scholarly journals Rapid Brain Death following Cardiac Arrest without Intracranial Pressure Rise and Cerebral Circulation Arrest

2018 ◽  
Vol 2018 ◽  
pp. 1-3
Author(s):  
Maxime Nguyen ◽  
Thomas Bièvre ◽  
Abdelouaid Nadji ◽  
Bélaïd Bouhemad
Keyword(s):  
Cardiac Arrest ◽  
Intracranial Pressure ◽  
Brain Death ◽  
Unusual Case ◽  
Neuronal Damage ◽  
Pressure Rise ◽  
Electric Activity ◽  
Cellular Toxicity ◽  
Intracranial Pressure Elevation ◽  
Brain Reperfusion

We describe here an unusual case of brain death following cardiac arrest. Brain electric activity had totally ceased, allowing the confirmation of brain death, despite normal cerebral blood flow (assessed by both transcranial doppler and tomodensitometry) and no evidence of intracranial hypertension. In our case, a residual electric activity was assessed at admission and lesions worsened on imaging during ICU stay, suggesting that part of the neuronal damage occurred after brain reperfusion. All these elements suggest BD rather by cellular toxicity than intracranial pressure elevation.

Transcranial Doppler ultrasonography in raised intra-cranial pressure and in intracranial circulatory arrest

1988 ◽  
Vol 68 (5) ◽  
pp. 745-751 ◽  
Author(s):  
Werner Hassler ◽  
Helmuth Steinmetz ◽  
Jan Gawlowski
Keyword(s):  
Intracranial Pressure ◽  
Brain Death ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Transcranial Doppler ◽  
Cerebral Perfusion ◽  
Doppler Ultrasonography ◽  
Perfusion Pressure ◽  
Circulatory Arrest ◽  
Transcranial Doppler Ultrasonography

✓ 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.

Chinese Pediatric Organ Donation With Scheduled Cardiac Arrest After Brain Death: A Novel China Classification Beyond Maastricht

2015 ◽  
Vol 47 (10) ◽  
pp. 2836-2840 ◽  
Author(s):  
Z. Wu ◽  
X. Gao ◽  
F. Chen ◽  
X. Tao ◽  
J. Cai ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Death ◽  
Organ Donation

scholarly journals Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

1993 ◽  
Vol 13 (4) ◽  
pp. 558-567 ◽  
Author(s):  
Douglas T. Ross ◽  
David I. Graham
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Neuronal Damage ◽  
Open Heart Surgery ◽  
Thalamic Reticular Nucleus ◽  
Global Cerebral Ischemia ◽  
Reticular Nucleus ◽  
Thalamic Nuclei ◽  
Attentional Processing ◽  
Thalamic Relay Nuclei

Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.

Difficulties in assessing brain death in a case of benzodiazepine poisoning with persistent cerebral blood flow

2004 ◽  
Vol 23 (10) ◽  
pp. 503-505 ◽  
Author(s):  
Frédéric Marrache ◽  
Bruno Megarbane ◽  
Stéphane Pirnay ◽  
Abdel Rhaoui ◽  
Marie Thuong
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Brain Death ◽  
Intracranial Hypertension ◽  
Multiorgan Failure ◽  
Deep Coma ◽  
Ventricular Drainage ◽  
Eeg Activity ◽  
Anoxic Injury

Assessing brain death may sometimes be difficult, with isoelectric EEG following psychotrope overdoses or normal cerebral blood flow (CBF) persisting despite brain death in the case of ventricular drainage or craniotomy. A 42-year-old man, resuscitated after cardiac arrest following a suicidal ingestion of ethanol, bromazepam and zopiclone, was admitted in deep coma. On day 4, his brainstem reflexes and EEG activity disappeared. On day 5, his serum bromazepam concentration was 817 ng/ml (therapeutic: 80-150). The patient was unresponsive to 1 mg of flumazenil. MRI showed diffuse cerebral swelling. CBF assessed by angiography and Doppler remained normal and EEG isoelectric until he died on day 8 with multiorgan failure. There was a discrepancy between the clinically and EEG-assessed brain death, and CBF persistence. We hypothesized that brain death, resulting from diffuse anoxic injury, may lead, in the absence of major intracranial hypertension, to angiographic misdiagnoses. Therefore, EEG remains useful to assess diagnosis in such unusual cases.

NEURONAL DAMAGE FROM TEMPORARY CARDIAC ARREST

The Lancet ◽  
1946 ◽  
Vol 247 (6397) ◽  
pp. 488-492 ◽  
Author(s):  
John Howkins ◽  
C.R. Mclaughlin ◽  
Peter Daniel
Keyword(s):  
Cardiac Arrest ◽  
Neuronal Damage

Cardiac arrest resuscitation: neurologic prognostication and brain death

2008 ◽  
Vol 14 (3) ◽  
pp. 261-268 ◽  
Author(s):  
Romergryko G Geocadin ◽  
Scott M Eleff
Keyword(s):  
Cardiac Arrest ◽  
Brain Death

Controlled Evaluation of Muscle Relaxation in the Ventilated Neonate

PEDIATRICS ◽  
1981 ◽  
Vol 67 (5) ◽  
pp. 641-646
Author(s):  
N. N. Finer ◽  
P. M. Tomney
Keyword(s):  
Birth Weight ◽  
Intracranial Pressure ◽  
Low Birth Weight ◽  
Muscle Relaxation ◽  
Control Period ◽  
Pancuronium Bromide ◽  
Intracranial Pressure Elevation ◽  
Controlled Evaluation ◽  
And Control ◽  
Inspiratory Oxygen

To assess the effects of muscle relaxation on the critically ill ventilated neonate, pancuronium bromide was administered for a 12-hour period to ten low-birth-weight neonates (960 to 2,000 gm) of 26 to 34 weeks gestation, all of whom required mechanical ventilation and were studied within 48 hours of birth (six to 39 hours). The infants were also studied for a 12-hour period during which no pancuronium bromide was administered. During both study periods, the order of which was randomized, heart rate, blood pressure, Po2, and intracranial pressure were continuously measured. The amounts of handling during the pancuronium and control periods were similar. The results revealed a significantly greater duration of hypoxia (P02 < 50 torr) (56.1 vs 23.6 minutes, P < .001) and hyperoxia (Po2 > 70 torr) during the control period (92.5 vs 13 minutes, P < .001). Durations of intracranial pressure elevation 10 cm H2O above the infant's baseline were significantly less during paralysis (6.7 vs 58.8 minutes, P < .001) as were spikes of intracranial pressure to greater than 25 cm H2O (1.6 vs 24.4, P < .05). There was no significant improvement in blood gas values, fractional inspiratory oxygen, or ventilator settings during muscle relaxation. Pancuronium reduced periods of nonoptimal oxygenation and elevated intracranial pressure and may therefore help to decrease adverse sequelae for the low-birth-weight, ventilated neonate.

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