Brain Death Leanne Johnson-Meeter PA-C Department of
Neurosurgery Gundersen Lutheran Medical Center 04/25/2013 Slide 2
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. Slide 3 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. Slide
4 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. Slide 5 Slide 6 Slide 7 Slide 8 Slide 9 Midbrain
(Mesencephalon) Connection: forebrain to the hindbrain Controls
response to sight Eye movement Pupil dilation Hearing Slide 10 Pons
(Latin for bridge) Connection: communication and coordination
center between the two hemispheres (right, left) and messages from
brain to spinal cord Arousal Sleep Slide 11 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
Slide 12 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 Slide 13
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.
Slide 14 GCS: Glasgow coma scale Slide 15 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? Slide 16 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 Slide 17 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 Slide 18 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
Slide 19 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 IVFs, now requiring pressors,
blood products Ventilation continues to deliver adequate O2 to the
brain, organs. +Pneumothorax requiring chest tube placement Slide
20 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 70s. Simultaneously, BP exceeded 200
systolic, then abruptly falls into the 100s systolic, requiring
pressors to maintain Slide 21 Slide 22 Now what? Slide 23 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 Slide 24 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? Slide 25 Test Brainstem reflexes 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) Slide 26 Dolls 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 Slide 27 Slide
28 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) Slide 29 . 1. Prerequisites: Core
Temperature 36.5C or 97F 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% O 2 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% O 2, 8 L per minute 5. Look closely for respiratory movements
(abdominal or chest excursions that produce adequate tidal volumes)
6. Measure PO 2, PCO 2, 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 PCO 2 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 Slide 30 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 patients primary
injury is in the brainstem Scenario 4: the patient has a false eye
on the right and has dense cataracts on the left Slide 31
Controversy #1 If the patients 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 Slide 32 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) Slide
33 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 Slide 34 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 brains
circulatory system Slide 35 Eeg: Electroencephalogram Slide 36 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 Slide 37 Cerebral Angiography Slide 38
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 Slide 39 Case
Presentation Going back to our trauma patient: 30 yo M with MCC,
severe TBI. Lets make him 75 years old, 125 kg, treat him with
hypothermia for 3 days in addition to paralytic, sedation, and
hypertonic saline gtt Hes now through the 3-5 day brain swelling
phase and Neurosurgerys asked for an examination Slide 40 How do
you start a car in cold weather? Slide 41 Hypothermia changes
everything Metabolism, insulin levels, adrenaline, noradrenlaine,
cortisol levels Cardiac renal and hematological function
Pharmaceutical clearance and metabolism Causes an encephalopathy
Slide 42 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 Slide 43 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 Slide 44 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 Slide 45 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) Slide 46
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 didnt
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 Slide 47 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) Slide 48 ~RIP~ Dying is like getting audited by
the IRS-something that only happens to other people... until it
happens to you. - JEROME P. CRABB
