Malleolar fractures are generally evaluated by physical examination and radiographs – they are then classified according to either the AO or Weber classification systems. In cases of dislocation, immediate reduction is mandatory to prevent skin necrosis and possible nerve damage. Correct treatment is chosen on the basis of:

Weber A fractures are usually treated conservatively, while Weber B and C fractures frequently require surgery. Specific attention should be given to the intraoperative evaluation of syndesmotic joint stability – up to 66% of Weber B and C ankle fractures have some degree of syndesmotic ligamentous injury [4, 19–25]. The most frequent complications are wound hematoma and wound necrosis. Postoperative infection rate is around 2%. Stufkens et al. analyzed the long-term outcomes of these fractures and concluded that over 10% of patients develop ankle arthrosis [19]. The evidence for optimal treatment strategies is low – especially in elite sports such as football. Arthroscopy – prior to open surgery – is shown to be effective in discovering hitherto undetected osteochondral defects in the ankle and enabling the surgeon to check the anatomical reduction [2, 4, 20, 25–29]. Up to 60–75% of ankle fractures (that require surgical fixation) have demonstrated evidence of articular cartilage damage – previously undiagnosed prior to surgery [19]. Such injuries are mostly cartilaginous in nature and therefore not radiographically visible (Fig. 13.2a–c). These lesions usually occur at locations not accessible through traditional fracture surgery incisions. Therefore, simultaneous arthroscopic assessment and management of these lesions is required to improve the rate and quality of recovery after fracture surgery.

Since radiographs are commonly used as the preferred diagnostic tool in acute ankle fractures, the very low sensitivity of plain radiography leads to many undiagnosed osteochondral lesions [4, 19, 20, 30–32].

In the only prospective randomized trial comparing arthroscopic-assisted with traditional non-assisted lateral malleolar fracture fixation, Takao et al. showed a very high rate of secondary pathology. This was mostly chondral damage and syndesmotic injury [20]. At average follow-up of 40 months, there was a small but significantly greater AOFAS outcome score in the arthroscopically assisted group compared with the traditional group [20].

Intra-articular fractures like triplane and Tillaux fractures clearly benefit from an arthroscopic-assisted approach because fracture site clearance and accurate intra-articular realignment check can be performed. The same applies to simple malleolar or distal tibial stress fractures that have an intra-articular fracture line. Complete cartilage assessment can also be performed without the need for large exposures. Any step-off into the joint line, comminution, or depressed fragment can be recognized and realigned (Fig. 13.3a–d). Percutaneous temporary K-wires are frequently used to manipulate and aid in fracture reduction before definitive osteosynthesis is performed [33, 34] (Fig. 13.4a–d). However, the technique can be demanding, and no studies comparing conventional open techniques are available [4, 28].

A substantial proportion of osteochondral injuries after ankle fracture will not cause long-term symptomatic problems. There remains a lack of studies over the need for combined arthroscopy as a standardized tool in fracture fixation treatment. A prospective randomized trial by Takao et al. showed no difference in outcome between patients undergoing arthroscopy and management of articular damage at the time of fixation and those that did not [20]. Ono et al. – in a larger prospective randomized trial of 72 patients – showed a statistically improved AOFAS score (91.0 vs 87.6) in patients that had arthroscopically assisted fixation [29]. Articular damage following ankle fracture may be an independent predictor for the development of post-traumatic arthritis. Hence, arthroscopic assessment at the time of fracture would be advantageous in predicting long-term outcome. Documentation of defect size, condition, and location (medial, central, lateral) can assist in adequate treatment decision-making. This is particularly true for defects over the medial malleolus that have been shown to have the poorest long-term outcomes [3, 20, 21, 31]. Frequently, acute osteochondral defects that are detected in combination with ankle fractures are amenable to arthroscopic treatment. Arthroscopy can help in decision-making and immediate treatment with regard to fragment fixation to anatomic fit or removal. Based upon the talar dome/tibial plafond defect size, bone marrow stimulation techniques (drilling, abrasion, or microfracture) can be used in the same procedure stage to treat osteochondral ankle lesions [35–39]. Cartilage regeneration procedures (autologous chondrocyte implantation [ACI], matrix-induced autologous chondrocyte implantation [MACI]) are becoming more popular in the treatment of football players with a chronic osteochondral defect of the talus [40, 41]. Arthroscopy can be beneficial in these cases – a cartilage biopsy can also be taken at the time of procedure for cell culture for cartilage implantation (ACI). The same treatment strategy is useful for the less frequent tibial plafond osteochondral lesions [33].

Injury to the syndesmosis after an ankle fracture is seen in 47–66% of patients and can result in chronic ankle problems [22]. Intraoperative stress views are more reliable – when compared to plain radiographs – at detecting definitive instability [23]. Nevertheless, borderline instability or partial injury to the syndesmotic complex without instability is difficult to detect. Magnetic ressonance imaging (MRI) has been shown to provide accurate information when documenting a syndesmotic injury, but has a significant false positive rate, whereas arthroscopic assessment has been shown to be more sensitive and specific [3, 4, 23, 24, 42]. In addition, arthroscopy can debride the extra-syndesmotic fibers of the ruptured ligaments that may otherwise produce chronic pain and impingement [10, 11, 43]. Good to excellent results have been reported in a few studies where arthroscopic assessment (with fixation) and/or debridement were used to manage such injuries [20, 21, 30, 32]. Arthroscopic evaluation may also detect sagittal and rotational ankle instability, which may not always be visualized on intraoperative stress radiography [3, 44]. Finally, damage to the medial area of the talocrural joint is an indirect finding commonly associated with syndesmotic injury.

Fractures of the talar neck and body (Fig. 13.5a–e) are rare injuries that can cause significant morbidity and complications. For the football player, these injuries can have a deleterious effect on their long-term functional outcome. Treatment efforts are aimed at the quality of fracture reduction and the preservation of talar blood supply. Arthroscopic-assisted surgery has been shown to be of value in both these aspects, but the technique is demanding and prolongs operative time and increases soft tissue swelling. Case reports, and small case series, provide some evidence to recommend this technique [19, 45–47]. The underlying principle in managing a talar fracture is to achieve anatomical reduction and stable fixation with minimal disturbance to the soft tissue – for the abovementioned reasons [45, 46]. Skin necrosis, infection, malunion, and post-traumatic arthritis are well-recognized complications of talar fractures, and management should be designed to minimize these. Subairy et al. have shown that arthroscopic-assisted surgical stabilization of these fractures is advantageous and reduces the time to union [46].

Stress fractures are the most common overuse bony injuries in football (Fig. 13.5), but stress fractures of the talar body are extremely rare and have only rarely been reported [5, 14, 48]. More common – but still rare – are stress fractures of the talar neck or lateral talar process [5, 15, 16]. Due to their minor displacement, most stress fractures of the talar body are treated nonsurgically [5, 14, 17]. Stress fractures in football are the result of excessive, repetitive cyclic loads traumatizing bones with normal form and structure [49]. Predisposing factors may be both intrinsic and extrinsic and include malalignment, lack of flexibility, increase in training, training of excessive volume and intensity, hard or soft activity surfaces, inappropriate shoes, and inadequate coaching [5, 14]. Additional factors to be considered include age, ethnicity, gender, fitness, skill level, and menstrual history [5, 50]. Mechanical factors that may lead to a stress fatigue fracture remain unclear but may result from repeated loading or from repetitive prolonged muscular action on bone not yet conditioned to such heavy and novel action.

In football players, significant pathogenetic movements predisposing to talar stress fracture can be identified in repetitive, restricted axial loading while sprinting, kicking a ball, or landing after heading. The load that has to be absorbed during these actions, the extremes in plantar-/dorsiflexion of the foot (kicking the ball), and other traumatic actions should be considered important pathogenetic factors in repetitive strain injuries. Moreover, when playing toward the end of a match, coordination is less precise as athletes are often fatigued [5, 50]. The diagnosis of stress fracture is based on clinical suspicion, a detailed history, and a physical examination, followed by appropriate imaging investigations. The role of conventional radiography is important, although initial findings are often minimal or absent (Fig. 13.5a). The earliest sign – often delayed until after the onset of symptoms – may be a lucent linear image (more often a sclerotic band, periosteal reaction, or callus formation) seen on X-ray [5, 14, 17]. MRI has a high sensitivity for the detection of stress fractures (Fig. 13.5b). In addition, MRI signs are evident several weeks before radiographic signs. Conservative treatment is preferred if there is no, or only minor, displacement at the fracture site. There is only limited scientific information on healing times for stress fractures of the talar body but overall, stress fractures are known for their prolonged healing period [5, 51]. Generally, treatment of stress fractures is immobilization for 4–8 weeks [14, 48, 50, 51]. Avascular necrosis remains a relatively high risk – given the suboptimal talar vascular status – even after an adequate immobilization period [51, 52]. Hawkins classified (nonstress) fractures of the talus in an attempt to predict the risk of avascular necrosis [53]. Hawkins type 1 fracture has a good prognosis as the risk of avascular necrosis is less than 15% [54]. If significant diastasis/displacement (Hawkins type 2) occurs, the risk of avascular necrosis rises to 50%, and surgical repositioning and fixation is indicated [54] (Fig. 13.5c–e).

If adequate measures – with rapid intervention to reposition the displaced fracture – are taken, it is possible to achieve a positive outcome without ongoing problems [5] (Fig. 13.5e). D’Hooghe et al. described the management of progressive talar body stress fractures in professional football players through posterior arthroscopy-assisted compression screw fixation with excellent healing results [5] (Fig. 13.5a–e). No other articles were found that combine arthroscopy with talar stress fracture fixation management.