Among portosystemic shunts, splenorenal shunts can cause increased portal pressure, which in turn can bring about hyperammonemia, resulting in hepatic encephalopathy. In recent years, it has been reported that oxaliplatin(OX), a key chemotherapy drug in colorectal cancer, can precipitate splenorenal shunts due to sinusoidal injury. We report a case of hyperammonemia post oxaliplatin therapy. A 72-year-old male patient who had undergone surgical resection for(RS)rectal cancer with hepatic metastasis had been receiving capecitabine plus OX(CAPOX)as adjuvant chemotherapy. During his 7th course of treatment, he visited the outpatient clinic with complaints of weakness, dysarthria, and urinary incontinence. Laboratory findings showed an elevated NH3 level (200 μg/dL), and subsequent abdominal computed tomography revealed a splenorenal shunt, which was attributed to OX. Balloon-occluded retrograde transvenous obliteration(BRTO)was then performed. The patient has been routinely followed up in the outpatient clinic and has had no recurrence of hyperammonemia or cancer 14 months after the procedure. In retrospect, the splenorenal shunt was present on his first visit, therefore, hyperammonemia could have been prevented at the time of commencement of chemotherapy. We report our case, along with the relevant literature.