Showing papers on "Sudden infant death syndrome published in 1991"

Defining the sudden infant death syndrome (SIDS): deliberations of an expert panel convened by the National Institute of Child Health and Human Development.

Abstract: (1991). Defining the Sudden Infant Death Syndrome (Sids): Deliberations of an Expert Panel Convened by the National Institute of Child Health and Human Development. Pediatric Pathology: Vol. 11, No. 5, pp. 677-684.

Results from the first year of the New Zealand cot death study.

Abstract: New Zealand's high mortality rate from the sudden infant death syndrome (SIDS) prompted the development of the New Zealand cot death study. This report of the preliminary analysis of the first year of the data gives the major identified risk factors. One hundred and sixty-two infants who died from SIDS were compared with 589 control infants, who were a representative sample of all hospital births in the study region. Obstetric records were examined and parental interviews were completed in 96% and 89% of subjects respectively. Data were available for all the variables in this study in 95% of those interviewed, thus 128 cases and 503 controls make up the subjects of this report. As expected we confirmed many risk factors for SIDS including: lower socioeconomic status, unmarried mother, young mother, younger school leaving age of mother, younger age of mother at first pregnancy, late attendance at antenatal clinic, nonattendant at antenatal classes, Maori, greater number of previous pregnancies, lower birth weight, shorter gestation, male infant, admission to neonatal intensive care unit. In addition, however, we identified three risk factors which are potentially amenable to modification. These were the prone sleeping position of baby (odds ratio = 3.53, 95% confidence interval 2.26, 5.54), maternal smoking (1-9 cigarettes/day OR = 1.87, 95% CI = 0.98, 3.54; 10-19/day OR = 2.64, 95% CI = 1.47, 4.74; 20+/day OR = 5.06, 95% CI = 2.86, 8.95) and breast feeding (OR = 2.93, 95% CI = 1.84, 4.67).(ABSTRACT TRUNCATED AT 250 WORDS)

Gastroesophageal reflux, as measured by 24-hour pH monitoring, in 509 healthy infants screened for risk of sudden infant death syndrome.

Abstract: Continuous long-term esophageal pH monitoring has become the preferred test to quantify acid gastroesophageal reflux. Because reflux to a limited extent is physiologic, the determination of optimal thresholds to separate normal from abnormal reflux is mandatory. Esophageal pH was measured during 24 hours in 509 healthy thriving infants, aged 3 days to 1 year, using a glass microelectrode with an external reference electrode connected to a portable recorder. Percentiles of the four parameters studied (reflux index or percent of the investigation time with a pH less than 4, number of episodes with a pH less than 4 during 24 hours, number of episodes lasting greater than 5 minutes, the duration of the longest episode (in minutes) are presented. A percentile curve of the reflux index regarding the age distribution shows that the normal range for the reflux index during the first 12 months of life is about 10% (95 percentile), decreasing from 13% at birth to 8% at 12 months. Application of an age-related percentile curve offers a close-to-reality possibility of data interpretation and illustrates that there is inevitably an overlap of data between normal and abnormal populations, because reflux is a phenomenon occurring to some extent in every human being.

Sudden death in infants sleeping on polystyrene-filled cushions.

Abstract: Background. Infants are at risk for both the sudden infant death syndrome (SIDS) and accidental suffocation. On postmortem examination, however, it is difficult to distinguish one from the other without information from the scene of death. Healthy infants are assumed to be able to turn their heads and, if not otherwise restrained, to obtain fresh air. We assessed this assumption in an investigation of infant deaths that occurred during sleep on cushions filled with polystyrene beads. Methods. We obtained data on 25 deaths from the U.S. Consumer Product Safety Commission. We also used mechanical and animal models to study physiologic aspects of ventilation relevant to these results, by simulating the effects on an infant of breathing into a cushion. We measured the effects of softness, malleability (molding of the cushion about an infant's head), airflow resistance, and rebreathing of expired gases. Results. All 25 study infants were prone when found dead, and at least 88 percent were face down wi...

Delayed central nervous system myelination in the sudden infant death syndrome.

Abstract: This study was designed to assess whether development of the central nervous system (CNS) is delayed in victims of the sudden infant death syndrome (SIDS). We selected the parameter of myelination because it is a continuously changing and readily accessible marker of CNS development in the SIDS age-range. We assessed myelination blindly in 61 SIDS and 89 autopsy controls. In 62 sites the degree of myelination was visually graded in myelin-stained histological sections on an ordinal scale of 0-4 using the inferior cerebellar peduncle as an internal standard of degree 3. Cases were stratified by postconceptional age at death and SIDS and controls were compared with respect to myelin degree at each site. Significantly delayed myelination (p less than 0.05) occurred in the SIDS group in 25 of the 62 sites examined. Hypomyelination affected fiber systems in which myelination is initiated before or after birth and which myelinate with different tempos and preferentially affect pyramidal and cerebellar (somatomotor) and prefrontal-temporal-limbic (visceromotor) systems. Hypomyelination was not associated with individual clinicopathologic variables in the SIDS group. Somatic growth and brain weight were significantly greater in SIDS than controls. Therefore, we suggest that SIDS is associated with a developmental CNS disorder. Although delayed CNS myelination most likely shares a common antecedent with sudden death and is not its cause, the role of somato- and viscero-motor systems in central cardiorespiratory control and arousal warrants further analysis in SIDS.

An overview of retrospective case-control studies investigating the relationship between prone sleeping position and SIDS.

Abstract: A critical overview of 19 case-control studies that have investigated the relationship between prone sleeping position and sudden infant death syndrome (SIDS) is presented. Issues relating to the non-comparability of the studies are described in terms of: (i) case definition; (ii) selection of controls; (iii) quality of the sleeping position data; (iv) recall bias; and (v) adjustment for confounding factors. All studies showed a positive association (2 out of the 19 studies were not significant) between prone sleeping position and SIDS. Meta-analysis techniques applied to six of these studies, based on 'usual' sleeping position in cases and population representative controls, has confirmed an overall higher risk of SIDS in infants who usually sleep prone. The most common odds ratio for an association between prone sleeping position and SIDS was 2.72 (95% confidence interval 2.27-3.26). The extent to which the methodological problems of retrospective case-control studies interfere with our interpretations of this association are discussed.

Comparison of Infant Mortality among Twins and Singletons: United States 1960 and 1983

Abstract: Infant mortality among US black and white twins and singletons was compared for 1960 and 1983 using the Linked Birth/Infant Death Data Sets from the National Center for Health Statistics. Both twin and singleton infant mortality rates showed impressive declines since 1960 but almost all of the improvement in survival for both twins and singletons was related to increased birth weight-specific survival rather than improved birth weight distribution. One-half of white twins and two-thirds of black twins weighed less than 2,500 g at birth, and 9% of white twin births and 16% of black twin births were in the very low (less than 1,500g) birth weight category. In 1983, twin infant mortality rates were still four to five times that of singletons. However, twins had a survival advantage in the 1,250-3,000 g range, which persisted after adjustment for gestational age. Cause-specific mortality among twins was considerably higher for every major cause of death: twin mortality risks due to newborn respiratory disease, maternal causes, neonatal hemorrhage, and short gestation/low birth weight were six to 15 times that of singletons. The lowest twin-to-singleton mortality ratios observed were for congenital anomalies and sudden infant death syndrome with relative risks twice that of singletons. The data underscore the need to develop effective strategies to decrease infant mortality among twins.

Hypoxanthine levels in vitreous humor: evidence of hypoxia in most infants who died of sudden infant death syndrome.

Abstract: Postmortem changes of the hypoxanthine in vitreous humor in humans were investigated. Hypoxanthine is formed from hypoxic degradation of adenosine monophosphate. Repeated sampling was performed in 13 deceased adults. Keeping the bodies at +6 degrees C, the increase of the hypoxanthine levels was estimated to 3.5 mumol/L per hour when sampling was started more than 12 hours after death (range 2.8 to 5.6 mumol/L per hour). Results of hypoxanthine measurements from vitreous humor in 73 infants with sudden infant death syndrome, 17 infants and children who died sudden violent deaths, and 6 neonates who died suddenly without hypoxemia prior to death were corrected according to the expected postmortem hypoxanthine increase. The time between death and autopsy was similar in the three groups studied. The corrected median hypoxanthine level in the group with sudden infant death syndrome was 227 mumol/L, which is significantly higher than in the other groups; 22 mumol/L in the group who had violent deaths (P less than .01), and 0 mumol/L in the neonate group (P less than .01). The findings seem to confirm that sudden infant death is preceded by a relatively long period of tissue hypoxia in most cases.

Exacerbation of Bacterial Toxicity to Infant Ferrets by Inftuenza Virus: Possible Role in Sudden Infant Death Syndrome

Abstract: Of several toxins examined, only staphylococcal alpha and gamma toxin, endotoxin, and diphtheria toxins were lethal for 5-day-old ferrets. Their toxicities were enhanced in animals infected at 1 day old with influenza virus, from 3-fold with staphylococcal gamma toxin through 14-fold for staphylococcal alpha toxin, 84-fold for endotoxin, and 219-fold for diphtheria toxin. No increased viral replication occurred in any tissue; thus the effects of the toxins were exacerbated by the infection, not vice versa. Neonates died suddenly without clinical symptoms as in human babies dying from the sudden infant death syndrome (SIDS). Pathologic examination showed inflammation in the upper respiratory tract, lung edema and collapse, and early bronchopneumonia in the toxin- and influenza virus-treated animals but not in those treated with toxin or virus alone. Thus, bacterial toxins could play a role in SIDS, this being more likely with a concomitant influenza virus infection.

Chronic Fetal Hypoxia and Sudden Infant Death Syndrome: Interaction Between Maternal Smoking and Low Hematocrit During Pregnancy

Abstract: To investigate the hypothesis that chronic fetal hypoxia contributes to the etiology of sudden infant death syndrome (SIDS), a possible interaction between the effect of maternal cigarette smoking and low hematocrit during pregnancy on the risk of SIDS was studied using the US Collaborative Perinatal Project cohort. The 193 SIDS cases identified in the cohort were analyzed with 1930 controls randomly selected from infants who survived the first year of life. After adjustment for maternal age, infants born to mothers who smoked 10 or more cigarettes per day and who were anemic (hematocrit less than 30%) during pregnancy were at a much higher risk of SIDS than infants born to mothers who did not smoke and were not anemic (odds ratio = 4.0; 95% confidence limits, 2.1 and 7.4). Smoking 10 or more cigarettes per day vs none increased the risk of SIDS by 70% among women with hematocrit at or above 30% but increased risk threefold among women with hematocrit below 30%. After adjustment for more potential confounders in a logistic regression model, the effect of smoking on SIDS continued to increase with lower levels of hematocrit during pregnancy. Birth weight accounted for very little of these associations. Low hematocrit was not a risk factor for SIDS among nonsmokers but became an important predictor among heavy smokers. These findings are in agreement with the hypothesis that chronic fetal hypoxia may predispose to SIDS, possibly by impairing the normal development of the fetal central nervous system.

Delayed dendritic development of catecholaminergic neurons in the ventrolateral medulla of children who died of sudden infant death syndrome.

Abstract: Catecholaminergic neurons were characterized by reaction with antiserum to tyrosine hydroxylase, by shape and location and by dendritic ramifications. In this population of cells in the ventrolateral medulla (VLM), the dendritic spines of fusiform and triangular neurons increased with gestational age and rapidly diminished after birth. However, in SIDS, the spines persisted notably in neurons in the VLM but also in the reticular formation and vagal nuclei. These findings suggest a delay in neuronal maturation and may be related to developmental disorders of respiratory, circulatory or sleep-wake regulation.

Sudden infant death syndrome related to climate.

Abstract: In Australia the single most important factor influencing the incidence of SIDS is the climate. The incidence in mid summer in South Australia is 0.7 per 1,000 live births, in mid winter in Tasmania it is 6.3 per 1,000 live births. It is predicted that if infants under 6 months of age in cold weather were tied into swaddling and placed supine to sleep as in Asia and Czechoslovakia, and older infants who may object to restriction of movement, had the cot made up with the infants' feet touching the lower end, warm clothing and no more than a single thin porous cover, the incidence of SIDS as in Asia and Czechoslovakia could be reduced to less than 1.0 per 1,000.

Early Parental Responses to Sudden Infant Death, Stillbirth or Neonatal Death

Abstract: OBJECTIVE To examine the mental health of parents after stillbirth (SB), neonatal death (NND) or sudden infant death syndrome (SIDS). DESIGN The sampling frame from southeast Queensland was observed over 2.5 years. Control families were matched for birth date, sex of child, hospital and health insurance status. SETTING Home interviews, by specially trained social workers, took place two months after the death of the infant. PARTICIPANTS Results were based on 918 responses from 260 bereaved families (99 SB, 109 NND, 52 SIDS) and 252 control families, with a 63.6% overall participation rate. MAIN OUTCOME MEASURES Questionnaires included standardised measures of anxiety, depression, biographic and demographic data. It was hypothesised that subject families would show more symptoms of anxiety and depression than control families, with mothers and parents affected by SIDS having the highest levels. RESULTS Affected parents report significantly more psychological symptoms than controls, mothers more than fathers (P less than 0.001). Parents affected by SIDS showed more symptoms than other affected parents. High levels of anxiety were 14 times more likely in mothers affected by SIDS than controls (95% confidence interval, 5.4-36.6), with depression 12 times more likely (95% confidence interval, 3.8-43.5). Anxiety for groups affected by SB and NND were respectively 3.9 (2.1-10.5) and 6.5 (2.6-16.3) times more likely than for controls, and depression 6.9 (2.1-22.5) and 8.5 (2.7-26.7) times more likely. Differences were less marked for fathers, except for fathers affected by SIDS. CONCLUSIONS Parents affected by stillbirth, neonatal death or sudden infant death syndrome manifest high levels of anxiety and depression two months after the death. Mothers have more symptoms than fathers, and parents affected by SIDS have the most symptoms of anxiety and depression.

Macrophages, microglial cells, and HLA-DR antigens in fetal and infant brain.

Abstract: Immunohistochemical reactions for macrophages, microglia, and HLA-DR antigens were tested on frozen sections of necropsy brain tissue from 20 fetuses and infants ranging in age from 18 weeks' gestation to 8 months post term No primary central nervous system disease was present but there were four cases of sudden infant death syndrome (SIDS) Macrophages were detected in all the samples studied and were located in the germinal matrix zone, in perivascular spaces throughout the brain, and in the leptomeninges and subependymal layer Well differentiated microglia were present in all cases examined after 35 weeks' gestation and less well ramified forms were seen at earlier stages of gestation HLA-DR antigens were detected on a small number of macrophages, chiefly in a perivascular location, in all but three cases The fewest reactive cells and the weakest reactions occurred in the youngest fetuses One case of SIDS showed increased foci of microglia in perivascular white matter: this case and one other case of SIDS were the only cases with well ramified microglia that expressed HLA-DR antigens These findings may be relevant to an understanding of local immune responses in fetal brain infections, including human immunodeficiency virus infection

Hyperplasia of bombesin-immunoreactive pulmonary neuroendocrine cells and neuroepithelial bodies in sudden infant death syndrome.

Abstract: The distribution and frequency of bombesin immunoreactive neuroendocrine (NE) cells including neuroepithelial bodies (NEB) was analyzed morphometrically in lung sections from 25 infants who died of sudden infant death syndrome (SIDS) and 25 control infants. The control group included infants age-matched to those with SIDS, as well as subjects ranging in age from early to late infancy, to define the postnatal development of pulmonary NE-cell system. Quantitative analysis was performed on lung sections immunostained with monoclonal antibody against bombesin and the contents of bombesin-like peptide in lung extracts were measured by a specific radioimmunoassay (RIA). In control infants, the frequency of NE cells was high at birth but decreased dramatically during the first year of life. In SIDS infants, the frequency of NE cells, the size of NEB, and the mean concentration of bombesin-like peptide detected by RIA were significantly increased compared to those values for age-matched controls. These findings s...

Gastroesophageal reflux in infants with a history of near-miss sudden infant death.

Abstract: From January 1984 through August 1986, 130 infants were referred to our department with a history of apnea, hypotonia, and cyanosis or pallor, suggesting near-miss sudden infant death syndrome. Protocol consisted of medical history, clinical examination, overnight polygraphic recording, and cardiologic, gastrointestinal, metabolic, neurologic, and toxicologic workups. In 49 of these infants who needed vigorous stimulation or mouth to mouth resuscitation, the event occurred shortly after feeding. Combined, continuous esophageal pH monitoring and polygraphic recording in these 49 infants showed pathologic gastroesophageal reflux (GER) in 34 patients. An abnormal overnight polygraphic recording was observed in 8 of 34 infants with pathologic GER. Other investigations led to etiologic diagnoses in 42 of the remaining infants. Severe GER was frequently found in children with apnea after feeding but clearly is not the only mechanism involved. Infants with a history of apnea after a feeding should be investigated for GER and appropriately treated.

Effect of prenatal cocaine on respiration, heart rate, and sudden infant death syndrome†

Abstract: We studied 114 neonates by pneumocardiogram recordings in order to examine the effects of cocaine with and without opiate exposure on neonatal respiration, heart rate, apparent life threatening events (ALTE), and sudden infant death syndrome (SIDS). In full-term infants exposed to cocaine without opiates we found increased longest apnea duration and more episodes of bradycardia, but decreased periodic breathing and average heart rate than in control full-term infants. Term infants prenatally exposed to cocaine with opiates also had less periodic breathing. Preterm infants exposed to cocaine with and without opiates had decreased apnea density and periodic breathing compared with preterm controls. Discriminant analysis to determine whether perinatal asphyxia or exposure to other drugs could predict cardiorespiratory abnormalities showed no consistent relationship. In 72 of 114 infants available for follow-up, no ALTE occurred but two were lost to SIDS. Our data support the hypothesis that prenatal cocaine exposure may perturb, albeit subtly, the maturation of respiratory control, resulting in disruption of postnatal respiration.

Possible mechanisms responsible for the sudden infant death syndrome.

Abstract: The accepted working definition of sudden infant death syndrome (SIDS), derived from the Second International Conference on Causes of Sudden Death in Infants held in Seattle in 1969. is ‘The sudden death of any infant or young child, which is unexpected by history, and in which a thorough post-mortem examination fails to demonstrate an adequate cause for death’.’ Sudden infant death syndrome has a variable incidence in different communities, usually ranging from 1 to 4 per 1000 live births. It is the largest single cause of death in the age group from 1 week to 1 year, is more common in lower socio-economic groups and during the winter months, and has a bias towards low birthweight infants, those born prematurely and males and infants born to single mothers. Maternal risk factors include young age, history of smoking, high parity and short interpregnancy intervals. Other risk factors include maternal opiate or barbiturate abuse, infection during pregnancy and high birth order. Further epidemiological features have been summarized in recent rev iew~.~~3 In spite of an extraordinary amount of world-wide research in recent years it has not been possible to find a unifying concept that can satisfactorily explain the cause of this enigmatic disorder4 It has been suggested that SlDS represents the end point of a heterogeneous group of interrelated predisposing factors, rather than a single disease en tit^.^-^ Failure to appreciate this heterogeneity has led some workers, who have discovered a condition that has presented clinically and pathologically as SIDS, to suggest that an identical mechanism must be responsible for most other SlDS cases. Alternatively, other authors have asked whether SlDS represents a diagnosis at all, or is just a ’convenient diagnostic dustbin’ that suits the very different needs and purposes of clinicians, pathologists, parents, public health authorities and researchers alike! The following review of current theories demonstrates the wide range of aetiological factors that have been under consideration recently in infants who have died suddenly and unexpectedly and who appear pathologically unremarkable at autopsy. Hypotheses must account for the consistent age range of SlDS victims and the other epidemiological features such

A review of epidemiological studies of sudden infant death syndrome in southern New Zealand.

Abstract: The rate of sudden infant death syndrome (SIDS) in Southern New Zealand has been very high with an apparent real increase in incidence from the early 1970s. Recent research is reviewed and the results of specific interventions aimed at preventing SIDS summarized. The intervention consisted of strongly advising new parents that their babies sleep on their back or side and that they avoid over-heating, especially during infections. For the Otago area, child-care practice has been documented and prone sleeping of 1 month old babies has declined from 41.8% in 1986 to 2.4% in 1989-90. There is also evidence that parental control of infants' thermal environment has improved, maternal smoking during pregnancy has slightly decreased and the number of babies breast fed at 1 month of age has increased by 11%. In Southern NZ there has been a decline in post-neonatal SIDS mortality from 6.3 deaths per 1000 live births 1979-84 to 1.3 per 1000 live births in 1990. There are grounds for supposing that the intervention has been causative of this change, a possibility being addressed by on-going studies.

Sleep apnea in infants who succumb to the sudden infant death syndrome.

Abstract: Previous studies have shown the frequency of respiratory pauses to be altered in groups of infants at risk for the sudden infant death syndrome (SIDS). In this study, we assess the frequency of apneic pauses during quiet sleep and rapid eye movement sleep in control infants and infants who subsequently died of SIDS. Sleep states were identified in 12-hour physiological recordings of SIDS victims and matched control infants, and the number of respiratory pauses from 4 to 30 seconds in duration was computed for quiet sleep and rapid eye movement sleep. SIDS victims 40 to 65 days of age showed significantly fewer apneic pauses than did age-matched control infants across the two sleep states. Fewer short respiratory pauses accounted for most of the reduction in number of apneic events in the SIDS victims during both sleep states. During the first month of life, SIDS victims did not differ significantly from control neonates on this measure. The finding that this respiratory difference exists during the second month of life, just before the period of maximal risk for SIDS, but not earlier, may have implications for the etiology of SIDS deaths.

Sudden infant death syndrome and small airway occlusion: facts and a hypothesis.

Abstract: Respiratory failure is almost certainly the cause of death in the majority of cases of sudden infant death syndrome (SIDS), but the mechanisms leading to it have not been elucidated. SIDS shares many environmental and socioeconomic risk factors with severe forms of bronchiolitis, and the age distribution of incident cases is similar. Present knowledge of lung and airway development during infancy, determinants of peripheral airway patency, changes in lung surface activity in infants with SIDS, and fluid film dynamics in small airways are reviewed. It is hypothesized that many cases of SIDS may be due to a final episode of progressive peripheral bronchial occlusion in infants with preceding critically diminished conductance of the smaller airways.

Maternal Smoking, Low Birth Weight, and Ethnicity in Relation to Sudden Infant Death Syndrome

Abstract: To determine independent effects of maternal smoking and infant low birth weight (less than 2,500 g) on risk of sudden infant death syndrome (SIDS) among different ethnic groups, the authors conducted a population-based case-control study based on the 1984-1989 Washington State birth record data. Two control groups were selected for 916 SIDS cases. The first one comprised 3,704 randomly selected controls, matched to cases by birth year, to describe the characteristics of the study population. In the second control group (n = 6,186), minorities were oversampled, by matching to cases on maternal race/ethnicity and birth year, to increase the power of analysis within each ethnic group. All subjects were classified into five groups on the basis of maternal race/ethnicity: white, black, American Indian, Asian, and Hispanic. After controlling for confounders, the authors found that maternal smoking was independently associated with SIDS among white (odds ratio (OR) = 2.2, 95% confidence interval (CI) 1.8-2.6), blacks (OR = 3.1, 95% CI 1.7-5.9), Asians (OR = 2.7, 95% CI 1.1-6.6, and Hispanics (OR = 5.5, 95% CI 1.4-22.0), but had little relation among American Indians (OR = 1.4, 95% Cl 0.9-2.4). Infant low birth weight was independently related to SIDS among whites (OR = 2.5, 95% Cl 1.8-3.4) and American Indians (OR = 5.5, 95% Cl 2.8-11.2) and to a lesser extent among blacks (OR = 1.9, 95% Cl 0.8-4.1), but not among Asians (OR = 1.1, 95% Cl 0.2-5.2) or Hispanics (OR = 1.2, 95% Cl 0.1-11.5). The misclassification that may occur because of the application of the same definition of low birth weight to all ethnic groups may be the main reason for the weaker association between infant low birth weight and SIDS among blacks and the absence of an association among Asians and Hispanics. Defining low birth weight as below population mean minus 1.96 standard deviations may provide better insight into the relation between low birth weight and SIDS. Understanding the reasons for the lack of a strong association between maternal smoking during pregnancy and SIDS among American Indians may enhance our knowledge of the etiology and pathogenesis of SIDS.

Esophageal pH monitoring data during chest physiotherapy.

Abstract: Sixty-three infants, aged from 1 to 4 months, were examined for gastroesophageal reflux (GER) using esophageal pH monitoring. Thirty were examined because of chronic vomiting, 21 were healthy controls examined for GER as part of a screening program for sudden infant death syndrome, and 12 had an acute respiratory disease (RD). The 24-h pH monitoring data were within normal ranges in 26 infants (20 controls, 2 babies with emesis, and 4 with RD). Data were abnormal in 37 infants (1 control, 28 infants with emesis, and 8 with RD). All babies were submitted during a fasting awake period to a 30-min chest physiotherapy session. In the three groups studied, the incidence of GER episodes detected by the pH probe was significantly higher during physiotherapy if compared (a) to the calculated mean incidence during a 30-min period of the 24-h investigation or (b) to the incidence during a fasting awake period such as that during which the physiotherapy was given (p less than 0.001; Wilcoxon rank-sum test). We conclude that chest physiotherapy significantly increases GER incidence. We therefore propose restricting chest physiotherapy to fasting periods. These data add to the confusion that already exists regarding the possible causal relationship between (acid) GER and respiratory disease.