Nukes Flashcards
Whole body scan > bones > spleen > hot spleen >
in-WBC
Whole body scan > bones > spleen > liver = spleen
sulfur colloid
Whole body scan > bones > spleen > light spleen
gallium
Whole body scan > no bones > heart > kidneys
MIBI
Whole body scan > no bones > heart > no kidneys
MIBG
Whole body scan > no bones > no heart > liver
MIBG
Whole body scan > no bones > no heart > no liver
iodine
MIBG with 1-123 is more likely to have heart than
I-131
Whole body scan > bones > liver > spleen > more photons
Tc99m sulfur colloid
Whole body scan > bones > (liver > spleen) > less photons
gallium
Whole body scan > (spleen > liver)
In - WBC
Whole body scan > no bones > liver and spleen > (liver > spleen)
I-131 MIBG
Whole body scan > no bones > liver and spleen > (liver > spleen) + intense renal
octreotide
Whole body scan > no bones > no liver or spleen
I123 or I131
Bones > lacrimal glands
with free TC
bones will be weak
Bones > lacrimal glands
with gallium
no spleen
bones > no lacrimal glands
sulfure colloid
liver=spleen
bones > no lacrimal glands
In 111 WBC
hot spleen
MIBG overview
I’ll talk about this more later in the chapter, but MIBG can be labeled with either 1-123 or 1-131.
The energy of the 1-123 (159 keV) is better for imaging, you can give a higher dose, and the
results are typically available within 24 hours (1-131 usually requires delated to optimize target to
background noise). Having said that 1-131 labeled MIBG is still used all over the place, especially
with adults. 1-131 may also be better for estimation of tumor uptake, for planning related to
MIBG therapy. The point of me rambling here is that you have two different MIBGs - so telling
which scan is which requires a little finesse.
MIBG
Cardiac
It has variable cardiac uptake, so it finds itself on multiple branch points. Cardiac activity is more
often seen on an 1-123 MIBG scan (as opposed to 1-131 MIBG). Another thing that helps me
remember this stuff: when you do a MIBG you are often looking for neuroblastoma. If the kidney
was also hot it would be hard to tell a mass near the kidney from the kidney - so part of the
reason the study works is that the kidney does NOT take up MIBG.
MIBG
adrenal glands
Normal adrenal glands are not seen. However, you can have faint uptake in the
adrenals in about 15% of 1-131 patients, and around 75% of 1-123 patients. So, if you see
adrenals and you are sure they are normal (faint and symmetric) it’s more likely to be 1-123.
DARK SPLEEN +
DARK KIDNEYS
knee jerk
octreotide
DARK SPLEEN +
DARK KIDNEYS
count study
This is a high count study, so the
images should be clearer (relative to
the normal “un-clear medicine.”
no bones + liver + dark spleen + dark kidneys
octreotide
Tc WBC vs In WBC
labeled
Just like MIBG can be labeled with either 1-123 or 1-131
you can label WBCs with Tc or Indium.
Tc WBC vs In WBC
Both will have hot spleens. Additionally,
Tc is a higher count study and
will typically look cleaner.
Tc WBC
The trick here can be imaging at 4 hours vs imaging at 24 hours. At 4 hours you can see lung uptake. At 24 hours the lungs are clearing up, but you start to get some bowel uptake. Just like an In-WBC the spleen is still darker than the Liver.
Tc WBC quick
Renal, GI
In WBC quick
no renal, no GI
18F - Sodium Fluoride vs Tc-MDP
You can do bone scans with several different tracers, the main two are 18F Sodium Fluoride and
Tc-MDP. If you were trying to differentiate the two, the primary take home point is F-18 PET is
way way way better than Tc-M DP. By “better” I mean that the image quality and sensitivity of F18
is multiple orders of magnitude better than Tc-MDP. It also has a shorter examination time. So,
why do you never see l8F? Because it costs more, and insurances won’t pay etc… Politics and
Finance are the reasons. Another potentially testable factoid would be which organ gets the
highest dose? The organ receiving the highest dose is Bone with MDP, and Bladder with ,8F
(overall l8F > Tc-MDP) — probably… honestly y o u ’ll read different things in different sources.
18F - Sodium Fluoride vs Tc-MDP
scan on scan on scan
This is a common trick, popular in case books & case conferences - asking you to distinguish F-18
bone scan vs Tc-MDP bone scan vs PET-FDG with marrow stimulation.
This is how you do it:
* Tc-MDP will have bone and kidney uptake. It will be a blurry fuzzy piece of crap.
* ,8F will be beautiful, super high resolution, and look like a MIP PET.
* FDG -PET with bone stimulation - will look similar to the F-l 8, but will have brain
uptake. Also, this can show increased uptake in the spleen.
the workhorse of
skeletal imaging is
methylene diphosphonate (MDP) tagged with
Tc-99m. This is prepared from a kit which has MDP and stannous
ion. You add free pertechnetate and the stannous ion reduces it so
it will bind to the MDP. If you don’t have enough stannous ion
(or you get air into the vial or syringe - that can cause oxidation)
you might get free Tc (salivary gland, thyroid, stomach uptake).
After you inject the tracer ( 15-25mCi) you wait 2-4 hours to let
the tracer clear from the soft tissues (so you can see them bones).
skeletal imaging mechanism
Phosphonate binding to bone (ehemisorption).
Distribution is based on blood flow and osteoblastic activity.
skeletal imaging gamesmanship
MDP and HDP are both bone agents so don’t get confused if they say HDP to
purposefully confuse you.
skeletal imaging what factors will affect tracer uptake
OsteoBLASTIC activity (why pure lytic lesions can be cold)
Blood Flow
skeletal imaging where is tracer uptake normal
Bone (dull), but also the Epiphyses in kids
Kidney (not seen *or very faint = Super Scan), Bladder
Breasts (especially in young women)
Soft tissues - low levels
skeletal imaging
abnormal distribution
Increased focal uptake is very nonspecific, and basically is just showing you bone turn over.
So a metastatic deposit can do that (and this is the classic indication). But, you can also see
it with arthritis (classically shoulder) and healing fractures (most commonly shown with
segmental ribs).
skeletal imaging Abnormal Distribution
skull sutures
It’s normal to see some persistent visualization of the skull
sutures, BUT when this is marked you may be thinking about renal
osteodystrophy.
skeletal imaging Abnormal Distribution
breast uptake
Some mild diffuse breast uptake is normal (especially in
younger women), BUT focal uptake can be cancer.
skeletal imaging Abnormal Distribution
renal cortex activity
You are supposed to have renal activity (not
seeing kidneys can make you think super scan), BUT when the renal
cortex is hotter than the adjacent lumber spine you should think
about hemochromatosis.
skeletal imaging Abnormal Distribution
diffuse renal uptake
This often occurs in the setting of chemotherapy
(especially if the study is looking for bone mets). This also can be seen
with urinary obstruction.
skeletal imaging Abnormal Distribution
liver uptake
This can be several things, but the main ones to think about arc (1) Too Much Al+3 contamination in the Tc, (2) Cancereither primary hepatoma or mets, (3) Amyloidosis, (4) Liver Necrosis
skeletal imaging Abnormal Distribution
spleen uptake
This is a common trick to show an auto-infarcted
spleen - common in sickle cell patients. These same patients are going
to have scattered hot and cold areas from multiple bone infarcts.
skeletal imaging Abnormal Distribution
lung uptake
In most cases this is some type of heterotopic calcification (dystrophic or mets).
The classic MDP hot lung met would be an osteosarcoma. Ultimately, it’s not specific and can be
seen in a ton of other random situations (fibrothorax, primarily tung tumors, radiation changes,
sarcoid, berylliosis, alveolar microlithiasis, Wegener’s, etc…).
skeletal imaging Abnormal Distribution
the single lesion
When you see a single hot lesion, the false positive rate for attributing the
finding to a met is high. Only about 15% to 20% of patients with proven mets have a single
lesion (most commonly in the spine). In other words, 80% of the time it’s benign. A classic
exception is a single sternal lesion in a patient with breast cancer. This is due to breast CA
80% of the time.
skeletal imaging Abnormal Distribution
sacral insufficiency fracture
This is a hot geographic area,
confined to the sacrum, often with a characteristic butterfly or “H”
shaped (Honda sign). Osteoporosis is the most common cause, but
it can also occur in a patient who has had radiation.
skeletal imaging Abnormal Distribution
diffusely decreased skeletal uptake
This can be seen with
(1) free Tc, or (2) Bisphosphonate therapy.
skeletal imaging Abnormal Distribution
fractures in the elderly (including abuse)
In older populations, bone scans may be negative for several days. A bone
scan obtained at 1 week will exclude a fracture.
skeletal imaging Abnormal Distribution
vertebral body fx (benign vs malignant)
A horizontal linear pattern of tracer uptake is the
classic look for an osteoporotic fracture (especially if they are multiple and of varying intensity).
If the tracer extends from the vertebral body into the posterior elements or just involves the
pedicles then you should think cancer. Lastly, followup of the osteoporotic fracture should show
tracer activity decreasing (cancer isn’t gonna do that).
skeletal imaging Abnormal Distribution
muscle
MDP is for bones, but it will also localize to injured skeletal muscle. The classic
way to show this is very hot quads, calfs, shoulders in a marathon runner (or military recruit) - as
a way to show rhabdomyolysis.
“Honda Sign”
sacral insufficiency fx
“Honda Sign”
sacral insufficiency fx
Hypertrophic Osteoarthopathy
This is a “Tramline” along the periosteum of long bones,
which is associated with conditions o f chronic hypoxia (CF,
Cyanotic Heart Disease, Mesothelioma, Pneumoconiosis).
However, when you see this - you need to think lung cancer.
Apparently it’s actually seen in 10% o f patients with lung cancer.
Next Step? CXR, Chest CT e tc …
Heterotopic ossification
the pattern is typically outside to
in, with the eventual development o f mature cortical bone. In some cases this abnormal
bone proliferation can reduce joint motility and cause pain. Therefore, in some cases
surgical resection is performed to preserve the function o f the joint.
Enter the MDP Bone Scan.
The main reason you image this is to see if it’s “mature.” Serial exams are used to
evaluate if the process is active or not (not = “mature”). If it’s still active it has a higher
rate o f recurrence after it’s resected. The idea is you can follow it with imaging until
it’s mature (cold), then you can hack it out (if someone bothers to do that).
AVN
Avascular Necrosis (AVN) as discussed in the MSK chapter, this can occur from a
variety of causes (EtOH, Steroids, Trauma, Sickle Cell, Gauchers).
The trick on bone scan is the timing.
• Early and late AVN is cold.
• Middle (repairing) will be hot.
PAgets
Seen primarily in older patients (8% at 80), it’s classically shown five ways
- Super Hot Enlarged Femur
- Super Hot Enlarged Pelvis,
- Super hot skull,
- Expanded hot “entire” vertebral body
- Metabolic Superscan - from widespread Pagets. Although, as a point of gamesmanship if they show you a metabolic superscan the answer is probably hyper PTH.
PAgets spine
Classically involves BOTH the vertebral body and posterior elements.
Primary Bone Tumors:
overview
Both Osteosarcoma and Ewings will be hot. Primary utility o f the bone scan is to see extent
of disease. With regard to benign bone tumors the only ones worth knowing are the HOT
ones and the COLD ones. Osteoid Osteoma is worth knowing a few extra things about
(because they lend themselves easily to multiple choice questions).
Osteoid osteoma
The lesion will be focal and three phase hot. A central hot nidus is often seen
(double density or hotter spot
within hot area). A normal bone
scan excludes this entity.
Fibrous Dysplasia
Be aware that in case books / case conference this is sometimes shown as a super hot mandible. Could also be shown as a leg that looks similar to Paget.
Specific Cancers - Specific Trivia
- Prostate Cancer Loves Bone Mets (85% of dying patients have it)
- Prostate Cancer bone mets are uncommon with a PSA less than 10 mg/ml
- Lung Cancer bone mets tend to be in the appendicular skeleton
- Lung Cancer can have hypertrophic osteoarthropathy (10%)
- Breast Cancer bone mets are most common to the spine, but the solitary sternal lesion is more specific
- Neuroblastoma frequently mets to the bones (metaphysis of long bones)
- 1-123 and 131 M1BG are superior for detection of neuroblastoma bone mets
Any bone uptake on
MIBG, 1-131, or Octreotide is abnormal, & concerning for mets.
Cold bone lesions
- Radiation Therapy (usually segmental)
- Early Osteonecrosis
- Infarction (very early or late)
- Anaplastic Tumor (Renal, Thyroid, Neuroblastoma, Myeloma)
- Artifact from prosthesis, pacemaker, spine stimulator, etc….
- Hemangioma ** this is variable
- Bone Cyst (without fracture)
Bone Island vs
Prostate Met:
• Both are sclerotic on plain film / CT • The Prostate Met should be very HOT on Bone Scan • The Bone Island should be cold, or faintly warm • Osteopoikilosis should be cold
Skeletal tumors
hot lesions
• Fibrous Dysplasia • Giant Cell Tumor • Osteoblastoma • Osteoid Osteoma • Aneurysmal Bone Cyst *donut sign (centrally cold)
Bone Scan vs Skeletal Survey (Trivia)
- Bone Scan is way better (more sensitive) than skeletal survey for blastic mets
- Skeletal Survey is superior (more sensitive) for lvtic mets
- Skeletal survey is the preferred evaluation for osseous involvement in myeloma
Equivocal Lesion N e x t S tep ?
If a bone scan “equivocal lesion” is found the next step is a plain film. If the plain film shows no corresponding lesion this is MORE suspicious for mets. Next step at that point would be a MRI.
Super Scans
overview
This is a common trick, where the scan shows no abnormal focal uptake, but you can’t see
the kidneys. The trick is that everything is hot.
Super Scans
types
diffuse mets
metabolic
Super Scans
duffuse mets
Diffuse skeletal
metastatic activity (breast and
prostate are the common culprits).
Super Scans
metabolic
From metabolic bone pathology; including hyperparathyroid, renal ® osteodystrophy, Pagets, or severe thyrotoxicosis.
Super Scans
how can you tell them apart
- The Skull will be asymmetrically hot on the metabolic super scan.
super scans
gamesmanship
A common sneaky move is to show you a bone scan, with no renals. But it’s
because there is a horseshoe kidney in the pelvis. Could be phrased as a next step question, with
the answer being look at prior CT to confirm normal anatomy.
Flair Phenomenon
This is a sneaky situation shown on bone scan, where a good response to therapy will mimic
a bad response. What happens is you have increased radiotracer uptake (both in number and
size of lesions) seen 2 weeks to 3 months after treatment.
So how can you tell it’s fla ir and not actually cancer getting worse?
- On plain film lesions should get more sclerotic
• After 3 months they should improve.
The Three Phase Scan
Bone scans can be done in a single delayed phase, or in 3 phases (flow, pool, and delayed). A
lot o f things can be “3 phase hot”, including osteomyelitis, fracture, tumor, osteoid osteoma,
charcot joint, and even reflex sympathetic dystrophy.
The Three Phase Scan
Cellulitis vs Osteomyelitis
The benefit of using 3 phases is to distinguish between cellulitis (which will be hot on flow
and pool, but not delays), and osteomyelitis (which is 3 phase hot). In children, a whole body
bone scan is often performed to evaluate extent. Additionally, because o f subperiosteal pus/
edema you can actually have decreased vascularity to the infected area (cold on initial phases)
but clearly hot on delayed phases.
In the spine, gallium (combined with bone scan) or MRI are the preferred imaging modalities
Three phase scan repsonse
You can also use a bone scan to evaluate response to treatment. Blood flow and blood pool
tend to stay abnormal for about 2 months, with delayed activity persisting for up to 2 years.
This is especially true when dealing with load bearing bones. Gallium67 and Indium111 WBC
are superior for monitoring response to therapy.
Three phase scan
Reflex Sympathetic Dystrophy (RSD):
Sometimes called “complex regional pain syndrome,” it can be seen after a stroke, trauma, or
acute illness. The classic description is increased uptake on flow and blood pool, with
periarticular uptake on delayed phase. The uptake often involves the entire extremity.
About one third o f adult patients with documented RSD do not show increased perfusion and
uptake (which probably means they are faking it, and need a rheumatology consult fo r
fibromyalgia). In children, sometimes you actually see decreased uptake.
Sulfur Colloid Bone Scan & WBC Imaging
Tc can be tagged to sulfur colloid with the idea o f getting a normal localization to the bone
marrow. You can actually perform Tc sulfur colloid studies to map the bone marrow in
patients with sickle cell (with the idea to demonstrate marrow expansion and bone infarct).
However, the major utility is to use it in combination with tagged WBC or Gallium.
Both Tc Sulfur Colloid and WBCs will accumulate in normal bone marrow, in a spatially
congruent way (they overlap). The principal is that infected bone marrow will become
photopenic on Tc-Sulfur Colloid. Now, this takes about a week after the onset of infection, so
you have to be careful in the acute setting. WBC, on the other hand, will obviously still
accumulate in an area o f infection.
Combined Tc-Sulfur Colloid and WBC study is positive fo r infection i f there
is activity on WBC image, without corresponding Tc S u lfu r Colloid activity on the bone marrow image
Tc sulfur colloid in infected bone
less uptake
In-WBc in infected bone
more uptake
Sulfur Colloid Bone Scan & WBC Imaging
the spine
When imaging the spine, WBC frequently fails to migrate showing a photopenic area
(WBC = False Negative in the Spinel. This is why gallium is preferred for osteomyelitis of
the spine.
gallium in infected bone
more uptake
ln-wbc less uptake in infected bone
false negative
Prosthesis Evaluation
Differentiating infection from aseptic loosening is challenging and the most common reason a
nuclear medicine doctor would get involved in the situation. Bone scan findings o f
periprosthetic activity is very nonspecific, because you can see increased tracer activity in a
hip up to 1 year after placement (even longer in cementless arthroplasty). Typically, there
would be diffusely increased activity on imaging with Tc-MDP in the case of infection (more
focal along the stem and lesser trochanter with loosening) - but this isn’t specific either.
Combined Tc-Sulfur Colloid and WBC imaging is needed to tell the difference.
Prosthesis evaluation is helful when negative
A negative bone scan excludes loosening or infection
Neuropathic Foot
Most commonly seen in the tarsal and tarsal-metatarsal joints (60%), in diabetics. When the
question is infection (which diabetics also get), it’s difficult to distinguish arthritis changes vs
infection with Tc-MDP. Again, combined marrow + WBC study is the way to go.
Neuropathic foot
next step
the need for a fourth phase
in diabetic feet. As these patient’s tend to have reduced peripheral blood flow, the addition of
a 4th phase at 24 hours may help you distinguish between bone and delayed soft tissue clearance.
When would you consider Tc99 HMPAO instead o f In-WBC for infection ? Two main reasons
(1) Kids - Tc99 will have a lower absorbed dose & shorter imaging time
(2) Small Parts - Tc99 does better in hands and feet
Why not use Tc99 HMPAO all the time ? The downsides to Tc99 HMPAO are:
(1) It has a shorter half life -6 hrs- which limits delayed imaging, and
(2) It has normal GI and gallbladder activity which obscures activity in those areas.
In-WBC Chem and Pharm
• The vast majority (like 90%) o f the labeled cells are Neutrophils. This allows you to
“trace” anything that triggers neutrophil migration (inflammation / infection).
• The radiation dose that the Indium deposits on the neutrophil doesn’t mess with its
function (supposedly). Lymphocytes on the other hand, tend to be killed by the radiation
(they don’t turn into cancer).
• In the normal situation the critical organ is the spleen.
• If the cells become fragmented - the Indium binds with transferrin and you see more
uptake in the liver and bone marrow.
If 1940 calls and wants to rule out a PE
you’ll want to get the angiography room ready. In 2014,
textbooks and papers still frequently lead with the following statement “Pulmonary’ angiography is
the definitive diagnostic modality and reference standard in the diagnosis o f acute PE. “ In reality,
pulmonary angiography is almost never done, and CTPA is the new diagnostic test of choice. V/Q
scan is usually only done if the patient is allergic to contrast or has a very low GFR. The primary
reason V/Q isn’t done is that it’s often intennediate probability, and the running joke is that if you
don’t know how to read one, just say it’s intermediate and you’ll probably be right.
The idea behind the test is that you give two tracers: one for ventilation and one for perfusion. If you
have areas of ventilated lung that are not being perfused, that may be due to PE. Normally
Ventilation and Perfusion are matched, with a normal gradient (less perfusion to the apex - when
standing).
Tracers
perfusion
For perfusion, Tc-99m macroaggregated albumin (Tc-99m MAA) is the most common
tracer used. MAA is prepared by heat denaturation of human serum albumin, with the size of the
particles commercially controlled. You give it IV and the tracer should stay in the pulmonary
circulation (vein-> SVC-> right heart -> pulmonary artery -> lung *STOP). The tracer should light up
the entire lung. A nonnal perfusion study excludes PE. Areas of perfusion abnormality can be from
PE or other things (more on this later). The biologic half life is around 4 hours (they eventually fall
apart, becoming small enough to enter the systemic circulation to eventually be eaten by the
reticuloendothelial system).
tracers
ventilation
There are two ways to do the ventilation; you can use a radioactive gas (Xenon-133) or a radioactive aerosol (Tc-99m DTPA).
xenon 133
The physical half-life is 5.3 days, the biologic half-life is 30 seconds (you breath it out). Because it has low energy (81 keV) it is essential to do this part of the test first (more on this in the physics chapter). Additionally, because the biologic half life is so short, you only can
do one view (usually posterior) with a single detector (dual detector can do anterior and posterior). There are 3 phases to the study: (1) wash in (single max inspiration and breath hold), (2) equilibrium (breathing room air and xenon mix), and (3) wash out (breathing normal air).
Tc99m DTPA
This one requires patient cooperation because they have to breath through a
mouth guard with a nose clamp for several minutes. It is also essential to do this part of the test first.
Quantitative Perfusion
overview
You can do quantitative studies typically to evaluate prior to lung resection, or prior to transplant.
You want to make sure that one lung can hold its own if you are going to take the other one out.
Quantitative Perfusion
testable trivia
Quantification is NOT possible if you use Tc-99 DTPA aerosol. You can do it with a
combined Xe + Tc MAA because the Xe will not interfere with the Tc.
Trivia Questions about Tc99m MAA
They show tracer in the brain
This is a classic way o f showing you a shunt (it got into the systemic circulation somehow, maybe an ASD, VSD, or Pulmonary AVM).
Trivia Questions about Tc99m MAA
How big are the particles?
A capillary is about 10 micrometers. You need your particles to stay in the lung, so they can’t be smaller than that. You don’t want them to be so big they block arterioles (150 micrometers). So the answer is 10-100 micrometers.
Trivia Questions about Tc99m MAA
When do you reduce the particle amount?
few situations. You don’t want to
block more than about 0.1% o f the capillaries, so anyone who has fewer
capillaries (children, people with one lung). Also you don’t want to block
capillaries in the brain, so anyone with a right to left shunt. Lastly anyone with
pulmonary hypertension (or who is pregnant).
Trivia Questions about Tc99m MAA
Is reduced particle the same as reduced dose?
Nope. The normal dose of Tc can be added to fewer particles.
Trivia Questions about Tc99m MAA
They show you multiple focal scattered hot spots
This is the classic way of showing “clumped MAA” , which happens if the tech draws blood into the syringe prior to injection.
Classic Trivia Questions for Xenon 133:
They show you persistent pulmonary activity during washout’.
This indicates Air Trapping (COPD)
Classic Trivia Questions for Xenon 133:
They show you accumulation o f tracer over the RUQ
This is fatty infiltration of the liver (xenon is fat soluble).
Classic Trivia Questions forTc-99m DTPA
Xenon
Quick Wash Out only one or two views
Activity homogenous in the lungs
Classic Trivia Questions forTc-99m DTPA
TC-99m DTPA
Slower Wash Out - multiple projections
“Clumping” common in the mouth,
central airways, and stomach (from
swallowing).
VQ scan
What i f you see tracer in the thyroid or stomach on VQ Scan??
You should think 2 things: (1) Free Tc, or (2) Right - to - Left Shunt
VQ scan
What do you need to call a Right - to - Left Shunt ?
tracer in the brain
VQ scan
I f you suspect a shunt (or the shunt is known) how do you alter the scan?
You reduce the number o f particles. If the normal amount o f particles is around 500K., you would reduce it to around 100K.
VQ scan
What i f the patient has pulmonary> hypertension?
reduce the particles
VQ scan
Particle reduction is the same as dose reduction?
Nope. You keep the dose the same - otherwise the study is non-diagnostic.
VQ scan
What about a neonate ? Do you do anything different?
What about a neonate ? Do you do anything different?
A: Yes - major particle reduction. Down to 10K- 50K particles (depending on who you
ask). The reason is that kids have less capillaries than adults. An adult number of
particles (500K) could functionally cause a PE - by blocking the majority of the
capillaries.
VQ scan
What i f you see a unilateral perfusion defect (o f the whole lung), but no ventilation defect ?
Get a CT or MRI. DDx is gonna be a mass, fibrosing mediastinitis, or Central PE.
O f those which is the MOST COMMON?
A: Most sources will say “central obstructing mass” i.e. “bronchogenic carcinoma”
VQ scan
How do you grade this unilateral perfusion defect (o f the whole lung), but no ventilation defect ?
te hnically low probability
Gallium 67 Scan
overview
The body handles Ga+3 the same way it would Fe+3 - which as you may remember from
step 1 gets bound (via lactoferrin) and concentrated in areas of inflammation, infection,
and rapid cell division. Therefore it’s a very non-specific way to look for infection or
tumor. Back in the stone ages this was the gold-standard for cancer staging (now we use
FDG-PET). 1 should point out that Gallium can also bind to neutrophil membranes even
after the cells are dead, which gives it some advantages over Indium WBC - especially in
the setting o f chronic infection.
Gallium 67 Scan
creation
Gallium is produced in a cyclotron via the bombardment
of Zn68, at which point it’s complexed with citric acid to
make Gallium Citrate. The half life is around 3 days
(78hours). It decays via electron capture, emitting gamma
rays at 4 photopeaks
Gallium 67 Scan
4 photopeaks
93 keV - 40%
184 k eV -2 0%
300 keV - 17%
393 keV - 5%
Gallium 67 Scan
imaging
Images are not typically done sooner than 24 hours -
because background is too high. The critical organ is the
colon. Remember “critical organ” = the first organ to be
subjected to radiation in excess o f the maximum allowable
amount.
Gallium 67 Scan
normal localization
Liver (which is the highest uptake), bone marrow ( “Poor Mans s
hone sca n”), spleen, salivary glands, lacrimal glands, breasts (especially if lactating, or
pregnancy). Kidneys and bladder can be seen in the first 24 (faintly up to 72 hours). Faint
uptake in the lungs can be seen in < 24 hours. After 24 hours you will see some bowel. In
children the growth plates and thymus.
Gallium 67 Scan
poor mans bone scan
Uptake is in both cortex (like regular bone scan) and marrow. Degenerative change, fractures, growth plates, all are hot - just like bone scan.
Gallium uptake is nonspecific and can be seen with a variety o f things
infection,
but also CHF, atelectasis, and ARDS.
Sarcoidosis
overview
The utility o f Gallium in Sarcoidosis patients is to help look for active disease. Increased
uptake in the lungs is 90% sensitive for active disease (scans are negative in inactive
disease). Additionally, Gallium can be used to help guide biopsy and lavage - if looking to
prove the diagnosis. The degree o f uptake is graded relative to surrounding tissue (greater
than lung is positive, less than soft tissue is negative).
Sarcoidosis
classic signs
- Lambda Sign - The nuke equivalent to the “ 1 -2-3 Sign” on Chest x-ray. You have
increased uptake in the bilateral hila, and right paratracheal lymph node. - Panda Sign - Prominent uptake in the nasopharyngeal region, parotid salivary gland,
and lacrimal glands. This can also been seen in Sjogrens and Treated Lymphoma.
Other Noninfectious Things
- Gallium can be used to show early drug reaction from chemotherapy (Bleomycin) or
other drugs (Amiodarone). - Gallium is elevated in IPF (idiopathic pulmonary fibrosis) and can be used to monitor
response to therapy.
PCP
Gallium Hot, Characteristic Gallium Pattern is Diffuse Bilateral Pulmonary Uptake
Kaposi Sarcoma
Gallium Negative, Thallium Positive
Galium 67 - Pneumonia
- Lung Uptake at 72 Hours
Bacterial Pneumonia
gallium?
Intense lobar configuration without parotid or nodal uptake.
Misc Infections That Gallium Can Pick Up:
• Abdominal and Pelvic Infections - In-111 WBC is superior to Gallium
(Gallium has some normal GI uptake).
• Malignant Otitis Media - Will be both Gallium and Bone Scan (Temporal Bone) Hot.
• Spinal Osteomyelitis - Gallium is superior to Indium WBC for spinal infections.
Thyroid overview
The thyroid likes to drink Iodine (it’s sort o f its job). Imaging takes advantage of this with
Iodine analogs. The distinction between “trapping” and “organification” is a common
question.
Thyroid
trapping
Analog is transported into gland. I23I, l3lI, and 99mTc all do this.
Thyroid tracer
I-131
The major advantage here is that it’s cheap as dirt. The disadvantage is that it has a
long half life (8 days), and that it’s a high energy (364 keV) beta emitter. The high energy
makes a crappy image with a ‘A inch crystal. It’s ideal for therapy, not for routine imaging.
It’s contraindicated in kids and pregnant women.
Thyroid tracer
Tc 99m
Remember that this guy is trapped but not organified. Background levels are higher
because only 1-5% o f the tracer is taken up by the thyroid gland. A common scenario to
choose Tc over Iodine is when they’ve had a recent thyroid blocker on board (iodinated
contrast is the sneaky one).
Thyroid
trivia
Thyroid formation takes place in fetus at 8-12 weeks
Thyroid tracer
I-123
This guy has a shorter half life (13 hours) and ideal energy (159 keV). It decays via
electron capture and all around makes a prettier image. The problem is that it costs more.
Thyroid
organification
Analog is oxidized by thyroid peroxidase and bound to tyrosyl
moiety. I23I and l3ll do this. 99mTc does NOT do this. Instead 99mTc slowly washes
out o f the gland.
Random Trivia on Breastfeeding
- Tc-99m: You can resume breast feeding in 12-24 hours
- 1-123: You can resume breast feeding in 2-3 days
- 1-131: You should not breast feed - pump and dump.
Iodine Uptake Test:
You give either 5 micro Ci o f 131 or 10-20 micro Ci o f 123. This is conventionally reported
at 4-6 hours, and 24 hours. Normals are 5-15% (4-6 hours), and 10-35% at 24 hours. A
correction for background is done on measurements prior to 24 hours (using the neck counts
- thigh counts).
Iodine Uptake Test:
factors affecting the test
Renal Function (increases stable iodine pool, reduces numbers)
Dietary Iodine - variable and controversial
Medications - thyroid blockers, Nitrates,
IV Contrast, Amiodarone
Iodine Uptake Test
increased uptake
graves
Early hashimoto
Rebound after Abrupt withdrawal of antithyroid medication
Dietary Iodine Deficiency
Iodine Uptake Test
decreased uptake
Primary or secondary causes of Hypothyroidism
Renal failure
Medications (thyroid blockers, Nitrates, IV Contrast, Amiodarone)
Dietary iodine overload
Graves disease
overview
About 75% of the time, if you have hyperthyroidism the
cause is going to be graves. Graves is an autoimmune
disease where an antibody to the thyrotropin receptor
stimulates the thyroid to produce hormone. TSH will be
very low, where T3 and T4 will be high. The classic
clinical scenario is a middle aged women with a protracted
course, pre-tibial edema, and exophthalmos. Scintigraphy
is going to give you a homogeneously increased gland,
with uptakes increased at both 4 hours and 24 hours.
Sometimes the 24 hour uptake is lower than the 4 hours (or
even at a normal range) - this is from rapid thyroid
hormone production.
Graves disease
visualization of the pyramidal lobe
The pyramidal lobe is seen in about 10%
o f normal thyroids. In patients with Graves disease it is seen as much as 45% of the time. Therefore, it’s suggestive when you see it.
Graves disease
quick
Diffuse homogenous uptake
Multi-nodular Toxic Goiter (Plummer Disease):
The classic scenario is an
elderly women with weight loss, anxiety, insomnia, and tachycardia. The gland is typically
heterogeneous, with uptake that is only moderately elevated. The nodules will be hot on the
background o f a cold gland.
Toxic Multi-nodular Goiter vs Non-Toxic Multi-nodular goiter
The toxic goiter will have hot nodules on a background o f cold thyroid. The Non-toxic one will have warm/hot nodules on a normal background of the thyroid.
Graves quick
Uptake High : 70s (typically > 50%)
homogenous
Toxic Multi-Nodular Goiter
quick
Uptake Medium High: 40s (typically <50%)
heterogenous
Hashimotos
The most common cause of goitrous hypothyroidism (in the US). It is an autoimmune
disease that causes hyper first then hypothyroidism second (as the gland bums out later). It’s
usually hypo - when it’s seen. It has an increased risk of primary thyroid lymphoma.
Step 1 trivia; associated with autoantibodies to thyroid peroxidase (TPO) and antithyroglobulin.
The appearance o f the hypothyroid gland is typically an inhomogeneous gland
with focal cold areas. The hyperthyroid (acute) gland looks very much like Graves with
diffusely increased tracer.
Subacute Thyroiditis
If you have a viral prodrome followed by hyperthyroidism, and then thyroid uptake scan
shows a DECREASED % RAIU you have de Quervains (Granulomatous thyroiditis).
During this acute phase, the disease can mimic Graves with a low TSH, high T3 and high T4
The difference is the uptake scan. After the gland bums out, it may stay hypothyroid or
recover. If they ask you about this, it’s most likely going to try and fool you into saying
Graves based on the labs, but have a low % RAIU.
Solitary Nodules
thyroid
20-40% Cold Nodules = Cancer
< 1% Warm Nodules = Cancer
Hot Nodule vs Cold Nodule
Most thyroid nodules are actually cold, and therefore most are benign (colloid, cysts, etc..).
In fact, cold nodules in a multi-nodular goiter are even less likely to be cancer compared to a
single cold nodule. Having said that, cold nodules are much more likely to be cancer when
compared to a functional (warm) nodule.
Discordant Nodule
This is a nodule that is HOT on Tc” but COLD on I123. Because some
cancers can maintain their ability to trap, but lose the ability to organify a hot nodule on Tc, it
shouldn’t be considered benign until you show that it’s also hot on I 123.
Gamesmanship: Iodine vs tc
A classic move is to show you a thyroid that will take up Tc, but NOT Iodine on 24 hour
imaging. This can be from a couple o f things: (1) congenital enzyme deficiency that
inhibits organification, (2) a drug like propylthiouracil that blocks organification.
Now if they just show you an Iodine Thyroid with low uptake on 24 hours, this is de Quervains, or a burned out Hashimotos.
I131 can be used to treat
both malignant and non-malignant thyroid disease.
Thyroid Cancer
overview
Papillary is the most common subtype (papillary is popular), and it does well with surgery + 1-131.
Medullary thyroid CA (the one the MENs get), does NOT drink the 1-131 and therefore
doesn’t respond well to radiotherapy. Prior treatment can also make you more resistant to
treatment, and re-treatment dosing is typically 50% more than the original dose.
Thyroid Cancer
things taht make you tratment resistan
- Medullary Subtype CA (will not drink the tracer)
- History of prior 1-131 (“easy gland has been killed o ff ’)
- History o f Methimazole treatment (even if years ago)
Thyroid Cancer
medullary subtype CA
Neuroendocrine in origin, so can occasionally (around 10%) have uptake on MIBG or Octreotide. They will be cold on thyroid scan and don’t drink the treatment 1-131. If forced to pick - I’d go with Octreoscan for medullary CA. Associated with MEN 2a and 2b
Thyroid Cancer
tratment timeline
So, normally the patient gets diagnosed and then they go for surgery. After surgery they will
come to nuclear medicine. You expect that they will have some residual thyroid (it’s really
hard to get it all out). Prior to actually treating them you will give them a tiny dose o f 1-131 to
see how much thyroid they have left. If the uptake is less than 5% this is ideal. Uptake more
than 5% will result in a painful ablation (may need steroids on top of the NSAIDs) and may
need to go back to the OR. Next, you will treat them. You want their TSH really ramped up.
The higher the TSH the thirstier the cancer /residual thyroid tissue. An ideal TSH is like 50
(30 would be a minimum).
Radioiodine Therapy
How do you get the TSH up?
o (1) is to stop the thyroid hormone (post op they are obviously hypothyroid),
o (2) is to give recombinant TSH “Thyrogen.”
Radioiodine Therapy
How do you decide on dosing?
Dosing is dependent on the stage of the disease; 100 for thyroid only, 150 for thyroid
+ nodes, 200 for distal. They are told about the precautions etc… Then you give them
the dose. Before you let them go home, you test them to see if they need to go to the
hospital.
Radioiodine Therapy
So when do patients need to he admitted to the hospital?
NRC limit is 7mR/h measured at 1 meter from the patient’s chest (some agreement
states use 5 mR/h). The number to remember is 33 mCi of residual activity (or 30
mCi in some strict agreement states).
Radioiodine Therapy
Possible Side Effects o f Treatment:
- Can cause pulmonary fibrosis if given to patient with lung mets. This is really only the case of macro-nodular disease (as opposed to micronodular disease). That isn’t necessarily a contraindication
- Sjogrens have a greater risk of salivary gland damage
- Salivary gland damage is dose related - so cancer treatment patients have a greater risk
Radioiodine Therapy
What routes does the body use to eliminate I, i l?
Urine is the main way it is eliminated but sweat, tears, saliva, and breast milk are other
routes.
Radioiodine Therapy
I f they don’t need to be admitted to the hospital, what precautions should they take?
There is a whole bunch of crap they are asked to do. Drink lots of water (increase renal excretion). Suck on hard candy (keep radiotracer from jacking your salivary glands). Patients are encouraged to stay away from people (distance principal). Sleep alone for 3 days (no sex, no kissing - keep that dirty dick in your pants!). Good bathroom hygiene (flush twice, and sit down if you are a guy). Use disposable utensils and plates. Clothes and linens should be washed separately. Most of these things are done for 3 days.
Radioiodine Therapy
Is it ok to breast feed? Is it ok to try> and get pregnant?
- No breast feeding. If you take I131 your breast feeding days are over (at least this time
around) . - No getting pregnant for at least 6-12 months after therapy
Radioiodine Therapy
other trivia
- If you participated in the therapy, you need your thyroid
checked 24 hours later. - If the patient got admitted to the hospital the RSO needs to
inspect the room after discharge before the janitor can
clean it or the next patient can move in. - Thyroglobulin is a lab test to monitor for recurrence.
Anything over zero - after thyroidectomy, is technically
abnormal, although the trend is more important (going up
is bad)
‘ Severe uncontrolled thyrotoxicosis and pregnancy are
absolute contraindications.
Radioiodine Therapy
gamesmanship for iodine post treatment
If you see an Iodine Scan,
and you see uptake in the
liver , this is ALWAYS a post
treatment scan.
Radioiodine Therapy
pt is on dialysis and needs I131 rx
Give I131 immediately following dialysis to maximize the time the I131 is on board. Decrease
dose as there is limited (essentially no) excretion until next dialysis. Dialysate can go down
sewer. Dialysis tubing needs to stay in storage.
Hyperthyroidism
treatment
I131 can also be used to treat hyperthyroidism. Dosing depends
on the etiology; 15 mCi for Graves (more vascular), 30 mCi
for multi nodular (harder to treat the capsule). Again the TSH
must be high for the therapy to be effective. By 3-4 months,
there should be clinical evidence of resolution of signs and
symptoms of hyperthyroidism, if 1-131 therapy was
successful.
Hyperthyroidism
emergent treatment
As an aside, there is no such thing as an “emergent
hyperthyroid treatment.” You can always use meds to cool it
down. The standard medication is Methimazole. However, if
there is an allergy to Methimazole, the patient is having WBC
issues (side effect is neutropenia) or the patient is pregnant
-use propylthiouracil (PTU). PTU is recommended during
pregnancy.
Hyperthyroidism
thyroid eye disease
It’s controversial, but some people believe that thyroid eye
disease will worsen after 1-131 treatment. If you are prompted, I would just have optho look at
their eyes, bad outcome is likely severity related. *You might not want to treat a bug-eyed dude
(depends on who you ask).
Hyperthyroidism
wolff-chaikoff effect
Since we are talking about hyperthyroid treatment, there is no better time than
to discuss the W.C. effect. Essentially, this is a reduction in thyroid hormone levels caused by ingestion
of a large amount of iodine. The Wolff-Chaikoff effect lasts several days (around 10 days), after which
it is followed by an “escape phenomenon.” The W.C. effect can be used as a treatment principle
against hyperthyroidism (especially thyroid storm) by infusion of a large amount of iodine to suppress
the thyroid gland. The physiology of the W.C. effect also explains why hypothyroidism is sometimes
produced in patients taking several iodine-containing drugs, including amiodarone.
What Causes Hyperparathyroidism ?
- Most common cause is a hyperfunctional adenoma (85%).
- Second most common cause is multiple gland hyperplasia (12%).
- Third most common cause is cancer (3%).
Parathyroid
Nuclear medicine can offer two techniques to localize these lesions;
dual phase and dual tracer
Dual Phase Technique
In dual phase technique, a single tracer (Tc”-Sestamibi) is administered, and both early (10
mins) and delayed (3 hours) imaging is performed. The idea is that sestamibi likes things with
lots of blood flow, and lots of mitochondria. Parathyroid pathology tends to have both of
these things, so the tracer will be more avid early, and stick around longer (after the tracer
washes out of normal tissue). SPECT can give you more precise localization.
Dual Phase Technique
initial phase
both thyroid and parathryroid
Dual Phase Technique
delayed phase
uptake remains in abnormal parathyroid (hyperplasia in this case)
Dual Phase Technique
trivia
Sestamibi parathyroid imaging depends on mitochondrial density and blood flow
Dual Phase Technique
false positives
Caused by things other than parathyroid pathology that like to drink Sestamibi.
• Thyroid Nodules
• Head and Neck Cancers
• Lymphadenopathy
Dual Tracer Technique
overview
In dual tracer technique two different agents are used and then subtraction is done. The first
agent is chosen because it goes to both thyroid and parathyroid (options are either Tc99-
Sestamibi or 201- Thallium Chloride). The second agent is chosen because it only goes to the
thyroid (options are either 1-123 or Pertechnetate). When subtraction is done, anything left hot
could be a parathyroid adenoma.
Dual Tracer Technique
problems
- Mo Tracers, Mo Problems
- Motion: subtraction imaging can’t tolerate much motion
- Stuff Messing with the Thyroid Tracers: recent iodinated contrast, etc…
Parathyroid
implantatio
The parathyroid gland can be surgically implanted into the forearm - typically done with hyperplasia surgery where they carve out 3 1/2 glands.
Parathyroid
what is considered successful treatment
Successful surgical treatment of hyperparathyroidism is often defined as intra-operative reduction of
PTH by 50%.
Parathyroid
false positive
Thyroid adenoma (most common), thyroid cancer, parathyroid cancer.
Parathyroid
false negative
Small sized adenoma (most common), 4 gland hyperplasia. A negative study in the setting of abnormal / suspicious labs should raise concern for these things (multiple gland
hyperplasia or a small adenoma).
Gamesmanship - MIBI - Lymph Nodes
On any study, parathyroid or a heart, if the tracer is MIBI than you should NOT see lymph
nodes. If you see lymph nodes they are suspicious (maybe cancer). Next step would be
ultrasound to further evaluate them.
Oh, and don’t forget about focal breast uptake (also cancer), - Breast Specific Gamma Imaging (BSGI) uses MIBI for a reason.
planar imaging is used for
brain death
planar imaig uses and is proportional to
lipophilic perfusion agents
proportional to blood flow
Spect imaging uses and is proportional to
lipophilic perfusion agents
proportional to blood flow
PET imagingis proportional to
metabolism
CNS Nukes agents
extracted
Can be used for Parenchymal Imaging)
HMPAO
ECD
CNS Nukes agents
not extracted
(Not used for Parenchymal Imaging - i.e. no SPECT)
DTPA
THIS vs THAT -HMPAOand ECD
Tc HMPAO (hexamethylpropyleneamine oxime) and Tc ECD (ethyl cysteinate dimer).
HMPAO and ECD can be used in both dementia imaging and for seizure focus localization.
These studies are typically performed with SPECT. The idea behind brain SPECT is that you
can look at brain blood flow, which should mimic metabolism. These two agents are neutral
and lipophilic, which lets them cross the blood brain barrier and accumulate in the brain.
Where and how much they accumulate should follow flow (and metabolism).
HMPAO overview
Neutral and Lipophilic
Accumulate in the cortex proportional to blood flow (Gray Matter > White Matter)
washout is fast
Uptake favors the frontal lobe, thalamus, and cerebellum
ECD Overview
Neutral and Lipophilic
Accumulate in the cortex proportional to blood flow (Gray Matter > White Matter)
Washout is slow (more rapid clearance
from blood p o o l)
Uptake favors the parietal and occipital lobes
* Makes comparison between HMPAO and
ECD difficult
HMPAO and ECD
Key points
Both agents pass blood brain barrier and stick to gray matter proportional to CBF
HMPAO washes out faster
ECD washout is slower, has better background clearance, and does not demonstrate intracerebral redistribution.
Tc- DTPA
overview
Unlike HMPAO or ECD, this agent is lipoPHOBIC - and is best thought o f as an “angiographic tracer” because it stays in the blood (or CSF if you put it there).
Tc- DTPA
key points
DTPA does NOT cross the blood brain barrier and therefore cannot be used for brain parenchymal imaging. *You can NOT do SPECT
Has the advantage over HMPAO and ECD in that it can be repeated without delay
DTPAs main utility is for shunt studies. NPH, and Brain Death.
Seizure Focus
The idea is that a seizure focus will be hot (hypermetabolic and hyperperfusion) during the seizure “ictal.” Then cold between seizures “interictal.” You need to inject tracer (HMPAO or ECD) within 30 seconds o f the seizure to get a good study. PET can be used, but is less practical.
Thallium 201
overview
Thallium is produced in a cyclotron, decays via electron capture, and has a half life of
around 3 days (73 hours). The major emissions are via the characteristic x-rays o f its
daughter product Mercury 201 - at 69 keV and 81 keV. The tracer is normally given as a
chloride and will therefore rapidly be removed from the blood
Thallium 201
behaves
Thallium behaves like potassium, crossing the cell membrane by active transport (Na+/
K pump). Tumors and inflammatory conditions will increase the uptake o f this tracer.
The higher the grade tumor, the more uptake you get. As Thallium requires active
transport, it can be thought o f as a viability marker - you need a living cell to transport it.
Thallium 201
normal distribution
Thyroid, salivary glands, lungs, heart, skeletal muscle, liver, spleen,
bowel, kidneys, and bladder. Any muscle twitching will turn hot.
Thallium 201
using with gallium
If you are going to use it with Gallium, you must use the Thallium first as the Gallium
will scatter all over the Thallium peaks.
Thallium 201
high yield
Toxoplasma Infection is Thallium Negative
Lymphoma is Thallium Positive
Kaposi Sarcoma is Thallium Positive (Gallium Negative)
Tumor is Thallium Positive
Necrosis is Thallium Negative
CNS
Tumor vs Necrosis
The tracers used for SPECT tumor studies are different than
those used for dementia or seizures. The tumor tracers are
20ITI (more common) and 99mTc Sestamibi (less common).
20ITI is a potassium analog, that enters the cell via the Na/K
pump. Inflammatory conditions will increase the uptake o f this
tracer, but not as much as tumors. The higher the tumor grade,
the more intense the uptake. Thallium can be thought o f as a
marker o f viability, as it will localize in living tumor cells, and
not necrosis. The control is the scalp (abnormalities will have
greater uptake than the scalp). You can use Thallium in
combination with perfusion tracers (HMPAO).
CNS tumor
Thallium Hot,
HMPAO Cold
CNS NEcrosis
Thallium Cold,
HMPAO Cold
CNS Lymphoma vs Toxoplasmosis:
As discussed in the neuro chapter CNS lymphoma
vs CNS Toxoplasmosis can be a diagnostic
dilemma. Thallium has a role in helping to distinguish the two (Toxo Cold, Lymphoma Hot).
Typically CNS lymphoma, toxoplasmosis,
bacterial abscess, cryptococcus infection,
and tuberculosis are all positive on
Ga-67 scintigraphy.
CNS lymphoma will be positive on
Tl-201.
Brain Death
You are looking for the absence of intracerebral perfusion to confirm brain death. So that you don’t keep Grandma around as a piece of broccoli, you need to have a tourniquet on the scalp - otherwise you might think scalp perfusion is brain perfusion and say she’s still alive. You have to identify tracer in the common carotid - otherwise the study must be repeated. In the setting of brain death, tracer should stop at the skull base. The hot nose sign, is seen secondary to perfusion through the external carotid to the maxillary branches. As a point o f trivia - the hot nose sign cannot be used to call brain death , it is a “Secondary Sign.” Some institutions will say you have to image the kidneys (to prove adequate systemic circulation / perfusion) and the injection site (to prove the tracer didn’t
extravasate).
Hot nose sign
brain death
Stroke
overview
There is no reason, ever, under any circumstances known to man, women, or beast to ever, ever
use SPECT to diagnose stroke. Having said that, you can look at stroke with SPECT and will
therefore likely be asked questions about it.
Stroke
take home points
- Acute Stroke is Cold
- Subacute Stroke can be warm - from luxury’ perfusion (blood flow is more than dead cells need)
- Chronic Stroke is Cold
Ischemia (TIAs)
overview
You can evaluate for cerebrovascular reserve by first giving acetazolamide (Diamox) - which
is a vasodilator , followed by a perfusion tracer. Normally you should get a 3-4x increase in
perfusion. However, in areas which have already maxed out their auto regulatory
vasodilation (those at risk for ischemia) you will see them as relatively hypointense. These
areas of worsening tracer uptake may benefit from some revascularization therapy.
Ischemia (TIAs)
bottom line
Ischemic Tissue Looks WORSE (relatively) compared to surrounding tissue, after vasodilation (Diamox / Acetazolamide)
Ischemia (TIAs)
gamesmanship
= Diamox = Acetazolamide… don’t just remember one.
You don’t know which one they will use.
Ischemia (TIAs)
post diamox
Worsening Uptake = Ischemia This might benefit from revascularization. Next Step = Angio
FDG-PET CNS overview
PET can assess perfusion (15O-H20) but typically it uses l8FDG to assess metabolism (which
is analogous to perfusion). Renal clearance o f l8FDG is excellent, giving good target to
background pictures. Resolution o f PET is superior to SPECT.
It’s important to remember that external factors can affect the results; bright lights
stimulating the occipital lobes, high glucose (>200) causes more competition for the tracer
and therefore less uptake, e tc …
FDG-PET cns most common indication
The most common indication for FDG Brain PET is dementia imaging. Because blood flow
mimics metabolism HMPAO, and ECD can also be used for dementia imaging and the
patterns of pathology are the same.
CSF Imaging
overview
The principle involved in imaging the CSF consists o f intrathecal administration that will
safely follow CSF and remains in the CSF compartment until it is absorbed through the
conventional pathways. The most common tracer used is IMln - labeled DTPA. So, you
have to do an LP on the dude (it’s intrathecal).
CSF Imaging
normal examination
- Time Zero - You do the LP
- 2-4 hours it ascends and reaches the basal cisterns
- 4 hours - 24 hours it flows around the sylvian fissures and interhemispheric cistern
- At 24 hours it should clear from the basilar cisterns and be over the cerebral
convexities
CSF Imaging
abnormal examination
- Tracer in the lateral ventricles
* Failure to clear from the cisterns and localize over the convexities by 24 hours
Communicating Hydrocephalus
overview
Normal pressure hydrocephalus is wet, wacky, and wobbly (incontinent, confused, and ataxic)
clinically, and demonstrates “ventricular enlargement out of proportion to atrophy” on CT. Since radiotracer shouldn’t normally enter the ventricles, a radionuclide cistemogram cannot be used
to distinguish communicating from noncommunicating hydrocephalus. Historically (1930s) you could
tell by injecting the material directly into the lateral ventricles.
Communicating Hydrocephalus
on scintigraphy your looking for
• Early entry (4-6 hours) o f tracer into the lateral ventricles
* Persistence o f tracer in the lateral ventricle > 24 hours
’ Delay in Assent to the parasagittal region > 24 hours
Communicating Hydrocephalus this vs that nph
NPH vs Non Obstructive (Communicating) Hydrocephalus.
NPH will have a normal opening pressure on LP.
NPH quick
Persistent
Tracer in the
Ventricles
> 24 Hours
CSF Leak
overview
You can use CSF tracers to localize a leak. The most common sites of CSF leak (fistulas) are between
the cribriform plate and ethmoid sinuses, from the sella turcica into the sphenoid sinus and from the
ridge of the sphenoid to the ear. The study is like a bleeding scan, in that the leak must be active
during the test for you to pick it up.
CSF Leak
how is it done
You image around the time the CSF is at the basilar cisterns (1-3 hours) and also
image pledgets (jammed up the nose prior to the exam). You compare tracer in the pledgets to serum
(ratio greater than 1.5 is positive).
Shunt Patency
imaging findings
- Normal Test will show tracer in the peritoneum - shows distal end is patent.
- You can manually occlude the distal limb to force tracer into the ventricles - shows proximal end is patent.
If the tracer fails to reflux into the ventricles, or it does but then doesn’t clear, you can think proximal obstruction
• If there is delayed tracer flow into the peritoneum (> 10 minutes = delayed), this can mean partial distal obstruction.
Shunt Patency
imaging findings
- Normal Test will show tracer in the peritoneum - shows distal end is patent.
- You can manually occlude the distal limb to force tracer into the ventricles - shows proximal end is patent.
If the tracer fails to reflux into the ventricles, or it does but then doesn’t clear, you can think proximal obstruction
• If there is delayed tracer flow into the peritoneum (> 10 minutes = delayed), this can mean partial distal obstruction.
Gastric Emptying
gamesmanship 1
One sneaky way to test this would be related
to the differences between solid food and liquid food curves. The main point is that solids have a
“lag phase” in which the stomach helps grind up the food into smaller parts (liquids don’t have
this). Lag Time can be increased
in diabetic patients.
Gastric Emptying
gamesmanship 2
Another possible question is that “attenuation correction” plays a role in calculation of emptying times, as movement from the back of the stomach to the front can increase counts due to attenuation.
Gastric Emptying
pharmacology trivia
• Prokinetic drugs (which enhance gastric emptying) metoclopramide (Reglan), tegaserod
(Zelnorm), erythromycin, and domperidone (Motilium) are stopped at least 2 days prior
to the test. - this can cause a false negative exam.
• Opiates (which delay gastric emptying) are stopped 2 days prior to the test. These can
cause a false positive exam.
• Anticholinergic/ Antispasmodic drugs such as Donnatal, Bentyl, Robinul, and Levsin, are
stopped for 2 days prior to the test
• Serotonin receptor antagonists - the classic one being Ondansetron (Zofran) are fine and can
be given prior to the exam.
Gastric Emptying
standard meal
" 4 oz o f Egg Whites ■ 2 Slices o f White Bread - Strawberry Jam ■ Water ■ Tc Sulfur Colloid
Esophageal Transit
Used (rarely) in the evaluation of esophageal motility disorders.
The supposed advantage is the ability to give quantitative information. The patient is made to
fast overnight, then fed Tc-99 sulfur colloid. Dynamic imaging is performed and transit time
and /or residual esophageal activity is measured.
GI Bleeding:
overview
The goal of a GI bleeding scan is to localize the bleed (not to say there
is one). Bleeding scan is sensitive to GI bleed rates as low as at 0.1
ml/min (Mesenteric angiography requires 1-1.5 ml/min bleeding).
Before the Tc-99 can be tagged to a RBC (beta chain o f the hemoglobin)’, it must first be reduced.
This is accomplished with stannous ion (tin). This is referred to as “tinning.” There are 3 methods
GI Bleeding:
sensitivity
GI bleed scan sensitivity
— 0.1 ml/min
Angiogram sensitivity =
1.0 ml/min
GI Bleeding:
invivo
- Tin (stannous ion) is injected into the patient
- Then Tc-99m pertechnetate is injected
- Tin binds to the hemoglobin then reduces the Tc (which then binds)
Although the process is super simple, you only get about 60-80% of it bound. So you have
a lot o f free Tc and a dirty image (poor target to background). Sometimes it fails miserably
(via drug interaction - heparinized tubing, or recent IV contrast). The images are too
crappy for cardiac wall motion studies, but can work for GI bleeding.
GI Bleeding:
In Vivo - In Vitro (Modified Method)
- Tin (stannous ion) is injected into the patient
- After 15-30 mins, you pull 3-5 cc o f blood out o f an IV line into a syringe with both
Tc-99m pertechnetate and an anticoagulant - It’s then re-injected 10 mins later
This one does a little better, binding close to 85%. Drug interactions (like heparin) are the
most common cause o f failure.
GI Bleeding:
invitro
Blood is withdrawn and added to a kit with both Tin (stannous ion) and Tc. It’s then reinjected.
This method works the best (98% binding), but is the most expensive
GI Bleeding:
invitro
Blood is withdrawn and added to a kit with both Tin (stannous ion) and Tc. It’s then reinjected.
This method works the best (98% binding), but is the most expensive
GI bleeding image acquisition
GI bleeding scan is acquired with DYNAMIC imaging (as opposed to 5
min static, transmission, SPECT, or dual tracer protocol). This allows the detection of
intermittent bleeds and better localization of the origin of the bleed.
GI Bleeding
reading the study
(1) Tracer outside the vascular distribution
(2) Tracer that Moves like bowel
(can be antegrade or retrograde)
(3) Tracer that Increases Intensity over time
The distal colon is an exception to the rule of
mobility — tracer here may not move.
GI Bleeding
normal
No Abnormal Tracer
Accumulation. Normal Uptake in Blood
Pool, Liver, & Heart.
GI Bleeding
abnormal
Abnormal Tracer
accumulation at the Hepatic Flexure,
increases over time. SMA territory 9could be anywhere or any territroy)
GI Bleeding
overview
You can get faked out by a lot of stuff; renal
or bladder excretion (possibly with hydro),
transplant kidney (classic trick - but again it
won’t move), varices or angiodysplasia (these
shouldn’t move), a penis with blood in it (this
will look like a penis), hemangioma (this will
be over the liver or spleen - and not move),
and the last trick - Free Tc in the stomach.
It you see gastric uptake * next look at the
salivary glands and thyroid to confirm it’s
free Tc, and not an actual bleed.
Rapid Review of Vascular Territories
- Celiac: Distal Esophagus, Stomach, 1st part of the Duodenum
- SMA: 2nd - 4th Parts o f the Duodenum, the rest o f the small and large bowel to the transverse colon at the level o f the splenic flexure.
- IMA: Distal 1/3 of the Transverse Colon to the Proximal Rectum
Alternative (Stone Age) Way o f Doing A Bleeding Scan;
Back when dinosaurs roamed the
earth, they used to do bleeding scans with Tc Sulfur Colloid. This had a variety of disadvantages: fast clearance (had to do scan in 30 mins), multiple blind spots (the stomach,
splenic flexure, and hepatic flexures - as sulfur colloid goes to the liver and spleen normally).
The only possible advantages are that it requires less prep and has good target to background
Meckel Scan
overview
The Meckel Diverticulum is a remnant of the
omphalomesenteric duct located near the
distal ileum. These things can have ectopic
gastric mucosa and present with painless
bleeding in the pediatric population.
Pertechnetate is used because it is taken up
by gastric mucosal cells. So you are looking
for tracer uptake in the pelvis (usually RLQ)
around the same time as the stomach.
Meckel Scan
gastric mucosa
Only about 10-30% o f Meckels diverticulum
will have eastric mucosa (these are the ones
most likely to bleed).
Meckel Scan
tricks
- You need to do the study when the patient is NOT bleeding (if they are bleeding -
then do a bleeding scan). - Pre-Treatment: You can use a bunch of different stuff to make the exam better:
O Pentagastrin - enhances uptake o f pertechnetate by gastric mucosa (also
stimulated GI activity)
0 H2 Blockers (Cimetidine and Ranitidine) block secretion of the pertechnetate
out o f the gastric cells making it stick around longer.
O Glucagon - slows gastric motility. - False Positive: Can occur from bowel irritation (recent scope, laxative use)
- False Negative: Recent In vivo labeling of RBCs , Recent Barium Study
(attenuated)
HIDA Scan
overview
Function and integrity of the biliary system can be evaluated by using Tc-99m labeled tracers that mimic
bilirubin’s uptake, transport, and excretion. All the tracers are basically analogs of this iminodiacetic acid
stuff.
Normally, the liver will have prompt tracer uptake (within 5 minutes), then you will have excretion into
the ducts, then the bowel - pretty much the same time you see the gallbladder. If the gallbladder is sick
(obstructed), it will still not have filled within 60 min. This is the basic idea.
HIDA Scan
trivia
You need higher doses o f tracer if the patient has hyperbilirubinemia
HIDA Scan
prep
Prep for the test is diet control. You need to have not eaten within four hours (so your gallbladder is ready
to fill), and have eaten within 24 hours (so your gallbladder isn’t so full, it can’t let any tracers in). If you
haven’t eaten for over 24 hours, then CCK can be given.
HIDA Scan
cck
makes teh GB contract
HIDA Scan
rim sign
A curved area of increased activity along the gallbladder fossa (hot rim, or pericholecystic hepatic activity sign) suggests a more angry gallbladder - (supposedly seen in 20% of gangrenous cholecystitis).
HIDA Scan
cystic duct sign
This sign is seen with acute
cholecystitis. The sign describes a
nub of activity in the cystic duct, with
the
HIDA Scan
mechanism of the rim sign
The mechanism is the result
o f inflammation causing regional hepatic hyperemia, with
more radiopharmaceutical being delivered to this area o f
hepatic parenchyma’.
HIDA Scan
chronic cholecystitis
This can be shown two ways; (1) delayed filling o f the GB (not seen at 1 hour, but seen at 4 hours), or (2) with a low EF (< 30%) with CCK stimulation. A reduced EF can also be seen in acute acalculous cholecystitis.
HIDA Scan
testable trivia
- The Dose o f CCK: 0.02 microgram/kg over 60 mins
- The Dose o f Morphine 0.02-0.04 mg/kg over 30-60 mins
HIDA Scan
biliary obstruction
The classic way to show this is a lack of visualization o f the
biliary tree - sometimes call a “Liver Seem S ig n ” It’s caused by back pressure in an
obstructed CBD.
HIDA Scan
P rom p t U p ta k e - W ith D e la y e d E x c re tio n (M e d ic a tio n )
Cholestatic jaundice can be drug induced. The classic offenders:
Chlorpromazine, Erythromycin. Birth Control (Estrogens), Anabolic
Steroids, and sometimes Statins. This can mimic biliary obstruction.
HIDA Scan
P rom p t U p ta k e - W ith D e la y e d E x c re tio n (M e d ic a tio n )
Cholestatic jaundice can be drug induced. The classic offenders:
Chlorpromazine, Erythromycin. Birth Control (Estrogens), Anabolic
Steroids, and sometimes Statins. This can mimic biliary obstruction.
THIS vs THAT: Biliary Atresia VS Neonatal Hepatitis
If you see a hepatobiliary scan (HIDA) in a kid, for sure this is the indication. Apparently,
these two things are hard to tell apart clinically. If you see tracer in the bowel it’s hepatitis,
but just remember that it might be slow so you need super delays (24 hours if necessary). If
you don’t see it in the bowel, you might still need to repeat the study if you didn’t charge up
those hepatocytes with some phenobarb (up regulates the cytochrome system). In other
words, a lot of places pre-medicate with phenobarbital to increase the utility o f the test. If
you operate early (Kasai procedure) they do a lot better, so it’s important not to screw this up.
THIS vs THAT: Biliary Atresia VS Neonatal Hepatitis
trivia
Dose of Phenobarb to prime the liver = 5 mg/kg x 5 days “5 fo r 5 keeps the liver alive ”
Technically it ’s 2.5 mg/kg twice a day - but that doesn t rhyme
Bile Leak
overview
You can use HIDA tracer after trauma or surgery to look for bile leak. The trick is that you need delayed images, and look in the right paracolic gutter / pelvis. You can get tracer in the gallbladder fossa, mimicking a gallbladder.
Bile Leak
reappearing liver sign
Labeled bile may track superiorly into the peri-hepatic space and coat the surface of the liver. This can give the appearance o f paradoxically increasing activity in the liver after an initial decrease in activity from liver emptying into the bowel.
HIDA Scan - Rapid Path Summary
No Bowel Activity, Persistent Blood Pool = Hepatocyte Dysfunction (Hepatitis)
No Bowel Activity, Blood Pool Goes Away Normally = Common Duct Obstruction
No Gallbladder Activity x 4 hours (or 1 hour + morphine) = Acute Cholecystitis
Abnormal GB emptying (EF < 30%) = Chronic Cholecystitis
HIDA Scan
narcotics
Most people will say something like - “hold the morphine for at least 6 hours — or 3 half lives -
prior to the HIDA scan.” Having said that narcotics alone should not prevent you from seeing the
gallbladder. What narcotics can do is delay bowel visualization by triggering the sphincter of oddi
to contract. This can mimic a biliary obstruction.
Don’t get it twisted - morphine is not the devil - it is a tool. Remember you will give morphine to
help promote visualization of the gallbladder in the scenario where there is dumping of the tracer
into the small bowel, but no GB activity seen.
Never inject CCK and morphine within 30 minutes of one another. Why Not ? It would be bad.
Try to imagine all life as you know it stopping instantaneously and every molecule in your
body exploding at the speed of light— Total protonic reversal.
HIDA Scan
elevated bilirubin overview
Elevated bilirubin (total > 5mg/dl) will increase the number of non-diagnostic/inconclusive and false negative exams.
HIDA Scan
elevated bilirubin gamesmanship
Increased renal activity can suggest elevated bilirubin
HIDA Scan
elevated biliribuin next step
Alternative agents DISIDA and BROM1DA are preferred over HIDA in the setting of
high levels of bilirubin
Sulfur Colloid Liver Scan
overview
Not frequently done because of the modem invention of CT. Sulfur Colloid tagged with Tc is quickly
eaten by the liver’s reticuloendothelial system. It can be used to see “hot” and “cold” areas in the liver.
Classically, the multiple choice question is Focal Nodular Hyperplasia is Hot on sulfur colloid
(although in reality it’s only hot 30-40% of the time).
Sulfur Colloid Liver Scan
lesions and results
Hepatic adenoma colid FNH 40% hot, 30% cold, 30% neutral Cavernous hemangioma cold (rbc scan hot) HCC cold (gallium hot) Cholangiocarcinoma cold mets cold abscess cold (gallium hot) focal fat cold (xe hot)
Sulfur Colloid Liver Scan
particle size
Particles for this scan need to be 0.1 - 1.0 micrometers. This
is the right size for the liver to eat them. If they are too big the spleen will eat them, and if they are too
small the bone marrow will eat them. Also, realize that if they were too big they would get stuck in the
lungs like a VQ on the first pass through.
Sulfur Colloid Liver Scan
colloid shift
In a normal sulfur colloid scan, 85% of the colloid is taken up by the liver (10%
spleen, 5% bone marrow). In the setting of diffuse hepatic dysfunction, portal hypertension,
hypersplcnism, or bone marrow activation you can see change in uptake - shift to the spleen and bone
marrow. The most specific causes of colloid shift are cirrhosis, diffuse liver mets, diabetes, and blunt
trauma to the spleen.
Sulfur Colloid Liver Scan
diffuse pulmonary activity
This is not normal localization of sulfur colloid. This is non-specific
and can be seen with a ton of things (most commonly diffuse liver disease), but the first thing you
should think (on multiple choice) is excess aluminum in the colloid. It can also be seen in primary
pulmonary issues (reflecting phagocytosis by pulmonary macrophages).
Sulfur Colloid Liver Scan
renal activity on sulfur colloid
The most common cause is CHF (maybe due to decreased renal
blood flow and’filtration pressure). Alternatively, in the setting of renal transplant - this can
indicate rejection (due to colloid entrapment within the fibrin thrombi o f the microvasculature).
Other more rare causes include coxsackie B viral infection, disseminated intravascular coagulopathy,
and thrombotic thrombocytopenic purpura.
Hemangioma Scan
overview
You can “prove” a liver lesion is a hemangioma with a Tc Labeled RBC scan.
Hemangioma Scan
why instead of using mri or ct
You can “prove” a liver lesion is a hemangioma with a Tc Labeled RBC scan.
Hemangioma Scan
how is it done
Using Tc labeled RBCs with anterior and posterior projection images . Delayed blood pool is typically done (30 mins - 3 hours).
Hemangioma Scan
what if it is small
“Small” is actually the most common reason for a false negative exam.
You need the thing to be at least 1,5cm, otherwise your sensitivity really drops off. You
could try SPECT but first you seriously need to consider what you are doing with your life.
Hemangioma Scan
what is the classic look
You want to see marked HOT on delays, with no real hot spot
on immediate flow or immediate pool. Angiosarcoma could be HOT on delays but would
also be hot on flow. A partially fibrosed hemangioma may be a false negative.
Spleen Scan
You can use Tc Sulfur Colloid or heat damaged Tc labeled RBCs to localize to the spleen. A
possible indication might be hunting ectopic spleen.
Fatty Changes
A fatty liver can alter the distribution o f several tracer. Examples:
• Reduced uptake in the Liver on Tc Sulfur Colloid - including the possible reversal of normal liver > spleen uptake pattern (Colloid Shift).
• There will be increased uptake in a fatty liver with Xenon 133.
• Trivia - FDG-PET uptake in the liver is not altered by background steatosis.
GU Function (Dynamic)
overview
Normal kidney function is 80% secretion and 20% filtration. Tracer choice is based on which o f these parameters you want to look at.
GU Function (Dynamic)
tc-dtpa
Almost all filtered and therefore a great agent for determining GFR. A piece of
trivia is that since a small (5%) portion of DTPA is protein bound (and not filtered) you are
slightly underestimating GFR. Critical organ is the bladder.
GU Function (Dynamic)
tc-mag3
This agent is almost exclusively secreted and therefore estimates effective renal plasma flow (ERPF). It is cleared by the proximal tubules. Critical organ is the bladder.
GU Function (Dynamic)
tc-gh
This agent can be used for structural imaging (discussed later in this
section), or functional imaging as it is filtered. Critical organ is the bladder.
GU Function (Dynamic)
indications
(1) Differential Function (2) Suspected Obstruction, (3) Suspected Renal Artery Stenosis, (4) Suspected Complication from Rental Transplant, (5) Suspected Urine Leak.
GU Function (Dynamic)
basics
Images are obtained posteriorly (anterior if patient has a transplant or horseshoe).
Typically dynamic exams have 3 phases: blood flow phase, cortical phase, and clearance phase.
Tc DTPA
quick
Filtered (GFR)
Good For Native Kidneys with Normal Renal Function
Critical Organ Bladder
Tc MAG 3
quick
Secreted (ERPF)
Concentrated better by kidneys with poor renal function
Critical Organ Bladder
Tc GH
quick
Filtered
Good for dynamic and cortical imaging.
Critical Organ Bladder
GU differenial function flow overview
Begins within 20 seconds o f injection. Flow will first be seen in the aorta. Then as it
reaches the renal arteries, the kidneys should enhance symmetrically and about equal to the
aorta (at that time).
GU differenial function flow
decreased (symmetric)
Technical Error - poor bolus
GU differenial function flow
decreased (asymmetric)
Renal Artery Thrombosis Renal Vein Thrombosis Chronic High Grade Obstruction Acute Rejection Acute Pyelonephritis
GU differenial function flow
indreased (asymmetric)
Renal Artery Aneurysm
GU differenial function flow
trivia
ATN, Interstitial Nephritis, and Cyclosporin toxicity
will all have normal perfusion/flow.
GU differenial function flow
cortical (parenchymal)
This is the most important portion of the exam (with regard to
differential function). An area o f interest in drawn around the kidneys and a background area
o f interest is also drawn (to correct for the background). This can be screwed up by drawing
your background against the liver or spleen (which is not true background since they will take
up some tracer). You want to measure this at a time when the kidney is really drinking that
contrast, but not so late that it is putting it in the collection system. Most places use around 1
min. A steep slope is good.
GU differenial function flow
Clearance (excretory):
Radiotracer will begin to enter the renal pelvis, collecting system, and
bladder. In a normal patient, you will be down to half peak counts at around 7-10 mins. If
you wanted to quantify retention of tracer you could look at a 20/3 or 20/peak ratio.
GU differenial function flow
20/3 or 20/peak ratio:
This is a method o f quantifying retention of radiotracer by comparing
the peak count at 20 minutes with the peak count at 3 mins (normal < 0.8) or the peak count (normal 0.3).
Suspected Obstruction (“The Lasix Renogram”)
overview
The exam is performed the same as a standard dynamic exam (blood flow, cortical, and
clearance), with a 30 minute wait after clearance. If there is still activity in the collecting
system, a challenge is performed with Lasix. The idea is that a true obstruction will NOT
respond to Lasix, whereas a dilated system will empty when overloaded by Lasix. The study
can be done with MAG-3 or DTPA. MAG-3 does better with patients with poor renal
function, and thus is used more commonly.
Suspected Obstruction (“The Lasix Renogram”)
no obstruction
* No obstruction = tracer clears from collecting system without need for Lasix * No obstruction = Washout o f 50% of the tracer within 10 minutes of Lasix administration
Suspected Obstruction (“The Lasix Renogram”)
indeterminate
Washout o f 50% of the tracer within 10-20 minutes of Lasix administration o The most common cause for this indeterminate result is a very dilated pelvis and subsequent “reservoir effect.”
Suspected Obstruction (“The Lasix Renogram”)
obstructed
Washout taking longer than 20 mins after Lasix administration
Suspected Obstruction (“The Lasix Renogram”)
false positive for obstruction
- Poor response to Lasix - secondary to bad renal function, or dehydration at baseline
- “Reservoir Effect” - very dilated renal pelvis, delaying transit time
Back Pressure Effects - Full or Neurogenic Bladder can generate back pressure and
not let the kidneys empty (can be resolved with a foley catheter).
Suspected Renal Artery Stenosis
dtpa
Remember this is a GFR tracer. A sick kidney will have decreased uptake and flow, because of loss of perfusion pressure.
Suspected Renal Artery Stenosis
mag3
Remember this is a Secreted tracer. A sick kidney will have marked tracer retention, with a curve similar to obstruction.
Suspected Renal Artery Stenosis
if its bilateral up or bilateral down
If it’s bilateral up or bilateral down, it’s not RAS. If the baseline study has asymmetrically
poor function, that isn’t positive for RAS, you need to see it worsen (> 10%).
Suspected Renal Artery Stenosis
Trivia related to ACE inhibitor administration
they need to stop their ACE inhibitor prior to
the renal study (3-5 days if captopril). They should be NPO for 6 hours prior to the test (for
PO ACE inhibitors).
Suspected Renal Artery Stenosis
normal exam
No Difference Between Pre and Post
Suspected Renal Artery Stenosis
normal exam
No Difference Between Pre and Post
Suspected Complication from Renal Transplant
The most common indication for nuclear medicine in the setting o f renal
transplant is to differentiate rejection from ATN. ATN is usually in the first week after
transplant, and is more common in cadaveric donors. There will be preserved renal perfusion
with delayed excretion in the renal parenchyma (elevated 20/3 ratio, delayed time to peak).
ATN usually gets better. There is an exception to this rule, but it will confuse the issue with
respect to multiple choice, so I’m not going to mention it. Cyclosporin toxicity can also look
like ATN (normal perfusion, with retained tracer) but will NOT be seen in the immediate post
op period. Rejection will have poor perfusion, and delayed excretion. A chronically rejected
kidney won’t really take up the tracer.
Suspected Complication from Renal Transplant
In a Normal DMSA or ATN
(with MAG 3 tracer),
the nephrographic appearance is
the same. Tracer in the
cortex, and that s it.
Suspected Complication from Renal Transplant
atn quick
Immediate Post OP (3-4 days post op)
Perfusion Normal
Excretion Delayed
Suspected Complication from Renal Transplant
cyclosporin toxicity
Long Standing
Perfusion Normal
Excretion Delayed
Suspected Complication from Renal Transplant
acute rejection
Immediate Post OP
Poor Perfusion
Excretion Delayed
Suspected Complication from Renal Transplant
fluid collections on imaging
Fluid collections seen after a transplant include urinomas, hematomas,
and lymphoceles. All 3 can cause photopenic areas on blood pool imaging.
Suspected Complication from Renal Transplant
urinoma
Usually found in the first 2 weeks post op. Delayed imaging will show
tracer between the bladder and transplanted kidney. The primary differential in this
time period is the hematoma. A hematoma is not going to have tracer in it.
O Urinoma = Hot with Tracer
O Hematoma = No Tracer
Suspected Complication from Renal Transplant
lymphocele
Usually found 4-8 weeks after surgery. The cause is a disruption o f
normal lymphatic channels during perivascular dissection. Most are incidental and
don’t need intervention. If they get huge, they can cause mass effect. This will look
like a photopenic area on the scan.
Suspected Complication from Renal Transplant
hematoma quick
Timing - Early (< Month)
Blood pool - COLD - No Tracer
delay - COLD - No Tracer
Suspected Complication from Renal Transplant
urinoma quick
Timing - Early (< Month)
Blood pool - COLD - No Tracer
delay - HOT with Tracer
Suspected Complication from Renal Transplant
lymphocele quick
Timing - Late (> Month)
Blood pool - COLD - No Tracer
delay - COLD - No Tracer
Renal cortex
overview
If you want to look at the renal cortex, you will want to use an agent that binds to the renal
cortex (via a sulfhydryl group). You have two main options with regard to tracer.
Renal cortex
Tc-DMSA
This is the more commonly used tracer. It binds to the renal cortex and is
cleared very slowly. Critical organ is the kidney (notice other renal tracers have the
bladder as their critical organ).
Renal cortex
Tc-GH (glucoheptonate)
This is less commonly used and although it binds to the
cortex, it is also filtered and therefore can be used to assess renal flow, the collecting
system, and the bladder. Critical organ is the bladder.
Renal cortex
pediatrics
DMSA is the preferred cortical imaging agent in pediatrics, because it has a lower dose to the
gonads (even though its renal dose is higher than TcGH).
Renal cortex
indications - pyelonephritis
Acute Pyelonephritis: Can appear as (a) fo ca l ill-defined area o f decreased uptake,
(b) multifocal areas o f decreased uptake, (c) diffuse decreased uptake - in an
otherwise normal kidney.
° Scarring and Masses can also appear as fo ca l areas o f decreased uptake -
although scarring usually has volume loss.
Renal cortex
indications - column of bertin vs mass
Simply put, the mass will be cold. The Column o f Bertin
(normal tissue) will be take up tracer.
Renal cortex DMSA acute vs chronic
- Defects on DMSA with acute renal problems = pyelo.
* Defects on DMSA with chronic renal problems = scar (or mass).
Renal cortex DMSA acute vs chronic
- Defects on DMSA with acute renal problems = pyelo.
* Defects on DMSA with chronic renal problems = scar (or mass).
Testicular
overview
This hasn’t been done in the United States since 1968, therefore it is very likely to be on the
test. The study is basically a blood flow study. The primary clinical question is testicular
torsion vs other causes of pain (epididymitis). The tracer used is sodium pertechnetate
(Na99mTc04). Oh, don’t forget to tape the penis out o f the way - tape it up, not down like is
required for the male residents on mammography rotations.
Testicular
normal
Symmetric low level flow to the testicles
Testicular
Acute (early) Torsion
Focal absence o f flow to the affected side (“nubbin sign”).
Testicular
Delayed (late) Torsion
Sometimes called a missed torsion. The appearance is a
halo of increased activity, with central photopenia.
Testicular
Testicular Abscess
Identical to delayed torsion - halo o f increased activity, with
central photopenia.
Testicular
Acute Epididymitis-
Increased flow and blood pool to the affected side.
P E T f o r C a n c e r
overview
As mentioned before, 18-FDG is cyclotron produced and decays via beta positive emission to
18-0. The positron gets emitted, travels a short distance, then collides with an electron
producing two 511 keV photons which go off in opposite directions. The scanner is a ring
and when the two photons land 180 degrees apart at the same time the computer does math
(which computers are good at) to localize the origin.
P E T f o r C a n c e r
A CT component is fused over the PET portion
(1) Anatomy - so you can see what the hell you are looking at.
(2) Attenuation Correction - Dense stuff will slow down the photons, and the CT
allows for correction o f that. It also leads to errors, the classic one being a metallic
pacemaker looks bright hot on the corrected image (the computer overcorrected). This
is a classic question. The answer is look at the source images (uncorrected).
P E T f o r C a n c e r
technical trivia
Some other technical trivia is that FDG enters the cell via a GLUT 1 transporter and is then
phosphorylated by hexokinase to FDG-6-Phosphate. This locks it in the cell. Normal bio
distribution is brain, heart, liver, spleen, GI, blood pool, salivary glands, and testes. The
collecting system and bladder (critical organ) will also be full of it, because that’s where it’s
getting excreted.
P E T f o r C a n c e r
variable areas of uptake
Muscles (classic forearm muscle uptake in the nervous chair
squeezing patient). Breast and ovaries in females at certain stages o f the menstrual cycle.
Thymus in younger patients. Lastly, brown fat around the neck, thorax, and adrenals
(especially in a cold room).
P E T f o r C a n c e r
ways to minimize brown fat uptake
Keep the room warm. Medications like
benzodiazepines or beta blockers.
P E T f o r C a n c e r
insulin
Insulin: So why not just give the patient some insulin??? It will drive it all into the
muscles. This is a classic trick. PET with diffuse muscle uptake = Insulin
Administration
P E T f o r C a n c e r
blood glucose
High Blood Glucose (> 150-200): The more glucose the patient has, the more
competition is created for the FDG and you will have artificially low SUVs.
P E T f o r C a n c e r
Consequences o f being fat
- Fat people will have HIGHER SUV values, because the fat takes up less glucose
- You leave the house in high heels… and come back home in flip flops
P E T f o r C a n c e r
When do you image? Following therapy
Following therapy; an interval of 2-3 weeks for chemotherapy and 8-12
weeks for radiation is the way to go. This avoids “stunning” - false negatives, and
inflammatory induced false positive.
P E T f o r C a n c e r
Who do you image
The main utility is extent o f disease, and distal metastatic spread. Local
invasion is tricky with a lot o f things. Usually straight up CT or MRI is better for local
invasion and characterization.
P E T f o r C a n c e r
What i f you see the right ventricle
The RV is not typically seen on PET unless it’s enlarged.
If you see the RV think about RVH.
SUV =
FDG Concentration at time “T”
/ -
(Dose / Body Weight)
Tumors that are PET COLD
BAC (Adeno In Situ) - Lung Cancer carcinoid rcc peritoneal/liver implants anything mucinous prostate
Not Cancer but PET HOT
infection inflammation ovaries in follicular phase muscles brown fat thymus
FDG PET Cancer Trivia
Focal Thyroid Uptake
Requires Further Workup - might be cancer, might be nothing
FDG PET Cancer Trivia
Diffuse Thyroid Uptake
Most often Autoimmune (Hashimoto) Thyroiditis
FDG PET Cancer Trivia
RCC and Oncocytoma
RCC are COLD (usually), Oncocytomas are FIOT
FDG PET Cancer Trivia
pulm nodulles
COLD Ground Glass Nodule = Cancer, HOT Glass Nodule = Infection
FDG PET Cancer Trivia
reason hcc is cold
The Reason HCC is often cold (60%) is that it has variable glucose-6- phosphatase and
can’t trap the FDG
FDG PET Cancer Trivia
testicular cancers
Testicular cancers skip right to the retroperitoneum. The trivia is the seminomatous CA is FDG hot, whereas non-seminomatous tends to be FDG COLD (or Luke Warm).
FDG PET Cancer Trivia
ovaries
While it’s OK for ovaries to be hot in functional (ovulating) young people, Grandma should NOT have FDG up-take in her dried-up raisin ovaries. This is suspicious - next step Ultrasound.
FDG PET Cancer Trivia
metformin
Metformin is classic for causing false positive bowel uptake. The uptake is typically intense and diffuse. It tends to favor the colon (small bowel to a lesser extent).
FDG PET Cancer Trivia
adrenal glands
mild uptake is normal. In general, an adrenal pathology is typically
considered malignant if the uptake is higher than the liver (used as an internal control).
Although this does not really hold up that well in my experience (especially since liver
uptake is variable). For example, Adrenal Adenomas can have moderate uptake (still
usually not super hot).
FDG PET Cancer Trivia
lymphoma
Most Lymphoma is Super Hot
FDG PET Cancer Trivia
Thymic Rebound v.v Recurrent Lymphoma
Thymic Hyperplasia (or Rebound) can be
“Warm” on PET, but recurrent Lymphoma should be HOT. Also, Rebound tends to
maintain the normal thymus look (it sorta drapes over the heart). Lymphoma is round
like a ball. A hot ball o f death, or a “great ball of fire”
FDG PET Cancer Trivia
extranodal marginal zone lymphomas
Extranodal marginal zone lymphomas, including the mucosa-associated lymphoid tissue (MALT) marginal zone lymphoma, have been shown to have LOW Avidity for FDG
GYN PET
False Positives
Physiologic FDG in the endometrium
Two described peaks of FDG
(1) Rag Week / Menstruation (first 4 days of cycle) and (2) Ovulation (~ day 14) and
menstruation may mimic disease.
Physiological uptake in the endometrium is usually diffuse. Cancer is usually more focal.
You won’t see this in postmenopausal women
GYN PET
False Positives
Physiologic FDG in the ovaries
Seen during ovulation
Typically appears as ovoid or a rim of activity with a photopenic center.
You won’t see this in postmenopausal women
GYN PET
False Positives
Endometrial or ovarian FDG activity in the
postmenopausal
suspicious (next step ultrasound)
GYN PET
False Positives
Benign lesions
- Uterine Fibroids
* Benign Endometriotic Cysts
GYN PET
False Positives
Misregistration
Focal uptake in the ureter or the
bladder - if mapped incorrectly can simulate disease.
Main strategy to reduce this artifact is to
minimize the time between the PET and CT acquisitions
GYN PET
False Positives
Vesicovaginal fistulas (common in advanced disease)
can falsely elevated SUV values by spilling urinary FDG excretion
GYN PET
False Negatives
overview`
Necrotic, Mucinous, Cystic, or
Low-grade Cancers — you gotta correlate with
US and/or MRI to avoid looking stupid.
50% of RCC may not be FDG avid
GYN PET
False Positives False Negatives
Small-volume peritoneal disease and small lymph nodes
can be missed because they
are small, can also be missed because the adjacent bowel (which has physiological uptake)
masks them
GYN PET
False Positives False Negatives
Perivesical disease
can be missed because of
the high uptake in the adjacent bladder — look at source images (uncorrected)
FDG PET Cancer Trivia
secondary osteosarcs
Remember secondary osteosarcomas (the ones from Pagets. Radiation, Multiple
Chondromas, e tc ….) are the bad mother fuckers. They have by far the worst outcome.
FDG PET Cancer Trivia bone tumors
back in the stone ages
Back in the stone ages - if you got diagnosed with an osteosarcoma they assumed that
80% of the time you had distal mets. This was prior to effective chemotherapy for
osteosarcoma… it was basically a death sentence. They do better now (little bit).
FDG PET Cancer Trivia bone tumors
typically mets go to
Typically mets go to (a) second bone sites, and (b) the lungs. Remember the classic
vignette of a spontaneous pneumothorax in an osteosarcoma patient = lung met.
FDG PET Cancer Trivia
with the modern addition of effective chemo
With the modem addition o f effective chemo, accurate staging and restaging actually
matters - and this is why I’m rambling on about osteosarcoma. PET may/could
actually play a key role in treatment and is therefore testable.
FDG PET Cancer Trivia
average suv
Average SUV is used at some institutions for describing tumor metabolism. Most
literature says you should use the SUV Max for describing osteosarcoma - because it’s
a very heterogenous tumor.
FDG PET Cancer Trivia
tumor grade and FDG uptake
Multiple papers have shown a correlation between tumor grade and FDG uptake (SUV
values). Higher SUV Max = Higher Tumor Grade.
FDG PET Cancer Trivia
baseline suv max
Baseline SUV Max is an independent and significant predictor of overall survival
(more = bad). Having said that PET is not typically used fo r baseline staging.
FDG PET Cancer Trivia
important bone stuff
An important point is that especially with bone stuff, nukes is highly non-specific.
Remember earlier in the chapter I said several B9 bones lesions are hot on Tc-MDP?
Same thing with PET. Giant Cell is the classic example. Lots o f cases o f GCTs have
higher SUV than sarcomas. Fibrous dysplasia is another classic that can be hot on
PET.
FDG PET Cancer Trivia
bone lesion cutoff
There is no cutoff to tell the difference between a B9 bone lesion and a bone sarcoma.
Same deal with infection. Osteomyelitis can have very high FDG uptake.
FDG PET Cancer Trivia
important point
Important point = Because PET is so nonspecific, it is NOT used clinically to avoid
biopsy…. but can sometimes guide biopsy.
FDG PET Cancer Trivia
most important prognostic factor
The most important prognostic factor = response to preoperative (neoadjuvant)
chemotherapy.
FDG PET Cancer Trivia
fdg uptake and viable tumor tissue
There is a proven positive correlation o f FDG uptake and viable tumor tissue. In other
words, F,8-FDG PET can be used to evaluate the effectiveness of neoadjuvant
chemotherapy.
In111- Octreoscan
overview
11’In Pentetreotide is the most commonly used agent for somatostatin receptor imaging. The
classic use is for carcinoid tumors, gastrinomas, paragangliomas, merkel cell tumors,
lymphoma, small cell lung cancer, medullary thyroid cancer, and meningiomas.
In111- Octreoscan
meningiomas
Meningiomas take up Octreotide (and Tc MDP).
In111- Octreoscan
trivia
As a point o f trivia, there are 5 somatostatin receptors but “ ‘In Pentetreotide can only bind to
two of them. The scan works because 80% o f neuroendocrine tumors express these two
receptors.
Meningiomas
Hot on Octreotide and Tc MDP
In111- Octreoscan
normal uptake
Normal uptake is in the thyroid, liver,
gallbladder, spleen, kidneys, bladder, and GI
tract. Imaging is done in early and delayed
phase. The advantage o f the early phase (4
hours) is that the bowel activity is absent.
The delayed is done to clarify that the
abdominal tracer is o f GI origin.
Indium111
overview
Indium is produced in a cyclotron and decays with a 67 hour half life via electron capture.
It produces two photopeaks at 173 keV and 247 keV. Just like Gallium, In”’ in a liquid
will carry a +3 valence and behaves like Fe+3, with the capability o f forming strong bonds
with transferrin.
Indium111
application
The most common application is to bind it to WBC,
although it can also be hooked to octreotide, or DTPA
for CNS imaging (cisternography). Basically, you can
hook indium to almost anything if you hook it first to
a strong chelator like DTPA. As a point of trivia, you
need to isolate the WBCs prior to labeling because the
transferrin in the blood binds with greater affinity and
will out-compete them.
MIBG
overview
MIBG is an analog o f nor adrenalin and is therefore taken up by adrenergic tissue. MIBG is
first line for tumors like pheochromocytoma, paraganglioma, and neuroblastoma. You can
have MIBG with either 1-123 or I -131. 1-123 is better because it has better imaging quality.
1-131 is cheaper, and the long half life allows for delayed imaging.
MIBG
blocking the thyroid gland
The thyroid gland should be blocked, to prevent unintended
radiation to the gland from unbound 1-123 or 1-131. This is accomplished with Lugol’s Iodine
or Perchlorate. Sometimes you’ll see “SSKT’ which is Super Saturated Potassium /odine
MIBG
biodistribution
Normal in liver, spleen, colon, salivary glands. The adrenals may be faintly visible. Note the kidneys are NOT seen.
MIBG
trivia
MIBG is superior to MDP bone scan for neuroblastoma bone mets. * I f you see a skeleton on MIBG the answer is diffuse bone mets.
MIBG
trivia 2
MIBG is better for Pheo than In-111 Octreotide. MIBG is better than CT or MRI for the extra-adenral Pheos.
Medication Interaction with MIBG - High Yield Trivia
Certain medications interfere with the workings o f MIBG and must be held.
Medications include calcium-channel blockers, labetalol (other beta-blockers have no
effect), reserpine, tricyclic antidepressants and sympathomimetics.
THIS vs THAT: MIBG Scans
What’s Different Between Patient “A” and “B” - who both recently got MIBG Scans? Patient B - Forgot to take her Lugol’s ! So, she ju s t cooked her thyroid.
Gamesmanship - MIBG
brown fat
Just like you can see it on FDG PET (around the shoulders / traps) you can also see
it with MIBG. In fact, it’s the MOST COMMON variant in I123 MIBG bio distribution.
Gamesmanship - MIBG
mechanism
Apparently brown fat has sympathetic innervation.
Gamesmanship - MIBG
utility
The classic use for MIBG is Neuroblastoma. But…. if someone wanted to get sneaky
they could also show you a pheochromocytoma, paraganglioma, or carcinoid on MIBG.
Essentially any catecholamine producing tumor. See the chart on the next page for specifics.
Gamesmanship - Octreotide
Octreotide Mechanism Nitty Gritty
Octreotide works as an analog to somatostatin and will
bind to the same receptors as somastostain. Well… sorta. Technically, there are 5 subtypes of
somatostatin receptors and Octreotide will only bind to 2 of them. As you can imagine, the
sensitivity of the agent is going to depend on which receptors are expressed by the tumor.
Fortunately, most tumors express those 2 receptors.
Gamesmanship - Octreotide
Suspected Insulinoma:
Some sources will say that Octreotide can trigger hypoglycemia in the
setting of an insulinoma. What to do about this seems to vary a lot on who you ask and what you
read. Some places will say to give them some IV solution with glucose before and during the
administration o f Octreotide. Other places will just say have D50 ready just in case.
Gamesmanship - Octreotide
Already on Octreotide Therapy
You will need to stop the treatment for 3 days prior to giving
the labeled agent.
M I B G Octreotide
Carcinoid
MIBG - Inferior (Sensitivity 50-70%)
Octreotide - Superior (Sensitivity 80-90%)
Misc - Octreotide and MIBG are similar for detection of Liver Mets
M I B G Octreotide
Insulinoma
MIBG -
Octreotide - SHIT (Sensitivity ~ 30%)
Misc - Insulinoma is usually B9
M I B G Octreotide
Gastrinoma
MIBG -
Octreotide - Good (Sensitivity ~ 85%)
Misc -
M I B G Octreotide
Non-Functional
Islet Cell Tumor
MIBG - Crap (No Function, No Fleceptors)
Octreotide - Crap (No Function, No Fleceptors)
Misc - FDG PET is the test of choice.
M I B G Octreotide
Pheo
MIBG - Superior For Non- Malignant (Adrenal) Types (which is like 90% of them)
Octreotide - Superior For Malignant (Extra-Adrenal) Types (which is a minority of them 10%)
Misc - FDG is also good - but Octreotide is cheaper - so people go that route first when malignancy is suspected
M I B G Octreotide
Paraganglioma
MIBG - Less Sensitive and Less Specific (*onty concentrates in the functional subtypes)
Octreotide - Superior (Sensitivity ~ 95%)
Misc -
M I B G Octreotide
Medullary
Thyroid CA
MIBG - Inferior (Sensitivity 30 %)
Octreotide - Superior - (Sensitivity 50-80%)
Misc - Octreotide is still the first line as a nukes agent. If it’s negative (in the setting of rising calcitonin) the next step is FDG-PET.
M I B G Octreotide
Neuroblastoma
MIBG - Superior (Sensitivity ~ 95%)
Octreotide - Inferior (Sensitivity ~ 64%)
Misc -
Gallium
overview
Gallium can be used for tumors. Remember, it’s very nonspecific with regard to infection, inflammation, or tumor.
Gallium
trivia 1
During the Cretaceous Period (when many o f your attendings trained); Gallium was used to differentiate residual tumor vs fibrosis, scarring, necrosis etc… in patients with Hodgkin’s disease and Malignant Lymphoma
Gallium
trivia 2
If you are going to use Gallium for treatment monitoring it’s important to have a pretreatment exam (to ensure that the tumor site is actually Gallium - avid).
ProstaScint
overview
11’In can be labeled to the antibody Capromab Pendetide (ProstaScint). Capromab is a
monoclonal antibody which recognizes PSA membrane antigen “PSMA” - which is slightly
different that PSA. Pendetide is the chelating agent. In my opinion, the exam is shit and
doesn’t work well.
ProstaScint
when to do the test
If you have a rising PSA and negative bone scan. The purpose o f the
study is to look for mets outside the prostate bed (soft tissue mets). If they do not have distal
mets, they can be offered salvage therapy (radiation to the surgical bed). It’s important to not
obsess over the surgical bed, the real question is distal mets. Having said that, the prostate bed
is best seen on the lateral between the bladder and penis.
ProstaScint
triia 1
ProstaScint will localize to soft tissue mets, NOT bone mets.
ProstaScint
trivia 2
ProstaScint’s critical organ is the LIVER.
ProstaScint
avoid this trap
This confuses some people. Avoid this trap: Indium = WBC. It’s slang to say “Indium Scan”
and people in Nukes just think tagged WBC with Indium. But…. Not all Indium is WBC.
Remember that Octreotide is actually labeled with Indium, and so is a bunch o f other stuff.
ProstaScint
Bottom Line: For Critical Organ Trivia
Indium ProstaScint = Liver
Indium WBC = Spleen
Indium Octreotide = Spleen
Sentinel Node Detection
overview
A sentinel node is the node which receives afferent drainage directly from a primary cancer.
Surgeons want to know where these are at; especially with melanoma and breast cancer. The
agent used for lymphoscintigraphy is 10-50 nm Tc99m sulfur colloid.
Sentinel Node Detection
melanoma
Sentinel node mapping is done when you have a lesion between 1 mm-4 mm deep.
Less than 1 mm you are typically safe. More than 4 mm you are totally screwed and it makes
no difference. The utility o f the test is to go after the ones in that middle zone (between
1-4 mm). Intradermal injection in 4 spots around the lesion / excision scar and imaging is done.
Sentinel Node Detection
breast cancer
Cancer drains to the internal mammary chain nodes about 3% o f the time.
Knowing this, and which axillary node to go for first, can help avoid aggressive lymph node
dissection. Injections can be done superficial or deep (into the pectoral muscle).
Sentinel Node Detection
Does particle size matter fo r sentinel node detection?
Yes and No.
The idea is that particles have to be small enough to travel through the lymphatics. A
particle that is 500 nm will not go anywhere. So any answer choice with 500 nm or larger
for a lymph node study is universally incorrect. Now this is where you will read different
stuff (and send me nasty emails). Some sources say < 200 nm. This will probably work,
but you will be waiting all day for the study. The larger the particles the slower the study.
More sources will say < 100 nm. This this will work, but again slow study. There is at
least one paper out that advocates for using a 0.22 mm filter (available in most hospital
pharmacies because it is commonly used for sterilization o f hyperalimentation solutions).
If you do that you end up with particles that are 10-100 nm. If you use this 0.22 mm filter
method you can routinely visualize lymphatic channels and sentinel nodes within 30 mins
after administration.
Sentinel Node Detection
gamesmanship
How do you know what the question writer does at his/her institution?
If it was me - 1 would pick a choice less than 100 nm. If forced to choose between 100 and
50 - 1 would pick 50, and there is literature to back you up (not that you’d have a chance to
defend yourself), but practically most places do filter the particles and use small ones.
Sentinel Node Detection
particle size
Lymphoscintigraphy < 0.2 microns (< 200 nm)
VQ 10-100 microns (10,000 - 100,000 nm)
Liver Spleen “Unfiltered” - so all sizes big and small
Breast Specific Gamma Imaging
overview
Tc99 Sestamibi will concentrate in a breast cancer 6 times more than normal background
breast tissue. It does pretty well, with the sensitivity supposedly near 90%. The technique is
to give 20-30 mCi o f Tc99 Sestamibi in the contralateral arm then image 20 mins later. A
foot injection is often done if you are going to image both breasts. You are supposed to use a
dedicated gamma camera that can mimic a mammogram and provide compression.
Breast Specific Gamma Imaging
Does Breast Density Affect Uptake / Distribution ?
Nope. The distribution is homogeneous regardless of density. Having said that, hormonal fluctuation can increase the background uptake
Breast Specific Gamma Imaging
When will background activity be lowest?
Around mid-cycle in premenopausal women.
Breast Specific Gamma Imaging
What are some causes o f fa lse positive studies ?
Fibroadenoma, fibrocystic change, or inflammation can give a false positive
Breast Specific Gamma Imaging
What are some causes o f false negative studies?
Lesions that are small (< 1 cm), or deep. Lesions located in the medial breast, and/or those overlapping with heart activity.
Breast Specific Gamma Imaging
What about lymph nodes?
You see lymph nodes on a “MIBI” scan - this is NOT normal, it is concerning for mets.
Myocardial Perfusion I SPECT:
Overview
Tc Sestamibi and Tc Tetrofosmin are the most common tracers. They work by crossing the cell
membrane and localizing in mitochondria (passive diffusion). They don’t redistribute (like
Thallium), giving better flexibility.
Myocardial Perfusion I SPECT:
Sestamibi vs Tetrofosmin
Tetrofosmin is cleared from the liver more rapidly and decreases the
chance of a hepatic uptake artifact.
Myocardial Perfusion I SPECT:
Thallium
This is historical with regard to cardiac imaging. It mimics potassium and crosses
the cell membrane first by distribution related to blood flow - second by delayed redistribution
(washout). Washout is delayed in areas with poor perfusion.
Myocardial Perfusion I SPECT:
Imaging Timing:
Tc studies (sestamibi and tetrofosmin) are done 30-90 mins after injection - allowing for clearance from background
Myocardial Perfusion I SPECT:
Thallium quick
old
Crosses cell via Na/K pump
redistributes
Imaging must be done immediately after
injection
Myocardial Perfusion I SPECT:`
Sestamibi and Tetrofosmin``
newer
Crosses cell via passive diffusion (localizes in mitochondria)
Does NOT redistribute
Imaging typically done 30-90 mins after injection to allow for background to clear
Myocardial Perfusion I SPECT:
Lung/ Heart Ratio
Only done with Thallium. If there is more uptake in the lungs, this correlates with multi-vessel disease or high grade LAD or LCX lesions.
Myocardial Perfusion I SPECT:
General Principal
You will see less perfusion distal to an area o f vascular obstruction (compared to normal myocardium). To improve sensitivity, the heart is stressed. Under stress you need about 50% stenosis to see a defect (it needs to be like 90% without stress).
Myocardial Perfusion I SPECT:
Preparation
Patient shouldn’t eat for 4 hours prior to imaging (decreases GJ blood flow). Patients
should (ideally) stop beta-blockers, calcium channel blockers, and long-acting nitrates for 24 hours
prior to the exam - as these meds mess with the sensitivity of the stress portion. There are reasons to
keep people on these meds (they might be getting risk stratification on medical therapy) - but I’d say
for the purpose of multiple choice just know that those medication classes mess with stress imaging
sensitivity.
Myocardial Perfusion I SPECT:
Protocols:
There are multiple ways to skin this particular cat. People will do two day exams; rest then
stress. People will do one day exams stress then rest. The advantage to doing stress first is that you can
stop if it’s normal. Typically the dosing is low for the rest and high for the stress.
Myocardial Perfusion I SPECT:
Chemical Stress
If you can’t exercise, the modem trend is to give you Regadenoson (coronary
vasodilator) - which is a specific adenosine receptor agonist. It’s specific to a certain receptor having
less bronchospasm than conventional adenosine or dipyridamole. If they get bronchospasm anyway you
need to give them albuterol.
Myocardial Perfusion I SPECT:
Known Left Bundle Branch Block
known LBBB will make ECG stress testing non-diagnostic. So
diagnostic imaging (radionuclide myocardial perfusion) is typically the way to go. The important trivia
is:
LBBB Classic Artifact
Pharmaceutic Choice
Myocardial Perfusion I SPECT:
LBBB Classic Artifact
= False Positive Reversible Perfusion Defect at the Septum (anteroseptal region). Supposedly this has something to do with the septum not relaxing correctly during diastolic coronary filling (because the rhythm is not totally coordinated with the left sided block).
Myocardial Perfusion I SPECT:
Known LBBB Pharmaceutic Choice
= Adenosine or Dipyridamole is supposedly better for LBBB patients than
Dobutamine. The reason is Dobutamine increases the HR more, and the more rapid the HR, the worse
the septal relaxation stuff is. Dobutamine = More False Positives.
Myocardial Perfusion I SPECT:
Findings
Fixed Defect (seen on stress and rest), Scar (prior infarct)
Reversible Defect (seen on stress, better on rest), Ischemia
Fixed Defect with Reversible Defect around it, Infarct with peri-infarct ischemia
Transient Ischemic Dilation (LV cavity is larger on stress), From diffuse subendocardial hypoperfusion producing an apparent cavity dilation. Correlated with high risk disease (left main or 3 vessel).
Fixed Cavity Dilation, Dilated cardiomyopathy
Right Ventricular Activity on Rest, If has intensity similar to LV then think right ventricular hypertrophy
Lots of splanchnic (liver and bowel) activity, Means you aren’t exercising hard enough - not shifting enough blood out of the gut.
THIS vs THAT: Stunned VS Hibernating Myocardium
stunned
This is the result of ischemia and reperfusion injury. It is an acute situation. The perfusion will be normal, but contractility will be crap. It will get better after a few weeks.
THIS vs THAT: Stunned VS Hibernating Myocardium
hibernating
This is a more chronic process, and the result of severe CAD causing chronic
hypoperfusion. You will have areas of decreased perfusion and decreased contractility even when
resting (just like scar). Don’t get it twisted, this is not an infarct. This tissue will take up FDG more
intensely than normal myocardium, and will also demonstrate redistribution of thallium.
Ischemia =
Will take up less tracer (relative to other areas) on stress, and the same amount of tracer (relative to other areas) on rest. It’s not normal heart so it won’t contract well.
scar =
Won’t take up tracer on rest or stress (it’s dead Jim). It’s scar not muscle, so it won’t contract normally either.
stunned=
The perfusion will be normal on both stress and rest, but the contractility is not normal.
hibernating =
Won’t take up tracer on rest or stress (it’s not dead,just asleep - like a bad soap
opera plot). The difference between hibernating muscle and scar is that the hibernating muscle will
take up FDG and redistribute thallium. The defect at rest will resolve / “redistribute” on delayed
thallium imaging. Remember thallium works with the Na/K pump - so cells need to be alive to
pump it in. A truly dead cell won’t have a functioning Na/K pump and therefore won’t be able to
redistribute / resolve the defect.
MUGA (Multigated Acquisition Scan):
overview
This is an equilibrium radionucleotide angiogram with cardiac pool images taken after the tracer has
equilibrated to the intravascular space. Drugs like Adriamycin and Doxorubicin can be cardiac toxic.
Oncologists will alter treatment protocols when the LVEF drops (usually by 10%).
MUGA (Multigated Acquisition Scan):
huh?
It’s an angiogram using tagged RBCs. You time (gate) the exam to get pictures that can be used
to estimate the Ejection Fraction (and evaluate motion etc…)
MUGA (Multigated Acquisition Scan):
general points
These studies requires gating (the “G” in MUGA). The study is done using Tc 99 labeled RBCs, and
the objective is to calculate an EF (MUGA is more accurate than myocardial perfusion for LVEF).
Photopenic halo around the cardiac blood pool is a classic look for pericardial effusion. Regional wall
motion abnormality on a resting MUGA is usually infarct (could be stunned or hibernating as well).
MUGA (Multigated Acquisition Scan):
false low EF
Screwed up LAO view can cause overlap of LV
with LA or RV or even great vessels - causing a false low EF.
Inclusion of the Left Atrium (which happens when it is enlarged) -
the result of LA inclusion is inclusion of the LA counts — this
falsely lowers the EF.
MUGA (Multigated Acquisition Scan):
False high EF
Wrong background ROI (over the spleen), will cause over subtraction of background and elevate the EF.
MUGA (Multigated Acquisition Scan):
best septal view
Left A nterior Oblique (LAO) is the “best septal view” - and the one usually used to measure the LVEF. A basic internal QA step when reading these studies is to confirm a good photopenic septum.
Rubidium 82
This is a potassium analog (mechanism is Na/K pump). This is similar to TI-201,
and can be used as a similar agent. You can use it for PET myocardial perfusion, although it’s
not used in most places because of cost limitations. Also, because o f the very short half life ( 75
seconds) it tends to give a dirtier image compared to PET o f NH?.
I say made with a g enerator, you say
Tc99 and Rubidium. * Rubidium is the only PET agent made like this, so that instantly makes it a testable fact.
Heart anatomy
anterior
LAD and apex
Heart anatomy
septal
between the LAD and RCA
Heart anatomy
inferior
RCA
Heart anatomy
LAteral
LCX
Cardiac Artifacts
Breast Tissue
“Soft Tissue Attenuation”
Decreased activity in anterior wall (may also affect septal and lateral - depending on body habitus)
Check for ECG changes and wall motion. If normal, then call it artifact. If not sure can repeat in prone position.
Cardiac Artifacts
Left Hemidiaphragm
“Soft Tissue Attenuation”
Decreased activity in inferior wall
Check for ECG changes and wall motion. If normal, then call it artifact.
Cardiac Artifacts
Subdiaphragmatic
Radiotracer Activity
Increased activity in inferior wall, can mask true defect. Can also mess with
“normalization” o f the ventricle and make the rest o f the LV look low.
Liver Excretes Tc, so you see it in the liver and bowel. Little bit o f exercise can be used to reduce GI blood flow.
Cardiac Artifacts
Patient Motion
usually respiration
Causes all kinds o f problems
You can repeat because tracer is fixed for around 2 hours
Cardiac Artifacts
Misregistration
Causes all kinds o f problems
Cardiac Artifacts
Left Bundle Branch Block
Reversible or Fixed Septal Defects , sparing the apex
Seen more in exercise or dobutamine stress compared to vasodilators
Cardiac Artifacts
Normal Apical Thinning
Normal variant
Look for matching stress and rest perfusion patterns with preserved wall function to show you this is normal (and not infarct)
Cardiac medication
Dipyridamole
Inhibits the breakdown of adenosine - which builds up.
Adenosine is a potent vasodilator.
No caffeine
Cardiac medication
Adenosine
Vasodilator
No caffeine
Side effects are worse than with dipyridamole. Rare side effect is AV block - which will get better when adenosine short half life runs out.
Cardiac medication
Regadenoson
Selective A2A - causes fewer
side effects
No caffeine
Cardiac medication
Dobutamine
Beta 1 agonist - acts like exercise by increasing heart rate and myocardial contraction.
Patient Can NOT be on a beta blocker. Best used in patients who cannot have Adenosine or Dipyridamole. Better in patients with COPD or Asthma, or who have taken caffeine in the last 12 hours.
Avoid with LBBB
Cardiac medication
Aminophylline
Antidote for Adenosine
Half life is shorter than Dipyridamole - so must continue to monitor.
Treatment for Bone Pain
overview
There are currently three approved agents for bone pain associated with metastatic disease from breast and prostate cancer: (1) Sr89-Chloride, (2) Sm153 EDTMP, and (3) Ra223-dichloride.
Treatment for Bone Pain
Why does cancer cause bone pain / bone problems?
Metastatic disease leads to a tumor derived factor that increases osteolytic activity. You end up with increased fracture risk, osteopenia, and hypercalcemia o f malignancy.
Treatment for Bone Pain
Can the patient get external radiation treatment with the therapy?
Yes, External radiation is not a contraindication and can be used with the therapy.
Treatment for Bone Pain
Absolute contraindications (for Sr and Sm) include’.
Pregnancy, Breastfeeding, and renal
Failure (GFR < 30). Patients with extensive bony mets (superscan) maybe shouldn’t be treated
either * controversial - and therefore not likely tested.
Treatment for Bone Pain
Strontium - Sr89(Metastron):
It works by complexing with the hydroxyapatite in areas where
bone turnover is the highest. It’s the oldest, and worst o f the three agents. It is a pure beta
emitter. It has a high myelotoxicitiy, relative to newer agents and therefore isn’t really used.
Treatment for Bone Pain
Samarium - Sm153 (Quadramet)
This is probably the second best o f the three agents;
“Samarium is a good Samaritan. ” It works by complexing with the hydroxyapatite in areas
where bone turnover is the highest. It is a beta decayer. The primary method o f excretion is
renal. Unlike Sr89, about 28% o f the decay is via gamma rays (103 kev) which can be used for
imaging. Does have some transient bone marrow suppression (mainly thrombocytopenia and
leukopenia), but recovers faster than Sr.
Treatment for Bone Pain
Sr89(Metastron) quick
15-30% drops in platelet and WBC from preinjection
8-12 weeks needed for full recovery
Treatment for Bone Pain
Sm153 (Quadramet) quick
40-50% drops in platelet and WBC from preinjection
6-8 weeks needed for full recovery
Treatment for Bone Pain
Radium - Ra223 (Xofigo): overview
This is the most recent o f the three agents, and probably the best.
The idea is that Ra223 behaves in a similar way to calcium. It is absorbed into the bone matrix
at the sites o f active bone mineralization. Its primary mechanism is the emission o f 4 alpha
particles, causing some serious double stranded DNA breaks.
Treatment for Bone Pain
Radium - Ra223 (Xofigo): why is it the best
(1) It’s an alpha emitter with a range shorter than Sr and Sm. This means less hematologic toxicity.
(2) At least one trial actually showed a survival benefit in prostate CA.
(3) It has a long half life (11.4 days), allowing for easy shipping.
Treatment for Bone Pain
Radium - Ra223 (Xofigo): trivia
The general population is safe, as the gamma effects are low. Soiled clothing and
bodily fluids should be handled with gloves, and clothes should be laundered separately. A 6
month period o f contraception is recommended although none o f this is evidence based (as per
usual).
Treatment for Bone Pain
Radium - Ra223 (Xofigo): side effects
Non-hematologic toxicities are generally more common than hematologic ones; diarrhea, fatigue, nausea, vomiting, and bone pain make the list.
SR 89 quick
Pure Beta Emitter
Most Bone Marrow Toxicity (longest recovery).
Renal excretion
SM 153 quick
Beta Emitter, with some imageable gamma rays
Less Bone Marrow Toxicity
Renal excretion
RA 223 quick
Alpha Emitter
Least Bone Marrow Toxicity
GI excretion
Improves Survival (prostate mets)
Yttrium-90
overview
This can be used as a radioembolization method for unresectable liver tumors. This is a pure Beta
emitter that spares most of the adjacent normal liver parenchyma (as the maximum tissue penetration is
about 10 mm).
Yttrium-90
prior to treatment
Prior to treatment with Y-90 the standard is to do a 99mTc MAA hepatic arterial injection. The primary
purpose of this injection is to look for a lung shunt fraction. This fraction needs to be < 10% under
ideal circumstances. You can still use Y-90 for 10-20% shunts but you need to decrease the dose.
Above 20% the risk of radiation pneumonitis is too large.
Yttrium-90
particle size
The optimal particle size is between 20-40 um, as this allows particles to trap in the
tumor nodules, but large enough to get stuck without totally obstructing. If you create a true
embolization the process actually doesn’t work as well because you need blood flow as a free radical
generation source.
Yttrium-90
radiation dose
The dose is typically 100-1000 Gy delivered. The current thinking is that lesions require at least 70 Gy for monotherapy success.
Yttrium-90
imaging
There are 175 Kev and 185 keV emissions you can use to image
Yttrium-90
trivia
The average half life is 2.67 days.
Radioimmune Therapy (RIT)
overview
Monoclonal antibodies can be used with Indium111 , such as ibritumomab tiuxetan (Zevalin) for
refractory non-Hodgkin lymphoma treatment or as a first line treatment.
The idea is that you can give the antibody labeled with Indium111 for diagnostic evaluation of the tumor
burden and then if the biodistribution is ok you can give the antibody labeled with Y-90 for treatment.
Radioimmune Therapy (RIT)
trivia 1
The antibody binds to the CD-20 receptors on B-cells.
Radioimmune Therapy (RIT)
trivia 2
Don’t give to patients with platelets less than 100K
Radioimmune Therapy (RIT)
what is considered altered distribution
(1) Uptake in the lungs is more intense than the heart day one, or more intense than liver on day 2 & 3.
(2) Uptake in the kidneys more than the liver on day 3.
(3) Uptake in the bowel that is fixed, and/or more than the liver
(4) Uptake in the bone marrow > 25%
Radioimmune Therapy (RIT)
most common side effect
Thrombocytopenia and neutropenia (about 90% of cases).
Radioimmune Therapy (RIT)
can you send them home post treatment
Dose to caretakers or persons near the patient is low, and they
can be released to the general population after treatment. Although some things like sleeping apart, no
kissing, etc… for about a week are still usually handed out.
Radioimmune Therapy (RIT)
protocol
You need to first give rituximab to block the CD20 receptors on the circulating B cells and
those in the spleen to optimize biodistribution. Then you can give the In111 labeled antibody to assess for
altered biodistribution. If you suspect altered distribution you should get delayed full body imaging at
90-120 hours. If altered you shouldn’t treat. If ok, then blast’em.
“Critical Organ ”
An organ that limits the dose of the radiopharmaceutical due to the increased
susceptibility of the critical organ for cancer. This may or may not be the “Target Organ.”
“Target Organ”-
This is the organ you want the tracer to accumulate in. It’s your organ of interest
A few generalizations on Critical Organs
If you are trying to
figure it out, it’s the organ that the tracer is going to spend the
most time in. For example, Gallium ends up in the bowel. Tc
RBC scans are going to end up passing through the heart a lot,
unless they are heat treated then the spleen eats them. Tc-
MAG3s and DTPA is going to be the bladder, but DMSA (which
sticks to the kidney) is going to be the kidney.
Liver
- In -P ro s taS c in t
- M31 m ib g
- S u lfur Colloid (IV)
Galbladder wall
HIDA
spleen
- -O ctre otid e
- -Damaged RBCs
- -In-WBC
stomach
pertechnetate
renal cortex
• Thallium
. DMSA
proximal colon
- Sulfur Colloid (oral)
* Sestamibi
bladder
MAG 3
• I123 MIBG
• MDP *some source
say bone
distal colon
Gallium
Tc - 99m
Analog -
Energy - “Low” - 140
Physical Half Life - 6 hours
Iodine -123
Analog - Iodine
Energy - “Low” - 159
Physical Half Life - 13 hours
Xenon - 133
Analog -
Energy - “Low” - 81
Physical Half Life - 125 hours (biologic tl/2 30 seconds)
Thallium - 201
Analog - Potassium
Energy - “Low” - 135 (2%), 167 (8%), use 71 MiHg daughter x-rays
Physical Half Life - 73 hours
Indium - 111
Analog -
Energy - “Medium” - 173 (89%), 247 (94%)
Physical Half Life - 67 hours
Gallium - 67
Analog - Iron
Energy - Multiple; 93 (40%), 184 (20%), 300 (20%), 393 (5%)
Physical Half Life - 78 hours
Iodine -131
Analog - Iodine
Energy - “High” - 365
Physical Half Life - 8 days
Fluorine -18
Analog - Sugar
Energy - “High” -511
Physical Half Life - 110 mins
Treatment Radionuclides Half Life
Strontium 89 50.5 DAYS (14 days in hone)
Samarium 153 46 Hours
Radium - 223 11 Days
Yttrium 90 64 Hours
Cardiac Radionuclides
Half Life
Rubidium 82 75 seconds
Nitrogen 13 10 mins
