2DefinitionDeep vein thrombosis is the formation of a blood clot in one of the deep veins of the body, usually in the leg
3ETIOLOGYDVT ususally originates in the lower extremity venous level ,starting at the calf vein level and progressing proximally to involve popliteal ,femoral ,or iliac system % pulmonary emboli originates here .
4Virchow triedMore than 100 years ago, Virchow described a triad of factors ofvenous stasis,endothelial damage, andhypercoagulable state
5Venous stasis prolonged bed rest (4 days or more) A cast on the leg Limb paralysis from stroke or spinal cord injuryextended travel in a vehicle
6HypercoagulabilitySurgery and trauma responsible for up to 40% of all thromboembolic diseaseMalignancyIncreased estrogen (due to a fall in protein ‘S) Increased estrogen occurs duringall stages of pregnancy—the first three months postpartum,after elective abortion, andduring treatment with oral contraceptive pills
7Inherited disorders of coagulation deficiencies of protein ‘S,’ protein ‘C,’ andantithrombin III.
8Acquired disorders of coagulation nephrotic syndrome results in urinary loss of antithrombin III, this diagnosis should be considered in children presenting with thromboembolic diseaseAntiphospholipid antibodies accelerate coagulation and include the lupus anticoagulant and anticardiolipin antibodies.
9Inflammatory processes, such as systemic lupus erythematosus (SLE), sickle cell disease, andinflammatory bowel disease (IBD),also predispose to thrombosis, presumably due to hypercoagulability
10Endothelial Injury Trauma, surgery, and invasive procedure may disrupt venous integrityIatrogenic causes of venous thrombosis are increasing due to the widespread use of central venous catheters, particularly subclavian and internal jugular lines. These lines are an important cause of upper extremity DVT, particularly in children.
11Clinical Pathophysiology The nidus for a clot is often an intimal defectWhen a clot forms on an intimal defect, the coagulation cascade promotes clot growth proximally. Thrombus can extend from the superficial veins into the deep system from which it can embolize to the lungs.
12Opposing the coagulation cascade is the endogenous fibrinolytic system Opposing the coagulation cascade is the endogenous fibrinolytic system. After the clot organizes or dissolves, most veins will recanalize in several weeks. Residual clots retract as fibroblasts and capillary development lead to intimal thickening.Venous hypertension and residual clot may destroy valves, leading to the postphlebitic syndrome, which develops within 5-10 years
13Edema, sclerosis, and ulceration characterize this syndrome, 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 hypertension Pulmonary embolism (PE) is a serious complication of DVT. Many episodes of pulmonary embolism go unrecognized, and at least 40% of patients with DVT have clinically silent PE on VQ scanning
14Presentation and Physical Examination Calf pain or tenderness, or bothSwelling with pitting oedemaSwelling below knee in distal deep vein thrombosis and up to groin in proximal deep vein thrombosisIncreased skin temperatureSuperficial venous dilatationCyanosis can occur with severe obstruction
15Palpate distal pulses and evaluate capillary refill to assess limb perfusion. Move and palpate all joints to detect acute arthritis or other joint pathology.Neurologic evaluation may detect nerve root irritation; sensory, motor, and reflex deficits should be notedHomans'’ sign: pain in the posterior calf or knee with forced dorsiflexion of the foot
16Search for stigmata of PE such as tachycardia (common), tachypnea or chest findings (rare), and exam for signs suggestive of underlying predisposing factors.
18Wells Clinical Prediction Guide The Wells clinical prediction guide incorporates risk factors, clinical signs, and the presence or absence of alternative diagnoses. Wells Clinical Prediction Guide for DVTClinical ParameterScoreActive cancer (treatment ongoing, or within 6 months or palliative)1Paralysis or recent plaster immobilization 1Recently bedridden for >3 days or major surgery <4 weeks1
19Localized tenderness along the distribution of the deep venous system1 Entire leg swelling1Calf swelling >3 cm compared to the asymptomatic leg 1Pitting edema (greater in the symptomatic leg)1Collateral superficial veins (nonvaricose)1Alternative diagnosis (as likely or > that of DVT)
20Total of Above Score High probability: Score ³3 Moderate probability: Score = 1 or 2 Low probability: Score £0Adapted from Anand SS, et al. JAMA. 1998; 279 ;1094
21Diagnostic StudiesClinical examination alone is able to confirm only 20-30% of cases of DVTBlood Teststhe D-dimerINR.Current D-dimer assays have predictive value for DVT, and theINR is useful for guiding the management of patients with known DVT who are on warfarin (Coumadin)
22D-dimerD-dimer is a specific degradation product of cross-linked fibrin. Because concurrent production and breakdown of clot characterize thrombosis, patients with thromboembolic disease have elevated levels of D-dimerthree major approaches for measuring D-dimerELISAlatex agglutinationblood agglutination test (SimpliRED
23False-positive D-dimers occur in patients with recent (within 10 days) surgery or trauma,recent myocardial infarction or stroke,acute infection,disseminated intravascular coagulation,pregnancy or recent delivery,active collagen vascular disease, or metastatic cancer
25venography gold standard” modality for the diagnosis of DVT Advantages Venography is also useful if the patient has a high clinical probability of thrombosis and a negative ultrasound,it is also valuable in symptomatic patients with a history of prior thrombosis in whom the ultrasound is non-diagnostic.
28Nuclear Medicine Studies Because the radioactive isotope incorporates into a growing thrombus, this test can distinguish new clot from an old clot
29PlethysmographyPlethysmography measures change in lower extremity volume in response to certain stimuli.
30Ultrasonographycolor-flow Duplex scanning is the imaging test of choice for patients with suspected DVTinexpensive,noninvasive,widely availableUltrasound can also distinguish other causes of leg swelling, such as tumor, popliteal cyst, abscess, aneurysm, or hematoma.
31clinical limitations expensive reader dependent Duplex scans are less likely to detect non-occluding thrombi.During the second half of pregnancy, ultrasound becomes less specific, because the gravid uterus compresses the inferior vena cava, thereby changing Doppler flow in the lower extremities
32Magnetic Resonance Imaging It detects leg, pelvis, and pulmonary thrombi and is 97% sensitive and 95% specific for DVT.It distinguishes a mature from an immature clot.MRI is safe in all stages of pregnancy.
33DIFFERENTIAL DIAGNOSIS Cellulitis ThrombophlebitisArthritis Asymmetric peripheral edema secondary to CHF, liver disease, renal failure, or nephrotic syndrome lymphangitis Extrinsic compression of iliac vein secondary to tumor, hematoma, or abscess Hematoma Lymphedema
34Muscle or soft tissue injury Neurogenic pain Postphlebitic syndrome Prolonged immobilization or limb paralysis Ruptured Baker cyst Stress fractures or other bony lesions Superficial thrombophlebitis Varicose veins
35ManagementUsing the pretest probability score calculated from the Wells Clinical Prediction rule, patients are stratified into 3 risk groups—high, moderate, or low.The results from duplex ultrasound are incorporated as follows:If the patient is high or moderate risk and the duplex ultrasound study is positive, treat for DVT.
36If the duplex study is negative and the patient is low risk, DVT has been ruled out. When discordance exists between the pretest probability and the duplex study result, further evaluation is required.If the patient is high risk but the ultrasound study was negative, the patient still has a significant probability of DVT
37a venogram to rule out a calf vein DVT surveillance with repeat clinical evaluation and ultrasound in 1 week.results of a D-dimer assay to guide managementIf the patient is low risk but the ultrasound study is positive, some authors recommend a second confirmatory study such as a venogram before treating for DVT
38EMERGENCY DEPARTMANT CARE The primary objectives of the treatment of DVT are toprevent pulmonary embolism,reduce morbidity, andprevent or minimize the risk of developing the postphlebitic syndrome.
39AnticoagulationThrombolytic therapy for DVTSurgery for DVTFilters for DVTCompression stockings
40Anticoagulation Heparin prevents extension of the thrombus Heparin's anticoagulant effect is related directly to its activation of antithrombin III. Antithrombin III, the body's primary anticoagulant, inactivates thrombin and inhibits the activity of activated factor X in the coagulation process.
41Heparin is a heterogeneous mixture of polysaccharide fragments with varying molecular weights but with similar biological activity. The larger fragments primarily interact with antithrombin III to inhibit thrombin.The low molecular weight fragments exert their anticoagulant effect by inhibiting the activity of activated factor X. The hemorrhagic complications attributed to heparin are thought to arise from the larger higher molecular weight fragments.
42The optimal regimen for the treatment of DVT is anticoagulation with heparin or an LMWH followed by full anticoagulation with oral warfarin for 3-6 monthsWarfarin therapy is overlapped with heparin for 4-5 days until the INR is therapeutically elevated to between 2-3.
43After an initial bolus of 80 U/kg, a constant maintenance infusion of 18 U/kg is initiated. The aPTT is checked 6 hours after the bolus and adjusted accordingly. .The aPTT is repeated every 6 hours until 2 successive aPTTs are therapeutic. Thereafter, the aPTT is monitored every 24 hours as well as the hematocrit and platelet count.
44Advantages of Low-Molecular-Weight Heparin Over Standard Unfractionated Heparin Superior bioavailabilitySuperior or equivalent safety and efficacySubcutaneous once- or twice-daily dosingNo laboratory monitoring*Less phlebotomy (no monitoring/no intravenous line)Less thrombocytopeniaEarlier/facilitated
45At the present time, 3 LMWH preparations, Enoxaparin,Dalteparin, andArdeparin
46warfarinInterferes with hepatic synthesis of vitamin K-dependent coagulation factorsDose must be individualized and adjusted to maintain INR between 2-32-10 mg/d POcaution in active tuberculosis or diabetes; patients with protein C or S deficiency are at risk of developing skin necrosis
47Thrombolytic therapy for DVT Advantages includeprompt resolution of symptoms,prevention of pulmonary embolism,restoration of normal venous circulation,preservation of venous valvular function,and prevention of postphlebitic syndrome.
48Thrombolytic therapy does not prevent clot propagation,rethrombosis, orsubsequent embolization.Heparin therapy and oral anticoagulant therapy always must follow a course of thrombolysis.
49Thrombolytic therapy is also not effective once the thrombus is adherent and begins to organize The hemorrhagic complications of thrombolytic therapy are formidable (about 3 times higher), including the small but potentially fatal risk of intracerebral hemorrhage.The uncertainty regarding thrombolytic therapy likely will continue
50Surgery for DVT indications when anticoagulant therapy is ineffective unsafe,contraindicated.The major surgical procedures for DVT are clot removal and partial interruption of the inferior vena cava to prevent pulmonary embolism.
51These pulmonary emboli removed at autopsy look like casts of the deep veins of the leg where they originated.
52This patient underwent a thrombectomy This patient underwent a thrombectomy. The thrombus has been laid over the approximate location in the leg veins where it developed.
53Filters for DVTIndications for insertion of an inferior vena cava filterPulmonary embolism with contraindication to anticoagulationRecurrent pulmonary embolism despite adequate anticoagulation
54Controversial indications: Deep vein thrombosis with contraindication to anticoagulationDeep vein thrombosis in patients with pre-existing pulmonary hypertensionFree floating thrombus in proximal veinFailure of existing filter devicePost pulmonary embolectomy
55Inferior vena cava filters reduce the rate of pulmonary embolism but have no effect on the other complications of deep vein thrombosis. Thrombolysis should be considered in patients with major proximal vein thrombosis and threatened venous infarction
58Further Inpatient Care Most patients with confirmed proximal vein DVT may be treated safely on an outpatient basis. Exclusion criteria for outpatient management are as follows:Suspected or proven concomitant pulmonary embolismSignificant cardiovascular or pulmonary comorbidityMorbid obesityRenal failureUnavailable or unable to arrange close follow-up care
59Patients are treated with a low molecular weight heparin and instructed to initiate therapy with warfarin 5 mg PO the next day. Low molecular weight heparin and warfarin are overlapped for about 5 days until the international normalized ratio (INR) is therapeutic.If inpatient treatment is necessary, low molecular weight heparin is effective and obviates the need for IV infusions or serial monitoring of the PTT.With the introduction of low molecular weight heparin, selected patients qualify for outpatient treatment only if adequate home care and close medical follow-up care can be arranged.
60Platelets also should be monitored and heparin discontinued if platelets fall below 75,000. While on warfarin, the prothrombin time (PT) must be monitored daily until target achieved, then weekly for several weeks. When the patient is stable, monitor monthly.Significant bleeding (ie, hematemesis, hematuria, gastrointestinal hemorrhage) should be investigated thoroughly since anticoagulant therapy may unmask a preexisting disease (eg, cancer, peptic ulcer disease, arteriovenous malformation).
61Duration of anticoagulation in patients with deep vein thrombosis Transient cause and no other risk factors: 3 monthsIdiopathic: 3-6 monthsOngoing risk for example, malignancy: 6 -12 monthsRecurrent pulmonary embolism or deep vein thrombosis: 6-12 monthsPatients with high risk of recurrent thrombosis exceeding risk of anticoagulation: indefinite duration (subject to review)
62Further Outpatient Care: Patients with suspected or diagnosed isolated calf vein DVT may be discharged safely on a nonsteroidal anti-inflammatory drug (NSAID) or aspirin with close follow-up care and repeat diagnostic studies in 3-7 days to detect proximal extension.At certain centers, patients with isolated calf vein DVT are admitted for full anticoagulant therapy.
63Patients with suspected DVT but negative noninvasive studies need to be reassessed by their primary care provider within 3-7 days.Patients with ongoing risk factors may need to be restudied at that time to detect proximal extension because of the limited accuracy of noninvasive tests for calf vein DVT.
65Prognosis:All patients with proximal vein DVT are at long-term risk of developing chronic venous insufficiency.About 20% of untreated proximal (above the calf) DVTs progress to pulmonary emboli, and 10-20% of these are fatal. With aggressive anticoagulant therapy, the mortality is decreased 5- to 10-fold.DVT confined to the calf virtually never causes clinically significant emboli and thus does not require anticoagulation
66Patient Education:Advise women taking estrogen of the risks and common symptoms of thromboembolic disease.Discourage prolonged immobility, particularly on plane rides and long car trips
67PROPHYLAXIS Ideidentify any patiant who is at risk. Prevent dehydration.During operation avoid prolonged calf compression.Passive leg exercises should be encourged whilst patient on bed.Foot of bed should be elevated to increase venous return.Early mobilization should be rule for all surgical patients.