Diagnostic de l’acidose métabolique à la naissance par la détermination du pH eucapnique

The identification of a metabolic acidosis is a key criterion for establishing a causal relationship between fetal perpartum asphyxia and neonatal encephalopathy and/or cerebral palsy. The diagnostic criteria currently used (pH and base deficit or lactatemia) are imprecise and non-specific.ObjectiveThe study aimed to determine among a low-risk cohort of infants born at term (n = 867), the best diagnostic tool of metabolic acidosis in the cordonal from the following parameters: pH, blood gases and lactate values at birth.Materials and methodsThe data were obtained from arterial blood of the umbilical cord by a blood gas analyser. The parameter best predicting metabolic analysis was estimated from the partial correlations established between the most relevant parameters.ResultsThe results showed a slight change in all parameters compared to adult values: acidemia (pH: 7.28 ± 0.01), hypercapnia (56.5 ± 1.59 mmHg) and hyperlactatemia (3.4 ± 0.05 mmol/L). From partial correlation analysis, pCO₂ emerged to be the main contributor of acidemia, while lactatemia was shown to be non-specific for metabolic acidosis. Seven cases (0.81 %) showed a pH less than 7.00 with marked hypercapnia. The correction of this respiratory component by EISENBERG's method led to the eucapnic pH, classifying six out of seven cases as exclusive respiratory acidosis.Discussion and conclusionIt has been demonstrated that the criteria from ACOG-AAP for defining a metabolic acidosis are incomplete, imprecise and generating errors in excess. The same is true for lactatemia, whose physiological significance has been completely revised, challenging the misconception of lactic acidosis as a specific marker of hypoxia. It appeared that eucapnic pH was the best way for obtaining a reliable diagnosis of metabolic acidosis. We proposed to adopt a simple decision scheme for determining whether a metabolic acidosis has occurred in case of acidemia less than 7.00.     

The evaluation of polycythemic newborns: efficacy of partial exchange transfusion

Objectives.?To evaluate the clinical characteristics and risk factors of symptomatic and asymptomatic polycythemic neonates performed partial exchange transfusion (PET) and to determine the time of resolution of symptoms and effect of PET on short-term morbidity.

Methods.?This prospective cohort study was conducted with symptomatic (hematocrit; Hct?>65% plus a clinical symptom) and asymptomatic (Hct level?>70% without any symptoms) neonates who underwent PET due to polycythemia.

Results.?Among the patients performed PET, 43 (69.3%) were symptomatic and 19 (30.7%) asymptomatic. Persistent pulmonary hypertension and minor problems like hypoglycemia, hypocalcemia, hyperbilirubinemia, and thrombocytopenia improved in all patients within 24?h, 2.5?±?1.0, 3.1?±?1.4, 56.2?±?16.9, and 53.5?±?10.5?h, respectively, after PET (in except one symptomatic neonate with hypoglycemia). In symptomatic group, in three patients with suspected necrotizing enterocolitis (NEC) prior to PET stage IIa NEC developed. No other clinical and ultrasonographic findings were observed after PET.

Conclusions.?Early morbidities, due to polycythemia may be reversed with PET within a short time. PET did not increase or cause any complications except NEC. The issue that either NEC was a sign of polycythemia or a complication of PET could not be definitely outlined.     

Neonatal seizure automatism and human inborn pattern of quadrupedal locomotion

Seizures in newborns do not always show a clear electro-clinical correlation. The real epileptic nature of some stereotyped rhythmic movements, included in the ‘subtle seizures’ and considered as brainstem release phenomena, is still debated. We report a brain injured newborn, who displayed several episodes of repetitive limb movements. The ictal EEG discharge, during one of these episodes, was associated with a motor pattern modification, which was endowed with quadrupedal locomotion kinematic features. This might represent an indirect evidence of cervical and lumbar Central Pattern Generators interconnection with in-phase coordination between diagonal limbs since the first hours of life in humans.     

Does newborn screening improve early lung function in cystic fibrosis?

Despite evidence showing an improvement in nutritional outcomes following diagnosis by newborn screening (NBS) for cystic fibrosis (CF), the impact on pulmonary outcomes has been less clear. In this review the approaches to measurement of early lung function and knowledge gained from NBS CF cohorts will be described. Studies which have compared outcomes in those diagnosed by NBS to those diagnosed following symptomatic presentation will be presented. Compiling the evidence base used to evaluate the impact of NBS on pulmonary outcomes has been complicated by improvements in clinical management, infection control practices, as well as public health interventions (such as tobacco smoking bans in public places) that have evolved substantially over recent decades. Forced expiratory volumes have been used as the main outcome but it is important not to draw conclusions for ‘early lung function’ from tests such as spirometry alone, which lack sensitivity in early lung disease. There is, at present, insufficient evidence to draw firm conclusions about the effect of NBS on early lung function. In an era of highly effective treatments targeting the underlying molecular defect responsible for CF, future opportunities for early initiation of treatment may mean that the impact of NBS on early lung function may yet to be realised.     

Rapid infusion of excessive phenytoin: A newborn autopsy case

The patient was a two-day-old female infant. The patient’s mother was a primigravid in her 20 s who developed premature abruption of the normal placenta on the first day of the 33rd week of gestation. The infant was born by emergency cesarean section with severe neonatal asphyxia with a birth weight of 1928 g. Spontaneous circulation was returned 11 min after birth. The infant was treated under mechanical ventilation in the neonatal intensive care unit, and phenobarbital was administered for repeated seizures. On day 2, spontaneous respiration was observed; however, the patient developed seizures repeatedly. The dose of phenobarbital reached the maximum and was switched to midazolam. In the early morning of day 3, while midazolam was administered up to the maximum dose, the infant developed status epilepticus, and the anticonvulsant drug was changed to phenytoin. Due to a calculation error, the intravenous administration of phenytoin was started at 400 mg/30 min, which is 10-fold of the normal dose. Six minutes later, after 80 mg was administered, the administration was stopped due to a drop in blood pressure; however, the infant died of cardiac arrest. An autopsy, which was performed approximately 25 h after death, revealed the blood phenytoin concentration in the heart was 63.85 μg/mL. The cause of death was determined to be acute phenytoin toxicity. This is the first fatal case reported of the blood concentration of phenytoin caused by rapid intravenous administration.