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OSTEOMALACIA

Definition
• Vitamin D deficiency that doesn’t allow bone to calcify normally
• Prognosis good with treatment
• Possible disappreance of bone deformities in children

AKA
• Also called rickets in infants and young children; osteomalacia in
adults

Incidences
• Rare in the United States
• Does appear occasionally in breast-fed infants who don’t receive a
vitamin D supplement or in infants fed a formula with a nonfortified
milk base
• Occurs in overcrowded, urban areas where smog limits sunlight
penetration
• Incidence of rickets is highest in children with darkly pigmented skin
who, 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 deficiency
and interfering with vitamin D activation in the kidneys

Manifestation
• 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
• Kyphoscoliosis

Pathophysiology
• Vitamin D regulates the absorption of calcium ions from the
intestine.
• When vitamin D is lacking, falling serum calcium concentration
stimulates synthesis and secretion of parathyroid hormone.
• This causes the release of calcium from bone, decreasing renal
calcium excretion and increasing renal phosphate excretion.
• When the concentration of phosphate in the bone decreases, ostid
may be produced but mineralization can’t proceed normally.
• This causes large quantities of ostoid to accumulate, coating the
trabeculae and linings of the haversian canals and areas beneath
the periosteum.
• When bone matrix mineralization is delayed or inadequate, bone is
didorganized in structure and lacks density. The result is gross
deformity of both spongy and compact bone.

Diagnostic studies
Laboratory
• 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/dl

Imaging
• X-rays showing characteristics bone deformities and
abnormalities such as Looser’s transformation zones
(radiolucent bands perpendicular to the surface of the bones
indicating reduced bone ossification confirm the diagnosis)

Pseudofracture
• is a diagnostic form of osteomalacia.
• Structure
A band of bone material of decreased density may form alongside
the surface of the bone. Thickening of the periosteum occurs. The
formation of callouses in the affected area is also common. This gives the
appearance of a false fracture. Typical sites of involvement are the axillary
margins of the scapula, ribs, pubic rami, proximal ends of the femora and
ulna.

Management
Medication
• Massive oral doses of vitamin D or cold liver oil
• For rickets refractory to vitamin D, or in rickets accompanied by
hepatic or renal disease, 25-hydroxycholecalciferol, 1,25-
dihydroxycholecalciferol, or a synthetic-analogue of active
vitamin D
Surgery
• Possible surgical intervention for intestinal disease
• Appropriate repair of bone fractures

Nursing Diagnosis

• Impaired Physical Mobility related to bone decalcification and


bone deformities and possible fractures
• High Risk for Injury related to weak bones due to
demineralization
• 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 treating


osteomalacia is collaborative. The goal in treating osteomalacia is to normalize
the clinical, biochemical, and radiologic abnormalities without producing
hypercalcemia, hyperphosphatemia, hypercalciuria, nephrolithiasis, or ectopic
calcification. The primary nursing responsibility, after assessment of causative
factors, is client education. If the cause of osteomalacia is related to a simple
dietary deficiency of calcium or vitamin D, these deficiencies need to be resolved.
Client education is useful in resolving such insufficiencies as well as educating
the health care community and families at risk. In more complex

Client 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 nutritional
balance, provide consultation with appropriate specialist, as
indicated (e.g, dietitian, psychiatrist)
• Teach client how to use ambulatory devices, with physical
therapist’s assistance, as necessary
• Teach client about high fracture risk, even with minor trauma,
related to fragile bone status
• Teach client to space activities and move slowly
• Review limitations in ADLs and promote ongoing independence
in ADLs within scope of limitations
• Review safety and fall precaution, and provide current literature
about occurrence of falls and how to create a safe home
environment
• Recommended reduction of daily alcohol intake
• As treatment progress, as evaluated by serial bone mineral
density scans, discuss gradual resumption of selected activities
• Recommend extra precautions in walking dog in neighborhood
and possibly walking on flat surfaces.

Illustration

Rickets of the knees demonstrates bowing of the femurs, metaphyseal cupping


and fraying,
coarsening of the trabecular pattern, increase in distance between end of shaft
and epiphyseal center,
poorly ossified epiphyseal centers
References
• Nurse’s Quick Check Disease 2005 (Marguerile Ambrose)
• Orthopaedic Nursing (Leona Mourad)
• Orthopaedic Nuring third edition (Ann B. Maher, Susan W.
Salmond and Teresa A. Pellino)