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Published by Lorebell

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Published by: Lorebell on Jul 24, 2009
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Vitamin D deficiency that doesn’t allow bone to calcify normally
Prognosis good with treatment
Possible disappreance of bone deformities in children
Also called rickets in infants and young children; osteomalacia inadults
Rare in the United States
Does appear occasionally in breast-fed infants who don’t receive avitamin D supplement or in infants fed a formula with a nonfortifiedmilk base
Occurs in overcrowded, urban areas where smog limits sunlightpenetration
Incidence of rickets is highest in children with darkly pigmented skinwho, because of their pigmentation, absorb less sunlight.
Risk/Precipitating factors
Inadequate dietary intake of vitamin D
Malabsorption of vitamin D
Inadequate exposure to sunlight
Inherited impairment of renal tubular reabsorption of phosphate(from vitamin D insensitivity) in vitamin D-resistant rickets(refractory rickets, familial hypophosphatemia)
Conditions reducing the absorption of fat-soluble vitamin D
Hepatic or renal disease
Malfunctioning parathyroid gland contributing to calcium deficiencyand interfering with vitamin D activation in the kidneys
Fractures of bones
Persistent skeletal pain
Progressive deformities of bones of extremities and spine
Progressive muscle weakness
May be asymptomatic until a fracture occurs
Leg and lower back pain due to vertebral collapse
Bowed legs
Knock knees
Rachitic rosary (beading of ends of ribs)
Enlarged wrists and ankles
Pigeon breast (protruding ribs and sternum)
Delayed closing of fontanels
Softening skull
Bulging forehead
Poorly developed muscles (pot belly)
Difficulty walking and climbing stairs
Vitamin D regulates the absorption of calcium ions from theintestine.
When vitamin D is lacking, falling serum calcium concentrationstimulates synthesis and secretion of parathyroid hormone.
This causes the release of calcium from bone, decreasing renalcalcium excretion and increasing renal phosphate excretion.
When the concentration of phosphate in the bone decreases, ostidmay be produced but mineralization can’t proceed normally.
This causes large quantities of ostoid to accumulate, coating thetrabeculae and linings of the haversian canals and areas beneaththe periosteum.
When bone matrix mineralization is delayed or inadequate, bone isdidorganized in structure and lacks density. The result is grossdeformity of both spongy and compact bone.
Diagnostic studies
Serum calcium concentration less than 7.5 mg/dl
Serum inorganic phosphorus concentration less than 3 mg/dl
Serum citrate level less than 2.5mg/dl
Alkaline phosphatase level less than 4 Bodansky units/dlImaging
X-rays showing characteristics bone deformities andabnormalities such as Looser’s transformation zones(radiolucent bands perpendicular to the surface of the bonesindicating reduced bone ossification confirm the diagnosis)Pseudofracture
is a diagnostic form of osteomalacia.
StructureA band of bone material of decreased density may form alongsidethe surface of the bone. Thickening of theperiosteumoccurs. Theformation of callouses in the affected area is also common. This gives the
appearance of a false fracture. Typical sites of involvement are the axillarymargins of thescapula, ribs, pubic rami, proximal ends of thefemoraand ulna.
Massive oral doses of vitamin D or cold liver oil
For rickets refractory to vitamin D, or in rickets accompanied byhepatic or renal disease, 25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol, or a synthetic-analogue of activevitamin DSurgery
Possible surgical intervention for intestinal disease
Appropriate repair of bone fractures
Nursing Diagnosis
Impaired Physical Mobility related to bone decalcification andbone deformities and possible fractures
High Risk for Injury related to weak bones due todemineralization
Acute Pain related to skeletal deformities and muscular stretching or strain or impingement of nerves.
Disturbed body image related to trauma
Risk for powerlessness related to deformed bones through body
Nursing Responsibility
Much of the orthopaedic nurse’s role in assessing and treatingosteomalacia is collaborative. The goal in treating osteomalacia is to normalizethe clinical, biochemical, and radiologic abnormalities without producinghypercalcemia, hyperphosphatemia, hypercalciuria, nephrolithiasis, or ectopiccalcification. The primary nursing responsibility, after assessment of causativefactors, is client education. If the cause of osteomalacia is related to a simpledietary deficiency of calcium or vitamin D, these deficiencies need to be resolved.Client education is useful in resolving such insufficiencies as well as educatingthe health care community and families at risk. In more complexClient teaching and nursing management for the client with osteomalacia
teach client about modes of treatment and prognosis
teach client about high-vitamin, high-protein, low-fat diet
Instruct client in importance of maintaining adequate nutritionalbalance, provide consultation with appropriate specialist, asindicated (e.g, dietitian, psychiatrist)

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