We have demonstrated that obese nulliparous women delivering a singleton infant at term have a twofold increase in risk of major PPH, regardless of mode of delivery, and that this risk is independent of many other recognised risk factors for major PPH. Contrary to our hypothesis we have found that obese nulliparous women who give birth vaginally have a twofold increase in risk of major PPH, similar in magnitude to those delivering by caesarean section. Previous studies have suggested that the increase in risk of PPH in obese women was largely explained by a concurrent increased caesarean section rate [35, 36]. Our findings identifying elevated risk for major PPH in obese women after vaginal birth are an important alert for clinicians. Active management of third stage is already recommended as standard practice for all women . We would recommend in this group of women who are obese, additional vigilance is required to prevent and manage PPH. No other studies have primarily investigated the role of maternal obesity on risk of major PPH among nulliparous women. The rate of major PPH (greater than or equal to1000mls) in this nulliparous cohort was 8.9%, (vaginal delivery [5.4%]; caesarean section [16.2%]). This is higher than the rate reported in a previous study in women of mixed parity (5.3%) where a higher threshold was used for major PPH, namely blood loss greater than 1000mls . If this same definition is applied to our population (i.e. >1000mls), the rates of major PPH are almost identical (5.1% in our cohort). Among the few previous publications reporting maternal obesity and general birth outcomes in nulliparous women, comparisons are difficult due to absent or differing definitions of PPH and none have assessed the risk of PPH after vaginal delivery and caesarean section separately. Our findings are consistent with the only study of nulliparous women that adjusted for confounding factors, and reported a two fold increase in risk of major PPH in obese women . However, in that study vaginal and caesarean births were not analysed separately, and no adjustment was made for perineal trauma or birthweight which are consistently reported as risk factors for PPH . Two other studies in nulliparous women have reported no association between obesity and major PPH but these studies were underpowered [38, 39]. In a further study, increased rates of PPH (blood loss greater than 500mls) were reported after vaginal birth in nulliparous obese women compared to those with a BMI of 20–30, but the magnitude of risk was not quantified .
Only one other study has primarily investigated the relationship between maternal obesity and PPH (defined as haemorrhage >1000mls) . Blomberg reported a small increased risk among obese women following vaginal delivery, but PPH risk was variable according to class of obesity following caesarean section. This study population was of mixed parity, and adjustment was only possible for very limited confounders (year of infant birth, maternal age, parity and smoking). Blomberg reported an increased rate of PPH in obese women predominantly associated with uterine atony, but also due to soft tissue trauma. No association was reported between obesity and PPH due to retained placenta. Although we did not have data available to identify the primary cause of PPH, when we performed a subgroup analysis amongst women who delivered vaginally excluding those with major perineal trauma (episiotomy or third/fourth degree laceration), and/or retained placenta, there was no significant difference in effect. We therefore demonstrated that the higher rates of PPH in obese women in our study were not attributable to either major perineal trauma or retained placenta and hence were most likely due to uterine atony. Other risk factors we found for major PPH after vaginal birth were similar to those previously identified, as seen in Table 2.
It is well established that obese women have higher rates of caesarean section, especially emergency intrapartum caesarean section,  and we confirmed that this mode of delivery was associated with the highest rates of PPH among the whole study population. We found that obese women who had a caesarean section had a 70% increase in risk for PPH. Challenging surgery in obese patients is associated with prolonged operative time, and consequently with increased blood loss . Other risk factors that we identified for PPH after caesarean section are consistent with previous studies [5, 33, 41–43].
Obesity was one of four factors we identified that independently increased risk for PPH after both vaginal and caesarean deliveries among nulliparous women (along with increasing birthweight, APH and Asian ethnicity). The relevance of our finding that increasing birthweight is associated with risk of PPH is that we have shown that the relationship is dose dependent and that there is not a cut off at which increased risk occurs, for example with macrosomic or large for gestational age infants, which has been reported previously [44, 45]. Contextualising this finding to the clinical setting, there is a 40% increase in risk for PPH with every 500g increase in birthweight in term infants.
Our novel finding that the independent risk for PPH was increased in women with a history of APH from any cause exclusive of placenta praevia is clinically significant as APH (predominantly of unknown origin) occurred in 5.2% of our nulliparous cohort. An association between PPH and Asian ethnicity has been reported previously [34, 45, 46].
A strength of our study was the ability to adjust for many known risk factors for PPH to better determine the independent effect of obesity for vaginal and caesarean delivery discretely. In keeping with other clinical studies, visual estimation was usual practice to estimate blood loss in our study . Visual estimation has been reported to underestimate higher volumes of blood loss,  it is therefore unlikely that we overestimated major PPH prevalence. We did not have data to further assess PPH defined by peripartum reduction in haemoglobin or requirement for blood transfusion.