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  1. 6. Rickets of vitamin D deficiency
  2. 7. <ul><li>Rickets is defined as the failure of osteoid to calcify in a growing person. </li></ul><ul><li>failure of osteoid to calcify in adult is called osteomalacia </li></ul>
  3. 8. Rickets of vitamin D deficiency is a common nutritional disorder under 3 yrs of age , is the term signifying a failure in mineralization of growing bone or osteoid tissue . Definition
  4. 9. Physical and metabolic property and source of VD
  5. 10. Characteristics Fat-soluble stable to heat, acid, alkali and oxidation bile is necessary for absorption.
  6. 11. 7-dehydrocholesterol in skin irradiated by ultraviolet rays converts into cholecalciferol (endogenous VD 3 ) fish-liver oils; egg yolks; butter; VD fortified milk; margarine Sources
  7. 12. Cod fish Mackerel salmon Sardines
  8. 13. Metabolism and regulation Dietary source 7-Dehydrocholesterol in skin Either vitamin D 2 or D 3 ultraviolet radiation (296 -- 310 nm ) Vitamin D 3 (--) Liver 25-hydroxylase 25(OH)D 3 Kidney 1- hydroxylase Hypocalcemia (+) Hypophosphatemia (+) (+) Parathyroid hormone Hyperphosphatemia (--) (--) Calcitonin (+) Hypercalcemia 1,25(OH) 2 D 3  
  9. 14. 296—310nm
  10. 15. Promotes intestinal calcium and phosphate absorption, presumably by affecting permeability of intestinal membrane Promotes bone dissolution and mineralization Promotes reabsorption of calcium and phosphorus from renal tubules Physical property ( 1, 25(OH) 2 VD 3 )
  11. 16. <ul><li>produced in one part of the body (the skin) </li></ul><ul><li>released into the blood </li></ul><ul><li>affect other tissues (the bones) </li></ul><ul><li>There is a feedback system with the </li></ul><ul><li>parathyroid to produce active vitamin D 3 </li></ul>Vitamin D hormone
  12. 17. Inadequate direct exposure to ultraviolet rays in sunlight Inadequate intake of VD Rapid growth Malabsorption Drugs Etiology
  13. 18. Inadequate direct exposure to ultraviolet rays in sunlight <ul><li>Less outdoor activity </li></ul><ul><li>The winter is longer </li></ul><ul><li>Sunlight pass way </li></ul><ul><li>Skin pigmentation </li></ul>
  14. 19. 日光照射不足
  15. 20. Inadequate intake of VD <ul><li>The diet contain small amounts </li></ul><ul><li>Improper ratio of Ca and P </li></ul>
  16. 21. the abundant laying down of osteoid tissue epiphyseal cartilage cells grow very rapidly widening of the epiphysis line Long bone Rachitic rosary Bracelets of wrist and ankle flat bone Craniotabes Square head disorder of new bone formation the bones are soft Bowlegs and knock-knees Pigeon breast Pathology
  17. 22. di c aphysis
  18. 23. Mechanism of rickets
  19. 24. VD deficiency reduction of intestinal absorption of calcium and phosphate Hypocalcemia   Parathyroid hormone hyperfunction hypofunction Excretion of urinary P↑ decalcification of mobilization of bone old bone↑ Calcium into blood Serum p ↓ Ca normal or slightly↓ Ca X p↓ Failure of Calcification of Osteoid tissue Ca++↓ Accumulation of osteoid tissue Rickets Tetany
  20. 25. skeletal deformities muscular relaxation psychoneurological symptoms Clinical manifestation
  21. 26. <ul><li>Four stage </li></ul><ul><li>Early active stage </li></ul><ul><li>Active stage </li></ul><ul><li>Recovery stage </li></ul><ul><li>Sequelae stage </li></ul>
  22. 27. Psychoneurological symptoms irritability restlessness night startle increased sweating occipital baldness Early active stage
  23. 28. <ul><li>Biochemical changes </li></ul><ul><li>Serum calcium normal (2.2 ~ 2.7mmol/l) </li></ul><ul><li>Phosphate normal or slightly low </li></ul><ul><li>(1.30 ~ 1.78mmol/l) </li></ul><ul><li>calcium multiply by phosphate slightly low </li></ul><ul><li>Alkaline phosphatase normal or high </li></ul>Early active stage
  24. 29. <ul><li>X-ray </li></ul><ul><li>there’s no obvious change in </li></ul><ul><li>x-ray of bone. </li></ul>Early active stage
  25. 30. occipital baldness
  26. 31. skeletal changes retardation of motor development Active stage
  27. 32. Craniotabes . 3-6 month old infants A pingpong ball sensation Square head over 5-9 months old saddle shaped or cross shaped head Delayed closure of anterior fontanel till 2-3 yrs old, or enlarged fontanel Delayed dentition till 10 months or 1 year old. defects of the enamel caries Head
  28. 33. Craniotabes
  29. 34. Active stage
  30. 35. Active stage
  31. 36. Frontal bossing Active stage
  32. 37. Vitamin D Deficiency: Rickets 1-1.5
  33. 38. Rachitic rosary Costochondral prominence or beading of the ribs the sides of the thorax become flattened the longitudinal grooves develop posterior to the rosary Harrison’s groove Along the lower border of the chest develops a horizontal depression, corresponds with the costal insertions of the diaphragm Pigeon breast deformity The sternum with its adjacent cartilage appears to be projected forward. . Thorax
  34. 39. Rachitic rosary
  35. 40. Rachitic rosary
  36. 41. Harrison’s groove
  37. 43. Funnel deformity
  38. 44. Bracelets of wrist and ankle The enlarged epiphysis can be seen or palpated Bowlegs and knock-knees bending of the softened shafts of the femur tibia and fibula. “ X” or “O” shaped legs coxa variation and greenstick fractures Extremities
  39. 45. Bracelets of wrist
  40. 46. Bracelets of ankle
  41. 50. Scoliosis kyphosis The pelvis entrance is narrowed by a forward projection of the promontory; The exit , by a forward displacement of the caudal part of the sacrum and the coccyx. Spinal column and pelvis
  42. 51. Scoliosis
  43. 52. kyphosis
  44. 53. relaxation of the ligaments the muscles are poorly developed and lack tone potbelly weakness Others the child is indifferent delayed speaking and dentition. Abdominal muscles Gastric and intestinal walls Ligaments and muscles
  45. 54. potbelly
  46. 55. Biochemical changes Serum calcium low < 2.2 mmol/l sometimes normal with the help of parathormone Serum phosphate below 1.5mmol/l calcium multiply phosphate low AKP elevated Active stage
  47. 56. The distal ends appear widened, concave, frayed. The distance from the distal ends of the ulna and radius to the metacarpal bones is increased doesn’t appear on the X-ray. The density of the shafts is decreased . X-ray changes Active stage
  48. 58. metacarpal
  49. 59. The symptoms disappear after treatment. Child becomes more active, normal muscular tone. Recovery stage
  50. 60. <ul><li>Serum Ca and P become normal </li></ul><ul><li>Akp recovers slowly in 1-1.5 month </li></ul>Recovery stage
  51. 61. <ul><li>X-ray improve in 2-3 weeks </li></ul><ul><li>reappearance and wide of line of </li></ul><ul><li>preparation calcification </li></ul><ul><li>increase in density of bone </li></ul><ul><li>gradually returns to normal </li></ul>Recovery stage
  52. 62. diaphyseal
  53. 63. Clinical symptoms disappear blood biochemistry normal x-ray examination different degrees of skeletal deformity Sequelae stage
  54. 65. Congenital rickets Pregnant women suffer from severe osteomalacia or VD deficiency due to less outdoor activity and poorer in dietary intake. The baby may be born with congenital rickets. two clinical types besides typical rickets
  55. 66. <ul><li>Congenital rickets </li></ul><ul><li>The typical symptoms are : </li></ul><ul><li>Enlarged anterior fontanel connect with </li></ul><ul><li>posterior one by a widened bony suture. </li></ul><ul><li>Posterior fontanel dose not close. </li></ul><ul><li>Typical rachitic change. </li></ul><ul><li>Hypocalcemic tetany. Ca and P are low. Akp </li></ul><ul><li>are high, x-ray of long bone reveals typical </li></ul><ul><li>rachitic changes. </li></ul>two clinical types besides typical rickets
  56. 67. Late rickets It occurs over 10-14 yrs. Females>males, with the symptoms of pain in both lower extremities i.e. ankle or knees, restlessness, increased sweating, delayed dentition, but less signs. X-ray reveals typical rachitic changes. two clinical types besides typical rickets
  57. 68. history of inadequate intake of VD clinical observation classical radiological biochemical changes Low serum 25(OH)D 3 is more reliable Diagnosis
  58. 69. Degree mild moderate severe Skeletal deformity none or abnormal exist obvious Skull and thorax Serum calcium normal Serum phosphate normal/ Akp normal/ x-ray normal typical signs deformity fracture clinical degree
  59. 70. Congenital hypothyroidism Characteristic features : dry and coarse skin myxedema subnormal body temperature the lower segment is shorter than the upper retardation of physical and mental development The serum calcium and phosphate are normal X-ray shows a delay in appearance of ossification centers in bone. Differential diagnosis
  60. 71. Congenital hypothyroidism
  61. 72. Chondrodystrophy Special features Protrusion of forehead broad with bulging of metaphysis short and broad fingers lordosis of lumbar spine, kyphosis of hip X-ray: long bones are short, broad and curved metaphysis are broad. Differential diagnosis
  62. 74. Recurrent respiratory infection Associated with iron deficiency anemia and malnutrition. Hypocalcemic tetany Bony deformities and fractures Stunted growth Complication
  63. 75. Aim: Control the development of rickets Prevent malformation Treatment
  64. 76. General therapy Insist on breast feeding from birth Supply with diet rich in VD Stay outdoor for enough sunlight Don’t sit ,stand and walk too much early for prevention of deformities in active rachitic infants Treatment
  65. 77. food VitaminD( µ g) (40iu=1 µ g) Cod liver oil 1tb 34.5 Most fish, 3.5 oz 8 Egg, cooked 0.65 Beef, 3.5 oz 0.18
  66. 78. VD therapy Preventive dosage: 400-800 Iu/day ① Treatment
  67. 79. <ul><li>General dosage </li></ul><ul><li>Oral medication </li></ul><ul><li>2000-6000 IU/d 2-4week 400IU </li></ul><ul><li>Intensive </li></ul><ul><li>30-60×10 4 IU /dose×1 </li></ul><ul><li>over 2-3 m then 400IU </li></ul>Treatment
  68. 80. Calcium therapy Calcium gluconate 1-3g/d 10% calcium chloride active calcium Treatment
  69. 81. Genaral therapy Prevention therapy     The daily requirement of VD is 400 Iu Prematurely born infants: The preventive dosage is 800 Iu/d in the first 3 m, then 400Iu/d No necessity for the child over 3 yrs old VD should also be pregnant and lactating mothers.  Prevention
  70. 82. Tetany of Vitamin D deficiency
  71. 83. rachitic tetany infantile tetany rachitic hypocalcemic convulsion characteristic convulsion carpopedal spasms laryngeal stridor Definition
  72. 84. VD deficiency reduction of intestinal absorption of calcium and phosphate Hypocalcemia   Parathyroid hormone hyperfunction hypofunction Excretion of urinary P↑ decalcification of mobilization of bone old bone↑ Calcium into blood Serum p ↓ Ca normal or slightly↓ Ca X p↓ Failure of Calcification of Osteoid tissue Ca++↓ Accumulation of osteoid tissue Rickets Tetany
  73. 85. Serum calcium is regulated by VD parathormone calcitonin normal lever 2.2-2.7 mmol/l. Chemical pathology
  74. 86. serum calcium <ul><li>Ionized calcium (Ca ++ ) 1.25 mmol/l </li></ul><ul><li>Calcium binding protein 1.13 mmol/l </li></ul><ul><li>Calcium citrate 0.13 mmol/l </li></ul>
  75. 87. Ca ++ is regulated by: blood pH serum protein serum phosphate
  76. 88. In early stage of VD deficiency, the serum calcium falls as with failure of parathyroid compensation The child receives more sunlight in the summer and spring, or at the beginning of VD therapy, large amount of calcium deposits on the bone with less decalcification of the old bone Serum phosphate release from tissues during infection, fever and hunger, the increase of serum phosphate lowers the level of serum calcium Ca ++ may be low when the child is injected with an alkaline drug or albumin Etiology
  77. 89. Typical symptom   Convulsion Carpopedal spasm Laryngospasm Clinical manifestation
  78. 91. Carpopedal spasm
  79. 93. Latent signs Chvostek’s sign Peroneal reflex Trousseau’s sign Clinical manifestation
  80. 94. <ul><li>Chvostek’s sign </li></ul>Tapping anterior to external auditory meatus Clinical manifestation
  81. 95. Systolic diastolic ischemia Clinical manifestation
  82. 96. symptoms of tetany the combined presence of rickets low serum calcium lever (especially Ca ++ ) Diagnosis
  83. 97. Other afebrile convulsion Hypoglycemia blood glucose is below 2.2mmol/l the convulsion can be controlled by glucose injection. Differential Diagnosis
  84. 98. Hypomagnesemia insufficient intake ( artificial feeding) infantile diarrhea, stearrhea hereditary magnesium malabsorptive defect blood magnesium is below 0.58 mmol/l treatment with magnesium can stop the seizures. (25%Mgso 4 , oral or injection) Differential Diagnosis
  85. 99. Epilepsy repeated attacks extremities bend loss of consciousness Electroencephalographic(EEG) changes no response to calcium therapy Differential Diagnosis
  86. 100. CNS Infection meningitis, encephalitis, cerebral abscess fever, poisoning symptoms, coma, intracranial hypertension cerebrospinal fluid (CSF) changes Differential Diagnosis
  87. 101. Acute laryngitis accompanies with upper respiratory infection characteristic hoarseness of voice whooping cough air way obstruction in severe cases Differential Diagnosis
  88. 102. Emergent therapy Stop the convulsion a. 5% chloral hydrate 1-2 ml/kg po/pr b. Luminal 5-7mg/kg im c. Valium 0.2-0.3 mg/kg im/iv Control the laryngospasm a. Oxygen inhalation b. Endotracheal intubation or trache’ostomy if necessary. Treatment
  89. 103. Calcium therapy a. 10% calcium Gluconate 10ml bid i.v; or more b. 10% calcium chloride 5-10ml tid p.o Caution a. Injective of calcium must slow, >10 min b. Don’t mixed with milk c. Other elements supplement i.e. K+, Na+, Mg++ Treatment
  90. 104. VD therapy See the rachitic VD therapy It will begin at 1 week after hypocalcemia is controlled . Treatment
  91. 105. Sources of VD Metabolism and regulation of VD Etiology of Rickets Symptoms and signs of Rickets in active stage Treatment of Rickets Clinical manifestation of Tetany Emergent therapy of Tetany EMPHASIS
  92. 106. THANK YOU