Hypoxic-Ischemic Encephalopathy: Biochemical and Physiological Aspects

Volpe, Joseph J.

doi:10.1016/b978-1-4160-3995-2.10006-8

Cited by 50 publications

(74 citation statements)

References 1,050 publications

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“…In our network the rates of neonatal asphyxia (1%), as well as of pH ≤ 7 (5‰) and HIE (0.7-1.7‰) were comparable to those described in literature when similar definitions are used [5,6,[18][19][20][21][22].…”

Section: Discussionsupporting

confidence: 87%

Is perinatal asphyxia predictable?

Locatelli

Lambicchi

Incerti

et al. 2020

BMC Pregnancy Childbirth

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Background: The objective of our study was to evaluate the association between perinatal asphyxia and hypoxicischemic encephalopathy (HIE) with the presence of ante and intrapartum risk factors and/or abnormal fetal heart rate (FHR) findings, in order to improve maternal and neonatal management. Methods: We did a prospective observational cohort study from a network of four hospitals (one Hub center with neonatal intensive care unit and three level I Spoke centers) between 2014 and 2016. Neonates of gestational age ≥ 35 weeks, birthweight ≥1800 g, without lethal malformations were included if diagnosed with perinatal asphyxia, defined as pH ≤7.0 or Base Excess (BE) ≤ − 12 mMol/L in Umbical Artery (UA) or within 1 h, 10 min Apgar < 5, or need for resuscitation > 10 min. FHR monitoring was classified in three categories according to the American College of Obstetricians and Gynecologists (ACOG). Pregnancies were divided into four classes: 1) low risk; 2) antepartum risk; 3) intrapartum risk; 4) and both ante and intrapartum risk. In the first six hours of life asphyxiated neonates were evaluated using the Thomson score (TS): if TS ≥ 5 neonates were transferred to Hub for further assessment; if TS ≥ 7 hypothermia was indicated. Results: Perinatal asphyxia occurred in 21.5‰ cases (321/14,896) and HIE in 1.1‰ (16/14,896). The total study population was composed of 281 asphyxiated neonates: 68/5152 (1.3%) born at Hub and 213/9744 (2.2%) at Spokes (p < 0.001, OR 0.59, 95% CI 0.45-0.79). 32/213 (15%) neonates were transferred from Spokes to Hub. Overall, 12/281 were treated with hypothermia. HIE occurred in 16/281 (5.7%) neonates: four grade I, eight grade II and four grade III. Incidence of HIE was not different between Hub and Spokes. Pregnancies resulting in asphyxiated neonates were classified as class 1) 1.1%, 2) 52.3%, 3) 3.2%, and 4) 43.4%. Sentinel events occurred in 23.5% of the cases and FHR was category II or III in 50.5% of the cases. 40.2% cases of asphyxia and 18.8% cases of HIE were not preceded by sentinel events or abnormal FHR. Conclusions: We identified at least one risk factor associated with all cases of HIE and with most cases of perinatal asphyxia. In absence of risk factors, the probability of developing perinatal asphyxia resulted extremely low. FHR monitoring alone is not a reliable tool for detecting the probability of eventual asphyxia.

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Section: Discussionsupporting

confidence: 87%

Is perinatal asphyxia predictable?

Locatelli

Lambicchi

Incerti

et al. 2020

BMC Pregnancy Childbirth

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“…All these factors can influence cerebral autoregulation and, therefore, blood supply to, and reperfusion of, ischemic areas. However, after HIE, the limited, available clinical evidence suggests that cerebral autoregulation is impaired 40,41 and that the cerebral circulation becomes dependent on arterial pressure to maintain adequate perfusion. This highlights the critical role of hemodynamic support of critically ill neonates.…”

Section: Secondary Energy Failurementioning

confidence: 99%

Preconditioning and Postinsult Therapies for Perinatal Hypoxic–Ischemic Injury at Term

et al. 2010

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Perinatal hypoxic-ischemic encephalopathy can be a devastating complication of childbirth. Herein, the authors review the pathophysiology of hypoxic-ischemic encephalopathy and the current status of neuroprotective strategies to ameliorate the injury centering on four themes: (1) monitoring in the perinatal period, (2) rapid identification of affected neonates to allow timely institution of therapy, (3) preconditioning therapy (a therapeutic that reduces the brain vulnerability) before hypoxic-ischemic encephalopathy, and (4) prompt institution of postinsult therapies to ameliorate the evolving injury. Recent clinical trials have demonstrated the significant benefit for hypothermic therapy in the postnatal period; furthermore, there is accumulating preclinical evidence that adjunctive therapies can enhance hypothermic neuroprotection. Advances in the understanding of preconditioning may lead to the administration of neuroprotective agents earlier during childbirth. Although most of these neuroprotective strategies have not yet entered clinical practice, there is a significant hope that further developments will enhance hypothermic neuroprotection.

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“…Hypoxic‐ischemic encephalopathy (HIE) after perinatal asphyxia is a common cause of neonatal morbidity and mortality and neurological disability among survivors 1–3 . Each year 1.2 million neonates die and about 1 million infants have permanent neurological disability caused by HIE 4 .…”

mentioning

confidence: 99%