Renal near-infrared spectroscopy use in the neonate

Review of near-infrared spectroscopy

NIRS is a bedside technology that has gained traction as a monitoring tool in the neonatal intensive care unit (NICU). Commercially available NIRS devices all function using the same principles. Near-infrared light with wavelengths between 685 and 880 nm is emitted from a sensor placed on an infant’s skin. The light passes through the underlying soft tissue or bone and penetrates to a depth of 1.5–3 cm depending on sensor configuration and number of wavelengths, where it is then partially absorbed by oxygenated and deoxygenated hemoglobin. Remaining light is reflected back to a detector on the sensor, and a tissue saturation level is calculated. Although similar in theory to pulse oximetry, NIRS does not rely on pulsatile blood flow and instead measures a heavily venous-weighted tissue saturation (approximately 75% venous and 25% arterial depending upon machine algorithm). Thus NIRS can be utilized for the simultaneous tissue oxygen saturation monitoring of various end organs. Fractional tissue oxygen extraction (fTOE) by the monitored organ can also be calculated with knowledge of overall systemic oxygenation (SpO ₂ ) and regional tissue oxygenation (rSO ₂ ) using the following formula: fTOE= (SpO ₂ − rSO ₂ )/SpO ₂ . Although several studies have demonstrated the utility of cerebral NIRS monitoring in reducing cerebral hypoxia with the potential for improving longer-term neurodevelopmental outcomes, ^, much less is known about NIRS monitoring of the kidney.

Renal near-infrared spectroscopy sensor placement and monitoring techniques

Appropriate placement of a renal NIRS sensor in a neonate has been described in a paravertebral location below the costal margin and above the iliac crest between the T12–L2 location but not crossing the spine. ^, Limited research has demonstrated that this placement correlates with ultrasound markers of renal blood flow. ^, Ongoing research into renal sensor placement is focused on left versus right differences, specific depth of measurement, simultaneous arterial and venous blood gas sampling, use of point of care ultrasound, and comeasurement of liver or intestinal oxygenation. At an even more granular level, renal tissue oxygenation may mostly be reflective of perfusion of glomeruli in the renal cortex, although there is less oxygen delivery to more distal segments of the collecting tubules, which are at particular risk for hypoxic injury. Kidney size will certainly be affected by gestational age and maturational processes, with implications for optimal depth of NIRS measurement.

Practical concerns of renal NIRS monitoring in the NICU must be considered. Skin integrity is of particular importance in the preterm infant with a thin stratum corneum. Use of a skin dressing or barrier such as Mepitel (Molnlycke, Gothenburg, Sweden) under an NIRS sensor has been described for preterm skin protection and has not altered the validity of NIRS measures. High-humidity conditions within a NICU isolette may also interfere with sensor adherence, although securing a renal NIRS sensor within the diaper may be feasible. As with any device in direct contact with infant skin, care must be taken to avoid pressure injuries, particularly if the infant is lying on the sensor for prolonged periods of time. Strict adherence to clinical protocols for turning and positioning infants in the NICU should be followed to reduce risk and for monitoring of skin integrity. Optimal duration of maintaining a renal NIRS sensor in one location is also unknown, but rotating sites is another described practice.

Correlation of renal NIRS data with other physiologic variables is also an important consideration. The neonatal kidney is exquisitely sensitive to cardiac output with 10% of cardiac output directed to the kidneys. As the kidney is not as well autoregulated as the brain, factors such as blood pressure and systemic oxygen saturation are likely to have a significant impact on renal NIRS measures. Time-synchronized evaluation of these vital signs may assist with clinician interpretation of renal NIRS. Moreover, simultaneous monitoring of cerebral NIRS values will provide insight into the relative effect of physiologic or pathologic processes on the kidney as compared with the brain. Optimal data capture practices and approach to missing values or artifacts have been described for cerebral or mesenteric NIRS monitoring, ^, and application to renal NIRS monitoring may be reasonable.

Normal renal saturation ranges

Several small studies have reported RrSO ₂ ranges in the neonatal period, although definitive thresholds based on renal sequelae have yet to be established. Literature from term infants describe RrSO ₂ values as being 10%–15% higher than concurrent cerebral saturation values. In term infants, beginning in the delivery room, RrSO ₂ has been measured at 40% in the first 2–3 minutes of age with a slow increase to ~85% by 10 minutes. A concomitant decrease in renal fTOE from ~40% down to <10% by 10 minutes after birth was observed in the transitional period and distinctly contrasts with a higher, preserved oxygen extraction by the brain. In a separate study measuring RrSO ₂ in the first 48 hours of life, RrSO ₂ peaked at about 92% on the first day and then gradually decreased to 89% on the second day. As the kidney is one of the most metabolically active organs, this finding may reflect increased kidney function and renal oxygen extraction over time.

Preterm infants exhibit a more complex trajectory of renal saturation ranges. Factors including gestational age, chronological age, growth restriction, patency of the ductus arteriosus, and severity of illness may influence RrSO ₂ values. In general, preterm infants tend to have lower and more variable RrSO ₂ levels compared with term infants. In a study of 80 preterm infants between 25 and 29 weeks’ gestational age, the median RrSO ₂ was between 63% and 72% in the first 48 hours of age. A two-center study of 109 preterm infants <32 weeks’ gestation found a 20% mean decrease in RrSO ₂ in the first 60 hours of life with a subsequent plateau in values for the remaining first week of life with median RrSO ₂ at 67% (interquartile range 59%–74%). These findings are similar to a small study of preterm infants <36 weeks’ gestation with RrSO ₂ decreasing from 80% down to mid-60% by 3 weeks after birth. The overall trend of a decrease in RrSO ₂ in the first few days may coincide with an increased glomerular filtration rate and subsequent increased oxygen utilization by the kidneys. Investigators also found increasing RrSO ₂ levels with higher gestational ages, with a 2.1% increase in baseline RrSO ₂ for each week of gestation between 24 and 32 weeks. The additional vascularization found in more mature kidneys may account for the increase in RrSO ₂ seen with advancing gestational age.

Acute kidney injury: At-risk populations and early detection

As previously described, there are no established thresholds for abnormal renal saturation. Notably, abnormal RrSO ₂ values have largely been extrapolated from cerebral NIRS studies in which a >20% decline or <40% threshold value has been associated with brain ischemia and injury. ^, However, limited data exist about renal thresholds of hypoperfusion and association with acute kidney injury (AKI). Measures appear to be dependent on the neonatal population being monitored, possibly indicating different mechanisms of renal injury. A compilation of abnormal RrSO ₂ values from studies of various neonatal populations at high risk for AKI is listed in Table 14.1 and described in the following sections. Measuring renal fTOE requires knowledge of simultaneous SpO ₂ values, but may potentially be a better marker for AKI risk than RrSO ₂ alone and deserves further investigation.