Brain Death
Leanne Johnson-Meeter PA-C
Department of Neurosurgery
Gundersen Lutheran Medical Center
04/25/2013
Disclaimer
• No financial relationships to disclose.
• All aspects surrounding coma and death are always
taken seriously and handled professionally. Any humor
injected is to lighten the mood of a dark topic.
Objectives
• Understand the definition of death.
• Through a case presentation, learn about the Neurologic
examination and the steps necessary to determine brain
death.
• Understand what the ancillary/confirmatory tests are to
determine brain death.
• Understand modern era controversy in determining brain
death.
Death
• Government
• UDDA: Uniform Determination of Death Act (1981)
– An individual who has sustained either
1) irreversible cessation of circulatory and
respiratory functions or
2) irreversible cessation of all functions of the entire
brain, including the brain stem, is dead.
Midbrain
(Mesencephalon)
•
•
•
•
•
Connection: forebrain to the hindbrain
Controls response to sight
Eye movement
Pupil dilation
Hearing
Pons
(Latin for “bridge”)
• Connection: communication and coordination center
between the two hemispheres (right, left) and messages
from brain to spinal cord
• Arousal
• Sleep
Medulla
• Connection: motor and sensory neurons from the
midbrain and forebrain pass through the medulla and
brain to spinal cord
• Autonomic functions: breathing, digestion, heart/blood
vessel function, swallow/sneeze
Case Presentation
•30 yo male, motorcycle collision, witnessed
•Highway speeds
•Unhelmeted
•Sustained severe TBI (traumatic brain injury) with a large
scalp laceration, actively bleeding
•Brought by air ambulance to GL, trauma activation
•Scene GCS 3(T); E1M1V1 with a left “blown pupil”
•Right forearm fracture
Trauma patient: maximum effort toward concurrent
resuscitation and diagnosis of multi-system injury:
– Securing airway and breathing, circulation: BP
support w/IVF, blood products, line placement (Art
line, central line)
– Determining further means of intervention: chest tube
for pneumothorax, ICP monitor for head injury, etc.
GCS: Glasgow coma scale
•
•
•
•
•
BP: 85/46, HR 98, T 34.5 deg C (94.1 deg F)
Potassium 3.2. Hemoglobin 8.2. Glucose 432
Trauma tox screen (urine): negative
Etoh: 301
Head CT findings of severe head injury: basilar skull
fracture (base of skull), Intraparenchymal bleeding,
bilateral SDH (subdural hematomas) 3-4 mm,
presence of brainstem blood, 2 mm hemorrhage
• Neurological examination: GCS 3T (1E, 1M, 1V)
• At this point, can you tell if this patient is brain
dead?
Determining Brain
Death
• 4 Approach Steps:
– Establish irreversible and proximate causes of coma
(i.e. Does the presentation of the patient result
from/match the pattern of a severe neurologic injury?
Is there anything present that potentially confounds
this presentation?)
– Achieve normal core temperature
– Achieve normal systolic blood pressure
– Perform neurologic examination
Determining Brain
Death
• Step 1: Irreversible and Proximate Causes of Coma
– Exclude drugs including etoh above the legal limit,
sedatives (trauma tox screen)
– No recent or persistent neuromuscular blocking
agents
– No severe electrolyte, acid-base, or endocrine
disturbance
Our patient: +etoh, K+ low, glucose high
Determining Brain
Death
• Step 2: Achieve Normal Core Temperature
– Core body temp >36 degrees C (96.8)
– Use warming blanket or warm IVF if necessary
Step 3: Achieve Normal Systolic Blood Pressure (BP)
- systolic bp > 100 mmHg
- fluid resuscitation and/or “pressors” medications
used to elevated the blood pressure
Our patient: temp 34.5 deg C (94.1 deg F), BP 85/46
Patient is taken to the ICU with continued management
of multisystem trauma:
– ICP monitor placed for real time monitoring of brain
injury. ICP measuring in the mid 20s. Sedation
(propofol, fentanyl)
– Electrolyte/endocrine replacement/treatment
– Blood pressure management initially with IVF’s, now
requiring pressors, blood products
– Ventilation continues to deliver adequate O2 to the
brain, organs. +Pneumothorax requiring chest tube
placement
• Despite aggressive management of injuries continues
over the next 48 hours: ICP 38, BP 198/110. The patient
is on a hypertonic saline and labetalol gtt. AM lytes are
normal, ventilation settings are unchanged
• On Day 4, the ICP exceeds 150 and then abruptly starts
to fall into the 70’s. Simultaneously, BP exceeded 200
systolic, then abruptly falls into the 100’s systolic,
requiring pressors to maintain
Now what?
Brain Death Exam
• Step 1:
– Sedation/pain medication/any drugs that can/could
interfere with neurological exam are discontinued for
adequate period of time to clear the system
• No severe electrolyte, acid-base or endocrine
disturbance
• Step 2: Achieve Normal Core Temperature
• Core body temp >36 degrees C (96.8)
• Use warming blanket or warm IVF if necessary
• Step 3: Achieve Normal Systolic Blood Pressure (BP
• Systolic BP > 100 mmHg
• Fluid resuscitation and/or pressors to elevate the
blood pressure
•
Step 4: Perform the Neurological Examination
• Start with the ventilator: is the patient over-breathing
the ventilator?
• Is there any motor response to painful stimulation?
• Test Brainstem reflexes
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–
–
–
Pupil reaction to light
Corneal reflex
Facial muscle movement to pain
Pharyngeal and tracheal reflexes (deep suction and
ET tube movement or tonsil tickle with q-tip: gag,
cough)
• Doll’s eyes
– Eye movements are absent
• Cold water calorics
– Head of bed 30 degrees, 50+ mL of ice water
irrigation of each ear canal with 5 mins observation
and 5 mins between tests. If there is a ruptured
Tympanic Membrane (Ear Drum) you must skip this
ear
Apnea Test
• Apnea = breathing is suspended
• Goal of test is to determine if the patient can breathe
without life support
• Creating an environment with the ventilator for the
patient to spontaneously breathe (exchange gas)
1. Prerequisites:
Core Temperature 36.5°C or 97°F
Systolic blood pressure 100 mm Hg
Corrected diabetes insipidus (Positive fluid balance)
Normal PCO2 (Arterial PCO2 of 35-45 mm Hg)
2. Preoxygenate with 100% O2 for 30 minutes .
3. Connect a pulse oximeter and disconnect the ventilator
4. Place a nasal cannula at the level of the carina and deliver 100% O2, 8 L per
minute
5. Look closely for respiratory movements (abdominal or chest excursions that
produce adequate tidal volumes)
6. Measure PO2, PCO2, and pH after 10 minutes and reconnect the ventilator
7. If respiratory movements are absent and arterial PCO2 is 60 mm Hg (option:
20 mm Hg increase in PCO2 over a baseline normal PCO2), the apnea test
result is positive (supports the diagnosis of brain death) Connect the
ventilator if during testing the systolic blood pressure becomes < 90 mm
Hg or the pulse oximeter indicates significant desaturation and cardiac
arrhythmias are present: immediately draw an arterial blood sample and
analyze ABG!
8. If PCO2 is 60 mm Hg or PCO2 increase is > 20 mm Hg over baseline normal
PCO2, the apnea test is positive [supports the clinical diagnosis of brain death]
9. If the PCO2 is < 60 mm Hg or PCO2 increase is < 20 mm Hg over baseline normal
PCO2, the result is indeterminate and an additional confirmatory test can be
considered
Trouble Shooting
Scenarios
• Scenario 1: the patient “fails” the apnea test
• Scenario 2: the patient is too unstable to perform the
apnea test
• Scenario 3: the patient’s primary injury is in the
brainstem
• Scenario 4: the patient has a false eye on the right and
has dense cataracts on the left
Controversy #1
• If the patient’s primary injury is in the brainstem, can
clinical brain death testing be performed?
• Example: 60 yo M with acute brainstem hemorrhage with
an examination consistent with brain death
Ancillary Testing
• Recommended by the AAN (American Academy of
Neurology) in uncertain situations and/or apnea test
cannot be performed
• Examples: severe facial trauma, pre-existing pupillary
abnormalities, toxic levels of drugs
• Severe pulmonary disease (resulting in retention of
carbon dioxide)
Ancillary Testing
• Nuclear Flow Study (Cerebral Scintigraphy)
– Injection of radionuclide tracers are used to establish
flow or lack of flow to the brain
– “Hollow Skull” sign
TCD
• Transcranial Dopplar
– Ultrasound used to establish cerebral circulatory
arrest
– Pros: inexpensive, portable
– Cons: requires an experienced operator and
interpreter. 10-20% of patients have inadequate bone
windows with which to examine the brain’s circulatory
system
Eeg:
Electroencephalogram
EEG
• Brain tracing of activity, much like the EKG for the heart.
Routinely used in Neurology for diagnosing/localizing
seizure disorders, sleep disorders
• No brain activity (flat waves) is diagnostic of brain death
Cerebral
Angiography
Cerebral
Angiography
• Contrast dye study to determine blood flow to the brain
• Dye is injected into the vessels of the brain by a small
catheter
• Presence of dye = blood flow. Absence of dye = brain
death
Case Presentation
• Going back to our trauma patient: 30 yo M with MCC,
severe TBI. Let’s make him 75 years old, 125 kg, treat
him with hypothermia for 3 days in addition to paralytic,
sedation, and hypertonic saline gtt
• He’s now through the “3-5 day brain swelling phase” and
Neurosurgery’s asked for an examination…
How do you start a
car in cold weather?
Hypothermia changes
everything…
• Metabolism, insulin levels, adrenaline, noradrenlaine,
cortisol levels
• Cardiac renal and hematological function
• Pharmaceutical clearance and metabolism
• Causes an encephalopathy
Hypothermia
• More on pharmacology in the setting of hypothermia:
– Cytochrome P450 activity is not only reduced, but the
duration of this reduction is significant: 72 hours!
– Sedatives, neuromuscular blockade
– Further exacerbated in elderly patients and those with
liver or kidney dysfunction
Hypothermia
• The effects of hypothermia on the physical examination:
– In the time before hypothermia, absent pupillary
reflexes and absent corneal reflexes predictions were
made for grim/poor outcomes with high specificity
– Now in the time of therapeutic hypothermia, care
must be taken
Hypothermia
• Corneal reflexes, when absent, have been found to be
less predictive of a poor outcome in the cooled
neurological patient compared to the normothermic
patient
• In one study the predictive value was 89% in cooled
patients v. 100% in normothermic patients
• Pupillary reaction does not seem to change, but absent
corneal reflexes is not as reliable
Hypothermia
• Motor response GCS (E,M,V)
• Reliability in predicting poor outcomes when
hypothermia has been applied is less v. not reliable
• Uncertainty exists for the etiology: hypothermia itself v.
prolonged effects of medications (sedatives, paralytics)
Imaging
• “Well, what did the CT / MRI scan show?”
• Everybody wants a picture…
– If there were mild or moderate changes in specific
sequences found on MRI scans in post-cardiac arrest
patients treated with hypothermia, it did not mean that
the patient didn’t ultimately have a good outcome
– Severe changes were more predictive of outcome
than the neurological examination, however (78%
compared to 48%)
– Imaging is not subject to vulnerability of hypothermia,
may be another tool
Conclusion
• Brain death requires a systematic and thoughtful
approach
• Recognition must be given to the effects of medications
and hypothermia on the brain death examination
• Ancillary studies should be considered when there is
doubt (based on resources, feasibility, cost)
• Careful discussion should occur with the family regarding
timing (this may be a limiting factor)
~RIP~
Dying is like getting audited by the IRS-something that only
happens to other people ... until it happens to you.
-JEROME P. CRABB