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Approximately 15% of deaths in developed nations are due to sudden cardiac arrest, making it the most common cause of death worldwide. Though high-quality cardiopulmonary resuscitation has improved overall survival rates, the majority of survivors remain comatose after return of spontaneous circulation secondary to hypoxic ischemic injury. Since the advent of targeted temperature management, neurologic recovery has improved substantially, but the majority of patients are left with neurologic deficits ranging from minor cognitive impairment to persistent coma. Of those who survive cardiac arrest, but die during their hospitalization, some progress to brain death and others die after withdrawal of life-sustaining treatment due to anticipated poor neurologic prognosis. Here, we discuss considerations neurologists must make when asked, “Given their recent cardiac arrest, how much neurologic improvement do we expect for this patient?”

ZusammenfassungZiel dieser Studie ist es, ein kritisches postnatales Outcome als Prädiktor für die Entwicklung einer hypoxisch ischämischen Enzephalopathie (HIE) zu evaluieren. Methodik Auf Basis der Daten der hessischen Perinatalerhebung aus dem Jahr 2016 mit 52 122 Geburten (Lebendgeborene Einlinge, ≥ 37+0 Schwangerschaftswochen) wurden die Fälle mit kritischem Outcome identifiziert. Kriterien waren ein APGAR-Score 16,0 mmol/L. Diese Fälle wurden mit den HIE-Fällen aus der Neonatalerhebung zusammengeführt. Es wurden die Odds Ratio sowie Sensitivität/Spezifität und positiver (ppW)/negativer(npW) Vorhersagewert berechnet. Durch Evaluation des Geburtsverlaufes und des subpartalen CTG wurde die potentielle Vermeidbarkeit des Kritischen Outcomes/hypoxisch ischämischen Enzephalopathie überprüft. Ergebnisse Die Inzidenz der Fälle mit kritischem Outcome (n=11) und derer mit hypoxisch ischämischen Enzephalopathie (n=29) ist gering. Nach Zusammenführung der Daten aus der Perinatal- respektive Neonatalerhebung ergaben sich eine Sensitivität von 10,34%, eine Spezifität von 99,98%, ein positiver bzw. negativer prädiktiver Wert von 27,35, bzw. 99,95%. In nahezu einem Drittel der Fälle mit kritischem Outcome (4/11) oder hypoxisch ischämischen Enzephalopathie (9/29) fanden sich Hinweise auf eine potentielle Vermeidbarkeit. Schlussfolgerungen Ein postnataler Depressionszustand führt häufiger zur Diagnose einer HIE als eine schwere Azidose im Nabelschnurblut. Da ein Drittel der Fälle vermeidbar erscheinen, kann die fachübergreifende Einzelfallanalyse bei kritischem Neugeborenenstatus zur Optimierung der Geburtshilfe auch im Rahmen der externen Qualitätssicherung (QS) zielführend sein.

Objective Hypoglycemia is a significant risk factor for perinatal brain injury and adverse outcomes, particularly in infants requiring resuscitation following hypoxic ischemic (HI) insult. We aimed to study blood glucose (BG) levels in physiologically stressed infants in the presence or absence of epinephrine (Epi) administration at resuscitation in the first 24 hours after birth. Study Design A retrospective chart review of all infants with heart rate (HR) Results By design, infants in the Epi group had lower cord pH and higher base deficit. BG was significantly lower overtime in premature infants ≤32 weeks of gestation in the Epi group. The BG was markedly higher in near-term and term infants in the Epi group compared with the PPV group. Hypoglycemia was more common despite administration of higher GIR in premature infants ≤32 weeks of gestation. Conclusion In the presence of physiological stress, premature infants are more at risk for hypoglycemia than term infants.

Hypoxic ischemic insult in early childhood can have a varied clinical presentation depending on the timing and severity of the insult, and magnetic resonance imaging plays a key role in identifying injury patterns. Dyskinetic cerebral palsy is commonly associated with injury to the basal ganglia and thalamus. We report two cases presenting in early childhood with signs and symptoms of dyskinetic cerebral palsy attributed to focal damage to the superior cerebellar vermis secondary to a hypoxic insult in the perinatal period in term infants.

Epilepsy is a frequent consequence of neonatal hypoxic–ischemic encephalopathy. It is not yet known if the introduction of therapeutic hypothermia modifies the rate and the characteristics of epilepsy. We report on 59 infants who suffered from hypoxic–ischemic encephalopathy and underwent therapeutic hypothermia. Birth, physiological and biochemical data, frequent electroencephalography (EEG) recordings or continuous EEG monitoring, and magnetic resonance imaging (MRI) were documented in the neonatal period. Prechtl's General Movements evaluation was performed and the Griffiths Scales of Mental Development were applied at 3 and 24 months of age, respectively. Children were followed up for at least 3 years (mean 5 ± 1.6 years). Six children (10%) developed epilepsy. All of them had a severe hypoxic–ischemic encephalopathy and were neurologically impaired at 2 years of age. Furthermore, all of them had a severe pattern of MRI injury and poor neonatal EEG backgrounds. Four of them suffered from neonatal status epilepticus. Four out of six showed a similar epileptic pattern: their epilepsy started early; it was drug resistant; it required an aggressive polytherapy; and it showed a spontaneous improvement after 2 years. The rate of epilepsy in our cooled infants was similar to those reported in other studies on noncooled ones. Only severe hypoxic–ischemic encephalopathy predisposed the cooled infants toward epilepsy. Neonatal status epilepticus and persisting poor EEG backgrounds were predictive of the development of epilepsy in our sample.

Background Hypoxic–ischemic injury (HII) is a significant cause of neonatal morbidity and mortality. It had been postulated that apparent diffusion coefficient (ADC) abnormalities in term neonatal HII generally peak at 3 to 5 days after birth and subsequently “pseudonormalize” by the end of the first week. Thus, ADC values may provide a clue for timing of HII. Objective In this study, we sought to assess whether ADC values can always predict time of hypoxic ischemic insult. Methodology We prospectively analyzed 34 full-term neonates with suspected HII by diffusion-weighted (DW) magnetic resonance imaging (MRI) within 14 days after birth. DW images (DWIs) were assessed for areas of restricted diffusion at different locations that could be encountered in HII. ADC maps were generated and ADC values were calculated. Spearman correlation coefficient and receiver operating characteristic (ROC) curve analyses were performed. Results The mean age of neonates at time of MRI was 8 (±4) days (range: 2–14 days). No significant correlation detected between ADC values and age of neonates at time of imaging (p = 0.183; R2 = 0.06). ROC curve analysis showed that ADC values could not discriminate between neonates who were imaged early (≤7 days) or later (p = 0.391; area under the curve = 0.633). Conclusion ADC values may not be capable to accurately predict time of onset in term neonates with HII. ADC values should always be interpreted in combination with both conventional and DWIs, and each case should be individualized instead of generalization.