Clinical characteristics associated with the onset of delirium among long-term nursing home residents.

BACKGROUND: Nursing home residents are frail, have multiple medical comorbidities, and are at high risk for delirium. Most of the existing evidence base on delirium is derived from studies in the acute in-patient population. We examine the association between clinical characteristics and medication use with the incidence of delirium during the nursing home stay. METHODS: This is a retrospective cohort study of 1571 residents from 12 nursing homes operated by a single care provider in Ontario, Canada. Residents were over the age of 55 and admitted between February 2010 and December 2015 with no baseline delirium and a minimum stay of 180 days. Residents with moderate or worse cognitive impairment at baseline were excluded. The baseline and follow-up characteristics of residents were collected from the Resident Assessment Instrument-Minimal Data Set 2.0 completed at admission and repeated quarterly until death or discharge. Multivariate logistic regression was used to identify characteristics and medication use associated with the onset of delirium. RESULTS: The incidence of delirium was 40.4% over the nursing home stay (mean LOS: 32 months). A diagnosis of dementia (OR: 2.54, p < .001), the presence of pain (OR: 1.64, p < .001), and the use of antipsychotics (OR: 1.87, p < .001) were significantly associated with the onset of delirium. Compared to residents who did not develop delirium, residents who developed a delirium had a greater increase in the use of antipsychotics and antidepressants over the nursing home stay. CONCLUSIONS: Dementia, the presence of pain, and the use of antipsychotics were associated with the onset of delirium. Pain monitoring and treatment may be important to decrease delirium in nursing homes. Future studies are necessary to examine the prescribing patterns in nursing homes and their association with delirium.

Neonatal hypocalcemia, neonatal seizures, and intellectual disability in 22q11.2 deletion syndrome.

PURPOSE: Hypocalcemia is a common endocrinological condition in 22q11.2 deletion syndrome. Neonatal hypocalcemia may affect neurodevelopment. We hypothesized that neonatal hypocalcemia would be associated with rare, more severe forms of intellectual disability in 22q11.2 deletion syndrome. METHODS: We used a logistic regression model to investigate potential predictors of intellectual disability severity, including neonatal hypocalcemia, neonatal seizures, and complex congenital heart disease, e.g., interrupted aortic arch, in 149 adults with 22q11.2 deletion syndrome. Ten subjects had moderate-to-severe intellectual disability. RESULTS: The model was highly significant (P < 0.0001), showing neonatal seizures (P = 0.0018) and neonatal hypocalcemia (P = 0.047) to be significant predictors of a more severe level of intellectual disability. Neonatal seizures were significantly associated with neonatal hypocalcemia in the entire sample (P < 0.0001), regardless of intellectual level. There was no evidence for the association of moderate-to-severe intellectual disability with other factors such as major structural brain malformations in this sample. CONCLUSION: The results suggest that neonatal seizures may increase the risk for more severe intellectual deficits in 22q11.2 deletion syndrome, likely mediated by neonatal hypocalcemia. Neonatal hypocalcemia often remains unrecognized until the postseizure period, when damage to neurons may already have occurred. These findings support the importance of early recognition and treatment of neonatal hypocalcemia and potentially neonatal screening for 22q11.2 deletions.

Prevalence of hypocalcaemia and its associated features in 22q11·2 deletion syndrome.

BACKGROUND: 22q11.2 deletion syndrome (22q11.2DS) is a relatively common yet under-recognized genetic syndrome that may present with endocrine features. We aimed to address the factors that contribute to the high prevalence of hypocalcaemia. METHODS: We investigated hypocalcaemia in a well-characterized sample of 138 adults with 22q11.2DS (65 m, 73 F; mean age 34.2, SD 11.8, years) using laboratory studies and lifelong medical records. Logistic regression modelling was used to identify features associated with lifetime prevalence of hypocalcaemia. RESULTS: Of the total sample, 111 (80.4%) had a lifetime history of hypocalcaemia. Eleven (84.6%) of 13 subjects with neonatal hypocalcaemia had documented recurrence of hypocalcaemia. Lifetime history of hypocalcaemia was associated with lifetime prevalence of hypoparathyroidism (P < 0.0001) and hypothyroidism (P = 0.04), as statistically independent factors. Hypomagnesaemia was associated with concurrent hypocalcaemic measurements, especially in the presence of concurrent hypoparathyroidism (P = 0.02). CONCLUSIONS: The results suggest that, in addition to the major effect of hypoparathyroidism, hypothyroidism may play a role in hypocalcaemia in 22q11.2DS and that there is a high recurrence rate of neonatal hypocalcaemia. Hypomagnesaemia may contribute to hypocalcaemia by further suppressing parathyroid hormone (PTH). Although further studies are needed, the findings support regular lifelong follow-up of calcium, magnesium, PTH and TSH levels in patients with 22q11.2DS. At any age, hypocalcaemia with hypoparathyroidism and/or hypothyroidism may suggest a diagnosis of 22q11.2DS.