Cause Of Sudden Infant Death Research Articles

Fetal Arrhythmia Detection Based on Labeling Considering Heartbeat Interval.

Arrhythmia is one of the causes of sudden infant death, and it is very important to detect fetal arrhythmia for fetal well-being. Fetal electrocardiogram (FECG) is one of the methods to detect a heartbeat. Fetal arrhythmia can be detected based on the heartbeat detection results from FECG signals such as heartbeat intervals. However, the accuracy of arrhythmia detection easily degrades depending on the accuracy of heartbeat detection. In this paper, we propose a deep learning-based fetal arrhythmia detection method using FECG signals. Recently, arrhythmia detection methods using adult ECG signals have achieved a high arrhythmia detection accuracy based on deep learning. Motivated by this fact, in the proposed method, the acquired FECG signals are segmented, and the segments are input into a deep learning model that classifies them into normal or arrhythmia ones. Based on the classification results of multiple segments, a subject is judged as a healthy or arrhythmia subject. Each segment of the training data is divided into three categories based on the estimated heartbeat interval: (i) normal, (ii) arrhythmia, and (iii) a segment that could be both normal and arrhythmic. Only segments labeled as normal or arrhythmia are used for training a deep learning model to achieve a higher classification accuracy of the model. Through these procedures, the proposed method detects fetal arrhythmia with fewer effects of heartbeat detection results. The experimental results show that the proposed method achieves 96.2% accuracy, 100% specificity, and 100% recall, improving the values of conventional methods based on heartbeat detection and feature detection.

ОСОБЕННОСТИ РЕАКЦИИ ДЫХАТЕЛЬНОГО ЦЕНТРА НОВОРОЖДЕННЫХ КРЫС, ПЕРЕНЕСШИХ ПРЕНАТАЛЬНОЕ ПАССИВНОЕ КУРЕНИЕ, НА ГИПОКСИЧЕСКОЕ ВОЗДЕЙСТВИЕ (IN VITRO)

It is expected that in neonates that underwent prenatal chronic effect of nicotine the identification of the reduction of intensiveness of respiratory response to hypoxic exposure may be the cause of sudden infant death. The effect of cigarette smoke may differ from the effect of nicotine. The study was performed on brain stem spinal cord preparations (BSS) in the brain of newborn rats (n=38) in vitro. In the experimental group (EG) the modeling of passive smoking was carried out by fumigation of cigarette smoke of rat females from the 1st to 20th day of gestation. Hypoxia was simulated by an artificial cerebrospinal fluid saturated with a gas mixture of 5% CO2 and 95% N2. Hypoxic depression of BSS respiratory rhythm of the control group (CG) occurred at the 5th minute; the restoration took place in 10 minutes at normoxia, at the same time there was an increase of the amplitude of the inspiratory discharges which did not return to baseline values (15 minutes). In preparations of CG at the 10th minute of hypoxia the duration of inspiratory discharges decreased and restored after 10 minutes at normoxia. The increase of the ratio of the power of low-frequency and medium-frequency oscillations was observed in the CG at the 15th minute of hypoxia with the restoration during 10 minutes. In the experimental group (EG) the increase of the duration of the respiratory cycle occurred at the 10th minute of hypoxia with the dynamics of recovery similar to that of CG. The increase of the amplitude of inspiratory discharges occurred at the 10th minute of hypoxia; a recovery period took 10 minutes. In the BSS of EG the reduction in the duration of the inspiratory discharges and the increase of the ratio of the power oscillations of low- and mid-range occurred at the 5th and 10th minutes of hypoxia and these parameters never returned to baseline values. Our data suggest that prenatal exposure to secondhand smoke has an effect on the mechanisms of central chemosensitivity in the offspring in the early postnatal period.

The mystery of the thymus gland.

The thymus is the last organ in the human body to have its mechanisms fully understood, having had its function fully delineated more than 50 years ago (Miller , Tissue Antigens 63:509-517). Prior to this, the thymus gland has had an interesting history with theories having included a role in fetal growth and development before becoming more sinisterly, a cause of sudden infant death in the late 19th century known as status lymphaticus (Paltauf , Wien Klin Wochenschr 2:877-881). Until Miller (, Lancet 278:748-749) eventually proved its primarily immunological role, the history of this mysterious gland has closely mirrored the history of medicine itself, troubling the minds of pathologists such as Virchow (, Ueber die Chlorose und die damit zusammenhängenden Anomalien im Gefässapparate, insbesondere über "Endocarditis puerperalis," vorgetragen in der Sitzung der Berliner Geburtshülflichen Gesellschaft vom 12) and Grawitz (, Deut Med Wochenschr 22:429-431), surgeons such as Astley Cooper (, The Anatomy of the Thymus Gland) and Keynes (1953, Ann R Coll Surg 12:88), and eminent medical epidemiologists such as Greenwood and Woods [, J Hyg (Lond) 26:305-326]. This article will hopefully be of interest therefore to both clinician and historian alike. Clin. Anat. 29:679-684, 2016. © 2016 Wiley Periodicals, Inc.

Postmortem diagnosis of infectious heart diseases: A mystifying cause of Sudden Infant Death

Sudden infant death (SID) is an unresolved problem of high relevance and previous studies have indicated a role of viral heart infections. The diagnosis remains difficult in clinical practice using routine diagnostic tests and must be substantially improved.A prospective study based on post-mortem samples from SID victims whose heart disease was not clinically recognized was conducted for 4 years in a Tunisian University Hospital. Pediatric cases of unnatural death served as controls. Both SID victims and controls were investigated for possible coxsackievirus-B (CV-B) infection in heart tissue.During the study period, 39 cases with a male predominance (77%) were reported. There was no positive family history of coronary artery disease among the victims. In 35 cases (90%), low birth weight and/or critical development period were reported. All SID victims had complained of mild fever and insomnia for a few days preceding death, which required infectious laboratory investigations marked with an elevated white blood cell count (WBC) and C-reactive protein (CRP). The cardiac biomarkers were also elevated. The histopathological investigations of the heart tissue samples revealed signs of myocardial and pericardial inflammation. Enterovirus was detected by immunohistochemistry (IHC) and PCR from myocardial samples from 6 cases (15.3%) having myocarditis and 3 cases (7.7%) having perimyocarditis.The current study is of great interest and is aimed at urging health professionals to adopt systematically long intensive heart care in infants with underlying vulnerability as well as new diagnostic approaches including histopathology complemented with IHC and molecular pathology.

Infant Ventricular Fibrillation After ST-Segment Changes and QRS Widening

Background— Ventricular arrhythmia–related sudden cardiac arrest in infants with structurally normal hearts is rare. There have been no previously published reports of infants <3 months of age with ventricular fibrillation in which a primary diagnosis could not be defined. Methods and Results— Retrospective chart review of 3 unrelated infants <2 months of age from 3 different tertiary care centers within the United States and Australia was conducted. All 3 infants survived sudden cardiac arrest secondary to multiple episodes of polymorphic ventricular tachycardia and ventricular fibrillation. Each infant demonstrated unique and transient ECG findings consisting of ST changes and QRS widening before arrhythmia onset, which have not been previously reported. Amiodarone, sedation, sodium channel–blocking agents, and ventricular pacing were effective in suppressing acute events. Despite thorough investigation, including genetic testing, the cause of ventricular arrhythmias in each of these infants remains unclear. Conclusions— This is the first report of idiopathic ventricular fibrillation in young infants preceded by stereotypical transient ECG changes. These findings may represent a new, potentially treatable cause of sudden infant death. Recognition of these prodromal changes may be important in future management and survival of these infants.

Prematurity and sudden infant death syndrome: United States 2005–2007

In 1987, the sudden infant death syndrome (SIDS) rate in the United States was 1.2 per 1000 live births. By the year 2005, the SIDS rate had dropped more than half to approximately 0.5 per 1000 live births. In 1987, the risk of SIDS was 2.32 times greater for extremely premature infants compared with term infants. The objective of this analysis was to determine if with the falling SIDS rate there has been a change in the risk for SIDS among preterm infants. Data were obtained from the United States Linked Infant Birth and Death Certificate Public User Period files for the years 2005 to 2007. The adjusted odds ratios (ORs) for postneonatal out-of-hospital death by gestational age were determined by logistic regression modeling. Over the 3-year period, there were 5203 postneonatal out-of-hospital deaths attributable to SIDS; 2010 attributable to other sudden deaths; 1270 attributable to suffocation in bed; and 3681 attributable to other causes. The adjusted OR for SIDS among the most preterm infants (24 to 28 weeks gestation) was significantly increased compared with term infants, OR(adj)=2.57 (95% confidence interval=2.08, 3.17), as were the adjusted ORs for the other causes of sudden infant death. Despite the marked drop in the incidence of SIDS since 1987, the risk for SIDS among preterm infants remains elevated. Other causes of sudden infant death for which SIDS is often mistaken reflect similar levels of increased risk among preterm infants.

Sudden death of an infant with coronary involvement due to Takayasu arteritis

We present an unusual case of sudden death of an 8-month-old female infant with coronary involvement due to Takayasu arteritis. She had been thought to be healthy, but died after presenting to a hospital with complains of vomiting. At autopsy, the aorta and its main branches were thickened and stenotic, with the abdominal aorta below the level of the orifice of renal arteries most severely affected. The ascending aorta was thickened and showed ostial stenosis in the coronary arteries bilaterally. The proximal segment of the left and right coronary arteries showed approximately 60% and over 90% occlusion, respectively. Microscopically, the intima was thickened due to an increase of intimal cells and fibers, and the adventitia showed thickening with fibrosis. In addition, remarkable infiltration of inflammatory cells, including multinuclear giant cells phagocytosing fragmented elastic fibers, and destruction of elastic fibers were observed in the media. We diagnosed the cause of death as coronary insufficiency induced by coronary involvement due to Takayasu arteritis. Takayasu arteritis was not considered as a cause of sudden infant death, although this disease can affect the coronary artery. This report suggests that Takayasu arteritis can be a life-threatening condition even in infants.

Post-mortem MRI reveals CPT2 deficiency after sudden infant death

Inherited metabolic disorders are the cause of a small but significant number of sudden infant deaths in infants. We report on a boy who suddenly died at 10 months of age during an acute illness. Parents declined autopsy; nevertheless, they accepted a whole body MRI, which revealed hepatomegaly with steatosis. Acylcarnitine profile of a blood sample from neonatal Guthrie screening led to the diagnosis of type 2 carnitine palmitoyltransferase deficiency. To conclude, whole body MRI is useful in the investigation of some inherited metabolic causes of sudden infant death, which might prevent future deaths in the family. It is a good alternative when autopsy is refused.

More evidence points to an infective cause of sudden infant death

More evidence points to an infective cause of sudden infant death

Gas dispersal potential of bedding as a cause for sudden infant death

We assessed the gas dispersal potential of bedding articles used by 14 infants diagnosed with sudden unexpected infant death at autopsy. Of these cases, eight exhibited FiCO 2 values greater than 10% within 2.5 min, six of which were found prone and two supine. The results demonstrated that these eight beddings had a high rebreathing potential if they covered the babies’ faces. We did not, however, take into account in our model the large tissue stores of CO 2. As some bicarbonate pools will delay or suppress the increase of FiCO 2, the time–FiCO 2 graphs of this study are not true for living infants. This model, however, demonstrated the potential gas dispersal ability of bedding. The higher the FiCO 2 values, the more dangerous the situation for rebreathing infants. In addition, FiO 2 in the potential space around the model's face can be estimated mathematically using FiCO 2 values. The FiO 2 graph pattern for each bedding item corresponded roughly to the inverse of the FiCO 2 time course. The FiO 2 of the above eight cases decreased by 8.5% within 2.5 min. Recent studies using living infants placed prone to sleep reported that some babies exhibited larger decreases in FiO 2 than increases observed in FiCO 2. While the decrease of FiO 2 in our model is still theoretical, CO 2 accumulation and O 2 deprivation are closely related. If a striking O 2 deficiency occurs in a short period, babies can lose consciousness before an arousal response is evoked and all infants could be influenced by the poor gas dispersal of bedding; the main cause of sudden death in infancy would thus be asphyxia. When the bedding is soft, the potential for trapping CO 2 seems to be high; however, it is impossible to assess it by appearance alone. We sought to provide some objective indices for the assessment of respiratory compromise in relation to bedding using our model. When a baby is found unresponsive with his/her face covered with poor gas dispersal bedding, we should consider the possibility of asphyxia.

Basilar artery insufficiency--a possible cause of sudden infant death? Results of a Doppler ultrasound study of 39 children with apparent life-threatening events

Hypoperfusion of the brain stem in dependence on head and body position followed by central bradycardia and apnea may be an important cause of sudden infant death syndrome (SIDS). 39 infants with a mean age of 10.6 +/- 10.2 weeks (6 days to 11 months) with apparent life threatening events (ALTE) were investigated by cranial Doppler sonography. Additionally 68 healthy infants aged 6 days to 5 months (m 3.7 +/- 4.1 weeks) were investigated. In all patients flow measurements were performed in one anterior cerebral artery (ACA), both internal carotid arteries (ICA), the basilar artery (BA), and both vertebral arteries (VA) in dependence on head (right/left/neutral) and body position (prone/supine). In healthy infants flow velocities within all intracranial arteries were independent of head and body position. In none of our infants with ALTE significant flow alterations in the ACA and both ICA in dependence on head and body position could be found. In 23 patients with ALTE no dependence of flow in the BA and both VA of head and body position could be shown. In 16 infants however pathologic flow profiles with low flow velocities could be found in the contralateral VA if the head was rotated to the other side. In 9 infants additionally pathologic flow profiles with a dramatic decrease of the flow velocities in the BA could be found. The reduction of the blood flow is caused by compression of the contralateral vertebral artery at the craniocervical junction. The reduction of blood flow in the VA and especially the BA may cause hypoperfusion of the brainstem followed by central bradycardia and apnea. Hypoperfusion of the brainstem in dependence on head and body position may be a significant cause of SIDS. By means of cerebral Dopplersonography infants at risk for SIDS may be detected. Body and head positions which should be avoided can be evaluated noninvasively.

Arrhythmogenic right ventricular dysplasia/cardiomyopathy as a cause of sudden infant death

Arrhythmogenic right ventricular dysplasia/cardiomyopathy is a rarely described cause of sudden death among infants. We report the case of a 4-month-old male infant who died suddenly in his sleep. Postmortem examination revealed the presence of arrhythmogenic right ventricular dysplasia/cardiomyopathy.

AAP report: Thorough investigation encouraged in SIDS cases

The role of pediatricians and medical examiners in carefully, thoroughly and compassionately investigating the cause of sudden infant death, especially in cases where child abuse is suspected, is outlined in a revised clinical report, released jointly by the Academy and the National Association of

Research and sudden infant death syndrome: definitions, diagnostic difficulties and discrepancies.

The diagnosis of causes of sudden infant death is an often complex and difficult process. Variable standards of autopsy practice and the use of different definitions for entities such as sudden infant death syndrome (SIDS) have also contributed to confusion and discrepancies. For example, the term SIDS has been used when the requirements of standard definitions have not been fulfilled. In an attempt to correct this situation recent initiatives have been undertaken to stratify cases of unexpected infant death and to institute protocols that provide frameworks for investigations. However, if research is to be meaningful, researchers must be scrupulous in assessing how extensively cases have been investigated and how closely cases fit with internationally recognized definitions and standards. Unless this approach is adopted, evaluation of research findings in SIDS will be difficult and the literature will continue to be beset by contradictions and unsubstantiated conclusions.

Il-10 gene polymorphisms are associated with infectious cause of sudden infant death

Cytokines are involved in regulating the intensity and duration of the immune response, and cytokine production is carefully regulated. With regard to sudden infant death, interleukin-10 (IL-10) is of special interest. This is an immunregulatory cytokine that plays an important role in the development of infectious disease. The purpose of this study was to elucidate the relationship between polymorphisms in the promoter region of the IL-10 gene and sudden infant death due to either sudden infant death syndrome (SIDS) or infection. The polymorphisms investigated include the SNPs in base pairs (bp) -1082, -819, -592, and the two microsatellites IL-10G and IL-10R. The main finding is an association between the ATA haplotype and the ATA/ATA genotype and infectious death. The group of infectious deaths also had a higher percentage of the genotypes G21/G22 and G21/G23, compared with the SIDS patients. In addition, G21/G22 was found in a higher percentage of the SIDS patients than in the controls. These findings lead us to speculate that, in some situations, an infant with an unfavorable IL-10 genotype may exhibit aberrant IL-10 production, which in turn leads to an imbalance in the immune response and renders the infant unable to cope with the infection.

Pathological changes of the heart in sudden infant death.

There are more than 120 different theories on the possible causes of sudden infant death (SID). In particular, dysfunctions of the central nervous system, cardiorespiratory insufficiency due to infections including atypical immune reactions, and cardiac dysregulation have been discussed during the previous decade. Reports on disturbances of the cardiac rhythmogenic function due to LQTS were among the most speculative. Based on gross histological, immunohistochemical and molecular genetic investigations of SID cases, the most important and most frequent findings of the heart are shown. The significance of different types of myocarditis, hypoxia-related changes, disturbances of the rhythmogenic function, cardiomyopathy, and other changes is discussed with regard to the cause of death. In conclusion, most of the changes reported in the literature are not sufficient to explain the cause of death. Problems in the diagnosis are shown which influence the classification of these disturbances as well as the classification of SID.

Cardiovascular causes for sudden infant death.

Although sudden infant death syndrome (SIDS) is a cause for sudden infant death, other causes should be ruled out before diagnosing SIDS. Cardiac causes for sudden infant death include viral myocarditis, congential heart disease particularly congential aortic stenosis, endocardial fibroelastosis, and anomalous origin of the left coronary artery from the pulmonary artery. Other cardiac conditions that may result in sudden death include rhabdomyomas of the heart in tuberous sclerosis and conduction system disorders. The most frequent conduction system disorders resulting in sudden death include histiocytoid cardiomyopathy, congential heart block that may be associated with maternal lupus erythematosus, arrhythmogenic right ventricular dysplasia, noncompaction of the left ventricle, and long QT syndromes.

Position dependent changes of cerebral blood flow velocities in premature infants.

The supine or prone positioning of infants has been a cause of much controversy. Recently it has been postulated that the position dependent hypoperfusion of the brainstem represents a possible cause of sudden infant death. To demonstrate position dependency and maturational changes of cerebral perfusion in premature newborn infants we investigated cerebral blood flow velocities (CBFV) in the main supratentorial and brainstem cerebral arteries. Measurements of CBFV were done with transfontanellar colour-coded Doppler sonography in the internal carotid artery (ICA), basilar artery (BA), and vertebral artery (VA) in the prone (head centered-baseline) and supine positions (maximal rotation to both sides) in 23 premature infants aged between 3-5 days of life. We performed follow-up measurements in 17 infants 7-10 days later and in 16 infants at the corrected age of 1 month. There was no difference in mean CBFVs between the prone and supine position at the first investigation. At the third investigation, CBFVs were significantly higher in the supine compared to the prone position. The CBFVs of the ICA were higher than in the BA and VA. This difference was not influenced by the body position but increased with post-natal age more in the VA (159%) than in the BA (129%) and ICA (128%). Position dependency was not seen in the ICA perfusion. In the prone position, five infants showed an incomplete steal effect in the contralateral VA. There was no significant side difference in the CBFVs of the ICA and VA, but in the resistance indices in the VA (left > right). in premature newborns, position dependent changes of cerebral blood flow velocity develop with maturation and are most pronounced in the vertebrobasilar system. These changes are possibly due to compression of the vertebral artery by neck movement and suggest an individual risk of brainstem perfusion deficits that may be aggravated with age and head rotation in a prone position.

Natural Rubber Latex Allergy Is Not a Cause of Sudden Infant Death

Background: The causes for sudden infant death (SID) remain unclear. As infants can become sensitized to NRL allergens by pacifiers and latex mattresses, we tried to establish whether there is a relationship between SID and natural rubber latex (NRL) allergy. Methods: We determined NRL–specific IgE concentrations in 112 unselected cases of SID by the CAP–FEIA method. Results: NRL–specific IgE could be detected only in 1 sample (0.64 kU/l; CAP class 1). Conclusions: We conclude that NRL allergy is not a cause of SID.

Compression of the vertebral arteries during head rotation—a possible cause of sudden infant death?

Eine lageabhangige Minderperfusion des Hirnstamms mit nachfolgenden zentralen Regulationsstorungen ist moglicherweise eine Ursache des plotzlichen Sauglingstodes. Zur Klarung dieser Frage wurden dopplersonographische Flusmessungen in der A. basilaris und in beiden Vertebralarterien in Abhangigkeit von Korperlage (Ruckenlage, Bauchlage) und Kopfposition (Mittelstellung, Rotation nach links und rechts) durchgefuhrt. Die Untersuchungen erfolgten mit den Computersonographiegeraten XP 10, Aspen und Sequoia der Firma Acuson mit einer Frequenz von 5 MHz. Aus dem Flu\profil wurde die maximale und mittlere Flusgescheindigkeit ermittelt. Untersucht wurden 39 Sauglinge (Alter 10,6±10,2 Wochen) mit anscheinend lebensbedrohlichen Ereignissen (ALE) und 68 gesunde Sauglinge (Alter 3,7±4,1 Wochen), die als Kontrollkollektiv dienten. Im Kontrollkollektiv war die Blutstromung in den Hirnbasisarterien unabhangig von der Korperlage und Kopfposition. Bei 41% der ALE-Patienten fiel die Blutstromung in der kontralateralen Vertebralarterie bei Kopfrotation ab. Bei 23% kam es zusatzlich zu einem Abfall der Blutstromung in der A. basilaris. Die Veranderungen waren in Bauchlage ausgepragter als in Ruckenlage. Der Abfall der Blutstromung im vertebrobasilaren System kommt durch Kompression der kontralateralen Vertebralarterie am kraniozervikalen Ubergang zustande. Ein nachfolgender Abfall der Durchblutung des Hirnstammes konnte somit eine Ursache des plotzlichen Sauglingstods sein.