Partial liquid ventilation with Perflubron in premature infants with severe respiratory distress syndrome.
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Fluorocarbons↗
Biomedical subjects
A R Spitzer
Publications and source records attributed to A R Spitzer.
The effects of patient volume and level of care at the hospital of birth on neonatal mortality.
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California↗
Clinical antecedents of neurologic and audiologic abnormalities in survivors of neonatal extracorporeal membrane oxygenation.
Extracorporeal membrane oxygenation is an effective rescue treatment for severe cardiorespiratory failure in term or near term neonates, although cerebral palsy, mental retardation, and sensorineural hearing loss are observed in 10 to 20% of survivors. The objective of the present study was to identify potential risk factors that may explain the neurologic and audiologic sequelae noted in 19% of 181 survivors of neonatal extracorporeal membrane oxygenation from our hospital. Our results suggest the following findings in survivors of severe cardiorespiratory failure treated with neonatal extracorporeal membrane oxygenation: (1) hypotension or the need for cardiopulmonary resuscitation before extracorporeal membrane oxygenation significantly increases the risk of spastic cerebral palsy, (2) profound hypocarbia before extracorporeal membrane oxygenation is associated with a significantly increased risk of hearing loss, (3) mental retardation in the absence of spastic cerebral palsy is unexplained except when due to abnormal fetal brain development, and (4) hypoxemia in the absence of hypotension does not increase the risk of neurologic or audiologic sequelae.
Brain↗
Safety and pharmacokinetics of multiple doses of recombinant human CuZn superoxide dismutase administered intratracheally to premature neonates with respiratory distress syndrome.
OBJECTIVES: To examine the safety and pharmacokinetics of multiple intratracheal (IT) doses of recombinant human CuZn superoxide dismutase (rhSOD) in premature infants with respiratory distress syndrome who are at risk for developing bronchopulmonary dysplasia (BPD). Methods. Thirty-three infants (700 to 1300 g) were randomized and blindly received saline, 2.5 mg/kg or 5 mg/kg rhSOD IT within 2 hours of surfactant administration. Infants were treated every 48 hours (as long as endotracheal intubation was required) up to 7 doses. Serial blood and urine studies, chest radiographs, neurosonograms, SOD concentration and activity measurements, and tracheal aspirate (TA) inflammatory markers were assessed throughout the 28-day study. RESULTS: SOD concentrations in serum (0.1 [0.05/0.15] microg/mL-geometric mean with lower/upper confidence intervals), tracheal aspirates (TA) (0.2 [0.1/0.3] microg/mL) and urine (0.3 [0.2/0.4] microg/mL) were similar at baseline in all 3 groups and did not change significantly in the placebo group. In the rhSOD treatment groups, SOD concentrations were increased on day 3 and did not change significantly thereafter over the 14-day dosing period (also measured on days 5, 7, and 13). SOD concentrations averaged 0.4 [0.3/0.5] microg/mL in serum, 0.8 [0.6/1.2] microg/mL in TA and 1.1 [1.0/1.3] microg/mL in urine for the low-dose group and 0.6 [0.5/0.7] microg/mL in serum, 1.1 [0.9/1.5] microg/mL in TA, and 2.2 [1.6/2.9] microg/mL in urine for the high-dose group over the 14-day dosing period. Enzyme activity directly correlated with SOD concentration and rhSOD was active even when excreted in urine. TA markers of acute lung injury (neutrophil chemotactic activity, albumin concentration) were lower in the rhSOD agroups compared with placebo. No significant differences in any clinical outcome variable were noted between groups. CONCLUSIONS: These data indicate that multiple IT doses of rhSOD increase the concentration and activity of the enzyme in serum, TA and urine, reduce TA lung injury markers and are well-tolerated. Further clinical trials examining the efficacy of rhSOD in the prevention of BPD are warranted.
Analysis of Variance↗
Placental leptin: an important new growth factor in intrauterine and neonatal development?
BACKGROUND: Leptin, the protein product of the ob gene, is produced by the adipocyte and seems to function as a link between adiposity, satiety, and activity. Leptin has also been found to be necessary for pubertal development, conception, and pregnancy in mice, and is increased in prepubertal children, independent of adiposity, suggesting a role in childhood growth and development. This study investigated 100 mother/newborn pairs to determine the role of leptin in neonatal development. Placental tissue was assayed for leptin mRNA to evaluate it as a source of leptin production in utero. METHODS: One hundred mother/newborn pairs were enrolled in this study. Radioimmunoassay was performed for leptin on maternal venous and newborn cord blood. Leptin concentrations were measured in 43 children in Tanner stages 1 and 2 as a control group. Placental tissue was obtained from five mothers and assayed for leptin mRNA by reverse transcription/polymerase chain reaction (RT/PCR). Human placental cell lines JAR and JEG-3 were also assayed for leptin mRNA expression. RESULTS: Leptin was present in all newborns studied at a mean concentration of 8.8 ng/mL (+/-9.6 standard deviations). Leptin concentrations in cord blood correlated with newborn weight (r = .51), body mass index (BMI) (r = .48), and arm fat (r = .42). There was no correlation between leptin and insulin. When statistically covarying for adiposity for newborns and Tanner stages 1 and 2 children, newborns had greater concentrations of leptin (mean, 10.57 ng/mL) than children (mean, 3.04 ng/mL). Leptin was present in all mothers at a mean value of 28.8 ng/mL (+/-22.2 standard deviations). Leptin concentration correlated with prepregnancy BMI (r = .56), BMI at time of delivery (r = .74), and arm fat (r = .73). Maternal leptin correlated with serum insulin (r = .49). There was no correlation between maternal and newborn leptin concentrations. Thirteen percent of newborns had higher leptin concentrations than their mothers. Placental tissue from five separate placentas expressed leptin mRNA at comparable or greater levels than adipose tissue. Two human trophoblastic placental cell lines, JAR and JEG-3, also expressed leptin mRNA. CONCLUSIONS: The correlation between leptin and adiposity found in children and adults was also found in newborns. Serum leptin concentrations in newborns were increased more than three-fold compared with children in Tanner stages 1 and 2 when controlling for adiposity, suggesting that leptin concentrations in the newborn are not explained by adiposity alone. Maternal leptin concentrations correlated with measures of adiposity at delivery but did not correlate with newborn adiposity or leptin. Leptin mRNA was expressed both in placental tissue and in two human placental cell lines. These data suggest that leptin has a role in intrauterine and neonatal development and that the placenta provides a source of leptin for the growing fetus.
Adipose Tissue↗
Exudative lung injury is associated with decreased levels of surfactant proteins in a rat model of meconium aspiration.
OBJECTIVE: Meconium aspiration syndrome remains a common cause of respiratory failure in neonates. The acute effects of meconium aspiration are inactivation of lung surfactant in vivo and in vitro. This study investigated the delayed effects of meconium on alveolar surfactant phospholipids and protein levels in spontaneously breathing animals. METHODS: Twenty-two adult rats were given 4.3 mg of dry weight human meconium after endotracheal intubation. Rats were briefly mechanically ventilated in room air, extubated, then killed after 16 (n = 6), 24 (n = 6), 48 (n = 6), and 72 hours (n = 4). Control animals received the same volume of normal saline (n = 7) or no meconium (n = 7). Bronchoalveolar lavage and tissue specimens were evaluated for inflammatory cells, total proteins, surfactant phospholipids, and surfactant proteins. RESULTS: Meconium caused exudative lung injury that was reflected in increased cell counts and proteins in alveolar lavage fluid. The peak injury occurred at 16 hours after instillation, whereas recovery occurred by 72 hours. Although total lavage fluid phospholipids did not change over time, phospholipid and dipalmitoyl phosphatidylcholine in large aggregates tended to decrease at 24 hours. Western blot analysis demonstrated time-dependent qualitative decreases in surfactant proteins A and B (SP-A, SP-B) in meconium-instilled animals compared with the controls. ELISA for SP-B confirmed the Western blot findings with total SP-B in large aggregate decreasing from 25 +/- 4 microg in controls to 6.6 +/- 0.8 microg at 24 hours of injury. CONCLUSIONS: Our study suggests that the exudative lung injury with meconium instillation is associated with decreased levels of SP-A and SP-B in the large aggregate fraction of lung surfactant. We speculate that decreased secretion and/or increased degradation accounts for lower levels of SP-B in bronchoalveolar lavage fluid.
Animals↗
Multi-motor unit action potential analysis (MMA)
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Action Potentials↗
Methylamine decreases trafficking and packaging of newly synthesized phosphatidylcholine in lamellar bodies in alveolar type II cells.
Lung lamellar bodies, the storage organelles for lung surfactant phosphatidylcholine (PC), maintain an acidic pH that can be increased with weak bases. This study investigates the effect of a weak base, methylamine, on the pH in lamellar bodies and on the trafficking and packaging of newly synthesized PC in lamellar bodies. Methylamine increased the pH of isolated lung lamellar bodies and of lamellar bodies in intact cells. Metabolic labelling of isolated type II cells with [methyl-3H]choline showed that although methylamine (2.5-10 mM) did not alter the labelling of cellular or microsomal PC and disaturated PC, it decreased the labelling of the PC and disaturated PC in lamellar bodies. The packaging of PC in lamellar bodies (the specific activities ratio between the PC in lamellar bodies and the microsomal PC) also decreased in a time- and concentration-dependent manner. The cellular synthesis of PC or its packaging into lamellar bodies was unaltered by brefeldin A, suggesting that the Golgi was not involved in PC packaging. Although methylamine also increased surfactant secretion, the inhibition of PC packaging in lamellar bodies seems unrelated to the secretagogue effect, (1) on the basis of metabolic consequences of increased secretion and (2) because ATP, another secretagogue, did not inhibit PC packaging. Methylamine seems to inhibit PC packaging by inhibiting trafficking of PC to lipid-rich light subcellular fractions. Together our results suggest that the trafficking of surfactant PC into lamellar bodies might be sensitive to changes in the pH of lamellar bodies.
Acridine Orange↗
Infant thoracic surgery: procedure-dependent pulmonary response.
Respiratory insufficiency is a common complication of thoracic surgery in infants. To better define this dysfunction, pulmonary compliance (CL) and resistance (R) were measured for 17 infants who underwent common thoracic procedures: Blalock-Taussing shunting (n = 7) repair of congenital coarctation of the aorta (n = 10). Measurements were obtained preoperatively and 0, 1, and 3 days postoperatively. Preoperatively, CL was lower and R was similar for the two groups. Both groups had decreased CL and increased R on postoperative day 0; infants with coarctation had recovery to preoperative values by postoperative day 1 for CL, and day 3 for R. CL and R did not return to the preoperative values by postoperative day 3 in infants with a shunt procedure. The changes in R were greater than those in CL for both groups in the postoperative period. These data indicate that such thoracic procedures are associated with pulmonary morbidity that is airway-predominant, and that the degree of compromise and the time until recovery are, in part, procedure-specific.
Airway Resistance↗
Documented home apnea monitoring: effect on compliance, duration of monitoring, and validation of alarm reporting.
The objectives of this study were to: (1) measure patient compliance with monitoring, (2) validate parental reports of alarms at home, (3) examine monitoring duration, and (4) compare documented monitor records with the traditional pneumogram to evaluate patients for monitor discontinuation. During the 1-year period from January through December, 1992, 114 infants were followed up with documented monitoring. Simultaneously, 113 infants were followed up with conventional monitors. Infants were premature, or victims of apparent life-threatening episodes (ALTE), or siblings of SIDS victims. Monitors recorded all episodes of apnea greater than 15 seconds and bradycardia less than 80 beats per minute. All families were contacted biweekly by telephone. Downloads were performed at regular intervals. Monitor downloads were compared with simultaneous pneumograms to assess the accuracy of a long-term, intermittent event-recording system versus short-term (6- to 12-hour) continuous recording. All families were highly compliant with the use of home monitoring. Although Caucasian families used the monitors more often than non-Caucasian families, all groups used the monitor > 75% of the time. True episodes were verified in 38% of patients by monitor downloads. Only 7.4% of all recorded events were true events. Of the real events, 51.2% were apneas of 16-20 seconds. No significant differences were found in overall duration of monitoring between documented and nondocumented monitors. In the premature infants, the duration of monitoring was significantly reduced in those infants found to have no true episodes over those with real events at home. Readmission for ALTE was reduced in infants with documented monitors. Premature infants without events were monitored an average of 24 fewer days (P = 0.03). Computerized monitor downloads were found to be equally, if not more, sensitive than pneumograms in evaluating infants for monitor discontinuation. Documented monitoring offers a viable alternative to traditional monitoring and pneumograms in assisting clinicians and families in evaluating their infant's progress. By accurately assessing compliance, distinguishing true from false alarms, and decreasing the need for pneumograms, these devices provide valuable information to clinicians and families.
Apnea↗
Meconium increases surfactant secretion in isolated rat alveolar type II cells.
One of the underlying causes of pathophysiology of meconium aspiration syndrome is access of meconium to the alveolar space and inhibition of activity of lung surfactant. This study examines the effects of meconium on type II cell function by following surfactant secretion. Isolated rat alveolar type II cells were labeled with [methyl-3H]choline during the initial 21-22 h of incubation. During the subsequent 150 min of incubation, phosphatidylcholine (PC) secretion in the presence of 1% meconium was increased 250 +/- 11% (mean +/- SE, n = 23) over controls. The secretagogue effect was concentration-dependent and reached a maximum at 0.5% meconium. The meconium effect was not due to cellular toxicity as evaluated by vital dye exclusion, lactate dehydrogenase release, and PC synthesis. The secretagogue effect of meconium was associated with the particulate fraction pelleted by centrifugation of the suspension for 1 h at 100,000 x g. Heat treatment of meconium decreased the effect, suggesting the active component to be a protein. The effect of meconium was additive with that of 0.1 mM terbutaline, or 1 mM ATP, suggesting different pathways of action of each agent. The effect of meconium was reduced in the presence of 0.1 mM 4,4'-diisothiocyanato-2,2'-disulfonic acid, or 100 ng/mL surfactant protein A. These agents were previously shown to inhibit surfactant secretion in a stimulus-independent manner. Our results suggest that meconium at low concentrations is not toxic to type II cells, and a component of meconium, possibly a protein, increases PC secretion.
Animals↗
Treatment of choice for carpal tunnel syndrome.
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Carpal Tunnel Syndrome↗
Effects of hypocarbia on the development of cystic periventricular leukomalacia in premature infants treated with high-frequency jet ventilation.
BACKGROUND AND OBJECTIVE: Previous data from our institution indicate that mechanically ventilated premature infants are at increased risk for cystic periventricular leukomalacia (CPVL), particularly if hypocapnia occurs. High-frequency jet ventilation (HFJV) may produce substantial hypocapnia. We sought to investigate whether hypocapnia during HFJV is associated with the development of CPVL. METHODS: Sixty-seven premature infants (mean gestational age, 27.2 weeks; mean birth weight, 1001 g) underwent HFJV for a mean of 44 (range, 8 to 70) hours during the first 3 days of life. All infants were followed with serial neurosonograms at least weekly until 6 to 8 weeks of age and every 2 to 4 weeks thereafter until discharge. To assess the cumulative effects of hypotension, acidosis, hypoxemia, and hypocarbia during the first 3 days of life on the development of PVL, we developed a quantitative assessment in which we assigned threshold levels at particular critical values of these parameters (such as a mean PaCO2 of 20 mm Hg) and calculated an area above the curve between longitudinally connected values of these parameters and the threshold levels. RESULTS: Nine of the 67 infants died before 21 days of life. Of the 58 who survived beyond 21 days, large CPVL (> 5 mm in size) developed in 18 infants. Infants with cysts were similar in birth weight, gestational age, and virtually all other antepartum, intrapartum, and postpartum parameters compared with the 40 neonates in whom CPVL did not develop. However, infants with CPVL were significantly more likely to have moderate or severe periventricular echodensities preceding development of CPVL and periventricular echodensities that persisted for a longer period. We did not find an effect of hypotension, acidosis, or hypoxemia on the development of CPVL. There were no differences in the mean PaCO2, the absolute low PaCO2 values, the ranges of low PaCO2 between groups, or area above the curve measurements at threshold levels of 15 and 20 mm Hg, respectively. However, logistic regression analysis revealed that infants with CPVL were independently significantly more likely to have greater cumulative hypocarbia below a threshold level of 25 mm Hg during the first day of life (odds ratio, 5.43; 95% confidence interval, 1.33 to 22.2). CONCLUSIONS: Hypocarbia produced by treatment with HFJV during the first 3 days of life is associated with the subsequent development of CPVL. The mechanisms for the development of CPVL among premature infants treated with HFJV need to be established.
Carbon Dioxide↗
High-frequency jet ventilation in the early management of respiratory distress syndrome is associated with a greater risk for adverse outcomes.
OBJECTIVE: The objective of this investigation was to determine if high-frequency jet ventilation (HFJV) used early in the treatment of premature infants with respiratory distress syndrome was effective in reducing pulmonary morbidity without increasing the occurrence of adverse neurologic outcomes. STUDY DESIGN: A total of 73 premature infants who met the inclusion criteria (gestational age of less than 33 weeks, birth weight of more than 500 g, age of less than 24 hours, need for assisted ventilation with peak inspiratory pressure of more than 16 and FIO2 more than 0.30, and roentgenographic evidence of respiratory distress syndrome) were randomized to either conventional (n = 36) or to high-frequency jet (n = 37) ventilation. Our goals were to maintain the infants on the assigned ventilator for at least 7 days unless they could either be extubated or meet crossover criteria. Univariate analyses were initially used to compare the two groups. Stepwise logistic regression was subsequently used to assess whether various factors independently influenced adverse outcomes. RESULTS: The two groups of infants were similar in all obstetrical, perinatal, and neonatal demographic characteristics. The mean birth weight and gestational age in the conventional group were 930 g and 26.6 weeks and in the HFJV group, 961 g and 26.9 weeks. The infants were randomized at similar ages (7.1 and 7.3 hours of life, respectively). Their prerandomization ventilator settings and arterial blood gases were nearly identical. There were no differences in pulmonary outcomes (occurrence of air leaks, need for oxygen or ventilation at 36 weeks postconception), and there were no differences in the mean number of days oxygen was required, number of days ventilated, or length of hospital stay. Infants ventilated with HFJV were significantly more likely to develop cystic periventricular leukomalacia (10 vs 2, P = .022) or to have a poor outcome (grade IV hemorrhage, cystic periventricular leukomalacia, or death) (17 vs 7, P = .016). Logistic regression analysis revealed HFJV to be a significant independent predictor of both cystic periventricular leukomalacia and a poor outcome. The presence of hypocarbia was not an independently significant predictor of adverse outcomes. CONCLUSIONS: With the HFJV treatment strategy that we used, use of the high-frequency jet ventilator in the early management of premature infants with respiratory distress syndrome resulted in significantly more adverse outcomes than in those treated with conventional mechanical ventilation.
Blood Pressure↗
Protein kinase C in ATP regulation of lung surfactant secretion in type II cells.
Previous studies provided indirect evidence for a role for protein kinase C (PKC) in ATP stimulation of surfactant secretion. The present study demonstrates that ATP increases PKC activity in the membrane fraction and decreases PKC activity in the cytosol fraction of alveolar type II cells, indicating translocation of PKC to the membranes. The kinetics of ATP concentration dependence of increases in phosphatidylcholine secretion and diacylglycerol content were similar, suggesting direct correlation between these two parameters. ATP also increased membrane PKC activity in a concentration-dependent manner. Almost one-half of the PKC activity in the cytosol and membrane fractions was Ca2+ independent. The ATP-induced increase was greater in membrane-associated Ca(2+)-dependent enzyme (233%) than in Ca(2+)-independent enzyme (121%). Desensitization of PKC by exposure of cells to phorbol esters decreased PKC activity in the membrane and cytosol fractions. In cells pretreated for 3 h with phorbol esters, PKC activity was near minimum, and ATP-stimulated secretion was lowest (< 40% of that observed in untreated cells). These results indicate that a major part of ATP-stimulated surfactant secretion in type II cells is mediated via activation of PKC.
Adenosine Triphosphate↗
The timing of SIDS deaths in premature infants in an urban population.
Previous reports have demonstrated that premature infants are at greatly increased risk for sudden infant death syndrome (SIDS). Although only 9% of infants are born at less than 36 weeks' gestation, 20% of SIDS victims are former premature infants. The objective of this study was to characterize the time course of SIDS in premature infants and to determine why SIDS occurs at such a high rate in this patient population. A database of all cases of SIDS in Philadelphia from 1987 through 1991 was used to establish the time course for SIDS deaths in term and preterm infants. Gestational age was established by Dubowitz exam. To evaluate distinctly different age groups, infants from 32-36 weeks were excluded from analysis. Age at death and postconceptional age of death were compared for both groups. Data are described in weeks (mean +/- SEM), and analyzed using unpaired t-test and log-rank test to compare survival rate between term and preterm infants. A significant difference (P < 0.01) was noted in age at death of term versus preterm infants. No difference was found in postconceptional age of death. The survival rates were also different (P < 0.001). Preterm infants showed a much wider distribution in age of death from SIDS. The term infants followed the classic SIDS curve. By 32 weeks' postnatal age, 95% of all SIDS had taken place in the term group, but only 75% in the preterm group. The age at death for SIDS differs in the preterm infant.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
Prognosis with preoperative pulmonary function and lung volume assessment in infants with congenital diaphragmatic hernia.
OBJECTIVES: To determine whether fatal pulmonary hypoplasia, as assessed by functional residual capacity (FRC), can be distinguished from other reversible causes of respiratory failure in infants with congenital diaphragmatic hernia (CDH). METHODS: In the present study, 25 term neonates having CDH without other anomalies (mean birth weight +/- SD, 3.25 +/- 0.50 kg) were enrolled prospectively into a protocol evaluating pulmonary function. Lung compliance (CL) and FRC were measured before diaphragmatic repair and compared with the highest oxygenation index (OI) and lowest PaCO2, also obtained preoperatively. Pulmonary function assessment was repeated after diaphragm repair on postoperative days 3 and 7. CL was determined by esophageal manometry and pneumotachography, and FRC was determined by helium dilution. RESULTS: Fifteen infants (60%) survived to hospital discharge. Eighteen (72%) required extracorporeal membrane oxygenation (ECMO) for support, and of these, 8 (44%) survived. PaCO2 was similar preoperatively in infants grouped as survivors without ECMO, survivors with ECMO, and nonsurvivors. In nonsurvivors (all of whom received ECMO), the preoperative OI was significantly higher (51 +/- 21), CL was less (0.11 +/- 0.04 mL/cm of water per kg), and FRC was smaller (4.5 +/- 1.0 mL/kg) than in the survivors who required ECMO (26 +/- 18, 0.18 +/- 0.08 mL/cm of water per kg, and 12 +/- 5 mL/kg, respectively), as well as in the survivors without ECMO, (6 +/- 2, 0.32 +/- 0.16 mL/cm of water per kg, and 15.8 +/- 4 mL/kg, respectively). The group surviving with ECMO had a higher OI than the infants surviving without ECMO. All nonsurviving infants had FRCs of less than 9.0 mL/kg preoperatively. In contrast, only 2 of the 15 survivors had preoperative FRCs less than 9 mL/kg. CONCLUSIONS: The results of this study suggest that preoperative assessment of FRC may predict fatal pulmonary hypoplasia in most infants with CDH.
Analysis of Variance↗
Infant sleep position following new AAP guidelines. American Academy of Pediatrics.
OBJECTIVE: This report examines the response of families to the American Academy of Pediatrics June 1992 recommendation that healthy term infants be put to sleep on their back or side to decrease the risk of sudden infant death syndrome. Parents at two clinics and private practices were interviewed to ascertain sleep position practices. METHODS: Parents of infants from 1 to 6 months of age who were in the waiting room for a well-child visit were eligible for study. A total of 760 interviews were conducted using a closed-ended questionnaire. Parents were asked about sleep position, positional changes during sleep, and factors that influenced their decision to position their infant prone, side, or supine. Interviews were conducted from September 1993 through April 1994. This interval was divided into two equal, 4-month time intervals. Sleep practices were compared during the first and second time periods. Differences between practice and clinic groups were measured. Groups were compared using the chi-square test, with results considered significant at P < .05. RESULTS: The number of infants placed side or supine for sleep increased significantly since the inception of the study, from 38.1% to 59.1%. Despite this increase, parents reported that the impetus for changing position came from family or the media, rather than from health professionals. Initially, the proportion of infants in private practices placed side or supine was greater than that of clinic patients. That difference disappeared by the end of the study. Prone positioning continued to be more prevalent in the 3- to 6-month-old infants than in the 1- to 3-month-old group. The majority of infants at all ages awoke in the same position that they were put to sleep. CONCLUSIONS: Side and supine positioning for sleep increased in all socioeconomic groups. A small number of infants placed side or supine for sleep are found prone on awakening. Health professionals need to increase their role in providing sleep position guidance. As the proportion of the population positioning their infants side or supine for sleep increases, it should be possible to examine the effect on the sudden infant death syndrome rate.
Cross-Sectional Studies↗