Hemosiderin findings in the liver, spleen and lung in newborn infants and infants

The content and distribution of hemosiderin in the liver, spleen and lungs of stillborn children, newborns and infants were determined histologically by Perl's method (Prussian blue reaction). We describe a study of 59 deaths up to the age of 2 years. The hemosiderin content depends on age and decreases with increasing age. No relevant differences were found in cases of sudden infant death syndrome (SIDS). In the liver hemosiderin is localized preponderantly in the periphery of the lobules. The spleen shows a diffuse siderosis of the red pulp. Minimal intrapleural, septal and perivasal depositions of hemosiderin can be found in the lung tissue. The significance of these findings is discussed.     

A comparison of respiratory symptoms and inflammation in sudden infant death syndrome and in accidental or inflicted infant death

Upper respiratory infection and pulmonary inflammation are common in sudden infant death syndrome, but their role in the cause of death remains controversial. Controlled studies comparing clinical upper respiratory infection and inflammation in sudden infant death syndrome with sudden infant deaths caused by accidents and inflicted injuries (controls) are unavailable. Our aim was to compare respiratory inflammation and upper respiratory infection within 48 hours of death and postmortem culture results in these two groups. A retrospective analysis of upper respiratory infection and pathologic variables in the trachea and lung of 155 infants dying of sudden infant death syndrome and 33 control infants was undertaken. Upper respiratory infection was present in 39% of sudden infant death syndrome cases and 40% of control cases. Upper respiratory infection was more likely to have occurred in association with more severe lymphocytic interstitial pneumonitis when sudden infant death syndrome cases and control cases were combined ( P=.04). Proximal and distal tracheal lymphocytic infiltration was more severe in control cases than in sudden infant death syndrome cases ( P=.01 and.01, respectively). Lymphocytic infiltrations of the bronchi, bronchioles, and pulmonary interstitium were similar between groups. Bronchial associated lymphoid tissue was more prominent in control cases ( P=.04). Cultures were positive in 80% of sudden infant death syndrome cases, 78% of which were polymicrobial. Among control cases, 89% were positive, with 94% being polymicrobial. This study confirms that microscopic inflammatory infiltrates in sudden infant death syndrome are not lethal.     

Laryngeal basement membrane thickening is not a reliable postmortem marker for SIDS: results from the Chicago Infant Mortality Study.

It has been suggested that laryngeal basement membrane (LBM) thickening is a pathognomonic postmortem marker for sudden infant death syndrome (SIDS) and is not seen in other causes of explained sudden infant death. To test this hypothesis, we evaluated longitudinal sections of the right hemilarynx taken through the midpoint of the true vocal cord from 129 SIDS cases and 77 postneonatal sudden infant death controls. Using a five-point semi-quantitative scale, maximum LBM thickness (LBMT) for SIDS cases and controls was not statistically different (mean, 2.39 + 0.69 and 2.40 + 0.77, respectively). Likewise, scores based on the average thickness along the entire basement membrane (i.e., "average" score), were not found to be different between SIDS cases and controls. Average and maximum LBMT increased with age in both SIDS cases and controls and were not different between SIDS cases and controls within each age interval. Similar trends in the distribution of maximum and average LBMTs were found between black and Hispanic SIDS and controls; the number of white/non-Hispanic infants was too low for meaningful comparisons. Maximum and average LBMTs were not different in SIDS cases and controls exposed to environmental tobacco compared with unexposed infants. The LBMTs also increased significantly with body weight and length in both SIDS cases and controls. Finally, there were no differences in LBMT in infants intubated prior to death compared with those who were not intubated. From these data, we conclude that LBMT is not pathognomonic of SIDS, is present or absent with equal frequency in SIDS and controls, increases with postnatal age, and does not correlate with passive smoke exposure. Therefore, LBMT should not be used to diagnose SIDS.     

Pulmonary interstitial emphysema in live birth determination: radiographic and gross pathologic features

Pulmonary interstitial emphysema (PIE) has previously been reported as a useful finding in the determination of live birth in cases where the birth and death were not attended. Herein, we present the radiographic and gross pathologic features of PIE in such a case. In this instance, in addition to parenchymal interstitial emphysema, there were subpleural air collections and a pneumothorax.     

Comparative analysis of differences by gender in sudden infant death syndrome in Hungary and Japan

We examined the sex ratio in sudden infant death syndrome (SIDS) cases in Hungary, in Tokyo and Japan between 1985 and 1996. From all the infant death cases in Hungary 395 (240 male, 155 female) were SIDS (odds ratio (OR)=1.179, with 95% confidence interval (CI)=0.961, 1.446), in Japan 4348 (2550 male, 1798 female) were SIDS (OR=1.145, with 95% CI=1.076, 1.218) and in Tokyo 307 (178 male, 129 female) were SIDS (OR=1.128, with 95% CI=0.894, 1.423). Male infants showed a significantly higher birth rate than females. The male infants are more vulnerable (p<0.005), however, higher mortality among male infants should not be considered a characteristic feature for SIDS.     

Diagnosis of sudden death in infants due to acute dehydration

When infants die suddenly of acute dehydration, clinical signs and autopsy findings may be equivocal or absent, and microbiologic cultures often are not helpful. Vitreous humor electrolyte and urea nitrogen concentrations were measured in 53 infants dying of gastrointestinal infections, sudden infant death syndrome (SIDS), other infectious diseases, and miscellaneous causes to determine whether these parameters would assist in the recognition and confirmation of deaths resulting from dehydration. Significant differences were found when comparing the mean sodium and urea nitrogen levels of infants dying of gastrointestinal infections with those succumbing to SIDS or other causes. We recommend that these determinations be routinely performed whenever the gross autopsy findings are insufficient to explain the death.     

Oronasal blood in sudden infant death.

Oronasal secretions are observed frequently in sudden infant death syndrome (SIDS), but overt blood is uncommonly reported. The literature on oronasal blood in sudden infant death is limited. The goal of this study was to determine the frequency of oronasal blood in sudden infant deaths and to examine possible causative factors. Oronasal blood was described in 28 (7%) of 406 cases of sudden infant death. Oronasal blood could not be attributed to cardiopulmonary resuscitation in 14 cases, including 10 (3%) of 300 cases of SIDS, 2 (14%) of 14 accidental suffocation cases, and 2 (15%) of 13 undetermined cases. Eight of the 10 infants in cases of sudden infant death were bedsharing: 5 with both parents, 2 between both parents. The infant in 1 SIDS case was from a family that had had three referrals to Child Protective Services. Oronasal blood not attributable to cardiopulmonary resuscitation occurs rarely in SIDS when the infant is sleeping supine in a safe environment. Bedsharing may place infants at risk of suffocation from overlaying. Oronasal blood observed before cardiopulmonary resuscitation is given is probably of oronasal skin or mucous membrane origin and may be a sign of accidental or inflicted suffocation. Sanguineous secretions that are mucoid or frothy are likely of remote origin, such as lung alveoli. The use of an otoscope to establish the origin of oronasal blood in cases of sudden infant death is recommended.     

Homicide as a cause of the sudden infant death syndrome

The homicidal asphyxiation of a 10 1/2-month-old male infant and the attempted asphyxiation of his 4-month-old sibling, documented by parental confession, is presented as evidence that murder may sometimes be mistaken as sudden infant death syndrome (SIDS). A review of the literature of the relationship between murder and SIDS deaths reveals the suspicions of some physicians but few published cases; this reflects not only the difficulties of making a determination of murder by suffocation, since no injuries may be present, but also a lack of awareness among physicians who must evaluate infant deaths. It is recommended that murder should be considered in the differential diagnosis of sudden, unexpected death in infants and that the autopsy should include full-body x-rays and at least an initial look at the social history of the child.     

The Institution of a Standardized Investigation Protocol for Sudden Infant Death in the Eastern Metropole,Cape Town,South Africa,,

The rate for the sudden infant death syndrome (SIDS) in Cape Town, South Africa, is estimated to be among the highest in the world (3.41/1000 live births). In several of these areas, including those of extreme poverty, only sporadic, nonstandardized infant autopsy, and death scene investigation (DSI) occurred. In this report, we detail a feasibility project comprising 18 autopsied infants with sudden and unexpected death whose causes of death were adjudicated according to the 1991 NICHD definitions (SIDS, n = 7; known cause of death, n = 7; and unclassified, n = 4). We instituted a standardized autopsy and infant DSI through a collaborative effort of local forensic pathology officers and clinical providers. The high standard of forensic investigation met international standards, identified preventable disease, and allowed for incorporation of research. We conclude that an effective infant autopsy and DSI protocol can be established in areas with both high sudden unexpected infant death, and elsewhere. (SUID)/SIDS risk and infrastructure challenges.     

Cocaine babies: the scourge of the '90s

Six cases of cocaine-related deaths of infants have covered the spectrum of potentially devastating effects. They include an intrauterine death of a 35-week-old fetus following acute maternal cocaine abuse; anoxic encephalopathy at birth with 3 months' vegetative survival from a similar episode; traumatic compression asphyxia in a 4-month-old; infectious cardiomyopathy with heart failure in a twin at age 21 months following maternal cocaine abuse at birth; malnutrition and dehydration in a 7-week-old during continuing cocaine abuse by the parents; and a teenage sibling's cocaine lacing of a baby milk bottle ingested by his 6-week-old brother. All the cases had positive toxicological screening for cocaine or metabolites or both in the mother at delivery or in the infant at birth, or both. There were no instances of sudden infant death syndrome (SIDS, or "crib death"). Pathologic and toxicologic, as well as birth, developmental, and social data are presented. An integrated medical, public health, law enforcement, and educational policy to prevent or at least ameliorate these tragic cases, now approaching epidemic proportions, has yet to be developed. A careful obstetrical history and examination of the mother, indication on the birth certificate of maternal drug abuse, and notification of health authorities (by birth certificate checking, among other ways) may send an early warning message to providers for intercession. Active ingestion/injection and passive inhalation by older children and teenagers require more intensive monitoring and aggressive interaction by pediatricians, social workers, school authorities, and employers.(ABSTRACT TRUNCATED AT 250 WORDS)     

Investigation of sudden infant deaths in the State of Maryland (1990-2000)

The Office of the Chief Medical Examiner (OCME) has recorded a significant decline in the deaths of sudden infant death syndrome (SIDS) in the state of Maryland since 1994. However, infants who died of accidental or non-accidental injuries remained consistent during the same time period. This report focuses on the epidemiological characteristics and scene investigation findings of infant victims who died suddenly and unexpectedly in Maryland between 1990 and 2000. A retrospective study of OCME cases between 1990 and 2000 yielded a total of 1619 infant fatalities. 802 infant deaths were determined to be SIDS, which represented 50% of the total infant deaths in our study population. Five hundred and twenty-three (31.8%) deaths were due to natural diseases, 128 (7.9%) deaths were accidents, and 74 (4.6%) were homicides. The manner of death could not be determined after a thorough scene investigation, review of history and a complete postmortem examination in 92 (5.7%) infants. SIDS deaths most often involved infants who were male and black. The peak incidence of SIDS was between 2 and 4 months of age. The majority of SIDS infants (60%) were found unresponsive on their stomach. Among SIDS infants, 269 (33.4%) were found in bed with another person or persons (bed sharing). Of the bed-sharing SIDS cases, 182 (68%) were African-American. In the past 11 years, 52 infants died of asphyxia due to unsafe sleeping environment, such as defective cribs, ill-fitting mattresses, inappropriate bedding materials. Of the 74 homicide victims, 53 (70%) involved infants less than 6 months of age. Twenty (27%) exhibited the classical abuse syndrome characterized by repeated acts of trauma to the infants.     

Simultaneous sudden infant death syndrome: a proposed definition and worldwide review of cases.

Epidemiologic studies of sudden infant death syndrome (SIDS), the leading cause of death of infants during the postperinatal period (7-365 days), have mainly focused on the deaths of single infants. Simultaneous sudden infant death syndrome (SSIDS), the death of a pair of twins occurring at the same time, has received limited attention within the medical community. To the authors' knowledge, this article is the first to describe the 41 SSIDS cases cited in the world literature from 1900 to 1998 by the location of death, a summary of the circumstances surrounding the deaths, and evaluation of these cases in terms of a proposed definition of SSIDS. This evaluation critiques whether the 41 pairs of SSIDS cases adhere to a newly proposed definition of SSIDS. Twin infant deaths must meet all three criteria to be considered SSIDS. The study found that only 12 pairs of twins met all three criteria (29.2%), nine pairs met two criteria (21.9%), alternative cause of death was offered in five pairs of twins (12.1%) and in the remaining 15 pairs (36.6%), only limited information was available; therefore, no conclusions could be reached.     

Cardiovascular malformations and sudden death in infancy

BACKGROUND: We survey the postmortem findings of cardiovascular malformations in infants under the age of 1 year who died suddenly and unexpectedly, in a way that mimicked sudden infant death syndrome (SIDS), and evaluate the importance of the malformation for the fatal outcome. METHODS: Four hundred fifty-seven infants under the age of 1 year, who died between 1982 and 2001, were investigated at the Department of Forensic Medicine in Stockholm, Sweden. RESULTS: Cardiovascular malformations were found in 18 infants (3.9%). Only 6 of 18 malformations, mostly severe, were clinically diagnosed before death. In the other 12 infants, cardiovascular malformations were found, such as atrial or ventricular septal defects, coarctation of aorta, stenosis of the aortic or pulmonary artery orifice, and aneurysm of the membranous portion of the interventricular septum. In all instances, the heart weight was increased. CONCLUSIONS: The observation of undiagnosed cardiovascular malformations as the only explanation for the cause of sudden and unexpected death in apparently healthy infants may advocate more examinations of the infant during early life. It is also important to enlarge the debate of the cause of death in infants with cardiovascular malformations. Should they be included in borderline SIDS?     

Cosleeping and sudden unexpected infant deaths in Kentucky: a 10-year retrospective case review

This retrospective case review investigates modifiable risk factors in sudden unexpected infant deaths, including those attributed to sudden infant death syndrome, and examines the impact of cosleeping with adults or siblings. The study examines sudden unexpected infant deaths from 1991 to 2000 in the state of Kentucky, excluding homicides and deaths from identifiable natural causes. Meta-analysis provides a cosleeping prevalence control in normal infants. Based on the findings described herein, we conclude that cosleeping may represent a risk factor in sudden unexpected infant deaths and that a full scene investigation, including whether the infant was cosleeping, should be sought in all cases of sudden infant death.     

Histologic thyroid gland findings in the newborn infant and infant, with special reference to sudden infant death

The morphological picture of the thyroid gland, the only endocrine organ with a follicle structure, allows a limited conclusion to be drawn with respect to the functional state in spite of any physiological variability. The thyroid of the newborn shows total colloid release and collapse of the follicles. The regular structure of the thyroid will be rebuilt within several weeks after birth. Total colloid absorption can be found in cases of stress-activated thyroids as well as in cases of death due to freezing. A histological examination was done on 88 thyroids of fetuses, newborns and infants. About 70% of the results on 27 cases of sudden infant death syndrome (SIDS) may be interpreted as a morphological correlate of a premortal chronic or recurrent stress reaction. The value of these results is discussed.     

An analysis of the usefulness of specific stages in the pathologic investigation of sudden infant death

Retrospective analysis of autopsy findings in 60 infants who had been found unexpectedly dead in their cribs or beds in South Australia from 1994 to 1998 was undertaken to determine the diagnostic usefulness of individual stages in the postmortem investigation. Positive findings occurred in 2 of 43 scene examinations (3%), 2 of 60 external examinations (3%), 2 of 11 radiologic examinations (18%), 8 of 60 internal examinations (13%), 7 of 60 histologic examinations (12%), and 3 of 58 microbiologic examinations (5%). No positive findings were detected on toxicologic screening. Not every case underwent each diagnostic step. This gave alternative diagnoses to sudden infant death syndrome (SIDS) in 15 cases (25%). This study demonstrates an increase in the percentage of cases of unexpected infant death due to causes other than SIDS; it also shows the diagnostic yield of individual stages in the postmortem evaluation of such cases. Negative findings were important in giving validity to the diagnosis in the 45 cases that were ultimately designated as SIDS.     

Beta-endorphin in the brainstem, pituitary, and spinal fluid of infants at autopsy: relation to sudden infant death syndrome

Immunohistochemical localization of beta-endorphin was studied in the pituitaries and medullas of forty human infants at autopsy. beta-Endorphin immunoreactivity was found in anterior pituitary cells in all cases. In the medulla, beta-endorphin immunoreactivity was found in the neurons of the medial and lateral cuneate nuclei in ten out of the forty cases. In eight of these ten cases, the infants died of causes other than sudden infant death syndrome (SIDS). Only two of 25 SIDS cases had demonstrable beta-endorphin in the brainstem nuclei. Beta-endorphin levels in the spinal fluids of all the cases showed no correlation to cause of death, age or gender.     

Failure to detect elevated levels of carboxyhemoglobin in infants dying from SIDS

Carboxyhemoglobin (COHb) levels were determined in stored blood samples from 91 infants diagnosed to have died from the sudden infant death syndrome (SIDS) (0.59+/-0.41%, excluding one outlying value of 10.83%); 48 age-matched controls (0.53+/-0.38%); and three individuals who died from fire related causes (41+/-20%). No statistical differences in COHb levels were detected between blood from SIDS and control infants (p = 0.43).     

Pulmonary hemosiderin in deceased infants: baseline data for further study of infant mortality

Infant lung samples were obtained prospectively at autopsy by medical examiner pathologists in five areas of the United States. Tissues were submitted regardless of the cause of death. Lung sections were stained with Prussian blue to detect deposits of hemosiderin. Fifty-nine cases were evaluated for the study. The four sections examined for each case were taken from the anterior and posterior aspects of the right and left upper lung. Three pathologists independently scanned the lung sections microscopically using a 10x objective lens (with 10x ocular lens) and indicated an "iron score" by indicating for each section if it showed no staining for iron-hemosiderin (Score 0), occasional staining with most fields negative (Score 1), focally abundant staining with most fields having no staining (Score 2), focally abundant staining with most fields showing positive staining (Score 3), or prominent staining throughout the section (Score 4). There was good agreement between pathologists on the iron score for each case. A total iron score was calculated by adding the scores based on each pathologist's observations. The mean total iron score was 6 (range, 1-44), with the range of possible total iron scores being 0 to 48. There was no significant difference between the four lung sections in a given case. Six cases had total iron scores that were at least twice the mean (i.e., total iron score > 12); in five of these cases death was caused by conditions other than sudden infant death syndrome, including one case in which asphyxia was the cause of death. These data are consistent with other reports that pulmonary hemosiderin in deceased infants is suggestive of a cause of death other than sudden infant death syndrome. The data may be useful as baseline data for further studies of infant mortality involving possible pathologic changes in the lungs.     

Sudden death of an infant with 'an early epileptic encephalopathy'.

This article reports an autopsy case of sudden death of an infant with an infrequent encephalopathy involving epileptic episodes. The infant was a 1-year and 10-month-old boy, who had a history of the first convulsive seizures in the third month after birth. The clinical diagnosis was described as 'an early infantile epileptic encephalopathy with suppression-bursts' (Ohtahara syndrome). On a winter day, he was collapsed following a high fever and was already dead on the arrival at a hospital. The body was small for the age and poorly nourished. The autopsy and postmortem magnetic resonance imaging scan (MRI) of formalin-fixed brain revealed advanced unsymmetric brain atrophy with cortical dysplasia, which were prominent in the left temporal and right occipital lobes, and sclerotic atrophy of the parahippocampal gyri, additionally showing a feature of the olivo-ponto-cerebellar atrophy. However, the cause of death was pathologically and microbiologically determined as bacterial bronchopneumonia following pulmonary infection of the influenza A virus. In sudden death cases of physically handicapped infants, the investigation of viral infection in consideration of an epidemiological survey is important even when the death can be pathomorphologically explained.