Hepatic encephalopathy (HE) is a complex neurological disorder characterized by a wide range of neuropsychiatric abnormalities, from subtle cognitive deficits to deep coma. While cirrhosis is the most common underlying condition, HE can also occur in other conditions. The pathogenesis of HE is multifactorial, but a key factor is the liver's impaired capacity to detoxify substances absorbed from the gut, notably ammonia. The resulting accumulation of these neurotoxins in the systemic circulation leads to their access to the central nervous system, where they disrupt neuronal function. We present a case report of a 62-year-old woman, with no cognitive impairment, with a relevant medical history of cholangiocarcinoma, surgically treated, with no signs of progression. She was admitted to the Emergency Department (ED) due to confusion and repetitive speech. On neurological examination, the patient presented prostration, with spontaneous eye opening but no directed gaze. She could not name objects upon request and could not repeat or follow commands. She had no cranial nerve deficits and no motor deficits in the limbs. Routine labs including liver function tests were normal except for high ammonia. There was no evidence of infection. A review of her medical history revealed a portal "arterialization" through an anastomosis between the hepatic artery and the portal vein. Subsequently, the patient was diagnosed with HE type B. This case highlights the importance of a thorough (meticulous) medical history, physical examination, and the patient's personal background, particularly in patients presenting with acute neurological changes and complex medical histories.