Simultaneous portosystemic shunt and proximal splenic artery embolization for patients with therapy-refractory hepatic encephalopathy at risk of portal hypertensive complications.

Background: Hepatic encephalopathy (HE) is a well-known complication of cirrhosis. When HE recurs despite optimal treatment or without a clear precipitant, a portosystemic shunt may be the culprit. We present a case of therapy-refractory HE caused by a spontaneous portosystemic shunt (SPSS).

Clinical case: A 69-year-old male with MASLD-related cirrhosis, with a medical history of biliopancreatic diversion and variceal bleeding, presented with his fifth episode of HE despite maximal pharmacological treatment. Initial lab tests and infectious screen were negative. Abdominal CT scan showed a paraesophageal shunt, supplied by the coronary vein. To address HE, SPSS closure was planned. Since SPSS closure could aggravate PHT and subsequently increase paracentesis frequency or induce variceal bleeding, this was combined with a proximal splenic artery embolization (pSAE). pSAE after SPSS closure resulted in a reduction of hepatic venous pressure gradient (HVPG) from 21mmHg to 15 mmHg. HE symptoms resolved, pharmacological treatment was stopped, and paracentesis became less frequent. Weeks later, the patient was readmitted with abdominal pain, and CT confirmed splenic infarction. Recurrent spontaneous bacterial peritonitis necessitated splenectomy, which was complicated by hemorrhage, septic shock, and death.

Conclusion: This case highlights the potential of combining SPSS closure and pSAE, two procedures that have not been combined before to our knowledge, to effectively reduce HE and HVPG, enabling cessation of anti-encephalopathic therapy and lowering paracentesis frequency. However, altered vascular anatomy can lead to complications such as splenic infarction. Although splenic infarction occurred as a complication, we believe this novel combined procedure warrants further investigation.