Perinatal hypoxic-ischemic encephalopathy (HIE) represents a major cause of neonatal death or long-term disability. Inflammation plays an important role in mediating brain damage induced by neonatal hypoxic-ischemic encephalopathy. The mechanisms underlying the inflammatory response in hypoxia and ischemia are complex and are still being extensively researched. The objective of this study was to determine the predictive value of peak lactate dehydrogenase (LDH), C-reactive protein (CRP), procalcitonin (PCT) and of the evolution of leukocytes, neutrophils and lymphocytes in the first 96 h after birth for the grade of encephalopathy and neurodevelopmental outcome in newborns with HIE. In order to reveal this relationship we used comparisons between the above mention parameters. The observed hematological changes were nonspecific. The vast majority of the 78 newborns included in the study had PCT values above normal in the first 24 h, contrasting with CRP values that were positive in only 15.8% of the patients. A total of 76.9% of the patients had LDH values higher than the upper limit of normal values. The mean LDH values in patients with an unfavorable prognosis were 1,235 U/l. We can conclude that LDH is a good predictor of HIE in the first 12/24 h after birth.

Newborns admitted to the Neonatal Intensive Care Unit (NICU) require increased attention regarding neurological assessment and monitoring, due to immaturity or certain conditions that occur during the perinatal and neonatal period. Hypoxic-ischemic encephalopathy (HIE) following perinatal asphyxia is one of the most studied clinical conditions due to the risk of medium-and long-term neurobehavioral outcome. We studied 43 newborns with HIE, for all 3 degrees of impairment, performed amplitude-integrated electroencephalography (aEEG) in the first hours of life and collected common laboratory tests, following serum glycemia at admission and creatinine, creatine kinase (CK) and lactate dehydrogenase (LDH) at admission and in the 3rd day of life. Newborns with mild HIE presented normal aEEG pattern and slightly elevated CK. A total of 80.9% of the newborns with moderate HIE had seizure patterns in aEEG, while among those with severe HIE, 71.4% had seizure patterns in aEEG and 28.5% burst suppression. CK and LDH were mean elevated in those with moderate HIE, and the newborns with severe HIE had also high creatinine values at admission and in the 3rd day of life. Statistically significant differences between the 3 degrees of HIE were noted in terms of creatinine (P=0.009) and CK (P=0.008) at admission and LDH in the 3rd day of life (P=0.036). Hypoglycemia was common in our study group. In conclusion, common blood tests in association with aEEG monitoring and rigorous neurological assessment can predict short-term outcome of HIE and multiorgan dysfunction and can help clinicians predict even long-term outcomes in severe HIE.

Hypoplastic left heart syndrome is a heterogeneous group of congenital cardiac malformations which associates hypoplastic/aplastic left ventricle, mitral and aortic valve, hypoplastic/atresia and severe aortic artery coarctation, and represents a medical-surgical emergency. We present a case of a newborn hospitalised in three clinics (two clinics from Timisoara and one from Vienna), and operated for hypoplastic left heart syndrome, without aortic coarctation, using a mixed technique cardiovascular repair surgery. The initial therapeutic conduct included maintaining the permeability of the arterial canal with prostaglandin E1. At the Vienna General Hospital, at the age of 17 days, bilateral banding of the pulmonary artery was performed and, at the age of 20 days, during the cardiac catheterisation, the Rashkind procedure (balloon atrial septostomy) was performed, with two stents being implanted in the arterial canal. Postoperative complications were postcardiotomy syndrome, pneumonia with Enterococcus faecalis and Stenotrophomonas maltophilia, sepsis with methicillin-resistant Staphylococcus aureus, coagulopathy, mixed anaemia, and metabolic acidosis. The patient died 1 month after the intervention due to cardiorespiratory arrest, bilateral congestive heart failure, left heart hypoplasia with shunt through the arterial canal and pulmonary artery banding, multiorgan failure, and severe secondary haemorrhagic disease. In conclusion, the initial cardiac surgical reconstruction consisted of a mixed technique, and anticoagulant medical treatment with heparin, antibiotics (bacterial endocarditis prophylaxis to be performed throughout life); postintervention hypoxic and infectious complications resulted in multiorgan failure and death.