Mortality and cause of death during inpatient psychiatric care in New South Wales, Australia: A retrospective linked data study.

BACKGROUND: Premature mortality in people with mental illness is well-documented, yet deaths during inpatient psychiatric care have received little research attention. This study investigates mortality rates and causes of death during inpatient psychiatric care in New South Wales (NSW), Australia. Risk factors for inpatient death were also explored. METHODS: A retrospective cohort study using linked administrative datasets with complete capture of psychiatric admissions in NSW from 2002 to 2012 (n = 421,580) was conducted. Univariate and multivariate random-effects logistic regression analyses were used to explore risk factors for inpatient death. RESULTS: The mortality rate during inpatient psychiatric care was 1.12 deaths per 1000 episodes of care and appeared to decline over the study period. Suicide accounted for 17% of inpatient deaths, while physical health causes accounted for 75% of all deaths. Thirty percent of these deaths were considered potentially avoidable. In the multivariate model, male sex, unknown address and several physical health diagnoses were associated with increased deaths. CONCLUSIONS: The mortality rate and number of avoidable deaths during inpatient psychiatric care were substantial and warrant further systemic investigation. This was driven by a dual burden of physical health conditions and suicide. Strategies to improve access to physical health care on psychiatric inpatient wards and prevent inpatient suicide are necessary. A coordinated approach to monitoring psychiatric inpatient deaths in Australia is not currently available and much needed.

Meta-Analysis of Longitudinal Cohort Studies of Suicide Risk Assessment among Psychiatric Patients: Heterogeneity in Results and Lack of Improvement over Time.

OBJECTIVE: It is widely assumed that the clinical care of psychiatric patients can be guided by estimates of suicide risk and by using patient characteristics to define a group of high-risk patients. However, the statistical strength and reliability of suicide risk categorization is unknown. Our objective was to investigate the odds of suicide in high-risk compared to lower-risk categories and the suicide rates in high-risk and lower-risk groups. METHOD: We located longitudinal cohort studies where psychiatric patients or people who had made suicide attempts were stratified into high-risk and lower-risk groups for suicide with suicide mortality as the outcome by searching for peer reviewed publications indexed in PubMed or PsychINFO. Electronic searches were supplemented by hand searching of included studies and relevant review articles. Two authors independently extracted data regarding effect size, study population and study design from 53 samples of risk-assessed patients reported in 37 studies. RESULTS: The pooled odds of suicide among high-risk patients compared to lower-risk patients calculated by random effects meta-analysis was of 4.84 (95% Confidence Interval (CI) 3.79-6.20). Between-study heterogeneity was very high (I2 = 93.3). There was no evidence that more recent studies had greater statistical strength than older studies. Over an average follow up period of 63 months the proportion of suicides among the high-risk patients was 5.5% and was 0.9% among lower-risk patients. The meta-analytically derived sensitivity and specificity of a high-risk categorization were 56% and 79% respectively. There was evidence of publication bias in favour of studies that inflated the pooled odds of suicide in high-risk patients. CONCLUSIONS: The strength of suicide risk categorizations based on the presence of multiple risk factors does not greatly exceed the association between individual suicide risk factors and suicide. A statistically strong and reliable method to usefully distinguish patients with a high-risk of suicide remains elusive.

Mood disturbance after infection.

OBJECTIVE: An aetiological link between acute infection and major depression has long been hypothesized, and is increasingly gaining recognition within contemporary literature. This review aims to examine the evidence for such a link, specifically between acute, self-limiting infection and major depression, and to summarize the current understanding of pathophysiological mechanisms underlying this link. METHODS: Relevant articles were sourced via an online search of published literature from Embase, MEDLINE, PsycINFO and PubMed using a variety of search terms including mood disorder, depression, infection and inflammation. Additionally, a search for articles from the bibliographies of retrieved papers was conducted. RESULTS: Findings from retrospective studies suggest an association between infection and subsequent mood disturbance, including major depression. This association has been confirmed by studies employing prospective observational or experimental challenge designs. The available evidence supports a multifactorial basis of vulnerability towards major depression in the context of acute infection. Genetic, neuroendocrine, autonomic and psychosocial factors may interact to potentiate the likelihood of a severe and prolonged depressive response to an immunological stressor in some individuals. CONCLUSION: Mood disturbance is likely to have a host-protective role in the context of an acute sickness response to infection. However, this usually adaptive and reversible response may progress in some vulnerable individuals into a more sustained and severe pattern of behavioural and physiological changes of major depression. Further research is needed to delineate the factors that predispose, precipitate and perpetuate depression in the context of acute infective illness. Such insights will inform effective prevention and treatment strategies.