limb length discrepancy in a child is a source of concern and anxiety for the parents and the attending pediatrician. This discrepancy may have a number of causes which also influence its natural history. A thorough clinical examination for the cause, magnitude of discrepancy and associated problem is important. This discrepancy has to be measured accurately and projection made of the expected discrepancy at skeletal maturity. Finally on this background, management decisions have to be taken.
In the past,
limb-lengthening surgery acquired a poor reputation because of lack of understanding of the biological principles involved and the poor technique and technology associated with it. In recent years many advances have taken place in these areas and utilizing these advances we can now achieve lengthening never possible before. Whereas formerly the recommended lengthening ranged up to 20% of the original length of the bone, currently 100% or more lengthening is possible. It is practical today to lengthen any long bone, even the phalanges and metacarpals. Besides this, diverse applications of lengthening devices have been found which can solve a number of complicated orthopedic problems in children e.g. correction of deformities of bones and joints with or without lengthening, simultaneous lengthening of different bones, double lengthening in single bone, bone transportation, healing of recalcitrant non unions and enhancement of the stature to name a few. The possibilities are immense and the field is poised at a very exciting stage with promise and potential for the future.
CAUSES OF LIMB LENGTH INEQUALITYTable 1 lists the
common causes of limb length inequality encountered in pediatric practice
Table 1: Causes of limb length discrepancy
Congenital causes are the best known reasons for a limb length discrepancy. They are the most difficult to treat also. Examples are congenital short femur and the spectrum of proximal focal femoral deficiencies which may exhibit a shortening in the range of 6% to 90% of the femoral length, partial or total absence of the tibia and fibula etc. Other congenital causes of discrepancy would be conditions like hemihypertrophy giving rise to a lengthening and the constriction band syndrome.
Infection can cause shortening in a variety of ways e.g. by causing joint dislocation or by damaging the growth plate. By asymmetric damage to the growth plate, angular and complex deformities can be produced along with shortening. Depending on the growth contribution of a growth plate, the age of the patient at the time of physeal damage and the extent of the growth plate damage whether partial or total, minimal or large amount of shortening can be produced. An example is complete damage to the lower femoral epiphysis inhibiting 70% of the femoral growth or 40% of the total lower limb length. Roughly an inhibition of 1 cm would take place per year of remaining growth. However, this is true only for the latter years of growth. A third way by which infection can cause limb length discrepancy is by causing a pathological fracture which mal-unites.
Posttraumatic malunions would cause an immediate discrepancy of limb length. However damage to growth following trauma would cause an insidious increase in the discrepancy. Interestingly, accurate reduction of fractures e.g. of the femur or tibia may give rise to a lengthening because of a growth stimulation.
Neoplasms and irradiation also act by causing growth plate damage. Some skeletal dysplasias e.g. Ollier's or hereditary multiple exostosis cause shortening of a limb by affecting the growth plate.
Miscellaneous causes of limb shortening would include paralytic causes e.g. poliomyelitis which causes an inhibition of growth. Reduced mass and activity coupled with an abnormal vasomotor control may be responsible for this. Perthes disease and slipped capital femoral epiphysis cause shortening by early fusion across the growth plate and by causing varus of the upper femur. Rarely shortening can be iatrogenic following surgery in the vicinity of a growth plate or following varus osteotomies of the upper femur which shorten the limb.
PATTERNS OF INCREASE IN LIMB LENGTH DISCREPANCYThis is can important factor to consider when planning treatment. If lengthening is carried out in a condition which is progressive e.g. Ollier's diseases, a repeat lengthening would be required at skeletal maturity. On the other hand, posttraumatic malunions may give rise to a static limb length discrepancy.
Shapiro has studied the growth patterns in lower extremity length discrepancies and classified them into 5 patterns. Important in this is type 1 or an upward slope pattern in which the length discrepancy increases with time at the same proportional rate. This happens for example in the proximal focal femoral deficiencies in Ollier's disease and with physeal damage.
Other patterns show varying response with time, e.g. Type V which shows a gradual reversal of the limb discrepancy with time. This underlines the importance of a repeated and regular evaluation and charting of the discrepancy to enable conclusions to be formed about the projected final limb length discrepancy.