Synopsis
Identify mineralisation failure behind bone pain, weakness and insufficiency fracture, protect mechanically vulnerable sites and correct the specific calcium, phosphate or vitamin-D defect safely.
- Osteomalacia is inadequate mineralisation of adult osteoid; high-yield clues are diffuse bone tenderness, proximal weakness, waddling gait and insufficiency or Looser-zone fractures.
- First-line bloods are adjusted calcium, phosphate, alkaline phosphatase, PTH, 25-hydroxyvitamin D, magnesium, renal and liver profiles, interpreted as one physiological pattern.
- Nutritional vitamin-D deficiency commonly produces low 25-hydroxyvitamin D, raised ALP and PTH and low phosphate, while adjusted calcium may remain low-normal through compensation.
- First-line imaging of focal pain is site-specific radiography; use MRI when a femoral-neck, sacral, pelvic or other insufficiency fracture remains suspected despite normal films.
- Protect weight bearing immediately across a painful high-risk femoral or pelvic site until an incomplete fracture has been excluded and orthopaedic stability is known.
- For uncomplicated adult deficiency requiring rapid correction, a guideline loading total near 300,000 units of colecalciferol over six to ten weeks is followed by 800 to 2,000 units daily maintenance.
- Do not prescribe phosphate blindly: persistent low phosphate requires fasting paired plasma and urine assessment to separate appropriate conservation from renal wasting.
- Biochemical correction precedes potent antiresorptive treatment because denosumab or intravenous bisphosphonate can worsen hypocalcaemia in inadequately mineralised bone.
Key red flags
Focal groin or thigh pain, pain on axial loading or sudden loss of walking may represent an incomplete femoral-neck or subtrochanteric insufficiency fracture.
Multiple symmetrical Looser zones, marked deformity or rapidly worsening pain requires protected loading and specialist metabolic-bone and orthopaedic review.
Perioral tingling, carpopedal spasm, seizure, stridor or arrhythmia suggests clinically important hypocalcaemia requiring urgent ECG and biochemical correction.
Severe weakness, respiratory compromise, rhabdomyolysis or haemolysis with very low phosphate requires urgent monitored phosphate management and investigation.
Weight loss, anaemia, hypercalcaemia or a solitary destructive lesion is inconsistent with simple nutritional deficiency and raises malignancy or myeloma.
Persistent hypophosphataemia despite corrected vitamin D suggests renal phosphate wasting, Fanconi syndrome or FGF23-mediated tumour-induced osteomalacia.
Investigation priorities
Distinguish vitamin-D deficiency, calcium deficit, kidney disease and phosphate loss while identifying acute treatment hazards.
Detect pseudofracture, complete fracture, deformity or a destructive alternative at the symptomatic site.
Management branches
Focal weight-bearing pain, loss of walking or a pseudofracture raises concern for impending completion.
- Stop provocative loading, document limb alignment and neurovascular findings and provide safe mobility aids.
- Obtain radiographs in two planes and use MRI promptly when a high-risk occult fracture remains possible.
- Refer tension-side, progressing, displaced or mechanically unsafe femoral lesions urgently for fixation assessment.
- Treat mineral deficiency and perform VTE-risk assessment alongside rather than after mechanical care.
Diffuse pain, proximal weakness or insufficiency fracture suggests mineralisation failure.
- Measure adjusted calcium, phosphate, ALP, PTH, vitamin D, magnesium and renal and liver function.
- Review diet, sunlight, bowel or bariatric disease, kidney disease and medicine exposures.
- Use ECG and monitored acute replacement for symptomatic severe calcium or phosphate disturbance.
- Avoid antiresorptive treatment until hypocalcaemia and important vitamin-D deficiency have been corrected.