1.SPECT thallium or sestamibi with reversible and fixed defects. They ask if it’s thal or
Tc, and the trick is that some of them are labeled redistribution, so thallium. They ask
vascular territory. They as about stunned vs hibernating and they show 3D images with
abnormal wall motion or LV dilation @ stress only
As far as vascular territories, there is a nice diagram of the 3 views(SA,HLA,VLA) with
the corresponding territories in Mettler 136. There are numerous examples of reversible
and fixed defects in the ACR Nucs disk and Mettler 144&145.
The difference between stunned and hibernating is that stunned has normal or near
normal perfusion, but it has decreased or absent motion temporarily. This does not need
revascularization, as it will recover on its own. It is due to ischemia that was relieved
(spontaneously or by TPA/cath) before significant injury occurred. Hibernating is
chronically ischemic myocardium which has reduced perfusion and contraction. It will
help to revascularize it, it will not recover on its own.(M160) The ways to assess for
hibernating myocardium are either with combined NH and FDG PET(discussed later) or
with 24 hr delayed thallium or a second injection for the thallium rest images(3 mCi
initially, then another 1.5 mCi at 4hrs).
LV dilation at stress only is indicative of a severe ischemic burden, generally multivessel
disease. It is one of the 5 bad outcome predictors, with the others being defects in
multiple vascular territories, left main distribution, lung accumulation of thallium, and
large, severe defect. See ACR disc case 508. On every case, before I look for perfusion
defects, I check for LV dilation, wall divergence toward apex(aneurysm) and lung and
Regarding the tracer used, I plan to initially call every SPECT study a “myocardial
perfusion study SPECT”, and if asked whether thal or Tc, then I will look if any of the
films are labeled “redistribution” which only applies to Tl. If you see gallbladder uptake
on the rotating man image, then you know it is Technetium
I was shown MPS with fixed defects anterior and inferior, and dilated LV. I said prior MI
with cardiomyopathy, and asked for gated SPECT to assess motion and EF. There was
hypo or akinesis anterior and inferior, and EF was 37%.
2.V/Q scan with various scenarios. Either multiple mismatched defect/high prob, or triple
match lower lobe, or COPD and patchy perfusion defects
High prob:2 or more large mismatched defect or 4 or more moderated defects is high
prob. For defect size, <25% of a segment is small, 25-75% is moderate, >75% is large.
See Mettler 214 and BH 1245.
Triple match:They show CXR with effusion and matched V/Q defect, which is a triple
match in the lower lobe, which is intermediate probability.See exact case ACR 424. In
the upper lobes, a triple match would be low prob.
COPD: COPD lowers the sensitivity and specificity of the exam. COPD may cause
segmental or nonsegmental defects. Even matched defects can be extensive enough to
warrant an indeterminant/intermediate prob, although some would still call this low prob.
Be sure to check the CXR, and check the ventilation for retention. Usually, you will need
another study such as CECT, or maybe venous dopplers. Some residents claim they were
shown COPD with stripe sign, with definite sparing of the pleura(M217) so they called it
low prob. See CR p175 for a low prob scan in COPD. Also see ACR case 404 which is
mild COPD with one moderate matched apical defect, low prob.
I was shown a V/Q sacn with heterogenous ventilation and perfusion, with the stripe sign.
I thought it was COPD and low prob, but the examiner said the pt had a history of CF, so
I said that would also explain the findings.
3.Thyroid: they ask solitary cold nodule, cold nodule in setting of MNG, hot nodule,
autonomous nodule. Have asked details on isotopes and doses.
Disc:The isotopes used for thyroid studies include Tc pertechnatate, I123 and I131. Tc
pertech is trapped but not organified. T1/2=6hrs keV=140. Can distinguish from Iodine
study b/c of the high salivary uptake with Tc, and the high background activity. Dose is
10mCi IV with imaging in anterior, LAO and RAO at 20 minutes. Some do flow images
at time of injection too. Cannot determine uptake with Tc. For I123, dose for scan(+/-
uptake) is 200-600uCi(that’s micro!). If only doing uptake, then only 20uCi. Uptakes are
measured at 4 and 24 hrs. Scanning is performed at 24 hrs. T1/2 13.2 hrs, 159keV. For
I131 (T1/2= 8 days keV=364)is not used for routine imaging b/c it has high dose, so I
doubt they would ask for the dose for “routine ” scan or uptake. It is used post
thyroidectomy to look for residual thyroid and nodes/mets. This can be done in 2 ways.
Either the pt stays off synthroid(T4) at least 4 weeks, or off cytomel(T3) for 2 weeks, in
which case the I131 dose is 2mCi. Alternatively, the pt can stay on meds and take
thyrogen for 2 days prior to the scan, in which case the dose is 4mCi. Imaging is at 72 or
96hrs post oral I131. Normal distribution in thyroid, stomach, salivary and
bladder(M120). In the rare instance that the post-thyroidectomy scan is completely
normal, then it is controversial whether to treat, just in case there are micromets which
you cant see on the scan. At Cooper, we don’t treat if the scan is completely normal.
However, in the overwhelming majority of cases there is either residual thyroid or
nodes/mets, in which case you treat. We start with 100mCi. If that doesn’t work, the next
treatment would have to be at least 150mCi. You can theoretically treat 5 or even 10
times, but if 3 are not successful it is usually not gonna work. Also, at 800mCi you start
to get significant bone marrow suppression. The rules of discharging a pt post I131
therapy are: Any dose <30mCi can go home right away. If >30 mCi, then can go home
when either: measured dose at 1 meter from pt is <7mrem/hr or calculated maximum
dose to another person would be no more than 0.5rem(500mrem). Pt goes back on
hormone replacement several days after treatment and follow up I131 whole body at 6
month intervals. For Graves dz, the I131 dose is 15mCi, and for toxic nodular goiter,
25mCi for solitary(may need 30 or more sometimes in MNG)ACR 707
Cold nodule:This has about a 15 or 20% risk of malignancy. The bulk of the other 80%
are colloid cysts or adenomas, with the being abscess, node, focal thyroiditis etc. risk is
higher if young male pt or prior neck radiation, or no response to a trial of hormone
suppression or adenopathy. See M114 F7-6, ACR 703
MNG with dominant cold nodule:These generally have less risk than isolated cold
nodules, but any cold dominant solid nodule still needs biopsy. If history of neck
radiation then higher risk. See ACR case 708
Hot nodule: this is a focal area of increased uptake, which usually is autonomous(Toxic)
and suppresses the rest of the gland, but not always, b/c it occasionally doesn’t produce
enough hormone to suppress. See CR p245 and M115 F7-7C, ACR 705 Less than 1%
chance of malignancy in hot nodule.
4.Lymphoma on a WB Gallium or PET scan. They usually show a young male with
inguinal nodes and chest or retroperitoneal nodes. Sometimes give Hx of HIV. One case
shows abnormal uptake in upper abdomen and hip. Another case has an incidental finding
of an absent spleen. DDx includes mets(young male seminoma, melanoma, rhabdomyo)
and infections such as TB or MAI
Disc:About gallium scanning:Gallium has T1/2 of 78.1 hrs and has 4 photpeaks of 93,
184, 296, &388. Dose is 5mCi for infection and 10mCi for tumor imaging. Imaging is
performed for tumor at 48 hrs(or 72), and then wait another 24 hrs or more if needed to
improve target to background(bowel). Normal distribution Liver>spl, marrow,
nasopharynx, lacrimal/salivary, and bowel, especially colon, breast, genital(M371).
Renal/bladder only in 1st 24 hrs, later not. Sensitivity for Hodgkins is about 90%, but
Nonhodgkins varies with cell type, and not as high. Should wait at least 4 weeks post
chemo to do a gallium b/c of stunning. Most places routinely do SPECT with the
planar(we do SPECT of neck and thorax) b/c of better sensitivity. Certainly if you are
unsure of something on the exam on planar, ask for SPECT. For examples of lymphoma,
see M373 and CR p55, ACR 302 F1&2, 5&6.(Also see SPECT in Film 15)
PET:Normal distribution for FDG is brain(only WB scan to have brain uptake!), kidneys,
bladder, and heart(but level in hrt varies with glucose levels), sometimes with lesser
uptake liver/spl. Dose is 10mCi FDG for most everything. Imaging is 1hr post injection,
so it is more convenient than gallium. Also, it has better target to background and better
image quality, and bowel is rarely a problem as it is with Ga. For lymphoma seen on
FDG PET see CR p191. The tumors with consistent PET uptake are lymphoma, lung,
breast, melanoma, Head/neck.
Staging for lymphoma is Ann Arbor. Stage 1=single lymph node region or single
extralymphatic site Stage 2=noncontiguous areas same side of diaphragm +/- one
extralymphatic site Stage 3=nodes or extralymphatic sites on different sides of the
diaphragm Stage 4=disseminated involvement of one or more extralymphatic
sites(usually marrow or liver) with or without lymph node involvement. Substage A does
not have systemic symptoms and B does(fever, wt loss, night sweats, pruritis). Although
this system is used for both hodgkin’s and NHL, it was designed for Hodgkins and does
not work as well for NHL in determining prognosis etc.
My case was PET with paraaortic, mediastinal right supraclaviular and right axillary
uptake, and I said most likely lymphoma and she said I was right.
5.Parathyroid adenoma: On Tc Sestamibi or Tl/Tc subtraction. Ask about sensitivity,
DDx, when to do these. Beware, they showed a few as incidental finding on sestamibi hrt
planar images, so if you see a planar heart, remember to check the neck
85% of cases of primary hyperpara are due to single or multiple hyperfunctioning
nodule(s), 15% are from hyperplasia. Many surgeons explore without prior imaging, but
some who are less experienced do not, and the rest use imaging when there was a
negative neck exploration or for persistent/recurrent hyperpara postop. There are 2 ways
to image parathyroid nodules. One is with combined Tc pertechnatate(6 mCi) and
Thallium 201 chloride(3mCi). This has about 71% sensitivity for primary hyperpara, but
much less in secondary hyperpara.Thallium is taken up by both thyroid and parathyroid,
whereas Tc is only taken up by thyroid. Thus, if you peak for Tl and separately for Tc
and then you do computer subtraction of the Tc from the thal, you should be left with
only parathyroid activity. False positives are due to thyroid cancer, coloid goiter, focal
hashimoto’s, or less likely, mets, sarcoid and lymphoma(M125, ACR 712)
For sestamibi, you give 20mCi and then image at 15 minutes and 2 or 3 hours. At 15
minutes, nl thyroid and thyroid or parathyroid adenomas or hyperplasia have uptake.
However, at 2-3 hrs, only parathyroid adenomas should be hot. Sensitivity 87%, so better
than the subtraction method. Again there are false positives, most commonly from
thyroid adenoma and lymphoma. See M126 and CR p105 c58, ACR 713. You know
MIBI was used if films are labelled 2 or 3 hours. Hrt activity could be MIBI or Tl
There is actually a 3rd way to image and that is with I123 and Tc-MIBI subtraction. The
idea is that I123 localizes only to thyroid, and MIBI to thyroid and para, so if you
subtract I123 from MIBI, you are left with parathyroid only.(CR p105 c59)
I got a parathyroid adenoma, but I thought the sestamibi was somewhat equivocal, as the
uptake was only slight on the 3 hr images. So I said I would do a subtraction to confirm
it, and then she showed me a I123/Thal subtraction which did confirm it.
6.Cardiomyopathy on SPECT or 3D recons demonstrating abnl motion, sometimes
MUGA with low EF of 35%. Ask causes of cardiomyopathy.
Dialted cardiomyopathy is suggested on SPECT when there is dilation of the LV at rest
and stress. This can be worse at stress if ischemic in origin. Also, if it is ischemic in
origin, then there will be multivessel perfusion defects, although these may be balanced
and therefore not easily detectable. In ischemia, findings are usually limited to the LV,
but with other types, findings are biventricular. See ACR 505. On gated SPECT, the
LVEF will be low(<55%) and wall motion will be diffusely diminished. 3D
reconstructions may show this better. Other causes of dilated CM include alcohol, chemo,
toxins, diabetes, thyroid dz, acromegaly, hypocalcemia,hypophoshatemia,
hemoglobinopathies and thiamine deficiency. Restrictive cardiomyopathy is totally
different, and has wall thickening, poor diastolic filling and high EF.
With MUGA, findings of cardiomyopathy include dilated LV(or biventricular) with low
EF(<55%) and sometimes low RVEF(<40%) with global hypokinesis. See ACR 523
(The nl LV should be slightly smaller than the RV). Methods for a tagged RBC scan will
be reviewed later under GI bleeding scan. However, in short, there are 3 possible
methods, in vivo, in vivtro and in vitro, which entail initially giving 1mg stannous ion to
reduce the RBCs(either in the body or in a tube), followed by 20mCi Tc pertechnatate
into the body or into blood taken from patient.
7.SPECT or PET with decreased uptake temporal or frontal. Sometimes it is an ACA or
MCA infarct, +/- crossed cerebellar diaschisis. One guy was shown abnormal with f/up
normal, probably a TIA.Sometimes Diamox study. Other times young person with AIDS
dementia or drug abuse, nl MRI with multiple defects
First, you cannot tell a good SPECT brain from a PET brain, so I will say “This is either a
PET brain scan or a Tc 99m HMPAO or ECD brain scan”. Hopefully they will help out.
Infarct:SPECT and PET are more sensitive for CVA in 1st hours than CT or MRI(except
diffusion imaging), can see almost all strokes within 8 hrs as cold areas(M89, ACR 619,
623& 624,. Cannot distinguish ischemic vs hemorrhagic though. Also, cannot see small
CVA, especially in WM. For 1st 3 days see reduced flow(SPECT) or metabolism(FDG)
including in the penumbra. By 1 to 3weeks, increased luxury perfusion is seen, but stable
defect by 1 month. Crossed cerebellar diaschisis is when the c/l cerebellar hemisphere
has decreased uptake, and does NOT represent a cerebellar infarct(ACR 622).
REMEMBER, if you see what looks like a cerebral CVA, check the c/l cerebellum.
Sometimes with luxury perfusion, you only see the cerebellar defect, which is the only
clue to the cerebral CVA.
With TIA, >60% will have decreased perfusion in 1st 24 hrs, but <40% detected by one
week. Hypoperfusion may persist even after symptoms have resolved, but are generally
reversible. Another cause of reversible perfusion defect would be vasospasm post SAH.
Sometimes, you cannot document ischemia unless you use Diamox(acetazolamide). Nl
brain blood flow increases 3-4 times post diamox, but ischemic areas cannot vasodilate
that much more b/c they are already maximally vasodilated, so they show up as
hypoperfused areas after diamox. This can identify high risk pts so medical or surgical
treatment can be started. See M91 f6-8. Another role of diamox is when there is an
aneurysm for which the best treatment option is sacrificing an ICA. You can do PET O-
15 first alone, then with balloon occlusion, then with diamox to see if the pt reaches the
ischemic threshold of <30% of flow, in which case you cannot sacrifice the ICA. See
AIDS dementia:It is important to distinguish the causes of altered MS in AIDS, which
can be from depression, tumor, infection or AIDS dementia. CT & MR are frequently
normal in AIDS dementia. However, SPECT will show multifocal patchy cortical and
subcortical hypoperfusion favoring the frontal, temporal, parietal and BG. These may
improve with therapy for AIDS. A similar pattern may be seen in cocaine or multidrug
users, and possibly vasculitis or multi-infarct dementia. I was shown a young person with
right frontal and left parietal defects, and I gave DDx of AIDS vs drugs vs vasculitis, and
she said it was a coke abuser.
8.Bile leak, postcholecystectomy or liver transplant, most to R gutter
First, I think it is best to call the study a “hepatobiliary scan” rather than a HIDA b/c you
don’t know which iminodiacetic acid agent they used(most today use DISIDA(a.k.a.
disofenin) or mebrofenin). Can’t go wrong with “hepatobiliary scan”.
Bile leak on IDA scan appears as an area of activity, usually beginning in the GB
fossa(from incomplete cystic duct ligation), that does not conform to normal shape of
liver or biliary tree, and which increases in size over time. It often tracks into the right
paracolic gutter and over the dome of the liver(M273, CR p69, ACR 307) Most leaks are
post surgical, especially cholecystectomy. Other causes are transplant, trauma,
interventional procedures, tumor or inflammatory processes. Bile leak is a serious
problem, and can result in peritonitis, subhepatic collection, abscess and fistula. If you
are not sure if there is a leak, get another view, such as a lateral. Sometimes need delayed
imaging(>1 hr) to detect a slow leak.
9.MAG3 +/- lasix either mechanical obstruction or functional obstruction. They ask about
pt preparation and how fluid status affects study. Ask about doses for DTPA or MAG3.
DTPA stands for diethylenetriaminepenta-acetic acid(I know WTF cares, but they asked
this) It is a GFR agent. Dose is 10mCi IV. Immediate flow study(1 frame per second for
60 seconds, tracer nl reaches kidney within 1 sec of aorta, which is about 5 or 6 sec) then
dynamic every 3 to 5 minutes for 30 minutes. MAG3 is a tubular secretion agent, and it
measures effective renal plasma flow. There are 3 phases on a MAG3 study, flow for 60
sec then tubular concentration phase during minutes 1 to 5 with peak cortical uptake, then
excretion. Normal time to peak is 3 to 5 minutes. Renal uptake ratios(R vs L) checked at
2-3 min and at 15 minutes. Normal T1/2 is 7 to 10 minutes. Patients need to be well
hydrated. If not, get an abnormal renogram(time-activity) curve with delayed peak
activity, delayed clearance or elevation of the excretion slope, and can alter response to
Lasix. In the setting of a dilated collecting system, a common clinical problem is to
distinguish mechanical obstruction from nonobstructive dilation due to reflux, UTI, prior
obstruction, noncompliant bladder. On a routine MAG3, both obstructive and
nonobstructive show decreased renal blood flow and a steeply rising curve without any
excretion. However, if you give Lasix (40mg in adult or 1mg/kg up to 40mg in kids) at
10 minutes(Cooper protocol, others do different), the nonobstructed collecting system
will empty, but the obstructed one will not(M347-349, & compare CR p91 to p365) Poor
hydration and overdistended bladder can give false + for obstruction. You should not
administer lasix if the collecting system is not filled, which usually occurs in the setting
of a high grade obstruction.
10.CSF leak on In111 DTPA into nose or ear. Ask how to do the study.
Most CSF leaks are the result of trauma or surgery. Most occur into the ear via the
sphenoid ridge or nose via the cribriform plate. The CSF leak study consists of 2 parts,
one is imaging to see the leak, and the other is to insert pledgets in ears, nose(wherever
suspected leak is)prior to the LP and measure their activity in a well counter at 4 to 24
hours and compare to a serum level obtained at the same time from a blood draw. A
pledget to serum ratio >1.5 is positive. In111 has T1/2 67hrs and keV of 173 and 247.
500uCi are instilled into the thecal sac via LP, and images for leak are obtained at 1 to 3
hours.See M99, CR p361. We do lateral and anterior imaging for rhinorrhea and posterior
11.IDA nonfilling GB at 1hr, ask what to do, give morphine, ends up being either acute
or chronic cholecystitis. Know technique/doses. What causes false + IDA? One guy
shown chronic cholecystitis with partial CBD obstruction from choledocholethiasis
Technique:Pt is NPO for at least 4 hrs prior to exam(o/w get nonfilling of GB, false +)
Inject 10mCi Tc labelled IDA. Image at 5 minute intervals for 60 minutes. Normally gb
seen within 30 minutes, &CBD and duodenum by 60 minutes. You know it’s an IDA b/c
you only see liver, and NO spleen uptake(so not SC or WBC) If no GB at 1 hr, either
continue hourly imaging to 4 hrs or give morphine 0.04mg/kg injection over 3-5 minutes.
GB should fill in 5-10 minutes post morphine in chronic cholecystitis(we image up to 30
minutes post), but not seen in acute(M264, and compare CR p65 to p67). Do not give
morphine in the setting of CBD obstruction(nonvis CBD/bowel) Besides non vis of GB,
another sign of acute cholecystitis is the “rim sign” of curvilinear increased activity
above the GB fossa(M265 f10-26). In 40% the rim sign means gangrenous cholecystitis.
The cystic duct sign is filling of a nubbin of cystic duct just proximal to an
obtruction(M266). Causes of false + IDA are recent meal, alcoholism, pancreatitis,
chronic chol, liver dysfxn, cholangioca of cystic duct and TPN or prolonged fasting
>24hrs. False – in acalculous chol, accessory cystic duct, duplication cyst mimicking GB
and duod tic mimicking GB. Partial CBD obstruction is due to stone, tumor, stricture or
sphincter of Oddi dysfxn or drugs like CCK. On scanning see persistent visualization of
CBD more than 60 minutes and delayed appearance of small bowel(if complete
obstruction, no vis of CBD b/c of high back pressure) see M272 and CRp205.
12.Superscan bone scan
This refers to a pattern of high bone to soft tissue uptake and absent renal and bladder
activity. Causes of a superscan include mets(#1 cause, mostly breast, prostate lung),
hyperparathyroidism(including renal osteodystrophy), and less likely myelofibrosis,
mastocytosis, fluorosis and pyknodysostosis. Mets tend to demonstrate more
inhomogeneity than the metabolic causes, some areas will be even more hot than the rest.
In renal osteodystrophy, there tends to be increased soft tissue uptake(not always) due to
the absence of functioning kidneys. Therefore if you see high bone uptake, absent
kidneys and high st uptake, (including stomach, lungs, kidneys)don’t say mets, say renal
osteodystrophy. Also, may see other findings in renal osteodystrophy, such as transplant
kidney, bowed bones, and railroad tracking along cortices. Also, mets tend to favor axial
skeleton with minimal distal appendicular uptake, but hyperpara favors face, calvarium
and mandible. For examples of superscan, see CR p129(mets) vs p267(renal),
M309(hyperpara) vs 295 f11-10(mets) and ACR cases 111 and 114
13.Acute AVN of femoral head. Also show OFF peak image on this case and the same
case shows a pelvic transplanted kidney and a hip replacement
Off peak imaging:The camera must be peaked before every study for the radionuclide
being used. For Tc, 140keV. If it is off peak, it produces an image with poor spatial
resolution. See M45. A similar appearance might be produced by pt motion,
nonuniformity, or poor spatial res of the camera. I would only mention these if you say
off peak and the examiner wants more.
Acute AVN produces a photopenic defect in the superior aspect of the femoral head.
Chronic AVN causes a hot focus, but some cases can have overall hot hip with small cold
focus. For example of acute see M320. For chronic see CR p273. Also, see ACR case
115, which shows AVN plus a transplant kidney(but not c/l hip replacement like on the
boards) and films 5&6 show an acute case. To put the whole case together, transplant pts
get steroids to immunosuppress and that leads to AVN(b/l in that case, c/l hip replaced).
14.ATN in transplant kidney, MAG3, nl perfusion, decr uptake/clearance DDx
The major complications post transplant(not talking about post op collections, they didn’t
ask that, and I am not getting into RVT and RAS or obstruction right now) are ATN,
rejection and cyclosporin toxicity. ATN usually occurs in the first 3-4 days. MAG3
shows normal or near normal perfusion but diminished function and progressive cortical
retention(M359, CR p97) Normal perfusion means that the kidney is visualized on the
flow portion on the same image that the iliac vessel is first seen, and intensity in kidney is
similar to the vessel. ATN resolves in 1 to 3 weeks. Rejection has 3 phases, hyperacute
within first 24 hrs, acute starts at 5 to 7 days and up to months, and chronic 6 months to
years. Rejection presents with decreased perfusion and decreased uptake and
clearance(M360). Cyclosporin tox is like ATN, with near normal perfusion, but it does
not occur for at least several weeks, so by asking when the transplant was, you can
differentiate the 2.
15.Graves’ dz on Tc pertechnatate. Doses to treat. How to tell it is Tc
With Tc you use 10mCi and get anterior, LAO, and RAO images at 20 minutes. Can tell
Tc from Iodine b/c of salivary activity about equal to thyroid, high background, and if
films are labelled with time, then easy, b/c Tc imaged at 20 minutes and I not until 24
hours. Dose to treat Graves is 15mCi and solitary nodule 25mCi and MNG sometimes 30
or more(would probably try 29.9 to avoid hassles) The pattern of uptake in Graves is
uniform increased activity often with prominent pyramidal lobe, and diminished salivary
gland uptake. Uptakes on a I123 typically at 24 hrs would be 40 to 70%(nl 10-30%) See
M118, CRp103. If pt cannot be irradiated(pregnant, child etc) then treat with beta
blockers and PTU or tapazol.
16.Paget’s dz on bone scan. They try to throw you off by hx of breast cancer(bastards)!
The lytic phase of Paget’s is always hot, the sclerotic phase is variable. In lytic, there is
typically a very hot bone, extending from epiphysis toward the other end of the
bone(blade of grass), but may involve whole bone, and the bone is thick. It is usually
positive on all 3 phases, but only need delayed imaging to diagnose. Can monitor
response to treatment with bisphosphanates w/ f/up bone scan(M326, CR p7) DDx would
include FBD, osarc or other primary bone tumor, chronic infection. Since I didn’t discuss
it previously, for bone scan, inject about 25mCi of Tc 99 MDP and obtain static images at
2 to 4 hrs. If concerned about osteomyelitis vs cellulitis then do immmediate
angiographic and blood pool images too. Hydrate pt preinjection, &void frequently
For pediatrics, the way to calculate doses for almost all radionuclides is the modified
Young’s rule, which is (age + 1/age + 7) X adult dose. For a 5 yo child’s bone scan, it is
(6/12) X 25=12.5mCi.
17.Alzheimer’s on PET or SPECT, decreased temporoparietal uptake.
SPECT and PET are useful for trying to distinguish among the different causes of
dementia(Alzheimer’s. multinfarct, Pick’s, AIDS) Inject 10 to 20mCi Tc HMPAO or
ECD and obtain SPECT images at 20 minutes post injection. For PET dose is 10mCi with
imaging at 1 to 2 hours. For both, minimize all sensory stimulation b/c it interferes with
study. In Alzheimer’s, SPECT shows decreased flow posterior temporal and parietal,
usually b/l(80%), but sometimes unilateral. PET shows diminished glucose metabolism
in same distribution. The b/l pattern is more than 80% predictive of Alzheimer’s. With
severe dz, the occiput, sensorimotor cortex and BG appear very hot. See M94, CR p233,
ACR case 617(PET) and 629(SPECT). Note that once the case also showed
ventriculomegaly. This is likely central atrophy, but could also be NPH or hydrocephalus.
18.Absent perfusion entire lung on MAA. Know DDx. May show CT or CXR.
I didn’t review it earlier, so I will now. The way to do a V/Q scan (using xenon b/c at
Cooper we only use xenon)is:Xenon is done first b/c it has a lower energy(81keV T ½ 5.3
days)It is performed upright with a posterior view. Pt inhales 10 to 20mCi of xenon as
deeply as possible, and holds breath 15 seconds while static image is taken. That is the
wash-in phase. The pt then rebreathes the same xenon(it is a closed system) for 2 to 5
minutes while image is taken(equilibrium phase). Next, fresh air is breathed while serial
15 second images are obtained for 2 to 3 minutes(washout). May need longer imaging for
washout in COPD pt. For perfusion, 5mCi MAA is injected into a peripheral vein during
quiet breathing in the supine position. The injection should be slow, over 3 to5
respiratory cycles. Upright images are obtained in the anterior, posterior, b/l anterior and
posterior obliques and laterals. In patients with severe pulmonary HTN, right to left
shunt, and kids, we reduce # of particles from 300,000 to 1 or 200,000.
Causes of unilateral absent perfusion include:tumor compressing PA, mediastinal
fibrosis(ACR 411), large pleural effusion, pneumothorax, large embolus(not as likely),
swyer james and pulmonary agenesis(M219 and 220 and ACR 412). Of those, the ones
that can cause V/Q mismatch include PE, effusion, tumor, and fibrosing mediastinitis.
The pattern should be called intermediate, but I will tell the examiner that this appearance
usually isnt related to PE, and ask for a CT to check for some of the above conditions.
19.RAS on captopril MAG3 renal scan.
Technique:At Cooper, we do the 2 day protocol, with captopril part done first. If this is
nl, then you don’t need to do the noncaptpril, but if abnl, then the next day pt gets the
noncaptopril. We give 25mg PO captopril and record BP at 15 minute intervals for 1
hour. (pt must not take any ACE for 2 to 4 days prior and BP must be >140 systolic o/w
might cause hypotension). One hour after captopril, inject 10mCi of Tc 99 MAG3 and do
the renogram. The hallmark of RAS is a renogram that becomes abnormal or more
abnormal after captopril. Findings are abnormal retention on the images, and continually
rising time activity curve(M353 and 354, CR p239) The theory behind the study is that
when there is a stenosis in the renal artery, the kidney produces more renin, which is
converted to angiotensin 1 and then 2, causing constriction of efferent arterioles, thus
maintaining GFR. When you give an ACE inhibitor, this cycle is disrupted, and A2
cannot be produced, so now the kidney with the RAS is not getting enough blood and
functions poorly. Sensitivity is over 90%, specificity 95%. Bilateral abnormal curves
after captopril could be b/l RAS, but if this is symmetric it suggests hypotension or
dehydration instead of RAS. With DTPA, the response to ACE is poor uptake by the
kidney w/ RAS.
20.Lymphoscintigraphy. Give history of breast or melanoma. Technique & Theory
Lymphoscintigraphy is used in breast, melanoma and prostate ca. The technique from
Case Review is: Inject 100uCi(at Cooper, we use a total of about 1 mCi) of filtered Tc
Sulfur colloid at multiple sites around the lesion in breast or skin, subdermally and
subcutaneously. Imaging is done in 2 phases; an early phase to map lymphatic channels
and to image the first node to take up tracer, and delayed images to see node retention.
The area over the node is marked preop. Also, many surgeons use a gamma probe in the
OR to find the sentinel node. The theory is that the first node(s) to drain a tumor are
indicative of the status of the nodes as a whole. If the first nodes are biopsied and tumor
free, then we can assume all are tumor free. However, if the first node is positive for
tumor, then a node dissection with sampling of multiple nodes needs to be done for
staging. In this way, we can avoid extensive node dissection in most pts, and thereby
spare them from lymphedema which often occurs after extensive node dissection, and the
cost of a more extensive procedure.See M384&385, CR p201&203.
21.Epididymo-orchitis on testicular scan
Inject 10mCi Tc 99 pertechnatate IV, or in kids, 300uCi/kg, with minimum of 3mCi. Pt
in supine position with scrotum supported from beneath. Penis taped superiorly to get it
out of the way(If Lisa is the tech, it moves itself up&outta the way). Use parallel hole or
converging collimator, but in kids, pinhole is better. Image immediately for flow and 15
minute delayed for static. In epididymitis, both perfusion and delayed activity are
inreased. It is important to ask which side hurts, b/c all flow is relative, comparing one
side to the other. If the painful side has high uptake, it is epidydimitis +/- orchitis. If the
painful side has less flow, it is torsion. See M364 and CR p367 row B. Note that
testicular appendage torsion can give a small focus of increased uptake on the painful
side, but it is much smaller and I don’t think they show this. Acute epididymitis mostly
occurs in adolescent boys due to STD with GC/chlamydia(ask Paul Shieh for details) It
can be localized to epididymis or also testicle.
22.Acute torsion or missed torsion on scrotal scan
See discussion for technique just above(10mCi pertech, flow and 15 min delay). Torsion
is due to the bell and clapper deformity allowing rotation of the testicle on the spermatic
cord, leading to strangulation. Sensitivity >90% in adults on nucs study, but less in kids.
In first few hours, perfusion is usually decreased, can look normal, or see “nubbin sign”
of tiny branch coming off internal iliac and terminating abruptly at the torsion
site(pathognomonic) On the static images, testicular activity is decreased but there is no
halo around it(ACR 325). Missed torsion produces a halo of increased activity around a
cold testicle(M363, CR 367 row C), with increased flow to the affected hemiscrotum.
Salvage rates for acute torsion 100% at 6 hrs, 70% to 12 hrs 20% at 12-24 hrs. Remember
to ask which side is painful, will prevent you from screwing up(except steve)!
23.Hot distal femur young pt +/- mets to spine and liver
If they show hot liver lesions on a bone scan in a young pt with abnormal focal bone
activity, this is by far most likely to be osteosarcoma, b/c not may things cause hot liver
lesion(DDx mucinous mets, artifact from overlying activity or prior SC scan, hepatic
necrosis, elevated aluminum, and osarc mets), especially in a young pt, but osarc mets
can. Also, multiple bone lesions in a young pt is more likely to be primary tumor with a
met than mets from a non-osseous primary, so DDx is Osarc vs Ewing’s. If there are no
mets, then there is a DDx for a focal bone lesion in young pt, including tumor, infection,
infarct in sickle cell pt, met from neuroblastoma or leukemia/lymphoma. Bone scan is not
good for determining extent of osarc b/ c there is often reactive hyperemia in the affected
limb. MRI is better. Ewing’s does not tend to have as much st uptake as osarc, so favor
osarc if lots of st uptake in the area. Favor osarc if there is a sunburst pattern(CR
117B)Remember that in a child the epiphyses are normally hot(nl scan M288), you need
to recognize when it is a skeletally immature pt, as it changes the DDx. See M297 f11-12,
CR p117 and p137(lung mets)
24.Splenosis on Tc SC or heat damaged RBC scan. See Nucs req 259 f10-47B
Splenosis is when splenic tissue seeds to other locations after
trauma(autotransplantation). The implants are often numerous and variable in size and
shape, located throughout the peritoneum and pleura. There are 2 ways to image for it.
One is with Tc SC(5 mCi for planar, 10mCi for SPECT), the other is with heat damged
RBCs labelled with Tc. These look different, b/c with heat damaged there is no liver
uptake, but with SC the liver is seen and is slightly hotter than spleen.
25.Biliary atresia on IDA. Liver uptake, but no CBD
When performing the IDA scan it is best to pretreat with phenobarb for 5 to 7 days,
2.5mg/kg PO BID. If there is no biliary uptake on intial images, then image to 24 hours.
However, even if there is no biliary activity at 24 hours, IDA cannot definitively diagnose
biliary atresia, b/c even if there is no biliary uptake, this could also occur in severe
hepatocellular dysfunction from neonatal hepatitis. However, if there is biliary uptake,
that exlcudes biliary atresia. See M275 f10-35, &compare to M274, and CR p215.
26.Quality control and artifacts
QC:Peaking(window seting) of the camera for a particluar isotope is done before every
exam. Uniformity testing is done every day using either a solid cobalt 57 source or a
liquid Tc source with the collimator on for extrinsic uniformity, and an intrinsic flood is
done with collimator off using planar or point source. Spatial resolution is done weekly
with a resolution phantom(quadrant bar phantom). Linearity is done weekly with bar
phantom Annual tests include energy resolution, count rate response, sensitivity,
collimator integrity, formatter performance and whole body accessory. For SPECT,
uniformity and center of rotation checks are done weekly and gantry and table alignment
is done quarterly. See M46 T3-1 for list.
Artifacts:we already discussed off peak. Others include cracked crystal(linear defect,
need new crystal M42&43, CR 151), nonfunctioning PMT(call service), Distorted
image=not circular, nonuniform image=inhomogeneous(need electronic tuning), and
contamination of crystal with radiopharmaceutical, need to clean or allow time to decay
10 half lives(all illustrated CR p151)
They added an artifact this year. It was a WBC scan with very poor resolution, could
hardly tell what study it even was. The correct answer was that the tech used the wrong
27.Nuclear VCUG/radionuclide cystography, with b/l reflux
Nuclear is more sensitive than fluoro, can detect even 1cc. Gonadal dose is 1 to 2 mrad,
which is about 100 times less than fluoro. Dose to bladder is under 50mrad. Technique is
to put 1mCi Tc SC in a volume of saline to fill bladder. This volume is calculated from
(age + 2) X 30. So for 2 year old =120cc. Fill bladder via a foley. Pt is supine during
filling, with camera posterior. Images obtained during filling and a single image at peak
filling. Catheter is removed and dynamic imaging is performed during voiding, with
static image postvoid. Reflux can be identified during filling, peak or voiding. Reported
as minimal(confined to ureter), moderate(involving renal pelvis), and severe(dilated
collecting system or tortuous ureter) See M357 for severe, CR 85 b/l moderate L>R
28.Perfusion scan with multiple hot spots in lungs and/or thyroid&stomach uptake
This question seems to be about artifacts on V/Q scans. Multiple hot spots can be from
pulling blood back into the syringe and allowing it to sit in the syringe for a little while.,
allowing clots to form. When these clots are then injected, they result in hot spots on the
perfusion scan. (M 196 f9-2) Another finding on an MAA scan could be uptake in the
kidneys or brain, which result from a right to left shunt(M196 f9-3) If you see uptake in
thyroid and stomach, that is from free pertechnatate(M 48 f3-12).
29.Ictal uptake in temporal lobe on PET or SPECT brain imaging, management
Most partial complex seizures arise from a focus of mesial temporal sclerosis in the
temporal lobe. The purpose of doing a PET/SPECT is to localize an abnormality for
surgical ablation, with partial temporal lobectomy. If a patient is injected during or within
30 seconds of a seizure, there will be increased uptake in the ictal focus. If the pt is
injected between seizures, then the focus will appear cold. Ictal studies are more
sensitive, about 90%, interictal 70%. See M92 and 93, and CR 229, ACR 625. The MRI
is usually negative when these studies are ordered. Mgmnt is surgery as above.
30.PET oncologic imaging. Recurrent colon ca, recurrent stomach uptake, liver mets in
lung ca. Some had cold center due to necrosis
Some of the uses for PET in cancer include: 1.When there is clinical or lab evidence of a
cancer or recurrence but CT etc are negative or equivocal. 2.Preoperative staging. For
instance, if there is a lesion on CT, but they want to know if it is a solitary lesion which
could be resected or if there is tumor elsewhere. For example of liver met in colon Ca,
see CR p195. For lung ca with met to R hilum and R retrocrural node, see ACR 324.
Remember, in PET see heart, brain and kidneys/bladder nrmally.
31.Discordant nodule, hot Tc, cold Iodine
Discordant nodules are the result of preservation of trapping but not of organification.
Therefore, on the Tc images done at 20 minutes, there is uptake, but it washes out by the
24hr iodine imaging since it cannot be organified. See M116. These should basically be
considered like cold nodules and require further work up.
32.Positive Meckel’s scan
Complications of Meckel’s tic are obstruction, intussusception, volvulus and hemorrhage.
Pretty much all bleeding Meckel’s tics have ectopic gastric mucosa(overall, CR says
about 20% of all meckel’s have gastric mucosa, but ACR says 50%), and therefore can be
imaged with Tc pertechnatate. Inject 10 mCi Tc Pertechnatate IV in adults or 300uCi per
kg in kids. Sequential anterior images are obtained for 60 minutes. A postive scan has a
focal area of increased activity in the RLQ or midabdomen, which appears at same time
as stomach(o/w could be sb activity that came from stomach) and has similar intensity as
stomach, and which does not move with time. Overall sensitivity and specificity about
90%. Several pharmacologic agents can be used to increase the sensitivity.
Cimetidine(300mg BID for 2 days prior or 20mg/kg/d for kids) blocks release of
pertechnatate from gastric mucsa, so it stays in the tic. Pentagastrin(6 ug/kg SC 5 minutes
before study) enhances mucosal uptake of Tc, and glucagon(0.5mg IV 10 minutes before
study) decreases small bowel motility so tracer doesn’t leave the tic. Normal
distribution=salivary, thyroid, gastric, bladder and breast. Can distinguish from Tc SC
RBC scan b/c Meckels has NO bone marrow uptake. See M261 and CR 75, ACR 317
I was shown a Meckel’s, and it looked very similar to the one in the books, but was a bit
more midline than some, lying just right of midline. The examiner did ask about what
meds could be used to increase sensitivity, thank god for recalls!
33.GI bleed, large or small bowel. Management
There are 2 choices for radiopharmaceuticals, Tc RBC or Tc SC. We use RBCs. This can
be done in vivo or in vitro. For in vivo, first give 10mg/kg of stannous ion, then 30
minutes later 20mCi of Tc pertechnatate(often problem with free pertechnatate with
kidney and stomach uptake) In modified vivo can also be done by drawing 10cc blood 30
minutes after the stannous is injected, and then agitate for 10 minutes and reinject as a
bolus. In vitro(“ultratag” kit) has better labeling efficiency, and we do this at Cooper. It
involves adding 3 cc blood to a tube containing stannous chloride. Then add sodium
citrate, citric acid and dextrose. Then add Tc pertech and after 20 minutes inject into pt.
Initial imaging 1 frame every 3 seconds for 60 seconds, then at 5 minute intervals for one
hour, then delayed imaging as needed. Common causes of GI bleed include diverticular
bleed, angiodysplasia, neoplasm, IBD, &ischemia. Nucs can detect around 0.2cc/min,
angio about 1cc/min. Sensitivity in active bleed >90%. The findings in a positive study
are a focus of activity that moves/changes with time. See M258 and 259, CR 221,
225,227, ACR 303(R colonic(F1) and sb(F7), ACR 304(Duodenum&R colon). Next step
in management is to do an anigogram to localize more accurately and perhaps embolize
34.PCP on a gallium scan and DDx
For infection, the gallium dose is 5mCi, and imaging is done at 6 hours, and 24 hours if
needed(ACR says to image @48 hrs). Normal distribution is liver, spleen, bowel/colon,
lacrimal, salivary, marrow. PCP appears as bilateral intense diffuse lung uptake, seen in
about 70% of cases. 90% sensitive, but not so specific, b/c other causes of diffuse lung
uptake include IPF, diffuse pneumonitis(CMV, MAI), sarcoid, lymphangitic
carcinomatosis, miliary TB, bleomycin toxicity and radiation pneumonitis. Specificity is
better when the CXR is negative or minimally abnormal and the lung gallium uptake is
intense, greater than liver. M391, ACR 427
35.Urinoma on MAG3 with extrav of MAG3 either posttrasplant or post lithotripsy. Both
cases also showed obstruction with decreased uptake and delayed clearance
Urinoma has 2 appearances. If it is a slow leak, it is a photopenic defect around the
kidney or ureter(DDx hematoma, abscess or lymphocele). In the case of slow leak,
delayed images may show tracer accumulation. If it is a rapid leak, then tracer will
appear within the collection right away. Remember to be on the lookout for transplant
kidneys in iliac fossa. See M361. CR 363 has stone related & CR93 transplant,ACR216
36.Pheochromocytoma with mets on Iodine MIBG
Metaiodobenzylguanidine(MIBG) is useful for imaging pheochromocytoma and
neuroblastoma, and to a lesser extent carcinoid, medullary thyroid ca and
paragangliomas. Sensitivity for pheo and NB is about 90%, specificity 95%. MIBG is
labelled with either 1mCi of I131 or 10mCi of I123. I123 is better b/c of resolution, lower
dose, can do SPECT, and shorter time to imaging. If I131 is used, then need to treat pt
with lugol solution for 3 days prior and 1 week after to prevent thyroid uptake. Normal
MIBG uptake in salivary, minimal heart, liver, renal, bladder, bowel and faint thyroid.
(Keys are liver without spl(only IDA also does this) and heart uptake, but honestly,
looking at various examples, it seems rather inconsistent. Maybe the best thing is that for
the most part you don’t see much uptake anywhere except in a mass.)Image at 24, 48 and
72 hours. Pheos will be focal areas of uptake. Some drugs such as tricyclics, reserpine,
insulin and amphetamines inhibit uptake and interfere with tumor imaging. Pheos are
more common in MEN 2A & 2B, VHL, NF, familial pheochromocytoma and Carney’s
triad. The diagnosis of pheo is usally made clinically and with urine VMA levels. Goal
of imaging is to localize. The 10% rule is that 10% multiple, 10% extra-adrenal, 10%
familial, 10% malignant. Mets go to bone, nodes, lung &peritoneum.See M366, CR249,
ACR 319 both neuro and pheo shown, F8 shows metastatic pheo like on boards.
37.Subacute thyroiditis. No uptake on Tc scan. DDx
Subacute thyroiditis presents as a painful swollen gland with high thyroid hormone levels
and markedly decreased uptake and no or minimal visualization of the thryroid on the
scan. With Tc, see salivary glands but no thyroid. See ACR 709. Other causes for nonvis
thyroid(decr uptake) include recent iodinated contrast, exogenous iodine in meds or food,
antithyroid meds, ectopic thyroid tissue, pt on synthroid/cytomel, prior surgery or rads to
38.Octreoscan, adrenal uptake from pheo or neuroblastoma
Octreoscan is In111 labelled pentreotide, a somatostatin analogue.(T ½ 67 hrs, keV
173&247) APUD/neuroendocrine tumors take up octreotide, and these include carcinoid,
pituitary adenomas, islet cell, medullary thyroid, pheo, NB, paraganlglioma and small
cell lung. Sensitivity 80 to 100% except lower for insulinomas and medullary thyroid.
Some non APUD tumors demonstrate variable uptake, including lymphoma, breast,
meningiomas and gliomas. Inject 6 mCi In111 octreotide, and image at 4 and 24 hrs(if
too much bowel, also 48hrs) We routinely use SPECT+planar. Nl distribution is blood
pool, thyroid, liver, spleen, kidneys, bladder, some bowel. Key is that kidneys and spl
very hot, no other scan does this(CEA has hot liver and kidneys but not spl). Potential
false + from TB, sarcoid,Crohn’s, UC&RA.
See M381, CR 187, ACR 327 F1-7=gastrinoma, F8-11=appy carcinoid w/ mets, F12-
15=pituitary prolactinoma, F16=hodgkins
39.Rib fractures in a breast cancer pt, involving consecutive ribs NOT mets. Incidentally,
the same case shows brain uptake on the bone scan from prior stroke.
Ribs are a common site of fracture and for mets, so it is not unusual to be presented with
rib abnormalities on bone scan and to be asked to determine if this is traumatic or mets.
The key is that trauma involves contiguous ribs, and the abnormalities can be connected
with a straight line(b/c of the mechanism of how the ribs came to be fractured) If you see
those 2 characteristics, it should be trauma, not mets. Another hint is that frxs are
punctate and mets are more linearly situated along the long axis. Also, can ask the pt for
history of trauma. See CR p9 row A, & CR p29, M313. Also compare BH 1228 f55.1 to
1235 and 1236.
40.Sacral insufficiency frx, sometimes b/l (Honda sign) sometimes unilateral, CT f/up
With b/l sacral insufficiency fractures, bone scan usually shows the classic Honda sign of
increased vertically oriented uptake b/l sacrum, with connection across the midline. Other
times, it is just on one side. Sometimes sacral frx can appear as transverse dots traversing
a sacral foramen. See M318 f11-38, ACR 135.
41.Malignant ascites from ovarian ca showing up on bone scan or thallium
Both malignant pleural effusion and malignant ascites can be hot on bone scan,
presenting with diffuse increased activity in thorax or abdomen. See M306 f11-23 and
M305. One resident said he saw ascites on a thallium study. He thought it was Tl b/c
there was heart uptake. I couldn’t find any mention of this, but it is possible, since Tl has
broad tumor affinity. Tl T1/2 73 hrs, 69 and 81 keV. Normal whole body distribution is
heart, muscle, liver, spleen, stomach, colon, salivary, testes, eyes, kidneys, choroid
plexus. The way to think of it is this: if see heart on a static image, choices are PET, Tc
sestamibi, thallium, MIBG, and Tc RBCs. PET should look much sharper, so not a
problem telling that, and see brain. Tc RBC easy to exclude b/c see all the vessels in that
one and the heart activity is in the chambers, not the myocardium. MIBG only has
minimal hrt uptake. MIBI should have strong GB uptake.
42.Bone scan w/ hot focus in arm and scatter artifact, with hot focus in axilla.
I suspect this is extravasation/infiltration of radiopharmaceutical at the injection site into
the soft tissues. Extravasated radiopharmaceutical can get into the lymphatics and be seen
in axillary lymph nodes. The extravasated agent in the arm can cause scatter artifact,
both at the site of infiltration, and in the adjacent soft tissue (of the thorax or butt), called
narrow angle effect. See nice examples CR p25 and M71
43.Spontaneous osteonecrosis(AVN, OCD) in the medial knee joint. +/- history of steroid
use(only gave hx if resident was flogging it and needed help)
Most bones have a dual blood supply, but the juxtaarticular bone does not b/c it has no
periosteum. This predisposes the juxtaarticular areas to infarction. Spontaneous
osteonecrosis of the knee is a disease of the elderly which has an acute onset. It can be
idiopathic or have predisposing factors, such as steroid use. In the knee, it usually
involves the medial distal femur, which shows increased uptake. The perfusion and blood
pool images are also abnormal, so all 3 phases are affected. Unlike OA, there is no
corresponding abnormality in the tibia. However, later on, there is often secondary OA
which confuses the picture. The XR is usually negative or shows sclerosis. CR p141 c76,
ACR case 116.
44.Brain death. Diagnosis and Management
There are 2 ways to do a brain death study, Tc pertechnatate or Tc HMPAO/ECD. Tc
pertechnatate normally goes to cerebral vessels, but not parenchyma, b/c of the BBB.
20mCi are injected, with images obtained for 2 to3 seconds each, up to 60 seconds. An
elastic band can be placed around the head prior to injection to decrease scalp uptake,
which can be confusing. In a normal study(M82), the caroitds are seen by 6 seconds, and
several seconds later the ACAs and MCAs are visualized(by 9 secs), and they look like a
“trident”. The SSS is visualized by 15 seconds. In the event of brain death(M84), tracer
is seen in the carotid, but none in the ACA, MCA or SSS. A single anterior or lateral
view is also obtained at 10 minutes to confirm lack of activity in SSS. A secondary sign
of brain death is increased flow to the nose via the IMAX. This causes the “hot nose”
SPECT uses Tc HMPAO or ECD, 10 mCi IV. Angiographic and 15 minute delay static
images should be obtained. Findings of brain death are absence of perfusion and lack of
cerebral activity on static images. You don’t really need to do SPECT, you can just get a
planar image showing no brain activity. The advantage of HMPAO/ECD is that they do
not rely on the angiographic phase, so timing and bolus are not as important.
Brain death should not be diagnosed on a nuclear scan in isolation. Correlation needs to
be made with the clinical findings (+/- EEG) before pronouncing death.
Also see CR p81 and especially ACR 610-613. Review these, as sometimes it is not so
easy to tell whether there is parenchymal uptake, and u do not wanna screw up brain
death. Especially case 613 with cerebellar flow only.
45.Osteomyelitis great toe on bone scan in DM. Also shows other hot areas in foot, but
the great toe is positive on gallium and the rest not.
Osteomyelitis(M323, CR p11) should be hot on all 3 phases (angiographic, blood pool,
and static 3 hour) of a bone scan. Cellulitis(M322) on the other hand, is only positive on
the early phases(angio and blood pool), but has zero or minimal uptake on the delayed
images. In the event of an equivocal bone scan(for instance, other reasons for positive 3
phase like trauma), correlation should be made with either Ga67 or a WBC scan. If
infection is the cause, then Ga or WBC uptake should exceed the bone scan uptake.
Remember, Ga T1/2=78 hrs, 4 photopeaks. Dose for infection 5mCi, imaging at 6 hrs and
24 hrs. WBC scan can be performed with In(T1/2 67hrs 173&247 keV). WBCs are
procured from 50cc of blood by allowing RBCs to settle to bottom and removing them.
WBCs then labelled with 1mCi of In111, and injected IV. Imaging at 24 hrs, medium
energy collimator. Early on have lungs, blood pool, liver and spleen. By 18 hrs, no more
lung and bllod pool, but have marrow, liver, spleen. Spl is hottest. With HMPAO, tag the
WBCs with 10mCi of Tc-HMPAO. Image at 30 minutes to 4 hours, with delayed at 18 or
24 hrs if needed. Similar distribution to In111 except that marow activity is seen early (3
hrs)and then disappears over next 24 hrs, and may get unbound Tc HMPAO going to GI,
kidneys, bladder, GB. For nice example of Bone scan, Gallium and WBC see ACR 122.
WBC more specific for infection than Ga, and more likely than Ga to be positive in an
acute infection, and in peripheral skeleton. Also better for abdomen b/c less bowel
activity. However, WBC not good for spine osteo, may be cold defect or normal.
46.Normal pressure hydrocephalus(NPH) on In111 DTPA
NPH has a clinical triad of ataxia, dementia and incontinence. CT shows dilated vents
with no evidence of atrophy, and opening pressures on LP are normal. Sometimes it is
difficult to tell atrophy from NPH, and then a cisternogram with In111 DTPA(T ½ 67hrs
173 and 247) can be instilled into the subarachnoid space by LP, 500uCi. Imaging is
preformed at 4, 24, 48 and 72 hours(if needed). On the normal cisternogram(M97), the
early images show a trident pattern of tracer in the basal cisterns, and sylvian and
interhemispheric fissures. By 24 hours, the tracer is distributed over the convexities There
is usually no flow into the ventricles, but occasionally may enter transiently in some
normal people. Findings in NPH are: 1.early entry of tracer into the lateral vents at 4
hours(looks heart shaped instead of trident), with persistence in the vents on later images.
2.Delay in ascent to the convexities +/- delayed clearance from basal cisterns. One thing
that helps me is that on the delayed Ant or post views, the normal shape should be round
at the top. Any other shape is abnormal.(M98 vs M97, CR p357, ACR 602 shows the
nonround appearance I am talking about)
47.Tibial plateau frx on bone scan
Frxs may be seen on bone scan as early as 24 hours, but this is variable, depending
mainly on the bone involved and pt age. Frxs are hot on all 3 phases. I would ask for XR
to correlate(always a good idea), although these can be subtle on XR. Activity in proimal
tibia only is likely a plateau frx, but need hx, b/c could be tumor too.
48.Hot pedicle on bone scan, DDx
I am not sure exactly what was shown in this case, but I suspect it centers on one of 2
issues. Either the point was to try to distinguish spondylolysis vs facet OA, or to
distinguish facet OA from met in pedicle/vertebral body. In the case of spondylolysis vs
OA, they can look the same on planar images and on axial and coronal SPECT. The best
way to tell is that on a sagittal SPECT, facet OA is at the level of the disc, and a pars
abnormality (spondylolysis) is at the level of the vertebral body(compare ACR case 106
F10 to F11) Spondylolysis is usually seen in a young pt (teenager especially), who has a
defect of the pars interarticularis, and the side opposite the pars is hot b/ c of increased
stress(CR 109), although the ipsilateral side can be hot too. Other DDx in young pt would
be osteoid osteoma and osteoblastoma.
In an older pt, facet degenerative change is much more likely, as it is very common.
However, metastatic disease can have a very similar appearance. The way to
distinguish these is on a SPECT axial or sagittal view. A met will localize to the pedicle
and vertebral body(anterior), but OA will localize to the facet(posterior). See CR p255.
49.Hyperparathyorid with metastatic calcification lung & soft tissue. DDx
Hyperparathyroidism leads to hypercalcemia, which causes metastatic calcification in
stomach/GI, lungs, kidneys, thyroid. When this pattern is seen, it is pretty much an aunt
minnie. Another cause of somewhat diffuse st uptake is amyloid, but this has a different
distribution, occuring in heart, skeletal muscle, liver and skin. For isolated uptake in one
organ or another, there are different DDx’s. See M309 f11-28B, CR p149. Regarding
renal uptake, there is normal renal uptake on every bone scan. However, this should be
less than the spine, and if >spine is abnormal(DDx hyperpara, radiation, chemo, sickle
cell, iron overload)
Another hint in hyperpara is that mandible, face and skull are sometimes very hot.
50.Pyelonephritis on SPECT renal study
The usual agent used for suspected pyelonephritis is Tc DMSA 5 mCi. Planar imaging of
kidneys performed at 2 hours after injection, in the posterior projection with a parallel
hole collimator, and in the posterior and posterior oblique projections with a pinhole
collimator. SPECT imaging can also be performed. The 3 main patterns of
pyelonephritis are focal defect, multifocal defect, or diffusely decreased activity. Also,
there may be bulging of the renal contour due to edema. Defects are usually reversible,
and may resolve on follow up, or go on to scar. See M355, and CR 243. The advantage of
DMSA over MAG3 is that it allows high resolution cortical imaging without interference
from collecting system. The way to recognize DMSA is that there is no collecting
system, bladder or ureteral activity(b/c no excretion). DDx includes scarring.
51.HIV with brain mass, positive on thallium= lymphoma
CT and MRI cannot definitively differentiate toxoplasmosis vs lymphoma, although
certain features do favor lymphoma, such as a solitary lesion, crossing midline(CC), size
>2cm. There are 3 nucs studies that can help differentiate them; PET, Thallium and Tc
Sestamibi. The same basic idea applies to all of them. Lymphoma will be hot with PET,
Tl, or Tc. See W1049 for toxo f46-3. The appropriate next step if the lesion is hot is a
biopsy, where if it is cold, the next step is antitoxo meds. See CR p325. Thallium and
PET can also be used for other brain tumors, and generally will have little or no uptake
in WHO grade 1 or2, but marked uptake in WHO 3 or 4.
52.Reflex sympathetic dystrophy(RSD) lower extremity
RSD(aka Sudeck’s atrophy) is a d/o which consists of pain, tenderness, swelling, and
vasomotor instability. It is not well understood, but tends to occur post trauma, MI or
stroke. XR shows osteopenia out of proportion to the patients other bones +/- soft tissue
swelling. 3 phase bone scan shows increase on angiographic and blood pool in about
50%, , with prominent increased periarticular activity(crosses joints) on the delayed
images in 95%. The typical(classic) pattern is hot on all 3 phases. When RSD is
reoslving, the perfusion images normalize 1st, then the blod pool, then the static. In kids,
can get a diffusely cold extremity instead of diffusely hot. When RSD involves the upper
extremity, it is called shoulder hand syndrome. The key is that it crosses joint, not limited
to one bone. The DDx might include inflammatory arthritides, such as RA, but those
should not involve as much area in a contiguous fashion(an entire limb), so RSD is
distinctive. Main DDx is disuse, such as post casting or stroke. See M321, CR p139,
53.Shin splints on bone scan. How do you distinguish from stress fracture?
Shin splints represent periosteal reaction in response to stress on the tibia. It is normal on
the angiographic and blood pool phases, but hot on the delayed images. B/c it involves
the periosteum, it has a linear, vertical orientation along the cortex. It usually involves the
posteromedial tibia, where the soleus inserts.The posterior location is key. There should
not normally be any activity along the posterior tibia, if there is it is probably splints.
Shin splints are usually less intense than fractures. See M315, CR p5A, ACR 107
Stress fractures are hot on all 3 phases. They are fusiform(not linear) in shape, and tend to
involve the proximal tibia.(CR p5B and C has both stress frx and shin splints, ACR 107).
They are more intense than splints. The 2 often coexist b/c both are related to increased
stress on bone.
54.PET in lung cancer showing parenchymal(RUL&RLL) and hilar/mediastinal uptake
Disc:Seems like a straightforward case of lung cancer, but they give the history of lung
cancer, which makes me wonder what’s the catch? Maybe they want you to recognize all
the abnormal areas, which will affect the staging. Specifically, c/l nodes or distant mets
will make it unresectable. PET is clearly superior to Chest CT for lung cancer staging .
PET sensitivity and specificity are 91 and 86%, whereas CT is 75 and 66%. PET is much
better at separating surgical from nonsurgical disease. See CR193 and ACR 324.
55.Hepatic uptake on bone scan, DDx
M304 T11-6 lists many possibilities. The main categories include 1.Artifact-recent Tc SC
study or overlying rib or abdominal wall uptake 2.Mets from mucinous cancers such as
ovary, breast&colon or SCC esophagus, small cell, melanoma, or osteosarcoma.
3.Diffuse hepatic necrosis 4.elevated serum aluminum 5.amyloid 6.HCC 7.cholangioca
8.microcolloid formation from improper preparation. I will say mets first, expecially
mucinous, as this is the classic cause. See M302 f11-19 and CR 141 c77.
56.Diaphragm attenuation on MPS. Looked worse at rest.
Diaphragm attenuation artifact causes an inferior wall perfusion defect which appears
worse on rest images b/c those are done with much less dose than the stress images. It is
usually seen in males. There are 2 ways to confirm something is DAA. One is with gated
SPECT evaluating wall motion. If wall motion is normal, then it is not an infarct. Also,
you can do attenuation correction using a transmission source. (M143, ACR 501 and 516)
57.Octreoscan with uptake in chest, DDx
Chest uptake on Octreosan can be from primary tumors such as carcinoid, small cell or
lymphoma, or it can be mets from other APUD tumors, such as islet cell, NB, pheo.
Remember In111 67hrs 173, 247. Normal octreoscan see spleen>>liver, and kidneys&
bladder. Image at 4 and 24 hrs after 6mCi injection.
For example of medullary thyroid with mets including lung and hilum, see CR 187. For
islet cell with liver mets, ACR 327.
58.Hibernating myocardium on PET ammonia
PET evaluation for hibernating myocardium includes stress/rest imaging with NH3(or
rubidium) and imaging with FDG. The basic premise is that normal heart uses fatty acids
for metabolism, not glucose, but ischemic heart uses glucose. Infarcted heart is cold on
NH3 and FDG b/c has no flow and no metabolic activity. Hibernating heart has no flow
with NH3 but has glucose metabolism, so is hot with FDG. See M186, ACR 518, Films 1
and 2 are hibernating, film 3 is infarct.
Ectopic thyroid tissue can occur in the base of the tongue(lingual), pelvis(struma ovarii in
an ovarian teratoma) or substernal. Lingual thyroid can be imaged adequately with Tc
pertechnatate, and has the advantage of lower radiation exposure, which is especially
important b/c most pts with suspected lingual thyroid(hypothyroid or tongue mass) are
children. However, other sites of ectopia are too deep, and the 140keV photons are
attenuated, so you need to use I123 or I131. In 70% of cases, a lingual thyroid is the only
thyroid tissue present. The other 30% also have some neck thyroid tissue.
Hypothyroidism occurs in 1/3 of lingual thyroid pts b/c it does not produce enough
hormone. Other symptoms include dysphagia, dysphonia and dyspnea. Treatment is with
synthroid which will correct the hypothyroidism and suppress growth of the lingual tissue
which may ameliorate mass effect. Typical Tc scan shows no tissue in the lower neck,
small thyroid tissue at base of tongue, and normal salivary uptake. See M112,CR245
c132, ACR 715.
60.Hodgkin’s on whole body thallium
Most lymphomas are thallium avid. The degree of thallium uptake is inversely
proportional to the aggressiveness of the lesions, with lower grade tumors demonstrating
more uptake than higher grade tumors. Gallium can be negative in low grade lymphomas,
which makes thallium particularly useful for them.
Thallium T ½=73 hrs, 69 and 81 keV. Normal distribution myocardium, skeletal muscle,
liver, spleen, stomach, colon, salivary, testes, eyes, kidney, choroid.
61.Types of collimators:
The collimator is placed b/w the pt and the camera, and its purpose is to aid in
localization of tracer, by decreasing scatter and only allowing photons arriving
perpendicular to the detector to be imaged. A pinhole collimator has a very small opening
to allow photons thru, is it has poor sensitivity, and must be placed very close to the
region of interest. It has very good resolution though, and is used to obtain high
resolution in small body parts such as thyroid or peds hip. Multihole collimators consist
of 3 types; parallel, converging and diverging. Parallel is used most, and has 3 energy
types based on energy levels that it images; low energy, medium and high. The difference
among these is in the thickness of the lead septa, higher is thicker. If you increase the
length of the septa, the sensitivity worsens but the resolution improves. With parallel
hole, neither size of image or count rate changes with distance of object from collimator,
but resolution worsens with increasing distance. A diverging collimator have septa that
diverge from the crystal face(or converge on the crystal, same thing) this increases the
imaged area, but minifies the image. Both sensitivity and resolution worsen with
increasing distance of object from collimator. Diverging is used to image large organs
like lungs. Converging has holes that converge as you move away from collimator
toward the pt.(or get closer together toward the pt) this results in magnification of the
image. Sensitivity increases as the object moves further from the cllimator. Resolution
decreases with distance(always does) It is used for small areas. M21&22) I was asked
about collimators on my test. Specifically, she asked me what types of collimators should
be used for thyroid imaging. I said either pinhole or converging, b/c it is a small body
part and you want to maximize resolution and magnify the image.
62.Congenital organification defect/dyshormogenesis. Cretinism workup
In an infant with clinical/lab hypothyroidism, there are 3 possibilites. One is absent
thyroid, the second is ectopic(lingual) thyroid, and the third is a congenital organification
defect. By using both Tc and I123 these can be differentiated. Do Tc first. This may
show absent or ectopic thyroid, in which case you are done. However, if it shows a
normal looking thyroid, then you have to do an I123. If thyroid is absent on I123 but
present on Tc, this means there is a thyroid in the normal location, and it is capable of
trapping, but there is an organification defect. M113 f7-5, ACR 714.
63.Colitis/IBD on WBC scan showing Left colonic uptake
WBC scan is much better for abdominal infection/inflammation than gallium, b/c there is
normal gallium uptake in bowel, and this limits detection of foci of
infection/inflammation. However, in the upper abdomen, detection is still limited even on
WBC scan, due to normal liver/spleen uptake. This can be subtracted out via Tc SC
imaging if necessary. The DDx for bowel uptake on a WBC scan includes
Crohn’s(discontinuous ACR 308 F2), UC(continuous, ACR 308 F1), infectious colitis,
pseudomembranous colitis, ischemic bowel and diverticulitis. False + from swallowed
WBCs and GI bleeding. The more intense a focus is vs liver, the more likely it is real.
See M397. Remember, there is no blood vessel tracer in WBC, so not a RBC scan.
Normal distribution SPl>liver and marrow. Also, we image earlier than usual for
IBD/bowel when In111 is used, at 6 hours instead of 24, b/c intestinal clearance increases
with time and confounds interpretation. With HMPAO we image at about 1 hour like
64.Hypertrophic pulmonary osteoarthropathy(HPO) on bone scan. Know causes
HPO causes periosteal reaction, especially in the long bones. Clinically it presents with
bone pain, arthralgia and clubbed fingers. On bone scan it shows linear increased
activity(“tram tracks”) along the medial and lateral aspects of the shafts of tibias, femurs,
and radii, especially around knees, ankles and wrists. Imaging findings usually precede
clinical and XR findings. It can be more focal and less linear, but will still be cortically
based and symmetric. The most common cause is lung cancer, with other causes
including mesothelioma, pulmonary mets, bronchiectasis, CF, mediastinal dz(hodgkin’s),
lung abscess, asthma, and heart disease and even some GI dz like IBD or biliary atresia.
Get a CXR! M328, CR257, ACR 119
65.CBD obstruction on hepatobiliary scan
An acute complete CBD obstruction on a DISDA scan will show a hot liver, with no
filling of bile ducts or bowel. This is called the “liver scan” sign, b/c it looks like a liver-
spleen scan without the spleen, only thing on the whole scan is liver. Also, there will be
delayed cardiac clearance(normally gone from heart by 10 minutes) The reason you know
it is not a liver spleen scan with an absent spleen is that in HIDA only get numerous
anterior images, at 5 minute intervals. For SC, only image once, but get obliques and
lateral in addition to anterior. See M271. Causes of complete obstruction include
mechanical things such as stone or tumor or pancreatic head mass or pancreatitis, and
functional things such as ascending cholangitis. Intrahepatic cholestasis from drugs
mimicks complete CBD obstruction. With partial CBD obstruction, tracer is visualized
to the level of the obstruction and then cut off. The CBD is visualized for a prolonged
period of time, and there is delayed appearance of bowel(>1 hr). Partial obstruction can
be due to stone, stricture(malignant or benign) and sphincter of oddi dysfxn or morphine
given before exam. CCK given prior to the exam is another cause of delayed biliary to
bowel transit. Also, delayed biliary to bowel is a normal variant in 20% of people.(M272,
CR p205, ACR 306) Remember that with complete bile obstruction the GB will not fill;
Do not call cholecystitis in that situation. In the setting of possible partial obstruction,
give CCK and if not truly obstructed will rapidly go to small bowel.
66.LeVeen or Denver shunt with patency or nonpatency
These shunts are used in pts with refractory ascites to drain the ascites to the SVC. It has
a one way valve to only allow flow from peritoneum to SVC. The shunt may occlude due
to fibrinous deposits at the valve in the peritoneal space. Patency is assessed by injecting
1 mCi of Tc MAA or Tc sulfur colloid into the peritoneum via paracentesis. Get
immediate images to show tracer scattered in peritoneum. If there is a normal functioning
shunt, activity should be seen in the lungs with MAA(M282) or liver/sleen with SC(CR
351) by 10 minutes. If there is no visualization in lungs by 30 minutes, then delayed
imaging should be performed to asess for partial obstruction vs complete. There seem to
be many protocols as far as time to imaging. The above was from CR, but ACR 320 says
to image immediate and at 2 and 5 hours. F1 is a nonfxning shunt and F2&3 are of a
functioning shunt. You should recognize an ascites shunt study b/c the initial images
show tracer in abdomen but not in any particular organ, just floating in peritoneum.
Lastly, don’t confuse peritoneal tracer at the superior peritoneum for liver/spleen on SC
scan. The liver and spleen should be well defined, you should see them as u would on a
normal SC scan.
67.Recurrent thyroid ca, positive on Tl or MIBI, negative on I131
I think this was an older question, and now it is much more likely they would show a
PET instead of Tl or MIBI, but it is the same idea. One of the most accurate methods for
detecting thyroid cancer recurrence is serum thyroglobulin level. This can be measured
beginning 2 months following thyroidectomy(it is normally high before then) A rising Tg
levl is suspicious for carcinoma. A level above 10ng/mL is associated with mets >85% of
the time. When the thyroglobulin is high, the next step is to get an I131 WB scan.
However, certain types of thyroid ca, such as anaplastic(dedifferentiated) and Hurthle cell
are sometimes I131 negative. However, they can be PET, Thal and Sestamibi positive.
The thyroid cancers that are positive on I131 tend to not be hot on PET, but those that are
I131 negative are hot. For pts who are I131 negative, but with elevated thyroglobulin,
PET is about 80% sensitive. Pts who are I131 negative cannot be treated with I131, and
will need other treatment such as external beam rads or chemo. See CRp375. You do not
need to stop thyroid meds for PET, Tl or MIBI.
68.Sacral lesion on bone scan mostly obscured by bladder.
This is a not uncommon scenario, in which the full bladder obscures pelvic lesions. That
is why it is important to always have the pt void just prior to imaging. If the scan does
have a full bladder, get rid of the interfering bladder activity by either emptying the
bladder and reimaging(best option), subtracting the bladder, or doing SPECT imaging. I
don’t know what the sacral lesion was, don’t have enough info. Could be a frx, a met, a
primary tumor like chordoma etc. Probably point was to empty bladder, and they might
not expect a specific diagnosis. I would recommend plain films.
69.Splenomegaly on Tc SC scan
There are 2 ways to identify splenomegaly. You can use a measuring device placed on
the patient over the area of interest, or you can Gestaldt it. Splenomegaly is a very
nonspecific finding, with many causes. The normal spleen should not measure more than
13cm long axis in adults on a posterior scan. In kids up to 18 yo, the max length is
calculated from 5.7 + (0.31 X age).The scan is helpful in confirming a clinical suspicion
of splenomegaly, but not in determining a cause. Causes can be broken down(M256 T10-
6) by massive enlargement-CLL, Myelofibrosis, thalassemia and GSD vs moderate-
cirrhosis, hepatitis, hemolytic anemia, Mono, lymphoma, and minimal such as CHF or
mets etc. ACR 311, M255 f10-19
70.Colloid shift on TC SC DDx
This refers to decreased concentration of Tc SC in liver, with increased activity in spleen
and bone marrow. It is a nonspecific finding, but the most common causes include
cirrhosis with portal hypertension and diffuse hepatic metastases. Other findings in
cirrhosis include small liver with large left lobe and caudate, splenomegaly,
inhomogeneous liver uptake(need to exclude superimposed HCC), persistence of colloid
in the blood pool due to poor hepatic uptake and clearance, especially evident in heart.
Ascites can be seen as separation of liver from ribs and right lateral abdominal wall.
Diffuse lung uptake may occur. Lastly, you can sometimes see caput medusae veins as
filling defects in the st of the abdomen(ACR 311,M245 f10-6)
71.Cold sacral lesion in a 17 yo
The DDx would include benign(hemangioma, bone cyst) or malignant tumors(including
some mets like thyroid, leukemia), radiation, osteomyelitis(may be cold, especially in
children), AVN from sickle cell or trauma or steroids etc, surgical defect, artifact from
object overlying the pt(clothes) or in the pt(barium). See CR p 147, M68 f5-7
72.HMPAO brain with activity only in BG and brain stem, no cerebral activity
This suggests trauma with diffuse edema or asphyxiation, anoxia or hypotension, some
global event leading to decreased perfusion to the entire telencephalon. This would not
constitute brain death since there is infratentorial and BG activity. See ACR 613
73.MAG3 or DTPA with hx of unilateral nephrectomy and cystectomy with creation of
an ileal loop. Shows activity in colon.
First of all, if you get this crazy case, I’d guess you passed and they are just having some
fun. Or you are the unluckiest SOB(Reggie, aka Reggie “Holiday” Denis) ever to take the
boards. In any event, there are 2 ways to divert urine after a cystectomy(usually for
TCC), and both involve reimplanting the ureter into some loop of bowel and pulling the
loop up to the skin. The most common type is the cutaneous ureteral ileal conduit, and it
entails reimplanting the ureter to an ileal loop and bringing the loop out to the skin as a
cutaneous stoma. These pts must wear a ureterostomy bag. In this situation, it would not
be normal to see tracer in the colon and the presence of tracer in the colon would suggest
a fistula from the ureter or ileal loop to the colon. I cannot think of any other possibilities
as to how it gets to the colon. Sorry, could not find an image of this anywhere, but if you
see a MAG3 with one kidney and no bladder and the urter going somewhere funny, just
guess fistula to colon!
74.Bone scan status post leg amputation, hot acetabulum and rib frxs
This question is also dubious. That being said, post amputation, it is normal to have
uptake in the stump b/c of the trauma and healing. However, it is not normal to have
increased activity in the acetabulum, so I would be concerned about tumor recurrence or
infection, or possibly RSD etc. I would get an XR to correlate(always a good idea) It
sounds like the ribs were coincidental trauma, he described them as contiguous levels.
M297 f11-12B, nl appearance. ACR 120 F8 shows a case of RSD post amputation.
75.I was shown a bone scan with a hot left kidney and dilated ureter. Also, the bladder
was compressed and deviated to the left by some mass, which was the cause of the
ureteral obstruction and “persistent nephrogram(nucs equivalent of it)” Said I would get
cross sxnal imaging, and she said US showed a huge fibroid uterus.
76.MAG3 with cine loop of the study, showing no tracer uptake in LP left, and then later
there was severe reflux to left lower pole. I said duplex left system with lower pole reflux
which led to scarring so the LP didn’t take up MAG3.