Acute hepatic encephalopathy (AHE) is a common form of delirium, a state of confusion, impaired attention, and decreased arousal due to acute liver failure. However, the neurophysiological mechanisms underlying AHE are poorly understood. In order to develop hypotheses for mechanisms of AHE, our work builds on an existing neural mean field model for similar EEG patterns in cerebral anoxia, the bursting Liley model. The model proposes that generalized periodic discharges, similar to the triphasic waves (TPWs) seen in severe AHE, arise through three types of processes a) increased neuronal excitability; b) defective brain energy metabolism leading to impaired synaptic transmission; c) and enhanced postsynaptic inhibition mediated by increased GABA-ergic and glycinergic transmission. We relate the model parameters to human EEG data using a particle-filter based optimization method that matches the TPW inter-event-interval distribution of the model with that observed in patients EEGs. In this way our model relates microscopic mechanisms to EEG patterns. Our model represents a starting point for exploring the underlying mechanisms of brain dynamics in delirium.