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Rickets
Rickets is caused by a lack of vitamin D, calcium, or phosphate which leads to softening and weakening of the bones due to defective mineralization of bone matrix. It results from vitamin D deficiency which prevents proper absorption of calcium and phosphate from the diet. Symptoms include bone pain, skeletal deformities, increased fractures, and impaired growth. Treatment involves addressing the underlying cause by increasing vitamin D, calcium, and phosphate intake.
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Rickets
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- 2. lack ofvitamin D, calcium, or phosphate, which leads to softening and weakening of the bones. Defective mineralization of bone matrix – excessive unmineralised osteoid
- 3. Vitamin Dhelps the body properly control calcium and phosphate levels in the body. When the body is deficient in vitamin D, it is unable to properly control calcium and phosphate levels calcium and phosphorous are found in milk and green vegetables.
- 4. Defective VitaminD metabolism – lowering of calcitriol - intestinal malabsorption of calcium - reduction of serum calcium – Parathyroid stimulation – normalised S.calcium at the expense of reduced S.Phosphate
- 5. Parathormone – Osteoblastic activity - ALP activity – Defective Osteoid mineralization
- 6. ultraviolet rays 7-Dihydrocholesterol Cholecalciferol(Vitamin D3)- in dermis Vit D2 absorbed thru small intestine Transport in serum- binds with X-globulin 25-Hydroxylation in Liver 1,25- Dihyroxylation in Kidney – active form
- 7. Nutritional Absorptive Renal Others
- 8. Decrease ineffect & amount of Sunlight Bread/Chapathi rich in Phytate bind dietary calcium – reduced absorption Infants who are exclusively breastfed may develop vitamin D deficiency. Poor Dietary intake of Ca & Vit D Malabsorption disorders – Coeliac d/s, hepatic osteodystrophy, lactose intolerance
- 9. Renal –Renal osteodystrophy, Nephrectomy, renal failure, hypoparathyroidism, X-linked hypophosphatemia/Vit D resistant rickets Vitamin dependant Type I (Inability to hydroxylate) Vitamin dependant Type II (Receptor insensitivity) Anticonvulsant therapy( 25OH in liver)
- 10. Failure ofdeposition of Ca along mature cartilage cell columns Disorderly invasion of cartilage by blood vessels Lack of reabsorption at the zone of provisional calcification Increased thickness of epiphyseal plate
- 11. Abundant osteoidwith Defective mineralization No resorption of uncalcified osteoid by osteoclasts Normal osteoblast – laid irregularly Abnormal arrangement of collagen bundles in compact bone
- 12. Long bonesbent when child starts crawling/walking
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- 22. Bone painor tenderness Arms Legs Spine Pelvis Skeletal deformities o Bowlegs o pigeon chest o rachitic rosary o Frontal bossing o Spine deformities (spine curves abnormally, including scoliosis or kyphosis ) o Pelvic deformities
- 23. Increased tendencytoward bone fractures Dental deformities o Delayed formation of teeth o Defects in the structure of teeth, holes in the enamel o Increased incidence of cavities in the teeth ( dental caries ) o Decreased muscle tone (loss of muscle strength) Muscle cramps Impaired growth Short stature
- 24. Acute stage Normal epiphyseal appearance clouded Metaphyseal splaying Thickened periosteum
- 25. Epiphysis Mottled& irregular Metaphysis ragged & broader Periosteal thickening disappears
- 26. Dense shadow Dense line at the end of metaphysis- deposition of Ca Stage of repair
- 27. Increase inbreadth of metaphysis Clearly defined bone Normal content of Ca salts Bone completely repaired
- 29. Serum Calow or normal. o Tetany -prolonged muscle spasm. o Chvostek's sign may be positive (a spasm of facial muscles occurs when the facial nerve is tapped) S.Phosphorus may be low. S.ALP may be high. ABG may reveal metabolic acidosis Urinary Ca may be low .
- 30. 24-hydroxylase assay– for vitamin D dependency rickets Serum 25-OH vitamin levels A bone biopsy is rarely performed but will confirm rickets.
- 31. Congenital syphilis Infantile scurvy
- 32. Goals -relieve symptoms and correct the cause of the condition. Underlying cause must be treated to prevent recurrence.
- 33. Medical treatment Prevention of deformity Treatment of existing deformity
- 34. Dietary sourcesof vitamin D include fish, liver, milk and cheese. Exposure to moderate amounts of sunlight is encouraged. Reduce cereal containing phytates Supplemention of Calcium and Vitamin D – 3000 i.u./day
- 35. Before treatment and2 years after treatment with calcium
- 36. Control ofmovements – reduced pressure upon limbs (soft bones easily bent by pressure / muscle strain) Positioning or bracing with ‘rickets’ splints may be used.
- 37. Correction bysplinting In young children below 4 yrs Useful in lower limbs Continuous supervision needed to prevent sores
- 38. Correction byosteotomy When deformity is near a joint At least stage 3 in radiograph
- 39. Chronic skeletalpain Skeletal deformities Skeletal fractures, may occur without cause
- 40. Rickets ofprematurity Very premature infants at risk Risk factors- hepatobiliary d/s, TPN, Diuretic therapy, chest percussion therapy Pathologic # in NICU Readily heal with treatment
- 41. Antiepileptic medications Induce microsomal P-450 enz Decreased Vit D Should be suspected in neurologic patients having seizures Start having frequent #
- 42. Familial hypophosphatemicrickets X-linked dominant (MC)- Mutn in PEX gene Aut dominant 12p13 – phosphatonins – fgf 23 – cause phosphaturia Aut recessive
- 43. Renal tubuleunable to retain PO4 End organ insensitivity to vit D (AR) Kidney unable to perform 2nd hydroxylation Renal tubular acidosis (kidney excretes fixed base and wastes bicarbonate) Ca ppt – renal calcinosis
- 44. Older age Delayed walking, angular deformities Systemic manifestn – irritability and apathy minimal Treatment – Oral Phosphorus , Vit D (Compl – nephrocalcinosis) Growth hormone – increased height, increased PO4, reduced Nephrocalcinosis
- 45. Surgery notefficacious – multilevel osteotomy to correct mechanical axis Recurrent deformity common Surgery when - gait compromised/severe pain
- 46. Oncogenic hypophosphatemic osteomalacia Asso with Neurofibromatosis, fibrous dysplasia Osteoblastoma, hemangiopericytoma of bone, skin tumors (disrupts renal tubular abs of po4) Secrete phosphatonins Resolve with excision of tumor
- 47. C/C pyelonephritis Congenital Abnormalities Polycystic kidney d/s Secondary hyperparathyroidism Leads to actvn of osteoclast and resorption of bone (high turn over d/s)
- 48. Glomerulus unableto excrete Phosphorus Vit D prodn reduced Ca abs from S.Intestine reduced PTH triggered Increased S.Ca – bone demineralization Precipitate in cornea, skin, blood vessels
- 49. C/F similarto Nutritional. Angular deformity, SCFE, AVN Radiography – cuppping of physis not present Subperiosteal resorption in phalanges, MC and ulna (feature of Hyperparathyroidism) Osteosclerosis of skull, rugger jersey spine Lytic areas in long bones (Brown tumors) Treat underlying d/s- Ca, Vit D, growth hormone, osteotomy, Ilizarov
- 50. Ca Normalor low in all Phosphate is reduced in all except Renal Osteodystrophy ALP and PTH high in all 25 OH Vit D N or high in all except nutritional (decreased) 1,25 (OH)2 N or low in all except Vit D dependent typeII (receptor insensitivity)
- 51. Maintain anadequate intake of calcium, phosphorus, and vitamin D. This may require dietary supplements in people who have gastrointestinal or other disorders Renal causes of vitamin D should be treated promptly.
- 52. Levels ofcalcium and phosphorus should be monitored regularly in people who have renal disorders . Genetic counseling may help people with a family history of inherited disorders that can cause rickets.