Abstract
Introduction:
Although the risk of pulmonary embolism (PE) or other embolic events associated with total joint arthroplasty have been recorded for some time, to date no direct means of these events in human arthroplasty have reported. This prospective study was designed to clarify the pathophysiologic mechanism of PE after total knee arthroplasty (TKA).
Methods:
Nine patients fulfilling the following selection criteria were included in this prospective study: diagnosis of osteoarthosis, age 60 to 75 years, cemented primary TKA. All patients had a baseline pulmonary perfusion scan 2 days prior to the surgery. TKA was performed in the standard manner under general anesthesia. Monitoring of the heart chambers during the course of the TKA was performed using a 5 MHz ultrasonic transducer placed into the esophagus. The 4-chamber view plane of the heart was then imaged using a 2-dimensional echocardiography. A tip of the catheter inserted from the contralateral femoral vein was also placed in the inferior vena cava to harvest the venous blood flowed from the suffered lower extremity before and after tourniquet release. All patients had pulmonary perfusion scans 3 hours after TKA and on the 21st postoperative day. The ventilation-perfusion scan was compared with the baseline perfusion scan.
Results:
No symptomatic PE were identified. Using transesophageal echocardiographic monitoring, the heaviest flow of embolic particles in the right heart was observed 2 seconds after tourniquet release and lasted approximately 30 seconds. By squeezing the calf muscle, the heavy flow of embolic particles was again observed. The venous blood harvested through the catheter after tourniquet release had fat droplets and white coagula. All of patients had pulmonary perfusion defects 3 hours after TKA, but no pulmonary perfusion defects on the 21st postoperative day.
Discussion and Conclusions:
Substantial amounts of embolic materials were seen in the right heart using transesophageal echocardiography in patients operated in the standard manner. It was demonstrated that these embolic materials consisted of fat droplets and white coagula. We also demonstrated that many embolic materials for PE and/or DVT originated in the calf. All of patients had pulmonary perfusion defects just after TKA. It was concluded that all of the patients who underwent TKA had asymptomatic PE just after the surgery. Therefore, all of the patients have a possibility of symptomatic PE just after TKA.
