This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Infants who have lower measures of gut oxygenation (compared to brain) are more likely to develop Necrotizing enterocolitis (NEC) or other intestinal disease and to have feeding intolerance. The primary objective of this project is to establish a baseline for normal values of NIRS measurements in premature infants and to establish what changes exist, if any with feeding. Because the incidence of NEC is around 5% in this patient population, we will be able to generate some pilot data on the usefulness of NIRS in predicting NEC. I. To obtain """"""""normal"""""""" intestinal tissue oxidation index values (TOI) in newborns weighing 750 to 1500g. 2. To obtain a cerebro-splanchnic oxgenation ration (CSOR) for each child in order to compare values at separate time points (at 1,2,3, and 4 weeks after birth). 3. To correlate decreasing CSOR and TOI with the development of NEC or other intestinal disease, if it occurs. 4. To obtain """"""""normal"""""""" values of increased intestinal TOI during feeding at 1,2,3, and 4 weeks after birth. 5. To correlate a blunted intestinal TOI increase with feeding with the onset of feeding intolerance, if it occurs. Premature infants are at risk for neurodevelopmental adverse outcomes from a number of causes, including hypotoxic-ischemic insults from the delivery process, respiratory distress syndrome, intraventricular hemorrhage, sedative and analgesic drugs, and apnea/bradycardia. In addition, premature infants frequently develop necrotizing enterocolitis (NEC), the etiology of which is still unclear, but may be related to decreased gut perfusion. Near-infrared spectroscopy (NIRS) measures cerebral and somatic oxygenation with two wavelengths of light to which oxy-and deoxyhemoglobin have distinct absorption characteristics. The oxyhemoglobin and total hemoglobin signals are measured, and a regional cerebral or intestinal oxyhemoglobin saturation ratio is calculated (tissue oxidation index, or TOI). Low intestinal TOI may help explain the high incidence of necrotizing enterocolitis in this population. Cerebral perfusion is autoregulated, therefore, a splanchnic: cerebral perfusion ratio should remain constant under normal conditions, but should be expected to fall during hypotension or sschemia. A recently published study showed a significant difference between the brain/gut ratio of TOI between neonates with NEC/acute abdomen and those without. However, there is no data to prove that a decreasing ration predicts these problems (i.e., is the decrease in gut perfusion as a result of the disease process, or is the disease process due to the decrease in gut perfusion?). As mentioned in our specific aims, obtaining normal values are critical for future studies. Without any data, it is difficult to speculate, but the ideal clinical situation would be to establish a """"""""cut off"""""""" point. Put in different terms, what we hope we will find is a number that defines abnormal gut perfusion and predicts feeding intolerance. The numbers will be presented as real values, which the machine expresses as percentage StO2. This value represents the percentage of oxygenated hemoglobin divided by the total hemoglobin. As this value is measured on the venous side of the capillary bed, it reflects blood oxygenation status after tissue oxygen extraction. The StO2 (5) will be compared to SPO2 (%) of the peripheral pulse oximeter (arterial side of peripheral capillary bed), as well as any ABGs that have been drawn per standard of care (if any). These vlaues will be examined with respect to oral feeds, respiratory rate, and any oxygenation and perfusion co-morbidities.
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