Significance: Pulse oximetry is widely used in clinical practice to monitor changes in arterial oxygen saturation (SpO2). However, decreases in SpO2 can be delayed relative to the actual clinical event, and near-infrared spectroscopy (NIRS) may detect alterations in oxygenation earlier than pulse oximetry, as shown in previous cerebral oxygenation monitoring studies.Aim: We aim to compare the response of transcutaneous muscle NIRS measures of the tissue saturation index with pulse oximetry SpO2 during hypoxia.Approach: Episodes of acute hypoxia were induced in nine anesthetized Yucatan miniature pigs. A standard pulse oximeter was attached to the ear of the animal, and a transcutaneous NIRS sensor was placed on the hind limb muscle. Hypoxia was induced by detaching the ventilator from the animal and reattaching it once the pulse oximeter reported 70% SpO2.Results: Twenty-four episodes of acute hypoxia were analyzed. Upon the start of hypoxia, the transcutaneous NIRS measures changed in 5.3 ± 0.4 s, whereas the pulse oximetry measures changed in 14.9 ± 1.0 s (p < 0.0001).Conclusions: Transcutaneous muscle NIRS can detect the effects of hypoxia significantly sooner than pulse oximetry in the Yucatan miniature pig. A transcutaneous NIRS sensor may be used as an earlier detector of oxygen saturation changes in the clinical setting than the standard pulse oximeter.
Introduction: We previously developed an implantable near-infrared spectroscopy (NIRS) sensor to provide real-time monitoring of spinal cord oxygenation and hemodynamics in a porcine model of acute SCI. Here, we present a method to fix an improved design of the sensor to the spinal cord for up to 14-days post-injury which will be important for its clinical application. Methods: Two Yucatan mini-pigs received a T2 contusion-compression injury. A multi-wavelength NIRS system with a custom-made miniaturized sensor was laid over the dura. The NIRS sensor consisted of a five wavelength LED and photodetector from the previous design. The placement of the LED and photodetector was reconfigured to create a sensor with a slimmer shape. The sensor was mounted on a flexible printed circuit board (PCB) and enclosed by an implantable soft silicone with thin flaps on its side. This allowed the sensor to sit flush on the dura and secured with a fibrin sealant material (TISSEEL), eliminating the need for additional spinal fixation devices. The surgical incision was sutured closed, and the sensor was fixed on the spinal cord while the animal recovered for 14-days post-injury. A fluoroscopy was performed on the surgery day, 7- and 14-days post-injury to assess the positioning of the sensor. Results/Conclusion: The implantable NIRS sensor appeared to remain fixed on the spinal cord after 14-days post-injury upon analysis of fluoroscopy images and examining the re-exposed surgical wound. Securing the NIRS sensor to the spinal cord with a fibrin sealant may provide a method for fixation for up to 14-days post-injury.
Background: We developed an implantable optical sensor based on near-infrared spectroscopy (NIRS) to continuously monitor spinal cord oxygenation and hemodynamics in patients with acute spinal cord injury (SCI). As a safety assessment measure, we aimed to study the effect of near-infrared (NIR) light emission and contact compression of the NIRS sensor on spinal cord tissue structure. Our previous in-vitro heat tests indicated no heat generation by the NIRS sensor. This study evaluated whether the NIRS sensor resulted in any potential compression damage to the spinal cord using histological analysis. Methods: Six Yucatan mini-pigs received a T10 SCI. A custom implantable NIRS sensor (version 2) was placed extradurally on the spinal cord and fixed with magnets and cross-connectors. After seven days of continuous data collection at 100Hz, the sensor was removed to allow for histological examination of the spinal cord tissue. Cellular damage was observed in the spinal cord at the NIRS sensor placement site in two animals. The design, shape, and material of the NIRS sensor were significantly revised to reduce the sensor footprint, minimize the compression on the cord, increase the sensor flexibility, and improve its clinical application. An in-vivo pilot experiment was performed on a Yucatan miniature pig with a T10 SCI to evaluate potential compression damage of the spinal cord tissue from placement and direct contact of the refined NIRS sensor (version 5). A fibrin sealant, TISSEEL, was utilized to fix the version 5 NIRS sensor on the spinal cord. Result: There were no signs of cellular damage, indentation, and significant flattening on the dorsal surface of the spinal cord where the version 5 NIRS sensor was placed for up to 4.5 hours. Conclusion: The refined NIRS sensor did not cause any compression damage to the porcine spinal cord after implantation for 4.5 hours. Implanting this sensor on the spinal cord of SCI patients requires further in-vivo examinations to ensure the sensor is safe to use for up to 14 days.
Background: A customized sensor, based on near-infrared spectroscopy (NIRS), was developed to non-invasively monitor spinal cord hemodynamics after acute spinal cord injury (SCI). However, the effect of direct contact and emission of the NIRS signals on the spinal cord tissue structure was not clear. This information is essential because even minimal heating or contact pressure from the NIRS sensor placed over the injured spinal cord may lead to further damage to the spinal cord tissue. Here, we evaluate the safety of the custom-made NIRS sensor as it is essential prior to its clinical translation. Methods: A custom-made multi-wavelength miniaturized NIRS sensor was placed extradurally on the spinal cord of six Yucatan mini-pigs who received a T10 SCI. After seven days of continuous data collection at 100 Hz, the sensor was removed and the spinal cord tissue was examined. Histological assessment of the spinal cord revealed evidence of cellular damage at the NIRS sensor placement in two animals. An in-vitro experiment was performed to evaluate the possibility of heat damage caused by the NIRS sensor. Using a digital thermometer with two probes, one directly touching the NIRS emitter and the other one at a control site one centimeter away from the emitter. The amount of heat generation of the NIRS emitter after seven days of continuous operation at 100 Hz was measured and compared with the control site. Results: In-vitro heat tests showed no heat generation by the NIRS sensor. The temperature measured from the emitter site of the NIRS sensor and control temperature probe was identical during the seven days. Conclusion: The custom-made NIRS sensor does not generate heat at the emitter site and physical damage observed with regards to histology is due to the compression applied from the sensor. By refining the sensor to be smaller and more flexible with an even surface, we will improve the safety of the NIRS sensor before translating this technology to human patients. The new sensor will be further examined.
Introduction: Pulse oximetry is commonly used in critical care to monitor changes in arterial oxygen saturation (SpO2). However, studies have reported that decreases in SpO2 may lag behind the actual clinical event. Previous studies have demonstrated that cerebral oxygenation monitoring using near-infrared spectroscopy (NIRS) can detect alterations in oxygenation earlier than pulse oximetry. Here, we compare responses of NIRS monitoring of spinal cord tissue oxygenation (TOI) to pulse oximetry SpO2 during hypoxia. Methods: During a study on optical monitoring of spinal cord hemodynamics in an animal model of spinal cord injury (SCI), episodes of acute (70-80% SpO2) hypoxia were induced. Six anesthetized Yucatan miniature pigs were studied. A standard pulse oximeter was attached to the ear of the animal and a custom-made NIRS sensor was placed extradurally on the spinal cord. Hypoxia was induced by removing the ventilator from the animal and reattaching it once SpO2 reached 70% or 80% as reported by the pulse oximeter. Results: 21 episodes of acute hypoxia were analyzed. Upon the start of hypoxia, NIRS TOI responded in 1.8 ± 0.5 seconds, while pulse oximetry SpO2 responded in 11.4 ± 0.6 seconds (p > 0.0001). Conclusion: NIRS can detect the effects of hypoxia on spinal cord tissue earlier than pulse oximetry can detect arterial oxygenation changes in the periphery. The NIRS sensor may be used as an earlier detector of oxygen saturation changes in the clinical setting than the standard pulse oximeter.
Introduction: By elevating intramuscular pressure and increasing muscle oxygen consumption, a sustained contraction of a limb muscle can compromise muscle metabolic status and function. In this study, we aimed to investigate the effect of isometric forearm muscle contractions at different intensities and isotonic contractions on muscle oxygenation dynamics using near-infrared spectroscopy (NIRS). Methods: The maximum voluntary contraction (MVC) force of forearm flexor muscles in the dominant arm was measured in ten healthy adult volunteers. A NIRS sensor was placed and fixed over the common flexor muscles of the forearm to monitor muscle rSO2. A reflectance pulse oximeter sensor was placed over the common extensor muscles, and a tourniquet cuff was placed loosely around the upper arm on the same side. Following a three-minute baseline measurement, each subject was instructed to perform a series of 30-second sustained isometric flexor muscle contractions at 10%, 30% and 50% MVC using a handgrip dynamometer. A 30-second isotonic muscle contraction followed by a 30-second episode of tourniquet-induced ischemia completed the experiment. Three minutes of recovery time were allowed after each episode. Results: Similar patterns of rSO2 changes were seen in all subjects during episodes of isometric contractions (30% MVC and 50% MVC), isotonic contractions, and ischemia. Isometric muscle contraction at 50% MVC induced the lowest level of muscle rSO2 (-16% ± 2.7%, p<0.0001). Conclusions: Isometric muscle contraction at 50% MVC induces a higher level of muscle hypoxia, in comparison to isotonic muscle contraction and limb muscle ischemia. Sustained isometric muscle contraction can compromise muscle oxygenation dynamics, which may expedite muscle fatigue and dysfunction.
Introduction: Current clinical guidelines recommend augmenting the mean arterial pressure (MAP) in acute spinal cord injury (SCI) patients to increase perfusion and oxygen delivery to the spinal cord, and potentially improve neurologic function. However, it is difficult for clinicians to hemodynamically manage acute SCI patients without real-time physiologic information about the effect of MAP augmentation within the injured cord. In this study, we investigated the utilization of a customized optical sensor, based on near-infrared spectroscopy (NIRS), to non-invasively monitor spinal cord oxygenation during the first week post-injury in a porcine model. Methods: Six Yucatan mini-pigs received a weight-drop T10 contusion-compression injury. A multi-wavelength NIRS system with a custom-made miniaturized sensor was placed directly onto the dura. The spinal cord tissue oxygenation index (TOI) and concentrations of oxygenated, deoxygenated, and total hemoglobin were monitored before and after SCI. To validate the NIRS measures, invasive intraparenchymal (IP) combined PO2/blood flow sensors were inserted into the spinal cord adjacent to the NIRS sensor. Episodes of MAP alteration and hypoxia were performed acutely after injury, 2 days post-injury, and 7 days post-injury to simulate the types of hemodynamic changes SCI patients experience post-injury. Results: Non-invasive NIRS monitoring identified changes in spinal cord oxygenation levels during the MAP alterations. Changes of TOI followed similar patterns of IP-derived oxygenation changes. Conclusion: Our novel NIRS sensor is feasible as a non-invasive technique to monitor real-time changes in spinal cord oxygenation 7 days post-injury in a porcine model of SCI.
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