Uterine Atony: Definition, Prevention,

Nonsurgical Management, and Uterine Tamponade

Fionnuala Breathnach, MD, MRCOG, MRCPI,* and Michael Geary, MD, MRCOG, FRCPI
Uterine atony, or failure of the uterus to contract following delivery, is the most common
cause of postpartum hemorrhage. This review serves to examine the prevention and
treatment of uterine atony, including risk-factor recognition and active management of the
third stage of labor. A range of uterotonic agents will be compared for efficacy, safety, and
ease of administration. Oxytocin and ergot alkaloids represent the cornerstone of uterotonic therapy, while prostaglandin therapy has been studied more recently as an attractive
alternative, particularly for resource-poor settings. Newer supplementary medical therapies, such as recombinant factor VII and hemostatic agents, and adjunctive nonsurgical
methods aimed at achieving uterine tamponade will be evaluated.
Semin Perinatol 33:82-87 Published by Elsevier Inc.
KEYWORDS uterine atony, oxytocic therapy, postpartum hemorrhage

critical step in the physiological prevention of postpartum hemorrhage is the simultaneous contraction and
retraction of myometrial fibers during and after the third
stage of labor. Resultant compression of the uterine vasculature serves to halt the 800 mL/min blood flow in the placental
bed. Despite the presence of effective medical interventions,
uterine atony today still claims thousands of maternal lives
and represents the most prevalent cause of postpartum hemorrhage. In the developing world, lack of access to uterotonic
therapies that have been available for almost a century represents a glaring disparity in global health today.

Definition
Uterine atony is defined as failure of the uterus to contract
adequately following delivery.1 Recognition of a soft, boggy
uterus in the setting of excessive postpartum bleeding can
alert the attendant to atony and should trigger a series of
interventions aimed at achieving tonic sustained uterine contraction that is maintained through the immediate postpartum period.

*Division of Maternal Fetal Medicine, Columbia University Medical Center,

New York, NY.
Department of Obstetrics and Gynecology, Rotunda Hospital, Dublin,
Ireland.
Address reprint requests to Fionnuala Breathnach, MD, MRCOG,
MRCPI, Division of Maternal Fetal Medicine, Columbia University,
Medical Center, 622 W 168th Street, New York, NY 10708. E-mail:
fmb2108@columbia.edu

82

0146-0005/09/$-see front matter Published by Elsevier Inc.

doi:10.1053/j.semperi.2008.12.001

Risk Factors
Astute risk assessment is crucial in identifying women at
increased risk of uterine atony, thereby allowing for preventive measures to be instituted and for delivery to take place
where transfusion and anesthetic facilities are available. The
established risk factors associated with uterine atony are outlined in Table 1. It is worth noting that multiparity, hitherto
believed to be a significant risk factor,2,3 has not been confirmed as having an association with uterine atony in recent
studies.4-6 Previous postpartum hemorrhage confers a 2- to
4-fold increased risk of hemorrhage compared to women
without such a history.6,7 Recommended prophylactic measures include appropriate hospital registration for women at
risk, active management of the third stage of labor, intravenous access during labor, and ensuring the availability of
cross-matched blood. However, up to 26% of patients in 1
study who underwent hysterectomy for hemorrhage had no
identifiable risk factors.8 Therefore, the unpredictability of
uterine atony in many cases underpins the need for strict
protocols for the management of postpartum hemorrhage to
be in place in every unit that provides obstetric care.

Active Management
of Third Stage of Labor
The 3 key components of the active management of the third
stage of labor are use of a prophylactic uterotonic agent, early
clamping of the umbilical cord, and controlled cord traction.

Uterine atony
Table 1 Risk Factors for Uterine Atony
Factors associated with uterine overdistension
Multiple pregnancy
Polyhydramnios
Fetal macrosomia
Labor-related factors
Induction of labor
Prolonged labor
Precipitate labor
Oxytocin augmentation
Manual removal of placenta
Use of uterine relaxants
Deep anesthesia (especially halogenated anesthetic
agents)
Magnesium sulfate
Intrinsic factors
Previous postpartum hemorrhage
Antepartum hemorrhage (placental abruption or previa)
Obesity
Age > 35 years
Adapted from Breathnach F, Geary M: in A Textbook on Postpartum
Hemorrhage. B-Lynch C, Louis K (eds): Sapiens Publishing,
2004.

Oxytocin, given as a 10 U bolus (either intravenous or intramuscular), is the first-line uterotonic for this purpose in most
settings. The prophylactic use of oxytocin in the third stage of
labor is the subject of a Cochrane review9 that compared
oxytocin alone to no uterotonic and to ergot alkaloids. This
review identified prophylactic oxytocin use (by either the
intravenous or the intramuscular route) as being associated
with a reduced risk of hemorrhage (relative risk (RR) 0.5;
95% confidence interval (CI) 0.43-0.59) and a reduced need
for therapeutic-dose uterotonics (RR 0.5; 95% CI 0.39-0.64)
when compared to no uterotonic use. In terms of efficacy,
little difference was demonstrated between oxytocin and ergot alkaloid use for active management of the third stage of
labor. However, ergometrine was associated with more manual removal of the placenta (RR 0.57; 95% CI 0.41-0.79) and
a statistically insignificant tendency toward hypertension (RR
0.53; 95% CI 0.19-1.58).

Oxytocin for
Treatment of Uterine Atony
A well-recognized initial reflex intervention in the setting of
uterine atony involves stimulation of uterine contraction,
usually achieved with bimanual uterine massage and the injection of oxytocin (either intramuscularly or intravenously),
with or without ergometrine. The mode of action of oxytocin
involves stimulation of the upper uterine segment to contract
in a rhythmic fashion. Owing to its short plasma half-life
(mean, 3 minutes), a continuous intravenous infusion is required to maintain the uterus in a contracted state.10 The
usual dose is 20 IU in 500 mL of crystalloid solution, with the
dosage rate adjusted according to response (typical infusion
rate 250 mL/h). When administered intravenously, the onset
of action is almost instantaneous and plateau concentration is

83
achieved after 30 minutes. By contrast, intramuscular administration results in a slower onset of action (3 minutes-7 minutes) but a longer lasting clinical effect (up to 60 minutes).
Metabolism of oxytocin is via the renal and hepatic routes.
Its antidiuretic effect can result in water toxicity if given in
large volumes of electrolyte-free solutions. Furthermore,
rapid intravenous bolus administration of undiluted oxytocin results in relaxation of vascular smooth muscle, which
can lead to hypotension.11 For therapeutic use, therefore,
where repeated doses may be necessary, it is best given intramuscularly or by dilute intravenous infusion.
Oxytocin is stable at temperatures up to 25C but refrigeration may prolong its shelf-life. A disadvantage of oxytocin
is its short half-life. The long-acting oxytocin analog carbetocin has been studied in this context as its more sustained
action, similar to that of ergometrine but without its associated side effects, may offer advantages over standard oxytocic
therapy.12 Comparative studies of intramuscular carbetocin
and intravenous infusion of oxytocin for the prevention of
postpartum hemorrhage have identified enhanced effectiveness (ie, a longer duration of activity) of the synthetic analog.13,14

Ergot Derivatives
(Ergometrine/Methylergonovine)
In contrast to oxytocin, the administration of methylergonovine (or its parent compound ergometrine) results in a sustained tonic uterine contraction via stimulation of myometrial -adrenergic receptors. Both upper and lower uterine
segments are thus stimulated to contract in a tetanic manner.10 Intramuscular injection of the standard 0.25 mg dose
of ergometrine (or 0.2 mg methylergonovine) acts within 2
minutes-5 minutes. Metabolism is via the hepatic route and
the mean plasma half-life is 30 minutes. Nonetheless, the
clinical effect of ergometrine persists for approximately 3
hours. Common side effects include nausea, vomiting, and
dizziness and these are more striking when given via the
intravenous route. Because of its vasoconstrictive effect via
stimulation of -adrenergic receptors, hypertension can occur. Contraindications to the use of ergot alkaloids therefore
include hypertension (including pre-eclampsia), heart disease, and peripheral vascular disease. If given intravenously,
where its effect is seen as being almost immediate, it should
be given over 60 seconds with careful monitoring of pulse
and blood pressure. Relevant to the developing world in particular is its heat lability. It is both heat- and light-sensitive
and should be stored at temperatures below 8C and away
from light.
Recommended first-line treatment of uterine atony, therefore, involves administration of oxytocin or an ergot alkaloid
as an intramuscular bolus, followed by repeat dosage of either of these agents if no effect is observed after 5 minutes
(Table 2). Bolus uterotonic therapy should be complemented
by continuous intravenous oxytocin infusion. Atony that is
refractory to these first-line uterotonics will warrant prostaglandin therapy.

F. Breathnach and M. Geary

84
Table 2 Medical Uterotonic Therapies
Agent

Dose

Cautions

Oxytocin (Pitocin,
Syntocinon)

10 IUs IM/IV followed by IV infusion of 20 IUs in 500 mL Hypotension if given by rapid IV bolus
crystalloid titrated versus response (eg, 250 mL/h)
Water intoxication with large
volumes
Contraindicated in hypertensive
Ergometrine (Ergonovine) 0.25 mg IM (ergometrine)
patients Can cause
0.20 mg IM (methergonovine)
Methergonovine
nausea/vomiting/dizziness
Can be repeated every 5 min to maximum of 5 doses
(Methergine)
Carboprost (15-methyl0.25 mg IM/intramyometrial. Can be repeated every 15
Bronchospasm (caution in patients
PGF2) (Hemabate)
min. Max. 2 mg.
with asthma, hypertension,
cardiorespiratory disease)
Dinoprostone (Prostin/
2 mg p.(r) 2-hourly
Hypotension
Prepidil)
Gemeprost (Cervagem)
1-2 mg intrauterine placement/1 mg p.r.
Gastrointestinal disturbance
Misoprostol (Cytotec)
600 g-1000 g p.(r)/intracavitary
Gastrointestinal disturbance,
shivering, pyrexia
Tranexamic acid
1g 8-hourly IV
Can increase risk of thrombosis
(Cyclokapron)
RFVIIa (novo Seven)
60-120 g/kg IV
Fever, hypertension
Adapted from Breathnach F, Geary M: in A Textbook on Postpartum Hemorrhage. B-Lynch C, Louis K (eds): Sapiens Publishing, 2004.

Carboprost
Carboprost (15-methyl PGF2) acts as a smooth muscle stimulant and is a second-line agent for use in the management
of postpartum uterine atony unresponsive to oxytocin/
ergometrine. It is an analog of PGF2 (dinoprost) with a
longer duration of action than its parent compound. Available in single-dose vials of 0.25 mg, it may be administered
by deep intramuscular injection or, alternatively, by direct
intramyometrial injection. The latter route of administration
is achieved either under direct vision at Cesarean section or
transabdominally or transvaginally following vaginal delivery
and has the advantage of a significantly quicker onset of
action.15,16 Peripheral intramuscular injection yields peak
plasma concentrations at 15 minutes in contrast to less than
5 minutes for the intramyometrial route. Using a 20-gauge
spinal needle, intravascular injection can be avoided by preinjection aspiration, and intramyometrial rather than intracavitary placement of the needle can be confirmed by observing resistance on injection, as described by Bigrigg and
colleagues.17 The dose may be repeated every 15 minutes up
to a maximum cumulative dose of 2 mg (8 doses).
The largest case series to date16 involved a multicenter
surveillance study of 237 cases of postpartum hemorrhage
refractory to standard uterotonics and reported an efficacy of
88%. Most women in this study required a single dose only.
Owing to its vasoconstrictive and bronchoconstrictive effects, carboprost can result in nausea, vomiting, diarrhea,
pyrexia, and bronchospasm. Contraindications therefore include cardiac and pulmonary disease. The cost and light- and
heat-sensitivity of carboprost render it unsuitable for consideration in low-resource settings.

tors. It may be given orally, sublingually, vaginally, rectally,

or via direct intrauterine placement and undergoes hepatic
metabolism. The rectal route of administration is associated
with a slower onset of action, lower peak levels, and a more
favorable side-effect profile when compared with the oral or
sublingual route. The results of an international multicenter,
randomized trial of oral misoprostol as a prophylactic agent
for the third stage of labor showed it to be less effective at
preventing postpartum hemorrhage than parenteral oxytocin.18 This observation may result from its longer onset of
action (20-30 minutes to achieve peak serum levels compared to 3 minutes for oxytocin). Misoprostol may, therefore,
be a more suitable agent for protracted uterine bleeding,
rather than as a prophylactic uterotonic agent.
The use of rectal misoprostol for the treatment of postpartum hemorrhage unresponsive to oxytocin and ergometrine
was first reported by OBrien and colleagues.19 A Cochrane
review has studied the performance of misoprostol compared
to standard oxytocic therapy and suggests that rectal misoprostol in a dose of 800 g could be a useful first-line drug
for the treatment of primary postpartum hemorrhage.20 As an
alternative to the aforementioned uterotonics, misoprostol
has the significant advantage of low cost, thermostability,
light stability, and lack of requirement for sterile needles and
syringes for administration, making it an attractive option for
use in the developing world. It has a shelf-life of several years.
Side effects of misoprostol are mainly gastrointestinal and are
dose-dependent. A frequently reported side effect of misoprostol is the occurrence of shivering and pyrexia. Side effects
are less marked when the rectal route of administration is
used.

Misoprostol

Other Prostaglandins
(Dinoprostone and Gemeprost)

Misoprostol is a synthetic analog of prostaglandin E1, which

selectively binds to myometrial EP-2/EP-3 prostanoid recep-

Dinoprostone (prostaglandin E2), despite its vasodilatory

properties, causes smooth muscle contraction in the preg-

Uterine atony

85

Figure 1 Lynch suture (A) anterior and and (B) posterior views of the uterus demonstrating the B-Lynch brace suture.
(C) Anatomical appearance after uterine closure. (Adapted from http://www.cblynch.com/HTML/bjog1.html). (Color
version of figure is available online.)

nant uterus, thus making it a potentially suitable uterotonic

agent. Its principal indication is in preinduction cervical
priming, but intrauterine placement of dinoprostone has been
successfully employed as a treatment for uterine atony.21 The
vasodilatory effect of dinoprostone, however, renders it unsuitable for use in the hypotensive or hypovolemic patient. It
may, however, be of use in women with cardiorespiratory
disease in whom carboprost is contraindicated.
Experience with gemeprost, a prostaglandin E1 analog, in
pessary formulation delivered directly into the uterine cavity
or placed in the posterior vaginal fornix, has been reported,
but its use in this setting is largely anecdotal.22,23 Its mode of
action resembles that of PGF2. Rectal administration has also
been reported.24

Hemostatics: Tranexamic
Acid and Recombinant Factor VII
The antifibrinolytic agent tranexamic acid, which prevents
binding of plasminogen and plasmin to fibrin, may have a
role in the control of intractable postpartum hemorrhage,
particularly where coagulation is compromised. However, to
date there is only 1 case report in the literature of the use of
this agent in the setting of postpartum hemorrhage; that particular case involved a placenta accreta where the source of
the persistent bleeding was the lower uterine segment and the
uterine body was described as being well contracted.25 The
dose employed was 1 g given intravenously every 4 hours to
a cumulative dose of 3 g.
The use of recombinant activated factor VII (rFVIIa) as a
hemostatic agent for refractory postpartum hemorrhage is
the subject of a northern European registry, which has re-

ported on a cumulative experience of 113 cases,26 80% of

whom were noted to have an improvement in hemorrhage
parameters after a single dose, with few reported side effects.
The mode of action of this agent involves enhancement of the
rate of thrombin generation, leading to formation of a fully
stabilized fibrin plug that is resistant to premature lysis.
Doses of 60-120 g/kg intravenously have been used. Adverse effects are reported predominantly from studies of rFVIIa use in patients with hemophilia and range from minor
complaints, such as headache and skin hypersensitivity, to
thrombosis. Deep-vein thrombosis, pulmonary embolism,
peripheral arterial thrombosis, and myocardial infarction
have all been described.27-29 Importantly, there is no current
information on safety in pregnancy and there are only limited
data from nonhemophiliac patients. Furthermore, the cost of
rFVIIa is considered prohibitive where resources are limited.
The comparative properties of all uterotonic agents discussed are outlined in Table 2.

Uterine Tamponade
The placement of uterine compression sutures to control
postpartum hemorrhage secondary to uterine atony has in
recent years been used as an adjunctive intervention aimed at
maintaining uterine contractility through tamponade. This
technique was first described by Christopher B-Lynch
(Fig. 1),30 and modified techniques have evolved in the
interim.31,32 B-Lynch suture placement can be easily
achieved at the time of Cesarean delivery, or if laparotomy is
required after vaginal delivery. Proponents of this brace suture recommend a test of bimanual compression once the
uterus is exteriorized, as a means of determining that the

86
suture should be effective if bimanual compression is successful at arresting the bleeding. In the setting of a vaginal
delivery, the B-Lynch suture requires a hysterotomy incision.
The rationale for hysterotomy in this case is 2-fold: first to
allow for exploration of the cavity with evacuation of placental fragments or clots, and furthermore, hysterotomy allows
for correct placement of the brace suture avoiding obliteration of the cavity. The latter complication has been associated
with blind modifications of the suture, such as those proposed by Hayman and coworkers31 and Cho and coworkers.32
Reported efficacy of the uterine brace suture is high. In a
review of 36 reported cases of women with severe postpartum hemorrhage treated with the B-Lynch suture, only 2
failed procedures were identified.30 B-Lynch reports on 7
failures in the literature,20,33 all of which involved either morbid placental adherence or disseminated intravascular coagulopathy. Safety concerns center on the potential for uterine
necrosis34,35; however, this complication is rare and is minimized by careful placement of the suture with direct visualization through a hysterotomy incision and with persistent,
even compression on the uterus, exerted by the operators
assistant, throughout the procedure of suture placement.
Balloon tamponade represents a further adjunctive strategy for achieving hemostasis in the setting of intractable hemorrhage unresponsive to conventional uterotonic therapy.
The commonly employed devices for this purpose are the
Rusch catheter,36 the Sengstaken-Blakemore37 (C.R. Bard,
Inc, Covington, GA) tube, and the Bakri catheter38 (Cook
Medical, Inc, Bloomington, IN). The Bakri catheter has the
advantage of a drainage port that allows for monitoring of
ongoing blood loss. Balloon tamponade is particularly effective where hemorrhage is attributed to atony,39 although also
advocated as a means of controlling lower segment bleeding
associated with placenta previa.38 In either event, concomitant use of uterotonic therapy is recommended as a means of
maximizing the tamponade effect of the balloon. When balloon tamponade is used in combination with a brace suture,
a sandwich effect is achieved.40,41 This combined maneuver
should be considered for synergistic benefit where 1 tamponade procedure does not confer optimal effect.

Conclusions
A stepwise approach to achieving effective uterine contractility is integral to any protocol on management of postpartum
hemorrhage. Such protocols should be established, disseminated, and regularly updated in every setting where obstetric
care is provided. Selection of appropriate uterotonic use must
take into account the resources available, safety profile of
these agents, and the fact that the combination of uterotonic
agents discussed here, with or without uterine tamponade, is
likely to work synergistically.

References
1. Cunningham FG, Leveno KJ, Bloom SL: Obstetrical hemorrhage, in
Cunningham FG, Leveno KJ, Bloom SL, et al (eds): Williams Obstetrics.
New York, McGraw-Hill, 2005, pp 809-854

F. Breathnach and M. Geary

2. Fuchs K, Peretz BA, Marcovici R, et al: The grand multipara: Is it a
problem? A review of 5785 cases. Int J Gynecol Obstet 23:321, 1985
3. Babinski A, Kerenyi T, Torok O, et al: Perinatal outcome in grand and
great-grand multiparity: Effects of parity on obstetric risk factors. Am J
Obstet Gynecol 181:669, 1999
4. Stones R, Paterson C, Saunders N: Risk factors for major obstetric
haemorrhage. Eur J Obstet Gynecol Reprod Biol 48:15-18, 1993
5. Tsu V: Postpartum hemorrhage in Zimbabwe: A risk factor analysis. Br J
Obstet Gynaecol 100:327-333, 1993
6. Waterstone M, Bewley S, Wolfe C: Incidence and predictors of severe
obstetric morbidity: Case control study. Br Med J 322:1089-1094,
2001
7. Hall MH, Halliwell R, Carr-Hill R: Concomitant and repeated happenings of complications of the third stage of labor. Br J Obstet Gynaecol
92:732-738, 1985
8. Clark SL, Yeh SY, Phelan JP, et al: Emergency hysterectomy for obstetric
hemorrhage. Obstet Gynecol 64:376-380, 1984
9. Elbourne DR, Prediville WJ, Carrolli G, et al: Prophylactic use of oxytocin in the third stage of labour. Cochrane Database Syst Rev 4:CD,
001808, 2001
10. Dollery C (ed): Therapeutic Drugs (ed 2). Edinburgh, Churchill Livingstone, 1999
11. Parker SL, Schimmer BP: Pituitary hormones and their hypothalamic
releasing hormones, in Gilman GA (ed): The Pharmacological Basis of
Therapeutics (ed 11). New York, NY, McGraw-Hill, 2006, pp 14891510
12. Hunter DJ, Schulz P, Wassenaar W: Effect of carbetocein, a long-acting
oxytocin analog on the postpartum uterus. Clin Pharmacol Ther 52:6070, 1992
13. Boucher M, Nimrod CA, Tawagi GF, et al: Comparison of carbetocin
and oxytocin for the prevention of postpartum hemorrhage following
vaginal delivery: A double-blind randomized trial. J Obstet Gynaecol
Can 26:481-488, 2004
14. Dansereau J, Joshi AK, Helewa ME, et al: Double-blind comparison of
cabetocin versus oxytocin in prevention of uterine atony after Cesarian
section. Am J Obstet Gynecol 180:670-676, 1999
15. Jacobs M, Arias F: Intramyometrial PGF in treatment of severe postpartum hemorrhage. Obstet Gynecol 55:665-666, 1980
16. Oleen MA, Mariano JP: Controlling refractory postpartum hemorrhage
with Hemabate sterile solution. Am J Obstet Gynecol 162:205-208,
1990
17. Bigrigg A, Chui D, Chissell S, et al: Use of intramyometrial 15-methyl
prostaglandin F2 to control atonic postpartum hemorrhage following
vaginal delivery and failure of conventional therapy. Br J Obstet Gynaecol 98:734-736, 1991
18. Gulmezoglu AM, Villar J, Ngoc NT, et al: WHO multicentre randomized trial of misoprostol in the management of the third stage of labor.
Lancet 358:689-695, 2001
19. OBrien P, El-Refaey H, Geary M, et al: Rectally administered misoprostol for the treatment of postpartum hemorrhage unresponsive to oxytocin and ergometrine: A descriptive study. Obstet Gynecol 92:212214, 1998
20. Mousa HA, Alfirevic Z: Treatment for primary postpartum hemorrhage.
Cochrane Database Syst Rev 1 CD:003249, 2003
21. Peyser MR, Kupferminc MJ: Management of severe postpartum hemorrhage by intrauterine irrigation with prostaglandin E2. Am J Obstet
Gynecol 162:694-696, 1990
22. Barrington JW, Roberts A: The use of gemeprost pessaries to arrest
postpartum hemorrhage. Br J Obstet Gynaecol 100:691-692, 1993
23. El-Lakany N, Harlow RA: The use of gemeprost pessaries to arrest
postpartum hemorrhage. Br J Obstet Gynaecol 101:277-278, 1994
24. Craig S, Chai H, Cho H: Treatment of severe postpartum hemorrhage
by rectally administered gemeprost pessaries. J J Perinat Med 27:231235, 1999
25. As AK, Hagen P, Webb JB: Tranexamic acid in the management of
postpartum hemorrhage. Br J Obstet Gynaecol 103:1250, 1996
26. Alfirevic Z, Elbourne DR, Pavord S: Use of recombinant activated factor
VII in primary postpartum hemorrhage: The Northern European registry 2000-2004. Obstet Gynecol 110(6):1270-1278, 2007

Uterine atony
27. Aledort L: RFVIIa: Its thrombogenicity. Thromb Haemost 84:522-523,
2000
28. Peerlinck K, Vermylen J: Acute myocardial infarction following administration of recombinant activated factor VII (novo seven) in a patient with
hemophilia A and inhibitor. Thromb Haemost 82:1775-1776, 1999
29. Roberts H: Clinical experience with activated factor VII: Focus on safety
aspects. Blood Coagul Fibrinolysis 9:S115-S118, 1998
30. B-Lynch C, Coker A, Lawal AH, et al: The B-Lynch surgical technique
for the control of massive postpartum hemorrhage: An alternative to
hysterectomy? Five cases reported. Br J Obstet Gynaecol 104:372-375,
1997
31. Hayman R, Arulkumaran S, Steer P: Uterine compression sutures: Surgical management of postpartum hemorrhage. Obstet Gynecol 99:502506, 2002
32. Cho J, Jun H, Lee C: Hemostatic suturing technique for uterine bleeding during Cesarean delivery. Obstet Gynecol 96:129-131, 2000
33. B-Lynch C: B-Lynch Brace suture (Tech Details). 2003 [updated 2003
Sept 25, 2003; cited]. Available from: http://www.cblynch.com/HTML/
technique.html
34. Treloar EJ, Anderson RS, Andrews HS, et al: Uterine necrosis following
B-Lynch suture for primary postpartum hemorrhage. Br J Obstet
Gynaecol 113:486-488, 2006

87
35. Joshi VM, Shrivastava M: Partial ischemic necrosis of the uterus following a uterine brace compression suture. Br J Obstet Gynaecol 111(3):
279-280, 2004
36. Johanson R, Kumar M, Obhrai M, Young P: Management of massive
postpartum hemorrhage: Use of a hydrostatic balloon catheter to avoid
laparotomy. Br J Obstet Gynaecol 108:420-422, 2001
37. Seror J, Allouche C, Elhaik S: Use of Sengstaken-Blakemore tube in
massive postpartum hemorrhage: A series of 17 cases. Acta Obstet
Gynecol Scand 84:660-664, 2005
38. Bakri YN, Amri A, Abdul Jabbar F: Tamponade-balloon for obstetrical
bleeding. Int J Gynecol Obstet 74:139-142, 2001
39. Dabelea V, Schultze PM, McDuffie RS: Intrauterine balloon tamponade
in the management of postpartum hemorrhage. Am J Perinatol 24:359364, 2007
40. Price N, Whitelaw N, B-Lynch C: Application of the B-Lynch brace
suture with associated intrauterine balloon catheter for massive hemorrhage due to placenta accreta following second-trimester miscarriage.
J Obstet Gynaecol 26:267-268, 2006
41. Danso D, Reginald P: Combined B-Lynch suture with intrauterine balloon catheter triumphs over massive postpartum hemorrhage. Br J
Obstet Gynaecol 109:963, 2002