An expert resource for medical professionals
Provided FREE as a service to women’s health

The Global Library of Women’s Medicine’s
Welfare of Women
Global Health Programme

An Educational Platform for

The global voice for women’s health

This chapter should be cited as follows:
Luna JMB, Escobar MF, Glob. libr. women's med.,
ISSN: 1756-2228; DOI 10.3843/GLOWM.409613

The Continuous Textbook of Women’s Medicine SeriesObstetrics Module

Volume 13

Obstetric emergencies

Volume Editor: Dr María Fernanda Escobar Vidarte, Fundación Valle del Lili, Cali, Colombia

Chapter

Evaluation and Management of Postpartum Hemorrhage: Hemostatic Reanimation

First published: October 2021

Study Assessment Option

By completing 4 multiple-choice questions (randomly selected) after studying this chapter readers can qualify for Continuing Professional Development awards from FIGO plus a Study Completion Certificate from GLOWM
See end of chapter for details

INTRODUCTION

Postpartum hemorrhage (PPH) is the leading cause of maternal morbidity and mortality worldwide. It is estimated that approximately 27% of maternal deaths are caused by this entity.1 When the cases of maternal deaths of PPH are analyzed, it has been found that the majority are preventable and many of the fatal outcomes are associated with delays in diagnosis and medical management.2

These types of delays are associated with the scarcity of resources principally in continents with low- and middle-income countries in Africa, Asia, and Latin America, where the prevalence of PPH reach 20%.3 High-income countries report a prevalence between 3 and 12%. This difference in prevalence has been achieved by applying integral or multifactorial "bundles" protocols that intervene at several critical points during the hemorrhage episode, optimizing logistics, improving the availability of resources, training personnel in the use of resources and generating continuous feedback, and updating of the emergency management guidelines. Within these strategies, one of the components with greatest impact is the improvement in resuscitation strategies to reduce the appearance of coagulopathy.

These concepts are based on the principle of what is known worldwide as "damage control resuscitation". These new concepts have been extrapolated from patients with severe hemorrhage with trauma and the appearance of coagulopathy.4,5

PATHOPHYSIOLOGY OF COAGULOPATHY IN POSTPARTUM HEMORRHAGE

The pathophysiology of coagulopathy in PPH is still uncertain. The coagulopathy is considered in most cases to be uncontrolled bleeding and a massive loss of coagulation factors, a condition that has been called coagulopathy of consumption.6,7 In the majority of cases of PPH the onset of coagulopathy is not usual, even in women who have bled 1000–2000 milliliters (ml). In the 98% of cases of PPH, values of coagulation and fibrinogen times are usually normal,15 however the onset of coagulopathy is associated with underestimation of the volume of losses, late diagnosis, and late management of PHH.

It is a fact that pregnancy physiologically prepares the women for postpartum bleeding; in the third trimester the levels of procoagulant factors rise (V, VII, VIII, IX, X, XII, von Willebrand, Fibrinogen), decreases the anticoagulant mechanisms (increases in heparin cofactor II, alpha-1 antitrypsin, protein S activity, and activated protein C resistance) and depressed the fibrinolytic activity.8,9 In the delivery of the placenta there is a controlled tissue injury, which exposes tissue factor and endothelial factors that initiate the coagulation cascade with the rapid formation of a clot on the area of placentation, which in conjunction with the uterine contraction limits bleeding. To protect the organism against a massive intravascular thrombus, the initial coagulation activation is followed by enhanced plasminogen activation and fibrinolytic activity. To prevent rebleeding by fibrinolysis, the plasminogen activator inhibitor (PAI)-1 level increases progressively.

However, during acute PPH there can occur a perpetuation of the activation of the coagulation system. The extensive tissue injury with hypovolemic shock induces a prothrombotic state that further promotes the consumption of coagulation factors, fibrinogen and platelet.10,11 The endothelial glycocalyx consists of a thick layer of proteoglycans and glycosaminoglycans, extremely sensitive to the endothelial damage. In shock/hypoxia status in severe hemorrhagic patients, this glycocalyx becomes degradation and secondary resulting in the release of heparan sulfate and similar constituents with heparin-like activity to the circulating blood, promoting the persistence of bleeding and loss of coagulation factors.12

Since obstetric hemorrhage is multifactorial, the appearance of disseminated intravascular coagulopathy (DIC) associated with hyper fibrinolysis has also been described. This type of coagulopathy is faster and has the same characteristics of DIC with amniotic fluid embolism, infection, and abruption of placenta where there is a massive release of tissue factor into the bloodstream.13,14

This usually is accompanied by what has been called dilutional coagulopathy that is caused by mistakes in the resuscitation strategies. It has been described that high volumes of crystalloids or colloids cause hemodilution of coagulation factors, platelets and fibrinogen, favoring the abnormal functioning of the coagulation system.16,17 The repositioning practices 3 : 1 (1 l of blood lost replace with 3 l of volume of crystalloids) favors the hypothermia, acidosis, and coagulopathy, a condition called death triad. This triad has been related to increased platelet dysfunction, alteration of the form platelet, reduction activity of coagulation factors, and inhibition of fibrinogen synthesis with acceleration of its degradation.20,21 Furthermore, colloids aggravate coagulopathy (colloid-induced coagulopathy) because they produce clot porous, which worsens outcome, increases bleeding, and transfusion requirements.18,19

Plasma as a resuscitation fluid offers numerous advantages as a potent intravascular fluid expander and reduces the risk of dilutional coagulopathy by providing a balanced mix of procoagulant and anticoagulant factors. It also appears to have protective effects on the endothelial glycocalyx border in animal and in vitro models. These properties are the reason why a central axis of hemostatic resuscitation is the implementation and early use of plasma and blood products.

In recent years, several studies have demonstrated that one of the principal markers of severity of PPH is the fibrinogen. It has been found that values below two gr/dl have a positive predictive value of 100% for the development of severe obstetric hemorrhage with the need for additional surgeries or the use of more than four units of red blood cells.22,23 For this reason, in all patients who present PPH, levels of fibrinogen must be evaluated.24 These findings have generated changes in the protocols of resuscitation with replenishment of fibrinogen early either with fibrinogen concentrates or with cryoprecipitate. These recommendations do not have a solid evidential basis since these recommendations arise from observational studies.25,26,27

HEMOSTATIC RESUSCITATION

The hemostatic resuscitation in PPH is a set of interventions that is aimed at diminishing the possibilities of the appearance of coagulopathy; it goes in direct link with early control of the cause and has these premises:

  • Limit the use of crystalloids with use of a permissive hypotensive resuscitation to decrease bleeding and support bleeding control.
  • Limit the use of crystalloids and promote the use of blood components always trying to achieve close transfusion relations close to 1 : 1.
  • Favor the early repositioning of fibrinogen.
  • Favor the rapid delivery of blood components and create massive transfusion protocols.
  • Optimize coagulation system with early use of antifibrinolytics.
  • Regaining homeostasis and avoid further coagulopathy related to hypothermia, acidosis and electrolyte disturbances (hypocalcemia, hyperkaliemia).

Resuscitation with endovenous liquids

The resuscitation with crystalloids is usually the method of choice in the first minutes of the PHH. However, it has been demonstrated in the last decade that the excessive use in loads over 2000 milliliters or 3 : 1 replacement according to the volume of bleeding are directly related to the appearance of coagulopathy by hemodilution.28 The strategies to reduce the use of crystalloids have been extrapolated from the trauma with severe hemorrhagic shock where "permissive hypotension" is recommended. These strategies indicate resuscitation boluses only when a critical point is reached, whether systolic pressure or mean arterial pressure, until the definitive control of bleeding was achieved. The first study that analyzed these restrictive strategies did not show differences in mortality but it did show that patients subjected to aggressive resuscitation had prolongation of PT, PTT, and minor platelet counts.29 Two recent randomized trials comparing the outcomes according to the strategies targeting higher or lower blood pressure goals (systolic blood pressure of 100 vs. 70 mmHg, mean arterial pressure of 65 vs. 50 mmHg) demonstrated that there is no survival advantage for the higher blood pressure targets. Nevertheless, there were no significant reductions in intraoperative blood transfusion volumes in the hypotensive arm.30,31

Given these findings, it is proposed that the strategy that would offer greater advantages in PPH would be the initial use of boluses 300–500 ml of crystalloids. This would have a subsequent evaluation of their hemodynamic response with markers such as systolic pressure and MAP (SBP 70 or MAP 50 mmHg) trying to use the least number of crystalloids to achieve adequate control of bleeding or have the possibility of using blood components.

Use of blood components

The early use of blood products with close relationships to the components of whole blood 1 : 1 : 1 has been proposed as the cornerstone of hemostatic resuscitation; in the last decade in trauma patients, severe hemorrhages and postpartum hemorrhage. The relationship of transfusion of blood components (red blood cells, plasma, and platelets) and the time in which this relationship is reached, have shown that there are improvements in survival and hemostatic control in these patients.32,33 Pasquier et al.34 demonstrated that in patients with PPH a higher use of plasma reduced the risk of hemostatic interventions. This evidence was strengthened with the appearance of trials with greater statistical power.

The PROMMTT study (Holcomb et al.) is a prospective, observational, multicenter study with 905 trauma patients, where they required at least three units of blood products in 24 h (major trauma transfusion).35 In this trial, they found that a moderate and high early dose of plasma and platelets (plasma: RBC ratio 1 : 1) was independently associated with improved 6 h mortality and that patients receiving low ratios are 3 to 4 times more likely to die. The pragmatic randomized optimal platelet and plasma ratios (PROPPR)36 randomized controlled trial comparing plasma, PLT, and RBC ratio of 1 : 1 : 1 (high-dose plasma and platelets) and 1 : 1 : 2 (half dose plasma and platelets) in trauma patients with hemorrhagic shock showed in the 1 : 1 : 1 group more patients achieved hemostasis (86 vs. 78%, P. 0.006), fewer exsanguinated in the first 24 h (9 vs. 15%, P. 0.03), but mortality was not significantly affected at 24 h (113 vs. 17, P. 0.120) or 30 days (22 vs. 26%, P. 0.26). Patients in the two groups received the same number of blood products during intervention and the same auxiliary fluid resuscitation, but achieved the desired difference in ratios signifying no presence of fluid dilution effects in the 1 : 1 : 2 group. Patients in the 1 : 1 : 2 group received more transfusions post intervention, and furthermore, cryoprecipitate was more frequently used (22 vs. 29%; P. 0.01) in the 1 : 1 : 2 in the first 24 h. These results support the decision to modify the resuscitation guidelines in hemorrhagic shock of the most important scientific societies, promoting the early achievement of 1 : 1 : 1 ratio in blood components trasfusion.37,38

Massive transfusion packages (MTP)

The relationship in the use is important, but it is fundamental to emphasize that the time in which this relationship is reached is equally determinant in order to obtain good results. The strategies of massive transfusion packages (MTPs) are a tool that facilitates the times when haemocomponents are delivered.39,40 MTP is coordinating with the blood bank of the institutions to always have available a certain number of units of red blood cells, plasma, platelets, and cryoprecipitate ready to be sent to the location where the bleeding is presented, whether in the delivery room, recovery, or surgery rooms. The initial units of red blood cells should be ideally O negative or failing O positive to reduce the chances of adverse reactions, and should be accompanied by units of fresh plasma, cryoprecipitate, or platelets that must start their warm-up and prepare immediately activate the verbal order for your shipment trying to guarantee the delivery of the ratio 1 : 1 in the first 10–15 min. Implementation of an MTP has been shown to improve the timeliness of blood transfusion (compared with historical controls) and to be cost-effective.41 Actually, this implementation is a standard in the quality of care of an institution that manages obstetric population.42,43

MTP in the non-obstetric population worldwide has been designed with 6 units of red blood cells, 6 units of plasma, and 1 platelet apheresis; however, the use of these large numbers of units in obstetric patients has been associated with events of volume overload or waste of blood components. Interestingly, several centers have designed MTP for obstetric population with fewer components (3 units of red blood cells, 2 plasma, 1 platelet apheresis, and 10 cryoprecipitate) with more quickly and efficiently correction in a fibrinogen levels, which as mentioned are directly related to less adverse outcomes. These initial "obstetric transfusion packages" were evaluated in a large intervention protocol in California and they proved to decrease the use of blood components and minor postpartum hysterectomy interventions with their implementation in conjunction with early diagnosis of PPH.44

There are new trends in rapidly replenishing fibrinogen even before plasma; the use of purified virally inactivated fibrinogen concentrates may be as efficacious as cryoprecipitate in correcting hyperfibrinogenemia and, if introduced into an algorithm for treating PPH-related coagulopathy, may reduce the need for massive transfusion of RBCs, plasma, and platelets.45,46 Further studies of fibrinogen concentrate in the setting of PPH are needed.

Use of antifibrinolytics

Tranexamic acid competitively inhibits fibrinolysis, blocking the binding sites of lysine in plasminogen molecules, thereby interfering with the activation of plasmin. The limitation of hyperactive fibrinolysis has been suggested to be the first step in the treatment algorithm for acquired coagulopathy in postpartum hemorrhage.47

The prophylactic use of tranexamic acid in doses of 1 g or 10 to 15 mg/kg is considered, it can generate reduction of blood loss without major complications, both in vaginal delivery and cesarean section.48 Current evidence derived from the WOMAN trial trial47 confirms the clinical relevance of the effect of treatment with tranexamic acid in postpartum hemorrhage in the earliest stages (first 3 h), achieving a reduction in mortality of 31% due to bleeding, and a 36% in the need for laparotomy to control bleeding, without significant side effects. This multicenter randomized study recommended a scheme with an initial dose of 1 g, followed by an additional dose of 1 g administered in cases of persistent bleeding 30 min later, a significant reduction in major obstetric outcomes was achieved regardless of the etiology of the bleeding or the mode of delivery. As a result of these findings, we suggest that its use be from minute zero of the diagnosis of bleeding with the intention of obtaining the best results.

Future interventions

The widening of the knowledge of the new coagulation cascade with the development of the cellular model and the predominant role of the platelet has generated many questions about the use of classical paraclinics to evaluate patients with severe obstetric hemorrhage, since the PT, PTT, INR, and platelet counts are paraclinical in a separate way that takes time to obtain results and we could be observing the picture of a clinical state that could be even more deteriorated or already optimized but inadequately reported.49 The current trends in the surveillance of patients with hemorrhage and coagulopathy are the point-of-care viscoelastic hemostatic assays (VHAs), thromboelastographic (TEG, Haemonetics Corp., Braintree, Massachusetts, USA) and thromboelastometry (ROTEM, Tem International GmbH, Munich, Germany), can assess and graphically display the viscoelastic properties of clot formation through to clot lysis, additionally provide information about thrombus generation, which correlates with thrombin-generation kinetics; these kinetic data cannot be evaluated with normal laboratory coagulation tests.50 TEG and ROTEM have shown to reduce bleeding, transfusions, and possibly mortality in different surgical populations.51,52

The viscoelastic methods have been tested in PPH obtaining interesting results, since they have validated the findings related to fibrinogen concentrations lower than 200 mg/dl and its association with adverse outcomes in PPH.53,54 The most important thing is that this type of intervention has been articulated with management protocols where the obtaining of results very early is combined with replenishments of guided hem compounds according to the deficiencies detected and not with a pre-established intervention package with the possibility of reducing the number of transfusions and progression to coagulopathy in severe PPH.55,56 This type of point-of-care technology is being implemented in most delivery rooms in high-income countries.

There are off-label practices reported in the management of coagulopathy as the early administration of fibrinogen concentrate and prothrombin complex concentrate (PCC), directed by the result of the VHA.57 Administration of pharmacological coagulation factor concentrates was used in these articles as alternatives to plasma and PLT transfusions together with clear volume resuscitation. This approach seeks to avoid any use of blood products and performs VHA monitoring of the existing and developing coagulopathy, with the purpose of goal-directed reversal of coagulopathy58 but this practice has no sufficient evidence in the obstetric population and the results of RETIC study59 that was made with trauma patients was very controversial; so this intervention still should not be recommended for general practice.

PRACTICE RECOMMENDATIONS

  • In postpartum hemorrhage it has been described that high volumes of crystalloids or colloids cause hemodilution of coagulation factors, platelets and fibrinogen, favoring the abnormal functioning of the coagulation system, The repositioning practices 3 : 1 (1 l of blood lost replace with 3 l of volume of crystalloids) must be eliminated.
  • The hemostatic resuscitation in PPH is a set of interventions that is aimed at diminishing the possibilities of the appearance of coagulopathy; it goes in direct link with early control of the cause and has these premises.
  • Limit the use of crystalloids with the use of a permissive hypotensive resuscitation to decrease bleeding and support bleeding control.
  • Limit the use of crystalloids and promote the use of blood components always trying to achieve close transfusion relations close to 1 : 1.
  • Favor the early repositioning of fibrinogen with fibrinogen concentrates or with cryoprecipitate.
  • Favor the rapid delivery of blood components and create massive transfusion protocols. The time of delivery is crucial.
  • Optimize the coagulation system with early use of antifibrinolytics. Use tranexamic acid.
  • Regain homeostasis and avoid further coagulopathy related to hypothermia, acidosis, and electrolyte disturbances (hypocalcemia, hyperkaliemia).


CONFLICTS OF INTEREST

The author(s) of this chapter declare that they have no interests that conflict with the contents of the chapter.

REFERENCES

1

World Health Organization. Maternal mortality: fact sheet 348 (www.who.int/mediacentre/factsheets/fs348/en) Accessed May 21, 2015.

2

Main EK, McCain CL, Morton CH, et al. Pregnancy-related mortality in California: causes, characteristics, and improvement opportunities. Obstet Gynecol 2015;125(4):938–47.

3

Khan KS, Wojdyla D, Say L, et al. WHO analysis of causes of maternal death: a systematic review. Lancet 2006;367(9516):1066–74.

4

Holcomb JB, Jenkins D, Rhee P, et al. Damage control resuscitation: directly addressing the early coagulopathy of trauma. J Trauma 2007;62:307–10.

5

Shapiro MB, Jenkins DH, Schwab CW, et al. Damage control: collective review. J Trauma 2000;49:969–78.

6

McLintock C, James AH. Obstetric hemorrhage. J Thromb Haemost 2011;9:1441–51.

7

Rattray DD, O’Connell CM, Baskett TF. Acute disseminated intravascular coagulation in obstetrics: a tertiary centre population review (1980 to 2009). J Obstet Gynaecol Can 2012;34:341–7.

8

Holmes VA, Wallace JM. Haemostasis in normal pregnancy: a balancing act? Biochem Soc Trans 2005;33:428–32.

9

Brenner B. Haemostatic changes in pregnancy. Thromb Res 2004;114:409–14.

10

Gando S, Sawamura A, Hayakawa M. Trauma, shock, and disseminated intravascular coagulation: lessons from the classical literature. Ann Surg 2011;254:10–9.

11

Levi M, van der PT. Inflammation and coagulation. Crit Care Med 2010;38:S26–S34.

12

Johansson PI, Stensballe J, Rasmussen LS, et al. A high admission syndecan-1 level, a marker of endothelial glycocalyx degradation, is associated with inflammation, protein C depletion, fibrinolysis, and increased mortality in trauma patients. Ann Surg 2011;254:194–200.

13

Collis RE, Collins PW. Haemostatic management of obstetric haemorrhage. Anaesthesia 2015;70:78–86.

14

Levi M. Pathogenesis and management of peripartum coagulopathic calamities (disseminated intravascular coagulation and amniotic fluid embolism). Thromb Res 2013;131(Suppl. 1):S32–6.

15

Wikkelsø AJ, Edwards HM, Afshari A, et al. FIB-PPH Trial Group. Pre-emptive treatment with fibrinogen concentrate for postpartum haemorrhage: randomized controlled trial. Br J Anaesth 2015;114:623–33.

16

Haut ER, Kalish BT, Cotton BA, et al. Prehospital intravenous fluid administration is associated with higher mortality in trauma patients: a National Trauma Data Bank analysis. Ann Surg 2011;253:371–7.

17

Shaz BH, Winkler AM, James AB, et al. Pathophysiology of early traumainduced coagulopathy: emerging evidence for hemodilution and coagulation factor depletion. J Trauma 2011;70:1401–7.

18

Fenger-Eriksen C, Tonnesen E, Ingerslev J, et al. Mechanisms of hydroxyethyl starch-induced dilutional coagulopathy. J Thromb Haemost 2009;7:1099–105.

19

Rasmussen KC, Hoejskov M, Johansson PI, et al. Coagulation competence for predicting perioperative hemorrhage in patients treated with lactated Ringer’s vs. dextran: a randomized controlled trial. BMC Anesthesiol 2015;15:178.

20

Meng ZH, Wolberg AS, Monroe DM. III, et al. The effect of temperature and pH on the activity of factor VIIa: implications for the efficacy of high-dose factor VIIa in hypothermic and acidotic patients. J Trauma 2003;55:886–91.

21

Djaldetti M, Fishman P, Bessler H, et al. pH-induced platelet ultrastructural alterations. A possible mechanism for impaired platelet aggregation. Arch Surg 1979;114:707–10.

22

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;5:266–73.

23

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;108:984–9.

24

De Lloyd L, Bovington R, Kaye A, et al. Standard haemostatic tests ollowing major obstetric haemorrhage. Int J Obstet Anesth 2011;20:135–141.

25

Mallaiah S, Barclay P, Harrod I, et al. Introduction of an algorithm for ROTEMguided fibrinogen concentrate administration in major obstetric haemorrhage. Anaesthesia 2015;70:166–75.

26

Ahmed S, Harrity C, Johnson S, et al. The efficacy of fibrinogen concentrate compared with cryoprecipitate in major obstetric haemorrhage: an observational study. Transfus Med 2012;22:344–9.

27

Collins P. Fibrinogen concentrate versus placebo for treatment of postpartum haemorrhage: a multicentre, prospective, double blind randomised controlled trial. ISRCTN46295339. http://www.controlled-trials.com/ ISRCTN46295339/ [Accessed 24 November 2014].

28

Duchesne JC, McSwain NE Jr, Cotton BA, et al. Damage control resuscitation: the new face of damage control. J Trauma 2010;69:976–90.

29

Bickell WH, Wall MJ Jr, Pepe PE, et al. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994;331(17):1105–9.

30

Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation during active hemorrhage: impact on in-hospital mortality. J Trauma 2002;52(6):1141–6.

31

Morrison CA, Carrick MM, Norman MA, et al. Hypotensive resuscitation strategy reduces transfusion requirements and severe postoperative coagulopathy in Modern resuscitation of hemorrhagic shock trauma patients with hemorrhagic shock: preliminary results of a randomized controlled trial. J Trauma 2011;70(3):652–63.

32

Johansson PI, Stensballe J. Effect of Haemostatic Control Resuscitation on mortality in massively bleeding patients: a before and after study. Vox Sang 2009;96:111–8.

33

Borgman MA, Spinella PC, Perkins JG, et al. The ratio of blood products transfused affects mortality in patients receiving massive transfusions at a combat support hospital. J Trauma 2007;63:805–13.

34

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;116:155–61.

35

Holcomb JB, del Junco DJ, Fox EE, et al. The Prospective, Observational, Multicenter, Major Trauma Transfusion (PROMMTT) Study: comparative effectiveness of a time-varying treatment with competing risks. Arch Surg 2012;1–10.

36

Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1 : 1 : 1 vs. a 1 : 1 : 2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA 2015;313:471–82.

37

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.

38

Practice guidelines for perioperative blood management: an updated report by the American Society of Anesthesiologists Task Force on Perioperative Blood Management. Anesthesiology 2015;122:241–75.

39

Burtelow M, Riley E, Druzin M, et al. How we treat: management of lifethreatening primary postpartum hemorrhage with a standardized massive transfusion protocol. Transfusion 2007;47:1564–72.

40

Goodnough LT, Spain DA, Maggio P. Logistics of transfusion support for patients with massive hemorrhage. Curr Opin Anaesthesiol 2013;26:208–14.

41

O’Keeffe T, Refaai M, Tchorz K, et al. A massive transfusion protocol to decrease blood component use and costs. Arch Surg 2008;143:686–90.

42

Kacmar RM, Mhyre JM, Scavone BM, et al. The use of postpartum hemorrhage protocols in United States academic obstetric anesthesia units. Anesth Analg 2014;119:906–10.

43

Lewis G. The Confidential Enquiry into Maternal and Child Health (CEMACH). Saving mothers’ lives: reviewing maternal deaths to make motherhood safer: 2003–2005. The Seventh Report on Confidential Enquiries into Maternal Deaths in the United Kingdom. London: CEMACH, 2007.

44

Shields LE, Smalarz K, Reffigee L, et al. Comprehensive maternal hemorrhage protocols improve patient safety and reduce utilization of blood products. Am J Obstet Gynecol 2011;205:368.e1–368.e8.

45

Mallaiah S, Barclay P, Harrod I, et al. Introduction of an algorithm for ROTEM guided fibrinogen concentrate administration in major obstetric haemorrhage. Anaesthesia 2015;70:166–75.

46

Ahmed S, Harrity C, Johnson S, et al. The efficacy of fibrinogen concentrate compared with cryoprecipitate in major obstetric haemorrhage: an observational study. Transfus Med 2012;22:344–9.

47

Shakur H, Haleema et al. The WOMAN Trial (World Maternal Antifibrinolytic Trial): Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum haemorrhage (WOMAN): an international, randomised, double-blind, placebo-controlled trial. Lancet 2017.

48

Novikova N, Hofmeyr GJ, Cluver C. Tranexamic acid for preventing postpartum haemorrhage. Cochrane Database Syst Rev 2015;6 CD007872.

49

Haas T, Fries D, Tanaka KA, et al. Usefulness of standard plasma coagulation tests in the management of perioperative coagulopathic bleeding: is there any evidence? Br J Anaesth 2015;114:217–24.

50

Ganter MT, Hofer CK. Coagulation monitoring: current techniques and clinical use of viscoelastic point-of-care coagulation devices. Anesth Analg 2008;106:1366–75.

51

Weber CF, Gorlinger K, Meininger D, et al. Point-of-care testing: a prospective, randomized clinical trial of efficacy in coagulopathic cardiac surgery patients. Anesthesiology 2012;117:531–47.

52

Stensballe J, Ostrowski SR, Johansson PI. Viscoelastic guidance of resuscitation. Curr Opin Anaesthesiol 2014;27:212–8.

53

Karlsson O, Jeppsson A, Hellgren M. Major obstetric haemorrhage: monitoring with thromboelastography, laboratory analyses or both? Int J Obstet Anesth 2014;23:10–7.

54

Huissoud C, Carrabin N, Audibert F, et al. Bedside assessment of fibrinogen level in postpartum haemorrhage by thromboelastometry. BJOG 2009;116:1097–102.

55

Collins PW, Lilley G, Bruynseels D, et al. Fibrin-based clot formation as anearly and rapid biomarker for progression of postpartum hemorrhage: a prospective study. Blood 2014;124:1727–36.

56

Mallaiah S, Barclay P, Harrod I, et al. Introduction of an algorithm for ROTEMguided fibrinogen concentrate administration in major obstetric haemorrhage. Anaesthesia 2015;70:166–75.

57

Schoechl H, Nienaber U, Hofer G, et al. Goal-directed coagulation management of major trauma patients using rotation thromboelastometry (ROTEM)- guided administration of fibrinogen and prothrombin complex concentrate. Crit Care 2010;14:R55.

58

Brenni M, Worn M, Bruesch M, et al. Successful rotational thromboelastometry- guided treatment of traumatic haemorrhage, hyperfibrinolysis and coagulopathy. Acta Anaesthesiol Scand 2010;54:111–7.

59

Innerhofer P, Fries D, Mittermayr M, et al. Reversal of trauma-induced coagulopathy using first-line coagulation factor concentrates or fresh frozen plasma (RETIC): a single-centre, parallel-group, open-label, randomised trial. Lancet Haematol 2017;4:e258–e271.

Online Study Assessment Option
All readers who are qualified doctors or allied medical professionals can now automatically receive 2 Continuing Professional Development credits from FIGO plus a Study Completion Certificate from GLOWM for successfully answering 4 multiple choice questions (randomly selected) based on the study of this chapter.
Medical students can receive the Study Completion Certificate only.

 

(To find out more about FIGO’s Continuing Professional Development awards programme CLICK HERE)