Determination of brain death
From the Ad Hoc C o m m i t t e e on Brain Death,* The Children's Hospital, Boston
The paper by Fackler and Rogers in this issue of The
Journal raises a very difficult and increasingly common
dilemma in the pediatric intensive care settiTig: How is
brain death to be defined under a variety of circumstances,
including differing developmental ages, causes, therapies,
and reasons for making such a determination. On the one
hand, organ donation programs have mandated require-
ments for a strict definition of brain death, whereas
humane treatment of patients, families, and staff dictates
that procedures be minimized that will unnecessarily delay
confirmation of that clinical determination, especially for
minimal technicalities.
To address these issues, The Children's Hospital in
Boston organized an ad hoc committee of clinicians with
legal counsel to make recommendations regarding the
determination of brain death in children. The Committee
report emphasized that the clinical examination is the most
important component of the criteria for determination of
brain death and that laboratory studies are to be used only
as adjuncts to the clinical examination or as a means of
confirming the irreversibility of the clinical state.
What follows are excerpts from that Committee report,
including a form to be completed by the patient's attending
physician, which becomes part of the medical record. This
procedure has helped to standardize the approach to the
determination of brain death in children in a teaching
hospital environment.
DETERMINATION OF B R A I N D E A T H
Brain death has occurred when cerebral and brainstem
functions are irreversibly absent. Absent cerebral function
is recognized clinically as the lack of receptivity and
responsivity, that is, no autonomic or somatic response to
Submitted for publication Sept._ 30, 1986; accepted Oct. 1,
1986.
Reprint requests: Robert K. Crone, M.D., Director, Multidisci-
plinary ICU, Department of Anesthesia, The Children's Hospital,
300 Longwood Ave., Boston, MA 02115.
*Ad Hoc Committee on Brain Death, The Children's Hospital,
Boston: Robert K. Crone, M.D., Chairman; Michael J. Bresnanl
M.D., Guiseppe Erba, M.D., E. Gary Fischer, M.D., S. Ted
Treves, M.D., Ellen Covner Weiss, Esq.
any sort of external stimulation, mediated through the
brainstem. Absent brainstem function is recognized clini-
cally when pupillary light, corneal, oculocephalic, oculo-
vestibular, oropharyngeal, and respiratory reflexes are
irreversibly absent. Procedures for testing these reflexes
are outlined below. Particularly in children, peripheral
nervous activity, including spinal cord reflexes, may persist
after brain death; however, decorticate or decerebrate
posturing is incons~ten t with brain death.
lrreversibility is recognized when the cause of coma is
established and is sufficient to account for the loss of brain
function, and when the possibility of recovery is excluded
by observation for an appropriate period of time. It is
important that the cause of coma be established when
possible. Absence of brain function resulting from head
trauma has different implications than that caused by a
metabolic abnormality or intoxication. Important revers-
ible causes that may mimic irreversibility are sedation,
hypothermia, neuromuscular blockade, and shock. If the
See related article, p. 84.
cause of coma cannot be established, these reversible
conditions must be ruled out by appropriate laboratory
studies, including analysis of blood and urine for clinically
significant levels of toxic substances that might produce
coma, such as sedative, hypnotic, and anesthetic agents;
measurement of core body temperature, which must be
higher than 32 ~ C; and measurement of peripheral neuro-
muscular function.
T h e period of observation will also vary, depending on
the circumstances and possible causes. In most cases in
which the cause is established and seems appropriate, such
as in severe inoperable head trauma, a period of 6 hours
seems reasonable and is commonly recommended, whereas
with hypoxic-ischemic encephalopathy, observation for 24
l~ours may be more appropriate.
Confirmatory laboratory findings may be appropriate in
determining primarily the irreversibility of brain death,
and possibly accelerating the determination of irreversibil-
ity. However, i f cause and irreversibility are established
and the clinical examination yields unequivocal findings,
Text continued on page 18.
15
16 A d H o c C o m m i t t e e on Brain Death The Journal o f Pediatrics
January 1987

USE PLATE OR PRINT

PT. NAME
LAST FIRST

DATE DIV.

MEDICAL REC. NO.

BRAIN DEATH EXAMINATION FORM

Date, time of examination

Diagnosis _ _ Probable cause of coma
1. Vital signs, chemistry values
a. BP (systolic/diastolic) / _
b. Temperature ( r e c t a l ) _
c. Serum sodium mEq/L Potassium mEq/L Osm/L
d. Urine sodium m E q / L Potassium mEq/L Osm/L
e. Urine volume for past 4 h r ml/hr
2, Drugs
a. Barbiturate level
b. Other drugs
c. Mydriatic drugs Yes No
d. Neuromuscular blocking agents: Peripheral nerve stimulation test normal Yes No
3. Metabolic abnormalities

4. Cerebral responsivity
a. Responsive to verbal commands Yes No
b. Responsive to painful stimulation delivered to each extremity and to both sides of face Yes No
5. Brainstem responsivity
a. Fundi R
b. Pupillary reaction R
c. pupil size R mm L mm
d. Ciliospinal reflex R
e. Doll's eyes reflex R
f. Corneal reflex R
g. Response to noxious nasal mucosa s t i m u l a t i o n
h. Iee water calories (25-50 ml, check tympanic membranes) R L
i. Gag, cough Yes No
j. Respirations Yes No
k. Apnea test (100% 0 2 for 5 min on ventilator with rate adjusted to give Paco2 >35. Turn off ventilator rate, leaving continual flow of
100% 02 for 5 min. Determine arterial blood gases at end of 5 min, or sooner if respirations or cyanosis occur, or if heart rate or BP
change >10%.)
Arterial blood gases at end of test: Pao2 Paco2 pH
Volume 110 Determination o f brain death 17
Number 1

6. Additional supplemental clinical examination

a- Deep tendon reflexes (0-4+)
Biceps R L
Triceps R L
Knee R L
Ankle R L
b. Clonus R L
c. Toes (t ~ 0) R L

7. Supplemental laboratory tests

a. Electroencephalogram
#1: Date/time Temperature _ _ Barbiturate level
Staff interpretation

~:2: Date/time Temperature _ _ Barbiturate level

Staff interpretation

b. Evoked potentials
Date/time Temperature _ _ Barbiturate level
Staff interpretation

c. CT scan results
Date/time
Results

d. Tc-99m cerebral radionuclide angiogram

Date/time
Results

8. Family members notified, relationship

9. Medical examiner's case
10. Organ donation

Signed Date/time
Attending physician

Signed Date/time
Concurring physician
18 A d Hoe Committee on Brain Death
confirmatory tests are unnecessary. When they are appro-
priate, confirmatory laboratory examinations that may
prove helpful include electroencephalography, radionu-
elide brain scan, and brainstem evoked potentials.
Tc-99m cerebral radionuelide angiogram. To determine
intracranial vascular perfusion, the cerebral radionuclide
angiogram is used as a confirmatory test in the diagnosis of
brain death, particularly when the EEG is equivocal or
barbiturates are present in the blood.
A bolus of Tc-99m as sodium pertechnetate (200 #Ci/
kg, minimum 5 mCi) is given intravenously in <3 seconds.
The patient is imaged in the anterior projection, using a
gamma, camera/computer system. Recording is begun at
the time of injection at one frame per second for 60
seconds. Evaluation of the studY is visual on the series of
images and on time-activity curves obtained from the
regions of interest over the cerebral hemispheres.
In cerebral death, the radionuelide cerebral angiogram
shows (1) bilateral absence of the arterial phase (anterior
and middle cerebral artery territories), (2) lack of visual-
ization of the sagittal sinus during the venous phase, (3)
lack of arterial peak of cerebral time-activity curves, and
(4) perfusion of the extracranial tissues only.
Electroencephalogram. The EEG is used to demonstrate
absence of any spontaneous activity in scalp records
whenever the clinical examination suggests that brain
functions are totally and persistently abolished. Available
data indicate that an isoelectric ("fiat") EEG, obtained
and interpreted according to stringent criteria,* provides
reliable evidence of cerebral death. Absence of electrical
response to rousing stimuli adds further evidence. The
EEG is particularly useful for assessing brain viability
when the clinical examination is limited by the use of
sedatives and muscle relaxants.
A repeating EEG after 24 hours is indicated:
1. When the first isoelectric EEG was obtained in
conditions of drug toxicity, especially CNS depressants;
hypothermia, especially temperature _+32~ C; or both
drug toxicity and hypothermia, even if body temperature is
>32 ~ C. At the time of the second EEG, drug blood levels
should be known to be below toxic levels, and body
temperature should be brought to 36 ~ C.
2. When, despite clinical evidence of persistent and
probably irreversible cerebral failure, the first EEG was
*EEG in the case of cerebral death is subject to much technicaland
interpretivebias.In complyingwiththe minimumstandardsoutlinedby the
AmericanEEG Societyrequiringmaximalamplificationof the signal,the
record oftenbecomescontaminatedby a varietyof environmentalartifacts.
To minimizesuch artifacts, equipmentmay have to be turnedoff tempo-
rarily, and personnelshouldbe expectedto withholdactivityin the vicinity
of the patientwhennecessary.
The Journal of Pediatrics
January 1987
not isoelectric but showed some activity, such as low-
voltage background or burst-suppression pattern, which
may represent agonal changes.
3. When the first EEG was isoelectric, but at the time
the clinical examination showed persistence of some brain-
stem or spinal reflexes.
4. When the interpretation of the first EEG as isoelec-
tric is controversial because of the presence of artifacts,
which may closely resemble cerebral activity.*
NOTE: When there is no doubt that an earlier EEG was
isoelectric, a repeat EEG after 24 hours is not mandatory
nor recommended (1) when clinical evidence points to
persistent loss of cerebral functions, including the auto-
nomic system; (2) when other factors that may temporarily
depress CNS activity can be excluded; and (3) when the
cause of death is known and well documented. However,
the decision is made entirely on the clinician's judgment.
For example, it is acceptable to repeat an isoelectric EEG
mainly for humanitarian reasons, because it is common
practice to prolong life-supporting measures beyond the
point of reasonable hope for recovery.
Brainstem (far field) evoked potentials
Indications. The indications for brainstem evoked
potentials are the same as for the EEG: to demonstrate
that reactivity to incoming stimuli (auditory, somatosenso-
ry) is absent in brainstem nuclei, except the first (cochlear)
wave. A "flat" auditory brainstem response in the presence
of viable peripheral conduction (cochlear wave) is consid-
ered unequivocal evidence of cerebral death because of the
proximity of auditory nuclei to vital centers. If acoustic
conduction is not demonstrable even at maximal stimulus
intensity, auditory brainstem evoked potentials should be
complemented by somatosensory brainstem evoked poten-
tialsto rule out the possibility that a flat response is caused
by peripheral deafness.
Brainstem sensory evoked potentials are not a substitute
for the EEG, but do effectively complement the informa-
tion derived from spontaneous electrical cortical activity
when cerebral death is suspected o n clinical grounds.
Brainstem evoked potentials have the advantage of being
free of artifact contamination and are less sensitive than
the EEG to the effect of CNS depressants. The disappear-
ance of activity from the EEG may precede the loss of
brainstem responses because the cortical structures are
*EEG in the case of cerebral death is subject to much technicaland
interpretivebias. In complyingwiththe minimumstandardsoutlinedby the
AmericanEEG Societyrequiringmaximalamplificationof the signal,the
record oftenbecomescontaminatedby a varietyof environmentalartifacts.
To minimizesuch artifacts, equipmentmay have to be turnedoff tempo-
rarily, and personnelshouldbe expectedto withholdactivityin the vicinity
of the patientwhennecessary.
Volume 110 Determination o f brain death 19
Number 1

more sensitive to the effects of severe insults than brain-
stem structures are. Thus, a t the time of an isoelectric
EEG, brainstem responses may be abnormal though not
completely absent. In this case, serial evoked potentials are
indicated to provide evidence of deterioration in brainstem
function.
Brainstem evoked potentials are recommended when (1)
the interpretation of the isoelectric EEG is controversial;
(2) the EEG is not completely isoelectric (agonal stage); or
(3) the EEG is isoelectric but the effects of CNS depres-
sants or hypothermia is present.
DOCUMENTATION OF BRAIN DEATH
Pertinent clinical examination and laboratory data are
summarized on the Brain Death Examination Form (see
example on pp. 16-17) dated and signed by the attending
physician of record and a concurring attending physi-
cian.

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