Abstract
PurposeThe aim of the presented study was to evaluate the differences between selected biochemical markers in infants with moderate or severe hypoxic-ischemic encephalopathy (HIE) and their impact on patient prognosis.MethodsA total of 57 cooled newborns were divided into groups according to Sarnat staging of HIE (A, moderate vs. B, severe). The differences between groups were evaluated depending on the mode of delivery, pregnancy and labor complications, gestational age at birth, birth weight, and Apgar score at 1.3 and 5 min. The differences in biochemical biomarkers of HIE (pH, base excess, serum lactate) as well as biomarkers of hepatic injury (aspartate transaminase, (AST), alanine transaminase (ALT), prothrombin time (PT), and activated partial thromboplastin time (APTT)), kidney failure (creatinine, urea), myocardial injury (troponin T (TnT)), levels of fibrinogen, and platelet counts were also examined. Univariate Kaplan-Meier method was used for survival analyses.ResultsThe biomarker levels in severe HIE newborns compared with moderate were as follows: pH (7.10 vs. 6.99), serum lactate (22.50 vs. 17.00 mg/dL), AST (109.50 vs. 270.55 IU/L), ALT (27.30 vs. 108.05 IU/L), PT (17.00 vs. 44.20 s), APTT (47.75 vs. 47.90 s), TnT (0.22 vs. 0.85 ng/mL), creatinine (0.68 vs. 1.15 mg/dL), urea (44.55 vs. 73.30 mg/dL), and fibrinogen (1.65 vs. 1.90 mg/dL). Survival analyses showed significantly reduced survival for severe HIE infants (75%) vs. moderate HIE (100%).ConclusionIn conclusion, the severity of HIE can be evaluated based on selected markers; however, their levels do not correspond with future prognosis of newborns.
Highlights
Neonatal encephalopathy (NE) is a term used to describe a neurological syndrome caused by a disorder of the brain
Patients frequently present a broad spectrum of other neurological symptoms, such as motor dysfunction, hearing loss, impaired vision, epilepsy, and behavioral problems, which occur as a consequence of a perinatal hypoxic-ischemic episode
Perinatal asphyxia, leading to moderate or severe hypoxic-ischemic encephalopathy (HIE), causes multiorgan injury and dysfunction of the brain, and the heart, liver, kidneys, and bone marrow [19, 20]. These pathophysiological disorders are related to the severity of encephalopathy and subsequent neurodevelopmental outcomes [21, 22]
Summary
Neonatal encephalopathy (NE) is a term used to describe a neurological syndrome caused by a disorder of the brain. NE occurs most often as a result of acute hypoxic-ischemic insult, intracranial. HIE is associated with increased risk of neonatal mortality; 15–20% of neonates die due to complications of perinatal asphyxia [3]. HIE often leads to sustained severe and irreversible brain damage. Further observations of infants affected by perinatal asphyxia revealed that 27–33% of them at an age of 6 to 7 years will develop features of intellectual disability (IQ under 70 and deficits in adaptive behaviors) [4]. Patients frequently present a broad spectrum of other neurological symptoms, such as motor dysfunction, hearing loss, impaired vision, epilepsy, and behavioral problems, which occur as a consequence of a perinatal hypoxic-ischemic episode. A diagnosis of cerebral palsy was confirmed in 17–29% of children with a history of perinatal asphyxia [4,5,6]
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