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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
CASE REPORT  
Year : 2021  |  Volume : 32  |  Issue : 1  |  Page : 255-260
Partial Splenic Embolization for Hypersplenism Associated with Steatohepatitis in a Hemodialysis Patient


1 Department of Medicine, Faculty of Medicine, Kuwait University, Kuwait
2 Department of Radiology, Nephrology Unit, Amiri Hospital, Ministry of Health, Kuwait
3 Department of Medicine, Nephrology Unit, Amiri Hospital, Ministry of Health, Kuwait

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Date of Web Publication16-Jun-2021
 

   Abstract 


Hypersplenism (HS) is a disorder characterized by a triad of splenomegaly, peripheral cytopenia due to premature destruction of blood cells and normocellular bone marrow. Its etiology is diverse and includes (a) primary autoimmune cytopenias, (b) secondary to congestion due to portal hypertension in cirrhosis and, other causes such asperiportal fibrosis, infections, autoimmune diseases, lymphoproliferative disorders, infiltrative diseases and hemolytic anemias. The latter diseases are common in patients with end-stage kidney disease. In severe cases, co-existence of multiple co-morbid conditions, coagulopathy of uremia and dialysis-anticoagulation, and their immunosuppressive state render surgical splenectomy at highrisk. Mid-segment partial splenic infarction and with an aim at 50%–70% splenic volume loss was shown to be a less invasive therapy for HS. In our case report, we describe its first successful trial in a hemodialysis patient with severe HS due to cirrhosis.

How to cite this article:
El-Reshaid K, Alabdulghani F, Al-Bader S. Partial Splenic Embolization for Hypersplenism Associated with Steatohepatitis in a Hemodialysis Patient. Saudi J Kidney Dis Transpl 2021;32:255-60

How to cite this URL:
El-Reshaid K, Alabdulghani F, Al-Bader S. Partial Splenic Embolization for Hypersplenism Associated with Steatohepatitis in a Hemodialysis Patient. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2021 Dec 8];32:255-60. Available from: https://www.sjkdt.org/text.asp?2021/32/1/255/318535



   Introduction Top


Hypersplenism (HS) is a disorder characterized by a triad of splenomegaly, peripheral cytopenia due to premature destruction of blood cells and normocellular bone marrow. Its etiology is diverse and includes: (a) primary autoimmune cytopenias, (b) secondary to congestion due to portal hypertension in cirrhosis and periportal fibrosis, and other causes such as infections, autoimmune diseases, lymphoproliferative disorders, infiltrative diseases, and hemolytic anemias.[1] While supportive blood transfusions and treatment of the underlying cause/s are essential in its early management, most cases present at late stage of disease and/or not amenable to therapy. Radiotherapy for HS can only increase the platelet counts but not increase white and red blood cells.[2] Open and lately laparoscopic splenectomies are the standard therapies for HS.[3] However, their perioperative risk increases with the severity of HS and the patient’s co-morbid conditions. Moreover, loss of splenic function is associated with impaired immunity and increased susceptibility to infections.[4] Splenic artery embolization has been used as an adjunct to non-surgical treatment of blunt splenic injury since 1981.[5] Recent improvement in this technique with partial splenic embolization (PSE) permitted its safe application in risky patients with HS.[6] In our case report, we describe its first successful trial in a hemodialysis (HD) patient with severe HS due to cirrhosis.


   Case Report Top


A 26-year-old-Pakistani girl was admitted, to our center, with progressive pancytopenia for four years. She was on maintenance HD for the past 10 years. Past history was significant for: (a) end-stage renal disease due to polycystic kidney disease, (b) morbid obesity, (c) hyperlipidemia for >10 years. The latter included; high serum cholesterol and trigly-cerides at 12 and 5 mmol/L with upper limit of normal values at 5 and 2.5, respectively. She was instructed to reduce her weight with multiple measures and had received statins and lately Evolocumab with Fibrates and Ursofalk. After weight reduction and treatment of her hyperlipidemia; serum alkaline phosphatase and gamma GT decreased from 1172 and 1265 IU/L in 2009 to 255 and 289 in December 2009 [Table 1]. However, due to non-compliance with medications and diet, her serum cholesterol and triglycerides had increased. The latter was associated with a progressive increase in serum alkaline phosphatase and gamma-glutamyltransferase. By December 2018, all liver parameters had worsened and she developed hepatosplenomegaly. Her peripheral leukocyte and platelet counts had decreased to 2.4 × 109/L and 58 × 109/L with hemoglobin at 88 g/L. She had negative blood culture, Widal test, Brucella slide agglutination test, antibodies to cytomegalovirus, Ebstein-Barr virus, Herpes virus, hepatitis C and hepatitis B surface antigen. Serum complements (C3 and C4) and protein electrophoresis were normal except for hypoalbuminemia. ANA, anti-ds DNA, ANCA, rheumatoid factor, cryo-globulins, and anti-mitochondrial antibodies were negative. Serum ceruloplasmin and ferritin were normal. Her condition deteriorated and by October 2019, the pancytopenia was severe with peripheral leukocyte and platelet counts at 1.9 and 20, respectively. At this stage, PSE had to be performed to halt her hypersplenism. Her pre-operative management included three sessions of daily HD. PSE was performed by an interventional radiologist. Access was obtained in the usual fashion via the right common femoral artery. A reverse visceral (Simmons I) catheter was used to select the coeliac axis, and angiography was performed [Figure 1]. A microcatheter (Direxion 2.4 French) with a microwire was then used to catheterize the splenic artery. The micro-catheter was advanced to the middle segment of the artery, to avoid non-target embolization through the pancreatic magna artery [Figure 2]. Embolization was then performed using spherical particles of 500–700 micrometer size (Embosphere). After sluggish flow was demonstrated in the distal splenic artery branches, digital subtraction angiography was repeated. This demonstrated reduced perfusion of the splenic parenchyma, which was considered the endpoint of the procedure [Figure 3]. After the procedure, the patient had two HD-free days following which, her usual HD sessions were restarted without heparin and just flushing the HD filter with 100 mL of saline every 30 min. After the procedure, the patient had moderate post-embolization syndrome (PES) in the form of pleurisy with mild pleural effusion and moderate pain for two weeks. The latter decreased after analgesics and methylprednisolone IV for three days followed by Prednisone 1 mg/kg for two weeks. Additionally, she received intravenous (IV) Cefoperazone 1 g IV every 12 h for two weeks to protect against chest and splenic infections. After the procedure, the peripheral leukocyte and platelet counts had increased and by the 5th postoperative day had reached 19 × 109/L and 320 × 109/L with hemoglobin to 100 g/L. The patient was discharged on the 5th postoperative day and had resumed her daily activities. Two months later, her peripheral leukocyte, platelet count, and hemoglobin remained stable at 6 × 109/L, 228 × 109/L, and 110 g/L, respectively [Table 1]. At that stage, a portal venous phase computed tomography was obtained and had shown non-enhancement (infarction) of nearly half of the spleen [Figure 4].
Figure 1: Initial angiography of the splenic artery showing a tortuous and enlarged splenic artery as well as splenomegaly.

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Figure 2: A Direxion 2.4F microcatheter advanced into the middle-segment of the splenic artery.

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Figure 3: Postembolization digital subtraction angiography showing reduced perfusion of the spleen.

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Figure 4: Coronal image from portal venous phase computed tomography angiogram, 2 months postsplenic infarction, showing non-enhancement of approximately 50% of the spleen (partial infarction).

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Table 1: A flow chart showing serial changes in laboratory tests in the patient following partial splenic embolization.

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The authors obtained all appropriate consent forms from the patient for the publication of the case report.


   Discussion Top


The spleen constitutes an important part of the body’s immune system. It is a site where antibodies, monocytes, and activated lymphocytes are produced.[7] The spleen is highly vascularized and is the most commonly injured visceral organ in blunt abdominal trauma.

PSE has been used in splenic injury, splenic artery aneurysms, splenic artery steal-syndrome and to improve liver perfusion in liver transplant recipients, and to administer targeted treatment to areas of neoplastic disease in the splenic parenchyma.[8] In non-traumatic cases, PSE has been used to improve the platelet count in patients with HS from idiopathic thrombo-cytopenic purpura, thalassemia, Gaucher disease, idiopathic HS, and cytopenia induced by anti-cancer chemotherapy.[9]

In patients with portal hypertension, PSE is used to improve liver function, decrease hepatic encephalopathy, improve blood count and decrease variceal bleed. Improvement in liver function is due to increase in hepatic arterial superior mesenteric blood flow.[9] PSE is superior to transjugular intrahepatic porto-systemic shunt since the latter stops variceal bleeds yet it increases the risk of hepatic encephalopathy.[10] PSE also increases all blood counts. The platelet count starts rising as early as 12–24 h after partial splenic embolization and peaks in one to two weeks. The count usually stabilizes in about two months at approximately double the value before embolization and then slowly decreases over the next several years. The red blood cell count increases significantly by six months after embolization and stays elevated for years.[9]

Nowadays, PSE is performed using 500–700 um particles suspended in contrast medium. The suggested volume of infarction is between 50–70% because the efficacy is reduced for a volume of less than 50% and the likely hood of complications increases with volumes >70% especially splenic abscess formation.[11] Angiography is performed following the procedure to estimate the approximate extent of infarction. Mid-segment embolizations are preferred to minimize pleurisy and post-procedure pleural effusions associated with upper pole ones and avoids accidental embolization of hepatic artery and pancreatic arteries associated with proximal sites. Distal-segments embolizations should be avoided since they are usually associated with a higher incidence of PES and massive splenic infarction (>70%) leading to higher incidence of splenic abscess and near-total splenic loss. Coils are avoided since the goal is parenchymal splenic embolization.

PES is an immune-mediated pleural effusion and ascites. However, severe PES syndrome leading to pneumonia and pulmonary emboli, splenic abscess formation, portal vein thrombosis, liver failure, and death has been reported in 3.7% of cases.[11] To decrease PES, corticosteroids are given to decrease PES, and IV cephalosporins are given to decrease chest and splenic infections. Vaccination against pneumococcal pneumonia, Hemophilus influenza type b, and meningococcal infection two weeks prior to the procedure is mandatory in splenectomy but not with PSE.

In conclusion, we have demonstrated that PSE is an effective intervention for HS associated with cirrhosis even in hemodialysis patients with risk of bleeding and low immunity. It provides minimal blood loss, small surgical wound, fewer postoperative systemic complications, and avoidance of general anesthesia.

Conflict of interest: None declared.



 
   References Top

1.
Dameshek W. Hypersplenism. Bull NY Acad Med 1955;31:113-36.  Back to cited text no. 1
    
2.
Liu MT, Hsieh CY, Chang TH, Lin JP, Huang CC. Radiotherapy for hypersplenism from congestive splenomegaly. Ann Saudi Med 2004;24:198-200.  Back to cited text no. 2
    
3.
Zhu JH, Wang YD, Ye ZY, et al. Laparoscopic versus open splenectomy for hypersplenism secondary to liver cirrhosis. Surg Laparosc Endosc Percutan Tech 2009;19:258-62.  Back to cited text no. 3
    
4.
Holdsworth RJ, Irving AD, Cuschieri A. Postsplenectomy sepsis and its mortality rate: Actual versus perceived risks. Br J Surg 1991; 78:1031-8.  Back to cited text no. 4
    
5.
Sclafani SJ. The role of angiographic hemostasis in salvage of the injured spleen. Radiology 1981;141:645-50.  Back to cited text no. 5
    
6.
Madoff DC, Denys A, Wallace MJ, et al. Splenic arterial interventions: Anatomy, indications, technical considerations, and potential complications. Radiographics 2005; 25Suppl 1:S191-211.  Back to cited text no. 6
    
7.
Mebius RE, Kraal G. Structure and function of the spleen. Nat Rev Immunol 2005;5:606-16.  Back to cited text no. 7
    
8.
Guan YS, Hu Y. Clinical application of partial splenic embolization. Scientific World Journal 2014;2014:961345.  Back to cited text no. 8
    
9.
Ahuja C, Farsad K, Chadha M. An overview of splenic embolization. AJR Am J Roentgenol 2015;205:720-5.  Back to cited text no. 9
    
10.
Dib N, Oberti F, Calès P. Current management of the complications of portal hypertension: Variceal bleeding and ascites. CMAJ 2006;174:1433-43.  Back to cited text no. 10
    
11.
Koconis KG, Singh H, Soares G. Partial splenic embolization in the treatment of patients with portal hypertension: A review of the English language literature. J Vasc Interv Radiol 2007;18:463-81.  Back to cited text no. 11
    

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Correspondence Address:
Kamel El-Reshaid
Department of Medicine, Faculty of Medicine, Kuwait University, P. O. Box 24923, 13110 Safat
Kuwait
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DOI: 10.4103/1319-2442.318535

PMID: 34145142

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