Of all the disorders podiatrists treat, I would bet good money that the most common ones experienced by all of us are the diabetic foot complications. Although I have always had a professional interest in the diabetic foot, and receive a lot of personal reward from helping these patients, I also find it very unfortunate because almost all of the complications that occur are entirely preventable.

Take, as an example, Mr Smith (names and some details modified for privacy), a 35-year-old Type 2 diabetic who ended up with an acquired adult clubfoot after surgical removal of his entire 5th metatarsal. He had a callus under the 5^th metatarsal head (from a pes cavus foot type) that became infected, abscessed, requiring a partial 5^th ray amputation that was later converted to an entire 5^th ray amputation. Any podiatrist could predict that loss of the attachment of the peroneus brevis tendon attachment would lead to an equinoadductovarus contracture. The extra strain while walking, combined with his uncontrolled diabetes resulted in Charcot arthropathy of the ankle, which is where I took over his care. A major reconstruction later (consisting of three surgeries), I was successful in saving his extremity.

However, two months ago, this same patient returned to my office with a plantar forefoot ulcer on the other side. As one might expect his blood sugars were very high, with a hemoglobin A1c above 14%. We’re now fighting to heal his wound before an infection leads to an amputation.

This patient’s situation highlights the highly preventable nature of this problem. Creating a diabetic foot ulcer is a multi-step process that could have been prevented at each of the steps. Consider these stages, one leading almost sequentially to the next:

There’s a world of detail between and within each of these numbered steps, but these eight cover the major stages reasonably well. Now, look at each step individually, and you’ll note most of them are preventable. In fact, not only is each one preventable, but stopping the process at one step eliminates all of the downstream complications from occurring. Prevent the diabetes and steps 2-8 don’t occur. Control the blood sugar, which prevents the neuropathy, and stop steps 3-8 from happening. Etc. Etc.

It’s also important to realize that preventing each step later in the process is progressively more difficult than the preceding step. Preventing an infected ulcer from becoming an amputation is much more difficult than preventing the ulcer in the first place.

The example above easily demonstrates these issues. If Mr Smith had taken better care of himself, he wouldn’t have become diabetic. If, after becoming diabetic, Mr Smith had worked to control his blood sugar, he wouldn’t have become neuropathic. If his cavus foot had been properly managed with appropriate shoes and regular podiatric care, he wouldn’t have acquired the ulcer. If he had sought care when he acquired the ulcer, it would have been treated, and the infection may not have occurred, which wouldn’t have led to the amputation, which wouldn’t have led to the acquired clubfoot deformity, which might not have led to the Charcot and the need for a reconstructive surgery. Notably, we stopped the leg amputation by reconstructing the deformity.

It’s really tragic that there are so many places in which we could intervene and yet the disease continues its rampage almost unabated. Until a cure for diabetes is found we are going to continue what appears to be an inexorable trail toward ever more severe limb complications in increasingly sick patients.

For all you diabetes researchers out there, I call on you to do the research project that has yet not been done: Testing what happens to foot ulcer rates when we intervene much more aggressively than we do now. There are two simple equations that are highly applicable to clinical practice:

Neuropathy + Deformity = Ulcer

Ulcer + Infection (or PAD) = Amputation

For a podiatrist these equations are like Newton’s laws of motion. Maybe we can call them the Diabetes Laws of Complications. The real key equation, though, is the first one because if the ulcer doesn’t occur then the infection doesn’t happen. You can effectively prevent the amputation by preventing the ulcer. It makes logical sense, then, for us to focus our podiatric prevention on the first equation. It’s also pretty obvious that podiatrists aren’t going to cure neuropathy. That leaves us with one final area to intervene: deformity. And that brings us to my research recommendation.

The research study that hasn’t been done yet is to see if surgically eliminating the deformity of a neuropathic foot will decrease the prevalence of ulcer formation. This might look like a trial in which neuropathic diabetic patients who all have some deformity (hammertoes, equinus, cavus, planus, limited joint motion, etc) but no ulcer history are randomized to a surgical group and a nonsurgical control group. They would then be observed for a set period of time (say, five years on average), watching for the prevalence of ulceration, infections, hospitalizations, and amputations.

This landmark study would, I predict, show an overall decrease in all negative outcomes and perhaps even an increase in life expectancy. This is clearly a hard study to perform, which is why it hasn’t been done yet (I doubt I’m the first person to think of it). Until the study is done we will be relegated to reacting to the disease’s complications rather than proactively eliminating deformity as a risk factor. Until we start proactively reconstructing high-risk feet, the medical community will not realize the true potential of podiatry and most effectively help our patients.

Best wishes.