The Effect of Lactic Acidosis on Neonatal Outcomes in Premature Infants

The aim of the study was to evaluate neonatal outcomes in preterm infants. Materials and methods. The study included 58 premature neonates divided into 2 groups: «A» ( N =34) with an adverse neonatal period ending in death and «B» ( N =24) who survived. Clinical assessment of the infant, measurement of blood gases, acid-base balance (ABB) and lactate, recording of lung ventilation parameters, calculation of mean airway pressure, oxygenation index (OI) and ventilation efficiency index (VEI), neurosonography and, in case of death, pathological and histological examination of the brain were performed. Results. Elevated lactate was found in 24 patients (70.5%) in group A and in 12 patients (50%) in group B. The mean lactate levels in groups A and B were 8.1±3.3 and 6.3±2.8 mmol/L, respectively. In group A, 19 (55.9%) infants had severe acidosis, corresponding to a pH of 7.19 to 6.80. In group B, only 8 (33.3%) infants had a pH between 7.0 and 7.19. At birth, neonates in both groups were found to have a base deficit (BD), which was significantly lower in group A than in group B ( P =0.004). There were no trends toward reduction of acidosis or normalization of ABB in infants in group A. Plasma BE levels in group B had returned to normal by 96 hours postpartum. The frequency of grade II, III peri/intraventricular hemorrhage (PIVH) and hemorrhage of other localization in group A were 8 (23.5%), 9 (26.5%), and 3 (8.8%), respectively. In group B, grade I PIVH and hemorrhage of other localization occurred in 5 (20.8%) and 1 (4.2%) cases, respectively. In neonates with grade II PIVH, severe lactic acidosis was diagnosed at birth: venous blood pH was 6.97 [6.8; 7.22], BE was (–21.6) [–30; –7.2] mmol/L, lactate level was 8.5 [6.3; 12.9] mmol/L, and pO₂ was 50.5 [20.5; 64] mm Hg. In infants with grade III PIVH, pH was –7.26 [7.12; 7.28], BE was (–8.1) [–8.9; –7] mmol/L, lactate was 7.6 [4.8; 8.9] mmol/L, and pO₂ was 33 [30; 50] mm Hg. Cell damage of varying severity affected all brain structures, as evidenced by absence or deformation of nuclei and nucleoli, and peripheral chromatin condensation. Morphological immaturity of brain structures was another negative factor. Conclusion. Lactic acidosis diagnosed at birth in premature infants is one of the indicators of perinatal hypoxia severity. Critical pH, BE, and lactate levels, as well as lack of response to treatment, contribute to structural brain damage and worsen prognosis. Severe changes in oxygen and lactate levels that persist for two days after birth lead to severe PIVH and irreversible brain changes.