Case Report

Disseminated Intravascular Coagulation Complicating the Conservative Management of Placenta Percreta Amy E. Judy, MD, MPH, Deirdre J. Lyell, MD, Maurice L. Druzin, MD, and Oliver Dorigo, MD, PhD BACKGROUND: Retention of the placenta is an option in the management of placenta percreta; however, it may be associated with significant morbidity. CASE: We present a case of conservative management of placenta percreta. Disseminated intravascular coagulation (DIC) developed 49 days after delivery. An urgent hysterectomy was performed, followed by rapid normalization of coagulation parameters. CONCLUSION: Disseminated intravascular coagulation may complicate the conservative management of placenta percreta and can manifest weeks after delivery in the absence of antecedent hemorrhage or infection. The time course and presentation of this case are similar to the development of DIC after prolonged retention of a fetal demise with a probable shared pathophysiology. Close follow-up may facilitate prompt diagnosis of DIC, thereby minimizing associated morbidity. (Obstet Gynecol 2015;126:1016–8) DOI: 10.1097/AOG.0000000000000960

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he incidence of abnormally adherent placenta, including placenta accreta, increta, and percreta, is increasing.1 These cases are associated with significant maternal morbidity and mortality.1 Given the increasing incidence and high rates of morbidity, conservative management of placenta accreta and percreta is becoming more common but is also associated with maternal morbidity.1,2 This report describes

From the Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, California. Corresponding author: Amy E. Judy, MD, MPH, 300 Pasteur Drive, Room HH333, Stanford, CA 94305; e-mail: [email protected]. Financial Disclosure The authors did not report any potential conflicts of interest. © 2015 by The American College of Obstetricians and Gynecologists. Published by Wolters Kluwer Health, Inc. All rights reserved. ISSN: 0029-7844/15

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Teaching Points 1. Conservative management of placenta percreta may be associated with disseminated intravascular coagulation, similar to disseminated intravascular coagulation observed after undelivered intrauterine fetal demise, and follow-up should include serial coagulation studies. 2. Prompt diagnosis and definitive management with hysterectomy may decrease morbidity.

the development of disseminated intravascular coagulation (DIC) after conservative management of placenta percreta and the subsequent diagnosis and management of this complication.

CASE The patient is a 32-year-old woman, gravida 2 para 1, with one prior low-transverse cesarean delivery for breech presentation. Ultrasonography performed at 31 weeks of gestation was highly suggestive of placenta percreta, demonstrating a complete central placenta previa with absence of the retroplacental clear space, moderate lacunae, and enlarged vessels with turbulent flow crossing tissue planes at the uterine serosa–bladder wall interface. Magnetic resonance imaging was also consistent with placenta percreta with signal inhomogeneity and irregularity of the bladder wall. A scheduled cesarean delivery was performed at 33 6/7 weeks of gestation with the intention to perform a concurrent hysterectomy. In anticipation of extensive placental invasion and possible massive blood loss, an intraaortic occlusion balloon catheter was placed preoperatively by vascular surgery. Under combined spinal– epidural anesthesia, a vertical skin incision was made, and a male neonate weighing 2,620 g with Apgar scores of 8 and 9 was delivered through a vertical incision of the uterine fundus. The umbilical cord was ligated and cut proximal to the cord insertion, and the hysterotomy was closed. Intraoperative examination identified a complete placenta previa with extensive involvement of the bladder and gross extension through the serosa with vascularity approaching the pelvic sidewall and filling the cul de sac. The decision was made to leave the placenta in situ. Estimated blood loss for the procedure was 500 mL. The intraaortic occlusion balloon was removed, and the hypogastric arteries were embolized in the immediate postoperative period. The initial postoperative course was uncomplicated. The patient received prophylactic antibiotics for 1 week and she did not require transfusion. Weekly ultrasonography demonstrated persistent vascularity of the placenta without significant change in size. b-hCG serum levels decreased from 5,406 mill-international units/m on postoperative day

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1 to 37 milli-international units/m on postoperative day 46. The patient was discharged on postoperative day 35 with clinic follow-up and weekly complete blood count and b-hCG level. Seven weeks postpartum, the patient presented with a hematoma on her hand, easy bruising, and bleeding of the gums. She reported scant brown discharge but no significant vaginal bleeding. Serum laboratory studies demonstrated significant coagulation abnormalities supporting the diagnosis of DIC (fibrinogen 46 mg/dL [normal 236–389 mg/dL], partial thromboplastin time 47.3 seconds [23.9–36.7 seconds], prothrombin time 19.5 seconds [11.5–14.2 seconds], international normalized ratio 1.7 [0.9–1.2], and D-dimer greater than 20,000 ng/mL [less than 500 ng/mL]). The patient had been asymptomatic on postoperative day 46, when complete blood count and b-hCG had been last assessed. Coagulation studies had been normal at last assessment on postoperative day 6 (Table 1). The patient was readmitted to the hospital and received 2 units of cryoprecipitate and 2 units of fresh-frozen plasma, with improvement in coagulation parameters (Table 1), and she was taken for surgery the day after readmission. Intraoperative findings revealed a moderate decrease in the size of the placenta with persistent, large-caliber vessels on the left aspect of the uterus and extension into the bladder. A total abdominal hysterectomy and partial bladder resection with left ureteral reimplantation were performed. Intraoperatively, the patient received an additional 5 units of freshfrozen plasma, 6 units of cryoprecipitate, 6 units of packed red blood cells, and 3 units of platelets. Final pathology confirmed placenta previa and percreta. She was admitted to the surgical intensive care unit and received 1 additional unit of packed red blood cells. Coagulation studies demonstrated rapid resolution of DIC with normalization of coagulation parameters on postoperative day 1 (Table 1). She was discharged home on postoperative day 8.

DISCUSSION Abnormal placentation is associated with significant morbidity during delivery and in the postoperative period.1 Conservative management as an alternative

to cesarean hysterectomy has been reported, but the morbidities associated with this approach are still poorly characterized and difficult to predict. Studies have demonstrated success rates of conservative management as high as 78% with serious morbidity as low as 6%,2 although a review of 57 published cases of conservatively managed placenta percreta by Pather et al3 reported major morbidity complicating 42% of patients with emergent hysterectomy required in 40% of patients. Series reporting low rates of morbidity may include less severe forms of abnormal placentation.3 Pather et al reported that DIC complicated 11% of conservatively managed cases; however, the most commonly reported indication for interval hysterectomy is hemorrhage followed by sepsis2 and in the absence of antecedent hemorrhage, DIC after the conservative management of abnormally adherent placenta has rarely been described. Coagulopathies have been reported to develop 7–9 weeks postpartum with clinical symptoms of increasing coagulation times, including ecchymosis or hematoma.3–6 The correction of DIC in these situations invariably requires a hysterectomy with removal of the placenta. The time course and presentation of our case are similar to the course and presentation described in the development of consumptive coagulopathy after intrauterine fetal demise with delayed delivery of the fetus.7 Disseminated intravascular coagulation largely presents 8–10 weeks after fetal death, although cases presenting up to 16 weeks after intrauterine fetal demise have been reported.7 In cases of intrauterine fetal demise, hypofibrinogenemia is the primary manifestation of coagulopathy, often with preservation of the platelet count,7 as was observed in this case. It has been hypothesized that an undelivered intrauterine fetal demise causes an accumulation of thromboplastin from the degenerating products of conception, which activates the extrinsic coagulation pathway and leads to a consumptive coagulopathy8; a similar

Table 1. Hematology and Coagulation Studies by Postoperative Day Postoperative Day Preoperative 0 6 46 49 50 1 or 51†

Hemoglobin Platelets (g/dL) (K/microliter) 12.7 10.4 9.5 12.0 12.4 11.4 7.6

227 187 275 180 185 168 171

Fibrinogen (mg/dL)

International Normalized Ratio

Prothrombin Time (s)

Partial Thromboplastin Time (s)

472 364 * * 46 165 448

1.0 1.1 1.0 * 1.7 1.4 1.2

12.4 13.5 12.5 * 19.5 16.7 14.7

26.4 33.5 35.9 * 47.3 37.5 32.6

* Only select studies assessed on these dates, where the asterisk represents no data available. † Postoperative day 1 after hysterectomy, postoperative day 51 after cesarean delivery.

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DIC With Conservatively Managed Percreta

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pathophysiology could similarly follow the retention of a morbidly adherent placenta. The extensive neovascularization that occurs with placenta percreta may facilitate access of the degenerating products to the systemic circulation. No bleeding or signs of infection preceded the diagnosis to provide alternative explanations for the development of DIC in this case. The similarity between intrauterine fetal demiseassociated DIC and DIC that manifests after the conservative management of placenta percreta has not previously been reported. This similarity underscores the importance of close monitoring of patients for which conservative management of placenta percreta is chosen as an alternative to cesarean hysterectomy. Given the timeframe and the notable hypofibrinogenemia observed in these cases, the conservative management of an abnormally adherent placenta might require serial complete blood counts and coagulation studies, particularly fibrinogen levels, for at least 10 weeks after cesarean delivery. Serial assessment of b-hCG appears to be of limited utility in postoperative monitoring of these patients, because only modest involution of the placenta was noted at the time of hysterectomy, despite a significant decline in serum b-hCG level. This patient remained hospitalized for 1 month postpartum as a result of a concern for unpredictable hemorrhage, but close outpatient followup with serial laboratory studies may be reasonable to avoid prolonged hospitalization. For patients managed conservatively who do not desire future fertility, interval hysterectomy might be considered to avoid the

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development of DIC, although the prevalence of this potentially rare complication is unknown. The decision to proceed with interval hysterectomy must be balanced against the significant risk of hemorrhage and organ injury that are known to be associated with hysterectomy for placenta percreta. REFERENCES 1. Publications Committee, Society for Maternal-Fetal Medicine, Belfort MA. Placenta accreta. Am J Obstet Gynecol 2010;203: 430–9. 2. Sentilhes L, Ambroselli C, Kayem G, Provansal M, Fernandez H, Perrotin F, et al. Maternal outcome after conservative treatment of placenta accreta. Obstet Gynecol 2010;115: 526–34. 3. Pather S, Strockyj S, Richards A, Campbell N, de Vries B, Ogle R. Maternal outcome after conservative management of placenta percreta at caesarean section: a report of three cases and a review of the literature. Aust N Z J Obstet Gynaecol 2014;54:84–7. 4. Wong VV, Burke G. Planned conservative management of placenta percreta. J Obstet Gynaecol 2012;32:447–52. 5. Jaffe R, DuBeshter B, Sherer DM, Thompson EA, Woods JR Jr. Failure of methotrexate treatment for term placenta percreta. Am J Obstet Gynecol 1994;171:558–9. 6. Silver LE, Hobel CJ, Lagasse L, Luttrull JW, Platt LD. Placenta previa percreta with bladder involvement: new considerations and review of the literature. Ultrasound Obstet Gynecol 1997; 9:131–8. 7. Pritchard JA. Fetal death in utero. Obstet Gynecol 1959;14: 573–80. 8. Romero R, Copel JA, Hobbins JC. Intrauterine fetal demise and hemostatic failure: the fetal death syndrome. Clin Obstet Gynecol 1985;28:24–31.

DIC With Conservatively Managed Percreta

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Disseminated Intravascular Coagulation Complicating the Conservative Management of Placenta Percreta.

Retention of the placenta is an option in the management of placenta percreta; however, it may be associated with significant morbidity...
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