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

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.

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.


1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).


PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245291
Author(s):  
Alexander Ruesch ◽  
Deepshikha Acharya ◽  
Samantha Schmitt ◽  
Jason Yang ◽  
Matthew A. Smith ◽  
...  

The brain’s ability to maintain cerebral blood flow approximately constant despite cerebral perfusion pressure changes is known as cerebral autoregulation (CA) and is governed by vasoconstriction and vasodilation. Cerebral perfusion pressure is defined as the pressure gradient between arterial blood pressure and intracranial pressure. Measuring CA is a challenging task and has created a variety of evaluation methods, which are often categorized as static and dynamic CA assessments. Because CA is quantified as the performance of a regulatory system and no physical ground truth can be measured, conflicting results are reported. The conflict further arises from a lack of healthy volunteer data with respect to cerebral perfusion pressure measurements and the variety of diseases in which CA ability is impaired, including stroke, traumatic brain injury and hydrocephalus. To overcome these differences, we present a healthy non-human primate model in which we can control the ability to autoregulate blood flow through the type of anesthesia (isoflurane vs fentanyl). We show how three different assessment methods can be used to measure CA impairment, and how static and dynamic autoregulation compare under challenges in intracranial pressure and blood pressure. We reconstructed Lassen’s curve for two groups of anesthesia, where only the fentanyl anesthetized group yielded the canonical shape. Cerebral perfusion pressure allowed for the best distinction between the fentanyl and isoflurane anesthetized groups. The autoregulatory response time to induced oscillations in intracranial pressure and blood pressure, measured as the phase lag between intracranial pressure and blood pressure, was able to determine autoregulatory impairment in agreement with static autoregulation. Static and dynamic CA both show impairment in high dose isoflurane anesthesia, while low isoflurane in combination with fentanyl anesthesia maintains CA, offering a repeatable animal model for CA studies.


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