Osteomalacia - Metabolic Bone Disorders

OSTEOMALACIA

Osteomalacia is a metabolic bone disease characterized by inade-quate mineralization of bone. As a result of faulty mineralization, there is softening and weakening of the skeleton, causing pain, tenderness to touch, bowing of the bones, and pathologic fractures. On physical examination, skeletal deformities (spinal kyphosis and bowed legs) give patients an unusual appearance and a waddling or limping gait. These patients may be uncomfortable with their appearance. As a result of calcium deficiency, muscle weakness, and unsteadiness, there is an increased risk for falls and fractures.

Pathophysiology

The primary defect in osteomalacia is a deficiency of activated vi-tamin D (calcitriol), which promotes calcium absorption from the gastrointestinal tract and facilitates mineralization of bone. The supply of calcium and phosphate in the extracellular fluid is low. Without adequate vitamin D, calcium and phosphate are not moved to calcification sites in bones.

Osteomalacia may result from failed calcium absorption (eg, malabsorption syndrome) or from excessive loss of calcium from the body. Gastrointestinal disorders (eg, celiac disease, chronic biliary tract obstruction, chronic pancreatitis, small bowel resec-tion) in which fats are inadequately absorbed are likely to produce osteomalacia through loss of vitamin D (along with other fat-soluble vitamins) and calcium, the latter being excreted in the feces with fatty acids. In addition, liver and kidney diseases can produce a lack of vitamin D because these are the organs that con-vert vitamin D to its active form.

Severe renal insufficiency results in acidosis. The body uses available calcium to combat the acidosis, and PTH stimulates the release of skeletal calcium in an attempt to reestablish a physio-logic pH. During this continual drain of skeletal calcium, bony fibrosis occurs and bony cysts form. Chronic glomerulonephritis, obstructive uropathies, and heavy-metal poisoning result in a re-duced serum phosphate level and demineralization of bone.

Hyperparathyroidism leads to skeletal decalcification and thus to osteomalacia by increasing phosphate excretion in the urine. Prolonged use of antiseizure medication (eg, phenytoin, pheno-barbital) poses a risk for osteomalacia, as does insufficient vitamin D (dietary, sunlight).

The malnutrition type of osteomalacia (deficiency in vitamin D often associated with poor intake of calcium) is a result of poverty, food faddism, and lack of knowledge about nutrition. It occurs most frequently in parts of the world where vitamin D is not added to food, where dietary deficiencies exist, and where sun-light is rare.

Gerontologic Considerations

A nutritious diet is particularly important in elderly people. Ad-equate intake of calcium and vitamin D is promoted. Because sunlight is necessary for synthesizing vitamin D, people should be encouraged to spend some time in the sun. Prevention, iden-tification, and management of osteomalacia in the elderly are es-sential to reduce the incidence of fractures. When osteomalacia is combined with osteoporosis, the incidence of fracture increases.

Assessment and Diagnostic Findings

On x-ray, generalized demineralization of bone is evident. Studies of the vertebrae may show a compression fracture with indistinct vertebral end-plates. Laboratory studies show low serum calciumand phosphorus levels and a moderately elevated alkaline phos-phatase concentration. Urine excretion of calcium and creatinine is low. Bone biopsy demonstrates an increased amount of osteoid.

Medical Management

The underlying cause of osteomalacia is corrected if possible. If osteomalacia is caused by malabsorption, increased doses of vita-min D, along with supplemental calcium, are usually prescribed. Exposure to sunlight for ultraviolet radiation to transform a cho-lesterol substance (7-dehydrocholesterol) present in the skin into vitamin D may be recommended.

If osteomalacia is dietary in origin, a diet with adequate protein and increased calcium and vitamin D is provided. The patient is instructed about dietary sources of calcium and vitamin D (eg, for-tified milk and cereals, eggs, chicken livers). The safe use of sup-plements is reviewed. Because high doses of vitamin D are toxic and enhance the risk of hypercalcemia, the importance of moni-toring serum calcium levels is stressed. Vitamin D raises the con-centrations of calcium and phosphorus in the extracellular fluid and thus makes these ions available for mineralization of bone.

Physical, psychological, and pharmaceutical measures are used to reduce the patient’s discomfort and pain. When assisting the patient to change positions, the nurse handles the patient gently, and pillows are used to support the body. As the patient responds to therapy, the skeletal discomforts diminish.

Frequently, skeletal problems associated with osteomalacia re-solve themselves when the underlying nutritional deficiency or pathologic process is adequately treated. Long-term monitoring of the patient is appropriate to ensure stabilization or reversal of osteomalacia. Some persistent orthopedic deformities may need to be treated with braces or surgery (eg, osteotomy may be per-formed to correct long bone deformity).