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PubMed1978

Pulsatile cerebral echo in diagnosis of brain death.

Conclusive diagnosis of brain death can be made by the demonstration of prolonged cessation of cerebral blood flow. This report describes a simple method to determine the presence or absence of the blood flow in the brain by recording the pulsatile midline echo on one channel of the electroencephalogram (EEG) or on any four-channel monitoring system in the intensive care unit. A firm transducer holder has been developed to eliminate artifacts caused by transducer motion, The pulsations of the midline echo are assumed to be the result of displacement of the midline structures by the arterial injection of each cardiac systole. Thus, the absence of these midline pulsatile echoes correlates with the absence of cerebral blood flow and, if the absence persists over 30 minutes in the presence of normal blood pressure, then the result is brain death. Twenty-eight cases of clinical brain death with electrocerebral silence of EEG and 18 obtained patients with various types of cerebral pathology were examined by the echo-pulsation technique. Twenty-six of the 28 cases showed no pulsation of the midline echo. The validity of the technique was documented in four cases by four-vessel cerebral angiogram.

Adolescent↗
PubMed1986

[Aspects of brain death].

The different aspects of brain death are discussed. It is pointed out that the diagnosis of poisoning as the cause of brain death can be checked by toxicological examination of brain tissue and of blood in the sinus of the dura mater, since the metabolism in the brain and sinus blood is markedly reduced while drugs and toxic substances continue to be broken down in the other organs. Particular importance attaches to this difference in the case of crimes of violence creating conditions that predispose to brain death when the significance of a further violent act, e.g. stabbing with resultant haemorrhage, has to be assessed. The simple vital reaction of bleeding does not of itself constitute proof in such a situation, unless it is possible to say with a good degree of certainty that brain death did not occur at the moment when the victim was stabbed. It may, however, be possible to state that brain death that could have been caused by violence has not yet occurred if complex vital reactions, such as inflammation of a wound, are seen.

Adult↗
PubMed1990

BRAINDEX: an interactive, knowledge-based system supporting brain death diagnosis.

BRAINDEX (Brain-Death Expert System) is an interactive, knowledge-based expert system offering support to physicians in decision making concerning brain death. The physician is given the possibility of communicating in almost natural language and, therefore, in terms with which he is familiar. This updated version of the system is implemented on an IBM-PC/AT with the expert system shell PC-PLUS and consists of about 430 rules. The determination of brain death is realized with backward chaining and for the optional coma-scaling a forward-chaining mechanism is used.

Brain Death↗
PubMed1988

Injury of myocardial conduction tissue and coronary artery smooth muscle following brain death in the baboon.

Experimental brain death was induced in 36 chacma baboons. In group A (n = 17), brain death was induced with no pharmacologic or surgical manipulation. Group B (n = 7) underwent bilateral vagotomy, unilateral left cardiac sympathectomy, or bilateral adrenalectomy before induction of brain death. Group C (n = 7) underwent total cardiac sympathectomy. Group D (n = 5) was pretreated with verapamil hydrochloride. Following induction of brain death, group A animals were maintained on a ventilator for a mean of 12 hr and 6 hr for the remaining groups. At the end of the experiment, the heart was excised, and tissue blocks were examined with light microscopy at (A) the atriaventricular node-bundle of His; (B) the major coronary arteries; and (C) myocardial tissue from the ventricular septum or left ventricular wall. In group A, 41% of the hearts showed histologic features of injury to the conduction tissue, 70% presented contraction band necrosis of the smooth muscle of the coronary arteries, and an incidence of 100% of the groups showed myocyte injury, more evident in the subendocardial area. In group B animals, conduction tissue injury was seen in 6 animals; the coronary arteries were not examined in this group; the incidence of myocyte injury was seen in 80% of the animals. Animals in groups C and D show no histopathologic injury in the conduction tissue (group A vs. C P less than 0.04), nor in the coronary arteries (group A vs. C P less than 0.002; group A vs. D P less than 0.01), preserving the myocytes (P less than 0.001). The catecholamine storm associated to acute increment of the endocranial pressure at the time of induction of brain death induces major histopathologic changes in the myocardium, as a result of endogenous catecholamines released inducing calcium overflow injury, affecting the conduction tissue, the smooth muscle of the coronary arteries, and the contractile myocardium. This can be prevented by calcium blockers or cardiac denervation.

Animals↗
PubMed1990

Reliability of electroencephalogram in the diagnosis of brain death.

The definition of brain death includes the irreversible loss of all brainstem and forebrain functions. The electroencephalogram (EEG), used to test forebrain functions, is part of the diagnostic armamentarium and is considered necessary even after primary infratentorial lesions. A review of both the current literature as well as new data on an interrater agreement and intrarater stability study provide the basis for a discussion on the reliability of EEG recording in this context and on the definition of brain death. Under normal conditions, the presence of an electrocerebrally inactive EEG is a valid indicator of brain death. However, the reliability and accordingly the validity of the EEG is restricted by technical problems and limited intrarater stability and interrater agreement.

Brain Death↗
PubMed2004

[Pediatric brain death and donation in Asturias].

BACKGROUND: Brain death is the irreversible cessation of intracranial neurologic function and is considered as the person's death. The objective of this study was to describe the characteristics of pediatric donors in the Hospital Central de Asturias from October 1995 to October 2002. METHODS: We performed a retrospective and descriptive study of the dead children who were potential donors in the pediatric intensive care unit (PICU). RESULTS: Of 43 dead children, 15 (34.9 %) were diagnosed with brain death. In four patients (family refusal in one, sepsis in two and brain tumor in one) there was no donation. In all patients, the diagnosis of brain death was based on clinical examination and electroencephalogram. Doppler ultrasonography and technetium-99m hexamethylpropyleneamineoxamine (Tc-99-HMPAO) scanning was also performed in three and nine patients respectively. The mean age of the donors was 8.1 years (range: 13 months-15 years). The male/female ratio was 3/1. The cause of death was multiple trauma in six children, brain hemorrhage in three, cardiac arrhythmias in three, lightning strike in one, diabetic ketoacidosis in one, septic shock in one and hypovolemic shock in one. The median interval between admission and brain death was 1.4 days (range: 3 hours-12 days). The time of organ support between brain death and donation was 8.4 hours (range: 6-13 hours). The most frequent complications after brain death were central diabetes insipidus in 90.9 % of the patients, hyperglycemia in 54.5 % and hypokalemia in 45.4 %. During support 72.7 % of the patients required inotropic aid. CONCLUSIONS: In our PICU more than one-third of the dead children suffered brain death, and most became donors. The most frequent cause of brain death was multiple trauma. Coordination with the transplant team and the training of medical staff are important to achieve a high percentage of donations.

Adolescent↗
PubMed1996

[Pragmatism versus metaphysics: a controversy about brain death].

The concept of brain death is still controversial. The Chilean case, as a result of a future transplantation law, seem to demonstrate this issue. The aim of this work is to contribute to the debate. A recent international polemic between metaphysic and pragmatic authors is approached, to establish bases to reject or accept the issue, after giving a brief history of the concept, from its medical origin to its transcendence to other areas as the law. The metaphysical rejection and the socio-cultural frame of the medical attitude that accepts brain death, are commented. It is concluded that the best defense of metaphysical point of view is the right to exclusion of minorities. Finally, brain death is criticized from a socio-cultural point of view of medical acts as a post-metaphysical concept of "useful death" and because of its relationship with "health production".

Brain Death↗
PubMed2002

A critique on the concept of "brain death".

Since the concept of "brain death" was introduced in medical terminology, enough evidence has come to light to show that the concept is based on an unclear and incoherent theory. The "brain death" concept suffers by internal inconsistencies in both the tests-criterion and the criterion-definition relationships. It is also evident that there are residual vegetative functions in "brain dead" patients. Since the content of consciousness is inaccessible in these patients who are in a profound coma, the diagnosis of "brain death" is based on an unproved hypothesis. A critical evaluation of the role and the limitations of the confirmatory tests in the diagnosis of "brain death" is attempted. Finally it is pointed out that a holistic approach to the problem of "brain death" in humans should necessarily include the inspection of the content of consciousness.

Brain↗
PubMed1992

[Changes of pupil size in brain death patients].

The representative criteria of brain death in Japan is Takeuchi Criteria (Koseisho Criteria), which is the definition of irreversible loss of brain function (functional brain death). The 3rd item of that criteria is "fixed pupil" and pupil size more than 4 mm. The 4th item is loss of the brain nerve reflexes including the light reflex. Three cases of brain death by whole brain destruction (organic brain death) who showed slow changes of pupil size were reported. Except fixed pupil, one case fulfilled Takeuchi Criteria. Other two cases fulfilled all items of Takeuchi Criteria, showing the same pupil size accidentally at the first and the second judgements. But, they changed their pupil size slowly and continuously after the examinations, showing tendencies toward mydriasis and/or miosis, repeatedly. They never decreased their pupil size less than 4 mm. The changes of pupil size were so slow that we could recognize them only after several hours or several days, and they were quite different from the light reflex. They did not receive any influences from turnover of day and night, darkness of the room, dopamine, etc. For the changes of pupil size were observed in the cases of organic brain death, it was elucidated that they were not due to the brain nerve activity. Then, it was considered that the changes of pupil size in the cases of functional brain death should be the same phenomena, because brain nerve function was lost.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
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

Changes of the cerebral mannitol concentrations in the course of brain death of a rodent model.

Determining the time of brain death is one of the critical issues in forensic examinations. Few authors have attempted to determine the time of brain death using pharmacokinetic approaches. We investigated cerebral concentrations of mannitol of which a single dose (1 g/kg) was administered in the course of brain death. The inflation of an epidural balloon was adopted as a rodent model of brain death. Brain death was determined using ordinary tests. Specimens were collected 4 h after brain death. Brain water content was higher in brain dead (BD) groups than those in control groups. Cerebral concentrations of mannitol in the BD group were significantly higher than those in the control group (P<0.01). In all areas of brain the concentration was the highest at the time when mannitol was administered during balloon inflation. Interhemispheric difference in the cerebrum was observed, followed by balloon inflation (P<0.05). Significant differences were observed in the average concentration of administered mannitol before and after brain death in the contralateral hemisphere (P<0.01) and in the brainstem (P<0.01). As the concentrations of mannitol in the brain are affected by cerebral trauma and brain death follows, mannitol can be used to determine the time of brain death at forensic examinations.

Animals↗
PubMed2000

Could heart rate variability analysis become an early predictor of imminent brain death? A pilot study.

UNLABELLED: Physiology of brain death is characterized by major disturbances of autonomic nervous system (ANS) activity which can lead to graft dysfunction. These findings exhibit the importance of early diagnosis of brain death to improve transplantation outcome. The aim of this prospective study was to assess whether heart rate variability (HRV) analysis, a noninvasive method to investigate ANS activity in comatose patients, could achieve this goal. A total of 14 brain-injured patients were included in the study as soon as they exhibited the clinical signs of imminent brain death. The electrocardiogram was then recorded from two leads with a Holter digital monitor. The clinical diagnosis of brain death was considered after an autonomic storm had occurred. HRV was assessed from 6 h before to 6 h after brain death in both time domain and spectral analysis, estimating either global ANS activity (index of variability, total power), parasympathetic activity (percentage of delta of R-R interval >50 ms, root mean square for successive interval differences, LnHF) or sympathetic activity (LnLF). Hourly averages of these variables were compared by using one-way analysis of variance. To assess whether HRV could per se diagnose brain death, receiver operating characteristic curves were generated for total power, root mean square for successive interval differences, and LnHF. We observed, for 6 h before brain death, a progressive extinction of the influence of the ANS on cardiovascular regulation. There was no activity in the two components of the ANS as soon as brain death occurred. HRV analysis appeared to be a very sensitive but a less specific method of diagnosing brain death. IMPLICATIONS: A total of 14 brain-injured patients with the clinical criteria of imminent brain death were enrolled for electrocardiogram recording and heart rate variability analysis (a noninvasive method to investigate autonomic nervous system activity). For 6 h before brain death, we observed a progressive extinction of autonomic nervous system activity which was not present as soon as brain death was clinically evoked.

Adult↗
PubMed2005

Organ-specific regulation of pro-inflammatory molecules in heart, lung, and kidney following brain death.

BACKGROUND: Nonspecific inflammatory events following brain death may increase the intensity of the immunological host response. The present study investigated the course of pro-inflammatory molecules in heart, lung, kidney, and plasma after brain death induction. MATERIALS AND METHODS: Brain death was induced in five pigs by inflation of an intracranial Foley catheter and five pigs were sham-operated as controls. Each experiment was terminated 6 h after brain death/sham operation and the organs were harvested. We measured the mRNA and protein levels for TNF-alpha, IL-1beta, and IL-6 in heart, lung, kidney, and plasma. Additionally, the mRNA expression for IL-6R, ICAM-1, MCP-1, and TGF-beta was determined in each organ. RESULTS: After 6 h, the plasma cytokine levels were higher in the brain-dead animals than in the sham-operated. In heart, lung, and kidney there was an increase in IL-6 and IL-1beta following brain death, while TNF-alpha was up-regulated in lung only (P < 0.05). MCP-1 and TGF-beta were significantly higher in heart and lung and IL-6R increased in heart after brain death (P < 0.05). CONCLUSIONS: Brain death was associated with non-uniform cytokine expression patterns in the investigated organs. These expression patterns may cause variable pro-inflammatory priming resulting in different degrees of damage and explain the organ-specific variation in outcomes after transplantations.

Animals↗
PubMed1988

99mTc-HM-PAO and 123I-amphetamine cerebral scintigraphy: a new, non invasive method in determination of brain death in children.

Determination of brain death in infants and children is difficult and criteria used in adult brain death are regarded insufficient in pediatric cases. In comatose children, clinical signs of brain death and EEG monitoring may be of limited value, while intercerebral blood flow estimations can provide more direct information. Beside radionuclide bolus angiography of polar radiopharmaceuticals with sequential technique, two radioisotopes are introduced for static brain images. Injection of 123I-amphetamine or the 99mTc labelled lipophilic complex HM-PAO into the peripheral venous circulation enables more precise static imaging of parenchymatous brain perfusion and cellular function in contrast to conventional dynamic imaging because of retention in the intact brain parenchyma. Critical deficits or complete loss of cerebral perfusion can be readily documented. These studies are particularly helpful when clinical signs and EEG alone cannot establish the definite diagnosis of brain death. Their easy application and wide availability renders them especially useful in children.

Adolescent↗
PubMed1984

[Brain death in a neurosurgical unit in Japan].

Walker states that the incidence of brain death accounts for approximately 1% of all deaths, so that brain death is a common state. According to Jennett et al, the occurrence of brain death is now a relatively frequent event, with about 4000 cases each year in Britain. But the actual circumstances of brain death can not be discovered from any published report. During the last 11 years (1973-1983) at Kyorin University Hospital, we studied 121 cases diagnosed as brain death according to Japanese criteria. The Japanese criteria requires that the pathology be a gross primary brain lesion, so did not concern ourselves with brain deaths due to secondary brain damage. We analysed the factors associated with brain death, that is the annual incidence, age, sex distribution, primary diagnosis and elapsed time from brain death to cardiac death. The increasing incidence of brain death in the last 5 years is probably due to a rise in severely brain-damaged patients (Table 1). In the age distribution, the high number of patients in their fifties presumably reflects the human age tendency for traumatic and vascular disorders respectively (Fig. 1 and Table 2). The fact that males predominate relates to the greater risk faced regarding cerebral trauma (Table 3). The primary diagnoses were cerebrovascular accidents in 60% of the cases especially subarachnoid hemorrhage in 41%, head injury in 31% and brain tumor in 9% (Tables 4 and 5). The elapsed time from brain deaths is measured from diagnosis of clinical brain death to cardiac asystole (Fig. 2). All patients had final cardiac asystole while still being ventilated.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1996

Brain death diagnosed by forensic analysis of drug distribution in human tissues-II--Distribution of caffeine in brain dead patients.

Caffeine concentrations in human tissues of 6 brain death cases as well as 5 non-brain death cases were examined in order to assess the possibility of diagnosing brain death based on an analysis of this compound. Concentrations of caffeine in human tissues were determined using gas chromatography/mass spectrometry. The tissue-to-blood concentration ratios were used to evaluate the distribution pattern in each case. In non-brain death cases, the ratios in all examined tissues were similar, and the values were close to 1 in all tissues except adipose, of which the value was near 0.3. In brain death cases, the ratios in all tissues except brain and adipose were similar to those in non-brain death cases. The ratios in the brain were higher than those of non-brain death cases, in 5 brain death cases, and lower in 1 brain death case to whom blood transfusion was done in a hospital. The ratios in the adipose were slightly higher in brain death cases than those in non-brain death cases. The discorded distribution of caffeine in brain death cases was presumably related to cessation of cerebral blood circulation at the time of brain death. Therefore, comparing caffeine concentrations in the brain with those in the other tissues can be useful for a forensic diagnosis of brain death.

Adult↗