Massive obstetric haemorrhage is a major contributor towards maternal morbidity and mortality. The main causes are abruptio placentae, placenta praevia and postpartum haemorrhage. Clinicians managing pregnant women should be equipped with the knowledge and skills for managing massive obstetric haemorrhage to institute timely and appropriate life-saving treatment. Prompt resuscitation and reversal of coagulopathy are critical while definitive measures are carried out to arrest the bleeding. Massive antepartum haemorrhage necessitates deliveries whereas interventions for postpartum haemorrhage range from medical to surgical measures. Algorithms such as haemostasis are useful aids to the systematic and stepwise management of postpartum haemorrhage. Surgical measures used to avoid peripartum haemorrhage include uterine compression sutures, uterine balloon tamponade, uterine artery, and internal iliac artery ligation. Tranexamic acid and recombinant factor VII are more recent medical interventions in massive postpartum haemorrhage. Education, regular drills and adherence to guidelines and protocols are important to reduce haemorrhage-related maternal deaths.
Introduction
Postpartum haemorrhage (PPH) continues to remain one of the leading causes of global maternal morbidity and mortality, especially in developing countries but also in developed countries. It is the most common single cause of maternal death in the developing countries, with an estimated 125,000 deaths every year, leading to one maternal death every 7 mins. Although the decreasing trend of obstetric haemorrhage during the 2006–2008 triennium in the UK is encouraging, sub-standard care was a factor in 66% of the deaths caused by obstetric haemorrhage in this latest triennium. More than one-half of these obstetric haemorrhage related deaths were, therefore, potentially preventable according to the two latest confidential enquires into maternal deaths in the UK. Uterine atony, placenta accreta and failure of routine postpartum observation and recognition of bleeding were the main reasons accounting for the substandard care. Clinicians managing pregnant women should be equipped with the knowledge and skills for managing obstetric haemorrhage to ensure institution of timely and appropriate life-saving treatment. This is particularly crucial in the current setting, as the incidence of massive PPH has been observed to increase as a result of factors such as increasing caesarean section rates leading to higher rates of placenta praevia and placenta accreta.
Definition
The Healthcare Commission defined ‘significant’ blood loss as greater than 1000 ml and ‘major’ blood loss as greater than 2500 ml in its recent review of maternity services in England and Wales. The Scottish Confidential Audit of Severe Maternal Morbidity (SCASMM) considered major haemorrhage to be blood loss of greater than 2500 ml, or transfusion of five or more units of blood or treatment for coagulopathy. Massive obstetric haemorrhage is therefore often based on the definition of greater than 2500 ml of blood loss (or more than 30% of blood volume). As underestimation of blood loss is almost invariable, however, additional resources should be mobilised if blood loss exceeds 1000 ml. This obstetric emergency requires immediate steps to arrest the bleeding, as well as a multidisciplinary approach to restore volume, reverse coagulopathy and improve oxygen-carrying capacity of the blood.
Massive obstetric haemorrhage contributes towards fetal and maternal mortality and also leads to short-term and long-term complications. Intrauterine fetal death, hypoxic ischaemic encephalopathy and cerebral palsy are the most severe fetal and neonatal complications. Immediate maternal implications include the need for operative interventions, such as caesarean section, peripartum hysterectomy and risks associated with blood transfusions. As massive haemorrhage leads to multi-organ failure, and complications include acute renal failure, pulmonary oedema and coagulopathy. Disseminated intravascular coagulopathy occurs as a result of active consumption of clotting factors or as a result of the dilutional effects of massive blood loss on clotting factors, platelets and fibrinogen (‘washout phenomenon’). Long-term maternal implications include issues with future fertility, Sheehan’s syndrome and psychological sequelae.
Definition
The Healthcare Commission defined ‘significant’ blood loss as greater than 1000 ml and ‘major’ blood loss as greater than 2500 ml in its recent review of maternity services in England and Wales. The Scottish Confidential Audit of Severe Maternal Morbidity (SCASMM) considered major haemorrhage to be blood loss of greater than 2500 ml, or transfusion of five or more units of blood or treatment for coagulopathy. Massive obstetric haemorrhage is therefore often based on the definition of greater than 2500 ml of blood loss (or more than 30% of blood volume). As underestimation of blood loss is almost invariable, however, additional resources should be mobilised if blood loss exceeds 1000 ml. This obstetric emergency requires immediate steps to arrest the bleeding, as well as a multidisciplinary approach to restore volume, reverse coagulopathy and improve oxygen-carrying capacity of the blood.
Massive obstetric haemorrhage contributes towards fetal and maternal mortality and also leads to short-term and long-term complications. Intrauterine fetal death, hypoxic ischaemic encephalopathy and cerebral palsy are the most severe fetal and neonatal complications. Immediate maternal implications include the need for operative interventions, such as caesarean section, peripartum hysterectomy and risks associated with blood transfusions. As massive haemorrhage leads to multi-organ failure, and complications include acute renal failure, pulmonary oedema and coagulopathy. Disseminated intravascular coagulopathy occurs as a result of active consumption of clotting factors or as a result of the dilutional effects of massive blood loss on clotting factors, platelets and fibrinogen (‘washout phenomenon’). Long-term maternal implications include issues with future fertility, Sheehan’s syndrome and psychological sequelae.
Aetiology
Antepartum haemorrhage
The two main causes of massive antepartum haemorrhage are placenta praevia and abruptio placentae. Placenta praevia occurs when the placenta is implanted over the lower uterine segment, leading to massive haemorrhage during the antepartum period or at the time of caesarean delivery. A morbidly adherent placenta includes placenta accreta, increta and percreta as it penetrates through the deciduas basalis into and then through the myometrium. One of the major changes in 21st-century obstetric practice has been rising caesarean section rates. The incidence of vaginal births after caesarean section has dropped from nearly 30% in 1996 to single-figure percentages in the USA. This suggests that some obstetricians have taken the ‘once a caesarean section, always a caesarean section’ view. This invariably increases the incidence of placenta praevia and abnormal placentation. In the largest study with over 30,000 women, the women with placenta accreta increased from 0.24% with no previous caesarean section to 2.13% with three previous caesarean deliveries. With the diagnosis of placenta praevia, the chance of placenta accreta is increased more than 20-fold after three previous caesarean sections. Abnormal placentation significantly increases the risk of obstetric haemorrhage, leading to significant morbidity, including peripartum hysterectomy.
Abruptio placenta is an obstetric emergency typically associated with massive haemorrhage, with high perinatal and maternal morbidity and mortality. The premature detachment of the placenta leads to extravasation of blood into the uterine musculature, resulting in couvelaire uterus. Mechanisms of haemorrhage in this condition include uterine atony and disseminated intravascular coagulopathy.
Postpartum haemorrhage
The traditional pneumonics ‘4Ts: tone, tissues, trauma and thrombin’ can be used to remember the potential causes. Masssive PPH may be caused by one or more causes and PPH from any cause will result in coagulopathy.
Tone
Uterine atony and failure of contraction and retraction of myometrial muscle fibres can lead to rapid and severe haemorrhage and hypovolemic shock. Risk factors for uterine atony could be divided into antenatal (e.g. uterine overdistension related to multiple pregnancy, polyhydramnios and fetal macrosomia) or intrapartum (e.g. precipitous labour, prolonged labour, augmentation of labour with oxytocin and placenta abruptio).
Tissue
Retained products of conception are more common after vaginal delivery. Bleeding from placenta praevia or placenta accrete, however, is often encountered during caesarean delivery. Placenta accreta should be suspected if the placenta does not separate readily, and vigilance should be exercised in women with placenta praevia who have had a previous caesarean section, even if it is not reported on antenatal ultrasounds.
Trauma
Trauma-related bleeding can be caused by lacerations of genital tract or uterine rupture. Apex of episiotomy or vaginal wall lacerations could be missed, resulting in persistent bleeding. Risk factors for significant cervical lacerations include precipitous labour, operative vaginal delivery and cerclage. Uterine rupture is often characterised by abdominal pain and persistent vaginal bleeding, despite the use of uterotonic agents. Although it is more common in the scarred uterus, rupture of an unscarred uterus can occur, particularly in multiparous women and if the labour is induced or augmented. The diagnosis should be considered if the woman has evidence of hypovolaemic shock, which is out of proportion to the amount of blood loss or if there is abdominal distension. For trauma that occurs at the time of caesarean delivery, bleeding is likely to be related to lateral extension of the incision. Cervical and vaginal lacerations, however, can occur when the operator attempts to dislodge a deeply engaged head during caesarean delivery.
Thrombin
Abnormalities of coagulation leads to massive PPH. Acquired causes for coagulopathy include severe pre-eclampsia, haemolysis, elevated liver enzymes and low platelets syndrome, abruptio placenta, fetal demise, amniotic fluid embolism and sepsis. Masssive PPH from any cause can lead to consumptive coagulopathy.
Management
In view of the potential rapid deterioration of massive haemorrhage, familiarisation and adherence to protocols and standard operating procedures are essential to maximise patient management. Development of a standardised institutional approach to managing massive obstetric haemorrhage is known to improve outcome. A management algorithm – ‘haemostasis’ has been proposed, which allows stepwise management of atonic PPH. A summary of the medical treatment and surgical interventions for massive PPH is shown in Fig. 1 .
Estimation of blood loss
Accurate visual estimation of blood loss is critical to activate the system to alert the multidisplinary team and to facilitate timely resuscitation. Participation in clinical reconstructions, as well as written and pictorial guidelines, allows early recognition of massive PPH.
Call for help
With massive haemorrhage, effective and clear communication with multidisciplinary team members is essential to improve patient outcome. Besides obstetricians, the personnel involved include senior anaesthetists, experienced midwives, consultant haematologists, blood transfusion laboratory staff, and porters for transporting specimens and blood. Interventional radiologists should be informed whenever necessary. The prevalence rate of peripartum intensive-care-unit admissions has been reported to be 0.4–0.6%, with the leading cause being haemorrhage. The full scope of intensive-care-unit resources should be available to the woman, as the maternal requirement for such care is not rare. Co-ordination can be facilitated by protocols and flow diagrams. Activation of ‘Code Blue’ or ‘Code Crimson’ allows various team members to be alerted early, and helps in organising the roles of physician, nurses and support staff to prioritise medical care and effectively manage resources.
Resuscitation
Early recognition and prompt resuscitation are essential in managing massive obstetric haemorrhage. Maternity early warning scoring systems has been recommended by The Confidential Enquiries into Maternal and Child Health to exercise vigilance to allow early recognition of bleeding or physiological derangement. The principal aims of resuscitation are to restore intravascular volume, maximise oxygen-carrying capacity and reverse coagulopathy. The basic ABC approach should be used as problems are being identified: (1) airway: carry out airway assessment to ensure the patency; (2) breathing: assess breathing adequacy and provide supplementation with 100% oxygen as needed; (3) circulation: assess circulatory status by continuously monitoring blood pressure, pulse rate, volume of peripheral pulses. Establish intravenous access with two large-bore cannulas for fluids, blood products and medications; (4) blood investigations should include full blood count and coagulation studies (prothrombin time, activated partial thromboplastin time, fibrinogen concentration). Women should be cross-matched for blood and other products such as fresh frozen plasma, platelets, and cryoprecipitate should be ordered; (5) Foley catheter: urine output should be maintained at greater than 30 ml/h.
Fluid resuscitation in massive haemorrhage is often conservative because of underestimation of blood loss and the rapid speed of blood loss. Clinical symptoms and signs of hypovolaemic shock include tachycardia, hypotension, tachypnoea, poor peripheral perfusion, confusion or unresponsiveness. These signs, however, are often delayed because of the compensatory mechanisms in these women who are young, fit and healthy. A loss of 1 L of blood requires replacement with 4–5 L of crystalloid (0.9% normal saline or lactated Ringer’s solution) or colloids until cross-matched blood is made available as a result of the shifting of intravenous fluid from the intravascular to the interstitial space. Failure to maintain optimal haematocrit during the acute event was associated with end organ dysfunction.
A ‘rule of 30’ has been proposed to monitor women with haemorrhage. If the systolic blood pressure falls by 30 mmHg, pulse rate rises by 30 beats/min, respiratory rate increases to more than 30 breaths/min and her haemoglobin or haematocrit drops by more than 30%, then the woman is likely to have lost at least 30% of her blood volume, and is in moderate shock leading to severe shock. The use of ‘shock index’ is invaluable in monitoring and managing women with PPH. It refers to heart rate divided by the systolic blood pressure. The normal value is 0.5–0.7. With significant haemorrhage, it increases to 0.9–1.1. A shock index of over 0.9 is associated with a need for intensive therapy on admission. The change in shock index of an individual woman seems to correlate better in the identification of early acute blood loss than other parameters, such as heart rate and blood pressure taken in isolation.
Arrest the bleeding
Delivery is indicated for massive antepartum haemorrhage. The mode of delivery should be caesarean section for placenta praevia, whereas placenta abruptio often results in rapid vaginal delivery.
For PPH, various methods are available to stop the bleeding. These range from pharmacological methods to aid uterine contraction to surgical interventions to stem the bleeding. Simple mechanical and physiological measures of uterine massage to stimulate uterine contraction are the first-line management of PPH. The bladder should be catheterised as a full bladder may interfere with uterine contraction. Massage should be maintained while other interventions are being initiated. The Royal College of Obstetricians and Gynaecologists have suggested that a non-pneumatic antishock garment may be useful in the UK for women with PPH who require transfer from midwife-led to consultant-led units. Use of an antishock garment may also be helpful in low-resource settings where there may be a delay in reaching emergency obstetrical care facilities, for reversing hypovolaemic shock and decreasing obstetric haemorrhage.
The medical team should initiate a sequence of non-operative and operative interventions for control of PPH. The obstetrician should promptly assess the success or failure of each measure. If an intervention does not succeed, the next treatment in the sequence must be swiftly instituted, to avoid unnecessary delay and arrest the woman from the morbidity and mortality of haemorrhagic shock.
The approach to treatment of PPH differs depending on the cause and whether haemorrhage occurs after a vaginal birth or after a caesarean delivery. After a vaginal birth, treatment begins with less invasive interventions and progresses to more invasive procedures until haemorrhage is controlled. The initial aim is to avoid laparotomy and its associated morbidity. By comparison, surgical inventions are more readily used with massive PPH after caesarean delivery. The likely causes also vary by the route of birth with retained products of conception more likely after a vaginal birth, but placenta praevia and accrete seen only after caesarean delivery.
Medical intervention
Active management of the third stage of labour has been proven to prevent and treat PPH. The following are the agents which are appropriate for use: (1) syntocinon 5 units can be given by slow intravenous injection and this may be repeated. Syntocinon can be given as an infusion of 40 units in 500 ml of Hartmann’s solution at 125 ml per h; (2) ergometrine 0.25 mg by slow intravenous injection or intramuscular injection can be added. Syntometrine (5 units of syntocinon and 0.5 mg of ergometrine) is another option. These are contraindicated in women with hypertension; (3) prostaglandin F2 alpha 0.25 mg can be given intramuscularly and can be repeated at 15-min intervals to a maximum of eight doses. It is contraindicated in women with asthma. The licensed route of administration is intramuscular, although intramyometrial route has been used; (4) misoprostol, a prostaglandin E1 analogue, has been used in several trials with good success in controlling PPH in cases refractory to oxytocin. A meta-analysis of the randomized-controlled trials showed that misoprostol significantly reduced the primary outcome of PPH (relative risk 0.57; 95% confidence interval 0.34 to 0.96). Another systematic review, however, concluded that the beneficial effects from addition of misoprostol to standard uterotonic treatment were insufficient. Where oxytocin use is not feasible, misoprostol is certainly a suitable alternative treatment for PPH ; and (5) carbetocin is a long-acting synthetic octapeptide analogue of oxytocin with agonist properties. It has been shown to reduce the need for additional oxytocics compared with syntocinon in women who undergo caesarean deliveries, and is similar in efficacy to syntometrine for preventing postpartum haemorrhage. Carbetocin is licensed for the indication of PPH prevention after caesarean deliveries. Further research into its use in the treatment of PPH allows another uterotonic agent to be explored.
Some clinicians prefer to use one medication over the others. There is no evidence that one sequence is better than another. The important point is not the sequence of drugs, but the prompt initiation of uterotonic therapy and the prompt assessment of its effect. Although medical intervention is often adequate in cases of PPH, the efficacy is lower with massive PPH. In the study by O’Brien et al., haemostatis was achieved with medical treatment in 15% of cases, whereas hydrostatic balloon and the B-Lynch suture arrested bleeding in 75% and 40% of cases.
Surgical management of postpartum haemorrhage
In massive PPH, early transfer of the woman to the operating theatre should be considered. Adequate assistance, exposure, lighting, instruments and anaesthesia are necessary to conduct a thorough examination. Consent should be taken from the woman or immediate family members for examination under anaesthesia, with the possibility of proceeding to laparotomy and additional life-saving measures, such as uterine artery ligation and hysterectomy.
Several techniques have been pioneered to avoid peripartum hysterectomy, including balloon tamponade, uterine compression suture, uterine artery embolisation and internal iliac artery ligation. The reported success rates for these techniques differ. These techniques were shown to be equally effective in controlling PPH, with the success rate being 84% for balloon tamponade, 90.7% for arterial embolisation, 91.7% for compression sutures and 84.6% for uterine or internal iliac artery ligation. A recent national cohort study looked at the specific second-line treatments for PPH; the first-line surgical intervention was uterine balloon tamponade. The study showed that uterine compression sutures and interventional radiological techniques have higher success rates than recombinant factor VIIa and pelvic vessel ligation. The cases managed with recombinant factor VIIa and pelvic vessel ligation, however, were more clinically complex. In deciding the surgical intervention, consideration should also be given to the experience and the skill of the operator, as well as familiarity with the chosen surgical procedure.
Examination under anaesthesia
If bleeding persists despite a firm, well-controlled uterus, the source of bleeding is likely to be from lacerations or retained products of conception. Examination under anaesthesia should be carried out to assess the genital tract and to explore the uterus. An assistant should use right angle retractors to optimise exposure. In cases in which it is difficult to visualise the apex of the laceration to begin suturing, the clinician can begin the suture line at the more distal end of the laceration first and sew toward the apex, while using the suture to pull the lacerated tissue toward the surgeon. One should avoid placing sutures cephalad to the fornix, as this can result in ureteral ligation. The cervix should be explored in a ‘circumferential approach’, using two round or ovum forceps moved sequentially in a clockwise direction, to allow visualisation of the entire lip of the cervix.
If the massive PPH is encountered at the time of caesarean delivery, bleeding from the incision can generally be controlled by suture ligation. Clear visualisation of the angles of the incision allows better haemostasis to be obtained. Care should be taken to identify the ureter to avoid any ureteric injuries.
Uterine tamponade
Successful use of uterine balloon tamponade has been reported using a number of devices, including Bakri balloon ( Fig. 2 ), Rusch urological hydrostatic balloon and the Sengstaken–Blakemore oesophageal catheter. Uterine tamponade works by exerting a counter pressure on the uterine cavity, reducing capillary and venous bleeding from the endometrium. This also creates a window of opportunity to allow correction of coagulopathy by replacement of blood products. The balloon could be inflated with 200–600 ml of warm sterile water or saline, depending on the size of the uterine cavity. After vaginal deliveries, uterine tamponade also serves as a ‘tamponade test’, which allows the obstetrician to identify women requiring the laparotomy. The tamponade test is positive if the uterine bleeding stops with uterine tamponade, indicating that the woman does not require a laparotomy. The advantages of this method include (1) easy and rapid insertion with minimal anaesthesia; (2) ease of removal and (3) rapid identification of failed cases.
