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ABSTRACT: Closed soft tissue injury induces progressive microvascular dysfunction and regional inflammation. The authors tested the hypothesis that adverse trauma-induced effects can be reduced by local cooling. While superficial cooling reduces swelling, pain, and cellular oxygen demand, the effects of cryotherapy on posttraumatic microcirculation are incompletely understood.
Controlled laboratory study.
After a standardized closed soft tissue injury to the left tibial compartment, male rats were randomly subjected to percutaneous perfusion for 6 hours with 0.9% NaCL (controls; room temperature) or cold NaCL (cryotherapy; 8 degrees C) (n = 7 per group). Uninjured rats served as shams (n = 7). Microcirculatory changes and leukocyte adherence were determined by intravital microscopy. Intramuscular pressure was measured, and invasion of granulocytes and macrophages was assessed by immunohistochemistry. Edema and tissue damage was quantified by gravimetry and decreased desmin staining.
Closed soft tissue injury significantly decreased functional capillary density (240 +/- 12 cm(-1)); increased microvascular permeability (0.75 +/- 0.03), endothelial leukocyte adherence (995 +/- 77/cm(2)), granulocyte (182.0 +/- 25.5/mm(2)) and macrophage infiltration, edema formation, and myonecrosis (ratio: 2.95 +/- 0.45) within the left extensor digitorum longus muscle. Cryotherapy for 6 hours significantly restored diminished functional capillary density (393 +/- 35), markedly decreased elevated intramuscular pressure, reduced the number of adhering (462 +/- 188/cm(2)) and invading granulocytes (119 +/- 28), and attenuated tissue damage (ratio: 1.7 +/- 0.17).
The hypothesis that prolonged cooling reduces posttraumatic microvascular dysfunction, inflammation, and structural impairment was confirmed.
These results may have therapeutic implications as cryotherapy after closed soft tissue injury is a valuable therapeutic approach to improve nutritive perfusion and attenuate leukocyte-mediated tissue destruction. The risk for evolving compartment syndrome may be reduced, thereby preventing further irreversible aggravation.
The American Journal of Sports Medicine 02/2007; 35(1):93-102. · 3.79 Impact Factor
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ABSTRACT: The application of radiofrequency energy to smooth and stabilize the cartilage surface has become increasingly controversial. There is little knowledge on extended-term effects, such as cartilage viability.
To analyze the effect of radiofrequency treatment on artificially created partial-thickness defects in the femoral cartilage of sheep knee joints 24 weeks after surgery.
Controlled laboratory study.
Grade II cartilage surface defects on the medial and lateral femoral condyles were artificially created in sheep for in vivo analysis. The cartilage lesions were treated alternately on the lateral or the medial condyle using a monopolar radiofrequency probe. Radiofrequency treatment was performed in a freehand technique until surface smoothing without change of cartilage color was seen. At 24 weeks after surgery, cartilage samples were harvested and were processed for macroscopic and histological evaluation. To analyze the effect of radiofrequency at time zero, samples of sheep femoral condyle cartilage with and without artificially created clefts were treated in vitro with radiofrequency. Evaluation was performed by scanning electron and confocal microscopy.
At 24 weeks after surgery, grade IV cartilage defects were detected in all radiofrequency-treated samples. The histological findings showed a central ulcer and dead chondrocytes in the radiofrequency-treated regions. The radiofrequency-treated cartilage revealed partial surface irregularities with partial-defect repair. After radiofrequency treatment in vitro, samples at time zero showed smoothing of the artificially created clefts, as seen by scanning electron microscopy. Confocal microscopy showed necrosis of chondrocytes over approximately one fourth of the upper cartilage thickness.
Even if chondrocyte death is seen only in approximately one fourth of the upper cartilage layers in the sheep femur after in vitro application, radiofrequency treatment can cause damage to cartilage 24 weeks after application.
Caution is recommended in the application of monopolar radiofrequency energy by visual control to partial-thickness cartilage defects. Irregular fronds of chondromalacia may be unattractive but represent viable articular cartilage. Using radiofrequency to obtain a more visually pleasing smooth surface may be counterproductive.
The American Journal of Sports Medicine 11/2005; 33(10):1472-8. · 3.79 Impact Factor
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ABSTRACT: Trauma-induced microcirculatory dysfunction, formation of free radicals and decreased endothelial release of nitric oxide (NO) contribute to evolving tissue damage following skeletal muscle injury. Administration of N-acetylcysteine (NAC) known to scavenge free radicals and generate NO is considered a valuable therapeutic approach. Thus, the objective of this study was to quantitatively analyze the acute effects of NAC on skeletal muscle microcirculation and leukocyte-endothelial cell interaction following severe standardized closed soft tissue injury (CSTI). Severe CSTI was induced in the hindlimbs of 14 male anesthetized Sprague-Dawley rats using the controlled impact injury technique. Rats were randomly assigned (n = 7) to high-dose intravenous infusion of NAC (400 mg/kg body weight) or isovolemic normal saline (NS). Non-injured, sham-operated animals (n = 7) were subjected to the same surgical procedures but did not receive any additional fluid. Creatin kinase (CK) activity was assessed at baseline, 1 h before and 2 h following posttraumatic NAC or NS infusion. Microcirculation of the extensor digitorum longus (EDL) muscle was analyzed using intravital microscopy and Laser-Doppler flowmetry (LDF). Edema index (EI) was calculated by measuring the EDL wet-to-dry weight ratio (EI=injured/contralateral limb). EDL-muscles were analyzed for desmin immunoreactivity and granulocyte infiltration. Microvascular deteriorations observed following NS-infusion were effectively reversed by NAC: Functional capillary density was restored to levels found in sham-operated animals and leukocyte adherence was significantly (p < 0.05) reduced compared to the NS group. NAC significantly (p < 0.05) increased erythrocyte flux determined by Laser-Doppler flowmetry. Posttraumatic serum CK levels and EI were significantly (p < 0.05) decreased by NAC. During the posttraumatic acute phase, single infusion of NAC markedly reduced posttraumatic microvascular dysfunction, attenuated both leukocyte adherence and tissue infiltration. NAC also decreased CSTI-induced edema formation and myonecrosis as reflected by attenuated serum CK levels and attenuated loss of desmin immunoreactivity. NAC may serve as an effective therapeutic strategy by supporting microvascular blood supply and tissue viability in the early posttraumatic period. Additional studies aimed at long-term analysis and investigation of injury severity--or dosage dependency are needed.
Journal of Orthopaedic Research 02/2005; 23(1):231-41. · 2.81 Impact Factor
