34 | CO NTRO VERSIES IN THE D ETERMINATIO N O F D EATH

4. The patient shows no drive to breathe during the apnea

test.

A result indicating that all of these conditions have been met must
be confirmed with a second examination some hours after the initial
positive results are obtained. The appropriate length of time be-
tween these examinations is a matter of some debate. According to
a consensus statement developed by the American Academy of
Neurology in 1995, “[A] repeat clinical evaluation [six] hours later is
recommended, but this interval is arbitrary.” 1 The six-hour interval
is far shorter than the interval recommended by the medical con-
sultants to the President’s Commission in 1981: they suggested
twelve hours in cases of a non-anoxic etiology (e.g., head trauma of
any kind, a stroke) and twenty-four hours in cases of an anoxic ori-
gin (e.g., a heart attack that leads to temporary cessation of
circulation to the brain).2 The standard interval between examina-
tions also varies from one country to another, ranging from two
hours to twenty-four hours.3

Q uestions about the appropriate interval between examinations are

related to questions about what laboratory or imaging tests are
needed to confirm the clinical diagnosis. These tests include the
electroencephalogram (EEG ), tests for evoked responses (brain-
stem auditory evoked potentials, somatic evoked potentials, and
motor evoked responses), and tests for blood flow through the ves-
sels that feed the brain (classic arteriography, radioisotope studies,
and transcranial D oppler ultrasonography).4 Standard practice in the
United States dictates that these tests should be optional, to be used
by the clinician in difficult cases— for example, when some factor
interferes with clinical testing or when there is a need to abbreviate
the interval before a second round of testing. In some other coun-
tries, the laboratory tests are mandatory.5

Neurologist James Bernat, a noted expert on the brain and its inju-
ries, has recommended that tests of intracranial blood flow be
included among the routine tests for total brain failure (or “brain
death”) in the United States.6 These imaging tests are particularly
useful for determining whether the pathophysiological events that
 CHAPTER THREE | 35

lead to total brain failure have in fact occurred. Those events will be
described and clarified in Part III.

First, however, we should make note of some well-known obstacles

to making the diagnosis of total brain failure in infants and children.
These obstacles have led to recommendations for longer observa-
tion times between clinical examinations, more extensive use of
imaging tests, and modifications to the tests themselves.7

For both children and adults, some studies have shown that testing
for the condition known as “brain death” is not always carried out
in a consistent way from one institution to another.8 In light of the
very serious consequences of this diagnosis, it is especially impor-
tant to ensure that variations in practice do not lead to errors or
abuse.

III. Total Brain Failure: Pathophysiology

The question addressed in Part II was, How can the clinician distin-
guish the patient with total brain failure from other brain-injured
patients? In this part we turn to the question, What events in the
brain and body of the patient lead to total brain failure? As we have
indicated, a diagnosis of total brain failure involves a judgment that
the brainstem and the structures above it have been destroyed and
therefore have lost the capacity to function ever again. In most
cases, however, this destruction did not accompany the initial injury
to the brain but instead came about through a self-perpetuating cas-
cade of events— events that progressively damaged more and more
tissue and finally destroyed the brainstem.

The source of this self-perpetuating cascade of damaging events is

the rigidity of the skull, which, after injury, can cause elevated pres-
sure in the cranial vault that holds and usually protects the brain.
Consider the three most common injuries leading to total brain fail-
ure. These are (1) head trauma (sustained, for example, in an
automobile accident or as a result of a gunshot wound), (2) cere-
brovascular accident (i.e., “stroke”), and (3) cerebral anoxia
(deprivation of oxygen) secondary to cardiac arrest. These three dif-
ferent causes have a common effect: severe damage to the cells
36 | CO NTRO VERSIES IN THE D ETERMINATIO N O F D EATH

comprising the tissues of the brain, that is, to the neurons and the
cellular networks that they form. This damage leads, in turn, to
edema, the abnormal accumulation of fluid. With little or no space
in which to expand, the swelling brain suffers steady increases in
intracranial pressure (ICP). Elevated ICP prevents oxygen-laden
blood from making its way up and into the cranial cavity and thus
deprives brain tissues of essential nutrients. This, in turn, leads to
additional damage, which leads to more edema and swelling. Neu-
rologist Alan Shewmon describes the result:

A vicious cycle is established in which decreasing cerebral

perfusion and increasing cerebral edema reinforce one an-
other until blood no longer enters the cranial cavity and
the brain herniates though the tentorium and foramen
magnum.9

The herniation that Shewmon refers to here can crush the brain-
stem, leading to the functional losses that are revealed by the
examination for total brain failure. That condition is the end point
of a vicious cycle— the point at which the brain, including its lower
centers in the brainstem, has been rendered permanently dysfunc-
tional.

This description of the physiological events that lead to total brain

failure shows the utility of yet another term for the clinical state un-
der discussion: “total brain infarction.” * An “infarction” is defined
as a “sudden insufficiency of arterial or venous blood supply… that
produces a macroscopic area of necrosis.” 10 When death is declared
based on the currently accepted neurological standard, the self-
perpetuating cascade of events in the brain following the initial in-
jury has run its full course. “Running its full course,” in this context,
means that total destruction of the brain has occurred due to infarc-
tion or lack of blood supply— hence, “total brain infarction.”

* See Chapter Two, Table 1.