All of us get in clinical ruts and occasionally manage our clinics on autopilot. Do not let your training get in the way of your intellect and clinical observational skills. Remember, your training was only a foundation to get you to the minimum level of competency, a gateway to real surgical learning so to speak. It is your experience (perhaps the most important quality of a great surgeon) and continued desire to improve your surgical technique, preoperative diagnosis and postoperative management that will make you a true master surgeon.
With this in mind, consider the following case study.
A woman presented initially with a painful lesion on the plantar aspect of her third metatarsal head. She previously had numerous conservative treatments consisting of repeated topical skin debridement, application of callus removers, orthotic devices and adjustment of shoes prior to seeing the “operator.” However, the patient has not gotten better and now seeks an opinion on a possible surgical remedy.
The surgeon notes there is significant scarring and nucleation within the hyperkeratotic lesion on the plantar aspect of the third metatarsal head. The surgeon obtained a marked lesion X-ray series. A very short gait analysis noted the patient had a limp with an antalgic gait. She had contracture to a mild extent to all of the lesser digits in addition to having a mild hallux valgus deformity.
The surgeon schedules the patient for surgery, confident that he has identified the correct metatarsal because of the marked lesion on AP radiograph. The scheduled surgery will include excision of the hyperkeratotic lesion and a condylectomy of the third metatarsal head plantarly through the same incision. The surgery goes well and the patient does well for approximately three to six months. Then the patient returns with the same pain and same hyperkeratotic lesion. Remember, great surgery based on poor diagnosis gives a less than desirable outcome in almost all situations.
The befuddled “operator” now has to reassess this less than desirable outcome. He decides that something biomechanical (can’t really figure it out exactly) must be happening to cause the lesion, especially since it has returned so quickly and that condyle is gone. The surgeon determines it is likely due to the slight contracture of the hammer digit, which must be putting retrograde pressure upon the metatarsal head. Is that why the condylectomy did not work on the plantarflexed third metatarsal?
After taking more X-rays, the practitioner notes a well healed stress fracture of the second metatarsal, which was present on the first pre-op films. However, the surgeon is not cognizant that the second and third metatarsals are long in comparison to the first and fourth rays, and that the well healed stress fracture could indicate a longstanding forefoot overload.
The surgeon schedules the patient for revision surgery. At this time, he will perform another “condylectomy” (because “some bone must have grown back on that met head”). In addition, he performs an arthroplasty of the second and third digits to reduce the overwhelming retrograde force due to the minimal digital deformity. (On AP views, the joint spaces of all the lesser MPJs are well maintained and there is no evidence of dorsal dislocation of the phalangeal bases.)
The surgeon takes the patient to the operating room again but she would like to have her mild hallux valgus deformity addressed as well this time. After performing a routine hallux valgus reconstruction, he performs an arthroplasty of the proximal interphalangeal joints of the second and third digits. The surgeon also excises the plantar lesion again, performing another condylectomy through that incision.
The surgeon seemed perplexed intraoperatively when he saw a well planed plantar metatarsal head surface and no real bony regrowth on the previously treated metatarsal head.
Guess what? Three months later, the patient returned to a full weight bearing status, albeit an antalgic one. However, six months after the revision surgery, the patient’s lesion returned. Now she has developed chronic pain with neuritic-type symptoms involving most of her forefoot because her lesser digits treated with arthroplasty look like ballpark franks.
The same practitioner now makes the diagnosis of a “neuroma.” (We have discussed the definition of a neuroma in previous blogs.) It cannot be a neuroma unless the surgeon had the unfortunate intraoperative accident of cutting one of the common plantar digital nerves during the previous surgery.
The patient has burning pain in the digits and inquires about a third surgery, a panmetatarsal head resection with second and third interspace neurectomies. This time, however, the patient, who has waning faith in this practitioner, decides that she needs another opinion. She decides to see another practitioner.
The problem is that this practitioner is one of law and not foot surgery.
Sadly, the patient still has pain and now so does the surgeon who has unsuccessfully operated on her twice. Yes, her surgeon is going to have to do a deposition.
How does it happen that this patient has global forefoot deformities and a posterior calcaneal exostosis at the insertion of the Achilles tendon, which was never mentioned in any record but was present all the time and big as life? Why did this practitioner never even consider that the patient could have some type of proximal contracture (i.e. equinus), which was the root of all of her problems? Is it really that difficult to figure out that maybe something else is causing excessive pressure in the forefoot when you have radiographic evidence of a stress fracture, which is well healed in the second metatarsal, as well as a monster exostosis on the posterior aspect of the calcaneus?
You perform a cheilectomy for very severe hyperkeratotic lesion and it keeps returning, and you do the losing surgery a second time? Wow. Is it really that hard, guys? Let us say, for example, that you take your car to the mechanic because the left front tire continues to wear out. You are probably not going to have a conceptual conundrum in figuring out that maybe noting is wrong with the tire and even though the tire may need to be changed, something else is causing the tire to wear out. This is conceptually a no-brainer.
Yet in the forefoot surgical arena, there are many who are afraid of cutting the gastrocnemius aponeurosis, reasoning that “you could injure the sural nerve.” Right. Isn’t that the nerve the neurologist routinely biopsies? I know my hand surgeon colleagues refer to it as the “donor nerve.” So I can repeatedly operate on the forefoot of the patient, get “ballpark frankitis” of the lesser digits and render the patient to a dysfunctional forefoot for the rest of her life. However, I did obviate that couple of percent of chance of injury to a small nerve that has no motor innervation.
Don’t get me wrong. I am a “save and preserve the nerve” guy. (I have the T-shirt and bumper sticker to prove it.)
However, this case illustrates that being afraid of the wrong thing can have devastating consequences.
Why is it then so difficult for the surgeons out there to wrap their cortices around the concept that it is very simple to diagnose equinus and surgically treat the equinus without surgically destroying the forefoot? There are numerous patients out there who cannot walk because they have had multiple osteotomies, pan-metatarsal head resections, arthroplasties of the digits, fusions of the digits with significant and permanent swelling and dysfunction, and digits heading in four different directions. All these patients needed in the first place, after conservative therapy has failed in some cases, is to be relieved of their bad alignment.
Is it really that conservative to perform multiple arthroplasties, extensive forefoot reconstruction on something that can be treated with a very minimally invasive surgery such as an endoscopic gastrocnemius recession? For that matter, isn’t it conservative to perform an open gastrocnemius recession?
What really is the downside? The most horrible event that can occur is a potential amputation neuroma to the sural nerve. Even if you transect this nerve, it will usually leave a small amount of numbness on the dorsal lateral aspect of the foot with the only resulting complication being a small area of cutaneous sensory loss.
Well, so what? The patient can't walk due to the intractable hyperkeratosis sub-second through fifth metatarsals and you are worried about the sural nerve. Why? Isn’t what we sometimes do surgically in complex cases a trade-off? Why not worry about the abnormal gait with subsequent lower extremity pathomechanics resulting from the compensation?
Try this for a self-experiment. Take a small BB pellet and tape it with duct tape to the bottom of your forefoot. You can pick the location. See how you compensate and how long you can stand it. Then block your sural nerve with some lidocaine. Which do you choose?
We have got to be kidding ourselves. “You cannot be serious,” as John McEnroe would say, that you are not going to take care of the truly deforming force with a minimal surgical intervention because your “paradigm” is focused and isolated only on the symptom rather than the cause.
The great comedian Dennis Miller is able to paint the ridiculousness of what our society sometimes fears and does in epics such as I Rant, Therefore I Am. I have to rant because I am tired of “seeing ballpark frankitis” and want to rave when I see the absolute surgical eloquence with exquisite outcome from simply doing the simple (in cases like these gastrocnemius recessions).