Incidence of Midfoot Instability in Patients with Achilles Tendon Ruptures (ATR): Why ATR is a Secondary Sign of Spring Ligament Laxity

Luisa Valentini¹, Md Abdul Aziz^1*, Simrin Chaudhri¹, Steven O Famure¹, Zhikai Li², Chandra Pasapula^1*

¹The Queen Elizabeth Hospital Kings Lynn NHS Foundation Trust, United Kingdom
²Corpus Christi College, University of Cambridge, United Kingdom

*Correspondence author: Md Abdul Aziz, Clinical Fellow Trauma and Orthopaedic, The Queen Elizabeth Hospital, King’s Lynn NHS Foundation Trust Gayton Rd, King’s Lynn, United Kingdom, PE30 4ET and Chandra Pasapula, T and O Consultant, The Queen Elizabeth Hospital, King’s Lynn NHS Foundation Trust, Gayton Rd, King’s Lynn, United Kingdom, PE30 4ET;
Email: [email protected]; [email protected]

Citation: Valentini L, et al. Incidence of Midfoot Instability in Patients with Achilles Tendon Ruptures (ATR): Why ATR is a Secondary Sign of Spring Ligament Laxity. J Ortho Sci Res. 2025;6(1):1-12.

Copyright^© 2025 by Valentini L, et al. All rights reserved. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Table 1: Demographics of the patients.

Table 2: Parameter comparison between ATR and non-ATR patients.

Table 3: Mechanism of injury of TA rupture.

Table 4: Parameters of the ATR foot.

Table 5: Patient information.

Discussion

The Achilles Tendon (AT), the largest tendon in the human body, consists of fibers from the gastrocnemius and soleus muscles, with its architecture optimized for strength and functional efficiency. Capable of withstanding forces up to 9 kN or approximately 12.5 times body weight during activities like running, its peak stress is estimated at 70 MPa [15]. The peak age of rupture is 37.5 years [16].

Anatomy favours the function. AT fibre spiralisation increases strength and allows wide origin fibres to act at a single insertion, medially at the heel. This allows the soleus to function as a net inverter at heel rise. The crescent shaped insertion dissipates tendon stress [17].

Numerous theories attempt to explain the pathogenesis of ATR. The degenerative theory by Langergren, et al., hypothesised that ATRs are localised 2-6 cm proximal to the calcaneal insertion. A hypovascular area with low presence of intratendinous vessels, coupled with repeated trauma, prevents regeneration leading to rupture [18]. Histopathological analysis is corroborative demonstrating hypoxic and mucoid degeneration, poor vascular supply, tissue and cell necrosis, calcification, lipomatosis and irregular, degenerated collagen fibres in nearly all rupture sites [19-21]. The torsional trajectory theory assumes that the tendon compresses the transverse vincula. The functional over-pronation theory by Clement states that AT injury occurs due to a functional over-pronation and gastrocnemius soleus insufficiency. Incomplete synergism of agonist muscles, inefficient plantaris contraction or differences in muscle-tendon thickness quotients have been assumed to be contributory. Oblique loading, short initial length and maximal muscle contraction are thought contributory [22]. Tendon stiffness has also been implicated in ATRs. 5 minutes of passive stretching (preload) differentially decreases tendon stresses more in women (22.4%) compared to men (8.8%), possibly explaining greater ATR rates in men [23-25]. Differences in TA dorsiflexion were not present in our study (Table 2).

Pre-existing diseases such as rheumatoid arthritis, gout, ankylosing spondylitis, chronic uraemia, hyperparathyroidism only account for 2% of ATR. Barfred demonstrated complete ruptures occur in the absence of pre-existing etiological factors in healthy tendons [26].

The TA spans 3 joints including the knee, ankle and subtalar joint, passing medially to the subtalar joint axis to act as a net inverter [27,28]. The interaction between the subtalar joint and Achilles tendon has important mutual biomechanical implications. The subtalar axis’ spatial location dynamically changes throughout the gait cycle [27]. Subtalar joint kinematics rather than heel varus or valgus position may play a greater role in ATR. Prior to toe off/heel rise the Center of Pressure [COP] line advances medially to the forefoot, the tibia externally rotates, externally rotating the talus and the subtalar axis spatial orientation, which is maximally lateralized distally towards the 4^th metatarsal or roughly 48% of the gait cycle [27]. The first ray thus generates a maximal net inversion forefoot moment (GRF) when transmitting 60% of weight in terminal stance. SL laxity defunctions this mechanism by allowing persistent medial talar head internal rotation, internally rotating the subtalar axis spatial orientation and changing the relationship of the medial calcaneal tuberosity and TA insertion to the subtalar axis [27].

Our study demonstrates significantly greater midfoot instability in terms of both Talonavicular laxity (TN) and first ray instability (p<0.05). Only 1 ATR foot had approximately equal first ray instability scores compared to the non-ruptured side and all ATR feet had greater TN laxity. This patient was about 3 months post ATR. Type 1 first ray instability occurs as a response to TN laxity. 2 patients had lateral radiographs demonstrating cavoid type feet.

8/14 had significant valgus impingement tenderness. Maximum tenderness was 8/10. Nine patients had coexisting retromalleolar tenderness. Both statically increased in ATR feet. Tenderness scores were between 2 and 8.

Our cohort of patients with TA ruptures didn’t have gross valgus and morphologically looked relatively normal physiological valgus despite having medial arch laxity, thus allowing the potential development of an internally generated conflict force/moment that acts against an inversion at heel rise which is when the TA ruptures.

We postulate several prerequisites that biomechanically predisposes the TA to rupture, which we summarise here.

1. Heel rise

At heel rise there is acceleration and muscles including tibialis posterior and the TA are at maximum voluntary contraction (roughly 48% of gait cycle). Jumping or starting to sprint is a form of ‘accelerated gait’ requiring greater TA force. Body weight and TA contraction increases joint reaction forces/pressures across the subtalar and Tibio Talar (TT) joint, which increases downward talar head pressure. Maximum TA contraction acts at 10 times body weight combined with the force of the weight acting down exerts pressure on the SL via the talar head. The downward force applied by the anterior tibia on the anterior talar neck is opposed by an equal and opposite force exerted by navicular as an anterior buttress and inferomedially by the SL keeps the talus in static equilibrium thus allowing heel rise.

At heel strike the TA does not rupture as muscles are relatively inactive generating minimal force. The medial calcaneal tubercle (weight-bearing calcaneus) at heel strike lies medial to the subtalar joint axis creating an inversion Ground Reaction Force (GRF) moment around the subtalar axis that augments the theoretical line of action of the TA. SL laxity allows increased heel valgus that theoretically acts against any inversion TA pull. However, Soleus (62% cross sectional area) acts at only about 15% maximal amplitude [27,29] and is relatively inactive at this stage of gait, reflecting why TA does not rupture at heel strike. Studies evaluating ATR patients have demonstrated greater calcaneal inversion on heel strike [30], possibly reflecting the body’s attempt to compensate for the midfoot laxity. Heel valgus / varus alone is therefore insufficient to explain if the TA would overload, with respect to the subtalar axis. A varus heel with SL laxity may still internally rotate the subtalar axis, therefore lateralise the forefoot GRF moment, thus generating an internal conflict moment.

2. Laxity of the SL

In our study all 14 patients had SL laxity or talonavicular axis laxity which allows greater non-physiological calcaneal eversion / valgus peaking in mid stance, at the point of increasing TA contraction. SL acts as a static restraint to heel valgus at the talonavicular axis. SL stability helps lock the midfoot and allows the stable first ray’s inversion GRF moment to lie maximal away from the subtalar axis and augment hindfoot TA pull, thus allowing all moments act as a single composite inversion moment unit around the subtalar axis. SL laxity and FRI internally rotates the talus/subtalar axis permitting the TA to remain as a net inverter, whilst placing the forefoot as an everter, thus creating a moment of conflict.  Progressive heel eversion due to increased SL strain puts the line of TA pull closer to the subtalar axis, diminishing its inverting moment for the same contraction force. Peak EMG soleus activity corresponds to heel raise, at just over 40% of the gait cycle, corresponding to when the TA commonly ruptures [7,32]. Increased EMG soleus activity demonstrated in Achilles tendinopathy representing sub-rupture overload pathology [31].

Eventually, excessive SL laxity increases heel valgus causing the calcaneal GRF and the TA to act lateral to the subtalar axis along with the forefoot GRF moment. As all act lateral to the subtalar axis thus there are no opposing moments at midstance or terminal stance from the latter two. The degree of SL laxity differentially changes the forefoot, hindfoot GRF and TA moments with respect to a progressively internally rotating subtalar axis. Furthermore, other factors such as foot length may play a role. Video analysis of TA ruptures demonstrate foot pronation (10 degrees) and external rotation consistent with deformities SL laxity produces [7,31].

3. Internal Rotation of the Subtalar Axis

A small degrees of SL strain amplifies subtalar axis arc of internal rotation of the at the forefoot, lateralising the forefoot GRF lateral to the subtalar axis, thus generating an eversion forefoot moment that opposes TA moment creating an internally generated zone of conflict. Evidence of subtalar axis internal rotation is seen in Achilles tendinopathy patients (representing sub-rupture TA overload) [33]. Reule demonstrated the subtalar joint’s spatial orientation is internally rotated by 18 degrees in subjects with Achilles Tendinopathy [AT] an internal conflict moment compared to 11 degrees in unaffected subjects [33]. Munteanu and Barton demonstrated decreased peak tibial external rotation in AT patients by approximately 40% lower compared to control non-AT group [34]. They demonstrated that the group with previous Achilles tendinopathy exhibited an uncharacteristic internal rotation moment of the tibia present just after heel strike and just before toe-off. Excess internal tibial rotation arises from talus internal rotation due to SL laxity’s failure to medially buttress the talus head. Williams showed 50% of Achilles tendinopathy patients demonstrated an internal rotation moment near heel strike and toe-off, correlating with our findings (Fig. 2,3) [35].

Figure 2: Small changes in talar spatial rotation changes the position of the subtalar axis in the forefoot significantly. (Approximately 9 degrees internal rotation for a 20 cm foot creates a 3 cm medial shift to the subtalar axis in the forefoot and loss of inversion moment). The third rocker puts greatest downward pressure on the talar head, with the TA maximally contracted.

Figure 3: Total inversion Moment: GRF at forefoot/hindfoot and TA pull.

Medial Column Instability and Lateral Force Transfer

First ray is destabilised at around 3 months from SL laxity development [36]. 4 patients were identified at 3 months from the injury date who had POP and boot immobilisation. 3 out of 4 patients had increased FRI and only 1 patient had a stable first ray, but all had increased lateral translation scores. Pressure studies demonstrate a lateral shift in the forefoot load in ATR. These changes have been demonstrated in patients with Achilles tendinopathy also. Dong, et al., found a laterally shifted plantar pressure, 18-24 months after in feet with unilateral ATR. They found an increased subtalar eversion angle and decreased total inversion [37]. Atik, et al., evaluated a single post Achilles rupture after 15 years follow up and demonstrated a lateral shift in the centre of pressure line [38]. Hahn and colleagues evaluated 13 patients using pedobarography and clinical assessment after flexor hallucis longus augmentation for TA ruptures (mean follow-up 46 months). A statistically increased forefoot pressure differences, force distribution and load transfer to the lateral foot were found when compared to the non-operated/injured leg. Whilst this was attributed to the FHL transfer, which diminishes phalanx power we believe unidentified SL laxity may have a role [39].

Coupling of Forefoot and Hindfoot Inverting Vectors

SL laxity decouples the forefoot and hindfoot moments. SL laxity differential changes the rate the forefoot and the hindfoot lose their inversion moment with respect to the subtalar axis. The maximum conflict arises when SL laxity causes persistent hindfoot/forefoot coupling with a maximum eversion moment at the forefoot with an inverting TA. None of our patients had gross valgus leading to no internal conflict moments. This explains why feet with gross valgus do not rupture, as the line of pull of the TA never enters the zone of conflict.

Susceptible Host

A sedentary host, despite having the above susceptible biomechanical profile may never rupture despite putting the TA into the ‘zone of conflict’ and therefore at risk. A host who plays basketball or sprints from still and with a maximally dorsiflexed foot, with no altered foot biomechanics may not generate an internal conflict moment to predispose the TA to rupture. The physiological strength of the collagen, BMI and level of activity would be additional factors determining SL laxity and rupture risk.

Peak ankle dorsiflexion and TA contraction exerts increased downward pressure on the talar neck. At peak dorsiflexion (40 degrees) the talar head hits the anterior part of the tibia, creating maximum downward pressure on the talar head and the SL, significantly exacerbated, during accelerated gait. A tight SL resists heel valgus at the midfoot rather and helps lock the midfoot and initiate a heel rise. The primary centre of rotation is at the metatarsal heads, but SL laxity creates a second centre of rotation in the midfoot, the primary one being at the metatarsal heads, creating a slight delay in dorsiflexion as confirmed by some studies. In our case 5 patients had a foot position described where the tibia was in the third rocker and the foot was about to generate a heel lift. This is consistent with Lemme, who showed that the foot was in dorsiflexion in 75% of cases [16].

Video evidence in basketball players demonstrates injury mechanisms [40]. The injured leg is loaded, with forward displacement of the centre of motion and an increase in hip and knee extension. There is an abrupt increase of ankle dorsiflexion, indicative of accelerated foot posture before forward and vertical propulsion. In one study, the ankle was abruptly dorsiflexed (29° at IF), externally rotated (15° at IF) and pronated (10° at IF) at the time of ATR. The measured maximum dorsiflexion angle of 40° was close to the range of physiological weight-bearing value. In addition, 48% demonstrated foot pronation. Just before take-off, when the foot is planted in dorsiflexion, the calf muscles eccentrically contract to prevent falling. 93% had no contact in their series of football injuries [7].

This is consistent with Lemme who evaluated 12 patients with video analysis and found peak rupture at toe off, consistent with peak acceleration when maximum thrust was about to be generated. Elastic energy stored in stretch then assists active contraction allowing the TA to generate an explosive propulsion force of 8 times body mass [40]. Tendon ruptures require greater force than this, intrinsically generated by an opposite GRF acting pathologically lateral to the subtalar axis. Intrinsic TA fibre arrangement may also play a role. More internal rotation of the TA fibres may rupture less as a greater inversion moment is generated. This has been insufficiently examined.

TA tightness may lead to an early heel rise and prolonged stance phase putting downward pressure on the talar head and therefore increase the duration of biomechanical risk profile for TA rupture. In our series there was no excessively tight TA. This was not found as a confounding factor in our cohort. Furthermore, TA thickness was not found to be significant in our study. TA thickness varies in its presentation depending on stage. Majewski, et al., demonstrated TA thickness peaked at 24 months regardless of whether treated percutaneously, open or non-operatively (17 mm) after an ATR. Initial thickness would increase due to hematoma, followed by organisation. Mature tendons then remodel to become relatively normal size (9-11mm). This is different to tendinopathic tendons which have a larger size [41].

Theoretically, medial column instability may have developed after the injury because of loss of the net inverting vector of the TA that may off load ligament stress. However, patient 14 is important to note, who was examined after their period of POP immobilisation and had not progressed onto loading the foot. This patient demonstrated medial column instability prior to mechanical loading. Patient 1 and 2 also finished their POP immobilisation time and were in their boot/just out of their boot. Both had evidence of medial column instability. Previous studies have implied first ray instability occurs approximately 3-6 months after injury to the SL [36].

Limitations

We accept that this study does not establish a temporal relationship between medial column instability onset and TA rupture. Formally algometry threshold testing was not performed in relation to the tibialis posterior tenderness.

Conclusion

Our study demonstrates increased medial column laxity is present in all ATR feet. The presence of signs of TP overload in some feet further suggests a common pathogenesis. Intrinsic foot biomechanics as a risk factor that predisposes the foot to ATR has not been described to date and helps rationally explain how huge intrinsic non-contact forces can be generated to overload the TA. We advocate using a medial arch support to help restore the subtalar axis and offload the midfoot to offload the TA. Midfoot laxity should be assessed in TA ruptures, to help restore biomechanics and protect the foot from future re-ruptures.

Conflict of Interests

The authors declare that they have no conflict of interest in this paper.

Acknowledgments

Not applicable

Funding/Sponsorship

Not applicable

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