Dvt In Preg

DVT in pregnancy - by Dr Kihara A.B. Epidemiology Thromboembolic diseases include thrombophlebitis, phlebothrombosis, septic pelvic thrombophlebitis and pulmonary embolism. They are a major cause of morbidity and mortality in the world. DVT and PE are distinct but related aspects of vascular venous thromboembolism. Incidence of thromboembolism is 0.2% in ante-natal period and 0.6% in postpartum. The incidence rises to 1-2% post caesarian section. Pulmonary embolism has a mortality rate of 15% in 50% of patients with DVT. Unfortunately only 5-10% are symptomatic. Pregnancy and venous thromboembolic disease • Pregnancy increases risk x 5-10 fold • 0.86/1000 deliveries • 0.71/1000 (DVT) : 0.15/1000 (PE) • Left leg>80% • Ileofemoral more common than calf vein (72% versus 9%) • Increased with age, caesarian section, bed rest and prior history of DVT/PE) Pathophysiology Virchow’s Triad: • Disorder of blood vessel wall • Disordered blood flow (stasis) • Abnormality of blood constituents ××Recap the clot forming physiological cascade and the fibrinolysis cascade Pregnancy and Virchow’s Triad • Venous stasis – changes in tone and obstruction • Vascular damage at time of delivery

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Decreased APTT, PS (free and total), APCr Increased FVIII:C, VWF, Fibrinogen Increased PAI-1 and PAI-2

Venous thrombosis – A multifactorial disease. Predisposing factors: A. Patient factors: 1. Age>40 : risk increase exponentially with age 2. Obesity : BMI > 30kg/m2 3. Varicose veins or venous thrombophlebitis 4. Previous D.V.T. 5. Oral contraceptives & Hormone replacement therapy; oestrogen is responsible for D.V.T. 6. Pregnancy: due to a. Hormonal changes b. Pressure on veins by fetus Highest incidence in puerperium especially just after childbirth 7. Dehydration: increase blood viscosity 8. Immobility: Stasis of blood 9. Long distance travel: due to a. Inactivity b. Dehydration Due to these factors blood becomes more sticky specially if journey is for more than 5 hours

B. Surgical conditions: • Especially includes surgery for more than half an hour duration • Abdominal, pelvis, orthopedic surgery to lower limb • Increased use of central venous line has caused more involvement of upper limbs in D.V.T. C. Medical Conditions 1. M.I./Heart failure 2. Inflammatory bowel disease 3. Malignancy or its treatment 4. Nephrotic syndrome 5. Behcet’s syndrome 6. Homocysteinemia 7. Major injuries/paralysis D. Hematological Disorders 1. Primary proliferative polycyathemia 2. Essential thrombocythemia 3. Myelofibrosis/Myeloproliferative diseases 4. Paraoxysmal nocturnal hemoglobinuria E. Anti-Coagulant Deficiences: 1. Antithrombin III: such patients are also relatively resistant to heparin Therapy 2. Factor II Leiden: Genetic polymorphism of P.T. gene 3. Factor V Leiden: Mutation leading to APC resistance 4. Heparin cofactor II 5. Prothrombin G20210 A mutation F. Increased Clotting factors: • XI and VIII G. Antiphospholipid Antibodies: 1. Lupus anticoagulant 2. Anti-Cardiolipin antibodies Signs and Symptoms D.V.T. of iliac, femoral or popliteal vein • leg swelling, warmth, erythema, increased, tissue turgor, distention of superficial veins and appearance of prominent venous collaterals. In some patients deoxyhemoglobin in straight veins gives it a cyanotic hue called as ‘Phlegmasia cerulea dolens’. • In markedly edematous legs, interstitial tissue pressure may exceed capillary perfusion pressure causing pallor – ‘Phlegmasia alba dolens’. • Tenderness is present along individual vein and a cord may be palpable. D.V.T. of calf vein: commonest complaint calf pain especially when standing or walking • There may be tenderness or warmth, increased tissue turgor or modest swelling. Homan’s Signs: positive C/I due to PE. 50% of clients are asymptomatic Diagnosis • Clinical Diagnosis unreliable due to differential diagnosis but serial limb measurements are suggestive of diagnosis and treatment follow-up • Screening investigations – impedance plethysmography • Definitive diagnosis – Doppler ultrasound, CT scan, MRI • PE – ventilation perfusions scan

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*** venograms and pulmonary angiograms not done in pregnancy

Differential Diagnosis 1. Muscle rupture 2. Trauma 3. Hemorrhage 4. Ruptured popliteal cyst 5. Lymphoedema 6. Post phlebitic syndrome 7. Streptococcal skin infections 8. Nerve compression 9. Arthritis 10. Tendonits 11. Fractures 12. Arterial occlusive disorders 13. Simple muscle strains Supportive Management 1. Bed rest with elevation of the affected limb 2. Exercise 3. Fluids 4. Avoid Deep Palpation 5. Compression stocking Specific Medical Treatment HEPARIN Acute phase heparin administration – it acts indirectly by activating plasma Antithrombin III. Dose :i.v. bolus 750010000 IU followed by continuous infusion so that 1000-1500 IU/Hr is maintained. Deep S.C. injection of 10,000-20,000 U every 8-12 hrs can also be given. This treatment is maintained for at least 5-7 days visa a vie clinical symptoms Test used to monitor heparin therapy include coagulation time, activated partial thromboplastin time, thrombin clotting time, and heparin assay. Heparin should not be given if the platelet count is below 50,000/µL. The partial thromboplastin time should be 1.5-2 times the control value during heparin therapy. Heparin is administered in the first trimester of pregnancy as warfarin causes embroyopathy S/E of heparin include: thrombocytopenia, osteoporosis and fatty necrosis Antidote of heparin, protamine sulphate 1mg per 100 units. Heparin must be stopped at least one day prior to delivery Low molecular weight heparin is equally effective used in fixed OD or BD doses for 6-14 days. Advantages of low molecular weight heparin includes: • Increased binding of plasma proteins or endothelium in turn leading to • Increased bioavailability • Predictable anticoagulant response

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Affinity for macrophages resulting in increase half life Affinity for platelets and platelet factor 4 binding to osteoblasts No monitoring required No hospitalization require Convenient O.D. doses Decreased incidence of thrombocytopenia

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Osteopenia Unknown

WARFARIN It is oral anticoagulant acts by indirectly interfering with the synthesis of Vit. K dependent clotting factors in liver, 5-15 mg is started during first week of heparin therapy as early as the first day if aPTT is in therapeutic range. Dose adjusted accordingly to P.T. INR should be maintained 1.5-2.5 times control. Heparin can then be withdrawn Embryopathy includes: nasal hypoplasia, skeletal abnormalities, and multiple central nervous system abnormalities. Antidote vitamin K 5mg I.V. Warfarin must be avoided in the first trimester and after 36 weeks gestation. PROPHYLAXIS 1. Extend use of warfarin throughout puerperium 2. Introduction of anticoagulant therapy in the next pregnancy 2 weeks prior to symptoms of previous pregnancy 3. Use of LMWH in clients with cardiac prosthesis and on bed rest during pregnancy 4. Avoid use of oestrogen containing contraceptives

NOTES