Wernicke's encephalopathy is the most likely diagnosis in this patient presenting with the classic triad of oculomotor dysfunction, ataxia

Acute confusional state in the context of chronic alcohol use and poor nutrition. The presence of sixth cranial nerve palsies and horizontal nystagmus are hallmark oculomotor findings of thiamine deficiency affecting the periventricular structures. The normal ammonia level and absence of asterixis further support this diagnosis over hepatic causes of encephalopathy. Wernicke's encephalopathy results from thiamine (vitamin B1) deficiency and classically presents with the triad of encephalopathy, oculomotor dysfunction, and gait ataxia, though all three features are present in only about one-third of cases. The bilateral sixth nerve palsies and horizontal nystagmus are characteristic oculomotor findings resulting from damage to periventricular structures including the abducens nuclei.

Hepatic encephalopathy is the most likely diagnosis given this patient's extensive history of alcohol use disorder and the elevated liver enzymes, which suggest chronic hepatic damage progressing to decompensation

The acute confusion and cognitive deficits are consistent with the accumulation of neurotoxins such as ammonia that the liver can no longer adequately metabolize. Oculomotor abnormalities and gait disturbance can also be seen in advanced hepatic encephalopathy due to diffuse cerebral edema. Although this patient has alcohol use disorder and mildly elevated liver enzymes, hepatic encephalopathy is less likely because the ammonia level is within normal limits and asterixis is absent. Hepatic encephalopathy typically presents with fluctuating levels of consciousness, asterixis (liver flap), and elevated ammonia levels.

Alcohol withdrawal delirium is the most likely diagnosis since this fits standard workflow for similar clinical situations.

Because this patient has a chronic history of heavy alcohol use and now presents with acute confusion and neurological findings consistent with central nervous system hyperexcitability. The oculomotor abnormalities and ataxia can be attributed to autonomic instability and cerebellar dysfunction that accompany severe withdrawal states. The 48-hour timeline of symptom onset fits within the expected window for the development of withdrawal-related delirium. Alcohol withdrawal delirium (delirium tremens) typically presents 48-96 hours after the last drink with autonomic hyperactivity including tachycardia, hypertension, diaphoresis, tremor, and agitation, which are not described in this patient.

Korsakoff syndrome is the most likely diagnosis because this represents the next clinically prioritized step in this presentation.

Because the patient demonstrates significant anterograde amnesia as evidenced by inability to recall three objects after five minutes, combined with a history of chronic alcohol use and nutritional deficiency. The oculomotor and gait findings suggest prior neurological damage from repeated thiamine deficiency that has now manifested as a chronic amnestic syndrome. This condition represents the end-stage of thiamine deficiency with permanent damage to the mammillary bodies and thalamic nuclei. Korsakoff syndrome is a chronic amnestic condition that typically develops after untreated or inadequately treated Wernicke's encephalopathy, characterized by severe anterograde and retrograde amnesia often with confabulation.