This author provides an intriguing case study detailing the diagnostic workup and treatment of a chronic wound complicated by Charcot foot and peripheral arterial disease (PAD).
A 60-year-old male presented to the clinic complaining of a recurrent ulcer on the bottom of his foot for the past six months. The patient states his ulcer heals when he does not put weight on his foot but the ulcer opens up again once he starts walking. The patient denies pain to the area and notes that he washes his foot with 1% betadine solution everyday.
He says he previously received treatment for the ulcer that included the use of VAC therapy (KCI) and a skin graft, which did not incorporate into his skin. The patient also notes a previous bone biopsy that was taken when the wound was deeper and it was negative for osteomyelitis.
The patient’s past medical history includes diabetes for the past 25 years, atrial fibrillation since 2007, congestive heart failure, hypertension, hypercholesterolemia and bilateral lower extremity edema. The patient also had Charcot neuroarthropathy of the left foot 15 years ago that is now inactive. He currently has Charcot neuroarthropathy of the right foot.
The patient’s past surgical history include coronary artery bypass graft (CABG) in 2002, cataract surgery for both eyes and surgery for a detached retina approximately eight years ago.
The patient’s medications include carvedilol (Coreg CR) 12.5 mg twice a day; 60 units of insulin during the day and 40 units at night; lisinopril 20 mg daily; gabapentin 600 mg twice daily; ezetimibe 10mg q PM; simvastatin (Zocor, Merck) 40 mg qhs; lansoprazole (Prevacid, Novartis) 30 mg qam; and furosemide 40mg daily.
The patient has no known drug allergies. He denies tobacco, alcohol and illicit drug use. The patient works as a Realtor and lives alone. He also has a family history of heart disease, diabetes and stroke.
Aside from the aforementioned findings from the past medical history, the remaining review of systems was unremarkable.
The patient had no hair growth bilaterally on the foot and ankle but there was hair growth present proximal to the ankle.
In regard to the vascular examination, capillary fill time was less than three seconds for all the toes. I noted mild non-pitting edema on the ankle bilaterally. The skin temperature was warm to cool, proximal to distal bilaterally on the lower extremity. The right foot temperature was 4ºF higher than the left foot. The patient’s dorsalis pedis and posterior tibial pulses were non-palpable bilaterally. In terms of the Doppler exam findings, the dorsalis pedis pulse was monophasic bilaterally and the posterior tibial pulse was biphasic bilaterally.
The ABI of the left extremity was 0.72 and the left lower thigh brachial index was 0.92 with a significant pressure gradient of 53 mmHg between the left lower thigh and left ankle segmental limb pressures. The right extremity ABI was 0.50 and the right lower thigh brachial index was 0.84. There were significant pressure gradients between the right lower thigh, right calf and right ankle segmental pressures of 29 mmHg and 38 mmHg respectively.
In regard to the dermatological exam, the patient had dry, scaly skin bilaterally on the foot and ankle. There were no interdigital macerations on either foot. The patient had a full thickness ulcer (3 cm x 3.5 cm in diameter) on the plantar right midfoot with a hyperkeratotic rim. There was no probing, tracking or odor. There were also no gross signs or symptoms of infection.
The neurological examination findings revealed absent protective sensation (0/10) after testing with the Semmes Weinstein 5.07/10 gram monofilament. The patient had diminished vibratory sensation at the level of the bilateral ankle. He had diminished sharp dull sensation at the level of the lower leg bilaterally. Proprioception was intact to the level of the first metatarsophalangeal joint bilaterally.
In regard to the musculoskeletal exam, the patient had muscle strength 5/5 for all gross lower extremity muscle groups. Patellar and Achilles reflexes were absent bilaterally. The ankle joint ROM was +8/+12 on the left and +10/+12 on the right. The first MPJ ROM was 36/30 on the left and 36/30 on the right. The first ray ROM was 1/3 on the left and 2/2 on the right. The patient had diminished range of motion about the ankle, subtalar joint and midtarsal joint bilaterally.
The patient has assisted gait with a wheelchair. He had a significantly flattened longitudinal arch on the right foot and a rectus left foot.
Dorsoplantar and lateral radiographs of the right foot (see Figures 1a and 1b) demonstrated collapse of the medial column along with degenerative changes throughout the midfoot area. There was diffuse osteopenia with calcification of blood vessels noted on the right foot. I noted collapse of the lesser tarsus with resulting plantar bony prominence, specifically with the navicular cuneiform joint, the cuneiform metatarsal joints and the metatarsal cuboid joints.
As revealed by the plantar pressures below (see Figure 2), the gait analysis showed that the heel never touched the ground because of equinus and the equinus and midfoot breakdown resulted synergistically in the midfoot bearing over 80 percent of the total weight in 80 percent of the stance phase of gait.
This exorbitant pressure in the midfoot area induces inflammation in the plantar skin below the osseous prominence almost immediately. The thermographic image (Figure 3) shows a 5 degree difference between the affected and unaffected foot after a three minute, mildly paced walk.
The patient’s left arterial findings were suggestive of moderate arterial occlusive disease with hemodynamically significant iliofemoral and tibioperoneal disease. His right arterial test showed moderate to severe right lower extremity arterial occlusive disease with multilevel disease by segmental limb pressure gradients. I referred the patient for a vascular consult.
I explained to the patient that his Charcot foot deformity had created a bony prominence that significantly increased the pressure on the plantar aspect of his foot in the location of his ulcer breakdown. While the patient was very interested in having Charcot reconstruction, I explained that he will most likely need bypass surgery to increase blood flow to the foot or he will likely not heal from the reconstructive surgery.
The patient received stenting of the bilateral thigh after an angiogram procedure and was scheduled for femoral popliteal bypass surgery following a cardiac stress test.
Following the patient’s bypass procedure, the dorsalis pedis/posterior tibial pulses show biphasic waveforms with the Doppler exam. Transcutaneous oximetry (tcPO2) testing showed 58 mmHg on the medial aspect of the right midfoot and 66 mmHg with the right medial ankle.
The patient subsequently underwent Charcot foot reconstruction on the right foot (see Figure 4a) with an external fixator (see Figure 4b). We dispensed an external bone stimulator and educated the patient on use of the device.
Four weeks after Charcot foot reconstruction, the patient developed a blood blister on the plantar forefoot that later progressed to an eschar. Subsequent debridement of the eschar revealed a full thickness ulcer, which was 10.5 cm x 5.6 cm in diameter and 0.5 cm in width (see Figure 5a). I subsequently applied a bioengineered skin equivalent to the wound on a weekly basis for eight weeks to facilitate wound closure. For a view of the wound five weeks after application of the bioengineered skin equivalent, see Figure 5b.
After wound closure, the patient’s radiographs (see figures 6a and 6b) and plantar pressures (see figure 6c) show a more plantigrade foot with a heel toe gait.
Dr. Wu is an Associate Professor of Surgery at the Dr. William M. Scholl College of Podiatric Medicine and Associate Professor of Stem Cell and Regenerative Medicine at the School of Graduate Medical Sciences at the Rosalind Franklin University of Medicine and Science in Chicago. She is also the Director for Educational Affairs and Outreach at the Center for Lower Extremity Ambulatory Research (CLEAR) in Chicago.