Splenic infarction is a rare clinical entity. Pancreas is a retroperitoneal organ in proximity to the spleen. The hypercoagulability that can occur during acute pancreatitis episodes and the pancreatic inflammatory process itself can affect neighboring vessels and produce vascular complications such as thrombosis or the formation of pseudoaneurysms. The thrombotic occlusion of splenic blood vessels may result in organ infarction. However, there was no splenic artery or venous thrombosis in the imaging findings of this patient. The presence of splenic infarct without any evident vessel thrombosis in the patient, further complicated by alcoholic hepatitis, portal hypertension, gastric, and paraesophageal varices merits a discussion of the case.
A 45-year-old male presented to the emergency department of the hospital with epigastric pain radiating to the back. He had a history of chronic alcohol abuse with no associated comorbidities.
Laboratory investigations revealed hemoglobin 10 g%, white cell count 14,000 per mm3, with 86% neutrophils, serum amylase 733 U/L, serum bilirubin 2 mg/dL, serum glutamic-oxaloacetic transaminase 150 U/L, and serum glutamic-pyruvic transaminase 211 U/L.
Contrast-enhanced computed tomography (CT) abdomen was done which revealed enlarged distal body and tail of pancreas with an irregularly marginated nonenhancing pancreatic parenchyma in the tail region, consistent with pancreatic necrosis (<30%). There was blurring of pancreatic margins with peripancreatic fat stranding and peripancreatic collections in relation to splenic hilum. Inflammatory changes extended to the splenic flexure in the form of colonic wall thickening. Nonenhancing areas were seen in the spleen in the anterior polar region: consistent with splenic infarct. Spleen measured more than 13 cm in span. Multiple dilated varices were seen in the left upper quadrant in communication with splenic vein. Gastric varices and paraesophageal varices were also noted. The portal vein measured up to 18 mm in diameter. The portal vein, superior mesenteric vein, splenic vein, and splenic artery demonstrated normal contrast opacification with no filling defects. The liver showed normal size and contrast enhancement with normal outline. The Modified CT Severity Index score of the patient was calculated to be 8/10.
Following [Figures 1-6] demonstrate the imaging findings from axial sections of CECT Abdomen relevant to the case.
The patient was managed conservatively in intensive care unit setting and gradually improved after 2 weeks. He was discharged to regular follow-up on outpatient department basis with strict instructions to abstain from alcohol.
Splenic infarction is the result of arterial and venous compromise in the splenic vessels, either intraluminal or extraluminal.
Various mechanisms have been described for splenic infarction in the course of acute pancreatitis. The most common cause is splenic vein thrombosis by direct extension of local inflammatory process or by hypercoagulable state induced by pancreatitis. It has been reported that vascular complications are significantly more common in alcohol-induced pancreatitis than in gallstone-induced pancreatitis. Thrombosis of the splenic vein develops because intrinsic damage to the intima of the vein occurs after inflammatory disease. However, in our patient, there was no luminal occlusion or identifiable narrowing/spasm of splenic vessels that would explain the etiology of spontaneous splenic infarct.
Further, congestive splenomegaly is a frequent finding in patients with portal hypertension. However, spontaneous splenic infarction has been rarely reported as a complication of portal hypertension. In a review of a large series of patients with splenic infarction, only 3 of 152 cases were the result of portal hypertension.
In view of the lack of evidence regarding the involvement of splenic vessels, it can be postulated that splenic infarct in our patient was due to hemodynamic changes leading to anoxia, rather than organic occlusion of splenic vasculature. First, an increase in the intravascular coagulability of splenic vessels secondary to pancreatitis can be a factor responsible for the areas of splenic infarction. Second, splenomegaly results from portal hypertension, and this is believed to increase splenic oxygen requirements disproportionate to the body’s oxygen delivering capacity. Consequently, the spleen suffers anoxic injury and subsequent infarction.
It is imperative that despite being a relatively infrequent complication, splenic infarct must be considered in the list of serious complications, arising out of multifactorial etiology in such complicated cases involving portal hypertension, acute pancreatitis, gastroesophageal varices, and alcoholic hepatitis.
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