A modified Bilirubin-induced neurologic dysfunction (BIND-M) algorithm is useful in evaluating severity of jaundice in a resource-limited setting.

BACKGROUND: Severe neonatal jaundice with associated acute bilirubin encephalopathy occurs frequently in low- and middle-income countries, where advanced diagnostic technology is in short supply. In an effort to facilitate the physical diagnosis of acute bilirubin encephalopathy, we pilot-tested a modified bilirubin induced neurologic dysfunction scoring algorithm in a group of pediatric trainees (residents) and their mentors (consultants) in a resource-constrained setting. METHODS: Jaundiced Nigerian infants were examined by consultant and resident pediatricians. The modified bilirubin induced neurologic dysfunction score assigned by residents was compared with the clinical diagnosis of acute bilirubin encephalopathy by expert consultants. Demographic information was obtained. Known risk factors were also evaluated among infants with and without acute bilirubin encephalopathy in addition to exploratory analyses. Data were analyzed by Statistical Analysis System; statistical significance was set at p < 0.05. RESULTS: Three hundred and thirty three paired modified bilirubin induced neurologic dysfunction scores (333) were analyzed and showed excellent agreement (weighted Kappa coefficient 0.7969) between residents and consultants. A modified bilirubin induced neurologic dysfunction score greater than or equal to 3 was highly predictive of a clinical diagnosis of acute bilirubin encephalopathy, with sensitivity of 90.7%, specificity of 97.7%, positive predictive value of 88.9%, and negative predictive value of 98.2%. Exposure to mentholated products was strongly associated with increased risk of acute bilirubin encephalopathy among those with known glucose-6-phosphate dehydrogenase deficiency (odds ratio = 73.94; 95% confidence interval = 5.425-infinity) as well as among those whose G6PD phenotype was unknown (odds ratio = 25.88; 95% confidence interval = 2.845-235.4). CONCLUSIONS: The modified bilirubin induced neurologic dysfunction score for neonatal jaundice can be assigned reliably by both residents and experienced pediatricians in resource-limited settings as reflected in the algorithm's sensitivity and specificity. It may be useful for predicting the development and severity of acute bilirubin encephalopathy in neonates.

Early neonatal bilirubin, hematocrit, and glucose-6-phosphate dehydrogenase status.

OBJECTIVE: To document the patterns of bilirubin and hematocrit values among glucose-6-phosphate dehydrogenase (G6PD)-deficient and G6PD-normal Nigerian neonates in the first week of life, in the absence of exposure to known icterogenic agents. METHODS: The G6PD status of consecutive term and near-term neonates was determined, and their bilirubin levels and hematocrits were monitored during the first week of life. Infants were stratified into G6PD deficient, intermediate, and normal on the basis of the modified Beutler's fluorescent spot test. Means of total serum bilirubin (TSB) and hematocrits of the 3 groups of infants were compared. RESULTS: The 644 neonates studied comprised 353 (54.8%) boys and 291 (45.2%) girls and 540 (83.9%) term and 104 (16.1%) near-term infants. They consisted of 129 (20.0%) G6PD-deficient, 69 (10.7%) G6PD-intermediate, and 446 (69.3%) G6PD-normal neonates. The G6PD-deficient and G6PD-intermediate infants had higher mean TSB than their G6PD-normal counterparts at birth and throughout the first week of life (P < .001). Mean peak TSB levels were 14.1 (9.48), 10.2 (3.8), and 6.9 (3.3) mg/dL for G6PD-deficient, G6PD-intermediate, and G6PD-normal neonates, respectively. Peak TSB was attained on approximately day 4 in all 3 groups, and trends in TSB were similar. Mean hematocrits at birth were similar in the 3 G6PD groups. However, G6PD-deficient and -intermediate infants had higher declines in hematocrit, bilirubin levels, and need for phototherapy than G6PD-normal infants (P < .001). CONCLUSIONS: The G6PD-deficient and G6PD-intermediate neonates had a higher risk of neonatal hyperbilirubinemia and would therefore need greater monitoring in the first week of life, even without exposure to known icterogenic agents.

Neonatal tetanus at the close of the 20th century in Nigeria.

The year 2000 marked another failed World Health Organization deadline for neonatal tetanus (NNT) eradication. Existing preventive strategies can be enhanced by exploring factors involved in the persistence of the scourge. Thus, records of neonates admitted between 1996 and 2000 into the Wesley Guild Hospital, Ilesa, were analysed. Of 3051 total neonatal admissions,162 (5.3%) had NNT. Eighty-nine (54.9%) mothers had clinic-based antenatal care (ANC), but only 59 (36.4%) had tetanus toxoid (TT) vaccines. The majority (66.7%) of them delivered at home or churches and others at either private clinics or primary health centres. Overall, the case fatality rate was 43.8%, though it was significantly higher among babies whose mothers had neither clinic-based ANC (odds ratio [OR] = 2.62; 95% confidence interval [CI] = 1.33-5.18) nor antenatal TT vaccination (OR = 2.41; 95% CI = 1.17-5.03). Thus, improvement on ANC, anti-tetanus immunization and ensuring hygienic deliveries are crucial for eliminating NNT in the 21st century.

Maternal factors in the etiology of fetal malnutrition in Nigeria.

BACKGROUND: The main objective of the study was to determine the role of maternal factors in the etiology of fetal malnutrition (FM) in Nigeria. Neonatal and Maternity Units of the Wesley Guild Hospital Ilesa, Nigeria, a unit of the Obafemi Awolowo University Teaching Hospitals Complex, Ile-Ife was the setting for the study. METHODS: This was a prospective study of consecutive, singleton, term live babies delivered between January and August 2001. Fetal malnutrition was diagnosed using Clinical Assessment of Fetal Nutritional Status (CANS) and the score (CANSCORE) adapted by Metcoff. The maternal prenatal record was checked and additional history was obtained from the mother. This included history of maternal illness and drugs taken during pregnancy. The socioeconomic class of the parents was also documented. Nutritional status of the mother was determined using mid arm circumference (MAC) and the body mass index (BMI). Babies were stratified into babies with FM and babies without FM. The two groups of babies were compared. RESULTS: Of the 473 studied, 89 [18.8%] had FM. Maternal factors found associated with FM were: lack of antenatal care, young mother (<18 years), primiparity, maternal undernutrition (BMI < 18.5 kg/m(2) and MAC < 23.5 cm), low socioeconomic status, pregnancy-induced hypertension, antepatum hemorrhage, and maternal infections especially malaria, urinary tract infections and HIV (P < 0.05). CONCLUSION: Improvement in the socioeconomic status of women and good antenatal care will reduce most of the maternal factors associated with FM in Nigeria. Therefore, antenatal should be made cheap and accessible to all pregnant mothers.

Use of biomarkers of sub-clinical infection, nutrition and neonatal maturity to interpret plasma retinol in Nigerian neonates.

Using the World Health Organization criterion, the prevalence of sub-clinical vitamin A deficiency can be assessed using plasma retinol concentrations <0.7 micromol/l. However, plasma retinol can be depressed by infection; thus, the use of this criterion alone may overestimate deficiency. In the present study, we investigated the usefulness of the acute-phase proteins (APP) alpha1-antichymotrypsin (ACT) and alpha1-acid glycoprotein (AGP), plasma carotenoids and anthropometric and gestational indices to interpret plasma retinol in the blood of 192 apparently healthy Nigerian neonates collected randomly during days 1-20 postpartum. The mean weight (2.64 kg) and length (0.458 m) of the neonates and plasma concentrations (geometric mean, micromol/l) of retinol (0.54), alpha-carotene (0.072), ss-carotene (0.076) and lutein (0.080) were low. The prevalence of vitamin A deficiency was 72 %, indicating a severe public health problem. Babies who were of low birth weight (P<0.003) or premature and low birth weight (P<0.023) had significantly lower retinol concentrations than full-term normal weight babies. Thirty-two neonates had abnormal ACT and forty-four abnormal AGP concentrations. Positive correlations between retinol and ACT (r 0.186, P=0.05) and AGP (r 0.31, P=0.0001) during days 1-5 may be due to the increasing plasma retinol from maternal milk and a coincidental increasing capacity to synthesise APP. Subsequently, negative correlations between retinol and ACT (r -0.28, P=0.02) and AGP (r -0.29, P=0.018) from day 6 onwards reflected the continuing increase in plasma retinol, but no further increase in the APP. Overall, weight, ACT, lutein and age explained 30 % of the variance in retinol, but lutein was the most significant (r(2) 0.18, P<0.0001). Hence, the distribution of plasma retinol concentrations in this group of neonates was more strongly linked with nutrition (via the surrogate marker lutein) than infection.