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Post-traumatic osteonecrosis of the lateral tibial plafond
Foot and Ankle Surgery 13 (2007) 24–29 www.elsevier.com/locate/fas
Post-traumatic osteonecrosis of the lateral tibial plafond Mathieu Assal a,*, Bruce J. Sangeorzan b, Sigvard T. Hansen a,b,c a
Me´decin adjoint du chef de service, Service de chirurgie orthope´dique et traumatologie de l’appareil moteur, Hoˆpitaux Universitaires de Gene`ve, rue Micheli-du-Crest 24, 1211 Gene`ve 4, Switzerland b Professor, Chief of Orthopaedics, Haborview Medical Center, 325 Ninth Avenue, Seattle, 98104-2499 WA, USA c Professor, STH Foot and Ankle Institute, Harborview Medical Center, 325 Ninth Avenue, Seattle, 98104-2499 WA, USA Received 20 February 2006; accepted 27 June 2006
Abstract We report a series of patients who presented with post-traumatic osteonecrosis of the lateral tibial plafond. Nine patients were identified with evidence of osteonecrosis limited to the lateral tibial plafond. All of them were seriously impaired with a mean valgus collapse of the ankle joint of 15.38. Seven patients had a Weber C open medial fracture-dislocation, and two had a closed Weber C fracture-dislocation. This series confirms that post-traumatic osteonerosis of the lateral tibial plafond is associated with Weber C fracture-dislocation. It evolves into a valgus deformity of the ankle due to collapse of the lateral tibial plafond. The prognosis is poor and required further reconstructive surgery in all cases. # 2006 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved. Keywords: Avn; Bone avascular necrosis; Ankle fracture; Ankle dislocation; Open fracture; Tibia plafond necrosis; Post-traumatic ankle disorders
1. Introduction Osteonecrosis in the foot and ankle is possible following trauma and has commonly been described in the talus, and to a lesser extent in the tarsal navicular and the sesamoids [1– 5]. The traumatic insult to the bone blood supply is believed to be responsible for the process of osteonecrosis [6,7], yet injuries to the distal epiphysis of the tibia, although frequent, have not been clearly identified as a possible cause and location for osteonecrosis. The goal of this study is to report a series of documented post-traumatic osteonecrosis of the distal tibial with a literature review in order to make this unrecognized and severe condition a more understandable and clear clinical entity.
2. Material and method Patients were selected from between August 2000 and January 2003. These patients were referred for second * Corresponding author. Tel.: +41 22 37 27 810; fax: +41 22 372 77 99. E-mail address: [email protected] (M. Assal).
opinion regarding the treatment of their ankle fracture after surgical management in other institutions. Each patient had a clinical history taken by the junior author and was further examined by one of the senior authors. To be enrolled in the study, patients had to fulfill each of the following inclusion criteria: (1) recent (less than 5 years) history of ankle fracture whether closed or open; (2) complete radiographic history including injury, immediate postoperative and follow-up films; (3) advancing radiographic signs of collapse and sclerosis of the tibial plafond on consecutive radiographs. The exclusion criteria were: (1) plafond fractures; (2) history of chronic inflammatory disease; (3) corticosteroid therapy; (4) clinical signs of ankle infection; (5) history of ankle septic arthritis. Radiographic signs of osteonecrosis of the tibial plafond were defined as follows: areas of loss of bone density adjacent to the talo-crural joint mixed with areas of spotty sclerosis, lacuna formation evolving in progressive tibia plafond collapse, joint space narrowing and eventually ankle joint malalignment. All these elements had to be present in order to make the radiological diagnosis of avascular necrosis. The lateral tibial plafond was arbitrarily defined as
1268-7731/$ – see front matter # 2006 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.fas.2006.06.007
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
25
Table 1 Data on the patients’ population Patient no.
Age (years)
Side
Fracture pattern
Time between injury and evidence of osteonecrosis (months)
Radiographic ankle valgus (angle)
1
35
L
5
88
2
31
L
8
238
3
22
R
6
118
4
45
L
5
228
5
56
L
7
208
6
56
R
6
98
7
54
R
4
238
8
36
L
Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, closed
3
188
9
36
R
Weber C fracture-dislocation, closed
7
48
Salvage surgical procedure
Histology and bacteriology of plafond bone biopsy
Structural bone graft and ankle fusion (surgery scheduled) Structural bone graft and total ankle arthroplasty Structural bone graft and ankle fusion Structural bone graft and total ankle arthroplasty Structural bone graft and total ankle arthroplasty Structural bone graft and ankle fusion Structural bone graft and ankle fusion Structural bone graft and ankle fusion (surgery scheduled) Structural bone graft and total ankle arthroplasty (surgery scheduled)
N/A Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection N/A N/A
the lateral half side of the mortise on an AP plain ankle radiograph. All radiographs were viewed by an attending radiologist. Some patients had a reconstructive surgery during the study period. These patients had bone biopsies performed at time of the surgery as well as several bacteriology swabs of their ankle fluid and distal tibia bone marrow. Bone biopsies were sent for histology and bacteriology. No patients received prophylactic antibiotics prior to completion of these studies, neither did they have a course of antibiotherapy during the preoperative weeks. For those patients who did not undergo surgery, infection was ruled out on the basis of clinical assessment and blood parameters (leucocytes count, ESR, C-reactive protein).
3. Results Nine patients were included in the study (Table 1). There were six females and three males. Their average age was 41.2 (22–56). Follow up was 1.2 (0.8–4.8) years. The initial injury was an open Weber C fracturedislocation in seven patients (Fig. 1). All seven had had a large medial transverse wound centered at the level of the medial malleolus (Fig. 2). The scar of the wound could be clearly differentiated from the scar left by the surgical incision because of its thickness as well as its transverse orientation (antero-posterior). Its mean measurement was 42 mm (32–91). Initial surgical management in all seven patients consisted in irrigation and de´bridement followed by open reduction and internal fixation. None of them was treated with external fixation and none had a medial flap. On
Fig. 1. AP radiograph of the ankle demonstrating a Weber C type fracturedislocation (patient 1, Table 1).
26
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
Fig. 2. Clinical appearance of the soft tissues injury on the medial side of the ankle (patient 3, Table 1). Note the transverse pattern of the traumatic wound.
their immediate postoperative radiographs, the reduction was found to be anatomic in five of nine cases. Two patients required a second procedure at an average 2 days postoperatively which consisted of fixation of a widened syndesmosis and lengthening of a malreduced fibula, respectively.
Two patients had a closed Weber C fracture-dislocation. One underwent open reduction and internal fixation and one was treated non-operatively with a below knee cast. Both patients had good reduction on immediate postoperative radiographs and did not undergo additional surgery. The nine patients referred for a second opinion all had their surgery in an outside institution. All expressed pain and were on chronic analgesic medication except one who had multiple allergies to analgesics. Functionally, none of them was able to run since the injury and seven required walking aids such as cane or crutches. All described worsening symptoms over the last months. In seven cases, there was obvious gross valgus malalignment of the ankle on clinical inspection (Fig. 3). Radiographs showed advanced signs of avascular necrosis of the lateral tibial plafond at a mean time of 5.9 (4–8) months following injury (Fig. 4), and a mean valgus collapse of the talo-crural joint of 15.38 (4–238) on the AP views. Remarkably three patients were in possession of photographs of their medial wound prior to surgery (Fig. 2); three had a CT-scan taken prior to their initial surgery which helped us to rule out fractures extending in the plafond; and interestingly one patient had an early MRI taken 3 months after the injury which showed early avascular changes in the lateral tibial plafond that were not yet apparent on the AP ankle radiograph (Fig. 5). All of them were offered further reconstructive surgery in view of the deteriorating clinical situation. Six patients had the surgery performed during the study period. The affected bone was removed and sent to pathology (Figs. 6 and 7). These showed evidence of avascular necrosis (Fig. 8) in all cases and no evidence of osteitis or osteomyelitis. The swabs were negative for infection in all cases.
Fig. 3. (A and B): Clinical inspection of the left hindfoot from the front and from behind reveals severe sagittal malalignment into valgus (patient 5, Table 1).
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
27
Fig. 4. (A and B): AP radiographs at three (A-left) and five (B-right) months postoperative (patient 1, Table 1). Radiographic signs of avascular necrosis with lateral tibia plafond collapse are observed on the lateral aspect of the tibia plafond (right). The syndesmotic screw was removed at three and a half months.
Fig. 6. Avascular bone removed from the lateral tibial plafond, and sent for pathology and histology (actual size 5.5 cm 1.6 cm 1.3 cm) (patient 5, Table 1).
4. Discussion
Fig. 5. Coronal T2-weighted magnetic resonance image taken three months after injury (patient 8, Table 1) demonstrates signal abnormality in the lateral tibia plafond.
Osteonecrosis of the distal tibia following ankle fracture is probably an infrequent issue and no clinical series of this pathology has been previously published. An isolated case was reported by Siffert and Arkin in 1950 and might be the first description of the pathology at this anatomical location [8]. A displaced closed bimalleolar fracture (Salter II-type) treated conservatively in a skeletally immature patient evolved into osteonecrosis of the distal epiphysis of the tibia. Remarkably the clinical, radiological and histological outcomes presented by this child were comparable to those observed in our study. However, it is well documented that fractures through growth plates are at increased risk of evolving into osteonecrosis by compromise of the critical blood supply to the epiphyseal segment. Thus, analogy to the
28
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
Fig. 8. Photomicrograph from surgical specimen (HE coloration, magnification 10). Bone fragment from lateral tibia plafond demonstrating bone avascular necrosis with areas of collapsed haversian systems, hypocellularity and lacking vascular sinuses. There are no inflammatory cells (patient 7, Table 1).
Fig. 7. Preoperative view of the tibia plafond from the front. The lateral portion of the plafond has been removed (arrow) and the ankle joint is prepared for fusion. The lateral defect will be filled with a structural autologous bone graft from the posterior iliac crest. The affected bone was removed (Fig. 6), and sent to pathology and histology (Fig. 8) (patient 5, Table 1).
adult population presented in our study may not be supported. In 1989, Lagier reported the case of an adult-onset osteonecrosis of the lateral distal tibia following a closed Maisonneuve-type ankle fracture—a pure syndesmotic injury without any evidence of bone lesions at the ankle level [9]. Although postoperative radiographs showed an anatomic reduction of the syndesmosis fixed by two oblique K-wires, signs of osteonecrosis were present on the radiographs at 4 months. Valgus collapse of the lateral tibial plafond with a 158 angulation was observed on the following radiographs at 6 months, although the AP radiograph still showed good reduction of the syndesmosis and no widening of the mortise. The patient had an ankle fusion performed and bone biopsies of the lateral tibial plafond revealed aseptic osteonecrosis. These two isolated case reports, together with our series may indicate that the lateral tibial plafond is an anatomical area that may be sensitive to avascular osteonecrosis. The vascular insult may be more obvious in those patients with
open injuries and extensive stripping and exposure of the distal tibia. However, two of our patients as well as Lagier’s case report had closed injuries. Remarkably in all cases there was tibio-talar dislocation that may indicate increased soft tissues displacement and higher energy trauma [10–13]. The distal tibia is richly supplied by nutrient arteries and by the perimalleolar arterial ring; this rich vascular supply was considered as an explanation to the rarity of bone osteonecrosis of the distal tibia. However, Menck et al. demonstrated that the lateral tibial epiphysis is relatively less vascularized than the medial part [11]. They found that the periosteal blood supply of the distal fifth of the tibia could be of two different types. In two thirds of the cases the lateral side is nourished by branches of the tibialis anterior artery, which are supported by vessels from the peroneal artery; in one third the latter branch was found to be absent so that the rami periostale arising from the tibialis anterior artery nourished the lateral aspect of the distal tibia alone. The relative restriction of blood supply to the distal and lateral extremity of the tibia could explain that osteonecrosis predominantly affects the lateral tibial plafond. Avascular necrosis of the distal tibia developing without a history of local trauma is a rare condition. Only one case reports has described this condition occurring in the setting of systemic lupus erythematosus (SLE) [14]. Bilateral distal
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
tibia histologically proven osteonecrosis occurred in a 42 years old patient with SLE and no clinical evidence of vascular insufficiency in her legs; the authors postulated that these bone infarctions developed as a consequence of the steroid therapy and/or the SLE itself. Six of our patients underwent reconstructive surgery during the study period. The avascular necrosis was documented on the basis of a histological analysis (Figs. 5 and 6). Histology showed cancellous bone and marrow necrosis of the epiphysis. Remarkably no cellularity evocative of inflammation such as would have been found in osteoarthritis, osteitis or osteomyelitis were observed. These findings together with the negative bacteriological cultures allow us to state that these were true post-traumatic aseptic osteonecrosis. Four patients did not receive optimal treatment initially and were left with some malreduction, but the other five were adequately treated. Therefore, it appears that avascular necrosis of the lateral tibial plafond can happen in spite of anatomic reduction and appropriate treatment. A limitation of this study is the small sample size (nine patients), which reflects the unusual nature of this pathology. To our knowledge, only two similar cases have been reported in the literature. The small number of cases makes it difficult to determine prognostic factors but a Weber C fracturedislocation appears to be clearly associated with posttraumatic osteonecrosis of the lateral tibial plafond.
29
References [1] Canale ST, Kelly FB. Fractures of the neck of the talus. J Bone Joint Surg Am 1978;60:143–56. [2] Haukins LG. Fractures of the neck of the talus. J Bone Joint Surg Am 1970;52:991–1002. [3] Smilie IS. Freiberg’s infraction (Ko¨hler’s second disease). J Bone Joint Surg Br 1957;39:580. [4] Ilfeld W, Rosen V. Osteochondritis of the first metatarsal sesamoid. Clin Orthop 1972;85:3841. [5] Jahss MH. The sesamoids of the hallux. Clin Orthop 1981;157:88–97. [6] Ficat RF, Arlet J. Ischemia and Necrosis of Bone Baltimore: Williams & Wilkins; 1980. pp. 32–35. [7] Sweet DE, Madewell JE. Osteonecrosis. Pathogenesis. In: Resnick D, Niwayama G, editors. 3rd ed., Diagnosis of Bone and Joint Disorders, vol. 5, 3rd ed. Philadelphia: WB Sauders; 1995. p. 3445–94. [8] Siffert RS, Arkin AM. Post-traumatic aseptic necrosis of the distal tibial epiphysis. J Bone Joint Surg Am 1950;32:691–5. [9] Lagier R. Case report 552: Post-traumatic remodelling of the distal tibial epiphysis: a form of aseptic osteonecrosis. Skeletal Radiol 1989; 18(4):331–3. [10] Giebel GD. The arterial supply of the ankle joint and its importance for the operative fracture treatment. Surg Radiol Anat 1997;19(4):231–5. [11] Menck J, Bertram C, Lierse W. Sectorial angioarchitecture of the human tibia. Acta Anat 1992;143(1):67–73. [12] Menck J. The arterial blood supply of the tibial and practical consequences. Langenbecks Arch Chir 1992;377(4):229–34. [13] Nelson GE, Kelly PJ, Peterson F, Janes J. Blood supply of the human tibia. J Bone Joint Surg Am 1960;42:625–32. [14] Outwater E, Oates E, Sarno RC. Bilateral distal tibial osteonecrosis in systemic lupus erythematosus [letter]. AJR Am J Roentgenol 1989; 152(4):895–6.
Post-traumatic osteonecrosis of the lateral tibial plafond Mathieu Assal a,*, Bruce J. Sangeorzan b, Sigvard T. Hansen a,b,c a
Me´decin adjoint du chef de service, Service de chirurgie orthope´dique et traumatologie de l’appareil moteur, Hoˆpitaux Universitaires de Gene`ve, rue Micheli-du-Crest 24, 1211 Gene`ve 4, Switzerland b Professor, Chief of Orthopaedics, Haborview Medical Center, 325 Ninth Avenue, Seattle, 98104-2499 WA, USA c Professor, STH Foot and Ankle Institute, Harborview Medical Center, 325 Ninth Avenue, Seattle, 98104-2499 WA, USA Received 20 February 2006; accepted 27 June 2006
Abstract We report a series of patients who presented with post-traumatic osteonecrosis of the lateral tibial plafond. Nine patients were identified with evidence of osteonecrosis limited to the lateral tibial plafond. All of them were seriously impaired with a mean valgus collapse of the ankle joint of 15.38. Seven patients had a Weber C open medial fracture-dislocation, and two had a closed Weber C fracture-dislocation. This series confirms that post-traumatic osteonerosis of the lateral tibial plafond is associated with Weber C fracture-dislocation. It evolves into a valgus deformity of the ankle due to collapse of the lateral tibial plafond. The prognosis is poor and required further reconstructive surgery in all cases. # 2006 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved. Keywords: Avn; Bone avascular necrosis; Ankle fracture; Ankle dislocation; Open fracture; Tibia plafond necrosis; Post-traumatic ankle disorders
1. Introduction Osteonecrosis in the foot and ankle is possible following trauma and has commonly been described in the talus, and to a lesser extent in the tarsal navicular and the sesamoids [1– 5]. The traumatic insult to the bone blood supply is believed to be responsible for the process of osteonecrosis [6,7], yet injuries to the distal epiphysis of the tibia, although frequent, have not been clearly identified as a possible cause and location for osteonecrosis. The goal of this study is to report a series of documented post-traumatic osteonecrosis of the distal tibial with a literature review in order to make this unrecognized and severe condition a more understandable and clear clinical entity.
2. Material and method Patients were selected from between August 2000 and January 2003. These patients were referred for second * Corresponding author. Tel.: +41 22 37 27 810; fax: +41 22 372 77 99. E-mail address: [email protected] (M. Assal).
opinion regarding the treatment of their ankle fracture after surgical management in other institutions. Each patient had a clinical history taken by the junior author and was further examined by one of the senior authors. To be enrolled in the study, patients had to fulfill each of the following inclusion criteria: (1) recent (less than 5 years) history of ankle fracture whether closed or open; (2) complete radiographic history including injury, immediate postoperative and follow-up films; (3) advancing radiographic signs of collapse and sclerosis of the tibial plafond on consecutive radiographs. The exclusion criteria were: (1) plafond fractures; (2) history of chronic inflammatory disease; (3) corticosteroid therapy; (4) clinical signs of ankle infection; (5) history of ankle septic arthritis. Radiographic signs of osteonecrosis of the tibial plafond were defined as follows: areas of loss of bone density adjacent to the talo-crural joint mixed with areas of spotty sclerosis, lacuna formation evolving in progressive tibia plafond collapse, joint space narrowing and eventually ankle joint malalignment. All these elements had to be present in order to make the radiological diagnosis of avascular necrosis. The lateral tibial plafond was arbitrarily defined as
1268-7731/$ – see front matter # 2006 European Foot and Ankle Society. Published by Elsevier Ltd. All rights reserved. doi:10.1016/j.fas.2006.06.007
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
25
Table 1 Data on the patients’ population Patient no.
Age (years)
Side
Fracture pattern
Time between injury and evidence of osteonecrosis (months)
Radiographic ankle valgus (angle)
1
35
L
5
88
2
31
L
8
238
3
22
R
6
118
4
45
L
5
228
5
56
L
7
208
6
56
R
6
98
7
54
R
4
238
8
36
L
Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, open with medial transverse wound Weber C fracture-dislocation, closed
3
188
9
36
R
Weber C fracture-dislocation, closed
7
48
Salvage surgical procedure
Histology and bacteriology of plafond bone biopsy
Structural bone graft and ankle fusion (surgery scheduled) Structural bone graft and total ankle arthroplasty Structural bone graft and ankle fusion Structural bone graft and total ankle arthroplasty Structural bone graft and total ankle arthroplasty Structural bone graft and ankle fusion Structural bone graft and ankle fusion Structural bone graft and ankle fusion (surgery scheduled) Structural bone graft and total ankle arthroplasty (surgery scheduled)
N/A Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection Osteonecrosis; no infection N/A N/A
the lateral half side of the mortise on an AP plain ankle radiograph. All radiographs were viewed by an attending radiologist. Some patients had a reconstructive surgery during the study period. These patients had bone biopsies performed at time of the surgery as well as several bacteriology swabs of their ankle fluid and distal tibia bone marrow. Bone biopsies were sent for histology and bacteriology. No patients received prophylactic antibiotics prior to completion of these studies, neither did they have a course of antibiotherapy during the preoperative weeks. For those patients who did not undergo surgery, infection was ruled out on the basis of clinical assessment and blood parameters (leucocytes count, ESR, C-reactive protein).
3. Results Nine patients were included in the study (Table 1). There were six females and three males. Their average age was 41.2 (22–56). Follow up was 1.2 (0.8–4.8) years. The initial injury was an open Weber C fracturedislocation in seven patients (Fig. 1). All seven had had a large medial transverse wound centered at the level of the medial malleolus (Fig. 2). The scar of the wound could be clearly differentiated from the scar left by the surgical incision because of its thickness as well as its transverse orientation (antero-posterior). Its mean measurement was 42 mm (32–91). Initial surgical management in all seven patients consisted in irrigation and de´bridement followed by open reduction and internal fixation. None of them was treated with external fixation and none had a medial flap. On
Fig. 1. AP radiograph of the ankle demonstrating a Weber C type fracturedislocation (patient 1, Table 1).
26
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
Fig. 2. Clinical appearance of the soft tissues injury on the medial side of the ankle (patient 3, Table 1). Note the transverse pattern of the traumatic wound.
their immediate postoperative radiographs, the reduction was found to be anatomic in five of nine cases. Two patients required a second procedure at an average 2 days postoperatively which consisted of fixation of a widened syndesmosis and lengthening of a malreduced fibula, respectively.
Two patients had a closed Weber C fracture-dislocation. One underwent open reduction and internal fixation and one was treated non-operatively with a below knee cast. Both patients had good reduction on immediate postoperative radiographs and did not undergo additional surgery. The nine patients referred for a second opinion all had their surgery in an outside institution. All expressed pain and were on chronic analgesic medication except one who had multiple allergies to analgesics. Functionally, none of them was able to run since the injury and seven required walking aids such as cane or crutches. All described worsening symptoms over the last months. In seven cases, there was obvious gross valgus malalignment of the ankle on clinical inspection (Fig. 3). Radiographs showed advanced signs of avascular necrosis of the lateral tibial plafond at a mean time of 5.9 (4–8) months following injury (Fig. 4), and a mean valgus collapse of the talo-crural joint of 15.38 (4–238) on the AP views. Remarkably three patients were in possession of photographs of their medial wound prior to surgery (Fig. 2); three had a CT-scan taken prior to their initial surgery which helped us to rule out fractures extending in the plafond; and interestingly one patient had an early MRI taken 3 months after the injury which showed early avascular changes in the lateral tibial plafond that were not yet apparent on the AP ankle radiograph (Fig. 5). All of them were offered further reconstructive surgery in view of the deteriorating clinical situation. Six patients had the surgery performed during the study period. The affected bone was removed and sent to pathology (Figs. 6 and 7). These showed evidence of avascular necrosis (Fig. 8) in all cases and no evidence of osteitis or osteomyelitis. The swabs were negative for infection in all cases.
Fig. 3. (A and B): Clinical inspection of the left hindfoot from the front and from behind reveals severe sagittal malalignment into valgus (patient 5, Table 1).
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
27
Fig. 4. (A and B): AP radiographs at three (A-left) and five (B-right) months postoperative (patient 1, Table 1). Radiographic signs of avascular necrosis with lateral tibia plafond collapse are observed on the lateral aspect of the tibia plafond (right). The syndesmotic screw was removed at three and a half months.
Fig. 6. Avascular bone removed from the lateral tibial plafond, and sent for pathology and histology (actual size 5.5 cm 1.6 cm 1.3 cm) (patient 5, Table 1).
4. Discussion
Fig. 5. Coronal T2-weighted magnetic resonance image taken three months after injury (patient 8, Table 1) demonstrates signal abnormality in the lateral tibia plafond.
Osteonecrosis of the distal tibia following ankle fracture is probably an infrequent issue and no clinical series of this pathology has been previously published. An isolated case was reported by Siffert and Arkin in 1950 and might be the first description of the pathology at this anatomical location [8]. A displaced closed bimalleolar fracture (Salter II-type) treated conservatively in a skeletally immature patient evolved into osteonecrosis of the distal epiphysis of the tibia. Remarkably the clinical, radiological and histological outcomes presented by this child were comparable to those observed in our study. However, it is well documented that fractures through growth plates are at increased risk of evolving into osteonecrosis by compromise of the critical blood supply to the epiphyseal segment. Thus, analogy to the
28
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
Fig. 8. Photomicrograph from surgical specimen (HE coloration, magnification 10). Bone fragment from lateral tibia plafond demonstrating bone avascular necrosis with areas of collapsed haversian systems, hypocellularity and lacking vascular sinuses. There are no inflammatory cells (patient 7, Table 1).
Fig. 7. Preoperative view of the tibia plafond from the front. The lateral portion of the plafond has been removed (arrow) and the ankle joint is prepared for fusion. The lateral defect will be filled with a structural autologous bone graft from the posterior iliac crest. The affected bone was removed (Fig. 6), and sent to pathology and histology (Fig. 8) (patient 5, Table 1).
adult population presented in our study may not be supported. In 1989, Lagier reported the case of an adult-onset osteonecrosis of the lateral distal tibia following a closed Maisonneuve-type ankle fracture—a pure syndesmotic injury without any evidence of bone lesions at the ankle level [9]. Although postoperative radiographs showed an anatomic reduction of the syndesmosis fixed by two oblique K-wires, signs of osteonecrosis were present on the radiographs at 4 months. Valgus collapse of the lateral tibial plafond with a 158 angulation was observed on the following radiographs at 6 months, although the AP radiograph still showed good reduction of the syndesmosis and no widening of the mortise. The patient had an ankle fusion performed and bone biopsies of the lateral tibial plafond revealed aseptic osteonecrosis. These two isolated case reports, together with our series may indicate that the lateral tibial plafond is an anatomical area that may be sensitive to avascular osteonecrosis. The vascular insult may be more obvious in those patients with
open injuries and extensive stripping and exposure of the distal tibia. However, two of our patients as well as Lagier’s case report had closed injuries. Remarkably in all cases there was tibio-talar dislocation that may indicate increased soft tissues displacement and higher energy trauma [10–13]. The distal tibia is richly supplied by nutrient arteries and by the perimalleolar arterial ring; this rich vascular supply was considered as an explanation to the rarity of bone osteonecrosis of the distal tibia. However, Menck et al. demonstrated that the lateral tibial epiphysis is relatively less vascularized than the medial part [11]. They found that the periosteal blood supply of the distal fifth of the tibia could be of two different types. In two thirds of the cases the lateral side is nourished by branches of the tibialis anterior artery, which are supported by vessels from the peroneal artery; in one third the latter branch was found to be absent so that the rami periostale arising from the tibialis anterior artery nourished the lateral aspect of the distal tibia alone. The relative restriction of blood supply to the distal and lateral extremity of the tibia could explain that osteonecrosis predominantly affects the lateral tibial plafond. Avascular necrosis of the distal tibia developing without a history of local trauma is a rare condition. Only one case reports has described this condition occurring in the setting of systemic lupus erythematosus (SLE) [14]. Bilateral distal
M. Assal et al. / Foot and Ankle Surgery 13 (2007) 24–29
tibia histologically proven osteonecrosis occurred in a 42 years old patient with SLE and no clinical evidence of vascular insufficiency in her legs; the authors postulated that these bone infarctions developed as a consequence of the steroid therapy and/or the SLE itself. Six of our patients underwent reconstructive surgery during the study period. The avascular necrosis was documented on the basis of a histological analysis (Figs. 5 and 6). Histology showed cancellous bone and marrow necrosis of the epiphysis. Remarkably no cellularity evocative of inflammation such as would have been found in osteoarthritis, osteitis or osteomyelitis were observed. These findings together with the negative bacteriological cultures allow us to state that these were true post-traumatic aseptic osteonecrosis. Four patients did not receive optimal treatment initially and were left with some malreduction, but the other five were adequately treated. Therefore, it appears that avascular necrosis of the lateral tibial plafond can happen in spite of anatomic reduction and appropriate treatment. A limitation of this study is the small sample size (nine patients), which reflects the unusual nature of this pathology. To our knowledge, only two similar cases have been reported in the literature. The small number of cases makes it difficult to determine prognostic factors but a Weber C fracturedislocation appears to be clearly associated with posttraumatic osteonecrosis of the lateral tibial plafond.
29
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