Tag Archives: Complex Regional Pain Syndrome

Case study of idiopathic degeneration of the talonavicular joint

Posted on March 31, 2020 | Comments Off on Case study of idiopathic degeneration of the talonavicular joint

by Ryan Allen, DPM1*; William Arthur, DPM1; Christina Ma, BS2; Charles Parks, DPM, FACFAS3; Monara Dini, DPM, FACFAS3

The differential diagnosis for chronic pain out of proportion is broad, and a final diagnosis of Mueller-Weiss syndrome is often a diagnosis of exclusion. We present a patient who experienced pain out of proportion following minor trauma. This progressed into worsening pain that affected his day-to-day activities and ability to perform work. Eventually, there was destruction of his talonavicular joint and early stages of idiopathic fusion. Multiple specialties were involved in this case including infectious disease, rheumatology, and neurology. Excluded diagnoses were septic joint, osteomyelitis, complex regional pain syndrome, Charcot arthropathy, and rheumatoid arthritis. We present a rare case of a patient who experienced idiopathic destruction and fusion of his talonavicular joint following minor trauma, with Mueller-Weiss syndrome suspected. The patient would make significant recovery following arthrodesis of the talonavicular joint.

Keywords: Mueller-Weiss-syndrome, complex regional pain syndrome, idiopathic fusion, talonavicular joint

ISSN 1941-6806
doi: 10.3827/faoj.2018.1301.0006

1 – Podiatric Surgery Resident, Department of Veteran Affairs at San Francisco
2 – Podiatric Medical Student, California School of Podiatric Medicine
3 – Assistant Professor, Department of Orthopaedic Surgery, University of California at San Francisco
* – Corresponding author: ryandylanallen@gmail.com

Müller-Weiss syndrome is a rare disease that is described as a spontaneous adult-onset tarsal navicular osteonecrosis [1]. Symptoms include chronic midfoot pain, swelling, and tenderness on the dorsal and medial midfoot. It is commonly found bilaterally and is found more frequently in women [1]. Its pathogenesis remains controversial. Some believe it to be caused by secondary compressive forces acting on the tarsus or possibly a congenital defect, while others believe it to be an ischemic process[2]. The characteristic findings for Müller-Weiss syndrome include a dorsomedial dislocation along with the collapse of the lateral navicular bone, resulting in a comma-shaped.

The first description of this condition was in the early twentieth century in Europe. In 1925, Schmidt reported on a patient with pluriglandular endocrine failure with deformities at the tarsal navicular. Walther Müller described this condition in 1927, where he suggested that the disease developed from a forceful compression of the lesser tarsus. Müller later suggested a congenital defect was the cause of the disease the following year [3]. Also, in 1927, an Austrian radiologist, Konrad Weiss, described similar findings in two patients suggesting osteonecrosis as the cause for the condition [4]. Although Schmidt was the first to describe this condition, the disease is named after Müller and Weiss.

The exact prevalence and incidence of this disease is currently unknown. However, there are isolated case reports throughout the literature. It is commonly present in the fourth to sixth decade of life. It is also frequently bilateral and usually found in patients with a higher body mass index. There is limited data suggesting an environmental and nutritional component [5]

The pathogenesis of this condition is poorly understood. However, the literature suggests that there are two contributing factors; a delay in ossification of the navicular and atypical compressive forces on the midfoot. 

There are multiple factors that can contribute to a delay in ossification including poor nutritional status, endocrinopathies, metabolic disease, or malabsorption disease [5]. When there is a delay in the ossification of the navicular, the weak outer chondral surface is susceptible to abnormal development from excessive compressive forces. Current literature suggests a large compressive force would contribute to plastic deformation of the navicular during ossification [5]. However, it is possible that persistent low compressive forces on the pliable chondral surface puts the navicular at risk of ossifying in an irregular orientation. 

The second contributing factor is a result of the biomechanical insult on the navicular. As mentioned previously, excessive compressive forces on the navicular is suggested to contribute to this condition. This is particularly true when these forces are applied to the lateral half of the navicular between the talar head and the cuneiforms. There are several conditions which can lead to compressive forces to the lateral aspect of the navicular including: primary subtalar joint varus, first ray brachymetatarsia (both congenital or acquired), and clubfoot deformities [5]. Other biomechanical factors such as a short hallux metatarsal, shortening of the entire medial column due to internal rotation of the navicular in the transverse plane, or retroposition of the first tarsometatarsal joint in relation to the second tarsometatarsal joint can also contribute to lateralization forces [5]. When the first ray is hypermobile, loading forces transfer to the second ray which may also lead to compressive forces into the intermediate cuneiform and lateral navicular [5]. 

Case Report

A 41-year-old male with a past medical history of right foot plantar fasciitis, depression, and insomnia was brought in by ambulance to the Emergency Department of San Francisco General Hospital with a chief complaint of 10/10 right foot pain accompanied by swelling. Two days prior, the patient had been exercising at his gym. He did not recall any particular injury apart from his right foot slipping off exercise equipment onto the floor, without any immediate pain. Several hours after exercising, he noticed a gradual increase in right foot pain. In the Emergency Department, plain films did not demonstrate fracture, there was diffuse soft tissue swelling on the dorsum of the foot (Figure 1),  labs were not drawn, however, the patient’s vital signs were all within normal limits. He was discharged from the ED with an ankle brace, crutches, and Tylenol for pain relief.

He again visited the ED 3 days later, with a further increase in pain and edema; he was not found to have any underlying fluctuance or erythema. He remained unable to bear weight on his right foot. He remained in an ankle brace and had been using ibuprofen without any significant pain relief, and he continued to not have any constitutional symptoms. Radiographs demonstrated increased soft tissue swelling from prior films, however, no evidence of fractures, soft tissue calcifications, or joint effusions were seen. He was recommended to continue use of the ankle brace, to stop ibuprofen, and trial Tylenol.  

Nearly one month later he presented to the ED with continued pain, however now able to bear weight. He had plain films which demonstrated even further increase in soft tissue swelling as well as a CT (Figure 2) with findings of prominent osteopenia involving the midfoot. Orthotics and Prosthetics was consulted and he was dispensed a CAM boot. The podiatry service was notified, and an appointment was made for the following day in the clinic. He was dispensed opioid pain medication, as well as ibuprofen, at discharge.

The next day, he presented to the Podiatry Clinic. His right dorsal foot was edematous and erythematous from the metatarsal heads to the level of the ankle joint. Fluctuance was not appreciated. The right dorsal foot was tender to palpation.


Figure 1 Radiographs of patient’s foot. Diffuse swelling on the dorsum of the foot without evidence of fracture or dislocation.

Figure 2 Sagittal CT demonstrating further soft tissue swelling with prominent osteopenia of the midfoot.

Allodynia was present. Pain increased with plantarflexion of the right ankle joint. Pain was also present with eversion and inversion of the right subtalar joint. He was unable to wear the CAM boot, dispensed to him the prior day, as this increased his pain. A CBC, ESR, CRP, BMP, and HgA1c, and a MRI with contrast were ordered to assess for abscess or osteomyelitis. His ESR and CRP were >130 mm/h and 198.0 mg/L, respectively. His HgA1C was 5.9%, and his uric acid level was 3.7 mg/dL. He was without leukocytosis and his remaining labs were unremarkable. An ACE wrap was applied from the foot to the tibial tuberosity to compress the foot. The patient was given strict instructions to elevate, do ROM exercises, and wear the CAM walker boot at a 90 degree angle to prevent worsening flexion contracture. He was given explicit instructions to return to the ED if he developed any fever, chills, nausea, and vomiting or any worsening pain. He was dispensed gabapentin to be taken at bedtime for pain. 

The previously ordered MRI was taken and reviewed. Findings were reviewed with radiology, and they were suggestive of broad diagnoses. Clinically and radiographically there was support of complex regional pain syndrome.  It showed destruction of joint spaces at the TN joint, subtalar joint, as well as deep marrow edema within the midfoot outside of the talonavicular joint (Figure 3). The navicular bone was almost entirely replaced with edema and enhancement.The MRI findings were also consistent to support Charcot arthropathy and osteomyelitis as well. Septic joint was also on the differential due to minimal fluid within joint spaces. Interventional Radiology was consulted for urgent bone biopsy. There would be no growth from the cultures of the specimen acquired.

The patient then underwent a right foot irrigation and debridement with bone biopsy approximately one week later with the presumption of infection versus complex regional pain syndrome. At this time the symptoms began 3 months prior. Gout was lowest on the differential due to a prior uric acid level of 3.7 mg/dL. In the operating room, a 4 cm incision was made dorsally to gain access to the talonavicular joint. A Rongeur forceps was used to collect a sample of synovial tissue which was noted to appear inflamed and thickened; this was sent to microbiology. The talus and navicular were assessed and noted to be hard and viable. A sample of cartilage and bone was taken from both the talus and the navicular and sent to microbiology. Bone specimens were also sent to pathology from both talus and navicular. The patient would subsequently be admitted to the hospital. 

Figure 3 Sagittal and transverse T2 MR imaging demonstrating destruction of the talonavicular joint with extensive marrow edema that was also present to the calcaneus and cuneiforms.

During his hospital stay, neurology was consulted to rule out CRPS. He was noted to not have any evidence of neuropathy with “intact afferent and efferent limbs of reflex arc.” Neurology assessed a low suspicion of neuropathic etiology of symptoms. In terms of the acquired specimens from the OR, there was no growth noted from any of the specimens (C&S, AFB, and fungal). The synovial tissue final pathologic diagnosis was noted to be “lymphoplasmacytic inflammation.” Excised bone of both the talus and the navicular were noted to be without any evidence of acute osteomyelitis.  

Figure 4 Radiographs demonstrating focal osteopenia and erosive changes of the talonavicular joint.

The patient remained in-house for 5 days; he was then discharged home. Two days after discharge he returned to the clinic; he was now one week status post biopsy. He remained without constitutional symptoms.  The differential diagnosis remained the same at this point, with complex regional pain syndrome as most likely diagnosis despite low suspicion from the Neurology team. New labs were ordered. Rheumatoid factor was noted to be within normal limits <3.5 IU/mL and antinuclear antibody was noted to be negative as well. His ESR had decreased to 68 mm/h and his CRP had decreased to 6.4 mg/L. The patient was encouraged to continue ambulating with a CAM boot and to practice ROM exercises. He would later follow up with the infectious disease clinic who noted that “osteopenia and marrow enhancement on imaging, elevated inflammatory markers, and absence of evidence for neuropathy on exam (making Charcot arthropathy unlikely) are concerning for infectious etiology.” 

Figure 5 Immediate post-operative films of the talonavicular fusion.

However, both cultures and pathology were without evidence of osteomyelitis and he did not have a systemic illness which could have led to hematologic seeding or skin breaks down allowing for direct inoculation. Serologies were sent to rule out less common infectious agents, such as TB and coccidioides. The serologies were noted to be negative for both TB and coccidioides.  The patient returned to the Podiatry Clinic two weeks later, now 3 weeks status postbiopsy and almost four months from the time of onset of symptoms. He attempted to ambulate in his CAM boot but was unable to do due 5/10 throbbing pain along his medial arch. He continued to not have any constitutional symptoms. He was encouraged to transition to regular shoes and discontinued the CAM boot. His sutures were removed at this visit. Since he had been discharged from the hospital, he had begun taking a new pain management regimen of gabapentin 300 three times daily which he noted to help alleviate some pain.

The patient returned to the clinic 5 weeks status post the open biopsy. He was still unable to walk in regular shoe wear and remained in his CAM boot utilizing a knee scooter. It had been two months since he last tried physical therapy and he wished to restart therapy. New plain film imaging was taken, and noted to be without any interval changes. He was encouraged to ambulate in regular shoe wear and to mobilize the foot as much as possible. It was stressed that weight bearing was imperative to make a recovery.

Two weeks later the patient returned to the clinic with new plain films. He was now 7 weeks status postbiopsy. He attempted to ambulate only utilizing the CAM boot but remained unable to bear weight on his right foot in regular shoe wear. On plain film imaging he was noted to have unchanged severe osteopenia from prior films, however with more focal osteopenia/erosion involving the talonavicular joint (Figure 4). X-ray findings correlated with TNJ degenerative joint disease.  

At this point in summary, neurology had evaluated the patient and had very low suspicion for complex regional pain syndrome. Medical workup had also been negative for inflammatory arthritis. Of note, the patient had no risk factors for Charcot arthropathy. The case was discussed on multiple accounts with the orthopaedic department and the patient was then placed in a short leg cast, made non-weight bearing, with a plan of serial casting with imaging to promote autofusion of the TNJ. If the patient was to continue to have pain, surgical fusion of the TNJ would be considered. 

The patient returned to the clinic 2 weeks, now 6 months status-post the initial onset of pain, and now with new assessment of TNJ degenerative joint disease secondary to unknown etiology with differential of CRPS, Müller-Weiss syndrome, septic joint, or osteomyelitis. 

Figure 6 Eight weeks post-operative films demonstrating trabeculation across the arthrodesis site.

He had remained in a short leg cast and NWB as instructed, and ambulating with a knee scooter. He remained without constitutional symptoms. At this time, surgery for fusion was discussed, as well as conservative treatment of serial casting. Patient opted to go with the latter. It was discussed that 6-8 weeks of serial casting may be adequate for fusion. Patient was again casted and he followed up again 2 weeks later. Again, surgery was discussed as the patient had no change in his symptoms, and was placed in a CAM boot with a plan for incisional biopsy.

The patient then opted to undergo a right foot incisional biopsy of the talus and a TN joint preparation for fusion. The patient returned to the operating room now just over 8 months from the initial onset of pain and symptoms. An incision was made through the prior incision site and deepend down to the talonavicular joint and a capsulotomy was performed. A pseudoarthrosis was noted. The articular surface of the navicular and talus were exposed and the surfaces were noted to have patchy areas of hyaline and fibrocartilage. A curette was then used to resect three separate specimens consisting of cortical bone from the articular surfaces of the navicular and the talus. This procedure’s goal was to prepare the joint for fusion and for a final biopsy. Fungal, bacterial, and acid fast bacilli would all be negative for growth.

The patient returned to the operating room for a third and final time, to undergo a right foot talonavicular arthrodesis with iliac crest bone graft at 9 months from onset of symptoms. An incision was made approximately 10 cm from the talar neck to the base of the first metatarsal. Dissection was carried down to the talonavicular joint was prepared utilizing curettes, fish scaled with osteotomes, and fenestrated using 0.062 K-wire. Attention was then directed to the right anterior superior iliac spine to acquire autograft. The talonavicular site was temporarily fixated and a combination of cancellous autograft, cancellous allograft bone chips, and 10 cc of Stimulan Biocomposite calcium sulfate were placed into the talonavicular arthrodesis site around the structural iliac crest autograft. Next, the talonavicular arthrodesis site was then fixated with a small Wright Medical medial column fusion plate and 3.5 mm fully threaded locking and nonlocking screws (Figure 5). The patient was then subsequently admitted for 48 hours for observation. Intraoperative bacterial cultures from bone were acquired but would be negative for growth.

The patient remained non-weight bearing for a total of 12 weeks, both with a short leg cast for the first 8 weeks followed by a CAM boot with ROM exercises for an additional 4 weeks. Serial radiographs demonstrated uneventful healing of the arthrodesis site (Figure 6). 

He continued to be followed weekly in the Podiatry Clinic. He continued to have interval changes of healing of the arthrodesis site on serial x-rays. The patient continued to work with physical therapy, primarily range of motion exercises. At 11 months he was noted to have significant improvement in pain during ambulation. He was able to transition to regular shoe wear at this time. At 13 months, he was noted to have 1/10 level of pain. At this point, he felt that he could return to day to day activities without restriction. There were no complications from any of the surgical interventions at his last follow up visit of this review, 13 months from the onset of symptoms. 

Discussion

This is an atypical presentation of Müller-Weiss. The inciting event was minor trauma, however, this is per the patient’s report, and therefore is subjective. The first ray mobility was not evaluated prior to the initial presentation. The patient had swelling and pain of the midfoot, however, this was unilateral. Although the patient did not have a higher than average BMI, he was athletic and he had exceedingly high midfoot torque on his foot during exercise routines. The appropriate steps in the management of other diseases including  complex regional pain syndrome were met.  Biopsies were taken to rule out infectious causes, and multiple serologies were taken, even to exclude TB.  Multiple imaging modalities were also used.  The patient was directed to pain management, and he was treated by physical therapy before and prior to the talonavicular fusion; he improved following the procedure of a talonavicular joint arthrodesis. 

Apart from minor trauma, the unilateral destruction of the talonavicular joint is what makes this case unique. Müller-Weiss syndrome is often bilateral and not following any incidence of trauma.  It is possible in this case that the initial inflammatory phase of this disease process leads to the eventual destruction of this patient’s talonavicular joint, resulting in the need for an arthrodesis. This would explain why he would make a recovery following this procedure in conjunction with continuing physical therapy. We therefore believe that this is an atypical case of complex  Müller-Weiss Syndrome, although atypical. 

Conflict of Interest Declaration

The corresponding and contributing authors have no relevant financial interest in this manuscript.

References

  1. Sharp RJ, Calder JDF, Saxby TS. Osteochondritis of the navicular: a case report. Foot Ankle Int 2003; 24:509–513  
  2. Müller W. Uber eine eigenartige doppelseitige Verãnderung des os naviculare beim Erwachsenen. Deutsche Zeitschrift fur chirurgie Leipzig 1927; 201:84-7.
  3. Nguyen, AS, Tagoylo GH, Mote GA. Diagnostic imaging of the Mueller-Weiss syndrome: findings of a rare condition of the foot.  J Am Podiatr Med Assoc. 2014 Jan-Feb;104(1):110-4.
  4. Weiss K. Über die “malaizie” des os naviculare pedis. Fortschritte auf dem Gebiete der Röntgenstrahlen 1927;45:63-7.
  5. Mohiuddin T, Jennison T, Damany, D. “Müller-Weiss disease. Review of Current Knowledge” Foot and Ankle Surgery, 2014, 20;79-84.
  6. Harden RN, et al. Complex Regional Pain Syndrome: Practical Diagnostic and Treatment Guidelines, 4th Edition. Pain Med 2013 Feb;14(2):180-229. doi: 10.1111/pme.12033. Epub 2013 Jan 17.

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Operating on patients with complex regional pain syndrome

Posted on July 31, 2018 | Comments Off on Operating on patients with complex regional pain syndrome

by Ryon Wiska DPM1*, Lawrence Fallat DPM FACFAS2

The Foot and Ankle Online Journal 11 (2): 3

Complex regional pain syndrome (CRPS) is a debilitating disorder characterized by widespread, chronic pain. While elective procedures should be held until acute CRPS flare ups have subsided, certain scenarios require immediate surgical care. Surgical management of patients with CRPS requires a team approach with several other specialties including pain management and anesthesiology.  In this article, we outline a pre-operative and post-operative management course for lower extremity surgery of patients with diagnosed CRPS. We also present several case reports where this protocol was utilized.

Keywords: Causalgia, Complex Regional Pain Syndrome, CRPS, Pain, Reflex Sympathetic Dystrophy, RSD, Surgical Management

ISSN 1941-6806
doi: 10.3827/faoj.2018.1102.0003

1 – Second year podiatric surgery resident at Beaumont Hospital, Wayne.
2 – Program director for podiatric surgery at Beaumont Hospital, Wayne.
* – Corresponding author: rwiska@gmail.com

Physicians have been documenting disorders of chronic pain for centuries, with earliest documentation spanning back to Ambroise Pare’s description of chronic pain with King Charles IX in the 17th century [1]. Mitchell and colleagues documented cases of chronic pain in soldiers secondary to gunshot wounds and injuries of peripheral nerves during the Civil War [2]. Complex regional pain syndrome (CRPS) has historically been known by multiple names including reflex sympathetic dystrophy, causalgia, Sudeck’s atrophy, and shoulder-hand syndrome. Most experts now abide by terminology introduced by the International Association for Study of Pain (IASP) in 1994, which subdivided CRPS into type 1 and type 2, with type 2 having an inciting nerve injury [3].

The diagnosis of CRPS is based on clinical findings. The original IASP diagnostic criteria for CRPS includes: 1) The presence of an initiating noxious event or a cause of immobilization. 2) Continuing pain, allodynia, or hyperalgesia with which the pain is disproportionate to any inciting event. 3) Evidence at some time of edema, changes in skin blood flow, or abnormal sudomotor activity in the region of pain. 4) This diagnosis is excluded by the existence of conditions that would otherwise account for the degree of pain and dysfunction [4]. More recent literature from the Reflex Sympathetic Dystrophy Association unveiled a clinical diagnostic criteria update, which reflects systemic findings that can be documented during patient visits (Table 1)[5]. Current management for active CRPS includes physical therapy, antidepressant agents, gabapentin, corticosteroids, topical analgesics, opioids, sympathetic blocks, somatic blocks, and neuromodulation [6-10].

  1. Continuing pain, which is disproportionate to any inciting event
  2. Must report at least one symptom in three of the four following categories Sensory: Reports of hyperalgesia and/or allodynia
    1. Vasomotor: Reports of temperature asymmetry and/or skin color changes and/or skin color asymmetry
    2. Sudomotor/Edema: Reports of edema and/or sweating changes and/or sweating asymmetry
    3. Motor/Trophic: Reports of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  3. Must display at least one sign* at time of evaluation in two or more of the following categories
    1. Sensory: Evidence of hyperalgesia (to pinprick) and/or allodynia (to light touch and/or deep somatic pressure and/or joint movement)
    2. Vasomotor: Evidence of temperature asymmetry and/or skin color changes and/or asymmetry
    3. Sudomotor/Edema: Evidence of edema and/or sweating changes and/or sweating asymmetry Motor/Trophic: Evidence of decreased range of motion and/or motor dysfunction (weakness, tremor, dystonia) and/or trophic changes (hair, nail, skin)
  4. There is no other diagnosis that better explains the signs and symptoms

* A sign is counted only if it is observed at time of diagnosis

Table 1 Clinical diagnostic criteria for complex regional pain syndrome.

In recent pain management literature, low dose naltrexone (LDN) has been shown to be efficacious in treating patients with CRPS [11].  LDN refers to doses approximately 50-fold lower than doses of naltrexone typically given to patients addicted to opioids [12]. It has been shown that LDN antagonizes the Toll-like receptor 4 (TLR 4) pathway and attenuate microglia. TLR 4 in both CNS neurons and microglia augments the production of pro-inflammatory cytokines via the nuclear factor kappa-light-chain-enhancer of activated B cells (NF- κB) pathway, which acts as a mediator for neuropathic pain [13]. In a double blind study of 30 women with chronic pain, twice daily administrations of 4.5 mg of Naltrexone resulted in 57% of the participants exhibiting a significant reduction in pain when compared to placebo [14].

The current paradigm of surgeons has been to avoid operating on patients with CRPS because symptoms could either recur or worsen. In 6-10% of patients, surgical intervention is warranted and should not be delayed. These conditions include painful deformity, displacement of fixation, fracture, trauma, tumors, and soft tissue masses [15].  Surgical management of patients with CRPS has been documented in orthopedic literature, with several papers discussing surgical intervention of the upper extremity and the knee [16,17]. Previous recommendations in the knee included waiting 5 months, with ranges from 2 months to 1 year. Prolonging surgery allows for subsidence of acute pain, as well as allowing time for treatment such as sympathetic blocks and physical therapy [16,17]. The purpose of this article is to outline a surgical management approach preoperatively and postoperatively for patients with active CRPS to provide the podiatric surgeon with management options, as well as review three cases in which this protocol was used.

Preoperative Management

Surgical management of patients with CRPS requires a team approach. It is imperative to coordinate with the physician who is actively managing the patient’s CRPS. If a patient does not have an active pain management specialist, consultation with a pain management specialist should be sought prior to operating. The surgeon should coordinate with the pain management physician as well as anesthesiologist regarding patient’s operative management course with clear understanding of preoperative and postoperative treatment.

Recent literature has found that low dose naltrexone (LDN) has been shown to be efficacious in treating patients with CRPS through its endorphin releasing and anti-inflammatory properties. However, it should be held at least 24-36 hours before surgery to ensure that opiate medication administered from anesthesia is able to reach full efficacy.

Anesthesia choice is critical in ensuring that CRPS flare-ups or increase in symptoms of active CRPS do not occur. Either epidural or spinal anesthesia should be utilized in patients with CRPS. This practice has been documented in orthopedic literature with studies showing recurrence rates of CRPS falling from 72% to 10% with the use of a preoperative spinal or epidural block [16]. It is believed that this may provide a clinical advantage by blocking the potential barrage of nociceptive afferent signals in the central nervous system during surgery [18].

When trying to evaluate whether epidural or spinal anesthesia should be performed, several variables should be considered such as time from start of induction to achievement of anesthesia, time for resolution of anesthesia, and possible side effects. In spinal anesthesia, the average time from intrathecal injection of local anesthetic to achievement of surgical anesthesia is 13 minutes in conventional spinal and 16 minutes in unilateral spinal [19]. In epidural anesthesia with insertion of catheter, the average time to achieve induction was noted to be 40 minutes [20]. When performing spinal anesthesia with 5 mg hypobaric bupivacaine, Ben-David reported two segment regression after 53 minutes and discharge after 180-190 minutes, with newer studies stating average PACU time following completion of procedure ranging between 65-98 minutes [21, 22]. Mulroy noted average PACU time for patients who received epidural prior to knee surgery as 92 ±18 minutes [23].

Epidural allows for the titration of short term local anesthetic which may lead to quicker discharge times following outpatient procedure, while still providing blockade to prevent CRPS flare-ups. In patients with CRPS, epidural catheter allows the option for continuous titration of anesthetic, which may be beneficial following the procedure, whereas spinal anesthesia employs a single dosage of anesthetic.

Common side effects noted in both spinal and epidural anesthesia are hypotension, bradycardia, post-dural puncture headaches, nausea, and vomiting.  In more severe side effects, prolonged neurological complications have been observed. In epidural anesthesia, urinary retention is also a common side effect, which may require catheterization and hospitalization.

Postoperative Management

Following the surgical procedure, patients are admitted for 24-48 hours of IV pain medication administration. Patients are given take-home oral analgesic medication for pain relief until acute surgical pain has subsided. Typical examples of oral medications include Percocet 10 mg/325 mg, 1-2 tablets by mouth every 4-6 hours, or Hydromorphone 2-4 mg, 1 tablet by mouth every 4-6 hours. If patients were previously taking LDN, they are to resume daily LDN when surgical pain is controlled and after 7 days have elapsed. We recommend early range of motion and aggressive physical therapy following procedure once the surgical site is stable. If symptoms of CRPS appear to be exacerbated following surgery, we recommend patients undergo intravenous Ketamine infusion therapy, under the management of their pain specialist.

Case Report No. 1

A 38-year-old male presented to our clinic one month after injuring his right foot when a 1000-pound roll of vinyl fell onto his foot. The patient was initially referred to our clinic for care of a nondisplaced fracture of the fifth metatarsal; however, radiographs and bone scan failed to reveal signs of fracture and a diagnosis of contusion to the right foot was made. The patient had been immobilized in a nonweightbearing below knee cast for one month and had subsequently developed increased pain out of proportion to injury as well as exhibited mottling of skin to dorsum of right foot in relation to left. The patient also began to exhibit rigid contractures of the right tibialis anterior, extensor digitorum longus, and extensor hallucis longus.  The patient was referred to a pain management specialist where the diagnosis of CRPS to the right lower extremity was made. The patient reported that since date of injury, the pain had progressively increased and at time of initial presentation, was so severe that even light touch to the right lower extremity was excruciatingly painful. On evaluation it was determined that the patient exhibited two distinct types of pain, a generalized CRPS pain to the affected lower extremity as well as a muscular pain secondary to rigid contractures. The patient was treated in our office monthly for peripheral nerve blocks at the level of the ankle joint consisting of 0.5% Marcaine plain, which the patient reported provided several hours of relief of contractures and pain before pain and contractures returned.  At the same time, he underwent 22 sympathetic blockades over the course of 3 years from 4 different pain clinics, but had no relief, despite multiple pain management treatment modality attempts including a spinal cord stimulator. The patient was treated noninvasively by pain management specialists as well as our clinic for approximately 3 years, at which time it was determined that pain level had plateaued and was not improving with the treatment.

The patient underwent three different manipulations of the right foot under epidural anesthesia. The extensor tendons were stretched for a period of 20 minutes, until relaxation of rigidly contracted muscles were noted. The patient was then placed in an anterior splint following the procedures. No acute flare up of CRPS was seen immediately after the procedure; however, the patient exhibited return of rigid contractures and pain 48 hours following each procedure and was unable to tolerate the anterior splint. No increase in CRPS pain was seen following procedures.

The patient then underwent a series of botox injections that provided some pain relief and reduction of contracture to right foot and ankle that lasted for approximately two to three weeks before the muscles returned to rigid clonus.

Surgical intervention to the right foot was discussed with the patient. The patient was offered procedures that included manipulation of the right foot under anesthesia, capsulotomy of the right first metatarsophalangeal joint, lengthening of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus tendons, and sectioning of extensor hallucis brevis, all of the right foot. The patient was advised that procedure may exacerbate symptoms of CRPS and that no guarantees were given or implied. The patient met with his pain management specialist prior to the procedure and was given provisions for oral analgesics following the procedure.

On the day of the procedure, anesthesia was obtained with spinal anesthesia. The patient was placed on the operating table in the supine position. Manipulation of the foot was first performed where attention was made to manually plantarflex the right ankle joint as well as toes 1-5, which were noted to be rigidly contracted in a dorsiflexed position. Following manipulation, the foot was noted to held in a plantarflexed position. Standard z-lengthening procedures were then performed to the extensor digitorum longus, extensor hallucis longus, and tibialis anterior tendons. The extensor hallucis brevis tendon was identified and then sectioned proximal to its insertion.  Attention was then directed to the first metatarsophalangeal joint where a dorsal and lateral capsulotomy was then performed and contracture of the first metatarsophalangeal joint was noted to be decreased. Closure was completed using a combination of dissolving and nondissolving suture. A postoperative block was then infiltrated around the incision sites consisting of 9 mL of 0.5% Marcaine plain and 2 mL of dexamethasone.

Following the procedure, the patient was admitted for 48-hour pain management. The patient reported a relief in pain following the procedure and was able to tolerate weight bearing to the right lower extremity without the use of an assistive device for the first time since the injury. Ultimately, the patient reported return of CRPS pain and contractures 2 weeks following the procedure; however, no increase in CRPS pain was noted. In addition, the patient noted that contractures to the right lower extremity were not as rigid or painful.

Case Report No. 2

A 31-year-old female with history of CRPS type 1 after sustaining multiple injuries from a motor vehicle accident presented to our clinic with complaints of right ankle pain. The patient had history of multiple surgeries to her right ankle with internal fixation after suffering a comminuted open right ankle fracture. The patient’s pain was actively cared for by a pain management specialist who had maintained the patients pain in a tolerable level with the use of LDN as well as IV Ketamine infusion therapy. The patient presented to our office with complaints of a painful right ankle, which had subsequently developed a severe valgus alignment of the right heel, subtalar joint arthritis, a nonunion of a right fibular fracture, as well as pain along course of retained hardware. Despite active pain management therapy, the patient admitted to 10/10 pain to the right ankle.  The patient related that pain to her right ankle was becoming debilitating to the point that she was unable to ambulate. Initial attempts were made to treat the patient conservatively with the use of padding, bracing, and offloading with patient reporting no relief of pain. When conservative treatment options were exhausted, the patient was advised of surgical correction. The patient was made aware that surgical correction risked the possibility of a CRPS flare-up. She was fully aware of this and wished to proceed with procedure. Prior to boarding procedure, multiple conversations were had with patient’s pain management specialist as well as anesthesia team at our institution with preoperative, perioperative, and postoperative management discussed at length. It was determined that prior to procedure, patient was to hold LDN. The day of the procedure, patient was to obtain a popliteal block prior to induction and then undergo general anesthesia. The patient was then to be admitted for extended stay pain monitoring.

Twenty-four hours prior to procedure, patient’s LDN was held. On the day of the procedure, the patient was to undergo a popliteal block prior to induction; however, she did not receive the block prior to procedure. The patient was brought to the operating room and placed on the hospital table in the supine position where general anesthesia was obtained. The patient then underwent removal of painful retained bone screws and plates of the ankle, open reduction and internal fixation of right fibular nonunion, resection of synostosis of right ankle, excision of scar tissue of right ankle, medial transpositional calcaneal osteotomy with internal fixation of right foot, as well as arthrotomy of right ankle.  The patient was then placed in a well-padded cast and was instructed to be non-weight bearing to the right lower extremity with the use of crutches.

Following the procedure, the patient awoke from anesthesia in intense pain to the surgical limb. An epidural was placed and pain was controlled. The patient was converted to 48 hour full admit due to epidural. After 24 hours, she related that epidural was starting to wear off and was admitting to increased pain to surgical limb. The patient was maintained on IV Dilaudid and oral Percocet, 10 mg. After 4 days postoperatively, her pain was maintained on oral Percocet and patient was discharged home.  The patient went on to achieve surgical union of fibular fracture, but continued to admit to CRPS pain to the surgical limb, which limited activities of daily living. The patient related to no increase in CRPS pain. Six months following her procedure, the patient successfully underwent a spinal cord stimulator trial. Following insertion of the stimulator, the patient was able to stand and walk around a department store, which she had been unable to do following the initial accident. Although the patient still relates to CRPS pain, the pain related to her foot and ankle condition has subsided and no increase in CRPS pain has been noted.

Case Report No. 3

A 65-year-old female presented to our office with history of CRPS, which she developed following a third intermetatarsal space neurectomy to the left foot. On clinical exam, the patient exhibited symptoms of a neuroma to the second intermetatarsal space to the left foot as well as a stump neuroma to the third intermetatarsal space of the left foot and admitted to 10/10 left pain with maximal tenderness to the forefoot. The patient admitted that pain to the left foot was so intense that her ability to ambulate was becoming limited. Conservative treatment was attempted with offloading, padding, and local steroid injections to the affected intermetatarsal spaces, which provided little to no relief. Once conservative options had failed, surgical intervention was discussed with the patient.  The patient was advised that the proposed procedures would be an excision of neuroma to second and third intermetatarsal space of the left foot. The patient was made aware that CRPS symptoms could be exacerbated by the procedure and that clear pain management goals were outlined with her pain management physician.

On the day of the surgery, anesthesia was obtained with spinal anesthesia as well as a local anesthetic block to the second and third intermetatarsal spaces of the left foot. Anatomic dissection was carried down to the level of the neuroma and nerve was tracked proximally until healthy nerve tissue was observed. Inflamed nerve was then resected from the second and third intermetatarsal space. A 4 cm x 2 cm x 0.5 cm nerve specimen was excised from the second intermetatarsal space and a 2 cm x 1.5 cm x 0.3 cm nerve specimen was excised from the third interspace.  Closure was then performed with a combination of dissolving and non-dissolving suture and a postoperative block was infiltrated to the incision site consisting of 9 mL of 0.5% Marcaine plain and 4 mL of dexamethasone. The patient was given Norco 7.5 mg/325 mg for pain control postoperatively and was partial weight bearing to the left heel in a surgical shoe. The patient declined postoperative observation for pain management and was discharged home once cleared by anesthesia.

Following the procedure, the patient reported no increased exacerbation of CRPS and admitted to decreased pain to the neuroma site on the left foot. While the patient still reports CRPS pain to the left lower extremity, she is now able to pursue activities of daily living and maintains a tolerable level of pain to the left lower extremity.

In conclusion, our outlined pre-operative and post-operative management course for lower extremity surgery of patients with diagnosed CRPS has proven effective in preventing flare-ups of CRPS and preventing increase of active CRPS pain.

Funding Declarations

No funding was used.

Conflict of Interest

None

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