Neonatal Bilirubin Production Estimated from “End-Tidal” Carbon Monoxide Concentration

Smith, David W.; Hopper, Andrew; Shahin, Susan; Cohen, Ronald S.; Ostrander, Clinton R.; Ariagno, Ronald L.; Stevenson, David K.

doi:10.1097/00005176-198401000-00017

Cited by 30 publications

(15 citation statements)

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“…A number of factors potentially could influence ETCO levels including maternal smoking (17), hemolysis (18,19), bilirubin levels (20,21), and infection (22,23). As a consequence, we recorded maternal smoking habits and on each measurement day, the serum bilirubin and hematocrit levels.…”

Section: Patientsmentioning

confidence: 99%

End-tidal Carbon Monoxide Levels in Prematurely Born Infants Developing Bronchopulmonary Dysplasia

et al. 2007

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Bronchopulmonary dysplasia (BPD) is associated with an early inflammatory response that persists after the first week of life. Inflammatory mediators can induce hemoxygenase-1 with a consequent increase in carbon monoxide (CO) production. End-tidal CO (ETCO) levels would be elevated in infants developing BPD. Serial measurements of ETCO levels were attempted on d 3, 5, 7, 14, 21, and 28 in 50 prematurely born infants (median gestational age 29 wk). Fourteen infants developed BPD [oxygen dependent beyond 36 wk post-menstrual age (PMA)] and had higher ETCO levels compared with the rest of the cohort on d 7, 14, 21, and 28. On d 14, the mean (SD) ETCO levels of the BPD group were 3.19 (1.11) ppm and 1.43 (0.61) ppm in the non-BPD group (p Ͻ 0.001). An ETCO level on d 14 Ͼ2.15 ppm had a sensitivity of 80% and specificity of 92% in predicting oxygen dependency at 36 wk PMA. Measurement of ETCO levels in prematurely born infants may be useful in the prediction of BPD.

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Section: Patientsmentioning

confidence: 99%

End-tidal Carbon Monoxide Levels in Prematurely Born Infants Developing Bronchopulmonary Dysplasia

et al. 2007

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“…Since maternal smoking may affect CO concentration in the fetus, infants who were exposed to maternal smoking were excluded from the study. In addition, infants with perinatal infection were also excluded since infection may also influence CO production [15,16,17,18]. …”

Section: Methodsmentioning

confidence: 99%

Early End-Tidal Carbon Monoxide Levels, Patency of the Ductus Arteriosus and Regional Cerebral Oxygenation in Preterm Infants

Dix¹,

Blok²,

Lemmers³

et al. 2013

Neonatology

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Background: Carbon monoxide (CO), a relaxant regulator of muscle tone and marker of oxidative stress and inflammation, can be measured in exhaled air by determination of end-tidal CO corrected for CO in ambient air (ETCOc). Objective: Increased endogenous production of CO may influence patency of the ductus arteriosus, cerebral perfusion and, subsequently, cerebral oxygenation. The aim was to study the relation between early ETCOc levels, hemodynamically significant patent ductus arteriosus (hsPDA) and cerebral oxygenation (rScO₂) in preterm infants <32 weeks' gestational age and determine predictive values of ETCOc for hsPDA. Methods: ETCOc was measured in 91 infants within the first 24 h after birth. A hsPDA was diagnosed according to echocardiographic indices. In 78/91 infants, rScO₂ was monitored with near-infrared spectroscopy to assess cerebral oxygenation. Results: ETCOc values were significantly higher in infants who subsequently developed hsPDA (2.3 ± 0.7 ppm) vs. no-hsPDA (1.7 ± 0.6 ppm), p < 0.001. With a cut-off value of 2.5 ppm, positive and negative predictive values of ETCOc for hsPDA were 55 and 88%, respectively. rScO₂ values were not different between the two groups (64 ± 1 vs. 65 ± 3%, NS). Conclusions: The higher ETCOc values in hsPDA infants early after birth reflect the early relaxant state of ductal muscular tone. ETCOc <2.5 ppm within 24 h after birth may predict the subsequent absence of hsPDA. ETCOc showed no correlation with cerebral oxygenation in both groups.

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“…The correlation between heme degradation and bilirubin production; carboxyhemoglobin, respiratory excretion of carbon monoxide, and end-tidal CO, was previously established and published. [17][18][19][20][21][22][23][24][25][26][27][28][29][30] Original Article…”

Section: Methodsmentioning

confidence: 99%

Phototherapy Increases Hemoglobin Degradation and Bilirubin Production in Preterm Infants

Aouthmany

1999

J Perinatol

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OBJECTIVE:To compare hemoglobin degradation and bilirubin production before and during phototherapy in preterm infants. BACKGROUND:Hemoglobin is catabolized into globin and heme, which is degraded by microsomal heme oxygenase into equimolar carbon monoxide and biliverdin. Biliverdin is then reduced into bilirubin. CO is excreted exclusively by the lungs; therefore, end-tidal carbon monoxide, corrected for inhaled CO (ETCO c ), reflects hemoglobin degradation and total bilirubin production.

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Neonatal Bilirubin Production Estimated from “End-Tidal” Carbon Monoxide Concentration

Cited by 30 publications

References 0 publications

End-tidal Carbon Monoxide Levels in Prematurely Born Infants Developing Bronchopulmonary Dysplasia

End-tidal Carbon Monoxide Levels in Prematurely Born Infants Developing Bronchopulmonary Dysplasia

Early End-Tidal Carbon Monoxide Levels, Patency of the Ductus Arteriosus and Regional Cerebral Oxygenation in Preterm Infants

Phototherapy Increases Hemoglobin Degradation and Bilirubin Production in Preterm Infants

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