The diagnosis of delirium in an acute-care hospital in Moscow: what does the Pandora’s box contain?

Olga N Tkacheva,1 Nadezda K Runikhina,1 Arkadiy L Vertkin,2 Irina V Voronina,1 Natalia V Sharashkina,1 Elen A Mkhitaryan,1 Valentina S Ostapenko,1 Elena A Prokhorovich,2 Tamar Freud,3 Yan Press3–5 1Russian Gerontology Clinical Research Center, Pirogov Russian National Research Medical University of Ministry of Healthcare of the Russian Federation, 2Moscow State University of Medicine and Dentistry named after AI Evdokimov, Moscow, Russia; 3Department of Family Medicine, Faculty of Health Sciences, Sial Family Medicine and Primary Care Research Center, Ben-Gurion University of the Negev, 4Comprehensive Geriatric Assessment Unit, Clalit Health Care Services, Yassky Clinic, 5Community-Based Geriatric Unit, Division of Community Health, Ben-Gurion University of the Negev, Beer-Sheva, Israel Background: Delirium, a common problem among hospitalized elderly patients, is not usually diagnosed by doctors for various reasons. The primary aim of this study was to evaluate the effect of a short training course on the identification of delirium and the diagnostic rate of delirium among hospitalized patients aged ≥65 years. The secondary aim was to identify the risk factors for delirium. Methods: A prospective study was conducted in an acute-care hospital in Moscow, Russia. Six doctors underwent a short training course on delirium. Data collected included assessment by the confusion assessment method for the intensive care units, sociodemographic data, functional state before hospitalization, comorbidity, and hospitalization indices (indication for hospitalization, stay in intensive care unit, results of laboratory tests, length of hospitalization, and in-hospital mortality). Results: Delirium was diagnosed in 13 of 181 patients (7.2%) who underwent assessment. Cognitive impairment was diagnosed more among patients with delirium (30.0% vs 6.1%, P=0.029); Charlson comorbidity index was higher (3.6±2.4 vs 2.3±1.8, P=0.013); and Barthel index was lower (43.5±34.5 vs 94.1±17.0, P=0.000). The length of hospitalization was longer for patients with delirium at 13.9±7.3 vs 8.8±4.6 days (P=0.0001), and two of the 13 patients with delirium died during hospitalization compared with none of the 168 patients without delirium (P=0.0001). Conclusion: Although the rate of delirium was relatively low compared with studies from the West, this study proves that an educational intervention among doctors can bring about a significant change in the diagnosis of the condition. Keywords: delirium, elderly, inpatients, Russi

Calcium signalling and pancreatic cell death: apoptosis or necrosis?

Secretagogues, such as cholecystokinin and acetylcholine, utilise a variety of second messengers (inositol trisphosphate, cADPR and nicotinic acid adenine dinucleotide phosphate) to induce specific oscillatory patterns of calcium (Ca2+) signals in pancreatic acinar cells. These are tightly controlled in a spatiotemporal manner, and are coupled to mitochondrial metabolism necessary to fuel secretion. When Ca2+ homeostasis is disrupted by known precipitants of acute pancreatitis, for example, hyperstimulation or non-oxidative ethanol metabolites, Ca2+ stores (endoplasmic reticulum and acidic pool) become depleted and sustained cytosolic [Ca2+] elevations replace transient signals, leading to severe consequences. Sustained mitochondrial depolarisation, possibly via opening of the mitochondrial permeability transition pore (MPTP), elicits cellular ATP depletion that paralyses energy-dependent Ca2+ pumps causing cytosolic Ca2+ overload, while digestive enzymes are activated prematurely within the cell; Ca2+-dependent cellular necrosis ensues. However, when stress to the acinar cell is milder, for example, by application of the oxidant menadione, release of Ca2+ from stores leads to oscillatory global waves, associated with partial mitochondrial depolarisation and transient MPTP opening; apoptotic cell death is promoted via the intrinsic pathway, when associated with generation of reactive oxygen species. Apoptosis, induced by menadione or bile acids, is potentiated by inhibition of an endogenous detoxifying enzyme NAD(P)H:quinone oxidoreductase 1 (NQO1), suggesting its importance as a defence mechanism that may influence cell fate

Cardiolipin exposure on the outer mitochondrial membrane modulates α-synuclein

Cardiolipin is a phospholipid component of the inner mitochondrial membrane. Here the authors demonstrate that cardiolipin interacts with mutant α-synuclein, and that impaired cardiolipin function can lead to spread of α-synuclein between neurons