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Biomedical subjects

K A Waters

Publications and source records attributed to K A Waters.

At least 19 recordsLinked to original sources

Outcome of noninvasive ventilation in children with neuromuscular disease.

OBJECTIVE: To assess the effect of institution of noninvasive ventilation (NIV) on clinical outcome and quality of life (QOL) in a cohort of children with severe neuromuscular disorders. METHODS: We reviewed records and obtained clinical data from the year prior to commencing NIV and annually thereafter. Data obtained included diagnosis, patient symptoms, mortality, NIV adverse effects, pulmonary function tests, polysomnographic data, length of hospitalizations, and health care costs. Patients and parents completed questionnaires assessing QOL with NIV and recalling QOL before NIV. RESULTS: Fourteen of 17 (82%) suitable patients were enrolled. Follow-up ranged from 6 to 84 months (median 30). Symptoms of daytime sleepiness (p = 0.003) and headache (p = 0.046) improved after initiation of NIV. Sleep quality assessed by polysomnography also improved. Hospitalization rates (p = 0.002) and health care costs (p = 0.003) decreased. QOL remained stable after NIV, despite disease progression. CONCLUSION: Treatment of respiratory failure, in children with neuromuscular disease, with noninvasive ventilation results in a reduction in symptoms, hospitalizations, and health care costs without adverse effects on quality of life.

Child↗

Postnatal nicotine and/or intermittent hypercapnic hypoxia effects on apoptotic markers in the developing piglet brainstem medulla.

The most important risk factors currently identified for the sudden infant death syndrome (SIDS) are prone sleeping and cigarette smoke exposure. In this study, we investigated the neuropathological sequelae of these risk factors by exposing piglets to intermittent hypercapnic-hypoxia (IHH) and/or nicotine (nic) in the early postnatal period. Our hypothesis was that either nic or IHH exposure could increase neuronal cell death, and that combined exposure (nic+IHH) would be additive. Four exposure patterns were studied: controls (n=14), IHH (n=10), nic (n=14), and nic+IHH (n=14). All groups had equal gender ratios. Nic exposure via an implanted osmotic minipump commenced within 48 h of birth and continued until age 13-14 days when animals were killed and brains collected. A total of 48 min of hypercapnic-hypoxia was delivered on the day immediately prior to killing in a pattern comprising 6 min of HH (8% O(2), 7% CO(2), balance N(2)) alternating with 6 min of air. Immunohistochemistry was performed to identify neurons positive for active caspase-3 and DNA fragmentation (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, TUNEL) in seven nuclei of the caudal medulla. Staining quantification showed that: 1. IHH induced neuronal death (increased both TUNEL and casapse-3) in more brainstem nuclei than nicotine. 2. Females were more severely affected by IHH than males. 3. Where IHH and nicotine were combined, TUNEL expression was approximately 5% less than IHH alone, but changes in caspase-3 were variable. We conclude that acute exposure to IHH in the postnatal period is more neurotoxic than exposure to nicotine alone. Combined exposure to IHH and nicotine produced variable responses with some results suggesting that nicotine can be neuroprotective. These results indicate that environmental insults attributable to prone sleeping can produce neurotoxic sequelae in SIDS, with some regional specificity in the response. However, no consistent relationship is evident when combining the two insults.

Analysis of Variance↗

N-methyl-D-aspartate receptor 1 changes in the piglet braintem after nicotine and/or intermittent hypercapnic-hypoxia.

Prone sleeping and cigarette smoke exposure are two major risk factors for the sudden infant death syndrome (SIDS). Utilizing piglet models of early postnatal nicotine and/or intermittent hypercapnic-hypoxia (IHH) exposure, we tested the hypothesis that these exposures, separately or combined, increase N-methyl-D-aspartate (NMDA) receptor 1 (NR1) expression in the brainstem medulla. We also tested for gender-specific effects. Three piglet exposure groups were compared against 14 controls; 1, nicotine [n = 14], 2, IHH [n = 10], and 3, nicotine+IHH [n = 14], with equal gender proportions in each group. Non-radioactive in situ hybridization and immunohistochemistry were performed for NR1 mRNA and protein expression, respectively, and were quantified in seven nuclei of the brainstem medulla. NR1 mRNA was significantly increased in the gracile and inferior olivary nucleus (ION) after nicotine exposure, in five of seven nuclei after IHH exposure, and in three of seven nuclei after nicotine+IHH. The increased mRNA changes were accompanied by increased protein only in the ION after IHH and nicotine+IHH (P = 0.019, and P = 0.008 respectively). By gender, control females had greater NR1 mRNA than males in the dorsal motor nucleus of vagus (P = 0.05) and for protein in the ION (P = 0.02). This gender difference was maintained after nicotine exposure in the ION with additional gender differences observed including greater mRNA in the cuneate nucleus (P = 0.04) and nucleus of the spinal trigeminal tract (P = 0.03) of males compared with females. Overall, more changes occurred at the mRNA level than protein, and IHH exposure induced more changes than nicotine or nicotine+IHH exposures. Together, these findings suggest that hypercapnic-hypoxic exposures (modeling prone sleeping or sleep apnea) are more likely to induce NMDA receptor changes in the developing brainstem than nicotine exposure alone.

Analysis of Variance↗

Effects of postnatal nicotine exposure on apoptotic markers in the developing piglet brain.

Exposure to cigarette smoke is a risk factor for the sudden infant death syndrome (SIDS), but the ability to distinguish between the neuropathological effects of pre- versus postnatal exposure is limited in the clinical setting. To test whether postnatal nicotine exposure could contribute to the increased neuronal expression of apoptotic markers that we have previously observed in SIDS infants, as well as including study of gender influences, we developed a piglet model to mimic passive smoking in the early postnatal period. Piglets were exposed to nicotine (2 mg/kg/day infused via an implanted osmotic minipump) within 48 h of birth until the age of 13-14 days, when the brain was collected for study. Four piglet groups included: control females (n=7), control males (n=7), nicotine females (n=7), and nicotine males (n=7). Apoptotic markers included immunohistochemistry for activated caspase-3, and for DNA fragmentation or terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL) in seven nuclei of the brainstem caudal medulla and two subregions of the hippocampus (CA4 and dentate gyrus). Among control females compared with males, there was less active caspase-3 and less TUNEL in the dorsal motor nucleus of vagus (DMNV), and there was less TUNEL in the nucleus of the spinal trigeminal tract (NSTT). Compared with controls, nicotine-exposed male piglets had increased TUNEL staining in the cuneate nucleus (P=0.05), and increased active caspase-3 in the hypoglossal, gracile and dentate gyrus (P<0.05 for each). Nicotine-exposed females showed no change in TUNEL staining in any of the nuclei studied, but increased active caspase-3 in the hypoglossal, DMNV and NSTT (P<0.05 for each). These results show for the first time that postnatal nicotine exposure can lead to an increase in apoptotic markers in the brain. In piglets, these effects showed regional and gender-specific differences, suggesting that passive, postnatal nicotine exposure may be responsible for some neuropathological changes observed in infants dying from SIDS.

Analysis of Variance↗

Correlations between brainstem NMDA receptor changes and active neuronal cell death after intermittent hypercapnic hypoxia in the developing piglet.

The role of the N-methyl-D-aspartate (NMDA) receptor in cell death was evaluated in the piglet brainstem after exposure to intermittent hypercapnic hypoxia (IHH). Study groups comprised controls (n=6) and piglets exposed to IHH on 2 (n=6) or 4 (n=5) successive days prior to euthanasia. All piglets had the caudal medulla evaluated at 13-14 days of age using double immunohistochemistry for TUNEL and the NMDA receptor 1 (NR1) subunit. The percent of TUNEL positive neurons amongst NR1 (% TUN in NR1) and non-NR1 neurons (% TUN in non-NR1) was determined in eight nuclei. After 2 days of IHH, %TUN in NR1 was increased in the dorsal motor nucleus of the vagus (DMNV, P=0.007) and the inferior olivary nucleus (ION, P=0.05). After 2 days IHH, %TUN in non-NR1 neurons was increased in the lateral reticular nucleus (LRt, P=0.05), nucleus of the solitary tract (NTS, P=0.004) and gracile nucleus (P=0.05). After 4days IHH, the increase of %TUN in NR1 was sustained in the ION (P=0.05), while %TUN in non-NR1 neurons was sustained in NTS (P=0.04) and LRt (P=0.006). Daily IHH exposure induces neuronal death within NR1 and non-NR1 neurons, but the neuronal phenotype is consistent within affected brainstem nuclei. Involvement of the NMDA receptor tended to occur in nuclei with higher basal NR1 expression, and thus occurred in nuclei relevant to cardiorespiratory function. We speculate that IHH exposures, such as occurs during obstructive apnea or facial entrapment in prone sleeping during infancy, can induce abnormalities of cardiorespiratory control.

Animals↗

Observer-blinded comparison of two nonopioid analgesics for postoperative pain in piglets.

Piglets are popular for studies of respiratory and cardiovascular function, but opioid analgesics are contraindicated in these studies because of central nervous system depression. We evaluated two nonopioid analgesics for postoperative pain relief following implantation of a central arterial catheter via an inguinal incision. Animals were randomly assigned to paracetamol-treated (n=8, rectal suppositories, 100 mg/kg) meloxicam-treated (n=8, 1 mg/kg meloxicam via the catheter) or untreated control group (n=8, placebo suppositories and normal saline). Additional controls received paracetamol or meloxicam, without pain (n=6 for both groups). Behavioral and physiological assessments, and blood sampling were undertaken at nine timed intervals until 24 h after surgery. Multifactorial numerical rating scale (NRS), behavioral and physiological pain scores (PPS) decreased over time for all groups (P<.001). On NRS and behavioral criteria, meloxicam was significantly better than paracetamol (P<.001), and both were better than control (p<.001 for each). Physiological parameters discriminated between the control and analgesia-treated groups, but not between paracetamol and meloxicam. Preliminary pharmacokinetics, determined by isocratic high-performance liquid chromatography (HPLC), revealed no difference in the half-life of paracetamol (2.5+/-0.3 h) vs. meloxicam (3.4+/-0.4 h). Paracetamol and meloxicam provided effective postoperative analgesia in piglets, with meloxicam superior to paracetamol on behavioral criteria.

Acetaminophen↗

Depression of ventilatory responses after daily, cyclic hypercapnic hypoxia in piglets.

Ventilatory responses (VRs) were measured via a sealed face mask and pneumotachograph in 30 unsedated, mixed-breed miniature piglets at 12.6 +/- 2.3 days of age (day 1) and then repeated after seven daily 24-min exposures to 10% O(2)-6% CO(2) [hypercapnic hypoxia (HH)]. Arterial blood was sampled at baseline, after 10 min of exposure, and after 10 min of recovery. VRs included hypoxia (10% O(2) in N(2)), hypercapnia (6% CO(2) in air), and HH (10% O(2)-6% CO(2)-balance N(2)). Treatment groups (n = 10 each) were exposed to 24 min of HH from day 2 to 8 as sustained HH (24 min of HH and then 24 min of air) or cyclic HH (4 min of HH alternating with 4 min of air). Day 1 and 9 data were compared in treatment and control groups. After cyclic HH, respiratory responses to CO(2) were reduced during hypercapnia and during HH (P < 0.001 vs. control for minute ventilation in both). In both treatment groups, time to peak minute ventilation was delayed in hypoxia (P = 0.02, ANOVA), and response amplitude was increased (P < 0.001 and P = 0.003, sustained and cyclic HH, respectively, vs. control). Respiratory pattern was also altered during the VRs and among treatment groups. Stimulus presentation characteristics exert effects on VRs that are independent of those elicited by daily HH.

Animals↗

Treatment of sleep-disordered breathing in children with myelomeningocele.

The prevalence of moderate to severe sleep-disordered breathing (SDB) in patients with myelomeningocele may be as high as 20%, but little information is available regarding treatment of these patients. To assess the efficacy and complications of treatments for these children, we collected data on 73 patients from seven pediatric sleep laboratories. Obstructive sleep apnea (OSA, n = 30) and central apnea (n = 25) occurred more frequently than central hypoventilation (n = 12). We also describe a sleep-exacerbated restrictive lung disease type of SDB in 6 patients who had hypoxemia during sleep without apnea or central hypoventilation. For each type of SDB, effective treatments were identified in a stepwise process, moving towards more complex and invasive therapies. For OSA, adenotonsillectomy was often ineffective (10/14), whereas nasal continuous positive airway pressure (CPAP) was usually successful (18/21). For central apnea, methylxanthines and/or supplemental oxygen proved sufficient in 2 of 9 and 3 of 6, respectively, but noninvasive positive pressure ventilation was required in 7 children. For central hypoventilation, supplemental oxygen (alone or with methylxanthines), noninvasive positive pressure ventilation, and tracheostomy with positive pressure ventilation were effective in 3, 2, and 2 patients, respectively. Sleep-exacerbated restrictive lung disease always required supplemental oxygen treatment, but in 2 cases also required noninvasive positive pressure ventilation; nutritional and orthopedic procedures also were helpful. Posterior fossa decompression was used for the first three types of SDB, but data were insufficient to delineate specific recommendations for or against its use. In summary, evaluation by an experienced, multidisciplinary team can establish an effective treatment regime for a child with myelomeningocele and SDB.

Adolescent↗

Site and mechanics of spontaneous, sleep-associated obstructive apnea in infants.

To examine the mechanics of infantile obstructive sleep apnea (OSA), airway pressures were measured using a triple-lumen catheter in 19 infants (age 1-36 wk), with concurrent overnight polysomnography. Catheter placement was guided by correlations between measurements of magnetic resonance images and body weight of 70 infants. The level of spontaneous obstruction was palatal in 52% and retroglossal in 48% of all events. Palatal obstruction predominated in infants treated for OSA (80% of events), compared with 38.6% from infants with infrequent events (P = 0.02). During obstructive events, successive respiratory efforts increased in amplitude (mean intrathoracic pressures -11.4, -15.0, and -20.4 cmH(2)O; ANOVA, P < 0.05), with arousal after only 29% of the obstructive and mixed apneas. The soft palate is commonly involved in the upper airway obstruction of infants suffering OSA. Postterm, infant responses to upper airway obstruction are intermediate between those of preterm infants and older children, with infrequent termination by arousal but no persisting "upper airway resistance" and respiratory efforts exceeding baseline during the event.

Airway Obstruction↗

Nocturnal pulse oximetry as an abbreviated testing modality for pediatric obstructive sleep apnea.

OBJECTIVE: To determine the utility of pulse oximetry for diagnosis of obstructive sleep apnea (OSA) in children. METHODS: We performed a cross-sectional study of 349 patients referred to a pediatric sleep laboratory for possible OSA. A mixed/obstructive apnea/hypopnea index (MOAHI) greater than or equal to 1 on nocturnal polysomnography (PSG) defined OSA. A sleep laboratory physician read nocturnal oximetry trend and event graphs, blinded to clinical and polysomnographic results. Likelihood ratios were used to determine the change in probability of having OSA before and after oximetry results were known. RESULTS: Of 349 patients, 210 (60%) had OSA as defined polysomnographically. Oximetry trend graphs were classified as positive for OSA in 93 and negative or inconclusive in 256 patients. Of the 93 oximetry results read as positive, PSG confirmed OSA in 90 patients. A positive oximetry trend graph had a likelihood ratio of 19.4, increasing the probability of having OSA from 60% to 97%. The median MOAHI of children with a positive oximetry result was 16.4 (7.5, 30.2). The 3 false-positive oximetry results were all in the subgroup of 92 children who had diagnoses other than adenotonsillar hypertrophy that might have affected breathing during sleep. A negative or inconclusive oximetry result had a likelihood ratio of.58, decreasing the probability of having OSA from 60% to 47%. Interobserver reliability for oximetry readings was very good to excellent (kappa =.80). CONCLUSIONS: In the setting of a child suspected of having OSA, a positive nocturnal oximetry trend graph has at least a 97% positive predictive value. Oximetry could: 1) be the definitive diagnostic test for straightforward OSA attributable to adenotonsillar hypertrophy in children older than 12 months of age, or 2) quickly and inexpensively identify children with a history suggesting sleep-disordered breathing who would require PSG to elucidate the type and severity. A negative oximetry result cannot be used to rule out OSA.

Adenoids↗

Head turning and face-down positioning in prone-sleeping premature infants.

BACKGROUND: Term infants may die of sudden infant death syndrome (SIDS) when they assume the face-straight-down or the face-near-straight-down head positions. Preterm infants have a higher SIDS rate, but it is not known how often they assume the face-straight-down and face-near-straight-down positions. OBJECTIVES: To determine the frequency and cardiorespiratory consequences of head turning and face-down head positioning in prone-sleeping premature infants. STUDY DESIGN: Supervised overnight cardiorespiratory and audiovisual recordings were conducted in 15 prone-sleeping preterm infants nearing hospital discharge: birth weight, 1178 101 (SEM) g, postconceptional age, 40 1.0 weeks. RESULTS: The preterm infants, studied at a younger postconceptional age than previously reported term infants, seldom turned their heads during sleep; therefore they rarely assumed the face-straight-down position (6 episodes in 3 infants) or the face-near-straight-down position (30 episodes in 6 infants). CONCLUSIONS: Prematurely born infants, known to be at increased risk of SIDS, rarely assume face-down positions when sleeping prone at approximately 40 weeks' postconceptional age. These results suggest that head turning during sleep is developmentally regulated and may have relevance to understanding the age distribution of SIDS.

Female↗

Neuronal apoptosis in sudden infant death syndrome.

Although evidence shows that victims of sudden infant death syndrome (SIDS) suffer repetitive episodes of hypoxemia, only subtle abnormalities have been found in their brains by light microscopy. The aim of the present study was to determine whether apoptosis, a form of cell death that can be triggered by hypoxemia and that leaves no scarring detectable by light microscopy, would be present in hypoxia-sensitive brain regions of SIDS victims. We looked for the presence of apoptosis with an in situ end-labeling method that detects DNA fragmentation. We studied 29 SIDS victims who were age-matched to nine control cases. We found significant neuronal apoptosis in 79% of the SIDS cases: 55% of the cases positive in the hippocampus and 96% positive in the brainstem. Whereas the distribution of apoptosis in the hippocampus was in hypoxia-sensitive subregions, the distribution in the brainstem was mostly in dorsal nuclei, including those involved with sensation in the face and position of the head (nucleus of the spinal trigeminal tract and vestibular nuclei). The control cases showed no significant apoptosis in the hippocampus and a mild degree in the brainstem in three cases. Our results indicate the occurrence of an acute insult at least several hours before death, an insult from which the infants had apparently recuperated. This suggests that SIDS victims suffered repeated apoptosis resulting in significant neuronal damage and, thus, functional loss in key brain regions. The involvement of specific nuclei in the brainstem may be linked to the fact that prone sleeping is a significant risk factor for SIDS. Enhanced neuronal death by apoptosis may thus have major implications for understanding the sequence of events leading to SIDS.

Apoptosis↗

Sleep-disordered breathing in children with myelomeningocele.

BACKGROUND: Although patients with myelomeningocele and the Chiari II malformation are known to have sleep apnea and respiratory control deficits, the prevalence, types, severities, and associations of sleep-disordered breathing (SDB) have not been adequately defined. METHODS: A cross-sectional study of our myelomeningocele clinic population was undertaken to correlate polysomnographic results with historical data and findings from magnetic resonance imaging of the Chiari malformation, pulmonary function results, and nocturnal pulse oximetry. RESULTS: A questionnaire survey of symptoms was available for 107 of 109 children (98% of the clinic population), and 83 patients agreed to undergo overnight polysomnography. Breathing during sleep was classified as normal in 31 cases (37%), mildly abnormal in 35 cases (42%), and moderately/severely abnormal in 17 cases (20%). Among the 17 patients with moderately/severely abnormal SDB, 12 patients had predominantly central apneas and 5 had predominantly obstructive apnea. Patients with a thoracic or thoracolumbar myelomeningocele, those who had previously had a posterior fossa decompression operation, those with more severe brain-stem malformations, and those with pulmonary function abnormalities were more likely to have moderately/severely abnormal SDB, relative risks (95% confidence intervals) 9.2 (2.9 to 29.3), 3.5 (1.3 to 8.9), 3.0 (0.9 to 10.5), and 11.6 (1.6 to 81.3), respectively. Failure of obstructive SDB to resolve after adenotonsillectomy in four patients suggested abnormal control of pharyngeal airway patency during sleep. Nocturnal pulse oximetry accurately predicted moderately/severely abnormal SDB with a sensitivity of 100% and a specificity of 67%. CONCLUSIONS: The pathogenesis of SDB in patients with myelomeningocele involves the functional level of the spinal lesions, congenital and acquired brainstem abnormalities, pulmonary function abnormalities, disorders of upper airway maintenance, and sleep state. Polysomnography and nocturnal pulse oximetry should be performed in high-risk patients to detect and classify SDB.

Arnold-Chiari Malformation↗

Curtailed respiration by repeated vs. isolated hypoxia in maturing piglets is unrelated to NTS ME or SP levels.

In early development, respiratory disorders can produce recurring hypoxic episodes during sleep. To examine possible effects of daily repeated vs. isolated hypoxic hypoxia, cardiorespiratory functions and central, respiratory-related neuromodulator levels in 21- to 32-day-old, chronically instrumented, unsedated piglets were compared between a fifth sequential daily hypoxia and an isolated hypoxia (10% O2-90% N2 for 30 min). Diaphragmatic electromyographic activity, heart rate and arterial pressure, and pH and gas tensions were measured. In vivo microdialysis, via chronically implanted guides, served to sample interstitial substance P (SP) and methionine-enkephalin (ME) at the level of the respiratory-related nucleus tractus solitarii (NTS). Compared with an isolated hypoxia, repeated hypoxia resulted in 1) lower respiratory frequency (f), ventilation equivalent, and arterial pH, higher arterial PO2 during hypoxia, and lower f in recovery from hypoxia; and 2) increased SP concentrations but no change in ME concentrations. We conclude that, in these maturing swine, repeated vs. isolated hypoxic exposure curtails respiratory responses to hypoxia by a mechanism(s) unrelated to SP or ME levels at the NTS.

Aging↗

Repeated microdialysis from the nucleus tractus solitarii of chronically instrumented, unsedated piglets.

Normal development of respiratory rhythm and control, and perturbations thereof, likely relate to neuromodulators in brainstem regions. To assess the feasibility of repeated neurochemical sampling by in vivo microdialysis from the respiratory-related nucleus tractus solitarii (NTS) during development. 19-24 day-old piglets (n = 7) were implanted under anesthesia with chronic microdialysis guides near NTS around obex. Unsedated piglets then underwent in vivo microdialysis twice, 3 days apart, through probes inserted acutely via the guides to abut against the NTS. The probe tips, surrounded by normal neurons and only diffuse gliosis, either intersected, or were within < or = 300 microns from the NTS. Thirty-min microdialysates were collected for 120 min in normoxia, HPLC-fractionated, and assayed for substance-P (SP), a respiratory excitatory neuropeptide. SP levels stabilized within 90 min from probe placement, and did not differ between the 2 experimental days. Thus, repeated in vivo microdialysis from NTS of conscious piglets is feasible, and can illuminate respiratory-related normal and pathological neurochemical processes during development.

Animals↗

Respiratory responses to rapid-onset, repetitive vs. continuous hypoxia in piglets.

Repeated, frequent hypoxic exposures may precede Sudden Infant Death. This study assessed whether such hypoxic modality, vs. continuous hypoxia, compromised compensatory cardiorespiratory responses. Following aseptic, chronic instrumentation, 10 to 20 day-old, unsedated piglets underwent measurements of arterial O2 saturation, pH and gas tensions, respiration, heart rate, physical activity, O2 consumption and rectal temperature on several experimental days. The piglets were exposed to 21 min of either 10% or 6% O2 in N2, each comprising either seven, 3-min exposures alternating with 3-min intervals in 21% O2 balance N2, or 7 consecutive hypoxic exposures. Responses to 6% hypoxia were greater than those to 10% hypoxia. In 10% hypoxia, responses to repetitive vs. continuous exposure differed only in PaCO2. In 6% hypoxia, repetitive vs. continuous exposure resulted in lower respiratory frequency (p < 0.05) and in lower ventilation equivalent (p = 0.07) despite higher activity levels. Thus, the mode of hypoxic exposure determines the extent of the respiratory response: Severe, repetitive hypoxia mitigates protective respiratory responses when compared to equivalent, but sustained hypoxia.

Animals↗

Face-straight-down and face-near-straight-down positions in healthy, prone-sleeping infants.

OBJECTIVE: To determine the frequency and physiologic consequences of the face-straight-down (FSD) position, a postulated mechanism for the sudden infant death syndrome in prone-sleeping infants. STUDY DESIGN: A survey of 151 infants, aged 1 to 7 months, in Montreal showed that 33% slept prone. Ten healthy prone-sleeping infants were studied in their homes at age 10 to 22 weeks. Infrared video and cardiorespiratory recordings were made on 3 consecutive nights in the prone (nights 1 and 3) and lateral (night 2) positions. RESULTS: Infants maintained the prone position during 17 of 19 studies, but only 4 of 9 infants maintained the lateral position. The FSD position was observed 27 times in 17 prone nights: median frequency, 0.6 times per night (interquartile range, 0 to 4), and median total duration, 3.3 minutes (0.8% of total sleep time). A related position, the face-near-straight-down (FNSD) position, occurred more often, 5.3 (1 to 10) time per prone night, for 22.4 minutes (5.8% of total sleep time). Most periods in the FSD and FNSD position had no physiologic consequences; however, 14% of FSD and 3% of FNSD episodes were associated with airway obstruction as indicated by snoring, paradoxical respiratory movements, apnea, and/or increased partial pressure of transcutaneous carbon dioxide. Spontaneous arousal and head turning terminated the FSD and FNSD episodes. CONCLUSION: The FSD and FNSD positions occur commonly in healthy prone-sleeping infants, and these positions can cause airway obstruction. We speculate that those infants with sudden infant death syndrome found in the FSD or FNSD position either have a congenital or an acquired defect in the arousal-head turning response or have encountered insurmountable environmental factors that prevent effective head turning.

Airway Obstruction↗

Assessment of the infant airway with videorecorded flexible laryngoscopy and the objective analysis of vocal fold abduction.

Accurate diagnosis of upper airway abnormalities by flexible laryngoscopy in infants is hampered by rapid laryngeal motion and lack of patient cooperation. This study evaluates the added role of videorecorded flexible laryngoscopy and the objective measurement of vocal fold abduction in improving the diagnosis of upper airway abnormalities in infants. Seventy-eight infants had videorecorded flexible laryngoscopy performed as part of their evaluation of a suspected airway disorder. These recordings were reviewed by three otolaryngologists for confirmation of the clinical diagnosis. From the video image, the maximum angle of vocal fold abduction was measured with image analysis software. Of 78 patients 40 had supraglottic or glottic abnormalities, 9 had nasal or nasopharyngeal obstruction, 9 had subglottic abnormalities (diagnosed subsequent to videolaryngoscopy), and 15 patients had normal findings on examination. Of those with laryngeal abnormalities, laryngomalacia was the most common diagnosis (23 of 78). Vocal fold paralysis was present in 4 patients. A separate group (9 of 78) of patients was identified as having symmetric bilateral limitation of vocal fold abduction. Laryngeal dyskinesia was diagnosed in these 9 patients. The mean values of maximal vocal fold abduction were as follows: (1) normals, 59.5 degrees; (2) laryngomalacia, 57.0 degrees; (3) paralysis, 26.6 degrees; and (4) incomplete abduction with laryngeal dyskinesia, 27.6 degrees. Videolaryngoscopy is a valuable tool for documentation, parent education, and analysis of infant laryngeal abnormalities. Repeat viewing of the video examination and frame-by-frame analysis improve the diagnostic accuracy. Using this approach, we have calculated the anterior glottic abduction angle in the normal and abnormal infant larynx. In addition, we have identified a group of infants with incomplete abduction of the vocal folds that appears to be different from that found in vocal cord paralysis.

Airway Obstruction↗