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Context Outpatients with suspected deep vein thrombosis (DVT) have nonspecific signs and symptoms. Missed DVT diagnosis may result in fatal pulmonary embolism. Since many patients may have DVT, a selective and efficient diagnostic process is needed.
Objective To systematically review trials that determined the prevalence of DVT using clinical prediction rules either with or without D-dimer, for the diagnosis of DVT.
Data Sources English- and French-language studies were identified from MEDLINE from 1990 to July 2004 and supplemented by a review of all relevant bibliographies.
Study Selection We included studies that prospectively enrolled consecutive, unselected outpatients with suspected DVT and applied clinical prediction rules before D-dimer testing or diagnostic imaging. All studies included sufficient information to allow the calculation of the prevalence of DVT for at least 1 of the 3 clinical probability estimates (low, moderate, or high). We required that patients be followed up for a minimum 3-month period. Unless the clinical model incorporated prior DVT, studies were excluded if patients with a history of prior DVT were enrolled.
Data Extraction Two reviewers independently reviewed and abstracted data for estimating the prevalence of DVT, sensitivity, specificity, and likelihood ratios (LRs) of D-dimer in each of the 3 clinical probability estimates. Data for the D-dimer in all studies were pooled and analyzed as high-sensitivity/low-specificity test or a moderate-sensitivity/moderate-specificity test.
Data Synthesis Fourteen studies involving more than 8000 patients used 1 clinical prediction rule for diagnosing DVT, of which 11 incorporated D-dimer testing in the diagnostic algorithm. The prevalence of DVT in the low, moderate, and high clinical probability groups was 5.0% (95% CI, 4.0%-8.0%), 17% (95% CI, 13%-23%), and 53% (95% CI, 44%-61%), respectively. The overall prevalence of DVT was 19% (95% CI, 16%-23%). Pooling all studies, the sensitivity, specificity, and negative LRs of D-dimer testing in the low probability group were 88% (95% CI, 81%-92%), 72% (95% CI, 65%-78%), and 0.18% (95% CI, 0.12-0.18); in the moderate probability group: 90% (95% CI, 80%-95%), 58% (95% CI, 49%-67%), and 0.19% (95% CI, 0.11-0.32); and in the high probability group: 92% (95% CI, 85%-96%), 45% (95% CI, 37%-52%), and 0.16% (95% CI, 0.09-0.30). The LRs for a normal result on a high or moderately sensitive D-dimer assay among patients with: (1) low clinical suspicion were 0.10 (95% CI, 0.03-0.37) and 0.20 (95% CI, 0.12-0.31); (2) moderate clinical suspicion were 0.05 (95% CI, 0.01-0.21) and 0.23 (95% CI, 0.13-0.39); and (3) high clinical suspicion were 0.07 (95% CI, 0.03-0.18) and 0.15 (95% CI, 0.10-0.38).
Conclusions Diagnostic accuracy for DVT improves when clinical probability is estimated before diagnostic tests. Patients with low clinical probability on the predictive rule have prevalence of DVT of less than 5%. In low-probability patients with negative D-dimer results, diagnosis of DVT can be excluded without ultrasound; in patients with high clinical suspicion for DVT, results should not affect clinical decisions
Deep Vein Thrombosis
Complete or partial occlusion of vein by thrombosis. Common cause of in-hospital mortality.
80% of time in calf muscles – usually around valve cusps or in soleal plexus --> 20% move proximally --> can result in fatal pulmonary embolism.
Risk Factors:
• Virchow’s triad (venous stasis, vessel wall injury, hypercoaguable state) --> primary mechanism for DVT
• age (increasing age increases risk, but mechanism is not known – may be related to mobility, the decreased fibrinolytic response)
• immobilisation > 3 days (venous stasis)
• pregnancy and postpartum period
• major surgery (trauma to blood vessels and period of immobilisation after)
• oral contraceptives
• obesity (impaired fibrinolytic activity and immobility)
• long plane or car trips
• medical conditions – cancer; previous DVT; CVA; CHF; nephrotic syndrome; ulcerative colitis
• fractures and other trauma (especially if immobilised)
Pathology:
Thrombus is composed or red blood cells, platelets and leukocytes bound together with fibrin.
Pathogenesis is due to vessel wall damage, venous stasis and increased activation of clotting factors (hypercoagulability) – Virchow’s triad.
Venous stasis/alteration in blood flow:
• occurs during immobility (eg loss of calf muscle venous pump; during surgery)
• also affected by arrhythmias, myocardial infarction, congestive heart failure, obesity, varicose veins
• arterial turbulence contributes
Injury to vessel wall:
• endothelial injury has a strong influence on the formation of a thrombus
• if vessel wall is damaged --> platelets adhere to exposed subendothelium collagen --> platelet aggregation --> activation of coagulation pathway
• eg may occur during surgery, trauma, burns, IV lines
Hypercoagulability:
• a number of acquired and hereditary hypercaogulable states have been identified
• eg postpartum, postoperative, severe trauma, cancer, oral contraceptives, obesity, nephrotic syndrome, congestive heart failure
Clinical Features:
Related to degree of venous obstruction – most do not produce significant venous obstruction and collaterals may rapidly develop. Many are asymptomatic but if symptomatic include: nonspecific painful swollen leg with dilated superficial veins; pulses usually present; unilateral oedema; nontender oedema of collateral superficial veins; Homan’s sign – dorsiflexion of foot causes pain in calf – only present in 1/3rd; venous distension; prominence of subcutaneous veins; may have low grade fever; may develop reddish purple hue to lower limb (phlegmasia cerulea dolens); 10% --> signs of pulmonary embolism.
Radiography – contrast venography; duplex ultrasound; MRI; nuclear medicine; 125 I-fribinogen scan
Differential diagnosis – muscle aches; muscle/tendon strain; fibromyalgia; cellulitis; thrombophlebitis; achilles tendonitis; calf strain; intermittent claudication; arthritis; haematoma; referred pain; varicose veins; ruptured Bakers cyst; lymphedoema; varicose veins.
Treatment:
Emergency treatment – aim is to prevent pulmonary embolism --> anticoagulation (heparin); thrombolytic therapy (stretokinase); compression stockings; surgery (thromboectomy) when anticoagulant is ineffective or can’t be used.
Does This Patient Have Deep Vein Thrombosis?
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