The iliotibial tract: imaging, anatomy, injuries, and other pathology

Abstract

The iliotibial tract, also known as Maissiat's band or the iliotibial band, and its associated muscles function to extend, abduct, and laterally rotate the hip, as well as aid in the stabilization of the knee. A select group of associated injuries and pathologies of the iliotibial tract are seen as sequela of repetitive stress and direct trauma. This article intends to educate the radiologist, orthopedist, and other clinicians about iliotibial tract anatomy and function and the clinical presentation, pathophysiology, and imaging findings of associated pathologies. Specifically, this article will review proximal iliotibial band syndrome, Morel-Lavallée lesions, external snapping hip syndrome, iliotibial band syndrome and bursitis, traumatic tears, iliotibial insertional tendinosis and peritendonitis, avulsion fractures at Gerdy's tubercle, and Segond fractures. The clinical management of these pathologies will also be discussed in brief.

Full text

REVIEW ARTICLE
The iliotibial tract: imaging, anatomy, injuries, and other
pathology
Russell Flato
1
&Giovanni J. Passanante
1
&Matthew R. Skalski
2
&Dakshesh B. Patel
1
&
Eric A. White
1
&George R. Matcuk Jr.
1
Received: 15 November 2016 /Revised: 6 February 2017 /Accepted: 9 February 2017 /Published online: 25 February 2017
#ISS 2017
Abstract The iliotibial tract, also known as Maissiat’sband
or the iliotibial band, and its associated muscles function to
extend, abduct, and laterally rotate the hip, as well asaid in the
stabilization of the knee. A select group of associated injuries
and pathologies of the iliotibial tract are seen as sequela of
repetitive stress and direct trauma. This article intends to edu-
cate the radiologist, orthopedist, and other clinicians about
iliotibial tract anatomy and function and the clinical presenta-
tion, pathophysiology, and imaging findings of associated pa-
thologies. Specifically, this article will review proximal
iliotibial band syndrome, Morel-Lavallée lesions, external
snapping hip syndrome, iliotibial band syndrome and bursitis,
traumatic tears, iliotibial insertional tendinosis and
peritendonitis, avulsion fractures at Gerdy’s tubercle, and
Segond fractures. The clinical management of these patholo-
gies will also be discussed in brief.
Keywords Iliotibial tract .Maissiat’sband.Fascia lata .
Gerdy’stubercle .Iliotibialband syndrome .Externalsnapping
hip
Introduction
The iliotibial (IT) tract is a portion of the fascia lata, the deep
fascia of the thigh investing the muscles of the hip and lower
extremity in this region. Specifically, the IT tract is a strong
band of the fascia lata located in the lateral thigh [1]. The IT
tract receives contributions from the tensor fascia lata (TFL)
and gluteus maximus muscles in the proximal thigh and in-
serts distally about the knee, including onto the proximal tibia
(Fig. 1)[2]. It transmits forces from the hip to the knee and
functions as one of the lateral stabilizers of the knee joint [3,
4]. Traumatic or overuse injuries of the IT tract can cause
significant pain and impairment of physical activity and occur
relatively commonly. A recent epidemiological study in the
USA concluded that the incidence of acute knee injuries pre-
senting to emergency departments is 2.29 per 1000 population
[5], and evidence suggests that perhaps roughly half of all
patients with acute knee injuries will demonstrate injury to
the IT tract on magnetic resonance imaging (MRI) [6].
Iliotibial band friction syndrome, caused by repetitive physi-
cal activity, is believed to be the most common running injury
to the lateral knee and accounts for 15–24% of overuse inju-
ries in cycling [7]. Imaging, particularly MRI, can aide in the
diagnosis of both acute and chronic injury to the IT tract. As
such, it is important for the radiologist to be familiar with the
normal anatomy of the IT tract as well as the clinical presen-
tation and imaging findings of its various pathologies.
Anatomy of the iliotibial tract
The fascia lata is the deep investing fascia of the thigh,
encasing the muscles of the hip and lower extremity in this
region [1]. The iliotibial (IT) tract is a strong longitudinal band
of this deep fascia in the lateral thigh [1]. Many investigators
have sought to characterize the anatomy of the IT tract, but
reports of its exact anatomy are still varied and inconsistent.
The anatomist Vesalius described the fascia lata as Bone of the
muscles of the tibia^in 1543 [2,8,9]. In 1855, Gerdy
*George R. Matcuk, Jr.
matcuk@usc.edu
1
Department of Radiology, Keck School of Medicine, University of
Southern California, 1520 San Pablo Street, Suite L1600, Los
Angeles, CA 90033, USA
2
Department of Radiology, Palmer College of Chiropractic-West
Campus, San Jose, CA 95134, USA
Skeletal Radiol (2017) 46:605–622
DOI 10.1007/s00256-017-2604-y

described the insertion of the fascia lata on the tibia [2,9,10].
Segond later termed this insertion point BGerdy’stubercle^[2,
9,11].
In 1958, Kaplan conducted a careful review of the histori-
cal literature and comparative anatomical dissections to fur-
ther elucidate the IT tract as a structure unique to humans,
likely representing adaptation to erect posture and bipedal gait
[2,12,13]. Kaplan characterized the IT tract as a ligament
connecting the ilium with the tibia [12]. He described the IT
tract as arising intimately from the tensor fascia lata and the
gluteus maximus in the region below the greater trochanter
and extending to its insertions on the lateral femoral condyle
and the lateral tibial tubercle (Gerdy’stubercle)[12].
Descriptions of the proximal anatomy of the IT tract have
been varied [13,14]. The IT tract is generally understood to be
comprised of a coalescence of the aponeurotic coverings of
the tensor fascia lata and gluteus maximus muscles, as well as
thefascialata(Fig.2)[2,9,12–16]. Along the lateral thigh,
the fascia lata receives expansions from gluteus maximus and
gluteal aponeurosis (i.e., aponeurotic fascia) posteriorly and
tensor fascia lata (TFL) anteriorly [13,15,16]. This lateral,
thickest region of the fascia lata is the IT tract [1,13,15,16].
Huang et al. recently described the proximal anatomy of
the IT tract, including its bony and muscular origins (Fig. 3)
[16]. The IT tract consists of three layers: the superficial layer,
intermediate layer, and deep layer [9,16]. These layers fuse in
the region of the greater trochanter to form the proximal IT
tract [14,16]. The superficial layer arises from the ilium su-
perficial to the TFL, while the intermediate layer arises from
the ilium slightly below the origin of the TFL and lies deep to
Fig. 1 Illustration of the lateral
view of the thigh demonstrating
the iliotibial tract and important
adjacent landmarks
Fig. 2 Illustration (a) and axial oblique PDFS MR image (b) of the cross-
sectional anatomy of the thigh demonstrating the iliotibial tract/band
made up of contributions from the aponeurotic fascia of the tensor
fascia lata anteriorly, gluteus maximus posteriorly, and the lateral
portion of the deep investing fascia (fascia lata)
606 Skeletal Radiol (2017) 46:605–622

the muscle [14,16]. The superficial and intermediate layers of
the IT tract merge at the distal end of the TFL and essentially
serve as the tendon for the TFL [14,16]. Huang et al. describe
the deep layer as a constant structure arising from the
supraacetabular fossa between the hip capsule and the tendon
of the reflected head of the rectus femoris [16]. This deep layer
merges just distal to where the superficial and intermediate
layers fuse [16].
Posteriorly, the IT tract receives contributions of tendi-
nous fibers from the gluteus maximus muscle and gluteal
aponeurotic fascia. The fibers of the superior gluteus
maximus and the superficial fibers of the inferior gluteus
maximus insert into the posterior IT tract [16]. The deep
fibers of the inferior gluteus maximus continue toward the
femur to insert onto the gluteal tuberosity of the linea
aspera [16]. The gluteal aponeurosis, arising from the iliac
crest, also contributes to the IT tract posteriorly [2,16].
The gluteal aponeurosis arises from the posterior iliac
crest and extends distally, covering the anterior two-
thirds of the gluteus medius, and inserts into the posterior
IT tract and onto the gluteal tuberosity [16].
While the layers of the IT tract merge over the area of the
great trochanter, the IT tract does not insert onto the greater
trochanter [14,16]. However, the IT tract attaches to the linea
aspera of the femur via the lateral intermuscular septum,
which arises from the IT tract [2,9,14,16]. The lateral
intermuscular septum also receives tendinous contributions
from the gluteus maximus [16].
At least five distal insertions of the IT tract about the knee
have been described (Fig. 4)[2,14]. These insertions extend
to an extensive periarticular area in the lateral knee, including
the distal femur, patella, proximal tibia, and joint capsule [2].
The IT tract courses over the vastus lateralis to terminate as
a ribbon-shaped insertion onto the infracondylar tubercle of
the tibia (Gerdy’stubercle)[2,14]. This direct insertion occurs
widely at and around Gerdy’stubercle[2]. Birnbaum et al.
also describe this portion of the IT tract as giving rise to in-
sertions on the fibular head [14].
The IT tract inserts onto the lateral portion of the femoral
diaphysis along the linea aspera through fibrous bundles
connecting the deep portion of the IT tract to the lateral
intermuscular septum [2,14]. The IT tract also inserts onto
the distal femur at the lateral epicondyle [2,14]. This insertion
is through a strong ligament at the superior aspect ofthe lateral
epicondyle near the lateral collateral ligament [2].
Fig. 4 Illustration of the distal iliotibial band insertions. 1 = Direct: wide
ribbon-shaped insertion at Gerdy’s tubercle; 2 = capsular-osseous:
posterior slip inserting on the tibia posterolateral to Gerdy’s tubercle
(lateral femorotibial ligament); 3 = lateral epicondyle: strong ligament
inserting at the upper edge of the lateral epicondyle near the lateral
collateral ligament; 4 = linea aspera: deepest portion inserts on lateral
portion of femoral diaphysis through the lateral intermuscular septum; 5
= patellar: wide fusiform insertion into the lateral patellofemoral
ligament/retinacular complex
Fig. 3 Illustration of the sites of the proximal origins of the iliotibial tract
and adjacent muscles: pink = superficial and deep (*) layers of the
iliotibial tract; yellow = gluteus minimus; light blue = gluteus medius;
green = gluteus maximus; dark blue = tensor fascia lata; red = gluteal
aponeurotic fascia
Skeletal Radiol (2017) 46:605–622 607

The IT tract has a patellar insertion that is wide and fuses
into the lateral transverse and longitudinal patellar retinaculum
[2,14]. Through this insertion, the IT tract contributes to the
lateral patellofemoral ligament complex [2].
The capsular-osseous insertion of the IT tract is a posterior
slip inserting onto the tibia posterolateral to Gerdy’stubercle
[2,9]. This insertion is also known as the lateral femorotibial
ligament [2]. Some authors argue that this capsular-osseous
insertion of the IT tract is the same structure as the anterolat-
eral ligament, only with different dissection protocols,and it is
discussed more thoroughly in the following section [17].
Function of the iliotibial tract
The IT tract and its associated muscles help extend, abduct,
and laterally rotate the hip [18]. The IT tract also serves an
important postural function, allowing for asymmetrical stand-
ing (pelvic slouch), with the upward pull of the lower attach-
ment of the IT tract locking the knee in hyperextension and
creating a rigid support pillar [19].
The IT tract is also a key structure contributing to the lateral
stability of the knee [3]. However, given the many compo-
nents and insertions of the IT tract, it is perhaps unsurprising
that the specific role of the IT tract in lateral knee stability has
been the subject of much investigation and debate. Recently,
the Bre-discovery^of the so-called anterolateral ligament of
the knee has prompted renewed interest in the anatomy and
function of the lateral stabilizers of the knee, including that of
the IT tract [20].
The IT tract has been relatively well defined as contributing
to anterolateral knee stability. Its fibers attaching to the lateral
femoral condyle divert forces of the tensor fascia lata and
gluteus maximus muscles. The distal IT tract is a dynamic
structure in its proximity to the knee; its posterior fibers are
isometric between 0° and 50° of knee flexion and increase in
length between 50° and 90° of flexion while its anterior fibers
increase in length between 0° and 40° of flexion and then are
essentially isometric from 40 to 90° [3].
Based on his studies of the IT tract, Kaplan advanced the
hypothesis that it provides anterolateral stability to the knee
[12]. This view was reinforced by subsequent biomechanical
studies that determined the distal IT tract was strong enough to
act as a ligamentous stabilizer and demonstrated the mecha-
nism by which this stabilizing action would occur [9,21–23].
However, Hughston et al. questioned the importance of the IT
tract in lateral stability based on their observations of patients
with posterolateral corner and lateral capsular injury with 3+
instability, but no concurrent lesion of the IT tract [24].
Terry et al. agreed with Kaplan’s assessment of the IT tract
as a lateral stabilizer of the knee [9]. Based on their cadaveric
study of 17 knee specimens, Terry et al. described the IT tract
as forming a sling posterior to the lateral femoral epicondyle
and acting to prevent posterior subluxation of the femur on a
fixed tibia. The layer of the IT tract they name the Bcapsular-
osseous layer^was taken to act synergistically with the ante-
rior cruciate ligament (ACL); when the knee extends, the dis-
tance between the femoral and tibial fixations of the IT tract
increases, tensing this segment of the IT tract, which restricts
anterolateral subluxation and anterior translation of the tibia.
Terry et al. also saw the IT tract as providing adduction stabil-
ity by preventing varus joint lengthening [2,9].
Subsequently, Hughston and Terry et al. produced a series
of 82 patients with anterolateral and anteromedial knee insta-
bility, which supported the hypothesis that the IT tract is vital
for anterolateral knee stability. In this study, 98% of patients
had an ACL lesion and 93% of patients had an IT tract lesion
of any kind. The authors posited that the number of possible
IT tract lesions accounts for the varied clinical presentation of
ACL rupture with regards to anterior tibial displacement [25].
Terry et al. also advanced the hypothesis that the combined
layers of the IT tract functionally constituted an anterolateral
ligament of the knee [9]. In a similar cadaveric study, Vieira
et al. largely supported this notion [2]. The authors found the
capsular-osseous layer of the IT tract to be a well-defined ana-
tomical structure that has a location and thickness to appropri-
ately constitute an anterolateral ligament of the knee [2]. In
earlier work, Hughston et al. suggested a capsuloligamentous
thickening of the anterolateral joint capsule was the true antero-
lateral ligament (ALL), distinct from the IT tract [3,24].
The ALL had previously been described, albeit inconsis-
tently, since at least 1879 by Segond [3,20], but Claes et al.
sought to define its anatomy through a rigorous cadaveric
study in 2013 [20]. The authors found the origin of the ALL
to be at the prominence of the lateral femoral epicondyle,
anterior to the origin of the lateral collateral ligament (LCL)
[20]. The ALL coursed toward the anterolateral proximal tib-
ia, attaching to the lateral meniscus and the tibia between
Gerdy’s tubercle and the fibular head [20]. The authors
asserted their dissections demonstrated the ALL as definitive-
ly distinct from the IT tract and hypothesized the function of
the ALL as being to control internal rotation of the tibia [20].
Subsequent qualitative and quantitative studies of the ALL
found similar but not wholly consistent anatomy, particularly
in regards to its origin being anterior, posterior, or at the lateral
femoral epicondyle [26–30]. Additionally, the ALL has been
variously implicated in resisting varus joint lengthening and
anteroposterior translation of the tibia in addition to internal
rotation of the tibia. Currently, the anatomy of the ALL and its
functional contribution to knee stability remain controversial
[31,32]. Thus, it is possible that the ALL in fact accounts, to
some degree, for the anterolateral stability previously attribut-
ed to the IT tract by Terry et al. [9,26].
Other major structures contributing to the lateral stability of
the knee are the biceps femoris and the other posterolateral
corner structures of the knee [4]. The biceps femoris is a
608 Skeletal Radiol (2017) 46:605–622

muscle of the posterior thigh composed of two parts: the long
head of the biceps and the short head of the biceps. Both the
long and short heads function act as knee flexors. The long
head arises from the posterior surface of ischial tuberosity. The
short head arises from middle third of linea aspera and the
lateral supracondylar ridge of femur. The main insertion site
of the biceps femoris is at the head and styloid process of the
fibula. In addition, it has several tendinous and fascial inser-
tional components, including one that inserts at the posterior
edge of the IT tract.
The additional structures usually described as being part of
the posterolateral corner structures of the knee are the fibular
(or lateral) collateral ligament (FCL), popliteus tendon,
popliteofibular ligament, lateral capsule, arcuate ligament,
and fabellofibular ligament [33]. These structures stabilize
the knee from posterolateral rotatory instability. The FCL is
the primary restraint to varus stress in early knee flexion. The
arcuate ligament fibers contribute to the lateral joint capsule.
The lateral aspect of the gastrocnemius muscle also contrib-
utes fibers to the joint capsule [4].
Imaging of the iliotibial tract
Proximally, the IT tract can be seen forming in the anterolat-
eral thigh with contributions from the deep fascia of the thigh,
gluteus maximus, and tensor fascia lata [16]. Distally, the IT
tract can be visualized as part of the soft tissue layers of the
lateral knee [4,6]. The soft tissue of the lateral knee is gener-
ally understood to be comprised of three layers; the IT tract
and biceps femoris tendon form the superficial layer, the pa-
tellar retinaculum forms the intermediate layer, and the LCL
and joint capsule form the deep layer (Fig. 5).
The IT tract is typically not well visualized on plan radio-
graphs but can sometimes be identified on anterior-posterior
(AP) radiograph of the lower extremity as a vertical linear
soft-tissue opacity [16]. On CT imaging, the IT tract will be a
hyperdense structure relative to adjacent muscular structures.
The IT tract is best visualized on MRI [6,16,34]. On MRI,
the IT tract is a hypointense, flat, linear structure in the lateral
hip, thigh, and knee [6]. In the absence of pathology, there
should be no adjacent edema or significant intrasubstance sig-
nal changes. Axial images help to differentiate intra-articular
fluid in the lateral joint space from signal changes associated
with IT tract pathology [34,35]. As with other ligamentous
structures, thickening and intrasubstance signal changes of the
IT tract on fat-suppressed fast spin-echo T2- or proton density
(PD)-weighted imaging suggest a sprain [4].
On MRI, the normal IT tract will typically measure
about 1 to 3 mm thick at the level of the lateral femoral
epicondyle [36,37]. Sonographic measurement of IT tract
thickness is generally consistent with MR measurement,
but studies using ultrasound (US) have reported slightly
lower average thicknesses [38,39]. Two sonographic in-
vestigations have attempted to determine whether age,
height, and or weight influence IT tract thickness in nor-
mal individuals; the studies differed as to whether aging
causes a baseline decrease in IT tract thickness, but nei-
ther study found a significant correlation between IT tract
thickness and height or weight [39,40].
Ultrasound is well regarded as an excellent imaging mo-
dality for superficial soft tissues, including the IT tract [41]. In
general, US offers an alternative imaging modality for the IT
tract that is more expedient and cost-effective than MRI; it
also allows for dynamic assessment of the IT tract [39,
41–45]. On sonographic examination, the IT tract is a relative-
ly hyperechoic linear structure that has a fibrillar pattern and is
Fig. 5 Illustration (a) and axial PDFS MR image (b) of the cross-
sectional layer anatomy of the lateral support system at the knee. Layer
1: superficial layer: anteriorly: IT band, posteriorly: superficial portion of
the biceps; layer 2: middle layer: anteriorly: lateral patellofemoral
ligament/retinacular complex; layer 3: deep layer: superficial: fibular
collateral ligament (FCL) and the fabellofibular ligament, intermediate:
lateral geniculate artery, deep: arcuate ligament, popliteus tendon,
popliteofibular ligament, and capsule
Skeletal Radiol (2017) 46:605–622 609

susceptible to anisotropy. Proximally, the IT tract can be easily
visualized in the axial plane as a stripe over the greater tro-
chanter [44]. Around the knee, the IT tract can readily be seen
in the coronal plane, with the distal insertion at Gerdy’stuber-
cle, and in the axial plane over the lateral formal epicondyle
[41,45]. The use of dynamic US examination at the greater
trochanter and lateral femoral epicondyle can be used to dem-
onstrate abrupt movement of the IT tract over these bony
landmarks as the cause of snapping hip or snapping knee
syndrome [43–46].
Proximal iliotibial band syndrome
Proximal iliotibial band syndrome (PITBS) is essentially
an overuse enthesopathy of the IT tract at its origin on the
iliac tubercle. Sher et al. first coined the term PITBS in
2011 in their discussion of a cohort of patients presenting
with pain and tenderness at the iliac tubercle. The authors
described MR findings in seven patients that were consis-
tent with a strain or tear of the proximal IT tract, positing
that these findings represented strain injury of the IT tract
iliac tubercle enthesis [13].
All of the patients Sher et al. described were female; four
were athletes who reported gradual onset pain localized to the
iliac tubercle, and three were older, non-athletes. None
recalled an inciting trauma. The authors hypothesized this
female predilection may be due to the greater hip width to
femoral length ratio leading to increased hip adduction torque
and/or greater peak hip adduction and internal rotation in all
walking and running conditions in women [13].
Huang et al. described similar presentations and imaging
findings in their patients with PITBS and agreed with Sher
et al. as to the pathophysiology of the condition [16].
Imaging
MR findings in PITBS include increased signal intensity
with fluid-sensitive sequences both superficial and deep
to the IT tract origin from the iliac crest, representing
edema about the IT tract enthesis (Fig. 6). MR can also
demonstrate thickening of the proximal IT tract attach-
ments and partial tearing (intrinsic hyperintense signal)
[13,16].
In contrast to Sher et al., Huang et al. described pa-
tients with PITBS as infrequently demonstrating marrow
edema in the iliac tubercle. They hypothesize marrow
edema in the iliac tubercle to be a manifestation of the
enthesopathy, similar to marrow edema in the calcaneus
of plantar fasciitis patients [16]. Sher et al. noted that
patients with PITBS often are misdiagnosed or treated
for presumed hip pathology, perhaps because the field of
view (FOV) for routine hip MRI does not always include
the proximal IT tract enthesis [13].
Treatment
As with other symptomatic fascial injuries, PITBS is usually
treated with rest, anti-inflammatory medications, and physical
therapy [16].
610 Skeletal Radiol (2017) 46:605–622
Fig. 6 A 56-year-old female with left hip pain. Coronal (a) and axial (b) STIR MR images demonstrate hyperintensity both superficial and deep to the
iliac origin of the iliotibial tract (arrows), consistent with proximal iliotibial band syndrome

Morel-Lavallée Lesion
The Morel-Lavallée lesion (MLL) is a closed internal
degloving soft tissue injury caused by a shearing separation
of the subcutaneous layer from the deep fascia and secondary
formation of a seroma, hematoma, or fat necrosis. This lesion
was first described by Maurice Morel-Lavallée in the proxi-
mal thigh, but the term has since been used to describe similar
lesions at other sites. However, the soft tissue of the proximal
thigh lateral to the greater trochanter remains the most com-
mon location for the MLL [47,48].
The abrupt separation of skin and subcutaneous fatty
tissue from the underlying fascia severs the lymphatics
and vasculature of the subdermal plexus, leading to a
hemolymphatic collection in the potential space created
between the two layers. The accumulation of this hetero-
geneous material can be slow or rapid. If left untreated, an
inflammatory reaction leads to the formation of a periph-
eral fibrous capsule. A superimposed infection of the le-
sion may ensue [47,48].
Lateral to the greater trochanter, the IT tract lies deep to the
dermis, subcutaneous fat, and superficial fascia. The dermis
and subcutaneous fat are more mobile than the firmer IT tract,
putting these superficial soft tissues at risk for a shearing in-
jury and subsequent MLL formation [47].
MLLs are usually due to severe pelvic or thigh trauma;
motor vehicle collisions are the most common mechanism.
MLLs can also be caused by low-velocity crush injuries, for
which the thigh is the most common site. Contact sports have
also been associated with MLLs [47].
MLLs may present acutely or remote to the trauma
depending on the rate and extent of hemolymphatic accu-
mulation. A patient’s body habitus or the presence of
distracting polytrauma may delay the clinical diagnosis
of MLLs, especially smaller lesions. Fractures of the
proximal femur, pelvis, and acetabulum may occur simul-
taneously [47,48].
Patients with MLLs typically report painful swelling. On
physical examination, MLLs can demonstrate ecchymosis,
soft tissue swelling, fluctuance, or skin hypermobility. As
the fibrous capsule forms, the area may become firm. The
overlying skin may also experience necrosis [47,48].
Imaging
MLLs are classified into six types based on the chronicity and
tissue composition of the collections and their appearance on
MRI. Specifically, this classification is based on lesion shape,
presence or absence of a capsule, overall T1 and T2 signal
characteristics, and enhancement features [47,49].
MLLs are described as either a seroma (type I), subacute
hematoma (type II), chronic organizing hematoma (type III),
perifascial dissection with closed fatty laceration and no
capsule (type IV), perifascial pseudonodular lesion (type V),
or having a superimposed infection with variable sinus tract
formation, internal septations, and a thick enhancing capsule
(type VI) [47,49].
A type I MLL appears as a homogeneous and hyperintense
collection on T2 and homogeneously hypointense on T1 with-
out evidence of outer capsule formation [47,49].
Type II MLLs are usually homogeneously hyperintense on
both T1 and T2. The T1 hyperintensity is due to the presence
of the methemoglobin characteristic of subacute hematomas.
Type II lesions can demonstrate intra-lesional heterogeneity
due to trapped fat globules, fluid-fluid levels from evolving
blood products, and/or internal septations (Fig. 7). If new or
residual capillaries are present within the lesion, patchy inter-
nal enhancement may be seen [47,49,50].
Type III MLLs demonstrate hypointensity on T1 and het-
erogeneous hypointensity/isointensity on fluid-sensitive im-
ages due to hemosiderin deposition, granulation tissue, necrot-
ic debris, fibrin, and blood clots. Type III lesions may show
internal enhancement secondary to neovascularization and or-
ganizing granulation tissue. A hypointense peripheral ring
may be seen, which represents a hemosiderin-laden fibrous
capsule with inflammatory infiltrate [47,49,50].
Type IV MLLs demonstrate T1 hypointensity, T2
hyperintensity, variable enhancement, and the absence of a cap-
sule, while type V MLLs will demonstrate variable T1 and T2
intensity as well as areas of both internal and peripheral enhance-
ment. Type V lesions have a small, rounded, pseudonodular
appearance. A type VI lesion will have thick enhancing capsule
with or without an associated sinus tract [47,49].
While MRI is the best modality to characterize a MLL,
patients are usually emergently evaluated with CT first. CT
can be helpful to localize the lesion to the interfascial plane
[47,51].
US also offers the ability to evaluate a suspected MLL
expediently, and it is also the modality of choice for
imaged-guided interventions [47]. MLLs will appear as
nonspecific fluid collections with heterogeneous
echogenicity; they will be compressible and fail to dem-
onstrate flow on color Doppler [47,52,53]. The chronic-
ity of the lesion will influence the US findings. Acute and
subacute (less than 1 month) lesions tend to have a het-
erogeneous appearance with irregular margins and a lob-
ular shape, while chronic lesions (greater than 18 months)
are more often homogeneous with smooth margins and a
flat or fusiform shape [47,52].
Treatment
Management of MLLs depends on the stage of the lesion as
well as its size and location. Treatment options include com-
pression banding, aspiration, or debridement and irrigation,
with or without injection of sclerosing agents. Smaller, more
Skeletal Radiol (2017) 46:605–622 611

acute lesions may be more amendable to nonsurgical manage-
ment (compression banding with or without sclerosants follow-
ed by percutaneous drainage if the lesion fails to resolve).
Percutaneous drainage with sclerotherapy can be used initially
for chronic lesions, but these may require subsequent surgical
debridement. Similarly, larger, symptomatic lesions may bene-
fit most from debridement and irrigation. Infected lesions ne-
cessitate open drainage and secondary closure [47,48].
External snapping hip syndrome
External snapping hip syndrome (ESHS) refers to a snapping,
popping, or clicking sensation over the greater trochanter with
hip motion [54]. ESHS itself is a form of snapping hip syn-
drome, which isdefined by a sensation of snapping during hip
motion (Bsnapping hip^or Bcoxa saltans^) with or without
associated pain [43,55,56]. For clarity, some have advocated
Fig. 7 Morel-Lavallée lesions in three separate patients with histories of
trauma. Coronal STIR MR image (a) demonstrates a thin hyperintense
serous fluid collection superficial to the iliotibial tract (curved arrows),
consistent with a type I Morel-Lavallée lesion. Coronal T1 MR image (b)
demonstrates a large heterogeneous collection superficial to the iliotibial
tract (curved arrow) with internal hypointense foci (arrow) corresponding
to blood products and hyperintense foci that followed fat signal intensity
on all pulse sequences (arrowhead) corresponding to fat globules,
consistent with a type II Morel-Lavallée lesion. Coronal T1 MR image
(c) demonstrates a hypointense organized hematoma superficial to the
iliotibial tract (curved arrows), representing a type III Morel-Lavallée
lesion
612 Skeletal Radiol (2017) 46:605–622

for reserving the term snapping hip syndrome only for those
cases where this snapping sensation is accompanied by pain
[46].
Snapping hip syndrome is typically classified as intra-
articular or extra-articular, depending on where the site of
pathology is located. Intra-articular snapping hip is caused
by any intra-articular derangement, such as acetabular labral
or ligamentum teres tears, or intra-articular bodies. Extra-
articular snapping hip is further divided into two forms: exter-
nal and internal [43,55,56]. The internal form of extra-
articular snapping hip has been attributed to the iliopsoas ten-
don moving over the iliopectineal eminence, producing an
audible snap emanating from the anterior hip [43,46].
However, some dynamic US studies suggest the actual source
of this snap to be the psoas tendon rolling laterally and ante-
riorly over the medial fibers of the iliacus muscle [57,58].
In the external form of snapping hip, the snap occurs in the
lateral hip as a result of abrupt forward movement of the
proximal IT tract or, less often, the distal gluteus maximus
over the greater trochanter during hip flexion [44,54,59,
60]. Passive movement from an adducted and internally rotat-
ed hip into flexion and external rotation may also elicit this
snap. Pain, which may reflect bursitis or tendonitis from re-
peated rubbing, often occurs at the moment of the sudden IT
tract translocation/snapping sound.
ESHS is typically associated with repetitive physical
activity/chronic overuse or activities that involve extremes of
hip motion [43]. Thickening of the posterior IT band or ante-
rior gluteus maximus is also associated with the development
of ESHS [43,54,59]. Variant anatomy, such as a smaller
femoral neck angle, narrower bi-iliac width, increased dis-
tance between the greater trochanters, or prominent greater
trochanters, may predispose patients to ESHS as well [55,
61]. Other rare causes of ESHS include anatomical and/or
biomechanical derangements resulting from surgery or other
pathological conditions [62–65].
ESHS is common among athletes and dancers. Patients are
typically young and physically active. Women may be more
affected than men, but this finding may be confounded by the
greater rates of intra-articular pathologies such as acetabular
labral tears and hip dysplasia in women. In addition to pain
and snapping, patients often report the feeling of hip sublux-
ation or dislocation. Patients may report difficulty with activ-
ities such as running, climbing stairs, or heavy lifting. On
examination, reproduction of the audible or palpable snap
should be possible with a provocative test of femoral flexion
and/or rotation [43].
Imaging
In practice, the diagnosis of ESHS is usually made by history
and physical examination, but imaging can be used to rule out
other diagnoses or confirm the diagnosis/involved structures.
In particular, dynamic US examination is increasingly used to
make the definitive diagnosis of ESHS. Plain radiographs are
usually normal in ESHS but are potentially useful in helping
exclude other pathologies [43].
More often, MRI will demonstrate findings suggestive of
ESHS. T1 imaging may demonstrate hypointense thickening
of the proximal IT tract, while T2 imaging may show thick-
ening and hyperintensity of the proximal IT tract.
Hyperintense greater trochanteric bursal inflammation or a
fluid collection may also be visualized on T2 (Fig. 8); how-
ever, this finding is non-specific and should only be consid-
ered pathologic when the appropriate clinical signs and symp-
toms are also present. Post-contrast imaging can show
peritendinous enhancement of involved structures [66].
A case series of three patients suggested that atrophy of the
gluteus maximus muscle on MRI could be a secondary sign of
ESHS. The authors hypothesized that this finding could be
due to gait changes made by patients to avoid pain [59].
Similar to MRI, a conventional sonographic examination
may reveal IT tract tendinopathy (increased thickness, hetero-
geneous echogenicity) or greater trochanteric bursitis [46,54,
59]. A dynamic US examination is usually successful in dem-
onstrating the translation of the IT tract/gluteus maximus over
the greater trochanter in ESHS; this movement can be corre-
lated in real time to the audible or palpable snap perceived by
the examiner or pain reported by the patient, allowing for the
definitive diagnosis of ESHS [44,46,54,59,60]. Dynamic
US can also visualize movement of the iliopsoas tendon over
the iliopectineal eminence (or the psoas tendon rolling over
the iliacus muscle), thus differentiating between internal and
external snapping hip when a physical examination is incon-
clusive [46,57,58].
In evaluating for ESHS, the US examination is performed
with the transducer transverse to the greater trochanter [57].
Fig. 8 A 21-year-old female runner with bilateral hip pain and snapping
sensation. Coronal T2FS MR image demonstrates hyperintensity in the
trochanteric bursae between the proximal iliotibial tracts and greater
trochanters (arrows), suggesting external snapping hip syndrome
Skeletal Radiol (2017) 46:605–622 613

The patient can be supine or standing, but normal gluteus
maximus contraction with weight bearing may be necessary
to reproduce the snap/abrupt translation of the IT tract or glu-
teus maximus [54,59]. Common maneuvers to elicit the
pain/snap include flexion of an adducted, extended hip and
external rotation of an adducted, internally rotated hip [54,
57]. It is recommended that both active and passive move-
mentsbeusedwhenevaluatingforESHS[57].
Treatment
ESHS is usually first treated conservatively with rest, avoid-
ance of aggravating activities, stretching of the IT tract, and
NSAIDs. Unresponsive patients can undergo injection of local
anesthetic and corticosteroids into the trochanteric bursa.
Between one-third and two-thirds of patients see symptom
response or resolution with conservative management.
Refractory cases are sometimes treated with surgical length-
ening of the IT tract with Z-plasty or endoscopic IT tract
release [43].
Iliotibial band syndrome and iliotibial bursitis
Iliotibial band syndrome (ITBS), sometimes referred to as
iliotibial band friction syndrome, refers to pain around the
lateral femoral epicondyle that is associated with lower limb
activity. Typically, this activity involves repetitive motion of
the lower limb, such as that encountered in running or cycling.
ITBS is usually due to chronic overuse, so that the classic
presentation of a patient with ITBS is an active young person
with lateral knee pain that increases throughout an episode of
physical activity.
ITBS is thought to be the most common running injury of
the lateral knee, and it is commonly diagnosed in other active
populations such as cyclists, soccer players, and basketball
players [67]. In an epidemiological study of military recruits
undergoing basic training, Linenger and West found ITBS to
account for 22% of all lower extremity injuries [68].
Renne first described ITBS in 1975 and thought it was due
to the IT tract rubbing back and forth across the lateral femoral
epicondyle during repetitive knee extension and flexion, caus-
ing friction and resultant irritation of the IT tract and perios-
teum or a possible bursa of the lateral epicondyle [69]. Renne
offered this etiology based on Kaplan [12], who concluded the
IT tract passed over the lateral epicondyle free of bony attach-
ments to insert on the tibia and moved anterior and posterior
with knee extension and flexion [69]. Thus, irritation of the IT
tract caused by friction of its movement against the lateral
epicondyle has been the historical understanding of the etiol-
ogy of ITBS.
This understanding has since been challenged [18,36,67,
70–73]. First, there is debate as to what direction and to what
extent the IT tract moves as the knee ranges. Fairclough et al.
considered the anatomy of the IT tract to preclude any
anterior-posterior movement about the lateral epicondyle
since the IT tract is simply a thickening of the lateral fascia
and is fixed to the linea aspera through the lateral
intermuscular septum [18]. On MR imaging, their study dem-
onstrated medial-lateral rather than anterior-posterior move-
ment of the IT tract about the lateral epicondyle with knee
flexion and extension. More recently, however, a sonographic
evaluation of the IT tract during knee flexion and extension
did demonstrate anterior-posterior movement of the IT tract
relative to the lateral epicondyle [74].
Second, several studies suggest that irritation of a cyst,
bursa, or synovial recess deep to the IT tract, rather than in-
flammation of the IT tract itself, is the true etiology of ITBS
[70–72]. In addition, one histological examination of tissue
from the lateral joint capsule in patients with chronic ITBS
demonstrated synovial tissue, which was inflamed and thick-
ened [70]. Further, documented successes with treating refrac-
tory ITBS with surgical resection of the lateral synovial recess,
surgical resection of the sometimes identified sub-IT tract bur-
sa, or surgical release of the IT tract attachment to the lateral
epicondyle have been used to support this etiology [72,
75–79].
However, other studies based on MRI findings in patients
with ITBS and cadavers show soft tissue signal changes in the
sub-IT tract space without demonstrating a distinct cyst, bursa,
or synovial recess [36,80]. It is possible that compression of a
vascularized fat pad in the sub-IT tract space is the cause of
ITBS pain [18,81]. Ultimately, ITBS may have multiple eti-
ologic subtypes [67] or at least be more accurately understood
as an impingement syndrome rather than a frictional one, giv-
en the relative lack of evidence for pathological changes oc-
curring within the IT tract itself, and the possibility that the IT
tract may not always move anterior-posterior relative to the
lateral epicondyle.
With these anatomical considerations concerning the etiol-
ogy of ITBS in mind, investigators have examined physical
and biomechanical risk factors for the development of ITBS
[67,82–85]. Factors thought to increase the compression of
structures underneath the IT tract, such as increased IT tract
tightness, have generated conflicting evidence [67,82].
However, the physical factors with the most robust association
with ITBS include limb length discrepancy, genu varum, foot
overpronation, hip adductor weakness, and myofascial restric-
tion [35,82,85–87].
Regardless of the etiology of ITBS, patients usually have a
consistent clinical presentation. Pain in the region of the distal
IT tract between the lateral femoral epicondyle and Gerdy’s
tubercle of the tibia is a consistent complaint, usually with a
history of regular athletic activity. Patients often notice the
onset of lateral knee pain late in or after completing an activity,
and as the syndrome progresses, pain begins earlier in the
614 Skeletal Radiol (2017) 46:605–622

course of activity. Running downhill is a typical and repro-
ducible aggravating factor. Physical examination reveals ten-
derness to palpation at the lateral epicondyle, approximately
2–3 cm proximal to the joint line [86].
Iliotibial bursitis is a rare sequela of chronic ITBS. As
discussed previously, MRI studies have demonstrated fo-
cal fluid collections between the IT tract and the lateral
femoral epicondyle in patients with ITBS, but anatomical
investigations of normal knees have failed to consistently
identify the gross and/or histological presence of a sub-IT
tract bursa [81]. However, the focal fluid collections often
identified on MRI in ITBS patients may represent the
formation of an adventitial bursa due to chronic inflam-
mation [36]. Continued irritation of this adventitial bursa
can lead to chronic ITBS symptoms, which can be under-
stood as iliotibial bursitis [72].
Surgical and histological case reports support the exis-
tence of pathological bursa in patients who suffer from
refractory ITBS [72,88]. Hariri et al. describe consistent-
ly identifying an apparent inflamed bursa underneath a
benign-appearing IT tract in a case series of 12 patients
undergoing surgery for recalcitrant ITBS. They also de-
scribe high rates of clinical relief in these patients after
surgical IT tract bursectomy [72].
The presentation of iliotibial bursitis is the same as ITBS.
Patients are typically physically active long distance runners
or cyclists with lateral knee pain localized to the lateral fem-
oral condyle that is exacerbated by activity. They may have a
history of being treated for ITBS. Physical examination usu-
ally reveals tenderness at the lateral femoral epicondyle that is
worst with 30° of flexion [72,88].
Imaging
The diagnosis of ITBS can typically be made by history and
physical examination, with imaging reserved for recurrent or
refractory cases [86]. In patients with ITBS, routine radio-
graphs, including anterior-posterior (AP), lateral, and sunrise
views, are typically normal, but can be used to help exclude
other knee pathology [69,86,89]. In contrast, characteristic
MRI findings associated with ITBS have been described [36,
86].
Most consistently, MR imaging demonstrates increased
fluid signal in the fat between the ITB and the lateral
femoral condyle (usually superolateral to the lateral joint
recess) (Fig. 9)[34,36,37,89,90]. However, mild
hyperintensity on fluid-sensitive sequences in this region
is not infrequently seen in older patients and should only
be considered pathologic when the appropriate clinical
signs and symptoms are also present. This area of edema
can be up to several centimeters in size. A discrete fluid
collection may be visualized in this space [34,36,37].
The IT tract may be thickened [37], but some studies have
questioned this finding, suggesting it only occurs in a
subset of chronic ITBS cases [36,89,90]. Additionally,
reactive edema in the lateral epicondyle may be present.
Less frequently, reactive bursitis can occur [36].
It should be noted that relatively few published studies
have sought to investigate what MR findings are associated
with ITBS. In 1992, Murphy et al. evaluated six patients with
ITBS by clinical history and physical examination. MR imag-
ing demonstrated ill-defined, decreased signalintensity on T1-
weighted images and increased signal intensity on T2-
weighted images deep to the IT tract adjacent to the lateral
femoral epicondyle; there were no signal intensity abnormal-
ities in the IT tract itself [34].
In a case series comparing MR imaging of ITBS pa-
tients and age-and-sex matched controls, Ekman et al.
similarly demonstrated increased fluid signal over the lat-
eral epicondyle of ITBS patients, but determined this sig-
nal to represent discrete, localized fluid collections. The
study also showed thickening of the distal IT tract in most
of the ITBS cases [37,86].
A subsequent case series of four ITBS patients by
Nishimura et al. suggested soft tissue inflammation and/or
edema rather than focal fluid collection in the space between
the IT tract and the lateral epicondyle. The ITB itself did not
show any signal alteration or increased thickness [89].
In 1999, Muhle et al. attempted to define MRI findings in
ITBS patients and to correlate these findings with anatomic
Fig. 9 A 28-year-old female with left knee pain after running a marathon.
Coronal STIR MR image demonstrates thickening of the iliotibial band
with increased intrasubstance signal intensity (arrowhead)withedema
both deep (arrow) and superficial (curved arrow) at the level of the lateral
femoral epicondyle, consistent with iliotibial band syndrome
Skeletal Radiol (2017) 46:605–622 615

features defined by MR arthrography in cadavers. This study
supported the findings of Murphy et al. and Nishimura et al.,
demonstrating ill-defined signal intensity alterations in the
fatty tissue deep to the IT tract in the majority of ITBS pa-
tients. A minority of ITBS patients had well-defined fluid
collections in the same distribution as this soft-tissue edema.
The authors concluded these well-defined fluid collections
likely represented secondary bursa formation as a result of
chronic inflammation. The study did not find a significant
difference in the thickness of the IT tract in ITBS patients
versus control patients [36].
While MRI is considered the gold-standard for diagnosing
ITBS in patients with unclear presentations and physical ex-
aminations, US has also been used successfully to diagnose
some cases. The use of US in diagnosing ITBS is not well
documented in the literature, but it has been proposed that US
findings in ITBS can correlate well with MRI findings. US has
been shown to demonstrate edematous swelling of the soft
tissues between the IT tract and the femoral epicondyle in
ITBS, similar to what is seen on MRI, although the sensitivity
is likely lower [42,91].
In iliotibial bursitis, MRI will demonstrate a well-defined
fluid collection between the IT tract and the lateral femoral
condyle (Fig. 10), although some sources suggest the adven-
titial bursa may be between the IT tract and the tibia, close to
its insertion onto the tibia [72,92,93]. This fluid collection is
best seen on short tau inversion recovery (STIR) or T2 fat-
suppressed (T2FS) imaging. Signal abnormalities within the
IT tract should be minimal or not visualized at all [92,93].
Treatment
ITBS is almost always managed non-surgically. Rest from the
inciting activity followed by gradual return to activity is a
mainstay of treatment [86]. Physical therapy and manual ther-
apy also play important roles [85,86]. Oral non-steroidal anti-
inflammatory drugs (NSAIDs), local corticosteroid injections,
or both can be used to control acute inflammation, although
corticosteroid injections have been shown to alleviate symp-
toms more effectively [86,94]. Response to corticosteroid
injection can be used to help diagnose ITBS as well [86,95].
Recalcitrant cases of ITBS with functional impairment are
sometimes treated with surgery [86]. As previously discussed,
favorable results have been reported with several surgical
treatments. These include surgical release of the IT tract, IT
tract bursectomy, and surgical resection of the lateral synovial
recess [72,75–79].
Similar to ITBS, iliotibial bursitis can initially be treated
conservatively with rest and NSAIDs to reduce inflammation
and potentially allow the bursa to heal. Truly refractory cases
in patients with poor symptom response despite adherence to
nonoperative measures can be treated with surgery. IT tract
bursectomy, as previously mentioned, has been used in these
patients as well as surgical IT tract release [72,88].
Iliotibial band injury in acute knee trauma
IT tract injury is common in the setting of acute knee trauma.
However, perhaps because the IT tract is rarely injured in
isolation, there is relatively little consideration of discrete IT
tract injury as a topic of inquiry in the literature. In addition,
while the IT tract presumably acts synergistically with the
other lateral stabilizers of the knee, the clinical significant of
its injury is unclear.
IT tract injury may occur in as many as 58% of cases of
acute knee trauma [6]. In patients undergoing surgery for
functional knee instability due to complete tears of a postero-
lateral structure, the deep layer of the IT tract may be the most
commonly damaged structure [96]. However, isolated injury
to the IT tract is rare as this is thought to require purely varus
force, which rarely occurs [97,98]. In acute knee trauma, the
incidence may be as low as 2% [6].
In up to two-thirds of cases of IT tract injury the ACL will
alsobetorn.Inupto20%ofcases, patellar dislocation will also
have occurred. Additionally, when an ACL tear or patellar dis-
location is identified, injury to the IT tract is common (∼70 and
∼74% of cases, respectively). As determined by MRI, most IT
tract injuries are sprains. Complete tears are rare [6].
Fig. 10 A 56-year-old male with left knee pain and swelling. Axial STIR
MR image demonstrates an oval hyperintense fluid collection deep tothe
iliotibial band (arrowhead) but separate from the lateral joint recess
(arrow), consistent with iliotibial bursitis
616 Skeletal Radiol (2017) 46:605–622

Imaging
MRI is well established as the first-line imaging modality in
evaluating traumatic internal derangement of the knee [99],
but discussion of IT injury, particularly sprains, as a discrete
imaging findings is lacking [6]. Mansour et al. classified IT
tract injuries as grade 0–3[6], similar to grading for other
ligamentous injuries [100].
The IT tract is classified as grade 0 if it is normal (thin,
intact, low signal intensity). Grade 1 injuries (minor
sprains) demonstrate edema superficial and deep to an
otherwise intact IT tract. Grade 2 injuries (severe sprains)
show edema adjacent to a partial tear of the IT tract, with
some intact fibers. Grade 3 injuries (tears) demonstrate a
grossly torn, discontinuous IT band with waviness of the
torn fibers (Fig. 11)[6].
Treatment
The clinical significance of IT tract injury in acute knee
trauma is unclear, but it likely contributes to knee insta-
bility, especially in cases with concomitant ACL tear [6,
25]. If the IT tract injury is part of a broader injury pattern
contributing to knee instability, surgical repair is generally
indicated [33].
Iliotibial tract insertional tendinosis
and peritendonitis
Most descriptions of IT Btendinitis,^Btendinosis,^or
Btendinopathy^in the literature are equated with ITBS.
However, this should occur only at or near the level of the
lateral femoral epicondyle. Unlike ITSB, insertional
tendinosis and peritendonitis are not related to chronic com-
pression or friction. The pathogenesis of insertional tendinosis
usually involves aging and overuse, particularly in unstable
joints, due to osteoarthrosis [101].
The IT tract lacks a tendon sheath, but can have inflamma-
tion of its paratenon, similar to the Achilles, quadriceps, and
patellar tendons. Presumably, its distal insertion may be affect-
ed by any disorder that causes enthesopathy, e.g., chronic
repetitive stress, spondyloarthropathies, diffuse idiopathic
skeletal hyperostosis (DISH), calcium pyrophosphate deposi-
tion disease (CPPD), or endocrine (hyperparathyroidism, ac-
romegaly) or metabolic (fluorosis) disorders. The incidence of
iliotibial insertional tendinosis/peritendonitis has not been de-
scribed in the literature, but is probably under-recognized and
under-reported.
Imaging
There are few reports describing the imaging findings associ-
ated with iliotibial insertional tendinosis/peritendonitis; how-
ever, the findings are the same as those reported with
tendinosis of other tendons, such as the Achilles tendon.
MRI may demonstrate thickening and increased
intrasubstance intermediate signal intensity, most prominent
on fluid-sensitive sequences (Fig. 12). In cases with associated
peritendonitis, there will be adjacent edema. On ultrasound,
the site of highest pain sensitivity will correspond to a region
of thickening and hypoechogenicity of the iliotibial band
[101].
Treatment
In general, treatment is conservative, consisting of rest, ice,
physical therapy, and NSAIDs. In refractory cases,
ultrasound-guided tenotomy or prolotherapy may improve pa-
tient symptoms [102].
Avulsion fracture at Gerdy’sTubercle
Avulsion fractures of the IT tract’s insertion at Gerdy’stuber-
cle are rare [33,97,98]. The mechanism of injury is thought to
be most commonly a direct blow to the anteromedial proximal
tibia, directed posterolaterally, with the knee near full exten-
sion [97,98]. However, case reports exist of isolated avulsions
with jumping [103].
Fig. 11 A 15-year-old female with right knee pain after an automobile
versus pedestrian accident. Coronal STIR MR image demonstrates
discontinuity of the distal iliotibial band (arrows) proximal to the
insertion on Gerdy’s tubercle with waviness of the torn fibers, consistent
with a complete (grade 3) tear
Skeletal Radiol (2017) 46:605–622 617

When encountered, avulsion fractures of Gerdy’s tuber-
cle are usually associated with injuries to the other pos-
terolateral corner structures of the knee. Isolated tears of
the IT tract are thought to require a pure varus force,
which is rarely seen. Patients will have severe pain with
weight bearing and point tenderness over Gerdy’s tuber-
cle. Concomitant ACL injury is a common finding in
these patients [97,98].
Imaging
Plain radiographs, CT, and MRI have potential roles in the
diagnosis and treatment of avulsion fractures at Gerdy’stuber-
cle. A plain radiograph can demonstrate the avulsed osseous
fragment at the IT band insertion site on Gerdy’s tubercle.
Associated findings may include a lipohemarthrosis, sugges-
tive of an intra-articular fracture, and/or widening of the lateral
compartment, suggestive of a ligamentous injury [98]. CT can
facilitate recognition of the extent of the fractured fragment as
well as aide in determining the surgical approach and methods
for internal fixation [103].
On MRI, there will be a linear T2 hyperintense/T1
hypointense fracture line with adjacent bone marrow edema
at Gerdy’s tubercle for non-displaced fractures (Fig. 13)[97].
There will be a gap between the ossific fragments for
displaced fractures with waviness of the retracted distal IT
band fibers.
Treatment
Conservative treatment for avulsion fractures at Gerdy’stu-
bercle is usually forgone in favor of open reduction with can-
cellous screw fixation of the fracture fragment to the tibia
using a lateral parapatellar approach [98,103].
Segond fracture
The Segond fracture is an avulsion fracture involving the
proximal tibia immediately distal to the lateral plateau as a
result of varus stress with internal rotation of the knee. It is
well established that Segond fractures are associated with
ACL tears, meniscal tears, and damage to the other structures
of posterolateral corner of the knee. Clinical diagnosis of
Segond fractures in the acute stage can be difficult because
of pain, muscle spasm, and/or swelling, so radiologic recog-
nition of this bony injury is important as it could reflect liga-
mentous derangement with significant instability of the knee
[104].
The mechanism of injury in Segond fractures is gener-
ally understood to be varus stress applied to an internally
rotated knee, which causes abnormal tension on the lateral
joint capsule at its midpoint [97,104]. Historically, this
tension was thought to produce an avulsion facture of the
lateral tibial plateau at the insertion of the lateral capsular
ligament. However, the precise anatomic structure causing
Fig. 12 A 61-year-old male with chronic left lateral knee pain. Coronal T2FS (a)andaxialPDFS(b) MR images demonstrate thickening and increased
intrasubstance intermediate signal intensity of the distal iliotibial band with adjacent edema, consistent with insertional tendinosis and peritendonitis
618 Skeletal Radiol (2017) 46:605–622

the avulsion has been extensively debated, and the path-
ogenesis is likely more complex than the historical under-
standing. In the past, this avulsion has been described as
being at the insertion of the capsular-osseous layer (pos-
terior slip) of the IT tract, lateral capsular ligament, and/or
anterior oblique band of fibular collateral ligament, but
recent literature suggests that this primary occurs at the
insertion of the anterolateral ligament [97,104–106].
Although there is likely overlap of the anterolateral liga-
ment with some of these other previously described struc-
tures based on differences in terminology and dissection
techniques, the course of this ligament from the lateral
femoral epicondyle to the lateral tibial plateau correlates
with the Segond fracture site, and there is general consen-
sus in the current literature that the anterolateral ligament
is the cause of the Segond fracture [107–111].
Patients with Segond fractures often present with pain at
the lateral joint line, swelling, and anterolateral rotational in-
stability [97,104,112]. In 75–100% of cases, patients will
have an associated ACL tear, and an associated medial
meniscal tear will be present in 66–75% of cases [104].
Segond fractures may also be associated with avulsion of the
fibular attachment of the long head of the biceps femoris ten-
don and the fibular collateral ligament [97,112]. More rarely,
patients will also have an avulsion of the ACL from its inser-
tion anterior to the tibial eminence [97,112].
Imaging
Plain radiographs may reveal an elliptical osseous fragment
parallel to the tibia, just distal to the lateral tibial plateau; this
finding has been referred to as the Blateral capsular sign^[97].
However, the avulsed fragment may not be visualized because
of its small size and/or projection inadequacies [112]. Proper
AP views may help visualize the fragment, but CT imaging
may be needed to demonstrate it best [47]. Additionally, case
reports exist of US revealing a chronic Segond fracture after
plain radiographs failed to demonstrate a fragment in a patient
presenting with persistent knee pain 6 months after a trauma
[113].
MRI should show abnormal signal intensity (low signal on
T1, high signal on T2) in the marrow along the lateral tibial
rim, representing bone marrow contusion/edema [97,112].
The avulsed fragment may or may not be visualized [97,
106,112]. Other associated findings include abnormal signal
intensities in the joint capsule (capsular edema) and
paracapsular connective tissue (paracapsular edema) [112],
including fluid surrounding the IT tract [106]. The anterolat-
eral ligament can be visualized in almostall cases, even at 1.5-
T MRI, with meniscal, femoral, and tibial portions, best visu-
alized as a thin, linear, hypointense structure in the coronal
plane attaching to the Segond fracture fragment [110,114]. A
joint effusion may also be present. In all cases of Segond
Fig. 13 A 33-year-old male with right knee pain after a fall. AP
radiograph (a) and coronal STIR MR image (b)demonstratea
minimally displaced avulsion fracture of Gerdy’s tubercle at the
iliotibial band insertion (arrows) with associated bone marrow edema
on the MRI. There is also a medial tibial plateau fracture (curved arrows)
Skeletal Radiol (2017) 46:605–622 619

fracture, MR imaging should be obtained to evaluate for con-
comitant ligamentous or meniscal injury [97].
Treatment
Segond fractures alone do not necessarily require operative
fixation. Patients have the option to be treated with physio-
therapy. However, operative treatment of any associated inju-
ry, such as an ACL tear, contributing to knee instability is
usually undertaken [113,115].
Conclusion
As an anatomical structure, the IT tract has been known in the
literature for quite some time, yet its precise anatomy remains
somewhat elusive. However, its contribution to knee stability
is relatively well established, and the pathologies related to the
IT tract are numerous and common. In addition, these pathol-
ogies often carry significant morbidity for patients. Plain radi-
ography, CT, MR, and US imaging potentially all have a role
in the diagnosis of the wide array of IT tract pathology. As
such, the radiologist should have a firm appreciation of the
complex anatomy of the IT tract, as well as the various imag-
ing findingsassociated with its pathology. A clear understand-
ing of the clinical presentation and pathophysiology of condi-
tions affecting the IT tract are often helpful in making a correct
diagnosis as well.
Compliance with ethical standards
Conflicts of interest The authors declare that they have no conflicts of
interest.
Grants received None
Disclosures None
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