Nutritional Rickets
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Direct answer
Nutritional rickets is defective mineralisation of growing bone from vitamin D deficiency, with or without dietary calcium deficiency, peaking in late infancy and the toddler years and again in adolescence. Vitamin D deficiency lowers calcium absorption and triggers secondary hyperparathyroidism — the biochemical signature of calcium low or normal, phosphorus low, alkaline phosphatase high and parathyroid hormone high, with low 25-hydroxyvitamin D confirming the cause. Treatment is vitamin D (daily replacement or supervised high-dose weekly regimens) with adequate calcium; prevention is 400 IU of vitamin D daily from infancy.
What you must remember
- Risk factors: exclusive breastfeeding without supplementation, dark or covered skin, indoor living, prematurity, malabsorption, and the cereal-heavy, calcium-poor weaning diets of India.
- Bony signs: craniotabes, frontal bossing with delayed fontanelle closure, rachitic rosary (beaded anterior rib ends), widening of wrists and ankles, Harrison's sulcus, bow legs or knock knees and delayed dentition.
- Non-osseous signs: hypocalcaemic seizures, tetany and carpopedal spasm, laryngospasm with stridor, Chvostek and Trousseau signs, and hypotonia with a protuberant abdomen.
- Biochemistry: low or normal calcium, low phosphorus, high alkaline phosphatase, high PTH and low 25-hydroxyvitamin D (below about 20 ng/mL defines deficiency).
- Radiology: cupping, fraying, splaying and widening of the metaphyses — best seen at the wrist (distal ulna and radius) and knee — with delayed bone age; healing appears within weeks.
- Treatment: daily vitamin D replacement for about three months (roughly 1,000-2,000 IU in infants, 3,000-4,000 IU in older children per international consensus) or supervised weekly high-dose courses favoured in Indian practice, always with dietary calcium ensured.
- Prevention: 400 IU vitamin D daily from the first weeks of life, maternal supplementation, sunlight and dietary diversification.
Common confusion
Nutritional rickets must be separated from causes that do not respond to vitamin D: X-linked hypophosphataemic rickets (very low phosphorus with normal calcium and PTH — vitamin D resistant), vitamin D-dependent rickets types 1 and 2 (the latter with alopecia), distal renal tubular acidosis and Fanconi syndromes, and chronic kidney disease (high phosphorus with low calcium — the reverse pattern). The second is calcium-deficiency rickets in Indian children on adequate vitamin D but cereal-bound, low-calcium diets — they need calcium as much as vitamin D.
Exam-focused takeaway
NEET-PG tests rickets in three registers: signs (rachitic rosary, craniotabes, wrist widening, Harrison's sulcus), biochemistry (the low-phosphorus, high-ALP, high-PTH pattern with 25-OH-D as the confirmatory test) and the differential against hereditary and renal rickets using calcium, phosphorus, PTH and acid-base. Treatment stems ask for vitamin D with calcium and the 400 IU daily prophylaxis; radiology stems name the wrist metaphysis with cupping and fraying. The Indian angle of calcium-poor diets feeds programme questions on supplementation and fortification.
Frequently asked questions
What are the classic bony signs?
Craniotabes, frontal bossing, rachitic rosary, widening of wrists and ankles, Harrison's sulcus, bow legs or knock knees, and delayed fontanelle closure with delayed dentition.
What is the typical biochemistry?
Low or normal calcium, low phosphorus, high alkaline phosphatase and high parathyroid hormone, with low 25-hydroxyvitamin D confirming vitamin D deficiency.
Which radiograph shows changes earliest?
The wrist — cupping, fraying and widening of the distal ulnar and radial metaphyses; the knee is the other classic site.
How does X-linked hypophosphataemic rickets differ?
Very low phosphorus with normal calcium and normal PTH, a family history and no response to usual vitamin D doses — hence vitamin D resistant — needing phosphate with active vitamin D analogues.
How is nutritional rickets treated?
Vitamin D daily for about three months (or supervised high-dose weekly regimens per local practice) with adequate dietary calcium, healing tracked by falling alkaline phosphatase and radiograph.