Sudden Infant Death Research Articles

A Closed Loop Feature Detection Platform for Automated Neonate Cardio‐Respiratory Measurements and Data Analysis

BackgroundSudden Infant Death Syndrome is thought to partly result from unseen brain abnormalities affecting cardio‐respiratory function, but for which no clear genetic or environmental mechanisms are known. Mouse genetic and exposure models present an opportunity to uncover molecular and environmental mechanisms. However, measuring cardio‐respiratory function in neonate mice is expensive, difficult, and inefficient. One major challenge is the time needed to carry out such measurements. The neonate autoresuscitation assay, consisting of repeated anoxic exposures followed by recovery, requires the full attention of an observer for the multi‐hour duration of a single‐subject assay, limiting throughput. To address this, we developed a closed‐loop feature detection platform for automated neonate cardio‐respiratory measurements.MethodsOur platform design consists of:1) a pneumotachograph face‐mask for precise respiratory measurements. 2) a micro‐controller automated bell‐housing gas switching system for rapid induction of respiratory challenges. 3) a micro‐computer‐based data‐acquisition system with real‐time feature detection and outputs for controlling gas exposure. 4) a data analysis suite that assists with study recordkeeping and provides a facile method to extract key outcome measures from acquired data.ResultsGas challenges are administered via the rotating bell housing system. A python program detects waveform features in real‐time, such as apnea and bradycardia. Upon apnea detection, the system switches to a rescue gas. Resumption of normal breathing and heart rate can also be detected and incorporated into criteria for automated initiation of the next anoxic exposure trial. Data is stored for later offline automated analysis using the data analysis suite.ConclusionsThe system offers a relatively inexpensive approach for automated high throughput neonate cardio‐respiratory assessment for facile screening to yield important clues in developmental pathophysiology.

The Role of Glutamatergic Signaling in Central Noradrenergic Neurons in Respiratory Control

Central noradrenergic (NA) neurons are key constituents of the respiratory homeostatic network. NA dysfunction is implicated in several developmental respiratory disorders such as the fatal Sudden Infant Death Syndrome (SIDS) and Rett Syndrome, in which abnormal chemosensory function is thought to play a role. However, which NA populations modulate respiratory chemoreflexes and the underlying mechanisms are still not fully understood. Histological evidence suggests that glutamate is co‐transmitted in subsets of brainstem NA neurons, some of which may contribute to regulating chemoreflexes. However, the extent of glutamate co‐transmission in the central NA system remains uncharacterized. Further, it remains unclear what role NA‐based glutamatergic signaling plays in various aspects of respiratory homeostasis.To anatomically map potential glutamate‐expressing NA neurons, we characterized the expression profile of all three known of Vesicular Glutamate Transporters (Vglut1, Vglut2 and Vglut3) in NA neurons by intersectional genetic fate mapping. For each Vglut1/2/3 transporter, acorresponding Cre knock‐in recombinase line was combined with DBH‐p2a_Flpomice. These Vglut1/2/3_Cre; DBH‐p2a_Flpocompound lines were crossed with the RC::F_TdTomato_P_GFPintersectional reporter mice. In each of the three intersectional reporter crosses, NA neurons co‐expressing either Vglut1, Vglut2, or Vglut3 are labeled by green fluorescent protein (GFP) while NA neurons without any Vglut1/2/3 expression are labelled by red fluorescent protein (tdTomato). Our preliminary fate maps, which reflect the cumulative expression profiles of glutamate markers in NA neurons throughout the development and lifetime of the mouse, found that about 80% NA neurons express Vglut2 at some point during their development and posterior medullary NA neurons express Vglut3 as well.Prior studies suggest that Vglut2‐based glutamatergic signaling may play a role in respiratory control. To determine what physiological role, if any, Vglut2‐based glutamatergic signaling may play in adult respiratory homeostasis, we conditionally ablated Vglut2 in central NA neurons by crossing DBH‐Cre/+with Vglut2flox/flox mice. Mutants and sibling controls (6‐8 weeks) were assessed for respiratory function by whole‐body barometric plethysmography. Ventilation and VO2 were assessed under room air (21%O2,79%N2), hypercapnia (21%O2, 74/72/69%N2, 5/7/10%CO2) and hypoxia (10% O2, 90% N2). Our preliminary data indicates that loss of Vglut2 in NA neurons does not significantly impact breathing under room air, hypercapnia, or hypoxia. Thus, our data suggests that Vglut2‐based glutamatergic signaling within the central NA system is dispensable for normal baseline breathing and hypercapnic, and hypoxic chemosensory reflexes.

Practicing What We Preach: An Effort to Improve Safe Sleep of Hospitalized Infants.

Introduction:To prevent sudden unexpected infant death, pediatric providers recommend the ABCs of infant sleep: Alone, on the Back, and in an empty Crib. This study’s objective was to document sleep practices of infants admitted to a large children’s hospital, examine adherence to American Academy of Pediatrics safe sleep guidelines, and develop interventions to improve guideline adherence.Methods:We conducted a pre/post quality improvement study at a single quaternary care medical center from 2015 to 2019. Infants 0 to younger than 12 months were observed in their sleeping environment pre- and post-implementation of multiple hospital-wide interventions to improve the sleep safety of hospitalized infants.Results:Only 1.3% of 221 infants observed preintervention met all ABCs of safe sleep; 10.6% of 237 infants met the ABCs of safe sleep postintervention. Significant improvements in the post-intervention cohort included sleeping in a crib (94% versus 80% preintervention; P < 0.001), avoidance of co-sleeping (3% versus 15% preintervention; P < 0.001), absence of supplies in the crib (58% versus 15% preintervention; P < 0.001), and presence of an empty crib (13% versus 2% preintervention; P < 0.001).Conclusions:Most infants hospitalized at our institution do not sleep in a safe environment. However, the implementation of a care bundle led to improvements in the sleep environment in the hospital. Further research is necessary to continue improving in-hospital safe sleep and to assess whether these practices impact the home sleep environment.

Non-polyalanine repeat mutation in PHOX2B is detected in autopsy cases of sudden unexpected infant death.

Congenital central hypoventilation syndrome (CCHS), which is caused by PHOX2B with phenotypic variations, has a point of controversy: CCHS is putatively involved in autopsy cases of sudden unexpected infant death (SUID) including sudden infant death syndrome. The relation of CCHS to SUID cases was investigated by extensive genotyping of PHOX2B. We analyzed 93 DNA samples of less than one-year-old SUID cases that were autopsied in our department. Unrelated adult volunteers (n = 942) were used as the control. No polyalanine tract expansion was detected in the SUID cases. The allelic frequencies of repeat contractions and SNP (rs28647582) in intron 2 were not significantly different from that in those control group. Further extensive sequencing revealed a non-polyalanine repeat mutation (NPARM) of c.905A>C in a sudden death case of a one-month-old male infant. This missense mutation (p.Asn302Thr), registered as rs779068107, was annotated to 'Affected status is unknown', but it might be associated with the sudden death. NPARM was more plausibly related to sudden unexpected death than expansions because of severe clinical complications. This finding indicates possible CCHS involvement in forensic autopsy cases without ante-mortem diagnosis.

Effects of sacubitril-valsartan on central and obstructive apneas in heart failure patients with reduced ejection fraction

ObjectiveThis study aimed to evaluate the effect of sacubitril-valsartan (SV) on central apneas (CA) and obstructive apneas (OA) in patients with heart failure with reduced ejection fraction (HFrEF).MethodsIn patients with HFrEF, SV initiation was titrated to the highest tolerable dosage. Patients were evaluated with portable apnea monitoring, echocardiography, and cardiopulmonary exercise testing at baseline and 3 months later.ResultsOf a total of 18 patients, 9 (50%) had OA, 7 (39%) had CA, and 2 (11%) had normal breathing. SV therapy was related to a reduction in NT-pro BNP and an improvement in LV function after 3 months. Portable apnea monitoring revealed a significant decrease of the respiratory event index (REI) after treatment with SV (20 ± 23 events/h to 7 ± 7 events/h, p = 0.003). When subgrouping according to type of apneas, REI, and time spent below 90% saturation (T90) decreased in patients with CA and OA (all p < 0.05).ConclusionIn this prospective study, SV treatment for 3 months in patients with CA and OA is associated with a significant decrease in REI.

Assessment of Nurses' Performance Regarding Infant Sleep Position on Sudden Infant Death Syndrome at Neonatal Intensive Care Units

Background: Sudden infant death syndrome (SIDS) is the sudden unexplained death of an infant during sleep. It is the most common cause of post neonatal mortality. Aim: This study aimed to assess nurses' performance regarding infant sleep position on sudden infant death syndrome at Neonatal Intensive Care Units (NICUs). Design: A descriptive research design was used to conduct this study. Settings: This study was carried out at NICUs in Helwan General Hospital affiliated to Ministry of health and Mustafa Hassan Pediatric Hospital affiliated to Fayoum University Hospitals. Sample: A convenience sample of seventy nurses who providing care for preterm and low birth weight infants admitted to NICUs in the previous mentioned settings. Tools: Two tools were used for data collection; 1st tool: A structured interview questionnaire sheet consists of two parts: Part (1) to assess characteristics of studied sample, Part (2) to assess nurses' knowledge regarding infant sleep position on SIDS, 2nd tool: Observational checklist to assess nurses' practice regarding infant sleep position on SIDS. Results: The mean age of studied nurses was 25.47±4.26 years and the mean gestational age of infants was 32.43±2.71 weeks, 55.7% of the studied nurses had unsatisfactory level of knowledge regarding infant sleep position on SIDS. Also, the study proved that, 58.6% of studied nurses had incompetent level of practice regarding infant sleep positions at NICUs. Conclusion: It can be concluded that, more than half of the studied nurses had unsatisfactory total level of knowledge regarding infant sleep position on SIDS and more than half of them had incompetent practice. Additionally, there were statistically significant differences between nurses’ total level of knowledge and their characteristics namely educational qualifications (P =0.033) and attendance of previous educational courses about the infant sleeping position at the NICUs (P =0.005), while there were highly statistically significant differences between nurses’ total level of practice and their years of experience at NICUs (P&lt;0.001).Recommendations: Continuous training program for nurses to improve their performance regarding infant sleep position on sudden infant death syndrome.

Differences in Mortality Among Infants With Neonatal Opioid Withdrawal Syndrome

Prior studies are mixed regarding whether infants diagnosed with neonatal opioid withdrawal syndrome have a higher risk of mortality than other infants. However, these studies have not accounted for whether mothers of infants with neonatal opioid withdrawal syndrome received medication for opioid use disorder in pregnancy. Linked data from 2016‒2018 North Carolina birth certificates, maternal and infant Medicaid claims, and infant death certificates were analyzed in summer 2021 to compare mortality and causes of mortality before age 1 year among infants diagnosed with neonatal opioid withdrawal syndrome whose mothers did and did not have claims for medication for opioid use disorder in pregnancy (N=4,480). Compared with mothers with medication for opioid use disorder claims in pregnancy (45.5%), mothers without medication for opioid use disorder claims (55.5%) were younger, more likely to be Black non-Hispanic, less likely to have paternity established, and more likely to have no prenatal care. The proportion (1.3%, n=31 vs 1.0%, n=21) and rate (3.5 vs 2.9 deaths per 100,000 infant days) of mortality was higher among infants of mothers without medication for opioid use disorder claims than infants of mothers with medication for opioid use disorder claims. Sudden unexpected infant death syndrome was the primary cause of death for infants of mothers with (90.5%) and without (58.1%) medication for opioid use disorder claims. Results highlight the importance of assessing for potential differences in outcomes according to whether infants with neonatal opioid withdrawal syndrome were exposed to medication for opioid use disorder. Efforts to ensure equitable access to medication for opioid use disorder and other support services in pregnancy are needed to promote healthy maternal and infant outcomes.

Variants in genes encoding the SUR1-TRPM4 non-selective cation channel and sudden infant death syndrome (SIDS): potentially increased risk for cerebral edema

Increasing evidence suggests that brain edema might play an important role in the pathogenesis of sudden infant death syndrome (SIDS) and that variants of genes for cerebral water channels might be associated with SIDS. The role of the sulfonylurea receptor 1 (SUR1)–transient receptor potential melastatin 4 (TRPM4) non-selective cation channel in cerebral edema was demonstrated by extensive studies. Therefore, we hypothesized that variants at genes of the SUR1-TRPM4 channel complex might be linked to SIDS. Twenty-four polymorphisms in candidate genes involved in the SUR1-TRPM4 non-selective cation channel were investigated in 185 SIDS cases and 339 controls. One (rs11667393 in TRPM4) of these analyzed SNPs reached nominal significance regarding an association with SIDS in the overall analysis (additive model: p = 0.015, OR = 1.438, 95% CI = 1.074–1.925; dominant model: p = 0.036; OR = 1.468, 95% CI = 1.024–2.106). In the stratified analysis, further 8 variants in ABCC8 (encoding SUR1) or TRPM4 showed pronounced associations. However, none of the results remained significant after correction for multiple testing. This preliminary study has provided the first evidence for a genetic role of the SUR1-TRPM4 complex in the etiology of SIDS, and we suggest that our initial results should be evaluated by further studies.

Prenatal smoking and drinking are associated with altered newborn autonomic functions.

Prenatal smoking and drinking are associated with sudden infant death syndrome and neurodevelopmental disorders. Infants with these outcomes also have altered autonomic nervous system (ANS) regulation. We examined the effects of prenatal smoking and drinking on newborn ANS function. Pregnant women were enrolled in Northern Plains, USA (NP) and Cape Town (CT), South Africa. Daily drinking and weekly smoking data were collected prenatally. Physiological measures were obtained during sleep 12-96 h post-delivery. In all, 2913 infants from NP and 4072 from CT were included. In active sleep, newborns of mothers who smoked throughout pregnancy, compared to non-smokers, had higher breathing rates (2.2 breaths/min; 95% CI: 0.95, 3.49). Quit-early smoking was associated with reductions in beat-to-beat heart rate variability (HRV) in active (-0.08 s) and quiet sleep (-0.11 s) in CT. In girls, moderate-high continuous smoking was associated with increased systolic (3.0 mmHg, CI: 0.70, 5.24) and diastolic blood pressure (2.9 mmHg, CI: 0.72, 5.02). In quiet sleep, low-continuous drinking was associated with slower heart rate (-4.5 beat/min). In boys, low-continuous drinking was associated with a reduced ratio of low-to-high frequency HRV (-0.11, CI: -0.21, -0.02). These findings highlight potential ANS pathways through which prenatal drinking and smoking may contribute to neurodevelopment outcomes. In this prospective cohort study of 6985 mother-infant dyads prenatal drinking and smoking were associated with multiple ANS parameters. Smoking was associated with increased neonatal breathing rates among all infants, and heart rate variability (HRV) and blood pressure (BP) among girls. Drinking was associated with reductions in HR and BP among all newborns, and reductions in the ratio of low to-high frequency HRV among boys. These findings suggest that prenatal smoking and drinking alter newborn ANS which may presage future neurodevelopmental disorders.

Hyperthermia and Heat Stress as Risk Factors for Sudden Infant Death Syndrome: A Narrative Review.

Background and ObjectivesHeat stress and hyperthermia are common findings in sudden infant death syndrome (SIDS) victims. It has been suggested that thermal stress can increase the risk of SIDS directly via lethal hyperthermia or indirectly by altering autonomic functions. Major changes in sleep, thermoregulation, cardiovascular function, and the emergence of circadian functions occur at the age at which the risk of SIDS peaks—explaining the greater vulnerability at this stage of development. Here, we review the literature data on (i) heat stress and hyperthermia as direct risk factors for SIDS, and (ii) the indirect effects of thermal loads on vital physiological functions.ResultsVarious situations leading to thermal stress (i.e., outdoors temperatures, thermal insulation from clothing and bedding, the prone position, bed-sharing, and head covering) have been analyzed. Hyperthermia mainly results from excessive clothing and bedding insulation with regard to the ambient thermal conditions. The appropriate amount of clothing and bedding thermal insulation for homeothermia requires further research. The prone position and bed-sharing do not have major thermal impacts; the elevated risk of SIDS in these situations cannot be explained solely by thermal factors. Special attention should be given to brain overheating because of the head's major role in body heat losses, heat production, and autonomic functions. Thermal stress can alter cardiovascular and respiratory functions, which in turn can lead to life-threatening events (e.g., bradycardia, apnea with blood desaturation, and glottal closure). Unfortunately, thermal load impairs the responses to these challenges by reducing chemosensitivity, arousability, and autoresuscitation. As a result, thermal load (even when not lethal directly) can interact detrimentally with vital physiological functions.ConclusionsWith the exception of excessive thermal insulation (which can lead to lethal hyperthermia), the major risk factors for SIDS appears to be associated with impairments of vital physiological functions when the infant is exposed to thermal stress.

The Science (or Nonscience) of Research Into Sudden Infant Death Syndrome (SIDS).

This Viewpoint paper presents a timely and constructive critique of mainstream SIDS research. It is concerning that twenty-first century medical science has not provided an answer to the tragic enigma of SIDS. The paper helps explain why this is so and illustrates possible shortcomings in the investigation of Sudden Infant Death Syndrome/Sudden Unexplained Infant Death (SIDS/SUID) by mainstream researchers. Mainstream findings are often based on questionable and dogmatic assumptions that return to founding notions such as the Triple Risk Hypothesis and the contention that the mechanisms underlying SIDS/SUID are heterogeneous in nature. The paper illustrates how the pathological findings in SIDS have been under-investigated (or ignored) and that key epidemiological risk factors have slipped from memory. This apparent amnesia has resulted in failure to use these established SIDS facts to substantiate the significance of various neuropathological, neurochemical, or other research findings. These unsupported findings and their derivative hypotheses are therefore ill-founded and lack scientific rigor.ConclusionThe deficits of SIDS “science” revealed in this paper explain why the SIDS enigma has not yet been solved. To make progress in understanding SIDS, it is important that researchers, as scientists, uphold standards of research. Encouragement for new directions of research is offered.

SIDS is associated with prenatal drug use: a meta-analysis and systematic review of 4 238 685 infants

ObjectiveTo conduct a meta-analysis to determine the association between prenatal drug exposure and risk of sudden infant death syndrome (SIDS).DesignStudies were searched using PubMed, Medline and Embase and restricted to...

Trigger role of infectious agents in the genesis of sudden infant death

Purpose. To increase the effectiveness of diagnostic predictors for the development of sudden infant death based on the study of the role of infectious agents.Materials and methods. A retrospective analysis of 120 cases of development of children, suddenly deceased, medical charts of pregnant women, histories of childbirth of mothers was carried out, and the morphological features of the suddenly deceased children were studied. The frequency of distribution and types of viruses detected using enzyme-linked immunosorbent assay (ELISA) and polymerase chain reaction test (PCR) in the examined children who died suddenly in their first year of life were analyzed. Statistical analysis of the research results was made in the MedStat software.Results. The frequency of detection of various infectious agents among the deceased from sudden infant death is (64.4 ± 4.2) %. Morphohistological study indicated characteristic signs of catarrhal tracheobronchitis (83.0 ± 5.5) %, focal intraepithelial inflammation of the larynx and trachea (48.9 ± 7.3) %, desquamative catarrhal pneumonia (31.9 ± 6.8) %, as well as acute focal bronchitis (27.7 ± 6.5) %.Conclusion. The performed study confirms that in the genesis of sudden infant death, along with a role of social and economic, medical and biological factors, there is an obvious negative effect of infectious agents, with the infectious activator working as the trigger and provoking sudden infant death.

The global burden of sudden infant death syndrome from 1990 to 2019: a systematic analysis from the Global Burden of Disease study 2019.

Sudden infant death syndrome (SIDS) still remains one of the leading causes of infant death worldwide, especially in high-income countries. To date, however, there is no detailed information on the global health burden of SIDS. To characterize the global disease burden of SIDS and its trends from 1990 to 2019 and to compare the burden of SIDS according to the socio-demographic index (SDI). Systematic analysis based on the Global Burden of Disease (GBD) 2019 data. Epidemiological data of 204 countries from 1990 to 2019 were collected via various methods including civil registration and vital statistics in the original GBD study. Estimates for mortality and disease burden of SIDS were modeled. Crude mortality and mortality rates per 100000 population were analyzed. Disability-adjusted life years (DALYs) and DALY rates were also assessed. In 2019, mortality rate of SIDS accounted for 20.98 [95% Uncertainty Interval, 9.15-46.16] globally, which was a 51% decrease from 1990. SIDS was most prevalent in Western sub-Saharan Africa, High-income North America and Oceania in 2019. The burden of SIDS was higher in males than females consistently from 1990 to 2019. Higher SDI and income level was associated with lower burden of SIDS; furthermore, countries with higher SDI and income had greater decreases in SIDS burden from 1990 to 2019. The burden of SIDS has decreased drastically from 1990 to 2019. However, the improvements have occurred disproportionately between regions and SDI levels. Focused preventive efforts in under-resourced populations are needed.

Forensic Autopsy Findings in Determination of the Risk Factors of Sudden Infant Death Syndrome

Introduction: Sudden infant death syndrome (SIDS) occurs when a seemingly healthy newborn under the age of one year dies unexpectedly while sleeping. SIDS is often known as crib death because neonates usually die in their cribs. Even after a thorough forensic examination and death site investigation, the general diagnosis of SIDS is made when the cause of infant death cannot be determined. According to the 1969 definition, SIDS is still an excluding diagnosis. Despite the fact that this syndrome has various distinguishing characteristics, such as an age distribution that only affects children under the age of one year and an apparent incidence during sleep, there has been a reluctance to include these characteristics in the classification. The aim of the study was to better understand the risk factors of sudden infant death syndrome (SIDS). Methods: This cross-sectional analytical study was conducted at the Department of Forensic Medicine, Pabna Medical College Hospital, Pabna, from March 2020 to April 2021, and the participants of the study were 25 sudden and unidentified infant death cases at the study hospital whose guardians had given authorization for inclusion in the study. Result: The male: female ratio of the present study was 1.27:1. 60% of the participants had died while at home, and no information regarding the activity of infant at time of death was available for 56% of cases. Initial forensic analysis confirmed SIDS in 76% of the cases. Among the SIDS cases, majority had no observable risk factors, but family history of ailments and habits such as heart disorders, respiratory distress and smoking were determined as possible risk factors. Previous history of SIDS in family was also considered as a risk factor. Conclusion: The location of the infants at the time of death is very important in properly determining cause of death. Better observation of the infants can help in conducting a proper forensic analysis.

Cerebrospinal Fluid Histamine Levels in Healthy Children and Potential Implication for SIDS: Observational Study in a French Tertiary Care Hospital.

ObjectiveA defect of the waking systems could constitute a factor of vulnerability for sudden infant death syndrome (SIDS). A decrease in orexin levels, which promotes wakefulness and activates histaminergic neurons (another hypothalamic wake-promoting system) has already been demonstrated between 2 and 6 months. This work aims to study the levels of histamine (HA), tele-methylhistamine (t-MeHA), its direct metabolite, and t-MeHA/HA ratio in the cerebrospinal fluid (CSF) of healthy children, to evaluate the maturation of the histaminergic system and its possible involvement in SIDS.MethodsSeventy Eight French children between 0 and 20 years (48.7% boys) were included, all of whom had a clinical indication for lumbar puncture, but subsequently found to be normal. Measurements of HA and t-MeHA in CSF were performed by reverse phase liquid chromatography coupled to mass spectrometry detection. Statistical analyses were performed using Spearman correlations and Non-parametric pairwise ranking tests.ResultsA negative correlation was found between age and CSF HA (r = −0.44, p < 10−4) and t-MeHA (r = −0.70, p < 10−4) levels. In pairwise comparisons, no difference in CSF HA and t-MeHA levels was observed between youngest age groups (i.e., 0–2 mo vs. 3–6 mo), but CSF HA and t-MeHA levels were significantly lower in older children (i.e., >6 mo vs. 0–6 mo). The CSF HA decrease with age was only observed in boys, who also presented global lower CSF HA levels than girls.ConclusionCSF HA and t-MeHA levels decrease with age in boys, and global levels are lower in boys than in girls. These results reveal changes in histaminergic transmission and metabolism during maturation. Whether lower CSF histamine values in boys compared to girls could contribute to their higher risk of SIDS warrants further research.

Commentary: Infant Mortality Among African Americans, Using Life Course Perspective to Encourage Transformation.

Commentary: Infant Mortality Among African Americans, Using Life Course Perspective to Encourage Transformation.

Positive Response of Alzheimer's Disease Patients to Antiviral Therapy-Case Reports

We have earlier reported findings of Ljungan virus (LV) antigen, a picornavirus causing neurological malformation in laboratory mice and also being associated with intrauterine death, sudden infant death.

Study protocol to assess de-implementation of the initial provider encounter for diagnosis and treatment of obstructive sleep apnea: the DREAM (Direct Referral for Apnea Monitoring) Project

BackgroundObstructive sleep apnea (OSA) is a very common and serious health condition which is highly prevalent among U.S. military Veterans. Because the demand for sleep medicine services often overwhelms the availability of such services, it is necessary to streamline diagnosis and treatment protocols. The goals of this study are to, (1) assess the efficacy of de-implementing the initial provider encounter for diagnosis and treatment of OSA; (2) determine the negative predictive value (NPV) of home sleep apnea testing (HSAT); (3) develop HSAT usage recommendations for various at-risk patient populations.MethodsThis is a large, pragmatic study that will take place in 3 VA sleep medicine programs: San Francisco, CA; Portland, OR; and Pittsburgh, PA. All Veterans referred for new sleep apnea evaluations at these sites will be included in this four-year study. Outcomes will include time from referral for OSA to sleep testing and treatment; positive airway pressure (PAP) treatment adherence measures; patient-reported clinical outcomes and measures of satisfaction; determination of the NPV of HSAT; HSAT usage recommendations for at-risk patient populations.DiscussionThe DREAM (Direct Referral for Apnea Monitoring) Project will inform sleep medicine providers and clinical organizations regarding strategies to streamline diagnosis and treatment protocols for OSA. Results of this study should have significant impact on clinical practices and professional guidelines.Trial registration The majority of this project is an observational study of clinical procedures. Therefore, clinical trial registration is not required.

Sudden infant death syndrome: The search for genetic predisposition

In approximately 80% of the infants who die unexpectedly in the first year of life no identifiable cause is found, and these infants are diagnosed with the sudden infant death syndrome (SIDS).1,2 The underlying cause is thought to be a combination of genetic predisposition and prenatal or postnatal environmental stressors.3 A failure to respond sufficiently to life-threatening hypoxic situation is commonly considered in various SIDS cases.4 A cardiac cause of death is also often suspected. Genetic testing efforts in SIDS cohorts have revealed genetic variants in cardiac genes.