Large tissue deficit in a neuroischaemic foot secondary to infection needing distal arterial bypass

A 43-year-old male with type 1 diabetes of 27 years' dura tion, with peripheral and autonomic neuropathy, was referred with indolent neuropathic ulceration complicated by local cellulitis over the left 5th metatarsal head His pedal pulses were palpable. He was treated with ora amoxicillin 500 mg tds and fludoxacillin 500 mg qds anc outpatient debridement. His deep wound swab hac grown Staphylococcus aureus and Streptococcus group G. The cellulitis resolved and he was given a total-contact cast. The ulcer healed after 8 weeks and he was given bespoke shoes with cradled insoles.

Two years later he was admitted with an infected ulcer on the plantar surface of the right heel where he had pulled off a piece of loose skin (Fig. 6.21a). His pedal pulses were now impalpable. He was admitted and given intravenous vancomycin 1 g bd, ceftriaxone 1 g bd and

Toe Venous Ulcer InfectedFemoral Popliteal Bypass Incision

metronidazole 400 mg tds. He had recently had a methi-cillin-resistant Staphylococcus aureus (MRSA) infection on the contralateral foot. Angiography showed occlusions of the right common iliac artery and superficial femoral artery. It was planned to perform an angioplasty of the right common iliac and right external iliac as a crossover procedure via the left femoral artery. However, whilst awaiting this the patient developed a critically ischaemic right foot. Urgent angiogram at this time showed thrombus in the right superficial femoral artery. He underwent thrombolysis. A check angiogram showed a patent superficial femoral artery, but significant stenoses in the popliteal artery with a good two-vessel run-off. He underwent a popliteal angioplasty. Following this, transcutaneous oxygen tension was 57 mmHg on the chest and 69 mmHg on the dorsum of the right foot. This was deemed adequate perfusion and no further vascular intervention was attempted. The ulceration on the right heel remained clean and a vacuum-assisted closure (VAC) pump was added to improve granulation.

The patient was followed up in the diabetic foot clinic and the ulcer had almost healed after 4 months. Despite careful education about the danger signs of deterioration he then presented very late with chills, sweating, infection of the heel ulcer and blue discolouration of the medial aspect of the right foot. He had spreading cellulitis and a 2-cm area of necrosis on the medial aspect of the right foot. Doppler waveforms were monophasic and damped. The working diagnosis was that he had mid-foot sepsis likely to be tracking from the ulcer and he underwent operative surgical debridement. There was a track leading from the heel ulcer along the extensor tendons to the midfoot and this was laid open. All dead and infected tissue was excised back to bleeding tissue. Deep tissue culture revealed MRSA and mixed anaerobes. Clinically, he was septic and was treated with vancomycin 1 g bd, rifampicin 600 mg bd (as an adjunctive treatment for MRSA), metronidazole 500 mg tds and Milton irrigation to the wound. In view of his sepsis he was also given gentamicin 5 mg/kg daily. Angiography showed further stenoses of the superficial femoral and popliteal artery.

Initially it was planned to carry out an angioplasty, but it was decided that distal bypass surgery had the best chance of restoring the pulsatile blood flow which was necessary to heal his large tissue deficit. He underwent a distal bypass from the right common femoral artery to the anterior tibial artery with a reversed lower saphenous vein. The reversed lower saphenous vein was tunnelled laterally to the knee subcutaneously. There was a good quality common femoral artery and a non-calcified anterior tibial artery in mid-shin of good calibre. The bypass was successful but the plantar wound was slow to heal.

His postoperative course was stormy. He developed a fever with productive cough associated with rigors and vomiting. He was treated with vancomycin 1 g bd and meropenem 1 g tds intravenously empirically and improved. He complained of back pain and X-ray showed evidence of vertebral collapse. He had magnetic resonance imaging (MRI) of his spine as a metastatic abscess was suspected. However, the MRI showed changes consistent with a haemangioma but this did not require neurosurgical intervention. An application of Apligraf finally healed the ulcer (Fig. 6.21b).

During this admission his wife visited the hospital every day, arriving early in the afternoon and leaving late in the evening. She took a great interest in his care and learned to clean and dress the foot. She was taught the danger signs of deterioration. Subsequently he never again presented late with severe infection because his wife checked his feet every day and brought him to the diabetic foot clinic at the first sign of a break in the skin.

Key points

• Patients admitted with severe infection need intense multidisciplinary care and frequent medical and surgical review

• Surgical debridement was needed on his second admission because of necrosis secondary to infection

• An arterial bypass was needed to restore pulsatile flow to heal a large tissue defect. The increase in blood flow after angioplasty may not have been sufficient

• The family of vulnerable patients should be taught to check the feet daily and respond rapidly at the first sign of a break in the skin

• Neuropathic feet eventually become neuroischaemic but this will need to be diagnosed by examination of the foot pulses at every visit

• Patients with neuroischaemic foot ulceration need long-term follow-up in a multidisciplinary diabetic foot service.

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