TACE-Associated Hepatic Encephalopathy in the Absence of Decompensated Liver Disease

Abstract

Hepatic encephalopathy is a common presentation of decompensated liver disease in patients with HCC, but occurs rarely outside the context of diffuse cirrhosis. We describe a case of severe encephalopathy in the setting of a routine TACE procedure for metastatic neuroendocrine tumor. This report seeks to raise awareness of the essential predilection for hepatic encephalopthy (HE) in patients with metastatic neuroendocrine tumor (NET), and may help to illuminate the mechanism of hepatic encephalopathy in the setting of NET. A 68 year old male with Grade II well-differentiated carcinoid tumor metastatic to the liver presented for chemoembolization of a hypervascular tumor in segment 4. He was known to have extremely high 5-HIAA and carcinoid syndrome. He had several ill-defined lesions in his liver without evidence of cirrhosis. Over the next 24 hours developed new confusion, dysarthria, and non-focal weakness. MRI was negative for any evidence of acute stroke or TIA. EEG revealed diffuse slowing and he was noted to have significant asterixis and clonus on exam. The patient did not have significantly elevated liver enzymes or fulminant hepatic failure. After several days he became increasingly obtunded with no localizing source. Lactulose was initiated for acute hepatic encephalopathy with gradual improvement in his asterixis, drowsiness, and confusion. Discussion We describe an unusual case of hepatic encephalopathy which occurred following localized chemoembolization of a NET in the absence of cirrhosis or widespread tumor burden. HE is known to occur in approximately 1% of patients with cirrhosis who undergo TACE, but occurs very rarely in the absence of cirrhosis. The exception to this is in patients with NET, who are known to have a poorly-understoond predilection for HE. In contrast to cirrhosis, patients with NET typically have well-preserved synthetic and detoxification function attributable to the remaining healthy hepatic tissue. This patient did not exhibit diffuse liver injury or elevated ammonia, but developed severe HE after TACE. This raises interesting questions about the mechanism of HE in NET -- arguing for a greater role of 5HIAA release in NET-associated HE, rather than transtumoral intrahepatic shunting of ammonia. Clinicians should be aware of the predilection towards hepatic encephalopathy in metastatic neuroendocrine tumors, and consider this etiology when neurologic symptoms arise in patients who have undergone recent embolization.2428 Figure 1 No Caption available.