Synopsis
During this talk MRI patterns of traumatic
muscle injuries in elite athletes will be covered with a special focus on
soccer injuries. The main topics will be: to give background information about
the frequency and relevance of muscle injuries (m.i.) in professional players; to
understand the mechanism of m.i. to discuss the MR imaging protocol needed to
diagnose m.i. including the role of new sequence developments and techniques in
daily practice; to discuss classification or grading systems and imaging predictors
regarding “time to return to play”; to demonstrate exercise induced changes and
differential diagnoses as well as complications.Background, mechanism
of injuries
MRI of muscle injuries in elite athletes
include a large variety of imaging patterns from very subtle signal changes to
complete muscle ruptures, from acute muscle strains to exercise-related chronic
changes or complications such as myositis ossificans or muscle hernia. A
comprehensive overview is provided in a book chapter by Dimmick and colleagues
(Dimmick et al. 2013), which is recommended for further reading. When imaging
elite athletes there are differences compared to non-athletes. First, we perform imaging that is often not
required in non-athletes and some subtle new diagnoses may be seen. On imaging
often multiple pathologies are present so we have to really figure out what's
clinically relevant. 35 % of all soccer
injuries are muscle injuries and they are the most frequent cause for missing a
game. They usually occur during the game where the risk is about six times
higher compared to the training (Ekstrand Br J Sports Med. 2011). The mechanism
in soccer is mostly an indirect mechanism (96%) and only in rare cases a direct
injury which are more common in so called collision sports, for instance rugby
or American football. Direct blunt forces cause contusion injuries in the
direction of the force an often lead to deep hematomas, for instance in the
quadriceps muscle group. Indirect m.i. typically occur after eccentric
contraction for instance during sprinting or kicking. Typical injury patterns in
indirect mechanisms include a muscle fibre disruption accompanied by muscle oedema
and hematoma. The location of the injury within the muscle-tendon-bone complex
mainly depends on the age. In youth players, the non-fused apophysis is at most
risk while in older individuals it is the degenerated tendon. The majority of
elite athletes are in the “intermediate” group with a mature skeleton and no
degeneration where the weakest link is the myotendinous junction. So, when
reading MR imaging in athletes, one should pay a special focus on the
myotendinous junction. In soccer players, 92% of m.i. affect the lower
extremity. In 37% the hamstrings are involved, in 18% the quadriceps and in 30%
the groin. Within these major muscle
groups there are specific “high risk” muscles that are most commonly affected:
The biceps femoris muscle (86%), Rectus femoris muscles (88%) and the adductors
within the groin complex (Ekstrand, Am J Sports Med 2011).
Imaging tools and protocols
In the assessment of m.i. and besides the
clinical examination, ultrasound and MRI are used, CT only in cases of bone
involvement (fractures) or heterotopic ossifications. A survey among 23
European soccer teams (Ekstrand, Br J Sports Med. 2012) revealed that 58% teams
used MRI to examine suspected m.i., 29% used ultrasound, 40% both and 13% used
solely the clinical examination. In elite players MRI is the “gold standard”. The
main advantages of MRI in the context of m.i. are: (1) Definite exclusion of a
severe injury. Especially the accuracy in diagnosing deep lesions is superior
in MRI versus ultrasound (Guillodo et al. 2011) (2) Prediction of time to
return to play and (3) Precise follow up and monitoring of muscle healing.
Fluid sensitive sequences are most efficacious
in rendering conspicuous the intramuscular oedema associated with acute muscle injury,
in demonstrating muscle fibre discontinuity and tendon injury. Thus, either Dixon
or frequency selective fat-saturated proton-density weighted or short-Tau-Inversion-Recovery
(STIR) sequences in long and short axis should be used. A T1 weighted TSE
sequence may be added to characterize haematomas and identify of muscle
atrophy. In some cases, a third sequence in a third orientation may be helpful,
e.g. a T2 weighted TSE sagittal sequence. The use of contrast agent is not
necessary in m.i. except rare cases of suspected tumours or septic conditions. Muscle
fibre tracking with diffusion tensor imaging (DTI) has been used to assess
muscle damage and to measure pennation angle. Normal muscle on DTI demonstrates
uniformity in bulk directionality and exhibits orderly arrangements. Disturbance
of normal arrangement of muscle fibres is demonstrated on DTI after injury. At present,
DTI remains an investigation/research tool and does not play a role in the
clinical MRI assessment of muscle injury (Dimmick S. et al. 2013).
Grading and prediction of time to return to play
The most commonly used grading
systems divide muscle injuries in 4 grades O’Donoghue et al. 1962, Ekstrand et
al. 2012). Grade 0: Normal MRI (“functional injury”), grade 1: oedema, grade 2:
partial rupture, grade 3: complete tear. It is obvious that this is only a
rough grading and that grade 2 injuries comprise a wide range of muscle
injuries from tiny fibre discontinuity to subtotal muscle ruptures. However,
surgical treatment is only necessary in grade 3 injuries. Grade I muscle strain
demonstrates intramuscular signal hyperintensity on fluid sensitive sequences
without discernible muscle fibre disruption. The oedema pattern is classically
‘‘feathery’’ in appearance typically around the myotendinous junction. In
partial tears (grade 2), disruption of muscle fibres is identified. Oedema and
haemorrhage is present within the muscle or at the muscle–tendon junction,
often with perifascial extension. Complete tears (grade 3) demonstrate complete
discontinuity of muscle fibres, usually with associated tendon fibre discontinuity
and an associated haematoma.
The “time to return to play” is a complex
estimation and many items have to be taken into account. Besides clinical
considerations, imaging predictors have shown to correlate with recovery time.
First, the grade of muscle injury is correlated, the higher the grade, the
longer the injury period. However, a study by Ekstrand (Ekstrand Br J Sports
Med. 2012) did not demonstrate significant differences between grade 1 and 2
injuries regarding time to return. One reason might be that –as stated above-
the grade 2 injuries comprise a wide range of injuries. Measures of the
longitudinal lengths as well as percentage and volume of muscle injury (Connell
et al. 2004) in MRI are strong predictors of the time to return to play. It has
been suggested that persistence of oedema defines the period of increased
vulnerability to develop a re-tear (Fleckenstein et al. 1989). Also the
presence of an intramuscular tendon tear may be associated with delayed return to
play (Linklater JM, et al Semin Musculoskelet Radiol 2010)
Differential
diagnoses, exercise related muscle changes and complications of m.i.
In general post exercise oedema
demonstrates a ground glass-like, mild degree of signal hyperintensity and
often demonstrates a somewhat patchy geographic distribution. This usually
resolves within minutes of cessation of activity but may persist to some degree
for several hours without symptoms (Fleckenstein et al. 1988). Delayed onset
muscle soreness (DOMS) is an indirect muscle injury with reversible structural damage
to the muscle at a cellular level resulting in an acute inflammatory response
and an increase in intracellular fluid. The differentiation to grade I injuries
are made clinically as DOMS typically commence at 1–2 days after the causative
activity, is greatest at 24–48 h and gradually resolves over the next 48–72 h. Chronic
exertional compartment syndrome is often bilateral and relieved with rest. This
entity is due to increased compartment pressure during exercise. In patients
with chronic exertional compartment syndrome, signal hyperintensity within the
muscle peaks after cessation of exercise, with a delay in return to the signal
intensity and water content of a resting state. Muscle hernias may present as focal
out-pouching of the muscle through the fascial defect. As this often occurs
during muscle contraction, ultrasound with its ability to visualize movement is
superior in this situation. Another complication is the development of myositis
ossificans or heterotopic ossification, respectively. Typical imaging features
can be seen after about 6 weeks and reflects the zonal composition with a
peripheral rim of ossification. In T2 or T2* weighted images, this peripheral
rim appears hypointens. In this stage the rim is calcified and is best
visualised on CT. The ossification then develops towards the centre. This
pattern of calcification in myositis ossificans may be differentiated from
osteosarcoma which typically demonstrates central ossification, which then
develops peripherally.
Acknowledgements
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