The diagnosis of musculo-aponeurotic or tendon lesion is primarily clinical.
It is either an acute artery suspecting a myo-aponeurotic or myotendinous lesion or pure tendinous lesion, or a progressive implant pain, typically in the overuse of the traction by oversensitivity (Overuse of the Anglo-Saxons).
The physician ‘s problem is to know his degree of severity, which directly depends on the time he has stopped working.
Imaging (Doppler – associated ultrasound and MRI) is used to confirm the diagnosis, to assess its severity and to guide the treatment.
Classifications of muscular, myo-aponeurotic and myotendinous lesions:
They are extrinsic (by direct shock) or intrinsic (by abrupt contraction or poorly controlled contraction or by excessive stretching).
Extrinsic muscle lesions:
They sit in the muscular body, typically at the expense of the vast lateral (vast external) or vast intermediate (crural) on the deep side of the muscle (in contact with the femur).
They create muscle contusion (Grade 1 lesion) characterized by minor ruptures of the collagen fibers associated with an interstitial edema and a hemorrhagic suffusion extending to the muscle. These minor lesions are the cause of the combed appearance with the MRI, in hypersignal in weighting T2. The use of sequences particularly sensitive to water is essential to the search for any muscular, myo – vuvenetic or myotendinous lesions: T2 STIR sequences (sequence in fat suppression by inversion recovery which makes it possible to cancel the signal of fatty protons). This sequence must be systematically realized in the three planes of space. On ultrasound, a small area of discretely heterogeneous intramuscular edema, which may be hypo- or hyperechoic, should be carefully examined on the axial sections perpendicular to the major axis of the muscle.
The macroscopic structure of the muscle is respected.
There may be partial intramuscular ruptures (Grade 2 lesions). These ruptures are sometimes responsible, due to the particularly abundant bleeding in these very richly vascularized muscles of sportsmen, of intramuscular hematic collections. These should be detected in imaging (ultrasound or MRI) to guide the evacuating puncture as soon as possible before the compartmentalization created by the healing process makes it difficult and less effective.
Intrinsic muscle damage:
They do not occur in the full muscular body, but in the areas of weakness that constitute the myoapeneurotic or myotendinous junctions. They are due to the stretching of the aponeurotic envelope or the tendon by the sudden contraction of the muscular fibers adhering to it.
Grading of lesions according to O ‘ Donoghue and correspondence to imagery:
Imaging allows the clinician to know the degree of severity of the lesion: from simple contracture to complete rupture with retraction.
The simple contracture will have no translation to MRI or ultrasound imaging.
Grade 1: Lesions comparable to muscular contusions after direct trauma
These minor lesions are the cause of the combed MRI aspect, in T2 – weighted hypersignal, at the expense of the muscle fibers adjacent to the aponeurotic or tendon blade.
On ultrasound, a small area of intramuscularly discretely heterogeneous intramuscular edema, which may be hypotensive, should be carefully investigated on the axial sections perpendicular to the major axis of the muscle, within the muscle fibers adjacent to the aponeurotic or tendon blade. or hyperechoic.
The macroscopic structure of the muscle is respected.
Clinically, we will speak of elongation without loss of function of the muscle.
Grade 2: partial failure without retraction
A hematoma of the myotendinous or myo-aponeurotic junction is frequently observed and a fluid suffusion is observed at the periphery of the muscle.
In both MRI and ultrasound, more definite signal anomalies (MRI) or echogenicity (ultrasound) appear, or even a detachment blade at the interface with the blade fibrous (aponeurotic or tendon), itself thickened in hypersignal T2 (MRI) and iso-, even hypoechoic (ultrasonography). With the progression of scarring, the fibrous plate thickens, appears better defined, and its signal and its echogenicity are modified attesting the fibrocicatricial process in progress: it appears in hyposignal T2 (MRI) and hyperechoic (ultrasound). The intravenous injection of a paramagnetic contrast agent (gadolinium) in MRI and the doppler mode coupled to the ultrasound make it possible to assess the activity of the healing process.
Imaging thus takes a prominent place in the follow – up of these lesions, particularly in high – level athletes.
Clinically, they result in the impossibility of practicing a sporting effort and require the interruption of activity.
Grade 3: complete rupture of the myotendinous or myoapenevrotic junction
The diagnosis is clinical.
Imaging, particularly MRI, provides an assessment of the extent of retraction for a preoperative assessment.
Clinically, there is total loss of muscle function.
Grade 3B: avulsion – fracture at tendon insertion.
The myo-aponeurotic disinsertions are of three types depending on their location:
* Perimuscular musculo-aponeurotic disintegration, between superficial aponeurosis and muscle fibers adherent to the aponeurosis, typically that of the deep side of the medial gastrocnemius (internal twin) to its distal third;
* it may result in tearing of the deep aponeurotic blade of the gastrocnemius, an intermuscular detachment with soleus (soleus). This aponeurotic tear favors bleeding (the aponeurosis being portal vessels), causing serohematic sheaths, or even hematomas collected, which delay healing;
* intramuscular musculo-aponeurotic disinsertion, typically along the sagittal aponeurotic septum of the rectus femoris (anterior right) at its anterior and superior part.
Musculotendinous disinfection occurring by detachment between the superficial tendon and the muscular body on unipenned muscles; typically distal lesions of the femoral biceps or rectus femoris.
Classification of mechanical tendon lesions:
Different pathological types:
It may be peritendinitis or tenosynovitis (if the tendon is protected by a synovial sheath), cellulitis or even bursitis slippage.
These are noninflammatory degenerative intratendinous lesions including mucoid degeneration and disorientation of collagen fibers, hypocellularity, foci of necrosis, fibrocicatrical nodules, cystic cavities, calcifications, and even ossifications (enthesophytes of traction).
There are very few cells of inflammation: the term “tendinitis” is forbidden!
This is the longitudinal separation of the bundles constituting the tendon. Is it still a sign of tendinosis or already a partial rupture?
It is a hole in the tendon.
This involves the complete rupture of the tendon, the two extremities of which can more or less deviate. It can lead to total functional impotence (eg quadriceps tendon), but can be followed by the disappearance of pain with no significant functional impairment (eg tendon of the epicondylians).
Microscopically, the symptomatic tendon consists of discontinuous and disorganized collagen fibers. Tenocytes take on a chondrocyte appearance within mucoid ranges, producing a total of fibrocartilaginous metaplasia. Fibroblastic proliferation and neoangiogenesis testify to the repair process, but there are no cells of inflammation. It is not a tendinitis!
Several mechanisms are possible:
Tendinopathies of traction by repeated hypersollicitations:
Repetitive hypersollicitation involves almost exclusively the extensor biarticular tendons: patellar tendon (patellar tendon) or quadriceps tendon on the knee and Achilles tendon (calcaneal tendon) on the foot.
It causes tendinosis. It may be due to extrinsic factors: training error (rapid and excessive modification of the activity on repetitive gestures), technical error (change of gesture resulting in a modification of the axis of the tendon), material defect , unsuitable land.
Intrinsic factors should also be investigated: static disorders, instability, muscle imbalance, myotendinous retractions.
The abrupt surtraction is the cause of a tendinous rupture and most often decomposes a chronic tendinopathy of traction by hypersollicitation. It can also be the cause of an avulsion of the tendon, a tendon rupture or a myotendinous tear.
Direct trauma by a penetrating object or contusion on superficial tendons (patellar and quadripital tendons).
Friction repeated by friction or by jumping:
They initially cause peritendinous pathologies (tenosynovitis, peritendinitis, cellulitis, bursitis), or even more exceptionally, of tendon lesions per se.
It is essentially the tendons of the feet of the goose and the tensor of the fascia lata.
The diagnosis of the myotendinous and aponeurotic lesions of the athlete is essentially clinical. Imagery is called upon to confirm and evaluate their severity in order to better guide treatment in stubborn forms.
Doppler ultrasound, when performed by specialized radiologists, has become increasingly reliable.
The MRI intervenes either first or secondarily after ultrasound, especially in professional sport and in severe forms, when a surgical procedure is discussed. However, it remains more sensitive for the diagnosis of small lesions, particularly in the acute phase, but also in the dismemberment of complex lesions, which are not uncommon in sports.
It also makes it possible, in the event of a diagnostic doubt, to rule out differential diagnoses by precisely exploring the intra – articular, osseous structures and the whole of the para – articular structures.
Imaging can also guide the treatment if it reveals a hematoma that should be evacuated at best under ultrasound control.
It also allows to check the quality of the healing before resumption of the activity thanks to the Doppler mode associated with the ultrasound and the use of sequences after intravenous injection of Gadolinium in MRI.