Hepatolenticular degeneration (HLD), also known as Wilson disease (WD), is an autosomal recessive disorder. The disease is caused by mutations in the causative genes that lead to impaired copper excretion and excessive copper accumulation in various organs of the body, especially in the liver, brain and kidney tissues, resulting in dysfunction of the corresponding organs. The progressive accumulation of copper in the liver causes hepatic sclerosis, secondary portal hypertension, clinical splenomegaly, hypersplenism, ascites, and gastrointestinal bleeding. We performed splenectomy on these patients from January 1996 to October 2002, and the postoperative results were satisfactory. In a retrospective analysis of 31 of these cases, we found that liver function improved to varying degrees 2 w after surgery without impairment of renal function. There was a significant correlation between the size of the giant spleen and liver function, and clinical practice showed that the giant spleen was involved in the formation of liver cirrhosis, and liver function improved significantly in most patients after splenectomy. In liver bean patients, liver function was impaired in the short term after splenectomy due to anesthesia and surgical trauma, and liver function improved significantly in most patients 2 w after surgery compared with that before surgery, and the improvement in liver function was more obvious than that reported in the literature for pathological splenectomy in post-hepatitis cirrhosis. In contrast, the pathological damage of copper to hepatocytes was terminated after effective copper repellent treatment in hepatocytes. Chen Shuang found that the spleen is involved in the cirrhosis process and has a significant role in promoting the formation of cirrhosis, and the removal of the spleen can partially alleviate the cirrhosis process. Wang Qian [11] further elucidated that the pathological spleen is involved in multiple immune regulation to promote cirrhosis formation in an animal model of cirrhosis in rats, and Murata found that the pathological spleen could promote hepatocyte regeneration after resection in a murine model of cirrhosis. The liver is the only organ in the body that receives a dual blood supply at the same time. Under normal conditions, the hepatic artery and portal vein each provide about 50% of the liver’s oxygen demand, while portal blood also provides fluid delivery substances rich in insulin and glucagon from the pancreatic veins to maintain normal liver tissue structure and physiological functions, as well as nutrients absorbed through the digestive tract from the superior mesenteric vein. Clinical studies have found that the outer diameter and blood volume of the hepatic artery increase in patients with cirrhosis compared with normal subjects, and the pressure and blood flow of the portal vein increase. The author believes that the venous wall is thinner than the arterial wall and more hepatic parenchyma is wrapped around the right lobe of the liver than the left lobe of the liver, and the expansion is limited by the expansion of the left lobe of the liver, which obviously provides more blood oxygen and nutrients, resulting in compensatory hypertrophy of the left outer lobe of the liver. Some scholars believe that the hypertrophy of the left liver causes the dilatation of the supplying vessels. In patients with hepatic sclerosis, hepatic artery blood flow increases after giant splenectomy. Because the hepatic artery and the splenic artery are both branches of the abdominal trunk, the blood flow of the hepatic artery increases by its own regulation after ligation of the splenic artery; in addition, after splenectomy, the blood flow and pressure of the portal vein decreases while the pressure of the hepatic sinusoids decreases, resulting in the expansion of the hepatic artery. There is a compensatory effect between splenic vein and superior mesenteric vein through visceral vascular neurological and hormonal regulation, and after splenectomy, there is a compensatory increase in blood flow in superior mesenteric vein so that more nutrients absorbed through the intestine are delivered to the liver. At the same time, the decrease in free portal vein pressure facilitates pancreatic venous reflux and increases the delivery of insulin and glucagon and other nutrients to the liver, which is conducive to the regeneration and repair of hepatocytes. The decrease in free portal vein pressure reduces the prehepatic shunt flow via the gastric coronary vein, ensuring effective perfusion of blood to the liver. After splenectomy, the decrease in free portal vein pressure effectively relieves gastrointestinal stasis and edema, which improves the patient’s appetite and facilitates the digestion and absorption of nutrients. All these factors are conducive to the regeneration and repair of hepatocytes and improvement of liver function. Copper excretion is impaired in liver and bean patients, and copper not only accumulates in the liver and brain tissue, but also in the kidneys, causing nephropathy. All 31 patients in our group had ultrasound changes of hepatocellular nephropathy in preoperative ultrasound examination. By comparing the pre- and post-operative status of renal function, we found that surgical trauma and anesthetic shock did not cause renal function damage. In conclusion, unless there is a history of severe esophageal varices or bleeding, simple splenectomy for hepatomegaly combined with hypersplenism is safe and reasonable, and it can effectively eliminate hypersplenism and significantly improve liver function without impairing renal function.