Nukes Flashcards
knee jerk for ocreotide scan
hot spleen & kidneys
I-123 vs I-131
- 1-123 lower E (159 keV)–> higher dose –> 24 hr imaging. 1/2 life 13 hrs. no b-emisison. Cardiac & adr act MC.
- I-131 high E (~364)–> crummier images. 1/2 life 8d. b-emission
Tc WBC vs In WBC
- both spleen > liver
- Tc-renal & GI. In does NOT. Higher count –> cleaner
- WBC- lung (<24 hrs)–> GI.
Tracer localization via chemisorption
- Tc-99 Medronate (MDP)
- binds HYDROXYAPATITE
Tracer localization via facilitated diffusion
F-18 FDG
Tracer localization via passive diffusion
T-99 sestamibi, tetrofosmin, HMPAO, ECD.
Tracer localization via secretion
-T-99 IDA, pertechniate
I-123, 131, T99 pertechnetate- mech of transport
I-analog transported via Na/I symported NIS.
K analogues
Thallium, Rb (transplant via Na/K ATP pump)
T-99 sestamibi-how is it transported
lipophilic cation with affinity to negatively charged mitochondria
ECD vs HMPAO
ECD faster clearance from blood pool
preparation bone scan
15-25mCi tracer
img at 2-4 hr (let ST clear)
MDP uptake dep on…
1) OB act (1˚at cortex)
2) blood flow
3) vitD
normal MDP uptake/localization
- bone
- kid, bladder
- breasts,
- ST
ways of getting free Tc
1) no enough Sn
2) air (oxide)
3) H2O–> clumping
Where is free Tc
- stomach
- thyroid
- salivary glad
making a good bone scan in setting of poor renal function
1) oral hydration 2-6 hrs before
2) 4th phase (24 hr delay)-problem=T99 half life is 6hrs
when does “flare phenomenon” occur. Why. How you know it’s flare?
2wk-3 mo
- bone healing
- xray: more sclerotis, start improving at 3 mo
persistent visualization skull sutures on bone scan
renal osteodystrophy
focal breast uptake on bone scan
-cancer
renal cortex hotter than adj lumbar spine on bone scan
hemochromatosis
diffuse renal uptake on bone scan
crx, urinary obstr
Liver uptake on bone scan
1) Al3+ contamination
2) hepatoma, mets
3) amyloidosis
4) liver necrosis
spleen uptake on bone scan
-autoinfarcted spleen
+ scattered hot & cold areas from mult bone infarcts
lung uptake on bone scan
- hetrotopic Ca (dystrophic or mets)-classically OS
- fibrothorax
- 1˚ lung tumor
- radiation change
- sarcoid, berrylliosis
- wegener’s
- alveolar microlithiasis
muscle uptake on bone scan
rhabomyolysis
diffusely decreased skel uptake on bone scan
1) Free Tc
2) bisphos
arterial intravasation on bone scan
arterial–> distal
causes insufficiency sacral fractures
- OP
- radiation
when should bone scan be performed to evaluate for fracture in elderly?
1 wk
AVN dx tests
MRi–> bone scan (if CI or need to image mult bones at once)
Donut sign-AVN femoral head
-hot on outside, cool in inside
AVN appearance on bone scan
dep on timing
- early=normal or cold (via interrupted bs)
- later-hot (at time that radiographs are becoming sclerotic)
hypertrophic osteoarthropathy affects what pt of bone
periosteum
donut sign-tumors
cystic (GCT, ABC, telangiectasia OS)
benign HOT bone lesions
- abc, gct
- oo, ob
- FD
use of PSA in predicting bone mets
<10 ng/ml nearly excludes
>100 highly predictive
MC loc for single metastatic lesion
spine
Mets on a bone scan
1) rarely single (15-20%)
2) super scan
3) MULT, randomly distributed into diff sites
how many dying prostate cancer pts have mets?
85%
which nuc medicine scan is bone uptake always abN
MIBG, 1-131, ocreotide
where does breast bone met usually go
spine
what pt of skeleton does lung cancer met to?
appendicular
which scan is most sup at detecting NB bone met?
MIBI
what pt of bone does NB met to?
metaphysis
what pt of skeleton does osteopokilosis spare?
spine & skull
next step: equivocal lesion on bone scan
plain film- no corresponding lesion=more concerning –> MRI
radiation change on bone scan
- acute (2-3 mo)-warm
- late (~6 mo)-cold. Persistent.
trickery re: bone scan and no kidneys
horseshoe
ways of showing FD on bone scan
- hot mandible
- leg that looks like pagets
superscan causes
1) diffuse mets-breast & prostate
2) metabolic-hyperPTH, renal osteodystrophy, Pagets, thyrotoxicosis
cold lesions on bone scan
1) late radiation change
2) early AVN
3) infarct (very early or late)
4) anaplastic/lytic tumor (renal, thyroid, NB, myeloma)
5) artifact-prosthesis, PM, etc
6) hemangioma-vairable
7) bone cyst (w/o fx)
8) mature HO
utility of bone scan re: heterotypic ossification
- serial exams to detect if process is active-resect once mature (cold)
- *still active=higher rate recurrence
F18-NA PET vs T99-MDP
F18-Na-cleaner, shorter exam time, more expensive. critical orgn=bladder
-MDP: bone (critical) & kidney, fuzzy
F18-NA vs FDG PET
will look similar in pts w/ GCSF or EPO (diffuse bmarrow) but brain uptake on FDG
when would you use Tc99 HMPAO instead of In-WBC for infection? Why not use it all the time?
Uses:
1) kids (lower absorbed dose & shorter imaging)
2) small pts-T99 does better in hands, feet
Not all the time:
1) .T99 shorter half life
2) GI and gb act obscures act in those areas
In-WBC-which cells are labeled?
90% NP (lymphocytes tend to be killed by radiation)
In-WBC critical orgn
spleen
what happens if In-labeled cells fragment?
indium binds transferrin-see liver and bmarrow uptake
How is MAA prepared?
denaturation of human serum albumin
-give via IV
MAA biologic half life
4 hrs
xenon 133 vs Tc99DTPA: gas vs aerosol
x=gas
DTPA=aerosol
Xenon 133: KeV, half life and bio halflife, critical orgn
- 81 KeV
- 5.2 d
- 30 s
- trachea
3 phases of xenon 133 administration
1) wash in (single max inspiration and breath hold)
2) equilibrium (breathing room air and xenon mix)
3) washout (Breathing normal air)
DTPA administration
- requires more pt cooperation (breath through mouth guard w/ nose clamp for several mins)
- must do this part before MAA?
quantification studies
- before lung resection/tx
- must use Xe + Tc MAA bc Xe won’t interfere w/ Tc
significance of tracer in brain during v/q scan
shunt
MAA particle size and #
- 10-100 micrometers
- 500K
when do you reduce particle amount and why?
- risk a functional PE
- anyone with fewer capillaries (don’t want to block more than 0.1% of caps, ie: children, 1 lung)- 10-50K in neonates
- R–>L shunt (don’t want to block caps in brain). 100K
- pulm HTN
- pregnant
- this does not reduce dose-normal dose of Tc added to fewer particles
clumped MAA moa, app
blood in syringe
multiple scattered focal hot spots
persistent pulmonary activity during xenon washout
air trapping (COPD)
accumulation Xe over RUQ
fatty liver
clumping Tc-99m DTPA
mouth, central airways, stomach (from swallowing)
what if tracer is in thyroid or stomach on VQ scan?
1) free Tc
2) R to L shunt
what do you need to call R to L shunt?
tracer in brain
if you suspect a R–>L shunt, how do you alter scan?
decreased particles
unilateral perfusion defect of whole lungg, no ventilation defect
CT or MR
Ddx= mass (MC), fibrosing mediastinitis, central PE
Gallium vs Indium WBC?
- gallium can bind to NP mets after cells are dead (helpful particularly in chronic inf)
- spine-gallium
- abd/pelvis-I-WBC
Gallium-67: production, half life, decay, emitting gamma photopeaks, when do you scan, critical orgn, normal localization?
- cyclotron via bombardment of Zn68 –> complexed with citric acid –> gallium citrate
- HL 78 hr
- electron capture
- 93 KeV (40%), 184 (20%), 300 (17%), 393 (5%)
- colon
- liver (highest), MARROW (and cortex), spleen, salivary/lacrimal glands, breasts, GP/thymus (kids)
- kid/bladder <24 hr (faintly up to 72 hr)
- <24 hr faint lung, >24 hr faint bowel
when is gallium uptake + in chest?
-infection
-sarcoid-active disease, guide bx/lavage graded ag bg lung
-CHF
-atelectasis
-ARDS
-idiopathic pulmonary fibrosis-monitor resp to rx
-immsupp: PCP, bacterial PNA. (-) for kaposi and ?lymphoma
-early drug run-bleomycin, amdiodarone)
-
lambda sign
1-2-3 (bilateral hila, R paratracheal LN)
panda sign
NP, parotid, lacrimal
*sarcoid, sjogrens, treated lymphoma
FDG-PET pleural talc
+ via granulomatous rxn
doses MAA, Xe and DTPA
- 3-5 mi
- 10-20
- 30
segmental defect size
- small <25%
- moderate 25-75%
- large: >75%
high probability PE (97%, PPV 88%)
- mismatched segmental defects. No associated radiographic abN (excludes clinical mimics).
- 2+ L
- 2 L & 2 mod
- 4 mod
intermediate probability (20-85%)
- 1L mismatch
- 1-4 M
- triple match LOWER lung
low probability (5-19%; NPV 84%)
- 1 L or M matched
- UPPER/MID lung triple match
very low probability (2-5%)
- 3- sm perfusion defects
- non segmental lesions-CMG, diaph elevation, aortic aneurism, pl eff, hila, PM artifact, fissure, bullae
- fissure/stripe sign-thin line MAA uptake btw perfusion defect and adjacent pleural surface representing intervening perfused lung
CTA vs VQ scan radiation doses to maternal breast and fetus
- CTA: breast 10-70mGy (ACR rec 3mGy/br). Fetal dose 0.1-0.66mGy
- VQ: breast <0.31 mGy, fetus 0.1-0.37
changes to routine VQ scan in the pregnant pt
-perfusion only
-adm 1/2 standard dose
~100K particles
what are the functions of the kidney?
80% secretion
20% filtration
Tracers used in renal scintigraphy
- DTPA- Filtration. GFR (small portion protein bound, not filtered–> slightly underestimation)
- MAG3-Secretion (ERPF)
- DMSA-binds prox tub cortex-ass cortical integrity
- GH (glucoheptonate)-structural (binds to cortex) or functional (filtered)
- critical orgn= bladder (exc dmsa-kid)
how is renal scintigraphy performed and phases
- pst (ant if tx or horseshoe)
- 3 phases-blood flow (~20s), cortical, clearance
symmetrically decreased flow to kidneys
technical error (poor bolus)
asymmetrically decreased flow to kidneys
- renal a/v thrombosis
- acute rejection
- acute pyelo
- chronic high grade obstruction
asymmetrically increased renal flow
renal artery aneurysm
kidney pathology in which flow is normal
- vasomotor nephropathy- imm after sx, should recover 1st 2 weeks
- ATN-~wks-mo’s
- interstitial nephritis
- cyclosporin tox
how is cortical function/phase of renal scan assessed?
- 1 min (really drinking up that contrast)
- steep slope :)
- draw area of interest and background area of interest-correct for background. Can be screwed up if obtained over liver or spleen
how is clearance/excretory function/phase of renal scan assessed?
- reach half peak counts ~7-10 mins
- quantify retention via 20/3 or 20/peak ratio
20/3 or 20/peak ratio
peak count at 20 mins vs peak count at 3 (Normal <0.8)
-peak count at 20 vs peak count (N 0.3)
what to do in setting of suspected obstruction. how does this differ from standard renal scintigraphy scan?
lasix renogram
- wait 30 mins after clearance phase. If act still in collecting system-give lasix
- MAG3 > DTPA (better in pts w/ poor renal function)
lasix renogram exam interpretation-no obs, indeterminate, obstructed
- no obstruction-clears w/o lasix
- no obs-50%+ w/i 10 mins after lasix
- indeterminate: w/o 50% 10-20 mins
- obstructed-w/o >20 mins
MCC indeterminate lasix renogram
-dilated pelvis (reservoir effect)
false positive “obstruction” on lasix renogram
- poor response to lasix-bad renal function or dyhydration
- reservoir effect-v dilated renal pelvis (MC)
- back pressure-full bl, neurogenic bladder (resolve w/ foley)
DTPA vs MAG3 renal fx
- DTPA-GFR, ie: decreased uptake and flow (loss of perfusion pressure)
- MAG3- secretion tracer (retention)
2 ways of performing ACE-i renogram
1) standard dynamic study –> ace-i
2) 1/2 dose baseline study –> full dose
(+) ACE-i renogram
->10% worsening
ACE-i renogram study preparation
- stop ACE-i (3-5 d if captopril), CCB
- NPO 6 hr (for PE ace-i)
- maintain IV access in case of hypoTN
how would a suspected fluid collection app on renal scintigraphy
photopenic (exc urinoma only on DELAYED phase)
renal scintigraphy chronic kidney transplant rejection
-no uptake
renal scintigraphy vascular complication (thromb) s/p kid tx
-no flow or function
indications for structural renal scintigraphy
acute pyelo- (-) uptake)
- scarring/mass- (-) uptake, scarring decr volume
- coumn of bertin vs mass-mass=cold
testicular scintigraphy
blood flow study
- torsion vs other cause of pain
- Na99m-TcO4
- tape penis up out of way
- normal= symmetric flow
- acute torsion=nubin sgx (focal decrease)
- delayed torsion-halo of increased activity w/ central photopenis
- abscess-same as delayed
- acute epididymitis-(+)
trapping vs organification of iodine analogues
- “trapping”-analog transported into glad. I-123, I-131, Tc-99
- organification-oxidized by thyroid peroxidase, bound to tyrosyl moiety. Tc-99 does not do this
- only 1-5% Tc-99 taken up by thyroid==> background levels higher
when would you choose Tc-99 over I-analogue?
if pt had recent I blocker (ex: I contrast)
when can you resume breastfeeding?: Tc-99, I-123, I-131, fdg 18
- Tc-99: 12-24 hrs
- I-123: 2-3 d
- I-131: nxt pregn
- fdg 18-8 hrs
how much I analogue do you give for uptake test? When do you image?
- 5 microCi 131
- 10-20 microCi 123
image at 4-6 hr and 24 hr
normal values I uptake. How do you correct for background?
4-6 hr: 5-15%
24 hr: 10-35%
correct background prior to 24 hr (use neck counts - thigh counts)
factors that affect I-uptake test
1) renal function- (+) stable I pool –> (-) numbers
2) dietary I-variable and controversial
3) meds-Thyroid blockser, nitrates, IV contrast, amiodarone
Causes of increased I uptakes
- graves
- early Hashimoto
- rebound after abrupt withdrawal of antithyroid mx
- dietary I deficiency
Decreased I uptakes
- hypoth
- renal fx
- mx (Th blockers, nitrates, IV contrast, amiodarone
- deiatry iodine overload
which meds decrease I uptake test?
- Thyroid blockers
- nitrates
- IV contrast
- amiodarone
MCC hyperTh
graves 75%!
nukes findings Graves
-diffuse homog uptakes
*24 hr may be lower/N than 6 hr via rapid TH production
+pyramidal lobe (45%)
Plummer dx
Multinodular toxic goiter
-wt loss, anxiety, niosmina, tachycardia
nukes findings multi nodular toxic goiter
-heterogenous, moderately elevated uptake
-
toxic vs non toxic MN goiter
- toxic=hot nodules, cold background
- non toxic= moderate/warm nodules, normal background
toxic MN goiter vs graves
- toxic MN goiter=medium high uptakes (<50%)
- graves= high uptake (>50%)
MCC goitrous hypothyroidism in US
-hashimotos
nukes appearance hashimotos
inhomogeneous focal cold areas
*acute= graves appearance
subacute thyroiditis (de Quervains) sequelae
-viral prodrome –> hyperTh –> decreased uptake
subacute thyroiditis vs graves
labs are the same: TSH (-), T3/T4 (+)
SAT low uptake
solitary thyroid nodule: how often cancerous if hot vs cold
20-40% cold
<1% warm
are most thyroid nodules warm/cold?
cold, ie: benign
discordant nodule
hot on Tc-99 but cold on I-123
Cancers can trap but lose ab to organify
need to prove it’s hot on I-123 before calling benign
may be caused by 1) congenital enz deficiency that int organification OR 2) drug blockage: propylthiouracil
which thyroid cancer does well with radiation?
papillary (+ sx)
which thyroid cancer does not do well with radiation?
medullary
who doesn’t resp well to I-131 radiation therapy
1) medullary cancer
2) prior rx- pretreatment dose 50% more
3) hx of methimazole rx (even if yrs ago)
ideal thyroid uptake after sx?
<5% (assume some thyroid is leftover after sx)
*>5% =painful ablation (steroids, NSAIDs), return to OR
ideal TSH prior to I-131 treatment
ideally 50 (30 is minimum) -want TSH super high--> residual cancer/thyroid tissue really thirsty
medullary subtype nukes
- cold on thyroid scan
- MIBG, ocreotide + (NE org)
- PET+ as aggressivenss/calcitonin+, ie: calcitonin > 1000 –> PET sensitive. Calcitonin <500, not good
how do you get post op TSH up?
1) stop thyroid med
2) recombinant TSH “Thyrogen”
how do you decide on post op I-131 dosing
depends on stage 100 for thyroid only 150 for thyroid + nodes 200 for distal *test before letting pt go home to see if they need to go to hospital
when do pts need to be admitted after I-131 rx?
- 33 mCi residual activity
- NRC: 7 mR/h measured 1 m from pt’s chest
possible side effects of I-131 rx
- pulmonary fibrosis if given with lung mets
- Sjogrens-salivary gland damage. DOSE RELATED
routes that body uses to eliminate I-131?
mainly urine
-sweat, tears, saliva, breast milk
precautions at home s/p I-131 rx
*for 3 days
- water
- hard candy (keep radio tracer from jacking your salivary glands)
- distance from others
- bathroom hygiene (flush twice, sit down if male)
- disposable uteinsils
- wash clothes separately
when to get pregnant and resume breast feeding s/p I-131 rx
- 6-12 mo before getting pregnant
- no more breast feeding this round
absolute CI to I-131 rx
- severe uncontrolled thyrotoxicosis
- pregnancy
healthcare workers participating in I-131 rx
- thyroid check 24 hrs later
- RSO inspect room after dc if admitted
uptake in liver on I-scan
post treatment scan
how to monitor for recurr s/p I-131 rx
thyroglobulin (anything >0!)
I-131 and dialysis
adm imm after dialysis to maximize time I-131 on board
- (-) dose (not excreted until next sash)
- dialysate down sewer. Tubing stay in store
I-131 for hyperTh- dosing
- 15 mCi for Graves (more vascular)
- 30 mCi for multi nodular (harder to treat the capsule)
-should resolve 3-4 mo
why don’t you treat if pt is in severe thyrotoxicosis
risk thyroid storm
-can cool them down w/ mx (bb, methimazole)
when do you not use methimazole?
- allergy
- neutropenia
- pregnancy (use PTU)
exophthalmos and I-131 rx
some say don’t
wolff-chaikoff Effect
large ingestion/infusion I –> TH (-)
MCC hyperPTH
- adenoma (85%)
- HP (12%)
- cancer (3%)
two techniques to localize PTH lesions
1) dual phase
2) dual tracer
dual phase PTH scan
- Tc-99 sestamibi
- 10 min (thyroid + PTH uptake) and 3 hrs img (abN PTH uptake)
what does sestamibi dep on?
- mitochondrial density
- blood flow
false positive dual phase PTH scan
1) thyroid nodule
2) h/n cancer
3) LAD
dual tracer PTH scan-tracers, positive
1) Something that goes to thyroid and PTH (Tc-99 sestamibi or 201-thallium chloride)
2) only to thyroid (I-123, pertechnetate)
(+) on subtraction = PTH abn
problems with dual tracer technique
1) more tracers
2) motion not tolerated well by subtract img
3) things that mess w/ thyroid img
False positives and negatives of dual tracer technique
FP: 1) thyroid adenoma (MC) 2) thyroid cancer 3) parathyroid cancer
FN: small sized adenoma (MC), 4 gland HP.
*consider if negative study in setting of abN labs
MIBI (+) LN
cancer
breast specific gamma img (BSGI)
uses MIBI bc focal uptake is abN
ways of img brain in nukes
1) planar (brain death only)
2) spect
3) PET
* planar and spect use lipophilic agents proportional to bf, which should mimic metabolism
- pet proportional to metabolism
agent of CNS nukes
*all perfusion (mimicking met)
- HMPAO, ECD
- extracted, used for parenchymal img
- neutral and lipophilic-cross BBB. Unstable lipophilic forms cover to hydrophilic state-trapped
- GM > WM
-DTPA-not extracted/used for parenchymal img, ie: no SPECT
HMPAO
hexamethylpropyleneamine oxime
ECD
ethyl cysteine dimer
SPECT
single positron emission CT
HMPAO vs ECD
ECD:
- slower washout, better blood clearance (better brain to background ratio), preferred in stroke img
- 15-30 mins ideal img
- parietal, occipital
- no intracerebral redistribution
HMPAO:
- faster washout
- 15 min-2 hr ideal img
- FL, thal, cerebellum
- Tc-99m HMPAO preferred since it accumulates in brain parenchyma within 2 min and takes several hours before significant redistribution
angiographic tracer of CNS nukes
Tc-DTPA (bc stays in blood)
-main uses: shunt, NPH, brain death
how soon after seizure is tracer adm?
30 s
tracers for seizure localization
- HMPAO, ECT
- PET less practical
Thallium 201-production, decay, half life, E peaks, route of transport, high yield uses, normal uptake
- cyclotron
- electron capture
- 3 d(73 hrs)
- 69 & 81 keV
- K analog, active transport (require living cell)
-thyroid, SG, lungs, heart, skel m, liver, spleen, bowel, kidneys, bladder
uses:
- cardiac viability
- toxo- (-)
- lymphoma (+)
- kaposi (+) (gallium-)
- tumor (+)
- necrosis (-)
cns nuke tracers for tumors (diff from dementia or seizures)
201 TI (mc) 99Tc-sestamibi
- in tumor > inflamm
- scalp=control
gallium+ cns
- CNS lymphoma
- Toxo
- bacterial abs
- cyrptococcus inf
- Tb
*kaposi= (-)
what to use to differentiate lymphoma from toxo?
thallium
Lymphoma (+)
Toxo (-)
“nose sign”
ext carotid –> maxillary branches
*can’t be used to call brain death
what should be checked to confirm brain death
kidneys (adequate uptake) injection site (no extrav)
stroke on SPECT-acute, subacute, chronic
acute= cold
SA- warm (luxury perfusion)
chronic=cold
luxury perfusion
paradoxical vascular dil/blood flow in relatively avascular infarcted brain
-48-72 hrs, aka “subacute stroke”
utility of nukes in TIA
cerebrovascular reserve via adm acetazolaide (Diamox) (vasodil) –> perfusion tracer
- areas maxed out on auto regulatory vasodilator less intense
- may benefit from revascularization
nukes study for dementia
FDG PET
*HMPAO and ECD can be used. FDG great renal clearance (good target to background images), resolution PET > SPECT)
normal brain on FDG PET
- symm
- BG >15% cortex
- cerebellum <15% cortex
- thal= cortex
FDG PET alzheimers
parietotemporal (-)
- pst cingulate gyrus first abN
- ID to PD!
FDG PET multi infarct dementia
scattered (-)
FDG PET dementia w/ Lewy bodies
- OL (-)
- preservation mid pst cingulate gyrus (“cingulate island sign”)
cingulate island sign
preservation of mid pst cingulate gyrus in dementia w/ lewy bodies
cingulate gyrus
The cingulate gyrus is the curved fold covering the corpus callosum. A component of the limbic system, it is involved in processing emotions and behavior regulation. It also helps to regulate autonomic motor function.
FDG-PET picks/frontotemporal dementia
FL/TL (-)
-mimics depression!
FDG-PET neurodegenerative disorders
spare motor strip
CSF nukes img-tracer
111 In - DTPA
*intrathecal adm
abN CSF nukes study
1) tracer in Vt (via reflux) (ex: NPH)
2) failure to clear from cisterns and localize over convexities by 24 hrs
normal CSF nukes study
1) 0 hr: adm
2) 2-4 hr: basal cistern
3) 4- 24 hr: Sylvian fissure, interhem cistern
4) 24 hr- over convexities, cleared from cisterns,
NPH CSF nukes study
early entrance and persistence in LVt
delayed ascent to parasag region (>24 hrs)
NPH MRI findings
- periVt T2/FLAIR +
- aquaducteal flow void
- thinning/bowing of cc
NPH vs non-obstructive communicating hydroceph
NPH has normal opening P on LP
CSF leak sites
1) cribriform plate and ethmoid sinus
2) sella turcica into sphenoid sinus
3) ridge of spehnoid to ear
how to test for CSF leak in nukes
1) img basilar cisterns (1-3 hrs)
2) nasal pledgets- (+) if tracer in pledgets:serum > 1.5
shunt patency
- tracer in peritnoeum=distal end patent
- tracer in Vt-proximal end paten (can force it in by squeezing distal limb)
shunt occlusion
- prox: no tracer in Vt or it’s there but doesn’t clear
- distal: delayed tracer in peritoneum (>10 mins)
gold standard for gastric motor function
gastric emptying study
what pt of menstrual cycle should gastric emptying be performed?
first 10 d
what’s more sensitive: solids or liquids
solids (but some emptying problems may be liquid only)
what has lag phase? solids or liquids
solids (stomach grinding up food)
-5-20 mins
artifactual increased counts in gastric emptying
attenuation correction as food moved back and forth btw stomach
which drugs should be stopped prior to gastric emptying study and when?
*2 d before
1) prokinetics (metoclopramide (reglan), tegaserod (zelnorm), erythromycin, domperidone (motilium)
2) opiates
3) anticholinergic/antispasmodic-donnatal, bentyl, robins, levsin
4) CCB
5) antacids
serotonin rec antags (classically ondansetron/zofran) are okay!
1/2 insulin morning dose (avoid hypoglycemia, schedule early morning)
GI bleed scan vs angiogram sensitivity
nukes: 0.1 ml/min
angiogram-1 ml/min
to what pt of Hbg is t-99 tagged?
b-chain
*must first be reduced via stannous ion (tin, tinning)
ways in which T99 is tagged to RBC
1) in vivo
- tin injected
- Tc-99 pertechnetate injected
- tin bind Hb –> reduces Tc –> Tc bind Hb
* 60-80% bound –> lots of free Tc ==> dirty images
* worse if tubing heparinized or recent IV contrast given
2) in vivo-in vitro–binds 85%
- tin injection
- blood withdrawn (15-30 mins). added to Tc-99 and anticoagulant
- reinfected 10 mins later
3) in vitro (98% binding, $$$)
- blood withdrawn –> added to tin & Tc-99 kit –> reinject
how is GI bleeding scan obtained?
dynamic (as opp to static, transmission, spect or dual tracer)
GI bleed fake outs
- hydro
- tx kid
- varices/angiodysplasia
- penis
- hemangioma (over liver or spleen)
- free Tc in stomach
*THESE THINGS SHOULD NOT MOVE
+ GI study
1) extravasc
2) move (distal colon=exception)
3) intensity +
alternative ways of doing a bleeding scan
Tc sulfur colloid-fast clearance (scan w/I 30 mins), blind spots (stomach, splenic flexure, hepatic flexure)
-pros: less prep, good target to background
how many meckel’s diverticulum will take up Tc99-pertechnitate
10-30%
when should you do a meckel’s scan?
when they’re not bleeding
how to make a Meckel’s scan better
- pentagastrin-(+) uptake pertechnetate by gastric mucosa
- H2 blockers (cimetidine, ranitidine)-block secret of pertechnetate out of gastric cells
- glucagon-slows gastric motility
false positive and negative Meckel’s scan
- FP: bowel irritate (recent scope, lax use)
- FN: recent in vivo labeling of RBCs, recent barium study (attenuated)
what changes about tracer dosing in setting of hyperbilirubinemia
give higher doses
HIDA scan prep
- NPO 4 hrs
- eaten w/I 24 hr (if too full, won’t let tracer in) (CCK)
- hold narcotic for 6 hr (or 3 half lives)-trigger sphincter of oddi contraction –> delays bowel visualizeion
time line normal hida scan
liver ~5 mins
GB/ bowel -20-60 mins
time line abN hida scan
bowel but no gb w/I 4 hrs
OR
no gb at 30mins-1 hr + morphine
cystic duct sign
nub of activity in cystic duct ass w/ acute cholecystits
rim sign
gangrenous cholecystitis (20%)
biliary obstruction
“liver scan sgx” via back P in CBD
-no gb, bile ducts, or bowel
showing chronic cholecystitis
1) delayed GB filling-not seen at 1 hr but seen at 4
2) EF < 30% w/ cck stim
Decreased EF
1) chronic cholecystiitis
2) acute acalculus cholecystitis
dosing cck and morphine
cck: 0.02 µg/kg over 30-60 mins, 15-30 min before the exam
morphine: 0.02-0.04 mg/kg over 30-60 mins, max 3mg
*should never inject these w/I 30 mins of one another
drug induced cholecystatic jaundice
prompt uptake, delayed excretion
- chlorpromazine, erythromycin, birth control (estrogens), anabolic steroids, statins (sometimes)
- may mimic biliary obstrcution
biliary atresia vs neonatal hepatitis
tracer in bowel=hepatitis
*if you don’t see it in bowel, delayed img at 24 hr
reappearing liver sign
-labeled dil track sup into peri-hepatic space, coat surface of liver giving appearance of paradoxically incr act in liver after initial decrease from livery emptying into bowel
elevated bilirubin
- > 5 mg/dl
- may be suggested with increased renal activity
- suggest DISIDA or BROMIDA over HIDA (increases non-dx/inconclusive/FN exams
sulfur colloid liver scan
- FNH 40% hot, 30% cold, 30% neutral
- regenerating nodule
- hot quadrate lobe (SVC/innominate vein obstr)
- hot caudate lobe (Budd-Chiari)
liver lesion RBC +
cavernous hemangioma
- > 1.5 cm
- ant, pst img; 30 mins-3 hr
- hot on delay, ø immediate flow or pool
- FN: small size (MC), partially fibrosed hemangioma, close to vascular structure, perceived increased act on flow img
Gallium + liver lesions
HCC
abscess
Xe hot liver lesions
focal fat
size of particles of sulfur colloid scan
- 1-1.0 µm
- too big-spleen eat them and stuck in lungs)
- too small-bone marrow eats them.
colloid shift
sulfur colloid uptake by spleen or bmarrow in setting of:
- diffuse hepatic dysfunction, portal HTN, hypersplenism, mbar activation
- most specific causes: cirrhosis, diffuse liver mets, DM, blunt spleen trauma
diffuse pulmonary activity in sulfur colloid scan
- excess aluminum
- primary pulm issues (reflecting phagocytosis by pulm MPs)
renal act on sulfur colloid scan
- CHF mc (decreased renal bf/filtration P)
- renal tx-rejection (colloid trapped in fibrin thrombi of microvasc)
- COxB, DIC, TTP
hemangioma vs Angiosarcoma
angio hot on immediate flow or pool
focal fat
Xe+
SC (-)
SUV =
(FDG concentration at time T) / (dose/body wt)
> 2 generally abN
high bg
> 150-200
eff of insulin
drives into m
when do you img fdg-pet ct following rx?
- 2-3 wks after crx
- 8-12 wk s/p radiation
- avoid stunning induced Fns and inflamm induced FPs
reducing brown fat
1) warm room
2) propranolol, reserpine, diazepam
3) high fat/low carb diet
hibernoma
focal brown fat
-ddx=liposarcoma, so resected
obesity eff on SUV
higher (fat takes up less llc)
Ki67 proliferation index
+ = more aggressive tumor
where do you inj FDG in setting of breast cancer?
- opp side
- pt supine, arms up
when do you use FDG-pet for breast cancer screening
if CI to MRI
FDG cold tumors
- BAC
- carcinoid/NE (low/intermed grade)
- 50% RCC
- perotneal bowel/liver implants-small and adj bowel
- perivesicular dx-missed by adj bladder
- mucinous anything
- prostate
- 60% HCC (variable g6p that can’t trap FDG
- nonseminomatous testicular CA (or Luke warm)
- MALT lymphoma
- necrotic or cystic tumors
which renal tumor is FDG hot
oncocytoma
diffuse thyroid FDG+
hashimotos
seminomatous vs non-sem CA
non-sem cold/Luke warm
-sem=hot
metformin eff on fdg
large > small bowel uptake
*hold for 48 hrs
FDG avid bowel spots
cancer
villous adenoma
FDG NETs
high grade
FDG pit adenomas
benign ones are hot
-horm w/u and MRI
when is adrenal FDG uptake abN
> liver…variable
-compare to non-con ct (<10hu)
FDG in sarcoid
cardiac
-can use as 1˚dx test or if bx failed
recurr lymphoma vs thymic rebound
recurr lymphoma=hot; round
-thymic rebound= warm; normal thymus shape
lymphoma fdg
usually hot
-MALT = low avidity
FDG endometrium
1) 1-4
2) ovulation (d 14)
- diffuse
- premeno
FDG endom: normal vs cancer
cancer= focal, post meno
FDG ovaries
ovulation
- ovoid rim w/ photogenic center
- premeno
benign FDG+ gyn lesions
-fibroids
endom cysts
-vesicovag fistula- urine spilled.
-misregistration in bladder/ureters-avoid by minimizing time btw PET and CT
use of FDG w/ osteosarcoma
- SUV Max (bc very heterog tumor); higher=higher grade; predictor of overall survival
- response to neoadj rx (FDG taken up by viable tumor)
- not used for screening bc so non-spec
Indium 111-prod, decay, peaks, half life, moa, uses, labelling process
- cyclotron
- electron capture
- 67 hr
- 173 and 247 keV
- Fe+ analog
-bind to WBC, ocreotide or DTPA (CNS img)
- must first be hooked to strong chelator.
- must isolate WBC prior to labeling (otherwise binds transferrin in blood!)
ocreotide scanning uses
- NE tumors:
- carcinoid
- gastrinoma
- PG
- SCLC
- medullary thyroid CA
- merkel cell tumor
- lymphoma
- meningioma
ocreotide scanning phases
early (4 hrs) and delayed
-early: no bowel
MIBG
- noradrenalin analog–> taken up by adrenergic tissue
- pheochromo, PG, NB (bone mets)
- link w/ I-123, I-131
- block thyroid with Lugol’s iodine or perchlorate
which meds interfere with MIBG?
- CCB
- labetalol (other bb’s have no eff!)
- reserpine
- TCA
- sympathomimetics
brown fat nukes
- FDG-PET-
- MIBG (sympathetic innervation
- shoulders, clavicles
ocreotide scan in setting of suspected insulinoma
- ocreo can trigger hypoglycemia
- give D50 bf and after or just have it ready
ocreotide scan prep if pt on ocreotide
stop rx for 3 d before
benignity vs malignancy gastronome vs insulinoma
gastronoma usually mal
insulinoma usually benign
when is ocreotide better than mibg?
everything except adrenal pheo, NB
what is best choice for non-functional islet cell tumor
fdg-pet
*mibg & ocreotide are both crap
prostascint
111-In label to Ab Capromab Pendetide (ProstaScint) –< PSA
- rising PSA + negative bone scan-looks for ST mets
- offers salvage rx (radiation to surgical bed)
- critical orgn=liver
various 111-In scans and critical orgn trivia
prostascint-liver
- wbc-spleen
- ocreotide-spleen
particle size: lymphoscintigraphy, VQ, liver spleen
<0.2 microns (<200 nm)
- 10-100 microns (10,000-100,000 nm)
- unfiltered-all sizes
sentinel node detection
10-50 nm Tcc99m-sulfur colloid for melanoma and breast cancer
sentinel node detection melanoma
- utility is in lesions 1-4mm depth
- intradermal int in 4 spots around lesion/excison scar–> img
sentinel node detection breast cancer
superficial or deep into pec m
breast specific gamma img
- 20-30 mCi Tc99-sestamibi in Cl arm –> img 20 mins later
- (foot injection if img both breasts)
- FP: FA, FC, inflamm
- FN: deep, <1cm, medial, overlying heart
cardiac img tracers
- t T99-sestamibi
- t99-tetrofosmin
- thallium (older, redistributes)
when to img cardiac tracers
- 30-90 mins for T99
- thallium-10 mins
cardiac stress test prep
- NPO 4 hrs (decreased GI bf)
- stop bb, cab, long acting nitrates for 24 hrs
- no caffeine ~12 hrs if using adenosine-related perfusion stress agents
chemical stressors
- regadenoson-less se’s/bronchospasm than others
- dipyridamole
- adenosine-AV block
- no caffeine
-dobutamine-beta 1 agonist. avoid in LBBB. pt cannot be on bb. Better in pts w/ COPD, asthma or have taken caffeine in 12 hrs
LBBB classic artifact on cardiac stress tests and which drug to use
- reversible perfusion defect at septum via improper relaxation during diastolic coronary filling bc discard rhythms
- need a perfusion drug.
- Dobumatin causes more FPs (incr HR–> decr septum relaxation)
fixed vs reversible defects on img
-fixed with surrounding reversible
- fixed=scar
- reversible=ischemia
- infarct w/ peri-infarct ischemia
LV cavity larger on stress vs rest
transient ischemic dilation
-diffuse SE hypo perfusion-correlates with hi risk dx (L main or 3 vess)
fixed cavity dilation
dilated cardiomyopathy
RV activity on rest
RV hypertrophy
lots of splanchnic act on cardiac stress
-not stressed enough
stunned myocardium
perfusion +, contractility (-)
hibernating
perfusion (-), contributed (-) , FDG+, thallium redistribution
hibernating vs scar
hibernating takes up FDG and redistributes thallium
multicoated acquisition scan (MUGA)
angiogram using tagged RBCs that is gated
- calculates EF (more accurate than myocardial perfusion for LVEF)
- performed in LAO (best septal view)
- falsely low EF: LV overlapped w/ LA or RV OR LA is big
- falsely high EF-ROI over spleen (wrong subtraction)
rubidium 82 & NH3
PET myocardial perfusion
1/2 life 75 s vs ~10 mins
Regadenoson
adenosine rec agonist
few se’s.
dipyridamole
inh bd of adenosine
adenosine
vasodilator
-aminophylline=antidone
agents for bone pain ass w/ metastatic disease from breast, prostate cancer
1) Sr 89-Cl
2) Sm-153 ETMP
3) Ra-223 dichloride
Absolute CIs to Sr and Sm bone pain rx
- pregnancy
- breast feeding
- renal fx
Strontium-Sr89 (Metastron)
- complexes with hydroxyapatite
- worst agent, highly myelotoxic
- b-emitter
samarium-Sm 153 (quadrate)
- complex w/ hydroxyapatite
- b-decay and 28% via gamma ray (103 kev), ie: used for img
- renal excretion
- myelotoxic
Sr89 vs Sm153
- SR89: 15-30% drop in platelet and WBC. 8-12 wk recovery
- Sm-153: 40-50% drop, 6-8 wks
radium-Ra 223 (xofigo)
- Ca-absorbed at sites of mineralization
- emits 4 alpha particles (shorter range than Sr, Sm–> less hematog.
- long half life- 11.4 d (shipping)
- non hematog tox mc than hematoma (diarr, fatigue, n/v, bone pain)
- GI excretion
- IMPROVES SURV! (prostate mets)
Yttrium-90
- beta emitter
- max tissue penetration ~10 mm-spares most of adj liver parenchyma
- pretreatment lung shunt check-10-20% decrease dose, >20% radiation pneumonitis
- 20-40 µm (trapped in tumor, but doesn’t block vess/bf
- dose: 100-1000 Gy delivered (need at least 70 for success)
- emission: 175 and 185 kev
- half life: 2.67 d
radioimmune rx + y90
-for refractory non-hodgkin lymphoma’
- preop with rituximab to block CD20 recs on circulating cells and in spleen
1) I-111 labeled Ab (ibritumomab tiuxetan/Zevalin) –< CD20 recs on Bcells==> eval tumor burden
2) Y90 rx - if altered bio distribution, don’t treat
- mc se’s: TCP, NP (90%), ie: don’t give to pts w/ PC < 100k
- can be discharged w/ proper care at home
% R –> L shunt
[(whole body count-lung count)/whole body] x 100%
LVEF calculation
(end diastolic count - end systolic count)/ (end diastolic counts - background counts)
thallium, cardiac img
- high 1st pass extraction 85%
- quick redistribution-dynamic exchange btw myocardial cytosol and vascular blood pool ie;: post stress img <10 mins post injection and delayed 24 img
ddx decreased pulmonary perfusion/absent perf
SAFE POEM: Swyer-James syndrome, pulmonary Agenesis/hypoplasia, mediastinal Fibrosis, pleural Effusion, Pneumonectomy, Obstruction by tumor, pulmonary Embolus, Mucous plug.
DTPA-uses
- Tc-DTPA-lung vent
- Tc-DTPA-kidney filtration
- Tc-DTPA-CSF
- In-DTPA- liquid emptying
Liver scan
- blood pool act, ø excr into bg, gb, or bowel at 60 min
- obtain 4 and 24 hr delayed img
-hepatitis
-biliary obstruction
-
captopril renogram FPs
dehydration
-captopril induced hypoT
CCBs
en block transplant
2 peds kidneys transplanted into adult
