Case 97: Osteomyelitic Calcaneous Heals and Remodels in Diabetic with Ischemic Neuropathic Leg

At age 58, this lady presented on August 3rd, 1994 with two persistent foot ulcers. She had a myocardial infarction in 1988 leading to the discovery of her diabetes. She stopped an eighteen year smoking habit in 1971. Her unregulated diabetes and elevated cholesterol levels were her major risk factors for her extensive atherosclerotic cardiovascular disease. Her foot ulcers had been present over a year and had taken her into her community hospital on six occasions in the previous several months. In early January she was treated with intravenous antibiotics, bedrest and foot soaks. In later January and in February, she had two attempts at bypass surgery. In the next few months, she had three attempts at skin grafts, a partial amputation of her big toe, heel debridements, and finally, an amputation of the rest of her big toe and the distal 3rd of her first metatarsal bone. The amputation and debridement sites broke down leaving new ulcers. In lieu of the further surgery advised by her vascular surgeon, she came to Bryn Mawr for another opinion.

A draining cavity was found over the end of her remaining first metatarsal.

The heel ulcer extended into obviously infected bone in the os calcis.

She had no palpable pulses below the groin in either leg. Light touch and vibration sense were absent. She could not feel the 6.10 fiber. Two point-discrimination was over six inches at the mid-calf. Photoelectricplethysmographic (PPG) tracings of the toes revealed no pulsatile arterial flow. Pulse volume tracings were low in the calf and flat in mid-foot. The posterior tibial and peroneal arteries were undetectable by Doppler at the ankle. The Doppler tracing of the anterior tibial was monophasic, low and broad; the ankle/arm blood pressure index was 0.357. She was presenting, self-referred, hence, with ulcers, osteomyelitis of her 1st metatarsal and calcaneous, advanced diabetic neuropathy and advanced arteriosclerosis obliterans....having left her vascular surgeon who advised her boot therapy had nothing to offer.

Cultures were taken and she was empirically begun on our usual program: an initial daily cleansing foot soak with dilute hydrogen peroxide in Sea Soaks, a broad spectrum oral antibiotic (Cipro) and Mini-Boot therapy with her foot immersed in Sea Soaks containing gentamicin. Her cultures and her antibiotic treatments are summarized in the table below. Likely because of her previous antibiotic treatments in the hospital environment, the cultured bacteria were usually quite resistant to antibiotics and in most instances there was no oral antibiotic available with appropriate coverage.

She had appeared to be doing well through the fall... but a Pseudomonas infection developed and as shown here necrosed the plantar aspect of the heel (the black area).

The ulcer on the end of her first metatarsal remnant was filling in... but she had ulcerated the end of her 2nd toe which had gotten infected also.

The Pseudomonas infection proved to be hard to eradicate and caused further damage if her treatments were interrupted. Infected bone is seen in the ulcer bed.

The Pseudomonas infected the 2nd toe also, March 25th, 1995.

X-ray of her ankle in December 1995 showed diffuse osteopenia.

Soft tissue swelling in the proximal arch and destruction of the inferior-posterior os calcis was also apparent.

The roentgenologist thought that the bone loss in the 4th and 5th metatarsal-phalangeal joints likely also represented osteomyelitis.

Twenty months later this area was significantly more calcified.

The locally infected area were infiltrated with antibiotics and her Mini-Boot treatments continued. The 2nd toe and the ulcer over the 1st metatarsal slowly healed., March 1st, 1996.

The necrotic bone and tissue were debrided by scraping and Mini-Boot treatments. Local injections were still aimed at seemingly infected areas.

The heel had been filling in nicely when again rubor pointing to a new cellulitis developed. The small ulcers in the reddened area may have been related to the trauma of our antibiotic injections.

The infection was beaten back and the induration secondary to the inflammation shown here is gradually receding. She is slowly increasing weight-bearing. Through much of the course of treatment, she used crutches to unweight her foot.

The left foot, of course, was also quite ischemic. It too was booted as necessary and has done well.

A fissure into the calcaneus developed as the bone continued to fill in. The positive cultures were obtained from the fissure where local measures were directed (irrigations, scraping, local antibiotic injections). She continues to be active and ambulatory.

Her August 1997 x-ray shows overall improvement in her bony structures but possible persistent osteomyelitis along her posterior calcaneal tuberosity. The soft tissue fissure is easily seen.

The right big toe area is seen to have done well.

A more lateral posterior view shows that the heel fissure continues to close.

Comments: Her case is included because of the great hurdles she overcame: marked ischemia, marked neuropathy, osteomyelitis of two uncovered bones (the end of the remnant of her 1st metatarsal and her calcaneous), recurrent infections with resistant organisms capable of badly damaging tissue, a lack of available effective oral antibiotics, the decreased control and supervision over her lesions attendant to outpatient treatments, occasional time gaps in therapy and the lack of support of her vascular surgeon. Her treatment was prolonged. It could have been shortened had inpatient therapy been allowed. Her capacity to heal and remodel her calcaneous is also to be appreciated. Her final pictures are still to be developed. While she is doing well at present, her feet obviously must be watched closely in the future. She has had the use of both legs for three years.