Retracted: Clinical Brain Death with False Positive Radionuclide Cerebral Perfusion Scans

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).

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

Journal of Neurosurgery ◽

10.3171/jns.1988.68.5.0745 ◽

1988 ◽

Vol 68 (5) ◽

pp. 745-751 ◽

Cited By ~ 28

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.

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Brain Tissue Oxygenation and Cerebral Perfusion Pressure Thresholds of Ischemia in a Standardized Pig Brain Death Model

Neurocritical Care ◽

10.1007/s12028-012-9675-3 ◽

2012 ◽

Vol 16 (3) ◽

pp. 462-469 ◽

Cited By ~ 17

Author(s):

Karlis Purins ◽

Per Enblad ◽

Lars Wiklund ◽

Anders Lewén

Keyword(s):

Brain Death ◽

Brain Tissue ◽

Cerebral Perfusion Pressure ◽

Cerebral Perfusion ◽

Tissue Oxygenation ◽

Perfusion Pressure ◽

Brain Tissue Oxygenation ◽

Pig Brain

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Oxygen and Carbon Dioxide in the Cerebral Circulation during Progression to Brain Death

Anesthesiology ◽

10.1097/00000542-200511000-00009 ◽

2005 ◽

Vol 103 (5) ◽

pp. 957-961 ◽

Cited By ~ 10

Author(s):

Nino Stocchetti ◽

Elisa Roncati Zanier ◽

Rita Nicolini ◽

Emelie Faegersten ◽

Katia Canavesi ◽

...

Keyword(s):

Carbon Dioxide ◽

Brain Death ◽

Cerebral Perfusion Pressure ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Brain Infarction ◽

Carbon Dioxide Tension ◽

Aerobic Metabolism ◽

Compensatory Mechanisms ◽

Oxygen Difference

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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Determination of cerebral perfusion by means of planar brain scintigraphy and99mTc-HMPAO in brain death, persistent vegetative state and severe coma

Intensive Care Medicine ◽

10.1007/bf01705036 ◽

1992 ◽

Vol 18 (2) ◽

pp. 76-81 ◽

Cited By ~ 19

Author(s):

H. -P. Schlake ◽

I. G. Böttger ◽

K. -H. Grotemeyer ◽

I. W. Husstedt ◽

W. Brandau ◽

...

Keyword(s):

Brain Death ◽

Cerebral Perfusion ◽

Vegetative State ◽

Persistent Vegetative State

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Detection of Brain Death in Barbiturate Coma: The Dilemma of an Intracranial Pulse

Neurosurgery ◽

10.1227/00006123-198908000-00019 ◽

1989 ◽

Vol 25 (2) ◽

pp. 275-278 ◽

Cited By ~ 8

Author(s):

Howard H. Kaufman ◽

Fred H. Geisler ◽

Thomas Kopitnik ◽

William Higgins ◽

Dan Stewart

Keyword(s):

Blood Flow ◽

Head Injury ◽

Intracranial Pressure ◽

Brain Death ◽

Cerebral Perfusion Pressure ◽

Cerebral Perfusion ◽

Perfusion Pressure ◽

Elevated Intracranial Pressure ◽

Barbiturate Coma ◽

The Face

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.

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