Chopart injuries

                                  Dr. KS Dhillon

Introduction

The transverse-tarsal or midtarsal joint is known eponymously as the Chopart joint after French surgeon François Chopart. He described an amputation through the articulation between the hindfoot and the midfoot(1). The Chopart joint is made up of the talonavicular joint (TNJ) and calcaneocuboid joint (CCJ). The TNJ is part of the coxa pedis (talocalcaneonavicular joint) which enables supination and pronation of the tarsus (2). The CCJ provides approximately 25° of rotation for hindfoot inversion and eversion (3). The Chopart joint complex allows the hindfoot to pivot while the forefoot remains still with inversion and eversion. The complex locks on heel inversion, stabilizing the midfoot during the push-off phase of gait (4). The Chopart joint is essential for normal foot function and requires strong ligamentous support. The TNJ is bridged superiorly by the dorsal talonavicular ligament and medial limb of the bifurcate ligament and inferiorly by the spring ligament (calcaenonavicular ligament). The spring ligament is comprised of the medioplantar oblique, inferoplantar longitudinal, and superomedial components (4) (fig 1). 

Superiorly the CCJ is supported by the dorsal calcaneocuboid ligament and the lateral limb of the bifurcate ligament and inferiorly by the short plantar ligament (plantar calcaneocuboid ligament) (4).

The cyma line divides the midfoot and the hindfoot. It represents the Chopart joint. It can be observed via dorsoplantar and lateral views (5), where radiological discrepancy indicates pathology. Initial imaging starts with radiographs in 3 views: dorsoplantar, lateral, and oblique (6). Oblique views are best for visualizing fractures of the anterior calcaneal process (4). 

The Chopart injuries can be divided into 4 broad groups:

• Ligamentous injury with dislocation

• Ligamentous injury without dislocation

• Fracture with dislocation

• Fracture without dislocation. 

Chopart dislocations can be pure-dislocations and fracture-dislocations. 

Pure dislocations are dislocations of the navicular and/or cuboid without an associated fracture. Fracture-dislocations are dislocations of the navicular and/or cuboid with associated fracture of the talus, navicular, calcaneus, or cuboid bones. Simultaneous dislocation of both the CCJ and TNJ is referred to as a complete Chopart dislocation. Swivel dislocations usually result from medial or lateral deforming forces causing CCJ and/or TNJ dislocation and the calcaneus ‘swivels’ on an intact talocalcaneal ligament (7). 

Fig 1.

Incidence and etiology

Ponkilainen et al (8) conducted a retrospective epidemiology cohort study of 307 midfoot injuries. They found that the incidence of midfoot injury is 12.1/100,000/year and Chopart injury 2.2/100,000/year. Motor vehicle accidents (MVA) are the main cause of Chopart dislocations. Chopart dislocations are more common in males (6,9). Richter et al. found that 16% of 155 midfoot fractures were Chopart fracture-dislocations(9). Richter et al in a follow-up study of 110 Chopart-dislocations found that 25% were pure-dislocations, 55% fracture-dislocations, and 20% combined Chopart-Lisfranc fracture-dislocations (6). A recent study by Rammelt et al (10) of 128 Chopart joint injuries found only 5 patients (3.7%) had pure-dislocations and the most frequent fracture-dislocation was transnavicular/transcuboidal in 21% of cases. The average age of patients in 5 studies was 36.8 years (11).

Diagnosis

Chopart injuries are clinically diagnosed through a careful history and physical examination. Radiographic evaluation is required to exclude fractures or assess syndesmotic integrity. 

Clinical signs

Clinical examination will show plantar ecchymosis. Plantar ecchymosis sign (PES) describes a central midfoot plantar ecchymosis that is pathognomic for relevant midfoot injuries. It indicates the rupture of strong plantar ligaments and resulting haematoma (12). PES has been seen following calcaneal fractures (13), Lisfranc (14), and Chopart injuries (15). The PES is rarely reported although it is a valuable clinical sign indicating underlying midfoot injury. A CT is useful when PES is positive and radiographs are negative. Compartment syndrome is common in Chopart injuries (9,10), especially dislocations (6). Palpation of the entire foot is necessary and conformation of the neurovascular statues is required.

Imaging

Up to 41% of Chopart injuries are missed at first presentation (5). Haapamaki et al (16) found that plain radiographs alone missed 33% of fractures in Chopart injuries. In Van Dorp et al (5) case series of 9 Chopart dislocations, 2 were initially missed from Xray alone and the severity of the injury was underestimated for 3 prior to CT. Alongside this 2/24 fracture-dislocations from case reports were initially missed on Xrays.  Rammelt et al found pure-dislocations to be very rare (4%). They encourage CT scanning to rule out associated fractures (10). Almeida et al (17) also found a significant improvement in identifying additional Chopart fractures missed on XR with CT. CT allows reconstructive modelling to determine the degree of dislocation (4). 

Management and outcomes

For Chopart dislocations, initial ORIF provides better outcomes than closed reduction prior to internal fixation (6). A study by Richter et al (6) found that a closed reduction can yield good results only with pure dislocations, when anatomic conditions can be restored, or if there were contraindications to surgery. Closed reduction alone was found to have statistically similar outcomes to operative treatment. Six of fourteen pure-dislocations required internal fixation following closed reduction and they should have undergone ORIF initially. Since there is a risk of requiring internal fixation following closed reduction, ORIF is advised and closed reduction is discouraged. 

Closed reduction is often challenging. It often fails and repeated attempts can cause further damage (18). Rammelt et al (10) found over a 10-year follow-up that ORIF generates significantly better results than closed reduction and percutaneous fixation in patients with Chopart injuries. According to Rammelt et al (10), pure-dislocations had the worst prognosis. 

Maintenance of foot column length is important. It significantly improves the gait quality (19). Correct alignment of the foot axes and correct length of medial and lateral columns should be a major goal of therapy (5). 

Secondary reconstruction improves outcomes in suitable patients with malunited Chopart fracture dislocations. Otherwise, joint fusion is required (20). Arthrodesis is carried out in patients who present late (21), in patients with diabetic arthropathy (22), or when other treatment strategies have failed. Arthrodesis can prevent midfoot collapse (23). TNJ arthrodesis can reduce the Chopart joint range of motion by 50%. It is a negative prognostic factor (10). It is considered as a last resort (24). Soft tissue conditions dictate treatment methods. External fixation can maintain reduction during soft tissue healing (10,25). It also maintains column length with unstable ORIF (26). Patients with Chopart injuries require long-term follow-up to monitor for complications which are common (5,27).

Conclusion

Pure dislocations tend to have inferior outcomes. It is probably due to the high energy required to disrupt the strong ligamentous anatomy at the Chopart joint. A general consensus is that closed reduction often fails and leads to poorer outcomes, even if followed by ORIF. Restoring and maintaining the medial and lateral foot columns by joint reconstruction is essential to obtain satisfactory results. Compartment syndrome evaluation and CT are highly recommended. Urgent ORIF with or without external fixation is the management of choice for these injuries. Negative prognostic factors include the severity of injury, delayed or staged treatment, arthrodesis, and MVA.

References

1. Wolf JH. Francois Chopart (1743–1795) – inventor of the partial foot amputation at the transtarsal articulation. Orthop Traumatol. 2000;8(4):314–317.

2. Kou JX, Fortin PT. Commonly missed peritalar injuries. J Am Acad Orthop Surg. 2009;17(12):775–786. doi: 10.5435/00124635-200912000-00006.

3. Walter WR, Hirschmann A, Alaia EF, Tafur M, Rosenberg ZS. Normal anatomy and traumatic injury of the midtarsal (Chopart) joint complex: an imaging primer. Radiographics. 2019;39(1):136–152. doi: 10.1148/rg.2019180102.

4. Walter WR, Hirschmann A, Tafur M, Rosenberg ZS. Imaging of Chopart (midtarsal) joint complex: normal anatomy and posttraumatic findings. AJR Am J Roentgenol. 2018;211(2):416–425. doi: 10.2214/AJR.17.19310.

5. Van Dorp KB, de Vries MR, van der Elst M, Schepers T. Chopart joint injury: a study of outcome and morbidity. J Foot Ankle Surg. 2010;49(6):541–545. doi: 10.1053/j.jfas.2010.08.005.

6. Richter M, Thermann H, Huefner T, Schmidt U, Goesling T, Krettek C. Chopart joint fracture-dislocation: initial open reduction provides better outcome than closed reduction. Foot Ankle Int. 2004;25(5):340–348. doi: 10.1177/107110070402500512.

7. Pillai A, Chakrabarti D, Hadidi M. Lateral swivel dislocation of the talo-navicular joint. Foot Ankle Surg. 2006;12:39–41.

8. Ponkilainen VT, Laine HJ, Mäenpää HM, Mattila VM, Haapasalo HH. Incidence and characteristics of midfoot injuries. Foot Ankle Int. 2019;40(1):105–112. doi: 10.1177/1071100718799741.

9. Richter M, Wippermann B, Krettek C, Schratt HE, Hufner T, Therman H. Fractures and fracture dislocations of the midfoot: occurrence, causes and long-term results. Foot Ankle Int. 2001;22(5):392–398. doi: 10.1177/107110070102200506.

10. Rammelt S, Missbach T. Chopart joint injuries: assessment, treatment, and 10-year results. J Orthop Trauma. 2023;37(1):e14–e21. doi: 10.1097/BOT.0000000000002465.

11. Metcalfe TSN, Aamir J, Mason LW. Chopart dislocations: a review of diagnosis, treatment and outcomes. Arch Orthop Trauma Surg. 2024 Jan;144(1):131-147. doi: 10.1007/s00402-023-05040-4. Epub 2023 Sep 15. PMID: 37715068; PMCID: PMC10774188.

12. Rammelt S. Chopart and lisfranc fracture-dislocations. In: Bentley G, editor. European surgical orthopaedics and traumatology: the EFORT textbook. Berlin, Heidelberg: Springer Berlin Heidelberg; 2014. pp. 3835–3857.

13. Richman JD, Barre PS. The plantar ecchymosis sign in fractures of the calcaneus. Clin Orthop Relat Res. 1986;207:122–125.

14. Ross G, Cronin R, Hauzenblas J, Juliano P. Plantar ecchymosis sign: a clinical aid to diagnosis of occult Lisfranc tarsometatarsal injuries. J Orthop Trauma. 1996;10(2):119–122. doi: 10.1097/00005131-199602000-00008.

15. Dewar FP, Evans DC. Occult fracture-subluxation of the midtarsal joint. J Bone Joint Surg Br. 1968;50(2):386–388.

16. Haapamaki VV, Kiuru MJ, Koskinen SK. Ankle and foot injuries: analysis of MDCT findings. AJR. 2004;183:615–622. doi: 10.2214/ajr.183.3.1830615.

17. Almeida RR, Mansouri M, Tso DK, Johnson AH, Lev MH, Singh AK, Flores EJ. The added value of cross-sectional imaging in the detection of additional radiographically occult fractures in the setting of a Chopart fracture. Emerg Radiol. 2018;25(5):513–520. doi: 10.1007/s10140-018-1615-x.

18. Honeycutt MW, Perry MD. The Chopart variant dislocation: plantar dislocation of the cuboid and navicular. Foot Ankle Orthop. 2019;4(3):2473011419876262. doi: 10.1177/2473011419876262.

19. Mittlmeier T, Krowiorsch R, Brosinger S, Hudde M. Gait function after fracture-dislocation of the midtarsal and/or tarsometatarsal joints. Clin Biomech (Bristol, Avon) 1997;12(3): S16–S17. doi: 10.1016/s0268-0033(97)88330-1.

20. Rammelt S, Zwipp H, Schneiders W, Heineck J. Anatomic reconstruction of malunited Chopart joint injuries. Eur J Trauma Emerg Surg. 2010;36(3):196–205. doi: 10.1007/s00068-010-1036-3.

21. Kumar A, Gaba S, Digge VK, Gautam D. Neglected medial swivel talonavicular dislocation treated with arthrodesis: a case report and literature review. J Clin Orthop Trauma. 2020;11(3):474–478. doi: 10.1016/j.jcot.2018.12.011.

22. Ansari MAQ. Isolated complete dislocation of the tarsal navicular without fracture: a rare injury. Ci Ji Yi Xue Za Zhi. 2016;28(3):128–131. doi: 10.1016/j.tcmj.2014.11.003.

23. Arain AR, Adams CT, Haddad SF, Moral M, Young J, Desai K, Rosenbaum AJ. Diagnosis and treatment of peritalar injuries in the acute trauma setting: a review of the literature. Adv Orthop. 2020;2020:1852025. doi: 10.1155/2020/1852025.

24. Johnstone AJ, Maffulli N. Primary fusion of the talonavicular joint after fracture dislocation of the navicular bone. J Trauma. 1998;45(6):1100–1102. doi: 10.1097/00005373-199812000-00025.

25. Klaue K. Treatment of Chopart fracture-dislocations. Eur J Trauma Emerg Surg. 2010;36(3):191–195. doi: 10.1007/s00068-010-1047-0.

26. Kutaish H, Stern R, Drittenbass L, Assal M. Injuries to the Chopart joint complex: a current review. Eur J Orthop Surg Traumatol. 2017;27(4):425–431. doi: 10.1007/s00590-017-1958-0.

27. Kösters C, Bockholt S, Müller C, Winter C, Rosenbaum D, Raschke MJ, Ochman S. Comparing the outcomes between Chopart, Lisfranc and multiple metatarsal shaft fractures. Arch Orthop Trauma Surg. 2014;134(10):1397–1404. doi: 10.1007/s00402-014-2059-8.

     Pigmented Villonodular Synovitis

                                        Dr. KS Dhillon

Introduction

Pigmented Villonodular Synovitis (PVNS) is a locally aggressive neoplastic synovial disease (not a true neoplasm) that affects joints, bursae, and tendon sheaths. It is characterized by synovial thickening, joint effusions, and bony erosions. Pigmented villonodular synovitis usually affects a single joint. Polyarticular cases are rare. Polyarticular involvement is more likely to occur in children.

Patients between the ages of 30 and 40 are usually affected. It can occur anytime between the 1st and 7th decade and equally affects men and women. 

Pigmented villonodular synovitis is rare. It accounts for less than 5% of all primary soft tissue tumors. Localized lesions are more common than diffuse lesions. 

Large joints are predominantly affected by diffuse PVNS, with the knee being the most common (66-80%). The hip, ankle, shoulder, and elbow are affected in descending frequency.

The intra-articular form of PVNS occurs almost exclusively in the knee. The tendon sheaths of the hand and wrist are affected more frequently. The volar aspect of the index and long fingers are the most common sites of disease.

Occasionally pigmented villonodular tenosynovitis can coexist with other synovial conditions such as synovial chondromatosis. Microscopically, PVNS synovitis has fibrohistiocytic origin.

Pigmented villonodular synovitis is usually benign. There are however a few cases of malignant transformation that have been reported. It may cause significant morbidity.

Types of Pigmented Villonodular Synovitis

Pigmented villonodular synovitis can be classified as extraarticular and intraarticular. 

Intraarticular

• Diffuse – Diffuse involvement of joint synovium

• Localized – Polypoid or nodular joint synovial lesion within the joint

Extraarticular

• Diffuse –   Diffuse multifocal involvement of extraarticular synovial membrane

• Nodular or Localized – Localized extraarticular nodular lesion, also referred to as giant-cell tumor of the tendon sheath

Both the localized intraarticular forms and diffuse forms predominantly involve the major weight-bearing joints of the lower extremities. The knee is the most common joint involved followed by the hip, ankle, foot, elbow, and shoulder. The nodular extraarticular variant typically involves the acral (limbs and fingers) soft tissues and is mainly found in the fingers and metacarpal/carpal areas. The forearm tendons are rarely involved.

When all types are taken into consideration, the fingers are involved in about 60% of the cases, the knee is involved in approximately 30% of cases and the toes are involved in about 10% of the cases.

Causes

The causes of PVNS include:

• Overexpression of CSF1 gene.

This leads to clusters of aberrant cells creating focal areas of soft tissue hyperplasia

• Mutations

Chromosome 1p13 in the majority of cases

5q33 chromosomal rearrangement

The Giant Cell Tumor of the tendon sheath is an associated condition.

Presentation of Pigmented Villonodular Synovitis

The symptoms are usually intermittent or steadily progressive. The knee is the most commonly affected large joint. Finger joints can present with localized swelling on the palmar aspect.

The patient usually presents with longstanding pain of insidious onset in the joints that are affected. In about 50% of the patients, there is a prior history of trauma to the area.

Other symptoms include:

• Swelling in the affected joint

• Stiffness in the affected joint

• Recurrent atraumatic hemarthrosis ( Hallmark of the disorder)

Examination would show joint effusion. The overlying skin may be erythematous. There would be joint line tenderness and movements of the joint would be limited. Fluid aspiration usually yields hemorrhagic fluid.

Laboratory Investigations

Bloodwork is usually normal. In patients with recurrent haemarthrosis, arthrocentesis will grossly show bloody effusion.

Diagnostic arthroscopy will show brownish or reddish inflamed synovium which is typical of PVNS. The frond-like pattern of papillary projections is the gold standard for diagnosis. During arthroscopy, synovial biopsy is obtained.

The biopsy will show that the synovium is covered with tan to brown, irregular papillary projections and larger nodular protrusions. Microscopic findings include fibrohistiocytic proliferations and mononuclear stromal cells infiltration into the synovium. It will also show hemosiderin stained multinucleated giant cells, pigmented foam cells (lipid-laden histiocytes), and mitotic figures. 

Imaging

X-rays

In the early stages, the X-rays may appear normal. AP and lateral view X-rays of the affected joint are usually done. The X-rays may show an ill-defined soft tissue mass around the joint. Often degenerative joint diseases are seen along with multiple subchondral cysts in the bones on both sides of the affected joint. 

Pressure erosion of the joints may occur leading to saucerization of the joint. Narrowing of joint space and osteophyte formation may be seen.

Sometimes, the effusion may be seen as a dense shadow which signifies the presence of hemosiderin.

CT Scan

A CT scan can reveal the extent of involvement and the extent of cystic lesion loss and bone erosions. A CT scan is also useful for guiding needle biopsy.

MRI

MRI is the imaging choice for PVNS. MRI can provide excellent demarcation of both intra and extra-articular disease. MRI will show joint effusion, hemosiderin deposits, synovial expansion, and bony erosions.

Nuclear Imaging

Bone and/or PET scans are not very useful in diagnosing pigmented villonodular synovitis.

Differential Diagnoses

The differential diagnosis includes:

• Rheumatoid arthritis

• Synovial hemangiomatosis

• Tuberculosis

• Gout

• Hemochromatosis

• Low-grade infectious arthritis

• Synovial Osteochondromatosis

• Synovial Sarcoma

• Hemophilia/hemarthrosis

Treatment of Pigmented Villonodular Synovitis

Excision of the affected synovium is the treatment of choice. In clinically aggressive cases, low-dose radiotherapy can be used to control the disease process. It is beneficial in preventing further destruction of the joint and in reducing the risk of recurrences.

In sporadic cases, transformation to a spindle-cell malignancy with metastases to the contralateral thigh has been reported. 

Although it is a benign condition, PVNS can result in significant morbidity if left untreated.

The primary treatment options include surgical resection or radiation therapy.

Nonoperative Treatment

Observation can be carried out in asymptomatic patients. 

CSF-1 receptor antagonist (pexidartinib) can be used in patients with extensive disease who are unlikely to benefit from the operative treatment.

Perxidartinib taken once daily for 24 weeks has significantly improved the disease burden in approximately 40% of patients. A major side effect is liver toxicity.

Radiotherapy

Radiotherapy is indicated in advanced disease. Radiotherapy reduces the rate of recurrence to less than 20%.

Operative Treatment

Partial synovectomy

For local form of PVNS that is accessible arthroscopic partial removal of synovium can be done. Otherwise, open surgery can be carried out.

Total synovectomy

Total synovectomy is done in patients with overtly symptomatic and painful disease. It can be done by arthroscopy or open surgery. Synovectomy improves the symptoms and function. Recurrence is common. It is often due to incomplete removal of the synovium.

Total synovectomy and total joint arthroplasty

It is done in patients with advanced disease with severe degenerative joint changes in the hip, knee, and shoulder.

Total synovectomy and arthrodesis

It is done in patients with severe disease of the ankle.

Amputation

In patients with a long course of the disease and numerous recurrences, an amputation may be required.

Complications of PVNS

Recurrence

Recurrence is the most common complication. Despite complete synovectomy, it occurs in about 50% of the patients. The rates are similar for both arthroscopic and open surgery. It can be reduced with addition of external beam radiation.

Joint destruction

PVNS can produce joint destruction which can result in moderate to severe joint deformity. It may lead to a need for arthrodesis or amputation. Skin necrosis can occur. Exposure to radiation can produce radiation-induced sarcoma

Prognosis

PVNS is associated with a high recurrence rate and accelerated degeneration of the knee. Often ultimately knee arthroplasty is required.

TKA in patients with PVNS is often associated with complications.

Conclusion

Pigmented Villonodular Synovitis is a locally aggressive synovial disease characterized by joint effusions, expansion of the synovium, and bony erosions. It usually presents in patients who are between 30 and 40 years of age, with recurrent atraumatic knee hemarthrosis.

The diagnosis is multifaceted, involving clinical assessment and MRI studies. Arthrocentesis reveals a brown fluid, and biopsy reveals hemosiderin-stained multinucleated giant cells.

Treatment generally consists of partial or total surgical synovectomy depending on the presence of localized or diffuse PVNS.