K.E.M. Radiology

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Seth G.S. Medical College and K.E.M. Hospital, Mumbai , India

Interventional Case Record

< Case 33 : February 2023 >

Contributed by : Harshitha Shetty

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Embolization of a spontaneous mesocaval shunt in a patient of liver cirrhosis and portal hypertension with recurrent episodes of hepatic encephalopathy

Introduction:

Liver cirrhosis causes increased intrahepatic vascular resistance to the portal flow leading to increased portal venous pressure and portal hypertension. Once portal hypertension develops, there is portosystemic collateral formation which can either be due to opening up of the pre-existing vessels or neo angiogenesis due to growth factors like VEGF (1, 2). These portosystemic collaterals divert a fraction of the portal blood into systemic circulation. With the progression of portal hypertension, these collaterals enlarge and form large vascular channels known as spontaneous portosystemic shunts (SPSS) (3). Though previously thought to be beneficial in decompressing the portal pressure, recent studies have shown an increased incidence of the development of hepatic encephalopathy, hepatorenal syndrome, gastroesophageal varices, ascites and spontaneous bacterial peritonitis (4). Large SPSS defined as those >8 mm diameter can be treated by embolization especially in the early stages (5).

Here, we describe a case of mesocaval shunt embolization in a patient presenting with recurrent episodes of hepatic encephalopathy.

Case presentation:

A 53 year old man, chronic alcoholic since the past 30 years, came with the complaints of altered sleep for one week in the form of excessive daytime sleepiness and tremors involving both upper limbs. The patient has had similar episodes occurring about every 20 days since the past six months for which he took some medications from a local practitioner, details of which were not available. There was no history of hematemesis/ malena/ jaundice/ altered sensorium. On examination, flaps were present in both upper limbs.(Video 1) An ultrasound of the abdomen showed altered echotexture of the liver suggestive of liver parenchymal disease with splenomegaly. LFTs showed Total bilirubin- 3 gm %, D. Bilirubin- 1.2 gm%, SGOT-73, SGPT-46, ALP-321. A contrast enhanced CT scan (Fig. 1) of the abdomen showed liver cirrhosis with portal hypertension (splenomegaly, portosystemic collaterals and minimal ascites). A serpiginous collateral was noted between the superior mesenteric vein and the IVC suggestive of a mesocaval shunt. Upper GI endoscopy showed small esophageal varices. A portosystemic shunt gram was performed which confirmed the presence of a mesocaval shunt at the level of L2 vertebral body from a tributary of SMV draining into IVC (Figure 1A and 1B). The patient was planned for mesocaval shunt embolization.

Video 1 : Flaps seen in the patient due to hepatic encephalopathy.

Fig 1 : Axial (Figure 1A) and coronal (Figure 1B) contrast enhanced CT images show a bunch of serpiginous tortuous collaterals connecting the tributary of the superior mesenteric vein with IVC suggestive of a mesocaval shunt.

An 8 Fr vascular access was taken through the right IJV. A 6 Fr Rabbe sheath was positioned at the opening of the mesocaval shunt in the IVC across the ostium. A 5 Fr SIM 1 catheter was placed deep in the collateral venous system. Shunt gram obtained by placing the catheter in the shunt with thelong sheath obstructing the shunt ostium shows retrograde filling of contrast into the collaterals which is seen draining into the portal vein confirming that it is a portosystemic shunt communicating the IVC with tributaries of SMV. Further selective canulation was performed using Terumo Progreat Microcatheter (Figure 2 and Video 2)

Figure 2: Portosystemic shunt gram shows the mesocaval shunt at the level of L2 vertebral body from a tributary of SMV draining into IVC.Teru

Video 2: Shunt gram taken by placing the catheter in the shunt and long sheath obstructing the shunt ostium shows retrograde filling of contrast into the collaterals which is seen draining into the portal vein confirming that it is a portosystemic shunt communicating the IVC with tributaries of SMV.

Multiple detachable coils both 0.035in and 0.018in system and COOK 0.035in pushable coils were used for the embolization of the mesocaval shunt. Check gram showed reflux of the contrast into IVC with non-filling of mesocaval shunt. (Figure 3A, 3B and Video 3)

Figure 3: Post-embolization shunt gram shows non-opacification of the mesocaval shunt with reflux of contrast into the IVC in the anteroposterior (Figure 3A) and lateral views (Figure 3B).

Video 3: Post-embolization check gram shows the reflux of the contrast into IVC with non-filling of mesocaval shunt.

Fig. 4 : Post-embolization axial (Figure 4A) and coronal (Figure 4B) contrast enhanced CT images show metallic artifacts of the embolization coils and non-opacification of the tortuous mesocaval shunt.

The patient tolerated the procedure well. No complications were encountered. The ward course was uneventful. MMSE examination was normal. The patient was afebrile, vitally stable and was discharged after 3 days.

Discussion:

Spontaneous portosystemic shunts are a marker of the severity of portal hypertension associated with higher mortality and complications including hepatic encephalopathy, variceal bleeding and portal vein thrombosis.

Spontaneous portosystemic shunts can be divided as left or right sided depending on their location with respect to the splenoportomesenteric confluence. The left sided include splenorenal shunt which is the most common portosystemic shunt, gastrorenal shunt and gastrocaval shunt. The right sided include recanalized paraumbilical vein which is commonly seen. The rare ones include mesocaval shunt, mesoazygous, portocaval, portorenal, mesoazygous and mesorenal shunts. (7,8).

Patients with cirrhosis and SPSS can develop hepatic encephalopathy in the absence of precipitating factors and stable liver functions due to bypass of the liver causing ineffective detoxification of ammonia and also due to decreased liver perfusion due to rerouting of the portal blood (9). Therefore, in the setting of recurrent or persistent hepatic encephalopathy, a large SPSS should be actively looked for. Shunt embolization is less invasive and is preferable over surgical treatments for patients with refractory hepatic encephalopathy (9). Large SPSS defined as >8mm diameter can be embolized through a variety of percutaneous endovascular techniques including balloon assisted retrograde transvenous occlusion (BRTO) and its modifications coil-assisted and plug-assisted retrograde transvenous obliteration (CARTO and PARTO). (10,11).

Studies show that the portal venous blood flow considerably increases in cirrhosis patients of Child Pugh class A and B after shunt embolization in 1-12 weeks. Improvement in the liver function measured by increase in serum albumin was also noted(12). However, in some patients who underwent shunt embolization worsening of portal hypertension was noted with new onset or worsening ascites and life threatening esophageal variceal bleeding. Therefore careful selection of patients for portosystemic shunt embolization is very important(13). One study concluded that to avoid the consequences of a sudden increase in portal pressure, embolization should be indicated only in patients with absent or mild esophageal varices and no signs of hepatic failure, such as ascites or jaundice(14).

A recent multicentre survey done by Laleman et al shows that shunt embolization in patients with a MELD < 11 has been shown to reverse chronic or recurrent hepatic encephalopathy and improve hepatic outcomes for at least a two-year follow-up(8). Further studies show that portosystemic shunt embolization result in reversal of hepatic encephalopathy in over 75% of cases. Mesocaval shunts are rare but when discovered have the potential for successful treatment with embolization that can lead to reversal and long-term clinical remission of hepatic encephalopathy (15).

Conclusion:

Large spontaneous portosystemic shunts are an ineffective compensatory mechanism and a marker of severe portal hypertension.

Early management of spontaneous portosystemic shunts with percutaneous endovascular embolization is beneficial in patients of liver cirrhosis with recurrent episodes of hepatic encephalopathy or variceal bleeding.

Careful selection of patients for portosystemic shunt embolization is required to prevent complications of worsening portal hypertension like life threatening acute esophageal bleeding and worsening ascites.

References:

1. Y. Iwakiri, “Pathophysiology of portal hypertension,” Clinics in Liver Disease, vol. 18, no. 2, pp. 281–291, 2014.

2. S. Bloom, W. Kemp, and J. Lubel, “Portal hypertension: pathophysiology, diagnosis and management,” Internal Medicine Journal, vol. 45, no. 1, pp. 16–26, 2015.

3. S. Nardelli, O. Riggio, S. Gioia, M. Puzzono, G. Pelle, and L. Ridola, “Spontaneous porto-systemic shunts in liver cirrhosis: clinical and therapeutical aspects,” World Journal of Gastroenterology, vol. 26, no. 15, pp. 1726–1732, 2020.

4. M. Sim´on-Talero, D. Roccarina, J. Mart´ınez et al., “Association between portosystemic shunts and increased complications and mortality in patients with cirrhosis,” Gastroenterology, vol. 154, no. 6, pp. 1694–1705, 2018.

5. C. A. Philips, S. Rajesh, P. Augustine, G. Padsalgi, and R. Ahamed, “Portosystemic shunts and refractory hepatic encephalopathy: patient selection and current options,” Hepatic Medicine: Evidence and Research, vol. 11, pp. 23–34, 2019.

6. A. Philips, A. Arora, R. Shetty, and V. Kasana, “A comprehensive review of portosystemic collaterals in cirrhosis: historical aspects, anatomy, and classifications,” International Journal of Hepatology, vol. 2016, Article ID

6170243, 15 pages, 2016.

7. R. Greinert, A. Zipprich, M. Sim´on-Talero et al., “Covert hepatic encephalopathy and spontaneous portosystemic shunts increase the risk of developing overt hepatic encephalopathy,”Liver International, vol. 40, no. 12, pp. 3093–3102, 2020.

8. 9 Rajesh S, Philips CA, Ahamed R, Abduljaleel JK, Nair DC, Augustine P. Friend or Foe? Spontaneous Portosystemic Shunts in Cirrhosis—Current Understanding and Future Prospects. Canadian Journal of Gastroenterology and Hepatology. 2021 Aug 12;2021.

9. 6 S. Nardelli, O. Riggio, L. Turco et al., “Relevance of spontaneous portosystemic shunts detected with CT in patients with cirrhosis,” Radiology, vol. 299, no. 1, pp. 133–140, 2021.

10. C. A. Philips, S. Rajesh, P. Augustine, G. Padsalgi, and R. Ahamed, “Portosystemic shunts and refractory hepatic encephalopathy: patient selection and current options,” Hepatic Medicine: Evidence and Research, vol. 11, pp. 23–34, 2019.

11. Y. Kako, K. Yamakado, W. Jomoto et al., “Changes in liver perfusion and function before and after percutaneous occlusion of spontaneous portosystemic shunt,” Japanese Journal of Radiology, vol. 35, no. 7, pp. 366–372, 2017.

12. S. Singh, P. S. Kamath, J. C. Andrews, and M. D. Leise, “Embolization of spontaneous portosystemic shunts for management of severe persistent hepatic encephalopathy,” Hepatology, vol. 59, no. 2, pp. 735-736, 2014.

13. Gupta S, Wong F, Sniderman K, Ryan S, Tsien C. A71 Mesocaval shunt embolization as a treatment for medically refractory hepatic encephalopathy in a patient with non-decompensated cirrhosis. J Can Assoc Gastroenterol. 2020 Feb;3(Suppl 1):84–5. doi: 10.1093/jcag/gwz047.070. Epub 2020 Feb 26. PMCID: PMC7043572.

14. Boixadera H, Tomasello A, Quiroga S, Cordoba J, Perez M, Segarra A. Successful embolization of a spontaneous mesocaval shunt using the Amplatzer Vascular Plug II. Cardiovasc Intervent Radiol. 2010 Oct;33(5):1044-8. doi: 10.1007/s00270-009-9739-8. Epub 2009 Nov 12. PMID: 19908090.

15. Sakurabayashi S, Sezai S, Yamamoto Y et al (1997) Embolization of portal-systemic shunts in cirrhotic patients with chronic recurrent hepatic encephalopathy. Cardiovasc Interv Radiol 20(2):120–124

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