[Fasciocutaneous bridge flap to cover defects on the lower leg after compartment syndrome with a complication-prone course : An "almost" forgotten safe flap procedure]. / Fasziokutane Brückenlappenplastik zur Defektdeckung im Komplikationsfall am Unterschenkel nach Kompartmentsyndrom : Eine "fast" vergessene, sichere Lappenplastik.

This article reports on a complicated case of a soft tissue defect with challenging soft tissue coverage on the lower leg. After a lower leg fracture and treatment with a tibial nail, a 29-year-old man developed compartment syndrome due to massive secondary bleeding with a lesion of the common peroneal nerve and muscle necrosis around the fibular muscles. The initial coverage with split skin showed no tendency to heal, so the patient was admitted to this hospital with a soft tissue defect of approximately 25 cm × 10 cm on the lateral lower leg with an exposed tibia over a length of 15 cm. The primary attempt was coverage with a split-thickness skin graft after secondary granulation; however, due to the previously damaged vascular supply, the wound demonstrated a delayed incomplete healing over 8 months. In addition, X­ray imaging revealed a nonunion and a resulting screw fracture of the two distal locking screws. The indications for revision surgery to treat the fracture and change the implant were fulfilled. In the same procedure, the residual cutaneous defects were closed. Given the previously complication-prone course and a difficult local blood flow situation, the choice of reconstruction procedures was limited. A bridge flap of the medial lower leg was performed in an interdisciplinary approach. The lifting defect was covered with split-thickness skin. In this way, the wound was finally adequately covered after 1 year.

Cell size induced bias of current density in hypertrophic cardiomyocytes.

Alterations in ion channel expression and function known as "electrical remodeling" contribute to the development of hypertrophy and to the emergence of arrhythmias and sudden cardiac death. However, comparing current density values - an electrophysiological parameter commonly utilized to assess ion channel function - between normal and hypertrophied cells may be flawed when current amplitude does not scale with cell size. Even more, common routines to study equally sized cells or to discard measurements when large currents do not allow proper voltage-clamp control may introduce a selection bias and thereby confound direct comparison. To test a possible dependence of current density on cell size and shape, we employed whole-cell patch-clamp recording of voltage-gated sodium and calcium currents in Langendorff-isolated ventricular cardiomyocytes and Purkinje myocytes, as well as in cardiomyocytes derived from trans-aortic constriction operated mice. Here, we describe a distinct inverse relationship between voltage-gated sodium and calcium current densities and cell capacitance both in normal and hypertrophied cells. This inverse relationship was well fit by an exponential function and may be due to physiological adaptations that do not scale proportionally with cell size or may be explained by a selection bias. Our study emphasizes the need to consider cell size bias when comparing current densities in cardiomyocytes of different sizes, particularly in hypertrophic cells. Conventional comparisons based solely on mean current density may be inadequate for groups with unequal cell size or non-proportional current amplitude and cell size scaling.