Diagnosis of deep venous thrombosis. A prospective study comparing duplex scanning to contrast venography.

Duplex scanning has been proposed as a safe alternative to contrast venography for diagnosing deep venous thrombosis, but its accuracy has not been proved. In this prospective, double-blind study of 47 patients, the sensitivity and specificity of duplex scan criteria were determined relative to contrast venography for lower extremity deep venous thrombosis. Criteria considered to show the presence of deep venous thrombosis included visualization of thrombus (T), absence of spontaneous flow by Doppler ultrasonography (F), absence of phasicity of flow with respiration (P), and incompressibility of the vein with probe pressure (VC). When analyzed individually, the variables T and F had low sensitivities (50% and 76%) but high specificities (92% and 100%). VC had low values for both (79% and 67%, respectively). The best single variable was P (sensitivity and specificity = 92%). The best combinations of variables were T+P (sensitivity = 95%, specificity = 83%), T+F+P (sensitivity = 95%, specificity = 83%), F+P (sensitivity and specificity = 92%), and F+T (sensitivity = 92%, specificity = 87%). The low specificity of vein incompressibility was secondary to cases in which normal veins were difficult to compress in the thigh. All false-negative cases were from isolated calf vein thrombi. We conclude that isolated criteria from duplex scanning should not be used to diagnose deep venous thrombosis. In cases of suspected calf vein thrombosis, repeat duplex examination should be obtained in 3-4 days to determine the most appropriate therapy. In equivocal cases of proximal vein thrombosis, a contrast venogram should be obtained.

Spontaneous lysis of deep venous thrombi: rate and outcome.

Ultrasonic duplex scanning was used to study the rates at which lysis of thrombi, valvular incompetence, and symptoms of the postthrombotic syndrome (edema) developed in 21 patients after deep venous thrombosis (DVT). Lysis of thrombi occurred rapidly in most patients. In 11 of 21 patients (53%), recanalization occurred in all segments by 90 days after presentation. In four patients, extension of the initial DVT occurred between 30 and 180 days, despite treatment with warfarin. Valvular incompetence developed in 13 patients during the study period. The number of patent venous segments with incompetent valves increased from the initial presentation to 180 days, at which time 25% of patent segments contained incompetent valves. Valvular incompetence developed in previously thrombosed segments that were initially competent after recanalization and in segments not previously thrombosed. This suggested that although incompetence may occur as a result of a direct effect of the thrombus on the valve, other mechanisms must also be involved. Patients with edema early after DVT (from 7 to 30 days) were more likely to have residual occlusion than valvular incompetence. The late development of edema (from 90 to 270 days) was more closely correlated with valvular incompetence.

Progression of lower-extremity arterial occlusive disease in type II diabetes mellitus.

The prevalence of lower-extremity arterial occlusive disease (LEAOD), the progression of LEAOD, and the incidence of new LEAOD were determined by noninvasive method in 410 volunteers between the ages of 50 and 70 yr; 252 individuals had type II (non-insulin-dependent) diabetes, 158 were control subjects. LEAOD was monitored with the ankle/arm systolic blood pressure index in combination with Doppler arterial velocity waveform analysis. LEAOD was much more prevalent in the type II patients (22%, 55 of 252) than in the control subjects (3%, 4 of 158) (P less than .00001). The prevalence of risk factors for LEAOD was much higher in the type II patients, including elevated triglyceride, depressed high-density lipoprotein (HDL) cholesterol, hypertension, smoking, and elevated systolic blood pressure. In type II diabetic patients the incidence of new LEAOD over a 2-yr period (14%, 28 of 197) was lower than the incidence of LEAOD progression (87%, 45 of 52). Type II patients with LEAOD also had a high incidence of mortality (22%, 12 of 55) compared with those without LEAOD (4%, 8 of 197) (P less than .0005). A risk score including smoking history, duration of diabetes, depressed HDL cholesterol, total cholesterol, elevated systolic blood pressure, and low obesity index is related to LEAOD. After accounting for the effect of all of the risk factors, we suggest that type II diabetes contributes additional risk for LEAOD.

Identification of mycobactins by nuclear-magnetic-resonance spectroscopy.

Details are given of the n.m.r. spectra of mycobactins F, H, M, N, P, S and T, and resonances are ascribed to all the protons in these molecules. A simplified system is described for identifying known mycobactins by the n.m.r. spectrum alone. This method will not distinguish mycobactins S and T, whose nuclei differ only in the configuration at an asymmetric centre.