Download Preeclamptic pregnancy complicated by huge retroplacental

Archives of Perinatal Medicine 20(4), 217-223, 2014
CASE REPORT
Preeclamptic pregnancy complicated by huge retroplacental
hematoma 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 weeks
of gestation because of pregnancy induced hypertension and IUGR. The ultrasound screening, Doppler blood flow
velocimetry, cardiotocography and 24-hour blood pressure monitoring was performed. Shortly after hospital
admission the BP suddenly increased up to 196/137 and the patient reported a solid abdominal pain. Immediately
performed ultrasound revealed a marginal placental abruption and a hematoma of 10 cm in the diameter located
on 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 cavity
were evacuated. Prematurely delivered neonate weighed 1580 grams, the Apgar score 3, 3 and 6 points in the
1st, 5th and 10th minute and was admitted to Neonatal Intensive Care Unit. The consequences and complication
linked 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 high
blood pressure during pregnancy [1]. One of its leading
causes is pregnancy induced hypertension, defined as
systolic blood pressure $140 and/or diastolic blood pressure $90 appearing after 20 weeks of gestation in a previously normotensive patient. Pregnancy induced hypertension (PIH) complicates about 6% of pregnancies and
its prevalence is constantly rising [2]. Not only PIH, but
every hypertension disorder in pregnancy increases the
risk of both maternal and fetal morbidity and mortality.
It concerns notably those patients who develop its severe forms – preeclampsia and eclampsia [2]. Preeclampsia, affecting 4.6% of pregnancies is diagnosed on the
basis of PIH concurrent with proteinuria and/or one of
the following: low platelet count (< 100 000/ml), high
serum creatinine, doubling of hepatic transaminases’ level, pulmonary edema, visual or cerebral symptoms
[3, 4]. Main fetal complications are intrauterine growth
restriction (IUGR) and prematurity, both resulting in
low birth weight and numerous diseases [5]. Possible
maternal after-effects concern hepatic, renal, central nervous system and coagulation disorders. Preeclampsia
and eclampsia cause 10-15% of direct maternal deaths
worldwide [1].
One of the significant life-threatening consequence
of preeclampsia is placental abruption, defined as partial
or total separation of the placenta occurring before
1
delivery of the fetus. The separated part of the placenta
ceases to exchange gas and nutrients, resulting in fetal
compromise. The risk of severe placental abruption in
pregnancies complicated by hypertension is five-fold
higher comparing to normotensive gravidas. What’s
more, many studies suggest that antihypertensive treatment of chronic hypertension in pregnancy do not reduce this risk [6]. Placental abruption may be caused by
maternal abdominal trauma, but mostly it is related to
the underlying process of chronic placental pathology.
Typical clinical features are abdominal pain, vaginal
bleeding, tenseness of the uterus, often concurrent with
hypertonic uterine contractions and non-reassuring FHR
tracings. Possible maternal consequences are: obstetrical haemorrhage, emergency cesarean section, emergency hysterectomy, DIC and renal failure. A very rare
complication is bleeding infiltrating the myometrium
that results in condition called Couvelaire’s uterus [42].
In case of placental abruption, the frequency of maternal
death increases seven fold. The adverse effects for the
fetus include preterm delivery, low birth weight, low
Apgar scores, perinatal asphyxia and death [7, 8]. Recently decreasing perinatal mortality in placental abruption nowadays amounts to approximately 12%. Almost
80% of perinatal deaths are intrauterine [9]. Although
obstetricians have wide and detailed knowledge on the
risk factors of placental abruption, still in most of the
cases it is very hard to establish its cause.
Department of Perinatology and Gynecology, Poznan University of Medical Sciences, Poznań, Poland
218
A. Roztocka, M. Ropacka-Lesiak, G.H. Bręborowicz
Case
A 28-year old female, gravida 2 para 1, was admitted
to the Department of Perinatology and Gynaecology,
University of Medical Sciences in Poznań because of
pregnancy induced hypertension and IUGR. Her previous pregnancy 8 years before was uncomplicated and
she gave vaginal birth at 41 week of gestation. The female infant weighed 3100 g and received 9 points in the
Apgar score. The patient had no relevant medical history. Her family history was positive for hypertension
and diabetes. Her partner was 33 years old and healthy.
Besides mild urinary tract infection treated with
Furagin, the first half of current gestation was asymptomatic and uncomplicated. She denied smoking tobacco,
drinking alcohol or using drugs, diet supplements or
herbs during this pregnancy. She also denied abdominal
trauma in the course of gestation. At 21 weeks of gestation, she noticed asymptomatic elevation of blood pressure (BP). The maximum BP was 140/100 mm Hg and
no medication was administered. At 28 weeks of gestation, the BP increased up to 150/100 mm Hg and the
ambulatory ultrasound revealed signs of fetal growth
restriction (IUGR). The Doppler examination demonstrated elevated resistance and notching in both uterine
arteries. Fetal anatomy was normal. At 29 weeks of pregnancy the patient was hospitalized in our Department for
the first time, because of mild hypertension and lower
limbs and face edema. She didn’t report any other symptoms. Obstetrical examination did not indicate any pathologies and the CTG tracings were reassuring. Results of
blood laboratory tests suggested no liver or kidney pathology. The total protein in urine was an equivalent of
1+ on dipstick test. On ultrasound, the estimated fetal
weight (EFW) using Hadlock formula was 931 g, which
was below the 3rd percentile for gestational age. There
was elevated resistance to blood flow and periodic notching in both uterine arteries. The biophysical profile was
8/8 points and the fetus’ presentation was cephalic. On
24-hour BP monitoring the mean BP values were 134
and 87.5 mm Hg for systolic and diastolic BP, respectively. The maximum BP was 180/136 mm Hg. The BP
was normalized with methyldopa and patient was discharged from the hospital. The therapy with methyldopa
was recommended, as well as BP monitoring 4 times
a day, counting fetal body movements and ambulatory
follow up in 7 days.
The patient was re-admitted at 33 weeks of gestation. She did not report any abnormal clinical symptoms
or elevated BP. However, on admission the value of BP
was 150/105 mm Hg. The vaginal discharge was normal,
there was 0.5 cm external dilation and there were no
signs of membranes rupture. The fundus of the uterus
appeared to be only 5 cm above the umbilicus. On ultrasound, the fetus was in cephalic position and EFW was
1488 g, below the 3rd percentile for gestational age.
Fig. 1. Marginal placental abruption resulting in huge
retroplacental hematoma
Fig. 2. Maternal surface of the placenta – notice huge
placental hematoma on the upper ring of the placenta
Fig. 3. The appearance of the uterus immediately after
delivery. Notice uteroplacental apoplexy characterized
by bleeding permeating myometrium casing its characteristic appearance – a bluish and purple colour mottled
by ecchymoses
Preeclamptic pregnancy complicated by huge retroplacental hematoma and Couvelaire uterus
Doppler ultrasound was normal. The gestational age was
verified on the basis of ultrasound measurement in the
I trimester. 4-hour BP monitoring was applied. Then,
suddenly the BP increased up to 199/137 mm Hg and
the patient complained of sharp, increasing abdominal
pain and mild scotomata. On CTG the basal FHR was
160 bpm with no decelerations and good variability and
regular, low-amplitude uterine contractions. The ultrasound performed rapidly revealed marginal placental abruption and a 10 cm in the diameter retroplacental hematoma. The emergency cesarean section was performed. During surgery, approximately 700 ml of sanguineous fluid was discovered in peritoneal cavity. The uterus appeared cyanosed with ecchymoses seen mainly in
both uterine horns. Signs of placental abruption occurred on placental surface. Approximately 700 ml of blood
clots were evacuated from the uterine cavity after placental extraction. On the basis of uterus’ appearance,
the Couvelaire syndrome was diagnosed. Intravenous
carbetocin and misoprostol per rectum were administered in order to constrict the uterus.
During puerperium patient suffered from anemia,
however it did not require blood transfusion. The delivered male infant weighed 1580 g and the Apgar score
was 3, 3, 6. The pH was 7.17 in the umbilical artery and
7.21 in the umbilical vein. The newborn was admitted to
the Neonatal Intensive Care Unit due to prematurity,
low birth weight and signs of perinatal hypoxia. Furthermore, anemia, neonatal respiratory distress syndrome,
congenital pneumonia and 1st degree intraventricular
haemorrhage were diagnosed. Additional findings were
small hemangiomas. The baby was discharged from the
hospital a month after birth. Currently, the infant is 10
months old, weighs 7700 g, requires regular surgeon
and cardiologist’s care due to the hemangiomas and periodically suffers from respiratory tract infections demanding hospitalization.
Discussion
Placental abruption, being the most common pathological cause of vaginal bleeding in late pregnancy, is a
life-threatening incident complicating 0,4-1% of pregnancies [7, 8]. The ethiopathogenesis is multifactoral and
still a subject of extensive research [7]. The incidence of
this complication is increasing, most likely due to augmentation of risk factors’ prevalence. Risk factors of placental abruption include those of acute etiology, such as
abdominal trauma or drug abuse. Others comprise of
hypertension disorders, especially severe preeclampsia
and eclampsia, polyhydramnios, prolonged rupture of
219
membranes, short umbilical cord, uterine tumors and
anomalies, chorioamnionitis, anemia, renal disorders,
intrapartum fever and prior cesarean delivery. Sociodemographic risk factors enclose maternal age, parity, tobacco use and male infant sex. Also a history of previous
ischemic placental disease, preeclampsia, IUGR or SGA
and placental abruption increase the risk [7, 8, 11-14].
Hypertension in pregnancy appears to be the most frequent pathology concurring with placental abruption.
Particularly a sudden increase of BP may result in acute
placental abruption [14].
Every pregnancy complicated by preeclampsia
should be considered high-risk. Early-onset preeclampsia
(commencing before 34th week of gestation) is more dangerous than late-onset and increases the risk of fetal
death almost 6 times. The risk of perinatal death or severe morbidity in this disorder is 16-fold higher than in
normal pregnancy [15]. What’s interesting, preeclampsia
occurs only in simultaneous presence of the placenta.
There is growing evidence that pathological vasculatory
development in the placental bed that begins early in
pregnancy leads to preeclampsia. These abnormalities
particularly concern remodeling and trophoblast invasion
of the uteroplacental spiral arteries. Altered development lead to lack of arterial dilation resulting in increased resistance in uteroplacental vasculature [16, 17].
Following abnormal deep placentation and hypoperfusion lead to placental insufficiency, a known cause of fetal hypoxia and ischemia. These events finally may result
in a wide range of pathologies – preeclampsia, IUGR,
preterm labor, preterm premature rupture of membranes, spontaneous abortion in late pregnancy and placental abruption [17, 18]. Excessive antiangiogenic and
inflammatory factors release following placental abnormal perfusion affect the function of the endothelium
leading to multi-system response [20]. The organs that
are exceptionally vulnerable to endothelial injury and inflammation are the brain, lungs, kidneys, liver, heart and
vessels [23]. The daily urine protein excretion rising
above or equal 0.3 g is a first sign of glomeruloendotheliosis [26]. There are also data that altered immunologic
response in the HLA system, recalling graft versus host
disease underlie preeclampsia [19]. Likewise, oxidative
stress occurring in ischemic conditions plays a significant role in preeclampsia, as it destroys the structure of
the syncytium [21, 22]. Genetic basis of this pathology,
suggesting the contribution of modifier genes and environmental factors is a subject of intensive research as
well [25].
220
A. Roztocka, M. Ropacka-Lesiak, G.H. Bręborowicz
A patient with preeclampsia should be hospitalized
and considering the often unusual symptoms of preeclampsia, every pregnant women who feels “poorly”
should be screened for this disorder [27]. In preeclamptic patients it is crucial to maintain the correct
blood pressure and avoid aggravation to eclampsia [23].
Magnesium sulfate is the medication of choice to
counteract eclampsia and it is proven to decrease maternal mortality [2, 24]. Moreover, a course of betamethasone for fetal lung maturation should be administered in
every case of early-onset preeclampsia. Both medications were administered to our patient.
It is widely known that delivery leads to recovery
from preeclampsia and eclampsia. Considering the mode
of labor in preeclamptic women, Steegers and colleagues
suggest vaginal birth after 30 weeks of pregnancy, if fetal
and cervical status allows it. However, when the fetus is
growth restricted, cesarean delivery appears to be more
safe [23]. Nassar et al. recommend labor induction for
the patients with severe preeclampsia at $ 34 weeks of
gestation, proving that almost 50% of them successfully
deliver vaginally after induction [28]. Physicians agree
that preeclampsia after 37 weeks of gestation is an unquestioned indication to deliver the fetus. Considering
the onset of preeclampsia prior to 36 weeks of gestation,
the management is still a subject of discussion. Commonly, expectant management with close surveillance is
recommended, unless the disease has severe features.
CTG non stress test, repeated ultrasound and Doppler
velocimetry assessments are the methods of choice to
monitor fetal well-being. Typical Doppler ultrasound
findings are: increased pulsatily index or/and notching in
the uterine arteries and alterations in umbilical artery
flows, such as AEDF and REDF [27].
According to Walker, placental insufficiency leads to
intrauterine growth restriction in 30% of preeclamptic
pregnancies. IUGR is referred as inability of the fetus to
reach its predetermined growth potential, resulting in
a SGA fetus (small for gestational age). Affected fetuses
are at higher risk of fetal, neonatal and perinatal morbidity and mortality [30-32]. Furthermore, the risk of intrauterine death rises 5 to 10-fold [29]. Sometimes poor
fetal growth in early pregnancy is the first symptom preluding preeclampsia. This less frequent form, referred as
early-onset IUGR is associated with preeclampsia and
pathological Doppler uterine artery pattern [33]. Severe
fetal growth restriction, hypertensive disorder and male
fetal sex – all found in our patient are proven to be
significant risk factors of placental abruption [34]. There
is enough research to state that most of the cases are
the consequence of alterations in placental development
resulting in chronic placental pathology [35, 36]. Large
retrospective cohort studies by Rasmussen et al. prove
that women whose first pregnancy was complicated by
IUGR are at higher risk of placental abruption in subsequent pregnancies [40].
Diagnosis of placental abruption is made upon clinical symptoms confirmed by ultrasound evaluation. Unfortunately, often there are no ultrasound findings despite
placental abruption – the sensitivity of USG in diagnosing this pathology is 25-50%, aproximately. However,
a presence of adverse ultrasound findings has a predictive value up to 88% [39]. Typical ultrasound finding is
a retroplacental hematoma. Its visualisation and large
diameter is prognostically unpropitious, likewise the percentage of the surface of placental detachment [37].
Other potential ultrasound findings are: subchorionic
fluid accumulation, echogenic debris in the amniotic
fluid and a so-called Jello sign. Jello sign is diagnosed
when a thickened layer of placenta shimmers as the patient moves during examination [39].
Severe placental abruption, referred as an abruption
concurrent with unstable maternal status and/or nonreassuring CTG tracing, is an indication for immediate
cesarean delivery. Because of the high risk of coagulopathy, blood, platelets, fresh frozen plasma and cryoprecipitate should be present at the operating room. Patients with severe abruption, DIC or hypovolemic shock
are at high risk of multiorgan failure and death. Close
surveillance of the mother and neonate is necessary also
postpartum. Prevention of uterine atony, monitoring
blood pressure, blood loss and laboratory tests are crucial. Uterine atony is managed by oxytocin, prostaglandine analogues and methylergonovine. It is important to
remember that methylergonovine is contraindicated in
preeclampsia as it increases the blood pressure [41].
In our patient, the ultrasound diagnosis of a retroplacental hematoma was confirmed during surgery. What’s
more, during c-section a Couvelaire uterus with blood
that reached the peritoneal cavity was diagnosed. Couvelaire uterus, also described as uteroplacental apoplexy,
is a rare, life threatening condition characterized by
bleeding permeating myometrium, rarely crossing to the
peritoneal cavity or infiltrating broad ligaments and
ovaries [42, 44, 47]. It was first described in 1911 by
French obstetrician, Alexandre Couvelaire. The diagnosis of Couvelaire uterus can only be established on the
basis of biopsy or visual examination during surgery
[42, 43]. Its characteristic appearance is a bluish or
purple colour, mottled by ecchymoses. In such case, the
Preeclamptic pregnancy complicated by huge retroplacental hematoma and Couvelaire uterus
risk of uterine rupture during constriction is very high,
as the myometrium is extremely weak. On the other
hand, the patients with a Couvelaire uterus are at higher
risk of uterine atony and haemorrhage, because the
blood-infiltrated myometrium is less able to contract
[42]. It also has lower susceptibility to pro-contracting
medication. Diagnosing Couvelaire uterus is an indication for aggressive treatment of atony to prevent severe
consequences such as DIC, emergency hysterectomy
and exsanguination. In our patient carbetocin and misoprostol with satisfactory effect was administered. Surgical methods of managing uterine atony and haemorrhage, applied when pharmaceutical methods fail, are uterine vessels ligation, uterine compression sutures, embolization and obstetrical hysterectomy as last resort.
The suture technique particularly recommended and
effective in managing haemorrhages in patients with
hypertensive disorders, placental abruption and Couvelaire uterus is the B-Lynch technique [52]. Hysterectomy
was the management of choice for many decades [44].
Nowadays the recommended treatment is conservative [42].
The etiology of Couvelaire uterus remains unidentified and few available reports link it with placental abruption, placenta previa, preeclampsia, coagulopathy,
amniotic fluid embolism and uterine rupture [42-45, 4748]. It is estimated that Couvelaire uterus develops in
5% of patients with placental abruption [51]. It is important to emphasise that Couvelaire uterus is not always a result of placental abruption. A very recent case
described by Shreedevi and colleagues presents a diagnosis of Couvelaire uterus in the absence of placental
abruption and any other pathologies [49]. A different recent case report describes a Couvelaire uterus that
developed after a dilation and curettage in missed abortion of 13 weeks old pregnancy. The mechanism suggested by authors is iatrogenic perforation of the uterine
wall during curettage, letting the blood infiltrate the
myometrium. Hysterectomy was indispensable [46]. In
the case reported by Gogola et al. the debris and air
bubbles in the uterine veins were concurrent with the
Couvelaire uterus and the authors suggest the bloodpermeated area of uterus to be the “portal” for the debris to reach maternal vessels and cause amniotic fluid
embolism [48]. Avery and Wells retrospectively describe
the ultrasound findings in Couvelaire syndrome confirmed during cesarean section. Those findings are large
retroplacental blood clot and blood dissecting into the
myometrium. They state that ultrasound diagnosis of
Couvelaire uterus is limited, but possible [50].
221
One should be aware that a patient diagnosed with
preeclampsia should control her blood pressure after discharge from the hospital. Sometimes hypertensives are
essential during puerperium. There are also reports that
these patients should avoid non-steroid anti-inflammatory drugs in treating post-cesarean pain. The metaanalysis from 2015 reports that among women who experienced preeclampsia, 20% will develop hypertension
and 16% will have preeclampsia in subsequent pregnancy
[10]. Low doses of ASA [53] and calcium supplementation [2] appear to be useful in prevention of preeclampsia among high-risk patients. What is important,
women with a history of preeclampsia have higher risk
of cardiovascular disorders in the future, most probably
as a result of systemic endothelial dysfunction [3, 54].
There is no scientific data on the recurrence of Couvelaire uterus.
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J
Anna Roztocka
Department of Perinatology and Gynecology
Poznan University of Medical Sciences
Polna 33, 60-535 Poznań, Poland
e-mail: [email protected]