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Recently attention has been called on the possible role of acidosis in the increased methemoglobin formation in the erythrocyte of newborn infant. In the present paper the relations between acidosis and methemoglobin content in the red cells of newborns has been investigated. No significant differences between the percent of methemoglobin in the normal newborns and percent of methemoglobin in the newborns with acidosis has been found. In addition, no correlations between the base excess and percent of methemoglobin has been observed. On the contrary, two newborns with low glucose-6-phosphate dehydrogenase activity demonstrated a significantly increased methemoglobin content in their red cells. The results of our study do not confirm a key role of acidosis in the mechanism of methemoglobin formation in the neonate. It is likely than impairment of red cell metabolism should be the main factor in the formation of methemoglobin in the first days of life.

One hundred eight pregnancies in 98 insulin-dependent diabetic women were managed according to a strict protocol calling for weekly postprandial blood sugar determinations, frequent prenatal contacts, and placental evaluation. Patients were cared for on an ambulatory basis with an average of 1 hospitalization during pregnancy exclusive of delivery. There were no fetal deaths and only 1 neonatal death related to diabetes, for a corrected perinatal mortality of 0.97%. White's classification was not helpful in identifying perinatal risks. The incidence of both perinatal and maternal morbidity was high; however, complications were not serious and the overall outcome was acceptable. In view of the financial and social benefits to patients, it is recommended, that an ambulatory approach to care of the pregnant diabetic patient be used and when feasible it should be the method of choice.

Volumes of plasma (PV), blood (BV), and red cells (RCV) were estimated within 32 hours of birth in 39 neonates with normal growth, 14 neonates with intrauterine growth retardation, and 20 neonates with macrosomia. Total PV, BV, and RCV increased linearly with birth weight and were unaffected by deviation in the quality of fetal growth. In proportion to body weight, PV/kg, BV/kg, and RCV/kg correlated neither with birth weight nor with the quality of intrauterine growth. Neonates with umbilical vein hematocrit (UV Hct) levels 51% to 60%, 61% to 65%, and 66% to 77% had progressively lower, but not statistically different, mean PV/kg (38.1 +/- 4.49, 37.6 +/- 5.41, and 34.8 +/- 5.16 ml/kg, respectively). On the other hand, they had progressively higher mean BV/kg (90 +/- 10.1 vs 101 +/- 13.7 ml/kg, P less than .002, and vs 110 +/- 19.0 ml/kg, P less than .001). They also had progressively higher mean RCV/kg (52 +/- 7.4, 64 +/- 8.7, and 75 +/- 16.4 ml/kg, P less than .001). Although PV/kg did not correlate with UV Hct, both BV/kg and RCV/kg increased linearly with increasing UV Hct (r = .58 and r = .79, respectively). Volume estimates were repeated after partial exchange transfusion in 29 neonates. Mean UV Hct decreased from 63 +/- 5.9% preexchange to 51 +/- 5.2% postexchange (P less than .001), mean PV increased from 37.7 +/- 5.56 to 47.6 +/- 7.99 ml/kg (P less than .001) and mean RCV decreased from 67 +/- 16.5 to 51 +/- 12.3 ml/kg (P less than .001). Despite precautions to keep the partial exchange isovolemic, mean BV decreased from 105 +/- 18.7 to 98 +/- 18.0 ml/kg (P = .001) and the mean PV increase (10 ml/kg) was less than the mean RCV decrease (16 ml/kg). These data suggest that neonates with polycythemic have normal PV but their RCV and BV are elevated in direct proportion to UV Hct. "Isovolemic" partial exchange transfusion decreases UV Hct, RCV, and BV and increases PV.

In a 3-yr period, eight infants among 43 survivors of acute NEC developed intestinal stricture. Four infants developed multiple stricture after proximal diversion procedures, and four had single strictures after medical therapy. Nineteen cases of intestinal stricture after NEC were collected from the literature. Radiographic examinations at the time of the acute disease were not predictive of the risk of subsequent stricture. Histologic examination showed various stages of wound healing, most prominently in the submucosa. Stricture should be considered as the cause of intestinal malfunction in any child who survives acute NEC.

Three-channel cassette electroencephalographic (EEG) recording for up to 24 hours was obtained from 37 neonates with clinically diagnosed or suspected seizures but no seizure activity on routine EEG. EEG seizures were recorded in seven patients, five of whom had experienced clinical seizures in the 24 hours prior to cassette EEG recording. EEG seizures were detected in only one of nine neonates with recurring clinical episodes believed unlikely to be seizures and in only one of 18 without recent clinical events. Cassette EEG can enhance the detection and differentiation of seizures in neonates with persistent clinical episodes but is of low yield otherwise.

Prenatal, intrapartum and postnatal factors are compared between 15 preterm infants, known to have periventricular leukomalacia (PVL) on ultrasound and 15 infants of similar birthweight and gestation who ultrasonographically showed no evidence of cystic lesions, and who are known to be neurologically normal at follow up. Prenatally, the incidence of antepartum haemorrhage was significantly higher in the PVL group. Intrapartum factors were similar between the two groups but postnatally, the PVL group had significantly lower PaCO2 readings during the first 72 h of life. It is postulated that a severe maternal bleed in late pregnancy and neonatal hypocarbia could significantly decrease cerebral perfusion and cause areas of ischaemia and infarction resulting in periventricular leukomalacia.

A total population of 29,395 neonates cared for in the six-year period from 1971 to 1976 was reviewed for evidence of autopsy-proven kernicterus. A total of 327 neonates died and 232 were autopsied. The only cases of kernicterus occurred in four near-term infants with antemortem proven sepsis. All four of these infants weighed more than 2,200 gm and were delivered after gestations of either 36 or 37 weeks. These cases of kernicterus occurred during a period when more aggressive management of hyperbilirubinemia in low-birth-weight infants had apparently eliminated immaturity as a predisposing factor in the development of kernicterus, uncovering bacterial infection as the major remaining etiologic co-factor.

A multivariate analysis of perinatal events occurring in infants with neonatal seizures who were enrolled in the National Collaborative Perinatal Project allowed prediction of outcome. This prediction of death or of mental retardation, cerebral palsy, or epilepsy was empirically confirmed 64% to 83% of the time. In an infant with neonatal seizures, a five-minute Apgar score of less than 7, the need for resuscitation after 5 minutes of age, the onset time of the seizures, and a seizure lasting more than 30 minutes are the best early predictors of which infants will die or will have significant neurologic sequelae. It is hypothesized that neonatal seizures may be a better indicator of the severity or duration of intrauterine asphyxia than the Apgar score. In the neonate with seizures, the use of the formula may allow identification of infants at high risk for adverse outcomes.

The hearing of 98 perinatal intensive care survivors with a mean birth weight of 1,540 g was assessed at a mean age of 6 1/2 years. They represented 73% of the long-term survivors with birth weights of 1,800 g or less who had been cared for in our neonatal unit during the three-year period 1971 through 1973. Nine of the 98 infants had sensorineural hearing loss, and 14 had exudative otitis media. During their neonatal period, the infants with hearing loss experienced more frequent apneic attacks, hyperbilirubinemia (serum bilirubin level, greater than 14 mg/dL), and hypothermia compared with their healthy counterparts. There was no evidence that the duration of stay in the incubator or the use of stay in the incubator or the use of ototoxic drugs had affected the hearing of these low-birth-weight infants.

Postmortem examination of the brain of a 5-week-old boy disclosed extensive thrombosis of the deep venous system and widespread necrosis of the cerebral parenchyma. As is characteristic of this uncommon form of cerebrovascular disease, malacia was present in the central gray matter but was only focal and incospicuous in contrast to a diffuse hemorrhagic softening of the centrum semiovale. This association of deep venous thrombosis and predominant white matter necrosis suggests that impairment of venous drainage should be considered in the pathogenesis of certain disorders of the cerebral white matter.

147 children with high risk of developing a prehepatic portal vein obstruction were reexamined. The children had survived during their neonatal period:--Serious umbilical infection and sepsis (n=33)--Multiple exchange transfusion (n=55)--Long-term umbilical vein catheter treatment for at least 24 hrs (n=59). The reexamination at the age of 2--4 years revealed one case of total occlusion of the vena lienalis with partial obstruction of the vena portae in a child with former umbilical sepsis. Even though the etiologic relation of neonatal umbilical disorders and prehepatic portal obstruction is evident, the risk for the individual case seems to be low.

In a group of 23 newborn infants with necrotizing enterocolitis receiving parenteral nutrition the serum triglyceride levels (347 samples), and the free to esterified cholesterol ratio (188 determinations) were studied. The relationship of both T, and FCH/ECH with bacterial infections were also studied. Mean T level increased significantly with the episodes of infection. In the group of infants with a birth weight less than 1,500 grs. a significantly greater percentage of T levels above 250 mg./dl. than in infants of a greater birth weight is found. FCH/ECH ratio was already abnormal in infants with necrotizing enterocolitis before parenteral nutrition was started. Authors also observed a positive correlation between abnormality of cholesterol esterification and days of parenteral nutrition.

Twelve infants with severe perinatal asphyxia were found to have elevated blood ammonia levels (302 to 960 microgram/100 ml). In the seven survivors, hyperammonemia was associated with CNS irritability, hyperthermia, hypertension, and wide neonatal heart rate oscillations. Follow-up examinations revealed severe neurologic dysfunction in five of seven infants. CNS depression, hyperthermia, hypertension, and a nonreactive, fixed heart rate characterized the infants that died. These findings suggest a clinical entity secondary to perinatal asphyxia whose signs and symptoms may be related to hyperammonemia.

The classification of the background EEG was performed in 132 fullterm neonates who had suffered perinatal hypoxia by visual inspection of whole polygraphic records of 2--3 h duration, i.e., maximally depressed, markedly depressed, moderately depressed, mildly depressed, minimally depressed, normal and other, according to the distribution of 7 EEG patterns. The quantitative analysis of the polygraphic record was made in 33 of the above and 10 control infants to investigate the effect of perinatal hypoxia on the background EEG and behavioral state cycle and to confirm the validity of the above classification. The calssification of the background EEG was well correlated with the disturbance of sleep cycle, which was also related to the interval after the hypoxic insult. The relation between sleep states and EEG patterns also had a close correlation with the classification and became progressively disrupted with increasing severity of the background EEG. Each grade of the background EEG abnormality had a different prognostic significance accordsing to the time of the recording. The one in the first week offered the best prognostic value.

Many etiologic factors have been implicated in delayed language development in the preschool child including: low birth weight, perinatal insults to the CNS, and chronic/recurrent middle ear disease with conductive hearing impairment during the first years of life. The results of an in-depth evaluation of 24 children, who manifested preschool language delay significant enough to require remedial intervention, are reported. A suggested early identification model employing High Risk Factors and a Developmental Screening Questionnaire for use by otolaryngologists, pediatricians and audiologists is presented.

Noxious insults interfering perinatally lead to disorganization of normal perinatal brain development characterized by growth acceleration and intensive histogenesis and known as a sensitive "vulnerable" period of CNS development. Thus induced abnormities, sometimes very discrete, give rise to functional pathology which becomes apparent gradually during maturation as neurobehavioural deviations. For the study of these pathogenetic processes, two experimental models were established. Rat was chosen as an advantageous model animal since the "brain growth spurt" occurring in man in the third trimester of gravidity is shifted postnatally in this altricial species. Prolonged neonatal malnutrition (days 1-40) lead in adult rats to behavioural abnormities (hyperactivity, stereotypy, decreased adaptability, aggressivity) associated with biochemical and electrophysiological alterations in the brain. But this multifactorial and long-term insult was not suitable for more precise analysis. Therefore short-term inhibition of protein synthesis was induced in 7-day-old rats by cycloheximide which resulted in delayed behavioural deviations (hyperactivity, decreased habituation, learning deficit, motor incoordination) connected with permanent morphological, biochemical and endocrinological alterations. These models were used for testing brain maldevelopment-regulatory action of nootropics. Pyritinol administered for 7-10 days following the noxious intervention prevented the brain maldevelopment and functional disturbances in both experimental models. Favourable effects of early and long-term pyritinol treatment on neuro-psycho-pathological sequels of perinatal distress were confirmed in clinical controlled prospective study of 128 high-risk newborns.

Authors analyse treatment and clinical and analytical evolution of 80 patients with hypertonic dehydration, depending on shock and acidosis. Several considerations concerning treatment and its' influence on evolution of different patients, emphasizing both therapeutic methods: with or without use of peritoneal dialysis, according to the values of initial natraemia, are made.

Thirteen infants with compartmentalization of the lateral ventricles diagnosed by air encephalography, computerized tomography, or autopsy are reported. In each case, the body of one or both lateral ventricles was completely divided by a membrane posterior to the foramen of Monro. Recognition of this entity is important from both therapeutic and prognostic standpoints.

Attention is called to a poorly recognized syndrome of neonatal renal arterial embolism, presumably from the ductus arteriosum, resulting in malignant hypertension, congestive heart failure, respiratory distress, and increased renin secretion. Radiographic studies revealed a ductus diverticulum and multiple narrowed arteries including the lower pole branches of the right renal artery. Renal scan showed poor imaging of the lower pole of the right kidney. Nephrectomy resulted in a prompt return of the blood pressure into the normal range. Eight cases recorded in the literature resemble the one reported here, and six of the eight had an associated thrombosis of the ductus arteriosum. Our patient appears to be the first case recognized by modern techniques followed by nephrectomy and clinical cure.

Burkitt's lymphoma (B.L.) is very restricted geographically, whereas the Epstein-Barr virus (E.B.V.), a very likely causal factor, exists all over the world. It is proposed that perinatal infection (either transplacental, or, more probably, neonatal) is an important risk factor for the development of B.L. This hypothesis arose when the epidemiological characteristics of E.B.V. infection were compared in different parts of the world and is supported by the preliminary results of a seroepidemiological prospective study of B.L. E.B.V. would behave in a manner similar to that of animal tumour viruses whose oncogenic potential is greatly enhanced by neonatal infection.

We investigated the contribution of brain growth failure to outcome in infants of very low birth weight (VLBW; less than 1.5 kg) who were appropriate for gestational age (AGA; n = 379) or small for gestational age (SGA; n = 102). Growth was assessed at birth, term, and 8 and 20 months' corrected age and results of a Bayley Mental Developmental Index (MDI) and neurologic examination were evaluated at 20 months of age. Both groups had similar 20-month MDI scores (93 vs 90) and similar rates of neurologic impairment (14% vs 10%). More SGA infants (25%) than AGA infants (14%) had a subnormal head circumference at 8 months' corrected age, indicating failure to catch up in head growth. Subnormal head size at 8 months predicted the 20-month MDI score for both groups. However, multivariate analysis indicated that, whereas subnormal 8-month head size was directly associated with the MDI score in AGA children, in SGA children 8-month head size was not significantly related to the MDI score when neonatal illness, neurologic impairment, socioeconomic status, and race were controlled for. We conclude that in AGA VLBW infants, subnormal head size at 8 months results from major neonatal illness and has adverse later effects. In SGA infants, subnormal head size at 8 months has many causes, including growth retardation in utero, which may not have an adverse effect on outcome; if subnormal head size is superimposed with neonatal illness, a poorer outcome is likely.

Nine infants with haematoma of the SCM muscle were evaluated. A review of previous reports and a comparison of the clinical features of this group of patients to ones considered in other reports is reported and a simple therapeutic program is outlined: during the first year of life, postures and simple exercises performed by the mother under the pediatrician's supervision are suggested. In the eight cases in which the therapeutic program was followed, the long-term outcome was satisfactory from both cosmetic and functional point of view. Therefore this method should be preferred during the first year of life, also taking into account the lack of negative influence on the mother-infant relationship and on the infant's neurological development.

Extracorporeal membrane oxygenation is an important technology in the treatment of high-risk infants whose long-term outcome is being followed prospectively at our institution. The extracorporeal membrane oxygenation procedure allows temporary cardiopulmonary support for critically ill full-term neonates who are refractory to maximum ventilatory and medical management as a consequence of severe persistent pulmonary hypertension. The technique necessitates both the permanent ligation of the right common carotid artery and jugular vein and systemic heparinization. The survivors constitute a unique group of high-risk infants, from the standpoint of the hypoxic-ischemic insults preceding extracorporeal membrane oxygenation and the risks associated with the procedure. Our results indicate that most of our survivors are developing normally at 1 year. Major morbidity, in terms of either significant developmental delay (Bayley mental and motor indices less than 70) or significant neuromotor abnormality, occurred in only 10% of these infants. Poor outcome was associated with major intracranial hemorrhage and chronic lung disease. Ligation of the right carotid artery and jugular vein was not associated with a consistent lateralizing lesion. Long-term follow-up through school age is essential.

Most frequent complications of infusion therapy in children include thrombosis and thrombophlebitis of the umbilical and subclavian veins. In the perinatal period thrombophlebitis of the umbilical vein is due to exogenous infection and becomes the source of umbilical sepsis. Thrombophlebitis of the subclavian vein in nurslings results more frequently from endogenous infection. Because of morpho-functional immaturity in infancy, hyperhydration of tissues is extreme, with vacuolar dystrophy of cells up to their necrosis, particularly in the liver and kidneys. Artificial pulmonary ventilation (APV), particularly in premature newborns, is frequently accompanied by breaks of alveolar septae, development of bullous and interstitial emphysema, pneumothorax. In deeply premature infants APV may be ineffective because of immaturity of the lung tissue.

5 infants with no growth of bacteria on cultures of blood and peritoneal fluid recovered from necrotising enterocolitis after medical treatment alone. 12 infants with positive cultures required surgery. 5 of these 12, who did not harbour clostridia, had a mild clinical course and all 5 survived segmental bowel resection. The 7 infants who harboured clostridia had a more severe clinical course and 4 died. In 3 of 4 infants with Clostridium perfringens, the necrotising enterocolitis was fulminant, characterised by severe pneumatosis intestinalis, extensive gangrene, early intestinal perforation, and a fatal outcome.

In relation to cochlear implants, the authors review the various etiologies of deafness in infancy and childhood, either genetic or acquired in order to determine the criteria for advising implantation. They put forward the necessity of complete evaluation of all the auditory pathways involved to determine if a premature who has sustained hypoxicischemic encephalopathy and a full term baby have the same chance to benefit from cochlear implants after meningitis. Defined criteria are urgent needs for patients and parents.

Fifteen-year-old children with a life-long history of epilepsy were examined. The epilepsy in these children was mostly due to ante- and perinatal pathology. It was revealed that the impact of pathogenic factors in the ante- and perinatal periods predetermined the development of foci of pathologically enhanced excitation in the brain. As the disease progressed, these foci got stabilized and the epileptic system began to form. Specific features of the systemogenesis arising under pathological situations in the early stages of the ontogenesis are shown to represent those factors which are implicated in the development of epilepsy as a whole.