A Closer Look At Redefining Charcot

Start Page: 107

Continuing Education Course #144 — August 2006

I am pleased to introduce the latest article, “A Closer Look At Redefining Charcot,” in our CE series. This series, brought to you by the North American Center for Continuing Medical Education (NACCME), consists of regular CE activities that qualify for one continuing education contact hour (.1 CEU). Readers will not be required to pay a processing fee for this course.

The standard of care for Charcot neuroarthropathy is “largely ill defined,” according to Molly Judge, DPM. Accordingly, Dr. Judge reviews the literature on this subject, emphasizing an understanding of the etiology of the disease process, and its potential ramifications in terms of degenerative changes, altered pathomechanics and musculoskeletal issues.

At the end of this article, you’ll find a nine-question exam. Please mark your responses on the enclosed postcard and return it to NACCME. This course will be posted on Podiatry Today’s Web site (www.podiatrytoday.com) roughly one month after the publication date. I hope this CE series contributes to your clinical skills.

Sincerely,

Jeff A. Hall
Executive Editor
Podiatry Today

INSTRUCTIONS: Physicians may receive one continuing education contact hour (.1 CEU) by reading the article on pg. 108 and successfully answering the questions on pg. 114. Use the enclosed card provided to submit your answers or log on to www.podiatrytoday.com and respond via fax to (610) 560-0502.
ACCREDITATION: NACCME is approved by the Council on Podiatric Medical Education as a sponsor of continuing education in podiatric medicine.
DESIGNATION: This activity is approved for 1 continuing education contact hour or .1 CEU.
DISCLOSURE POLICY: All faculty participating in Continuing Education programs sponsored by NACCME are expected to disclose to the audience any real or apparent conflicts of interest related to the content of their presentation.
DISCLOSURE STATEMENTS: Dr. Judge has disclosed that she has no significant financial relationship with any organization that could be perceived as a real or apparent conflict of interest in the context of the subject of her presentation.
GRADING: Answers to the CE exam will be graded by NACCME. Within 60 days, you will be advised that you have passed or failed the exam. A score of 70 percent or above will comprise a passing grade. A certificate will be awarded to participants who successfully complete the exam.
TARGET AUDIENCE: Podiatrists
RELEASE DATE: August 2006
EXPIRATION DATE: August 31, 2007
LEARNING OBJECTIVES: At the conclusion of this activity, participants should be able to:
• discuss the findings from Elosser’s study and criticisms of the study;
• review the potential effects of nerve damage on bone healing;
• describe how anesthetic joint pathomechanics impact Charcot neuroarthropathy;
• review key musculoskeletal factors involved with Charcot neuroarthropathy; and
• discuss key characteristics of hypertrophic and atrophic bone destruction in neuropathic joints.

Sponsored by the North American Center for Continuing Medical Education.

Here one can see a 59-year-old female with diabetic neuropathy who fell and sustained a fracture. These photos were taken one day after the fall. The author questions whether care for fractures should vary depending on whether a patient has diabetic neuro
Here one can see a 59-year-old female with diabetic neuropathy who fell and sustained a fracture. These photos were taken one day after the fall. The author questions whether care for fractures should vary depending on whether a patient has diabetic neuro
This patient underwent open reduction internal fixation and surgeons applied an Ilizarov frame for the treatment of a Charcot ankle. She thought she had chosen the frame procedure in lieu of a primary ankle fusion. After four months of non-weightbearing i
This patient underwent open reduction internal fixation and surgeons applied an Ilizarov frame for the treatment of a Charcot ankle. She thought she had chosen the frame procedure in lieu of a primary ankle fusion. After four months of non-weightbearing i
114
Author(s): 
By Molly Judge, DPM

   For foot and ankle specialists, the diagnosis and complete management of neuropathic arthropathy ranks among the most daunting challenges. Currently, one makes the clinical diagnosis when there is a compilation of clinical and radiographic findings suspicious for the condition. The diagnosis relies upon the histopathology to identify the neuropathic joint destruction.

   Once one makes a diagnosis, either definitively or clinically, the treatment approach remains the discretion of the physician. Those best trained for treating this condition rely on the literature completed by some of the world’s most renowned authorities in the fields of diabetes research and foot and ankle surgery.1 Although there are numerous articles on managing the condition, many are case reports and isolated accounts of individual experience.2 The traditional academic approach considers the etiology of Charcot neuroarthropathy, possible triggers of the disease process and focuses on arresting the acute, destructive phase of this condition.

   While there are numerous conditions that lend themselves to the development of neuroarthropathy, the prevailing thinking is there are at least two essential components that incite neuropathic joint destruction: a significant sensory nerve deficit (somatic and autonomic); and trauma (trivial or otherwise).3

Understanding The Degenerative Changes With Neuropathic Joints

   The historical literature reveals significant insight regarding the neuropathic joint and how it behaves. In 1917, Eloesser designed animal research testing to answer critical questions regarding how and why a neuropathic joint undergoes degenerative changes.4 One of the first questions he posed was: Is a nerve lesion the primary cause of Charcot joint? For example, does a degenerative change in nerve result in bone atrophy?

   To study this, he sectioned a dorsal nerve root to the extremity in 42 cats, producing total analgesia, anesthesia and ataxia in a unilateral fashion. Each animal developed a degenerative posterior column, producing unilateral neuropathy and allowing for the contralateral limb to serve as a control. All animals developed ataxia, hypotonia in gait and loss of pain perception.

   Seventy percent developed spontaneous lesions of bone including multiple fractures and dislocations while 30 percent developed typical Charcot joint changes. While nerve damage produced a dysfunctional limb, this study did not identify the cause of the Charcot joint.4

   These findings only prompted further questions. Is the Charcot joint the result of trophic bone changes due to a nerve lesion or is it the result of abnormal movements of ataxia in an anesthetic limb?

   Eloesser studied this question in two parts. First, he looked at the ribs of normal controls and denervated cats. In vitro chemical analysis and stress studies of the ribs failed to reveal evidence of atrophy or weakness on these non-weightbearing bones. These findings seem to discount the theory of Charcot that a trophic nerve disturbance resulted in the wasting of bone.4

   Eloesser further noted in stress testing the ribs that the affected bone was usually a little stronger than the unaffected side. He chose not to speculate if these findings were due to a trophic nerve disturbance affecting bone metabolism. He related that the denseness one sees in tabetic bone on X-ray might be the result of ataxia and loss of normal muscle function that increases weightbearing stress on bone. The experiment did not answer the question of whether trophic nerve injury itself caused bone to become more dense, sclerotic and susceptible to bone and joint damage.4

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