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British Medical Journal, 03 December 1966, 2, 1391 (Correspondence)

Sir,

We do not agree with Dr. S. T. Anning's statement (12 November, p. 1183) that deep-vein thrombosis, and the recanalization of the veins which follows, is the commonest reason for failure of the leg muscle pump.

One hundred and six consecutive patients suffering from venous leg ulcers, who first attended the Varicose Vein Clinic at Sir Patrick Dun's Hospital between 14 September 1964 and 22 March 1965, were questioned carefully about previous incidents of deep-vein thrombosis. Of these cases 84 were women, of whom 45 had an ulcer on the left leg, 37 had an ulcer on the right leg, and two had bilateral ulcers. Of 22 men, 15 had an ulcer on the left leg, and seven had an ulcer on the right. The predominance of left-sided ulcers would appear to support the explanation of their origin as deep-vein thrombosis, since post-thrombotic iliac-vein occlusion is more common on the left side.¹ However, only 23 patients (22 women, one man) gave a history of deep-vein thrombosis in the ulcerated limb, and in only 11 cases (all women) was this definite. The others gave histories of varying degrees of uncertainty, our notes ranging from "probably not" to "yes, but can't remember which leg". In these 23 patients the deep-vein thrombosis had preceded ulceration in only 16; in five of the others the ulcer had appeared first, and two patients were uncertain of the order of events. Of seven patients with definite history of deep-vein thrombosis preceding ulceration three had the ulcer on the left leg, and four had the ulcer on the right. Of nine patients with an uncertain history of deep-vein thrombosis preceding ulceration, five had the ulcer on the left leg, and four had the ulcer on the right.

These figures suggest that deep-vein thrombosis, with or without proximal obstruction, is not the most important cause of venous ulceration, and that the failure of the muscle pump which produced the ulcer has its origin elsewhere. We believe that the commonest derangement of the muscle pump is incompetence of the valves in the perforating veins, in many cases following thrombosis and recanalization in these veins. These incompetent valves form leaks in the muscle pump, reducing its efficiency. Whether or not the deep veins also are damaged, closure of these incompetent perforating veins, wither by compression sclerotherapy or by ligation, increases the efficiency of the muscle pump and improves venous return.

If the venous disorder is treated, the necessity for wearing elastic stockings or webbing bandages indefinitely, as advised by Dr. Anning, is avoided. It is of great importance that treatment should be directed at the incompetent perforating veins. We join Dr. Anning in stressing that mere trreatment of the superficial varicosities will do little to improve venous return from the lower limb.

We are, etc.

W. G. Fegan

J. M. Pegum                                                                        Sir Patrick Dun's Hospital, Dublin

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