PET-CT Indications
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Direct answer
Positron emission tomography combined with CT (PET-CT) uses fluorine-18 fluorodeoxyglucose (FDG), a glucose analogue trapped in metabolically active cells, to image glucose metabolism fused with CT anatomy in a single examination. Its principal indications are oncological — characterising indeterminate solitary pulmonary nodules, staging and response assessment of lymphoma, melanoma and many solid tumours, detecting recurrence with rising tumour markers, and differentiating radiation necrosis from recurrent brain tumour — plus selected infection and inflammation imaging and, with FDG or amyloid tracers, dementia and epilepsy evaluation. False positives from physiological uptake, infection and inflammation, and false negatives in hyperglycaemia, slow-growing or small tumours are the key pitfalls NEET-PG expects.
What you must remember
- Principle: F-18 FDG is transported like glucose and phosphorylated by hexokinase but not further metabolised, so it accumulates intracellularly in proportion to glucose use; F-18 half-life is about 110 minutes.
- PET detects the two 511 keV photons from positron annihilation; CT fusion provides anatomical correlation and attenuation correction in one visit.
- Patient preparation: fast typically four to six hours, blood glucose controlled (elevated glucose reduces tumour uptake), physical inactivity before injection to minimise muscle uptake; diabetic protocols adjust insulin timing.
- High-yield oncology uses: solitary pulmonary nodule characterisation; staging and restaging of Hodgkin and non-Hodgkin lymphoma (replaced gallium-67); melanoma and head-neck cancer staging; unknown primary with cervical nodal metastasis; rising tumour markers with negative conventional imaging; glioma recurrence versus radiation necrosis.
- Lower or variable utility: prostate carcinoma (FDG-avidity poor; PSMA PET is preferred in current practice), mucinous and low-grade gastrointestinal tumours, and renal cell carcinoma detection within the urinary tracer background.
- Non-oncological uses: fever of unknown origin and prosthetic or vascular graft infection evaluation, sarcoidosis activity, epilepsy focus localisation (FDG interictal hypometabolism) and amyloid PET in dementia assessment.
- Pitfalls: physiological uptake in brain, heart, bowel, urinary tract and brown fat; false positives from tuberculosis, other granulomatous disease and post-chemotherapy thymic or marrow rebound; false negatives from hyperglycaemia, tiny lesions below resolution and indolent histology.
- Reporting pairs uptake intensity (standardised uptake value) with CT morphology — the SUV is semiquantitative, not absolute proof of malignancy.
Common confusion
The predictable mistake is treating FDG uptake as synonymous with cancer — tuberculosis, sarcoidosis and healing fractures are FDG-avid, a serious issue in India where TB mimics lymphoma on PET. The second error is forgetting hyperglycaemia: competing glucose drives FDG out, causing false negatives, hence the fasting and glucose-control protocol. Finally, remember PET-CT is a problem-solving and staging tool; it does not replace biopsy for histology, and its resolution limits miss subcentimetre disease.
Exam-focused takeaway
Expect the FDG principle (glucose analogue, trapped after phosphorylation), the F-18 half-life (about 110 minutes), and indication matching — lymphoma staging, unknown primary, radiation necrosis versus recurrence. Pitfall questions contrast TB granulomas and malignancy uptake, and glucose loading effects. Distinguish PET-CT from bone scan (metabolic versus osteoblastic) and know PSMA has superseded FDG for prostate cancer.
Frequently asked questions
What is FDG and how does it work?
Fluorine-18 fluorodeoxyglucose, a glucose analogue transported into cells and phosphorylated by hexokinase without further metabolism, so it remains trapped in proportion to glucose utilisation, making hypermetabolic tumours bright on PET.
Which tumours are best evaluated by FDG PET-CT?
Lymphoma, melanoma, lung cancer, head and neck cancers and most aggressive solid tumours for staging, response and recurrence. FDG is unreliable for prostate and low-grade mucinous tumours, where PSMA or conventional imaging is preferred.
Why must patients fast before FDG PET?
Fasting lowers insulin and blood glucose so tumours take up FDG competitively; hyperglycaemia and recent insulin drive tracer into muscle and reduce lesion visibility, producing false-negative studies.
Can PET-CT distinguish tumour recurrence from radiation necrosis?
In glioma, recurrent tumour shows FDG hypermetabolism whereas necrosis is hypometabolic; amino-acid tracers such as methionine and FET perform even better in current practice.
What are the common false-positive causes of FDG uptake?
Physiological brain, myocardial, bowel, urinary and brown-fat activity; infection and inflammation including tuberculosis and sarcoidosis; and post-therapy changes such as thymic rebound and marrow stimulation — clinical correlation and CT morphology resolve most.