Shoulder:Rotator Cuff Pathology/Thickness Rotator Cuff Tears/Traumatic versus degenerative tears

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Bullet points

  • Accidental lesion and lesion assimilated to an accidental lesion are two legal concepts.
  • They require expert medical knowledge to determine whether the lesion is of degenerative or traumatic nature.
  • Minor degenerative disorders, symptomatic or asymptomatic depending on the individual, are frequent over age 30 and should no longer be taken into account in deciding whether the origin of a lesion was traumatic or degenerative.
  • The prevalence of full-thickness degenerative lesions has significantly decreased over the last 15 years.
  • Full-thickness and anterior lesions are often accidental in younger subjects.
  • Demographic, anamnestic, clinical, radiographic and intraoperative data should be used to distinguish between degenerative and traumatic lesions.

Key Words

Rotator Cuff Pathology; Full Thickness Rotator Cuff Tears; Traumatic; Degenerative.


Traumatic lesion and lesion assimilated to a traumatic lesion are in some countries two legal concepts. The criteria allowing differentiation between degenerative lesions and lesions probably due to an accident sometimes lead to interminable legal quarrels between patients, the insured and insurance companies. Legal disputes are thus legion and risk delaying treatment, to the detriment of both patient and employer. The issue is medically critical, as rapid treatment of traumatic rotator-cuff lesions is the key to good functional outcome.[1][2][3][4][5][6][7]

The main difficulty is to distinguish between a traumatic rotator-cuff lesion, acute exacerbation of a pre-existing degenerative lesion, and simple painful or functional decompensation of a pre-existing degenerative lesion.[8] It is important to collate and distinguish objective and indisputable demographic, anamnestic, clinical and radiographic rotator-cuff lesion data (e.g., fatty infiltration) as a basis to decide whether in a given case the tear was traumatic (or assimilated) or more likely of degenerative or disease-specific nature. It is thus a question of defining the clinical and paraclinical data that formally confirm or exclude accidental status. A single risk factor, such as smoking,[9][10] hypercholesterolemia,[11] alcohol abuse,[12] high blood pressure,[13] hyperthyroidism,[14] critical shoulder angle,[15][16] or morphology of the greater tuberosity[17] is not necessarily a criterion.

Natural phenomena

Minor degenerative disorders, which may be symptomatic or asymptomatic depending on the individual, are frequent over 30 years old[18][19] and should probably no longer be taken into account in deciding whether a given lesion is degenerative or accidental. An ultrasound study of 51 asymptomatic patients aged 40 to 70 years reported abnormalities such as tendinosis (65%), acromioclavicular osteoarthritis (65%), labral pathology (14%) and partial tear of the bursa side of the supraspinatus tendon (22%).[8] The supraspinatus tendon insertion on the greater tuberosity may show degeneration that is probably multifactorial: vascular,[20] mechanical,[21] morphologic,[22][23] and genetic.[24]

The prevalence of full-thickness rotator-cuff tear in the population under age 70 who has never shown symptoms is at most 15%.[8][25]


Demographic criteria

Several studies have demonstrated that the prevalence of degenerative full-thickness tear is not as important as previously though (Table).

Table: Prevalence of degenerative full-thickness tear

20–30 y 30–40 y 40–50 y 50–60 y 60–70 y 70–80 y >80 y
Tempelhof et al.[26] 13% 20% 31% 51%
Abate et al.[27] 25% 25%
Fehringer et al.[28] 22% 22%
Moosmayer et al.[29] 2,1% 5,7% 15%
Yamamoto et al.[30] 0% 0% 0% 10,7% 15,2% 26,5% 36,8%
Liem et al.[31] 0% 0% 0% 0% 13% 37.5% 0%

In an ultrasound study of asymptomatic subjects over 65 years old, Abate et al. reported the prevalence of rotator-cuff lesions:[27] only 3.1% of non-diabetic patients had partial or full thickness tears of less than 1 cm, and 7.8% had tears greater than 1 cm. In a study of 200 shoulders in 100 patients with a mean age of 71.4 years (range, 65-87 years), Fehringer et al. found 22% prevalence of full-thickness rotator-cuff lesions in patients consulting for lower-limb issues, whether the shoulder was symptomatic or not.[28] Another ultrasound and magnetic resonance imaging (MRI) assessment of 420 asymptomatic volunteers found a prevalence of full-thickness rotator cuff tear of 2%, 6% and 15% in the 50-59, 60-69 and 70-79 year-old age-groups respectively,[29] with location in the supraspinatus tendon in 78% of cases. In a similar study of 664 volunteers in a single village, prevalence of full-thickness tear was 22.1%:[30] 0% between 20 and 49 years of age, 10.7% for subjects in their 50s, 15.2% in the 60s, 26.5% in the 70s and 36.6% in over-79 year-olds; only 34.7% of these lesions were symptomatic. Liem et al. reported no rotator-cuff lesions in a control group of 55 under 60 years old.[31]

In summary, lesions are rarely full-thickness before the age of 60 (in fewer than 10% of cases even in the elderly), and involve the supraspinatus tendon in 85% of cases. Between 70 and 79 years of age, 74-89% of subjects have a functional rotator cuff. Traumatic tears concern younger subjects, with a mean age of 54 years.[5] A traumatic event was recorded in 79.2% of cases (57/72 shoulders) in a study of full-thickness cuff tear in subjects under 50 years old.[32]

Clinical criteria

Immediate impairment of active flexion or external rotation or onset of pseudoparalytic shoulder (loss of active anterior forward flexion) due to rotator-cuff tear are typical consequences of a trauma.[2][33][34][35][36] Berhouet et al. reported on 112 patients under 65 year old patients with rotator-cuff lesions. More than half had clearly been involved in an accident,[35] and all these patients showed loss of forward flexion or external rotation. Denard et al. prospectively studied 58 patients with pseudoparetic shoulder and rotator cuff tear;[36] 78% of the cases (45 out of 58) involved a trauma. There is thus a high rate of traumatic events associated with acute loss of function. Loew reported severe pain after traumatic rotator-cuff injury, subsiding after 3 days, which may account for delayed consultation and treatment.[33][34]

Factorial criteria

Only 5 studies reported the mechanism of traumatic rotator cuff lesions.[1][37][38][39][40] This mainly involves falling onto the arm in extension.[41] Other associated actions causing injury comprise external rotation against resistance, violent traction while trying to avoid a fall or lifting a heavy weight, or shoulder dislocation. However, the mechanism is usually unclear, especially in road accidents. The following actions should be considered:[33][34]

  • Significant trauma with violent passive backward and inward movement of the arm, or arm stabilized by muscle action: for example, trying to avoid a fall from scaffolding or on stairs.
  • Shoulder dislocation causes full-thickness cuff tear in 41% of cases in 40-to-55 year-olds, in 71% in 56-to-70 year-olds, and systematically in older subjects.[42]
  • Suddenly hanging with the arm in suspension bearing full body-weight.
  • Violent passive traction in adduction, antepulsion or abduction, as in wrenching the arm or trying to avoid a fall with arms outstretched.
  • Axial impact during a fall on the elbow or hand.
  • Direct shock to the shoulder without necessarily involving the arm in extension can also cause full-thickness tear.

Radiologic criteria

Correct analysis of assessment comprising conventional X-ray, ultrasound and magnetic resonance imaging (MRI) or computed tomography (CT) is often decisive and, in the light of present knowledge, can distinguish between degenerative and accidental lesions.

Conventional radiologic criteria

Acromion morphology and acromioclavicular osteoarthritis

Whether acromion morphology is a risk factor for rotator-cuff lesion is controversial. Acromion morphology according to Bigliani,[43] acromial slope in the frontal and parasagittal planes, lateral protrusion[44] and critical shoulder angle are debated factors.[15][16] Anterior coraco-acromial ligament spur,[45] presence of an os acromiale[46] and acromioclavicular arthropathy[47] do not correlate with rotator-cuff lesion; the only clear association is with acromial acetabulization.

Proximal humeral remodeling

Subchondral sclerosis and greater tuberosity subchondral cysts do not seem to be signs of chronic rotator-cuff lesion, having wide interobserver variability and poor predictive value.[48][49] They are thus not reliable signs of chronic or degenerative lesion, an seem to be related to age.[50] Chronic partial or retracted cuff lesions are associated with major remodeling of the greater tuberosity in the form of “femoralization” and osteopenia.[21][51][52][53] Localized greater tuberosity osteopenia on AP X-ray is the bone response to lack of mechanical stress (Wolff’s law).[54]

Acromio-humeral distance

Acromio-humeral distance <7 mm on anteroposterior shoulder view is a sign of chronic rotator-cuff tear.[55][56] Saupe et al. correlated this 7 mm threshold with computed tomography (CT)-arthrography evidence of lesion, and found full-thickness supraspinatus tear in 90% of cases, infraspinatus tear in 67% and subscapularis tear in 47%.[56] Distance <7 mm generally corresponds to a massive tear of several months’ progression, associated with altered muscle trophicity.[55][56]

Magnetic resonance imaging (MRI) and computed tomography (CT) criteria

The only irrefutable signs of accidental lesion are fractures and stigmata of glenohumeral or acromioclavicular dislocation.[57] Magnetic resonance imaging (MRI) and, to a lesser extent, computed tomography (CT) are now contributive to confirming or ruling out accidental etiology. Above all, they can rule out occult fracture, notably of the greater tuberosity.

Rotator-cuff muscle atrophy

Supraspinatus atrophy is assessed via the tangent sign.[58] A positive tangent sign is risk factors for incomplete rotator cuff repair repair.[59]

Rotator-cuff fatty infiltration

Magnetic resonance imaging (MRI)[60] and computed tomography (CT)[61] quantify fatty infiltration in the rotator-cuff muscles. This quantification is essential, as initial fatty infiltration exceeding grade 2 generally contraindicates repair surgery, because of a very high risk of healing failure. It is thus a decisive prognostic factor for clinical and radiological outcome.[62] For the supraspinatus muscle, it is more reliably assessed in the axial plane.[63] The fish backbone sign also indicates a chronic lesion (Figure).[63]

The fish backbone sign illustrates Goutallier grade 3 or 4 fatty infiltration. Left: The supraspinatus muscle in the horizontal (axial) plane with grade 3 fatty infiltration. Right: Note the resemblance to the backbone of a fish.

Fatty infiltration has several potential origines such as age or rotator cuff lesion.

  • Fatty infiltration of rotator cuff muscles increased naturally with age, with a significant acceleration after 40 years. A fatty infiltration graded 2, a common threshold for management decision, is commonly found in those aging patients with intact cuff on computed tomography (CT) arthrography.[64] A fatty infiltration graded 2 or below is thus not always associated with a rotator cuff lesion.
  • Fatty infiltration seem to appear quickly after a rotator cuff lesion, as soon as 3 weeks in animal models.[65][66] In humans, significant fatty infiltration is observed only after 6 months or if there is no traumatic etiology.[35] In both traumatic and non-traumatic cases, grade 2 fatty infiltration sets in at 3, 2.5 and 2.5 years after symptom onset in the supraspinatus, infraspinatus and subscapularis muscles, respectively; progression to grades 3 and 4 takes respectively 5, 4 and 3 years (Table).[67][68] Isolated supraspinatus lesions showed no significant fatty infiltration at 4 years’ follow-up.[69] In contrast, massive lesions become irreparable after the same period of time.[70]

Time to onset (months) Supraspinatus fatty infiltration Infraspinatus fatty infiltration Subsacapularis fatty infiltration
Minimal Intermediate Severe Minimal Intermediate Severe Minimal Intermediate Severe
Overall series 24 46 70 26 44 67 24 34 46
Traumatic onset 19 35 58 19 31 46 17 31 39
Progressive onset 29 54 84 33 56 84 33 36 55

Table: Average time to onset of different fatty infiltration stages assessed in overall series and traumatic versus progressive onset.

According to Goutallier,[61] significant fatty infiltration (grade 3 or 4, generally contraindicating repair) at the time of the accident probably involves decompensation or acute extension of a pre-existing lesion. Severe fatty infiltration may however develop within months of accidental massive lesion, particularly if the anterior rotator cuff is involved (Figure).

T1-weighted sagittal slices without fat-sat: pseudoparalytic left shoulder 4 months (A) and 7 months (B) post-trauma. Infiltration became severe by 3 months, contraindicating repair.
Bone and muscle edema

Greater tuberosity edema used to be thought of as being associated with full-thickness rotator-cuff tear,[71] but this was not confirmed in a more recent study.[57] Screening for muscle edema, on the other hand, is crucial. Except in real involvement of the muscle-tendon junction,[72] rare denervation phenomena as found in suprascapular nerve compression (<2%)[73] or Parsonage-Turner syndrome and other infrequent entities,[74] muscle edema is associated with acute retraction and indicates accidental etiology (Figure).[57] Onset is within days, unlike neurologic edema, where onset is a matter of weeks.

Examples of acute posterosuperior rotator-cuff edema in traumatic tear with chronic anterior cuff lesion. A: Posterosuperior rotator-cuff edema on frontal T1 slices. The persistence of a tendon remnant on the greater tuberosity is also indicative of traumatic etiology.[75] B: T1-weighted sagittal slice, showing significant fatty infiltration only in the subscapularis.
Changes in subacromial and subdeltoid bursa

Fluid or hematoma in the bursa is more frequently found in acute than chronic lesions, and is generally associated with lesions of the tendon rather than of the tendon-bone junction (mid-substance tear). Blood signal following an accident is a sign of traumatic rotator-cuff lesion.[76]

Location and type of tendon lesion

Location of the lesion is also an important factor. In the frontal plane, traumatic lesions generally involve the tendon itself.[76] Medial tendon retraction according to Patte[77] (Table) then develops,[71] generally with slow progression. Braune et al. found no retracted tendons in the glenoid or beyond 12 weeks after trauma.[78] However, some cases of grade 3 retraction at the glenoid without fatty infiltration may be found during the weeks following a trauma, suggesting acute massive lesions with severe muscle and tendon retraction. In the sagittal plane, subscapularis tendon lesions are typical of accidents.[3][37][79] Moreover, 80% of asymptomatic lesions involve the supraspinatus tendon.[29] Anterior or posterior extension in a previously asymptomatic patient suggests a traumatic etiology.

Intraoperative criteria

Lesion type alone may not be a sufficient criteria to determine a traumatic or non-traumatic etiology.[78] The most significant criteria for traumatic origin are hemarthrosis, tendon remnant on the greater tuberosity, frayed and bleeding tendon edge, and subscapularis involvement.[75][78]


Rotator-cuff tears are most often degenerative but some may nevertheless be caused or aggravated by a traumatic event. It is not recommended to apply just a single criterion, such as age, to determine whether a causal relation is above or below the threshold of likelihood. The field of application of the concept of causality (no accident, no injury) is deliberately wide; ruling it out requires an exhaustive argumentation using all of the criteria defined above. 


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