ACR Codes: 9.9
The diagnosis of brain death (BD) must respect all the guarantees required by law and be precise and certain since this situation is often related with a possible organ transplantation or removal of "life support" measures. The prerequisites for confirming a diagnosis of BD vary in different countries and as such clinical criteria +/- different neurophysiological and neuroradiological methods (used as confirmatory tests) have been established for the documentation of this diagnosis.
Clinical criteria for the diagnosis of BD include deep unresponsive coma, no brain stem function and no spontaneous respiration. Of course, confounding factors that may result in a misdiagnosis, such as severe electrolyte, acid-base, or endocrine disturbances, severe hypothermia, hypotension and the presence of drug intoxication, poisoning or neuromuscular blocking agents, must first be ruled out.
British and Australian legislations rely only on the clinical confirmation of brain stem death (without taking into any consideration the function of the cortex or requesting documentary confirmatory tests) for making the diagnosis of BD. Two neurophysiological methods are used to demonstrate the cessation of brain function: electroencephalography (EEG) and brain stem auditory evoked potentials; limitations have been cited for both of these modalities.
Various imaging techniques (most of which assess cerebral blood flow) have been used to confirm the diagnosis. Among these, conventional angiography of the four cerebral arterial axes is the reference standard for imaging brain death. Blood flow may also be imaged with nonselective intra-arterial (IA) angiography (via catheterization and injection of the aortic arch), intravenous digital subtracton angiography (IV DSA), transcranial doppler (TCD), magnetic resonance imaging (MRI) or MRA, radionuclide cerebral angiography, xenon CT or spiral CT (with IV contrast). Brain perfusion can be quantified with SPECT or HMPAO scintigraphic techniques.
As mentioned earlier different countries use differing guidelines, an isoelectric EEG or lack of intracranial circulation documented by selective cerebral angiography may be mandatory for the confirmation of BD in some countries. Sometimes confirmatory tests may be requested in special circumstances, such as situations in which clinical and EEG examinations cannot be reliably performed (eg, the use of barbiturate sedation in acute brain trauma) or in order to reduce the duration of the requisite period of observation.
The following cerebral angiographic findings - whether selective/nonselective IA or IV - have been demonstrated in patients with clinical signs of brain death (it has been suggested that a sudden and severe increase in intracranial pressure first affects the cerebrum leading to complete arrest in carotid arterial flow, which results in transtentorial herniation (followed by cerebellar herniation) and consequent raised infratentorial pressure with resultant compression of the infratentorial arteries):
Anterior arterial circulation: slow filling and interruption of blood flow in the internal carotid arteries. This arrest of flow could be seen at different levels of this artery: cervical portion, the carotid siphon, or even the proximal segments of the anterior or middle cerebral arteries. When present, opacification of the anterior or middle cerebral arteries was always very slow and restricted to their first or second segments. Delayed opacification and stagnation of contrast medium in basal arachnoidal arterial segments has been referred to as subarachnoid "stasis filling". No evidence of capillary or venous filling was demonsrated in these patients.
Posterior arterial circulation: stagnation and arrest of contrast medium at the level of the vertebral arteries, contrast medium stasis within the basilar (which showed compression against the clivus) or posterior cerebral arteries without evidence of flow during the filming sequence, and delayed and very slow vertebrobasilar blood flow with venous opacification.
Venous drainage: normal external carotid venous drainage may result in opacification of the superior sagittal sinus (via meningeal vessels or emissary veins), cavernous sinus (through the superior ophthalmic vein, which may also appear prominent), and transverse sinus (via the mastoid emissary vein). Jugular venous return may also be observed in some cases.
Of note is the possible occurence of false-negative results, using angiographic criteria in BD patients. An example of such a case was presented by Braun et al in a patient who had undergone craniotomy for acute subdural hematoma; this patient had clinical and EEG criteria compatible with brain death but IV angiography showed persistent circulation especially on the side of the vault defect.
Compared with IV DSA, selective angiography is more invasive, time-consuming, costly and also requires greater expertise. Also increases in intra-arterial pressure associated with arterial injections may push the contrast medium higher in the neck or into the intracranial arteries, giving a false impression of intracranial blood circulation. Drawbacks cited for both IA and IV DSA include the following: patients need need to be transported out of the ICU with major medical risks; and the use of contrast media can be detrimental for the already compromised patient's organs, such as the kidneys.
Reference(s): 1-Wijdicks FM. The Diagnosis of Brain Death. N Eng J Med. 2001 Apr;344(16):1215-21.
2-Dupas B, Gayet-Delacroix M, Villers D. Diagnosis of Brain Death Using Two-Phase Spiral CT. Am J Neuroradiol AJNR. 1998 Apr;19(4):641-7.
3-Braun M; Ducrocq X, Huot JC. Intravenous angiography in brain death: report of 140 patients. Neuroradiology. 1997 Dec;10(6):402-5.
4-Paolin A, Manuali A, Di Paola F. Reliability in diagnosis of brain death. Intensive Care Med. 1995 Aug;21(8):657-62.
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