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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 4  |  Issue : 1  |  Page : 38-39

Portosystemic encephalopathy in a noncirrhotic patient treated by vascular plug embolization of mesoiliac shunt


Department of Radiodiagnostics and Medical Imaging, Prince Sultan Military Medical City, Riyadh, Saudi Arabia

Date of Submission09-Aug-2019
Date of Acceptance28-Oct-2019
Date of Web Publication12-Dec-2019

Correspondence Address:
Othman Alshehre
Department of Radiodiagnostics and Medical Imaging, Prince Sultan Military Medical City, Riyadh
Saudi Arabia
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/AJIR.AJIR_19_19

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  Abstract 


Mesoiliac shunts in the absence of liver cirrhosis are rarely reported as a cause of hyperammonemia with encephalopathy. Here, we report the case of a 65-year-old female patient with no history of liver disease, who developed significant confusion. Workup showed hyperammonemia and encephalopathy due to spontaneous mesoiliac shunt with no imaging signs of portal hypertension. Liver biopsy showed no evidence of cirrhosis. The shunt was occluded using a vascular plug, resulting in complete resolution of symptoms with no recurrence at 8-year follow-up.

Keywords: Embolization, hepatic encephalopathy, mesoiliac shunt, portal hypertension, portosystemic shunts, shunt occlusion


How to cite this article:
Alshehre O, Alahmari F, Alammari S, Almathami A, Alobaidi H, Alrashidi I, Alosaimi M, Garad F. Portosystemic encephalopathy in a noncirrhotic patient treated by vascular plug embolization of mesoiliac shunt. Arab J Intervent Radiol 2020;4:38-9

How to cite this URL:
Alshehre O, Alahmari F, Alammari S, Almathami A, Alobaidi H, Alrashidi I, Alosaimi M, Garad F. Portosystemic encephalopathy in a noncirrhotic patient treated by vascular plug embolization of mesoiliac shunt. Arab J Intervent Radiol [serial online] 2020 [cited 2020 Apr 3];4:38-9. Available from: http://www.arabjir.com/text.asp?2020/4/1/38/272861




  Introduction Top


Portosystemic shunts without liver disease could be potentially induced by abdominal trauma, prior surgery, and postnatal viral or hepatotoxic injuries. Congenital shunts are related to incomplete involution of the omphalomensenteric venous system.[1]


  Case Report Top


A 65-year-old female patient presented to the emergency department with acute confusion, lethargy, dysarthria, nausea, and vomiting. Brain computed tomography (CT) showed no acute intracranial lesions. Serum ammonia level was elevated at 119 μmol/L (normal range: 11–32 μmol/L). There was slight elevation in transaminases (aspartate aminotransferase [AST] 59 U/L and alanine aminotransferase [ALT] 56 U/L) with normal total bilirubin (13 μmol/L).

Abdominal CT revealed a patent portal vein and an enlarged superior mesenteric vein with a 10-mm portosystemic shunt connecting the superior mesenteric vein to the right common iliac vein [Figure 1] and [Figure 2].
Figure 1: Computed tomography images of the mesoiliac shunt at inflow (superior mesenteric vein) and outflow (right common iliac vein)

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Figure 2: Angiographic images of the mesoiliac shunt before (a) and after intervention (b)

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Through left common femoral vein access, the shunt was catheterized [Figure 3] with 65-cm long, 7-Fr sheath that was used for the deployment of Amplatzer Vascular Plug (18 mm × 14 mm) near the shunt inflow. This resulted in complete remission of symptoms and normalization of transaminases (AST 19 U/L and ALT 14 U/L) and ammonia level at 44 μmol/L without additional medical therapy. The patient remained free of symptoms after 8-year follow-up.
Figure 3: Three-dimensional reconstructed computed tomography image of the mesoiliac shunt (a) and postintervention coronal computed tomography image (b)

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  Discussion Top


Liver cirrhosis is the most common cause of hepatic encephalopathy (HE). It leads to portal-systemic venous shunts, in which the neurotoxic substances, such as ammonia, bypass the liver into the systemic circulation, affecting the brain.[2] However, there are various less frequent causes of high ammonia level not associated with liver disease such as high protein diet, constipation, and gastrointestinal bleeding.[2],[3],[4],[5]

In our case, all the common causes of liver disease and causes of hyperammonemia in the absence of liver disease were excluded, and porto-systemic shunt was diagnosed on the basis of CT findings.

Interventional radiology treatment was first attempted by Nagino et al. in 1992 using fibrin glue to close a large shunt between the inferior mesenteric vein and the internal iliac vein; this offered amelioration of hypoproteinemia and reduction of serum ammonia levels without any complications.[3]

Other similar cases of noncirrhosis-related HE reported in literature were treated with percutaneous occlusion using coils to treat inferior mesenteric-caval shunt in patients with disturbed consciousness and Amplatzer plug for spontaneous spleno-renal shunt in patients presented with confusion and violent behavior. Plug and coils were used in combination to close inferior mesenteric-caval shunt in patients with relapsing confusion, lethargy, and dysartheria.[4],[5]

Endovascular approaches represented an alternative treatment option to the usual surgical ligation.[6]


  Conclusion Top


Extrahepatic portosystemic shunts are rare, but should be considered in patients presenting with altered consciousness and an elevated ammonia level in the absence of liver disease. In portosystemic shunts associated with encephalopathy, endovascular embolization may provide complete remission.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that her name and initial will not be published, and due efforts will be made to conceal her identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Raskin NH, Price JB, Fishman RA. Portal-systemic encephalopathy due to congenital intrahepatic shunts. N Engl J Med 1964;270:225-9.  Back to cited text no. 1
    
2.
Watanabe A. Portal-systemic encephalopathy in non-cirrhotic patients: Classification of clinical types, diagnosis and treatment. J Gastroenterol Hepatol 2000;15:969-79.  Back to cited text no. 2
    
3.
Nagino M, Hayakawa N, Kitagawa S, Katoh M, Komatsu S, Nimura Y, et al. Interventional embolization with fibrin glue for a large inferior mesenteric-caval shunt. Surgery 1992;111:580-4.  Back to cited text no. 3
    
4.
Otake M, Kobayashi Y, Hashimoto D, Igarashi T, Takahashi M, Kumaoka H, et al. An inferior mesenteric-caval shunt via the internal iliac vein with portosystemic encephalopathy. Intern Med 2001;40:887-90.  Back to cited text no. 4
    
5.
Rogal SS, Hu A, Bandi R, Shaikh O. Novel therapy for non-cirrhotic hyperammonemia due to a spontaneous splenorenal shunt. World J Gastroenterol 2014;20:8288-91.  Back to cited text no. 5
    
6.
Ali S, Stolpen AH, Schmidt WN. Portosystemic encephalopathy due to mesoiliac shunt in a patient without cirrhosis. J Clin Gastroenterol 2010;44:381-3.  Back to cited text no. 6
    


    Figures

  [Figure 1], [Figure 2], [Figure 3]



 

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Discussion
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