In Reply:—

We appreciate the interest of Drs. Stöllberger and Finsterer regarding our article, and we thank the Editor for the opportunity to reply to their remarks. Small echogenic findings were not stained with Sudan or Giemsa, so we can only speculate that they represented air or cold blood. The large echogenic findings were strongly suspected of being thrombi, on the basis of their inhomogeneous internal structure. Because echogenic materials were observed in all patients subjected to basically the same operational procedure, they were not considered artifacts. We considered small materials, 2.33 mm (inner diameter of the central catheter) or less, to be air or cold blood. In the tourniquet group, both two patients who had previously undergone total hip arthroplasty in ipsilateral leg showed no echogenic findings during tourniquet inflation. It is impossible to avoid generation of the echogenic materials observed after each manipulation, because they could directly flow from the drainage vein to the inferior vena cava. In the recovery room, cardiopulmonary function returned to its preoperative state in all patients, so we simply observed patients. But we relied on perfusion lung scans in all patients (n = 4) with a postoperative decrease in Pao2. Hagen et al.  reported a patent foramen or atrial septal defect in approximately 27% of individuals, but no atrial septal defects was detected by color flow Doppler in any patient in our study. 1The considerable increase in right atrial and pulmonary artery pressure favored right-to-left shunt flow via  atrial septal defect, but in the one patient in whom large, grade 3 echogenic materials were detected and atrial septum bulged toward the left atrium, we found no echogenic materials in the left atrium. Considering reports that emboli reduce the cross-sectional area of the pulmonary arterial bed by at least 40% to produce hemodynamic changes, we agree with the hypothesis that these phenomena may have been caused not only by mechanical obstruction but also by vasoconstriction of the pulmonary vasculature due to the release of neurohumoral substances, such as serotonin released from platelets adhering to the embolus. 2,3We consider that other factors (e.g. , inflow of bone marrow components and cement monomer) to the systemic circulation and limited mobility in the ward can also lead to activation of the clotting cascade. We think that venous thromboembolism formation can be easily avoided without tourniquet inflation. A high risk of blood transfusion is the only drawback to this method. The most important preventive measure is to be aware of the possibility of this complication, so the real-time investigation, safety, portability, and reproductivity of the evidence provided by transesophageal echocardiography in the operating room offer advantages over the standard technetium-99m lung scans and angiography diagnostic techniques. Furthermore, transesophageal echocardiography is useful for the rapid diagnosis of paradoxical embolism.

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McIntyre KM, Sasahara AA: The hemodynamic response to pulmonary embolism in patients without prior cardiopulmonary disease. Am J Cardiol 1971; 28: 288–94
Malik AB: Pulmonary microembolism. Physiol Rev 1983; 63: 1114–207