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* From the Department of Clinical Neurological Sciences, London Health Sciences Centre, University of Western Ontario, London, Ontario; the
Division of Pediatric Care, Montreal Children’s Hospital, McGill University Health Centre, Montreal, Quebec, the
Adult Critical Care, University of Calgary, Alberta; and the
Division of Neurology, Montreal Neurological Institute, Montreal, Quebec, Canada.
Address correspondence to: Dr. G. Bryan Young, Department of Clinical Neurological Sciences, London Health Sciences Centre, 339 Windermere Road, London, Ontario N6A 5A5, Canada. Phone: 519-663-2911; Fax: 519-663-3753; E-mail: bryan.young{at}lhsc.on.ca
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Methods: A literature review based on a MEDLINE search of relevant articles published between January 1966 to January 2005 was undertaken.
Results: Tests of whole brain perfusion/intracranial blood circulation are the only ones that meet stated criteria.
Conclusions: At present only cerebral angiography and nuclear medicine tests of perfusion are accepted by Canadian standards, but computed tomography and magnetic resonance angiography should prove to be suitable. Transcranial Doppler studies may be suitable for specific cases once appropriate guidelines are established.
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Sometimes clinical criteria cannot be applied reliably, e.g., when the cranial nerves cannot be adequately examined, when neuromuscular paralysis or heavy sedation is present, or in some patients for whom the apnea test is precluded (respiratory instability or high cervical spine injury) or not valid (high carbon dioxide retainers). In these situations ancillary tests are necessary. The recently adopted Canadian guidelines for neurological determination of death state that for both adults and children, ancillary tests are not required unless the minimum clinical criteria cannot be applied, or confounding factors remain unresolved.
Truly confirmatory ancillary tests for brain death should meet the following criteria:
Care must be taken to avoid "self-fulfilling prophesies" in developing tests for brain death; some type of confirmation is desirable. Verification methods include the continued support of the patient for a suitable time after the test has been applied, with observation and outcome determination and/or a neuropathological examination of the brain.
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Electrophysiologic tests
ELECTROENCEPHALOGRAPHY
A component of brain death declaration with the first guidelines for brain death declaration,7 remains strongly recommended in the United States and is an essential part of the American criteria for the diagnosis of brain death in children.8 When continuous, raw or quantified EEG monitoring reveals generalized voltage suppression, this can prompt clinicians to consider brain death.9 Electroencephalography is, however, too anatomically and physiologically limited to be a suitable tool. Electroencephalography records activity from only the cortical layers immediately beneath the scalp; it does not record from subcortical structures, such as the brain stem or thalamus, and offers only crude, limited coverage of the convexity surface of the cerebrum. Furthermore, not all EEG frequencies are faithfully captured: recording characteristics of the machine and the attenuation of the skull attenuate frequencies < 0.5 Hz and > 35 Hz.10 Because of this, the EEG may be flat or isoelectric in the presence of viable neurons in the brain stem and elsewhere.
There are few studies that examine the validity of EEG in brain death. Studies to determine the false negative rate (in which EEG activity is present in the presence of clinically declared brain death) are of limited usefulness: agonal EEG activity was found in seven of 15 adults and 15 of 29 children at the time these patients met clinical criteria for brain death.11,12 Grigg et al. found EEG waves in 11 (19.6%) of 56 patients who had been diagnosed as brain dead.13 In another series one of 50 adult patients had residual EEG activity.14 Alvarez et al. found no false negatives for EEG in 28 children who met clinical criteria for brain death.15 Studies to determine the false positive rate (in which the EEG is flat in patients who are not brain dead) are lacking, except for isolated case reports.16,17
There are other problems with EEG. Electroencephalography is vulnerable to confounders: it may be flat or isoelectric in massive barbiturate overdose or in deep anesthesia, conditions that are completely reversible. Thus, there is a "double dissociation" in that EEG activity can be absent without brain death, either from surviving subcortical neurons or completely reversible conditions (false positives), and agonally present in patients who meet the criteria for brain death (false negatives for the "brain stem death" concept). Furthermore, in the hostile electrical environment of the ICU, some electrical signals are recorded for which the source cannot be identified, even though they probably do not arise from the brain (more false negatives). This probably leads to the considerable variation in inter-rater agreements as to whether electrocerebral silence is present or not.18 Thus, the EEG is far from an ideal or even a suitable test for brain death; it meets very few of the desired criteria for a suitable ancillary test. At best EEG, when applied to brain death, is mildly confirmatory; at worst it is misleading or irrelevant. Thus, despite official recommendations in some countries, EEG seems poorly suited as a necessary component of brain death declaration in children. When confirmation is needed, a test of blood flow to the brain is more appropriate.
EARLY COMPONENT EVOKED POTENTIALS
Somatosensory evoked potentials (up to N20 with median nerve stimulation) and BAERs (up to wave V), recordings from scalp electrodes use computer averaging to detect "far field potentials deep in the brain. These, like EEG, have limitations in their suitability as ancillary tests.19 Each test activates a discrete sensory pathway.20 Evoked potentials (EPs) thus allow examination of specific areas of interest in the brainstem, but these are individually highly restricted specific pathways. Therefore EPs do not test the functional integrity of other central nervous system structures. Discretely placed proximal lesions along the pathway may selectively eliminate the evoked responses from that site onwards, while sparing other brain stem structures. Thus, the clinical exam that tests functionally and anatomically independent cranial nerve reflexes is superior to EPs in principle. Unlike EEG signals, the early components of SSEPs and BAERs are minimally affected by sedative drugs and anesthetics. However, drugs and metabolic derangements affect middle and late somatosensory and auditory potentials. Wave I of BAERs, generated in the cochlear nuclei outside the brain stem, assures that the auditory signal has been processed up to the brain stem. Its absence could relate to end organ dysfunction, e.g., damage to the inner ear by trauma. Thus, when wave 1 is absent, BAERs are not appropriate for assessment for brain death.21 Thus, while EPs offer some advantages over EEGs, they do not appear to be sufficient stand-alone tests for brain death. Some have argued that the combination of BAERs and SSEPs offer greater assurance of an accurate diagnosis of brain death.22 However, since BAERs can only be applied in a minority of patients because of the necessity of requiring wave I to be present bilaterally, it is unlikely that this will be practical. The sensitivity and specificity of the combined use also needs to be determined.
Studies of the value of EPs in brain death are very limited in scope. Most have examined a group of clinically brain dead patients to examine the association with the presence or absence of responses. There is thus ambiguity as to what is the "gold standard" of brain death. This approach does not allow for the detection of false positives, in which the EPs argue for brain death when the latter is not present, but examine only the sensitivity of the test (at times greater than 100% if the presence of brainstem signals overrules the clinical diagnosis of brain death). For example, of 130 clinically brain dead patients, BAER waves III or V (generated in the brain stem) were present in six patients; with SSEPs waves following the cervical potential wave were present in four.19 In another series of 30 brain dead patients, the BAERs and the N20 SSEP responses were absent in all cases.23 Of 51 clinically brain dead children, all those tested for BAERs and SSEPs had absent brain stem potentials.12 In a small series of 18 patients who were comatose but not brain dead, the SSEP N18 response, generated in the medulla, was present in each case, but was lost when the same patients became brain dead.24 One study involved 17 patients with brain death; in all the SSEPs were absent. Of the seven patients with deep coma or appalic state, SSEPs were absent in four (false positives). Furthermore, in many patients with severe brain injuries but who are not brain dead, the N20 cortical response is absent.25–27
The electroretinogram is not useful a test, as the retina is spared in brain death. The cortical visual evoked response is probably not suitable, as its absence often relates to technical and other factors.
Tests of brain blood flow
Tests that show absent blood flow to the brain are generally accepted as establishing whole brain death with certainty, as it is axiomatic that the brain without a blood supply over a suitable period of time is dead. Of course, hypothermia and transient, reversible hypotension should be excluded. However, because these tests have been used to define brain death, there are no reliable studies to assess their validity. It does not always follow, however, that the presence of some arterial blood flow in the intracranial compartment precludes the diagnosis of brain death. Preservation or restoration of intracranial blood flow can occur when intracranial pressure is relieved by a ventricular drain, a craniotomy with duraplasty, in neonates and very young infants with open fontanelles and unfused sutures, or with recanalization of the intracranial circulation after a period of time.28,29 However, proof of absent blood flow to brain should achieve the goal of avoiding false positives in brain death declaration.
Brain death may be accompanied by either tissue edema or mass effect that causes intracranial pressure to equal or exceed systolic and mean arterial blood pressure. Consequently, blood does not enter the intracranial compartment, or does so only during systole (systolic peak only, or reverberating flow). Either result does not allow for perfusion of brain tissue, which would produce death of the brain’s neurons and glial cells.30 Tests of brain blood flow thus provide evidence of global brain death; i.e., both cerebral hemispheres and posterior fossa structures can be assessed. Tests of brain blood flow provide an acceptable, stand-alone method of declaring brain death. The tests are not confounded by drugs, metabolic disorders or hypothermia. A caveat is that the systemic blood pressure should be adequate, i.e., the patient should not be in shock, when these tests are applied. Tests of brain blood flow include four-vessel (carotid and vertebral) angiography, TCD, MRI and MRA, computed tomographic angiography, and nuclear medicine tests of brain.31
More precise tests of perfusion are preferable, e.g., angiography and single photon emission computed tomography (SPECT), compared with two-planar imaging of brain circulation. As many of the clinical tests should be applied as feasible, including apnea testing, to confirm the presence or absence of lower medulla functioning.
Rarely, perfusion tests give "false negative" results, in which some perfusion of arterial or venous intracranial structures is found in the presence of clinically and pathologically confirmed brain death.32 This occurs principally in those conditions in which intracranial pressure is lowered through some decompressive mechanism, e.g., decompressive craniectomies, skull fractures, ventricular shunts or infants with pliable skulls. Such false negatives are not a major concern in view of their rarity, and the fact that brain death could still be confirmed clinically or with other methods. It should be recognized that preservation of flow does not always exclude the possibility of brain death. The main vascular endpoint should be lack of brain tissue perfusion rather than lack of arterial perfusion. Some neuro-imaging tests address this better than others. It should be remembered, in principle, that in developing ancillary tests of brain death, false negatives are much less problematic than are false positives; i.e., it is far worse to falsely declare someone brain dead than to find the brain to be viable when it is not.
FOUR-VESSEL CEREBRAL ANGIOGRAPHY
Four-vessel cerebral angiography is the traditional "gold standard" among ancillary tests for brain death. The test is invasive and requires transportation of the patient to the radiology department. When this is done, it is imperative that the blood pressure be monitored, as such patients can be hemodynamically unstable, and severely damaged brain may have lost autoregulation and blood flow will vary with changes in perfusion pressure. The absence of any intracranial filling of internal carotid or vertebral arteries requires the intracranial pressure to exceed mean arterial blood pressure. Early recommendations suggested that a certain amount of time, e.g., one minute, should elapse before concluding that the contrast material does not enter the intracranial cavity.33 It is possible however, for brain death to exist without intracranial pressure exceeding mean arterial blood pressure; there can also be a gradual evolution from some intracranial arterial filling ("siphon, partial and delayed filling") to no filling, even though brain death can be present from the onset.
TRANSCRANIAL DOPPLER
Transcranial Doppler is safe, non-invasive, relatively inexpensive, and can be done without transporting the patient out of the ICU. The test requires skill and rigor in its application to insonate the major intracranial arteries. Usually two tests are done at least 20 min apart. One looks for systolic peaks or an oscillating or reverberating flow pattern, or disappearance of systolic flow on the second test. Patients with external ventricular drains or large craniotomies should be excluded. Caution should be exercised with very young children, at least until further studies are done in this population. In a series of 37 consecutive patients with Glasgow coma scale scores < 7, the specificity was 100% and the sensitivity was over 90%.34 False positives have been reported in some series in 10–15%.35 Transcranial Doppler showed no flow in the vertebrobasilar system, yet scintigraphic techniques and selective angiography revealed arterial perfusion.36 The false positive rate is lower when using a transorbital approach than a transtemporal technique.37 Thus, absence of flow with TCD is not sufficiently reliable to confirm brain death, while a reverberating pattern without diastolic forward flow in all vessels should be sufficient. Because of numerous caveats and lack of precise guidelines, TCD is not, at this time, recommended as the sole test of brain perfusion in cases of suspect brain death.
MAGNETIC RESONANCE ANGIOGRAPHY WITH MRI
Loss of intracranial perfusion with MRA is the most definitive aspect of MRI perfusion (Figure 1
). In addition, there is loss of intracranial flow void on MRI, transtentorial and tonsillar herniation, variable gray-white differentiation and relative contrast enhancement of the nose and scalp, similar to that found with nuclear medicine tests.
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Xenon CT is an older technique that involves inhalation of xenon with imaging in a quantitative manner. The test allows quantification of brain perfusion. Flows of < 5 mL/100 g·min–1 are confirmatory of brain death.39
NUCLEAR MEDICINE IMAGING TECHNIQUES
Nuclear medicine imaging techniques have long been applied to brain death7 assessment. Initially 99mTc pertechnetate was used with two-planar imaging to detect blood flow into the intracranial compartment. Now 99mTc-labelled hexamethylpropyleneaminoxime (HMPAO) or ethyl cysteinate dimer, agents that penetrate into the brain parenchyma in proportion to regional blood flow with SPECT, have been utilized. This demonstrates the presence or absence of brain perfusion rather than just intracranial circulation, and comes nearer to the ideal.40 The agents used for SPECT show no significant redistribution for several hours, making it easy to perform and interpret functional imaging.41 In a study that compared HMPAO-SPECT with dynamic flow studies in 41 cases of severe head injury, there were no false positives or false negatives in the SPECT-studied patients, while dynamic studies were equivocal in five patients, four of whom showed no uptake with static images.42 No studies were equivocal and HMPAO-SPECT demonstrated brainstem perfusion in those patients who were not brain dead. In brain death the lack of signal from the intracranial compartment and the normal uptake in other parts of the head produce the "empty light bulb" and "hot nose" signs.43,44
Currently only cerebral angiography and nuclear medicine tests of perfusion are accepted as confirmatory tests in the neurological determination of death. However, CT and MRA should prove to be suitable and await further consideration for consensus or trials. Transcranial Doppler requires further definition.
Other tests
There are no other serious contenders as ancillary tests. The atropine test allows a limited assessment of medullary function. Atropine, an anticholinergic drug, will abolish any residual vagal tone, as evidenced by an increase in heart rate.45 An atropine test compatible with brain death demonstrates a heart rate increase of < 3%.45 As the dorsal motor vagal nucleus is in the medulla, the test provides a limited assessment of caudal medullary function. Although this is probably one of the last functions to be lost in brain death, the test provides a far too restricted assessment to be very useful.46 Determination of venous oxygen saturation in the jugular bulb (in which the ratio between central venous and jugular bulb oxygen saturation was < 1) was shown to have 96.6% sensitivity and 99.3% specificity in brain death.47 The authors found one survivor whose ratio of central venous blood oxygen to internal jugular oxygen concentration was less than 1; others in this category were brain dead using clinical criteria. The test is not available in many centres, carries a small risk, and requires special training for catheter insertion. Other tests of brain metabolism and neurochemistry, including magnetic resonance spectroscopy, have not been sufficiently explored.48
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Accepted for publication August 10, 2005. Revision accepted November 6, 2005.
This article is accompanied by an editorial. Please see Can J anesth 2006; 53: 533–39.
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9 Vivien B, Paqueron X, Le Cosquer P, Langeron O, Coriat P, Riou B. Detection of brain death onset using the bispectral index in severely comatose patients. Intensive Care Med 2002; 28: 419–25.[Medline]
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11 Paolin A, Manuali A, Di Paola F, et al. Reliability in diagnosis of brain death. Intensive Care Med 1995; 21: 657–62.[Medline]
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33 Braun M, Ducrocq X, Huot JC, Audibert G, Anxionnat R, Picard L. Intravenous angiography in brain death: report of 140 patients. Neuroradiology 1997; 39: 400–5.[Medline]
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36 Paolin A, Manuali A, Di Paola F, et al. Reliability in diagnosis of brain death. Intensive Care Med 1995; 21: 657–62.[Medline]
37 Lampl Y, Gilad R, Eschel Y, Boaz M, Rapoport A, Sadeh M. Diagnosing brain death using the transcranial Doppler with a transorbital approach. Arch Neurol 2002; 59: 58–60.
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39 Pistoia F, Johnson DW, Darby JM, Horton JA, Applegate LJ, Yonas H. The role of xenon CT measurements of cerebral blood flow in the clinical determination of brain death. AJNR Am J Neuroradiol 1991; 12: 97–103.[Abstract]
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43 Flowers WM Jr, Patel BR. Radionuclide angiography as a confirmatory test for brain death: a review of 229 studies in 219 patients. South Med J 1997; 90: 1091–6.[Medline]
44 Bonetti MG, Ciritella P, Valle G, Perrone E. 99mTc HM-PAO brain perfusion SPECT in brain death. Neuroradiology 1995; 37: 365–9.[Medline]
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47 Diaz-Reganon G, Minambres E, Holanda M, Gonzalez-Herrera S, Lopez-Espadas F, Garrido-Diaz C. Usefulness of venous oxygen saturation in the jugular bulb for the diagnosis of brain death: report of 118 patients. Intensive Care Med 2002; 28: 1724–8.[Medline]
48 Kato T, Tokumaru A, O’uchi T, et al. Assessment of brain death in children by means of P-31 MR spectroscopy: preliminary note. Radiology 1991; 179: 95–9.
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