While improvements in the understanding of plantar fasciopathy and advances in diagnosis and treatment have reduced the need for endoscopic plantar fasciotomy (EPF), it remains an efficacious procedure for properly selected patients.
Endoscopic plantar fasciotomy (EPF) emerged in the literature in 1991 and has remained an efficacious, minimally invasive technique to this day.1-6 There is no doubt that EPF is still a viable and efficacious procedure. What has changed is our understanding of plantar fasciopathy and that has forced a paradigm shift in the treatment of plantar fasciopathy, which has given EPF a different space in that paradigm.
No longer is it good enough to get a cursory history of present illness, press on the bottom of the patient’s heel, make a diagnosis of plantar fasciitis and provide a “cookie cutter approach” to treatment.
First, we are still using fallacious nomenclature when referring to plantar fasciitis when Lemont so eloquently pointed out in 2003 that this is not an inflammatory condition but rather one of a degenerative condition.7 This is the similar case for the myth of “tendonitis,” which is actually “tendinopathy.”8,9
The fact of the matter is that while the surgical technique of EPF has been a mainstay in the treatment of severe plantar fasciopathy and is probably one of the most peer-reviewed surgical techniques in the podiatric surgical armamentarium, the understanding of the condition that surgeons developed the modality to treat has radically changed for the better.
With the advent of musculoskeletal ultrasound, we can effectively diagnose plantar fasciopathy with a high degree of specificity and individually design treatment plans for the level of pathology present in the patient.10 High-resolution sonography allows the practitioner to grade the level of degeneration. Then one should tailor treatment to the level of tissue degradation. For example, sonograms can clearly reflect different levels of severity, requiring different treatment approaches ideally for optimal results. Those practitioners who do not assess the level of tissue degeneration with high-resolution diagnostic ultrasound are pretty much forced to use a cookie-cutter approach as they do not really know what they are treating. Visualization is everything from diagnosis to surgical technique.
Surgeons are performing fewer EPFs today for primarily one reason: better technology. Due to the paradigm shift from viewing this condition as resulting from inflammation rather than tissue degeneration, new techniques have become available that have decreased the number of ultimately recalcitrant cases of plantar fasciopathy.
A Shift Toward Favoring Regenerative Medicine Options Over Steroid Injections
Additionally, this paradigm shift should also cause the practitioner to pause and question modalities that are theoretically anti-inflammatory. For example, consider the widespread and, in my opinion, injudicious use of the injection of steroids. Monto and colleagues showed that the injection of steroids was inferior to the injection of platelet-rich plasma (PRP).11 In fact, after 24 months, patients using only steroids were only 4 points better at 56 on the American Orthopedic Foot and Ankle Society (AOFAS) scoring system. This is in comparison to a score of 92 at 24 months for patients using PRP, who began with a score of 37.
Now this is truly astounding. With a steroid injection, we have a treatment that gives an initial benefit for just three months before starting the plunge back to the baseline score in comparison to a score of 95 at three months with the injection of PRP.11 By the way, the highest AOFAS score reached with the steroid in the study was 81. The average end score with PRP: 92 at 24 months. Other studies have shown similar short-term results for steroid infiltration.12
The study by Monto and colleagues illustrates the power of regenerative medicine for a degenerative condition. This is why fewer EPFs are necessary at this time. By implementing amniotic tissue allograft (stem cells), I have found more profound effects in treating plantar fasciopathy. While I reserve EPF for patients in a IVB or IVC category on the Barrett Plantar Fasciopathy Ultrasound Grading System (see left), I still recommend intervening with ultrasound-guided partial plantar fasciotomy with amniotic tissue allograft, even for those patients who are likely to need an EPF.
Steroid injections likely demonstrate a temporary effect due to the fact that they may decrease cellular products of degeneration that interrupt nociception via this biochemical mechanism.13 Significant complications are associated with the use of corticosteroids and combining them with lidocaine has a synergistic effect, making them more toxic to tenocytes.14 Steroids also have long-term, deleterious effects on tendon tissue.15 Accordingly, when incorporating steroid injections into a “cookie cutter” treatment approach, the practitioner should weigh the benefits of short-term pain relief versus long-term tissue damage.
Key Insights On The Efficacy Of EPF
Nevertheless, EPF is highly efficacious, minimally invasive and safe. The long-term efficacy of EPF is well established.16 Additionally, patients reportedly have fewer complications with EPF in comparison to open heel surgery or even ESWT.4 As with any surgery, complications can occur and this is no different with EPF. Most complications with EPF are due to excessive activity in the postoperative period before the fascia has had enough time to heal. Close monitoring by the surgeon can mitigate this factor. I usually recommend no more than five minutes of standing or walking per hour for the first four weeks without a walking boot, and minimizing ambulation as much as possible during the first two weeks after EPF. I cannot emphasize enough the avoidance of performing bilateral surgery.
The primary reason an endoscopic plantar fasciotomy does not have a desired outcome is coexisting pathology that the surgeon has not recognized prior to intervening with the technique. Occasionally, there is a misdiagnosis but this is rare with the use of high-resolution diagnostic sonography.
There is a very high association of plantar fasciopathy with medial calcaneal nerve entrapment.17 Rose and coworkers found a 72 percent association of nerve entrapment with patients who presented with plantar fasciopathy.18 This means that without an excellent diagnostic workup, the simple case of “plantar fasciitis” that has not resolved with the plethora of conservative modalities and proceeds to an EPF could very likely have neurogenic pathology. Underlying nerve entrapment can sometimes be very subclinical and release of the plantar fascia exacerbates it.
Endoscopic plantar fasciotomy is a very viable alternative to open heel surgery with less complication and pain for the patient. As with any surgical technique that alters the biomechanics of the foot, clinicians should exhaust less invasive techniques prior to intervening with release of the plantar fascia. Interestingly, as pointed out by Bader and colleagues in 2012, patients with the most severe plantar fasciopathy had the higher mean improvements with EPF in comparison to those patients with milder symptoms.19 These findings support my contention that in order to treat plantar fasciopathy ideally, one should grade it to the severity of the degeneration and treat it with a specific intervention tailored to the level of pathology.
Dr. Barrett is an Adjunct Professor within the Arizona Podiatric Medicine Program at the Midwestern University College of Health Sciences. He is a Fellow of the American College of Foot and Ankle Surgeons. Dr. Barrett has disclosed that he holds the patent to the EPF procedure and has a consulting agreement with Vilex for the manufacture of endoscopic instrumentation.
1. Barrett SL, Day SV. Endoscopic plantar fasciotomy for chronic plantar fasciitis/heel spur syndrome: surgical technique--early clinical results. J Foot Surg. 1991; 30(6):568-570.
2. Barrett SL, Day SV, Brown MG. Endoscopic plantar fasciotomy: preliminary study with cadaveric specimens. J Foot Surg. 1991; 30(2):170-172.
3. Chou AC, Ng SY, Koo KO. Endoscopic plantar fasciotomy improves early postoperative results: a retrospective comparison of outcomes after endoscopic versus open plantar fasciotomy. J Foot Ankle Surg. 2015; epub May 22.
4. Othman AM, Ragab EM. Endoscopic plantar fasciotomy versus extracorporeal shock wave therapy for treatment of chronic plantar fasciitis. Arch Orthop Trauma Surg. 2010; 130(11):1343-1347.
5. Radwan YA, Mansour AM, Badawy WS. Resistant plantar fasciopathy: shock wave versus endoscopic plantar fascial release. Int Orthop. 2012; 36(10):2147-2156.
6. Saxena A, Fournier M, Gerdesmeyer L, Gollwitzer H. Comparison between extracorporeal shockwave therapy, placebo ESWT and endoscopic plantar fasciotomy for the treatment of chronic plantar heel pain in the athlete. Muscles Ligaments Tendons J. 2012; 2(4):312-316.
7. Lemont H, Ammirati KM, Usen N. Plantar fasciitis: a degenerative process (fasciosis) without inflammation. J Am Podiatr Med Assoc. 2003; 93(3):234-237.
8. Almekinders LC. Tendinitis and other chronic tendinopathies. J Am Acad Orthop Surg. 1998; 6(3):157-164.
9. Maffulli N, Wong J, Almekinders LC. Types and epidemiology of tendinopathy. Clin Sports Med. 2003; 22(4):675-692.
10. Tassone JB, Barrett SL (eds.). Diagnostic Ultrasound of the Foot and Ankle, First Edition, Data Trace, New York, 2013.
11. Monto RR. Platelet-rich plasma efficacy versus corticosteroid injection treatment for chronic severe plantar fasciitis. Foot Ankle Int. 2014; 35(4):313-18.
12. McMillan AM, Landorf KB, Gilheany MF, Bird AR, Morrow AD, Menz HB. Ultrasound guided corticosteroid injection for plantar fasciitis: randomised controlled trial. Br Med J. 2012; 344:e3260.
13. Wong MW, Tang YY, Lee SK, Fu BS. Glucocorticoids suppress proteoglycan production by human tenocytes. Acta Orthopaedica. 2005; 76(6):927-931.
14. Yang SL, Zhang YB, Jiang ZT, Li ZZ, Jiang DP. Lidocaine potentiates the deleterious effects of triamcinolone acetonide on tenocytes. Med Sci Monit. 2014; 20:2478-2483.
15. Poulsen RC, Watts AC, Murphy RJ, Snelling SJ, Carr AJ, Hulley PA. Glucocorticoids induce senescence in primary human tenocytes by inhibition of sirtuin 1 and activation of the p53/p21 pathway: in vivo and in vitro evidence. Ann Rheum Dis. 2014; 73(7):1405-1413.
16. Nery C, Raduan F, Mansur N, Baunfeld D, Del Buono A, Maffulli N. Endoscopic approach for plantar fasciopathy: a long-term retrospective study. Int Orthoped. 2013; 37(6):1151-1156.
17. Chang CW, Wang YC, Hou WH, Lee XX, Chang KF. Medial calcaneal neuropathy is associated with plantar fasciitis. Clin Neurophysiol. 2007; 118(1):119-123.
18. Rose JD, Malay DS, Sorrento DL. Neurosensory testing of the medial calcaneal and medial plantar nerves in patients with plantar heel pain. J Foot Ankle Surg. 2003; 42(4):173-177.
19. Bader L, Park K, Gu Y, O’Malley MJ. Functional outcome of endoscopic plantar fasciotomy. Foot Ankle Int. 2012; 33(1):37-43.
For further reading, see “Point-Counterpoint: Recalcitrant Plantar Fasciitis: Is Fasciotomy Ever Necessary?” in the November 2011 issue of Podiatry Today or “A Closer Look At Endoscopic Plantar Fasciotomy” in the May 2002 issue.
For an enhanced reading experience, check out Podiatry Today on your iPad or Android tablet.
Maintaining that endoscopic plantar fasciotomy has a long list of potential sequelae and does not truly address the biomechanical etiology of heel spur syndrome plantar fasciitis, this author suggests that subtalar stents may emerge as a viable option for this condition.
Biomechanics has taught us that pronation is the major deforming force in the foot. It is pronation, or excessive hypermobility, that creates the majority of the pathology that we treat on a daily basis. Heel spur syndrome plantar fasciitis is a biomechanically induced pathologic symptom complex causing heel and arch pain. The presenting clinical history and physical symptoms are well known. For the sake of debating the use of endoscopic plantar fasciotomy (EPF) for recalcitrant heel spur syndrome plantar fasciitis, let us assume that there has been an accurate diagnosis of plantar fasciitis and that we are not dealing with anything other than a biomechanically induced etiology.
My stance against EPF is not founded on any lack of technical merit of the procedure itself. It is based on the primary belief that EPF does not address the true etiology of heel spur syndrome plantar fasciitis and therefore surgeons should not use it.
Weil once coined the phrase “the rape of the plantar fascia” and promoted extracorporeal shockwave therapy (ESWT) as an alternate treatment to avoid destructive and detrimental fascia disruption.1 This was the first step away from traditional surgical fascia disruption.
In addition to avoiding surgery on the fascia, we must identify the true etiology of plantar fasciitis symptoms, treat the etiology at its source and not concentrate on symptom treatment. Currently, most of our treatment protocols are symptom-oriented toward the plantar fascia and plantar medial calcaneal tubercle area. We need to stop treating the most common podiatric deformity with a symptom-based approach and treat the true biomechanical alignment deviation that causes heel spur syndrome plantar fasciitis.
Reviewing The Plantar Fasciitis Treatment Options
Let us look at how podiatric medicine treats heel spur syndrome plantar fasciitis as outlined by the 2010 practice guidelines of the American College of Foot and Ankle Surgeons (ACFAS).2 The treatment algorithm for plantar fasciitis includes a long list of conservative treatment options including custom or over-the-counter orthotics, proper shoe gear, non-steroidal anti-inflammatory drugs (NSAIDs), cortisone injections, strapping, bracing, casting, stretching, night splints, physical therapy, platelet-rich plasma (PRP), botulinum toxin injection, radiofrequency Coblation, radiofrequency nerve ablation and cryosurgery.
Surgical intervention options traditionally involve cutting the plantar fascia with or without spur resection. Most surgeons now leave the plantar spur alone as it is commonly agreed to be an incidental finding that does not require excision.3-8 Most clinicians agree that when there is insufficient symptomatic improvement following a reasonable timeframe with conservative treatment, surgery is then a reasonable option. One can attempt ESWT if conservative treatment options prove less effective.
All conservative and surgical treatment options for heel spur syndrome plantar fasciitis, if one examines them closely and honestly, should lead us to the realization that we are treating the symptoms of plantar fasciitis, not the true pathologic etiology. This is a major shortcoming in the approach taken by the podiatric and orthopedic communities.
The etiology is hypermobility, pronation, STJ instability or talotarsal mechanism instability. Call it what you like but all of these terms attempt to explain the congenital, structural, functional, adaptive, compensatory etiologic symptom complex that we know as heel spur syndrome plantar fasciitis.
Understanding The Limitations And Potential Sequelae Of EPF
I do not support EPF for the treatment of heel spur syndrome plantar fasciitis. I choose to offer my patients an alternative option that addresses the primary etiology of their plantar fasciitis and leaves the plantar fascia intact and functional. Endoscopic plantar fasciotomy does not treat the primary etiology. Endoscopic plantar fasciotomy reduces the tension of the plantar fascia at the medial calcaneal tubercle and structurally weakens the arch. The same disruption and resultant weakness applies to any plantar fascia cutting procedure.
The plantar fascia is a biologic structure that exists to provide support and structural integrity to the arch of the foot. It is there for a reason. Cutting it creates arch instability, reduces the windlass effect and creates possible lateral column overload. Sharkey, Tweed and their respective coauthors identified increased arch weakness, lowering of the medial arch and an increased peak pressure under the metatarsal heads as consequences of plantar fascia release.5-7
Endoscopic plantar fasciotomy reduces forefoot and digital stability, similar to the possible effects of performing radical plantar fasciectomy for plantar fibroma resection. One must apply known biomechanical principles of the relationship of digits and metatarsals at the metatarsophalangeal joints (MPJs). It would then follow that the risks of submetatarsal head/MPJ retrograde buckling, hammertoe formation, nerve irritation and first ray elevatus with hallux limitus or hallux rigidus could be potential sequelae of plantar fascia cutting and the resulting arch instability.
Farabeuf’s axis identifies a central axis of the STJ, around which hypermobility and its resultant pathology develop.9 There are various biomechanical theories — involving the pedal axes of the STJ, the midtarsal joint and the first and fifth rays — of planar dominance and of tissue stress that attempt to explain and define normal and abnormal foot alignment and function. The notion of the neutral STJ, the mantra and core of the podiatric profession, has been the subject of debate and research for decades with no definitive conclusion accepted as to what constitutes the true neutral position of the STJ. Research studies show a high level of inconsistency in quantifying numeric values of joint range of motion (ROM) among multiple examiners.10 Manual examination with the use of measuring devices provides inconsistently reproducible intra-examiner results. Each biomechanical theory attempts to develop an explanation of foot motion and function, although difficult to quantitate, that leads to pathologic foot symptoms.
Where Subtalar Stents Can Have An Impact
I believe that EPF does not effectively treat the abnormal functional alignment of the STJ complex that causes heel spur syndrome plantar fasciitis. I believe a more effective way to treat the abnormal STJ alignment is to utilize a subtalar stent. This provides more stability in several planes of motion. More current terminology for subtalar stenting is extra-osseous talotarsal stabilization, which is commonly equated with the historic pediatric flatfoot corrective procedure arthroereisis. The historic procedures by Chambers, Grice and Green, with specific attention to the sinus tarsi, exemplify the importance of and the need for sinus tarsi and STJ control of pronatory hypermobility within the sinus tarsi/subtalar joint.11-13 While this thought process existed 70 years ago, the primary application was in the treatment of pediatric flatfoot. Arthroereisis was therefore synonymous with flatfoot correction as opposed to STJ stabilization in general.14-17 It was not until after 2006 that authors began to discuss the use of extra osseous talotarsal stabilization or arthroereisis in the adult foot.18-20
Differences in classification exist when considering design, location within the sinus tarsi and the function of newer stents. A review of current and historic literature clarifies these important differences and the evolution of sinus tarsi altering devices.21-27 Historically, arthroereisis began as a bone blocking procedure with autogenous bone graft to centrally fuse the sinus tarsi. There were subsequent attempts to alter the height of the posterior facet with inferior STJ calcaneal osteotomy. Surgeons devised procedures to stop anterior displacement of the talus with the placement of blocking devices on the calcaneal floor distal to the lateral talar process. The move toward sinus tarsi implantation evolved from bone to plastic to silastic to stainless steel to titanium devices. Newer generation implants offer longer medial stems that, in my opinion, provide more long-term stability by engaging more of the canalis tarsi in addition to occupying the sinus tarsi.
The literature supports the use of sinus tarsi stenting in both children and adults.26 Improved clinical symptoms, improved rearfoot alignment, reduced tension in the posterior tibial tendon and reduced pressure in the tarsal tunnel are results of this procedure.
A Closer Look At The Author’s Experience With Sinus Tarsi Stents
I have utilized sinus tarsi implants as a standalone procedure as well as in conjunction with other bone and joint corrective procedures. I have over 100 cases of patients treated with stents for hypermobility-induced heel spur syndrome plantar fasciitis. I have not cut a strip of plantar fascia in six years. I am not reserving stents only for patients with end-stage recalcitrant heel spur syndrome plantar fasciitis. I offer patients what I feel is a less invasive surgical procedure and the best alternative to treat their hypermobility-induced foot symptoms. Many patients choose this before plantar fasciitis symptoms ever become recalcitrant. I also use stents on patients who have recalcitrant plantar fasciitis.
Stents are a treatment option that I present at the same time as I discuss all treatment options including orthotics. Many of these patients with plantar fasciitis have concomitant early- and mid-stage bone and soft tissue deformities including bunions, hammertoes, neuromas, metatarsal or tendinopathy symptoms. While these secondary deformities were mildly or not symptomatic, they were not the primary pathology for which patients sought treatment. Their primary symptoms were heel, arch, generalized foot and leg pain or fatigue. Many also report a history of knee, hip or back symptomatology common with many podiatric and orthopedic patients.
In over six years of addressing hypermobility with implants (over 350 cases), I have found that many of my patients’ secondary foot and proximal upper level joint-related symptoms show significant improvement. Yes, I regularly see symptomatic improvement with orthotics. That is why I have so few patients requiring end-stage EPF or other fascia release procedures. I see consistently more symptom improvement at multiple levels with stenting than I did with orthotics alone during my preceding 23 years in practice.
I have seen numerous patients who had worn orthotics for many years return with recurrent heel spur syndrome plantar fasciitis and advancing secondary pedal symptoms from other bone and joint pathologies. By the time patients returned with recurrent heel spur syndrome plantar fasciitis, they frequently had secondary pronatory-induced proximal pathology in their knees, hips and back. Often, some of their earlier non-symptomatic secondary foot pathology had progressed, leading one to conclude that orthotics did not provide enough internal alignment correction and control. We also see patients return later with recurring heel spur syndrome plantar fasciitis — which was previously asymptomatic — after previous fascial cutting procedures, proof of a lack of biomechanical control through surgical fasciotomy. Many patients still wore orthotics postoperatively.
Sinus tarsi implants address and change STJ alignment. Endoscopic plantar fasciotomy cuts the symptomatic fascia, weakens and destabilizes the arch. I also use standalone implants for the treatment of painful posterior calcaneal spurs and Achilles tendinopathy (15 cases with up to a five-year follow-up), leaving the tendon attached and no spur excision. Is the posterior insertional calcaneal spur any different from the plantar calcaneal spur that most surgeons now leave untouched?
One cannot manage all cases with a single procedure. Some will require adjunct procedures. Over time, I saw a level of symptomatic improvement high enough that my comfort level with standalone implants grew.
What You Should Know About The Subtalar Joint
Growing interest in gastrocnemius recession prompts a closer look at the location of its effect on the sinus tarsi and STJ. Tight heel cords exert their effect on the calcaneus and plantarflex it. The proverbial chicken and egg question becomes: Is hypermobility more a result of the talus moving anteriorly, adducting and plantarflexing, or is it a result of the calcaneus everting? Is it a combination of both or one more than the other?
I feel that talar motion drives the navicular downward (navicular drop sign) and causes the medial column instability. One sees no increase in calcaneal inclination angles with implants yet there are reports that it is not always necessary to perform posterior tendo-aponeurosis lengthenings.28 This may be a functional result of STJ stability achieved by the implant, effectively elevating the talus and reducing pronatory shortening of the rearfoot. The question then remains: Is equinus congenital or is it partially acquired or progressive from pronatory compensation?
Specific adjunctive procedures to address multi-level deformity may be indicated. The surgeon has the option of presenting a less invasive stenting procedure initially with the understanding that revision or additional, more aggressive procedures may be necessary in the future. One could attempt revisional osteotomy while fusion revision would be most difficult with higher morbidity.
Stabilization of the STJ is paramount to creating a more stable functional foot.
Biomechanical principles, clinical practice experience and a growing body of evidence-based medicine literature confirm my beliefs that hypermobility-induced foot pain improves with increased foot stability. Increasing scientific literature among multiple medical specialties connects hypermobility and pronation with a variety of foot, ankle, knee (meniscus, anterior cruciate ligament), hip and back (disk, sciatica) pathology. I consistently see these symptoms improve with better biomechanical control of foot function.
I feel that orthotics decelerate foot pronation outside the foot by applying resistance to the foot as it pronates against the orthotic inside the shoe. I believe that we are not altering the STJ axes or planes of motion with orthotics. I feel that EPF does not change these same axes or planar relationships. During closed kinetic chain stance, the STJ pronates and the midtarsal joint unlocks within the foot on top of orthotics. Therefore, neither orthotics nor EPF create major improvement of STJ alignment and stability.
In the hypermobile flatfoot including the foot with heel spur syndrome plantar fasciitis, the majority of osseous and soft tissue corrective procedures work around the sinus tarsi and subtalar joint. Posterior calcaneal osteotomies, distal calcaneal osteomies and medial arch suspension procedures do not address the STJ or sinus tarsi alignment and function. Tendo-Achilles lengthening and gastrocnemius recession for equinus reduce the deforming pull at the posterior calcaneus. The effects of these procedures on the STJ and sinus tarsi alignment are peripheral effects around the STJ-sinus tarsi versus direct effects within the sinus tarsi that one can obtain with an implant.
I have seen consistent postoperative weightbearing X-ray changes in bone alignment using sinus tarsi stenting. During most of the first year of performing stenting for hypermobility, I obtained postoperative weightbearing X-rays to document stent placement. In a lateral X-ray view, typical changes included opening of the sinus tarsi, elevation of the navicular and improved alignment of the CYMA line. The talocalcaneal angle was reduced. On an AP X-ray view, I saw more talar head coverage by the navicular, lowered talocalcaneal angles and lowered talar second metatarsal angles. I stopped taking routine postoperative weightbearing foot X-rays after the first six to eight months as I had consistent symptomatic improvement and felt I did not require X-ray proof of alignment change. I routinely take intraoperative C-arm views to document proper guide wire and stent placement. The improved angular alignment I saw occurred through axis shifts created by talotarsal stabilization with sinus tarsi stenting.
I am against EPF because it does not address the etiology of heel spur syndrome plantar fasciitis, damages the natural integrity of the plantar fascia and alters the inherent stability the fascia provides the foot. The biomechanical principles of the past, more current theories and future research will change the understanding of foot function.
The basic premise should be that the majority of rearfoot function and its resultant effects on the forefoot stem from the STJ-sinus tarsi alignment. One must recognize this and continually study it. Sinus tarsi implants provide a less invasive, less bone and joint disruptive, modifiable and reversible means of gaining STJ stability. Stenting offers a more favorable long-term outcome over EPF by treating the etiology, not the symptomatology of heel spur syndrome plantar fasciitis. Appropriate patient selection and technique improve our outcomes. Standalone stenting has become my highest outcome treatment for plantar fasciitis. I believe sinus tarsi stenting, alone or in conjunction with other procedures, will with time most likely become a mainstay in treating hypermobility-induced foot pathology.
Dr. Fishman is in private practice in Bridgeton, NJ. He is a Diplomate of the American Board of Podiatric Surgery and a Fellow of the American College of Foot and Ankle Surgeons.
1. Weil LS. The rape of the plantar fascia. Biomechanics. 1994; 1:37.
2. Thomas JL, Christensen JC, Kravtiz SR, et al. The diagnosis and treatment of heel pain: a clinical practice guideline- revision 2010. J Foot Ankle Surg. 2010; 49(3 Suppl):S1-19.
3. Gegenschein A. Stress analysis of the standing foot following surgical plantar release. J Biomech. 2002; 35(5):629-637.
4. Cheung JT, An KN, Zhang M. Consequences of partial and total plantar fascia release: a finite element study. Foot Ankle Int. 2006; 27(2):125-132.
5. Tweed JL, Barnes MR, Allen MJ, Campbell JA. Biomechanical consequences of total plantar fasciotomy, review of the literature. J Am Podiatr Med Assoc. 2009; 99(5):422-430.
6. Sharkey NA, Ferris L, Donahue SW. Biomechanical consequences of plantar fascial release or rupture during gait: part I- disruptions in longitudinal conformations. Foot Ankle Int. 1998; 19(12):812-820.
7. Sharkey NA, Donahue SW, Ferris L. Biomechanical consequences of plantar fascial release or rupture during gait: part II- Alterations in forefoot loading. Foot Ankle Int. 1999; 20(2):86-96.
8. Brugh A, Fallat LM, Savoy-Moore RT. Lateral column symptomatology following plantar fascial release- a prospective study. J Foot Ankle Surg. 2002; 41(6):365-371.
9. Farabeuf LH. Précis de Manuel Operatoire, Ligatures, Amputations. G Masson, Paris, 1893.
10. LeLievre J. Current concepts and correction in the valgus foot. Clin Ortho Relat Res. 1970; 70:43.
11. Chambers RB, Cook TM, Cowell HR. Surgical reconstruction for calcaneonavicular coalition. Evaluation of function and gait. J Bone Joint Surg Am. 1982;64(6):829-36.
12. Grice DS. Further experience with extra-articular arthrodesis of the subtalar joint. J Bone Joint Surg Am. 1955;37-A(2):246-59.
13. Forg P, Feldman K, Flake E, Green DR. Flake-Austin modification of the STA-Peg arthrodesis: a retrospective study. J Am Podiatr Med Assoc. 2011;91(8):394-405.
14. Lepow GM, Smith SD. A modified subtalar arthroeresis implant for the correction of flexible flatfoot in children: the STA- Peg procedure. Clin Podiatr Med Surg. 1989; 6(3):585-590.
15. Thompkins MH, Nigro JS, Mendicino S. The Smith STA-Peg: a 7 year retrospective study. J Foot Ankle Surg. 1993; 32(1):27-33.
16. Brancheau S, Maxwell J, Ritchey KL, et al. The Valentin DTJ arthroeresis implant: a ten-year retrospective study. In: Vickers NS, Miller SJ (eds): Reconstructive Surgery of the Foot and Leg. Podiatry Institute Inc., Tucker, GA, 1996, pp. 44-53.
17. Dockery GL, Crawford ME. The Maxwell-Brancheau (MBA) implant in pediatric and adult flexible flatfoot conditions. Foot Ankle Q. 1999; 12(1):107-120.
18. Needleman RL. A surgical approach for flexible flat feet in adults including a subtalar arthroeresis with the MBA sinus tarsi implant. Foot Ankle Int. 2006; 27(1):9-18.
19. Kooning PM, Heesterbeek PJ, de Visser E. Subtalar arthroereisis for pediatric flexible pes planovalgus: fifteen years’ experience with the cone-shaped implant. J Am Podiatr Med Assoc. 2009; 99(5):447-453.
20. Scharer BM, Black BE, Sockrider N. Treatment of pediatric flatfoot with MBA subtalar arthroereisis implant. A retrospective radiographic review. Foot Ankle Specialist. 2010; 3(2):67-72.
21. Graham ME, Jawrani NT, Goel VK. Effect of extra-osseous talotarsal stabilization on posterior tibial tendon strain in hyper pronating feet. J Foot Ankle Surg. 2011; 50(6):676-681.
22. Viladot R, Pons M, Alvarez F, Omana J. Subtalar arthroereisis for posterior tibial tendon dysfunction: a preliminary report. Foot Ankle Int. 2003; 24(8):600-606.
23. Chang TJ, Lee J. Subtalar joint arthroereisis in adult acquired flatfoot and posterior tibial tendon dysfunction. Clin Podiatr Med Surg. 2007; 24(4):687-697.
24. Graham ME, Jawrani NT, Goel VK. Evaluating plantar fascia strain in hyperpronating cadaver feet following extra-osseous talotarsal stabilizing procedure. J Foot Ankle Surg. 2011; 50(6):682-686.
25. Graham ME, Jawrani NT, Goel VK. Effect of extra-osseous talotarsal stabilization on posterior tibial nerve strain in hyperpronating feet: a cadaveric evaluation. J Foot Ankle Surg. 2011; 50(6):672-675.
26. Graham ME, Jawrani NT, Goel VK. The effect of HyProCure sinus tarsi stent on tarsal tunnel compartment pressures in hyperpronating feet. J Foot Ankle Surg. 2011; 50(1):44-49.
27. Graham ME. Surgical treatment of hyperpronation using an extra-osseous talotarsal stabilization device: radiographic outcomes in 70 adult patients. J Foot Ankle Surg. 2012; 51(5):548-55.
28. Personal communication with Michael Graham, DPM.
For further reading, see “Understanding The Biomechanics Of Subtalar Joint Arthroereisis” in the April 2011 issue of Podiatry Today or “Dispelling The Misconceptions About Subtalar Arthroereisis” in the May 2010 issue.
For an enhanced reading experience, check out Podiatry Today on your iPad or Android tablet.
I have to simply restate the facts. There are at least four Level 1, randomized controlled trials verifying that foot orthoses have significant positive effects in treating plantar fasciitis. There are no such studies showing any positive effects of subtalar implants treating this condition.
Doug Richie, Jr., DPM, FACFAS