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Objective. Alkaptonuria is a genetic disorder of tyrosine metabolism, resulting in elevated circulating concentrations of homogentisic acid. Homogentisic acid is deposited as a polymer, termed ochronotic pigment, in collagenous tissues, especially cartilages of weightbearing joints, leading to a severe osteoarthropathy. We undertook this study to investigate the initiation and progression of ochronosis from the earliest detection of pigment through complete joint failure.Methods. Nine joint samples with varying severities of ochronosis were obtained from alkaptonuria patients undergoing surgery and compared to joint samples obtained from osteoarthritis (OA) patients. Samples were analyzed by light and fluorescence microscopy, 3-dimensional scanning electron microscopy (SEM), and the quantitative backscattered electron mode of SEM. Cartilage samples were mechanically tested by compression to determine Young's modulus of pigmented, nonpigmented, and OA cartilage samples.Results. In alkaptonuria samples with the least advanced ochronosis, pigment was observed intracellularly and in the territorial matrix of individual chondrocytes at the boundary of the subchondral bone and calcified cartilage. In more advanced ochronosis, pigmentation was widespread throughout the hyaline cartilage in either granular composition or as blanket pigmentation in which there is complete and homogenous pigmentation of cartilage matrix. Once hyaline cartilage was extensively pigmented, there was aggressive osteoclastic resorption of the subchondral plate. Pigmented cartilage became impacted on less highly mineralized trabeculae and embedded in the marrow space. Pigmented cartilage samples were much stiffer than nonpigmented or OA cartilage as revealed by a significant difference in Young's modulus.Conclusion. Using alkaptonuria cartilage specimens with a wide spectrum of pigmentation, we have characterized the progression of ochronosis. Intact cartilage appears to be resistant to pigmentation but becomes susceptible following focal changes in calcified cartilage. Ochronosis spreads throughout the cartilage, altering the mechanical properties. In advanced ochronosis, there is aggressive resorption of the underlying calcified cartilage leading to an extraordinary phenotype in which there is complete loss of the subchondral plate. These findings should contribute to better understanding of cartilage-subchondral interactions in arthropathies.

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We have developed an in vitro model of ochronosis that should contribute to understanding joint destruction in AKU and to the aetiology of OA.

While the majority of AFX presentations are benign, there is a real possibility of metastatic spread. Invasion beyond the dermis and a rapid rate of recurrence are suggestive of a more aggressive clinical course.

Postoperative wound infection, most often with, is of ubiquitous concern in surgical practice, occurring in an average of 1.5 to 5 percent of all procedures. The antimicrobial properties of local anesthetics have been documented over the past 25 years by in vitro studies. This study evaluates the effects of lidocaine preparations on in an in vivo setting. In a wound infection model using live albino guinea pigs, inoculum was introduced for the reproducible bacterial colonization of clean surgical wounds. One of two sites on the dorsum of each animal was infiltrated with a commercial lidocaine preparation (with and without epinephrine) prior to inoculation with (10 cfu/ml). The other site, inoculated with without preinfiltration with lidocaine, served as the control. Cultures from the sites treated with lidocaine were then compared with cultures from the control sites. All control sites had a consistent presence >or=10 cfu/ml, the threshold for bacterial inhibition of wound healing. Infiltration of the wound with 2 ml of 2% lidocaine prior to inoculation was associated with an average decrease in bacterial count of >70 percent ( n= 19). On the other hand, the addition of epinephrine (1:100,000) to lidocaine was associated with a 20-fold in bacterial counts compared with control values ( n= 10). This is the first study to demonstrate inhibition of by a local anesthetic agent in an in vivo model of a surgical wound. This information suggests a possible role for local anesthetics in prophylaxis against surgical wound infection.

No abstract

Purpose We conducted a retrospective review following concerns involving a suspected increase in the requirement for surgical re-exploration for hematoma evacuation when ketorolac was administered perioperatively in patients undergoing reduction mammoplasty. Methods Following ethics approval, a retrospective chart review was conducted of all patients who underwent reduction mammoplasty at our two institutions from the time ketorolac became available in 2004 until surgeons requested its use discontinued in 2007. The data we collected included patient demographics, ketorolac administration, requirement for surgical re-exploration, documented hematoma formation not requiring surgical re-exploration, and excessive bleeding in the perioperative period. Three hundred and seventy-nine patient records were reviewed; 127 of the patients received a single intravenous dose of ketorolac (15 or 30 mg), and 252 of the patients did not receive ketorolac.Results Patients who received ketorolac were at an increased risk of requiring surgical re-exploration for hematoma evacuation (relative risk [RR] = 3.6; 95% confidence interval [CI], 1.4 to 9.6) and hematoma formation not requiring re-exploration (RR = 2.2; 95% CI,