Acute Fulminant Liver Failure Research Articles

A295 A CHALLENGING DIAGNOSTIC CASE - SEVERE ACUTE HEPATITIS POTENTIALLY ASSOCIATED WITH COVID-19 IN AN IMMUNOCOMPETENT YOUNG ADULT

Abstract Background Severe hepatitis with liver enzymes in the thousands is usually associated with viral etiologies, toxins, vascular aetiologies, acute gall stones, autoimmune hepatitis, and Wilson disease. Acute hepatitis in the moderate range has been associated with COVID19 infection. Aims A potential case of severe hepatitis with initial ALT of 6863, who tested positive for COVID19. Acetaminophen ingestion confounded the presentation. Methods Case Report Results A 48-year-old woman, with history of Insomnia on Zopiclone, presented to Hospital with a 6-day history of fatigue, malaise, muscle aches and subjective fevers. She had a ten pack-years smoking history, consumed 8 alcoholic beverages weekly, used marijuana infrequently, and denied any herbal or naturopathic supplement usage. She was double vaccinated against COVID19 over a year ago. On the 2nd day of symptoms, she ingested 5 grams of Acetaminophen over a 24-hour period. Subsequently, she continued to use Acetaminophen, but did not exceed a daily dosage of 4 grams. On the 5th day, she presented to clinic and was found to have elevated liver enzymes: ALT 6863, AST 5785, ALP 62, GGT 60, and INR 1.1 with Bilirubin 8. She had nausea and emesis, prompting her to present to the hospital on the 6th day. The patient was alert and oriented, with mild tenderness in the right upper quadrant with no jaundice, ascites, peripheral edema, or encephalopathy. She had reactive lymphocytosis consistent with a potential viral infection. Testing for acute hepatitis A, B, and C, HIV, EBV, CMV, herpes simplex virus, and varicella-zoster was negative. COVID19 was detected by rapid antigen testing and confirmed via PCR. Blood and urine toxicology screens were unremarkable. Acetaminophen was detected at a low level of 67 μg/mL at presentation and given the diagnostic dilemma & concern for concomitant acetaminophen-associated liver injury she was started on N-acetylcysteine (NAC) infusion. Acetaminophen level was trended until undetectable. Ceruloplasmin and alpha-1 antitrypsin were unremarkable. Iron studies showed an elevated Ferritin 1032. Autoimmune workup was negative except for anti-dense fine speckled autoantibodies with 1:80 (low) titre. Abdominal ultrasound with doppler was normal. Her liver enzymes improved (Figure1) without signs of acute fulminant liver failure. She was discharged after 48 hours (day 7). In follow-up, her labs were: ALT 11, AST 16, INR 1.1, Bilirubin 6, and Ferritin 61. Conclusions To our knowledge, this is one of the first case reports of severe hepatitis, possibly due to COVID-19 in an immunocompetent adult, however, concerns for concomitant unintentional acetaminophen toxicity complicate the diagnosis. NAC was given to mitigate diagnostic error given the risk of anchoring bias. If patient condition had deteriorated liver biopsy would have been considered. Funding Agencies None

Acute fatty liver of pregnancy with transient resolution preceding postpartum liver failure requiring liver transplant

Abstract Objectives Acute fatty liver of pregnancy (AFLP) is a rare, potentially fatal complication of unknown etiology that occurs in the third trimester or early postpartum and can be associated with adverse maternal and fetal outcomes. The purpose of this report is to share a case of AFLP in which a period of objective and symptomatic resolution preceded delayed postpartum liver failure and liver transplant. Case presentation A 35-year-old G3P0020 female experienced preterm premature rupture of membranes (PPROM) at 32 weeks’ gestation and AFLP. She delivered vaginally and despite apparent initial disease resolution, was found 22 days later to have fulminant acute liver failure that required liver transplantation. Conclusions AFLP should be monitored closely postpartum even if disease parameters initially appear to resolve after delivery.

A curious case of expanded dengue syndrome.

Dengue fever (DF) primarily presents with fever, headache, malaise, bleeding manifestations and haemoconcentration. World Health Organization (WHO) classifies DF according to levels of severity: (a) without warning signs; (b) with warning signs, such as abdominal pain, persistent vomiting, fluid accumulation, mucosal bleeding, lethargy, liver enlargement, increasing haematocrit and thrombocytopenia; and (c) severe dengue with severe plasma leakage, severe bleeding or organ failure. Atypical clinical presentations of DF are defined as expanded dengue syndrome: this includes renal, cardiac, hepatic or cerebral damage. We report such a severe case where a young man developed acute kidney injury, acute fulminant liver failure and acute pancreatitis secondary to DF, but recovered.

A Case of Zinc Phosphide-Induced Acute Fulminant Liver Failure

A Case of Zinc Phosphide-Induced Acute Fulminant Liver Failure

Acute fatty liver of pregnancy About 20 cases

Our retrospective study concerned acute hepatic steatosis in pregnancy: diagnostic problems, severity and therapeutic perspectives in the Moroccan context. It concerns a series of 20 cases of SHAG collected in the department of gynecology-obstetrics and maternal resuscitation of the CHU MOHAMED VI in Marrakech over a 5-year period from January 2017 to December 2021. We included in this sample women admitted during pregnancy or post partum for management of SHAG. In our series, the frequency of SHAG was 1 case per 4340 deliveries. The age of the patients ranged from 18 to 45 years, with an average of 28 years and an average gestational age of 32 days and 3 weeks. Thus the majority of patients were multiparous and multigestational with a frequency of 55%. Clinically: polyuria-polydipsia syndrome was present in 20% of patients, nausea-vomiting in 70% and epigastralgia in 60%. Biologically: Hypoglycaemia present in 60%, hyperleukocytosis in 85%, creatinine level above 12mg/l in 70%, hyperuricaemia in 75%, hepatic cytolysis in 90%, hyper bilirubinaemia in 95% with conjugated predominance, prolonged PT in 50% and hyperammonia in 10%. Concerning complications, acute fulminant liver failure was observed in 30% of our patients, it is the most serious and fatal complication. The therapeutic management of SHAG requires, in addition to uterine evacuation associated with adequate medical and surgical resuscitation.

Acute Fulminant Liver Failure Secondary to Yellow Phosphorus Poisoning: Role of Extended N-acetylcysteine Therapy

Acute Fulminant Liver Failure Secondary to Yellow Phosphorus Poisoning: Role of Extended N-acetylcysteine Therapy

Near-fatal ferrous sulfate poisoning

Rationale: Acute iron poisoning is commonly seen in a pediatric population caused by accidental ingestion of iron syrups. We describe a case of iron poisoning who presented to the hospital following intentional near-fatal ingestion of ferrous sulfate. Patient’s Concern: A 14-years-old previously healthy female patient presented to the emergency department with a history of an intentional overdose of 80 ferrous sulfate tablets. Diagnosis: Ferrous sulfate poisoning. Interventions: The patient developed acute fulminant liver failure 24 h after of the overdose. She was managed conservatively, mainly with deferoxamine and N-acetylcysteine while awaiting transfer to a liver transplant facility. Outcomes: The patient responded well to medical therapy and was discharged on the 9th day of intensive care unit admission. Lessons: This case highlights the patient’s successful recovery with prompt conservative therapy. Severe iron toxicity can be treated with early use of deferoxamine and N-acetylcysteine where a liver transplant facility is not available.

420.6: Transplantation of Organs From SARS-CoV-2-Positive Donors To Uninfected (Non-lung) Solid Organ Transplant Recipients Has Not Resulted in Significant SARS-CoV-2 Related Morbidity Or Mortality

Introduction: The SARS-CoV-2 pandemic has conferred significant morbidity and mortality across the globe, especially for solid organ transplant (SOT) recipients. This has led to reluctance of using organs from SARS-CoV-2 infected donors due to concerns of disease transmission. However, this must be offset with an increase in wait list mortality. We sought to evaluate the use of organs from SARS-CoV-2 donors into (non-Lung) Solid Organ Transplant Recipients in a prospective fashion. Methods: We evaluated the use of organs from SARS-CoV-2 donors between 6/17/2021 to 2/24/2022. 18 patients were transplanted with SARS-CoV-2-positive donor (COVID+) organs: 3 heart, 4 liver, and 11 kidney recipients. SOT recipients were tested for presence of SARS-CoV-2 by RT-PCR prior to and after their operations. Induction immunosuppression was standard and not altered from protocol. Postoperatively, recipients were kept in modified droplet precautions and received post-exposure treatment recommended by Transplant Infectious Disease. Treatment regimens included remdesivir and monoclonal antibodies directed against SARS-CoV-2 (Figure 1). Perioperative and post discharge care was administered by a multidisciplinary care team with no significant alterations in care protocols. Results: SOT recipients of COVID+ organs at our institution have not experienced any significant morbidity or mortality from SARS-CoV-2. All patients are alive at current follow up with excellent allograft function with a median follow up for heart, liver, and kidney recipients of 235, 67, and 86 days respectively. All patients were vaccinated except for one liver patient who was status 1A due to fulminant acute liver failure. 13/18 patients had post-operative nasopharyngeal swabbing for RT-PCR based viral testing and two tested positive for SARS-CoV-2 at POD #8. Neither patient experience clinical symptoms of disease. Use of of SARS-CoV-2 did not appear to increase inpatient hospital stay. Median LOS for heart, liver, and kidney recipients was 40, 12.3, and 7.4 days respectively. Neither pre-transplant vaccination, use of COVID+ organs, nor post exposure prophylaxis resulted in increased risk of immunologic complications as only one recipient (heart) has experienced an acute cellular rejection episode to date Conclusion: Our experience indicates that COVID+ organs can be utilized successfully. The decision to use these organs was based on organ quality, individual patient need at the time the organ offer was made and whether a potential similar quality, COVID negative organ would be available to the patient in the near future. As evidenced by our data, successful use of COVID+ organs is dependent on multidisciplinary wait list and perioperative management to ensure appropriate donor:recipient selection and mitigation of transmission risk with use of post-exposure prophylaxis.

Non-hepatotropic viral hepatitis and its causative pathogens: The ongoing need for monitoring in children with severe acute hepatitis of unknown etiology.

Non-hepatotropic viral hepatitis and its causative pathogens: The ongoing need for monitoring in children with severe acute hepatitis of unknown etiology.

Acute fulminant liver failure, COVID -19 and 2-day intensive care unit follow-up period: A Case Report

We aimed to share our case who developed liver failure due to covid-19, which is more severe than we have ever encountered. A 67-year-old male patient was brought to our hospital by ambulance with complaints of weakness and eating and drinking disorder. In the first examination, the patient was conscious, oriented and cooperative. The liver and kidney function tests and whole blood parameters of the patient at the first admission were within normal limits. The patient was admitted to the intensive care unit because of comorbidities and oxygen support may be required. It was found that the patient’s liver function tests were found to be elevated in the examinations on the first intensive care unit day. Transplantation and Plasmapheresis could not be performed due to the patient's general condition. In the follow-up, orotracheal intubation was performed for the patient whose general condition deteriorated, blood pressure decreasing and positive inotropic therapy was initiated on the second ICU day. The patient whose general condition deteriorated could not be saved despite all interventions. Although our knowledge about SARS-CoV-2 is not sufficient yet, we think that it should be kept in mind that it may also cause fulminant liver failure.

Role of Corticosteroids in Drug-Induced Liver Injury. A Systematic Review.

Introduction: Apart from cessation of the implicated agent leading to drug-induced liver injury (DILI), there is no standard therapy for DILI. Corticosteroids have been used in DILI, although their efficacy is unclear. Published data showed either beneficial effects or no improvement associated with steroid therapy. The aim of the current study was to perform a systematic review of the role of corticosteroids in the treatment of DILI. Methods: A search was performed in PubMed, searching for the terms: “corticosteroids” and “drug-induced liver injury”. Observation studies were included, but case reports excluded. Results: A total of 24 papers were retrieved. Most of these were observational studies on the effects of corticosteroids in moderate/severe DILI (n = 8), reports on the corticosteroid treatment in patients with drug-induced autoimmune hepatitis (DI-AIH) (n = 5), and effects of corticosteroids in drug-induced fulminant acute liver failure (ALF, n = 2). Furthermore, treatment of corticosteroids in patients with liver injury due to check point inhibitors (CPIs) was addressed in nine studies. In moderate/severe DILI, six out of eight studies suggested steroid treatment to be beneficial, whereas two studies showed negative results. All five observational studies on the effects of corticosteroids in DI-AIH showed good therapeutic response with rapid and long lasting effects after discontinuation of corticosteroids and without evidence of relapse. Steroid therapy was not associated with improved overall survival in patients with drug-induced fulminant ALF. CPIs-induced liver injury was found to improve spontaneously in 33–50% without corticosteroids, and the rate of patients who were treated responded to steroids in 33–100% (mean 72%). Conclusions: The majority of studies analyzing the effects of corticosteroids in moderate/severe DILI have demonstrated beneficial effects. However, this was not the case in drug-induced fulminant ALF. Patients with DI-AIH had an excellent response to corticosteroids. The majority of those with CPIs-induced liver injury responded to corticosteroids; however, patients without treatment usually recovered spontaneously. The observational design and comparison with historical controls in these studies makes it very difficult to draw conclusions on the efficacy of corticosteroids in DILI. Therefore, there is a strong need for a randomized controlled trial to properly assess the role of corticosteroids in DILI.

Fatal Fulminant Hepatic Failure in a Case of Zinc Phosphide Poisoning: A Case Report

Rodenticide is the term given for the compounds that are used in the killing of rats. The commonest compounds that are available as rodenticides are Aluminum phosphide, Zinc Phosphide, Yellow Phosphorus and Coumarins. Due to their easy availability in the general stores, these also have been used as a source of inflicting self-harm by the patients in order to commit suicide. Most of the patients escape the poisonous side effects with a mild course, but some cases progress to a state of Acute liver failure or fulminant liver failure. Due to the broad range of symptoms that can occur with the compounds, it is important to discuss the course of progression of symptoms from mild to severe in order to understand the treatment protocols to treat the patient appropriately. Some patients progress to such a severe form of symptoms that there is an urgent indication of liver transplantation. Here we report a case of rodenticide poisoning in a young female which started off with a mild course and ultimately progressed to fulminant liver failure leading to a fatal outcome.

HYPEREOSINOPHILIA, MYELOPHITISIS AND CUTANEOUS METASTASES: ATYPICAL PRESENTATION OF NON-SMALL CELL LUNG CARCINOMA

Hypereosinophilia is defined as an eosinophil count greater than 1.500 cells/mm. It is usually associated with organ dysfunction due to visceral eosinophilic infiltration or tissue damage mediated by eosinophilopoietic cytokines, like IL-5. Determining its etiology represents a diagnostic challenge, as numerous conditions are associated with its occurrence, especially parasitic diseases, allergic disorders, medications and neoplasms. Paraneoplastic eosinophilia usually develops in the context of tumors of the lower gastrointestinal tract, lung, Hodgkin's lymphoma, peripheral T-cell lymphomas (PTCL), and its pathophysiology is associated with interleukin-5 (IL-5) secretion, an eosinophil proliferation-inducing cytokine. To describe a clinical case of paraneoplastic hypereosinophiliadue to lung cancer, a rare laboratory manifestation, in a case with an advanced stage of the disease and catastrophic evolution. A 68-year-old woman, with a history of obesity and SAH, presents to the health service of the HC/FMUSP due to adynamia, dyspnea on exertion and perception of multiple violaceous cutaneous nodules on the scalp, thorax, abdomen and extremities, 45 days long. On physical examination, she had cutaneous-mucosal pallor, poor general condition, hypoxemia, and disseminated cutaneous nodules of up to 5 cm. Blood count revealed: Hb 8.9 g/d, Ht 26%, MCV 89 fl, 75.980 leukocytes/mm 3 (31.920 neutrophils with left shift to promyelocytes/ 40.270 eosinophils/ 0 basophils/ 2.280 lymphocytes/ 1.520 monocytes) and 107.000 platelets/mm 3 ; LDH = 592 U/L (NSV up to 214 U/L); IgE = 496 IU/mL (NSV up to 100 IU/mL). Myelogram showed hypercellular bone marrow with massive infiltration by elements of non-hematopoietic origin, as well as prominent medullary eosinophilia. Computed tomography (CT) showed an irregular lung mass, 5 cm in diameter, in the right upper lobe, suggestive of a primary neoplastic site, as well as secondary implants in the liver parenchyma, adrenal glands and subcutaneous cellular tissue/skin. Biopsy of subcutaneous nodules showed undifferentiated malignant neoplasm of epithelioid pattern, with immunohistochemistry: AE1/AE3 positive, 34BE12 positive, MELAN-1 negative, HMB45 negative, S100 negative, p63 negative, characterizing squamous cell carcinoma. During hospitalization, the patient rapidly evolved with tumor lisis syndrome, acute renal failure and fulminant liver failure, and died after a short period of hospitalization. We report an atypical case of pulmonary squamous cell carcinoma, marked by paraneoplastic eosinophilia, bone marrow infiltration, cutaneous metastasis, spontaneous tumor lysissyndrome and acute liver failure. Paraneoplastic hyperosinophilia is a marker associated withpoor prognosis in solid tumors, usually reflecting an elevated tumor mass, with multi-metastatic disease, as presented in our case. Although it is a rare condition, paraneoplastic eosinophilia mustfall within the differential scope of causes of sustained elevation of eosinophils. Rapid recognition and prompt treatment of the underlying neoplasm may provide a more favorable evolution.

S2909 A Rare Case of Acute Fulminant Liver Failure Caused by Body Building Supplements

Introduction: Creatine monohydrate is an ergogenic supplement that has been utilized by athletes to increase strength and performance. Creatine supplementation increases stores in muscle to facilitate ATP and phosphocreatine production, delaying onset of muscle fatigue. The use of Creatine has been linked to cases of cholestatic liver injury. We present a rare case of drug induced liver injury (DILI) leading to acute liver failure. Case Description/Methods: A 27 year old male with no PMH presented for evaluation of fatigue, chills, emesis and abdominal pain. He was hospitalized at another facility for markedly elevated transaminases and was transferred to our transplant liver center for evaluation of acute fulminant hepatic failure. On physical exam, the patient was altered with scleral icterus, his abdomen was soft and distended, with no significant organomegaly or signs of spider angiomas and asterixis, however, he was found to have stage 3 or 4 hepatic encephalopathy and required intubation. History was negative for alcohol use, ingestion of significant tylenol use, over-the-counter medications or prior liver disease history. Lab Work was significant for a total bilirubin at 26.9, AST 2829, ALT 3091, ammonia level 80, WBC count of 3.6, hemoglobin at 14.8, platelets 227,00, INR 6.4, PTT of 76.3 and tylenol level of 10. Workup for hepatitis, Wilson's disease, Alpha-1 Antitrypsin, and autoimmune serologies were all noted to be negative. He was given FFP and factor VII to help correct his coagulopathy. He started on lactulose and xifaxan. He ultimately required liver transplantation and developed post transplant complications of acute renal failure which eventually resolved. The patient was extubated and while seen in the outpatient setting where it was revealed that he took high doses of Creatine supplementation as an aid for basketball training. Discussion: Creatine induced liver injury is a rare complication only reported by a handful of case reports in the literature. Our case is unique and highlights a rare cause of DILI, as well as, the detrimental effects of ingesting a significant amount of Creatinine which ultimately caused Acute Liver Failure in a previously healthy patient. This case highlights the need for future studies that show accurate dosing for athletes in order to avoid liver toxicity as well as the importance of FDA regulations of such supplements. It is also important for physicians to keep in mind rarer causes of liver failure.

Современные подходы к диагностике и лечению острой печеночной недостаточности у взрослых (по данным EASL Clinical Practical Guidelines of the management of acute (fulminant) liver failure 2018–2019 in adult)

В статье приведены данные об этиологии, патогенезе, клинике, диагностике и лечении острой печеночной недостаточности как неотложного состояния в гепатологии, с которым приходится работать врачам-анестезиологам в отделении интенсивной терапии. Перечислены основные причины возникновения острой печеночной недостаточности, основные различия в постановке диагноза, приведены критерии оценки кандидатов на трансплантацию печени, а также основные подходы к лечению острой печеночной недостаточности и печеночной энцефалопатии согласно современным мировым рекомендациям.

Moving Forward to New Trends in Liver Transplantation

Liver transplantation (LT) is the only recognized effective treatment for end-stage liver disease (ESLD) and acute fulminant liver failure [...]

Survivor of maternal dengue shock syndrome with acute fulminant liver failure following liver dialysis

Survivor of maternal dengue shock syndrome with acute fulminant liver failure following liver dialysis

Thyroid Storm Treated With Nonconventional Therapy

Background: Thyroid storm is a rare sequela of thyrotoxicosis with mortality rate of 10-30%. Management of thyroid storm is heavily dependent on thionamides. Cholestyramine and potassium iodide (SSKI) are used as adjunctive therapy and not as the sole treatment for storm. We present a case of thyroid storm treated with cholestyramine and SSKI. Clinical Case: A 45 year old male with past medical history of atrial fibrillation, congestive heart failure, hypertension, substance abuse and grave’s disease presented to the emergency department (ED) for diarrhea. During the course of ED, patient went into atrial fibrillation with rapid ventricular rate. Chest X-ray showed pulmonary edema. Labs were: TSH <0.0025 mIU/L (0.35-4.94 mIU/L) and free T4 3.52 ng/dl (0.7-1.40 ng/dl). Patient was noncompliant with methimazole. Upon admit, ACLS was initiated due to hypoxia and transferred to ICU for ventilator and pressor support. Wartofsky score was 60, suggestive of thyroid storm. Management included methimazole 20mg every 4hours, hydrocortisone 100mg every 8 hours, cholestyramine 4mg every 6 hours, and SSKI 250mg every 6 hours for thyrotoxicosis and amiodarone infusion for afib. Despite normal liver enzymes on admit, day 3 AST increased to 2740 U/L (5-34) and ALT 2684 U/L (0-55). Methimazole was stopped due to potential hepatotoxicity. Day 3 free T4 remained high at 4.16 ng/dl and patient remained critically ill. Plasmapheresis was offered as methimazole was stopped and patient was hemodynamically unstable to undergo surgery. However, family declined this intervention; SSKI and cholestyramine were continued. Free T4 was monitored over the course of treatment; by day 5 free T4 trended down to 1.93 ng/dl. SSKI was eventually stopped on day 8 of treatment as free T4 had normalized and cholestyramine reduced to 4mg twice daily. By day 15, free T4 was 0.8 ng/dl, so cholestyramine was stopped. Due to clinical improvement, patient was weaned off the ventilator and pressor support along with hydrocortisone. Liver enzymes normalized by Day 17. Patient was restarted on methimazole 5mg daily before discharge. Discussion: Thyroid storm is associated with varying degree of liver dysfunction, which can pose a challenge to treatment. In our case, acute fulminant liver failure was multifactorial in the setting of shock, thyroid storm and potential drug toxicity. Thus, thionamides were contraindicated. Radioactive iodine treatment was contraindicated due to use of amiodarone. Plasmapheresis and emergent thyroidectomy could not be done. Thus, nonconventional therapy was used and patient responded well to treatment. This case emphasizes the use of cholestyramine along with SSKI as an effective treatment in patients who are critically ill the setting of a thyroid storm, especially when thionamides are contraindicated and other avenues of treatment are limited.

Acute (fulminant) liver failure: a clinical and imaging review.

Acute liver failure (ALF) is a rare clinical entity with high morbidity and mortality frequently requiring liver transplantation for survival. Imaging, particularly with ultrasound, plays an important role, especially to distinguish patients with underlying chronic liver disease who have lower transplant priority. We discuss the clinical and imaging findings in the three subtypes of ALF using a multi-modality approach with an emphasis on ultrasound.

S2509 Aortic Dissection - A Rare Cause of Acute Liver Failure

INTRODUCTION: Acute liver failure (ALF) is a medical emergency which needs to be treated urgently. An atypical presentation might delay appropriate medical care. ALF as a result of aortic dissection presents atypically, and requires high clinical suspicion. CASE DESCRIPTION/METHODS: A 37-year-old female was admitted for deranged liver function test (LFT) associated with her first onset of complex generalized tonic clonic seizure. She had no past medical history. There were no family history of seizure or liver disease, in particular Wilson’s disease or hemochromatosis. There was no recent acetaminophen or excessive alcohol consumption. Upon admission, her blood pressure was 99/75 mmHg and there were no clinically detectable jaundice, hepatic flap, Kayser-Fleischer rings or chest pain. Her transaminases showed a hepatitic pattern of deranged LFT (ALT 388 U/L and AST 378 U/L with normal serum bilirubin, ALP and INR). Abdominal Ultrasound excluded the presence of liver cirrhosis or biliary obstruction. Serologies for viral hepatitis (A, B, C, E; EBV and CMV) and anti-liver panel were all negative. Computed Tomography (CT) of the brain excluded intracranial bleeding or mass. Chest radiography showed soft-tissue opacity over right upper mediastinum (Figure 1a). ECG showed sinus tachycardia. Urgent bedside echocardiography excluded acute myocardial infarction and valvular heart disease. Within 12 hours after admission, she started to developed features of ischemic hepatitis and acute liver failure (new asterixis, prolonged INR of 1.7, worsening LFT with ALT 3430 U/L, AST 3000 U/L, bilirubin 170umol/L). She also developed oliguric AKI. Intravenous N-acetylcysteine was given in view of early hepatic encephalopathy and rapidly progressing acute liver failure. While she had no chest pain, her rising serum troponin and widened mediastinum prompted an urgent CT Aortogram. The CT Aortogram showed a 4.3cm dilatation of the ascending thoracic aorta with acute hemopericardium and cardiac tamponade (Figure 1b). She underwent an emergent ascending aorta and aortic arch repair and temporary renal dialysis. Both her kidney, liver and neurological function recovered following surgical repair. DISCUSSION: This case highlighted the importance of prompt identification of acute aortic dissection as the etiology of fulminant acute liver failure. Delayed or missed diagnosis could have been catastrophic. The presence of neurological sequelae very early in the clinical presentation is a harbinger for an ischemic cause.Figure 1.: Chest X-ray showed a soft tissue opacity over the upper right mediastinum. This was further delineated on CT Aortogram to be an ulcerated ascending aorta dilatation.Figure 2.: Patchy diffuse hypoenhancement of the liver, gallbladder edema and ascites were seen on CT.