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Buerger's disease (BD) is characterised by segmental inflammation of medium and small size arteries, affects mainly young adult men, and is more prevalent in the southeast Mediterranean and the Far East. Its pathogenesis remains unclear, but cigarette smoking is strongly implicated. Autoimmune diseases, hypercoagulable states, diabetes, and emboli need exclusion before a diagnosis is made. The tibial and leg digital arteries are usually affected, and arteriography shows typically “corkscrew” peripheral obstructions. The best treatment is stopping smoking. Prostacyclin infusion is currently the most effective treatment for pain control and healing of ischaemic lesions.1 In selected cases, regional guanethidine block may have good results.2 Sympathectomy does not always provide longstanding benefit,3 and arterial bypass is difficult due to poor run-off in the diseased arteries.3,4 Limited amputations are often necessary to remove necrotic tissue.
New methods are being tested for pain relief and ulcer healing, including pedicled omental transfer5 and induction of angiogenesis using vascular endothelial growth factor gene transfer.6 Spinal cord stimulators (SCS) are used extensively in refractory peripheral atherosclerotic disease. Experience in BD is limited but suggests that SCS have favourable effects on pain and healing of digital ulcers, comparable with those noted in other arteriopathies.4
We present our experience of the use of SCS in three patients with BD. They were all male, middle aged smokers, who had presented with painful ischaemic ulcers of the legs at least six years earlier, had typical angiographic appearances of BD, no evidence of other relevant diseases and had been (and still are) unable to stop smoking. Over that period, they had all required repeated admission to hospital and had unsuccessfully tried various treatments to relieve pain and promote healing of their ischaemic ulcers, including analgesics, vasodilators, antiplatelet agents, epidural analgesia, prostacyclin, and local guanethidine infusions. One patient had needed amputation of gangrenous toes and another a below-knee amputation after these treatments failed. SCS were used in all three patients to manage intractable pain, poor wound healing, and recurrence of ischaemic lesions occurring postoperatively. Within four months of treatment with SCS, the pain resolved completely and the wounds healed in all three patients and they were able to return to work. One of them requires oral analgesia after prolonged periods of standing, but none of them has required further admission to hospital.
SCS may modulate painful stimuli through several mechanisms. According to the gate control theory of pain, stimulation of large diameter, type A fibres at the posterior horns of the spinal cord by low amplitude electric current inhibits simultaneous transmission of painful stimuli through the same spinal cord segment. Similarly, inhibition of sympathetic vasoconstriction improves the peripheral microcirculation. Nitric oxide and γ-aminobutyric acid systems in the spinal cord may be important intermediaries in SCS-induced pain relief.7,8 In arterial insufficiency, SCS have been shown to decrease rest pain (Fontaine class III), improve claudication distance, raise skin temperature, and increase transcutaneous oxygen tension in the forefoot, with values of >10 mmHg before treatment being associated with significantly better outcome.9,10
SCS may be a useful therapeutic option in BD, particularly for pain control and wound healing and may delay the need for amputation in selected patients who have exhausted all other therapeutic options. Return to work and reduced need for repeated hospital admissions may balance the overall expense of the procedure. Further studies are required to determine the exact indications for the use of SCS in BD, while stopping smoking should continue to be emphasised as the most important treatment.
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