When A Blister Becomes An Ulcer: The Perils Of Insufficient Testing

There is a great deal of satisfaction when our diabetic foot care team gets referrals for patients who were previously seen by doctors from surrounding regions and other nations. However, there is also a great deal of difficulty with poorly or improperly managed cases. In this diagnostic dilemma, I’d like to focus on one patient who was sent to us after one year of care by several doctors. The patient in question is a 70-year-old male, who was previously seen by two podiatrists and an orthopedist. His initial complaint was a small blister plantar to the first metatarsal head of his left foot. He had just returned from a business trip in which he had done excessive amounts of walking. Near the end of the trip, he noticed the blister and followed up with his local podiatrist two days later. The blister had ruptured when he saw the podiatrist and evolved into a small eschar with dry blood covering the site. The patient has had diabetes for 20 years that he has controlled with oral medication. He also has peripheral neuropathy of the feet to the ankle. Pulses were not palpable but the foot was warm to touch and the capillary fill time was five seconds. His foot type was a high arch foot with a plantarflexed first ray and a mild equinus deformity. His doctor debrided the local wound and noticed minimal bleeding. He started wet to dry dressing changes and told the patient to wear only tennis shoes for the next week. At one week follow-up, the patient’s foot was warm and swollen, and the blister had become an ulcer. There was edema locally at the first metatarsal head region, yet there was no drainage. The patient was complaining of mild pain and difficulty sleeping. The doctor debrided the wound of necrotic borders and started levofloxacin for antibiotic care. He instructed the patient to call if he got fever or chills, and to continue wet to dry dressing changes. The patient in question is a 70-year-old male, who was previously seen by two podiatrists and an orthopedist. His initial complaint was a small blister plantar to the first metatarsal head of his left foot. He had just returned from a business trip in which he had done excessive amounts of walking. Near the end of the trip, he noticed the blister and followed up with his local podiatrist two days later. The blister had ruptured when he saw the podiatrist and evolved into a small eschar with dry blood covering the site. The patient has had diabetes for 20 years that he has controlled with oral medication. He also has peripheral neuropathy of the feet to the ankle. Pulses were not palpable but the foot was warm to touch and the capillary fill time was five seconds. His foot type was a high arch foot with a plantarflexed first ray and a mild equinus deformity. His doctor debrided the local wound and noticed minimal bleeding. He started wet to dry dressing changes and told the patient to wear only tennis shoes for the next week. At one week follow-up, the patient’s foot was warm and swollen, and the blister had become an ulcer. There was edema locally at the first metatarsal head region, yet there was no drainage. The patient was complaining of mild pain and difficulty sleeping. The doctor debrided the wound of necrotic borders and started levofloxacin for antibiotic care. He instructed the patient to call if he got fever or chills, and to continue wet to dry dressing changes. The patient returned the following week with no erythema or edema of the ulcer site. However, he did have an increase in pain and continued necrotic skin edges. The ulcer had become full thickness with penetration of the subcutaneous fat and palpable flexor tendon. His local podiatrist took radiographs that showed no bone involvement and the patient received pain medication for his nighttime pain complaints. This process of weekly visits continued with no change in treatment and a continued increase in the size and depth of the ulceration for the next two months. At two months, the patient went to a local orthopedist for a second opinion. He suggested a hallux amputation to close the ulcer. He thought the ulcer was deep and probed to bone and suggested treatment with removal of any infected bone. When The Patient Sought Second Opinions This scared the patient. He then saw a recommended local podiatrist, who suggested continued local wound care. Since the ulcer did not look infected and there was no edema or erythema of the region, the doctor started wet to dry dressing changes with a topical wound healing agent and saw the patient for two more months in this same manner. After seven months of treatment, the podiatrist obtained a second radiograph of the ulcer site. This revealed mild bony changes of the tibial sesamoid. The plantar axial view revealed a mild fragmentation of the plantar tibial sesamoid with no other bony changes. The doctor blindly debrided the tibial sesamoid in the office through the ulceration site with minimal bleeding. He then placed the patient on a combination of oral levofloxacin and clindamycin for six weeks. During this six-week period, the doctor saw the patient at one-week intervals for wound checks and local debridement. Serial X-rays showed minimal change in the tibial sesamoid. The ulcer was still not closing and bone was palpable through the ulcer site. The patient continued to complain of pain at night with bed rest and his wife noted he had difficulty sleeping and would sleep in a La-Z-Boy chair at night from time to time. What More Thorough Testing And Consults Revealed At one year of treatment, the patient came to see our diabetic foot team for care. We received all of the paperwork from the doctors and began to question why the patient had not healed. It was unfortunate to find this gentleman had endured one year of care and many months of costly antibiotics without any improvement in this ailment. As part of our treatment, we performed a series of non-invasive testing on the patient, including transcutaneous oximetry (TcPO2), segmental pressures of the extremity and an MRI of the left foot. The results of the tests showed a stenosis of the common femoral artery and reconstitution at the ankle with mild inflow into the foot. TcPO2 studies showed levels of 10 or lower within the foot and only levels of 15 at the ankle. Toe brachial index studies showed a level of .18 with severe occlusive disease including moderate small vessel disease of the foot. MRI studies showed osteomyelitis of both sesamoids and the base of the great toe proximal phalynx. A vascular consult and angiography revealed a bypass potential to the peroneal artery with good inflow to the foot. A bypass would require a plastic vein substitute since the patient’s own vein had been used for bypass surgery several years earlier. This meant the bypass would not last as long, yet it was felt that without a bypass, no chance of healing existed. The bypass was performed and the patient felt immediate relief of his aching foot and leg pain. His TcPO2 levels increased to 28 at the ulcer site and 45 at the ankle level. His capillary fill time was still found to be five seconds. Why Severe Occlusive Disease Must Be Taken Into Account Due to the long travel involved, the patient was referred home to his local doctor with recommendations of six weeks of intravenous antibiotics and observation of the bypass results and ulcer site. Unfortunately, during this period, the patient underwent a Keller-type bunionectomy and bilateral sesamoid removal by his local doctor. This treatment was not part of our suggested care due to the patient’s severe occlusive disease. Immediately following surgery, the patient’s hallux began to look dusky and cold. We saw him one week later in our clinic. He had dry gangrene of the entire hallux and part of the first metatarsal head region. He also was complaining of pain in the leg again. An ultrasound of the bypass revealed a mild blockage which was reopened. A repeat TcPO2 of the foot revealed a level of 24 at the gangrene proximal edge and 46 at the ankle level. The patient underwent a Chopart’s amputation with anterior tibial tendon transfer to the talus and an Achilles lengthening. He healed without complication and returned to work in a lace-up ankle brace with forefoot filler and diabetic shoes. He is seen monthly for check-ups. Seven months after the surgery, the patient has continued working without problems. The issue with this case is a small percentage of diabetic patients have both severe large and small vessel disease. Although they may have enough circulation to prevent spontaneous gangrenous changes, they do not have enough circulation to heal wounds. It is essential that we test these patients prior to initiating any debridement or local wound care as this will only make the problem worse. Final Recommendation My recommendation to anyone who deals with diabetic foot ailments is to obtain non-invasive vascular (NIV) studies prior to any care in order to comprehend the level of disease. Furthermore, do not be aggressive until you know the overall picture including the patient’s healing potential, bypass potential and level of infection. Do not hesitate to order several tests if necessary. Also make appropriate referrals to vascular surgeons, infectious disease specialists and diabetic foot specialists in order to get other ideas on the care of your patient. Once you have the entire picture, try to perform only one surgery at the level of highest healing potential versus the best ambulation potential. This will allow patients to return to their lives more rapidly and decreases the risks to you of caring for these high-risk patients. Dr. Baravarian is an Assistant Clinical Professor in the Department of Surgery/Division of Podiatric Surgery of the UCLA School of Medicine.