Cases Of Sudden Infant Death Research Articles

Suspended rocking cradles, positional asphyxia, and sudden infant death.

To describe the risk of unexpected death in infants who are placed in suspended rocking cardles. Ten cases of sudden infant death and 5 cases of infant asphyxia with successful resuscitation reported to the Consumer Product Safety Commission were analyzed. The death scene investigation reports and autopsy material were made available for evaluation. All 15 cases implicated a suspended head-to-toe rocking cradle. Infants were aged 3 months or younger and were found in the facedown prone position when discovered. The cradle was tilted at greater than 5 degrees, and the head was wedged at one end of the cradle. A locking pin was not used in 14 cases. Ten of the 15 infants died. The autopsy reports listed sudden infant death syndrome as the cause of death. Suspended rocking cradles represent a potentially lethal sleeping environment and should not be used without a locking pin in place. Infants should be placed in the supine position for sleep.

Routine microbiological testing in sudden and unexpected infant death.

To evaluate the significance of microbiological test results in a series of infants who had died suddenly and unexpectedly. Following a review of all cases of sudden natural death in infants presenting to the Adelaide Children's Hospital (ACH) division of the Women's and Children's Hospital (WCH) over the 10 year period between 1983 and 1992, specific evaluation of microbiological test results was undertaken. There were 329 cases of sudden infant death syndrome (SIDS) and 23 cases in which sudden infant death was either attributed to other conditions or was unclassifiable. Positive microbiological results were recorded in the majority of cases, most being considered to be due to postmortem overgrowth or to contamination at autopsy. Of the remaining cases, microbiological results were essential to the establishment of the diagnosis in three cases, and were a useful adjunct to the diagnosis in a further six cases. Routine microbiological testing in cases presenting as SIDS did not reveal occult sepsis in most instances. Such testing did, however, add support to the diagnosis of SIDS where no pathogens were isolated and, if not undertaken, would have resulted in a small percentage of cases of sudden infant death due to infections remaining undiagnosed.

Retarded heart growth in the victims of sudden infant death: possible implications for lethal mechanisms.

The study was aimed to compare the weight of the heart at death in infants who died of sudden infant death (SID) and in control infants under 1 year old. The study included 227 infants who died in St. Petersburg in 1983 to 1990 and who met the criteria of SID. One hundred and thirty-eight infants who died within 24 h out of hospital of defined respiratory infections within the same period of time constituted a control group. Infants with signs of malformations, tumours, and intrauterine infections were excluded from the study. A linear regression model was used in data analysis. No statistically significant association was found between the weight of the heart by the time of death and the following variables: gender, birth weight and length, ponderal index at birth, gestational age, calendar age at death, and length at death. Two variables which significantly influenced the heart weight and entered the linear regression model were infant's weight by the time of death and the cause of death (whether SID or not). No statistically significant interaction was found for these two parameters. It was found that each increase in total body weight by 1000 g brought with it an increase in the heart weight by 4 g (95% CI = 3.6-4.4); for the SID babies, the weight of the heart was less than for the control ones by 1.6 g (95% CI = 0.3-2.9 g). Retarded heart growth may lead to functional disturbances and may contribute to possible mechanisms in some SID cases.

CO2 rebreathing: a possible contributory factor to some cases of sudden infant death?

Physical and geometrical conditions influencing carbon dioxide (CO2) accumulation near the face of a sleeping infant positioned deep in a cot or pram (open cot shaft) or underneath bedding (closed cot shaft) were investigated. By means of mathematical and data-based simulation, and an experimental rebreathing model, both hypothetical (dry, exhaled air +20 degrees C) and more physiological conditions (heated, humidified exhaled air, room temperature +20 degrees C; with and without pooling of cold air within the shaft) were tested. With exhaled air at +20 degrees C, the CO2 concentration increased to about 10% within 5 min. The increase was faster the smaller the volume, and the smaller the opening of the cot shaft. When expiratory air was heated, the CO2 concentration increased with the same speed as when the shaft was closed, but to only 0.1-0.3% when the shaft was open. Pooling of cold air in the shaft increased CO2 accumulation 70-200 times the concentration in air (to <5.5%) when the shaft was open. Turbulence of the air outside the open shaft reduced the increase in CO2 concentration. The experiments imply that CO2 may accumulate around an infant's head when placed deep in a cot or pram with the bedding and walls creating a narrow, vertical, shaft-like tunnel to the surrounding air. Although the CO2 concentration may theoretically attain dangerous levels in such circumstances, a rapid equilibrium between the air within and outside the cot usually occurs due to convection of the expiratory air and turbulence from drafts, the infant's body movements and breathing. Such factors will largely eliminated any significant rebreathing with the exception of the extreme situation when expired air is contained within a closed space.

Sudden infant death and maternal cigarette smoking: results from the Lower Saxony Perinatal Working Group.

Maternal smoking has long been identified as a risk factor for sudden infant death (SID). However, only few studies analysed the biological plausibility of the relationship between maternal smoking and SID. In Lower Saxony (North Germany), detailed information concerning the perinatal period is routinely obtained for almost all infants born in this region. The perinatal data sets from 190 SID cases who had died between 1986 and 1990 and in whom a full autopsy had been performed were identified and compared to data sets from 5920 random controls, frequency matched to cases on year of birth. After adjusting for potential confounders (socio-economic status, birth weight, maternal age and nationality), smoking during pregnancy was still associated with a significantly increased risk of SID (odds ratio (OR) 2.7, 95% confidence interval (CI) 1.7-4.5). There was a clear dose-effect relationship between the number of cigarettes smoked and the risk of SID: adjusted ORs were 2.6 (1.5-4.4) for 1-10 cigarettes/day, 2.8 (1.8-6.0) for 11-20 cigarettes/day, and 6.9 (1.9-25.5) for > 20 cigarettes/day. There also appeared to be an interaction between smoking during pregnancy and maternal anaemia: the risk of SID almost doubled if mothers not only smoked, but were also anaemic (haemoglobin < 100 g/l). These results support the concept that smoking during pregnancy has direct biological effects on the fetus which are associated with an increased risk of SID later in life. The exact mechanism(s) whereby smoking increases the risk of SID, however, remains to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Is partial deletion of the complement C4 genes associated with sudden infant death?

The two C4 loci C4A and C4B in 61 cases of sudden infant death (SID), 93 living controls and 7 cases of infectious death were studied. In the SID group 13.1% showed deletion of the C4A gene, while 2.5% of the cases showed deletion of the C4B gene. This was not significantly different from neither the controls nor the infectious death group. We were not able to confirm that deletion of the C4B gene is associated with SID. However, in the SID group deletion of either the C4A or the C4B gene was associated with signs of infections prior to death (P = 0.035). This observation may indicate that a proportion of SID victims are more vulnerable to infections than other infants.

Morphologic variations in 180 cases of sudden infant death and 180 controls.

The incidence of morphologic variations (MVs) was investigated in 180 infants who died unexpectedly and suddenly and in 180 age-matched nonsuddenly deceased infants. The same person (G.M.) performed a full postmortem and histologic examination on all of the infants, none of whom had significant malformations. The test group (TG) consisted of 146 infants whose death was unexplained, whereas group 3 (G3) consisted of 34 infants with adequately determined causes of death. The principal findings in the control group were prematurity, inflammatory and metabolic diseases, tumors, and traumatic lesions. MVs were present in 62% of the TG infants, in 47% of the G3 children, and in 22% of the controls. The differences between the TG and G3 on the one hand and the controls on the other are statistically significant (p < 0.001 and 0.05, respectively). In the TG, anomalies were twice, dysplasias three times, and dysmorphisms four times as common as in controls; in G3, four times as many dysplasias and dystropics were found as in controls. In the TG, 23% of the MVs were multiple as compared with 9% in G3 and 5% in controls. The pattern of distribution was not confined to certain organs. Among the relative high percentage of dysplasias, the large number of neuroblastomas is striking.

Pathophysiological mechanisms of sudden infant death syndrome

AbstractThere is a consensus that sudden infant death syndrome, the leading cause of mortality in the first year of life, is multifactorial. Most of the cases are probably due to respiratory or cardiac disorders. It has been proposed that some cases of sudden infant death might result from ventricular fibrillation triggered by a sudden increase in sympathetic activity affecting the heart with reduced electrical stability. This impairment can be due to an insufficient or delayed development of cardiac vagal innervation, with the resultant lack of its protective effect that has been demonstrated to be present since the third week of life. Clinical studies suggest that some of the sudden infant death victims may have a reduced heart rate variability that could be interpreted as a decreased parasympathetic activity to the heart. On the other hand, a reduced cardiac electrical stability may be provoked by a developmental imbalance in sympathetic innervation such to create a dominance of left-sided nerves. We have demonstrated that an imbalance of this type experimentally induced in puppies increases the susceptibility to ventricular fibrillation and prolongs QT interval. In order to demonstrate a significant relationship between prolonged QT interval and sudden infant death, we performed a large prospective study on 18,832 neonates. QT interval corrected for heart rate (QTc) measured from an electrocardiogram on the fourth day of life, was within the normal limits in nine victims from known causes, while it was exceeding the mean by two standard deviations (&gt;433 msec) in six of 12 sudden infant death victims. If these data are confirmed by a larger multicenter study started in Italy, it will be possible to identify some of the sudden infant death victims by the observation of a prolonged QT interval on the electrocardiogram. In this case a preventive strategy based on a time-limited administration of beta adrenergic blocking agents to the infants at risk, might reduce the incidence of sudden infant death.

Airway resistance of the posterior nasal pathways in sudden infant death victims

In order to test the hypothesis that infectious swelling of parts of the inner nose causes airway obstruction and is of aetiological significance for sudden infant death (SID), we measured the airway resistances of the prepared posterior nasal pathways of 55 SID victims and 7 infants who died of other causes. About 25% of the SID victims but none of the control cases had strongly elevated nasal resistances; over 4000 kPa.s.m-3 up to unmeasurable values. A histological survey showed that about 50% of the SID cases and only 1 of the control cases exhibited distinct to severe signs of inflammation of the nasal mucous membranes. No correlation was found between nasal resistance and age, sex, body weight, body length, head circumference, or histological findings. We conclude that an elevated nasal resistance plays a role in some SID cases and that SID is rather the result of different processes than a monocausal disease.

The association of lingual thyroglossal duct remnants with sudden death in infancy

Two cases of sudden infant death are described in which relatively large posterior lingual midline cysts were demonstrated at autopsy. Death in both patients was attributed to upper airway obstruction due to the cysts, both of which represented thyroglossal duct remnants.

Simple urinary acylcarnitine profiling by gas chromatography mass spectrometry

In many cases of sudden infant death, victims have been shown to be deficient in medium-chain acyl-CoA dehydrogenase (MCAD), a key enzyme for (3-oxidation of fatty acids. This disease, and several other inborn errors of metabolism leading to organic aciduria, are characterized by concentrations of certain acylcarnitines 1 in urine of the order of 1 pmol ml -1 . Normal levels of acylcarnitines are of the order of 1 nmol ml -1 . An affordable, routine analytical procedure for traces of urinary acylcarnitines would facilitate diagnosis of acidurias and acidemias. Acylcarnitines are essential to P-oxidation because they carry the fatty acyl units (RCO-) across the mitochondrial membrane. Carnitine detoxifies mitochondria of excesses of acyl groups by carrying them, as acylcarnitines, into urine. Thus profiling of urinary acylcarnitines would also allow the biochemistry of some currently ill-defined diseases, and the metabolic routes of acidic drugs, to be elucidated.

Suffocation, recurrent apnea, and sudden infant death

We reviewed the cases of 27 young children from 27 different families who were suffocated by their mothers. The certainty, or near certainty, of suffocation was based on reliable observation or recording of the suffocation, maternal confession, or successful prosecution in a criminal court. Eighteen of the children are alive, although one has severe brain damage; nine are dead. Twenty-four were reported to have had previous episodes of apnea, cyanosis, or seizure, and 11 had had 10 or more such episodes that were either invented or caused by the mother. Repetitive suffocation usually began between the ages of 1 and 3 months and continued until it was discovered, or the child died, 6 to 12 months later. The 27 children had 15 live elder siblings and 18 who had died suddenly and unexpectedly in early life; 13 of the dead siblings had had recurrent apnea, cyanosis, or seizures, and, although most of them at the time of death were certified as having sudden infant death syndrome, it is probable that some were suffocated. Repetitive suffocation has a characteristic clinical presentation that should allow identification before brain damage or death occurs. The characteristics should also allow the cause of death of some cases of sudden infant death to be established more accurately.

Histologische Lungenbefunde beim pl�tzlichen Kindstod

The lungs of 79 children who had died between the ages of 1 week and 2 years old were histologically examined. 59 of these children could be categorized as cases of Sudden Infant Death because of the history and postmortem findings. In the remaining 20 cases a definite cause of death could be established. This is the same collective on which the histological investigations of the lymphatic tissue has been carried out. Morphological changes which are typical for a virus pneumonia were found in a substantially higher frequency in the cases of Sudden Infant Death than in the control cases. The validity of these findings and their possible significance for the cause of death are discussed.

Autopsies and Sudden Infant Death Syndrome

Sir .—In their article in the May 1989 issue of AJDC , Chasnoff et al 1 are misled in their belief that an autopsy can rule out lethal trauma in an infant who is presumptively diagnosed to have died of sudden infant death syndrome (SIDS). It is recognized in forensic pathology that young infants who die of external airway obstruction, accidental or otherwise, may have no pathologic changes on autopsy that indicate lethal injury by suffocation or smothering. In many cases of sudden infant death, death-scene investigation may be the only way to determine why a healthy infant died suddenly and unexpectedly at home. 2,3 The data described by Chasnoff and coworkers are based on live infants. However, these infants are unsuitable controls for a study of infants who die of SIDS. The selection of controls in any prospective study of infants who died of SIDS should be restricted to healthy

Prospective study on the prevalence of sudden infant death and possible risk factors in Brussels: Preliminary results (1987–1988)

A prospective study was carried out to assess the frequency of sudden infant death (SID) in the Brussels area. The study was conducted between January and December 1987 on infants presented to the health clinics of the Brussels "Office de la Naissance et de l'Enfance" (ONE). The infants entered the study if: (a) they were born between January 1 and December 31, 1987; (b) they attended an ONE consultation in the Brussels area between January 1987 and December 1988; (c) visits were repeated monthly during the first 12 months of life, or until death occurred; and (d) standard questionnaires were completed for each visit. For 4,064 infants these four criteria were fulfilled. During the study period 7 infants died of SID. Their deaths were unexpected and remained unexplained despite post-mortem investigations. For each SID case, 10 control infants were selected from the same health clinics. Controls matched the SID cases in the following respects: (a) dates of visits; (b) sex; (c) gestational age; (d) legal age; and (e) the profession of both parents. For most of the 65 items studied no significant difference was seen between the 7 SID infants and their 70 matched controls. Only two variables significantly differentiated the two groups. Repeated fatigue during feeding was seen in 4 of the 7 SID cases, but only in 10 of the 70 control infants (Fisher P = 0.017). Profuse sweating during sleep was reported in 2 of the 7 SID infants, and in none of the 70 controls (Fischer P = 0.007). These two infants' bedclothes were repeatedly wet with sweat.(ABSTRACT TRUNCATED AT 250 WORDS)

Possible association of sudden infant death with partial complement C4 deficiency revealed by post-mortem DNA typing of HLA class II and III genes

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

Postmortem cerebrospinal fluid pleocytosis.

We show that postmortem cerebrospinal fluid (CSF) pleocytosis is a common event. Postmortem cerebrospinal or ventricular fluid was obtained from children and adults. The cells were counted and morphologically characterized using several histochemical markers. Infants exhibit a brisk postmortem CSF pleocytosis. Sudden infant death cases have relatively high CSF counts. Typeable cells are mononuclear and consist of approximately 60%-70% lymphocytes and 20%-40% macrophages. When postmortem duration is greater than 12 h, the cells become vacuolated and cannot be identified. The etiology of these findings requires further study.

Relationship between periventricular hemorrhage, leukomalacia and brainstem lesions in prematurely born infants

The brain pathology in very prematurely born infants with intraventricular hemorrhage (IVH) was studied particularly as to the severity and site of the complicated brain lesions responsible for the prognosis. A high frequency of leukomalacia, pontosubicular necrosis and/or olivocerebellar neuronal loss was found in the cases of IVH, and these non-hemorrhagic brain lesions showed an increasing frequency with the grade of IVH. However, there was marked reduction of IVH, periventricular leukomalacia and, in particular, brainstem lesions in prematurely born cases of sudden infant death. These IVH and associated conditions have different pathogenesis, but factors responsible for their occurrence may be present together in each case.

Haemosiderin-laden mescrophages in the interstitial tissue of the lung of sudden infant death cases – a mark of previous “near-miss” events?

In a series of 24 consecutive cases of Sudden Infant Death Syndrome (SIDS) the lungs of 10 infants showed foci of haemosiderin-laden macrophages in the interstitial and subpleural tissue without extravasated red cells nearby, indicating that petechial haemorrhages had occurred at some time prior to the last and fatal event. These lungs were free from inflammatory changes and therefore can be considered to be true cases of SIDS. In contrast the lungs of 11 infants showed inflammatory changes including bronchiolitis and interstitial pneumonia. The remaining 3 infants showed both inflammatory changes and interstitial haemosiderin in macrophages without red cells in the proximity. Fresh petechiae and alveolar haemorrhage sometimes with haemosiderin-laden macrophages are seen in all groups. It is suggested that in true SIDS the lungs are not only free from inflammatory changes, but also show signs of previous events causing petechial haemorrhages, for example near-miss episodes. Haemosiderin-containing macrophages in the interstitium, without free red cells nearby may be the mark of such an event.

Occlusive Lesions of Cardiac Conducting Tissue Arteries in Sudden Infant Death Syndrome

Cardiac conducting tissue from the hearts of 40 victims of sudden infant death syndrome was examined microscopically by serial section. In five hearts there were marked narrowing of the major artery supplying the atrioventricular node. In another there was similar narrowing of the artery supplying the sinus node. The arterial lesions were focal and characterized by cellular intimal thickening which severely narrowed the vessel lumen. This arterial anomaly may be a contributory factor in the pathogenesis of some cases of sudden infant death.