Archives of Perinatal Medicine 20(4), 217-223, 2014 CASE REPORT

Preeclamptic pregnancy complicated by huge retroplacentalhematoma and Couvelaire uterus – a case report

ANNA ROZTOCKA, MARIOLA ROPACKA-LESIAK, GRZEGORZ H. BRĘBOROWICZ1

Abstract

The paper presents a case of 28-year old pregnant woman, gravida 2 para 1, referred to the hospital at 33 weeksof gestation because of pregnancy induced hypertension and IUGR. The ultrasound screening, Doppler blood flowvelocimetry, cardiotocography and 24-hour blood pressure monitoring was performed. Shortly after hospitaladmission the BP suddenly increased up to 196/137 and the patient reported a solid abdominal pain. Immediatelyperformed ultrasound revealed a marginal placental abruption and a hematoma of 10 cm in the diameter locatedon the posterior uterine wall. During urgent cesarean section a Couvelaire uterus syndrome was diagnosed.Approximately 700 ml of blood clots from the uterine cavity and 700 ml of sanguineous fluid from peritoneal cavitywere evacuated. Prematurely delivered neonate weighed 1580 grams, the Apgar score 3, 3 and 6 points in the1st, 5th and 10th minute and was admitted to Neonatal Intensive Care Unit. The consequences and complicationlinked to retroplacental hematoma and Couvelaire uterus are also described.

Key words: preeclampsia, IUGR, placental abruption, Couvelaire uterus, uteroplacental apoplexy

Introduction

Ten percent of women worldwide experience highblood pressure during pregnancy [1]. One of its leadingcauses is pregnancy induced hypertension, defined assystolic blood pressure $140 and/or diastolic blood pres-sure $90 appearing after 20 weeks of gestation in a pre-viously normotensive patient. Pregnancy induced hyper-tension (PIH) complicates about 6% of pregnancies andits prevalence is constantly rising [2]. Not only PIH, butevery hypertension disorder in pregnancy increases therisk of both maternal and fetal morbidity and mortality.It concerns notably those patients who develop its seve-re forms – preeclampsia and eclampsia [2]. Preeclamp-sia, affecting 4.6% of pregnancies is diagnosed on thebasis of PIH concurrent with proteinuria and/or one ofthe following: low platelet count (< 100 000/ml), highserum creatinine, doubling of hepatic transaminases’ le-vel, pulmonary edema, visual or cerebral symptoms[3, 4]. Main fetal complications are intrauterine growthrestriction (IUGR) and prematurity, both resulting inlow birth weight and numerous diseases [5]. Possiblematernal after-effects concern hepatic, renal, central ner-vous system and coagulation disorders. Preeclampsiaand eclampsia cause 10-15% of direct maternal deathsworldwide [1].

One of the significant life-threatening consequenceof preeclampsia is placental abruption, defined as partialor total separation of the placenta occurring before

delivery of the fetus. The separated part of the placentaceases to exchange gas and nutrients, resulting in fetalcompromise. The risk of severe placental abruption inpregnancies complicated by hypertension is five-foldhigher comparing to normotensive gravidas. What’smore, many studies suggest that antihypertensive treat-ment of chronic hypertension in pregnancy do not re-duce this risk [6]. Placental abruption may be caused bymaternal abdominal trauma, but mostly it is related tothe underlying process of chronic placental pathology.Typical clinical features are abdominal pain, vaginalbleeding, tenseness of the uterus, often concurrent withhypertonic uterine contractions and non-reassuring FHRtracings. Possible maternal consequences are: obstet-rical haemorrhage, emergency cesarean section, emer-gency hysterectomy, DIC and renal failure. A very rarecomplication is bleeding infiltrating the myometriumthat results in condition called Couvelaire’s uterus [42].In case of placental abruption, the frequency of maternaldeath increases seven fold. The adverse effects for thefetus include preterm delivery, low birth weight, lowApgar scores, perinatal asphyxia and death [7, 8]. Re-cently decreasing perinatal mortality in placental abrup-tion nowadays amounts to approximately 12%. Almost80% of perinatal deaths are intrauterine [9]. Althoughobstetricians have wide and detailed knowledge on therisk factors of placental abruption, still in most of thecases it is very hard to establish its cause.

1 Department of Perinatology and Gynecology, Poznan University of Medical Sciences, Poznań, Poland

A. Roztocka, M. Ropacka-Lesiak, G.H. Bręborowicz218

Case

A 28-year old female, gravida 2 para 1, was admittedto the Department of Perinatology and Gynaecology,University of Medical Sciences in Poznań because ofpregnancy induced hypertension and IUGR. Her pre-vious pregnancy 8 years before was uncomplicated andshe gave vaginal birth at 41 week of gestation. The fe-male infant weighed 3100 g and received 9 points in theApgar score. The patient had no relevant medical his-tory. Her family history was positive for hypertensionand diabetes. Her partner was 33 years old and healthy.

Besides mild urinary tract infection treated withFuragin, the first half of current gestation was asympto-matic and uncomplicated. She denied smoking tobacco,drinking alcohol or using drugs, diet supplements orherbs during this pregnancy. She also denied abdominaltrauma in the course of gestation. At 21 weeks of gesta-tion, she noticed asymptomatic elevation of blood pres-sure (BP). The maximum BP was 140/100 mm Hg andno medication was administered. At 28 weeks of gesta-tion, the BP increased up to 150/100 mm Hg and theambulatory ultrasound revealed signs of fetal growthrestriction (IUGR). The Doppler examination demon-strated elevated resistance and notching in both uterinearteries. Fetal anatomy was normal. At 29 weeks of preg-nancy the patient was hospitalized in our Department forthe first time, because of mild hypertension and lowerlimbs and face edema. She didn’t report any other symp-toms. Obstetrical examination did not indicate any patho-logies and the CTG tracings were reassuring. Results ofblood laboratory tests suggested no liver or kidney pa-thology. The total protein in urine was an equivalent of1+ on dipstick test. On ultrasound, the estimated fetalweight (EFW) using Hadlock formula was 931 g, whichwas below the 3rd percentile for gestational age. Therewas elevated resistance to blood flow and periodic notch-ing in both uterine arteries. The biophysical profile was8/8 points and the fetus’ presentation was cephalic. On24-hour BP monitoring the mean BP values were 134and 87.5 mm Hg for systolic and diastolic BP, respec-tively. The maximum BP was 180/136 mm Hg. The BPwas normalized with methyldopa and patient was dis-charged from the hospital. The therapy with methyldopawas recommended, as well as BP monitoring 4 timesa day, counting fetal body movements and ambulatoryfollow up in 7 days.

The patient was re-admitted at 33 weeks of gesta-tion. She did not report any abnormal clinical symptomsor elevated BP. However, on admission the value of BPwas 150/105 mm Hg. The vaginal discharge was normal,

there was 0.5 cm external dilation and there were nosigns of membranes rupture. The fundus of the uterusappeared to be only 5 cm above the umbilicus. On ultra-sound, the fetus was in cephalic position and EFW was1488 g, below the 3rd percentile for gestational age.

Fig. 1. Marginal placental abruption resulting in hugeretroplacental hematoma

Fig. 2. Maternal surface of the placenta – notice hugeplacental hematoma on the upper ring of the placenta

Fig. 3. The appearance of the uterus immediately afterdelivery. Notice uteroplacental apoplexy characterized

by bleeding permeating myometrium casing its characte-ristic appearance – a bluish and purple colour mottled

by ecchymoses

Preeclamptic pregnancy complicated by huge retroplacental hematoma and Couvelaire uterus 219

Doppler ultrasound was normal. The gestational age wasverified on the basis of ultrasound measurement in theI trimester. 4-hour BP monitoring was applied. Then,suddenly the BP increased up to 199/137 mm Hg andthe patient complained of sharp, increasing abdominalpain and mild scotomata. On CTG the basal FHR was160 bpm with no decelerations and good variability andregular, low-amplitude uterine contractions. The ultra-sound performed rapidly revealed marginal placental ab-ruption and a 10 cm in the diameter retroplacental he-matoma. The emergency cesarean section was per-formed. During surgery, approximately 700 ml of sangui-neous fluid was discovered in peritoneal cavity. The ute-rus appeared cyanosed with ecchymoses seen mainly inboth uterine horns. Signs of placental abruption occur-red on placental surface. Approximately 700 ml of bloodclots were evacuated from the uterine cavity after pla-cental extraction. On the basis of uterus’ appearance,the Couvelaire syndrome was diagnosed. Intravenouscarbetocin and misoprostol per rectum were adminis-tered in order to constrict the uterus.

During puerperium patient suffered from anemia,however it did not require blood transfusion. The deli-vered male infant weighed 1580 g and the Apgar scorewas 3, 3, 6. The pH was 7.17 in the umbilical artery and7.21 in the umbilical vein. The newborn was admitted tothe Neonatal Intensive Care Unit due to prematurity,low birth weight and signs of perinatal hypoxia. Further-more, anemia, neonatal respiratory distress syndrome,congenital pneumonia and 1st degree intraventricularhaemorrhage were diagnosed. Additional findings weresmall hemangiomas. The baby was discharged from thehospital a month after birth. Currently, the infant is 10months old, weighs 7700 g, requires regular surgeonand cardiologist’s care due to the hemangiomas and pe-riodically suffers from respiratory tract infections de-manding hospitalization.

Discussion

Placental abruption, being the most common patho-logical cause of vaginal bleeding in late pregnancy, is alife-threatening incident complicating 0,4-1% of pregnan-cies [7, 8]. The ethiopathogenesis is multifactoral andstill a subject of extensive research [7]. The incidence ofthis complication is increasing, most likely due to aug-mentation of risk factors’ prevalence. Risk factors of pla-cental abruption include those of acute etiology, such asabdominal trauma or drug abuse. Others comprise ofhypertension disorders, especially severe preeclampsiaand eclampsia, polyhydramnios, prolonged rupture of

membranes, short umbilical cord, uterine tumors andanomalies, chorioamnionitis, anemia, renal disorders,intrapartum fever and prior cesarean delivery. Sociode-mographic risk factors enclose maternal age, parity, to-bacco use and male infant sex. Also a history of previousischemic placental disease, preeclampsia, IUGR or SGAand placental abruption increase the risk [7, 8, 11-14].Hypertension in pregnancy appears to be the most fre-quent pathology concurring with placental abruption.Particularly a sudden increase of BP may result in acuteplacental abruption [14].

Every pregnancy complicated by preeclampsiashould be considered high-risk. Early-onset preeclampsia(commencing before 34th week of gestation) is more dan-gerous than late-onset and increases the risk of fetaldeath almost 6 times. The risk of perinatal death or se-vere morbidity in this disorder is 16-fold higher than innormal pregnancy [15]. What’s interesting, preeclampsiaoccurs only in simultaneous presence of the placenta.There is growing evidence that pathological vasculatorydevelopment in the placental bed that begins early inpregnancy leads to preeclampsia. These abnormalitiesparticularly concern remodeling and trophoblast invasionof the uteroplacental spiral arteries. Altered develop-ment lead to lack of arterial dilation resulting in in-creased resistance in uteroplacental vasculature [16, 17].Following abnormal deep placentation and hypoperfu-sion lead to placental insufficiency, a known cause of fe-tal hypoxia and ischemia. These events finally may resultin a wide range of pathologies – preeclampsia, IUGR,preterm labor, preterm premature rupture of membra-nes, spontaneous abortion in late pregnancy and placen-tal abruption [17, 18]. Excessive antiangiogenic andinflammatory factors release following placental abnor-mal perfusion affect the function of the endotheliumleading to multi-system response [20]. The organs thatare exceptionally vulnerable to endothelial injury and in-flammation are the brain, lungs, kidneys, liver, heart andvessels [23]. The daily urine protein excretion risingabove or equal 0.3 g is a first sign of glomeruloendothe-liosis [26]. There are also data that altered immunologicresponse in the HLA system, recalling graft versus hostdisease underlie preeclampsia [19]. Likewise, oxidativestress occurring in ischemic conditions plays a signifi-cant role in preeclampsia, as it destroys the structure ofthe syncytium [21, 22]. Genetic basis of this pathology,suggesting the contribution of modifier genes and envi-ronmental factors is a subject of intensive research aswell [25].

A. Roztocka, M. Ropacka-Lesiak, G.H. Bręborowicz220

A patient with preeclampsia should be hospitalizedand considering the often unusual symptoms of pre-eclampsia, every pregnant women who feels “poorly”should be screened for this disorder [27]. In preec-lamptic patients it is crucial to maintain the correctblood pressure and avoid aggravation to eclampsia [23].Magnesium sulfate is the medication of choice tocounteract eclampsia and it is proven to decrease mater-nal mortality [2, 24]. Moreover, a course of betametha-sone for fetal lung maturation should be administered inevery case of early-onset preeclampsia. Both medica-tions were administered to our patient.

It is widely known that delivery leads to recoveryfrom preeclampsia and eclampsia. Considering the modeof labor in preeclamptic women, Steegers and colleaguessuggest vaginal birth after 30 weeks of pregnancy, if fetaland cervical status allows it. However, when the fetus isgrowth restricted, cesarean delivery appears to be moresafe [23]. Nassar et al. recommend labor induction forthe patients with severe preeclampsia at $ 34 weeks ofgestation, proving that almost 50% of them successfullydeliver vaginally after induction [28]. Physicians agreethat preeclampsia after 37 weeks of gestation is an un-questioned indication to deliver the fetus. Consideringthe onset of preeclampsia prior to 36 weeks of gestation,the management is still a subject of discussion. Com-monly, expectant management with close surveillance isrecommended, unless the disease has severe features.CTG non stress test, repeated ultrasound and Dopplervelocimetry assessments are the methods of choice tomonitor fetal well-being. Typical Doppler ultrasoundfindings are: increased pulsatily index or/and notching inthe uterine arteries and alterations in umbilical arteryflows, such as AEDF and REDF [27].

According to Walker, placental insufficiency leads tointrauterine growth restriction in 30% of preeclampticpregnancies. IUGR is referred as inability of the fetus toreach its predetermined growth potential, resulting ina SGA fetus (small for gestational age). Affected fetusesare at higher risk of fetal, neonatal and perinatal mor-bidity and mortality [30-32]. Furthermore, the risk of in-trauterine death rises 5 to 10-fold [29]. Sometimes poorfetal growth in early pregnancy is the first symptom pre-luding preeclampsia. This less frequent form, referred asearly-onset IUGR is associated with preeclampsia andpathological Doppler uterine artery pattern [33]. Severefetal growth restriction, hypertensive disorder and malefetal sex – all found in our patient are proven to besignificant risk factors of placental abruption [34]. Thereis enough research to state that most of the cases are

the consequence of alterations in placental developmentresulting in chronic placental pathology [35, 36]. Largeretrospective cohort studies by Rasmussen et al. provethat women whose first pregnancy was complicated byIUGR are at higher risk of placental abruption in sub-sequent pregnancies [40].

Diagnosis of placental abruption is made upon clini-cal symptoms confirmed by ultrasound evaluation. Unfor-tunately, often there are no ultrasound findings despiteplacental abruption – the sensitivity of USG in diagno-sing this pathology is 25-50%, aproximately. However,a presence of adverse ultrasound findings has a predic-tive value up to 88% [39]. Typical ultrasound finding isa retroplacental hematoma. Its visualisation and largediameter is prognostically unpropitious, likewise the per-centage of the surface of placental detachment [37].Other potential ultrasound findings are: subchorionicfluid accumulation, echogenic debris in the amnioticfluid and a so-called Jello sign. Jello sign is diagnosedwhen a thickened layer of placenta shimmers as the pa-tient moves during examination [39].

Severe placental abruption, referred as an abruptionconcurrent with unstable maternal status and/or non-reassuring CTG tracing, is an indication for immediatecesarean delivery. Because of the high risk of coagulo-pathy, blood, platelets, fresh frozen plasma and cryopre-cipitate should be present at the operating room. Pa-tients with severe abruption, DIC or hypovolemic shockare at high risk of multiorgan failure and death. Closesurveillance of the mother and neonate is necessary alsopostpartum. Prevention of uterine atony, monitoringblood pressure, blood loss and laboratory tests are cru-cial. Uterine atony is managed by oxytocin, prostaglan-dine analogues and methylergonovine. It is important toremember that methylergonovine is contraindicated inpreeclampsia as it increases the blood pressure [41].

In our patient, the ultrasound diagnosis of a retropla-cental hematoma was confirmed during surgery. What’smore, during c-section a Couvelaire uterus with bloodthat reached the peritoneal cavity was diagnosed. Cou-velaire uterus, also described as uteroplacental apoplexy,is a rare, life threatening condition characterized bybleeding permeating myometrium, rarely crossing to theperitoneal cavity or infiltrating broad ligaments andovaries [42, 44, 47]. It was first described in 1911 byFrench obstetrician, Alexandre Couvelaire. The diagno-sis of Couvelaire uterus can only be established on thebasis of biopsy or visual examination during surgery[42, 43]. Its characteristic appearance is a bluish orpurple colour, mottled by ecchymoses. In such case, the

Preeclamptic pregnancy complicated by huge retroplacental hematoma and Couvelaire uterus 221

risk of uterine rupture during constriction is very high,as the myometrium is extremely weak. On the otherhand, the patients with a Couvelaire uterus are at higherrisk of uterine atony and haemorrhage, because theblood-infiltrated myometrium is less able to contract[42]. It also has lower susceptibility to pro-contractingmedication. Diagnosing Couvelaire uterus is an indica-tion for aggressive treatment of atony to prevent severeconsequences such as DIC, emergency hysterectomyand exsanguination. In our patient carbetocin and miso-prostol with satisfactory effect was administered. Surgi-cal methods of managing uterine atony and haemorrha-ge, applied when pharmaceutical methods fail, are ute-rine vessels ligation, uterine compression sutures, em-bolization and obstetrical hysterectomy as last resort.The suture technique particularly recommended andeffective in managing haemorrhages in patients withhypertensive disorders, placental abruption and Couve-laire uterus is the B-Lynch technique [52]. Hysterectomywas the management of choice for many decades [44].Nowadays the recommended treatment is conservati-ve [42].

The etiology of Couvelaire uterus remains uniden-tified and few available reports link it with placental ab-ruption, placenta previa, preeclampsia, coagulopathy,amniotic fluid embolism and uterine rupture [42-45, 47-48]. It is estimated that Couvelaire uterus develops in5% of patients with placental abruption [51]. It is im-portant to emphasise that Couvelaire uterus is not al-ways a result of placental abruption. A very recent casedescribed by Shreedevi and colleagues presents a diag-nosis of Couvelaire uterus in the absence of placentalabruption and any other pathologies [49]. A different re-cent case report describes a Couvelaire uterus thatdeveloped after a dilation and curettage in missed abor-tion of 13 weeks old pregnancy. The mechanism sug-gested by authors is iatrogenic perforation of the uterinewall during curettage, letting the blood infiltrate themyometrium. Hysterectomy was indispensable [46]. Inthe case reported by Gogola et al. the debris and airbubbles in the uterine veins were concurrent with theCouvelaire uterus and the authors suggest the blood-permeated area of uterus to be the “portal” for the deb-ris to reach maternal vessels and cause amniotic fluidembolism [48]. Avery and Wells retrospectively describethe ultrasound findings in Couvelaire syndrome con-firmed during cesarean section. Those findings are largeretroplacental blood clot and blood dissecting into themyometrium. They state that ultrasound diagnosis ofCouvelaire uterus is limited, but possible [50].

One should be aware that a patient diagnosed withpreeclampsia should control her blood pressure after dis-charge from the hospital. Sometimes hypertensives areessential during puerperium. There are also reports thatthese patients should avoid non-steroid anti-inflamma-tory drugs in treating post-cesarean pain. The meta-analysis from 2015 reports that among women who ex-perienced preeclampsia, 20% will develop hypertensionand 16% will have preeclampsia in subsequent pregnancy[10]. Low doses of ASA [53] and calcium supplemen-tation [2] appear to be useful in prevention of pre-eclampsia among high-risk patients. What is important,women with a history of preeclampsia have higher riskof cardiovascular disorders in the future, most probablyas a result of systemic endothelial dysfunction [3, 54].There is no scientific data on the recurrence of Couve-laire uterus.

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J Anna RoztockaDepartment of Perinatology and GynecologyPoznan University of Medical SciencesPolna 33, 60-535 Poznań, Polande-mail: anroztocka@gmail.com