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At least 19 recordsLinked to original sources
PubMed1998

"Brainstem death," "brain death" and death: a critical re-evaluation of the purported equivalence.

The author challenges brain-based diagnoses of death by re-examining the concept of death, its definition, the anatomical criterion, and the clinical signs or tests. Dr. Shewmon challenges the fundamental assumptions underlying brain death: (1) that the brain is the body's "critical system"; and (2) that the body even has a localized "critical system." He does not redefine death, but shifts the anatomical criterion from a single focus (the brain) to the entire body. The clinical tests correspondingly shift from those implying loss of brain function to those implying thermodynamically supracritical microstructural damage diffusely throughout the body. He concludes that the notion of "brain death" as bodily death is logically and physiologically incoherent, and that its replacement by something scientifically more credible would promote not only the sanctity of life, but ironically even transplantation as well.

Age Factors↗
PubMed2005

The concept and practice of brain death.

Brain death, the colloquial term for the determination of human death by showing the irreversible cessation of the clinical functions of the brain, has been practiced since the 1960s and is growing in acceptance throughout the world. Of the three concepts of brain death--the whole-brain formulation, the brain stem formulation, and the higher brain formulation--the whole-brain formulation is accepted and practiced most widely. There is a rigorous conceptual basis for regarding whole-brain death as human death based on the biophilosophical concept of the loss of the organism as a whole. The diagnosis of brain death is primarily a clinical determination but laboratory tests showing the cessation of intracranial blood flow can be used to confirm the clinical diagnosis in cases in which the clinical tests cannot be fully performed or correctly interpreted. Because of evidence that some physicians fail to perform or record brain death tests properly, it is desirable to require a confirmatory test when inadequately experienced physicians conduct brain death determinations. The world's principal religions accept brain death with a few exceptions. Several scholars continue to reject brain death on conceptual grounds and urge that human death determination be based on the irreversible cessation of circulation. But despite the force of their arguments they have neither persuaded any jurisdictions to abandon brain death statutes nor convinced medical groups to change clinical practice guidelines. Other scholars who, on more pragmatic grounds, have called for the abandonment of brain death as an anachronism or an unnecessary prerequisite for multi-organ procurement, similarly have not convinced public policy makers to withdraw the dead-donor rule. Despite a few residual areas of controversy, brain death is a durable concept that has been accepted well and has formed the basis of successful public policy in diverse societies throughout the world.

Brain Death↗
PubMed1990

[Hemodynamic, coagulation and glycoregulation changes induced by brain death].

Brain death results in various changes in circulation haemostasis, acid-base balance and glycoregulation. This study was carried out between February 1988 and December 1988 in 91 patients with brain death. Age range was between 6 and 58 years. The cause of brain death was brain trauma (71%) and vascular malformations (26%). In all patients a cardio-vascular collapse occurred at the moment of brain death, requiring an intravascular loading (466.3 +/- 240.3 ml.h-1) with crystalloids and albumin. Dopamine was used in 70% of cases at the dose of 3 micrograms.kg.min-1 to improve kidney and splanchnic perfusion. No alterations of acid-base balance were observed in these patients who admitted for organ donation in a short delay (17.1 +/- 6 h). Haemostasis was modified in all patients but the alterations occurred before the brain death and were related to brain injury. Further investigations are required for a better understanding of glycoregulation changes as they could influence pancreatic transplant survival. Hormonal changes have also to be more extensively studied for possible physiopathologic causes of the variations. A better understanding of these alterations will be of benefit for management of patients in brain death and potential organ donors.

Adolescent↗
PubMed1995

Desensitization of myocardial beta-adrenergic receptors and deterioration of left ventricular function after brain death.

Brain death often results in a series of hemodynamic alterations that complicate the treatment of potential organ donors before transplantation. The deterioration of myocardial performance after brain death has been described; however, the pathophysiologic process of the myocardial dysfunction that occurs after brain death has not been elucidated. This study was designed to analyze the function of the myocardial beta-adrenergic receptor and the development of left ventricular dysfunction in a porcine model of experimental brain death. Analysis of the beta-receptor included determination of receptor density and adenylate cyclase activity after stimulation independently at the receptor protein, the G protein, and the adenylate cyclase moiety. Myocardial beta-receptor density did not change after the induction of brain death. A decrease in stimulated adenylate cyclase activity was observed within the first hour after brain death at the level of the beta-receptor, the G protein, and the adenylate cyclase moiety, which suggests the occurrence of rapid desensitization of beta-receptor function. Significant deterioration of myocardial performance also occurred within the first hour after brain death, represented by a decrease in preload-recruitable stroke work compared with the baseline value. The deterioration of myocardial performance after brain death correlates temporally with desensitization of the myocardial beta-receptor signal transduction system. The mechanism of impairment appears to be localized to the adenylate cyclase moiety itself.

Adenylyl Cyclases↗
PubMed2001

No evidence of NO-induced damage in potential donor organs after brain death.

Brain death induces multiple-organ dysfunction, with undesirable consequences for organ transplantation. However, the mechanisms are not completely clear. In the hearts, lungs, livers, and kidneys of rats, we investigated whether brain death leads to changes in nitric oxide (NO) production or to the formation of nitrotyrosine (the footprint of peroxynitrite, formed from NO and superoxide) or to lipid peroxidation products. To produce a rat model of brain death, we inflated a subdurally placed balloon catheter. We used the Griess reaction to assay plasma nitrite and nitrate. Proteolytic digestion followed by high-performance liquid chromatography (HPLC) with electrochemical detection determined nitrotyrosine formation in the tissues. Tissues were also examined immunohistochemically with anti-nitrotyrosine antibody. We used a thiobarbituric acid method to assay lipid peroxidation. An intense, transient hemodynamic activation occurred at the onset of brain death (heart rate, 496 beats/min; mean arterial pressure (AP), 181 mm Hg; dP/dt(max), 11,500 mm Hg/sec). A constant hypotensive phase (mean AP, 50 mm Hg; dP/dt(max), 2,674 mm Hg/sec) followed. Plasma concentration of nitrite plus nitrate remained unchanged 2 hours after brain death (32.8 +/- 1.5 vs 31.3 +/- 2.2 micromol/liter at zero time). Neither HPLC nor immunohistochemistry detected significant nitrotyrosine formation in the tissues. We detected no increase in lipid peroxidation products.Our results indicate that changes in the generation of reactive nitrogen and active oxygen species do not play an important role in post-brain-death organ dysfunction, at least not at the early stage.

Animals↗
PubMed2001

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.

Adult↗
PubMed1986

Brain death.

Brain death is a condition widely recognized by philosophers, theologians, the public, and the law. Criteria for the determination of brain death have been progressively refined for almost 30 years. They involve clinical evidence of the loss of brain function and various periods of observation, which can often be shortened by confirmatory tests, particularly cerebral blood flow studies or electroencephalography. Prompt declaration of brain death is therefore possible. In addition, it is important for physicians to offer the possibility of organ donation to the patient's family both because organs are desperately needed and because many families desire this. A model algorithm for the determination of brain death, explanatory text, and appropriate references are presented to aid the development of protocols for individual and hospital use.

Algorithms↗