Indications for operative versus nonoperative treatment of tarsometatarsal joint injuries depend on the specific injury pattern and disruption of normal anatomy, which may be evident on physical examination or radiographs but may also present more subtly.
By Andrew Rosenbaum, MD, John DiPreta, MD, and Richard Uhl, MD
Jacques Lisfranc (1790-1847), a field surgeon in Napoleon’s army, described an amputation involving the tarsometatarsal (TMT) joint due to a severe gangrene that developed when a soldier fell from a horse with his foot caught in a stirrup.1-3 Although this is one type of TMT joint injury, it must be understood that the so-called Lisfranc injury does not delineate any one specific fracture or dislocation, but instead a spectrum of processes involving the TMT joint complex.
Injuries to the Lisfranc joint occur in 1 of 55,000 persons each year in the US and are two to three times more common in men than women.4,5 Approximately 20% of these injuries are misdiagnosed or missed on initial radiographic assessment, leading to potentially devastating consequences for patients, including degenerative arthritis, loss of arch height, and chronic instability and pain at the midfoot-forefoot articulation.5 The most commonly cited causes of Lisfranc injury are high energy mechanisms, with motor vehicle accidents accounting for 40% to 45% of the injuries.5 Low energy mechanisms, such as those sustained in athletic competition, account for approximately 30%.5
Lisfranc’s joint divides the midfoot and the forefoot, forming an oblique line through the foot’s TMT joints, which consist of the articulations between the first metatarsal and medial cuneiform, second metatarsal and middle cuneiform, third metatarsal and lateral cuneiform, and the fourth and fifth metatarsals with the cuboid. It runs from the lateral aspect of the proximal forefoot to the medial aspect of the distal forefoot. Both osseous and ligamentous structures contribute to joint stability, with the bony structures producing a stable configuration resembling a Roman arch.1 Of note, the middle cuneiform–second metatarsal articulation forms the keystone of the arch, preventing mediolateral metatarsal motion at the Lisfranc joint. This transverse arch also prevents plantar displacement of the three medial metatarsals.
The joint capsule and TMT ligaments provide limited soft-tissue support to the Lisfranc joint. Ligaments are grouped according to anatomic location (dorsal, plantar, and interosseous). Additionally, the lesser metatarsals are bound together by intermetatarsal ligaments. There are no ligamentous connections between the first and second metatarsal bases. The most significant and strongest ligamentous structure is the oblique interosseous ligament. Lisfranc’s ligament, as it is called, originates on the lateral surface of the medial cuneiform and passes in front of the intercuneiform ligament, ultimately inserting on the medial aspect of the second metatarsal base near the plantar surface. In a biomechanical study by Solan et al,6 the strength of the dorsal, plantar, and interosseous ligaments was evaluated by stressing each to failure. The Lisfranc ligament was strongest, followed by the plantar and then the dorsal ligaments.6
Mechanism of injury
The Lisfranc joint is susceptible to both direct and indirect mechanisms of injury. Direct injuries are due to high energy blunt trauma to the dorsum of the foot, such as a crush injury. These often result in poorer clinical outcomes than indirect injury types because of the soft tissue trauma associated with direct injuries. Indirect mechanisms can be stratified into high energy and low energy subtypes. Motor vehicle accidents are the most common cause of high energy Lisfranc injury. In a 2005 study investigating the mechanism by which the forefoot is injured in motor vehicle accidents, Smith et al performed impact testing on postmortem human lower legs and feet. The authors determined that Lisfranc injuries result from the forefoot being forcefully plantar flexed, as occurs during sudden braking in a car accident.7 Low energy injuries include those incurred during athletic competition.
Axial loading of a plantar flexed foot causes indirect injuries, such as those incurred in football players when one player falls onto the heel of another whose foot is in equinus and planted. Of note, approximately 4% of professional football players suffer Lisfranc injuries each year.1 Indirect Lisfranc injuries have also been observed in gymnasts and soccer and basketball players.8 Less common low-velocity mechanisms include forced forefoot abduction and nonspecific twisting or falling injuries seen with jumping or falls from a height.9
With direct injuries, the force vector dictates the fracture pattern and direction of dislocation. The more predictable indirect injuries most commonly involve failure of the weaker dorsal TMT ligaments in tension with subsequent dorsal or dorsolateral metatarsal dislocation.5
Quenu and Kuss10 published the earliest classification scheme for Lisfranc injuries (1909). It was subsequently modified by Hardcastle et al in 1982 and Myerson et al in 1986.3,11 These classifications are all based on TMT joint congruency and displacement of the metatarsal bases. While they are useful for standardizing descriptions of Lisfranc injuries, clinicians have not found these classifications helpful for management and prognosis.5,11
In an attempt to develop a classification scheme with strong prognostic implications, Chiodo and Myerson established a columnar classification in 2001 based on the three mechanical columns of the foot: the medial column, consisting of the first TMT and medial naviculocuneiform joints; the middle column, consisting of the second and third TMT joints and the articulation of the middle and lateral cuneiforms with the navicular; and the lateral column, formed by the articulations between the fourth and fifth metatarsals and the cuboid.12 The clinical utility of this classification relates to its emphasis on midfoot motion and the fact that TMT joint incongruity, which can occur following a Lisfranc injury, is best tolerated at the medial and lateral columns.1 Further, the second TMT joint is most vulnerable to post-traumatic arthritis.1 In other words, medial and lateral column injuries may have a better prognosis than those involving the middle column.
The diagnosis of high energy Lisfranc injuries is straightforward, as physical exam will reveal swelling and obvious deformity, including widening or flattening of the forefoot. A positive gap sign, or abnormal space between the first and second toes, is also suggestive of a TMT joint injury or intercuneiform disruption.13 Although associated vascular injury is rare, it may be difficult to palpate a dorsalis pedis pulse in the presence of swelling.14
In a case of low energy injury, physical examination may reveal only a patient with an inability to bear weight and evidence of minimal midfoot and forefoot swelling. An additional finding may be plantar arch ecchymosis, which is considered pathognomonic for Lisfranc injury.15 Various tests and stress maneuvers have been described, including pain on passive abduction and pronation of the forefoot, to aid in identification of Lisfranc injury.4,8,16 Although it is possible that physical exam alone can identify a Lisfranc injury, diagnostic adjuncts are usually required in this setting.
Nonweight bearing anteroposterior (AP), lateral, and 30° oblique views of the foot should comprise the initial radiographic series. However, 50% of subtle Lisfranc injuries will appear normal on nonweight bearing imaging.13 Thus, to diagnose these injuries, clinicians should obtain a weightbearing film with both feet on a single cassette or an abduction-pronation stress view.1 In practice, however, clinicians rarely do this because of patients’ inability to bear weight without pain. Therefore, in the setting of nondiagnostic plain radiographs a bone scan or magnetic resonance imaging (MRI) can be useful. Computed tomography is also useful for delineating fractures and preoperative planning.1
Findings consistent with a Lisfranc injury on AP radiographs include incongruity at the first and second metatarsal joints, misalignment between the medial border of the second metatarsal and the medial border of the middle cuneiform, and a diastasis of 2 mm or more between the first and second metatarsals when compared with the contralateral foot (Figures 1, 2). It is important to note, however, that on AP views, the first-second metatarsal interspace has been shown to vary between individuals, with a diastasis of up to 3 mm at times considered normal.17,18 In such instances, radiographic comparison with the contralateral foot should be obtained.
The oblique radiograph of a normal foot should depict a well-aligned medial border of the fourth metatarsal and medial border of the cuboid. The presence of a small bony fragment between the base of the second metatarsal and the medial cuneiform may be observed and represents an avulsion of either the proximal or distal attachment of the Lisfranc ligament. This “fleck” sign, as described by Myerson et al, is suggestive of a TMT joint complex injury.11
Flattening of the longitudinal arch, dorsal displacement, or both at the second TMT joint may be observed on lateral weightbearing radiographs.1 In the uninjured patient, the fifth metatarsal is normally plantar in relation to the medial cuneiform. Flattening of the midfoot arch positions the medial cuneiform plantar to the fifth metatarsal. Although the radiographic findings listed are those most commonly encountered with Lisfranc injuries, as mentioned, their absence does not definitively rule one out.
Indications for both operative and nonoperative treatment exist, all with the goal of re-establishing a painless and stable foot. Nonoperative treatment is limited to stable TMT joint complex injuries and include those that are nondisplaced, without fracture, and stable under radiographic stress examination.5 Treatment of these injuries involves protected weightbearing in a controlled ankle motion (CAM) walking boot for six to 10 weeks, with frequent follow-up radiographs to ensure no change in alignment.1
Any disruption of normal anatomy warrants surgical correction. In most cases, surgeons perform open reduction and internal fixation (Figure 3). The first, second, and third TMT joints are typically stabilized using screw fixation, while the fourth and fifth are pinned with K-wires. Although this is one approach to operative management, many forms of fixation are available and selection depends on both the nature of the injury and the surgeon’s preference. Additional options include bridge plating and primary fusion, particularly in the setting of significant cartilage damage.1
A period of nonweightbearing follows surgery, with progression to protected and then full weightbearing at around three and eight weeks, respectively. Four to six weeks of postoperative physical therapy focusing on balance and gait training is initiated only after a patient is advanced to full weightbearing.1
Regardless of the treatment modality used for Lisfranc injury, failure to achieve anatomic alignment increases the risk of complications. Post-traumatic arthritis, chronic instability, gait abnormalities, and pain result from the suboptimal TMT joint mechanics associated with nonanatomic reduction.
There is very little motion at the TMT joint complex during walking, as it predominantly functions as a structure for regulating and dispersing loading forces during weightbearing.19 Therefore, it is not uncommon for patients to have abnormal gait biomechanics following a Lisfranc injury, particularly when anatomic reduction is not accomplished. Several studies have evaluated this.19-21 In a 2010 investigation by Schepers et al, plantar pressure and foot position variables were compared in patients’ injured and uninjured feet.20 An altered walking pattern was observed, with reduced contact times and surfaces in the injured forefoot and concurrently increased contact pressures in the midfoot. This suggests a compensatory role of the midfoot during gait in the setting of Lisfranc injury.20
Additionally, it has been shown that a dorsolateral displacement of the second metatarsal base by 1 or 2 mm results in a reduction of the TMT articular contact area by 13.1% and 25.3%, respectively.22 Such malalignment, which can occur following nonanatomic reduction, increases the risk of developing posttraumatic arthritis.
Despite these complications, good or excellent outcomes, as based on results from the American Orthopaedic Foot and Ankle Society midfoot score and the long-form Musculoskeletal Function Assessment score, have been achieved in 50% to 95% of patients with anatomic alignment, compared with 17% to 30% of patients with nonanatomic alignment following injury.3,11,23-25
The management of a Lisfranc injury requires a familiarity with the osseoligamentous anatomy of the TMT joint complex, the common mechanisms of injury, and classification systems. It is important to recognize that these injuries can refer to any one of several processes that affect the TMT joint, and understand the approach to both diagnosis and treatment.26 While physical examination and plain radiographs are the cornerstones of the workup, injuries of the TMT joint complex may also present more subtly, requiring a high level of suspicion to diagnose. The indications for operative versus nonoperative treatment depend on the specific injury pattern and disruption of normal anatomy. Regardless of treatment, good outcomes are achievable and contingent upon anatomic restoration and stabilization.
Andrew Rosenbaum, MD, is a resident, John DiPreta, MD, is an associate professor, and Richard Uhl, MD, is chair in the Division of Orthopaedic Surgery at Albany Medical College in Albany, NY.
1. Watson TS, Shurnas PS, Denker J. Treatment of Lisfranc joint injury: Current concepts. J Am Acad Orthop Surg 2010;18(12):718-728.
2. Cassebaum WH. Lisfranc fracture-dislocations. Clin Orthop Relat Res 1963;30:116-129.
3. Hardcastle PH, Reschauer R, Kutscha-Lissberg E, Schoffmann W. Injuries to the tarsometatarsal joint: Incidence, classification and treatment. J Bone Joint Surg Br 1982;64(3):349-356.
4. Mantas JP, Burks RT. Lisfranc injuries in the athlete. Clin Sports Med 1994;13(4):719-730.
5. Thompson MC, Mormino MA. Injury to the tarsometatarsal joint complex. J Am Acad Orthop Surg 2003;11(4):260-267.
6. Solan MC, Moorman CT III, Miyamoto RG, et al. Ligamentous restraints of the second tarsometatarsal joint: A biomechanical evaluation. Foot Ankle Int 2001;22(8):637-641.
7. Smith BR, Begeman PC, Leland R, et al. A mechanism of injury to the forefoot in car crashes. Traffic Inj Prev 2005;6(2):156-169.
8. Curtis MJ, Myerson M, Szura B. Tarsometatarsal joint injuries in the athlete. Am J Sports Med 1993;21(4):497-502.
9. Hawkes NC, Flemming DJ, Ho VB. Subtle Lisfranc injury: Low energy midfoot sprain. Military Med 2007;172(9):12-13
10. Wilppula E: Tarsometatarsal fracture-dislocation: Late results in 26 patients. Acta Orthop Scand 1973;44(3):335-345.
11. Myerson MS, Fisher RT, Burgess AR, Kenzora JE. Fracture dislocations of the tarsometatarsal joints: End results correlated with pathology and treatment. Foot Ankle 1986;6(5):225-242.
12. Chiodo CP, Myerson MS. Developments and advances in the diagnosis and treatment of injuries to the tarsometatarsal joint. Orthop Clin North Am 2001;32(1):11-20.
13. Davies MS, Saxby TS. Intercuneiform instability and the “gap” sign. Foot Ankle Int 1999;20(9):606-609.
14. Wilson DW. Injuries of the tarsometatarsal joints: Etiology, classification and results of treatment. J Bone Joint Surg Br 1972;54(4):677-686.
15. Ross G, Cronin R, Hauzenblas J, Juliano P. Plantar ecchymosis sign: A clinical aid to diagnose occult Lisfranc tarsometatarsal injuries. J Orthop Trauma 1996;10(2):119-122.
16. Trevino SG, Kodros S. Controversies in tarsometatarsal injuries. Orthop Clin North Am 1995;26(2):229-238.
17. Coss HS, Manos RE, Buoncristiani A, Mills WJ. Abduction stress and AP weightbearing radiography of purely ligamentous injury in the tarsometatarsal joint. Foot Ankle Int 1998;19(8):537-541.
18. Potter HG, Deland JT, Gusmer PB, et al. Magnetic resonance imaging of the Lisfranc ligament of the foot. Foot Ankle Int 1998;19(7):438-446
19. Teng AL, Pinzur MS, Lomasney L, et al. Functional outcome following anatomic restoration of tarsal-metatarsal fracture dislocation. Foot Ankle Int 2002;23(10):922-926.
20. Schepers T, Kieboom B, van Diggele P, et al. Pedobarographic analysis and quality of life after Lisfranc fracture dislocation. Foot Ankle Int 2010;31(10):857-864.
21. Mittlmeier T, Krowiorsch R, Brosinger S, Hudde M. Gait function after fracture-dislocation of the midtarsal and/or tarsometatarsal joints. Clin Biomech 1997;12(3):S16-S17.
22. Ebraheim NA, Yang H, Lu J, Biyani A. Computer evaluation of second tarsometatarsal joint dislocation. Foot Ankle Int 1996;17(11):685-689.
23. Arntz CT, Hansen ST Jr. Dislocations and fracture dislocations of the tarsometatarsal joints. Orthop Clin North Am 1987;18(1):105-114.
24. Kuo RS, Tejwani NC, DiGiovanni CW, et al. Outcome after open reduction and internal fixation of Lisfranc joint injuries. J Bone Joint Surg Am 2000;82(11):1609-1618.
25. Arntz CT, Veith RG, Hansen ST Jr. Fractures and fracture-dislocations of the tarsometatarsal joint. J Bone Joint Surg Am 1988;70(2):173-181.
26. Rosenbaum A, Dellenbaugh S, DiPreta J, Uhl R. Subtle injuries to the Lisfranc joint. Orthopedics 2011;34(11):882-887.