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OSTEOMALACIADefinition
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Vitamin D deficiency that doesn’t allow bone to calcify normally
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Prognosis good with treatment
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Possible disappreance of bone deformities in children
AKA
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Also called rickets in infants and young children; osteomalacia inadults
Incidences
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Rare in the United States
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Does appear occasionally in breast-fed infants who don’t receive avitamin D supplement or in infants fed a formula with a nonfortifiedmilk base
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Occurs in overcrowded, urban areas where smog limits sunlightpenetration
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Incidence of rickets is highest in children with darkly pigmented skinwho, because of their pigmentation, absorb less sunlight.
Risk/Precipitating factors
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Inadequate dietary intake of vitamin D
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Malabsorption of vitamin D
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Inadequate exposure to sunlight
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Inherited impairment of renal tubular reabsorption of phosphate(from vitamin D insensitivity) in vitamin D-resistant rickets(refractory rickets, familial hypophosphatemia)
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Conditions reducing the absorption of fat-soluble vitamin D
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Hepatic or renal disease
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Malfunctioning parathyroid gland contributing to calcium deficiencyand interfering with vitamin D activation in the kidneys
Manifestation
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Fractures of bones
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Persistent skeletal pain
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Progressive deformities of bones of extremities and spine
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Progressive muscle weakness
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May be asymptomatic until a fracture occurs
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Leg and lower back pain due to vertebral collapse
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Bowed legs
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Knock knees
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Rachitic rosary (beading of ends of ribs)
 
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Enlarged wrists and ankles
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Pigeon breast (protruding ribs and sternum)
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Delayed closing of fontanels
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Softening skull
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Bulging forehead
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Poorly developed muscles (pot belly)
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Difficulty walking and climbing stairs
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Kyphoscoliosis
Pathophysiology
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Vitamin D regulates the absorption of calcium ions from theintestine.
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When vitamin D is lacking, falling serum calcium concentrationstimulates synthesis and secretion of parathyroid hormone.
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This causes the release of calcium from bone, decreasing renalcalcium excretion and increasing renal phosphate excretion.
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When the concentration of phosphate in the bone decreases, ostidmay be produced but mineralization can’t proceed normally.
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This causes large quantities of ostoid to accumulate, coating thetrabeculae and linings of the haversian canals and areas beneaththe periosteum.
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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
Laboratory
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Serum calcium concentration less than 7.5 mg/dl
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Serum inorganic phosphorus concentration less than 3 mg/dl
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Serum citrate level less than 2.5mg/dl
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Alkaline phosphatase level less than 4 Bodansky units/dlImaging
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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
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is a diagnostic form of osteomalacia.
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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.
Management
Medication
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Massive oral doses of vitamin D or cold liver oil
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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
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Possible surgical intervention for intestinal disease
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Appropriate repair of bone fractures
Nursing Diagnosis
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Impaired Physical Mobility related to bone decalcification andbone deformities and possible fractures
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High Risk for Injury related to weak bones due todemineralization
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Acute Pain related to skeletal deformities and muscular stretching or strain or impingement of nerves.
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Disturbed body image related to trauma
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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
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teach client about modes of treatment and prognosis
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teach client about high-vitamin, high-protein, low-fat diet
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Instruct client in importance of maintaining adequate nutritionalbalance, provide consultation with appropriate specialist, asindicated (e.g, dietitian, psychiatrist)
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