Magnus NM Master Reference

Bone Scan (Tc-99m MDP)

Tc-99m MDP

Adult Dose

740–925 MBq (20–25 mCi)

Paediatric Dose

9.3 MBq/kg (min 37 MBq)

Physical T½

6 h (Tc-99m)

Mechanism: Adsorption onto calcium hydroxyapatite at sites of osteoblastic activity; 50% skeletal uptake at 2–3 h

Normal findings: Homogeneous symmetric uptake in axial skeleton, long bones, flat bones. Mild uptake kidneys, bladder. Growth plates prominent in children. Slight asymmetry skull base/facial bones normal. Renal activity should be symmetric.

Ensure adequate hydration (500 mL water before and after injection)
Void bladder immediately before imaging
Remove metallic objects, prosthetics if possible
Delay scan if recent barium study (streak artifact)
Inform of any recent fracture, surgery, or radiation therapy

0 min

IV injection of Tc-99m MDP

0–5 min

Flow phase: dynamic images (2 s/frame × 60 frames) over region of interest — THREE-PHASE only

5–10 min

Blood pool phase: static images of ROI — THREE-PHASE only

2–4 h

Whole-body delayed scan: ant + post (anterior + posterior); spot views of equivocal areas; SPECT/CT of any lesion

Void

Patient voids before whole-body scan to clear pelvic activity

Freq	Finding	Context	Key Features
Common	Metastases (blastic)	Prostate, breast, lung	Multiple foci · axial > appendicular · hot spots
Common	Degenerative joint disease	Facet joints, knees, hips, shoulders	Periarticular uptake · bilateral but asymmetric
Common	Fracture (acute)	Trauma, insufficiency, stress	Focal intense · linear pattern for insufficiency fx
Common	Arthritis (OA/RA)	Peripheral joints	Periarticular, symmetric in RA; asymmetric in OA
Classical	Osteomyelitis	Any bone, children > adults	THREE-PHASE all positive; flow > pool > delayed
Classical	Paget's disease	Pelvis, spine, skull, femur	Expanded bone, intense uptake, 'tam-o'-shanter' skull
Classical	Superscan	Disseminated mets (prostate/breast), renal osteodystrophy	Intense skeletal uptake, absent kidney/bladder activity — easy to miss
Classical	Reflex sympathetic dystrophy (CRPS)	Post-trauma extremity	Periarticular uptake all 3 phases; asymmetric flow
Classical	Avascular necrosis (cold phase)	Femoral head, scaphoid, talus	Photopenic area early → later hot rim
Classical	Primary bone tumour	Any bone	Intense focal uptake ± soft tissue extension
Rare	Fibrous dysplasia	Ribs, long bones, skull	Intense focal · 'shepherd's crook' deformity
Rare	Hypertrophic osteoarthropathy	Periosteum, long bones	Parallel track sign — bilateral periosteal uptake
Rare	Heterotopic ossification	Post-surgery, burns, spinal injury	All 3 phases hot; soft tissue location
Rare	Flare phenomenon	Post-chemotherapy response	Increased uptake at known mets 3–6 months post-Rx; indicates response not progression
Rare	Renal osteodystrophy (metabolic)	Hyperparathyroidism, CKD	'Tie sternum' · Calvarial uptake · Absent kidneys

Superscan — absent renal/bladder activity is the clue; very uniform bone uptake
Cold lesions early in AVN or rapidly destructive myeloma (photopenic)
Urine contamination mimics pelvic pathology — repeat with catheter
Bone islands (enostoses) cause mild focal uptake — correlate with CT
Soft tissue uptake: myositis ossificans, rhabdomyolysis, calcific metastases (breast, ovarian, mucinous)
Breast uptake in gynecomastia or tamoxifen therapy
Flare post-therapy — do not report as disease progression without clinical correlation

Three-phase bone scan differentiates osteomyelitis (all 3 phases +) from cellulitis (flow + pool + only, delayed negative)
Bone scan sensitivity ~95% for metastases but specificity low — correlate CT/MRI for solitary lesion
SPECT/CT is mandatory for spine, pelvis, and any equivocal focus
Tc-99m MDP also accumulates in myocardial infarction, pericardial calcification, amyloid (cardiac)
In children, symmetry of growth plates is key — asymmetric uptake at any physis is abnormal

NaF PET/CT (F-18 Sodium Fluoride)

F-18 NaF

Adult Dose

185–370 MBq (5–10 mCi)

Paediatric Dose

2.2 MBq/kg (min 37 MBq)

Physical T½

110 min (F-18)

Mechanism: NaF exchanges with hydroxyl groups in hydroxyapatite; faster bone kinetics than MDP; higher extraction (100% first pass vs 50% MDP)

Normal findings: Symmetric skeletal uptake; higher SUVmax than background soft tissue. Growth plates in children. Mild renal pelvis and bladder activity.

Hydration (500 mL before and after)
No specific dietary restriction (no glucose loading needed)
Void before scan
Delay if recent Tc-99m study (count rate interference)

0 min

IV injection of F-18 NaF

45–90 min

PET/CT acquisition: skull vertex to mid-thigh or whole body

Low-dose CT for attenuation correction and anatomic correlation

Optional

Dynamic early acquisition for perfusion assessment

Freq	Finding	Context	Key Features
Common	Bone metastases	Prostate, breast, lung, thyroid	Higher sensitivity than MDP bone scan · SUVmax quantification useful
Common	Degenerative disease	Spine, large joints	Periarticular · osteophyte uptake
Common	Fracture	Insufficiency, traumatic, stress	Focal linear intense · resolution over months
Classical	Paget's disease	Pelvis, spine, skull	Intense, expanded bone · very high SUVmax
Classical	Metabolic bone disease	Hyperparathyroidism, osteomalacia	Diffuse uptake increase · pseudofractures in osteomalacia
Rare	Primary bone tumour	Osteosarcoma, Ewing's	Intense focal with soft tissue extension
Rare	Superscan	Diffuse mets	Intense uniform skeletal uptake

Higher cost than MDP bone scan; not universally available
Bowel activity can mimic lumbosacral pathology on coronal images
No blood pool phase — cannot assess soft tissue vascularity
Higher radiation dose than MDP if whole-body acquisition

Superior sensitivity to planar bone scan and comparable to SPECT/CT MDP
Quantitative SUVmax enables response monitoring
Can be combined with FDG PET on same day (sequential protocol) for comprehensive oncology staging
Rapid scan time (45–90 min vs 3–4 h for MDP)

MAG3 / DTPA Renal Scintigraphy

Tc-99m MAG3

Adult Dose

185–370 MBq MAG3; 370 MBq DTPA

Paediatric Dose

3.7 MBq/kg MAG3 (min 18.5 MBq)

Physical T½

6 h (Tc-99m)

Mechanism: MAG3: tubular secretion (~80% first pass); DTPA: glomerular filtration (GFR measurement); MAG3 superior in poor renal function

Normal findings: Peak cortical activity 3–5 min; prompt washout post-Lasix (T½ <10 min); split renal function 45–55% each kidney; no urinary tract dilatation; symmetric curves

Hydrate well — 2 glasses water 30 min before; IV saline 10 mL/kg if paediatric
No caffeine 12–24 h (vasoactive effect on GFR)
Stop ACE-I / ARBs 3–5 days before CAPTOPRIL study (not routine)
Catheterize neonates/infants to avoid bladder effect on drainage
Furosemide protocol: F+0 (Lasix at injection), F-15 (Lasix 15 min before), F-20 (Lasix at 20 min after injection)

0 min

Patient supine; inject tracer IV; start dynamic acquisition

0–3 min

Blood flow phase: 2 s/frame

3–30 min

Functional phase: 30 s/frame; plot time-activity curves

15–20 min

Furosemide injection (F+0, F-15, or F-20 per protocol)

Post-Lasix

Continue acquisition 30 min post-Lasix

Optional

Post-micturition image to assess bladder reflux

Freq	Finding	Context	Key Features
Common	Obstruction (hydronephrosis)	UPJ, UVJ, ureter stricture	T½ >20 min post-Lasix; dilated pelvicalyceal system; flat/rising curve
Common	Impaired renal function	CKD, ATN, RAS	Reduced GFR; slow cortical transit; poor excretion; low differential function
Common	Vesicoureteral reflux	Children, recurrent UTI	Rising ureter curve on micturition; bladder to ureter/kidney reflux
Classical	Renovascular hypertension (RAS)	Renal artery stenosis	Captopril: worsening perfusion + function on affected side; RI rising
Classical	Acute tubular necrosis (ATN)	Post-transplant, ischaemia	Good perfusion (flow normal); poor function (uptake high, excretion nil) — 'reverse perfusion pattern'
Classical	Urine leak	Post-surgery, trauma	Focal tracer accumulation outside collecting system
Rare	Duplex kidney	Congenital anomaly	Two separate peaks/curves from single renal unit
Rare	Horseshoe kidney	Midline isthmus	Asymmetric position; isthmus uptake on anterior view
Rare	Ureterocele	Cobra-head filling defect	Photopenic focus within bladder

Dehydration causes apparent 'obstruction' — always hydrate well
Full bladder obstructs drainage — ensure voiding or catheterise
Poor renal function limits Lasix response — use F-15 protocol
Dilated non-obstructed system (resolved VUR) shows slow drainage without true obstruction
Split function unreliable if <20% differential — kidney may be non-functioning

MAG3 is preferred over DTPA in neonates, renal failure, single kidney (better signal)
F-15 protocol (Lasix 15 min BEFORE injection) reduces 'indeterminate' results by ensuring peak Lasix effect during excretion phase
Differential renal function: <40% on one side = significant impairment
Transplant kidney: anterior position; use anterior camera; immediate post-transplant ATN has good perfusion but poor function

DMSA Renal Cortical Scintigraphy

Tc-99m DMSA

Adult Dose

185 MBq

Paediatric Dose

1.85 MBq/kg (min 18.5 MBq)

Physical T½

6 h (Tc-99m)

Mechanism: 40–50% binds to proximal tubular cells; fixed cortical agent; images cortex directly; best agent for scarring and pyelonephritis

Normal findings: Uniform cortical uptake; smooth renal outline; symmetric bilateral uptake (40–60% split); normal column of Bertin = prominent medial cortical extension — do not mistake for mass

No specific preparation required
Scan at 2–4 h post-injection
SPECT acquisition mandatory for definitive scar assessment

0 min

IV injection Tc-99m DMSA

2–4 h

Posterior + posterior oblique views; SPECT/CT ideally

Optional

Anterior view for horseshoe or ectopic kidney

Freq	Finding	Context	Key Features
Common	Acute pyelonephritis	UTI, febrile, children	Focal photopenic area; acute oedema; resolves with treatment
Common	Renal scar	Post-infection, reflux nephropathy	Peripheral cortical defect; contour deformity; volume loss
Common	Renal mass (cyst/tumour)	RCC, simple cyst	Photopenic defect; no cortical uptake
Classical	Duplex kidney	Congenital	Two DMSA concentrating moieties; upper pole often poor function
Classical	Renal infarction	Vascular occlusion, vasculitis	Wedge-shaped photopenic defect; peripheral cortical location
Classical	Horseshoe kidney	Congenital	Medially positioned kidneys; isthmus visible on anterior view
Rare	Renal vein thrombosis	Hypercoagulable, dehydration	Enlarged kidney; globally reduced uptake
Rare	Dromedary hump	Normal variant	Focal bulge left lateral cortex opposite spleen — smooth; normal function

Column of Bertin mimics scar on planar — SPECT differentiates (normal cortical tissue, no defect)
Dromedary hump (left kidney) is normal variant — spleen impression
Acute oedema resolves; rescan 4–6 months to confirm scar vs acute pyelonephritis
Split function assessment less reliable than MAG3 for GFR measurement

Gold standard for renal scarring detection — superior to ultrasound and CT
In children with febrile UTI: acute DMSA detects pyelonephritis; delayed DMSA (3–6 months) confirms scar
VUR grade correlates poorly with DMSA scarring — DMSA is better predictor of long-term renal damage
Small photopenic defect at lower pole — always rule out VUR-related scar

Captopril Renography

Tc-99m MAG3 or Tc-99m DTPA

Adult Dose

185–370 MBq

Paediatric Dose

3.7 MBq/kg

Physical T½

6 h

Mechanism: ACE inhibition → reduces efferent arteriolar tone → drops GFR in RAS-affected kidney; functional effect detected on renogram curves

Normal findings: No significant change in renogram curves or split function post-captopril

Stop ACE inhibitors 3–5 days; ARBs 7 days
Stop NSAIDs 3 days
Hydrate well (2 glasses water 30 min pre)
Oral captopril 25–50 mg (weight-based) given 60 min before study
Monitor BP throughout — hypotension risk; have saline available

Day 1

Baseline renogram — MAG3/DTPA standard protocol

Day 2

Captopril renogram: captopril 60 min pre-injection; repeat identical protocol

Alternative

Single-day: captopril study only if pre-test probability high

Freq	Finding	Context	Key Features
Common	Renovascular hypertension (unilateral RAS)	Atherosclerosis, FMD	Post-captopril: peak delayed >11 min; cortical retention; split function worsens >10% on affected side
Common	Bilateral RAS	Atherosclerosis	Both kidneys worsen post-captopril; may see bilateral RI elevation
Classical	Fibromuscular dysplasia (FMD)	Young women	Mid/distal renal artery; unilateral captopril effect
Classical	Transplant renal artery stenosis	Post-transplant HTN	Anterior study; single kidney; captopril worsening
Rare	Renal artery dissection	Trauma, aortic dissection	Acute unilateral deterioration

Normal captopril scan does not exclude RAS — sensitivity 75–90% (anatomy not function)
False positive: dehydration, bilateral disease, renal failure (GFR <30)
False negative: mild RAS (<70% stenosis), bilateral equal disease
Hypotension post-captopril — monitor BP every 15 min; avoid in known bilateral RAS without BP support

Duplex US is first-line investigation; captopril renography reserved for equivocal cases or pre-revascularisation assessment
If pre-test probability high and scan positive → proceed to CTA/MRA → revascularisation
ACE-I-induced acute kidney injury post-revascularisation implies haemodynamically significant RAS

VUR Scintigraphy (Radionuclide Cystography)

Tc-99m pertechnetate

Adult Dose

37–74 MBq intravesical (direct)

Paediatric Dose

74 MBq (direct); weight-based MAG3 (indirect)

Physical T½

6 h

Mechanism: Direct: catheter instillation of tracer into bladder; continuous dynamic imaging during fill and void. Indirect: post-MAG3 renogram — tracer cleared to bladder, then void phase

Normal findings: No retrograde tracer in ureter or kidney during any phase

Catheterisation required for direct method
Informed consent for catheterisation in children
Indirect: performed as final phase of MAG3 scan; patient must be continent

Direct

Catheterize bladder; fill with saline + tracer until capacity (or discomfort); continuous 30 s/frame imaging during fill + void + post-void

Indirect

After MAG3 renogram; patient void; image continuously during void

Freq	Finding	Context	Key Features
Common	Grade I–II VUR	Children with UTI/febrile	Tracer fills ureter only (I) or pelvis (II) during void
Common	Grade III–V VUR	High-grade reflux	Marked dilatation of collecting system; intrarenal reflux (grade V)
Classical	Bilateral VUR	Both kidneys	Bilateral ureteric filling; may be asymmetric
Rare	Spontaneous fill-phase reflux	High-grade VUR	Reflux during bladder filling, not only voiding

Direct RNC most sensitive but catheter required — radiation dose very low
Indirect less sensitive for low-grade VUR but catheter-free
Cannot grade VUR anatomically as well as fluoroscopic VCUG — combine if exact grading needed
Bladder spasm during void can simulate reflux on dynamic images

Radiation dose 50–200× lower than fluoroscopic VCUG — preferred for follow-up studies
Direct RNC: detection threshold much lower than VCUG (any intravesical tracer entering ureter = VUR)
Paediatric VUR follow-up: use direct RNC to monitor resolution with lower radiation exposure

Scrotal Scintigraphy

Tc-99m pertechnetate

Adult Dose

370–555 MBq

Paediatric Dose

4 MBq/kg

Physical T½

6 h

Mechanism: Pertechnetate reflects blood flow; increased flow = hyperaemia (epididymo-orchitis); decreased flow = ischaemia (torsion)

Normal findings: Symmetric blood flow and parenchymal uptake bilaterally; equal photon density each testis

Urgent study — do not delay
Tape testes upward; shield penis
Flow study essential

0 min

Dynamic flow: 2 s/frame × 60 frames over scrotal region

5 min

Static images: anterior + bilateral markers

Markers

Lead markers on medial side of each testis for lateralisation

Freq	Finding	Context	Key Features
Common	Epididymo-orchitis	Sexually active males, UTI	Increased flow + increased uptake on affected side; 'halo' sign with central hypoperfusion = late torsion/abscess
Common	Testicular torsion	Pre-pubertal males, acute scrotum	Decreased/absent flow + photopenic area on affected side — SURGICAL EMERGENCY
Classical	Missed torsion (>24h)	Late presentation	'Halo sign': peripheral hyperaemia surrounding cold centre
Classical	Hydrocele	Any age	Photopenic rim around testis; testis normal
Classical	Varicocele	Young males	Increased flow left > right
Rare	Testicular tumour	Any age	Variable — often cold (necrosis) or normal flow
Rare	Torsion of appendix testis	Pre-pubertal	Focal increased uptake adjacent to testis

Ultrasound with Doppler is first-line and faster — scrotal scan used when US equivocal or unavailable
Any clinical suspicion of torsion = surgical exploration; do NOT delay surgery for scan
In missed torsion (>24h): paradoxical halo of hyperaemia around cold testis — do not mistake for orchitis

Classic torsion: absent flow + cold testis on static images
Classic epididymo-orchitis: hot testis + hot epididymis on both flow and static
Scrotal scan has high sensitivity/specificity in pre-Doppler era — still used in select cases
Bilateral torsion is rare but described — check both sides

Thyroid Scan + RAI Uptake

Tc-99m pertechnetate

Adult Dose

185 MBq Tc-99m; 7.4–14.8 MBq I-123; 370 kBq–1.85 MBq I-131 (diagnostic)

Paediatric Dose

Weight-based; I-123 preferred in children

Physical T½

6 h Tc-99m; 13.2 h I-123; 8 days I-131

Mechanism: Pertechnetate trapped by NaI symporter (not organified); iodine isotopes trapped AND organified — better correlation with function; uptake at 4h and 24h

Normal findings: Homogeneous symmetric thyroid lobes; isthmus visible; uptake 10–35% at 24h (I-123); Tc-99m scan shows trap pattern only

Stop thyroid medications: PTU/carbimazole 5–7 days; levothyroxine 4–6 weeks; amiodarone 3–6 months
Stop iodine-containing drugs: IV contrast 4–6 weeks; amiodarone 3–6 months
No iodised salt or seafood for 1–2 weeks
TSH stimulation: stop T4 4–6 weeks or give recombinant TSH if metastatic disease follow-up

Tc-99m

Inject; image at 20 min: anterior, obliques, markers over chin and sternal notch

I-123

Oral capsule; image at 4h and 24h (uptake); scan at 4h or 24h

Uptake

Neck and thigh counts at 4h and 24h; calculate %uptake: (neck-thigh/dose)×100

Freq	Finding	Context	Key Features
Common	Multinodular goitre	Middle-aged women	Patchy inhomogeneous uptake; multiple hot/cold nodules; enlarged gland
Common	Graves' disease	Young women; autoimmune	Diffuse homogeneous enlarged gland; elevated uptake >35%
Common	Toxic adenoma	Single hot nodule	Autonomous 'hot' nodule with suppressed surrounding tissue — benign; RAI curative
Common	Cold nodule	Cyst, malignancy, adenoma	Focal photopenia — 5–15% risk of malignancy; correlate with US + FNA
Classical	Hashimoto's thyroiditis	Autoimmune; hypothyroid	Patchy heterogeneous; normal or low uptake; anti-TPO positive
Classical	Subacute thyroiditis (De Quervain's)	Post-viral; painful	Very low/absent uptake — key to differentiate from Graves'
Classical	Ectopic thyroid	Lingual, sublingual, substernal	Uptake outside normal neck position; absent or reduced normal gland
Classical	Post-partum thyroiditis	Post-partum hyperthyroid	Low uptake thyrotoxicosis; recovery expected
Rare	Toxic multinodular goitre	Older patients	Multiple hot nodules; elevated uptake; normal or enlarged gland
Rare	Struma ovarii	Ovarian dermoid	Pelvic uptake on whole-body scan; low/absent neck uptake
Rare	Thyroid malignancy	Well-differentiated	Cold nodule; post-thyroidectomy whole-body I-131 scan for metastases

Tc-99m: trapping only — does not correlate with function as well as I-123
Recent iodine load suppresses uptake — always check history
'Hot' nodule on Tc-99m may be 'discordant' (cold on I-123) → risk of malignancy not excluded
Photopenic area behind sternum may be substernal goitre — get thoracic inlet/chest views
Uptake elevated in rebound hypothyroidism (post-medication stop) — interpret with TSH level

Low uptake + hyperthyroidism = thyroiditis or exogenous T4 or iodine excess
High uptake + hyperthyroidism = Graves' or toxic nodule → RAI therapy candidate
Cold nodule: always perform US + FNA — scan alone cannot exclude malignancy
Post-thyroidectomy I-131 whole-body scan: stimulated TSH >30 mIU/L (stop T4 or rhTSH); NaClO4 not needed with I-131

Parathyroid Scintigraphy (Sestamibi)

Tc-99m sestamibi

Adult Dose

740–925 MBq sestamibi

Paediatric Dose

Rarely performed in children

Physical T½

6 h

Mechanism: Sestamibi accumulates in mitochondria-rich cells; parathyroid adenoma retains tracer longer than thyroid (washout difference); SPECT/CT provides 3D localisation

Normal findings: Uniform washout of sestamibi from thyroid by 2 h; no residual focal activity

No specific dietary prep
SPECT/CT preferred — localises to mediastinum or ectopic adenoma
No withdrawal of calcium-lowering drugs

0 min

Inject sestamibi

15–30 min

Early images: thyroid + parathyroid uptake — anterior neck

2–3 h

Delayed images: thyroid washed out; adenoma retained — hot focus

Subtraction

Inject Tc-99m pertechnetate (thyroid only); subtract from sestamibi early images

SPECT/CT

3D localisation mandatory for operative planning

Freq	Finding	Context	Key Features
Common	Solitary parathyroid adenoma	80% of primary HPT	Focal hot focus at 2h; may be inferior pole thyroid, ectopic mediastinal, or retrooesophageal
Common	Multigland disease (hyperplasia)	Secondary/tertiary HPT; MEN	Multiple foci; 4-gland disease; poor sensitivity of scan
Classical	Ectopic parathyroid adenoma	Mediastinum, paraesophageal, intrathymic	Mediastinal focus on SPECT/CT — critical pre-operative finding
Classical	Double adenoma	5–10% of primary HPT	Two separate hot foci; important not to miss
Rare	Parathyroid carcinoma	Severe hypercalcaemia; large adenoma	Large intense focus; locally invasive on CT
Rare	Intrathyroidal adenoma	Within thyroid tissue	Focal hot area on subtraction; identified on CT

4-gland hyperplasia: scan sensitivity only 40–60% — surgical exploration still required
Multigland disease common in renal failure (secondary HPT) — scan may underestimate disease extent
Thyroid nodule mimics parathyroid adenoma on planar — SPECT/CT differentiates
Negative scan: does not exclude adenoma — consider 4D CT parathyroid or selective venous sampling

Sensitivity 80–90% for solitary adenoma; falls to 40–60% for multigland disease
SPECT/CT is essential — changes operative approach in 15–20% of cases (ectopic adenoma)
Combined sestamibi SPECT/CT + 4D CT = best pre-operative localisation
Post-failed surgery: 4D CT or selective venous sampling for PTH gradient essential

HIDA / Hepatobiliary Scintigraphy

Tc-99m DISIDA or Tc-99m Mebrofenin

Adult Dose

185–370 MBq

Paediatric Dose

1.85–3.7 MBq/kg

Physical T½

6 h

Mechanism: IDA agents undergo hepatocyte uptake and biliary excretion like bilirubin; image entire hepatobiliary system including gallbladder ejection fraction

Normal findings: Hepatic extraction fraction >90%; bile ducts visible 15–30 min; gallbladder fills by 60 min; bowel activity by 60 min; GBEF ≥35% (some centres ≥38%)

Fast 4–6 h (must have fasted gallbladder for CCK test)
NPO >24 h: give IV morphine 0.04 mg/kg to contract sphincter of Oddi — ensures GB filling
Avoid opioids 6 h before (can delay excretion)
Cholecystokinin (CCK/sincalide): for GBEF measurement — give after GB fills

0 min

IV injection

0–60 min

Dynamic anterior images; 1 min/frame

15 min

Hepatic extraction should occur; bile ducts should be visible

30–60 min

Gallbladder should fill

60 min

If no GB filling: give morphine 0.04 mg/kg over 3 min; continue 30 min

CCK phase

After GB fills: sincalide 0.02 μg/kg IV over 60 min; measure GBEF

4–24 h

Delayed views if no bowel activity initially

Freq	Finding	Context	Key Features
Common	Acute cholecystitis	Cystic duct obstruction	GB non-visualised at 4 h with morphine augmentation; 'rim sign' (pericholecystic hyperaemia)
Common	Chronic cholecystitis / biliary dyskinesia	Low GBEF	GB fills but GBEF <35%; reproduces patient's symptoms with CCK
Common	Common bile duct obstruction	Stone, stricture, cholangiocarcinoma	Dilated intrahepatic ducts; no bowel activity at 4–24 h; tracer pools in ducts
Classical	Biliary leak	Post-surgery, trauma	Tracer outside biliary tree; accumulates in abdomen/peritoneum
Classical	Sphincter of Oddi dysfunction	Post-cholecystectomy pain	Delayed drainage; dilated CBD; high time-to-peak biliary excretion
Classical	Biliary atresia (neonates)	Neonatal jaundice	No bowel activity at 24 h despite good hepatic extraction — key differentiator from neonatal hepatitis
Classical	Neonatal hepatitis	Neonatal jaundice	Poor hepatic extraction; eventual (delayed) bowel activity
Rare	Choledochal cyst	Young females	Photopenic mass with delayed filling then retention
Rare	Accessory hepatic duct	Surgical variant	Tracer leak from accessory duct post-cholecystectomy

GB visualised = acute cholecystitis EXCLUDED (>97% NPV)
GB non-visualised: could be chronic cholecystitis (if fasted <4h or fasted >24h); use morphine augmentation protocol
High bilirubin >5 mg/dL: Mebrofenin preferred over DISIDA (higher hepatocyte extraction)
False positive GBEF: if patient not adequately fasted; use CCK pre-treatment to empty GB then measure refilling

Rim sign (pericholecystic hepatic hyperaemia) = gangrenous cholecystitis; requires urgent surgery
GBEF <35% + reproduction of symptoms = biliary dyskinesia = cholecystectomy candidate
For neonatal jaundice: phenobarbital pretreatment (5 mg/kg/day × 5 days) increases biliary excretion; any bowel activity = atresia excluded
Liver extraction fraction can serve as functional hepatic reserve marker pre-hepatectomy

GI Bleeding Scintigraphy

Tc-99m labelled RBCs

Adult Dose

740–925 MBq

Paediatric Dose

9.25–11.1 MBq/kg

Physical T½

6 h

Mechanism: Labelled RBCs remain intravascular; extravasation at bleeding site detected as early focal accumulation that moves along bowel lumen on sequential images

Normal findings: Vascular pool activity only: heart, great vessels, liver, spleen, kidneys; bowel activity absent in early phase

No bowel prep required
In vitro labelling (UltraTag kit) preferred over in vivo — higher labelling efficiency >97%
Establish IV access
Continuous acquisition most sensitive — do not stop at 1h if bleeding suspected

0 min

IV injection labelled RBCs

0–90 min

Dynamic 1 min/frame × 90 min; immediately review for active bleed

If negative

Static images at 2, 4, 6, 18, 24 h; patient remains in department during early phase

Positive

Report site, movement pattern; proceed to CTA angiography or colonoscopy

Freq	Finding	Context	Key Features
Common	Active small bowel bleed	Obscure GI bleed; Crohn's	Focal activity appears in small bowel; moves aborally — jejunum/ileum pattern
Common	Colonic bleed	Diverticulosis, angiodysplasia, cancer	Focal colonic activity; moves orally and aborally — colonic haustral pattern
Classical	Meckel's diverticulum bleed	Young patients	Right lower quadrant; may show Meckel's uptake; confirm with Meckel's scan
Classical	Angiodysplasia	Elderly, cecum/ascending colon	Focal cecal/right colon; often episodic
Rare	Bleeding rate <0.1 mL/min	Occult bleed	Sensitivity limit; may miss very slow bleeds on early images — use delayed scans
Rare	Varices (gastric/oesophageal)	Cirrhosis portal HTN	Upper GI distribution; rarely needs RBC scan

Movement of tracer over time is key to localisation — single static images misleading
Penis/urine contamination mimics pelvic bowel bleed — shield penis; void before
Free pertechnetate from poor labelling = gastric mucosa + bladder activity — appears as 'bleed'
Bleeding must be active at time of scan — negative scan does not exclude GI bleed if bleeding stopped
Accessory spleen or genitalia uptake can mimic ectopic bleed

Sensitivity 0.1–0.5 mL/min (vs CTA 0.3–0.5 mL/min; colonoscopy requires >0.5 mL/min)
RBC scan guides colonoscopy/angiography to correct colonic segment — critical for emergency haemostasis
Continuous real-time imaging superior to intermittent static views for localisation
Positive scan → CTA → interventional radiology or surgical segmental resection

Meckel's Diverticulum Scan

Tc-99m pertechnetate

Adult Dose

185–370 MBq

Paediatric Dose

5.55 MBq/kg (min 37 MBq)

Physical T½

6 h

Mechanism: Pertechnetate is concentrated by mucin-secreting cells (gastric mucosa); ectopic gastric mucosa in Meckel's diverticulum accumulates tracer simultaneously with stomach

Normal findings: Gastric activity (stomach), bladder, and kidneys only; no ectopic focus

Fast 4 h minimum
Cimetidine pretreatment: 20 mg/kg/day × 2 days before scan — blocks secretion, increases mucosal retention (key for sensitivity)
Pentagastrin can be used to stimulate uptake (2 μg/kg SC 15 min before)
Glucagon to reduce bowel peristalsis (0.1 mg IV)
Empty bladder before scan

0 min

IV injection

0–30 min

Dynamic 1 min/frame anterior images including abdomen and pelvis

30 min

Spot views: anterior, posterior, right lateral; bladder shielded or patient voids

Freq	Finding	Context	Key Features
Common	Meckel's diverticulum with ectopic gastric mucosa	Young patients; painless rectal bleeding; right lower quadrant pain	Right lower quadrant focal activity appearing simultaneously with stomach — constant position; does not move with peristalsis
Classical	Meckel's without gastric mucosa	Asymptomatic or fibrous band	Scan negative — gastric mucosa must be present for detection
Rare	Ectopic gastric mucosa (non-Meckel's)	Duplication cysts, enteric cysts	Focal activity at other sites — Barrett's oesophagus; enteric duplication
Rare	False positive	Urinary tract, AVM, intussusception	Activity moves with peristalsis or corresponds to bladder/ureter on lateral view

Sensitivity 80–90% IF gastric mucosa present; only 60% of Meckel's have sufficient gastric mucosa
Cimetidine pretreatment is ESSENTIAL — improves sensitivity significantly
Bladder overlaps right lower quadrant — void before scan; use lateral view
Activity moves = bowel or ureter; activity fixed = Meckel's or ectopic mucosa
Negative scan does NOT exclude Meckel's — capsule endoscopy or surgical exploration may be needed

Classic presentation: painless PR bleed in child <2y → first investigation after clinical exam
'Rule of twos': 2% prevalence; 2 inches long; 2 feet from ileocecal valve; presents before age 2; 2 types of ectopic mucosa
Sensitivity highest with cimetidine + glucagon + pentagastrin triple preparation
Small bowel series may show filling defect but Meckel's scan is more specific for gastric mucosal content

Gastric Emptying Scintigraphy

Tc-99m sulphur colloid labelled eggs

Adult Dose

18.5 MBq Tc-99m per 120 kcal meal

Paediatric Dose

As adult — standardised meal required

Physical T½

6 h Tc-99m; 2.8 days In-111

Mechanism: Labelled solid meal tracks solid-phase gastric emptying; T½ and % retention measured; dual-isotope allows simultaneous solid + liquid assessment

Normal findings: % retention at 4h: <10% (solid meal — SNMMI standardised protocol). T½ emptying: 50–109 min. Liquid phase: T½ 10–20 min

NPO 4–6 h (6–12 h for diabetics — better baseline)
Stop prokinetics (metoclopramide, domperidone) 48 h; opioids 2 days; anticholinergics 2 days
Standardised meal: 2 large eggs (scrambled) + toast + water — 120 kcal; mix tracer in eggs before cooking
BSG/SNMMI protocol: images at 0, 1, 2, 4 hours post-meal

0 min

Patient eats standardised meal within 10 min; start timing

0, 1, 2, 4 h

Anterior + posterior images; 1 min static; geometric mean counts

Calculate

% retention = (counts at time T / counts at 0 min) × 100

Freq	Finding	Context	Key Features
Common	Gastroparesis	Diabetics, post-vagotomy, idiopathic, post-viral	% retention >10% at 4h (mild 10–15%; moderate 15–35%; severe >35%)
Common	Rapid gastric emptying (dumping syndrome)	Post-gastrectomy/fundoplication	T½ <30 min; rapid clearance; early dumping symptoms
Classical	Diabetic gastroparesis	Long-standing diabetes	Severe; >35% at 4h; bezoar formation; erratic glucose control
Classical	Post-surgical gastroparesis	Post-vagotomy, post-Nissen	Moderate; functional; may improve with time
Rare	Opioid-induced GI dysmotility	Chronic opioid use	Delayed T½; improvement with opioid reduction
Rare	Connective tissue disease	Scleroderma, SLE	Delayed or rapid depending on enteric neuropathy pattern

Hyperglycaemia delays gastric emptying — blood glucose must be <180 mg/dL before study; treat if higher
Non-standardised meal = non-reproducible results — must use validated protocol
Images at 4h only — inadequate to calculate T½ or category severity accurately
Opioids, anticholinergics must be stopped — check full medications list

4-hour protocol (SNMMI/ASNC consensus) is gold standard — do not use 2h only protocols
Solid phase more clinically relevant than liquid; liquid emptying is usually preserved until late disease
% retention at 4h >10% = gastroparesis; 2–3% of normal controls have borderline results
Wireless motility capsule (Smartpill) complements or replaces scintigraphy in equivocal cases

Salivary Gland Scintigraphy

Tc-99m pertechnetate

Adult Dose

185 MBq

Paediatric Dose

2 MBq/kg

Physical T½

6 h

Mechanism: Pertechnetate is concentrated by serous acini of salivary glands (as iodide analogue); lemon juice/citric acid stimulates secretion — functional test

Normal findings: Symmetric uptake parotid and submandibular glands bilaterally; symmetric stimulated secretion (decreased uptake after lemon = secretion intact); thyroid and gastric mucosa also visible

No specific preparation
Lemon juice/swabs for stimulation phase

0 min

Inject pertechnetate; supine; camera over face/neck

0–30 min

Dynamic 1 min/frame — uptake phase

20 min

Lemon juice × 3 cycles — observe secretion

30 min

Static images: AP + lateral

Freq	Finding	Context	Key Features
Common	Sjögren's syndrome	Dry eyes + dry mouth; autoimmune	Reduced uptake bilaterally; impaired or absent secretion post-stimulation
Common	Unilateral parotid mass	Parotid tumour, Warthin's, pleomorphic adenoma	Focal photopenic defect (most tumours cold); Warthin's may be warm/hot
Classical	Warthin's tumour (papillary cystadenoma lymphomatosum)	Older males; bilateral 15%	'Hot' nodule on pertechnetate scan — one of very few hot salivary masses; bilateral in 15%
Classical	Post-radiation sialadenitis	Post-head/neck RT	Globally reduced uptake and secretion; bilateral if bilateral RT
Classical	Sialolithiasis	Stone in duct	Delay in secretion post-stimulation on affected side; asymmetric
Rare	Sarcoidosis	Bilateral parotid enlargement	Bilateral diffusely reduced uptake; correlate with bilateral hilar lymphadenopathy on CXR

Most parotid masses are cold — cannot distinguish benign from malignant
Warthin's is the exception — 'hot' on scan; useful characteristic
Thyroid visible as potential confounding activity in lower neck

Sjögren's diagnosis: reduced uptake + absent stimulated secretion; quantitative analysis useful
Warthin's tumour: bilateral warm nodules in older male = classic presentation
Combined US + scintigraphy most useful diagnostic approach for salivary gland pathology

Myocardial Perfusion Imaging (MPI) SPECT

Tc-99m sestamibi or Tc-99m tetrofosmin

Adult Dose

Stress: 925–1110 MBq Tc-99m; Rest: 296–370 MBq Tc-99m

Paediatric Dose

Rarely performed

Physical T½

6 h Tc-99m; 73 h Tl-201

Mechanism: Tc-99m agents: passive diffusion into myocytes proportional to flow; fixed in mitochondria; minimal redistribution (unlike Tl-201). Tl-201: K+ analogue; redistribution 3–4h post-injection reflects viability

Normal findings: Homogeneous myocardial uptake all segments; EF ≥50%; normal wall motion; no perfusion defect

Fast 4–6 h before stress test
Stop beta-blockers 48 h (if testing for ischaemia, not viability)
Caffeine products 12–24 h (if vasodilator stress)
IV access; 12-lead ECG monitoring; resuscitation available
Stress types: exercise (Bruce protocol) or pharmacological: adenosine/regadenoson (vasodilator) or dobutamine (contraindication to vasodilator)

Day 1 or same-day

1-day protocol: rest low-dose → stress high-dose; 2-day: stress Day1 / rest Day2

Stress phase

Inject at peak stress (85% max HR or max tolerated workload); image 30–60 min post

Rest phase

Separate injection 3–4 h later or next day; image 30–60 min post

SPECT/CT

Gated SPECT: wall motion + EF + perfusion

Calcium score and/or CT coronary angiography optional

Freq	Finding	Context	Key Features
Common	Fixed defect (scar/infarct)	Previous MI; CTO	Perfusion defect present on BOTH stress and rest — no change (scar)
Common	Reversible defect (ischaemia)	CAD; significant stenosis	Defect on stress; normalises on rest — classic ischaemia pattern
Common	Partially reversible defect	Mixed scar + viable	Partial normalisation at rest — mixed territory
Classical	Transient ischaemic dilatation (TID)	Severe multivessel disease; LMS disease	LV cavity larger on stress than rest images — high-risk finding
Classical	Increased lung uptake	LV failure during stress; severe ischaemia	Increased Tl-201 or sestamibi in lungs on stress — high risk
Classical	Right ventricular uptake	RV hypertension; severe LV disease	RV prominence on stress images
Rare	Balanced ischaemia	Severe 3-vessel or LMS disease	'Normal' appearing scan but globally reduced uptake; EF drops on stress; TID present
Rare	Coronary artery anomaly	Young athlete with chest pain	Normal variant anatomy; may show ischaemia
Rare	Microvascular disease (syndrome X)	Women; typical chest pain; normal coronaries	Patchy or diffuse perfusion abnormality; normal coronaries on angiography

Artefacts: breast/diaphragm attenuation (inferior wall in males; anterior in females) — use prone imaging or CT AC
Balanced ischaemia may appear 'normal' — look for TID and lung uptake
Image quality degraded by obesity or large breasts — Rb-82 PET superior
Normal MPI does not exclude non-obstructive coronary disease

Gated SPECT provides both perfusion AND function — EF drop from rest to stress = high risk
SSS (Summed Stress Score) ≥13 = severe ischaemia → revascularisation likely beneficial
Duke Treadmill Score integrates ST changes, symptoms, and exercise time for risk stratification
PET MPI (Rb-82 or N-13 ammonia) superior to SPECT: higher resolution, absolute flow quantification, lower radiation dose

MUGA / Radionuclide Ventriculography (RNV)

Tc-99m RBCs

Adult Dose

740–925 MBq

Paediatric Dose

10 MBq/kg

Physical T½

6 h

Mechanism: Labelled RBCs fill cardiac chambers; ECG-gated acquisition over 16–32 frames per cardiac cycle; measures LVEF, RVEF, wall motion

Normal findings: LVEF ≥50%; RVEF ≥35%; normal wall motion (septal, anterior, inferior, lateral, apical); peak filling rate; time to peak filling

In vitro RBC labelling (UltraTag kit) or modified in vivo method
ECG electrodes — gating required
Rest study (no stress)
No specific dietary restrictions

0 min

Inject labelled RBCs

10 min

ECG-gated dynamic acquisition: 30–45° LAO view (best septal separation); anterior + left lateral

Frames

16 frames/cycle standard; 32 for diastolic analysis

Calculate

LVEF = (end-diastolic counts - end-systolic counts)/end-diastolic counts × 100

Freq	Finding	Context	Key Features
Common	Reduced LVEF	Cardiomyopathy, post-chemotherapy cardiotoxicity	LVEF <50% — anthracycline toxicity threshold: >10% drop or absolute <50%
Common	Regional wall motion abnormality	Coronary artery disease, MI	Hypokinesis, akinesis, dyskinesis in specific territories
Classical	Dilated cardiomyopathy	Idiopathic, alcohol, viral	Globally reduced LVEF; dilated LV; diffuse hypokinesis
Classical	Anthracycline cardiotoxicity monitoring	Oncology — doxorubicin, epirubicin	Serial MUGA most sensitive and reproducible for EF drop; stop/modify chemotherapy if drop >10% or EF <50%
Classical	LV aneurysm	Post-STEMI	Dyskinetic bulge inferior or apical — opposite phase to normal contraction on phase image
Rare	RVEF reduction	PE, right heart failure, ARVC	RVEF <35% with right ventricular wall motion abnormality

Irregular rhythm (AF) degrades gating accuracy — average cycle length approach; report rhythm
EF highly dependent on loading conditions and heart rate — compare under same conditions
MUGA underestimates EF compared with echo — use same modality for serial monitoring (reproducibility ±3–5%)
Obesity and large body habitus: image quality degraded

MUGA is gold standard for LVEF reproducibility in chemotherapy monitoring — CV ±3–5% vs echo ±10%
SNMMI guideline: Anthracycline monitoring — baseline MUGA before cumulative dose 300 mg/m²; repeat at 400, 500 mg/m²
Phase analysis maps regional timing of contraction — useful for LBBB, pre-excitation, CRT assessment
Concurrent assessment of LV volumes, peak filling rate (diastolic function parameter)

V/Q Lung Scan

Ventilation: Tc-99m DTPA aerosol or Tc-99m Technegas

Adult Dose

Perfusion: 185–370 MBq MAA; Ventilation: 40 MBq Technegas or 40 MBq DTPA aerosol

Paediatric Dose

Perfusion: 1.85–3.7 MBq/kg (min 40 MBq); Ventilation reduced proportionally

Physical T½

6 h Tc-99m; MAA particles ~3 h biological

Mechanism: MAA particles (10–40 μm) impact in pulmonary capillaries proportional to blood flow; aerosol/Technegas distributes to ventilated alveoli; mismatch = PE until proven otherwise

Normal findings: Homogeneous perfusion and ventilation all lobes; matched pattern; no segmental perfusion defects

CXR within 24 h (essential for PIOPED interpretation)
Recent CTPA if available — compare
Pregnancy: safe if CTPA contraindicated; reduce dose
Perfusion scan done first if ventilation unavailable
Note: 200,000–700,000 MAA particles injected — no significant haemodynamic effect

Ventilation

Technegas: inhale 6–10 breaths; 8 views (ant, post, 2 laterals, 4 obliques)

Perfusion

MAA injection supine; 8 matched views immediately

PIOPED II

Interpret ventilation and perfusion together with CXR per PIOPED II criteria

Freq	Finding	Context	Key Features
Common	Pulmonary embolism	DVT, malignancy, immobility	≥1 segmental V/Q mismatch; ventilation normal, perfusion absent
Common	Chronic PE	Unresolved acute PE	Multiple bilateral mismatches; pulmonary hypertension pattern
Common	Matched defects	Pneumonia, COPD, tumour	V/Q match — low probability for PE; indicates intrinsic lung disease
Classical	Stripe sign	COPD with bullae vs PE	Rim of perfused lung at periphery — against PE (unlikely to have peripheral perfusion in PE)
Classical	PIOPED II High probability	Major PE	≥2 large segmental mismatches; high clinical specificity 97%
Classical	PIOPED II Low probability	COPD + matched defects	<1 small mismatch segment; low PE probability
Rare	Saddle embolus	Massive PE	Bilateral large central perfusion defects; preserved peripheral ventilation
Rare	Pulmonary AVMs	Hereditary haemorrhagic telangiectasia	Perfusion without ventilation — REVERSED mismatch
Rare	Vasculitis (Takayasu's)	Large vessel vasculitis	Unilateral absent perfusion; preserved ventilation

'Intermediate/indeterminate probability' on PIOPED II still common — requires clinical pre-test probability (Wells score)
Triple match (opacity on CXR + matched V/Q defect) does not exclude PE — consider CTPA
MAA injection with free flow — avoid poor injection technique (clot or bolus effect)
Cardiac shunt: paradoxical embolism (renal, cerebral, splenic uptake of MAA) — right-to-left shunt

PISAPED criteria (alternative): any perfusion defect not matching CXR opacity = PE (simplified approach)
V/Q SPECT/CT (SPECT-CT): emerging gold standard — higher sensitivity/specificity than planar; replaces PIOPED criteria
Pregnancy: V/Q preferred over CTPA — lower breast dose; equivalent fetal dose
Normal perfusion scan: PE effectively excluded (NPV ~99%)

Brain Perfusion SPECT

Tc-99m HMPAO

Adult Dose

555–1110 MBq

Paediatric Dose

5.55–7.4 MBq/kg

Physical T½

6 h

Mechanism: Lipophilic agents cross blood-brain barrier; ECD cleaved by esterases and retained; HMPAO converted to hydrophilic form; distribution fixed at injection — 'brain snapshot' at time of injection

Normal findings: Symmetric cortical perfusion; relative hypoperfusion cerebellum compared with cortex; grey > white matter; thalami and basal ganglia prominent

Quiet room; dim light; eyes open/closed per protocol
IV cannula inserted 10–15 min before injection (acclimatisation)
Inject tracer then patient waits 15 min before scanning (quietude maintained)
Sedation only if unavoidable (use benzodiazepine — minimal effect on perfusion)
ICTAL injection: inject at onset of seizure (clinician must be present); image within 1–4 h

0 min

Inject HMPAO/ECD in quiet room

15–30 min

Transfer to scanner

SPECT/CT

High-resolution SPECT; CT for AC and anatomical correlation

Views

Transaxial, coronal, sagittal reconstruction; compare with MRI

Freq	Finding	Context	Key Features
Common	Alzheimer's dementia	Bilateral temporoparietal hypoperfusion (posterior predominant)	Precuneus + posterior cingulate early; frontal lobes later; MMSE correlates
Common	Vascular dementia	Multi-infarct pattern	Scattered cortical + subcortical photopenic areas; follows vascular territories
Common	Frontal lobe dementia (FTD)	Bilateral frontal ± temporal hypoperfusion	'Frontal lobe' pattern; personality changes; disinhibition
Classical	Epilepsy — ictal SPECT	Seizure focus localisation	ICTAL: hyperperfusion at seizure focus; INTERICTAL: hypoperfusion
Classical	Epilepsy — interictal SPECT	Pre-surgical evaluation	Relative hypoperfusion at epileptogenic zone; SISCOM (subtraction ictal-interictal SPECT) most useful
Classical	Lewy body dementia (DLB)	Occipital hypoperfusion; DaTscan abnormal	Posterior visual cortex reduction early; DaTscan differentiates from Alzheimer's
Classical	Transient ischaemic attack (TIA)	Acute — perfusion asymmetry	Focal cortical hypoperfusion in ischaemic territory; may be normal MRI
Rare	Crossed cerebellar diaschisis	Supratentorial lesion (infarct/tumour)	Contralateral cerebellar hypoperfusion — neural network disconnection phenomenon
Rare	PRES (posterior reversible encephalopathy syndrome)	Hypertensive emergency, eclampsia	Posterior occipitoparietal hyperperfusion — vasogenic oedema

SPECT perfusion reflects perfusion at TIME OF INJECTION — not at scan time (HMPAO/ECD fixed)
Ictal injection must be within 30 s of seizure onset — requires experienced bedside team
Patient motion degrades SPECT — use HMPAO (faster fixation) for agitated patients
Crossed cerebellar diaschisis is a secondary effect — do not report as primary cerebellar disease

SISCOM (Subtraction Ictal-Interictal SPECT Coregistered with MRI) improves surgical planning sensitivity 80–90%
Alzheimer's pattern: bilateral temporoparietal; FTD pattern: frontal; DLB: occipital + DaTscan
Perfusion SPECT combined with FDG PET and MRI = most comprehensive dementia workup
Brain death: absent cerebral perfusion bilaterally on HMPAO SPECT = confirmatory test

DaTscan / DAT SPECT (Dopamine Transporter Imaging)

I-123 Ioflupane

Adult Dose

185 MBq I-123

Paediatric Dose

Not approved for children

Physical T½

13.2 h I-123

Mechanism: Ioflupane binds to dopamine transporter (DAT) on presynaptic dopaminergic neurons in striatum; loss of nigrostriatal neurons → reduced striatal binding

Normal findings: Symmetric 'comma' or 'D-shaped' bilateral striatal (caudate + putamen) uptake; putamen uptake ≥ caudate

Thyroid block MANDATORY: potassium iodide (KI) 100 mg or potassium perchlorate 400 mg given 60 min before injection
Stop drugs that affect DAT for 5–7 days: cocaine, amphetamine, methylphenidate
Serotonin reuptake inhibitors, buproprion can interfere — discuss with neurologist
Antipsychotics (D2 blockers) do not affect DAT scan

0 min

Thyroid block then IV injection of I-123 ioflupane

3–6 h

SPECT acquisition: 40 min; reconstruct transaxial slices at level of basal ganglia

Report

Visual analysis + SBR (specific binding ratio) calculation; compare with age-matched normal database

Freq	Finding	Context	Key Features
Common	Parkinson's disease	Rest tremor, rigidity, bradykinesia	Asymmetric reduction putamen > caudate; 'full stop' shape (caudate only); contralateral to clinically affected side
Common	DLB (Lewy body dementia)	Dementia + parkinsonism + hallucinations	Bilateral striatal reduction; similar pattern to PD but bilateral early
Classical	MSA (multiple system atrophy)	Autonomic failure + parkinsonism	Bilateral putamen reduction; clinical features differentiate from PD
Classical	PSP (progressive supranuclear palsy)	Vertical gaze palsy + falls	Bilateral symmetrical striatal reduction; clinical differentiation required
Rare	Normal DaTscan	Essential tremor, drug-induced parkinsonism, DIP	NORMAL scan in essential tremor = rules out nigrostriatal disease; reassurance
Rare	SWEDD (scans without evidence of dopaminergic deficit)	Clinical PD features but normal DAT	Normal scan; alternative diagnosis — dystonia, psychogenic, essential tremor

DaTscan differentiates presynaptic (PD, DLB, MSA, PSP) from postsynaptic (drug-induced, ET) parkinsonism
Drug-induced parkinsonism (DIP) from antipsychotics — DAT normal
Essential tremor — DAT normal; very useful to reassure patient
DAT reduction does not differentiate PD from MSA, PSP, DLB — clinical assessment essential
Thyroid block MUST be given — iodine-123 will damage thyroid if not blocked

Asymmetry index: >20% asymmetry in putamen = highly suggestive of PD
Progressive reduction in serial DaTscans correlates with disease progression
DaTscan is NOT a diagnostic substitute for clinical assessment — it confirms presynaptic dopaminergic deficit
FP-CIT SPECT (DaTscan) sensitivity 78% / specificity 90% for Parkinson's-spectrum disorders

Radionuclide Cisternography (In-111 DTPA)

In-111 DTPA

Adult Dose

18.5–37 MBq intrathecal

Paediatric Dose

3.7–7.4 MBq intrathecal

Physical T½

2.8 days (In-111)

Mechanism: In-111 DTPA injected intrathecally (lumbar puncture); follows CSF flow craniocaudally; normal: reaches basal cisterns 2–4 h, sylvian fissures 4–6 h, convexity 12–24 h; absorbed over convexity by 24–48 h; ABSENT lateral ventricle entry in normal

Normal findings: 2–4 h: basal cisterns (prepontine, perimedullary); 4–6 h: sylvian fissures; 24 h: convexity activity + absent lateral ventricles; 48–72 h: cleared

Informed consent for lumbar puncture
Neurological team performs LP; nuclear medicine provides radiopharmaceutical
Patient supine post-LP 30–60 min to allow tracer to migrate
No anticoagulation at time of LP
Trefhine/butterfly needle 22G; inject slowly with CSF mixing

Lumbar puncture; verify free flow; inject In-111 DTPA in 1 mL CSF

2–4 h

First images: posterior spine + base of skull; basal cisterns should be visible

4–6 h

Second images: sylvian fissure filling expected

24 h

Convexity filling expected; lateral ventricles SHOULD NOT be visible

48 h

Clearance from convexity; minimal residual

72 h

Essentially cleared; persistent activity = abnormal

CSF leak

Additional views head, nose, ears per clinical question; cotton pledgets nasal/ear placed before injection; count pledgets at 4–24h

Freq	Finding	Context	Key Features
Common	Normal pressure hydrocephalus (NPH)	Triad: gait, cognition, incontinence	Ventricular reflux at 24–48 h persisting; absent/delayed convexity filling — 'holdup' pattern; positive VP shunt response predictor
Common	CSF leak (rhinorrhoea/otorrhoea)	Post-trauma, post-surgery, spontaneous	Tracer detected in nasal/ear pledgets; >3:1 pledget:serum ratio = positive; direct visualisation of leak site on planar/SPECT
Classical	Communicating hydrocephalus	Post-meningitis, SAH, malignant meningitis	Ventricular entry of tracer; slow convexity clearance; enlarged ventricles
Classical	Obstructive hydrocephalus	Aqueductal stenosis, mass	Tracer does not reach ventricles or fills asymmetrically; obstruction level identified
Classical	Spinal CSF leak (intracranial hypotension)	Spontaneous; orthostatic headache	Absent or very slow cranial migration; tracer pools in lumbar region; subdural hygromas on MRI
Rare	CSF shunt patency	VP/VA shunt evaluation	Tracer injected at shunt reservoir; patent = flow into peritoneum/atrium; blocked = no distal flow
Rare	Arachnoiditis	Post-infection/surgery	Irregular CSF flow; 'loculation' pattern; asymmetric distribution

LP must be confirmed free-flowing CSF before injection — do not inject if bloody or blocked
In-111 long half-life allows imaging up to 72h — plan accordingly
Patient must avoid bending/stooping 24h after LP (headache/leak prevention)
Pledget-based CSF leak: meticulous technique — no contamination by blood, saliva; count immediately when removed
Normal variant: mild transient ventricular entry at 24h may occur — persistence to 48h is significant
Spinal CSF leak: reduced cranial activity may be subtle; compare with expected progression times

NPH cisternogram: ventricular reflux + delayed convexity filling predicts positive shunting outcome (positive predictive value 75–85%)
CSF leak localisation: SPECT/CT superior to planar for precise anatomical site (cribriform plate, tegmen tympani, skull base)
Intracranial hypotension (spinal leak): tracer stays lumbar; urgent MRI spine with contrast (epidural enhancement, venous engorgement, subdural hygroma)
In-111 DTPA: no concerns re: radionuclide toxicity at these doses; DTPA is biologically inert
Always collect pledgets in pre-weighed tubes; count promptly and calculate pledget:serum activity ratio

CSF Shunt Patency Study

Tc-99m DTPA

Adult Dose

18.5–37 MBq into shunt reservoir

Paediatric Dose

3.7–7.4 MBq

Physical T½

6 h

Mechanism: Tc-99m DTPA injected directly into shunt reservoir by neurosurgeon/radiologist under sterile conditions; flow into peritoneal/atrial end assessed by imaging

Normal findings: Prompt flow from reservoir to distal end; peritoneal spread (VP) or cardiac entry (VA); no proximal backflow into ventricle

Neurosurgical team must tap shunt reservoir — sterile technique
Confirm shunt type (VP, VA, VPL) before scan
Have neurosurgeon available — do not perform without their knowledge

0 min

Reservoir tap; inject tracer; release; begin imaging

0–30 min

Sequential images head + abdomen; confirm flow direction

30 min

Distal end: peritoneal spread (VP) or right atrium/SVC (VA)

Freq	Finding	Context	Key Features
Common	Distal shunt obstruction	Fibrin, debris, peritoneal loculation	Tracer stalls at distal end; no peritoneal spread; proximal reflux
Common	Proximal shunt obstruction	Choroid plexus occlusion; catheter blockage	No flow from reservoir; manual pumping resistance
Classical	Partial obstruction	Fibrin, protein clot	Slow flow; partial distal spread
Rare	Abdominal pseudocyst	Peritoneal scarring	Tracer confined to loculated abdominal cyst; no free spread

Must be sterile procedure — CSF infection risk
Flow assessment requires real-time imaging — not single static images
Bilateral VP shunts: image both sides

Combined with manometric measurement of reservoir pressure for functional assessment
Positive shunt tap (CSF aspirated) confirms proximal patency before tracer injection

FDG PET/CT (F-18 Fluorodeoxyglucose)

F-18 FDG

Adult Dose

370–555 MBq (3.7–5.5 MBq/kg, weight-based, BSA-based)

Paediatric Dose

3.7–5.18 MBq/kg (min 26 MBq; max 444 MBq)

Physical T½

110 min (F-18)

Mechanism: FDG = glucose analogue; phosphorylated by hexokinase → FDG-6-phosphate (trapped); no further metabolism; accumulates in proportion to glucose utilisation; cancer, infection, inflammation all hypermetabolic

Normal findings: Physiological uptake: brain cortex, heart (variable), liver, spleen, GI tract (variable), kidneys/bladder, blood pool, tonsils (mild), bone marrow (diffuse mild)

Fast 4–6 h (water allowed)
Blood glucose <11 mmol/L (200 mg/dL) — measure before injection
Diabetics: insulin protocols per local policy; do not inject if glucose >200 mg/dL
Rest quietly 30–60 min post-injection (uptake phase); avoid talking (reduces laryngeal/masseteric uptake)
Warm room or warm blanket (reduces BAT uptake)
Void before scan; catheter if pelvic disease
No vigorous exercise 24 h before (muscle uptake)

0 min

IV injection of FDG; rest 45–60 min

45–60 min

PET/CT: skull base to thighs standard; vertex to toes if bone/lower extremity disease; vertex = brain tumour/dementia

Low-dose or diagnostic CT; IV contrast if diagnostic staging CT required

Optional

Delayed 2–3 h images for difficult cases (liver mets, head/neck)

Brain

Dedicated brain PET if dementia/epilepsy workup: vertex-only, high-resolution reconstruction

Freq	Finding	Context	Key Features
Common	Lymphoma (Hodgkin's and high-grade NHL)	Staging and response assessment	Avid nodal + extranodal uptake; Deauville score for response
Common	Lung cancer (NSCLC)	Primary + nodal + distant staging	Primary FDG-avid; mediastinal nodes; adrenal; bone; brain (poor FDG)
Common	Colorectal cancer	Staging, recurrence, CEA rise	Hepatic metastases; peritoneal disease; pelvic recurrence
Common	Oesophageal cancer	Staging; response	Primary + nodal; peritoneal + liver mets
Common	Breast cancer	High grade/triple negative; recurrence	Avidity variable; HER2+ and TNBC most avid
Classical	Melanoma	Staging; recurrence	Highly FDG-avid primary and metastases; brain mets less visible
Classical	Infection/inflammation	Fever of unknown origin; vasculitis	FDG hot in infected/inflamed tissue; aortitis; spondylodiscitis; endocarditis
Classical	Sarcoidosis	Hilar + mediastinal + extrapulmonary	FDG hot in granulomas; complements Ga-67 scan; cardiac sarcoid
Classical	Brain glioma (high grade)	GBM, anaplastic astrocytoma	FDG avid high-grade tumours vs low-grade; differentiate recurrence vs radiation necrosis
Rare	Low-grade malignancy (low FDG)	Prostate, mucinous CA, lobular breast, HCC	May be false negative — use PSMA/DOTATATE/specific tracers
Rare	Brown adipose tissue (BAT)	Young patients, cold exposure	Bilateral symmetric cervical/supraclavicular FDG uptake — normal; avoid by warming
Rare	Treatment-induced inflammation	Post-RT, post-surgery, colitis	Hot areas at treatment sites — must interpret with clinical timeline

Hyperglycaemia: reduces tumour FDG uptake (competitive inhibition) — glucose must be <200 mg/dL
Brain metastases: FDG PET poor sensitivity due to high normal brain uptake — use MRI
Prostate, mucinous tumours, lobular breast: low FDG avidity — false negative
BAT (brown fat): bilateral symmetric cervical/supraclavicular — use warming protocol
Thymic rebound post-chemotherapy (young patients): diffuse thymic FDG uptake — correlate CT shape

Deauville score (lymphoma response): 1–2 = complete metabolic response; 4–5 = residual disease; score 3 = institution-specific
PERCIST (SULpeak): ≥30% reduction = partial metabolic response; complete = normalisation to liver background
FDG PET/CT superior to CT alone for nodal staging in lung, oesophageal, head/neck cancers
For solitary pulmonary nodule: FDG-avid → high risk; non-avid → follow (but false negative in ground glass, carcinoid, <1cm lesions)

PSMA PET/CT (Prostate-Specific Membrane Antigen)

Ga-68 PSMA-11 or F-18 DCFPyL

Adult Dose

150–250 MBq Ga-68; 333 MBq F-18

Paediatric Dose

Not standard

Physical T½

68 min Ga-68; 110 min F-18

Mechanism: PSMA = type II transmembrane glycoprotein overexpressed 100–1000× on prostate cancer cells; radioligand binds PSMA → allows whole-body staging of prostate cancer at very low PSA levels

Normal findings: Physiological: salivary glands (major), lacrimal glands, liver, spleen, kidneys, small bowel, duodenum; ganglia (celiac, stellate); penis/testes (mild)

Fast 4–6 h (water permitted)
No testosterone-lowering therapy hold required
Adequate hydration; void before scan
Imaging at 60 min post-injection

0 min

IV injection

60 min

PET/CT: skull vertex to thighs; include skull for Ga-68; include feet if bone mets suspected

Delayed

90–120 min images for pelvic lymph nodes if equivocal — improves contrast due to bladder clearance

Freq	Finding	Context	Key Features
Common	Prostate cancer — primary staging	High-risk PCa: Gleason ≥7, PSA ≥10	Primary prostate intense uptake; pelvic nodes; seminal vesicle invasion
Common	Biochemical recurrence post-prostatectomy	Rising PSA >0.2 ng/mL	Detects recurrence at PSA 0.2–0.5 ng/mL — superior to conventional imaging
Common	Bone metastases	Any PSA level	Bone lesions FDG-cold but PSMA-hot; sclerotic on CT
Classical	Pelvic lymph node metastases	Obturator, external/internal iliac, presacral	Small nodes (<8mm) may still be PSMA-positive — size criteria inadequate
Classical	Para-aortic/retroperitoneal nodes	Spread beyond pelvis	Upstages treatment intent; changes to systemic therapy
Classical	Oligometastatic disease	1–5 lesions	Identifies candidates for metastasis-directed therapy (SABR) or salvage lymph node dissection
Rare	Ganglia mimics	Celiac, stellate, inferior mesenteric ganglia	Intense PSMA uptake; round; correlate with CT — normal neural tissue; do NOT report as nodes
Rare	PSMA-negative disease	Neuroendocrine differentiation, CRPC	Absence of PSMA expression — use FDG PET instead; NE-PCa is FDG-avid PSMA-poor

Ganglia (celiac, inferior mesenteric, stellate, paravertebral) are intensely PSMA-positive — very common false positive; correlate CT anatomy
Bladder activity obscures pelvic nodes — delayed imaging at 90 min helps
PSMA expression varies — poorly differentiated PCa may lose PSMA; concurrent FDG for aggressive/NE disease
Bone marrow signal can be diffusely increased with G-CSF treatment — mimic of diffuse mets

OSPREY, CONDOR, ProPSMA trials confirm superiority over bone scan + CT for staging and recurrence
Lutetium-177 PSMA-617 therapy (Pluvicto): PSMA PET is required diagnostic gateway
SUVmax >3 × liver background = PSMA-positive lesion (guideline threshold)
If PSMA negative but high clinical suspicion: check FDG PET for dedifferentiated/NE component

Ga-68 DOTATATE PET/CT (SRS)

Ga-68 DOTATATE

Adult Dose

100–200 MBq

Paediatric Dose

2 MBq/kg (min 25 MBq)

Physical T½

68 min Ga-68

Mechanism: DOTATATE binds somatostatin receptor subtype 2 (SSTR2); NETs overexpress SSTR2; high-affinity binding allows detection of very small NET lesions; superior to In-111 Octreoscan

Normal findings: Physiological: pituitary, salivary glands, thyroid, spleen (intense), adrenal glands, kidneys, liver (mild), uncinate process pancreas, bowel (mild); uterus in menstrual phase

Stop somatostatin analogues (octreotide, lanreotide) 4–6 weeks before (long-acting) or 24h (short-acting) — competes with DOTATATE binding
Fast 4–6 h; water permitted
Void before scan

0 min

IV injection

40–90 min

PET/CT: vertex to thigh; extend to knees/feet if bone disease

Delayed

Optional 2–3 h images for better liver contrast if hepatic disease

Freq	Finding	Context	Key Features
Common	Gastroenteropancreatic NETs	GI carcinoids, pancreatic NETs	Highly avid primary + nodes + liver mets + bone mets; grade 1/2 most avid
Common	Carcinoid tumour	Ileal origin most common	Primary ileal primary often small; mesenteric mass with desmoplastic reaction; liver mets
Common	Pancreatic NET	Non-functioning (incidental) or functional	Intense focal pancreatic uptake; assess for liver mets; correlate with MRI
Classical	Phaeochromocytoma/paraganglioma	SDHA/B/C/D mutations; extra-adrenal	Adrenal or paraganglionic site; very high SUVmax; SDH-mutated: DOTATATE >>> MIBG
Classical	Medullary thyroid cancer	High calcitonin; recurrence	Neck/node recurrence; distant mets; DOTATATE variable — try if MIBG/FDG negative
Classical	Meningioma	Intracranial; SSTR2-high	Intense DOTATATE uptake; useful for radiation planning; pitfall with brain lesion characterisation
Rare	Grade 3 NET / NEC	Poorly differentiated; high Ki-67	May lose SSTR2 → DOTATATE negative; use FDG PET (high grade usually FDG-avid DOTATATE-poor)
Rare	Breast cancer (some)	ER+ tumours express SSTR	Moderate uptake; investigational

Spleen intense uptake — do not mistake for adrenal or lateral left-sided lesion
Uncinate process pancreas: physiological uptake — compare with pancreatic body/tail
Meningioma: intracranial DOTATATE-avid lesion — may be primary finding on staging scan; correlate MRI
Grade 3 NEC: DOTATATE may be negative; always combine with FDG for high-grade disease
Long-acting SSA (octreotide LAR): must be withheld 6 weeks — receptor competition

DOTATATE > Octreoscan by sensitivity (2–5× more lesions detected) — now standard of care
'Flip-flop' phenomenon: grade 1/2 NET: DOTATATE+/FDG−; grade 3 NEC: DOTATATE−/FDG+
Lu-177 DOTATATE therapy (Lutathera): DOTATATE PET required — must show adequate SSTR2 expression (≥ spleen)
Somatostatin receptor score (Krenning): liver > spleen = very high expression = best PRRT response

MIBG Scintigraphy (I-123 / I-131)

I-123 MIBG

Adult Dose

I-123: 370–400 MBq; I-131 diagnostic: 37–74 MBq

Paediatric Dose

I-123: 5.18 MBq/kg (min 37 MBq)

Physical T½

13.2 h I-123; 8 days I-131

Mechanism: MIBG (metaiodobenzylguanidine) = guanethidine analogue; taken up by catecholamine-secreting cells via noradrenaline transporter; accumulates in adrenergic tissue and tumours derived from neural crest

Normal findings: Physiological: salivary glands, liver, spleen, myocardium (I-123), adrenals (mild), lungs (mild), bladder; bowel (variable)

Thyroid block ESSENTIAL: KI 1–2 mg/kg (min 130 mg) daily from 24 h before until 3 days after I-123; 7 days for I-131
Stop medications affecting MIBG uptake for appropriate duration: tricyclics, cocaine, labetalol, calcium-channel blockers, reserpine (see full list)
Antihypertensive management if phaeochromocytoma — inform anaesthesia team

I-123

Inject; image at 24 h (planar WB); SPECT/CT at 24 h of lesion site; additional 48 h if needed

I-131

Image at 24, 48, 72, 120 h

Views

Anterior + posterior whole body; SPECT/CT of any lesion area

Freq	Finding	Context	Key Features
Common	Phaeochromocytoma	Hypertensive crises, sweating, palpitations	Adrenal (90%) or extra-adrenal (10%); intense focal uptake; SPECT/CT for localisation
Common	Neuroblastoma (paediatric)	Abdominal mass; children <5 years	Intense primary + metastatic uptake; bones, liver, nodes; Curie score for burden
Common	Paraganglioma	Extra-adrenal; head/neck/chest/pelvis	Focal uptake at para-aortic, carotid body, glomus sites
Classical	Carcinoid / NET (MIBG-positive subtype)	Foregut/midgut carcinoids	MIBG uptake variable; DOTATATE generally superior for NET
Classical	Medullary thyroid cancer	Post-thyroidectomy; high calcitonin	Variable MIBG avidity; useful if DOTATATE/FDG negative
Rare	Merkel cell carcinoma	Skin; neuroendocrine	Variable MIBG uptake
Rare	Cardiac MIBG (for heart failure)	Cardiac sympathetic innervation	Reduced cardiac MIBG = poor sympathetic innervation; predictor of SCD in CHF; 123I-MIBG heart-to-mediastinum ratio (HMR) used

Medications causing false-negative MIBG: labetalol, tricyclics, calcium channel blockers, cocaine, reserpine — MUST STOP
Thyroid block failure: I-123 uptake in thyroid — check for thyroid activity
Myocardial uptake of I-123 MIBG is normal and prominent — do not mistake for cardiac tumour
Extra-adrenal phaeochromocytoma: carefully review organ of Zuckerkandl, bladder wall, mediastinum

I-123 preferred over I-131 for staging: higher image quality, lower radiation dose, 24h protocol
In neuroblastoma: MIBG is most sensitive agent (90%); DOTATATE superior for MIBG-negative NB
SDH-mutated paraganglioma: DOTATATE > MIBG — check genetics
Cardiac I-123 MIBG (AdreView): HMR <1.6 = high risk of arrhythmic death in CHF; ICD implantation decision

OctreoScan / In-111 Pentetreotide

In-111 DTPA-octreotide

Adult Dose

222 MBq

Paediatric Dose

3.7 MBq/kg

Physical T½

2.8 days In-111

Mechanism: Somatostatin analogue; binds SSTR2,5; accumulates in NET and other SSTR-expressing tumours; now largely superseded by Ga-68 DOTATATE PET

Normal findings: Liver, spleen, kidneys, bladder, pituitary (faint), normal adrenal glands; bowel variable

Stop SSA 4 weeks (long-acting); 24h (short-acting)
Laxatives 12–24 h before imaging (bowel activity prominent)
No specific dietary restriction

0 min

IV injection

Early images: WB planar; SPECT/CT lesion site

24h

Standard imaging: WB planar + SPECT/CT

48h

Delayed if bowel activity interfering

Freq	Finding	Context	Key Features
Common	Gastroenteropancreatic NETs	All grades G1/2	Focal uptake primary + metastases; lower sensitivity than DOTATATE
Classical	Pituitary adenoma	GH-secreting, TSH-secreting	Supra-physiological pituitary uptake
Rare	Small cell lung cancer	SSTR2 expression variable	Focal pulmonary uptake

In-111 pentetreotide largely replaced by Ga-68 DOTATATE PET where available
Bowel activity interferes with abdominal lesion detection at 24h — use laxatives and delayed 48h images
Spleen uptake intense — perisplenic lesion may be obscured

Where Ga-68 DOTATATE unavailable, In-111 OctreoScan remains valid alternative
Sensitivity for pancreatic NETs 50–70% (DOTATATE: 80–90%)
SSTR2 expression required — grade 3 NECs often negative

Lymphoscintigraphy / Sentinel Node

Tc-99m sulphur colloid

Adult Dose

37–74 MBq peritumoral injection

Paediatric Dose

Proportionally reduced

Physical T½

6 h

Mechanism: Colloidal particles drain via lymphatics to first-draining (sentinel) lymph node; identification with gamma probe in theatre guides targeted biopsy/excision

Normal findings: Prompt lymphatic drainage to regional sentinel node; may see multiple SLNs

Injection by surgeon/interventional radiologist under US guidance or clinical palpation
Image acquisition 30–120 min post-injection
Patient goes directly from nuclear medicine to operating theatre — same-day protocol standard

0 min

Peritumoral/intradermal injection of filtered Tc-99m colloid

30–120 min

Dynamic and static images; mark SLN on skin with felt tip; provide map to surgeon

Theatre

Gamma probe intraoperatively; blue dye (patent blue/isosulphan) simultaneously for visual confirmation

SPECT/CT

Mandatory if unexpected drainage pattern (e.g., interval nodes, in-transit)

Post-excision

Ex vivo counting of excised node to confirm sentinel

Freq	Finding	Context	Key Features
Common	Breast cancer SLN	Standard of care	Axillary SLN; internal mammary or supraclavicular in medial tumours
Common	Melanoma SLN	Standard of care	Drainage pattern variable; head/neck melanoma may drain to parotid, occipital, cervical nodes
Classical	Failed mapping	Obesity, prior axillary surgery, large tracer volume	No drainage seen — proceed to axillary dissection
Classical	Internal mammary drainage	Medial breast tumour	SLN in internal mammary chain — important but often skipped surgically
Rare	In-transit nodes	Interval nodes between primary and regional basin	SPECT/CT identifies unexpected in-transit or deep nodes

Injection technique critical — must be peritumoral or intradermal
Shine-through from injection site can mask nearby SLN — use shielding block
Blue dye allergy (patent blue): rare but severe anaphylaxis possible — have adrenaline ready
SPECT/CT essential for unusual drainage patterns (melanoma head/neck)

Combined radiocolloid + blue dye: SLN identification rate >95%
False negative SLN biopsy ~5–8% — depends on tumour location, technique, and learning curve
ICG (indocyanine green) fluorescence increasingly used as third agent
Hybrid tracer (99mTc-labelled albumin-ICG) allows preoperative scintigraphy + intraoperative fluorescence

WBC Scan (Radiolabelled Leucocytes)

In-111 oxine WBC

Adult Dose

In-111: 18.5 MBq labelled WBCs; Tc-99m HMPAO: 185–370 MBq

Paediatric Dose

In-111: 3.7–7.4 MBq; Tc-99m proportionally reduced

Physical T½

2.8 days In-111; 6 h Tc-99m

Mechanism: WBCs (predominantly neutrophils) labelled ex vivo; infused back; migrate to sites of infection/inflammation by normal leucocyte trafficking; 60 mL blood required for labelling; 2–3 h procedure

Normal findings: In-111 24h: liver, spleen, bone marrow (normal distribution); some bowel at 24h acceptable. Tc-99m HMPAO 4h: liver, spleen, marrow; gallbladder activity; bowel by 4h (renders abdominal WBC unreliable)

40–60 mL blood withdrawn into ACD (acid citrate dextrose) anticoagulation
WBC isolation and labelling — 2–3 h procedure
Reinfusion of labelled cells
In-111: image at 4h and 24h; Tc-99m HMPAO: image 1h and 4h (NOT for bowel — bowel excretion)

Blood draw

Venepuncture; label WBCs over 2–3h; reinfuse

In-111: 4h

Early images to localise GI bleed or acute foci

In-111: 24h

Delayed: better target-to-background; confirm persistence of foci

Tc-99m: 1h

Acute foci; excellent for orthopaedic prosthesis infection — combine with Tc-99m sulphur colloid bone marrow scan

Freq	Finding	Context	Key Features
Common	Prosthetic joint infection	Post-arthroplasty pain, raised CRP	Focally increased WBC activity at prosthesis site beyond bone marrow distribution; compare with Tc-99m sulphur colloid
Common	Osteomyelitis	Acute bone infection	Increased WBC activity at site; 3-phase bone scan usually also positive
Common	Diabetic foot infection	Soft tissue + bone	Focal plantar/digital uptake; extent assessment for amputation level
Classical	Inflammatory bowel disease (IBD)	Active Crohn's/UC	In-111 WBC shows bowel wall activity in proportion to disease activity; extent mapping
Classical	Fever of unknown origin (FUO)	After conventional work-up negative	Localises occult infection; abscesses; endocarditis; vascular graft infection
Classical	Vascular graft infection	Post-aortic surgery; infected aortic graft	Intense WBC uptake along graft; requires CT correlation
Rare	Pulmonary sequestration / atelectasis	Post-operative lung collapse	Physiological increased WBC — false positive; correlate CXR/CT

Tc-99m HMPAO WBC: NOT for abdominal infection — bowel excretion at 4h gives false positives
In-111: long acquisition time (24h delayed); better for abdominal/bowel disease
Prosthetic infection: compare with Tc-99m sulphur colloid bone marrow scan — normal marrow distribution at prosthesis is benign; focal WBC beyond marrow = infection
False negative: high-grade WBC (>15,000/mm³) in sepsis — too many unlabelled cells dilute the labelled fraction
Steroid therapy reduces WBC migration — lower sensitivity

Dual-isotope WBC (In-111) + Tc-99m sulphur colloid: gold standard for hip/knee prosthesis infection; sensitivity 85%, specificity 95%
In-111 WBC for bowel disease: extent correlates with endoscopic grade; guides therapy
Spinal osteomyelitis: WBC scan often FALSE NEGATIVE (indolent infection, vertebral vascularity); use Ga-67 or FDG PET instead
FDG PET increasingly replacing WBC scan for many indications (faster, no labelling, better resolution)

Gallium-67 Scan

Gallium-67 citrate

Adult Dose

185–370 MBq

Paediatric Dose

2.04 MBq/kg (min 37 MBq)

Physical T½

78 h Ga-67

Mechanism: Ga-67 behaves like Fe3+ (ferric iron); binds transferrin → lactoferrin in areas of infection; directly taken up by tumour cells; multi-energy gamma emitter (93, 184, 296, 388 keV)

Normal findings: Liver (intense), spleen, bone marrow, lacrimal glands, salivary glands, nasopharynx; bowel (variable — requires laxatives); breast (lactating); kidneys (24h only)

Bowel prep 24h before imaging (bowel activity prominent)
Stop iron supplements 4 weeks (competitive binding)
Laxatives before each imaging session

0 min

IV injection Ga-67 citrate

24h

Initial images: may show blood pool; tumour sites

48h

Standard images: WB planar; SPECT/CT lesion site

72h

Delayed: best contrast; bowel interference minimum

96h+

Optional delayed if bowel confusion persists

Freq	Finding	Context	Key Features
Common	Lymphoma (active)	Hodgkin's, high-grade NHL	Nodal and extranodal uptake; largely superseded by FDG PET
Common	Sarcoidosis	Bilateral hilar adenopathy; pulmonary infiltrate	Classic patterns: 'panda sign' (bilateral lacrimal + parotid) + 'lambda sign' (bilateral hilar + right paratracheal) — highly specific
Common	Hepatocellular carcinoma (HCC)	Cirrhosis; AFP elevated	Avid Ga-67 uptake in HCC — differentiates from benign hepatic lesions
Classical	Fever of unknown origin	After blood cultures, CT, etc. negative	Identifies infection sites: endocarditis, abscesses, osteomyelitis, pyelonephritis
Classical	Opportunistic infections in HIV	PCP pneumonia, disseminated MAI	Diffuse pulmonary uptake; abdominal nodes
Classical	Vertebral osteomyelitis/discitis	Spondylodiscitis	Hot at disc-vertebral junction; superior to WBC scan for spine
Rare	Primary hepatic lymphoma	Rare lymphoma	Avid hepatic uptake

Bowel activity major limitation — laxatives and delayed images mandatory
Multi-day protocol (48–72h) is inconvenient
Largely replaced by FDG PET/CT for oncology and infection/inflammation — Ga-67 used where PET unavailable
False positive: recent surgery, radiation therapy sites
Renal activity normal at 24h — persists longer in renal disease

Panda sign (lacrimal + parotid) + Lambda sign (bilateral hilar + right paratracheal) = essentially pathognomonic for sarcoidosis
HCC: Ga-67 avid; FNH: Ga-67 negative or equal to liver — helps differentiate HCC from FNH in cirrhotic liver
Vertebral osteomyelitis: Ga-67 > In-111 WBC — use Ga-67 or FDG for spine infection
Ga-67 still useful where FDG PET unavailable (resource-limited settings; PET contraindicated)

PIOPED II Criteria — V/Q Lung Scan

Probability Classification

PIOPED II (2006) — combine with clinical pre-test probability (Wells score) for final PE likelihood. V/Q SPECT/CT increasingly preferred over planar PIOPED II criteria.

Planar V/Q — PIOPED II Categories

Category	Criteria	PE Prevalence
High Probability	≥2 large segmental mismatches (perfusion defect with normal ventilation), OR ≥2 moderate + 1 large mismatch, OR ≥4 moderate mismatches	~85–90%
Intermediate (Indeterminate)	Findings that do not fit high or low categories; 1 moderate mismatch; difficult to categorise	~20–40%
Low Probability	Non-segmental defects; matched V/Q defects with no CXR abnormality; 1 small segmental mismatch; any perfusion defect smaller than CXR abnormality	~15–20%
Very Low Probability	≤3 small segmental mismatches; non-segmental, non-perfusion defects only	~5–10%
Normal	Perfusion scan completely normal	~0–2%

Defect Size Definitions

Size	% of Segment
Large	>75% of a pulmonary segment
Moderate	25–75% of a segment
Small	<25% of a segment

Triple Match Rule

Opacity on CXR + ventilation defect + perfusion defect in same segment = "triple match." Does NOT exclude PE — only lowers probability category. Consider CTPA if clinical suspicion remains high.

V/Q SPECT Criteria (EANM/SNMMI)

Any wedge-shaped perfusion defect (≥1 segment or ≥2 subsegments) with normal ventilation = PE. Sensitivity 96%, specificity 97%. Reduces indeterminate rate from ~20% (planar) to <3%. V/Q SPECT now preferred over planar.

Cisternogram Normal Progression & Pathological Patterns

In-111 DTPA

Normal CSF flow: lumbar injection → basal cisterns (2–4h) → sylvian fissures (4–6h) → convexity (12–24h) → clearance (24–48h). Lateral ventricles should NEVER be visualised in a normal study.

Normal Progression Timetable

Time Post-Injection	Expected Location of Tracer	Significance if Absent
2–4 h	Basal cisterns (prepontine, interpeduncular, perimedullary cisterns, sylvian base)	Obstruction at basal level; check LP injection
4–6 h	Sylvian fissures bilaterally; interhemispheric fissure beginning	Subdural or subarachnoid space obstruction
12 h	Convexity reaching vertex; interhemispheric activity	Delayed convexity = communicating hydrocephalus / NPH pattern
24 h	Convexity well-established; NO lateral ventricular activity	Ventricular reflux at 24h = NPH (if symptoms); pathological
48 h	Decreasing convexity; essentially cleared	Persistent activity = impaired CSF absorption
72 h	Nearly complete clearance	Persistent activity = severely impaired absorption or obstruction

Pathological Patterns

Pattern	Key Features	Likely Diagnosis
Type A — NPH	Ventricular reflux at 24h + absent/delayed convexity filling	Normal pressure hydrocephalus (NPH) — responds to VP shunt
Type B — Communicating Hydrocephalus	Ventricular entry + slow convexity; usually clears by 72h	Post-SAH/meningitis communicating hydrocephalus
Type C — Arachnoid Granulation Obstruction	Stalled convexity; activity pools over convexity; fails to reach sagittal sinus	Absorptive defect; post-SAH; malignant meningitis
CSF Leak	Tracer in nasal pledgets; pledget:serum ratio >3:1 at 4h; direct visualisation of leak on SPECT/CT	CSF rhinorrhoea / otorrhoea
Intracranial Hypotension	Minimal cranial migration; tracer pools in lumbar region; very slow ascent	Spinal CSF leak (spontaneous or post-LP)
Loculation	Irregular distribution; asymmetric collections	Post-meningitis arachnoiditis; loculated CSF spaces

Pledget Technique — CSF Leak Localisation

Site	Pledget Placement	Positive Threshold
Anterior rhinorrhoea	Middle meatus, inferior meatus, nasopharynx	Pledget:serum activity ratio >3:1 at 2–4h
Posterior rhinorrhoea	Nasopharynx, sphenoethmoidal recess	Ratio >3:1; nasal endoscopy + SPECT/CT for site
Otorrhoea	Ear canal (both ears)	Ratio >3:1 on affected side

Radiopharmaceutical Dose Reference

Adult + Paediatric

Adult doses below are standard ranges. Paediatric doses follow EANM paediatric dosage card (weight-based). Minimum doses apply to ensure adequate image quality.

Adult Doses

Study	Agent	Adult Dose (MBq)	Route
Bone Scan	Tc-99m MDP	740–925	IV
NaF PET	F-18 NaF	185–370	IV
MAG3 Renal	Tc-99m MAG3	185–370	IV
DTPA Renal	Tc-99m DTPA	370	IV
DMSA Cortical	Tc-99m DMSA	185	IV
Thyroid Scan	Tc-99m pertechnetate	185	IV
Thyroid Scan	I-123	7.4–14.8	Oral
Parathyroid	Tc-99m sestamibi	740–925	IV
HIDA	Tc-99m mebrofenin	185–370	IV
GI Bleed	Tc-99m RBCs	740–925	IV
Meckel's	Tc-99m pertechnetate	185–370	IV
Gastric Emptying	Tc-99m S-colloid in food	18.5 (in meal)	Oral
MPI SPECT (stress)	Tc-99m sestamibi	925–1110	IV
MPI SPECT (rest)	Tc-99m sestamibi	296–370	IV
MUGA	Tc-99m RBCs	740–925	IV
V/Q Perfusion	Tc-99m MAA	185–370	IV
V/Q Ventilation	Tc-99m Technegas	40 (inhaled)	Inhaled
Brain Perfusion	Tc-99m HMPAO	555–1110	IV
DaTscan	I-123 ioflupane	185	IV
Cisternogram	In-111 DTPA	18.5–37	Intrathecal
FDG PET	F-18 FDG	370–555	IV
PSMA PET (Ga-68)	Ga-68 PSMA-11	150–250	IV
DOTATATE PET	Ga-68 DOTATATE	100–200	IV
MIBG (diagnostic)	I-123 MIBG	370–400	IV
OctreoScan	In-111 pentetreotide	222	IV
WBC Scan	In-111 WBC	18.5	IV
Gallium-67	Ga-67 citrate	185–370	IV
Salivary	Tc-99m pertechnetate	185	IV
Scrotal	Tc-99m pertechnetate	370–555	IV
Lymphoscintigraphy	Tc-99m nanocolloid	37–74	Peritumoral

Paediatric Dosing Principles (EANM)

Agent	Dose/kg	Minimum	Maximum
Tc-99m MDP	9.3 MBq/kg	37 MBq	740 MBq
Tc-99m MAG3	3.7 MBq/kg	18.5 MBq	185 MBq
Tc-99m DMSA	1.85 MBq/kg	18.5 MBq	185 MBq
Tc-99m HMPAO	5.55–7.4 MBq/kg	100 MBq	500 MBq
F-18 FDG	3.7–5.18 MBq/kg	26 MBq	444 MBq
Ga-68 DOTATATE	2 MBq/kg	25 MBq	200 MBq
I-123 MIBG	5.18 MBq/kg	37 MBq	400 MBq
In-111 DTPA (cisternogram)	3.7–7.4 MBq total	3.7 MBq	37 MBq

Renal Scintigraphy Reference Tables

MAG3 · DMSA · Captopril

Diuretic Renography — T½ Interpretation

T½ Post-Furosemide	Interpretation	Action
<10 min	Normal drainage — obstruction excluded	No further action
10–20 min	Equivocal — indeterminate result	Repeat with optimised hydration; F-15 protocol; MR urography
>20 min	Obstruction present	Urological review; consider retrograde pyelogram; surgical planning
Rising curve	Severe obstruction — no response to Lasix	Urgent urological referral

Split Renal Function Interpretation

Differential Function	Interpretation	Clinical Implication
45–55% each kidney	Normal, symmetric function	No significant unilateral impairment
40–45% on one side	Mild reduction	Monitor; treat underlying cause
30–40%	Moderate reduction	Significant — review for obstruction, RAS, scarring
<30%	Severe reduction	Severely impaired; consider total function; nephrectomy decision
<10–15%	Near non-functioning kidney	Non-contributer; nephrectomy threshold

Captopril Renography — Positive Criteria

Parameter	Positive for RAS
Time to peak activity (Tmax)	Post-captopril Tmax >11 min on affected side, OR increase >2 min vs baseline
20-min/peak ratio (20-min retention)	>0.30 post-captopril (increased cortical retention)
Differential function change	Drop >10% in affected kidney post-captopril
Curve morphology	Post-captopril curve: plateau or rising vs baseline normal washout

Furosemide Protocols Compared

Protocol	Timing	Advantage	When to Use
F+0	Lasix at same time as tracer injection	Simple; single injection	Standard adult; good renal function
F-15	Lasix 15 min BEFORE tracer	Peak Lasix effect during excretion phase; reduces indeterminate results	Preferred for paediatric; marginally impaired function
F+20	Lasix at 20 min post-tracer	Allows assessment of spontaneous drainage before Lasix	Assessing baseline drainage pattern

Gastric Emptying Scintigraphy — Normal Values

SNMMI/ASNC Consensus Protocol

Standardised 4-hour solid-phase protocol (2 scrambled eggs + toast, 120 kcal, Tc-99m sulphur colloid labelled). All values are for solid-phase meal. Liquid phase T½ 10–20 min (independently assessed if dual-isotope protocol).

Normal Retention Values (% activity remaining)

Time Point	Normal Upper Limit (% Retention)	Interpretation if Exceeded
0 min (baseline)	100% (by definition)	—
1 hour	<90%	Delayed if >90%
2 hours	<60%	Delayed if >60%
4 hours	<10% (primary endpoint)	Gastroparesis if >10% at 4h

Severity Classification at 4 Hours

% Retention at 4h	Severity	Clinical Notes
0–9%	Normal	No gastroparesis
10–15%	Mild gastroparesis	Diet modification; review medications
15–35%	Moderate gastroparesis	Medical therapy (prokinetics); dietitian referral
>35%	Severe gastroparesis	Hospitalisation risk; consider enteral/parenteral nutrition; specialist referral

Rapid Gastric Emptying (Dumping)

Criterion	Value
T½ solid meal	<30 min (normal 50–109 min)
1h retention	<30% (suggests >70% emptied in 1h)

Pre-study Requirements

Parameter	Requirement
Blood glucose	<180 mg/dL (10 mmol/L) — treat hyperglycaemia before study
Fasting	4h minimum (6–12h for diabetics)
Opioids stopped	48–72h
Prokinetics stopped	48h (metoclopramide, domperidone, erythromycin)
Anticholinergics stopped	48h

PERCIST & RECIST — PET Response Criteria

Oncology Response Assessment

PERCIST 1.0 (PET Response Criteria in Solid Tumours)

Measure SULpeak (SUV normalised to lean body mass) in the most active lesion (highest SULpeak). Compare same lesion pre- and post-treatment.

Response Category	PERCIST Criterion
Complete Metabolic Response (CMR)	Complete resolution of FDG uptake to <1.5× mean liver SUL; no new lesions
Partial Metabolic Response (PMR)	≥30% decrease in SULpeak of target lesion; no new lesions
Stable Metabolic Disease (SMD)	Neither CMR/PMR nor PMD — change <30% decrease or <30% increase
Progressive Metabolic Disease (PMD)	≥30% increase in SULpeak OR new FDG-avid lesion

Deauville Score (Lymphoma Response — FDG PET)

Score	Uptake Relative to Reference	Interpretation
1	No uptake above background	Complete metabolic response
2	Uptake ≤ mediastinal blood pool	Complete metabolic response
3	Uptake > mediastinal but ≤ liver	Likely CMR (institution-dependent — some treat as complete)
4	Uptake moderately > liver	Partial response — residual disease
5	Markedly > liver or new lesions	Progressive/no response
X	New areas of uptake unlikely lymphoma	Evaluate separately

RECIST 1.1 (CT-based — for comparison)

Response	Criterion
Complete Response (CR)	Disappearance of all target lesions; nodes <10mm short axis
Partial Response (PR)	≥30% decrease sum longest diameter (SLD) of target lesions
Stable Disease (SD)	Neither PR nor PD
Progressive Disease (PD)	≥20% increase in SLD; or new lesions; or unequivocal progression non-target lesions

Typical Tracer Background Reference Values

Structure	Typical SUVmax Range	Used as Reference in
Liver	2.0–3.5	Deauville (lymphoma); PSMA (ganglion threshold)
Mediastinal blood pool	1.5–2.5	Deauville score 2 threshold
Brain cortex	8–15	Normal — masks small cortical mets
Bone marrow (diffuse)	1.5–2.5	Baseline; elevated post-G-CSF

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