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Fracture healing, a critical and complex biological process, often presents challenges in clinical practice with the current standards failing to fully address the medical needs for rapid and effective recovery. In this work, a localized cold therapy is investigated as an alternative approach to expedite bone healing. We hypothesized that optimized cold application can enhance bone healing within a fracture model by inducing hypoxia, leading to accelerated angiogenesis along with improved osteogenesis. A short, localized cold exposure is directly applied to the fracture site over a 4-week period in a mouse fracture model, aiming to assess its impact on bone formation through mechanisms of angiogenesis and osteogenesis. Our results revealed a significantly greater volume of new bone tissue and enhanced vascularity at the fracture site in the cold-treated group compared with controls. Calcified tissue histology analysis showed that the accelerated callus maturation and development of the vascular network following cold exposure were associated with an activity increase of alkaline phosphatase and transient receptor potential vanilloid 1. These biological changes were accompanied by a hypoxic environment induced during cold therapy. The study provides compelling evidence supporting the efficacy of intermittent cold therapy in accelerating fracture healing. These promising results highlight the need for further research in larger-scale studies and diverse fracture models, underlining the potential of cold therapy as a novel, noninvasive treatment strategy in orthopedic care.
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Compartment syndrome (CS) occurs in several clinical scenarios. Reperfusion injury and tissue swelling are common causes. This can occur after trauma but also is seen post revascularization of extremities. CS is a difficult diagnosis to make in a timely fashion that avoids permanent tissue damage. The treatment for CS is immediate fasciotomy, but fasciotomy is not a complication-free procedure. Previous care pathways usually resulted in fasciotomy being performed in a disproportionate number of normal legs. These false positives and prophylactic releases are costly to the health system because of protracted hospital stays and increased surgery numbers. The desirable tool for surgeons would be one that decreases false positives and negatives while ensuring a diagnosis in a timely fashion with true positives. A new technology that allows continuous pressure monitoring seems to be the best aid to make a diagnosis. We present our experience in decreasing the time to diagnosis in a CS case post revascularization despite the neurological blockade.
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OBJECTIVES: Acute compartment syndrome is a devastating condition associated with lasting consequences or even death if not treated in a timely fashion. Current preclinical modeling is inadequate. Ideally a model should mimic human disease. There should be a trauma-induced reperfusion or direct muscle event that causes gradual increased pressure and is amenable to release with fasciotomy. We have attempted to reproduce this mechanism and outcome in a porcine model. METHODS: Anterior tibial musculature was injured with vascular occlusion plus exterior tourniquet crush or direct intracompartmental crush through balloon inflation. The injury was maintained for over 5 hours. At that time, the tourniquet or balloon was removed. The injuries were continuously monitored with an intramuscular continuous pressure sensor. Pressure changes were recorded and after 2 hours of postinjury observation, a fasciotomy was performed for the muscle compartment. RESULTS: Pressures were brought to 100 mm Hg during the injury phase. During the two-hour observation period, the balloon catheter technique achieved an average pressure of 25.1 ± SD 8.8 mm Hg with a maximum reading of 38.2 mm Hg and minimum reading of 14.1 mm Hg. During this same period, the ischemia-reperfusion + direct crush technique achieved an average pressure of 33.7 ± SD 7.3 mm Hg, with a maximum reading of 43.5 mm Hg and minimum reading of 23.5 mm Hg. Average pressure postfasciotomy for the balloon catheter technique was 2.4 ± SD 2.5 mm Hg; and for the crush technique, average value postfasciotomy was 4.9 ± SD 3.7 mm Hg-both representing a return to physiologic levels. CONCLUSION: This is the first preclinical model that shows the same response to injury and treatment as is observed in human physiology. Surgical and nonsurgical therapies for compartment syndrome can now be tested reliably.
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Síndromes Compartimentales , Humanos , Animales , Porcinos , Síndromes Compartimentales/etiología , Síndromes Compartimentales/cirugía , Fasciotomía , Tibia , PresiónRESUMEN
CASE: A 34-year-old man had an injury which resulted in pilon fracture and acute compartment syndrome of his forefoot. The case report describes the use of a novel minimally invasive dorsal approach for decompression of the lateral, central, medial, and interosseous compartments. The release was performed through multiple small incisions on the dorsal foot. The patient had complete relief with normal function of all muscle groups at 6 weeks and is now 18 months after surgery. He has returned to full activity. CONCLUSION: The successful decompression of the forefoot compartments through a percutaneous approach avoided known complications of muscle death, toe clawing, and secondary surgeries.
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Síndromes Compartimentales , Adulto , Síndromes Compartimentales/complicaciones , Síndromes Compartimentales/cirugía , Pie/cirugía , Humanos , MasculinoRESUMEN
BACKGROUND: Clinical case series have indicated that 1 or 2-compartment decompression of the anterior or lateral leg may be sufficient for release, but, currently, no cadaveric model has verified that approach. The objective of this study was to investigate the functional relationship between compartments by alternating sequences of infusion and fasciotomy release. METHODS: This study utilized multicompartment sequential pressurization with simultaneous monitoring by continuous pressure sensors to model compartment syndrome in a human cadaver leg. Subsequent sequential release of compartments and continuous streaming of pressure readings permitted unique insights. RESULTS: A leg model allowed the examination of pressure changes in all 4 compartments as treated with sequential fasciotomies. The successful modeling of lower-leg pressures consistent with compartment syndrome showed that discrepancies relative to accepted concepts were seen when the deep posterior compartment was pressurized in isolation. Also, release of 1 of the 2 of either the anterior or lateral compartments seems to be sufficient for decompression to acceptable pressure levels. CONCLUSIONS: The deep posterior compartment does not appear to be completely discrete and instead follows the pressurization curve of the posterior muscle group. This indicates that release of the deep posterior compartment may not be needed in all acute compartment syndrome scenarios. CLINICAL RELEVANCE: Surgical techniques can be modified for treatment of acute compartment syndrome to avoid large scar lengths, deep dissection, and multiple exposures that could improve patient outcomes.
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Síndromes Compartimentales , Cadáver , Síndromes Compartimentales/etiología , Síndromes Compartimentales/cirugía , Fasciotomía/métodos , Humanos , Pierna/cirugía , PresiónRESUMEN
BACKGROUND: Acute compartment syndrome of the foot is a controversial topic. Release of the foot has been seen as complicated because of large incisions and postoperative morbidity, and there has been debate over whether this procedure is actually effective for releasing all areas of increased pressure. New sensor technology affords the opportunity to advance our understanding of acute compartment syndrome of the foot and its treatment. The purpose of the present study was to determine whether percutaneous decompression could be performed for the treatment of compartment syndrome in a forefoot model. METHODS: The present study utilized a validated continuous pressure sensor to model compartment syndrome in human cadaveric feet. We utilized a pressure-controlled saline solution infusion system to induce increased pressure. A novel percutaneous release of the forefoot was investigated to assess its efficacy in achieving decompression. RESULTS: For all cadaveric specimens, continuous pressure monitoring was accomplished with use of a continuous pressure sensor. There were 4 discrete compartment areas that could be reliably pressurized in all feet. The average baseline, pressurized, and post-release pressures (and standard deviations) were 4.5 ± 2.9, 43.8 ± 7.7, and 9.5 ± 3.6 mm Hg, respectively. Percutaneous decompression produced a significant decrease in pressure in all 4 compartments (p < 0.05). CONCLUSIONS: With use of continuous compartment pressure monitoring, 4 consistent areas were established as discrete compartments in the foot. All 4 compartments were pressurized with a standard pump system. With use of 2 small dorsal incisions, all 4 compartments were successfully released, with no injuries identified in the cutaneous nerve branches, extensor tendons, or arteries. These results have strong implications for the future of modeling compartment syndrome as well as for guiding clinical studies. CLINICAL RELEVANCE: A reproducible and accurate method of continuous pressure monitoring of foot compartments after trauma is needed (1) to reliably identify patients who are likely to benefit from compartment release and (2) to help avoid missed or evolving cases of acute compartment syndrome. In addition, a reproducible method for percutaneous compartment release that minimizes collateral structural damage and the need for secondary surgical procedures is needed.
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PURPOSE: To examine the ability of surgeons to identify the osseous landmarks associated with the femoral anterior cruciate ligament (ACL) footprint and locate optimal tunnel placement on 3-dimensional (3D) printed models compared with intraoperative placement. METHODS: Twelve sports fellowship-trained orthopaedic surgeons were asked to identify a femoral landmark and an ACL footprint on 10 different 3D printed knees. The 3D models were made based on 20 real patients with different anatomical morphology who later received ACL reconstructive surgery using independent drilling. ImageJ software was used to quantify the measurements, which were then analyzed using descriptive statistics. RESULTS: Overall, none of the surgeons were able to consistently identify the junction of the bony ridges. The mean error per participant ranged from 2.81 to 7.34 mm in the proximal direction (P = 3.30e-05) and from 2.42 to 8.05 mm in the posterior direction (P =4.88e-12). None of the surgeons were able to appropriately identify the center of the femoral footprint on the anatomic 3D models. The difference between the center of the footprint surgeons identified on the 3D model and the tunnel graft location in surgery was significantly different (P = .0046). On average, the magnitude of the error when the surgeons performed the actual surgery was 3.72 ± 2.43 mm, whereas on the 3D models it was 5.82 ± 1.97 mm. CONCLUSIONS: Experienced sports fellowship-trained orthopaedic surgeons were unable to correctly identify the junction of the intercondylar and bifurcate ridges and the native ACL footprint on 3D models. Operatively placed tunnels were more accurate implying that looking either through a scope or soft-tissue landmarks play a significant role in surgeons ACL footprint localization. CLINICAL RELEVANCE: The graft position for ACL reconstruction plays an important role on the kinematics of the knee. This paper shows that soft tissue landmarks are needed to provide reliable reference points for reconstruction.
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Genetic studies have been instrumental in the field of orthopaedics for finding tools to improve the standard management of fractures and delayed unions. The Wnt signaling pathway that is crucial for development and maintenance of many organs also has a very promising pathway for enhancement of bone regeneration. The Wnt pathway has been shown to have a direct effect on stem cells during bone regeneration, making Wnt a potential target to stimulate bone repair after trauma. A more complete view of how Wnt influences animal bone regeneration has slowly come to light. This review article provides an overview of studies done investigating the modulation of the canonical Wnt pathway in animal bone regeneration models. This not only includes a summary of the recent work done elucidating the roles of Wnt and ß-catenin in fracture healing, but also the results of thirty transgenic studies, and thirty-eight pharmacological studies. Finally, we discuss the discontinuation of sclerostin clinical trials, ongoing clinical trials with lithium, the results of Dkk antibody clinical trials, the shift into combination therapies and the future opportunities to enhance bone repair and regeneration through the modulation of the Wnt signaling pathway.