Atraumatic instability is a condition in which the shoulder starts to slip part way out of joint without having had a significant injury.
Atraumatic instability may arise from a variety of causes. A flat or small socket weak muscles stretchy ligaments periods of disuse and loss of normal coordination may contribute to atraumatic instability.
A persistent program of stabilizing exercises is the best place to start with managing atraumatic instability.
Uncommonly if a prolonged dedicated exercise program is not successful capsular tightening by surgery may be considered.
The postoperative rehabilitation after this surgery is particularly important.
A shoulder that has been stable may become unstable after a minor injury or a period of disuse. Certain shoulders may be more susceptible to atraumatic instability.
- A flat or small glenoid fossa may jeopardize the balance concavity compression adhesion-cohesion and glenoid suction cup stability mechanisms. Attenuation of the glenoid labrum may further compromise these stabilizing mechanisms.
- Thin excessively compliant capsular tissue may invaginate into the joint when traction is applied limiting the effectiveness of stabilization from limited joint volume.
- An extensive glenohumeral joint capsule may allow humeroscapular positions outside the range of balance stability.
- Weak muscles may provide insufficient compression for the concavity compression stabilizing mechanism.
- Poor neuromuscular control may fail to position the scapula to balance the net humeral joint reaction force.
- Voluntary or inadvertent malpositioning of the humerus in excessive anterior or posterior scapular planes may cause the net reaction force to lie outside the confines of the glenoid fossa.
Any of these factors individually or in combination could contribute to instability of the glenohumeral joint. For example posterior glenohumeral subluxation may result from the combination of a relatively flat posterior glenoid and the tendency to retract the scapula during anterior elevation of the arm resulting in use of the elevated humerus in anterior scapular planes. Excessively compliant capsular tissue in combination with relatively weak rotator cuff muscles could contribute to inferior subluxation on attempted lifting of objects with the arm at the side. If the lateral scapula is allowed to droop (whether voluntarily or involuntarily) the superior capsular structures are relaxed permitting inferior translation of the humerus with respect to the glenoid (see figure 1).
Because they usually result from loss of midrange stability atraumatic instabilities are more likely to be multidirectional. Pathogenetic factors such as a flat glenoid weak muscles and a compliant capsule may produce instability anteriorly inferiorly posteriorly or a combination. Although the onset of atraumatic instability may be provoked by a period of disuse or a minor injury many of the underlying contributing factors may be developmental. As a result the tendency for atraumatic instability is likely to be bilateral and familial as well.
It is now apparent that atraumatic instability is not a simple diagnosis but rather a syndrome that may arise from a multiplicity of factors. To help recall the various aspects of this syndrome we use the acronym "AMBRII". The instability is Atraumatic usually associated with Multidirectional laxity and with Bilateral findings. Treatment is predominantly by Rehabilitation directed at restoring optimal neuromuscular control. If surgery is necessary it needs to include reconstruction of the rotator Interval capsule-coracohumeral ligament mechanism and tightening of the Inferior capsule.
The age distribution of 51 patients presenting to our service with the atraumatic (AMBRII) instability shows that this appears to be a condition which presents predominantly under the age of 30 (see figure 2).
AMBRII instability often begins with some minor event or series of events which lead to progressive decompensation of the glenohumeral stability mechanisms.
An awkward lift reaching over the back seat of the car or a sneeze may be all that is necessary to launch the predisposed but compensated shoulder down the path toward instability. The patient notices that the shoulder has become loose and may feel it slip out and clunk back in with different activities. These episodes almost never require manipulative reduction.
The instability may be sufficiently subtle that the patient is unaware of the humerus translating on the glenoid. The patient may only be aware of a feeling that the shoulder does something unnatural in certain positions or that certain functions cannot be performed such as reaching out in front or lifting at the side.
In contrast to the situation in traumatic instability discomfort with activities of daily living may be a significant component of the complaint. A patient may volunteer that he or she can make the shoulder "pop out" and that at times the shoulder feels as if it "needs to be popped out" on purpose.
The patient should indicate each and every position in which problems with instability have been noted. Instability with the arm out in front of the body and problems lifting or reaching down are particularly suggestive of the AMBRII condition. It is important to note how frequently the problem occurs and whether the problem is "avoidable" if the patient concentrates on how the shoulder is used.
Finally we record the extent and effectiveness of previous non-operative and operative treatment and the presence or absence of instability symptoms in the opposite shoulder or other joints.
Simple shoulder test
The Simple Shoulder Test provides a minimal data set for characterizing some of the functional impairment from atraumatic multidirectional glenohumeral instability. These patients had greatest difficulty sleeping lifting overhead and throwing (see figure 3).
Particular emphasis is placed on the patient's functional goals with respect to work and sport. We try to determine whether these goals are realistic considering the condition of the shoulder.
In summary patients with atraumatic instability are usually young perhaps with a family predisposition to "loose shoulders." The instability is most prevalent in midrange positions those commonly used in activities of daily living such as lifting at the side or raising the arm to the front. The contralateral shoulder may also seem "loose." The patient may have difficulty defining exactly what it is about the shoulder that is bothersome. The history does not reveal an injury of sufficient magnitude to tear the capsule or ligaments.
The physical examination of patients with AMBRII syndrome is usually started by asking them to demonstrate the positions in which the shoulder feels unstable. They may demonstrate a spontaneous jerk test by bringing the elevated arm horizontally across the chest causing the humeral head to subluxate posteriorly. Then by returning the elevated humerus to the coronal plane they produce a "clunk" on reduction of glenohumeral joint (much like the Ortolani and Barlow signs of the hip). Using the palpable scapular coordinates we can estimate the scapular plane in which the shoulder subluxes and the plane in which it reduces. Patients may also demonstrate that when they attempt to lift an object or tie their shoes the shoulder subluxates inferiorly. They may demonstrate that when they lie on the affected shoulder it is pushed forward out of joint. Finally they may demonstrate by elevating the arm in a posterior humerothoracic plane that they can produce anterior subluxation with spontaneous reduction on return to the coronal plane. By allowing the patient to demonstrate the symptomatic positions and motions of instability our hands are free to define the humeroscapular positions at the moments of interest. These observations may reveal faulty patterns of scapulohumeral mechanics such as allowing the lateral scapula to droop during lifting or retracting the scapula during anterior elevation of the humerus.
We have described our investigations of classic clinical laxity tests showing that in a small group of subjects the magnitude of translation for shoulders with atraumatic instability is essentially the same as that of normal shoulders or shoulders with traumatic instability. Therefore we pay particular attention to the patient's response during laxity testing: we are seeking to reproduce the translations which duplicate the symptoms that brought the patient in for treatment. Our best diagnostic confirmation occurs when during a laxity test the patient states "that's it that's the thing that's bothering me." We refer to this as recognition of the symptomatic event when it is reproduced during the examination.
We always make a point of examining the laxity of the contralateral glenohumeral joint. Occasionally laxity tests will yield different results on the symptomatic side. More often however examination of the contralateral shoulder is similar to the symptomatic one. This allows us the opportunity to demonstrate to the patient and the family that while both shoulders demonstrate similar degrees of laxity the patient is able to control one of them using good mechanics. This demonstration helps set the foundation for our discussion of the need to regain stabilizing neuromuscular control of the symptomatic shoulder.
Finally we examine the strength of abduction and rotation to gauge the power of the muscles contributing to stability through concavity compression. We also examine the strength of the scapular protractors and elevators which are necessary to position the scapula securely.
In atraumatic instability shoulder radiographs characteristically show no bony pathology. Because these patients characteristically demonstrate midrange instability radiographs may show translation of the humeral head with respect to the glenoid. The axillary view may show posterior subluxation. Occasionally radiographs may suggest factors underlying the atraumatic instability such as a relatively small or hypoplastic glenoid or a posteriorly inclined or otherwise dysplastic glenoid. The bony glenoid fossa may appear quite flat; however it is difficult to relate the apparent depth of the bony socket to the effective depth of the fossa formed by cartilage and labrum covering the bone.
We do not use stress radiographs arthrography MRI or arthroscopy in the diagnosis of atraumatic instability.
Surgery is not always an option
The goal of treatment for patients with atraumatic instability is the restoration of shoulder function.
Many patients with the AMBRII syndrome have simply become deconditioned from their normal state of dynamic glenohumeral stability. They have lost the proper neuromuscular control of humeroscapular positioning; concavity compression has become dysfunctional.
Neuromuscular control cannot be restored surgically; rather it requires prolonged adherence to a well-constructed reconditioning program. The patient may need to be convinced that training and exercises constitute a reasonable therapeutic approach. Many would prefer a surgical "cure." We have found it useful to demonstrate that often the contralateral shoulder has substantial laxity on examination yet is clinically stable. In this way we try to educate the patient and family that a loose shoulder is not necessarily clinically unstable. We emphasize that gymnasts usually have very lax yet very stable shoulders.
There are two aspects of the non-operative management of atraumatic instability:
- strengthening the compressor muscles and
- training for humeroscapular balance.
First it is essential to optimize the strength and endurance of the muscles compressing the head of the humerus into the glenoid concavity. Weakness or poor endurance of the rotator cuff muscles can usually be managed by a regular exercise program. The second component of the exercise program emphasizes regaining stability through neuromuscular control of humeroscapular positions. If an major and protracted effort with the exercise program is not successful in improving shoulder function a surgical repair may be considered.