EXPLORE PAST ISSUES
Maternal Death
Vol. 15 No 1 | Autumn 2013
Feature
Postpartum haemorrhage


This article is 7 years old and may no longer reflect current clinical practice.

A typographical error in lecture notes that described postpartum haemorrhage as ‘one of the moist testing situations for the labour ward team’ has since seemed to me a very appropriate summary of postpartum haemorrhage.

Globally, it is estimated that half a million women die annually from causes related to pregnancy and childbirth and that half of these deaths are related to obstetric haemorrhage. The risk of death from obstetric haemorrhage in Australasia and the UK is rare, and has declined in the UK over the past two triennia from rates of 0.85/100 000 to 0.39/100 000. Unfortunately, surveys have shown more than two-thirds of cases of severe maternal morbidity, or near misses, are attributable to haemorrhage and the incidence of major obstetric haemorrhage seems to be increasing. Furthermore, substandard care was cited as a major contributor to the nine deaths in the UK from haemorrhage in the most recent Centre for Maternal and Child Enquiries (CMACE) report.1,1a,19

WHO defines primary postpartum haemorrhage (PPH) as genital tract blood loss greater than or equal to 500ml within 24 hours after birth, while secondary PPH occurs from 24 hours to 12 weeks postpartum.2 This is a very arbitrary definition that fails to take into account the subjective nature and inaccuracy of visual estimations of blood loss. It fails to acknowledge differences in losses between vaginal and caesarean birth or that losses of this magnitude rarely compromise maternal wellbeing in our population, although this is dependent on pre-existing medical conditions. Perhaps a more clinically relevant (separate from data-collection requirements and audit) definition is blood loss that causes haemodynamic instability (even if loss is less than 500ml), is in excess of 1000ml or necessitates red cell transfusion.3,6,7,9,10,13

So what makes a difference to outcome in PPH?

Table 1. Risk factors PPH

Antenatal Intra/peripartum
Polyhydramnios
Multiple pregnancy
Fibroids
Past PPH
Previous retained placenta
Previous Caesarean Section/uterine surgery
Placenta praevia/percreta/increta
APH
High parity
Maternal Age
Obesity
Drugs e.g. Nifedipine/MgSO4/salbutamol
Hypertensive disorders
Pre-existing coagulation disorder e.g. Von Willebrand’s
Therapeutic anticoagulation
Anaemia
Fetal demise in utero
Abruption
Induction/augmentation of labour
Prolonged labour
Pyrexia
Prolonged ruptured membranes Instrumental delivery
Episiotomy
Retained placenta/membranes
Physiological third stage
Drugs e.g. inhaled anaesthetic agents
Therapeutic anticoagulation/DIC

Prevention

There are many risk factors that can be identified at booking.2a,12,13,18,19 Health professionals must be aware of specific antenatal risk factors for PPH (see Table 1) and should take these into account when counselling women about place of delivery and type of care. Care plans must be modified when risk factors are identified. Anaemia identified antenatally should be treated. Women with bleeding disorders should have a clear plan of intrapartum management documented after consultation with an obstetric physician or haematologist. Any woman with a previous caesarean section should have an ultrasound scan to identify placental site and, if it is praevia or of any concern, referred to a tertiary centre.1,2a,6,7,9,13 Women with placenta accreta/percreta are at very high risk of major PPH. If placenta accreta or percreta is diagnosed antenatally, there should be consultant-led multidisciplinary planning for delivery.

More often overlooked are those risk factors which develop intrapartum (see Table 1). There is clear evidence from randomised controlled trials that active management of the third stage (including use of a uterotonic) results in reduced blood loss and therefore reduced risk of PPH. Plans for active management of the third stage should be documented for those identified at risk antenatally and consideration given to routine use of preventative measures in intrapartum situations known to increase risk, for example, pyrexia or assisted delivery.

WHO recommends active management should be offered to all women attended by a skilled practitioner.2 Prophylactic use of oxytocics reduces the risk of PPH by 60 per cent.3,4,11,12

Recognition

You would think it should be easy to identify a PPH, but minor blood loss can gradually become major haemorrhage, visual estimations frequently underestimate loss5,17 and haemorrhage may be concealed. It is vital to take and react to patient observations. The most common site of concealed haemorrhage is the uterus, hence the importance of monitoring uterine tone and fundal height postnatally.

By the time a woman drifts into unconsciousness she will have lost around 40 per cent of her circulating volume. It is the hypovolaemia, rather than anaemia, that kills women during an acute haemorrhage. It seems appropriate that PPH protocols should be instituted at an estimated blood loss well below this figure, as the aim of management is to prevent haemorrhage escalating to the point where it is life threatening.

Tone Abnormalities of uterine contraction
Tissue Retained products of conception
Trauma Genital tract trauma
Thrombin Abnormalities of coagulation

Prompt, appropriate intervention

An empty contracted uterus will not bleed in the absence of a coagulopathy. The four Ts, developed by ALSO (see Table 2), are a good aide mémoire when managing PPH and thinking of cause. By far the most common cause of PPH is uterine atony, with genital tract trauma and retained products of conception often co-existing. A clotting diathesis is rarely primary. Disseminated intravascular coagulation (DIC) is usually secondary to significant blood loss and loss of clotting factors secondary to a condition such as abruptio placantae or pre-eclamptic toxaemia, which is the trigger for DIC.

Accepting that antenatal risk assessment at best identifies only 40 per cent of those who have a PPH and that delay(s) in initiating appropriate management is the major factor resulting in adverse outcomes after PPH, it is essential to have a clear, logical sequence for management.1,2,18 Protocols and flow charts may be helpful. In the seventh Confidential Enquiry into Maternal Deaths report, failure of identification and management of intra-abdominal bleeding, uterine atony and placenta percreta were the main reasons for substandard care (Confidential Enquiry into Maternal and Child Health, 2006). Furthermore, a reduction in length of postgraduate training programs and reduced hours have led to less practical experience, which may result in failure to recognise even the clear signs and symptoms of intra-abdominal bleeding.1 The UK Royal College of Obstetricians and Gynaecologists and the Royal College of Midwives have thus recommended annual ‘skill drills’, including maternal collapse. RANZCOG is also encouraging development of multidisciplinary obstetric emergency courses (for example, PRactical Obstetric Multi-Professional Training) to ensure that everyone knows how to work together to ensure swift and efficient treatment in such an emergency.

Management of the acute presentation of PPH requires multiple tasks to be performed simultaneously. The basic principles can be grouped under the following principles of assessing the maternal condition and extent of the bleeding, arresting the bleeding and replacing her circulating volume and blood products.7

Once a PPH has been identified, appropriate help should be called. Early involvement of appropriate senior staff, including laboratory specialists, is fundamental to the management of major PPH. It is vital that trainee obstetricians and anaesthetists do not perceive calling for senior colleagues as involving ‘loss of face’. Senior staff must be receptive to concerns expressed by juniors and midwives.

A primary survey of a collapsed or severely bleeding woman should follow a structured approach of simple ‘ABC’ (airway, breathing, circulation), with resuscitation taking place as problems are identified; that is, a process of simultaneous evaluation and resuscitation. Simple measures such as laying the patient flat, keeping her warm and administering oxygen should not be overlooked. The urgency and measures undertaken to resuscitate and arrest haemorrhage need to be tailored to the degree of shock.

It is important to assess both the extent of prior bleeding and ongoing loss. Blood loss is usually visible at the introitus and this is especially true if the placenta has been delivered. If the placenta remains in situ, then a significant amount of blood can be retained in the uterus behind a partially separated placenta, the membranes or both. Loss may be concealed in kidney dishes on the delivery trolley, in linen or beneath the patient.

The cause of bleeding should be established as best able (see Table 2). The most common cause of primary PPH is uterine atony. Fundal massage should expel clot, improve uterine tone and provide an assessment of contracted fundal height. An in-dwelling catheter will keep the bladder empty and may later be useful for fluid management.

A further ecbolic should be given: 5iu syntocinon as a slow intravenous (IV) infusion is recommended as first-line treatment. In addition, Ergometrine, a syntocinon infusion or Carboprost (prostaglandin F2α) may be needed.2,3,9,10,13

If pharmacological measures are failing to control the haemorrhage, arrangements to transfer to theatre, then interventional/surgical measures should be instituted until the bleeding stops.

Contemporaneously, fluid resuscitation should be underway. The aim is to rapidly restore circulating blood volume. Two large-bore IV catheters should be sited and bloods drawn for complete blood count, coagulation studies, baseline renal and liver function and cross match.

Fluid resuscitation in obstetrics is often overly conservative either owing to underestimating loss, delay in symptoms of hypovolaemia in women with good compensatory mechanisms or because of concern that over resuscitation will cause pulmonary oedema. Until blood is available, infuse up to 3.5 litres of warmed fluid solution, crystalloid and/or colloid, as rapidly as required. The best equipment available should be used to achieve rapid, warmed infusion of fluids. Special care needs to be taken in patients with pre-eclampsia. Once adequate clear fluids are given, think O2 carrying capacity.

Compatible blood should be given as soon as available, but if 3.5 litres clear fluid and bleeding is massive and ongoing then un-cross-matched blood should be given. Fresh frozen plasma, platelets and cryoprecipitate should be given if the clinical situation or clotting results warrant this. After six units of red cells, clotting is likely to be altered. Clinicians and blood transfusion staff should liaise at a local level to agree on a standard form of words (such as ‘we need compatible blood now’ or ‘group-specific blood’) to be used in cases of major obstetric haemorrhage and also a timescale in which to produce various products.6,7,8,13 Most large units will have a massive transfusion protocol that, when activated, will ensure appropriate blood and products are delivered to theatre.

Once in theatre there should be a systematic exploration of the genital tract, repairing tears and identifying any factors contributing to ongoing loss. The judgment of senior clinicians, taking into account the individual woman’s future reproductive aspirations, is required in deciding the appropriate sequence of interventions. Balloon tamponade has replaced uterine packing in the management of PPH secondary to atony. A variety of hydrostatic balloons are available with similar efficacy. Studies suggest successful avoidance of hysterectomy in up to 78 per cent of cases using a balloon. Haemostatic sutures (B-Lynch, Hayman, Cho and so forth)14,15 placed at laparotomy have been shown to be effective in controlling severe PPH from atony, reducing the need for hysterectomy. Uterine artery ligation may significantly reduce bleeding and is relatively simple to perform; while internal iliac ligation is best left to those comfortable operating in the pelvic sidewall and not undertaken by generalists ‘occasionally’ during an emergency. While there are no studies making direct comparisons, it would seem balloon tamponade and haemostatic uterine sutures are equally effective as internal artery ligation in reducing the need for hysterectomy and may be more appropriate as first-line procedures. In large centres, there may be facilities for radiological intervention and selective uterine or internal iliac embolisation in the stable patient with ongoing loss. In the face of life-threatening PPH, recombinant factor VIIa may have a useful adjuvant role to surgical treatment.13

Most literature supports early recourse to hysterectomy, particularly in situations of uterine rupture or accreta/percreta. Ideally, the decision should be made by a senior obstetrician and surgery performed by a surgeon.1,6,8,13,16 Once the bleeding has been controlled and initial resuscitation has been completed, continuous close observations in either a high-dependency unit on the labour ward or an intensive care unit is required. The recording of observations on a flowchart helps in the early identification of continuous bleeding.

It is also important that once the bleeding is arrested and any coagulopathy is corrected, thromboprophylaxis is administered, as there is a high risk of thrombosis.

Debriefing of patients and relatives is an important aspect of management that is often overlooked. Complications following massive PPH are diverse and may not be immediately apparent. They range from surgical complications (synechiae, uterine necrosis, sepsis) through to delayed lactation (Sheehan’s syndrome) and post-traumatic stress disorder.

Stalin said: ‘One death is a tragedy. One million is a statistic.’ By preventing one, we may improve the other.

References

  1. Saving Mothers’ Lives. March 2011 The Eighth Report of the Confidential Enquiries into Maternal Deaths in the United Kingdom Centre for Maternal and Child Enquiries (CMACE), BJOG 118 (Suppl. 1), 1–203 1.
  2. WHO guidelines for the management of postpartum haemorrhage and retained placenta. 2009.
  3. Mousa HA, Alfirevic Z. Treatment for primary postpartum haemorrhage (Review) The Cochrane Library 2007, Issue 4.
  4. Tunçalp Ö, Hofmeyr GJ, Gülmezoglu AM. Prostaglandins for preventing postpartum haemorrhage. Cochrane Database Syst Rev. 2012 Aug 15;8.
  5. Bose P, Regan F, Paterson-Brown S. Improving the accuracy of estimated blood loss at obstetric haemorrhage using clinical reconstructions. BJOG 2006; 113:919–924.
  6. Clinical and Practice Guideline. Management and Treatment of Postpartum Haemorrhage. Institute of Obstetricians and Gynaecologists Royal College of Physicians of Ireland June 2012.
  7. PROMPT Course Manual. Edition 2. 2012.
  8. National Women’s Health Clinical Guidance/Recommended Best Practice. Postpartum Haemorrhage. 2009. ADHB Policies and guidelines.
  9. American College of Obstetricians and Gynecologists. ACOG Practice Bulletin: Clinical Management Guidelines for Obstetrician- Gynecologists Number 76, October 2006: postpartum hemorrhage. Obstet Gynecol. Oct 2006;108(4):1039-47.
  10. ACOG Practice Bulletin: Technical Bulletin number 143, July 1990:Diagnosis and Management of Post Partum Haemorrhage. Int J Gynaecol Obstet 1991 Oct;36(2):159-63.
  11. Prendiville WJ, Elbourne D, McDonald S. Active versus expectant management in the third stage of labour. Cochrane Database Syst Rev. 2000.
  12. Combs CA., Murphy EL. & Laros RK Jr. (1991) Factors associated with postpartum hemorrhage with vaginal birth. Obstet Gynecol 77, 69–76.
  13. RCOG Green top guideline No 52. May 2009
  14. Cho JH, Jun HS, Lee CN. Hemostatic suturing technique for uterine bleeding during cesarean delivery. Obstet Gynecol. Jul 2000;96(1):129-131.
  15. Hayman RG, Arulkumaran S, Steer PJ. Uterine Compression sutures: surgical management of post partum haemorrhage. Obstet Gynecol. Mar 2002;99(3):502-6.
  16. John R Smith. Postpartum Haemorrhage in eMedicine 2006.
  17. Blood loss at delivery: how accurate is your estimation? Glover P. Aust J Midwifery, 2003 Jun :16(2):21-4.
  18. Al-Zirqi I, Vangen S, Forsen L, Stray-Pedersen B. Prevalence and risk factors of severe obstetric haemorrhage. BJOG 2008;115:1265–72.
  19. Michael S. Kramer, Mourad Dahhou, Danielle Vallerand, Robert Liston, K.S. Joseph, Risk Factors for Postpartum Hemorrhage: Can We Explain the Recent Temporal Increase? J Obstet Gynaecol Can 2011;33(8):810–819.

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