Snapping Hip (Coxa Saltans)

                                    DR KS Dhillon

Introduction

Snapping hip syndrome is also known as coxa saltans or dancer’s hip. It is a clinical condition characterized by an audible or palpable snapping sensation that is heard during movement of the hip joint. The snapping hip has multiple etiologies and is classified based on the anatomic structure that is causing the snapping sensation. Two main snapping hip categories have been recognized namely:

• Extra-articular

• Intra-articular

There is now increasing knowledge of intra-articular pathologies and the term intra-articular snapping hip has relatively fallen out of favor. These etiologies include labral tears of the hip and loose bodies (e.g. secondary to synovial chondromatosis) [1,2,3].

Extra-articular snapping hip has become subclassified into:

• External snapping hip

• Internal snapping hip

External snapping hip is usually attributed to the iliotibial band moving over the greater trochanter of the femur during hip movements. Other causes include: 

• The proximal hamstring tendon rolling over the ischial tuberosity.

• The fascia lata or the anterior aspect of the gluteus maximus rolling over the greater trochanter.

• The psoas tendon rolling over the medial fibers of the iliacus muscle. 

A combination of defects is also possible. Thickening of both the posterior iliotibial band and anterior gluteus maximus can snap over the greater trochanter at the same time [4,5].

Internal snapping hip is usually caused by the iliopsoas tendon snapping over underlying bony prominences, such as the iliopectinal eminence or the anterior aspect of the femoral head. Other causes include partial or complete bifurcation of the iliopsoas tendon and paralabral cysts. The snapping sensation can closely mimic intra-articular pathology. Proper physical exams and imaging can differentiate the two. In approximately 50% of internal snapping hip cases, an additional intra-articular hip pathology is present.

Etiology

Snapping hip is most often an overuse phenomenon. It may be precipitated by trauma due to intramuscular injection into the gluteus maximus and surgical procedures. Coxa vara following total hip arthroplasty has been linked to the development of external snapping hip syndrome. There are other anatomical variations that may predispose to coxa saltans. These include an increased distance between the greater trochanters, prominent greater trochanters, and narrow bi-iliac width. Iliotibial band tightness, muscle tightness, shorter muscle or tendon lengths, or inadequate relaxation of the muscles may contribute to the development of snapping hip. Sometimes no etiology can be found resulting in an idiopathic classification [6].

Epidemiology

Approximately 5% to 10% of the population is affected by coxa saltans. The majority of patients experience painless snapping. The prevalence is slightly higher in women than in men. The individuals typically affected include those who do repetitive extreme hip motions. These include competitive and recreational ballet dancers, soccer players, weight lifters, and runners. Ninety percent of the competitive ballet dancers have reported symptoms of snapping hip syndrome and 80% have bilateral involvement. Movements that provoke snapping include external hip rotation and abduction at or over 90 degrees.

Pathophysiology

The external snapping hip syndrome is usually caused by the iliotibial band snapping over the greater trochanter of the femur during movements such as flexion, extension, and internal or external rotation.

Internal snapping hip is usually caused by the iliopsoas tendon snapping over underlying bony prominences, such as the iliopectinal eminence or the anterior aspect of the femoral head.

History and Physical

A good history and physical examination often can help pinpoint the correct anatomic region of the snapping. The patient usually can point with a finger to the area that is painful upon snapping and may even be able to recreate the snap. Symptoms develop and increase over a long period, typically months to years. 

External snapping hip is usually obvious on clinical examination. The patient experiences snapping or a sensation of subluxation of the hip. Sometimes the patient can even palpate the snapping phenomenon under the skin. The area over the greater trochanteric region can be painful due to abductor tendon pathology, greater trochanter bursitis, or inflammation of the iliotibial band. Tests to provoke the snap usually include femoral flexion or rotation. During the examination of the hip, the patient is placed in a lateral position, and the Ober test is done to test for iliotibial band tightness. With the patient in the same position, the knee and hip can be cycled through flexion and extension to provoke the snapping.

In patients with internal snapping hip, there is snapping or locking of the hip with an audible snap. Gluteus medius weakness is sometimes found. For examination of the hip, the patient is placed in the supine position with the affected hip guided by the examiner into an externally rotated and flexed position. From this position, the leg is extended into a neutral position next to the other resting leg. This test is positive if the snapping is reproduced at the anterior part of the hip.  

Evaluation

In the event that history and physical examination fails to diagnose coxa saltans, imaging can be used to help rule out other hip pathology and confirm the diagnosis. Plain radiographs are usually of not much value to confirm the diagnosis. They, however, are done to rule out anatomical variations, developmental dysplasia, or other hip pathology. A positive response to anesthetic injection into the joint in the affected area can help distinguish between external and internal snapping hip syndrome [3,6,7,8,9].

External snapping hip syndrome can be confirmed on T1 weighted axial MRI as a thickened iliotibial band or thickened anterior edge of the gluteus maximus muscle. If the snapping is not felt on physical examination, dynamic ultrasonography can be used to demonstrate the snapping of the iliotibial band over the greater trochanter. Dynamic ultrasonography can also reveal associated iliopsoas bursitis, tendonitis, and muscle tears. 

The diagnosis of internal snapping hip syndrome can be confirmed using iliopsoas bursography combined with fluoroscopy, magnetic resonance imaging, dynamic ultrasonography, or magnetic resonance arthrography. Magnetic resonance arthrography is preferred because it can also detect intra-articular hip pathology, which often accompanies internal snapping hip syndrome.

Management

When there is no pain treatment is not needed. When there is pain with snapping, treatment is conservative. It consists of rest, physical therapy, stretching, steroid injections, oral anti-inflammatory medications, and activity modification. In most patients, these measures are effective in relieving the pain.

Surgery may be warranted if the pain persists despite these conservative measures. For external snapping hip syndrome, iliotibial band loosening is usually the goal. This can be accomplished with either open or arthroscopic procedures. The iliotibial tendon can be lengthened or completely released using various procedures such as Z-lengthening, a cross-shaped release, a Z-shaped release, or a gluteus maximus release. If the release is excessive or there is damage to the surrounding area, weakness in abduction may be a complication [10].

For the internal snapping hip syndrome open or arthroscopic procedures are also available to lengthen or release the iliopsoas tendon. Usually,

arthroscopic methods are preferred to avoid complications of open surgery. The most common side effect of iliopsoas release is hip flexor weakness. This can occur if there is excessive release or there is damage to the surrounding area. 

Surgeries for external and internal snapping hip can result in other complications such as infection, muscle atrophy, heterotopic ossification, continued symptoms, or nerve damage.

Differential Diagnosis

The differential diagnosis of snapping hip includes:

• Acetabular Labral Tear

• Femoral Head Avascular Necrosis

• Hip Tendonitis

• Iliopsoas Tendinitis

• Bursitis; Greater Trochanteric or Iliopsoas

• Iliotibial Band Syndrome

• Intra-Articular Loose Body of the Hip

• Synovitis

Conclusion

Snapping hip syndrome is a primarily asymptomatic hip disorder that is characterized by a snapping sound or sensation upon specific hip movements. It has several etiologies that are classified based on the anatomical structure causing the snapping sensation. Extra-articular snapping hip syndrome (SHS) comprises two main classes i.e. external SHS, involving the iliotibial tendon, and internal SHS, involving the iliopsoas tendon. It is important to distinguish intra-articular pathologies from extra-articular SHS. Intra-articular processes are more acute, trauma-related, and largely more painful and debilitating.

Internal (iliopsoas) snapping is typically audible, while external (iliotibial) snapping is usually palpable. The etiologies are multifactorial. Both present with a broad spectrum of symptoms, including pain and decreased mobility. The true prevalence, however, remains unknown. It is estimated that about  5-10% of the population has some degree of SHS. Specific populations such as avid runners, ballet dancers, and gymnasts are more prone to develop this condition due to overuse and hypertrophy of involved anatomy. The most sensitive diagnostic tool is reproducing the snap with physical examination and movement. X-rays, MRI, dynamic ultrasound, and CT scans can supplement the diagnosis and confirm the underlying cause. Symptomatic patients are usually managed with NSAIDs, rest, physical therapy, and corticosteroid injections or analgesics. If pain and snapping persist, endoscopic disengagement of the iliopsoas or iliotibial tendon is carried out.

References

1. Hyland S, Graefe SB, Varacallo M. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL): Aug 8, 2023. Anatomy, Bony Pelvis and Lower Limb, Iliotibial Band (Tract). 

2. May O. Arthroscopic techniques for treating ilio-psoas tendinopathy after hip arthroplasty. Orthop Traumatol Surg Res. 2019 Feb;105(1S):S177-S185. 

3. Nolton EC, Ambegaonkar JP. Recognizing and Managing Snapping Hip Syndrome in Dancers. Med Probl Perform Art. 2018 Dec;33(4):286-291. 

4. Snapping Hip Syndrome. Orthop Nurs. 2018 Nov/Dec;37(6):361-362. 

5. Badowski E. Snapping Hip Syndrome. Orthop Nurs. 2018 Nov/Dec;37(6):357-360.

6. Flato R, Passanante GJ, Skalski MR, Patel DB, White EA, Matcuk GR. The iliotibial tract: imaging, anatomy, injuries, and other pathology. Skeletal Radiol. 2017 May;46(5):605-622.

7. Macke C, Krettek C, Brand S. [Tendinopathies of the hip : Treatment recommendations according to evidence-based medicine]. Unfallchirurg. 2017 Mar;120(3):192-198. 

8. Chang CY, Kreher J, Torriani M. Dynamic sonography of snapping hip due to gluteus maximus subluxation over greater trochanter. Skeletal Radiol. 2016 Mar;45(3):409-12. 

9. Potalivo G, Bugiantella W. Snapping hip syndrome: systematic review of surgical treatment. Hip Int. 2017 Mar 31;27(2):111-121. 

10. Ilizaliturri VM, Camacho-Galindo J. Endoscopic treatment of snapping hips, iliotibial band, and iliopsoas tendon. Sports Med Arthrosc Rev. 2010 Jun;18(2):120-7.

 

   Radioulnar Synostosis

                                DR KS Dhillon

Introduction

Osseous union or synostosis, of any two bones adjacent to each other, can involve any part of the upper extremity. Synostosis between the ulna and radius can take two general forms i.e. posttraumatic and congenital. Each form may be further classified into subtypes.

Sandifort in 1793, provided the initial description of congenital radioulnar synostosis. This condition is caused by a failure of segmentation between the ulna and the radius [1,2,3].  

Posttraumatic radioulnar synostosis and the congenital form are separate entities, having different causes, treatments, and prognoses [4].  The traumatic form can occur anywhere along the length of the interosseous membrane between the radius and ulna. Gros first described posttraumatic radioulnar synostosis in 1864, in autopsy specimens. Later Groves postulated that the success of treatment depended on where in the forearm synostosis had occurred [5,6].

The indications for surgical treatment of congenital radioulnar synostosis remain somewhat controversial. They are related to bilaterality and to the degree of deformity. They must be based on individual functional limitations. Surgery is recommended to be performed in childhood before patients reach school age.

The indication for surgery in posttraumatic radioulnar synostosis is the functional limitation of forearm rotation. Surgery is performed after the synostosis has matured and distinct radiographic borders are observed. Waiting for more than 3 years affects the final outcome.

The only contraindication for surgical treatment is the presence of mild deformity in an older patient if the patient has only minimal functional deficit. 

Pathophysiology

The skeletal anomaly in radioulnar synostosis includes varying degrees of proximal radial and ulnar fusion, with or without involvement of the radial head. If the radial head is involved, it may be dislocated posteriorly or anteriorly [7]. In patients with fibrous synostosis limited motion can be present. In severe cases, regional soft-tissue hypoplasia is often present, including those in which atrophy and fibrosis of the brachioradialis, pronator quadratus, pronator teres, and supinator muscles occur. The interosseous membrane may also be abnormal.

In the embryo, the upper limb bud arises from the unsegmented body wall at 25 to 28 days. The elbow becomes visible at 34 days, and the humerus, ulna, and radius become visible at 37 days. In the initial stages, the three cartilaginous analogues of the humerus, ulna, and radius are connected before segmentation. Hence, for a short time, the ulna and radius share a common perichondrium. At this time abnormal events can lead to a failure of segmentation. The severity and duration of the insult can determine the degree of subsequent synostosis.

Endochondral ossification then proceeds. The cartilaginous synostosis ossifies, either partially or completely, in the transverse or longitudinal plane. Congenital radioulnar synostosis in the forearm usually occurs between the proximal radius and the ulna. The condition is present at birth but is usually not discovered until early adolescence when the patient presents to the doctors with a lack of supination and pronation. 

In the initial stages, the union may be more of a synchondrosis. As the skeleton matures, the osseous bridge between the radius and the ulna becomes more radiographically apparent. Usually, if there is motion between the two adjacent bones it is minimal [8,9,10,11,12,13].

Etiology

Commonly, the cause of posttraumatic radioulnar synostosis is an operatively treated forearm fracture. Patients who have high-energy comminuted open fractures appear to be more likely to develop this condition. Proximal forearm fractures and Monteggia fractures also appear to have a higher incidence of synostosis [14]. The use of bone grafts and the presence of screws protruding through the opposite cortex also increase the incidence of synostosis.

Other causes of radioulnar synostosis include soft-tissue injury, any trauma causing hematoma formation between the radius and ulna, reconstructive procedures, or injury to the interosseous membrane [15]. Patients with closed head injuries appear to be more prone to this complication. This is presumably so for the same reason that they develop heterotopic ossification [16,17].

Epidemiology

Congenital radioulnar synostosis occurs rarely. There are only a few hundred cases reported in the literature. The rarity often leads to a delay in clinical diagnosis. Cleary and Omer [18] reported that the average patient age at diagnosis was 6 years. It ranged from 6 months to 22 years. There is no sex predilection and no particular inheritance pattern is apparent. In about 60% of cases the condition is bilateral.

Since congenital radioulnar synostosis is caused by an in-utero insult, its association with other abnormalities is to be expected. About a third of cases are associated with general skeletal abnormalities, such as hip dislocation, clubfoot, polydactyly, syndactyly, knee anomalies, Madelung deformity, ligamentous laxity, thumb hypoplasia, carpal coalition, and problems of the renal, cardiac, neurologic, and GI systems.

Some of the associated syndromes and abnormalities are genetically determined. These include acrocephalosyndactyly, Apert syndrome, arthrogryposis, mandibulofacial dysostosis, Carpenter syndrome, William syndrome, Klinefelter syndrome, Holt-Oram syndrome, microcephaly, multiple exostoses, and fetal alcohol syndrome [19,20]. Cleary and Omer found a genetic basis for an autosomal dominant form of congenital radioulnar synostosis in 20% of their patients [18].

Prognosis

The results of surgical treatment for posttraumatic radioulnar synostosis are fair at best.  There is a high failure rate with a loss of approximately one half of the intraoperative rotation. The use of postoperative indomethacin or low-dose limited field irradiation within the first 5 days after surgery is effective in reducing the recurrence of synostosis.

History and Physical Examination

The functional deficits associated with congenital radioulnar synostosis depend on the severity of the deformity as well as on whether or not it is bilateral. Patients who have severe fixed forearm pronation deformity cannot compensate for the resulting functional limitations by using scapular and glenohumeral motion. The forearm will usually lie in the pronated or hyperpronated position.

Hypermobility at the radiocarpal and midcarpal joints can disguise the lack of forearm rotation, especially with neutral or mild pronation deformities. Usually, there is a full or nearly full range of elbow motion, with flexion contractures rarely exceeding 30º. A shortening of the forearm or an abnormal carrying angle of the elbow may be seen.

Usually, there is no pain until the teenage years, when progressive and symptomatic radial head subluxation may be seen. This accounts for the delayed clinical diagnosis in many cases.  The disability is usually most significant in bilateral cases that have severe pronation. Children can initially have a normally located radial head and in adolescence, the children may develop symptomatic radial head subluxation. Radiographic follow-up is necessary.

Classification

Wilkie [21] divided congenital synostosis into two types based on the proximal radioulnar junction:

Type 1 - There is complete synostosis with the radius and ulna fused proximally for a variable distance.

Type 2 - There is less involvement. There may be a partial union. This type involves the region just distal to the proximal radial epiphysis and is associated with radial head dislocation.

Cleary and Omer [18] described four types of congenital synostosis:

• Bony synostosis

• Fibrous synostosis

• Associated posterior dislocation of the radius

• Associated anterior dislocation of the radius

Simmons et al [22] believed congenital synostosis to be a spectrum of anomalies in which the synostosis occurred in varying lengths, with or without the involvement of the radial head.

Posttraumatic radioulnar synostosis has been classified into three types based on location:

• Type 1 - Occurs in the distal forearm (least common)

• Type 2 - Occurs in the mid-forearm

• Type 3 - Occurs in the proximal forearm

Imaging Studies

Plain posteroanterior (PA) and lateral radiographs of the forearm are taken (fig 1). The X-rays will show bony ankylosis of the proximal radius and ulna. In patients with congenital proximal radioulnar synostosis, the radial pronation angle, which is easily measured on the flexed PA view, maybe a useful indicator of the severity of the condition [23].

Fig 1.

Management

Indications for surgical treatment of congenital radioulnar synostosis are controversial.  They are related to bilaterality and to the degree of deformity. Patients who have neutral rotation, mild pronation, or rare supination positions can compensate with ipsilateral shoulder motion. Wrist hypermobility can allow further functional compensation. Severe pronation deformities especially those more than 60º cause significant functional difficulty, especially with activities requiring supination. Hence, indications for surgery must be based more on individual functional limitations than on absolute forearm position.

Surgery should be performed in childhood before patients reach school age. In patients who have symptomatic subluxation of the radial head, the radial head may be excised at maturity. 

The indication for surgery in posttraumatic radioulnar synostosis is forearm limitation of rotation. Surgery is performed after the synostosis has matured and distinct radiographic borders are seen. This will reduce the likelihood that the synostosis will recur. A too-long wait of more than 3 years will adversely affect the final outcome due to soft-tissue contracture. A 100º arc of motion is desirable so that the patient can perform all activities of daily living (ADLs), and a 60º arc is required to perform most ADLs without assistance.

The only contraindication for surgical correction is the presence of mild deformity in an older patient who has only minimal functional deficit. 

Surgical Therapy

Attempts to achieve and maintain motion at the synostosis site are usually unsuccessful. Synostosis tends to recur despite excision, the use of various medications, or the interposition of fat, silicone, or muscle. Success, however, has been reported with excision of the bony bridge and the interposition of vascularized fat graft. An average rotation range of 74º can maintained at 2 years after surgery [24].

Some of the mobilization procedures are combined with tendon transfers to achieve supination. The extensor carpi radialis longus can be transferred to the volar aspect of the wrist and the flexor carpi ulnaris can be transferred dorsally around the ulna. 

Congenital radioulnar synostosis

The preferred surgical procedure for the treatment of congenital radioulnar synostosis has been osteotomy and derotation through the fusion mass, along with fixation with transcutaneous pins [25,26,27].

The optimal position of correction will vary according to the degree of involvement present, the bilaterality of the synostosis, and the amount of compensatory shoulder or radiocarpal motion that the patient has. Severe deformities do not permit one-stage correction, because of the tension on fibrous and vascular structures. Gradual correction using a multiplanar external fixator decreases the risk of neurovascular injury and it allows the patient to select the most functional position.

Generally, neutral rotation is used for unilateral deformities, and for bilateral deformities, one side is placed in 20-30º of pronation and the other in 20-30º of supination [28]. Shortening of the forearm is recommended to decrease the risk of neurovascular compromise. 

Postoperatively a long arm cast with 90º of elbow flexion is utilized for 8 weeks. After derotation, transcutaneous pins have generally been recommended for fixation. This pinning can easily be reversed if postoperative vascular compromise develops [8,29].

Simcock et al [30] reported the use of derotational osteotomy to treat 31 forearms in 26 children who had congenital radioulnar synostosis and functional limitations. In all cases, the union was successfully achieved within 8 weeks. There were no cases of compartment syndrome, vascular compromise, or loss of fixation. The overall rate of complications was 12%. This included two transient anterior interosseous nerve palsies in patients with rotational corrections of more than 80º, one transient radial nerve palsy, and one symptomatic muscle herniation.

Hwang et al [31] reported the use of one-stage rotational osteotomy of the proximal third of the ulna and the distal third of the radius with segmental bone resection to treat congenital radioulnar synostosis in 25 patients (28 forearms). There were 2 groups in this study. In group 1, the ulnar osteotomy was stabilized with an intramedullary pin. In group 2, no fixation was used. The surgical outcomes did not differ significantly between the two groups. The authors were of the opinion that one-stage rotational osteotomy of the proximal third of the ulna and the distal third of the radius with segmental bone resection was simple and safe and that internal fixation at the osteotomy site was not necessary.

Bishay [32] carried out a prospective study involving 12 consecutive pediatric patients (14 forearms) with severe congenital proximal radioulnar synostosis with a mean pronation deformity of 70.7° with a range of 60-85° that was corrected through single-session double-level rotational osteotomy and percutaneous placement of intramedullary Kirschner wires (K-wires) in both radius and ulna. At a mean follow-up of 30.4 months (range, 24-36 months), the patients had a mean pronation deformity correction of 59.8°. All 12 patients showed improvement in functional activities. None of the patients had any loss of correction or nonunion, neuropathies, circulatory disturbances, or hypertrophic scars.

Satake et al [33] carried out a study to assess the long-term (≥10 y) results of simple rotational osteotomy for congenital radioulnar synostosis in nine patients (12 forearms). Following the procedure, the forearm was fixed at an average of 4.2° of supination. At the final follow-up, the average motion arc of the palm ranged from 62° of supination to 26° of pronation. There were no postoperative neurologic or circulatory complications. The patients were better able to perform ADLs, and all were satisfied with the surgery results. The average score on the 11-item version of the Disability of the Arm, Shoulder, and Hand (DASH) score was 3.79 points at the final follow-up.

Pei et al [34] conducted a retrospective study of 31 patients (36 forearms) with congenital radioulnar synostosis. They found that proximal radioulnar derotational osteotomy followed by plate fixation was a safe and feasible procedure with a low complication rate. They were of the opinion that the technique could effectively improve the function of the forearm. Hamiti et al [35] also reported good results with this approach. 

Posttraumatic radioulnar synostosis

The surgery for posttraumatic synostosis is different from that for congenital radioulnar synostosis. Surgery for posttraumatic synostosis restores motion through excision of the synostosis area [5,6,36]. Numerous interposition materials such as fat, fascia, silicone, muscle, and cellophane have been used after resection to prevent a recurrence of synostosis, but these have met with varying degrees of success. Kelikian and Doumanian [37] have developed a metallic swivel prosthesis to restore motion, but no large series has been reported that supports its effectiveness. 

The goal of treatment involves resection of the entire bony synostosis. 

The dissection should be carefully carried out with minimal periosteal disruption to prevent the further stimulation of bone, limiting recurrence. The protection and identification of neurovascular structures are essential. The final range of motion should be assessed intraoperatively. There should be minimal postoperative immobilization.

Giannicola et al [38] carried out a study to evaluate 12 patients with posttraumatic proximal radioulnar synostosis (two with a double synostosis) who were treated surgically. The synostosis was excised in 10 cases. Radial head excision was done in one case, radial head arthroplasty in three, and proximal radial diaphyseal resection in two. The mean extension-flexion and pronation-supination arcs were 116° and 123°, respectively. There were significant improvements in the Mayo Elbow Performance Score (mean, 24), modified American Shoulder and Elbow Surgeons score (mean, 28), and QuickDASH score (mean, 17). One patient had synostosis recurrence and one had late disassembly of the radial head arthroplasty.

Abdul Azeem et al [39] reported good functional and prophylaxis against recurrence results with a triple therapy consisting of preoperative radiation therapy, tissue interposition after heterotopic ossification resection, and postoperative adjuvant indomethacin.

Complications

Although the surgical procedure that is used to treat congenital radioulnar synostosis is quite straight forward, it is associated with significant complications [40,41]. These include neurovascular compromise and recurrence of ankylosis. Soft-tissue contracture and neurovascular compromise can occur. Simmons et al [22] were of the opinion that derotations of more than 85º should be performed in two stages. For suspected compartment syndromes a low threshold for fasciotomies should be maintained. 

References

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2. Wang E, Wenger DR, Zhang L, Zhao Q, Ji S, Li J. The mechanism of acute elbow flexion contracture in children with congenital proximal radioulnar synostosis. J Pediatr Orthop. 2010 Apr-May. 30 (3):277-81. 

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6. Watson FM Jr, Eaton RG. Post-traumatic radio-ulnar synostosis. J Trauma. 1978 Jun. 18 (6):467-8.

7. Mital MA. Congenital radioulnar synostosis and congenital dislocation of the radial head. Orthop Clin North Am. 1976 Apr. 7 (2):375-83.

8. Dawson HG. A congenital deformity of the forearm and its operative treatment. Br Med J. 1912. 2:833-5.

9. Hansen OH, Andersen NO. Congenital radio-ulnar synostosis. Report of 37 cases. Acta Orthop Scand. 1970. 41 (3):225-30. 

10. Kelikian H. Congenital Deformities of the Hand and Forearm. Philadelphia: WB Saunders; 1974.

11. Lewis WH. The development of the arm in man. Am J Anat. 1901. 1:145-83.

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13. Spritz RA. Familial radioulnar synostosis. J Med Genet. 1978 Apr. 15 (2):160-2.

14. Bauer G, Arand M, Mutschler W. Post-traumatic radioulnar synostosis after forearm fracture osteosynthesis. Arch Orthop Trauma Surg. 1991. 110 (3):142-5.

15. Henket M, van Duijn PJ, Doornberg JN, Ring D, Jupiter JB. A comparison of proximal radioulnar synostosis excision after trauma and distal biceps reattachment. J Shoulder Elbow Surg. 2007 Sep-Oct. 16 (5):626-30. 

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20. Giuffrè L, Corsello G, Giuffrè M, Piccione M, Albanese A. New syndrome: autosomal dominant microcephaly and radio-ulnar synostosis. Am J Med Genet. 1994 Jul 1. 51 (3):266-9.

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23. Liu L, Liu C, Rong YB, Bai F, Chen SL. Radial Pronation Angle: A Novel Radiological Evaluation Index of Congenital Proximal Radioulnar Synostosis. Ann Plast Surg. 2020 May. 84 (5S Suppl 3):S196-S201. 

24. Sonderegger J, Gidwani S, Ross M. Preventing recurrence of radioulnar synostosis with pedicled adipofascial flaps. J Hand Surg Eur Vol. 2012 Mar. 37 (3):244-50.

25. Ogino T, Hikino K. Congenital radio-ulnar synostosis: compensatory rotation around the wrist and rotation osteotomy. J Hand Surg Br. 1987 Jun. 12 (2):173-8. 

26. Khalil I, Vizkelety T. Osteotomy of the synostosis mass for the treatment of congenital radio-ulnar synostosis. Arch Orthop Trauma Surg. 1993. 113 (1):20-2. 

27. El-Adl W. Two-stage double-level rotational osteotomy in the treatment of congenital radioulnar synostosis. Acta Orthop Belg. 2007 Dec. 73 (6):704-9.

28. Green WT, Mital MA. Congenital radio-ulnar synostosis: surgical treatment. J Bone Joint Surg Am. 1979 Jul. 61 (5):738-43. 

29. Smith RJ, Lipke RW. Treatment of congenital deformities of the hand and forearm (second of two parts). N Engl J Med. 1979 Feb 22. 300 (8):402-7. 

30. Simcock X, Shah AS, Waters PM, Bae DS. Safety and Efficacy of Derotational Osteotomy for Congenital Radioulnar Synostosis. J Pediatr Orthop. 2015 Dec. 35 (8):838-43.

31. Hwang JH, Kim HW, Lee DH, Chung JH, Park H. One-stage rotational osteotomy for congenital radioulnar synostosis. J Hand Surg Eur Vol. 2015 Oct. 40 (8):855-61. 

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