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PubMed2001

Care of the patient close to death.

The recognition that the patient is close to death is essential and usually possible. Assessment must be meticulous, goals clearly articulated, and strategies for symptom relief and comprehensive care defined and monitored. Death should not be obstructed by futile measures. The wish of a patient to be allowed to die needs to be respected, as well as a patient's anguish in the face of imminent and unwanted death. The final phase of life (hours or days) should not be seen as a time of treatment failure, but as a time for completion of tasks in peace and dignity, even in the mist of weakness and profound surrender.

Analgesics↗

PubMed1989

[An investigation of sudden cardiac death in apparently healthy young men by annual health examination].

We have clinically compared the health records of 58 apparently healthy men who succumbed to sudden cardiac death (SCD) against the same number of control subjects (CS) with similar physical and social backgrounds. SCD, for our purpose, was defined as a death that occurred from a non-traumatic cause within one hour after the SCD onset. The clinical examination of our SCD cases consisted of evaluating the findings derived from their health records covering a span of 13 years such as their ECGs, the blood pressure data, chest x-rays, serum chemical analysis, and their obesity indexes. Heart weights were estimated from their ECGs by the quantification of a multivariate analysis. Of the total SCD cases studied, eleven hearts also were examined pathologically. With respect to the physical conditions of the SCD cases and the CS cases, the systolic blood pressure in the SCD cases was found to be higher, whereas no significant variances in the diastolic values were found, and both the systolic and diastolic values were within normal ranges in the two groups. A greater number of hearts weighing more than 420 g were found in the SCD group. Similarly the frequency of premature contraction and the serum cholesterol level was higher. No further appreciable differences, however, were found. Myocardial cell hypertrophy, degeneration, and interstitial edema were observed in all eleven hearts. Our data have revealed that the greater the heart weight, the greater the risk of succumbing to SCD. The risk becomes more evident if the systolic and cholesterol levels are also found to be high.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed2004

Caspases, the enemy within, and their role in oxidative stress-induced apoptosis of inner ear sensory cells.

This review covers the general roles of members of the cysteine protease family of caspases in the process of apoptosis (programmed cell death) looking at their participation in both the "extrinsic" cell death receptor and the "intrinsic" mitochondrial cell death pathways. It defines the difference between initiator and effector caspases and shows the progression of caspase activations that ends up in the apoptotic cell death and elimination of a damaged cell. The review then presents what is currently know about the participation of caspases in the programmed cell death of inner ear sensory cells during the process of normal development and maturation of the inner ear and their importance in this process as illustrated by the results of caspase-3 gene knockout experiments. The participation of specific caspases and the sequence of their activation in the elimination (apoptosis) of damaged sensory cells from adult inner ears after an injury that generates oxidative stress are reviewed. Both the possibility and the potential efficacy of caspase inhibition with a broad-spectrum pancaspase inhibitor as an interventional therapy to treat and rescue oxidative stress-damaged inner ear sensory cells from apoptosis are presented and discussed.

Adult↗

PubMed2005

Melatonin prevents hydrogen peroxide-induced Bax expression in cultured rat astrocytes.

During oxidative stress, cell apoptosis is promoted through the mitochondrial death pathway. Increased reactive oxygen species (ROS) are linked to excess cell loss and mediate the induction of apoptosis in various cell types. However, the role of ROS in the apoptotic pathway has not been clearly established. The aims of this study were to investigate the biochemical and morphological responses of rat astrocytes to hydrogen peroxide-mediated cell death and to define the role that melatonin might play in the apoptotic cascade. Hydrogen peroxide (H2O2; 0.1-1.0 mM) significantly reduced cell viability. Astrocyte death was associated with enhanced ROS production in a dose-dependent manner, as measured by 2',7'-dichloro-fluorescein fluorescence. H2O2-induced cell death was found to be mediated through an apoptotic pathway as treated cells exhibited cell shrinkage, nuclear condensation and marked DNA fragmentation. H2O2 also triggered caspase-3 activation and Bax expression. The ability of different antioxidants to prevent H2O2-induced apoptosis was examined by pre-incubating rat astrocytes with N-acetylcysteine (10 mM), glutathione (0.5 mM) or melatonin (0.1 mM and 10 nM). Results showed that N-acetylcysteine and glutathion can protect astrocytes against ROS accumulation and caspase-3 activation, whereas 0.1 mM melatonin can inhibit H2O2-induced apoptosis by regulating Bax expression and by inhibiting caspase-3 activation. Antiapoptotic effect of 10 nM melatonin associated to inhibition of Bax expression, give rise to new therapeutic approaches.

Animals↗

PubMed2006

Causes of death and determinants of outcome in critically ill patients.

INTRODUCTION: Whereas most studies focus on laboratory and clinical research, little is known about the causes of death and risk factors for death in critically ill patients. METHODS: Three thousand seven hundred patients admitted to an adult intensive care unit (ICU) were prospectively evaluated. Study endpoints were to evaluate causes of death and risk factors for death in the ICU, in the hospital after discharge from ICU, and within one year after ICU admission. Causes of death in the ICU were defined according to standard ICU practice, whereas deaths in the hospital and at one year were defined and grouped according to the ICD-10 (International Statistical Classification of Diseases and Related Health Problems) score. Stepwise logistic regression analyses were separately calculated to identify independent risk factors for death during the given time periods. RESULTS: Acute, refractory multiple organ dysfunction syndrome was the most frequent cause of death in the ICU (47%), and central nervous system failure (relative risk [RR] 16.07, 95% confidence interval [CI] 8.3 to 31.4, p < 0.001) and cardiovascular failure (RR 11.83, 95% CI 5.2 to 27.1, p < 0.001) were the two most important risk factors for death in the ICU. Malignant tumour disease and exacerbation of chronic cardiovascular disease were the most frequent causes of death in the hospital (31.3% and 19.4%, respectively) and at one year (33.2% and 16.1%, respectively). CONCLUSION: In this primarily surgical critically ill patient population, acute or chronic multiple organ dysfunction syndrome prevailed over single-organ failure or unexpected cardiac arrest as a cause of death in the ICU. Malignant tumour disease and chronic cardiovascular disease were the most important causes of death after ICU discharge.

Adult↗

PubMed2005

HIV disease progression in a patient cohort treated via a clinical research network in a resource limited setting.

OBJECTIVE: To examine HIV disease progression in a cohort of adult patients treated with antiretroviral therapy (ART) via a clinical research network in Thailand. DESIGN, SETTING, PARTICIPANTS AND INTERVENTION: A cohort of 417 patients enrolled in a series of randomized ART trials, between 1996 and December 2002. MAIN OUTCOME MEASURES: Progression to combined endpoint of AIDS defining illness or death according to baseline characteristics, ART used, immunological and virological responses to initial 6 months of ART. RESULTS: During 1677 person years of follow-up, 29 of 417 patients progressed; tuberculosis was the most common event defining progression (14 of 29 events). The rates of progression to combined endpoint or death alone were 1.7 [95% confidence interval (CI), 1.1-2.4] and 0.7 (95% CI, 0.3-1.3) per 10 person years respectively. Compared to patients with baseline CD4 cell counts > or =350 x 10/l, the adjusted hazard ratio (HR) for progression was 3.67 (95% CI, 1.31-10.27) for patients with <200 x 10 cells/l. Responses to 6 months of therapy were the strongest predictors of disease progression; compared to patients with undetectable viral load at 6 months, HR for progression was 4.95 (95% CI, 2.14-11.46) for viral load >4 log10. Compared to patients with a 6-month CD4 cell count > or =350 x 10/l, HR for progression was 5.22 (95% CI, 1.90-14.37) for patients with <200 x 10 cells/l. CONCLUSIONS: HIV-infected patients in Thailand who had access to ART, appropriate care, CD4 cell and viral load monitoring facilities via a clinical research network had progression rates comparable to those in developed countries. In this setting, ART initiation could generally be delayed until the CD4 cell count approaches 200 x 10/l.

AIDS-Related Opportunistic Infections↗

PubMed1997

Pulmonary myelomonocyte subtypes in drowning and other causes of death.

Three immunohistochemically different myelomonocytic subtypes, i.e. MRP8, MRP14 and 27E10 were quantitatively evaluated in the intraalveolar, alveolar-interstitial and alveolar-intracapillary lung compartments. Lung sections from 5 major groups with defined causes of death, i.e. drowning and death during immersion (DI), cerebral/intracranial haemorrhages (CH), sudden cardiac deaths (SCD), hanging and throttling (HT) and immediate trauma deaths (ITD) were stained and the positive cells counted. The results show clear differences of the cell numbers on average. Among the different compartments the intracapillary cell count exhibits the highest numbers. If the cell counts are compared to the different causes of death, DI shows the highest values and ITD the lowest. The individual values, however, show considerable variations in all compartments and especially in the low cell count range. Within the DI group two subgroups can be differentiated, one having low and the other one having high cell numbers. This can be due to the type of agony, i.e. drowning versus immersion/hydrocution, or to resuscitation attempts or to a combination of both factors.

Adult↗

PubMed1999

Cell death in acromegalic cardiomyopathy.

BACKGROUND: Prolonged untreated acromegaly leads to a nonspecific myopathy characterized by ventricular dysfunction and failure. However, the mechanisms responsible for the alterations of cardiac pump function remain to be defined. Because cell death is implicated in most cardiac disease processes, the possibility has been raised that myocyte apoptosis may occur in the acromegalic heart, contributing to the deterioration of ventricular hemodynamics. METHODS AND RESULTS: Ten acromegalic patients with diastolic dysfunction and 4 also with systolic dysfunction were subjected to electrocardiography, Holter monitoring, 2-dimensional echocardiography, cardiac catheterization, and biventricular and coronary angiography before surgical removal of a growth hormone-secreting pituitary adenoma. Endomyocardial biopsies were obtained and analyzed quantitatively in terms of tissue scarring and myocyte and nonmyocyte apoptosis. Myocardial samples from papillary muscles of patients who underwent valve replacement for mitral stenosis were used for comparison. The presence of apoptosis in myocytes and interstitial cells was determined by confocal microscopy with the use of 2 histochemical methods, consisting of terminal deoxynucleotidyl transferase (TdT) assay and Taq probe in situ ligation. Acromegaly was characterized by a 495-fold and 305-fold increase in apoptosis of myocytes and nonmyocytes, respectively. The magnitude of myocyte apoptosis correlated with the extent of impairment in ejection fraction and the duration of the disease. A similar correlation was found with the magnitude of collagen accumulation, indicative of previous myocyte necrosis. Myocyte death was independent from the hormonal levels of growth hormone and insulin-like growth factor-1. Apoptosis of interstitial cells did not correlate with ejection fraction. CONCLUSIONS: Myocyte cell death, apoptotic and necrotic in nature, may be critical for the development of ventricular dysfunction and its progression to cardiac failure with acromegaly.

Acromegaly↗

PubMedDate not supplied

[When should a brain scan with HMPAO be performed to diagnose brain death?].

INTRODUCTION: Current Spanish law defines the criteria to be met in the case of brain death (BD) and the complementary tests to confirm it, although they do not always need to be carried out. In Spain one of the most frequently used methods is the electroencephalogram (EEG), which has its shortcomings in patients who are under sedation with barbiturates. Transcranial Doppler (TCD) offers a number of advantages in the diagnosis of BD, but it also has certain limitations. In these cases, a cerebral perfusion scan (CPS) with HMPAO can be very useful. CASE REPORTS: We describe the case of two patients who were admitted to the Intensive Care Unit with serious traumatic brain injuries. Progress was unfavourable and the findings of the clinical exploration were compatible with BD. Since we were dealing with patients under barbiturate therapy, the EEGs were complex and difficult to interpret. TCD was difficult to perform in both cases because of loss of brain matter and displacement of intracranial structures, respectively. CPS, however, allowed us to confirm the diagnosis of BD. CONCLUSION: Although it has obvious advantages, TCD cannot always be performed to confirm BD diagnosis. In these cases, CPS can be an extremely valuable tool

Adult↗

PubMed1992

Racial differences in ill defined cancer mortality in the United States and in the District of Columbia.

STUDY OBJECTIVE: The aim was to examine the epidemiology of unknown primary cancer mortality in the USA during 1979 to 1988 by age, sex, race, year, and geographical area. DESIGN: National (US) and state data were abstracted for deaths due to ill defined cancer (ICD-9 195.0 to 199.1) and all cancers combined (ICD-9 140.0-209.9). Age adjusted mortality rates were calculated using the 1980 USA population as the standard, and standardised rate ratios were derived. National total cancer incidence data were obtained from the surveillance, epidemiology and end results (SEER) program, and age and sex specific relative (black/white) cancer incidence rates were derived and compared to relative (black/white) mortality rates for ill defined cancer. State and regional median family income levels were obtained from the 1980 census and compared to corresponding mortality rates. SETTING: This study used data for the US population, the 50 states, and the District of Columbia. MEASUREMENTS AND MAIN RESULTS: During 1984-1988, ill defined cancers accounted for an average of 34,921 deaths each year in the USA (13.7 per 100,000 population). The mortality rate due to ill defined cancers is greater among blacks (19.3 per 100,000) than whites (13.2 per 100,000) (RR = 1.5) and has not declined since 1979. There is considerable geographical variation in the ill defined cancer mortality rate. Thus among blacks the highest rates were clustered in the central states (23 per 100,000) and the lowest rates were seen in the mountain and western states (17 per 100,000). The District of Columbia had the highest overall rate (21.7 per 100,000) when compared to all other states. The black/white relative mortality rate due to ill defined cancer was consistently greater than the black/white relative incidence of all cancers. CONCLUSIONS: Ill defined cancer mortality is the fourth leading site of cancer mortality in the USA, and accounts for 7.4% of cancer deaths annually. The large proportion of ill defined cancer deaths may have biased the accuracy of national and local cancer incidence and mortality statistics. The higher mortality of ill defined cancer among blacks is not explained by the higher overall cancer incidence among blacks and suggests the influence of socioeconomic or cultural barriers that may result in underutilisation of health services or substandard health care. Ill defined cancer mortality may be a sentinel indicator of deficiencies in the health care delivery system as well as a measure of progress against cancer.

Adult↗

PubMed2003

N-acetylcysteine does not prevent bronchopulmonary dysplasia in immature infants: a randomized controlled trial.

OBJECTIVE: To evaluate whether N-acetylcysteine (NAC) infusion during the first week of life reduces the risk of death or bronchopulmonary dysplasia (BPD) in infants with extremely low birth weight. Study design In a Nordic multicenter, double-blind trial, infants (n=391) weighing 500 to 999 g and on ventilator or nasal continuous positive airway pressure were randomized before the age of 36 hours to receive NAC 16 to 32 mg/kg/d (n=194) or placebo (n=197) intravenously for 6 days. Primary end points were death or BPD, defined as supplementary oxygen requirement at 36 weeks' gestational age. RESULTS: There was no difference in the combined incidence of the primary end points death or BPD, 51% vs. 49%, between the NAC group and control group. Also similar was the incidence of BPD in survivors at 36 weeks' gestational age, 40% vs. 40%, and the mean oxygen requirement at the age of 28 days, 31.2% vs. 30.7%, respectively. The severity of BPD was similar in both groups. CONCLUSIONS: A 6-day course of intravenous N-acetylcysteine at the dosage used does not prevent BPD or death in infants with extremely low birth weight.

Antioxidants↗

PubMed1999

CD4 cell counts at the third month of HAART may predict clinical failure.

OBJECTIVE: To evaluate the influence of immunological and virological markers on clinical outcome in patients receiving their first highly active antiretroviral therapy (HAART) regimen. DESIGN AND METHODS: Observational study of 585 patients initiating HAART in a clinical setting. Clinical failure was defined as the occurrence of new or recurrent AIDS-defining events or death, and was analysed by means of intention-to-treat, univariate and multivariate analyses. An adjusted Cox regression model was used to evaluate the effect of 3-month CD4 cell counts on clinical outcome. RESULTS: Clinical failure occurred in 55 patients (9.4%) during a median follow-up of 483 days (range 33-1334 days): 45 new AIDS-defining events (ADEs) in 38, ADE recurrence in six, and death in 11. Twenty-four of the 45 new ADEs (53.4%) occurred during the first 3 months of HAART, and 11 of 45 (24.4%) in the presence of CD4 cell counts > 200 x 10(6) cells/l. The mean (median, range) CD4 counts were 144 x 10(6) cells/l (128, 4-529) in patients with and 322 x 10(6) cells/l (288, 14-1162) in patients without clinical failure (P < 0.0001). Moreover, the proportion of patients with mean CD4 cell counts < 200 x 10(6) cells/l was higher in those experiencing subsequent clinical failure (X2 test: 26.75; P < 0.00001). Multivariate analysis showed that baseline CD4 cell counts < 50 x 10(6) cells/l and AIDS at enrolment predicted failure; after adjusting for 3-month CD4 cell counts, this marker was the only one independently associated with clinical failure (hazard risk, 4.79; 95% confidence interval, 1.40-16.47). CONCLUSIONS: The 3-month immunological response is a reliable predictor of long-term clinical outcome.

AIDS-Related Opportunistic Infections↗

PubMed2005

Cost-effectiveness of implanted defibrillators in young people with inherited cardiac arrhythmias.

BACKGROUND: The implanted cardioverter-defibrillator (ICD) has been shown to improve survival in adult patients with high risk acquired cardiac disease, with a cost-effectiveness ratio in the range of $30,000 to $185,000 per quality-adjusted-life-year saved. However, data on the benefit and cost-effectiveness of device therapy in high-risk patients with inherited cardiac disorders are limited. METHODS: We developed two separate computer-based analytical models to compare non-ICD with ICD therapy in patients (age range: 10-75 years) with long QT syndrome (LQTS) and hypertrophic cardiomyopathy (HCM). In each disease entity patients were stratified into low-risk (no known risk factors); high-risk (known risk factors [primary prevention]); and very high-risk (prior near-fatal events [secondary prevention]). Net costs were defined as the difference between costs resulting from treatment of the disease and savings due to gained productivity attributable to prevention of sudden cardiac death. Outcome was defined as costs per quality-adjusted life-years saved. RESULTS: In LQTS, defibrillator therapy was shown to be cost effective in high-risk male patients (incremental cost-effectiveness ratio [ICER]=$3328 per quality-adjusted-life-year saved), and cost saving in high-risk females (ICER=$7102 gained per quality-adjusted-life-year saved) and very high-risk males and females (ICER=$15,483 and 19,393 gained per quality-adjusted-life-year saved, respectively). In HCM, defibrillator therapy was cost saving in both male and female high-risk (ICER=$17,892 and $17,526 gained per quality-adjusted-life-year saved, respectively) and very high-risk (ICER $22,944 and $22,329 gained per quality-adjusted-life-year saved, respectively) patients. Defibrillator therapy was not shown to be cost effective in low-risk patients with either LQTS or HCM (ICER in the range of $400,000 to $600,000 lost per quality-adjusted-life-year saved). Sensitivity analyses were consistent with the results in each risk group. CONCLUSIONS: In appropriately selected patients with inherited cardiac disorders, early intervention with ICD therapy is cost-effective to cost saving due to added years of gained productivity when the lifespan of an individual at risk is considered.

Arrhythmias, Cardiac↗

PubMed1985

Sepsis score and complement factor B for monitoring severely septic surgical patients and for predicting their survival.

Sepsis score and complement factor B (FB) have been measured in 66 severely septic surgical patients in the intensive care unit, with the aim of monitoring their clinical course and predicting their outcome. Sepsis score correlated well with clinical course. 82% of patients with initial sepsis score less than 20 progressively improved and survived. Only 6% of patients with sepsis score greater than or equal to 20 survived. FB plasma level was significantly higher (p less than 0.01) in patients who subsequently survived. Two indices were identified which could predict patient outcome several days in advance with 100% accuracy: (1) the index of survival from sepsis defined as the combination of sepsis score less than 20 and FB greater than or equal to 45 mg/dl, and (2) the index of death from sepsis defined as sepsis score greater than or equal to 20 and FB less than 40 mg/dl.

Adolescent↗

PubMed2006

Acute ischemic stroke care and outcome in centers participating in the Polish National Stroke Prevention and Treatment Registry.

BACKGROUND AND PURPOSE: Significant intercenter variability in quality of care and stroke outcomes was found in many countries. The aim of the study was to compare the acute ischemic stroke care and outcomes in centers participating in the Polish National Stroke Prevention and Treatment Registry. METHODS: The World Health Organization Stepwise Approach to Stroke Surveillance-based questionnaire was used to collect data on patients admitted to participating centers between December 1, 2001, and July 31, 2002. To ensure data quality, only centers reporting representative sample of patients were analyzed. Ischemic stroke patient characteristics, in-hospital care, and early outcomes (adjusted for case mix) were compared for participating centers. RESULTS: There were 26 of 48 centers that met inclusion criteria, with a total of 8736 patients (52% women; mean age 71 years, with a range among institutions from 68 to 75 years). Significant differences between centers were observed for distribution of risk factors and in-hospital care. The rates for death and poor outcome (defined as a Rankin score > or =3 or death) ranged from 8.0% to 31.8% and from 44.2% to 74.7%, respectively. After adjusting for case mix, the death or poor outcome prognoses remained significantly different between centers. CONCLUSIONS: The observed significant differences between Polish stroke centers indicate the need for improvement of patient education, effective stroke risk factor control, and standardized in-hospital care.

Acute Disease↗

PubMed2000

Impact of new highways on road deaths: a case study in risk assessment.

Epidemiologists have generally avoided to assess risk for road deaths from high-speed highways. We examined the validity of the claim that the Trans-Israel Highway, a six-lane 320 km toll road with higher design speed, and raised speed limits (120 kph), will reduce road deaths. We used models showing that death tolls vary with the fourth power of rise in driving speed. Risk assessments was derived from estimates of increase in the highway-induced traffic, the impact of higher speed limits (from 110 to 120 kph) and the so-called spillover effect from speed habituation. We predict a large rise in the number of killed or injured, even if the death risks per vkm is low on the Highway itself. With the Trans-Israel Highway, death tolls--some 550 fatalities per year in 1995, could rise to as high as 900-1000 per year in 2010. Congestion produced by induced traffic will partially offset these effects. By contrast, death tolls from alternative strategies based on sustainable transportation policies could be reduced to less than 300 deaths per year. Risk assessment based on explicitly defined assumptions predicts high death tolls from the nationwide impact of raised speed on the Highway and its connecting roads. There is a need for new frameworks which impose the Code of Helsinki type requirements for the assessment and authorization of social decisions with adverse public health impacts.

Accidents, Traffic↗

PubMed2002

Sudden unexpected death in epilepsy.

Sudden unexpected death in epilepsy is the most common category of seizure-related death for patients who develop chronic epilepsy, accounting for up to 17% of epilepsy deaths. Sudden unexpected death in epilepsy is defined as a sudden, unexpected, non-accidental death in an individual with epilepsy with or without evidence of a seizure having occurred (excluding documented status epilepticus) and where autopsy does not reveal an anatomical or toxicological cause of death. Incidence rates range between 0.35 and 2.70 per 1000 person-years in the population-based studies and between 1.50 and 9.30 per 1000 person-years in selected cohorts. Seizure frequency appears to be an important factor in sudden unexpected death in epilepsy, although the exact pathogenetic mechanisms involved are unclear.

Cause of Death↗

PubMed1996

[Analysis of a novel gene expressed in apoptotic T-cell hybridoma treated with dexamethasone].

Developmentally and physiologically controlled cell deaths are called programmed cell death (PCD), and distinguished from accidental cell death while apoptosis is defined morphologically as a certain type of cell death (i.e. chromatin condensation, DNA fragmentation, organella compaction, and blebing of cell and nuclear membranes). Apoptosis is often associated with PCD. Most of cells undergoing PCD have been shown to require de novo synthesis of mRNA and protein. A number of genes have been reported to be expressed in apoptotic cells. In the immune system programmed cell death plays an important role in negative selection of immature T cells. Situations that result in programmed cell death include the withdrawal of cytokine from cultures of cytokine dependent cells, lysis of target cells by cytotoxic T cells, and activation of T cells. In T cells, another well described means of inducing apoptosis is an exposure to glucocorticoids. We cloned a novel gene expressed in apoptotic 2B4. 11 mouse T-cell hybridoma treated with steroid. This gene was not detected in vivo, but was so in mouse thymocytes and splenocytes cultured with dexamethasone and IgM stimulated mouse preB cell line WEHI-231. Thirty-six amino acids, position 2-37, has a 37% homology to mouse intracisternal A-particle gag p27 protein.

Amino Acid Sequence↗