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At least 55 records · Page 3Linked to original sources
PubMed1996

[From death concepts to brain death diagnostic criteria].

The authors present considerations about death and brain death concepts, as well the legal aspects for its diagnosis in Brazil. They also present the UNICAMP Protocol for the Diagnosis of Brain Death, revised and according with the current law, with standard techniques for the diagnostic exam. They emphasize the importance of a mature ethical position for this frequent and challenging situation.

Attitude to Death↗
PubMed1983

[Brain death in secondary brain lesion].

The criteria of brain death established by Japanese Society of EEG in 1974, necessitates a prerequisite; be applicable only to "acute destructive, primary gross lesion of brain". Namely, because of insufficient clinical data, secondary brain lesion such as post-anoxia, intoxication, metabolic coma and some kinds of CNS infection were excluded for the object to determine brain death. The criteria published by others also describe that etiology of coma should be clarified, and that careful measures are necessary to diagnose brain death if the cause of coma is unknown. In the present study, it was investigated that whether a clinico-pathological entity of brain death could exist universally regardless of the etiology, and by what means it could be defined clinically. The patients suffering from nondestructive, secondary brain lesions and who showed "brain death-like state" were selected for the study. ("Brain death-like state" requires coma, dilated nonreactive pupis and arrest of respiration concomitantly for more than 6 hours.) And 25 patients were collected, whose underlying diseases were post-anoxia or shock, CO intoxication, Paraquat poisoning, near-drowning or suffocation, hepatic coma, accidental hypothermia and sepsis, with or without the episode of cardiac arrest. Though all the patients died from 1 to 13 days after the insult, clinical signs of brain death-like state were not always irreversible. Isoelectric EEG was obtained on that state in 11 patients and repeated EEG revealed no return on those patients. But another 5 patients showed EEG activity when brain death was strongly suspected clinically.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

Brain death: determination with brain stem evoked potentials and radionuclide isotope studies.

Thirty-three patients fulfilling the clinical criteria for brain death were tested by Brainstem Auditory Evoked Potentials (BAEP) and Radionuclide Cerebral Angiography and Brain Perfusion Studies. There was a significant correlation between the BAEP and radionuclide study outcomes. All patients with absence of BAEP showed no cerebral perfusion. These findings, added to the clinical findings, resulted in a final diagnosis of brain death in all patients. It is concluded that BAEP and Radionuclide Cerebral Perfusion studies are useful adjuncts for proving that brain death has really occurred.

Adolescent↗
PubMed2004

Endothelial activation through brain death?

BACKGROUND: Brain death induces myocardial dysfunction and multifocal microscopic myocardial necrosis in dogs; however, the pathogenetic pathways between brain death and cardiac damage remain incompletely understood. We hypothesized that brain death might induce a propensity toward coronary vasospasms, possibly by endothelial dysfunction. We therefore studied the effect of serotonin and acetylcholine on tension generated by isolated coronary artery segments from control and brain dead dogs. METHODS: Coronary segments were isolated 1 hour after brain death that was induced by the inflation (15 ml saline) of an extradurally placed balloon or from sham-operated time-matched controls. Studied were the effect of serotonin on isometric tension, with and without pre-constriction with prostaglandin F(2alpha) (PGF(2alpha)), and the effect of acetylcholine after pre-constriction. RESULTS: Coronary segments from brain dead dogs exhibited severe vasoconstriction when serotonin (10(-7), 10(-6), and 10(-5) mol/liter) was administered, a reaction that was barely detectable in control segments. After pre-construction with PGF(2alpha), serotonin caused only significant vasodilation in a concentration of 10(-5) mol/liter, unlike in control segments where 10(-6) mol/liter had already induced a highly significant vasodilation. The reaction on acetylcholine was identical in both groups. CONCLUSION: Brain death induces changes in coronary vasoreactivity in dogs, with a highly increased sensitivity for the vasospastic effects of serotonin. It is, however, not merely caused by aspecific endothelial dysfunction, as evidenced by the normal reaction on acetylcholine. These alterations in coronary artery properties might contribute to the myocardial damage seen after brain death.

Acetylcholine↗
PubMed1993

[Neurological problems in the diagnosis of brain death--observation of spinally-mediated movements in brain-dead patients and proposal of a "brain death judging doctor" system].

We report two cases in which neurological examination met the Second Tentative Criteria for Brain Death of Chiba University Medical School, except for spontaneous contractions of the rectus abdominis muscle during apnea testing. In Case 1, a 54-year-old man with brainstem infarction, judgement of brain death was suspended initially, but was ultimately declared after the contractions were deemed to be spinal in origin. MRI findings after declaration and autopsy were compatible with brain death. In Case 2, a 27-year-old man with fulminant hepatitis and subsequent severe brain edema, judgement was postponed due to detection of the contractions at the second testing, and was ceased with family intent. Several cases of abnormal gross and fine movements in brain-dead patients have been reported. These paradoxical phenomena may confuse an inexperienced examiner and delay the declaration of brain death. Whether brain death should be considered real death of the person or not, neurologists should be aware of the occasional presence of neurological problems in the diagnosis of brain death, such as spinally-mediated movements. Since the major opposition to brain death is the distrust of medical doctors, we propose a pilot system of a "brain death judging doctor".

Adult↗
PubMed1999

Modulation of coronary perfusion pressure can reverse cardiac dysfunction after brain death.

BACKGROUND: Brain death results in a rapid decline in left ventricular function, which has clinical relevance for organ transplantation. The aim of the present study was to investigate coronary perfusion changes during brain death and their role in cardiac dysfunction. METHODS: In an in situ isolated canine heart model, brain death was induced by inflation of a subdural balloon catheter. The heart was perfused separately with the animal's own blood by a pressure-controlled roller pump that was coupled to the measured aortic pressure. Myocardial contractility was estimated by the slope of the end-systolic pressure-volume relation. RESULTS: Induction of brain death resulted in a transient hyperdynamic response, followed by a significant decrease in systemic vascular resistance, coronary blood flow, and the end-systolic pressure-volume relation (p<0.05). However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death levels, coronary blood flow and the end-systolic pressure-volume relation were also restored to baseline levels. CONCLUSION: Severe impairment of coronary blood flow may contribute to decreased contractility after brain death that can be reversed by modulation of coronary perfusion pressure.

Animals↗
PubMed1992

Acute endocrine failure after brain death?

After brain death, 32 potential organ donors were studied to determine serum and plasma concentrations of hypothalamic-pituitary hormones, thyroid hormones, and cortisol over a period of up to 80 hr. Diagnosis of brain death was established either on the basis of clinical criteria (n = 16) or by angiography (n = 16). While 78% of the organ donors developed diabetes insipidus, none of the circulating hormones of the anterior pituitary gland showed a progressive decline in concentration according to their plasma half-lives. With the exception of arginine vasopressin (AVP), no hormone concentration was found to be subnormal due to the onset of brain death. The subnormal free triiodothyronine (FT3) values in 62% of cases (median FT3 of 2.2 pmol/L within the first 24 hr) and the cortisol concentration of 6.9 micrograms/dl correlate with the frequency of similar findings in patients with severe head injuries. While the adrenocorticotropic hormone (ACTH) concentrations of 10-53 pg/ml remained constant during the study period, thyroid-stimulating hormone (TSH) and human growth hormone (hGH) concentrations showed a 12- and 35-fold increase from baseline values after 30-40 hr. These results suggest that, despite the now generally accepted criteria of brain death, there is still some residual function, and thus also perfusion of the hypothalamic-pituitary neuroendocrine system. This residual function appears to be sufficient to maintain hormonal plasma levels at least in the low reference range in most donors. Hormonal depletion in organ donors subsequent to brain death, as suggested repeatedly in the literature, could not be confirmed. The analysis of serum or plasma concentration patterns of a number of hormonal parameters following brain death does not support the rationale for a routine replacement therapy of total triiodothyronine (TT3) or cortisol to maintain endocrine homeostasis prior to organ harvest. However, dexamethasone therapy may be followed by suppression of the adrenal cortex of the organ donor. In these cases, cortisol substitution may be indicated.

Adrenocorticotropic Hormone↗
PubMed1985

Brain death and bioelectrical brain activity.

The effect of mechanical vibration and light stimulation on the ongoing and evoked bioelectrical activity was studied in two cases with clinically defined brain death and two other patients with severe head injury, one of them with an isoelectric EEG. The importance of such stimulation sequences for the definition of brain death is discussed, with particular emphasis on mechanical vibration.

Adult↗
PubMed1997

[Organ transplantation and brain death. A critical contribution to the definition of brain death].

The following article is based on a lecture held in February 1996 in Bremen on the occasion of the 6. International Symposium of Intensive Medicine. Some arguments of the discussion about Brain-Death Definition are inquired. The main points are not the identification-methods (diagnosis) of brain-death but the function of Brain-Death-Definition. On one hand it is possible to demonstrate that the points of criticism are not plausible; on the other hand that the discussion about Brain-Death-Definition is a substitute that can't give an answer to the real ethical problem. The question is: "Which kind of medicine does the society want?" The main objective is to get to the matters of facts in the current discussion to create the presupposition reasonable orientation.

Brain Death↗