Tag Archives: Rheumatoid Arthritis

Dextrose Prolotherapy Treatment for Unresolved “Morton’s Neuroma” Pain

Posted on June 1, 2012 | Comments Off on Dextrose Prolotherapy Treatment for Unresolved “Morton’s Neuroma” Pain

by Ross A. Hauser, MD1, Wayne A. Feister2, DO, Debra K. Brinker, RN3

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

This study investigates the effectiveness of Dextrose Prolotherapy injections on a group of patients with “Morton’s neuroma.” These patients had failed previous conservative therapies, including surgical and non-surgical procedures as well as steroid injections. In this study, seventeen patients with neuroma pain were treated for six months. Every month, 10 to 20 injections containing 0.5 to 1 milliliter of Dextrose solution were given based on patient response. Pre- and post-treatment surveys utilized both objective data (i.e., solutions used, length and number of treatments, etc.) and subjective data (post-treatment visual analog scale or VAS ratings of pain relief/reduction). The results of this short-term study suggest that Prolotherapy, using injections of Dextrose into weakened ligaments, tendons, and joints, is a promising option among current treatment choices. Prolotherapy works by stimulating the body to repair these soft tissues. Future studies must confirm not only the efficacy but also the reduced risks of Dextrose Prolotherapy for one of the most common foot ailments.

Key words: Morton’s neuroma, neuralgia, metatarsalgia, paresthesias, intermetatarsal bursitis, inflammatory arthritis, osteomyelitis, rheumatoid arthritis, localized vasculitis, ischemia, tarsal tunnel syndrome, peripheral neuritis, synovitis, tendonitis, avascular necrosis, metatarsophalangeal joint capsulitis, Hackett-Hemwall Dextrose Prolotherapy

Accepted: March, 2012
Published: June, 2012

ISSN 1941-6806
doi: 10.3827/faoj.2012.0506.0001

Morton’s neuroma (MN) is a painful condition that affects the ball of the foot. First described in the 1800s, this affliction continues to be a common cause of forefoot pain [1]. Seemingly benign, MN pain can cause extreme discomfort, making it difficult to walk. Those affected become so cautious that they are afraid to place the afflicted foot (or feet) on the ground to take a step.

The word “neuroma” suggests a tumor of the nerve; however, the term is actually a misnomer since the condition is not necessarily an abnormal growth of the nerve [2, 3]. Also, the term neuroma does not describe what is seen with a microscope. Over time, other terms have been used to describe aspects of this pathology. Based on the shape, size, and structure (morphology) of tissues noted under the microscope, other terms may apply: perineural fibrosis, endoneural edema, neurofibromata, angioneurofibromata, local demyelination, and local vascular degeneration [4, 5] (Fig. 1).

Figure 1 Possible tissue pathologies that explain interdigital pain.

What circumstances give rise to the onset of neuromas in the foot? Chronic irritation, trauma, or excessive motion induces a severe, intermittent pain between a pair of the five metatarsal heads in the bones of the fore foot. MN pain may then radiate through the nerves to the tip of the toes [6]. The shooting pain follows a path from that web space to the touching halves of adjacent toes. Seen most commonly in the second and third web space—any interdigital space between toes can be affected [7-9] (Fig. 2).

Figure 2 Interdigital spaces.

Typical symptoms in the region of the intermetatarsal spaces include sharp pains, burning sensations, and paresthesias (abnormal sensation) with weight-bearing activity. (Fig. 3) In fact, the sensation is often described as walking with a stone in the shoe or on a folded or creased sock. As the condition progresses, the pain becomes debilitating; and walking becomes more apprehensive, even to an observer. Noting these typical symptoms, an accurate diagnosis can then be made after a thorough review of the patient’s history and a physical assessment.

Figure 3 Inflamed interdigital nerve.

Evidence on the frequency of this condition is minimal; however, a foot clinic computed the incidence of patients diagnosed with a “neuroma” at a rate of 9.3% of 4000 patients who complained of foot pain [10-12]. Although neuromas in both feet and multiple neuromas in one foot occur, both conditions are rare [13, 14]. Furthermore, neuromas are seen among patients of all ages; even so, they are more prevalent in middle-aged adults [15-17]. The condition most often affects women who frequently wear pointed, high-heeled, close-toed, ill-fitting shoes poorly designed for foot mechanics [18]. Footwear that transfers body weight to the metatarsal heads may be the reason women suffer from MN more frequently than men at a documented rate of eighteen to one [19]. The pain generally intensifies with walking, weight-bearing movement, and tight-fitting shoes.

The discomfort, however, eases with rest and the removal or change of footwear [20, 21] At the onset of the condition, additional relief may be gained by removing the shoe, massaging the foot, and wiggling the toes.

The etiology (cause) of Morton’s neuroma is controversial. A longstanding entrapment theory maintains that the third digital nerve, which is large and formed by a branch of the medial and lateral plantar nerves, is compromised by mechanical irritation. With dorsiflexion—when the toes or foot are bent upward toward the nose—the unyielding transverse ligament fixates the proximal end of the digital nerve [22, 23] (Fig. 4). However, this pinching does not always occur in one nerve; other intermetatarsal spaces can be affected [24]. Since it is not a true neuroma (tumorous nerve), some refer to the condition as Morton’s metatarsalgia [25]. Metatarsalgia is pain related to the metatarsal bones of the foot [26]. Another explanation for the pain is an ischemia or lack of blood flow through the plantar digital artery, which precedes a fibrous thickening around the nerve, called a perineural fibrosis [27]. In addition, a pathophysiological theory for MN claims that the intermetatarsal bursa—distally located to the transverse metatarsal ligament and close to the neurovascular bundles—is irritated. Thus inflamed, secondary fibrosis in the bursa can lead to the symptoms of neuroma. Lateral compression of the foot will then invariably cause pain, probably due to the inflamed bursa—not the nerve—being squeezed between the metatarsal heads [28] (Fig. 4).

Figure 4 Cross sectional view of the fore foot displaying the interdigital points of irritation/inflammation.

The inflamed and enlarged bursa causes a click when the metatarsals are squeezed. This distinctive click, called “Mulder sign,” can be used when diagnosing Morton’s neuroma [29].

A clear knowledge of conditions that affect the metatarsal region is critical to making a definitive diagnosis. Initially, possible diagnoses include metatarsal stress fracture, intermetatarsal bursitis, inflammatory arthritis, osteomyelitis, rheumatoid arthritis, localized vasculitis, ischemia, tarsal tunnel syndrome, peripheral neuritis, synovitis, tendonitis, avascular necrosis, metatarsophalangeal joint capsulitis, and others [30-32] (Fig. 5).

Figure 5 Diagnoses to consider when interdigital pain is the main symptom.

Many treatments have been developed for relief of the symptoms of Morton’s neuroma, but initially, non-surgical approaches are preferred. Among these conservative treatments from simple to complex are changing the footwear; avoiding high-heeled shoes; resting the feet; applying ice; elevating the foot; taking anti-inflammatory medications; taping and strapping, padding, and immobilizing the foot; receiving physical therapy; wearing orthotics or other shoe gear; and injecting steroids. When conservative approaches are unsuccessful, surgery is generally sought as the next step. Surgical approaches include resection, transection, decompression, excision of the involved nerve, and cryogenic nerve ablation.

Another conservative treatment for Morton’s neuroma pain is Prolotherapy, which has a longstanding record of success with hypermobility, when joints are unusually loose or abnormally flexible.

If the goal of padding and strapping is to reduce forefoot motion and pain, it is reasonable to utilize a treatment, such as Prolotherapy, that not only reduces hypermobility, but also results in joint stabilization [33].

Additionally, recent studies demonstrate that injection therapy, utilizing 4% sclerosing alcohol, has success rates of 84 – 89% [34-36]. Dextrose Prolotherapy injections will induce a proliferative response without the risk of alcohol infiltrating the surrounding tissue. The overall purpose of this study was to record the outcomes of Dextrose Prolotherapy on a group of patients with Morton’s neuroma in a private pain clinic.

Patients and Methods

In the study, an attending physician treated seventeen patients with Morton’s neuroma at a private medical clinic. All subjects signed a consent form, stating that a minimum of three and a maximum of six monthly treatments might be needed.

To meet the criteria for inclusion in the study, patients had to be at least 18-years-old, to have suffered unresolved Morton’s neuroma at any intermetatarsal space, and to have failed previous conservative treatment.

At the clinic, a search of electronic medical records (EMR) to find patients with the diagnosis of Morton’s neuroma was conducted.

To be included in the study, two criteria were paramount: 1) a diagnosis of Morton’s neuroma, which had to be the primary condition, and 2) a six-month time lapse, since the patient’s last Prolotherapy injections. The search revealed 31 patients diagnosed with Morton’s neuroma; of these, five could not be contacted by phone (three attempts were made before discontinuing phone calls). Two patients chose not to participate.

Five patients were excluded because of multiple foot problems that took priority over Morton’s neuroma: previous surgeries, osteoarthritis, and ankle problems. Two patients were excluded because not enough time had elapsed—at least six months—since their last Prolotherapy session.

Patients selected for the study had to complete preliminary oral, written, and visual surveys. Demographic information was obtained. Then the patient completed a visual analog scale (VAS), which includes ratings of pain at rest; pain with normal activities; pain while walking barefoot; ability to walk distances without pain; as well as stiffness and numbness/burning (Fig. 6). Finally, an assessment interview with clinical staff members collected both subjective and objective data, such as the type and duration of symptoms, previous treatments and tests, limitations to activity, and previous medical opinion.

Figure 6 Questionnaire used by patients to assess levels of pain.

Next, a physical examination determined objective data by checking for the following: the precise location of the pathology or point of maximal tenderness by palpating (light and/or deep touch) the affected web space; the presence or absence of Mulder’s click; and the severe pain that results with lateral compression of the forefoot.

The end of the Prolotherapy treatment was determined when patients indicated a zero to 1 on the pain scale, or their personal goals for pain relief or for the ability to function were met. Although some had little pain, their main goal was to eradicate numbness, which they found disturbing. Some patients wanted to achieve a zero to 1 level of pain while walking, even with level 4 pain while jumping. Therefore, they would stop treatment with a low level of walking discomfort.

Following treatment, interviews and surveys were completed on a monthly basis. Monthly data collection included the total percentage of improvement; VAS score of pain; level of pain intensity; level of stiffness; degree of crepitation (grating sensations from a joint); range of motion; ability to perform the ADLs (activities of daily living) and to exercise the affected body part.

Six months after the last visit, patients were called to obtain information and answered detailed questions. Interviews provided data on the level of foot/toe pain (VAS scale), percent of overall improvement, limitations/improvements in activities and walking, duration of post-treatment pain relief, and assessment of the treatment by the patient.

For data analysis, patient responses were collected, calculated, and compared at three different times: prior to Prolotherapy, during monthly visits, and in phone interviews conducted six months after Prolotherapy. Statistical analysis using Graph Pad Software calculated the paired student t-test before and after Prolotherapy.

Technique

The Hackett-Hemwall technique of Prolotherapy (www.hacketthemwall.org) was used. Each patient received 10 – 20 injections of 15% Dextrose, 0.2% Procaine, and a 10% Sarapin solution, for a total of 10 to 20 cubic centimeters of solution per foot. Each injection consisted of 0.5 to 1 cubic centimeter of solution and used a two-inch, 27-gauge needle. Injected areas were web spaces one through four—with attention given to metatarsophalangeal joints, dorsal and plantar surfaces, and joint capsules and ligaments (Fig. 7). If applicable, patients were advised to reduce or discontinue non-steroidal anti-inflammatory (NSAID), steroidal and narcotic medications, and other therapies. Prolotherapy treatments were discontinued, once a patient reached a clinical resolution of symptoms.

Figure 7 Prolotherapist injecting the third interdigital space with sclerosant solution.

Results

The final study group included 17 patients but 19 feet, since some patients suffered from MN in both feet. Ten right feet and nine left feet were treated. The average age of the 17 patients was 57 years: eleven were women, and six were men.

Before introducing Prolotherapy, study patients reported previous treatments. No one used pain medications for their symptoms. Some patients had tried wide-toed shoes, orthotics, padding, chiropractics, acupuncture, and steroid injections. Some patients had had MRI and radiographic diagnosis. One of seventeen had seen a podiatrist. A physician told three patients that surgery was required, but only one had surgery to remedy the pain on the other foot.

From patient questionnaires, averages were determined for periods of time. The average length of time patients experienced the pain of Morton’s neuroma was 20 months before entering the clinic. Patients received an average of 3.7 Prolotherapy treatments.

The average time of follow-up was 13.3 months. To determine the efficacy of treatments, only those patients with follow-up more than 6 months were included.

Patients’ subjective experience of pain offers the best measure for statistical accuracy. Patients were asked to rate their pain levels on a scale of 0 to 10—with 0 being no pain and 10 being severe crippling pain. All 17 patients reported pain as a symptom. Thus, patients were asked to report pain levels before and after Prolotherapy in these four categories: 1) pain at rest; 2) pain with normal activities; 3) pain with exercise, and 4) pain while walking barefoot.

Concerning 1) pain at rest: prior to Prolotherapy treatment, VAS pain levels averaged 4.68. None of the patients had a starting pain of less than three. After Prolotherapy treatment, VAS pain levels averaged 0.95.

Concerning 2) pain with normal activity and mobility: prior to Prolotherapy treatment, 15 of the 17 participants reported walking with some degree of pain, and a VAS pain level of 6.89. Eleven of 17 patients were unable to walk fifty feet without pain; 14 of 17 could not walk a half-mile without pain. Four of 17 patients reported an inability to walk barefoot. After Prolotherapy, all patients reported improvements in walking without pain, and a VAS pain level of 1.89. Fourteen of the 17 participants walked normally again and rated their pain relief at greater than 74%. Sixteen of the 17 could walk one block or more.

Concerning 3) pain with exercise: prior to Prolotherapy, 15 of the 17 patients reported decreased ability to exercise, and a VAS pain level of 7.27. Of those 15, eight were totally compromised and unable to exercise; five were moderately (only 30 to 60 minutes possible) to severely compromised (only 0 to 30 minutes possible). Nearly half of the patients were totally compromised in their athletic abilities prior to treatment. After Prolotherapy, 5 of the 17 patients reported being able to exercise as much as they wanted without impediments and with satisfaction, with a VAS pain level of 1.73. Other physical improvements occurred, notably, decreases in stiffness and numbness (burning). Thirteen to 14 patients reported a 100% improvement in the activities of daily living that continued to the end of the study. None reported an inability to exercise.

Concerning 4) pain while walking in bare feet: prior to Prolotherapy treatment, 10 of 17 patients could not walk barefooted without severe pain at levels eight, nine, or ten, and an average VAS pain level of 6.47. Furthermore, 12 of 17 patients could walk less than 50 feet before they experienced noticeable pain, with or without shoes. Only 3 of the 17 patients could walk more than a half-mile without pain.

After Prolotherapy, all patients had a pain level of four or less walking barefooted, and a VAS pain level of 1.65. As for walking distances without pain, all patients could walk at least one block or more. One patient was restricted to walking between 50 feet and one block. Among the 19 treated feet of the 17 patients in the study, eighteen feet could manage walking a half-mile or more, eight of the treated feet reported no walking restrictions.

When comparing the four previous categories before and after Prolotherapy, all reached a statistically significant outcome with a paired student t-test of p = <0.0001. This p-value confirms that the numerical results, when compared and tallied, exceed the mathematical probability of mere chance.

Thus, this prospective, non-controlled study demonstrates that Hackett-Hemwall Dextrose Prolotherapy decreases pain and improves the quality of life for patients with Morton’s neuroma, which was unresolved by previous therapies, medications, and interventions. Prolotherapy provided a relief of 74% for 14 out of 17 of the patients. Among the three patients who were told they needed surgery, two patients felt sufficient pain relief with Prolotherapy to avoid surgery. After the study period, patients experienced overall improvement in range of motion, ability to walk and exercise, as well as relief of stiffness and numbness/burning (Fig. 8).

Figure 8 Survey responses before and after Prolotherapy on levels of pain with various activities.

Discussion

This study should not be compared to a clinical trial in which a treatment is studied under controlled conditions. Instead, the projected goal was to document the responses of patients with unresolved Morton’s neuroma pain to the Hackett-Hemwall technique of Dextrose Prolotherapy. Clearly, the study’s strength was the number of quality of life parameters examined. Quality of life conditions—such as the ability to walk and exercise, enhanced range of motion, reduced stiffness, enjoyment of activities of daily life, and reduced levels of pain—are all important factors affecting the person with Morton’s neuroma.

Improvements in a large number of variables were most likely the result of Prolotherapy treatment. There is no medical test to quantify pain relief. However, observable, documented changes—such as the ability to walk or walk barefoot, to exercise, to work, and to use less pain therapies—are valid measures of success for patients whose health and vitality have considerably improved.

This study noted two empirical shortcomings. One is the subjective nature of the data gathered by the most reliable methods available. Surveys, for instance, relied on the patients to rate their pain, stiffness, and degree of disability. A second obvious weakness is the small number of patients involved in the study. However, on the positive side, this small study group made it possible to see results in a relatively short time span.

Many treatments for the relief of Morton’s neuroma symptoms have developed over time. Although conservative, non-surgical, and surgical approaches have been used, their effectiveness as a treatment is variable, often leaving patients with mixed results and questionable improvement.

A review of three trials that involved 121 people was not able to determine the effectiveness of conservative, surgical, and non-surgical interventions because, as the authors noted, there was insufficient evidence and research flaws. For instance, there were only three randomized controlled studies of the various treatments. The authors were also unable to find any studies to identify the incidence or prevalence of this condition. In the review of the three trials, researchers found no evidence to support the use of pronation insoles, which are routinely used as a conservative approach. Furthermore, they found no evidence supporting the effectiveness of corticosteroids (non-surgical); and they gave a poor grade to the surgical approach due to high risks of amputation neuroma (minimum of 20%), painful plantar scars, and postoperative complications [37].

Histomorphological findings are accepted as the gold standard for diagnosing Morton’s neuroma. Of consequence is a histomorphologic study of 23 nerve biopsies from patients with typical Morton’s neuroma symptoms compared to 25 plantar nerve autopsies of individuals with no record of forefoot problems. The study revealed that nerve biopsies from MN patients had the same characteristics as those removed from autopsies. Tissue samples were identical and could not be distinguished one from the other. However, none of the excised tissue in this study was found to be normal; all had the pathological features of fibrotic tissue (thickened, scarred) [38]. Another study found identical histology when comparing Morton’s neuroma and control patients, observing the same fibrotic changes in the symptomatic patients as in the asymptomatic patients [39] From this research , the question arises as to whether the “neuroma” is actually the cause of the condition, caused by other conditions, or present in normal plantar nerves?

Searches with magnetic resonance imaging (MRI) for typical pathologies of Morton’s neuroma did not discover any diagnostic features (symptomatology). In a retrospective study of 85 foot MRI examinations, 33% of patients with no clinical evidence of Morton’s neuroma showed diagnostic “lesions” suggestive of the condition [40] In a study of 70 asymptomatic volunteers, 30% were diagnosed with Morton’s neuromas [41].

In MR imaging after neuroma resection, a neuroma was found in 26% of the asymptomatic and 50% in the symptomatic web spaces [42]. Thus, MRI reveals neuroma-like abnormalities in both symptomatic and asymptomatic patients [43].

Another retrospective study of steroid injections showed a 47% improvement in the recipients [44]. A study gauging symptom relief from a series of corticosteroid injections reported that 30% of the patients attested to total symptom relief [45]. In another study involving 60 patients, the results of conservative treatment were considered poor in 73% of the cases; thus, the authors recommended surgery as the initial treatment of choice [46].

Surgical removal of the neuroma is reported to provide satisfactory relief in 76 – 85% of the patients [47, 48]. Nonetheless, there were exceptions. In a study of 56 patients with excised neuromas, two thirds of the satisfied patients continued to have tenderness at the cut end of the common digital nerve; 75% were still limited in their choice of footwear; and 14% failed to demonstrate any notable improvement. Those who did not respond to surgery continued their pre-surgical use of steroids, lidocaine, and broad-toed shoes [49]. Other complications of surgery include numbness of the affected toes, postoperative infection, tenderness at the incision, keratosis (scarring) of the sole of the foot, recurrence of pain, and an amputation neuroma. Nearly 20% of the patients continued to feel pain after the first surgery, and few found pain relief with additional surgery [50]. In view of these findings, patients should be informed of the possible results of surgery, since adverse outcomes are common.

Patients searching for alternatives to the mainstream medical care are prudent to consider Prolotherapy for reasons of which practitioners of Prolotherapy are aware. First, Prolotherapists know that ligaments need to be tighter, shorter, and stronger. If the intermetatarsal ligament is weak and loose, however, the interdigital nerve rises up between the metatarsal heads where they can be compressed and, thereby, traumatized [51]. Abnormal metatarsal mobility that results from such weakened ligaments inflames the bursa (cushioning sac) between the heads, creating a space into which tissue from the plantar side of the foot can enter and is subsequently pinched by the metatarsal heads [52]. A fibrous build-up can occur when the weak ligaments allow tissue between bones to be rubbed and irritated. Because Prolotherapy strengthens weakened ligaments and connective tissues, it is a viable treatment option.

For Prolotherapists, Morton’s “neuroma” is most likely mechanically-induced from excessive motion between the metatarsals, combined with excessive weight-bearing stress on the forefoot [53]. Hypermobility of the forefoot predisposes a person to this condition, and Prolotherapy injections at the plantar and dorsal structures of the affected metatarsals will benefit the patient [54].

Prolotherapy has a long history of being utilized for unresolved foot and toe pain [55]. In a study of 19 patients with unresolved foot and toe pain, 63% of patients noted 75% pain relief from Prolotherapy [56] In a study undertaken precisely to evaluate the effectiveness of Dextrose Prolotherapy on Morton’s neuroma pain, 16 of the 20 patients with chronic plantar fasciitis who had failed previous conservative treatment reported good to excellent results from the Prolotherapy [57].

As a treatment, Prolotherapy has been utilized for approximately 100 years, with its modern injection protocols being formalized by George S. Hackett, MD in the 1950s [58, 59]. Increasingly popular in the US, Prolotherapy is used nationally and internationally in both alternative (integrative) and allopathic (orthodox) medical practice [60] The treatment is simple. When therapeutic solutions are injected into painful and tender ligaments, tendons, and joints—an inflammation develops, which causes healing cells to proliferate and strengthen damaged ligament, tendon, and joint structures [61], These injections improve both joint stability and biomechanics, ultimately decreasing pain [62]. In this way, Prolotherapy is a safe and practical option for hypermobile joints of the foot that cause persistent pain [63].

Conclusion

While the exact cause of Morton’s neuroma (MN) is still debated, this study confirms that the Hackett-Hemwall technique of Dextrose Prolotherapy not only reduces levels of pain for patients with MN, but also enhances other quality of life concerns. Conventional therapies, on the other hand—rest, weight loss, exercises for muscle strengthening, orthotics, massage therapy, physiotherapy, manipulation, analgesics, non-steroidal anti-inflammatory drugs, anti-depressant medications, trigger point and steroid injections, and various surgical treatments—often result in residual pain for the patients [64-66]. Patients with MN, therefore, are searching for alternative treatments to relieve the pain [67]. Patients unable to find relief with traditional treatments are also hesitant to use options like surgery.

Surgery for Morton’s neuroma, for instance, presents these significant risks: numbness of the affected toe, postoperative infection, incisional soreness, scarring, and recurring stump neuromas [68, 69]. Instead of these traditional options, patients dealing with Morton’s neuroma are now trying Prolotherapy [70]

As a promising option, Prolotherapy—using injections of an irritant—tightens, shortens, and strengthens ligaments, tendons, and joints. Prolotherapy works by stimulating the body to repair these soft tissues. The solution starts and accelerates healing through inflammation, triggering a healing cascade of effects. Initially, fibroblasts—immature cells capable of producing collagen fibers—proliferate. Hence, the term Prolotherapy arose from this observable process. Once collagen forms, it is woven (reticulated) into ligament and tendon tissue. In this manner, Prolotherapy has the potential to stop the disease process.

In some cases, preliminary, anecdotal evidence suggests that Prolotherapy can reverse Morton’s neuroma. In one double-blind animal study over a six-week period, for instance, Prolotherapy was shown to increase ligament mass by 44%, ligament thickness by 27%, and ligament-bone attachment by 28% [71]. In human studies on Prolotherapy, biopsies performed after the completion of Prolotherapy showed significant increases in collagen fiber and ligament diameter of 60% [72, 73]. These finding are especially significant since a potential cause of Morton’s neuroma is weakened ligaments [74, 75].

In this prospective study, the Hackett-Hemwall technique of Dextrose Prolotherapy used on patients averaging 1.5 years of unresolved pain with Morton’s neuroma was shown to improve their quality of life, which continued 13.3 months after their last session. The 17 patients treated with Prolotherapy reported significantly less pain, stiffness, disability, or use of other pain therapies, as well as improvements in walking, range of motion, ability to exercise, and performing activities of daily living.

Patients told that there were no other treatments for pain or that surgery was their only option achieved the same positive results. This study justifies the desirability and use of Prolotherapy for Morton’s neuroma pain. Future studies need to further substantiate these findings, especially if Prolotherapy enables Morton’s neuroma sufferers to avoid surgery and its possible adverse effects. Although a study with more patients in a controlled empirical setting is needed to document the efficacy of Hackett-Hemwall Dextrose Prolotherapy, this treatment should be considered, based on the substantial advantages and minimal drawbacks (e.g., aversion to needles), as well as the reduced risks and increased rewards of Prolotherapy over conventional treatments.

References

  1. Morris MA. Morton’s metatarsalgia.clinical orthopaedics and related research. 1977 127: 203-207. [PubMed]
  2. Spina R, et al. The effects of functional fascial taping on Morton’s neuroma: A case report. Australasian Chiropractic July 2002 10: 45-50. [Website]
  3. Hassouna H, Singh D. Morton’s metatarsalgia: pathogenesis, aetiology and current management. Acta Orthop Belg 2005 71: 646-655. [PubMed]
  4. Rout R, Tedd H, Lloyd R, Ostlere S, Lavis GJ, Cooke PH, Sharp RJ. Morton’s neuroma: diagnostic accuracy, effect on treatment time and costs of direct referral to ultrasound by primary care physicians. Pual Prim Care 2009 17: 277-282. [PubMed]
  5. Morscher E. Ulrich J, Dick W. Morton’s intermetatarsal neuroma: morphology and histological substrate. Foot Ankle Int 2000 21: 558-562. [PubMed]
  6. Decherchi P. Thomas George Morton’s metatarsalgia. Presse Med 2007 36: 1098-1103. [PubMed]
  7. Pastides P, El-Sallakh S, Charalambides C. Morton’s neuroma: A clinical versus radiological diagnosis. Foot Ankle Surg. 2012 18 :22-4. [PubMed]
  8. Beltran LS, Bencardino J, Ghazikhanian V, Beltran J. Entrapment neuropathies III; lower limb. Semin Musculoskelet Radiol 2010 14: 501-111. [PubMed]
  9. Nissen Kl. Plantar digital neuritis: Morton’s metatarsalgia. JBJS 1948 30: 84-93. [PubMed]
  10. Pace A, Scammell B, Dhar S. The outcome of Morton’s neurectomy in the treatment of metatarsalgia. Int Orthop. 2010 April; 34:511-5. [PubMed]
  11. Hassouna H, Singh D. Morton’s metatarsalgia: pathogenesis, aetiology and current management. Acta Orthop Belg 2005 71: 646-655. [PDF]
  12. Banks A, et al. McGlamry’s comprehensive textbook of foot and ankle surgery. Vol 2.Philadelphia,PA. Lippincott, Williams, and Wilkins 2001.
  13. Lee KT, Lee YK, Young KW, Kim HJ, Park SY. Results of operative treatment of double Morton’s neuroma in the same foot. 2009, J Orthop Sci 2009 14: 574-578. [PubMed]
  14. Kay D, Bennett GL. Morton’s neuroma. Foot Ankle Clin. 2003 Mar;8(1):49-59. [PubMed]
  15. Thomas JL, Blitch EL 4th, Chaney DM, Dinucci KA, Eickmeier K, Rubin LG, Stapp MD, Vanore JV. Diagnosis and treatment of forefoot disorders. Morton’s intermetatarsal neuroma. J Foot & Ankle Surgery 2009 48: 251-256. [PubMed]
  16. Adams WR 2nd. Morton’s neuroma. Clin Podiatr Med Surg. 2010 27: 535-545. [PubMed]
  17. MollicaMB. Morton’s neuroma: Getting patients back on track. Physician Sportsmedicine 1997 25: 76-82. [PubMed]
  18. Wu KK. Morton neuroma and metatarsalgia. Current Opinion Rheumatology 2000 12: 131-142.[PubMed]
  19. Terk M, Kwong PK, Suthar M, Horvath BC, Colletti PM. Morton neuroma: Evaluation with MR imaging performed with contrast enhancement and fat Suppression Radiology 1993 189:239-241. [PubMed]
  20. Clinical Practice Guideline Forefoot Disorders Panel, Thomas JL, Blitch EL 4th, Chaney DM, Dinucci KA, Eickmeier K, Rubin LG, Stapp MD, Vanore JV. Diagnosis and treatment of forefoot disorders. Morton’s intermetatarsal neuroma. J Foot & Ankle Surgery 2009 4: 251-256. [PubMed]
  21. Coady CM, Gow N, Stanish W. Foot problems in middle-aged patients: keeping active people up to speed. Phys Sportsmed 1998  26: 31-42. [PubMed]
  22. Lee KS. Musculoskeletal ultrasound: how to evaluate for Morton’s neuroma. AJR Am J Roentgenol. 2009 Sep; 193(3):W172. [PubMed]
  23. Fabie F, Accadbled F, Tricoire JL, Puget J. Anatomic danger of percutaneous section of the inter-metatarsal ligament for the treatment of Morton’s neuroma. Rev Chir Orthop Reparatrice Appar Mot 2007 93: 720-724.French. [Pubmed]
  24. Bossley CJ, Cairney PC. The intermetatarsophalangeal bursa – its significance in Morton’s metatarsalgia. JBJS 980 62B: 184-187. [PubMed]
  25. Schuh R, Trnka HJ. Metatarsalgia: distal metatarsal osteotomies Foot Ankle Clin. 2011 16: 583-595. [PubMed]
  26. Birbilis T, Theodoropoulou E, Koulalis D. Forefoot complaints-the Morton’s metatarsalgia. The role of MR imaging. Acta Medica (Hradec Kralove) 2007 50: 221-222. [PubMed]
  27. Nissen Kl. Plantar digital neuritis: Morton’s metatarsalgia. JBJS 1948 30: 84-93. [PubMed]
  28. Claustre J, Bonnel F, Constans JP, Simon L. The intercapital metatarsal space: anatomical and pathological aspects. Rev Rhum Mal Osteoartic 1983 50: 435-440. [PubMed]
  29. Mendicino SS, Rockett MS. Morton’s neuroma. Update on diagnosis and imaging. Clin Podiatr Med Surg 1997 14: 303-311. [PubMed]
  30. Schreiber K, Khodaee M, Poddar S, TweedEM. Clinical Inquiry. What is the best way to treat Morton’s neuroma? 2011 60: 157-158. [PubMed]
  31. Lee M, Kim S, Huh YM, Song HT, Lee SA, Lee JW, Suh JS. Morton neuroma: Evaluated with ultrasonography and MR imaging. Korean J Radiolog 2007 8: 148-155. [PubMed]
  32. Summers A. Diagnosis and treatment of Morton’s neuroma. Emerg Nurse  2010 18: 16-17. [PubMed]
  33. Hackett GS, Henderson DG. Joint stabilization: An experimental, histologic study with comments on the clinical application in ligament proliferation. Amer J Surg 1955 89: 968-973. [PubMed]
  34. Hughes R; Ali K; Jones H; Kendal S; Connell D. Treatment of  Morton’s neuroma with alcohol injection under sonographic guidance: Follow-up of 101 cases. Am J Roentgenology 2007 188:1535-1539.[PubMed]
  35. Hyer C, Mehl LR, Block AJ, Vancourt RB. Treatment of recalcitrant intermetatarsal neuroma with 4% sclerosing alcohol injection: A pilot study. J Foot & Ankle Surgery 2005 44: 287-291. [PubMed]
  36. Dockery GL. The treatment of intermetatarsal neuromas with 4% alcohol sclerosing injections. Journal of Foot and Ankle Surgery 1999 38:403-408. [PubMed]
  37. Thomas CE, et al. Interventions for the treatment of Morton’s neuroma (review). The Cochrane Library 2005 Issue 2:1-14.
  38. Morscher  E, Ulrich J, Dick W. Morton’s intermetatarsal neuroma: Morphology and histological substrate. Foot Ankle Int 2000 21: 558-562. [PubMed]
  39. Bourke G, Owen J, Machet D. Histological comparison of the third interdigital nerve in patients with Morton’s metatarsalgia and control patients. Aust NZ J Surg 64: 421-424. [PubMed]
  40. Bencardino J, Rosenberg ZS, Beltran J, Liu X, Marty-Delfaut E. Morton’s neuroma: Is it always symptomatic? Am J Roentgenology 2000 175: 649-653. [PubMed]
  41. Zanetti M, Strehle JK, Zollinger H, Hodler J. Morton neuroma and fluid in the intermetatarsal bursae on MR images of 70 asymptomatic volunteers. Radiology 1997 203: 516-120. [PubMed]
  42. Espinosa N, Schmitt JW, Saupe N, Maquieira GJ, Bode B, Vienne P, Zanetti M. Morton neuroma: MR imaging after resection—postoperative MR and histologic findings in asymptomatic and symptomatic intermetatarsal spaces. Radiology 2010 255: 850-856. [PubMed]
  43. Resch S, Stenstrom A, Jonsson A, Jonsson K.  The diagnostic efficacy of magnetic resonance imaging and ultrasonography in Morton’s neuroma: a radiological-surgical correlation. Foot Ankle Int 1994 15: 88-92. [PubMed]
  44. Bennett GL, Graham CE, Mauldin DM. Morton’s interdigital neuroma: A comprehensive treatment protocol. Foot Ankle Int 1995 16: 760-763. [PubMed]
  45. GreenfieldJ,  Rea J Jr, Ilfeld FW. Morton’s interdigital neuroma: Indications for treatment by local injections versus surgery. Clinical Orthopaedics Rel Research 1984 185:142-144. [PubMed]
  46. Gaynor R, Hake D, Spinner SM, Tomczak RL. A comparative analysis of conservative versus surgical treatment of Morton’s neuroma JAPMA  1989 79: 27-30. [PubMed]
  47. Monacelli G, Cascioli I, Prezzemolo G, Spagnoli A, Irace S. Surgical treatment of Morton’s neuroma: our experience and literature review. Clin Ter 2008 159: 165-167. Article in Italian. [PubMed]
  48. Faraj A, Hosur A.  The outcomes after using two different approaches for excision of Morton’s neuroma. Chinese Medical Journal 2010 123: 2195-2198. [PubMed]
  49. Mann R, Reynolds JC. Interdigital neuroma-a critical clinical analysis. Foot & Ankle 1983 3: 238-243. [PubMed]
  50. Johnson J, Johnson KA, Unni KK. Persistent pain after excision of an interdigital neuroma – results of reoperation. JBJS 1988 70A: 651-657. [PubMed]
  51. Read JW, Noakes JB, Kerr D, Crichton KJ, Slater HK, Bonar F. Morton’s metatarsalgia: sonographic findings and correlated histopathology. Foot Ankle Int. 1999  2093:153-161. [PubMed]
  52. Mulder JD. The causative mechanism in Morton’s metatarsalgia. JBJS 1951 33B: 94-95. [PubMed]
  53. Wu KK. Morton interdigital neuroma: A clinical review of it etiology, treatment and results. J of Foot and Ankle Surgery 1996 35(2): 112-119; discussion 187-8. [PubMed]
  54. Hackett G, et al. Ligament and tendon relaxation treated by prolotherapy. 5th ed.Oak Park,IL. Gustav A. Hemwall 1992
  55. Hauser R, et al. Prolo your pain away! 3rd edition.Oak Park,IL.BeulahLand Press 2007 139-147.
  56. Hauser R,  A retrospective observational study on Hackett-Hemwall dextrose prolotherapy for unresolved foot and toe pain at an outpatient charity clinical in rural Illinois. J of Prolotherapy 2011 3: 543-551. [Website]
  57. Ryan M. Sonographically guided intratendinous injections of hyperosmolar dextrose/lidocaine: A pilot study for the treatment of chronic plantar fasciitis. Brit J Sports Medicine 2009 43: 303-306.  [Website]
  58. Hauser RA. Punishing the pain. Treating chronic pain with Prolotherapy. Rehab Manag 1999 12: 26-28. [PubMed]
  59. Rabago D. Prolotherapy in primary care practice. Primary Care 2010 37: 65-80. [PubMed]
  60. Schnirring L. Are your patients asking about prolotherapy? Physician Sportsmedicine 2000 28:15-17.
  61. Rabago D, Best TM, Beamsley M, Patterson J. A systematic review of prolotherapy for chronic musculoskeletal pain. Clin J Sports Medicine 2005 15: 376-380. [PubMed]
  62. Centeno CJ, Elliott J, Elkins WL, Freeman M. Fluoroscopically guided cervical prolotherapy for instability with blinded pre and post radiographic reading. Pain Physician 2005 8: 67-72.  [PubMed]
  63. Tsatsos G. Prolotherapy in the treatment of foot problems. JAPMA 2002  92: 366-368. [PubMed]
  64. Martin E. Pharmacologic management of foot pain in the older patient. J Am Podiatr Med Assoc 2004 94(2):98-103.
  65. Drury AL. Use of homeopathic injection therapy in treatment of Morton’s neuroma. Altern Ther Health Med. 2011 17:48. [PubMed]
  66. Jannink M. Effectiveness of custom-made orthopaedic shoes in the reduction of foot pain and pressure in patients with degenerative disorders of the foot. Foot Ankle Int 2006 27: 974-979. [PubMed]
  67. Kay D, Bennett GL. Morton’s neuroma Foot Ankle Clin. 2003  8: 49-59. [PubMed]
  68. Singh SK, Loli JP, Chiodo CP. The surgical treatment of Morton’s neuroma. Current Orthopaedics 2005: 19 379-384.
  69. Hughes R; Ali K; Jones H; Kendal S; Connell D. Treatment of Morton’s neuroma with alcohol injection under sonographic guidance: Follow-up of 101 cases. American Journal of Roentgenology 2007 188: 1535-1539. [PubMed]
  70. Hauser, RA, Hauser, MA. Prolo Your Pain Away!, 2007 3rd edition Beulah Land Press,Oak ParkIL pg 144-145.
  71. Liu Y. An in situ study of the influence of a sclerosing solution in rabbit medial collateral ligaments and its junction strength. Connective Tissue Research1983 2: 95-102. [PubMed]
  72. Maynard JA, Pedrini VA, Pedrini-Mille A, Romanus B, Ohlerking F. Morphological and biochemical effects of sodium morrhuate on tendons. J  Orthopaedic Research. 1985 3: 236-248.  [PubMed]
  73. Hauser R, et al. Prolo your pain away! 3rd edition.Oak Park,IL.BeulahLand Press 2007 139-147.
  74. Wu KK. Morton’s interdigital neuroma: a clinical review of its etiology, treatment and results. J Foot Ankle Surg 1996 35:187-188. [PubMed]
  75. Hauser RA, Hauser MA, Cukla JK. A retrospective observational study on Hackett-Hemwall Dextrose Prolotherapy for unresolved foot and toe pain at an outpatient charity clinic in rural Illinois. J Prolotherapy. 2011 3: 543-551.  [Website]
  76. Ravin T, Cantieri M, Pasquarello G. Principles of Prolotherapy. Denver,CO:AmericanAcademy of Musculoskeletal Medicine; 2008.

Address Correspondence to: : Ross Hauser, MD, Caring Medical, 715 Lake St., Suite 600, Oak Park, IL 60301

1Medical Director, Caring Medical & Rehabilitation Services; Editor-in-Chief, Journal of Prolotherapy
2Private Practice, Medical Editor, Ohio University Clinical Assistant Professor, Bowling Green State University Adjunct Assistant Professor
3Registered Nurse, Caring Medical & Rehabilitation Services

© The Foot and Ankle Online Journal, 2012

Comments Off on Dextrose Prolotherapy Treatment for Unresolved “Morton’s Neuroma” Pain

Posted in Uncategorized

Tagged , , , , , , , , , , , , , , , , ,

First Metatarsalphalangeal Joint Arthrodesis in Rheumatoid Arthritis: A Case Report of Non-Union

Posted on April 1, 2008 | Comments Off on First Metatarsalphalangeal Joint Arthrodesis in Rheumatoid Arthritis: A Case Report of Non-Union

by Evan F. Meltzer, MS, DPM, FACFAS1

The Foot & Ankle Journal 1 (4): 3

The author presents a case report of an attempted arthrodesis of the first metatarsophalangeal joint in a patient with rheumatoid arthritis. Reasons for non union were explored. These include the primary disease process and associated medical and surgical complications. There is conflicting data regarding any direct correlation of patients with rheumatoid arthritis and ethnicity affecting the outcome of surgical arthrodesis.

Key words: Non-Union, rheumatoid arthritis, arthrodesis

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) 

Published: April 1, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0104.0003

Rheumatoid arthritis (RA) affects people worldwide with a consistent prevalence of 1%. It is most prevalent in highly developed countries such as the United States, England, and Scandinavia. [1] The prevalence of the disease varies in some populations, and may exceed 5% in several Native American tribes such as the Yakima, Chippewa and Pima tribes of the United States. [1,2] In contrast, RA is less common in Japan and Hong Kong and relatively rare in Indonesia and sub-Saharan Africa. [1] This case report illustrates a surgical non union 8 months following an arthrodesis procedure in a patient with rheumatoid arthritis.

Case Report

A 35 year old female with a history of rheumatoid arthritis presented to the podiatry clinic with a chief complaint of pain in the right great toe for the previous 6 months. Her systemic disease was adequately controlled by her primary physician with Etanercept (Enbrel®), 25 mg injected subcutaneously twice per week. The patient was also taking Alendronate (Foxamax®)70mg by mouth weekly. We also prescribed naproxen, 500 mg twice per day, and hydrocodone, 5mg with acetaminophen 500 mg as needed for breakthrough pain. The patient’s primary provider also prescribed a baseline daily dose of prednisone, 10 mg daily, in addition to an increase, then tapering schedule with an endpoint of 20 mg daily.

The patient is a non-smoker and did not have diabetes or peripheral neuropathy. Medical treatment failed to provide pain relief, and shoe therapy combined with corticosteroid arthrocentesis was recommended. The patient’s symptoms progressed and she was presented with several surgical options.

The patient underwent a first MTP arthrodesis procedure using the CHARLOTTE™ MTP Fusion System (Wright Medical Technology, Inc.). The surgery was uneventful, and radiographs taken 7 weeks postoperatively demonstrate adequate correction (Figs 1, 2).

Figure 1  The 7 week postoperative anteroposterior radiograph demonstrating satisfactory placement of the CHARLOTTE™ MTP plate with screw fixation.  The CHARLOTTE™ Multi-Use Compression screw is also visible from medial distal to lateral proximal.

Figure 2    The 7 week postoperative lateral radiograph illustrating the low profile of the construct, with good purchase of all screw threads.

The patient was kept immobilized for 3 months, ambulating in a cam walker for that entire time, and was subsequently discharged from postoperative care. Shortly after discharge, the patient relocated to another city in Montana.

The patient returned to the podiatry clinic 8 months later with a screw head percutaneously visible. There were no complaints of pain other than the concern over a visible screw head and associated dorsal edema. There was no reported history of trauma to the affected foot during the intervening time. Subsequent radiographs demonstrated loosening of the other screws and a failed union of the first MTP joint (Figs 3, 4).

Figure 3     The 8 month postoperative anteroposterior radiograph clearly showing the non union, exuberant bone medial to the plate, and lucency of bone around the screws.

Figure 4    The 8 month postoperative lateral radiograph demonstrating the position of the percutaneous screw and loosening of the entire construct.  The dorsal edema and visible screw head prompted the patient to return to the clinic.

The percutaneous screw was easily removed in the clinic with a hemostat. The patient returned to the operating room where all hardware was removed except for the initial transverse screw. The region of the non union and first metatarsal shaft was remodeled with demineralized bone matrix using Allomatrix® DR (Wright Medical Technology, Inc.). This was applied within the pseudo joint space along with another CHARLOTTE™ Multi-Use Compression screw.

An Orthofix bone growth stimulator was fitted and dispensed to promote bone healing. Radiographs taken prior to the author’s relocation indicated adequate progression of primary bone healing of the revised surgical site.

Discussion

The incidence of non union following arthrodesis of painfully diseased joints in rheumatoid arthritis patients is not unusual. [3,4] However, there is conflicting data suggesting a direct correlation between RA and surgical non union. [9,10] Maenpaa et al [9] state that non unions are more common among patients with severe deformity and osteoporosis (RA, neuromuscular arthropathy). In contradiction to the previous statement, Bogoch and Moran [10] state that the relatively rapid and reliable bone healing and arthrodesis in RA may be attributable to the preexisting rapid turnover of bone with an increase in osteogenesis. These authors speculate that the phase of induction of osteogenesis initiated by surgical arthrodesis is enhanced by the preconditioned state of bone formation in this patient group. Other possible primary surgical approaches to consider in this case were hemi or total first implant arthroplasty verses resection arthroplasty (Keller procedure). This patient desired a rigid fusion. Another approach to revision could have been to remove all hardware and leave the non union alone, since she had no pain. Some studies show that non unions are not always painful. [5] If successful, first MTP arthrodesis is a satisfactory procedure with good long-term results. [5,6] The effects of poor bone healing with the use of oral prednisone are widely recognized. [7] This may be considered a causative factor in this surgical result, but is purely speculative. The effect of an intra-articular corticosteroid injection in the final result of this case is also unknown. It is unlikely that joint injection with corticosteroid would have such a widespread effect on the massive failure of the entire construct.

What is known is the increased risk of non union due to the patient’s comorbidity of rheumatoid arthritis. The literature [1,2] supports the notion that the incidence of rheumatoid arthritis in certain Native American tribes exceeds 5%. While this author could not locate a specific reference to the incidence of RA in the Blackfeet Tribe of Montana, obeservations by two family doctors on this reservation over a 20 year period concur a similar incidence of the disease in the Blackfeet members they have treated. [8] The pharmacy budget at the Blackfeet Community Hospital is significantly impacted by the cost of RA mitigating drugs.

In addition to medical morbidities, the foot and ankle surgeon must recognize rheumatoid arthritis as a factor that may impact the outcome of planned surgical procedures. High risk patients should be adequately counseled regarding risk factors and benefits verses possible adverse results. This should be carefully considered during the informed consent process. There seems to be a general consensus among foot and ankle surgeons that patients with RA have a higher risk of non union following surgical arthrodesis. The possibility of the increased risk of non union associated with RA in conjunction with ethnic ancestry cannot be positively correlated by this report and may merit further study of bone healing and genetic background.

References

1. Cush, JJ, Kavanaugh, A. Rheumatoid Arthritis: Early Diagnosis and Treatment. Professional Communications, Inc., p 29. 2005.
2. Peschken, CA, Esdaile, JM. Rheumatic diseases in North America’s indigenous peoples. Seminars in Arthritis and Rheumatism 28 (6), pp.368-391. 1999.
3. Anderson, T, Maxander, P, Rydholm, U, Besjakov, J, Carlsson, A. Ankle arthrodesis by compression screws in rheumatoid arthritis: Primary nonunion in 9/35 patients. Acta Orthopaedica 76 (6), pp. 884-890. 2005.
4. Salai, M, Hakerem, D, Pritch, M, Chechick, A, Goshen, E. Non-union of undisplaced radial neck fracture in a rheumatoid patient. Archives of Orthopaedic and Trauma Surgery 119 (1-2), pp.119-120. 1999.
5. Goucher, NR, Coughlin, MJ. Hallux Metatarsophalangeal joint Arthrodesis using dome-shaped reamers and dorsal plate fixation: A prospective study. Foot and Ankle International 27 (11), pp. 869-876. 2006.
6. Brodsky, JW, Passmore, RN, Pollo, FE, Shabat, S. Functional outcome of Arthrodesis of the first metatarsalphalangeal joint using parallel screw fixation. Foot and Ankle International 26 (2), pp. 140-146. 2005.
7. Waters, RV, Gamradt, SC, Asnis, P, Vickery, BH, Avnur, Z, Hill, E, Bostrom, MPG. Systemic corticosteroids inhibit bone healing in a rabbit ulnar osteotomy model. Acta Orthopaedica Scandinavica 71 (3), pp. 316-321. 2000.
8. Personal communication, R. Rottenbiller, MD and R. Odegaard, MD. Blackfeet Community Hospital, Browning, Montana. 2007.
9. Maenpaa, H, Lehto, MUK, Belt, EA. Why Do Ankle Arthrodeses Fail in Patients with Rheumatic Disease? Foot & Ankle International 22 (5), pp403-408. 2001.
10. Bogoch, ER, Moran, EL. Bone Abnormalities in the Surgical Treatment of Patients with Rheumatoid Arthritis. Clin. Orthop., 366, pp8-21. 1999.

Address correspondence to: Evan F. Meltzer, MS, DPM, FACFAS
G.V. (Sonny) Montgomery VA Medical Center, Surgical Service (112)
1500 Woodrow Wilson Drive, Jackson, MS 39216

1G.V. (Sonny) Montgomery VA Medical Center, Surgical Service (112), 1500 Woodrow Wilson Drive, Jackson, MS 39216

© The Foot & Ankle Journal, 2008

[Download PDF File for Printing]

Comments Off on First Metatarsalphalangeal Joint Arthrodesis in Rheumatoid Arthritis: A Case Report of Non-Union

Posted in Uncategorized

Tagged , , ,

An Unusual Case Report of Two Bone Osteomyelitis With Long-Term Follow-up

Posted on April 1, 2008 | Comments Off on An Unusual Case Report of Two Bone Osteomyelitis With Long-Term Follow-up

by Brian Carpenter, DPM, FACFAS1, Jeffrey Taylor, DPM2, Travis Motley, DPM, FACFAS3, Jason Smith, DPM4

The Foot & Ankle Journal 1 (4): 1

A 49 year-old patient, with a history of rheumatoid arthritis, presents with suspected septic arthritis of the ankle and subtalar joints. The patient was found to have osteomyelitis of both the talus and calcaneus. The patient was treated by debridement, antibiotic impregnated PMMA beads, and ultimately, a subtalar joint fusion. This case illustrates the importance of the early recognition and diagnosis, the possible sequelae, and the need for aggressive treatment of a septic joint.

Key words: Osteomyelitis, rheumatoid arthritis, subtalar joint, PMMA beads

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)  

Published Online: April 1, 2008

ISSN 1941-6806
doi: 10.3827/faoj.2008.0104.0001

Osteomyelitis is traditionally subdivided into three categories based on etiology. The first type is hematogenous osteomyelitis. This form is commonly monomicrobial, with staphylococcal organisms isolated most frequently. [7] The second type is direct extension osteomyelitis. It is usually polymicrobial in origin and seen more frequently in the general population. [6] Sources of direct extension osteomyelitis include puncture wounds, surgery, implants, contiguous ulcerations, and septic arthritis.

The third type is osteomyelitis secondary to vascular insufficiency. It is also polymicrobial in origin and seen mostly in those over 55 years of age as the result of tissue hypoxia. [1]

Septic arthritis is the most destructive form of arthritis. It is classified by its offending pathogen or etiology. Neisseria gonorrhea is commonly isolated from sexually active adults with associated superficial lesions. [8] Haemophilus influenza is commonly isolated from children under the age of two. [8] Staphylococcus and Streptococcus species, which are the most common offending pathogens overall, are seen in children over the age of two and in adults. [8] The etiologies are very similar to osteomyelitis.

Hematogenous septic arthritis may be secondary to upper respiratory and skin infections, most frequently encountered with gram-positive organisms. [8]

A joint is susceptible to infection because of the profound vascular supply within the synovial joint lining. The joint may be even more prone to an infective process given an existing arthritide, such as rheumatoid arthritis.

Arthritis not only causes direct damage to the joint, but may also be treated with repeated corticosteroid injections that can decrease the joint’s immunocompetence.

Direct extension septic arthritis shares its etiologies with direct extension osteomyelitis, but septic arthritis may also originate from an adjacent osteomyelitis. [1]

The following case report describes a middle-aged female with a history of rheumatoid arthritis, who developed osteomyelitis of the talus and calcaneus. The joints were never proven to be septic by joint aspiration and culture. The ensuing destructive sequelae raises many questions about the origin and the development of the infective process. [1]

Case Report

A 49 year-old white female with a past medical history of long term rheumatoid arthritis and a sedentary lifestyle, presented to the clinic complaining of a painful left ankle. The ankle became painful, erythematous, and edematous three months prior, and was accompanied by fever and chills. The patient did not initially seek treatment. Ten to fourteen days later, with rest and a decrease in activity, the erythema and edema subsided without the use of antibiotics, however, the pain persisted. The patient then went to see her rheumatologist, who treated her with physical therapy, an NSAID, and a steroid injection of the left ankle. The patient denied trauma, but did note a superficial cat scratch to the anterior aspect of her left lower leg one to two weeks prior to the onset of pain, which she treated with a topical antibiotic.

On initial physical examination significant findings revealed a globally edematous left ankle. The swelling was markedly more edematous on the lateral aspect of the ankle. There was pain on palpation of the anterior, lateral, and posterior aspect of the ankle joint. Pain was elicited with eversion and dorsiflexion of the ankle and there was no pain of the subtalar joint with range of motion. The neurovascular status of both extremities was intact.

Plain films of the left foot and ankle, taken on a previous presentation did not reveal a fracture or dislocation, although there was significant degenerative joint disease of the left ankle joint.

The patient returned to the clinic two weeks later with an additional complaint of a painful left heel on weightbearing. Physical exam revealed severe pain with compression to the body of the left calcaneus. There was no apparent cellulitis of the left foot or ankle. Computerized tomography (CT) scan findings of the left foot and ankle revealed degenerative joint disease of the subtalar joint with an irregular calcaneal-cuboid joint that includes significant destruction of bone. A large lytic lesion in the posterior inferior aspect of the calcaneus is seen with a small lytic lesion of the medial talar dome. There were trabecular changes of the lateral talar body with surrounding soft tissue inflammation. (Fig. 1)

Figure 1  CT scan revealed joint narrowing consistent with degenerative arthritis.  A large area of bone lysis is seen in the body of the os calcis.

Plain films, taken shortly after that time, corresponded with the CT findings. We concluded that degenerative changes of the talus, calcaneus, and subtalar joint were probably the result of an infective process.

Five days later, surgical debridement of osteomyelitic bone of the left talus and calcaneus was performed to an intra-operative viable periphery. Tobramycin impregnated beads were inserted into the dead space, and the patient was placed on cephazolin 2 gm IV every 8 hours. (Fig. 2)

Figure 2  Following surgical debridement of osteomyelitic bone, antibiotic impregnated PMMA beads were inserted.  Cultures revealed staphylococcus aureus osteomyelitis.

The wound was closed over the implanted beads with a drain in place. Bone biopsy of debrided bone was positive for osteomyelitis, and biopsy of peripheral bone and residual bone was negative. Cultures of the debrided necrotic bone were positive for Staphylococcus aureus. The postoperative period was unremarkable. A Ceretec WBC-labeled bone scan performed six weeks after the initial debridement. This was negative for osteomyelitis (Fig. 3)

Figure 3  Ceretec white blood cell bone scans performed six weeks after insertion of PMMA beads were negative for any signs of active osteomyelitis.

Ten weeks after debridement of the left talus and calcaneus, the beads were removed. The residual bone of the talus and calcaneus were clinically viable, and a subtalar joint fusion with talar and calcaneal reconstruction using autogenic iliac bone graft was performed. The patient was placed in a below-the-knee cast. Plain film findings two weeks after STJ fusion demonstrated intact internal fixation from anterior dorsal to plantar posterior with good placement and joint alignment. A portion of increased density of both the talus and calcaneus corresponded to generalized osteopenia of the bone grafts. (Fig. 4)

Figure 4 Iliac bone graft is used with a single cannulated cancellous screw to fuse the subtalar joint.

Intravenous antibiotics were discontinued and the patient was put on a two-week course of oral cephalexin.

The postoperative course involved a non-weightbearing, below-the-knee cast for eight weeks with progression to a non-weightbearing removable cast walker (RCW) for three weeks. The patient was then placed in a weightbearing RCW for another three weeks. Proper foot orthoses and ankle brace was fitted when the patient progressed to her shoes.

After casting, the patient underwent eight weeks of physical therapy to increase range of motion, proprioception, and strength. The patient was pain free six months after fusion. The plain films demonstrated approximately 90% fusion of the left subtalar joint with the heel in rectus position. (Fig. 5)

Figure 5 Six months after fusion, the subtalar joint is stable and without pain on ankle and foot range of motion. 

The patient is now ten years post surgery. She is enjoying a healthy lifestyle that includes jogging without pain.

Discussion

There are many questions that arise from this case report and should be addressed to make any pertinent conclusions.

The patient’s history suggests clinical sepsis prior to presenting and the etiology remains unclear. First of all, the cat scratch she reported was probably not the cause. We were unable to isolate the most common organism isolated from cat scratches or bites, Pasteurella multiocida. [2] Also, the location and depth of the laceration are not consistent with an infectious introduction of the ankle or subtalar joint. Secondly, a steroid injection, which has been demonstrated as a source of joint sepsis in the literature, was administered to the patient early in the presentation. Injections of corticosteroid into a septic joint may increase the propagation of the infectious process, but cannot be labeled as the cause due to the onset of symptoms prior to the injection. [3,4] Finally, the patient’s long term rheumatoid arthritis must be recognized as a significant factor as to increased risk of joint sepsis, but cannot be labeled as a cause. [5,6] Given the exclusion of these three factors and the absence of other complicating trauma, although rarely seen in middle aged adults, we hypothesize the septic arthritis must be attributed to a hematogenous route. [5,6]

Assuming bacteremia one must decide on the location of the infection. Given the patient’s report, it is easy to assume ankle joint sepsis. The suspicion is heightened by the possible propagating of infection by a local joint injection to the ankle joint. The clinical and radiographic findings also suggest extra-tibiotalar sepsis. An effusion of the subtalar joint may present with ankle joint swelling that is more prominent below the lateral malleolus, given the communicating lateral anatomy of the subtalar and ankle joints. [7] Computerized tomography of the foot and ankle further supports the hypothesis of subtalar sepsis by displaying adjacent boney lesions located in the inferior talus and superior calcaneus.

Therefore, the original septic joint may have been the subtalar joint in isolation or in combination with the ankle joint. It appears the detrimental sequelae of osteomyelitis developed only in the subtalar joint.

Sequelae of septic arthritis may include persistence of the infection secondary to inadequate drainage. It can also be caused by damage to the articular cartilage, tenosynovitis, and secondary osteomyelitis. As intra-articular exudate increases, the joint attempts to accommodate its increased volume through posture, which causes more pain and stiffness. When the joint can no longer handle the intra-articular pressure, the corresponding cartilage is compressed, synovial blood supply is compromised, capsular erosions and sinus tracts form, and contiguous spread to underlying bone results. [5]

When osteomyelitis is recognized secondary to joint sepsis, joint resection arthroplasty, staged arthrodesis, or even amputation can be performed to alleviate the patient’s symptoms and stop further spread of the infection. [5] Surgical debridement of all necrotic bone must be performed. In this case, it was followed by implantation of PMMA antibiotic beads for the treatment of existing infection and prophylaxis of further infection in the anatomical dead space. The use of antibiotic laden beads is efficacious in the treatment of acute and chronic osteomyelitis. [8] PMMA beads have been in use for over 30 years. The beads are typically left in the wound for 5 to 14 days after debridement or until soft tissure coverage or primary closure can be achieved. [13] Studies have shown that minimum inhibitory concentration of antibiotics are released from PMMA beads from the first 2 days after implantation up to multiple weeks. [12] Following proper debridement and antibiotic prophylaxis, a Ceretec bone scan, which is a sensitive and specific for osteomyelitis, can be utilized to confirm the absence of infection or persistent infection. An isolated talocalcaneal arthrodesis, employing an iliac crest bone graft, has been described by many authors as an excellent way to treat various degenerative processes of the subtalar joint, and has proven to be a more functional alternative to a pan-talar fusion. [9,10]

This patient most likely developed subtalar septic arthritis from an uncommon hematogenous route. The infection was not drained and may have been even propagated with a corticosteroid injection and spread contiguously to the talus and calcaneus. Once recognized, the osteomyelitis was aggressively treated with surgery and appropriate intravenous antibiotic therapy. The case illustrates three important points about the septic joint. First, the suspicion of a septic joint must be diagnosed and treated appropriately and aggressively by joint aspiration, if possible, and proper cultures and definitive antibiotics. Secondly, early intervention in these cases is paramount, as demonstrated graphically by this case. Finally, if complications, such as osteomyelitis, do occur, proper aggressive surgical treatment must be performed promptly.

References

1. Joseph, W. : Infections, in Principles and Practice of Podiatric Medicine, Levy, Hetherington (eds.),
2. New York, Churchill Livingstone, 1990, 275-313.
3. Chodakewitz, J., Bia, F. : Septic Arthritis and Osteomyelitis form a Cat Bite. Yale Journal of Biology and Medicine, 61:513-518, 1988.
4. Kothari, T. et al. : Pseudomonas cepacia Septic Arthritis due to Intra-articular Injections of Methylprednisolone. Canadian Medical Association Journal. 116(11): 1230, 1232, 1235, June 1977.
5. Gowans, J., Granieri, P. : Septic Arthritis. Its Relation to Intra-articular Injections of Hydrocortisone Acetate. New England Journal of Medicine 261: 502-503, 1959.
6. Freeland, A., Senter, B. : Septic Arthritis and Osteomyelitis. Hand Clinics 5: 533-552, November 1989.
7. Cunningham, R., Cockayne, A., Humphreys, H. : Clinical and Molecular Aspects of the Pathogenesis of Staphylococcus aureus and Bone and Joint Infections. Journal of Medical Microbiology 44(3): 157-164, March 1996.
8. Sternbach, G., Baker, F. : The Emergency joint: Arthrocentesis and Synovial Fluid Analysis. JACEP 5: 787-792, October 1976.
9. Calhoun, J., Mader, J. : Antibiotic Beads in the Management of Surgical Infections. American Journal of Surgery 157: 443-449, April 1989.
10. Russotti, G. et al. : Isolated Talocalcaneal Arthrodesis. Journal of Bone and Joint Surgery 79-A: 1472-1478, December 1988.
11. Thomas, F. : Arthrodesis of the Subtalar Joint. Journal of Bone and Joint Surgery 49-B: 93-97, February 1967.
12. Perry, A. et al : Antimicrobial Realease Kinetics From Polymethylmethacrylate in a Novel Continous Flow Chamber. Clinical Orthopaedics and Related Research 403, pp. 49-53 2002.
13. Walenkamp, G. et al : Osteomyelitis Treated With Gentamicin-PMMA Beads. Acta Orthop Scand 69 (5): 518-522, 1998.

1Director of Residency Training, Associate Professor, University of North Texas Health Science Center, John Peter Smith Hospital, Department of Orthopaedics, 1500 South Main Street, Ft.Worth, Texas 76104.

2Private Practice; North Texas Podiatry, 401 Westpark Way, Euless. Texas

3Staff Physician, Assistant Professor, University of North Texas Health Science Center, Department of Orthopaedics. 1500 South Main Street, Ft. Worth, Texas 76104.

4Resident, PGY-2,John Peter Smith Hospital, Department of Orthopaedics. 1500 South Main Street, Ft. Worth, Texas 76104

© The Foot & Ankle Journal, 2008

[Download PDF File for Printing]

Comments Off on An Unusual Case Report of Two Bone Osteomyelitis With Long-Term Follow-up

Posted in Uncategorized

Tagged , , , ,