Diseases Info

Rickets

Overview | Symptoms | Treatment | Prevention

Overview

Alternative names

osteomalacia in children; deficiency - vitamin D; renalosteodystrophy; pediatric osteomalacia; vitamin D deficiency; renal rickets

Definition

A disorder involving softening and weakening of the bones ofchildren, primarily caused by lack of vitamin D and/or lack of calcium orphosphate.

Causes, incidence, and risk factors

Rickets is a disorder caused byinsufficiency or inefficient action of activated vitamin D in the body duringchildhood. Vitamin D is a fat-soluble vitamin that may be absorbed from theintestines or may be produced by the skin when the skin is exposed toultraviolet light (particularly sunlight). It is converted to its active form bythe body in 2 steps, occurring first in the liver and completed in the kidneys.In its active form, vitamin D acts as a hormone to regulate calcium absorptionfrom the intestine and to regulate levels of calcium and phosphate in the bones.Active vitamin D is assisted by the actions of other body hormones.

Because vitamin D is fat soluble, conditions that reducedigestion or absorption of fats will decrease the ability of vitamin D to beabsorbed from the intestines. Sunlight is important to skin production ofvitamin D, and environmental conditions where sunlight exposure is limited mayreduce this source of vitamin D. Lack of vitamin D production by the skin mayoccur with indoor confinement or working indoors during the daylight hours, orit may occur in climates with little exposure to sunlight.

When the body is deficient in vitamin D, it is unable toproperly regulate calcium and phosphate levels. If the blood levels of theseminerals becomes low, the other body hormones may stimulate release of calciumand phosphate from the bones to the bloodstream.

Rickets is a bone disease of children. It causes progressivesoftening and weakening of the bone structure. There is a loss of calcium andphosphate from the bone, which eventually causes destruction of the supportivematrix. The parathyroid gland may increase functioning to compensate fordecreased levels of calcium in the bloodstream, resulting in even more loss ofcalcium and phosphorous as it is reabsorbed from the bones. In severe cases,cysts may develop in the bones.

Rickets is fairly rare. It is most likely to occur duringperiods of rapid growth where the body demands high levels of calcium andphosphate. It is usually seen in young children 6 to 24 months old and isuncommon in newborns.

Nutritional causes of rickets occur with a lack of vitamin Din the diet or with malabsorption disorders characterized by poor fatabsorption, including steatorrhea, sprue, and short bowel syndrome. A dietarylack of vitamin D may occasionally occur in people on a vegetarian diet who donot drink milk products or in people who are lactose intolerant (those who havetrouble digesting milk products). A dietary lack of calcium and phosphorous mayalso play a part in nutritional causes of rickets. Rickets from a dietary lackof these minerals is rare because calcium and phosphorous are present in milkand green vegetables. A dietary lack of calcium causes osteoporosis (an adultdisorder causing brittle bones) more often than it causes rickets.

Hereditary rickets is a vitamin D-resistant form of ricketscaused when the kidney is unable to retain phosphate. It is an inherited,sex-linked disorder.

Rickets may also be caused by kidney disorders involvingrenal tubular acidosis. The acidic condition of the body causes the calcium inthe bones to dissolve, leaving soft, weak bones.

Occasionally, rickets may be caused in children withdisorders of the liver or biliary (liver secretion) system, when fats andvitamin D are inadequately absorbed or when the vitamin D is not converted toits active form.

Renal osteodystrophy occurs in people with chronic renalfailure. The manifestation is virtually identical to that of rickets inchildren, and that of osteomalacia or osteoporosis in adults.

Symptoms

• bone pain or tenderness
  arms, legs, spine, pelvis
• skeletal deformities
  • bowlegs
  • forward projection of the breastbone (pigeon chest)
  • "bumps" in the rib cage ("rachitic rosary")
  • asymmetrical or odd-shaped skull
  • spine deformities (spine curves abnormally, including scoliosis orkyphosis)
  • pelvic deformities
• increased tendency toward bone fractures
• dental deformities
  • delayed formation of teeth
  • defects in the structure of teeth, holes in the enamel
  • painful teeth, aching aggravated by sweets, or by cold/hot food ordrinks
  • increased incidence of cavities in the teeth (dental caries)
• fever, especially at night
• restlessness, especially at night
• weakness, progressive
  • decreased muscle tone (loss of muscle strength)
  • decreased muscle development
• muscle cramps
• impaired growth
  • short stature (adult is less than 5 feet tall)
  • growth, slow (child 0-5 years)
• pectus excavatum
• sutures - separated

Signs and tests

A musculoskeletal examination reveals tenderness or pain ofthe bone itself, rather than joints or muscles. In some cases, tetany (prolongedmuscle spasm) may occur if serum levels of calcium are low. Chvostek's sign maybe positive (a spasm of facial muscles with tapping over the facial nerve)indicating low serum levels of calcium.

• Serum calcium and serum phosphorus may be low.
• Serum alkaline phosphatase may be high.
• Arterial blood gases may reveal metabolic acidosis.
• Bone X-rays may show decalcification or changes in the shape/structure ofthe bones.
• A bone biopsy is rarely performed but will confirm rickets.

Other tests and procedures to determine cause may beperformed, such as:

• a PTH
• a calcium; urine
• a calcium (ionized)
• ALP (alkaline phosphatase) isoenzyme

Treatment

The treatment goals are the relief ofsymptoms and the correction of the cause. The replacement of deficient calcium,phosphorous, and/or vitamin D causes symptoms to disappear. There may be a needto use the biologically active form of vitamin D in people who have vitaminD-resistant rickets or who have difficulty converting vitamin D to its activeform. Dietary sources of vitamin D include fish, liver, and processed milk.Exposure to moderate amounts of sunlight is encouraged. The underlying causemust be treated to prevent recurrence. Maintaining good posture helps to correctskeletal deformities. Positioning or bracing may be used to reduce or preventdeformities. A surgical correction of some skeletal deformities may benecessary.

Expectations (prognosis)

The disorder may be corrected withreplacement of deficient minerals and vitamin D. Laboratory values and X-raysusually improve after about 1 week, although some cases may be resistant andrequire large doses of minerals and vitamin D.

If rickets is not corrected while children are still growing,skeletal deformities and short stature may be permanent, but if it is correctedwhile the child is young skeletal deformities often reduce or disappear withtime.

Complications

• chronic skeletal pain
• skeletal deformities
• skeletal fractures, may be spontaneous (without a cause such as trauma)

Calling your health care provider:

Call your health care provider if symptoms indicate ricketsmay be present.

Prevention

Rickets may be avoided by maintaining anadequate intake of calcium, phosphorous, and vitamin D. This may require dietarysupplements in people with associated gastrointestinal or other disorders.

Renal causes of vitamin D should be treated promptly. Levelsof calcium and phosphorous should be monitored regularly in people with renaldisorders.

• Rickets involving hands
• Rickets involving legs
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• Bone Scan (Radioisotope)