The difference in the length of any limb, upper or lower, is called limb-length discrepancy (LLD) or, depending on your author, limb length inequality (LLI). Usually, upper limb LLD causes few problems, unless the discrepancy is really significant and leads to subsequent changes in arm function. I will, therefore, focus on LLD in the legs. For ease of reference and, as it is often seen this way, LLD will be used to mean leg-length discrepancy.
Overview
LLD is typically divided into two broad categories:
1. Structural discrepancies. These occur when either the thigh (femur) or shin (tibia) bone or both bones in one leg are different lengths to the corresponding bones in the other leg. Small discrepancies between the length of bones on each side of the body are common; the problem occurs when the difference in length is more pronounced (usually .5 to 1 inch difference is considered within normal limits). A structural LLD also is called a true leg length discrepancy and is considered a true discrepancy because the cause is an actual physical length difference in the lower extremity bones. Structural LLD is usually as a result of genetic conditions, nutritional deficiency or traumatic cause such as fracture or disease loss of bone. A fuller guide is shown below:
a. Previous injury to bone. A broken bone can cause an LLD if the bone heals in a shortened position. This typically occurs if the bone fractures into several shards and is more likely in an open fracture. Remarkably, broken bones in children can lead to overgrowth of bone few years after healing, resulting in a longer than normal bone. Overgrowth commonly occurs in young children with femoral fractures. However, if the break runs through the growth centre near the end of a bone and damages the cells responsible for growth of the bone, this may cause slower growth, resulting in a shorter leg.
b. Bone diseases. Bone disease such as osteomyelitis, can also injure the growth plate, where growth in length occurs, so that a discrepancy occurs gradually over time. Others include neurofibromatosis, multiple hereditary exostoses and Ollier disease. Bone tumours and the treatments designed to eradicate them can also be related to leg length discrepancy. Tumours, like an infection, can invade the growth plate and treatments, like chemotherapy, can also damage the plate.
c. Bone infection. Bone can occur in children while they are growing can cause significant LLD, especially if the infection happens in infancy. Inflammation of joints during growth, such as juvenile arthritis, can cause LLD.
d. Hemihypertrophy (one side too big) or hemiatrophy (one side too small) are rare limb length discrepancy conditions. In these conditions, the arm and leg on one side of the body are either longer or shorter than the arm and leg on the other side of the body. There may also be a difference between the two sides of the face.
e. Other causes. Other causes include inflammation (arthritis) and neurologic conditions.
f. Idiopathic difference. Sometimes the cause of limb length discrepancy is unknown. These conditions are usually present at birth, but the leg length difference may be too small to be detected. As the child grows, the limb length discrepancy increases and becomes more noticeable.
2. Functional discrepancies. These occur when the leg lengths are equal but the symmetry is altered usually somewhere above the hip which in turn disrupts the symmetry of the legs. Functional LLD is more common than the structural form, however the causes can be harder to determine. In functional LLD it appears that one leg may be longer than the other, but there is no significant difference in the length of the lower extremity bones. Instead, a postural distortion above the hip joints has caused one lower extremity to appear longer or shorter than the other.
The causes of functional LLD are numerous with the most common set out below:
a. Sacroiliac joint dysfunctions leading to pelvic obliquity – and I think the most common, at least in my clinic. This is one of the key findings from a massive study carried out by one of our co-authors, Augusto Manganiello was that just a small LLD can lead to significant pelvic torsion and further sine biomechanical problems.
b. Hip joint dysfunction causing compensatory alterations by the joint and muscles that move the joint. Congenital (present at birth) problems that alter alignment of the hips, such as coxa vara and developmental dislocation of the hip fall into this category.
c. Neuromuscular problems, such as cerebral palsy, which causes problems with alignment and posture can also lead to a functional discrepancy.
d. I am told that a growth in muscle mass itself may lead to LLD. Apparently, the Vastus lateralis muscle seems to push the iliotibial band (ITB) laterally leading to femoral angle compensations to maintain a line of progression during the gait cycle. This is bound to be misdiagnosed as ITB syndrome and subsequently treated incorrectly.
e. And the internal rotators of the lower limb being chronically short or in a state of contracture though I hate this sort of diagnosis as there’s never a decent answer to the why?
f. And apparently, failure or incorrect loading of the Back Force Transmission System (the longitudinal-muscle-tendon-fascia sling and the oblique dorsal muscle-fascia-tendon sling). See the proceedings of the first and second Interdisciplinary World Congress on Low Back Pain.
g. And one I found last week with a patient who has uber lax ligaments and has developed one hyperflexed knee leading to a subsequent low hip on that side.
It is important to distinguish between the two as they are treated differently.
Incidence
One study reported that 32% of 600 military recruits had a 1/5 inch to a 3/5 inch difference between the lengths of their legs. In a study by a bloke called Knutson, who is no slouch, he concluded:
“Using data on leg-length inequality obtained by accurate and reliable x-ray methods, the prevalence of anatomic inequality was found to be 90%, the mean magnitude of anatomic inequality was 5.2 mm (SD 4.1). The evidence suggests that, for most people, anatomic leg-length inequality does not appear to be clinically significant until the magnitude reaches ~ 20 mm (~3/4″).
Conclusion
Anatomic leg-length inequality is near universal, but the average magnitude is small and not likely to be clinically significant.”
The most accurate way to identify a structural LLD is with a lower extremity radiograph that allows a comparison of bone measurement with the other limb. If this is not an option, a comparison of the measurement between bony landmarks on each side with a tape measure is another option, although it is somewhat less accurate.
Treatment
Structural discrepancies
For structural LLD the therapeutic goal must be to flatten the pelvis. Treatment of structural LLDs depends on the severity of discrepancy and the requirements of the patient. Treatment is done in the following ways:
1. Orthotics: A shoe lift can be used to treat discrepancies up to 2 cm. The lift should be large enough to allow the patient to walk normally.
2. Shortening procedures: The following procedures, used to shorten the longer leg, may be recommended for some children, in cases where the leg length discrepancy is expected to be between 2 and 6 cm at maturity. Shortening is considered safer and results in less complications than lengthening procedures:
a. Epiphysiodesis – This procedure slows the rate of growth of the long leg, allowing the short leg to catch up. The operation involves the creation of bony ridge, usually by repositioning a block of bone in the region, that tethers the growth plate, preventing future growth. The disadvantages of this procedure include shortened stature, surgery on the unaffected extremity, and the irreversibility of the procedure.
b. Epiphyseal stapling – This operation is performed to slow the rate of the growth temporarily. Staples are surgically inserted on each side of the growth plate. Once equalization has been achieved, the staples are removed.
c. Bone resection – This operation, removal of a section of bone to equal out the discrepancy, can be performed in adults or adolescents who are no longer growing.
3. Lengthening procedures are usually reserved for discrepancies that are more than 4 cm. While one of the obvious advantages of lengthening is the achievement of height, it is not always the method of choice because the process used is technically difficult and has a significant rate of complications, discussed further below.
For this procedure, a customized apparatus that encircles the leg is surgically attached to the limb that will be lengthened by pins. Limb lengthening correction works on the principle of bone regeneration (osteogenesis) as segments of the bone are pulled apart (distracted). To achieve this, a bone is first cut in two during surgery. Days after surgery, the two ends of the bone are very gradually pulled apart through continual adjustments that are made to the apparatus, usually at a rate of 1 mm per day. This gradual distraction leads to formation of new bone between the two ends, at the site of lengthening. After the process is complete, and the bone is given a chance to harden, the apparatus is surgically removed. A cast or brace may be required for some time for further protection. Common complications associated with lengthening procedures include pin tract infection, wound infection, hypertension, partial dislocation of the hip and knee, a delayed union of the bone and fatigue fractures after removal of the lengthening apparatus.
4. Prosthetics: These devices, which are typically used to treat a child who has had to have an amputation, may be satisfactory for some patients with very large discrepancies, who would not benefit from other lengthening or shortening procedures
But, any structural LLD <20 mm and LLD caused by supra-pelvic muscle hypertonicity may interact in a standing posture, but not in an prone or supine posture as they are unloaded postures. So, any LLD due to suprapelvic muscular hypertonicity should be eliminated before any necessary treatment of structural LLD starts.
The lateral flexion of the lumbar spine was assessed in a group of subjects 10 years after structural LLD caused by femoral fracture that occurred after they were skeletally mature. Despite the compensatory lumbar scoliosis, these subjects had symmetrical lumbar lateral flexion, prompting the authors to comment that the “…acquired leg-length discrepancy produced little permanent structural abnormality in the lumbar spine…”. So, significant anatomic LLD acquired after skeletal maturity does not result in adaptive structural changes within a 10-year period.
However, another study from the same orthopaedic centre looked at the effects of significant (so about 3 cm) structural LLD acquired prior to skeletal maturity in mature subjects (so between 17–38 years old). In this group, there was considerable asymmetry of lumbar lateral flexion after placing a lift under the short leg to level the pelvis. This indicates that the body had permanently compensated to the structural changes in the spine/pelvis.
This type of permanent compensation in preskeletal maturity LLD was also found in subjects with pelvic obliquity. Young et al. found that placing a lift under the foot of a subject with no pelvic obliquity resulted in greater lumbar lateral flexion towards the now high iliac crest side. In subjects with pelvic obliquity, when the lift was put under the foot on the side of the low iliac crest in order to level the crest, lateral flexion was increased towards the formerly low crest side. If the body remodels and adapts to the pelvic obliquity or torsion caused by anatomic LLI, then by putting a lift under the side of the “low” iliac crest, one is actually raising what the body has adapted to as level. In other words, the unlevel pelvis of those with anatomic LLI has been adapted to and is now “normal”, and putting a lift under the low side has the same effect as putting a lift under the leg of an even pelvis!
