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case review/SF Nucs


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Patient for HIDA, question must be asked?
Time of last meal
Patient for HIDA, been fasting 36 hours
Administer Sincalide

Low dose since only one organ gets all the tracer
Tracers for HIDA?
GB not visualized after 1 hour
Do NOT call it acute chole

Must give Morphine
When is MS04 given if GB not seen?
45 min
Dose MSO4?
3 mg IV
How long after MSO4 do you image before calling it quits?
another 45 min
baby with HIDA
Biliary atresia vs. hepatitis
Diagnosis of atresia
No filling of small bowel after 24 hours.
No ACE inhibitor for 3 days

Preferably no BP medicine at all and pt must be well hydrated. These steps to prevent hypotension, which is dangerous. If it occurs, you stop scan and treat the patient. If it occurs, it does suggest that the patient is relying on AII to maintain BP.
To make kid with neonatal hepatitis's liver pick up and excrete better, thus can hopefully r/o atresia
R/O GI bleed; tracers
Tc99m labeled RBCs


Tc99m sulfur colloid
Dose of RBCs?
20 mci
Dose of Sulf colloid
10 mci
RBC labeling
In vivo - worst - inject Stannous pp to reduce RBCs, then inject TcO4 into blood. Too much free pertechnetate.

In vitro -- Best, but time consuming. Draw blood, put in stannous, add Tc, reinject into pt.

In vivtro -- our choice. Balance. >95% labeling. Inject stannous, wait, then draw up aliquot of blood into same tube as TcO4, mix, reinject.
Diagnosis of bleed
Activity that increases over time. Movement is icing on cake.
Scan with uptake in stomach
Tc 99m pertechnetate scan

--if focusing on abdomen, Meckel scan

-- If focusing elsewhere, probably neck for thyroid scan (not for uptake)
Normal Meckel scan
Blood pool, then stomach uptake that gets excreted into small bowel, then renal excretion (so should see bladder)
Abnormal meckel scan
Tracer activity increases on same timeframe as stomach upkate.

If you see uptake on first image, its not a meckels.

Also, there can be other structures with ectopic mucosa, such as duplication cyst
Reasons for whole body scans?
Look for tumor (FDG, bone scan, octreoscan, MIBG)

Look for infection (gallium, indium)
Agents used for tumor imaging

I-123 or I-131 MIBG

Best application of PET
Lymphoma imaging, because reverts to negative post chemo when in remission. If negative PET but no change in CT, still good sign. Likewise if recurrence on PET, same size on CT, badness.
Caveat in PET tumor imaging
Reactive lymph nodes. Put in your DDx if unsure. Usually not as dark as tumor. Tumor darker than mediastinum.

Also, thymic rebound post chemotherapy
False pos FDG
Infection (granuloma, pneumonia)

Inflamm (sarcoid, rheum nodules, divertic)




Gallium energies



(I95 highway, double it, 300 miles to gainesville)

Another photopeak of 395, but not used in imaging
Gallium T1/2
76 hours

(I-76 in Philly)
Identifying a Ga scan
Soft tissues prominent

Bone/bone marrow


Large bowel excretion

NO cardiac uptake. Don't see kidneys/bladder.
MIBG label, uses
I 123 or I 131


Recognizing MIBG

Liver (no spleen)


Octreotide -- what is the radiolabel
Uses for Octreoscan


Other neuroendocrine (pheo, neuroblastoma, etc)
Recognizing Octreoscan
Intense uptake in



Mild uptake in liver (SPLEEN>liver)
Inflammation imaging tracers
WBC scan

When is Ga better than WBC?
Imaging spinal osteomyelitis (although MRI better)

Imaging lung inflammation (sarcoid, interstitial pneumonia, drug toxicity)
WBC radiolabels
In111 oxime

Dose of In111 labeled WBC

0.5 mCi
When image Gallium?
Start at 24, often wait until 48 hours. Better SNR. Give enema.
When image In111 WBC scan?
Can image at 4 hours, but usually wait until next day.
In111 photopeaks


1 plus 7 is 8, divided by 2 is 4 which is one half or .5 of what you started with
Normal 111In WBC scan


SPLEEN > LIVER (makes sense, as spleen is the filter for all blood cells)


Little soft tissue (unlike Ga)

Spleen > liver (unlike Ga)

No bowel activity (unlike Ga)

Bone MARROW uptake (like Ga)
Indications for labeled WBC
Confirm osteomyelitis

Abdominal infection or inflammatory bowel disease

Vascular graft infection
Reversible defect on cardiac stress
Always means ischemia

Except for one small caveat: some pts with LBBB can get reversible septal defect not related to ischemia.
Mild to moderate fixed defect
Does not always mean infarct


Incomplete infarct

Hibernating myocardium

Attenuation artifact
Hib myoc
Chronic low flow state to myocardium, resulting in decreased metabolism. Looks like an incomplete infarct, with poor uptake on rest images and wall motion abnormality.
Severe fixed defect

Hibernating myoc will not go all the way to no uptake
Bruce endpoints
1) Most people stop due to symptoms (fatigue, dyspnea)

2) Angina or hypotension

3) Severe ECG changes or arrhythmia

4) Attain 85% of target (this is enough to unmask ischemia)
Pt who cannot exercise enough to unmask ischemia
Pharmacologic stress

1) Adenosine or persantine -- both work not by increasing workload, but by causing vasodilation, which causes steal from stenosed vessel, resulting in ischemia.

2) Dobutamine -- positive inotrope and chronotrope, so increases myocardial workload.
When dobutamine used
Patient taking THEOPHYLLINE -- antagonizes persantine and adenosine, or patient with ASTHMA not on theophylline, because these drugs can exacerbate asthma.
Difference in imaging for Bruce, adenosine, or dobutamine

You dont even have to know how patient was stressed in order to interpret the study, as long as the stress was adequate
How adenosine given?
Continuous IV infusion for 3 min, then inject tracer, and continue adenosine infusion for another 2 min
How dobutamine given?
Keep giving dobutamine via infusion until target HR reached, then maintin for 1 minute BEFORE tracer injection (JUST LIKE FOR BRUCE)
201 Tl characteristics
Analogue of K

Long half life, which limits dose that can be given (4mCi)

Low energy (80keV = x-ray range)

Our institution
Tl first as resting study

Mibi as stress tracer (overpowers Tl with higher energy and higher dose, locks in place, so dont have to image them right after like you do on the rest images with Tl for fear of redistribution)
Dose of sestamibi
20 mCi
Waiting time to image?
30-60 min (waiting for liver to clear)
Sign of ischemia besides uptake
Stress dilatation of the LV cavity

Long - long axis views are named opposite of the way the heart is oriented: Heart laying on it side = VLA; Heart standing up = HLA
septal defect near base
Normal membranous septum
6 segments: Anterior, anteroseptal, inferoseptal, inferior, inferolateral, anterolateral (just look at the polar maps)

LAD is centered over RV insertion (interventric groove), so LAD territory is anterior and anteroseptal.

RCA is inferior, so it supplies the 2 segments counterclockwise to LAD: inferoseptal and inferior. Circ is lateral, so circ supplies the 2 segments clockwise to the LAD = anterolateral and inferolateral.
PET perfusion
Use Rb -- disadv = 1.3 minute half life, so all stress is pharmacologic, very expensive.
When is viability assessment needed?
When fixed defect is at least 1/2 of normal uptake, can be sure its viable. But if questionable, then

1) Thallium redistribution (inject extra 1mCi and image next day for redistrib)

2) FDG -- the best choice if there is any question remaining
99mTc-MAA dose
4 mci

About 1 million particles total
Injection instructions
When is vent scan done with 99mTc-DTPA? With Xe?
BOTH DONE BEFORE MAA INJECTED, because once MAA is in there, it aint goin anywhere and you cant give enough Xe or aerosol to see through it
Protocol for Xe
3 stages: Imaging is performed throughout all 3 stages. All imaging is from POSTERIOR view.

Wash-in: Pt holds breath for 30s, or takes deep breaths.

Equilib: Pt breathes normally through closed system.

Washout: System turned to exhaust, patient breathes normal air, exhaling out the Xe.
Protocol for DTPA

Breathe from nebulizer 3-5 min

Images recorded after breathing (shit aint goin anywhere)

ADVANTAGE: Get to take multiple projections, unlike with Xe
Slow wash-in and washout on Xe study
Suggests COPD, especially if patchy
Nonsegmental defect
Does not conform to segments

Hilar defect, costophrenic angle defect, etc
Small defect
Lies within a segment, but involves LESS THAN 1/4 OF IT
Low probability
Nonsegmental defects (very low)

Any perf abnl substantially smaller than CXR abnl (very low)

Small defects

Matched defects with clear CXR (probably due to COPD)

Triple match in upper or midlung (very low)

Markedly heterogeneous perfusion

Stripe sign (very low)
Medium size defect
1/2 of segment
Large defect
whole segment
High prob
at least 2 unmatched perfusion defects or the equivalent with CLEAR CXR

So, you MUST ASK FOR CXR as soon as you see a V/Q scan, just like in real life
DDx of V/Q mismatch
Acute PE

Chronic PE

Node or tumor in hilum compressing vessel (airway more rigid, wont compress)

Thats why you need MULTIPLE defects in order to call it High prob
Intermediate prob
Single large or medium defect, unmatched, normal CXR

Triple match lower lobes (intermediate because could be atelectasis, pneumonia, or infarct, and you cant tell them apart, especially infarct and pneumonia)

Any other abnormality not in high or low categories
High prob PPV
Low prob PPV
Very low prob
V/Q scan with uptake throughout body
When is bone scan hot more often? Lytic or blastic lesion

Doesnt matter what xray shows. As long as there is new bone formation going on, there will be uptake
Bone scan tracer
Tc Methylenediphosphonate

Wt dependent

.05 mCi/kg.

So, 10 kg baby, give 0.5 mCi
When imaged?
4 hours later
Where is most of dose then
In toilet. Reason you have to wait is to clear out the soft tissues, which occurs via the kidneys. So in older people and those with renal failure, bad bone scans with lots of background.
Purpose of 3 phase scan
Blood flow and pool images tell you what is going on in the SOFT TISSUES. It tells you about hyperemia. So you would want to do it for r/o RSD or osteo.
Problem with 3 phase
Very nonspecific. Doesnt tell you anything diagnostic except that there is hyperemia in the soft tissues.
metastatic disease
Central distribution, as it goes to bones with red marrow. Acral lesions are not likely to be mets.
Multiple lesions random distn but predominantly central
Pathognomonic for mets
Very hot long segment uptake

Goes from one end of bone to other end, and no skip lesion.

May have associated deformity.

Blade of grass appearance when starting out
Skull with hot uptake and sharp zone of transition to normal uptake
Pagets osteoporosis circumscripta
Increased uptake in an extremity. Uptake increased on all 3 phases. Periarticular bone especially hot.

Usually post-traumatic.

Reverts to normal 6 months after sx resolve.
Diffuse increased cortical uptake, with tram-track appearance

Almost always pulm dz, and usu lung CA.
Distribution of HO
Lower extremities > Upper
DDx of HO
When it occurs in lumpy patchy uptake variety, could be peripheral vascular dz. NOT METS, too far peripheral.
Isolated acral medullary lesion.
Not going to be met. Will have to do plain film. If not visible, CT to better define.
Bone imaging

When should you request a CT?
When looking for matrix
Bone imaging

When should you request an MRI?
When you want to evaluate soft tissues
Bone imaging

When should you request a bone scan?
When you want to determine whether there is multiplicity of lesions, or evaluate lesion distribution.
Cold lesion DDx
Unicameral bone cyst


Eosinophilic granuloma

Myeloma (causes little bone response)

Mets (so destructive that there is not even enough time to make bone) = Thyroid and RCCA


Surgical defect
Cold lesion: What they want to hear on boards
Myeloma, thyroid met, RCCA met

Also, just by sheer prevalence, breast can as an unusual manifestation
What does a cold lesion require
A cold lesion is tough to see on bone scan. A significant amount of bone has to be destroyed in order for it to be visible
See bone scan with mets. Then few months later, repeat, lesions have gotten hotter.

Pt was given chemo in interim, which killed tumor cells, and now bone is repairing, but laying down more new bone to do it. So scan temporarily (3-6 mo) shows increase.
When fx hot
by 24 hours
How long fx stay hot?
Ribs 6 mo to years

Wt bearing up to 10 years, slowly fading away
Stress fx, positive on what phases?
All 3
Bilat uptake or unilat uptake at L5
Think spondylolysis
Diffuse linear uptake in tibia
Shin splints.

If uptake was more focal, stress fx.
WBC scan to r/o osteo
WBCs are in marrow, and there is very modest uptake in fracture, but not a lot. If you have a lot of uptake on WBC scan, you can suspect that the bone is infected.
How long can bone scan be abnormal after placement of a prosthesis?
1 year or more. So during this time, you can't really diagnose anything. But years out, if there is a question of infection, then imaging becomes more useful
What is best way to screen a prosthesis for infection?
Compare a baseline MDP to a current one.
Prosthesis imaging
You normally do a WBC scan to rule in or out osteomyelitis. But in the case of prosthesis, there can be expansion of the marrow in that region. Thus, when you do a WBC scan, you will see increased uptake in the same area as the prosthesis, and suspect infection. But it might just be marrow expansion. How do you tell?

By doing a sulfur colloid scan, you can evaluate the marrow volume in that area. So, lets say you get a TcMDP bone scan which is very hot in the region of the prosthesis. You then do a WBC scan, and it is normal. Then you don't have to worry about infection. Its either postop changes or osteolysis. But what if the WBC scan is positive? Then you can't just say its infected so tap the joint, you go on to sulfur colloid to evaluate marrow in that region. If the sulfur colloid shows increased uptake in the same regions, you are probably just dealing with marrow expansion. But if the sulfur colloid scan is not hot in that region, that is suggestive of WBC infiltration exclusive of marrow proliferation, and thus suspicious for infection. You would recommend tapping the joint.
Case with distinct bones, no kidneys, no bladder, minimal soft tissue
Superscan. Bone has extracted more tracer than it normally does, so that by 3-4 hours when you are imaging, there is minimal left in soft tissues, including kidneys and even sometimes bladder.
Superscan ddx
Metabolic bone disease

Metastatic disease
Metabolic causes of superscan
#1 Renal osteodystrophy

#2 Osteomalacia


Rare for hyperparathyroidism to be so bad as to cause superscan
Metastatic causes of superscan
Breast or Prostate

Even in diffuse metastatic dz, should still be able to see some irregularity to suggest metastatic disease over metabolic
Suspect superscan, but not sure
Ask for any plain film.
Intense uptake in humeral or femoral head
Think AVN

Could be other bones too of course
MDP scan with focal liver uptake
Metastatic disease
Diffuse liver uptake
Due to colloid formation in the MDP. Occurs when there is excess aluminum coming out with the Tc from the moly generator
Why aluminum?
Aluminum is used as a reducing eluting agent for the moly generator.
Splenic uptake on MDP scan
Splenic infarct (sickle cell)
Myocardial uptake
MI (occurs a few days out from an MI. Can also get uptake in calcified aneurysm)
Brain uptake

Chest uptake, diffuse
Pleural effusion
Uptake in stomach, kidneys and lungs
Metastatic calcification due to hypercalcemia
Focal muscle uptake
Myositis ossificans

Soft tissue tumor
Diffuse muscle uptake
Inflammatory (rhabdomyolysis or polymyositis)
Lost 15 cards for renal
Types of renal scanning - basic
standard -- typified by MAG-3

Cortical -- typified by DMSA
Tracers for standard imaging

Dose of tracer for study
10 mCi, whether DTPA or MAG3
Differences between MAG3 and DTPA
DTPA is filtered only. Thus it is excreted proportionally to the glomerular filtration rate.

MAG3 is filtered and secreted. It is excreted proportionally to the ERPF - effective renal plasma flow. This is the entire volume of plasma available for clearance by the kidney. 20% of ERPF is due to the filtration (GFR), the other 80% is due to tubular secretion. Thus MAG 3 can be excreted at 5 times the rate of DTPA. This results in better count density and better excretion, which makes for better images, which makes MAG 3 studies more accurate and easier to read.
What is renal scan not used for
to "check" the kidneys.

It is used for specific purposes only
What are those purposes?
Determining split function

Assessing degree of obstruction

Evaluation of RVH (captopril)

Eval of suspected ATN

Transplant eval (limited)
What does decreased renal flow indicate
Totally nonspecific. Decreased renal function results in decreased renal flow.
What is exception to this
ATN. Renal perfusion is classically preserved when there is ATN, despite poor function. That is why it so frequently recovers function.
When is split function calculated
2 minutes, before tracer in coll system
Normal split function

40/60 definitely abnormal

In between is equivocal
Patient with hydronephrosis
Use diuresis renography to determine if hydro is obstructive or nonobstructive.

Give lasix, if you can "flush" out activity through the collecting system, it is not obstructed
Dose of lasix
Adult = 40mg IV

Kid -- 1mg/kg IV
Caveat to this
If bladder distended, may not be able to flush out kidneys, so pt must be able to pee
Interpreting diuresis renography
Draw ROI over entire kidney, including coll system.

Measure half-time of emptying s/p administering lasix

T1/2 < 10 min = NORMAL

T1/2 > 20 min = ABNORMAL

T1/2 in between is equivocal
When is lasix given
Usually 20 min s/p tracer, but can give when coll system full, at same time as tracer (babies) and even 15 minutes BEFORE injection (if you know the entire purpose is to evaluate hydronephrosis for obstruction, this way is best, because you are giving tracer 3 minutes before peak lasix activity (18 min), thus allowing 3 minutes for perfusion/split fcn calculation, then you immediately begin to calculate the T1/2 of emptying 3 min into the study).
Why is captopril scan necessary to evaluate for RVH
2 Reasons

1) You can't just calculate renal blood flow as estimate of RAS, because renal blood flow is preserved until the stenosis is very very severe. It is preserved by the renin angiotensin system. By knocking out this mechanism, and comparing perfusion to the kidney after knocking out the system to before knocking out the system, you can then get an accurate estimation, not of renal artery stenosis, but of renovascular hypertension. This is because if you have a renal artery stenosis that is not physiologically significant, there will be no change in perfusion after giving captopril. So what you are evaluating is for RENOVASCULAR HTN.

2) Renal blood flow can be diminished due to non-vascular causes, i.e. anything except ATN that reduces renal function
How does renin angiotensin system work
Compensates for decreased renal perfusion by causing increased constriction of the efferent arteriole, which increases filtration pressure at the glomerulus, maintaining GFR
What happens when captopril given
Efferent arteriole opens, decreasing pressure across glomerulus, and less filtration occurs, which can result in renal failure. On scan, see it as decreased perfusion (delayed uptake)
What is goal of captopril scan
Get a baseline,

Then induce transient renal failure, and get picture of it happening
When is captopril given relative to tracer?
Given P.O., 1 hour prior to tracer and scan time
Contraindication to captopril scan
Elevated creatinine. If patient already in renal failure, since goal is to induce renal failure, it is going to be hard to tell if there is any difference.
What does positive study look like
MAG-3 -- Initial uptake not affected because GFR is only 20% of uptake with MAG3. But there is delayed washout looking like a prolonged nephrogram.

DTPA -- Decreased initial uptake (split function falls), also slow washout.
Bilateral prolonged nephrogram with MAG3 post capto

Severe Hypotension

Bilateral symmetric RAS

So if you see this appearance, check the BP
Transplant evaluation
Simply do renal scan to visualize perfusion to the kidney.

Compare level of oliguria with perfusion. If there is good perfusion but oliguria, suggests ATN, and lower liklihood of rejection.

If there is diminished perfusion, suggests rejection.

But the distinction between ATN and rejection is not clear cut.

Other complications of transplant (urinoma) are not well defined with renal scintigraphy
Appearance of rejection
= appearance of renal failure

MAG3 -- Prolonged nephrogram phase = prolonged washout

DTPA -- Fades to background, without excretion visible
Role of renal scan in chronic renal failure

Will have poor perfusion to both kidneys, poor excretion, no information given
Difference in DMSA renal cortical scan
More like a bone scan. DMSA gets adsorbed to the tubules, so you wait for it to adsorb and for background to clear out, and then get your delayed images of cortex
Evaluate pyelonephritis or scarring

Inject DMSA

No dynamic imaging

Wait 4 hours.

Take pictures.
Pinhole is desired because need high resolution. Also SPECT.
RN cystography -- protocol
Inject tracer into bladder catheter first

Then hook up bag of saline, and drip it in

Image continuously during filling and voiding
Indications for RNC
Follow-up after positive VCUG

Primary screening tool in girls, since no chance of urethral abnormality as cause of reflux (but if positive, would have to do more eval to look for Hutch divertic, etc)

Screening for sibling of pt with reflux (20% incidence in sibs)
Testicular torsion protocol
Inject Tc pertechnetate

Look at blood flow and pool images

Normally dont see anything. But if torsed, you see a large cold region, with ring of hyperemia around it if it is a late torsion.

If inflammed due to epididymoorchitis, you will see large round area of hyperemia
Indications for brain PET
only 2 reasons clinically:

1) Epileptogenic foci

2) Eval of dementia
Parietal decreased uptake bilaterally, no other abnormality
Early alzheimers
Frontal decreased uptake bilaterally, no other abnormality
Picks disease. If there is just frontal or frontotemoral decreased uptake, its Picks.
Bilateral decreased parietal with decreased frontal uptake also
More advanced Alzheimers.

When very advanced, decreased uptake in whole cortex.
DDx diffuse decreased cortical uptake
Lewy body dementia

Advanced alzheimer

High serum glucose levels causing competetive inhibition
Goal of PET in epilepsy
For refractory cases, localize focus for surgical planning
Identifying Sz focus
FDG used for identifying foci in interictal period

See cold focus, usually right or left temporal lobe.
Complementary tests

How is PET for intraictal imaging?
FDG gets locked into cells once it is phosphorylated by hexokinase. If seizure occurs sometime in the 40 min between injection and imaging, you will see the focus and all of the places it generalized to, making it useless for intraictal imaging.
DDx for hot foci on brain PET
Tumor - met or primary

Epileptogenic focus plus wherever it generalizes to if that occurred

Motor-sensory activation
Other big use of brain PET
Differentiating radiation changes from recurrent tumor
Setup of gamma camera
Top layer = collimator

Next layer = scintillation crystal -- converts high energy photon to light

Next layer -- lots of photomultiplier tubes -- amplify the light

Next layer -- a wire coming out of each PMT going to computer to give information to make the image
Tests for Gamma camera
1) Field uniformity

2) Resolution

3) Center of rotation
Field uniformity frequency
Done daily
Extrinsic flood
Collimator kept on

Cobalt SHEET source put below camera, where patient would be

Should see salt and pepper appearance
Causes of abnormalities on extrinsic flood
Collimator damage

Collimator contamination

Crystal crack

PMT out
Intrinsic flood
Collimator taken off

Point source
What can you see with intrinsic flood?
Cracked crystal

PMT out
Failed PMT
Round defect with no bright around it
Appearance of cracked crystal
Jagged or linear area of no counts, with rim of increased counts due to confused PMTs
Thyroid scan with large nodule
Hot -- benign

Cold -- If it is a dominant nodule (larger than the others), it must be biopsied by FNA
Given 2 images from scan. Performed 30 min apart. One scan very blurry. Next one looks normal.
Off peak image.

You can predict this was done as first case of the day, because the technologist does the flood with Cobalt 57, which has peak of 122 keV. This is close enough to Tc to image it, but all you are imaging is the scatter.
No excretion after 24 hours into bowel on HIDA in kid
Cannot exclude biliary atresia. Recommend biopsy.
Telling difference between Tc and I thyroid scans
If Tc, imaged immediately, and see background plus salivary glands

If Iodine, no background, just thyroid.

So if given scan with two adjacent structures, and no background, its probably thyroid, or maybe DMSA renal scan with lots of defects making it look like a thyroid.
Thyroid scan with decreased uptake
Subacute (Hashimoto) thyroiditis

Extrinsic thyroid hormone suppressing TSH

Large iodine load

PTU or methimazole
How can you tell difference
1) Does patient have thyrotoxicosis -- if yes, eliminates PTU, methimazole as cause
How else can you tell if decrease activity is related to PTU/methimazole
Tc scan:

TcO4 is trapped by the thyroid, not organified, like Iodine is. PTU and methimazole block organification, thus blocking Iodine from being concentrated. But they do not block trapping, so Tc can still accumulate in there.
Gallium face
Normally see lacrimal glands and nose. Do not NORMALLY see salivary glands.
Soft tissues, no bones, liver, no spleen, heart, salivary glands, bladder

When you see salivary glands and myocardium on same scan you are looking at autonomic innervated organs, which should make you think MIBG. MIBG is the only normal whole body scan that you will see heart on except for PET.

Should also be able to see adrenal faintly, although if shown it will probably be the adrenal that is the mass
MIBG scan with mass
Adult -- PHEO

Kid -- Neuroblastoma
Brain uptake on whole body scan
Spleen and liver, central bone marrow activity
Could be sulfur colloid or In111 WBC scan
How do you tell difference
InWBC scan -- No bladder activity

Sulfur colloid -- get bladder activity
Liver, hot spleen, very hot kidneys, soft tissue but no bone
Octreotide scan

Carcinoid or islet cell tumor
I131 indications
Pre-therapy to look for mets

S/P ablation therapy, to get a baseline, and because with such a high dose given, will see everything that takes up I131

Screening for recurrence
What scan can look like gallium?
MIBG. Both have soft tissue uptake, both have uptake in face.

Differentiate by observing for bone marrow uptake. If bones are visible, its gallium. If not, its MIBG.
DDx diffuse lung uptage on gallium
Sarcoidosis (stage 2 or 3)



Hypersensitivity pneumonitis


Drug toxicity (bleomycin)
Diffuse homogeneous liver uptake on MDP bone scan
Colloid formation by MDP, due to too much alumina in eluate
Focal or multifocal liver uptake on MDP bone scan
Metastatic lesions. Adenocarcinomas (breast, colon) commonly do it. Of course any met with calcification also.
Gallium dose
Depends whether imaging for tumor or inflammatory disease

If for tumor, give 10 mCi

For inflammation, give 5 mCi
Size for hemangioma on RBC scan
2 cm
Not seen on immediate, seen on delayed images
What type of hemangioma is this
CAVERNOUS. Think it has to slowly fill in the caverns. Capillaries fill immediately, so those are the flash fillers.
When are delayed images taken for hemangioma
1 to 2 hours
Bleeding scan tracers
Tc labeled RBCs

Sulfur colloid -- no ability for delayed imaging but better signal to noise since blood pooc clears rapidly
drugs for enhancement of meckel scan
Pentagastrin -- increases rapidity of uptake, used with glucagon to decrease motility

2% of popn

2 cm from ileocecal junction
Gastric emptying study
GOO vs. diabetic gastroparesis
position acquired
Ant and posterior or just LAO
characterizing reflux
Milk study

high -- more than 1/2 way to mouth

low and short

long -- greater than 10 seconds
differentiate DTPA from HMPAO brain death study
HMPAO has salivary gland uptake
Binds irreversibly to brain cells on first pass
Advantage of HMPAO
Do not need good bolus
Luxury perfusion
cerebral blood flow increased or not decreased 3-7 days after stroke because of loss of autoregulation even though brain dead
agents for radionuclide VCUG
sulfur colloid or DTPA
methods for performing
direct or indirect

Direct -- put in catheter

indirect -- do renal flow study first, then image
why kids reflux
short intramural UVJ segment
limitations of renography
dehydration limits study

as does renal insufficiency
quantitative side
washout half time post lasix
patient with UPJ obstruction for follow up renal scan shows persistent dilatation of collecting system
Will look like this for life. The coll system will never return to normal. BUT on post lasix imaging, will still have NORMAL WASHOUT.
COllections around transplant kidneys
Urinoma, hematoma, abscess -- first 2 weeks postop

Lymphocele -- 4 to 8 weeks
Complications after transplant


hyperacute/acute rejection

Cyclosporin toxicity -- months after
Photopenic kidney 24 hours post transplant
renal vein thrombosis

Renal artery thrombosis -- more common after 2 months

Hyperacute rejection -- rare because of prescreening

Acute cortical necrosis
Post transplant renal scan with good uptake. No excretion.
common first week complications

Accelerated acute rejection

Urinary leak

Urinary obstruction
When does acute rejection begin
5 to 7 days = accelerated

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