scholarly journals Frequent Preservation of Neurologic Function in Brain Death and Brainstem Death Entails False-Positive Misdiagnosis and Cerebral Perfusion

2021 ◽  
pp. 1-14
Author(s):  
Michael Nair-Collins ◽  
Ari R. Joffe
CHEST Journal ◽  
2014 ◽  
Vol 146 (4) ◽  
pp. 283A
Author(s):  
Sara Qasim Bughio ◽  
Gilda Diaz-Fuentes ◽  
Sindhaghatta Venkatram

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Sindhaghatta Venkatram ◽  
Sara Bughio ◽  
Gilda Diaz-Fuentes

Practice guidelines from the American Academy of Neurology for the determination of brain death in adults define brain death as “the irreversible loss of function of the brain, including the brainstem.” Neurological determination of brain death is primarily based on clinical examination; if clinical criteria are met, a definitive confirmatory test is indicated. The apnea test remains the gold standard for confirmation. In patients with factors that confound the clinical determination or when apnea tests cannot safely be performed, an ancillary test is required to confirm brain death. Confirmatory ancillary tests for brain death include (a) tests of electrical activity (electroencephalography (EEG) and somatosensory evoked potentials) and (b) radiologic examinations of blood flow (contrast angiography, transcranial Doppler ultrasound (TCD), and radionuclide methods). Of these, however, radionuclide studies are used most commonly. Here we present data from two patients with a false positive Radionuclide Cerebral Perfusion Scan (RCPS).


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.


Author(s):  
G. T. Laurie ◽  
S. H. E. Harmon ◽  
E. S. Dove

This chapter begins with a discussion of concepts of death. It considers the mostly philosophical arguments against the use of the term ‘brain death’ as applied to the person and then explains the medico-legal effects of applying brainstem death criteria. The chapter also discusses post-mortem pregnancy.


1987 ◽  
Vol 22 ◽  
pp. 231-249
Author(s):  
David Lamb

This paper examines the development of the concept of brain death and of the criteria necessary for its recognition. Competing formulations of brain death are assessed and the case for a ‘brainstem’ concept of death is argued. Attention is finally drawn to some of the ethical issues raised by the use of neurological criteria in the diagnosis of human death.


Author(s):  
Hui Yang

Carotid endarterectomy and carotid artery stenting have been performed worldwide to reduce neurologic symptoms and prevent stroke. Preoperative cardiovascular and neurologic evaluations are essential to optimize a patient for surgery and guide the intra- and postoperative management. The primary goals of anesthetic management are to maintain cerebral perfusion and prevent perioperative myocardial ischemia. A shunt may be placed to provide antegrade cerebral blood flow if signs of cerebral ischemia develop during carotid cross-clamping. An awake patient is the gold standard for monitoring the adequacy of cerebral perfusion, although neurologic monitoring may be used if a patient is under general anesthesia. Rapid emergence allows immediate assessment of neurologic function. Any delayed emergence necessitates prompt management and communication to surgeon. All patients need to be closely monitored postoperatively for any neurologic, cardiovascular, or respiratory complications.


Author(s):  
Sheila Adam ◽  
Sue Osborne ◽  
John Welch

This chapter provides an overview of the care and management of neurological disorders commonly seen in critical care, starting with an outline of the anatomy and physiology of the nervous system. The concepts of awareness, consciousness, and arousal, and the use of the Glasgow Coma Scale (GCS) to assess conscious level are discussed. The management and monitoring of raised intracranial pressure, cerebral perfusion pressure, and the impact on cerebral blood flow are detailed. The management of sodium and water balance, including diabetes insipidus, is outlined. There are overviews of the management and nursing of patients who have suffered traumatic brain injury, subarachnoid haemorrhage, status epilepticus, myasthenia gravis, Guillain–Barré syndrome, meningitis, encephalitis, and intracranial abcess. The concept, ethics, and testing of brainstem death, organ donation, and the care of the family are detailed.


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.


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