Partial Splenic Artery Embolization Research Articles

New methods for the management of gastric varices

Bleeding from gastric varices has been successfully treated by endoscopic modalities. Once the bleeding from the gastric varices is stabilized, endoscopic treatment and/or interventional radiology should be performed to eradicate varices completely. Partial splenic artery embolization is a supplemental treatment to prolong the obliteration of the veins feeding and/or draining the varices. The overall incidence of bleeding from gastric varices is lower than that from esophageal varices. No studies to date have definitively characterized the causal factors behind bleeding from gastric varices. The initial episodes of bleeding from esophageal varices or gastric varices without prior treatment may be at least partly triggered by a violation of the mucosal barrier overlying varices. This is especially likely in the case of varices of the fundus. In view of the high rate of hemostasis achieved among bleeding gastric varices, treatment should be administered in selective cases. Among untreated cases, steps to prevent gastric mucosal injury confer very important protection against gastric variceal bleeding.

Long-Term Results of Partial Splenic Artery Embolization as Supplemental Treatment for Portal-Systemic Encephalopathy

To present long-term results of angiographic partial splenic artery embolization (PSE) as a supplemental treatment of portal-systemic encephalopathy. Twenty-five patients with portal-systemic encephalopathy were divided into two groups: 14 patients underwent transportal obliteration and/or balloon-occluded retrograde transvenous obliteration (BRTO) of portal-systemic shunts (PSS), followed by PSE (PSE(+) group), and 11 patients underwent only transportal obliteration and/or BRTO of PSS (PSE(-) group). Portal venous pressures pretreatment was similar to posttreatment in the PSE(+) group, but lower than posttreatment in the PSE(-) group. Serum ammonia levels were higher at pretreatment than at 1 wk posttreatment in both groups, but the levels in the two groups were similar at pretreatment, 1 wk, 3 months, 3 yr, 4 yr, and 5 yr posttreatment. However, serum ammonia levels were lower in the PSE(+) group than in the PSE(-) group 6 months, 9 months, 1 yr, and 2 yr posttreatment. Grades of encephalopathy were higher at pretreatment than at 1 wk posttreatment in both groups, but the levels in the two groups were similar at pretreatment, 1 wk, 2 yr, 3 yr, 4 yr, and 5 yr posttreatment. However, grades of encephalopathy were lower in the PSE(+) group than in the PSE(-) group 3 months, 6 months, 9 months, and 1 yr posttreatment. Obliteration of PSS followed by PSE benefit patients with portal-systemic encephalopathy.

Emergency splenic arterial embolization for massive variceal bleeding in liver recipient with left-sided portal hypertension

Splenic vein thrombosis with gastric variceal bleeding is difficult to manage, and splenectomy may be necessary to stop variceal bleeding. The authors report the case of a post-orthotopic liver transplant patient with bleeding gastric varices secondary to splenic vein thrombosis treated by partial splenic artery embolization. Successful embolization was performed via transcatheter approach depositing Gianturco coils into the intrasplenic artery resulting in immediate cessation of variceal bleeding. No recurrence of bleeding was noted postembolization. In conclusion, splenic artery embolization can be used as treatment for postliver transplant variceal bleeding with hypersplenism.

Clinical evaluation for treatment of thrombocytopenia using partial splenic arterial embolization

Clinical evaluation for treatment of thrombocytopenia using partial splenic arterial embolization

Mechanisms for increment of platelet associated IgG and platelet surface IgG and their implications in immune thrombocytopenia associated with chronic viral liver disease

In addition to hypersplenism, immunological destruction of platelets by elevated platelet associated IgG (PAIgG) and platelet surface IgG (PSIgG) has been proposed as a causative factor for thrombocytopenia in chronic liver disease (CLD), although the implication of PAIgG may be debatable since recent investigations on idiopathic thrombocytopenic purpura disclosed the fact that PAIgG largely relates to the intra-platelet IgG in α-granules and not to PSIgG. Further, with regard to the elevated PSIgG of CLD, characterization as to whether it mainly represents anti-platelet glycoprotein (GP) antibodies or IgG contained in the immune complex has not been elucidated. Thirty-seven patients with chronic viral liver disease (CVLD); 31 hepatitis C and 6 hepatitis B were included in this study. First we monitored the changes in levels of PAIgG, α-granule IgG, PSIgG and mean platelet volume (MPV) during the course of partial splenic arterial embolization (PSE). The elevated level of PAIgG decreased after PSE, paralleling that of α-granule IgG, while PSIgG showed no change; MPV decreased reciprocally with the increase of platelet count. These results indicate that the increment of PAIgG in CVLD may be caused by accelerated destruction of platelets; this generally evokes hyperproduction of large-sized thrombocytes, which have an increased capability to uptake circulating IgG. To characterize PSIgG, we then tested CVLD patients for antiplatelet GP antibodies and found only a 5.4% positivity. It was also found that circulating immune complex levels in CVLD patients were clearly elevated, correlating with the levels of PSIgG. Thus, it was surmised that immune complexes bound to the platelet surface, and not platelet specific GP antibodies, may be playing a crucial role in platelet destruction of CVLD, possibly through phagocytosis by macrophages.

Portal-systemic encephalopathy in non-cirrhotic patients: classification of clinical types, diagnosis and treatment.

Hepatic encephalopathy is suspected in non-cirrhotic cases of encephalopathy because the symptoms are accompanied by hyperammonaemia. However, the cause of the large portal-systemic shunt formation observed in these cases is not clear, as cirrhosis and portal hypertension are absent. The frequency of such cases reported in the literature is increasing with progress and spread of abdominal imaging diagnostic techniques. Some cases have been misdiagnosed as psychiatric diseases (dementia, depression and others) and consequently patients have been hospitalized in psychiatric institutions or geriatric facilities. Some paediatric cases have also been misdiagnosed. Therefore, the importance of accurate diagnosis of this disease should be strongly emphasized. Some paediatric cases have also been misdiagnosed. When psychoneurological symptoms are suggestive of hepatic encephalopathy but objective and subjective symptoms or abnormal values of liver function tests are not sufficiently indicative of liver cirrhosis, portal-systemic encephalopathy should be suspected. Abnormal angiograms of the portal vein, superior mesenteric vein or splenic vein are conclusive evidence of portal-systemic encephalopathy. Transrectal portal scintigraphy also provides information useful for detection of shunts and a quantitative estimation of shunt index. We classified the disease into five types based on whether the shunt is formed inside or outside the liver. Type I (intrahepatic type) designates cases in which shunts are located between the portal and systemic veins. Type II designates a type of intra/extrahepatic shunt that originates from the umbilical part of the portal vein and serpentines in the liver, then leaves the liver. Type III (extrahepatic type) occurs most frequently. Type IV (extrahepatic) is accompanied by shunts similar to those in type III, but hepatic pathology presents as idiopathic portal hypertension. Type V (extrahepatic) represents the congenital absence of the portal vein, where the superior mesenteric vein joins the intrahepatic inferior vena cava or the left renal vein. The prevalence of each type in our country was examined by a nationwide investigation. In addition to the conventional diet or drug treatments, obliteration by less invasive interventional radiology using a metallic coil and ethanol has recently been used more frequently than surgical occlusion of shunts. Shunt-preserving disconnection of portal and systemic circulation and partial splenic artery embolization are also performed. International investigation of the disease status and establishment of diagnostic and therapeutic methods for the disease are awaited and investigation of long-term prognosis after therapy is also necessary.

Successful treatment of severe thrombocytopenia in a cirrhotic patient with portal hypertension using partial splenic artery embolization

INTRODUCTION: Patients with cirrhosis and portal hypertension frequently have splenomegaly, thrombocytopenia, anemia and coagulopathy. Splenectomy is an accepted treatment for thrombocytopenia in patients without portal hypertension, however, splenect0my carries a high risk of intraoperative bleeding in those with underlying portal hypertension. Several studies and case reports advocate partial splenic artery embolization for the management of thrombocytopenia due to splenomegaly. CASE: A 69 year old male with Laennec's cirrhosis, portal hypertension (splenomegaly, ascites), presented with severe thrombocytopenia, coagulopathy, anemia, epistaxis, and melena. He was a poor surgical candidate because of comorbidities of insulin dependent diabetes meUitus, chronic renal failure, coronary artery disease, and sip right pneumonectomy for lung cancer 26 years ago. Hg/Hct were 7.6/22.4, platelets: 16,000, PT: 14.2. EGD revealed grade 4 esophageal varices, and portal hypertensive gastropathy. He received 4 units of packed cells. Initially, he underwent a partial splenic artery embolization using polyvinyl alcohol particles. His platelets increased to a range of 26-36,000 one week post embolization, H/H were stable and no additional blood transfusions were needed. Twelve days later a second partial splenic artery embolization was done, which led to a further increase in platelet count to a range of 60-70,000. CT and MRI of the abdomen showed a 50% decrease in spleen size. His H/H at discharge were 9.9/27.9, WBC 4.4 (preadmission was 2.8). CONCLUSION: Partial splenic artery embolization may be a useful procedure for the management of splenomegaly and thrombocytopenia in cirrhotic patients with portal hypertension. It may decrease the frequency of bleeding and blood replacement therapy by increasing platelets count and function. More controlled studies are warranted before considering this procedure as a standard approach for this patient population. [1] Hideya Noguchi. Changes in platelet kinetics after a partial splenic arterial embolization in cirrhotic patients with hypersplenism. Hepatology 1995 Dec;22(6): 1682-1688. [2] Sangro B. Partial splenic embolization for the treatment of hypersplenism in cirrhosis. Hepatology 1993 Aug;18(2):309-314.

Changes in platelet kinetics after a partial splenic arterial embolization in cirrhotic patients with hypersplenism

We performed a partial splenic arterial embolization in 22 patients with cirrhosis associated with thrombocytopenia and then evaluated the changes in platelet kinetics after undergoing the procedure using 111In-tropolone-labeled platelets. The controls consisted of eight chronic hepatitis patients who showed a normal platelet count and normal spleen size. The mean splenic infarction ratio after the procedure was 54.9%. A platelet kinetics study was performed before and 2 months after the procedure. Before the procedure, the cirrhotic patients showed increases in the splenic volume and the spleen/liver uptake ratio of the 111In-labeled platelets on both the third and seventh days, and a decrease in the platelet recovery compared with the controls, which suggested an increased platelet pool in the spleen. In addition, the platelet survival time in cirrhotic patients was shortened, whereas the platelet-associated immunoglobulin G (PA-IgG) was higher than that of the controls, which suggested the involvement of immunologic mechanisms in the thrombocytopenia. With an increase of the platelet count after a partial splenic arterial embolization, the spleen/liver uptake ratio of the 111In-labeled platelets decreased, whereas the platelet recovery increased. Furthermore, the platelet survival time was prolonged, whereas the PA-IgG decreased. The platelet count showed a positive correlation with the platelet survival time and a negative correlation with PA-IgG before and after the procedure. These results suggest that a transcatheter splenic arterial embolization not only may reduce the increased platelet pool in the spleen but also may improve the thrombocytopenia induced by immunologic mechanisms in patients with cirrhosis.

Changes in platelet kinetics after a partial splenic arterial embolization in cirrhotic patients with hypersplenism

We performed a partial splenic arterial embolization in 22 patients with cirrhosis associated with thrombocytopenia and then evaluated the changes in platelet kinetics after undergoing the procedure using 111In-tropolone-labeled platelets. The controls consisted of eight chronic hepatitis patients who showed a normal platelet count and normal spleen size. The mean splenic infarction ratio after the procedure was 54.9%. A platelet kinetics study was performed before and 2 months after the procedure. Before the procedure, the cirrhotic patients showed increases in the splenic volume and the spleen/liver uptake ratio of the 111In-labeled platelets on both the third and seventh days, and a decrease in the platelet recovery compared with the controls, which suggested an increased platelet pool in the spleen. In addition, the platelet survival time in cirrhotic patients was shortened, whereas the platelet-associated immunoglobulin G (PA-IgG) was higher than that of the controls, which suggested the involvement of immunologic mechanisms in the thrombocytopenia. With an increase of the platelet count after a partial splenic arterial embolization, the spleen/liver uptake ratio of the 111In-labeled platelets decreased, whereas the platelet recovery increased. Furthermore, the platelet survival time was prolonged, whereas the PA-IgG decreased. The platelet count showed a positive correlation with the platelet survival time and a negative correlation with PA-IgG before and after the procedure. These results suggest that a transcatheter splenic arterial embolization not only may reduce the increased platelet pool in the spleen but also may improve the thrombocytopenia induced by immunologic mechanisms in patients with cirrhosis.

Giant iatrogenic splenic pseudocyst

Partial splenic arterial embolization was used to treat hypersplenism in a 10-year-old boy with portal hypertension secondary to congenital hepatic fibrosis. After embolization the spleen remained enlarged, but the boy's platelet count increased and his variceal bleeding ceased. One month later, he returned with vomiting and an abdominal mass. Computed tomography showed a large cyst of the spleen with a small rim of residual splenic tissue. Percutaneous drainage with ultrasound guidance yielded 2,800 mL of brown fluid. Wedge-shaped infarctions are described early after splenic embolization, and these areas eventually fibrose and contract. In this case, the embolization resulted in splenic necrosis and liquefaction with pseudocyst formation. This unusual complication was effectively treated without surgery.