Patients with diabetes and neuropathy can develop devastating foot and ankle complications, such as Charcot foot. An expert in the surgical reconstruction of the foot and ankle explains how collaborative care can prevent chronic or recurrent ulcers and bone destruction.
By the time “Peter,” 48, was referred to me, his ankle bone had completely dislocated from his tibia and calcaneus, he had osteomyelitis, a 10-cm ulcer caused by his ankle joint dislocating from his foot, a collapsed midfoot, and he hadn’t walked in 13 months. Peter’s diabetes was well-controlled, but a severe ankle sprain from stepping into a hole had precipitated the most extreme case of Charcot neuropathic osteoarthropathy I’ve seen in my 30 years of practice.
Reconstruction of Peter’s foot and ankle was a lengthy process involving treatment of his osteomyelitis, 6 months in an external fixator to slowly stretch his skin, moving soft tissue and vessels back into position, 3 surgeries with internal and external hardware to stabilize the foot and ankle, and debridement of the ankle ulcer that was filled with fluid and scar tissue from his ankle having been dislocated for many months.
The repair of Peter’s diabetic Charcot foot was limited by the extent of his injuries and the prolonged delay in receiving surgery. Peter also lost 2.5 years of his life when he couldn’t work, walk or drive. The rest of his body was affected by his immobility, causing him to lose muscle mass strength and coordination.
It’s now been 30 months since Peter’s initial injury and 11 months since his first surgery, and he’s making progress. Peter is able to walk with a brace, he is able to drive, and he is in rehab to strengthen his body.
Peter’s suffering and loss of ankle function was totally preventable, however. Peter had sought treatment at a wound care center for the huge ulcer resulting from the ankle joint dislocation and complete destruction of the talus jutting out of his foot 2 months after he sprained his ankle. Had he been referred for reconstructive surgery at that time, we may have prevented his osteomyelitis and complete Charcot breakdown of the ankle, hindfoot and midfoot. The repair of his foot and ankle would also have been far better with less extensive procedures and complications, and Peter would have had considerably less disability and a better quality of life.
A Closer Look At The Plantar Ulcers That Can Result From Charcot
Although Peter’s case was extreme, many patients with diabetic Charcot foot require reconstructive surgery or a custom ankle-foot orthosis, braces, and/or a Charcot restraint orthotic walker (CROW) to heal and prevent the chronic plantar ulcers that result from the classic rocker-bottom foot deformity of this condition. Uncontrolled inflammation causes the midfoot to collapse, pushing the bottom of the foot into the ground. Individuals with Charcot foot often have neuropathy, causing them to be unaware of the constant irritation of the plantar tissue, which eventually breaks down and creates an ulcer that either won’t heal or recurs.
People with diabetes also can have multiple comorbidities, such as poor circulation, kidney function problems, and malnourishment, which can lead to an increased risk of infection. A foot infection is the primary reason patients with diabetes are hospitalized, while 5% to 24% of foot ulcers will require limb amputation.1 Some studies suggest that as many as 13% of all patients with diabetes and 29% of patients with diabetic neuropathy will develop Charcot arthropathy.2
Up to a quarter of cases of Charcot foot are misdiagnosed or diagnosed late, after the foot develops a deformity.3 The first symptom of Charcot foot is acute local inflammation, and many patients visit wound care clinics for treatment of a warm and swollen foot that is often mistaken for osteomyelitis, aggressive septic osteoarthritis, or sepsis. These patients are frequently treated unnecessarily with antibiotics, which fail to arrest the uncontrolled inflammation of Charcot foot.
What Are The Most Effective Solutions For Charcot?
Ninety percent of the patients with Charcot foot that I evaluate have rejected the use of a CROW for offloading. The device is intended to stabilize the foot and ankle while accommodating the pressure points caused by the deformity, thereby diffusing weight throughout the foot and preventing progression to deformity. However, the CROW is heavy and difficult to maneuver, especially in patients with heart disease and atrophy of their leg muscles. Offloading the foot can also create unnatural stress patterns in the opposite foot, leading to ulcers and even fractures.
The surgical options for Charcot foot are exostectomy to shave the bony prominences and remove infected bone, or reconstruction of the foot using external and internal fixators. Exostectomy is a less optimal strategy, since the shaved bone is a symptom of an imbalanced foot. Reconstructive surgery rebuilds a substructure for the foot and each reconstruction is unique.
I always do a bone biopsy and a rapid bacterial genomic DNA assay prior to surgery to determine which bacteria are present so the patient can be started on appropriate antibiotics. I don’t want to administer a broad-spectrum antibiotic, which can lead to unnecessary toxicity and complications in a patient with diabetes. While the wound is healing, I may first remodel the bone, followed by reconstruction. We use either external fixators or a new technology called the Salvation External Fixation System (Wright Medical, Memphis, TN), which allows us to drill through the metatarsal and put metal bolts from the metatarsal through the midfoot to the talus. This concept, known as beaming, was invented by William Grant, DPM.
After cutting out the ulcer and secondary scar tissue, often there may not be sufficient tissue to close the wound. Recently I’ve been using a cryopreserved human umbilical cord and amniotic membrane wound allograft (Neox; Amniox Medical, Miami, FL), which is a source of antfibrotic and anti-inflammatory cytokines and unique matrix proteins that guide rapid healing while reducing inflammation, adhesion, and scarring. Neox modulates inflammation, which allows the wound to close and heal rapidly while decreasing the risk of infection.
I will follow patients who live locally for wound care; patients who live more than an hour to my clinic are followed by their local wound care center.
In addition to treating Charcot foot, another way I collaborate with wound care clinicians is to do prophylactic surgical procedures (tenotomies, digital arthroplasty, and joint destructive procedures) on patients with diabetes to heal and prevent recurrence or onset of ulcers. These patients are referred to me from wound care clinicians when the clinician understands the medical benefits of surgically stabilizing the patient. These elective procedures can be effective in staving off further complications and returning the patient to a more productive lifestyle.
Patients with diabetes can be fragile due to the many complications of their disease. Every decision made on the treatment of the diabetic foot is critical to preventing morbidity and mortality. By working together, wound care physicians and podiatrists can make the right decisions to treat early so that preservation and rather than salvage is the option for the patient.
Alan Block, a nationally recognized expert and educator in amputation prevention and peripheral artery disease, practices at Columbus Podiatry and Surgery in Columbus, Ohio. He serves as a board member of the Ohio College of Podiatric Medical Foundation. He is a former member of the advisory board of Kent State University College of Podiatric Medicine, former editor-in-chief of the Journal of the American Society of Podiatric Surgeons, and the current Past President of the Ohio Foot and Ankle Medical Association.
1. Alexiadou K, Doupis J. Management of diabetic foot ulcers. J Diabetes Ther. 2012;3(1):4.
2. Kaynak G, Birsel O, Guven MF, Ogut T. An overview of the Charcot foot pathophysiology. Diabet Foot Ankle. 2013;4(1):21117.
3. Korzon–Burakowska A, Jakóbkiewicz-Banecka J, Fiedosiuk A, Petrova N. Osteoprotegerin gene polymorphism in diabetic Charcot neuroarthropathy. Diabet Med. 2012;29(6):771–775.