Mental stress is associated with higher mortality, but it remains controversial whether the association is causal or a consequence of a higher physical disease burden in those with a high mental stress load. Understanding causality is important when developing targeted interventions. We aimed to estimate the effect of mental stress on mortality by performing a ‘natural’ experiment using spousal bereavement as a disease-independent mental stressor.

We followed a population-based matched cohort, including all individuals in Denmark bereaved in 1997–2014, for 17 years. Prospectively recorded register data were obtained for civil and vital status, 39 mental and physical diagnoses, and socioeconomic factors.

In total, 389 316 bereaved individuals were identified and 137 247 died during follow-up. Bereaved individuals had higher all-cause mortality than non-bereaved references in the entire study period. The relative mortality in the bereaved individuals was highest shortly after the loss (adjusted hazard ratio (aHR), first month: 2.50, 95% confidence interval (CI) 2.37–2.63; aHR, 6–12 months: 1.38, 95% CI 1.34–1.42). The excess mortality rate associated with bereavement rose with increasing number of physical diseases (1.33 v. 7.00 excess death per 1000 person-months for individuals with 0 v. ⩾3 physical conditions during the first month) and was exacerbated by the presence of mental illness. The excess mortality among bereaved individuals was primarily due to death from natural causes.

Bereavement was associated with increased short-term and long-term mortality, even after adjustment for morbidities, which suggests that mental stress may play a causal role in excess mortality.

Universal screening for postpartum depression is recommended in many countries. Knowledge of whether the disclosure of depressive symptoms in the postpartum period differs across cultures could improve detection and provide new insights into the pathogenesis. Moreover, it is a necessary step to evaluate the universal use of screening instruments in research and clinical practice. In the current study we sought to assess whether the Edinburgh Postnatal Depression Scale (EPDS), the most widely used screening tool for postpartum depression, measures the same underlying construct across cultural groups in a large international dataset.

Ordinal regression and measurement invariance were used to explore the association between culture, operationalized as education, ethnicity/race and continent, and endorsement of depressive symptoms using the EPDS on 8209 new mothers from Europe and the USA.

Education, but not ethnicity/race, influenced the reporting of postpartum depression [difference between robust comparative fit indexes (∆*CFI) < 0.01]. The structure of EPDS responses significantly differed between Europe and the USA (∆*CFI > 0.01), but not between European countries (∆*CFI < 0.01).

Investigators and clinicians should be aware of the potential differences in expression of phenotype of postpartum depression that women of different educational backgrounds may manifest. The increasing cultural heterogeneity of societies together with the tendency towards globalization requires a culturally sensitive approach to patients, research and policies, that takes into account, beyond rhetoric, the context of a person's experiences and the context in which the research is conducted.

The loss of a close relative is one of the most stressful life events. In pregnancy, this experience has been associated with a higher risk of fetal death and under-five mortality, but little is known about potential effects on long-term mortality in offspring. We examined the association between prenatal maternal bereavement and mortality in a cohort of 5.3 million children followed until up to 37 years of age.

The population-based cohort study included 5 253 508 live singleton births in Denmark (1973–2004) and Sweden (1973–2006). Children born to mothers who lost a child, spouse, sibling, or parent during or 1 year before pregnancy were categorized as exposed.

Prenatal maternal bereavement was associated with a 10% increased all-cause mortality risk in offspring [mortality rate ratio (MRR) 1.10, 95% confidence interval (CI) 1.03–1.18]. The association was the most pronounced for children of mothers who lost a child/spouse (MRR 1.28, 95% CI 1.14–1.44) and was stronger during the first 10 years of life. Prenatal maternal bereavement may have stronger effects on natural causes of death in offspring, including infectious/parasitic disease (MRR 1.86, 95% CI 1.07–3.23), endocrine/nutritional/metabolic diseases (MRR 3.23, 95% CI 2.02–5.17), diseases of nervous system (MRR 3.36, 95% CI 2.47–4.58), and congenital malformations (MRR 1.39, 95% CI 1.08–1.80). No excess mortality risk in offspring was observed for unnatural causes of death.

Prenatal maternal bereavement was associated with an increased long-term mortality risk in offspring, particularly for selected natural causes of diseases and medical conditions. Our results support the fetal programming hypothesis that prenatal stress may contribute to ill health from physical diseases later in life.

Maternal stress during pregnancy may increase the risk of preterm delivery (PD), but the associations between stress and subtypes of PD are not clear. We investigated maternal loss of a close relative and risks of very and moderately PD (<32 and 32–36 weeks, respectively) and spontaneous and medically indicated PD.

We studied 4 940 764 live singleton births in Denmark (1978–2008) and Sweden (1973–2006). We retrieved information on death of women's family members (children, partner, siblings, parents), birth outcomes and maternal characteristics from nationwide registries.

Overall, the death of a close family member the year before pregnancy or in the first 36 weeks of pregnancy was associated with a 7% increased risk of PD [95% confidence interval (CI) 1.04–1.10]. The highest hazard ratios (HR) for PD were found for death of an older child [HR (95% CI) 1.20 (1.10–1.31)] and for death of a partner [HR (95% CI) 1.31 (1.03–1.66)]. These losses were associated with higher risks of very preterm [HR (95% CI) 1.61 (1.29–2.01) and 2.07 (1.15–3.74), respectively] than of moderately preterm [HR (95% CI) 1.14 (1.03–1.26) and 1.22 (0.94–1.58), respectively] delivery. There were no substantial differences in the association between death of a child or partner and the risk of spontaneous v. medically indicated PD.

Death of a close family member the year before or during pregnancy was associated with an increased risk of PD, especially very PD. Possible mechanisms include both spontaneous and medically indicated preterm birth.

Maternal stress during pregnancy is associated with a modestly increased risk of fetal growth restriction and pre-eclampsia. Since placental abruption shares similar pathophysiological mechanisms and risk factors with fetal growth restriction and pre-eclampsia, we hypothesized that maternal stress may be implicated in abruption risk. We investigated the association between maternal bereavement during pregnancy and placental abruption.

We studied singleton births in Denmark (1978–2008) and Sweden (1973–2006) (n = 5 103 272). In nationwide registries, we obtained data on death of women's close family members (older children, siblings, parents, and partners), abruption and potential confounders.

A total of 30 312 (6/1000) pregnancies in the cohort were diagnosed with placental abruption. Among normotensive women, death of a child the year before or during pregnancy was associated with a 54% increased odds of abruption [95% confidence interval (CI) 1.30–1.82]; the increased odds were restricted to women who lost a child the year before or during the first trimester in pregnancy. In the group with chronic hypertension, death of a child the year before or in the first trimester of pregnancy was associated with eight-fold increased odds of abruption (odds ratio 8.17, 95% CI 3.17–21.10). Death of other relatives was not associated with abruption risk.

Loss of a child the year before or in the first trimester of pregnancy was associated with an increased risk of abruption, especially among women with chronic hypertension. Studies are needed to investigate the effect of less severe, but more frequent, sources of stress on placental abruption risk.

To evaluate the use of inpatient pharmacy and administrative data to detect surgical site infections (SSIs) following hysterectomy and colorectal and vascular surgery.

Retrospective cohort study.

Five hospitals affiliated with academic medical centers.

Adults who underwent abdominal or vaginal hysterectomy, colorectal surgery, or vascular surgery procedures between July 1, 2003, and June 30, 2005.

We reviewed the medical records of weighted, random samples drawn from 3,079 abdominal and vaginal hysterectomy, 4,748 colorectal surgery, and 3,332 vascular surgery procedures. We compared routine surveillance with screening of inpatient pharmacy data and diagnosis codes and then performed medical record review to confirm SSI status.

Medical records from 823 hysterectomy, 736 colorectal surgery, and 680 vascular surgery procedures were reviewed. SSI rates determined by antimicrobial- and/or diagnosis code-based screening followed by medical record review (enhanced surveillance) were substantially higher than rates determined by routine surveillance (4.3% [95% confidence interval, 3.6%—5.1%] vs 2.7% for hysterectomies, 7.1% [95% confidence interval, 6.7%–8.2%] vs 2.0% for colorectal procedures, and 2.3% [95% confidence interval, 1.9%–2.9%] vs 1.4% for vascular procedures). Enhanced surveillance had substantially higher sensitivity than did routine surveillance to detect SSI (92% vs 59% for hysterectomies, 88% vs 22% for colorectal procedures, and 72% vs 43% for vascular procedures). A review of medical records confirmed SSI for 31% of hysterectomies, 20% of colorectal procedures, and 31% of vascular procedures that met the enhanced screening criteria.

Antimicrobial- and diagnosis code-based screening may be a useful method for enhancing and streamlining SSI surveillance for a variety of surgical procedures, including those procedures targeted by the Centers for Medicare and Medicaid Services.

To evaluate the use of routinely collected electronic health data in Medicare claims to identify surgical site infections (SSIs) following hip arthroplasty, knee arthroplasty, and vascular surgery.

Retrospective cohort study.

Four academic hospitals that perform prospective SSI surveillance.

We developed lists of International Classification of Diseases, Ninth Revision, and Current Procedural Terminology diagnosis and procedure codes to identify potential SSIs. We then screened for these codes in Medicare claims submitted by each hospital on patients older than 65 years of age who had undergone 1 of the study procedures during 2007. Each site reviewed medical records of patients identified by either claims codes or traditional infection control surveillance to confirm SSI using Centers for Disease Control and Prevention/ National Healthcare Safety Network criteria. We assessed the performance of both methods against all chart-confirmed SSIs identified by either method.

Claims-based surveillance detected 1.8–4.7-fold more SSIs than traditional surveillance, including detection of all previously identified cases. For hip and vascular surgery, there was a 5-fold and 1.6-fold increase in detection of deep and organ/space infections, respectively, with no increased detection of deep and organ/space infections following knee surgery. Use of claims to trigger chart review led to confirmation of SSI in 1 out of 3 charts for hip arthroplasty, 1 out of 5 charts for knee arthroplasty, and 1 out of 2 charts for vascular surgery.

Claims-based SSI surveillance markedly increased the number of SSIs detected following hip arthroplasty, knee arthroplasty, and vascular surgery. It deserves consideration as a more effective approach to target chart reviews for identifying SSIs.

Infect Control Hosp Epidemiol 2012;33(1):40-49

In April 2009, 2009 pandemic influenza A (H1N1) (hereafter, pH1N1) virus was identified in California, which caused widespread illness throughout the United States. We evaluated pH1N1 transmission among exposed healthcare personnel (HCP) and assessed the use and effectiveness of personal protective equipment (PPE) early in the outbreak.

Cohort study.

Two hospitals and 1 outpatient clinic in Southern California during March 28-April 24, 2009.

Sixty-three HCP exposed to 6 of the first 8 cases of laboratory-confirmed pH1N1 in the United States.

Baseline and follow-up questionnaires were used to collect demographic, epidemiologic, and clinical data. Paired serum samples were obtained to test for pH1N1-specific antibodies by microneutralization and hemagglutination-inhibition assays. Serology results were compared with HCP work setting, role, and self-reported PPE use.

Possible healthcare-associated pH1N1 transmission was identified in 9 (14%) of 63 exposed HCP; 6 (67%) of 9 seropositive HCP had asymptomatic infection. The highest attack rates occurred among outpatient HCP (6/19 [32%]) and among allied health staff (eg, technicians; 8/33 [24%]). Use of mask or N95 respirator was associated with remaining seronegative (P = .047). Adherence to PPE recommendations for preventing transmission of influenza virus and other respiratory pathogens was inadequate, particularly in outpatient settings.

pH1N1 transmission likely occurred in healthcare settings early in the pandemic associated with inadequate PPE use. Organizational support for a comprehensive approach to infectious hazards, including infection prevention training for inpatient- and outpatient-based HCP, is essential to improve HCP and patient safety.