Clinical features analysis of 105 children with liver failure

Clinical features analysis of 105 children with liver failure | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Research Article Clinical features analysis of 105 children with liver failure Leilei Chen, Yucan Zheng, Guorui Hu, chen leilei, Yan Lu, Zhi-feng Liu This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-4158601/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Objective To study the clinical features of pediatric liver failure and provide reference for diagnosis and prevention. Methods Clinical data of children diagnosed with liver failure at XX Hospital from 2012 to 2023 were collected and statistically analyzed. Results Among 105 cases of liver failure in children, the age ranged from 1 day to 14 years and 11 months, with a median age of 1 year and 9 months. There were 67 males and 38 females, with acute and subacute liver failure accounting for 82.8%. The most common causes were hereditary metabolic diseases (24 cases, 22.9%), followed by infection factors (12 cases, 11.4%), and biliary diseases (10 cases, 9.5%). However, the cause remained unknown in 34.3% of cases. The most common clinical manifestations were poor appetite, fever, and jaundice. The main complications were hepatic encephalopathy, electrolyte disorders, and infection. There was no statistically significant difference in age, albumin, blood ammonia, presence of hepatic encephalopathy, ALT, and GGT between the survival group and the 28-day mortality group (P>0.05). The survival group had lower PELD/MELD scores, total bilirubin, and INR, and higher platelet count compared to the 28-day mortality group, with statistically significant differences (P<0.05). Conclusion Hereditary metabolic diseases, infection, and biliary diseases are common causes of pediatric liver failure. MELD/PELD scores can predict the prognosis of liver failure. Clinical feature analysis and MELD/PELD scores are helpful in guiding clinical diagnosis, treatment, and prognosis assessment. Children liver failure hereditary metabolic disease infection biliary malformation Introduction Liver failure is a severe liver damage caused by various factors, leading to severe impairment or compensation failure of synthesis, detoxification, metabolism, and biotransformation functions, resulting in a group of clinical syndromes characterized by jaundice, coagulation dysfunction, hepatorenal syndrome, hepatic encephalopathy, and ascites [1]. As one of the rare clinical diseases, pediatric liver failure is difficult to treat clinically and has a high mortality rate. To explore the clinical features of pediatric liver failure, we conducted a retrospective analysis of the data of 105 cases of pediatric liver failure admitted to XX Hospital, and the results are reported as follows. Objects and Methods 1.1 Objects From February 2012 to February 2023, a total of 105 cases of diagnosed liver failure in children were admitted to XX Hospital. The age range was from 1 day to 14 years and 11 months, with a median age of 1 year and 9 months. There were 67 males and 38 females.1.2 observed indicator 1.2 Observation indicators The laboratory tests conducted during the diagnosis of liver failure in admitted patients included complete blood count (leukocyte, WBC; platelet, PLT), biochemical markers (glutamic-pyruvic transaminase, ALT; total bilirubin, TBIL; glutamic oxaloacetic transaminase, AST; albumin, ALB), prothrombin time/Prothrombin activity (PT/PA), fasting blood sugar (GLU), international normalized ratio (INR), and glutamyl transferase (GGT). In addition, some patients underwent blood and urine genetic metabolic and gene testing using gas chromatography-mass spectrometry (GC-MS). Complications that occurred during the course of the disease included multiple organ dysfunction syndrome (MODS), infection, electrolyte imbalance, hypoglycemia, hepatic encephalopathy, ascites, gastrointestinal bleeding, and hepatorenal syndrome. 1.3 Diagnostic criteria The Diagnosis and Treatment Guidelines for Liver Failure (2018 Edition) formulated by the Chinese Society of Infectious Diseases, currently serve as the basis for the diagnosis, treatment, and classification of pediatric liver failure in China. 1.4 Treatment approach: Firstly, treatment is based on the etiology. For all cases, measures are taken to correct coagulation disorders, preserve liver function, alleviate jaundice, administer albumin, reduce intracranial pressure, lower blood ammonia levels, provide anti-infection protect vital organs, etc. 1.5 Statistical methods Statistical analysis was conducted using EXCEL 2000 and SPSS 26.0 software. Normally distributed continuous data were expressed as mean ± standard deviation (x ± SD), and between-group comparisons were performed using the t-test. Non-normally distributed continuous data were expressed as median (interquartile range), and between-group comparisons were performed using the Mann-Whitney U test. Categorical data between two groups were compared using the chi-square test. A p-value < 0.05 was considered statistically significant. Results 2.1 General information From February 2012 to February 2023, XX Hospital admitted a total of 105 pediatric patients diagnosed with liver failure, with ages ranging from 0.09 to 14.92 years, with an average age of 4.17 years and a median age of 1.75 years. Among them, there were 67 males and 38 females. Among the patients, there were 37 cases (35.2%) younger than 1 year old, 26 cases (24.8%) between 1 and 3 years old, 13 cases (12.4%) between 3 and 7 years old, 18 cases (17.1%) between 7 and 12 years old, and 11 cases (10.5%) between 12 and 18 years old. The length of hospital stay ranged from 1 to 64 days, with an average of 19.25 days and a median of 17 days (Table 1 ). Table 1 Age distribution characteristics of 105 pediatric patients Age(years) Cases Age distribution rate(%) 0 ~ 1 37 35.2 1 ~ 3 26 24.8 3 ~ 7 13 12.4 7 ~ 12 18 17.1 12 ~ 18 11 10.5 合计 105 100 2.2 Disease classification Acute liver failure accounted for 60 cases (57.1%), subacute liver failure for 27 cases (25.7%), subacute-on-chronic liver failure for 8 cases (7.6%), and chronic liver failure (cirrhosis) for 10 cases (9.5%). Acute and subacute liver failure together accounted for 82.8% of all liver failure cases. (Table 2 ). Table 2 Distribution characteristics of disease subtypes in 105 pediatric patients Disease classification Cases rate(%) Acute liver failure 60 57.1 subacute liver failure 27 25.7 acute-on-chronic liver failure 8 7.6 chronic liver failure 10 9.5 total 105 100 2.3 Etiology analysis Among the 105 patients, there were 24 cases (22.9%) of genetic metabolic diseases, including 2 cases of urea cycle disorders, 3 cases of citrullinemia, 1 case of tyrosinemia, 1 case of arthrogryposis, renal dysfunction, and cholestasis syndrome (ARC syndrome), 2 cases of progressive familial intrahepatic cholestasis, 5 cases of Wilson's disease, and 2 cases of type 2 infantile liver failure syndrome. There was 1 case of congenital bile acid synthesis disorder, 1 case of Alagille syndrome, and 6 cases of other genetic metabolic diseases. In terms of infection factors, there were 12 cases (11.4%), including 6 cases of sepsis, 2 of which were combined with Epstein-Barr virus infection, 1 case of hepatitis B virus infection, 1 case of measles virus infection, 1 case of varicella-zoster virus combined with Epstein-Barr virus infection, 1 case of influenza virus infection, and 2 cases of other hepatotropic virus infections. There were 10 cases (9.5%) of biliary diseases, including 8 cases of cholestasis, 1 case of choledocholithiasis, and 1 case of cholangitis. There were 6 cases (5.7%) of congenital malformations, 4 cases (3.8%) of autoimmune hepatitis, 3 cases (2.9%) of circulatory failure, 3 cases (2.9%) of drug-related liver injury, including 1 case caused by acetaminophen, 1 case caused by anti-tuberculosis drugs, and 1 case caused by traditional Chinese medicine. There were 2 cases (1.9%) of anorexia nervosa, 2 cases (1.9%) of hemophagocytic syndrome, 1 case (1%) of autoimmune disease, 1 case (1%) of poisoning, 1 case (1%) of tumor, and 36 cases (34.3%) with unknown causes (Table 3 ). Table 3 Clinical characteristics of children with different etiologies metabolic disorders(n = 24) Infection(n = 12) biliary tract disease(n = 10) Malformation(n = 6) Other Diagnostics(n = 17) known cause (n = 69) unknown cause(n = 36) P Gender (male/female) 13/11 10/2 9/1 4/2 7/10 46/23 21/15 0.143 a Age (years), median 2.6(0.5,9.1) 1.7(0.8,6.5) 1.5(0.7,9.8) 0.7(0.6,2.6) 5.8 ± 5.6 1.6(0.8,8.7) 2.1(0.9,5.1) 0.766 b Infant (n=) 7 5 4 4 4 24 13 Kindergarten(n=) 5 2 3 1 5 16 10 preschool period(n=) 2 1 0 1 2 6 7 school age(n=) 7 4 2 0 3 16 2 adolescence(n=) 3 0 1 0 3 7 4 INR 2.5(1.9,3.0) 2.2 ± 1.3 2.0 ± 0.8 2.1 ± 0.9 2.0(1.2,3.4) 2.0(1.5,3.0) 2.0(1.4,2.9) 0.893 b ALT 315.0(70.0,1140.0) 1519.5(428.3, 3507.5 ) 153.0(103.8,1674.8 339.0 ± 347.4 1505.0(136,4431.0) 491.0(104.5,2092.5) 1508.0(593.5,3129.6) 0.001 b hepatic encephalopathy(n=) 7(36.8%) 6(50%) 3(30%) 1(16.7%) 4(36.4%) 26(37.7%) 16(44.4%) 0.412 b TBIL 139.3 ± 135.9 74.6 ± 60.4 275.4 ± 265.6 347.7 ± 229.1 50(25.8,97.1) 123.1(32.9,249.3) 114.3(35.9,185.0) 0.926 b GGT 56(29,157) 144.3 ± 125.1 119.1 ± 81.2 110 ± 88.1 136.0 ± 117.6 82.0(39.5,176.0) 95.5(56.8,156.8) 0.223 b blood ammonia 92.6 ± 61.2 85.4 ± 51.1 100.8 ± 57.4 38.5(28.3,81.0) 62(46.5,86) 69.0(46.3,113.5) 76 ± 44.9 0.708 b PLT 87.0(51.0,324.0) 226.5 ± 147.2 233.6 ± 132.6 107.0 ± 54.2 160.8 ± 152.6 153.0(71.0,312.0) 207.6 ± 139.0 0.421 b albumin 35.4 ± 7.0 37.5 ± 5.5 38.1 ± 4.6 33.9 ± 6.7 40.2(36.1,43.5) 36.4 ± 6.8 39.6 ± 6.6 0.049 b a Comparing total diagnosis and uncertainty using independent sample t-tests b Comparing total diagnosis and uncertainty using Mann Whitney U-test INR: International normalized ratio ; ALT:glutamic-pyruvic transaminase;ALT:glutamic-pyruvic transaminase; TBIL: total bilirubin; GGT: Glutamyl transferase;PLT: Blood platelet 2.4 Clinical manifestations of liver failure at onset include a decrease in appetite, which is the most common presentation (96.2%), followed by fever (75.3%), visible jaundice (71.4%), and various neurological abnormalities such as lethargy, seizures, irritability, consciousness and behavioral disorders (53.3%). Other common symptoms include nausea, vomiting, diarrhea, and abdominal distension (52.4%).In terms of physical signs, hepatomegaly (enlarged liver) is observed in 75.2% of cases, splenomegaly (enlarged spleen) in 39.0% of cases, and hepatosplenomegaly (enlarged liver and spleen) in 34.3% of cases. 2.5 Analysis of the Characteristics of Complications. Electrolyte disturbances were observed in 63 cases (60%), which were the most common. Among these 63 cases, 35 cases (33.3%) had hyponatremia, 47 cases (44.8%) had hypocalcemia, 26 cases (24.8%) had hypokalemia, 4 cases (3.8%) had hyperkalemia, 23 cases had hypochloremia, and 15 cases (14.3%) had hypophosphatemia. Additionally, there were 62 cases (59%) of hypoalbuminemia. In 42 cases (40%), hepatic encephalopathy was observed. Ascites was present in 37 cases (35.2%), and pleural effusion was present in 32 cases (30.5%). Among them, 23 cases (21.9%) had both ascites and pleural effusion. Other site infections were observed in 62 cases (59%), with sepsis, respiratory tract infections, and gastrointestinal infections being the most common. Petechiae and ecchymosis were present in 35 cases (33.3%). Peripheral edema was observed in 26 cases (24.8%). Thrombocytopenia was seen in 32 cases (30.5%). Hypoglycemia was present in 34 cases (32.4%). Multiple Organ Dysfunction Syndrome (MODS) was observed in 19 cases, accounting for 18.1%. 11 cases (10.5%) presented with gastrointestinal bleeding, characterized by vomiting of coffee-colored material, melena, and the presence of red blood cells and positive fecal occult blood tests. There were 9 cases (8.6%) of liver cirrhosis. Liver-kidney syndrome was observed in 9 cases (8.6%), all of which exhibited oliguria (reduced urine output) and elevated levels of blood urea nitrogen and serum creatinine. 2.6 Outcome and prognosis. Among the 105 cases, 83 cases (79%) showed improvement, 20 cases (19.1%) resulted in death, and 2 cases (1.9%) were transferred to another hospital. Based on the survival status of the children on the 28th day, they were categorized as follows: Survival group (83 cases): Patients whose condition improved, transferred from the ICU to a general ward, and discharged. Death group (20 cases): Patients who died during the 28-day observation period. In the survival group, the PELD/MELD score, total bilirubin, and INR (International Normalized Ratio) were lower compared to the death group, while platelet count was higher, with statistically significant differences (P 0.05) between the two groups in terms of age, albumin level, blood ammonia level, presence of hepatic encephalopathy, ALT (alanine aminotransferase), and GGT (gamma-glutamyl transferase), as shown in Table 4 .Among the 89 cases with a PELD/MELD score below 30, 13 cases (14.6%) resulted in death. Among the 10 cases with a score between 30 and 40, 5 cases (50%) resulted in death. Among the 4 cases with a score above 40, 2 cases (50%) resulted in death. As the score increased, the mortality rate also increased ( Table 5 ).The prognostic evaluation of liver failure in children, as assessed by the ROC curve, yielded an AUC (Area Under the Curve) value of 0.753 (P < 0.001). The standard error was 0.064, with a 95% confidence interval of (0.627–0.879). Table 5 The outcome of the disease in the PELD/MELD scoring system PELD/MELD n death(n, %) 0～30 89 13(14.6%) 30～40 10 5(50%) >40 4 2(50%) Discussion Pediatric liver failure is a rare clinical condition with a low incidence rate but a high mortality rate. Currently, there is a lack of epidemiological studies on pediatric liver failure in China. Some related studies only focus on acute liver failure in children. In the United States, it is estimated that there are 500–600 cases of acute liver failure in children per year in the entire population. The incidence of Pediatric Acute Liver Failure (PALF) in the United States does not vary by region and has remained stable over the past decade [ 2 ]. There is no statistically significant difference in the incidence rates between different regions over a span of six years [ 2 ]. The etiology of pediatric liver failure is complex and difficult to determine. The most common cause of liver failure is genetic metabolic disorders, accounting for 24 cases (22.9%). Infection factors are the second most common, accounting for 12 cases (11.4%), followed by biliary diseases in 10 cases (9.5%), congenital malformations in 6 cases (5.7%), and autoimmune hepatitis in 4 cases (3.8%), among others. However, approximately 34.3% of the cases still have an unknown etiology. This conclusion is consistent with the research findings from the National University of Singapore, Institute of Pediatrics [ 3 ]. Consistent with the results of a prospective, multicenter study conducted abroad, over one-third of pediatric acute liver failure patients have an unknown etiology. Despite advancements in diagnostic methods, this proportion reaches two-thirds in patients between the ages of 1 and 5 with acute liver failure [ 4 – 6 ]. Given the fact that children, especially infants and young children, have a lower immune function and lower levels of peripheral blood antibodies, it becomes difficult to detect pathogen-specific antibodies. Additionally, children with liver failure have impaired coagulation function, increasing the risk of bleeding. Pathological examination cannot determine the cause through liver puncture. Studies in the United States and Europe have observed that acetaminophen poisoning is the most common cause of acute liver failure in children [ 6 – 8 ]. Inherited metabolic liver diseases can occur at any age, such as Wilson's disease (hepatolenticular degeneration), tyrosinemia, and infantile liver failure syndrome.According to reports, Wilson's disease is the most common inherited metabolic disease causing liver failure in children [ 9 ]. In this study, all 5 cases of hepatolenticular degeneration occurred during the school-age period, accounting for 27.8% of liver failure cases in this age group. Therefore, Wilson's disease should be a particular focus for children with liver failure in this age group. A high proportion of infectious etiology was observed in school-age children (22.2%), while in all other age groups, the percentage of infectious causes was roughly similar among all cases (11.8% in infancy, 7.6% in early childhood, 7.7% in preschool period, and 9.1% in adolescence). Congenital developmental abnormalities generally manifest in infancy (4 cases in infancy, accounting for 66.7% of congenital developmental abnormalities). Prolonged jaundice after birth leads to complications such as liver cirrhosis, ascites, and infections, ultimately resulting in liver failure. The most common causes of liver failure in infants with congenital developmental abnormalities are biliary atresia and congenital choledochal cysts. In this study, all 6 cases of congenital developmental abnormalities were biliary atresia, which is an important cause of liver failure in the infant group. It has been observed that an increasing number of autosomal recessive inherited monogenic diseases affect intracellular transport and vesicular trafficking, which are becoming important factors in patients with acute liver failure (ALF) of unknown etiology. Reducing the proportion of liver failure cases with unknown causes remains a challenge. Out of 34 patients, whole-genome sequencing was performed. Diagnosis was established in 18 children, and genetic variants associated with inherited metabolic liver diseases were identified, including SLC25A13 , JAG1 , USP53 , AKR1D1 , NBAS , OTC , ATP7B , VPS33B , ABCB4 , among others. Additionally, gene variations in GPR82 , ATP11C , NCOA6 , ALMS1 , etc., were discovered, but there are currently no related literature reports on their association with childhood liver failure. More research is needed to elucidate the potential of whole-exome/genome sequencing in the management of childhood liver failure, including its use as a means for early diagnosis and assessment. Early diagnosis of liver function failure is crucial for treatment and prognosis. The most common presenting symptom is decreased appetite, accounting for 96.2%. Fever is the second most common symptom (75.3%), followed by jaundice (71.4%). Among these cases, sepsis, respiratory tract infections, and gastrointestinal infections are the most frequently observed, with some cases involving biliary infections. One case of bile peritonitis was identified. These findings are similar to those reported by the PLA General Hospital [ 10 ] and studies from Turkey [ 9 ]. Currently, effective treatment options for pediatric acute liver failure include medication, artificial liver support, and even liver transplantation. However, the overall mortality rate of pediatric acute liver failure is reported to range between 20% and 50%, indicating poor clinical outcomes [ 11 – 14 ]. In this dataset, there were 20 deaths (19.1%), which is consistent with international reports. In this study, the serum total bilirubin levels of the deceased children were significantly higher than those of the surviving children, which is consistent with previous research findings [ 15 , 16 ]. The massive necrosis of liver cells inhibits the conversion of unconjugated bilirubin to conjugated bilirubin, and the accumulation of bile can lead to elevated levels of conjugated bilirubin in the blood. The combined effect of these factors results in an elevation of total bilirubin levels [ 17 ]. This plays an important role in predicting prognosis. The liver synthesizes most of the clotting factors, and the significant decrease in clotting factors due to liver cell necrosis leads to abnormal coagulation function. This results in an increased INR (international normalized ratio) value, which is an important diagnostic and prognostic indicator for liver failure. In this study, the INR levels of the deceased children were significantly higher than those of the surviving children, which is consistent with related research findings [ 18 , 19 ]. The PELD/MELD scoring system utilizes objective parameters to assess the condition of liver failure patients and provides an accurate reflection of their disease severity. It is widely used in the management of end-stage liver disease patients [ 20 ]. Studies suggest that the PELD/MELD system is superior to other scoring systems in predicting patient prognosis [ 11 , 21 ]. The relationship between PELD/MELD scores and the 3-month mortality rate of end-stage liver disease patients is as follows: ≤30 points, 40% mortality rate; >30 to < 40 points, 72% mortality rate; ≥40 points, 100% mortality rate. This indicates that PELD/MELD can accurately assess the severity of end-stage liver disease and effectively predict the short-term prognosis of liver failure patients [ 22 ]. The PELD/MELD scores in the deceased group were higher than those in the surviving group (P < 0.001), and the higher the score, the higher the mortality rate (Table 5 ). Furthermore, the area under the receiver operating characteristic (ROC) curve (AUC) for the prognostic evaluation of pediatric liver failure patients was 0.753 (P < 0.001), with a standard error of 0.064 and a 95% confidence interval of 0.627 to 0.879. This suggests that the PELD/MELD scoring system has a good evaluation performance. The receiver operating characteristic (ROC) curve analysis of the PELD/MELD scoring system confirms its good evaluation capability. conclusion Currently, both the basic and clinical research on pediatric liver failure lag behind that of adults. So far, there is no globally accepted guideline for pediatric liver failure. It is essential to pay attention to clinical and basic research related to pediatric liver failure. This study indicates that genetic metabolic disorders, infections, and biliary anomalies are common causes of pediatric liver failure. The MELD or PELD scoring systems can predict the prognosis of liver failure in children. The clinical characteristic analysis of pediatric liver failure and the application of MELD or PELD scores will help guide clinical diagnosis, treatment, and prognosis assessment. Declarations ETHICS APPROVAL AND CONSENT TO PARTICIPATE We have cancelled the patient's details.We have obtained the parents’ consent and signatures on the informed consent form. This study was approved by the Ethics Committee of Nanjing Children's Hospital, Nanjing, China(202311016-1). CONSENT FOR PUBLICATION Not applicable. AVAILABILITY OF DATA AND MATERIALS The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request. COMPETING INTERESTS The authors declare that they have no competing interests. AUTHOR CONTRIBUTIONS LC and YZ contributed to the study design, data collection, analysis, and manuscript preparation. GH,JZ and YL contributed to data analysis, manuscript preparation, and revised the manuscript. ZL contributed to the study design and critically revised the manuscript. All authors read and approved the final manuscript. References Liver Failure And Artificial Liver Group Chinese Society Of Infectious, Severe Liver Disease And Artificial Liver Group Chinese Society Of Hepatology. 肝衰竭诊治指南(2018年版)[J]. 实用肝脏病杂志, 2019,22(02):164-171. Kulkarni S, Perez C, Pichardo C, et al. Use of Pediatric Health Information System database to study the trends in the incidence, management, etiology, and outcomes due to pediatric acute liver failure in the United States from 2008 to 2013[J]. Pediatr Transplant, 2015,19(8):888-895. Chiou F K, Logarajah V, Ho C, et al. Demographics, aetiology and outcome of paediatric acute liver failure in Singapore[J]. Singapore Med J, 2022,63(11):659-666. Alonso E M, Horslen S P, Behrens E M, et al. Pediatric acute liver failure of undetermined cause: A research workshop[J]. Hepatology, 2017,65(3):1026-1037. Lenz D, Horby J M, Kelly D, et al. Etiology and Outcome of Adult and Pediatric Acute Liver Failure in Europe[J]. J Pediatr Gastroenterol Nutr, 2023,77(1):115-120. Di Giorgio A, Gamba S, Sansotta N, et al. Identifying the Aetiology of Acute Liver Failure Is Crucial to Impact Positively on Outcome[J]. Children (Basel), 2023,10(4). Kathemann S, Bechmann L P, Sowa J P, et al. Etiology, outcome and prognostic factors of childhood acute liver failure in a German Single Center[J]. Ann Hepatol, 2015,14(5):722-728. Fontana R J. Acute liver failure including acetaminophen overdose[J]. Med Clin North Am, 2008,92(4):761-794. Baris Z, Saltik T I, Uslu N, et al. Acute liver failure in children: 20-year experience[J]. Turk J Gastroenterol, 2012,23(2):127-134. 朱世殊张鸿飞陈菊梅杨晓晋徐志强. 儿童肝衰竭临床特征的研究[J]. 中华实验和临床病毒学杂志, 2004(04). Nunez-Ramos R, Montoro S, Bellusci M, et al. Acute Liver Failure: Outcome and Value of Pediatric End-Stage Liver Disease Score in Pediatric Cases[J]. Pediatr Emerg Care, 2018,34(6):409-412. Chapin C A, Horslen S P, Squires J E, et al. Corticosteroid Therapy for Indeterminate Pediatric Acute Liver Failure and Aplastic Anemia with Acute Hepatitis[J]. J Pediatr, 2019,208:23-29. Wands D, Tayler R, Kelly D, et al. Infantile acute liver failure in the West of Scotland[J]. Arch Dis Child, 2020,105(8):794-796. Yankol Y, Ertugrul M, Kanmaz T, et al. Management of Pediatric Acute Liver Failure in a Region With Insufficient Deceased Donor Support: A Single-Center Experience[J]. Exp Clin Transplant, 2016,14(5):535-541. 苗敏, 钱素云. 儿童急性肝衰竭病因及转归相关因素分析[J]. 中华实用儿科临床杂志, 2019,34(19):1462-1466. 罗兰, 刘萍萍, 隆彩霞, 等. 重症儿童急性肝衰竭预后的相关因素[J]. 中华实用儿科临床杂志, 2019,34(18):1390-1393. Lopez-Velazquez J A, Chavez-Tapia N C, Ponciano-Rodriguez G, et al. Bilirubin alone as a biomarker for short-term mortality in acute-on-chronic liver failure: an important prognostic indicator[J]. Ann Hepatol, 2013,13(1):98-104. 姜涛, 欧阳文献, 谭艳芳, 等. 儿童急性肝衰竭120例病因和预后分析[J]. 中华实用儿科临床杂志, 2020,35(6):422-425. 苗敏, 钱素云. 儿童急性肝衰竭流行病学研究进展及预后因素分析[J]. 中华急诊医学杂志, 2018,27(11):1302-1307. 张东敬, 周彬, 侯金林. 慢加急性肝衰竭预后模型的研究进展[J]. 临床肝胆病杂志, 2018,34(06):1351-1356. Zheng Y X, Zhong X, Li Y J, et al. Performance of scoring systems to predict mortality of patients with acute-on-chronic liver failure: A systematic review and meta-analysis[J]. J Gastroenterol Hepatol, 2017,32(10):1668-1678. Wu C H, Tian G S, Xu X Y, et al. Assessment of prognosis and curative effect in patients with chronic severe hepatitis using the model for end-stage liver disease scores[J]. Chin Med J (Engl), 2006,119(2):148-150. Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. 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Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-4158601","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Research Article","associatedPublications":[],"authors":[{"id":285785839,"identity":"24f2eb36-5f21-469d-8c25-fe482d0e299b","order_by":0,"name":"Leilei Chen","email":"","orcid":"","institution":"Nanjing University","correspondingAuthor":false,"prefix":"","firstName":"Leilei","middleName":"","lastName":"Chen","suffix":""},{"id":285785840,"identity":"fa9fa1e1-29c9-490c-91e2-f8fd96c6f2d3","order_by":1,"name":"Yucan Zheng","email":"","orcid":"","institution":"Children’s Hospital of Nanjing Medical University","correspondingAuthor":false,"prefix":"","firstName":"Yucan","middleName":"","lastName":"Zheng","suffix":""},{"id":285785841,"identity":"e6ef3066-954a-4112-aedb-89f335712699","order_by":2,"name":"Guorui Hu","email":"","orcid":"","institution":"Children’s Hospital of Nanjing Medical University","correspondingAuthor":false,"prefix":"","firstName":"Guorui","middleName":"","lastName":"Hu","suffix":""},{"id":285785842,"identity":"49e5d12d-98ad-4170-a5c1-ef567cb71959","order_by":3,"name":"chen leilei","email":"","orcid":"","institution":"Children’s Hospital of Nanjing Medical University","correspondingAuthor":false,"prefix":"","firstName":"chen","middleName":"","lastName":"leilei","suffix":""},{"id":285785843,"identity":"72bea41c-5606-4584-ab0d-6541f6a97cf2","order_by":4,"name":"Yan Lu","email":"","orcid":"","institution":"Children’s Hospital of Nanjing Medical University","correspondingAuthor":false,"prefix":"","firstName":"Yan","middleName":"","lastName":"Lu","suffix":""},{"id":285785844,"identity":"8a1ff408-85fd-4166-8af9-f9dec92963ac","order_by":5,"name":"Zhi-feng Liu","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAwklEQVRIiWNgGAWjYDAC5sMNBxgqGJjBHB6itLAlArWcIVULA2MblEOUFvk2xsbDvPPusOvOSGB88LaNQd6ckBbGNsaGw7zbnjGb3UhgNpzbxmC4s4GAFmb5RpCWwyAtbNK8bQwJBgcIaGFjA9kyB6yF/TdRWnjAWhogtjATpUUCqOXgnGNALWceNkvOOSdhuIGQFvk25sMf3tQcTjY7nnzww5syG3mCtsBAMjDwGkC2EqkeCOyIVzoKRsEoGAUjDgAAaIU+eDcP2gEAAAAASUVORK5CYII=","orcid":"","institution":"Nanjing Children’s Hospital, Nanjing University","correspondingAuthor":true,"prefix":"","firstName":"Zhi-feng","middleName":"","lastName":"Liu","suffix":""}],"badges":[],"createdAt":"2024-03-24 15:14:20","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-4158601/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-4158601/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":54769034,"identity":"d1b1f794-9e91-415b-b382-3ed31eac11a3","added_by":"auto","created_at":"2024-04-16 13:42:40","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":276898,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-4158601/v1/93ea5830-78b0-4c49-af5d-aa1b7cf12746.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Clinical features analysis of 105 children with liver failure","fulltext":[{"header":"Introduction","content":"\u003cp\u003eLiver failure is a severe liver damage caused by various factors, leading to severe impairment or compensation failure of synthesis, detoxification, metabolism, and biotransformation functions, resulting in a group of clinical syndromes characterized by jaundice, coagulation dysfunction, hepatorenal syndrome, hepatic encephalopathy, and ascites [1]. As one of the rare clinical diseases, pediatric liver failure is difficult to treat clinically and has a high mortality rate. To explore the clinical features of pediatric liver failure, we conducted a retrospective analysis of the data of 105 cases of pediatric liver failure admitted to XX Hospital, and the results are reported as follows.\u003c/p\u003e\n"},{"header":"Objects and Methods ","content":"\u003cp\u003e1.1\u0026nbsp;\u0026nbsp;Objects\u003c/p\u003e\n\u003cp\u003eFrom February 2012 to February 2023, a total of 105 cases of diagnosed liver failure in children were admitted to XX Hospital. The age range was from 1 day to 14 years and 11 months, with a median age of 1 year and 9 months. There were 67 males and 38 females.1.2 observed indicator\u0026nbsp;\u003c/p\u003e\n\u003ch3\u003e1.2 Observation indicators\u003c/h3\u003e\n\u003cp\u003eThe laboratory tests conducted during the diagnosis of liver failure in admitted patients included complete blood count (leukocyte, WBC; platelet, PLT), biochemical markers (glutamic-pyruvic transaminase, ALT; total bilirubin, TBIL; glutamic oxaloacetic transaminase, AST; albumin, ALB), prothrombin time/Prothrombin activity (PT/PA), fasting blood sugar (GLU), international normalized ratio (INR), and glutamyl transferase (GGT). In addition, some patients underwent blood and urine genetic metabolic and gene testing using gas chromatography-mass spectrometry (GC-MS). Complications that occurred during the course of the disease included multiple organ dysfunction syndrome (MODS), infection, electrolyte imbalance, hypoglycemia, hepatic encephalopathy, ascites, gastrointestinal bleeding, and hepatorenal syndrome.\u003c/p\u003e \u003cdiv id=\"Sec2\" class=\"Section2\"\u003e \u003ch2\u003e1.3 Diagnostic criteria\u003c/h2\u003e \u003cp\u003e The Diagnosis and Treatment Guidelines for Liver Failure (2018 Edition) formulated by the Chinese Society of Infectious Diseases, currently serve as the basis for the diagnosis, treatment, and classification of pediatric liver failure in China.\u003c/p\u003e \u003cp\u003e1.4 Treatment approach: Firstly, treatment is based on the etiology. For all cases, measures are taken to correct coagulation disorders, preserve liver function, alleviate jaundice, administer albumin, reduce intracranial pressure, lower blood ammonia levels, provide anti-infection protect vital organs, etc.\u003c/p\u003e \u003c/div\u003e \u003cdiv id=\"Sec3\" class=\"Section2\"\u003e \u003ch2\u003e1.5 Statistical methods\u003c/h2\u003e \u003cp\u003eStatistical analysis was conducted using EXCEL 2000 and SPSS 26.0 software. Normally distributed continuous data were expressed as mean\u0026thinsp;\u0026plusmn;\u0026thinsp;standard deviation (x\u0026thinsp;\u0026plusmn;\u0026thinsp;SD), and between-group comparisons were performed using the t-test. Non-normally distributed continuous data were expressed as median (interquartile range), and between-group comparisons were performed using the Mann-Whitney U test. Categorical data between two groups were compared using the chi-square test. A p-value\u0026thinsp;\u0026lt;\u0026thinsp;0.05 was considered statistically significant.\u003c/p\u003e \u003c/div\u003e"},{"header":"Results","content":"\u003cp\u003e2.1 General information From February 2012 to February 2023, XX Hospital admitted a total of 105 pediatric patients diagnosed with liver failure, with ages ranging from 0.09 to 14.92 years, with an average age of 4.17 years and a median age of 1.75 years. Among them, there were 67 males and 38 females. Among the patients, there were 37 cases (35.2%) younger than 1 year old, 26 cases (24.8%) between 1 and 3 years old, 13 cases (12.4%) between 3 and 7 years old, 18 cases (17.1%) between 7 and 12 years old, and 11 cases (10.5%) between 12 and 18 years old. The length of hospital stay ranged from 1 to 64 days, with an average of 19.25 days and a median of 17 days (Table \u003cspan\u003e1\u003c/span\u003e).\u003c/p\u003e\n\u003cdiv\u003e\u0026nbsp;\u003ctable id=\"Tab1\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 1\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eAge distribution characteristics of 105 pediatric patients\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eAge(years)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCases\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eAge distribution rate(%)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u0026thinsp;~\u0026thinsp;1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e37\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e35.2\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1\u0026thinsp;~\u0026thinsp;3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e26\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24.8\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3\u0026thinsp;~\u0026thinsp;7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e12.4\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7\u0026thinsp;~\u0026thinsp;12\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e18\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e17.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e12\u0026thinsp;~\u0026thinsp;18\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e合计\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e105\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e100\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e2.2 Disease classification Acute liver failure accounted for 60 cases (57.1%), subacute liver failure for 27 cases (25.7%), subacute-on-chronic liver failure for 8 cases (7.6%), and chronic liver failure (cirrhosis) for 10 cases (9.5%). Acute and subacute liver failure together accounted for 82.8% of all liver failure cases. (Table \u003cspan\u003e2\u003c/span\u003e).\u003c/p\u003e\n\u003cdiv\u003e\u0026nbsp;\u003ctable id=\"Tab2\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 2\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eDistribution characteristics of disease subtypes in 105 pediatric patients\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eDisease classification\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eCases\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003erate(%)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAcute liver failure\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e60\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e57.1\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003esubacute liver failure\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e27\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e25.7\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eacute-on-chronic liver failure\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7.6\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003echronic liver failure\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9.5\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003etotal\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"char\"\u003e\n \u003cp\u003e105\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e100\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e2.3 Etiology analysis Among the 105 patients, there were 24 cases (22.9%) of genetic metabolic diseases, including 2 cases of urea cycle disorders, 3 cases of citrullinemia, 1 case of tyrosinemia, 1 case of arthrogryposis, renal dysfunction, and cholestasis syndrome (ARC syndrome), 2 cases of progressive familial intrahepatic cholestasis, 5 cases of Wilson\u0026apos;s disease, and 2 cases of type 2 infantile liver failure syndrome. There was 1 case of congenital bile acid synthesis disorder, 1 case of Alagille syndrome, and 6 cases of other genetic metabolic diseases. In terms of infection factors, there were 12 cases (11.4%), including 6 cases of sepsis, 2 of which were combined with Epstein-Barr virus infection, 1 case of hepatitis B virus infection, 1 case of measles virus infection, 1 case of varicella-zoster virus combined with Epstein-Barr virus infection, 1 case of influenza virus infection, and 2 cases of other hepatotropic virus infections. There were 10 cases (9.5%) of biliary diseases, including 8 cases of cholestasis, 1 case of choledocholithiasis, and 1 case of cholangitis. There were 6 cases (5.7%) of congenital malformations, 4 cases (3.8%) of autoimmune hepatitis, 3 cases (2.9%) of circulatory failure, 3 cases (2.9%) of drug-related liver injury, including 1 case caused by acetaminophen, 1 case caused by anti-tuberculosis drugs, and 1 case caused by traditional Chinese medicine. There were 2 cases (1.9%) of anorexia nervosa, 2 cases (1.9%) of hemophagocytic syndrome, 1 case (1%) of autoimmune disease, 1 case (1%) of poisoning, 1 case (1%) of tumor, and 36 cases (34.3%) with unknown causes (Table \u003cspan\u003e3\u003c/span\u003e).\u003c/p\u003e\n\u003cdiv\u003e\u0026nbsp;\u003ctable id=\"Tab3\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 3\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eClinical characteristics of children with different etiologies\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\u0026nbsp;\u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003emetabolic disorders(n\u0026thinsp;=\u0026thinsp;24)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eInfection(n\u0026thinsp;=\u0026thinsp;12)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ebiliary tract disease(n\u0026thinsp;=\u0026thinsp;10)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eMalformation(n\u0026thinsp;=\u0026thinsp;6)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eOther Diagnostics(n\u0026thinsp;=\u0026thinsp;17)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eknown cause (n\u0026thinsp;=\u0026thinsp;69)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eunknown cause(n\u0026thinsp;=\u0026thinsp;36)\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eP\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eGender (male/female)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13/11\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10/2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e9/1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4/2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7/10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e46/23\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e21/15\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.143\u003csup\u003ea\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eAge (years), median\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.6(0.5,9.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.7(0.8,6.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.5(0.7,9.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.7(0.6,2.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.8\u0026thinsp;\u0026plusmn;\u0026thinsp;5.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1.6(0.8,8.7)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.1(0.9,5.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.766\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eInfant (n=)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e24\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eKindergarten(n=)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003epreschool period(n=)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eschool age(n=)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eadolescence(n=)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\u0026nbsp;\u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eINR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.5(1.9,3.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.2\u0026thinsp;\u0026plusmn;\u0026thinsp;1.3\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.0\u0026thinsp;\u0026plusmn;\u0026thinsp;0.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.1\u0026thinsp;\u0026plusmn;\u0026thinsp;0.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.0(1.2,3.4)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.0(1.5,3.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2.0(1.4,2.9)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.893\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eALT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e315.0(70.0,1140.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1519.5(428.3, 3507.5 )\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e153.0(103.8,1674.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e339.0\u0026thinsp;\u0026plusmn;\u0026thinsp;347.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1505.0(136,4431.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e491.0(104.5,2092.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1508.0(593.5,3129.6)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.001\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ehepatic encephalopathy(n=)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e7(36.8%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e6(50%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e3(30%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e1(16.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4(36.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e26(37.7%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e16(44.4%)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.412\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eTBIL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e139.3\u0026thinsp;\u0026plusmn;\u0026thinsp;135.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e74.6\u0026thinsp;\u0026plusmn;\u0026thinsp;60.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e275.4\u0026thinsp;\u0026plusmn;\u0026thinsp;265.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e347.7\u0026thinsp;\u0026plusmn;\u0026thinsp;229.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e50(25.8,97.1)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e123.1(32.9,249.3)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e114.3(35.9,185.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.926\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eGGT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e56(29,157)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e144.3\u0026thinsp;\u0026plusmn;\u0026thinsp;125.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e119.1\u0026thinsp;\u0026plusmn;\u0026thinsp;81.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e110\u0026thinsp;\u0026plusmn;\u0026thinsp;88.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e136.0\u0026thinsp;\u0026plusmn;\u0026thinsp;117.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e82.0(39.5,176.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e95.5(56.8,156.8)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.223\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eblood ammonia\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e92.6\u0026thinsp;\u0026plusmn;\u0026thinsp;61.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e85.4\u0026thinsp;\u0026plusmn;\u0026thinsp;51.1\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e100.8\u0026thinsp;\u0026plusmn;\u0026thinsp;57.4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e38.5(28.3,81.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e62(46.5,86)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e69.0(46.3,113.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e76\u0026thinsp;\u0026plusmn;\u0026thinsp;44.9\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.708\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ePLT\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e87.0(51.0,324.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e226.5\u0026thinsp;\u0026plusmn;\u0026thinsp;147.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e233.6\u0026thinsp;\u0026plusmn;\u0026thinsp;132.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e107.0\u0026thinsp;\u0026plusmn;\u0026thinsp;54.2\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e160.8\u0026thinsp;\u0026plusmn;\u0026thinsp;152.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e153.0(71.0,312.0)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e207.6\u0026thinsp;\u0026plusmn;\u0026thinsp;139.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.421\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003ealbumin\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e35.4\u0026thinsp;\u0026plusmn;\u0026thinsp;7.0\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e37.5\u0026thinsp;\u0026plusmn;\u0026thinsp;5.5\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e38.1\u0026thinsp;\u0026plusmn;\u0026thinsp;4.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e33.9\u0026thinsp;\u0026plusmn;\u0026thinsp;6.7\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e40.2(36.1,43.5)\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e36.4\u0026thinsp;\u0026plusmn;\u0026thinsp;6.8\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e39.6\u0026thinsp;\u0026plusmn;\u0026thinsp;6.6\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0.049\u003csup\u003eb\u003c/sup\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"9\"\u003e\n \u003cp\u003ea\u0026nbsp;Comparing total diagnosis and uncertainty using independent sample t-tests\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\" colspan=\"9\"\u003e\n \u003cp\u003eb\u0026nbsp;Comparing total diagnosis and uncertainty using Mann Whitney U-test\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003ctfoot\u003e\n \u003ctr\u003e\n \u003ctd colspan=\"9\"\u003eINR: International normalized ratio ; ALT:glutamic-pyruvic transaminase;ALT:glutamic-pyruvic transaminase; TBIL: total bilirubin; GGT: Glutamyl transferase;PLT: Blood platelet\u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tfoot\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003e\u003cspan\u003e2.4 Clinical manifestations of liver failure at onset include a decrease in appetite, which is the most common presentation (96.2%), followed by fever (75.3%), visible jaundice (71.4%), and various neurological abnormalities such as lethargy, seizures, irritability, consciousness and behavioral disorders (53.3%). Other common symptoms include nausea, vomiting, diarrhea, and abdominal distension (52.4%).In terms of physical signs, hepatomegaly (enlarged liver) is observed in 75.2% of cases, splenomegaly (enlarged spleen) in 39.0% of cases, and hepatosplenomegaly (enlarged liver and spleen) in 34.3% of cases.\u003cbr\u003e\u003c/span\u003e\u003cspan\u003e2.5 Analysis of the Characteristics of Complications. Electrolyte disturbances were observed in 63 cases (60%), which were the most common. Among these 63 cases, 35 cases (33.3%) had hyponatremia, 47 cases (44.8%) had hypocalcemia, 26 cases (24.8%) had hypokalemia, 4 cases (3.8%) had hyperkalemia, 23 cases had hypochloremia, and 15 cases (14.3%) had hypophosphatemia. Additionally, there were 62 cases (59%) of hypoalbuminemia. In 42 cases (40%), hepatic encephalopathy was observed. Ascites was present in 37 cases (35.2%), and pleural effusion was present in 32 cases (30.5%). Among them, 23 cases (21.9%) had both ascites and pleural effusion. Other site infections were observed in 62 cases (59%), with sepsis, respiratory tract infections, and gastrointestinal infections being the most common. Petechiae and ecchymosis were present in 35 cases (33.3%). Peripheral edema was observed in 26 cases (24.8%). Thrombocytopenia was seen in 32 cases (30.5%). Hypoglycemia was present in 34 cases (32.4%). Multiple Organ Dysfunction Syndrome (MODS) was observed in 19 cases, accounting for 18.1%. 11 cases (10.5%) presented with gastrointestinal bleeding, characterized by vomiting of coffee-colored material, melena, and the presence of red blood cells and positive fecal occult blood tests. There were 9 cases (8.6%) of liver cirrhosis. Liver-kidney syndrome was observed in 9 cases (8.6%), all of which exhibited oliguria (reduced urine output) and elevated levels of blood urea nitrogen and serum creatinine.\u003cbr\u003e\u003c/span\u003e\u003cspan\u003e2.6 Outcome and prognosis. Among the 105 cases, 83 cases (79%) showed improvement, 20 cases (19.1%) resulted in death, and 2 cases (1.9%) were transferred to another hospital. Based on the survival status of the children on the 28th day, they were categorized as follows:\u003cbr\u003e\u003c/span\u003e\u003c/p\u003e\n\u003cp\u003eSurvival group (83 cases): Patients whose condition improved, transferred from the ICU to a general ward, and discharged.\u003c/p\u003e\n\u003cp\u003eDeath group (20 cases): Patients who died during the 28-day observation period.\u003c/p\u003e\n\u003cp\u003eIn the survival group, the PELD/MELD score, total bilirubin, and INR (International Normalized Ratio) were lower compared to the death group, while platelet count was higher, with statistically significant differences (P\u0026thinsp;\u0026lt;\u0026thinsp;0.05). There were no statistically significant differences (P\u0026thinsp;\u0026gt;\u0026thinsp;0.05) between the two groups in terms of age, albumin level, blood ammonia level, presence of hepatic encephalopathy, ALT (alanine aminotransferase), and GGT (gamma-glutamyl transferase), as shown in Table \u003cspan\u003e4\u003c/span\u003e.Among the 89 cases with a PELD/MELD score below 30, 13 cases (14.6%) resulted in death. Among the 10 cases with a score between 30 and 40, 5 cases (50%) resulted in death. Among the 4 cases with a score above 40, 2 cases (50%) resulted in death. As the score increased, the mortality rate also increased ( Table \u003cspan\u003e5\u003c/span\u003e).The prognostic evaluation of liver failure in children, as assessed by the ROC curve, yielded an AUC (Area Under the Curve) value of 0.753 (P\u0026thinsp;\u0026lt;\u0026thinsp;0.001). The standard error was 0.064, with a 95% confidence interval of (0.627\u0026ndash;0.879).\u003c/p\u003e\n\u003cp\u003e\u003cimg src=\"https://myfiles.space/user_files/122228_c8a1650c59388082/122228_custom_files/img1711959104.png\"\u003e\u003cbr\u003e\u003c/p\u003e\n\u003cdiv\u003e\u003cbr\u003e\u003c/div\u003e\n\u003cdiv\u003e\u0026nbsp;\u003ctable id=\"Tab5\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv\u003eTable 5\u003c/div\u003e\n \u003cdiv\u003e\n \u003cp\u003eThe outcome of the disease in the PELD/MELD scoring system\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003ePELD/MELD\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003en\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003edeath(n, %)\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e0～30\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e89\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e13(14.6%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e30～40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e10\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5(50%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u0026gt;40\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e4\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e2(50%)\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e"},{"header":"Discussion","content":"\u003cp\u003ePediatric liver failure is a rare clinical condition with a low incidence rate but a high mortality rate. Currently, there is a lack of epidemiological studies on pediatric liver failure in China. Some related studies only focus on acute liver failure in children. In the United States, it is estimated that there are 500\u0026ndash;600 cases of acute liver failure in children per year in the entire population. The incidence of Pediatric Acute Liver Failure (PALF) in the United States does not vary by region and has remained stable over the past decade [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. There is no statistically significant difference in the incidence rates between different regions over a span of six years [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eThe etiology of pediatric liver failure is complex and difficult to determine. The most common cause of liver failure is genetic metabolic disorders, accounting for 24 cases (22.9%). Infection factors are the second most common, accounting for 12 cases (11.4%), followed by biliary diseases in 10 cases (9.5%), congenital malformations in 6 cases (5.7%), and autoimmune hepatitis in 4 cases (3.8%), among others. However, approximately 34.3% of the cases still have an unknown etiology. This conclusion is consistent with the research findings from the National University of Singapore, Institute of Pediatrics [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Consistent with the results of a prospective, multicenter study conducted abroad, over one-third of pediatric acute liver failure patients have an unknown etiology. Despite advancements in diagnostic methods, this proportion reaches two-thirds in patients between the ages of 1 and 5 with acute liver failure [\u003cspan additionalcitationids=\"CR5\" citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Given the fact that children, especially infants and young children, have a lower immune function and lower levels of peripheral blood antibodies, it becomes difficult to detect pathogen-specific antibodies. Additionally, children with liver failure have impaired coagulation function, increasing the risk of bleeding. Pathological examination cannot determine the cause through liver puncture. Studies in the United States and Europe have observed that acetaminophen poisoning is the most common cause of acute liver failure in children [\u003cspan additionalcitationids=\"CR7\" citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. Inherited metabolic liver diseases can occur at any age, such as Wilson's disease (hepatolenticular degeneration), tyrosinemia, and infantile liver failure syndrome.According to reports, Wilson's disease is the most common inherited metabolic disease causing liver failure in children [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e]. In this study, all 5 cases of hepatolenticular degeneration occurred during the school-age period, accounting for 27.8% of liver failure cases in this age group. Therefore, Wilson's disease should be a particular focus for children with liver failure in this age group. A high proportion of infectious etiology was observed in school-age children (22.2%), while in all other age groups, the percentage of infectious causes was roughly similar among all cases (11.8% in infancy, 7.6% in early childhood, 7.7% in preschool period, and 9.1% in adolescence). Congenital developmental abnormalities generally manifest in infancy (4 cases in infancy, accounting for 66.7% of congenital developmental abnormalities). Prolonged jaundice after birth leads to complications such as liver cirrhosis, ascites, and infections, ultimately resulting in liver failure. The most common causes of liver failure in infants with congenital developmental abnormalities are biliary atresia and congenital choledochal cysts. In this study, all 6 cases of congenital developmental abnormalities were biliary atresia, which is an important cause of liver failure in the infant group. It has been observed that an increasing number of autosomal recessive inherited monogenic diseases affect intracellular transport and vesicular trafficking, which are becoming important factors in patients with acute liver failure (ALF) of unknown etiology. Reducing the proportion of liver failure cases with unknown causes remains a challenge. Out of 34 patients, whole-genome sequencing was performed. Diagnosis was established in 18 children, and genetic variants associated with inherited metabolic liver diseases were identified, including \u003cem\u003eSLC25A13\u003c/em\u003e, \u003cem\u003eJAG1\u003c/em\u003e, \u003cem\u003eUSP53\u003c/em\u003e, \u003cem\u003eAKR1D1\u003c/em\u003e, \u003cem\u003eNBAS\u003c/em\u003e, \u003cem\u003eOTC\u003c/em\u003e, \u003cem\u003eATP7B\u003c/em\u003e, \u003cem\u003eVPS33B\u003c/em\u003e, \u003cem\u003eABCB4\u003c/em\u003e, among others. Additionally, gene variations in \u003cem\u003eGPR82\u003c/em\u003e, \u003cem\u003eATP11C\u003c/em\u003e, \u003cem\u003eNCOA6\u003c/em\u003e, \u003cem\u003eALMS1\u003c/em\u003e\u003c/p\u003e \u003cp\u003e, etc., were discovered, but there are currently no related literature reports on their association with childhood liver failure. More research is needed to elucidate the potential of whole-exome/genome sequencing in the management of childhood liver failure, including its use as a means for early diagnosis and assessment.\u003c/p\u003e \u003cp\u003eEarly diagnosis of liver function failure is crucial for treatment and prognosis. The most common presenting symptom is decreased appetite, accounting for 96.2%. Fever is the second most common symptom (75.3%), followed by jaundice (71.4%). Among these cases, sepsis, respiratory tract infections, and gastrointestinal infections are the most frequently observed, with some cases involving biliary infections. One case of bile peritonitis was identified. These findings are similar to those reported by the PLA General Hospital [\u003cspan citationid=\"CR10\" class=\"CitationRef\"\u003e10\u003c/span\u003e] and studies from Turkey [\u003cspan citationid=\"CR9\" class=\"CitationRef\"\u003e9\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eCurrently, effective treatment options for pediatric acute liver failure include medication, artificial liver support, and even liver transplantation. However, the overall mortality rate of pediatric acute liver failure is reported to range between 20% and 50%, indicating poor clinical outcomes [\u003cspan additionalcitationids=\"CR12 CR13\" citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e\u0026ndash;\u003cspan citationid=\"CR14\" class=\"CitationRef\"\u003e14\u003c/span\u003e]. In this dataset, there were 20 deaths (19.1%), which is consistent with international reports.\u003c/p\u003e \u003cp\u003eIn this study, the serum total bilirubin levels of the deceased children were significantly higher than those of the surviving children, which is consistent with previous research findings [\u003cspan citationid=\"CR15\" class=\"CitationRef\"\u003e15\u003c/span\u003e, \u003cspan citationid=\"CR16\" class=\"CitationRef\"\u003e16\u003c/span\u003e]. The massive necrosis of liver cells inhibits the conversion of unconjugated bilirubin to conjugated bilirubin, and the accumulation of bile can lead to elevated levels of conjugated bilirubin in the blood. The combined effect of these factors results in an elevation of total bilirubin levels [\u003cspan citationid=\"CR17\" class=\"CitationRef\"\u003e17\u003c/span\u003e]. This plays an important role in predicting prognosis. The liver synthesizes most of the clotting factors, and the significant decrease in clotting factors due to liver cell necrosis leads to abnormal coagulation function. This results in an increased INR (international normalized ratio) value, which is an important diagnostic and prognostic indicator for liver failure. In this study, the INR levels of the deceased children were significantly higher than those of the surviving children, which is consistent with related research findings [\u003cspan citationid=\"CR18\" class=\"CitationRef\"\u003e18\u003c/span\u003e, \u003cspan citationid=\"CR19\" class=\"CitationRef\"\u003e19\u003c/span\u003e]. The PELD/MELD scoring system utilizes objective parameters to assess the condition of liver failure patients and provides an accurate reflection of their disease severity. It is widely used in the management of end-stage liver disease patients [\u003cspan citationid=\"CR20\" class=\"CitationRef\"\u003e20\u003c/span\u003e]. Studies suggest that the PELD/MELD system is superior to other scoring systems in predicting patient prognosis [\u003cspan citationid=\"CR11\" class=\"CitationRef\"\u003e11\u003c/span\u003e, \u003cspan citationid=\"CR21\" class=\"CitationRef\"\u003e21\u003c/span\u003e]. The relationship between PELD/MELD scores and the 3-month mortality rate of end-stage liver disease patients is as follows: \u0026le;30 points, 40% mortality rate; \u0026gt;30 to \u0026lt;\u0026thinsp;40 points, 72% mortality rate; \u0026ge;40 points, 100% mortality rate. This indicates that PELD/MELD can accurately assess the severity of end-stage liver disease and effectively predict the short-term prognosis of liver failure patients [\u003cspan citationid=\"CR22\" class=\"CitationRef\"\u003e22\u003c/span\u003e]. The PELD/MELD scores in the deceased group were higher than those in the surviving group (P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), and the higher the score, the higher the mortality rate (Table\u0026nbsp;\u003cspan refid=\"Tab5\" class=\"InternalRef\"\u003e5\u003c/span\u003e). Furthermore, the area under the receiver operating characteristic (ROC) curve (AUC) for the prognostic evaluation of pediatric liver failure patients was 0.753 (P\u0026thinsp;\u0026lt;\u0026thinsp;0.001), with a standard error of 0.064 and a 95% confidence interval of 0.627 to 0.879. This suggests that the PELD/MELD scoring system has a good evaluation performance. The receiver operating characteristic (ROC) curve analysis of the PELD/MELD scoring system confirms its good evaluation capability.\u003c/p\u003e"},{"header":"conclusion","content":"\u003cp\u003eCurrently, both the basic and clinical research on pediatric liver failure lag behind that of adults. So far, there is no globally accepted guideline for pediatric liver failure. It is essential to pay attention to clinical and basic research related to pediatric liver failure. This study indicates that genetic metabolic disorders, infections, and biliary anomalies are common causes of pediatric liver failure. The MELD or PELD scoring systems can predict the prognosis of liver failure in children. The clinical characteristic analysis of pediatric liver failure and the application of MELD or PELD scores will help guide clinical diagnosis, treatment, and prognosis assessment.\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eETHICS APPROVAL AND CONSENT TO PARTICIPATE \u0026nbsp; \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWe have cancelled the patient\u0026apos;s details.We have obtained the parents\u0026rsquo; consent and signatures on the informed consent form. This study was approved by the Ethics Committee of Nanjing Children\u0026apos;s Hospital, Nanjing, China(202311016-1).\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eCONSENT FOR PUBLICATION\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eAVAILABILITY OF DATA AND MATERIALS \u0026nbsp; \u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eCOMPETING INTERESTS \u0026nbsp; \u0026nbsp;\u0026nbsp;\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u0026nbsp;\u003c/strong\u003e\u003cstrong\u003eAUTHOR CONTRIBUTIONS\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eLC and YZ contributed to the study design, data collection, analysis, and manuscript preparation. GH,JZ and YL contributed to data analysis, manuscript preparation, and revised the manuscript. ZL contributed to the study design and critically revised the manuscript. All authors read and approved the final manuscript.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eLiver Failure And Artificial Liver Group Chinese Society Of Infectious, Severe Liver Disease And Artificial Liver Group Chinese Society Of Hepatology. 肝衰竭诊治指南(2018年版)[J]. 实用肝脏病杂志, 2019,22(02):164-171.\u003c/li\u003e\n\u003cli\u003eKulkarni S, Perez C, Pichardo C, et al. Use of Pediatric Health Information System database to study the trends in the incidence, management, etiology, and outcomes due to pediatric acute liver failure in the United States from 2008 to 2013[J]. Pediatr Transplant, 2015,19(8):888-895.\u003c/li\u003e\n\u003cli\u003eChiou F K, Logarajah V, Ho C, et al. Demographics, aetiology and outcome of paediatric acute liver failure in Singapore[J]. Singapore Med J, 2022,63(11):659-666.\u003c/li\u003e\n\u003cli\u003eAlonso E M, Horslen S P, Behrens E M, et al. Pediatric acute liver failure of undetermined cause: A research workshop[J]. Hepatology, 2017,65(3):1026-1037.\u003c/li\u003e\n\u003cli\u003eLenz D, Horby J M, Kelly D, et al. Etiology and Outcome of Adult and Pediatric Acute Liver Failure in Europe[J]. J Pediatr Gastroenterol Nutr, 2023,77(1):115-120.\u003c/li\u003e\n\u003cli\u003eDi Giorgio A, Gamba S, Sansotta N, et al. Identifying the Aetiology of Acute Liver Failure Is Crucial to Impact Positively on Outcome[J]. Children (Basel), 2023,10(4).\u003c/li\u003e\n\u003cli\u003eKathemann S, Bechmann L P, Sowa J P, et al. Etiology, outcome and prognostic factors of childhood acute liver failure in a German Single Center[J]. Ann Hepatol, 2015,14(5):722-728.\u003c/li\u003e\n\u003cli\u003eFontana R J. Acute liver failure including acetaminophen overdose[J]. Med Clin North Am, 2008,92(4):761-794.\u003c/li\u003e\n\u003cli\u003eBaris Z, Saltik T I, Uslu N, et al. Acute liver failure in children: 20-year experience[J]. Turk J Gastroenterol, 2012,23(2):127-134.\u003c/li\u003e\n\u003cli\u003e朱世殊张鸿飞陈菊梅杨晓晋徐志强. 儿童肝衰竭临床特征的研究[J]. 中华实验和临床病毒学杂志, 2004(04).\u003c/li\u003e\n\u003cli\u003eNunez-Ramos R, Montoro S, Bellusci M, et al. Acute Liver Failure: Outcome and Value of Pediatric End-Stage Liver Disease Score in Pediatric Cases[J]. Pediatr Emerg Care, 2018,34(6):409-412.\u003c/li\u003e\n\u003cli\u003eChapin C A, Horslen S P, Squires J E, et al. Corticosteroid Therapy for Indeterminate Pediatric Acute Liver Failure and Aplastic Anemia with Acute Hepatitis[J]. J Pediatr, 2019,208:23-29.\u003c/li\u003e\n\u003cli\u003eWands D, Tayler R, Kelly D, et al. Infantile acute liver failure in the West of Scotland[J]. Arch Dis Child, 2020,105(8):794-796.\u003c/li\u003e\n\u003cli\u003eYankol Y, Ertugrul M, Kanmaz T, et al. Management of Pediatric Acute Liver Failure in a Region With Insufficient Deceased Donor Support: A Single-Center Experience[J]. Exp Clin Transplant, 2016,14(5):535-541.\u003c/li\u003e\n\u003cli\u003e苗敏, 钱素云. 儿童急性肝衰竭病因及转归相关因素分析[J]. 中华实用儿科临床杂志, 2019,34(19):1462-1466.\u003c/li\u003e\n\u003cli\u003e罗兰, 刘萍萍, 隆彩霞, 等. 重症儿童急性肝衰竭预后的相关因素[J]. 中华实用儿科临床杂志, 2019,34(18):1390-1393.\u003c/li\u003e\n\u003cli\u003eLopez-Velazquez J A, Chavez-Tapia N C, Ponciano-Rodriguez G, et al. Bilirubin alone as a biomarker for short-term mortality in acute-on-chronic liver failure: an important prognostic indicator[J]. Ann Hepatol, 2013,13(1):98-104.\u003c/li\u003e\n\u003cli\u003e姜涛, 欧阳文献, 谭艳芳, 等. 儿童急性肝衰竭120例病因和预后分析[J]. 中华实用儿科临床杂志, 2020,35(6):422-425.\u003c/li\u003e\n\u003cli\u003e苗敏, 钱素云. 儿童急性肝衰竭流行病学研究进展及预后因素分析[J]. 中华急诊医学杂志, 2018,27(11):1302-1307.\u003c/li\u003e\n\u003cli\u003e张东敬, 周彬, 侯金林. 慢加急性肝衰竭预后模型的研究进展[J]. 临床肝胆病杂志, 2018,34(06):1351-1356.\u003c/li\u003e\n\u003cli\u003eZheng Y X, Zhong X, Li Y J, et al. Performance of scoring systems to predict mortality of patients with acute-on-chronic liver failure: A systematic review and meta-analysis[J]. J Gastroenterol Hepatol, 2017,32(10):1668-1678.\u003c/li\u003e\n\u003cli\u003eWu C H, Tian G S, Xu X Y, et al. Assessment of prognosis and curative effect in patients with chronic severe hepatitis using the model for end-stage liver disease scores[J]. Chin Med J (Engl), 2006,119(2):148-150.\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":true,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"Children, liver failure, hereditary metabolic disease, infection, biliary malformation","lastPublishedDoi":"10.21203/rs.3.rs-4158601/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-4158601/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eObjective\u003c/strong\u003e \u0026nbsp;To study the clinical features of pediatric liver failure and provide reference for diagnosis and prevention. \u003cstrong\u003eMethods\u003c/strong\u003e \u0026nbsp;Clinical data of children diagnosed with liver failure at XX Hospital from 2012 to 2023 were collected and statistically analyzed.\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eResults\u003c/strong\u003e Among 105 cases of liver failure in children, the age ranged from 1 day to 14 years and 11 months, with a median age of 1 year and 9 months. There were 67 males and 38 females, with acute and subacute liver failure accounting for 82.8%. The most common causes were hereditary metabolic diseases (24 cases, 22.9%), followed by infection factors (12 cases, 11.4%), and biliary diseases (10 cases, 9.5%). However, the cause remained unknown in 34.3% of cases. The most common clinical manifestations were poor appetite, fever, and jaundice. The main complications were hepatic encephalopathy, electrolyte disorders, and infection. There was no statistically significant difference in age, albumin, blood ammonia, presence of hepatic encephalopathy, ALT, and GGT between the survival group and the 28-day mortality group (P\u0026gt;0.05). The survival group had lower PELD/MELD scores, total bilirubin, and INR, and higher platelet count compared to the 28-day mortality group, with statistically significant differences (P\u0026lt;0.05).\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e Hereditary metabolic diseases, infection, and biliary diseases are common causes of pediatric liver failure. MELD/PELD scores can predict the prognosis of liver failure. Clinical feature analysis and MELD/PELD scores are helpful in guiding clinical diagnosis, treatment, and prognosis assessment.\u003c/p\u003e","manuscriptTitle":"Clinical features analysis of 105 children with liver failure","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-04-01 08:20:24","doi":"10.21203/rs.3.rs-4158601/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"fa451016-5aeb-4717-9958-84b842e8e313","owner":[],"postedDate":"April 1st, 2024","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"posted","subjectAreas":[],"tags":[],"updatedAt":"2024-04-16T13:34:33+00:00","versionOfRecord":[],"versionCreatedAt":"2024-04-01 08:20:24","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-4158601","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-4158601","identity":"rs-4158601","version":["v1"]},"buildId":"qtupq5eGEP_6zYnWcrvyt","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}