đ§â Childhood Tumours
đ Key Learning
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Wilms tumour is the most common renal tumour in childhood, presenting as a painless abdominal mass, haematuria and flank pain in children < 4 years.
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Neuroblastoma arises from neural crest cells of the sympathetic nervous system, often secretes catecholamines and presents variably depending on site.
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Retinoblastoma presents in children < 3 years, often with leukocoria and strabismus, and is linked to RB1 tumour suppressor gene mutations.
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All three conditions require urgent specialist referral for further investigation and management.
đ„Ź Wilms Tumour (Nephroblastoma)
Pathophysiology
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The most common renal tumour in childhood (5% of all childhood malignancies). Â
Clinical Features
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Age < 4 years in 75% of cases.
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Painless, rapidly growing abdominal mass.
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Haematuria.
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Hypertension.
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Flank pain or fever.
Red Flags & Referrals
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Palpable abdominal mass or organomegaly OR unexplained visible haematuria â very urgent referral (within 48 hours).
Investigations
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Abdominal ultrasound (initial test).
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Followed by CT or MRI for staging.
Management
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Neoadjuvant chemotherapy followed by surgical resection.
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Further chemotherapy ± radiotherapy based on staging.
đ§ Neuroblastoma
Pathophysiology
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Malignant tumour of sympathetic nervous system.
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Derived from neural crest cells.
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Common primary sites: adrenal medulla, sympathetic ganglia  (abdomen, thorax, pelvis, neck).
Clinical Features
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Usually diagnosed at around 2 years of age.
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Abdominal mass: pain, distension.
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Thoracic mass: respiratory symptoms, dysphagia.
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Cervical tumour: Hornerâs syndrome.
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Metastases to bone marrow: fatigue, pallor, bruising.
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Systemic symptoms due to catecholamine secretion: flushing, sweating, tachycardia, hypertension.
Red Flags & Referrals
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Palpable abdominal mass or organomegaly â very urgent referral (within 48 hours).
Investigations
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Urine catecholamines: elevated VMA/HVA levels.
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Imaging: CT/MRI.
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Biopsy to confirm diagnosis.
Management
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Risk-adapted multimodal therapy: surgery, chemotherapy, radiotherapy, immunotherapy, stem cell transplant (if high-risk).
đïž Retinoblastoma
Pathophysiology
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Malignancy of retinal cells.
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Caused by mutations in the RB1 tumour suppressor gene on chromosome 13.
Genetic Subtypes
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Germline mutation: bilateral tumours, high risk of additional malignancy (e.g. osteosarcoma).
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Sporadic mutation: unilateral tumour, no increased risk of other cancers.
Clinical Features
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Presents < 3 years (often < 1 year if bilateral).
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Leukocoria â white pupillary reflex.
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Strabismus (squint).
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Decreased visual acuity.
Retinoblastoma. Leukocoria.
Red Flags & Referrals
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Absent red reflex â urgent referral (suspected cancer pathway).
Investigations
- MRI orbit/brain (for extent).
Management
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Chemotherapy (systemic or intra-arterial).
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Local therapies (cryotherapy, laser photocoagulation).
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Enucleation if extensive disease.
đ Exam Clues & Clinchers
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Toddler with painless abdominal mass, haematuria and HTN â Wilms tumour â US abdomen, very urgent referral.
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Flushing, abdominal mass, bone marrow failure signs in child < 5 â Neuroblastoma â urine VMA/HVA.
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White pupil in infant photo â Retinoblastoma â absent red reflex â urgent ophthalmology referral.