Managing Ulcers On The Charcot Foot

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Continuing Education Course #110 — July 2003

I am very pleased to introduce the latest article, “Managing Ulcers On The Charcot Foot,” in our CE series. This series, brought to you by HMP Communications, 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.

Charcot arthropathy is a significant problem. If it is not recognized and treated early and aggressively, it can lead to significant damage to bones and joints, reulceration and infection. In this article, Pamela M. Jensen, DPM, and John S. Steinberg, DPM, offer perspective on the etiology of the condition, key diagnostic markers, conservative treatment options and surgical procedures.

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


Jeff A. Hall
Podiatry Today

INSTRUCTIONS: Physicians may receive one continuing education contact hour (.1 CEU) by reading the article on pg. 74 and successfully answering the questions on pg. 80. Use the postage-paid card provided to submit your answers or log on to and respond electronically.
ACCREDITATION: HMP Communications, LLC 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 HMP Communications, LLC are expected to disclose to the audience any real or apparent conflicts of interest related to the content of their presentation.
DISCLOSURE STATEMENTS: Drs. Jensen and Steinberg have disclosed that they have 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 their presentation.
GRADING: Answers to the CE exam will be graded by HMP Communications, LLC. 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.
RELEASE DATE: July 2003.
EXPIRATION DATE: July 31, 2004.
LEARNING OBJECTIVES: At the conclusion of this activity, participants should be able to:
• discuss the neurotraumatic and neurovascular theories on the etiology of Charcot arthropathy;
• discuss ancillary diagnostic procedures for Charcot;
• differentiate between Charcot and osteomyelitis;
• identify indications for conservative and surgical treatment of ulcers on the Charcot foot; and
• discuss potential complications of reconstruction and arthrodesis procedures.

Sponsored by HMP Communications, LLC.

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Here is a chronic midfoot ulceration that resulted from a Charcot deformity.
As you can see, this patient has a chronic Charcot midfoot deformity with a fracture/dislocation at the LisFranc’s joint complex.
Here is the same patient three weeks after undergoing a midfoot fusion with reconstruction using internal and external fixation.
Another view of a patient who underwent a midfoot fusion.
This radiograph reveals insufficient reduction and insufficient fixation of Charcot midfoot deformity in a patient who has diabetes.
Here is a clinical view of the same patient, who has severe midfoot abduction and ulcer risk due to focal increased pressures.
Here one can see a chronic midfoot plantar Charcot ulceration after the patient underwent an I&D with split thickness skin grafting to the plantar foot. Exostectomy and probably percutaneous tendo-Achilles lengthening are often indicated with this foo
By Pamela M. Jensen, DPM, and John S. Steinberg, DPM

Neuropathic osteoarthropathy, or Charcot arthropathy, is a condition associated with a loss of sensory nerve function and concurrent vascular dynamic changes. In the acute setting, Charcot can result in bone and joint deformation and fragmentation. If it is not treated early and aggressively, the collapse of involved joints will cause instability, deformity and subject bony prominences to ulceration and infection.
The incidence in the United States and internationally of those with diabetes who have Charcot arthropathy ranges from 7.5 to 13 percent. Internationally, 10 to 20 percent of those with tabes dorsalis and 20 to 25 percent of patients with syringomyelia have some degree of Charcot arthropathy. The age of onset is usually between the fourth and fifth decade with a diagnosed duration of diabetes greater than 15 years. Presentation is usually unilateral but bilateral involvement has been noted at 5.9 to 39.3 percent. Ethnic groups are equally susceptible to having a Charcot arthropathic event.

Understanding The Etiology Of Charcot Arthropathy
Two independent theories, the “neurotraumatic” and the “neurovascular” theories, have been proposed as to the cause of this deformity. However, the consensus of current literature indicates a combination of factors from both theories is generally present in Charcot arthropathy.

The neurotraumatic theory (German theory) proposes that an unperceived trauma to an insensate foot renders the patient unaware of osseous destruction that occurs during ambulation. The resulting trauma leads to progressive destruction and significant damage to bone and joints.
The neurovascular theory (French theory) proposes that autonomic neuropathy, caused by the underlying nervous system impairment and degeneration, results in hyperemic demineralization that leads to osteopenia. The combination of these theories with initial abnormal bone formation due to autonomic deformity and the following microtrauma of the insensate foot, results in multiple fractures and joint subluxation.
Shapiro, et. al., (1988) concluded blood flow in Charcot patients is intact and loss of blood flow in patients with diabetes is protective against Charcot. While this may be worthy of further investigation, our clinical experience has demonstrated significant limb ischemia in the face of chronic Charcot. While blood flow may have been intact at the time of the initial Charcot episode, it may be deficient several years later when treating the chronic Charcot foot deformity. This is of particular importance when evaluating the non-healing Charcot ulceration and also in considering surgical alternatives in the management of this patient population.

Key Clinical Signs And Symptoms
The clinical presentation of Charcot arthropathy generally begins with inflammation, localized warmth to extremity (3 to 7ºF when compared to the non-affected foot or otherwise normal skin temperature), diffuse erythema, joint effusion, intact skin without ulceration and loss of protective sensation. Up to 75 percent of acute Charcot arthropathy patients will present with some level of pain. However, many present with no pain or pain that is significantly less than expected when one considers the clinical and radiographic findings. These patients may have instability, deformity and loss of joint function. In extreme cases, the foot may present as a “loose bag of bones.” Approximately 40 percent of Charcot arthropathy patients have a concomitant ulceration, thereby complicating the diagnosis and raising concern for osteomyelitis.1

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