Abstract
Postpartum hemorrhage (PPH) is one of the most important issues in obstetrics, for which hemostatic transarterial embolization has been widely used. As Grönvall et al. 1 concluded: “embolization is an effective and safe procedure to control PPH when other procedures (including surgery) have failed”. This is true for PPH in general. Treatment of uterine artery pseudoaneurysm (UAP), also an important cause of PPH, shows a stark contrast to this general concept. UAP requires transarterial embolization 2, 3; surgical procedures including uterine curettage are principally contraindicated. UAP has been considered to be a rare disorder, occurring after cesarean section or traumatic abortion/deliveries: cesarean incision injures the uterine artery wall and blood escapes around the site. When surrounding tissue covers this blood accumulation and when it still has continuity with the uterine artery, UAP forms 2, 3. We broadened this concept 3. UAP can occur even without “apparent” traumatic procedures: it can occur after non-traumatic vaginal deliveries. It is not as rare as previously believed, with an estimated incidence of 0.2–0.3% 3. We suggested that underlying vascular abnormality may be one possible cause of UAP 4; however, this does not explain all causes of UAP after non-traumatic delivery. Why do some patients develop UAP after normal vaginal delivery while many others do not? We hypothesized that “strong shear” or “acute stretching” of the artery, and not direct injury to it, may account for the occurrence of this type of UAP. Rapid delivery and dystocia have been reported as a cause of genital tract injury including pelvic hematoma 5. Especially in rapid delivery, strong and acute stretching of the pelvic artery is expected to occur, which may cause vessel tear, leading to pelvic hematoma formation. We hypothesized that a similar mechanism may function in UAP occurrence after non-traumatic delivery. We examined whether patients with UAP showed rapid deliveries or dytocia. Of the 22 UAP patients we treated, six suffered UAP after normal term, or near term, vaginal deliveries (median: 37.5 weeks, range: 34–42 weeks) 3. Intervals from onset to delivery and the second stage of labor were a median of 514 min (range: 150–645) and 36 min (range: 14–43), respectively (primi- and multiparous women grouped together). There were no rapid or protracted (prolonged) deliveries (S. Matsubara, Y. Baba, unpublished data). None of the women had clinical or histological chorioamnionitis (unpublished data), and thus intrauterine infection was also rejected as an underlying mechanism of this type of UAP. A report on three UAP women 6 associated rapid delivery with UAP; however, two were delivered preterm (27–30 weeks). Rapid delivery may result from (a) low resistance of the pelvic canal compared with the fetus (encountered at preterm delivery) or (b) abnormally strong uterine contractions. A “strong shear” or “acute stretching” of the artery may occur in scenario (b) but not (a). That report also did not support our hypothesis. Based on the diversity of its clinical features, I stated, “UAP may behave as a chameleon, with its skin color easily changing in a patient-by-patient manner, and sometimes deceives physicians” 7. One important reason for this deception may be that UAP can occur “unexpectedly” after non-traumatic delivery. Furthermore, the treatment strategy differs between PPH general and UAP. Clarification of some risk factors of post non-traumatic delivery UAP will enable obstetricians to prepare for its occurrence. We should not be “deceived”.
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