Gathering a history from other caregivers can clarify baseline mentation. Other mental illnesses: Some mental illnesses, such as a manic episode of bipolar disorder, depersonalization disorder, or some types of acute psychosis may cause a rapidly fluctuating impairment of cognitive function and ability to focus. These, however, are not technically causes of delirium per DSM-5 criteria D (i.e. fluctuating cognitive symptoms occurring as part of a primary mental disorder are results of the said mental disorder itself), while physical disorders (e.g. infections, hypoxia, etc.) can precipitate delirium as a mental side-effect/symptom. Psychosis: Consciousness and cognition may not be impaired (however, there may be overlap, as some acute psychosis, especially with mania, is capable of producing delirium-like states). Prevention
Using a tailored multi-faceted approach as outlined above can decrease rates of delirium by 27% among the elderly. At least 30–40% of all cases of delirium could be prevented, and high rates of delirium reflect negatively on the quality of care. Episodes of delirium can be prevented by identifying hospitalized people at risk of the condition. This includes individuals over age 65, with a cognitive impairment, with hip fracture, or with severe illness. Close observation for the early signs is recommended in such populations. Delirium may be prevented and treated by using non-pharmacologic approaches focused on risk factors, such as constipation, dehydration, low oxygen levels, immobility, visual or hearing impairment, sleep deprivation, functional decline and removing or minimizing problematic medications. Ensuring a therapeutic environment (e.g.
After basal levels have been measured, confirmation is done by administering ACTH, and comparing 17-OHP pre and post test. 17-OHP levels over 10 ng/mL at the 60th minute post stimulation is considered diagnostic for LOCAH. Androgen backdoor pathway
In 21-hydroxylase deficiency, especially in mild cases (LOCAH), the androgen "backdoor" pathway may be the reason of androgen excess. This backdoor pathway is not always considered in the clinical evaluation of patients with hyperandrogenism conditions such as LOCAH and may be a source of diagnostic pitfalls and confusion. One case study demonstrated the importance of considering serum 5α-dihydrotestosterone (DHT) levels and the androgen backdoor pathway in a LOCAH diagnosis that would have not been apparent from testosterone levels alone. 11β-Hydroxylase deficiency
The activity of 11β-hydroxylase can be determined by observing the basal  11-deoxycortisol level. A level over 10 ng/mL, indicates followup with ACTH stimulation test. The 60th minute post-stimulation 11-deoxycortisol levels higher than 18 ng/mL are diagnostic of LOCAH. 3β-Hydroxysteroid dehydrogenase deficiency
The activity of 3β-hydroxysteroid dehydrogenase can be determined by observing the basal 17α-hydroxypregnenolone level. A level above 30 ng/mL and 17α-hydroxypregnenolone/cortisol ratio above 10 SD are diagnostic of LOCAH. Management
Management and treatment of LOCAH is case specific and the application of glucocorticoid treatment is not standard as it is in classic CAH. LOCAH is not a life-threatening medical condition and the risks of treatment given prenatally or to asymptomatic children outweigh potential benefits.