Pulmonary embolism after hip or knee replacement: postoperative changes on pulmonary scintigrams in asymptomatic patients

Serial pulmonary imaging has proved to be effective in the evaluation of patients undergoing total joint arthroplasty. A clinical dilemma arises in asymptomatic patients whose postoperative pulmonary images differ from the preoperative images. The authors prospectively evaluated 403 patients with serial imaging to determine the significance of changed postoperative images in asymptomatic patients undergoing total hip or knee arthroplasty. Twenty-two (5.5%) patients had significant changes on postoperative images. Seventeen were asymptomatic; all but one underwent pulmonary angiography. Documented pulmonary emboli were demonstrated in 100% of patients whose postoperative images changed to indicate a high probability of pulmonary embolism, 71% whose images changed to a moderate probability, and 0% whose images changed to indeterminate probability. Overall, pulmonary emboli occurred in 76% of all asymptomatic patients with significantly change postoperative images. Asymptomatic pulmonary embolism is a significant occurrence after total hip or knee repair, and a changed lung scan with appropriate clinical evaluation is an accurate indicator of pulmonary emboli in asymptomatic postarthroplasty patients.     

Osteomyelitis: detection with US

To evaluate the role of ultrasound (US) in the detection of osteomyelitis, the authors prospectively studied 48 patients clinically suspected of having osteomyelitis. A sonographic diagnosis was made if fluid was seen directly in contact with bone, without intervening soft tissues. Twelve of the 48 patients were subsequently found to have osteomyelitis. In 10 of them, US demonstrated abnormal fluid adjacent to the bone. This fluid was thought to represent an inflammatory exudate dissecting in a subperiosteal and/or extraperiosteal location. Eight of the 48 patients had soft-tissue fluid collections. The rest of the patients either had no abnormalities or had cellulitis. The authors conclude that US can be useful in the detection of osteomyelitis.     

Biological and Biomechanical Evaluation of Autologous Tendon Combined with Ligament Advanced Reinforcement System Artificial Ligament in a Rabbit Model of Anterior Cruciate Ligament Reconstruction

Objective

To compare the biomechanical and histological changes in a rabbit model after reconstructing the anterior cruciate ligament (ACL) with solely autologous tendon and with autologous tendon combined with the ligament advanced reinforcement system (LARS) artificial ligament.

Methods

Anterior cruciate ligament reconstruction was performed in 72 knees from 36 healthy New Zealand white rabbits (bodyweight, 2500–3000 g). The Achilles tendons were harvested bilaterally. The left ACL were reconstructed solely with autografts (autologous tendon group), while the right ACL were reconstructed with autografts combined with LARS ligaments (combined ligaments group). The gross observation, histological determination, and the tension failure loads in both groups were evaluated at 12 weeks (n = 18) and 24 weeks (n = 18) postoperatively.

Results

Gross examination of the knee joints showed that all combined ligaments were obviously covered by a connective tissue layer at 12 weeks, and were completely covered at 24 weeks. Fibrous tissue ingrowth was observed between fascicles and individual fibers in the bone–artificial ligament interface at both time points; this fibrovascular tissue layer localized at the bone–artificial ligament interface tended to be denser in specimens obtained at 24 weeks compared with those obtained at 12 weeks. The tension failure loads of the knees were similar in the autologous tendon group and the combined ligaments group at 12 weeks (144.15 ± 3.92 N vs. 140.88 ± 2.75 N; P > 0.05), and at 24 weeks (184.15 ± 1.96 N vs. 180.88 ± 3.21 N; P > 0.05).

Conclusion

Reconstructing the ACL in rabbits using autologous tendon combined with the LARS artificial ligament results in satisfactory biointegration, with no obvious immunological rejection between the autologous tendon and the artificial ligament, and is, therefore, a promising ACL reconstruction method.

     

Studies on the mechanism of bacterial resistance to complement-mediated killing. II. C8 and C9 release C5b67 from the surface of salmonella minnesota S218 because the terminal complex does not insert into the bacterial outer membrane

The mechanism for consumption of terminal complement components and release of bound components from the surface of serum-resistant salmonella minnesota S218 was studied. Consumption of C8 and C9 by S218 occurred through interaction with C5b67 on the bacterial surface because C8 and C9 were consumed when added to S218 organisms previously incubated in C8-deficient serum and washed to remove all C5b67 on the bacterial surface because C8 and C9 were consumed when added to S218 organisms previously incubated in C8- deficient serum and washed to remove al but cell bound C5b67. Rapid release of (125)I C5 and (125)I C7 from the membrane of S218 was dependent on binding of C8 because (125)I C5 and (125)I C7 deposition in C8D serum was stable and was twofold higher in C8D than in PNHA, and addition of purified C8 or C8 and C9 to S218 previously incubated in C8D serum caused rapid release of (125)I C5 and (125)I C7 from the organism. Analysis by sucrose density gradient ultracentrifugation of the fluid phase from the reaction of S218 and 10 percent PNHS revealed a peak consistent with SC5b-9, in which the C9:C7 ratio was 3.3:1, but the NaDOC extracted bound C5b-9 complex sedimented as a broad peak with C9:C7 of less than 1.2:1. Progressive elution of C5b67 and C5b-9 from S218 but not serum-sensitive S. minnesota Re595 was observed with incubation in buffers of increasing ionic strength. Greater than 90 percent of the bound counts of (125)I C5 or (125)I C9 were released from S218 by incubation in 0.1 percent trypsin, but only 57 percent of (125)I C9 were released by treatment of Re595 with trypsin. These results are consistent with the concept that C5b-9 forms on the surface of the serum-sensitive S. minnesota S218 in normal human serum, but the formed complex is released and is not bactericidal for S218 because it fails to insert into hydrophobic outer membrane domains.