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Updated: Mar 1, 2026

Non-invasive Optical Measurement of Cerebral Metabolism and Hemodynamics in Infants
Published on: March 14, 2013
Does metabolic alkalosis influence cerebral oxygenation in infantile hypertrophic pyloric stenosis?
Matthias Nissen1, Grigore Cernaianu2, Rene Thränhardt1
1Department of Pediatric Surgery, St. Mary's Hospital, St. Elisabeth Group, Ruhr-University of Bochum, Herne, Germany.
Insights
Metabolic alkalosis in infants with pyloric stenosis impacts cerebral oxygenation. Correcting metabolic alkalosis normalized regional cerebral oxygenation (rSO2) measured by NIRS, suggesting its utility in perioperative care.
Area of Science:
- Pediatric Surgery
- Neonatology
- Medical Technology
Background:
- Infantile hypertrophic pyloric stenosis (IHPS) often presents with metabolic alkalosis (MA).
- Perioperative regional tissue oxygenation (rSO2) in IHPS patients is not well understood.
- MA's influence on cerebral and renal oxygenation requires investigation.
Purpose of the Study:
- To investigate the effect of MA correction on cerebral (c-rSO2) and renal (r-rSO2) oxygenation in infants with IHPS.
- To assess the utility of near-infrared spectroscopy (NIRS) in monitoring perioperative oxygenation in this population.
Main Methods:
- Retrospective analysis of 12 infants with IHPS.
- NIRS used to measure c-rSO2 and r-rSO2 at multiple perioperative time points.
- Comparison of oxygenation parameters before and after MA correction, and before/after surgery.
Main Results:
- Correction of MA led to a significant increase in c-rSO2.
- Cerebral oxygenation positively correlated with sodium and inversely with bicarbonate/base excess.
- Renal oxygenation showed no significant changes, but a negative correlation with hematocrit suggested increased renal blood flow under hemodilution.
Conclusions:
- NIRS is suitable for detecting impaired cerebral oxygenation in infants with IHPS and MA.
- Correction of MA normalizes c-rSO2, highlighting NIRS's potential in optimizing perioperative management.
- Monitoring c-rSO2 may be crucial for neurodevelopmental outcomes after pyloromyotomy.
Background:
This pilot study focuses on regional tissue oxygenation (rSO2) in patients with infantile hypertrophic pyloric stenosis in a perioperative setting. To investigate the influence of enhanced metabolic alkalosis (MA) on cerebral (c-rSO2) and renal (r-rSO2) tissue oxygenation, two-site near-infrared spectroscopy (NIRS) technology was applied.
Materials And Methods:
Perioperative c-rSO2, r-rSO2, capillary blood gases, and electrolytes from 12 infants were retrospectively compared before and after correction of MA at admission (T1), before surgery (T2), and after surgery (T3).
Results:
Correction of MA was associated with an alteration of cerebral oxygenation without affecting renal oxygenation. When compared to T1, 5-min mean (± standard deviation) c-rSO2 increased after correction of MA at T2 (72.74 ± 4.60% versus 77.89 ± 5.84%; P = 0.058), reaching significance at T3 (80.79 ± 5.29%; P = 0.003). Furthermore, relative 30-min c-rSO2 values at first 3 h of metabolic compensation were significantly lowered compared with postsurgical states at 16 and 24 h. Cerebral oxygenation was positively correlated with levels of sodium (r = 0.37; P = 0.03) and inversely correlated with levels of bicarbonate (r = -0.34; P = 0.05) and base excess (r = -0.36; P = 0.04). Analysis of preoperative and postoperative cerebral and renal hypoxic burden yielded no differences. However, a negative correlation (r = -0.40; P = 0.03) regarding hematocrite and mean r-rSO2, indirectly indicative of an increased renal blood flow under hemodilution, was obtained.
Conclusions:
NIRS seems suitable for the detection of a transiently impaired cerebral oxygenation under state of pronounced MA in infants with infantile hypertrophic pyloric stenosis. Correction of MA led to normalization of c-rSO2. NIRS technology constitutes a promising tool for optimizing perioperative management, especially in the context of a possible diminished neurodevelopmental outcome after pyloromyotomy.
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