Bottle feeding and the sudden infant death syndrome.

OBJECTIVE--To determine whether the risk of the sudden infant death syndrome is increased in bottle fed babies. DESIGN--Population based case-control study matching for age and time. SUBJECTS--All babies aged 1 week to 1 year dying of sudden infant death syndrome during November 1987 to April 1989 or February 1990 to June 1991 and two live controls. SETTING--Avon and north Somerset. MAIN OUTCOME MEASURES--Breast or bottle feeding, sleeping position, maternal smoking, parental employment, and length of gestation. RESULTS--Compared with being fully breast fed, the crude odds ratio for sudden infant death in fully bottle fed babies was 3.1 and for mixed breast and bottle fed babies 1.5. These odds ratios fell to 1.8 (95% confidence interval 0.7 to 4.8) and 1.2 (0.5 to 2.7) respectively after maternal smoking, parental employment, preterm gestation, and sleeping position had been adjusted for. Sleeping position partly masked the effect of being bottle fed on sudden infant death as breast fed babies were more likely to have slept prone than bottle fed babies. CONCLUSIONS--Bottle feeding is not a significant independent risk factor for the sudden infant death syndrome. Patterns of maternal smoking, preterm gestation, and parental employment status account for most of the apparent association with bottle feeding.     

Endpiece: Genius (1815)

ObjectiveTo examine the proposition that a used infant mattress is associated with an increased risk of sudden infant death syndrome.DesignCase-control study.SettingScotland (population 5.1 million, with about 53 000 births a year).Participants131 infants who died of sudden infant death syndrome between 1 January 1996 and 31 May 2000 and 278 age, season, and obstetric unit matched control infants.ResultsRoutine use of an infant mattress previously used by another child was significantly associated with an increased risk of sudden infant death syndrome (multivariate odds ratio 3.07, 95% confidence interval 1.51 to 6.22). Use of a used infant mattress for last sleep was also associated with increased risk (6.10, 2.31 to 16.12). The association was significantly stronger if the mattress was from another home (4.78, 2.08 to 11.0) than if it was from the same home (1.64, 0.64 to 4.2).ConclusionA valid significant association exists between use of a used infant mattress and an increased risk of sudden infant death syndrome, particularly if the mattress is from another home. Insufficient evidence is available to judge whether this relation is cause and effect.

What is already known about this topic

The major risk factors for sudden infant death syndrome are sleeping prone and parental smokingOne study has suggested that the syndrome is associated with sleeping on an infant mattress previously used by another child

What this study adds

New case-control data show that the association between a previously used infant mattress and sudden infant death syndrome is validWhen source of used mattress is categorised, the association is significant only if the mattress is from another homeInsufficient evidence is available to judge whether this is a cause and effect relation     

Interaction between bedding and sleeping position in the sudden infant death syndrome: a population based case-control study.

OBJECTIVE--To determine the relation between sleeping position and quantity of bedding and the risk of sudden unexpected infant death. DESIGN--A study of all infants dying suddenly and unexpectedly and of two controls matched for age and date with each index case. The parents of control infants were interviewed within 72 hours of the index infant''s death. Information was collected on bedding, sleeping position, heating, and recent signs of illness for index and control infants. SETTING--A defined geographical area comprising most of the county of Avon and part of Somerset. SUBJECTS--72 Infants who had died suddenly and unexpectedly (of whom 67 had died from the sudden infant death syndrome) and 144 control infants. RESULTS--Compared with the control infants the infants who had died from the sudden infant death syndrome were more likely to have been sleeping prone (relative risk 8.8; 95% confidence interval 7.0 to 11.0; p less than 0.001), to have been more heavily wrapped (relative risk 1.14 per tog above 8 tog; 1.03 to 1.28; p less than 0.05), and to have had the heating on all night (relative risk 2.7; 1.4 to 5.2; p less than 0.01). These differences were less pronounced in the younger infants (less than 70 days) than the older ones. The risk of sudden unexpected death among infants older than 70 days, nursed prone, and with clothing and bedding of total thermal resistance greater than 10 tog was increased by factors of 15.1 (2.6 to 89.6) and 25.2 (3.7 to 169.0) respectively compared with the risk in infants of the same age nursed supine or on their side and under less than 6 tog of bedding. CONCLUSIONS--Overheating and the prone position are independently associated with an increased risk of sudden unexpected infant death, particularly in infants aged more than 70 days. Educating parents about appropriate thermal care and sleeping position of infants may help to reduce the incidence of the sudden infant death syndrome.     

Ethnic differences in mortality from sudden infant death syndrome in New Zealand.

OBJECTIVES--To examine the factors which might explain the higher mortality from sudden infant death syndrome in Maori infants (7.4/1000 live births in 1986 compared with 3.6 in non-Maori children). DESIGN--A large nationwide case control study. SETTING--New Zealand. 485 infants who died of sudden infant death syndrome were compared with 1800 control infants. There were 229 Maori and 240 non-Maori cases of sudden infant death syndrome (16 cases unassigned) and 353 Maori and 1410 non-Maori controls (37 unassigned). RESULTS--Maori infants had 3.81 times the risk (95% confidence interval 3.06 to 4.76) of sudden infant death syndrome compared with non-Maori infants. The risk factors for sudden infant death syndrome within groups were remarkably similar. When Maori and non-Maori controls were compared the prevalence of many of the known risk factors was higher in Maori infants. In particular, mothers were socioeconomically disadvantaged, younger, and more likely to smoke and their infants were of lower birth weight and more likely to share a bed with another person. Multivariate analysis controlling for potential confounders found that simply being Maori increased the risk of sudden infant death syndrome by only 1.37 (95% CI = 0.95 to 2.01), not statistically significantly different from 1. Population attributable risk was calculated for prone sleeping position, maternal smoking, not breast feeding, and infants sharing a bed with another person. In total these four risk factors accounted for 89% of deaths from sudden infant death syndrome in Maori infants and 79% in non-Maori infants. CONCLUSION--The high rate of sudden infant death syndrome among Maori infants is based largely on the high prevalence in the Maori population of the major risk factors. Other risk factors, not related to ethnicity, probably explain remaining differences between Maori and non-Maori children.     

Thermal environment and sudden infant death syndrome: case-control study.

OBJECTIVE--To compare the thermal environment of infants who died of the sudden infant death syndrome with that of age matched control infants. DESIGN--Case-control study. Infants who died were matched with two controls, one for age and one for age and birth weight. Thermal measurements were conducted at the death scene for cases and at the scene of last sleep for control infants, who were visited unexpectedly within four weeks of the index infant''s death on a day of similar climatic conditions. A follow up questionnaire was administered to parents of cases and controls. SETTING--The geographical area served by the professional Tasmanian state ambulance service, which includes 94% of the Tasmanian population. SUBJECTS--41 infants died of the sudden infant death syndrome at home; thermal observations at death scene were available for 28 (68%), parental questionnaire data were available for 40 (96%). 38 controls matched for age and 41 matched for age and birth weight. RESULTS--Cases had more excess thermal insulation for their given room temperature (2.3 togs) than matched controls (0.6 togs) (p = 0.009). For every excess thermal insulation unit (tog) the relative risk of the sudden infant death syndrome was 1.26 (95% confidence interval 1.05 to 1.52). The average thermal bedding value calculated from parental recall was similar to that observed by attendant ambulance officers (mean difference = 0.4 tog, p = 0.39). Cases were more likely to have been found prone (odds ratio 4.58; 1.48 to 14.11). Prone sleeping position was not a confounder or effect modifier of the relation between excess thermal insulation and the syndrome. CONCLUSIONS--Overheating and the prone sleeping position are independently associated with an increased risk of the sudden infant death syndrome. Further work on infant thermal balance and sudden infant death is required and guidelines for appropriate infant thermal care need to be developed.     

The common bacterial toxins hypothesis of sudden infant death syndrome

The background to the common bacterial toxin hypothesis of sudden infant death syndrome is presented. The idea is that some cases of sudden infant death syndrome are due to the lethal effects of nasopharyngeal bacterial toxins which can act synergistically to trigger the events leading to death. The concept is consistent with the age distribution of sudden infant death syndrome, the winter excess of cases and the role of prone sleeping and passive exposure to cigarette smoke. A number of laboratory-based investigations are described. There is an increased isolation of staphylococci and Gram-negative bacilli from sudden infant death syndrome infants compared with age- and season-matched healthy infants. Bacteria from sudden infant death syndrome infants interact synergistically to cause sudden death in gnotobiotic weanling rats. Bacterial toxins implicated in sudden infant death syndrome interact synergistically to cause death in chick embryos. Nicotine in very low doses potentiates the lethal effect of toxin combinations in chick embryos. Staphylococcal toxins and endotoxins have been demonstrated in sudden infant death syndrome tissues, antibodies to endotoxins are low in sudden infant death syndrome cases and the prone sleeping position leads to pooling of secretions in the upper airways, increasing the risk of bacterial growth and toxin production. If the hypothesis is correct, then there is the possibility of a further reduction in the incidence of sudden infant death syndrome based on immunisation against the toxins involved.     

Bed sharing,smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group.

OBJECTIVES--To investigate why sharing the bed with an infant is a not consistent risk factor for the sudden infant death syndrome in ethnic subgroups in New Zealand and to see if the risk of sudden infant death associated with this practice is related to other factors, particularly maternal smoking and alcohol consumption. DESIGN--Nationwide case-control study. SETTING--Region of New Zealand with 78% of all births during 1987-90. SUBJECTS--Home interviews were completed with parents of 393 (81.0% of total) infants who died from the sudden infant death syndrome in the postneonatal age group, and 1592 (88.4% of total) controls who were a representative sample of all hospital births in the study region. RESULTS--Maternal smoking interacted with infant bed sharing on the risk of sudden infant death. Compared with infants not exposed to either risk factor, the relative risk for infants of mothers who smoked was 3.94 (95% confidence interval 2.47 to 6.27) for bed sharing in the last two weeks and 4.55 (2.63 to 7.88) for bed sharing in the last sleep, after other confounders were controlled for. The results for infants of non-smoking mothers were inconsistent with the relative risk being significantly increased for usual bed sharing in the last two weeks (1.73; 1.11 to 2.70) but not for bed sharing in the last sleep (0.98; 0.44 to 2.18). Neither maternal alcohol consumption nor the thermal resistance of the infant''s clothing and bedding interacted with bed sharing to increase the risk of sudden infant death, and alcohol was not a risk factor by itself. CONCLUSION--Infant bed sharing is associated with a significantly raised risk of the sudden infant death syndrome, particularly among infants of mothers who smoke. The interaction between maternal smoking and bed sharing suggests that a mechanism involving passive smoking, rather than the previously proposed mechanisms of overlaying and hyperthermia, increases the risk of sudden infant death from bed sharing.     

Babies sleeping with parents: case-control study of factors influencing the risk of the sudden infant death syndrome. CESDI SUDI research group

ObjectiveTo investigate the risks of the sudden infant death syndrome and factors that may contribute to unsafe sleeping environments.DesignThree year, population based case-control study. Parental interviews were conducted for each sudden infant death and for four controls matched for age, locality, and time of sleep.SettingFive regions in England with a total population of over 17 million people.Subjects325 babies who died and 1300 control infants.ResultsIn the multivariate analysis infants who shared their parents'' bed and were then put back in their own cot had no increased risk (odds ratio 0.67; 95% confidence interval 0.22 to 2.00). There was an increased risk for infants who shared the bed for the whole sleep or were taken to and found in the parental bed (9.78; 4.02 to 23.83), infants who slept in a separate room from their parents (10.49; 4.26 to 25.81), and infants who shared a sofa (48.99; 5.04 to 475.60). The risk associated with being found in the parental bed was not significant for older infants (>14 weeks) or for infants of parents who did not smoke and became non-significant after adjustment for recent maternal alcohol consumption (>2 units), use of duvets (>4 togs), parental tiredness (infant slept ⩽4 hours for longest sleep in previous 24 hours), and overcrowded housing conditions (>2 people per room of the house).ConclusionsThere are certain circumstances when bed sharing should be avoided, particularly for infants under four months old. Parents sleeping on a sofa with infants should always be avoided. There is no evidence that bed sharing is hazardous for infants of parents who do not smoke.

Key messsages

• Cosleeping with an infant on a sofa was associated with a particularly high risk of sudden infant death syndrome
• Sharing a room with the parents was associated with a lower risk
• There was no increased risk associated with bed sharing when the infant was placed back in his or her cot
• Among parents who do not smoke or infants older than 14 weeks there was no association between infants being found in the parental bed and an increased risk of sudden infant death syndrome
• The risk linked with bed sharing among younger infants seems to be associated with recent parental consumption of alcohol, overcrowded housing conditions, extreme parental tiredness, and the infant being under a duvet

     

Environment of infants during sleep and risk of the sudden infant death syndrome: results of 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers.

OBJECTIVE--To investigate the role of sleeping arrangements as risk factors for the sudden infant death syndrome after a national risk reduction campaign. DESIGN--Two year population based case-control study. Parental interviews were conducted for each infant who died and for four controls matched for age and date of interview. SETTING--Three regions in England with a total population of 17 million people. SUBJECTS--195 babies who died and 780 matched controls. RESULTS--Prone and side sleeping positions both carried increased risks of death compared with supine when adjusted for maternal age, parity, gestation, birth weight, exposure to smoke, and other relevant factors in the sleeping environment (multivariate odds ratio = 9.00 (95% confidence interval 2.84 to 28.47) and 1.84 (1.02 to 3.31), respectively). The higher incidence of side rather than prone sleeping led to a higher population attributable risk (side 18.4%, prone 14.2%). More of the infants who died were found with bed covers over their heads (21.58; 6.21 to 74.99). The use of a dummy had an apparent protective effect (0.38; 0.21 to 0.70). Bed sharing for the whole night was a significant risk factor for infants whose mothers smoked (9.25; 2.31 to 34.02). No protective effect of breast feeding could be identified on multivariate analysis. CONCLUSIONS--This study confirms the importance of certain risk factors for the sudden infant death syndrome and identifies others-for example, covers over the head, side sleeping position-which may be amenable to change by educating and informing parents and health care professionals.     

Respiratory viruses and sudden infant death.

Viruses were shown to be present in the respiratory tract in 200 of 763 cases of the sudden infant death syndrome studied in the nine years 1974-82. Epidemiological and pathological evidence suggested that the distribution of viruses in the sudden infant death syndrome differs between infants aged 3 months or less and those aged over 3 months: the incidence of detection of virus was 14% in the younger group compared with 39% in the older group. The distribution of the viruses in these two groups was compared with that in 1341 live infants with respiratory virus infections. Adenovirus, influenza virus, parainfluenza virus, and rhinovirus had similar distribution among the victims of the sudden infant death syndrome and live controls. The incidence of detection of respiratory syncytial virus was increased in the older infants dying of the sudden infant death syndrome (90% of the cases detected) compared with the older group of live infants (53%). Antibody studies, detection of virus, and epidemiological data suggest that respiratory syncytial virus may be a precipitating factor of sudden death in older infants.     

Immunological evidence for a bacterial toxin aetiology in sudden infant death syndrome

Toxin-specific antibodies to clostridial, enterobacterial and staphylococcal toxins implicated in sudden infant death syndrome were studied in sera from sudden infant death syndrome infants and a comparison group of infants (babies with phenylketonuria). The results indicated a higher proportion of sera from sudden infant death syndrome infants contained IgA that bound to clostridial and enterobacterial toxins but a higher proportion of sera from the phenylketonuria comparison group contained IgA that bound staphylococcal toxins. The higher proportion of serum samples with IgG and IgM in the healthy comparison babies serum probably indicated immunity in this group of babies to these toxins. The effect of gender and age had a minimal effect on the incidence of these antibodies. The presence of toxin-specific antibodies in sudden infant death syndrome and the of comparison infants suggests that all infants are exposed to these toxins and most babies successfully overcome the toxic challenge. Some infants with predisposing risk factors (temperature change, smoking, infection, immune development, sleeping position, etc.) that could affect the baby's immune competency could succumb to these and possibly other toxins. This immunological evidence further strengthens the view that bacterial toxins are a significant cause of sudden infant death syndrome.     

Can the fall in Avon's sudden infant death rate be explained by changes in sleeping position?

OBJECTIVE--To examine the impact of changing practice with regard to infant sleeping position on mortality from the sudden infant death syndrome. DESIGN--A population based study of all infants dying suddenly and unexpectedly during February 1990 to July 1991, and two groups of controls; one comprising every 125th baby born to Avon residents and the other comprising pairs of infants matched to each index case for age, neighbourhood, and date of study. Information about sleeping position was collected at home visits soon after the index baby''s death or, for the population based controls, on several occasions in the first six months of life. The design was comparable to that of an earlier study of the same population. SETTING--County of Avon. SUBJECTS--35 infants who died suddenly and unexpectedly (32 of the sudden infant death syndrome), 70 matched controls, and 152 population based controls. RESULTS--The prevalence of prone sleeping in the matched controls was much lower than that found in an earlier study in Avon (28% (18/64) 1990-1 v 58% (76/131) 1987-9; p less than 0.001) and was comparable with the prevalence in population based controls (29%). This would be expected to lead to a reduction in the incidence of the sudden infant death syndrome to 2.0/1000 live births (95% confidence interval 1.8/1000 to 2.5/1000). The actual mortality fell from 3.5/1000 in 1987-9 to 1.7/1000. CONCLUSION--The fall in mortality can be almost entirely accounted for by the reduction in prone sleeping, suggesting a causal relation exists between them. Side and supine positions confer protection but the side position is unstable and the infant may roll prone. We therefore recommend supine as the safest sleeping position for babies.     

Aerial release of bacteria from cot mattress materials and the sudden infant death syndrome

AIM: To investigate aerial release of bacteria from used cot mattresses and to assess factors that may influence this process. METHODS AND RESULTS: Movement on used mattresses, simulating that of an infant's head, significantly enhanced aerial release of naturally acquired bacteria from the polyurethane foams (total count data, P = 0.008; Staphylococcus aureus, P = 0.004) or from polyvinyl chloride covers (total count data, P = 0.001). Aerial release of naturally acquired bacteria from used cot mattresses showed high variability and was poorly correlated (R2 < or = 0.294) with bacterial cell density within the materials. In experiments involving inoculation of S. aureus and Escherichia coli onto the polyurethane of unused cot mattresses, aerial release of the species correlated well (R2 > or = 0.950) with inoculation density when simulated infant head movement was applied. Aerial release of these bacterial species from the material decreased with increase in width or aqueous content of the material, and was lower from polyurethane foam of a used cot mattress. CONCLUSIONS: Simulated infant movement and mattress related factors influence aerial release of bacteria from cot mattress materials. With simulated infant movement on cot mattress polyurethane foam, levels of airborne bacteria above the material are proportional to bacterial population levels inoculated onto the material. SIGNIFICANCE AND IMPACT OF THE STUDY: Cot mattresses harbouring relatively high levels of naturally acquired toxigenic bacteria, such as S. aureus, could pose a relatively high risk of infection to the infant's respiratory tract through increased aerial contamination. This has impact in the context of recent findings on cot mattress related risk factors for sudden infant death syndrome.     

Smoking and the sudden infant death syndrome: results from 1993-5 case-control study for confidential inquiry into stillbirths and deaths in infancy. Confidential Enquiry into Stillbirths and Deaths Regional Coordinators and Researchers.

OBJECTIVE--To investigate the effects of exposure to tobacco smoke and of parental consumption of alcohol and illegal drugs as risk factors for the sudden infant death syndrome after a national risk reduction campaign which included advice on prenatal and postnatal avoidance of tobacco smoke. DESIGN--Two year population based case-control study. Parental interviews were conducted for each infant who died and four controls matched for age and date of interview. SETTING--Three regions in England with a total population of 17 million people. SUBJECTS--195 babies who died and 780 matched controls. RESULTS--More index than control mothers (62.6% v 25.1%) smoked during pregnancy (multivariate odds ratio = 2.10; 95% confidence interval 1.24 to 3.54). Paternal smoking had an additional independent effect when other factors were controlled for (2.50; 1.48 to 4.22). The risk of death rose with increasing postnatal exposure to tobacco smoke, which had an additive effect among those also exposed to maternal smoking during pregnancy (2.93; 1.56 to 5.48). The population attributable risk was over 61%, which implies that the numbers of deaths from the syndrome could be reduced by almost two third if parents did not smoke. Alcohol use was higher among index than control mothers but was strongly correlated with smoking and on multivariate analysis was not found to have any additional independent effect. Illegal drug use was more common among the index parents, and paternal use of illegal drugs remained significant in the multivariate model (4.68; 1.56 to 14.05). CONCLUSIONS--This study confirms the increased risk of the sudden infant death syndrome associated with maternal smoking during pregnancy and shows evidence that household exposure to tobacco smoke has an independent additive effect. Parental drug misuse has an additional small but significant effect.     

Cot mattresses as reservoirs of potentially harmful bacteria and the sudden infant death syndrome

Cot mattress materials were investigated as potential reservoirs of bacteria in relation to the sudden infant death syndrome (SIDS). The sleeping position of the infant significantly influenced bacterial population density of cot mattress polyurethane foams (p<0.0000001) and their covers (p<0.004). Staphylococcus aureus was isolated at significantly higher frequency (p<0.03) from the infant's head region of cot mattress materials. Significantly higher bacterial population densities (p<0.001) were associated with polyurethane foams from non-integral mattresses (exposed polyurethane foam), when compared to those from mattresses completely covered by polyvinyl chloride (integral type mattress). The frequency of isolation of S. aureus from polyurethane foams from non-integral mattresses was also significantly higher (p=0.03) than from foams from the integral type. The following factors were significantly associated with increased frequency of isolation of S. aureus: from the polyurethane foam, previous use of non-integral mattresses by another child (p=0.03 for all sample sites, p=0.01 for torso region); from the covers, sleeping in the prone position (p=0.003 head region, p=0.001 torso region). Prone sleeping was also significantly associated with increased bacterial population levels (p=0.01) and increased frequency of isolation of Escherichia coli (p=0.02) from the torso region of cot mattress covers. These findings could explain some recently identified risk factors for SIDS associated with type and previous use of cot mattresses. Clostridium perfringens was isolated at very low frequency and Streptococcus pyogenes was not isolated from any cot mattress materials tested.     

Assessment of dry heat exchanges in newborns: influence of body position and clothing in SIDS.

A dramatic decrease of sudden infant death syndrome (SIDS) has been noted following the issuance of recommendations to adopt the supine sleeping position for infants. It has been suggested that the increased risk could be related to heat stress associated with body position. In the present study, the dry heat losses of small-for-gestational-age newborns nude or clothed were assessed and compared to see whether there is a difference in the ability to lose heat between the prone and supine positions. An anthropomorphic thermal mannequin was exposed to six environmental temperatures, ranging between 25 and 37 degrees C, in a single-walled, air-heated incubator. The magnitudes of heat losses did not significantly differ between the two body positions for the nude (supine 103.46 +/- 29.67 vs. prone 85.78 +/- 34.91 W/m(2)) and clothed mannequin (supine 59.35 +/- 21.51 vs. prone 63.17 +/- 23.06 W/m(2)). With regard to dry heat exchanges recorded under steady-state conditions, the results show that there is no association between body position and body overheating.     

Clinical and angiographic predictors of stroke and death from carotid endarterectomy: systematic review.

OBJECTIVE: To identify risk factors for operative stroke and death from carotid endarterectomy. DESIGN: Systematic review of all studies published since 1980 which related risk of stroke and death to various preoperative clinical and angiographic characteristics, including unpublished data on 1729 patients from the European carotid surgery trial. MAIN OUTCOME MEASURE: Operative risk of stroke and death. RESULTS: Thirty six published studies fulfilled our criteria. The effect of 14 potential risk factors was examined. The odds of stroke and death were decreased in patients with ocular ischaemia alone (amaurosis fugax or retinal artery occlusion) compared with those with cerebral transient ischaemic attack or stroke (seven studies; odds ratio 0.49; 95% confidence interval 0.37 to 0.66; P < 0.00001). The odds were increased in women (seven studies; 1.44; 1.14 to 1.83; P < 0.005), subjects aged > or = 75 years (10 studies: 1.36; 1.09 to 1.71; P < 0.01), and with systolic blood pressure > 180 mm Hg (four studies; 1.82; 1.37 to 2.41; P < 0.0001), peripheral vascular disease (one study; 2.19; 1.40 to 3.60; P < 0.0005), occlusion of the contralateral internal carotid artery (14 studies; 1.91; 1.35 to 2.69; P < 0.0001), stenosis of the ipsilateral internal carotid siphon (five studies; 1.56; 1.03 to 2.36; P = 0.02), and stenosis of the ipsilateral external carotid artery (one study; 1.61; 1.05 to 2.47; P = 0.03). Operative risk was not significantly related to presentation with cerebral transient ischaemic attack versus stroke, diabetes, angina, recent myocardial infarction, current cigarette smoking, or plaque surface irregularity at angiography. Multiple regression analysis of data from the European carotid surgery trial identified cerebral versus ocular events at presentation, female sex, systolic hypertension, and peripheral vascular disease as independent risk factors. CONCLUSIONS: The risk of stroke and death from carotid endarterectomy is related to several clinical and angiographic characteristics. These observations may help clinicians to estimate operative risks for individual patients and will also facilitate more meaningful comparison of the operative risks of different surgeons or at different institutions by allowing some adjustment for differences in case mix.     

The social origins of infantile colic: questionnaire study covering 76,747 infants.

OBJECTIVE: To describe risk factors for infantile colic. DESIGN: Questionnaire administered by health visitors. SETTING: Sheffield. SUBJECTS: Mothers of 76,747 infants born between 1 August 1975 and 31 May 1988, interviewed when the infant was 1 month old. MAIN OUTCOME MEASURES: Reporting of infantile colic and its duration; weight of infant leeding, state of the home, socioeconomic characteristics of the parents, parents'' age, and mother''s parity. RESULTS: The odds of reporting infantile colic were increased with breast feeding (odds ratio of breast v bottle feeding 1.35 (95% confidence interval 1.28 to 1.43)), increasing parental age, lower parity, increasing parental age at leaving full time education, and more affluent homes and districts of residence. In a logistic regression analysis, mother''s age and parity and socioeconomic factors remained the most important risk factors for the reporting of infantile colic (each P < 0.005), and the effect of breast feeding was attenuated (odds ratio of breast v bottle feeding 1.09 (1.02 to 1.15)). CONCLUSION: At a population level, dietary factors contribute little to mothers'' reporting of infantile colic, and dietary change should not be the primary intervention.     

Prenatal nicotine alters vigilance states and AchR gene expression in the neonatal rat: implications for SIDS

Maternal smoking is a major risk factor for sudden infant death syndrome (SIDS). The mechanisms by which cigarette smoke predisposes infants to SIDS are not known. We examined the effects of prenatal nicotine exposure on sleep/wake ontogenesis and central cholinergic receptor gene expression in the neonatal rat. Prenatal nicotine exposure transiently increased sleep continuity and accelerated sleep/wake ontogeny in the neonatal rat. Prenatal nicotine also upregulated nicotinic and muscarinic cholinergic receptor mRNAs in brain regions involved in regulating vigilance states. These findings suggest that the nicotine contained in cigarette smoke may predispose human infants to SIDS by interfering with the normal maturation of sleep and wake.     

The effect of prone posture on nasal temperature in children in relation to induction of staphylococcal toxins implicated in sudden infant death syndrome

The incidence of sudden infant death syndrome (SIDS) has declined in response to campaigns discouraging the prone sleeping position. Recent work suggests some SIDS death may be in response to bacterial toxins produced in the upper airway. A minimal temperature of 37 degrees C is required for induction of the pyrogenic toxins of Staphylococcus aureus identified in many SIDS infants. This aim of this study was to test the hypothesis that the prone position raises the temperature of the upper airways in children. A pilot study of 10 children (aged 3-8) and a main study of 30 children were carried out. Nasal septal temperatures were measured with an infra-red thermometer with the subjects in upright and prone positions under controlled conditions of ambient temperature and humidity. In both the pilot study and main study, nasal temperatures in the prone position were significantly higher (P < 0.01) Five subjects' prone readings were 37 degrees C or higher. These findings suggest that lying prone raises the upper airway surface temperature towards that required for toxin production. This could be one means by which the prone sleeping position contributes to the risk of SIDS.