Case 93: Managed Care: Noncompliant Diabetic with Multiple Successfully-Treated Episodes of Callus, Ulcers and Osteomyelitis Limited in Access to Boot and Comes to Surgery

At age 58 this professional man was referred 1/11/93 with a foot ulcer of 8 days duration and a history of having had his right 2nd toe removed at an academic wound-healing center in Philadelphia in April 1992. He had a long history of obesity and uncontrolled type 2 diabetes. His light touch sensation was diminished, his two-point discrimination over 15 cm and he could not feel either the 5.05 or the 6.10 fibers in either foot. He had an ulcer at the site of his 2nd toe amputation. The transcutaneous PO2 (TcPO2) over the 2nd metatarsal head was 2 mm Hg, a value incompatible with healing and perhaps related to cellulitis and/or small vessel disease in his foot. The ulcer fissure tunneled towards the 1st metatarsal head providing a portal for infection to the mid-foot. He also had dark spots in his plantar callus. A foot x-ray showed a piece of wire imbedded in the foot. The wire was removed in the office and he was given 15 treatments with local gentamicin injections followed by Mini-Boot therapy with his foot immersed in Sea Soaks containing urecholine and gentamicin. Subsequently, his treatments were tapered first to two per week, then one per week and finally to one a month. In spite of the documented hypoxia and significant infection in his foot from which Pseudomonas areuginosa resistant to Cipro was cultured, he was spared the costs of hospitalization and the inconvenience and risk of long term intravenous medications. Unfortunately, the ease with which we cured his foot did not impress upon him his need to obtain our prescribed shoewear and to practice preventive care.

He returned 11/5/93 with infected calluses on both feet draining foul-smelling pus. A culture probe was introduced 1.25 cm into the 0.75x0.5 cm ulcer in the right foot. The ulcer in the left foot was 0.5 cm across. Abundant E-Coli and abundant Enterococci were cultured from both feet. Again, he was treated as an outpatient with oral Bactrim-DS and local antibiotic injections before his boot therapy. He did not appreciate the gravity of his situation and through most of November kept but a few appointments. In late November and December he was more compliant. Sample treatments included (1) an initial cleansing foot soak in Sea Soaks containing dilute hydrogen peroxide; (2) vancomycin and/or gentamicin injections locally into the ulcer beds and around the underlying bone; and finally, (3) Mini-Boot therapy with his foot immersed in Sea Soaks containing both antibiotics and urecholine. His feet did well and by early January, 1994 were close to healed. The patient disappeared from care. On January 18th, 1994 he returned requesting boot therapy. He had a 1 cm ulcer in the planar callus under his right 1st metatarsal head and a 2.5 cm pigmented plantar callus on the left foot. His skin was dry and flaky. The skin flakes were soaked off and his calluses trimmed. He received yet another lecture on foot care and seemed to have a good prognosis.

He returned April 13th, 1994, but 6 weeks later. He had developed new lesions but delayed coming for help because of worry about his insurance coverage. The culture probe entered 5 cm into his foot. His x-ray showed dislocation of the 1st metatarsal-phalangeal joint with probable osteomyelitis.

His foot was vastly improved within a few weeks but in view of his bony involvement, therapy was continued for another 2.5 months.

His culture grew out Enterococci, Streptococcus viridans and methicillin-resistant Staphylococcus aureus. He was treated with oral Cipro, joint irrigations with Sea Soaks containing Vancomycin and gentamicin, local antibiotic injections (Vancomycin, gentamicin and Fortaz) and, of course, Mini-Boot therapy with his foot immersed in antibiotic solution.

He continued to work during these outpatient treatments. He disappeared with intact feet 7/12/94 for vacation, when he spent his time walking on the beach and visiting tourist attractions!!! He returned 8/2/94 again with new lesions: thick ulcerated plantar callus under both first metatarsal heads. Again he was given appropriate antibiotics locally and Mini-Boot treatments. Again, he was prescribed molded inserts, several pairs of extra depth shoes with box toes and lubricating creams. He was exhorted to watch his feet daily and attempt to get off them at least 15-20 minutes an hour... preferably sitting at work as much as possible. And again he healed and disappeared.

He did well only a few months and returned 8/11/95 with purulent ulcers penetrating calluses under both first metatarsal heads. Heavy growths of Acinebacter baumannii and methicillin-resistant Staphylococcus aureus were cultured from both feet.

The callus was pared back and his routine begun again (initial cleansing soak, local injections now with Ticar and Vancomycin and Mini-Boot therapy). His feet healed again.

His insurance carrier, however, was questioning the frequency and nature of his relapses. He changed insurance carriers and sought means to spread his medical costs among various covered providers. When his ulcers and calluses recurred, he went to his podiatrist who trimmed his callus and prescribed Ceftin. The ulcers and infection on his left foot enlarged bringing him back for boot therapy January 26th, 1996.

The plantar ulcer had enlarged and had a small tract into the space between the 1st and 2nd toes.

The infection appeared to have followed the tendon sheaths up the foot and penetrated the skin in two areas on the dorsum of the foot.

He was begun on his outpatient routine but in view of systemic symptoms (sweats and nausea), his missing appointments and a question of leg swelling, he was hospitalized. In addition to his usual outpatient therapies, intravenous antibiotics were administered. His left foot did well but he was left with a dorsiflexed big toe. His first extensor tendon was surgically cut releasing his toe which then fell into a normal position. The problem of insurance coverage again dictated his behavior. He had been advised he was to be allowed but a given number of boot treatments a year. His visits fell off. His infection relapsed. He again sought the help of other providers and was hospitalized by his orthopedic surgeon. When last contacted, he had been in the hospital two weeks, had had an amputation of his big toe and metatarsal head and was to receive a course of outpatient intravenous antibiotics.

Comments: This man has had recurrent neuropathic ulcers as did case #89. The latter, however, was lucky enough to have no breaks in insurance coverage; he had no major surgery and required no hospitalizations while under our care. Case #93 did well when he was regularly attended. His major illnesses were associated with delays directly related to the policy of his insurance carriers. Instead of the modest costs of our outpatient care, the carriers incurred the costs of three hospitalizations. Surgical ablation procedures are commonly viewed by the general physician as definitive courses of action. "Get it off and get on with life," the surgeon might advise. Unfortunately, lesions recur on neuropathic feet and are more likely to recur as the weight-bearing surface of the foot becomes smaller and more abnormal in shape. Primary prevention is, of course, the most desirable solution. The insurance companies would do well to support diabetes care by competent and interested physicians. Again, once the lesions develop, the cases presented in this series show that the patients can be effectively handled as outpatients in most situations. Inpatient care may still be necessary as in case #92 who could not properly accomplish the outpatient program. The insurance company makes a big mistake in attempting to enforce procedures that for the sake of costs delay care. For a boot service to properly design therapy, accurate noninvasive tests are necessary; the capitated vascular testing site rarely provides the desired information. Requiring the patient to go to such a site may be too great an inconvenience for some patients and in all cases delays treatment. Again, provided only with information from the capitated site, we have found some patients in the position where the insurance would not pay for our specific noninvasive tests but would pay for a brief hospital admission for an arteriogram. The latter, of course, satisfies the patient and other doctors that the vascular surgeon may or may not have a role in the case. The same information, however, may be obtained in the non-invasive vascular laboratory where costs and risks are greatly reduced. Again, when the arteriogram is performed and shows that some vascular operative procedure is possible, it becomes very difficult in chronic patients to avoid the procedure and its risks... both major costs for the insurer and occasionally an unnecessary disaster for the patient.