RE: Treatment for Metastatic Cancer Spread to Feet
From: Roody Samimi, DPM
First of all, a biopsy is indicated. Any suspicions for metastatic cancer should be sent to an orthopedic oncologist. Surgery by us is only indicated in benign cases.
Roodabeh Samimi, DPM Stockton, CA
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RE: Arthrogram of the 2nd MPJ for Partial Plantar Tear
From: Kevin A. Kirby, DPM
Regarding the diagnosis of plantar plate tears, of course diagnostic ultrasound (US) and MRI are often helpful in ruling out larger plantar plate injuries. I believe that here in Northern California, arthrogram is now rarely used to diagnose plantar plate tears. However, podiatrists who are only using US to examine the symptomatic plantar plate, and are not also examining the other lesser metatarsophalangeal joint (MPJ) plantar plates with US, should be well aware of the research literature regarding frequency of plantar plate tears in symptomatic and asymptomatic MPJs.
In an excellent US and MRI study by Gregg and colleagues from 12 years ago, plantar plate tears were present in...
Editor's note: Dr. Kirby's extended-length letter can be read here.
RE: Arthrogram of the 2nd MPJ for Partial Plantar Tear
From Kenneth Meisler, DPM
In my office, we almost exclusively use ultrasound to diagnose 2nd MPJ plantar plate tears. We have done this many hundreds of times. In addition, I have seen many patients who were treated by other doctors for 2nd MPJ pain. Many of those patients had MRIs or ultrasounds performed to rule out a plantar plate tear. I have not seen a patient who had an arthrogram of the 2nd MPJ in many years.
I use two Hospital for Special Surgery fellowship-trained musculoskeletal radiologists for my MRIs and CT scans, each from a different radiology practice. They both prefer ultrasound to evaluate the 2nd MPJ for plantar plate tears. In spite of the lower payment they receive as compared to MRI, they feel that in most cases, it is better for evaluating plantar plate tears.
A podiatrist should be able to perform these ultrasounds in his/her office. However, it requires a very good ultrasound machine plus experience and/or training in evaluating for this injury. Every podiatrist will not be able to perform this because they will not have been trained to do it, have enough patients that require it regularly, or have an ultrasound machine that can evaluate for it. My suggestion is to get trained to diagnose plantar plate tears or refer the patient out to a radiologist, ideally fellowship-trained in musculoskeletal ultrasound, and ask them which works better in their hands.
When I suspected a torn plantar plate, I injected Marcaine into the dorsum of the capsule and tried to overfill the joint. If the joint became tense and required more effort than expected, then a tear was very unlikely. If the plantar soft tissues became engorged, then a tear existed. It is easy to do, costs pennies versus thousands of dollars, and is easy for the patient to understand and see.
I have always used a 50/50 mixture of local anesthetic and Renographin under "C" arm guidance. Use a small needle and inject dorsally until the joint is full. Any leakage from the medial/lateral/plantar aspect is evidence of a capsular tear. Make sure you visualize it in multiple planes.
If it’s a true plantar plate tear, the combination of a positive modified Lachman test in combination with a thin slice (2mm) sagittal plane MRI will confirm the diagnosis. A 3T MRI is the optional magnet size for best resolution. I also recommend that you have the tech call you when the patient arrives so you can confirm the exact location of the 2nd MTPJ pathology.
Regarding arthrograms, you should use 1/2cc lidocaine mixed with 1/2cc hypaque in a 23g needle or whatever radiology has in stock. Use an ultrasound or fluoroscopy to ensure that you’re in the joint and to observe extravasation which, depending on the severity of the tear, would confirm the diagnosis.
There are neurologists and podiatrists in my own geographic area who do not prescribe any of the varied vitamin compounds for diabetic neuropathy. I respect their right to their opinions.
The way I handle these compounds in my practice is that I give the patient a one-month supply of one of the compounds (and there are many) and tell him or her to try it for a month. If the patient feels that it helps them, they will come back every month for a new supply. If it does not help them, they won't buy it again. Some patients will want to run it past their neurologists, endocrinologists, or primary care doctors first; and in some cases, those doctors will give them a green light and in some cases they are told not to try it. I don't lose any sleep over either decision.
I 100% concur with Lancing Malusky, DPM. I use Metanx as my frontline in treatment of neuropathy. I actually prefer Metanx’s sister formulation of Deplin. It’s labeled for depression, but it’s the same stuff – just pure 15mg L-methyl folate. I typically prescribe it as 1/2 tablet qd to 1/2 bid. I then supplement with Jarrow-Brand methylated B12 to prevent anemia. Aside from being contra-indicated in history of cancer or history of seizure, patients can take it with any of their meds. If anything, they are able to take lower doses of their other neuropathy meds.
Anecdotally, I noticed that their Raynaud’s symptoms also resolves. Therefore, I use it with good success as a front liner in treating my Raynaud's patients, without the side-effects of calcium channel blockers. One can use it on children as well as adults. You can start and stop on a dime and use it seasonally. I would love to know why the neurologist thinks it’s so bad.
Is it possible to get clarification as to this post? Why was the neurologist so adverse to Metanx? Was it the B6? The L-methyl folate? The B12? Why is Metanx “the worst thing you can take?” Is it the attitude of an all-knowing neurologist? Is it legitimate? What are the studies?
Paul Jones, DPM, Portland, OR
I recently developed type 2 diabetes. My current A1c level went from 6.2 to 5.3. More importantly though, I requested Metanx for night time foot neuropathy from my PCP (who had never heard of it). The non-generic Metanx resolved my night pain. The A1c change may be coincidental, but the resolution of my neuropathy is not.
It is difficult to tell, but those lesions look like pitted keratolysis. Have the specimens been analyzed for bacterial identification and sensitivity? Is Corynobacterium a possibility? Is the patient diabetic?
Martin V. Sloan, DPM, Abilene, TX
RE: Body Identity Integrity Disorder (BIID)
From: George Jacobson, DPM
This is a rare disorder where the patient wants to get rid of a body part. In this case, amputate the foot. The patient gets happiness at the loss of a body part. To read more about this, look it up or click this link. Could you imagine having a patient that has this disorder and does everything they can to lose their foot or leg.
This appears to be purpura due to a hypersensitive vasculitis due to the antibiotics. One can also see a transient rash from endocarditis. This does not appear to be embolic, which usually occurs at the tips of the toes. Ask the internist if they can put the patient on another antibiotic.
The characteristic radiographic appearance of chronic gouty arthritis in the foot is the presence of clearcut, “punched-out” erosions with dense, sclerotic margins in a juxta-articular distribution, often with overhanging edges. What's going on in the proximal interphalangeal joint of the second toe and the distal-medial tuft of the distal phalanx in the great toe is highly suspicious.
Arthrocentesis with even just a couple of drops of synovial fluid enables microscopic examination which can make the diagnosis. If crystals are seen, their shape and appearance under polarized light are diagnostic. Way back when I taught in the classrooms and clinics of the Illinois College of Podiatric Medicine, when we saw this kind of arthropathy on an x-ray, we used to say, "When in doubt, think of gout."
There have been a number of posts dealing with gout and diabetic patients, most recently that by Dr. Udell on the differential between gout and infection.
Strange as it may seem, gout has been misdiagnosed when the actual pathology is early onset of Charcot foot disease. This is more common than might otherwise be recognized and most often [misdiagnosed] by family practice type physicians who are not educated enough for the index of suspicion needed to diagnose early onset of this osteoarthropathy.
In particular is a case that was seen by a family practice physician for several months, referred back to radiology, then to orthopedics, all of which has confirmed gout without supportive serological testing, etc. With the patient apparently not improving, the family practice physician...
Editor's note: Dr. Kravitz's extended-length letter can be read here.
It is not that uncommon for diabetics to experience gout attacks. After all, diabetes does/can affect the renal function in diabetics causing increase in uric acid. Regarding the radiographs submitted, there is not enough evidence in the pictures to suggest chronic attacks of gout in that particular toe. Obtaining labs is recommended.
Two conditions that share clinical appearances are acute gout and acute bacterial infection. A sixty five year old diabetic patient could have acute gout or an infection, and missing the correct diagnosis could be problematic. It is not out of the question that the patient could even be presenting with acute gout combined with a bacterial infection.
This case calls for a needle biopsy of the affected joint and ask the lab to not only look for urate crystals but have them do a culture and gram stain. You will have to send the fluid tapped in two different types of media (Call your lab). In the interim, place the patient on a broad spectrum antibiotic and monitor the patient carefully for any signs of ascending cellulitis.
I had a similar case many years ago. What was most annoying is that the patient would come in every four weeks to have the lesions debrided and enucleated. Can you imagine what it was like debriding and enucleating 30 or 40 punctate lesions every four weeks. What finally worked was that I casted the patient for fully functional rigid foot orthotics. After using the orthotics, the lesions all went away. That was 25 years ago. Today, I would have done a punch biopsy first and sent the specimen to the Derm Path lab.
EMLA works best placing it under occlusion. I tried it in practice on young apprehensive teens, some younger children, and apprehensive older patients. My experience is it takes too long to work. Also, the patch or occlusion preparation seems to work on certain areas better than others. When I tried it on the plantar foot, forget it. The flexor side (anterior) surfaces are somewhat better. EMLA takes too long in any case. Use the freezing sprays instead.
In clinical practice, I have in the past recommended EMLA cream topically BID over small surface areas of the tarsal tunnel, sural, or deep peroneal nerve trunks for neuropathic pain reduction, especially in diabetic patients or those with radiculopathy. Pre-treatment topically of younger patients, or the use of vibration devices, often lessens apprehensive fear of local nerve blocks. Finally, we have had patients with hypersensitive feet or reduced pain thresholds benefit from topical EMLA under occlusion 45 minutes prior to the office visit for sharp debridement of IPKs.
In my 13 years of clinical practice, I estimate that 2-3 people out of every 100 experience the metallic taste in the mouth with oral terbinafine. Most of these patients were able to deal with it. I do recall one patient several years ago to whom it became very bothersome. It took a couple of weeks to resolve after stopping the medication.
At the time, I did a Google search on this and found a case of a gentleman, in I believe the UK, who was actually hospitalized because he didn't want to eat due to the taste disturbance. In my experience, the taste disturbance with oral terbinafine is rare and to become a big problem is incredibly rare.
I have used EMLA for my kids when they were young, prior to injections and blood draws. I then used it for electrolysis. If used as directed from a fresh tube, it is very effective and leaves the skin completely numb. I suggest applying a liberal amount under occlusion for 30 to 45 minutes. This is all my personal experience. I have never used it on patients prior to nail debridement.
I must admit to “shock and awe" at the recent discussion regarding loss of taste with oral terbinafine. Loss of taste is one on the most common adverse sequels of this medication, occurring in greater than 1/50 patients. Although typically reversed with discontinuation of terbinafine, loss of taste may be permanent. I suggest that in the future, practitioners might familiarize themselves with the FDA package insert before prescribing medications, or offering commentary regarding potential medication side-effects.
Allen Jacobs, DPM, St. Louis, MO
After over writing 200 scripts for terbinafine, I have seen 3 cases of taste disorder that caused the patient to stop its use. Taste came back within days of stopping. No ill effects were noted thereafter. As an aside, not one case of elevated liver functions was found in those patients tested.
Neil Barney, DPM, Brewster, MA
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