Transcript TWO BASIC QUESTIONS - National Center for State Courts

BRAIN DEATH AND STATES OF
CONSCIOUSNESS
Laurence Tancredi, MD, JD
New York University School of Medicine
TWO BASIC QUESTIONS
Does the essence of life reside throughout all
organs or is it represented in a single organ of
the body?
How can we avoid the inaccurate diagnosis of
death with maximum certainty?
REASONS FOR SHIFT TO BRAIN DEATH
The mechanical ventilator (Bjorn Ibsen: mid-20th.
Century)
especially combination of mechanical ventilator and
new cardiac stimulation measures)
The creation of intensive care units (ICUs)
The issue of organ procurement for transplantation
purposes.
FORMULATIONS OF BRAIN DEATH
Whole-brain: complete and irreversible
cessation of all brain function, including that
of the brain stem
Brain-stem formulation: complete and
irreversible cessation of brain-stem function
alone
LOCATION OF BRAIN STEM
BRAIN STEM
HARVARD CRITERIA (1968)
•
•
•
•
Unreceptivity and unresponsivity
No movements or breathing
No reflexes
Flat electroencephalogram (EEG)
All of the above four tests are to be repeated at, at least, 24 hrs
with no change.
Exclusion of hypothermia (below 90 F or 32.2 C) or
Central nervous system depressants
American Academy of Neurology Guidelines
(1995)
Demonstration of coma
Evidence for the cause of coma
Absence of confounding factors, including hypothermia, drugs,
electrolyte, and endocrine disturbances
Absent brainstem reflexes
Absent motor responses
Apnea
A repeat evaluation in 6 hrs is advised, but the time period is
considered arbitrary
Confirmatory laboratory tests are only required when specific
components of the clinical testing cannot reliably be evaluated.
PREREQUISITES BEFORE DETERMINATION
OF BRAIN DEATH
Acute catastrophic event involving both hemispheres
or brainstem and irreversibility
Exclusion: medical conditions that may confound
clinical assessment, particularly severe electrolyte,
acid-base, or endocrine disturbances
Core temperature equal to or greater than 32 degrees C
No documented evidence of drug intoxication,
poisoning, or neuromuscular blocking agents
CONFIRMATORY TESTS OF BRAIN DEATH IN
ADULTS
Electroencephalography (EEG)
Cerebral Angiogram
Transcranial Doppler Sonography
Magnetic Resonance Imaging (MRI)
Single Photon Emission Computed Tomography
(SPECT)
Evoked Potentials
Brainstem Auditory Evoked Potentials (BAEP)
Somatosensory Evoked Potentials (SSEP)
Spiral Computed Tomography Scan (Spiral CT Scan)
BRAIN DEATH DETERMINATION IN CHILDREN
No reports of children recovering neurological function who have
met adult brain death criteria on clinical examination
Guidelines for children emphasize history and clinical
examination in determining etiology of coma to eliminate
reversible conditions
Age-related observation periods and need for specific tests
recommended in guidelines for children under 1 year of age
7 days to 2 months: Two examinations and EEGs 48 hrs apart
2 months to 1 year: Two examinations and EEGs 24 hrs apart,
or one examination and an initial EEG showing ECS combined
with a radionuclide angiogram showing no CBF or both
More than 1 year: Two examinations 12-24 hrs apart, EEG and
isotope angiography are optional
NEUROLOGIC STATES RESEMBLING BRAIN
DEATH
Hypothermia
Acute Poisoning
Acute Metabolic Encephalopathies
Akinetic Mutism
Persistent Vegetative State
Locked-in-Syndrome
PERSISTENT PERMANENT VEGETATIVE
STATE
Time Duration: 1 month; if persistent more than 1 year,
almost always permanent
Function lost:
No cognition: consistent responses to linguistic,
symbolic, or mimetic instruction are absent
No semantically meaningful sounds or goal-directed
movements
No sustained head-ocular pursuit activity
PERSISTENT PERMANENT VEGETATIVE
STATE
Function usually or often preserved:
Brainstem and autonomically controlled visceral
functions: homeothermia; osmolar homeostasis;
breathing; circulation; gastrointestinal functions
Pupillary and oculovestibular reflexes usually remain
and are accentuated
Brief, inconsistent shifting of head or eyes toward
new sounds or sights may occur
Smiles, tears, or rage reactions may occur either
spontaneously or to nonverbal sounds
Reflex postural responses to noxious stimuli remain
HYPOTHERMIA: CLINICAL FEATURES
Body Core Temperature
35 – 32 degrees C
Central Nervous System: apathy; dysarthria,
impaired judgment
Cardiovascular: tachycardia, then progressive
bradycardia; cardiac cycle prolongation;
vasoconstriction
Respiratory: tachypnia, to progressive bradypnea;
bronchorrhea; bronchospasm
HYPOTHERMIA: CLINICAL FEATURES
32 – 28 degrees C
Central Nervous System: decreased level of
consciousness; hallucinations; papillary dilation
Cardiovascular: Progressive decrease in pulse and
cardiac output; increased cardiac arrhythmias;
Respiratory: Hypoventilation; 50% decrease in
carbon dioxide production per 8 degree C drop
in temperature; absence of protective airway
reflexes; 50% decrease in oxygen consumption
Neuromuscular: hyporeflexia; diminishing shivering,
rigidity
HYPOTHERMIA: CLINICAL FEATURES
Under 28 degrees C
Central Nervous System: coma; absent
oculocephalic, corneal and bulbar reflexes
Cardiovascular: hypotension, bradycardia,
dysrhythmias, decreased ventricular arrhythmia,
asystole
Respiratory: pulmonic congestion and edema; apnea
Neuromuscular: amobile; areflexia
RESEARCH DIRECTIONS FOR BRAIN DEATH
Improvements in use of MRI and MRI angiography
Use of multimodality evoked potentials (MEPs), which
test cerebral cortex as well as the brain stem, and
include:
brain-stem auditory evoked potentials (BAEP)
flash-visual evoked potentials (flash VEPs), and
median somatosensory evoked potentials
(median SEPs)
Refinements of imaging technologies (PET, MRI,
SPECT) to achieve greater sensitivity and specificity
Improvements in MEG (magnetoencephalography) to
detect cellular activity in the brain stem
FUTURE DEVELOPMENTS AND BRAIN
DEATH
Use of electrodes on motor cortex to translate motor
control commands, opens possibilities of translating
and transferring ideas to a computer during process
of dying
Use of electrodes may also provide means for
determining that any organized activity doesn’t exist,
which in the absence of mechanical disruption,
would demonstrate the brain is dead.
Understanding the process of neuronal death
(apoptosis) may provide opportunities for
intervention
SOURCES
Wijdicks EFM., (ed.): Brain Death. Philadelphia, Lippincott
Williams & Wilkins (2001)
Faymonville ME, Pantke KH, Berre J et. Al (2004): Cerebral
functions in brain-damaged patients. What is meant by
coma, vegetative state, minimally conscious state, locked-in
syndrome and brain death? Anaesthesist 53: 1195-1202
Karantanas AH, Hadjigeorgiou GM, Paterakis K et al. (2002:
Contribution of MRI and MR angiography in early diagnosis
of brain death. Eur Radiol 2710-2716.
Munari M, Zuchetta P, Carollo C et al. (2005): Confirmatory
tests in the diagnosis of brain death: Comparison between
SPECT and contrast angiography. Critical Care Medicine 33:
2068-2073
Yuan J, Yanker BA (2000): Apoptosis in the nervous system.
Nature 407: 802-809