Case 191: Osteomyelitis, an Open Joint, Focal Necrosis of toe, Extensive Cellulitis of an Arteriosclerotic Neuropathic Foot... Healed in the Outpatient Clinic.

Born August 1st, 1943, this man was found to have diabetes in 1983. While weighing but 190 pounds (86.4Kg) in his early twenties, he had achieved a weight of 290 pounds (131.8 Kg) when he presented for boot therapy on the 19th of April, 1999. He was then taking 10 mg of glyburide twice daily. He gave a history of having developed a Charcot foot which led him to an orthopedic specialist in a Philadelphia teaching center who performed a mid-foot fusion in 1997. He had seen this specialist for a routine follow-up just before departing for Las Vegas on business. There he developed a draining ulcer on his left third toe leading to a one-day hospitalization and the administration of intravenous antibiotics. He chose to return to his Philaldephia physicians and left Las Vegas with a prescription for Ceftin. His orthopedic specialist recommended hospitalization, intravenous antibiotics and surgery. He came to the Bryn Mawr Circulator Boot Clinic for another opinion.

April 19th, 1999: He presented with a swollen left foot that was reddened over the distal dorsal area over the 2nd to 5th metatarsals. The 3rd toe was swollen and rotten over its distal lateral aspect.

April 20th, 1999: At the time of his second day of treatment, a gap through his tissue into his distal interphalangeal joint was noted when his toe was bent towards his big toe; the joint appeared to be obviously infected.

Doppler sounds were diminished but biphasic at the ankle. High pitched sounds over the posterior tibial suggested streaming and partial arterial obstruction. Bio-thesiometer readings were elevated pointing to advanced peripheral neuropathy: the maximal 50 voltage of the apparatus in the big toe and 35 volts in the little toe. He presented, hence, with advanced diabetic neuropathy, modest peripheral arteriosclerosis obliterans, necrotizing cellulitis of the third toe, cellulitis of the distal foot and likely osteomyelitis of the distal interphalangeal joint. We advised him that as his physicians in Philadelphia and Las Vegas had advised, patients so afflicted are commonly hospitalized for intravenous antibiotics and for consideration of revascularization procedures in communities with aggressive vascular surgery services. These things, we advised, we could do also, but we advised him we would likely do just as well with our outpatient booting program. He chose the latter.

We first cultured his toe. We gave him an oral broad spectrum antibiotic, Trovan (it had not yet been recalled). Then, we proceeded immediately with our treatments. First, we cleaned his foot with a bath of Sea Soaks and dilute hydrogen peroxide. Then, we injected gentamicin and vancomycin locally into the infected areas of his distal foot and 3rd toe. We then placed his foot in a bag containing Sea Soaks, vancomycin and gentamicin and put the bagged foot in the Circulator Mini-Boot where its pulsations further scrubbed his lesion, disseminated the injected antibiotics throughout his foot and toe, reduced the swelling of his foot and toe and augmented/maintained the arterial circulation in the foot. We advised him that such treatments should be performed daily until it was clear that his foot would heal on its own. As his blood sugars were grossly elevated, we stopped his oral agents and gave him an insulin program. On April 24th, his culture report returned. He had a heavy growth of Staphylococcus aureus, a heavy growth of Enterococcus species, moderate growth of Pseudomonas aeruginosa and moderate growth of Streptococcus viridans. All of the organisms were covered by the locally administered vancomycin and gentamicin. The Trovan was ineffective against the Staphylococcus and the Enterococcus. His foot, however, was improved, albeit still at risk. In view of his advanced neuropathy, Urecholine (bethanechol chloride) was also added to our therapeutic regimen, both injected locally and included in his Mini-Boot baths.

June 3rd, 1999: Some of the fatty material had just been debrided from the edge of his ulcer prior to this picture. His sedimentation rate was 71mm/hr.

His cellulitis and swelling slowly receded and he was left with a clean ulcer with an exposed distal interphalangeal joint. By early May his options included continued outpatient treatment to heal his ulcer or hospitalization to remove his toe with a good chance the amputation site would heal. His insurance company allowed his choice of continued outpatient treatments. Coming to the program with his blood sugars constantly in the 200-300 range, he required frequent insulin adjustments. By June, his sugars averaged closed to 100 and his glycohemoglobin A1c was 6.8% (June 29th).

July 20th, 1999

During June, he received 20 outpatient treatments. Before the first nine he was given local injections of ceftazidime, Vancomycin and Urecholine. Throughout the month, gentamicin and Vancomycin were placed in his Mini-Boot bath. When in mid-June his joint gap was covered and only a clean ulcer remained, his local injections were discontinued but the antibiotics along with Urecholine and amphotericin-B (a culture showed yeast) were still added to his Mini-Boot bath. Although it did not provide coverage of all of his infecting bacteria, he was continued on oral Cipro during June and July to replace the Trovan, which had been recalled from the market.

September 9th, 1999

His foot color was largely restored and the 3rd toe swelling greatly reduced. His sedimentation rate, however, remained elevated at 44 mm/hr. In requesting additional coverage for his treatments, we advised his insurance company that in spite of the seeming intactness of his toe, we could not declare him healed because of his increased sed rate. We proposed that it would be appropriate to x-ray his foot and target any suspicious areas with local antibiotics and boot therapy. If there were no suspicious areas, we would plan to continue him on oral antibiotics (? which ones) and follow his sed rate at monthly intervals.

September 9th, 1999

His hammertoe deformities made it difficult to clearly see the distal IP joint of the 3rd toe even with a bright light. Multiple screws are seen traversing the metatarsotarsal joints from his previous surgery. The radiologist noted a loss of the cortex of the tuft of the distal 3rd phalanx suggesting a small focus of persisting osteomyelitis. Some lucency was also noted about the tip of the more lateral screw again possibly reflecting a small area of inflammation or infection.

September 11th, 1999

His insurance company discontinued his coverage on September 11th. He was discharged from the boot clinic with a prescription for Cipro.

Comments: This man did well. In spite of his advanced neuropathy, moderate arteriosclerosis and screws in his foot, he has recovered from a large area of cellulitis, focal necrosis of the toe and osteomyelitis. He was able to grow skin over an exposed infected joint. The latter feat is commonly said to be impossible by many surgeons who would have amputated this man's toe. Gaining permission of insurance carrriers is a new burden for physicians today. Here we were grateful to be allowed to treat our patient six days a week, five days a week and then three days a week as we and the patient saw fit. The patience of the insurance company did wear thin, however, and they did not allow his "wrap-up" treatments. Hopefully, it will not prove to be a mistake. The insurance company made out well also. Note that there were no charges for MRI's, bone scans, hospital days, operating room procedures, intravenous antibiotics, visiting nurses or multiple consultations of a "wound-healing team". Nor were there expenses for complications. The use of local gentamicin as opposed to intravenous gentamicin reduced the risk of gentamicin-induced ototoxicity and nephropathy. There were charges for the boot therapy, of course. But the "boot" is the reason we succeed in healing these cases while others fail.