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Serial examination and direct measurement of intracompartmental pressure (ICP) are suboptimal strategies for the detection of acute compartment syndrome (CS) because they are operator‐dependent and yield information that only indirectly reflects intracompartmental muscle perfusion. As a result, instances of unnecessary fasciotomy and unrecognized CS are relatively common. Recently, near‐infrared spectroscopy (NIRS)‐based systems for compartment monitoring have generated interest as an adjunct tool. Under ideal conditions, NIRS directly measures the oxygenation of intracompartmental muscle (StO2), thereby obviating the challenges of interpreting equivocal clinical examination or ICP data. Despite these potential advantages, existing NIRS sensors are plagued by technical difficulties that limit clinical utility. Most of these limitations relate to their transcutaneous design that makes them susceptible to both interference from intervening skin/subcutaneous tissue, underlying hematoma, and instability of the skin‐sensor interface. Here, we present a flexible, wireless, Bluetooth‐enabled, percutaneously introducible intramuscular NIRS device that directly and continuously measures the StO2 of intracompartmental muscle. Proof of concept for this device is demonstrated in a swine lower extremity balloon compression model of acute CS, wherein we simultaneously track muscle oxygenation, ICP, and compartment perfusion pressure (PP). The observed StO2 decreased with increasing ICP and decreasing PP and then recovered following pressure reduction. The mean change in StO2 as the PP was decreased from baseline to 30 mmHg was −7.6%. The mean difference between baseline and nadir StO2 was −17.4%. Cross‐correlations (absolute value) describing the correspondence between StO2 and ICP were >0.73. This novel intramuscular NIRS device identifies decreased muscle perfusion in the setting of evolving CS. Statement of Clinical Significance: This novel intramuscular near‐infrared spectroscopy device can directly measure the perfusion of intracompartmental muscle and holds promise as a potential clinical tool to facilitate early and accurate diagnosis of acute compartment syndrome of the limb. [ABSTRACT FROM AUTHOR]

The asymmetric unit of the title compound, [Zn(C3H7NO)2(H2O)4][Zn(C13H10N2O5)Cl]2, is composed of a single anion and half a cation. The ZnII atom in the monoanion has a distorted triganol–pyramidal geometry, being coordinated by three O atoms and one N atom from one 2-{3-[2-(carboxylatomethoxy)phenyl]pyrazol-1-yl}acetate ligand and one Cl atom. In the dication, the ZnII atom is located on an inversion center and is coordinated by six O atoms in a slightly distorted octahedral geometry. In the crystal, the ions are linked by O—H...O hydrogen bonds, forming a two-dimensional network lying parallel to the ab plane. There are also C—H...O and C—H...Cl interactions present, which lead to the formation of a three-dimensional structure.

Laser speckle contrast imaging (LSCI) was used to monitor thermal-induced changes in the blood flow and the diameter of mesenteric microvessels of normal and tumor bearing mice under 60 min treatment at different constant temperatures between 41[degrees]C and 45[degrees]C. The results show that the blood flow and the diameter increase at the beginning and then reach a plateau and finally start to decrease. The lower the temperature, the longer the plateau stays. A t-test indicates that there is no significant difference in plateau values of relative blood flow and relative diameter for the same group. For normal mice, the relative increases in the blood flow and the diameter are 1.26 and 1.41, respectively, while for tumor-bearing mice they are 1.08 and 1.13, respectively. At higher treatment temperature or under longer heat treatment, there are decreases in the blood flow and the diameter, such changes in tumor-bearing mice are more obvious than those in normal mice, which means tumor microvessels are more sensitive to heat than normal. Moreover, thermal induced shrink of microvessel usually occurs sooner than the decrease in blood flow, and the relative change in diameter is larger than that in blood flow. Therefore we may conclude that deformation of vessel is a main factor for changing the blood perfusion of a microvessel. OCIS codes: 170.3880, 170.1470, 170.6480, 280.2490, 120.6150.

Background  Current near-infrared spectroscopy (NIRS)-based systems for continuous flap monitoring are limited to flaps which carry a cutaneous paddle. As such, this useful and reliable technology has not previously been applicable to muscle-only free flaps where other modalities with substantial limitations continue to be utilized. Methods  We present the first NIRS probe which allows continuous monitoring of local tissue oxygen saturation (StO 2) directly within the substance of muscle tissue. This probe is flexible, subcentimeter in scale, waterproof, biocompatible, and is fitted with resorbable barbs which facilitate temporary autostabilization followed by easy atraumatic removal. This novel device was compared with a ViOptix T.Ox monitor in a porcine rectus abdominus myocutaneous flap model of arterial and venous occlusions. During these experiments, the T.Ox device was affixed to the skin paddle, while the novel probe was within the muscle component of the same flap. Results  The intramuscular NIRS device and skin-mounted ViOptix T.Ox devices produced very similar StO 2 tracings throughout the vascular clamping events, with obvious and parallel changes occurring upon vascular clamping and release. The normalized cross-correlation at zero lag describing correspondence between the novel intramuscular NIRS and T.Ox devices was >0.99. Conclusion  This novel intramuscular NIRS probe offers continuous monitoring of oxygen saturation within muscle flaps. This experiment demonstrates the potential suitability of this intramuscular NIRS probe for the task of muscle-only free flap monitoring, where NIRS has not previously been applicable. Testing in the clinical environment is necessary to assess durability and reliability. [ABSTRACT FROM AUTHOR]