doi:10.1111/j.1447-0756.2007.00567.x J. Obstet. Gynaecol. Res. Vol. 33, No.

4: 557–560, August 2007

B-Lynch suture after the failure of hypogastric artery

ligation to control post-partum hemorrhage due
to placenta increta in a patient with the factor V
Leiden mutation

Asli Somunkiran1, Ismail Ozdemir1, Yavuz Demiraran2 and Oguz Yucel1

Departments of 1Obstetrics and Gynecology and 2Anesthesiology, Duzce University, School of Medicine, Duzce, Turkey

Abstract
Post-partum hemorrhage may be a life-threatening condition. A case of a patient receiving antithrombotic
therapy for the factor V Leiden mutation, in whom post-partum hemorrhage had occurred due to placenta
increta, is described. In this case, the post-partum hemorrhage did not respond to bilateral hypogastric artery
ligation, while the B-Lynch surgical technique was successful in obtaining hemostasis.
Key words: B-Lynch brace suture, factor V Leiden mutation, hypogastric artery ligation, placenta accreta,
post-partum hemorrhage.

Introduction
Post-partum hemorrhage is a serious complication that
often occurs unexpectedly. Major post-partum hemor-
rhages occur in approximately 4% of vaginal and 6% of
cesarean deliveries.1 The most common causes of major
hemorrhage are uterine atony, retained or morbidly
adherent placenta, coagulopathy, uterine rupture, and
uterine inversion. Effective action is required to
prevent major morbidity or mortality. When the con-
servative management of post-partum hemorrhage
fails to control the blood loss, operative interventions,
such as embolization and ligation of the uterine or
internal iliac arteries, are required. However, failure of
uterine arterial embolization and hypogastric artery
ligation have been reported in cases with placenta
accreta.2 We report a case of placenta accreta/increta, in
which post-partum hemorrhage was unresponsive to
hypogastric artery ligation, while the B-Lynch tech-
nique was used successfully. We also review the pub-
lished literature on the B-Lynch technique.
Case
A 32-year-old patient was in her fourth pregnancy. Two
of her previous three pregnancies had ended with
second trimester pregnancy loss and one with first tri-
mester abortion. She had undergone curettage follow-
ing all her previous pregnancies. While she was being
evaluated for recurrent pregnancy loss, the factor V
Leiden mutation was diagnosed. In order to prevent
miscarriage and other complications related to the
factor V Leiden mutation, low-molecular-weight
heparin (Tinzaparin sodium 10 000 IU; Innohep, Abdi
Ibrahim, Istanbul, Turkey) was started immediately
after she became pregnant, during her current preg-
nancy. Her current pregnancy was uneventful, with
daily injections of Tinzaparin sodium 10 000 IU. She
was admitted to hospital at 36 weeks’ gestation with
spontaneous rupture of the membranes. Vaginal
examination on admission revealed a 4-cm dilated,
80% effaced cervix and breech presentation. A provi-
sional ultrasound examination confirmed the breech

Received: August 29 2006.

Accepted: November 23 2006.
Reprint request to: Assistant Professor Asli Somunkiran, Duzce University, School of Medicine, Department of Obstetrics and
Gynecology, 81620 Konuralp, Duzce, Turkey. Email: aslisomunkiran@yahoo.com

© 2007 The Authors 557

Journal compilation © 2007 Japan Society of Obstetrics and Gynecology
A. Somunkiran et al.
presentation; the estimated fetal weight was 2750 g.
Considering her poor pregnancy outcomes and the
breech presentation of the foetus, cesarean section was
planned. Her last Tinzaparin sodium injection was
2 hours before surgery.
A lower segment cesarean section was performed
under general anesthesia. Following the induction of
anesthesia with propofol (2 mg/kg, iv), rocuronium
bromide 0.6 mg/kg was intravenously administered to
facilitate tracheal intubation. Desflurane (6–8%) with
50% oxygen in 50% nitrous oxide was used to maintain
anesthesia. After delivering the infant, fentanyl
(1 mg/kg iv) was administered. Immediately after
delivering a 2700-g girl with an Apgar score of 8, 10 IU
oxytocin and 1 g cephazolin sodium were infused
intravenously. The placenta was implanted on the
anterior uterine wall, and attempts to remove it using
controlled cord traction were unsuccessful. Digital
exploration confirmed a degree of morbid adherence
to the underlying myometrium, but not penetration
through the myometrium, indicating placenta increta.
We administered 20 IU of oxytocin in 1000 mL normal
saline intravenously. The uterus was exteriorized and,
with difficulty, the placental tissue was removed manu-
ally as far as possible. The remaining placental tissue
triggered uterine relaxation and post-partum hemor-
rhage, which did not respond to oxytocin infusion and
uterine massage. Metilergometrin injection was not
considered because the patient also had mild pre-
eclampsia (blood pressure 140/90 mmHg, proteinuria
800 mg/day). At the 20th minute of the operation, the
estimated blood loss was 2750 mL, and control hemo-
globin and hematocrit values were 8.33 g/dL and
23.2%, respectively. Two units of suspended erythro-
cytes and two units of fresh frozen plasma were trans-
fused intraoperatively. Bilateral hypogastric artery
ligation was performed, but the procedure failed to
control the hemorrhage. There was profuse bleeding
from the placental bed on the anterior uterine wall.
Over-sewing the implantation site with 0-chromic
sutures did not provide hemostasis. A B-Lynch com-
pression suture was placed with Chromic catgut no. 2.
In the meantime, the patient was given an infusion of
125 mg of methylprednisolone, 1000 mL of succiny-
lated gelatine plasma expander (Gelofusine, Biofarma
Ilac, Istanbul, Turkey), and 3000 mL of normal saline,
in addition to blood and oxytocin. After the B-Lynch
suture, the bleeding was controlled, the cesarean inci-
sion was sutured, and the operation was completed.
The patient was admitted to the intensive care unit
(ICU) postoperatively, and five units of fresh whole
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blood and two units of fresh frozen plasma were trans-
fused in the ICU. She was discharged from the ICU the
next day with hemoglobin of 11.3 g/dL, hematocrit of
31.4%, 185 ¥ 103/mm3 platelets, prothrombin time 13.6,
activated partial thromboplastin time 4.7, and interna-
tional normalized ratio 1.12. After an uneventful recov-
ery, the patient was discharged from the hospital 7 days
postoperatively.
Discussion
Factor V Leiden is a common genetic mutation that
predisposes its carriers to venous thromboembolism. It
is reported in 5% of the healthy white population3 and
3% of low-risk obstetric patients.4 When combined with
the hypercoagulable state that characterizes pregnancy,
there is an increased risk of severe, recurrent preg-
nancy complications. Factor V Leiden is the most
common cause of primary and recurrent venous
thromboembolism in pregnancy. It has consistently
been shown to increase the risk of early onset gesta-
tional hypertension and HELLP syndrome in preg-
nancy. Maternal carriage of factor V Leiden is also
associated with severe placental abruption, fetal
growth disturbances, and stillbirth.5,6 It is not known
whether prophylactic treatment of asymptomatic car-
riers improves the outcome, although some observa-
tional studies have suggested a benefit.7 In addition, no
randomised prospective studies have examined the
efficacy of antithrombotic therapy in women with
previous obstetric complications. Vossen et al.8 in-
vestigated the relationship between inherited throm-
bophilia and fetal loss, and the influence of
thromboprophylaxis on pregnancy outcome in a pro-
spective study. They reported that prophylaxis with
low-molecular-weight heparin had no clear benefit
with respect to the risk of fetal loss. In our case, low-
molecular-weight heparin was started because of the
patient’s history of second trimester pregnancy losses.
Unlike her previous pregnancies, her current preg-
nancy was uneventful with regard to prophylaxis,
except for mild pre-eclampsia.
An abnormally adherent placenta, although an
uncommon condition, is one of the main causes of
post-partum hemorrhage, and has considerable signifi-
cance clinically, because of the morbidity and occa-
sional mortality from severe hemorrhage, uterine
perforation, and infection.9 Risk factors for abnormal
placental adherence include implantation in the lower
uterine segment over a previous cesarean section scar
or other previous uterine incisions, or after uterine
© 2007 The Authors

curettage. Nearly one fourth of women with placenta
accreta have a history of previous curettage.9 Our case
had three previous curettages because of recurrent mis-
carriages, due to the factor V Leiden mutation, which
was a possible cause of the placenta increta. Successful
treatment depends on immediate blood replacement
therapy and nearly always prompts hysterectomy.
Alternative treatment modalities include uterine or
internal iliac artery ligation or angiographic emboliza-
tion. The use of argon beam coagulation for hemostasis
in the lower uterine segment has also been reported.10
Nevertheless, the failure of conservative treatments,
uterine arterial embolization, and hypogastric artery
ligation has been reported in cases with placenta
accreta.2,11–13
B-Lynch et al.14 introduced the B-Lynch suturing
technique (brace suture) in 1997, with five successful
cases. This surgical technique is useful for controlling
massive post-partum hemorrhage because of its sim-
plicity of application, life-saving potential, relative
safety, and its capacity for preserving the uterus and
fertility. Satisfactory hemostasis can be assessed imme-
diately after application.14 Unlike hypogastric artery
ligation, which requires a relatively high degree of
skill, this procedure is relatively simple, and gynecolo-
gists, generally, could easily learn this life-saving
procedure from the illustrations and video that are
available at the website of Dr Christopher B-Lynch.15 As
far as we could determine, 60 successful cases have
been reported to date, including the series of B-Lynch
et al.16–20 one failure was reported in a case where a
patient had undergone hysterectomy.21 In a very recent
case, uterine necrosis, following its application for
primary post-partum hemorrhage, was reported.22
The technique has been used for bleeding that was
unresponsive to vascular ligation in three patients.19,23
Of these, O’Leary uterine artery ligation and utero-
ovarian branch ligations were unsuccessful in control-
ling the hemorrhage in one case.23 In the series of
Holtsema et al.19 it was performed in one patient
because adequate hemostasis could not be achieved,
despite bilateral internal iliac artery ligation, and in
another patient for bleeding that was unresponsive to
bilateral uterine artery ligation. In our case, we used
the brace suture because the bleeding from the placen-
tal bed could not be controlled with bilateral hypogas-
tric artery ligation. The brace technique was reported to
be successful in a patient with placenta accreta; in this
case, the B-Lynch suture was the first-line treatment.17 It
was also applied successfully with an intrauterine
balloon catheter for massive hemorrhage, due to pla-
© 2007 The Authors
Journal compilation © 2007 Japan Society of Obstetrics and Gynecology
B-Lynch suture in placenta increta
centa accreta, following a second-trimester miscar-
riage.20 Therefore, it may be helpful to consider the
B-Lynch technique before artery ligation in cases of
abnormal placental adherence.
It is possible to diagnose placenta increta antepar-
tum. Cox et al.24 hypothesized that the absence of a
subplacental sonolucent area was consistent with the
presence of a placenta increta. They were able to iden-
tify placenta increta ultrasonically from the lack of the
usual subplacental sonolucent space in a case with pla-
centa previa. Pasto et al.25 confirmed that the absence of
a subplacental sonolucent or hypoechoic retroplacental
zone was consistent with placenta increta. Magnetic
resonance imaging has also been used to diagnose pla-
centa accreta.26 Given that there is a possibility for
antepartum diagnosis, further methods could be used
to diagnose this life-threatening condition in patients
who are at increased risk (previous cesarean section,
curettage) for abnormal placental adherence. Thus,
these patients could be advised to give birth in tertiary
care hospitals, where they could be treated adequately
in case of post-partum hemorrhage.
In conclusion, care must be taken while giving low-
molecular-weight heparin to patients with the factor V
Leiden mutation, because these patients are already
candidates for post-partum hemorrhage due to prob-
able abnormal placental adherence caused by recurrent
curettages. In cases of abnormal placental adherence,
the B-Lynch suture may be considered before artery
ligation.
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