Respiratory symptoms are the most common manifestation of COVID-19 across all age groups and it is most often associated with radiographical findings consistent with pneumonia.2 A recent systematic review estimated that 16% of children with SARS-CoV-2 infection are asymptomatic,3 or others may present with seizures, gastrointestinal bleeding or jaundice. This reports a 2-year old boy with no known co-morbidity who had a 2-week history of abdominal pain and jaundice then had a rapidly progressive course of neurological deterioration and eventual demise. He had markedly elevated liver enzymes and deranged bleeding parameters with elevated ammonia and ferritin levels. Hepatitis B and hepatitis A titers were non-reactive. He was managed as a case of hepatic encephalopathy secondary to cholestatic jaundice. His chest x-ray was normal but his SARS-CoV-2 RT PCR result was positive with a low cycle threshold. Locally, this is the first reported case of SARS-CoV-2 RT-PCR positive pediatric patient presenting as fulminant hepatic failure with no associated respiratory manifestations. Clinicians should be mindful that such presentation, however uncommon, is possible and a high index of suspicion should be maintained.
COVID-19 ; SARS-CoV-2 ; Liver Failure ; Massive Hepatic Necrosis

No abstract available.
Adult ; Female ; Humans ; Liver Transplantation ; Magnetic Re ; Massive Hepatic Necrosis/*pathology ; Tomography, X-Ray Computed

Two cases in which postoperative hepatic necrosis followed by halothane(fulthane) anesthesia are presented. Case 1 was 3 dar-old neonate who was performed corrective surgery for jejunal atresia under the halothane anesthesia. He was placed with hyperalimentation just after operation, and was relatively well. He died on postoperative 11 days. Necropsy matrial was obtained from liver. Histologic finding of liver disclosed massive cental hemorrhagic necrosis. Case 2 was a 17 year-old boy who was performed corrective open heart surgery for TOF under the halothane anesthesia, He developed oliguria just after operation. On postoperative 1 day, hepatocellular and renal dysfunction were found, and peritoneal diaysis performed. He died on postoperative 3 day. Necropsy matrials were obtained from liver and kidney-Liver disclosed massive central hemorrhagic necrosis. Kidney showed intact glomeruli and proximal and distal convoluted tubular cells were degenerated. The configuration of tubular basement membrane was not clear. These considered to be acute tubular necrosis, ischemic type.
Adolescent ; Anesthesia* ; Basement Membrane ; Halothane* ; Humans ; Infant, Newborn ; Intestinal Atresia ; Kidney ; Liver ; Male ; Massive Hepatic Necrosis* ; Necrosis ; Oliguria ; Thoracic Surgery

BACKGROUND: To the best of our knowledge, the report on Amanita subjunquillea poisoning has not been found in the medical literature. We investigated the clinical aspects of Amanita subjunquillea poisoning. METHODS: Sixteen subjects who had ingested the mushroom (A. subjunquillea) were examined for clinical features, laboratory and radiologic findings prospectively. RESULTS: The mean incubation period was 11.5 hours(range: 3 to 17 hours). The initial presentations were gastrointestinal symptoms which persisted for 2 to 4 days. The transaminase levels were elevated in all subjects and peaked on day 3 after ingestion of the mushrooms (mean AST/ALT levels : 3241 IU/L and 3741 IU/L, respectively). Biochemical evidence of pancreatitis and disseminated intravascular coagulation were frequent (83.3% and 62.5%, respectively). Liver ultrasonography and scintigraphy revealed abnormalities in most cases. Massive hepatic necrosis was confirmed by liver biopsy in one subject. The overall mortality was 12.5%. CONCLUSION: Clinical manifestations of A. subjunquillea poisoning were similar to those of other poisonous Amanitaceae intoxication. However, the mortality rate was lower in A. subjunquillea poisoning. Our data showed strong evidence that A. subjunquillea should be classified in the group of poisonous mushrooms.
Agaricales ; Amanita* ; Biopsy ; Disseminated Intravascular Coagulation ; Eating ; Liver ; Massive Hepatic Necrosis ; Mortality ; Pancreatitis ; Poisoning* ; Prospective Studies ; Radionuclide Imaging ; Ultrasonography

The incidence of severe hepatitis A virus (HAV) infection has been increasing. However, clinicopathologic features of severe HAV infection that lead to liver transplantation (LT) have not been reported in Korea. We retrieved 16 LT cases with HAV infection during the last 3 years at Asan Medical Center, Seoul, Korea. Fifteen cases progressed to hepatic encephalopathy. Thirteen cases survived with or without complications, and three patients died of sepsis. The explanted liver showed massive or zonal necrosis with moderate to severe cholestasis. The zonal distribution of necrosis was frequently associated with endothelialitis of portal and/or central veins. Degenerative changes of hepatocytes were various in degree and distribution. Viral inclusions were suspected in two cases. Although HAV infection is usually confirmed by serological tests, significant venulitis of central and/or portal veins and viral inclusions, which are rarely observed, can suggest an HAV infection as a cause of massive hepatic necrosis of unknown mechanism.
Cholestasis ; Fluconazole ; Hepatic Encephalopathy ; Hepatitis ; Hepatitis A ; Hepatitis A virus ; Hepatocytes ; Humans ; Incidence ; Korea ; Liver ; Liver Transplantation ; Massive Hepatic Necrosis ; Necrosis ; Portal Vein ; Sepsis ; Serologic Tests ; Veins

Animals ; Immunoglobulin A, Secretory ; metabolism ; Intestines ; drug effects ; metabolism ; Male ; Massive Hepatic Necrosis ; metabolism ; Mice ; Mice, Inbred BALB C ; Tumor Necrosis Factor-alpha ; pharmacology

Despite recent improvements in operative techniques, immunosuppression and organ procurement, failure of a hepatic allograft remains an important risk to liver recipients. In the absence of any effective method of extracorporeal support, the only alternative to death for these patients is retransplantation. The causes of hepatic allograft failure were listed as primary nonfunction, technical included hepatic artery thrombosis or portal vein thrombosis, and rejection. Hepatic artery thrombosis remain one of most serious complication after liver transplantation and can be associated with one of three typical syndrome: acute, massive hepatic necrosis, biliary tract necrosis and leakage, relapsing bacteremia. The early diagnosis of hepatic artery thrombosis is very important and screening with duplex ulrtasound can allow the recognition of early hepatic artery thrombosis. The emgent revascularization of hepatic artery thrombosis in asymptomatic patient and retransplantation in symptomatic patient lead to improved graft salvage and patient survival. We report one case of hepatic retransplantation due to hepatic artery thrombosis. The patient with 30 years old man underwent primary hepatic transplantation due to liver cirrhosis with hepatocellular carcinoma. After 6th postoperative day of primary transplantation, liver transaminase began to elevate and not responded to steroid pulse therapy. Thereafter bile leakage, evident in T-tube cholangiogram was noted. Explolaparotomy was performed and showed hepatic artery thrombosis and necrosis of donor aspect of extrahepatic biliary tree. On next day, retransplantation was performed. Thereafter secondary graft function was slowly regained but the patient was recoverd and discharged.
Adult ; Allografts ; Bacteremia ; Bile ; Biliary Tract ; Carcinoma, Hepatocellular ; Early Diagnosis ; Hepatic Artery ; Humans ; Immunosuppression ; Liver ; Liver Cirrhosis ; Liver Transplantation ; Mass Screening ; Massive Hepatic Necrosis ; Necrosis ; Thrombosis ; Tissue and Organ Procurement ; Tissue Donors ; Transplants ; Venous Thrombosis

PURPOSE: Although there has been recent progress in surgical techniques, such as perioperative management, immunosuppresive regimen and intervention radiology, a liver retransplantation remains as the only therapeutic option for patients with a failing liver allograft. The purpose of this study was to review our clinical experiences of liver retransplantation, performed at the Asan Medical Center. METHODS: Between August 1992 and March 2001, 400 cases of liver transplantations, including 331 in adults and 69 in pediatrics, were performed. Of the 331 adult cases, 10 cases of liver retransplantation, during the same period, were retrospectively analyzed. RESULTS: In the 331 cases of adult liver transplantation, 232 cases of living donor and 99 of cadaveric liver transplantations were carried out. The 331 adult cases also included 10 liver retransplantations. Therefore, the overall liver retransplantation rate was 3%. Primary non-function (PNF) was the leading cause of retransplantation. The conversion of living donor liver transplantation to a cadaveric liver retransplantation was the most common type of retransplantaion, with a cadaveric to cadaveric type the second most common. The in-hospital mortality was 40%. The causes of in-hospital mortality were hepatic artery pseudoaneurysm rupture, Aspergillus pneumonia, and multiple organ failure, initiated by jejuno-jejunostomy site bleeding and massive hepatic necrosis. CONCLUSION: In the current era of extreme organ shortage, retransplantation is the only therapeutic alternative for irreVersible graft failure, especially if the patient has no multiple organ failure (MOF) prior to the operation. Therefore, the careful selection of patients for a retransplantation is required. They should be given superurgent priority if the circumstances permit, and living donor liver transplantation (LDLT) offer a promising alternative.
Adult ; Allografts ; Aneurysm, False ; Aspergillus ; Cadaver ; Chungcheongnam-do ; Hemorrhage ; Hepatic Artery ; Hospital Mortality ; Humans ; Liver Transplantation ; Liver* ; Living Donors ; Massive Hepatic Necrosis ; Multiple Organ Failure ; Pediatrics ; Pneumonia ; Retrospective Studies ; Rupture ; Transplants

Aplastic anemia following acute hepatitis or acute hepatic failure is an uncommon disease and has a poor prognosis. We experienced a case of aplastic anemia following acute hepatic failure in a 10- year-old girl. She was admitted because of jaundice and lethargy for 8 days. Laboratory findings revealed marked elevated serum transaminases and bilirubin levels, prolonged prothrombin time and partial thromboplastin time, and massive hepatic necrosis on the pathological study. There was no evidence of metabolic, toxic or autoimmune hepatitis. During the treatment of acute hepatic failure, pancytopenia developed and marked hypocellularity of all hematopoietic elements in bone marrow was revealed. She recovered partially from aplastic anemia after treatment with anti-thymocyte globulin, corticosteroid and cyclosporine.
Anemia, Aplastic* ; Antilymphocyte Serum ; Bilirubin ; Bone Marrow ; Cyclosporine ; Female ; Hepatitis* ; Hepatitis, Autoimmune ; Humans ; Jaundice ; Lethargy ; Liver Failure* ; Liver Failure, Acute ; Massive Hepatic Necrosis ; Pancytopenia ; Partial Thromboplastin Time ; Prognosis ; Prothrombin Time ; Transaminases

We report the computed tomographic and angiographic findings in the case of a recently obtained successful clinical outcome after embolization of the hepatic artery in the case of a snakebite causing hemoperitoneum associated with hepatic necrosis and rupture with active bleeding.
Aged, 80 and over ; Contrast Media/administration & dosage ; Embolization, Therapeutic/*methods ; Female ; Fibrin Foam/therapeutic use ; Follow-Up Studies ; Hemoglobins ; Hemoperitoneum/*etiology/therapy ; Hemorrhage/etiology/therapy ; Hepatic Artery/radiography ; Humans ; Korea ; Liver/*injuries/pathology/radiography ; Massive Hepatic Necrosis/complications/*etiology/therapy ; Radiographic Image Enhancement/methods ; Rupture, Spontaneous ; Snake Bites/*complications ; Tomography, X-Ray Computed/*methods ; Treatment Outcome ; Viper Venoms/adverse effects