DF-008

Despite the increase in research on delirium, it remains underdiagnosed and difficult to manage, and the outcome is poor especially in older people.

To identify the clinically diagnosed rates of delirium, the possible aetiologies, to describe treatment, number and type of psychotropic medication used and to investigate the reasons for referral to a liaison psychiatric team.

Retrospective study of medical records of inpatients admitted to Sligo Regional Hospital during an 18-month period.

One hundred and fifty-six files had a documentation of delirium (time prevalence 2%). Mean age of the sample was 82 years (SD = 7.2), 66 (42%) were male. Sixty-nine (44.2%) of the total sample had a previous history of dementia, and 57 (36.5%) had a previous history of delirium. In 67 (43.2%) samples, the cause was infection, while in 4, no specific cause was identified. Ninety (58%) were referred to the liaison service, but only in 26 (28.9 %), the reason for referral was "acute confusion" or "delirium". In a majority of referrals, the reason was an affective disorder more often depression. There were no significant differences between delirium subtypes and referrals (χ(2) = 3.868, df 3, p = 0.28). Examination of the amount of antipsychotics prescribed before, during and after delirium shows that there was a significant increase in use during the delirium (χ(2) = 17.512, df 8, p = 0.025) and decrease in z-hypnotics medication (zopiclone/zolpidem), (χ(2) = 20.114, df 4, p < 0.001), while benzodiazepines and antidepressants remained the same.

Delirium is often misdiagnosed and unrecognized in hospital settings; however, when identified the pharmacological management is appropriate.

Though it is well recognized that the pharmacological actions of benzodiazepines are mediated by facilitation of GABAergic neurotransmission, the consequences of these changes in regional brain function are not well understood. This study measured regional brain glucose metabolism using Positron Emission Tomography and 2-deoxy-2[18F]fluoro-D-glucose in normal controls (n = 21) investigated with and without lorazepam (30 micrograms/kg IV) and with flumazenil given after lorazepam (n = 9). Lorazepam markedly decreased metabolism in thalamus (23 +/- 8%) and occipital cortex (19 +/- 8%), and flumazenil partially reversed these changes. Changes in metabolic activity in thalamus were significantly correlated with lorazepam-induced sleepiness (r = .69, df 20, p < .0005) and there was a trend of an association between the reversal by flumazenil of lorazepam-induced change in thalamus and in sleepiness (r = .63, df 8, p = .07). Benzodiazepine-induced changes in thalamic activity may account for their sedative properties.