Showing papers in "Clinics in haematology in 1981"

Prevention of venous thromboembolism.

Abstract: : The aim of prophylaxis in venous thromboembolism is firstly to prevent fatal pulmonary embolism and secondly to reduce the morbidity associated with deep vein thrombosis and the post-phlebitic limb. Particularly high-risk groups are identifiable and include those over 60 years of age undergoing major surgery, patients with malignancy and those undergoing hip operations. Low-dose subcutaneous heparin (5000 U s.c. commenced two hours preoperatively and continued eight to twelve hourly until the patient is fully mobile) is unequivocally effective in preventing deep vein thrombosis in medical and surgical patients and, most importantly, significantly reduces the incidence of fatal postoperative pulmonary embolism and total mortality. Furthermore, in established deep vein thrombosis, low-dose heparin limits proximal clot propagation, which is the prelude to pulmonary embolism. Despite this, surveys have demonstrated an alarming deficiency amongst clinicians in the application of measures to prevent venous thromboembolism. Heparin prophylaxis carries a small risk of increased bleeding complications, mostly evidenced by the frequency of wound haematoma rather than major haemorrhage. Low molecular heparin fragments (e.g. Fragmin, Choay, Enoxaprin) are now emerging as useful alternative agents, having the advantage of once daily administration and yet providing similar efficacy in the prevention of deep vein thrombosis. However, protection against fatal pulmonary embolism has yet to be demonstrated. Mechanical methods of prophylaxis designed to counteract venous stasis, such as graduated elastic compression stockings, are also beneficial in protection against deep vein thrombosis but by themselves do not achieve such consistently good prophylaxis as low-dose heparin. However, clinical trials with combinations of mechanical methods and low-dose heparin indicate that this may be the optimum approach to very high-risk patients. In the presence of established acute deep vein thrombosis, anticoagulant therapy is the mainstay in preventing pulmonary embolism. Vena caval interruption procedures should be reserved for patients in whom anticoagulation is contraindicated or for those who develop recurrent pulmonary embolism despite adequate anticoagulation.

Tropical splenomegaly. Part 1: Tropical Africa.

Abstract: The emergence of tropical splenomegaly syndrome as a distinct entity in tropical medical practice has been briefly described, together with its link with malaria. The clinical and haematological aspects of the syndrome have been reviewed with some emphasis on local experience. No attempt has been made to give details of the immunological aspects, but the mechanisms by which the established immunological features of the disease help to understand the pathogenesis of the syndrome have been highlighted.

Endothelium and arteriosclerosis.

Abstract: Endothelium, platelets and macrophages can each provide growth factors that may participate in atherosclerotic lesion initiation or progression, or both. These mitogens, coupled with alternations in endothelial integrity or function resulting from a variety of different risk-associated factors, such as hyperlipidaemia, hypertension, tobacco smoke, antibodies, infections, or homocystinaemia, may provide the basis for the intimal proliferative smooth muscle cell response of atherosclerosis. Platelets, endothelium or macrophages may be important in lesion initiation and progression in some circumstances but not in others, depending upon the extent and type of endothelial "injury'.

Thrombotic disorders associated with pregnancy and the pill.

Abstract: A wide range of procoagulant changes has been observed with oral contraceptive (OC) therapy during pregnancy. The thrombotic disorders which are clinically important during pregnancy and the puerperium are venous thromboembolism thrombosis as a component of preeclamptic toxemia myocardial infarction and cerebral infarction and thrombosis. Changes observed in blood coagulability/rheology/flow platelet function glucose/lipid metabolism and blood pressure partially explain the relative tendency towards arterial events. On the other hand cyclical changes in hemorrheological/hemodynamic factors observed in nonpill users prevent in some way the development of arterial diseases; however it is possible that cessation of these cyclical changes over a long period may remove the protection from arterial events normally enjoyed by women. The 1977 Royal College of General Practitioner study found that duration of pill use affected risk of circulatory disease: women who had been on the pill continuously for more than 5 years had twice the age-adjusted death rate from circulatory diseases than women who had taken it for a shorter period. Although epidemiological evidence supports the association between pregnancy OC and thrombotic disorders and many procoagulant changes have been demonstrated in both pregnancy and combined pill use many questions need to be resolved regarding pathogenesis such as the protective mechanism of menstrual cycle against vascular thrombotic disease and the importance of cyclical variation in hormonal concentration. Because retrospective prevalence studies can not distinguish cause and consequence and cannot provide data on sudden death (perhaps the 1st manifestation of a thrombotic disorder) further prospective studies on OCs with varying chemical formulations should be done.

The role of haemostatic mechanisms.

Abstract: SUMMARY One factor that has been proposed to explain the pathogenesis of thrombosis is the existence of a hypercoagulable state that favours intravascular clotting. Evidence in support of such a construct is convincing in only a few situations. Patients with neoplasm may have intravascular coagulation because the blood is exposed to clot-promoting agents; thrombosis after the transfusion of preparations of the vitamin K-dependent clotting factors may have a similar origin. In a few instances, thrombosis has been related to decreasedtitres of antithrombin III, the presence of an abnormal form of plasminogen, or the presence of increased titres of inhibitors of the generation or action of plasmin. In the majority of cases, no present data relate a hypercoagulable state to the evolution of thrombi. We need a fresh paradigm.

Nutritional anaemias. Part 1: Tropical Africa.

Abstract: SUMMARY A review of nutritional anaemia in Africa is presented above. It has been noted that nutritional anaemia, including iron-deficiency anaemia, megaloblastic anaemia due to folate deficiency or vitamin B12 deficiency, or both, and protein deficiency-anaemia, is widespread throughout Africa. It is particularly common in growing children, women of child-bearing age, pregnant women and lactating mothers. The anaemia is also especially common during the second half of the dry season and the first Half of the wet season, when food supplies are limited. In all cases the anaemia is caused either by limited dietary intake, excessive loss of nutrients or excessive utilization. The anaemia is associated with a number of sequelae including both structural changes, like mitochondrial swelling and mucosal atrophy, and functional abnormalities, such as cardiac failure, decreased work output, increased pregnancy risks and increased susceptibility to infections. The evidence in favour of increased susceptibility to infections in megaloblastic anaemia and protein-deficiency anaemia is overwhelming, but in iron-deficiency anaemia the available information argues in favour of reduced susceptibility to infections, except after initiation of iron therapy. The treatment of nutritional anaemia includes replacement of the deficient nutrients (and blood transfusion in severe cases), prevention of further nutrient losses and treatment of associated complications.