Presentation on theme: "VENOUS THROMBOSIS Dr Narisha Ramparsad Department of Haematology and Molecular Medicine."— Presentation transcript:
VENOUS THROMBOSIS Dr Narisha Ramparsad Department of Haematology and Molecular Medicine
Normal haemostasis Ensures fluid state of blood in vasculature Prevents blood loss – site of injury – by forming haemostatic plug Clot removal – when healing is complete
Overview of Haemostasis THROMBOSIS BLEEDING
Definitions A blood clot that forms in a blood vessel or within the heart and remains there is called a thrombus. A thrombus that travels from the blood vessel or heart to another location in the body is called an embolus, and the disorder, an embolism. For example, an embolus that occurs in the lungs is called a pulmonary embolism. Sometimes, a piece of atherosclerotic plaque, small pieces of tumor, fat clumps, air, amniotic fluid, or other materials can act in the same manner as an embolus. (MEDLINE PLUS)atherosclerotic
Pathogenesis -Thrombosis Normally - balance between clotting and bleeding With thrombosis - imbalance with procoagulant state manifesting Risk increases when > 1 risk factor present Venous thrombi – fibrin & RBCs mainly, leucocytes & plts also present Virchow’s triad 1) vessel wall damage 2) blood flow (stasis) 3) hypercoaguability of blood Venous thrombosis can affect any part of venous system but deep veins most commonly affected.
Venous thromboembolism (VTE) VTE = Deep Vein Thrombosis (DVT) and/or Pulmonary Embolism (PE) Incidence increases with age 117 cases/ Increasing health problem – prevention important, potentially fatal
Thrombosis commonly occurs in deep veins of limbs. Can also affect superficial veins Venous system leg – 2 important categories 1- deep calf vein involvement only 2- proximal vein thrombosis (involving popliteal, femoral or iliac veins) – give rise to clinically significant PE Pulmonary emboli ( majority arise from deep veins of leg >90%) Other sources of PE include – upper extremity thrombosis, deep pelvic veins, renal veins, IVC
DEEP VEINS OF THE LEG
DEEP VEIN THROMBOSIS – clinical features Leg pain, swelling, tenderness, palpable cord (thrombosed vessel), phlegmasia cerulea dolens in occasional patients. Non specific signs and symptoms.
Differential Diagnosis DVT Cellulitis Popliteal cyst Lymphatic obstruction Muscle strain/tear Direct twisting injury to leg If think about DVT – MUST objectively exclude
Pulmonary Embolism – Clinical Features Symptoms variable Transient Dyspnoea, tachypnoea Tachycardia Pleuritic chest pain, cough, haemoptysis, CVS collapse with hypotension, syncope ( massive pulmonary embolism) Clinically silent Clinical features are non specific ONCE again must objectively exclude
Laboratory investigations D-Dimer assay Compression ultrasound(DVT) Venography (DVT) Spiral CT (highly sensitive for PE MRI Work up for thrombophilic state when confirm diagnosis
Clinical course Untreated proximal vein thrombosis – potentially lethal – fatal PE Extension of thrombus proximally Post thrombotic syndrome frequent complication of deep DVT. Heaviness, swelling cramps, itching, ulceration Chronic thromboembolic pulmonary hypertension.
Treatment – Anticoagulant Therapy Heparin: Unfractionated or Low Molecular Weight Heparins e.g Enoxaprin(Clexane), Dalteprin, Fondaparinux Vitamin K antagonists e.g Warfarin Oral anti Xa (clinical trials) Direct thrombin inhibitors
Initiation of treatment Must cover with Clexane when initiating Rx with Warfarin – Why? ( short T1/2, Protein C) – relative prothrombotic state
Treatment – how long? Individualise each case Look at risk factors present Transient vs permanent vs no risk factors 1 st episode vs recurrent thrombosis Reassess D-Dimer levels Risk –Benefit ratio of anticoagulant therapy
Treatment – how long ? First onset,transient risk factor – 6 months, recheck D-Dimer levels. If raised continue ? Indefinite therapy. First onset, idiopathic thrombosis – consider life long Warfarin. Reassess risk-benefit ratio Recurrent DVT – indefinite anticoagulation Patients with APL antibodies or 2 more inherited risk factors – 12 months anticoagulation and reassess
Treatment how long First episode thombosis – with deficiency of natural anticoagulants e.g. antithrombin, Prot C, Prot S or FVLeiden/Prothrombin gene mutation – 12 months and reassess ? indefinite therapy
Side effects of anticoagulant therapy Bleeding Heparin Induced thrombocytopenia and thrombosis Heparin induced osteoporosis, increased transaminase levels, hypersensitivity reactions e.g. necrosis, alopecia, hyperkalaemia
Treatment – Thrombolytic therapy – When? Indicated in patients with PE – haemodynamically unstable, evidence of R ventricular failure Threatened limb in setting of DVT
Prophylaxis – venous thrombosis Important to identify those patient at increased risk of thrombosis Prevention Use of LMWH, compression stockings Awareness – patients and health care professionals
CONCLUSION Venous thromboembolism – major cause of morbidity and mortality Identify risk factors early -institute prophylaxis Prophylaxis imperative measure to decrease incidence of thrombotic events If suspect thrombosis must objectively test Duration of treatment – varies -individualise