The Problem
Quadrangular space syndrome (QSS) or Quadrilateral space syndrome is a compressive neuropathy of the axillary nerve (AN) and/or the posterior circumflex humeral artery (PCHA) in the shoulder. The most frequent cause is a fibrous band(s) in the quadrilateral wpace (QS) and/or surrounding muscle hypertrophy. The QS is bordered by the teres major and teres minor muscles, the humeral shaft, and triceps (long head) muscle. Dilated veins can also place compression on the AN.
Clinical Presentation
Patients will typically present with vague posterior shoulder pain especially in the overhead athlete including baseball pitchers, tennis, and volleyball players. Patients may also complain of paresthesias in a non-dermatomal distribution. Generally, QSS is seen in the dominant arm and is not associated with direct trauma.
Patients may have undergone previous shoulder procedures with continued posterior shoulder pain, often more inferior to the posteriorly placed portal. Throwing athletes may describe dull, burning pain especially when in the late cocked position (abducted/externally rotated) of throwing. Physical exam can elicit tenderness posteriorly 2-3 cm distal to the typical posterior arthroscopy portal site. Differential diagnosis includes thoracic outlet syndrome, axillary artery occlusion or aneurysm, effort thrombosis, suprascapular nerve entrapment, complex regional pain syndrome, brachial plexitis, internal impingement, glenohumeral internal rotation deficit (GIRD), cervical disc disease, and glenohumeral arthritis.
Diagnostic Workup
Physical exam findings include point posterior shoulder tenderness and/or weakness to external rotation/abduction. In late presentation, there may be some atrophy of the deltoid muscle.
MRI may demonstrate isolated denervation of the teres minor muscle and/or deltoid muscle; angiography and MR angiography can assess occlusion of the PCHA; subclavian arteriography is performed with the arm first at the patient’s side followed by injection with the arm in abduction/external rotation. The PCHA can be patent at the side and occluded with the arm abducted/externally rotated; more recently Doppler ultrasound (US) can show evidence of blockage or significant stenosis of the PCHA with abduction/external rotation of the shoulder; x-rays of the shoulder should be taken to evaluate for any inferior bony osteophyte that can impinge on the AN and cause QSS type symptoms. A paralabral cyst which can be seen on MRI has been reported as a cause for QSS. An osteochondroma of the proximal humerus has been reported as a cause for QSS confirmed by CT. CT angiography is also used for diagnostic workup. A 1% lidocaine injection test in QSS can be diagnostic if it eliminates posterior shoulder pain; ensure that the PCHA is not injected.
EMG is used for diagnostic work up of AN compression in chronic cases of QSS although the AN may show no signs of denervation in acute/subacute cases.
Diagnosis can be challenging with many patients misdiagnosed. While the condition is rare, it should be considered for patients and athletes with posterior shoulder pain.
Non–Operative Management
Patients should be told that most cases are “self limiting” and complete resolution with rest can occur. In the overhead thrower, the athlete should be “shut down” for at least 6-8 weeks with an assessment of the thrower’s pitching mechanics. As symptoms improve, core strengthening, rotator cuff stretching, and stabilization should progress. Active release therapy (ART) may be helpful. Some advocate “complete rest” for at least 6 months.
Indications for Surgery
Persistent symptoms greater than 6 months with significant symptoms would be an indication for surgical exploration with confirmation with MR angiogram or arteriogram.
Surgical Technique
With the patient in a lateral decubitus position a 3.5-4.0 cm longitudinal incision is made over the posterior shoulder. The posterior aspect of the deltoid is identified and elevated. The deltoid is not detached. The humeral neck is palpated laterally and the fat overlaying the teres major and minor muscles is identified and the neurovascular bundle is carefully dissected. Any fibrous bands or adhesions overlaying the AN and PCHA are dissected free, a vessel loop is placed around the AN, and the neurovascular (NV) bundle is released.
Examine for any venous dilation that can sometimes compress the AN. This should be examined with the shoulder abducted and externally rotated. The vein should then be ligated and tied off. Dissection has been achieved when a finger can be easily passed through the QS. Some authors advocate partial release of the teres major muscle (though rarely necessary).
Pearls and Pitfalls of Technique
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Confirm QSS with arteriogram that may require the addition of the patient’s shoulder in abduction and external rotation.
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Look for dilation of the vein in QSS.
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Elevate posterior deltoid for identification of the teres major and minor muscles.
Potential Complications
With non-operative treatment, pain and disability can persist; a baseball thrower may be unable to throw; with operative treatment neurovascular injury can occur; shoulder pain may persist if the diagnosis of QSS is incorrect.
Post–operative Rehabilitation
A sling is maintained for comfort for 10 days, avoiding hyperabduction and external rotation for the first 4 weeks. Perform pendulum exercises immediately to prevent the formation of new adhesion. Following removal of the sling, range of motion (ROM) exercises commence along with strengthening with physical therapy (PT).
Outcomes/Evidence in the Literature
Cahill, B.. “QSS”. J. Hand Surg. vol. 8. 1983. pp. 65-9. (A study of 18 patients with 8 patients with QSS with complete relief, 8 with improvement and 2 without improvement. Seminal article describing QSS with four "cardinal signs": pain poorly localized to the shoulder, paresthesia in a non-dermatomal distribution, discrete point tenderness in the quadrilateral space, and a positive arteriogram finding in abduction and external rotation.)
Francel, T.. “QSS”. Plast Recon Surg. vol. 87. 1991. pp. 911-16. (A study showing relief of pain but without functional return.)
Tubbs, R.. “Surgical anatomy of the axillary nerve within the QS”. J Neurosurg. vol. 102. 2005. pp. 912-914. (QSS in a 20 year old pitcher.)
McAdams, T.. “Surgical decompression of the QS in overhead athletes”. AJSM. vol. 36. 2007. pp. 528-532. (Review of 4 overhead athletes that underwent successful decompression for QSS. Fibrous bands were found in 3 patients and venous dilatation in one patient.)
Lester, B.. “QSS: diagnosis, pathology and treatment”. vol. 28. 1999. pp. 718-725. (Review of QSS cases where only 30% of patients had ongoing symptoms that required surgical intervention.)
McClelland, D.. “A case of QSS with involvement of the long head of the triceps”. AJMSM. vol. 36. 2008. pp. 1615-1617. (Signs and symptoms of QSS presenting in the long head of the triceps tendon with axillary nerve innervation of the long head of the triceps in 24/35 shoulder dissections.)
Cothran, R.. “QSS: Incidence of imaging findings in a population referred for MRI of the shoulder”. AJR. vol. 184. 2005. pp. 989-992. (This study suggests that MRI findings of teres minor atrophy or abnormal signal may be present in as many as 0.8% of patients referred for shoulder MRI. The study suggests that most of these patients have other shoulder abnormalities on MRI apart from atrophy or abnormal signal to the teres minor or deltoid muscles or both.)
Amin, M.. “An unusual cause of the QS impingement syndrome by a bone spike”. Skel. Rad. vol. 35. 2006. pp. 956-958. (A reported case of QSS relating to a bone spike following a malunited old scapular fracture. The bone spike was well demonstrated by multidetector CT scan. Teres minor atrophy was caused by the impinging bone spike in a prolonged and intermittent course resulting from a previous malunited fracture of the scapula.)
Apaydin, N.. “Review of the surgical anatomy of the axillary nerve and the anatomic basis of its iatrogenic and traumatic injury”. Surg. Radiol. Anat. vol. 32. 2010. pp. 193-201. (A review of QSS and helpful anatomic figures showing the landmarks of the axillary nerve; EMG is the test of choice to evaluate for abnormal function of the teres minor and/or deltoid.)
Robinson, D.. “Ultrasound of the PCHA”. J. Med. Imaging Radiation Oncol. vol. 54. 2010. pp. 219-23. (A new technique is described to use US to identify the PCHA. The scan was performed from a posterolateral approach just above the level of the surgical neck.)
Summary
QSS, though rare and usually “self-limiting”, should be in the differential for sources of posterior shoulder pain. This is especially true for the overhead throwing athlete. A careful history should be obtained including duration of symptoms and position of shoulder when pain is heightened. Physical exam should examine for localized atrophy, point tenderness, and associated weakness. Imaging modalities should include MRI of the shoulder and MR angiography to examine for arterial occlusion. EMG should likewise be obtained but will often be within normal limits. Surgical decompression should be considered for continued symptoms and failed non-operative treatment with expected surgical findings to include fibrous bands and possible venous dilatation. Results of surgery are generally good to excellent.
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