PubMed Health⌕ Search

Biomedical subjects

R G Meny

Publications and source records attributed to R G Meny.

17 recordsLinked to original sources

Gasping and other cardiorespiratory patterns during sudden infant deaths.

To gain information on the cardiorespiratory changes occurring immediately before sudden infant death (SID), recordings of heart rate and chest wall impedance were analyzed in nine infants who had died at a median age of 4.8 mo (range 1-6 mo) while attached to a memory monitor. Postmortem diagnoses were sudden infant death syndrome in seven infants and mild bronchopulmonary dysplasia in two infants. Primary cause of the monitor alarm was bradycardia in all but two infants. Heart rate fell to < or = 15 bpm 7.5 min (range 1.4-25.2 min) after the first alarm; there was no indication of heart block or ventricular tachycardia. Apnea (> 20 s) began 0.3 to 13.7 min (median 2.7 min) after this alarm in five infants and 7 to 20 s before it in three infants; in the remaining infant, stimulation occurred before any apnea. Gasping was already present at the time of the first monitor alarm in three infants and occurred within 2.7 min after it in a further four infants. One infant only began to gasp 13 min after the first monitor alarm. The duration of gasping ranged from 3 s to 11 min in those five infants in whom it was not interrupted by resuscitation. The latter was given to three infants 4, 21, and 228 s after the monitor alarm but had no effect on the ongoing decrease in heart rate. Since gasping only occurs if PaO2 is < 5-15 mm Hg, it is most likely that the seven infants who gasped at or shortly after the first monitor alarm were already severely hypoxemic at that time. This hypoxemia developed in the absence of prolonged central apnea. The role of other mechanisms potentially resulting in severe hypoxemia, such as upper airway obstruction or rebreathing, remains to be determined.

Apnea↗

Asystoles during infancy recorded by home memory monitors. Benign events?

OBJECTIVES: To assess the frequency and clinical significance of asystole (sinus arrest > or = 2.0 seconds) and the incidence of bradycardia in infants prescribed home cardiorespiratory monitors and to test the hypothesis that asystoles are more likely to occur in preterm infants. DESIGN: Prospective, consecutive sample of monitor printouts. METHODS: All 291 printouts from the memory monitors of 161 patients received during a 2-month period were analyzed. SETTING: University hospital providing primary and referral care. MAIN OUTCOME MEASURES: Asystoles and bradycardias; clinical course of patients with asystoles. RESULTS: Eight patients (5.0%) had 32 episodes of asystole lasting 2.0 to 4.3 seconds (group 1). Fifty-three patients (32.9%) had true bradycardia alarms but no asystoles (group 2). One hundred patients (62.1%) had neither asystoles nor bradycardias (group 3). Preterm infants constituted 88% of group 1 and 81% of group 2 but only 58% of group 3. Infants were more likely to be full-term in group 3 than in the other 2 groups (chi 2, P = .02). Birth weights were lower in group 1 than in group 3 (P < .05, 1-tailed t test). There were 479 true bradycardias; 72.2% lasted 10 seconds or less, 26.3% were longer than 10 seconds but no more than 20 seconds, and 1.5% were longer than 20 seconds. None of the 8 patients with asystoles required resuscitation for their asystoles; all survived and were free of any life-threatening events after their monitors were discontinued and up until their first birthday. CONCLUSIONS: Asystoles occur more commonly in preterm infants; those pauses in the 2.0- to 4.0-second range seem to be benign. Studies of long-term recordings are needed to redefine asystole in both normal preterm and fullterm infants. These data would help further refine current guidelines for pacemaker implantation during infancy.

Birth Weight↗

Cardiorespiratory recordings from infants dying suddenly and unexpectedly at home.

OBJECTIVE: Little is known about the mechanism of death during sudden infant death. To study the mechanism, we obtained data on six infants who died while on a memory-equipped cardiorespiratory monitor. METHODS: Waveforms of respiration and heart rate trend were available for five infants; an alarm log only was available for the sixth. These printouts were reviewed with attention to mechanism and time to death. RESULTS: All infants were born prematurely; autopsies reported the cause of death as sudden infant death syndrome in three cases and bronchopulmonary dysplasia in the others. Bradycardia, which played a more prominent role than central apnea, was preceded by tachycardia in two deaths. Resuscitation occurred within 1 minute in four cases; no response to alarms occurred in the other two cases, apparently because the parents were desensitized by prior meaningless alarms. Five patients died within 20 minutes, whereas one death due to sudden infant death syndrome was prolonged. CONCLUSION: Bradycardia is an important feature in all six of these infant deaths. Although its etiology is unknown, hypoxemia or obstructive apnea may precede bradycardia. Home monitors equipped to detect these possible antecedents will yield further insight into sudden infant death.

Bradycardia↗

Codeine and the breastfed neonate.

Codeine is an analgesic commonly used to relieve pain in the early post partum. Its metabolite, morphine, is probably responsible for its effectiveness in this use. However, morphine may also cause neonatal apnea. We studied free codeine and morphine levels in breastmilk of 17 samples from seven mothers and neonatal plasma of 24 samples from 11 healthy, term neonates. Levels were determined by radioimmunoassay. Milk codeine levels ranged from 33.8 to 314 ng/ml 20 to 240 minutes after codeine; morphine levels ranged from 1.9 to 20.5 ng/ml. Infant plasma samples one to four hours after feeding had codeine levels ranging from < 0.8 to 4.5 ng/ml; morphine ranged from < 0.5 to 2.2 ng/ml. Low infant plasma levels are secondary to low excretion into milk and the small amounts of milk available in the first few days. Moderate codeine use during this time (< or = four 60 mg doses) is probably safe.

Breast Feeding↗

Home apnea monitoring and disruptions in family life: a multidimensional controlled study.

We used data from telephone interviews and mailed questionnaires to examine 12 aspects of family life among 93 families with infants considered at high risk for sudden infant death syndrome and on home apnea monitors and a matched comparison group with infants not requiring monitoring. Using logistic regression to control confounding variables, we found that case mothers were at an increased risk of poor health, but we found no other significant differences in family life between the two groups.

Apnea↗

Normal fetal hemoglobin levels in the sudden infant death syndrome.

It has been reported that infants who die of the sudden infant death syndrome (SIDS) have elevated fetal hemoglobin levels. To test this hypothesis, we determined the level of fetal hemoglobin in dead and living infants in three different laboratories by three methods: high-performance liquid chromatography, polyacrylamide-gel electrophoresis, and cell-based immunofluorescence assays for fetal hemoglobin-containing red cells (F cells). Our infant study population consisted of 67 infants who had died of SIDS, 22 control infants examined at autopsy, and 80 living infants. The fetal hemoglobin level was not higher in the infants who had died of SIDS than in the control infants for any age group analyzed. Immunofluorescence assays for F cells were also performed in blood samples from 105 mothers of infants who had died of SIDS, 55 adult female controls, 52 fathers of infants who had died of SIDS, and 67 adult male controls. The percentage of fetal hemoglobin-containing red cells in the parents of infants who had died of SIDS was not statistically different from that in sex-matched adults in the control groups. We conclude that elevated fetal hemoglobin levels in infants or their parents are not suitable for use as indicators of the risk of SIDS in the infants. Furthermore, the fetal hemoglobin level is not useful as a postmortem marker of an infant's having died of SIDS.

Adult↗

Sudden infant death and home monitors.

During a two-year period, ten infants died suddenly and unexpectedly with a home cardiorespiratory monitor available. We investigated the compliance with appropriate monitoring technique as well as the medical and demographic factors associated with these deaths (90% were due to sudden infant death syndrome). At least six and probably eight of these ten families were noncompliant with appropriate monitoring technique. The main comparison group consisted of 211 patients for whom care with home cardiorespiratory monitors was initiated and continued. Bronchopulmonary dysplasia and severe, apparent life-threatening events were significantly increased in the subjects, as were the following characteristics: black race; lack of private medical insurance; unmarried mother; maternal age of less than 25 years; cigarette smoking by mother during pregnancy; and low Apgar scores. These diagnostic and demographic factors may be useful in predicting the infant at highest risk for sudden and unexpected death when a home monitor is prescribed. Noncompliance with proper monitoring technique patients; methods of educating parents of infants at high risk of sudden infant death syndrome with the necessity for compliance need to be developed.

Bronchopulmonary Dysplasia↗

Mass spectrometer monitoring of expired carbon dioxide in critically ill neonates.

Seventy-five paired comparisons of expired carbon dioxide tension (PECO2) and PaCO2 were obtained to evaluate the clinical usefulness of a mass spectrometer for monitoring PECO2 in critically ill neonates and to explore the factors that influence the PaCO2-PECO2 gradient. Nine neonates with a mean birth weight of 2.18 kg and a mean gestational age of 34 wk were studied during continuous positive-pressure ventilation. When PaCO2 was between 26 and 50 torr, this variable was linearly related to PECO2 by the equation: PaCO2 = 23.42 + .50 PECO2, r = +0.69 (p less than .001). Mean daily gradients for severe pulmonary disease (n = 9; mean 10.5 +/- 4.4 [SD] torr) were significantly (p less than .01) higher than those for moderate disease (n = 10; mean 3.9 +/- 3.1 torr); however, 61.3% of the gradients were no greater than 10 torr. Expiratory times no greater than 1.0 sec were associated with significantly (p less than .001) higher gradients (n = 33; mean 12.2 +/- 3.8 torr) than those over 1.0 sec (n = 42; mean 5.4 +/- 4.9 torr). This was, in part, due to the response time of the mass spectrometer system (0.68 sec to 63% of a step change in CO2). The continuous monitoring of PECO2 was especially helpful in the care of two neonates. We hypothesize that a decrease in the response time would improve the correlation between PaCO2 and PECO2 and thereby enhance the usefulness of this device as a trend monitor.

Carbon Dioxide↗

Fatal adenoviral (type 7) respiratory disease in neonates.

Two cases of fatal neonatal adenoviral type 7 respiratory disease are described. The clinical, laboratory, x-ray, and pathological features of these two neonates and those reported in the literature are highlighted. Suggestions are made regarding how to diagnose this disease early so that the patients can be isolated and further spread of the disease prevented.

Adenoviridae Infections↗

Alimentary absorption of gentamicin in preterm infants.

Fifty-two preterm neonates receiving oral gentamicin from birth, as prophylaxis against necrotizing enterocolitis (NEC), had serum gentamicin levels measured on the second day of life (52 infants) and on the seventh to tenth days (43 infants). The serum gentamicin concentrations on the second day were 0.5 microgram/ml or less in 21 percent, 0.6 to 1.0 microgram/ml in 15 percent, 1.1 to 2 micrograms/ml in 34 percent, 2.1 to 5 micrograms/ml in 25 percent, and 5 to 7.1 micrograms/ml in 4 percent of the infants. Paired serum gentamicin levels were significantly lower (p less than 0.001) on the seventh to tenth day as compared to the second day. We conclude that preterm infants in the first few days of life absorb orally administered gentamicin. Concomitant use of systemic gentamicin under such circumstances may potentially lead to toxic serum gentamicin concentration.

Enterocolitis, Pseudomembranous↗

Hypermethioninemia in an infant.

We discuss an infant with hepatitis and hypermethioninemia. An inborn error of metabolism, such as methionine adenosyltransferase deficiency or hereditary tyrosinemia, was originally thought to be the basis for these abnormalities. The infant's subsequent clinical course, however, was incompatible with such a diagnosis; the hypermethioninemia was instead due to the trilogy of prematurity, hepatitis, and a high-protein, high-methionine diet.

Amino Acid Metabolism, Inborn Errors↗

Use of home apnea monitors.

OBJECTIVE: To examine the frequency of use of home apnea monitors, reasons for not using them, and factors associated with their use among families of infants for whom home monitoring had been prescribed. DESIGN: Cross-sectional study, including a telephone interview to collect demographic data and a mailed questionnaire to obtain data on monitor use. SETTING: The apnea clinics in two tertiary-care centers. PARTICIPANTS: Ninety-three families (representing an 80.9% response rate) with infants considered at increased risk of sudden infant death syndrome and requiring home monitors. Infants with tracheostomies or bronchopulmonary dysplasia and families with monitored twins, a mother known to be drug addicted, or no home telephone were excluded. RESULTS: Of concern were that 23.1% of mothers reported using the monitor 12 or fewer hours per day and that 10.8% believed their infants did not need a monitor. Of 11 variables examined, only color change in the infant was associated with frequency of monitor use. CONCLUSIONS: Clear, consistent communication with families regarding the use of apnea monitors is essential to improve compliance with proper monitoring techniques.

Cross-Sectional Studies↗

Home apnea monitoring and risk factors for poor family functioning.

As part of a comprehensive study on the impact of home apnea monitoring on family functioning, we undertook an in-depth analysis of risk factors for poor family functioning in 93 families of monitored infants. A multistep correlation and regression analysis was used to examine the ability of 16 demographic, infant, family, and monitor-related variables to predict poor functioning in each of 12 different aspects of family life. Of note was the fact that monitor-related variables failed to be important predictors of poor family functioning. Rather, previous family problems and low satisfaction with social support were the most broad and powerful predictors of poor functioning. To enhance the capabilities of families to manage the added responsibility of home monitoring, clinicians might wisely assess both of these aspects of family life and then target extra support services to families identified to be at risk in these areas.

Adult↗