Controversies about irreversible loss of brain functions and cerebral perfusion in brain death

2016 ◽  
Vol 23 (2) ◽  
pp. e8-e8 ◽  
Author(s):  
C. Roth ◽  
W. Deinsberger ◽  
J. Kleffmann ◽  
A. Ferbert
2010 ◽  
Vol 2 (1) ◽  
pp. 2 ◽  
Author(s):  
Calixto Machado

Brain death (BD) should be understood as the ultimate clinical expression of a brain catastrophe characterized by a complete and irreversible neurological stoppage, recognized by irreversible coma, absent brainstem reflexes, and apnea. The most common pattern is manifested by an elevation of intracranial pressure to a point beyond the mean arterial pressure, and hence cerebral perfusion pressure falls and, as a result, no net cerebral blood flow is present, in due course leading to permanent cytotoxic injury of the intracranial neuronal tissue. A second mechanism is an intrinsic injury affecting the nervous tissue at a cellular level which, if extensive and unremitting, can also lead to BD. We review here the methodology of diagnosing death, based on finding any of the signs of death. The irreversible loss of cardio-circulatory and respiratory functions can cause death only when ischemia and anoxia are prolonged enough to produce an irreversible destruction of the brain. The sign of such loss of brain functions, that is to say BD diagnosis, is fully reviewed.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Ari R. Joffe ◽  
Gurpreet Khaira ◽  
Allan R. de Caen

AbstractBrain death has been accepted worldwide medically and legally as the biological state of death of the organism. Nevertheless, the literature has described persistent problems with this acceptance ever since brain death was described. Many of these problems are not widely known or properly understood by much of the medical community. Here we aim to clarify these issues, based on the two intractable problems in the brain death debates. First, the metaphysical problem: there is no reason that withstands critical scrutiny to believe that BD is the state of biological death of the human organism. Second, the epistemic problem: there is no way currently to diagnose the state of BD, the irreversible loss of all brain functions, using clinical tests and ancillary tests, given potential confounders to testing. We discuss these problems and their main objections and conclude that these problems are intractable in that there has been no acceptable solution offered other than bare assertions of an ‘operational definition’ of death. We present possible ways to move forward that accept both the metaphysical problem - that BD is not biological death of the human organism - and the epistemic problem - that as currently diagnosed, BD is a devastating neurological state where recovery of sentience is very unlikely, but not a confirmed state of irreversible loss of all [critical] brain functions. We argue that the best solution is to abandon the dead donor rule, thus allowing vital organ donation from patients currently diagnosed as BD, assuming appropriate changes are made to the consent process and to laws about killing.


1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski

✓ Transcranial Doppler ultrasonography was used to monitor 71 patients suffering from intracranial hypertension with subsequent brain death. Among these, 29 patients were also assessed for systemic arterial pressure and epidural intracranial pressure, so that a correlation between cerebral perfusion pressure and the Doppler ultrasonography waveforms could be established. Four-vessel angiography was also performed in 33 patients after clinical brain death. With increasing intracranial pressure, the transcranial Doppler ultrasonography waveforms exhibited different characteristic high-resistance profiles with first low, then zero, and then reversed diastolic flow velocities, depending on the relationship between intracranial pressure and blood pressure (that is, cerebral perfusion pressure). This study shows that transcranial. Doppler ultrasonography may be used to assess the degree of intracranial hypertension. This technique further provides a practicable, noninvasive bedside monitor of therapeutic measures.


2010 ◽  
pp. 4847-4850
Author(s):  
P.J. Hutchinson ◽  
J.D. Pickard

Death can be defined as the irreversible loss of the capacity for consciousness and brain stem function, combined with irreversible loss of the capacity to breathe. The irreversible cessation of brainstem function, whether caused by a primary intracranial catastrophe (e.g. trauma, haemorrhage) or the result of extracranial cranial events (e.g hypoxia), will result in the same clinical state, hence brain stem death is the same as death of the patient....


2005 ◽  
Vol 103 (5) ◽  
pp. 957-961 ◽  
Author(s):  
Nino Stocchetti ◽  
Elisa Roncati Zanier ◽  
Rita Nicolini ◽  
Emelie Faegersten ◽  
Katia Canavesi ◽  
...  

Background The authors propose that for a moderate reduction of perfusion during progressive irreversible ischemia, oxygen extraction increases to maintain aerobic metabolism, and arteriojugular oxygen difference (AJDo2) increases. Because of reduced carbon dioxide washout, venoarterial difference in carbon dioxide tension (DPco2) increases, with no change in the DPco2/AJDo2 ratio. With further reduction of cerebral perfusion, the aerobic metabolism will begin to decrease, AJDo2 will decrease while DPco2 will continue to increase, and the ratio will increase. When brain infarction develops, the metabolism will be abated, no oxygen will be consumed, and no carbon dioxide will be produced. Methods The authors studied 12 patients with acute cerebral damage that evolved to brain death and collected intermittent arterial and jugular blood samples. Results Four patterns were observed: (1) AJDo2 of 4.1 +/- 0.7 vol%, DPco2 of 6.5 +/- 1.9 mmHg, and a ratio of 1.55 +/- 0.3 with cerebral perfusion pressure of 62.5 +/- 13.4 mmHg; (2) a coupled increase of AJDo2 (5.8 +/- 0.7 vol%) and DPco2 (10.1 +/- 1.0 mmHg) with no change in ratio (1.92 +/- 0.14) and cerebral perfusion pressure (57.9 +/- 5.8 mmHg); (3) AJDo2 of 4.7 +/- 0.4 vol% with an increase in DPco2 (11.8 +/- 1 mmHg) and correspondingly higher ratio (2.7 +/- 0.2); in this phase, cerebral perfusion pressure was 39.7 +/- 10.5 mmHg; (4) immediately before diagnosis of brain death (cerebral perfusion pressure, 17 +/- 10.4 mmHg), there was a decrease of AJDo2 (1.1 +/- 0.1 vol%) and of DPco2 (5.3 +/- 0.6 mmHg) with a further ratio increase (5.1 +/- 0.8). Conclusions Until compensatory mechanisms are effective, AJDo2 and DPco2 remain coupled. However, when the brain's ability to compensate for reduced oxygen delivery is exceeded, the ratio of DPco2 to AJDo2 starts to increase.


1992 ◽  
Vol 18 (2) ◽  
pp. 76-81 ◽  
Author(s):  
H. -P. Schlake ◽  
I. G. Böttger ◽  
K. -H. Grotemeyer ◽  
I. W. Husstedt ◽  
W. Brandau ◽  
...  

2019 ◽  
Vol 86 (4) ◽  
pp. 347-358 ◽  
Author(s):  
James L. Bernat

Death can be defined as the permanent cessation of the organism as a whole. Although the organism as a whole is a century-old concept, it remains better intuited than analyzed. Recent concepts in theoretical biology including hierarchies of organization, emergent functions, and mereology have informed the idea that the organism as a whole is the organism’s critical emergent functions. Because the brain conducts the critical emergent functions including conscious awareness and control of respiration and circulation, the cessation of brain functions is death of the organism. A newer concept, the brain as a whole, may offer a superior criterion of death to the whole-brain criterion, because it more closely matches accepted clinical brain death tests and confirms the cessation of the organism’s emergent functions. Although the concepts of organism as a whole and brain as a whole remain vague and in need of rigorous biophilosophical analysis, their future precision will be restricted by the categorical limitations intrinsic to theoretical biological models.


Neurosurgery ◽  
1989 ◽  
Vol 25 (2) ◽  
pp. 275-278 ◽  
Author(s):  
Howard H. Kaufman ◽  
Fred H. Geisler ◽  
Thomas Kopitnik ◽  
William Higgins ◽  
Dan Stewart

Abstract Patients treated with barbiturate coma for elevated intracranial pressure after head injury may suffer brain death. Since such patients have an iatrogenically induced absence of neurological function, brain death cannot be diagnosed clinically. Furthermore, as demonstrated by two of our patients, monitoring of intracranial pressure, even in the face of brain death, may show a low intracranial pressure and an intracranial pulse, suggesting the presence of adequate cerebral perfusion pressure and, therefore, brain viability. Under these circumstances. however, significant intracranial blood flow may be absent. Therefore, we suggest that a patient in barbiturate coma should undergo serial blood flow studies. even when the intracranial pressure is low and an intracranial pulse is present. to determine whether brain death has occurred.


Sign in / Sign up

Export Citation Format

Share Document