Quantitative assessment of the midcarpal shift test.

The subjective, clinical midcarpal shift test was compared with a quantitative measurement of carpal volar/dorsal translation versus ulnar deviation using a mechanical testing system. Testing was performed on 19 healthy volunteers (mean age, 33 years) and 3 patients (four wrists; mean age, 23 years) who had been diagnosed with ulnar midcarpal instability, a nondissociative form of carpal instability. During physical examination, each subject's wrist was graded I to V using the previously described classification of the degree of laxity and clunk observed with the midcarpal shift test. Each subject was also evaluated using a quantitative mechanical testing system that simulates the subjective clinical test. The testing system measures displacement of the distal carpal row, more specifically, the capitate, as the wrist is moved from neutral to ulnar deviation under a constant axial load of 44 N directed volarly at the head of the capitate. Reflective markers were attached to the skin above the proximal and distal ends of the third metacarpal and at the point where the 44-N load was applied to the carpus. Motion of the markers was used to calculate ulnar deviation and dorsal/volar translation of the carpus. The maximum slope of the carpal translation versus ulnar deviation curve was measured for each subject and compared with the results of the clinical midcarpal shift test. Higher maximum slopes were seen in subjects with the higher grades of carpal laxity. There were also differences with regard to the point at which the clunk occurred; the higher the clinical grade of laxity, the greater the ulnar deviation of the wrist at the point at which the clunk was observed. These differences were not significant, however. These data confirm the validity of the clinical test and establish its usefulness as a diagnostic indicator of midcarpal nondissociative carpal instability. The mechanized test also may be useful as a biomechanical marker, enabling the results of ligament sectioning to be effectively compared with defined clinical laxity.

Anatomic alignment of the patellar groove.

The variability in alignment of the natural patellar groove was determined about various anatomic axes of the femur, using 3 plane radiographs and electronic digitization. After the patellar groove was identified and marked on 15 anatomic specimen femurs, radiographs were taken in the coronal, sagittal, and transverse planes so that principal anatomic axes could be outlined. Through electronic digitization, a 3-dimensional representation of the patellar groove was constructed about the distal anatomic axis, mechanical axis, transepicondylar axes, and transcondylar axes. Regarding these 4 principal anatomic axes, the variability in orientation of the patellar groove was profound in both coronal and transverse planes, typically involving a range of 11 degrees to 16 degrees about the mean. The average orientation most closely approximated the perpendicular to the transepicondylar axis in the coronal plane; however, the range varied extensively. None of the anatomic axes tested proved reliable as a reference axis for proper position of the patellar groove, and this study shows that the orientation of the natural patellar groove is more variable than previously suspected. The failure of femoral components to accommodate this variability may explain many complications associated with the patellar component in total knee arthroplasty.

The production of experimental cholecystitis by endotoxin.

Acute acalculous cholecystitis (AAC) is a severe inflammatory disorder of the gallbladder. It occurs primarily in patients acutely ill from other disorders and is related to sepsis and shock. We previously found that platelet-activating factor (PAF), a phospholipid autacoid purported to be a mediator of the shock response, produced AAC. This study was performed to determine the effect of intravenous lipopolysaccharide (LPS) on feline gallbladders. Anesthetized cats underwent LPS administration with and without administration of a cyclooxygenase inhibitor and PAF antagonist. Gallbladder inflammation was evaluated by quantitation of luminal water transport and tissue myeloperoxidase levels. In an attempt to understand the mechanisms of the response, gallbladder perfusate and tissue prostanoid and PAF levels were quantitated as were serum PAF levels. LPS administration resulted in alteration of the normal absorptive pattern of the gallbladder mucosa to exsorption of fluid into the gallbladder lumen, increased tissue myeloperoxidase levels and increased serum PAF levels. This was associated with increased gallbladder tissue and perfusate prostanoid levels and increased perfusate PAF levels. Indomethacin prevented the pro-inflammatory changes in the gallbladder produced by LPS. The PAF antagonist, alprazolam, increased gallbladder prostanoid production when administered alone and with LPS. The administration of LPS resulted in the production of acute changes in the gallbladder consistent with cholecystitis. These changes being prevented by a cyclooxygenase inhibitor suggests that development of AAC may be related to the release of systemic and local pro-inflammatory substances.