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Keywords:

  • Cohort studies;
  • family;
  • generation;
  • obstetric anal sphincter injuries;
  • recurrence;
  • siblings

Abstract

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

Objective

To investigate the aggregation of obstetric anal sphincter injuries (OASIS) in relatives.

Design

Population-based cohort study.

Setting

The Medical Birth Registry of Norway from 1967 to 2008.

Population

All singleton, vertex-presenting infants weighing 500 g or more. Through linkage by national identification numbers, 393 856 mother–daughter pairs, 264 675 mother–son pairs, 134 889 mothers whose sisters later became mothers, 132 742 fathers whose brothers later became fathers, 131 702 mothers whose brothers later became fathers and 88 557 fathers whose sisters later became mothers were provided.

Methods

Comparison of women with and without a history of OASIS in their relatives.

Main outcome measure

Relative risk of OASIS after a previous OASIS in the family.

Results

The risk of OASIS was increased if the woman's mother or sister had OASIS in a delivery (aRR 1.9, 95% CI 1.6–2.3; aRR 1.7, 95% CI 1.6–1.7, respectively). If OASIS occurred in one brother's partner at delivery, the risk of OASIS in the next brother's partner was modestly increased (aRR 1.2, 95% CI 1.1–1.4). If OASIS occurred in one sister at delivery, the risk of OASIS in the brother's partner was also increased a little (aRR 1.2, 95% CI 1.1–1.4). However, there was no excess occurrence in sisters whose brothers' partners had previously had OASIS (aRR 1.1, 95% CI 0.9–1.3).

Conclusions

There appears to be increased familial aggregation of OASIS. These risks are stronger through the maternal rather than the paternal line of transmission, suggesting a strong genetic role that shapes aggregation of OASIS within families. These observations must be cautiously interpreted because of bias from unmeasured confounding factors may have impacted the findings.


Introduction

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

Obstetric anal sphincter injuries (OASIS) may result in severe complications, such as perineal pain, dyspareunia, and anal and urinary incontinence.[1-4] In recent years, an increase in the occurrence has been reported in several countries.[5] In Norway the reported occurrence of OASIS in vaginal deliveries has increased from 0.5% in 1967 to 4.1% in 2004.[6] Probably as result of increased attention and several intervention programmes,[7] this figure was reduced to 2.5% in 2009.[8]

Previous studies have identified important risk factors for OASIS, such as primiparity, instrumental delivery, high birthweight and high maternal age.[6, 9, 10] Although earlier studies have reported that OASIS tends to recur between deliveries in the same mother,[11, 12] and have also indicated a paternal influence on recurrence,[13] knowledge about aggregation of OASIS in families is limited. Such knowledge might have both clinical and etiological importance. The observed recurrence suggests that there might be a genetic predisposition for OASIS, possibly involving both maternal and fetal genes, thus increasing the aggregation of OASIS in families. However, environmental factors may also be involved.

To extend our understanding of familiar aggregation of OASIS, we investigated the aggregation of OASIS within generations and among sisters or brothers' partners.

Methods

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

In this registry-based cohort study, we used data from the Medical Birth Registry of Norway, which is based on compulsory notification of all live births and stillbirths in the country after 16 weeks of gestation, and comprises records of more than 2 200 000 births since 1967. A notification form including data on maternal health before and during pregnancy, interventions and complications during delivery and health of the newborn is completed by the midwives and attending doctors. Except for a modest decrease in the annual numbers of births during the 1970–80s, the number of births in Norway was fairly stable, around 60 000 births per year during the study period.[8]

The notification form remained almost unchanged until 1999, when a revised version was introduced. The national identification number is provided soon after birth by the population registry of Norway. Routine record linkage between the Medical Birth Registry and the population registry is established by means of the mother's identification number, and ensures the registration of all births in the medical birth registry.

Classified according to the International Classification of Diseases, OASIS includes third-degree injuries (ICD–10: O70.2) involving the sphincter muscle, and fourth-degree injuries (ICD–10: O70.3) involving rectal mucosa. In the period 1967–1998, OASIS was reported to the medical birth registry as plain text and recorded in the registry as ‘Rupture of anal sphincter’ or ‘Total rupture’, whereas from 1999 onwards it was recorded by checking a box in the form. The registration of OASIS has been validated with a satisfactory result.[14]

From 1967 up to June 2005, more than 2 270 000 births were registered in the medical birth registry. Female newborns were subsequently recorded as mothers, with 498 318 births (Figure 1). Similarly, 334 069 newborns were recorded as fathers (Figure 1). The study was confined to singleton vertex-presenting vaginal births with birthweights of 500 g or more in both generations, leaving 393 856 mother–offspring and 264 675 father–offspring units for study (Figure 1). The number of fathers with data on their own births was considerably lower than for mothers, because they were on average 2 years older. Thus, fewer of their births were recorded in the medical birth registry from 1967: 55% of mothers were born during 1967–1971, whereas 63% of fathers were born during the same period. Additionally, 7% of the fathers were unknown and could not be identified. We used these data to study whether women and men whose own births were complicated by OASIS had an excess risk of parenting deliveries complicated by OASIS.

image

Figure 1. Flow charts of the study population in the generational file, Norway, 1967–2005.

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In the population registry of Norway all full sisters and brothers in Norway were identified and linked with the Medical Birth Registry, establishing a file in which each record holds data on all consecutive births among full sisters and partners of full brothers from 1967 to 2008. We identified 175 550 mothers with at least one sister who later became a mother, 173 886 fathers with at least one brother who later became a father, 171 947 mothers with at least one brother who later became a father, and 116 267 fathers with at least one sister who later became a mother (Figure 2). The study was confined to singleton, vaginal, vertex-presenting births with birthweights of 500 g or more, leaving 134 889 mothers whose sisters later became mothers, 132 742 fathers whose brothers later became fathers, 131 702 mothers whose brothers later became fathers and 88 557 fathers whose sisters later became mothers for study (Figure 2). We also included pairs of births among sisters or brothers' partners in the study. The first birth in each pair was the first occurring among sisters or brothers' partners. The second birth in the pair was a later birth in another sibling: 170 183 pairs of births in mothers whose sisters later became mothers, 167 044 pairs of births in partners of fathers whose brothers later became fathers, 166 800 pairs of births in mothers whose brothers later became fathers and 107 374 pairs of births in partners of fathers whose sisters later became mothers (Figure 2). We used these data to assess the aggregation of OASIS among sisters and brothers' partners.

image

Figure 2. Flow charts of study population in full sisters and brothers, Norway, 1967–2008.

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From the generation file we also identified 25 568 pairs of sisters whose mother did not have OASIS. This enabled us to study the ‘pure’ aggregation of OASIS among sisters.

Statistical analysis

The aggregation of OASIS within families was estimated as the relative risk of occurrence of OASIS. Relative risks (RRs) with 95% confidence intervals (95% CIs) were calculated by log-binomial regression. We calculated the likelihood of OASIS in daughters whose mothers had OASIS. Similarly, we calculated the likelihood of OASIS in partners of sons whose mothers had OASIS. We also calculated the likelihood of OASIS in women whose sisters previously had OASIS and the likelihood of OASIS in partners of men whose brothers' partners previously had OASIS. Because analyses of aggregation in generations or siblings could include two or more births in the same woman, we used multilevel log-binomial regression analysis in order to avoid biased risk estimates and standard errors caused by the nested structure of data (births nested within women). Log-binomial regression was used to adjust for possible confounding factors such as period of delivery (before 1996, 1996–2000 and 2001–2005 for generations; 1967–77, 1978–88, 1989–98 and 1999–2008 for pairs of siblings), maternal age (<20, 20–29, 30–34, 35–39, 40 years or older), instrumental delivery (yes or no), birthweight (<2500, 2500–2999, 3000–3499, 3500–3999, 4000–4449, 4500 g or greater) or head circumference (<33, 33–34, 35–36, 37–38, 39–40, 41 cm or greater). The effects of adjusting for birth order (one or greater than one) in the second generation and in the last sibling in pairs of siblings were negligible, and this was not included in the final models. Time trends in aggregation of OASIS were assessed by adding an interaction term between year of delivery and OASIS to the models. The statistical analyses were carried out with spss (SPSS Inc., Chicago, IL, USA) and MlWin (Centre for Multilevel Modelling, University of Bristol, UK). The regional committee for medical research ethics approved the study protocol (REK Vest no. 247.09).

Results

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

The majority of births in the first generation occurred during 1967–80 and in the second generation during 1992–2005 (Table 1). There were more women of birth order 1, more heavy newborns and more frequent use of instrumental vaginal delivery in the second generation (Table 1).

Table 1. Maternal and obstetric characteristics in the generational data, with mother–daughter pairs as the observational units, with vertex-presenting vaginal deliveries with birthweights of 500 g or more (393 856 units), Norway, 1967–2005
CharacteristicsFirst generationSecond generation
Year of delivery
1967–1980381 249 (96.8%)
1981–199112 607 (3.2%)39 384 (10.0%)
1992–2005354 472 (90.0%)
Birth order
Birth order 1153 286 (38.9%)215 888 (54.8%)
Birth order 2+240 570 (61.1%)177 968 (45.2%)
Median maternal age 24 years26 years
Birth weight more than 4000 g52 145 (13.3%)83 886 (21.3%)
Instrumental vaginal delivery 10 996 (2.8%)34 338 (8.7%)
OASIS 1486 (0.4%)13 264 (3.4%)

Intergenerational risk of OASIS

Women who were born in a delivery complicated by OASIS had twice the risk of having OASIS in their own delivery compared with women with no family history of OASIS (aRR 1.9, 95% CI 1.6–2.3; Table 2). For men who were born in a delivery complicated by OASIS, the risk of OASIS in their partner was moderately increased compared with other men (aRR 1.4, 95% CI 1.1–1.7; Table 2). Stratifying data for the first or second generation's birth order did not alter the results. No significant time trends in relative risks were observed.

Table 2. Aggregation of obstetric anal sphincter injuries (OASIS) across generations, Norway, 1967–2005
Intergenerational aggregation of OASISOASIS in first generationSecond generation (daughters/partners of sons)
Total no. of deliveries in second generationNo. (%) of OASISCrude RR (95% CI)Adjusted RR (95% CI)a
  1. a

    Adjusted for period of delivery (before 1996, 1996–2000, 2001–2005), maternal age (<20, 20–29, 30–34, 35–39, 40 years or older), instrumental delivery (yes or no), and birthweight (<2500, 2500–2999, 3000–3499, 3500–3999, 4000–4449, 4500 g or greater) in second generation.

Mother and daughterNo OASIS392 37013 158 (3.4)ReferenceReference
OASIS1486106 (7.1)2.1 (1.7–2.6)1.9 (1.6–2.3)
Mother and partner of sonNo OASIS263 4559572 (3.6)ReferenceReference
OASIS122068 (5.6)1.5 (1.2–2.0)1.4 (1.1–1.7)

Risk of OASIS in siblings

Sisters who delivered subsequently to a sister with a history of OASIS had almost twice the risk of having OASIS compared with women with no family history of OASIS (aRR 1.7, 95% CI 1.6–1.7; Table 3). If OASIS occurred in one brother's partner at delivery, the risk of OASIS in the next brother's partner was modestly increased (aRR 1.2, 95% CI 1.1–1.4; Table 3). If OASIS occurred in one sister at delivery, the risk of OASIS in the brother's partner was also modestly increased (aRR 1.2, 95% CI 1.1–1.4; Table 3).

Table 3. Aggregation of obstetric anal sphincter injuries (OASIS) in Siblings, Norway, 1967–2008
Aggregation of OASIS among siblingsOASIS in siblings with first deliverySiblings with subsequent delivery
Total no. of deliveriesNo. (%) of OASISCrude RR (95% CI)Adjusted RR (95% CI)a
  1. a

    Adjusted for period of delivery (1967–77, 1978–88, 1989–98 or 1999–2008), maternal age (<20, 20–29, 30–34, 35–39, 40 years or older), instrumental delivery (yes or no), and birthweight (less than 2500, 2500–2999, 3000–3499, 3500–3999, 4000–4449, 4500 g or greater) in sibling with subsequent delivery.

Among sistersNo OASIS131 1385042 (3.8)ReferenceReference
OASIS3751316 (8.4)2.1 (1.9–2.4)1.7 (1.6–1.7)
Among partners of brothersNo OASIS129 1834872 (3.8)ReferenceReference
OASIS3559215 (6.0)1.6 (1.4–1.8)1.2 (1.1–1.4)
Among sisters and their brothers' partnersNo OASIS128 1384838 (3.8)ReferenceReference
OASIS3564210 (5.9)1.5 (1.3–1.7)1.2 (1.1–1.4)
Among brothers' partners and sistersNo OASIS86 2553358 (3.9)ReferenceReference
OASIS2302124 (5.4)1.5 (1.3–1.8)1.1 (0.9–1.3)

By contrast, there was no excess occurrence in the sisters of brothers whose partners had OASIS previously (aRR 1.1, 95% CI 0.9–1.3; Table 3).

In the subgroup of sisters whose mother had no history of OASIS, we found the same aggregation of OASIS (aRR 1.6, 95% CI 1.3–2.0, data not shown).

There was no time trend in the aggregation of OASIS among siblings, except for a decreased aggregation among brother's partners with time, and this was not significant from 1978 onwards.

In all the analysis, the year of delivery was the single adjusting variable with significant effect. Adjusting the relative risks for head circumference instead of birthweight did not alter the results.

Discussion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

The risk of OASIS was two-fold if the woman's mother or sister had sustained OASIS in a delivery. There was also excess risk, but less so, in the partners of brothers whose sister or brother's partner had sustained OASIS, whereas in the sisters of brothers whose partners had sustained OASIS there was no excess risk.

The strengths of our study were the population-based design, the large study size and the long follow-up period. The prospective collection of data reduced selection and recall bias, and provided a high precision in effect estimates. The national identification number made the linkage of births between generations and between siblings reliable, and the outcome variable has a high validity.[14]

This study was population based and the findings would thus be applicable to the Norwegian population; however, the Norwegian birth population is relatively homogenous and the external validity of our results in other populations needs to be assessed by further studies.

Furthermore, data on several possible confounding factors like instrumental delivery, birthweight, head circumference, maternal age and parity were available. A weakness was that the lack of data precluded adjusting for factors like maternal smoking, delivery position, body mass index (BMI) and duration of second stage, which have been associated with OASIS and may have confounding effects on the occurrence of OASIS.[6, 10, 15-17]

We have previously reported a time trend in OASIS,[6] resulting in increasing occurrence from 1967 to 2004. Possible explanations for the increase of OASIS in this period include: (1) improved routines for the registration of OASIS in the medical birth registry; (2) improved diagnostic attention and routines; (3) a change of classification during this time period; and (4) changes in obstetric and demographic risk factors.

In a previous study, we have assessed the validity of OASIS in the Norwegian Medical Birth Registry in 1990–1992 and 2000–2002, and found 85.3–91.8% sensitivity and 91.4–95.4% positive predictive value in the respective periods.[14] The new notification form used from 1999 onwards may have improved the recording of OASIS in the birth registry, but we observed no sudden change in the occurrence after the introduction of the new form.[6] It cannot be ruled out that Martius' previous classification of perineal tears into three degrees, including partial rupture of anal sphincter as a second-degree tear, might also have influenced the observed increase in OASIS.[18] If so, we would expect more severe rather than mild cases of OASIS to have been registered in the early period. Such ‘misclassification’ is not likely to significantly affect the observed association in siblings, as they generally occurred in the same period of time; however, the observed intergenerational association could represent an association between more severe OASIS and OASIS irrespective of severity.

Although the occurrence of OASIS tends to decrease by birth order,[6, 9] the aggregation among women whose mothers or sisters had OASIS was regardless of birth order. The risk of OASIS between sisters remained unchanged even if their mother's own deliveries were not complicated by OASIS. Consistent with the results of the present study, we have previously reported recurrence in the same woman, and that men who fathered a delivery complicated by OASIS in one woman were more likely to father a subsequent delivery with OASIS in another.[13]

Obstetric anal sphincter injuries (OASIS) may be inherited through maternal or paternal susceptibility genes for OASIS. If OASIS is inherited through paternal as well as maternal susceptibility, paternal alleles passed through the fetus might increase the mother's risk of OASIS. The higher maternal than paternal risk may be explained by a stronger maternal than paternal genetic susceptibility, including the possible contribution of mitochondrial gene susceptibility, which is exclusively transmitted through the maternal line.[19]

Birthweight and head circumference could be influenced by paternal genes and increase the risk of OASIS[20, 21]; however, such effects are likely to be negligible because adjusting for birthweight or head circumference had no effect.

Additionally, nutritional, lifestyle or other environmental factors shared by generations or siblings might explain the observed familiar aggregation of OASIS. Factors such as education, smoking, marital status and BMI have previously been studied without showing a consistent association with the risk of OASIS.[6, 10, 15, 16, 22]

In a previous study based on the same population as in the present study,[6] we reported no association between OASIS and maternal education and marital status. Additionally, we reported a 40% reduction in the occurrence of OASIS among women who smoked until the end of their pregnancy; however, the results were not significant when we adjusted for a number of variables, including birthweight. Our results were in line with a recent study from Finland that showed nulliparous women who smoked during pregnancy had a 28% lower incidence of OASIS than non-smokers, but this association was observed regardless of birthweight.[17] It is well established that women who smoke deliver smaller infants, and this may explain why smoking protects against OASIS.[17, 23] Another explanation could be the influence of smoking on the connective and collagen tissue. Smoking appears to be highly hereditable, and could present a confounding factor in our study.[24] Smoking habits were not registered in the Norwegian birth registry before 1999, and we could not control our results for this variable.

Our database also lacked information on ethnicity, which has been associated with the occurrence of OASIS.[6, 10, 15] In our previous study we reported an increased risk for OASIS in African and Asian mothers giving birth in Norway.[6] However, our study population consisted only 1.0% African and Asian mothers in the earliest period and 5.4% in the latest period.[6] Hence, ethnicity could hardly affect our results.

Body mass index and physical activity are among other environmental factors that could influence our results. In previous studies, the association between BMI and OASIS has not been reported consistently,[15, 16, 22] thus the effect of BMI on our results is uncertain. A recent Norwegian study has shown an increased risk of OASIS in women with pregestational physical inactivity.[22]

We are not aware of any other studies on the aggregation of OASIS within families; however, several studies have suggested a genetic basis for the development of female pelvic floor disorders (genital prolapse, and urinary and fecal incontinence).[25-28] There is also evidence that OASIS is strongly associated with pelvic floor disorders.[29] Magdi suggested that the ‘elastic index’, measured by the degree of abdominal striae, was predictive of perineal laceration.[30] Our study supports the hypotheses that there might be inherited biological differences in women resulting in an increased risk for OASIS.

Based on the present study, the underlying mechanism of the aggregation of OASIS in families remains unclear. Further studies are warranted to investigate whether the aggregation of OASIS within families is influenced by shared environmental factors. A classic twin study or comparing the structure of connective tissue between women with and without OASIS are some possible designs for future studies. The similar aggregation in generations and siblings support a role for genetic susceptibility in OASIS. If aggregation of OASIS in generations and siblings were exclusively explained by environmental factors, one would expect higher aggregation among sisters than in generations whose births were more spaced in time. Additionally, one would suspect similar maternal and paternal aggregations. The weaker and inconsistent paternal risk, compared with maternal risk, in the present study is consistent with our previous results indicating that a man who fathered a birth with OASIS in one woman was more likely to father a subsequent birth with OASIS in another; however, the maternal risk was higher.[13]

Conclusion

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

The present study indicates that both maternal and paternal factors contribute to the risk of OASIS. The maternal risk is likely to be caused, at least in part, by genetic susceptibility. The paternal contribution seems to be weaker, probably because it is passed only through the fetus. This study provides a new perspective on the cause of OASIS, and should stimulate research into the genetic etiology. Genetic susceptibility, along with other risk factors of OASIS, could help clinicians identify women at risk and prevent OASIS during vaginal deliveries. These observations must be interpreted cautiously, as bias from unmeasured confounding factors may have impacted the findings.

Disclosure of interests

All authors declare that they have no relevant interests to declare.

Contribution to authorship

EB contributed by writing the article, performing statistical analyses, assisting with the conception and design of the study, and with interpreting the data. LMI and PEB contributed by supervising, drafting the article and revising it for important intellectual content. SR, the main supervisor, revised the article, contributed to the conception and design of the study, assisted with the interpretation of data and supervised the statistical analyses. All authors approved the final version of the article.

Details of ethics approval

The regional committee for medical research ethics approved the study protocol (REK Vest no. 247.09).

Funding

The study was funded by the Norwegian Foundation for Health and Rehabilitation and the Norwegian Women's Public Health association.

Acknowledgements

The authors want to thank the Norwegian Foundation for Health and Rehabilitation and the Norwegian Women's Public Health association for funding the study.

References

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’

  1. Top of page
  2. Abstract
  3. Introduction
  4. Methods
  5. Results
  6. Discussion
  7. Conclusion
  8. References
  9. Reviewer's Commentary on ‘Familial risk of obstetric anal sphincter injuries: registry-based cohort study’
  10. Disclosure of interests

For many women, the birth of a baby is an empowering, fulfilling, extraordinary and life-changing event. For some, it is not.

The potential for pelvic floor trauma is one of women's major fears as they approach childbirth. It is an ongoing concern throughout and beyond pregnancy care provided by midwives, obstetricians, colorectal surgeons and urogynaecologists (Turner et al., BJOG 2008;115:1494–02). For some women, self-efficacy, along with midwifery and obstetric support and coaching, contribute to minimising perineal trauma, so alleviating the potential realisation of these fears and concerns. However, despite this, many women experience perineal tears or have an episiotomy. Although such trauma may heal without long-term impact, there are also women with longer-term psychological, psychosexual, social or physical concerns arising from the experiences of childbirth and perineal trauma, and particularly so following severe perineal trauma.

Severe trauma involves anal sphincter injuries, i.e. third-degree tears (International Classification of Diseases 10th revision: 070.2) and fourth-degree tears (International Classification of Diseases 10th revision: 070.3), collectively referred to as obstetric and anal sphincter injuries (OASIS). Known risks for OASIS include, for example, primiparity, advancing maternal age, high birthweight, instrumental birth and OASIS in a previous birth (Porat et al., Int Urogynecol J 2012:DOI 10.1007/s00192-012-1923-8). The protective or causative influence of episiotomy remains controversial (Baumann et al., Int Urogynecol J 2007;18:985–90; Räisänen et al., Am J Obstet Gynecol 2012;206:e1–6).

Baghestan et al. build on their previous work and provide here a unique approach to considerations around such trauma, through analysis of aggregation of OASIS in families within the rich database of the Norwegian birth register. Should such an association exist, they propose, this would provide the impetus for further research into maternal, paternal and fetal genetic influences on this important outcome.

The extensive and complex analyses of a relatively homogeneous ethnic group yielded many interesting trends. For example, if a woman experienced OASIS during the birth of her daughter, the daughter had an adjusted relative risk of 1.9 for experiencing OASIS when she gave birth. Knowledge of such risks may empower women to consider their options: dare it be said, have an elective caesarean section, or plan to enter labour well aware of strategies with the potential to reduce the risk, such as remaining upright, use of warm compresses on the perineum, avoiding active pushing and so on. Readers will also be interested in further analyses presented, including (i) the suggested influence of being born through OASIS and fathering a child in the future, with the associated 40% increased risk of the birth of that child being complicated by OASIS, and (ii) that having a sister who experienced OASIS increased a woman's risk by 70% for this complication during childbirth.

The authors wisely recommend caution in overinterpretation of their findings, particularly in different ethnic populations, suggesting instead, that further research should address the potential impact of unmeasured confounders, such as smoking and other environmental factors, along with genetic studies.