|Year : 2014 | Volume
| Issue : 1 | Page : 54-56
Wandering spleen as acute abdomen
Basant Kumar1, Vijai D Upadhyaya1, Sheo Kumar2, Ram N Rao3
1 Department of Pediatric Surgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Department of Radio diagnosis, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
3 Department of Pathology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India
|Date of Web Publication||14-Jul-2014|
Department of Pediatric Surgery, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh
Source of Support: None, Conflict of Interest: None
Wandering spleen is a rare clinical entity that accounts for only 0.1-0.2% of all splenectomies. Early diagnosis and intervention is necessary for the preservation of the spleen, especially in children. However, most of the times in acute settings a precise clinical diagnosis is difficult because of its similarity of presentation with other causes of acute abdomen resulting in delayed diagnosis. We present a 12-year-old boy with left-sided abdominal pain following a fall from a bed. His abdominal examination revealed an enlarged tender spleen. Abdominal ultrasound and computed tomography showed enlarged spleen with multiple areas of infarction and thrombosis of the splenic vein. At laparotomy a diagnosis of torsion of a wandering spleen with infarction was confirmed and splenectomy done. We present the management of the patient with wandering spleen that presented as acute abdomen with lower abdominal mass and briefly review the literature.
Keywords: Acute abdomen, splenic torsion, splenopexy, wandering spleen
|How to cite this article:|
Kumar B, Upadhyaya VD, Kumar S, Rao RN. Wandering spleen as acute abdomen. Arch Int Surg 2014;4:54-6
| Introduction|| |
Wandering spleen is a rare clinical entity that accounts for only 0.1-0.2% of all splenectomies.  It occurs either due to laxity in supporting ligaments (in adult) or because of congenital abnormalities in the development of splenic supporting ligaments leading to incomplete or complete failure of splenic attachment with peritoneal surface. ,,,,, It allows the spleen to move freely in the abdominal cavity. Clinical presentation varies from asymptomatic, or asymptomatic mobile abdominal mass to acute abdomen caused by torsion of the vascular pedicle, well described in the literature. ,,,,, Early diagnosis and intervention is necessary for the preservation of the spleen, especially in children. However, most of the times, in acute settings it is impossible due to its similarity of presentation with other causes of acute abdomen resulting in delayed diagnosis. We present the management of a 12-year-old boy with wandering spleen that presented as acute abdomen with lower abdominal mass and briefly review the literature.
| Case Report|| |
A 12-year-old boy presented with complaints of pain and a progressively enlarging lump in the abdomen, 4 days after a trivial trauma following a fall from a bed. Pain was moderate, continuous, peri-umbilical, mostly over upper part of abdominal lump, non-colicky and non-radiating in nature. Pain had no relation with feeds and position. No other associated symptoms were noted except two episodes of fever and vomiting in last 4 days. He also had previous history of recurrent mild to moderate abdominal pain during running or playing in the past 5 years which resolves spontaneously after rest. He was pale, dehydrated and afebrile having blood pressure of 100/56 mm Hg, pulse rate 100 bpm and respiratory rate 20 breaths/min. On examination, the abdomen was not distended and no muscle guarding. There was peri-umbilical tenderness and a firm, tender mobile mass with a notch, in the mid and lower abdomen [Figure 1]. A clinical diagnosis of abdominal tumor with inta-tumoral bleed was made.
|Figure 1: Pre-operative photograph showing bulging in mid and lower abdomen due to enlarged wandering spleen|
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Laboratory results were all within the normal ranges, except decreased hematocrit (hemoglobin-8.3 g%). The plain abdominal radiograph was un-remarkable while abdominal ultrasonography with color Doppler showed empty splenic fossa, elongated splenic hilum with engorged and thrombosed splenic vessels. The spleen was massively enlarged of about 26 cm × 12 cm × 8 cm diameter. About 100 ml peri-splenic fluid with debris suggestive of blood was present. Contrast-enhanced computed tomography (CECT) of the abdomen revealed empty splenic fossa with enlarged spleen in the left lower abdomen and peri-splenic fluid. The splenic parenchyma showed multiple, poorly-enhanced areas, suggestive of infarction. No enhancement of the elongated splenic vascular pedicle (suggestive of thrombus formation) with whirlpool-appearance was detected [Figure 2]a-c. The pancreatic tail and liver were normal. A final diagnosis of wandering spleen with acute torsion of the vascular pedicle was made.
|Figure 2: Axial (a) and coronal images (b and c) of abdominal computed tomography-scan showing empty splenic fossa with whirl-sign at splenic hilum and enlarged wandering spleen reaching up to pelvis. Note the|
hypo intensity of spleen due to loss of vascularity (c)
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Child was resuscitated and emergency exploration performed. On exploration, the spleen was enlarged with multiple black patches over it. Peri-splenic collection of about 150 ml was present. Elongated splenic hilum was inflamed, thickened, appeared as a mass and was quite fragile [Figure 3]. Splenic pedicle was ligated carefully to avoid pancreatic injury but in spite of all care, bleeding started from the incised vascular pedicle. It was an arterial bleed probably occurred due to clot dislodgement. A blind 3-0 prolene suture was taken through pancreas to control the bleeding. Post-operative course was uneventful and child was discharged on the 8 th day. Histology showed congested spleen with multiple areas of necrosis with thrombosed vessels. He was vaccinated against Pneumococcus, Meningococcus and Haemophilus influenzae in post-operative period. After 1 year of follow-up, child is doing well.
|Figure 3: Operative picture showing enlarged spleen with multiple patchy areas of discolorations. Note the thick mass-like inflamed fragile splenic hilum|
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| Discussion|| |
Wandering spleen is an extremely rare clinical entity, characterized by splenic hyper mobility that results from elongation or mal-development of its suspensory ligaments. It is also known as aberrant, floating, displaced, prolapsed, ptotic, dislocated or dystopic spleen. , Ectopic spleen, splenosis and accessory spleens are separate clinical entities and must be distinguished from it.  Actual incidence of wandering spleen is unknown because of its asymptomatic presentation but an incidence of 0.16% is reported in the literature.  Male to female ratio is 1:1 below 10 years but after that, female predominates with ratio of 1:7; especially females within child bearing age (70-80%).  It occurs in two forms; congenital or acquired. ,,,,, Congenital mal-development or lack of splenic suspensory ligaments is responsible for almost all of the floating spleen in children less than 10 years of age. In adults, multiparity, female hormones and splenomegaly are considered as etiological factors for the acquired form of wandering spleen. ,,,,,
Clinical presentation varies from asymptomatic cases detected incidentally to acute abdomen due to vascular pedicle torsion and ischemia as occurred in our patient. However the most common presentation is an abdominal mass with non-specific abdominal symptoms or intermittent abdominal pain due to spontaneous rotation and de-rotation of the vascular pedicle. ,,,,, Diagnosis can be made by careful history and examination but most of the time it is missed because of rarity of condition. In our patient, there was typical history of recurrent abdominal pain during playing or running with spontaneous resolution after rest and on examination we palpated a tender mobile mass with a notch but we missed the diagnosis even with all these signs and symptoms. Child did not give history of previously detected abdominal lump and it is the factor which misguided us. We thought about intra-abdominal tumor with sudden intra-tumor bleed and never thought about wandering spleen during evaluation, but screening ultrasonography clinched the diagnosis.
Barium meal or enema may give indirect evidence of wandering spleen but is not used routinely. Ultrasonography with color Doppler and triple phase abdominal CECT is sufficient for diagnosis and plan for management. , Visceral angiography is usually not required. Isotope studies with Tc-99m sulfur colloid is usually used to visualize the vascularity of post-operative spleen after splenopexy for wandering spleen. , The recommended treatment of wandering spleen is operative; either splenopexy or splenectomy. , Recently, laparoscopic management is preferred over open splenopexy or splenectomy. ,,, Conservative management is traditional and reported to have very high complication rate up to 65%.  The reported complications in acute torsion of wandering spleen includes gangrene or splenic abscess, acute or recurrent pancreatitis, pancreatic tail necrosis, intestinal obstruction, gastric outlet obstruction, gastric volvulus, thrombocytopenia, hypersplenism and rarely variceal hemorrhage. ,,,,,,,
Progressive splenic enlargement is the unique feature in our case. It occurs probably because of early venous thrombosis followed by arterial thrombosis. Trivial trauma led to torsion of the vascular pedicle with congestive splenomegaly. Peri-splenic hemoperitoneum; occurred due to venous rupture or splenic rupture, causes peri-splenic inflammation resulted into mass-like, thrombosed and fragile splenic hilum. In conclusion, wandering spleen is rare but should be kept in mind, when investigating a "curious" abdominal mass presenting as acute abdomen, especially in young females and children. The diagnosis should be confirmed with abdominal ultrasound scanning or CECT and handle the splenic hilum with care during surgery.
| References|| |
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[Figure 1], [Figure 2], [Figure 3]