Brain death scintigraphy

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					Brain Death study with Tc99m-
   exemetazine (Ceretec®)
             Mike Durkan
          Fall Term 2008-09
     Nuclear Medicine Externship
       On Monday October 20th, I participated in a “Brain Death” study of a 19yr old
male. The patient was riding his bike to school when he was struck by a car. The
emergency response team resuscitated the patient during transport and established
necessary life support equipment. The accident dislocated the patient’s skull from
his spine, Atlanto-occipital dislocation. The trauma caused by this event left the
patient quadriplegic and critically damaged his vertebral arteries. The level of
cerebral trauma caused from the cerebrovascular accident was unable to be
evaluated using Radiologic angiography.
       Before the nuclear medicine brain scan was ordered; Electroencephalograms
and an Ultrasound study were done to evaluate blood flow and electrical activity in
the brain. The Tc99m-exametazine (Ceretec) Brain Death study was done and it was
concluded the patient was conscious but lacked Cerebellum and Pons function,
indicating “Locked-In Syndrome” or Cerebro-medullospinal disconnection. Over the
course of two days the patient’s condition deteriorated and another nuclear
medicine study was done to evaluate brain function. The study showed complete
brain death.
       After talking with a radiologist, he said the patient was very indicative of
locked-in syndrome however EEG activity is usually normal in these patients. At the
time of the nuclear medicine study the patient’s EEG was negative, indicating no
brain function. The radiologist mentioned an idiosyncratic increased uptake of
Tc99m-exametazine caused by Luxury perfusion or Misery perfusion. This case study
will follow the Nuclear medicine Technologist’s role in this diagnosis and explain the
anomaly seen from luxury perfusion in Tc99m-exametazine brain studies.
    Tc99m-examatazine (Ceretec®) for
           Brain Scintigraphy
• Exametazine is the active lipophilic -moiety
  (i.e. complex) labeled to Tc99m
• When labeled with Tc99m-Stannous ion, this
  lipophilic characteristic allows Blood Brain
  Barrier (BBB) penetration.
• Brain Cells “actively” take up Tc99m-
• ≈5.25% of the IV injected dose is taken up
  within 1 minute post injection and first pass.
• The molecule doesn’t undergo wash-out
  following neuronal uptake.
• Radiopharmaceutical shelf life is 30 minutes
  after reconstitution with Tc99m-stannous
• Repeat Brain studies require 48hrs of delay
  between Tc99m-Ceretec studies.
            Brain Death Procedure
• Standard USP and ALARA
• X1: Adsorbent <.05µM filter.
• X2: 15%NaCl in 10mL of Sterile
  Water (Saline).
• X2: tube extensions with
  0.6mL volume. (1.2ml total
• Absorbent chucks
• X1: Large rubber band or
  knotted tourniquet.
                  Brain Death Procedure
Acquisition Parameters                         Injection of Tc99m-exametazine
•   Use a large FOV detector with a LEHR or    •   The patient should have the rubber band or
    LEGP collimator.                               knotted tourniquet placed.
     –   NOTE: Converging collimators like;         –   This decreases facial and skull perfusion
         fanbeam, astigmatic, and conbeam               artifact.
         collimators are preferred.            •   The filter should be placed between the dose
•   Position pt. supine with head first.           syringe and 1.6mL tubing.
                                                    –   The Tc99m-Ceretec is suspended in a neutral
•   Place a rubber band or knotted                      mixture of Methylene Blue. This mixture is
    tourniquet around forehead and                      filtered to prevent deactivation of the
                                                        lipophilic compound.
    inferior occipital region.
                                               •   To create an ideal flow of cerebral perfusion,
•   Bolus 10-25mCi of filtered Tc99m-              a modified Oldendorf method of IV
    exametazine intravenously no longer            administration is used.
    than 30minutes after reconstitution.            –   A bolus administration of Tc99m-Ceretec
•   Acquire a 30 second - 6 minute flow                 needs to be used to provide a diagnostically
                                                        accurate Flow series of images.
    with 1-20 seconds/frame.                        –   This is done by filling the 1.6mL of tubing with
•   15 minutes post injection acquire static            the dose then bolusing the
    planar lateral and anterior images for              radiopharmaceutical with 5ml saline.
    250kcounts or 180 seconds.
                 Brain Death Procedure
•   Only do SPECT if recommended by
•   Physical obstructions like critical life
    support equipment may limit SPECT
•   Acquire SPECT 30-90 minutes post
    injection of Tc99m-exametazine.
•   Using a 128x128 matrix, set-up SPECT
    for 64 projections at 20 secs/stop.
•   Reconstruct with a minimum of 8mm
    slice thickness.
•   If three plane reconstruction is required
    use iterative algorithmic reconstruction,
    ie. OSEM/MLEM.
•   Use a low-pass HANN or Butterworth
    filter with a cutoff frequency of 0.4,
    0.45, or 0.5 cycles per second.
          Results of Patient’s Scan
• Normal procedure indicates SPECT acquisition. SPECT would have
  demonstrated the severity of cerebral damage caused by decreased
  vertebral artery supply. Because imaging was limited by the
  patient’s respiratory tube and other equipment, no SPECT was
• Image acquisition parameters for the flow were extended to 6
• The Brain Death study was quickly read by the radiologist.
• “Cerebellar activity was absent but cerebral activity was present.
  Abnormal brain scan but negative for Brain Death.”
• After a later transcription and further consultation with the
  Intensive care doctor the patient was thought to have
  Cerebromedullospinal disconnection. This was revealed on the
  Tc99m-Ceretec when activity was absent in the cerebellum and
  parts of the brainstem, specifically the Pons. The Medulla
  Oblongata had perfusion.
Negative Brain Death Images
Anterior Dynamic    Right Lateral

      Atlantooccipital Dislocation
• In a normal patient, the
  gap pointed out in the
  image should be three
  times less.
• Accompanying this injury
  the patient became
  quadriplegic and lost
  blood flow from his
  vertebral arteries.
• The Brain scan evaluated
  the severity of the
  Cerebral vascular accident
                Locked in Syndrome
• Cerebromedullospinal
  disconnection or “locked-in”
  syndrome is caused by
  obstruction or damage to the
  basilar artery.
• The basilar artery supplies blood
  to the Pons and parts of the
• The Pons and Cerebellum have
  major roles in the body’s control   Pons
  of motor/sensory function.
• Common causes of this condition            Cerebellum
  are Lou Gehrig’s disease, CVA,
  Amyotrophic lateral sclerosis,
  drug overdose, and a variety of
  neurodegenerative diseases.
              Locked in Syndrome
• In one case of locked in
  syndrome, a famous French
  journalist and editor of ELLE
  magazine had a stroke that
  caused this condition.
• He was left with a small
  amount of muscle control in
  his left eye. This allowed him
  to communicate by blinking at
  letters alphabetically spoken
  to him. Over a few years he
  used this method to write a
  book, “The Diving Bell and
        Repeating the Brain Scan
• The 19yr old patient was diagnosed with locked in
  syndrome. Later the next day however, the patient
  began having seizures and coded twice.
• The patient suffered a major change in body
  temperature and EEG pattern.
• After a persistent negative EEG, the ICU doctors
  ordered another Tc99m-Ceretec brain scan.
• Because 3.5-7% Tc99m-exematazine was possibly left
  in the patients neurons, repeat images would need to
  be done 48 hours after the last Brain Death study.
• The leftover radioactivity had enough counts to create
  a false negative 24hrs after the study.
              Positive for Brain Death
•   On October 22nd, 48hrs after the initial
    study, I came in late to help the on-call
    technologist with the study.
•    After we positioned the patient we
    acquired a five minute static to determine
    the amount of activity left in the patient’s
•   The Radiologist determined the activity was
    insignificant so we repeated the study.
•   Because the patient was an organ donor, a
    variety of instruments and life preserving
    medicines were being used to keep the
    patient and his organs from atrophy.
•   To mitigate organ harvesting the study was
    reported as a “call dictation”.
•   A respiratory therapist and ICU nurse
    accompanied the patient.
•   After the study, the Radiologist determined
    Brain Death.
            Cerebral Luxury Perfusion
•   The Brain Stem functions as an auto
    regulator of normal bodily functions
    like: breathing, digestion,
    sensory/motor refluxes,
    consciousness, and our circadian
•   The rare occurrence of Luxury
    perfusion is associated with
    autonomic deregulation of cerebral
•   This condition accompanies cerebral
    vascular events (CVA) that may
    damage the brain stems control over
    this function.
•   Luxury perfusion is defined as an
    increase in cerebral blood flow that
    exceeds metabolic needs of the
   The Luxury Perfusion Artifact with
    Tc99m-exematzine Brain Studies
• There’s a couple of theories about why luxury perfusion
  causes increased uptake of Tc99m-exametazine in
  damaged neurons.
    1) With an increased amount of blood flow comes an increased
       uptake of the lipophilic compound. The molecule passively
       diffuses across infarcted cells’ membranes.
    2) When acute trauma damages the blood brain barrier, the
       Tc99m-exametazine molecule pools in cerebral vasculature.
    3) Permanent blood brain barrier damage causes cerebral
       extravasation of the injected dose; showing not cerebral
       uptake but hemorrhagic pooling.
  Authors suggest that blood brain barrier disruption or permanent
  damage in combination with deregulated cerebral blood flow
  causes the increased Brain uptake of tc99m-exametazine. This
  causes a False-negative nuclear medicine brain death study.
        False Negative Brain Death
• With the information from the
  above slide and the history of the
  19yr old patient in mind, I
  consulted the radiologist about his
• He told me that this could be a
  possible result because of the
  correlation between the patient’s
  vertebral artery CVA but there’s no
  way of telling without another
  nuclear medicine study, a Tc99m-
  bicisate /ECD (Neurolite®).
• The bicisate compound has been
  shown to differentiate between
  ischemic and infarcted tissue
  better than exametazine.
      Due to the condition and changed state of the patient
after the initial study, the radiologist said it is unknown
whether the study indicated brain death, even though activity
was seen in the brain.
      Had the patient’s state remained unchanged from the
initial Tc99m-HMPAO images the radiologist would have
suggested the possibility of luxury perfusion causing an
idiosyncratic “false negative”. Locked-in syndrome was further
ruled out because the patient lacked Electroencephalogram
(EEG) activity. Luxury perfusion would have to be further
evaluated with a Tc99m-ECD Acetazolamide brain study. Also
the patient’s blood brain barrier would have to be evaluated
either with a Tc99m-DTPA study or Pertechnetate study.
References continued

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