Offspring of diabetic mothers experience an increased risk for type 2 diabetes but it is not known whether diabetic pregnancies also confer a higher inter-generational risk for diabetic complications. Because microalbuminuria is a sensitive indicator of glomerular damage, we compared the urine albumin:creatinine ratios (ACRs) between 65 infants of diabetic mothers (InfDM+) and 59 infants of non-diabetic mothers (InfDM−), and repeated the comparisons in 21 InfDM+ and 19 InfDM− when children were 5–19 months old. ACRs were higher among neonates compared with normal reference values for adults, but declined with increasing age. The only independent predictor of higher ACRs in a logistic regression model (⩾13 mg/mmol v. <13 mg/mmol) was the presence of delivery complications (odds ratio 2.95; P = 0.015). Neither high nor low birth weight was associated with higher neonatal ACRs. The most unique finding of the study was that InfDM+ had significantly lower ACRs than InfDM− [mean = 12.9 (median = 6.0) v. mean = 16.6 (median = 11.5), respectively at P = 0.05] even after adjusting for other variables using logistic regression (odds ratio 0.25; P = 0.001). In contrast, by 5–19 months, there was a trend toward higher ACRs among InfDM+ compared with InfDM− [mean = 6.3 mg/mmol (median = 1.9) v. mean = 3.0 mg/mmol (median = 2.5), respectively at P = 0.25]. Lower ACRs in InfDM+ may be due to developmental changes in fetal kidneys induced by hyperinsulinemia. Although the implications of this observation are unclear, it is possible that exposure to a diabetic intrauterine environment might influence the later risk for renal disease.

Campylobacter fetus is a rare cause of meningitis in the pediatric age group and, in particular, among neonates. The clinical presentation of campylobacter meningitis in high-risk neonates is not well-described. A review of campylobacter meningitis by Lee et al 1 in 1985 reported nine cases occurring in neonates, of which only one case was caused by C. fetus. In the ensuing six years only three more confirmed cases of neonatal meningitis caused by C. fetus have been reported. 2,3 We here report another confirmed case of C. fetus meningitis in a neonate.

Life-threatening events such as prolonged apnea and severe bradycardia are uncommon in infants. When such events occur in a family, however, the results may be disastrous. Over a period of 3 years ending June 1986, we have looked after 111 such infants aged 4 weeks to 40 weeks with a mean age of 14 weeks (male-female ratio 1.26:1). Of these infants, 33 had an identifiable cause and were treated according to the diagnoses. A structural approach to this problem yielded good results. Only 10 infants were treated with a home monitor (4 prescribed by physician and 6 by parental request). Sleep and pneumogram (polysomnogram) studies showed fewer apneic episodes with advancing age (P less than .01). Giving theophylline seemed to abolish pneumogram abnormalities. No infants died.

We examined the records of 14 patients aged 7 months to 10 1/4 years who were treated for bacterial tracheitis from May 1982 to December 1987; the management protocol for 13 of the patients included the use of nasotracheal intubation. The infection was caused by Staphylococcus aureus in seven, Haemophilus influenzae in three, Branhamella catarrhalis in one and Streptococcus pneumoniae in one. Both H. influenzae and B. catarrhalis were isolated in another patient, and no organism was found in the remaining patient. In addition to the bacteria, viruses were cultured from the tracheal secretions of two patients. The mean duration of intubation was 7.6 days and of hospital stay 9.2 days. Twelve of the cases occurred during the cold months of the year (October to March). Of the three deaths only one occurred in the pediatric intensive care unit and was due to severe bronchospasm and an air leak that caused bilateral pneumothorax and pneumomediastinum. In one patient subglottic stenosis developed that necessitated tracheostomy. Healing began 5 to 9 days after the onset of symptoms, as demonstrated with the use of repeated fibreoptic bronchoscopy. We found that the airway could be safely managed with the use of a nasotracheal tube. Bronchoscopy helped to confirm the diagnosis, to remove adherent secretions and to monitor the course of the disease. The ventilation tube can be removed after the patient's temperature returns to normal, if there is an air leak around the tube, if the quantity and viscosity of the secretions decrease and if healing is observed at bronchoscopy.

A two-year-old child dying of pulmonary hypertension and cor pulmonale secondary to bronchopulmonary dysplasia, was demonstrated to have reactive pulmonary hypertension in response to 100% oxygen and isoproterenol infusion. In an attempt to find an oral medication to maintain pulmonary vasodilatation, experimental trials were done using hydralazine, salbutamol, nifedipine and diltiazem. Cardiac index, pulmonary and systemic vascular resistances and intrapulmonary shunts were monitored during the trials. Hydralazine, salbutamol and nifedipine were ineffective. Diltiazem 2.0 mg given every 6 h resulted in a profound and sustained decrease in pulmonary pressures and resistance, and a reversal of the cor pulmonale.

Congenital tracheal occlusion, though seemingly rare, is generally fatal if not attended to immediately. A high index of suspicion should help to make the diagnosis in a neonate when there are respiratory distress at birth and no audible cry and an endotracheal tube cannot be advanced beyond the vocal cords. We present our experience with cases of congenital tracheal obstruction due to various causes during a period of four years.

Two cases with unusual primitive foregut anomalies are described. Both children, born within 24 hours of each other, had complete tracheal atresia, proximal esophageal atresia, and distal tracheoesophageal fistula along with some minor anomalies; both needed immediate tracheostomy for adequate ventilation. At 15 months of age, both patients are thriving and developing normally with the exception of their speech. A review of the literature revealed no other survivors with this condition. Diagnosis of tracheal atresia should be kept in mind when a newborn infant exhibits respiratory distress without an audible cry associated with failure to advance the endotracheal tube beyond the vocal cords. An immediate tracheostomy can be lifesaving in these children.

6 preterm infants with birth weights ranging from 790 to 1,040 g and gestational ages of 26-35 weeks were given metoclopramide at a mean postnatal age of 35 days. The infants were selected only after fulfilling rigid clinical criteria. All infants were spontaneously breathing and were on parenteral nutrition with 3% Vamin and 10% Neutralipid. Metoclopramide, 0.1 mg/kg/day, was given intravenously in three divided doses. Progress was monitored using abdominal girth, gastric residual aspirate before each feed, intestinal transit times, daily weight gain, number of episodes of vomiting or regurgitation and assessment of tolerance to increasing amounts of feeds. Excellent response was seen in all infants. Withdrawal of the drug led to prompt recurrence of all symptoms and signs which again disappeared on reinstitution of the medication. No untoward side-effects were noted during the administration of the drug. We conclude that, in selected cases, metoclopramide may be used for persistent functional feeding intolerance and gastric stasis.