Secondary postpartum hemorrhage following ...

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drome, coagulopathy and Sheehan's syndrome. PPH is one of the top five causes of maternal mortality in both high- income and low-income countries, with a ...

Arch Gynecol Obstet DOI 10.1007/s00404-008-0625-4

C A S E RE P O RT

Secondary postpartum hemorrhage following placental site vessel subinvolution: a case report Lama Al-Mehaisen · Oqba Al-Kuran · Zouhair O. Amarin · Ismail Matalka · Soha Beitawi · Alia Muhtaseb

Received: 22 December 2007 / Accepted: 4 March 2008 © Springer-Verlag 2008

Introduction Postpartum hemorrhage (PPH) is an obstetric emergency that can follow vaginal or cesarean delivery. It is a major cause of shock, renal failure, acute respiratory distress syndrome, coagulopathy and Sheehan’s syndrome. PPH is one of the top Wve causes of maternal mortality in both highincome and low-income countries, with a much lower absolute risk of death in the former [1]. The true incidence of PPH is unknown, but a reasonable estimate is 1–5% of deliveries. Figures vary according to the criteria used to deWne the disorder [1]. The most common deWnition of PPH is an estimated blood loss of 500 ml after vaginal birth or 1,000 ml after cesarean delivery [2], yet accurate measurement of blood loss is rarely possible or practicable. PPH can also be deWned as 10% change in haematocrit from admission assessment to postpartum data, or the need to administer a transfusion of red blood cells [3]. PPH is classiWed as primary or secondary. Primary PPH occurs within 24 h after delivery, and secondary PPH occurs 24 h to 6 weeks after delivery. Bleeding after delivery is controlled by a combination of contraction of the myometrium, which constricts the blood

L. Al-Mehaisen · O. Al-Kuran · Z. O. Amarin (&) · S. Beitawi Department of Obstetrics and Gynaecology, King Abdullah University Hospital, Jordan University of Science and Technology, POB 600017, Irbid 22110, Jordan e-mail: [email protected] I. Matalka · A. Muhtaseb Department of Pathology, King Abdullah University Hospital, Jordan University of Science and Technology, Irbid, Jordan

vessels supplying the placental bed, and local decidual haemostatic factors, including tissue factor, type-1 plasminogen activator inhibitor and systemic coagulation factors [4]. DeWcient contraction of the myometrium is manifested clinically as uterine atony. Defective decidual homeostasis is associated with inadequate decidualization or bleeding diatheses.

Case report A 21-year-old woman in her Wrst pregnancy was admitted at 39 weeks gestation with a 2-h history of prelabor spontaneous rupture of the amniotic membranes. The antenatal course had been unremarkable. Erythromycin was prescribed. Four hours later, she went into labor and epidural analgesia was administered. Full cervical dilatation was achieved 6 h later, but the fetal head remained palpable abdominally in spite of good uterine contractions. A straightforward caesarean section was performed for failure to progress in second stage, and a 3 kg female infant was delivered in good condition. The estimated blood loss was 900 ml. The postoperative period was uneventful. Postoperative hemoglobin was 12 g/dl. The patient was discharged with the recommendation that she Wnishes her course of oral antibiotics. Two weeks later, she was admitted through accident and emergency department with severe vaginal bleeding. Her hemoglobin was 7 g/dl. Four units of blood were transfused. There was no pyrexia, but the uterus was subinvoluted. No retained products of conception were evident on ultrasound examination. Examination under anesthesia conWrmed uterine subinvolution with no other cause for the bleeding. ESR, CRP, high and low vaginal swabs, clotting

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Arch Gynecol Obstet

proWle, liver and kidney function tests were within normal ranges. Intravenous cephalosporin and Xagyl were administered. Five days later, the bleeding settled and she was discharged home on oral antibiotics. Two days later, the patient was readmitted with further mild vaginal bleeding. Repeat examination was unremarkable. Complete blood count, kidney and liver function tests were normal, and serum hCG was negative. Thrombophilia screen and pelvic ultrasound scan were unremarkable. The patient remained on the postnatal ward for observation when suddenly she developed severe bleeding of about 1,500 ml. Emergency total abdominal hysterectomy was performed. At operation, the uterus was subinvoluted, pale and soft. Eight units of blood and three units of fresh frozen plasma were administered intra- and postoperatively. The postrecovery was uneventful and she was discharged 10 days later. Histopathological examination revealed the classical features of subinvoluted placental bed vessels. Microscopic sections showed large, patent, dilated superWcial myometrial blood vessels. Their walls were distorted and thickened due to deposition of hyaline material replacing the media, and there was partial absence of the endothelial lining (Fig. 1). Additionally, these vessels exhibited partial intravascular thrombosis of variably aged thrombi (Fig. 2). Fig. 1 A grossly congested uterus showing ruptured blood vessel (arrow, left). Thickened dilated blood vessels after Wxation (arrow, right)

Fig. 2 Large, patent superWcial myometrial blood vessel, containing an organized thrombus (left). Clusters of patent partially thrombosed arteries (right)

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There was little intervening myometrial tissue in between them. However, clearly demarcated from the surrounding myometrium, there were a few normally involuted vessels adjacent to the subinvoluted vessels. These vessels showed loose adventitia, brightly eosinophilic media, thickened intima and identiWable endothelial lining, with small slitlike vascular lumina.

Discussion In cases of subinvolution of the placental bed, the uteroplacental spiral arteries and the musculature of the placental bed fail to involute and revert to their nonpregnant state. The aVected vessels are usually widely dilated and tortuous and partially hyalinized with loss of endothelial lining and internal elastic lamina. Subinvolution may recur in subsequent pregnancies [5]. In their review, Weydert and Benda concluded that subinvolution of the placental site was an important diagnosis, as this process implied an idiopathic cause, rather than an iatrogenic cause of postpartum uterine bleeding [6]. Khong et al. studied various causes of delayed PPH including subinvolution of the placental bed and its association with other pregnancy disorders. Hyalinized fragments of uteroplacental (spiral) arteries that were either collapsed

Arch Gynecol Obstet

or completely thrombosed were seen in involution of the placental bed. Widely distended and patent uteroplacental arteries characterized subinvolution of the placental bed with only partial occlusion by thrombosis. While concluding that subinvolution of the placental bed is an important cause of delayed PPH, no clear relation with other pregnancy disorders was seen [5]. Assessing the placental bed by examining the whole uterus is the only way to make the diagnosis of subinvolution; placental examination on its own is not helpful. This condition may therefore be underdiagnosed due to both low clinical suspicion and the diYculty in conWrming the underlying pathological process. It has been reported that the expression of bcl-2 oncoprotein is associated with inhibition of apoptosis and prolonged cell survival. The bcl-2 oncoprotein is not detected in the uteroplacental arteries during the third trimester of pregnancy but is seen in involution, and more strongly in subinvolution, of the placental bed. The involution and subinvolution of the placental bed are perhaps morphologic entities that lie in the spectrum between complete resolution and subinvolution of pregnancy-induced changes, where bcl-2 is associated with subinvolution of the uteroplacental arteries. It has been suggested that subinvolution of placental site vessels may represent an abnormal interaction between maternal uterine cells and fetal trophoblast [7]. Clinically, the speed and severity of the bleeding necessitate immediate action with little time for procedures such

as emergency uterine embolization. The clinical management of the severe forms of cases similar to the presented one is based on relatively small series of sporadic case reports. The condition lacks reliable predictive criteria; it also lacks consensus on strategy due to the imperfect understanding of the pathogenesis. EVective measures other than hysterectomy remain controversial. The rarity of the condition obviates from conducting randomized controlled trials.

References 1. Lu MC, Fridman M, Korst LM (2005) Variations in the incidence of postpartum hemorrhage across hospitals in California. Matern Child Health J 9:297 2. Lockwood CJ, Schatz F (1996) A biological model for the regulation of peri-implantational hemostasis and menstruation. J Soc Gynecol Investig 3:159–165 3. American College of Obstetricians and Gynecologists (1998) ACOG educational bulletin. Postpartum hemorrhage. Number 243, January 1998 (replaces no. 143, July 1990). Int J Gynaecol Obstet 61(1):79–86 4. Lockwood CJ, Krikun G, Schatz F (1999) The decidua regulates hemostasis in human endometrium. Semin Reprod Endocrinol 17:45 5. Costa MA, Calejo LI, Martinez-de-oliveira J, Laurini R (2005) Late-onset postpartum hemorrhage from placental bed subinvolution: a case report. J Reprod Med 50:557–560 6. Weydert JA, Benda JA (2006) Subinvolution of the placental site as an anatomic cause of postpartum uterine bleeding: a review. Arch Pathol Lab Med 130:1538–1542 7. Khong TY, Abdul Rahman H (1997) Bcl-2 expression delays postpartum involution of pregnancy-induced vascular changes in the human placental bed. Int J Gynecol Pathol 16:138–142

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