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Journal of Obstrectic Anaesthesia and Critical Care
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 Table of Contents  
CASE REPORT
Year : 2018  |  Volume : 8  |  Issue : 1  |  Page : 46-49

A maternal near-miss case of massive obstetric hemorrhage: Recent trends in management of hemostatic failure


1 Department of Anaesthesiology, Pain and Perioperative Medicine, Sir Ganga Ram Hospital, New Delhi, India
2 Department of Blood Transfusion Medicine, Pain and Perioperative Medicine, Sir Ganga Ram Hospital, New Delhi, India

Date of Web Publication13-Apr-2018

Correspondence Address:
Dr. Neetu Jain
Department of Anaesthesiology, Pain and Perioperative Medicine, Sir Ganga Ram Hospital, Old Rajinder Nagar, New Delhi - 110060
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/joacc.JOACC_49_17

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  Abstract 


Obstetric hemorrhage is a leading cause of maternal mortality and morbidity. Uterine atony is the major cause of postpartum hemorrhage (PPH) accounting for 79% of all cases besides genital trauma, placental causes and coagulation disorders. We present a case of massive obstetric hemorrhage secondary to uterine atony that was referred to our center in a state of hemorrhagic shock with severe metabolic acidosis, hypothermia and coagulopathy. Prompt activation of massive transfusion protocol, use of thromboelastography guided correction of coagulopathy and early hysterectomy to control hemorrhage played a vital role in successful patient management. Postoperative intensive management of ventilatory function, haemodynamics, kidney function and sepsis led to a favourable outcome. This case highlights the importance of multi-disciplinary team management involving anesthesiologist, emergency medical personnel, obstetrician, blood transfusion services and critical care team in optimizing the clinical condition of the critical patient.

Keywords: Massive transfusion protocol, obstetric hemorrhage, post-partum hemorrhage, thromboelastography, uterine atony


How to cite this article:
Jain N, Gupta AK, Sood J, Khillan K. A maternal near-miss case of massive obstetric hemorrhage: Recent trends in management of hemostatic failure. J Obstet Anaesth Crit Care 2018;8:46-9

How to cite this URL:
Jain N, Gupta AK, Sood J, Khillan K. A maternal near-miss case of massive obstetric hemorrhage: Recent trends in management of hemostatic failure. J Obstet Anaesth Crit Care [serial online] 2018 [cited 2019 Dec 7];8:46-9. Available from: http://www.joacc.com/text.asp?2018/8/1/46/230065




  Introduction Top


The maternal mortality ratio is 239 in developing countries versus 12 in developed countries per 100,000 live births.[1] There is a huge disparity in mortality rate between the countries as well as within a country, based primarily on availability and access of health care facilities. Obstetric hemorrhage accounts for 27% of all maternal deaths.[2] Postpartum hemorrhage (PPH) complicates 2.9% of all deliveries. PPH is further exacerbated by hemostatic failure.[3] Early judicious use of blood component therapy guided by thromboelastography (TEG) point-of-care testing (POCT) and multidisciplinary approach helps in achieving a favourable patient outcome.


  Case Report Top


A 30-year-old G3P2 female with previous two uncomplicated vaginal deliveries and an uneventful course of pregnancy underwent third vaginal delivery at 39 weeks of gestation. She developed atonic PPH, not responding to first line uterotonics (oxytocin) and uterine massage; and refractory to ergometrine, 15-methyl PGF and rectal misoprostol. She was brought to our tertiary care centre in a state of hemorrhagic shock five hours post-delivery, in an unresponsive state with feeble peripheral pulses, unrecordable blood pressure and extreme pallor. After securing the airway with an endotracheal tube and intravenous fluid resuscitation, noradrenaline infusion was started at 0.5 μg/kg/min.

Blood samples were sent for complete blood count, coagulation profile, renal function tests, blood grouping and cross matching. Massive transfusion protocol (MTP) was activated as per the hospital blood transfusion policy. Four units each of uncrossmatched O negative packed red blood cells (PRBC), fresh frozen plasma (FFP) and platelet concentrate were promptly released from the blood bank. Two PRBCs were transfused in the emergency room (ER) and decision for emergency hysterectomy was taken.

She was immediately transferred to the operating room (OR) wherein scrub team, surgeons and anaesthesiologists were ready. On arrival in OR, her pulse rate was 160–170 beats per minute and blood pressure 70/40 mm Hg. Oesophageal temperature probe was inserted which recorded an initial temperature of 34.6°C. Anaesthesia was maintained with intermittent fentanyl, atracurium and a mixture of oxygen, nitrous oxide (50:50) with sevoflurane. Tranexamic acid 1 gm was given intravenously. As the surgery proceeded, intravenous infusion of vasopressin 0.04 IU/kg/hr was added to augment blood pressure. Clinical coagulopathy was evident and TEG in the operating suite [Figure 1] detected an abnormal R time (23.1 minutes), K time (11.2 minutes), α angle (20.8°) and maximum amplitude (MA 45.6 minutes). She was transfused cryoprecipitate 2 pools (8 units), FFP 8 units, platelet concentrate 4 units and PRBC 7 units. Arterial blood gas revealed severe metabolic acidosis and hypocalcaemia with pH 6.993, PaCO2 19.7 mm Hg, base deficit -26.7mmol/L, HCO -3 5.8 mmol/L, lactate 18.37 mmol/L and ionized calcium 0.68 mmol/L. Calcium gluconate and sodium bicarbonate supplementation were given as a supportive measure. Active warming was done with the help of fluid warming devices and forced air warming blankets to raise the core temperature to 36.0°C over two hours. Her urine output was 250 ml intraoperatively. Blood reports received intraoperatively revealed haemoglobin 3.9 g/dL, platelet count 70,000/μl, activated partial thromboplastin time (aPTT) >400 secs, prothrombin time >300 secs and serum fibrinogen 0.8 g/L. She was transferred to critical care unit for elective ventilation and further management.
Figure 1: Intraoperative thromboelastrograph. R value = reaction time (s); K = kinetics (s); α = angle (slope between R and K); MA = maximum amplitude (mm); LY30 = amplitude at 30 minutes (%)

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Postoperatively, she was managed in critical care unit wherein further blood and blood products were transfused. Gradually, her condition stabilized and coagulopathy improved [Figure 2]. Her serum fibrinogen levels rose to 1.34 g/L on second postoperative day. Procalcitonin levels (161.51ng/ml) were indicative of severe sepsis. She responded to antibiotics and was extubated on 7th postoperative day. She developed acute kidney injury (AKI) for which intermittent renal replacement therapy was given on 10th, 14th and 19th day of surgery after which she recovered from AKI. Her procalcitonin level showed a decreasing trend and came down to 2.37 ng/ml by 26th day of surgery. She was discharged from the hospital on 32nd day in a stable condition. Overall, 24 units PRBCs, 16 units FFP, 22 units platelet concentrate and 3 pools (12 units) of cryoprecipitate were transfused during her hospital stay.
Figure 2: Postoperative thromboelastrograph on day 1. R value = reaction time (s); K = kinetics (s); α = angle (slope between R and K); MA = maximum amplitude (mm); LY30 = amplitude at 30 minutes (%)

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  Discussion Top


Uterine atony is the major cause of PPH. Known risk factors for atonic PPH include age <20 years or >40 years, cesarean delivery, hypertensive disorders of pregnancy, polyhydramnios, chorioamnionitis, multiple gestations, retained placenta and antepartum hemorrhage.[4] Prolonged labor and augmentation of labor are other proposed risk factors but more data is needed to corroborate the hypothesis.[4] Absence of risk factors in 40% cases of atonic PPH makes this complication unpredictable, as seen in our case. Vigilance in all the cases, especially in peripheral maternity centres, accurate estimation of blood loss during delivery to allow prompt, timely intervention (escalation of management or transfer to a higher facility) is the key to successful management.

Prompt communication and pre-existing MTP as part of the transfusion services play a game changer role in such near-miss cases. Early use of uncrossmatched/type specific blood; FFP to packed cells in the ratio 1:1 or 1:2 with platelets and cryoprecipitate as used in our case, has been advocated as per the MTP in acute obstetric hemorrhage.[5] The intraoperative use of crystalloids and colloids was restricted to prevent further worsening of dilutional coagulopathy.

Intraoperative TEG [Figure 1] showed evidence of coagulopathy with poor initiation of clot formation and decreased clot strength and stability. Early goal directed transfusion of FFP, cryoprecipitate and platelets was done for increased R time, decreased α angle and decreased MA respectively. Follow up TEG [Figure 2] after appropriate transfusion evidenced correction of coagulopathy which was reflected in considerable improvement in clinical condition of the patient. These POCT devices are invaluable in guiding medical management of hemorrhage and avoiding loss of time waiting for routine laboratory results.

Early activation of fibrinolysis is known within one hour of childbirth possibly because of associated tissue damage. Early use of tranexamic acid, as used in our case, has been advocated for the treatment of PPH. Tranexamic acid reduces death due to bleeding in women with PPH without any adverse effects.[6]

The role of fibrinogen in PPH is also being increasingly acknowledged. Fibrinogen levels increase with advancing gestation to 4.5–5.8 g/L at term compared to a normal value of 2.0–4.5 g/L.[7] Fibrinogen level less than 2.0 g/L is the only marker associated with 100% positive predictive value for severe PPH.[8] Likewise, administration of cryoprecipitate is advocated when fibrinogen levels fall below 1.0 g/L.[9] In our case, cryoprecipitate was administered based on the TEG findings with a markedly increased K time and decreased α angle indicating poor thrombin burst.

It has been advocated to maintain a platelet count of 50,000/μl during active bleeding.[9] Johansson and Stensballe advocated that proactive administration of platelets during acute hemorrhage is associated with lower mortality.[10]

Franchini et al. advocated the use of recombinant factor VIIa in life threatening PPH before considering hysterectomy.[11] However, in our case of severe hemorrhagic shock with ongoing bleeding, it was deemed that the administration of rFVIIa would be inappropriate with low arterial pH and/or co-factors. So, decision for hysterectomy was taken.

Uncontrolled hemorrhage leads to the lethal triad of hypothermia, acidosis and coagulopathy each of which exacerbates the other.[12] To abort this vicious cycle and ensure optimal function of transfused coagulation factors; prevention and treatment of hypothermia, acidosis and hypocalcaemia is absolutely essential. Early use of active fluid warming devices and forced air warming blankets, calcium gluconate and sodium bicarbonate supplementation aided in correcting hypothermia, hypocalcaemia and metabolic acidosis, respectively. Besides optimal intraoperative management, the role of seamless continuation of care into the postoperative period cannot be overstated to achieve favourable outcome. Massive hemorrhage and transfusions may be associated with significant complications.[12] In our case, the intensive management in critical care unit by supporting ventilation, maintaining fluid and electrolyte balance, optimizing kidney function and control of sepsis led to a positive outcome.

This case highlights the early use of point-of-care TEG, tranexamic acid, timely implementation of massive transfusion protocol, damage control resuscitation and surgery, which was lifesaving in our critical emergency scenario. The multidisciplinary approach involving anaesthesiologists, obstetricians, blood transfusion services, nephrologists and critical care team remains the cornerstone of optimal patient care in the management of massive obstetric hemorrhage.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient has given her consent for her images and other clinical information to be reported in the journal. The patient understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Maternal mortality. WHO Media centre. Fact sheet, Updated November 2016. Available from: http://www.who.int/mediacentre/factsheets/fs348/en/. [Last accessed on 2017 Jun 07].  Back to cited text no. 1
    
2.
Bateman BT, Berman MF, Riley LE, Leffert LR. Epidemiology of postpartum haemorrhage in a large, nationwide sample of deliveries. Anesth Analg 2010;110:1368-73.  Back to cited text no. 2
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3.
Collins PW, Cannings-John R, Bruynseels D, Mallaiah S, Dick J, Elton C, et al. Viscoelastometric-guided early fibrinogen concentrate replacement during postpartum haemorrhage: OBS2, a double-blind randomized controlled trial. Br J Anaesth 2017;119:411-21.  Back to cited text no. 3
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4.
Kramer MS, Berg C, Abenhaim H, Dahhou M, Rouleau J, Mehrabadi A, et al. Incidence, risk factors, and temporal trends in severe postpartum haemorrhage. Am J Obstet Gynecol 2013;209:449.e1-7.  Back to cited text no. 4
    
5.
Holcomb JB, Tilley BC, Baraniuk S, Fox EE, Wade CE, Podbielski JM, 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.  Back to cited text no. 5
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6.
Effect of early tranexamic acid administration on mortality, hysterectomy, and other morbidities in women with post-partum hemorrhage (WOMAN): An international, randomised, double-blind, placebo-controlled trial. Lancet 2017;389:2105-16.  Back to cited text no. 6
    
7.
Levy JH, Welsby I, Goodnough LT. Fibrinogen as a therapeutic target for bleeding: A review of critical levels and replacement therapy. Transfusion 2014;54:1389-405.  Back to cited text no. 7
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8.
Charbit B, Mandelbrot L, Samain E, Baron G, Haddaoui B, Keita H, et al. PPH Study Group. The decrease of fibrinogen is an early predictor of the severity of postpartum haemorrhage. J Thromb Haemost 2007;5:266-73.  Back to cited text no. 8
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9.
Mercier FJ, Bonnet MP. Use of clotting factors and other prohemostatic drugs for obstetric haemorrhage. Curr Opin Anaesthesiol 2010;23:310-6.  Back to cited text no. 9
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10.
Johansson PI, Stensballe J. Hemostatic resuscitation for massive bleeding: the paradigm of plasma and platelets-a review of the current literature. Transfusion 2010;50:701-10.  Back to cited text no. 10
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11.
Franchini M, Franchi M, BergaminiV, Salvagno GL, Montagnana M, Lippi G. A critical review on the use of recombinant factor VIIa in life-threatening obstetric postpartum haemorrhage. Semin Thromb Hemost 2008;34:104-12.  Back to cited text no. 11
    
12.
Sihler KC, Napolitano LM. Complications of massive transfusion. Chest 2010;137:209-20.  Back to cited text no. 12
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