Portal vein thrombosis and hepatic infarction due to hepatic mobilization after primary debulking surgery for advanced ovarian cancer: A case report.

Hepatic mobilization is essential in debulking surgery for resecting diaphragmatic lesions in advanced ovarian cancer. However, hepatic mobilization potentially induces postoperative portal vein thrombosis and hepatic infarction. No reports exist regarding these postoperative complications of gynecological surgeries. Thus, we reported a case of portal vein thrombosis and hepatic infarction after ovarian cancer surgery with upper abdominal surgery. The 51-year-old female patient who had been diagnosed with advanced ovarian and early endometrial cancer underwent primary debulking surgery. Ultimately, she underwent the following surgical procedures: a hysterectomy, bilateral salpingo-oophorectomy, total parietal peritonectomy, low anterior resection, ileostomy, and appendicectomy. The hepatic enzymatic and D-dimer levels were elevated, postoperatively. Contrast-enhanced computed tomography revealed portal vein thrombosis and an infarction of the hepatic S3 region. The portal vein thrombosis resolved post-administration of unfractionated heparin. The hepatic infarction improved. Meticulous intra- and postoperative management should encompass the deliberation of the potential risk of these postoperative complications.

Fulminant liver failure resulting from massive hepatic infarction associated with hemolysis, elevated liver enzymes, and low platelets syndrome.

Hepatic infarction is an extremely rare and fatal complication associated with hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. It can develop into fulminant liver failure, which increases both maternal and neonatal mortality rates. A 34-year-old woman with no remarkable past medical history developed eclampsia after delivery at 40 weeks of gestation. Imaging indicated massive hepatic infarction and rupture followed by cardiac arrest and fulminant liver failure. Despite liver replacement therapy with plasma exchange and continuous hemodiafiltration, the patient gradually deteriorated with persistent bacterial infection until death at 98 days after delivery. The management of fulminant liver failure complicated with HELLP syndrome should be multidisciplinary. Liver transplantation, the only radical treatment for fulminant liver failure, is worth attempting, if applicable.

Hepatic infarction in pregnancy: a systematic review.

OBJECTIVE: Hepatic infarction is a rare complication of pregnancy most often associated with hemolysis, elevated liver enzymes, and low platelets syndrome. The objective of this review is to identify risk factors, present signs and symptoms, identify methods of diagnosis, and identify best management practices on the basis of published case reviews. DATA SOURCES: PubMed and MEDLINE (Ovid) databases were searched for citations regarding hepatic infarction in pregnancy or the postpartum period from database inception until the study date of December 18, 2023. Key words included "liver infarction" or "hepatic infarction" and "pregnancy" or "obstetrics." STUDY ELIGIBILITY CRITERIA: Case reviews or case series published in the English language were included. Our study was registered with the Prospective Register of Systematic Reviews (registration number CRD42023488176) and was conducted in accordance with the published Prospective Register of Systematic Reviews and Meta-analyses Of Observational Studies in Epidemiology guidelines. METHODS: Included papers were evaluated for bias using a previously published tool. RESULTS: A total of 38 citations documenting 50 pregnancies published between 1979 and 2023 were included. Of these, 34% had a history of hypertensive disease, 26% had antiphospholipid syndrome, and 22% had a history of thrombus. Of those without a preexisting diagnosis of antiphospholipid syndrome, 24% tested positive during hospitalization. Most patients presented with epigastric or right upper quadrant pain (78%), and 32% and 16% had severe blood pressure or mild blood pressure, respectively. Sixty-four percent of patients presented with transaminitis. Forty-six percent of patients delivered preterm, and 32% of pregnancies ended in intrauterine fetal demise, abortion, or early termination of pregnancy for maternal benefit. Computed tomography scans were used to confirm diagnosis of hepatic infarction in 58% of cases, magnetic resonance imaging in 14%, and ultrasound in 6%. In cases that described management, treatment was always multimodal, including antihypertensives (18%), therapeutic anticoagulation (45%), blood product transfusion (36%), plasma exchange or intravenous immunoglobulin (20%), and steroids (39%). Transfer to the intensive care unit was required in 20% of cases. CONCLUSION: Hepatic infarction should be considered in all cases of hemolysis, elevated liver enzymes, and low platelets syndrome, but specifically in patients with a history of antiphospholipid syndrome who present with epigastric or right upper quadrant pain. The diagnosis can usually be confirmed with a computed tomography scan alone, and management should be prompt with supportive care, therapeutic anticoagulation, and steroids.

Hypervirulent Klebsiella pneumoniae Mediated Hepatic Infarction Septic Shock After Rectal Cancer Surgery: A Case Report.

The liver receives blood from both the hepatic artery and portal vein. Hepatic infarction is rare in clinical practice as both the hepatic artery and portal vein can supply blood to the liver. Here, we reported a case of a 75-year-old man who underwent radical laparoscopic surgery for rectal cancer and subsequently developed hepatic infarction. The patient experienced severe infection, as well as circulatory and respiratory failure on the third day after surgery. The patient presented with high fever, chest tightness, shortness of breath, decreased blood oxygen saturation and blood pressure. The leukocyte count decreased from 8.10 × 10^9/L to 1.75 × 10^9/L. Procalcitonin (PCT) levels increased from 1.02 ng/mL to 67.14 ng/mL, and eventually reaching levels over 200 ng/mL. Enhanced abdominal computed tomography (CT) confirmed the presence of hepatic infarction, but no thrombosis was observed in the hepatic artery or portal vein. Metagenomic next-generation sequencing (mNGS) identified hypervirulent Klebsiella pneumoniae (hvKp) in the patient's blood and ascites, one day earlier than the detection results using traditional culture methods. The patient was diagnosed with hepatic infarction combined with septic shock caused by hvKp. This case emphasizes that in the high-risk group of thrombosis, infection can trigger exacerbated hepatic infarction events, particularly in cases after surgical procedures. For severely ill patients with infectious diseases who are admitted to the ICU with worsening symptoms, it is important to collect appropriate samples and send them for pathogen detection using mNGS in a timely manner. This may aid in early intervention and improve clinical outcomes.

Hepatic infarction occurred after 125I particle stent treatment for hepatocellular carcinoma with portal vein tumor thrombus: A case report.

BACKGROUND: Hepatic infarction is a rare liver condition. The purpose of this study is to report a case of hepatic infarction caused by thrombus formation following portal vein stent implantation in a patient with hepatocellular carcinoma and portal vein tumor thrombus, and to explore the underlying causes. CASE REPORT: The patient in this study was a 52-year-old male admitted with diffuse hepatocellular carcinoma involving the right lobe and portal vein tumor thrombus. After undergoing portal vein stent implantation and 125I particle strand implantation treatment, the portal vein was patent, and the pressure decreased. However, multiple instances of hepatic artery chemoembolization combined with targeted immunotherapy resulted in gradual reduction in the diameter of the hepatic artery and affecting hepatic arterial blood flow. Two months post-stent implantation, thrombus formation within the stent was noted, and the patient's condition did not improve with anticoagulant therapy, as evidenced by follow-up CT scans showing an increase in thrombi. Six months later, the patient suffered from gastrointestinal bleeding and, despite emergency esophagogastric variceal ligation and hemostatic treatment, developed hepatic parenchymal infarction and liver function failure. CONCLUSIONS: We reveal the underlying cause is that (1) thrombus formation within the portal vein stent, leading to portal vein embolism and obstructed blood flow due to exacerbate portal hypertension after various treatments; and (2) the effect of hepatic artery chemoembolization, immunotherapy, and targeted therapy on tumor angiogenesis, causing reduced hepatic artery diameter and impaired arterial blood flow. These factors disrupt the liver's dual blood supply system, ultimately contributing to hepatic infarction. To our knowledge, this is the first report of hepatic infarction as a complication following portal vein stent implantation for hepatocellular carcinoma with portal vein tumor thrombus, and it holds significant reference value for guiding the treatment of hepatocellular carcinoma with concurrent portal vein tumor thrombus in a clinical setting.

Congenital syphilis and hepatic infarction, a not previously reported association. A pediatric case report. / Sífilis congénita e infarto hepático, una asociación no reportada. Descripción de un caso pediátrico.

Congenital syphilis is caused by Treponema pallidum infection of the fetus during pregnancy. Symptoms are variable. While endothelial damage is common, it is not usually present in congenital cases. Here we report the case of a 42-day-old infant hospitalized due to an abdominal mass. Imaging studies confirmed the presence of an injury in the left lobe of the liver without mass effect. Biopsies showed changes compatible with infarction and neonatal hepatitis. The patient's and his mother's serologies confirmed the diagnosis of congenital syphilis, and he was treated with intravenous penicillin. The liver is protected from ischemic injury by its double irrigation, but the accumulation of harmful agents may have caused this unusual presentation. Three months later, the patient was symptom-free, and the control MRI showed atrophy of the left lobe, while the rest of the parenchyma was unchanged.

La sífilis congénita es causada por la infección del feto con Treponema pallidum durante el embarazo. Los síntomas son variables. Si bien es común el daño endotelial, no suele estar presente en los casos congénitos. Reportamos el caso de un lactante de 42 días de vida hospitalizado por masa abdominal. Las imágenes confirmaban la presencia de una lesión en el lóbulo hepático izquierdo sin efecto de masa. Las biopsias mostraron cambios compatibles con infarto y hepatitis neonatal. Las serologías del paciente y de su madre confirmaron el diagnóstico de sífilis congénita, y recibió tratamiento con penicilina intravenosa. El hígado se encuentra protegido de los daños isquémicos gracias a su doble irrigación, pero la acumulación de noxas puede haber provocado dicha presentación inusual. Tres meses más tarde, el paciente se encontraba libre de síntomas y la resonancia de control mostró atrofia del lóbulo izquierdo, mientras el resto del parénquima no presentaba alteraciones.

Acute Liver Infarct with a Superimposed Liver Abscess as a Consequence of Hypercoagulable State in a Patient with COVID-19 without Respiratory Manifestations.

COVID-19 infection has been associated, particularly in severely ill patients requiring hospitalization, with a hypercoagulable state. The case presented herein was a 66-year-old man with SARS-CoV-2 infection who did not have any respiratory symptoms. He presented with the following clinical manifestations: portal vein and hepatic artery thrombosis, liver infarction, and a superimposed abscess of the liver. In this case, early detection and the administration of anticoagulants and antibiotics led to a significant improvement within weeks of the diagnosis. We encourage physicians to be aware of COVID-19-associated hypercoagulable state and its potential complications, regardless of the acuity of the presentation or the absence of respiratory symptoms.

Liver involvement in patients with COVID-19 infection: A comprehensive overview of diagnostic imaging features.

During the first wave of the pandemic, coronavirus disease 2019 (COVID-19) infection has been considered mainly as a pulmonary infection. However, different clinical and radiological manifestations were observed over time, including involvement of abdominal organs. Nowadays, the liver is considered one of the main affected abdominal organs. Hepatic involvement may be caused by either a direct damage by the virus or an indirect damage related to COVID-19 induced thrombosis or to the use of different drugs. After clinical assessment, radiology plays a key role in the evaluation of liver involvement. Ultrasonography (US), computed tomography (CT) and magnetic resonance imaging (MRI) may be used to evaluate liver involvement. US is widely available and it is considered the first-line technique to assess liver involvement in COVID-19 infection, in particular liver steatosis and portal-vein thrombosis. CT and MRI are used as second- and third-line techniques, respectively, considering their higher sensitivity and specificity compared to US for assessment of both parenchyma and vascularization. This review aims to the spectrum of COVID-19 liver involvement and the most common imaging features of COVID-19 liver damage.

Hepatic Infarction in a Patient With Sickle Cell Trait Presenting With HELLP Syndrome.

Hepatic infarction is uncommon due to the dual blood supply from the hepatic artery and portal vein. The majority of the cases are caused following liver transplant or hepatobiliary surgery, hepatic artery occlusion, or shock. Hepatic infarction is a rare complication of hemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome. HELLP is an obstetrical emergency requiring prompt delivery. The presence of elevated liver enzymes, mainly alanine aminotransferase and aspartate aminotransferase in pre-eclampsia, should warrant diagnosis and treatment in the line of HELLP syndrome. Our patient with underlying sickle cell trait presented with features of HELLP syndrome in her third trimester of pregnancy. She underwent cesarean delivery on the same day of the presentation. The liver enzymes continued to rise following delivery and peaked on postoperative day two. Contrast computed tomography scan showed multifocal hepatic infarctions. Pre-eclampsia by itself is a state of impaired oxygenation and can lead to hepatic hypoperfusion, and appeared to be a clear contributor to the hepatic infarction in this case. However, this case also raises the question of whether the underlying sickle cell trait might have potentiated the hepatic infarction. Although sickle cell disease is well known to cause hepatic infarctions, it is unknown whether the sickle cell trait affects the liver to a similar extent as sickle cell disease. In addition, there have been case reports of sickle cell trait causing splenic infarcts and renal papillary necrosis, but it remains unclear if it can be directly associated with hepatic infarction.

Multiple hepatic infarctions secondary to diabetic ketoacidosis: A case report.

BACKGROUND: Hepatic infarctions (HI) are ischemic events of the liver in which a disruption in the blood flow to the hepatocytes leads to focal ischemia and necrosis. Most HI are due to occlusive events in the liver's blood vessels, but non-occlusive HI may occur. They are associated with disruption of microvasculature, such as in diabetic ketoacidosis. While HI usually presents as peripheral lesions with clear borders, irregular nodular lesions may occur, indistinguishable from liver neoplasms and presenting a diagnostic challenge. CASE SUMMARY: We report a case of multiple extensive HI in a patient with poorly controlled diabetes mellitus, who first presented to the emergency room with diabetic ketoacidosis. He then developed jaundice, thrombocytopenia, and a marked elevation of serum aminotransferases. An ultrasound of the liver showed the presence of multiple irregular lesions. Further investigation with a computerized tomography scan confirmed the presence of multiple hypoattenuating nodules with irregular borders and heterogeneous appearance. These lesions were considered highly suggestive of a primary neoplasm of the liver. While the patient was clinically stable, his bilirubin levels remained persistently elevated, and he underwent an ultrasound-guided percutaneous biopsy of the largest lesion. Biopsy results revealed extensive ischemic necrosis of hepatocytes, with no signs of associated malignancy. Three months after the symptoms, the patient showed great improvement in all clinical and laboratory parameters and extensive regression of the lesions on imaging exams. CONCLUSION: This case highlights that diabetic ketoacidosis can cause non-occlusive HI, possibly presenting as nodular lesions indistinguishable from neoplasms.

Efficacy and safety of endovascular therapy for delayed hepatic artery post-pancreatectomy hemorrhage: development of extrahepatic collateral circulation and complications of post endovascular therapy.

BACKGROUND: Endovascular therapy (ET) for delayed hepatic artery post-pancreatectomy hemorrhage (HA-PPH) may require complete hepatic artery occlusion (HAO). Nonetheless, the development of extrahepatic collateral circulation (EHC) and the relationship between radiological factors (EHC, portal vein stenosis, and HAO) and adverse hepatic events after ET remain unclear. This study aimed to evaluate the efficacy and safety of ET for delayed PPH and examine the development of EHC. METHODS: A total of 19 ET cases for delayed HA-PPH were reviewed. Hepatic adverse events, portal vein stenosis, HAO, and mortality rate after ET were evaluated. Moreover, EHC from the left gastric artery (LGA), right inferior phrenic artery (RIPA), left inferior phrenic artery (LIPA), right internal thoracic artery (RITA), left internal thoracic artery (LITA), renal artery (RA), omental artery (OA), intercostal artery (IA), and branch of superior mesenteric artery (BSMA) was assessed using angiogram and computed tomography angiography (CTA). RESULTS: All cases were successfully treated using transcatheter arterial embolization (n = 17) and stent-graft placement (n = 2) without mortality. EHC from the LGA (8/19), RIPA (10/19), LIPA (4/19), and RITA (3/19) was observed on post-ET CTA. The incidence of hepatic adverse events was significant in the group with both HAO and portal vein stenosis (p < 0.001) and absence of EHC from LIPA and RITA (p < 0.05). CONCLUSION: ET for delayed HA-PPH might be effective and safe. While avoiding both HAO and portal vein stenosis is important, the development of EHCs from LIPA and RITA may prevent hepatic adverse events after ET.

The findings of the contrast-enhanced CT and risk factors for hepatic infarction after pancreatoduodenectomy.

PURPOSE: Hepatic infarction is a relatively rare life-threatening complication after pancreatoduodenectomy (PD). Computed tomography (CT) findings and risk factors for hepatic infarctions after PD were investigated. METHODS: One hundred-fifty three patients who underwent contrast-enhanced CT (CECT) after PD between January 2011 and August 2016 were retrospectively analyzed. Hepatic infarction was defined as the non-contrast enhanced area expanding to the liver surface without mass effect on CECT. The relationships between infarctions and preoperative laboratory data or surgical procedures using uni- and multivariate analyses were examined. RESULTS: Twenty-nine patients showed 47 hepatic infarctions on CT. Infarctions most commonly appeared in segment 7 (S7) (17 lesions, 36.2%). Lesions were wedge-shaped in 12 patients and spread over multiple hepatic segments in 11 patients. Univariate analysis identified celiac artery (CA) or common hepatic artery (CHA) resection (p = 0.0029) and portal vein (PV) resection (p = 0.013) as risk factors for infarctions. CA or CHA resection (p = 0.038) remained as a significant factor after multivariate logistic analysis. CONCLUSIONS: Hepatic infarctions after PD were most frequently seen in S7 and PV penetrating sign was characteristic CT findings. CA or CHA resection or PV resection were revealed as risk factors for hepatic infarctions.

A case of massive hepatic infarction in severe preeclampsia as part of the HELLP syndrome.

Hepatic infarction is a rare and fatal complication associated with hemolysis, elevated liver enzymes and low platelets syndrome. It can develop into fulminant liver failure and lead to death in 16% of cases. A 25-year-old woman, with unremarkable prenatal history, was sent to gynecological emergency unit for management of severe preeclampsia at 30 weeks and 4 days of pregnancy. Initial laboratory studies revealed aspartate aminotransferase at 290 U/L, alanine aminotransferase at 193 U/L and a normal value of hemoglobin, platelets and the prothrombin time. Behind the persistence of high blood pressure despite dual therapy, an emergent cesarean section was performed. However, two days after surgery, the patient accused an epigastric pain and was subsequently noted to have developed HELLP syndrome: thrombocytopenia (77000 /ul), anemia (hemoglobin 9.1 g/dL) and worsened liver injury (aspartate aminotransferase 2809 U/L; alanine aminotransferase 2502 U/L). A thoraco-abdominopelvic computed tomography (CT) was performed, which revealed massive hepatic infarction more marked on the right lobe, by showing the existence of diffuse hypodense plaques, poorly limited, not enhanced after injection, interesting all hepatic segments. The vascular permeability of the portal and subhepatic was preserved. During the surveillance, the laboratory tests worsened (hemoglobin = 4,6 g/dl; platelets count = 20000 /ul; WBC = 26000 /ul; CRP = 340 mg/l; albumin = 16 g/l, prothrombin time (PT) = 50%). The patient received antibiotics, she was transfused by red blood cells and platelets concentrates, she also received albumin with the pleural effusion drainage. The damaged hepatic areas stayed stable in control CT and the patient gradually improved here biological test, to become normal at 11 days after delivery. Hepatic infarction is an extraordinarily rare complication of preeclampsia. The diagnosis should be suspected by noting elevated liver enzymes, thrombocytopenia and typical images of hepatic infarction on abdominal CT. Early recognition and multidisciplinary management is necessary to prevent hepatic failure and death.

Venous thrombosis and segmental hypoperfusion in amebic liver abscess: MDCT demonstration and its implications.

PURPOSE: To report venous thrombosis and associated perfusion defect in amebic liver abscess (ALA) using MDCT. METHOD: MDCT images of 62 patients with ALA were reviewed for venous thrombosis and associated perfusion abnormalities. RESULT: The study found 43 (69%) patients with venous thrombosis: portal vein thrombosis (PVT) occurred in 39, hepatic vein thrombosis (HVT) in 37 and inferior vena cava (IVC) thrombosis in 4. Combined PVT and HVT occurred in 33 (77%) patients. The portal vein thrombi remained localized in subsegmental branches in 25 patients and extended to segmental branches in 14. The hepatic vein thrombi were confined to peripheral branches in 18 patients; they progressed to the main trunk in 19 and to the IVC in 4. A wedge-shaped hypoattenuating zone suggesting ischemia was identified in 33 (77%) patients in portal phase: 31 had combined PVT and HVT, 2 had HVT alone, but none had PVT alone. It occurred significantly more often with combined PVT and HVT than HVT alone (p = 0.05). Arterial phase enhancement occurred in 2 of 13 patients with multiphasic CT. All patients were symptomatic despite medical therapy and therefore required percutaneous drainage. About half of the patients were identified with ruptured abscesses. Segmental atrophy was observed in seven of nine patients who underwent follow-up CT. CONCLUSION: Combined PVT and HVT commonly occur with ALA and often manifests as segmental hypoperfusion in portal venous phase, indicating ischemia. The detection of such events by CT may be indicative of severe disease that requires aggressive management involving percutaneous drainage.

Acute liver failure and infarction complicating TIPS placement.

Here in we report a case of acute liver failure with hepatic infarction after transjugular intrahepatic portosystemic shunt (TIPS). An upper gastrointestinal hemorrhage patient with a medical history of alcoholic cirrhosis underwent a TIPS procedure. One day after TIPS, his alanine aminotransferase and aspartate aminotransferase levels increased to 1214 U/L and 1511 U/L, respectively. Two days after TIPS, they peaked at alanine aminotransferase 8389 U/L and aspartate aminotransferase >7500 U/L, respectively. An emergent stent occlusion was performed on the second day. Portography showed that there were no portal vein branches or parenchymal stains on the edge of the right liver lobe. A CT scan demonstrated diffuse hepatic parenchyma, homogeneous hypodense lesion, and bilateral pleural effusion. The patient died of liver failure and multiple organ dysfunction syndrome 6 hours after the stent occlusion.

Sífilis congénita e infarto hepático, una asociación no reportada. Descripción de un caso pediátrico / Congenital syphilis and hepatic infarction, a not previously reported association. A pediatric case report

La sífilis congénita es causada por la infección del feto con Treponema pallidum durante el embarazo. Los síntomas son variables. Si bien es común el daño endotelial, no suele estar presente en los casos congénitos. Reportamos el caso de un lactante de 42 días de vida hospitalizado por masa abdominal. Las imágenes confirmaban la presencia de una lesión en el lóbulo hepático izquierdo sin efecto de masa. Las biopsias mostraron cambios compatibles con infarto y hepatitis neonatal. Las serologías del paciente y de su madre confirmaron el diagnóstico de sífilis congénita, y recibió tratamiento con penicilina intravenosa. El hígado se encuentra protegido de los daños isquémicos gracias a su doble irrigación, pero la acumulación de noxas puede haber provocado dicha presentación inusual. Tres meses más tarde, el paciente se encontraba libre de síntomas y la resonancia de control mostró atrofia del lóbulo izquierdo, mientras el resto del parénquima no presentaba alteraciones.

Congenital syphilis is caused by Treponema pallidum infection of the fetus during pregnancy. Symptoms are variable. While endothelial damage is common, it is not usually present in congenital cases. Here we report the case of a 42-day-old infant hospitalized due to an abdominal mass. Imaging studies confirmed the presence of an injury in the left lobe of the liver without mass effect. Biopsies showed changes compatible with infarction and neonatal hepatitis. The patient's and his mother's serologies confirmed the diagnosis of congenital syphilis, and he was treated with intravenous penicillin. The liver protected from ischemic injury by its double irrigation, but the accumulation of harmful agents may have caused this unusual presentation. Three months later, the patient was symptom-free, and the control MRI showed atrophy of the left lobe, while the rest of the parenchyma was unchanged.

Successful management of brain abscess and paradoxical embolization caused by huge pulmonary arteriovenous malformation: a case report / 中国医师杂志

Objective:The purpose of this case report is to improve the understanding of pulmonary arteriovenous malformation (PAVM) and its related complications by reviewing case data and literature.Methods:A case of huge PAVM complicated with brain abscess and paradoxical embolization of liver, spleen and kidney is reported, and then we summarize its clinical characteristics, diagnosis and treatment, and review the relevant references.Results:Brain abscess and paradoxical embolization are the most common complications of PAVM. The diagnosis and process of this patient was timely and clear. The patient received interventional embolization for PAVM and achieved good results.Conclusions:PAVM can cause brain abscess and paradoxical embolization. We should be vigilant to avoid missed diagnosis and misdiagnosis.

Spontaneous Hepatic Infarction in a Patient with Gallbladder Cancer.

Hepatic infarction is known as a rare disease entity in nontransplant patients. Although a few cases of hepatic infarction have been reported to be linked with invasive procedures, trauma, and hypercoagulability, a case of spontaneous hepatic infarction in a nontransplanted patient has hardly ever been reported. However, many clinical situations of patients with cancer, in particular biliary cancer, can predispose nontransplant patients to hepatic infarction. Besides, the clinical outcome of hepatic infarction in patients with cancer can be worse than in patients with other etiologies. As for treatment, anticoagulation treatment is usually recommended. However, because of its multifactorial etiology and combined complications, treatment of hepatic infarction is difficult and not simple. Herein, we report a case of fatal hepatic infarction that occurred spontaneously during the course of treatment in a patient with gallbladder cancer. Hepatic infarction should be considered as a possible fatal complication in patients during treatment of biliary malignancies.

Hepatic infarction in a pregnant woman with antiphospholipid syndrome and triple antibody positivity: A case report focusing on catastrophic antiphospholipid syndrome.

Pregnant women with antiphospholipid syndrome (APS) carry a high risk of arterial or venous thrombosis. Such thrombotic conditions occur more frequently in patients with triple positivity to antiphospholipid antibodies or with high antibody titers. Hepatic infarction is a rare complication in pregnant women with APS, and it sometimes mimics HELLP syndrome. This report describes a preeclamptic pregnant woman with APS who had high titers of three antiphospholipid antibodies. She experienced severe epigastric pain with elevated liver enzymes; in addition, she had tachycardia and tachypnea. The clinical findings suggested hepatic infarction and pulmonary thromboembolism, a partial manifestation of catastrophic APS. Therefore, she underwent emergent cesarean section at 25+2 weeks of gestation. After the delivery, her laboratory test indicated HELLP-like features, and computed tomography confirmed hepatic infarction and pulmonary micro-thromboembolism. Here, we report a case of a partial manifestation of catastrophic APS in a pregnant woman with triple antibody positivity, including a brief literature review.