Incidence and Risk Factors of Postoperative Delirium in Patients with Esophageal Cancer

Background

Postoperative delirium is a common complication after major surgery and is characterized by acute confusion with fluctuating consciousness. The aim of this study was to investigate the incidence and risk factors of postoperative delirium in patients with esophageal cancer.

Methods

We conducted a retrospective cohort analysis of 306 consecutive patients who had undergone an esophagectomy at Keio University Hospital from January 1998 to December 2009. All data were assessed by psychiatrists, and delirium was diagnosed according to criteria of the Diagnostic and Statistical Manual Disorder, fourth edition. Univariate and multivariate analyses were performed.

Results

Postoperative delirium developed in 153 (50.0?%) of 306 patients. One hundred fourteen (37.3?%) of the 306 patients required psychoactive medication for symptoms associated with delirium. Univariate analyses showed that older age, male gender, additional flunitrazepam for sedation in intensive care unit (ICU) after surgery, longer periods of time under mechanical ventilation after surgery, longer ICU stays, occurrence of postoperative complications, and longer hospital stays were significantly associated with postoperative delirium. Multivariate analysis revealed that development of delirium was linked to older age, additional flunitrazepam in ICU, and occurrence of postoperative complication.

Conclusions

The development of postoperative delirium in patients with esophageal cancer is a problem that cannot be ignored. Our results suggest that the risk of developing delirium is associated with older age, use of flunitrazepam in ICU, and postoperative complications.     

The validity of revised death certificates (ICD-10) for ischemic heart disease in Oita City, Japan

PURPOSE: Mortality statistics have recorded an increased number of deaths from ischemic heart disease (IHD) since death certificates were revised to reflect the International Classification of Diseases, tenth revision (ICD-10) in Japan, in 1995. However, it remains unclear whether the validity of IHD diagnosis improved after this revision. METHODS: We conducted the Oita Cardiac Death Survey to validate IHD certified deaths that occurred among residents aged 25-74 in Oita City, Japan (mean population = 273,000). Of the eligible 342 fatalities, 328 cases (95.0%) were examined by a review of the medical records and/or interviews with physicians. The MONICA criteria were applied and provided a reference standard against which to assess the validity of certified fatal IHD. Sensitivity (Se), positive predictive value (PPV), specificity (Sp) and negative predictive value (NPV) for IHD as the cause of death were analyzed, assuming that all validated IHD deaths were true. Multivariate logistic models were used to determine associations of false positive and false negative cases with sex, age at time of death and place of death. RESULTS: Vital statistics revealed 273 fatalities to be due to cardiac disease, including 143 from acute myocardial infarctions (AMI), 27 from other IHD, 52 from heart failure and 51 from other heart diseases. After validation, 25 'definite fatal AMI' and 71 'possible fatal AMI or IHD death' were identified among all subjects according to the MONICA criteria. In all, Se, PPV, Sp and NPV for IHD certified as the cause of death were 86.5% (95% Cl: 77.6-92.3), 50.3% (42.5-58.1), 64.7% (58.1-70.7), and 92.0% (86.5-95.5), respectively. PPV among persons aged 25-54 years was remarkably decreased. PPV and Sp among out-of-hospital deaths were significantly lower than for in-hospital deaths. Multivariate logistic models revealed out-of-hospital deaths and being aged 25-54 years to be significant predictors of false positive cases (odds ratio (OR) = 2.03, P < 0.001 versus in-hospital deaths and OR = 2.79, P < 0.05 versus ages of 65-74 years, respectively). CONCLUSIONS: Because false positive cases increased among certified IHD deaths after the revision, PPV and Sp percentages decreased. Out-of-hospital deaths and being aged 25-54 years were associated with increased possibility of false positive. Given our findings, IHD deaths in vital statistics may increase due to the tendency of physicians to certify IHD as the cause of death in cases without clear sign suggestive of other causes.     

Study of liver‐targeted regulatory T cells in hepatitis B and C virus in chronically infected patients

Introduction: Regulatory T cells (Tregs) play a critical role in chronic viral infections. The role of Tregs in chronic hepatitis B (CHB) and chronic hepatitis C (CHC) is unknown. This study examined the distribution and frequency of forkhead box p3⁺ (Foxp3⁺) Tregs in the liver tissue and compared the clinicopathological characteristics of CHB and CHC patients. Methods: Liver needle biopsies were obtained from 26 patients who were hepatitis B surface antigen positive and 27 patients who were hepatitis C virus antibody positive. Results: The ratio of Foxp3⁺ Tregs in CD3⁺ T cells was similar in HBV and in HCV cases. In HBV cases, the variables that were positively associated with the ratio of Foxp3⁺ Tregs in CD3⁺ T cells included the serum alanine aminotransferase level (R=0.402, P=0.025) and the ratio of CD8⁺ T cell plus CD56⁺ NK cell against CD4⁺ T cell (R=0.53, P=0.005). The ratio of Foxp3⁺ Tregs in CD3⁺ T cells increased more in the severe activity group than in the mild activity group (P=0.04). In HCV cases, the ratio of Foxp3⁺ Tregs in CD3⁺ T cells increased significantly in terms of the genotype2 (P=0.0002) and male gender (P=0.04). In addition, the ratio of Foxp3⁺ Tregs in CD3⁺ T cells showed a negative correlation with the ratio of CD8⁺ T cell plus CD56⁺ NK cell against CD4⁺ T cell (R=?0.508, P=0.005) and HCV viral load (R=?0.482, P=0.001). Conclusions: Liver‐targeted regulatory T cells present similarly in CHB and CHC, but their relationship with the effector cell population, the inflammation grade or the viral load is different between CHB and CHC.     

Stimulatory Effect of Calcitonin Gene-Related Peptide on Adrenocorticotropin Release from Rat Anterior Pituitary Cells

In the present study, we examined the direct regulatory effect of rat calcitonin gene-related peptide (CGRP) on adrenocorticotropin (ACTH) release from rat cultured anterior pituitary cells. CGRP significantly increased ACTH release at concentrations of 10⁻⁸–10⁻¹¹ M. The ACTH release was gradually increased by CGRP concentrations lower than 10⁻¹⁰ M, and was decreased at concentrations higher than 10⁻⁹ M, presenting a bell-shaped dose-response curve. As well as having an additive effect on corticotropin-releasing factor-induced ACTH release, CGRP stimulated the accumulation of intracellular cAMP. The CGRP-induced ACTH release was inhibited by a protein kinase A inhibitor, suggesting that its stimulatory effect on the ACTH release was mediated via an adenylate–cyclase–protein kinase system. CGRP-like immunoreactive nerve fibers have been reported to innervate the anterior pituitary, so that the stimulatory effect of CGRP on the ACTH release suggests that this peptide may be involved in neural regulation of hormone secretion in the anterior pituitary.     

Chlamydia pneumoniae: comparison with findings of Mycoplasma pneumoniae and Streptococcus pneumoniae at thin-section CT

PURPOSE: To retrospectively compare thin-section computed tomographic (CT) findings of Chlamydia pneumoniae pneumonia with those of Streptococcus pneumoniae pneumonia and Mycoplasma pneumoniae pneumonia. MATERIALS AND METHODS: Institutional review board and patient informed consent were not required. Twenty-four patients with C pneumoniae pneumonia (17 men, seven women; age range, 19-89 years) underwent thin-section CT; 41 patients with S pneumoniae pneumonia (28 men, 13 women; age range, 19-91 years) and 30 patients with M pneumoniae pneumonia (20 men, 10 women; age range, 16-67 years) were also enrolled. Thin-section CT scans of each patient were retrospectively and independently assessed by two chest radiologists for consolidation, ground-glass opacity (GGO), bronchovascular bundle thickening, nodules, pleural effusion, lymphadenopathy, reticular or linear opacity, airway dilatation, pulmonary emphysema, and bilateral lung involvement. Consensus was reached for disagreements. The frequency of each finding was compared among the three types of pneumonia by using the chi2 test. RESULTS: For C pneumoniae pneumonia, CT demonstrated consolidation in 20 patients, GGO in 13, bronchovascular bundle thickening in 17, nodules in 18, pleural effusion in six, lymphadenopathy in eight, reticular or linear opacity in 15, airway dilatation in nine, pulmonary emphysema in 11, and bilateral lung involvement in 12. Bronchovascular bundle thickening (P = .022) and airway dilatation (P = .034) were significantly more frequent in patients with C pneumoniae pneumonia than in those with S pneumoniae pneumonia. Reticular or linear opacity (P = .017), airway dilatation (P = .016), and associated pulmonary emphysema (P = .003) were significantly more frequent in patients with C pneumoniae pneumonia than in those with M pneumoniae pneumonia. CONCLUSION: C pneumoniae pneumonia demonstrates a wide spectrum of thin-section CT findings that are similar to those of S pneumoniae pneumonia and M pneumoniae pneumonia; airway dilatation and bronchovascular thickening were significantly more frequent in patients with C pneumoniae pneumonia.     

Phylogenetic variations of highly pathogenic H5N6 avian influenza viruses isolated from wild birds in the Izumi plain,Japan, during the 2016–17 winter season

During the 2016–2017 winter season, we isolated 33 highly pathogenic avian influenza viruses (HPAIVs) of H5N6 subtype and three low pathogenic avian influenza viruses (LPAIVs) from debilitated or dead wild birds, duck faeces, and environmental water samples collected in the Izumi plain, an overwintering site for migratory birds in Japan. Genetic analyses of the H5N6 HPAIV isolates revealed previously unreported phylogenetic variations in the PB2, PB1, PA, and NS gene segments and allowed us to propose two novel genotypes for the contemporary H5N6 HPAIVs. In addition, analysis of the four gene segments identified close phylogenetic relationships between our three LPAIV isolates and the contemporary H5N6 HPAIV isolates. Our results implied the co‐circulation and co‐evolution of HPAIVs and LPAIVs within the same wild bird populations, thereby highlighting the importance of avian influenza surveillance targeting not only for HPAIVs but also for LPAIVs.