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PubMed2002

Programmed cell death is required for palate shelf fusion and is regulated by retinoic acid.

The actual role of programmed cell death (PCD) in embryonic processes and the extrinsic signals that define the death fate in developing cells are still poorly understood. Here, we show that during secondary palate shelf fusion in the mouse, PCD appeared in the medial edge epithelia (MEE) of the anterior region only after shelf contact. Contact was necessary for efficient cell death activation in the MEE. However, exogenous all-trans-retinoic acid (RA) increased cell death independently of contact. Competence to induce cell death by contact or by RA exposure was obtained when the MEE were close to touch. Endogenous RA is a relevant regulator of the secondary palate PCD since this was reduced by a retinol dehydrogenase inhibitor and an RAR specific antagonist. Bmp-7 expression was positively regulated by RA. However, BMP-7 was unable to activate cell death within the palate tissue and NOGGIN, a natural BMP antagonist, did not block PCD. Reduction of PCD at the MEE directly with a caspase inhibitor or by inhibiting retinol dehydrogenase resulted in unfused palate shelves, but adhesion was not affected. In contrast, exogenous RA also blocked fusion, but in this situation the increased cell death within the MEE appeared to affect adhesion, thereby causing cleft palate in vivo.

Animals↗

PubMed2005

Temporal variation in deaths related to alcohol intoxication and drinking.

BACKGROUND: Temporal variation in deaths related to alcohol intoxication is examined using two approaches. First, we examine the risk of these deaths during festivals, on the day preceding them, and on the three days that immediately follow them. Second, we assess the weekday variation in deaths, and compare this with survey-based data on weekday variations in drinking. Previously no data existed on the temporal association between intoxication-related deaths and drinking occasions according to the severity of intoxication. METHODS: We used population registration data on 15-69-year-old men and women, linked with the national cause of death register for the years 1987-2001, and the Finnish Drinking Habits Survey carried out in 2000. Intoxication-related deaths were defined on the basis of underlying and contributory causes of death. RESULTS: The largest increased risk of intoxication-related deaths was observed for Midsummer Day [Observed deaths/Expected deaths (O/E) = 2.88 (95% confidence interval 2.48-3.31) for men and O/E = 2.21 (1.43-3.27) for women respectively], Midsummer Eve [O/E = 2.70 (2.32-3.12) and 3.18 (2.23-4.41)], May Day [O/E = 1.80 (1.50-2.16) and 2.65 (1.79-3.79)], Christmas Eve [O/E = 1.58 (1.29-1.91) and 2.21 (1.43-3.27)], and New Year's Day [O/E = 1.48 (1.20-1.80) and 1.77 (1.08-2.74)]. Among men, the increased risk at Midsummer lasted for three consecutive days. The weekday distribution of different levels of intoxication and of intoxication-related deaths was similar, with a clear increase observed on Friday, Sunday, and, particularly, Saturday. CONCLUSIONS: Intoxication-related deaths peak during weekends and around festival days when alcohol is widely consumed in excess. Public awareness of the risks attached to binge drinking should be increased.

Adolescent↗

PubMed2000

Flow cytometric investigation of filamentation, membrane patency, and membrane potential in Escherichia coli following ciprofloxacin exposure.

Ninety-eight percent of the cells in a population of Escherichia coli in log-phase growth lost colony-forming ability after being exposed for 3 h to the quinolone antibiotic ciprofloxacin at four times the MIC in nutrient broth, a concentration easily reached in vivo. Flow cytometric analysis, however, demonstrated that only 68% of this bacterial population had lost membrane potential, as judged by the membrane potential-sensitive dye bis-(1,3-dibutylbarbituric acid) trimethine oxonol [DiBAC(4)(3)], and only 30% could no longer exclude the nucleic acid-binding dye propidium iodide (PI), reflecting lost membrane integrity, efflux mechanisms, or both. Subsequent removal of ciprofloxacin and resuspension in nutrient broth resulted in renewed cell division after 2 h, with a calculated postantibiotic effect (PAE) time of 57 min. The proportion of DiBAC- and PI-fluorescent cells in this recovering population remained stable for more than 4 h after antibiotic removal. Eighty percent of cells present at drug removal were filamentous. Their number subsequently decreased with time, and the increase in particle count seen at the end of the PAE resulted from the division of short cells. Exposure to ciprofloxacin in the presence of the protein synthesis inhibitor chloramphenicol increased colony-forming ability to 60% of starting population numbers. In contrast to ciprofloxacin alone, this antibiotic combination resulted in insignificant filamentation and no dye uptake. Subsequent drug removal and resuspension in nutrient broth resulted in the appearance of filaments within 1 h, with 69% of the population forming filaments at 3 h. Dye uptake was also seen, with 20% of the population fluorescing with either dye after 4 h. We were unable to relate dye uptake to the viable count. Cell division resumed 240 min after removal of both drugs, yielding a PAE calculated at 186 min. Inhibition of protein synthesis with chloramphenicol prevented ciprofloxacin-induced changes in bacterial morphology, cell membrane potential, and ability to exclude nucleic acid-binding dye. These changes persisted beyond the end of the classically defined PAE and were not a definite indicator of cell death as defined by loss of colony formation, which related at least in part to filamentation.

Anti-Infective Agents↗

PubMed1993

Diversification in the concept of "birth and death": the controversy about "brain death and organ transplantation" in Japan.

There is a lot of hesitation in Japan in defining brain death as the death of the individual and in proceeding to organ transplantation. Regarding the diagnostic criteria of brain death, those issued by the Japanese Ministry of Health and Welfare in 1985 are sufficient for judgment of brain death. Many people, however, do not accept brain death as death of the individual, and even those who admit brain death as death of the individual hesitate to approve of the actual removal of organs from brain dead patients. Thus, the controversy about brain death in Japan appears to be separated from the objective of organ transplantation.

Brain Death↗

PubMed2004

Malignancy-related causes of death in human immunodeficiency virus-infected patients in the era of highly active antiretroviral therapy.

BACKGROUND: Before the introduction of highly active antiretroviral therapy (HAART), malignancies accounted for less than 10% of all deaths among human immunodeficiency virus (HIV)-infected patients. This figure may have increased, and the observed types of malignant disease may have been modified, as a result of decreased occurrence of opportunistic infections, the chronicity of HIV infection, the possible oncogenic role of HIV itself, and the aging of the HIV-infected population. METHODS: All French hospital wards involved in the management of HIV infection were asked to prospectively document the deaths of HIV-infected patients in the year 2000. Underlying causes of death were defined using a standardized questionnaire. RESULTS: Of a total of 964 deaths, 269 (28%) were attributable to malignancies. Acquired immunodeficiency virus (AIDS)-related malignancies were the underlying cause of 149 deaths (15%); among these malignancies were non-Hodgkin lymphoma (n = 105 [11%]), noncerebral lymphoma (n = 78 [median CD4 count, 86 x 10(6) per liter; interquartile range [IQR], 35-231 x 10(6) per liter), and primary cerebral lymphoma (n = 27 [median CD4 count, 20 x 10(6) per liter; IQR, 4-109 x 10(6) per liter). Kaposi sarcoma was associated with 40 deaths (4%), and cervical carcinoma was associated with 5 (0.5%). Non-AIDS-related malignancies were the underlying cause of 120 deaths (13%); these non-AIDS-related malignancies included 103 solid tumors (50 respiratory tumors, 19 hepatocarcinomas, 9 digestive tumors, and 6 anal tumors; median CD4 count, 218 x 10(6) per liter; IQR, 108-380 x 10(6) per liter) and 17 hemopathies (12 Hodgkin lymphomas, 4 myeloid leukemias, and 1 myeloma; median CD4 count, 113 x 10(6) per liter; IQR, 56-286 x 10(6) per liter). Compared with patients who died of other causes, patients who died of solid tumors were more likely to be male, to smoke, to be older, and to have higher CD4 counts. CONCLUSIONS: Malignant disease has been a major cause of death among HIV-infected patients in industrialized nations since the introduction of HAART. Whereas lethal hemopathies and Kaposi sarcoma are associated with advanced immunosuppression, lethal solid tumors can occur in patients with controlled HIV infection.

Acquired Immunodeficiency Syndrome↗

PubMed1994

Brain death: neuropathological findings and forensic implications.

'Brain death' is defined pathophysiologically as intracranial circulatory arrest. The morphological features of brain death include cerebral edema, absence of reactive changes, and--after an interval of 15-36 h--the morphological hallmarks of respirator brain: edema, global softening of the brain, dusky discoloration of the gray matter, and often necrotic and sloughing tonsillar herniations. The following implications of brain death for forensic medicine are discussed: discriminating between respirator and autolytic brain, declaration of death, determining the time of brain death versus the time of the traumatic event leading to brain death, and neuropathological control of the clinical diagnosis of brain death. These issues are elucidated and their bearing on forensic practice is illustrated by several real-life situations. Thus, neuropathological examination in the case of clinically diagnosed brain death is--without doubt--necessary in order to answer several questions often or regularly expected.

Brain↗

PubMed2004

Factors associated with out-of-hospital coronary heart disease death: the national longitudinal mortality study.

PURPOSE: A significant portion of coronary heart disease deaths occur out of the hospital, prior to access to life saving medical care. Improving the immediacy of care could have important impact on coronary mortality. METHODS: The objective of this research is to identify factors associated with the occurrence of out-of-hospital coronary heart disease death as compared with in-hospital. Identification of these factors could lead to additional strategies for rapid treatment of coronary attack symptoms. A large national cohort study with individually identified characteristics was matched to the National Death Index to identify deaths by cause occurring in up to 11 years of follow-up. Approximately 60,000 deaths occurred in the cohort of approximately 700,000 participants aged 25 years or more. Location of death was defined as either in- or out-of-hospital. RESULTS: Among deaths classified as coronary heart disease (CHD), multivariate logistic models of the association between selected demographic and socioeconomic characteristics of individuals prior to death and place of death show that black persons are more likely to die out of hospital, as are persons who live alone or are unmarried, persons at the lowest end of the income distribution, and persons who live in rural areas vs. urban areas. CONCLUSIONS: The factors most strongly associated with a CHD death occurring out-of-hospital as compared with in-hospital are race (black persons are 1.23 times more likely to die out of hospital than white persons, net of demographic and socioeconomic differentials) and living status (persons who are not married are 1.60 times more likely to die out of hospital than persons who are married, net of demographic and socioeconomic characteristics). Attention should be paid to these groups to emphasize the need for rapid attention to the signs of a coronary attack so that rapid and potentially life saving intervention can be implemented.

Adult↗

PubMed2002

Trends in maternal mortality and assessment of substandard care in a tertiary care hospital.

OBJECTIVE: To assess the trends in maternal mortality and factors affecting substandard care at a tertiary care hospital in a developing country. METHOD: All maternal deaths during a period of 11 years in a tertiary care hospital were studied. Maternal deaths were defined according to ICD-10. The principal cause and category of death, chief contributory factor, nature of care (standard or substandard), relationship to outcome and responsibility for substandard care (if any) were determined. RESULTS: Among the 133 maternal deaths, 92 (69%) were due to direct causes, 38 (29%) were indirect and 3 (2%) were accidental deaths. Genital tract sepsis (26%), hypertension in pregnancy (24%) and obstetric hemorrhage (20%) accounted for over 70% of deaths. In 79% of deaths, the care was substandard and in 73% of deaths substandard care was felt to have influenced the adverse outcome. Overall maternal mortality rate was 98.5 per 100,000 deliveries. An increasing but insignificant (P=0.08) trend in maternal mortality was noted after 1991. CONCLUSIONS: The majority of maternal deaths remain due to preventable and treatable obstetric complications. Maternal death enquiries of this nature facilitate identification of factors contributing to substandard care. It is important to ascertain that life threatening obstetric complications receive high quality emergency obstetric care at all levels.

Adult↗

PubMed2006

Cell cycle molecules define a pathway required for neuron death in development and disease.

We review here evidence defining a molecular pathway that includes cell cycle-related molecules and that appears to play a required role in neuron death during normal development as well as in disease and trauma. The pathway starts with inappropriate activation of cyclin dependent kinase 4 (Cdk4) in neurons which leads to hyper-phosphorylation of the pRb family member p130. This in turn results in dissociation of p130 and its associated chromatin modifiers Suv39H1 and HDAC1 from the transcription factor E2F4. Dissociation of this complex results in de-repression of genes with E2F binding sites including those encoding the transcription factors B- and C-Myb. Once elevated in neurons, B- and C-Myb proteins bind to the promoter for the pro-apoptotic BH3-only protein Bim and promote its induction. Bim then interacts with the core cellular apoptotic machinery, leading to caspase activation and apoptotic death. This pathway is supported by a variety of observations and experimental findings that implicate it as a required element for neuron loss in development and in many nervous system traumas and disorders. The components of this pathway appear to represent potential therapeutic targets for prevention of disease-associated neuron death.

Animals↗

PubMed2002

Drowning and near-drowning.

Water immersion is a frequent cause of accidental death and hospital admission. This article outlines the pathogenesis and principles of treatment. Drowning is defined as death by asphyxia due to submersion in a liquid medium. Near-drowning is defined as immediate survival after asphyxia due to submersion.

Adolescent↗

PubMed2003

Urinary outflow obstruction increases apoptosis and deregulates Bcl-2 and Bax expression in the fetal ovine bladder.

During organogenesis, net growth of tissues is determined by a balance between proliferation, hypertrophy, and apoptotic death. Human fetal bladder outflow obstruction is a major cause of end-stage renal failure in children and is associated with complex pathology in the kidney and lower urinary tract. Experimental manipulation of the fetal sheep urinary tract has proved informative in understanding the pathobiology of congenital obstructive uropathy. In this study we used an ovine model of fetal bladder outflow obstruction to examine effects on apoptotic cell death in the developing urinary bladder. While 30 days of obstruction in utero between 75 and 105 days gestation resulted in overall growth of the fetal bladder as assessed by weight, protein, and DNA measurements, we found that apoptosis, as assessed by in situ end-labeling, was up-regulated in fetal bladder detrusor muscle and lamina propria cells and that this was accompanied by a down-regulation of the anti-death protein Bcl-2 and an up-regulation of the pro-death protein Bax. Moreover, activated caspase-3, an effector of apoptotic death, was increased in obstructed bladders. This is the first study to define altered death in an experimental fetal model of bladder dysmorphogenesis. We speculate that enhanced apoptosis in detrusor smooth muscle cells is part of a remodeling response during compensatory hyperplasia and hypertrophy. Conversely, in the lamina propria, an imbalance between death and proliferation leads to a relative depletion of cells.

Animals↗

PubMed1999

Predictors of clinical events or restenosis during follow-up after percutaneous mitral balloon valvotomy.

AIMS: The purpose of this study is to define predictors of events or restenosis during follow-up after percutaneous mitral balloon valvotomy. METHODS AND RESULTS: Percutaneous mitral balloon valvotomy was attempted in 137 patients with severe mitral valve stenosis. In 127 patients follow-up was complete with a mean of 4.2 +/- 2.6 years. Events during follow-up were defined as death, mitral valve surgery or repeat percutaneous mitral balloon valvotomy. Restenosis was defined as a decrease in mitral valve area from > or = 1.5 cm2 following percutaneous mitral balloon valvotomy to < 1.5 cm2. There was 80 +/- 4% event-free survival 4 years after percutaneous mitral balloon valvotomy. Multivariate analysis showed chronic atrial fibrillation at baseline (P = 0.039, relative risk (RR) = 2.5) and a high residual maximal gradient after percutaneous mitral balloon valvotomy (P = 0.004, RR = 2.0 per 5 mmHg) to be independent predictors of an event during follow-up. The restenosis rate was 28.3% after 4 years. Chronic atrial fibrillation at baseline (P = 0.0338, RR = 2.2), a small mitral valve area after percutaneous mitral balloon valvotomy (P = 0.0003, RR = 0.8/0.1 cm2) and a high residual maximal transmitral gradient (P = 0.0252, RR = 1.6/5 mmHg) were all independent predictors of restenosis. CONCLUSION: Patients with chronic atrial fibrillation and a high maximal transmitral gradient after percutaneous mitral balloon valvotomy have a higher risk for events during follow-up. Restenosis is related to the presence of chronic atrial fibrillation at baseline and a suboptimal percutaneous mitral balloon valvotomy result.

Adult↗

PubMed2003

Drowning.

PURPOSE OF REVIEW: To summarize current knowledge on pathophysiology and treatment of drowning accidents. Studies and case reports were searched using the keywords drowning, near-drowning, asphyxia, hypoxia and hypothermia in conjunction with organ systems and specific treatment options. RECENT FINDINGS: Drowning is defined as death by suffocation in a liquid. In contrast, near-drowning is defined as survival beyond 24 h after a drowning accident. Drowning is a frequent preventable accident with a significant morbidity and mortality in a mostly healthy population. In the majority of patients the primary injury is pulmonary, resulting in severe arterial hypoxemia and secondary damage to other organs. Damage to the central nervous system is most critical in terms of patient survival and subsequent quality of life. Therefore, prompt resuscitation and aggressive respiratory and cardiovascular treatment are crucial for optimal survival. Immediate interruption of hypoxia, aggressive treatment of hypothermia and cardiovascular failure are the cornerstones of correct medical treatment. Unfortunately, accurate neurologic prognosis cannot be predicted from initial clinical presentation, laboratory, radiological or electrophysiological examinations. SUMMARY: Several case studies have convincingly demonstrated that drowning victims may survive neurologically intact even after prolonged submersion times, in particular in cold water. Therefore, aggressive initial therapeutic efforts are indicated in most near-drowning victims.

Journal Article↗

PubMed1997

Low doses of zidovudine plus didanosine are less effective than higher doses of didanosine monotherapy: a randomized trial in patients pretreated with zidovudine.

OBJECTIVE: To compare the clinical efficacy and tolerance of didanosine (ddl) monotherapy with low-dose zidovudine/didanosine (AZT/ddl) therapy among HIV-infected patients previously treated with AZT. METHODS: A randomized controlled trial was carried out of ddl 400 mg daily versus AZT/ddl 300/200 mg daily among patients with CD4 cell counts </=350 mm3 and prior AZT treatment for at least 16 weeks. Fifty eight patients received ddl monotherapy and 66 combined treatment. RESULTS: Patients were similar with respect to demographic, clinical and laboratory characteristics, and prior AZT treatment. Median duration of follow-up was 17.3 months. In the ddl group, 20 patients (34%) discontinued treatment because of toxicity, compared to 19 (29%) in the AZT/ddl group (p=0.38). There was no statistically significant difference in CD4 change between the two groups. In the ddl group, 16 patients (28%) developed a clinical endpoint (death or AIDS-defining opportunistic infection), compared to 33 (50%) in the combined therapy group (relative risk 1.8; 95% confidence interval 1.1-2.9; p=0.01). CONCLUSIONS: For fairly advanced AZT-pretreated patients, monotherapy with ddl was clinically and statistically superior to the low-dose AZT/ddl combination in preventing AIDS-defining illness and death. When access to drugs is limited, e.g. in under-resourced countries, combining available drugs and reducing dosage may be less effective than a single drug at the conventional dosage.

Journal Article↗

PubMed2002

An investigation of unexplained infant deaths in houses contaminated with methyl parathion.

In Lorain County, Ohio, unexplained infant deaths in homes sprayed with methyl parathion (MP), an organophosphate (OP) pesticide, prompted an investigation to determine whether infants living in treated homes are at higher risk for unexplained death. A case was defined as any death of an infant (12 months of age) in Lorain County between 1 January 1990 and 31 December 1994, attributed to sudden infant death syndrome (SIDS) or other unknown natural causes. For each case infant, birth certificate data were used to identify two control infants matched with regard to date of birth, sex, city of residence, and maternal race and educational level. Wipe samples from the home address listed on the birth certificate of control infants or the death certificate of case infants were analyzed for MP. Birth certificates provided additional risk factor information. The relationship between MP contamination and unexplained death was analyzed by exact conditional logistic regression. Wipe samples were collected from the residences of 34 case infants and 72 control infants. MP (>0.02 mg/100 cm2) was detected in five homes, three of which had been occupied by case infants. Case infants were 4.6 times more likely than control infants to have lived in MP-treated homes, but the confidence interval (CI) was wide (95% CI: 0.2, 274.7) and included 1. Maternal smoking, young maternal age, and the presence of other siblings in the family were each independently predictive of case status. In a multivariate model adjusting for these other variables and the matching variables, the estimated risk associated with MP exposure was 13.0 (95% CI: 0.2, 2,685.0). Although this association was not statistically significant and should be interpreted cautiously, it suggests an increased risk for unexplained death among infants living in MP-contaminated homes. The relationship between children's health and exposure to OP pesticides including MP should be evaluated further.

Cause of Death↗

PubMed2007

Familial premature coronary artery disease mortality and obstructive sleep apnea.

BACKGROUND: Obstructive sleep apnea (OSA) is linked to both coronary artery disease (CAD) and sudden death, but any causal role remains unclear. A family history of premature CAD and related mortality is an independent risk factor for the development of CAD. We hypothesized that OSA is associated with a family history of premature mortality from ischemic heart disease. METHODS: We prospectively studied 588 subjects who underwent polysomnography from May 2000 to June 2004. Demographics, comorbidities, family history of cardiovascular disease, and the ages and causes of death for 10 strata of family members were recorded for all subjects. We excluded those subjects with known causes of premature cardiac death, such as hypertrophic cardiomyopathy and long-QT syndrome. OSA was defined by American Academy of Sleep Medicine criteria (ie, apnea-hypopnea index >or= 5). Premature CAD mortality was defined as death due to ischemic heart disease or sudden cardiac death before 55 years of age (men) or 65 years of age (women). RESULTS: Polysomnography confirmed OSA in 316 subjects and excluded it in 202 subjects. The unadjusted odds ratio (OR) for OSA and a family history of premature CAD mortality was 2.11 (95% confidence interval [CI], 1.10 to 4.31; p = 0.031). After adjusting for each subject's sex, body mass index, and history of CAD, there was a significant and independent association between OSA and family history of premature CAD mortality (OR, 2.13; 95% CI, 1.04 to 4.66; p = 0.046). CONCLUSIONS: Regardless of their own CAD status, people with OSA are more likely than those without OSA to have a family history of premature CAD mortality.

Cause of Death↗

PubMed1997

[Sudden infant death].

Sudden infant death [SID] is defined as the "sudden death of an infant under one year of age that remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene and the review of the clinical history". This definition, given by the National Institute of Child Health and Human Development in the USA. recognized SID as a diagnostic entity, however, SID remains a pathological diagnosis of exclusion. SID-cases are divided into three categories: group 1 in which autopsy does not reveal any cause of death, group 2 in which postmortem findings are not sufficient to be the cause of death; group 3 in which the death is adequately explained, is classified as "non-SID". The purpose of the study was to analyse the situation about SID over a 25-year period, from 1969 through 1993, looking for changes in frequency and developmental trends. The study includes 364 SID-infants which were examined according to a standard method. Histological, microbiological, virological and immunological studies were performed and data of the death scene investigation and of the clinical history were collected, 284 infants who had died due to clinical diseases served as one control group, a second group consisted of 6397 newborns of the city of Zürich. Of the SID-infants, almost every third infant [29%] was grouped in group 1, more than half of the infants [52%] with signs of mild infections in group 2, whereas almost every fifth child [19%] was grouped in group 3. With regard to epidemiological parameters the peak of mortality was found at about three months of age; the percentage of boys and twins, of third and later born infants was higher compared to the general population. SID probands were born twice as often in October as in March. The percentage of mothers of first, second and third born SID-infants at an age younger than 20, 22 and 24 years was higher compared to the general population. All these parameters were also found in group 3. The risk of familial recurrence in group 1 and group 2 was 0.8%. Between 1969 and 1993 the rate of SID deaths dropped from 1.1 to 0.9 per thousand live births, whereas SID as a percentage of postneonatal mortality increased to 34 per cent.

Adult↗

PubMed2002

Causes of death for patients with community-acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team cohort study.

BACKGROUND: To our knowledge, no previous study has systematically examined pneumonia-related and pneumonia-unrelated mortality. This study was performed to identify the cause(s) of death and to compare the timing and risk factors associated with pneumonia-related and pneumonia-unrelated mortality. METHODS: For all deaths within 90 days of presentation, a synopsis of all events preceding death was independently reviewed by 2 members of a 5-member review panel (C.M.C., D.E.S., T.J.M., W.N.K., and M.J.F.). The underlying and immediate causes of death and whether pneumonia had a major, a minor, or no apparent role in the death were determined using consensus. Death was defined as pneumonia related if pneumonia was the underlying or immediate cause of death or played a major role in the cause of death. Competing-risk Cox proportional hazards regression models were used to identify baseline characteristics associated with mortality. RESULTS: Patients (944 outpatients and 1343 inpatients) with clinical and radiographic evidence of pneumonia were enrolled, and 208 (9%) died by 90 days. The most frequent immediate causes of death were respiratory failure (38%), cardiac conditions (13%), and infectious conditions (11%); the most frequent underlying causes of death were neurological conditions (29%), malignancies (24%), and cardiac conditions (14%). Mortality was pneumonia related in 110 (53%) of the 208 deaths. Pneumonia-related deaths were 7.7 times more likely to occur within 30 days of presentation compared with pneumonia-unrelated deaths. Factors independently associated with pneumonia-related mortality were hypothermia, altered mental status, elevated serum urea nitrogen level, chronic liver disease, leukopenia, and hypoxemia. Factors independently associated with pneumonia-unrelated mortality were dementia, immunosuppression, active cancer, systolic hypotension, male sex, and multilobar pulmonary infiltrates. Increasing age and evidence of aspiration were independent predictors of both types of mortality. CONCLUSIONS: For patients with community-acquired pneumonia, only half of all deaths are attributable to their acute illness. Differences in the timing of death and risk factors for mortality suggest that future studies of community-acquired pneumonia should differentiate all-cause and pneumonia-related mortality.

Cause of Death↗