Monday, 30 October 2023

 

     Management of Hand Extensor Tendon Injuries


                             Dr. KS Dhillon


Introduction

The extensor tendons function to transmit tension from the muscle belly to the specific joints of the hand. Extensor tendons are divided into two groups namely the intrinsic and extrinsic groups [1]. The intrinsic muscles are located within the hand itself. The extrinsic muscles are located proximally in the forearm and insert into the hand by long tendons [1]. The extensor muscles are all extrinsic except for the interosseous-lumbrical complex [1]. The lumbrical muscles produce flexion of the metacarpophalangeal (MP) joints and extension of the interphalangeal (IP) joints [1]. The interossei group forms the lateral bands with the lumbricals muscles and they adduct and abduct the fingers [1]. The radial nerve innervates all the extrinsic extensors. The extrinsic extensors consists of 3 wrist extensors as well as a larger group of thumb and digit extensors [1]. The extensor carpi radialis brevis (ERCB) is the main wrist extensor. Other extensors include extensor carp radialis longus (ECRL) and extensor carpi ulnaris (ECU) which also provide radial and ulnar movement of the wrist respectively [1]. The ECRB inserts at the base of the third metacarpal. The ECRL inserts at the base of the second metacarpal and the ECU at the base of the fifth metacarpal [2].

The extensor digitorum communis, extensor digiti minimi, and extensor indicis proprius extend the digits [2]. These muscles insert at the base of the middle phalanges as central slips and to the base of the distal phalanges as lateral slips [2]. Extension of the thumb is carried out by the extensor pollicus longus, abductor pollicis longus, and extensor pollicis [1]. There is an extensor retinaculum at the wrist which prevents bowstringing of the tendons at the wrist level and separates the tendons into 6 compartments [1]. The extensor digitorum muscle (also known as extensor digitorum communis) is a muscle of the posterior forearm. It extends the medial four digits of the hand. It is innervated by the posterior interosseous nerve, which is a branch of the radial nerve. The index and little fingers are also extended by the extensor indicis proprius and extensor digiti minimi [1]. The first extensor compartment of the wrist contains the extensor pollicis brevis and the abductor pollicis longus. The second contains the extensor carpi radialis longus and extensor carpi radialis brevis. The third, compartment contains the extensor pollicis longus; the fourth, the four tendons of the extensor digitorum communis plus the extensor indicis proprius; the fifth, the extensor digiti quinti; and the sixth, the extensor carpi ulnaris [1].


Extensor Tendon Injuries

Extensor tendon injuries are more common than flexor tendon injuries [3]. They are very common (61%) [4] since they are not protected as well as the flexor tendons due to their superficial location under the the skin. Extensor tendon injuries are known to cause serious functional impairment. They have, however, not received as much attention in the literature as flexor tendon injuries [5]. To repair the extensor tendons the surgeon needs the same skills as required for flexor tendon repair. It is not a simple challenge, which is a common misconception [6-8]. 

Lacerations of the extensor tendon can occur at any site. Extensor tendons are difficult for surgeons to repair because of their small size compared to the flexors and their lack of collagen-bundle linkage, which reduces the grip strength available for the suture material [9]. The flat tendon profile in zones I to IV increases the surface area between the repaired tendon and the adjacent tissue, particularly bone. This makes it susceptible to adhesion formation. Furthermore, the cross-section of the extensors changes from semicircular to bioconcave disk in zones I to IV making durable repair difficult because of the thin but broad characteristics of the tendon [10].


Clinical Presentation

A detailed history is essential. It is important to know the mechanism of injury, the position of the finger during the injury, age, occupation, and handedness of the patient. There are several reasons why the mechanism of injury is important. Most lacerations on the dorsum of the hand and fingers are clean. If there is any contamination wound debridement would be needed. History should elicit whether there was a human bit. The patient should also be asked about the presence of a foreign body in the wound. 

Physical examination should include a systemic and in-depth examination of both hands. The site of the laceration and the inability to extend a joint distal to it indicates that the extensor tendon has been divided. If the extensor tendon is completely divided the finger would be resting in flexion. 

When testing the function of the extensor muscle of the hand, the extension must be against resistance. Extension of the hand digits is performed by several muscles in the forearm that insert onto the digits. The extensor digiti minimi extends the fifth digit. It can be tested by asking the patient to lay the hand flat on a surface and hyperextension the fifth digit. The extensor digitorum tendons extend the 2nd to 5th digits. With the hand lying flat on a surface the tendon of each finger can be tested by having the patient hyperextend the digits against resistance. Extension of the second finger is also performed by extensor indicis. Extension of the first digit is controlled by two muscles i.e. the extensor pollicis longus and brevis. The path of these two tendons defines the anatomical snuffbox that contains the radial artery and the scaphoid bone. Extension of the thumb at the interphalangeal joint and the metacarpophalangeal joint can be tested separately. 

Central slip injuries may not be immediately apparent on cursory examination after trauma. The Elson test can be useful in the identification of possible central slip injuries. The patient places the hand over the edge of a surface with the digits flexed at the proximal interphalangeal (PIP) joint and hanging freely. The examiner applies firm, constant pressure to the digit in question at the level of the middle phalanx. The patient then attempts to extend the finger at the PIP joint in opposition to the examiner’s applied force. If the patient is able to extend the PIP joint while the distal interphalangeal (DIP) joint remains pliable, it can be concluded that the central slip is intact. If there is an injury to the central slip, the patient will only be able to extend the PIP joint through the use of the lateral bands, which will lead to DIP joint rigidity and concomitant extension or even hyperextension at the DIP joint.

Sensation testing can be carried out to rule out radial nerve injury. The median and ulnar nerve should also be tested. Radiographs are done to assess any associated fracture that needs to be fixed before tendon and nerve injuries are treated. Human bites are also known to cause metacarpal fractures. Foreign objects including glass can be picked up on X-rays.

The extrinsic and intrinsic components of the extensor system can act independently. Hence full extension of the digits at the individual small joint of the hand is possible even after a laceration. The extension of the distal IP joint of the finger is still possible with complete severance of the main extrinsic extensor tendon at or proximal to the metacarpophalangeal joints. Furthermore, oblique retinacular ligaments can produce weak distal extension through the tenodesis effect. 

The extensor mechanism usually fails at the insertion of the central slip and the terminal tendon producing characteristic deformities including the mallet and boutonniere deformity. In addition, mallet fingers can be complicated by extensor lag at the distal IP joint. A swan neck deformity can result as excess tension builds at the central slip insertion into the base of the middle phalanx.


Repair Of Extensor Inuries

Kleinert and Verdan [11] have created a classification system for extensor tendon lacerations according to the eight zones of the hand, wrist, and forearm. This classification has been widely accepted. Verdan defined eight zones (fig 1). Four odd-numbered zones overlie each of the joints and four even-numbered zones overlie the intervening tendon segments, increasing from distal to proximal. The type of injury, the surgical approach, and potential deformity vary according to the zone [11]. 

Zone I refers to the area from the DIP joint to the fingertip; zone II encompasses the middle phalanx; zone III refers to the PIP joint; zone IV is over the proximal phalanx; zone V refers to the MP joint; zone VI encompasses the metacarpal and zone VII is over the wrist [11]. 

According to Rockwell et al [12], the treatment of tendon injuries is dependent on the location and type of injury. Repair should be done very soon after the injury, especially within the first 2 weeks.

Extensor tendon repair techniques are not as complicated as flexor tendon repairs. This is because the extensor tendon is smaller with a relatively flat cross section. Its collagen is longitudinally orientated. There is little or no cross-linking. Due to the size differential and surrounding paratendon, except in zone VII, extensor tendons are not as capable of withstanding multiple-stranded, strong repair approaches, especially in the distal zones.

Unfortunately, there are very few studies that have investigated the strength of extensor repairs. The four-strand repair by Howard et al [13] has been shown to be the strongest. The biomechanical features including shortening, and loss of motion and strength were not evaluated in the study. 

Compared with augmented Massachusetts General Hospital (MGH) Becker extensor tendon repair, or the traditional modified bunnel repair, two-strand locked bunnell repair has been found to be immediate in strength. It was evaluated further by Newport et al [14]. In these studies the locked bunnell improved the quality of strength over the traditional bunnell (17% versus 58% pullout) but less than the MGH repair (0% pullout) and the four-strand Bunnell or Kracjkow-Thomas (0% pullout) repair that was described by Howard et al [9]. 

The strength and the quality of the repair compared to the traditional two-stranded technique differs in the smaller, thinner tendons of zone IV as compared to repair in zone VI [9,15].

The tension strength of the extensor repair has not been studied in depth. Ketchum et al [15] investigated the tension strength via a force transducer on the proximal phalanx. They found that normal subjects could generate a force of 2.99 kg for the index finger. This decreased ulnarly to 1.97kg for the little finger. Studies in animal models have illustrated that tendon shortening can affect how the extensor tendon repair works by causing a loss of composite flexion and increasing the force required to obtain full flexion. Newport and Williams [9] showed that the modified bunnell technique can produce an average of at least 7mm of shortening resulting in 35 degrees or more loss of composite flexion when the wrist is held in a neutral position [9]. Minamikawa et al [16] also showed that there was a loss of 6.4 mm tendon over the metacarpal when the wrist was extended 45 degrees or more and they recommended that this could be amended if the wrist was appropriately extended. However, these are only animal studies so further research is still needed. The animal models cannot take into account muscle tone, adhesion formation, friction of edema, skin closure, or bulk of repair.






Fig 1.


Zone I Injuries

Zone I injury is referred to as a mallet finger. In this injury, there is disruption to the extensor tendon over the distal interphalangeal joint causing a flexion deformity of the distal interphalangeal joint [17]. It is usually a close injury but it can be open at times. The most likely cause is forceful flexion of the distal interphalangeal joint which is extended. This will result in a rupture of the extensor tendon or avulsion from its insertion at the distal phalanx. When it is left untreated hyperextension of the proximal interphalangeal joint may develop due to the retraction of the central band causing a swan neck deformity [18]. Mallet fingers are classified into 4 types:

  • Type 1: Close injury with or without avulsion fracture

  • Type 2: Laceration at or proximal to the distal interphalangeal joint with loss of tendon continuity

  • Type 3: Deep abrasion with loss of skin, subcutaneous tissue, and tendon substance

  • Type 4: (A) Transepiphyseal plate fracture in children; (B) hyperflexion injury with fracture of the articular surface of 20 to 50%; and (C) hyperextension injury with fracture of the articular surface greater than 50% and with early or late palmar subluxation of the distal phalanx.

Closed type I mallet injury is treated with an immobilization splint in extension or slight hyperextension for 8 weeks. This would include 2 weeks of night splinting. Exercises start by blocking exercises of the profundus involving the proximal interphalangeal joint active motion. A Cochrane review found that patient compliance was the most important factor in the success of splinting [19]. Another Cochrane review found that there was no evidence of difference in the outcomes between splints [20]. After 8 weeks the fingers should be reexamined to see if active extension is present.  Splinting can now be reduced to high-risk times such as manual work, sleeping, or athletic performance. Splinting can be useful even after 3 months of the injury [21,22]. 

Type 2-4 injuries should be treated surgically. Type 2 requires a simple suture through the tendon alone or a roll-type suture incorporating the tendon and skin in the same suture and then splinting for 6-8 weeks [23]. Type 3 fractures include loss of tendon substance which requires immediate soft tissue coverage and primary grafting or reconstruction with a free tendon graft [23]. Type 4A injuries are best treated with closed reduction followed by splinting. These are the most likely fractures in children [23]. Type 4B injuries are usually treated by splinting for 6 weeks with 2 weeks of night splinting. This treatment yields good results. Type 4C with palmar subluxation of the distal phalanx is treated surgically with open reduction and internal fixation using a Kirschner wire and sometimes a pull-out wire or suture. A splint is used for 6 weeks. After 6 weeks the Kirschner wire is removed and motion started. The fracture fragment’s location is very important as proximally displaced fragments not in continuity with the distal phalanx may also require open reduction and internal fixation.

Chronic mallet finger is common. This is because some patients accept the deformity and never see a doctor for treatment. For those who present late splinting is the first line of treatment. Several reports have shown good outcome in patients who present late and are treated by splinting. Surgery is offered if conservative treatment fails or patients present with recurrent chronic mallet deformities. The treatment includes immobilization with transartilcular Kirschner wire fixation across the affected joint, fowler central slip release, excision of tendon scar, and fixation in hyperextension. Amputation and distal interphalangeal joint arthrodesis are the only two salvage procedures available [24-26].


Zone II injuries

Zone II injuries or middle phalanx injuries are usually due to a laceration or crush injury rather than avulsion as in zone I. If examination shows an extensor lag then exploration and repair is needed. If there is active extension with only a degree of weakness then splinting can be used for 3-4 weeks. Injuries with greater than 50% of the tendon torn or cut should be repaired. The tendon is repaired with a fashion-of-eight suture.


Zone III injuries

Zone III Injury produces a boutonniere deformity. It is caused by disruption of the central slip at the proximal interphalangeal joint. Examination shows absent or weak active extension of the proximal interphalangeal joint [27]. Active extension is initially retained by the lateral bands but the head of the proximal phalanx eventually goes through the central slip resulting in migration of the lateral bands. This then results in loss of extension at the proximal interphalangeal joint and hyperextension at the distal interphalangeal joint leading to boutonniere deformity. The injury can be open or close and the central slip can avulse with or without the bony fragment. The boutonniere deformity usually occurs 10-14 days after the initial injury [8]. Closed deformities require splinting for 4-6 weeks of the PIP joint in extension with the wrist joint and DIP joint left free. Surgery should be carried out for closed fractures when:

  • When there is a displaced avulsion fracture at the base of the middle phalanx

  •  When there is axial and lateral instability of the PIP joint associated with loss of active or passive extension of the joint  

  • When non-operative treatment fails. 

During surgery, a suture is passed through the central tendon and secured to the middle phalanx with or without the bony fragment.  Kirschner wire fixation of the proximal interphalangeal joint is maintained for 10 to 14 days. This is followed by an extension splint until union. If a primary repair is not possible then the lateral bands can be sutured in the dorsal midline of the finger to reconstruct the central slip. A flap can be raised from the proximal portion of the central slip to restore active extension. For open injuries, surgical repair is sometimes not required if splinting is used. However, in a true boutonniere deformity, both central slip and lateral band injuries can be expected. In the elderly, the period of immobilization can be reduced to 2 weeks to help in returning of full flexion.


Zone IV injuries

Zone IV injuries are proximal phalanx injuries. They usually involve the broad extensor mechanism. The injuries are usually partial and spare the lateral bands. They are usually diagnosed by inspection [28]. Splinting the PIP joint in extension for 3-4 weeks without repair has shown to have the same outcome as repairing it with 5 zero nonabsorbable sutures [29]. However, if the laceration is complete primary surgical repair has to be performed followed by 6 weeks of splinting in extension [30]. In the first 3 weeks, volar splinting is used with passive extension allowed. At week 4 gentle active extension is started but no passive flexion is allowed. In the last two weeks, active flexion is started, and graded resisted exercises are carried out.


Zone V injuries

Injuries in zone V are nearly always open. They are treated as human bites until examination proves otherwise. After wound irrigation primary tendon repair is required. The sagittal bands have to be repaired to prevent lateral migration of the extensor digtorum communis tendon and subsequent metacarpophalangeal extension loss [8,29].

After surgery, splinting of the wrist in 30-45 degrees of extension and the metacarpophalangeal joint in 20-30 degrees of flexion is done with the proximal interphalangeal joint free. If there is a human bite the wound should be extended for inspection and debrided, irrigated, and should be left open [30]. Cultures are taken before irrigation and patients are started on broad-spectrum antibiotics. The bite wound usually heals within 5 to 10 days. Secondary repair is rarely required.


Zone VI injuries

The tendons in this area are close to the thin subcutaneous tissue and thin paratendon. Injuries in this zone are situated in the dorsum of the hand. These injuries may not always result in loss of the extension at the MP joint. Surgical repair is done with stronger core-type sutures followed by splinting. The splinting should be placed in extension for 4-6 weeks. If the extensor digitorum communis is involved, all the fingers should be splinted. If the proprius tendon is solely involved, only the affected finger needs to be splinted with the wrist joint [31]. Degloving injuries that require grafting and flaps are not uncommon. Since the tendons in this area are larger, stronger core suture has to be used.


Zone VII injuries

There is still debate about releasing the retinaculum for visualization and repair of the tendon when injuries occur in this area. Such a release can produce postoperative adhesions [32,33]. Part of the extensor retinaculum has to be maintained to prevent tendon bowstringing [9]. With early dynamic splinting adhesions are less likely. A four-strand suture is appropriate for zone VII injuries.


Zone VIII injuries

Injuries to the dorsal forearm can produce laceration of many tendons, including the musculotendinous junction and tendon bellies. The thumb and wrist extensors should be repaired first [34]. Multiple figure of eight sutures are used to repair the muscle bellies. Static immobilization of the wrist in 45 degrees of extension and metacarpophalangeal joints in 15-20 degrees is maintained for 4-5 weeks [35].


Thumb injuries

Mallet injuries are uncommon in the thumb. This is because the terminal extensor tendon is thicker on the thumb [36]. For open injuries primary repair with splinting for 6 weeks is carried out. For closed injuries splinting for 6 weeks without surgical repair is a suitable alternative [37]. The broad expansion of the metacarpophalangeal joint of the thumb makes laceration of all components in this area uncommon. Extensor pollicis brevis is rarely lacerated in isolation. Its repair is debatable because extension of the metacarpophalangeal joint is possible with an intact extensor pollicis longus. Extensor pollicis longus injury causes extension lag in both metacarpophalangeal and interphalangeal joints. It has to be repaired. Splinting is done for 3 to 4 weeks, with the thumb metacarpophalangeal joint in full extension and the wrist in 40 degrees of extension with slight radial deviation. For injuries in zones VI and VII, the abductor pollicis longus retracts when divided. It has to be released for successful repair [28]. Splinting is done for 4-5 weeks with the wrist in radial deviation and the thumb in maximal abduction [28].


Rehabilitation of Extensor Injuries

The aim of rehabilitation is to obtain healing with minimal gapping in the tendon and to prevent adhesions. Static mobilisation has been the traditional method of postoperative rehabilitation. There can be several complications including tendon rupture, adhesion formation requiring tenolysis, extension lag, loss of flexion, and decreased grip strength [32,38-40].

Early mobilization was introduced for flexor tendon injuries to decrease adhesions and subsequent contractures. Mobilization has been shown to enhance DNA synthesis at the repair site, improve tensile strength, and increase the vascularity [41-43]. Now it has been shown to be more useful in certain areas for extensor injuries as well [44]. 

Mowlavi et al [45] studied early controlled mobilization versus static splinting for zone V and zone VI injuries [45]. They found that functional outcomes at 4,6 and 8 weeks were better after early controlled mobilization compared to static splinting [45]. However, the outcomes were not improved after 6 months [45]. The authors were of the opinion that dynamic splinting should be available to those who are motivated to return early to functional capacity. 

Bulstrode et al [46] also found that ROM for the early mobilization group at 6 weeks postoperatively was greater than the static mobilization group but the differences disappeared at 12 weeks. The grip strength was also assessed at 12 weeks postoperatively [46]. They found that the difference in grip strength was significantly greater in the early-mobilized group compared to the immobilized [46]. 

Russell et al [47] also compared immobilization with early controlled mobilization but they found no significant difference in hand function between the groups.

Early mobilization rehabilitation programs can be of 2 types. 

  • (1) early active mobilisation

  • (2) early controlled mobilization using a dynamic splint.

Early controlled motion with a dynamic extensor splint has been found to reduce adhesions and contractures. There are only two randomized controlled trial studies that have compared early mobilization versus early active mobilization. Chester et al [48] studied extensor injuries from zone IV to VIII and found significantly better ROM in the patient group treated with early controlled mobilization as compared to early active mobilization at 4 weeks. Khandwala et al [49] compared early active mobilization with early controlled mobilization in zones V and VI and they found no difference in total active motion at 4 or 8 weeks postoperatively. There are only a few studies that have tried to evaluate the specific mobilization regime that has the best functional outcome.

A recent review by Talsmaby et al [50] confirmed that short-term evidence shows early controlled mobilization is superior over immobilization for extensor tendons. There is no conclusive evidence regarding the long-term effectiveness of the different rehabilitation programs. In addition, the study highlighted that there is a wide variety in the duration of splinting, splinting technique, and frequency and force intensity of exercises used for rehabilitation. Evaluation of the cost-effectiveness of the treatment regimes' showed that dynamic splinting is more expensive and requires more hand therapist input. This is why some authors prefer early active mobilization for proximal zone injuries [51,52]. 


Complications

Complications can occur after extensor tendon repair. These include loss of flexion due to extensor tendon shortening, loss of flexion and extension due to adhesions, and a weak grip. When the extensor tendon becomes shortened or adherent, tenodesis restraint occurs. Flexion of the digit at the MP joint causes extension force at the PIP joint. Hand therapy has to be started and it should focus on extrinsic excursion exercises. Splinting should be started immediately.

If there is no improvement following 6 months of conservative treatment then surgery may be needed. Tenolysis is appropriate when tenodesis occurs as a result of scarring with no significant loss of tendon length. If the tendon is shortened, Littler’s technique of extensor tendon release can be used [53]. Eggli et al [54] evaluated the clinical outcomes in 23 patients after tenolysis and they found that on average follow-up of 5 years, significant improvement occurred in 88% of the digits in extensor and flexor injuries in zone II. Extensor tenolysis was also found to be a safe procedure [54].

In Zone VII and VIII injuries, there can be multiple tendon lacerations. These injuries can lead to decreased wrist mobility. Human bite injuries in zone V can be complicated by infection. Zone I, II and III injuries can be complicated by deformities. Newport et al [32] retrospectively reviewed 62 patients with 101 extensor tendon injuries and they found that patients without associated injuries achieved 64% good to excellent results and total active motion of 212 degrees which was statistically significant. Distal zones (I to IV) had poorer outcomes as compared to proximal zones (V to VIII). The percentage of fingers losing flexion was greater than those losing extension. This study showed that the loss of flexion was a more significant complication of extensor tendon injuries. 

Staged extension tendon repair can be carried out after failed primary repair. It involves tendon reconstruction using a silicone implant. Small skin incisions are made over the dorsum of the finger and a silicone rod is placed along the pretendious fascia to create a tunnel. Soft tissue defects are treated by split-thickness skin grafts or by secondary suture. Once the wounds have healed, the silicone rod is exchanged for a tendon graft. Adams [55] used this technique in 6 fingers to restore proximal joint extension in patients with severe injuries to the dorsal skin and extensor mechanism. He restored active extension of all proximal interphalangeal joints. He recommended it as a reliable alternative for severely injured fingers with extensor mechanism loss.


Conclusion

The literature has not focused on extensor tendon injuries to the same extent as flexor tendon injuries. Rehabilitation methods have been researched and it is clear that mobilization techniques are more favored. The surgical approach to each zone has not been fully researched. There are very few papers looking at the outcomes of different approaches. More research is needed to work out the optimal approach to extensor tendon injuries and to study the complication rates after different approaches.




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Wednesday, 18 October 2023

     Quadrilateral Space Syndrome



                               Dr. KS Dhillon



Introduction

Quadrilateral space syndrome (QSS) is a rare disorder characterized by axillary nerve and posterior humeral circumflex artery (PHCA) compression within the quadrilateral space. It was first described by Cahill and Palmer in 1983 [1]. In the original description by Cahill, there were four distinct features of QSS. These included diffuse pain around the shoulder; paresthesia in a nondermatomal distribution; point tenderness above the quadrilateral space; and positive angiogram finding in provocative positioning [1]. The condition is usually attributed to repeated overhead activity such as seen in baseball and volleyball. However, a variety of other pathologies including hematomas, lipomas, and labral cysts may cause compression in the quadrilateral space [2].

Neurovascular compression accounts for the acute findings in QSS. These include pain, paraesthesia, and atrophy. It is uncertain whether this is primarily a problem of neural entrapment or vascular compression [3,4]. Compression may occur at rest or with movement. QSS should be considered in all patients with a complaint of shoulder pain, neck pain, lateral arm paraesthesia, and/or quadrilateral space tenderness [5].


Anatomy

The quadrilateral space lies between the teres minor muscle superiorly, the teres major muscle inferiorly, the long head of the triceps medially, and the humeral shaft laterally (Fig 1) [3]. The PHCA and axillary nerve reside in the quadrilateral space. 

The axillary nerve innervates the teres minor and deltoid muscles. These two muscles are primarily responsible for abduction and external rotation. There are fibrous bands within the quadrilateral space, which exacerbate symptoms, particularly pain that is elicited by movements associated with the deltoid and teres minor muscles [6,7]. The anatomical differences in innervation patterns in the glenohumeral joint can make it difficult to distinguish whether the pain is due to suprascapular nerve palsy or axillary nerve compression [8]. Since the PHCA stretches around the neck of the humerus, repetitive tension and mechanical stress to the PHCA wall can lead to thrombosis and aneurysmal degeneration [9,10,11].


Fig 1.




Etiology

The etiology of QSS is not clear. Impingement is usually due to trauma, fibrous bands, or hypertrophy of a muscular border. Occasionally, QSS can also be caused by lipomas, labral cysts, hematoma resulting from fracture, osteochondroma, and axillary schwannomas. Compression of the axillary nerve can also be caused by aneurysms and traumatic pseudoaneurysms of the posterior circumflex humoral artery [11-14]. Anatomical variations can also predispose patients to QSS.

Abnormal origin of the radial collateral artery from the PHCA can also mimic the symptoms of QSS [15]. An accessory subscapularis muscle that originates from the anterior surface of the subscapularis, courses under the axillary nerve, and inserts onto the shoulder joint, can also serve as a risk factor for QSS [16]. QSS has also been seen as a rare complication of thoracic surgery [17].


Clinical Presentation

QSS is typically seen in younger patients who are less than forty years of age. Patients usually present with a history of repeated overhead activities as seen in athletes involved in volleyball, baseball, or swimming [18-25]. Symptoms can be vague. There can be neurogenic or vascular symptoms. Neurogenic symptoms include paresthesias, fasciculations, weakness, or neurogenic pain. Vascular symptoms include signs of acute ischemia such as pain, pallor, and absent pulses. Symptoms of thrombosis, or embolism such as coolness or cyanosis of the hand or digits may also be present. Besides vascular and neurogenic symptoms, patients with QSS can experience muscular atrophy and accompanying weakness. This is believed to be due to denervation. There can be tenderness over the quadrilateral space. In some severe cases, thrombosis of the PHCA can block flow from the axillary artery, leading to embolization and subsequent digital ischemia, cyanosis, and cold intolerance [9,26,27].


Differential Diagnoses

The symptoms of QSS are nondescript. This often makes QSS a diagnosis of exclusion since it can mimic other vascular, musculoskeletal, or nerve-related syndromes in the area. A review of the patient’s medical history can be useful; particularly the absence of significant relief following attempted therapeutic interventions. 

In the workup of QSS, some conditions have to be ruled out. These include cervical spine pathologies, rotator cuff injuries, referred pain syndromes, and labral injuries [5]. The other important conditions in the differential include brachial plexus pathologies, such as thoracic outlet syndrome and brachial neuritis, suprascapular nerve injury, and glenohumeral joint arthritis [3]. Anterior shoulder dislocation, fracture of the head of the humerus, and blunt trauma can all be sources of axillary nerve injury independent of axillary nerve compression. 

Koga et al [28] reported about a patient who presented with QSS symptoms of shoulder pain and upper limb numbness when throwing. The patient was ultimately found to have compression of the axillary nerve between the proximal humerus and the latissimus dorsi tendon. The clinical sequelae can be identical in this situation, but the nerve compression occurs outside of the quadrilateral space.


Imaging and Other Workup

Compression of the axillary nerve may be intermittent and hence imaging of QSS can be challenging. The diagnosis of QSS can be confirmed by imaging [5].

Computed tomography angiography, digital subtraction angiography, and magnetic resonance angiography have all been used to visualize PHCA occlusion [29,30]. There is no “gold standard” diagnostic test for QSS.  Magnetic resonance imaging (MRI) is usually the first choice of imaging [31]. MRI can show focal fatty atrophy of the teres minor muscle. It can also exclude pathological causes of shoulder pain [3,31,32]. Arteriography is the cornerstone of diagnosis in QSS. It will reveal compression of the PHCA while the patient’s arm is in abducted and externally rotated [5]. Bilateral upper extremity arteriography is useful in establishing the patient’s baseline healthy anatomy. Decreased outflow from the PHCA would indicate compression of the adjacent axillary nerve [3,5]. In one controlled study, 80% of asymptomatic controls demonstrated PHCA occlusion on arteriography, leading to low specificity [30].

Ultrasound can be used for the diagnosis of QSS. It will show a dilated PHCA and mild atrophy of the deltoid muscle [33]. Occlusion and stenosis of PHCA were detected using ultrasound in another report [14]. Although not so common, teres minor atrophy can also be seen [34,35,36]. Color Doppler sonography has also been used to compare differences in the posterior humeral circumflex arterial flow between provocative and neutral positions [37]. Sonoelastography has also been used in the diagnosis of QSS in patients with axillary schwannoma [38]. 

Electromyogram (EMG) is also useful in the diagnosis of QSS. The EMG can detect denervation of muscles supplied by the compressed axillary nerve, such as the deltoid and teres minor muscles. The test, however, has a high false-negative rate. In a study by McAdams and Dillingham, four patients with established QSS underwent EMG and MRI testing. They found that all four EMG scans were negative and half of the MRI scans were normal [39]. Although EMG can yield false negative results, it can however eliminate other etiologies of neuropathic pain, such as neurogenic thoracic outlet syndrome.


Treatment

In the literature, there is great variability in the management and treatment of QSS. This is due in part to its recent description and because case reports dominate the literature. The initial treatment is usually conservative. Conservative treatment includes physical therapy and physical activity modification [19]. Physical activity modification can be useful but some patients may find this hard to do. Physical therapy can include transverse friction massage and active release soft tissue massage to the quadrilateral space [5]. Besides therapeutic massage, active shoulder range of motion and scapular stabilization exercises, stretching of the posterior rotator cuff, and the use of nonsteroidal anti-inflammatories have shown success in the treatment of QSS [5]. There has been mild success with the use of ultrasound-guided perineural steroid injections. Pain and other symptomatic relief including tingling, and sensation of coldness following the injection of local anesthetic or steroids can be a diagnostic of QSS. It can also be used with physical therapy for symptomatic treatment [2].


Surgery is considered when patients are unresponsive to conservative treatment for at least six months [40]. Surgical decompression is carried out in such patients. It has proven successful in reversing radial sensory neuropathy secondary to QSS [26]. Since other conditions such effort thrombosis (also known as Paget–Schroetter syndrome) and arterial thoracic outlet syndrome can mimic QSS, imaging and pertinent follow-up testing is essential before planning surgical decompression [41,42]. Despite its lack of specificity, arteriography demonstrating compression of the PHCA and the accompanying presentation of QSS symptoms should raise the suspicion for QSS and surgical decompression may be indicated. 

During surgical decompression, the axillary nerve is dissected free to ensure its competency. During the procedure, the axillary nerve and PHCA is palpated while the patient’s arm is placed in external rotation and abduction. This is to verify a freely gliding uncompressed nerve and a consistently strong pulse in the artery [43]. It is also useful to check for fibrous bands around the neurovascular structures, which may be indicative of structural compression [39]. Postoperatively, patients are placed in an arm sling for comfort. Physical therapy is started to prevent the development of adhesions. Physical therapy is an important part of the postoperative recovery [39]. After a successful operation, most athletes can return to their sports [19].

There are several other treatment modalities reported in the literature. These include thrombolysis when there is a thrombus, thrombectomy when there is a distal embolus, aneurysm resection, and endovascular treatment with coiling [44,45,46,47]. In rare instances, quadrilateral space syndrome can resolve spontaneously [48].


Conclusions

QSS is a rare disorder. It can be associated with significant morbidity. Since many symptoms of QSS are nonspecific, there may be a delay in diagnosis and hence delay in treatment. There is one study that showed that the mean interval from the commencement of symptoms to surgical decompression was 14.5 months, with a range from 6–24 months [39]. Medical practitioner awareness of QSS as a differential diagnosis especially in at-risk populations such as athletes, is critical for timely and accurate diagnosis. Careful review of imaging studies is necessary to exclude differential diagnoses, understand etiology, and to devise the best treatment strategy for patients with QSS. Future investigations in patients with QSS could include studies on the prevalence of QSS and a more thorough analysis on the barriers of diagnosis, including limited practitioner awareness of the condition, nonspecific presentation, and the absence of a gold standard workup.

Patients are usually treated conservatively with physical therapy and activity modification. Patients who are non-responsive to conservative therapy after 6 months are subjected to surgery. 


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