Formal retrospective case review and sudden infant death

A review of 24 consecutive sudden infant deaths was undertaken to evaluate the importance of the various stages in the postmortem assessment of such cases. Death in three cases was caused by obvious trauma. Of the remainder, 16 were attributed to sudden infant death syndrome (SIDS), 4 to accidental asphyxia (identified by death scene examination and/or formal case review) and 1 to a lingual thyroglossal duct cyst. Three (14%) of 21 deaths thought to be SIDS after postmortem examination were attributed to asphyxia following subsequent formal case review.     

Housing and sudden infant death syndrome. The New Zealand Cot Death Study Group

AIMS: This paper examined factors relating to the infants' place of domicile to see whether they increased the risk of sudden infant death syndrome (SIDS) beyond social and environmental effects previously published. METHODS: A case control study was undertaken in New Zealand between the years 1987-90. From all sudden infant death syndrome diagnoses over this time, parents of 393 (81%) sudden infant death syndrome infants consented to participate and these derive the cases. Controls were ascertained by randomly sampling 1800 infants from all babies born over 78% of the country. Parents of 1592 (88%) control infants consented to participate in the study. RESULTS: The relative risk of sudden infant death for infants usually residing in houses rented from the government (State houses) was 1.73 (95% CI: 1.13, 2.66) times that of infants with parents owning their house, after adjusting for likely social, economic and environmental confounding factors. However, the type of housing, construction of housing, heating and age of housing was not associated with sudden infant death syndrome. Although house size, measured in terms of bedroom numbers, was similar for sudden infant death syndrome and control infants (chi 2 = 0.40, df = 2, p = 0.82), the number of people normally residing within these houses was different. Sudden infant death syndrome infants' houses were less likely to have two adults and more likely to have more children normally resident. Density calculations (derived by calculating the children and/or adult numbers divided by bedroom numbers) revealed a non significant increase in relative risk, suggesting that housing overcrowding was not associated with sudden infant death syndrome in New Zealand. CONCLUSIONS: Infants domiciled in State houses are more likely to experience sudden infant death syndrome. However, this increased relative risk for sudden infant death syndrome appears to have little to do with the house per se and, perhaps, more to do with socioeconomic characteristics.     

DTP vaccine and infant sudden death syndrome. Meta-analysis

BACKGROUND: At the beginning of 1994, five cases of sudden infant death syndrome after DTP immunization appeared in Spain. In order to study a causal relationship a meta-analysis of the different studies that assess this possibility has been conducted. METHODS: The selection criteria was epidemiological study, case-control or cohort, assessing risk of sudden infant death syndrome in immunized versus non-immunized infants or risk of sudden infant death syndrome in recently immunized infants versus immunized infants beyond 30 days. Pooled risk ratios were calculated from adjusted risk ratios, when available, of the different studies, by a meta-analysis according the method described by Greenland. RESULTS: One cohort and four case-control studies were selected. Pooled risk ratio for immunized versus non-immunized infants was 0.67 (95% CI = 0.60-0.75). When comparing risk of sudden death syndrome in up to 30 days immunized infants versus more than 30 days immunized infants, the pooled risk ratio was 1.00 (95% CI = 0.84-1.20). CONCLUSIONS: DTP-immunization does not seem to increase the risk of sudden infant death syndrome. The risk of sudden infant death syndrome is not greater in the first thirty days following immunization. These data indicate a lack of association between DTP immunization and sudden infant death syndrome.     

Activation of p70 S6 protein kinase is necessary for angiotensin II-induced hypertrophy in neonatal rat cardiac myocytes

Infants with mandibular hypoplasia are at risk of sudden death from cardiorespiratory arrest secondary to upper airway obstruction. To evaluate diagnostic difficulties that may occur at autopsy in such infants, the autopsy files at the Adelaide Children's Hospital (ACH) for 36 years, 1959 to 1994, were reviewed. Eight cases were identified (age range, 2 days to 10 months; mean age, 2.2 months; male/female ratio, 5:3). In all cases, death was considered most likely due to airway obstruction related to mandibular hypoplasia or its treatment. Although death occurred in the hospital in five cases, one infant suddenly collapsed at home while feeding and died, and two infants were unexpectedly found dead in their cribs at home. Three infants had defined genetic syndromes. Although all the infants had histories of antemortem airway obstruction, one infant had normal oxygen saturation studies before hospital discharge, and one infant had a tracheostomy. Acute bronchopneumonia was an exacerbating factor in one case. Assessment of mandibular size is important in any infant who dies unexpectedly; and if hypoplasia is found, careful review of the clinical details for evidence of airway obstruction is necessary to help distinguish these cases from sudden infant death syndrome (SIDS). Sudden death may, however, occur in infants with mandibular hypoplasia in spite of apparent clinical stability before death with no significant recent episodes of oxygen desaturation.     

Pathological fear of cot death

Cot death (sudden infant death syndrome) is one of the most common causes of death in the first year of life. Four cases with a pathological fear of cot death are presented. All the patients were depressed and in 2 cases the fear of cot death had an obsessional quality. In all cases there were complications during pregnancy (miscarriage, threatened abortion, recurrent vomiting in last trimester). In 1 case, the patient knew 3 mothers who had suffered cot deaths; in another, the infant was gravely ill in the neonatal period. Pathological fear of cot death can be recognised by the presence of two central features - overvigilance and excessive nocturnal checking of the baby's breathing. Therapeutic interventions are discussed.     

Hashimoto''s thyroiditis and HLA in Caucasian Italians

Sudden infant death syndrome is the sudden, unexpected death of an apparently healthy infant, accounting for 7,000 to 10,000 deaths per year. For the parents, the unexpectedness and guilt can be overwhelming. The long, difficult grief process has a great effect on marital relationships, surviving siblings, and subsequent children. Increasing the nurse's understanding of the effects of sudden infant death syndrome can enhance the support the parents receive. A caring attitude and follow-up throughout the grief process are necessary.     

Central nervous system damage as a possible component of unexpected deaths in infancy

A longitudinal study of 1553 infants, designed to provide early indicators of gross developmental problems by using a behavioral assessment scale, included 12 infants who later died suddenly and unexpectedly. In a retrospective examination of neonatal records, considerable evidence of central nervous system damage was found. Anoxic conditions and even possible seizure activity were implicated. Abnormalities of muscle tonus, skin color and cry were found, together with some visual problems. These findings on behavioral assessment in the neonatal period appear to identify a population which is at greater risk of sudden death in infancy. The need for oxygen therapy as a high-risk indicator of sudden unexpected death has been reported in a previous study and is further substantiated by the present findings: they are also compatible with thos of Naeye (1973), who found long-term hypoxic conditions in autopsy studies on the sudden infant death syndrome. It is suggested that the possibility of central nervous system involvement in the aetiology of the sudden infant death syndrome should be more thoroughly investigated.     

The story of the internal carotid artery of mammals: from Galen to sudden infant death syndrome

Some anatomical aspects of the blood supply of the brains of mammals have been examined to illuminate their functions. A fundamental explanation of sudden infant death syndrome (cot death) is suggested following experimental observations. Speculative contributions have been made to comparative physiological ideas concerning mammals of pronograde and erect habitus, their vascular pressure adaptations and temperature management. Neuro- and interventional radiologists may make some significant future applications of these ideas. Of immediate practical interest is the possibility of influencing the well-being of human embryos' neural tube development in utero by a comprehensive study of their temperature environment.     

Development of a new introduction technique for the pulsatile catheter pump

Hypoplastic pineal glands and decreased melatonin levels are found in sudden infant death syndrome. Excess oxygen radical production and inadequate radical quenching is suggested to cause oxidative stress in the brain of sudden infant death syndrome victims. Loss of intraventricular cerebrospinal fluid melatonin could play an important role in the disease process. Infants at risk might be protected by exogenous melatonin.     

Increase in the incidence of occipital plagiocephaly

INTRODUCTION: The diagnosis and treatment of posterior plagiocephaly is one of the most controversial aspects of craniofacial surgery. PATIENTS AND METHODS: The purpose of this study is to describe a recent increase in the incidence of occipital plagiocephaly without synostosis in our hospital during the last 6 months. The shift in the referral patterns is roughly contemporaneous with the American Academy of Pediatrics recommendations regarding infant sleep position. The temporal coincidence of this increase with the recommendation to avoid the prone sleeping position, to reduce the risk of sudden infant death syndrome, suggests a possible causal relationship. If the association is causal, education regarding the need of head position rotation coupled with that for sudden infant death syndrome should obviate positional occipital plagiocephaly. CONCLUSIONS: The feature of true lambdoid synostosis versus those of deformational plagiocephaly secondary to positional molding are inadequately described in the literature and poorly understood; the differential diagnosis is important in relation to a conservative diagnostical and therapeutical intervention in patients with positional molding.     

Retrospective biochemical screening of fatty acid oxidation disorders in postmortem livers of 418 cases of sudden death in the first year of life

OBJECTIVE: Fatty acid oxidation (FAO) disorders are frequently reported as the cause of sudden and unexpected death, but their postmortem recognition remains difficult. We have devised a biochemical protocol in which informative findings in liver tissue are microvesicular steatosis, elevated concentrations of C8-C16 fatty acids, glucose depletion, and low carnitine concentration. STUDY DESIGN: We analyzed 27 cases representing five FAO disorders and compared the results with those obtained in a retrospective blinded analysis of 418 cases of sudden infant death (313 SIDS, 45 infections, and 34 accidents and abuse). RESULTS: All cases of accidents and abuse correctly tested negative. Among the others, 25 (6%) showed at least two abnormal findings. Of these, 14 closely matched the biochemical profiles seen in specific FAO disorders. These included 2 cases with medium-chain acyl-CoA dehydrogenase deficiency, 4 cases consistent with glutaric acidemia type 2, 4 cases with either very long-chain acylcoenzyme A dehydrogenase deficiency or long-chain 3-hydroxy-acyl-coenzyme A dehydrogenase deficiency, and 4 cases predicted to be affected with carnitine uptake defect. CONCLUSION: The results of this study support the view that approximately 5% of all cases of sudden infant death are likely caused by an FAO disorder.     

Hypoxanthine in vitreous humor and cerebrospinal fluid--a marker of postmortem interval and prolonged (vital) hypoxia? Remarks also on hypoxanthine in SIDS

Hypoxanthine (Hx) is a degradation product of adenosine. Increased concentrations were reported in cases of hypoxia as well as with prolonged postmortem interval (PMI). Hx is recommended as an indicator of prolonged (cerebral) hypoxia, for example in vitamins of sudden infant death as well as a new biochemical method for estimation of postmortem time. The correlation of vitreous Hx values with the time since death was reported to be even higher than the vitreous potassium (K+) values. The authors' investigations on 92 bodies with known time since death gave a completely opposite result: a much higher correlation between vitreous K+ and time since death than vitreous Hx. The possible discrepancies between these different results will be discussed (disturbing of intra-ocular fluid dynamics by repeated sample-taking in the study of Rognum et al. The results published so far on vitreous Hx values in sudden infant death syndrome (SIDS) cases as an indicator for a prolonged cerebral hypoxia are also not convincing. When vitreous concentrations of newborn infants or infants of age < 6 months are compared to those of older infants or adults the vitreous diameter must be taken into consideration (diffusion gradient; Fick's law of diffusion). The discrepant results on vitreous Hx as a measure of vital hypoxia and PMI will be discussed. The authors' results on Hx determinations on cerebrospinal fluid in comparison to cerebrospinal spinal (CSF) potassium will also be briefly addressed.     

Genetic counseling in a case of Takayasu arteritis

Two cases affected with Takayashu arteritis are presented. The adult probanda born in 1960 after genetic counselling and appropriate prenatal care had a healthy liveborn boy. Her previous six pregnancies were terminated on the basis of forced medical reason. The infant probanda died at the age of 4 months with the features of sudden infant death syndrome (SIDS). Pathohistological examination detected her Takayashu arteritis. It seems to be the youngest published case in the international literature and Takayashu arteritis may be the rare cause of SIDS.     

Travel and changes in routine do not increase the risk of sudden infant death syndrome

We investigated the relationship between travel and changes in routine and the sudden infant death syndrome (SIDS) among 485 SIDS cases compared with 1800 randomly selected control infants. There was no increased risk of SIDS with travel. Special events, such as christenings, were not associated with an increased risk of SIDS. However, visits to and by friends or relatives were associated with a significantly reduced risk of SIDS after controlling for potential confounders (odds ratios = 0.70; 95% confidence interval = 0.52, 0.96). These findings may indicate less social support in SIDS cases.     

Sudden deaths in yearling feedlot cattle

A survey of the causes for fatal diseases of yearling feedlot cattle was conducted on more than 407,000 cattle during a 14-month period. Of the 4,260 (1%) cattle that died during this period, 1,358 (32%) were categorized as cases of "sudden death syndrome." Of the 11 most frequent causes of the syndrome, as determined at necropsy, only 4--bloat, pulmonary aneurysms, riding injury, and hemopericardium--were considered as short-course problems and true causes of sudden death. The largest number of cases of sudden death were attributed to pneumonia (113 animals). Consequently, the sudden death syndrome is a misnomer for many long-course diseases and, in some instances, a mask for neglect because, as clinically used, the name frequently includes cattle that have been sick, often with pneumonia, for several days.     

Cocaine use in women from a defined population: prevalence at delivery and effects on growth in infants

Adverse health effects associated with intrauterine cocaine exposure (prematurity and its associated morbidity, intrauterine growth retardation, possible risk of sudden infant death syndrome) are based on studies from large urban hospitals, but few data exist from other sources. The current study, set in a community hospital, was designed to (1) estimate the prevalence of maternal cocaine use at delivery, (2) describe neonatal outcomes, and (3) evaluate physiological growth in exposed children. The study was conducted over 30 months (total births were 14,074) at The Children's Hospital of Greenville Memorial Hospital, the major source of neonatal care for Greenville County, South Carolina (1990 population: 320,000). A child was considered exposed to cocaine if there was documented evidence of use in the mother's medical record or if one member of the pair had a positive urine drug screen. Growth data were abstracted from clinical records. Overall prevalence of exposure was 1.0%. Of the 137 subjects (89, positive urine drug screen; 48 self-reported exposure), 21 (15%, 95% confidence interval, 9% to 21%) were premature (gestational age < 37 weeks) and 2 died of sudden infant death syndrome. Mean age- and sex-adjusted percentiles for weight, length, and head circumference increased from 23%, 29%, and 18%, respectively, at birth to 43%, 49%, and 54% in children followed for 12 months; however, 50% of the cohort were lost to follow-up, and these children were smaller at birth than those under active follow-up. Rates of prematurity and infant death were similar to those reported in urban hospitals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Minor inflammatory lesions and sudden infant death: cause, coincidence, or epiphenomena?

Minor inflammatory changes are often found in tissues of infants who die suddenly. Recently it has been proposed that these infiltrates signal significant underlying infectious disease and are responsible for death. Currently there is no unanimity about the percentage of cases in which inflammatory infiltrates occur and no international consensus in regard to the minimal criteria required for their diagnosis or their significance. We recommend that the presence of minor inflammatory infiltrates should not detract from the diagnosis of sudden infant death syndrome (SIDS) until further study has determined otherwise.     

Tritiated-naloxone binding to brainstem opioid receptors in the sudden infant death syndrome

The sudden infant death syndrome (SIDS) is defined as the sudden death of an infant under 1 year of age that remains unexplained after a thorough case investigation, including a complete autopsy. We hypothesized that SIDS is associated with altered 3H - naloxone binding to opioid receptors in brainstem nuclei related to respiratory and autonomic control. We analyzed 3H - naloxone binding in 21 regions in SIDS and control brainstems using quantitative tissue receptor autoradiography. Three groups were analyzed: SIDS (n = 45); acute controls (n = 14); and a chronic group with oxygenation disorders (n = 15). Opioid binding was heavily concentrated in the caudal nucleus of the solitary tract, nucleus parabrachialis medialis, spinal trigeminal nucleus, inferior olive, and interpeduncular nucleus in all cases analyzed (n = 74). The arcuate nucleus on the ventral medullary surface contained negligible binding in all cases (n = 74), and therefore binding was not measurable at this site. We found no significant differences among the three groups in the age-adjusted mean 3H - naloxone binding in 21 brainstem sites analyzed. The only differences we have found to date between SIDS and acute controls are decreases in 3H - quinuclidinyl benzilate binding to muscarinic cholinergic receptors and in 3H - kainate binding to kainate receptors in the arcuate nucleus in alternate sections of this same data set. The present study suggests that there is not a defect in opioid receptor binding in cardiorespiratory nuclei in SIDS brainstems.     

Parasomnias in infants below one-year old of age

INTRODUCTION: Certain sleep disorders which occur in children and adults show the same phenomena, although presentation, significance, cause and treatment are all different. However, there are some disorders which are only found in infancy, as in the four conditions which we review below. In spite of great variation between individuals, the general way in which the wakefulness-sleep states mature during the first months of life is well known. In general the physiological patterns of REM and NREM are in general the same in children as in adults. However, the pathological patterns are similar, but there are major differences between them. These differences are mainly physiological, behavioural, parent-child relationship and specific disorders. We shall see that the central alveolar hypoventilation syndrome of infants is not the same as that of adults. The sleep apnea syndrome of the newborn is different to the apneas seen in older children. Benign neonatal myoclonia of sleep are not present in adults, and finally the sudden death of an infant is not like the unexplained nocturnal sudden death or sinus arrest linked to paradoxical sleep in adults.     

Religion's role in adjustment to a negative life event: Coping with the loss of a child.

Parents (N?=?124) who had lost an infant to sudden infant death syndrome were interviewed 3 wks and 18 mo postloss. Two components of religion (religious participation and religious importance) were assessed, and their relations with 3 coping-process variables (perceived social support, cognitive processing of the loss, and finding meaning in the death) were examined. Greater religious participation was related to increased perception of social support and greater meaning found in the loss. Importance of religion was positively related to cognitive processing and finding meaning in the death. Furthermore, through these coping-process variables, religious participation and importance were indirectly related to greater well-being and less distress among parents 18 mo after their infants' deaths. Results suggest that further study of the social and cognitive aspects of religion would be profitable. (PsycINFO Database Record (c) 2010 APA, all rights reserved)