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Sem dvt

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whom that have sx of swelling leg, painful when walking and raise up leg, redness of leg skin, have history of accident or long journey u are suspected had deep vein thrombosis.

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Sem dvt

  1. 1. NOOR AFIFAH BT ABDRAHMANAZIZAH BT MAJIDMOHD NAQIB B BAJURIDEEP VEINTHROMBOSIS
  2. 2. Definition• Deep vein thrombosis is theformation of a blood clot in one ofthe deep veins of the body, usuallyin the leg
  3. 3. • 2 types of VT– Superficial• Occur in tortuous dilated varicose vein ; pregnancy– Deep• may be referred to as proximal DVT or distal DVT.• Occasionally, DVT also occurs in the veins of theupper extremities.• DVT can occur spontaneously without knownunderlying cause (idiopathic thrombosis) or afterprovoking events, such as trauma, surgery or acuteillness (provoked thrombosis).
  4. 4. EPIDEMIOLOGY• Untreated Proximal DVT– 30-50% risk PE– 12-15% mortality• Untreated ProximalDVT– 30-50% risk PE– 12-15% mortality• Treated DVT– <8% risk PE– Mortality <2%
  5. 5. RISK FACTORS• Principal Risk Factors– Immobilization– Trauma– Surgery– Infection– Post-partum period• Other Factors– Age– Obesity– Malignancy– Previous VTE– Varicose Veins– Dehydration– smoking– Hormonal Therapy
  6. 6. SFJSPJ
  7. 7. ETIOLOGY• DVT usually originates in the lower extremityvenous level ,starting at the calf vein level andprogressing proximally to involve popliteal,femoral ,or iliac system. .80 -90 % pulmonaryemboli originates here .
  8. 8. Virchow triad• More than 100 years ago, Virchow described atriad of factors of• venous stasis,• endothelial damage, and• hypercoagulable state
  9. 9. DVT:PathogenesisClinical featuresAzizah Binti Majid027653
  10. 10. More than 100 years ago, Virchow described a triad offactors ofvenous stasis,endothelial damage, andhypercoagulable stateVirchow triad
  11. 11. • deficiencies of protein ‘S,• ’ protein ‘C,’ and• antithrombin III.Inheriteddisorders ofcoagulation• nephrotic syndrome results in urinaryloss of antithrombin III, this diagnosisshould be considered in childrenpresenting with thromboembolic disease• Antiphospholipid antibodies acceleratecoagulation and include the lupusanticoagulant and anticardiolipinantibodies.Acquireddisorders ofcoagulation
  12. 12. The nidus for a clot is often an intimal defectRBC, WBC, Platelets, and Fibrin adhere (stick together) toform a clot (thrombus.)The thrombus enlarges as blood products accumulateforming a large clot that occludes the vein lumen.When a clot forms on an intimal defect, the coagulationcascade promotes clot growth proximally. Thrombus canextend from the superficial veins into the deep systemfrom which it can embolize to the lungs.Clinical Pathophysiology
  13. 13. Two different types of thrombus can form:• Arterial thrombus (white thrombus)• Venous thrombus (red thrombus)Arterial and venous thrombi differ in compositionand appearance.Arterial thrombi are typically composed mainly ofplatelet aggregates, giving the appearance of ‘whitethrombi’.Venous thrombi largely consist of fibrin and redblood cells so are known as ‘red thrombi’.Cont…
  14. 14. Opposing the coagulation cascade is the endogenousfibrinolytic system. After the clot organizes or dissolves,most veins will recanalize in several weeks. Residual clotsretract as fibroblasts and capillary development lead tointimal thickening.Venous hypertension and residual clot may destroyvalves, leading to the postphlebitic syndrome- a statecharacterized by edema,pain, and skin discoloration mostoften as a complication of DVT- which develops within 5-10 yearsCont…
  15. 15. Edema, sclerosis, and ulceration characterize thissyndrome, which develops in 40-80% of patients with DVT.patients also can suffer exacerbations of swelling and pain,probably as a result of venous dilatation and hypertensionPulmonary embolism (PE) is a serious complication ofDVT. Many episodes of pulmonary embolism gounrecognized, and at least 40% of patients with DVT haveclinically silent PE.Cont…
  16. 16. Clinical feature of DVT and PEDVT• Swelling of the leg• Pain or tenderness in the leg; thepain is usually in 1 leg and mayonly be present when standing orwalking• Skin that is warm to the touch inthe leg• Red or discolored skin• Swelling with pitting oedema• Swelling below knee in distaldeep vein thrombosis and up togroin in proximal deep veinthrombosis• Superficial venous dilatation• Cyanosis can occur with severeobstruction• Positive Homan’s Sign-pain onforced dorsiflexion of the footwhen the leg is raised• Low Grade Fever• Unequal Leg Measurements???• Pallor- Phlegmasia Alba Dolens• Cyanosis-Phlegmasia CeruleaDolensPE• Unexplained shortness of breath• Chest pain and/or palpitations• Anxiety and/or sweating• Hemoptysis• Fever• Fatigue and/or fainting• tachycardia (common),• tachypnea• Massive Emboli- Shock, Pallor,Severe Dyspnea, Crushing ChestPainNot all people with DVThave signs or symptomsIf the inferior vena cava is involved – lowerextremities edematous and cyanoticIf the superior vena cava is involved – upperextremities, back, neck and face show signs
  17. 17. • Phlegmasia Alba Dolens• known as milk leg orwhite leg)• deep vein thrombosisthat progresses to totalocclusion of the deepvenous system.• sudden (acute) process.• The leg, then, must relyon the superficial venoussystem for drainage• Phlegmasia Cerulea Dolens• painful blue edema,• occlusion of the superficialvenous system, therebypreventing all venousoutflow from the extremity• Sudden occurrence -edematous cyanotic painfulleg.• May result in gangrene andhigh risk for massivepulmonary embolism
  18. 18. PE• From the thrombi originating in the deep venous systemof the lower extremities• Rarely, they may originate in the pelvic, renal, or upperextremity veins and the right heart chambers.• Large thrombi lodge at the bifurcation of the mainpulmonary artery or the lobar branches, accumulate andmay cause haemodynamic compromise.• Smaller thrombi continue distally, occluding smallervessels in the lung periphery. These are more likely toproduce pleuritic chest pain by initiating an inflammatoryresponse adjacent to the parietal pleura.• Most pulmonary emboli are multiple, and the lower lobesare involved more commonly than the upper lobes
  19. 19. The Wells clinical prediction guide incorporates risk factors, clinical signs, and thepresence or absence of alternative diagnoses
  20. 20. Investigation
  21. 21. • D-dimer measurement• Duplex ultrasoundexamination afterraised D-dimer• Filling defects in flowand a lack ofcompressibilityindicate the presenceof a thrombosis
  22. 22. • Ascending venography (rarely)• Pulmonary embolism is diagnosedby ventilation–perfusion scanningshows mismatched defects• Computerised tomographic(CT) scanning of thepulmonary arteries,which can show fillingdefects in pulmonary arteries• Pulmonary angiography (rarely)
  23. 23. Management
  24. 24. • low molecular weight heparin• Warfarin– started at a dose of 10 mg on day one, 10 mg on daytwo and 5 mg on day three• Thrombolysis– Iliac vein thrombosis– tissue plasminogen activator administered directlyinto thrombus via popliteal vein or by direct puncturein groin• stent grafting for iliac vein compression syndrome• Thrombectomy (rarely)
  25. 25. • pulmonary emboli– Anticoagulation– severe right heart strain & shortness of breathneed for fibrinolytic treatment

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