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DOI: 10.1148/rg.232025110
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(Radiographics. 2003;23:305-308.)
© RSNA, 2003


AFIP ARCHIVES

Best Cases from the AFIP

Splenic Torsion1

Simmi Chawla, MD, Danielle K. B. Boal, MD, Peter W. Dillon, MD and Ronald T. Grenko, MD

1 From the Department of Radiology, Penn State University, Milton S. Hershey Medical Center, 500 University Dr, Hershey, PA 17033-0850. Received June 13, 2002; revision requested August 20 and received September 24; accepted September 25. Address correspondence to S.C. (e-mail: simmic@hotmail.com).

Index Terms: Spleen, CT, 775.1211 • Spleen, infarction, 775.795 • Spleen, US, 775.1298


    History
 Top
 History
 Imaging Findings
 Pathologic Evaluation
 Discussion
 References
 
A 4-year-old girl presented with a 2-day history of vomiting, abdominal pain, and fever. Physical examination showed a nondistended abdomen with good bowel sounds. There was moderate diffuse abdominal tenderness, more pronounced on the left side than on the right, with a palpable left upper quadrant mass. Laboratory data were remarkable for an elevated white blood cell count.


    Imaging Findings
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 History
 Imaging Findings
 Pathologic Evaluation
 Discussion
 References
 
Supine and upright abdominal radiographs revealed dilated loops of bowel without air-fluid levels or evidence of pneumoperitoneum. Abdominal computed tomography (CT) demonstrated an enlarged spleen without enhancement (Fig 1a). There was a marked degree of stranding within the region of the splenic hilum and a whorl of concentric arcs involving the splenic pedicle (Fig 1b). The splenic artery could not be followed to the splenic hilum. The pancreatic tail was displaced inferiorly and posteriorly (Fig 1c). In addition, there was a small left pleural effusion associated with posterior left lung atelectasis (not shown). Ultrasonography (US) revealed an enlarged spleen with a patchy heterogeneous echotexture. The spleen demonstrated multiple areas of hypo- and hyperechogenicity (Fig 2) and little Doppler flow.



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Figure 1a.  Abdominal CT scans obtained with intravenously and orally administered contrast material demonstrate an enlarged, nonenhancing spleen (a); stranding and a whorl of concentric arcs in the region of the splenic hilum (arrow) (b); and posterior, medial, and inferior displacement of the pancreatic tail (*) (c).

 


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Figure 1b.  Abdominal CT scans obtained with intravenously and orally administered contrast material demonstrate an enlarged, nonenhancing spleen (a); stranding and a whorl of concentric arcs in the region of the splenic hilum (arrow) (b); and posterior, medial, and inferior displacement of the pancreatic tail (*) (c).

 


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Figure 1c.  Abdominal CT scans obtained with intravenously and orally administered contrast material demonstrate an enlarged, nonenhancing spleen (a); stranding and a whorl of concentric arcs in the region of the splenic hilum (arrow) (b); and posterior, medial, and inferior displacement of the pancreatic tail (*) (c).

 


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Figure 2.  US image of the left upper quadrant demonstrates an enlarged spleen with a patchy, heterogeneous echotexture. There are multiple areas of hypo- and hyperechogenicity that represent areas of hemorrhage (clot), infarction, and congestion. The spleen is superior to the stomach (ST) and left kidney (LK).

 

    Pathologic Evaluation
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 History
 Imaging Findings
 Pathologic Evaluation
 Discussion
 References
 
The patient underwent splenectomy. The spleen was identified intraoperatively at the costal margin in the left upper quadrant of the abdominal cavity with a moderate amount of surrounding serous fluid (Fig 3a). The vascular pedicle was twisted at least 720° (Fig 3b). There were absolutely no attachments of the spleen to the abdominal wall or to the undersurface of the diaphragm. The pancreas was normal. A counterclockwise rotation was used to derotate the spleen. Upon reduction of the torsion, aberrant vascular anatomy was noted. The splenic vessels appeared to originate from the middle colic artery, and a narrow splenic pedicle was noted. Gross pathologic examination revealed an enlarged spleen that measured 11.0 x 8.0 x 5.4 cm and was congested and dusky (Fig 4). Thrombosis of the hilar vessels was noted. The texture of the spleen was heterogeneous, a finding that corresponded to the heterogeneous echotexture seen at US. Histopathologic evaluation of the spleen revealed nearly complete infarction of the parenchyma except for small islands of residual white matter. Marked splenic congestion was also evident (Fig 5a). Thrombosis of the hilar veins was confirmed and appeared to be acute without histologic evidence of organization or recanalization (Fig 5b).



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Figure 3a.  Intraoperative photographs demonstrate an enlarged, engorged spleen with no tethering visceral attachments (a) and torsion of the vascular pedicle of at least 720° (b). The arc of pink tissue to the left (arrow) represents the colon, and the purple tissue superiorly (*) represents the stomach.

 


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Figure 3b.  Intraoperative photographs demonstrate an enlarged, engorged spleen with no tethering visceral attachments (a) and torsion of the vascular pedicle of at least 720° (b). The arc of pink tissue to the left (arrow) represents the colon, and the purple tissue superiorly (*) represents the stomach.

 


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Figure 4.  Photograph of the enlarged, engorged spleen (split longitudinally) demonstrates a large area of central hemorrhage and irregular texture that corresponds to the echotexture seen at US (cf Fig 2).

 


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Figure 5a.  (a) Photomicrograph of the spleen reveals nearly complete infarction of the parenchyma and marked splenic congestion with necrosis. (b) Photomicrograph of the spleen helps confirm thrombosis of the hilar vessels.

 


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Figure 5b.  (a) Photomicrograph of the spleen reveals nearly complete infarction of the parenchyma and marked splenic congestion with necrosis. (b) Photomicrograph of the spleen helps confirm thrombosis of the hilar vessels.

 
The radiologic, intraoperative, and histopathologic findings were all consistent with splenic infarction secondary to torsion.


    Discussion
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 History
 Imaging Findings
 Pathologic Evaluation
 Discussion
 References
 
Splenic torsion is a rare cause of acute or recurrent abdominal pain. A hypermobile spleen is caused by the absence or abnormal development of the splenic suspensory ligaments, either of which predisposes the spleen to torsion. The splenic ligaments include the gastrolienal and lienorenal ligaments. The former attaches the spleen to the greater curvature of the stomach, whereas the latter attaches the spleen to the posterior abdominal wall; both ligaments attach to the hilum of the spleen medially (1). The phrenicocolic ligament supports the spleen inferiorly.

Incomplete development or laxity of the anchoring ligaments of the spleen leads to splenic hypermobility, which causes the spleen to "wander" and to assume an ectopic position (2,3). The spleen typically migrates inferiorly and is usually intraperitoneal (2). Many investigators believe that incomplete fusion of the dorsal mesogastrium (from which the spleen and the pancreatic tail develop) with the peritoneum that overlies the left kidney contributes to hypermobility. Intraperitoneal inclusion of the pancreatic tail in a number of reported cases of wandering spleen supports this belief (2). Normal fusion causes both the spleen and the pancreatic tail to be retroperitoneal (2,3). Other causes of splenic hypermobility include postpartum laxity, splenomegaly, previous abdominal trauma, and surgery (4).

Splenic torsion is rare, having been diagnosed in approximately 0.3% of 1,413 cases of splenectomy in one study (5). Most of the splenectomies in this survey were performed for reasons other than acute, chronic, or recurrent abdominal pain. Instead, most were performed for hematologic disease, such as congenital hemolytic anemia or idiopathic thrombocytopenia (5). Symptoms of splenic torsion vary depending on the degree of torsion. Mild torsion manifests as chronic abdominal pain associated with splenic congestion, moderate torsion as severe intermittent abdominal pain related to intermittent rotation and derotation, and severe torsion as an acute abdomen caused by acute torsion with infarction and mass effect on adjacent organs (3,6). Torsion can vary from 90° to 2,160°. Pain is caused by capsularstretching and local peritonitis (4). At radiography, if the spleen is intraperitoneal, it may appear as a large, central abdominal mass or as a mass in the left flank (7). Color Doppler US shows decreased perfusion of the spleen, whether the spleen is ectopic or, as in this case, in the left upper quadrant. The spleen is enlarged, with a patchy, heterogeneous echotexture that represents areas of infarction and congestion (8). CT findings include splenic enlargement from engorgement with little or no contrast material enhancement (8,9). Swischuk et al (2) describe twisting of the pedicle with or without twisting of the pancreatic tail as having a whorled appearance, a finding that is valuable in making the diagnosis at CT. The current recommended treatment for splenic torsion associated with infarction is splenectomy (3,7).

The patient in this case had an uneventful recovery after undergoing splenectomy. The Infectious Disease Service was consulted, and the patient was given Haemophilus influenzae B, meningococcal, and pneumococcal vaccinations. Long-term prophylactic antibiotic therapy was initiated.


    Footnotes
 
Editor's Note.— Everyone who has taken the course in radiologic pathology at the Armed Forces Institute of Pathology (AFIP) remembers bringing two beautifully illustrated cases for accession to the Institute. In recent years, the staff of the Department of Radiologic Pathology has judged the "best cases" by organ system, and recognition is given to the winners on the last day of the class. With each issue of RadioGraphics, one or more of these cases are published, written by the winning resident. Radiologic-pathologic correlation is emphasized, and the causes of the imaging signs of various diseases are illustrated.


    References
 Top
 History
 Imaging Findings
 Pathologic Evaluation
 Discussion
 References
 

  1. Moore KL. The abdomen. In: Satterfield TS, eds. Clinically oriented anatomy. 3rd ed. Baltimore, Md: Williams & Wilkins, 1992; 127-242.
  2. Swischuk LE, Williams JB, John SD. Torsion of wandering spleen: the whorled appearance of the splenic pedicle on CT. Pediatr Radiol 1993; 23:476-477.[CrossRef][Medline]
  3. Balm R, Willekens FGJ. Torsion of a wandering spleen. Eur J Surg 1993; 159:249-251.[Medline]
  4. Peitgen K, Schweden K. Management of intermittent splenic torsion ("wandering spleen"): a review. Eur J Surg 1995; 161:49-52.[Medline]
  5. Eraklis AJ, Filler RM. Splenectomy in childhood: a review of 1413 cases. J Pediatr Surg 1972; 7:382-388.[CrossRef][Medline]
  6. Robinson AP. Wandering spleen: case report and review. Mt Sinai J Med 1988; 55:428-434.[Medline]
  7. Gordon DH, Burrell MI, Levin DC, Mueller CF, Becker JA. Wandering spleen: the radiological and clinical spectrum. Radiology 1977; 125:39-46.[Abstract]
  8. Nemcek AA, Miller FH, Fitzgerald SW. Acute torsion of a wandering spleen: diagnosis by CT and duplex Doppler and color flow sonography. AJR Am J Roentgenol 1991; 157:307-309.[Free Full Text]
  9. Herman TE, Siegel MJ. CT of acute splenic torsion in children with wandering spleen. AJR Am J Roentgenol 1991; 156:151-153.[Free Full Text]




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