Apnoea and seizures.

We report two infants with near miss sudden infant death syndrome events exhibiting seizure disorders after caffeine treatment, suggesting there is an infant subgroup diagnosed as near miss sudden infant death syndrome who have apnoea possibly with seizures whose seizure threshold may be lowered by central nervous system stimulants like caffeine.     

Risk of sudden infant death syndrome in subsequent siblings

To determine the risk of recurrence of sudden infant death syndrome in families, we studied 251,124 live births by linked birth and death certificates from Oregon for a 10-year period. We found five recurrences among 385 subsequent siblings, for a rate of 13/1000 live births and a relative risk of 6. When the recurrences were adjusted separately for birth order and maternal age, the risk was still five times that expected (p less than 0.001). Families with infant deaths from causes other than sudden infant death syndrome had similar recurrence rates, suggesting that the phenomenon was not specific to sudden infant death syndrome. The overall mortality rate for subsequent siblings after a sudden death event totaled 20.8/1000. We believe that a risk of 2%, although small in the design of studies of infants at risk for sudden infant death syndrome, is not trivial in the counseling of parents.     

Neonatal long QT syndrome and sudden cardiac death

Neonatal sudden cardiac death most often results from cardiac electrical diseases, cardiomyopathies, or sudden infant death syndrome. In infants without a known premortem diagnosis or abnormalities identified at autopsy, sudden infant death syndrome accounts for the vast majority of sudden deaths. Potential cardiac causes of some sudden infant death syndrome cases may include malignant brady- or tachyarrhythmias and congenital long QT syndrome. The possible mechanisms include abnormal brain stem respiratory control of arousal, dysautonomia and malignant cardiac bradyarrhythmias or tachyarrhythmias. Screening for neonatal sudden cardiac death may not be feasible, but hopefully through careful review of history, physical examination, and family health history, and judicious diagnostic testing, can the risk of cardiac sudden death be reduced. Further comprehension of the genetic basis of inherited arrhythmia disorders may help elucidate the mechanisms of arrhythmogenesis and etiologies of sudden infant death. Prevention and treatment of these disorders may also be improved through more detailed understanding of the molecular basis of cardiac electrical pathophysiology.     

Oxygen desaturation complicates feeding in infants with bronchopulmonary dysplasia after discharge.

Recurrent episodes of hypoxemia may affect the growth, cardiac function, neurologic outcome, and survival of infants with bronchopulmonary dysplasia (BPD). As oral feeding might stress these infants by compromising pulmonary function even after hospital discharge, we measured oxygen saturation (SaO2) via pulse oximetry before, during the initial 10 minutes of, and immediately after oral feeding in 11 patients with BPD, 12 very low birth weight infants, and 23 healthy full-term infants. All infants with BPD had been previously discharged from the hospital after weaning from supplemental oxygen. Studies were done at a mean postconceptional age of 43 weeks while the infants were fed at home by one of their parents. Levels of SaO2 for the three groups were comparable before and during feeds. After feeding, the infants with BPD had significantly lower mean levels of SaO2 (84 +/- 8% [SD] vs 93 +/- 4% and 93 +/- 3%, respectively; P less than .01). They also spent more time after feeding with an SaO2 less than 90% (64 +/- 34% of time vs 27 +/- 33% for the very low birth weight and 22 +/- 20% for the term group; P less than .01) and greater time with an SaO2 less than 80% (37 +/- 28% vs 4 +/- 10% and 4 +/- 8%, respectively; P less than .01). Desaturation in infants with BPD was related to larger volume and faster oral intake during feeding. Thus, the data indicate that desaturation after feeding remains a recurrent problem for survivors of BPD after discharge.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distinguishing sudden infant death syndrome from child abuse fatalities

Fatal child abuse has been mistaken for sudden infant death syndrome. When a healthy infant younger than 1 year dies suddenly and unexpectedly, the cause of death may be certified as sudden infant death syndrome. Sudden infant death syndrome is more common than infanticide. Parents of sudden infant death syndrome victims typically are anxious to provide unlimited information to professionals involved in death investigation or research. They also want and deserve to be approached in a nonaccusatory manner. This clinical report provides professionals with information and suggestions for procedures to help avoid stigmatizing families of sudden infant death syndrome victims while allowing accumulation of appropriate evidence in potential cases of infanticide. This clinical report addresses deficiencies and updates recommendations in the 2001 American Academy of Pediatrics policy statement of the same name.     

Bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is the most common sequelae of preterm birth. It has proven a difficult condition to define as improving early management of the premature infant has led to a changing clinical picture over time. However, despite the advances in neonatal care, rates of BPD are at best unchanged and may even have risen. As BPD has significant long-term consequences, particularly from respiratory, cardiovascular and neurodevelopmentary perspectives, effective early management is key to improving long term outcomes. In this review the various definitions of BPD, and their limitations, are discussed alongside the evidence behind effective management of preterm infants, including the long-term management needed after discharge from hospital.     

Survey of sleeping position recommendations for prematurely born infants on neonatal intensive care unit discharge

Prematurely born infants are at increased risk of sudden infant death syndrome, particularly if slept prone. Yet, some prematurely born infants are slept prone despite the high risk age for sudden infant death syndrome and this may reflect the advice given by neonatal unit staff. The aim of this study was to determine neonatal units' recommendations regarding sleeping positions for premature infants prior to and after discharge. A questionnaire survey was sent to all 224 neonatal units in the United Kingdom, of which 81% responded. Analysis of their responses demonstrated that 43% of units started to sleep infants supine 1 to 2 weeks prior to discharge, but oxygen-dependent infants were slept non-supine until an older age. Non-supine sleeping was recommended by 40% of units for infants with Pierre Robin syndrome or gastro-oesophageal reflux. All units advised supine sleeping at discharge, but 29% additionally recommended side sleeping and only 58% positively discouraged prone sleeping. Written information was given to parents by 70% of the units, but few provided information which was specifically about prematurely born infants. Conclusion: The worrying lack of consistency in recommending non-prone sleeping emphasises that evidence-based guidelines for the sleeping position of convalescent prematurely born infants are required.     

Sudden infant death syndrome and secretin treatment for autism

The Back to Sleep Campaigns remain the greatest influence on the reduction of sudden infant death syndrome. Blatt and Meguid review updates on the effectiveness of these campaigns in reducing sudden infant death syndrome. They also review studies on why parents do not follow this proven advice. The contribution of the risks of other environmental factors are also reviewed. Also discussed are commentaries from a study reviewed last on the link between a prolonged QT electrocardiogram interval and sudden infant death syndrome. Church provides a cogent and timely review of the reported effectiveness of hormone secretin effectiveness in treating children with autism. This newly proposed treatment has been in the spotlight of the lay public, the popular media, and the scientific community. In short order, secretin as a treatment for autism has moved from a chance observation to the subject of a double-blind, placebo-controlled study.