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1
Q

DIFFUSE INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
(‘SUPERSCAN’) 4

A
  1. Widespread bone metastases—most common sources include
    prostate and breast. Uptake is diffuse but often patchy/
    asymmetrical. Long bones less commonly involved.
  2. Metabolic bone disorders—osteomalacia, hyperparathyroidism
    and renal osteodystrophy. Uptake is diffuse and symmetrical.
    Proximal long bones usually involved, with prominent uptake in
    the skull and mandible. May have focal areas of very high uptake
    due to brown tumours in hyperparathyroidism.
  3. Myeloproliferative disorders—e.g. myelofibrosis, mastocytosis,
    leukaemia, lymphoma and Waldenstrom’s macroglobulinaemia.
  4. Widespread polyostotic Paget’s disease or fibrous dysplasia—
    usually multifocal rather than diffuse
2
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Neoplastic 5

A
  1. Metastatic—multiple randomly scattered lesions especially in the
    axial skeleton. Solitary lesions in typical locations, e.g. sternum in
    breast cancer, pelvis/sacrum/lower lumbar spine in prostate cancer.
  2. Hypertrophic pulmonary osteoarthropathy—tramline sign:
    linear, symmetrical uptake along the periphery of the long bones
    (distal > proximal). Corresponds to the periosteal reaction seen on
    plain film. See Section 1.24 for a list of causes.
  3. Primary bone tumours—e.g. Ewing sarcoma, osteosarcoma.
    Solitary, but may also have distant bone metastases
  4. Erdheim-Chester disease*—skeletal involvement in 96%, typically
    femur, tibia and fibula. Less commonly ulna, radius and humerus.
    Bilateral symmetrical increased metadiaphyseal uptake
    corresponding to osteosclerosis on plain film.
  5. Eosinophilic granuloma/Langerhans cell histiocytosis*—variable
    uptake (increased or decreased). Most common sites include skull,
    pelvis and femur. Less common sites include ribs, humerus,
    mandible and spine
3
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Joint disease 2

A
  1. Degenerative—most common sites include:
    (a) Cervical and lumbar spine—facet joint arthropathy is often
    best seen on posterior views, in the lumbar spine appearing to
    lie between two adjacent vertebrae. Arthropathy at the
    intervertebral disc is often best seen on anterior views due to
    cervical and lumbar lordosis.
    (b) Hips and knees—most commonly seen in the superior aspect
    of the hip joints and medial compartment of the knees at the
    site of maximal load.
    (c) Shoulders—three potential sites of focal arthropathic uptake:
    glenohumeral joint, acromioclavicular joint and greater
    tuberosity (due to rotator cuff impingement).
    (d) Other common sites—sternoclavicular joints, hands, ankles
    and feet.
  2. Inflammatory arthropathies—uptake is related to increased blood
    flow to the affected joint, resulting in diffuse tracer accumulation
    surrounding the joint rather than the focal uptake associated with
    degenerative change. Distribution depends on the underlying
    arthropathy.
4
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Fractures 4

A
  1. Traumatic—80% of fractures demonstrate tracer uptake on
    bone scan 24 hours after injury (may be delayed in elderly/
    osteoporotic patients). By 1 week, 100% of fractures are visible
    on bone scan. Aligned fractures in ribs are always traumatic (i.e.
    not pathological). With single lesions elsewhere, always ask if
    history of trauma ± correlate with plain film. As the fracture
    evolves, the bone scan appearances change with three distinct
    phases:
    (a) Phase 1—0 to 4 weeks: diffuse increased uptake at the fracture
    site ± fracture line.
    (b) Phase 2—4 to 12 weeks: intense linear uptake at the fracture
    site.
    (c) Phase 3—12 weeks to 2 years: gradual reduction in uptake.
  2. Stress—caused by abnormal stress on a normal bone. Bone scans
    are commonly used in their detection and can be combined with
    SPECT-CT when evaluating smaller bones, e.g. hallux, sesamoids and pars defects. Bone scans can differentiate between tibial stress
    fractures (focal uptake usually at the junction of the mid-distal
    thirds of the tibia) and shin splints (periostitis at the insertion of
    tibialis and soleus muscles causing longitudinal linear increased
    uptake involving ≥ one-third of the posterior tibial cortex).
    Enthesopathy and periosteal reactions related to stress will all show
    increased uptake, e.g. plantar fasciitis shows focal uptake at the
    inferior aspect of the calcaneum.
  3. Insufficiency—caused by normal stress on an abnormal bone, e.g.
    osteoporosis, metabolic bone disorders. Common sites include
    tibial plateau, calcaneum, sacrum (H-shaped ‘Honda’ sign), lesser
    trochanter of femur (especially in metabolic bone disorders) and
    vertebral bodies (compression fractures).
  4. Nonaccidental injury*—bone scans can detect radiologically
    occult fractures and may be considered if the clinical suspicion
    is high.
5
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Paget’s disease

A

Can affect any bone, but most commonly seen in the spine
(especially lower lumbar spine), femora, skull and pelvis.
Characterized by diffuse increased uptake within the affected
bone, often starting from one end and progressing until the entire
bone is involved. The associated bony expansion and
flame-shaped advancing edge may also be visible on bone scan.
The exception to this rule is in the skull, where the increased
uptake starts in the skull base and progresses to the vertex during
the lytic/active phase of the disease, corresponding to the classic
‘osteoporosis circumscripta’ on plain film.
70% of patients have polyostotic disease. On a bone scan the
intensity of tracer uptake can vary depending on the phase and
treatment of the disease. Complications—bone deformity, fracture
and malignant degeneration (e.g. osteosarcoma)—are often well
seen on bone scan due to the increased uptake in the underlying
Pagetic bone

6
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Infection 4

A
  1. Periprosthetic infection—see Section 15.3.
  2. Dental infection/sinusitis—including Garre’s sclerosing
    osteomyelitis of the mandible. Focal uptake in the mandible or
    maxilla.
  3. CRMO/SAPHO—multifocal areas of uptake; CRMO usually occurs
    in children or adolescents and favours metaphyses of long bones (especially femur and tibia, also clavicle); SAPHO usually occurs in
    adults and favours sternoclavicular joints (commonest site of
    involvement, bull’s head sign), manubriosternal joint,
    costochondral joints, spine (paravertebral hyperostosis) and
    sacroiliac joints (often unilateral).
  4. Paediatric polyostotic osteomyelitis—6.8% of osteomyelitis in
    infants is polyostotic (up to 22% in neonates) due to
    haematogenous spread of infection. Bone scan is largely replaced
    by MRI (whole-body STIR) but can still be useful in patients unable
    to tolerate MRI
7
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Benign lesions

A
  1. Osteomas—skull and mandible; also ivory osteomas in paranasal
    sinuses.
  2. Fibrous cortical defect/nonossifying fibroma—variable uptake,
    increased in healing or fracture.
  3. Bone island—usually no uptake; low-grade uptake has been
    reported in larger lesions.
  4. Osteoid osteoma—increased uptake on blood pool images and
    late (bone phase) images, ± a central intense focus of uptake
    corresponding to the nidus on anatomical imaging, surrounded by
    less intense uptake corresponding to the surrounding sclerosis.
  5. Fibrous dysplasia—persistent increased uptake on bone scan;
    20%–30% polyostotic, commonly unilateral and monomelic (one
    limb).
  6. Melorheostosis—monostotic or polyostotic, monomelic,
    commonly involves long bones.
  7. Osteochondroma—increased uptake in an adult suggests growth
    or malignant degeneration.
  8. Enchondroma.
  9. Heterotopic bone formation.
8
Q

FOCAL INCREASED UPTAKE ON
WHOLE-BODY BONE SCANS
Avascular necrosis (AVN

A
  1. <1 month—photopenia at the site of AVN.
  2. 1–4 months—increased uptake around the area of AVN due to
    peripheral revascularization (e.g. ‘donut’ sign in the hip).
  3. 4–10 months—diffuse increase at the site of AVN as healing
    occurs.
  4. > 10 months—either the scan returns to normal (uncomplicated
    healing) or there is increased uptake due to sclerosis and
    secondary degenerative changes
9
Q

INCREASED UPTAKE ON LOCAL VIEW

BONE SCANS 2

A
  1. Joint replacement—two-phase bone scans (blood pool and late)
    are used to look for evidence of loosening or infection. Normal
    scans have a high negative predictive value, but a significant
    number of normal prosthetic joints continue to accumulate tracer
    years after surgery.
    (a) Loosening—typically shows increased uptake only on the late
    phase images with normal uptake on the blood pool phase.
    (i) Hips—focal increased uptake in the greater and lesser
    trochanters and at the tip of the femoral prosthesis
    suggests loosening.
    (ii) Knees—normal uptake can persist for up to 4 years.
    Uptake at the femoral prosthesis normalizes first, followed
    by the lateral tibial prosthesis, with the medial tibial
    prosthesis normalizing last. Any focal uptake not
    conforming to this pattern is suspicious for loosening.
    (b) Infection—increased uptake surrounding the prosthesis on
    both the blood pool and late phase images.
    (c) Synovitis/capsulitis—following knee replacement. Increased
    uptake in the synovium/capsule on the blood pool phase
    only.
  2. Complex regional pain syndrome—two- or three-phase (dynamic
    flow, blood pool and late) bone scan. Increased uptake in the
    affected limb on all three phases in a periarticular distribution.
    Over time this increased uptake normalizes; in chronic cases
    decreased uptake may be seen on all phases
10
Q

INCREASED UPTAKE ON BONE SCANS
NOT DUE TO SKELETAL ABNORMALITY
Artefacts 6

A
  1. Urine contamination—can be anywhere.
  2. Extravasated injection in the arm/leg—± uptake in the draining
    sentinel node.
  3. Post surgery—increased uptake due to hyperaemia.
  4. Arterial injection—increased uptake in the injected arm distal to
    the injection site.
  5. Tracer preparation problems.
    (a) Free pertechnetate—uptake in stomach, thyroid, GI tract and
    salivary glands.
    (b) Colloid formation due to aluminium—liver uptake, reduced
    bone uptake.
    (c) High pH—uptake in liver, gallbladder and GI tract.
  6. Equipment.
    (a) Edge effect—apparent increased uptake at the edges of the
    field.
    (b) Distance from camera/rotation of patient—bones closer to
    the camera will appear to show increased uptake.
    (c) Summation artefact—contamination of the collimator/
    camera
11
Q

INCREASED UPTAKE ON BONE SCANS
NOT DUE TO SKELETAL ABNORMALITY
Physiological variants 6

A
  1. Epiphyses.
  2. Calcification of costal cartilages.
  3. Bladder diverticulum.
  4. Nipples.
  5. Renal anomalies.
  6. Hyperostosis frontalis.
12
Q

INCREASED UPTAKE ON BONE SCANS
NOT DUE TO SKELETAL ABNORMALITY
Soft-tissue uptake 2

A
  1. Calcification—e.g. myositis ossificans, dermatomyositis,
    hyperparathyroidism, calcified tumours/metastases, vascular
    calcification, calcific tendonitis, tumoural calcinosis, calcified
    abscess and alveolar microlithiasis.
  2. Others (noncalcified):
    (a) Infarcts—cardiac, cerebral.
    (b) Renal uptake—long term antibiotics, chemotherapy,
    hypercalcaemia and hypercalciuria.
    (c) Malignant pleural effusions and ascites.
    (d) Metastases—commonly liver metastases from colon, breast or
    small cell carcinoma.
    (e) Amyloidosis—cardiac uptake.
    (f) Tumour—e.g. inflammatory breast cancer.
    (g) Hypercalcaemia with metastatic calcification—uptake in lungs
    and stomach.
    (h) Amiodarone lung
13
Q

PHOTOPENIC AREAS ON BONE SCANS

6

A
  1. Artefacts—the most common cause.
    (a) External—metal objects, e.g. coins, belts, lockets and buckles.
    (b) Internal—joint prostheses, pacemakers.
  2. Lytic metastases—e.g. renal, thyroid and lung.
  3. Avascular lesions—e.g. bone cysts.
  4. Spinal haemangiomas—occasionally slightly increased uptake.
  5. Radiotherapy fields—nonanatomical, usually oblong in shape.
  6. Multiple myeloma*—bone scan often normal due to the lack of
    osteoblastic activity; larger lesions may be photopenic or show
    increased uptake.
14
Q
VENTILATION-PERFUSION MISMATCH ON 
V/Q SCANS
Mismatched perfusion defects
Perfusion defect > ventilation defect
8
A
  1. Pulmonary embolus—especially if multiple and segmental.
  2. Bronchial carcinoma—but more commonly matched.
  3. Tuberculosis*—typically affects an apical segment.
  4. Vasculitis—polyarteritis nodosa, SLE, etc.
  5. Tumour/fat embolus.
  6. Post radiotherapy.
  7. Pulmonary hypertension.
  8. Pulmonary artery narrowing.
15
Q

VENTILATION-PERFUSION MISMATCH ON
V/Q SCANS
Mismatched ventilation defects 5

A
  1. Chronic obstructive pulmonary disease (COPD).
  2. Pneumonia.
  3. Lung collapse—of any cause.
  4. Pleural effusion.
  5. Bronchial carcinoma—the rarest appearance
16
Q

MATCHED VENTILATION-PERFUSION
DEFECTS ON V/Q SCANS
Multiple 9

A
  1. Chronic bronchitis.
  2. Pulmonary infarct/chronic pulmonary embolus (PE)—do not confuse with the mismatched perfusion defect of acute PE.
  3. Asthma or acute bronchitis—may also show mismatched ventilation or perfusion defects.
  4. Bullae—long-standing bullae have scarce vessels and hypoventilation results in vascular constriction.
  5. Collagen vascular disease.
  6. Lymphangitis carcinomatosa.
  7. Pulmonary hypertension.
  8. Sarcoidosis*.
  9. Intravenous drug abuse.
17
Q

MATCHED VENTILATION-PERFUSION
DEFECTS ON V/Q SCANS
Solitary 3

A
  1. Pneumonia—results in hypoventilation and compensatory
    hypoperfusion with a corresponding area of opacification on CXR
    (triple match). This cannot be distinguished from a pulmonary
    infarct on V/Q scan or CXR alone.
  2. Bulla.
  3. Pulmonary infarct
18
Q

ARTEFACTS ON V/Q SCANS 7

A
  1. Breast prostheses—matched defect.
  2. Cardiomegaly—matched defect.
  3. Pacemaker—matched defect.
  4. Clumping—technical problem causing focal areas of increased
    uptake on perfusion images due to clumping of tracer particles.
  5. Central airways deposition—areas of focal increased uptake seen
    centrally on ventilation images due to precipitation of aerosol,
    secondary to turbulent air flow in the major bronchi, commonly
    in COPD.
  6. Right to left cardiac shunt—uptake seen in the brain and
    abdominal viscera on the perfusion images.
  7. Renal uptake on the ventilation images—in pneumonitis or
    smokers.
19
Q

CAUSES OF A PERFUSION DEFECT ON A

MYOCARDIAL PERFUSION SCAN 6

A
  1. Inducible/reversible ischaemia.
  2. Infarction.
  3. Hibernating myocardium—often reduced activity during stress
    and at rest.
  4. Breast-related artefact—particularly anterior defects.
  5. Inferior wall defects—may result from diaphragmatic motion or
    the increased distance of this wall from the camera.
  6. Apical thinning
20
Q

SCINTIGRAPHIC LOCALIZATION OF
GI BLEEDING
Common sites 8

A
  1. Ulcers—benign or malignant.
  2. Vascular lesions—angiodysplasia (most common in right colon),
    varices (oesophageal or gastric), fistula (including aortoenteric),
    telangiectasia (e.g. in HHT, vasculitis, scleroderma), intramural
    haematoma.
  3. Tumours—malignant (primary or metastatic) and benign (e.g.
    adenoma, leiomyoma).
  4. Inflammatory lesions—gastritis, duodenitis.
  5. Diverticula—e.g. colonic or Meckel’s.
  6. Surgical anastomosis.
  7. Intussusception.
  8. False-positive scintigraphy—uptake may be seen in renal tract,
    liver, spleen (including splenunculi), uterus, bone marrow and
    hypervascular small bowel.
21
Q

MECKEL’S SCAN

A

Positive scan
1. Meckel’s diverticulum containing ectopic gastric mucosa—note
that the timing of tracer uptake in the diverticulum should match
the timing of normal gastric uptake.
False positive scan
1. Duplication cyst containing ectopic gastric mucosa.
2. Bowel inflammation or obstruction—including intussusception.
3. GI bleeding—e.g. peptic ulcer.
4. Vascular lesions with increased blood pool.
5. Radioactive tracer in the renal collecting systems—including
tracer in a bladder diverticulum.
False negative scan
1. Meckel’s containing no gastric mucosa—or nonfunctioning
gastric mucosa.
2. Meckel’s hiding behind the bladder—may be masked by normal
bladder uptake.
3. Technical problem with the scan—always check for normal
gastric uptake

22
Q
Abnormal HIDA SCAN
Delayed uptake 1
Delayed excretion 2
Abnormal GB uptake/EF 3
Pooling of tracer in liver parenchyma 2
Others 2
A

Delayed uptake:
Any cause of hepatocellular failure/dysfunction

Delayed excretion into the biliary tree:

  1. Infants—biliary atresia.
  2. Adults—biliary obstruction; if there is focal dilatation of the bile duct this may be due to a choledochal cyst.

Abnormal gallbladder uptake/ejection fraction:
Gallbladder uptake is normally seen within 1 hour, and after a
fatty meal the gallbladder ejection fraction should be >40%.
1. Acute cholecystitis—no gallbladder uptake.
2. Chronic cholecystitis—delayed tracer uptake by the gallbladder
with poor gallbladder ejection fraction.
3. Gallbladder dyskinesia—normal gallbladder uptake with poor
ejection fraction. Also consider acalculous cholecystitis.

Pooling of tracer within the liver parenchyma:

  1. Biloma—HIDA scan can be used to diagnose postoperative bile leaks.
  2. Focal biliary dilatation/choledochal cyst.

Other findings:

  1. Sphincter of Oddi dysfunction—delayed passage of tracer into the bowel.
  2. Biliary reflux—tracer passes from the duodenum into the stomach
23
Q

PHOTOPENIC DEFECTS ON

RADIONUCLIDE (DMSA) RENAL IMAGES 5

A
  1. Scars—note that defects present during infection may resolve later,
    hence imaging is routinely delayed until 3 months after the acute
    infective episode.
  2. Hydronephrosis—central defect.
  3. Focal renal lesions—cysts, tumours (e.g. RCC, lymphoma, Wilms
    tumour, metastases) and abscesses.
  4. Trauma—subcapsular or intrarenal.
  5. Infarct/ischaemi
24
Q

ABNORMAL RADIONUCLIDE
RENOGRAM (MAG3)
Delayed tracer uptake 5

A
  1. Renal artery stenosis.
  2. Poor renal function.
  3. Dehydration—particularly children.
  4. Renal tubular acidosis.
  5. Renal transplant rejection
25
Q

ABNORMAL RADIONUCLIDE
RENOGRAM (MAG3
Delayed excretion 3

A
  1. All of the above.
  2. Nephritis.
  3. Obstruction—together with delayed drainage.
26
Q

ABNORMAL RADIONUCLIDE
RENOGRAM (MAG3
Delayed drainage 4

A
  1. Obstruction—including PUJ and ureteric obstruction.
  2. Baggy renal pelvis – drains with posture/diuretic.
  3. Nephritis.
  4. Megaureter
27
Q

PHOTOPENIC AREAS ON RADIONUCLIDE
THYROID IMAGING
Localized 8

A
  1. Colloid cyst.
  2. Nonfunctioning adenoma.
  3. Carcinoma—papillary, follicular; medullary may be bilateral.
  4. Multinodular goitre.
  5. Marine-Lenhart syndrome—cold thyroid stimulating hormone
    (TSH)-dependent nodule in the presence of Graves disease.
  6. Vascular.
  7. Abscess.
  8. Artefact
28
Q

PHOTOPENIC AREAS ON RADIONUCLIDE
THYROID IMAGING
Generalized 5

A
  1. Concurrent medication for hyperthyroidism.
  2. Hypothyroidism.
  3. Thyroiditis—e.g. acute (infectious), De Quervain’s, Riedel’s and
    Hashimoto’s (later stages). Shows diffusely reduced/absent uptake.
  4. Ectopic hormone production—e.g. ectopic thyroid tissue.
  5. Amiodarone induced thyroiditis type 2—subacute inflammatory
    thyroiditis
29
Q

INCREASED UPTAKE ON RADIONUCLIDE
THYROID IMAGING
Focal increased uptake 2

A
  1. Toxic nodule—± suppression of the rest of the gland.

2. Artefact—e.g. swallowed tracer activity in the oesophagus

30
Q

INCREASED UPTAKE ON RADIONUCLIDE
THYROID IMAGING
Diffuse increased uptake 5

A
  1. Graves disease—very hot, uniform and both lobes.
  2. Multinodular goitre—mildly increased, heterogeneous.
  3. Hashimoto’s thyroiditis—in the early stages.
  4. Amiodarone-induced thyrotoxicosis type 1—exacerbation of a
    preexisting thyroid condition by amiodarone. May be normal or
    show diffuse increased uptake. ( Type 2 -slow destruction of thyroid tissue, low/absent uptake on scinti)
  5. Lithium therapy
31
Q

FOCAL INCREASED UPTAKE ON A
PARATHYROID SESTAMIBI SCAN
Physiological 9

A
  1. Salivary glands.
  2. Oral cavity—due to secretions from the salivary glands.
  3. Thyroid gland.
  4. Heart.
  5. Liver.
  6. Bone marrow.
  7. Thymus.
  8. Brown fat.
  9. Uptake in the arm vein used for injection
32
Q

FOCAL INCREASED UPTAKE ON A
PARATHYROID SESTAMIBI SCAN
Pathological 6

A
  1. Parathyroid adenoma.
  2. Parathyroid carcinoma.
  3. Thyroid adenoma/carcinoma.
  4. Other malignancies—adenocarcinoma (e.g. lung), squamous cell
    cancers (e.g. head and neck), bronchial carcinoid, lymphoma and
    breast cancer.
  5. Sarcoidosis*.
  6. Parathyroid hormone secreting paraganglioma
33
Q

BRAIN DATSCAN

Normal 4

A
  1. Normal patient.
  2. Drug-induced or vascular Parkinsonism.
  3. Essential tremor.
  4. Drug interactions—e.g. cocaine, anti-ADHD (attention-deficit
    hyperactivity disorder) drugs and antidepressants. These can cause
    a false negative scan
34
Q

BRAIN DATSCAN

Abnormal 5

A
  1. Parkinson’s disease.
  2. Multiple system atrophy.
  3. Progressive supranuclear palsy.
  4. Corticobasal degeneration.
  5. Lewy body dementia.
35
Q
BRAIN DATSCAN ( I - Dopamine scan for Parkinsons Dx)
Asymmetrical/unilateral reduced uptake 3
A
  1. Early Parkinson’s disease—NB: other Parkinsonian syndromes (see
    earlier) are less likely to be asymmetrical.
  2. Cerebral infarct—causes punched-out defects.
  3. Brain tumour
36
Q

DEMENTIA IMAGING BY FDG PET-CT 4

A
  1. Alzheimer’s disease—temporoparietal reduced uptake, starts in
    mesotemporal and posterior cingulate gyrus.
  2. Lewy body dementia—same as in Alzheimer’s disease, except it
    can also involve the occipital lobes.
  3. Frontotemporal dementia—disproportionate frontal reduced
    uptake.
  4. Vascular dementia—patchy reduced uptake
37
Q

MIBG SCINTIGRAPHY 6

A

Abnormal uptake

  1. Phaeochromocytoma.
  2. Neuroblastoma—in children.
  3. Paraganglioma.
  4. Medullary thyroid carcinoma.
  5. Ganglioneuroma.
  6. Neuroendocrine neoplasms—less avid than with SRS
38
Q

SOMATOSTATIN RECEPTOR

SCINTIGRAPHY (OCTREOTIDE SCAN 7

A

Abnormal uptake

  1. Neuroendocrine neoplasms—carcinoid tumours, pancreatic NETs.
  2. Inflammation—e.g. sarcoidosis, rheumatoid arthritis and IBD.
  3. Scar tissue—e.g. postsurgical.
  4. Phaeochromocytoma—less avid than with MIBG.
  5. Neuroblastoma—less avid than with MIBG.
  6. Paraganglioma—less avid than with MIBG.
  7. Medullary thyroid carcinoma—less avid than with MIBG
39
Q

Causes of nonmalignant FDG uptake on PET-CT

13

A
  1. Physiological uptake—liver, spleen, kidneys, bowel, urine,
    endometrium (ovulatory and menstrual phases) and ovaries/
    corpus luteum (ovulatory phase).
  2. Skeletal uptake—degenerative, fractures, Paget’s disease,
    inflammatory arthropathy and reactive bone marrow (GCSF,
    anaemia, infection etc.)
  3. Inflammation—e.g. recent surgery (especially <6 weeks), foreign
    body reaction, diverticulitis, gastritis, pancreatitis and
    retroperitoneal fibrosis.
  4. Granulomatous disease—e.g. TB, sarcoidosis and sarcoid-like
    tumour reaction (immune phenomenon by host’s defense against
    tumour cells, most common in mediastinal and hilar nodes).
  5. Infection/abscesses.
  6. Fat.
    (a) Brown fat—common in young thin women; seen in
    supraclavicular fossae, posterior thorax, mediastinum and
    upper abdomen. Also in hibernoma (benign tumour of
    brown fat).
    (b) Lipomatous hypertrophy of the interatrial septum—1%–
    8% of the population.
    (c) Fat necrosis.
  7. Metformin—diffuse increased GI tract uptake.
  8. Benign tumours—e.g. adrenal adenoma (5%), pituitary
    adenoma and parathyroid adenoma.
  9. Uterine fibroid—18% show uptake.
  10. Thyroid nodules—2.1% incidence; 36% malignant, the rest are
    benign.
  11. Parotid nodules—0.5% incidence; 50% benign, commonly
    Warthin tumours or pleomorphic adenomas.
  12. Venous thrombosis.
  13. Attenuation correction artefacts
40
Q

Malignancies with poor FDG PET avidity 8

A
  1. HCC—up to 50% show no uptake.
  2. Lymphoma* subtypes—e.g. MALT.
  3. Necrotic or mucinous adenocarcinoma.
  4. Renal cell carcinoma—around 60% sensitivity.
  5. Early-stage pancreatic cancer.
  6. Prostate cancer—but may take up choline.
  7. Well-differentiated neuroendocrine tumours—e.g. carcinoid;
    gallium-based tracers such as DOTATOC are useful.
  8. Well-differentiated thyroid malignancy.
41
Q

CHOLINE PET-CT

Causes of malignant uptake 4

A
  1. Prostate cancer—main indication for the scan.
  2. Lymphoma*.
  3. Mucinous adenocarcinoma.
  4. Lung cancer—small cell and adenocarcinoma (including low-grade
    tumours that only show minimal uptake on FDG PET).
42
Q

CHOLINE PET-CT

Causes of nonmalignant uptake 5

A
  1. Skeletal uptake—same as with FDG (see Section 15.22).
  2. Inflammation—same as with FDG (see Section 15.22).
  3. Granulomatous disease—same as with FDG (see Section 15.22).
  4. Infection/abscesses.
  5. Benign tumours—e.g. adrenal adenoma (5%), pituitary
    macroadenoma (larger focus of uptake than normal pituitary
    uptake) and parathyroid adenoma.
43
Q

GALLIUM-68 DOTA PET-CT

Causes of malignant uptake 8

A
  1. Neuroendocrine tumours—main indication for the scan. Higher avidity with well-differentiated tumours (the opposite of FDG PET). Includes pancreatic NETs (insulinoma, glucagonoma, gastrinoma, VIPoma), ACTH-secreting carcinoids and Merkel cell tumours.
  2. Phaeochromocytoma and paraganglioma.
  3. Medullary and iodine negative thyroid carcinomas.
  4. Small-cell lung cancer.
  5. Meningioma.
  6. Medulloblastoma.
  7. Invasive lobular breast cancer.
  8. Benign phosphaturic mesenchymal tumour—causes oncogenic osteomalacia
44
Q

GALLIUM-68 DOTA PET-CT

Causes of nonmalignant uptake 5

A
  1. Skeletal uptake—seen in osteoblastic processes, e.g. degenerative,
    fractures, Paget’s disease, inflammatory arthropathy, epiphyseal
    growth plates, haemangioma and enchondroma.
  2. Inflammation—white blood cells (including leukocytes and
    macrophages) express somatostatin receptors. Seen in recent
    surgery (especially <6 weeks), foreign body reaction, diverticulitis,
    gastritis, pancreatitis, prostatitis, post radiotherapy and reactive
    nodes.
  3. Infection/abscesses.
  4. Splenunculi and splenosis