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    DR Amanullah Lail: Assistant Professor Paediatrics Duhs/Dmc/Chk

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    Rickets is a disease of growing bones in children caused by a lack of vitamin D and calcium, which prevents proper mineralization of bone. This results in soft, weak bones and skeletal deformities. Symptoms include bowed legs, skull swelling, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels, and x-rays revealing widened growth plates and bone abnormalities. Treatment involves high dose vitamin D supplements to correct deficiencies. Prevention focuses on breastfeeding, adequate milk intake, vitamin D supplementation, and sun exposure to maintain healthy vitamin D levels in both children and mothers.

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    DR Amanullah Lail: Assistant Professor Paediatrics Duhs/Dmc/Chk

    Uploaded by

    paqard
    307 views36 pages
    Rickets is a disease of growing bones in children caused by a lack of vitamin D and calcium, which prevents proper mineralization of bone. This results in soft, weak bones and skeletal deformities. Symptoms include bowed legs, skull swelling, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels, and x-rays revealing widened growth plates and bone abnormalities. Treatment involves high dose vitamin D supplements to correct deficiencies. Prevention focuses on breastfeeding, adequate milk intake, vitamin D supplementation, and sun exposure to maintain healthy vitamin D levels in both children and mothers.

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    Rickets

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    Rickets is a disease of growing bones in children caused by a lack of vitamin D and calcium, which prevents proper mineralization of bone. This results in soft, weak bones and skeletal deformities. Symptoms include bowed legs, skull swelling, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels, and x-rays revealing widened growth plates and bone abnormalities. Treatment involves high dose vitamin D supplements to correct deficiencies. Prevention focuses on breastfeeding, adequate milk intake, vitamin D supplementation, and sun exposure to maintain healthy vitamin D levels in both children and mothers.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    307 views36 pages

    DR Amanullah Lail: Assistant Professor Paediatrics Duhs/Dmc/Chk

    Uploaded by

    paqard
    Rickets is a disease of growing bones in children caused by a lack of vitamin D and calcium, which prevents proper mineralization of bone. This results in soft, weak bones and skeletal deformities. Symptoms include bowed legs, skull swelling, and bone pain. Diagnosis involves blood tests showing low calcium and vitamin D levels, and x-rays revealing widened growth plates and bone abnormalities. Treatment involves high dose vitamin D supplements to correct deficiencies. Prevention focuses on breastfeeding, adequate milk intake, vitamin D supplementation, and sun exposure to maintain healthy vitamin D levels in both children and mothers.

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    of 36

    DR AMANULLAH LAIL

    ASSISTANT PROFESSOR
    PAEDIATRICS
    DUHS/DMC/CHK
    RICKETS
    LEARNING OBJECTIVES
    Identify cases of rickets clinically
    Explain Lab Diagnosis
    X-ray findings
    Enumerate preventive measures
    Define osteomalacia
    DEFINITION
    Rickets
    A disease of growing bones
    occurs in children
    before fusion of epiphysis
    due to
    un mineralized matrix
    at the growth plates.
    .

    Osteomalacia

    Failure of mature bones to mineralize
    due to
    prolonged deficiency
    dietary lack of vitamin D
    or
    lack of ultraviolet rays of sun.
    VITAMIN D METABOLISM
    Maintenance of normal plasma levels of
    Calcium & phosphorus.

    Two forms of Vit D are present
    1 Vit D2 (ergocalciferol)
    2.Vit D3 (cholecalciferol)



    Types of Rickets
    Vitamin D Deficient Rickets(nutritional)
    Vitamin D Dependent rickets
    Vitamin D Resistant Rickets
    Renal Rickets
    Hepatic Rickets
    Congenital Rickets


    Normal bone development
    Bone consists of protein matrix osteoid
    Mineral phase-calcium and phosphorus.
    Ossification
    Intramembranous ossification-flat bones
    mesenchymal cells differentiate into
    osteoblasts
    Enchondral ossification long tubular
    bones


    Endochondral ossification
    Growing cartilage at the epiphyseal plates
    is mineralized and resorbed
    and
    replaced by osteoid matrix
    which undergoes mineralization
    to create bone.

    In Rickets
    Mineralization is delayed or inadequate
    osteoid thickens and increase in
    circumference of growth plate.

    Softening of the bones-----Deformities
    CLINICAL FEATURES
    Peak incidence 6 months 2 years
    Irritability
    profuse sweating while asleep
    hypotonia
    frequent respiratory infections.
    Failure to thrive
    Delay in walking,delayed dentition
    Fits,tetany.

    SIGNS
    HEAD
    Larger than normal.
    Frontal bossing (due to excess osteoid)
    Craniotabes (ping pong ball sensation)
    due to thinning of outer table of skull.
    Delayed closure of anterior fontanel
    caput quadratum (square like head)


    THORAX
    Rachitic Rosery (prominent costochondral
    junctions)
    Harrisons sulcus (depression above the
    subcostal margin at the site of diaphragm)
    Pulling of softened ribs by the diaphragm during
    inspiration.
    Pigeon chest deformity.(The weakened ribs
    bend inwards due to the pull of respiratory
    musclesand ,causing anterior protrusion of
    sternum.


    Extremities
    1. Widening of wrists and ankles
    2. Bending of long bones
    results in
    bow legs
    knock knees,(genu valgum)
    3. Green stick fractures
    Widening of wrist joints

    Widening of ankle joints




    LAB DATA
    1.Serum Calcium low (normal 9-11mg/dl)
    2.Serum phosphorus low (normal-5-7mg/dl
    3.Alkaline phosphatase is raised.
    This is the most striking feature,shows
    increased but ineffective activity of
    osteoblasts.
    4. 25-(OH) D levels less than 20 ng/dl
    Confirms of Vitamin D deficiency

    TREATMENT
    STOSS THERAPY
    300,000-600,000 units i/m
    Indrop D 200,000 units
    Repeat x-ray after 3 weeks
    Another dose
    HIGH DOSE VITAMIN D THERAPY
    2000-5000 IU/day over 4-6 weeks
    Followed by intake o 400 I/U daily

    VITAMIN D DEPENDENT
    RICKETS
    Inborn error of vitamin D metabolism
    Autosomal Recessive
    Type 1 and 2
    TYPE 1
    Defect in 1 alpha-hydroxylase responsible for
    the synthesis of 1-25-dihydroxy vit D
    Symptoms in the 1
    st
    year of life
    Tetany,convulsions,musle weakness andgrowth
    failure
    TYPE 2 VIT D DEPENDENT
    End Organ resistance to effects to
    1,25.(OH) D3
    ALOPECIA
    1-25(OH) VIT D is high
    TREATMENT
    Physiological doses of one alpha Leo
    1-2 micrograms per day.
    VITAMIN D RESISTANT RICKETS
    X linked dominant
    Males are more severely effected than
    females
    Vitamin D activation & tubular
    reabsorption of phosphate are impaired
    resulting in hypophosphatemia .
    TREATMENT
    Oral Phosphate and 1 ,25-(OH)2 D3
    0.05micrograms /kg/day.
    PREVENTION
    To prevent rickets, health experts
    recommend
    a child should be breast-fed
    weaned and put on to cow's milk and
    other foods rich in vitamin D and calcium,
    like eggs and dairy products such as
    butter and leafy vegetables.
    Fish
    PREVENTION
    1.Exposure to sunlight (ultraviolet light)
    Early morning and evening 30 minutes per
    week or 2 hours per week maintains
    adequate sun exposure.
    2.Food fortified with Vit A and Vit D
    specially butter,ghee and milk.
    Children under 5 should 500ml of milk
    daily or youghart or cheese daily.
    PREVENTION
    Daily intake of 400 i.u.vitamin D by
    supplemention.
    Lactating mothers should receive
    supplemention with milk or vitamin D to
    ensure prevention of rickets in their
    babies.
    Sun exposure to mothers.

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