Sudden Infant Death Syndrome

To examine (1) sleep architecture of infants at varied risk for sudden infant death syndrome, (2) delays or advances in preterm infants at term postmenstrual age, (3) whether ventilatory support and gestational age alter sleep, (4) whether steroids alter sleep, (5) confounding influences of sex, small for gestational age, and maternal smoking. Design: Overnight polysomnography. Dependent variables: Percentage of active sleep, quiet sleep, indeterminate, and awake time per total recording time; mean and longest duration of state epochs; number of episodes ≥ 10 minutes; and sleep efficiency. Setting: Collaborative Home Infant Monitoring Evaluation (CHIME). Participants: Two hundred one preterm and 198 term infants between 33 and 58 weeks postmenstrual age during polysomnography. Fifty-one term infants with an apparent life-threatening event without known etiology (apnea of infancy), 59 subsequent siblings of babies who died of sudden infant death syndrome, and 88 healthy term infants. Results: Tracings of infants with apnea of infancy and healthy term infants were similar. Subsequent siblings of babies who died of sudden infant death syndrome spent less time in quiet sleep. Preterm infants (≤ 37 weeks postmenstrual age) exhibited immature architecture compared with infants of term postmenstrual age. The latter exhibited similar sleep except that they had a lower percentage of quiet sleep and longer mean indeterminate and longest indeterminate episodes. Preterm infants with the youngest gestational age lagged behind older preterm infants. Neither sex nor use of steroids affected sleep. Assisted ventilation was associated with a delay in maturation, small-for-gestational age status with increased active sleep, and smoking with increased awake time. Conclusion: With few exceptions, asymptomatic premature infants do not exhibit significant delays in sleep architecture compared with term infants at comparable postmenstrual age. The preterm infant with an early gestational age and morbidity exhibited delayed sleep architecture.

Background: Sudden infant death syndrome (SIDS) is a tragic incident which remains a mystery even after post-mortem investigation and thorough researches.Methods: This comprehensive review is based on the genes reported in the molecular autopsy studies conducted on SIDS so far. A total of 20 original studies and 7 case reports were identified and included in this analysis. The genes identified in children or adults were not included. Most of the genes reported in these studies belonged to cardiac channel and cardiomyopathy. Cardiac channel genes in SIDS were scrutinized for further analysis.Results: After screening and removing the duplicates, 42 unique genes were extracted. When the location of these genes was assessed, it was observed that most of these belonged to Chromosomes 11, 1 and 3 in sequential manner. The pathway analysis shows that these genes are involved in the regulation of heart rate, action potential, cardiac muscle cell contraction and heart contraction. The protei...

The epidemiological features of SIDS reflect an infection-related aetiology. The main pathological findings (heavy fluid-laden lungs, intrathoracic petechial hemorrhages, heavy brain, thymus and liver) are observed in the majority of cases. The reason for this paper is to emphasize an extraordinary aspect of mainstream research: that it tends to ignore (or misinterpret) the epidemiology and the anatomical pathology of SIDS and through these omissions or misinterpretations has entered into the domain of dogma by following lines of research that follow unproven ideas such as the Triple Risk Hypothesis. Such research does not consider the abovementioned key features of SIDS which still stand as the best guide to the underlying cause or causes of this tragic enigma. This article explores the possible ©2022 by the authors -Open Access -Distributed under CC BY 4.0

Infants with unexplained apneic episodes (Near-Miss for Sudden Infant Death Syndrome (SIDS)), are presumably at increased risk of subsequently dying of SIDS. It has been proposed that these infants exhibit prolonged sleep apnea which contributes to the mechanism leading to death. The objective of this study was to document the incidence of apnea during sleep recordings in 16 Near-Miss infants and compare the findings with those obtained from age and sex matched controls. Polygraphic records of 4 sleep and 3 cardiopulmonary variables were obtained during a 12 hour overnight recording. Successive minutes were classified as quiet sleep, active sleep, waking or indeterminate states by trained observers using standard scorin criteria. Respiratory rate and variability were calculated by computer for each minute across the night and related to sleep state. Pauses in breathing 3 3 seconds were identified in both groups. There was a tendency for Near-Miss infants to breathe faster with fewer apnea than controls, but this finding was not statistically significant. A1 though one half of the Near-Miss infants had recurrent prolonged apneic spells, all survived and were normal at 2 years. The proposed relationship between SIDS and apnea is not confined by this study.

Introduction: Patients with a history of gestational diabetes have a greater susceptibility to recurrence in subsequent pregnancies, as well as a higher risk of developing glucose intolerance and, of course, type 2 diabetes in the future. The present study aimed to determine the prevalence of diabetes and glucose intolerance disorder in patients with gestational diabetes in the postpartum period in Iran. The he following databases were searched for all the published articles: Irandoc, Iranmedex, SID, Magiran, Scopus, as well as Google search engine using the keywords of diabetes, gestational diabetes, pregnancy, type II diabetes, pregnancy diabetes, multiple sclerosis, and epidemiology. The study data was entered the STATA statistical software and was analyzed. The forest plot was used to demonstrate the results of the meta-analysis. Results: A number of 6497 participants within the age range 18-45 years from 6 studies were assessed in the current study. According to the results of the meta-analysis, the prevalence rate of postpartum diabetes in 6497 patients with a history of gestational diabetes (9.4%) and a confidence interval of 95% was obtained at 9.0 -10.0. Conclusion: Postpartum Glucose Metabolism Disorders are common in women with gestational diabetes. Therefore, the cases of gestational diabetes should be initially screened, identified, and treated during pregnancy to prevent fetal complications. Thereafter, these mothers need to be followed up in the postpartum period to identify diabetes and glucose intolerance and prevent and treat these disorders.

Based on evidence of an increased rate of respiratory infections in sudden infant death (SID) infants as well as the observation of familial occurrence, we analysed in a retrospective study class II and class III genes of the major histocompatibility complex in 40 cases of SID by Southern blot analysis of DNA obtained post mortem from tissue samples. In 24 cases, the parents were interviewed and confirmatory human lymphocyte antigen (HLA) and DNA typing was carried out. Using HLA-DRJ3 and -DQI3 probes, no evidence of an abnormal HLA-DR frequency distribution in SID infants was detected (P = 0.97). Using DNA probes for the tandemly arranged complement CA and steroid 21-hydroxylase genes, an increased number of C4B gene deletions in SID cases was found. The increase in C4 gene deletions was significant (P = 0.0125) in infants with recurrent infections. These data indicate a possible role of partial C4 deficiency as a genetically predisposing risk factor in SID.

Congenital cystic adenomatoid malformation (CCAM) is a developmental lesion of the lungs and terminal respiratory structures, which is characterized by pseudocysts, lesions, and cystically dilated airways. CCAM is also known as congenital pulmonary airway malformation (CPAM). Various classification systems for CCAM have been described, and based on a recent classification, CCAMs are classified morphologically into five different types (Type 0, I, II, III, and IV) based on lesion sizes. The most common manifestation of CCAM in neonates and children is respiratory distress (RD). Spontaneous pneumothorax is a rare manifestation of CCAM. In this case report, we discuss a CCAM type-II case of a 38-day-old female infant with a radiological post-mortem diagnosis of a large left-side spontaneous pneumothorax. The gross examination of the lungs revealed multiple emphysematous air bubbles up to 0.5 cm in diameter, and the histological examination revealed focal pleural fibrosis, accompanied by thickened septa and atelectasis. In this scenario, the routine use of prenatal ultrasonography would be important to obtain a timely prenatal diagnosis. At the same time, improvements in surgical techniques, as well as greatly improved imaging techniques, have improved the outcome of these patients. Finally, it is important to remark on the importance of autopsy in the case of sudden infant death with a suspected CCAM.

Thirteen infants with achondroplasia and sudden unexpected death or unexplained apnea were discovered through nonsystematic retrospective case collection. Most were initially thought to have died from sudden infant death syndrome. However, historical and pathologic findings suggest that many of these infants had apnea and sudden unexpected death secondary to acute or chronic compression of the lower brainstem or cervical spinal cord. lhfants with achondroplasia evidently are at considerably increased risk for such deaths between 1 month and I year of age. Appropriate intervention, given these previously unrecognized risks, may include cer~'ical restraint, polysomnographic evaluation, and apnea monitoring. (J PEDI,4rR 104:342. 1984

During the 1980s a high sudden infant death syndrome (SIDS) incidence was reason for concern among paediatricians in many countries. In Sweden, the SIDS incidence in 1973 was 0.3 per 1000. During the late 1970s and early 1980s, it increased and reached a maximum in 1991 of 1.1 per 1000. Much effort was devoted to research on SIDS pathogenesis, but effective proposals how to bring the incidence down were scarce. Before the 1970s, babies in Sweden were put to sleep on their back or side. At the beginning of the 1970s, this custom changed, however, as in other Western countries, and the babies were put to sleep prone instead. In 1985, Davies reported an astonishingly low SIDS incidence in Hong Kong. 1 He asked whether the custom of the babies sleeping supine in Hong Kong could contribute to the low incidence. Unfortunately, this report was received with scepticism. However, observations pointing in the same direction started to appear. In 1988, Beal showed that there was a consistent association between SIDS and prone sleeping position. De Jonge and Engelberts demonstrated that the rise in SIDS incidence in the Netherlands had come when parents started to put their babies to sleep in prone position. A prospective case control-study done in Avon in southwest England provided strong evidence of an association between prone sleeping and SIDS. Mitchell in New Zealand conclusively brought the different epidemiological observations together. He and co-workers demonstrated that prone sleeping, passive smoking and non-breastfeeding was over-represented in infants dying of SIDS. Abandoning the prone sleeping position in infants was paralleled by a clear-cut decrease in SIDS incidence in New Zealand. These results were rapidly spread internationally and non-prone sleeping was widely implemented. Norway and Denmark had seen an even more pronounced rise in SIDS incidence than Sweden. This prompted a large, joint Scandinavian case-control study of risk factors of SIDS 1992SIDS -1995. 7,8 . 7,8

Sudden and unexpected infant deaths can be unexplained [sudden infant death syndrome (SIDS)] or explained (non-SIDS) but risk factors including lower birthweight are similar in both groups. Mutations in the glucokinase (GK) gene result in Maturity Onset Diabetes of the Young type 2 (MODY 2) and are associated with lower birthweight. Low hepatic glucose-6-phosphatase (G6 PC1) expression occurs in both low birthweight and SIDS infants. We investigated whether polymorphisms are prevalent in the GK and G6PC1 genes in infants who died suddenly and unexpectedly. Mutation analysis was performed by polymerase chain reaction (PCR) and denaturing high-performance liquid chromatography (DHPLC) in samples from 126 infants who died suddenly and unexpectedly (78 SIDS, 48 non-SIDS) and from 70 healthy, living infants. G6PC1 promoter polymorphism significance was investigated by transfection of reporter gene constructs into a H4IIE cell line. Heterozygous GK polymorphisms were identified in 17.9% of SIDS and 20.8% of non-SIDS infants: two rare silent polymorphisms, Y215Y and S263S, in the coding region; a third rare polymorphism, -45G>A, in the hepatic promoter and the most prevalent polymorphism, c.484-29G>C, in a non-coding region upstream from the intron 4-exon 5 junction. A novel heterozygous polymorphism -77G>A in the G6PC1 promoter in 6.3% of non-SIDS and 2.9% of control infants decreased basal G6PC1 promoter activity (p<0.001). We describe three novel polymorphisms in the GK gene, S26 3S, -45G>A, and a common (14.3%) intronic substitution, c.484-29G>C, in infants who died suddenly and unexpectedly. We identified the first G6PC1 promoter polymorphism, which lowers expression, potentially increasing risk of hypoglycaemia and hence risk of sudden and unexpected death.

The incidence of sudden infant death syndrome (SIDS) has declined in response to campaigns discouraging the prone sleeping position. Recent work suggests some SIDS death may be in response to bacterial toxins produced in the upper airway. A minimal temperature of 37³C is required for induction of the pyrogenic toxins of Staphylococcus aureus identified in many SIDS infants. This aim of this study was to test the hypothesis that the prone position raises the temperature of the upper airways in children. A pilot study of 10 children (aged 3^8) and a main study of 30 children were carried out. Nasal septal temperatures were measured with an infra-red thermometer with the subjects in upright and prone positions under controlled conditions of ambient temperature and humidity. In both the pilot study and main study, nasal temperatures in the prone position were significantly higher (P 6 0.01) Five subjects' prone readings were 37³C or higher. These findings suggest that lying prone raises the upper airway surface temperature towards that required for toxin production. This could be one means by which the prone sleeping position contributes to the risk of SIDS.

A 67 kDa protein was isolated from cell membrane preparations of Staphylococcus aureus (NCTC 10655) by affinity adsorption with synthetic Lewis a antigen conjugated to Synsorb beads. Pre-treatment of buccal epithelial cells expressing Lewis a with the purified protein reduced binding of the staphylococcal strain to a greater extent than the material not bound to the Synsorb beads. The significance of this work is discussed with reference to expression of Lewis a antigen in infants and the proposed role of toxigenic strains of staphylococci in some cases of sudden infant death syndrome.

Epidemiological factors associated with susceptibility to respiratory infections are similar to those associated with Sudden Infant Death Syndrome. Here we review the evidence that respiratory pathogens might be involved in some cases of Sudden Infact Death Syndrome in the context of factors identified in epidemiological studies of cot deaths: the age range affected; mother's smoking; respiratory viral infections; immunisation status. Both laboratory and epidemiological evidence suggests that vulnerability of infants to infectious agents depends on interactions between genetic, developmental and environmental factors that contribute to colonisation by microorganisms, the inflammatory and specific immune responses and the infants' physiological responses to inflammatory mediators. A model is proposed to explain how microorganisms might trigger a series of events resulting in some of these unexpected deaths and discusses how the the present recommendations regarding child care practices might help reduce the numbers of Sudden Infant Death Syndrome cases associated with infectious agents.

Purpose-Sudden Infant Death Syndrome (SIDS) and suffocation account for more than half of all Sudden Unexpected Infant Deaths (SUID). The American Academy of Pediatrics (AAP) recommendations describe the safest environments to protect infants. This study compared parent responses on the Newborn Sleep Safety Survey and observational assessments (N=72) of infant sleep environments in families thought to be at high-risk for non-compliance with AAP recommendations. Design and Methods-A naturalistic study of participants enrolled in two home visitation support programs was used. Observed risks ranged from 36.6% (never use pacifier) to 4.3% (never use firm mattress). Results-Results comparing report to observation demonstrated acceptable concordance. Five items had fair concordance (Kappa > .4), four showed moderate concordance (Kappa > .6), and one excellent concordance (Kappa > .8). Although direct observation of safety behaviors is the gold standard in the injury prevention field, direct observation is logistically difficult, time consuming, and costly. Syndrome (SIDS) and suffocation require accurate assessment of the infant sleep environment. This study provides acceptable evidence for the use of the Newborn Sleep Safety Survey as an alternative to direct observation to assess parent adherence to recommendations. Limitations are discussed.

Purpose-Sudden Infant Death Syndrome (SIDS) and suffocation account for more than half of all Sudden Unexpected Infant Deaths (SUID). The American Academy of Pediatrics (AAP) recommendations describe the safest environments to protect infants. This study compared parent responses on the Newborn Sleep Safety Survey and observational assessments (N=72) of infant sleep environments in families thought to be at high-risk for non-compliance with AAP recommendations. Design and Methods-A naturalistic study of participants enrolled in two home visitation support programs was used. Observed risks ranged from 36.6% (never use pacifier) to 4.3% (never use firm mattress). Results-Results comparing report to observation demonstrated acceptable concordance. Five items had fair concordance (Kappa > .4), four showed moderate concordance (Kappa > .6), and one excellent concordance (Kappa > .8). Although direct observation of safety behaviors is the gold standard in the injury prevention field, direct observation is logistically difficult, time consuming, and costly. Syndrome (SIDS) and suffocation require accurate assessment of the infant sleep environment. This study provides acceptable evidence for the use of the Newborn Sleep Safety Survey as an alternative to direct observation to assess parent adherence to recommendations. Limitations are discussed.

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...

Background: Vaccination is a fundamental strategy in public health for controlling and eradicating infectious diseases. However, the undesirable Adverse Events Following Immunization (AEFI) should be effectively monitored, prevented, and managed in societies. Previously, Sudden Infant Death (SID) has been reported as a serious AEFI. We present a rare case of SID in an 18-month-old girl due to severe myocarditis following vaccination. Case Presentation: An 18-month-old girl presented to the Emergency Department (ED) with a history of the injection of Diphtheria-Tetanus-Whole Cell Pertussis (DTwP); Measles, Mumps, and Rubella (MMR), and oral poliovirus vaccines. She expired one-hour post ED admission after the episodes of vomiting and cardiopulmonary arrest. Postmortem histopathological examination signified marked congestion and the destruction of muscle fibers in the myocardium with inflammatory cells infiltration predominantly eosinophils. Given the postmortem histopathological findings, the cause of death was concluded as severe myocarditis following vaccination. Finally, the causality assessment was performed according to the Naranjo scale; the relevant data revealed a probable association in this regard (Naranjo score 6). Conclusion: Myocarditis is a rare and probable AEFI; thus, cardiac monitoring should be recommended as a diagnostic measure in managing postvaccinal adverse effects.

Heart  abnormalities  are  the  most  prevalent  congenital  defects, with Hypoplastic Left Heart Syndrome (HLHS) being a critical type  marked  by  the  left  heart's  underdevelopment.  Immediate diagnosis and intervention are crucial to avert dire consequences like sudden infant death. The report described the sudden death of  a  4.5-month-old  female  infant,  who  showed  symptoms  like cyanosis, dyspnea, and distress while crying and breastfeeding. On the day of the incident, the infant experienced a seizure after crying  for  10  minutes.  She  passed  away  in  the  Emergency Department due to resistant bradycardia. The case highlights the devastating  effects  of  misdiagnosis  and  the  difficulties  in detecting complex HLHS, underlining the urgency for increased vigilance, and the use of diagnostic techniques

The laryngeal chemoreflex exists in infants as a primary sensory mechanism for defending the airway from the aspiration of liquids. Previous studies have hypothesized that prolonged apnea associated with this reflex may be life threatening and might be a cause of sudden infant death syndrome. In this study we quantified the output of the respiratory neural network, the diaphragm EMG signal, during the laryngeal chemoreflex and eupnea in early postnatal (3-10 days) piglets. We tested the hypothesis that diaphragm EMG activity corresponding to reflex-related events involved in clearance (restorative) mechanisms such as cough and swallow exhibit lower complexity, suggesting that a synchronized homogeneous group of neurons in the central respiratory network are active during these events. Nonlinear dynamic analysis was performed using the approximate entropy to asses the complexity of respiratory patterns. Results: Diaphragm EMG, genioglossal activity EMG, as well as other physiological signals (tracheal pressure, blood pressure and respiratory volume) were recorded from 5 unanesthetized chronically instrumented intact piglets. Approximate entropy values of the EMG during cough and swallow were found significantly (p < 0.05 and p < 0.01 respectively) lower than those of eupneic EMG. Reduced complexity values of the respiratory neural network output corresponding to coughs and swallows suggest synchronous neural activity of a homogeneous group of neurons. The higher complexity values exhibited by eupneic respiratory activity are the result of a more random behaviour, which is the outcome of the integrated action of several groups of neurons involved in the respiratory neural network.

Forty-four isolates consisting of Fusarium solani (Mart.) Sacc. f.sp. glycines Roy, Fusarium solani f.sp. phaseoli (Burkholder) W.C. Snyder & H.N. Hans., and F. solani, collected from a variety of hosts and locations, were compared based on pathogenicity on soybean and mitochondrial DNA (mtDNA) restriction fragment length polymorphisms (RFLPs). The 24 isolates of F. solani f.sp. glycines caused more severe sudden death syndrome (SDS) foliar symptoms and root rot on soybean compared with all other isolates. All isolates of F. solani f.sp. glycines belonged to a single mtDNA RFLP haplotype. The other isolates of F. solani belonged to nine mtDNA RFLP haplotypes distinct from that of the SDS pathogen and did not cause significant levels of SDS. Three isolates of F. solani f.sp. phaseoli in a single mtDNA RFLP haplotype were very similar to isolates of F. solani f.sp. glycines in culture. One of these isolates consistently produced SDS-like symptoms in pathogenicity tests, although at a ...

It has been suggested that reflux laryngitis (RL) is involved in apneas-bradycardias of the newborn. The aim of the present study was to develop a unique RL model in newborn lambs in order to test the hypothesis that RL enhances the cardiorespiratory components of the laryngeal chemoreflexes (LCR) in the neonatal period. Gastric juice surrogate (2 mL HCl + pepsin, pH 2) (RL group, n = 6) or saline (Control group, n = 6) was repeatedly injected onto the posterior aspect of the larynx, 3 times a day for 6 consecutive days, via a retrograde catheter introduced into the cervical esophagus. Lambs instilled with gastric juice surrogate presented clinical signs of RL, as well as moderate laryngitis on histological observation. Laryngeal chemoreflexes were thereafter induced during sleep by injection of 0.5ml of HCl (pH 2), milk, distilled water or saline into the laryngeal vestibule via a chronic, transcutaneous supra-glottal catheter. Overall, RL led to a significantly greater respiratory inhibition compared to the Control group during LCR, including longer apnea duration (p = 0.01), lower minimal respiratory rate (p = 0.002) and a more prominent decrease in SpO2 (p = 0.03). No effects were observed on cardiac variables. In conclusion, 1) our unique neonatal ovine model presents clinical and histological characteristics of RL; 2) the presence of RL in newborn lambs increases the respiratory inhibition observed with LCR, at times leading to severe apneas and desaturations.

The objective of this work was to identify genomic regions that underlie resistance to Fusarium tucumaniae sp. nov., the causing agent of sudden death syndrome (SDS) in soybean in South America, using a population with a genetic background different from that previously reported for Fusarium virguliforme sp. nov. (F. solani f. sp. glycines), also responsible for SDS in soybean. Although major genes and quantitative trait loci (QTL) for SDS resistance have been identified, little is known about the same disease caused by Fusarium tucumaniae sp. nov., in South America. To identify genetic factors related to resistance to F. tucumaniae and DNA markers associated with them, a QTL analysis was performed using recombinant inbred lines. The map locations of the four loci, here identified, differed from those SDS resistance QTL previously described. It was screened a residual heterozygous line (RHL), which was heterozygous around the most effective QTL, RSDS1, and homozygous for the other g...

Sudden unexpected infant death (SUID) is a major cause of death in infants &lt; 1 year of age. Sudden infant death syndrome (SIDS) is a SUID still unexplained after post-mortem examination. In 2014, a protocol of post-mortem investigation was introduced to assess both the prevalence and the etiopathogenesis of SUID. Our aim was to compare SUID data before and after the application of a standardized autopsy protocol of investigation. In the time interval 2004–2018, SUID cases occurring in the Veneto Region, North-East Italy, were referred to our Core Lab. Since 2014, a complete autopsy was performed, including gross and histological study with toxicologic and molecular analysis carried out at the referral center. A total of 36 SUIDs (22 M, mean age 95.5 ± 80 days), 17 before (group A) and 19 after (group B) 2014, were collected. In group A, only 1 (6%) resulted as explained SUID, due to lymphocytic myocarditis and 16 (94%) were SIDS. In group B, 8 were SIDS (42%) and 11 (58%) explain...

Introduction/Objective. Sudden death in children may occur as a result of many diseases and accidents, while the cause often remains unknown. There are different terms in the literature that represent the causes of sudden death in children. The aim of our study was to determine the most common cause of sudden death in children admitted to the Clinic of Pediatrics. Methods. The retrospective study was conducted in the period from January 1, 1995 to December 31, 2015 and included 49 patients, aged from 10 days to 17 years, in whom death occurred in the Emergency Department and in the first 48 hours of hospitalization. Results. In 23 patients (47%) the cause of death was infection, in 10 patients (20%) heart failure, four patients (8%) died due to status epilepticus, the same number of patients (8%) died due to aspiration of a foreign body, while the rest of the patients died due to diabetic ketoacidosis (2%), rickets (2%), carbon monoxide poisoning (2%), hemolytic anemia (2%), suicide...

The rate of sudden infant death syndrome (SIDS) declined significantly in Canada and the US between the late 1980s and the early 2000s. In the US, this decline was shown to be due in part to a shift in diagnosis, as deaths from accidental suffocation and strangulation in bed and from other ill-defined and unspecified cause increased concurrently. This study was undertaken to determine whether there was such a shift in diagnosis from SIDS to other causes of death in Canada, and to quantify the true temporal decrease in SIDS. Cause-specific infant death rates were compared across three periods: 1991-95, 1996-2000 and 2001-05 using the Canadian linked livebirthinfant death file. The temporal decline in SIDS was estimated after adjustment for maternal and infant characteristics such as maternal age and small-for-gestational age using logistic regression. Deaths from SIDS decreased from 78.4 [95% confidence interval (CI) 73.4, 83.4] per 100 000 livebirths in 1991-95, to 48.5 [95% CI 44.3, 52.7] in 1996-2000 and to 34.6 [95% CI 31.0, 38.3] in 2001-05. Mortality rates from other ill-defined and unspecified causes and accidental suffocation and strangulation in bed remained stable. The temporal decline in SIDS between 1991-95 and 2001-05 did not change substantially after adjustment for maternal and infant factors. It is unlikely that the temporal decline of SIDS in Canada was due to changes in cause-of-death assignment practices or in maternal and infant characteristics.

The drive on respiration mediated by the peripheral arterial chemoreceptors was assessed by the hyperoxic test in 3-day-old rat pups. They accounted for 22.5 +/- 8.8% during control conditions, but only for 6.9 +/- 10.0% after nicotine exposure, an effect counteracted by blockade of peripheral dopamine type 2 receptors (DA2Rs). Furthermore, nicotine reduced dopamine (DA) content and increased the expression of tyrosine hydroxylase (TH) in the carotid bodies, further suggesting that DA mediates the acute effect of nicotine on arterial chemoreceptor function. During postnatal development TH and DA2R mRNA levels in the carotid bodies decreased. Thus, nicotine from smoking may also interfere with the postnatal resetting of the oxygen sensitivity of the peripheral arterial chemoreceptors by increasing carotid body TH mRNA, as well as DA release in this period. Collectively these effects of nicotine on the peripheral arterial chemoreceptors may increase the vulnerability to hypoxic episod...

In situ hybridization was used to characterize respiration-related areas of the brainstem activated around the time of birth as well as Ž . their postnatal sensitivity to CO . Levels of mRNA corresponding to the immediate early genes IEG , c-fos and c-jun, and of substance P 2 Ž . Ž . precursor, ppt-A, were determined in rat fetuses E21 and neonatal pups 1 h, 1 day and 6 days after normal birth and after exposure to Ž . hypercapnia 12% CO for 1 h . Transient increases in c-fos mRNA were observed in the central chemoreceptor area of the ventral 2 Ž . Ž . Ž . medullary surface VMS , in the lateral reticular nucleus LRN , in the nucleus of the solitary tract NTS , and in the nucleus raphe Ž . pallidus RPA 1 h after birth. Increased expression of c-fos mRNA in the VMS could also be evoked by hypercapnia and this response was particularly pronounced 1 day after birth. On the other hand, c-jun mRNA could be detected already at E21 in the hypoglossal Ž . nucleus XII and LRN and these levels were not significantly altered at 1 h after birth. There was, however, an increase in the expression of c-jun mRNA in the pia mater surrounding the brainstem after birth. At 1 day after birth, c-jun mRNA levels had decreased in the LRN Ž . and pia mater, and later on 6 days after birth in XII. Furthermore, the ppt-A mRNA level in NTS increased immediately after birth and Ž . remained high 1 and 6 days later. These results suggest that a the central chemoreceptor area of the VMS, as well as the NTS, LRN, Ž . RPA and pia mater are activated following birth; b the VMS, but not the other structures examined, can be activated immediately after Ž . birth by hypercapnia; and c increased expression of ppt-A mRNA may be related to the transition of respiratory control at birth.

Sudden infant death syndrome (SIDS) is an irreparable loss for the parents and has life-long consequences for the grieved family Objective: This systematic review aims to compile all the researches conducted so far on the possible involvement of respiratory neuronal structures of brainstem in SIDS Methods: Studies were extracted by using MeSH words “Sudden infant death syndrome, neuropathology” on Pubmed database and also search through hand screening. Results: A total of 114 studies were identified which were later further screened for inclusion criteria such as SIDS cases, original articles and case reports and brain nuclei involved in SIDS, while review articles and editorials were excluded. After further screening 40 studies were shortlisted. All the data was analyzed through excel, yearwise, country wise comparison was also conducted. Maximum studies (24) were published from Italy, most publications were from 2010-2020 (27). Upon final screening according to the inclusion of ne...

The mechanisms underlying the sudden infant death syndrome (SIDS) appear to have origins in the fetal environment resulting in neural damage which later compromises responses to breathing or blood pressure challenges during sleep. The deficits appear to involve alterations in neurotransmitter receptors within regions involved in chemoreception and cardiovascular control. SIDS risk is enhanced by pre-and postnatal nicotine exposure, and possibly by hypoxic experiences. The prone sleeping position plays a significant role in risk, as do head positions that minimize facial escape from enclosed spaces; elevated body temperature may also be a factor. Compensatory mechanisms, including diminished gasping ability, relative failure to arouse to a safer state, or a failure to recruit respiratory efforts to overcome a blood pressure loss have been the object of recent research efforts. The findings suggest that the fatal event involves a neurally-compromised infant, circumstances that challenge vital physiology, most likely during sleep, at a particular developmental period.

Any attempt to determine the mechanisms of failure in the sudden infant death syndrome (SIDS) should consider the role of functional circumstances that appear to accompany fatal episodes. An association of SIDS events with sleep states appears to be one such major circumstance, although that association may be only an approximate, temporal one, with the fatal event occurring during waking following a sleep episode. Knowledge of the association of sleep states with SIDS should direct our attention to those brain mechanisms that are modified by sleep state and might affect respiratory and cardiac control mechanisms. Moreover, even the name of the syndrome indicates that SIDS occurs suddenly; the circumstances of death normally do not include prolonged respiratory failure or signs indicative of life-threatening, prolonged cardiac failure. Thus, one would expect that a cataclysmic event, or a very unique combination of events, perhaps compounded by long-standing conditions, would be associated with death. The combination of circumstances of sleep state and sudden failure would suggest disturbance of central integration mechanisms. Structures within the brain are affected differently by sleep and waking states, and some of these areas of the brain have profound effects on cardiac and respiratory patterning. The pontine brainstem, for example, gives rise to large phasic EEG spikes during rapid eye movement (REM) sleep that are coincident in time with large changes in motor membrane potentials, Phasic movements of the extremity involved, and alterations in tone of the diaphragm.'.** 3 4 These pontine structures appear to alter reflex and motor patterning during REM sleep in such a fashion as to dissociate influences from more rostra1 brain areas and to exert, compared to the standards of control patterns during waking, unusual, all-encompassing modulation of motor reflex activity. The dissociative effects are great enough to abolish or greatly reduce large blood pressure rises elicited by electrical stimulation of the central nucleus of the amygdala5 or respiratory-cycle timing elicited by electrical stimulation of the orbital frontal cortex.6 Forebrain structures underlie a synchronization of brain electrical activity during quiet sleep that provides the potential for interaction between brain structures but elicits a burst-pause mode of neuronal discharge in motor areas which accompanies considerable regularity in respiratory and cardiac motor control. Quiet sleep can greatly diminish both the cxcitatory properties of single-pulse stimulation to forebrain areas' and the phasic diwharge rclationships of neurons to the respiratory cycle.8 However, the very large diswciative effects observed during REM sleep are not apparent in this state. Thus, in T h i \ u o r h wa\ \upported by Grant HL-22418 from the National Heart, Lung, and Blood Institute and <;rant HI)-'?hM from the National Institute of Child Health and Human Development, National ln\[itu[c\ 01 Hedlth ' Auihor lo uhom corre\pondence 5hould be Fent.

Background. Pneumocystis without obvious accompanying pathology is occasionally reported in autopsied infant lungs. Its prevalence and significance are unknown. Interestingly, this mild infection induces a strong activation of mucus secretion-related genes in young immunocompetent rodents that has not been explored in infants. Excess mucus is induced by multiple airway offenders through nonspecific pathways and would explain a cofactor role of Pneumocystis in respiratory disease. We undertook characterization of the prevalence of Pneumocystis and associated mucus in infant lungs. Methods. Samples from 128 infants (mean age, 101 days) who died suddenly and unexpectedly in Santiago during 1999-2004 were examined for Pneumocystis using nested polymerase chain reaction (nPCR) amplification of the P. jirovecii mtLSU ribosomal RNA gene and immunofluorescence microscopy (IF). Pneumocystis-negative infants 28 days and older and their age-closest positives were studied for MUC5AC expression and Pneumocystis burden by Western blot and quantitative PCR, respectively. Results. Pneumocystis DNA was detected by nPCR in 105 of the 128 infants (82.0%) and Pneumocystis organisms were visualized by IF in 99 (94.3%) of the DNA-positive infants. The infection was commonest at 3-4 months with 40 of 41 (97.6%) infants of that age testing positive. MUC5AC was significantly increased in Pneumocystis-positive tissue specimens (P = .013). Death was unexplained in 113 (88.3%) infants; Pneumocystis was detected in 95 (84.0%) of them vs 10 of 15 (66.7%) with explained death (P = .28). Conclusions. A highly focal Pneumocystis infection associated to increased mucus expression is almost universally present in the lungs of infants dying unexpectedly in the community regardless of autopsy diagnosis.

Brugada syndrome is an inherited arrhythmogenic disorder, characterised by coved-type ST-segment elevation in the right precordial leads, and is associated with increased risk of sudden death. It is genetically and clinically heterogeneous, presenting typically in the fourth or fifth decade of life. The prevalence of Brugada syndrome in the paediatric population is low compared with the adult population. Interestingly, over the last several years, there has been growing evidence in the literature of onset of the disease during childhood. Most of the paediatric cases reported in the literature consist of asymptomatic Brugada syndrome; however, some patients manifest the disease at different regions of the cardiac conduction system at a young age. Early expression of the disease can be affected by multiple factors, including genetic substrate, hormonal changes, and still unknown environmental exposures. The initial manifestation of Brugada syndrome in children can include sinus node d...

Sudden infant death syndrome (SIDS) was first defined in the USA as: 'The sudden death of an infant under one year of age which remains unexplained after a thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of the clinical history'. More recently, diverse studies have shown that some cases of SIDS can be explained, when an accurate post-mortem examination is performed. The primary objective of the present paper was to delineate possible causes of SIDS as derived from a review of autoptic studies reported in the literature.

The Back to Sleep Campaign was initiated in 1994 to implement the American Academy of Pediatrics' (AAP) recommendation that infants be placed in the nonprone sleeping position to reduce the risk of the Sudden Infant Death Syndrome (SIDS). This paper offers a challenge to the Back to Sleep Campaign (BTSC) from two perspectives: (1) the questionable validity of SIDS mortality and risk statistics, and (2) the BTSC as human experimentation rather than as confirmed preventive therapy. The principal argument that initiated the BTSC and that continues to justify its existence is the observed parallel declines in the number of infants placed in the prone sleeping position and the number of reported SIDS deaths. We are compelled to challenge both the implied causal relationship between these observations and the SIDS mortality statistics themselves.

Sudden infant death syndrome (SIDS) continues to be one of the top causes of infant death in the U.S. Despite significant public health initiatives focused on high-risk populations to enhance sleep environments and techniques. The SIDS rate has remained stable in recent years. Risk factors and newer risk reduction strategies for SIDS are the focus of this review article. We conducted a comprehensive literature search on Medline, Cochrane, Embase, and Google Scholar until July 2022. The following search strings and Medical Subject Heading (MeSH) terms were used: "SIDS," "Sudden Infant Death" and "SUID". We explored the literature on SIDS for its epidemiology, pathophysiology, the role of various etiologies and their influence, associated complications leading to SIDS, and preventive and treatment modalities. Despite a more than 50% drop-in rates since the start of the "Back to Sleep" campaign in 1994, sudden infant death syndrome (SIDS) continues to be the top cause of post-neonatal mortality in the United States, despite continued educational initiatives that support safe sleep and other risk reduction strategies. The new American Academy of Pediatrics guidelines for lowering the risk of SIDS include a lot of emphasis on sleeping habits, bedding, and environment but also include elements that are frequently ignored (i.e., prenatal care, smoking, alcohol and drug use, and childhood vaccinations). This study highlights these less-frequently discussed aspects and identifies treatments that have produced beneficial behavioral shifts that benefit newborns as well as their mothers' health and wellbeing.

Post-perinatal infant mortality in Yorkshire 1991-1993 was higher among non-whites (mainly Pakistanis) than among whites (5.7/1000 vs. 4.9/1000 live births). Pakistani families had more deaths from congenital or metabolic abnormalities, and from perinatal factors, but far fewer than sudden infant death syndrome.

Objective-To investigate the role of sleeping arrangements as risk factors for the sudden infant death syndrome after a national risk reduction campaign. Design-Two year population based case- control study. Parental interviews were conducted for each infant who died and for four controls matched for age and date of interview. Setting-Three regions in England with a total population of 17 million people. Subjects-195 babies who died and 780 matched controls. Results-Prone and side sleeping positions both carried increased risks of death compared with supine when adjusted for maternal age, parity, gestation, birth weight, exposure to smoke, and other relevant factors in the sleeping environment (multivariate odds ratio = 9.00 (95% confidence interval 2.84 to 28.47) and 1.84 (1.02 to 3.31), respectively). The higher incidence of side rather than prone sleeping led to a higher population at- tributable risk (side 18.4%, prone 14.2%). More of the infants who died were found with bed covers over their heads (21.58; 6.21 to 74.99). The use of a dummy had an apparent protective effect (0.38; 0.21 to 0.70). Bed sharing for the whole night was a significant risk factor for infants whose mothers smoked (9.25; 2.31 to 34.02). No protective effect of breast feeding could be identified on multivariate analysis. Conclusions-This study confirms the im- portance of certain risk factors for the sudden in- fant death syndrome and identifies others-for example, covers over the head, side sleeping position-which may be amenable to change by educating and informing parents and health care professionals. Key messages * Despite the success of the "Back to Sleep" cam- paign, the sudden infant death syndrome remains a major cause of death in infancy * This large case-control study is the first after the national campaign to reduce the risk of the syndrome * The risk of sudden infant death is increased by prone or side sleeping position; loose bedding (particularly duvets), which can slip over the baby's head; and bed sharing by mothers who smoke * The risk may be reduced by supine sleeping position; placing the baby with feet at the foot of the cot ("feet to foot"); ensuring that bedding is securely tucked in; and avoiding the use of duvets

The three year study of sudden unexpected death in infancy (SUDI), recently completed as part of the programme of the Confidential Enquiry into Stillbirths and Deaths in Infancy (CESDI), includes the largest and most comprehensive study of cot death yet conducted in the UK. Over 450 sudden deaths, of which 80% were classified as sudden infant death syndrome (SIDS) were investigated in five (former) NHS regions between 1993 and 1996, both by confidential inquiry and by case-control technique. Outline results for the first two years were given in the third report of the National Advisory Body for CESDI 1 while more detailed reports on various aspects of the case-control study are being published in professional journals. 2 3 The national intervention on sleeping position in 1991 was followed by a marked and most welcome fall in the incidence of cot death, the national rate declining from 1.61/1000 live births in 1990 to 0.6 in 1993. However SIDS is still the largest category of deaths in the postperinatal period, and the SUDI study has shown that several major problems remain to be addressed. Some of these I should like to discuss.