Up to one-third of healthy individuals present asymptomatic LLD, ranging from 5 mm to 2 cm (4). These patients are not aware of their leg’s inequality because, most likely, it existed since childhood or was established gradually over time. The true prevalence of LLD following THA is difficult to quantify because of the variability in definitions and measurement methods (5). Since obtaining stability takes precedence over attaining equal leg length, and based on the intraoperative difficulty of accurate leg length assessment, LLD is relatively common after THA, with overlengthening being more common and less tolerated than residual shortened leg (3). The current estimation of the incidence of this complication derives from small cohort reports. Williamson and Reckling (6) reported an LLD incidence as high as 96% (144/150 patients), with an average lengthening of 1.6 cm (15.9 ± 9.54 mm), where 27% of the patients subjectively noticed the inequality and required heel lift on the opposite side to improve the gain pattern. More recently in a series of 68 patients, Edeen et al. (7) reported an average discrepancy of 9.7 mm, and poor correlation between clinical and roentgenographic measures. Thirty-two percent of the patients were aware of the LLD with more than half being disturbed by it, and the average LLD in this group was 14.9 mm. Jasty et al. (8) reported an incidence of preoperative limb inequality of 50.6% (43/85 patients), ranging from 0.5 to 7.25 cm, compared to only 16% (14/85 patients) postoperatively. Love and Wright (9) reported that 18% of their patients presented postoperative limb lengthening of more than 1.5 cm, out of them 6% only necessitated shoe correction. Parvizi et al. (1) identified 21 patients, out of 6,954 primary and revision THAs, who underwent revision surgery for symptomatic LLD. Condensing the literature reports, the incidence of LLD after THA ranges from 1% to 27% with inequality value varying from 3 to 70 mm, with a mean of 17 mm (3). Indisputably, the literature evidence had revealed that LLD is quite common following THA and that it cannot be completely eliminated. The boundaries between acceptable and unacceptable inequality remain poorly defined. In general, it has been shown that up to 10 mm of limb disparity may be well tolerated by most patients (3) and that more than 1.5 cm of lengthening is associated with backache, uncomfortable gait, and nerve palsy, compromising an otherwise excellent outcome of hip arthroplasty. A reasonable target is to obtain a stable prosthesis with LLD less than 7 mm (10).

LLD is basically divided into two major categories: structural (or true LLD) and functional (or apparent LLD) (4).
Management and prognosis is different for each type, therefore it is crucial to discern between the two etiologies. Most of the time, LLD is attributable to functional causes and not to true lengthening (11). The prognosis of functional LLD is favorable, where in most circumstances, the condition resolves over time with physical therapy (11). Combination of the two discrepancies may coexist magnifying or balancing each other. It is important to recognize functional discrepancy, which constitutes the subjective perception of the patient, to avoid unnecessary revision surgery and to reassure the patient.

True LLD consists of concrete differences in the cumulative length of bony structures and/or thickness of the cartilaginous surfaces of the lower limb (4). Structural LLD may be present before surgery or may result from the prosthesis implantation. Common causes of preoperative LLD include dysplastic hips (DDH), protrusion acetabuli, coxa vara, flexion contractures, spinal deformities, previous osteotomies for treatment of dysplasia, uncorrectable pelvic tilts, neuromuscular disorders, malunion of previous fractures resulting in distorted anatomy of the proximal femur, or sequelae of any pediatric conditions which contributed to true LLD (physeal arrest or other growth abnormalities). In advanced osteoarthritis, complete obliteration of the joint space as a result of full thickness loss of the cartilage may cause shortening of the more affected side, which is often unnoticed by the patients. Similarly, advanced osteoarthritis of the ipsilateral knee may cause shortening of the affected limb through subsequent coronal deformity of the joint (severe varus or valgus) or frontal deformity (knee flexion contracture). Patients presenting any of the aforementioned pathologies are at risk for developing postoperative LLD, and should undergo thorough preoperative clinical and radiographic evaluation. True LLD may ensue from the technical aspect of the procedure, and is more commonly related to overlengthening of the operated limb. The main cause of postoperative LLD is component malpositioning which may affect LLD either directly or indirectly (1). Common causes of inappropriate component positioning directly affecting the LLD include inferiorization of the acetabular component (placement of the socket inferior to the teardrop) and superiorization of the femoral component (placement of the center of the femoral head proximal to the tip of the greater trochanter).

Other, more subtle, but important potential cause of indirect limb lengthening comprises retroversion of the acetabular socket leading to intraoperative instability that is addressed by increasing the femoral neck length and/or the femoral stem offset, to improve the soft tissue tension, hence stabilizing the hip at the price of limb length inequality.

Functional LLD is the consequence of postural asymmetry of the lower limbs resulting from soft tissue contractures or spinal deformity which may cause pelvic obliquity (4). Functional length of lower limbs is measured clinically from umbilicus or metasternum (xiphisternum) to medial malleolus, whereas true length is measured from the anterior-superior iliac spine (ASIS) to medial malleolus. Hip flexion contracture, which is tightness of the anterior structures crossing the hip (anterior capsule, rectus femoris muscle, iliopsoas muscle), may be the leading cause of apparent LLD. Abduction contracture of the ipsilateral hip or contralateral adduction contracture may tilt the pelvis, relatively lengthening the abducted limb and subsequently causing functional LLD. Primary or degenerative lumbar scoliosis may cause pelvic obliquity which leads to functional LLD through adduction or abduction contracture. In opposite, true LLD may cause pelvic tilt with subsequent compensatory lumbar scoliosis. Cummings et al. (12) showed that the amount of pelvic obliquity increases in a linear pattern as the leg length disparity increases; the authors demonstrated that “posterior innominate bone rotation occurs on the side of the lengthened limb, and anterior rotation occurs on the shorter limb.” Deformities distal to the hip joint, that is, knee frontal or coronal deformities or foot/ankle deformities, may contribute to apparent LLD and limp (10). In cases where LLD exists before surgery, patients’ expectations must be understood, and the patient should be counseled that the goal of surgery is to attempt to correct structural LLD and not necessarily functional LLD. Preoperative oral and written communication between the patient and the surgeon outlining the potential residual LLD after surgery and reiterating on the fact that equality may need to be sacrificed for stability, may be helpful in avoiding unrealistic expectations, patient’s dissatisfaction, and medicolegal implications (2,10).

In the majority of cases, LLD after THA is minor and is associated with no or few symptoms; likewise, moderate LLD, whenever symptomatic, is associated with manageable and untroublesome symptoms. However, significant LLD may cause substantial disability as a result of pain, neurologic symptoms, or functional impairment (1). Common presentations include hip pain, low back pain, paresthesia, abnormal gait, and dislocation (hip instability) (1). Symptomatic LLD may be associated with morbidity including lumbago, sciatica, limp, need for heel lifts, and eventually revision THA (1,10). It is worthy to note that there is no threshold of discrepancy beyond which disability can be predicted. White and Dougall (13) demonstrated no statistical correlation between LLD and functional outcome; in their series of 200 patients, 71.5% had leg length within 10 mm with overall LLD ranging from −11 to +35 mm. In contrast, Gurney et al. (14) reported that there is a breakpoint between 2 cm and 3 cm regarding the effects of LLD on physiologic parameters (oxygen consumption and rating of perceived exertion); the authors showed that LLD of 3 cm induces significant quadriceps fatigue in the longer limb, and that a discrepancy as small as 2 cm may greatly affect the walking capacity of elderly patients with multiple comorbidities. The literature is plush in reporting the clinical repercussion of LLD, including gait abnormalities, disabling low back pain, and sciatic, femoral, and peroneal nerve palsy (12,14,15

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