Spontaneous Rupture of Uterine Vessels Complicated with Placental Abruption: A Rare Case Report

A 23‑year‑old Sundanese primigravid woman at 33–34 weeks of pregnancy presented to Waled General District Hospital, Cirebon, West Java, Indonesia because of progressive abdominal tension 14 hours before admission, followed by regular labor pain 12 hours before admission. No bloody show or watery discharge from the birth canal was observed. Fetal movements were felt by the mother. The patient had no history of urinary tract infection, chronic disease including hypertension and preeclampsia, fever, abdominal massage, or trauma. The patient attended eight prenatal visits: seven with a midwife and one with an obstetrician/gynecologist, during which no varices were found nor hypertension and preeclampsia. Physical examination showed blood pressure within the normal limit of 125/94 mmHg, tachycardia at 140 bpm, and no fever was recorded. Despite preserved blood pressure, the presence of marked tachycardia and severe anemia was indicative of compensated hemorrhagic shock, emphasizing that significant and life-threatening intra-abdominal bleeding in pregnancy may occur without evident hypotension. Obstetrical examination revealed a tense abdomen with tenderness and muscular defense. Cardiotocography examination revealed a type III category based on FIGO classification, which indicated a high probability of fetal hypoxia or acidosis and required immediate intervention ( Figure 1 ), hence raising a suspicion of placental abruption. Ultrasound findings showed a single intrauterine viable fetus with part of the placenta detached, retroplacental hematoma, and intra-abdominal free fluid ( Figure 2 ). Computed tomography (CT) or magnetic resonance imaging (MRI) were not performed in this case because of resource limitations and poor specificity and cannot be used to investigate the origin of the hemorrhage. Figure 1 A cardiotocography (CTG) was done to observe the fetus’ condition. There was evidence of fetal distress throughout the assessment, which placed the CTG in the third category. Cardiotocography strip with two multi-line line graphs. Graph 1: legend shows “FHR1” and “Pulse”. Horizontal axis: time, unit 1 centimeter per minute. Vertical axis: numeric scale 60 to 200. FHR1 line values described: rises from 130 to 155, drops to 110, returns to 145-155; later drops from 160 to 120, recovers to 150-160; later oscillates 140-170, dips to 135-140, recovers to 160. Pulse line runs near 130-140 with small fluctuations. Graph 2: legend shows “FMP” and “Toco”. Horizontal axis: time, unit 1 centimeter per minute. Vertical axis: numeric scale 0 to 100. Toco line shows repeated peaks 50-60 with troughs 10-20. Text near peaks: “FMP 12 percent (12)” and “FMP 3 percent (72)”. Pulse annotations: “Pulse 39 bpm”, “Pulse 140 bpm”, “Pulse 41 bpm”, “Pulse 139 bpm”. Multi-line cardiotocography graphs showing fetal heart rate, pulse and uterine activity over time. Figure 2 Placenta was inserted at fundus extending to the anterior corpus of the uterus with retroplacental hemorrhage. Ultrasound showing placenta and retroplacental hematoma. A cardiotocography (CTG) was done to observe the fetus’ condition. There was evidence of fetal distress throughout the assessment, which placed the CTG in the third category. Placenta was inserted at fundus extending to the anterior corpus of the uterus with retroplacental hemorrhage. Her hemoglobin level was 6.8 gr/dL and hematocrit level was 22%, suggesting severe anemia. She was diagnosed with G1P0A0 parturient at 33–34 weeks of pregnancy and 1 st stage latent phase with suspected placental abruption. The patient was scheduled to undergo an emergency caesarean section due to fetal distress and possible intra-abdominal bleeding. She exhibited significant anemia and tachycardia with maintained blood pressure, consistent with compensated hemorrhagic shock. Blood transfusion was initiated for hemodynamic optimization prior to surgery. A massive transfusion protocol was considered; however, given the patient’s compensated state and the rural hospital setting, targeted transfusion with three units of packed red cells (PRC) with one unit were administered immediately, and the remaining units were administered intraoperatively along with two units of fresh frozen plasma (FFP), which was considered more appropriate. We aimed to achieve a hemoglobin level of 10 g/dL. Clotting time was 8 minutes and bleeding time was 3 minutes, both were in normal limit. However, comprehensive coagulation studies were not performed in this case due to limitations of the resources. The initial differential diagnoses included placental abruption, uterine rupture, and other causes of acute abdominal pain, such as appendicitis or ovarian torsion. The absence of a uterine scar, nausea, vomiting, fever, lack of vaginal bleeding, and ultrasound findings of a retroplacental hematoma favored placental abruption over uterine rupture and other causes of an acute abdomen. Given the rarity of SHiP in the absence of maternal hypotension and trauma, preoperative diagnosis of SHiP remains challenging and, therefore, is only established intraoperatively. The patient underwent emergency cesarean section approximately 2 hours after admission under spinal anesthesia. During the surgery, approximately 1000 cc of blood was found in the peritoneal cavity immediately, confirming the suspicion of pre-existing intra-abdominal bleeding before uterine manipulation. A female baby was born with a body weight of 1,920 g and a body length of 48 cm. Her APGAR score was poor: 3 in the 1st minute and 4 in the 5th minute. Intramural oxytocin injection (10 IU) was administered, and the contraction was adequate. The placenta was delivered immediately, and the two layers of the uterine segment were closed. Further exploration revealed active bleeding from the rupture of the right uterine venous plexus ( Figure 3A ), confirming the etiology of SHiP in this patient. A fibrin sealant patch (TachoSil Nycomed) was applied as an adjunctive topical hemostatic agent following control of the active venous bleeding to enhance local hemostasis and minimize the likelihood of persistent minor bleeding. Hemostasis was successfully achieved thereafter. A uterine fibroid (LO-6) was also found in the left fundal uterus with a size of 2×2 cm ( Figure 3B ). The bilateral adnexa were within the normal limits. Intraoperative blood loss was estimated at approximately 1,000 cc, according to 900 cc suctioned into the tube and an additional 100 cc from the gauze pads used during the procedure ( Figure 4 ). A 4 × 4-cm gauze hold approximately 8–10 cc of blood, and 15 gauze pads were used during the surgery. Figure 3 An emergency caesarean section was performed. ( A ) Rupture of uterine venous plexus as the source of bleeding. ( B ) A uterine fibroid present at the left fundal uterine (LO-6) with a size of 2×2 cm. Part A shows gloved hands actively grasping and manipulating a large, rounded biological mass. The mass has a smooth outer surface with visible vascular markings and areas of hemorrhage. Its size is substantial relative to the gloved hands holding it. Part B shows the same large rounded mass fully exposed within an open surgical field. Surgical retractors are positioned at the lower portion of the operative site, holding the cavity open. The surface of the mass is smooth and glistening, with visible vascular streaks running across it. The mass occupies the majority of the frame. Two intraoperative photograph shows surgical handling and exposure of a uterine fibroid and rupture of uterine venous plexus. Figure 4 During the surgery, intra-abdominal hemorrhage was measured about 1,000 cc. The specimen is a dark reddish-brown to nearly black mass of biological tissue, irregular and lobulated in form, covered with blood and fluid. It is roughly palm-sized with an uneven, folded surface consistent with a soft organ or portion thereof. The tissue rests on a green surgical drape, the upper portion of which shows bloodstaining. A metal surgical instrument with a flat, broad tip is positioned at the upper right, partially contacting the specimen and is stained with blood. Surgical specimen consistent with intra-abdominal hemorrhage, shows a dark, irregular mass of excised biological tissue. An emergency caesarean section was performed. ( A ) Rupture of uterine venous plexus as the source of bleeding. ( B ) A uterine fibroid present at the left fundal uterine (LO-6) with a size of 2×2 cm. During the surgery, intra-abdominal hemorrhage was measured about 1,000 cc. Postoperatively, the baby was transferred to a regular perinatology ward; however, owing to a poor APGAR score, CPAP was required. The baby was monitored for eight days in the perinatology ward. After her condition had improved, she was discharged. The patient was subsequently transferred to a regular ward for close postoperative monitoring, including serial hemodynamic assessment, supportive care, and follow-up laboratory evaluation. Her hemoglobin level increased to 10.1 mg/dL and her hematocrit was measured at 30% after transfusion. The patient recovered well and was discharged after two days of observation in a stable condition.

Untreated spontaneous hemoperitoneum in pregnancy (SHiP) can be fatal. It is a rare disorder that occurs during pregnancy. 1 , 2 SHiP is associated with a reported maternal mortality rate of 1.7% and a perinatal mortality rate of 26.9%. 3 In SHiP, several etiologies have been reported, which vary depending on the gestational age. 2 First trimester SHiP usually correlates with ectopic pregnancy rupture, whereas second‑ and third‑trimester SHiP are usually linked with aberrant vascular rupture. 4–8 There is evidence that a hypertrophic utero-ovarian vessel, caused by increased blood flow to the uterine arteries during the second trimester, is the cause of the higher incidence of SHiP. 2 Predisposing factors, such as increased age and multipara, could increase the likelihood of uterine vein rupture in SHiP. 9 Given its rarity and nonspecific presentation, as it often mimics other causes of acute abdomen during pregnancy, such as placental abruption or uterine rupture and appendicitis. 2 , 10 SHiP due to rupture of the uterine veins remains a diagnostic challenge that can easily be overlooked without surgical exploration. Reporting such cases is essential to raise clinical awareness, emphasize the importance of early suspicion, and guide prompt management through surgical intervention and blood transfusion to improve maternal–fetal outcomes. Caesarean delivery is the preferred approach in late pregnancy. 1 We present a rare case of a 23‑year‑old Sundanese primigravid woman at 33–34 weeks of gestation with SHiP due to rupture of the uterine venous plexus and placental abruption.

Spontaneous hemoperitoneum in pregnancy (SHiP) is an unpredictable and potentially life-threatening condition. As preoperative findings are often nonspecific, this case highlights the importance of maintaining a high index of suspicion and considering SHiP in the differential diagnosis of acute abdomen during pregnancy, particularly when there is a decline in maternal or fetal status. Early recognition and timely operative procedures may improve maternal and perinatal outcomes, particularly in resource-limited or rural areas. Early identification of spontaneous hemoperitoneum in pregnancy (SHiP) is challenging because its presentation may overlap with that of other causes of acute abdomen. In this case, rapid clinical deterioration and fetal distress required prompt surgical intervention, which ultimately confirmed the diagnosis and allowed definitive management. The considerations outlined are based on singular experience and aim to generate hypotheses rather than provide evidence-based recommendations. However, increased clinical vigilance, prompt surgical intervention when necessary, and adequate hemodynamic support may improve maternal and fetal outcomes under similar circumstances. Further studies are required to better understand the diagnostic mechanisms and to establish optimal management strategies for this rare condition.

Spontaneous hemoperitoneum in pregnancy (SHiP) remains an exceptionally rare but life-threatening event, if not treated carefully. 1 , 2 Diaz-Murillo reported that the incidence of SHiP from rupture of uterine veins is exceedingly rare, accounting for only 1/10,000 births. 11 Most cases described in the literature occur in multiparous women or those with endometriosis, uterine varicosities, or assisted reproductive technology. 7 , 8 , 11 In contrast, our patient was a young primigravid woman without any predisposing factors. This distinction makes this case clinically instructive rather than solely rare, emphasizing that SHiP can occur outside the typical risk profile and thus highlights the importance of maintaining a high index of suspicion even in low-risk pregnancies. Various etiologies have been described for SHiP, which may vary according to the age of gestation. 2 First trimester SHiP is associated with ectopic pregnancy rupture, whereas the second and third trimesters are more often associated with abnormal vascular rupture, such as splenic artery, uterine arteries, varicose veins, or even aneurysm rupture. 4–8 A higher incidence of SHiP during the second trimester is reported to be due to increased blood supply to the uterine arteries, causing hypertrophic utero-ovarian vessels. 2 The most frequent sites were the broad ligament, comprising 78.3% of cases, posterior wall of the uterus (18.3%), and anterior uterus (3.3%). 11 Several mechanisms have been hypothesized to explain the spontaneous rupture of uterine vessels in SHiP during the later trimester of pregnancy. The proposed predisposing factors for spontaneous rupture of uterine veins include physical exertion, defecation, sports, and violent coitus. 8 , 12 This may lead to vascular dilatation of the uterus and elevated venous pressure, especially in the varicose veins of the broad ligament of the uterus. Increasing blood volume during pregnancy can demonstrate a varicose vein, while valves are absent from the small and medium veins, and the superficial and thin outer sheaths of the parauterine and subserosal veins lack inherent elasticity and fascia. An enlarged uterus during pregnancy also compresses the inferior vena cava, leading to blockage and increased venous pressure by up to 2–3 times, creating a higher likelihood of spontaneous rupture of the veins. Uterine venous malformations or congenital uterine venous dysplasia may also play a role in this condition. Endometriosis and inflammation during pregnancy may cause rupture in the subserosal and parauterine veins. 13–15 Furthermore, in cases of spontaneous rupture of the uterine arteries, the exact cause is unknown. However, various conditions, such as aneurysm, pseudoaneurysm, congenital malformation, alteration within the vascular intima caused by inflammation or estrogen, and local erosion of the arteries associated with endometriosis, may lead to vessel rupture. 16 Other risk factors, such as in vitro fertilization technology and connective disease, can also induce spontaneous rupture of uterine vessels. 8 , 11 , 17 , 18 Patients may experience acute abdominal pain and low hemoglobin levels due to hemorrhage, sometimes leading to hypovolemic shock. 3 , 19 Physical examination and ultrasonography are required to establish a profound diagnosis and rule out any other possible causes, such as uterine scar rupture and placental etiologies, as the clinical findings may be similar. 19 Placental etiologies may be considered if maximum tenderness is felt at the site of the placental location and is not influenced by the patient’s position. However, in hemoperitoneum, the intensity of pain increases when the patient lies on their side. In this case, the symptoms may overlap, as the patient experiences placental abruption along with hemoperitoneum. 19 Bertholdt et al reported a similar case of hemoperitoneum associated with placental abruption, but the patient had no uterine vessel rupture; thus, the hemoperitoneum originated from backflow of intrauterine blood through the left intrauterine tube. These mechanisms prevent complete detachment of the placenta, causing a missed diagnosis of placental abruption and delayed treatment. 20 However, whether placental abruption contributed to the development of the SHiP or represents a concurrent obstetric event remains uncertain. In this case, we also found a uterine fibroid at the left fundal uterine with the size of 2×2 cm. In a study by Pegu et al, the patient had SHiP due to rupture of the venous plexus overlying the fibroid. The patient was 32 years old with gravida 2 at 32 weeks of gestation, with no history of trauma or injury. She presented with tachypnea, and ultrasonography showed fetal demise; hence, labor was induced. Pegu et al hypothesized that the hemorrhage was the result of misoprostol administration for labor induction. 12 Additionally, Chen et al postulated a theory regarding the mechanism of hemoperitoneum from non-ruptured uterine fibroids, such as if the mass size is fairly large, which in their case is 10 cm, it may overstretch and split the overlying vessels between the uterine masses, causing a disruption of the vessels and hemorrhage. 9 , 21 , 22 Although previous studies have suggested a possible association between uterine fibroids and SHiP, the uterine fibroid in this case (LO-6) was only 2×2 cm in size, and its contribution to the development of SHiP remains uncertain. Moreover, the fibroid in our patient was relatively small and located contralateral to the site of the venous rupture. Therefore, a direct causal relationship cannot be established, and the fibroid should be interpreted as a possible associated finding. Furthermore, a meta-analysis by Jenabi et al demonstrated a significant association between uterine fibroids and placental abruption. 23 It is also presumed that the association between these two events is determined by the location of the fibroids. If large submucosal fibroids are located near the placental insertion site, placental abruption may be induced as a result of ischemia and necrosis due to restriction of blood flow. 24 Due to the limitations of the research and the fact that the symptoms are mostly equivocal, it is quite challenging to diagnose SHiP from a ruptured uterine vein with placental abruption. Ultrasonography may reveal fluid collection in the abdominal cavity, but this is not specific. Other investigations using computed tomography (CT) or magnetic resonance imaging (MRI) are not recommended because of poor specificity and cannot be used to investigate the origin of the hemorrhage, including the presence of varicose veins. 9 Although laparoscopy is occasionally required to determine the etiology of bleeding, avoiding the presence of certain risk factors, such as uterine manipulation, violent coitus, and lifting heavy weights, may reduce excess tension on the uterus due to the presence of fibroids, leading to hemoperitoneum. 25 The decision to perform an emergency caesarean section was based on the presence of a category III cardiotocography tracing indicating fetal distress, consistent with the current obstetric guidelines recommending immediate delivery in such circumstances. Surgical exploration also serves dual diagnostic and therapeutic purposes, confirming the presence of hemoperitoneum and allowing direct hemostasis. 26 Intraoperatively, a small uterine fibroid was identified, but it was not removed because of the high risk of intraoperative bleeding and postpartum hemorrhage. This conservative approach aligns with the recommendations of Chen et al, who emphasized deferring myomectomy until hemodynamic stability is achieved. Chen et al also recommended urgent laparoscopy to establish a diagnosis in uncertain cases. 9 We focused on controlling the hemorrhage and improving the patients’ general condition since the patient had severe anemia. If the fibroids enlarge, myomectomy is performed after the patient is stable. Nonetheless, the patient will have an increased risk of uterine fibroid recurrence of up to 2.8 times if myomectomy is performed. However, in multiparous women, the incidence of recurrence declines as pregnancy creates a protective effect. 27 , 28 Given the rarity and unpredictability of SHiP, this case did not support routine screening for uterine fibroids or vascular anomalies as a preventive measure. However, awareness of such possible associations may prompt clinicians to consider SHiP earlier in patients with similar acute presentations. Due to the intricacy of her condition and probable obstetric risks in future pregnancies, follow-up in a higher-level maternal care setting was deemed appropriate for this patient. This case is clinically significant as it illustrates the rare coexistence of spontaneous hemoperitoneum in pregnancy and placental abruption in a primigravid patient without classical predisposing factors. The overlapping presentation with more common obstetric emergencies illustrates the diagnostic challenge of SHiP and emphasizes the importance of maintaining a high index of suspicion. In resource-limited settings, prompt clinical assessment and timely surgical exploration remain essential for achieving favorable maternal and fetal outcomes. Future research should aim to establish diagnostic algorithms or imaging markers to facilitate earlier recognition of SHiP and reduce maternal–fetal morbidity.