Failure of uterine arterial embolization: placenta accreta with profuse postpartum hemorrhage

Uterine artery embolization (UAE) has been developed as a first-line alternative treatment for postpartum hemorrhage refractory to medication. The incidence of failure is approximately 5% (1), of which abnormal placentation corresponds to more than 50% 2-4). The success rate of UAE for management of abnormal placentation with postpartum hemorrhage was reported to be 62-71% in the literature(2, 3). Rare reports of UAE failure caused by abnormal placentation have been documented. We present a case of placenta previa accreta, where the patient underwent hysterectomy following repeated failure of internal iliac artery embolization for the treatment of postpartum hemorrhage. Reviewing relevant English-written literature, according PubMed, we sought to explore the underlying mechanisms of UAE failure in abnormal placentation-induced postpartum hemorrhage. A 22-year-old, gravida 2 para 1, 39-week pregnant woman had a history of uncomplicated lower-segment cesarean section. Antenatal care was uneventful until 31 weeks of gestation when persistent placenta previa totalis was detected (Fig. 1A) at a local obstetric clinic, from where she was referred to our hospital. Under general anesthesia, a 2710-g male fetus was delivered by lower segment transverse cesarean section with Apgar scores of 9 and 10 at 1 and 5 min, respectively. A scarred uterus and placenta accreta involving > 30% of the cotyledons over the entire lower segment were noted. Intrapartum hemorrhage with blood loss in excess of 3000 ml ensued. No signs of uterine atony or genital tract laceration were observed. On the basis of the patient's strong desire to preserve her uterus, vigorous manual removal of placenta fragments was followed by hemostatic suturing. Unfortunately, subsequent vaginal blood loss exceeding 2000 ml commenced 2 h after the cesarean section while in the recovery room, and the response to medication was poor. After informed consent was obtained from the family, aorto-iliac angiography via the femoral approach disclosed a spasm of branches of the internal iliac artery (IIA), with no contrast extravasation. We found selective embolization of uterine arteries was very difficult because of spasmodical vessels. Under the impending shock condition, proximal embolization of the right-anterior and left divisions of IIA was performed using pledgets of absorbable gelatin sponge (Gelfoam) for effective bleeding control, with the patient's blood pressure subsequently recovered from 50/30 to 110/55 mmHg. (A) Prenatal sonography at 33 weeks. The placenta previa totalis, absence of retroplacenta hypoechogenicity (arrow head) and local lacunae vascular sign (→) were evident. Placenta adherence potential was suspected. (B) Angiography before secondary internal iliac artery embolization. Revascularization of the left-internal pudendal artery without contrast extravasation was evident (→). Slowly, vaginal bleeding was subsequently observed, but with more than 1000 ml of blood loss 2 h after the embolization procedure. When the vital signs had been stabilized, the radiologist urged exploration to establish the causes of the embolization failure, and a second attempt was made. Revascularization of the left internal pudendal artery with the spasm slightly relieving showed no extravasation of dye and in situ gelfoams (Fig. 1B). Catheterization of the left internal pudendal artery failed and secondary embolization of the bilateral IIA was performed using gelfoam. Disappointingly, external bleeding was still present, and severe anemia (hemoglobin 3.8 mg/dl) was diagnosed with developing disseminated intravascular coagulopathy. Then an emergent hysterectomy was smoothly performed 11 h after the cesarean section, with a blood loss of only 150 ml. Total blood loss was in excess of 10 480 ml, with a transfusion of 34 units of blood (250 ml per unit). Gross inspection revealed a tonic uterus with no obvious oozing. Microscopic examination revealed retained placenta fragments over the lower segment and an intact myometrium. One day after the operation, epigastria followed by abdominal pain and ileus were noted, subsiding 1 week later. During follow up at the outpatient clinic, the patient developed hot flushes and vaginal and skin dryness 4 months after the hysterectomy. Serum hormonal levels indicated menopausal status (follicle stimulating hormone 39.83 mIU/ml, luteinizing hormone 16.15 mIU/ml, and estradiol 24.1 pg/ml), and a prescription of estrogen replacement therapy was then started. Unfortunately, her menopausal status persisted 8 months after the hysterectomy, implying permanent ovarian failure. An English-written PubMed search was completed for the years 1979-2001 and revealed only five cases of postpartum hemorrhage resulting from placenta accreta or increta where UAE failure was experienced and a hysterectomy performed (Table I). No maternal mortality or complications were documented. Repeated arterial embolization was performed in two cases 3, 5), however, vaginal bleeding was still not controlled. Abnormal placentation is one of the major causes of hysterectomy following arterial embolization because of persistent bleeding. From the literature review and our findings, the underlying causes of UAE failure for the treatment of abnormal placentation-induced postpartum hemorrhage appear to be independent of age and are associated with: iatrogenic myometrial injury caused by vigorous digital separation of the placenta; severe disseminated intravascular coagulopathy after sudden onset of massive blood loss; delayed or incomplete embolization; and unrecognized bleeding from collateral circulation. Deux et al. have reported that spasm of the IIA branches makes selective embolization difficult, resulting in a high frequency of no extravasation of dye (7). Proximal embolization of IIA may be ineffective for controlling severe postpartum hemorrhage as a result of numerous collateral vessels in distal IIA early recovery, which may have been the main cause of failure of the repeated IIA embolization in our case. The secondary angiography disclosed revascularization of the left internal pudendal artery, implying that collateral vessels in the distal IIA had constituted in less than 2 h. Emergent catheterization of collateral vessels in itself is a very strenuous procedure because of the characteristic of a small caliber, tortuous and even spasm. Prophylactic, gentle handling catheterization into the target artery or other alternatives may alleviate the spasm. Further prospective studies are needed. Uterine artery embolization has been a beneficial alternative procedure for the treatment of postpartum hemorrhage refractory to conservative nonsurgical treatment. For patients at high risk of abnormal placentation, prophylactic catheterization before childbirth and, if necessary, selective embolization in the operating room with secondary placenta removal when intractable hemorrhage indeed occurs could be a good choice of effective bleeding cessation and of preserving fertility (2, 8). Gelfoam (pledgets of gelatin sponge), which provide temporary occlusion, are particularly suitable because the injury and coagulopathy should be resolved in a relatively short period. We also use Ivalon (polyvinyl alcohol) in some cases. It is a short-term occlusive agent with a more limited potential for recanalization, is less-likely to transmit Creutzfeldt-Jakob disease and preserves the smaller branches and collateral vessels because of the large diameter, and may be used instead of gelfoam. Serious complications of UAE, although rare, have been reported. Ankum et al. reported that the disadvantages of UAE for uteri myoma have become apparent, in that subsequent ovarian failure and sepsis are the most worrisome complications (9). Amato et al. reported a case that underwent UAE treatment for uterine fibroids. Transient ovarian failure developed 3 months after UAE, with recovery of ovarian function 4 months later (10). Our patient developed hot flushes, vaginal and skin dryness, and menopausal serum-hormone levels, 4 and 8 months after her hysterectomy, suggesting permanent ovarian failure. The vascular supply to the ovaries may have been compromised by the repeated proximal embolization of the IIA, the hysterectomy, or both. Simultaneously, massive and rapid blood loss of more than 10 000 ml may cause the ovary, irreversible ischemia or infarction. In conclusion, abnormal placentation accounts for the majority of UAE failures in the treatment of postpartum hemorrhage. Uterine artery embolization could be used as the first-line alternative treatment when medication is refractory. If UAE failure has actually ensued, a timely hysterectomy can still control bleeding effectively without maternal mortality. But the complication of subsequent ovarian failure may occur. Candidates for UAE or hysterectomy should be counseled. Address. for. correspondence:Fu-Tsai Kung Department of Obstetrics and Gynecology Chang Gung Memorial Hospital Kaohsiung Taiwan e-mail: ftkung@ksts.seed.net.tw