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Nuclear magnetic resonance spectroscopy: biochemical evaluation of brain function in vivo and in vitro.
Nuclear magnetic resonance spectroscopy (MRS) offers a unique opportunity to monitor mmolar concentrations of high energy phosphates, glucose, lactate and amino acids. The possibility of obtaining information about chemical constituents noninvasively is of great importance. MRS and chemical shift imaging (CSI) are emerging as tools for tumor grading, monitoring of treatment, ischemia research, in pediatric research for follow-up of children with borderline mental retardation, for defining brain death and to define epileptic foci. It is important to know which cell type (neuronal or glial) shows changes as a result of external manipulations (e.g. excitotoxins) or internal changes (brain pathology). Metabolic studies have been carried out on brain cell cultures. By using 13C labeled glucose and acetate in combination with 13C MRS it was shown that astrocytes release lactate, glutamine, citrate and alanine and that cerebral cortical neurons use glutamine released from astrocytes as a precursor for GABA synthesis. An important feature in MRS is the localization of N-acetyl aspartate in neurons, since this enables monitoring of neuronal reactions, such as survival after neurotoxic insults. Recent advances have yielded high speed functional echo planar imaging (EPI) techniques that are sensitive to changes in cerebral blood volume, blood flow and blood oxygenation (Functional MRI). During cognitive task performance, local alterations in neuronal activity induce local changes in cerebral metabolism and cerebral perfusion, which can now be detected with MRI.
Defining and redefining death.
The definition of death, brain death in particular, is increasingly important to critical care professionals. There are essentially three definitions of death from a theoretical perspective: the traditional heart-lung definition, the whole-brain definition, and the higher-brain definition. These definitions use different underlying assumptions within their own theoretical framework. The differing definitions and theoretical frameworks have encouraged physiological, philosophical, spiritual, and ethical analyses, which have led to spirited debate throughout the healthcare community and especially in critical care.
[Sudden cardiac death: definition, mechanisms and risk factors].
Sudden cardiac death is defined as natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour after the onset of symptoms. The mechanisms are the following: 1. ventricular fibrillation, 2. ventricular tachycardia and flutter with subsequent ventricular fibrillation, 3. torsade de pointe, 4. bradyarrhythmias and asystolic arrest. White the main risk factor is the presence of coronary artery disease, any organic or functional disease of the heart can predispose for sudden cardiac death. To evaluate the risk of sudden cardiac death noninvasive (Holter, echocardiography, exercise test and signal averaged (ECG) and often invasive (electrophysiological study) tests are necessary. The therapy is based on drugs (mainly beta blockers and amiodarone), coronary revascularization, catheter ablation techniques and the implantation of a cardioverter defibrillator; the latter appears to be the most promising approach.
On defining a 'natural death'.
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Pro/con ethics debate: when is dead really dead?
Contemporary intensive care unit (ICU) medicine has complicated the issue of what constitutes death in a life support environment. Not only is the distinction between sapient life and prolongation of vital signs blurred but the concept of death itself has been made more complex. The demand for organs to facilitate transplantation promotes a strong incentive to define clinical death in a manner that most effectively supplies that demand. We consider the problem of defining death in the ICU as a function of viable organ availability for transplantation.
Bioethics for clinicians: 24. Brain death.
Brain death is defined as the complete and irreversible absence of all brain function. It is diagnosed by means of rigorous testing at the bedside. The advent of neurologic or brain death criteria to establish the death of a person was a significant departure from the traditional way of defining death and remains ethically challenging to some. We review the ethical, cultural, religious and legal issues surrounding brain death and outline an approach to establishing a diagnosis of brain death in clinical practice.
Can pediatricians define and apply the concept of brain death?
OBJECTIVE: We sought to determine pediatric residents' and attending physicians' ability to define brain death, their ability to apply this standard of death to a clinical scenario, and their knowledge regarding the legal necessity of confirmatory testing when determining death by brain criteria. We compared resident and attending self-confidence at discussing brain death with their ability to define brain death and apply this concept to a clinical scenario. METHODOLOGY: A questionnaire was sent to 136 residents, postgraduate years 1 through 3, at four accredited pediatric training programs in the United States. Participation was tracked by return address. One follow-up request for participation was made. A similar procedure was followed for 140 faculty pediatricians at two of the institutions. Demographic information including level of training, subspecialty training, training program, and formal ethics training was collected. Respondents defined brain death, interpreted a clinical scenario, and stated whether confirmatory testing is legally required to determine death by brain criteria. Respondents rated their confidence at explaining brain death to a patient's family on a scale from 1 to 5. RESULTS: Eighty-seven percent (118/136) of resident surveys were returned. Thirty-six percent (42/118) of the residents correctly defined brain death. Forty-three percent (51/118) of residents correctly interpreted the clinical scenario. Fifty-five percent (65/118) of the residents correctly recognized that brain death could be determined without a confirmatory test. Residents who correctly defined brain death were as confident as those who did not (2.8 +/- 1 vs 1.5 +/- 1). Residents who correctly interpreted the clinical scenario were as confident as those who did not (2.6 +/- 1 vs 1.9 +/- 0.9). Eighty percent (112/140) of attending physician surveys were returned. Thirty-nine percent (44/112) of attending physicians correctly defined brain death. Fifty-three percent (59/112) correctly interpreted the clinical scenario. Fifty-eight percent (65/112) recognized that brain death can be diagnosed without confirmatory testing. All pediatric intensivists (n = 12) correctly answered all three questions. Their performance was significantly better than other pediatricians. Attendings who correctly defined brain death were more confident than those who did not (4.2 +/- 1 vs 1.1 +/- 0. 9). Attendings who correctly interpreted the clinical scenario were more confident than those who did not (3.8 +/- 1.2 vs 2.2 +/- 1.2). CONCLUSIONS: Pediatric residents and attendings have difficulty defining and applying the concept of brain death. This concept is difficult to grasp and internalize for many pediatricians. To ensure that critical decisions are made by knowledgeable physicians and well-informed families, more effective educational strategies need to be identified.
Relative mortality from overdose of antidepressants.
OBJECTIVE: To compare the fatal toxicities of antidepressant drugs in 1987-92. DESIGN: Retrospective epidemiological review of prescription data of the Department of Health, Scottish Office Home and Health Department, and Welsh Health Common Services Authority (excluding data from most private general practices and most hospitals), and mortality data from the Office of Population Censuses and Surveys and General Register Office in Scotland. SETTING: General practice, England, Scotland, and Wales. MAIN OUTCOME MEASURES: Deaths per million prescriptions and deaths per defined daily dose. RESULTS: 81.6% (1310/1606) of deaths from antidepressant overdose were due to two drugs, amitriptyline and dothiepin. The overall average of deaths per million prescriptions was 30.1. The overall rate for tricyclic drugs was 34.14 (95% confidence interval 32.47 to 38.86; P < 0.001), monoamine oxidase inhibitors 13.48 (6.93 to 22.19; P < 0.001), atypical drugs 6.19 (4.04 to 8.80; P < 0.001), and selective serotonin reuptake inhibitors 2.02 (0.64 to 4.17; P < 0.001). The numbers of deaths per million prescriptions of amoxapine, dothiepin, and amitriptyline were significantly higher than expected, while nine drugs had a significantly lower number of deaths per million prescriptions than expected. Analysis of deaths per defined daily dose showed a similar pattern. CONCLUSIONS: Safety in overdose should be considered in risk-benefit and cost-benefit considerations of antidepressants. A switch in prescribing, from drugs with a high number of deaths per million prescriptions to drugs with a low number, could reduce the numbers of deaths from overdose. Although this form of suicide prevention can be implemented easily and immediately, its introduction needs to be considered against the higher costs of some of the newer drugs.
Querying the ill-defined stroke diagnoses on death certificates and their effects on type-specific mortality in Taiwan.
In Taiwan, the high proportion of stroke deaths of which the underlying causes of death (UCD) has been classified to ill-defined categories, has impeded valid type-specific mortality studies. The aim of this study was to assess the extent of changes in the distributions of stroke subtypes and mortality after querying the certifying physicians. There were 2632 death certificates issued from January through June 1998 in Taiwan of which the UCD was classified to ill-defined cerebrovascular disease categories (International Classification of Diseases, 9th Revision ICD-9 code 436 or 437.9). Staff of the Office of Statistics, Department of Health copied 2035 death certificates issued by hospitals and mailed them back to the certifying physicians to request more specific information on the stroke subtype. Responses were obtained for 1505 (74%) of the 2035 queries sent. Four fifths of these (1191/1505) resulted in a change to a more specific code. In most cases, the ICD-9 code was changed to 431 (cerebral hemorrhage, CH, 239/1505) or 433-4 (cerebral infarction, CI, 819/1505). After the querying, the percentage changes in the age-adjusted death rate (per 100,000 population) for CH were +16% for men and +20% for women; and for CI the percent changed were +100% for men and +130% for women. The changes increased as the age of the deceased increased. The changes in the CH/CI death ratios resulting from querying were greater in younger (less than 65 years old) age groups than in older age groups. Given the large gains of more specific information on stroke subtypes, querying is a useful method to improve the quality of cause of death statistics. However, the large changes in distributions and death rates of different stoke subtypes as a result of querying, show the non-querying mortality data are not suitable for type-specific analysis.
Sudden cardiac death--can it be defined with precision?
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Treatment and outcome of severe intraventricular extension in patients with subarachnoid or intracerebral hemorrhage: a systematic review of the literature.
Severe intraventricular hemorrhage caused by extension from subarachnoid hemorrhage or intracerebral hemorrhage leads to hydrocephalus and often to poor outcome. We conducted a systematic review to compare conservative treatment, extraventricular drainage, and extraventricular drainage combined with fibrinolysis. We carried out a search in Medline of the literature between January 1966 and December 1998 and an additional hand-search from January 1990 to December 1998. Pharmaceutical companies were contacted to gather unpublished data. We reviewed the reference lists of all relevant articles. Two authors independently assessed eligibility of the studies and extracted data on characteristics of study design, patients, and treatment. Patients with primary intraventricular hemorrhage were excluded. Main outcome measures were death and poor outcome (defined as death or dependency) at the end of follow-up. No randomized clinical trial has yet been conducted so far, and we therefore reviewed only observational studies. The case fatality rate for conservative treatment (ten studies) was 78%. For extraventricular drainage (seven studies) it was 58% [relative risk versus conservative treatment (RR) 0.74; 95% confidence interval (CI) 0.55-0.99]. For extraventricular drainage with fibrinolytic agents (five studies) the case fatality rate was 6% (RR 0.08; 95% CI 0.02-0.24). The poor outcome rate for conservative treatment was 90%, that for extraventricular drainage 89% (RR 0.98; 95% CI 0.75-1.30) and that for extraventricular drainage with fibrinolytic agents 34% (RR 0.38; 95% CI 0.21-0.68). All RR values remained essentially the same after adjusting for age, sex, World Federation of Neurological Surgeons scale, study design, and year of publication for the studies that provided these data. Outcome is thus poor in patients with intraventricular extension of subarachnoid or intracerebral hemorrhage. This meta-analysis suggests that treatment with ventricular drainage combined with fibrinolytics may improve outcome for such patients, although this impression is derived only from an indirect comparison between observational studies. A randomized clinical trial is warranted.
The influence of chronic prearrest health conditions on mortality and functional neurological recovery in cardiac arrest survivors.
PURPOSE: To study the impact of chronic prearrest health conditions on mortality and neurological recovery in patients after witnessed cardiac arrest and primary successful resuscitation. PATIENTS AND METHODS: The study was set in the community of Vienna, Austria. Data concerning cardiopulmonary resuscitation of adult patients who survived a witnessed cardiac arrest were collected according to an internationally recommended protocol (Utstein-Style). Chronic prearrest health conditions and New York Heart Association (NYHA) functional classes were evaluated. All patients were followed up for 6 months after the event or death. Adverse outcome was defined as death or severe neurological impairment. A forward stepwise logistic regression model was applied to assess the impact of pre-arrest morbidity on unfavorable outcome, expressed as odds ratio (OR) with 95% confidence intervals (CI). RESULTS: Of 411 patients, 269 (66%) had one or more of the following pre-arrest diseases: coronary heart disease (45%), hypertension (26%), congestive heart failure (20%), diabetes mellitus (14%), chronic pulmonary disease (6%), and cerebrovascular disease (5%). In 22% a NYHA class of III or IV was present before cardiac arrest. At 6-month follow-up, 161 (40%) of the patients were alive with favorable neurological recovery; overall mortality was 57% (n = 233). Increasing NYHA classes (OR 1.4 per NYHA class increase; CI 1.1 to 1.7) and increasing age were independent predictors of adverse outcome (OR 1.03 per 10-year increase; CI 1.01 to 1.05), as were durations of cardiac arrest (OR 1.10 per 5-minute increase; CI 1.07 to 1.12) and the presence of ventricular fibrillation or tachycardia (OR 0.3; CI 0.2 to 0.5). The remaining health conditions, as listed above, were not independently associated with outcome. CONCLUSIONS: A large proportion of patients with cardiac arrest had chronic diseases before the event. The presence of impaired functional performance in patients with structural heart disease increased unfavorable outcome within 6 months in primary cardiac arrest survivors. However, the impact of chronic prearrest conditions on outcome seems to be very small, and should not influence decisions whether to withhold or withdraw therapy.
Prediction of sudden cardiac death by fractal analysis of heart rate variability in elderly subjects.
OBJECTIVES: The aim of this study was to test the hypothesis that abnormal scaling characteristics of heart rate (HR) predict sudden cardiac death in a random population of elderly subjects. BACKGROUND: An abnormality in the short-term fractal scaling properties of HR has been observed to be related to a risk of life-threatening arrhythmias among patients with advanced heart diseases. The predictive power of altered short-term scaling properties of HR in general populations is unknown. METHODS: A random sample of 325 subjects, age 65 years or older, who had a comprehensive risk profiling from clinical evaluation, laboratory tests and 24-h Holter recordings were followed up for 10 years. Heart rate dynamics, including conventional and fractal scaling measures of HR variability, were analyzed. RESULTS: At 10 years of follow-up, 164 subjects had died. Seventy-one subjects had died of a cardiac cause, and 29 deaths were defined as sudden cardiac deaths. By univariate analysis, a reduced short-term fractal scaling exponent predicted the occurrence of cardiac death (relative risk [RR] 2.5, 95% confidence interval [CI], 1.9 to 3.2, p < 0.001) and provided even stronger prediction of sudden cardiac death (RR 4.1, 95% CI, 2.5 to 6.6, p < 0.001). After adjusting for other predictive variables in a multivariate analysis, reduced exponent value remained as an independent predictor of sudden cardiac death (RR 4.3, 95% CI, 2.0 to 9.2, p < 0.001). CONCLUSIONS: Altered short-term fractal scaling properties of HR indicate an increased risk for cardiac mortality, particularly sudden cardiac death, in the random population of elderly subjects.
Timing of aneurysm surgery in subarachnoid hemorrhage: a systematic review of the literature.
OBJECTIVE: Many practitioners favor early operation after aneurysmal rupture, but sound data supporting this practice are lacking. A systematic review was conducted to compare early aneurysm surgery (Days 0-3), intermediate surgery (Days 4-7), and late surgery (more than 7 d after subarachnoid hemorrhage). METHODS: We performed a MEDLINE search of the literature published between January 1974 and December 1998 and an additional manual search of selected journal titles from January 1998 to December 1998. Main outcome measures were death and poor outcome (defined as death or dependency) at the end of the follow-up period. Risk ratios (RRs) and corresponding 95% confidence intervals (CIs) were calculated; patients planned for late surgery were used as the reference. RESULTS: Identified were 1 randomized clinical trial and 268 observational studies, of which only 10 studies (assessing a total of 1814 patients) fulfilled a set of minimum requirements for methodological quality. In the trial, the RR of poor outcome was 0.42 (95% CI, 0.17-1.04) for patients planned for early surgery and 1.07 (95% CI, 0.56-2.05) for intermediate surgery. In analyses with data from the 11 included studies, the RR of poor outcome for patients in good clinical condition at admission was 0.41 (95% CI, 0.34-0.51) for early surgery and 0.47 (95% CI, 0.32-0.69) for intermediate surgery. For patients in poor clinical condition at admission, the RR of poor outcome was 0.84 (95% CI, 0.67-1.05) for early surgery and 0.54 (95% CI, 0.24-1.22) for intermediate surgery. Adjustment of the RRs for year of publication, study design, and aneurysm location yielded essentially the same results, as did a sensitivity analysis after exclusion of the data from the randomized trial. CONCLUSION: This meta-analysis suggests that both early and intermediate surgical treatment improve outcome after aneurysmal subarachnoid hemorrhage--in particular for patients in good clinical condition at admission. However, this impression is derived only from an indirect comparison between different cohorts of patients. Sound evidence on the best timing of surgery is still lacking. Observational studies with better methods--and ideally a new randomized trial--are needed.
Maternal caffeine consumption and fetal death: a case-control study in Uruguay.
The objective of this study was to examine the association between caffeine intake during pregnancy and fetal mortality in Montevideo, the capital city of Uruguay, taking into account several potential confounding factors. A population-based case-control study was conducted between 1 August 2002 and 31 December 2003. A total of 382 cases and 792 controls were recruited. Cases consisted of women hospitalised with a medically confirmed diagnosis of spontaneous antepartum fetal death, in all maternity hospitals during the study period. Antepartum fetal death was defined as a fetal death in which the attending doctor certified that the death occurred prior to the onset of labour. Fetal deaths were included if they were of at least 20 weeks' gestational age or weighed >350 g. Controls were women who had a live, vigorous and term adequate-for-gestational-age newborn. Multiple gestations and fetuses/newborns with evident congenital malformations were excluded. Only a small proportion of the mothers (8.1% of the cases and 9.5% of the controls) did not consume caffeine during pregnancy. Among consumers, mate drinking was the most frequent source of caffeine in both cases and controls. After controlling for mother's and her partner's education, history of abortions and/or fetal deaths, vomiting/nausea during the first trimester of gestation and attendance for prenatal care, the category of mean caffeine intake of > or = 300 mg/day showed a significantly increased risk of fetal death (OR 2.33 [1.23; 4.41]) compared with no caffeine consumption during pregnancy. The study also found that less-educated women, mothers who did not attend for prenatal care and women with a history of abortions and fetal death were at an increased risk of fetal death. As mate drinking is highly consumed among pregnant women in Uruguay, the association found with fetal death makes it a preventable risk factor.
Outcome in familial subarachnoid hemorrhage.
BACKGROUND AND PURPOSE: The outcome of subarachnoid hemorrhage in patients with familial occurrence of subarachnoid hemorrhage (familial SAH) is an important but neglected factor in balancing the risks of screening for asymptomatic aneurysms and repairing these in unaffected members of such families. METHODS: We studied the outcome of familial SAH in a prospective, hospital-based series of patients with at least one first-degree relative with SAH and compared it with the outcome in a prospectively collected hospital series of patients selected for the absence of SAH in first- and second-degree relatives. Outcome was graded in three categories: independence, dependence, or death. Poor outcome was defined as death or dependence. RESULTS: Of 29 patients with familial SAH, 52% had a poor outcome, whereas only 37% of 125 patients with sporadic SAH had a poor outcome. The crude relative risk for poor outcome in familial SAH was 1.4 (95% confidence interval [CI], 0.9 to 2.1; P = .14); the odds ratio adjusted for age and sex was 2.5 (95% CI, 1.0 to 6.0; P = .04). This risk is probably an underestimation due to our strict patient selection criteria. CONCLUSIONS: Patients with familial SAH have a greater risk of poor outcome than patients with sporadic SAH. This adds to the factors in favor of screening unaffected first-degree relatives of patients with familial SAH.
[The genetic disorders responsible for sudden cardiac death].
Sudden cardiac death is defined as an unpredictable death within 24 hours. It is estimated to occur with a frequency of more than 50,000 per year in Japan. The inherited arrhythmogenic diseases associated with the transmembranous ionic channels, anchoring proteins or intracellular calcium regulating proteins are thought to be responsible for sudden cardiac death in infants, children, and young adults who have structurally normal hearts. Recent genetic analyses have identified congenital diseases such as the long-QT syndrome (LQTS), the Jervell and Lange-Nielsen syndrome (JLNS), the Brugada syndrome (BrS), the short-QT syndrome (SQTS), the arrhythmogenic right ventricular cardiomyopathy type 2 (ARVC2), and the catecholamine-induced polymorphic ventricular tachycardia (CPVT) /familial polymorphic ventricular tachycardia (FPVT). Loss of function in the slow component of the delayed rectifier potassium current (I(Ks)) channels (KCNQ1, KCNE1), the rapid component of the potassium current (I(Kr)) channels (KCNH2, KCNE2) and the inward rectifier potassium current (I(Kl), Kir2.1) channel (KCNJ2) is linked to the LQTSs (type 1, 2, 5, 6, and 7 (Andersen syndrome)) and the JLNSs (type 1 and 2). Changes of function in the alpha-subunit of cardiac sodium channels (SCN5A) is also linked to the LQTS type 3 and the BrS. A mutation in the ankyrin-B, anchoring proteins, has been identified as cause of the LQTS type 4. The SQTS is caused by gain of function in the KCNH2. Further, the missense mutations in the gene encoding ryanodine receptor 2 (RyR2) or calsequestrin 2 (CASQ2) that regulate intra-cardiac calcium handling is possibly implicated in the ARVC2 and the CPVT/FPVT. Herein, we present a review of the literature regarding the genetic mechanisms of the inherited arrhythmogenic diseases.