outcome and bias the outcome of SAE in this study. However the organization of peri-natal care worldwide will not allow the setting of technical facilities for SAE in all hospitals, and patient’s transfer will therefore be a necessity in most cases. Vaginal delivery was associated with a higher success rate than was caesarean delivery (77.7% and 47.5% respectively, p,0.05). Of the causes of PPH, uterine atony was associated with the highest success rate (88.6%). Vaginal or cervical tears were associated with a trend towards SAE failure (p = 0.06). Shock was also associated with a significantly lower success rate: SAE failed in 28 of 72 (38.3%) patients with shock. Disseminated intravascular coagulopathy was not correlated with SAE outcome. Severe PPH is a complex situation, often involving a combination of characteristics (mode of delivery, PPH causes, and haemodynamic and coagulation status). Accordingly we conducted a multivariate analysis to identify independent factors that may influence SAE outcome. Uterine atony remains an independent predictor of SAE success in the multivariate analysis, with an odds ratio of 4.13 (95% CI, 1.35–12.6). Caesarean delivery was correlated with poor results, with an odds ratio of 0.16 (95% CI, 0.04–0.5). Surgical methods, in particular uterine artery ligation, have been shown to be successful and may thus be more appropriate for PPH after caesareans [3,13,19]. The causes of PPH after caesarean are different from causes after vaginal delivery: for example, only 22.7% of the PPH in the caesarean group were due to uterine atony, compared with 48.1% in the vaginal delivery group (p = 0.03). Similarly, 40.9% of the haemorrhages after caesareans were due to abnormal placentation 40.9% but only 8.6% for the vaginal delivery group (p,0.003). These differences in the causes of PPH can explain the discrepancy of the oucome of SAE. Shock was also a negative predictor of SAE success: the OR was 0.21 (95% CI, 0.07–0.6). Although SAE can be used in haemodynamically unstable patients as surgery can be more challenging for these patients, anything that may delay treatment and foreclose options for these patients should be avoided. Emergency hysterectomy must always be considered an option in this life-threatening situation. We reported two deaths in this study. The causes of PPH in those cases were surgical (one occurred after a caesarean delivery and the other was caused by genital tears. As the case descriptions make clear, these patients were in extremely grave condition at the time of the SAE. The first patient stopped bleeding after the SAE, References 1. Bouvier-Colle MH, Pequignot F, Jougla E (2001) [Maternal mortality in France: frequency, trends and causes]. J Gynecol Obstet Biol Reprod (Paris) 30: 768–775. 2. Bouvier-Colle MH, Varnoux N (2001) [Maternal mortality and severe morbidity in 3 French regions: results of MOMS, a European multicenter investigation]. J Gynecol Obstet Biol Reprod (Paris) 30: S5–9. 3. Tamizian O, Arulkumaran S (2002) The surgical management of post-partum haemorrhage. Best Pract Res Clin Obstet Gynaecol 16: 81–98. 4. den Hertog CE, de Groot AN, van Dongen PW (2001) History and use of oxytocics. Eur J Obstet Gynecol Reprod Biol 94: 8–12. 5. Gilbert L, Porter W, Brown VA (1987) Postpartum haemorrhage–a continuing problem. Br J Obstet Gynaecol 94: 67–71. 6. Prendiville WJ (1996) The prevention of post partum haemorrhage: optimising routine management of the third stage of labour. Eur J Obstet Gynecol Reprod Biol 69: 19–24. 7. Prendiville WJ, Elbourne D, McDonald S (2000) Active versus expectant management in the third stage of labour. Cochrane Database Syst Rev. pp CD000007. 8. Poeschmann RP, Doesburg WH, Eskes TK (1991) A randomized comparison of oxytocin, sulprostone and placebo in the management of the third stage of labour. Br J Obstet Gynaecol 98: 528–530. 9. Burchell RC (1968) Physiology of internal iliac artery ligation. J Obstet Gynaecol Br Commonw 75: 642–651. 10. Evans S, McShane P (1985) The efficacy of internal iliac artery ligation in obstetric hemorrhage. Surg Gynecol Obstet 160: 250–253. Arterial Embolisation but the second required a hysterectomy. The procedure itself did not change these patients’ outcome. Both, however, were transferred to our institution for SAE, and we must wonder whether this medical transfer was justified, or if it delayed optimal surgical management. Recent studies report a return of normal menses and preservation of future fertility with successful uneventful pregnan- cies after SAE [20–22]. However, we focused on outcome of SAE in severe PPH. Our study is the first large trial to assess the results of SAE in treating life-threatening PPH in a large population. It suffers from methodological and statistical limitations because it was neither controlled nor randomised, but it is extremely difficult to conduct such a trial in this rare, life-threatening emergency situation. The success rate in a large population with extremely severe PPH is not as good as the overall rates reported in the literature. PPH due to uterine atony after vaginal delivery remains an optimal indication for SAE; caesarean deliveries and hemodynamic shock are not associated with good success rates. Several reports have confirmed the efficacy of uterine artery ligature in the treatment of PPH after caesarean [3,13,19]. Whether surgery should be preferred to SAE is still unknown. However it seems very difficult for both ethical and technical reasons to organize a randomised controlled trial in such a life- threatening disease that need immediate management. However as SAE does not always guarantee haemostasis in cases of severe PPH; the indications of transfer if needed for this treatment should be carefully discussed in light of the patient’s haemodynamic status to minimise the risks. In conclusion, SAE appears to be an effective method for treating PPH, but the situations in which SAE or surgical treatments such as vascular ligature or emergent hysterectomy are indicated should be clarified with a larger clinical trial. Acknowledgments We would like to acknowledge Dr. Patrick Rozenberg for his precious advices during the elaboration and writing of this study. Author Contributions Conceived and designed the experiments: CT WB JPP ART. Performed the experiments: CT WB JS JPP DP EV. Analyzed the data: CT WB JS JPP DP EV DJ ART. Wrote the paper: CT WB DJ ART. 11. Clark SL, Phelan JP, Yeh SY, Bruce SR, Paul RH (1985) Hypogastric artery ligation for obstetric hemorrhage. Obstet Gynecol 66: 353–356. 12. Chattopadhyay SK, Deb Roy B, Edrees YB (1990) Surgical control of obstetric hemorrhage: hypogastric artery ligation or hysterectomy? Int J Gynaecol Obstet 32: 345–351. 13. Vedantham S, Goodwin SC, McLucas B, Mohr G (1997) Uterine artery embolization: an underused method of controlling pelvic hemorrhage. Am J Obstet Gynecol 176: 938–948. 14. AbdRabbo SA (1994) Stepwise uterine devascularization: a novel technique for management of uncontrolled postpartum hemorrhage with preservation of the uterus. Am J Obstet Gynecol 171: 694–700. 15. Nizard J, Barrinque L, Frydman R, Fernandez H (2003) Fertility and pregnancy outcomes following hypogastric artery ligation for severe post-partum haemor- rhage. Hum Reprod 18: 844–848. 16. Pelage JP, Le Dref O, Jacob D, Soyer P, Herbreteau D, et al. (1999) Selective arterial embolization of the uterine arteries in the management of intractable post-partum hemorrhage. Acta Obstet Gynecol Scand 78: 698–703. 17. Corr P (2001) Arterial embolization for haemorrhage in the obstetric patient. Best Pract Res Clin Obstet Gynaecol 15: 557–561. 18. Pelage JP, Le Dref O, Mateo J, Soyer P, Jacob D, et al. (1998) Life-threatening primary postpartum hemorrhage: treatment with emergency selective arterial embolization. Radiology 208: 359–362. 19. O’Leary JA (1995) Uterine artery ligation in the control of postcesarean hemorrhage. J Reprod Med 40: 189–193. PLoS ONE | www.plosone.org 5 November 2008 | Volume 3 | Issue 11 | e3819