Genu Valgus

Question 1:This is a clinical photograph and x-ray of a child who was referred with genu valgus(Figure 1). What is your approach?

Figure 1.1 a child with bilateral genu valgum

It is important to fully assess such a child. Although, this can be physiological, but it is important to rule out other causes of genu-valgus without unduly worrying the child and the family. Thorough history to explore:

1. Possible aetiology (see table 1.1)
2. The impact of genu valgus on activities
1. Gait disturbance
2. Difficulty running
3. Pain or discomfort
4. Patellar dislocation / subluxation
5. Ligamentous instability
6. Cosmosis

3. The progress
1. Is the deformity getting worse or better
2. Are the symptoms (if any) are getting worse or better
3. What treatments have been tried and the response for it.

My clinical examination is to:

1.     Assess the deformity

a.     Is it bilateral? Is it symmetrical?

b.     Is it severe (measure the intermalleolar distance and tibio-femoral angle). Assess the lower limb rotational profile as other abnormalities may cause an apparent increase in valgus of the knee as the case when there is an increased femoral anteversion. 

c.     Is it in the femur, tibia or both? (Deformity of the proximal tibia is not masked by bending the knee)

2.     Look for potential causes

a.     Weight, BMI

b.     Bony lumps (ostoechdromas

c.     Syndromic appearance

3.     The impact of my potential treatment

a.     Quality of skin, length of the limb and presence of other deformity that may preclude bracing.

b.     Stiffness of joints below that need to be considered when correcting deformity

Investigations are not necessary if the condition is mild or moderate, bilateral and symmetrical and asymptomatic. If not, I would request radiograph (long leg alignment views and blood bone profiles). Further investigations will be guided by my differential diagnosis.

Question 2: What is you indication for surgical intervention?

 Having ruled out secondary causes and observed it long enough to allow for natural correction, my indication will be:

1. Severe (intermalleolar distance > 10 cm at 10 years or > 15 cm at 5 years).
2. Symptoms
3. Unilateral

 Question 3: What will you do? When?

My preferred option is guided growth provided there is enough growth left (boys younger than age 12, girls younger than age 10), and there is no physeal disorder. Alternative is corrective osteotomy or a combination of both, particularly if the deformity is severe.

 In general there are two options of epiphysiodesis:

• Control (reversible):

1.     8 Plates ( Steven’s)

2.     Staples (Blount)

3.     Screw ( Metaizeau)

• Ablation (irreversible):

1.     Bone block (phemister)

2.     Drill and curratte ( Canale)

In osteotomy, three options:

1. Closing wedge ( most preferred as it is inherently stable, no overlengthening, quickier to heal)
2. Opening wedge
3. Neutral wedge

 The site of deformity is established by careful deformity planning. In this patient the mLDFA is reduced. He has a normal mMPTA. This means the deformity is femoral only. He is 10 years old with significant growth remaining, there is no known or apparent physeal disorder so guided growth is appropriate.

 There are two approaches regarding the timing of the surgery:

1. Timed 

Based on the growth remaining in the physis (can be obtained from Green-Anderson growth charts) and the width of the physis, appropriate timing of surgery can be established with reasonable accuracy. The principle is that after hemi-apiphysiodesis, the continued growth at the physis is not linear but represents an arc’ with the radius equals to the width of the physis and the centre is at the tethered end of the physis. The arc of remaining growth, the angle of deformity and the radius of the arc (which is the width of the physis) can be formulated to predict the timing of surgery. There is user friendly software such as Multiplier which can be used for this purpose. Inaccuracy in estimating the skeletal age and measuring the width of physis can lead to overcorrection or under correction which is main disadvantage of this method.

2. Untimed

Perform a reversible hemi-apiphysiodesis when indicated and the patient is monitored closely at 4- to 6-month intervals, and if correction is completed while growth still remains, either reverse the hemiepiphysiodesis or complete the remaining lateral portion of the physis to prevent overcorrection.

Question 4: Figure 1.2 shows x-rays of a two years, Asian, walking with marked leg bowing. Also, his grandmother noted prominent ankles (more marked on the right).  What can you see on this child plain x ray?

The clinical picture and the radiological findings are very characteristic for Rickets. The physis are widened, bulky and irregular (Clearly visible in the ankle, distal and proximal femur). There is splaying ("cupping") of the bone at the junction of the metaphysis and physis. The widened growth plate is due to lack of mineralization of the cartilage matrix, and this weakens the growth plate.

Rickets usually affects the fastest growing bones in the body. Therefore, I look at the costochondral junctions of the middle ribs, the distal femur, the proximal humerus, both ends of the tibia and finally, the distal ulna and radius. The classic "rachitic rosary" of the chest is due to cartilage overgrowth and metaphyseal splaying at the costochondral junction of the ribs and it is readily visible and palpable.

Figure 1.2 Radiographs of a child with bowed legs

Question 5: How would you manage this child?

There are various causes for Rickets; nutritional, vitamin D resistant Rickets and vitamin D dependent Rickets. These need to be identified and treated accordingly. I usually liaise with the paediatricians who are usually keen to deal with medical side of this condition.

Question 6: What do you expect his biochemical profile?

I expect this child to have low calcium (Ca), phosphate (PO₄ ) and Vitamin D level and high alkaline phosphate (ALP).

Question 7: These are his blood results. Are they consistent with your diagnosis?

Table 1.1 Blood result of the 2 year old Asian child

He has normal Ca, PO_4, high ALP and low vitamin D and these findings are consistent with Rickets. The calcium and PO₄ are usually low early on in the course of rickets; however, their levels normalize as a consequence of increased parathyroid hormone (PTH) secretion (secondary hyperparathyroidism). (Note: this child PTH level was 583.3 ng/L (normal range 12-72)).