Presentation on theme: "Brain Death Leanne Johnson-Meeter PA-C Department of Neurosurgery Gundersen Lutheran Medical Center 04/25/2013."— Presentation transcript:
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.
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
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 – 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% 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
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 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
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…
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