ORIGINAL ARTICLE
Major obstetric haemorrhage: monitoring with thromboelastography, laboratory analyses or both?

https://doi.org/10.1016/j.ijoa.2013.07.003Get rights and content

Abstract

Background

Haemorrhage is a common cause of morbidity and mortality in the obstetric population. The aim of this study was to compare the use of thromboelastography and laboratory analyses to evaluate haemostasis during major obstetric haemorrhage. A secondary aim was to evaluate correlations between the results of thromboelastography, laboratory analyses and estimated blood loss.

Methods

Forty-five women with major obstetric haemorrhage and 49 women with blood loss <600 mL were included. The following thromboelastography analyses were performed: time to start of clotting (TEG-R), time to 20 mm of clot firmness (TEG-K), rate of clot growth (TEG-Angle), maximum amplitude of clot (TEG-MA) and lysis after 30 min (TEG-LY30). In addition, platelet count, activated partial thromboplastin time, prothrombin time, fibrinogen, antithrombin and D-dimer were measured.

Results

Thromboelastography variables reflecting clot stability and fibrinolysis were decreased in women with massive obstetric haemorrhage compared to women with normal bleeding, while clot initiation was accelerated. Laboratory analyses also showed impaired haemostasis with the most pronounced differences in platelet count, fibrinogen concentration and antithrombin activity. The strongest correlations existed between fibrinogen and TEG-MA and between estimated blood loss and TEG-MA, fibrinogen and antithrombin, respectively.

Conclusions

Impaired haemostasis, demonstrated by thromboelastography and laboratory analyses, was found after an estimated blood loss of 2000 mL. Thromboelastography provides faster results than standard laboratory testing which is advantageous in the setting of on-going obstetric haemorrhage. However, laboratory analyses found greater differences in coagulation variables, which correlated better with estimated blood loss.

Introduction

Haemorrhage is still a common cause of morbidity and mortality in the obstetric population. The latest UK Confidential Enquiry into Maternal Deaths reported a decline in mortality from postpartum haemorrhage (PPH) but it is still the sixth most common direct cause of death.1 Several reports have described substandard care and stated the need for guidelines for managing PPH.2, 3, 4 Postpartum haemorrhage has been reported to be responsible for 73% of all severe morbidity during pregnancy and is the most common obstetric cause of intensive care admission.5 Laboratory analyses are usually used for diagnosis of haemostatic disorders in cases of obstetric haemorrhage and serve as a basis for decision-making and follow-up treatment. As the results of these analyses are reported with variable delay, immediate knowledge of the haemostatic condition has previously been unavailable, making early specific treatment difficult.

Two viscoelastic methods, thromboelastography (TEG) and thromboelastometry (TEM), have now been re-evaluated and technically improved. These global point-of-care tests simultaneously measure coagulation and fibrinolysis in whole blood and can detect haemostatic derangement within 10–20 min.6 In a recent prospective longitudinal study in healthy pregnant women, TEG demonstrated faster blood coagulation with increased strength of the fibrin clot and less fibrinolysis during the pregnancy compared to eight weeks postpartum.7 These results are supported by other studies reporting changes in TEG/TEM variables during the puerperium.8, 9 Few studies have evaluated TEG/TEM in women with PPH10 and the significance of these methods in connection with obstetric haemorrhage is unclear.11, 12, 13, 14

The primary aim of this prospective observational study was to describe the results of coagulation testing using TEG and traditional laboratory analyses during major obstetric haemorrhage (MOH) and to compare the findings with results of parturients with normal postpartum blood loss. A secondary aim was to study whether the results of TEG or laboratory analyses correlated with estimated blood loss (EBL).

Section snippets

Methods

The Regional Ethical Review Board in Gothenburg, Sweden approved this study. Written informed consent was obtained from all participants. Women with MOH and women with blood loss <600 mL were included. Women with MOH were brought to the operating room, if not already there because of caesarean section, and blood sampling was performed after an EBL of ⩾2000 mL. The first sample was performed after admission to the operating room or when the decision to assess coagulation was made. Women were asked

Results

Forty-five women with MOH and 49 women with blood loss <600 mL were included. Patient characteristics are shown in Table 1. Treatments at the time of blood sampling are shown in Table 2. Major obstetric haemorrhage was secondary to placental retention (n = 17), caesarean section (n = 14), uterine atony (n = 6), uterine rupture (n = 2), placenta praevia (n = 2), cervical or vaginal lacerations (n = 2), abruptio placentae (n = 1) and placenta accreta (n = 1).

Thromboelastography variables are shown in Table 3.

Discussion

The main finding in this study is that haemostasis is impaired when blood loss exceeds 2000 mL during MOH, demonstrated by both TEG and laboratory analyses. Thromboelastography can provide rapid and clinically important information about haemostatic changes in connection with MOH; perhaps revealing indications for specific blood product therapy at an earlier point compared with traditional laboratory testing. Laboratory analyses can verify and specify these haemostatic changes. TEG showed faster

Disclosure

This work was financially supported by Sahlgrenska University Hospital and grants from the Västra Götaland Region, the Göteborg Medical Society and Elsa and Gustav Lindhs Foundation. Kaolin, reagent, cups and pins were supplied by the Haemoscope Corporation. The company had no impact on study design, data collection, analysis and interpretation of data, writing of report or decision to submit the paper for publication. The authors have no conflicts of interest to declare.

References (37)

  • B. Charbit et al.

    The decrease of fibrinogen is an early predictor of the severity of postpartum hemorrhage

    J Thromb Haemost

    (2007)
  • C. Rourke et al.

    Fibrinogen levels during trauma hemorrhage, response to replacement therapy, and association with patient outcomes

    J Thromb Haemost

    (2012)
  • A.A. Hanke et al.

    Long-term safety and efficacy of a pasteurized nanofiltrated prothrombin complex concentrate (Beriplex P/N): a pharmacovigilance study

    Br J Anaesth

    (2013)
  • C. Oelschlager et al.

    Antithrombin III inhibits nuclear factor kappaB activation in human monocytes and vascular endothelial cells

    Blood

    (2002)
  • A. Mizutani et al.

    Antithrombin reduces ischemia/reperfusion-induced renal injury in rats by inhibiting leukocyte activation through promotion of prostacyclin production

    Blood

    (2003)
  • R. Cantwell et al.

    Saving Mothers’ Lives: Reviewing maternal deaths to make motherhood safer: 2006–2008. The Eighth Report of the Confidential Enquiries into Maternal Deaths in the United Kingdom

    BJOG

    (2011)
  • Lennox C, Marr L. Scottish confidential audit of severe maternal morbidity: reducing avoidable harm. Ninth Annual...
  • R.J. Luddington

    Thrombelastography/thromboelastometry

    Clin Lab Haematol

    (2005)
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