Thrombotic microangiopathy complicate with the severe sudden-onset liver ruptures in a pre-eclampsia patient after the caesarean section: a case report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Thrombotic microangiopathy complicate with the severe sudden-onset liver ruptures in a pre-eclampsia patient after the caesarean section: a case report Zhenzhen Chen, Yuqing Wang, Shibing Zhao, Kaixuan Niu, Huaxue Wang This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8374429/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 12 You are reading this latest preprint version Abstract Background The sudden-onset life-threatening liver rupture is a rare complication of pregnancy-associated thrombotic microangiopathy. Patients with both HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome and atypical haemolytic uraemic syndrome (aHUS) are very rare, who are always in a significantly urgent situation and hard to treat. We herein report a case of successfully treating a patient who experienced a severe liver rupture with HELLP syndrome and aHUS after the caesarean section. Case presentation: A 37-year-old woman had a sudden-onset hypertension and proteinuria; thus, she was diagnosed as pre-eclampsia and then a caesarean section was performed. After that, she had the continuous hemolysis, significantly elevated liver enzymes and low platelet count with oliguria and increased creatinine. During the treatment, we organized the multi-disciplinary treatment twice to make decisions of an intervention and an exploratory laparotomy. Combined with the other active treatment, blood transfusion, plasma exchange, and continuous renal replacement therapy, the patient finally survived and returned to a healthy state. Conclusions Physicians should pay special attention to the possibility of a severe liver rupture in pre-eclampsia and thrombotic microangiopathy patients during pregnancy or post-partum. The active life support and the good multi-disciplinary treatment help a lot for survival. pre-eclampsia thrombotic microangiopathy HELLP syndrome atypical haemolytic uraemic syndrome Figures Figure 1 Figure 2 Background Pre-eclampsia is a complex multisystem disease characterized by sudden-onset hypertension and other organ dysfunction. The pathology of pre-eclampsia may lead to severe pregnancy or postpartum thrombotic microangiopathy (TMA), which is a rare syndrome caused by endothelial cell injuries, mainly complicating kidney injuries. The severe liver rupture is rarely complicated with TMA. It is significantly difficult to treat the patients with both HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome and atypical haemolytic uraemic syndrome (aHUS). We herein report a case of successfully treating a pre-eclampsia patient who experienced a severe liver rupture after a caesarean section, lately diagnosed as HELLP syndrome and aHUS. Case presentation A 37-year-old woman was admitted to this hospital because of oliguria, abdominal pain, anemia, thrombocytopenia, liver dysfunction and renal dysfunction after a caesarean section. The patient had been in her healthy pregnant state until two weeks before the current presentation, when she had the blood pressure as 150/100 mmHg and proteinuria detected by one routine prenatal appointment, however, with no symptoms. Two days before the current presentation, the patient was considered as the severe pre-eclampsia because of the increasing blood pressure up to 170/101 mmHg with the high alanine aminotransferase (235 U/liter) and the aspartate aminotransferase (320 U/liter); thus, she had a caesarean section in the local hospital. The next two days, the woman had the oliguria with dark urine, short of breath and the abdominal pain with nausea and vomiting. On evaluation, the low hemoglobin and platelet with the high alanine aminotransferase, alanine aminotransferase and creatinine were shown in Table 1 in detail. The data revealed anemia, thrombocytopenia, the liver dysfunction and the kidney dysfunction. For the further treatment, the woman was referred to our hospital. The first day of our hospital, the temperature was 36.5°C, the pulse 116 beats per minute, the blood pressure 113/80 mmHg, the respiratory rate 26 breaths per minute, and the oxygen saturation was 95%. The patient showed a pale appearance and coarse crackles in the biliteral lower lung fields. And she had the abdominal distension, tenderness and rebound tenderness, however, the abdominal incision was clean. Ultrasound imaging revealed the perihepatic, perisplenic and pelvic fluid collections with the air-fluid level up to 98 mm. Computed tomography (CT) of the abdomen showed that ascites and pelvic fluid collections (Figure 1). But no evidence of visceral hemorrhage was found. We indwelled a pelvic drain and observed an output of pale yellow fluid. Initially, the patient was diagnosed as HELLP syndrome, severe hemolytic anemia, thrombocytopenia, multiple organ dysfunction syndrome (MODS) (kidney, liver, respiratory). Dexamethasone was immediately administered via intravenous injection (30 mg). We used therapeutic plasma exchange and continuous renal replacement therapy (CRRT). After the transfusion of red blood cells (6 U), plasma (800 mL), and cryoprecipitate (20 U), the hemoglobin was still decreasing without the improved platelet count. And the blood pressure was also decreasing. Those hinted the continuous bleeding. CT imaging revealed a heterogeneous hepatic density, accompanied by multiple hypodense lesions and massive hemoperitoneum in abdominal and pelvic cavity (Figure 2). After a multi-disciplinary treatment, we considered an ongoing liver hemorrhage and planned to control bleeding through an interventional procedure. Intraoperative findings revealed no evidence of vascular rupture or contrast agent extravasation in the detected main blood vessels. After the intraoperation, we observed that the hemoglobin and platelets were continuously decreasing even after she received the transfusion of red blood cells (6.5 U), platelets (3 U) and plasma (800 mL). To clarify the bleeding reason, we decided to perform an exploratory laparotomy after another multi-disciplinary treatment. It was found that the massive hemorrhage from ruptures in the left lateral lobe and the capsular ruptures of segments S7/S8 of the liver, with tear lengths of approximately 12 cm and 15 cm, respectively. No active bleeding was observed at the uterine incision site. The operation was very difficult. During the operation, the hemoglobin, blood glucose and lactic acid maintained the low level in that case of the continuous transfusion of frozen plasma. The postoperative arterial blood gas analysis revealed a lactate level of 11.4 mmol/L, glucose of 1.9 mmol/L, and total hemoglobin below 30 g/L. The first day after the operation, the patient remained anuria and edema; thus, we continuously performed CRRT. The laboratory data showed the hemoglobin and platelet count still had the trend to decrease, revealing the hemolysis. We performed the transfusion of red blood cells (24.5 U), platelet (2 U), cryoprecipitate (40 U) and fresh frozen plasma (1400 mL). The abdominal drain fluid is 1700 mL bloody fluid and the pelvic drain fluid is 1200 mL bloody fluid. Hemodynamic management targeted a mean arterial pressure of 70-75 mmHg, supported by norepinephrine at a maximum dose of 0.5 μg/kg/min, which was subsequently tapered. Considering the high liver enzymes, increased bilirubin, abnormal coagulation indexes, and continuous low blood glucose, an intravenous bolus of concentrated glucose and 10 mg of dexamethasone were administered. Moreover, the reduction on the white cells and lymphocytes hinted her infectious state. For that, we used imipenem and vancomycin for the anti-infection therapy. Fortunately, the second day after the operation, the drain fluid is 2300 mL blood fluid in total; thus, we performed the plasma transfusion. The laboratory tests showed that the hemoglobin and platelet increased, total bilirubin decreased, and all of liver function indexes turned good. Considering continuous anuria, hemolytic anemia and increasing lactatedehydrogenase (LDH), the laboratory tests detecting immune system functions were administered. The results were shown on Table 2. We diagnosed the patient as aHUS, not thrombotic thrombocytopenic purpura (TTP) and Shiga toxin E. coli hemolytic uremic syndrome (STEC-HUS). In the following treatment, we performed the therapeutic plasma exchange four times, 3000 mL per time, and high-dose intravenous immunoglobulin five days, 20 g per day. The fourth day after the operation, considering that the patient kept alert, we performed the high-flow nasal oxygen instead of intubation. We continuously performed the plasma transfusion (400 mL per day). However, the white cell count was up to 30.98×10 9 /L, and Burkholderia cepacian and Staphylococcus epidermidis were isolated from the sputum culture and the blood culture, respectively, which revealed the catheter-related blood stream infection. Thus, we exchanged the central venous catheter and dialysis catheter, with subsequent adjustment of the antimicrobial regimen to cefpirome combined with sulfamethoxazole-trimethoprim. On post-operative day 14, the urine output increased to 1500 mL, so we stopped CRRT. Considering the patient maintained the stable condition, she was transferred to the Nephrology Department for the continuous care. On post-operative day 30, the patient was discharged. For her net three-month follow-up consultation, the hemoglobin, platelet and creatinine returned to a healthy state. Discussion We herein report a case of successfully treating aHUS and HELLP syndrome in a patient with a life-threatening liver rupture. The most uncommon disorder of the patient is the sudden-onset life-threatening liver rupture-derived massive hemorrhage and continuous severe hemolytic anemia, which are the most challengeable to treat. TMA syndrome is a pattern of extraordinarily complicated disorders caused by endothelial cell injuries, clinically characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and ischemic organ injury 1 . Kidney is the most injured organ. In the case, it is rare that the patient’s liver rupture caused massive hemorrhage. Liver rupture complicated with HELLP syndrome is mainly caused by subcapsular liver hematoma 2 . The hypertension-induced vasospasm and endothelial injuries may lead to the liver rupture 3 . When hepatic ruptures cause the low blood pressure and severe hemolysis, the first choice is to stabilize blood pressure through blood transfusion and stop bleeding through intervention or exploratory laparotomy. HELLP syndrome is a subtype of TMA affecting mainly the liver and more rarely the kidney. In the case, pregnancy TMA in the patient was characterized by the continuous hemolysis, liver failure, coagulopathy dysfunction, and kidney injury. The high creatinine is hard to be explained by HELLP syndrome. TMA can be divided into HUS, TTP, and other factor-induced TMA. The typical HUS is mainly caused by the Shiga toxin. And other types of HUS were recognized as aHUS. Pregnancy and postpartum have been viewed as high-risk factors for TMA 4 . The patient in our case had the preeclampsia during her pregnancy, which is one of the commonest causes of aHUS for pregnant women 4 . The symptoms of aHUS and HELLP syndrome are similar, which are part of TMA with different injured organs and severity. HELLP syndrome is rarely life-threatening if patients are treated early while aHUS is continuous and more severe. In the case, the patient maintained the low hemoglobin, platelet count and the elevated creatinine, liver enzymes and bilirubin for one month after the caesarean section. And until her discharge, she had anemia. Moreover, the immune function tests showed the heterozygous CFI, CF8, C1R, C3, CFP; thus, there is no evidence to exclude aHUS. The renal biopsy can be helpful to confirm the diagnosis. Eculizumab, a monoclonal antibody inhibiting complement protein C5, has been proved to be efficient to treat life-threatening aHUS and improve the long-term clinical outcomes 5 . In the case, the data of blood tests, liver function tests, kidney function tests maintained normal 2 weeks after discharge. Considering the expensive cost, the patient refuse to receive eculizumab treatment. However, we suggest that aHUS patients should receive eculizumab treatment to improve the long-term survival. Conclusion Physicians should pay special attention to the possibility of the severe liver rupture in pre-eclampsia and thrombotic microangiopathy patients during pregnancy or post-partum. The active life support and the good multi-disciplinary treatment help a lot for treatment. Abbreviations TMA: thrombotic microangiopathy; HELLP: hemolysis, elevated liver enzymes, and low platelets; aHUS: atypical haemolytic uraemic syndrome; CT: computed tomography; MODS: multiple organ dysfunction syndrome; CRRT: continuous renal replacement therapy; LDH: lactatedehydrogenase. TTP: thrombotic thrombocytopenic purpura; STEC-HUS: Shiga toxin E. coli hemolytic uremic syndrome; MAHA: microangiopathic hemolytic anemia Declarations Consent to participate Informed consent was obtained from the patient for publication Informed consent was obtained from the patient for participation in this study. Availability of data and materials Please contact the corresponding author for data requests. Competing interests The authors declare that they have no competing interests. Funding This work was supported by Clinical Research and Translation Program of Anhui Province [grant number 202304295107020073]. Authors’ contributions ZC, YW, SZ, KN and HW provided medicine for the patient and edited the draft of the manuscript. HW provided medicine for the patient and reviewed the manuscript as a corresponding author. All authors read and approved the final manuscript. Acknowledgements Clinical trial number: not applicable Ethical Approval and accordance The protocol was approved by The Clinical Medical Research Ethics Committee of the First Affiliated Hospital of Bengbu Medical University in accordance with the ICH GCP and CHINA GCP. References James NG, Carla MN. Syndromes of thrombotic microangiopathy. N Engl J Med. 2014;371(7):654-66. S Ainslie M, Rebecca S, Kelle H, Sunette C. Preeclampsia and HELLP syndrome complicated by subcapsular liver hematoma and rupture. CMAJ. 2023;195(45):E1543-E1545. McCormick PA, Higgins M, McCormick CA, Nolan N, Docherty JR. J Matern Fetal Neonatal Med. 2022;35(25):7942-7947. Fadi F, Marie S, François P, Miquel B, Paul C, et al. Management of thrombotic microangiopathy in pregnancy and postpartum: report from an international working group. Blood. 2020;136(19):2103-2117. Yahiya YS. Ravulizumab: A Review in Atypical Haemolytic Uraemic Syndrome. Drugs. 2021;81(5):587-594. Tables Tables 1 and 2 are available in the Supplementary Files section. Additional Declarations No competing interests reported. Supplementary Files Table1.docx Table2.docx CAREchecklistEnglish2013.pdf12.20.pdf Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 13 Mar, 2026 Reviews received at journal 12 Mar, 2026 Reviewers agreed at journal 22 Feb, 2026 Reviews received at journal 19 Feb, 2026 Reviews received at journal 15 Feb, 2026 Reviewers agreed at journal 11 Feb, 2026 Reviewers agreed at journal 09 Feb, 2026 Reviewers invited by journal 02 Feb, 2026 Editor invited by journal 22 Jan, 2026 Editor assigned by journal 22 Jan, 2026 Submission checks completed at journal 22 Jan, 2026 First submitted to journal 22 Jan, 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. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. 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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-8374429","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":584147164,"identity":"ad4f3f97-e281-47ba-82af-26dda94b813f","order_by":0,"name":"Zhenzhen Chen","email":"","orcid":"","institution":"the First Affiliated Hospital of Bengbu Medical University","correspondingAuthor":false,"prefix":"","firstName":"Zhenzhen","middleName":"","lastName":"Chen","suffix":""},{"id":584147165,"identity":"69915b10-efe2-41fa-85a4-e32efad1ffc6","order_by":1,"name":"Yuqing Wang","email":"","orcid":"","institution":"The Second Affiliated Hospital, Army Medical University","correspondingAuthor":false,"prefix":"","firstName":"Yuqing","middleName":"","lastName":"Wang","suffix":""},{"id":584147166,"identity":"8650b84e-62e2-4ac9-8295-c5e598087533","order_by":2,"name":"Shibing Zhao","email":"","orcid":"","institution":"the First Affiliated Hospital of Bengbu Medical University","correspondingAuthor":false,"prefix":"","firstName":"Shibing","middleName":"","lastName":"Zhao","suffix":""},{"id":584147167,"identity":"4504e6b3-8f22-4b69-bd69-b1c75e02f08b","order_by":3,"name":"Kaixuan Niu","email":"","orcid":"","institution":"the First Affiliated Hospital of Bengbu Medical University","correspondingAuthor":false,"prefix":"","firstName":"Kaixuan","middleName":"","lastName":"Niu","suffix":""},{"id":584147168,"identity":"b8522241-e6ae-4479-9ff7-406bf8853ba1","order_by":4,"name":"Huaxue Wang","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAA0UlEQVRIiWNgGAWjYBACAygtx8bM2PggoaKGeC3G/OzMhw0enDlGvJbEmf1saZIPW5gJazGXSH4mzVNxmHHDYR6zisQGNgb+9u4EvFosZ6QZG/OcOcxsANRyI3GHDIPEmbMb8DvsRoLhY96222wQLWfYGAwkcglpSf9wmPffbR6QloLENmZitOQAbWm4LSHZzJbGQJyWM2+KDecc+2/Az8x8WCLhzDEewn45nr5N4k1NWn0b/8HGjz8qauT423vxa8EAPKQpHwWjYBSMglGAFQAA15NJlYbUBlIAAAAASUVORK5CYII=","orcid":"","institution":"the First Affiliated Hospital of Bengbu Medical University","correspondingAuthor":true,"prefix":"","firstName":"Huaxue","middleName":"","lastName":"Wang","suffix":""}],"badges":[],"createdAt":"2025-12-16 09:39:44","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8374429/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8374429/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":101826865,"identity":"9c4b2f0f-1ad8-48f7-a388-e4640bfe3273","added_by":"auto","created_at":"2026-02-04 05:18:55","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":210229,"visible":true,"origin":"","legend":"\u003cp\u003eAbdominal CT imaging after hospitalization.\u003c/p\u003e\n\u003cp\u003eAn abdominal CT was administered after the patient was referred to our hospital. The imaging demonstrated the diffusely decreased attenuation throughout the liver parenchyma (the white row) without the evidence of focal lesions.(A,B,C).\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-8374429/v1/944f3a8eabb33eef0d106617.png"},{"id":101943163,"identity":"7d48f658-dd9c-490b-b16a-fbe2eaaec938","added_by":"auto","created_at":"2026-02-05 09:40:51","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":359604,"visible":true,"origin":"","legend":"\u003cp\u003eAbdominal CT imaging before the interventional procedure.\u003c/p\u003e\n\u003cp\u003eThe abdominal CT imaging showed intraparenchymal and subcapsular hemorrhage within the liver (the red row) both in arterial and venous phase in the axial plane (Fig 2A, B, and C) and in the coronal plane (Fig 2D and E).\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-8374429/v1/c86e7e664db7f6e672d60972.png"},{"id":101944618,"identity":"f92e86ac-3420-4c39-b8e6-5ab7b0e15c0d","added_by":"auto","created_at":"2026-02-05 09:53:09","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1050899,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8374429/v1/2ed97a8c-4449-4708-87d7-55f3f6a70419.pdf"},{"id":101826867,"identity":"7310aaf3-7a22-4ee6-9e44-5a132e8559ea","added_by":"auto","created_at":"2026-02-04 05:18:55","extension":"docx","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":19443,"visible":true,"origin":"","legend":"","description":"","filename":"Table1.docx","url":"https://assets-eu.researchsquare.com/files/rs-8374429/v1/8d3287108481de82d228f4cb.docx"},{"id":101826868,"identity":"705ac726-e777-4ddd-8a32-04705771ed67","added_by":"auto","created_at":"2026-02-04 05:18:55","extension":"docx","order_by":2,"title":"","display":"","copyAsset":false,"role":"supplement","size":17355,"visible":true,"origin":"","legend":"","description":"","filename":"Table2.docx","url":"https://assets-eu.researchsquare.com/files/rs-8374429/v1/a47c385ff6fb197e89e250e9.docx"},{"id":101880816,"identity":"0dd732bc-fa45-4e41-9e6a-2b8f58cab62a","added_by":"auto","created_at":"2026-02-04 15:06:39","extension":"pdf","order_by":3,"title":"","display":"","copyAsset":false,"role":"supplement","size":789078,"visible":true,"origin":"","legend":"","description":"","filename":"CAREchecklistEnglish2013.pdf12.20.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8374429/v1/2353979b6c9cfb52d41217bd.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Thrombotic microangiopathy complicate with the severe sudden-onset liver ruptures in a pre-eclampsia patient after the caesarean section: a case report","fulltext":[{"header":"Background","content":"\u003cp\u003ePre-eclampsia is a complex multisystem disease characterized by sudden-onset hypertension and other organ dysfunction. The pathology of pre-eclampsia may lead to severe pregnancy or postpartum thrombotic microangiopathy (TMA), which is a rare syndrome caused by endothelial cell injuries, mainly complicating kidney injuries. The severe liver rupture is rarely complicated with TMA. It is significantly difficult to treat the patients with both HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome and atypical haemolytic uraemic syndrome (aHUS). We herein report a case of successfully treating a pre-eclampsia patient who experienced a severe liver rupture after a caesarean section, lately diagnosed as HELLP syndrome and aHUS.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 37-year-old woman was admitted to this hospital because of oliguria, abdominal pain, anemia, thrombocytopenia, liver dysfunction and renal dysfunction after a caesarean section.\u003c/p\u003e\n\u003cp\u003eThe patient had been in her healthy pregnant state until two weeks before the current presentation, when she had the blood pressure as 150/100 mmHg and proteinuria detected by one routine prenatal appointment, however, with no symptoms. Two days before the current presentation, the patient was considered as the severe pre-eclampsia because of the increasing blood pressure up to 170/101 mmHg with the high alanine aminotransferase (235 U/liter) and the aspartate aminotransferase (320 U/liter); thus, she had a caesarean section in the local hospital. The next two days, the woman had the oliguria with dark urine, short of breath and the abdominal pain with nausea and vomiting. On evaluation, the low hemoglobin and platelet with the high alanine aminotransferase, alanine aminotransferase and creatinine were shown in Table 1 in detail. The data revealed anemia, thrombocytopenia, the liver dysfunction and the kidney dysfunction. For the further treatment, the woman was referred to our hospital.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe first day of our hospital, the temperature was 36.5\u0026deg;C, the pulse 116 beats per minute, the blood pressure 113/80 mmHg, the respiratory rate 26 breaths per minute, and the oxygen saturation was 95%. The patient showed a pale appearance and coarse crackles in the biliteral lower lung fields. And she had the abdominal distension, tenderness and rebound tenderness, however, the abdominal incision was clean. Ultrasound imaging revealed the perihepatic, perisplenic and pelvic fluid collections with the air-fluid level up to 98 mm. Computed tomography (CT) of the abdomen showed that ascites and pelvic fluid collections (Figure 1).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eBut no evidence of visceral hemorrhage was found. We indwelled a pelvic drain and observed an output of pale yellow fluid. Initially, the patient was diagnosed as HELLP syndrome, severe hemolytic anemia, thrombocytopenia, multiple organ dysfunction syndrome (MODS) (kidney, liver, respiratory). Dexamethasone was immediately administered via intravenous injection (30 mg). We used therapeutic plasma exchange and continuous renal replacement therapy (CRRT). After the transfusion of red blood cells (6 U), plasma (800 mL), and cryoprecipitate (20 U), the hemoglobin was still decreasing without the improved platelet count. And the blood pressure was also decreasing. Those hinted the continuous bleeding. CT imaging revealed a heterogeneous hepatic density, accompanied by multiple hypodense lesions and massive hemoperitoneum in abdominal and pelvic cavity (Figure 2).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eAfter a multi-disciplinary treatment, we considered an ongoing liver hemorrhage and planned to control bleeding through an interventional procedure. Intraoperative findings revealed no evidence of vascular rupture or contrast agent extravasation in the detected main blood vessels. After the intraoperation, we observed that the hemoglobin and platelets were continuously decreasing even after she received the transfusion of red blood cells (6.5 U), platelets (3 U) and plasma (800 mL). To clarify the bleeding reason, we decided to perform an exploratory laparotomy after another multi-disciplinary treatment. It was found that the massive hemorrhage from ruptures in the left lateral lobe and the capsular ruptures of segments S7/S8 of the liver, with tear lengths of approximately 12 cm and 15 cm, respectively. No active bleeding was observed at the uterine incision site. The operation was very difficult. During the operation, the hemoglobin, blood glucose and lactic acid maintained the low level in that case of the continuous transfusion of frozen plasma. The postoperative arterial blood gas analysis revealed a lactate level of 11.4 mmol/L, glucose of 1.9 mmol/L, and total hemoglobin below 30 g/L.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eThe first day after the operation, the patient remained anuria and edema; thus, we continuously performed CRRT. The laboratory data showed the hemoglobin and platelet count still had the trend to decrease, revealing the hemolysis.\u0026nbsp;We performed the transfusion of red blood cells (24.5 U), platelet (2 U), cryoprecipitate (40 U) and fresh frozen plasma (1400 mL). The abdominal drain fluid is 1700 mL bloody fluid and the pelvic drain fluid is 1200 mL bloody fluid. Hemodynamic management targeted a mean arterial pressure of 70-75 mmHg, supported by norepinephrine at a maximum dose of 0.5 \u0026mu;g/kg/min, which was subsequently tapered. Considering the high liver enzymes, increased bilirubin, abnormal coagulation indexes, and continuous low blood glucose, an intravenous bolus of concentrated glucose and 10 mg of dexamethasone were administered. Moreover, the reduction on the white cells and lymphocytes hinted her infectious state. For that, we used imipenem and vancomycin for the anti-infection therapy.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eFortunately, the second day after the operation, the drain fluid is 2300 mL blood fluid in total; thus, we performed the plasma transfusion. The laboratory tests showed that the hemoglobin and platelet increased, total bilirubin decreased, and all of liver function indexes turned good. Considering continuous anuria, hemolytic anemia and increasing lactatedehydrogenase (LDH), the laboratory tests detecting immune system functions were administered. The results were shown on Table 2. We diagnosed the patient as aHUS, not thrombotic thrombocytopenic purpura (TTP) and Shiga toxin E. coli hemolytic uremic syndrome (STEC-HUS). In the following treatment, we performed the therapeutic plasma exchange four times, 3000 mL per time, and high-dose intravenous immunoglobulin five days, 20 g per day. The fourth day after the operation, considering that the patient kept alert, we performed the high-flow nasal oxygen instead of intubation. We continuously performed the plasma transfusion (400 mL per day). However, the white cell count was up to 30.98\u0026times;10\u003csup\u003e9\u003c/sup\u003e/L, and \u003cem\u003eBurkholderia cepacian\u003c/em\u003e and \u003cem\u003eStaphylococcus epidermidis\u003c/em\u003e were isolated from the sputum culture and the blood culture, respectively, which revealed the catheter-related blood stream infection. Thus, we exchanged the central venous catheter and dialysis catheter, with subsequent adjustment of the antimicrobial regimen to cefpirome combined with sulfamethoxazole-trimethoprim. On post-operative day 14, the urine output increased to 1500 mL, so we stopped CRRT. Considering the patient maintained the stable condition, she was transferred to the Nephrology Department for the continuous care. On post-operative day 30, the patient was discharged. For her net three-month follow-up consultation, the hemoglobin, platelet and creatinine returned to a healthy state.\u0026nbsp;\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eWe herein report a case of successfully treating aHUS and HELLP syndrome in a patient with a life-threatening liver rupture. The most uncommon disorder of the patient is the sudden-onset life-threatening liver rupture-derived massive hemorrhage and continuous severe hemolytic anemia, which are the most challengeable to treat.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eTMA syndrome is a pattern of extraordinarily complicated disorders caused by endothelial cell injuries, clinically characterized by microangiopathic hemolytic anemia (MAHA), thrombocytopenia, and ischemic organ injury\u003csup\u003e1\u003c/sup\u003e. Kidney is the most injured organ. In the case, it is rare that the patient\u0026rsquo;s liver rupture caused massive hemorrhage. Liver rupture complicated with HELLP syndrome is mainly caused by subcapsular liver hematoma\u003csup\u003e2\u003c/sup\u003e. The hypertension-induced vasospasm and endothelial injuries may lead to the liver rupture\u003csup\u003e3\u003c/sup\u003e. When hepatic ruptures cause the low blood pressure and severe hemolysis, the first choice is to stabilize blood pressure through blood transfusion and stop bleeding through\u0026nbsp;intervention or exploratory laparotomy.\u003c/p\u003e\n\u003cp\u003eHELLP syndrome is a subtype of TMA affecting mainly the liver and more rarely the kidney. In the case, pregnancy TMA in the patient was characterized by the continuous hemolysis, liver failure, coagulopathy dysfunction, and kidney injury. The high creatinine is hard to be explained by HELLP syndrome. TMA can be divided into HUS, TTP, and other factor-induced TMA. The typical HUS is mainly caused by the Shiga toxin. And other types of HUS were recognized as aHUS. Pregnancy and postpartum have been viewed as high-risk factors for TMA\u003csup\u003e4\u003c/sup\u003e. The patient in our case had the preeclampsia during her pregnancy, which is one of the commonest causes of aHUS for pregnant women\u003csup\u003e4\u003c/sup\u003e. The symptoms of aHUS and HELLP syndrome are similar, which are part of TMA with different injured organs and severity. HELLP syndrome is rarely life-threatening if patients are treated early while aHUS is continuous and more severe. In the case, the patient maintained the low hemoglobin, platelet count and the elevated creatinine, liver enzymes and bilirubin for one month after the caesarean section. And until her discharge, she had anemia. Moreover, the immune function tests showed the heterozygous CFI, CF8, C1R, C3, CFP; thus, there is no evidence to exclude aHUS. The renal biopsy can be helpful to confirm the diagnosis.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003eEculizumab, a monoclonal antibody inhibiting complement protein C5, has been proved to be efficient to treat life-threatening aHUS and improve the long-term clinical outcomes\u003csup\u003e5\u003c/sup\u003e. In the case, the data of blood tests, liver function tests, kidney function tests maintained normal 2 weeks after discharge. Considering the expensive cost, the patient refuse to receive eculizumab treatment. However, we suggest that aHUS patients should receive eculizumab treatment to improve the long-term survival.\u0026nbsp;\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003ePhysicians should pay special attention to the possibility of the severe liver rupture in pre-eclampsia and thrombotic microangiopathy patients during pregnancy or post-partum. The active life support and the good multi-disciplinary treatment help a lot for treatment.\u0026nbsp;\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003eTMA: thrombotic microangiopathy; HELLP: hemolysis, elevated liver enzymes, and low platelets; aHUS: atypical haemolytic uraemic syndrome; CT: computed tomography; MODS: multiple organ dysfunction syndrome; CRRT: continuous renal replacement therapy; LDH: lactatedehydrogenase. TTP: thrombotic thrombocytopenic purpura; STEC-HUS: Shiga toxin E. coli hemolytic uremic syndrome; MAHA: microangiopathic hemolytic anemia\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eConsent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eInformed consent was obtained from the patient for publication\u003c/p\u003e\n\u003cp\u003eInformed consent was obtained from the patient for participation in this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003ePlease contact the corresponding author for data requests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThis work was supported by Clinical Research and Translation Program of Anhui Province [grant number 202304295107020073].\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026rsquo; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eZC, YW, SZ, KN and HW provided medicine for the patient and edited the draft of the manuscript. HW provided medicine for the patient and reviewed the manuscript as a corresponding author. All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eClinical trial number: not applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eEthical Approval and accordance\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe protocol was approved by The Clinical Medical Research Ethics Committee of the First Affiliated Hospital of Bengbu Medical University in accordance with the ICH GCP and CHINA GCP.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eJames NG, Carla MN. Syndromes of thrombotic microangiopathy. N Engl J Med. 2014;371(7):654-66.\u003c/li\u003e\n\u003cli\u003eS Ainslie M, Rebecca S, Kelle H, Sunette C. Preeclampsia and HELLP syndrome complicated by subcapsular liver hematoma and rupture. CMAJ. 2023;195(45):E1543-E1545.\u003c/li\u003e\n\u003cli\u003eMcCormick PA, Higgins M, McCormick CA, Nolan N, Docherty JR. J Matern Fetal Neonatal Med. 2022;35(25):7942-7947.\u003c/li\u003e\n\u003cli\u003eFadi F, Marie S, Fran\u0026ccedil;ois P, Miquel B, Paul C, et al. Management of thrombotic microangiopathy in pregnancy and postpartum: report from an international working group. Blood. 2020;136(19):2103-2117.\u003c/li\u003e\n\u003cli\u003eYahiya YS. Ravulizumab: A Review in Atypical Haemolytic Uraemic Syndrome. Drugs. 2021;81(5):587-594.\u003c/li\u003e\n\u003c/ol\u003e"},{"header":"Tables","content":"\u003cp\u003eTables 1 and 2 are available in the Supplementary Files section.\u003c/p\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":"discover-medicine","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"","sideBox":"Learn more about [Discover Medicine](https://link.springer.com/journal/44337)","snPcode":"44337","submissionUrl":"https://submission.springernature.com/new-submission/44337/3","title":"Discover Medicine","twitterHandle":"","acdcEnabled":true,"dfaEnabled":true,"editorialSystem":"stoa","reportingPortfolio":"Discover Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"pre-eclampsia, thrombotic microangiopathy, HELLP syndrome, atypical haemolytic uraemic syndrome","lastPublishedDoi":"10.21203/rs.3.rs-8374429/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8374429/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eThe sudden-onset life-threatening liver rupture is a rare complication of pregnancy-associated thrombotic microangiopathy. Patients with both HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome and atypical haemolytic uraemic syndrome (aHUS) are very rare, who are always in a significantly urgent situation and hard to treat. We herein report a case of successfully treating a patient who experienced a severe liver rupture with HELLP syndrome and aHUS after the caesarean section.\u003c/p\u003e\u003ch2\u003eCase presentation:\u003c/h2\u003e \u003cp\u003eA 37-year-old woman had a sudden-onset hypertension and proteinuria; thus, she was diagnosed as pre-eclampsia and then a caesarean section was performed. After that, she had the continuous hemolysis, significantly elevated liver enzymes and low platelet count with oliguria and increased creatinine. During the treatment, we organized the multi-disciplinary treatment twice to make decisions of an intervention and an exploratory laparotomy. Combined with the other active treatment, blood transfusion, plasma exchange, and continuous renal replacement therapy, the patient finally survived and returned to a healthy state.\u003c/p\u003e\u003ch2\u003eConclusions\u003c/h2\u003e \u003cp\u003ePhysicians should pay special attention to the possibility of a severe liver rupture in pre-eclampsia and thrombotic microangiopathy patients during pregnancy or post-partum. The active life support and the good multi-disciplinary treatment help a lot for survival.\u003c/p\u003e","manuscriptTitle":"Thrombotic microangiopathy complicate with the severe sudden-onset liver ruptures in a pre-eclampsia patient after the caesarean section: a case report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-02-04 05:18:49","doi":"10.21203/rs.3.rs-8374429/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-03-13T10:05:17+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-03-12T06:33:43+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"315262580365958619778019010214768848343","date":"2026-02-22T13:55:38+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-19T21:39:01+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-02-15T12:05:30+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"256891866939835470774129434557957789272","date":"2026-02-11T16:25:21+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"248816094501685403144491553338778794348","date":"2026-02-10T01:39:38+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-02-02T07:13:11+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-01-23T04:39:37+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-01-22T16:26:19+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-01-22T07:41:04+00:00","index":"","fulltext":""},{"type":"submitted","content":"Discover Medicine","date":"2026-01-22T07:19:24+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"
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