Bowlegs (Genu Varum) & Tibia Vara
Children with bowlegs, when standing straight with toes pointed forward, have ankles that can touch each other, but knees that do not. If they are more than 3 inch apart, they are considered not normal.
Bowlegs is a condition involving the shin and thigh (tibia and femur) bones. Having
- Bow legs at birth with tibia vara
bowlegs is considered a normal part of growth in young children, as are ‘knock-knees’ in which both knees point inward but ankles are away, again more than 3 inches is not normal. Bowlegs usually correct by the time the child is 3-7 years old.
But if the child remains bowlegged, it may be a sign of an underlying bone disease, such as Blount’s disease or rickets, which is caused by a Vitamin D deficiency. Vitamin C deficiency could be contributory.
Approach to treatment.
Bowlegs cannot be corrected permanently without first treating the basic cause for the condition. In the meantime, doctors try to make sure that the child’s legs can straighten themselves naturally with growth. If this doesn’t work, doctors may require the child to wear corrective leg braces. Severe cases would require surgery.
Knock-Knees (Genu Valgum)
The standing child whose knees touch but whose ankles do not and are atleast 3 inches apart are said to have knock knees. During childhood, knock knees are a normal stage of development and growth (physiologic valgus) and is slightly more common in girls, although boys do develop it.
Between birth – 18 months, an outward-turning (varus) alignment from hip to knee to ankle is normal.
Between about 18 – 24 months, this alignment normally becomes neutral.
Between 2 and 5 years old, an inward-turning (valgus) alignment is normal.
The alignment returns to neutral as the child grows.
1 in 1,000 won’t straighten naturally. 99 percent of the time, a 3 or 4 year-old with physiologic genu Valgum would be near normal.
Approach to treatment
Doctors should closely monitor the child’s leg development, to make sure that the legs straighten themselves naturally. If the condition doesn’t self-correct, the child may require corrective leg braces. Severe cases may require surgery.
Apparent when a child is 2 – 3 years old and it may increase in severity until age 4. An abnormal walking gait can also be a sign.
Self-corrects by the time a child is about 7 – 8 years. Knock-knees actually help a child to maintain balance in the initial period. Occasionally, they persist into adolescence.
• Some cases, especially in a child who’s 6 or older, may be a sign of an underlying bone disease, such as osteomalacia or rickets.
• Obesity can contribute to knock knees—or can cause gait (walking) problems.
• The condition can occasionally result from an injury to the growth area of the shin bone (tibia), which may result in just one knocked knee.Knock-knees actually help a child to maintain balance in the initial period and all children have this for a certain period.
The doctor’s checkup for diagnosing Knock knees and Bow legs can include measurements of
child’s length and height
weight and body mass index (BMI)
knee extensions and rotations
leg-lengths and leg symmetry
observation and assessment of gait
Radiology: One X-Ray preferably only an AP view is initially recommended, avoid more.
Night brace, particularly if a family history of knock knees exists; the brace attaches to a shoe and works by pulling the knee up into a straight position
Orthotics: Shoes with inner heel wedge and/or an arch pad.
Genu Recurvatum
If the defect is isolated, conservative treatment is preferred, using casts, corrective splints, physical therapy, braces, and gait training. Of these physical therapy is the mainstay and done mostly by the parents who are well tutored before by the treating doctors.
Surgery is usually the last option.
In our case, given the fact that it was an isolated deformity, it was treated early with conservative intervention, and the prognosis has appeared good. The infant, 18 months old at the time of this writing, was walking with no apparent difficulty, continued to be monitored by a pediatric orthopedic surgeon, and was receiving physical therapy.
Rickets
Rickets is a disorder caused by a prolonged deficieny of mainly vitamin D, calcium, or phosphate. It leads to softening and weakening of the bones in children
Causes
Vitamin D helps the body absorb calcium and phosphate from the intestines. If the blood levels of these minerals become too low, the body may produce hormones that cause calcium and phosphate to be released from the bones. This leads to weak and soft bones.
Symptoms: (When to see a doctor)
Delayed growth
Aches and pains
Muscle weakness
Skeletal deformities
Source:
Vitamin D is absorbed from food or produced by the skin when exposed to sunlight. Lack of vitamin D production by the skin may occur in people who:
Keep themselves covered in black clothing with little exposure to sunlight
Stay and work indoors most of the time, dark- skinned children
Vitamin D deficient diet
Are lactose intolerant (have trouble digesting milk products)
Do not drink milk or take milk products
Follow a vegetarian diet
Infants who are breastfed only.
Hereditary rickets is a form of the disease that can runs through families. It occurs when the kidneys are unable to retain the mineral phosphate. Rickets may also be caused by kidney disorders that involve renal tubular acidosis.
If a vitamin D or calcium deficiency causes rickets, adding vitamin D or calcium to the diet generally corrects any resulting bone problems for the child. Rickets due to a genetic condition may require additional medications or other treatment. Occasionally skeletal deformities caused by rickets may need surgery.
Bowed legs. Thickened wrists and ankles
Breastbone (sternum)projection Delayed Fontanelle closure
Infants who are breastfed only may develop vitamin D deficiency. Human breast milk does not supply the proper amount of vitamin D. This can be a particular problem for darker-skinned children in winter months (when there are lower levels of sunlight).
Fat digestion or absorption disorders and liver disorders will make it more difficult for vitamin D to be absorbed or converted to active form.
Blood Tests
Serum calcium
Bone x-rays
Serum alkaline phosphatase
Serum phosphorus
Other tests and procedures include the following:
Alkaline phosphatase (ALP) isoenzyme
Calcium (ionized)
PTH
Urine calcium
Treatment
The aim of treatment are to relieve symptoms and correct the cause.
Replacing calcium, phosphorus, or vitamin D that is lacking will eliminate most symptoms of rickets.
Dietary sources of vitamin D include fish, liver, and processed milk. Exposure to moderate amounts of sunlight is encouraged. If rickets is caused by a metabolic problem, a prescription for vitamin D supplements may be needed.
Positioning or bracing may be used to reduce or prevent deformities. Some skeletal deformities may require corrective surgery.
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Scurvy
Scurvy is a state of dietary deficiency of vitamin C (ascorbic acid). The human body lacks the ability to synthesize and make vitamin C and therefore depends on exogenous dietary sources to meet vitamin C needs. Consumption of fruits and vegetables or diets fortified with vitamin C is essential to avoid ascorbic acid deficiency. Although scurvy is uncommon, it still occurs and can affect adults and children who have chronic dietary vitamin C.
The body’s pool of vitamin C can be depleted in 1-3 months.
Poor wound healing and breakdown of old scars may be seen. Capillary fragility can beseen, beading may be present at the costochondral junctions of the ribs. This finding is known as the scorbutic rosary (ie, sternum sinks inward) and may occur in children. The scorbutic rosary is distinguished from rickety rosary (which is knobby and nodular) by being more angular and having a step-off at the costochondral junction. Fractures, dislocations, and tenderness of bones are common in children.
Metaphyseal flaring and Pelken Spur can be seen on X-Rays with pencil thinning of cortex.
Bleeding into the joints causes painful swelling of joints (hemarthroses). Sub-periosteal hemorrhage may be palpable, especially along the distal portions of the femurs and the proximal parts of the tibias of infants. Bleeding into the femoral sheaths may cause femoral neuropathy and bleeding into the muscles of the arm and the leg may cause woody edema.
After 1-3 months of severe vitamin C deficiency, patients may develop short breath and bone pain. Myalgias may occur because of reduced carnitine production. Skin changes with roughness, gum bruising, loose teeth, poor wound healing, easy bruising and petechiae, and emotional changes and irritability may occur. Dry mouth and dry eyes like Sjögren syndrome may occur.
Blood Tests: Plasma Vitamin C level
Plasma ascorbic acid level may help in establishing the diagnosis, but this level generally reflects the recent dietary intake rather than the actual body levels of vitamin C. Signs of scurvy can occur with low -to-normal serum levels of vitamin C.
The best confirmation of the diagnosis of scurvy is its resolution of symptoms and improved radiological evidence following vitamin C administration.