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Article ID: WMC004821
ISSN 2046-1690
Atypical Placement Abruption: Clinical suspicion
and management
Peer review status:
No
Corresponding Author:
Dr. A. Isabel M Fernandez,
Ana Isabel M.Fernandez, Obtetrics & Gynecology Laredo, 39009 - Spain
Submitting Author:
Dr. A. Isabel M Fernandez,
Ana Isabel M.Fernandez, Obtetrics & Gynecology Laredo, 39009 - Spain
Article ID: WMC004821
Article Type: Case Report
Submitted on:28-Jan-2015, 11:15:58 PM GMT
Published on: 29-Jan-2015, 12:27:41 PM GMT
Article URL: http://www.webmedcentral.com/article_view/4821
Subject Categories:OBSTETRICS AND GYNAECOLOGY
Keywords:Placental, abruption, morbidity, pregnancy, metrorrhagia
How to cite the article:Fernandez AM. Atypical Placement Abruption: Clinical suspicion and management.
WebmedCentral OBSTETRICS AND GYNAECOLOGY 2015;6(1):WMC004821
Copyright: This is an open-access article distributed under the terms of the Creative Commons Attribution
License(CC-BY), which permits unrestricted use, distribution, and reproduction in any medium, provided the
original author and source are credited.
Source(s) of Funding:
No funding details. No compensation or any economic funding was received by the authors.
Competing Interests:
Author has not any relevant financial relationships to disclosure in relationship to this article. Nothing to disclose.
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Atypical Placement Abruption: Clinical suspicion
and management
Author(s): Fernandez AM
Abstract
PA is a serious obstetric complication; it is responsible
for an important maternal and perinatal morbidity and
mortality. Its risk factors have been identified but it is
often unpredictable. The classic clinical triad is present
in only a few cases. Suitable obstetric management is
the key to avoid maternal and perinatal unwished
outcomes. It is reported a case of a pregnant woman,
without risk factors except for multiparity, who
submitted a PA with incomplete triad of symptoms and
its decisive management.
Introduction
Placental abruption (PA) is a serious multifactorial
obstetric complication; it occurs in 0.4-1% of
pregnancies, although its real frequency is difficult to
estimate, because it varies depending on the
population studied and diagnostic factors selected. (1,2)
PA refers to bleeding at the decidual-placental
interface that causes partial or total placental
detachment prior to delivery of the fetus. PA gives rise
to considerable maternal and perinatal morbidity and
mortality (clotting disorders, hemorrhagic shock and
rarely death, are the most common maternal
complications) but also rises fetal complications; the
principal cause is prematurity, with its associated
morbidity, but also intrauterine growth restriction and
intrauterine fetal death (2,6). Neonatal morbidity and
mortality rates have fallen over the past few decades
because of improvements in obstetrical management,
the liberal use of cesarean delivery and improved
neonatal care; in fact, perinatal mortality has
decreased from 20% in the 1970s to 9-12% currently. (3,7)
Several risk factors for PA have been identified:
smoking, chronic hypertension, preeclampsia,
pregnancy induced hypertension, a maternal age
above 35 years, multiparity, PROM, polyhydramnios,
previous PA, in vitro fertilization, addictive behavior
(alcohol, cocaine), male-sex fetuses… ( 2 , 5 , 8 )
Identification of these factors is a critical issue;
appropriate monitoring and prevention measures to be
offered to that at-risk population. The presence of
some of them may help to make the diagnosis of PA.
At first, diagnosis is clinical, based on the classic triad
of metrorrhagia in the second and third trimester
associated with abdominal pain and uterine hypertonia;
a non-reassuring fetal status is often associated.
However, PA occurrence is often unpredictable and
asymptomatically; metrorrhagia, pain or hypertonia are
not specific for PA, so diagnosis is then made by the
discovery of fresh or longstanding clots on placental
examination, during hysterotomy. It has been
described the classic form was found in only one-third
of cases (10). Ultrasonography, which is not carried out
systematically, has an excellent specificity (92-96%)
but its sensitivity is low (24%) (2, 11, 12), so it can be
useful when diagnostic is uncertain but only if it does
not delay the patient’s management. Moreover,
histological confirmation is not constant, especially
when PA occurs suddenly because detachment has
been so recent and sudden that clots have not had
time to form (9, 14). The lack of sensitivity of pathological
examinations underlies the importance of clinical
examination for PA diagnosis.
Fetal vitality and maternal condition guide obstetric
management of PA (2) . If the fetus is living, and
emergence caesarean should be performed unless
vaginal delivery is imminent (caesarean section rates
between 74-94%) (7,13) and in case of fetal bradycardia,
extraction by caesarean within 20 min significantly
reduces neonatal mortality and the incidence of
cerebral palsy. In case of intrauterine fetal death,
vaginal delivery is possible with close clinical and
laboratory monitoring.
In developed countries, maternal mortality has
become rare but there is still significant morbidity
linked to the hemorrhagic risk due to hematoma
formation, which is readily associated with
disseminated intravascular coagulation. In these cases,
an early management should be performed, including
an intensive care team. Neonatal mortality in PA is
mainly associated with prematurity. Although up to 26
or 32 weeks, there is no mortality difference whether
PA is present or not, after 26-32 weeks, PA is a risk
factor for neonatal mortality independent of the
gestational age. (2)
Case Report
A 32-year Caucasian woman, gravid 3 para 2, was
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admitted at gestational age of 37 weeks, due to
sudden labor pains which started one hour prior to her
admission; there was no history of bleeding per vagina.
Fetal movements decreased in the last hours. She had
previously normal pregnancies and vaginal births. In
the current pregnancy there were no complications
and baby’s scans were reported to be normal.
On examination: she was not pale, pulse 89/minute,
maternal blood pressure was 142/88 mmHg,
temperature 36.8ºC, bilateral edema of lower limbs but
she denied headache, flickering in front of eyes or
epigastric pain. Uterus was tender and woody hard
with palpable contractions. Its size corresponded to
the period of gestation. It was difficult to hear the fetal
heart by Sonicaide. An ultrasound scan was
performed; it revealed a bradycardic fetus in cephalic
presentation; the placenta was located in the fundus
and in the left anterolateral wall and a doubtful
hypoechogenic image (85 x 55 mm) suggested the
presence of a deciduate placental hematoma.
On speculum examination: there was no bleeding, no
leaking of liquor, cervix was 2 cm dilated with
membranes intact.
Laboratory test results were hemoglobin 12,3 g/dL,
hematocrit 31.1 %, platelets 175 x 109 /mm3 and
parameters of coagulation were normal.
She was catheterized, cross matched and given
intravenous fluid; in view of the above findings,
abruption of placenta was suspected. An emergent
uncomplicated caesarean section under general
anesthesia was performed and a female infant
weighing 2730 g was delivered. The ultrasound
suspicion of PA was confirmed intraoperatively. The
fetal APGAR score was 7 and 9 at the 1st and 5th
minute, respectively and any kind of resuscitation was
necessary. Cord blood pH was 7.26 in the artery.
The postoperative course was uneventful without
coagulation disorders or transfusion. There was a drop
in hemogolobin from 12.3 to 9.8 g/dL. She was
discharged home with her baby on the 5th
postoperative day. The only medication she received
on discharge was iron supplementation. Her postnatal
obstetric and medical appointments revealed no
obvious pathology. Histologial examination confirmed
the diagnosis (placental infarctions and decidual
vasculopathies).
Discussion
PA is serious case of maternal morbidity and fetal
morbidity and mortality. Risk factors that cause PA
include hypertension and preeclampsia, smoking,
WebmedCentral > Case Report
trauma to the abdomen, gestational diabetes mellitus,
preterm labor, age older than 40 years… In this case,
no risk factors had been identified in the present
pregnancy except for multiparity.
The timely attendance to the hospital and timely
admission with suspicion of abrution allowed us to
intervene very early and quickly, thereby preventing
and adverse outcome. In our case, there was no
external bleeding and no maternal compromise; the
only symptom was abdominal pain and the only
clinical sign was a tense and tender abdomen.
Conclusion
The risk factors for PA are clearly identified, but its
occurrence often remains unpredictable and the
classic clinical triad is rarely observed.
Ultrasonography has a limited value to diagnostic PA.
It is very important to educate patients and clinicians
about symptons of abruption. Obstetric management
is guided by fetal and maternal condition, so a
multidisciplinary management (obstetrician,
anesthesiologist, pediatrician, nurses…) can limit
maternal morbidity and mortality, although perinatal
mortality, which occurs essentially in utero, remains
high.
References
1. Tikkanen M.: Etiology, clinical manifestations, and
prediction of placental abruption. Acta Obstet Gynecol
Scand 2010; 89: pp. 732-740
2. Oyelese Y., and Ananth C.V.: Placental Abruption.
Obstet Gynecol 2006; 108: pp. 1005-1016
3. Ananth C.V., and Wilcox A.J.: Placental abruption
and perinatal mortality in the United States. Am J
Epidemiol 2001; 153: pp. 332-337
4. Kåregård M., and Gennser G.: Incidence and
recurrence rate of abruptio placentae in Sweden.
Obstet Gynecol 1986; 67: pp. 523-528
5. Tikkanen M., Riihimäki O., Gissler M., et al:
Decreasing incidence of placental abruption in Finland
during 1980–2005. Acta Obstet Gynecol Scand 2012;
91: pp. 1046-1052
6. Ananth C.V., Berkowitz G.S., Savitz D.A., and
Lapinski R.H.: Placental abruption and adverse
perinatal outcomes. JAMA 1999; 282: pp. 1646-1651
7. Tikkanen M., Luukkaala T., Gissler M., et al:
Decreasing perinatal mortality in placental abruption.
Acta Obstet Gynecol Scand 2013; 92: pp. 298-305
Page 3 of 4
WMC004821
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8. Tikkanen M.: Placental abruption: epidemiology, risk
factors and consequences. Acta Obstet Gynecol
Scand 2011; 90: pp. 140-149
9. Elsasser D.A., Ananth C.V., Prasad V., and
Vintzileos A.M.: Diagnosis of placental abruption:
relationship between clinical and histopathological
findings. Eur J Obstet Gynecol Reprod Biol 2010; 148:
pp. 125-130
10. Hurd W.W., Miodovnik M., Hertzberg V., and Lavin
J.P.: Selective management of abruptio placentae: a
prospective study. Obstet Gynecol 1983; 61: pp.
467-473
11. Glantz C., and Purnell L.: Clinical utility of
sonography in the diagnosis and treatment of
placental abruption. J Ultrasound Med 2002; 21: pp.
837-840
12. Kikutani M., Ishihara K., and Araki T.: Value of
ultrasonography in the diagnosis of placental abruption.
J Nippon Med Sch 2003; 70: pp. 227-233
13. Kayani S.I., Walkinshaw S.A., and Preston C.:
Pregnancy outcome in severe placental abruption.
BJOG 2003; 110: pp. 679-683
14. Elsasser D.A., Ananth C.V., Prasad V., and
Vintzileos A.M.: Diagnosis of placental abruption:
relationship between clinical and histopathological
findings. Eur J Obstet Gynecol Reprod Biol 2010; 148:
pp. 125-130
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