MODULE 2: Glenohumeral Joint Instability: History and Subjective Examination

Welcome to the training modules

History of Patient Presentation and Primary Mechanism of Injury.

The patient history (particularly the mechanism of injury) can determine the patient’s sub-group of
instability (maco-traumatic, mico-traumatic or atraumatic instability), and assist in formulating an
evidence-based treatment pathway(Sadi et al., 2020).


 

1.1 Macro-traumatic (traumatic) Instability.

  • As mentioned in MODULE 1, macro-traumatic instability is the result of an acute trauma to
    the shoulder, such as a fall or collision in contact sport or it can be due to a sudden
    increase in overload leading to a “moment in time” when a structural lesion develops
    (such as the last repetition of a bench press after an overloaded session in the gym or
    the last few serves after doubling training duration in a tennis session).
  • There are variations as to how any an individual’s GHJ will be impacted by any one traumatic
    event, dependent in part due to the variability of an individual’s anatomy and presence
    of any underlying GHJ hypermobility. In some circumstances the exact position of the
    arm at the time of injury is known, in others it is unclear.
  • Once a traumatic event has occurred, then this will affect the individual’s movement
    strategies, particularly if there is structural damage to the joint.

 

1.1.1   Macro-traumatic Anterior Instability

  • In traumatic anterior instability, the history is usually one of contact with the arm in 90° or
    above, such as a fall, collision or tackling incident where the arm is forced back into a
    combination of elevation, external rotation +/- extension (McCluskey & Getz, 2000).
    This mechanism of injury is very typical of a sporting scenario but could also occur
    in a workplace or home setting.
  • In traumatic anterior instability, particularly in a high-speed collision scenario, the humeral
    head will dislocate anterior-inferiorly, creating damage to the anterior-inferior capsuloligamentous
    and labral complex, plus or minus the anterior glenoid rim (Boney Bankart lesion)
    and/or posterior humeral head (Hills-Sachs lesion).
  • If the HH locks out, (HH shifts over the glenoid rim and does not spontaneously reduce;
    grade 3+) then it will need to be reduced (relocated) and the patient may report having to
    have their shoulder relocated or “put back in” either by someone present at the scene or
    in hospital (plus or minus the use of anaesthetic). In other scenarios, the HH may
    spontaneously reduce once the patient moves, particularly if the underlying joint is hypermobile.
  • In some other macro-traumatic situations, the GHJ may not dislocate, but sublux, where
    the humeral head has translated enough to almost come out over the glenoid rim but
    fails to meet a grade 3+ dislocation.
  • A traumatic subluxation can also result in damage to the anterior inferior capsuloligamentous
    and labral complex, plus or minus injury to the anterior glenoid rim and/or humeral head.
  • In some, less common scenarios, an anterior dislocation or subluxation in lesser ranges
    of elevation, such as a collision or fall with the arm tucked in by the patient’s side.
  • In some situations, the HH can be displaced more anterior superiorly. Examples
    include a fall onto the point of the elbow (which drives the HH anterosuperior) or a fall onto
    an outstretched arm with the arm behind the body ( e.g. slipping over on ice). This can
    result in a traumatic SLAP lesions or combined SLAP and superior glenohumeral
    ligament (SGHL).
  • Patients with macro-traumatic anterior instability will typically report apprehension,
    weakness, positional specific pain, and/or avoidance in combined positions of abduction
    and ER at 90° of elevation; such as reaching back behind their head or getting their arm
    back to throw a ball (see more in aggravating factors and symptomology section).

 

1.1.2   Macro-traumatic Posterior Instability

  • In maco-traumatic posterior shoulder instability (PSI), the history is usually one with arm
    in a position of flexion, horizontal flexion (adduction) and internal rotation usually at or above
    90° of GHJ flexion, where the force of the mechanism subluxes or dislocates the HH posteriorly.
    Examples are a fall onto an outstretched arm in a forwards (flexed) position or tackle or
    fall with the arm coming across the body (shoulder in adducted position). A fall in a workplace
    scenario can also result in a similar injury.
  • Damage typically occurs to the posterior capsuloligamentous and labral complex,
    plus or minus the posterior glenoid rim (reverse bony bankart lesion) and/or anterior
    humeral head (reverse Hill Sachs)
  • Spontaneous relocation of posterior dislocations is much more common in posterior
    instability as only 23 % of traumatic posterior instabilities require reduction. (Goubier,
    Iserin, Duranthon, Vandenbussche, & Augereau, 2003; L. F. McIntyre, Caspari, & Savoie,
    1997; Williams, Strickland, Cohen, Altchek, & Warren, 2003; Xu et al., 2015). This may
    be due to the posterior aspect of the shoulder having more anatomical variations
    (e.g. glenoid retroversion, glenoid dysplasia, variations in labral shape and attatchments)
    (Ogul, Taydas, Sakci, Altinsoy, & Kantarci, 2021) and a thinner capsulolabral complex
    compared to the anteriorly(Dashottar & Borstad, 2012); allowing for less restraint
    to spontaneous relocation of the HH when the patient moves.
  • After a maco-traumatic PSI incident, the patient will often report that they experienced
    a specific incident where their arm was injured but have no awareness that a dislocation
    or subluxation occurred. The next day, the patient may report difficulty using their arm
    and significant pain that lasts for weeks. This is often from the bleeding that has occurred
    overnight from damage to the capsuloligamentous, labral and/or bony structures that results
    in joint effusion (swelling), limiting range and creating pain.
  • The spontaneous relocation of many posterior dislocations,(Goubier et al., 2003;
    L. Watson et al., 2023; Williams et al., 2003) reduced awareness of posterior dislocations
    by the patient, and a low level of clinical suspicion of the condition,(Valencia Mora et al.,
    2017; L. Watson et al., 2023) often leads to PSI being missed or misdiagnosed when the
    patient presents to the health practitioner.(Schubert & Duralde, 2021)
  • Patients with macro-traumatic posterior instability may report pain rather than apprehension
    (ref) (though apprehension and avoidance may still be reported) in combined positions
    of flexion, HF and IR (see more in aggravating factors and symptomology section).

 

1.2   Micro-traumatic Instability

  • As mentioned in MODULE 1, micro-traumatic instability is caused by a gradual or acute
    overload of musculature +/- capsuloligamentous structures (ref) This type of instability
    is common in patients who regularly go to the gym or participate in repetitive overhead
    sports such as swimming and tennis.
  • With microtraumatic Instability this can be acquired by gradual over use or loading
    in a repetitive scenario – such as throwing sports, swimming or gym
  • Or it can be as a result of an acute overloading incident such as mistiming a throw
    or use of the racquet (in tennis) at a particular moment in time (usually with a high load of
    force +/- awkward or end range of motion) – Or in a scenario where there is acute
    overloading in a situation such in gym where the patient loses control of a motion – usually
    under high weight load or in an awkward motion – such as a bench press, incline press or
    overhead press. The same stressors could apply in an overuse scenario in a heavy
    manual loading job such as a line man or construction worker
  • Due to the history of micro-trauma, compared to the atraumatic sub-group, this group
    have a higher likelihood of acquired structural lesions. Theses structural lesions typically
    include small labral tears (anterior, posterior or SLAP lesions) plus or minus stretched
    (volumised) and attenuated capsulolabral structures.
  • Patients often have a previous a history of shoulder pain, especially with high-volume,
    activities, such as increasing training loads or high-level tournaments. These episodes
    may have been previously conservatively managed (with an ability for the patient to continue
    participating in sport) but recently there has been a definite increase pain levels, [pain frequency or
    both.
  • Both non-modifiable and modifiable factors impact on the micro-traumatic shoulder
    presentation.
  • Non-modifiable factors include patient anatomy, age and gender.
  • Although shoulder hypermobility is a characteristic feature of atraumatic instability
    (ref), the presence of shoulder hypermobility is not uncommon in the micro-
    traumatic group.
  • In the sporting population, up to 13 % of males and up to 42 % of females will have
    underlying joint hypermobility(Nathan, Davies, & Swaine, 2018). Hypermobility increases
    the prevalence of overuse sporting injuries(Liaghat et al., 2021; Mise et al., 2022)
    and increases the risk of macro-traumatic instability in a contact senario
    (Cameron et al., 2010; Chahal, Leiter, McKee, & Whelan, 2010)
  • In the setting of underlying GHJ hypermobility, patients can often present with combined
    instability, usually anterior inferior or posterior. Swimming(Pink & Tibone, 2000) (McMaster,
    Roberts, & Stoddard, 1998; Zemek & Magee, 1996) and tennis (L. Watson et al., 2023)
    in particular, are populations that have an increased incidence of posterior-
    inferior laxity and micro-instability.
  • Alterations in bony anatomy have also been shown to have as association with predisposition
    towards instability (Bradley, Baker, Kline, Armfield, & Chhabra, 2006; Hohmann & Tetsworth,
    2015; Owens et al., 2007; Weishaupt, Zanetti, Nyffeler, Gerber, & Hodler, 2000) and have
    a higher incidence in certain sporting populations.(Greenberg, Fernandez-
    Fernandez, Lawrence, & McClure, 2015)
  • For example, the dominant shoulder of baseball pitchers have a higher incidence
    of glenoid retroversion when compared to the non-dominant side(Wyland et al., 2012)or
    the shoulders of the non-throwing population(Rassi, Subhas, Bullen, Forney, & Polster,
    2019) A significant increase in glenoid retroversion (above 10 degrees) is associated
    with the development of PSI. (ref)
  • Unilateral overhead sportspeople may also have bony adaptation to the humerus which
    is often normal and not associated with the development of shoulder pathology. One adaption
    that has been found in baseballers and tennis players is an increase in humeral retroversion
    (or retrotorsion) where the humerus is oriented in a posterior-medial direction)
    (Greenberg et al., 2015). This bony adaptation results in an increase in shoulder ER range
    of motion
    and a concomitant decrease in shoulder IR range of motion compared to the contralateral
    side, which is thought to favour the serving or throwing motion. (Hibberd, Oyama, & Myers,
    2014; Reagan et al., 2002; Wyland et al., 2012) Clinicians should be cautious when
    screening for and implementing interventions for soft tissue motion deficits based on
    clinical ROM measures and mistaking humeral retroversion for pathological glenohumeral
    internal rotation deficit (GIRD) (See more in Module 3).
  • To date, it is unknown if a patient’s anatomy creates a biomechanical advantage for enhanced
    performance in particular sports (for example, patients with inherent GHJ hypermobility
    have a biomechanical advantage for stroke length in swimming (ref)); or if the acquired
    forces and loads of a particular sport alters a patient’s anatomy for enhanced performance
    over time (for example, the humeral retrotorsion that occurs in baseballers who commence
    throwing at a young age before humeral head physis has occurred). (Wyland et al., 2012)
  • Volume of play, shoulder muscle strength, scapula position, player position, and participation
    in prevention programs are examples of modifiable risk factors.
  • A recent systematic review(Hoppe et al., 2022) found moderate level evidence that the
    following was associated with shoulder injuries in overhead sports:

    • Player position (e.g.: baseball pitcher in baseball= increased risk of injury)
    • Gender (females more likely to sustain a shoulder injury)
    • Shoulder rotation ROM (ER ROM deficit only= more likely to have shoulder injury and
      more likely to have surgery).
    • Shoulder rotation strength (reduced ER/IR strength = increased risk of injury)
    • Scapula dyskinesia (presence of scapula dyskinesia in abduction =increased
      risk of injury)
    • Prevention programs (decreased the risk to sustain shoulder problems by 28%,
      except if the injury was moderate and severe).
    • Playing volume (increased volume = increased risk of injury)
    • Adolescents may be at higher risk for shoulder injuries due to an immature musculoskeletal
      system; particularly in regards to playing volume(Zaremski, Zeppieri, & Tripp, 2019)
      For example, high levels (volume) of early sports specialisation in baseball, independent
      of fatigue, age, and workload, place adolescent athletes at increased risk of injury and
      serious overuse injury. (Jayanthi, LaBella, Fischer, Pasulka, & Dugas, 2015)
    • Certainly throwing (overhead loading) more than 3 hours per week before 10 years
      of age has been shown to result in a greater likelihood of shoulder injury (ref)
    • If a patient has developed anterior dominant microtraumatic instability they will report
      positional specific pain in positions of abduction / external rotation at 90° of elevation
      such as the cocking phase of throwing or serving in tennis, backstroke in swimming &
      opening their arms out in pec fly positions in the gym(Kuhn, 2010)
    • If a patient has developed posterior dominant microtraumatic instability then they will
      report pain with deceleration or letting go of the ball in throwing or follow through or backhand
      in tennis or push up into a bench press or overhead press position at the gym(Kuhn,
      2010; L. Watson et al., 2023; L. A. Watson et al., 2017)
    • If a component of inferior instability is present the patient will report not liking or avoiding
      carrying things by their side (especially if they are heavy) & often lying on their side at night
      (Kuhn, 2010; L. Watson, Pizzari, Balster, Lenssen, & Warby, 2022)
    • If the instability is chronic or if the underlying joint is hypermobile then patients may
      complain of anterior & inferior instability symptoms, posterior inferior instability symptoms
      or a combination of all 3 (anterior, posterior & inferior)
    • The clinician should question the patient on any changes in technique (e.g. changing
      serving action in a tennis player) or equipment (e.g. increasing or decreasing the weight of
      a racquet by more than 5kg).
    • Again, the patient can usually determine the worst position for their shoulder or in which
      position the shoulder was overloaded – indicating their primary direction of instability
      (Kuhn, 2010; Kuhn, Helmer, Dunn, & Throckmorton, 2011).

 

1.3  Atraumatic Instability

  • As mentioned in MODULE 1, atraumatic instability has no seemingly obvious mechanism
    of injury or cause of onset. Atraumatic shoulder instability is characterised by aberrant
    motor patterning of the scapula and humeral head superimposed on a background
    of congenital capsular hypermobility (Ref).
  • This sub-group of instability is associated with a higher rate of congenital anomalies
    such as glenoid retroversion, glenoid hypoplasia, absent labral tissue, a voluminous
    joint capsule and wide rotator intervals (ref).
  • There is a higher incidence of GLL and collagen disorders (Ehler’s Danlos and Marfan’s
    Syndrome) in patients with atraumatic shoulder instability.
  • In atraumatic instability the patient may be aware that they have hypermobile shoulders
    as well other hypermobility in other synovial joints if generalized ligamentous laxity is
    present. In this case, they may report that they have always had clicking or clunking
    shoulders and may even be able to demonstrate spontaneous voluntary subluxations
    of the humeral head which called “volitional instability” (ref).
  • In other situations, the patient may have no awareness of any hypermobility in their
    shoulder girdle.
  • It is common for patients with atraumatic instability to report that they have always
    had poor posture as they typically sit with their scapula in depression and downward
    rotation at rest. This creates a “dropped” shoulder girdle position which contributes
    to poor posture.
  • Hypermobile shoulders often have less shoulder girdle muscle bulk than other populations,
    (Simmonds & Keer, 2007) which is possibly due to alterations in hormonal
    (Denko & Boja, 2001), collagen(Malfait et al., 2006) (Child, 1986)and muscle fibre (ref)
    type proportions.
  • Symptoms are typically a combination of pain, avoidance, feelings of “looseness”
    or that the joint is “out of place”, loss of control in certain motions and restriction of range
    of motion (due to uncontrolled and excessive HH translations blocking motion) (ref).
    Apprehension may be reported but is less common (ref). Shoulder range of motion
    (particularly those that cause symptoms) can produce GHJ clicking (see more in aggravating
    factors and symptomology section).
  • As patients with atraumatic shoulder instability will typically have two or more directions
    of instability (ref) patients may report symptoms in multiple GHJ positions (ref). Most patients
    will have a primary direction of instability where their symptoms are more severe (ref)
  • In some patients, spontaneous subluxations are reported that can be voluntary (controlled
    by the patient) or involuntary (uncontrolled by the patient) or a combination of both.
  • Pain is often due to secondary rotator symptoms. The rotator cuff may be overloaded
    due to excessive fatigue from trying to control the HH (often in a poor length tension
    relationship due to poor scapula position),(ref) or the subluxing or translating HH causes
    excessive compression and/or traction on the rotor cuff tissues (particularly the articular
    surface) which generates pain (ref)
  • Patients may also describe a deep, vague pain inside the GHJ that can hard to localize.
    This pain is often associated with a particular movement in which there is loss of HH control;
    such as reaching across the body in posterior dominant atraumatic instability (ref).
  • The history of onset is usually associated with increased symptoms after an increase
    in activity level (such as swimming) or commencement of an unfamiliar activity such as
    taking on a new sport or gym which they have not previously done
  • Onset can also occur with waking up one morning with pain after sleeping awkwardly
    on their shoulder
  • It can be associated with increased fatigue levels such as carrying a heavy school
    bag or backpack
  • Or there can be spontaneous onset of subluxation events that don’t seem to have
    any provocation factor – such picking up a school bag or taking off a tight top
  • In atraumatic instability the patient will have symptoms in two directions (posterior-
    inferior or anterior-inferior) or all three directions (anterior, posterior and inferior).

Shifting sub-groups

  • It is important to be aware that patients can shift sub-groups within their clinical history.
    For example, a patient may have a history of atraumatic instability (reporting they’ve
    always been “loose and clunky” since a child and been able to voluntarily sublux their shoulder
    free from pain). Later, they’ve fallen over in the shower, dislocated their shoulder (which
    required reduction) and sustained a structural lesion. The patient now presents with maco-
    traumatic instability superimposed on a background of atraumatic instability.
  • Patients may also develop macro-traumatic instability on a background of mico-
    traumatic instability. For example, a swimmer that has been having significant shoulder
    pain from over training may have a sudden posterior subluxation event diving into the
    pool at the start of their race. This patient now has macro-traumatic instability superimposed
    on a previous history of micro-traumatic instability.
  • Patients may develop micro-traumatic instability on a background of atraumatic instability.
    The hypermobile, MDI type patient may start a boot-camp or push up challenge in the gym
    and develop micro-traumatic instability (and possibly acquire structural lesions) over a period
    of weeks or months.

 

Aggravating Factors and Directions of Instability

  • A patient’s reports of their shoulder position of aggravation (or avoidance) can assist
    with determination of the direction or directions of instability (Kuhn et al., 2011) as these
    reported positions of aggravation (or avoidance) have a good correlation (82 % agreement)
    with objective testing (Kuhn et al., 2011)
  • This has been shown for anterior, posterior and inferior instability as well as combinations.

Anterior instability

  • If a patient has anterior instability, they will typically report their worst symptoms
    (apprehension/avoidance/positional specific pain) in positions of combined abduction
    and external rotation at 90° of elevation (ref).
    Examples include:

    • cocking position for throwing (baseball, cricket, rugby) or serve (i.e.: tennis)
    •  latissimus (“Lat”) pull-downs behind the head or pectoralis (“pec”) flies in the gym.
    • Swinging actions with the arm above your head such as monkey bars, gymnastics,
      rock climbing or bouldering
    • Catching a ball behind the head in overhead sports (AFL, NFL, rugby, basketball,
      netball).
    • reaching back behind their head for a light in bed/seatbelt
    • Sleeping with your arms up and over the head 

Posterior instability

  • If a patient has posterior instability, they will typically report symptoms
    (apprehension/ avoidance, positional specific pain) in positions of flexion, horizontal
    flexion (adduction) and/or internal rotation (IR). (ref)
    Examples include:

    • reaching across the body to pull down a seatbelt, 
    • crossing the arms across the body to pull off a tight top, 
    • driving with the arm up on the steering wheel,
    •  the follow through phase of a throw or serve, 
    • the pull phase of the swim stroke 
    • bench press, overhead press or push ups in the gym.  
    • a plank  or downward dog yoga pose.
    • Sleeping on the affected arm at night or having the affected arm in horizontal
      flexion (across the body) while sleeping.

Inferior instability

  • Inferior instability will not be present in isolation. It will be present in combination
    with anterior or posterior instability. If a component of inferior instability is present,
    the patient will report apprehension, avoidance or positional specific pain with forces
    that create inferior translation of the HH.
    Examples include:

    •  carrying heavy shopping or weights by their side with the affected limb. (ref) 
    • carrying a heavy backpack on the shoulders or in the hand
    • prolonged computer use or writing
  • A patient may have inferior instability as a component of multidirectional instability,
    as part of a SGHL capsuloligamentous complex injury, as part of a traumatic SLAP
    lesion (especially if combined SLAP), an extensive anterior or posterior labral injury
    involving the superior and inferior aspects of the labrum or due to any structural lesion
    superimposed on a hypermobile joint.

Bi-directional instability

  • Bi- directional instability (instability in more than one direction) such as anterior inferior
    or posterior inferior instability has been described as part of the symptomatic hypermobile
    or MDI patient presentation (MODULE 1) and can also occur as a result of patients
    with extensive structural lesions.
  • Patients may also develop bi-directional instability as part of ongoing anterior or posterior
    dominant instability, especially once it becomes chronic or recurrent(Curl & Warren,
    1996) Curl and Warren (1996) first brought this to clinical light when they reported
    that it was really impossible for the shoulder to traumatically dislocate or sublux anteriorly
    without the posterior GHJ being affected. This phenomenon is commonly highlighted
    with an anterior GHJ dislocation, with a bony Bankart lesion occurring on the anterior
    glenoid, and a Hill Sachs lesion occurring on the posterior HH. Similarly, with a first time
    anterior dislocation – the majority of the force will impact the anterior band of the IGHL but
    some force will still be taken by the posterior band IGHL (ref – Terry ?)
  • Equally, the shoulder cannot sublux posteriorly without the anterior GHJ noticing, especially
    subscapularis. This is why many patients with posterior instability also report anterior
    shoulder pain due to anterior pathology such as partial tears around subscapularis
    (K. McIntyre et al., 2016)
  • In the context of recurring anterior instability, increasing stress is placed on the posterior IGHL,
    often leading to a secondary posterior instability. Patients will still report symptoms
    in their primary (anterior) direction of instability (abduction, external rotation and 90° of
    elevation) but start to develop symptoms in positions that are more representative
    of PSI (flexion, horizontal flexion and/or IR).
  • If the underlying joint is already hypermobile then bi-directional or even tri-directional
    instability is more likely to develop as there may already be a component of inferior
    laxity that becomes more obvious and symptomatic once trauma is imposed.
  • Understanding the patient’s direction/s of instability is imperative for planning exercise
    selection, and for the surgeon to understand, should surgery be warranted.

 

Symptomology

3. 1  Instability symptoms

  • The classic instability symptom reported is one of apprehension and/or avoidance in a specific
    position, such as abduction and ER 90° of elevation for anterior instability and flexion/HF
    and IR for posterior instability. (ref). Patients with instability may also experience sharp pain
    (plus or minus a sensation of the shoulder “giving way”) and weakness with quick or unguarded
    movements, such as suddenly changing direction of a throw.
  • While apprehension (including avoidance) is typically with traumatic structural instability (ref)
    (particularly anterior macro-instability) (ref), other sub-groups are more likely to experience
    pain because of their GHJ instability.
  • Patients with micro-traumatic instability may experience sharp pain, catching, loss of control
    and/or a loss of power with certain positions in their sport, such as the cocking phase of
    the throw for anterior instability or the follow through phase of a serve/preparation for a backhand
    in tennis for posterior instability.
  • Patients with atraumatic instability may also experience sharp pain, catching, and loss of
    control in certain motions, but also report feeling subluxations and feelings of “looseness”
    in the shoulder.

 

3. 2  Dead Arm Symptoms

  • The use of the arm forcefully in a position of abduction, ER at 90° elevation and extension
    may be associated with the feeling of the arm going “dead” or sudden onset of weakness.
    This is referred to as “dead arm” (ref). The patient reports a sudden onset of loss of control of
    their arm in the position of abduction and ER 90°, often with the need to “shake their arm out”
    before a feeling of control returns.
  • “Dead arm symptoms” have been attributed to episodes of anterior instability where the HH
    has translated enough to impact the axillary nerve but not create any permanent neurological
    injury.
  • More than 3 episodes of “dead arm” are considered equivalent to a full anterior dislocation
    event (ref).
  • A reverse “dead arm” has been described for posterior instability of the shoulder which
    typically causes a sudden shooting pain down the lateral aspect of the humerus into the forearm
    (ref). This is thought to occur due to pressure of the posterior HH translating posteriorly
    onto the axillary nerve in the posterior quadrilateral space.
  • Intermittent neurological symptoms in the C8 to T1 distribution can also be associated
    inferior GHJ laxity or instability as the depressed scapula/shoulder girdle cause traction of
    the brachial plexus. Inferior instability can co-exist in any of the sub-groups of instability
    described above.

 

3. 3  Clicking

  • Clicking in the shoulder is quite common in GHJ instability and may be associated
    with varying causes, some of which may have high clinical significance some may not.
  • Clicking may be due to subluxation events, labral lesions and/or secondary stress
    on the sub-acromial bursa and AC joint.
  • MacFarland(McFarland, Kim, & Savino, 2002) showed in SLAP lesions that only 48% (?)
    patients reported clicking and that it didn’t have a significant statistical impact on the diagnosis
    of a SLAP lesion.
  • Clicking of the shoulder and its relative significance needs to be analysed in conjunction
    with objective examination of the shoulder girdle.
  • If a patient reports a painful clicking or clunking symptom associated with a specific
    movement then this clinically relevant and needs to be considered in the overall management
    plan

 

4. Pain Sites

  • Pain intensity, type and location can vary with GHJ instability and depends on several
    factors. The “acuteness” of macro-traumatic instability, with the possibility of bony damage
    (i.e.: a bony Bankart lesion) often causes high levels of pain for the patient when the joint is
    dislocated. In more chronic GHJ instability cases (such as micro-traumatic and atraumatic
    instability) pain is often associated with secondary cuff overload symptoms and may be described
    as “aching” or “burning” pain.
  • In some instances, the pain location can be vague, with the patient reporting symptoms
    deep inside the joint which is hard to localise but associated with specific positions that create
    excessive or uncontrolled translations of the HH. These aggravating positions may or may
    not be associated with a clicking or clunking of the GHJ.
  • Once any secondary irritation of the rotator cuff or the GH joint surface has occurred then
    more localised symptoms develop
  • Often with micro-traumatic and atraumatic instability there are multiple pain sites as chronic
    uncontrolled translation of the HH affects tissues structures on both sides of the GHJ (ref).

 

4.1  Anterior Instability

  • In anterior instability there may be pain in the anterior part of the joint (due to damage
    to the anterior capsuloligamentous or labral structures) but this can often be vague and hard
    to localise. The patient often indicates pain deep inside the front of the joint.
  •  In anterior instability, there may also be pain in the posterior aspect of the GHJ as the posterior
    HH may receive a bone compression injury (Hills Sach lesion) as part of the anterior instability event.
  • In micro-traumatic instability, the supraspinatus tendon may also get compressed between
    the HH and the posterior superior glenoid or have some fibres torn due to the excessive
    translation of the HH

 

4.2  Posterior Instability

  • In posterior instability there is frequently pain in both sides of the GHJ.
  • Pain may be present in the posterior joint line due to pressure of the HH on either the posterior
    labrum, capsuloligamentous complex or posterior chondral surface. There can be a tightening
    feeling in the posterior musculature due to the posterior cuff guarding against the excessive
    posterior HH translation
  • Posterior instability is often associated with compression pain in the anterior cuff. As the
    HH slides posteriorly, the subscapularis is compressed against the HH and the anterior
    glenoid fossa. (ref)
  • With more extensive posterior HH translation the subscapularis can be further traumatised
    setting up subscapularis tenopathology or partial thickness tear (refs)
  • A bony compression injury may occur between the anterior superior HH and the glenoid
    (a reverse Bankart lesion) which can also create pain in the front of the joint.
  • In posterior instability, due to the HH sliding excessively posteriorly, there often can be secondary
    stress reactions in the ACJ. This can result in the patient reporting ACJ pain that may or
    may not be associated with clicking. On MRI there is often oedema reported on the ACJ or
    early development of osteoarthritic change (ref).
  • Posterior instability of the shoulder is often associated with significant scapula winging (ref)
    so it is not uncommon for the patient to resport pain around the shoulder blade, typically
    with the arm in combinations of flexion, adduction (horizontal flexion) and internal rotation

 

4.3  Inferior Instability

  • If significant components of inferior instability are present, there is often more generalised
    pain around the rotator cuff; in particular the biceps and supraspinatus due to the humeral
    head creating a traction effect of these tendons.
  • With inferior instability the scapula typically sits in depression and downward rotation
    at rest, creating more traction around the medial scapula and into the cervical spine; hence
    symptoms are often reported in these areas.
  • This depressed scapula position can also be associated with clicking around the scapula
    and the thoracic spine (snapping scapula) due to the scapula rubbing against the thorax and
    creating irritation in either the bursa or soft tissues in the region (refs)

 

5.  Age

  • The age of the patient is relevant in any shoulder pathology and should be determined
    at the initial assessment.
  • The patient’s age is one factor that will increase the likelihood of a recurrence and the type
    of structural lesion present after a traumatic GHJ dislocation.
  • During a GHJ dislocation, younger patients (<40 years) are more likely to sustain capsuloligamentous
    injuries, after which the primary concern is a recurrence of instability (ref).
  • Traditional studies (ref) reporting on risk factors for recurrence of instability after a first-time
    traumatic event report that recurrence of instability significantly reduces over 40 years.
    However, there is limited evidence on the recurrence rates of patients over 40 years,
    with many studies (ref) limiting their inclusion criteria to an upper limit of 40.
  • A 2015 review (Shah et al., 2017) of GHJ dislocation risk in the United Kingdom by gender
    and age (including 16 to 70 year olds) found that while most primary GHJ dislocations
    occurred in young men (16-20 years), the incidence in women increased beyond 50 years
    (to a maximum at 61-70 years) thought this pattern was not observed in men. The reasons for
    this were unknown, however the authors hypothesised that these differences may be due to
    possible gender differences in falls risk(Gale, Cooper, & Aihie Sayer, 2016), joint proprioception,
    soft tissue tendon quality and protective muscle bulk.
  • The higher rates of dislocation among young males (16-20 years) in this study(Shah et al., 2017)
    is similar to that reported in other studies (based in Canada, Denmark, USA and Norway)
    (Leroux et al., 2014; Liavaag et al., 2011; Zacchilli & Owens, 2010)and is strongly associated
    participation of collision sports such as Ice Hockey or American Football.
  • The results of this UK review show that patients over the age of 40 (particularly females)
    can still have a traumatic GHJ dislocation, especially given that over 40-year-olds are more
    active today than when much of the recurrence studies were conducted (ref).
  • In some clinical cases, the over 40-year-old may still experience the typical dislocation
    event you might see in a 20-year-old, with pain, apprehension and increased risk of recurrence;
    especially if their dislocation resulted in a classic instability lesion such as a soft tissue
    Bankart tear.
  • However, during a traumatic GHJ event, the over 40-year-old is more likely to dislocate
    their shoulder primarily through the capsule without avulsing the ligaments and has a 7 times
    greater likelihood of sustaining a greater tuberosity facture(Shields, Jefferies, Brooksbank,
    Millar, & Jenkins, 2018).
  • This population are therefore more likely to have greater pain compared to a typical younger
    instability patient as they will experience pain from the fracture site as well as from any capsulitis
    response that may develop secondary to the capsule injury or fracture site bleeding into the
    GHJ. In this case, the patient is much more likely to have increased anterior and generalised
    shoulder pain, with significant night pain and increased aching during the day.

 

6.  Family History and Other Joint Involvement

  • It is imperative during the subjective to establish arm dominance and if symptoms
    are bilateral. Bilateral symptoms may indicate the presence of systemic hyperlaxity
    (e.g.: GLL) though hyperlaxity may also just be confined to the shoulders(Rupp, Rutledge,
    Quinn, & Millett, 2023; Schenk & Brems, 1998).
  • A family history of instability is important to note as this may indicate a hereditary component
    (e.g. due to GHJ retroversion, GLL) that predisposes the patient to developing instability
    (Guerrero, Busconi, Deangelis, & Powers, 2009; Johnson & Robinson, 2010).
  • Heredity, congenital and systemic factors can have implications for the management
    of a patient’s instability, including treatment timelines and discussions around expectations
    of outcome and return to sport, especially in the setting of a contact sport.
    ( See MODULE 3: Treatment).

 

7. Medical History

  • The medical history is important to note as part of standard medical care. Any previous
    or present diseases such as diabetes, cancer or auto immune and inflammatory disorders
    may be relevant to the patient’s instability presentation and treatment plan.
  • The patient’s current or previous history of any mental health issues, and whether they are
    receiving counselling +/- adequate medication) is also relevant to the patient’s presentation.
  • The clinician should question the patient on current or past medications and what condition
    they relate to.
  • The clinician should question the patient on a history of trauma to any part of the body
    which may lend insight to the initial mechanism of injury for a current shoulder problem.
    For example, a patient may not think its relevant that they had a major fall off their skateboard
    onto an outstretched arm and fractured their wrist when they were 16 years old. However,
    since then they haven’t felt comfortable pushing considerable weight through the shoulder
    and now 20 years on, they are experiencing shoulder pain when performing higher loads
    of bench press in the gym and a recent MRI confirms a chronic posterior labral tear.
  • Not only is the family history of GHJ instability, shoulder and/or generalised joint hypermobility
    important to discuss, but also if there are any symtpoms that may be associated with
    pathological alterations in the systemic collagen structure of the body, such as Hypermobility
    type Ehler’s Danlos Syndrome (EDHS).
  • Ehler’s Danlos Syndrome (EDS) a (likely) hereditary connective tissue disorder that affects
    musculoskeletal joints as well as other systemic systems. There are different sub-groups
    of EDS(Gensemer et al., 2021) but one of the most common types to be associated with GHJ
    instability is Hypermobility type EDS (hEDS)(Rupp et al., 2023) or EDS type III (Gensemer
    et al., 2021). Over 95 % of patient with hEDS/EDS III experience joint subluxations, with the
    shoulder being the most common(Tinkle et al., 2017) Due to alterations in collagen structure,
    patients with EDS commonly experience other systematic disorders such as gastric intestinal
    dysmotility, irritable bowel syndrome, autonomic nervous system dysfunction (such as postural
    orthostatic tachycardia syndrome (POTS)) cardiac value changes and skin alterations
    (Gensemer et al., 2021; Miller et al., 2020; Rupp et al., 2023).
  • Clinicians should query the patient on the presence of any night pain. While shoulder-
    specific night pain is often associated with the inflammatory phase of a shoulder condition
    (e.g.: acute injury, reactive tenopathology, reactive capsulitis), any unrelenting night pain or
    night pain not altered by a change in position, unexplained weight loss and/or night sweats,
    may indicate a more sinister condition. In such cases, a referral to the patient’s general
    practitioner (GP) and/or current medical specialist is warranted for further investigations,
    usually with MRI plus or minus CT scan.

 

8. Sporting, Activity and Occupational Objectives

  • It is vital to ascertain what the patients sport (elite, representative, recreational) activity
    and occupational participation (part time/full time) is as well as their goals and expectations
    (including timelines) around these activities.
  • Understanding the patient’s goals assists the physiotherapist to have a conversation
    about which treatment options will provide the best long-term outcomes or highest rate
    of success (eg: surgery vs conservative management), realistic timelines (when to expect
    return to training or play) and sport/ADL and occupational modifications in the immediate
    or long term.
  • Establishing hared goals between the patient and the physiotherapist will assist in patient
    motivation and drive the rehabilitation pathways(Gennarelli, Brown, & Mulcahey, 2020).

 

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