Journal of Epidemiology and Community Health, 1989, 43, 133-139

Epidemiology of babies dying at different ages from thesudden infant death syndromeJONATHAN P NICHOLL AND ALICIA O'CATHAINFrom the Medical Care Research Unit, Department of Community Medicine, University of Sheffield MedicalSchool, Sheffield.

ABSTRACr An analysis of data from the United Kingdom multicentre study of postneonatalmortality has been made to assess whether there are causally distinct groups of babies dying from theSudden Infant Death Syndrome (SIDS), and to develop explicit risk factor profiles for the subgroups.The 303 SIDS babies in the multicentre study were divided into four subgroups by age at death:

weeks 1-7, 8-15, 16-23, and 24 or more weeks. Contrasts between these subgroups with respect to 28epidemiological characteristics and to pathology findings were investigated. Significant contrasts inthe number of previous pregnancies, duration of the 2nd stage of labour, gestational length, familyfinances and repair of housing were found. Overall, very strong evidence of epidemiologicaldifferences was found (Xi = 29-3, p < 0-001), and of contrasts in the nature and degree of anyacquired terminal disease.

It is concluded that there are different causes ofSIDS with different distributions according to ageat death.

The majority of sudden unexpected infant deaths (cotdeaths) are also unexplained at necropsy,' and suchunexplained cot deaths (Sudden Infant DeathSyndrome, SIDS, deaths) made up about 35% of allpostperinatal deaths in the UK in 1985.2 In 1986 therewas an unusual increase in the infant death ratespecific to the postneonatal period3 which waspartially accounted for by a 15% increase in thenumber of recorded SIDS deaths.4

It is now widely believed that SIDS may not be asingle entity, and that a number of differentmechanisms can lead to SIDS deaths. If this is truethen there are important implications for developingstrategies for prevention. Since the causes of SIDSdeaths are, by definition, not known, the usual routefor prevention is not open, at least in the short term.The options, then, are either to identify infants in highrisk groups and to intervene in the health care ofindividual babies during the early months of theirlives5 or to adopt a broader population approach bytrying to lower the incidence of risk factors.6 Theadvantages of small reductions in risk throughout thewhole population have been described in relation toother causes of mortality.7 Both strategies requireidentification of risk factors for SIDS. However, ifSIDS is a syndrome with not one but several causes,then considering all SIDS cases together may haveconfused the epidemiology and blurred theidentification of the risk factors. Some factors

important in the deaths of one group of babies mayhave been missed through pooling all the subgroups.

Since appropriate subgroups cannot be identified bytheir actual underlying causes, it is necessary to usesome proxy variable(s) which are most likely to differbetween any causal groups. The most obviouscandidates for such proxy measures are age at deathand the necropsy findings.With respect to age at death, it is prima facie

reasonable to suppose that if there are different causesof SIDS then they will have distinct, though probablyoverlapping, age at death distributions. Sosubdividing the babies into different age at deathgroups will result in subgroups with different mixturesof causes of death and different epidemiologicalprofiles. Indeed, whether or not age at deathsubgroups have distinct epidemiology might be usedto assess the multiple cause hypothesis.On the other hand, the question of whether or not

pathologically distinct subgroups ofSIDS would havedifferent mixtures ofcauses ofdeath is complicated bylack of knowledge about the pathology of live babieswho survive infancy.

Accordingly, we have investigated theepidemiological evidence for the multiple causehypothesis with respect to age at death, and developedexplicit epidemiological, or risk factor, profiles foreach of the subgroups.

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134Methods

The data on 988 babies who died at between I weekand 2 years old and 773 controls matched for date andplace of birth which were collected for the UKMulticentre Study of Post Neonatal Mortality8 havebeen further analysed in this study. The data andmethods have been thoroughly described previously.Eight centres were included in the study, which ranbetween 1976 and 1979, and data were obtained oneach death from hospital records, home interviews,general practitioner and health visitor records, andnecropsy findings.

Excluding babies who did not have a thoroughnecropsy, there were 303 babies in the study (31% ofthe total) whose deaths were not explained orexpected, and which would usually be labelled "SIDS"in accordance with the definition of Beckwith.9 Theseare the subject of this enquiry. Nearly half (42%) ofthese babies were completely symptomless beforedeath, a fifth (21%) had non-specific symptoms andthe remainder had symptoms of specific illnesses(typically of upper respiratory tract infections) notsufficient to explain the deaths.

In these 303 cases the relevance of the pathologyfindings to the death under the headings "terminaldisease", "metabolic disturbance" and "tissuedamage" has further been assessed as "major","minor", or "none" (see the Multicentre Study report,appendix 1). The last group includes a few babies inwhom pathology, though present, was not assessed ashaving any bearing on the deaths.

Infants with acquired terminal disease were alsogrouped by the anatomical system in which the diseasewas recognised. The main sites being the upper andlower airways (URT, LRT respectively,) thegastrointestinal system (GI), and "other" sites.For the purposes ofcomparing the epidemiology of

older and younger SIDS deaths, the age at deathdistribution has often been dichotomised at 12 weeks,and in order that our results should be directlycomparable with these studies we also dichotomisedthe age distribution at 12 weeks. However, mostpopulation studies show little evidence of a bimodaldistribution in age at death,'0 and we did not observetwo peaks in the distribution on either side of 12 weeksin the multicentre data either (see fig 1). Accordingly,for the main analysis, the age distribution was firstdivided at the median (15 weeks), and then the lowerage group was subdivided into two intervals of equallength (less than 8 weeks, and 8 to 15 weeks), and theupper interval divided to give a third interval of thesame length (16 to 23 weeks). The remainder of thedeaths comprise one group ofolder deaths. The use offour intervals chosen in this way avoided any selection

Jonathan P Nicholl and Alicia O'Cathain

biases and enabled any trends in the associatedepidemiology to be identified.

0

0

z

0

Age at death (weeks)

Fig 1 Observed and estimated age at death distribution. Thesmooth curve gives the relative frequency with which deathsoccur at diferent ages estimated by a log-normal distributioncurve fitted by equating moments.

The Multicentre Study collected information on anextensive range of characteristics of the infant, themother, the pregnancy and the infant's social andfamilial environment. Twenty eight characteristicswhich are widely thought to be risk factors for SIDS orwhich have recently been discussed in the literature aspossible factors in SIDS, and for which there was atleast weak evidence (p<0 1) that the cases andcontrols differed, were included in the analysis (seetable 1).

Table I Characteristics included in the analysis

1 Birthweight2 Length of gestation3 Feeding4 Attendance at a special care

baby unit (SCBU)5 Time in SCBU6 Singleton/multiple birth7 Number of home contacts with

GP8 Number of contacts with GP

before death9 Sex10 Mother's age at delivery11 Mother's smoking habits12 Number of previous pregnancies13 Interval between births14 Other infant deaths

15 Duration of 2nd stage of labour16 Number of antenatal

consultations17 Time of first antenatal

consultation18 Weeks delay in seeing GP19 Time of first hospital contact20 Ownership of accommodation21 Type of accommodation22 State of repair of

accommodation23 Cleanliness of accommodation24 Financial circumstances25 Social class of father26 Family problems27 Employment status of father28 Ratio of people to rooms in

home

Epidemiology of sudden infant death syndrome

The question of whether the distribution of each ofthe epidemiological characteristics differed betweenthe age at death subgroups was investigated bycomparing the distributions using x2 tests (aftercategorising those characteristics measured oncontinuous scales), and a multivariate discriminantanalysis was carried out to assess the evidence as awhole for whether there are differences in theepidemiology of babies dying at different ages (withthe categorical variables dichotomised and treated ascontinuous).

Multiple logistic regression models have also beenfitted separately to each subgroup of cases andcontrols to identify a group of factors which takenjointly appear to discriminate most sharply betweenthe cases and controls. The resulting models identify asmall group of factors which, taken together, areassociated with an increased risk of a SIDS deathwithin that subgroup.

Results

The numbers of cases and pathology profiles of eachof the four age at death subgroups are shown in table2.

Table 2 Pathology profiles of age at death subgroups

Age at death, weeks (%)

Pathology findings 1-7 -S15 16-23 24-103

Acquired terminal disease:None 34-6 24-0 14-7 9-6MinorURT 38-5 32-0 36-8 21-7LRT 5-8 140 162 157GI 1-9 2-0 5-9 6-0Other 19 0 0 0 0 2 4

All 481 48-0 58-8 45-8MajorURT 5-8 7 0 7-4 8-4LRT 7 7 11-0 11.8 22-9GI 1-9 7 0 5-9 9-6Other 19 3-0 1-4 3-7

All 17.3 28-0 26-5 44-6

Metabolic disturbance:None/Minor 59-6 640 72-1 590Major 40-4 36-0 27-9 40 0

Tissue damage:None 25-0 26-0 26-5 19-3Minor 61-5 67-0 66-2 60-2Major 13-5 7-0 7-4 20-5

All casesn = 100% 52 100 68 83

There is a striking contrast between the pathologyprofiles of the subgroups. Whilst 35% of babies dyingbetween 1 and 7 weeks old had no acquired disease and39% had only minor URT infections at the time of

135

death, only 10% of babies dying at over 24 weeks hadno evidence of disease and only 22% had minor URTinfections. Babies dying at intermediate ages hadintermediate levels of disease.

Five characteristics (number of previouspregnancies, duration of the 2nd stage of labour,gestational length, family finances, and repair ofhousing) discriminated significantly between the fourage at death groups of SIDS deaths. Some weakevidence was also found that family problemsdiscriminated between the subgroups. When thesevariables were entered into a multivariate discriminantanalysis, the number of previous pregnancies, familyfinances, and the state of repair of the family's housingwere found to discriminate independently between thesubgroups. Overall, very strong evidence was foundthat these three characteristics, taken jointly,discriminated between babies dying at different ages(X= 29-3, p<0-001).

Given, then, that the subgroups areepidemiologically distinct, a risk profile was drawn upfor each group separately. The only characteristicfound to be (significantly) associated with increasedrisk in all four groups was birthweight. The riskassociated with multigravidity and young mothersincreased with age (see figs 2 and 3) and a similar effect

4-

r.r.

2-

01

r.r.

10-

5-

0

I

16 21 26 31 36Mother's age

. .. . -

..

No of cigarettesFig 2 Estimated relative risk of death by mother's age andnumber of cigarettes smokedper day during pregnancy. Risksare estimated relative to infants of mothers aged 26 andnon-smokers in four age groups.

1-7 weeks,. 8-15 weeks, ---- 16-23weeks, - * over 24 weeks.

20 25 30

was seen with regard to the state of housing of the young babies included only mother's smoking duringinfant (fig 3). In contrast, the risks associated with pregnancy as a significant risk factor (see table 3) formothers smoking during pregnancy and attendance at which the risk ofdeath was found to increase threefolda special care baby unit (figs 2 and 3) show the for every 10 cigarettes smoked per day. In the older age

groups the profiles are not dissimilar from each other.

(weeks) They all include birthweight or gestational age and

some indicator of possible socio-economicdeprivation (family problems in peak age infant

4 l deaths, repair of housing in the post-peak age group,r.r. and family finance in the oldest group). The number of27n _ previous pregnancies considerably increased the risk

in both the middle age groups but was not included inthe risk profile of the oldest group of infants.

Attendance at SCBU Comparing the two age groups 1-1 1 weeks and 12 +weeks, six characteristics (number of previous

10 pregnancies, financial problems, gestational age andr.r. l v . three aspects of housing) discriminated significantly

51 T [ ~ l r between infants who died at the younger ages (n = 102)o I w -_ v 2 |and the others (n = 201). When multivariate profiles

~ .,, were drawn up separately for the two groups,

Birth order multigravidity and a poor state of repair of housingwere found to be associated with a substantiallyincreased risk only in the older babies (see table 4),

r.r. 10 whilst maternal smoking during pregnancy was only asignificant risk factor in the profile of babies under 12

weeks of age.

&O$<08i QF; o Discussion

State of repair of housing EVIDENCE FOR SEVERAL CAUSES

~~~~~~~~~Someprevious authors have commented onFig 3 Estimated relative risk ofdeath by number ofprevious dife between or and youngerbiepregnancies, house repair andattendance at a special care baby dfferences between older and younger babiesunit (SCBU). Relative risks are estimatedfrom odds ratios following the observations of Kraus et al,'1 whorelative to infants ofprimigravid mothers, in housing ofgood noticed that SIDS was associated with weather factorsrepair, who did not attend an SCBU. Vertical lines give only in older babies, and Fedrick"2 who found that,approximate 95% confidence intervals. relative to younger groups, older SIDS deaths

commonly occurred in winter in male babies. Neitheropposite effect, the risk decreasing at increasing ages. of these factors was found to be significantly moreWhen all the characteristics were entered into the pronounced in the multicentre study in SIDS deathslogistic regression models, the resulting risk profile for occurring after 12 weeks. Fedrick,13 however, also

Table 3 Risk profiles

Age at death Characteristics with signifcant relative risks.* Values are relative risk (95% confidence interval)

1-7 weeks Number of cigarettes smoked by mother during pregnancyn=52 1-81 (1-25, 2 62)

8-15 weeks Family problems + birthweight + at least one previous pregnancyn = 100 5-59 (2-16, 14 51) 1 57 (1-15, 2 16) 2-76 (1 37, 5 55)

16-23 weeks At least oneprevious pregnancy + housing in poor repair + birthweight + other infant death

n = 68 7-53 (2-38, 2383) 1337 (181, 9871) 172 (1-81, 208) 411 (148, 1138)

24+ weeks Inadequate family finance + length of gestation + mother's agen = 83 3-92 (1 62, 9 50) 1 43 (1-15, 1 78) 1 65 (1 11, 2-44)

Te increase in risk for smoking is given for an increase of5 cigarettes smoked per day, for birthweight for a decrease of 500g, for gestational period for I week less, andfor mother's age for 5 years younger.

136 Jonathan P Nicholl and Alicia O'Cathain

Epidemiology of sudden infant death syndrome

Table 4 Risk profiles

Age at death Characteristics with significant relative risks.* Values are relative risk (95% confidence interval)

1-11 weeks Number of cigarettes smoked bymother during pregnancy + birthweight + family problems

n = 102 1-30 (107, 1-59) 1-44 (103, 202) 309 (1-18, 8 08)+ attendance at SCBU + smoking x SCBU

2-50 (1-14, 5 50) 2-39 (1-02, 5 60)

12 + weeks Housing in poor repair + length of gestation + mother's agen = 201 6-99 (2-62, 18-63) 1-32 (1-15, 1-52) 1-93 (1-47, 2-53)

+ at least one previous + family problems + first contact withpregnancy hospital4-25 (2-37, 7-63) 261 (1 33, 5-14) 1 42 (1-04, 204)

SCBU = special care baby unit.The increase in risk for smoking is given for an increase of 5 cigarettes smoked per day, for birthweight for a decrease of 500g, for gestational period for 1 week less, formother's age for 5 years younger and for first contact with hospital for 10 weeks later.

noted that low maternal age, high parity and lowsocial class were features only of older babies, just aswe have observed. The theme of respiratory infectionsor a winter preponderance playing a comparativelymajor role only in older deaths is common to manystudies which have contrasted age groups, 1418although some other studies have not found theseeffects. 19-21One possible reason for the difference between the

findings of various studies is that they have not alwaysused the same age groups. Beal22 used 0-8, 8-16 and16-24 weeks, Macarthur and Bartholomew21 used4-19 and 20-52 weeks, Kraus et al used 1-4 and 5-11months, Carpenter and Gardner,15 and Goldberget al9 used monthly divisions. Others have usedFedrick's original division at 12 weeks or variations ofit such as 3 months or 13 weeks. 14 16 18 20 23-28 Itwouldbe appropriate to divide the babies at 12 weeks if theage at death distribution was bimodal with peakseither side of 12 weeks, as has sometimes been found.'0However, a bimodal distribution is not usually found.Indeed, commonly, 12 weeks is the unique modal ageat death and a division at this age may thus be entirelyinappropriate. The advantage of using several agegroups is that it has been possible to identify theobvious patterns and trends in the epidemiologyassociated with death at different ages seen in figs 2and 3. On the other hand, using just two largersubgroups, some factors with small associated riskshave been revealed as significant.On balance, the evidence for epidemiological

contrasts at different ages available both from thepatterns revealed using several age groups and thesignificance of the differences between the twosubgroups is similar. Both analyses show strongcontrasts between the risk factors for SIDS at differentages. If we were to suppose that there was a singlecommon underlying cause of SIDS then it would benecessary to explain why this cause is only associated

with certain characteristics, such as multigravidity, insome groups of babies. Plainly the contrasts in theepidemiology ofSIDS at different ages are most easilyexplained by supposing that there are different causesor mixtures of causes of SIDS operating at differentages.The contrast in the epidemiology of older and

younger SIDS is to be found not just in what factorsare significant but in the type offactor. Factors such aslow birthweight, maternal smoking during pregnancy,and attendance at a special care baby unit areassociated with, or indicate, a vulnerability at birth,and it is perhaps not surprising that they are associatedwith the deaths of very young babies. On the otherhand in the older babies factors associated with thelikelihood of infections-dirty housing in poor repair,and the possible presence of other children in thehouse-were found to be associated with the risk ofSIDS. Whether as a cause or an effect, the associationsare clearly reflected in the contrasting pathology ofinfants dying at different ages. Young SIDS infantshave little pathology at the time of death compared toolder SIDS infants, many of whom had LRT and GIinfections. Overall, the conclusion that there are anumber of different underlying causes of SIDS, withdifferent age at death distributions, seems certain.

IMPLICATIONS FOR THE AETIOLOGY OF SIDSWith regard to younger SIDS infants, theepidemiological characteristics present few clues to thecause(s) of death. The strong association withmaternal smoking during pregnancy presumablywould be allied with smoking after pregnancy andaround the time of the infant's death. It is known thatsmoking leads to an increased incidence of LRTinfections29-3' but since comparatively few youngbabies were found to have any necropsy evidence oflower respiratory disease, it may be antenatal smokingwhich is the risk factor in young infants. Indeed, when

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antenatal smoking was taken into account, otherindicators of neonatal vulnerability-low birthweightand time spent in a special care baby unit-no longercontributed to identifying very young babies at risk.

In infants aged between 8 and 24 weeks and inbabies with some evidence of terminal disease, wetypically found poor housing and multigravid mothersto be associated with the risk of SIDS. Both of thesefactors are likely to be associated with an increasedincidence of infections and other disease in babies.Poor housing and "another" child might also beindicative of many other things, including neglect.However, other well known characteristics, such as thewinter excess of SIDS, are also indicative of aninfectious aetiology, at least in some SIDS cases.

IMPLICATIONS FOR THE PREVENTION OF SIDSOne possible strategy for the prevention ofSIDS relieson identifying babies at risk, and in this context it hasbeen widely reported that risk scores for SIDS as awhole often fail to identify some subgroups ofSIDS.32A discriminant analysis for all the 303 SIDS cases inthis study taken together yielded eight independentlysignificant risk factors. Among infants less than eightweeks old the positive predictive value of thediscriminant function (that is, the proportion ofpredicted cases that were actually deaths) was 72%compared to 81% in babies aged 16-24 weeks. Incontrast, a discriminant based on the singlecharacteristic "smoking during pregnancy", identifiedfrom the multivariate profiles as a risk factor in younginfants, had a positive predictive value of 79% in thatgroup.However, overall little improvement in the

sensitivity and positive predictive values of thediscriminant could be achieved by using separatesubgroups functions.The viability of the alternative approach to

preventing SIDS by reducing the incidence of riskfactors in the population, for example by reducing theprevalence of smoking during pregnancy, depends onthe relation that the risk factors have to SIDS.Although it is neither a necessary nor a sufficientcondition that the risk factor actually be a "cause" ofSIDS, this would certainly make populationintervention more likely to succeed. Of the fewattempts to identify what qualities associations musthave for them to be labelled causes, Bradford Hill's33 isthe most well known. It is important, therefore, toassess the qualities of strength, consistency and so onthat the epidemiological associations have. On thesegrounds, smoking both during and after pregnancy,and high parity might well be justifiably labelled ascauses of SIDS, at least until Bradford Hill's lastcriterion of experimental evidence, in the form of theresults of a population intervention study, could beassessed.

Jonathan P Nicholl and Alicia O'Cathain

We are very grateful for the advice and assistance ofDrs Jean Keeling and Mike Murphy and also ofProfessors Brian Williams and John Knowelden. Weare also grateful to Lynne Schofield and JanetMorrison for their help.

This secondary analysis of the multicentre data hasbeen supported by the Foundation for the Study ofInfant Deaths. The original study and analysis wassupported by the DHSS, who, together with TrentRegional Health Authority, maintain the MedicalCare Research Unit. We are grateful for their support.

Correspondence to: J P Nicholl, Medical CareResearch Unit, Department ofCommunity Medicine,University ofSheffield Medical School, Beech Hill Rd,Sheffield S1O 2RX.

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Acceptedfor publication December 1988