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?

My patient with cirrhosis has hypohonia and cogwheel rigidity. Is there a connection between cirrhosis and Parkinson’s disease?

There is a high prevalence of extra-pyramidal or Parkinson-like (PL) clinical findings in patients with cirrhosis. In fact, over 75% of patients with cirrhosis may exhibit PL signs, such as tremor, rigidity, and akinesia, with 88% also showing hyperintensity in the globus pallidus of basal ganglia on T1-weighted brain MRI.1

What’s even more interesting is the similarity between PL clinical and MRI findings among patients with cirrhosis and those with Manganese (Mn) toxicity.2,3 More specifically, similar MRI findings involving the globus pallidus have been reported in Mn-exposed workers, patients with cirrhosis, and those undergoing total parenteral nutrition with excessive Mn replacement. 4 These observations seem more than coincidental as 67% of patients with cirrhosis have been reported to have elevated blood Mn concentrations, with significantly higher levels in patients with previous portacaval anastomoses or transjugular intrahepatic portosystemic shunt (TIPS).1

Mn-induced parkinsonism is distinguishable from classic Parkinson’s disease in several ways, including the absence of Lewy bodies, more frequent dystonia, and less resting tremor.5 Also, remember that Mn-induced PL disease does NOT respond to L-dopa, a drug used to treat early stages of PD. 5 This finding can be explained by the fact that, in contrast to Parkinson’s disease where many of the dopamine-producing cells in the substantia nigra of the brain degenerate resulting in dopamine deficiency, in Mn-induced PL disease the problem is release of dopamine into synapses not its production.5

Bonus Pearl: Did you know that due to its paramagnetic properties, manganese can be effectively seen by MRI!

References

  1. Spahr L, Butterworth RF, Fontaine S, et al. Increased blood manganese in cirrhotic patients: relationship to pallidal m agnetic resonance signal hyperintensity and neurological symptoms. Hepatology 1996;24:1116-1120. https://www.ncbi.nlm.nih.gov/pubmed/8903385
  2. Hauser RA, Zesiewicz TA, Rosemurgy AS, et al. Manganese intoxication and chronic liver failure. Ann Neurol 1994;36:871-75. https://www.ncbi.nlm.nih.gov/pubmed/7998773
  3. Krieger S, Jaub M, Jansen O, et al. Neuropsychiatric profile and hyperintense globus pallidus on T1-weighted magnetic resonance images in liver cirrhosis. Gastroenterol 1996;111:147-55. https://www.ncbi.nlm.nih.gov/pubmed/8698193
  4. Lucchini R, Albini E, Placidi D, et al. Brain magnetic resonance imaging and manganese exposure. Neurotoxicity 2000;21:769-75. https://www.ncbi.nlm.nih.gov/pubmed/11130281
  5. Kwakye GF, Paoliello MMB, Mukhopadhyay S, et al. Manganese-induced parkinsonism and Parkinson’s disease: Shared and distinguishable features. Int J Environ Res Public Health 2015;12;7519-40. https://www.ncbi.nlm.nih.gov/pubmed/26154659

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My patient with cirrhosis has hypohonia and cogwheel rigidity. Is there a connection between cirrhosis and Parkinson’s disease?