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Nov 8, - Perinatal asphyxia is a lack of blood flow or gas exchange to or from the fetus in the period immediately before, during, or after the birth process  ‎Introduction · ‎Etiology · ‎History and Physical · ‎Treatment / Management.
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But when something goes wrong, like a birth injury , it can quickly turn into one of the scariest. One of the most common birth injuries is known as birth asphyxia. When a baby is deprived of oxygen, their cells cannot work properly, allowing waste products acids to build up in the cells, causing temporary or permanent damage.

“Risk factors of birth asphyxia” | Italian Journal of Pediatrics | Full Text

All these possibilities are extremely scary. Birth Asphyxia during pregnancy may be recognized during delivery or just before by monitoring the vital signs of the baby. In these cases, an emergency c-section is often performed. In other cases, the condition may not be recognized, causing a baby to be born vaginally while in distress.

Often, this distress shows up as a silent birth, with the baby making no noise immediately after delivery.

BIRTH ASPHYXIA

Asphyxia may occur from several causes, some of which are unavoidable, while others result from negligent or improper medical care. Lowered respiration after anesthesia, such as an epidural, can lead to a depleted oxygen supply to the baby. Sudden drops in blood pressure, prior to or during birth, are also risk factors for asphyxia.

In other cases, the oxygen can be cut off due to placental detachment from the uterus, a condition known as placental abruption. A pinched or obstructed umbilical cord during pregnancy may also lead to birth asphyxia. Birth asphyxia may still occur after the baby is born. This may be due simply to a difficult pregnancy. Blood pressure or respiratory abnormalities may cause asphyxia.

Birth Asphyxia

Also, blood disorders such as anemia in the infant may prevent the blood from carrying enough oxygen. Two types of chemical changes may happen when oxygen levels in the newborn are decreased. The first is known as hypoxemia , which are low levels of blood oxygen. The second is acidosis , which is the presence of too much acid in the blood.

Left untreated, the baby could suffer severe brain damage. If the baby is still in the uterus, the mother can be given oxygen throughout the delivery.


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A cesarean section may be required if the problems persist. An evident impairment in motor coordination is monitored by rotarod performance; however, no significant difference in intensity of non-finalised motor behaviour and time-course of gross motor activity can be observed between the asphyxiated and control rats [ 28 ].

Taken together, the experimental rates exposed to the birth asphyxia, evidently, demonstrate altered fine movement functions, reflecting deficits in motor coordination and balance, whereas the locomotion and general motor activity remained non-affected. The cognitive and motor deficits observed in rats indicate the deleterious effects of birth asphyxia similar to those observed in human newborns suffered from perinatal asphyxia. The above described experimental model allows for monitoring of the deficits in cognitive performance, specific asphyxia-induced changes in motoric and stress-mediated behaviour [ 31 , 32 ].


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Metabolic particularities, impairments and individual outcomes by perinatal asphyxia. Asphyxia is characterised by hypoxia mild or severe oxygen deficiency and the pH-values reduced below 7. Depending on the grade of oxygen deficits see previous subchapters in the manuscript perinatal asphyxia causes either severe brain injury or subtle perturbations affecting further development of the central nervous system CNS [ 40 , 41 , 42 ].

Global hypoxia impairs the general availability of oxygen [ 45 , 46 ], affecting the electron transport pathways [ 47 ], increasing calcium influx and triggering fragmentation of both chrDNA and mtDNA [ 48 ]. The consequently triggered cascade of biochemical events creates a significant imbalance in central oxygen-dependent molecular pathways. Even more damaging is the reversion to normal oxygen levels during the post-asphyxic re-oxygenation associated with an extensive production of highly reactive oxygen species.

Respectively, suppression and over-activation of the affected molecular pathways occur during both periods: hypoxia and re-oxygenation [ 36 , 38 ]. Established chronic deficits underlie severe pathologies developed as individual long-term outcomes of perinatal asphyxia.

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Hypoxic-ischaemic encephalopathy [ 55 , 56 , 57 ], CNS damage [ 58 , 59 ], epilepsy [ 60 , 61 ], nephropathy [ 43 ], cardiomyopathy [ 62 , 63 ], vascular pathologies [ 64 ], senescence [ 32 , 65 ], diabetes mellitus [ 66 , 67 ], cancer [ 68 ], neurodegenerative diseases [ 58 ], morbidity and mortality [ 69 ] and tissue remodelling [ 70 ] all belong to individual short- and long-term outcomes of birth asphyxia. Furthermore, the discovered blood-brain barrier permeability in hypoxic-ischaemic encephalopathy well explains potential correlations in pathology specific molecular profiles between brain and blood, justifying the high prognostic value of non-invasive blood examinations [ 81 ].

This result is of clinical interest offering a potential inexpensive and safe prognostic marker in newborn infants with perinatal asphyxia [ 82 ]. The oxidative stress markers as measured in blood, are well recognised as the good predictors of poor outcomes in newborns with asphyxic deficits [ 83 ]. Therefore, the pathology specific biomarkers are of great clinical value being currently under extensive consideration by researchers [ 84 ].

Potentially the brain tissue of the mesencephalon area overproducing SB can be also the source of the increased SB levels in the blood-serum, due to the blood-brain-barrier breakdown that is characteristic for hypoxic-ischalmic encephalopathy. However, the proteins of Sfamily cannot be considered as asphyxia specific biomarkers, since significantly increased expression levels of them have been detected in blood of several patient cohorts, who suffer from different types of pathologies—neurodegenerative and vascular disorders [ 90 , 91 , 92 ], cardiomyopathy [ 93 ], several cancer types [ 94 , 95 ].

Transcription levels of the TAU-protein as measured in experimental rats exposed to birth asphyxia versus control animals normoxia. The transcriptome-profies are specific for the brain-regions — Mesencephalon, Hypothalamus and Telencephalon. Data taken from [ 96 ]. Moreover, there is an evident correlation between the expression peaks in individual brain-regions and appearance of the TAU-transcripts in blood of asphyxiated pups.

Transcription levels of the HER-2 protein as measured in experimental rats exposed to birth asphyxia versus control animals normoxia. According to the above given results, both TAU-protein and HER-2 can be considered as biomarker-candidates for further validating tests in clinical studies. Re-oxygenation of newborns with asphyxic deficits triggers a cascade of compensatory biochemical events to restore function, which may be accompanied by improper homeostasis and oxidative stress.

In the clinical setting, after resuscitation of an infant with birth asphyxia, the emphasis is on supportive therapy. Several interventions have been proposed to attenuate secondary neuronal injuries elicited by asphyxia, including hypothermia. Hypothermia has been pointed out to be an effective intervention against the secondary neuronal injury, elicited by the birth asphyxia [ 98 ].

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Applied immediately after birth asphyxia, hypothermia generally lowers metabolic rates, and diminishes the glutamate levels in brain [ 98 , 99 , ]. Although promising, the clinical efficacy of hypothermia has not been fully demonstrated. It is evident that new approaches are warranted. In the context of neuroprotection, several sentinel proteins have been described to protect the integrity of the genome e.

They act by eliciting metabolic cascades leading to i activation of cell survival and neurotrophic pathways; ii early and delayed programmed cell death, and iii promotion of cell proliferation, differentiation, neuritogenesis and synaptogenesis. It is proposed that sentinel proteins can be used as markers for characterising long-term effects of perinatal asphyxia, and as targets for novel therapeutic development and innovative strategies for neonatal care [ ].

Therefore, this approach is currently considered as the therapeutic strategy against the long-term deleterious consequences of birth asphyxia as well as for several pathophysiologic conditions such as myocardial reperfusion injury, stroke, neurotrauma, arthritis, multiple sclerosis and severe complications secondary to Diabetes mellitus [ ]. The application of low concentrations of NO-inhibitors is beneficial against extensive ischaemic lesions in brain [ ].

Pre- and post-hypoxic treatment with NMDA-receptor antagonists appears to reduce cerebral tissue injury [ , ].

Perinatal Asphyxia

Calcium-channel blockers have also been demonstrated to have beneficial effects [ ] by reducing post-asphyxic lesions in brain. Pretreatment with barbiturates may improve survival and reduce the severity of brain injury [ ]. It reduces cerebral metabolism [ ] and decreases oxygen consumption [ ].

By lowering the oxygen consumption, it prevents free-radical destruction of the cell membranes [ ].

Causes of Birth Asphyxia

The barbiturate pretreatment reduces the intra- and extra-cellular accumulation of water and, in this way, prevents convulsions [ ]. Postnatal treatments with free-radical scavengers such as dimethylthiourea, xanthine-oxidase, and allopurind-inhibitor improve clinical outcomes after perinatal asphyxic insults [ , ].

The authors thank to DAAD for the support. Also, the authors would like to thank M. Viktoriya Peeva for the literature search to the topic performed in — Skip to main content Skip to sections.