Todd O. McKinley

Complications of Locking Plate Fixation in Complex Proximal Tibia Injuries

Objectives: To report the complications and pitfalls in the treatment of complex injuries of the proximal tibia when locking plates are used. Design, Setting, and Patients: This was a retrospective case series conducted at a university Level I trauma center. Thirty-seven patients with complex proximal tibia fractures (41C1, 41C2, 41C3, 41A2, 42A2) were treated with locking plates. Intervention: All fractures were treated with locking plates (Less Invasive Stabilization System (LISS); Synthes, Paoli, PA). Main Outcome Measurements: Healing, alignment, infection, and other complications. Results: Twelve fractures (32%) healed without any complications. Eight patients (22%) developed deep infections that required operative debridements, and 5 of them had a hardware removal; 1 eventually required an above-knee amputation. Eight cases (22%) had postoperative malalignment, with hyperextension as the most common deformity. Three cases (8%) had loss of alignment into varus during healing. Other complications were 1 superficial wound dehiscence, 1 delayed soft-tissue breakdown, 4 hardware irritations, 1 peroneal nerve injury at the distal part of a 9-hole plate, 1 tibial tubercle nonunion, and 1 postoperative compartment syndrome. Conclusion: The complication rate, particularly infection, was higher than in previous reports. Other complications such as hardware prominence, malalignment, and loss of alignment were similar to those of historical controls. Some of the complications may reflect the techniques that were used and should decrease with more experience; however, some may be inherent in the treatment of high-energy fractures using locking plates.

Kinematic and contact stress analysis of posterior malleolus fractures of the ankle.

Objective: To determine if there are measurable dynamic contact stress aberrations and kinematic abnormalities (instability) that have not been observed in conventional static loading studies of posterior malleolar ankle fractures. Design: Cadaveric fracture model. Setting: Biomechanics laboratory. Intervention: Seven fresh cadaveric specimens were fixed in an unconstrained testing apparatus and loaded to one body weight. The ankle was moved from 25° of plantarflexion to 15° of dorsiflexion. The model included the intact ankle and four fracture simulations (50% fracture without internal fixation, 2 mm gap and step malreductions, and anatomically fixed). Main Outcome Measure: Motion at the ankle was monitored with an electromagnetic tracking device, and intra-articular contact stresses were measured using a real-time stress sensor. Results: There were no kinematic abnormalities suggestive of tibiotalar subluxation in any of the fracture simulations. There was no increase in peak contact stress in any of the fracture models compared with the unfractured model. However, there was a shift in the location of the contact stresses to a more anterior and medial location following the fracture. When summed over the range of motion, these areas of cartilage bore significantly higher cumulative contact stresses relative to the nonfracture situation. Conclusions: We found no talar subluxation and no increase in contact stresses near the articular incongruity, making it unlikely that these factors explain the increased incidence of arthrosis after trimalleolar fractures (OTA/AO classification 44 B3 fractures). Rather, we found that the joint remaining bears increased stress and that the center of stress shifts anteriorly, loading cartilage that normally sees little load.

N-Acetylcysteine Inhibits Post-Impact Chondrocyte Death in Osteochondral Explants

BACKGROUND Chondrocyte death has been linked to injury-induced oxidative damage, suggesting that antioxidants could substantially improve viability. However, since reactive oxygen species play roles in normal physiology, there are concerns that antioxidants may have deleterious side effects. To address these issues, we studied the effects of N-acetylcysteine, a potent free radical scavenger, on chondrocyte viability and cartilage proteoglycan content in an in vitro cartilage injury model. We hypothesized that treatment with N-acetylcysteine soon after an impact injury would have significant chondrocyte-sparing effects and would prevent injury-induced proteoglycan losses. METHODS Bovine osteochondral explants were subjected to a single impact load with use of a drop-tower device. Chondrocyte viability was measured at multiple time points post-impact with use of fluorescent probes and confocal microscopy. Forty-eight hours after impact, the effects on viability of immediate post-impact treatment with N-acetylcysteine were compared with the effects of the caspase inhibitor N-CBZ-Val-Ala-Asp(O-Me) fluoromethyl ketone and those of the cell-membrane-stabilizing surfactant poloxamer 188. The effect of N-acetylcysteine on proteoglycan content was determined at seven and fourteen days post-impact. RESULTS Chondrocyte viability declined sharply within an hour and reached a steady state within six to twelve hours after impact. Immediate treatment with N-acetylcysteine doubled the number of viable chondrocytes assayed forty-eight hours after impact, and this effect was significantly greater than that of N-CBZ-Val-Ala-Asp(O-Me) fluoromethyl ketone. Even when N-acetylcysteine treatment was delayed for up to four hours after injury, it still had significant positive effects on cell viability at forty-eight hours. Moreover, N-acetylcysteine treatment significantly improved proteoglycan content at the impact sites at both seven and fourteen days after injury. CONCLUSIONS Treatment with N-acetylcysteine soon after a blunt impact injury can reduce chondrocyte death and proteoglycan loss measured seven to fourteen days after injury.

Percutaneous reduction and fixation of displaced intra-articular calcaneus fractures.

Objectives: The purpose of this study is to assess the initial results of percutaneously reducing and fixing calcaneus fractures compared with a concurrent control group that was openly reduced and internally fixed through an extensile lateral approach. Design: Retrospective cohort study, consecutive series. Setting: Level I trauma center. Patients/Participants: One hundred twenty patients with 125 intra-articular calcaneus fractures were selected as a consecutive series with treatment method randomized by surgeon and time of presentation. Intervention: Patients treated with open reduction and internal fixation (OR group) had an extended lateral approach and fractures were fixed with plates and screws. Patients treated with percutaneous reduction (PR group) had small incisions with indirect fragment manipulation, and the reduction achieved was secured with screws alone. Main Outcome Measurement: Clinical and radiographic assessment. Results: There were 41 patients with 42 fractures in the OR group and 79 patients with 83 fractures in the PR group. There were no significant differences in sex, age, open fractures, fracture classification, or initial Bohlers angle between the two groups. Bohlers angle was improved after surgery by an average of 22.4° in the OR group and 25.3° in the PR group (P = 0.31). The average loss of reduction at healing (minimum 4 months postoperatively) was not significantly different between the two groups. Deep infection occurred in six of 42 of the OR group and zero of 83 of the PR group (P = 0.002). The incidence of minor wound complications was nine of 42 in the OR group and five of 83 in the PR group (P = 0.03). The need for late subtalar fusions (two of 26 and three of 41 with full 2-year follow-up) and implant removal (five of 42 and 10 of 83) was not significantly different. Conclusions: The results of this study suggest that in comparison to open reduction, this method of percutaneously reducing and fixing calcaneus fractures minimizes complications and achieves and maintains extra-articular reductions as well as the standard extensile open reduction and internal fixation. Further study of this technique is warranted. This should include assessment of articular reduction and longer follow-up of a larger number of patients.

Incongruity versus instability in the etiology of posttraumatic arthritis.

The etiology of posttraumatic arthritis is understood poorly but it clearly has a pathomechanical component. Posttraumatic arthritis likely results from irreversible cartilage damage sustained at the time of injury and chronic cartilage overloading resulting from articular incongruity and instability. However, the relative importance of instability and incongruity is unknown. Clinical studies show that the hip, knee, and ankle tolerate incongruity differently. However, all three joints poorly tolerate instability. Basic mechanical studies have shown that static loading of articular surface incongruities have caused relatively modest increases in contact pressure. However, static testing poorly replicates normal viscoelastic properties of cartilage, which may mask important transient stress elevations that occur during motion. Static tests also ignore potential abnormal loads that may accumulate throughout a motion cycle. We review the clinical and basic scientific evidence linking incongruity and instability to posttraumatic arthritis. Preliminary data from a newly developed dynamic ankle testing device are presented. Dynamic testing allows measurement of transient contact loads and loading rates that occur through the entire motion cycle and it opens the door to measure mechanical abnormalities associated with instability.

Basic science of intra-articular fractures and posttraumatic osteoarthritis.

Intra-articular fractures represent the primary etiologic factor leading to posttraumatic osteoarthritis. The pathomechanisms linking intra-articular fractures to end-stage cartilage destruction are poorly understood. However, fracture-related chondrocyte death has been linked to posttraumatic osteoarthritis. Researchers have made significant progress in understanding the pathomechanical link between injury and chondrocyte death. This article reviews recent basic scientific progress investigating intraarticular fractures and fracture-related chondrocyte death and dysfunction.

Instability Dependency of Osteoarthritis Development in a Rabbit Model of Graded Anterior Cruciate Ligament Transection

BACKGROUND Joint instability has long been empirically recognized as a leading risk factor for osteoarthritis. However, formal mechanistic linkage of instability to osteoarthritis development has not been established. This study aimed to support a clinically accepted, but heretofore scientifically unproven, concept that the severity and rapidity of osteoarthritis development in unstable joints is dependent on the degree of instability. In a survival rabbit knee model of graded joint instability, the relationship between the magnitude of instability and the intensity of cartilage degeneration was studied at the organ level in vivo. METHODS Sixty New Zealand White rabbits received either complete or partial (medial half) transection of the anterior cruciate ligament or sham surgery (control) on the left knee. At the time that the animals were killed at eight or sixteen weeks postoperatively (ten animals for each treatment and/or test-period combination), the experimental knees were subjected to sagittal plane stability measurement, followed by whole-joint cartilage histological evaluation with use of the Mankin score. RESULTS Sagittal plane instability created in the partial transection group was intermediate between those in the complete transection and sham surgery groups. The partial and complete transection groups exhibited cartilage degeneration on the medial femoral and/or medial tibial surfaces. The average histological score (and standard deviation) for the medial compartment in the partial transection group (2.9 ± 0.9) was again intermediate, significantly higher than for the sham surgery group (1.9 ± 0.8) and significantly lower than for the complete transection group (4.5 ± 2.3). The average histological scores for the medial compartment in the partial transection group correlated significantly with the magnitude of instability, with no threshold effect being evident. The significance level of alpha was set at 0.05 for all tests. CONCLUSIONS The severity of cartilage degeneration increased continuously with the degree of instability in this survival rabbit knee model of graded instability.

Trabecular bone strain changes associated with subchondral stiffening of the proximal tibia

Subchondral stiffening is a hallmark pathologic feature of osteoarthritis but its mechanical and temporal relationship to the initiation or the progression of osteoarthritis is not established. The mechanical effect of subchondral stiffening on the surrounding trabecular bone is poorly understood. This study employs a relatively new application of digital image correlation to measure strain in the trabecular region of the proximal medial tibia in normal specimens and in specimens with simulated subchondral bone stiffening. Coronal sections from eight normal human cadaveric proximal tibiae were loaded in static compression and high resolution contact radiographs were made. Repeat contact radiographs were collected after the subchondral bone near the jointline was stiffened using polymethylmethacrylate. Digital images, made from loaded and unloaded contact radiographs, were compared using in-house software to measure trabecular displacement and calculate trabecular bone strain. Overall strain was higher in the stiffened specimens suggesting experimental artifiact significantly affected our results. Consistent increases in median maximum shear strain, median maximum principal strain, median minimum principal strain, and peak shear strain were measured near the inner and outer edges of the stiffened segment. Our experiment provides direct experimental measurement of increases in trabecular bone strain caused by subchondral stiffening, however, the clinical and biologic importance of strain increases is unknown.

Correlation of dynamic cartilage contact stress aberrations with severity of instability in ankle incongruity.

Joint instability is presumed to cause abnormality in cartilage contact mechanics, which accumulatively damages the articular surface, leading to osteoarthritis. The purpose of this study was to clarify the effect of instability on dynamic cartilage contact mechanics. Using human ankle cadaver specimens, potentially unstable ankles were modeled by introducing a coronally directed step‐off incongruity of the anterior tibial surface and/or by transecting the anterior talofibular ligament. Specimens were subjected to a duty cycle with quasi‐physiologic stance‐phase motion and loading. AP tibial forces were modulated, causing a controlled, quantifiable ankle subluxation during the duty cycle. Instantaneous changes in local articular contact stresses were continuously measured using a thin, flexible pressure transducer. Tests were repeated while varying the tibial surface condition (anatomic, 1‐mm step‐off, and 2‐mm step‐off), both before and after transection of the anterior talofibular ligament, with various AP force magnitudes, so that situations of various degrees of instability were created for each specimen. Instability events occurred when the step‐off incongruity was introduced, with the abnormality in joint kinematics being greater after ligament transection. Contact stress data revealed that these instability events involved distinctly abrupt increases/decreases in local articular contact stresses, and that the degree of abruptness was correlated nearly linearly with the abnormality in kinematics. The severity of contact stress aberration appeared to be correlated with the degree of instability. Given this linear relationship, even small instability events presumably involve appreciable abnormality in dynamic joint contact mechanics.

Mitochondrial electron transport and glycolysis are coupled in articular cartilage

OBJECTIVE Although the majority of the adenosine triphosphate (ATP) in chondrocytes is made by glycolysis rather than by oxidative phosphorylation in mitochondria there is evidence to suggest that reactive oxygen species produced by mitochondrial electron transport (ET) help to maintain cellular redox balance in favor of glycolysis. The objective of this study was to test this hypothesis by determining if rotenone, which inhibits ET and blocks oxidant production inhibits glycolytic ATP synthesis. DESIGN Bovine osteochondral explants were treated with rotenone, an ET inhibitor; or oligomycin an ATP synthase inhibitor; or 2-fluoro-2-deoxy-D-glucose, a glycolysis inhibiter; or peroxide, an exogenous oxidant; or mitoquinone (MitoQ), a mitochondria-targeted anti-oxidant. Cartilage extracts were assayed for ATP, nicotine adenine dinucleotide (NAD+/H), and culture medium was assayed for pyruvate and lactate after 24 h of treatment. Imaging studies were used to measure superoxide production in cartilage. RESULTS Rotenone and 2-FG caused a significant decline in cartilage ATP (P < 0.001). In contrast, ATP levels were not affected by oligomycin. Peroxide treatment blocked rotenone effects on ATP, while treatment with MitoQ significantly suppressed ATP levels. Rotenone and 2-FG caused a significant decline in pyruvate, but not in lactate production. NADH:NAD+ ratios decreased significantly in both rotenone and 2-FG-treated explants (P < 0.05). Rotenone also significantly reduced superoxide production. CONCLUSIONS These findings showing a link between glycolysis and ET are consistent with previous reports on the critical need for oxidants to support normal chondrocyte metabolism. They suggest a novel role for mitochondria in cartilage homeostasis that is independent of oxidative phosphorylation.