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Journal of the Irish Medical Association, April 1964., Vol. LIV. No. 332, pp. 110
PROPHYLAXIS OF SUPERFICIAL AND DEEP VENOUS
THROMBOSIS IN THE LOWER LIMBS
W. G. FEGAN, M.Ch., F.R.C.S.I., W. H. BEESLEY, M.B., B.Ch.
D. E. FITZGERALD, M.Sc., L.R.C.P.I., S.I.
Venous Insufficiency Unit, Sir Patrick Dun's Hospital, Dublin
Venous thrombosis in the lower limbs can be a crippling disease, and it may be fatal should pulmonary embolism result. The object of this paper is to formulate a comprehensive regime of prophylaxis.
It is apparent from many post mortem studies of the veins of the lower limbs that venous thrombosis in them is a much more common occurrence than the ante mortem clinical state of patients indicates. Roberts (1963), in cases of 108 consecutive deaths, performed dissections of the lower limbs after death. He found venous thrombosis in 58 cases (53%), the highest incidence being in the intramuscular veins of the soleus muscle, followed by the posterior tibial veins and then the veins of the gastrocnemius. Sulma (1949) reports 170 cases of venous thrombosis in whom 20 died; but in 14 of these 20, thrombosis was not diagnosed during life. McLachlin and Paterson (1962) describe 100 people complete post mortem dissections of pelvic and leg veins in a random series of patients - 34% of the cases had venous thrombosis. Sevitt and Gallagher (1961) state that only about one third of cases with thrombi at necropsy have relevant symptoms during life.
Aetiology
Much has been written about the causes of venous thrombosis - the classification from the Nomenclature of Diseases of the Blood and Lymph Vessels is probably the most comprehensive:
Thromboangeitis obliterans
Recurrent or migrating
Essential
Mechanical injury (contusion, laceration, surgery)
Chemical injury (Sclerosants, drugs, diagnostic solutions)
Muscular strain
Inflammatory lesions -
Infectious diseases
Chronic diseases of the vein wall (varices, phlebosclerosis)
Blood dyscrasias (polycythaemia, leukaemia, pernicious anaemia)
Congestive heart failure
Carcinoma
This is an extensive and varied list of causes.
In the present state of knowledge the two aetiological factors which appear to be of prime import are (1) venous stasis, and (2) endothelial injury, and the clinician is able to reduce the incidence of these factors.
Diagnosis
Venous thrombosis may involve either the deep or the superficial veins of the leg, or both. This distinction between the two systems of venous drainage is often erroneous, since both may be involved, albeit one much more than the other.
Pain is often the first symptom of thrombosis, especially in the superficial veins, where it usually occurs in large tortuous varicosities. Tenderness, increase in heat and swelling along the course of the superficial thrombosed vein may accompany the pain. The major problem of diagnosis is presented by deep vein thrombosis. Pain is often slight and frequently absent. Many of these cases are completely "silent". A positive Homan's sign, tenderness along the course of the deep veins, oedema, cyanosis, dilatation of collateral veins, fever or increased E.S.R. may be present, but equally these may all be absent and the first indication that the patient has suffered a thrombotic episode may be the catastrophe of a pulmonary embolus. The doctor who daily looks for a positive Homan's sign is accepting defeat in so far as he is expecting to find instituting and supervising prophylactic measures.
There are no reliable tests available for the prediction of intravascular clotting. A past history of a thrombosis or embolism would make one anticipate another episode.
Prophylaxis
If we can prevent or minimize venous stasis and endothelial injury, then we have gone a long way towards reducing the morbidity and mortality associated with venous thrombosis. An attempt will now be made to formulate a plan of prophylaxis with these objects in mind.
Obviously this can only be put into practice in elective, non-acute cases. It cannot be stressed too highly that varices in pregnant women should be treated adequately before delivery. For many years one of us has been responsible for treating chronic venous insufficiency in expectant mothers at the Rotunda Hospital. In the past five years there has been no case of post partum deep vein thrombosis, or pulmonary embolism, in patients treated in this clinic and only five cases of superficial venous thrombosis, all of whom failed to complete treatment at the clinic.
Thus it is advocated that all patients who have to be hosptalized and who fall within these five groups should have both their legs securely and comfortably bandaged from toes to upper thighs with crepe bandages and over these they should wear a full-length two-way stretch elastic stocking. It is well established that these measures go a long way towards stimulating an adequate venous return from the lower limbs. Great care must be exercised when applying bandages to patients with arterial inadequacy in their legs.
Venous thrombosis is of frequent occurrence following pelvic procedures, and some obstetricians, although performing similar manoeuvres, are more plagued with venous thrombosis than others. All pelvic procedures should be performed with the utmost care in order to minimize damage to the veins.
Adult patients confined to bed are comparatively inactive and prone to venous thrombosis. Conversely, children confined to bed are usually active and very seldom develop venous thrombosis. It would be ideal if every bed were equipped with a cheap form of pedalling machine with a light aluminium cradle over it. In this way a patient can exercise his legs while in bed, and thus diminish the likelihood of venous thrombosis. There should also be an overhead handle available so that the patient can regularly rotate the position from side to side. Even if unable to actually rotate themselves, the effort of attempted rotation is almost as efficient in increasing venous return from the limbs by its pumping action on the abdominal veins. We have only recently become aware of the full significance of this abdominal pump. In this department we have taken a large series of deep intravenous pressure recordings in the active patient and find that the abdominal pump is of great importance in boosting venous return from the lower limbs.
We found the classical paper by Sevitt and Gallagher (1961) from the Birmingham Accident Hospital immensely instructive. In cases of fractured neck or femur treated with Phenindione they were able to eliminate completely pulmonary embolism and significant vein thrombosis. They also reported that there were no clinically important cases of post-operative bleeding in patients so treated. The decision to use anti-coagulants pro-phylactically rests with the clinician. It would certainly appear to be less necessary if the measures described above (1-13) are applied. However, should a susceptible patient be confined to bed for more than two to three days then prophylactic anticoagulant therapy should be commenced as soon as the patient enters hospital and continued at least until the patient is fully ambulent.
Anti-coagulant therapy is contra-indicated in cases of bleeding into the brain, meninges, spinal cord and gastro-intestinal tract, and in patients with thoracic or abdominal injuries or with blood disorders. In some of these cases delayed anti-coagulation may be of benefit (Sevitt and Gallagher, 1961).
We have been aware that pulmonary embolism has been non-existent following the technique of injection therapy for varicose veins which we have been using for fourteen years in upwards of 14,000 patients. We deliberately produce a small controlled venous thrombosis at each injection site. As far as we are aware we have had no case of pulmonary embolism in this series. We attribute this to the fact that after treatment we apply compression and insist on immediate ambulation. We have endeavoured to examine, to the best of our ability, the reported incidence of deaths following operation for varicose veins. Fig. 1., is a synopsis of our efforts in this direction. The majority of these mortalities were due to pulmonary embolism.
DIAGRAM HERE
The largest series is from McPheeters (1946), who made a survey among a group of American surgeons, and obtained 7,771 cases. There were 54 deaths, i.e. 7 per thousand.
Using immediate ambulation following our continuous pressure injection technique in the treatment of chronic venous insufficiency, we have had no deaths in a series twice as large as McPheeters (1946). If our mortality rate had been the same as in his series, we should have been indirectly responsible for the death of one hundred patients, and probably caused somewhat in the region of five hundred non-fatal pulmonary emboli. We are convinced that our freedom from pulmonary embolism is due to compression after injection and to insistence on immediate ambulation.
Summary
The incidence and causes of venous thrombosis in the lower limbs are briefly reviewed. Diagnosis of this condition is discussed, and stress laid on the fact that diagnosis is often not made before death. A comprehensive scheme of prophylaxis is outlined with special emphasis on compression and immediate ambulation.
It is shown that using our continuous compression injection technique in treating venous insufficiency , despite causing upwards of 70,000 minimal localized thromboses, we are able by pressure and immediate ambulation to control the thromboses and prevent pulmonary embolism.
References
Browse, N. L. (1962). Brit. Med. J., 1, 1714-1721.
Browse, N. L. (1962). Brit. Med. J., 1, 1721-1723.
Butkiewicz, T. (1962). Bull. Soc. Int. Chir., 5.
Cherry, J. C. (19947). Irish J. Med. Sci., 225, 101.
Fegan, W. G. (1952, '53, '54, '55, '56, '57, '62). Clin. Rep. Rotunda Hospital.
Fegan, W. G. (1961). Minerva Cardioangiol. Europ., p. 481.
Fegan W. G., FitzGerald, D. E. (1963). Irish J. Med. Sci., 439-443.
Hermann, Louis G. (1961). Industrial Med. & Sci., 30, 11, p. 489-494.
Hughes, E. S. R., Goble, A. J. (1962). Lancet, 1080-1081.
Kilbourne, N. J. (1931). Ann. Surg., 83, 691.
Ludbrook, J. (1962). Fundamentals of Clinical Cardiology.
Mathiesen, F. R. (1955). Acta. Chir. Scand., 108, 6.
Meyerowitz, B. R., Crook, A. (1960). Lancet.
McLachlin, J. et al. (1962). Arch. Surg., 85, 738-744.
McPheeters , H. O., Anderson, J. (1946). Phil.
Nilsson, N. J. et al. (1963). Scand. J. Clin. & Lab. Invest., 15, Suppl. 69.
Roberts, G. Hefin (1963). Scot. Med. J., 8, 11.
Schmukler, J. (1963). Angiology, 14, 2.
Scott, D. B. (1963). Anaesthesia, 18, 2.
Sevitt, S., AND Gallagher, N. (1961). Brit. J. Surg., XLVIII, 211, p. 475-489.
Sulma, M., Penti, A. (1949). Acta Chir. Scand., 98, 130.
Thorbjarnarson, B. (1961). Surg. Clin. N. Amer., 41, 2.
Walker, W. F., Pickard, C. (1962). Bull. Soc. Int. Chir., XXI, 3, pP. 257-264.
Wright, I. S. (1963). J.A.M.A., 183, 194-198.