Tag Archives: Achilles tendon

Effects of high and low cut on Achilles tendon kinetics during basketball specific movements

by Jonathan Sinclair1*, Benjamin Sant1pdflrg

The Foot and Ankle Online Journal 9 (4): 5

The aim of the current investigation was to examine the influence of high and low-cut specific basketball footwear in relation to minimalist and conventional athletic footwear on the loads experienced by the Achilles tendon during basketball specific movements. Ten males performed run and 45˚ cut movements whilst wearing low-cut, high-cut, minimalist and conventional athletic footwear. Achilles tendon forces were calculated using Opensim software allowing the magnitudinal and temporal aspects of the Achilles tendon force to be quantified.  Differences in Achilles tendon load parameters were examined using 4 (footwear) x 2 (movement) repeated measures ANOVA. The results show that a main effect was evident for peak Achilles tendon force, which was significantly larger in the minimalist (run = 5.74 & cut = 5.85 BW) and high-cut (run = 6.63 & cut = 6.01 BW) footwear in relation to the low-cut (run = 5.79 & cut = 5.47 BW) and conventional (run = 5.66 & cut = 5.34 BW) conditions. In addition a main effect was also evident for Achilles tendon load rate, which was significantly larger in the minimalist (run = 48.84 & cut = 43.98 BW/s) and high-cut (run = 54.31 & cut = 46.51 BW/s) footwear in relation to the low-cut (run = 43.15 & cut = 31.57 BW/s) and conventional (run = 44.74 & cut = 31.15 BW/s) conditions. The current investigation indicates that minimalist and high-cut footwear may place basketballers at increased risk for Achilles tendon pathology as a function of their training/ competition. Furthermore, it appears that for basketballers who may be susceptible to Achilles tendinopathy that low-cut and conventional conditions are most appropriate.

Keywords: basketball, Achilles tendon, biomechanics

ISSN 1941-6806
doi: 10.3827/faoj.2016.0904.0005

1 – Centre for Applied Sport and Exercise Sciences, School of Sport and Wellbeing, College of Health & Wellbeing, University of Central Lancashire, Lancashire, UK.
* – Corresponding author: jksinclair@uclan.ac.uk


At all levels of play basketball is becoming a uniquely popular athletic discipline throughout the world [1]. Basketball is regarded as a physiologically demanding sport in which players are required to perform a series of different motions that typically include running, jumping and rapid changes of direction [2]. A typical competitive basketball season will require players to train frequently and perform >60 games, a regimen which serves to place high physical and mechanical demands on those involved [3].

Basketball has in recent years gained more research attention from the scientific community regarding players’ susceptibility to injury. Research investigating the prevalence of injuries in basketball players has shown that in relation to other non-contact sports basketball is associated with a comparatively high rate of injury. Information from aetiological analyses indicates that 11.6 injuries occur per 1000 appearances, and that the vast majority (65 %) are confined to the lower extremities [4]. Athletic disciplines which include frequently jumps, foot strikes and changes in direction such as basketball, place high loads on the Achilles tendon placing it at high risk from injury [5].

Given the highly physical nature of modern basketball, court footwear must now fulfill a range of biomechanical parameters such as traction, support, stability and shock attenuation [6]. Traditionally basketball specific footwear designs were available only with high-cut ankle supports which are utilized in order to promote mediolateral stability during landing [7]. In recent times however, low-cut footwear models have also been introduced and utilized at all levels of play, meaning court specific footwear can be selected based on individual preference. Recreational level players are also known to use low-cut conventional athletic footwear which may serve to enhance improve impact loading but at the expense of medio-lateral stability [7]. In comparison to other sports such as running there is currently a paucity of scientific research examining the efficacy of basketball footwear.

Appropriate footwear selection has been cited as a mechanism by which the risk from Achilles tendon pathologies during sport can be mediated. Considerable research has examined the effects of different footwear on the forces experienced by the tendon during different sports. Sinclair examined the effects barefoot and in minimalist footwear on Achilles tendon kinetics in relation to conventional running shoes [8]. Their results showed that conventional footwear significantly reduced peak Achilles tendon forces in relation to barefoot and minimalist conditions. Similarly, Sinclair et al., [9] examined the effects of minimalist and netball specific conditions on the forces experienced by the Achilles tendon during running and cutting movements. They showed that the peak force and rate of force application was significantly reduced in the netball specific condition. Finally, Sinclair et al [10] investigated the effects of minimalist energy return and convention athletic footwear on Achilles tendon loads during depth jumping. They showed the footwear did not significantly affect Achilles tendon forces during this movement. However, despite the wealth of peer reviewed literature examining the effects of different footwear on Achilles tendon kinetics there is currently no information available regarding the influence of basketball specific shoes.

Therefore, the aim of the current investigation was to examine the influence of high and low-cut specific basketball footwear in relation to minimalist and conventional athletic footwear on the loads experienced by the Achilles tendon during basketball specific movements. The findings from the current investigation may provide basketball players with important clinical information regarding the selection of appropriate footwear, which may ultimately help to attenuate their risk from developing Achilles tendon pathologies.

Methods

Participants

Ten male participants, volunteered to take part in this study. All were free from musculoskeletal pathology at the time of data collection and provided written informed consent. The mean characteristics of the participants were; age 24.26 ± 4.05 years, height 1.77 ± 0.07 cm and body mass 78.66 ± 7.43 kg. The procedure utilized for this investigation was approved by the University of Central Lancashire, Science, Technology, Engineering and Mathematics, ethical committee.

Footwear

The footwear used during this study consisted of minimalist (Vibram five-fingers Original;), high-cut (Nike Lebron XII), low-cut (Nike Lebron XII Low) footwear and conventional (New Balance 1260 v2) (shoe size 9–10 in UK men’s sizes).

Procedure

Participants completed five repeats of two sport specific movements; run and cut in each of the four footwear conditions. To control for any order effects the order in which participants performed in each footwear/ movement condition were counterbalanced. Kinematic information from the lower extremity joints was obtained using an eight camera motion capture system (Qualisys Medical AB, Goteburg, Sweden) using a capture frequency of 250 Hz. To measure kinetic information an embedded piezoelectric force platform (Kistler National Instruments, Model 9281CA) operating at 1000 Hz was utilized. The kinetic and kinematic information were synchronously obtained and interfaced using Qualisys track manager.

To define the anatomical frames of the thorax, pelvis, thighs, shanks and feet retroreflective markers were placed at the C7, T12 and xiphoid process landmarks and also positioned bilaterally onto the acromion process, iliac crest, anterior superior iliac spine, posterior superior iliac spine, medial and lateral malleoli, medial and lateral femoral epicondyles, greater trochanter,  calcaneus, first metatarsal and fifth metatarsal. Carbon-fibre tracking clusters comprising of four nonlinear retroreflective markers were positioned onto the thigh and shank segments. Static calibration trials were obtained with the participant in the anatomical position in order for the positions of the anatomical markers to be referenced in relation to the tracking clusters/markers. A static trial was conducted with the participant in the anatomical position in order for the anatomical positions to be referenced in relation to the tracking markers, following which those not required for dynamic data were removed.

Data were collected during the run and cut movements according to below procedures:

Run

Participants ran at 4.0 m.s-1 ±5% and struck the force platform with their right (dominant) limb. The average velocity of running was monitored using infrared timing gates (SmartSpeed Ltd UK). The stance phase of running was defined as the duration over > 20 N of vertical force was applied to the force platform[11].

Cut

Participants completed 45° sideways cut movements using an approach velocity of 4.0 m.s-1 ±5% striking the force platform with their right (dominant) limb. In accordance with McLean et al.,[12] cut angles were measured from the centre of the force plate and the corresponding line of movement was delineated using masking tape so that it was clearly evident to participants. The stance phase of the cut-movement was similarly defined as the duration over > 20 N of vertical force was applied to the force platform [11].

Processing

Dynamic trials were digitized using Qualisys Track Manager in order to identify anatomical and tracking markers then exported as C3D files to Visual 3D (C-Motion, Germantown, MD, USA). Ground reaction force and kinematic data were smoothed using cut-off frequencies of 25 and 12 Hz with a low-pass Butterworth 4th order zero lag filter.

Data during the stance phase were exported from Visual 3D into OpenSim software (Simtk.org), which was used give to simulations of muscles forces. Simulations of muscle forces were obtained using the standard gait 2392 model within Opensim v3.2. This model corresponds to the eight segments that were exported from Visual 3D and features 19 total degrees of freedom and 92 muscle-tendon actuators.

We firstly performed a residual reduction algorithm (RRA) within OpenSim, this utilizes the inverse kinematics and ground reaction forces that were exported from Visual 3D. The RRA calculates the joint torques required to re-create the dynamic motion. The RRA calculations produced route mean squared errors <2°, which correspond with the recommendations for good quality data.  Following the RRA, the computed muscle control (CMC) procedure was then employed to estimate a set of muscle force patterns allowing the model to replicate the required kinematics 13. The CMC procedure works by estimating the required muscle forces to produce the net joint torques.

Achilles tendon force was estimated in accordance with the protocol of Almonroeder et al [14] by summing the muscle forces of the medial gastrocnemius, lateral, gastrocnemius, and soleus muscles. Achilles tendon load rate was quantified as the peak Achilles tendon force divided by the time to peak force. All Achilles tendon load parameters were normalized by dividing the net values by body weight (BW).

Analyses

Differences in kinetic and kinematic parameters between footwear were examined using 4 (footwear) x 2 (movement) repeated measures ANOVAs, with significance accepted at the P≤0.05 level. Effect sizes were calculated using partial eta2 (pη2). Follow up comparisons on significant interactions were examined using simple main effects and post-hoc pairwise comparisons were conducted on all significant main effects. The data was screened for normality using a Shapiro-Wilk which confirmed that the normality assumption was met. All statistical actions were conducted using SPSS v22.0 (SPSS Inc., Chicago, USA).

Results

Tables 1 and Figure 1 present the footwear differences in Achilles tendon kinetics both movements. The results indicate that the experimental footwear significantly affected Achilles tendon load parameters.

 

Minimalist High-cut Low-cut Conventional
Run Cut Run Cut Run Cut Run Cut
Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD Mean SD Mean
Peak Achilles tendon force (BW) 5.74 0.75 5.85 1.03 6.63 1.19 6.01 0.69 5.79 0.78 5.47 1.00 5.66 0.90 5.34
Time to peak Achilles tendon force (s) 0.12 0.01 0.16 0.04 0.13 0.02 0.16 0.02 0.14 0.01 0.19 0.04 0.13 0.02 0.18
Achilles tendon load rate (BW/s) 49.84 8.70 43.98 18.68 54.31 17.49 46.51 14.71 43.15 9.16 31.57 11.96 44.74 11.97 31.15

Table 1 Achilles tendon kinetics as a function of footwear and movement conditions.

fig1

Figure 1 Achilles tendon kinetics during the stance phase (a. = run & b. = cut) (black = minimalist, black dash = high-cut, grey dot = low-cut & grey = conventional).

For peak Achilles tendon force a significant main effect (P<0.05, pη2 = 0.64) was observed for footwear. Post-hoc pairwise comparisons showed that peak Achilles tendon force was significantly larger in the high-cut footwear in relation to the minimalist, low-cut and conventional athletic conditions. In addition it was also revealed that peak force was significantly larger in the minimalist footwear in comparison to the conventional condition.

For time to peak Achilles tendon force significant main effects were observed for both footwear (P<0.05, pη2 = 0.55) and movement (P<0.05, pη2 = 0.70). Post-hoc analysis for footwear showed that time to peak force was significantly greater in the low-cut footwear in comparison to the minimalist, high-cut and conventional conditions. Furthermore, it was also demonstrated that time to peak force was significantly greater in the conventional athletic footwear in relation to the minimalist and high-cut conditions. Finally, it was shown that time to peak force was significantly greater in the high-cut footwear in comparison to the minimalist condition. In addition post-hoc analysis for movement indicated that time to peak Achilles tendon force was significantly greater when performing the cut movement.

For Achilles tendon load rate significant main effects were observed for both footwear (P<0.05, pη2 = 0.42) and movement (P<0.05, pη2 = 0.47). Post-hoc analysis for footwear showed that Achilles tendon load rate was significantly larger in the minimalist and high-cut footwear in relation to the low-cut and conventional conditions.  

Discussion

The current study aimed to examine the effects of different basketball footwear on the loads experienced by the Achilles tendon during sport specific movements. To the authors knowledge this investigation is the first comparative examination of the effects of different footwear on Achilles tendon kinetics during basketball specific movement. The findings from this work may provide basketball players with important information regarding the selection of appropriate footwear to attenuate their risk from developing Achilles tendon pathologies.

The primary observation from the current work is that Achilles tendon loading parameters were shown to be significantly larger in the minimalist and high-cut footwear in comparison to the conventional low-cut conditions. This observation is in agreement with those of Sinclair [8] and Sinclair et al [9] who showed that minimalist footwear were associated with significant increases in Achilles tendon loading.

This observation may provide important clinically meaningful information regarding the aetiology of Achilles tendon pathologies. Achilles tendon pathologies are considered to be initiated by high loads which are experienced too frequently by the tendon itself 15. Tendon loading at an appropriate level can initiate collagen synthesis and positively influence the mechanical properties of the tendon [16]. However, when mechanical loads exceed the physiological threshold for collagen synthesis and the remodeling threshold is exceeded, this facilitates tendon degradation and ultimately leads to injury [16]. Therefore the findings from the current investigation indicate that minimalist and high-cut footwear may place basketballers at a greater risk from Achilles tendon pathologies as a function of their training/ competition.

In conclusion, although the effects of different footwear on Achilles tendon forces have been examined previously, our current knowledge of differences in Achilles tendon kinetics when performing sport specific movements in basketball footwear is limited. The current study therefore sought to provide an evaluation of Achilles tendon forces when performing sport specific movements in different basketball specific footwear. This work shows importantly that peak Achilles tendon force and the rate of Achilles tendon load rate were significantly larger in minimalist and high-cut footwear in relation to the low-cut and conventional conditions. As such given the association between Achilles tendon loading and tendon pathology the current investigation indicates that minimalist and high-cut footwear may place basketballers at increased risk for Achilles tendon pathology as a function of their training/ competition. Furthermore, it appears that for basketballers who may be susceptible to Achilles tendinopathy that low-cut and conventional conditions are most appropriate.

References

  1. Cumps, E, Verhagen R, and Meeusen R. “Prospective epidemiological study of basketball injuries during one competitive season: ankle sprains and overuse knee injuries.” J Sport Sci Med 6: 204-211, 2007. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3786241/
  2. Montgomery PG, Pyne DB and Minahan CL. The physical and physiological demands of basketball training and competition. Int J Sports Physiol Perform. 15: 75-86, 2010. https://www.ncbi.nlm.nih.gov/pubmed/20308698
  3. Narazaki K, Berg K, Stergiou N and Chen B. Physiological demands of competitive basketball. Scand J Med Sci Sport. 19: 425-322, 2009. https://www.ncbi.nlm.nih.gov/pubmed/18397196
  4. Deitch JR, Starkey C, Walters SL and Moseley JB. Injury Risk in Professional Basketball Players; A Comparison of Women’s National Basketball Association and National Basketball Association Athletes. Am J Sport Med. 34: 1077-1083, 2006. https://www.ncbi.nlm.nih.gov/pubmed/16493173
  5. Wertz, J., Galli, M., and Borchers, J. R. Achilles Tendon Rupture Risk Assessment for Aerial and Ground Athletes. Sport Health. 5: 407-409, 2013. https://www.ncbi.nlm.nih.gov/pubmed/24427410
  6. Caselli MA. Selecting the proper athletic shoe. Pod Manag. 25: 147-149, 2006.
  7. Commons AT and Low DC. Understanding the effect of high-cut shoes, running shoes and prophylactic supports on ankle stability when performing a v”-cut movement. Sport Exerc Med Open J. 1: 1-7, 2014.
  8. Sinclair, J. Effects of barefoot and barefoot inspired footwear on knee and ankle loading during running. Clin Biomech. 29: 395-399, 2014. https://www.ncbi.nlm.nih.gov/pubmed/24636307
  9. Sinclair, J., Atkins, S., Taylor, P. J., and Vincent, H. Effects of conventional and minimalist footwear on patellofemoral and Achilles tendon kinetics during netball specific movements. Comp Ex Phys. 11: 191-199, 2015.
  10. Sinclair, J., Hobbs, S. J., and Selfe, J. (2015). The Influence of Minimalist Footwear on Knee and Ankle Load during Depth Jumping. Research in Sports Medicine, 23(3), 289-301. https://www.ncbi.nlm.nih.gov/pubmed/26053415
  11. Sinclair, J., Edmundson, C.J., Brooks, D., and Hobbs, S.J. Evaluation of kinematic methods of identifying gait Events during running. Int J Sport Sci Eng. 5: 188-192, 2011.
  12. Thelen, D.G., Anderson, F.C., and Delp, S.L. Generating dynamic simulations of movement using computed muscle control. J Biomech. 36: 321–328, 2003. https://www.ncbi.nlm.nih.gov/pubmed/12594980
  13. Almonroeder, T., Willson, J.D., and Kernozek, T.W. The effect of foot strike pattern on Achilles tendon load during running. Annals Biomedical Eng. 41: 1758-1766, 2013. https://www.ncbi.nlm.nih.gov/pubmed/23640524
  14. Selvanetti, A.C.M., and Puddu, G. Overuse tendon injuries: basic science and classification. Op Tech Sport Med. 5: 110–17, 1997.
  15. Kirkendall, D.T., and Garrett W.E. Function and biomechanics of tendons. Scandinavian. J Med Sci Sport. 7: 62–66, 1997. https://www.ncbi.nlm.nih.gov/pubmed/9211605

The effects of CrossFit and minimalist footwear on Achilles tendon kinetics during running

by Jonathan Sinclair1, and Benjamin Sant1pdflrg

The Foot and Ankle Online Journal 9 (4): 2

The aim of the current investigation was to comparatively assess the influence of barefoot, CrossFit, minimalist and conventional footwear on the loads experienced by the Achilles tendon during running. Twelve male runners (27.81 ± 7.02 years, height 1.77 ± 0.11 cm and body mass 76.22 ± 7.04 kg) ran at 4.0 m·s-1 in each of the four footwear conditions. Achilles tendon forces were calculated using a musculoskeletal modelling approach allowing the magnitudinal and temporal aspects of the Achilles tendon force to be quantified. Differences between footwear were examined using one-way repeated measures ANOVA. The results showed the peak Achilles tendon force was significantly larger when running barefoot (5.81 ± 1.21) and in minimalist footwear (5.64 ± 1.03 BW) compared to conventional footwear (5.15 ± 1.05 BW). In addition it was revealed that Achilles tendon impulse was significantly larger when running barefoot (0.77 ± 0.22 BW.s) and in minimalist footwear (0.72 ± 0.16 BW.s) in comparison to both conventional footwear (0.64 ± 0.15 BW.s). Given the proposed association between high Achilles tendon forces and tendon degradation, the outcomes from the current investigation indicate that CrossFit athletes who select barefoot and minimalist footwear for their running training may be at increased risk from Achilles tendon pathology in comparison to conventional footwear conditions.

Keywords: Footwear, Achilles tendon, running, CrossFit

ISSN 1941-6806
doi: 10.3827/faoj.2016.0904.0002

1 – Centre for Applied Sport and Exercise Sciences, School of Sport and Wellbeing, College of Health & Wellbeing, University of Central Lancashire, Lancashire, UK.
* – Corresponding author: jksinclair@uclan.ac.uk


CrossFit represents a relatively new activity associated with aerobic exercises, calisthenics, and Olympic weightlifting [1]. CrossFit as a discipline has expanded to become an international sport which has been linked to significant gains in aerobic and anaerobic fitness [1]. Given the novelty of CrossFit in relation to more established sports it has received a paucity of published attention in the sports science and strength and conditioning literature.

A key feature of CrossFit training is aerobic conditioning and the manner in which this is examined during competition is via distance running events. Engagement in distance running mediates numerous physiological benefits but it is known to be associated with a high rate of chronic pathologies, with around 70 % of runners experiencing an injury injured during the course of a year [2,3]. Shorten proposes that athletic footwear with suitable mechanical features may be able to manage the incidence of chronic running related injuries [4].

CrossFit athletes are able to select from a wide range of different footwear conditions with distinct design characteristics. There has been no peer reviewed research which has examined the biomechanical influence of different footwear available to CrossFit athletes. CrossFit specific footwear represents a hybrid footwear designed to incorporate the stability characteristics of a weightlifting shoe with the cushioning and flexibility of a running trainer. Currently, there is a trend for CrossFit athletes to opt to train and compete either barefoot or minimalist footwear in lieu of traditional footwear options, although the efficacy of barefoot and minimalist footwear is not yet fully established.

The effects of different footwear on the loads experienced by the Achilles tendon have been examined previously. Sinclair examined the effect running barefoot had on minimalist and conventional footwear on Achilles tendon kinetics during the stance phase of running [5]. The findings showed that peak Achilles tendon kinetics were significantly larger when running barefoot and in minimalist footwear. Similarly Sinclair et al, examined the effects of minimalist, maximalist and conventional footwear on the loads borne by the Achilles tendon during running[6] . Their findings confirmed that peak Achilles tendon force and Achilles tendon impulse were significantly larger in minimalist footwear in relation to the conventional and maximalist conditions. Currently there are no published scientific investigations regarding the effects of barefoot, CrossFit, minimalist and conventional footwear on the loads experienced by the Achilles tendon.    

Therefore the aim of the current study was to comparatively examine the influence of barefoot, CrossFit, minimalist and conventional footwear on the loads experienced by the Achilles tendon during the stance phase of running. Given that running activities are associated with a high incidence of chronic Achilles tendon pathologies, the current investigation may deliver key information to CrossFit athletes concerning the selection of suitable footwear.

Methods

Participants

Thirteen male participants took part in this investigation. All uninjured at the time of data collection and written informed consent was obtained. The mean and standard deviation (SD) characteristics of the participants were: age 27.81 ± 7.02 years, height 1.77 ± 0.11 cm and body mass 76.22 ± 7.04 kg. The research design utilized for this investigation was approved by the University of Central Lancashire, Science, Technology, Engineering and Mathematics, ethical committee. 

Procedure

Participants ran at 4.0 m·s-1 (±5%), while striking an embedded piezoelectric force platform (Kistler, Kistler Instruments Ltd., Alton, Hampshire) which sampled at 1000 Hz. Participants struck the platform with their right foot which was used for analysis. Running velocity was monitored using infrared timing gates (Newtest, Oy Koulukatu, Finland). The stance phase was delineated as the duration over which 20 N or greater of vertical force was applied to the force platform. Runners completed five trials in each footwear condition. The order that participants ran in each footwear condition was randomized. Kinematics and ground reaction forces data were synchronously collected. Kinematic data was captured at 250 Hz via an eight camera motion analysis system (Qualisys Medical AB, Goteburg, Sweden). Dynamic calibration of the motion capture system was performed before each data collection session.

Lower extremity segments were modelled in 6 degrees of freedom using the calibrated anatomical systems technique [7]. To define the segment coordinate axes of the foot and shank, retroreflective markers were placed unilaterally onto the 1st metatarsal, 5th metatarsal, calcaneus, medial and lateral malleoli, medial and lateral epicondyles of the femur. A carbon fiber tracking cluster was positioned onto the shank segment and the foot was tracked using the 1st metatarsal, 5th metatarsal and calcaneus markers. The center of the ankle joint was delineated as the midpoint between the malleoli markers[8] . Static calibration trials were obtained allowing for the anatomical markers to be referenced in relation to the tracking markers/ clusters. The Z (transverse) axis was oriented vertically from the distal segment end to the proximal segment end. The Y (coronal) axis was oriented in the segment from posterior to anterior. Finally, the X (sagittal) axis orientation was determined using the right hand rule and was oriented from medial to lateral.

Processing

Dynamic trials were digitized using Qualisys Track Manager in order to identify anatomical and tracking markers then exported as C3D files to Visual 3D (C-Motion, Germantown, MD, USA). Ground reaction force and marker trajectories were smoothed using cut-off frequencies of 50 and 12 Hz using a low-pass Butterworth 4th order zero lag filter. All data were normalized to 100% of the stance phase then processed trials were averaged. Joint kinetics were computed using Newton-Euler inverse-dynamics. To quantify net joint moments anthropometric data, ground reaction forces and angular kinematics were used.  

Achilles tendon force (BW) was determined using a musculoskeletal modelling approach. This model has been used previously to resolve differences in Achilles tendon force between different footwear [5, 6]. Achilles tendon force was quantified as a function of the plantarflexion moment (PFM) divided by the Achilles tendon moment arm (MA). The moment arm was quantified as a function of the ankle sagittal plane angle (ak) using the procedure described by Self and Paine [9]:

Achilles tendon force = PFM / MA

MA = -0.5910 + 0.08297 ak – 0.0002606 ak2

Average Achilles tendon load rate was quantified as the Achilles tendon force divided by the time over which the peak force occurred. Instantaneous Achilles tendon load rate was also determined as the peak increase in Achilles tendon force between adjacent data points. In addition to this Achilles tendon force, impulse  was quantified during running by multiplying the Achilles tendon force estimated during the stance phase by the stance time.

Experimental footwear

The footwear used during this study consisted of conventional footwear (New Balance 1260 v2), minimalist (Vibram five-fingers, ELX) and CrossFit (Reebok CrossFit CR) footwear, (shoe size 8–10 in UK men’s sizes).

Analyses

Means and standard deviations were calculated for all footwear conditions. Differences in Achilles tendon parameters between footwear were examined using one-way repeated measures ANOVAs, with significance accepted at the P≤0.05 level. Effect sizes were calculated using partial eta2 (pη2). Post-hoc pairwise comparisons were conducted on all significant main effects. The data was screened for normality using a Shapiro-Wilk which confirmed that the normality assumption was met. All statistical actions were conducted using SPSS v22.0 (SPSS Inc., Chicago, USA).

Results

Table 1 and Figure 1 present the Achilles tendon loads during the stance phase of running, as a function of the different experimental footwear. The results indicate that the experimental footwear significantly influenced Achilles tendon force parameters.

Barefoot CrossFit Conventional Minimalist
Mean SD Mean SD Mean SD Mean SD
Peak Achilles tendon force (BW) 5.81 1.21 5.50 1.32 5.15 1.05 5.64 1.03
Time to peak Achilles tendon force (s) 0.13 0.02 0.14 0.02 0.15 0.02 0.14 0.02
Achilles tendon average load rate (BW/s) 45.54 12.76 42.37 14.44 35.76 10.49 40.84 9.07
Achilles tendon instantaneous load rate (BW/s) 128.84 42.10 153.23 51.56 115.45 40.08 136.21 25.93
Achilles tendon impulse (BW.s) 0.77 0.22 0.69 0.20 0.64 0.15 0.72 0.16

Table 1 Achilles tendon forces as a function of footwear.

fig1

Figure 1 Achilles tendon forces during the stance phase as a function of footwear (black = barefoot, dash = minimalist, grey = conventional, grey dot = CrossFit).

A main effect (P<0.05, pη2 = 0.21) was shown for the magnitude of peak Achilles tendon load. Post-hoc pairwise comparisons showed that peak Achilles tendon force was significantly larger in the barefoot (P=0.01) and minimalist (P=0.04) conditions in relation to conventional footwear. A main effect (P<0.05, pη2 = 0.43) was shown for the time to peak Achilles tendon load. Post-hoc pairwise comparisons showed that time to peak Achilles tendon force was significantly larger in the barefoot (P=0.001) and minimalist (P=0.007) conditions in relation to conventional footwear. In addition time to peak Achilles tendon force was significantly shorter in the barefoot condition (P=0.007) in relation to the CrossFit footwear.  In addition a main effect (P<0.05, pη2 = 0.29) was evident for average Achilles tendon load rate. Post-hoc analysis showed that average load rate was significantly larger in the barefoot (P=0.004), CrossFit (P=0.04) and minimalist (P=0.02) conditions in relation to the conventional footwear. A main effect (P<0.05, pη2 = 0.25) was found for instantaneous Achilles tendon load rate. Post-hoc pairwise comparisons showed that instantaneous Achilles tendon load rate was significantly larger in the barefoot (P=0.01), CrossFit (P=0.003) and minimalist (P=0.01) conditions in relation to the conventional footwear. Finally, a main effect (P<0.05, pη2 = 0.34) was observed for Achilles tendon impulse. Post-hoc analyses indicated that Achilles tendon impulse was significantly larger in the barefoot (P=0.007) and minimalist (P=0.04) conditions in relation to conventional footwear.

Discussion

The aim of the current investigation was to comparatively examine the influence of barefoot, CrossFit, minimalist and conventional footwear on the loads experienced by the Achilles tendon during running. To the authors knowledge the current study represents the first comparative examination of Achilles tendon kinetics when running in these specific footwear conditions.

The key observation from the current study is that Achilles tendon force parameters were significantly larger in the barefoot and minimalist conditions in relation to the conventional running shoes. This observation is in agreement with those of Sinclair [5] and Sinclair et al. [6] who similarly noted that barefoot and minimalist footwear conditions were associated with significant increases in Achilles tendon kinetics in relation to more substantial running footwear. This observation may provide important clinical information with regards to the etiology of Achilles tendon pathologies as a function of running activities in CrossFit athletes. The initiation and progression of Achilles tendonitis is mediated by excessive tendon loads that are applied without sufficient cessation between activities [10]. Mechanisms of tendon loading that are above the systematic threshold for collagen related synthesis lead ultimately to degradation of the collagen network as the rate of resynthesis is not able to keep pace with the rate of breakdown [11]. Therefore the findings from the current investigation indicate that running barefoot and in minimalist footwear may place CrossFit athletes performing running activities at a greater risk from Achilles tendon pathology.

The specific findings from the current study may be explained by taking into account the effects of running barefoot and in minimalist footwear on the sagittal plane mechanics of the ankle joint. When running barefoot and wearing minimalist footwear, runners adopt a more plantarflexed foot position throughout the stance phase in relation to more structured running shoes [12, 13].  Increased ankle plantarflexion serves to reduce the length of moment arm of the Achilles tendon [9]. If the moment arm is shortened, this mediates an increase in the load which must be borne by the tendon when running barefoot and in minimalist footwear.

Research which has examined the influence of different footwear condition on the loads borne by the Achilles tendon during the stance phase of running, habitually examines only the peak forces experienced per footfall. Because running barefoot and in minimalist footwear mediates alterations in stance times and step frequencies, the time integral of loads experienced by the Achilles tendon are not quantified. The current study addresses this by quantifying the impulse experienced by the Achilles tendon during the stance phase which is a reflection of both the load experienced and the time interval of the load. The findings from the current investigation in relation to the Achilles tendon impulse mirror those of Sinclair et al., in that barefoot and minimalist footwear were associated with significantly larger impulse in relation to conventional running shoes [6]. This therefore further supports the notion outlines above that running barefoot and in minimalist footwear may increase the likelihood of experiencing an Achilles tendon injury compared to conventional running shoes.   

In conclusion, although differences in Achilles tendon loading as a function of different footwear conditions has been examined previously, the current knowledge with regards to the effects of minimalist, barefoot, CrossFit and conventional footwear on Achilles tendon forces is limited. As such the present study therefore adds to the current knowledge by providing a comprehensive evaluation of Achilles tendon load parameters when running in minimalist, barefoot, CrossFit and conventional footwear. On the basis Achilles tendon load and impulse parameters were shown to be significantly greater when running barefoot and in minimalist footwear, the outcomes from the current investigation indicate that CrossFit athletes who select barefoot and minimalist footwear for their running training may be at increased risk from Achilles tendon pathology in comparison to conventional footwear conditions.

References

  1. Weisenthal, B. M., Beck, C. A., Maloney, M. D., DeHaven, K. E., & Giordano, B. D. (2014). Injury rate and patterns among CrossFit athletes. Orthopaedic Journal of Sports Medicine (In press).
  2. Taunton, JE, Ryan, MB, Clement, DB, McKenzie, DC, Lloyd-Smith, DR, Zumbo, BD. A retrospective case-control analysis of 2002 running injuries. Br J Sp Med. 2002; 36: 95-101. doi: 10.1136/bjsm.36.2.95  
  3. van Gent, R, Siem DD, van Middelkoop M, van Os TA, Bierma-Zeinstra SS, Koes, BB. Incidence and determinants of lower extremity running injuries in long distance runners: a systematic review. British Journal of Sports Medicine 2007: 41: 469-480. http://www.ncbi.nlm.nih.gov/pubmed/17473005
  4. Shorten, MA. Running shoe design: protection and performance. pp 159-169 in Marathon Medicine (Ed. D. Tunstall Pedoe). 2000; London, Royal Society of Medicine.
  5. Sinclair J. Effects of barefoot and barefoot inspired footwear on knee and ankle loading during running. Clinical Biomechanics 2014; 29: 395-399. http://www.ncbi.nlm.nih.gov/pubmed/24636307
  6. Sinclair, J., Richards, J., & Shore, H. (2015). Effects of minimalist and maximalist footwear on Achilles tendon load in recreational runners. Comparative Exercise Physiology, 11(4), 239-244.
  7. Cappozzo A, Catani F, Leardini A, Benedeti MG, Della CU. Position and orientation in space of bones during movement: Anatomical frame definition and determination. Clinical Biomechanics 1995; 10: 171-178. http://www.ncbi.nlm.nih.gov/pubmed/11415549
  8. Graydon, R, Fewtrell, D, Atkins, S, Sinclair, J. The test-retest reliability of different ankle joint center location techniques. Foot Ankle Online J. 2015; 8: 1-11. doi: 10.3827/faoj.2015.0801.0011
  9. Self, BP, Paine, D. Ankle biomechanics during four landing techniques. Medicine & Science in Sports & Exercise 2001; 33: 1338–1344.
  10. Selvanetti, ACM, Puddu, G. Overuse tendon injuries: basic science and classification. Operative Techniques in Sports Medicine 1997; 5: 110–17. http://www.sciencedirect.com/science/article/pii/S1060187297800317
  11. Kirkendall, DT, Garrett W.E. Function and biomechanics of tendons. Scandinavian. Journal of Medicine & Science in Sports 1997; 7: 62–66. http://www.ncbi.nlm.nih.gov/pubmed/9211605
  12. Lieberman, D.E., Venkadesan, M., Werbel, W.A., Daoud, A.I., D’Andrea, S., Davis, I.S., & Pitsiladis, Y. (2010). Foot strike patterns and collision forces in habitually barefoot versus shod runners. Nature, 463, 531-535.
  13. Sinclair, J., Greenhalgh, A., Brooks, D., Edmundson, C. J., & Hobbs, S. J. (2013). The influence of barefoot and barefoot-inspired footwear on the kinetics and kinematics of running in comparison to conventional running shoes. Footwear Science, 5, 45-53.

Lumpy bumpy Achilles with gait instability could be cerebrotendinous xanthomatosis: Two case reports

by Iftikhar H Wani, MBBS MS Ortho1; Munir Farooq, MBBS MS Ortho1; M Shafi Bhat, MBBS MS Ortho1; Ansar-ul-haq Lone1; Younis Kamal, MBBS MS Ortho1; Irfan latoo, MBBS MS Ortho1pdflrg

The Foot and Ankle Online Journal 7 (1): 3

Cerebrotendinous xanthomatosis is a rare genetic metabolic disorder of cholesterol and bile acid metabolism that results in systemic and neurologic abnormalities. We report two cases of bilateral painful enlargement of the Achilles tendons who subsequently were diagnosed with cerebrotendinous xanthomatosis. It is important that orthopaedic surgeons be aware of this condition because the initial presentation may be symmetric, painful enlargement and deformity of the Achilles tendons. Early diagnosis is the key to treatment because medical therapy is effective in halting progression of, although not reversing, the devastating neurological lesions of this condition.

Keywords: Xanthomatosis; ataxia; Achilles tendon; genetic disorder; early diagnosis.

ISSN 1941-6806
doi: 10.3827/faoj.2014.0703.0003

Address correspondence to:Iftikhar H Wani MBBS MS Ortho
Registrar Hospital for Bone and Joint Surgery Barzulla Srinagar Kashmir India.
Email: drihwani@yahoo.co.in


Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive lipid-storage disease secondary to a disruption in cholesterol metabolism caused by a mutation in the sterol 27-hydroxylase (CYP27) gene [1,2]. In the absence of the key enzyme, sterol 27-hydroxylase, other metabolites are increased such as cholestanol. This elevated concentration results in characteristic clinical findings such as bilateral cataracts, tendon xanthomas, and neurologic impairments including debilitating cerebellar ataxia and cerebral degeneration.

Case 1

A 27-year-old male presented to our hospital with a four-year history of bilateral, slowly progressive, painful swelling of the Achilles tendon, but showed rapid progression in size for last 3 months to the extent that it interfered with his ability to walk. The pain was exacerbated by walking, was relieved somewhat by rest, and progressively restricted the patient’s walking distance to a maximum of two blocks at present.

The patient had been previously operated on for bilateral cataracts thirteen years before. No other family members have shown similar symptoms or signs of hypercholesterolemia.

On physical exam, each fusiform mass measured 10 cm in length starting approximately 1.5 cm proximal from the Achilles tendon insertion (Figure 1 and Figure 2). Patient had ataxic gait and exhibited symmetrical 2+ deep tendon reflexes. His muscle strength and ankle range of motion were normal. General physical examination did not disclose cutaneous xanthomas or yellowish discoloration.

Picture1

Figure 1 Bilateral Achilles tendon swelling (case 1).

Picture2

Figure 2 Bilateral Achilles tendon swelling (case 1).

Case 2

A 33-year-old male presented complaining of slowly enlarging masses overlying both distal Achilles tendons (Figure 3). They were soft and non-tender to palpation, however he did complain that closed countered shoes caused significant pain over the area. Despite being treated with nonsteroidal anti-inflammatory as well as oral steroid regimens, growth continued over the past six years.

Picture3

Figure 3 Bilateral Achilles tendon swelling (case 2).

A neurologist had previously diagnosed multiple sclerosis on the basis of the clinical findings of neuropathy in the extremities, an ataxic gait, and plaque-like changes in the cerebral cortex on magnetic resonance imaging (Figure 4). The patient had a family history of type-2 diabetes mellitus but no other inherited disorders.

No osseous pathology was noted on plain radiographs (Figure 5). Magnetic resonance images revealed a soft tissue mass on each Achilles tendon exhibiting a heterogeneous signal (Figure 6). Biopsy was done and tissue was examined under light microscopy. Fatty yellow deposits were seen infiltrating the tendinous fibers. Innumerable foamy macrophages were visualized with cleft-like spaces consistent with dissolved cholesterol secondary to cellular processing under light microscopy (Figure 7).

Picture5

Figure 4 Brain MRI (case 2).

Picture6

Figure 5 Anteroposterior and lateral radiographs and ankle showing bilateral soft tissue swelling without bony abnormality.

Blood investigations revealed a normal complete hemogram. Liver enzymes and a lipid panel found no abnormalities except for an elevated cholestanol level of 25.8 ug/mL (normal value is 4.2 +/- 1.2 ug/mL).

Picture7

Figure 6 Magnetic resonance image revealed a soft tissue mass on each Achilles tendon exhibiting a heterogeneous signal.

Picture8

Figure 7 Light Microscopy image showing innumerable foamy macrophages with cleft-like spaces (Stain, hematoxylin and eosin, original magnification ×200).

The patient was started on bile acid replacement therapy with chenodeoxycholic acid and atorvastatin. There is no further progression of swellings after treatment. There was no improvement of neurological dysfunction as seen clinically after treatment.

Discussion

Cerebrotendinous xanthomatosis was first described in 1937 by Van Bogaert and colleagues and has since been characterized clinically, biochemically, and genetically [3]. In 1968, Menkes et al described the accumulation of cholestanol, the primary metabolite found in elevated concentrations in cerebrotendinous xanthomatosis, in tissues of the CNS [4]. In 1971, Salen found that chenodeoxycholic acid (CDCA), an important bile acid, was virtually absent in patients with clinical symptoms of the disease [5]. This led to successful trials of therapy with CDCA replacement by Salen and colleagues in 1971 [6]. In 1980, defects in mitochondrial 27-hydroxylase were implicated in the biochemical pathophysiology of the disease by Oftebro et al [7]. In 1991, mutations in the gene CYP27A1 were discovered as causative [8-10].

Typically, untreated cerebrotendinous xanthomatosis follows a progressive course. Chronic, sometimes intractable diarrhea occurs, with onset typically in infancy. The diarrhea continues through adulthood if left untreated [11]. This typical presentation was not seen in our cases. Juvenile cataracts may be a presenting sign as was seen in one of our cases but the patient was not evaluated properly for the cause leading to delayed diagnosis [12]. Xanthomas are rarely seen before age 20 years, as was in our cases, although an exaggerated phenotype may be observed in patients with heterozygous familial hypercholesterolemia and cerebrotendinous xanthomatosis [13]. They are usually found on the Achilles tendon but may also be found on the patella, elbow, hand, and neck tendons. They have also been reported on the parenchyma of the lungs and brain, as well as in the bones.

Cerebrotendinous xanthomatosis is classically characterized by (1) bilateral Achilles tendon xanthoma; (2) bilateral cataract formation; and (3) progressive neurological dysfunction with mainly pyramidal tract signs, cerebellar ataxia, and cognitive impairment. Other orthopaedic manifestations of cerebrotendinous xanthomatosis include osteoporosis with an increased risk of fracture [14-16] and peripheral neuropathy [17] with secondary neuropathic deformity and/or ulceration of the feet [18,19].

The diagnosis of CTX is mostly clinical as most biochemical parameters are normal. Diagnosis depends on elevated serum cholestanol levels. MRI shows evidence of cerebral and cerebellar atrophy. T2-weighted image may show focal or diffuse high signal intensities in vertebral and cerebellar white matter. Dentate nuclei could be hyperintense on FLAIR images [20]. More recently, molecular biological techniques have been developed to assist in the diagnosis of cerebrotendinous xanthomatosis in asymptomatic homozygote family members of symptomatic patients. Heterozygotes can also be identified in these families, which is important for genetic counseling and prenatal diagnosis [21].

The differential diagnosis for a patient presenting with xanthomas of Achilles tendon and other tendons includes familial hypercholesterolemia and sitosterolemia [22]. Patients have accelerated atherosclerosis with tendon xanthomas, but absence of neurological symptoms and diarrhea differentiates them from CTX.

Conclusion

Xanthomatous Achilles tendon deposits have been reported to regress with chenodeoxycholic acid therapy [23-26]. Early diagnosis of CTX is essential and key to the treatment as pharmacological management with CDCA and HMG COA reductase inhibitors (Simvastatin) has shown to slow or even reverse the progression of disease [23-24]. Patients with childhood cataract should be thoroughly screened for this problem. Medical therapy, therefore, should be instituted at the time of diagnosis, and family members should be screened for subclinical disease. The benefits of genetic testing should be given to asymptomatic subjects for the early diagnosis of this rare disease.

References

1. Lee MH, Hazard S, Carpten JD et-al. Fine-mapping, mutation analyses, and structural mapping of cerebrotendinous xanthomatosis in U.S. pedigrees. J Lipid Res. 2001;42 (2): 159-69. [Pubmed]
2. Bjorken I, Boberg KM, Leitersdoef E. Inborn errors in bile acid biosynthesis and storage of sterols other than cholesterol. In: Scriver CR, Beaudet AL, editors. The metabolic and molecular bases of inherited disease. 8th ed. New York: McGraw-Hill; 2001. p 2970-8.
3. Van Bogaert L, Scherer HJ, Epstein E. Une forme cerebrale de la cholesterinose generalisee [dissertation/master’s thesis]. Paris: Masson et Cie. 1937.
4. Menkes JH, Schimschock JR, Swanson PD. Cerebrotendinous xanthomatosis. The storage of cholestanol within the nervous system. Arch Neurol. 1968;19 (1): 47-53. [Pubmed].
5. Salen G. Cholestanol deposition in cerebrotendinous xanthomatosis. A possible mechanism. Ann Intern Med. 1971;75 (6): 843-51. [Pubmed]
6. Salen G, Meriwether TW, Nicolau G. Chenodeoxycholic acid inhibits increased cholesterol and cholestanol synthesis in patients with cerebrotendinous xanthomatosis. Biochem Med. 1975;14 (1): 57-74. – [Pubmed]
7. Oftebro H, Björkhem I, Skrede S et-al. Cerebrotendinous xanthomatosis: a defect in mitochondrial 26-hydroxylation required for normal biosynthesis of cholic acid. J Clin Invest. 1980;65 (6): 1418-30. [Pubmed]
8. Clayton PT, Verrips A, Sistermans E et-al. Mutations in the sterol 27-hydroxylase gene (CYP27A) cause hepatitis of infancy as well as cerebrotendinous xanthomatosis. J Inherit Metab. Dis. 2002;25 (6): 501-13. [Pubmed]
9. Gallus GN, Dotti MT, Federico A. Clinical and molecular diagnosis of cerebrotendinous xanthomatosis with a review of the mutations in the CYP27A1 gene. Neurol Sci. 2006;27 (2): 143-9. [Pubmed]
10. Sugama S, Kimura A, Chen W et-al. Frontal lobe dementia with abnormal cholesterol metabolism and heterozygous mutation in sterol 27-hydroxylase gene (CYP27). J Inherit Metab. Dis. 2001;24 (3): 379-92. [Pubmed]
11. Von bahr S, Björkhem I, Van’t hooft F et-al. Mutation in the sterol 27-hydroxylase gene associated with fatal cholestasis in infancy. J Pediatr Gastroenterol Nutr. 2005;40 (4): 481-6. [Pubmed]
12. Monson DM, Debarber AE, Bock CJ et-al. Cerebrotendinous xanthomatosis: a treatable disease with juvenile cataracts as a presenting sign. Arch Ophthalmol. 2011;129 (8): 1087-8. [Pubmed]
13. Huijgen R, Stork AD, Defesche JC et-al. Extreme xanthomatosis in patients with both familial hypercholesterolemia and cerebrotendinous xanthomatosis. Clin Genet. 2012;81 (1): 24-8. [Pubmed]
14. Berginer VM, Shany S, Alkalay D et-al. Osteoporosis and increased bone fractures in cerebrotendinous xanthomatosis. Metab Clin Exp. 1993;42 (1): 69-74. [Pubmed]
15. Chang WN, Lui CC. Failure in the treatment of long-standing osteoporosis in cerebrotendinous xanthomatosis. J Formos Med Assoc. 1997;96 (3): 225-7. [Pubmed]
16. Kuriyama M, Fujiyama J, Kubota R et-al. Osteoporosis and increased bone fractures in cerebrotendinous xanthomatosis. Metab Clin Exp. 1993;42 (11): 1497-8. [Pubmed]
17. Kuritzky A, Berginer VM, Korczyn AD. Peripheral neuropathy in cerebrotendinous xanthomatosis. Neurology. 1979;29 (6): 880-1. [Pubmed]
18. Kuriyama M, Fujiyama J, Yoshidome H et-al. Cerebrotendinous xanthomatosis: clinical and biochemical evaluation of eight patients and review of the literature. J Neurol Sci. 1991;102 (2): 225-32. [Pubmed]
19. Katz DA, Scheinberg L, Horoupian DS et-al. Peripheral neuropathy in cerebrotendinous xanthomatosis. Arch Neurol. 1985;42 (10): 1008-10. [Pubmed]
20. Vadapalli S. Cerebrotendinous xanthomatosis. Indian J Orthop. 2013;47 (2): 200-3. [Pubmed]
21. Meiner V, Meiner Z, Reshef A et-al. Cerebrotendinous xanthomatosis: molecular diagnosis enables presymptomatic detection of a treatable disease. Neurology. 1994;44 (2): 288-90. [Pubmed]
22. Brodsky JW, Beischer AD, Anat D et-al. Cerebrotendinous xanthomatosis: a rare cause of bilateral Achilles tendon swelling and ataxia. A case report. J Bone Joint Surg Am. 2006;88 (6): 1340-4. [Pubmed]
23. Nakamura T, Matsuzawa Y, Takemura K et-al. Combined treatment with chenodeoxycholic acid and pravastatin improves plasma cholestanol levels associated with marked regression of tendon xanthomas in cerebrotendinous xanthomatosis. Metab Clin Exp. 1991;40 (7): 741-6. [Pubmed]
24. Kuriyama M, Tokimura Y, Fujiyama J et-al. Treatment of cerebrotendinous xanthomatosis: effects of chenodeoxycholic acid, pravastatin, and combined use. J Neurol Sci. 1994;125 (1): 22-8. [Pubmed]
25. Watts GF, Mitchell WD, Bending JJ et-al. Cerebrotendinous xanthomatosis: a family study of sterol 27-hydroxylase mutations and pharmacotherapy. QJM. 1996;89 (1): 55-63. [Pubmed]
26. Peynet J, Laurent A, De liege P et-al. Cerebrotendinous xanthomatosis: treatments with simvastatin, lovastatin, and chenodeoxycholic acid in 3 siblings. Neurology. 1991;41 (3): 434-6. [Pubmed]

Infected Gouty Tophous at the Posterior Ankle, Leg, and Achilles Tendon in a Diabetic Patient: A Case Report

by Sutpal Singh, DPM, FACFAS, FAPWCA1, Long K. Truong, DPM2, pdflrgMaria Mejia, DPM3, W. Scott Davis, DPM4, Jennifer Chen, DPM5, Kamran Chaudhary, MD6, Marie Cleto-Quiaoit, MD7

The Foot and Ankle Online Journal 6 (5): 1

The clinical presentation of a diabetic patient with an open infected lesion and concomitant chronic tophaceous gout of the Achilles tendon is evaluated and treatment is described. The 42-year-old man suffered from chronic tophaceous gout with multilobular, solid, tender, enlarged subcutaneous nodules affecting the right hand and both feet. The patient was neuropathic and wearing tight shoes which resulted in laceration of the posterior skin near the soft tissue mass. This resulted in an infected ulcer and cellulitis. He was treated by incision and drainage with removal of the tophaceous mass from the Achilles tendon, sural nerve decompression, as well as debridement of the Achilles tendon.

Keywords: Achilles tendon, Gout, Diabetic foot, surgical debridement

Accepted: April, 2013
Published: May, 2013

ISSN 1941-6806
doi: 10.3827/faoj.2013.0605.001


Address correspondence to: Sutpal Singh, DPM, FACFAS, FAPWCA,
Currently at St. Alexius Medical Center, Hoffman Estates, IL

1Chief Ilizarov Surgical Instructor at Doctors Hospital West Covina, California.
2,3,4,5Residency, Doctors Hospital of West Covina, California. (PM&S 36).
6Greater Chicago Rheumatology, Chicago, Illinois.
7Pathologist, St Alexius Medical Center, Hoffman Estates, Illinois.


Gout is a condition characterized by deposition of monosodium urate crystals in tissues. Acute gout is preceded by elevated serum uric acid levels, although hyperuricemia is often not present during a gouty attack.[4] It is also important to note that most patients with hyperuricemia never experience a gout flare.[1]

As crystal deposition favors areas of the body with lower temperatures, and therefore further from the heart, it has a high tendency to affect the foot, particularly the first metatarsal-phalangeal joint, in about 56-78% of patients.[10] This is known as podagra. An acute gout flare is often characterized by a red, hot, and swollen joint that is very painful to touch, representing a similar clinical presentation as cellulitis.[4]

InfGtFig1a InfGtFig1b

Figure 1 Infected right posterior ankle and lower leg area.

Definitive diagnosis of acute gout is made by observation of negatively birefringent crystals in fluid aspirated from the affected joint. Joint aspirate analysis has been shown to have sensitivity of 85 percent and specificity of 100 percent.[2,13] In the absence of joint aspirate analysis, clinical diagnosis may be made based on meeting certain criteria which include podagra, hyperuricemia, history of monoarticular arthritis followed by asymptomatic periods, palpable tophi and knowledge of certain known co-morbidities associated with gout.[15]

Gout is a multifactorial condition, and as such, must be treated in a multifactorial manner. Gout is caused by altered purine metabolism, but other factors, including high purine diet, alcohol intake, and reduced renal clearance may also contribute. Therefore, lifestyle modification must be a part of any treatment regimen.[4] Acute gout attacks usually resolve without treatment within days to weeks. However, treatment can decrease the duration of an attack and decrease frequency of future attacks. NSAIDs (i.e. indomethacin), corticosteroids (i.e. Prednisone) and colchicine are first-line therapies in cases of acute gout. Colchicine is less commonly used due to the potential side effects.[4] Uric acid lowering agents are often used to treat chronic hyperuricemia.

InfGtMRIFig2a

Figure 2 Magnetic resonance image (MRI) of the right lower extremity shows a large mass engulfing the Achilles Tendon.

These agents are not started during an acute gouty attack, as they can exacerbate the symptoms. These include allopurinol, which is the most commonly prescribed, as well as probenecid and febuxistat (Uloric®, Takeda Pharmaceuticals U.S.A., Inc).[4] The primary treatment for tophaceous gout is to lower the uric acid level with dietary and medical therapy but this may not be easy to achieve therefore, surgical treatment maybe indicated. Surgical intervention has been shown to have a high incidence of complications6, therefore it is mainly recommended when tophi cause pain, skin necrosis, ulcerations, sinuses, nerve compression, interference with tendon function, or when joints are being destroyed and painful.[12]

InfGtFig3

Figure 3 Right hand.

It is important to distinguish gout from other conditions, as symptoms of acute gout may mimic those of other conditions, and vice versa. Septic arthritis may display the involvement of a single joint, with leukocytosis and elevated erythrocyte sedimentation rate (ESR). Septic arthritis and acute gout may even occur simultaneously.[1] This report describes a case of lower extremity infection in the presence of gouty tophi in a diabetic neuropathic patient with infiltration into the sural nerve.

Case Report

A 42-year-old diabetic patient was seen in the hospital for pus draining from the ankle and back of the leg. He said that he was wearing boots and that it may have cut the back of the leg several weeks ago. He noticed large amounts of pus draining from the posterior ankle and lower leg. He was subsequently admitted. His past medical history was significant for gout and insulin diabetes mellitus. Physical examination showed an infected abscess at the posterior ankle and leg on the right, with pus draining from the ulcerated area. (Fig 1) magnetic resonance imaging (MRI) shows the extent of infiltration of the tophus on the right lower extremity. (Fig 2)

InfGtFig4

Figure 4 Left posterior ankle without any infection.

On the right hand (Fig 3) as well as the left posterior ankle (Fig 4), there were indurated soft tissue masses for which the patient denied any pain. He had a large non-infected tophi on the left lower extremity.

Surgical Technique

The patient was placed in a prone position under general anesthesia with a thigh tourniquet. A curvilinear incision was made from the middle of the leg on the medial side, going inferiorly across the open wound and ulcer and then crossing over onto the inferior lateral heel area. The incision was deepened down to the subcutaneous tissue and then down to the deep tissue. There was a tremendous amount of brown pus draining from the wound area. Culture and sensitivity for gram positive, gram negative, anaerobic and aerobic organisms were performed. There was a large amount of adhesions noted at the subcutaneous and deep tissue. There was also a large soft tissue mass engulfing the Achilles tendon and sural nerve (Fig. 5 and Fig. 6). Neuroplasty of the sural nerve with surgical loupes was performed.

InfGtFig5 InfGtFig5b

Figure 5 Infiltration of the soft tissue mass engulfing the Achilles tendon.

The entire mass from the posterior, medial, lateral and anterior aspect of the Achilles tendon was removed. The Achilles tendon was also debrided of any degenerative tissue (Fig. 7 and Fig. 8). The necrotic skin was debrided and the skin edges were approximated using 3-0 ProleneTM, Ethicon Inc in simple as well as horizontal mattresses. The open wound area was loosely approximated and packed with Iodoform gauze. The surgical site was dressed with XeroformTM, Covidien, gauze, and KerlixTM, Covidien.

Discussion

Gout, a common metabolic disorder has increased in prevalence worldwide and is estimated to have doubled in the US alone within the last three decades.[9] Though gouty tophi are typically found in joints, it may also be present in tendons and soft tissue such as Achilles tendon, ear helices, sclera, and sub conjunctivae.[2] Despite many studies which report that gout may be found in these places, there are currently little to no studies reporting the epidemiology of gout present in places like the soft tissue or rearfoot.

InfGtFig6

Figure 6 Sural nerve entrapment (forceps) with the soft tissue mass.

In this case study, we reported on an infected tophaceous wound. (Fig 7) Histology of the mass is shown in Fig 9-12. Culture and sensitivity revealed infiltration by Streptococcus agalactiae, also known as Group B streptococcus or GBS, which is a beta-hemolytic Gram-positive streptococcus. Though rare, it is important to note that tophi, when left untreated for a long duration, may accumulate and can lead to ulceration which can become infected. A 2011 case study reported a patient who was noncompliant with his allopurinol regimen, and resulted in a tophaceous ulcerated nodule overlying the dorsal first and second metatarsophalangeal joint of the left foot.[5]

InfGtFig7

Figure 7 Removal of the soft tissue mass. Gross description: 17.2 gm of dark brown to pale yellow soft tissue mass. Sectioning reveals cystic mass with chalky white substance.

The nodule and resulting ulceration were so large that amputation of the left foot was strongly considered.[5] Though bacterial cultures were negative for septic arthritis in this case, ciprofloxacin was given as prophylaxis and the patient healed well with adequate surgical debridement. [5]

It is important to monitor gout, especially in manifestations at the Achilles tendon because if left untreated it may exhibit traumatic effects. Though not as common as in the joints, tophi have been known to be found in the Achilles tendon. A 1981 case study of an acute Achilles rupture alluded to the rupture possibly being caused by gout with deposits consistent with tophi found throughout the tendon, especially at the rupture site.[14]

Often times when assessing the aspirate of a red, hot, swollen joint, if synovial crystals are found a diagnosis of a crystal arthritis such as gout or CPPD is automatically assumed. However, a retrospective study based at a US urban medical center looked at records of all the joint synovial crystal aspirates from a seven year span, containing a total of 265 synovial crystal joint aspirates.[11]

InfGtFig8

Figure 8 Surgical appearance after removal of the mass from the Achilles tendon as well as debridement of the Achilles tendon.

Of those 265 aspirates, 4, or 1.5%, came back positive for bacterial cultures confirming concomitant septic arthritis with crystal arthritis.[11] While this may seem a small amount, if left untreated may have deleterious effects on the patient.

Another study of 30 cases of concomitant septic and gouty arthritis in 2003 from Taiwan stated that wounds as the result of subcutaneous tophi rupture were the most common source of concomitant septic and gouty arthritis, with the most common infectious organism being Staphylococcus aureus.[14] Fourteen went on to receive surgical debridement with 9 having no reported complications.[14]

InfGtFig9

Figure 9 Low power of chronic gouty inflammatory reaction with foreign body giant cell proliferation.

InfGtFig10

Figure 10 Formalin Fixation has destroyed the uric acid crystals to leave amorphous eosinophilic material. Note the multinucleated giant cells indicating chronic inflammatory process (upper right).

With the degeneration in Western diet consisting of increased intake of fast food, soft drinks, and meat it is no surprise that gout and diabetes are common co morbidities. A 2008 study based at the University of Pennsylvania Medical Centre expanded on the notion that hyperuricemia, gout, and metabolic syndrome are associated with each other. This suggests that gout in men with a high cardiovascular risk profile is at a higher risk of developing type 2 diabetes.[3]

InfGtFig11

Figure 11 Low power of acute gouty inflammation showing gouty casts.

InfGtFig12

Figure 12 Note the inflammatory neutrophils.

When dealing with diabetic patients, wounds and resulting infection can lead to limb loss or even death.[9] Therefore it is pertinent to monitor both gout and diabetes, because gout left untreated could be a means for ulceration.

InfGtFig13

Figure 13 Several months after surgery shows complete healing with good Achilles tendon strength.

The case study presented in this article highlighted the significance of the necessity of a thorough examination for patients with numerous risk factors. While our outcome was positive (Fig 13), without a thorough debridement and attentive follow up, this case had the potential to result in a below the knee amputation. This is especially true with the known potentially poor healing capacity of diabetics. Moreover, it vital that in order to prevent recurrence patients with gout must be tightly controlled.

Conclusion

As discussed before, infected gouty tophus of the Achilles tendon is a rare finding even though gout commonly affects the foot and ankle. A thorough history and physical examination with assistance of advanced diagnostic tools and laboratory studies is essential to properly diagnose this condition. Differential diagnosis of gout should always be considered in patients with a history of hyperuricemia even if symptoms are masked by cardinal signs of infection. Medical and surgical therapy has been reported to successfully treat this condition. Our case report demonstrates good prognosis with early recognition and successful surgical debridement.

References

1. Becker M. Clinical manifestations and diagnosis of gout. In: UpToDate. Basow DS (Ed), Waltham, MA, 2012.
2. Chen LX, Schumacher HR. Current trends in crystal identification. Current Opinion  Rheum 2006 18: 171-73. [PubMed]
3. Choi HK, De Vera MA, Kishnan E. (2008). Gout and risk of type 2 diabetes among men with a high cardiovascular risk profile. Rheumatology 2008  47: 1567-1570. [PubMed]
4. Eggebeen AT. Gout: an update. American family Physician 2007 76: 801-808. [PubMed]
5. Falidas E, Rallis E, Bournia V, Mathioulakis S, Pavlakis E, Villas C. Multiarticular chronic tophaceous gout with severe and multiple ulcerations: a case report. J Medical Case Reports 2011 5: 1-4. [PubMed]
6. Kumar S, Gow P. A Survey of indications, results, and complications of surgery for tophaceous gout. J New Zealand MedAssoc 2002 23: 115(1160). [PubMed]
7. Larmon WA,  Kurtz JF. The surgical management of chronic tophaceous gout. JBJS 195840 :743-772. [PubMed]
8. Mahoney PG, James PD, Howell CJ, Swannell AJ.  Spontaneous rupture of the Achilles tendon in a patient with gout. Annals Rheumatic Dis 1981 40: 416-418. [PubMed]
9. Ramsey SD, Newton K, Blough D, McCullouch DK, Sandhu NS, Reiber GE, Wagner EH. Incidence, outcomes, and cost of foot ulcers in patients with diabetes. Diabetes Care 1999 22: 382-387. [PubMed]
10. Roddy E. Revisiting the pathogenesis of podagra: why does gout target the foot? JFAR 2011 4:13. [PubMed]
11. Shah K, SpearJ, Nathanson LA, McCauley J, Edlow JA.  Does the presence of crystal arthritis rule out septic arthritis? J Emergency Med 2007 32: 23-26. [PubMed]
12. Terkeltaub R. (2010). Update on gout: New therapeutic strategies. Nature Reviews: Rheumatology 2010 6: 30-38.[PubMed]
13. Wallace SL, Robinson H, Masi AT,  Decker JL, McCarty DJ, Yü T. Preliminary criteria for the classification of the acute arthritis of primary gout. Arthritis Rheumatism 1977 20:  895-900. [PubMed]
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15. Zhang W. EULAR evidence based recommendations for gout. Part I: Diagnosis. Report of a task force of the standing committee for international clinical ctudies including Therapeutics (ESCISIT). Annals Rheumatic Dis (2006) 65: 1301-311.  

Management of Open Chronic Tendo Achilles Injuries: A case report

by Anil Thomas Oommen MS Orth1 , Pradeep Mathew Poonnoose MS Orth2 ,
Debabrata Padhy MS Orth3 , Ravi Jacob Korula MS Orth4

The Foot and Ankle Online Journal 3 (1): 2

Delayed presentation of an open Tendo Achilles injury with segmental loss of tendon and soft tissue is a challenging problem for the Orthopaedic surgeon. We present a patient who presented with a 4 x 5 cm open wound and a 4cm segmental loss of the tendon 6 months after the injury. To bridge the defect in the tendon, lengthening of the proximal tendon was done using a tongue in groove sliding technique, and a reverse sural artery flap was used to cover the soft tissue defect. At 9 months follow up, the patient was able to perform a single limb toe stance. The technique and the relative merits of this simple procedure are discussed.

Key words: Achilles tendon, Sural artery flap, Bakers slide, Tendo Achilles, tendon rupture.

Accepted: December, 2009
Published: January, 2010

ISSN 1941-6806
doi: 10.3827/faoj.2010.0301.0002


Open Tendo Achilles injuries commonly occur following cycle spoke injuries or after a fall into ‘Indian style’ closets. [1] If patients present within 6 to 12 hours of the injury a thorough wash followed by primary or delayed repair of the tendon can be done. Management of delayed presentation of open Tendo Achilles injuries is more complex, as there is a loss of soft tissue cover in addition to the tendon defect.

An effective surgical procedure is required to bridge the defect in the Tendo Achilles, as well as to achieve adequate soft tissue cover. [1,2] A number of procedures have been described for reconstruction of the Tendo Achilles. These include lengthening the aponeurotic tendon either in a ‘tongue in groove’ fashion as described by Baker, or the V-Y technique popularized by Abraham and Pankovich. [1,2] The other methods described for repair of neglected rupture include augmentation with the peronei (Teuffer’s modification of White and Kraynick technique), or with a strip from the median raphe of the proximal tendon (Bosworth’s technique). [2] Management of the defect in an open injury is more complex because of the associated loss of soft tissue cover. The use of vascularised extensor digitorum brevis and various composite free flaps have been described for such defects. [2] These require the expertise of a micro vascular surgeon.

We present the case of a patient who presented with a 4 x 5 cm open wound and a 4 cm segmental loss of the tendon six months following a fall. Following a thorough debridement, we opted to bridge the defect by lengthening the tendon with a Baker’s procedure, and cover the skin defect with a reverse sural artery flap. The technique and relative merits of this simple procedure are discussed.

Surgical Procedure

With the patient in prone position, the wound was debrided and the residual skin defect measured. Swabs taken from the wound confirmed the absence of active infection.

The reverse sural artery flap was elevated before the tendon was lengthened. (Fig 1) The flap was marked proximally on the calf, with the edges 0.5 cm more than the measured recipient area.

Figure 1  Presentation of injury. Elevation of the reverse sural artery flap, with insert (A) showing the skin defect over the ruptured Tendo Achilles. The flap has been cut back to a bleeding edge.

The small saphenous vein, sural artery and nerve were cut at the proximal edge of the flap and raised along with the fascio-cutaneous flap. The deep fascia was anchored to the epidermis prior to elevating the flap, in order to prevent shearing between the deep fascia and the skin. Distally, the incision was extended up to the medial border of the wound. Laterally, the flap was raised to 7.5 cm short of the lateral malleolus, in order to preserve the perforators from the peroneal artery that supply the elevated flap. At this stage, the tourniquet was released, and bleeding from the flap edge was noted. As the bleeding from the leading edge of the flap was inadequate, the flap had to be cut back until a bleeding edge was obtained. (Fig. 1) The flap was then turned over its pedicle, and laid over the defect.

Following the elevation of the flap, the aponeurosis and tendinous portion of the Tendo Achilles was exposed. The proximal edge of the defect was freshened, and a no. 5 ethibond (ETHICON, Inc.) Bunnel suture was passed through the distal end of the tendon. Care was taken not to disturb the mesotenon near the defect. A ‘tongue in groove’ lengthening of the tendon was done at the musculotendinous junction. For the defect of 4 cm, a 9 cm cut was made in the aponeurosis, to ensure adequate overlap after the lengthening. Traction was applied to the tendon with the ethibond suture to lengthen the tendon, and the defect was closed with the ankle in 10 degrees of plantarflexion. (Fig. 2)

Figure 2 Repair of the tendon using a ‘tongue in grove lengthening’ of the aponeurosis.

There was no distal remnant of the Tendo Achilles, and hence the tendon was anchored on to the calcaneum directly. The insertion site on the calcaneum was freshened, and the ethibond suture was threaded through the calcaneum using a Beath pin, and anchored tightly onto the sole of the foot over a button. (Fig. 2) Additional bony sutures were placed between the tendon and the calcaneum.

After anchoring the tendon, the flap was rotated and sutured over the defect. Multiple corrugated drains were used under the flap to ensure good drainage. The donor site was covered with split thickness skin graft. An anterior plaster splint was applied to keep the ankle in plantarflexion. Once the sutures were removed after 2 weeks, the leg was casted in 20 degrees of flexion at the ankle for 2 months, followed by another 2 months in neutral position. The button used to anchor the ETHIBOND suture was removed at 4 months. He was then allowed to bear weight, though the repair had to be protected with a cast for another 2 months. At 9 months, he was able to perform a single limb toe stance. (Fig. 3)

Figure 3 Nine months following surgery, the patient was able to stand on one leg without support.

Discussion

Delayed presentation of open Tendo Achilles injuries require careful repair of the tendon defect, and adequate soft tissue cover. [1,2] Reconstruction of the defect can be challenging, as the blood supply of the Tendo Achilles at its insertion is extremely poor. [3] The reconstruction of Tendo Achilles injuries require meticulous handling of the remnant segments. The mesotenon of the tendon segment near the defect should be preserved in order to maintain vascularity and achieve healing at the site of reconstruction. [3] Bosworth advocated elevation of a full thickness central strip of the proximal tendon, which is turned over and sutured to the distal end of the defect. The ‘turned over’ section of the graft has poor vascularity, and the healing at the repair site could potentially be compromised.

If the defect is bridged by lengthening the tendon proximally, the dissection of the mesotenon near the defect is less extensive, and hence the vascularity at the repair site is relatively well preserved. The repair is more biological and is more appropriate for reconstruction of the Tendo Achilles. The repair is also less bulky near the insertion site.

For protection of the reconstructed tendon, a full thickness soft tissue cover is necessary, as split thickness skin graft is unlikely to heal over the repair site.

The options for soft tissue cover include free vascularised composite tensor fascia lata flap, medial plantar flap with plantar aponeurosis or a free flap. [1,4] These free flaps often require micro vascular expertise.

The reverse sural artery flap is a neuro-cutaneous flap that has the advantages of having a fairly constant blood supply with associated ease of elevation and preservation of major vascular trunks in the lower extremity. [2,3] This flap is based on the distribution of the sural nerve and the retrograde perfusion is maintained by the anastomoses of the cutaneous perforating branches of the peroneal artery and the median superficial sural artery. [2,3]

This flap remains the workhorse for soft tissue cover over the posterior distal third of the leg and heel. [2,3] It is a relatively simple flap that can be performed by most orthopaedic surgeons. [2,4] The Tendo Achilles slide can be done through the same incision used for elevation of the flap. The resultant flap is however, often quite bulky. Where expertise is available, an adipo-fascial flap can be used to make the repair more aesthetic. [1]

Conclusion

The sliding technique for bridging defects in the Tendo Achilles followed by a reverse sural artery flap is an excellent option for management of delayed presentation of open Tendo Achilles injuries.

Acknowledgements

No benefits in any form have been received or will be received from any commercial party related directly or indirectly to the subject of this article.

References

1. Mohanty A, Jain P: Reconstructing and resurfacing open neglected Achilles tendon injury by distal posterior tibial artery based adipofascial flap. Eur J Plastic Surgery 27: 196 – 199, 2004.
2. Bullocks JM, Hickey RM, Basu CB, Hollier LH, Kim JY: Single-stage reconstruction of Achilles tendon injuries and distal lower extremity soft tissue defects with the reverse sural fasciocutaneous flap. J Plast Reconstr Aesthet Surg 61(5): 566 – 572 , 2008.
3. Carr AJ, Norris SH: The blood supply of the calcaneal tendon. J Bone Joint Surg 71B (1):100 – 101, 1989.
4. Jeng SF, Wei, FC: Distally based sural island flap for foot and ankle reconstruction. Plastic and Reconstructive Surgery 99 (3): 744 – 750,1997.


Address Correspondence to : Anil Thomas Oommen, Assistant Professor, Unit 2,Department of Orthopaedics,Christian Medical College and Hospital, Vellore, India, 632004 Email : lillyanil@cmcvellore.ac.in

Assistant Professor,Unit 2, Department Of Orthopaedics, Christian Medical College and Hospital, Vellore 632004, India +914162282172.
Associate Professor, Unit 2, Department Of Orthopaedics, Christian Medical College and Hospital, Vellore 632004, India +914162282173.
Assistant Professor,Unit 2, Department Of Orthopaedics, Christian Medical College and Hospital, Vellore 632004, India +914162282081.
Professor and Head, Unit 2, Department Of Orthopaedics, Christian Medical College and Hospital, Vellore 632004, India +914162282167.

© The Foot and Ankle Online Journal, 2010

The Achilles Musculotendinous Junction: A Survey of Orthopaedic Surgeons

by Richard Cove1 , David Weller2, Mark Westwood3

The Foot and Ankle Online Journal 2 (12): 4

Background: Achilles tendon rupture is a common injury, which can frequently affect young, active people. Consequently, there are important socio-economic implications in choosing the correct treatment. There is considerable debate in the literature concerning surgical versus non-surgical treatment and most surgeons would elect not to repair a rupture within the muscle belly above the musculotendinous junction. There is a wide anatomical variation in the exact location of the Achilles musculotendinous junction, which can lead to confusion among surgeons when trying to identify the location of a rupture and treatment plan.
Materials and Methods: Delegates at a regional orthopaedic meeting were asked to fill in a questionnaire, which showed a photograph of a lower limb. They were asked to draw two transverse lines, the first identifying the musculotendinous junction, and the second marking the highest level at which they would consider a surgical repair. They were asked about their understanding of the term “musculotendinous junction”.
Results: Twenty two delegates (n =22) of various degrees of seniority responded. There was a wide variety of answers, with the average level of the musculotendinous junction identified as being 10.1cm above the insertion into the calcaneum. The average highest level for considering surgical intervention was 8.71cm above the insertion into the calcaneum. Cadaveric measurements have shown that in fact the Achilles musculotendinous junction lies on average 5.51cm above the tendons attachment to the calcaneum.
Conclusion: There is confusion regarding the exact location and nature of the Achilles musculotendinous junction among the orthopaedic surgeons in our survey. Although most surgeons stated that they would not operate on a rupture above the musculotendinous junction, almost all identified a point higher than this region as their highest point for repair. Particular care is advised if an ultrasound reports the location of any rupture relative to the musculotendinous junction.

Key Words: Achilles tendon, rupture, surgical repair, conservative treatment, musculotendinous zone.

Accepted: November, 2009
Published: December, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0212.0004


The most common site for Achilles tendon rupture is 2-6cm from the calcaneal insertion, [1,2] although avulsion fractures of the os calcis have been described. [3] The Achilles tendon rupture is a common injury, affecting approximately 18 in 100,000 people [4,5], typically males between 30 and 50 years of age.

There is considerable debate in the orthopaedic literature about the benefits of surgical versus conservative treatment. However, it is generally accepted that surgical repair offers a lower rate of re-rupture, and conservative treatment avoids wound complications. [4,6,7] Many surgeons would elect to treat a rupture proximal to the musculotendinous junction (i.e. within the muscle belly) conservatively. The aim of this study was to investigate the confusion among surgeons of the exact nature and location of the musculotendinous junction.

Subjects and Methods

Delegates at the 2008 British South West Orthopaedic Club (SWOC) were asked to fill in an anonymous questionnaire, which showed a photograph of an exposed lower leg (male, 177cm tall – age and weight of the subject?). They were firstly asked their level of seniority, and then asked to draw two lines on the photograph; the first (labeled “line 1”) at the level of musculotendinous junction, and the second (labeled “line 2”) at the upper limit of where they thought surgical repair of an Achilles tendon rupture could be beneficial. They were also asked what they understood by the term “musculotendinous junction” for the Achilles tendon, and what they considered as the clinical significance of this junction.

The original photograph included a tape measure which was cropped out of the image shown to the delegates. The exact location of the Achilles tendon insertion was established using ultrasound and a mark on the subjects’ skin, which was digitally removed on the image shown to the delegates. A scaled ruler was used to directly measure the delegates’ markings on the photograph.

Results

Twenty-two (out of 35) surgeons returned a completed form- 7 Consultants (2 with an interest in foot and ankle surgery), thirteen Specialist registrars (SpR), 1 Associate Specialist, 1 ST1 trainee, and 1 respondent not specifying their grade.

The average level at which the musculotendinous junction was identified was 10.1cm (Standard Deviation [SD] 3.9cm) above the calcaneal attachment, with the average for consultants slightly higher than SpRs, at 11.5cm and 8.8cm respectively. The average highest level at which people thought surgery would be beneficial was 8.7cm (SD 2.7cm), with little difference between consultants and SpRs (8.8cm compared to 8.6cm). This meant that overall, those that responded thought that the highest level at which a patient might benefit from surgery was on average 1.4cm (SD 1.4cm) below the level of the musculotendinous junction.

There was a wide disparity in answers, with levels identified for the musculotendinous junction varying between 5.5cm and 24.5cm, with the level identified for considering surgery varying between 5.5cm and 17.5cm. The variation in differences between the two levels was also large, from people identifying the highest level for surgery at 3.5cm below the musculotendinous junction through to 2.5cm above it.

When asked what their understanding of the term “musculotendinous junction” was, virtually all respondents stated that it was where the muscle fibres were replaced by tendon, with a few people identifying it as a zone of transition rather than a discrete “junction”. When asked what they felt its clinical significance was, comments varied from “the muscle enhances healing/vascularity”, “the suture in the muscle belly is less likely to hold”, to “nil”, and “arbitrary”. However, most comments (thirteen out of twenty two) suggested that tears above the musculotendinous junction should be treated non-operatively, with comments such as “ruptures proximal to this don’t benefit from surgery”, and “repair at or above will be difficult due to suture cut out”. The results are summarized in figures 1 and 2.

Figure 1 Survey Results.

Figure 2 Results Key.

Discussion

In 2007 Pichler, et al. [8], directly measured the distance from the soleus musculotendinous junction to the attachment of the tendon to the posterior surface of the calcaneal tuberosity in series of cadavers.

Although they reported a wide anatomical variation, ranging from 0 to 11.75cm, they showed that the overall average distance was 5.51cm, with 70% of their subjects having a musculotendinous junction between 2.54cm and 7.62cm from the attachment to the calcaneus. [8] This is considerably lower than the level identified by the surgeons in our survey (where the average was 10.1cm). This suggests that orthopaedic surgeons consistently overestimate the level of the musculotendinous junction. This disparity is of concern as it may lead to misinterpretation of ultrasound reports that make reference to the musculotendinous junction.

It is interesting to note that the surgeons surveyed are prepared to consider operative repair more proximal than the anatomical musculotendinous junction. It would suggest that there is adequate quality tendon to repair proximally. This is despite the fact that the majority of respondents defined the musculotendinous junction as a level beyond which sutures would not hold.

We would suggest that the term musculotendinous junction should continue to define the point at which the last fibres of soleus attach to the Achilles tendon. Proximal to this there is a ‘musculotendinous zone’. This study has identified an ‘Achilles surgical zone’ which is approximately 0-10cm from the calcaneal insertion. Further research is required to discover the true value of surgery for high Achilles ruptures.

In the light of our findings, and bearing in mind the considerable anatomical variation identified by Pichler, et al., [8] we suggest that, to avoid confusion, any ultrasound scan on a suspected Achilles tendon rupture should identify the level of a rupture relative to the calcaneal insertion.

References

1. Carr AJ, Norris SH: The blood supply of the calcaneal tendon. J Bone Joint Surg 71B:100 – 101, 1989.
2. Lagergren C, Lindholm A: Vascular distribution in the Achilles tendon. Acta Chir Scand 116: 491 – 495, 1958/59.
3. Arner O, Lindholm A: Avulsion fracture of the os calcaneus. Acta Chir Scand 117: 258 – 260, 1959.
4. Khan RJK, Fick D, Keogh A, Crawford J, Brammar T, Parker M: Treatment of acute Achilles tendon ruptures. J Bone Joint Surg 87A (10) 2202 – 2209, 2005.
5. Bhandar M, Guyatt GH, Siddiqui F, Morrow F, Busse J, Leighton RK, Sprague S, Schemitsch EH: Treatment of acute Achilles tendon ruptures: a systematic overview and metaanalysis. Clin Orthop Relat Res. 400:190-200, 2002.
6. Lea RB, Smith L: Non-Surgical Treatment of Tendo Achilles Rupture. J Bone Joint Surg 54A (7): 1398 – 1407, 1972.
7. Strauss EJ, Ishak C, Jazzrawi L, Sherman O, Rosen J: Operative treatment of acute Achilles tendon ruptures: An institutional review of clinical outcomes. Injury 38: 832 – 838, 2007.
8. Pichler W, Tesch NP, Grechenig W, Leithgoeb O, Windisch, G: Anatomical variations of the musculotendinous junction of the soleus muscle and its clinical implications. Clin Anat 20: 444 – 447, 2007.


Address Correspondence to: Richard Cove FRCS(orth)
Email: richard_cove@yahoo.com

Orthopaedic Registrar, Royal Cornwall Hospital, Truro, UK.
Orthopaedic SHO, Derriford Hospital, Plymouth. UK.
Othopaedic Consultant, Plymouth. UK.

© The Foot and Ankle Online Journal, 2009

Surgical Correction of Subluxing Peroneal Tendons Utilizing a Lateral Slip of the Achilles Tendon: A case report

by Mark Mendeszoon, DPM, FACFAS, FAFAOM,1 , J. Todd McVey, DPM2, Adam MacEvoy, DPM3  

The Foot and Ankle Online Journal 2 (8): 3

Subluxation of the peroneal tendon can be either an acute or chronic condition. As an acute injury, it can quite often be misdiagnosed as a lateral ankle sprain. This case report describes a technique using the lateral slip of the Achilles tendon as a retinacular graft to repair subluxation and dislocation of the peroneal tendons.

Key words: Tubularization, Achilles tendon graft, modified Brostrom repair, subluxation, dislocation, peroneal tendons.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot and Ankle Online Journal (www.faoj.org)

Accepted: July, 2009
Published: August, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0208.0003

 


The peroneal tendons course around the lateral ankle at the distal aspect of the fibula. These tendons which include the tendons of the peroneus longus and brevis move through a tunnel created of both fibrous and osseous structures. [2] The borders of this tunnel include the lateral malleolus, posterior talofibular ligament, calcaneal fibular ligament, and superior peroneal retinaculum. Both tendons run together until they are distal to the fibula where they split and enter separate sheaths. Most important to us is the superior peroneal retinaculum (SPR) which is the primary restraint to subluxation and dislocation of the peroneal tendons. [1,8,9]

 

First Described in 1803 by Monteggia, peroneal subluxation and dislocation can be categorized as either acute or chronic injuries. Most acute injuries are caused by a sudden dorsiflexion and inversion of the ankle while the peroneals are contracting. Acute injuries occur most often during sporting activities.

The most common injury occurs during downhill skiing. If the injury is left untreated, it can lead to chronic pain or ankle pain that will require surgical correction. Pain is caused by splitting or fraying of the peroneal tendons which occur when the tendon continues to sublux over the posterior lateral edge of the fibula causing micro tears to the tendon. Chronic injuries are also associated with patients who are prone to multiple ankle sprains. These sprains can lead to lateral ankle weakness which can lead to inflammation of the peroneal tendon sheath. [6,8,9] The sustained inflammation of the sheath can lead to weakening and stretching of superior peroneal retinaculum which will allow the peroneal tendons to leave the peroneal tunnel. Echard and Davis created a classification system for peroneal subluxation.

This system includes for subtypes which are as follows:

I-Periosteum is elevated form underlying malleolus.
II-Superior peroneal retinaculum is torn from the anterior insertion.
III-Superior peritoneal retinaculum is avulsed with a small piece of bone.
IV-Superior peroneal retinaculum is avulsed from posterior attachment and tendon dislocates.

Conservative treatment of this condition can be used however the literature shows there is a high failure rate for this course of action. [2] Most conservative treatment includes casting for 4-6 weeks. Other treatment includes taping which as a lower success rate than casting. Usually primary repair is indicated for tears in the tendon involving 50% or less. [11] Considering the majority of these patients are athletes, most want a speedy return to activity and expect a high success rate. [1,8,9,10]

Case Report

A male patient reported that he was racing his motocross bike when he landed a jump with his foot in an awkward position. He recalls extreme pain at his ankle and noted that a bone was protruding under his skin, which he states that he pushed the bone back in to place and went to the emergency room (ER).

At the ER it was noted that patient had significant swelling, pain on palpation, ecchymosis, popping sensation along with extreme instability. Patient was immobilized, obtained a magnetic resonance image (MRI) and sent to the office the next day for consultation. After educating the patient on conservative and surgical options, the patient chose the latter. MRI showed extreme poster lateral edema, and anterior talofibular ligament (ATFL) tear, avulsion fracture of fibula, with a high suspicion of SPR tear.

Clinical evaluation reveals a 5’11” male who is 195 lbs. The patient’s neurovascular status remains intact. There is significant ecchymosis, positive Mondor sign, pain on palpation of fibula, pain with range of motion and the fibula is mobile at the lateral ankle. Stress films in the operating room while the patient is under general anesthesia reveals a positive anterior drawer and talar tilt.

Surgical Technique

An incision is made over the lateral aspect of the leg following the peroneal tendons, approximately 10-12cm in length. (Fig 1.) Significant hematoma and disruption of the tissue is encountered during blunt dissection. The peroneal tendon sheath is completely ruptured, and the peroneus brevis is lying on top of the lateral aspect of the fibula. The peroneal retinaculum is ruptured with an associated fleck of bone. On closer inspection, the peroneal groove is noted to be disrupted, rough, and shallow.

Figure 1  10-12 cm incision along the peroneal tendons.

The calcaneofibular ligament is intact and stable, and the posterior capsule gapped open. The ATFL is attenuated and the origin is slightly disrupted. The peroneal tendons are intact distally.

The damaged peroneal tendon are then tubularized using #2 fiber wire and placed back onto the fibular groove (Figs. 3,4). Subluxation and popping of the tendon is still noted. Because of this a reconstruction using the lateral 20% of the Achilles tendon is performed. A transverse incision is made into the Achilles tendon approximately 8 cm proximal to the insertion. The tendon is split distally and dissected through blunt means and used to protect the sural nerve and lateral structures. The low-lying muscle belly of the peroneus brevis, which is dissected away from the tendon just enough to pass the Achilles slip through its course. (Fig. 2) The cut end of the Achilles tendon is passed under the muscle belly of the peroneus brevis and over the peroneus longus and brevis tendons. (Figs. 5 and 6)

Figure 2  Resection of low lying muscle belly.

 

Figures 3 and 4 Repair of the peroneal tendons through tubularization.

 

Figures 5 and 6  A tunnel is made through the peroneus brevis muscle belly and the slip of the Achilles tendon is then passed over the peroneal tendons.

This bridge of tendon over the peroneal tendons is then anchored to the lateral malleolus using an Arthrex® bioabsorbable anchor. (Figs. 7,8 and 9) At completion of this reconstruction, there is no sign of subluxation of the peroneal tendons.

The wound is then irrigated and a modified Brostrom technique is used to repair and tighten the ligaments in a pants-over-vest fashion. This greatly increases the tension strength of the repair. The wound is then closed in layers.

  

Figures 7, 8 and 9  Bone anchor is used to anchor the repair.  The procedure is strengthened with a Modified Brostrom repair.

Discussion

There have been many options reported for surgical repair of peroneal subluxation or dislocation. These include direct repair of peroneal retinaculum, reconstruction of peroneal retinaculum, bone block (lateral malleolus, sliding graft), and groove deepening and rerouting procedures. [1,2,4,6,9]   Each of these procedures have their strengths and weaknesses. Acute repair of the superficial peroneal retinaculum is a simple repair however it may not be able to fix the underlying problem if there is a shallow grove, or the superior peroneal retinaculum itself is inherently weak due to prolonged inflammation. Reconstruction of the peroneal tendon can be accomplished using the peroneus brevis, plantaris, and/or Achilles tendons. There have been few studies reported on these techniques. A concomitant soft tissue procedure is a rerouting technique using the calcaneal fibular ligament. Bone block procedures incorporate part of an osteotomy used to deepen the fibular grove. This was first described by Kelly, and then modified by DuVries. [1,6,9,10] Complications associated with these techniques include graft fracture, tendonitis, pain and re-subluxation. Groove deepening procedures are performed by removing bone from the posterior aspect of the fibula. The result of deepening this grove is a more stable tunnel for the peroneus brevis and longus tendon sheath for gliding.

Peroneal tendon subluxation and dislocation is a condition which can be easily misdiagnosed as an ankle sprain and may cause a chronic painful condition requiring surgical intervention. As foot and ankle specialists we need to have a high suspicion, particularly in the younger athletic patients prone to such injuries.  The two most inherent causes of peroneal subluxation are multiple lateral ankle sprains and a shallow peroneal grove at the distal aspect of the tibia. Conservative treatment for this condition does not report a high success rate. The patient healed satisfactorily utilizing a lateral slip of the Achilles tendon in a tissue transfer technique and at the short term 6 month post op visit the patient had no complaints of pain.

References

1. Butler BW, Lanthier J, Wertheimer SJ: Subluxing peroneals: A review of the literature and case report. J Foot Ankle Surg 32: (2):134 – 139, 1993.
2 Oliva F, Ferran N, Maffulli N: Peroneal retinaculoplasty with anchors for peroneal tendon subluxation. Bull Hosp Joint Disease 63: (3 – 4): 113 – 116, 2006.
3. Ferran NA, Maffulli N, Oliva F: Management of recurrent subluxation of the peroneal tendons. Foot Ankle Clinics 11: (3) 465 – 474, 2006.
4. Kollias SL, Ferkel RD: Fibular grooving for recurrent peroneal tendon subluxation. Am J Sports Medicine 25: (3):329 – 335, 1996.
5. Brage ME, Hansen ST Jr: Traumatic subluxation/dislocation of the peroneal tendons. Foot Ankle Online 13: (7): 423 – 431, 1992.
6. Tan V, Lin SS, Okereke E: Superior peroneal retinaculoplasty: a surgical technique for peroneal subluxation. Clinical Ortho Rel Res [serial online] 410: 320 – 325, 2003.
7. Krause JO, Brodsky JW: peroneus brevis tendon tears: Pathophysiology, surgical reconstruction, and clinical results. Foot Ankle Int 19: (5): 271 – 279, 1998.
8. Ferran NA, Maffulli N, Oliva F: Management of recurrent subluxation of the peroneal tendons. Foot Ankle Clinics [serial online]11: (3):465 – 474, 2006.
9. Niemi WJ, Savidakis J Jr, DeJesus JM: Peroneal subluxation: a comprehensive review of the literature with case presentations. J Foot Ankle Surg 36: (2): 141 – 145, 1997.
10. Porter D, McCarroll J, Knapp E, Torma J: Peroneal tendon subluxation in athletes: fibular groove deepening and retinacular reconstruction. Foot Ankle Int 26: (6): 436 – 441, 2005.
11. Heckman DS, Reddy S, Pedowitz D, Wapner KL, Parekh SG: Operative treatment for peroneal tendon disorders. J Bone Joint Surg 90A: (2): 404 – 418, 2008.
12. Mendicino RW, Orsini RC, Whitman SE, Catanzariti AR: Fibular groove deepening for recurrent peroneal subluxation. J Foot Ankle Surg 40: (4):252 – 263, 2001.


Address correspondence to:Adam MacEvoy, DPM. PGY III, Department Of Veterans Affairs. Louis Stokes Cleveland Medical Center. Podiatry Surgery . Cleveland Ohio 44106. (216) 791-3800 Ext 5891

1 Precision Orthopedics, 150 7th Ave, Chardon , Ohio 44024.
2 Department Of Veterans Affairs. Louis Stokes Cleveland Medical Center
Podiatry Surgery. Cleveland, Ohio 44106.
3 PGY III, Department Of Veterans Affairs. Louis Stokes Cleveland Medical Center. Podiatry Surgery . Cleveland, Ohio 44106.

© The Foot and Ankle Online Journal, 2009

Aberrant Tendo-Achilles Tendon in Club Foot: A case report

by J. Terrence Jose Jerome, MBBS, DNB (Ortho), MNAMS (Ortho)1, Mathew Varghese, M.S. (Ortho)2, Balu Sankaran, FRCS, FAMS3, Rajendra Kumar Gupta4, Simon Thomas, MBBS, DNB (Ortho), MNAMS (Ortho)5, Amit Mittal6

The Foot & Ankle Journal 2 (2): 2

This case report discusses the presentation and treatment of a baby boy with club foot deformity. He was initially treated by Ponseti’s method of weekly plaster of paris casting. The club foot did not reduce after 6 weeks of serial casting. The boy then underwent percutaneous Achilles tendon lengthening and placed in a Steinbek Splint. After 12 weeks, the equinus persisted and we decided to perform an open Achilles lengthening. An aberrant tendo-achilles tendon was discovered during open tenotomy and this was released. Once the aberrant tendon was released, the club foot reduced and at 9 months, the baby could walk with good heel strike and the foot was supple with no residual deformity.

Key words: Aberrant tendo-Achilles tendon, club foot, talipes equinus, Ponseti’s casting method

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: January, 2009
Published: February, 2009

ISSN 1941-6806
doi: 10.3827/faoj.2009.0202.0002

Congenital club foot is a complex deformity that is difficult to correct. It has a tendency to recur until the age of six or seven years. While there may be a so-called recurrence in an adolescent, this is usually associated with incomplete initial correction rather than being secondary to growth alone. We present a case report of a 15 day-old boy with aberrant tendo-Achilles tendon of the right side which caused an incomplete correction of club foot.

Case Report

A 15 day- old baby was referred by a pediatrician for the management of right clubfoot. The baby was a full-term, normal delivery in a governmental hospital. On examination the baby was found to have a 3-dimensional deformity (CAVE) with four components in the right foot (Figs. 1)

 

Figures  1   A 15 day- old baby presents with right club foot deformity.  The deformity is 3-dimensional with 4 components including cavus, forefoot adduction, heel varus and equinus (CAVE).

C-Cavus-increased longitudinal arch of foot.
A-Adduction-tarsal bones are directed towards the median plane
V-Varus-inversion and adduction of calcaneum
E-Equinus-increased plantar flexion of foot

The spine and pelvis were clinically normal. The baby was treated by Ponseti’s method of weekly POP (plaster of paris) cast. Simultaneous correction of the three components of deformity (Cavus, Forefoot, Adduction and heel varus) was achieved in 6 weeks. (Fig. 2)

Figure 2   The baby is treated with serial casting  by Ponseti’s method of weekly plaster of paris cast.

The baby had persistent equinus (Fig. 3A) after 6 weeks of serial POP casting. The foot could be abducted and externally rotated to 60 degrees.A percutaneous tenotomy of the tendo-Achilles was done under local anesthesia. Postoperatively, toe to groin cast with knee in 90 degrees of flexion to maintain the corrected position and to allow tendon healing was applied for 3 weeks. Then the foot was maintained in 60-70 degrees of abduction, external rotation and 15-20 degrees of dorsiflexion by Steinbek Splint (open toe high top straight shoes attached to bar of length equal to shoulder width). This splint is usually worn 23 hours/day for the first 3 months and 14-16 hours/day up to 3-4 years of age.

Twelve weeks later, the parents were complaining that their baby touches the floor only with tip of the right toe. On examination, the heel cord was found tight. (Fig. 3B)

 

Figures 3A and 3B  The boy presents with persistent equines following 6 weeks of serial casting. (3A)  After 12 weeks, the heel cord was still found to be tight and open Achilles tendon lengthening was planned. (3B)

Equinus was found to be persistent. We decided to do an open tendo-Achilles lengthening. Intra-operatively, we found an aberrant tendo-Achilles tendon (Fig. 4) attaching just posterior to the tendo-Achilles tendon and the calcaneal tuberosity. This was released from the calcaneum and the foot could be dorsiflexed to 20 degrees on the operating table. The baby was given an above- knee POP cast for 3 weeks and followed with Steinbek Splint in 70 degrees of abduction, external rotation on affected side and 45 degrees on normal side with 15 degrees of dorsiflexion.

Figure 4  An aberrent tendo-Achilles tendon was discovered during open tenotomy.  The aberrent tendon was located just posterior to the Achilles tendon and calcaneal tuberosity.

At 9 months, the baby could walk with a good heel strike and the foot was supple with no residual deformity. (Fig. 5) At 18 months follow up the baby was found to have a pain-free, plantigrade foot, with good mobility. (Fig. 6) The parents were advised to continuously use the brace for the baby, 14 to 16 hours a day until 3 to 4 years of age.

Figure 5  At 9 months, the boy could walk with good heel strike and the foot was supple with no deformity.

Figure 6  At 18 months follow-up, the baby was found to have a pain-free, plantigrade foot, with good mobility.

Discussion

Club foot deformity has four components [3-5,6,14,15]: equinus, varus, adductus, and cavus. The goal of treatment is to reduce or eliminate these four deformities so that the patient has a functional, pain-free, plantigrade foot, with good mobility and without calluses, and does not need to wear modified shoes. The most severe deformities in a club foot occur in the hind part of the foot. The talus and calcaneus are generally deformed and in severe equinus, the calcaneus is in varus angulation and medially rotated, and the navicular is severely displaced medially. [2,11,12,17,18,20,21] These components of the deformity are inextricably inter-related. The ligaments of the posterior aspect of the ankle and of the medial and plantar aspects of the foot are shortened and thickened. The muscles and tendons of the gastrocnemius tibialis posterior, and toe flexors are shortened. [4,14,15,20]

Most orthopedists have agreed that the initial treatment of a club foot should be non-operative. [4,5,8,11,12,14,15] The preferred method is manipulation and application of a plaster cast at weekly intervals. Less favored methods of initial treatment are use of a Denis Browne splint, stretching and adhesive strapping, and physiotherapy. Manipulation and serial application of casts, supported by limited operative intervention, yielded satisfactory functional results in 89 percent of the feet. [8,14,15] However, at other institutions, manipulative treatment has resulted in increased cavus deformity, rocker-bottom deformity, a longitudinal breach, flattening of the proximal surface of the talus, lateral rotation of the ankle, and increased stiffness of the ligaments and joints. [1,2,3,4] To avoid these distressing outcomes, early and even primary operative treatment of club foot is practiced in some centers [5,7,9,10,12,15,19,23], often with equally disturbing failures and complications, such as wound infection, necrosis of the skin, severe scarring, stiff joints, overcorrection and under correction, dislocation of the navicular, flattening and beaking of the talar head, talar necrosis, and weakness of the plantar flexors of the ankle with major disturbances of gait.

The reported results of operations in newborns have been either short term and not encouraging. Early operative treatment often results in reduced motion of the ankle and foot, whereas manipulation and the application of plaster casts with proper technique lead to greater mobility and less disability. [7,9,10,13,15]

Most orthopedists have agreed that an operation [3,4,5,11,12,15,21] should be considered only after manipulation and serial application of casts have failed to obtain correction in a specified period of time, preferably not more than three months. The poor results of manipulative treatment of most club feet in many clinics suggest that the attempts at correction have been inadequate or that the technique has been faulty. [8,14,15] Books and papers on pediatric orthopedics have devoted scant space to manipulative technique in the treatment of this deformity, and often the descriptions have been incorrect. The correction of the cavus component of the deformity is usually not addressed. [14,15] The equinus is corrected by dorsiflexion of the foot with the heel in valgus after the adduction of the foot and the varus deformity of the heel has been corrected. The correction entails stretching of the tight posterior capsules and ligaments of the ankle and subtalar joints and the tendo-Achilles. [4,5,8,12,14,15] Two or three plaster casts that carefully mold the heel, applied after manipulation, are usually needed to correct the equinus deformity. Care should be taken not to cause a rocker-bottom deformity, which can occur when dorsiflexion of the foot is attempted with pressure under the metatarsals rather than under the mid-part of the foot, particularly when the varus deformity of the heel has not been corrected. [1,8]

A simple subcutaneous tenotomy of the tendo-Achilles, performed with the patient under local anesthesia, facilitates correction of the equines. [8,14,15] This tenotomy is done in about 70 percent of patients, when 15 degrees of dorsiflexion has not been obtained with the use of the casts. Dorsiflexion of the ankle to more than 10 to 15 degrees is rarely possible because of the talar and calcaneal malformations and tight ligaments. A posterior capsulotomy of the ankle and subtalar joint is rarely done, because the few additional degrees of correction that are obtained may be completely lost later due to retraction of the scar tissue. [4,5,13,14,15]

Regardless of treatment, a club-foot deformity tends to relapse until the child is about seven years old. [3,4,5,8,12,14,15] To prevent relapse, some orthopedists hold the foot in maximum correction with a series of plaster casts or with splints. Denis Browne splints and high-top shoes with well-molded heels that hold the feet in lateral rotation are the most effective means for maintenance of the correction. The splints are worn full time for two to three months and thereafter at night for two to four years. The splint should maintain the foot in 60 to 70 degrees of external rotation, to prevent recurrence of varus deformity of the heel, adduction of the foot, and in-toeing. [8,14,15] With careful supervision and with cooperative and responsible parents who follow instructions faithfully; relapse can be prevented in about 50 percent of patients. In the other 50 percent, a relapse will occur between the ages of ten months and seven years (average age, two and one-half years). A relapse is detected when slight equinus and varus deformity of the heel is observed, usually without increased cavus and adduction deformity of the fore foot. [16,18,22,23]

The original correction may be recovered in four to eight weeks with manipulations followed by application of a toe-to-groin plaster cast, with the foot held in marked lateral rotation, every ten to fourteen days. This treatment is often followed by lengthening of the tendo-Achilles, if the tendon prevents dorsiflexion of the ankle to at least 15 degrees, and by use of the Denis Browne splint at night. [3,4,5,8,12,14,15] A large proportion of club feet that are treated with this procedure found the correction of the equinus, varus deformity of the heel, was obtained with manipulation and application of casts. If this can be maintained, the anteroposterior talocalcaneal angle will become normal. Cavus component of the club-foot deformity rarely recurs. [8,14,15] When this deformity is resistant to manipulation, it should be treated with plantar fasciotomy and recession of the extensor hallucis longus tendon to the neck of the first metatarsal. The adductus component of the club-foot deformity does not recur in patients who have received good treatment and follow-up care. When proper treatment with manipulation and casting has been started shortly after birth, operative release of the tarsal joints is seldom needed. [19]

An early operation (not later than the second month of life) is indicated only in the small percentage of patients who have short, rigid feet, with very severe equino varus deformity, that do not respond to proper manipulations. Many orthopedists also favor release of the tarsal joints in less rigid feet when manipulations have failed to completely correct the displacement of the navicular and the talocalcaneal alignment to a normal talocalcaneal index. Extensive posteromedial release, with or without internal fixation of the tarsal bones, is the preferred procedure, but there has been much disagreement about the timing of the operation. Recently, more radical [19,22,23] techniques have been tried in younger patients. The objective of all of these operations is release of the tight capsules and ligaments of the ankle and tarsal joints, and lengthening of the shortened tendons of the foot to facilitate placement of the tarsal bones in normal alignment.

The baby in this case report had a persistent eqinus deformity even after percutaneous tenotomy. Intra-operatively an aberrant tendo-Achilles was noted and was released from its calcaneal attachment. This could be the reason for the resistant equinus deformity. The literature rarely describes the aberrant tendo-Achilles tendon and the management.

Conclusion

The initial treatment of club foot should be non-operative. Corrective manipulation and serial application of casts, followed by calcaneal tenotomy and release of an aberrant tendo-Achilles tendon if found, should be successful in at least 85 percent of patients who are initially treated a few days after birth. High index of suspicion for an aberrant tendon should be there, if there is a resistant equinus deformity alone, especially after manipulation, POP cast correction and percutaneous tendo-Achilles tenotomy.

The orthopedist and podiatrist must have a thorough understanding of the deformity and be highly skilled with regard to manipulation and the application of plaster casts. Most relapses can be treated successfully with additional manipulations and applications of casts for four to eight weeks. Operative correction of a club foot is indicated when the deformity has not been treated successfully with proper manipulation and serial application of casts, supported by limited operative intervention. Most of these resistant club feet can be corrected with the use of an extensive posteromedial release and release of aberrant tendo-Achilles tendon with satisfactory functional results.

References

1. Altar D, Lehman WB, Grant AD.: Complications in clubfoot surgery. Orthop Rev 20: 233 – 239, 1991.
2. Beatson TR, Pearson JR. A method of assessing correction in club feet. J Bone Joint Surg 44B( 1): 40 – 50, 1966.
3. Brockman EP. Congenital Club-Foot (Talipes Equinovarus). Bristol, John Wright. 1930.
4. Carroll NC. Congenital clubfoot: patho anatomy and treatment. In Instructional Course Lectures, in American Academy of Orthopedic Surgeons. Vol. 36. pp. 117 – 121. Park Ridge, Illinois. The American Academy of Orthopaedic Surgeons, 1987.
5. Cummings RJ, Lovell WW. Current concepts review. Operative treatment of congenital idiopathic club foot. J Bone Joint Surg 70A: 1108 – I112, 1988.
6. Evans D. Relapsed club foot. J Bone Joint Surg 43B(4): 722 – 733, 1961.
7. Green ADL, Lloyd-Roberts C. The results of early posterior release in resistant club feet. A long-term review. J Bone Joint Surg 67B (4): 588 – 593, 1985.
8. Laaveg SJ, Ponseti IV.: Long-term results of treatment of congenital club foot. J Bone Joint Surg 62A: 23-31, 1980.
9. Lau JHK, Meyer LC, Lau HC. Results of surgical treatment of talipes equinovarus congenita. Clin Orthop. 248:219 – 226. 1989.
10. Levin MN, Kuo KN, Harris CF, Matesi DV. Posteromedial release for idiopathic talipes equinovarus. A long-term follow-up study. Int Orthop 242: 265 – 268, 1989.
11. Lovell WW. Bailey T, Price CT, Purvis JM. The non-operative management of the congenital clubfoot. Orthop. Rev 8: 1l3 – 115, 1979.
12. McKay DW. New concept of and approach to clubfoot treatment: section I principles and morbid anatomy. J. Pediat Orthop. 2: 347 – 356, 1982.
13. Main BJ, Cnder RJ. An analysis of residual deformity in club feet submitted to early operation. J Bone Joint Surg 60B (4): 536 – 543, 1978.
14. Ponseti IV, Campos J. Observations on pathogenesis and treatment of congenital clubfoot. Clin Orthop. 84: 50 -60, 1972.
15. Ponseti IV, Smoley EN. Congenital club foot: the results of treatment. J Bone Joint Surg 45A (344): 261 – 275, 1963.
16. Porter RW. Congenital talipes equinovarus: Resolving and resistant deformities. J Bone Joint Surg 69B (S): 822- 825, 1987.
17. Porter RW, Roy A, Rippstein J. Assessment in congenital talipes equinovarus. Foot and Ankle Int 1: 16 – 21, 1990.
18. Scott WA, Hosking SW, Catterall A. Club foot. Observations on the surgical anatomy of dorsiflexion. J Bone Joint Surg 66B (1): 71-76. 1984.
19. Simons CW. Complete subtalar release in clubfeet. Part I- a preliminary report. J Bone Joint Surg 67A: 1144 – 1055, 1985.
20. Swann M, Lloyd-Roberts G, Catterall A. The anatomy of uncorrected club feet. A study of rotation deformity. J Bone Joint Surg 51B (2): 263 – 269, 1969.
21. Tachdjian MO. The Child’s Foot. Philadelphia, W. B. Saunders, 1985.
22. Thompson GH., Richardson AB, Westin GW. Surgical management of resistant congenital talipes equinovarus deformities. J Bone Joint Surg 64A 652 – 665, 1982.
23. Turco VJ. Resistant congenital club foot – one-stage postero medial release with internal fixation. A follow-up report of a fifteen-year experience. J Bone Joint Surg 61A: 805 – 814, 1979.


Address correspondence to: Dr. J. Terrence Jose Jerome, MBBS.,DNB (Ortho), MNAMS (Ortho)
Registrar in Orthopedics, Dept. of Orthopedics
St. Stephen’s Hospital, Tiz Hazari, Delhi 54, India

Registrar in Orthopedics, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India.
Head Professor, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India.
Professor Emeritus, Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India. E-mail: pasle@bol.net.in
Consultant in Orthopedics, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India. Phone: 991-23966021-27.
5-6  Registrar in Orthopedics, Department of Orthopedics, St. Stephens Hospital, Tiz Hazari, Delhi, India. Phone: 991-23966021-27.

© The Foot & Ankle Journal, 2009

An Unusual Second Rupture of the Achilles Tendon: A case report

by Oladejo A. Olaleye, MRCS Ed., DOHNS, MBBS1 , Helmut Zahn, FRCS (Tr&Ortho)2

The Foot & Ankle Journal 1 (12): 3

This case report describes an unusual second rupture sustained after conservative treatment of an initial Achilles tendon rupture at the musculotendinous junction. The initial injury was successfully managed conservatively with an equinus cast for 6 weeks. The patient developed a tendonitis 10cm below the initial rupture and subsequently sustained a second traumatic rupture of the Achilles tendon at a new site after tripping on a curb. The patient had no known systemic diseases and was not on steroid or fluoroquinolone therapy. The site of this second rupture was repaired surgically using an open technique without any long term complications.

Key words: Achilles tendon, rupture, traumatic

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org)

Accepted: November, 2008
Published: December, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0112.0003

Case report

A 37 year-old male, dog-handler from the police force was chasing a suspect when he experienced acute pain to the right posterior leg in the Achilles region. He was unable to ambulate after the initial injury. No previous leg injuries or tendinitis were reported. The patient did not report any history of taking corticosteroids or fluoroquinolone antibiotics. Clinically, the patient had a positive Simmond’s test and rupture of the Achilles tendon was isolated to the musculo-tendinous junction.

A clinical diagnosis of Achilles rupture was rendered. No magnetic resonance imaging (MRI) was initially performed and the patient was managed conservatively in an equinus cast for 6 weeks and then in an adjustable boot to bring the foot to ankle range of motion to 90 degrees over the following 6 weeks. The adjustable boot was initially put in 20 degrees of dorsiflexion for 3 weeks then adjusted to 90 degrees over the following course of treatment.

The adjustable boot was removed and he managed to walk without crutches. The patient had regained total range of motion of the ankle with no gap or tenderness along the Achilles tendon and good plantarflexion power.

Reinjury

He subsequently developed a painful lump in his Achilles tendon 10cm inferior to the initial rupture location. Clinically, he had a fusiform swelling of the tendon which was slightly fluctuant and tender to palpation. He was placed on a course of anti-inflammatory medication and referred to physiotherapy for ultrasound. To confirm the diagnosis, an MRI scan was scheduled. During this period, the patient sustained a second injury to the same tendon while waiting for the MRI scan. The patient had been walking on the road with a group of friends when he tripped on a curb and felt a sharp pain along his right Achilles tendon. MRI confirmed a second injury more inferior to the original site of injury. (Fig. 1)

Figure 1 Region of second rupture as identified on MRI (arrow).  More proximally, the initial injury can be seen at the musculo-tendinous junction. 

MRI of the site of injury revealed an abnormally high signal change and thickening within a somewhat retracted Achilles tendon 3 cm above its insertion as well as at the musculo-tendinous junction of the gastrocnemius muscle.

This was consistent with a full-thickness, high-grade tear or rupture of the Achilles tendon at the musculo-tendinous junction. Intra-tendinous edema associated with the presence of fluid was located within and about the Achilles tendon suggesting the presence of intra-tendinous hematoma. There was also swelling of the posterior surrounding subcutaneous soft tissues.

There was little fluid noted within the retrocalcaneal bursa or along the lower aspect of the Achilles tendon about 2.5cm from its insertion.

A small region of marrow edema was noted in the posterior aspect of the talus. The tibia and fibula were intact and no fracture of ankle was reported.

On his second presentation to the hospital, there was a palpable gap to the Achilles tendon with a positive Simmond’s test. At this time, he was scheduled for primary surgical repair of the tendon.

Intraoperatively, the patient had a general anaesthetic, positioned in a prone position with tourniquet applied. The incision was limited to the second rupture site and the initial injury was not visualised as it was at the musculotendinous junction. The tendon was exposed demonstrating the second rupture with obvious complete rupture 3 cm above the calcaneus with high attenuation. (Figs. 2A and B)

 

Figure 2A and B  Intra-operatively, substantial attenuation of reinjury is identified with a forcep holding distal end of achilles tendon rupture, 3cm above its calcaneal insertion (A)  The proximal end of the ruptured tendon is also identified with a forcep. (B)

The ruptured edges were identified and re-apposed by a modified Kessler locking core stitch using No.5 Ethibond and a running suture using No.1 Vicryl. (Fig. 3) Postoperatively, he was placed in an equinus cast with DVT (deep vein thrombosis) prophylaxis and gradual rehabilitation with good recovery.

Figure 3 Repair after closure of the Achilles paratenon.

Discussion

Achilles tendon rupture is a complete disruption of the Achilles tendon most commonly affecting 30-50 year old males with the rupture about 4-5cm above the calcaneus (a zone of poor blood flow in the tendon). [7] There is a male:female predisposition of 6:1. Predisposing factors include chronic tendonitis or tendinopathy and prior cortisone injection treatments. The majority of these injuries occur during some athletic event requiring forceful push-off of the foot. Other associating risk factors include gout, patient with blood type O, systemic lupus erythematosus, rheumatoid arthritis, patients on steroid medication and fluoroquinolone-type antibiotics. [7]

Achilles tendon rupture is often characterized by an acute onset of pain in the distal posterior portion of the lower leg. Patients often think they have been kicked, cut or hit in the back of the leg with subsequent difficulties ambulating or putting weight down on the affected foot.

Pathophysiological theories include chronic degeneration of the tendon and failure of the inhibitory mechanism of the musculotendinous unit. [5] Some believe that it may be due to the whipping action or bowstring effect caused by ankle pronation, or by the Achilles tendon’s relatively weak blood supply. Others consider the cause to be the combination and frequency of eccentric shortening when the heel hits the ground followed rapidly by concentric contraction when the toes push off. [9]

There is obvious leg swelling with a palpable defect in the Achilles tendon and a positive Thompson’s test. The Thompson’s test usually reveals absence of plantar flexion on squeezing the calf with the patient lying in the prone position.

The diagnosis is often made clinically. Plain radiographs, ultrasonography, and MRI can also be useful to confirm the diagnosis. The MRI is the gold-standard for diagnosing acute Achilles tendon ruptures and can also confirm the diagnosis of a partial rupture which may not be clinically apparent.

Achilles tendon injuries can occur in different locations along the Achilles tendon. Tennis leg is a rupture between the Achilles tendon and the gastrocnemius. Achilles tendinosis, Achilles tendonitis, Achilles tenosynovitis, Achilles tendon rupture and medicine side effects are most often felt an inch or two above the heel. Insertional Achilles tendinosis, tendonitis, and tenosynovitis occur where the Achilles tendon and heel connect. Achilles tendon laceration or crushing could occur anywhere along the Achilles tendon. [9]

Achilles tendon ruptures can be managed conservatively or operatively and several methods have been employed with varying results. Lower re-rupture rates and slightly improved strength and functional ability may be expected with surgical repair. The rate of minor surgical complications is higher than that of non-operative treatment. [5] With careful attention to the surgical wound and patient compliance to post-operative rehabilitation protocols, operative repair of acute Achilles tendon ruptures is a reliable treatment for active patients. [8] Three partial Achilles tendon re-ruptures and one complete rupture were documented in a series of 74 patients that had operative repair. [8] A known benefit of surgical repair is the decreased re-rupture rate. One study showed a 4% re-rupture rate for operative repair compared to an 8% re-rupture rate for conservative management. [6] Re-rupture rates of 1.4% and 13.4% for surgical and conservative management respectively have been reported. [1] A meta-analysis found re-rupture rates of 1% and 18% for surgical and conservative repair. [3] There were no re-ruptures for 44 patients treated surgically as opposed to 9 of the 44 for those treated conservatively. [2]

Recent studies have suggested better outcomes with early postoperative functional rehabilitation. An unusual type rupture, where the Achilles tendon was ruptured in two places requiring several innovative techniques to repair has been described. [4]

In our institution, we prefer operative approach with early mobilisation in an adjustable air cast boot. The usual regime is to apply a dorsal slab until the wound has healed. An adjustable air cast boot is then applied starting at 45 degrees of equinus aiming to reach 90 degrees by 6 weeks, at which point, weight bearing is allowed. Passive dorsiflexion is continued until range of movement equals contralateral side. The air cast is discarded 3 months after surgical repair.

Conclusion

This case report highlights an unusual second rupture of the Achilles tendon at a different site on the same tendon following an initial traumatic rupture at the musculotendinous junction. This is a rarely reported injury in the literature. This previously fit and healthy patient had a traumatic rupture of his right Achilles tendon at the musculotendinous junction which was treated conservatively in an equinus cast. He subsequently developed a tendonitis and then traumatic rupture at a site 10cm below the initial rupture on the same tendon. This was treated with open surgical repair and rehabilitation.

In conclusion, the presentation of this case study has highlighted the potential role for routine MRI scanning to assess Achilles tendon ruptures and identification of risk for a second rupture.

References

1. Cetti R, Christensen SE, Ejsted R, Jensen NM, Jorgensen U. Operative versus non-operative treatment of Achilles tendon rupture. A prospective randomized study and review of the literature. Am J Sports Med. 21 (6): 791 – 799, 1993.
2. Inglis AE, Scott WN, Sculco TP, Patterson AH. Ruptures of the tendo Achilles: an objective assessment of surgical and non-surgical treatment. J Bone Joint Surg 58A (7): 990 – 993, 1976.
3. Kellam JF, Hunter GA, McElwain JP. Review of the operative treatment of Achilles tendon rupture. Clin Orthop 201: 80 – 83, 1985.
4. Kuwada GT. A severe acute Achilles rupture and repair. J Foot Ankle Surg 34 (3): 262 – 5, 1995.
5. Leppilahti J, Orava S. Total Achilles tendon rupture. A review. Sports Med 25(2): 79 – 100, 1998.
6. Nistor L. Surgical and non-surgical treatment of Achilles tendon rupture: a prospective randomized study. J Bone Joint Surg 63A (3): 394 – 399, 1981.
7. Saglimbeni AJ & Fulmer CJ. Achilles tendon injuries and tendonitis. Emedicine, 2008.
8. Strauss EJ, Ishak C, Jazrawi L, Sherman O, Rosen J. Operative treatment of acute Achilles tendon ruptures: an institutional review of clinical outcomes. Injury 38(7): 832 -838, 2007.
9. Everything about Achilles tendons (2004-2006). Online, accessed 24th November 2008.


Address correspondence to: Olaleye MRCS Ed., DOHNS, MBBS
Trauma and Orthopaedic Surgery Department
William Harvey Hospital, Ashford
Kent, United Kingdom. TN24-OLZ
Email: dejolaleye@yahoo.com

1 CT1 Trauma and Orthopaedic Surgery, William Harvey Hospital. Ashford, Kent. UK.
2 Consultant, Trauma and Orthopaedic Surgery, William Harvey Hospital, Ashford, Kent. UK.

© The Foot & Ankle Journal, 2008

Repair of Nelgected Achilles Tendon Rupture with Monofilament Polypropylene Mesh: A Case Study of 12 Patients

by Robert Fridman, DPM, AACFAS1, Fred Rahimi, DPM, FACFAS2, Paul Lucas, DPM, FACFAS3, Rob Daugherty, DPM, AACFAS4, Heidi Hoffmann, DPM5

The Foot & Ankle Journal 1 (5): 2

The purpose of this study is to evaluate the effectiveness of polypropylene mesh as an alternative to autogenous grafts and/or tendon transfers for neglected Achilles tendon rupture. Twelve patients with neglected Achilles tendon rupture underwent surgical repair using monofilament polypropylene mesh graft from 1999-2003. The average follow-up was 1.5 years. All patients were placed in a non-weight bearing, below-knee cast for 3 weeks, followed by 3 weeks of partial weight bearing in walking boot. All patients healed uneventfully, with three patients complaining of mild pain, one of moderate pain, and five with stiffness that resolved with physical therapy. The adjunctive use of monofilament polypropylene mesh is an appropriate method for the treatment of neglected Achilles tendon ruptures.

Key words: Achilles Tendon Rupture, Achilles Tendon Repair, Marlex ® Mesh

This is an Open Access article distributed under the terms of the Creative Commons Attribution License.  It permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ©The Foot & Ankle Journal (www.faoj.org

Accepted: April 1, 2008
Published: May 1, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0105.0002

Degeneration, tendon contracture, and a high re-rupture rate are frequent sources of failure in non-operative treatment of neglected Achilles tendon ruptures. [1] Bosworth previously noted that retraction of the gastrocnemius-soleus complex may occur within three days of injury, making re-approximation of the tendon ends difficult. [2] Current clinical practice supports surgical repair of the tendon in this condition. End-to-end [3], percutaneous [4] and limited-open repairs [5] may not be as effective in neglected ruptures due to excessive tendon contracture and degeneration of the tendon ends.

Therefore, tendon augmentation is routinely employed in cases of neglected rupture. The flexor hallucis longus tendon is most commonly used to augment reconstruction. [6,7,8] Mann and others described using the tendon of the flexor digitorum longus as a graft. [9] Fascia lata, [10] peroneus brevis, [11] gracilis, [12] and plantaris [13] tendon grafts have also been described in the literature.
Synthetic grafts may also be used to augment the surgical repair in situations where surrounding autogenous tissues are weak or unable to span the defect. The advantages of synthetic grafts over autogenous grafts include absent donor site morbidity and unlimited material available for sizable defects.

A distinct disadvantage of synthetic grafts is possible foreign body reaction after implantation. Dacron® vascular graft, [14] carbon fiber composites, [15] collagen tendon prosthesis, [16] and GraftJacket® [17] have all been described as alternatives to autogenous grafts. Ozaki, et al, reported that polypropylene mesh had little to no tissue reaction when implanted during rotator cuff repair [18] and subsequently used this material for repair of Achilles tendon with satisfactory results. [19] This case study reports on a series of neglected Achilles ruptures repaired with Marlex ® polypropylene mesh.

Materials and Methods

Twelve patients with neglected Achilles tendon rupture were treated surgically by the same surgeon using Marlex ® polypropylene mesh (Davol Inc., Rhode Island, USA) as described by Ozaki, et al. The diagnosis of neglected Achilles tendon rupture was based on history, clinical and MRI findings.

Neglected tears were defined as a closed rupture of 10 or more days duration without previous surgical treatment for the affected tendon. MRI findings were all indicitive for complete rupture of the Achilles tendon with fatty degeneration. (Fig.1)

Figure 1  MRI of neglected rupture of Achilles tendon shows significant gapping and degeneration of tendon ends.

The average patient age was 52.5 years (range = 31 to 70 years). There were 8 males and 4 females included in the study, with an average follow-up period of 1.5 years (range = 0.5 – 4 years). Table 1 summarizes the demographic data.

TABLE 1  Demographics of 12 patients with neglected Achilles tendon rupture.

Patients were either contacted by telephone or interviewed in the clinic. A modified VISA-A Questionnaire was used for clinical evaluation.20 (Table 2)

TABLE 2  The modified VISA-A (Victorian Institute of Sport Assessment-Achilles) Questionnaire.

Surgical Procedure

The procedure is performed under general anesthesia with a pneumatic thigh tourniquet. Both lower extremities are prepped and draped, so as to have an appropriate reference point when tensioning the repaired tendon. Prophylactic antibiotics are given prior to inflating the tourniquet. The patient is positioned prone and local anesthetic is infiltrated into the surgical site. A posteromedial incision is made along the Achilles tendon extending proximally and distally past the defect (Fig. 2).

Figure 2   A posteromedial incision is made along the Achilles tendon extending proximally and distally past the defect.

The sural nerve is retracted laterally, and the paratenon is incised and tagged for later closure. The ruptured ends of the tendon are identified, and fibrotic and/or degenerated tendon is excised (Fig. 3).

Figure 3   The ruptured ends of the tendon are identified and degenerated tendon is removed.

The tendon ends are prepared for insertion into the mesh graft by incising the tendon 2-3 cm in the frontal plane. The mesh is prepared by tri-folding it to a slightly smaller width than the tendon itself. The folds are secured with 3-0 non-absorbable suture (Fig. 4).

Figure 4  The mesh is prepared by folding it 3 times to a slightly smaller width than the tendon itself.  The folds are secured with 3-0 non-absorbable suture.

To assess the length of graft, the gastrocnemius-soleus complex is pulled distally and then compared to the resting tension of the contralateral limb. The mesh is then measured and cut to fit the defect. The mesh is held in place with heavy non-absorbable suture, securing all knots anteriorly to prevent scarring and stenosis with the underlying superficial fascia and skin. The proximal portion is secured first (Fig.5), which allows for easier tensioning adjustments prior to securing the distal end.

Figure 5  The proximal portion of the mesh-tendon interface is first secured. 

A portion of the plantaris tendon is resected and fanned out to cover the anterior and posterior portion of the graft, and is secured using 3-0 non-absorbable suture (Fig. 6).

Figure 6  A portion of the plantaris tendon is resected and fanned out to cover the anterior and posterior portion of the graft and is secured.

The tendon and graft are reinforced with calcaneal bone anchors inserted medially and laterally (Fig. 7).

Figure 7  Bone anchors secure the repaired tendon to the calcaneus.

The anchor sutures are then braided along the sides of the tendon creating a finger-trap stitch. The paratenon is repaired with an interlocking baseball stitch and the skin is reapproximated using 5.0 absorbable suture. (Figs. 8,9)

Figure 8 The paratenon is reapproximated.

Figure 9  Absorbable suture is used for closure and surgical strips are placed across the surgery site.

All patients were placed in a non-weight bearing, short leg cast in gravity equinus for 3 weeks, and then advanced to a non-weight bearing walking boot with passive range of motion exercises for an additional 3 weeks. Progressive weight bearing with active physical therapy was initiated post-operatively at 6 weeks.

Results

The average time for follow-up was 1.5 years (range 0.5 – 4 years; mean = 2 years; standard deviation 1.515; median 1.5 years; 25th percentile = 0.75 years; 75th percentile = 4 years). There were no cases of foreign body reaction following implantation of the mesh graft. All patients were able to return to work or to their level of activity before the injury. Of the twelve patients involved in the study, eight related no pain at the time of the interview.

Three patients related mild pain. One patient presented to the surgeon five months after surgery complaining of moderate pain at the operative site, and stated that he heard a “pop” when ambulating and began to experience pain at the surgical site. This patient was immobilized in a non-weightbearing walking boot with crutches and follow-up MRI showed evidence of diffuse thickening at the site of the repair with no evidence of a recurrent tear. He then returned to pre-operative activities of daily living without incident. Five patients related mild ankle joint stiffness upon waking in the morning. Two patients complained of mild weakness to the calf muscle.

Four patients stated that they were limited in their shoe gear, with one patient stating that she was no longer able to wear high heel shoes. All patients were satisfied with the overall results of the procedure. (Table 3)

TABLE 3 Data Results.

Discussion

A number of surgical techniques have been described for the repair of neglected Achilles tendon ruptures. Autogenous grafts in the form of local tendons or free fascia may be used when the donor tissue is healthy and where the gaps are manageable. Synthetics grafts are useful when autogenous grafts cannot be used.

Lieberman, et al, [14] described repair of Achilles tendon ruptures with Dacron® vascular graft in 7 patients, with a follow-up of ten to 38 months. The graft was woven from distal to proximal and across the rupture in a Bunnell-type fashion, and the patients were immobilized in a short-leg cast for two weeks and then fitted with a posterior fiberglass splint.

Patients were allowed to return to their normal level of activity approximately five months after surgery. There was no incidence of re-rupture, wound infection, or skin adhesion. All of the patients had normal gait, normal range of motion of the ankle, and had returned to their pre-injury level of activity. Two patients noted weakness in the injured leg and two years after the repair; however, their activity levels had not been altered. Another patient complained of tightness in the tendon area and discomfort after a significant amount of exercise.

Parsons, et al, [15] described repair of Achilles tendon using a composite carbon implant in 48 patients/51 procedures with an average follow-up of 2.1 years. Three cohort groups were observed on a temporal basis and quantitatively evaluated at 1 year (N = 29), 18 months (N = 22), and 2 years (N = 20), respectively. These three groups demonstrated continuous improvement during the first postoperative year, with 86% having a good to excellent result. A high level of function was maintained throughout the second year.

Lee [17] described a case-report using GraftJacket ® for augmentation of a gastrocnemius recession repair in a chronic Achilles rupture. The augmentation obviated the need for tendon transfer or free tendon graft, and early return to activity and good plantarflexion strength was noted postoperatively.

This series reports on 12 patients who were repaired using Marlex ® polypropylene mesh. This material has been extensively used in general and cardiovascular surgery with predictable results. Hosey, et al, studied the Marlex ® -tendon complex in rabbits and reported that it had similar physical properties to a normal tendo Achilles. [20] There was no reported incidence of foreign body reaction. The potential risk of donor site morbidity was eliminated through use of a synthetic graft. All patients were satisfied or very satisfied with their surgical outcome. Ozaki [19] and Choskey [22] reported findings that were similar to those in our set.

There are a number of limitations in this study. The sample size is small, and our results are compared to historical controls, which inherently introduces bias between the two groups. Additionally, we did not consider any independent variables, such as weight or length of the tendon defect, which may have added confounders or bias to the overall outcome of the study.

The VISA-A (Victorian Institute of Sport Assessment-Achilles) questionnaire provides a valid and reliable index of severity of Achilles tendinopathy. [20] It was modified in this study to include questions about return to work and footwear restrictions. Additionally, it qualifies VISA-A pain, stiffness, and weakness score of 0 as none, 1-3 as mild, 4-6 as moderate, and 7-10 as severe. This modification may alter the operating characteristics of the questionnaire, however, it is quite unlikely.

In conclusion, the results demonstrated above suggest that polypropylene mesh graft is an effective alternative to autogenous grafts and/or tendon transfers in the treatment of neglected Achilles tendon rupture.

This investigation was not funded by any commercial or other outside agency or corporation. The investigators do not have any potential conflicts of interest, actual or perceived, to this investigation.

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Address correspondence to: Robert Fridman, DPM, AACFAS, Department of Orthopaedics, New York-Presbyterian Hospital, University Hospitals of Columbia and Cornell, New York, NY.

1Private Practice, Foot Associates of New York, New York, NY.
2Fahey Medical Center, Des Plaines, IL.
3Alexian Brothers Medical Center, Hoffman Estates, IL.
4Private Practice, Daugherty Foot and Ankle Clinic, Cape Girardeau, MI.
5Private Practice, Northwest Suburban Podiatry, Arlington Heights, IL.

© The Foot & Ankle Journal, 2008