The diagnosis and management of brain death is a frequently encountered clinical scenario,
particularly within the intensive care unit.
The diagnostic criteria of brain death have been included in guidelines,
both for adults and infants,
however testing for and determination of brain death is still subject of uncertainty and constant debate.(1,2)
Brain death corresponds to the irreversible cessation of all brain functions,
including the brainstem,
due to severe brain damage.(3) The process of diagnosing brain death involves neurologic testing,
consideration of confounders and,
if necessary,
performance of confirmatory tests.
A triad of coma,
brainstem areflexia and apnea must be met in order for brain death to be clinically reported. Particular bioclinical circumstances,
such as shock,
hypothermia,
drug intoxications,
acid-base disorders,
electrolyte abnormalities,
locked-in syndrome and Guillan Barre syndrome are mimickers of brain death and require further tests for confirmation.
The same goes for paediatric patients,
disturbing residual movements,
family discomfort and the possibility of the patient serving as donor for organ transplantation may also require confirmatory tests.(4)
Ancillary tests are based on either the absence of the cerebral blood flow or on the lack of brain electrical activity.
The three most commonly performed confirmatory tests are cerebral scintigraphy,
cerebral angiography and electroencephalogramm.
Transcranial Doppler US,
CT angiography and MR angiography are also used,
but to a lesser extent.
Although there is no global consensus in respect to which confirmatory test should be used,
CT-angiography and MR-angiography have proven to be useful ancilllary imaging tests in the diagnosis of brain death,
with absence of blood flow being compatible with the clinical diagnosis of brain death.(5) Four-vessel cerebral angiography is the reference method in the diagnosis of brain death,
however it is invasive and expensive.
In brain dead patients,
no intracerebral flow is discernable above the entry levels of the carotid and vertebral arteries in the skull,
whereas the flow at the level of the external carotid circulation serves as positive reference.
SPECT with technetium 99m-HMPAO as radiotracer shows no uptake within the brain,
creating the so-called ”hollow skull phenomenon” in brain dead patients.
Transcranial Doppler ultrasound (TCD) is noninvasive,
and widely available,
however it is operator-dependent and does not quantify cerebral circulation.
At computed tomography angiography (CTA) and magnetic resonance angiography (MRA) the diagnostic criterion of brain death is the lack of intracranial arterial contrast opacification.
The disadvantage of the CTA is the potential harmful effect of contrast medium on donor organs,
whereas at MRA the monitors must be MRI-compatible and potential of Gadolinium-based contrast agents to induce nephrogenic systemic fibrosis has been reported.(6)
Diffuse gyral and cerebellar cortex swelling,
parenchymal hemorrhage,
diffuse axonal injury and tonsillar herniation are commonly encountered findings at MRI in brain death.
Also loss of flow void in the petrous portions of the ICA hast been reported.(7)
At Gadolinium-enhanced MRA,
failure of intracranial vessels to fill with contrast with extracranial vessels having normal blood flow as postive reference,
attests brain death.
The absence of the cerebral circulation above the supraclinoid segment of internal carotid artery and its intracranial ramifications,
more exactly above the level of the A2-portion of the anterior cerebral artery (ACA) and the M1-portion of the middle cerebral artery (MCA),
are unequivocal signs of brain death.(8–10)