Postpartum hemorrhage: Clinical and radiologic aspects

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European Journal of Radiology 74 (2010) 50–59

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European Journal of Radiology journal homepage: www.elsevier.com/locate/ejrad

Review

Postpartum hemorrhage: Clinical and radiologic aspects Nam Kyung Lee a , Suk Kim a,∗ , Jun Woo Lee a , Yu Li Sol a , Chang Won Kim a , Hyun Sung Kim b , Ho Jin Jang c , Dong Soo Suh c a

Department of Radiology, Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, Pusan National University, #1-10, Ami-Dong, Seo-Gu, Busan 602-739, Republic of Korea b Department of Surgery, Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, Pusan National University, Busan 602-739, Republic of Korea c Department of Obstetrics and Gynecology, Pusan National University Hospital, Pusan National University School of Medicine and Medical Research Institute, Pusan National University, Busan 602-739, Republic of Korea

a r t i c l e

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Article history: Received 16 October 2008 Accepted 23 April 2009 Keywords: Pregnancy Complications Uterus Hemorrhage CT MR

a b s t r a c t Postpartum hemorrhage (PPH) is a potentially life threatening condition, and it remains the leading cause of maternal morbidity. Uterine atony, lower genital tract lacerations, uterine rupture or inversion, retained products of conception and underlying coagulopathy are some of the common causes of PPH. Most conditions can be diagnosed based on clinical and laboratory evaluation supplemented by ultrasound information. Computed tomography (CT) or magnetic resonance (MR) imaging can provide information for the detection, localization and characterization of PPH in some difficult cases. CT can accurately demonstrate the anatomic location of significant arterial hemorrhage as sites of intravenous contrast material extravasation, which can be as a guide for angiographic intervention. The presence of focal or diffuse intravenous contrast extravasation or a hematoma within the enlarged postpartum uterine cavity on CT can help the diagnosis of uterine atony when the clinical diagnosis of uterine atony is unclear. CT can also provide the information of other alternative conditions such as a puerperal genital hematoma, uterine rupture and concealed hematoma in other sites. MR imaging may be considered as a valuable complement to ultrasound where the ultrasound findings are inconclusive in the diagnosis and differential diagnosis of retained products of conception. Knowledge of the various radiologic appearances of PPH and the correlation with clinical information can ensure correct diagnosis and appropriate and prompt treatment planning in the patients with PPH. © 2009 Elsevier Ireland Ltd. All rights reserved.

1. Introduction Postpartum hemorrhage (PPH) is an obstetrical emergency that can follow vaginal or cesarean delivery. Ultrasound (US) is considered as the primary imaging modality for the assessment of patients with PPH as the modality is safe and inexpensive to perform and it can be routinely performed at the bedside. However, US may be limited by bowel gas and pain, and US also has difficulty to identify active hemorrhage [1–3]. Computed tomography (CT) or magnetic resonance (MR) imaging is not an appropriate first-line diagnostic procedure for the evaluation of PPH. CT and MR imaging can demonstrate the anatomic location and the extent of a concealed hematoma or a puerperal genital hematoma [1,4]. Unlike other modalities such as US and MR, contrast-enhanced CT can accurately demonstrate the anatomic location of a significant arterial hemorrhage as

∗ Corresponding author. Tel.: +82 51 240 7354; fax: +82 51 244 7534. E-mail address: [email protected] (S. Kim). 0720-048X/$ – see front matter © 2009 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrad.2009.04.062

sites of intravenous contrast material extravasation. Demonstration of active arterial bleeding on contrast-enhanced CT may help interventional radiologists to perform a precise angiographic investigation and embolization of specific arteries [5–7]. In this article, we review the basic concepts of PPH including the etiology, hemodynamic changes in pregnancy, an overview of management, and the relevant pelvic vascular anatomy and CT anatomy. We also discuss the pathological conditions that cause PPH, particularly for primary, potentially life-threatening PPH. Briefly, we also illustrate the retained products of conception (RPOC), which is the most common cause of secondary or late PPH. 2. Basic concepts 2.1. Etiology PPH is a major cause of maternal morbidity, with sequelae such as shock, renal failure, coagulopathy and adult respiratory distress syndrome. There is no single, satisfactory definition of PPH. An estimated blood loss in excess of 500 mL following a vaginal birth or a

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blood loss of greater than 1000 mL following cesarean birth often has been used for the diagnosis of PPH, but the average volume of blood lost at a routine delivery can approach these amounts [3,8]. PPH can also be defined as primary or secondary. Primary PPH occurs within 24 h after delivery (also called early PPH) and secondary PPH occurs 24 h to 12 weeks after delivery (also called late PPH). Primary PPH, which occurs in 4–6% of pregnancies, is caused by uterine atony in 80% or more of the cases. Other causes of primary PPH include lower genital tract lacerations, RPOC, uterine rupture or inversion and underlying coagulopathy. In contrast to primary PPH, secondary PPH is most commonly caused by RPOC. Other causes of secondary PPH include infection, placental site subinvolution and underlying coagulopathy [3,8]. 2.2. Hemodynamic changes in pregnancy The maternal blood volume increases markedly during pregnancy to fulfill the perfusion demands of the low resistant uteroplacental unit. Uterine atony or trauma to the genital region in pregnancy results in significantly more bleeding than would occur in the non-pregnant state due to an increased blood supply to these tissues. It is well recognized that excessive obstetric hemorrhage may lead to disseminated intravascular coagulopathy (DIC) [9,10]. DIC is characterized by acute widespread activation of coagulation, the consumption of procoagulants and platelets, and intravascular deposition of fibrin, resulting in thromboembolic complications. Concomitant diffuse hemorrhage occurs due to an overwhelming consumption of platelets and coagulation factors [9,10]. Rarely, acute massive PPH in the peritoneal cavity or extraperitoneal cavity may lead to the development of abdominal compartment syndrome [11]. Abdominal compartment syndrome is defined as an acute rise in intraabdominal pressure with multiorgan dysfunction, which includes the cardiovascular, pulmonary, renal, gastrointestinal and hepatic systems. Reported CT findings of abdominal compartment syndrome include increased abdominal girth secondary to tense fluid accumulation in the retroperitoneum or peritoneum, a collapsed inferior vena cava (IVC), shock bowel, and a raised hemidiaphragm (Fig. 1) [12–14]. The most widely accepted method of measurement of intraabdominal pressure is measurement of the intravesical pressure. In patients with abdominal compartment syndrome, the intravesical pressure usually rises above 20 mmHg [12–14]. 2.3. Overview of management The treatment of PPH is centered on resuscitation of the patient and arrest of the bleeding. Initially, the administration of fluid and blood products is required in patients with PPH. Subsequently, more directed therapy including intravenous administration of uterotonics and uterine massage to promote uterine contraction in uterine atony, vaginal packing, removal of RPOC and surgical repair of lacerations should be performed [3,8,9]. If bleeding cannot be successfully controlled with conservative treatment, there are a number of other treatment options. In order of increasing invasiveness, the options include selective arterial embolization, ligation of the uterine or internal iliac arteries, and, as a last resort, a hysterectomy [15–19]. Surgical ligation of the uterine or internal iliac artery may not be effective to control PPH in 50% of patients due to an abundant collateral blood supply of the uterus [15]. Hysterectomy should be considered only when all conservative measures fail to achieve hemostasis following a life-threatening PPH. This procedure is associated with high morbidity and loss of subsequent fertility [16]. Transcatheter arterial embolization has emerged as a highly effective technique for controlling PPH. The rate of success is as high as 90%, with the added advantage of preserving

Fig. 1. Abdominal compartment syndrome in a 35-year-old woman as a complication of postpartum hemorrhage. (a) Contrast-enhanced CT image after a subtotal hysterectomy for the treatment of intractable postpartum hemorrhage at the level of the root of the superior mesenteric artery shows increased abdominal girth secondary to massive hemoperitoneum, compression of the inferior vena cava (arrow) and subcutaneous edema. (b) Contrast-enhanced CT image at the level of the pelvis shows intravenous contrast extravasation (arrow) in the pelvic peritoneal cavity, gas bubbles at the recent incision site, bilateral rectus sheath hematomas (arrowheads) and hemoperitoneum.

fertility, few complications and avoidance of surgical exploration [17–19]. 2.4. Vascular anatomy of the pelvis The vascular supply of the uterus is primarily derived from the uterine artery, with a potential collateral supply from the ovarian artery. The uterine artery originates from the anterior division of the internal iliac artery. The uterine artery crosses over the ureter as it passes medially in the parametrium. In the parametrium, the uterine artery divides into a smaller descending vaginal branch (cervicovaginal artery) and a larger ascending branch, which tortuously ascends along the uterine margin at the medial edge of the broad ligament (Fig. 2). The ascending branch is divided into two terminal branches. The ovarian branch of the uterine artery forms anastomosis with the terminal branch of the ovarian artery, and the tubal branch makes its way through the mesosalpinx and supplies part of the uterine tube (Fig. 2) [20–23]. In the uterine wall, uterine arteries divide and run circumferentially as a group of anterior and posterior arcuate arteries between the outer and middle thirds of the myometrium. The radial arteries arise from the arcuate arteries and the radial arteries are directed toward the uterine cavity to become the spiral arteries in the endometrium [24,25]. The vaginal artery may arise either from the anterior trunk of the internal iliac artery or from the uterine artery. There are extensive anastomoses with the vaginal branches of the uterine artery [20–25]. The ovarian arteries originate from the aorta, just below the origin of the renal arteries. The ovarian arteries cross over the external or common iliac vessels as they approach the pelvic brim. The ovarian artery descends to the suspensory ligament of the ovary, and

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Fig. 2. Drawing illustrates the arterial blood supply to the female reproductive organs.

runs through the suspensory ligament to enter the ovary at the mesovarian border. At the ovarian hilum, it divides into a number of smaller branches that enter the ovary. Its main stem, however, traverses the entire length of the broad ligament and forms anastomoses with the branches of the uterine artery (Fig. 2). The ovarian vein drains into the IVC on the right side and into the left renal vein on the left side [20–26].

Fig. 3. Normal postpartum uterus in a 27-year-old woman with right ureteral injury during a cesarean delivery. Contrast-enhanced CT images obtained during the arterial phase (a) and the delayed phase (b) demonstrate an enlarged uterus with a small amount of intrauterine fluid and gas bubbles. There is no evidence of intravenous contrast material extravasation in the uterine cavity.

2.5. Normal CT appearance of the postpartum On CT images, the normal postpartum uterus often appears as an enlarged uterus and then gradually returns to a nongravid size within 6–11 weeks. The uterine cavity may have a small amount of blood or fluid. However, there is no evidence of intravenous contrast material extravasation in the uterine cavity on the contrast-enhanced CT (Fig. 3) [22,27]. The uterine and ovarian arteries can be more easily identified in postpartum women rather than in non-pregnant women as the uterine and ovarian blood flow is increased during the postpartum period. On CT images, the uterine artery and its branches can be depicted as tortuously enhancing tubular structures in the parametrium. The ascending branch of the uterine artery is depicted as a dot-like enhancing structure between layers of the broad ligament, near the lateral margin of the body on the axial contrast-enhanced CT images owing to a vertical course (Fig. 4) [6,22]. The ovarian artery is smaller and less confidently identifiable than the ovarian vein, whereas the ovarian vein can be readily identified on CT images. At the level of the inferior mesenteric artery origin, both ovarian vessels are seen medial to the ureters. Traced inferiorly, both vessels cross the ureters anteriorly and come to lie lateral to the ureters along the anterior surface of the psoas muscle. In the pelvis, both vessels descend to the suspensory ligament of the ovary, and run through the suspensory ligament to enter the ovary at the mesovarian border [22,26]. 3. Imaging techniques At our institution, CT examinations are performed with a multidetector row scanner. Unenhanced scans are obtained with a section thickness of 5 mm and a scan range from the kidney to the inferior pubic ramus. After obtaining the unenhanced CT

Fig. 4. Normal uterine artery. (a) Contrast-enhanced CT image at the level of the parametrium shows that the normal uterine arteries (arrows) appear as tortuously enhancing tubular structures in the parametrium. (b) Contrast-enhanced CT image (b at a higher level than a) shows the normal uterine arteries (arrows) appearing as dot-like enhancing structures tortuously near the lateral margin of the uterine body. Note the active contrast extravasation within the uterine cavity (asterisk) secondary to the uterine atony.

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scan, 150 mL of contrast material is administered at a flow rate of 3–4 mL/s using a mechanical injector. Oral contrast material is not administered. Two-phase contrast-enhanced CT including arterial phase and delayed phase is performed. Delayed phase scanning is performed at a fixed delay of 75 s. The scan range for arterial phase CT is identical to that for unenhanced CT and the scan range for delayed phase CT is from the hepatic dome to the inferior pubic ramus. Three-phase CT technique we have employed may require a significant amount of radiations exposure to patients. To reduce the radiation exposure, in our opinion, an alternative protocol such as a two-phase CT technique (unenhanced and enhanced phase) with the use of low dose unenhanced CT seems to be effective. However, further studies will be needed to evaluate the clinical effectiveness of this protocol. Despite radiation hazard, we prefer CT to MR because CT is cost effective and quick at examination compared with MR. MR is usually reserved for clarifying problems encountered on US and CT or to examine patients who cannot tolerate intravenous administration of iodine contrast material. Pelvic MR imaging is performed using a superconductive 1.5-T scanner and a phased array multi-coil at our institution. The protocol consists of an axial T1-weighted spin-echo sequence and T2-weighted turbo spin-echo sequences obtained in the sagittal and axial planes. Axial image includes the pelvis from the aortic bifurcation to below the vulva. Dynamic gadoliniumenhanced T1-weighted images are obtained after an intravenous bolus injection of 10 mL of gadolinium. 4. Abnormal imaging appearances of postpartum 4.1. Uterine atony As mentioned previously, the most common cause of primary PPH is uterine atony (i.e., the lack of effective contraction of the

Fig. 5. Uterine atony in a 33-year-old woman after a cesarean section. Unenhanced CT (a) and contrast-enhanced CT images obtained during the arterial phase (b) at the level of the uterine body demonstrate the presence of focal intravenous contrast extravasation (arrow) in the uterine cavity and the presence of a hematoma within the uterus.

Fig. 6. Uterine atony in a 33-year-old woman after a vaginal delivery. Contrast enhanced CT images obtained during the arterial phase (a) and the delayed phase (b) at the level of the uterine body demonstrate the presence of diffuse intravenous contrast extravasation in the uterine cavity (arrow), probably caused by oozing of a vein or small artery. Note the change in the uterine shape due to uterine contraction on the delayed phase CT image.

uterus after delivery), which complicates approximately 1 in 20 deliveries [2,3,8]. Uterine atony is caused by ineffective uterine contraction, ultimately leading to serious bleeding from the uterine vessels. Any condition that predisposes to poor uterine contraction such as a retained placenta, uterine fatigue after prolonged or induced labor, a blood clot within the uterus, uterine overdistention (multiple gestation, polyhydramnios or macrosomia), placental previa and a uterine infection will increase the possibility of uterine atony immediately after delivery [2,3,8]. From a clinical aspect, the presence of a boggy uterus with either heavy vaginal bleeding or an increasing uterine size is a highly indicative finding of uterine atony [8,9]. CT is not an appropriate first-line diagnostic procedure for the evaluation of PPH caused by uterine atony. When the clinical diagnosis of uterine atony is not convincing, CT may be helpful to detect the presence of arterial or venous oozing in the uterine cavity secondary to ineffective myometrial contraction, thereby directly confirming the presence of uterine atony. Active bleeding, that is typically identified on contrast-enhanced CT images, can manifest as intravenous contrast material extravasation. A comparison with unenhanced images allows differentiation of intravenous contrast material extravasation from other preexisting high-attenuation materials. Significant arterial bleeding can be identified on the contrast-enhanced CT images during the arterial phase, whereas small arterial or venous oozing can often be identified on the delayed phase. Therefore, the presence of focal or diffuse intravenous contrast extravasation and/or a hematoma within the cavity of an enlarged postpartum uterus on CT images can assist in the diagnosis of uterine atony when the clinical diagnosis of uterine atony is unclear (Figs. 5–8) [5–7]. CT may be helpful in the detection of other alternative conditions such as a puerperal genital hematoma and a concealed hematoma in other sites (Fig. 9) [5–7].

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Fig. 7. Uterine atony in a 31-year-old woman. (a) Contrast-enhanced CT image obtained during the arterial phase demonstrates focal intravenous contrast material extravasation (arrow) into the uterine cavity. (b) Selective left uterine arteriogram shows hypertrophy of the left uterine artery with intravenous contrast material extravasation (arrow).

Fig. 8. Uterine atony and intractable postpartum hemorrhage after a vaginal delivery in a 28-year-old woman. (a) Contrast-enhanced CT image obtained during the delayed phase shows extravasation of contrast media in the lower uterine segment (arrow). (b) Common iliac arteriogram that was performed 2 h after the CT examination shows both engorged and tortuous uterine arteries without extravasation of contrast media.

Fig. 9. Ruptured angiomyolipomas in a 32-year-old woman. (a) Contrast-enhanced CT image shows an enlarged uterus without evidence of intravenous contrast material extravasation in the uterine cavity. However, fluid accumulation is seen in the broad ligament (arrow). (b) Contrast-enhanced CT image (b at a higher level than a) shows a large fat-containing mass in the right kidney with an intratumoral hematoma and retroperitoneal hematoma. Note the intravenous contrast extravasation in the fat-containing mass (arrow) in the right kidney. It was difficult to diagnosis the ruptured angiomyolipomas prior to the CT examination.

As mentioned previously, DIC is more common in patients with PPH than in non-pregnant patients. If there is any uncontrollable bleeding from the recent incision sites, the possibility of DIC in relation to PPH should be recognized (Fig. 10). It has been reported that the hematocrit (cellular-fluid level) sign could be a suggestive sign of coagulopathic hemorrhage such as DIC rather than bleeding in patients with normal coagulation (Fig. 11). This sign indicates a setting of the cellular elements in the dependent position of a hematoma [28,29]. Although there has been no report that the hematocrit sign is present in postpartum patients with DIC, based on our experience, the hematocrit sign is more commonly observed in the PPH with DIC. The rectus sheath is a common extrauterine site of PPH, particularly in patients who recently underwent a cesarean delivery. In patients with PPH, most rectus sheath hematomas result from injury of the inferior epigastric arteries secondary to DIC or inadequate hemostasis and occur in the lower abdomen, particularly in a recent incision site [30–32]. The inferior epigastric artery arises from the external iliac artery just superior to the inguinal ligament to enter the posterior rectus sheath. It enters the lower rectus abdominis and forms an anastomosis with the superior epigastric artery. Contrast extravasation and/or a heterogeneous high-attenuating hematoma in the rectus sheath are highly suggestive findings of the inferior epigastric artery injury on the CT images (Fig. 12). Progressing hematomas may expand into the preperitoneal, prevesical, and perivesical space [30–32]. Active contrast extravasations outside the uterus on CT images can affect the therapeutic approach, especially the angiographic approach as additional selective arterial embolotherapy should be included for the sites of active bleeding foci outside the uterus [2,29].

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Fig. 10. Uterine atony in a 33-year-old woman. (a) Contrast-enhanced CT image obtained during the arterial phase at the level of the uterine fundus demonstrates focal intravenous contrast extravasation in the uterine cavity (arrow) and the presence of a hematoma within the uterus (asterisk) and a small amount of ascites. (b) Contrast-enhanced CT image obtained during the arterial phase at the level of the uterine cervix demonstrates intravenous contrast extravasation in the uterine cervix (arrow), a small amount of ascites, and multifocal intravenous contrast extravasations (arrowheads) and gas bubbles in the rectus muscle secondary to a recent cesarean section.

4.2. Puerperal genital hematoma Puerperal genital hematomas are relatively uncommon but can be a cause of serious morbidity and even maternal death. They can be difficult to diagnose, as symptoms can be nonspecific and bleeding is often concealed. A puerperal genital hematoma can result from episiotomy trauma or birth canal trauma [9,33]. From a clinical standpoint, puerperal genital hematomas can be classified as vulvar, vulvovaginal, paravaginal or supravaginal hematomas. Vulvar, vaginal, cervical or uterine tears may lead to the inferior pudendal, vaginal or uterine vessel injury and consequently

Fig. 11. Hematocrit sign in a 36-year-old woman with DIC. Contrast-enhanced CT image after a cesarean delivery at the level of vagina shows two loculated hematomas in the prevesical space. Note the hematocrit sign (arrows).

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Fig. 12. Rectus sheath hematomas in a 33-year-old woman after a cesarean delivery. (a) Contrast-enhanced CT image shows a large rectus sheath hematoma in a recent incision site that contains multifocal extravasation of intravenous contrast media (arrows) and gas bubbles. (b) Selective right inferior epigastric arteriogram shows extravasation of contrast material (arrows) at the level of the cervix and mid-vagina.

to vulvar, vulvovaginal, paravaginal and supravaginal hematomas. For vulvar hematomas, bleeding is limited to the vulvar tissues superficial to the urogenital diaphragm. Paravaginal hematomas arise from damage to the descending branch of the uterine artery or vaginal artery. The hematomas are confined to the paravaginal tissues in the space bounded inferiorly by the levator ani muscle and superiorly by the cardinal ligament (Fig. 13) [4,27,33]. Supravaginal hematomas are the result of damage to the uterine artery branches in the broad ligament. Supravaginal hematomas can dissect retroperitoneally or develop within the broad ligament. Supravaginal hematomas can be clinically occult despite significant blood loss [4,27,33].

Fig. 13. Drawing illustrates paravaginal hematoma.

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Fig. 14. Paravaginal hematoma in a 30-year-old woman. (a) Contrast-enhanced CT image shows the hematoma (arrows) confined to the right paravaginal space and hemoperitoneum (asterisk) from a right uterine artery pseudoaneurysm. Note a small area containing extravasated contrast material (arrowhead) in an area of disruption of the right vaginal wall. The right uterine artery pseudoaneurysm is not shown in this figure. V = vagina. (b) Contrast-enhanced CT image (b at a higher level than a) shows the hematoma confined to the right paravaginal space (arrows) and the pelvic extraperitoneal space (asterisks). U = uterus.

US is able to detect pelvic extraperitoneal hematomas in patients with a suspected puerperal genital hematoma. CT and MR imaging can show the exact extent of a puerperal genital hematoma. Contrast-enhanced CT can detect the presence of a hematoma and extravasation of intravenous contrast material in the perivaginal region and/or broad ligament. A puerperal genital hematoma can often extend into the paravesical, pararectal, or presacral space (Figs. 14–16) [4,27,33]. 4.3. Uterine rupture Uterine rupture is a potentially life threatening complication, carrying an increased risk of maternal and perinatal morbidity and mortality. The incidence is approximately 1 in 3000 deliveries. The most common cause of uterine rupture is separation of a previous cesarean hysterectomy scar. However, uterine ruptures have also been known to occur in some women who have never had a cesarean delivery, which can be caused by weak uterine muscles after several pregnancies, excessive use of labor inducing agents, a prior surgical procedure on the uterus, a congenital uterine anomaly or fetal macrosomia [34]. Uterine rupture typically is classified as complete or incomplete rupture. Complete rupture is defined that all layers of the uterine wall including the membrane, decidua, myometrium and serosa are separated that results in direct communication between the uterine and peritoneal cavity. While incomplete rupture does not extend through the entire thickness of the uterus and overlying peritoneum. Incomplete rupture is also commonly referred to as a uterine dehiscence. The morbidity and mortality are appreciably

Fig. 15. Puerperal genital hematoma secondary to slipped ligation of a uterine artery during a cesarean section in a 31-year-old woman. (a) Contrast-enhanced CT image shows bilateral broad ligament hematomas (asterisks) and a retroperitoneal hematoma (arrow). U = uterus. (b) Contrast-enhanced CT image (b at a lower level than a) demonstrates intravenous contrast material extravasation from a branch of the left uterine artery (arrowhead). The gas-filled structure with a stripe like configuration is consistent with a gelatin bioabsorbable sponge (asterisk). U = uterus.

greater for complete uterine rupture than for incomplete uterine rupture [35]. Early diagnosis of uterine rupture may be difficult as uterine rupture has no distinguishable clinical features prior to hypovolemic shock. CT may be a useful imaging modality for the detection and diagnosis of postpartum uterine rupture, especially if a patient presents with nonspecific symptoms or signs such as pelvic pain or fullness and shock that cannot be explained after delivery. CT features of uterine rupture include focal disruption of the uterine wall, a hematoma in the broad ligament and hemoperitoneum. Focal disruption of the uterine wall appears as a hypoattenuating lesion within the densely enhancing myometrium. Hypoattenuating fluid with or without air bubbles in the disrupted site often extends into the endometrial cavity and extrauterine region (Fig. 17). When uterine rupture is suspected, surgical treatment should be performed [36–38]. 4.4. Retained products of conception Retained products of conception (RPOC) is the most common cause of secondary or late PPH, occurring with a greater frequency after termination of pregnancy than after vaginal or cesarean delivery. The incidence of RPOC increases in a patient with placenta accreta. Common symptoms include pelvic pain and vaginal bleeding [8,9]. US can help in the diagnosis of RPOC, but the reported diagnostic accuracy of US is variable. On US images, RPOC often appears as an echogenic intracavitary mass attached to the endometrium. Another imaging feature indicative of RPOC is high-velocity, low-resistance flow at color Doppler US [39–41]. However, it is

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Fig. 16. Puerperal genital hematoma from a vaginal wall injury caused by an episiotomy in a 26-year-old woman. (a) Contrast-enhanced CT image shows intravenous contrast material extravasation and a large hematoma (arrows) in the right perivaginal space. Note the intravenous contrast material extravasation (arrowhead) adjacent to the vagina (V). The presence of contrast medium in the bladder is noted (asterisk). V = vagina. (b) Selective left internal iliac arteriogram shows a pseudoaneurysm (arrow) in the right vaginal artery.

sometimes difficult to diagnose RPOC as normal postpartum involution of the uterus, necrotic deciduas and blood clots may mimic residual tissues. Clinical information and US findings can be usually sufficient to suggest a diagnosis of RPOC. MR imaging should be reserved for the cases where the US findings are inconclusive and patient care depends on further imaging. On MR images, RPOC is often seen as an intracavitary soft-tissue mass with variable degrees of enhancing tissue and with variable degrees of myometrial thinning, and obliteration of the junctional zone. Although MR findings of RPOC reveal variations in signal intensity and contrast enhancement, RPOC usu-

Fig. 17. Complete uterine rupture in a 34-year-old woman. Contrast-enhanced CT image shows the postpartum uterus with disruption of the left lateral wall due to rupture (arrow). Fluid and gas bubbles are seen within the uterine cavity and broad ligament.

Fig. 18. Retained products of conception in a 41-year-old woman with vaginal bleeding on postpartum day 13 and serum ␤-human chorionic gonadotropin level of 21 mIU/mL. (a) Axial T1-weighted image shows a slightly enlarged uterus with high-signal-intensity fluid in the endometrial cavity, which is consistent with blood products. (b) Sagittal T2-weighted image shows an irregular intrauterine mass of heterogeneous intensity with thinning of the myometrium. (c) Sagittal gadoliniumenhanced T1-weighted image shows enhancing tissue within the intrauterine mass (arrows).

ally shows very high intensity areas on T2-weighted images. This observation suggests that the normally vascularized placenta can show very high intensity on T2-weighted images, as seen with the normal prepartum placenta. Variable amounts of enhancing tissue may suggest the presence of at least partially viable chorionic and decidual tissue as well as vascularized granulation tissue (Fig. 18) [42–44]. A failed pregnancy, RPOC, first trimester mole and uterine arteriovenous malformation (AVM) could have overlapping appearances (Figs. 18 and 19). Differentiating RPOC from gestational trophoblastic disease (GTD) and uterine AVM is not usually relevant in the immediate postpartum period. This differential diagnosis is crucial during the first trimester when a patient presents with bleeding. The serum level of ␤-human chorionic gonadotropin (␤-HCG) is a

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Fig. 19. Uterine arteriovenous malformation in a 33-year-old woman after a dilatation and curettage. (a) Axial T2-weighted image shows a cluster of serpentine flow-related signal voids (arrowheads) in the uterine wall, in the parametrium, and protruding into the endometrial cavity. (b) Coronal dynamic subtraction MR angiogram shows prominent vascular lesions in the parametrium with dilated bilateral uterine and ovarian vessels. Note the markedly engorged left ovarian vein (arrow).

helpful distinguishing factor. The serum ␤-HCG level may be only mildly elevated or normal with RPOC. In contrast to RPOC, GTD usually results in markedly elevated levels of the hormone and uterine AVM results in negative ␤-HCG findings [44–47]. Images suggesting RPOC should be evaluated carefully in association with serum ␤-HCG level assessment and a pertinent patient history, which is helpful in the differentiation of RPOC from GTD and uterine AVM. 5. Conclusion Selective arterial embolization for the control of intractable PPH is a well-established procedure. The key to successful selective arterial embolization is the accurate identification of the bleeding site. CT imaging is not an appropriate first-line diagnostic procedure for the evaluation of PPH. However, CT can demonstrate the anatomic location of a significant arterial hemorrhage as sites of intravenous contrast material extravasation. Therefore, a CT examination before an angiographic procedure may reduce the total radiation burden of the patient by decreasing the time and radiation exposure during diagnostic and interventional angiography. Moreover, CT can be useful to detect a concealed hematoma in other sites and differentiate the cause of postpartum hemorrhage such as uterine atony, puerperal genital lacerations, and uterine rupture. MR imaging may be considered a valuable complement to US or CT where the US or CT findings are inconclusive in the evaluation of PPH. Conflicts of interest All authors have no financial relationship to disclosure. Acknowledgement This study was supported by a Medical Research Institute grant from Pusan National University. References [1] Nagayama M, Watanabe Y, Okumura A, Amoh Y, Nakashita S, Dodo Y. Fast MR imaging in obstetrics. Radiographics 2002;22:563–80. [2] Dildy III GA. Postpartum hemorrhage: new management options. Clin Obstet Gynecol 2002;45:330–44. [3] Gilbert L, Porter W, Brown VA. Postpartum haemorrhage: a continuing problem. Br J Obstet Gynaecol 1987;94:67–71. [4] Yamashita Y, Torashima M, Harada M, Yamamoto H, Takahashi M. Postpartum extraperitoneal pelvic hematoma: imaging findings. AJR Am J Roentgenol 1993;161:805–8. [5] Shanmuganathan K, Mirvis SE, Sover ER. Value of contrast-enhanced CT in detecting active hemorrhage in patients with blunt abdominal or pelvic trauma. AJR Am J Roentgenol 1993;161:65–9.

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