Charcot Foot Phase 1.2

At least one account I encountered estimates that approximately 3% of diabetics will "come down with" Charcot Foot. In bygone eras it used to afflict others, but nowadays it’s all but exclusively a diabetic problem. Brief basics, normally the diabetic breaks or fractures a foot bone, usually does not feel the injury due to diabetic neuropathy and the foot swells up in response. Treatment is typically immobilization to prevent the broken bone from displacing. The displaced bone can rip through the foot from the inside.
My injury and affliction was atypical. I had tendon and/or nerve damage (and still do) but not breaks or fractures. (Breaks and fractures are both breaks, just of different severity and separation of the pieces.) The reports that cleared me came from both X-ray and MRI. Doctors at an urgent care center and a sports medicine practice, my GP and "Dr. Dumbass" all gave diagnoses of "no breaks."
So imagine my surprise when Dr. Dumbass–aka podiatrist David Greenberg–told me on the second visit that I did have breaks and fractures.
I had resumed bowling as exercise with limits on frequency and duration based on the "no breaks" diagnosis. This tail-spun me into stressful second guessing and worries of what further damage I could have inflicted to myself. Bowling was neither particularly successful nor painless, but it remained one of the few things I could still do and just about my only social interaction.
The bowling may seem haphazard. Maybe it was. My reasoning was that Phase Two of Charcot Foot is typically a long duration of rebuilding strength and integrity in the foot, things lost by a combination of inactivity and poor circulation that limit the flow of nutrients to the foot. Basically, immobilized and unused feet tend to atrophy during Phase One. I experienced the most evident ankle collapse in the month that I did stay off the foot almost entirely, and little to no evident progression when I did get the limited exercise. The human body is an odd machine: it works better the more it is responsibly used.
Dr Dumbass gave the new diagnosis without the benefit of any new X-ray or scan. Subsequent images ordered and reviewed by a later doctor showed structural damage that is natural progression of Charcot but seemed to confirm that there had been no initial bone damage.
I rectified Dr. Dumbass’s inconsistencies as statistical generalizations of the overall condition rather than any result of examination.
I started seeing Dr. Thomas Mancini when the foot swelled back up in response to discontinuation of prednisone.
Doctor Mancini had some concerns after a thorough examination of my foot, which is something Dr. Dumbass never really bothered to do. Dr. Mancini wanted me to consider Boniva type drugs and wanted me to pick up the leg brace that Dr. Dumbass had prescribed and I had been fitted for custom manufacture before the leg and foot re-inflated.
The toe infection that sent me to the hospital for four days interfered with those plans. The hospital, deeming a blind gimpy guy as a trip and fall hazard, kept me immobilized for the weekend. That proved a long enough time of absolute inactivity for the ankle to suffer further collapse. This change for the worse could be seen in the shape of the foot, felt when the foot was used or moved on its own, and it could be heard when I tried walking on it.