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DVT Presentation.ppt

  1. Samuel Ngigi K. KMTC
  2.  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.
  3.  Pregnancy increases risk x 5-10 fold  0.86/1000 deliveries  0.71/1000 (DVT) : 0.15/1000 (PE)  Left leg>80%  Ileo-femoral more common than calf vein (72% versus 9%)  Increased with age, caesarian section, bed rest and prior history of DVT/PE)
  4. 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
  5.  Venous stasis – changes in tone and obstruction  Vascular damage at time of delivery  APTT, PS (free and total), APCr  FVIII:C, VWF, Fibrinogen  PAI-1 and PAI-2
  6. Predisposing factors: A. Patient factors:  Age>40 risk increase exponentially with age  Obesity (BMI > 30kg/m2  Varicose veins or venous thrombophlebitis  Previous D.V.T.  Oral contraceptives & HRT; estrogen is responsible  Pregnancy: due to (i) Hormonal changes (ii) Pressure on veins by fetus
  7.  Highest incidence in puerperium especially just after childbirth  Dehydration: increase blood viscosity  Immobility: Stasis of blood  Long distance travel: due to (i) Inactivity (ii) Dehydration  Due to these factors blood becomes more sticky specially if journey is for more than 5 hours
  8. 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.
  9. C. Medical Conditions  M.I./Heart failure  Inflammatory bowel disease  Malignancy or its treatment  Nephrotic syndrome  Behcet’s syndrome  Homocysteinemia  Major injuries/paralysis
  10. D. Hematological Disorders  Primary proliferative polycyathemia  Essential thrombocythemia  Paraoxysmal nocturnal hemoglobinuria
  11. E. Anti-Coagulant Deficiences:  Antithrombin III: such patients are also relatively resistant to heparin Therapy  Factor II Leiden: Genetic polymorphism of P.T. gene  Factor V Leiden: Mutation leading to APC resistance  Heparin cofactor II  Prothrombin G20210 A mutation
  12. F. Increased Clotting factors:  XI and VIII G. Antiphospholipid Antibodies:  Lupus anticoagulant  Anti-Cardiolipin antibodies
  13. 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  50% of clients are asymptomatic
  14.  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 *** venograms and pulmonary angiograms not done in pregnancy
  15.  Muscle rupture  Trauma  Hemorrhage  Ruptured popliteal cyst  Lymphedema  Post phlebitic syndrome  Streptococcal skin infections (CELLULITIS)  Nerve compression  Arthritis  Tendonits  Fractures  Arterial occlusive disorders  Simple muscle strains
  16. ◦ Bed rest with elevation of the affected limb ◦ Exercise ◦ Fluids ◦ Avoid Deep Palpation ◦ Compression stocking
  17. 1. HEPARIN  Acute phase heparin administration – it acts indirectly by activating plasma Antithrombin III. Dose: i.v. bolus 7500-10,000 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 vis a vis clinical symptoms
  18. 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 if administered in the first trimester of pregnancy as WARFARIN causes embryopathy
  19. 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
  20.  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: i. Increased binding of plasma proteins or endothelium in turn leading to a. Increased bioavailability b. Predictable anticoagulant response ii. Affinity for macrophages resulting in increase half life iii. Affinity for plts and platelet factor 4 binding to osteoblasts iv. No monitoring required v. No hospitalization require vi. Convenient O.D. doses vii. Decreased incidence of thrombocytopenia viii. Osteopenia Unknown
  21. 2. WARFARIN  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.
  22. ◦ Extend use of warfarin throughout puerperium ◦ Introduction of anticoagulant therapy in the next pregnancy 2 weeks prior to symptoms of previous pregnancy ◦ Use of LMWH in clients with cardiac prosthesis and on bed rest during pregnancy ◦ Avoid use of estrogen containing contraceptives
  23. Thank You

Notas do Editor

  1.  Partial thromboplastin time (PTT) and activated partial thromboplastin time (aPTT) Activated protein C resistance (APCR) describes a hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). This results in an increased risk of venous thrombosis, including deep vein thrombosis and pulmonary embolism. von Willebrand factor (VWF) is a blood glycoprotein involved in hemostasis.
  2. Thrombophlebitis (throm-boe-fluh-BY-tis) is an inflammatory process that causes a blood clot to form and block one or more veins, usually in your legs. The affected vein might be near the surface of your skin (superficial thrombophlebitis) or deep within a muscle (deep vein thrombosis, or DVT) Hormone replacement therapy(HRT)
  3. Nephrotic syndrome is a kidney disorder that causes your body to pass too much protein in your urine. Nephrotic syndrome is usually caused by damage to the clusters of small blood vessels in your kidneys that filter waste and excess water from your blood. Behcet's syndrome, is a rare disorder that causes blood vessel inflammation throughout your body. Homocysteinemia, a separate but related entity, is defined as elevation of the homocysteine level in blood. This condition has also been referred to as homocyst(e)inemia to reflect metabolites that may accumulate. In fact, a high level of homocysteine is a risk factor for heart disease.
  4. Polycythemia refers to an increase in the number of red blood cells in the body. The extra cells cause the blood to be thicker, and this, in turn, increases the risk of other health issues, such as blood clots. Thrombocythemia is a disease in which your bone marrow makes too many platelets. Platelets are blood cell fragments that help with blood clotting. Having too many platelets makes it hard for your blood to clot normally. This can cause too much clotting, or not enough clotting. Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired, life-threatening disease of the blood. The disease is characterized by destruction of red blood cells (hemolytic anemia), blood clots (thrombosis), and impaired bone marrow function (not making enough of the three blood components).
  5. Resistance to activated protein C (APC resistance) is a term used to describe abnormal resistance of human plasma to the anticoagulant effects of human APC. APC resistance is characterized by a reduced anticoagulant response of patient plasma after adding a standard amount of APC.
  6. Thrombocytopenia is a condition characterized by abnormally low levels of platelets
  7. Osteopenia is a condition that begins as you lose bone mass and your bones get weaker.