Six weeks of leg pain and a limp in a well-grown child. Build the differential with the case team — one piece of evidence at a time — toward a diagnosis hiding in plain sight.
June 12, 2026 · 15 min
1. The Presentation
A previously well 7-year-old girl is brought in with 6 weeks of pain in both legs and a limp, with no fall or injury beforehand. The pain started around the knees and shins, tends to be worse later in the day, and has gradually intensified — she now finds it hard to climb stairs or get up from sitting. Paracetamol and ibuprofen help only briefly. There has been no warmth, redness or swelling.
What is the highest-yield initial step?
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Growing pains are bilateral and evening-predominant — but they are intermittent, never cause a limp or functional loss, and do not progress over weeks. Pain that worsens steadily with gait disturbance is a red flag that mandates evaluation, not reassurance.
✓ Correct
In a child with chronic atraumatic limp the differential is broad — bone, joint, marrow, infection, nutrition. A structured history (fevers, night pain, weight loss, morning stiffness, and crucially diet) reshapes the pre-test probabilities before you commit to tests. Dietary history is the step most often skipped — and here it proves pivotal.
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Imaging will come, but advanced imaging before a history and examination risks anchoring, often needs sedation in children, and is best directed by cheaper discriminators. History first.
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There is no fever and no focal warmth or swelling. Treating blindly for infection is premature and would muddy the picture.
2. The Targeted History
On systematic questioning she has had no fevers, and no recent sore throat, diarrhoea, skin infection or tick exposure. There is no night pain waking her from sleep, no weight loss, night sweats, easy bruising or unusual fatigue. She does not feel stiffer in the mornings than later in the day — if anything the pain worsens through the day with activity.
The combination of no morning stiffness and pain that worsens with activity argues most against which diagnosis?
✓ Correct
Inflammatory arthritis classically causes morning stiffness that eases with movement. Pain that worsens with activity and through the day is the opposite — a mechanical/bone pattern. Combined with a later joint exam showing no effusion, this makes JIA unlikely.
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Bone pathology (tumour, chronic nonbacterial osteomyelitis, metabolic disease) is entirely compatible with activity-related, evening-predominant pain — this history does not argue against it.
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Absence of night pain and weight loss lowers but does not exclude malignancy — leukaemia can present without systemic features. One reassuring feature can’t rule it out.
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Scurvy and rickets cause activity-related bone pain without morning stiffness, so this pattern is compatible with nutritional disease, not against it.
3. The Examination
Her vital signs are normal and she is afebrile, and she is growing normally (23 kg and 122 cm, both 50th percentile; BMI 15.5). She walks with an antalgic gait and will not put full weight through the left leg, where bending the knee is sharply painful and restricted. On palpation both lower limbs are tender over the metaphyseal regions — the lower femurs and upper tibias — but the joints themselves are quiet: no effusion, warmth or redness. Her skin is dry and free of rash, petechiae or purpura, with no enlarged lymph nodes or organomegaly, and the neurological examination is unremarkable.
Which examination finding is most diagnostically localising?
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It tells you she is in pain and protecting the limb, but is non-specific — almost any painful leg process produces it.
✓ Correct
This localises the problem to bone (the metaphyses), not the joint. Symmetric, multifocal metaphyseal tenderness with no effusion, warmth or erythema points toward a systemic bone process — metabolic/nutritional, autoinflammatory (CNO), or marrow infiltration — rather than arthritis or a single focal lesion.
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Without effusion or warmth this is pain-limited movement driven by adjacent bone tenderness — not a true arthritic sign.
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Their absence lowers suspicion for leukaemia and for the cutaneous signs of scurvy — but early scurvy and early leukaemia can both have a normal skin and abdomen. Reassuring, not localising.
4. Choosing the First Investigation
She is otherwise systemically well. The working differential spans musculoskeletal, malignant, inflammatory, infectious, nutritional and haematologic causes. You need a first test that can separate a joint process from a bone process and flag tumour, infection or metabolic bone disease.
Which is the most informative first investigation?
✓ Correct
Cheap, fast and high-yield: a radiograph distinguishes joint from osseous disease and shows characteristic patterns — permeative lysis and periosteal reaction (tumour), cortical destruction or new bone (infection), and the metaphyseal changes of metabolic bone disease. It is the right first imaging step and directs everything after it.
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More sensitive for marrow disease, but expensive, often needs sedation in young children, and is best directed by the radiograph. Usually the second step, not the first.
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There is no effusion to aspirate, and the exam points to bone rather than joint — low yield and invasive.
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Far too invasive as a first step, before non-invasive imaging and labs have had a chance to narrow the field.
5. The Radiograph
Plain radiography of the left knee shows subtle sclerosis of the distal femoral metaphysis, with no periosteal reaction, no cortical destruction, no lytic lesion and no soft-tissue mass.
How does this most change the differential?
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Osteosarcoma shows aggressive features — a mixed lytic/sclerotic lesion with a Codman triangle or “sunburst” periosteal reaction. Their absence argues against it.
✓ Correct
Aggressive tumours produce permeative “moth-eaten” lysis, cortical disruption, periosteal reaction (“onion-skin” in Ewing’s) and soft-tissue masses. A film showing only subtle metaphyseal sclerosis with none of these makes a destructive primary tumour unlikely — and that subtle metaphyseal sclerosis is itself a clue toward metabolic bone disease.
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CNO is multifocal and characterised on MRI; a single subtle plain-film finding cannot establish it.
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Plain films are insensitive early. A near-normal film does not exclude marrow disease (leukaemia, CNO) or early metabolic change — which is exactly why MRI and labs follow.
6. The MRI
MRI of the lower limbs shows symmetric, multifocal bone-marrow and soft-tissue oedema involving several regions — the sacroiliac regions, acetabula and proximal femoral physes — with preserved joint spaces. There is no abscess and no large soft-tissue mass.
Which diagnosis is least consistent with this pattern?
✓ Correct
Pyogenic osteomyelitis is typically focal, with marrow oedema plus a subperiosteal collection or adjacent soft-tissue abscess, and usually fever with high inflammatory markers. A symmetric, multifocal marrow-oedema pattern with no abscess is the opposite picture — making single-organism pyogenic osteomyelitis the least consistent option.
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CNO classically produces multifocal, often symmetric metaphyseal marrow-oedema lesions without abscess or mass — highly consistent, and stays on the list.
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Subperiosteal haemorrhage with marrow and soft-tissue oedema in scurvy can produce exactly this multifocal pattern and mimic infection or autoinflammation — consistent.
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Leukaemia can give diffuse marrow signal abnormality, so it remains possible on imaging alone — not the least consistent. Labs are needed to exclude it.
7. The Laboratory Results
Bloods show mild anaemia (Hgb 10.9 g/dL) with normal white-cell and platelet counts. The peripheral smear shows no blasts and only scant neutrophil hypersegmentation; haemoglobin electrophoresis is normal. ESR 36 and CRP 6.9 are mildly elevated; ANA negative; LDH normal. Lyme and Mycoplasma serologies are negative and two blood cultures show no growth. Calcium, alkaline phosphatase and renal/liver panels are normal.
Which result most lowers concern for leukaemia?
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Non-specific — mild inflammation occurs across infection, autoinflammation, malignancy and even scurvy. It neither supports nor refutes leukaemia.
✓ Correct
Leukaemia usually shows cytopenias and/or circulating blasts. A smear with no blasts and preserved white-cell and platelet counts (only mild anaemia) substantially lowers the probability. (Caveat: early leukaemia can occasionally have a clean smear — so vigilance continues — but this meaningfully de-prioritises it.)
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ANA addresses connective-tissue disease and JIA, not leukaemia.
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Supportive but non-specific — LDH can be normal in leukaemia and raised in many benign states. Weaker evidence than the smear and counts.
8. The Dietary History
You return to the history and take a detailed dietary account. Her diet consists largely of dairy products and refined carbohydrates, with minimal intake of fruits, vegetables, fruit juices or any vitamin supplementation. Until her symptoms began she played volleyball and gymnastics, she attends school normally, and her growth sits on the 50th percentile.
This dietary pattern raises concern for deficiency of which nutrient as the cause of her bone pain?
✓ Correct
Fruits and vegetables are the principal dietary source of vitamin C; a diet of dairy and refined carbohydrate with almost no fruit or veg is the classic set-up for deficiency. Lack of vitamin C impairs collagen formation → capillary fragility, subperiosteal haemorrhage and bone pain, mimicking infection or autoinflammation on imaging. Crucially, normal growth does not exclude it — selective diets can be calorie-sufficient yet micronutrient-poor.
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Worth checking (restrictive diets cause multiple deficiencies), but her dairy-heavy diet supplies some vitamin D, calcium and ALP are normal, and there are no growth-plate changes — making rickets less likely. Keep it on the list pending the level.
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The scant neutrophil hypersegmentation makes B12/folate worth measuring, but B12 deficiency causes macrocytic anaemia and neurological signs — not a subperiosteal-haemorrhage bone-pain syndrome.
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Iron deficiency causes anaemia but not the bone-pain / subperiosteal pattern seen here; her anaemia is mild and not the presenting problem.
9. Narrowing Down, and the Next Step
The differential now narrows to two leading considerations: chronic nonbacterial osteomyelitis and vitamin C deficiency. You want to confirm or exclude nutritional deficiency before contemplating an invasive step such as bone biopsy, while continuing to watch for any new fever.
What is the best next step to confirm the leading nutritional diagnosis?
✓ Correct
A markedly low ascorbic acid gives biochemical confirmation of scurvy. Because restrictive diets cause multiple deficiencies — and the smear shows neutrophil hypersegmentation — checking vitamin D, B12 and folate at the same time is sensible. (Interpret vitamin C with care: levels fall with recent intake and with delayed sample handling, so early supplementation can begin while testing is pending.)
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Invasive — reserved for when malignancy or CNO cannot be excluded non-invasively, or if fevers emerge. Premature when a cheap blood test can confirm a strongly suspected nutritional cause.
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CNO often improves with NSAIDs, but a response is non-specific and would not distinguish it from scurvy. Biochemical testing is more direct.
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Adds radiation and non-specific uptake data, and cannot confirm a nutritional deficiency.
10. Making the Diagnosis
The results return. 25-hydroxyvitamin D is normal, and vitamin B12 and folate are not suggestive of deficiency. The serum vitamin C concentration is markedly reduced at <0.5 mg/L.
What is the unifying diagnosis?
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CNO was the main alternative, but it is a diagnosis of exclusion and would not explain a markedly low vitamin C. The dietary history plus biochemistry point elsewhere.
✓ Correct
The long-standing diet with negligible vitamin C, the clinical course (progressive limb pain, limp, metaphyseal tenderness), the imaging (multifocal marrow and soft-tissue oedema from subperiosteal haemorrhage) and a markedly low ascorbic acid together establish scurvy as the unifying diagnosis. Normal vitamin D, B12 and folate exclude the main co-deficiencies.
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Vitamin D is normal, calcium and ALP are normal, and there are no growth-plate (physeal) changes — rickets is excluded.
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No blasts, no significant cytopenias and a normal LDH — and a low vitamin C does not fit leukaemia. Already de-prioritised.
11. Why It All Fits
Vitamin C (ascorbic acid) is an essential cofactor for the hydroxylation of proline and lysine during collagen synthesis.
Which mechanism best explains her bone pain and imaging findings?
✓ Correct
Without vitamin C, collagen is unstable: vessels become fragile (bleeding) and osteoid formation fails. In growing children this produces subperiosteal haemorrhage and metaphyseal injury → prominent limb pain, limp and refusal to bear weight, with marrow and soft-tissue oedema on MRI that mimics infection or autoinflammation. Gingival and cutaneous signs may be absent early.
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That is an arthritis mechanism — she has no synovitis and the ANA is negative.
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That is osteomyelitis — cultures are negative and the pattern is symmetric and multifocal without abscess.
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That is leukaemia/malignancy — the smear shows no blasts and counts are largely preserved.
12. Management
The diagnosis is established. You plan treatment and follow-up.
What is the appropriate management?
✓ Correct
Scurvy is treated by replacing vitamin C (oral preferred; parenteral if oral aversion or vomiting) alongside correcting the underlying selective diet. No single standardised regimen exists — commonly higher oral doses for several days to a week, then a lower daily dose until symptoms resolve. Clinical improvement often begins within days, with recovery of pain and function over 1–3 weeks; radiographic changes resolve over weeks to months. Screen for coexisting deficiencies.
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Appropriate for inflammatory or autoinflammatory disease — not nutritional deficiency. They would not correct the cause and would add harm.
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For osteomyelitis, which has been excluded here (negative cultures, non-pyogenic imaging pattern).
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NSAIDs gave only brief relief and do not address the deficiency. Analgesia is adjunctive, not the treatment.
13. Outcome and Take-Aways
What happened next. Vitamin C supplementation was started, with dietitian-guided counselling to address the dietary selectivity. Over the next 3 weeks her pain resolved and her gait returned to normal. Inflammatory markers normalised and the peripheral-blood smear abnormalities resolved.
Key learning points
Take a dietary history in any child with chronic limb pain or limp. Selective eating can cause micronutrient deficiency even when growth and weight appear entirely normal.
Bilateral metaphyseal bone tenderness with a clean joint exam localises the problem to bone, not joint — and points toward systemic processes (metabolic, autoinflammatory, marrow) rather than arthritis.
Scurvy is a great mimic. It can produce mildly raised inflammatory markers and multifocal marrow/soft-tissue oedema on MRI that resemble osteomyelitis or chronic nonbacterial osteomyelitis — so dietary history and biochemical confirmation matter.
Early scurvy can lack the classic gingival and cutaneous signs; progressive limb pain and refusal to bear weight may dominate the early picture.
Interpret the serum vitamin C with care (recent intake and sample handling affect it), and when suspicion is high, start repletion while confirmatory testing is pending.
Vitamin C repletion plus dietary correction is highly effective, usually with rapid symptomatic improvement — and screen for coexisting deficiencies in any restrictive diet.