Atypical amniotic fluid embolism presenting with isolated coagulopathy: A case report

Atypical amniotic fluid embolism presenting with isolated coagulopathy: A case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Atypical amniotic fluid embolism presenting with isolated coagulopathy: A case report xue huang, xinli zhong, jinjing long, xingya liu This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8191695/v1 This work is licensed under a CC BY 4.0 License Status: Published Journal Publication published 05 Feb, 2026 Read the published version in BMC Pregnancy and Childbirth → Version 1 posted 31 You are reading this latest preprint version Abstract Background Amniotic fluid embolism (AFE) is a rare but catastrophic obstetric emergency characterised by the sudden entry of amniotic fluid or fetal components into the maternal circulation, triggering severe cardiorespiratory collapse, coagulopathy, or both. While most patients exhibit abrupt hypotension and hypoxia, a coagulopathy-dominant subtype has increasingly been recognised but remains easily overlooked. Its insidious onset and absence of overt cardiopulmonary signs often delay recognition and appropriate intervention. Case presentation: We report a 30-year-old Chinese woman (gravida 2, para 1) who developed severe coagulopathy-dominant AFE shortly after the vaginal delivery of a term singleton infant at a tertiary comprehensive hospital. She presented exclusively with massive postpartum bleeding and precipitous drops in fibrinogen (3.21→ 0.37 g/L within 15 minutes) and platelets (96→46×10⁹/L), without hypoxia or cardiopulmonary compromise. Recognising the disproportionate coagulopathy, clinicians rapidly initiated a protocol involving massive transfusion emphasising early fibrinogen supplementation, followed by timely surgical intervention. Despite profound disseminated intravascular coagulation and recurrent haemorrhage, coordinated multidisciplinary management resulted in complete recovery without sequelae. Conclusions This case highlights an atypical, coagulopathy-dominant case of AFE in which rapid recognition of isolated coagulopathy and early fibrinogen-guided transfusion likely avoided a fatal outcome. Vigilant monitoring and prompt, team-based intervention are essential to improving survival in such non-classical AFE presentations. Amniotic fluid embolism coagulopathy-dominant subtype postpartum haemorrhage massive transfusion multidisciplinary management Figures Figure 1 Figure 2 Background Amniotic fluid embolism (AFE) is a rare but life-threatening obstetric complication that poses a serious threat to both maternal and foetal survival. Although its global incidence is extremely low—recent population-based data estimate approximately 6 cases per 100,000 deliveries( 1 )—AFE remains a leading cause of maternal morbidity and mortality because of its abrupt onset and rapidly progressive haemodynamic and coagulopathic collapse ( 2 , 3 ). Typical AFE can often be diagnosed promptly because of its characteristic presentation with abrupt cardiopulmonary collapse and disseminated intravascular coagulation (DIC). However, atypical forms of AFE are far more insidious and diagnostically challenging, as they may lack the hallmark respiratory or cardiovascular manifestations, leading to delayed recognition and missed opportunities to intervene in a timely manner. Recent studies have suggested that AFE represents not merely a mechanical embolic event but rather a complex immunologic and haemostatic reaction involving the activation of inflammatory and coagulation cascades ( 4 ). Among its variants, the coagulopathy-dominant type – characterised by early and profound consumptive coagulopathy – remains particularly rare and difficult to recognise ( 5 ). Successful management is highly reliant on clinical vigilance, rapid multidisciplinary coordination and decision-making tailored to the particular case. Here, we report a case of atypical, coagulopathy-dominant AFE occurring after vaginal delivery, in which the patient developed abrupt and severe coagulopathy with massive postpartum haemorrhage but no cardiopulmonary collapse. Prompt recognition of the severity of the condition and initiation of a protocol involving massive transfusion emphasising early fibrinogen replacement, combined with immediate surgical intervention and multidisciplinary management, led to full recovery. This case highlights the importance of early diagnosis and team-based management in improving outcomes in atypical presentations of AFE. Case presentation A 30-year-old Chinese woman, gravida 2 para 1, at 40 weeks of gestation was admitted to our hospital—a tertiary general hospital in China—because of a 2-day history of slightly decreased fetal movement. On admission, her vital signs were stable (temperature 36.6°C, pulse 78 beats/min, respiratory rate 20 breaths/min and blood pressure 109/78 mmHg). Her body mass index was 24.2 kg/m². The antenatal course had been uneventful, with no hypertensive disorders, diabetes or other complications. The diagnosis on admission was decreased foetal movement, suspected nuchal cord and intrauterine singleton pregnancy at 40 weeks with signs of impending labour. After admission, routine examinations revealed no abnormalities. Labour was induced with a conventional protocol of intravaginal dinoprostone (Cervidil) followed by intravenous oxytocin for cervical ripening and augmentation of uterine contractions. On the third day of induction, owing to minimal labour progress, an artificial rupture of membranes was performed at 13:20 to promote labour progression, releasing clear amniotic fluid. Within 20 min, uterine contractions intensified, and labour progressed rapidly. The cervix became fully dilated at 17:48, and the patient delivered a healthy live infant vaginally at 18:29. The neonate had Apgar scores of 9, 10, and 10 at 1, 5, and 10 minutes, respectively, and the labour and delivery progressed smoothly without complications. Onset of event and initial management Six minutes after foetal delivery, the placenta and membranes were expelled spontaneously but appeared slightly incomplete, and uterine curettage was performed to remove residual tissue. Within 15 min postpartum, the total estimated blood loss reached approximately 400 ml. During this time, the patient experienced sudden chest tightness, although her oxygen saturation remained normal, and her symptoms improved rapidly after supplemental oxygen. Uterine atony was initially suspected, and uterotonic agents—including oxytocin, carboprost tromethamine, and methylergometrine—were administered at standard doses according to routine clinical protocols. Laboratory tests, including complete blood count, coagulation profile and blood cross-matching, were ordered, and two intravenous lines were established. Cervical and vaginal lacerations were identified and promptly sutured. Despite these interventions, bleeding persisted, reaching approximately 1200 mL by 19:00 and increasing to about 1500 mL by 19:21. Uterine balloon tamponade was applied, accompanied by the transfusion of 4 units of packed red blood cells and 400 mL of fresh frozen plasma. Approximately 1 h after delivery, the patient developed progressive pallor, decreased responsiveness, thready pulse and hypotension, indicating worsening haemodynamic instability. By 20:18, the cumulative blood loss exceeded 3000 mL, and the patient was transferred to the operating room for surgical management. At that time, laboratory results from the initial 400 mL bleeding episode became available, revealing marked thrombocytopenia and hypofibrinogenaemia, confirming severe coagulopathy as the underlying cause of the haemorrhage. Intraoperative management and outcome Owing to persistent vaginal bleeding and rapidly worsening coagulopathy, the patient was taken for an emergency exploratory laparotomy at 20:18. Given the uncontrolled haemorrhage and severe coagulation dysfunction, a total hysterectomy was performed to achieve haemostasis. The patient received massive transfusion, including packed red blood cells, fresh frozen plasma, cryoprecipitate, and fibrinogen concentrate, with detailed transfusion volumes provided in Figure 1. After surgical intervention and aggressive correction of coagulopathy, the bleeding was brought under control and the patient was transferred to the intensive care unit (ICU) for close postoperative monitoring. The first operation concluded at 01:00 the next day. However, at 05:00, ICU staff noted a large volume of fresh blood in the abdominal drainage bag. Bedside ultrasound and urgent computed tomography revealed massive intra-abdominal and pelvic bleeding, accompanied by a sharp drop in haemoglobin, falling from 58 g/L on postoperative assessment to 44 g/L despite ongoing transfusion (4 units of packed red blood cells and 400 mL of fresh frozen plasma). The patient was immediately returned to the operating room for re-exploration. Intraoperatively, diffuse oozing from the vascular plexus of the ovarian ligament and adjacent pelvic peritoneum was identified, while the hysterectomy stump remained haemostatic. Vascular ligation and extensive compression suturing were performed, along with additional massive transfusion and haemostatic therapy. The total cumulative blood loss reached approximately 6500 ml. The clinical course and major interventions are summarised in Figure 1, whereas Figure 2 illustrates the dynamic changes in key coagulation parameters characteristic of coagulopathy-dominant amniotic fluid embolism. Following the second surgery, haemostasis was successfully achieved, and the patient was returned to the ICU for continued monitoring and supportive care. Over the following days, coagulation parameters and haemoglobin levels gradually normalised, and the patient showed steady improvement without further bleeding episodes. She showed steady postoperative improvement and was discharged in good condition without complications 2 weeks after surgery. Discussion AFE is a rare but life-threatening obstetric emergency, accounting for approximately 5%–15% of maternal deaths in developed countries ( 6 ). Approximately 70% of AFE cases occur during labour, 11% occur following vaginal delivery and 19% occur after caesarean section ( 2 ). The condition is characterised by the entrance of amniotic fluid or foetal components into the maternal circulation, triggering a clinical triad of sudden hypotension or cardiopulmonary collapse, respiratory distress and disseminated coagulopathy ( 6 ). Although traditionally regarded as a single catastrophic embolic event, emerging evidence suggests that AFE represents a complex syndrome involving immune-mediated inflammatory responses and haemostatic dysregulation, rather than purely mechanical obstruction of the pulmonary vasculature ( 4 , 7 ). Recent evidence suggests that AFE encompasses two major clinical phenotypes with distinct pathophysiological mechanisms: a cardiopulmonary-collapse type, characterised by sudden hypoxia, hypotension and cardiac arrest caused by pulmonary vasospasm and right ventricular failure( 8 ),and a coagulopathy-dominant type, in which disseminated intravascular coagulation and massive obstetric haemorrhage are the predominant manifestations. ( 9 , 10 ). Although the precise pathogenesis of AFE remains unclear, Weiner et al. ( 11 ) demonstrated in vitro that amniotic fluid possesses strong procoagulant activity. Subsequent experimental studies have shown that amniotic fluid can directly activate factor X through the extrinsic coagulation pathway and induce platelet–neutrophil aggregation and activation, supporting its potential role in triggering systemic coagulation dysfunction ( 12 , 13 ). In the coagulopathy-dominant pattern, it has been hypothesised that bioactive components of amniotic fluid – such as tissue factor, cytokines and complement factors – initiate widespread activation of coagulation and fibrinolysis, leading to the rapid consumption of clotting factors and platelets ( 14 ). This cascade may result in abrupt hypofibrinogenaemia and thrombocytopenia, occasionally preceding any overt cardiopulmonary compromise ( 15 ).The diagnosis of AFE remains primarily clinical and one of exclusion, as there are no pathognomonic laboratory markers or imaging findings. In the present case, the patient developed sudden chest tightness without oxygen desaturation, accompanied by persistent vaginal bleeding shortly after delivery. Moreover, laboratory tests for coagulatory function were delayed, resulting in temporary misattribution of the haemorrhage to uterine hypotonia rather than to an underlying AFE-associated coagulopathy. Such diagnostic uncertainty is common in coagulopathy-dominant AFE, where the absence of cardiopulmonary collapse can obscure the true aetiology of bleeding. In this patient, several features were highly suggestive of coagulopathy-dominant AFE. The extent of haemorrhage was insufficient to account for the marked deterioration in coagulatory function, as evidenced by a precipitous fall in fibrinogen (from 3.21 g/L to 0.37 g/L within 15 min) and thrombocytopenia (platelets decreased from 96 × 10⁹/L to 46 × 10⁹/L). These findings indicated an acute, DIC-like coagulopathic process triggered by AFE. The rapid improvement in haemostasis following aggressive replacement of fibrinogen and platelets further supported this interpretation. Differential diagnoses included uterine atony, retained placental tissue, placenta accreta spectrum disorders and obstetric DIC secondary to other causes such as HELLP syndrome, acute fatty liver of pregnancy or sepsis. However, these conditions were ruled out based on both the absence of hypertension, elevated liver enzymes or evidence of infection and the temporal sequence – acute coagulation failure within minutes of delivery – being more consistent with AFE. Although a definitive diagnosis of AFE still relies on the correlation between characteristic clinical manifestations and supportive laboratory findings, alongside the exclusion of other causes, this case highlights that sudden, disproportionate declines in fibrinogen and platelet levels after delivery should prompt suspicion for AFE-associated coagulopathy, even in the absence of cardiopulmonary compromise. Prompt recognition and decisive management are essential in improving outcomes for patients with AFE, particularly in the coagulopathy-dominant form. In the present case, once persistent bleeding and worsening laboratory parameters were recognised, a massive transfusion protocol was promptly activated, accompanied by an immediate multidisciplinary response. Timely surgical intervention and targeted haemostatic resuscitation were key to survival. When conservative measures failed, emergency exploratory laparotomy and total hysterectomy were performed to control the bleeding. Intraoperative management followed the principles of damage-control resuscitation, emphasising balanced transfusion of packed red blood cells, plasma, cryoprecipitate and fibrinogen concentrate to restore haemostatic competence ( 16 ). In the early phase of resuscitation, early fibrinogen supplementation should be prioritised ( 17 ), with the goal of maintaining levels above those acceptable in non-pregnant individuals, as physiological fibrinogen concentrations during pregnancy normally range from 400 to 600 mg/dL (4–6 g/L) ( 18 ). Cryoprecipitate or fibrinogen concentrate provides a more concentrated source of fibrinogen and allows rapid correction ( 16 ). Management of massive transfusion should be guided by the current cumulative blood loss, the anticipated rate of ongoing haemorrhage and the feasibility of achieving surgical control. In cases of AFE-related DIC, a transfusion strategy focusing on the early replacement of fibrinogen and other coagulation factors is critical, accompanied by continuous monitoring and dynamic assessment of coagulation-related parameters throughout the progression of the disease ( 19 ). Following intensive postoperative care, the patient’s coagulatory function gradually normalised, leading to complete recovery without complications. This case highlights that early recognition of atypical, coagulopathy-dominant AFE – together with prompt fibrinogen-centred resuscitation, timely surgical intervention and coordinated multidisciplinary management – is critical to improving maternal survival. Although most reported AFE cases involve the cardiopulmonary-collapse form, this experience reinforces the concept that disproportionate coagulopathy can be the initial and predominant manifestation, requiring heightened clinical vigilance and goal-directed correction of abnormalities of coagulation to achieve a favourable outcome. Conclusion This case demonstrates that coagulopathy-dominant AFE can manifest primarily as acute disseminated coagulopathy without cardiopulmonary collapse. Here, early recognition of disproportionate coagulation dysfunction, rapid activation of a multidisciplinary team and implementation of a protocol involving massive transfusion emphasising early fibrinogen replacement together with timely surgical intervention were pivotal to maternal survival. Prompt decision-making and coordinated team management remain the cornerstone of improving outcomes in this rare but life-threatening obstetric emergency. Abbreviations AFE: amniotic fluid embolism APTT: activated partial thromboplastin time Cryo: cryoprecipitate DIC: disseminated intravascular coagulation Fbg: fibrinogen Fbg concentrate: fibrinogen concentrate FFP: fresh frozen plasma ICU: intensive care unit INR: international normalised ratio MTP: massive transfusion protocol Plt: platelets PT: prothrombin time RBC: red blood cells TXA: tranexamic acid Declarations Ethics approval and consent to participate Ethical approval for this case report was waived by the Ethics Committee of The First People’s Hospital of Shuangliu District, Chengdu (West China Airport Hospital, Sichuan University) in accordance with institutional policy. Written informed consent for participation was obtained from the patient. Consent for publication Written informed consent for publication of this case report and any accompanying images was obtained from the patient. Availability of data and materials All data generated or analyzed during this study are included in this published article. No additional datasets are available. Competing interests The authors declare that they have no competing interests. Funding This work was supported by the Technological Innovation and R&D Project of the Chengdu Science and Technology Bureau (No. 2024-YF05-02147-SN). Authors’ contributions Huang X was primarily responsible for the conception and design of the study, data acquisition, analysis, and drafting of the manuscript. Zhong XL contributed to clinical data collection and assisted with the interpretation of clinical findings. Long JJ assisted in manuscript revision and provided important clinical insights. Liu XY supervised the project, ensured adherence to reporting standards, and provided overall guidance throughout the research and manuscript preparation process. All authors have read and approved the final manuscript. Acknowledgements We sincerely thank the patient and her family for their cooperation and for granting permission to publish this case. Their support made this work possible and contributes to clinical understanding of atypical presentations of amniotic fluid embolism. References Mazza GR, Youssefzadeh AC, Klar M, Kunze M, Matsuzaki S, Mandelbaum RS, et al. Association of Pregnancy Characteristics and Maternal Mortality With Amniotic Fluid Embolism. JAMA Network Open. 2022/11/01;5(11). Clark SL, Hankins GDV, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: Analysis of the national registry. American Journal of Obstetrics & Gynecology. 1995/04/01;172(4). KE F, D T, JJ K, M K. Incidence, risk factors, management and outcomes of amniotic-fluid embolism: a population-based cohort and nested case-control study - PubMed. BJOG : an international journal of obstetrics and gynaecology. 2016 Jan;123(1). Baxter FJ. Amniotic Fluid Embolism: A Narrative Review. 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Cite Share Download PDF Status: Published Journal Publication published 05 Feb, 2026 Read the published version in BMC Pregnancy and Childbirth → Version 1 posted Editorial decision: Revision requested 26 Dec, 2025 Reviews received at journal 25 Dec, 2025 Reviews received at journal 24 Dec, 2025 Reviewers agreed at journal 24 Dec, 2025 Reviews received at journal 23 Dec, 2025 Reviews received at journal 22 Dec, 2025 Reviewers agreed at journal 22 Dec, 2025 Reviews received at journal 21 Dec, 2025 Reviews received at journal 21 Dec, 2025 Reviewers agreed at journal 20 Dec, 2025 Reviews received at journal 20 Dec, 2025 Reviews received at journal 19 Dec, 2025 Reviewers agreed at journal 19 Dec, 2025 Reviewers agreed at journal 19 Dec, 2025 Reviewers agreed at journal 19 Dec, 2025 Reviewers agreed at journal 19 Dec, 2025 Reviewers agreed at journal 19 Dec, 2025 Reviewers agreed at journal 18 Dec, 2025 Reviewers agreed at journal 18 Dec, 2025 Reviews received at journal 18 Dec, 2025 Reviewers agreed at journal 18 Dec, 2025 Reviewers agreed at journal 18 Dec, 2025 Reviewers agreed at journal 18 Dec, 2025 Reviews received at journal 17 Dec, 2025 Reviewers agreed at journal 17 Dec, 2025 Reviewers agreed at journal 17 Dec, 2025 Reviewers invited by journal 17 Dec, 2025 Editor invited by journal 27 Nov, 2025 Editor assigned by journal 26 Nov, 2025 Submission checks completed at journal 26 Nov, 2025 First submitted to journal 24 Nov, 2025 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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10:04:55","extension":"html","order_by":14,"title":"","display":"","copyAsset":false,"role":"acdc-reference","size":61310,"visible":true,"origin":"","legend":"","description":"","filename":"earlyproof.html","url":"https://assets-eu.researchsquare.com/files/rs-8191695/v1/d55668ecb3a187bcd052043e.html"},{"id":98763618,"identity":"f99837f9-335c-4cc8-b67e-8076a0e19323","added_by":"auto","created_at":"2025-12-22 10:04:54","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":344798,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cem\u003eClinical timeline of haemorrhage progression, laboratory changes, and key interventions in the patient with suspected coagulopathy-dominant amniotic fluid embolism.\u003c/em\u003e\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8191695/v1/59c07138247c52ab0d979c0a.png"},{"id":98763617,"identity":"abaae5f6-b779-45f6-971a-bc4795ca7d51","added_by":"auto","created_at":"2025-12-22 10:04:54","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":69988,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cem\u003eDynamic changes in key coagulation parameters in a patient with coagulopathy-dominant amniotic fluid embolism.\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cem\u003ePanel A shows fibrinogen levels (g/L); Panel B shows platelet counts (×10⁹/L);\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003e\u003cem\u003ePanel C shows INR; and Panel D shows APTT (s).\u003c/em\u003e\u003c/p\u003e\n\u003cp\u003eTimepoints (T0–T8):\u003c/p\u003e\n\u003cp\u003eT0–Admission; T1 – Delivery (18:29); T2 – 15 min postpartum; T3 – Before surgery (massive haemorrhage \u0026gt;3000 mL); T4 – Intraoperative laboratory results (during hysterectomy); T5 – Postoperative laboratory results on ICU admission; T6 – Re-bleeding at 05:00; T7 – Post-second surgery (ICU stage); T8 – Postoperative Day 2.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8191695/v1/501b5abfa288ed2351f4a2e2.png"},{"id":102235034,"identity":"2aa5e796-7a60-478f-9bc8-c10a6a957256","added_by":"auto","created_at":"2026-02-09 16:14:54","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":772041,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8191695/v1/dd9d305b-9196-4526-905c-6a514643b83a.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Atypical amniotic fluid embolism presenting with isolated coagulopathy: A case report","fulltext":[{"header":"Background","content":"\u003cp\u003eAmniotic fluid embolism (AFE) is a rare but life-threatening obstetric complication that poses a serious threat to both maternal and foetal survival. Although its global incidence is extremely low\u0026mdash;recent population-based data estimate approximately 6 cases per 100,000 deliveries(\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e)\u0026mdash;AFE remains a leading cause of maternal morbidity and mortality because of its abrupt onset and rapidly progressive haemodynamic and coagulopathic collapse (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e, \u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e). Typical AFE can often be diagnosed promptly because of its characteristic presentation with abrupt cardiopulmonary collapse and disseminated intravascular coagulation (DIC). However, atypical forms of AFE are far more insidious and diagnostically challenging, as they may lack the hallmark respiratory or cardiovascular manifestations, leading to delayed recognition and missed opportunities to intervene in a timely manner.\u003c/p\u003e \u003cp\u003eRecent studies have suggested that AFE represents not merely a mechanical embolic event but rather a complex immunologic and haemostatic reaction involving the activation of inflammatory and coagulation cascades (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). Among its variants, the coagulopathy-dominant type \u0026ndash; characterised by early and profound consumptive coagulopathy \u0026ndash; remains particularly rare and difficult to recognise (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e). Successful management is highly reliant on clinical vigilance, rapid multidisciplinary coordination and decision-making tailored to the particular case.\u003c/p\u003e \u003cp\u003eHere, we report a case of atypical, coagulopathy-dominant AFE occurring after vaginal delivery, in which the patient developed abrupt and severe coagulopathy with massive postpartum haemorrhage but no cardiopulmonary collapse. Prompt recognition of the severity of the condition and initiation of a protocol involving massive transfusion emphasising early fibrinogen replacement, combined with immediate surgical intervention and multidisciplinary management, led to full recovery. This case highlights the importance of early diagnosis and team-based management in improving outcomes in atypical presentations of AFE.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003e\u003cspan lang=\"EN-GB\"\u003eA 30-year-old Chinese woman, gravida 2 para 1, at 40 weeks of gestation was admitted to our hospital\u0026mdash;a tertiary general hospital in China\u0026mdash;because of a 2-day history of slightly decreased fetal movement. On admission, her vital signs were stable (temperature 36.6\u0026deg;C, pulse 78 beats/min, respiratory rate 20 breaths/min and blood pressure 109/78 mmHg). Her body mass index was 24.2 kg/m\u0026sup2;. The antenatal course had been uneventful, with no hypertensive disorders, diabetes or other complications. The diagnosis on admission was decreased foetal movement, suspected nuchal cord and intrauterine singleton pregnancy at 40 weeks with signs of impending labour. After admission, routine examinations revealed no abnormalities. Labour was induced with a conventional protocol of intravaginal dinoprostone (Cervidil) followed by intravenous oxytocin for cervical ripening and augmentation of uterine contractions. On the third day of induction, owing to minimal labour progress, an artificial rupture of membranes was performed at 13:20 to promote labour progression, releasing clear amniotic fluid. Within 20 min, uterine contractions intensified, and labour progressed rapidly. The cervix became fully dilated at 17:48, and the patient delivered a healthy live infant vaginally at 18:29. The neonate had Apgar scores of 9, 10, and 10 at 1, 5, and 10 minutes, respectively, and the labour and delivery progressed smoothly without complications.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eOnset of event and initial management\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-GB\"\u003eSix minutes after foetal delivery, the placenta and membranes were expelled spontaneously but appeared slightly incomplete, and uterine curettage was performed to remove residual tissue. Within 15 min postpartum, the total estimated blood loss reached approximately 400 ml. During this time, the patient experienced sudden chest tightness, although her oxygen saturation remained normal, and her symptoms improved rapidly after supplemental oxygen. Uterine atony was initially suspected, and uterotonic agents\u0026mdash;including oxytocin, carboprost tromethamine, and methylergometrine\u0026mdash;were administered at standard doses according to routine clinical protocols. Laboratory tests, including complete blood count, coagulation profile and blood cross-matching, were ordered, and two intravenous lines were established. Cervical and vaginal lacerations were identified and promptly sutured.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-GB\"\u003eDespite these interventions, bleeding persisted, reaching approximately 1200 mL by 19:00 and increasing to about 1500 mL by 19:21. Uterine balloon tamponade was applied, accompanied by the transfusion of 4 units of packed red blood cells and 400 mL of fresh frozen plasma. Approximately 1 h after delivery, the patient developed progressive pallor, decreased responsiveness, thready pulse and hypotension, indicating worsening haemodynamic instability. By 20:18, the cumulative blood loss exceeded 3000 mL, and the patient was transferred to the operating room for surgical management. At that time, laboratory results from the initial 400 mL bleeding episode became available, revealing marked thrombocytopenia and hypofibrinogenaemia, confirming severe coagulopathy as the underlying cause of the haemorrhage.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eIntraoperative management and outcome\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-GB\"\u003eOwing to persistent vaginal bleeding and rapidly worsening coagulopathy, the patient was taken for an emergency exploratory laparotomy at 20:18. Given the uncontrolled haemorrhage and severe coagulation dysfunction, a total hysterectomy was performed to achieve haemostasis. The patient received massive transfusion, including packed red blood cells, fresh frozen plasma, cryoprecipitate, and fibrinogen concentrate, with detailed transfusion volumes provided in Figure 1. After surgical intervention and aggressive correction of coagulopathy, the bleeding was brought under control and the patient was transferred to the intensive care unit (ICU) for close postoperative monitoring. The first operation concluded at 01:00 the next day.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003eHowever, at 05:00, ICU staff noted a large volume of fresh blood in the abdominal drainage bag. Bedside ultrasound and urgent computed tomography revealed massive intra-abdominal and pelvic bleeding, accompanied by a sharp drop in haemoglobin, falling from 58 g/L on postoperative assessment to 44 g/L despite ongoing transfusion (4 units of packed red blood cells and 400 mL of fresh frozen plasma). The patient was immediately returned to the operating room for re-exploration. Intraoperatively, diffuse oozing from the vascular plexus of the ovarian ligament and adjacent pelvic peritoneum was identified, while the hysterectomy stump remained haemostatic. Vascular ligation and extensive compression suturing were performed, along with additional massive transfusion and haemostatic therapy. The total cumulative blood loss reached approximately 6500 ml. The clinical course and major interventions are summarised in Figure 1, whereas Figure 2 illustrates the dynamic changes in key coagulation parameters characteristic of coagulopathy-dominant amniotic fluid embolism.\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-GB\"\u003eFollowing the second surgery, haemostasis was successfully achieved, and the patient was returned to the ICU for continued monitoring and supportive care. Over the following days, coagulation parameters and haemoglobin levels gradually normalised, and the patient showed steady improvement without further bleeding episodes. She showed steady postoperative improvement and was discharged in good condition without complications 2 weeks after surgery.\u003c/span\u003e\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eAFE is a rare but life-threatening obstetric emergency, accounting for approximately 5%\u0026ndash;15% of maternal deaths in developed countries (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). Approximately 70% of AFE cases occur during labour, 11% occur following vaginal delivery and 19% occur after caesarean section (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). The condition is characterised by the entrance of amniotic fluid or foetal components into the maternal circulation, triggering a clinical triad of sudden hypotension or cardiopulmonary collapse, respiratory distress and disseminated coagulopathy (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). Although traditionally regarded as a single catastrophic embolic event, emerging evidence suggests that AFE represents a complex syndrome involving immune-mediated inflammatory responses and haemostatic dysregulation, rather than purely mechanical obstruction of the pulmonary vasculature (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eRecent evidence suggests that AFE encompasses two major clinical phenotypes with distinct pathophysiological mechanisms: a cardiopulmonary-collapse type, characterised by sudden hypoxia, hypotension and cardiac arrest caused by pulmonary vasospasm and right ventricular failure(\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e),and a coagulopathy-dominant type, in which disseminated intravascular coagulation and massive obstetric haemorrhage are the predominant manifestations. (\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e, \u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e). Although the precise pathogenesis of AFE remains unclear, Weiner et al. (\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e) demonstrated in vitro that amniotic fluid possesses strong procoagulant activity. Subsequent experimental studies have shown that amniotic fluid can directly activate factor X through the extrinsic coagulation pathway and induce platelet\u0026ndash;neutrophil aggregation and activation, supporting its potential role in triggering systemic coagulation dysfunction (\u003cspan citationid=\"CR12\" class=\"CitationRef\"\u003e12\u003c/span\u003e, \u003cspan citationid=\"CR13\" class=\"CitationRef\"\u003e13\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn the coagulopathy-dominant pattern, it has been hypothesised that bioactive components of amniotic fluid \u0026ndash; such as tissue factor, cytokines and complement factors \u0026ndash; initiate widespread activation of coagulation and fibrinolysis, leading to the rapid consumption of clotting factors and platelets (\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e). This cascade may result in abrupt hypofibrinogenaemia and thrombocytopenia, occasionally preceding any overt cardiopulmonary compromise (\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e).The diagnosis of AFE remains primarily clinical and one of exclusion, as there are no pathognomonic laboratory markers or imaging findings. In the present case, the patient developed sudden chest tightness without oxygen desaturation, accompanied by persistent vaginal bleeding shortly after delivery. Moreover, laboratory tests for coagulatory function were delayed, resulting in temporary misattribution of the haemorrhage to uterine hypotonia rather than to an underlying AFE-associated coagulopathy. Such diagnostic uncertainty is common in coagulopathy-dominant AFE, where the absence of cardiopulmonary collapse can obscure the true aetiology of bleeding.\u003c/p\u003e \u003cp\u003eIn this patient, several features were highly suggestive of coagulopathy-dominant AFE. The extent of haemorrhage was insufficient to account for the marked deterioration in coagulatory function, as evidenced by a precipitous fall in fibrinogen (from 3.21 g/L to 0.37 g/L within 15 min) and thrombocytopenia (platelets decreased from 96 \u0026times; 10⁹/L to 46 \u0026times; 10⁹/L). These findings indicated an acute, DIC-like coagulopathic process triggered by AFE. The rapid improvement in haemostasis following aggressive replacement of fibrinogen and platelets further supported this interpretation.\u003c/p\u003e \u003cp\u003eDifferential diagnoses included uterine atony, retained placental tissue, placenta accreta spectrum disorders and obstetric DIC secondary to other causes such as HELLP syndrome, acute fatty liver of pregnancy or sepsis. However, these conditions were ruled out based on both the absence of hypertension, elevated liver enzymes or evidence of infection and the temporal sequence \u0026ndash; acute coagulation failure within minutes of delivery \u0026ndash; being more consistent with AFE. Although a definitive diagnosis of AFE still relies on the correlation between characteristic clinical manifestations and supportive laboratory findings, alongside the exclusion of other causes, this case highlights that sudden, disproportionate declines in fibrinogen and platelet levels after delivery should prompt suspicion for AFE-associated coagulopathy, even in the absence of cardiopulmonary compromise.\u003c/p\u003e \u003cp\u003ePrompt recognition and decisive management are essential in improving outcomes for patients with AFE, particularly in the coagulopathy-dominant form. In the present case, once persistent bleeding and worsening laboratory parameters were recognised, a massive transfusion protocol was promptly activated, accompanied by an immediate multidisciplinary response. Timely surgical intervention and targeted haemostatic resuscitation were key to survival. When conservative measures failed, emergency exploratory laparotomy and total hysterectomy were performed to control the bleeding. Intraoperative management followed the principles of damage-control resuscitation, emphasising balanced transfusion of packed red blood cells, plasma, cryoprecipitate and fibrinogen concentrate to restore haemostatic competence (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eIn the early phase of resuscitation, early fibrinogen supplementation should be prioritised (\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e), with the goal of maintaining levels above those acceptable in non-pregnant individuals, as physiological fibrinogen concentrations during pregnancy normally range from 400 to 600 mg/dL (4\u0026ndash;6 g/L) (\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e). Cryoprecipitate or fibrinogen concentrate provides a more concentrated source of fibrinogen and allows rapid correction (\u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e). Management of massive transfusion should be guided by the current cumulative blood loss, the anticipated rate of ongoing haemorrhage and the feasibility of achieving surgical control. In cases of AFE-related DIC, a transfusion strategy focusing on the early replacement of fibrinogen and other coagulation factors is critical, accompanied by continuous monitoring and dynamic assessment of coagulation-related parameters throughout the progression of the disease (\u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eFollowing intensive postoperative care, the patient\u0026rsquo;s coagulatory function gradually normalised, leading to complete recovery without complications. This case highlights that early recognition of atypical, coagulopathy-dominant AFE \u0026ndash; together with prompt fibrinogen-centred resuscitation, timely surgical intervention and coordinated multidisciplinary management \u0026ndash; is critical to improving maternal survival. Although most reported AFE cases involve the cardiopulmonary-collapse form, this experience reinforces the concept that disproportionate coagulopathy can be the initial and predominant manifestation, requiring heightened clinical vigilance and goal-directed correction of abnormalities of coagulation to achieve a favourable outcome.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case demonstrates that coagulopathy-dominant AFE can manifest primarily as acute disseminated coagulopathy without cardiopulmonary collapse. Here, early recognition of disproportionate coagulation dysfunction, rapid activation of a multidisciplinary team and implementation of a protocol involving massive transfusion emphasising early fibrinogen replacement together with timely surgical intervention were pivotal to maternal survival. Prompt decision-making and coordinated team management remain the cornerstone of improving outcomes in this rare but life-threatening obstetric emergency.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eAFE:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;amniotic fluid embolism\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eAPTT: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003eactivated partial thromboplastin time\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eCryo: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003ecryoprecipitate\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eDIC:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;disseminated intravascular coagulation\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eFbg:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;fibrinogen\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eFbg concentrate:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;fibrinogen concentrate\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eFFP:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;fresh frozen plasma\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eICU: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003eintensive care unit\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eINR:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;international normalised ratio\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eMTP: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003emassive transfusion protocol\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003ePlt: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003eplatelets\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003ePT: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003eprothrombin time\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eRBC:\u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003e\u0026nbsp;red blood cells\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-GB\"\u003eTXA: \u003c/span\u003e\u003c/strong\u003e\u003cspan lang=\"EN-GB\"\u003etranexamic acid\u003c/span\u003e\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eEthics approval and consent to participate\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eEthical approval for this case report was waived by the Ethics Committee of The First People\u0026rsquo;s Hospital of Shuangliu District, Chengdu (West China Airport Hospital, Sichuan University) in accordance with institutional policy. Written informed consent for participation was obtained from the patient.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eConsent for publication\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eWritten informed consent for publication of this case report and any accompanying images was obtained from the patient.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eAvailability of data and materials\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eAll data generated or analyzed during this study are included in this published article. No additional datasets are available.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eCompeting interests\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eThe authors declare that they have no competing interests.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eFunding\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eThis work was supported by the Technological Innovation and R\u0026amp;D Project of the Chengdu Science and Technology Bureau (No. 2024-YF05-02147-SN).\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eAuthors\u0026rsquo; contributions\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eHuang X was primarily responsible for the conception and design of the study, data acquisition, analysis, and drafting of the manuscript. Zhong XL contributed to clinical data collection and assisted with the interpretation of clinical findings. Long JJ assisted in manuscript revision and provided important clinical insights. Liu XY supervised the project, ensured adherence to reporting standards, and provided overall guidance throughout the research and manuscript preparation process. All authors have read and approved the final manuscript.\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cspan lang=\"EN-US\"\u003eAcknowledgements\u003c/span\u003e\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003e\u003cspan lang=\"EN-US\"\u003eWe sincerely thank the patient and her family for their cooperation and for granting permission to publish this case. Their support made this work possible and contributes to clinical understanding of atypical presentations of amniotic fluid embolism.\u003c/span\u003e\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eMazza GR, Youssefzadeh AC, Klar M, Kunze M, Matsuzaki S, Mandelbaum RS, et al. Association of Pregnancy Characteristics and Maternal Mortality With Amniotic Fluid Embolism. JAMA Network Open. 2022/11/01;5(11).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eClark SL, Hankins GDV, Dudley DA, Dildy GA, Porter TF. Amniotic fluid embolism: Analysis of the national registry. American Journal of Obstetrics \u0026amp; Gynecology. 1995/04/01;172(4).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eKE F, D T, JJ K, M K. Incidence, risk factors, management and outcomes of amniotic-fluid embolism: a population-based cohort and nested case-control study - PubMed. BJOG : an international journal of obstetrics and gynaecology. 2016 Jan;123(1).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eBaxter FJ. Amniotic Fluid Embolism: A Narrative Review. Journal of Obstetric Anaesthesia and Critical Care. Jul-Dec 2023;13(2).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eKanayama N, Tamura N. OBGYN. Journal of Obstetrics and Gynaecology Research. 2014/06/01;40(6).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eSultan P, Seligman K, Carvalho B. Amniotic fluid embolism: update and review. Current Opinion in Anesthesiology. June 2016;29(3).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eA P, P P, V T, A S, A T, E S, et al. Amniotic fluid embolism managed with success during labour: report of a severe clinical case and review of literature - PubMed. Archives of gynecology and obstetrics. 2008 Mar;277(3).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eM K, C B, P B, M K, G L, J O, et al. Amniotic fluid embolism incidence, risk factors and outcomes: a review and recommendations - PubMed. BMC pregnancy and childbirth. 02/10/2012;12(1).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003eJB L. Amniotic fluid embolism. Report of two cases with coagulation disorder - PubMed. Acta obstetricia et gynecologica Scandinavica. 1997 Sep;76(8).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e IT A, GD S. Amniotic fluid embolism and isolated coagulopathy: atypical presentation of amniotic fluid embolism - PubMed. European journal of anaesthesiology. 2001 Jun;18(6).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e AE W, DE R. The pathogenesis of amniotic-fluid embolism. III. Coagulant activity of amniotic fluid - PubMed. The New England journal of medicine. 10/19/1950;243(16).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e MJ H, DL H, S D, BS K. Effect of amniotic fluid on coagulation and platelet function in pregnancy: an evaluation using thromboelastography - PubMed. Anaesthesia. 2005 Nov;60(11).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e Bao W, Chen C, Zhang K, Zeng L, Qiu H, Liao C, Ho M, et al. Amniotic fluid induces platelet-neutrophil aggregation and neutrophil activation. Am J Obstet Gynecol. 2013;208(4):e1\u0026ndash;e8. doi:10.1016/j.ajog.2012.12.041\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e Levi M. Pathogenesis and management of peripartum coagulopathic calamities (disseminated intravascular coagulation and amniotic fluid embolism). Thrombosis Research. 2013/01/01;131.\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e O E, F G, S M-T, E V, JP K, CJ K, et al. Evidence of maternal platelet activation, excessive thrombin generation, and high amniotic fluid tissue factor immunoreactivity and functional activity in patients with fetal death - PubMed. The journal of maternal-fetal \u0026amp; neonatal medicine : the official journal of the European Association of Perinatal Medicine, the Federation of Asia and Oceania Perinatal Societies, the International Society of Perinatal Obstetricians. 2009 Aug;22(8).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e LD P, GR S, MM C, SL C, GD H. An update on the use of massive transfusion protocols in obstetrics - PubMed. American journal of obstetrics and gynecology. 2016 Mar;214(3).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e JH L, K G, QJ Q, RR B, I W. Adjuncts to Blood Component Therapies for the Treatment of Bleeding in the Intensive Care Unit - PubMed. Transfusion medicine reviews. 2017 Oct;31(4).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e FG C, DB N. Disseminated Intravascular Coagulation Syndromes in Obstetrics - PubMed. Obstetrics and gynecology. 2015 Nov;126(5).\u003c/span\u003e\u003c/li\u003e\n\u003cli\u003e\u003cspan lang=\"EN-US\"\u003e JA L, TL K, S S, M A, M A, EJ K. Rotational thromboelastometry (ROTEM\u0026reg;)-guided diagnosis and management of amniotic fluid embolism - PubMed. International journal of obstetric anesthesia. 2019 May;38.\u003c/span\u003e\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":true,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-pregnancy-and-childbirth","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"prch","sideBox":"Learn more about [BMC Pregnancy and Childbirth](http://bmcpregnancychildbirth.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/prch/default.aspx","title":"BMC Pregnancy and Childbirth","twitterHandle":"@BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Amniotic fluid embolism, coagulopathy-dominant subtype, postpartum haemorrhage, massive transfusion, multidisciplinary management","lastPublishedDoi":"10.21203/rs.3.rs-8191695/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8191695/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eAmniotic fluid embolism (AFE) is a rare but catastrophic obstetric emergency characterised by the sudden entry of amniotic fluid or fetal components into the maternal circulation, triggering severe cardiorespiratory collapse, coagulopathy, or both. While most patients exhibit abrupt hypotension and hypoxia, a coagulopathy-dominant subtype has increasingly been recognised but remains easily overlooked. Its insidious onset and absence of overt cardiopulmonary signs often delay recognition and appropriate intervention.\u003c/p\u003e\u003ch2\u003eCase presentation:\u003c/h2\u003e \u003cp\u003eWe report a 30-year-old Chinese woman (gravida 2, para 1) who developed severe coagulopathy-dominant AFE shortly after the vaginal delivery of a term singleton infant at a tertiary comprehensive hospital. She presented exclusively with massive postpartum bleeding and precipitous drops in fibrinogen (3.21\u0026rarr; 0.37 g/L within 15 minutes) and platelets (96\u0026rarr;46\u0026times;10⁹/L), without hypoxia or cardiopulmonary compromise. Recognising the disproportionate coagulopathy, clinicians rapidly initiated a protocol involving massive transfusion emphasising early fibrinogen supplementation, followed by timely surgical intervention. Despite profound disseminated intravascular coagulation and recurrent haemorrhage, coordinated multidisciplinary management resulted in complete recovery without sequelae.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003eThis case highlights an atypical, coagulopathy-dominant case of AFE in which rapid recognition of isolated coagulopathy and early fibrinogen-guided transfusion likely avoided a fatal outcome. Vigilant monitoring and prompt, team-based intervention are essential to improving survival in such non-classical AFE presentations.\u003c/p\u003e","manuscriptTitle":"Atypical amniotic fluid embolism presenting with isolated coagulopathy: A case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2025-12-22 10:04:50","doi":"10.21203/rs.3.rs-8191695/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision 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