Heel pain is arguably the most common complaint that foot and ankle specialists hear. The majority of these complaints are linked to plantar fasciitis and we all have developed our own unique treatment algorithms for this condition. What happens when we are months into our treatment algorithm and the patient has not had much improvement or a fasciotomy has been performed and the heel pain returns? Is it still plantar fasciitis? No. In both of these scenarios, we must revert back to our differential diagnoses. While heel pain is commonly caused by plantar fasciitis, it is also attributed to heel pad atrophy, seronegative arthritis-induced inflammation, tarsal tunnel syndrome, medial calcaneal neuritis, heel spurs, calcaneal stress fractures, periosteal inflammation and entrapment of the first branch of the lateral plantar nerve (Baxter’s nerve). Baxter says as much as 20 percent of heel pain is caused by entrapment of the first branch of the lateral plantar nerve.1 While this is not new information for many, too many patients continue to slip under the radar with a diagnosis of plantar fasciitis that is refractory to exhaustive conservative and sometimes surgical care.
Understanding The Anatomy And Etiology
The first branch of the lateral plantar nerve has sensory components to the calcaneal periosteum, the long plantar ligament and the lateral plantar skin, and motor fibers to the abductor digiti minimi, flexor digitorum brevis and quadratus plantae. The first branch of the lateral plantar nerve originates from the lateral plantar nerve near the bifurcation of the tibial nerve or it may arise from the tibial nerve prior to its bifurication. It then dives through the superficial fascia at the superior border of the abductor. At this level, the investing fascia of the abductor is thicker laterally because of the reinforcement from the interfasicular ligament in continuity with the medial intermuscular septum.2 It travels distally between the lateral abductor fascia and the medial edge of the quadratus. When it reaches the lower border of the abductor hallucis, it turns and courses laterally, passing 5.5 mm anterior to the medial calcaneal tuberosity (or spur) and between the quadratus and the underlying flexor brevis until it reaches its distal target of the abductor digiti minimi.3 This is a true entrapment neuropathy. Sammarco reported histological evidence of perineural fibrosis and hypertrophy of affected nerves.4 Researchers have cited two primary points of potential entrapment.5,6 The first is the point where the nerve turns laterally between the medial edge of the quadratus plantae and the thick lateral fascia of the abductor hallucis. The second is the point where the nerve courses anterior to the tuberosity and/or spur. An increase in cubic contact of this passage (via a spur or muscle hypertrophy) and/or pronation of the rearfoot/midfoot complex, causing impingement at the nerve’s sharp turn are both possible predisposing conditions. When one sees entrapment neuropathy of the Baxter’s nerve after a plantar fasciotomy, it is typically caused by distal migration of the fascia which can entrap the nerve or is the result of scar tissue which has bound the nerve down. Be aware that overzealous spur resection can also cause iatrogenic nerve damage.
How To Ensure An Accurate Diagnosis
Whenever a patient presents with a complaint of heel pain, one must ask several questions of the patient. Subjectively, you want to know if the pain is worse after rest or after activity. Does the pain radiate distally or laterally? How long have the symptoms been present? When conducting the physical exam, one should: • palpate the proximal and distal plantar fascia; • palpate and percuss the tibial and medial calcaneal nerve; • palpate the abductor hallucis origin; • assess for pain with compression of the heel from side to side; and • see if engaging the windlass mechanism induces symptoms. By systematically gathering this information on every heel pain patient, you will have screened for all the differentials. Initially, Baxter’s nerve entrapment might not declare itself as a distinct entity. This is particularly true in the face of chronic plantar fasciitis cases in which adjacent fascial edema can lead to nerve entrapment. This can create a mixed or combined clinical picture. Classically, clinicians will note distinct, exquisite tenderness over the origin on the abductor hallucis, which can cause laterally radiating pain and/or parathesias. Many times, one can also elicit symptoms by using Phalen’s maneuver. To perform this maneuver, you invert and plantarflex the foot. This causes the porta pedis to narrow at the superior margin of the abductor hallucis and compress the nerve. You will also want to assess the patient’s ability to abduct the fifth digit. Some patients lack this ability inherently so be sure to compare the affected side with the contralateral side. If Baxter’s nerve entrapment is present, the patient may not be able to abduct the fifth digit. Clinically, we have not found this to be a reliable indicator. Patients with classic Baxter’s nerve entrapment often will deny first step pain but, on the contrary, will complain of symptoms worsening with prolonged activity. They may also complain of laterally radiating pain. During the biomechanical exam, clinicians will typically note a pronated foot structure. Plain radiographs and bone scans can help rule out osseous pathology. If you suspect systemic arthropathy, you may employ serologic testing. Obtaining a MRI can be helpful in a couple of ways. It will determine the presence or absence of inflammation around the proximal fascia as well as fascial thickness. If you see little inflammation, you can assume the heel pain is related to nerve entrapment. Another interesting finding reported by Seidelmann is increased water signal and fatty replacement of the abductor digiti minimi, which would indicate atrophy secondary to chronic nerve entrapment.7 In our opinion, NCVs and EMG are rarely helpful in making the diagnosis. It has also been our experience that the classic signs and symptoms of Baxter’s nerve entrapment are often superimposed with those of plantar fasciitis. This is logical as the same pronated foot structure, which is a probable cause for Baxter’s nerve entrapment, is often the cause of plantar fascial strain and overload as well. Fortunately, the initial treatment is virtually identical for both conditions.
A Guide To Initial Treatment
In our practice, almost all patients with plantar heel pain receive the same initial treatment. We use taping to control pathologic motion, initiate an aggressive Achilles/plantar fascia stretching program and reduce inflammation with a Medrol dose pack or, less frequently, NSAIDs. Subsequent visits incorporate combinations of plantar fascia injections, a custom orthosis, night splints and physical therapy. The majority of the patients with plantar fasciitis will respond to these treatments. We have found that although these same conservative treatments are indicated for both Baxter’s nerve entrapment and plantar fasciitis, patients with nerve entrapment traditionally have a much poorer response. In patients who have concomitant nerve entrapment and plantar fasciitis, you will most likely see a delineation of nerve entrapment symptoms as the plantar fascia calms down. If complaints persist after four to six months of the aforementioned conservative therapy, we often will inject Baxter’s nerve with a corticosteroid/local anesthetic mixture. We will also use this injection earlier if the signs and symptoms are clearly indicative of nerve entrapment. The injection is sometimes therapeutic, but almost always becomes primarily diagnostic. It is important the injection only block Baxter’s nerve and is not fanned out. One should insert the needle over the origin of the abductor at the point where you elicit symptoms with palpation. Once the needle has penetrated the skin, the patient should tell you at the point that he or she feels paresthesias crossing laterally through the heel. At that moment, you are on the nerve and should inject in that location only. If the nerve is successfully blocked, patients will often relate to you that it feels like they are walking on a rope once they stand. If the pain ceases and there is no recurrence, continue your current conservative care and monitor the injection. If the pain ceases only for a short time before returning, then a surgical release is warranted. If there is no change in the pain after the injection, the primary diagnosis would point to plantar fasciitis once one has ruled out other differential diagnoses. At this point, clinicians should consider surgical management of the plantar fascia, according to one’s preference.
Pertinent Pointers On Surgical Treatment
Although researchers have described an isolated external neurolysis of Baxter’s nerve, we typically perform the neurolysis with a plantar fasciectomy.6 This has been a well documented technique and covers both bases for those patients with mixed symptomatology. One would ensure the patient is in a supine position on the operating table with the knee and hip flexed, and the foot externally rotated. Typically, general anesthesia and a thigh tourniquet are preferred for hemostasis, but they are not required. Proceed to make a 4 cm incision on the medial heel over the proximal abductor hallucis and curving plantarly just anterior to the weightbearing surface of the heel. Making the incision directly over the course of Baxter’s nerve prevents damage to the medial calcaneal or tibial nerves, although one must watch for stray nerve branches. (See “What You Should Know About The Tibial Nerve Release” below.) Carry the dissection through the subcutaneous tissue to the abductor fascia. Proceed to release the abductor fascia superficially, dorsally and plantarly. Using a senn retractor, retract the abductor muscle belly dorsally and then plantarly to release the fascia between the abductor and quadratus plantae. At this point, surgeons will often see the venae comitantes that accompany Baxter’s nerve but they often won’t be able to see the actual nerves. Proceed to release the distal portion of the flexor retinaculum. Direct attention toward the plantar fascia, resecting a 0.5 to 1.0 inch section of the central band. Incorporate the small medial band, which is intimately related to the deep fascia between the abductor and quadratus at this point, in this excision. Be aware that overzealous fascial resection will lead to arch destabilization. One should subsequently perform careful spur resection even though this is usually not the cause of the pain. Then retract the abductor dorsally, retract the flexor brevis plantarly and palpate the course of the nerve to ensure the release of all entrapments. It is critical to avoid injuring any of the small communicating veins as this will lead to postoperative bleeding, subsequent fibrosis and scar tissue proliferation. This could set the stage for re-entrapment. Irrigate the wound and close with 4-0 nylon interrupted horizontal mattress sutures. Apply a bulky compressive dressing and release the tourniquet. Postoperatively, one should emphasize protected weightbearing in a CAM walker for four weeks. Remove the sutures at two weeks and use an Ace-type bandage. After four weeks, allow the patient to transition into a soft tennis shoe or a clog. The average period for full recovery is about three months although it may take up to six months. After about the 12th week, the patient can wear his or her orthotic again. Earlier attempts are normally unsuccessful due to pain with the plantar portion of the scar. Occasionally, one may employ a medrol dose pack in the sub-acute postoperative period to decrease deep edema.
What You Should Know About The Tibial Nerve Release
Some authors advocate extending the incision more proximally and releasing the terminal branches of the tibial nerve.8 The senior author performed a brief, unpublished prospective study in which 25 patients were divided into a concomitant tibial nerve release group and a group of just Baxter’s neurolysis and plantar fasciectomy. He found that the tibial nerve release group fared much more poorly with increased post-op discomfort, persistent edema and more frequent return of symptoms believed to be secondary to increased fibrosis and subsequent re-entrapment.
While Baxter’s nerve entrapment was once considered a controversial diagnosis for heel pain, it has experienced copious validation in the literature. Henricson and Westlin reported 10 of 11 athletes with chronic heel pain with nerve entrapment symptoms were asymptomatic after decompression and returned to their sports in an average of five weeks.8 Confitti and Tarquino reported 61 percent of patients had complete relief and 35 percent had at least a 50 percent reduction in symptoms when they combined plantar fasciectomy with external neurolysis in 26 feet with an average follow up of 25.3 months.9 Goecker and Banks reported on 18 feet with a follow-up of 32.8 months. Nine patients were completely asymptomatic and nine had mild pain after prolonged activity.10 Many other studies have similar findings.1,6,11,12 Baxter himself reports an overall success rate of 92 percent over the past 15 years.1 Few debate its existence, but Baxter’s nerve entrapment is still a diagnostic dilemma that can be overlooked by the foot and ankle specialist. By performing a systematic heel exam every time you see a patient presenting with heel pain and by keeping the diagnosis in your differentials, we can prevent this under-diagnosed condition from slipping through the cracks. An old adage noted by James Losito, DPM, brilliantly conveys the sometimes perplexing condition of heel pain: The eyes only see what the mind knows. Dr. DeHeer is a Fellow of the American College of Foot and Ankle Surgeons and is a Diplomate of the American Board of Podiatric Surgery. He is also a team podiatrist for the Indiana Pacers and the Indiana Fever. Dr. DeHeer is in private practice with various offices in Indianapolis. Dr. Offutt is a member of the American College of Foot and Ankle Surgeons. He is in private practice at various offices in Indianapolis.
1. Baxter DE. “Release of the Nerve to the Abductor Digiti Minimi” in Master Techniques in Orthopaedic Surgery of The Foot and Ankle, ed by HB Kitaoka, p 359, Lippincott Williams and Wilkins, Philadelphia, PA, 2002.
2. Sarrafian SK: “Nerves” in Anatomy of the Foot and Ankle, p 381, J.B. Lippincott, Philadelphia, PA, 1993.
3. Arenson DJ, Cosentino GL, Suran SM: The inferior calcaneal nerve. JAPA 70: 552, 1980.
4. Sammarco GJ, Helfrey RB: Surgical treatment of recalcitrant plantar fasciitis. Foot Ankle 17: 520, 1996.
5. Rondhuis JJ, Huson A: The first branch of the lateral plantar nerve and heel pain. Acta Morphol Neerl Scand 24: 269, 1986.
6. Baxter DE, Thigpen CM: Heel Pain – operative results. Foot Ankle 5: 16, 1984.
7. Seidelmann FE: “MRI evaluation of Tibialis Posterior Tendinopathy” at the International Foot and Ankle Congress, New Orleans, LA. April 30, 2004.
8. Hendrix CL, Jolly GP, Garbalosa JG, et al: Entrapment neuropathy: the etiology of intractable help pain syndrome. J Foot Ankle Surg 37: 237, 1998.
9. Confitti JA, Tarquinio TA: Operative outcome of partial plantar fasciectomy and neurolysis to the nerve of the abductor digit minimi muscle for recalcitrant plantar fasciitis. Foot Ankle Int 25: 482, 2004.
10. Goecker RM, Banks AS: Analysis of release of the first branch of the lateral plantar nerve. JAPMA 90; 281, 2000.
11. Baxter DE, Pfeffer GB: Treatment of chronic heel pain by surgical release of the first branch of the lateral plantar nerve. Clin Orthop 279: 229, 1992.
12. Kenzora JE: The painful heel syndrome: an entrapment neuropathy. Bull Hosp Jt Dis 47: 178, 1987.
13. Henricson AS, Westlin NE: Chronic calcaneal pain in athletes: entrapment of the calcaneal nerve? Am J Sports Med 12: 152, 1984.