Overview Traditionally, the most definitive option for treating active gastric variceal bleeding from splenic vein obstruction is splenectomy. Herein, we report a successful case of splenic vein stent placement to remedy sinistral portal hypertension with refractory gastric variceal bleeding resulting from splenic vein occlusion.
Splenic Vein Stent Placement For Refractory Gastric Variceal Bleeding
Amanda V Hayman, MD, Matthew J Fisher, MD, Robert K Ryu, MD, David J Bentrem, MD, Anton I Skaro, MD, Reed A Omary, MD
Departments of Surgery and Radiology, Northwestern University, Chicago, Illinois.
Contact: Amanda Hayman, MD E-mail
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Citation: Hayman AV, Fisher MJ, Ryu RK, Bentrem DJ, Skaro AI, and Omary RA. Splenic Vein Stent Placement For Refractory Gastric Variceal Bleeding. J Surg Radiol. 2010 Oct 1;1(2).
Received June 29, 2010. Accepted July 29, 2010. Epub August 5, 2010. Copyright: © 2010 Surgisphere Corporation. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
Contents - Introduction- Discussion - Disclosures - References |
Introduction
Splenic vein thrombosis (SVT) or occlusion has multiple etiologies, including chronic or acute pancreatitis, hypercoagulable and hemolytic states, portal hypertension, and extrinsic occlusion from an intraabdominal mass, either benign or malignant.1 The most common cause is pancreatitis, which has up to a 20% incidence of SVT.2 Other etiologies are less common, especially in the absence of portal vein thrombosis.
Splenic vein thrombosis or occlusion leads to splenomegaly and sinistral portal hypertension. Gastric varices develop as a consequence of elevated venous pressure within the short gastric veins, which are the remaining outflow of the spleen in the setting of SVT.3 Portal venous involvement can result in both esophageal and gastric varices in the region of the gastro-esophageal junction. Persistent gastric variceal (GV) bleeding from SVT poses a therapeutic challenge. Unlike esophageal varices (EV), GVs are not amenable to endoscopic intervention via banding, balloon tamponade,4 or esophageal stenting.5 Transjugular intrahepatic portosystemic shunts (TIPS), another tool used for persistent EV and GV bleeding from portal hypertension, is also ineffective, as the obstruction is proximal to the portal system, so-called sinistral portal hypertension.
Therapeutic options for persistent GV bleeding from SVT have classically been limited to splenectomy with or without distal pancreatectomy, splenic artery embolization, or, rarely, a distal splenorenal shunt. However, operative treatment can be technically difficult due to the presence of the varices and massive splenomegaly. To the best of our knowledge, we present the first known case report of successful splenic vein stent placement to treat persistent GV bleeding.
Case Report
A 42-year-old man with a past medical history of possible myelodysplastic syndrome presented to his primary care provider with a six-day history of melena. He had no history of peptic ulcer disease or heavy alcohol use. He developed hematemesis and was admitted for further workup. Upper endoscopy revealed active bleeding in the gastric fundus. A Dieulafoy lesion was suspected and was unsuccessfully clipped. He was transferred to our institution’s medical intensive care unit for further care. Prior to transfer he had received five units of blood in the previous 48 hours.
On physical exam, he had splenomegaly, was hemodynamically stable, and in no acute distress. Radiographic records from the referring institution included a duplex ultrasound record that showed a patent hepatic and portal venous system with hepatopedal flow, as well as splenomegaly with a longitudinal span of 17 cm. An abdominal and pelvic computed tomography scan again showed splenomegaly, as well as venous congestion without evidence of portal vein thrombosis or cirrhosis (Figure 1). On admission to the ICU, his laboratory studies included a hemoglobin level of 9.8 gm/dl, an international normalized ratio of 1.1, a serum lipase of 41 units/L (normal 7- 60), and a serum amylase of 212 units/L (normal 20-115).
Figure 1. Pre-procedure CT image of the splenic vein.
Due to ongoing need for blood transfusion and persistent, large volume hematemesis, the patient was brought emergently to the interventional radiology (IR) suite for diagnostic and potentially therapeutic evaluation. Celiac arteriography via the right common femoral artery showed no arterial extravasation. The splenic artery was accessed, showing patent arterial flow to the spleen. Delayed imaging demonstrated that the splenic vein was patent near the portal confluence, but distal patency was difficult to assess.
To better image the splenic vein closer to the splenic hilum, transhepatic portal vein access was obtained and the splenic vein accessed. A venogram showed a segmental occlusion of the splenic vein near the splenic hilum and filling of multiple gastric varices (see movies available online at www.SurgRad.com). A 0.014-inch diameter guidewire was placed across the lesion and angioplasty performed with a 5 mm diameter x 4 cm length balloon catheter.
Next, a 12 mm diameter x 60 mm length S.M.A.R.T.® stent (Cordis Endovascular, Miami Lakes, FL) was deployed and dilated using a 10 mm diameter balloon catheter. A completion venogram showed a widely patent stent without filling of any collateral branches (see movies available online at www.SurgRad.com). Patient was subsequently placed on full antiplatelet therapy (daily aspirin 325 mg and clopidogrel 75 mg.).
Subsequently, the patient had no more hematemesis, nor did he require any further blood transfusions. He was transferred out of the intensive care unit to the regular floor. Subsequent triphasic pancreatic computed tomography and a magnetic resonance cholangio-pancreatography scans were performed that demonstrated normal pancreas parenchyma with hypoenhancement of the pancreatic tail. Both studies were limited due to artifact from the stent. He was discharged hospital day six. The presumptive cause of his SVT was compression of the splenic vein from a distal pancreatic tail mass. He is scheduled to undergo endoscopic ultrasound as an outpatient.
Figure 2. Images showing intact arterial flow to the spleen and subsequent filling.
Figure 3. Images showing splenic vein occlusion near the hilum of the spleen.
Figure 4. Patency of the splenic vein demonstrated with stent in place within this vessel.
Figure 5. Closer view of the stent with contrast flowing through the splenic vein. This venogram was completed through transhepatic portal vein access with the catheter terminating near the splenic hilum.
Discussion
Previous reports have demonstrated success with stenting portal venous obstructions from gastrointestinal malignancies,6 for obliterating surgically created splenorenal shunts,7 or for repairing traumatic arteriovenous fistulae involving the splenic vein.8 Also, there have been many cases of iliac vein stenting for May-Thurner syndrome,9 caused by obstruction from the iliac vein. However, to be the best of our knowledge, this case represents the first known report of splenic venous stent placement for the treatment of actively bleeding gastric varices from isolated SVT.
Stenting the splenic vein is a quicker and much less invasive procedure than the alternative surgical options. It also avoids the risk of pancreatic leak that can complicate a distal pancreatectomy, as well as the increased risk of infection and sepsis after splenectomy. Drawbacks to stenting include the risk of contrast nephropathy and of stent occlusion, although this may be mitigated by antiplatelet medications. Further, if the patient fails endovascular therapy, he would likely require distal pancreatectomy and splenectomy after all, especially given the concern for a mass in the pancreatic tail. The presence of the stent could make the resection, especially if performed laparoscopically, technically more difficult as the margin would have to be more proximal on the splenic vein than is usual. The stent can also make the dissection more hazardous.
As our facility with interventional techniques increases, we will continue to expand the indications for venous stent placement to treat a wider variety of disorders and subsequently spare patients from potentially more morbid and invasive procedures.
Disclosures
The authors have no disclosures or conflicts of interest related to this manuscript.References
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