Minimal Percutaneous Release for Acute Compartment Syndrome of the Foot: A Case Report.

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.

Percutaneous Forefoot Decompression in a Foot Compartment Syndrome Model.

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.

Effects of rosiglitazone (PPAR†γ agonist) on the myocardium in non-hypertensive diabetic rats (PPAR γ).

BACKGROUND: There is ongoing controversy regarding the safety of rosiglitazone and its effects on the myocardium, in some cases causing severe cardiac pathology and even in some instances mortality. In this study we aimed at examining the effects of pharmacologic doses of rosiglitazone on cardiomyocytes in diabetic non-cardiac rats receiving sub-optimal doses of insulin. METHODS: Animals were distributed into six groups: normal, diabetic, and diabetic receiving insulin, each subdivided into a control group and an experimental group receiving pharmacologic doses of rosiglitazone. Cardiomyocyte hypertrophy was assessed using heart to body weight index and microscopic examination using the number of cardiomyocytes per quadrant of high power field and intercalated disks in a sector of 100 × field. Fibrosis was assessed using Masson Trichrome staining. A number of sections of each group were stained with periodic acid Shiff and others with Sudan III for glycogen and fat accumulation, respectively. One way ANOVA was used for statistical analysis as appropriate. RESULTS: Diffuse cardiomyopathic changes in diabetic control animals were observed consisting of cardiomyocyte hypertrophy, loss of striations and widespread vacuolation. These changes were reduced and even prevented by treatment with insulin and rosiglitazone. Masson staining showed that all rat groups had no more than +1 fibrosis that is equal to what was present in the normal controls. CONCLUSION: Rosiglitazone, in combination with even sub-optimal doses of insulin therapy, has protective effects on cardiac muscle in diabetic animals especially those expressed as muscle hypertrophy, muscle cell death, and fibrosis.

Polymeric binders suppress gliadin-induced toxicity in the intestinal epithelium.

BACKGROUND & AIMS: Celiac disease is a prevalent immune disorder caused by the ingestion of gliadin-containing grains. We investigated the ability of a polymeric binder to reverse the toxic effects induced by gliadin in human intestinal cells and gliadin-sensitive HCD4-DQ8 mice. METHODS: Gliadin was neutralized by complexation to a linear copolymer of hydroxyethylmethacrylate (HEMA) and sodium 4-styrene sulfonate (SS). The ability of the polymeric binder to abrogate the damaging effect of gliadin on cell-cell contact was investigated in IEC-6, Caco-2/15, and primary cultured differentiated enterocytes. The efficacy of the polymeric binder in preventing gliadin-induced intestinal barrier dysfunction was assessed using gliadin-sensitive HLA-HCD4/DQ8 transgenic mice. RESULTS: Poly(hydroxyethylmethacrylate-co-styrene sulfonate) [P(HEMA-co-SS)] complexed with gliadin in a relatively specific fashion. Intestinal cells exposed to gliadin underwent profound alterations in morphology and cell-cell contacts. These changes were averted by complexing the gliadin with P(HEMA-co-SS). More importantly, the P(HEMA-co-SS) hindered the digestion of gliadin by gastrointestinal enzymes, thus minimizing the formation of immunogenic peptides. Coadministration of P(HEMA-co-SS) with gliadin to HLA-HCD4/DQ8 mice attenuated gliadin-induced changes in the intestinal barrier and reduced intraepithelial lymphocyte and macrophage cell counts. CONCLUSIONS: Polymeric binders can prevent in vitro gliadin-induced epithelial toxicity and intestinal barrier dysfunction in HCD4/DQ8 mice. They have a potential role in the treatment of patients with gluten-induced disorders.

FTIR study of polycaprolactone chain organization at interfaces.

Polycaprolactone (PCL), extensively known as a biomaterial, is the subject of this paper. Knowing well that some biomaterial applications exhibit specific chain organization, we focused our study on the orientation of PCL chains when this polymer is adsorbed (spin-coated) on inert substrates such as gold-coated glass slides. The main technique allowing adsorbed thin films analysis that we chose is polarization-modulation infrared reflection-absorption spectroscopy (PM-IRRAS), which permits qualitative and quantitative determination of chain anisotropy in the confined layers at the interface. Based on our spectroscopic results, we achieved an adsorption model of PCL chains and we calculated orientation angles with respect to the substrate normal. Calculated values show a quasi-perpendicular deposition of PCL chains on the gold substrate. Moreover, PCL thin films remain highly crystalline, a fact which could be the basis of the important anisotropy of PCL chains.