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Clinical, Biological and Electroencephalographic Monitoring of Newborns with Neurological Risk in the Neonatal Intensive Care Unit

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Clinical, Biological and Electroencephalographic Monitoring of Newborns with Neurological Risk in the Neonatal Intensive Care Unit EXPERIMENTAL AND THERAPEUTIC MEDICINE 22: 760, 2021 Clinical, biological and electroencephalographic monitoring of newborns with neurological risk in the Neonatal Intensive Care Unit FLORINA MARINELA DOANDES1,2, ANIKO‑MARIA MANEA1,2, NICOLETA LUNGU1,2, DANIELA CIOBOATA1,2, TIMEA BRANDIBUR1,2, OANA COSTESCU1,2, ANCA HUDISTEANU1, EUGEN RADU BOIA3 and MARIOARA BOIA1,2 1Neonatology and Puericulture Department, ‘Victor Babeş’ University of Medicine and Pharmacy of Timisoara, 300041 Timisoara; 2Neonatology and Preterm Department, ‘Louis Ţurcanu’ Children Emergency Hospital, 300011 Timisoara; 3Department of Oto‑Rhino‑Laryngology, ‘Victor Babeş’ University of Medicine and Pharmacy of Timisoara, 300041 Timisoara, Romania Received March 12, 2021; Accepted April 14, 2021 DOI: 10.3892/etm.2021.10192 Abstract. Newborns admitted to the Neonatal Intensive group. In conclusion, common blood tests in association with Care Unit (NICU) require increased attention regarding aEEG monitoring and rigorous neurological assessment can neurological assessment and monitoring, due to immaturity predict short‑term outcome of HIE and multiorgan dysfunc‑ or certain conditions that occur during the perinatal and tion and can help clinicians predict even long‑term outcomes neonatal period. Hypoxic‑ischemic encephalopathy (HIE) in severe HIE. following perinatal asphyxia is one of the most studied clinical conditions due to the risk of medium‑ and long‑term neurobe‑ Introduction havioral outcome. We studied 43 newborns with HIE, for all 3 degrees of impairment, performed amplitude‑integrated Due to immaturity or certain conditions that occur during the electroencephalography (aEEG) in the first hours of life and perinatal and neonatal period, newborns from the Neonatal collected common laboratory tests, following serum glycemia Intensive Care Unit (NICU) have a high risk of neurological at admission and creatinine, creatine kinase (CK) and lactate and developmental sequelae. The fetal brain is vulnerable to dehydrogenase (LDH) at admission and in the 3rd day of life. severe and sustained hypoxia during birth, which can lead to Newborns with mild HIE presented normal aEEG pattern and hypoxic‑ischemic encephalopathy (HIE) (1). The incidence of slightly elevated CK. A total of 80.9% of the newborns with perinatal asphyxia is reported to be between 1 and 6 per 1,000 moderate HIE had seizure patterns in aEEG, while among live full‑term births (2) and it has been determined to be those with severe HIE, 71.4% had seizure patterns in aEEG the third most common cause of neonatal death (23%), after and 28.5% burst suppression. CK and LDH were mean elevated preterm birth (28%) and severe infections (26%) (3,4). HIE, in those with moderate HIE, and the newborns with severe following perinatal asphyxia, remains an important problem, HIE had also high creatinine values at admission and in the in both full‑term and near‑term newborns (5). Early diagnosis 3rd day of life. Statistically significant differences between the and proper treatment of neurological problems in neonatal 3 degrees of HIE were noted in terms of creatinine (P=0.009) period and especially of neonatal seizures can reduce adverse and CK (P=0.008) at admission and LDH in the 3rd day of neurological outcome in early infancy (1,6,7). life (P=0.036). Hypoglycemia was common in our study HIE is a term to define the disturbed neurological function in the earliest days of life in the term newborn, consisting in the alteration of the level of consciousness, tone and neonatal reflexes, including the sucking and swallowing reflex, the pres‑ ence of seizures in moderate and severe stages of HIE (5,8) Correspondence to: Dr Florina Marinela Doandes or and cardiovascular (bradycardia, hypotension) and respiratory Dr Aniko‑Maria Manea, Neonatology and Puericulture Department, disorders (irregular respiration, apnea) in severe HIE (5,9). ‘Victor Babeş’ University of Medicine and Pharmacy of Timisoara, 2 Eftimie Murgu Square, 300041 Timisoara, Romania Furthermore, severe HIE includes multisystem involve‑ E‑mail: [email protected] ment, not only neurological, but also cardiac, renal, liver E‑mail: [email protected] damage (4,5,10‑12) and fluctuations in the glycemic values (generally, hypoglycemia) (4). Key words: hypoxic‑ischemic encephalopathy, neonatal seizures, For the detection of cerebral insult secondary to peri‑ amplitude‑integrated electroencephalography, creatinine, lactate natal hypoxia, electroencephalographic monitoring (EEG) is dehydrogenase, creatine kinase used, both to detect and monitor seizure activity and also to define abnormal patterns such as ‘burst suppression’ pattern 2 DOANDES et al: MONITORING OF NEWBORNS WITH NEUROLOGICAL RISK found in severe stages of HIE, low voltage or flat, isoelectric (stage 2) was defined in the case of lethargic newborns, with trace (13). Neonatal seizures are often subclinical and difficult decreased activity, hypotonia, distal flexion and complete to diagnose, and the initiation of anticonvulsant therapy may extension, weak sucking reflex, incomplete Moro reflex, be delayed to the detriment of the neurological status of the miosis, bradycardia, and periods of apnea. Severe encepha‑ newborn (14). Sometimes some abnormal movements of the lopathy (stage 3) has been associated with stupor or coma, no newborn (jitteriness) can be interpreted as seizures and, thus, spontaneous activity, intermittent decerebration posture, flac‑ treated incorrectly (15). Therefore, in NICU departments, cidity, absent Moro and suck reflex, pupils deviated/dilated, amplitude‑integrated electroencephalography (aEEG) is valu‑ poor reaction to light, variable heart rate and apnea. able. The aEEG bedside monitoring utilizes a reduced number of electrodes that are maintained for at least 24 h (13‑15). aEEG monitoring. The newborns were aEEG monitored in The hypoxic‑ischemic insult is usually systemic, not only the the NICU using Natus Cerebral Function Monitor‑ Olympic brain being affected. Severity of HIE may vary, and concurrent Brainz Monitor. Cross cerebral 1 or 2 channel monitoring was multiorgan dysfunctions are commonly observed (4,11,16,17). used (3 or 5 electrodes), with linear display of low‑voltage The aim of this study was to assess newborns with HIE clini‑ activity (0‑10 µV) and logarithmic display of activity cally, biologically and electroencephalographically following between 10‑100 µV, aEEG displayed as a time‑compressed perinatal asphyxia in the NICU, knowing that the severity of trend at 6 cm/h. The aEEG was classified as: a) Continuous the disease reflects the medium‑ and long‑term outcome of the normal voltage (CNV) and discontinuous normal voltage patients. Neurological recovery is fast in the mild form, while (DNV) without abnormal changes: normal; b) burst suppres‑ stages 2 and 3 of HIE require long‑term medical support, sion (BS) and inactive flat trace (FT): Abnormal; c) single or depending on the degree of organ compromise (9,13). repeated seizures (Sz) and status epilepticus (SE): epileptic activity (18,19). Patients and methods Laboratory tests. Laboratory common tests were processed Newborns. This single‑center prospective study performed in our hospital laboratory upon admission to the NICU. In over a period of 2 years included newborns with HIE admitted our study, we considered serum creatinine, creatine kinase to the regional level III Neonatal Intensive Care Unit (NICU) and LDH nonspecific markers of kidney and brain damage of ‘Louis Turcanu’ Emergency Clinical Hospital for Children following perinatal hypoxia. We also evaluated serum in Timisoara, Romania. glycemia at admission. Analyses in the 3rd day of life were The inclusion criteria were: Gestational age (GA) also collected. Normal values (from hospital laboratory ≥36 weeks, clinical and biological history of perinatal devices) consisted of: Glycemia, 3.88‑6.38 mmol/l; creatinine, asphyxia, not more than 48 h of life at admission, clinical 21‑75 µmol/l; LDH, 225‑600 U/l; and total creatine kinase, criteria of mild, moderate or severe HIE, aEEG monitoring for 24‑228 U/l. If several determinations of the same analysis at least 24 h, in the first 72 h of life. were performed, the highest or lowest value was recorded as Exclusion criteria were: GA <36 weeks, inability to perform significant, depending on the case. aEEG in the first 72 h of life, acute meningitis or encepha‑ litis, other severe infections (sepsis or pneumonia), neonatal Statistical analysis. Statistical analyses were performed using encephalopathy of other causes than perinatal asphyxia, severe Epi Info 7 for Windows (https://www.cdc.gov/epiinfo/pc.html). malformations. We used ANOVA test to analyze the variation of laboratory The study was approved by Ethics Committee for Scientific tests according to HIE stage. If ANOVA test could not be Research of the Emergency Hospital for Children ‘Louis applied, we used Mann‑Whitney or Kruskal‑Wallis test. A Turcanu’ (approval no. 78/2020). The authors ensure that the P‑value of <0.05 was considered indicative of a statistically study was carried out in accordance with the Declaration of significant difference. Helsinki. Demographic variables and clinical data were collected Results (sex, gestational age, Apgar scores, neonatal resuscitation, mechanical ventilation, neonatal seizures), aEEG, and usual Assessment of HIE. Forty‑three newborns with gestational laboratory tests [glycemia, creatinine, creatine kinase, lactate age ≥36 weeks and HIE were enrolled in the study. Of these, dehydrogenase
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