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Journal of Ultrasound logoLink to Journal of Ultrasound
. 2021 Feb 16;25(1):83–87. doi: 10.1007/s40477-021-00565-z

Iliotibial band enthesopathy: an unusual cause of lateral knee pain post total knee replacement

G Hegde 1, A Subramanian 1, C Azzopardi 1, A Patel 1, S L James 1, Rajesh Botchu 1,
PMCID: PMC8964855  PMID: 33591565

Abstract

Iliotibial band (ITB) pathology is one of the main causes of lateral knee pain. The enthesopathy of the ITB at its insertion post total knee replacement (TKR) is a rare cause of lateral knee pain. We describe a series of cases of ITB enthesopathy with sonographic findings and management.

Keywords: Iliotibial band, Enthesopathy, TKR

Introduction

Total knee replacement (TKR) is one of the most commonly performed arthroplasty procedures, with approximately 94,500 cases in 2019 in the United Kingdom [1]. Chronic pain following TKR is frequently encountered, leaving almost 20% of the patients unsatisfied with the surgery [2]. This could be secondary to a number of articular or extra-articular pathologies. Imaging is routinely performed to identify the possible cause for it, and frequently, the focus is on the prosthesis, bone, or joint-related abnormalities [3]. Soft tissue abnormalities can also result in pain, which is often localised to a particular region. The iliotibial band (ITB) is one of the lateral structures of the knee joint, and ITB friction syndrome is a well-known cause for lateral knee pain, even post operation. ITB enthesopathy at the insertion site, especially following TKR, is less common and not well described in the literature. This, however, can be a cause of lateral knee pain and can be easily diagnosed with sonography. This study is aimed at describing sonographic abnormalities in ITB enthesopathy which can cause lateral knee pain in post-TKR patients.

Materials and methods

This retrospective study was carried out in the ultrasound department of a tertiary orthopaedic hospital. The cases were identified by searching for the key words “iliotibial band enthesopathy” in the reports of ultrasound (USG) knee scans performed from 2014 to 2020. Patients who had undergone knee surgery other than TKR and patients with lateral knee pain without any history of TKR were excluded from this study. Patients with a history of spondyloarthropathy and crystal deposition disease were also excluded to avoid the non-mechanical causes of ITB enthesopathy. The demographics of the patients, presenting symptoms, imaging findings, time elapsed after TKR to the onset of symptoms, and subsequent treatment were noted through the perusal of electronic medical records. All the USG examinations were carried out by consultant musculoskeletal radiologists using the Siemens Acuson S2000 machine with a 5–14 MHz linear transducer. The ITB at its insertion site was assessed in both the transverse and longitudinal sections using a 2D greyscale and power Doppler USG. Each USG evaluation of the ITB was performed in supine position, with the knee slightly flexed and the hip mildly internally rotated [4]. The ITB was identified by locating the patellar tendon in the long axis and then moving the probe laterally, where it appears as the first identifiable longitudinal structure [4]. It was also directly visualised by placing the probe in the coronal plane on Gerdy’s tubercle [5].

Results

Seven patients fulfilled the search criteria. Four of them were females, and three of them were males. The patient’s age ranged from 49 to 79 years, with an average age of 65 years. All the patients presented with a history of lateral knee pain. The average time elapsed from TKR to the onset of symptoms was 3.6 years, with the shortest surgery-to-symptom duration being 1 year and the longest being 6 years. The imaging findings included the thickening of the tendon, the loss of fibrillar appearance of the tendon, increased vascularity, and heterotopic ossification. Some of the associated findings were minimal joint effusion with or without synovial thickening and chronic lateral collateral ligament sprain with no history of recent trauma. Six of these patients were successfully treated with USG-guided steroid and local anaesthetic injection, and the other patient underwent physiotherapy (Table 1).

Table 1.

Cases with demographics, sonographic findings, associated findings and treatment

Case Age/sex Imaging findings Associated findings if any Treatment
Case 1 49/male

ITB Thickening +

Neovascularity +

None

40 mg triamcinolone

2 ml Ropivacaine(7.5 mg/ml)

Case 2 66/female

ITB Thickening +

Neovascularity +

Heterotopic ossification +

Mild chronic LCL sprain Physiotherapy
Case 3 67/female ITB Thickening + Mild chronic LCL sprain

40 mg triamcinolone

2 ml Ropivacaine(7.5 mg/ml)

Case 4 50/male

ITB Thickening +

Tibial osteophyte +

Minimal Knee joint effusion and synovitis

40 mg triamcinolone

2 ml Ropivacaine(7.5 mg/ml)

Case 5 79/female ITB Thickening + None

40 mg triamcinolone

2 ml Ropivacaine(7.5 mg/ml)

Case 6 66/female ITB Thickening + Minimal Knee joint effusion and synovitis

40 mg triamcinolone

2 ml Ropivacaine(7.5 mg/ml)

Case 7 77/male ITB Thickening + None

40 mg triamcinolone

2 ml Ropivacaine(7.5 mg/ml)

Discussion

Chronic post-operative pain after TKR is often considered as pain persisting for 3 to 6 months that increases in intensity, affecting the quality of life [6]. Although the reasons for this are not fully understood and may be multifactorial, possible causes of post-operative pain can be broadly categorised into intra-articular (joint related) and extra-articular types. While intra-articular causes can be related to implant failure, aseptic loosening, or infection, extra-articular causes could be due to soft tissue abnormalities and neurovascular or psychological factors [3]. Some of the most commonly described aetiologies for chronic pain in the lateral aspect of the knee joint after TKR are popliteal tendinopathy [7], ITB friction syndrome, impingement caused by malposition of the prosthesis [8], and soft tissue impingement in the lateral gutter of the knee [9]. ITB enthesopathy is uncommon and can result in pain in the lateral aspect of the knee joint. This may potentially be an overlooked condition on clinical grounds, and imaging for chronic pain following TKR should routinely examine this aetiology.

The ITB is a strong band formed by the thickening of the fascia lata on the lateral aspect of the thigh. In the proximal aspect, it splits into two layers. The superficial layer is attached to the iliac crest, whereas the deeper layer blends with the lateral part of the capsule of the hip joint. Distally, the iliotibial tract is attached to the anterolateral facet on the lateral condyle of the tibia (Gerdy’s tubercle) [10] (Fig. 1). Along its course in the thigh, it is anchored to the femoral shaft by the lateral intermuscular septum and is continuous with the patellar retinacula. The ITB is also firmly attached to the distal femur by strong, obliquely oriented, fibrous strands [11].

Fig. 1.

Fig. 1

Graphical representation of distal ITB anatomy with insertion at Gerdy’s tubercle of tibia

USG is a particularly good modality to evaluate ITB abnormalities in the post-operative knee given its excellent diagnostic capability, low cost, and wide availability. MRI, although frequently used in evaluating the ITB, is often limited following TKR because of magnetic susceptibility artefacts from metal hardware. Dynamic assessment with USG is an added advantage to evaluate the ITB. Being a superficial structure, the ITB can be very well visualised using a linear high-frequency transducer (up to 18 MHz). On USG, the ITB appears as a linear, relatively hyperechoic structure with a fibrillar appearance [12, 13]. The thickness of the ITB varies from 1.1 to 1.9 mm at the level of the lateral femoral condyle and 3.4 mm ± 0.5 mm at the level of the tibial condyle [13, 14] (Fig. 2).

Fig. 2.

Fig. 2

Longitudinal (a) and transverse (b) USG images demonstrating the normal fibrillar appearance of the ITB (arrow) at Gerdy’s tubercle

ITB enthesopathy is the inflammation of the ITB at its insertion into Gerdy’s tubercle. On USG, all our patients demonstrated abnormal thickening of the ITB near its insertion, with the loss of normal echogenicity, appearing more hypoechoic (Fig. 3). Neovascularity with an increased Doppler signal on power Doppler was visible in three of our patients (Fig. 4). Three other patients demonstrated heterotopic calcification in the ITB at its insertion (Fig. 5). Cortical irregularity of Gerdy’s tubercle was noted in one patient (Fig. 6). Most of the patients complained of tenderness on sonographic compression. There was no evidence of partial or complete tear. We successfully treated six of these patients with USG-guided steroid and local anaesthetic injection. Apart from diagnosis, USG is also extremely useful in providing guidance for needle placement.

Fig. 3.

Fig. 3

Longitudinal USG images of two different patients (a and b) at the level of Gerdy’s tubercle demonstrating hypoechoic, diffusely thickened ITB at its insertion with the loss of normal fibrillar appearance (arrows)

Fig. 4.

Fig. 4

Longitudinal (a) and transverse USG images with power Doppler at the level of Gerdy’s tubercle demonstrating thickened heterogenous ITB with neovascularity

Fig. 5.

Fig. 5

Calcification in ITB enthesopathy. a Longitudinal USG image demonstrating thickened heterogenous ITB with a small focal calcification (arrow). b Large dense focus of calcification at ITB insertion (arrow)

Fig. 6.

Fig. 6

Longitudinal USG image demonstrating bony irregularity (arrow) at the site of ITB insertion

ITB friction syndrome is a well-known condition. Insertional ITB tendinopathy has been described in the literature [15] as an abnormality with a thickened hypoechoic ITB in the region of tibia, distal to the lateral femoral condyle in patients without TKR. This appears similar to ITB enthesopathy, which is characterised by inflammatory changes centred on the ITB insertion/enthesis. Although the exact aetiology is unknown, we hypothesise that this is due to an overuse-related inflammation at the enthesis with possible increased load on the ITB caused by the altered biomechanics following TKR. Further research is needed to explain the exact mechanism of occurrence of this enthesopathy. To the best of our knowledge, no other descriptions of other peer-reviewed studies describe ITB enthesopathy as a cause of pain in post-TKR patients. As pain after TKR is a relatively common complaint and ITB enthesopathy is an easily diagnosable and treatable cause of lateral knee pain post TKR, awareness of this entity for early diagnosis and appropriate management to minimise morbidity are necessary.

Our study had a few limitations. The number of patients in our study was small; however, the USG findings were characteristic. Some of our patients had other associated abnormalities, such as joint effusion and lateral collateral ligament sprain, which could have contributed to the pain, but most of the patients had localised pain over the lateral aspect of the knee with tenderness on sonographic compression. In addition, the response to the corticosteroid injection reiterates that ITB enthesopathy was the primary cause of the pain.

Conclusions

We describe ITB enthesopathy as one of the causes of chronic lateral knee pain in post-TKR patients that can be diagnosed with USG. Post-TKR pain can be attributed to various causes, and ITB enthesopathy should be considered along with other possibilities when lateral knee pain is encountered. USG is a quick, easy, and accurate method of demonstrating ITB enthesopathy. The USG-guided injection of local anaesthesia and steroids is an effective treatment option for this condition in the appropriate clinical setting.

Funding

No financial disclosures.

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

Ethical approval

All the images and the data have been retrospectively obtained from already performed radiological examinations. The examinations were performed with complete ethical standards and patient consent.

Informed consent

Informed consent was obtained from all individual participants included in the study.

Footnotes

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

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