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Sudden unexpected infant death (SUID) is the leading cause of death for infants. Physician advice on safe sleep is an important source of information for families. We sought to evaluate the safe sleep knowledge, attitudes, and behaviors of physicians by distributing a cross-sectional survey at a freestanding children’s hospital. The survey included demographics, knowledge items, attitudinal assessment, and frequency of providing safe sleep guidance. Multivariable linear regression and logistic regression were used to evaluate associations between variables. 398 physicians were surveyed with 124 responses (31%). Females, those who received safe sleep training, and those who see infants in daily practice had higher knowledge scores. Physicians with higher knowledge scores had more positive attitudes toward safe sleep and provided safe sleep education to patients more often. Our study underlies the importance of education and repeated exposure in forming positive attitudes toward safe sleep recommendations and leads to increased provision of safe sleep guidance.

Objective Higher mortality among full-term infants (term infant deaths) contributes to disparities in infant mortality between the United States and other developed countries. We examined differences in the causes of term infant deaths across county poverty levels and urban–rural classification to understand underlying mechanisms through which these factors may act. Methods We linked period birth/infant death files for 2012-2015 with US Census poverty estimates and county urban–rural classifications. We grouped the causes of term infant deaths as sudden unexpected death in infancy (SUDI), congenital malformations, perinatal conditions, and all other causes. We computed the distribution and relative risk of overall and cause-specific term infant mortality rates (term IMRs) per 1000 live births and 95% CIs for county-level factors. Results The increase in term IMR across county poverty and urban–rural classification was mostly driven by an increase in the rate of SUDI. The relative risk of term infant deaths as a result of SUDI was 1.6 (95% CI, 1.5-1.8) times higher in medium-poverty counties and 2.3 (95% CI, 1.2-2.5) times higher in high-poverty counties than in low-poverty counties. Cause-specific IMRs of congenital malformations, perinatal conditions, and death from other causes did not differ by county poverty level. We found similar trends across county urban–rural classification. Sudden infant death syndrome was the main cause of SUDI across both county poverty levels and urban–rural classifications, followed by unknown causes and accidental suffocation and strangulation in bed. Conclusions Interventions aimed at reducing SUDI, particularly in high-poverty and rural areas, could have a major effect on reducing term IMR disparities between the United States and other developed countries.

Sudden infant death syndrome (SIDS; also known as crib death) describes the sudden unexpected death of an infant under one year of age, which remains unexplained after a thorough investigation. SIDS is a public health concern. It is the fourth leading cause of infant death in Canada. Newspapers are a major source of health information for the public, shape public perceptions and can direct the discussion around issues. Despite the potential influence of newspapers, no study has examined the portrayal of SIDS in Canadian newspapers over time. The purpose of our study was to gain an understanding of SIDS coverage in Canadian English language newspapers using the Canadian Newsstream database from 1970 to 2015 and the historical database: The Globe and Mail from 1844 to 1977. Generating descriptive quantitative and qualitative data, we noted a decline in SIDS coverage over time. Blame and misdiagnosis were two dominant themes in the coverage of SIDS with many other aspects around SIDS missing; for example, indigenous people, who are at higher risk for SIDS, were rarely mentioned. Our findings suggest problems in the content and frequency of coverage of SIDS that have the potential to shape the public understanding of SIDS.

We evaluated images in popular stock photography websites for adherence with American Academy of Pediatrics (AAP) guidelines for safe infant sleep practices. Three top stock photo websites were used to collect photographs generated from key phrases. All images depicting an infant sleep environment were analyzed for consistency with AAP guidelines. Descriptive statistics, chi-square and z test of proportions, were conducted. A total of 1233 of 1947 stock photographs showed sleeping infants on a flat surface. In all, 627 (50.8%) photographs showed the infant in the supine position and 79 (5%) of all infant sleep environments were adherent with AAP recommendations. Bedding inconsistent with safe sleep recommendations was identified in 1133 images (71.3%), with blankets noted in 49.5%. Images depicting sleeping infants on stock photography sites do not routinely adhere to AAP recommendations. Media messages inconsistent with health care messages create confusion and misinformation about infant sleep safety and may lead inadvertently to unsafe practices.

This study aimed to establish the number of deaths in infants under 1 year of age that were being reported for medico-legal examination at a single large academic centre in Hungary, as well as the method of these investigations with special emphasis on histopathology, ancillary techniques and the adherence of our current practice to international recommendations. A single-centre, retrospective audit was conducted on all suspected sudden infant death cases. After the review there were eight infectious background sudden infant death syndrome (SIDS) cases, infectious respiratory tract disease in 14 cases, cardiac septal tumour in one case, and hepatic, possibly metabolic, disorder in one case. Our study has highlighted that even in a single institution there is a huge heterogeneity of approaches which needs standardisation. A reclassification of infant cases according to the San Diego definition resulted in a decreased number of SIDS cases in our material. The San Diego definition and related international recommendations were found to be practical and the classification provides a guide to the standardisation of current practice.

Abnormal muscularization of acinar arteries is the hallmark of persistent pulmonary hypertension of newborn (PPHN), an uncommon disease with high rate of morbidity and mortality. PPHN presents with signs of respiratory distress immediately following birth. We herein report 2 cases presenting as a witnessed sudden unexpected death in the late neonatal period, preceded by respiratory deterioration and in whom the presence of abnormal muscularization of the acinar pulmonary arteries was reminiscent of PPHN. The significance of this report is twofold: to increase the awareness among pediatricians and pathologists of this feature that can present in some cases of Sudden Unexpected Death in Infancy/Sudden Infant Death Syndrome, and to highlight the importance of performing a thorough autopsy in order to identify the abnormality.

Sudden infant death syndrome (SIDS) is the leading cause of death among infants aged 1 to 12 months. The purpose of this study was to assess prenatal and postnatal physicians' knowledge about SIDS in a county with high rates of SIDS deaths. A cross-sectional survey was conducted of pediatricians, family practitioners, and obstetricians in Sedgwick County, Kansas. Most physicians reported correctly that there were effective measures to reduce SIDS. Most respondents agreed it was important to discuss SIDS with parents. Pediatricians were more likely than family practitioners and obstetricians to recognize that pacifier use is important for infants in their first year to reduce SIDS and 2 to 4 months is the age range for peak incidence of SIDS. Pediatricians, family practitioners, and obstetricians are knowledgeable about SIDS and SIDS risk reduction. However, they are not allocating adequate time for discussing SIDS and SIDS reduction efforts with patients.

Nicotinic acetylcholine receptors (nAChRs) are cationic channels of the neuronal cell membrane, differentially expressed in the central nervous system which, when activated by endogenous acetylcholine or exogenous nicotine, are able to enhance cholinergic transmission. The aim of this study was to investigate in human perinatal age the immunohistochemical expression of the α7-nAChR subtype, given its involvement in neuronal differentiation and its significant vulnerability to the toxic effects of nicotine. Thirty fetuses (with a gestational age between 25 and 40 weeks) and 35 infants (1-6 months old), suddenly died of known (controls) and unknown causes (unexplained deaths), with smoking and nonsmoking mothers, were included in this study. A negative or low immunoexpression of α7-nAChRs, indicative of their inactivation, was observed in the granular layers of the cerebellar cortex in 66% of the sudden unexplained perinatal deaths and 11% of the controls. A high correlation was also observed between these findings and maternal smoking. Apart from the well-known adverse effects of nicotine exposure during pregnancy, it may also cause significant alterations in cerebellar cholinergic transmission in areas of the brain involved in vital functions. These events may give us insights into the pathogenetic mechanisms leading to sudden unexplained fetal and infant death.

We evaluated a comprehensive hospital-based infant safe sleep education program on parental education and safe sleep behaviors in the home using a cross-sectional survey of new parents at hospital discharge (HD) and 4-month follow-up (F/U). Knowledge and practices of infant safe sleep were compared to the National Infant Sleep Position Study benchmark. There were 1092 HD and 490 F/U surveys. Supine sleep knowledge was 99.8% at HD; 94.8% of families planned to always use this position. At F/U, 97.3% retained supine knowledge, and 84.9% maintained this position exclusively ( P < .01). Knowledge of crib as safest surface was 99.8% at HD and 99.5% F/U. Use in the parents’ room fell to 91.9% (HD) and 68.2% (F/U). Compared to the National Infant Sleep Position Study, the F/U group was more likely to use supine positioning and a bassinette or crib. Reinforcing the infant sleep safety message through intensive hospital-based education improves parental compliance with sudden infant death syndrome risk reduction guidelines.

Early and prolonged skin-to-skin contact (SSC) after birth between a mother and her newborn has been shown to generate beneficial effects on the mother-infant relationship and breastfeeding. Close mother-infant body contact immediately after birth positively enhances exclusive breastfeeding during the hospital stay, with a dose-response relationship. Skin-to-skin contact may ease the infant’s transition to extra-uterine life and helps regulate the infant’s body temperature and nursing behavior. However, reports of sudden unexpected postnatal collapse (SUPC) soon after birth, in healthy term neonates, in association with SSC, have raised concerns about the safety of this practice. Based on available evidence, we developed a surveillance protocol in the delivery room and postnatal ward of the Institute for Maternal and Child Health of Trieste (Italy). The aim of our protocol is (a) to promote safe mother and infant bonding and (b) to establish successful breastfeeding, without increasing the risk of SUPC. As there is no known effective intervention to prevent SUPC, our protocol has been conceived as a potential best practice.

Working hypothesis: benign febrile seizures seen in 7% of infants before 6 months play a role in the terminal pathway in a subset of sudden infant death syndrome victims. Supporting evidence: (1) lack of 5-hydroxitryptamine, one consistent finding in sudden infant death syndrome that Kinney et al coined a developmental serotonopathy, is consistent with risk for seizures. (2) Non–rapid eye movement sleep increasing during the age of highest risk for sudden infant death syndrome facilitates some seizures (seizure gate). (3) Sudden unexpected death in epilepsy is associated with severe hypoxemia and hypercapnia during postictal generalized electroencephalographic (EEG) suppression. In toddlers, sudden unexplained deaths are associated with hippocampal abnormalities and some seizures. (4) The sudden nature of both deaths warrants an exploration of similarities in the terminal pathway. Moreover, sudden infant death syndrome, febrile seizures, sudden unexplained death in childhood, and sudden unexpected death in epilepsy share some of the following risk factors: prone sleeping, infections, hyperthermia, preterm birth, male gender, maternal smoking, and mutations in genes that regulate sodium channels. State-of-the-art molecular studies can be exploited to test this hypothesis.

The investigation of infant death is complex and requires synergy between multiple agencies including law enforcement, Child Protective Services, medicolegal death investigators, and forensic pathologists. Prior to the forensic pediatric autopsy, the death investigator must identify the types of death scenes involved (e.g., hospital, residence, daycare) and document the details of the scene. Interviews must be conducted with the caregivers and other family members (including doll reenactments), law enforcement, pediatricians, and emergency medical personnel. The forensic pathologist must be able to conduct a comprehensive pediatric forensic autopsy and be aware of the specific challenges related to cases of sudden unexpected infant deaths. This article provides an overview of infant death investigation, discussing the roles and responsibilities of the medicolegal death investigator and the forensic pathologist.

The organ weights in cases of sudden infant death syndrome (SIDS) and undetermined deaths in previously healthy infants do not correspond to “the normal range” of organ weights in international standard charts for infants currently in use in some institutions. The aim of our study was to ascertain the organ weights of infants dying suddenly and unexpectedly in England and for whom a cause of death was not found, therefore falling under the category of SIDS or undetermined. We collated the organs weights from 2 institutions covering between them the South East and North of England including London, Yorkshire, and Derbyshire. The cases from The Royal London Hospital were autopsied between 1997 and 2013, and the cases from Sheffield Children's Hospital were autopsied between 2006 and 2013. There were 188 babies who had been born at term (62 female and 126 male) and 26 ex-premature babies (15 female and 11 male). Organs of male babies were slightly heavier than those of female babies but as there was no significant differences male and female babies were considered together. Comparison with standard charts (from 1932 and 1962) and with more recent charts confirmed the discrepancy between the older charts commonly in use with more recent measurements, including ours. The main reason for these differences is that babies in the recent charts were previously healthy babies with no long term disease and improved in the health of the population.

Congenital diaphragmatic hernia is a congenital malformation of the diaphragm, resulting in the herniation of the abdominal organs into the thoracic cavity. The most common types of congenital diaphragmatic hernia are Bochdalek hernia (postero-lateral hernia), Morgagni hernia (anterior defect), and diaphragm eventration (abnormal displacement of part or all of an otherwise intact diaphragm into the chest cavity). Congenital diaphragmatic hernia is a life-threatening pathology in infants, and a major cause of death due to pulmonary hypoplasia and pulmonary hypertension. We present a fatal case of congenital diaphragmatic hernia in a newborn. At the autopsy, a central defect of the diaphragm was found, 8 × 5 cm in size, that led to a herniation of the small intestine, the right lobe of the liver, and the right adrenal gland into the thorax. An esophageal atresia was associated with the congenital diaphragmatic hernia. The lungs showed severe hypoplasia and atelectasia. Physicians should pay attention to a prenatal diagnosis of congenital diaphragmatic hernia in order to prevent newborn fatalities.

Our primary objective was to compare parents of infants cared for in newborn intensive care units (NICUs) and infants cared for in well-baby (“general”) nurseries with regard to knowledge and practice of safe sleep practices/sudden infant death syndrome risk reduction measures and guidelines. Our secondary objective was to obtain qualitative data regarding reasons for noncompliance in both populations. Sixty participants (30 from each population) completed our survey measuring safe sleep knowledge and practice. Parents of NICU infants reported using 2 safe sleep practices—( a) always placing baby in crib to sleep and ( b) always placing baby on back to sleep—significantly more frequently than parents of well infants. Additional findings and implications for future studies are discussed.

Objective. Following the “Back to Sleep” campaign, deaths from sudden infant death syndrome (SIDS) were reduced. However, SIDS and sleep-related deaths continue to occur. Studies demonstrate that modeling by health care workers influences parents to place infants supine for sleep. Recently, additional emphasis has been placed on environment. The purpose of this study was to improve sleep position and environment in the hospital. Methods. A Plan-Do-Study-Act cycle was initiated. Sleeping infants were observed at baseline. A bundled intervention was implemented; infants were again observed. Parents were surveyed. Results. At baseline, 25% (36/144) of sleeping infants were safe; the majority of unsafe sleep was a result of environment. Postintervention, significantly more (58%; 145/249) had safe sleep ( P < .0001). Most parents planned to use the supine position (95%; 96/101); none planned to cosleep. Many intended to adjust their infants’ home sleep environment. Conclusion. Using a multifaceted approach significantly improved infant safe sleep practice in the hospital setting.

We sought to (1) determine if there is an increased prevalence of vitamin D deficiency (VDD) in cases of sudden death in infancy and childhood; (2) establish whether there is a link between VDD and infection; and (3) assess if the level of vitamin D can be related to abnormalities in the skeletal survey and rib histology in our cohort. The postmortem reports of cases in which vitamin D levels were measured in 2009 and 2010 were retrieved. When parental consent for audit had been granted, rib histology and skeletal surveys were reviewed. Plasma 25-hydroxyvitamin D levels were measured in 41 postmortem cases. Ten (24.5%) had adequate levels, 5 (12%) had suboptimal levels, 16 (39%) had moderate deficiency, and 10 (24.5%) had severe deficiency. We had only 4 cases with VDD and infection. There were 25 cases of unexplained death in our cohort, and 76% of these had inadequate vitamin D levels. The rib histology was abnormal in 69% of cases that had inadequate vitamin D levels, while the radiology was abnormal in 19% of cases. A significant proportion of infants and children who died suddenly and unexpectedly had inadequate levels of vitamin D. We were unable to confirm or exclude an association between VDD and infection due to the small number of cases with confirmed infection. Further multicenter studies are needed to confirm our findings and explore possible associations between VDD and other known risk factors for sudden unexplaineddeath in infancy and childhood.

The peak age at which sudden infant death syndrome (SIDS) occurs corresponds to the developmental period in which infants are dependent on their innate responses to infection. There is a growing body of evidence indicating that dysregulation of inflammatory responses might contribute to the physiological changes leading to these sudden deaths. This study examined the effects of three important risk factors for SIDS on inflammatory responses: cigarette smoke, virus infection and male sex. Cytokine responses of peripheral monocytic blood cells of healthy, non-smoking males and females to endotoxin were measured. Surrogates for virus infection or cigarette smoke were assessed using IFN-γ or water-soluble cigarette smoke extract (CSE). For most conditions, cells from males had lower pro-inflammatory cytokine responses than those of females. An opposite trend was observed for IL-10. Significantly lower levels of some cytokines were noted for cells from male donors exposed to CSE. In females, there were significant correlations between testosterone levels and levels of pro-inflammatory cytokines, but none for males. Testosterone levels in females correspond to those among male infants in the age range at greatest risk of SIDS. The effects of the testosterone surge in male infants need to be examined in relation to changes in cortisol levels that occur during the same period of infant development.

Congenital diaphragmatic hernia (CDH) presenting beyond the neonatal period is commonly perceived to be rare. With reported frequencies of 2.6% to 20% of all CDH, it may be an overlooked cause of mortality. Variable symptomatology makes its diagnosis challenging. We report the sudden death of a 3-month-old patient shortly after hospital discharge following congenital heart surgery. Autopsy findings associated the patient’s demise with migrated abdominal contents in the chest through a Bochdalek hernia defect. No indications of CDH existed before hospital discharge. Relevant issues pertaining to congenital heart disease, CDH, and importance of autopsy in this context are discussed.

Truncus arteriosus is a rare congenital heart defect characterized by a single common arterial trunk giving rise to both the pulmonary and systemic arteries. Concurrent cardiac abnormalities are common. In the absence of surgical intervention, the condition is associated with extremely high infant mortality, with the mechanism of death being either arrhythmia or congestive heart failure. We report the case of a previously healthy and reportedly normal two-week-old infant who was found dead in his crib. At autopsy he was found to have truncus arteriosus communis persistens, a rare subtype of truncus arteriosus with associated valve atresia and left ventricular hypoplasia. This case highlights that forensic pathologists may encounter severe cardiac malformations in previously normal infants, and the necessity for thorough evaluation and accurate diagnoses.

Abnormal muscularization of intra acinar pulmonary arteries is a histological hallmark of persistent pulmonary hypertension of newborn (PPHN), an uncommon disease with high morbidity and mortality. PPHN presents with signs of respiratory distress immediately following birth. The disease is multi-factorial in origin and can be idiopathic as well associated with a variety of conditions such as congenital heart disease and both congenital and acquired lung diseases. We report two cases presenting as sudden unexpected death in late neonatal period (SUDI) showing abnormal muscularization of acinar pulmonary arteries reminiscent of PPHN. The significance of this report is twofold; to increase the awareness amongst pediatricians and pathologists of this feature not previously described in SUDI/Sudden Infant Death Syndrome (SIDS) and to highlight the importance of performing a thorough autopsy in order to identify the diagnosis.

The purpose of this study was to examine the infant bed-sharing practices of mothers from the birth of the infant to three months of age. The study was a longitudinal descriptive design using a self-report instrument immediately after delivery with follow-up phone interviews at one and three months after discharge. While no mothers intended to bed-share with their infants immediately after delivery, 60 percent reported bed-sharing at some time at one month after discharge and 9 percent at three months. Only 19 percent of mothers reported receiving information about infant sleeping practices from their physician and 22 percent from their nurse. One month post discharge was identified as a high-risk period for infant bed-sharing. Interventions aimed at teaching new mothers about responding to infant cues and ways to manage a fussy infant may minimize the rate of bed-sharing.

We present 4 cases of sudden infant death in which we believe that gastroesophageal reflux (GOR) was a contributory, if not a causative, factor. Two of our patients had documented GOR reflux disease during life, and all 4 cases showed histologic evidence of GOR. No other cause of death was identified in any of the patients. Gastroesophageal reflux can cause sudden death in a vulnerable infant during a critical period of development through failure of “autoresuscitation” mechanisms.

Simultaneous sudden infant death syndrome (SSIDS) is death of both twins within 24 hours which is compatible with the sudden infant death syndrome criteria and death is independent of each other. A pair of twin babies, approximately two months old, was found dead in the supine position in bed by their mother. After scene, autopsy, toxicological and histopathological investigations, specific cause of death could not be found. There were 41 pairs of twin babies with SSIDS reported in the literature between 1900 and 1998. This is the second case report from Turkey.

We studied the dialogue between telephone operators at medical emergency communication centres in Norway and parents of children later diagnosed with sudden infant death syndrome. The aim was to understand how the parents experienced the communication with the telephone operators. The qualitative method involved semi-structured interviews. We interviewed six respondents from urban areas and five from rural areas. An important finding was that all the parents were satisfied with the resuscitation instructions they received. It was also perceived as important that the emergency operators expressed empathy and care. We believe that it is not merely the quality of the resuscitation attempts that the operators' efforts should be measured against. It is also important that the operators provide good explanations and express emotional support. Our findings indicate that this will be enormously appreciated, even if callers do not feel that they are capable of performing optimum resuscitation.

This study compared pathological findings from a neonatal rat model of sudden death with those from 40 sudden infant death syndrome (SIDS) infants collected at autopsy. In the rat model, influenza A virus was administered intranasally on postnatal day 10, and on day 12 a sublethal, intraperitoneal dose of Escherichia coli endotoxin; mortality was 80%. Tissue samples from the animals and infants were fixed in formaldehyde, embedded in paraffin, and sections stained with hematoxylin and eosin. Tissues from the SIDS specimens were additionally cultured for bacteria and viruses; post-mortem blood samples were evaluated for signs of inflammation. All sections were examined by a pediatric forensic pathologist familiar with SIDS pathology. Comparisons between the rat model and the human SIDS cases revealed that both exhibited gross and microscopic pathology related to organ shock, possibly associated with the presence of endotoxin. Uncompensated shock appeared to be a likely factor that caused death in both infants and rat pups. Response to a shock-inducing event might have played an important role in the events leading to death. The similarities between the neonatal rats and the human cases indicate that further research with the model might elucidate additional aspects of SIDS pathology.

Richard Nobles and David Schiff revisit the Sally Clark case and consider the presentation by non-statisticians of statistical evidence in court.

The potential diagnostic significance of prior family referral to Child Protective Services (CPS) in cases of sudden infant death is unknown. Therefore, the authors retrospectively searched for CPS data for the 5-year referral history on all 533 families whose infants died suddenly from Sudden Infant Death Syndrome (SIDS), other natural diseases, accidents, or inflicted injuries and underwent postmortem examination by the medical examiner during a 10-year period. No family had more than one infant death. At least 27% of the families in each group had at least one CPS referral. The data suggest that a family's referral to CPS prior to their sudden death of their infant does not increase the likelihood that it was caused by inflicted injuries, and prior referral should not preclude a diagnosis of SIDS. The authors recommend future prospective studies that include refined exposure histories and that are large enough to have sufficient statistical power to compare family CPS referrals and outcomes in groups of infants who died suddenly with a matched group of living infants.

Pulmonary intra-alveolar siderophages (PS) have been suggested as a marker of previous attempts at imposed suffocation in infants dying suddenly and unexpectedly. The aims of this study were to (1) compare PS counts between cases of sudden infant death syndrome (SIDS) and a control group comprised of infants whose deaths were attributed to accidental or inflicted suffocation, (2) compare clinical variables in SIDS and control suffocation cases, and (3) review individual cases irrespective of the cause and manner of death with an average PS count greater than 200 per 20 high-power fields (hpf) per lung lobe. Retrospective assessment of siderophages in available iron-stained lung sections was undertaken in 91 SIDS cases and 29 cases of death due to suffocation (27 accidents and 2 homicides) from the San Diego SIDS and Sudden Unexplained Death in Childhood (SUDC) Research Project (SDSSRP) database. Neither the means of the log-transformed PS counts nor the medians of the raw PS counts were significantly different between the SIDS and control suffocation groups. The distributions of the PS data were different, however—the range was wider in the SIDS group. Only 6% of each group had a history of prior apparent life-threatening events. Approximately three fourths of the families from both groups had no prior referral to Child Protective Services. The number of PS varies widely in cases of sudden infant death caused by SIDS and accidental or inflicted suffocation and cannot be used as an independent variable to ascertain past attempts at suffocation.

The investigation of sudden death of infants varies, and death rates may depend on local practices of death certification. We studied the extent of the investigation and the final cause of death (COD) in 3 regions: New York, New York, USA (NY); King County, Washington, USA (KC); and Montevideo, Uruguay (MU). We conducted a retrospective review of 543 cases (NY 258, KC 56, MU 229) of previously healthy babies who died suddenly without obvious trauma, at ages 0 to 12 months, over a 3-year period (1998 to 2001). All cases included a complete autopsy and histologic examination. Cases were assessed for completion of special studies (including radiographs, photos, toxicology and metabolic sampling, cultures, and vitreous humor chemistry), measurements, and scene investigation. Specialized pediatric measurements and testing were done less often than routine procedures, and were done less often in cases overall compared with cases certified as sudden infant death syndrome (SIDS). Fifty-five percent of SIDS cases in NYC and 12% of SIDS cases in KC had no scene investigation. Manhattan had a complete workup in 42% of SIDS cases, whereas the remaining sites had fewer that 15% of cases completely worked up. The most common non-natural COD was suffocation at all 3 sites. The overall most common COD were respiratory infection in MU (22%) and SIDS in NY (45%) and KC (86%). We conclude that the sudden death of infants requires special consideration and still lacks consistency. SIDS investigations are not done completely in all cases and rates may depend on regional differences in certifying infant deaths.

A 26-day-old male infant who had been fussy and feeding poorly for a period of several hours died suddenly despite efforts at resuscitation. Postmortem examination revealed eosinophilic endomyocarditis unassociated with disease in other organs. The etiology remained unexplained after review of the medical and family histories and circumstances of death, extensive light and immunofluorescence microscopies, and microbiological, metabolic, and toxicologic testing. This appears to be the youngest reported case of eosinophilic endomyocarditis, a disorder that typically occurs in middle-age males and is often associated with benign or malignant hypereosinophilic conditions. The medical literature is reviewed.

Deposits of hemosiderin are found frequently in the interstitium of the lungs of infants who die suddenly and have been a suggested marker for hypoxia during previous episodes of apnea. We studied the epidemiology of pulmonary interstitial hemosiderin (PIH) in 94 infants with a diagnosis of the sudden infant death syndrome that was established during the New Zealand Cot Death Study. Twenty-seven infants (29%) had widely distributed PIH. Associations were sought between PIH and variables on which information had been obtained from parental interviews or from medical records. Previous suggestions of associations with increasing birth weight and decreasing age at death were confirmed in multivariate analysis ( P = 0.0018 and P = 0.03, respectively) and with increasing gestation in univariate analysis ( P < 0.0001). PIH was not found in any of the 13 infants delivered by elective cesarean section compared with a 33% incidence in those exposed to labor ( P = 0.02). There was no association with previous apnea. We consider that the likely explanation of these findings is that PIH is a residue of interstitial hemorrhage caused by chest compression during labor that occurs particularly in larger infants of greater gestational age and then clears gradually during early infancy.

A wandering or ectopic spleen, a rare congenital condition caused by improper fixation of the ligamentous attachments, was identified during a postmortem examination of a 10-month-old female who had died of Streptococcus pneumoniae sepsis. The wandering spleen was autoinfarcted and adherent to the left hepatic lobe, with resultant functional hyposplenism.

Inherited metabolic disorders account for a small but significant number of sudden unexplained deaths in neonates, infants and occasionally older children. In particular, inherited disorders of fatty acid oxidation may closely mimic sudden infant death syndrome. Post-mortem investigations offer the final opportunity to establish a diagnosis. Such diagnoses are of great importance to the families concerned and provide the opportunity for genetic counselling and antenatal diagnosis. Current advances in technology, particularly in the case of electrospray ionization tandem mass spectrometry, have revolutionized the investigation of metabolic disease at post-mortem, facilitating the identification of a wide range of metabolic diseases in tiny samples of blood, plasma and bile. Such analyses may provide vital clues to diagnosis, usually in the form of acylcarnitine profiles. Accurate diagnosis relies on the timely collection of appropriate samples and the subsequent selection of informative testing. In order to maximize the chances of a diagnosis, a collaborative approach between the various disciplines is vital. A brief description of the more frequently encountered inherited disorders, collection and processing of appropriate samples and available investigations that may lead to accurate diagnosis are clearly described.

The World Health Organization (WHO) reports that nonsmokers experience disease and death due to secondhand smoke (SHS) exposure in the home. We estimated the total excess burden and costs to society due to SHS exposure in U.S. public housing.We quantified the public health burden for outcomes causally related to SHS exposure for nationally representative never-smoking residents in U.S. public housing using (1) WHO-recommended health outcomes and methodology, (2) publicly available and other large databases, and (3) published estimates of morbidity and mortality rates. We used published estimates of direct medical and nonmedical care costs and the value of productivity losses to estimate SHS-related societal costs for disease and death. We estimated the public health and economic burden for two serum cotinine limits of detection (LODs): 0.05 nanograms per milliliter (ng/mL) and 0.015 ng/mL.In 2011, an estimated 37,791 never-smoking child and adult U.S. public housing residents experienced illness and death due to SHS exposure at home based on an LOD=0.05 ng/mL (50,967 residents at LOD=0.015 ng/mL). Costs incurred by society for these illnesses and deaths totaled $183 million (LOD=0.05 ng/mL) and $267 million (LOD=0.015 ng/mL) annually. Of the total costs, direct costs (medical and nonmedical) accounted for $128 million and $176 million for LOD=0.05 ng/mL and LOD=0.015 ng/mL, respectively. Medical care accounted for the majority of direct costs-$110 million at LOD=0.05 ng/mL and $153 million at LOD=0.015 ng/mL. Adverse respiratory health outcomes accounted for approximately one-half (56% at LOD=0.05 ng/mL and 52% at LOD=0.015 ng/mL) of total societal costs.Implementing smoke-free policies in all U.S. public housing could save lives and decrease SHS-related morbidity and mortality in never-smoking residents, resulting in annual societal savings of $183 million at LOD=0.05 ng/mL and $267 million at LOD=0.015 ng/mL.

Studies in various settings reveal that a significant percentage of autopsies demonstrate findings that were not previously clinically diagnosed. In the pediatric and adolescent age group, forensic examinations comprise a large percentage of total autopsies performed. We hypothesized that a similar number of previously undiagnosed findings would be present in this population and thus reviewed a series of autopsy reports from the Medical Examiners Office in the Arkansas Crime Laboratory. During 1997 through 1999, we performed 439 complete forensic autopsies on children and adolescents (age range 1 day to 19 years; median 18 months). Previously undiagnosed lesions were found in 173 (39%). Of these subjects, 68 (39%) had clinically significant pathology, 60 (35%) had insignificant pathology, and 45 (26%) had pathology of undetermined significance. Thirty-six subjects had lesions expected from a previously diagnosed condition. Of the total number of lesions found, 168 were inflammatory, 58 were congenital anomalies (48 unexpected), and 88 comprised miscellaneous other conditions. Infants < 6 months of age were significantly more likely to have a previously undiagnosed lesion than children > 6 months ( P < 0.0001). Previously undiagnosed findings, mostly inflammatory, occur relatively frequently in pediatric and adolescent forensic autopsies and are more likely to occur in infants.

The past decade and a half has seen marked changes in the epidemiology of sudden infant death syndrome (SIDS). The avoidance of certain risk factors such as sleeping prone and cigarette smoke exposure has resulted in the death rate falling dramatically. Careful evaluation of environmental factors and endogenous characteristics has led to a greater understanding of the complexities of the syndrome. The development and implementation of death scene and autopsy protocols has led to standardization in approaches to unexpected infant deaths with increasing diagnoses of accidental asphyxia. Despite these advances, there is still confusion surrounding the diagnosis, with deaths being attributed to SIDS in many communities and countries where death scene investigations and autopsies have not been conducted. The following review provides a brief overview of the historical background, epidemiology, pathology, and pathogenesis of SIDS. Contentious issues concerning the diagnosis and current problems are discussed. Despite calls to abandon the designation, SIDS remains a viable term for infants who die in their sleep with no evidence of accident, inflicted injury, or organic disease after a full investigation has been conducted according to standard guidelines.

Sudden Infant Death Syndrome (SIDS) is the most common cause of death in children between 1 and 6 months of age. Recent data suggest that a prolonged QTc interval on the 12-lead electrocardiogram (ECG) is associated with SIDS. Prone body position during sleep is also known to be a risk factor for SIDS; this has prompted the American Academy of Pediatrics to promote the "Back to Sleep" campaign. We postulated that the QTc interval in infants might change as a function of body position, linking the observations relating body position and QTc interval to SIDS. We recorded ECGs in a group of infants in both the supine and prone position to determine if the QTc interval and QT dispersion differ between the 2 positions. Forty-seven standard 12-lead EGGs and high-amplitude, rapid-sweep 12-lead EGGs were performed on 45 healthy infants (mean age 26 +/- 40 days) in both the supine and prone positions. The infants were asleep in a quiet, restful state. The ECGs were reviewed by 2 investigators blinded to the position of the infants during recording. Measurements included the average QTc interval (using Bazett's correction) and QT dispersion (the difference between the longest and the shortest QT intervals on a standard 12-lead EKG). The study was designed to detect a 3% difference in QTc interval with 80% power and alpha = 0.05. All subjects had telephone or clinical follow-up at 1 year. The average QTc interval was 403 +/- 20 milliseconds (msec) in the supine position and 405 +/- 27 msec in the prone position (p = NS). The QT dispersion was 20 +/- 12 msec in the supine position and 22 +/- 13 msec in the prone position (p = NS). One infant in the study group died of SIDS at the age of 3 months. The EGG of this patient revealed a QTc interval of 382 msec in the supine position and 407 msec in the prone position; the QT dispersion was 34 msec in the supine position and 34 msec in the prone position. We found no difference in QTc interval or QT dispersion as a function of body position in healthy infants resting quietly. Prolongation of the QTc interval is unlikely to explain the increased risk for SIDS associated with prone body position in the general population of healthy infants, unless patients with long QT syndrome are somehow more influenced by body position than normal patients are.

Increased relative medial thickness (RMT) of smooth muscle in small pulmonary arteries, peripheral extension of smooth muscle into the alveolar wall arteries, and right ventricular hypertrophy (RVH), in response to purported prolonged hypoxia, have been reported in sudden infant death syndrome (SIDS). Prone sleep position, an important risk factor for SIDS, predisposes infants to hypoxia from airway obstruction or rebreathing. Since publication of the earlier pulmonary artery studies, the SIDS definition has been expanded, and sudden infant death investigational protocols have been implemented. Our aims in this study were to (1) compare RMT in preacinar arteries (PA), intra-acinar arteries accompanying small airways (SIA), and alveolar wall arteries (AW) in SIDS infants and controls; (2) correlate RMT with postmortem variables; (3) determine if peripheral extension occurred more often in SIDS infants than in controls; and (4) determine if RVH occurred in SIDS. Movat-stained sections from standardized tissue blocks taken prospectively from the apex of the right upper lobe from 88 SIDS cases and 17 controls were evaluated using a computer-assisted digitizing system with images obtained from a microscope with an attached video camera. When adjusted for age, the RMT values for the SIA arteries were significantly greater in controls, while the PA and AW arteries were not statistically different between the SIDS cases and controls. Peripheral medial smooth muscle extension did not differ between the groups, and RVH was not seen in SIDS cases. Given the recent identification of brain stem abnormalities interfering with protective cardiorespiratory responses against acute life-threatening hypoxia perhaps precipitated by prone sleeping, our data suggest that SIDS is an acute event not preceded by recurrent or prolonged apnea and hypoxia.

This article combines a philosophical critique of the idea that public health nurses are primary technicians who neutrally hand over scientifically established facts on risks to the public and an empirical analysis of the actual work of public health nurses. It is argued that the relationship between facts and values in public health is complex and that, despite the introduction of several scientifically-based standards and guidelines, public health nurses are not technicians. They do moral work and experience ethical dilemmas. To get a grip on the specific character of this moral work, we distance ourselves from the idea that there are ethical dilemmas in public health nursing for which we can provide general ethical rules and principles. Instead we suggest a contextual ethical approach, in which several different kinds of consideration may be important. To illustrate this, we analysed 15 in-depth interviews with nurses involved in the prevention of cot deaths in the Netherlands. It is shown that these nurses do not neutrally pass on the epidemiological facts on the risks of prone sleeping, warm bedclothes and passive smoking, but they are the moral architects of this preventive practice. It is also shown that this moral work and the ethical dilemmas they experience cannot be characterized in terms of general ethical rules and principles. It becomes clear that the moral work of nurses differs according to the three main risks at stake: the balance between virtue, risk taking and responsibility depends on the specific context.

Forensic evidence is often given in terms of a mathematical probability. However, it is easy to make a particular type of error, ‘the prosecutor's fallacy’, in the interpretation of such probability. This paper highlights the source of this error and briefly introduces Bayes Theorem as the correct theoretical basis for interpreting such evidence. The first Californian legal case in which this error was committed is discussed, followed by all cases in the UK in which this error was highlighted and rectified by the Court of Appeal. It is important for all parties concerned — expert witnesses, lawyers and judges — to understand these principles correctly. Furthermore, the criminal courts face dilemmas when juries are involved. This paper concludes by discussing recent guidance from the Court of Appeal on how such evidence should be presented to the jury and the implications of this guidance.

Using a cohort study of all deaths in infants under 12 months in Dundee bom between 1882–91 we set out to compare the aetiology of sudden unexpected infant deaths in Dundee at the end of the 19th Century with the aetiology of present day Sudden Infant Death Syndrome (SIDS). During. 1882–1891, 361 infants died suddenly and unexpectedly and without obvious cause while in bed with their parents. The sex ratio of deaths was even (0.51 male) whereas the typical male fraction of SIDS today is 0.61. The mean age at death was almost two and one-half weeks younger in the Dundee cohort than for SIDS in modern Scotland. The infants in the Dundee cohort were discovered more frequently early in the morning than is typical. Their social class distribution was different in that no overlying cases were found in the higher classes whereas SIDS affects all classes. The overlying rate for illegitimate infants was lower than that reported for SIDS today. The epidemiological characteristics of the Dundee cohort and of those dying from present day SIDS differ considerably. The Dundee cohort apparently died from overlying rather than from SIDS as it is classified today. Present day advice that co-sleeping is safe should be given more cautiously until the safety of co-sleeping is resolved. It might be prudent to inform parents that co-sleeping is a risk factor for SIDS and that it should therefore be avoided.

Sudden infant death syndrome is the leading cause of death in infants in the United States. The laryngeal chemoreflex (LCR) is thought to contribute to its pathogenesis. In adult animals, increasing levels of intralaryngeal CO2result in a decrease in ventilatory activity. Intravenous acetazolamide (AZ) abolishes this response. The purpose of this study was to determine the effects of intralaryngeal CO2and AZ on the LCR and respiratory physiology of piglets under normoxic and hypoxic conditions. We applied 0% or 10% CO2in a randomized order to the larynx of 26 piglets. Intubation via tracheotomy prevented inhalation of the gas mixtures. Laryngeal stimulation was performed under normoxic conditions (Pao2 of >70 mm Hg) in 15 animals and under hypoxic conditions (Pao2 of 50 to 65 mm Hg) in 11 animals both with and without intravenous AZ (5 mg/kg). Respiratory and cardiovascular response data were recorded. Ten percent intralaryngeal CO2has no significant effect on mean baseline respiratory rate, systemic Paco2 or Pao2 levels, or apnea duration (p > .05). The use of AZ (versus no AZ) resulted in significantly higher baseline respiratory rates (64 versus 51 breaths per minute; p = .016), a decreased baseline systemic Paco2 level (38.8 versus 45.9 mm Hg; p < .001), a higher baseline Pao2 level (97.9 versus 82.8 mm Hg; p < .001), shorter mean apnea durations (15.5 versus 24.8 seconds; p = .001), a higher lowest O2saturation level after the stimulus (78.0% versus 68.4%;p = .003), and fewer profound apneas (10 of 90 versus 41 of 90 trials; p < .001). We conclude that 10% intralaryngeal CO2does not decrease ventilatory activity in piglets and has no significant effect on the LCR. Acetazolamide, however, appears to have a protective effect against the LCR, resulting in shorter and less severe apneas. The protective effect of AZ against the LCR appears to be related to its ability to stimulate the respiratory drive and increase oxygenation at baseline.

In victims of sudden infant death syndrome (SIDS), renal development has been reported to be significantly impaired. In the present study, we used stereological techniques to estimate volume of kidney cortex and total number of glomeruli in a group of human infants. Infants were classified according to cause of death—SIDS or non-SIDS. Cases were further subdivided according to birth weight—normal birth weight (NBW) or low birth weight (LBW) (we were unable to identify any non-SIDS LBW infants for our study). No significant differences were found between NBW and LBW infants (irrespective of cause of death) for cortical volume, glomerular density, or total glomerular number ( p > 0.140). Kidney cortical volume, glomerular density, and total glomerular number were not significantly different between SIDS and non-SIDS infants (p > 0.510). Glomerular number was only significantly less in SIDS infants of LBW (p = 0.032) than in controls according to the Wilcoxon rank sum test; using the Kruskal-Wallis for one-way analysis, no significant difference was found (p > 0.010). These results contrast with those from previous studies, as a reduction in glomerular number was not noted in SIDS NBW infants, and the mean value for the control (non-SIDS NBW) group was significantly reduced ( p < 0.01) from those of previous studies. This indicates that glomerular number reduction is seen in SIDS NBW and non-SIDS NBW cases and is therefore directly associated with growth retardation rather than with SIDS.