Prophylaxis to prevent venous thromboembolism Medical Assignment Help

Prophylactic measures to prevent venous thrombosis during surgery are aimed at procedures for preventing stasis, such as early mobilization, elevation of the legs, compression stockings, and possibly calf-muscle stimulation and passive calf-muscle exercises during surgery, and methods for preventing hypercoagulability, usually using heparin.
Low-risk patients (Table 6.26) require no specific measures other than early mobilization. Moderate-risk patients should receive specific prophylaxis such as low-dose heparin at a dose of 5000 units subcutaneously every 8 or 12 hours until the patient is ambulatory; no laboratory monitoring is required.
Low molecular weight heparin once daily has been shown to be more effective than standard low-dose heparin in preventing thrombosis in high-risk patients. However, in general surgical practice there is no clear evidence that low molecular weight heparin is superior to low-dose heparin and it is much more expensive. Before the introduction of low molecular weight heparin, other approaches were used in high-risk surgical patients such as low-dose warfarin and higher doses of subcutaneous heparin to keep the PTTK between 1.25 and 1.5 times the control value.

Treatment of established venous thromboembolism.

Treatment of established venous thromboembolism.

Treatment of established venous thromboembolism (Information box 6.2) The aim of anticoagulant treatment is to prevent further thrombosis and pulmonary embolization while resolution of venous thrombi occurs by natural fibrinolytic activity. Anticoagulation is started with heparin as it produces an immediate anticoagulant effect. There is no evidence  that it is necessary to use heparin for any longer than it takes for simultaneously administered warfarin to produce an anticoagulant effect, usually about 3-4 days. Anticoagulation for 6 weeks is sufficient for patients after their first thrombosis as long as there are no persisting risk factors. Long-term treatment should be considered in patients with repeated episodes or continuing risk factors. Outpatient anticoagulation is best supervised in anticoagulant clinics. Patients are issued with national booklets for recording INR results and anticoagulant doses. The role of thrombolytic therapy in the treatment of venous thrombosis is not established. It is sometimes used in patients with massive pulmonary embolism and in patients with extensive deep venous thrombi. For these conditions it is necessary to give a bolus dose of streptokinase, 250000 units over 30 min to inactivate antibodies formed by previous streptococcal infection followed by a continuous infusion, approximately 100000 units every hour, for 24-72 hours. The dose of streptokinase is adjusted to maintain the TT between two and four times the control value.
Thrombolytic therapy should be followed by anticoagulation with heparin for a few days and then by oral anticoagulants for a few months to prevent rethrombosis. New agents are being evaluated as antithrombotic agents including direct inhibitors of thrombin such as hirudin. Hirudin can inactivate thrombin bound to fibrin more efficiently than AT-III potentiated by heparin. Clinical studies are required to establish the antithrombotic effect in relation to the risk of bleeding.

Further reading

Bloom Al., Forbes CD, Thomas DP and Tuddenham EGD (1994) Haemostasis and Thrombosis, 2nd edn. Edinburgh: Churchill Livingstone. Chanarin I (1979) The Megablastic Anaemias, 3rd edn.
Oxford: Blackwell Scientific Publications. Dacie ]V (1985 (volume 1), 1988 (volume 2), 1992 (volume 3)) The Haemolytic Anaemias, 3rd edn. Edinburgh:

Churchill Livingstone.

Firkin F, Chesterman C, Pennington D & Rush B (eds) (1989) de Gruchy’s Clinical Haematology in Medical Practice, 5th edn. Oxford: Blackwell Scientific. Furie B & Furie BC (1992) Molecular and cellular biology of blood coagulation. New England Journal of Medicine 326, 800-806.
Groopman JE, Molina JM & Scadden DT (1989) Haemopoietic growth factors: Biology and clinical applications. New England Journal of Medicine 321, 1449- 1459.
Hows JM (1991) Severe aplastic anaemia: The patient without a HLA-identical sibling. British Journal of Haematology 77, 1-4.
Mollison PL, Engelfriet CP & Contreras M (1993) Blood Transfusion in Clinical Medicine, 9th edn. Oxford: Blackwell Scientific Publications.
Pippard MJ, Hughes RT & Cotes PM (1992) Erythropoietin. In: Recent Advances in Haematology 6 (ed. Hoffbrand AV & Brenner MK). Edinburgh: Churchill

Livingstone.

Thein SL & Weatherall DJ (1988) The thalassaemias. In: Recent Advances in Haematology 5 (ed. Hoffbrand AV). Edinburgh: Churchill Livingstone. Williams WI, Beutler E, Erslev AJ & Lichtman MA (1990) Hematology, 4th edn. New York: McGraw-Hill.

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