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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.

Laryngeal closure following hypoxic gasps has been documented, but its efficacy in improving autoresuscitation capacity is unknown. We studied SWR/J mice who normally cannot autoresuscitate and the C57/BLJ strain who can. We evaluated the effects of elevated end-inspiratory lung volume immediately following a gasp. We compared upper airway-intact mice with tracheostomized mice in which the vocal cords are bypassed. We used the techniques of repeated autoresuscitate trials to test autoresuscitation capability. Both SWR/J and C57/BLJ mice could maintain elevated lung volume immediately after a gasp (breath holding). Such breath holding increased autoresuscitation ability in C57/BLJ mice but did not in SWR/J mice. In SWR/J mice, the duration of the breath holds was less than that in the C57/BLJ mice. These findings indicate that gasp-associated breath holding improves autoresuscitation capability during repeated autoresuscitation trials. Also, they show that SWR/J mice have a deficiency in central nervous system mechanisms regulating glottic closure during hypoxic gasping.

Rebreathing may impair ventilation and lead to sudden death among sleeping infants. To estimate the potential for rebreathing imposed by an infant's sleep microenvironment, we developed a mechanical model to assess the rate of CO2 dispersal away from an infant's face. We compared the mechanical model results with changes in arterial blood gases of rabbits. The rabbits breathed into the same microenvironments used for the model studies. In the rabbits, rebreathing (documented by capnometry) caused hypercarbia and in some cases death. The mechanical model consisted of the mannequin head positioned as in the rabbit studies and connected to a 100-ml syringe filled with CO2. CO2 was washed out of the system using 30-ml “breaths” (rate = 15/min). The half times (t1/2) for CO2 dispersal served to quantify the rebreathing potential of 16 items of bedding. The t1/2 values correlated with increments in the rabbits' arterial PCO2 (r = 0.789). The threshold for the increase in the rabbits' arterial PCO2 corresponded to t1/2 values of > or = 18.7 s; the 90% point for lethality in the rabbit model was 28.1 s. The mechanical model was also used to show the independent effects of softness and porosity of bedding on its rebreathing potential. By describing the potential for rebreathing within bedding, the mechanical model should be useful in future quantitative studies of infants' respiratory adaptation to sleep microenvironments.

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?

Severe hypoxia produces a state of neural depression known as hypoxic coma in which reflex activity is believed to be absent but from which spontaneous recovery (“autoresuscitation”) still can occur. We evaluated the swallowing reflex during hypoxic coma by employing mechanical and chemosensory stimuli. BALB/c mice were given 97% N2-3% CO2 to breathe. At onset of coma, a 0.05-ml bolus of saline or water was infused into the pharynx. Unlike mechanical stimulation (sham infusion), fluid infusion usually was followed by rapid swallowing, more so with water than with saline. This model allowed examination of interactions among swallowing, hypoxic gasping, airway fluid removal, and autoresuscitation. Compared with sham infusion, saline and water reduced gasping rate equally. Saline, however, prolonged the process of autoresuscitation more than did water, an effect possibly related to an observed increased retention of saline in the airway. Occasionally, mice failed to swallow after infusions, in which case airway obstruction during gasping and autoresuscitation failure was repeatedly observed. These studies suggest that the swallowing component of the laryngeal chemoreflex is present during hypoxic coma and that swallowing facilitates autoresuscitation when upper airway fluid is present.

Mechanisms underlying failure of autoresuscitation from hypoxic apnea were investigated. Failure was induced by repeated exposure to hypoxia. The influence of maturation was studied in adults, weanlings, and 10- and 5-day-old mice. Mice successful at autoresuscitation (BALB/c) as well as those prone to autoresuscitation failure (SWR weanlings) were studied. Hypoxic apnea was induced with 97% N2–3% CO2, and 21% O2 was given at its onset; electrocardiogram and ventilation were recorded. Hypoxic exposure was repeated if autoresuscitation (recovery of eupnea) occurred. Autoresuscitation failure (death) was induced in all mice. Young BALB/c mice tolerated more trials than older mice. SWR weanlings frequently failed to autoresuscitate on the initial exposure and tolerated fewer repeat trials overall than age-matched BALB/c mice. Induced autoresuscitation failure in all mice appeared to be unrelated to gasping regulation, because both gasp number and amplitude were similar during the failed trial and the previous successful trial. In most mice, failure was associated with absent recovery of heart rate during gasping. In BALB/c mice in particular, this persistent bradycardia was usually due to heart block, which occurred in 95% of failed trials. In addition, heart block occurred with increasing frequency on later successful trials, but conversion to sinus rhythm always preceded successful autoresuscitation. Heart block was also frequent in SWR mice and had similar consequences. BALB/c mice exposed to continuous anoxia survived longer than SWR mice, indicating increased endurance of components of the autoresuscitation mechanism not directly related to the ventilatory function of gasping (e.g., cardiovascular components).(ABSTRACT TRUNCATED AT 250 WORDS)

We unknowingly "screened" all NICU infants for elevated levels of serum benzyl alcohol (Bz-OH) over a three-month period. The fortuitous "screening" procedure resulted from the interference by Bz-OH with a routine blood CO2 assay used for all infants; validity was proved by (1) replication of the interference pattern with Bz-OH or benzoic acid; (2) confirmation of elevated benzoic acid levels in serum in two of the four screening positive infants tested but not in control infants, and (3) disappearance of the interference patterns when Bz-OH solutions were discontinued in affected infants. Screened Bz-OH-positive infants were compared to screened negative control infants, matched for weight (less than 1000 g), severity of RDS (on respirators), exposure to Bz-OH, and survival for longer than 48 hours. Intraventricular hemorrhage (IVH), metabolic acidosis appearing prior to IVH, and mortality were increased in Bz-OH-positive infants (P less than .05 in each case); hyperbilirubinemia and thrombocytopenia were not. Gasping respirations were not a major symptom. It is concluded that Bz-OH poisoning was a major cause of morbidity and mortality in NICU infants weighing less than 1000 g at birth during the three-month screening period. A retrospective review of patient records covering a 16-month period showed significant improvement in the survival rate of infants weighing less than 1000 g following the discontinuation of Bz-OH solutions.

The upper airway is vulnerable to collapse from negative intraluminal pressures during inspiration. The tongue muscles, the genioglossi and geniohyoids, by contracting during inspiration, appear to function to resist this collapse. This study supports the hypothesis that two cervical strap muscles, the sternohyoid and sternothyroid, have a similar function. First, phasic inspiratory electromyographic activity was recorded from the sternohyoid and sternothyroid muscles of nine anesthetized rabbits during tidal breathing. Furthermore, each muscle showed a progressive increase in electromyographic activity with airway occlusion. Second, in eight rabbits, by determining the amount of negative pressure required to collapse the upper airway (airway closing pressure determination), it was shown that upper airway stability improved with electrical stimulation of either the paired sternohyoid or sternothyroid muscles. In addition, in 12 freshly killed rabbits, mechanical tension, mimicking the contraction of either the sternohyoid or sternothyroid, improved airway stability. Finally, observations of the pharyngeal lumen utilizing a fiber-optic endoscope, revealed concentric narrowing of the oro- and nasopharynx when airway pressure was lowered and concentric widening when tension was increased in the sternohyoid or sternothyroid muscles. These findings support the hypothesis that phasic inspiratory contraction of the sternohyoid and sternothyroid muscles functions to resist pharyngeal airway collapse due to negative intraluminal pressures.

Tonic and phasic inspiratory genioglossus (GG) electromyographic activity (EMG) was recorded from 13 anesthetized rabbits during unstimulated breathing. Integrated GG EMG peaked earlier in inspiration and presented a more rounded contour than integrated diaphragmatic (DIA) EMG. Spontaneous augmented deep inspirations (sighs) showed a biphasic pattern in both GG and DIA EMGs. Hyperventilation abolished phasic inspiratory activity in the GG before the DIA, suggesting that the GG has a higher CO2 apneic point. Hypercapnia increased both EMGs; however, GG EMG increased more, as a percent of base line, than did DIA EMG. Oxygen breathing decreased GG more than DIA EMG; sodium cyanide injection and brief nitrogen breathing increased GG more than DIA EMG; carotid body denervation abolished these responses. Vagotomy abolished the Hering-Breuer inflation-inhibition reflex in both muscles, and tactile, visual, and auditory stimulation increased GG more than DIA EMG. Thus, the GG responses to chemoreceptor input and to nonspecific respiratory stimuli are qualitatively similar but quantitatively different from DIA responses. The relevance to mixed and obstructive apnea is discussed.

The ability of the extrathoracic airway (ETA) to remain open when exposed to negative pressure was investigated in rabbits. Postmortem, the ETA collapsed at -6.3 +/- 0.6 cmH2O whereas, during airway occlusion maneuvers in lightly anesthetized animals, it remained patent at pressures as low as -80 cmH2O. This discrepancy suggested that a neuromuscular mechanism maintains ETA patency. Four findings indicated that the genioglossus and geniohyoid muscles, which pull the tongue and hyoid bone anteriorly, help maintain ETA patency: 1) anterior movement of the hyoid bone increased the negative pressure at which the ETA collapsed postmortem, 2) ETA closure during occluded inspirations occurred after 12th nerve section abolished electromyographic activity in these muscles and 3) after deep anesthesia depressed such activity, and 4) closing pressure was linearly related to peak integrated electromyograms of the two muscles. After 12th nerve section, ETA closing pressure became more negative with progressive asphyxia greatly exceeding postmortem closing pressure, which suggests that other muscles also help maintain ETA patency. Blood gas tensions, respiratory system mechanoreceptors, and depth of anesthesia appear to influence genioglossus and geniohyoid activity.

To learn how increased cervical adipose tissue might affect upper airway function, we studied effects of mass loading on upper airway dimensions, stability, and resistance. Eight rabbits were studied (anesthetized and postmortem) using lard-filled bags to simulate cervical fat accumulation. Additionally, a handheld device was used to apply measured loads at localized sites along the airway. Upper airway resistance and closing pressure (a reflection of airway stability) were determined before and after loading. Endoscopy revealed concentric narrowing of the pharynx during loading in anesthetized and postmortem preparations. Upper airway resistance was increased by mass loads, with larger loads having greater effects. Loading caused decreased airway stability as reflected by closing pressures. The area over the thyrohyoid membrane was more vulnerable to mass loading than adjacent areas. Because mass loading of the upper airway causes changes in its configuration and function similar to those seen in obstructive sleep apnea syndrome (OSA), we speculate that such loading may contribute to the pathogenesis of OSA associated with obesity.

A nasal flowmeter suitable for preterm infants is described. It is made from a commercially available nasal cannula and 400-mesh stainless steel screen. Low dead space (0.35 ml) and low resistance (1.3 cmH2O . 100 ml-1 . s) are advantages. Light weight and compact design have eliminated the need for extensive restraint of the subject. Also, the investigator need not hold the flowmeter in place. These features make accurate measurement of respiratory airflow and tidal volume possible during polygraphic monitoring studies lasting several hours.

The effective elastance of the respiratory system (E‣rs) is a measure of its ability to resist a change in tidal volume under conditions of changing elastic loads. E‣rs was measured while subjects breathed air and 2% CO2 and 4% CO2 in air in two groups of premature infants of different gestational ages at 1 day 3–4 days, and 7–10 days of age. E‣rs was shown to decrease with increasing maturation and was independent of changes in control tidal volume. The decrease of E‣rs with increased gestational age could be accounted for by differences in calculated thoracic gas volumes in all but one instance, where E‣rs was lower in one group on the 3rd day of life. The activity of the Hering-Breuer reflex, as measured by the degree of slowing of inspiratory time after occlusion at FRC, has been previously reported to be normal to increased in similar infants. This suggests that differences related to size account for most of the maturational changes of E‣rs in newborns.

The effect of maturation and motor activity on recovery from hypoxic apnea by gasping (autoresuscitation) was investigated in Swiss Webster mice and a SW-related strain. Apnea was induced with 97% N2–3% CO2 and air given at its onset. In 69 Swiss Webster-related strain mice that gasped for at least 5s, the survival rates were 100% in 1- to 16-day-old mice, 19% in 17- to 23-day-old mice, and 90% in adults. The rates in 81 Swiss Webster mice were 100, 70, and 95%, respectively. The decrease in survival in 17- to 23-day-old mice was statistically significant for both strains, as was the difference in survival in 17- to 23-day-old mice between the two strains. Gasping was absent or of brief (less than 5s) duration in 15 Swiss Webster mice that failed to recover. Seizure-like activity was observed during hypoxic apnea and gasping but was not seen significantly more often in mice that died. Simultaneous recordings of limb movement (electromyogram) and breathing pattern indicated that movement did not interfere with the occurrence of gasping. We conclude that in adults and very young mice autoresuscitation is a powerful mechanism for recovery from hypoxia, but at an intermediate age, it is frequently unsuccessful.

The progressive respiratory response to occlusion of the airway at FRC was measured in a group of full-term and premature human infants. The sleep state of the full-term infants was shown to affect the response primarily through variations in the phase of thoracic and abdominal movements. The weakest responses were seen in those infants who demonstrated parodoxical respiration prior to occlusion. Most infants developed paradoxical respiratory movements after occlusion, but this did not affect the strength of the load-compensatory response. An increase in response related to both gestationaland postnatal age was observed. This increase could not be accounted for byvariations in the amount of paradoxical and in-phase respiration and thus may represent an increase in the sensitivity of infants to chemical stimuli with maturation.

To investigate the reflex mechanisms of sighs (spontaneous large breaths)(VT greater than 2 X control VT) in infants, recordings of respiratory flow and tidal volume (VT) were made during sleep. The frequency of sighs was greater at 1 than at 5 days of age, while respiratory frequency and controlVT did not change. Most sighs (93%) had a biphasic pattern of inspiratory flow characterized by an inspiratory duration nearly twice that of control breaths, with an abrupt change in flow rate halfway through inspiration. Interruption of ventilation (3–7 s of airway occlusion) appeared to generate astimulus for biphasic sighs, since sighs occurred during the first breath after termination of airway occlusion more frequently after long thanafter brief occlusions. However, a biphasic inspiratory pattern in airway pressure was rarely observed while the airways were occluded, regardless of occlusion duration. This suggests that increase in lung volume during the initialpart of the biphasic inspiration following occlusion is a stimulus for the second part. Thus the underlying reflex mechanism of sighs in human infantsappears to be the same as occurs in the so-called Head's paradoxical response to lung inflation.

Breathing variability and apnea characteristic of rapid eye movement (REM) sleep was investigated in a newborn infant with complete interruption of intercostal to phrenic neural pathways due to intrapartem transection of the cervical spinal cord. Breath-to-breath variability in inspiratory duration (TI), breath duration (Ttot), tidal volume (VT), and ventilation (VI) was significantly greater in REM than in quiet sleep and was similar to the variability in these parameters seen in normal infants. In addition, brief periods of diaphragmeatic apnea were observed during REM sleep. The phenomenon of shortened TI during airway occlusion previously attributed to intercostal-to-phrenic reflexes was examined in the quadriplegic infant and in seven healthy term infants. The frequency of this response was increased when airway occlusion was delayed until after onset of inspiration. Shortening of TI by occlusion occurred no less frequently in the quadriplegic than in the control infants. The constant paradoxical inward movement of the rib cage during inspiration observed in the quadriplegic infant suggests that supraspinal innervation of intercostal muscle limits such paradoxical movements in the normal infant. The quadriplegic infant's end-expiratory volume was consistently above his passive functional residual capacity, as inferred from respiratory volume and pressure measurements.

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)