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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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Yuanfei Li,1,* Yong Yang,1,* Yafeng Zheng,2,* Yang Gao,3 Guoliang Shu,4 Wei Gai,2 Yuxin Guo,2 Xianghui Deng1 1Department of Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, People’s Republic of China; 2WillingMed Technology (Beijing) Co., Ltd, Beijing, People’s Republic of China; 3Department of Radiology, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, People’s Republic of China; 4Department of General Surgery, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xianghui Deng, Department of Critical Care Medicine, The Affiliated Changsha Central Hospital, Hengyang Medical School, University of South China, Changsha, People’s Republic of China, Tel +8613974833075, Email 853275395@qq.comAbstract: 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.Keywords: hepatic infarction, mNGS, hypervirulent Klebsiella pneumoniae, septic shock

Abstract 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

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. [ABSTRACT FROM AUTHOR]

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., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Purpose: To investigate the association between hepatic ischemic complications and hepatic artery (HA) collateral vessels and portal venous (PV) impairment after HA embolization for postoperative hemorrhage.Materials and Methods: From October 2003 to November 2019, 42 patients underwent HA embolization for postoperative hemorrhage. HA collateral vessels were classified according to visualization after embolization (grade 1, none; grade 2, 1-4 segmental HA; and grade 3, ≥4 segmental HA). Transhepatic portal vein stent placements were performed in the same session for 5 patients (11.9%) with poor HA collateral vessels (grade 1 or 2) and compromised PV flow (>70% stenosis). Hepatic ischemic complications were analyzed for relevance to HA collateral vessels and PV compromise.Results: After HA embolization, HA flow was found to be preserved (grade 3) through intra- and/or extrahepatic collateral vessels in 23 patients (54.8%), and hepatic complications did not occur regardless of PV flow status (0%). Of the 19 patients (45.2%) with poor HA collateral vessels (grade 1 or 2), segmental hepatic infarction occurred in 2 of 15 patients (13.3%) with preserved PV flow (10 naïve and 5 stented). The remaining 4 patients with poor HA collateral vessels and untreated compromised PV flow experienced multisegmental hepatic infarction (n = 3) or hepatic failure (n = 1) (100%) (P < .005).Conclusions: After HA embolization, preserved HA flow (≥4 segmental HA) lowered the risk of hepatic complications regardless of the PV flow. Based on these findings, transhepatic PV stent placement seems to be an effective intervention for the prevention of hepatic complications in cases of poor HA collateral vessels and compromised PV flow. [ABSTRACT FROM AUTHOR]

Polycythemia vera (PV) is one of the three BCR-ABL1-negative myeloproliferative neoplasms characterized by activating mutations in JAK2, which clinically presents as erythrocytosis and has an increased risk of both thromboembolic events and progression to myelofibrosis and acute myeloid leukemia. Splanchnic vein thrombosis is a rare manifestation of venous thromboembolism involving one or more abdominal vessels and is strongly associated with PV. We herein report a case in which hepatic infarction due to PV was saved by conservative treatment.

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.

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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.

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., (Sociedad Argentina de Pediatría.)

In this second part of the topic the hepatic pseudoaneurysm, hepatic infarction, and pylephlebitis are discussed as acute and potentially life-threatening hepatic vascular diseases. The focus is on their appearance on B-mode ultrasonography, duplex ultrasonography, and contrast-enhanced ultrasonography. Zahn's pseudo infarction is an important differential diagnosis to wedge-shaped hepatic infarction in this context. Knowledge of the data should help raise awareness of these rare findings, to come up with relevant differential diagnoses in the corresponding clinical situation, to interpret the ultrasound images correctly and thus to initiate the appropriate diagnostic and therapeutic steps in time.

Hepatic infarction is a rare complication of radiofrequency ablation (RFA) for hepatocellular carcinoma. Hepatic infarction is thought to be caused by injury to either the hepatic arterial system or to both the hepatic arterial and portal venous supply. The efficacy of RFA is reduced in the presence of nearby vessels larger than 3 mm in diameter due to a heat-sink effect. Such an effect can be diminished by performing percutaneous pure ethanol injection prior to RFA. Although larger vessels are unlikely to be ablated or obliterated by RFA alone, it can happen and cause massive liver damage, particularly if RFA was preceded by other therapies such as percutaneous pure ethanol injection and/or transcatheter arterial embolization. Here, we report a case of massive liver infarction after sequential use of both treatment modalities for hepatocellular carcinoma.

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Objective: We describe the serial computed tomography (CT) findings of extensive hepatic infarction and successful plasma exchange therapy in a severe preeclamptic woman with postpartum HELLP syndrome. Case Report: A 38 year-old woman presented with elevated blood pressure of 140–180/90–120 mmHg and 3+ proteinuria at 28 weeks of gestation. Two days after admission, the patient suddenly complained of severe epigastric pain and headache. Her blood pressure rose sharply to 195/120 mmHg. A 980 g female was delivered by emergency cesarean section. Following delivery, the patient's clinical condition and laboratory values deteriorated, with progressive liver insufficiency (peak AST level = 4246 IU/L, ALT = 3685 IU/L, LDH = 6237 IU/L, platelets = 72,000/mm3). Two consecutive plasma exchanges (PEX) were undertaken on the 3rd and 4th postpartum day. A contrast-enhanced CT of the abdomen performed 8 days postpartum showed geographically wedge-shaped areas of low attenuation, with a mottled appearance in the right hepatic lobe. Shortly thereafter, the patient recovered and all laboratory parameters gradually normalized 3 weeks after delivery. Follow-up CT-scan of the liver 2 months postpartum showed no evidence of infarction, with complete recovery. Conclusion: We recommend that severely ill patients with HELLP syndrome having epigastric pain should undergo CT imaging of the liver. A trial of postpartum PEX therapy should be considered for treatment of the HELLP syndrome complicated with hepatic infarction, which is recalcitrant to conventional medical management, and fails to abate within 72–96 hours of delivery.

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., Competing Interests: Conflict-of-interest statement: Authors declare no conflict of interests for this article., (©The Author(s) 2023. Published by Baishideng Publishing Group Inc. All rights reserved.)

Purpose : HELLP syndrome is a relatively uncommon pregnancy-related condition characterized by hemolysis, elevated liver function tests, and low platelets. It can be accompanied by life-threatening hepatic complications including hepatic infarction, hematoma formation, and hepatic rupture. HELLP syndrome occurs in approximately 0.2% of pregnancies. Major hepatic complications occur in less than 1% of HELLP patients suggesting an incidence of 1/50,000. The pathogenesis is incompletely understood and in particular, it is difficult to understand a disorder with both major thrombotic and bleeding manifestations. Methods : Literature review. Results : On the basis of reports in the published literature, and our own clinical experience, we suggest that vasospasm is one of the principal drivers with hepatic ischemia, infarction, and hemorrhage as secondary events. It is known that vasoactive substances are released by the failing placenta. We suggest these cause severe vasospasm, most likely affecting the small post-sinusoidal hepatic venules. This leads to patchy or confluent hepatic ischemia and/or necrosis with a resultant increase in circulating liver enzymes. Reperfusion is associated with a fall in platelet count and microvascular hemorrhage if the microvasculature is infarcted. Blood tracks to the subcapsular space causing hematoma formation. If the hematoma ruptures the patient presents with severe abdominal pain, intra-abdominal hemorrhage, and shock. Conclusions : We suggest that hepatic and other complications associated with HELLP syndrome including placental abruption, acute renal failure, and posterior reversible encephalopathy syndrome (PRES) may also be due to regional vasospasm.

Purpose: To describe the imaging findings of hepatic infarction after transjugular intrahepatic portosystemic shunt (TIPS) placement and identify risk factors, clinical manifestations, and outcomes of infarction after TIPS., Materials and Methods: In this retrospective analysis of a TIPS registry (1995-2021), cirrhotic patients with hepatic infarction (n = 33) and control patients without infarct (n = 33) after TIPS were identified. Laboratory values, ultrasound findings, and clinical variables were compared between groups to identify risk factors and differences in outcomes. A Cox proportional hazards regression model with propensity score was used to assess the effect of hepatic infarction on mortality and acute-on-chronic liver failure (ACLF) score., Results: Hepatic infarction involved the right posterior segments (segments VI or VII) in 32 of 33 patients. Prolonged vasopressor requirement (p = 0.003) and intensive care unit stay (p = 0.001) were seen in patients with hepatic infarct, as well as trends toward lower post-TIPS portosystemic pressure gradient (p = 0.061) and higher risk of ACLF (p = 0.056). Procedure-related portal vein thrombosis or hepatic artery injury was identified in 12 and 5 patients with infarct, respectively. Patients with infarct had higher postprocedural aspartate aminotransferase (p < 0.001) and alanine aminotransferase (p < 0.001) levels, higher international normalized ratio (p = 0.016), lower platelet count (p = 0.042), and a greater decrease in hemoglobin level (p = 0.003)., Conclusion: Hepatic infarction most frequently affects the right posterior hepatic segments after TIPS and results in a worse postprocedural course. Procedure-related complications and critically low portosystemic pressure gradient may contribute to TIPS-associated hepatic infarct., (© 2022. Springer Science+Business Media, LLC, part of Springer Nature and the Cardiovascular and Interventional Radiological Society of Europe (CIRSE).)