Article, Obstetrics

Management of postpartum hemorrhagic shock and disseminated intravascular coagulation with damage control resuscitation

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American Journal of Emergency Medicine

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Management of postpartum hemorrhagic shock and disseminated intravascular coagulation with Damage control resuscitation

Abstract

Damage control resuscitation (DCR) that addresses all aspects of the lethal triad (ie, acidosis, hypothermia, and coagulopathy) is a resuscitation strategy originally developed for combat casualties and subsequently used for civilian trauma patients. However, its Survival benefits in obstetric emergencies have yet to be evaluated. Here, we report successful management of a life-threatening case of postpar- tum hemorrhagic shock associated with disseminated intravascular coagulation with DCR. A 35-year-old fifth gravida woman delivered a healthy full-term baby boy at 17:50 on February 7, 2013, through the vagina following oxytocin induction at 9:00. Immediately after the placenta expulsion at 17:55, massive postpartum hemor- rhage with DIC occurred, and hemorrhagic shock developed. Conventional colloid and crystalloid transfusion and hysterectomy were performed, but the bleeding persisted. Given the life-threaten- ing nature of the condition, a team of experts were called in from the entire hospital, and DCR was performed at 23:40. At 0:30 on February 8, clotting was seen in the intraVaginal bleeding with coagulation- related variables gradually improving. At 6:20, the patient returned to consciousness. By 15:30, urine amount started to increase with all the test parameters continuing to improve. On February 9, near-normal values were seen for hemoglobin level, platelets, fibrinogen, and other related parameters. Five days after DCR, all variables were restored to the normal value range, and the patient was transferred out of intensive care unit. This case report suggests that DCR may be considered as a life-saving solution to patients with postpartum hemorrhagic shock with DIC in obstetric emergencies.

Postpartum hemorrhage (PPH) is the leading cause of maternal death worldwide, claiming approximately 342900 lives in 2008 alone [1]. Nevertheless, PPH-associated death in many cases is believed to be avoidable by optimized management [2]. Currently, transfusion is the mainstay of management for PPH [3]. However, today’s transfu- sion strategies routinely used in obstetric emergencies are those developed in the United States military in the Korean and Vietnam wars based on observational data rather than randomized clinical trial results [4,5]. In these classical or conventional strategies, large volumes of crystalloid and red blood cells are used, and little attention is paid to coagulopathy [6]. Over the past decade, significant advances have been made in the understanding of posttrauma biology and pathophysiology, in parallel with accumulation of clinical data [7]. As a result, a new concept, “damage control resuscitation” (DCR), has emerged. Despite existence of differences in the definition of DCR, the central tenet of this evolving resuscitation strategy is the same, that is, to control (or ideally prevent) the development of coagulopathy in the severely injured through early proactive treatment [8,9]. Damage

control resuscitation was born in the military and is now being implemented in the civilian setting as well. However, the survival benefit of DCR has been rarely evaluated in obstetric emergencies. Here, we report successful management of a life-threatening case of postpartum hemorrhagic shock with disseminated intravascular coagulation by DCR.

A 35-year-old fifth gravida woman was admitted to the Depart- ment of Obstetrics and Gynecology of our tertiary hospital on February 6, 2013. In her 4 previous pregnancies, missed abortion occurred twice (in 2003 and 2005, respectively), natural miscarriage occurred once (in 2007) at 6 months due to premature rupture of membranes, and only the fourth pregnancy lasted to term with a healthy baby girl delivered through vagina in 2008. During the present pregnancy, she first felt fetal movements 5 months after her last period (May 2, 2012) and was hospitalized at 31 weeks for 7 days in response to signs of miscarriage. Later examinations at her regular prenatal visits showed normal glucose tolerance, indicating no pregnancy diabetes. At admission, she had a body temperature of 36.5?C, a pulse rate of 90 per minute, a respiratory rate of 20 per minute, and blood pressures of 110/80 mm Hg. An antepartum obstetric examination showed that her fundal height was 35 cm, her abdominal circumference was 105 cm, and the fetal heart rate was 144 beats per minute; no uterine contractions were detectable, and no extremity edema was evident.

Labor induction with oxytocin was performed at 9:00 on February 7, 2013. A healthy baby boy (3600 g) was born at 17:50, and the placenta came out at 17:55. Excessive vaginal bleeding occurred instantaneously after the placenta expulsion. Cervical and perineal lacerations were sutured, and uterine contraction-promoting treat- ments and colloids- and crystalloids-based Volume expansion measures were performed. However, no improvement in the bleeding was achieved. By 11:20, the total amount of blood loss was close to 2000 mL; her blood pressures dropped to 80/50 mm Hg, and her heart rate increased to 136 beats per minute from 90 beats per minute before labor induction.

Postpartum hemorrhage is defined by the American College of Obstetricians and Gynecologists as the loss of more than 500 mL of blood after vaginal delivery or 1000 mL after cesarean delivery [10]. Based on the timeframe, PPH is classified as primary (within the first 24 hours of delivery) and secondary (N 24 hours after delivery but b 12 weeks) [11]. Apparently, the patient in this case report had severe primary PPH. Moreover, the patient had severe DIC, a disorder characterized by systemic intravascular activation of the coagulation system, leading to overconsumption of coagulation factors and platelets [12]. When the uterus was pressed, steady stream of unclotted dark red blood came out of the vagina; bedside ultrasound revealed no Blood clots in the cavity of the corpus uteri and a slight

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Table 1

Time course changes in the major blood variables indicative of the severity of coagulopathy Variable Time between 21:20, February 7, and 15:30, February 8, 2013

21:20

22:20

23:05

23:50

00:30

03:10

06:20

09:20

13:45

19:05

22:15

01:05

07:15

15:30

HB (g/L)

64

35

32

32

39

48

60

62

63

51

63

71

75

77

PLTs (x109/L)

172

131

60

84

70

141

62

45

36

36

85

68

56

47

Fib (g/L)

ND

0.27

0.32

0.73

2.08

2.27

1.59

1.48

1.83

2.19

2.40

2.65

2.82

3.50

PT (s)

N 320

27.5

29.7

24.6

22.3

20.1

17.1

15.4

15.1

13.6

12.3

12.2

11.8

11.6

TT (s)

N 300

32.3

26.3

20.7

N 300

N 300

43.7

26.3

33.3

17.5

16.2

16.1

15.5

14.5

APTT (s)

N 400

N 400

N 400

N 400

N 400

119.4

99.2

63.9

70.1

48.2

42.9

40.6

38.8

37.9

D-dimer (ng/mL)

ND

ND

ND

ND

ND

42380

17080

11470

10840

9540

10615

10410

11105

10530

FDP (mg/L)

289.2

342.8

328.1

275.3

246.6

237.8

169.4

84.5

88.8

82.3

86.1

80.1

87.3

97.4

Abbreviations: HG, hemoglobin; PLTs, platelets; FIB, fibrinogen; PT, prothrombin time; TT, thromboplastin time; APTT, activated partial thromboplastin time; FDP, Fibrin degradation products.

deposit of blood in the lower part of the uterus; and laboratory tests showed severely abnormal values in the major coagulation function variables including hemoglobin level, platelets, fibrinogen, prothrom- bin time, activated partial thromboplastin time, fibrin degradation products, and D-dimer that was undetectable (Table 1).

Given the severity of the patient’s condition (hemorrhagic shock with DIC and weakened uterine contractions), measures including accelerating the fluid transfusion rate and performing component transfusion (plasma and coagulation factors) were taken. Neverthe- less, bleeding was not mitigated. At 21:40, a decision on hysterectomy was made. During the hysterectomy procedure, another 3100 mL blood was lost. After hysterectomy, intraperitoneal bleeding contin- ued. As a result, the abdomen had to be kept open. When intravenous drips of red blood cells together with plasma, platelets, and fibrinogen were given at an accelerated rate and intra-Abdominal compression was attempted to control bleeding, still no success was achieved. By 23:00, blood pH dropped to 7.03, and all laboratory test variables stayed abnormal (Table 1).

It has been proposed that successful management of exsanguinat- ing PPH requires a team effort [6]. In our case, experts were called in from the relevant departments of the entire hospital after the failure in the control of bleeding with all the measures described above. The Chair of the Critical Care Department was in at 23:30. A consensus was reached on an immediate DCR, which consisted of the following measures: (1) termination of crystalloid transfusion, (2) resuscitation with packed blood products, (3) control of hypotension with norepinephrine, (4) minimization of coagulants with low-dose anticoagulation heparin, (5) use of methylprednisolone for possible amniotic fluid embolism, and (6) correction of acidosis. Half hour after the DCR procedure, intraperitoneal bleeding started to reduce gradually, and the abdomen was closed. By 0:30 on February 8, 2013, clotting was seen in intravaginal bleeding, and most of the coagulation function variables were improving (Table 1). At 6:20, the patient returned to consciousness. By 15:30 PM, urine amount increased to 150 mL/h, and the coagulation function variables continued to improve. Five days after DCR, all variables were restored to the normal value ranges, and the patient was transferred out of intensive care unit.

In summary, we successfully saved the life of the patient with DCR after the conventional resuscitation strategies and hysterectomy

failed to control bleeding. This case report suggests that DCR may be considered as a life-saving strategy for patients with hemorrhagic shock and DIC in obstetric emergencies.

Xiaoyan Xue MD Lina Liu MD Zhiguo Rao MD

Department of Critical Care Aerospace Central Hospital Beijing, 100049 China

E-mail address: [email protected] http://dx.doi.org/10.1016/j.ajem.2013.03.051

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