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Our aim was to evaluate programs promoting bed sharing on maternity wards and determining ways to reduce these risks. Members of the National Association of Medical Examiners were contacted requesting information on deaths of healthy infants while bed sharing on maternity wards. Fifteen deaths and three near deaths are reported. One or more factors that increase the risk of bed sharing were present in all cases. Accidental suffocation was deemed the most likely cause of these incidents. Cases of infant deaths and near deaths while bed sharing on maternity wards are under reported. The ‘Baby Friendly’ (BF) initiative in maternity hospitals to promote breastfeeding is endorsed by the American Academy of Pediatrics and the US Center for Disease Control and Prevention. The BF initiative encourages prolonged skin-to-skin contact and bed sharing. Education of mothers and more efficient monitoring should significantly reduce the risk of maternity ward bed sharing.

Autoresuscitation (AR) is a highly conserved response among mammals, which allows survival from transient extreme hypoxia. During hypoxia, bradycardia, and hypoxic gasping develop after a brief period of hyperactivity. Normally, AR occurs if oxygen is restored during the gasping period where an initial heart rate increase is rapidly followed resumption or eupneic breathing. Humans and other mammals can survive multiple immediately repeated AR. A defective AR capacity has been implicated in Sudden Infant Death Syndrome. We had reported earlier that inbred strains of mice such as BALB/cJ could survive a characteristic number of immediately repeated AR trials, but that SWR/J mice failed to AR from a single hypoxic episode. We now report that strains closely related to SWR/J, FVB/N and SJL/J exhibit partial resuscitation defects relative to BALB/cJ or other mouse strains, establishing a genetic basis for variation in AR failure. The AR trial phenotype of BALB/cJ x SWR/J intercross F(1) and F(2) mice was consistent with BALB/cJ dominance and a discrete number of loci. Genome-wide mapping conducted with 60 intercross F(2) animals linked two loci to the number of AR trials survived, including one sex-specific locus with male expression, consistent with the observed 50% male bias for Sudden Infant Death Syndrome in humans. A locus carried on SWR/J chromosome 10 seems to be particularly important in AR failure and was confirmed in a partial consomic line. These results establish a genetic basis for AR failure phenotype in mice, with relevance to Sudden Infant Death Syndrome.

Dr. Paviotti and his associates are to be commended for developing a program that intends to improve newborn infant safety while promoting mother–infant contact and breast feeding.1 I agree on the need to prove the effectiveness of this protocol as in my report a few infants, who died, had awake mothers and room visitors at the time. The scheduled observations may prove valuable, but an infant can become dangerously hypoxic when its airway is obstructed for only a few minutes. I agree that bed sharing should be discouraged.

Recurrent laryngeal nerve injury during patent ductus ligation: can this common complication be reduced?

We have previously demonstrated that fluctuating cerebral blood flow velocity and arterial blood pressure (ABP) are associated with intraventricular hemorrhage (NEJM 309, 1983). The cause of these ABP fluctuations (ABP Flues) is unknown. In the present study we determined the relation of respiratory muscle activity to fluctuations in ABP. We studied four preterm infants on ventilators for RDS with ABP Flucs. We monitored esophageal (Pes), gastric (Pg), and ABP pressure. Consistent findings were: 1) ABP flucs have the same frequency and direction of change as Pes and Pg changes associated with spontaneous breathing; 2) spontaneous apneic pauses were accompanied by sudden and complete cessation of ABP Flucs; 3) large cough-like swings in Pes and Pg, seen in all infants were associated with the largest ABP Flucs; 4) cutaneous stimulation had no effect on ABP Flucs provided no change in Pes and Pg occurred; 5) respirator pressure swings had only small effects on ABP Flucs in one infant; 6) the effects of change in Pes and Pg on ABP were nearly simultaneous (0.05-.2 s.), thus respiratory pressure changes appeared to be superimposed on cardiac swings in ABP. These findings suggest that the fluctuations in ABP are caused by two mechanisms: 1) direct transmission of pleural and abdominal pressure to the cardiovascular system during spontaneous breathing and/or 2) fluctuations in venous return produced by breathing pressures. (Funding NIH HD 10993)