CASE 82
By: Dr. Amna Kashgari MD,SSC-Rad
HISTORY: A 4-year-old boy with sever right ankle pain after minor trauma.
What are your findings?
What is your differential diagnosis?
What is you diagnosis?
What are the causes of the underlying disease?
FINDINGS:
AP and lateral X-Ray of the right ankle demonstrate generalized underemineraliztion of the bone with irregular widened epiphyseal plates. Cupping and fraying of the metaphyseal region is also noted.
There is incomplete fracture line noted in the distal metaphysis of the right tibia with adjacent periosteal reaction. Another possible incomplete fracture noted in the anterior cortex of the tibia.
DIFFERENTIAL DIAGNOSIS:
Rickets.
Osteogenesis imperfecta.
Hypovitaminosis C (scurvy).
Metaphyseal chondrodysplasia.
DIAGNOSIS:
Rickets with pathological fracture.
Causes of Rickets:
Nutritional: commonest cause in the developing countries
Malabsorption.
Drugs that increases metabolism of vitamin D in the liver.
Chronic liver disease.
Renal rickets – Chronic renal failure – RTA.
Hereditary rickets:
Vitamin D dependent rickets (Type 1 & 2).
Vitamin D resistant rickets.
Primary hypophosphatemia.
PEARLS AND DISCUSSION:
Rickets is due to defective mineralization occurs in both bone and cartilage of epiphyseal growth plate, associated with growth retardation and skeletal deformities.
Vitamin D (cholecalciferol) is formed in the skin after exposure to ultraviolet light.
Vitamin D is converted to 25(OH) vitamin D (calcidiol) in the liver. Plasma concentration of 25(OH) vitamin D reflects vitamin D status derived from both endogenous and exogenous sources.
In the kidney, 25(OH) vitamin D is converted to the active hormone 1,25(OH)2 vitamin D (calcitriol), which increases the concentrations of calcium and phosphate in extracellular fluid leading to the calcification of osteoid. When calcitriol levels are low, hypocalcaemia develops. This stimulates parathyroid hormone (PTH) and some of the changes seen in bone are those of hyperparathyroidism.
Early in the course of the rickets, the calcium concentration in serum decreases. However, after stimulation of PTH, calcium returns to the normal range, but phosphate usually falls. Alkaline phosphatase released into the extracellular fluid resulting in elevated serum levels.
| Types |
Ca Serum |
Phosphate Serum |
Alkaline phosphatase |
Ca Urine |
PTH |
|---|---|---|---|---|---|
|
Vitamin D deficiency rickets |
Low-Normal | Low-Normal | High | High | High |
| Hypophosphatemic rickets | Normal | Low | High | Normal |
Manifestations of rickets:
Head:
Craniotabes.
Delayed closure of anterior fontanel.
Frontal and parietal bossing.
Delayed eruption of primary teeth.
Skeletal manifestations:
Generalized Osteopenia.
Widening of the epiphyseal growth plates due to loss of normal ‘zone of provisional calcification’ adjacent to the metaphysis lead to indistinctness of metaphyseal margin, progressing to a ‘frayed’ appearance.
Splaying and cupping of the metaphysis due to cartilage overgrowth in the ‘zone of maturation’ secondary to stress.
Bowing of legs.
Rachitic rosary: enlargement of the cartilage at costochondral junction.
FURTHER READING:
Lane F Donnelly. Fundamental of pediatric radiology. ISBN-13: 978-0721690612
Johan G Blickman, Bruce R Parker, Patrick D Barnes. Pediatric Radiology: The Requisites, 3e. ISBN-10: 0323031250
