Sep 032012
 

This is a non-inflammatory deformity of the femoral head caused by a vascular insult leading to osteonecrosis of the capital femoral epiphysis.

Incidence

  • It affects more boys than girls (4:1)
  • Usually presents between 4 and 8 years of age. ( can have a secondary peak between 10 and 12 years ).
  • Caucasians are affected more frequently than other races.
  •  Occurs in approximately 5.5 of 100,000 children per year (and therefore a lifetime risk of developing the disease is about 1 per 1200 individuals)

Etiology

Although the cause is not clear it occurs in those with a delayed skeletal maturation and also there is an increased incidence with a positive family history or in children with a history of low birth weight.

Clinical Features

  • Pain (may present with referred pain in the knee).
  • Decreased range of motion.
  • Limping gait.
  • There are 4 clinical stages: Initial stage, fragmentation, healing and residual.

Differential Diagnosis

Differential Diagnosis includes:

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Aug 012012
 

Rickets is a disease of growing bone that is unique to children and adolescents. It is caused by a deficiency or impaired metabolism of vitamin D, magnesium, phosphorus or calcium. It leads to softening and weakening of the bones.

Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets .

Types of Rickets

Different types have been described and may include:

  • Nutritional Rickets
  • Vitamin D Resistant Rickets
  • Vitamin D Dependent Rickets
    • Type I
    • Type II
  • Congenital Rickets

Pathophysiology

Vitamin D deficiency rickets occurs when the metabolites of vitamin D are deficient. Less commonly, a dietary deficiency of calcium or phosphorus may also produce rickets. Vitamin D-3 (cholecalciferol) is formed in the skin from a derivative of cholesterol under the stimulus of ultraviolet-B light. It is converted into the active metabolite calcitriol after final hydroxylation in the kidney. Calcitriol acts to regulate the body’s calcium metabolism by the following mechanisms:

(1) it promotes absorption of calcium and phosphorus from the intestine; (2) it increases reabsorption of phosphate in the kidney; and, (3) it acts on bone to release calcium and phosphate. Calcitriol may also directly facilitate calcification. These actions result in an increase in the concentrations of calcium and phosphorus in extracellular fluid.

This increase of calcium and phosphorus in extracellular fluid, in turn, leads to the calcification of osteoid, primarily at the metaphyseal growing ends of bones but also throughout all osteoid in the skeleton. Parathyroid hormone facilitates the 1-hydroxylation step in vitamin D metabolism.

In the vitamin D deficiency state, hypocalcemia develops, which stimulates excess secretion of parathyroid hormone. In turn, renal phosphorus loss is enhanced, further reducing deposition of calcium in the bone.

Etiology

The body needs vitamin D to absorb calcium and phosphorus from food. Rickets can occur if thechild’s body doesn’t get enough vitamin D or if his or her body has problems using vitamin D Continue reading »

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Aug 102011
 
The most common congenital disorder of the lower extremities, clubfoot, or talipes, is marked primarily by a deformed talus and shortened Achilles tendon, which give the foot a characteristic clublike appearance. In talipes equinovarus, the foot points downward (equinus) and turns inward (varus), and the front of the foot curls toward the heel (forefoot adduction).
Clubfoot, which has an incidence of about 1 per 1,000 live births, usually occurs bilaterally and is twice as common in boys as it is in girls. It may be associated with other birth defects, such as myelomeningocele, spina bifida, and arthrogryposis. Clubfoot is correctable with prompt treatment.
Causes
A combination of genetic and environmental factors in utero appears to cause clubfoot. Heredity is a definite factor in some cases, although the mechanism of transmission is undetermined. If a child is born with clubfoot, his sibling has a 1 in 35 chance of being born with the same anomaly. Children of a parent with clubfoot have 1 chance in 10.
In children without a family history of clubfoot, this anomaly seems linked to arrested development during the 9th and 10th weeks of embryonic life, when the feet are formed. Researchers also suspect muscle abnormalities, leading to variations in length and tendon insertions, as possible causes of clubfoot.
Signs and symptoms
Talipes equinovarus varies in severity. Deformity may be so extreme that the toes touch the inside of the ankle, or it may be only vaguely apparent.
In every case, the talus is deformed, the Achilles tendon shortened, and the calcaneus somewhat shortened and flattened. Depending on the degree of the varus deformity, the calf muscles are shortened and underdeveloped, with soft-tissue contractures at the site of the deformity. The foot is tight in its deformed position and resists manual efforts to push it back into normal position.
Clubfoot is painless, except in older, arthritic patients. In older children, clubfoot may be secondary to paralysis, poliomyelitis, or cerebral palsy, in which case treatment must include Continue reading »
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