CARBON MONOXIDE IN PREGNANCY - keywords
CO intoxication
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brain damage by carbon monoxide intoxication during pregnancy
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Alehan F, Erol I, Onay OS. Cerebral palsy due to nonlethal maternal carbon monoxide intoxication. Birth Defects Res A Clin Mol Teratol. 2007 Aug;79(8):614-6. (CO intoxication at 20 weeks PMA)
Bekiesinska-Figatowska M, Mierzewska H, Jurkiewicz E. Basal ganglia lesions in children and adults. Eur J Radiol. 2013 May;82(5):837-49.Brunetti-Pierri N, Wilfong AA, Hunter JV, Craigen WJ. A severe case of dentatorubro-pallidoluysian atrophy (DRPLA) with microcephaly, very early onset of seizures, and cerebral white matter involvement. Neuropediatrics. 2006 Oct;37(5):308-11.
Ginsberg MD, Myers RE. Fetal brain injury after maternal carbon monoxide intoxication. Clinical and neuropathologic aspects. Neurology. 1976 Jan;26(1):15-23.
Guzman JA. Carbon monoxide poisoning. Crit Care Clin. 2012 Oct;28(4):537-48.
Hager B. Hydranencephaly following carbon monoxide poisoning during pregnancy: An uncommon and potentially fatal complication in infant. Birth Defects Res. 2023 Sep 1;115(15):1450-1453.
Mohammad SS, Angiti RR, Biggin A, Morales-Briceño H, Goetti R, Perez-Dueñas B, Gregory A, Hogarth P, Ng J, Papandreou A, Bhattacharya K, Rahman S, Prelog K, Webster RI, Wassmer E, Hayflick S, Livingston J, Kurian M, Chong WK, Dale RC; Basal Ganglia MRI Study Group. Magnetic resonance imaging pattern recognition in childhood bilateral basal ganglia disorders. Brain Commun. 2020 Oct 26;2(2):fcaa178.
Passi GR, Pandey S, Devi ARR, Konanki R, Jain AR, Bhatnagar S, Tripathi R, Jain V. Cerebral creatine deficiency disorders - A clinical, genetic and follow up study from India. Brain Dev. 2022 Apr;44(4):271-280.
Tuoni C, Nuzzi G, Scaramuzzo RT, Fiori S, Filippi L. Neonatal hypoxic-ischemic encephalopathy after acute carbon monoxide intoxication during pregnancy. A case report and brief review of the literature. Front Pediatr. 2023 Nov 3;11:1264855.
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disorders of the newborn globus pallidus
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--> kernicterus
The pallido-subthalamic pattern of kernicterus is different than the thalamo-striate pattern that is typical of acute total asphyxia.
Some neurodegenerations, only exceptionally starting in early childhood, may affect globus pallidus: pallidopyramidal degeneration (Hunt-van Bogaert: globus pallidus and pyramidal tract; panthotenate kinase associated neurodegeneration), pallido-Luysian atrophy (pallidum externum and subthalamus)(Brunetti-Pierri et al. 2006).
Intensity changes of pallidum on MRI may also occur in the absence of injury, with manganese storage due to long term parenteral nutrition (reversible) and with polycythaemia (T1 hypersignal). Children with Wilson disease may have changed globi pallidi due to cupper storage.
putamen, pallidum, subthalamus and brainstem in Leigh phenotype
mitochondrial disorder
∆∆ altered signal of pallidum on MRI in newborns and infants
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kernicterus
asphyxia
CO intoxication ———————————>
PRES
hypoglycaemia
organic acidaemias like glutaric aciduria, methylmalonic aciduria
mitochondrial disorder ----------------------------------------------------------------->
neurofibromatosis I
succinic semialdehyde dehydrogenase deficiency (late infancy)
https://www.ncbi.nlm.nih.gov/books/NBK560724/
Canavan disease (white matter plus pallidum)
Krabbe disease
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destruction of striatum (Alehan et al. 2007)
brain damage by carbon monoxide intoxication during pregnancy
Vulnerability increases with duration of gestation due to multiple mechanisms: indirect effect of maternal hypoxaemia due to binding of CO to maternal Hb; direct effect of transplacental CO binding much intenser with fetal Hb with shift to left of the dissociation curve; direct effect of CO by interfering with ATP synthesis through binding on cytochromes; indirect effect of fetal heart failure.
CO also causes inflammation by increasing levels of cytosolic heme and the protein heme oxygenase-1, resulting in intracellular oxidative stress, causes platelet-neutrophil aggregation and neutrophil degranulation, with the production and release of reactive oxygen species (ROS)(Guzman 2012).
Intoxication in pregnancy leads to fetal tissue hypoxia via two mechanisms. The decreased oxygen level in the fetal umbilical vein causes tissue hypoxia. In addition, the elimi-
nation of CO is slower in fetuses (Cramer, 1982).
Consequently several lesion patterns related to hypoxia have been reported:
- specific vulnerability of globus pallidus internum and of substantia nigra (iron concentration high); also neuronal cell death in hippocampus, Purkinje cells, thalamus, subthalamic nucleus and putamen
- non-specific ischaemic lesions in cortex and white matter.
Dystonic cerebral palsy has been reported in exposed fetuses, because of slow CO elimination in utero, even though the CO intoxication of the mother was mild (Alehan et al. 2007).
Neuropathological substrate (Ginsberg and Myers 1976)(references to Hallervorden 1949, Solcher 1957)(Alehan et al. 2007, Hager 2023).
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hydranencephaly
septal agenesis (end of first trimester exposure)
polymicrogyria
bilateral cystic white matter and cortex destruction
selective injury to pallidum, hypothalamus and substantia
nigra; in some also to thalamus
∆∆ globus pallidus changes in imaging
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rhesus monkey with tissure rarefaction in putamen and pallidum following CO intoxication (Ginsberg and Myers 1976)
CO poisoning in pregnancy is particularly relevant because the fetus may be more affected than the mother by CO exposure, due to the over 200 x higher affinity of fetal hemoglobin for CO.
CO diffuses across the placenta either by passive diffusion or through a transporter-mediated mechanism and this diffusion increases with gestational age and in proportion to fetal weight.
Because of the lower baseline PaO2 of fetal blood compared with maternal blood, and the natural left shift of the fetal hemoglobin dissociation curve, the fetus is more susceptible to CO-related insults. Binding ability of CO to fetal hemoglobin is almost 3 times greater than the adult hemoglobin, thus fetal CO-Hb levels are about 10%–15% higher than maternal levels, because clearance from the fetal compartment is slower.
Hence maternal CO-Hb levels do not accurately reflect fetal hemoglobin or tissue levels.
Hyperbaric oxygen therapy has effects, such as CNS oxygen toxicity leading to seizures and retrolental fibroplasia in preterm neonates delivered before 35 weeks of gestation, which should be taken into account before starting this treatment.
CO intoxication: several pregnancy-specific effects
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