Recent advances in the management of chronic ankle instability

Abstract

Ankle sprains are the most common lesion of the ankle joint which might result in chronic ankle instability (CAI). Significant strides have been taken to enhance our comprehension of the underlying mechanisms of CAI, as the exploration of novel surgical techniques and the identification of previously unrecognized anatomical components. The present review aims to provide an extensive overview of CAI, encompassing its pathophysiology, epidemiology, clinical assessment, treatment, and rehabilitation. Treatment of CAI requires a multifaceted algorithm, involving historical analysis, clinical evaluations, and diagnostic imaging. Surgical interventions for CAI primarily involve the anatomical and/or non-anatomical reconstruction and/or repair of the anterior talofibular ligament. Anatomical repair has exhibited superior functional outcomes and a reduced risk of secondary osteoarthritis compared to non-anatomical repair. Non-anatomical approaches fall short of replicating the normal biomechanics of the anterior talofibular ligament, potentially leading to postoperative stiffness. This review seeks to academically review and up-to-date literature on this issue, tailored for clinical practice, with the intent of aiding surgeons in staying abreast of this critical subject matter.

1. Introduction

Ankle ligament injury is frequent and imposes a notable socioeconomic burden. Chronic ankle instability (CAI) denotes the development of clinical and functional impairments in the ankle joint following an initial acute ankle injury.¹ Acute lateral ankle instability might progress to a chronic state when the ankle fails to regain its normal functional and mechanical stability after the injury. This is primarily due to inadequate healing or incorrectly tensioned healing of the damaged or stretched anterior talofibular ligament (ATFL) and/or the calcaneofibular ligament (CFL).^1,2 CAI can develop either subsequent to the initial ankle sprain or as a result of recurring injuries.³ A previous report has delineated 7 subsets of CAI, with the broad classification being either mechanical or functional instability.⁴

The diagnosis of ankle functional instability relies on the evaluation of the clinical manifestations and symptoms exhibited by the patient. This clinical presentation is attributed to impaired proprioception nerve receptors within the ligaments. Accurate diagnosis necessitates a clinical assessment, as treatment approaches vary. Arthroscopic examination has no revealed morphological abnormalities in the ATFL, even in cases where noticeable abnormal lateral laxity is observed depending on physical examination. Moreover, there is corroborating evidence suggesting that functional instability may be attributed, in part, to a degree of microinstability stemming from ATFL insufficiency.

Mechanical ankle instability is assessed through physical and radiological examinations, primarily arising from ligament laxity. Mechanical instability is marked by the definitive inadequacy of ligamentous stabilizers, supported by objective evidence of ligament laxity during physical examinations. Within the realm of mechanical ankle instability, the concept of microinstability involving a superior fascicle tear of the ATFL is gaining prominence.⁵ Recently, the ATFL's superior fascicle is found to reside within the joint.⁶ Due to this anatomical feature, adequate healing of the ATFL's superior fascicle is hindered, as it does not possess inherent self-healing properties. Individuals with this condition add to the risk of recurrent ankle sprains, and they may subsequently develop CAI or classical ankle instability as involving the ATFL's inferior fascicle and the CFL tear. Therefore, the identification of ankle microinstability is crucial as it serves as an initial phase and a precursor to the onset of ankle instability.⁷

Some authors have established a connection between functional and mechanical instability, marking a significant advancement in our understanding of these phenomena.^8,9 His concept revolved around the idea that a ligament injury, a key factor contributing to mechanical instability, also being a causative factor for functional instability. It arises as a result that ligament damage can lead to partial deafferentation, leading to sensorimotor impairment, ultimately giving rise to ankle functional instability. Building upon this foundation, Hertel and his colleagues⁸ have put forth a comprehensive model of CAI that encompasses all recognized mechanical and functional factors. It comprises 8 primary parts and these components interact through 3 overarching constructs: self-organization, perception-action, and neurosignature. The ankle mechanical instability pertains to anatomical structure deformities, while the functional instability is more closely associated with proprioceptive and neuromuscular deficits, absent increased ligament laxity.⁹ This CAI model underscores the intricate interplay among its various components, taking into account the holistic perspective of the individual. Once a patient experiences an ankle sprain, they become part of a dynamic loop where these 8 components collectively influence the development of CAI. They are interactive within what is referred to as self-organization, a unique configuration for each patient that governs their motion, affected by diverse constraints. These diverse pathological factors also interconnect through perception-action cycles and the neurosignature. It is crucial to recognize that the mechanical and functional dimensions of CAI are closely intertwined and should be considered as a unified entity rather than isolated phenomena.¹⁰

2. Epidemiology of CAI

The occurrence of ankle sprains is estimated at approximately 7‰ in the general population, although it can escalate substantially to as high as 10%–30% in the context of all sports-related injuries.¹¹ Recent findings from a thorough systematic review conducted by Lin and collaborators¹² have revealed an overall CAI prevalence of approximately 25% following an ankle sprain. For otherwise healthy adolescent athletes, the incidence of CAI hovers at around 20% after experiencing an ankle sprain.^12,13 Notably, in the United Kingdom, the prevalence of ankle sprains is documented at 52.7 cases per 10,000 individuals, while in the United States, it is slightly lower, at 21.5 cases per 10,000.¹⁴

Besides, the occurrence of acute ankle sprains exhibits distinct prevalence patterns among males and females. It reaches its peak incidence among males aged 15–19 years, while a peak incidence is observed among females aged 10–14 years.¹⁵ In terms of comparable sports activities, women are more likely to sprain an ankle than men. However, men tend to sprain the medial ankle and develop symptoms. Factors such as increased average height and weight, greater body mass index, and participation in specific athletic endeavors may also contribute to the risk of ankle injury.¹⁴

3. Mechanism and pathologies of CAI

In sports settings, an inversion ankle sprain stands out as the most commonly encountered cause of acute ankle injuries.¹⁶ This abrupt onset of inversion, accompanied by internal rotation forces, and occurring in conjunction with either dorsi- or plantar-flexion, generates significant strains that can lead to the tear of the lateral ankle ligaments. Additionally, it may lead to concurrent osteochondral lesions or exacerbate anterior or posterior joint impingement. Notably, the ATFL is typically the first ligament to rupture in over three-quarters of acute ankle sprains. This is primarily because the ATFL is the least robust component within the lateral collateral ligament complex, particularly its superior fascicle.17, 18, 19 As the forces applied during the injury escalate, the damage can propagate further, causing ruptures in the inferior fascicle of the ATFL and the CFL.¹⁴ Ultimately, continued energy imparted can result in the rupture of the posterior tibiofibular ligament (PTFL), leading to lateral dislocation of the ankle. Roughly 65%–80% of cases involve an isolated ATFL injury, whereas 20% of cases encompass combined tears of the ATFL and CFL.^18,20 Based on the increased attention regarding the CFL, Li et al.²¹ provided detailed and objective data regarding the types of injuries of the ATFL and the CFL. They found that nearly half (44%) of the ATFL injuries were accompanied by CFL injuries, yet the total count of absorbed CFL in patients with affected ATFL was relatively low (18%). Among all cases of complex ATFL and CFL injuries, nearly three-quarters (72%) showed thickening solely at the CFL body, while approximately one-fifth (21%) exhibited tearing at the fibular side (3%) or the calcaneal side (18%), leaving only 7% with CFL absorption. Thus, the percentage of cases involving CFL absorption amounted to a mere 3%.

It's worth noting that injuries to the PTFL are uncommon at the occurrence of inversion sprains.^5,17,19 A ligamentous injury occurring in an ankle sprain can potentially initiate sensorimotor alterations through the action of inflammatory and pain mediators. These changes can manifest as non-specific sensory-perceptual and motor-behavioral deficits.⁸ The response to such an injury varies from person to person, and some individuals may go on to develop CAI. Nonetheless, several factors might change this progression. CAI is often linked to various other pathological conditions.²² Research suggested that more than half of affected individuals might experience associated peroneal tendinopathy, while a smaller portion may develop concurrent sinus tarsus syndrome.²³ Underlying deformities, like cavovarus hindfoot deformity and misalignment of the fibula, can increase the likelihood of individuals developing CAI.²⁴ As a result of CAI, ankle osteoarthritis may develop over time, with being responsible for a significant 80% of cases.

A recent study by Michels and their colleagues²⁵ shed light on concerning outcomes observed 1 year after individuals experienced an ankle sprain. According to their research, 15.8% of cases experienced a relapse, 8.1% still reported subjective instability, and 6.7% continued to endure lingering pain.²⁵ They seem to persist over an extended duration. In a subsequent study that spanned 6.5 years and focused on ankle sprains, it was discovered that 6% of patients could not continue to pursue their occupational activities, and 15% of patients were only able to maintain their initial occupation with certain restrictions.²⁶ One potential underlying cause for these persistent limitations lies in articular lesions. The occurrence of osteochondral lesions subsequent varies widely, ranging from 37% to 89% based on available literature.^27,28 Some authors conducted arthroscopic evaluations of the cartilage in 99 ankles affected by CAI. Their findings indicated that 23.2% of patients had cartilage in good condition, while the remaining 76.8% exhibited cartilage damage, and 41.4% presenting serious lesions.²⁹

4. Physical examination tests

Clinicians utilize specific physical examination techniques to diagnose and evaluate the severity of CAI. Typical examination findings encompass instability observed during stress tests (evaluated either through radiography or clinical assessment) and tenderness localized over the affected ligament. Additionally, clinicians may look for signs of subluxation within the tendoachilles ligament complex.²⁴ One commonly employed test is the anterior drawer test, designed to assess the integrity of the ATFL. Another valuable tool is Romberg's Maneuver, which assists in assessing proprioception abnormalities. The talar tilt test has excellent specificity and serves as a valuable tool for diagnosing CFL injuries, and caution is required when interpreting a negative test.^30,31 It is crucial to conduct a comprehensive assessment to identify any associated injuries or foot deformities in the patient.

Frey and colleagues³² conducted a study that revealed physical examination to be highly accurate, with a 100% success rate in diagnosing grade III ligament injuries. However, its accuracy dropped significantly to just 25% when distinguishing grade II injuries, as compared to findings from MRI.³² Beynon and associates³³ conducted a systematic review, and the findings highlighted the anterolateral talar palpation test as the most diagnostically accurate. Specificity, on the other hand, tests such as the anterior drawer test, anterolateral drawer test demonstrated the highest specificity. Nevertheless, in a systematic review conducted by Beynon and her colleagues,³³ they presented evidence regarding the reliability and validity of orthopedic tests for diagnosing ankle sprains and instability. As a result, they advise against relying solely on physical examination tests for diagnosing an ankle sprain but suggest using them in combination with the patient's clinical history.³³

5. Radiological investigations

Imaging plays an important role in the evaluation of CAI. Various imaging modalities, including radiography, ultrasound, and MRI, are utilized to diagnose chronic lateral ankle ligament injuries. Standard plain radiographs for evaluating ankle stability may also provide valuable insights. When assessing ATFL-deficient ankles under weight-bearing conditions, several distinct alterations become noticeable. These alterations include increased anterior translation, internal rotation, and superior translation of the talus.⁶ However, it's essential to acknowledge that this method may yield false negatives due to muscle contraction, and it may not effectively capture functional ankle instability, potentially diminishing its reliability.³⁴ Incorporating ankle mortise radiographs can facilitate the performance of the talar tilt test. Furthermore, weight-bearing radiographs are valuable for ruling out underlying bony pathologies and arthritic conditions.

Stress radiography is an objective instrument for evaluating chronic lateral ankle instability. Choi et al.³⁵ have investigated its consistency and reliability in patients with chronic lateral ankle instability. The study revealed that the interobserver reliability of the radiographic measurements was satisfactory, but the consistency of the ankle stress radiographs needs to be interpreted cautiously.³⁵ The consistency of stress radiographs might be compromised by the magnitude of the force applied to the foot, muscle guarding result of patient discomfort during the stress test and variations in soft tissue tension caused by changes in ankle effusion or inaccuracies in stress testing apparatus and the X-ray beam alignment.^35,36

Stress ultrasound has been used as an alternative tool for the diagnosis of CAI, but the subjective influence on the measurement and the relatively high error of the mean may limit its applicability and reliability, especially in longitudinal or interventional studies. Wenning et al.³⁷ assessed specificity and sensitivity for stress ultrasound (Table 1). In addition, manual stress ultrasound is more precise than other traditional methods to examine CAI, such as stress radiography or the manual anterior drawer test.³⁶ Its sensitivity is very high, akin to that of MRI. More importantly, manual stress ultrasound allows physicians to accurately visualize and quantify changes in the location of the ATFL origin and insertion.³⁶

Table 1.

Outcomes of stress ultrasound.³⁷

Method	Cut-off value	Sensitivity	Specificity
Stress sonography	3.6 mm	1.0	0.4
	5.2 mm	0.92	0.6
	6.6 mm	0.71	0.68
	7.2 mm	0.71	0.8
	8.3 mm	0.5	0.92

Stress ultrasound as the cumulative difference between ligament lengths of anterior talofibular ligament and calcaneofibular ligament at rest vs. 150 N stress.

Advancements in MRI technology, particularly more robust 3-dimensional studies, have significantly enhanced the precision of diagnosing CAI.³⁸ The application of axial MRI, which incorporates a localized gradient, offers the most favorable angles for evaluating crucial ligaments like the ATFL and PTFL. Additionally, MRI coronal imaging provides a comprehensive visualization of ligaments. MRI proves invaluable for confirming the presence of chronic ligamentous injuries, osteochondral lesions, or other soft tissue pathologies.³⁹ In a recent systematic review, the high diagnostic accuracy of MRI in detecting ATFL lesions was highlighted, with reported diagnostic sensitivity and specificity of 1.0 (with a 95% confidence interval of 0.58–1.00) and 0.9 (with a 95% confidence interval of 0.79–0.96), respectively, underscoring its effectiveness in diagnosing ATFL injuries.⁴⁰ Furthermore, ultrasound serves as another valuable tool for diagnosing CAI and demonstrates almost equivalent sensitivity to MRI in assessing soft tissue pathologies. Ultrasound achieves an impressive level of accuracy, boasting a sensitivity of 93.8% and a specificity of 100% in detecting ATFL tears, comparable to the 97% accuracy achieved with MRI.41, 42, 43

Evolving surgical techniques for lateral ankle instability focus on the importance of restoring the ATFL, but current practices vary in terms of whether the CFL is repaired during lateral ligament repair.⁴⁴ While some surgeons argue that repair of the CFL is unnecessary, an expert consensus indicated that most of the respondents routinely repair the CFL during a lateral ligament repair.⁴⁵ However, some authors refrain from advocating CFL repair based on biomechanical data and clinical outcome data.^21,43 Several retrospective clinical studies have shown that repairing only the ATFL could achieve favorable outcomes, irrespective of whether the surgeries were conducted using an open approach or arthroscopic assistance.46, 47, 48 Additionally, the control study had indicated comparable results between repairing or reconstructing the ATFL alone and addressing both the ATFL and CFL concurrently.⁴⁹ The absence of a clear consensus regarding the necessity of CFL repair is further exacerbated as the scarcity of biomechanical studies in the literature elucidating the role of CFL in maintaining lateral ankle stability.

6. Management of CAI

The optimal management of CAI remains an area of ongoing exploration. Conservative treatment is typically initiated during the first 2 months following injury. Nonsteroidal anti-inflammatory drugs, might offer short-term pain relief and reduce swelling, but they do not lead to sustained improvements in CAI symptoms.⁵⁰ Athletes with CAI often benefit from ankle bracing or taping, which enhances both functional and mechanical stability. Rehabilitation incorporates physiotherapy and orthotics, supplemented by proprioceptive training and strengthening exercises for the evertor muscles (peroneus brevis).⁵¹ However, despite an appropriate conservative approach, approximately 20%–30% of patients may continue to experience CAI with continuous symptoms, including activity limitations, a feeling of instability, and recurrent ankle injury. Surgical intervention becomes a consideration when CAI lasts for 3–6 months without responding to conservative treatment. Surgical management of CAI can be mainly defined as non-anatomic and anatomic direct repair, anatomic reconstruction with an autograft or allograft, and non-anatomic reconstruction procedures (dynamic and static tenodesis) of ATFL and/or CFL. Compared with dynamic tenodesis, static tenodesis obtained better clinical satisfaction and fewer subsequent sprains. Non-anatomic reconstruction abnormally increased inversion stiffness at the subtalar level as compared with anatomic repairment. Anatomic repair has been shown to have better functional outcomes and less secondary osteoarthritis when compared to nonanatomic repair. Non-anatomic methods do not replicate the normal anatomical course of ATFL/CFL and may lead to stiffness. Direct repair is commonly used when the quality of the damaged ligaments permits. When the torn ligaments are not adequate, reconstruction incorporating either an autograft or allograft is another promising option in the short term, although the longevity of this procedure remains unclear. The use of an allograft avoids donor site morbidity, but it comes with inherent risks. Ankle arthroscopy is a useful adjunct to ligamentous procedures, performed at the time of repair to identify and treat intra-articular conditions that may be associated with CAI, providing good to excellent short- and long-term clinical outcomes.

In general, anatomic repair means the utilization of the native tissue for ATFL repair.⁵² However, it is crucial to note that there remains controversy in establishing the superiority of any specific technique for the surgical treatment of CAI. Nonetheless, non-anatomic reconstructions, such as the classic Evans, Watson-Jones, or Chrisman-Snook procedures, have been demonstrated to markedly disrupt the biomechanics of the normal ankle, especially to the subtalar joint.^53,54 Due to these concerns and the favorable outcomes observed with anatomic techniques, the latter currently serve as the primary surgical treatment choice.^48,50,55,56 Anatomic open repair, as initially introduced by Broström in 1966, adheres to the native anatomy by tightening the torn ankle joint lateral collateral ligament.⁵⁷ Over time, various modifications have been put forward to enhance this technique. Additionally, some authors suggested shortening the ligaments that were often elongated rather than torn.⁵⁸ In contemporary practice, a previous report proposed augmentation with fiber tape, suggesting that it might achieve reduced immobilization and earlier rehabilitation. However, it remains a considerable controversial tissue in demonstrating its clinical advantage.59, 60, 61 Previous report concluded that the emerging trend of exclusively addressing the ATFL demonstrated comparable results to those procedures involving both the ATFL and CFL.^48,62, 63, 64, 65 Overall, these various anatomical repair techniques, along with numerous modifications, consistently achieved excellent functional outcomes, with success rates ranging from 87% to 95%.^58,66,67 It is essential to emphasize that the efficacy of these techniques hinges on the quality of the remaining ligaments for achieving an effective repair. Karlsson and colleagues⁵⁸ identified risk factors for less favorable outcomes.

7. Arthroscopic lateral ankle ligament repair

Arthroscopy plays a prominent role in both the assessment and treatment of ankle instability.68, 69, 70 Kashuk et al.⁷¹ were among the pioneers in describing the use of arthroscopic techniques with suture anchors for managing CAI. These techniques may include all-inside, all-arthroscopic, or arthroscopic-assisted approaches.⁷¹ Arthroscopic repair of lateral ankle ligaments has demonstrated favorable clinical outcomes. A recent systematic review revealed that patients undergoing this procedure experienced a substantial enhancement in the American orthopaedic foot & ankle society (AOFAS) score, with scores improving from 22.8 to 54.2 during an average follow-up period of 17.1 months. Notably, all the patients return to sports. Nevertheless, it is essential to acknowledge that an overall complication rate of 11.6% was realized, which is in line with what is observed with open techniques.⁷²

Batista et al.⁷³ conducted a study revealing that there was no instance of recurrent lateral ankle instability, and no documented complications were recorded within a patient cohort undergoing arthroscopic repair. Over 25 years, there was a notable improvement in the mean AOFAS score.⁷³ Furthermore, long-term studies have reported enhancements in AOFAS scores, Karlsson scores, and visual analog scale scores.⁷⁴ Nonetheless, it is important to note that there is a scarcity of available literature to examine the frequency of revision procedures following arthroscopic repair. Significant complications associated with arthroscopic repair primarily encompass postoperative nerve injuries or issues related to suture entrapment. Nevertheless, with specialized training and advancements in arthroscopic techniques, the occurrence of nerve injury can be reduced. In contemporary practice, arthroscopic evaluation is considered a crucial prognostic factor. Consequently, most authors recommend a comprehensive arthroscopic evaluation, along with the management of any intra-articular pathology, before proceeding with ligament surgery.^55,56

8. Risk factors for CAI

Numerous risk factors contribute to ankle sprains and CAI.⁷⁵ The accumulation of these risk factors may, to some extent, explain the presence and seriousness of CAI, underscoring the need for a thorough assessment of potential contributing factors.⁷⁶ These risk factors can be categorized into mechanical, functional, personal, and environmental factors. One of the prominent mechanical risk factors consistently highlighted is ligamentous laxity.¹⁰ Much emphasis has been placed on the involvement of the ATFL and CFL, both of which are frequently associated with laxity and have been extensively studied, receiving substantial and moderate levels of evidential support, respectively.⁷⁷ Syndesmotic and subtalar laxity have also been identified as possible risk factors for CAI, although with varying levels of supporting evidence.⁷⁸ The role of deltoid ligament laxity in relation to lateral instability remains a topic of debate. More frequently, medial insufficiency is linked to deltoid laxity, often in the context of conditions like flatfoot.⁷⁸ It is plausible that syndesmotic laxity serves as the primary hazard factor, while deltoid insufficiency may indirectly contribute to CAI due to its correlation with syndesmotic lesions. Additionally, reduced ankle dorsiflexion has garnered recognition as a hazard factor, supported by adequate evidence in the literature.^79,80

Functional risk factors for CAI were categorized into 3 distinct groups: compromised neuromuscular control, deviations in gait patterns, and deficiencies in strength.^8,81 Neuromuscular control impairments encompassed issues such as proprioception deficits, balance irregularities, and delayed peroneal reaction times. Altered gait patterns were characterized by functional challenges experienced during walking, running, or jumping activities.^82,83 Strength deficits were primarily attributed to weaknesses in the evertor muscles and, to a lesser extent, weaknesses in the plantarflexor muscles.⁸⁴ Additionally, certain factors such as increased body mass index, multiligament relaxation, youth, and sports activity were also identified as potential risk factors for CAI.⁸⁵ Lalevée et al.¹⁰ proposed a cumulative model that incorporates, categorizing as either inherent or consequential. This model recognizes the cumulative impact of hazard factors and, in contrast to prior models, offers opportunities for intervention and proactive management of inherent hazard factors to mitigate the risk of initial ankle sprains.¹⁰

9. Complications after surgical treatment for CAI

While the complications arising from surgical treatment of CAI are relatively rare, they present specific problems, including nerve damage, incision healing, and the possibility of recurrent instability. Incision undesirable healing, although occurring in a minority of cases, is generally superficial.⁸⁶ Nerve damage is another potential complication, manifesting as either self-subsiding acroparesthesia or the formation of a neuroma that may necessitate surgical excision. This complication is recognized in both arthroscopic and invasive open operations. According to the research conducted by Sammarco and colleagues,⁸⁶ there was an overall rate of postoperative nerve dysfunction reported at 6.2%, with more often occurring in patients who endured non-anatomic repair procedures.

The occurrence of recurrent instability varies with various types of repair techniques. However, non-anatomic approaches tend to be more commonly linked to subjective instability compared to anatomic methods.⁸⁶ For cases of subjective instability that do not respond to conservative treatment, physiotherapy is typically recommended as the initial approach. However, in instances of recurrent instability that persist despite conservative measures, revision surgery may become necessary. Stiffness is a common post-reconstruction complication, albeit generally manageable. It is crucial to promote early post-surgery motion to mitigate the risk of stiffness. In some cases, over-tightening of grafts might result in ongoing pain and stiffness. Ongoing advancements in the field are continually exploring new techniques. These innovations encompass investigations into arthroscopic anatomy reconstruction, potential applications of synthetic scaffold support, and even the utilization of nano scaffolds. Nevertheless, the implementation of these practices requires further research and validation.⁸⁷

Several forms of cognitive dysfunction can occur in the perioperative period all of which are characterized by problems in thinking and perception. The earliest of these, delirium, occurs 24 – 96 h after a procedure and is manifest as an acute confusional state with disturbance in attention and reduced awareness of the environment. Unlike delirium and dementia, no formal definition of postoperative cognitive dysfunction (POCD) has been codified. The Diagnostic and Statistical Manual of Mental Disorders does not mention POCD as a separate disease entity. The definition of POCD varies markedly across studies but is typically inferred from a comparison of pre-to post-operative cognitive function. POCD developing in the postoperative period can largely be reversible and rarely persists in the longer term. Increasing age was the most common risk factor.⁸⁸ Paredes et al.⁸⁸ found that approximately 12% of apparently previously cognitively well patients undergoing anaesthesia and noncardiac surgery will develop symptoms of cognitive dysfunction after their procedure. Little is known about the pathogenesis of this disorder. Mechanisms that have been proposed to explain this phenomenon are hyperventilation, hypotension, cerebral microemboli, and inflammatory mechanisms.⁸⁹ The links between anaesthesia and cognitive dysfunction are unclear, in part because of the lack of consistency regarding definition and diagnosis. As yet no individual anaesthetic technique, drug, or mode of monitoring has been proven to reduce the incidence of POCD. To date, there are no specific treatments available for POCD, but the condition is of concern to some elderly patients, and it is important that anaesthetists and surgeons consider ways to reduce its incidence and engage in discussion of the risks with patients preoperatively. As POCD is likely to be multifactorial, the prevention approach should be multidisciplinary and include consultation with care of the elderly specialists where appropriate. Vascular risk factors such as hypertension, obesity, diabetes mellitus, and smoking are linked with cognitive decline in the general population. It is therefore logical that optimisation of these features would assist in lowering the risk of POCD and dementia. These are also risk factors for postoperative complications such as wound infections and respiratory deterioration that are also linked to delirium and POCD.

10. Rehabilitation and return to activities

Postoperative rehabilitation plays a pivotal role in the restoration of a patient's initial functional state. Traditional postoperative management typically initiates with joint rest, followed by gradual mobilization supported by physiotherapy exercises aimed at enhancing muscle strength, particularly the peroneal muscles, and enhancing balance and proprioception.⁹⁰ Additionally, prophylactic ankle bracing may be employed to enhance joint position awareness and provide extra support.⁹⁰ Certain factors, such as advanced age, heightened swelling, diminished range of motion, and persistent pain, may indicate a less favorable prognosis for recovery.

In 2012, Donovan and colleagues⁸¹ conducted a literature review and categorized the presence of impairments in CAI into 4 distinct domains. They have developed a tailored rehabilitation protocol aimed at treating these 4 impairment domains, which has proven beneficial for enhancing CAI management. Nonetheless, conflicting evidence exists concerning the suitable weight-bearing status and postoperative physiotherapy guidelines.⁹¹ Previous reports that compared early mobilization and delayed mobilization found that early mobilization enhances functional outcomes but is associated with increased complication rates. Generally, it is not recommended to have prolonged immobilization, as it could potentially restrict range of motion. Instead, a relatively delayed approach to weight-bearing is recommended.

11. Medial ankle instability

The complex of medial ankle ligaments fulfills a range of essential functions in preserving the natural biomechanics of the ankle joint. Among these ligaments, the deltoid ligament plays a particularly vital role in ensuring stability.⁹² The deep layer of the deltoid ligament primarily restricts talar translation, while the superficial layer of the deltoid ligament primarily counters talar rotation.⁹³ It is noteworthy that around 5% of ankle sprains involve the deltoid ligament.¹⁴ Hintermann and colleagues¹⁸ reported a deltoid ligament injury prevalence of 40% among patients who underwent arthroscopic surgery to address ankle lateral instability. Although only a small percentage of deltoid ligament damage requires surgical intervention, individuals with chronic medial ankle instability might ultimately opt for surgical procedures.⁹⁴

The diagnostic process for a medial ankle injury initiates with a comprehensive evaluation of the patient's history and a physical examination. In the case of a trauma-induced acute injury to the medial ankle ligaments due to trauma, typically arising from either valgus stress or external rotation injury, it commonly manifests as symptoms such as ankle pain, swelling, and difficulty in weight-bearing. The management of acute deltoid ligament injury should follow a treatment approach akin to that used for acute injury to the ankle lateral ligament injury. Managing acute deltoid injuries should follow a treatment approach akin to that of acute lateral ligament sprains. In the case of non-surgical management, the standard protocol involves an initial treatment of rest and immobilization.⁹⁵ This period of immobilization generally extends for a duration of 1–3 weeks, until the pain and swelling have subsided. As with lateral ligament injuries, surgical intervention becomes a consideration for patients who continue to experience instability symptoms despite a dedicated nonoperative treatment regimen. The primary objective of surgical intervention for deltoid ligament injuries is to restore medial ankle stability, which can be achieved through ligament repair or reconstruction, depending on the severity of the ligament injury and the condition of the surrounding soft tissues.⁹⁵ The primary surgical option involves adjustment of deltoid ligament tension and securing it to the medial malleolus, providing that the quality of the deltoid tissue is sufficient. In cases where the soft tissues are unsuitable for a secure direct repair, alternative reconstruction methods become a viable option.

12. Conclusion

Ankle instability is a very prevalent pathology. Accurate diagnosis involves careful combined assessment of history, examination findings, and imaging findings. Failed rehabilitation is an indication of operative repair. The results of anatomic repair are favorable compared with those of nonanatomic tenodesis reconstruction, which has been reported to be associated with higher rates of sural nerve impairment and wound complications. Augmenting the primary repair by tendon transfer protects the repair and adds to the stability. Arthroscopy is ready to lend a hand to diagnose and treat the ankle instability.

CRediT authorship contribution statement

Yimeng Yang: Conceptualization. Yang Wu: Writing–review & editing. Wenhui Zhu: Conceptualization, Writing–review & editing.

Ethical statement

Not applicable.

Funding

This work was supported by the National Natural Science Foundation of China (No.82202708), the Shanghai Sailing Program (21YF1404100), and the Natural Science Foundation of Shanghai Committee of Science and Technology (21ZR1446000). Open Research Program of State Key Laboratory of Molecular Engineering of Polymers of Fudan University (K2023-22).

Declaration of competing interest

The authors declare that there is no conflict of interest.