Should my patient with cirrhosis and esophageal varices be considered for partial splenic embolization?

 

Although limited, the weight of the evidence suggests that patients with cirrhosis and esophageal varices may benefit from partial splenic embolization (PSE).

A 2006 small randomized-controlled trial comparing PSE and endoscopic ligation vs. endoscopic ligation alone in patients with cirrhosis, thrombocytopenia and esophageal varices reported reduced risk of recurrence of varices, progression to variceal bleeding and death over a mean follow-up of 4.8 years. 1

A 2016 meta-analysis of PSE in the management of gastroesophageal variceal hemorrhage arrived at a similar conclusion with respect to reducing the risk of recurrence of varices, variceal hemorrhage and mortality. 2 The studies included in this meta-analysis, however, were small with only 1 randomized-controlled trial (RCT) in the series.

A 2019 small retrospective of patients undergoing transjugular intrahepatic portosystemic shunt (TIPS) placement with or without PSE found a significant benefit in primary shunt patency (period between placement and first shunt dysfunction), but not secondary shunt patency (period between placement and permanent shunt dysfunction) or mortality over a 5-year follow-up.3

Adverse effects of PSE include post-embolization syndrome—a constellation of symptoms such as fever, pain, and nausea/vomiting— reported in 78%-100% of patients. More severe complications up to 15%-30% may also occur with PSE, particularly when around 70% or more of splenic volume is embolized. These complications include pleural effusion/ascites, spontaneous bacterial peritonitis, pulmonary embolism, liver failure, portal vein thrombosis and splenic abscesses which may develop between 10 days to 3 months following the procedure.  Up to 6% of patients undergoing PSE may die of the procedure-related complications. 4-6  

For these reasons, careful selection of patient for PSE and limiting the extent of splenic necrosis to 50% with close monitoring of clinical and ultrasound follow-up, particularly in patients with a volume of splenic necrosis >50%,  have been suggested.6

 

Fun fact: Did you know that splenic embolization was first performed by Frank E. Maddison of Madison, Wisconsin, in 1973 using autologous clot to treat recurrent gastrointestinal hemorrhage arising from esophageal varies?

 

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References

 

  1. Ohmoto K, Yoshioka N, Tomiyama Y, et al. Improved prognosis of cirrhosis patients with esophageal varices and thrombocytopenia treated by endoscopic variceal ligation plus partial splenic embolization. Digestive Diseases and Sciences 2006;51:352-58. https://link.springer.com/article/10.1007/s10620-006-3137-8
  2. Wang P, Liu R, Tong L, et al. Partial splenic embolization has beneficial effects for the management of gastroesophageal variceal hemorrhage. Saudi J Gastroenterol 2016;22:399-406. http://europepmc.org/articles/PMC5184739/
  3. Wan Y-M, Li Y-H, Xu Z-Y, et al. Comparison of TIPS alone and combined with partial splenic embolization (PSE) for the management of variceal bleeding. European Radiology 2019; https://doi.org/10.100/s00330-019-06046-6
  4. N’Kontchou G, Seror O, Bourcier V, et al. Partial splenic embolization in patients with cirrhosis: efficacy, tolerance, and long-term outcome in 32 patients. Eur J Gastroenterol Hepatol 2005;17:179-84. https://www.ncbi.nlm.nih.gov/pubmed/15674095
  5. Hadduck TA, McWilliams JP. Partial splenic artery embolization in cirrhotic patients. World J Radiol 2014;28:6:160-168. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4037542/
  6. Smith M, Ray CE. Splenic artery embolization as an adjunctive procedure for portal hypertension. Semin Intervent Radiol 2012;29:135-39. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3444868/
  7. Maddison FE. Embolic therapy of hypersplenism. Invest Radiol 1973;8:280-281. https://journals.lww.com/investigativeradiology/Citation/1973/07000/Embolic_Therapy_of_Hypersplenism.54.aspx

 

Contributed in part by Theodore R. Pak, MD, PhD, Mass General Hospital, Boston, Massachusetts.

Should my patient with cirrhosis and esophageal varices be considered for partial splenic embolization?

Should I continue nadolol in my patient with cirrhosis and refractory ascites?

Under certain circumstances, you may need to! Although nonselective beta blockers (NSBBs), such as nadolol and propranolol, have been the cornerstone of medical treatment of portal hypertension in preventing variceal bleeding in patients with cirrhosis for decades, recent reports of their association with worsening survival, increased risk of hepatorenal syndrome and acute kidney injury in patients with refractory ascites or spontaneous bacterial peritonitis [SBP]) 1,2 have added controversy to their routine use in end-stage cirrhosis.

This is because patients with end-stage cirrhosis may be highly dependent on their cardiac output (particularly the heart rate) in maintaining an adequate arterial blood pressure 3-5 and the negative inotropic and chronotropic effects of NSBBs blunt this compensatory mechanism. The result is a drop in the cardiac output that may be particularly significant in the presence of conditions already associated with hypotension, such as sepsis, spontaneous bacterial peritonitis (SBP), or hemorrhage, further increasing the risk of renal hypoperfusion and hepatorenal syndrome.3

Although 2 meta-analysis studies failed to find an association between NSBBs and increased mortality among patients with cirrhosis and ascites, 6,7 serious concerns over the adverse effects of these drugs in at least a subset of patients has not waned.  Some have recommended reducing NSBB dose or discontinuing treatment in patients with refractory ascites or SBP and any of the following parameters: 4

  • Systolic blood pressure <90 mmHg
  • Serum creatinine >1.5 mg/dL
  • Hyponatremia <130 mmol/L

Similar recommendations were made by a 2015 consensus conference on individualizing the care of patients with portal hypertension.

In the absence of randomized-controlled studies, it seems prudent to proceed with more caution when using NSBBs in patients with end-stage cirrhosis and watch closely for any signs of hypotension or renal function deterioration.

References

  1. Serste T, Njimi H, Degre D, et al. The use of beta-lackers is associated with the occurrence of acute kidney injury in severe hepatitis. Liver In 2015;35:1974-82. https://www.ncbi.nlm.nih.gov/pubmed/25611961
  2. Mandorfer M, Bota S, Schwabl P, et al. Nonselective beta blockers increase risk of hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterol 2014;146:1680-90. https://www.sciencedirect.com/science/article/pii/S0016508514003060?via%3Dihub
  3. Garcia-Tsao G. The use of nonselective beta blockers for treatment of portal hypertension. Gastroenterol Hepatol 2017;13: 617-19. http://www.gastroenterologyandhepatology.net/archives/october-2017/the-use-of-nonselective-beta-blockers-for-treatment-of-portal-hypertension/
  4. Reiberger T, Mandorfer M. Beta adrenergic blockade and decompensated cirrhosis. J Hepatol 2017;66: 849-59. https://www.ncbi.nlm.nih.gov/pubmed/27864004
  5. Giannelli V, Lattanzi, Thalheimer U, et al. Beta-blockers in liver cirrhosis. Ann Gastroenterol 2014;27:20-26. https://www.ncbi.nlm.nih.gov/pubmed/24714633
  6. Facciorusso A, Roy S, Livadas S, et al. Nonselective beta-blockers do not affect survival in cirrhotic patients with ascites. Digest Dis Sci 2018;63:1737-46. https://link.springer.com/article/10.1007%2Fs10620-018-5092-6
  7. Njei B, McCarty TR, Garcia-Tsao G. Beta-blockers in patients with cirrhosis and ascites: type of betablocker matters. Gut 206;65:1393-4. https://gut.bmj.com/content/gutjnl/65/8/1393.full.pdf
  8. De Franchis R. Expanding consensus in portal hypertension. Report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.  J Hepatol 2015;63:743-52.  https://www.ncbi.nlm.nih.gov/pubmed/26047908  

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Should I continue nadolol in my patient with cirrhosis and refractory ascites?