, Argentina
Okan Akinci, MD, Istanbul, Turkey
Erhan Akpinar, MD, Ankara, Turkey
Canan Altay, MD, Izmir, Turkey
Roger L. Antonelli, MD, Dayton, Ohio
John M. Barkley, MD, Boston, Mass
H. Scott Beasley, MD, Pittsburgh, Pa
Richard Beedie, Auckland, New Zealand
Amy S. Bokal, MD, Bixby, Okla
Adrian Brady, FFRRCSI, Cork, Ireland
Eric L. Bressler, MD, Minnetonka, Minn
Jorge Brito, Coimbra, Portugal
Jean-Michel C. Bruel, MD, Montpellier, France
Michael P. Buetow, MD, Okemos, Mich
Peter Buetow, Bellingham, Wash
Marcio Bustamante, Rio de Janeiro, Brazil
Rogério Pedreschi Caldana, MD, São Paulo, Brazil
Océlio Cartaxo, Recife, Brazil
Dr Tirso Cascajares Murillo, Los Mochis, Mexico
Filipe Caseiro Alves, MD, Coimbra, Portugal
Nelson M. G. Caserta, MD, Campinas, Brazil
Antonio Cavalcanti, MD, São Paulo, Brazil
Can Cevikol, MD, Antalya, Turkey
Marcos Nogueira Chagas, MD, Brasilia, Brazil
Chris Chernesky, MD, Springfield, Mo
Haris Chrysikopoulos, MD, Kerkyra, Greece
Pablo Cikman, MD, Cordoba, Argentina
Marc G. de Baets, MD, Lugano, Switzerland
Wagner Diniz de Paula, MD, Brasilia, Brazil
Paolo Della Vigna, Villa Guardia, Como, Italy
Mustafa Kemal Demir, MD, Istanbul, Turkey
Susana Dias, Porto, Portugal
Christopher Dorvault, MD, Pensacola, Fla
Juliet Fallah, MD, Chicago, Ill
Francis Flaherty, MD, Ridgefield, Conn
Ricardo B. Fonseca, MD, Nashville, Tenn
Lee Foo Cheung, MD, Saint Michel, France
Akira Fujikawa, Tokyo, Japan
Ann S. Fulcher, MD, Richmond, Va
Cristine Norwig Galvão, Barretos, Brazil
Vasco Ernesto Gálvez, Salta, Argentina
Juan Francisco Garcia, MD, Monterrey, Mexico
Roberto Garcia Figueiras, MD, Santiago de Compostela, Spain
Douglas Gardner, MD, Windsor, Ontario, Canada
William Gawman, Waterloo, Ontario, Canada
Gilles Genin, MD, Annecy, France
Alvaro Gomez Naar, Salta, Argentina
Manish Goyal, MD, Massillon, Ohio
Aleksandar Grgic, MD, Homburg, Germany
Daniel Gridley, Goodyear, Ariz
John D. Grizzard, MD, Midlothian, Va
Kathleen R. Groom, Fort Campbell, Ky
Flavius Guglielmo, MD, Basking Ridge, NJ
Dr Jean Haddad, Cairns, Australia
Satoshi Hamatake, Kumamoto, Japan
Andreas Harzheim, MD, Cologne, Germany
Nobushige Hayashi, MD, PhD, Fukui, Japan
Karin Herrmann, MD, Munich, Germany
Marla R. Hersh, Tampa, Fla
Steven W. Hetts, MD, San Mateo, Calif
John J. Hines, MD, New Hyde Park, NY
Helen T. Ho, MD, Chicago, Ill
Alvaro Huete, MD, Santiago, Chile
Gloria L. Hwang, MD, San Mateo, Calif
Alberto Iaia, MD, Wilmington, Del
Waleed Ibrahim, MD, Rochester Hills, Mich
Andrew J. Kapustin, Merion, Pa
Kamil Karaali, MD, Antalya, Turkey
Nurettin Katranci, MD, Antalya, Turkey
Takuji Kiryu, MD, Gifu, Japan
Mitchell A. Klein, MD, Milwaukee, Wis
Steven A. Klein, MD, Shrewsbury, Mass
Arlene M. Klink, MD, Irvine, Calif
Glenn Krinsky, New York, NY
Supika Kritsaneepaiboon, MD, Songkla, Thailand
Mark Kutler, MD, Dallas, Tex
Mario Laguna, West Allis, Wis
Daniel Lahan Martins, MD, Campinas, Brazil
Roger Lao, MD, Dix Hills, NY
Iñigo Lecumberri, Bilbao, Spain
John T. Lim, MD, Newport Coast, Calif
David A. Lisle, Brisbane, Australia
Jaume Llauger, MD, Barcelona, Spain
Walter Mak, MD, Peoria, Ill
N. B. S. Mani, MD, Nassau, Bahamas
John A. Mattingly, MD, Belleville, Ill
Frank McKowne, MD, Vancouver, Wash
Luis Mendez-Uriburu, Tucuman, Argentina
Ur Metser, MD, Tel-Aviv, Israel
Manabu Minami, MD, Ibaraki, Japan
Sankar Ranjan Mondal, MD, Nassau, Bahamas
Eduardo Mondello, MD, Buenos Aires, Argentina
Annamalai Muthiah, Jr, MD, Charlottesville, Va
Tammam Nehme, East Wenatchee, Wash
Mizuki Nishino, MD, Boston, Mass
Michael T. O’Loughlin, MD, West Hartford, Conn
Sanford M. Ornstein, MD, Phoenix, Ariz
Ann B. Owen, MD, Murfreesboro, Tenn
David M. Panicek, MD, New York, NY
Harish K. Panicker, MD, Washington, DC
Narendrakumar P. Patel, MD, Newburg, NY
Constantino S. Pena, Key Biscayne, Fla
Siriporn Pinaikul, MD, Songkla, Thailand
Adilson Prando, MD, Campinas, Brazil
Lorenzo Preda, Milan, Italy
Klaus W. Preidler, MD, Graz, Austria
Daniel Rappaport, MD, FRCPC, Etobicoke, Ontario, Canada
Denis M. Regent, Nancy-Brabois, France
Enrique Remartinez Escobar, MD, Melilla, Spain
Pietro Renda, Padova, Italy
Jordi Rimola, MD, Sabadell, Spain
Mathieu H. Rodallec, Paris, France
Kris Saadeh, Mount Pleasant, SC
Guis Saint-Martin, Rio de Janeiro, Brazil
Satyajit Sarangi, MD, Lewers, Del
Robert Sauer, St Poelten, Austria
Pierre J. Sauvage, MD, Mâcon, France
Stephen Irwin Schabel, MD, Charleston, SC
Mahomed Seedat, Toowoomba, Australia
Hülya Sezer, Istanbul, Turkey
Anthony Shadid, Peoria, Ill
Janet R. Shaefer, MD, Rapid City, SD
Matt Shapiro, MD, Charlottesville, Va
Taro Shimono, MD, Osaka, Japan
Hiroshi Shinmoto, MD, Tokyo, Japan
S. Horatio Slawson, RPh, MD, Peoria, Ill
David F. Sobel, MD, La Jolla, Calif
Scott D. Steenburg, MD, Mount Pleasant, SC
Dr Anne Stroh-Marcy, Soissons, France
Kouichi Sugiyama, Hamamatsu, Japan
Norio Takahashi, MD, Fukui, Japan
Satoru Takahashi, MD, Osaka, Japan
Yumiko Oishi Tanaka, MD, Ibaraki, Japan
Luis Tata, MD, Amadora, Portugal
Eugene Tong, MD, Austin, Tex
William Torreggiani, MB, FFRRCSR, Dublin, Ireland
Baris Turkbey, MD, Ankara, Turkey
Meric Tuzun, Ankara, Turkey
Hiroyuki Ueda, Kyoto, Japan
Noriaki Usuki, Kobe, Japan
Jose R. Varela Romero, La Coruña, Spain
Mayra Veloso Soares, MD, Brasilia, Brazil
Geert Verswijvel, MD, Genk, Belgium
Joan C. (Kai) Vilanova, MD, Girona, Spain
Dr Silvio Alejandro Vollmer, Neuquen, Argentina
Ronald H. Wachsberg, MD, Newark, NJ
Yukari Wakabayashi, MD, Tokyo, Japan
Edward Williams, Jersey, Channel Islands, British Isles
Tatsuya Yamamoto, Tochigi, Japan
Sasan Yasharpour, MD, Staten Island, NY
Satoru Yoshida, MD, Muroran City, Japan
Joe Yut, Olathe, Kan
Jeffrey H. Zapolsky, MD, Oshkosh, Wis




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