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Management of massive

postpartum haemorrhage
and coagulopathy
Jessica Moore
Edwin Chandraharan
Abstract
Postpartum haemorrhage (PPH) continues to remain the leading cause of
maternal morbidity and mortality worldwide. Whilst this is especially true
in resource limited countries, it also remains a signicant problemin devel-
oped countries. The traditional denition of primary PPHis blood loss from
the genital tract of 500 ml or more within 24 h of delivery (or >1000 ml
during caesarean section). Secondary PPH refers to an excessive blood
loss between 24 h and 6 weeks, postnatally. Massive PPH refers to
a blood loss of over 2000 ml (or >30% of blood volume) and hence, is an
obstetric emergency that requires a systematic, multi-disciplinary approach
to restore the volume, clotting system and the oxygen carrying capacity of
blood, whilst steps are taken to arrest bleeding as quickly as possible.
The last condential enquiry into maternal deaths (CEMACH, 2003e2005)
in the UK cited haemorrhage as the third highest cause of direct maternal
deaths with 6.6 deaths per million maternities. This report found that 58%
of these deaths may have been preventable and too little being done, too
late (failuretoappreciateclinical picture, delayininstitutingappropriatetreat-
ment, delay is summoning senior help and system failures) continues to
contribute to maternal morbidity and mortality, even in the developed world.
Massive obstetric haemorrhage may occur in the antepartum (placenta
praevia, placental abruption and placenta accreta) or postpartum period.
It is has been observed that the incidence of massive PPH is likely to be
increasing due to the increased incidence of risk factors such as morbidly
adherent placenta secondary to previous caesarean sections and maternal
obesity. However, massive obstetric haemorrhage and the resultant coagul-
opathy can occur in women deemed to be at low risk and hence, all clini-
cians managing women during pregnancy and labour need to possess
knowledge and skills to recognize symptoms, signs and complications of
massive obstetric haemorrhage. This may ensure institution of timely and
appropriate treatment that could save lives.
Keywords coagulopathy; communication; massive obstetric haemor-
rhage; shock index; resuscitation
Introduction
The Royal College of Obstetricians and Gynaecologists (RCOG)
guidelines on PPH describe major PPH as a blood loss of more
than 1000 ml. This is further subdivided into moderate PPH of
1000e2000 ml and severe PPH with a blood loss of over 2000 ml.
There are varying denitions of what constitutes massive PPH,
however, two important points need to be considered. Firstly,
even a smaller blood loss may cause compromise in a patient
who is anaemic prior to delivery or in a patient with a low body
mass index (BMI), who is likely to have a smaller circulating
blood volume. Secondly, the denition of massive PPH relies on
an estimation of blood loss. It is well recognized that the esti-
mation of blood loss by clinicians by visual inspection of the
blood is notoriously inaccurate. Moreover, various terms such as
severe PPH and major PPH have been used interchangeably
with massive PPH and this may contribute to lack of clarity
during communication during obstetric emergency. The inci-
dence of PPH of over 1000 ml is thought to be around 1.86%
worldwide. Data from Scotland on massive PPH of over 2500 ml
or women who received more than 5 l of blood is estimated at
3.7/1000 maternities.
Massive PPH may result in immediate or long-term implica-
tions and these are listed in Table 1.
Whilst risk factors may predispose some women to massive
PPH, up to 40% of cases will occur in women classed as low
risk. It is therefore vital that all health care professionals are
trained in the recognition and management of massive post-
partum haemorrhage. Local protocols for systematic, multi-
disciplinary management of massive obstetric haemorrhage (e.g.
Code Blue) are invaluable and may help to save lives.
Coagulopathy refers to an abnormality in the blood coagula-
tion system that increases the tendency for bleeding and may be
due to hereditary or acquired factors. In the context of this
article, coagulopathy is most likely to arise as a consequence of
massive PPH and hence, would be acquired. This occurs due to
the consumption of clotting factors (disseminated intravascular
coagulation or DIC) or due to the dilutional effects of massive
blood loss on clotting factors, platelets and brinogen (washout
phenomenon). Massive PPH may also occur, albeit less
commonly, in the context of a patient predisposed to bleeding by
an underlying coagulopathy (e.g., von Willebrands disease,
abnormally functioning platelets or patients receiving treatment
Immediate and long-term implications of PPH
Immediate implications
C
Blood transfusions and effects of multiple blood transfusions
including transfusion reactions, risk of infections and transfusion
associated acute lung injury (TRALI)
C
Acute renal failure
C
Pulmonary oedema
C
Coagulopathy
C
Risk of peripartum hysterectomy
C
Intensive care treatment
Long-term implications
C
Future fertility
C
Long-term anaemia
C
Psychological sequelae e delayed bonding with baby,
posttraumatic stress disorder
C
Sheehans syndrome (pituitary failure)
Table 1
Jessica Moore MBBS MD MRCOG is a Consultant Obstetrician at St. Georges
Healthcare NHS Trust, London, UK. Conicts of interest: none declared.
Edwin Chandraharan MBBS MS (Obs & Gyn) DFFP DCRM MRCOG is a Consultant
Obstetrician and Gynaecologist at St. Georges Healthcare NHS Trust,
London, UK. Conicts of interest: none declared.
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with anticoagulants). Acquired coagulopathy is likely once 80%
of the blood volume has been lost; this equates to approximately
4.5 l in the average size woman.
Case history
Background
A 33-year-old woman was booked in her second pregnancy at
16weeks. She hadpreviouslydelivereda2690-gbabyat 37weeks of
gestation by elective caesarean section for breech presentation. Her
current pregnancy was uneventful and after appropriate counsel-
ling, she opted for vaginal birth after caesarean section (VBAC).
Delivery
She went into spontaneous labour at 39 weeks gestation after
rupturing her membranes and showed a rapid progress of labour.
Partograph showed a cervical dilation from 3 cm to full dilatation
in 2 h. Her second stage of labour lasted only 19 min with the
spontaneous delivery of a live infant weighing 3310 g. Synto-
metrine was given prior to delivery of the placenta by controlled
cord traction.
Immediate postpartum period
Immediately after delivery of the placenta, she started to bleed
vaginally. On examination in the delivery room, the uterus was
noted to be atonic and she had sustained a second degree tear
with multiple vaginal lacerations. The placenta and membranes
appeared complete. Resuscitation with intravenous (i.v.) uids
(crystalloids and colloids) was commenced and blood was sent
for urgent full blood count (FBC) and cross-match and clotting
screen. A repeat dose of oxytocics was given and a 40-unit syn-
tocinon infusion in 500 ml normal saline was commenced (125
ml/h). Her blood pressure was 130/67 mmHg and her pulse was
114 beats/min. An attempt was made to suture the vaginal tear in
the delivery room, however, the heavy bleeding continued and
the estimated blood loss (EBL) was 1200 ml. Hence, a decision
was made to transfer her to theatre.
Management in theatre
In theatre she received a spinal anaesthetic and was examined in
lithotomy position after catheterization of her bladder. The on-call
consultant obstetrician and consultant anaesthetist were in atten-
dance. Examination of the uterine cavity excluded retained
placental tissue or membranes. There were no signs of uterine
rupture. However, signicant bleeding was noted from a large
laceration in the posterior vaginal fornix. Despite attempts to
achieve haemostasis with suturing, she continued to bleed and the
hospital emergency protocol for massive PPH was activated. At
that time her bloodpressure droppedto90/40 mmHg andher pulse
was 120/min. In view of massive haemorrhage, the difculties in
achieving haemostasis and ongoing bleeding, two more consultant
obstetricians attended the theatre to provide support. A haemacue
blood sample was found to have a haemoglobin of 3.6 g/dl and
hence, 2 units of O-negative blood were given. Results of FBC from
the haematology labsoonafter conrmeda haemoglobinof 3.2g/dl
and platelets of 102 10
9
/l. Her coagulation prole was normal at
this stage (except for the falling platelet count). At this time the
vagina was packed with gauze to aid in haemostasis from a large
vascular area in the posterior vaginal wall and also to allow
replacement of blood and clotting factors.
In total she received the following blood products and clotting
factors:
2 units O-negative blood
6 units of cross-matched blood
12 units of fresh frozen plasma (FFP)
2 units of cryoprecipitate
2 pools of platelets.
As profuse bleeding continued and was not responding to
surgical measures (application of sutures), a multi-disciplinary
discussion took place between the obstetric, anaesthetic and
the haematology teams. It was felt that the risks of activated
Factor VII would outweigh the benets at this stage as the
coagulation parameters were normal. A joint decision was made
for uterine artery embolization and the on-call interventional
radiology team was contacted. The patient was intubated, kept
warm and arterial access was established in addition to venous
access. The rest of the vaginal walls were sutured and then
packed with a balloon containing 350 ml of normal saline and
gauze pack to apply pressure. Once the patient was haemody-
namically stable, she was transferred to the interventional radi-
ology department, where she underwent bilateral femoral artery
catheterization and embolization of both uterine arteries.
Subsequent management
She was transferred to ITU and ventilated. On day 1, she had the
vaginal pack and vaginal balloon removed with no signicant
blood loss. The embolization catheters were removed from the
femoral arteries by the interventional radiology team.
Case discussion
This case highlights an example of massive PPH in a high risk
pregnancy (vaginal birth after caesarean section or VBAC).
However, this did not prove to be related to the underlying cause
of her massive PPH, as multiple vaginal lacerations, most likely
secondary to precipitate labour, resulted in massive PPH. This
patient was cared for in appropriate setting for a woman
attempting VBAC, with immediate availability of skilled staff and
supporting facilities to ensure optimum outcome.
Aetiology of massive PPH
These may be subdivided according to site of blood loss or
according to the mechanism of blood loss (Table 2). However it
is important to remember that there may be more than one
reason for a massive PPH and that any large PPH will result in
a coagulopathy.
Principles of management
The RCOG guidelines on the management of PPH identify four
components, all of which must be undertaken simultaneously.
These are effective communication, resuscitation, monitoring
and investigation as well as arresting of bleeding. In addition to
these, prompt diagnosis of the aetiology, a multi-disciplinary
approach, appropriate post PPH care in ITU or HDU setting and
communication with relatives and debrieng of patient, form the
cornerstones of good clinical care to optimize outcome.
Prompt diagnosis is obviously important as the quicker the
bleeding is arrested the better the outcome for the mother with
reduced risk of coagulopathy. In many cases the blood loss may
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be obvious, however, a patient may present with signs of shock
or there may be insidious bleeding over a period of time which
has gone unnoticed. In addition, the extent of the bleeding may
not be revealed if bleeding is intra-abdominal as with a ruptured
uterus. In this case discussed, a diagnosis of traumatic PPH was
made early and the patient was transferred to the theatre for
further management.
A multi-disciplinary approach is essential at every stage of
management of PPH from initial communication to relevant team
members, throughout the resuscitation process, monitoring and
treatment to arrest bleeding.
The use of algorithms is a useful way of remembering a safe
and methodical approach to the problem whilst confronted with
a stressful and demanding situation. One such algorithm is
HAEMOSTASIS (Table 3). Our patient was managed by a multi-
disciplinary team comprising senior clinicians (senior midwives,
three consultant obstetricians, consultant anaesthetist, haema-
tologist and consultant radiologist) to ensure optimum care.
Another key aspect of management is training and re-drills.
Fire drills involve role play of a clinical scenario involving rele-
vant team members followed by debrieng and implementation
of any recommendations. Such multi-disciplinary simulated
training needs to be repeated at regular intervals and must all
involve all team members, who would be normally involved in
the management of PPH.
Communication
Effective and clear communication is essential between the
members of the multi-disciplinary team, who will manage
a massive PPH. These include senior obstetrician(s), senior
anaesthetist, experienced midwife, consultant haematologist,
interventional radiology team, blood transfusion laboratory staff,
porters for transporting specimens and blood as well as other
team members to document events and to provide assistance, as
required. Code Blue (major PPH Protocol) was activated in this
case when the visually estimated blood loss was over 2 l. This is
a useful way of alerting all the team members quickly and
ensures that senior clinicians are involved early in the manage-
ment. Establishing roles within each team is important as is
identifying a team leader, who will oversee the management and
a scribe who documents events and timings for future reference.
Resuscitation
The principle aims of resuscitation are to restore intravascular
volume and then maximize oxygen carrying capacity and coag-
ulability. Using the ABC approach resuscitation can take place as
problems are identied. This starts with assessing the airway and
breathing and supporting as appropriate with assistance from the
anaesthetist. A mother who is able to talk gives vital information
about the airway and breathing. High ow oxygen (10e15 l/min)
should be administered via a face mask. Circulation is assessed
through pulse rate, blood pressure and capillary return. Maternal
signs of shock include tachycardia, tachypnoea, poor peripheral
perfusion, confusion or unresponsiveness, oliguria and
biochemical evidence of metabolic acidosis. However, it is
important to appreciate that young, t and healthy pregnant
women are able to withstand signicant blood loss before signs
of hypovolaemic shock may be apparent. Whilst assessing
circulation two large bore (14 G) cannulae should be inserted and
blood should be taken for FBC, urgent cross match of at least
4 units, coagulation screen and urea and electrolytes.
Our patient received immediate uid resuscitation with 2 l of
crystalloids followed by 1 l of colloid, as the bleeding was rapid,
Classication of PPH according to sites and
mechanisms
The possible sites of bleeding include:
Uterine causes
C
Atonic uterus
C
Ruptured uterus
C
Uterine inversion
C
Trauma at caesarean section e.g., extension to angle
of uterine incision
Placental causes
C
Placenta praevia
C
Placenta abruption
C
Retained placenta
Vaginal
C
Lacerations and tears
C
Haematoma
Coagulopathy
C
Pre-existing coagulopathy, e.g., von Willebrands disease
C
Treatment with anticoagulants
C
Obstetric causes e HELLP (haemolysis, elevated liver
enzymes and low platelets), amniotic uid embolism,
chorioamnionitis, placental abruption
C
Consumptive coagulopathy as result of massive blood loss
The mechanisms by which bleeding occur include the 4 Ts:
C
Tone of uterus e abnormalities of uterine contractions
C
Tissue e retained tissue inside the uterus
C
Trauma e lacerations to any part of the genital tract
C
Thrombin e abnormalities of coagulation
Table 2
Management algorithm of PPH HAEMOSTASIS
H Ask for Help and hands on uterus (uterine massage)
A Assess and resuscitate
E Establish aetiology, ensure availability of blood and ecbolics
M Massage uterus
O Oxytocin infusion/prostaglandins e IV/IM/per rectal
S Shift to theatre e aortic pressure or anti-shock
garment/bimanual compression as appropriate
T Tamponade balloon/uterine packing e after exclusion
of tissue and trauma
A Apply compression sutures e B-Lynch/modied
S Systematic pelvic devascularization e uterine/ovarian/
quadruple/internal iliac
I Interventional radiology and, if appropriate uterine artery
embolization
S Subtotal/total abdominal hysterectomy
Table 3
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profuse and ongoing. In view of the low haemoglobin concentra-
tion (3.6 g/dl), uncross-matched O-negative blood was adminis-
tered to restore the oxygen carrying capacity, whilst awaiting
group specic, cross-matched blood. In viewof massive blood loss
and multiple blood transfusions, she received platelets and clot-
ting factors, to offset the effects of dilutional coagulopathy (the
washout phenomenon). The patient was also kept warm.
Shock index (SI) refers to pulse rate divided by systolic blood
pressure and its normal value is 0.5e0.7. In severe haemorrhage,
the SI increases to 0.9e11.1 and it has been reported that a shock
index of >0.9 was associated with a need for intensive therapy
on admission. Our patients pulse rate was 120/min and the
systolic blood pressure was 90 mmHg, with the SI of 1.33.
Indeed, she did require intensive therapy.
Monitoring and investigation
During the initial resuscitation it is essential to record the uid-
response by measuring pulse, blood pressure, respiration rate,
oxygen saturation and uid balance. A urinary catheter will help
with accurate uid balance and also will ensure that a full
bladder will not prevent uterus from contracting. Bed side testing
for haemoglobin may be of use, however, this should not replace
clinical judgement. Repeated FBCs and coagulation screens will
also guide resuscitation. All measurements must be clearly
documented and an intensive care monitoring chart is useful.
Continued communication between team members is an essen-
tial part of evaluating the response to resuscitation and the need
for additional measures such as arterial and central venous
pressure lines.
Arresting of bleeding
Managing the cause of bleeding requires a methodological
approach to exclude the potential causes, which have been
already described. Although uterine atony accounts for 80% of
PPH, careful clinical examination should be carried out to
exclude other or additional causes such as retained placenta or
products of conception, vaginal or cervical lacerations or hae-
matoma, ruptured uterus, uterine inversion, broad ligament
haematoma and rarely, bleeding from outside the genital tract
such as ruptured liver or splenic artery aneurysm.
In massive PPH, early transfer to theatre should be considered
as additional measures may be required to arrest bleeding.
During examination, if a uterus is found to be atonic, bimanual
compression may be used to control bleeding whilst oxytocic
agents are administered. Consent should be taken for examina-
tion under anaesthesia with proceed to laparotomy and addi-
tional life saving measures such as uterine artery embolization
and hysterectomy. It may not be always possible to obtain
a written consent in such an emergency. If verbal consent is also
not possible, it is good practice to keep the immediate family
informed of the clinical situation.
Key aspects of the management of massive PPH
Blood and blood products
In massive PPH, blood transfusion is essential to replace volume
and oxygen carrying capacity and blood products replace clotting
factors, brinogen and platelets. Guidelines from the British
Committee for Standards in Haematology summarize the main
therapeutic aims of management of massive blood loss, which
are to maintain the following levels:
Haemoglobin > 8 g/dl
Platelet count > 75 10
9
/l
Prothrombin time < 1.5 mean control
Activated prothrombin time < 1.5 mean control
Fibrinogen > 1.0 g/l
Blood
Concentrated red blood cells (RBC) are the rst line of therapy in
massive PPH. Each unit of RBC will increase the haemoglobin by
1 g/dl and the haematocrit by 3%. All blood is screened for
infectious diseases and as a result of storage contains depleted
number of platelets and clotting factors. It is appropriate to
replace uids with crystalloid and colloid up to 3.5 l in which
time cross-matched blood should be available. The decision to
commence transfusion of blood should be a clinical decision and
it is not necessary to wait for results of FBC.
Management of coagulopathy
The management of a coagulopathy requires effective commu-
nication with the haematologist who will advise on the use of
clotting factors. Ideally, coagulopathy should be prevented by
anticipating depletion in clotting factors and transfusing appro-
priately. It is not necessary to wait for laboratory clotting results
if a developing coagulopathy is suspected. A prothrombin time
(PT) and APTT ratios of >1.5 are associated with an increased
risk of a clinical coagulopathy; in the presence of ongoing
bleeding this requires correction with FFP. Disseminated intra-
vascular coagulation (DIC) is a type of coagulopathy character-
ized by widespread intravascular activation of the coagulation
system leading to vascular deposition of brin and a consump-
tion of clotting factors. It is associated with certain obstetric
complications including amniotic uid embolization, placental
abruption and severe chorioamnionitis. It may also be triggered
by massive blood loss.
Fresh frozen plasma
Fresh frozen plasma (FFP) is derived from whole blood and
contains clotting factors. It is stored at 30

to prevent the
clotting factors from decaying and needs to be defrosted thor-
oughly prior to administration.
Cryoprecipitate
Cryoprecipitate contains more brinogen than FFP and is useful
in correcting hypobrinogenaemia.
Platelet infusions
Platelet infusions are derived from the whole blood of donors and
can be stored for up to 5 days at room temperature. Platelet
infusions are seldom required if platelets are above 50 10
9
/l
but may be required in these circumstances if surgical interven-
tion is anticipated. Each pool of platelets contains 4e6 units of
platelets which should produce an increment of 50 10/l in the
average size patient.
Other coagulation factors
Recombinant Factor VIIa (rFVIIa) is the activated form of Factor
VII made in hamster kidney cells. It is licensed for use in patients
with haemophilia. It is not licensed for use in massive PPH and
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there are no randomized controlled trials on its use in post-
partum haemorrhage. Most of the data comes from case reports
and therefore requires cautious interpretation as there may be
bias towards only reporting successfully managed cases. One
review of 65 case studies of women in whom rFVIIa was used in
massive haemorrhage showed it to be effective in PPH, however,
the review highlighted the lack of good data. There is a need for
further evaluation of its use and the appropriate dose as well as
the costebenet ratio. Efcacy may be affected by haemodilution
and some studies show that adequate levels of brinogen and
platelets are needed for it to be effective. The RCOG guidelines
on PPH suggest a dose of 90 mg/kg which may be repeated in
the absence of a clinical response in 15e30 min. In this case, the
possible use of activated Factor VII was discussed with the
Consultant Haematologist and it was felt that the risks (thrombo-
embolic complications, myocardial infarction and ischaemic
stroke) would outweigh the benets.
Medical management
Medical management is the mainstay of treatment for uterine
atony. Active management of the third stage of labour has been
proven to reduce the risk of PPH. The following agents are
appropriate for use:
Syntocinon 5 units by slow intravenous injection e this may
be repeated
Ergometrine 0.5 mg by slow intravenous injection or intra-
muscular injection (contraindicated in women with
hypertension)
Syntocinon infusion of 40 units in 500 ml Hartmanns solu-
tion at 125 ml/h
Carboprost 0.25 mg by intramuscular injection which may be
repeated at 15 min intervals to a maximum on eight doses
(contraindicated in asthmatics). Carboprost may also be
given intramyometrially, however, it is not licensed to be
given by this route
Misoprostol 800e1000 mg rectally
Our patient initially received ergometrine and syntocinon infu-
sion. However, the aetiology of PPH was due to genital tract
trauma and the uterus well contracted. Hence, she did not
require intramuscular or rectal prostaglandins.
Surgical management
Failure to control bleeding with medical treatment or if surgical
causes (retained products, uterine or genital tract trauma) are
suspected, should prompt the patient to be transferred to the
theatre. Bimanual compression of the uterus may be appropriate
prior to full examination under anaesthesia (EUA) to allow the
replacement of uids, blood and blood products. EUA should
include a thorough and systematic examination of the genital
tract including the uterus, cervix and vagina. The uterus must be
examined to exclude retained products, uterine inversion or
rupture. The cervix and vaginal walls be closely inspected for
lacerations and haematomas. The abdomen must also be exam-
ined for signs of increasing distension suggesting intra-
abdominal bleeding. Similarly, massive PPH at the time of
caesarean section must involve identication of bleeding vessels,
particularly if there is extension to the angles of the uterine
incision.
Surgical management of massive PPH will depend on the
underlying cause. Balloon tamponade of the uterus has been
proven to be an effective measure. Available balloons include
gastric balloon of the SengstakeneBlakemore tube or Rusch
balloon which may be inserted into the uterine cavity and lled
with 200e600 ml of warm water or saline depending on the size
of the uterine cavity. In earlier gestations it may be appropriate to
use a Foley catheter balloon. Overall the reported success rates
are between 70 and 100%. If bleeding is arrested, 80e85% of
cases, the patient will not require laparotomy. Hence, this
Tamponade Test may be very useful in determining the indi-
cation for a laparotomy. There are no reported complications in
either the short or long-term with the use of uterine balloons and
they may be removed after 6e12 h, or earlier, if the coagulopathy
has been corrected.
Other steps in initial surgical management may be to repair
cervical or vaginal lacerations. Tamponade may also be appro-
priate for arresting bleeding from multiple vaginal lacerations
and may involve the use of a balloon or vaginal pack, as in this
case.
Should these techniques fail, it is appropriate to proceed to
laparotomy through a Pfannenstiel incision (a midline incision
may be required if upper abdominal pathology such as rupture of
the liver is suspected). The most experienced obstetrician should
be present and the availability of an experienced gynaecological
surgeon is desirable, if measures such as internal iliac artery
ligation are contemplated. Direct aortic compression may be
useful reduce bleeding, while coagulation parameters are cor-
rected. If the cause of PPH is uterine atony, compression sutures
such as B-lynch suture or modied compression sutures (vertical
or horizontal) may be attempted. Data from the Scottish Con-
dential Audit of Severe Maternal Morbidity identied 52 cases
where the haemostatic brace suture was used in cases of massive
PPH with 81% of these women avoiding hysterectomy.
Complications of compression sutures include erosion of the
sutures through the uterus, uterine necrosis, pyometria and
uterine adhesions.
Other surgical techniques include systematic pelvic devascu-
larization (ligation of the uterine arteries, ovarian arteries and or
internal iliac arteries). The simplest ligation is uterine artery
ligation which is useful if the bleeding is coming from the body of
the uterus but not if the source of haemorrhage is the lower
uterine segment, cervix or vagina. Ligation of the internal iliac
arteries is a more complex procedure which will also arrest
bleeding from the lower uterine segment, broad ligament and
vagina. It requires a surgeon who is familiar with the anatomy of
the pelvic side wall to ensure the ureters and other major vessels
are not damaged. Success rates have been quoted as between 40
and 100%.
If the above surgical techniques fail or are not appropriate to
perform, the options are to proceed to hysterectomy or if the
patients condition is not immediately life threatening, or to
consider the use of interventional radiology as discussed below.
The decision to proceed to hysterectomy is ideally made by two
senior clinicians. If possible and appropriate, it may be benecial
to involve the womens partner in this decision. Early recourse to
hysterectomy is recommended in cases of massive PPH resulting
from placenta accreta and ruptured uterus. Subtotal hysterec-
tomy is the most suitable option, unless there is trauma to the
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cervix or lower segment. It is desirable that an appropriately
experienced gynaecological surgeon should be present during
a peripartum hysterectomy as complications include bladder
damage, ureteric damage, ovarian damage which may necessi-
tate an oophorectomy, infection as well as long-term psycho-
logical consequences of loss of femininity and fertility. Following
hysterectomy and correction of coagulopathy there may be
persistent ooze from small pelvic vessels which may require
temporary abdominal packing.
Data published by UK Obstetric Surveillance System (UKOSS)
looked at the management of all women in UK who underwent
hysterectomy between February 2006 and February 2007. A total
of 318 women had peripartum hysterectomy most commonly
secondary to uterine atony (53%) and morbidly adherent placenta
(39%). The case fatality rate was 0.6% with two women dying.
The study also highlighted the consequences of peripartum
hysterectomy with 20% of women suffering damage to other
structures, 20% requiring further surgery to control bleeding and
nearly 20% reporting additional signicant morbidity. The study
also highlighted that massive obstetric haemorrhage was managed
in a variety of ways and not always following existing guidelines. It
concluded, however, that for each woman who dies in the UK
following peripartum hysterectomy, 150 women survived.
Interventional radiology
The use of an angiographic approach to PPH has evolved over
the last 30 years. In addition to a high success rate, it also
improves the likelihood of preserving fertility. The procedure is
performed by an interventional radiologist; the anterior division
of the internal iliac artery is catheterized via the femoral
approach under uoroscopic guidance, allowing access to the
uterine and vaginal arteries. It may be performed prophylacti-
cally in cases of anticipated haemorrhage, for example suspected
placenta accreta in patient with previous caesarean section scar.
Such prophylactic uterine artery balloon placement allows
immediate ination of balloons after delivery to provide
a temporary occlusion. Should occlusion be required for a period
longer than 12 h it is recommended to perform embolization.
Prior to embolization in massive PPH, the patient must be hae-
modynamically stable enough to be transferred to the radiology
department. Such a decision must be undertaken by the senior
obstetrician and anaesthetist, after discussion with the on-call
interventional radiologist. In our patient, balloon tamponade
and vaginal packing was carried out to control the bleeding and
the patient was made haemodynamically stable, prior to embo-
lization. Embolization of uterine or vaginal arteries can be per-
formed if the source of bleeding can be identied. If this is not
possible, empiric embolization of the anterior division of the
internal iliac artery may be performed. A gelatin sponge is the
preferred agent as it causes temporary arterial occlusion for
approximately 3 weeks. Bilateral embolization is usually per-
formed. Despite interventional radiology emerging as a treatment
for massive PPH there are no randomized controlled trials. The
best available data come from a review of summarized case
series which reported a 97% success rate with selective arterial
embolization. Other data suggest a 70e100% success rate for
cases of persistent atony. There are risks involved with emboli-
zation including gluteal claudication, possible reduction in future
fertility and rarely sepsis and femoral artery occlusion, in addi-
tion to the failure to control bleeding necessitating hysterectomy.
Post PPH management
Our patient was transferred to the intensive treatment unit (ITU)
to ensure multi-organ support and continued observation for
bleeding, to assess response to treatment and recovery (full
blood count, coagulation prole, renal and liver function tests),
as well as for prophylaxis against thrombo-embolism. She made
a good recovery and the tamponade balloon and the emboliza-
tion catheters were removed once haemostasis was achieved.
Midwifery support for bonding with baby and for establishment
of breast feeding was provided on a daily basis. The patient and
her family were fully debriefed and were offered psychological
support. Advice on the management of future pregnancies was
also given and the patient was offered a postnatal appointment.
Risk management issues
Massive PPH is an obstetric emergency which is associated with
increased maternal morbidity and mortality. Clear and appro-
priate documentation and a root cause analysis through the risk
management process are essential to learn lessons and to improve
clinical care. This case was declared as a Serious Untoward Inci-
dent (SUI), as per the criteria of NHS London and was fully
investigated. The SUI Panel felt that the case was very well
managed with clear communication, and with multi-disciplinary
input involving senior clinicians (including three consultant
obstetricians). These ndings were disseminated to all the
members of the team through the Joint Clinical Governance Day.
Conclusion
Massive PPH is an obstetric emergency that is associated with
increased maternal morbidity and mortality. In some cases it may
be anticipated and measures could be taken to prevent it.
However, it is often unpredictable and will require rapid mobi-
lization of a multi-disciplinary team with senior input to ensure
optimum management. The aims of management are to resus-
citate the patient, stop further bleeding and replace blood and
clotting factors. The use of locally agreed guidelines will support
this process. Our patient had a traumatic postpartum haemor-
rhage which resulted in over 8 l of blood loss. She was aggres-
sively resuscitated and had a multi-disciplinary management that
ensured a good outcome with retention of fertility. Regular
departmental simulated training with drills for massive PPH
followed by appropriate debrieng will optimize practice. A
FURTHER READING
Baskett T, Clader A, Arulkumaran S. Munro Kerrs operative obstetrics.
11th edn. Saunders Elsevier, 2007.
Brace V, Kernaghan D, Penney G. Learning from adverse clinical outcomes:
major obstetric haemorrhage in Scotland, 2003e2005. BJOG 2007;
114: 1388e96.
British Committee for Standards in Haematology, Stainsby D,
MacLennan S, Thomas D, Isaac J, Hamilton PJ. Guidelines on
management of massive blood loss. London: British Society of
Haematology, 2008.
REVIEW
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 20:6 179 2010 Elsevier Ltd. All rights reserved.
Chandraharan E, Arulkumaran S. Management algorithm for atonic post-
partum haemorrhage. J Paediatr Obstet Gynaecol; June 2005: 106e12.
Chandraharan E, Arulkumaran S. Massive postpartum haemorrhage and
management of coagulopathy. Obstet Gynaecol Reprod Med 2007 Apr;
17: 119e22.
Chandraharan E, Arulkumaran S. Surgical aspects of postpartum
haemorrhage (review article). Best Pract Res Clin Obstet Gynaecol
2008 Dec; 22: 1089e102.
Condous GS, ArulkumaranS, Symonds I, et al. Thetamponadetest for massive
postpartum haemorrhage. Obstet Gynecol 2003 Apr; 104: 767e72.
Dildy GA. Postpartum haemorrhage: new management options.
Clin Obstet Gynaecol 2002; 45: 330e44.
Knight M, on behalf of UKOSS. Peripartum hysterectomy in the UK:
management and outcomes of the associated haemorrhage. BJOG
2007 Nov; 114(11): 1380e7.
Lefkou E, Hunt B. Haematological management of obstetric haemorrhage.
Obstet Gynaecol Reprod Med 2008 Aug; 18: 217e23.
The Condential Enquiry into Maternal and Child Health (CEMACH). Saving
mothers lives: reviewing maternal deaths to make motherhood safer e
2003e2005. In: Lewis G, ed. Theseventhreport oncondential enquiries
into maternal deaths in United Kingdom. London: CEMACH, 2007.
Managing obstetric emergencies and trauma. 2nd edn. RCOG Press, 2007.
Mukerjee S, Arulkumaran S. Post partum haemorrhage. Obstet Gynaecol
Reprod Med 2009 May; 19: 121e6.
RCOG Guidelines. Prevention and management of postpartum
haemorrhage. Green-top Guideline No. 52, May 2009.
Searle E, Pavord S, Alrevic Z. Recombinant factor VIIa and other
pro-haemostatic therapies in primary postpartum haemorrhage. Best
Pract Res Clin Obstet Gynaecol 2008; 22: 1075e88.
Winograd RH. Uterine artery embolization for postpartum haemorrhage.
Best Pract Res Clin Obstet Gynaecol 2008; 22: 1119e32.
USEFUL WEBSITES
British Committee for Standards in Haematologym, www.bcshguidelines.
com
UKOSS, www.npeu.ox.ac.uk
Practice points
C
Massive PPH is associated with increase in maternal morbidity
and mortality and hence a multi-disciplinary approach is
essential.
C
Underlying causes of massive PPH include uterine atony,
retained placental tissues and membranes, genital tract
trauma and coagulopathy.
C
Shock index (pulse rate divided by systolic blood pressure)
may give an indication regarding the need for immediate
resuscitation.
C
Coagulopathy may result from washout phenomenon and
requires replacement of platelets and clotting factors.
C
Interventional radiology may be considered, if the patient is
haemodynamically stable.
REVIEW
OBSTETRICS, GYNAECOLOGY AND REPRODUCTIVE MEDICINE 20:6 180 2010 Elsevier Ltd. All rights reserved.

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