Case Report
 
Atraumatic rupture of spleen
 
Ashish Kumar Jha, Rupesh Pokharna,Sandeep Nijahwan, Subhash Nepalia, Pankaj Jain, Arya Suchismita, Bharat Sapra, Amit Mathur
Department of Gastroenterology,
SMS Medical College, Jaipur, India


Corresponding Author
: Ashish Kumar Jha
Email: ashishjhabn@yahoo.co.in


Abstract

Splenic rupture is a rare life threatening complication usually occurring after trauma. Atraumatic splenic rupture (ASR) can occur in diseased (pathologic rupture) or normal spleen (spontaneous rupture).[1,2,3] ASR is associated with varied etiologies including, neoplastic, infectious, inflammatory, noninfectious, drug-and treatment-related and mechanical disorders.[1,2,3] A recent study showed secondary metastatic neoplastic disorders and pancreatitis to be associated in 3.8% and 9.2% of ASR respectively.[2]

We report here two cases of ASR. The first case describes ASR subsequent to disseminated duodenal adenocarcinoma, while the second is a rare case of acute on chronic pancreatitis. To the best of our knowledge the former is the first case of its kind to be reported in literature.

Case 1

A 68 year old male presented with history of severe abdominal pain in left hypochondrium and epigastrium. There was no history of trauma. He had tachycardia, pallor and mild tenderness in left hypochondrium. His hemoglobin was 6.5 gm/dl and serum alkaline phosphatase (SAP) level raised by 1.5 times. Contrast enhanced computed tomography (CECT) scan (Figure 1) showed a large subcapsular splenic hematoma and dilatation of biliary radicals.

Esophagogastroduodenoscopy revealed an irregular ulcer of less then 1cm size in second part of duodenum (D2). Histopathological examination (H&E) of biopsy from the ulcer showed chronic inflammatory cells without any evidence of malignancy. The patient was instituted intravenous fluids, analgesics, proton pump inhibitor, antibiotics and blood transfusion. The patient showed clinical improvement and reduction in the size of the hematoma and was discharged on treatment for H. pylori infection and analgesics.

Six weeks later, he presented with vomiting suggestive of gastric outlet obstruction (GOO). He also had mild pain in his right flank and right hip. His hemoglobin was 8.5 gm/dl and SAP level raised by 3 times. Esophagogastroduodenoscopy revealed polypoidal lesion with friability in the D2 segment. Histopathology of the duodenal lesion showed moderately differentiated duodenal adenocarcinoma. CECT scan with angiography showed infiltrative growth involving second and third part of duodenum, circumferential thickening of gastric wall, dilatations of common bile duct (CBD), biliary radicals and main pancreatic duct (MPD), perinephric and retroperitoneal collection encasing the right renal hilum, destructive lesion in right femoral head and small resolving splenic haematoma. A diagnosis of disseminated duodenal adenocarcinoma with femoral head metastasis and resolving splenic hematoma was made. Treatment options including palliative surgery, chemotherapy and enteral stenting were not opted because of his poor general condition and refusal to give consent. Patient was managed with feeding jejunostomy, analgesics and nutritional supplements. Five weeks later, the patient died because of general debility.


Case 2

A 45 year old chronic alcoholic male presented with six days history of moderate epigastric pain radiating to the back and two days history of sudden, severe left hypochondrial pain radiating to the left shoulder. There was no history of trauma. His two-month old medical records revealed hemoglobin of 11gm/dl and ultrasonographic evidence of chronic pancreatitis. He had tachycardia, pallor and tender left hypochondrium and epigastrium. His hemoglobin was 4.5 gm/dl and serum amylase raised by 2.5 times. CECT scan showed a 8 × 10 × 10 cm3 heterogeneous lesion along the splenic capsule compressing the spleen and the posterior wall of stomach, mild atrophic pancreas with dilated MPD and presence of fluid along the pancreatic tail, ascites and left sided pleural effusion. Peritoneal fluid aspiration revealed hemoperitoneum. He required laparotomy which revealed a hematoma extending from splenic parenchyma through the capsule into the perisplenic area (Figure 2) and presence of free fluid along the edematous pancreatic tail. Splenectomy was performed with satisfactory postoperative course. Pathological study showed capsular disruption with adherent blood clots, subcapsular hemorrhage and a tear in the spleen tissue with hemorrhages. He is currently on alcohol deaddiction therapy, pancreatic enzyme supplements and oral analgesics and is under our follow up since last four months.


Discussion

ASR associated with neoplasms are mostly caused by hematological malignancies however, malignancies of various solid organs like ovary, lungs, skin, stomach, liver, pancreas, urinary bladder, prostate, rectum and breast have been rarely described.[1,2,3] There is no case report of ASR associated with duodenal adenocarcinoma. The pathological processes described for ASR in hematological malignancies include capsular distention due to infiltration of the splenic parenchyma and capsule, coagulation defects and splenic infarct with subsequent capsular hemorrhage.[1,4,5] However, the mechanisms implicated in solid tumors are direct invasion or metastases and disruption of the splenic blood flow secondary to thrombosis.[1,6]

Duodenal adenocarcinoma is a rare gastrointestinal malignancy, having tendency of local invasion and metastasis commonly to lymph nodes, liver, peritoneum and lung. At presentation, over 45% of patients may have metastasis.[7] The systemic spread of tumor cells into the spleen is the possible explanation of rupture. Metastasis to bone is unusual and the locations of bone metastases are not well described.[8,9] We did not find any report of metastasis to femoral head.ASR is a rare complication of pancreatitis.[10,11,12,13] The exact etiology and natural history of this complication is not well described. The likely mechanisms of splenic rupture in pancreatitis include splenic vessels thrombosis, dissection of a pseudocyst into the splenic hilum, splenic artery pseudoaneurysm erosion by the pseudocyst contents, extension of the inflammatory process from the pancreatic tail into the splenic hilum and perisplenitis.[11] Treatment strategies for ASR include total splenectomy, organ-preserving surgery or conservative measures.[2] ASR carries a mortality rate of 12.2%, but splenomegaly, advancing age and neoplastic disorders are associated with higher mortality.[2]

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