REVIEW

CURRENT
OPINION New approaches to obstetric hemorrhage: the
postpartum hemorrhage consensus algorithm
Thierry Girard a, Manfred Mörtl b, and Dietmar Schlembach c

Purpose of review
Postpartum hemorrhage is increasingly frequent and a major contributor to maternal morbidity and
mortality. Although individual steps, such as coagulation or surgical management, have been reviewed,
there is little information on treatment algorithms.
Recent findings
A treatment algorithm for postpartum hemorrhage was developed by the experts from three different
specialties and from three countries. The algorithm describes symptoms, diagnosis, general measurements,
medication, and organizational aspects.
Summary
The algorithm is thought to serve as a template for local adaptation. It will hopefully improve the
management of postpartum hemorrhage.
Keywords
massive bleeding, postpartum hemorrhage, uterine atony

INTRODUCTION however, is to provide the clinicians with inter-

Postpartum hemorrhage (PPH) is a major cause of
maternal mortality and morbidity. The prevalence
of PPH is rising and the contributing factors are not
completely understood, although this might be in
part because of a detection bias, as the knowledge of
risk factors and treatment options is increasing [1].
The majority of fatal obstetric hemorrhages
are potentially avoidable, as ‘major sub-standard
care’ has been associated with 60–80% of these
cases [2–4]. The following contributors to adverse
outcome have been identified [4–7]:
(1) delayed treatment because of underestimation
of blood loss;
(2) delayed availability of blood products;
(3) lack of treatment algorithms;
(4) lack of knowledge and training;
(5) insufficient interdisciplinary communication;
and
(6) inadequate organization.
D-A-CH ALGORITHM
In previous reviews, the use of clotting factors and
other prohemostatic drugs as well as the manage-
ment of abnormal placentation have been addressed
[8,9]. The aim of the proposed algorithm (Fig. 1),
disciplinary guidance throughout PPH, including
the initial minutes after diagnosis or suspicion.
The working group is of the strong opinion that
early recognition and treatment can prevent
many patients from progressing into massive PPH
with the concomitant coagulopathy and circulatory
instability.
As a result of the lack of a unanimous guide-
line for the treatment of PPH, experts from the
German-speaking countries Austria, Germany, and
Switzerland have decided to compile a treatment
algorithm. This effort was based on both national
and international algorithms on the treatment of
PPH. The expert group consisted of obstetricians,
anesthesiologists, and hemostasis specialists (see list
a
Department of Anesthesiology, University Hospital Basel, Basel, Swit-
zerland, bInterdisciplinary Centre for Gynecology, Gynecooncology and
Feto-Maternal Medicine, Klagenfurt, Austria and cDepartment of Obstet-
rics/Prenatal Diagnosis and Fetal Physiology, University Hospital Jena,
Jena Germany
Correspondence to Professor Dr med. Thierry Girard, Department of
Anesthesiology, University Hospital Basel, Spitalstrasse 21, CH-4031,
Basel, Switzerland. Tel: +41 61 265 25 25; e-mail: thierry.girard@
unibas.ch
Curr Opin Anesthesiol 2014, 27:267–274
DOI:10.1097/ACO.0000000000000081

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Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
 Obstetric and gynecological anesthesia
KEY POINTS

The treatment of PPH should be fast and focused.

Organizational measures are as important as
medication and surgical treatment.

Uterine (balloon) tamponade can temporarily stop
bleeding and allow for transfer.

Tranexamic acid and fibrinogen concentrate seem to
be valuable treatment options, large trials are about
to be completed.

Hemodynamic instability must be corrected before
extended surgery, such as peripartum hysterectomy.
below). A timely and accurate diagnosis of the cause
of hemorrhage is key for a causative treatment.
A stepwise diagnostic approach allows for a fast
identification of the cause of bleeding. Knowledge
of risk factors for PPH allows for the elaboration
of interdisciplinary treatment plans in patients at
risk. These patients should be consulted by an
anesthesiologist as soon as the risk factors have
been identified. Table 1 summarizes the pre-existing
risk factors and intrapartum or postpartum factors
influencing the risk of PPH [5,10]. Members of the
consensus group are given below:
(1) PD Dr med. Wolfgang Arzt, Abt. für Geburt-
shilfe und Pränatalmedizin, Landesfrauen-
und Kinderklinik Linz (A).
(2) Professor Dr med. Ernst Beinder, Klinik für
Geburtsmedizin, Charite – Universitätsmedi-
zin Berlin (D).
(3) Professor Dr med. Christoph Brezinka, Univer-
sitätsklinik für Gynäkologische Endokrino-
logie und Reproduktionsmedizin, Department
Frauenheilkunde (A).
(4) Professor Dr med. Kinga Chalubinski, Univer-
sitätsfrauenklinik, Medizinische Universität
Wien (A).
(5) Professor Dr med. Dietmar Fries, Klinische Abt.
für Allgemeine & Chirurgische Intensivmedi-
zin, Medizinische Universität Innsbruck (A).
(6) Professor Dr med. Thierry Girard, Departement
Anästhesie, Universitätsspital Basel (CH).
(7) Professor Dr med. Wiebke Gogarten, Klinik
für Anästhesiologie, operative Intensivmedizin
Notfallmedizin und Schmerztherapie, Klini-
kum Bielefeld, Bielefeld (D).
(8) Professor Dr med. Bernd-Joachim Hackelöer,
Amedes Experts, Hamburg (D).
(9) Professor Dr med. Hanns Helmer, Univer-
sitätsfrauenklinik, Medizinische Universität
Wien (A).
268 www.co-anesthesiology.com
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(10) Professor Dr med. Wolfgang Henrich, Klinik
für Geburtsmedizin, Charite – Universitätsme-
dizin Berlin (D).
(11) Professor Dr med. Irene Hösli, Abt. Geburtshilfe
& Schwangerschaftsmedizin, Universitätsspital
Basel (CH).
(12) Professor Dr med. Peter Husslein, Univer-
sitätsfrauenklinik, Medizinische Universität
Wien (A).
(13) Professor Dr med. Franz Kainer, Diakonie Neu-
endettelsau – Klinik Hallerwiese, Geburtshilfe
und Pränatalmedizin, Nürnberg (D).
(14) Professor Dr med. Uwe Lang, Universitätskli-
nik für Geburtshilfe und Frauenheilkunde,
Medizinische Universität Graz (A).
(15) Dr med. Manfred G. Mörtl (Head of the
consensus team), Klinik für Gynäkologie
und Geburtshilfe, Perinatalzentrum, Klinikum
Klagenfurt am Wörthersee (A).
(16) Dr med. Georg Pfanner, Abt. für Anästhesio-
logie und Intensivmedizin, LKH Feldkirch (A).
(17) Professor Dr med. Werner Rath, Universitäts-
frauenklinik, Universitätsklinikum RWTH
Aachen (D).
(18) Professor Dr med. Dietmar Schlembach (Head
of the consensus team), Universitätsfrauenkli-
nik, Universitätsklinikum Jena, Jena (D).
(19) Professor Dr med. Ekkehard Schleussner,
Universitätsfrauenklinik, Universitätsklinikum
Jena, Jena (D).
(20) Professor Dr med. Horst Steiner, Salzburg (A).
(21) Professor Dr med. Daniel Surbek, Univer-
sitätsklinik für Frauenheilkunde, Inselspital
Medizinische Universität Bern (CH).
(22) Professor Dr med. Roland Zimmermann, Klinik
für Geburtshilfe, Universitätsspital Zürich
(CH).
The suggested algorithm outlines a common
denominator of the current practice in Austria,
Germany, and Switzerland, and does not necessarily
concur with the clinical practice in other countries.
For many recommendations, the underlying evi-
dence is scarce and relies on ‘expert opinion’.
The algorithm is intended to be as general as
possible, but local organizational adaptations are
probably needed. It is aimed at all professionals
involved with labor, that is, midwives, obstetricians,
anesthesiologists, and intensivists. The algorithm
consists of four steps. At the beginning of each step,
the requirements for organization and staffing are
summarized. Horizontally, the algorithm is organ-
ized in three columns: clinical symptoms, general or
surgical measures, and medication or target values.
The presentation of four single steps does
not imply that these measures must be performed
Volume 27
Number 3
June 2014
 New approaches to obstetric hemorrhage Girard et al.

Postpartum hemorrhage
treatment algorithm
After vaginal delivery or postoperatively after cesarean section
© 2014: PPH-CONSENSUS-Group (D-A-Ch)

Clinical symptoms General/surgical measures Medication

Maximal duration:
30 minutes after diagnosis
Call for senior obstetrician/inforn anesthesiologist
• Vaginal bleeding • 2 intraevnous accesses (at least 1 large bore) • OXYTOCIN
> 500 ml after vaginal delivery • Cross match blood/emergency labs 3–5 U as short infusion and
> 1000 ml after cesarean section • Volume (e.g. crystalloids/colloids) P 40 U in 30 min (controlled infusion)
S • Foley catheter
A OR
T • Measure blood loss
R • CARBETOCIN (off-label use)
E beware: underestimation A 100 µg as short infusion
• Fast detection of bleeding cause (4 Ts)
P !use measuring system!
• Uterine tone (Tone)
L
• Placental inspection (Tissue) L
1 • Inspect via speculum (Trauma) E Severely persistent hemorrage STEP 2,
• Stable hemodynamics
• Coagulation (Thrombin) L moderately persistent hemorrhage consider

• MISOPROSTOL (off-label use)

• Uterine compression - ultrasound 800 µg sublingual/rectal

Duration maximal further 30 min. Call for anesthesiologist/alert OR-team/organize operating room
(= 60 min after diagnosis) consider transfer
• Persistente severe bleeding • Prepare operating room Order RBC, plasma, platelets
• Stable hemodynamics • Exclude uterine rupture (Cross match, prepare blood products)
S •
•
Palpation/ultrasound
Suspected placentral retention
• Sulprostone
T 500 µg (maximum 1500 µg/24h)
• Manual removal
as controlled infusion only
E • Curettage (controlled by ultrasound)
P • 2 g tranexamic acid i.v.
before fibrinogen
2
In case of persistent severe hemorrhage
approx. 1500 ml blood loss
• Fibrinogen 2–4 g
• Consider RBC, plasma

Consider transfer/call for senior anesthesiologist

Inform the persons with the best clinical expertise
• Refractory severe bleeding Uterine tamponade
with hemodynamic stability Balloon: Target values:
OR • Insert balloon under ultrasound control • Hemoglobin > 80–100 g/l (5–6.2 mmol/l)
sufficient filling of balloon • Platelets > 50 Gpt/l
• Hemodynamic shock
(continue sulprostone) • Systolic BP > 80 mmHg
S • Use slight traction • pH ≥ 7.2
T AIM • Alternatively: Gauze packing of the uterus • Temperature > 35° C
E • Hemodynamic stability • Calcium > 0.8 mmol/l
P • (Temorary) cessation of Cessation of bleeding:
bleeding • Intermediate/high-dependency care
3 • Improve coagulation and • Deflate balloon after 12–24 hours
anemia (potentially after transfer to large center)
• Organize STEP 4

Persistence or resurgence of bleeding:

(bleeding with balloon in situ or after deflation)
• Consider repeating balloon (”bridging”)
• Go to STEP 4

Call in the persons with the best clinical expertise

• Persistent bleeding Definite treatment/(surgical) therapy
S In-stable hemodynamics Stable hemodynamics
T Stop the bleeding Definite surgical therapy
E Laparotomy/vascular clamps/compression • Compression sutures
P • Vascular ligation
Stabilization • Hysterectomy
4
Hemodynamics/temperature/coagulation
Embolisation
consider rFVIIa

Criteria for transfer

• Lack of surgical or interventional equipment Recombinant FVIIa (Off-label use!)
or lack of experienced personel • Initial 60–90 µg/kg (bolus)
• Temporary stop of bleeding through tamponade • Might be repeated after 20 min
• Hemodynamic stability for transport in case of persistent bleeding
• Existing SOP with the target hospital

FIGURE 1. Consensus algorithm for the treatment of PPH. The algorithm consists of four steps. At the beginning of each step,
the requirements for organization and staffing are summarized. Horizontally the algorithm is organized in three columns:
clinical symptoms, general or surgical measures, and medication or target values. The presentation of four single steps does
not imply that these measures must be performed sequentially. The clinical condition of the patient, e.g. hemodynamic
instability, might demand deviation from the given sequence.

sequentially. The clinical condition of the patient, STEP 1

for example, hemodynamic instability, might The aim of step 1 is to recognize PPH, establish
demand deviation from the given sequence. monitoring, identify the cause of bleeding, and

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 Obstetric and gynecological anesthesia
Table 1. Risk factors for postpartum hemorrhage
‘T’ Prepartal
Tonus, trauma Previous uterine atony
Previous uterine surgery
Uterus myomatosus
Overdistension of the uterus, for example
Multiple pregnancy
Polyhydramnios
Fetal macrosomia
Tissue Previous placental abruption
Placenta previa
Abnormality of placentation
(placenta accreta, increta, and percreta)
Thrombin Hereditary or acquired coagulopathy
Other causes Previous postpartum hemorrhage
Multipara
Pregnancy-associated hypertension
Amniotic infection
Smoking
increase uterine tone. Step 1 must not last more
than 30 min.
An obstetric consultant has to be called in and
the anesthesiologist on call should be informed.
Clinical symptoms
Before PPH can be treated, a correct diagnosis has to
be made. It is well known that estimations of blood
loss are inadequate and, therefore, usage of a simple
measuring system is advocated [11–13]. PPH is
defined as blood loss exceeding 500 and 1000 ml
after vaginal and cesarean delivery, respectively.
During step 1, the patient is in stable hemody-
namic condition. Should cardiovascular instability
occur, then the algorithm shortcuts to step 3.
General measures
The parturient needs at least two intravenous
accesses (as large a bore as possible) and blood
should be drawn to cross-match blood products.
Further measures are substitution of intravascular
volume and a Foley catheter. The discussion about
optimal volume resuscitation strategy is almost
endless, especially as far as crystalloid or colloidal
&&
solutions are concerned [14 ]. Colloidal fluids have
a more pronounced effect on intravascular volume,
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Intrapartal or postpartal
Uterine atony
Uterine rupture
Uterine inversion
Lacerations
Placental retention
Disseminated intravascular coagulation (DIC)
Because of complications of pregnancy (preeclampsia,
HELLP syndrome, and amniotic fluid embolism)
Because of hematological diseases (dilution coagulopathy
and hyperfibrinolysis)
Prolonged labor
Induced labor
Prolonged augmentation with oxytocin
Instrumented delivery
Cesarean section
but they can inhibit platelet aggregation and
interact with the measurement of fibrinogen levels
[15]. Excessive amounts of fluids lead to dilution
coagulopathy [8]. Should larger amounts of fluid
be used, then these should be warmed.
Identification of the cause of bleeding is of
paramount importance, and the 4 Ts are a valuable
mnemonic: Tonus (uterine atony), Tissue (placental
retention), Trauma (lacerations to the cervix or
vagina), and Thrombin (primary coagulopathy)
[16].
Medication
Step 1 focuses on increasing the uterine tone, as
the cause of PPH is most frequently uterine atony.
Oxytocin is administered as a short infusion of 3–5
international units, followed by an infusion pump
with up to 40 units over 30 min. A bolus adminis-
tration of oxytocin receptor agonists should be
discouraged, as this leads to a fast decrease of peri-
pheral resistance and a drop in blood pressure.
Therefore, oxytocin should only be given as a short
infusion [3,17,18].
Alternatively, carbetocin 100 mg can be given as
a short infusion intravenously. It must be noted
that the administration of carbetocin to treat PPH
is off-label.
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June 2014

In the case of persistent severe bleeding, step 2
follows immediately. But if the bleeding is moder-
ately persistent, then misoprostol 800 mg can be
given rectally or sublingually [19].
STEP 2
In the case of persistent severe hemorrhage and
cardiovascular stability, step 2 follows step 1 after
at most 30 min. The development of a coagulopathy
has to be anticipated and treatment initiated. The
duration of step 2 is limited to another 30 min.
Clinical symptoms
Clinically, the patient remains hemodynamically
stable despite the persistent severe hemorrhage.
Should hemodynamics become unstable, then step
3 is to be started immediately.
General measures
The anesthesiologist should be called into the labor
ward. The operation room and its staff should be
alerted, and preparations for emergency surgery
should be initiated. In smaller hospitals, this might
be a valuable moment to consider transfer of the
patient to a larger medical center.
If there is suspicion of placental retention, then
a manual placental removal or curettage of the
uterine cavity should be performed. Depending
on the local circumstances, that is, duration from
order entry until delivery of red blood cells, fresh
frozen plasma, or platelets, blood products might
have to be ordered at this moment.
Medication
Step 2 focuses on the interdisciplinary management
of uterine tone, coagulation, temperature, and
hemodynamic stability.
Uterine tone
After using oxytocin receptor agonists in step 1,
there is now a switch to prostaglandins. Sulprostone
(a prostaglandin E2 analog) is given via an infusion
pump. The maximal dose of 1500 mg per 24 h must
not be exceeded. The initial dose is up to 500 mg in
the first 60 minutes. Side-effects of prostaglandins
include a decrease of peripheral vascular resistance,
shivering, fever, nausea, and vomiting [1,20 ].
& seem to have a lower mortality [29]. As is true with
Coagulation and anemia
Physiological changes of coagulation during preg-
nancy and delivery are complex. Pregnancy is
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New approaches to obstetric hemorrhage Girard et al.
characterized by a state of hypercoagulability
[21,22]. Traditional laboratory analyses of coagu-
lation, such as activated partial thromboplastin time
(aPTT) and international normalized ratio (INR),
are frequently only available after 45–60 min. With
point-of-care monitoring of coagulation, such as
thromboelastography (TEG) and rotational throm-
boelastometry (ROTEM), whole-blood coagulation
as well as fibrinolysis can be monitored within
&
minutes [23 ]. Normal values in term pregnant
patients have recently been published with a
maximal amplitude of 64–86 mm for TEG and a
maximal clot firmness of 15–38 mm for the clot
&
firmness of the fibrin clotFIBTEM [24 ]. Impairment
of hemostasis in PPH is seen by a 39% decrease in
fibrinogen concentration and a 20% decrease in
TEG clot firmness, whereas aPTT and INR changed
&
by only 12–15% [23 ]. Fibrin polymerization, as
monitored in the FIBTEM, had a good correlation
with fibrinogen concentration (R2 ¼ 0.75) and was
detectable after 5 min [25].
Antifibrinolysis
A review of tranexamic acid in surgical patients
has shown a significant reduction in the need
for red blood cell transfusion and the need for
reoperation [15,26]. In obstetric patients with PPH,
a recent prospective trial has shown a significant
reduction of secondary measures in severe PPH
treated with tranexamic acid [27]. Although fibrino-
lytic capacity decreases during the last trimester
of pregnancy, fibrinolysis is increased during
delivery [21]. A large, randomized, double-blind
controlled trial, the World Maternal Antifibrinolytic
Trial (WOMEN), is about to be completed and
will hopefully shed more light on the importance
of tranexamic acid in PPH [28].
In the proposed algorithm, the recommended
dose of tranexamic acid in step 3 is 2 g. Current
recommendations for tranexamic acid vary from
1 to 3 g. Therefore, the working group has agreed
on the intermediate dose of 2 g. It is also recom-
mended to administer tranexamic acid before any
supplementation of fibrinogen.
Red blood cells to fresh frozen plasma ratio
Patients transfused with a high ratio of red blood
cells to fresh frozen plasma (RBC : FFP), that is, >1 : 2,
most research on massive hemorrhage, the major
proportion of the research on this has been acquired
from trauma patients. Pasquier et al. [30] performed
a retrospective chart review of patients with severe
PPH. Patients with a higher RBC : FFP ratio were less
www.co-anesthesiology.com 271
 Obstetric and gynecological anesthesia
likely to receive further interventions in addition to
sulprostone administration [30]. On the other hand,
differences in RBC : FFP ratios between patients with
and without additional interventions were small
(1 : 1.2 vs. 1 : 1.6).
There are currently two practices in massive
hemorrhage: fixed product ratio or individualized
procoagulant intervention and factor substitution
&&
[14 ]. The coagulopathy associated with massive
blood loss is because of loss of coagulation factors,
activation of coagulation, and dilutional coagulo-
pathy [31]. FFP is an inefficient measure to restore
coagulation factors, because the concentration of
&&
coagulation factors in FFP is low [14 ,32].
Fibrinogen
During massive hemorrhage, factor I (fibrinogen)
is one of the first coagulation factors to decrease
&&
beyond critical levels [33 ,34]. Term pregnant
women have an increased concentration of fibrino-
gen of approximately 4.5–5.8 g/l compared with
&&
the normal value of 2.0–4.5 g/l [33 ]. Retrospective
investigations have identified a fall of fibrinogen to
be predictive of major blood loss in PPH [35,36]. It is
logical to assume that early substitution of fibrino-
gen in PPH could reduce total blood loss and the
need for secondary interventions such as surgery
or embolization. First investigations in nonobstetric
populations have been performed, and a double-
blind, placebo-controlled investigation in cardiac
&
surgery has recently been published [37 ]. The
fibrinogen group had not only fewer blood trans-
fusions than the placebo group, but total avoidance
of allogeneic blood was 13 of 29 (45%) in the
fibrinogen group compared to 0 of 32 patients in
&
the placebo group [37 ]. Hopefully, the results
of a randomized controlled trial in PPH will soon
provide more data on the usefulness of fibrino-
&
gen concentrate in PPH [38 ]. The use of fibrinogen
concentrate in PPH is off-label.
In the UK and in North America, cryoprecipitate
is used as a source of fibrinogen. The drawbacks of
cryoprecipitate are that it has to be thawed and that
&&
it is not virally inactivated [33 ].
Recombinant activated factor VII
Following early case reports, recombinant activated
factor VII (rFVIIa) has been occasionally used
in severe obstetric hemorrhage. A recent review
article on this topic concludes that rFVIIa cannot
compensate for inadequate transfusion policy [39].
In order to achieve a firm clot formation, rFVIIa
needs the crucial substrate of platelets and fibrino-
&&
gen [14 ,15,39]. Therefore, control of fibrinolysis,
transfusion of red blood cells, and a minimal
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concentration of fibrinogen are essential before
considering a treatment with rFVIIa. As rFVIIa is
an enzyme, temperature and acid–base status (pH)
should be as close to physiological values as possible.
Temperature
Hypothermia is often associated with major blood
loss and is mainly because of infusion of cold fluids
and blood products. Hypothermia of 348C or below
&&
induces coagulopathy [14 ]. Therefore, early and
aggressive warming, in addition to an adequate
room temperature, is of great importance.
STEP 3
The aim of step 3 is to establish hemodynamic
stability and to (temporarily) stop bleeding. Coagul-
opathy and anemia are treated. An anesthesia con-
sultant should be in the room, and the individuals
with the best expertise should be notified.
The goal of uterine tamponade is to stop
bleeding. This might be a temporary stop and, thus,
uterine tamponade serves to bridge until the patient
is hemodynamically stabilized and coagulopathy is
treated. Once hemodynamic stability is reached,
there should again be a consideration to transfer
the parturient into a larger center. There are com-
mercially available balloons with drainage systems
for uterine tamponade. These have the advantage to
allow for visual monitoring of ongoing bleeding.
STEP 4
Persistent bleeding leads to step 4: invasive measures,
such as surgery or interventional radiology. At this
point, the patient is potentially hemodynamically
unstable, coagulopathic, hypothermic, and acidotic.
This situation needs urgent interdisciplinary
management. Step 4 distinguishes between hemo-
dynamic instability and hemodynamic stability.
Hemodynamic instability
In case of hemorrhagic shock and persistent
bleeding, it might be unavoidable to proceed to
surgery. The prevailing opinion among obstetricians
to proceed to hysterectomy as a last resort must be
scrutinized. This surgery has an average duration of
157  75 min, with a blood loss of 3325  1839 ml
[40]. To perform such a surgery in cases of hemo-
dynamic instability, coagulopathy, and acidosis
with limited training (frequency of postpartum
hysterectomy is 0.8–1.39 per 1000 births [40,41])
is potentially hazardous.
Therefore, the algorithms advocate a three-
phase approach.
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June 2014

Phase 1
Laparotomy (Pfannenstiel or vertical). Eventration
of the uterus and cranial traction with uterine mas-
sage. Atraumatic vascular clamps are placed in the
region of the arteria uterina and hypogastric vessels
to minimize uterine perfusion.
Phase 2
Pausing the surgery and stabilizing the patient as far
as hypovolemia, coagulopathy, acidosis, and hypo-
thermia are concerned. This can be done within the
operation room or in the ICU.
Phase 3
Definite surgery with compression sutures (e.g.
B-Lynch), vessel ligation, or hysterectomy on the
hemodynamically stable patient by a surgeon with
the appropriate expertise is advocated. If the infra-
structure allows, then invasive radiology and embo-
lization is an alternative approach [42].
Hemodynamic stability
The hemodynamically stable patient is brought to
definite surgical repair (or invasive radiology)
according to phase 3 above.
CONCLUSION
In conclusion, a treatment algorithm for PPH has
been developed by an interdisciplinary, international
working group. The aim is to provide the basis for
rapid and adequate treatment of this dangerous
condition. Although the prevalence of PPH has inc-
reased, severe hemorrhage fortunately remains an
infrequent event. But the severity of the condition
and the velocity of deterioration demand immediate
and interdisciplinary action. This requires training in
multidisciplinary teams at regular intervals [43,44].
Acknowledgements
The author wishes to acknowledge the members of the
consensus group who are listed in this article, as well as
Allison Dwileski for editorial assistance.
Conflicts of interest
There are no conflicts of interest.
REFERENCES AND RECOMMENDED
READING
Papers of particular interest, published within the annual period of review, have
been highlighted as:
& of special interest
&& of outstanding interest
1. Samangaya R, Pennington R, Vause S. Factors relating to a rising incidence of
major postpartum haemorrhage. BJOG 2010; 117:370.
0952-7907 ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
New approaches to obstetric hemorrhage Girard et al.
2. RCOG. Green-top Guideline No. 52 [Internet]. [Cited 3 February 2014].
Available at http://www.rcog.org.uk/files/rcog-corp/GT52PostpartumHaemor
rhage0411.pdf.
3. Haeri S, Dildy GA. Maternal mortality from hemorrhage. Semin Perinatol
2012; 36:48–55.
4. Farquhar C, Sadler L, Masson V, et al. Beyond the numbers:
classifying contributory factors and potentially avoidable maternal deaths
in New Zealand, 2006–2009. Am J Obstet Gynecol 2011; 205:331.
e1–331.e8.
5. Driessen M, Bouvier-Colle M-H, Dupont C, et al. Postpartum hemorrhage
resulting from uterine atony after vaginal delivery: factors associated with
severity. Obstet Gynecol 2011; 117:21–31.
6. Upadhyay K, Scholefield H. Risk management and medicolegal issues related
to postpartum haemorrhage. Best Pract Res Clin Obstet Gynaecol 2008;
22:1149–1169.
7. Dupont C, Touzet S, Colin C, et al. Incidence and management of
postpartum haemorrhage following the dissemination of guidelines in a
network of 16 maternity units in France. Int J Obstet Anesth 2009;
18:320–327.
8. Mercier FJ, Bonnet M-P. Use of clotting factors and other prohemostatic
drugs for obstetric hemorrhage. Curr Opin Anaesthesiol 2010; 23:310–
316.
9. Snegovskikh D, Clebone A, Norwitz E. Anesthetic management of patients
with placenta accreta and resuscitation strategies for associated massive
hemorrhage. Curr Opin Anaesthesiol 2011; 24:274–281.
10. Henrich W, Surbek D, Kainer F, et al. Diagnosis and treatment of peripartum
bleeding. J Perinat Med 2008; 36:467–478.
11. Kadri Al HMF, Anazi Al BK, Tamim HM. Visual estimation versus gravimetric
measurement of postpartum blood loss: a prospective cohort study. Arch
Gynecol Obstet 2011; 283:1207–1213.
12. Prata N, Gerdts C. Measurement of postpartum blood loss. BMJ 2010;
340:c555.
13. Schorn MN. Measurement of blood loss: review of the literature. J Midwifery
Womens Health 2010; 55:20–27.
14. Kozek-Langenecker SA, Afshari A, Albaladejo P, et al. Management of
&& severe perioperative bleeding: guidelines from the European Society of
Anaesthesiology. Eur J Anaesthesiol 2013; 30:270–382.
These guidelines of the European Society of Anaesthesiology summarize the
different methods to prevent transfusions as well as the possibilities for treatment
in many different clinical scenarios.
15. Bolliger D, Görlinger K, Tanaka KA. Pathophysiology and treatment of
coagulopathy in massive hemorrhage and hemodilution. Anesthesiology
2010; 113:1205–1219.
16. Anderson JM, Etches D. Prevention and management of postpartum
hemorrhage. Am Fam Physician 2007; 75:875–882.
17. Thomas JS, Koh SH, Cooper GM. Haemodynamic effects of oxytocin given as
i.v. bolus or infusion on women undergoing caesarean section. Br J Anaesth
2006; 98:116–119.
18. Moertl MG, Friedrich S, Kraschl J, et al. Haemodynamic effects of
carbetocin and oxytocin given as intravenous bolus on women under-
going caesarean delivery: a randomised trial. BJOG 2011; 118:1349–
1356.
19. International Federation of Gynecology And Obstetrics. Treatment of post-
partum hemorrhage with misoprostol. Int J Gynaecol Obstet 2012; 119:215–
216.
20. Tang J, Kapp N, Dragoman M, de Souza JP. WHO recommendations for
& misoprostol use for obstetric and gynecologic indications. Int J Gynaecol
Obstet 2013; 121:186–189.
Given the controversies about misoprostol, these recommendations are very
welcome to clarify the current position of obstetric experts.
21. Hellgren M. Hemostasis during normal pregnancy and puerperium. Semin
Thromb Hemost 2003; 29:125–130.
22. Levy JH, Dutton RP, Hemphill JC, et al. Multidisciplinary approach to the
challenge of hemostasis. Anesth Analg 2010; 110:354–364.
23. Karlsson O, Jeppsson A, Hellgren M. Major obstetric haemorrhage:
& monitoring with thromboelastography, laboratory analyses or both? Int J
Obstet Anesth 2014; 23:10–17.
This study compares the results from thromboelastography with traditional
laboratory values in women with a peripartum blood loss of more than 2000 ml.
The results underline the value of point-of-care testing.
24. Macafee BB, Yentis SM, Campbell JPJ, et al. Reference ranges for thrombo-
& elastography (TEG) and traditional coagulation tests in term parturients
undergoing caesarean section under spinal anaesthesia. Anaesthesia
2012; 67:741–747.
As a result of the hypercoagulability toward the end of pregnancy, it is important to
define normal values of term pregnant women.
25. Huissoud C, Carrabin N, Audibert F, et al. Bedside assessment of fibrinogen
level in postpartum haemorrhage by thrombelastometry. BJOG 2009;
116:1097–1102.
26. Dunn CJ, Goa KL. Tranexamic acid: a review of its use in surgery and other
indications. Drugs 1999; 57:1005–1032.
27. Ducloy-Bouthors A-S, Huissoud C, Jude B, et al. High-dose tranexamic acid
reduces blood loss in postpartum haemorrhage. Crit Care 2011; 15:R117–
R127.
www.co-anesthesiology.com 273
 Obstetric and gynecological anesthesia
28. Shakur H, Elbourne D, Gülmezoglu M, et al. The WOMAN Trial (World
Maternal Antifibrinolytic Trial): tranexamic acid for the treatment of postpartum
haemorrhage: an international randomised, double blind placebo controlled
trial. Trials 2010; 11:40.
29. Shaz BH, Dente CJ, Nicholas J, et al. Increased number of coagulation
products in relationship to red blood cell products transfused improves
mortality in trauma patients. Transfusion 2010; 50:493–500.
30. Pasquier P, Gayat E, Rackelboom T, et al. An observational study of the fresh
frozen plasma: red blood cell ratio in postpartum hemorrhage. Anesth Analg
2013; 116:155–161.
31. Spahn DR, Ganter MT. Towards early individual goal-directed coagulation
management in trauma patients. Br J Anaesth 2010; 105:103–105.
32. Kozek-Langenecker S, Sorensen B, Hess J, Spahn DR. Clinical effectiveness
of fresh frozen plasma compared with fibrinogen concentrate: a systematic
review. Crit Care 2011; 15:R239.
33. Levy JH, Welsby I, Goodnough LT. Fibrinogen as a therapeutic target for
&& bleeding: a review of critical levels and replacement therapy. Transfusion
2014. [Epub ahead of print]
A review article on the function of fibrinogen and the importance of this coagulation
factor for hemostasis. The article critically discusses the different therapeutic
options for the substitution of fibrinogen. Different clinical situations, such as
trauma, surgery, and obstetrics, are discussed.
34. Fries D, Martini WZ. Role of fibrinogen in trauma-induced coagulopathy. Br J
Anaesth 2010; 105:116–121.
35. Cortet M, Deneux-Tharaux C, Dupont C, et al. Association between fibrinogen
level and severity of postpartum haemorrhage: secondary analysis of a
prospective trial. Br J Anaesth 2012; 108:984–989.
36. Charbit B, Mandelbrot L, Samain E, et al. The decrease of fibrinogen is an early
predictor of the severity of postpartum hemorrhage. J Thromb Haemost 2007;
5:266–273.
274 www.co-anesthesiology.com
Copyright © Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
37. Rahe-Meyer N, Solomon C, Hanke A, et al. Effects of fibrinogen concentrate
& as first-line therapy during major aortic replacement surgery: a randomized,
placebo-controlled trial. Anesthesiology 2013; 118:40–50.
In this study, the authors randomly assigned patients with aortic surgery to either
fibrinogen concentrate or placebo. Although the number of patients was only
approximately 30 patients per group, the effect of fibrinogen on the avoidance of
transfusion is impressive.
38. Wikkelsoe AJ, Afshari A, Stensballe J, et al. The FIB-PPH trial: fibrinogen
& concentrate as initial treatment for postpartum haemorrhage: study protocol
for a randomised controlled trial. Trials 2012; 13:110.
A study protocol for the investigation of fibrinogen in PPH. Hopefully, the results of
the study will soon improve our knowledge in this field.
39. Ahonen J. The role of recombinant activated factor VII in obstetric
hemorrhage. Curr Opin Anaesthesiol 2012; 25:309–314.
40. Forna F, Miles AM, Jamieson DJ. Emergency peripartum hysterectomy:
a comparison of cesarean and postpartum hysterectomy. Am J Obstet
Gynecol 2004; 190:1440–1444.
41. Lau WC, Fung HY, Rogers MS. Ten years experience of caesarean and
postpartum hysterectomy in a teaching hospital in Hong Kong. Eur J Obstet
Gynecol Reprod Biol 1997; 74:133–137.
42. Rath W, Hackethal A, Bohlmann MK. Second-line treatment of
postpartum haemorrhage (PPH). Arch Gynecol Obstet 2012; 286:549–
561.
43. Merién AER, van de Ven J, Mol BW, et al. Multidisciplinary team training in a
simulation setting for acute obstetric emergencies: a systematic review.
Obstet Gynecol 2010; 115:1021–1031.
44. Crofts JF, Ellis D, Draycott TJ, et al. Change in knowledge of midwives and
obstetricians following obstetric emergency training: a randomised controlled
trial of local hospital, simulation centre and teamwork training. BJOG 2007;
114:1534–1541.
Volume 27
Number 3
June 2014