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Brain-stem auditory evoked potential monitoring. Variations of stimulus artifact in brain death.

Brain-stem auditory evoked potentials (BAEPs) were recorded in 20 subjects with brain death (mean age, 33.2 +/- 15.1 years) and 20 healthy volunteers (mean age, 29.8 +/- 6.8 years). Brain death was due to head injury (n = 14), encephalitis (n = 3), brain-stem hemorrhage (n = 1), cerebellar hemorrhage (n = 1) or cerebral infarction (n = 1). The presence, latency and amplitude of the individual BAEP components and variations of the stimulus artifact were evaluated. The mean (+/- S.D.) amplitude of the stimulus artifact was 0.26 +/- 0.12 microV in the brain-dead subjects and 0.09 +/- 0.05 microV in the control group (P < 0.001, t test). The causes of the phenomenon of increasing stimulus artifacts in the evolution of brain death remain unclear.

Acoustic Stimulation↗

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↗

Phenomenological diversity of spinal reflexes in brain death.

In brain death, spinal reflexes and automatisms are observed which may cause irritation and even doubt in the diagnosis. In the literature there are no dedicated descriptions of the diversity and of neuroanatomical considerations. In 278 examinations of 235 patients for the determination of brain death, on 42 occasions obvious spinal reflexes and/or spinal automatisms were observed in 27 brain dead bodies. Because they were not systematically searched for, minute forms have probably been missed. The reflexes (R) and automatisms (A) are described according to the time of observation in relation to the development of brain death, the presumable spinal localization and the possible phylogenetical interpretation. Especially disquieting examples are discussed in more detail, e.g. monophasic EndotrachealSuction-ThoracicContraction-R supposedly switched in segments C2-6 or TrapeziusPinch-ShoulderProtrusion-R conveyed by the accessory nerve (terminology according to the scheme: for the reflexes, Trigger-Response-R: for the automatisms, Movement-A). After these experiences a more thorough examination showed frequent observations of rather minute forms of spinal reflexes, as well as automatisms and even the Lazarus sign (in possibly more than two thirds of the examinations). An estimation of the factual frequency would necessitate special attention to those much more frequent but less obvious minute spinal reflexes and automatisms.

Adult↗

What can be learned from brain-death models?

Brain death of the donor is an important risk factor influencing graft outcome. In addition to its nonspecific effects, it potentiates graft immunogenicity and increases host alloresponsiveness. Thus brain death in addition to other unspecific injuries such as organ procurement, preservation and consequences of ischemia/reperfusion injury, contributes towards the change of an inert organ to an immunological altered graft. Prior to engraftment, brain death initiates a cascade of molecular and cellular events including the release of proinflammatory mediators leading to cellular infiltrates. Those events may affect the incidence of both acute and chronic changes, developing and contributing to reduced graft survival. Consequently, strategies to reduce the immunogenicity or the pro-inflammatory status of the graft are becoming more attractive and might even help to improve organ quality and graft function.

Brain Death↗

Brain death after severe traumatic brain injury: the role of systemic secondary brain insults.

Secondary brain insults predominantly due to hypotension are frequent among patients with fatal traumatic brain injury. We assessed the correlation between different systemic secondary brain insults and brain death in 404 patients admitted to our intensive care unit (ICU) after severe traumatic brain injury. We collated data on hypoxemia and hypotension prior to as well as the occurrence of hypoxemia, hypotension, shock, anemia, hyperglycemia, and hyperthermia within the first 24 hours after ICU admission. We also considered both the presence of extracranial injuries and the category of traumatic brain injury using computerized tomography. The 59 patients (14.6%) who developed brain death, were significantly older than patients without a fatal neurological outcome (46.1 +/- 22 vs 29.5 +/- 14.9 years; P < .0001). Intracranial mass lesions, whether surgically evacuated were more frequent among brain-dead patients. The systemic secondary brain insults significantly associated with brain death were hypoxemia, hypotension, shock, anemia, and hyperglycemia within the first 24 hours after ICU admission. After multivariate analysis, the factors that independently predicted brain death were the occurrence of shock (odds ratio [OR], 6.74; 95% confidence interval [CI], 2.85-15.84; P = .001) and older age (OR, 1.05; 95% CI, 1.03-1.07; P = .003). In conclusion, early shock seems to be the major systemic secondary brain insult associated with brain death in patients with severe traumatic brain injury. Prevention of or correction of shock might help to either decrease the occurrence of a fatal neurological outcome or in brain-dead patients to preserve organs in better condition for procurement.

Adult↗

Activation of inflammatory mediators in rat renal isografts by donor brain death.

BACKGROUND: Brain death (BD) has been thought to influence the early course of transplanted organs by triggering a series of nonspecific inflammatory events that in turn may increase the kinetics and intensity of the immunological host responses. In this study early nonspecific, cellular, and molecular changes occurring in kidney isografts from BD donors are compared with those from normal anesthetized, ventilated controls. METHODS: After induction of brain death, the animals were mechanically ventilated for 6 hr before organ removal. Only rats with stable blood pressure (mean arterial pressure >80 mmHg) were included. Serum creatinines were measured daily. Representative grafts were harvested 6 hr after brain death and between 1 hr and 5 days after engraftment for morphology, immunohistology, and reverse transcriptase-polymerase chain reaction. The presence of serum cytokines was assessed by enzyme linked immunoabsorbant assay. RESULTS: Serum creatinine levels rose slightly in recipients from BD donors. Serum interleukin-1beta levels increased within 6 hr versus controls (P<0.05). mRNA levels of interleukin-1beta and macrophage inhibitory protein-1 in the kidneys were up-regulated transiently before engraftment (6 hr after BD) and 1 hr after revascularization (P<0.05). By immunohistology, numbers of infiltrating polymorphonuclear leukocytes peaked at 24 hr in parallel with intragraft induction of P- and E-selectin, complement, and other proinflammatory chemokines and cytokines. At 5 days, the isografts from BD donors were highly infiltrated by host leukocyte populations associated with intense up-regulation of their products. In contrast, those from control donors remained relatively normal through this initial follow-up period. CONCLUSIONS: The intense nonimmune inflammation produced in isografts after donor BD may represent the initial stages of a continuum between an initial nonspecific and later immune reactivity, when placed in the context of allotransplantation.

Animals↗

[Criteria of brain death: 3d generation. Interpretation of criteria established by the Federal Chamber of Physicians in determining brain death].

The criteria of brain death published by the Federal Chamber of Physicians in 1982 in their second generation have stood the test of time and remain valid. The most important amendments in issuing a third generation are the following: In primary cerebral lesions supratentorial lesions have to be distinguished from infratentorial processes. In primarily the infratentorial processes EEG activities of the cortex max outlast apneic brain stem areflexia. Therefore in infratentorial processes controls of the EEG are indispensable. The extinction of evoked potentials, certain conditions being observed, may prove the loss of brain stem function and therefore may allow to shorten observation time, and may offer an alternative to isoelectricity in the EEG or cerebral perfusion stop as a diagnostic procedure. Additional tests for brain death are commented on. Special considerations are necessary in brain death in children.

Brain Damage, Chronic↗

Problems associated with the apnea test in the diagnosis of brain death.

BACKGROUND: Brain death is the absence of all cortical functions, including the brainstem. The apnea test (AT) is a necessary requisite to complete this diagnosis. Anecdotal reports describing hypotension and acidosis due to apnea test have been reported. However, there are few studies that evaluate complications or difficulties related to this procedure. OBJECTIVE: To analyze medical problems associated with the apnea test. METHODS AND PATIENTS: We analyzed clinical features, potential risk conditions, and problems in 129 brain dead patients during the apnea test. The diagnosis of brain death was made according to the American Academy of Neurology recommendations. RESULTS: Clinical problems during the apnea test were detected in more than two thirds of patients, including: arterial hypotension (12%), acidosis (68%), and hypoxemia (23%). Four patients developed major complications, including: pneumothorax, cardiac arrest, bradycardia, atrial fibrillation and myocardial infarction. CONCLUSION: The apnea test is not an innocuous procedure. Complications during the AT are more common than reported and limit organ procurement for transplantation. Guidelines for performing the AT should be followed in order to avoid clinical complications.

Adult↗

A consideration of the ethics of brain death--what are the ethical guidelines for physician, family and society in dealing with brain death?

There is at present considerable confusion with respect to ethical guidelines that should govern the behavior of society and the physician confronted by problems resulting from recent attainments of medicine and science. The use of life supporting devices raises the problem of determining when death has occurred and what is proper ethical procedure in dealing with the deficient half life caused by "Brain Death." Some guidance is obtained from a consideration of the nature of life, the nature of death, the nature of man, and the essence lost in death of man. A parallel consideration of the nature of ethics, the bases of ethics and of ethical decision can be helpful. An individual may have ideals which control behavior, even elevate ethical standards; others entertain concepts that destroy social ethics. Ethics control and direct social interactions; ethics determine the quality of social behavior--ethics are established by societies not by individuals. Numerous commissions have endeavored to define the requirements of physicians for diagnosing brain death and for appropriate subsequent actions. The rationales presented, however, are not invariably accepted by lay society. The problem is created by numerous trends. Among them are the "rightest" movement which, though possessing many virtues, has its excesses such as expressed in the "right to life movement." These have not been beneficial and have necessitated "right to death movements." Opposition is also due to the fact that society's concepts of the medical profession have changed. The practice of organ transplantation has created problems. Finally, the concept of death as other than evil is no longer generally accepted. As more biological manipulations are possible ever more difficult ethical problems will arise. It is a certainty, however, that when brain death has occurred life of man and that of the individual has ended. Although others might not agree, our ethic requires us to use life assist techniques to preserve the vegetative man, the individual who can still breathe spontaneously though lacking consciousness and behavioral ability. All the codes of medical ethics state that a physician shall not kill--this does not mean he cannot permit the terminal phases of death when the essence of human life is lost. A major question is the ethical responsibility of one society toward another. Can an affluent society squander its resources in the preservation of ineffectual life in the body after "brain death" when others are without the medical assistance which would permit total living?

Attitude to Death↗

[Early brain stem auditory evoked potentials in brain death].

Brain-stem auditory evoked potentials (BAEPs) are realized after the first flat EEG in 50 patients. BAEPs were absent in 70% of the patients. In 22% of the patients, one- or two-sided peak I persists. In 8% the peaks I, II and IV exist after the first flat EEG. BAEP evolution with the course of time is realized. A complete disappearance is established after 24 h. The useful advantage of BAEPs in the early diagnosis of brain death is discussed.

Adolescent↗

Brain death.

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Brain Death↗

Brain death.

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Brain Death↗

Brain death.

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Brain↗

Brain death.

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Brain Death↗