Cardiac Arrest Caused by Amniotic Fluid Embolism: a Report of Two Clinical Cases

Abstract

Background:

Amniotic fluid embolism (AFE) is a rare and catastrophic obstetric complication that can lead to sudden cardiac arrest, respiratory distress, and disseminated intravascular coagulation. Recognizing and managing this condition promptly is crucial for improving maternal and neonatal outcomes.

Objective:

This report includes two case studies describing the timely detection, prompt delivery of medical treatment, and the interdisciplinary approach essential for achieving better outcomes for mothers and children confronting with this catastrophic condition.

Case presentation:

Case 1: A 39-year-old pregnant woman at 36 weeks and 5 days of gestation with central placenta previa was admitted due to antepartum hemorrhage. She developed convulsions and cardiac arrest during a cesarean section, requiring cardiopulmonary resuscitation. Laboratory tests revealed severe anemia, thrombocytopenia, coagulopathy, severe acidosis, and myocardial injury. Bedside echocardiography and CT scan identified high-risk pulmonary embolisms. Intensive care included VA-ECMO, CRRT, transcatheter arterial embolization, and mechanical thrombectomy. Histopathology confirmed amniotic fluid components making up the emboli. Case 2: A 31-year-old female was transferred following a cesarean section for central placenta previa complicated by severe hemorrhage, cardiac arrest, and pulmonary embolism. Laboratory results showed severe anemia, thrombocytopenia, significant coagulopathy, myocardial injury, and hepatic injury. Histopathology confirmed amniotic components in the embolism. Management involved extensive blood transfusions, and pulmonary thromboendarterectomy. She was discharged in improved condition.

Conclusion:

Early diagnosis and prompt intervention are crucial to optimizing outcomes for patients with amniotic fluid embolism, utilizing a comprehensive multidisciplinary approach.

1. BACKGROUND

Amniotic fluid embolism (AFE) is a major cause of maternal morbidity and mortality, posing significant challenges in managing obstetric patients. The mechanism of this syndrome is not well understood, but it is believed to be anaphylactoid due to the entry of amniotic fluid into the maternal circulation (1-3). Early recognition and immediate multidisciplinary intervention are critical for improving outcomes in such cases. Because of the rapid course and high mortality rate, prompt diagnosis and comprehensive control by obstetricians, anesthetists, intensivists, and cardiologists are crucial (1-3).

2. OBJECTIVE

This report includes two case studies describing the timely detection, prompt delivery of medical treatment, and the interdisciplinary approach essential for achieving better outcomes for mothers and children confronting with this catastrophic condition.

3. CASE PRESENTATION

Case 1

The patient was a 39-year-old gravida 5, para 2 (GTPAL 22002) female at her 36 weeks and 5 days of gestation. She was brought to the Emergency Department after experiencing antepartum hemorrhage caused by a central placenta previa that was detected during her routine prenatal check-ups. The patient underwent a cesarean section under spinal anesthesia. Right after the fetal delivery, the she abruptly developed convulsions, cyanosis, and cardiac arrest. Cardiopulmonary resuscitation was initiated immediately and spontaneous circulation was recovered after 30 minutes. She was then transferred to the Intensive Care Unit for further monitoring and management.

Figure 1. CT-scan findings of chest.

Bedside echocardiography revealed a significantly dilated right ventricle with reduced tricuspid annular plane systolic excursion (TAPSE) of 10 mm, and interventricular septal displacement. There was also severe tricuspidal regurgitation with a vena contracta of 9 mm and pulmonary hypertension with a pulmonary artery systolic pressure (PASP) of 45 mmHg. Left ventricular function was preserved as assessed by echocardiography. The results highly suggest an acute right ventricular failure, therefore, we decided to perform a contrast- enhanced chest computed tomography for exploring the diagosis of high-risk PE. The result revealed partial thrombosis in the pulmonary artery trunk and a complete occlusion of the right pulmonary artery. The CT also demonstrated an enlarged right ventricle with right-to-left ventricle ratio greater than 1 (Figure1). Given the circumstances relating to the cardiac arrest following the cesarean section, we suspected that the high-risk PE was attributed to amniotic fluid embolism

An acute thrombus (arrow) produces partial obstruction of the main pulmonary artery, right pulmonary artery, left pulmonary artery, and lower lobe branches.

Laboratory tests revealed severe anemia with hemoglobin (Hb) levels dropping to 57 g/L and thrombocytopenia indicated by a platelet count of 53 G/L. Coagulation studies show a significant increase in the international normalized ratio (INR) from 1.66 to over 12, prothrombin time (PT) extending beyond 180 seconds, and fibrinogen levels critically low at less than 0.4 g/L; additionally, arterial blood gas analysis indicated severe acidosis with a pH of 7.06, partial pressures of carbon dioxide and oxygen at 41 mmHg and 363 mmHg respectively, critically low bicarbonate at 11.9 mmol/L, and significantly elevated lactate levels at 15.0 mmol/L. Cardiac biomarkers also rose, high-sensitivity troponin T 3171 ng/L and NT-proBNP 717 ng/L, reflecting myocardial injury.

The patient post-resuscitation condition was deteriorated and become more complicated with postpartum hemorrhage due to central placenta previa. Vasopressors including epinephrine and norepinephrine were given with escalating dose. Arterial blood gas analysis indicated severe metabolic acidosis and elevated lactate levels, prompting the initiation of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) and continuous renal replacement therapy (CRRT). PERT was alerted and the management strategies were made by the consensus of the team, including an operation involving bilateral uterine artery ligation and transcatheter arterial embolization of the uterine arteries to control the bleeding. As the patient also suffered from a hemorrhagic shock, systemic thrombolysis was contraindicated. We performed mechanical thrombectomy for high-risk PE treatment. Pulmonary angiography post-thrombectomy showed restored pulmonary blood flow and patient oxygen saturation remarkably improved (Figure 2C). Histopathological evaluation of the thrombus confirmed the presence of amniotic fluid components (Figure 3). In parallel with all the invasive procedure, the patient was also received extensive blood transfusion to address severe anemia and coagulopathy with 6 units of packed red blood cells (PRBCs), 1 kit of platelets, 6 units of fresh frozen plasma (FFP) and 12 units of cryoprecipitate.

Figure 2. Pre- and post-thrombectomy pulmonary angiography: a 5 French (5F) multipurpose catheter was advanced to the right and left pulmonary arteries, revealed Five days later, the patient’s hemodynamic status improved, allowing for the weaning from VA-ECMO and mechanical ventilation. Then, repeated echocardiography showed improved TAPSE, normalized pulmonary artery pressure, and restored right ventricular function. The patient was extubated and unfractionated heparin was converts to a direct oral anticoagulant (DOAC). A numerous large thrombi in both branches (Figure 2A and 2B); Pulmonary angiography post-thrombectomy showed restored pulmonary blood flow (Figure 2C).

Figure 3. The sample comprises keratin (Figure 3A, arrow), amorphous mucinous material, mature squamous cells, thrombus interspersed with polymorphonuclear leukocytes (Figure 3B, arrow).

Five days later, the patient’s hemodynamic condition improved enough to let mechanical breathing and VA-ECMO be weaned. A repeated echocardiogram seven days following therapy revealed better TAPSE, normalized pulmonary artery pressure, and recovered ventricular function. The patient was extubated; unfractionated heparin was changed to a direct oral anticoagulant (DOAC).

Case 2

A 31-year-old female pregnant underwent a cesarean section at 37 weeks of gestation due to severe vaginal bleeding caused by a central placenta previa at a local hospital. She had two pregnancies and two deliveries (GTPAL 21011). Immediately after the baby was delivered, a cardiac arrest occurred. She was successfully resuscitated after approximately 1 minute of advanced life support. Bedside echocardiography reviewed a dilated right ventricle, highly suspected an acute high- risk pulmonary embolism complicated cardiac arrest. Therefore, a contrast chest- computed tomography (CT) was performed. The CT confirmed the present of partial embolism of the main pulmonary artery trunk and its branches on both sides. She further received transfusions of 6 units of packed red blood cells, 2 units of whole blood, and 3 units of fresh frozen plasma before being transferred to University Medical Center of Ho Chi Minh city for further advanced management

At arrival in our hospital, she was alert with a heart rate of 162 bpm, blood pressure of 106/78 mmHg, respiratory rate of 32 breaths per minute, temperature of 37.1°C, and oxygen saturation (SpO2) of 90%. Her laboratory results reveal a severe anemic condition with hemoglobin 6.9 g/dL, platelet count 50 x 10^9/L, INR 2.17 and an aPTT of 43.3 seconds. Myocardial injury and cardiac strain was evidenced by troponin T hs 8213 ng/L and NT-proBNP 2825 ng/L. Renal function was declined and hepatic enzymes rose as a consequence of cardiac arrest.

The Pulmonary Embolism Response Team (PERT) including obstetricians, cardiac surgeons, intensivists, interventional and non-interventional cardiologists was alerted for multidisciplinary approach of this challenging case. Our patient was prediagnosed with a massive PE complicated cardiac arrest immediately after a cesarean section. Given her post-operative and severe anemic and thrombocytopenic condition, she was absolutely contraindicated for fibrinolytic therapy. After a deliberate discussion, PERT members reached a concensus to perform a complete hysterectomy to control the excessive bleeding, along with a pulmonary thromboendarterectomy, and extensive blood transfusions. The operation was performed under general anesthesia with cardiopulmonary bypass. The patient was afterwards transferred to the Intensive Care Unit for postoperative care, involving continuous renal replacement therapy (CRRT) for acute kidney injury, liver function monitoring, and coagulopathy management. She received a total of 9 units of packed red blood cells, 10 units of fresh frozen plasma, 10 units of cryoprecipitate, and 6 platelet kits. Her hemodynamic was supported by vasoactive agents, dobutamine, milrinone, and noradrenaline. The histopathology of the surgical removed clot revealed thrombus tissue with keratin debris, consistent with amniotic fluid embolism (Fig 4). After approximately 3 weeks, the patient was completely recovered and appeared well at follow-up visits.

Figure 4. Histopathology report. The sample consists of keratinized masses (Figure 4A, arrow) accompanied by thrombotic tissue (Figure 4B, arrow).

4. DISCUSSION

Amniotic fluid embolism is a rare and fatal obstetric complication characterized by sudden cardiac arrest, respiratory distress, and disseminated intravascular coagulation. These cases emphasize the importance of early identification and multidisciplinary treatment to improve outcomes for mothers and children.

Amniotic fluid embolism occurs in about 1 in 8,000 to 1 in 80,000 pregnancies. The condition often arises during labor in 70% of cases, following vaginal delivery in 11% of cases, and during or after a cesarean section in 19% of cases (1). The challenging nature of diagnosing and uniquely identifying character makes it difficult to accurately determine the actual incidence, perhaps leading to an underrepresentation of non-fatal cases (1).

Steiner and Lushbaugh were the first to document eight cases of sudden mother death caused by “obstetric shock” coming from the presence of embryonic debris in the pulmonary arteries. They identified amniotic fluid embolism as the underlying cause. The hallmark of this condition is the presence of fetal waste in the lungs, which leads to sudden and severe respiratory failure (2). The death rates in the United Kingdom and the United States were found to be 21.6% and 19%, respectively. Initial studies showed that the prevalence of the condition was 1.7 cases per 100,000 pregnancies in the United Kingdom and 7.7 cases per 100,000 pregnancies in the United States. Major risk factors include the black race, pregnancy, labor induction, advanced maternal age, placenta previa, and cesarean delivery (2).

Amniotic fluid embolism (AFE) is often accompanied with disseminated intravascular coagulopathy (DIC). Clinically, AFE is diagnosed by ruling out other potential causes in pregnant or recently postpartum women who are having sudden cardiovascular collapse, acute respiratory distress, low oxygen levels, and seizures. AFE often occurs during labor or shortly after delivery, and is often confirmed retrospectively. The Society for Maternal-Fetal Medicine and the Amniotic Fluid Embolism Foundation recommends using specific diagnostic criteria for identifying amniotic fluid embolism, including the occurrence of rapid cardiorespiratory arrest or hypotension with respiratory failure, evident disseminated intravascular coagulation (DIC), onset of symptoms during labor or within 30 minutes after placenta delivery, and the absence of fever during labor.

Although the precise pathophysiology of amniotic fluid embolism remains uncertain, it is thought to include the infiltration of amniotic fluid into the mother’s bloodstream, leading to an abnormal humoral and immunological reaction. The production of vasoactive and procoagulant substances leads to acute pulmonary hypertension, right ventricular failure, and perhaps left ventricular failure and systemic hypotension. Pulmonary hypertension leads to significant ventilation-perfusion mismatch, cardiogenic pulmonary edema, and hypoxemic respiratory failure. Noncardiogenic pulmonary edema caused by endothelial damage and capillary leak syndrome. The initiation of the coagulation cascade may lead to the development of multiple organ failure, ischemic organ dysfunction, and DIC. While changes in inflammatory markers may not have significant diagnostic value, postmortem findings have shown the existence of inflammatory cells and fetal cells in the lungs (3, 4).

Increasing the chances of stabilization and preventing additional deterioration in patients presenting with acute cardiorespiratory compromise, hypoxemia, and hemorrhage due to disseminated intravascular coagulation depends on a multidisciplinary, team-based approach involving obstetricians, anesthesiologists, intensivists, and both interventional and non-interventional cardiologists. The first emergency management objectives are reversing coagulopathy, managing bleeding, and doing high-quality cardiopulmonary resuscitation. Recommendations are for tranexamic acid administration and starting a major transfusion program. Eliminating other possible diagnoses helps one to confirm the presumed diagnosis of amniotic fluid embolism. Prompt delivery of the fetus should be taken under consideration whether the fetus is alive and has reached the gestational age of ex utero viability or if delivery will help in mother resuscitation (5, 6).

Usually, extracorporeal membrane oxygenation should not be employed in treating amniotic fluid embolism. Particularly in patients with amniotic fluid embolism, who often present with disseminated intravascular coagulation, the need for anticoagulation with this operation carries a major bleeding risk. However, several case studies of patients with refractory amniotic fluid embolism–especially those who are unresponsive to conventional ventilatory maneuvers or those undergoing protracted cardiac arrest where oxygenation is essential for fetal delivery—have shown successful results with extracorporeal membrane oxygenation. The need to send patients to specialized facilities with knowledge of extracorporeal membrane oxygenation could restrict the feasibility of this technique (7).

The 39-year-old patient in Case 1 developed a post-resuscitation state that grew more complicated and manifested as cardiovascular collapse. Veno-arterial extracorporeal membrane oxygenation was used to maintain a hemodynamic state in severe metabolic acidosis, rising lactate levels, and increasing vasopressor dosages. Five days later, the patient’s illness cleared up.

The paper “Impact of Pulmonary Embolism Response Teams on Acute Pulmonary Embolism: A Systematic Review and Meta-Analysis” examined how Pulmonary Embolism Response Teams (PERT) affected treatment decisions and outcomes for patients suffering from acute pulmonary embolism (8). Without a rise in bleeding complications, data analysis of 16 studies comprising 3,827 PERT-treated patients, and 3,967 control patients revealed PERT patients were more likely to receive advanced treatments, including catheter-directed interventions, systemic thrombolysis, and surgical embolectomy (8). Among PERT patients, the utilization of inferior vena cava filters was much reduced. The PERT group demonstrated a nonsignificant trend toward decreased mortality despite having more intermediate and high-risk cases, implying that PERT improves the use of advanced medicines and might cut mortality in patients with higher-risk pulmonary embolism (8).

The research conducted at the University Medical Center of Ho Chi Minh city, Vietnam, assessed the effects of establishing a Pulmonary Embolism Response Team to enhance outcomes for patients with acute pulmonary embolism. This observational study, done at a single center from January 1, 2019, to August 1, 2021, involved patients diagnosed with pulmonary embolism with computed tomography (9). Patients were divided into two groups: those treated before the founding of the Pulmonary Embolism Response Team (51 patients) and those treated after its organization (79 patients) (9). The analysis indicated that the post-pulmonary Embolism Response Team cohort exhibited a markedly reduced occurrence of both primary and clinically significant non-major hemorrhagic events (11.3% versus 31.4%, p = 0.005) and underwent a higher frequency of interventional treatments, including aspiration embolectomy and catheter-directed thrombolysis (16.5% compared to 3.9%, p = 0.046)9. The in-hospital mortality rate significantly decreased in the post-pulmonary Embolism Response Team sample (8.9% versus 21.6%, p = 0.041)9. The data indicate that the interdisciplinary strategy employed by the Pulmonary Embolism Response Team, even in a resource-constrained hospital environment, markedly enhanced clinical outcomes, including decreased hemorrhagic complications and fatality rates (9). The research highlights the advantages of forming a Pulmonary Embolism Response Team in emerging healthcare systems to improve the management and outcomes of acute pulmonary embolism cases (9).

Alerts were sent to obstetricians, intensivists, interventional, non-interventional cardiologists, and cardiac surgeons. Therapeutic approaches were formulated in accordance with the consensus of the team. In the first case, a mechanical thrombectomy was performed for high-risk pulmonary embolism therapy; in the second one, a pulmonary thromboendarterectomy was executed. After surgery and intervention, both patients’ oxygen saturation raised, restoring pulmonary blood flow. The patient’s hemodynamic conditions improved; successive echocardiograms revealed normal pulmonary artery pressure and tricuspid annular plane systolic excursion, therefore indicating restored right ventricular function.

Analyzing data from the National Inpatient Sample (2010–2014), Edward D. Percy, MD, and associates investigated the safety and efficacy of surgical embolectomy for acute pulmonary embolism (10). The study comprised 58,974 individuals and revealed that more severe cases–such as those involving saddle emboli and increased death risk–were treated with surgical embolectomy (10). While death rates for surgical embolectomy have greatly dropped, in-hospital mortality rates were greater than those of systematic thrombolysis and catheter-directed treatment. These results imply that surgical embolectomy is now a safer and more efficient treatment for patients with high-risk pulmonary embolism, especially in large urban teaching hospitals with the required knowledge and tools (10).

Moreover, among other types, amniotic fluid embolism might present itself as cardiac collapse and widespread intramobile coagulation. These conditions demand specific, aggressive treatment plans. Obstetricians, anesthesiologists, intensivists, interventional and non-interventional cardiologists, and cardiac surgeons make up a multidisciplinary team that guarantees a complete strategy to treat issues like heart malfunction and disseminated intravascular coagulation. In both cases, the Pulmonary Embolism Response Team was critically essential in planning therapy and carrying out advanced life-saving procedures. Among these procedures were extracorporeal membrane oxygenation, mechanical and surgical thrombectomy, continuous renal replacement treatment, and major blood transfusions.

5. CONCLUSION

Early diagnosis, quick intervention, and thorough multidisciplinary treatment successfully managed AFE in these cases. Improving patient outcomes mostly depends on constant monitoring, sophisticated surgical methods, and customized postoperative management; thus, patients with AFE can show notable recovery with prompt and efficient treatment.

Abbreviations:

AFE: amniotic fluid embolism; APTT: activated partial thromboplastin time; CT: computed tomography; DBP: diastolic blood pressure; DIC: disseminated intravascular coagulation; DVT: deep vein thrombosis; FDP: fibrin degradation products; FFP: fresh frozen plasma; HE: hematoxylin-eosin; HR: heart rate; ICU: intensive care unit; PE: pulmonary embolism; PRBCs: packed red blood cells;

Ethical Statement:

Our institution does not require ethical approval for reporting individual cases or case series.

Pattient Consent Form:

Patient was informed about subject of the study.

Author’s contribution:

The all authors were involved in all steps of preparation this article. Final proofreading was made by the first author.

Conflicts of interest:

The authors declared that they have no conflicts of interest in this work.

Financial support and sponsorship:

None.