A previous prospective study of neonatal mortality in babies receiving special care at the University College Hospital, Ibadan, revealed that respiratory failure associated with prematurity, perinatal asphyxia, sepsis, and congenital malformations were the major causes of high neonatal mortality. To improve survival, selective measures were taken to improve care of low-birth-weight infants and prevent or treat intrapartum and postnatal hypoxia, metabolic acidosis, hypoglycemia, and hypothermia. A change in the initial antibiotic management of suspected septicemia to the use of cloxacillin and an aminoglycoside was also introduced, based on the current knowledge of etiologic agents and their antimicrobial sensitivities. In the 5-year period (1976 to 1980), the neonatal mortality in babies weighing 2,500 g and more at birth dropped significantly from 1.2% to 0.7% (P < .02). The case fatality rates from birth asphyxia and neonatal sepsis dropped by 48% and 32%, respectively. Despite therapeutic interventions, however, the neonatal mortality in babies with birth weight of 1,000 g or less, 1,001 to 1,500 g, 1,501 to 2,000 g, and 2,001 to 2,499 g remained unchanged at about 82%, 25%, 9%, and 3%, respectively. These results suggest that early identification of infants at risk of developing birth asphyxia or neonatal septicemia and institution of prompt and appropriate management could produce a significant reduction in mortality in infants of normal birth weight. Survival of low-birth-weight infants requires additional high technical, financial, and manpower resources, which most centers in developing countries cannot afford at the present time. Therefore, efforts are probably better concentrated on decreasing the incidence of low birth weight.

Lomotil liquid in a dose of 0.3 mg/kg/day has been compared with plain mist kaolin in controlling acute diarrhoea in young children aged 6 weeks to 2 years. Lomotil was found to stop the diarrhoea faster and significantly shorten the period of hospital admission than kaolin (P less than 0.05) in children whose diarrhoea was complicated by moderate dehydration. In those with mild dehydration lomotil had no advantage over kaolin. Children with severe dehydration treated with lomotil spent on the average much shorter period in hospital than those on kaolin, but the numbers were too small to allow for useful comparison. There was no adverse effect observed in any of subjects at the dose of lomotil used.

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a major cause of severe neonatal jaundice in Nigeria, but not all G6PD-deficient babies become jaundiced. Neonatal jaundice not attributable to G6PD deficiency nor to any other known aetiology is also common. In an effort to explain these two facts, we have measured the levels of the three enzymes G6PD, glutathione peroxidase (GSHPX), and glutathione reductase (GSSGR) in 38 jaundiced newborns, 26 control newborns, and 44 normal adults, all of them males. We could not yet prove an additive effect of GSSGR or GSHPX deficiency with G6PD deficiency in causing jaundice. There was no evidence that low levels of GSHPX per se are associated with jaundice. However, jaundiced newborns with normal G6PD had significantly lower levels of GSSGR than control newborns with normal G6PD. These data suggest that a relatively low activity of GSSGR, a riboflavin-dependent enzyme, may predispose the red cells to accelerated destruction in the neonatal period.

A retrospective study of birthweights, the incidence, and possible aetiology of low birthweight in 31,490 Nigerian children, delivered in two hospitals at Ibadan, is reported. The important findings were: (a) mean birthweights for males (3,000 gm), and for females (2,880 gm) in a non-teaching hospital were significantly higher than 2,980 gm and 2,860 gm for males and females respectively in the teaching hospital; (b) the mean birthweights for boys were significantly higher than those for girls in both hospitals; (c) these mean birthweights, though generally higher than previous reports from Nigeria, were significantly lower than those for North American Caucasian and Negro babies, and of babies of three different racial groups in Malaysia. Other interesting, though expected findings were: (a) a high incidence of low birthweight (15.5 per cent) and (b) a high incidence of small for dates babies (60 per cent). It is suggested that since birthweights, the incidence of low birthweight and its aetiology are vital in the planning of health care in any country, a prospective study involving many urban and rural areas of the country and including factors known to influence birthweight should be undertaken.

Journal Article Neonatal Morbidity and Mortality in Ibadan: A Review of Cases seen in the Out-patient Clinic Get access C. E. EFFIONG, M.B., M.R.C.P., D.C.H. C. E. EFFIONG, M.B., M.R.C.P., D.C.H. Senior Lecturer in Paediatrics University of IbadanIbadan, Nigeria Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Tropical Pediatrics, Volume 22, Issue 6, December 1976, Pages 265–267, https://doi.org/10.1093/tropej/22.6.265 Published: 01 December 1976

A study of haematological levels (haematocrits, reticulocyte and white cell counts) in healthy singleton full-term Nigerian neonates has shown significantly lower values than those of some previous reports but similar to others. The mean haematocrit of 60.8% on the 1st day dropped quite rapidly to 39.3% by the 4th week of birth. The mean reticulocyte count ranged from 3.8 to 1.9% on the 1st and 5th postnatal days, respectively. Adult level of less than 1 % was reached on the 6th day. Mean leucocyte count on the 1st day for males (12,400/mm3) was significantly lower than that for females (15,860/mm3). The mean total white cell count stabilized by the 3rd day at approximately 9,000/mm3 and showed no significant differences between the sexes beyond the 1st day values. The polymorphonuclear leucocytes and lymphocytes formed 61 and 36%, respectively, on the 1st day but by the 3rd day the lymphocytes were the predominant white cells.

633 platelet counts are reported on 338 full-term healthy Nigerian babies aged 1 hour to 28 days. Platelet counts for the first week (207,000 +/- 72,000 cumm) are significantly lower (P less than .001) than in the subsequent 3 weeks (282,000 +/- 94,000 cumm). Platelet counts of 100,000-400,000/cumm during the first week and 100,000-450,000/cumm during the rest of the neonatal period include 95% of the respective age groups of Nigerian infants studied and these ranges can therefore be regarded as standard for healthy Nigerian neonates. Platelet counts in Nigerian neonates are essentially similar to those reported elsewhere but significantly higher than in Nigerian adults.

ABSTRACT. The association of erythrocyte G6PD deficiency (type A‐) and hyperbilirubinaemia in two groups of Nigerian male newborns has been examined. The results provide evidence that the enzyme deficiency is the single most important factor in the pathogenesis of severe neonatal jaundice in this West African population.

This male baby was spontaneously delivered after 32 weeks gestation to a 26-year-old eclamptic mother. The mother, who had had five normal babies before this pregnancy, had severe pre-eclamptic toxemia with a blood pressure of 240/140 mm Hg, albuminuria, and edema. At the time of delivery, her blood pressure could only be reduced to 160/100 despite very intensive therapy. The baby had an Apgar score of 6 and weighed 2,200 gm at birth. He had an edematous, blue and cold right forearm and hand, with numerous blisters on the dorsum of the hand. The right forearm, which was limp, had a line about 5 cm below the elbow demarcating the healthy proximal portion from the dead distal part (Fig. 1). The right brachial and radial arteries were not palpable. All other systems were normal.

The glucose 6-phosphate dehydrogenase (G6PD) genotype was determined in 100 male patients with homozygous sickle cell anemia (SS) by a combination of quantitative assay, cytochemical testing, and starch-gel electrophoresis. Of the 100 patients tested, 16 were found to be G6PD deficient (GdA-), AND 84 G6PD normal (22GsA and 62 GdB). This distribution of G6PD genotypes did not differ significantly from that observed in the general population. The level of G6PD activity in GdA- SS patients was nearly always higher than in G6PD-deficient subjects who did not have an associated hemolytic state, but it was nearly always lower than in G6PD-normal subjects. The clinical course of sickle cell disease, including the degree of anemia, was not milder in GdA- than in G6PD-normal patients but could not be proved to be significantly more severe. It was concluded that in this community the incidence of G6PD deficiency in sickle cell anemia was not greater than would be expected by chance, and there was no evidence that the coexistence of the GdA- gene in SS patients ameliorated their disease.