ABSTRACT
Lumbar sympathectomy was first performed and described in 1923 by Dr D.Royal in the Lewisham Hospital, Sidney to treat spastic paralysis secondary to a cerebral cortical bullet injury in a 30-year old man.1 The result was dramatic with respect to the spasticity, but it was also noted that the treated limb became much warmer and developed capillary dilatation. In subsequent years, an increasing body of surgeons documented the vascular changes associated with sympathetic denervation and use of the procedure was extended to treat conditions such as atherosclerotic occlusions, Raynaud’s phenomenon, and thromboangiitis obliterans.2, 3
Surgical sympathectomy remained the mainstay of the treatment of lower limb occlusive disease until open vascular reconstruction became possible in the early 1950s, after which its use steadily declined. This has become even more apparent over the past 20 years, as reconstructive surgery has developed and the role of endoluminal therapy has advanced. Despite this, there are still some clinical situations in which sympathetic denervation remains a valuable treatment option; these include lower extremity causalgic pain4-6 hyperhydrosis,7 distal arterial occlusive disease not amenable to direct surgical attack and selected patients with vasospastic disorder.8-10
Functions of the sympathetic nervous system
The primary functions of the sympathetic nervous system are to prevent heat loss, through reduction of superficial extremity blood flow, and to modify basal organ function. Resting sympathetic activity primarily antagonizes the vasodilating influence of the parasympathetic nervous system on arteriolar resistance vessels, cutaneous precapillary sphincters and capacitance vessels. Local increase in sym pathetic outflow causes decreased skin blood flow, piloerection and sweating. These responses are mediated by the constricting influence of norephinephrine on vascular smooth muscle. Abolition or opposition of sympathetic efferents leaves the parasympathetic nervous system unopposed and leads to theoretical increases in cutaneous blood flow as great as 40-100%.11 Controversy remains about the precise mechanisms of flow improvement, if any, in chronically ischaemic extremities and there are wide variations in the degree of clinical improvement observed by different authors. Both clinical and experimental
studies indicate that the major circulatory effect of sympathectomy is increased skin blood flow caused by shunting of blood through cutaneous arteriovenous anastomoses,11 without alteration in overall limb perfusion.
