Evidence of Occurrence of Intradural and Subdural Hemorrhage in the Perinatal and Neonatal Period in the Context of Hypoxic Ischemic Encephalopathy: An Observational Study from Two Referral Institutions in the United Kingdom

2009 ◽  
Vol 12 (3) ◽  
pp. 169-176 ◽  
Author(s):  
Marta C. Cohen ◽  
Irene Scheimberg
Keyword(s):  
Thin Film ◽  
Hypoxic Ischemic Encephalopathy ◽  
Subdural Hemorrhage ◽  
Intrauterine Death ◽  
Venous Plexus ◽  
Neonatal Deaths ◽  
The United Kingdom ◽  
Degrees Of Severity ◽  
The Brain ◽  
Ischemic Encephalopathy

The occurrence of subdural hemorrhage (SDH) on the convexities of the cerebral hemispheres is not an unusual finding in the setting of intrauterine, perinatal, or neonatal deaths, the hemorrhage usually presenting either as a thin film over the occipital poles or as a small infratentorial bleed. Working in 2 referral centers with over 30 000 deliveries per year, we routinely examine the dura macroscopically and histologically in nonmacerated fetuses over 24 weeks in gestation and in neonates. This paper describes our experience of intradural hemorrhage (IDH) and SDH associated with hypoxia. Our series comprises 25 fetuses and 30 neonates with obvious macroscopic intradural hemorrhage and hypoxia of varying degrees of severity diagnosed by systematic examination of the brain. Fetal gestational age ranged from 26–41/40 weeks (all no more than 24 hours from intrauterine death), while the 30 neonates lived for between 1 hour and 19 days. Simultaneously with IDH, frank SDH was seen in 2 of 3 of all cases (16 fetuses and 20 neonates). Intradural hemorrhage was more prominent in the posterior falx and tentorium, most likely because of the existence of 2 venous plexus at these sites. Our findings demonstrate that SDH and cerebral hypoxia are common associations of IDH and that SDH (often seen as a thin film of hemorrhage) almost always occurs in association with diffuse falcine IDH. Diffuse IDH with SDH are more frequently associated with severe or moderate hypoxic ischemic encephalopathy (HIE), while mild or early HIE is more common with focal IDH without SDH.

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

2010 ◽  
Vol 113 (1) ◽  
pp. 233-249 ◽  
Author(s):  
Robert D. Sanders ◽  
Helen J. Manning ◽  
Nicola J. Robertson ◽  
Daqing Ma ◽  
A. David Edwards ◽  
...  
Keyword(s):  
Perinatal Period ◽  
Rapid Identification ◽  
Postnatal Period ◽  
Hypoxic Ischemic Encephalopathy ◽  
Current Status ◽  
Neuroprotective Agents ◽  
Period 2 ◽  
Neuroprotective Strategies ◽  
The Brain ◽  
Ischemic Encephalopathy

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.

scholarly journals Lipid Profiles from Dried Blood Spots Reveal Lipidomic Signatures of Newborns Undergoing Mild Therapeutic Hypothermia after Hypoxic-Ischemic Encephalopathy

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4301
Author(s):  
Rebekah Nixon ◽  
Ting Hin Richard Ip ◽  
Benjamin Jenkins ◽  
Ping K. Yip ◽  
Paul Clarke ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Peripheral Blood ◽  
Univariate Analysis ◽  
Dried Blood Spots ◽  
Hypoxic Ischemic Encephalopathy ◽  
Perinatal Brain Injury ◽  
Blood Spots ◽  
Lipid Species ◽  
The Brain ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is associated with perinatal brain injury, which may lead to disability or death. As the brain is a lipid-rich organ, various lipid species can be significantly impacted by HIE and these correlate with specific changes to the lipidomic profile in the circulation. Objective: To investigate the peripheral blood lipidomic signature in dried blood spots (DBS) from newborns with HIE. Using univariate analysis, multivariate analysis and sPLS-DA modelling, we show that newborns with moderate–severe HIE (n = 46) who underwent therapeutic hypothermia (TH) displayed a robust peripheral blood lipidomic signature comprising 29 lipid species in four lipid classes; namely phosphatidylcholine (PC), lysophosphatidylcholine (LPC), triglyceride (TG) and sphingomyelin (SM) when compared with newborns with mild HIE (n = 18). In sPLS-DA modelling, the three most discriminant lipid species were TG 50:3, TG 54:5, and PC 36:5. We report a reduction in plasma TG and SM and an increase in plasma PC and LPC species during the course of TH in newborns with moderate–severe HIE, compared to a single specimen from newborns with mild HIE. These findings may guide the research in nutrition-based intervention strategies after HIE in synergy with TH to enhance neuroprotection.

scholarly journals Neuronal apoptosis can be prevented by the combined therapy with melatonin and hypothermia in a neonatal rat model of hypoxic-ischemic encephalopathy

2021 ◽  
Author(s):  
Alina Mihaela Toader ◽  
Oana Hoteiuc ◽  
Cristina Bidian ◽  
Dan-Daniel Oltean ◽  
Flaviu Tabaran ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Brain Regions ◽  
Hypoxic Ischemic Encephalopathy ◽  
Newborn Rats ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
The Brain ◽  
Ischemic Encephalopathy

Introduction. Birth hypoxia is a leading cause of perinatal mortality and neurological morbidity, resulting in central nervous system injury. Cerebral hypoxia and ischemia can produce a severe brain damage following a typical pattern, defined by selective vulnerability of the brain regions. The neonates are most prone to hypoxic-ischemic injuries due to the lack of efficient antioxidant defense. Neonatal hypoxia–ischemia (HI) in a 7-day-old rat HI model can produce cell death by apoptotic or necrotic mechanisms. The degree of apoptotic or necrotic mechanisms responsible for cell death in neonatal hypoxia–ischemia are not very clear as yet. The form of neuronal death may also depend on the severity of ischemic injury. Necrosis predominates in more severe cases, whereas apoptosis occurs in areas with milder ischemic injury. A human study demonstrated apoptotic and necrotic forms of cell death after hypoxic injury, whereas in some brains from stillbirths, only apoptotic figures were observed. The expression of activated caspase-3 reflects the role of apoptosis in neonatal hypoxic ischemic brain injury. Objectives. The aim of this study was to evaluate the possible neuroprotective effect of melatonin and hypothermia in hypoxic-ischemic encephalopathy in newborn rats. Local damages induced by hypoxia and ischemia were assessed by evaluating the changes in terms of histology and apoptosis. Methods. The experiment was conducted on 20 newborn Wistar rats premedicated for seven days with melatonin in a dose of 20 mg/kg/day. On the 7th postnatal day (P7), the newborn rats were exposed to ischemia (by clamping the right carotid artery) and hypobaric hypoxia (8% O2 for 90 minutes) and some groups to hypothermia. Results. In this experimental model of neonatal encephalopathy, melatonin, in a dose of 20 mg/kg/day has neuroprotective effect by reducing the number of cells expressing apoptosis in Cornu Ammonis (CA) (Ammon’s Horn) CA1, CA2, CA3 and dentate gyrus of the hippocampus when combined with hypothermia. Conclusion. The results of this study prove that melatonin is protective in ischemic-hypoxic brain injuries, but the protection is conditioned in most of the brain regions (excepting cerebral cortex) by conjugation with post-injury hypothermia treatment.  

scholarly journals Apgar Scores at 10 Minutes and Outcomes in Term and Late Preterm Neonates with Hypoxic-Ischemic Encephalopathy in the Cooling Era

2018 ◽  
Vol 36 (05) ◽  
pp. 545-554 ◽  
Author(s):  
Marina Ayrapetyan ◽  
Kiran Talekar ◽  
Kathleen Schwabenbauer ◽  
David Carola ◽  
Kolawole Solarin ◽  
...  
Keyword(s):  
Therapeutic Hypothermia ◽  
Brain Mri ◽  
Brain Magnetic Resonance Imaging ◽  
Hypoxic Ischemic Encephalopathy ◽  
Preterm Neonates ◽  
Short Term ◽  
Apgar Scores ◽  
Significant Difference ◽  
The Brain ◽  
Ischemic Encephalopathy

Objective To determine the short-term outcomes (abnormal brain magnetic resonance imaging [MRI]/death) in infants born with a 10-minute Apgar score of 0 who received therapeutic hypothermia and compare them with infants with higher scores. Study Design This is a retrospective review of 293 neonates (gestational age ≥ 35 weeks) born between November 2006 and October 2015 admitted with hypoxic-ischemic encephalopathy who received therapeutic hypothermia. Results of brain MRIs were assessed by the basal ganglia/watershed scoring system. Short-term outcomes were compared between infants with Apgar scores of 0, 1 to 4, and ≥5 at 10 minutes. Results Eight of 17 infants (47%) with an Apgar of 0 at 10 minutes survived, having 4 (24%) without abnormalities on the brain MRI and 7 (41%) without severe abnormalities. There was no significant difference in the combined outcomes of “death/abnormal MRI” and “death/severe abnormalities on the MRI” between infants with Apgar scores of 0 and 1 to 4. Follow-up data were available for six of eight surviving infants, and none had moderate or severe neurodevelopmental impairment. Conclusion In the cooling era, 47% of infants with no audible heart rate at 10 minutes and who were admitted to the neonatal intensive care unit survived; 24% without abnormalities on the brain MRI and 41% without severe abnormalities.

Bacteriophage carriers localize in the brain of a rat model of neonatal hypoxic‐ischemic encephalopathy

2021 ◽  
pp. 2100226
Author(s):  
Abdullah K. Alshememry ◽  
Jung‐Lynn Jonathan Yang ◽  
Edward A. Armstrong ◽  
Jerome Y. Yager ◽  
Larry D. Unsworth
Keyword(s):  
Rat Model ◽  
Hypoxic Ischemic Encephalopathy ◽  
The Brain ◽  
Ischemic Encephalopathy

scholarly journals Thiamine as a Possible Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Encephalopathy

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 42
Author(s):  
Gian Pietro Sechi ◽  
Flaminia Bardanzellu ◽  
Maria Cristina Pintus ◽  
Maria Margherita Sechi ◽  
Maria Antonietta Marcialis ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Hypoxic Ischemic Encephalopathy ◽  
Neuroprotective Strategy ◽  
Pathophysiological Role ◽  
High Doses ◽  
The Many ◽  
The Brain ◽  
Thiamine Treatment ◽  
Ischemic Encephalopathy

On the basis that similar biochemical and histological sequences of events occur in the brain during thiamine deficiency and hypoxia/ischemia related brain damage, we have planned this review to discuss the possible therapeutic role of thiamine and its derivatives in the management of neonatal hypoxic-ischemic encephalopathy (HIE). Among the many benefits, thiamine per se as antioxidant, given intravenously (IV) at high doses, defined as dosage greater than 100 mg IV daily, should counteract the damaging effects of reactive oxygen and nitrogen species in the brain, including the reaction of peroxynitrite with the tyrosine residues of the major enzymes involved in intracellular glucose metabolism, which plays a key pathophysiological role in HIE in neonates. Accordingly, it is conceivable that, in neonatal HIE, the blockade of intracellular progressive oxidative stress and the rescue of mitochondrial function mediated by thiamine and its derivatives can lead to a definite neuroprotective effect. Because therapeutic hypothermia and thiamine may both act on the latent period of HIE damage, a synergistic effect of these therapeutic strategies is likely. Thiamine treatment may be especially important in mild HIE and in areas of the world where there is limited access to expensive hypothermia equipment.

Lack of Evidence for a Causal Relationship between Hypoxic-Ischemic Encephalopathy and Subdural Hemorrhage in Fetal Life, Infancy, and Early Childhood

2007 ◽  
Vol 10 (5) ◽  
pp. 348-350 ◽  
Author(s):  
Roger W. Byard ◽  
Peter Blumbergs ◽  
Guy Rutty ◽  
Jan Sperhake ◽  
Jytte Banner ◽  
...  
Keyword(s):  
Sudden Infant Death ◽  
The United States ◽  
Hypoxic Ischemic Encephalopathy ◽  
Sudden Infant ◽  
Subdural Hemorrhage ◽  
Fetal Life ◽  
Female Ratio ◽  
Infancy And Early Childhood ◽  
Age Range ◽  
Ischemic Encephalopathy

It has been asserted that hypoxic-ischemic encephalopathy (HIE) with cerebral swelling in the absence of marked trauma may be responsible for subural hemorrhage in the young. As this may have considerable implications in determining both the mechanism of death and the degree of force required to cause injury in certain cases of inflicted head injury in infancy, clarification is required. A retrospective study of 82 fetuses, infants, and toddlers with proven HIE and no trauma was undertaken from forensic institutes in Australia, the United Kingdom, Germany, Denmark, and the United States. The age range was 35 weeks gestation to 3 years, with a male to female ratio of 2:1. All cases had histologically confirmed HIE. Causes of the hypoxic episodes were temporarily resuscitated sudden infant death syndrome with delayed death (N = 30), drowning (N = 12), accidental asphyxia (N = 10), intrauterine/delivery asphyxia (N = 8), congenital disease (N = 6), aspiration of food/gastric contents (N = 4), inflicted asphyxia (N = 3), epilepsy (N = 1), dehydration (N = 1), drug toxicity (N = 1), complications of prematurity (N = 1), and complications of anesthesia (N = 1). The initiating event was not determined in 4 instances. In no case was there macroscopic evidence of subdural hemorrhage. In this study no support could be given to the hypothesis that HIE in the young in the absence of trauma causes subdural hemorrhage.

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