Pregnancy-related acute liver failure with HELLP–AFLP overlap requiring intensive care

Pregnancy-related acute liver failure with HELLP–AFLP overlap requiring intensive care | 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 Pregnancy-related acute liver failure with HELLP–AFLP overlap requiring intensive care Mr Mangalabarathi Nagaraj, Dr Priyadharshini Rajasekaran This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8934627/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 29 You are reading this latest preprint version Abstract Pregnancy-related acute liver failure is an uncommon but life-threatening obstetric emergency that may overlap with HELLP syndrome and disseminated intravascular coagulation. We describe a patient presenting in presenting at 36 weeks of gestation with fever, jaundice, severe anemia, thrombocytopenia, markedly elevated bilirubin, acute kidney injury, and profound coagulopathy. Imaging revealed fetal growth restriction with oligohydramnios and mild ascites. A diagnosis of HELLP syndrome with acute liver failure and multiorgan dysfunction was considered. The patient required intensive critical care management including massive transfusion support, N-acetylcysteine therapy, correction of coagulopathy, and continuous multidisciplinary monitoring. She underwent vacuum-assisted vaginal birth after previous cesarean delivery, complicated by postpartum hemorrhage and transient respiratory compromise. With aggressive ICU-based supportive care, hepatic and renal function gradually improved, and she was discharged in stable condition. This case highlights the importance of early recognition and critical care intervention in pregnancy-associated acute liver failure. Figures Figure 1 Figure 2 BACKGROUND Pregnancy-related acute liver failure is an uncommon but severe complication of the third trimester, associated with high maternal and perinatal morbidity if not recognized early. The most important pregnancy-specific hepatic disorders leading to acute liver failure include HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) and acute fatty liver of pregnancy (AFLP). Both conditions may present with overlapping clinical and biochemical features such as jaundice, thrombocytopenia, coagulopathy, renal impairment, and rapid progression to multiorgan dysfunction, making timely diagnosis challenging in emergency and critical care settings(1,2) HELLP vs AFLP overlap HELLP syndrome and acute fatty liver of pregnancy (AFLP) are rare but life-threatening hepatic complications of late pregnancy. Although traditionally described as distinct entities, both conditions share overlapping clinical and biochemical features, including jaundice, thrombocytopenia, coagulopathy, renal dysfunction, and rapid progression to multiorgan failure. Increasing evidence suggests that HELLP syndrome and AFLP may represent a spectrum of pregnancy-related liver failure rather than completely separate disorders. Diagnostic difficulty in ICU-level ALF Diagnosing acute liver failure in pregnancy is particularly challenging in the critical care setting because physiological changes of pregnancy, overlapping laboratory abnormalities, and concurrent complications such as sepsis, thrombotic microangiopathy, or disseminated intravascular coagulation can obscure the primary etiology. Timely differentiation is often less important than early recognition of severity, prompt intensive care support, and urgent delivery to prevent maternal mortality. CASE PRESENTATION A pregnant patient in her 20s, with a history of one previous cesarean delivery, presented in presenting at 36 weeks of gestation to the emergency department with complaints of fever, progressive yellow discoloration of the eyes, generalized weakness, and reduced fetal movements. There was no documented history of chronic liver disease, pre-existing hypertension, diabetes mellitus, autoimmune illness, or alcohol use. Family history was non-contributory. The pregnancy had been complicated by reduced fetal growth on prior antenatal evaluation. On initial examination, the patient appeared acutely ill with marked pallor and icterus. She had bilateral pedal edema and signs of systemic involvement. Early clinical assessment raised concern for pregnancy-related hepatic dysfunction with evolving multiorgan impairment. Initial laboratory evaluation demonstrated severe anemia, with hemoglobin approximately 5.7 g/dL, thrombocytopenia of around 110 ×10³/µL, and biochemical evidence of acute liver injury with markedly elevated total bilirubin near 20 mg/dL (direct fraction 14.2 mg/dL). Coagulation testing revealed profound derangement with an international normalized ratio above 2.0 and hypofibrinogenemia consistent with consumptive coagulopathy. Renal function was significantly impaired, with serum creatinine approaching 2.9 mg/dL and reduced estimated glomerular filtration rate. Key laboratory abnormalities at admission are summarized in Table 1 . Table 1 Key laboratory abnormalities on admission Parameter Result Reference range Hemoglobin ~ 5.7 g/dL 12–15 g/dL Platelets ~ 110 ×10³/µL 150–400 ×10³/µL Total bilirubin ~ 20 mg/dL 0.3–1.2 mg/dL Direct bilirubin ~ 14.2 mg/dL 2.0 0.9–1.2 Fibrinogen ~ 123 mg/dL 200–400 mg/dL Serum creatinine ~ 2.9 mg/dL 0.5–1.1 mg/dL Estimated GFR ~ 21 mL/min > 90 mL/min Obstetric ultrasonography showed severe fetal growth restriction with oligohydramnios, while abdominal imaging revealed mild ascites without focal hepatic structural abnormality. Echocardiography demonstrated preserved left ventricular systolic function without valvular pathology. Infectious etiologies including viral hepatitis, dengue, malaria, leptospirosis, and scrub typhus were excluded through appropriate serological testing. Based on the clinical presentation of hemolysis, thrombocytopenia, hepatic failure, renal dysfunction, and severe coagulopathy, a working diagnosis of pregnancy-associated acute liver failure with overlap of hemolysis, elevated liver enzymes, and low platelets syndrome and disseminated intravascular coagulation was established. The patient was transferred to the medical intensive care unit for multidisciplinary critical care management. She required aggressive transfusion support including packed red blood cells, fresh frozen plasma, and cryoprecipitate to correct life-threatening anemia and coagulopathy. Supportive hepatic therapy with N-acetylcysteine was initiated. Broad-spectrum antimicrobial therapy was administered due to persistent fever and risk of sepsis. Two days after intensive care admission, the patient progressed into spontaneous labor. Due to worsening maternal condition and fetal compromise, assisted vaginal birth after previous cesarean delivery was performed using a vacuum extraction device. Delivery was complicated by postpartum hemorrhage requiring uterotonic therapy, vaginal packing, and additional transfusion support. In the immediate postpartum period, the patient developed transient respiratory compromise with desaturation and hemoptysis, consistent with pulmonary edema, requiring critical care monitoring and respiratory support. With continued multidisciplinary ICU care, hepatic and renal parameters gradually improved, coagulation stabilized, and the patient was discharged in stable condition with planned follow-up. Clinical Timeline of Diseases Progression are illustrated in Fig. 1. Investigations for Infectious causes of acute liver failure were excluded, obstetric ultrasonography showed fetal growth restriction with oligohydramnios, abdominal imaging revealed mild ascites without structural liver disease, and transthoracic echocardiography was normal. Serial laboratory trends during ICU stay are summarized in Table 2 and Trends in hepatic, coagulation, and renal biomarkers during ICU stay are illustrated in Fig. 2 . Table 2 . Serial laboratory trends during intensive care stay Table 2 summarizes the dynamic changes in hepatic, coagulation, and renal biomarkers, demonstrating gradual recovery following multidisciplinary critical care support and delivery. Hospital day Total bilirubin (mg/dL) International normalized ratio Serum creatinine (mg/dL) Interpretation Day 1 (Admission) 20.0 2.2 2.9 Severe acute liver failure with coagulopathy and acute kidney injury Day 2 18.0 2.0 2.7 Persistent hepatic dysfunction; ongoing transfusion requirement Day 3 15.0 1.8 2.3 Early biochemical improvement following intensive supportive care Day 4 12.0 1.5 1.9 Post-delivery stabilization with improving coagulation profile Day 5 9.0 1.3 1.6 Continued recovery of liver and renal function Day 6 6.0 1.2 1.3 Near normalization of coagulation parameters Day 7 (Discharge phase) 4.0 1.1 1.2 Significant resolution of hepatic and renal dysfunction Differential Diagnosis The patient presented in presenting at 36 weeks of gestation with jaundice, severe anemia, thrombocytopenia, acute kidney injury, and profound coagulopathy progressing to multiorgan dysfunction. Several pregnancy-related and non–pregnancy-related conditions were considered. HELLP syndrome was strongly suspected based on thrombocytopenia, hemolysis-related anemia, hepatic dysfunction, renal impairment, and rapid clinical improvement following delivery. These features are characteristic of severe HELLP syndrome complicated by disseminated intravascular coagulation and acute liver failure. Acute fatty liver of pregnancy (AFLP) was considered because of marked hyperbilirubinemia, coagulopathy, renal dysfunction, and ascites. However, the diagnosis of isolated AFLP was less likely. Formal application of the Swansea criteria was limited by incomplete data in the setting of critical illness. Importantly, there was no documented hypoglycemia, which is a key feature of AFLP, and serum ammonia levels were not available. In addition, the presence of thrombocytopenia and hemolysis, along with postpartum recovery without prolonged hepatic failure, favored a HELLP spectrum disorder rather than AFLP alone. Thrombotic microangiopathy (TMA) , including thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome, was also considered due to anemia, thrombocytopenia, and acute kidney injury. However, the absence of neurological manifestations and the rapid clinical and biochemical improvement after delivery without plasma exchange made TMA unlikely. Sepsis-associated liver dysfunction was considered because of fever at presentation. Broad infectious screening was performed and empirical antibiotics were initiated; however, negative infectious work-up and subsequent recovery following delivery argued against sepsis as the primary cause. Other causes of acute liver failure in pregnancy, including viral hepatitis, autoimmune hepatitis, drug-induced liver injury, and biliary obstruction, were excluded through serological testing, clinical history, and imaging. Final diagnosis pregnancy-related acute liver failure secondary to severe HELLP syndrome complicated by disseminated intravascular coagulation and multiorgan dysfunction. Swansea criteria: Against the Swansea criteria , the patient met jaundice, coagulopathy, renal dysfunction, and ascites, but lacked hypoglycemia, hyperammonemia (ammonia 21 µmol/L), encephalopathy, leukocytosis, imaging evidence of steatosis, or delayed recovery, and therefore did not meet diagnostic criteria for AFLP. Differential diagnoses considered are summarized in Table 3 Table 3 Summary of differential diagnoses considered in pregnancy-related acute liver failure This table outlines the key conditions evaluated, supporting findings, and reasons they were excluded or considered less likely. Differential diagnosis Supporting clinical features in this patient Key investigations/considerations Reason final diagnosis favored against/for HELLP syndrome (Hemolysis, Elevated liver enzymes, Low platelets) Severe anemia, thrombocytopenia, hepatic dysfunction, renal impairment Platelet reduction, hemolysis, liver injury pattern Strongly supported; common cause of pregnancy-related multiorgan dysfunction requiring ICU care [ 1 ] Acute fatty liver of pregnancy Marked jaundice, severe coagulopathy, acute liver failure, ascites, renal dysfunction Hyperbilirubinemia, hepatic failure, overlap with HELLP Considered highly likely due to profound bilirubin elevation and acute liver failure features [ 2 ] Disseminated intravascular coagulation Severe coagulopathy, low fibrinogen, postpartum hemorrhage risk INR > 2.0, hypofibrinogenemia Strongly supported as a major complication of HELLP/AFLP overlap [ 3 ] Sepsis-associated hepatic dysfunction Fever, systemic illness, thrombocytopenia Infection screening, empirical antibiotics Infectious etiologies excluded by negative serology; sepsis less likely primary cause [ 4 ] Thrombotic thrombocytopenic purpura / atypical hemolytic uremic syndrome Hemolysis, thrombocytopenia, acute kidney injury Clinical overlap with HELLP Less likely due to postpartum recovery and absence of neurologic involvement [ 5 ] Viral hepatitis Jaundice, acute liver injury Viral hepatitis markers negative Excluded through serological evaluation [ 4 ] Autoimmune or drug-induced hepatitis Acute liver dysfunction possible No autoimmune history or hepatotoxic drug exposure Unlikely given clinical context and imaging findings Biliary obstruction / structural liver disease Jaundice could suggest obstruction Ultrasound showed no biliary obstruction or hepatic mass Excluded through abdominal imaging Key Message for Readers The final diagnosis of pregnancy-related acute liver failure with HELLP syndrome–AFLP overlap and disseminated intravascular coagulation was made after exclusion of infectious, thrombotic microangiopathic, and structural hepatic TREATMENT Management was initiated immediately after admission with the primary goals of stabilizing maternal physiology, correcting life-threatening coagulopathy, preventing progression of multiorgan failure, and planning timely delivery. A multidisciplinary team involving obstetrics, critical care, hepatology, transfusion medicine, and neonatology coordinated the therapeutic strategy, as pregnancy-related acute liver failure associated with hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy requires urgent supportive care and definitive delivery(1,2). The patient required admission to the intensive care unit for multiorgan dysfunction, where she received massive transfusion support, N-acetylcysteine therapy, empirical broad-spectrum antibiotics, and close multidisciplinary monitoring. Definitive management consisted of urgent delivery following partial correction of coagulopathy. Intensive care management interventions are summarized in Table 4 . Table 4 Summary of intensive care treatments and transfusion support This table summarizes the major pharmacological, supportive, and transfusion-based interventions provided during the critical care course. Treatment category Intervention provided Clinical indication Outcome/response Critical care monitoring Admission to medical intensive care unit with continuous hemodynamic and respiratory monitoring Multiorgan dysfunction with acute liver failure and coagulopathy Allowed early detection of hemorrhage, pulmonary edema, and renal deterioration Red blood cell transfusion Packed red blood cells (multiple units) Severe anemia (hemoglobin ~ 5.7 g/dL) and suspected hemolysis Improved oxygen-carrying capacity and hemodynamic stability Plasma replacement therapy Fresh frozen plasma (> 10 units) Correction of markedly prolonged international normalized ratio (> 2.0) Gradual improvement in coagulation parameters Fibrinogen replacement Cryoprecipitate (> 20 units) Hypofibrinogenemia (~ 123 mg/dL) consistent with disseminated intravascular coagulation Reduced bleeding risk and supported stabilization prior to delivery Coagulation support Intravenous vitamin K Support of hepatic clotting factor synthesis Adjunctive improvement in coagulation profile Hepatic supportive therapy N-acetylcysteine infusion followed by oral continuation Supportive management of acute liver failure Associated with biochemical improvement in bilirubin levels Antimicrobial therapy Broad-spectrum antibiotics (piperacillin–tazobactam + metronidazole) Persistent fever and risk of sepsis complicating liver failure Prevented secondary infection while infectious causes were excluded Obstetric intervention Vacuum-assisted vaginal birth after previous cesarean delivery (Kiwi® OmniCup, Clinical Innovations, USA) Fetal compromise and worsening maternal condition Definitive management enabling disease stabilization postpartum Postpartum hemorrhage management Uterotonic therapy, vaginal packing, additional transfusion support Delivery complicated by postpartum hemorrhage Controlled bleeding with improved maternal recovery Respiratory supportive care Oxygen therapy and intensive monitoring Postpartum pulmonary edema with transient desaturation Resolved with critical care support Step-down and discharge therapy Oral supportive medications and outpatient follow-up planning Recovery phase after stabilization Discharged in stable condition with improving liver and renal function OUTCOME AND FOLLOW-UP Following delivery and continued multidisciplinary intensive care support, the patient demonstrated gradual clinical and biochemical recovery. Over the first week of hospitalization, hepatic dysfunction progressively improved, with a steady decline in total bilirubin levels and stabilization of liver synthetic function. Coagulation parameters normalized with cessation of transfusion requirements, and fibrinogen levels recovered after correction of disseminated intravascular coagulation. Renal function also improved, with serum creatinine decreasing from severe acute kidney injury range to near-baseline values, consistent with reversal of pregnancy-related multiorgan dysfunction. Respiratory compromise observed in the immediate postpartum period, consistent with pulmonary edema, resolved with supportive oxygen therapy and careful fluid balance monitoring. Postpartum hemorrhage was successfully controlled with uterotonic therapy, vaginal packing, and additional transfusion support, with no recurrent bleeding episodes. The patient was stepped down from intensive care once hemodynamically stable and transferred to the general obstetric ward for continued monitoring. At the time of discharge, she was clinically stable, ambulatory, tolerating oral intake, and independent in daily activities. She was discharged on oral supportive therapy including ursodeoxycholic acid, lactulose, and antioxidant supplementation, with advice for rest and gradual return to routine activity. Follow-up was arranged with obstetrics, hepatology, and nephrology services. Surveillance included repeat liver function testing, coagulation profile, renal function assessment, and blood pressure monitoring within 2–4 weeks after discharge, consistent with recommended postpartum follow-up for hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy recovery(1,2). Long-term counseling was provided regarding recurrence risk in future pregnancies and the importance of early antenatal surveillance. DISCUSSION Pregnancy-related acute liver failure represents one of the most severe obstetric emergencies, with rapid progression to multiorgan dysfunction if diagnosis and delivery are delayed. The most important pregnancy-specific hepatic disorders causing acute liver failure in the third trimester include hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy. Both conditions share overlapping clinical manifestations such as jaundice, thrombocytopenia, coagulopathy, and renal dysfunction, often making early differentiation difficult in emergency and critical care settings(1,2). This case describes a woman presenting at 36 weeks of gestation with rapidly progressive acute liver failure manifested by jaundice, profound coagulopathy, thrombocytopenia, acute kidney injury, and systemic instability necessitating intensive care admission. Initial evaluation excluded infectious and structural hepatic causes, and pregnancy-related liver failure was considered most likely. The clinical course was complicated by disseminated intravascular coagulation, high transfusion requirements, and evolving maternal–fetal compromise. Management focused on aggressive supportive critical care, close multidisciplinary coordination, and timely delivery, after which the patient demonstrated prompt clinical stabilization and progressive biochemical recovery. Establishing a definitive diagnosis was challenging because pregnancy-specific liver disorders share substantial clinical and biochemical overlap, particularly in critically ill patients. Features such as jaundice, thrombocytopenia, coagulopathy, and renal dysfunction can be seen in HELLP syndrome, acute fatty liver of pregnancy, sepsis, and thrombotic microangiopathies. In this case, the severity of liver dysfunction and coagulopathy raised concern for acute fatty liver of pregnancy; however, incomplete fulfillment of Swansea criteria, absence of hyperammonemia or severe hypoglycemia, and rapid improvement after delivery favored a HELLP-spectrum disorder. The urgency of maternal stabilization and delivery further limited reliance on exhaustive diagnostic testing, underscoring the pragmatic challenges of diagnosis in obstetric critical care. Brief review of similar published cases Several published reports describe acute liver failure in pregnancy complicated by disseminated intravascular coagulation and acute kidney injury requiring intensive care management. Knight and colleagues reported that acute fatty liver of pregnancy frequently presents with coagulopathy and renal dysfunction, with maternal outcomes improving significantly with early diagnosis and delivery(2). Ch’ng et al. emphasized the diagnostic challenge of pregnancy-related liver dysfunction and the importance of distinguishing pregnancy-specific syndromes from viral hepatitis and thrombotic microangiopathies(1). Case-based evidence also demonstrates that intensive care support and transfusion-based correction of coagulopathy are critical determinants of survival in severe hemolysis, elevated liver enzymes, and low platelets syndrome(6). Comparison with previously published cases is summarized in Table 5 Table 5 Summary of published pregnancy-related acute liver failure cases with critical care involvement Study Condition Major complications Key management Outcome Knight et al. (2008) [ 2 ] Acute fatty liver of pregnancy Coagulopathy, renal failure Early delivery + ICU support Improved maternal survival Ch’ng et al. (2002) [ 3 ] Pregnancy liver dysfunction spectrum Diagnostic overlap with HELLP Multidisciplinary evaluation Better outcomes with early recognition Sibai (2004) [ 1 ] HELLP syndrome DIC, hepatic rupture risk Delivery + supportive transfusion ICU often required in severe cases Present case HELLP/AFLP overlap DIC, AKI, pulmonary edema, PPH Massive transfusion + ICU + assisted delivery Full maternal recovery Clinical lessons and conclusions This case highlights several important learning points. First, pregnancy-related acute liver failure should be suspected in third-trimester patients presenting with jaundice, thrombocytopenia, renal dysfunction, and severe coagulopathy. Second, overlap between hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy is common, and management should prioritize supportive intensive care stabilization and urgent delivery rather than delayed diagnostic separation. Third, aggressive correction of disseminated intravascular coagulation and postpartum critical care monitoring are essential to prevent fatal maternal complications. Although causality between assisted delivery and recovery cannot be inferred, the favorable outcome in this patient was most likely attributable to timely multidisciplinary intensive care intervention, transfusion support, and definitive delivery. LEARNING POINTS / TAKE HOME MESSAGES Pregnancy-related acute liver failure should be promptly suspected in third-trimester patients presenting with jaundice, thrombocytopenia, severe coagulopathy, and acute kidney injury, as rapid progression to multiorgan dysfunction is common. Significant clinical overlap exists between hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy: management should prioritize urgent stabilization and timely delivery rather then delayed diagnostic separation. Early admission to intensive care with aggressive correction of disseminated intravascular coagulation using fresh frozen plasma and cryoprecipitates is essential to prevent catastrophic hemorrhagic complications. Delivery remains the definitive treatment for pregnancy-specific acute liver failure syndromes, and multidisciplinary coordination between obstetrics, critical care, hepatology, and transfusion services improves maternal outcomes. Postpartum complications such as hemorrhage, pulmonary edema, and persistent organ dysfunction require continued critical care surveillance even after delivery to ensure full recovery. Declarations Ethics approval and consent to participate: Ethics approval was not required for this case report as per institutional policy. Written informed consent was obtained from the patient. Consent for publication Informed consent was obtained from the patient for publication of this case report and any accompanying images or clinical data. Competing interests The author declares that there are no competing interests. Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Author Contribution MN conceptualized the case report, participated in patient care, conducted the literature review, and drafted the initial manuscript. PR contributed to clinical supervision, critical revision of the manuscript for important intellectual content, and validation of clinical accuracy. Both authors read and approved the final manuscript. Acknowledgement The authors would like to acknowledge the multidisciplinary intensive care, obstetrics, hepatology, transfusion medicine, and nursing teams at Narayana Health City, Bengaluru, for their coordinated clinical support in the management of this patient. We also thank the patient and her family for providing informed consent for publication of this case report. Data Availability All relevant clinical data supporting the findings of this case report are included within the manuscript. References Anitha G, Shivamurthy G, Krishnappa TK, Chethan R. Maternal and Fetal Outcome in HELLP Syndrome: An Observational Study. J South Asian Fed Obstet Gynaecol. 2020;12(3):122–32. Morrison MA, Chung Y, Heneghan MA. Managing hepatic complications of pregnancy: practical strategies for clinicians. BMJ Open Gastroenterol. 2022;9(1):e000624. Nelson DB, Byrne JJ, Cunningham FG. Acute Fatty Liver of Pregnancy. Clin Obstet Gynecol. 2020;63(1):152–64. Anand AC, Nandi B, Acharya SK, Arora A, Babu S, Batra Y, et al. Indian National Association for the Study of Liver Consensus Statement on Acute Liver Failure (Part-2): Management of Acute Liver Failure. J Clin Exp Hepatol. 2020;10(5):477–517. Seetharam A. Intensive Care Management of Acute Liver Failure: Considerations While Awaiting Liver Transplantation. J Clin Transl Hepatol. 2019;7(X):1–8. Levi M, Toh CH, Thachil J, Watson HG. Guidelines for the diagnosis and management of disseminated intravascular coagulation. Br J Haematol. 2009;145(1):24–33. PATIENT’S PERSPECTIVE. I remember. feeling unwell for several days before coming to the hospital. I had fever, extreme weakness, and my eyes and skin became yellow. I was very worried because I could not feel my baby moving normally and I felt something was seriously wrong. When I. arrived at the emergency department, I was frightened after hearing that my blood levels were very low and that my liver and kidneys were affected. I was transferred to the intensive care unit, where I received blood transfusions and many medications. The doctors explained that my condition was serious and that close monitoring was needed to protect both me and my baby. A few days later. I went into labor, and the delivery was difficult. After delivery, I experienced heavy bleeding and breathing difficulty, which was very scary for me. The critical care team supported me throughout this period, and I gradually started improving. Over the following days. I felt stronger, and my jaundice reduced. I was relieved to recover and to be able to return home. This experience made me realize the importance of seeking urgent medical care when serious symptoms occur during pregnancy. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 23 Mar, 2026 Reviews received at journal 22 Mar, 2026 Reviews received at journal 22 Mar, 2026 Reviews received at journal 22 Mar, 2026 Reviewers agreed at journal 22 Mar, 2026 Reviews received at journal 22 Mar, 2026 Reviews received at journal 21 Mar, 2026 Reviewers agreed at journal 21 Mar, 2026 Reviews received at journal 20 Mar, 2026 Reviewers agreed at journal 20 Mar, 2026 Reviews received at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviews received at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviews received at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers agreed at journal 19 Mar, 2026 Reviewers invited by journal 19 Mar, 2026 Editor invited by journal 09 Mar, 2026 Editor assigned by journal 02 Mar, 2026 Submission checks completed at journal 02 Mar, 2026 First submitted to journal 21 Feb, 2026 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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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8934627","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":610157120,"identity":"9b0b2556-c51b-4d87-8940-5038482e1e7e","order_by":0,"name":"Mr Mangalabarathi Nagaraj","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABGUlEQVRIiWNgGAWjYNCCAoYEEMXMYMDAwA9iJRQQ0mIA1sLYDNIi2QDSYkC0FhD7AEQEJ9BtP3v4xQ8Duzz+2YefPy4ouJNnfH514ocHBgzy/GIHsGoxO5OXZtljkFwscS7NsHmGwbNisxtvN0sAHWY4c3YCdi0HcswMeAyYExvOMBg28xgcTtx24+wGkJYEg9s4tJx/Y2b4x6A+cf4Z9o9gLZtnnN38A6+WGznGj0EqN5zhgdiygb93G35bbrwxY5YxOF5seIancDZQS7HEDd5tFgkGErj9cj7H+OObiuo8uTPsGz7z/Dmcx99/dvPNHxU28vzS2LUAAZsEMi+BQQKsUgKrWihg/oCqhf8APtWjYBSMglEwAgEAttZmpkE9Sx4AAAAASUVORK5CYII=","orcid":"","institution":"Narayana Health","correspondingAuthor":true,"prefix":"Mr","firstName":"Mangalabarathi","middleName":"","lastName":"Nagaraj","suffix":""},{"id":610157122,"identity":"cae22537-316d-476e-af7a-e3f7b197f9ba","order_by":1,"name":"Dr Priyadharshini Rajasekaran","email":"","orcid":"","institution":"Narayana Health","correspondingAuthor":false,"prefix":"Dr","firstName":"Priyadharshini","middleName":"","lastName":"Rajasekaran","suffix":""}],"badges":[],"createdAt":"2026-02-21 16:08:51","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8934627/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8934627/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":105297276,"identity":"d6961790-4473-40fe-ab2f-217df4db2235","added_by":"auto","created_at":"2026-03-24 13:18:30","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":463536,"visible":true,"origin":"","legend":"\u003cp\u003eSee image above for figure legend\u003c/p\u003e","description":"","filename":"floatimage1.png","url":"https://assets-eu.researchsquare.com/files/rs-8934627/v1/4b46bd8adbf741ca9ece1729.png"},{"id":105297275,"identity":"b422b953-208a-4554-8d42-534a45e9e49c","added_by":"auto","created_at":"2026-03-24 13:18:30","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":65992,"visible":true,"origin":"","legend":"\u003cp\u003e\u003cstrong\u003eTrends in liver, coagulation, and renal biomarkers during intensive care stay.\u003c/strong\u003e\u003cbr\u003e\nSerial laboratory monitoring demonstrated progressive improvement in hepatic dysfunction with declining total bilirubin levels, correction of severe coagulopathy with normalization of the international normalized ratio, and recovery of renal function with decreasing serum creatinine values from admission through the discharge phase. These trends reflect clinical stabilization following multidisciplinary critical care support, transfusion therapy, and delivery. This figure was created by the authors for this manuscript.\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8934627/v1/a080d14fcb127b9c1ff52588.png"},{"id":105564526,"identity":"74ff9eec-b4a4-496e-ab5e-c6a09d97cd8d","added_by":"auto","created_at":"2026-03-27 12:49:54","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1766170,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8934627/v1/f5c332c5-01fa-4635-aa87-54945001b163.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Pregnancy-related acute liver failure with HELLP–AFLP overlap requiring intensive care","fulltext":[{"header":"BACKGROUND","content":"\u003cp\u003ePregnancy-related acute liver failure is an uncommon but severe complication of the third trimester, associated with high maternal and perinatal morbidity if not recognized early. The most important pregnancy-specific hepatic disorders leading to acute liver failure include HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) and acute fatty liver of pregnancy (AFLP). Both conditions may present with overlapping clinical and biochemical features such as jaundice, thrombocytopenia, coagulopathy, renal impairment, and rapid progression to multiorgan dysfunction, making timely diagnosis challenging in emergency and critical care settings(1,2)\u003c/p\u003e \u003cp\u003e \u003cstrong\u003eHELLP vs AFLP overlap\u003c/strong\u003e \u003cp\u003eHELLP syndrome and acute fatty liver of pregnancy (AFLP) are rare but life-threatening hepatic complications of late pregnancy. Although traditionally described as distinct entities, both conditions share overlapping clinical and biochemical features, including jaundice, thrombocytopenia, coagulopathy, renal dysfunction, and rapid progression to multiorgan failure. Increasing evidence suggests that HELLP syndrome and AFLP may represent a spectrum of pregnancy-related liver failure rather than completely separate disorders.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eDiagnostic difficulty in ICU-level ALF\u003c/strong\u003e \u003cp\u003eDiagnosing acute liver failure in pregnancy is particularly challenging in the critical care setting because physiological changes of pregnancy, overlapping laboratory abnormalities, and concurrent complications such as sepsis, thrombotic microangiopathy, or disseminated intravascular coagulation can obscure the primary etiology. Timely differentiation is often less important than early recognition of severity, prompt intensive care support, and urgent delivery to prevent maternal mortality.\u003c/p\u003e \u003c/p\u003e"},{"header":"CASE PRESENTATION","content":"\u003cp\u003eA pregnant patient in her 20s, with a history of one previous cesarean delivery, presented in presenting at 36 weeks of gestation to the emergency department with complaints of fever, progressive yellow discoloration of the eyes, generalized weakness, and reduced fetal movements. There was no documented history of chronic liver disease, pre-existing hypertension, diabetes mellitus, autoimmune illness, or alcohol use. Family history was non-contributory. The pregnancy had been complicated by reduced fetal growth on prior antenatal evaluation.\u003c/p\u003e \u003cp\u003eOn initial examination, the patient appeared acutely ill with marked pallor and icterus. She had bilateral pedal edema and signs of systemic involvement. Early clinical assessment raised concern for pregnancy-related hepatic dysfunction with evolving multiorgan impairment. Initial laboratory evaluation demonstrated severe anemia, with hemoglobin approximately 5.7 g/dL, thrombocytopenia of around 110 \u0026times;10\u0026sup3;/\u0026micro;L, and biochemical evidence of acute liver injury with markedly elevated total bilirubin near 20 mg/dL (direct fraction 14.2 mg/dL). Coagulation testing revealed profound derangement with an international normalized ratio above 2.0 and hypofibrinogenemia consistent with consumptive coagulopathy. Renal function was significantly impaired, with serum creatinine approaching 2.9 mg/dL and reduced estimated glomerular filtration rate. Key laboratory abnormalities at admission are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eKey laboratory abnormalities on admission\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"3\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eParameter\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eResult\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eReference range\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHemoglobin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;5.7 g/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e12\u0026ndash;15 g/dL\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePlatelets\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;110 \u0026times;10\u0026sup3;/\u0026micro;L\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e150\u0026ndash;400 \u0026times;10\u0026sup3;/\u0026micro;L\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTotal bilirubin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;20 mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.3\u0026ndash;1.2 mg/dL\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDirect bilirubin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;14.2 mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026lt;\u0026thinsp;0.3 mg/dL\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eInternational normalized ratio\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;2.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.9\u0026ndash;1.2\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eFibrinogen\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;123 mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e200\u0026ndash;400 mg/dL\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSerum creatinine\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;2.9 mg/dL\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e0.5\u0026ndash;1.1 mg/dL\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eEstimated GFR\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e~\u0026thinsp;21 mL/min\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;90 mL/min\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eObstetric ultrasonography showed severe fetal growth restriction with oligohydramnios, while abdominal imaging revealed mild ascites without focal hepatic structural abnormality. Echocardiography demonstrated preserved left ventricular systolic function without valvular pathology. Infectious etiologies including viral hepatitis, dengue, malaria, leptospirosis, and scrub typhus were excluded through appropriate serological testing. Based on the clinical presentation of hemolysis, thrombocytopenia, hepatic failure, renal dysfunction, and severe coagulopathy, a working diagnosis of pregnancy-associated acute liver failure with overlap of hemolysis, elevated liver enzymes, and low platelets syndrome and disseminated intravascular coagulation was established.\u003c/p\u003e \u003cp\u003eThe patient was transferred to the medical intensive care unit for multidisciplinary critical care management. She required aggressive transfusion support including packed red blood cells, fresh frozen plasma, and cryoprecipitate to correct life-threatening anemia and coagulopathy. Supportive hepatic therapy with N-acetylcysteine was initiated. Broad-spectrum antimicrobial therapy was administered due to persistent fever and risk of sepsis.\u003c/p\u003e \u003cp\u003eTwo days after intensive care admission, the patient progressed into spontaneous labor. Due to worsening maternal condition and fetal compromise, assisted vaginal birth after previous cesarean delivery was performed using a vacuum extraction device. Delivery was complicated by postpartum hemorrhage requiring uterotonic therapy, vaginal packing, and additional transfusion support.\u003c/p\u003e \u003cp\u003eIn the immediate postpartum period, the patient developed transient respiratory compromise with desaturation and hemoptysis, consistent with pulmonary edema, requiring critical care monitoring and respiratory support.\u003c/p\u003e \u003cp\u003eWith continued multidisciplinary ICU care, hepatic and renal parameters gradually improved, coagulation stabilized, and the patient was discharged in stable condition with planned follow-up. Clinical Timeline of Diseases Progression are illustrated in Fig.\u0026nbsp;1.\u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cp\u003eInvestigations for Infectious causes of acute liver failure were excluded, obstetric ultrasonography showed fetal growth restriction with oligohydramnios, abdominal imaging revealed mild ascites without structural liver disease, and transthoracic echocardiography was normal. Serial laboratory trends during ICU stay are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e and Trends in hepatic, coagulation, and renal biomarkers during ICU stay are illustrated in Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e2\u003c/span\u003e.\u003c/p\u003e \u003cp\u003eTable\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e. \u003cb\u003eSerial laboratory trends during intensive care stay\u003c/b\u003e\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003esummarizes the dynamic changes in hepatic, coagulation, and renal biomarkers, demonstrating gradual recovery following multidisciplinary critical care support and delivery.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"char\" char=\".\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHospital day\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eTotal bilirubin (mg/dL)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eInternational normalized ratio\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eSerum creatinine (mg/dL)\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eInterpretation\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 1 (Admission)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e20.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e2.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eSevere acute liver failure with coagulopathy and acute kidney injury\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e18.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e2.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2.7\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ePersistent hepatic dysfunction; ongoing transfusion requirement\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e15.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.8\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e2.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eEarly biochemical improvement following intensive supportive care\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 4\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e12.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.9\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003ePost-delivery stabilization with improving coagulation profile\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 5\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e9.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eContinued recovery of liver and renal function\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 6\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e6.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.3\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eNear normalization of coagulation parameters\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDay 7 (Discharge phase)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c2\"\u003e \u003cp\u003e4.0\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c3\"\u003e \u003cp\u003e1.1\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"char\" char=\".\" colname=\"c4\"\u003e \u003cp\u003e1.2\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eSignificant resolution of hepatic and renal dysfunction\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003e \u003c/p\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003eDifferential Diagnosis\u003c/h2\u003e \u003cp\u003eThe patient presented in presenting at 36 weeks of gestation with jaundice, severe anemia, thrombocytopenia, acute kidney injury, and profound coagulopathy progressing to multiorgan dysfunction. Several pregnancy-related and non\u0026ndash;pregnancy-related conditions were considered.\u003c/p\u003e \u003cp\u003e \u003cb\u003eHELLP syndrome\u003c/b\u003e was strongly suspected based on thrombocytopenia, hemolysis-related anemia, hepatic dysfunction, renal impairment, and rapid clinical improvement following delivery. These features are characteristic of severe HELLP syndrome complicated by disseminated intravascular coagulation and acute liver failure.\u003c/p\u003e \u003cp\u003e \u003cb\u003eAcute fatty liver of pregnancy (AFLP)\u003c/b\u003e was considered because of marked hyperbilirubinemia, coagulopathy, renal dysfunction, and ascites. However, the diagnosis of isolated AFLP was less likely. Formal application of the Swansea criteria was limited by incomplete data in the setting of critical illness. Importantly, there was no documented hypoglycemia, which is a key feature of AFLP, and serum ammonia levels were not available. In addition, the presence of thrombocytopenia and hemolysis, along with postpartum recovery without prolonged hepatic failure, favored a HELLP spectrum disorder rather than AFLP alone.\u003c/p\u003e \u003cp\u003e \u003cb\u003eThrombotic microangiopathy (TMA)\u003c/b\u003e, including thrombotic thrombocytopenic purpura and atypical hemolytic uremic syndrome, was also considered due to anemia, thrombocytopenia, and acute kidney injury. However, the absence of neurological manifestations and the rapid clinical and biochemical improvement after delivery without plasma exchange made TMA unlikely.\u003c/p\u003e \u003cp\u003eSepsis-associated liver dysfunction was considered because of fever at presentation. Broad infectious screening was performed and empirical antibiotics were initiated; however, negative infectious work-up and subsequent recovery following delivery argued against sepsis as the primary cause.\u003c/p\u003e \u003cp\u003eOther causes of acute liver failure in pregnancy, including viral hepatitis, autoimmune hepatitis, drug-induced liver injury, and biliary obstruction, were excluded through serological testing, clinical history, and imaging.\u003c/p\u003e \u003cp\u003e \u003cstrong\u003eFinal diagnosis\u003c/strong\u003e \u003cp\u003epregnancy-related acute liver failure secondary to severe HELLP syndrome complicated by disseminated intravascular coagulation and multiorgan dysfunction.\u003c/p\u003e \u003c/p\u003e \u003c/div\u003e\n\u003ch3\u003eSwansea criteria:\u003c/h3\u003e\n\u003cp\u003e \u003cb\u003eAgainst the Swansea criteria\u003c/b\u003e, the patient met jaundice, coagulopathy, renal dysfunction, and ascites, but lacked hypoglycemia, hyperammonemia (ammonia 21 \u0026micro;mol/L), encephalopathy, leukocytosis, imaging evidence of steatosis, or delayed recovery, and therefore did not meet diagnostic criteria for AFLP. Differential diagnoses considered are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab3\" class=\"InternalRef\"\u003e3\u003c/span\u003e\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab3\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 3\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003e\u003cb\u003eSummary of differential diagnoses considered in pregnancy-related acute liver failure\u003c/b\u003e This table outlines the key conditions evaluated, supporting findings, and reasons they were excluded or considered less likely.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eDifferential diagnosis\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSupporting clinical features in this patient\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eKey investigations/considerations\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eReason final diagnosis favored against/for\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eHELLP syndrome (Hemolysis, Elevated liver enzymes, Low platelets)\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSevere anemia, thrombocytopenia, hepatic dysfunction, renal impairment\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePlatelet reduction, hemolysis, liver injury pattern\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eStrongly supported; common cause of pregnancy-related multiorgan dysfunction requiring ICU care [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eAcute fatty liver of pregnancy\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eMarked jaundice, severe coagulopathy, acute liver failure, ascites, renal dysfunction\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eHyperbilirubinemia, hepatic failure, overlap with HELLP\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eConsidered highly likely due to profound bilirubin elevation and acute liver failure features [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eDisseminated intravascular coagulation\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSevere coagulopathy, low fibrinogen, postpartum hemorrhage risk\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eINR\u0026thinsp;\u0026gt;\u0026thinsp;2.0, hypofibrinogenemia\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eStrongly supported as a major complication of HELLP/AFLP overlap [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eSepsis-associated hepatic dysfunction\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFever, systemic illness, thrombocytopenia\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eInfection screening, empirical antibiotics\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eInfectious etiologies excluded by negative serology; sepsis less likely primary cause [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eThrombotic thrombocytopenic purpura / atypical hemolytic uremic syndrome\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eHemolysis, thrombocytopenia, acute kidney injury\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eClinical overlap with HELLP\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eLess likely due to postpartum recovery and absence of neurologic involvement [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eViral hepatitis\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJaundice, acute liver injury\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eViral hepatitis markers negative\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eExcluded through serological evaluation [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eAutoimmune or drug-induced hepatitis\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAcute liver dysfunction possible\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eNo autoimmune history or hepatotoxic drug exposure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eUnlikely given clinical context and imaging findings\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eBiliary obstruction / structural liver disease\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eJaundice could suggest obstruction\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eUltrasound showed no biliary obstruction or hepatic mass\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eExcluded through abdominal imaging\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e\n\u003ch3\u003eKey Message for Readers\u003c/h3\u003e\n\u003cp\u003e \u003cem\u003eThe final diagnosis of pregnancy-related acute liver failure with HELLP syndrome\u0026ndash;AFLP overlap and disseminated intravascular coagulation was made after exclusion of infectious, thrombotic microangiopathic, and structural hepatic\u003c/em\u003e \u003c/p\u003e\n\u003ch3\u003eTREATMENT\u003c/h3\u003e\n\u003cp\u003eManagement was initiated immediately after admission with the primary goals of stabilizing maternal physiology, correcting life-threatening coagulopathy, preventing progression of multiorgan failure, and planning timely delivery. A multidisciplinary team involving obstetrics, critical care, hepatology, transfusion medicine, and neonatology coordinated the therapeutic strategy, as pregnancy-related acute liver failure associated with hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy requires urgent supportive care and definitive delivery(1,2).\u003c/p\u003e \u003cp\u003eThe patient required admission to the intensive care unit for multiorgan dysfunction, where she received massive transfusion support, N-acetylcysteine therapy, empirical broad-spectrum antibiotics, and close multidisciplinary monitoring. Definitive management consisted of urgent delivery following partial correction of coagulopathy. Intensive care management interventions are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab4\" class=\"InternalRef\"\u003e4\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab4\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 4\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003e\u003cb\u003eSummary of intensive care treatments and transfusion support\u003c/b\u003e This table summarizes the major pharmacological, supportive, and transfusion-based interventions provided during the critical care course.\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"4\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTreatment category\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eIntervention provided\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eClinical indication\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eOutcome/response\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCritical care monitoring\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAdmission to medical intensive care unit with continuous hemodynamic and respiratory monitoring\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eMultiorgan dysfunction with acute liver failure and coagulopathy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eAllowed early detection of hemorrhage, pulmonary edema, and renal deterioration\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eRed blood cell transfusion\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePacked red blood cells (multiple units)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eSevere anemia (hemoglobin\u0026thinsp;~\u0026thinsp;5.7 g/dL) and suspected hemolysis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eImproved oxygen-carrying capacity and hemodynamic stability\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003ePlasma replacement therapy\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFresh frozen plasma (\u0026gt;\u0026thinsp;10 units)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCorrection of markedly prolonged international normalized ratio (\u0026gt;\u0026thinsp;2.0)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eGradual improvement in coagulation parameters\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eFibrinogen replacement\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCryoprecipitate (\u0026gt;\u0026thinsp;20 units)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eHypofibrinogenemia (~\u0026thinsp;123 mg/dL) consistent with disseminated intravascular coagulation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eReduced bleeding risk and supported stabilization prior to delivery\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eCoagulation support\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eIntravenous vitamin K\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eSupport of hepatic clotting factor synthesis\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eAdjunctive improvement in coagulation profile\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eHepatic supportive therapy\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eN-acetylcysteine infusion followed by oral continuation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eSupportive management of acute liver failure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eAssociated with biochemical improvement in bilirubin levels\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eAntimicrobial therapy\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eBroad-spectrum antibiotics (piperacillin\u0026ndash;tazobactam\u0026thinsp;+\u0026thinsp;metronidazole)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePersistent fever and risk of sepsis complicating liver failure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003ePrevented secondary infection while infectious causes were excluded\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eObstetric intervention\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eVacuum-assisted vaginal birth after previous cesarean delivery (Kiwi\u0026reg; OmniCup, Clinical Innovations, USA)\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eFetal compromise and worsening maternal condition\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eDefinitive management enabling disease stabilization postpartum\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003ePostpartum hemorrhage management\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eUterotonic therapy, vaginal packing, additional transfusion support\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDelivery complicated by postpartum hemorrhage\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eControlled bleeding with improved maternal recovery\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eRespiratory supportive care\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eOxygen therapy and intensive monitoring\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003ePostpartum pulmonary edema with transient desaturation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eResolved with critical care support\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003e\u003cb\u003eStep-down and discharge therapy\u003c/b\u003e\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eOral supportive medications and outpatient follow-up planning\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eRecovery phase after stabilization\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eDischarged in stable condition with improving liver and renal function\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e\n\u003ch3\u003eOUTCOME AND FOLLOW-UP\u003c/h3\u003e\n\u003cp\u003eFollowing delivery and continued multidisciplinary intensive care support, the patient demonstrated gradual clinical and biochemical recovery. Over the first week of hospitalization, hepatic dysfunction progressively improved, with a steady decline in total bilirubin levels and stabilization of liver synthetic function. Coagulation parameters normalized with cessation of transfusion requirements, and fibrinogen levels recovered after correction of disseminated intravascular coagulation. Renal function also improved, with serum creatinine decreasing from severe acute kidney injury range to near-baseline values, consistent with reversal of pregnancy-related multiorgan dysfunction.\u003c/p\u003e \u003cp\u003eRespiratory compromise observed in the immediate postpartum period, consistent with pulmonary edema, resolved with supportive oxygen therapy and careful fluid balance monitoring. Postpartum hemorrhage was successfully controlled with uterotonic therapy, vaginal packing, and additional transfusion support, with no recurrent bleeding episodes.\u003c/p\u003e \u003cp\u003eThe patient was stepped down from intensive care once hemodynamically stable and transferred to the general obstetric ward for continued monitoring. At the time of discharge, she was clinically stable, ambulatory, tolerating oral intake, and independent in daily activities. She was discharged on oral supportive therapy including ursodeoxycholic acid, lactulose, and antioxidant supplementation, with advice for rest and gradual return to routine activity.\u003c/p\u003e \u003cp\u003eFollow-up was arranged with obstetrics, hepatology, and nephrology services. Surveillance included repeat liver function testing, coagulation profile, renal function assessment, and blood pressure monitoring within 2\u0026ndash;4 weeks after discharge, consistent with recommended postpartum follow-up for hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy recovery(1,2). Long-term counseling was provided regarding recurrence risk in future pregnancies and the importance of early antenatal surveillance.\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003ePregnancy-related acute liver failure represents one of the most severe obstetric emergencies, with rapid progression to multiorgan dysfunction if diagnosis and delivery are delayed. The most important pregnancy-specific hepatic disorders causing acute liver failure in the third trimester include hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy. Both conditions share overlapping clinical manifestations such as jaundice, thrombocytopenia, coagulopathy, and renal dysfunction, often making early differentiation difficult in emergency and critical care settings(1,2).\u003c/p\u003e \u003cp\u003eThis case describes a woman presenting at \u003cb\u003e36 weeks of gestation\u003c/b\u003e with rapidly progressive acute liver failure manifested by jaundice, profound coagulopathy, thrombocytopenia, acute kidney injury, and systemic instability necessitating intensive care admission. Initial evaluation excluded infectious and structural hepatic causes, and pregnancy-related liver failure was considered most likely. The clinical course was complicated by disseminated intravascular coagulation, high transfusion requirements, and evolving maternal\u0026ndash;fetal compromise. Management focused on aggressive supportive critical care, close multidisciplinary coordination, and timely delivery, after which the patient demonstrated prompt clinical stabilization and progressive biochemical recovery.\u003c/p\u003e \u003cp\u003eEstablishing a definitive diagnosis was challenging because pregnancy-specific liver disorders share substantial clinical and biochemical overlap, particularly in critically ill patients. Features such as jaundice, thrombocytopenia, coagulopathy, and renal dysfunction can be seen in HELLP syndrome, acute fatty liver of pregnancy, sepsis, and thrombotic microangiopathies. In this case, the severity of liver dysfunction and coagulopathy raised concern for acute fatty liver of pregnancy; however, incomplete fulfillment of Swansea criteria, absence of hyperammonemia or severe hypoglycemia, and rapid improvement after delivery favored a HELLP-spectrum disorder. The urgency of maternal stabilization and delivery further limited reliance on exhaustive diagnostic testing, underscoring the pragmatic challenges of diagnosis in obstetric critical care.\u003c/p\u003e\n\u003ch3\u003eBrief review of similar published cases\u003c/h3\u003e\n\u003cp\u003eSeveral published reports describe acute liver failure in pregnancy complicated by disseminated intravascular coagulation and acute kidney injury requiring intensive care management. Knight and colleagues reported that acute fatty liver of pregnancy frequently presents with coagulopathy and renal dysfunction, with maternal outcomes improving significantly with early diagnosis and delivery(2). Ch\u0026rsquo;ng et al. emphasized the diagnostic challenge of pregnancy-related liver dysfunction and the importance of distinguishing pregnancy-specific syndromes from viral hepatitis and thrombotic microangiopathies(1). Case-based evidence also demonstrates that intensive care support and transfusion-based correction of coagulopathy are critical determinants of survival in severe hemolysis, elevated liver enzymes, and low platelets syndrome(6). Comparison with previously published cases is summarized in Table\u0026nbsp;\u003cspan refid=\"Tab5\" class=\"InternalRef\"\u003e5\u003c/span\u003e\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab5\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 5\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eSummary of published pregnancy-related acute liver failure cases with critical care involvement\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"5\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c3\" colnum=\"3\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c4\" colnum=\"4\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c5\" colnum=\"5\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eStudy\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eCondition\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c3\"\u003e \u003cp\u003eMajor complications\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c4\"\u003e \u003cp\u003eKey management\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c5\"\u003e \u003cp\u003eOutcome\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eKnight et al. (2008) [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eAcute fatty liver of pregnancy\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eCoagulopathy, renal failure\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eEarly delivery\u0026thinsp;+\u0026thinsp;ICU support\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eImproved maternal survival\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCh\u0026rsquo;ng et al. (2002) [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePregnancy liver dysfunction spectrum\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDiagnostic overlap with HELLP\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eMultidisciplinary evaluation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eBetter outcomes with early recognition\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSibai (2004) [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eHELLP syndrome\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDIC, hepatic rupture risk\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eDelivery\u0026thinsp;+\u0026thinsp;supportive transfusion\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eICU often required in severe cases\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePresent case\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eHELLP/AFLP overlap\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c3\"\u003e \u003cp\u003eDIC, AKI, pulmonary edema, PPH\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c4\"\u003e \u003cp\u003eMassive transfusion\u0026thinsp;+\u0026thinsp;ICU\u0026thinsp;+\u0026thinsp;assisted delivery\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c5\"\u003e \u003cp\u003eFull maternal recovery\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e\n\u003ch3\u003eClinical lessons and conclusions\u003c/h3\u003e\n\u003cp\u003eThis case highlights several important learning points. First, pregnancy-related acute liver failure should be suspected in third-trimester patients presenting with jaundice, thrombocytopenia, renal dysfunction, and severe coagulopathy. Second, overlap between hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy is common, and management should prioritize supportive intensive care stabilization and urgent delivery rather than delayed diagnostic separation. Third, aggressive correction of disseminated intravascular coagulation and postpartum critical care monitoring are essential to prevent fatal maternal complications.\u003c/p\u003e \u003cp\u003eAlthough causality between assisted delivery and recovery cannot be inferred, the favorable outcome in this patient was most likely attributable to timely multidisciplinary intensive care intervention, transfusion support, and definitive delivery.\u003c/p\u003e \u003cdiv id=\"Sec11\" class=\"Section2\"\u003e \u003ch2\u003eLEARNING POINTS / TAKE HOME MESSAGES\u003c/h2\u003e \u003cp\u003e \u003cul\u003e \u003cli\u003e \u003cp\u003ePregnancy-related acute liver failure should be promptly suspected in third-trimester patients presenting with jaundice, thrombocytopenia, severe coagulopathy, and acute kidney injury, as rapid progression to multiorgan dysfunction is common.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eSignificant clinical overlap exists between hemolysis, elevated liver enzymes, and low platelets syndrome and acute fatty liver of pregnancy: management should prioritize urgent stabilization and timely delivery rather then delayed diagnostic separation.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eEarly admission to intensive care with aggressive correction of disseminated intravascular coagulation using fresh frozen plasma and cryoprecipitates is essential to prevent catastrophic hemorrhagic complications.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003eDelivery remains the definitive treatment for pregnancy-specific acute liver failure syndromes, and multidisciplinary coordination between obstetrics, critical care, hepatology, and transfusion services improves maternal outcomes.\u003c/p\u003e \u003c/li\u003e \u003cli\u003e \u003cp\u003ePostpartum complications such as hemorrhage, pulmonary edema, and persistent organ dysfunction require continued critical care surveillance even after delivery to ensure full recovery.\u003c/p\u003e \u003c/li\u003e \u003c/ul\u003e \u003c/p\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e \u003cstrong\u003eEthics approval and consent to participate:\u003c/strong\u003e \u003cp\u003eEthics approval was not required for this case report as per institutional policy. Written informed consent was obtained from the patient.\u003c/p\u003e \u003cp\u003e \u003cstrong\u003eConsent for publication\u003c/strong\u003e \u003cp\u003eInformed consent was obtained from the patient for publication of this case report and any accompanying images or clinical data.\u003c/p\u003e \u003ch2\u003eCompeting interests\u003c/h2\u003e \u003cp\u003eThe author declares that there are no competing interests.\u003c/p\u003e \u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eThis research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eMN conceptualized the case report, participated in patient care, conducted the literature review, and drafted the initial manuscript. PR contributed to clinical supervision, critical revision of the manuscript for important intellectual content, and validation of clinical accuracy. Both authors read and approved the final manuscript.\u003c/p\u003e\u003ch2\u003eAcknowledgement\u003c/h2\u003e\u003cp\u003eThe authors would like to acknowledge the multidisciplinary intensive care, obstetrics, hepatology, transfusion medicine, and nursing teams at Narayana Health City, Bengaluru, for their coordinated clinical support in the management of this patient. We also thank the patient and her family for providing informed consent for publication of this case report.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eAll relevant clinical data supporting the findings of this case report are included within the manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eAnitha G, Shivamurthy G, Krishnappa TK, Chethan R. Maternal and Fetal Outcome in HELLP Syndrome: An Observational Study. J South Asian Fed Obstet Gynaecol. 2020;12(3):122\u0026ndash;32.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMorrison MA, Chung Y, Heneghan MA. Managing hepatic complications of pregnancy: practical strategies for clinicians. BMJ Open Gastroenterol. 2022;9(1):e000624.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eNelson DB, Byrne JJ, Cunningham FG. Acute Fatty Liver of Pregnancy. Clin Obstet Gynecol. 2020;63(1):152\u0026ndash;64.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eAnand AC, Nandi B, Acharya SK, Arora A, Babu S, Batra Y, et al. Indian National Association for the Study of Liver Consensus Statement on Acute Liver Failure (Part-2): Management of Acute Liver Failure. J Clin Exp Hepatol. 2020;10(5):477\u0026ndash;517.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSeetharam A. Intensive Care Management of Acute Liver Failure: Considerations While Awaiting Liver Transplantation. J Clin Transl Hepatol. 2019;7(X):1\u0026ndash;8.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eLevi M, Toh CH, Thachil J, Watson HG. Guidelines for the diagnosis and management of disseminated intravascular coagulation. Br J Haematol. 2009;145(1):24\u0026ndash;33.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePATIENT\u0026rsquo;S PERSPECTIVE.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eI remember. feeling unwell for several days before coming to the hospital. I had fever, extreme weakness, and my eyes and skin became yellow. I was very worried because I could not feel my baby moving normally and I felt something was seriously wrong.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eWhen I. arrived at the emergency department, I was frightened after hearing that my blood levels were very low and that my liver and kidneys were affected. I was transferred to the intensive care unit, where I received blood transfusions and many medications. The doctors explained that my condition was serious and that close monitoring was needed to protect both me and my baby.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eA few days later. I went into labor, and the delivery was difficult. After delivery, I experienced heavy bleeding and breathing difficulty, which was very scary for me. The critical care team supported me throughout this period, and I gradually started improving.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOver the following days. I felt stronger, and my jaundice reduced. I was relieved to recover and to be able to return home. This experience made me realize the importance of seeking urgent medical care when serious symptoms occur during pregnancy.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"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":"","lastPublishedDoi":"10.21203/rs.3.rs-8934627/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8934627/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003ePregnancy-related acute liver failure is an uncommon but life-threatening obstetric emergency that may overlap with HELLP syndrome and disseminated intravascular coagulation. We describe a patient presenting in presenting at 36 weeks of gestation with fever, jaundice, severe anemia, thrombocytopenia, markedly elevated bilirubin, acute kidney injury, and profound coagulopathy. Imaging revealed fetal growth restriction with oligohydramnios and mild ascites. A diagnosis of HELLP syndrome with acute liver failure and multiorgan dysfunction was considered. The patient required intensive critical care management including massive transfusion support, N-acetylcysteine therapy, correction of coagulopathy, and continuous multidisciplinary monitoring. She underwent vacuum-assisted vaginal birth after previous cesarean delivery, complicated by postpartum hemorrhage and transient respiratory compromise. With aggressive ICU-based supportive care, hepatic and renal function gradually improved, and she was discharged in stable condition. This case highlights the importance of early recognition and critical care intervention in pregnancy-associated acute liver failure.\u003c/p\u003e","manuscriptTitle":"Pregnancy-related acute liver failure with HELLP–AFLP overlap requiring intensive care","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-24 13:18:25","doi":"10.21203/rs.3.rs-8934627/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision 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