Header bg
  • Users Online: 187
  • Print this page
  • Email this page
Header bg

Table of Contents
Year : 2022  |  Volume : 6  |  Issue : 3  |  Page : 191-195

Amniotic fluid embolism with cardiac arrest and coagulopathy during Cesarean section: A case report

Department of Women’s Anaesthesia, KK Women’s and Children’s Hospital, Singapore

Date of Submission25-Mar-2022
Date of Decision28-Apr-2022
Date of Acceptance07-May-2022
Date of Web Publication27-Jul-2022

Correspondence Address:
Lan Fern Michele Lim
Department of Women’s Anaesthesia, KK Women’s and Children’s Hospital, 100 Bukit Timah Rd
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bjoa.bjoa_96_22

Rights and Permissions

Amniotic fluid embolism (AFE) is a rare but potentially fatal condition of pregnancy. It is a diagnosis of exclusion and its management largely supportive. We present a case of a 36-year-old patient who was admitted at 32 weeks gestational age with an acute abdomen. She underwent an emergency Cesarean section for fetal distress secondary to possible placental abruption. This was complicated by post-delivery cardiac arrest and respiratory failure from suspected AFE, disseminated intravascular coagulation and severe postpartum hemorrhage. She was managed with vasopressors, point-of-care coagulation testing, massive transfusion, anti-fibrinolytics, fibrinogen concentrate and eventual hysterectomy. Post-operatively, she was treated for acute respiratory distress syndrome in the intensive care unit. She and her neonate survived with good outcome. We discuss the practical constraints faced in the diagnosis and management of AFE, due to a lack of specific diagnostic tests and the need for prompt high-quality resuscitation, simultaneous management of coagulopathy and massive hemorrhage, timely activation of senior personnel and the involvement of a multi-disciplinary team in a crisis situation.

Keywords: Amniotic fluid, embolism, intensive care unit, pregnancy, respiratory distress syndrome

How to cite this article:
Lim LF, Sim XL, Sng BL. Amniotic fluid embolism with cardiac arrest and coagulopathy during Cesarean section: A case report. Bali J Anaesthesiol 2022;6:191-5

How to cite this URL:
Lim LF, Sim XL, Sng BL. Amniotic fluid embolism with cardiac arrest and coagulopathy during Cesarean section: A case report. Bali J Anaesthesiol [serial online] 2022 [cited 2022 Aug 10];6:191-5. Available from: https://www.bjoaonline.com/text.asp?2022/6/3/191/352407

  Introduction Top

Amniotic fluid embolism (AFE) is a rare but potentially catastrophic complication of pregnancy. Its incidence ranges from 1.9 - 6.1 cases per 100 000 maternities,[1] and case-fatality rates from 11 – 44%.[1],[2] Previously hypothesized to result from amniotic fluid passing into and obstructing the pulmonary circulation, an anaphylactoid reaction with activation of proinflammatory mediators is now thought to be the likely mechanism.[3] The resulting pulmonary vasoconstriction and right heart failure causes hypoxia, hypotension and adverse fetal effects. Activation of the coagulation cascade results in disseminated intravascular coagulation (DIC). Complications like left heart failure, acute lung injury and multi-organ failure may ensue.

Its clinical presentation is variable.[4] Classically it presents with a triad of hypotension, acute respiratory failure and coagulopathy during labour and delivery. Those presenting with cardiorespiratory arrest have higher risks of neurologic sequelae and death. The respiratory system is compromised by pulmonary edema or acute respiratory distress syndrome (ARDS).

Our case report presents a patient who underwent an emergency Cesarean section for fetal distress secondary to placental abruption, which was complicated by post-delivery cardiac arrest from suspected AFE, DIC and massive postpartum hemorrhage (PPH), culminating in hysterectomy. She and her neonate survived with good outcome. The practicalities in diagnosis and management of AFE are discussed.

  Case Report Top

A 36-year-old gravida-3 parous-2 patient, with a history of 2 previous Cesarean deliveries, presented at 32 weeks gestational age with acute abdominal pain. Fetal bradycardia with heart rate (HR) of 96/min was detected. Decision was made for a category 1 Cesarean section in view of non-assuring fetal status.

Rapid sequence intubation was performed. A Couvelaire uterus was noted on surgical entry without scar rupture. The fetus was delivered with low APGAR scores, intubated and transferred to the neonatal intensive care unit (ICU). Retroplacental clots with estimated 80% placental abruption were noted, with uterine atony. Uterotonics included IV carbetocin, oxytocin infusion, IM Syntometrine®, IM carboprost and PR misoprostol. B-lynch suture was performed. At closure, there was adequate uterine tone and hemostasis and estimated blood loss (EBL) of 1 L. With 2.5 L of crystalloid infused, she maintained stable mean arterial pressures above 70 mmHg and HR around 90/min without vasopressors. Hemoglobin concentration (Hb) was 8 g/dL (using HemoCue®). One unit of packed red blood cells (RBC) and IV tranexamic acid 1g were administered.

After skin closure, hypotension was noted with blood pressure (BP) of 90/55 mmHg, decreasing rapidly despite phenylephrine and fluids. There was sinus tachycardia, an acute drop in end-tidal C02 from 35 to 10 mmHg and unrecordable oxygen saturation (SpO2). FiO2 was increased to 1.0. Lung compliance was normal, and no rash noted. The carotid pulse became impalpable. Code blue was activated and cardiopulmonary resuscitation (CPR) started for cardiac arrest with pulseless electrical activity (PEA).

After return of spontaneous circulation (ROSC), she remained hypotensive despite adrenaline boluses. The provisional diagnosis was AFE or pulmonary thromboembolism. There was subsequent bradycardia and a second cardiac arrest with PEA. CPR was restarted and IV adrenaline 1 mg given. Post ROSC, central venous and arterial catheters were inserted and adrenaline infusion started at 0.3mcg/kg/min. She remained hypotensive (systolic BP 60 – 80 mmHg), tachycardic and hypoxemic (Sp02 41 – 86%). Arterial blood gas (ABG) showed metabolic and respiratory acidosis and hypoxemia. [Table 1]
Table 1: Arterial blood gas results

Click here to view

A referral for extracorporeal membrane oxygenation (ECMO) was made in view of prolonged hypoxemia. However, she was not a suitable candidate due to high bleeding risks. Fifty minutes after initial collapse, sudden hematuria and massive per-vaginal bleeding were noticed. Significant coagulopathy was presumed. Decision was made for re-laparotomy and hysterectomy.

Coagulation test results, albeit not available immediately, painted a picture of DIC: prothrombin time (PT): >120 s (INR incalculable), activated partial thromboplastin time (aPTT): > 180s, fibrinogen: < 0.4 g/L. Rotational thromboelastometry (ROTEM®) [Figure 1] showed flat lines in all tests and unrecordable FibTEM A5 and ExTEM A5. 4 units of RBC, 500 ml of fresh frozen plasma (FFP), 2 units of platelet concentrate and IV fibrinogen 2g were given.
Figure 1: ROTEM result

Click here to view

At surgical closure, EBL was 2.5 L. Hypoxemia persisted, responding intermittently to recruitment maneuvers and tracheal suctioning. Repeat ABG [Table 1] showed improved metabolic and respiratory acidosis, Hb 10.5 g/dL and coagulation profile was improved after targeted transfusion, with PT 17.3s (INR 1.49), aPTT 49.9s, and fibrinogen 1.54 g/L.

She was kept intubated and ventilated in ICU over 2 days. ARDS was diagnosed. Chest radiography (CXR) showed bilateral pulmonary infiltrates. CT pulmonary angiogram showed extensive pulmonary edema, without evidence of pulmonary embolism. Electrocardiogram (ECG) showed non-specific T inversions. [Figure 2]. Increased serum troponins and transaminitis were attributed to myocardial and liver injury respectively. With clinical improvement, she was extubated on post-operative day (POD) 3. Transthoracic echocardiogram performed then showed normal left ventricular (LV) systolic function and ejection fraction, normal right ventricular (RV) systolic function and low probability of pulmonary hypertension. She was discharged on POD 9 without clinical neurologic deficits. The neonate was discharged well a month later.
Figure 2: Post-operative ECG

Click here to view

  Discussion Top

There are specific practical learning points in our case:

AFE is a clinical diagnosis of exclusion. The Society of Maternal Fetal Medicine and AFE Foundation proposed four criteria[5]:

  • (1) sudden onset of cardiorespiratory arrest, or both hypotension and respiratory compromise

  • (2) overt DIC

  • (3) absence of fever

  • (4) onset during labour or within 30 min of placental delivery

Not all these criteria were present initially in our patient. The sudden onset of hemodynamic collapse and respiratory failure focused our diagnoses to AFE and pulmonary thromboembolism. Differential diagnoses included: (1) Cardiac arrest: myocardial infarction (2) Acute respiratory failure with hemodynamic instability: venous air embolism, sepsis, anaphylaxis (3) Coagulopathy: sepsis, hemorrhage, severe preeclampsia. The development of significant coagulopathy made AFE most likely, as it is a highly specific hallmark distinguishing it from differentials like anaphylaxis or pulmonary thromboembolism.[5] While placental abruption likely contributed to DIC, it was unlikely it had primarily caused cardiac arrest with persistent hypoxemia.

There are no diagnostic tests of sufficient accuracy for AFE. Proposed biomarkers such as insulin-like growth factor binding protein-1, zinc coproporphyrin-1, sialyl-Tn antigen, complement C3, C4 and interleukin-8[6] are not widely available. Standard laboratory tests aiding in diagnosis require turnover time. Point-of-care ABG guides management of ventilation and acid-base derangement, but arterial puncture is challenging in patients in extremis. Coagulation tests to diagnose DIC take time, and may not markedly change in early DIC.[7] Point-of-care coagulation tests are thus more useful, and may demonstrate hyperfibrinolysis or hypofibrinogenemia,[8] and aid in blood product management. Changes in ECG and CXR are non-specific to AFE. Investigations to exclude pulmonary thromboembolism may be performed. Echocardiography may be recommended[9] in the acute phase for diagnosis.

Management of AFE requires a well-coordinated, multi-disciplinary team comprising members from anaesthesia, critical care, maternal-fetal medicine, respiratory medicine, cardiology and haematology. Manpower required for resuscitation should not be under-estimated. Our hospital has protocols for the activation of senior staff during acute emergencies.

After initial stabilization of the patient, early echocardiography can determine the nature of cardiac injury for tailored treatment.[9] RV failure is exacerbated by high positive end-expiratory pressure, hypoxemia, hypercarbia, acidosis and excessive fluids. The failing RV may be supported pharmacologically by milrinone, dobutamine or inhaled nitric oxide. If LV failure predominates, preload, contractility and afterload should be optimized. ECMO, intra-aortic balloon counter-pulsation, cardiopulmonary bypass, RV assist device, continuous hemofiltration and plasma exchange transfusion[10],[11],[12],[13],[14] are currently experimental. ECMO may be considered in AFE for severe respiratory failure or persistent hemodynamic instability,[9],[14] but there is no definite evidence of significantly improved outcomes.[14] There were concerns using ECMO in this case due to development of DIC and uncontrolled PPH.

Massive PPH must be managed in close communication with the surgical team, and blood products given according to institution-based massive blood transfusion protocols. Transfusing a higher ratio of FFP to RBC may increase survival in obstetric hemorrhage.[15] Fibrinogen should be maintained above 1.5g/dL in bleeding obstetric patients,[7] and anti-fibrinolytic agents considered.[9] Off-label use of recombinant factor VIIa should be discussed with the hematologist, due to its possible thrombotic risks.[7]

A department review after critical incidents is key to highlight issues and obstacles encountered. AFE is rare and likely highly educational for the disciplines involved. Incident reporting, departmental review and interdisciplinary reviews involving anesthesia, maternal-fetal medicine and nursing were conducted here. Thorough review of protocols is important to further improve established workflows. Prompt recognition and resuscitation, familiarity with institutional protocols, timely activation of senior staff and a multi-disciplinary team approach enhanced our patient’s and neonate’s outcome.

  Conclusion Top

Though rare, AFE remains a leading cause of direct maternal death in developed countries. Its associated neurologic injury in survivors[4] and perinatal morbidity is significant.[1] This case report adds insight into current clinical management of AFE. A high index of suspicion is required for diagnosis, and prompt high-quality resuscitation is essential. Familiarity with institutional protocols and preparation for such rare yet potentially lethal events through incident reporting, inter-disciplinary review, education and simulations will ensure smooth and successful resuscitation.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

  References Top

Knight M, Berg C, Brocklehurst P, Kramer M, Lewis G, Oats J, et al. Amniotic fluid embolism incidence, risk factors and outcomes: A review and recommendations. BMC Pregnancy Childbirth 2012;12:7.  Back to cited text no. 1
Benson MD Amniotic fluid embolism mortality rate. J Obstet Gynaecol Res 2017;43:1714-8.  Back to cited text no. 2
Shamshirsaz AA, Clark SL Amniotic fluid embolism. Obstet Gynecol Clin North Am 2016;43:779-90.  Back to cited text no. 3
Clark SL, Hankins GD, Dudley DA, Dildy GA, Porter TF Amniotic fluid embolism: Analysis of the national registry. Am J Obstet Gynecol 1995;172:1158-67; discussion 1167-9.  Back to cited text no. 4
Clark SL, Romero R, Dildy GA, Callaghan WM, Smiley RM, Bracey AW, et al. Proposed diagnostic criteria for the case definition of amniotic fluid embolism in research studies. Am J Obstet Gynecol 2016;215:408-12.  Back to cited text no. 5
Stawicki SP, Papadimos TJ Challenges in managing amniotic fluid embolism: An up-to-date perspective on diagnostic testing with focus on novel biomarkers and avenues for future research. Curr Pharm Biotechnol 2014;14:1168-78.  Back to cited text no. 6
Erez O, Mastrolia SA, Thachil J Disseminated intravascular coagulation in pregnancy: Insights in pathophysiology, diagnosis and management. Am J Obstet Gynecol 2015;213:452-63.  Back to cited text no. 7
Collins NF, Bloor M, McDonnell NJ Hyperfibrinolysis diagnosed by rotational thromboelastometry in a case of suspected amniotic fluid embolism. Int J Obstet Anesth 2013;22:71-6.  Back to cited text no. 8
Pacheco LD, Clark SL, Klassen M, Hankins GDV Amniotic fluid embolism: Principles of early clinical management. Am J Obstet Gynecol 2020;222:48-52.  Back to cited text no. 9
Viau-Lapointe J, Filewod N Extracorporeal therapies for amniotic fluid embolism. Obstet Gynecol 2019;134:989-94.  Back to cited text no. 10
Hsieh YY, Chang CC, Li PC, Tsai HD, Tsai CH Successful application of extracorporeal membrane oxygenation and intra-aortic balloon counterpulsation as lifesaving therapy for a patient with amniotic fluid embolism. Am J Obstet Gynecol 2000;183:496-7.  Back to cited text no. 11
Stanten RD, Iverson LI, Daugharty TM, Lovett SM, Terry C, Blumenstock E Amniotic fluid embolism causing catastrophic pulmonary vasoconstriction: Diagnosis by transesophageal echocardiogram and treatment by cardiopulmonary bypass. Obstet Gynecol 2003;102:496-8.  Back to cited text no. 12
Weksler N, Ovadia L, Stav A, Ribac L, Iuchtman M Continuous arteriovenous hemofiltration in the treatment of amniotic fluid embolism. Int J Obstet Anesth 1994;3:92-6.  Back to cited text no. 13
Pacheco LD, Saade GR, Hankins GDV Extracorporeal membrane oxygenation (ECMO) during pregnancy and postpartum. Semin Perinatol 2018;42:21-5.  Back to cited text no. 14
Tanaka H, Matsunaga S, Yamashita T, Okutomi T, Sakurai A, Sekizawa A, et al. A systematic review of massive transfusion protocol in obstetrics. Taiwan J Obstet Gynecol 2017;56:715-8.  Back to cited text no. 15


  [Figure 1], [Figure 2]

  [Table 1]


    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

  In this article
Case Report
Article Figures
Article Tables

 Article Access Statistics
    PDF Downloaded14    
    Comments [Add]    

Recommend this journal